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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > F ro nt o f Bo o k > Edito rs
Editors
Jeffrey Schaider MD Associate Professor of Em ergency Medicine Rush Medical College; Chairm an, Departm ent of Em ergency Medicine, Cook County Hospital, Chicago, Illinois Stephen R. Hayden MD Professor of Clinical Medicine, Program Director, Residency Program Departm ent of Em ergency Medicine, University of California San Diego; Editor-in-Chief, Journal of Em ergency Medicine, Medical Center, San Diego, California Richard Wolfe MD Associate Professor Division of Em ergency Medicine, Harvard Medical School; Chief of Em ergency Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts Roger M. Barkin MD Professor of Surgery Division of Em ergency Medicine, University of Colorado Health Science Center; Vice President for Pediatric and Newborn Program s and Vice President of Medical Services, Healthone, Denver, Colorado Peter Rosen MD Associate Professor Harvard University; Attending Physician, Beth Israel Deaconess Hospital, Boston, Massachusetts; Attending Physician, St. John's Hospital, Jackson Hole, Wyom ing; Visiting Professor, University of Arizona, Tucson, Arizona
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Secondary Editors Frances R. DeStefano Acquisitions Editor Nicole Demoski Managing Editor David Murphy Project Manager Benjamin Rivera Senior Manufacturing Manager Angela Panetta Marketing Manager Teresa Mallon Design Coordinator TechBooks Production Service Courier Westford Printer
Contributors Barrett Adams M.D. Physician Departm ent of Em ergency Medicine, University of Arizona, Tucson, Arizona James Adams M.D. Professor and Chair Departm ent of Em ergency Medicine, Northwestern University, Feinberg School of Medicine, Northwestern Mem orial Hospital, Chicago, Illinois Mitchell Adelstein M.D. Assistant Professor Departm ent of Em ergency Medicine, St. Luke's Hospital, New York, New York
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Steven Aks D.O. Associate Professor Departm ent of Em ergency Medicine, Rush University; Director, The Toxikon Consortium , Section of Toxicology, Departm ent of Em ergency Medicine, John H. Stroger Hospital of Cook County, Chicago, Illinois Amer Aldeen M.D. Attending Physician Departm ent of Em ergency Medicine, Feinburg School of Medicine, Northwestern Mem orial Hospital, Chicago, Illinois Nadeem Al-Duaij M.D. Clinical Fellow Departm ent of Em ergency Medicine, Harvard Medical School, Harvard Affiliated Em ergency Medicine Residency, Beth Israel Deaconess Medical Center, Boston, Massachusetts Paul Allegretti D.O., F.A.C.O.E.P. Associate Professor and Program Director Departm ent of Em ergency Medicine, Midwestern University/Chicago College of Osteopathic, Medicine, Downers Grove, Illinois; Attending Physician, Departm ent of Em ergency Medicine, Provident Hospital of Cook County, Chicago, Illinois Marilyn Althoff M.D. Faculty Departm ent of Medicine, Morristown Mem orial Hospital, Morristown, New Jersey Philip D. Anderson M.D. Assistant Professor Departm ent of Em ergency Medicine, Harvard Medical School; Attending Physician, Departm ent of Em ergency Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts Paul A. Andrulonis M.D. Assistant Medical Director
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Departm ent of Em ergency Medicine, Mem orial Hospital West, Pem broke Pines, Florida Rebecca Apollon M.D. Clinical Associate Departm ent of Em ergency Medicine, Tufts University School of Medicine, Boston, Massachusetts, Post-Graduate Year 2, Departm ent of Em ergency Medicine, Baystate Medical Center, Springfield, Massachusetts L. Kristian Arnold M.D. Chief Medical Officer Arlac Health Services, Lexington, Massachusetts Paul Arnold M.D., B.Sc. Clinical Instructor Departm ent of Surgery, University of Toronto; Staff Physician, Departm ent of Em ergency Medicine, University of Health Network, Toronto, Ontario Andrew A. Aronson M.D. Attending Physician Departm ent of Em ergency Medicine, Allegheny General Hospital, Pittsburgh, Pennsylvania Veronique Au M.D. Departm ent of Em ergency Medicine, Alta Bates Sum m it Medical Center, Berkeley, California Elisa Aumont M.D. Departm ent of Em ergency Medicine, University of Mississippi Medical Center, Jackson, Mississippi Brandon H. Backlund M.D. Attending Physician Departm ent of Em ergency Medicine, Wahiawa General Hospital, Wahiawa, Hawaii; Attending Physician, Departm ent of Em ergency Medicine, Castle Medical Center, Kailua, Hawaii John Bailitz M.D.
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Assistant Professor Departm ent of Em ergency Medicine, Rush Medical College; Assistant Program Director, Departm ent of Em ergency Medicine, Cook County Hospital, Chicago, Illinois Amy Baldwin M.D. Physician Departm ent of Em ergency Medicine, University of Arizona, Tucson, Arizona Adam Z. Barkin M.D. Instructor Departm ent of Medicine, Harvard Medical School; Attending Physician, Departm ent of Em ergency Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts Roger Barkin M.D., M.P.H., F.A.A.P., F.A.C.E.P. Professor of Surgery Division of Em ergency Medicine, University of Colorado Health Science Center; Vice President for Pediatric and Newborn Program s, and Vice President of Medical Services Healthone, Denver, Colorado Suzanne Z. Barkin M.D. Associate Professor of Radiology (Pediatrics) Departm ent of Radiology, Denver Health Medical Center, Denver, Colorado David Barlas M.D. F.A.C.E.P. Assistant Professor Departm ent of Em ergency Medicine, Cornell University College of Medicine, New York, New York; Associate Program Director, Departm ent of Em ergency Medicine, New York Hospital Medical Center of Queens, Flushing, New York Eric Barton M.D. Associate Professor of Surgery (EM), Chief Division of Em ergency Medicine, University of Utah Health Sciences Center, Salt Lake City, Utah
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Kathleen Bassett M.D. Assistant Professor of Pediatrics University of Utah School of Medicine, Salt Lake City, Utah Beverly Bauman M.D. F.A.A.P., F.A.C.E.P. Assistant Professor Departm ent of Em ergency Medicine, Oregon Health and Sciences University, Portland, Oregon Jamil D. Bayram M.D. Assistant Professor Departm ent of Em ergency Medicine, Rush University Medical Center, John H. Stroger Hospital of Cook County, Chicago, Illinois B. J. Beck M.S.N., M.D. Clinical Instructor Departm ent of Psychiatry, Harvard Medical School; Clinical Assistant, Departm ent of Psychiatry, Massachusetts General Hospital, Boston, Massachusetts; Staff Psychiatrist, Departm ent of Psychiatry, Anna Jaques Hospital, Newburyport, Massachusetts Kyan J. Berger M.D., F.A.A.E.M. Em ergency Physician Departm ent of Em ergency Medicine, Beverly Hospital and Addison Gilbert Hospital, Beverly, Massachusetts Matthew R. Berkman M.D. Resident Departm ent of Em ergency Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts Herbert G. Bivins M.D. Clinical Professor Departm ent of Em ergency Medicine, University of California at Fresno; Program Director, Departm ent of Em ergency Medicine, University Medical Center, Fresno, California Adam Black M.D. Assistant Director
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Departm ent of Em ergency Medicine, St. Elizabeth's Hospital, Chicago, Illinois Paul Blackburn D.O., F.A.C.O.E.P., F.A.C.E.P. Program Director Departm ent of Em ergency Medicine, Maricopa Medical Center, Phoenix, Arizona Keith S. Boniface M.D. Assistant Professor, Assistant Residency Director Departm ent of Em ergency Medicine; Director, Sonography; Assistant Medical Director, Maritim e Medical Access, The George Washington University, Washington, D.C. Michael J. Bono M.D., Ph.D. Professor, Associate Director Departm ent of Em ergency Medicine and Em ergency, Medicine Residency Program , Eastern Virginia Medical School, Norfolk, Virginia Steven H. Bowman M.D. Assistant Professor Departm ent of Em ergency Medicine, Rush Medical College; Program Director, Departm ent of Em ergency Medicine, John H. Stroger Hospital of Cook County, Chicago, Illinois Jefferson D. Bracey D.O. Clinical Assistant Professor Departm ent of Surgery, University of Nevada School of Medicine, Las Vegas, Nevada; Assistant Medical Director, Departm ent of Em ergency Medicine, St. Rose Dom inican Hospital, Henderson, Nevada Andrea Bracikowski M.D. Associate Professor Departm ents of Em ergency Medicine and Pediatrics, Vanderbilt University Medical Center; Attending Physician, Departm ent of Pediatric Em ergency Medicine, Vanderbilt Children's Hospital, Nashville, Tennessee Kenneth Bramwell M.D.
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Departm ent of Pediatric Em ergency, Medicine, University of Arizona, Tuscon, Arizona Harminder Brar M.D. Resident Physician Departm ent of Em ergency Medicine, John H. Stroger Hospital of Cook County, Chicago, Illinois Lorna M. Breen M.D. Assistant in Clinical Medicine Departm ent of Medicine, Colum bia University College of Physicians and, Surgeons; Assistant Attending Physician, Departm ent of Em ergency Medicine, New York Presbyterian Hospital, New York, New York Allison V. Brewer M.D. Senior Resident Departm ent of Em ergency Medicine, Tufts University School of Medicine; Senior Resident, Departm ent of Em ergency Medicine, Baystate Medical Center, Springfield, Massachusetts Judith C. Brillman M.D. Professor of Em ergency Medicine, Assistant Dean Graduate Medical, Education, University of New Mexico, Albuquerque, New Mexico Calvin A. Brown III M.D. Clinical Instructor Harvard Medical School; Attending Physician, Departm ent of Em ergency Medicine, Brigham and Wom en's Hospital, Boston, Massachusetts David F. M. Brown M.D. Assistant Professor Departm ent of Em ergency Medicine, Harvard Medical School; Vice Chairm an, Departm ent of Em ergency Medicine, Massachusetts General Hospital, Boston, Massachusetts Lance Brown M.D., M.P.H.
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Associate Professor of Em ergency Medicine and, Pediatrics Departm ent of Em ergency Medicine, Lom a Linda University; Chief, Division of Pediatric Em ergency Medicine, Departm ent of Em ergency Medicine, Lom a Linda University Medical Center and Children's, Hospital, Lom a Linda, California Brian Browne M.D., F.A.C.E.P. Professor Departm ent of Em ergency Medicine and, Medicine; Acting Chairm an, Director, Em ergency Medical Services, University of Maryland Medical Center, Baltim ore, Maryland Sean Bryant M.D. Assistant Professor Departm ent of Em ergency Medicine, Rush Medical College; Attending Physician, Departm ent of Em ergency Medicine, Section of, Medical Toxicology, John H. Stroger Hospital of Cook County, Chicago, Illinois Gary Bubly M.D., F.A.C.E.P. Clinical Associate Professor Departm ent of Em ergency Medicine, Brown University School of Medicine; Associate Director, Departm ent of Em ergency Medicine, The Miriam Hospital, Providence, Rhode Island Ann Buchanan M.D. St. David's Hospital, Austin, Texas Robert G. Buckley M.D., M.P.H., F.A.C.E.P Chairm an Departm ent of Em ergency Medicine, Naval Medical Center, San Diego, San Diego, California Colleen J. Buono M.D. Em ergency Medical Services Fellow Departm ent of Em ergency Medicine, University of California, San Diego; Clinical Faculty, Departm ent of Em ergency Medicine, University of California, San Diego Medical Center, San Diego,
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California Jeffrey A. Bush M.D. Professor of Clinical Medicine Departm ent of Em ergency Medicine, University of California, San Diego; Em ergency Departm ent Medical Director, Departm ent of Em ergency Medicine, University of California, San Diego, San Diego, California Colleen Campbell M.D. Associate Professor of Em ergency Medicine Departm ent of Em ergency Medicine, University of California San Diego, San Diego, California Michelle Canham M.D. Assistant Professor Departm ent of Em ergency Medicine, Rush University; Attending Physician, Departm ent of Em ergency Medicine, John H. Stroger Hospital of Cook County, Chicago, Illinois Taylor Young Cardall M.D. Em ergency Physician Departm ent of Em ergency Medicine, Scottsdale Healthcare, Scottsdale, Arizona Martin J. Carey M.D. Departm ent of Em ergency Medicine, University of Arkansas for Medical Sciences, Little Rock, Arkansas Keri L. Carstairs M.D. Attending Physician Departm ent of Em ergency Medicine, Naval Medical Center, San Diego, San Diego, California Shaun D. Carstairs M.D. Attending Physician Departm ent of Em ergency Medicine, Naval Medical Center, San Diego, San Diego, California Ingrid D. Carter D.O.
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Attending Physician Departm ent of Em ergency Medicine, John H. Stroger Hospital of Cook County, Chicago, Illinois Wallace Carter M.D. Associate Professor Departm ent of Em ergency Medicine, Weill Medical College of Cornell University; Residency Director, Departm ent of Em ergency Medicine, New York Presbyterian Hospital, New York, New York Austen Chai M.D. Departm ent of Em ergency Medicine, John H. Stroger Hospital of Cook County, Chicago, Illinois Michael Chamales M.D. Departm ent of Surgery, Texas Tech University Health Sciences Center, Lubbock, Texas Jennifer Chan M.D. Resident Departm ent of Em ergency Medicine, Beth Israel Deaconess Medical Center, Harvard Affiliated Em ergency Medicine Residency, Boston, Massachusetts Theodore C. Chan M.D. Associate Professor of Medicine Departm ent of Medicine; Medical Director, Departm ent of Em ergency Medicine, University of California, San Diego, San Diego, California Andrew Chang M.D. Assistant Professor Departm ent of Em ergency Medicine, Albert Einstein College of Medicine; Attending Physician, Departm ent of Em ergency Medicine, Montefiore Medical Center, Bronx, New York Robert S. Chang M.D. Attending Physician Departm ent of Em ergency Medicine, South Shore Hospital, South Weym outh, Massachusetts
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Anna Cheh M.D. Departm ent of Em ergency Medicine, Beth Israel Deaconess Hospital, Boston, Massachusetts David Cherkas M.D. Instructor Departm ent of Em ergency Medicine, Mt. Sinai School of Medicine, New York, New York Michele Chetham M.D. Physician Departm ent of Pediatric Medicine, Carepoint, Swedish Medical Center, Denver, Colorado Gordon Chew M.D. Senior Physician Departm ent of Em ergency Medicine, Kaiser Vallejo Medical Center, Vallejo, California Hong K. Choi M.D. Assistant Professor Departm ent of Em ergency Medicine, Albert Einstein College of Medicine; Residency Site Director, Departm ent of Em ergency Medicine, Montefiore Medical Center, Bronx, New York Yi-Mei Chng M.D., M.P.H. Clinical Fellow Departm ent of Em ergency Medicine, Harvard Medical School; Resident, Departm ent of Em ergency Medicine, Massachusetts General Hospital, Boston, Massachusetts Teriggi J. Ciccone M.D. Departm ent of Em ergency Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts Gregory Ciottone M.D. Director International Section, Departm ent of Em ergency Medicine, Harvard Medical School; Director, Division of Disaster Medicine, Departm ent
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of Em ergency Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts Brian Clyne M.D. Assistant Professor Departm ent of Em ergency Medicine, Brown Medical School; Residency Program Director, Departm ent of Em ergency Medicine, Rhode Island Hospital, Providence, Rhode Island Stewart Coffman M.D., F.A.C.E.P. Clinical Assistant Professor Departm ent of Em ergency Medicine, Southwestern University of Texas, Dallas, Texas; Chairm an, Departm ent of Em ergency Medicine, Medical Center of Lewisville, Lewisville, Texas James Colletti M.D. Associate Residency Director Departm ent of Em ergency Medicine, Regions Hospital, St. Paul, Minnesota Christopher B. Colwell M.D., F.A.C.E.P. Associate Professor Departm ent of Surgery, University of Colorado Health Sciences, Center; Associate Director, Departm ent of Em ergency Medicine, Denver Health Medical Center, Denver, Colorado Jim Comes M.D. Associate Professor Departm ent of Em ergency Medicine, University of California-Fresno Medical Education, Program ; Associate Residency Director, Departm ent of Em ergency Medicine, University Medical Center, Fresno, California Matthew D. Cook M.D. Marco Coppola D.O., F.A.C.E.P. Professor Departm ent of Em ergency Medicine, Texas A & M University Health Science System College, of Medicine, College Station, Texas; Medical
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Director, Departm ent of Em ergency Medicine, Las Colinas Medical Center and Questcare Partners, Irving, Texas Kelly Corrigan M.D. Departm ent of Em ergency Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts Brian N. Corwell M.D. Departm ent of Em ergency Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts Francis L. Counselman M.D. Professor and Chairm an Departm ent of Em ergency Medicine, Eastern Virginia Medical School, Norfolk, Virginia Linda C. Cowell M.D. Newton Wellesley Hospital, Norfolk, Massachusetts Richard A. Craven M.D., F.A.C.O.E.M. Associate Professor Departm ent of Fam ily Medicine, Eastern Virginia Medical School, Norfolk, Virginia Kirk Cumpston D.O. Assistant Professor Departm ent of Em ergency Medicine; Assistant Medical Director, Virginia Com m onwealth University, Virginia Poison Center, Richm ond, Virginia Liesl A. Curtis M.D., F.A.C.E.P. Assistant Professor Departm ent of Em ergency Medicine, Georgetown University Hospital, Washington, D.C. Seric Cusick M.D. Chief Resident Harvard Affiliated Em ergency Medicine; Residency, Departm ent of Em ergency Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts; Fellow, Division of Em ergency Ultrasound; Clinical
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Instructor, Departm ent of Em ergency Medicine, University of California Irvine Medical Center, Irvine, California Rita Cydulka M.D., M.S. Associate Professor Departm ent of Em ergency Medicine, Case Western Reserve University School of, Medicine; Vice Chair, Departm ent of Em ergency Medicine, MetroHealth Medical Center, Cleveland, Ohio Daniel Davis M.D. Associate Clinical Professor of Medicine Departm ent of Em ergency Medicine; Faculty Physician, Departm ent of Em ergency Medicine, University of California, San Diego, San Diego, California Joanne Davis M.D. Departm ent of Em ergency Medicine, Lom a Linda University Medical Center, Lom a Linda, California Jennifer E. De la Pena M.D. Resident Departm ent of Em ergency Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts Peter DeBlieux M.D. Professor of Clinical Medicine Departm ent of Em ergency Medicine, LSUHSC New Orleans; Director of Resident and Faculty Developm ent, Departm ent of Em ergency Medicine, MCLNO Charity Hospital, New Orleans, Louisiana David Della-Giustina M.D., F.A.C.E.P. Departm ent of Military and Em ergency Medicine, Uniform ed Services University of the Health Sciences, Bethesda, Maryland; Chairm an, Departm ent of Em ergency Medicine, Madigan Arm y Medical Center, Tacom a, Washington Paul H. Desan M.D., Ph.D. Assistant Professor Departm ent of Psychiatry, Yale University School of Medicine;
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Director, Psychiatric Consultation Service, Yale New Haven Hospital, New Haven, Connecticutt Paul L. DeSandre D.O. Assistant Professor Departm ent of Em ergency Medicine, Albert Einstein College of Medicine, Bronx, New York; Associate Residency Director, Departm ent of Em ergency Medicine, Beth Israel Deaconess Medical Center, New York, New York Diane Devita M.D., F.A.C.E.P. Assistant Clinical Professor Departm ent of Em ergency Medicine, University of Washington; Staff Physician, Departm ent of Em ergency Medicine, Madigan Arm y Medical Center—Fort Lewis, Fort Lewis, Washington Michael K. Doney M.D., M.S., M.P.H. Fellow in International Em ergency Medicine, Adjunct Instructor Departm ent of Em ergency Medicine, The George Washington University, Washington, D.C. Danielle J. Douglas M.D., Ph.D. Associate Professor Departm ent of Surgery, Colum bia University; Chief, Departm ent of Surgery, New York Hospital—Cornell Medical Center, New York, New York Susan Dufel M.D. Associate Professor Traum atology and Em ergency Medicine, University of Connecticut, Farm ington, Connecticut; Residency Director, Hartford Hospital, Hartford, Connecticut Jonathan A. Edlow M.D. Associate Professor Departm ent of Medicine, Harvard Medical School; Vice Chairm an, Departm ent of Em ergency Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts
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Arunachalam Einstein M.D. Departm ent of Em ergency Medicine, John H. Stroger Hospital of Cook County, Chicago, Illinois Norbert Elsner M.D. Assistant Professor Departm ent of Em ergency Medicine, Albert Einstein College of Medicine; Associate Director, Departm ent of Em ergency Medicine, Jacobi Medical Center, Bronx, New York Janet Eng D.O., F.A.C.E.P., F.A.C.O.E.P. Medical Toxicologist, Assistant Program Director Massachusetts State University Em ergency Medicine; Residency, Ingham Regional Medical, Lansing, Michigan Stephen K. Epstein M.D., M.P.P. Instructor Departm ent of Em ergency Medicine, Harvard Medical School; Physician, Departm ent of Em ergency Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts Timothy Erickson M.D., F.A.C.E.P., F.A.C.M.T., F.A.A.C.T. Professor Departm ent of Em ergency Medicine, University of Chicago at Illinois, Chicago, Illinois Eva Escatel M.D. Senior Resident Em ergency Medicine Residency Program at, MetroHealth Clinic Foundation, Case Western University, Cleveland, Ohio Barnet Eskin M.D., Ph.D. Clinical Assistant Professor Departm ent of Surgery, UMDNJ-New Jersey Medical School, Newark, New Jersey; Attending Em ergency Physician, Departm ent of Em ergency Medicine, Morristown Mem orial Hospital, Morristown, New Jersey Brian Euerle M.D.
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Assistant Professor Division of Em ergency Medicine, University of Maryland School of Medicine; Attending Physician, Departm ent of Em ergency Medicine, University of Maryland Medical Center, Baltim ore, Maryland James Feldman M.D. Associate Professor of Em ergency Medicine Departm ent of Em ergency Medicine, Boston University School of Medicine; Research Director, Departm ent of Em ergency Medicine, Boston Medical Center, Boston, Massachusetts Robert Feldman M.D. Assistant Professor Departm ent of Em ergency Medicine, Rush University; Attending Physician, Departm ent of Em ergency Medicine, John H. Stroger Hospital of Cook County, Chicago, Illinois Donna Felsenstein M.D. Assistant Professor of Medicine Harvard Medical School, Physician, Departm ent of Medicine/Division of Infectious Disease, Massachusetts General Hospital, Boston, Massachusetts Ian Glen Ferguson D.O. Attending Physician/Clinical Faculty Departm ent of Surgery/Division of Em ergency Medicine, Stanford University Medical Center, Palo Alto, California; Attending Physician/Clinical Faculty, Departm ent of Em ergency Medicine, Santa Clara Valley Medical Center, San Jose, California Maggie Ferng M.D. Departm ent of Em ergency Medicine, John H. Stroger Hospital of Cook County, Chicago, Illinois David Feldman M.D. Departm ent of Em ergency Medicine, Boston, Massachusetts James Feldman M.D., F.A.C.E.P. Departm ent of Em ergency Medicine, Boston Medical Center, Boston
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University School of Medicine, Boston, Massachusetts Michelle A. Finkel M.D. Attending Physician Departm ent of Em ergency Medicine, Little Com pany of Mary Hospital, Torrance, California Daniel Firestone M.D. Resident Departm ent of Em ergency Medicine, University of California, San Diego, San Diego, California Christopher Fischer M.D. Chief Resident Beth Israel Deaconess Medical Center, Harvard Affiliated Em ergency Medicine; Residency, Boston, Massachusetts Jonathan Fisher M.D., M.P.H. Instructor of Medicine Departm ent of Em ergency Medicine, Harvard Medical School; Physician, Departm ent of Em ergency Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts Steven F. Fisher M.D. Physician Departm ent of Em ergency Medicine, Abington Mem orial Hospital, Abington, Pennsylvania Megan Fix M.D. Chief Resident Harvard Affiliated Em ergency Medicine; Residency, Massachusetts General Hospital, Brigham and Wom en's Hospital, Boston, Massachusetts Kelly Anne Foley M.D., F.A.C.E.P. Associate Professor Departm ent of Em ergency Medicine, Eastern Virginia Medical School, Norfolk, Virginia Jessica Freedman M.D.
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Departm ent of Em ergency Medicine, Mt. Sinai School of Medicine, New York, New York Franklin D. Friedman M.D., M.S. Assistant Professor Departm ent of Em ergency Medicine, Tufts University School of Medicine; Director, Em ergency Clinical Operations, Departm ent of Em ergency Medicine, Tufts—New England Medical Center, Boston, Massachusetts Steven Furer M.S., F.A.C.E.P. Attending Physician Departm ent of Em ergency Medicine, The Medical Center of Aurora South, Aurora, Colorado Mary Anne Fuchs M.D. Departm ent of Em ergency Medicine, University of California, San Diego, San Diego, California Ara Gabrielian M.D. Delaram Ghadishah M.D. Assistant Professor Departm ent of Em ergency Medicine, University of California Irvine, Irvine, California Adit A. Ginde M.D. Resident Physician Departm ent of Em ergency Medicine, Harvard Medical School; Resident Physician, Departm ent of Em ergency Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts Bret Ginther M.D. Assistant Medical Director Departm ent of Em ergency Medicine, Inland Valley Medical Center, Wildom ar, California Daren Girard M.D. Associate Director Departm ent of Em ergency Medicine, Landm ark Medical Center,
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Woonsocket, Rhode Island Robyn Heister Girard M.D. Kaiser Perm anente South, San Francisco, California Eric Glasser M.D. Clinical Instructor Departm ent of Em ergency Medicine, Georgetown University Hospital, Washington, D.C. Judd L. Glasser M.D. Clinical Instructor Departm ent of Em ergency Medicine, University of California, San Diego; Attending Staff, Director of Pre-Hospital Care, Departm ent of Em ergency Medicine, Tri-City Medical Center, Oceanside, California Laura B. Glicksman M.S., D.M.D. Orthodontist, (Private Practice) Laura B. Glicksm an, M.S., D.M.D., P.C., Needham , Massachusetts Donald C. Goff M.D. Harvard Medical School, Psychotic, Disorders Program , Massachusetts General Hospital, Boston, Massachusetts Jessica R. Goldstein M.D. Senior Instructor Departm ent of Em ergency Medicine, MetroHealth Hospital, Cleveland, Ohio Dolores Gonthier M.D. Consultant MD2 Healthcare Consulting, Inc., Wexford, Pennsylvania J. Scott Goudie M.D. Chief Resident Harvard Affiliated Em ergency Medicine Residency, Departm ent of Em ergency Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts Matthew N. Graber M.D., Ph.D. Assistant Professor
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Departm ent of Em ergency Medicine and Departm ent, of Biochem istry, Em ory University School of Medicine, Atlanta, Georgia Charles S. Graffeo M.D. Clinical Professor of Em ergency Medicine, Assistant Program Director Departm ent of Em ergency Medicine, Eastern Virginia Medical School, Norfolk, Virginia Ruth Granlund M.D. Physician Departm ent of Em ergency Medicine, Feather River Hospital, Paradise, California Henry J. Grazioso M.D., F.A.A.E.M. Clinical Assistant Professor Departm ent of Em ergency Medicine, Boston University School of Medicine, Boston, Massachusetts; Attending Physician, Department of Em ergency Services, Brockton Hospital, Brockton, Massachusetts Ian Greenwald M.D. Assistant Professor Departm ent of Em ergency Medicine, Em ory University, Atlanta, Georgia Shamai A. Grossman M.D., M.S. Assistant Professor of Medicine Departm ent of Em ergency Medicine, Harvard Medical School; Director, Departm ent of Em ergency Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts Ian R. Grover M.D. Assistant Clinical Professor of Medicine Departm ent of Em ergency Medicine, University of California, San Diego, San Diego, California Kama Guluma M.D. Assistant Clinical Professor Departm ent of Em ergency Medicine/Medicine, University of California San Diego, San Diego, California
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Atul Gupta D.O., F.A.A.E.M. Departm ent of Em ergency Medicine, Long Beach Mem orial Medical Center, Miller Children's Hospital, Long Beach, California David A. Guss M.D. Professor Departm ent of Em ergency Medicine, University of California, San Diego; Director, Departm ent of Em ergency Medicine, University of California, San Diego, San Diego, California Robert S. Hamilton M.D., F.A.A.E.M. Volunteer Clinical Faculty University of California, Davis; Medical Director, Em ergency Services, Merry Medical Center, Redding, Redding, California David Harter M.D. Assistant Residency Director Departm ent of Em ergency Medicine, John H. Stroger Hospital of Cook County, Chicago, Illinois Stephen R. Hayden M.D. Professor of Clinical Medicine, Program Director Departm ent of Em ergency Medicine Residency, University of California, San Diego; Editor-in-Chief, Journal of Em ergency Medicine, San Diego, California Robin R. Hemphill M.D., M.P.H. Associate Professor Departm ent of Em ergency Medicine, Vanderbilt University Medical Center, Nashville, Tennessee Sean O. Henderson M.D. Associate Professor Departm ent of Em ergency Medicine, Keck School of Medicine, University of Southern, California; Vice Chair, Departm ent of Em ergency Medicine, Lactuse Medical Center, Los Angeles, California Gregory W. Hendey M.D., F.A.C.E.P. Associate Professor of Clinical Medicine
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Departm ent of Medicine, University of California, San Francisco, San Francisco, California; Research Director, Departm ent of Em ergency Medicine, University of California, San Francisco, Fresno University Medical Center, Fresno, California David B. Herzog M.D. Professor of Psychiatry (Pediatrics) Departm ent of Psychiatry, Harvard Medical School; Director, Eating Disorders Unit; Child Psychiatry, Services at Massachusetts General Hospital, Departm ent of Psychiatry, Massachusetts General Hospital, Boston, Massachusetts Ra'ed A. Hijazi M.D., M.H.A., F.A.C.E.P. Assistant Professor Departm ent of Em ergency Medicine, King Saud University of Health Sciences; Deputy Chairm an, Em ergency Departm ent; Division Head, Traum a and Critical Care Director, of Disaster Medicine; Medical Director, Em ergency Medical Services, King Abdulaziz Medical City, National Guard, Riyadh, Saudi Arabia Scot Hill M.D. Assistant Professor Departm ent of Em ergency Medicine, The Mount Sinai School of Medicine; Associate Director, Departm ent of Em ergency Medicine, The Mount Sinai Medical Center, New York, New York Doodnauth Hiraman M.D. Assistant Professor of Medicine Weill Medical College of Cornell University, Departm ent of Em ergency Medicine, New York Presbyterian Hospital, New York, New York Forrest Holden M.D. Em ergency Residency Program Maricopa Medical Center, Phoenix, Arizona Patrick Cline Holland M.D., F.A.C.E.P. Clinical Associate Professor Departm ent of Medicine, University of Washington, Medical
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Student/Intern Coordinator, Madigan Arm y Medical Center, Tacom a, Washington Danielle A. Hoover D.O., M.S. Resident Physician Departm ent of Em ergency Medicine, Case Western Reserve University; Resident Physician, Departm ent of Em ergency Medicine, MetroHealth Medical Center/Cleveland Clinic, Foundation/CWRU, Cleveland, Ohio Jeffrey Horton M.D. Physician Departm ent of Em ergency Medicine, Mem orial Hospital, Martinsville, Virginia Mark A. Hostetler M.D., M.P.H Chief Em ergency Medicine, Departm ent of Pediatrics, The University of Chicago School of Medicine; Medical Director, Departm ent of Pediatric Em ergency, The University of Chicago, Com er Children's Hospital, Chicago, Illinois Renee Hsia M.D., M.Sc. Resident Departm ent of Surgery, Division of Em ergency, Medicine, Stanford/Kaiser Em ergency Medicine Residency, Stanford, California Carl K. Hsu M.D. Weill Medical College of Cornell University, New York, New York, Departm ent of Em ergency Medicine, The Brooklyn Hospital Center, Brooklyn, New York J. C. Huffman M.D. Psychiatric Consultation Service, Departm ent of Psychiatry, Massachusetts General Hospital, McLean Hospital and Harvard Medical School, Boston, Massachusetts Timothy Hurtado D.O. Departm ent of Em ergency Medicine, Madigan—University of
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Washington, Tacom a, Washington Anwer Hussain D.O., F.A.A.E.M., F.A.C.O.E.P. Clinical Instructor Departm ent of Em ergency Medicine, Midwestern University, Downers Grove, Illinois; Attending Physician, Departm ent of Em ergency Medicine, Provident Hospital of Cook County, Chicago, Illinois Alec Tuan Huynh M.D. Resident PGY-4 Departm ent of Em ergency Medicine, University of California San Diego, San Diego, California Anthony Huynh M.D. Em ergency Physician Departm ent of Em ergency Medicine, San Clem ente Regional Medical Center, San Clem ente, California James Hwang M.D. Em ergency Ultrasound Fellow Section of Em ergency Medicine/Departm ent of Surgery, Yale University School of Medicine, New Haven, Connecticut Wender Hwang M.D. Departm ent of Em ergency Medicine, Lom a Linda University Medical Center, Lom a Linda, California Jason Imperato M.D., Ph.D. Instructor Departm ent of Em ergency Medicine, Harvard Medical School, Boston, Massachusetts; Staff Physician, Departm ent of Em ergency Medicine, Mount Auburn Hospital, Cam bridge, Massachusetts Paul Ishimine M.D. Hagop Isnar M.D. Associate Director Departm ent of Em ergency Medicine, Auburn Mem orial Hospital, Auburn, New York Kenneth Jackimczyk M.D.
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Attending Physician Departm ent of Em ergency Medicine, Maricopa Medical Center, Phoenix, Arizona Safia C. Jackson B.S. Research Assistant Departm ent of Psychiatry, Massachesetts General Hospital, Boston, Massachusetts Irving Jacoby M.D., F.A.C.E.P., F.A.C.P. Professor of Medicine Departm ent of Medicine, University of California, San Diego School of Medicine, La Jolla, California; Attending Physician, Departm ent of Em ergency Medicine, University of California, San Diego, San Diego, California Liudvikas Jagminas M.D., F.A.C.E.P. Assistant Physician Departm ent of Em ergency Medicine, Brown Medical School, Providence, Rhode Island; Physician in Chief, Departm ent of Em ergency Medicine, Mem orial Hospital of Rhode Island, Pawtucket, Rhode Island Thea James M.D. Departm ent of Em ergency Medicine, Boston University School of Medicine, Boston, Massachusetts Gregory D. Jay M.D., Ph.D. Associate Professor of Medicine and Em ergency, Medicine, Associate Professor of Engineering Departm ent of Em ergency Medicine, Brown Medical School; Research Director, Departm ent of Em ergency Medicine, Rhode Island Hospital, Providence, Rhode Island David Jerrard M.D. Associate Professor Departm ent of Em ergency Medicine, University of Maryland, Baltim ore, Maryland
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Albert Jin M.D. Staff Physician Departm ent of Em ergency Medicine, Irvine Regional Hospital and Medical Center, Irvine, California Gary Johnson M.D., F.A.C.E.P. Associate Professor Departm ent of Em ergency Medicine, SUNY Upstate Medical University, Syracuse, New York Jennifer S. Johnson M.D. Resident Physician Departm ent of Em ergency Medicine, University of California, San Diego, San Diego, California Beth Anne Joseph M.D. Assistant Professor University of Connecticut School of Medicine, Departm ent of Em ergency Medicine and Traum atology, Manchester Mem orial Hospital, Manchester, Connecticut Madeline M. Joseph M.D. Associate Professor Departm ent of Em ergency Medicine, University of Florida Health Science Center, Jacksonville; Chief, Departm ent of Pediatric Em ergency Medicine, Shands Hospital, Jacksonville, Florida Pascal Juang M.D. Em ergency Care Unit, Hoag Hospital, Newport Beach, California Joseph H. Kahn M.D., F.A.C.E.P. Associate Clinical Professor Departm ent of Em ergency Medicine, Boston University School of Medicine; Director, Medical Student Education, Departm ent of Em ergency Medicine, Boston Medical Center, Boston, Massachusetts Christopher S. Kang M.D. Madigan Arm y Medical Center, Tacom a, Washington Tarina Lee Kang M.D.
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Harvard Affiliated Em ergency Medicine Residency, Senior Resident Departm ent of Em ergency Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts A. Antoine Kazzi M.D., F.A.A.E.M. Chief of Service Em ergency Medicine; Medical Director, The Em ergency Unit, The Am erican University of Beirut, Beirut, Lebanon Ziad N. Kazzi M.D., F.A.A.E.M. Assistant Professor Departm ent of Em ergency Medicine, University of Alabam a, Birm ingham , Birm ingham , Alabam a Samuel Keim M.D. Residency Director Departm ent of Em ergency Medicine, University of Arizona, Tucson, Arizona Sean P. Kelly M.D. Instructor of Medicine Departm ent of Em ergency Medicine, Harvard Medical School; Medical Student Clerkship Director, Departm ent of Em ergency Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts Mamata Kene M.D. Resident Physician Departm ent of Em ergency Medicine, University of California, San Diego; Resident Physician, Departm ent of Em ergency Medicine, University of California San Diego Medical Center, San Diego, California Elicia Sinor Kennedy M.D., F.A.C.E.P Assistant Professor Clinical Faculty Departm ent of Em ergency Medicine, University of Arkansas for Medical Sciences, Little Rock, Arkansas Kevin Kern D.O. Attending Physician
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Departm ent of Em ergency Medicine, John H. Stroger Hospital of Cook County, Chicago, Illinois James P. Killeen M.D. Assistant Clinical Professor of Medicine Departm ent of Em ergency Medicine, University of California, San Diego; Clinical Faculty, Departm ent of Em ergency Medicine, University of California, San Diego Medical Center, San Diego, California Grace Kim M.D. Assistant Professor Departm ent of Em ergency Medicine, Lom a Linda University; Attending Physician, Departm ent of Em ergency Medicine, Division of Pediatric Em ergency Medicine, Lom a Linda University, Lom a Linda, California Tamaki Kimbro M.D. Departm ent of Em ergency Medicine, Mendocino Coast District Hospital, Fort Bragg, California Jeffrey King M.D., F.A.C.E.P. Clinical Associate Professor Departm ent of Em ergency Medicine, Wayne State University; Interim Chief, Departm ent of Em ergency Medicine, Harper University Hospital, Detroit, Michigan Matthew Kippenhan M.D. Clinical Instructor Departm ent of Em ergency Medicine, Northwestern University, Feinberg School of Medicine; Staff Physician, Department of Em ergency Medicine, Northwestern Mem orial Hospital, Chicago, Illinois Barry J. Knapp II M.D., F.A.C.E.P. Associate Professor Departm ent of Em ergency Medicine, Eastern Virginia School of Medicine, Norfolk, Virginia
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Leo Kobayashi M.S Assistant Professor Departm ent of Em ergency Medicine, Brown Medical School; Attending Physician, Departm ent of Em ergency Medicine, Rhode Island Hospital, Providence, Rhode Island Paul Kolecki M.D., F.A.C.E.P. Assistant Professor; Director of Undergraduate Em ergency Medicine Departm ent of Em ergency Medicine, Thom as Jefferson University, Jefferson Medical College, Philadelphia, Pennsylvania Jennifer L. Kolodchak M.D. Clinical Instructor Departm ent of Em ergency Medicine, Rush University Medical School; Attending Physician, Departm ent of Em ergency Medicine, Rush University Medical Center, Chicago, Illinois Amy V. Kontrick M.D. Assistant Professor Departm ent of Em ergency Medicine, Northwestern University, Feinberg School of Medicine, Chicago, Illinois Richard S. Krause M.D. Residency Program Director Departm ent of Em ergency Medicine, University of Buffalo School of Medicine and, Biom edical Sciences, Buffalo, New York Joel Kravitz M.D., F.A.C.E.P., F.R.C.P.S.C. Assistant Professor Departm ent of Em ergency Medicine, Thom as Jefferson University; Assistant Residency Director, Departm ent of Em ergency Medicine, Albert Einstein Medical Center, Philadelphia, Pennsylvania Lara Kulchycki M.D. Attending Physician Departm ent of Em ergency Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts Alan M. Kumar M.D., F.A.C.E.P.
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Clinical Instructor Departm ent of Medicine, University of Chicago; Attending Physician, Departm ent of Em ergency Medicine, Lutheran General Hospital, Park Ridge, Illinois Dick Kuo M.D. Assistant Professor Departm ent of Surgery, Division of Em ergency, Medicine, University of Maryland School of Medicine; Medical Director, Departm ent of Adult Em ergency Medicine, University of Maryland Medical Center, Baltim ore, Maryland Gregory W. Lampe M.D. Em ergency Physician Departm ent of Em ergency Medicine, Mission Hospital Regional Medical Center, Mission Viejo, California Owen Lander M.D. Assistant Professor Departm ent of Em ergency Medicine, Robert C. Byrd Health Sciences Center, West Virginia University, Morgantown, West Virginia Mark Langdorf M.D., M.H.P.E. Departm ent of Em ergency Medicine, University of California, Irvine Medical Center, Orange, California Emi Latham M.D. Departm ent of Em ergency Medicine, University of California, San Diego, San Diego, California Minh V. Le M.D. Departm ent of Em ergency Medicine, University of California, San Diego Medical Center, San Diego, California James M. Leaming M.D. Assistant Professor Departm ent of Em ergency Medicine, Tufts School of Medicine; Attending Physician, Departm ent of Em ergency Medicine, Tufts—New England Medical Center, Boston, Massachusetts
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Jason M. Lebwohl M.D. Conrow Regional Medical Center, Conrow, Texas JiWon E. Lee M.D. Resident Physician Departm ent of Em ergency Medicine, Rush Medical College; Resident Physician, Departm ent of Em ergency Medicine, John H. Stroger Hospital of Cook County, Chicago, Illinois Moses S. Lee M.D., F.A.C.E.P., F.A.A.E.M. Assistant Clinical Professor Departm ent of Em ergency Medicine, Rush Medical College; Senior Attending Physician, Departm ent of Em ergency Medicine, John H. Stroger Hospital of Cook County, Chicago, Illinois Tomas C. Lee Em ergency Physician, Active Staff Physician Departm ent of Em ergency Medicine, Sierra Nevada Mem orial Hospital, Sierra, Nevada Eric Legome M.D. Assistant Professor Departm ent of Em ergency Medicine, New York University School of Medicine, Bellevue Hospital Center; Director/Bellevue Em ergency Medicine Residency, Departm ent of Em ergency Medicine, New York University Hospital/Bellevue Hospital Center, New York, New York Steven Lelyveld M.D., F.A.A.P., F.A.C.E.P. Associate Professor Departm ents of Pediatrics and Medicine, University of Chicago Pritzker School of Medicine; Attending Physician, Departm ents of Pediatric Em ergency Medicine, and Medicine, University of Chicago Corner Children's Hospital, Chicago, Illinois Amy LePage M.D. Chief Resident Departm ent of Em ergency Medicine, Mayo Clinic, Rochester, Minnesota
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Roneet Lev M.D., F.A.C.E.P. Voluntary Assistant Clinical Professor Departm ent of Em ergency Medicine, University of California, San Diego; Director of Operations, Departm ent of Em ergency Medicine, Scripps Mercy Hospital, San Diego, California Hope W. Levin M.D. Child and Adolescent Psychiatry Fellow Departm ent of Psychiatry, Harvard Medical School; Child and Adolescent Psychiatry Fellow, Departm ent of Psychiatry, Massachusetts General Hospital, Boston, Massachusetts David Levine M.D., F.A.C.E.P. Assistant Professor Departm ent of Em ergency Medicine, Rush University; Medical Director, Departm ent of Em ergency Medicine, John H. Stroger Hospital of Cook County, Chicago, Illinois Saul Levine M.D. Assistant Physician Departm ent of Em ergency Medicine, University of California, San Diego, San Diego, California Trevor Lewis M.D., F.A.C.E.P. Assistant Professor Departm ent of Em ergency Medicine, Rush Medical College; Director, Observation Em ergency Medicine, Departm ent of Em ergency Medicine, John H. Stroger Hospital of Cook County, Chicago, Illinois Lazaro Lezcano M.D., F.A.A.P Clinical Assistant Professor of Pediatrics Departm ent of Pediatrics, Weill Medical College of Cornell University, New York, New York; Director of Neonatology, Departm ent of Pediatrics/Division of Neonatology, St. Barnabas Hospital, Bronx, New York Richard Lichenstein M.D. Associate Professor
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Departm ent of Pediatrics, University of Maryland School of Medicine; Director, Pediatric Em ergency Medicine, Departm ent of Pediatrics, University of Maryland Hospital for Children, Baltim ore, Maryland Jason Liebzeit M.D. Chief Resident Departm ent of Em ergency Medicine, Northwestern University, McGaw Medical, Center, Chicago, Illinois Alexander T. Limkakeng Jr. M.D. Assistant Professor Departm ent of Em ergency Medicine, Thom as Jefferson University, Jefferson, Medical College; Attending Physician, Department of Em ergency Medicine, Thom as Jefferson University Hospital, Philadelphia, Pennsylvania David A. Listman M.D. Departm ent of Pediatric Em ergency, Medicine, St. Barnabas Hospital, Bronx, New York Shan Liu M.D., M.P.H. Instructor Departm ent of Surgery, Harvard Medical School; Faculty, Departm ent of Em ergency Medicine, Massachusetts General Hospital, Boston, Massachusetts Angela Loh M.D. Assistant Chief Departm ent of Em ergency Medicine, Kaiser Perm anente San Jose, San Jose, California Frank LoVecchio M.D. Banner Health, Phoenix, Arizona Lisa Lowe M.D., M.P.H. Resident Physician Departm ent of Em ergency Medicine, University of California, San Diego, San Diego, California Jenny Lu M.D., M.S.
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Resident Physician Departm ent of Em ergency Medicine, University of Illinois at Chicago; Physician, Departm ent of Em ergency Medicine, John H. Stroger Hospital of Cook County, Chicago, Illinois Boris Lubavin M.D. Departm ent of Em ergency Medicine, University of California, Irvine Medical Center, Orange, California Jon Ludwig M.D. Pacific Em ergency Providers Scripps Mercy Hospital Em ergency, Departm ent, San Diego, California Binh T. Ly M.D. Associate Clinical Professor of Medicine Departm ent of Surgery, University of California, San Diego; Director, Medical Toxicology Fellowship; Associate Director, Em ergency Medicine; Residency, Division of Medical Toxicology, San Diego, California Elizabeth L. Lynch M.D. Assistant Professor Departm ent of Em ergency Medicine, Lom a Linda University Medical Center; Assistant Medical Director, Departm ent of Em ergency Medicine, Lom a Linda University Medical Center, Lom a Linda, California Gene Ma M.D., F.A.C.E.P. Assistant Clinical Professor Departm ent of Medicine, University of California, San Diego, San Diego, California; Quality Assurance Chairm an, Departm ent of Em ergency Medicine, Tri-City Medical Center, Oceanside, California John MacKay Jr. M.D. Assistant Professor Departm ent of Em ergency Medicine, Texas Tech University; Attending Physician, Departm ent of Em ergency Medicine, Thom ason Hospital, El
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Paso, Texas Laura Macnow M.D. Instructor Departm ent of Em ergency Medicine, Harvard Medical School; Attending Physician, Departm ent of Em ergency Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts Timothy J. Mader M.D. Associate Professor Departm ent of Em ergency Medicine, Tufts University School of Medicine, Boston, Massachusetts; Associate Director of Em ergency, Medicine, Departm ent of Em ergency Medicine, Research, Baystate Medical Center, Springfield, Massachusetts John Mahoney M.D. Associate Professor Departm ent of Em ergency Medicine, University of Pittsburgh School of Medicine; Attending Physician, Departm ent of Em ergency Medicine, UPMC Presbyterian, Pittsburgh, Pennsylvania Mamta Malik M.D. Departm ent of Em ergency Medicine, Rush Medical Center, Chicago, Illinois Gerald Maloney Jr. D.O. Clinical Instructor Departm ent of Em ergency Medicine, Rush Medical College, Medical Toxicology Fellow, Toxikon Consortium , Chicago, Illinois Mark Mandell M.D. Chairm an Departm ent of Em ergency Medicine, Morristown Mem orial Hospital, Morristown, New Jersey Alex Manini M.D. Departm ent of Em ergency Medicine, Massachusetts General Hospital, Boston, Massachusetts Julie Marmon M.D.
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Jeffrey Manko M.D. Departm ent of Em ergency Medicine, New York University/Bellevue Medical Center, New York, New York Robert Marsan Jr. M.D., B.S. University of Pennsylvania, Philadelphia, Pennsylvania Kevin J.L. Martens M.D. Resident Physician Departm ent of Em ergency Medicine, Lom a Linda University Medical Center, Lom a Linda, California Jon D. Mason M.D. Associate Professor Departm ents of Em ergency Medicine and Pediatrics, Eastern Virginia Medical School; Attending Physician, Departm ent of Em ergency Medicine, Sentara Norfolk General Hospital, Norfolk, Virginia Laura Matzkin M.D. Senior Resident Tufts University School of Medicine, Departm ent of Em ergency Medicine, Baystate Medical Center, Springfield, Massachusetts Madeline Matar Joseph M.D. Associate Professor, Director, Pediatric Em ergency Medicine Fellowship Program , Chief Division of Pediatric Em ergency Medicine, University of Florida College of Medicine, Jacksonville, Florida Amal Mattu M.D. Associate Professor and Program Director Departm ent of Em ergency Medicine, University of Maryland School of Medicine, Baltim ore, Maryland Suzan Mazor M.D. Assistant Professor Departm ents of Em ergency Medicine and Pediatrics, Children's Hospital and Regional Medical Center, Sand Point Way, Nebraska Christopher M. McCarthy II M.D.
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Resident Departm ent of Em ergency Medicine, Harvard University, Beth Israel Deaconess Medical Center, Boston, Massachusetts Robert F. McCormack M.D. Instructor Departm ent of Em ergency Medicine, Harvard Medical School; Attending Physician, Departm ent of Em ergency Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts Daniel C. McGillicuddy M.D. Instructor Departm ent of Em ergency Medicine, Harvard Medical School; Attending Physician, Departm ent of Em ergency Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts Murray J. McLachlan M.D. Michelle S. McMahon-Downer M.D. Instructor in Pediatrics Division of Pediatric Em ergency Medicine, Departm ent of Pediatrics, Boston University School of Medicine; Attending Physician, Pediatric Em ergency Medicine, Boston Medical Center, Boston, Massachusetts Anthony J. Medak M.D. Departm ent of Em ergency Medicine, University of California, San Diego, San Diego, California Howard K. Mell M.D., M.P.H. Resident Departm ent of Em ergency Medicine, Mayo School of Graduate, Medical Education; Resident Physician, Departm ent of Em ergency Medicine, Saint Mary's Hospital/Mayo Clinic, Rochester, Minnesota Moss Mendelson M.D., F.A.C.E.P. Associate Professor Departm ent of Em ergency Medicine, Eastern Virginia Medical School; Chief, Departm ent of Em ergency Medicine, Sentara Hospitals, Norfolk, Norfolk, Virginia
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Fernando G. Mendoza M.D. Instructor in Pediatrics Division of Pediatric Em ergency Medicine, Boston University School of Medicine, Boston, Massachusetts Nathan Mick M. D. Medical Director Departm ent of Pediatric Em ergency Medicine, Maine Medical Center, Portland, Maine Scott A. Miller M.D. Clinical Instructor Departm ent of Em ergency Medicine, Rush University Medical Center, Chicago, Illinois Shayle Miller Ph.D., F.A.C.E.P. Assistant Professor Departm ent of Em ergency Medicine, Rush Medical College; Voluntary Attending Physician, Departm ent of Em ergency Medicine, John H. Stroger Hospital of Cook County, Chicago, Illinois Trevor J. Mills M.D. Program Director Louisiana State University Em ergency Medicine; Residency, Associate Clinical Professor, Louisiana State University Health Science Center, New Orleans, Louisiana Leslie Milne M.D. Departm ent of Em ergency Medicine, Massachusetts General Hospital, Sports Medicine Departm ent, Children's Hospital, Boston, Massachusetts Andrew Milstein M.D., M.S., F.A.C.E.P. Clinical Assistant Professor Departm ent of Surgery, Division of, Em ergency Medicine, University of Maryland, Baltim ore, Maryland; Attending Physician, Departm ent of Em ergency Medicine, Baltim ore Washington Medical Center, Glen Burnie, Maryland
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Elizabeth L. Mitchell M.D. Assistant Professor Departm ent of Em ergency Medicine, Boston University, Boston, Massachusetts Christy Rosa Mohler M.D., F.A.C.E.P., F.A.A.E.M. Em ergency Physician Departm ent of Em ergency Medicine, Scripps Mercy Hospital Chula Vista, Chula Vista, California Robert C. Montana M.D. Providence Everett Medical Center, Everett, Washington Maria Moreira M.D. Associate Program Director The Denver Health Medical Center Residency in, Em ergency Medicine; Clinical Instructor, Departm ent of Surgery, Division of Em ergency Medicine, The University of Colorado Health Sciences Center, Denver, Colorado John W. Morehouse M.D. Jordan Moskoff M.D. Assistant Professor Departm ent of Em ergency Medicine, Rush University Medical College; Assistant Director, Adult Em ergency Services, Departm ent of Em ergency Medicine, John H. Stroger Hospital of Cook County, Chicago, Illinois Matthew B. Mostofi D.O. Assistant Professor Departm ent of Em ergency Medicine, Tufts University School of Medicine; Attending Physician, Departm ent of Em ergency Medicine, Tufts-New England Medical Center, Boston, Massachusetts Linda Mueller M.D. Departm ent of Em ergency Medicine, Munster Com m unity Hospital, Munster, Indiana David W. Munter M.D., M.B.A.
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Assistant Clinical Professor Departm ent of Em ergency Medicine, Eastern Virginia Medical School; Director and Chair, Departm ent of Em ergency Medicine, DePaul Medical Center, Norfolk, Virginia Michael S. Murphy M.D. Medical Director for Pre-Hospital Care Departm ent of Em ergency Medicine, South Shore Hospital, South Weym outh, Massachusetts Scott B. Murray M.D. Clinical Fellow in Medicine Departm ent of Medicine, Harvard Medical School; Chief Resident, Harvard Affiliated Em ergency Medicine, Beth Israel Deaconess Medical Residency Center, Boston, Massachusetts Veronique Murray M.D. Mark B. Mycyk M.D. Assistant Professor Departm ent of Em ergency Medicine, Northwestern University; Attending Physician, Departm ent of Em ergency Medicine, Northwestern Mem orial Hospital, Chicago, Illinois Eric S. Nadel M.D. Departm ent of Em ergency Medicine, Brigham and Wom en's Hospital, Boston, Massachusetts Kathleen Nasci M.D. Medical Director Departm ent of Em ergency Medicine, Pennsylvania Hospital, Philadelphia, Pennsylvania Isam Nasr M.D., F.A.C.E.P. Assistant Professor Departm ent of Em ergency Medicine, Rush Medical College; Senior Attending Physician, Departm ent of Em ergency Medicine, John H. Stroger Hospital of Cook County, Chicago, Illinois Larry A. Nathanson M.D.
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Instructor of Medicine Departm ent of Medicine, Harvard Medical School; Director of Em ergency Medicine Inform atics, Departm ent of Em ergency Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts Sean-Xavier Neath M.D., Ph.D. Assistant Professor Departm ent of Em ergency Medicine, University of California, San Diego, San Diego, California James Nelson M.D. Resident Physician Departm ent of Em ergency Medicine, University of California, San Diego, San Diego, California Edward Newton M.D. Professor Departm ent of Em ergency Medicine, Keck School of Medicine, University of Southern, California; Chairm an, Departm ent of Em ergency Medicine, Los Angeles California and University of Southern, California Medical Center, Los Angeles, California Ann P. Nguyen M.D. Assistant Professor Departm ent of Em ergency Medicine, New York University School of Medicine; Attending Physician, Departm ent of Em ergency Medicine, Bellevue Hospital Center and, New York Medical Center, New York, New York Michael W. Nielson M.D. Sean Patrick Nordt M.D. University of California, San Diego, San Diego, California Yasuharu Okuda M.D. Assistant Professor Departm ent of Em ergency Medicine, Mt. Sinai School of Medicine; Associate Residency Director, Departm ent of Em ergency Medicine,
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The Mt. Sinai Hospital, New York, New York Jonathan S. Olshaker M.D. Professor Departm ent of Em ergency Medicine, Boston University School of Medicine; Chief, Departm ent of Em ergency Medicine, Boston Medical Center, Boston, Massachusetts Jennifer Oman M.D. Associate Clinical Professor of, Em ergency Medicine Departm ent of Em ergency Medicine, University of California Irvine School of, Medicine, Orange, California David Palafox M.D. Assistant Professor Departm ent of Em ergency Medicine, Texas Tech University Health Science Center; Faculty, Departm ent of Em ergency Medicine, Urgent Care Center, Thom ason General Hospital, El Paso, Texas Peter Pang M.D. Assistant Professor Departm ent of Em ergency Medicine, Northwestern University Feinberg, School of Medicine; Staff Physician, Departm ent of Em ergency Medicine, Northwestern Mem orial Hospital, Chicago, Illinois Jennifer M. Park M.D. Instructor of Psychiatry Harvard University; Director, Acute Psychiatry Service, Departm ent of Psychiatry, Massachusetts General Hospital, Boston, Massachusetts Lawrence T. Park M.D. Instructor Departm ent of Psychiatry, Harvard Medical School; Director, Inpatient Psychiatry, Departm ent of Psychiatry, Massachusetts General Hospital, Boston, Massachusetts Peter J. Park M.D. Attending Physician
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Departm ent of Em ergency Medicine, Naval Medical Center San Diego, San Diego, California Robert A. Partridge M.D., M.P.H., D.T.M., F.A.C.E.P. Associate Professor Departm ent of Em ergency Medicine, Brown Medical School; Attending Physician, Departm ent of Em ergency Medicine/Sam uels 2, Rhode Island Hospital, Providence, Rhode Island Raj J. Patel M.D. Assistant Professor Departm ent of Em ergency Medicine, University of California San Diego, San Diego, California; Staff Physician, Departm ent of Em ergency Medicine, Palom ar Medical Center, Escondido, California Rahul Patwari M.D. Attending Physician Departm ent of Em ergency Medicine, Rush University Hospital, Chicago, Illinois Timothy Pavek M.D. St. Vincent Hospital Medical Center, Green Bay, Wisconsin David A. Peak M.D. Instructor Departm ent of Em ergency Medicine, Harvard Medical School; Staff Physcian, Departm ent of Em ergency Medicine, Massachusetts General Hospital, Boston, Massachusetts John Pease M.D. Staff Physician Departm ent of Em ergency Medicine, Tripler Arm y Medical Center, Honolulu, Hawaii Bradley F. Peckler M.D. Associate Professor Internal Medicine, Division of Em ergency Medicine, University of South Florida; Attending Physician, Departm ent of Em ergency Medicine, Tam pa General Hospital, Tam pa, Florida
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David A. Perlstein M.D. Clinical Instructor Departm ent of Pediatrics, Weill Medical College of Cornell University, New York, New York; Associate Medical Director, Director of Am bulatory Pediatrics, Departm ent of Pediatrics, St. Barnabas Hospital, Bronx, New York Aaron Pessl M.D. Resident Departm ent of Em ergency Medicine, University of California, San Diego, San Diego, California Kelly Pettit M.D. Resident Physician Departm ent of Em ergency Medicine, University of California, San Diego, San Diego, California Benjamin Z. Philips M.D. Departm ent of Em ergency Medicine, Rhode Island Hospital, Providence, Rhode Island Charles V. Pollack Jr. M.A., M.D., F.A.C.E.P. Professor Departm ent of Em ergency Medicine, University of Pennsylvania School of Medicine; Chairm an, Departm ent of Em ergency Medicine, Pennsylvania Hospital, Philadelphia, Pennsylvania Janet M. Poponick M.D. Assistant Professor Departm ent of Em ergency Medicine, Cast Western Reserve University, MetroHealth Medical Center, Cleveland, Ohio William Porcaro M.D. EMS/Disaster Medicine Fellow Departm ent of Em ergency Medicine, University of Massachusetts Medical School; Attending Physician, Departm ent of Em ergency Medicine, University of Massachesetts Mem orial Healthcare, Worcester, Massachusetts
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Jason J. Prystowsky M.D., M.P.H. Clinical Instructor Departm ent of Em ergency Medicine, Em ory University, Atlanta, Georgia Michelle E. Pyka M.D. Departm ent of Em ergency Medicine, Lom a Linda University Medical Center, Lom a Linda, California Vittorio Raho M.D. Resident Departm ent of Em ergency Medicine, Harvard Medical School; Resident, Departm ent of Em ergency Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts Niels Rathlev M.D. Associate Professor Departm ent of Em ergency Medicine, Boston University School of Medicine; Vice Chair, Departm ent of Em ergency Medicine, Boston Medical Center, Boston, Massachusetts Wende R. Reenstra M.D., Ph.D. Instructor Departm ent of Medicine, Harvard Medical School; Director Basic Science Research, Departm ent of Em ergency Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts Kristine Reid M.D. Departm ent of Em ergency Medicine, York Hospital, York, Maine Ian Reilly M.D. Em ergency Physician Departm ent of Em ergency Medicine, Sharp Mem orial Hospital, San Diego, San Diego, California James W. Rhee M.D. Clinical Instructor Departm ent of Em ergency Medicine, University of Illinois at Chicago, Toxicology Fellow, Toxikon Consortium , Chicago, Illinois
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Christopher Richards M.D. Associate Professor Departm ent of Em ergency Medicine, Oregon Health and Science University, Portland, Oregon Kathy Richardson M.D. Residency Coordinator Departm ent of Em ergency Medicine, University of California, San Diego, San Diego, California Mark Richmond M.D. Assistant Medical Director Departm ent of Em ergency Medicine, Santa Barbara Cottage Hospital, Santa Barbara, California Steven Riley M.D. Assistant Professor Departm ents of Em ergency Medicine and, Pediatrics, Vanderbilt University School of Medicine, Nashville, Tennessee Jaime B. Rivas M.D. Physician Departm ent of Em ergency Medicine, Palom ar and Pom erado Hospitals, Escondido, California Matthew Robinson M.D. Clinical Instructor Departm ent of Em ergency Medicine, Naval Medical Center, San Diego, San Diego, California Colleen N. Roche M.D. Assistant Professor, Assistant Residency Director Departm ent of Em ergency Medicine, The George Washington University, Washington, D.C. Jedd E. Roe M.D., M.B.A. M.S.F. Residency Director, Associate Professor Departm ent of Em ergency Medicine, University of Alabam a at Birm ingham , Birm ingham , Alabam a
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Joshua Roffman M.D. Carlo L. Rosen M.D. Assistant Professor Departm ent of Medicine, Harvard Medical School; Program Director, Harvard Affiliated Em ergency Medicine Residency, Departm ent of Em ergency Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts Peter Rosen M.D. Associate Professor, Attending Physician Beth Israel Deaconess Hospital, Boston, Massachusetts; Attending Physician, St. John's Hospital, Jackson Hole, Wyom ing, Visiting Professor, University of Arizona, Tucson, Arizona Lawrence S. Rosenthal M.D., Ph.D. Associate Professor Departm ent of Cardiology; Director, Section Cardiac Pacing and Electrophysiology, University of Massachusetts Mem orial Medical Center, Worchester, Massachusetts Christopher Ross M.D. Assistant Professor Departm ent of Em ergency Medicine, Rush University; Assistant Program Director, Departm ent of Em ergency Medicine, John H. Stroger Hospital of Cook County, Chicago, Illinois Todd C. Rothenhaus M.D. Departm ent of Em ergency Medicine, Boston University Medical Center, Boston, Massachusetts David H. Rubin M.D. Professor of Clinical Pediatrics Departm ent of Pediatrics, Weill Medical College of Cornell University, New York, New York; Chairm an and Program Director, Departm ent of Pediatrics, St. Barnabas Hospital, Bronx, New York Scott Rudkin M.D., M.B.A., R.D.M.S. Assistant Clinical Professor
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Departm ent of Em ergency Medicine, University of California, Irvine; Vice Chief of Em ergency Medicine, Departm ent of Em ergency Medicine, University of California, Irvine Medical Center, Orange, California Nate Rudman M.D. Em ergency Physician Departm ent of Em ergency Medicine, Cape Cod Hospital, Hyannis, Massachusetts Gary S. Sachs M.D. Associate Professor of Psychiatry Departm ent of Psychiatry, Massachusetts General Hospital; Director of Bipolar Clinic and, Research Program , Harvard Medical School, Boston, Massachusetts Mark Sagarin M.D. Mt. Auburn Hospital, Cam bridge, Massachusetts Erich Salvacion M.D. Hospitalist, Departm ent of Internal Medicine, Kaiser Perm anente, Bellflower, California Leon D. Sanchez M.D., M.P.H. Clinical Instructor Departm ent of Medicine, Harvard Medical School; Attending Physician, Departm ent of Em ergency Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts Arthur Sanders M.D., M.H.A. Professor Departm ent of Em ergency Medicine, University of Arizona College of Medicine; Attending Physician, Departm ent of Em ergency Medicine, University Medical Center, Tucson, Arizona Kathy Sanders M.D. Assistant Professor Departm ent of Psychiatry, Harvard Medical School; Training Director, Departm ent of Psychiatry, Massachusetts General Hospital, Boston,
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Massachusetts Marcelo Sandoval M.D. Assistant Professor Departm ent of Em ergency Medicine, Albert Einstein College of Medicine, Bronx, New York; Chair, Com m ittee on Em ergency/Disaster, Managem ent, Beth Israel Medical Center, New York, New York John Santamaria M.D., F.A.A.P., F.A.C.E.P. Affialiate Professor Departm ent of Medicine, USF School of Medicine, Tam pa, Florida Sally Santen M.D. Assistant Professor Departm ent of Em ergency Medicine, Vanderbilt School of Medicine, Nashville, Tennessee Elaine Sapiro M.D., M.P.H. Assistant Clinical Professor Departm ent of Em ergency Medicine, University of California, San Diego, San Diego, California Daniel L. Savitt M.D. Associate Professor Departm ents of Em ergency Medicine and Internal, Medicine, Brown University; Director, Departm ent of Em ergency Medicine, The Miriam Hospital, Providence, Rhode Island Assaad J. Sayah M.D., F.A.C.E.P. Assistant Clinical Professor Departm ent of Em ergency Medicine, Tufts University School of Medicine, Boston, Massachusetts; Chairm an, Departm ent of Em ergency Medicine, Caritas Good Sam aritan Medical Center, Boston, Massachusetts Shari Schabowski M.D. Assistant Professor Departm ent of Em ergency Medicine, Rush Medical College; Senior
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Attending Physician, Departm ent of Em ergency Medicine, John H. Stroger Hospital of Cook County, Chicago, Illinois Jeffrey Schaider M.D. Associate Professor of Em ergency Medicine Rush Medical College; Chairm an, Departm ent of Em ergency Medicine, Cook County Hospital, Chicago, Illinois Michael Schmidt M.D. Assistant Professor Departm ent of Em ergency Medicine, Feinburg School of Medicine; Assistant Professor, Departm ent of Em ergency Medicine, Northwestern Mem orial Hospital, Chicago, Illinois Jeffrey I. Schneider M.D. Assistant Professor, Assistant Residency Director Departm ent of Em ergency Medicine, Boston University School of Medicine; Attending Physician, Boston Medical Center, Boston, Massachusetts Hugh Schuckman M.D. Clinical Professor Departm ent of Em ergency Medicine, North East Ohio Universities, College of Medicine, Rootstown, Ohio; Attending Physician, Sum m a Health System s, Akron, Ohio Suzanne Schuh M.D., F.R.C.P.(C), F.A.A.P., A.B.P.E.M. Professor of Paediatrics University of Toronto; Staff Paediatrician and Research Director, Division of Paediatric Em ergency Medicine; Senior Associate Scientist, Research Institute, Hospital for Sick Children, Toronto, Canada Theresa Schwab M.D. Departm ent of Em ergency Medicine, Christ Medical Center, Oak Lawn, Illinois Gary Schwartz M.D. Assistant Professor
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Departm ent of Em ergency Medicine, Vanderbilt University Medical Center, Nashville, Tennessee James Scott M.D. Dean School of Medicine and Health Sciences, Deans Office SMHS, George Washington University, Washington, D.C. Michelle Sergel M.D. Assistant Professor Departm ent of Em ergency Medicine, Rush University Medical Center; Attending Physician, Departm ent of Em ergency Medicine, John H. Stroger Hospital of Cook County, Chicago, Illinois Nathan Shapiro M.D., M.P.H. Assistant Professor Harvard Medical School, Research Director, Beth Israel Deaconess Medical Center, Boston, Massachusetts Ghazala Q. Sharieff M.D., F.A.C.E.P., F.A.A.E.M., F.A.A.P. Assistant Clinical Professor Children's Hospital and Health Center/University of, California, San Diego, California; Director of Pediatric Em ergency Medicine, Palom ar-Pom erado Hospitals/California Em ergency, Physicians, San Diego, California Philip Shayne M.D. Associate Professor and Residency Director Departm ent of Em ergency Medicine, Em ory School of Medicine, Atlanta, Georgia Lorne Sherman M.D. North Shore University Hospital, Manhasset, New York Scott C. Sherman M.D. Assistant Professor Departm ent of Em ergency Medicine, Rush Medical College; Assistant Residency Director, Departm ent of Em ergency Medicine, John H. Stroger Hospital of Cook County, Chicago, Illinois
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Chet Shermer M.D. Clinical Assistant Professor Departm ent of Em ergency Medicine, University of Mississippi Medical Center; Staff Physician, Departm ent of Em ergency Medicine, Mississippi Baptist Medical Center, Jackson, Mississippi Patricia Shipley M.D. Rush-Presbyterian-St. Luke's Medical Center, Chicago, Illinois Lee Shockley M.D. Associate Professor Departm ent of Surgery, Division of Em ergency Medicine, University of Colorado; Medical Director, Departm ent of Em ergency Medicine, The Denver Health Medical Center, Denver, Colorado Robert Sidman M.D. Departm ent of Em ergency Medicine, Rhode Island Hospital, Providence, Rhode Island Christine Tsien Silvers M.D., Ph.D. Research Associate Children's Hospital Inform atics Program , Children's Hospital, Boston, Massachusetts; Attending Physician, Departm ent of Em ergency Medicine, Caritas Good Sam aritan Medical Center, Brockton, Massachusetts Alison K. Sisitsky M.D. Attending Physician Departm ent of Em ergency Medicine, Newton Wellesley Hospital, Newton, Massachusetts Christian M. Sloane M.D. Assistant Clinical Professor Departm ent of Em ergency Medicine, University of California, San Diego, Medical Center, San Diego, California James Smith M.D. Resident Physician Departm ent of Em ergency Medicine, Harvard Affiliated Em ergency
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Medicine Residency, Beth Israel Deaconess Medical Center, Boston, Massachusetts Rebecca Smith-Coggins M.D. Associate Professor Departm ent of Surgery/Em ergency Medicine, Stanford University, Stanford, California Brian K. Snyder M.D. Associate Clinical Professor of Medicine Departm ent of Em ergency Medicine, University of California, San Diego, San Diego, California Matthew Solley M.D. Chief Resident Departm ent of Em ergency Medicine, University of California Irvine Medical Center, Orange, California Julia Sone M.D. Physician Departm ent of Surgery, INOVA Fairfax Hospital, Falls Church, Virginia Camie J. Sorensen M.D., M.P.H. Physician Departm ent of Em ergency Medicine, Harvard Affiliated Em ergency Medicine Residency, Beth Israel Deaconess Medical Center, Boston, Massachusetts Matthew T. Spencer M.D. Assistant Professor Departm ent of Em ergency Medicine, University of Rochester School of Medicine and, Dentistry, Rochester, New York Linda L. Spillane M.D. Associate Professor Departm ent of Em ergency Medicine, University of Rochester; Residency Program Director, Departm ent of Em ergency Medicine, Strong Mem orial Hospital, Rochester, New York
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Blake Spirko M.D., F.A.C.E.P., F.A.A.P. Fellowship Director Pediatric Em ergency, Medicine, Departm ent of Em ergency Medicine, Tufts University School of Medicine, Boston, Massachusetts; Associate Professor, Departm ent of Em ergency Medicine, Baystate Medical Center, Springfield, Massachusetts Timothy Stallard M.D. Assistant Professor Departm ent of Em ergency Medicine, Texas A & M System Health Sciences Center; Program Director, Em ergency Medicine Residency, Scott and White Mem orial Hospital, Tem ple, Texas Dale W. Steele M.D. Associate Professor Departm ents of Em ergency Medicine and, Pediatrics, Brown Medical School; Attending Physician and Fellowship Director, Departm ent of Pediatric Em ergency Medicine, Hasbro Children's Hospital, Providence, Rhode Island James T. Steen M.D. Senior Resident Departm ent of Em ergency Medicine, University of Iowa, Iowa City, Iowa James M. Stephen M.D. Assistant Professor Departm ent of Em ergency Medicine, Tufts University School of Medicine; Director—Medical Inform atics; Associate Director—Pediatric Traum a Service, Departm ent of Em ergency Medicine, Tufts-New England Medical Center, Boston, Massachusetts T. A. Stern M.D. Psychiatric Consultation Service Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts Edward Stettner M.D.
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Assistant Professor Departm ent of Em ergency Medicine, Em ory University; Attending Physician, Departm ent of Em ergency Medicine, Grady Mem orial Hospital, Atlanta, Georgia Helen Straus M.D., M.S. Assistant Professor Departm ent of Em ergency Medicine, Rush University; Attending Physician, Departm ent of Em ergency Medicine, John H. Stroger Hospital of Cook County, Chicago, Illinois Stacey A. Suecoff M.D. Assistant Professor Departm ent of Pediatrics, Weill Medical College of Cornell University, New York, New York; Director, Departm ent of Pediatric Em ergency Medicine, St. Barnabas Hospital, Bronx, New York John Sullivan M.D. Attending Physician and Core Faculty Departm ent of Em ergency Medicine, Jackson Mem orial Hospital, Miam i, Florida Paul A. Szucs M.D. David Tanen M.D. Director Em ergency Medicine Residency Program , Departm ent of Em ergency Medicine, Naval Medical Center San Diego, San Diego, California Guy Tarleton M.D. Departm ent of Em ergency Medicine, St. Francis Medical Center, Santa Barbara, California Elizabeth Temin M.D. Instructor Departm ent of Em ergency Medicine, Harvard Medical School; Adjunct Instructor, Departm ent of Em ergency Medicine, Boston University Medical School; Attending Physician, Departm ent of Em ergency Medicine, Massachusetts General Hospital, Boston, Massachusetts
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Kristine Thompson M.D. Clinical Instructor Departm ent of Em ergency Medicine, Mayo Clinic College of Medicine, Jacksonville, Jacksonville, Florida Trevonne M. Thompson M.D. Medical Toxicology Fellow Toxikon Consortium , John H. Stroger Hospital of Cook County, Division of Occupational Medicine; Clinical Instructor, Departm ent of Em ergency Medicine, University of Illinois at Chicago, Chicago, Illinois Carrie Tibbles M.D. Associate Program Director Departm ent of Em ergency Medicine, Harvard Affiliated Em ergency Medicine Residency; Physician, Beth Israel Deaconess Medical Center, Bostson, Massachusetts Mercedes Torres M.D. Senior Resident Surgery, Departm ent of Em ergency Medicine, University of Maryland Medical Center, Baltim ore, Maryland Susan P. Torrey M.D., F.A.C.E.P. Assistant Professor Departm ent of Em ergency Medicine, Tufts University School of Medicine, Boston, Massachusetts; Associate Residency Director, Departm ent of Surgery, Baystate Medical Center, Springfield, Massachusetts Shirin Trachiotis M.D. Departm ent of Em ergency Medicine, Sibley Mem orial Hospital, Washington, D.C. Jason Tracy M.D. Instructor in Medicine Harvard Medical School; Assistant Program Director, Beth Israel Deaconess Medical Center, Boston, Massachusetts
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Clyde Turner M.D. Attending Physician Departm ent of Em ergency Medicine, Darnall Arm y Com m unity Hospital, Fort Hood, Texas Edward Ullman M.D. Attending Physician Departm ent of Em ergency Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts Thomas A. Utecht M.D. Associate Professor of Clinical Medicine University of California, San Francisco; Chief Quality Officer, Com m unity Medical Centers, Fresno, California Sami Uwaydat M.D. Resident Physician Harvey & Bernice Jones Eye Institute, University of Arkansas for Medical Sciences, Little Rock, Arkansas Federico E. Vaca M.D., M.P.H. Associate Professor Departm ent of Em ergency Medicine, University of California, Irvine School of, Medicine, Orange, California Tyler F. Vadeboncoeur M.D. Senior Associate Consultant Departm ent of Em ergency Medicine, Mayo Clinic College of Medicine, Em ergency Physician, Departm ent of Em ergency Medicine, St. Luke's Hospital, Jacksonville, Florida Carla Valentine M.D. Attending Physician Departm ent of Em ergency Medicine, Santa Barbara College Hospital, Santa Barbara, California Verena Valley M.D. Departm ent of Em ergency Medicine, University of Mississippi Medical Center, Jackson, Mississippi
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Karen B. Van Hosen M.D. Clinical Professor of Medicine Departm ent of Em ergency Medicine, University of California, San Diego, San Diego, California James T. Vandenberg M.D., F.A.A.E.M. Adjunct Clinical Associate Professor Departm ent of Em ergency Medicine, University of Iowa, Iowa City, Iowa; Medical Director, Departm ent of Em ergency Medicine, Great River Medical Center, West Burlington, Iowa P. Yannis Venieris M.D. Gary M. Vilke M.D., F.A.C.E.P., F.A.A.E.M. Professor Departm ent of Em ergency Medicine, University of California, San Diego, San Diego, California Robert Vissers M.D., F.A.C.E.P. Adjunct Associate Professor Oregon Health & Sciences University; Director, Departm ent of Em ergency Medicine, Legacy Em anuel Hospital, Portland, Oregon David A. Vitberg M.D. Clinical Fellow Critical Care Medicine, Critical Care Medicine Departm ent, National Institutes of Health, Bethesda, Maryland James Walker D.O., M.S. Clinical Professor Departm ent of Surgery, University of Oklahom a HSC; Em ergency Physician, Departm ent of Em ergency Medicine, Oklahom a Heart Hospital, Oklahom a City, Oklahom a Michael Waters M.D. Academ ic Chief Resident Departm ent of Em ergency Medicine, University of California, Irvine School of Medicine, Orange, California Joseph Weber M.D.
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Assistant Professor Departm ent of Em ergency Medicine, Rush Medical College; Em ergency Medicine Service Director, Departm ent of Em ergency Medicine, John H. Stroger Hospital of Cook County, Chicago, Illinois Bruce A. Webster M.D., Ph.D. Chief Departm ent of Em ergency Medicine, Swedish Medical Center, Seattle, Washington Scott G. Weiner M.D., M.P.H. Assistant Professor Departm ent of Em ergency Medicine, Tufts University School of Medicine; Attending Physician, Departm ent of Em ergency Medicine, Tufts-New England Medical Center, Boston, Massachusetts Kurt Whitaker M.D. Rebecah M. Wilks M.D. Adjunct Assistant Professor Departm ent of Em ergency Medicine, George Washington University School of Medicine, Washington, D.C. Seth K. Williams M.D. Chief Resident Departm ent of Orthopaedic Surgery, University of California, San Diego, San Diego, California Brandon K. Wills D.O., M.S. Clinical Assistant Professor Departm ent of Em ergency Medicine, University of Washington; Staff Physician, Departm ent of Em ergency Medicine, Madigan Arm y Medical Center, Tacom a, Washington Tracy Wimbush M.D. Departm ent of Em ergency Medicine, Massachusetts General Hospital, Boston, Massachusetts Kathleen A. Wittels M.D. Chief Resident
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Harvard Affiliated Em ergency Medicine Residency; Chief Resident, Massachusetts General Hospital, Brigham and Wom en's Hospital, Boston, Massachusetts Peter J. Witucki M.D. Assistant Clincal Professor Departm ent of Em ergency Medicine, University of California, San Diego, San Diego, California Richard Wolfe M.D. Associate Professor Division of Em ergency Medicine, Harvard Medical School; Chief, Departm ent of Em ergency Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts Jeannette M. Wolfe M.D., F.A.C.E.P. Clinical Assistant Professor Departm ent of Em ergency Medicine, Tufts University School of Medicine, Baystate Hospital, Springfield, Massachusetts Jason K. Wong M.D. Resident Departm ent of Em ergency Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts Robert Wollard M.D. Adam Wos M.D. Resident Departm ent of Em ergency Medicine, University of California, San Diego, San Diego, California Daniel T. Wu M.D. Assistant Professor Departm ent of Em ergency Medicine, Em ory University School of Medicine, Atlanta, Georgia Christine Yang-Kauh M.D. Clinical Instructor Departm ent of Em ergency Medicine, Weill Medical College of Cornell
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University, New York, New York; Attending Assistant Residency Director, Departm ent of Em ergency Medicine, New York Methodist Hospital, Brooklyn, New York Sandra S. Yoon M.D. Christian Young M.D. Resident Physician Departm ent of Em ergency Medicine, Northwestern University School of Medicine; Resident Physician, Departm ent of Em ergency Medicine, Northwestern Mem orial Hospital, Chicago, Illinois Timothy Young M.D. Richard Zane M.D. Vice Chairm an Departm ent of Em ergency Medicine, Brigham and Wom en's Hospital, Harvard Affiliated Em ergency Medicine Residency, Boston, Massachusetts Michelle Zell-Kanter Pharm.D., A.B.A.T. TOXIKON Coordinator Section of Clinical Toxicology, Division of Occupational Medicine, John H. Stroger Hospital of Cook County, Chicago, Illinois Julie Zeller M.D. Departm ent of Em ergency Medicine, Beth Israel Deaconess Medical Center, Boston, Massachusetts Aviva Jacoby Zigman M.D. Physician Departm ent of Em ergency Medicine, Portland Adventist Medical Center, Portland, Oregon Andrew Zigman M.D. Departm ent of Em ergency Medcine, Portland Adventist Medical Center, Portland, Oregon Gary D. Zimmer M.D., F.A.C.E.P. Assistant Professor Departm ent of Em ergency Medicine, Johns Hopkins University,
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Baltim ore, Maryland; Chairm an, Departm ent of Em ergency Medicine, St. Mary Medical Center, Langhorne, Pennsylvania Karen P. Zimmer M.D. Assistant Professor of Pediatrics Johns Hopkins University, Baltim ore, Maryland David N. Zull M.D., F.A.C.E.P., F.A.C.P. Associate Professor Departm ents of Medicine and Em ergency Medicine, Northwestern University; Co-Director, Em ergency Departm ent, Observation Unit, Departm ent of Em ergency Medicine, Northwestern Mem orial Hospital, Chicago, Illinois
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > F ro nt o f Bo o k > Preface
Preface
Rosen and Barkin's 5-Minute Em ergency Medicine Consult uniquely reflects our clinical practices and specialty of em ergency m edicine. It's focus is to provide concise, form atted inform ation that will allow the busy clinician to respond to challenges in a tim ely fashion. The book is m eant to be readily accessible and frequently used in the m idst of the clinical environm ent rather than be read at one's leisure. It is written and edited by practicing clinicians for practicing clinicians. As em ergency physicians, we need references to rem ind us of clinical presentations, differential diagnoses, drugs and dosages and m anagem ent principles that facilitate our clinical judgm ent in synthesizing the vast array of available data. We have attem pted to supplem ent this data bank with a perspective gained through m any years of practice. The book is not m eant to be a diagnostic engine, but rather a place to turn to confirm a diagnosis that is supported by the clinical presentation. Our talented authors discuss each topic as if they were in the m iddle of a busy ED, trying to present a precise and clinically relevant sum m ary to a resident who had queried them on a topic, or with whom they m ight be seeing a patient with a particular problem . We are indebted to them for their com m itm ent to this task. The book is intended to be accurate, pointed, and readily integrated into practice, rather than definitive. This 3rd edition incorporates new inform ation and approaches to m anagem ent, while allowing us to develop new topics that reflect som e of the new challenges we face.
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Rosen and Barkin's 5-Minute Em ergency Medicine Consult will be useful to both novices in em ergency m edicine and experienced clinicians. The inform ation and organization of the book is designed to be optim al in the m iddle of the “chaos― that surrounds our clinical settings. The form at and content focuses on the key inform ation that you will need in patient m anagem ent. Clinical acum en, judgm ent, and experience rem ain as the foundation for our clinical practices. It is our hope that this book will serve as a useful and readily used resource and enhance the fulfillm ent of practicing em ergency m edicine. Jeffrey Schaider Stephen R. Hayden Richard Wolfe Roger M. Barkin Peter Rosen
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > F ro nt o f Bo o k > Ackno w ledgem ents
Acknowledgements
To m y loving wife, Anna, and m y sons Jacob and Isaac, who have always supported and inspired m e. I would like to thank the Cook County Em ergency Medicine Residents and Attendings for their contributions to this textbook and to enhancing m y knowledge and understanding of our unique field. Finally, I want to extend a special thanks to m y friend, Dr. Robert Sim on, who continues to be a role m odel and m entor. J. S. To m y residents, I hope this book helps you where it is needed m ost and gives you the inform ation you need to take better care of your patients. To m y children, Connor, Maia, and Kenny and m y wife Marina thank you for all the love and support and your willingness to allow m e to do the work I love. S. R. H. To the Em ergency Medicine faculty and residents at Beth Israel Deaconess Medical Center R. W. This book is dedicated to the m any talented and devoted clinicians who will hopefully find it useful in their pursuit of excellence in patient care. Your constant focus on your patient's welfare and health is an inspiration to provide tools that facilitate the challenges of working in the em ergency and urgent care setting. Thanks are especially due to the m any authors who help to m ake this book com prehensive, accurate and tim ely. Lippincott's entire editorial team have m ade the process m ove sm oothly through m any steps
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with special thanks to Nicole Dernoski who coordinated the com m unication and com pletion of the m anuscript. R. M. B.
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↑ Table of Contents
[+] Abdominal Aortic Aneurysm [+] Abdominal Pain [+] Abdominal Trauma, Blunt [+] Abdominal Trauma, Imaging [+] Abdominal Trauma, Penetrating [+] Abortion, Spontaneous [+] Abruptio Placentae [+] Abscess, Skin/Soft Tissue [+] Abuse, Elder [+] Abuse, Pediatric (Nonaccidental Trauma [NAT]) [+] Acetaminophen Poisoning [+] Acidosis [+] Acromio-Clavicular Joint Injury [+] Acute Coronary Syndrome: Coronary Vasospasm [+] Acute Coronary Syndrome: Drug Induced [+] Acute Coronary Syndrome: Myocardial Infarction [+] Acute Coronary Syndrome: Non–Q-Wave (Non-ST Elevation) MI
Page 107
[+] Acute Coronary Syndrome: Stable Angina [+] Acute Coronary Syndrome: Unstable Angina [+] Adrenal Insufficiency [+] Airway Management [+] Alcohol Poisoning [+] Alcoholic Ketoacidosis [+] Alkalosis [+] Altered Mental Status [+] Amebiasis [+] Amenorrhea [+] Amphetamine, Poisoning [+] Amputation Traumatic/Replantation [+] Amyotrophic Lateral Sclerosis [+] Anal Fissure [+] Anaphylaxis [+] Anemia [+] Angioedema [+] Ankle Fracture/Dislocation
Page 108
[+] Ankle Sprain [+] Ankylosing Spondylitis [+] Anterior Cruciate Ligament Injury [+] Anticholinergic Poisoning [+] Antidepressant Poisoning [+] Aortic Dissection, Thoracic [+] Aortic Rupture, Traumatic (TAI) [+] Aphthous Ulcers [+] Apnea [+] Appendicitis [+] Arsenic Poisoning [+] Arterial Gas Embolism (AGE) [+] Arterial Occlusion [+] Arthritis, Degenerative [+] Arthritis, Juvenile Idiopathic [+] Arthritis, Monoarticular [+] Arthritis, Rheumatoid [+] Arthritis, Septic
Page 109
[+] Ascites [+] Asthma, Adult [+] Asthma, Pediatric [+] Asystole [+] Ataxia [+] Atrial Fibrillation [+] Atrial Flutter [+] Atrioventricular Blocks [+] Babesiosis [+] Back Pain [+] Bacterial Tracheitis [+] Barbiturates, Poisoning [+] Barotrauma [+] Bartholin Abscess [+] Bell's Palsy [+] Benzodiazepine, Poisoning [+] Beta-Blocker Poisoning [+] Biologic Weapons
Page 110
[+] Bipolar Disorder [+] Bite, Animal [+] Bite, Human [+] Bladder Injury [+] Blow-Out Fracture [+] Boerhaave Syndrome [+] Botulism [+] Bowel Obstruction [+] Bradyarrhythmias [+] Bronchiolitis [+] Bronchitis [+] Bundle Branch Blocks [+] Burns [+] Bursitis [+] Calcium Channel Blocker, Poisoning [+] Candidiasis, Oral [+] Carbamazepine, Poisoning [+] Carbon Monoxide, Poisoning
Page 111
[+] Cardiac Arrest [+] Cardiac Pacemakers [+] Cardiac Testing [+] Cardiac Transplantation Complications [+] Cardiogenic Shock [+] Cardiomyopathy [+] Cardiomyopathy, Hypertrophic [+] Cardiomyopathy, Peripartum [+] Carpal Fractures [+] Carpal Tunnel Syndrome [+] Cauda Equina Syndrome [+] Caustic Ingestion [+] Cavernous Sinus Thrombosis [+] Cellulitis [+] Cerebral Aneurysm [+] Cerebral Vascular Accident [+] Cervical Adenitis [+] Cesarean Section, Emergency
Page 112
[+] Chancroid [+] Chemical Weapons Poisoning [+] Chest Pain [+] Chest Trauma, Blunt [+] Chest Trauma, Penetrating [+] Cholangitis [+] Cholecystitis [+] Cholelithiasis [+] Chronic Obstructive Pulmonary Disease [+] Cirrhosis [+] Clavicle Fracture [+] Cocaine, Poisoning [+] Colon Trauma [+] Coma [+] Compartment Syndrome [+] Congenital Heart Disease, Acyanotic [+] Congenital Heart Disease, Cyanotic [+] Congestive Heart Failure
Page 113
[+] Conjunctivitis [+] Conscious Sedation [+] Constipation [+] Contact Dermatitis [+] Cor Pulmonale [+] Corneal Abrasion [+] Corneal Burn [+] Corneal Foreign Body [+] Cough [+] Croup [+] Cushing Syndrome [+] Cyanide Poisoning [+] Cyanosis [+] Cystic Fibrosis [+] Dacryoadenitis [+] Dacryocystitis [+] Decompression [+] Deep Vein Thrombosis
Page 114
[+] Defibrillators, Implantable [+] Delirium [+] Delivery, Uncomplicated [+] Dementia [+] Dengue Fever [+] Dental Truama [+] Depression [+] Dermatomyositis/Polymyositis [+] Diabetes Insipidus [+] Diabetes Mellitus, Juvenile [+] Diabetic Ketoacidosis [+] Dialysis Complications [+] Diaper Rash [+] Diaphragmatic Trauma [+] Diarrhea, Adult [+] Diarrhea, Pediatric [+] Digoxin, Poisoning [+] Disseminated Intravascular Coagulation
Page 115
[+] Disulfirum Reaction [+] Diverticulitis [+] Diverticulosis [+] Dizziness [+] Domestic Violence [+] Duodenal Trauma [+] Dysfunctional Uterine Bleeding [+] Dysphagia [+] Dyspnea [+] Dystonic Reaction [+] Eating Disorder [+] Ectopic Pregnancy [+] Eczema/Atopic Dermatitis [+] Edema [+] Ehrlichiosis [+] Elbow Injuries [+] Electrical Injury [+] Encephalitis
Page 116
[+] Endocarditis [+] Endometriosis [+] Epididymitis/Orchitis [+] Epidural Abscess [+] Epidural Hematoma [+] Epiglottitis, Adult [+] Epiglottis, Pediatric [+] Epiphyseal Injuries [+] Epistaxis [+] Erysipelas [+] Erythema Infectiosum [+] Erythema Multiforme [+] Erythema Nodosum [+] Esophageal Trauma [+] Ethylene Glycol, Poisoning [+] External Ear Chondritis/Abscess [+] Extremity Trauma, Penetrating [+] Facial Fractures
Page 117
[+] Failure to Thrive [+] Fatigue [+] Feeding Problems, Pediatric [+] Feeding Tube Complications [+] Femur Fracture [+] Fever, Adult [+] Fever, Pediatric [+] Fibrocystic Breast Disease [+] Fibromyalgia [+] Flail Chest [+] Foot Fracture [+] Forearm Fracture, Shaft/Distal [+] Foreign Body, Ear [+] Foreign Body, Esophageal [+] Foreign Body, Nasal [+] Foreign Body, Rectal [+] Fournier Gangrene [+] Fracture, Open
Page 118
[+] Fractures, Pediatric [+] Frostbite [+] Gallstone Ileus [+] Gangrene [+] Gastric Outlet Obstruction [+] Gastritis [+] Gastroenteritis [+] Gastroesophageal Reflux Disease [+] Gastrointestinal Bleeding [+] γ-GHB, Poisoning [+] Giardia [+] Glaucoma [+] Globe Rupture [+] Glomerulonephritis [+] Gonococcal Disease [+] Gout/Pseudogout [+] Granulocytopenia [+] Guillain-Barré Syndrome
Page 119
[+] Hallucinogen Poisoning [+] Hand Infection [+] Hazmat [+] Head Trauma, Blunt [+] Head Trauma, Penetrating [+] Headache [+] Headache, Cluster [+] Headache, Migraine [+] Heart Murmur [+] HELLP Syndrome [+] Hematuria/Proteinuria [+] Hemophilia [+] Hemoptysis [+] Hemorrhagic Fevers [+] Hemorrhagic Shock [+] Hemorrhoid [+] Hemothorax [+] Henoch Schönlein Purpura
Page 120
[+] Hepatic Encephalopathy [+] Hepatic Injury [+] Hepatitis [+] Hepatorenal Syndrome [+] Hernia [+] Herpes, Genital [+] Herpes Simplex [+] Herpes Zoster [+] Hiccups [+] High Altitude Illness [+] Hip Injury [+] Hirschsprung Disease [+] HIV/AIDS [+] Hordeolum and Chalazion [+] Horner Syndrome [+] Humerus Fracture [+] Hydatidiform Mole [+] Hydrocarbon Poisoning
Page 121
[+] Hydrocele [+] Hydrocephalus [+] Hyperbaric Oxygen Therapy [+] Hypercalcemia [+] Hyperemesis Gravidarum [+] Hyperkalemia [+] Hypernatremia [+] Hyperosmolar Syndrome [+] Hyperparathyroidism [+] Hypertensive Emergencies [+] Hyperthermia [+] Hyperthyroidism [+] Hyperventilation [+] Hyperviscosity Syndrome [+] Hyphema [+] Hypocalcemia [+] HypoGlycemia [+] Hypoglycemic Poisoning
Page 122
[+] Hypokalemia [+] Hyponatremia [+] Hypoparathyroidism [+] Hypothermia [+] Hypothyroidism [+] Idiopathic Thrombocytopenic Purpura [+] Immunizations [+] Immunosuppression [+] Impetigo [+] Inborn Errors of Metabolism [+] Inflammatory Bowel Disease [+] Influenza [+] Intracerebral Hemorrhage [+] Intussusception [+] Iritis [+] Iron Poisoning [+] Irritable Bowel [+] Irritable Infant
Page 123
[+] Irritant Gas Exposure [+] Isoniazid Poisoning [+] Isopropanol Poisoning [+] Jaundice [+] Kaposi Sarcoma [+] Kawasaki Disease [+] Knee Dislocation [+] Labor [+] Labyrinthitis [+] Laceration Management [+] Laryngitis [+] Larynx Fracture [+] Lead Poisoning [+] Legg-Calvé-Perthes Disease [+] Leukemia [+] Lightning Injuries [+] Lithium Poisoning [+] Ludwig's Angina
Page 124
[+] Lunate Dislocation [+] Lyme Disease [+] Lymphadenitis [+] Lymphangitis [+] Lymphogranuloma Venereum [+] Malaria [+] Malgaigne Fracture [+] Mallory-Weiss Syndrome [+] Malrotation [+] Mandibular Fractures [+] Marine Envenomation [+] Mastitis [+] Mastoiditis [+] MDMA Poisoning [+] Measles [+] Meckel Diverticulum [+] Medial Collateral Ligament Strain [+] Medial Meniscus Injury
Page 125
[+] Ménière Disease [+] Meningitis [+] Meningococcemia [+] Mercury Poisoning [+] Mesenteric Ischemia [+] Metacarpal Injuries [+] Methanol Poisoning [+] Methemoglobinemia [+] Mitral Valve Prolapse [+] Molluscum Contagiosum [+] Monoamine Oxidase Inhibitor, Poisoning [+] Mononucleosis [+] Multiple Myeloma [+] Multiple Sclerosis [+] Mumps [+] Munchausen's Syndrome [+] Mushroom, Poisoning [+] Myasthenia Gravis
Page 126
[+] Myocardial Contusion [+] Myocarditis [+] Nasal Fractures [+] Near Drowning [+] Neck Injury by Strangulation/Hanging [+] Neck Trauma, Blunt, Anterior [+] Neck Trauma, Penetrating, Anterior [+] Necrotizing Soft Tissue Infections [+] Necrotizing Ulcerative Gingivitis [+] Needle Stick [+] Neonatal Jaundice [+] Neonatal Sepsis [+] Nephritic Syndrome [+] Nephrotic Syndrome [+] Neuroleptic Malignant Syndrome [+] Neuroleptic Poisoning [+] Noncardiogenic Pulmonary Edema [+] Nonsteroidal Anti-inflammatory Poisoning
Page 127
[+] Nursemaid's Elbow [+] Oculomotor Nerve Palsy [+] Opiate Poisoning [+] Opportunistic Infection [+] Optic Artery Occlusion [+] Optic Neuritis [+] Organophosphate Poisoning [+] Osgood-Schlatter Disease [+] Osteogenesis Imperfecta [+] Osteomyelitis [+] Osteoporosis [+] Otitis Externa [+] Otitis Media [+] Otologic Trauma [+] Ovarian Cyst/Torsion [+] Paget's Disease [+] Pancreatic Pseudocyst [+] Pancreatic Trauma
Page 128
[+] Pancreatitis [+] Panic Attack [+] Paraphimosis [+] Parkinson's Disease [+] Paronychia [+] Patellar Injuries [+] Patent Ductus Arteriosus [+] Pediatric Trauma [+] Pediculosis [+] Pelvic Fracture [+] Pelvic Inflammatory Disease [+] Pemphigus [+] Penile Shaft Fracture [+] Peptic Ulcer [+] Perforated Viscous [+] Pericardial Effusion/Tamponade [+] Pericarditis [+] Perilunate Dislocation
Page 129
[+] Periodontal Abscess [+] Periorbital and Orbital Cellulitis [+] Peripheral Neuropathy [+] Peripheral Vascular Disease [+] Perirectal Abscess [+] Peritonsillar Abscess [+] Pertussis [+] Phalangeal Injuries, Foot [+] Phalangeal Injuries, Hand [+] Pharyngitis [+] Phencyclidine, Poisoning [+] Phenytoin, Poisoning [+] Pheochromocytoma [+] Phimosis [+] Pityriasis Rosea [+] Placenta Previa [+] Plant, Poisoning [+] Pleural Effusion
Page 130
[+] Pneumocystis Carinii Pneumonia [+] Pneumomediastinum [+] Pneumonia, Adult [+] Pneumonia, Pediatric [+] Pneumothorax [+] Poisoning [+] Poisoning, Antidotes [+] Poisoning, Gastric Decontamination [+] Poisoning, Toxidromes [+] Polio [+] Polycythemia [+] Postpartum Hemorrhage [+] Postpartum Infection [+] Pre-Eclampsia/Eclampsia [+] Pre-excitation Syndromes [+] Pregnancy, Trauma in [+] Pregnancy, Uncomplicated [+] Priapism
Page 131
[+] Prostatitis [+] Pruritis [+] Pseudotumor Cerebri [+] Psoriasis [+] Psychiatric Commitment [+] Psychosis, Acute [+] Psychosis, Medical vs. Psychiatric [+] Pulmonary Contusion [+] Pulmonary Edema [+] Pulmonary Embolism [+] Purpura [+] Pyelonephritis [+] Pyloric Stenosis [+] QT Syndrome, Prolonged [+] Rabies [+] Radiation Injury [+] Rapid Sequence Intubation [+] Rash
Page 132
[+] Rash, Pediatric [+] Reactive Arthritis [+] Rectal Prolapse [+] Rectal Trauma [+] Red Eye [+] Renal Calculus [+] Renal Failure [+] Renal Injury [+] Reperfusion Therapy, Cardiac [+] Reperfusion Therapy, Cerebral [+] Respiratory Distress [+] Resuscitation, Neonate [+] Resuscitation, Pediatric [+] Retinal Detachment [+] Retropharyngeal Abscess [+] Reye Syndrome [+] Rhabdomyolysis [+] Rheumatic Fever
Page 133
[+] Rib Fracture [+] Ring/Constricting Band Removal [+] Rocky Mountain Spotted Fever [+] Roseola [+] Rubella [+] Sacral Fracture [+] Salicylate Poisoning [+] Sarcoidosis [+] Scabies [+] Scaphoid Fracture [+] Schizophrenia [+] Sciatica/Herniated Disc [+] Seborrheic Dermatitis [+] Seizure, Adult [+] Seizure, Febrile [+] Seizure, Pediatric [+] Sepsis [+] Serum Sickness
Page 134
[+] Sexual Assault [+] Shock [+] Shoulder Dislocation [+] Sick Sinus Syndrome [+] Sickle Cell Disease [+] Sinusitis [+] Skin Cancer [+] Sleep Apnea [+] Slipped Capital Femoral Epiphysis [+] Small-Bowel Injury [+] Smoke Inhalation [+] Snake Envenomation [+] Spider Bite, Black Widow [+] Spider Bite, Brown Recluse [+] Spinal Cord Syndromes [+] Spine Injury: Cervical, Adult [+] Spine Injury: Cervical, Pediatric [+] Spine Injury: Coccyx
Page 135
[+] Spinal Injury: Lumbar [+] Spine Injury: Thoracic [+] Splenic Injury [+] Spondylolysis/Spondylolisthesis [+] Spontaneous Bacterial Peritonitis [+] Sporotrichosis [+] Staphylococcal Scalded Skin Syndrome [+] Sternoclavicular Joint Injury [+] Stevens-johnson Syndrome [+] Sting, Bee [+] Sting, Scorpion [+] Streptococcal Disease [+] Stridor [+] Subarachnoid Hemorrhage [+] Subdural Hematoma [+] Sudden Infant Death Syndrome (SIDS) [+] Suicide, Risk Evaluation [+] Supraventricular Tachycardia
Page 136
[+] Sympathomimetic Poisoning [+] Syncope [+] Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH) [+] Synovitis, Toxic [+] Syphilis [+] Systemic Lupus Erythematosus [+] Tachydysrhythmias [+] Temporal Arteritis [+] Temporal Mandibular Joint Injury/Syndrome [+] Tendon Laceration [+] Tendonitis [+] Tenosynovitis [+] Testicular Torsion [+] Tetanus [+] Theophylline Poisoning [+] Thoracic Outlet Syndrome [+] Thrombotic Thrombocytopenic Purpura [+] Thumb Fracture
Page 137
[+] Tibial Plateau Fracture [+] Tibial/Fibular Shaft Fracture [+] Tick Bite [+] Tinea Infections, Cutaneous [+] Toluene Poisoning [+] Toothache [+] Torticollis [+] Toxic Epidermal Necrolysis [+] Toxic Shock Syndrome [+] Toxoplasmosis [+] Transfusion Complications [+] Transient Global Amnesia [+] Transient Ischemic Attack [+] Transplant Rejection [+] Trauma, Multiple [+] Trichomonas [+] Tricyclic Antidepressant, Poisoning [+] Trigeminal Neuralgia
Page 138
[+] Tuberculosis [+] Tularemia [+] Tumor Compression Syndromes [+] Tympanic Membrane Perforation [+] Ultraviolet Keratitis [+] Urethral Trauma [+] Urethritis [+] Urinary Retention [+] Urinary Tract Fistula [+] Urinary Tract Infections, Adult [+] Urinary Tract Infections, Pediatric [+] Urticaria [+] Vaginal Bleeding [+] Vaginal Bleeding in Pregnancy [+] Vaginal Discharge/Vaginitis [+] Valvular Heart Disease [+] Varicella [+] Varices
Page 139
[+] Vasculitis [+] Venous Insufficiency [+] Ventilator Management [+] Ventricular Fibrillation [+] Ventricular Peritoneal Shunts [+] Ventricular Tachycardia [+] Vertebrobasilar Insufficiency [+] Vertigo [+] Violence, Management of [+] Visual Loss [+] Vitreous Hemorrhage [+] Volvulus [+] Vomiting, Adult [+] Vomiting, Pediatric [+] Von Willebrand Disease [+] Warfarin/Coumadin Overdose [+] Warts [+] Weakness
Page 140
[+] West Nile Virus [+] Wheezing [+] Wilms’ Tumor [+] Withdrawal, Alcohol [+] Withdrawal, Drug [+] Wolff-Parkinson-White Syndrome [+] Wound Ballistics ↑ Back of Book
[+] Appendix
Page 141
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Abdo m inal Ao rtic Aneurysm
Abdominal
Aortic Aneurysm Jason Imperato Carlo L. Rosen
Basics Description
Focal dilation of the aortic wall with an increase in diam eter by at least 50% (>3 cm )
95% are infrarenal.
Gradual expansion or rupture causes sym ptom s.
Rupture can occur into the intraperitoneal or retroperitoneal spaces.
Intraperitoneal rupture is usually im m ediately fatal.
Average growth rate of 0.2 to 0.5 cm per year
5-year risk of rupture: o
Aneurysm s 65 years old
o
Fam ily history
o
Cigarette sm oking
o
Atherosclerosis
o
Hypertension
o
Diabetes m ellitus
o
Connective tissue disorders:
Ehlers-Danlos syndrom e
Marfan syndrom e
Uncom m on causes: o
Blunt abdom inal traum a
o
Infections of the aorta
o
Mycotic aneurysm secondary to endocarditis
Diagnosis Signs and Symptoms
Unruptured: o
Most often asym ptom atic
o
Abdom inal, back, or flank pain:
Vague, dull quality
Pa ge 1 4 3
Constant, throbbing, or colicky
o
Abdom inal m ass or fullness
o
Palpable, nontender, pulsatile m ass
o
Intact fem oral pulses
Ruptured: o
o
o
Classic triad:
Pain
Hypotension
Pulsatile abdom inal m ass
Present in only 30–50% of patients
System ic:
Syncope
Hypotension
Tachycardia
Evidence of system ic em bolization
Abdom en:
Abdom inal, back, or flank pain
Acute, severe, constant
Radiates to chest, thigh, inguinal area, or scrotum
o
Flank pain radiating to the groin in 10% of cases
Pulsatile, tender abdom inal m ass
Only 75% of aneurysm s >5 cm are palpable
Abdom inal tenderness
Abdom inal bruit
Gastrointestinal (GI) bleeding
Extrem ities:
Lower-extrem ity pain
Dim inished or asym m etric pulses in the lower extrem ities
Com plications: o
Large em boli: acute painful lower extrem ity
Pa ge 1 4 4
o
Microem boli: cool, painful, cyanotic toes (“blue toe syndrom e―)
o
Aneurysm al throm bosis: acutely ischem ic lower extrem ity
o
Aortoenteric fistula: GI bleeding
Essential Workup
Unstable patients: o
Explorative surgery without further ancillary studies
o
Bedside abdom inal ultrasound
Stable sym ptom atic patients: o
Abdom inal CT
Tests Lab
CBC
Type and cross-m atch blood
Creatinine
Urinalysis
Coagulation studies
Imaging
Plain radiographs: o
Abdom inal or lateral lum bar radiographs
o
Only if other tests are unavailable
o
Curvilinear calcification of the aortic wall or a paravertebral soft-tissue m ass indicates abdom inal aortic aneurysm (AAA) in 75% of patients.
o
Cannot identify rupture
o
Negative study does not rule out AAA.
Abdom inal ultrasound: o
Highly sensitive for detecting AAA prior to rupture
o
In em ergent setting, useful to determ ine presence of
Pa ge 1 4 5
AAA only. o
Ultrasound findings consistent with AAA are enlarged aorta greater than 3 cm or focal dilatation of the aorta.
o
Sensitivity has been reported as low as 10% following rupture.
o
Indicated in the unstable patient
Abdom inal CT scan: o
Contrast is not necessary.
o
Will dem onstrate both aneurysm and site of rupture (intraperitoneal versus retroperitoneal)
o
Allows m ore accurate m easurem ent of aortic diam eter
o
Indicated in stable patients only
Aortography: o
No use in em ergent evaluation
o
The presence of m ural throm bi can lead to underestim ation of the size of the aorta.
Diagnostic Procedures/Surgery Explorative laparotom y by vascular surgeon P.3
Differential Diagnosis
Other abdom inal arterial aneurysm s (i.e., iliac or renal)
Renal colic
Biliary colic
Musculoskeletal back pain
Pancreatitis
Cholecystitis
Appendicitis
Pa ge 1 4 6
Bowel obstruction
Perforated viscus
Mesenteric ischem ia
Diverticulitis
GI hem orrhage
Aortic throm boem bolism
Myocardial infarction
Addisonian crisis
Sepsis
Treatment Pre Hospital
Establish two large-bore IV lines
Rapid transport to the nearest facility with surgical backup
Alert ED staff as soon as possible to prepare the following: o
Operating room
o
Universal donor blood
o
Surgical consultation
Initial Stabilization
Two large-bore IV lines
Crystalloid infusion
Cardiac m onitor
Early blood transfusion
ED Treatment For patients suspected of sym ptom atic AAA:
Avoid overaggressive fluid resuscitation; this leads to increased bleeding.
Em ergent surgical consult and operative intervention
Diagnostic tests should not delay definitive treatm ent.
Pa ge 1 4 7
Follow-Up Disposition Admission Criteria All patients with sym ptom atic AAA require em ergent surgical intervention and adm ission.
Discharge Criteria Asym ptom atic patients only
Issues for Referral
Close vascular surgery follow up m ust be arranged prior to discharge.
Instructions to return im m ediately: o
With any pain in the back, abdom en, flank, or lower extrem ities
o
With dizziness or syncope
References 1. Bessen HA. Abdom inal aortic aneurysm s. In Marx JA, et al, eds. Rosen's em ergency m edicine: concepts and clinical practice. 5th ed. St. Louis, MO.: Mosby, 2002:1176–1186. 2. Ernst CB. Abdom inal aortic aneurysm . N Engl J Med. 1993;328:1167–1172. 3. Hallet JW. Managem ent of abdom inal aortic aneurysm s. Mayo Clin Proc. 2000;75:395–399. 4. Rogers RL, McCorm ack R. Aortic disasters. Em erg Med Clin N Am . 2004;22:887–908. 5. Tayal VS, Graf CD, Gibbs MA. Prospective study of accuracy and outcom e of em ergency ultrasound for abdom inal aortic aneurysm over two years. Acad Em erg Med. 2003;10:867–871.
Pa ge 1 4 8
6. Walker JS, Dire DJ. Vascular abdom inal em ergencies. Em erg Med Clin N Am . 1996;14:571–591.
Codes ICD9-CM 441.3
ICD10 171.4
Pa ge 1 4 9
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Abdo m inal Pain
Abdominal Pain
Michelle A. Finkel
Basics Description
Parietal pain: o
Irritating m aterial causing peritoneal inflam m ation
o
Pain transm itted by som atic nerves
o
Exacerbated by changes in tension of the peritoneum
o
Pain characteristics:
Sharp
Well localized
Abdom inal tenderness
Involuntary guarding
Rebound tenderness
Exacerbated by m ovem ent and coughing
Visceral pain: o
Distention of a viscous or organ capsule or spasm of intestinal m uscularis fibers:
o
Pain is generally poorly localized.
Colicky with intestinal distention
Constant with a distended gallbladder or kidney
Inflam m ation:
Initially, the pain is poorly localized.
Pa ge 1 5 0
Focal tenderness develops as the inflam m ation extends to the peritoneum or localizers.
o
Ischem ia from vascular disturbances:
Pain is severe and diffuse with catastrophic vascular em ergencies
Pain is disproportional to the abdom inal exam ination
Referred pain: o
Felt at distant location from diseased organ
o
Due to an overlapping supply by the affected neurosegm ent to the perceived location of pain
Abdom inal wall pain: o
Constant
o
Aching
o
Muscle spasm
o
Involvem ent of other m uscle groups
Etiology
Peritoneal irritants: o
Gastric juice
o
Fecal m aterial
o
Pus
o
Blood
o
Bile
o
Pancreatic enzym es
Visceral obstruction: o
Sm all intestines
o
Large intestines
o
Gallbladder
o
Ureters and kidneys
o
Visceral ischem ia
o
Intestinal
o
Renal
Pa ge 1 5 1
o
Splenic
Visceral inflam m ation: o
Appendicitis
o
Inflam m atory bowel disorders
o
Cholecystitis
o
Hepatitis
o
Peptic ulcer disease
o
Pancreatitis
o
Pelvic inflam m atory disease
o
Pyelonephritis
Abdom inal wall pain
Referred pain: o
The possibility of intrathoracic disease m ust be considered in every patient with abdom inal pain.
Diagnosis Signs and Symptoms
General: o
Anorexia
o
Malaise
o
Tachycardia
o
Hypotension
o
Fever
o
Nausea
o
Vom iting:
Etiology requiring surgical intervention is less likely when vom iting precedes the onset of pain
Abdom inal: o
Diarrhea
o
Constipation
Pa ge 1 5 2
o
Distended abdom en
o
Abnorm al bowel sounds:
High-pitched rushes with bowel obstruction
Absence of sound with ileus or peritonitis
Often unreliable
o
Pulsatile abdom inal m ass
o
Rovsing sign:
Palpation of left lower quadrant causes pain in right lower quadrant (RLQ)
o
Suggestive of appendicitis
McBurney point tenderness associated with appendicitis:
Palpation in RLQ two-thirds distance between um bilicus and right anterior superior iliac crest causes pain
o
Murphy sign:
Pause in inspiration while exam iner is palpating under liver
o
o
Suggestive of cholecystitis
Psoas sign:
Pain on extension of the thigh
Suggests inflam m ation around psoas m uscle
Obturator sign
Pain on rotation of the flexed thigh, especially internal rotation
Inflam m ation around internal obturator m uscle
o
Tender or discolored hernia site
o
Rectal and pelvic exam ination:
Tenderness with pelvic peritoneal irritation
Cervical m otion tenderness
Adnexal m asses
Rectal m ass or tenderness
Pa ge 1 5 3
Genitourinary: o
Flank pain
o
Dysuria
o
Hem aturia
o
Vaginal bleeding
o
Tender adnexal m ass on pelvis
o
Testicular pain
May be referred from renal or appendiceal pathology
o
Testicular swelling
o
High-riding testes
o
Transverse lie of testis
Extrem ities: o
Shoulder pain:
o
Referred pain from diaphragm atic involvem ent
Pulse deficit or unequal fem oral pulses
Skin: o
Jaundice
o
Herpes zoster
o
Cellulitis
Essential Workup Historical characteristics define the type of pain and suggest underlying causes:
Nature of onset of pain
Tim e of onset and duration of pain
Location of pain initially and at presentation
Extra-abdom inal radiations
Quality of pain (e.g., sharp, dull, cram py)
Palliative or provocative factors
Relation of associated finding to onset of pain
Changes in bowel habits
History of traum a
Pa ge 1 5 4
Gynecologic history
Visceral obstruction
Tests Lab
CBC: o
WBC is a poor predictor of surgical disease
Urinalysis
Serum lipase: o
More accurate than a serum am ylase in diagnosing pancreatic disorders
hCG
Serum electrolytes and glucose
Liver function tests
Gonorrhea and chlam ydia cultures should be obtained if a pelvic exam ination is perform ed.
Imaging
ECG: o
Indicated in patients with epigastric pain with risk factors for coronary artery disease
Kidney, ureter, and bladder (KUB) and upright: o
Indicated prim arily if bowel obstruction is suspected
o
Air-fluid levels and intestinal distention: Bowel obstruction
Ileus
Volvulus
Intussusception
Upright chest radiograph: o
Pneum operitoneum
Perforated viscus
Extra-abdom inal causes
Ultrasound:
Pa ge 1 5 5
o
Biliary abnorm alities
o
Hydronephrosis
o
Intraperitoneal fluid
o
Aortic aneurysm
o
Pelvic ultrasound
P.5
Abdom inal CT: o
Spiral CT without contrast:
Determ ines location and size of stone in patients with renal colic
o
CT with IV contrast only:
o
Vascular rupture suspected in a stable patient
CT with IV and oral contrast:
Indicated when there is a suspicion of a surgical etiology involving bowel or intraperitoneal hem orrhage
o
CT with rectal contrast only:
High accuracy reported in detecting appendicitis
IVP: o
Indicated in patients with suspected ureteral calculi
o
More tim e-consum ing than spiral CT
Barium enem a: o
Intussusception
o
Volvulus
Differential Diagnosis
Parietal pain: o
Abdom inal arterial aneurysm
o
Appendicitis
o
Diverticulitis with perforation or abscess
o
Ruptured ectopic pregnancy
Pa ge 1 5 6
o
Ruptured ovarian cyst
o
Pancreatitis
o
Perforated peptic ulcer
o
Perforated viscus
o
Splenic rupture
Visceral pain: o
Abdom inal epilepsy
o
Abdom inal m igraine
o
Adrenal crisis
o
Early Appendicitis
o
Bowel obstruction
o
Cholecystitis
o
Constipation
o
Depression
o
Diabetic ketoacidosis
o
Diverticulitis
o
Dysm enorrhea
o
Ectopic pregnancy
o
Esophagitis
o
Fecal im paction
o
Fitz-Hugh–Curtis syndrom e
o
Gastroenteritis
o
Hepatitis
o
Hirschsprung disease
o
Incarcerated hernia
o
Inflam m atory bowel disease
o
Intussusception
o
Irritable bowel syndrom e
o
Ischem ic bowel
o
Lactose intolerance
o
Lead poisoning
o
Meckel diverticulitis
Pa ge 1 5 7
o
Neoplasm
o
Ovarian torsion
o
Pancreatitis
o
Pelvic inflam m atory disease
o
Peptic ulcer disease
o
Renal/ureteral calculi
o
Sickle cell crisis
o
Splenic infarction
o
Spontaneous abortion
o
Testicular torsion
o
Urinary tract infection
o
Volvulus
Referred pain: o
Myocardial infarction
o
Pneum onia
Abdom inal wall pain: o
Abdom inal wall hem atom a or infection
o
Black widow spider bite
o
Herpes zoster
Pediatric Considerations
5 years: o
Appendicitis
o
Ectopic pregnancy
o
Inflam m atory bowel disease
o
Pelvic inflam m atory disease
Treatment Initial Stabilization
Em ergent laparotom y: o
Patients who are hem odynam ically unstable with suspected vascular rupture
IV fluids
ED Treatment
Antiem etics are im portant for com fort.
Narcotics or analgesics should not be withheld.
Antibiotics are needed in potential perforation and in peritonitis.
Surgical consultation based on suspected etiology
Medication (Drugs)
Am picillin: 0.5–2 g IV
Cefotetan 1–2 g IV
Cefoxitin: 1–2 g IV
Com pazine 5–10 m g PO prn nausea
Gentam icin: 1–1.7 m g/kg IV
Levofloxacin: 500 m g IV
Metronidazole 15m g/kg IV, loading dose
Pa ge 1 5 9
Ondansetron 4 m g IV prn nausea
Prom ethazine: 12.5–25 m g PO/IM/IV
Follow-Up Disposition Admission Criteria
Surgical intervention
Peritoneal signs
Patient unable to keep down fluids
Lack of pain control
Medical cause necessitating in-house treatm ent (m yocardial infarction, diabetic ketoacidosis)
IV antibiotics needed
Discharge Criteria No surgical or severe m edical etiology found in patient who is able to keep fluid down, has good pain control, and is able to follow detailed discharge instructions.
References 1. Graff LG 4th, Robinson D. Abdom inal pain and em ergency departm ent evaluation. Em erg Med Clin North Am . 2001;19(1):123–136. 2. Hendrickson M, Naparst TR. Abdom inal surgical em ergencies in the elderly. Em erg Med Clin North Am . 2003;21(4):937–969. 3. Kam in RA, Nowicki TA, Courtney DS, Powers RD. Pearls and pitfalls in the em ergency departm ent evaluation of abdom inal pain. Em erg Med Clin North Am . 2003;21(1):61–72 4. Kizer KW, Vassar MJ. Em ergency departm ent diagnosis of abdom inal disorders in the elderly. Am J Em erg Med.
Pa ge 1 6 0
1998;16(4):357–362. 5. Mason JD. The evaluation of acute abdom inal pain in children. Em erg Med Clin North Am . 1996;14(3):629–643.
Codes ICD9-CM 789.0
ICD10 R10.4
Pa ge 1 6 1
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Abdo m inal Traum a, Blunt
Abdominal
Trauma, Blunt Stewart Coffman
Basics Description
Injury results from a sudden increase of pressure to abdom en.
Solid organ injury usually m anifests as hem orrhage.
Hollow viscous injuries result in bleeding and peritonitis from contam ination with bowel contents.
Etiology
Sixty percent result from m otor vehicle collisions.
Solid organs are injured m ore frequently than hollow viscous organs.
The spleen is the m ost frequently injured organ (25%), followed by the liver (15%), intestines (15%), retroperitoneal structures (13%), and kidney (12%).
Less frequently injured are the m esentery, pancreas, diaphragm , urinary bladder, urethra, and vascular structures.
Pediatric Considerations
Pa ge 1 6 2
Children tend to tolerate traum a better because of the m ore elastic nature of their tissues.
Owing to the sm aller size of the intrathoracic abdom en, the spleen and liver are m ore exposed to injury because they lie partially outside the bony rib cage.
Diagnosis Signs and Symptoms
Spectrum from abdom inal pain, signs of peritoneal irritation, to hypovolem ic shock
Nausea or vom iting
Labored respiration from diaphragm irritation or upper abdom inal injury
Left shoulder pain with inspiration (Kehr sign) from diaphragm atic irritation owing to bleeding
Delayed presentation possible with sm all bowel injury
Essential Workup
Evaluate and stabilize airway, breathing, and circulation (ABCs).
Prim ary objective is to determ ine need for operative intervention.
Exam ine abdom en to detect signs of intra-abdom inal bleeding or peritoneal irritation.
Injury in the retroperitoneal space or intrathoracic abdom en is difficult to assess by palpation.
Rem em ber that the lim its of the abdom en include the diaphragm superiorly (nipples anteriorly, inferior scapular tip posteriorly) and the intragluteal fold inferiorly and encom pass entire circum ference.
Pa ge 1 6 3
Abrasions or ecchym oses m ay be indicators of intra-abdom inal injury: o
Roll the patient to assess the back.
Bowel sounds m ay be absent from peritoneal irritation (late finding).
Foley catheter (if no blood at the m eatus, no perineal hem atom a, and norm al prostate exam ) to obtain urine and record urinary output
Plain film of the pelvis: o
Fracture of the pelvis and gross hem aturia m ay indicate genitourinary injury.
o
Further evaluation of these structures with retrograde urethrogram , cystogram , or intravenous pyelogram
CT m ost useful in assessing need for operative intervention and for evaluating the retroperitoneal space and solid organs: o
Patient m ust be stable enough to m ake trip to scanner.
o
Also useful for suspected renal injury
FAST (focused abdom inal sonography for traum a) to detect intraperitoneal fluid o
Ultrasonography is rapid, requires no contrast agents, and is noninvasive.
o
Operator dependent
Diagnostic peritoneal lavage (useful for revealing injuries in the intrathoracic abdom en, pelvic abdom en, and true abdom en) prim arily indicated for unstable patients: o
Positive with gross blood, RBC count of >100,000/m m 3 , WBC count of 500/m m 3 , or presence of bile, feces, or food particles
Tests
Pa ge 1 6 4
Lab
Hem oglobin/hem atocrit, which initially m ay be norm al owing to isovolem ic blood loss
Type and cross is essential.
Urinalysis for blood: o
Microscopic hem aturia in the presence of shock is an indication for genitourinary evaluation.
Arterial blood gases: o
Base deficit m ay suggest hypovolem ic shock and help guide the resuscitation.
Imaging See Essential Workup.
Diagnostic Procedures/Surgery See Essential Workup.
Differential Diagnosis Lower thoracic injury m ay cause abdom inal pain.
Treatment Pre Hospital
Aggressive fluid resuscitation is still considered standard of care.
Norm al vital signs do not preclude significant intra-abdom inal pathology.
Initial Stabilization
Ensure adequate airway: o
Intubate if needed.
o
O 2 100% by nonrebreather face m ask
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Two large-bore intravenous lines with crystalloid infusion
Begin infusion of packed RBCs if no response to 2 L of crystalloid.
If patient is in profound shock, consider transfusion of O-negative or type-specific blood.
P.7
ED Treatment
Continue stabilization begun in field.
Nasogastric tube to evacuate stom ach, decrease distention, and decrease risk of aspiration: o
May relieve respiratory distress if caused by a herniated stom ach through the diaphragm
Medication (Drugs)
Tetanus toxoid booster: 0.5 m L IM for patients with open wounds
Tetanus im m une globulin: 250 units IM for patients who have not had com plete series
Intravenous antibiotics: broad-spectrum aerobic with anaerobic coverage such as a second-generation cephalosporin
Pediatric Considerations
Crystalloid infusion is 20 m L/kg if patient in shock.
Packed RBC dose is 1 m L/kg.
Follow-Up
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Disposition Admission Criteria
Postoperative cases
Equivocal findings on diagnostic peritoneal lavage, FAST exam , or CT
Many blunt abdom inal traum a patient benefit from adm ission, m onitoring, and serial abdom inal exam inations.
Discharge Criteria No patient in whom you suspect intra-abdom inal injury should be discharged hom e without an appropriate period of observation despite negative exam ination or im aging studies.
References 1. Am oroso TA. Evaluation of the patient with blunt abdom inal traum a: an evidence based approach. Em erg Med Clin North Am . 1999;17:63–75. 2. Brasel KJ, et al. Incidence and significance of free fluid on abdom inal CT in blunt traum a. J Traum a. 1995;44(5):889–892. 3. Davis JJ, Cohn I Jr, Nance FC. Diagnosis and m anagem ent of blunt abdom inal traum a. Ann Surg. 1976;183:672–678. 4. Holm es JF, et al. Perform ance of helical CT without oral contrast for the detection of gastrointestinal injuries. Ann Em erg Med. 2004;43(1):120–128. 5. McGahan JP, Wang L, Richards JR. Focused abdom inal ultrasound for traum a. Radiographics. 2001;21:91–99. 6. Stengel D, Bauwens K, Sehouli J, et al. System atic review and m eta-analysis of em ergency ultrasonography for blunt abdom inal traum a. Br J Surg. 2001;88:901–912.
Codes
Pa ge 1 6 7
ICD9-CM 868.00
ICD10 S39.9
Pa ge 1 6 8
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Abdo m inal Traum a, Im aging
Abdominal
Trauma, Imaging Christopher Richards
Basics Description This is a diagnostic procedure; basis for its use will vary with results of exam ination.
Diagnosis Signs and Symptoms
Abdom inal traum a m ay present in an unstable patient with m ultiple associated injuries or as an isolated injury in a stable patient with no physical findings.
Assessm ent of the abdom en focuses on the need for early surgical m anagem ent; the diagnosis of specific organ injuries should be handled later.
History
History should include m echanism of injury, restraint use and type, airbag or helm et use, prehospital vital signs, initial m ental status and change in m ental status, and any
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prehospital treatm ents perform ed and their effect on patient status.
AMPLE history (allergies, especially to radiographic contrast agents, m edications, past m edical history, last m eal, events leading up to the injury)
Physical Exam
Com prehensive physical exam should include com plete bodily exposure and perineal and digital rectal exam s.
Abdom inal stab wounds should be locally explored after local anesthesia; penetration of the abdom inal wall fascia requires further evaluation.
Caution should be taken because the physical exam is accurate in determ ining serious abdom inal injury in only 45–50% of cases.
Essential Workup
See Abdom inal Traum a (Blunt) and Abdom inal Traum a (Penetrating)
Tests General approach to im aging in blunt abdom inal traum a:
The ideal abdom inal im aging study is rapid, inexpensive, sensitive for operative injury; identifies m any nonoperative injuries requiring close observation and follow-up; requires m inim al training to perform and interpret; and does not exist yet.
Ultrasound has becom e the initial screening test of choice for hem odynam ically stable patients; it has replaced diagnostic peritoneal lavage in m any clinical settings.
CT scan is the definitive test for m ost patients, especially children, but requires intravenous contrast m aterial: o
Unstable patients should not be transported for a CT scan.
Pa ge 1 7 0
Most patients require serial physical exam inations and a period of observation even after negative im aging studies.
Imaging Ultrasound
Advantages: o
Rapid
o
Noninvasive
o
Can be perform ed at patient's bedside
o
Does not require contrast agents or ionizing radiation
Disadvantages: o
Operator dependent
o
Does not reliably identify specific organ injury
o
Not sensitive enough to exclude all injuries. Serial exam ination and observation are required if ultrasound is the sole im aging study.
o
Is not well suited for penetrating injuries; m ay m iss significant bowel injuries not accom panied by hem operitoneum
o
Indications: o
Does not evaluate spinal or retroperitoneal injuries
Blunt traum a in either stable or unstable patients
Contraindications: o
Absolute:
Pre-existing indication for exploratory laparotom y
o
Relative:
Obesity
Subcutaneous em physem a
Positive test: o
Dem onstration of free fluid or obvious solid organ injury (approxim ately 250 m L free fluid required in
Pa ge 1 7 1
adults)
Adequate exam includes visualization of Morrison pouch, pericardium , both paracolic gutters, and the pelvic rectouterine pouch (pouch of Douglas), and exam of the liver and spleen for parenchym al injuries.
Considerations: o
Positive test result should be followed by CT in a stable patient or by laparotom y in an unstable patient.
o
Institutional factors determ ine which clinical departm ent perform s the study.
CT scan:
Advantages: o
Sensitivity of 85–98%
o
Provides specific organ injury inform ation
o
Allows for sim ultaneous reform atting and reconstruction of spinal structures
o
Fosters nonoperative approach to solid organ injuries
o
Diagnoses retroperitoneal and bony injuries m issed by other m odalities.
Disadvantages: o
Requires intravenous contrast (acute contrast reactions and renal failure)
o
Isolated diaphragm atic, pancreatic, bowel injuries m ay be m issed, especially if perform ed im m ediately after injury.
Indications: o
Hem odynam ically stable patients
Contraindications: o
Absolute:
Pre-existing indication for exploratory laparotom y
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o
Hem odynam ic instability
Previous contrast reaction
Relative:
Multiple allergies
Considerations: o
Modality of choice in children
o
Many m ultiple-injury patients require CT im aging of the head, spine, chest, or pelvis; m odern equipm ent provides for rapid scanning of m ultiple anatom ic regions in one session.
o
Monitoring m ust be continued in the CT suite; patients should be accom panied by appropriate m edical personnel.
o
Water m ay be substituted for oral contrast, but optim al detection of intestinal injury requires oral contrast and a 2- to 4-hour delay for intestinal opacification.
Diagnostic Procedures/Surgery
Gunshot wounds to the abdom en require evaluation by a surgeon and will require laparotom y: o
Selective laparotom y is an option for experienced centers.
Diagnostic peritoneal lavage: o
o
Advantages:
Rapid
Relatively sim ple to perform
97.8% accurate in diagnosing injury
Disadvantages:
Invasive
Does not identify specific organ injury
1–2% com plication rate
May m iss retroperitoneal injuries and
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intraperitoneal bladder rupture o
Indications:
Hem odynam ically unstable patients
Patients requiring em ergent surgery for other conditions (e.g., craniotom y for epidural hem atom a)
Stab wounds that penetrate the abdom inal fascia
o
Contraindications:
Absolute: pre-existing indication for exploratory laparotom y
Relative: previous abdom inal surgery, severe abdom inal distention, pregnancy, pediatric patients
o
Nasogastric tube and Foley catheter placem ent m andatory before beginning procedure P.9
o
Positive test:
Aspiration of >10 m L of blood, bile, bowel contents, or urine
Diagnostic peritoneal lavage fluid in the urine or chest tube
o
Blunt traum a with >100,000 erythrocytes/m m 3
Penetrating traum a >1,000 erythrocytes/m m 3
Considerations:
Favored in stab wound patients when local wound exploration is confirm atory
Favored in unstable blunt traum a patients because it m ay be perform ed sim ultaneously with other em ergency-basis surgical
Pa ge 1 7 4
interventions (e.g., craniotom y for epidural hem atom a)
Must always be accom panied by serial abdom inal exam s after procedure
In the presence of pelvic fractures, use supraum bilical location.
In pregnancy, consider supraum bilical or open technique.
False-positive results m ay be obtained if perform ed >8 hours after injury.
Differential Diagnosis See Abdom inal Traum a (Blunt) and Abdom inal Traum a (Penetrating).
Treatment Pre Hospital All patients with a significant m echanism of injury or suspicion of m ajor traum a should be triaged to a facility equipped to m anage such injury.
Pediatric Considerations
Pediatric patients should be triaged to a pediatric traum a center or to an adult traum a center equipped to m anage children.
CT scan should be considered the diagnostic test of choice in children as a greater percentage of injuries in children will be m anaged nonoperatively.
Diagnostic peritoneal lavage (DPL) is relatively contraindicated.
Initial Stabilization
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In unstable patients, m anagem ent of the airway, breathing, and circulation; treatm ent of hypovolem ic shock; and control of m ajor hem orrhage m ust take precedence.
See Abdom inal Traum a (Blunt) and Abdom inal Traum a (Penetrating).
ED Treatment See Abdom inal Traum a (Blunt) and Abdom inal Traum a (Penetrating).
Follow-Up Disposition Admission Criteria See Abdom inal Traum a (Blunt) and Abdom inal Traum a (Penetrating).
Discharge Criteria See Abdom inal Traum a (Blunt) and Abdom inal Traum a (Penetrating).
References 1. Am oroso TA. Evaluation of the patient with blunt abdom inal traum a: an evidence based approach. Em erg Med Clin North Am . 1999;17:63–75. 2. Chiquito PE. Blunt abdom inal injuries. Diagnostic peritoneal lavage, ultrasonography and com puted tom ography scanning. Injury. 1996;27:117–124. 3. Pryor JP, Reilly PM, Dabrowski GP, et al. Nonoperative m anagem ent of abdom inal gunshot wounds. Ann Em erg Med. 2004;43(3):344–353. 4. Rose JS. Ultrasound in abdom inal traum a. Em erg Med Clin North Am . 2004;22(3):581–599. 5. Stengel D, Bauwens K, Sehouli J, et al. Em ergency
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ultrasound-based algorithm s for diagnosing blunt abdom inal traum a. Cochrane Database Syst Rev. 2005;18(2):cd004446.
Miscellaneous SEE ALSO: Abdom inal Traum a, Blunt; Abdom inal Traum a, Penetrating
Codes N/A
Pa ge 1 7 7
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Abdo m inal Traum a, Penetrating
Abdominal
Trauma, Penetrating Stewart Coffman
Basics Description
Solid organ injury usually results in hem orrhage.
Hollow viscus injury can lead to spillage of bowel contents and peritonitis.
Associated conditions: o
Injury to both thoracic and abdom inal structures occurs in 25% of cases.
Etiology
Eighty percent of gunshot wounds and 20–30% of stab wounds result in significant intra-abdom inal injury. Com m only injured structures include: o
Liver (37%)
o
Sm all bowel (26%)
o
Stom ach (19%)
o
Colon (17%)
o
Major vessel (13%)
o
Retroperitoneum (10%)
o
Mesentery/om entum (10%)
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o
Other:
Spleen (7%)
Diaphragm (5%)
Kidney (5%)
Pancreas (4%)
Duodenum (2%)
Biliary (1%)
Diagnosis Signs and Symptoms
Penetrating wound from knife, gun, or other foreign object
Spectrum of presentation ranging from localized pain to peritoneal signs: o
High-velocity projectile can cause extensive direct tissue dam age.
o
Secondary m issiles and tem porary cavitation of effected structures
o
Exit wound m ay be larger than entrance wound, but sm all entrance and exit wounds can conceal m assive internal dam age.
Rem em ber the borders of the abdom en: superior from the nipples (anteriorly) or inferior tip of scapula (posteriorly) to inferior gluteal folds.
Essential Workup
Diagnosis of intra-abdom inal injury from gunshot wounds to the abdom en are m ade by celiotom y in the operating room .
Locally explore stab wounds to abdom en: o
If the wound penetrates anterior fascial layer, the
Pa ge 1 7 9
patient should undergo diagnostic peritoneal lavage or bedside ultrasound.
Diagnostic laparoscopy is useful in diagnosing diaphragm atic injury and spleen and liver lacerations: o
May help avoid unnecessary surgery.
CT is useful in the evaluation of patients with a suspected retroperitoneal injury: o
Not reliable for detection of hollow viscus or diaphragm atic injuries.
If 10,000 RBC/m m 3 or m ore are found in the diagnostic peritoneal lavage fluid, the patient should undergo laparotom y.
If Table o f C o ntents > Abuse, Elder
Abuse, Elder
Helen Straus
Basics Description Elder abuse m ay include the following:
Em otional abuse: o
Insults
o
Hum iliation
o
Threats to institutionalize or abandon
Physical and/or sexual abuse: o
Hitting
o
Slapping
o
Pushing
o
Burning
o
Inappropriate restraining
o
Forced sexual activity
Material exploitation: o
Stealing or coercion involving patient m onies or property
Neglect: o
Behaviors by a patient or caregiver that com prom ise the patient's health or safety
o
Failure to provide adequate food, shelter, hygiene,
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and/or m edical attention
Epidemiology Incidence In the United States, one m illion known cases annually (estim ated 5 m illion cases):
2% reported by physicians
Etiology
Caregiver stress, dependency, or psychopathology
Victim dependency or dim inishm ent of ability to perform activities of daily living
Diagnosis Essential Workup
Obtain history without fam ily m em bers/caregivers present: o
Abused elders m ay fear institutionalization if they report caregivers
o
Many m ay feel em barrassm ent and responsibility for abuse
o
Frequently will not volunteer inform ation
o
Ask patient specifically about abuse or neglect (in private)
o
Patient's m edical condition m ay influence quality of history obtained
Obtain history from caregivers/other relatives/friends/neighbors
Docum ent a clear and detailed description of findings including the following: o
Statem ents of the patient as they pertain to the
Pa ge 2 1 0
abuse o
o
Psychosocial history:
Fam ily and other social relationships
Caregiver burdens/coping m echanism s
Drug/ethanol (EtOH) use
Prior adult protective services reports
Skin and other physical findings:
Photographic docum entation
Safety assessm ent
Signs and Symptoms Variable, possibly inconsistent, history or physical findings
History
Not willing or able to obtain adequate food/clothing/shelter
Not providing for personal hygiene/safety
Delay in obtaining m edical care/previously untreated m edical condition
Vague (or im plausible/inappropriate) explanations
Disparities between histories given by patient and caregiver
Caregiver who insists on giving the patient's history
Medication difficulties:
o
Incorrect doses
o
Lost m edications
o
Unfilled prescriptions
Altered interpersonal interactions: o
Withdrawn
o
Indifferent
o
Dem oralized
o
Fearful
o
Substance abuse
Caregiver with:
Pa ge 2 1 1
o
Financial dependence on patient
o
Substance abuse or psychiatric or violence history
o
Controlling behavior (m ay refuse to leave elder alone with physician) or poor knowledge
o
Significant life stressors
o
Relationship issues
o
Financial difficulties
o
Legal problem s
Physical Exam
Inconsistent findings: o
Patterns or variable-age bruises, burns, lacerations/abrasions
o
Unusual sites of bruising (inner arm , torso, buttocks, scalp)
o
Poor hygiene (inadequate care of skin, nails, teeth)
Unexplained injuries: o
Bruised or bleeding genital or rectal area
o
Wrist or ankle lesions suggestive of restraint use
Findings perhaps consistent with neglect or delay in seeking/obtaining m edical attention: o
Dehydration
o
Weight loss
o
Decubitus ulcer
o
Malnutrition
Tests Perform any exam ination and laboratory or radiographic studies as indicated by the patient's condition.
Differential Diagnosis Patient m ay present with any chief com plaint:
Potential differential diagnosis is nonspecific
Abuse best identified by asking patient directly in a setting
Pa ge 2 1 2
apart from caregivers/fam ily and correlating with risk factors and provider findings
Differentiate findings consistent with other disease causes from abuse/neglect: o
Dehydration
o
Ill-fitting dentures
o
Burns
o
Ecchym oses
o
Insom nia
o
Medication noncom pliance
o
Dem entia
o
Depression
Treatment Pre Hospital Observe details of the patient's environm ent that m ay not be im m ediately available to the hospital care team , including the following:
Interpersonal interactions at the scene: o
Em barrassm ent
o
Sham e
o
Fear of reprisal, abandonm ent, and/or institutionalization
Conditions in the physical environm ent to determ ine potential danger areas
P.19
Initial Stabilization
Pa ge 2 1 3
ABCs (airway, breathing, circulation)
Treat life-threatening m edical/traum atic conditions as appropriate.
ED Treatment
May require separation of the patient and the caregiver or fam ily m em ber
Social work referral: o
Safety planning
o
Respite planning for caregiver
o
Adult protective services referral
Com petent elder patients are free to accept or decline treatm ent or disposition despite risks they m ay incur.
General m easures appropriate to the m edical/traum atic conditions identified, including: o
Fluids
o
Medications
o
Surgery
o
Diet
o
Activity
o
Nursing care
o
Physical therapy
Follow-Up Disposition Disposition determ ined by m edical condition and hom e environm ent
Admission Criteria
Medical condition requiring adm ission
Abuse or neglect renders hom e conditions unsafe.
Pa ge 2 1 4
Discharge Criteria
Medical condition(s) addressed
Safe environm ent available
Abuse or neglect successfully countered by social services and/or law enforcem ent
Issues for Referral
Many states have m andatory reporting requirem ents: o
Com ply with area legal requirem ents.
EtOH/drug treatm ent as appropriate
Notify adult protective services.
References 1. Clarke ME, Pierson W. Managem ent of elder abuse in the em ergency departm ent. Em erg Med Clin North Am . 1999;17:631–644. 2. Kruger RM, Moon CH. Can you spot the signs of elder m istreatm ent? Postgrad Med. 1999;106:169–183. 3. Lachs MS, Pillem er K. Elder abuse. Lancet. 2004;364:1263–1272. 4. Levine JM. Elder neglect and abuse—a prim er for prim ary care physicians. Geriatrics. 2003;58(10):37–40, 42–44. 5. Marshall CE, Benton D, Brazier JM. Elder abuse: using clinical tools to identify clues of m istreatm ent. Geriatrics. 2000;55:42–53.
Codes ICD9-CM V61.3
ICD10 T74.1
Pa ge 2 1 5
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Abuse, Pediatric (No naccidental Traum a [NAT])
Abuse, Pediatric (Nonaccidental Trauma [NAT]) Suzanne Z. Barkin
Basics Description
Child abuse effects up to 14 m illion or 2–3% of U.S. children each year.
1,200–1,400 children die of m altreatm ent each year in the United States, 80% 4 hours in overdose
Toxic dose >150 m g/kg acutely
Probable toxic level is 140 µg/m L at 4 hours postingestion (see Fig. 1 nom ogram for acute intoxication).
Therapeutic plasm a concentration is 5–20 µg/m L.
Diagnosis Signs and Symptoms Acute Overdose
Phase 1: 0.5–24 hours postingestion: o
Nausea, vom iting, m alaise
o
Occurs with large overdoses
o
May not be present with sm aller toxic doses
Phase 2: 24–72 hours postingestion: o
Decreased GI sym ptom s
o
Hepatic dam age is occurring.
o
Right upper quadrant pain and tenderness
o
Elevation of liver enzym es, PT/INR, bilirubin
o
Oliguria
o
Prolonged (>4 hours) acetam inophen (APAP) half-life im plies hepatic toxicity.
Phase 3: 72–96 hours postingestion: o
Critical tim e period in the prognosis
o
Peak liver function abnorm alities
o
Hepatic encephalopathy develops.
o
If the PT/INR continues to rise and/or renal
Pa ge 2 2 6
insufficiency develops beyond the third day postingestion, there is high likelihood that the patient will require hepatic transplantation.
Phase 4: 96 hours to 10 days postingestion: o
Resolution of hepatic injury or progression to com plete hepatic failure
Fig. 1. Rum ack-Matthew nom ogram . (Adapted from Rum ack BH, Matthew H. Acetam inophen poisoning and toxicity. Pediatrics. 1975;55:871–876.
Pa ge 2 2 7
)
Essential Workup
Ingestion history of all APAP-containing products
Tim e of ingestion
APAP level: o
Obtain 4-hour postingestion level or im m ediately on presentation if >4 hours postingestion.
o
Use Rum ack-Matthew nom ogram as therapeutic guide for single acute overdose.
o
Obtain level, but do not use nom ogram for therapeutic guidance in chronic ingestions or very late ingestions (>24 hours)
Call poison center ([800] 222-1222) or toxicologist.
Tests Lab
APAP level
Electrolytes, BUN, creatinine, glucose
Liver enzym es: o
Elevated AST is the first abnorm ality detected.
o
AST/ALT levels m ay rise >10,000 in stage III of toxicity.
o
Bilirubin
PT/INR
Pregnancy test
Differential Diagnosis
Suspect APAP as coingestant with other drugs in overdose.
Causes of acute onset hepatotoxicity: o
Infectious hepatitis
o
Reye syndrom e
o
Am anita sp. m ushroom s toxicity
Pa ge 2 2 8
o
Herbal and dietary supplem ents
o
Other drug ingestions
P.23
Treatment Pre Hospital
Transport all pill bottles/pills involved in overdose for identification in ED.
Over-the-counter cold rem edies often contain acetam inophen.
Initial Stabilization Airway, breathing, circulation (ABCs):
Adm inister supplem ental oxygen.
Adm inister naloxone, thiam ine, D50 (or Accu-Chek) for altered m ental status.
ED Treatment
Supportive care: o
IV fluids
o
Antiem etics
Gastric decontam ination: o
Adm inister a single dose of activated charcoal if recent ingestion.
NAC Administration
Adm inister if toxic level detected as defined by Rum ack-Matthew nom ogram .
NAC virtually 100% hepatoprotective if initiated within 8
Pa ge 2 2 9
hours of an acute overdose
NAC available in oral form or IV form
24 hours postingestion or chronic repeated APAP ingestion o
Initiate NAC if:
Ingestion >150 m g/kg APAP
Sym ptom atic
Abnorm al hepatic screening panel
Discontinue NAC if APAP falls to nondetectable level and no AST elevation occurs by 36 hours postingestion.
Call poison center ([800] 222–1222) or toxicologist for help.
Pregnancy Considerations
No teratogenicity with NAC
NAC m ay be effective in protecting fetal liver: o
Fetal liver m etabolizes APAP to toxic NAPQI after 14 weeks of gestation.
Alert A shortened oral NAC protocol m ay be considered with poison center or toxicology consultation.
NAC Preparations
Pa ge 2 3 0
Oral NAC: o
Poor taste and odor:
Dilute to 5% with fruit juice or soft drink to increase palatability.
o
Use antiem etics (m etoclopram ide or ondansetron) liberally to facilitate PO adm inistration.
o
If the patient vom its NAC within 1 hour of adm inistration, repeat the dose.
o
Adm inister NAC as a drip through nasogastric (NG) tube if vom iting continues.
o
Given q4h
IV NAC (two options): o
Acetadote infusion given per m anufacturer's instructions
o
Oral NAC given by IV route if:
Oral form not tolerated because of vom iting
Acetadote not available
Contact local poison center or toxicologist for help.
Medication (Drugs)
Activated charcoal: 1–2 g/kg PO
Dextrose: D 5 0 W 1 am p (50 m L or 25 g; peds: D 2 5 W 2–4 m L/kg) IV
Metoclopram ide: Start with 10 m g (peds: 1 m g/kg) IV (1 m g/kg m ax.)
N-acetylcysteine (NAC): 140 m g/kg PO loading (adult and pediatric) followed by 70 m g/kg q4h for 17 additional doses
Acetadote: 21-hour IV infusion (see package insert for dosing)
Pa ge 2 3 1
Naloxone (Narcan): 0.4–2 m g (peds: 0.1 m g/kg) IV or IM initial dose
Ondansetron: >80 kg, 12 m g; 45–80 kg, 8 m g (peds 0.15 m g/kg) IV
Thiam ine (vitam in B 1 ): 100 m g (peds: 50 m g) IV or IM
Follow-Up Disposition Admission Criteria
Hepatotoxic level of APAP requiring full course of NAC therapy (see Treatm ent)
Nontoxic suicide attem pt requiring psychiatric treatm ent
Discharge Criteria Asym ptom atic patients with nontoxic ingestions not requiring full course of NAC therapy
Issues for Referral
Evidence of significant hepatotoxicity at tim e of ED arrival warrants early evaluation by hepatology and/or transplant service.
Consider substance abuse referral for patients with oral narcotic abuse.
Patients with unintentional (accidental) poisoning require poison prevention counseling.
Patients with intentional (e.g., suicide) poisoning require psychiatric evaluation.
References 1. Anker AL. Acetam inophen. In: Ford MD, Delaney KA, Ling LJ, et al., eds. Clinical Toxicology. Philadelphia: WB Saunders;
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2001:265–274. 2. Buckley NA, Whyte IM, O'Connell DL, et al. Oral or intravenous N -acetylcysteine: which is the treatm ent of choice for acetam inophen (paracetam ol) poisoning? J Toxicol Clin Toxicol. 1999;37(6):759–767. 3. Dargan PI, Jones AL. Acetam inophen poisoning: an update for the intensivist. Crit Care. 2002;6(2):108–110. 4. Jones AL. Mechanism of action and value of N-acetylcysteine in the treatm ent of early and late acetam inophen poisoning: a critical review. J Toxicol Clin Toxicol. 1998;36:277–285. 5. Rum ack BH. Acetam inophen m isconceptions. Hepatology. 2004;40(1):10–15. 6. Sm ilkstein MJ, Knapp GL, Kulig KW, et al. Efficacy of oral n -acetylcysteine in treatm ent of acetam inophen overdose. Analysis of the national m ulticenter study. N Engl J Med. 1988;319:1557–1562. 7. Yip L, Dart RC, Hurlbut KM. Intravenous adm inistration of oral N -acetylcysteine. Crit Care Med. 1998;26:40–42.
Codes ICD9-CM 965.4
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Acido sis
Acidosis
Matthew Robinson
Basics Description Respiratory Acidosis
Reduced pH owing to alveolar hypoventilation with elevated PaCO 2
Defined as PaCO 2 >45 m m Hg or higher than expected for calculated respiratory com pensation for m etabolic acidosis
Divided into three broad categories: o
Prim ary failure in central nervous system drive to ventilate:
o
Sleep apnea
Anesthesia
Sedative overdose
Prim ary failure in transport of CO 2 from alveolar space:
o
Chronic obstructive pulm onary disease
Myasthenic crisis
Severe hypokalem ia
Guillain-Barré syndrom e
Prim ary failure in transport of CO 2 from tissue to alveoli:
Pa ge 2 3 4
Severe heart failure
Metabolic Acidosis
Process that reduces serum pH by decreasing plasm a bicarbonate levels
Prim arily caused by: o
Gain of a strong acid through ingestion or m etabolism
o
Loss of bicarbonate from the body
Metabolic acidosis is clinically evaluated by dividing into two m ain groups: o
Elevated anion gap m etabolic acidosis:
Bicarbonate reduced through buffering of added strong acid
Anion gap is increased owing to retention of the unm easured anion from the titrated strong acid.
o
Norm al anion gap m etabolic acidosis owing to:
Kidneys fail to reabsorb or regenerate bicarbonate.
Losses of bicarbonate from gastrointestinal tract (diarrhea)
Ingestion or infusion of substances that release hydrochloric acid
o
No anion gap is observed owing to the absence of any unm easured anion of a titrated acid and secondary chloride retention with HCO 3 - loss.
Etiology Anion Gap Acidosis To rem em ber possible causes, use m nem onic A CAT MUD PILES:
Alcohol ketoacidosis
Carbon m onoxide or cyanide
Aspirin
Toluene
Pa ge 2 3 5
Methanol
Urem ia
Diabetic ketoacidosis
Paraldehyde
Iron/isoniazid
Lactic acidosis
Ethylene glycol
Starvation
Increased Osmolar Gap To rem em ber possible causes, use m nem onic ME DIE:
Methanol
Ethylene glycol
Diuretics (m annitol; no acidosis)
Isopropyl alcohol (no acidosis)
Ethanol
Non-Anion Gap Metabolic Acidosis
Gastrointestinal losses of bicarbonate: o
Diarrhea
o
Villous adenom a
o
Rem oval of sm all bowel, pancreatic or biliary secretions
o
Tube drainage
o
Sm all bowel/pancreatic fistula
Anion exchange resins (i.e., cholestyram ine): o
Ingestion of calcium chloride or m agnesium chloride
Renal loss of bicarbonate
Renal tubular acidosis: o
Type I (distal): hypokalem ic hyperchlorem ic m etabolic acidosis:
Decreased ability to secrete hydrogen
Serum HCO 3 15 m Eq/L
Norm al/elevated potassium
Carbonic anhydrase inhibitors
Tubulointerstitial renal disease
Hypoaldosteronism
Addition of hydrochloric acid such as: o
Am m onium chloride
o
Arginine hydrogen chloride
o
Lysine hydrogen chloride
Diagnosis Signs and Symptoms
Nonspecific findings
Vital signs: o
Tachypnea or Kussm aul respirations with m etabolic acidosis
o
Hypoventilation with respiratory acidosis
Pa ge 2 3 7
o
Tachycardia
Som nolence
Confusion
CO 2 narcosis
Myocardial conduction and contraction disturbances
Essential Workup
Electrolytes, BUN, creatinine, glucose: o
Decreased bicarbonate with m etabolic acidosis
o
Hyperkalem ia and hypercalcem ia with severe m etabolic acidosis
Arterial blood gases: o
pH
o
CO 2 retention in respiratory acidosis
o
CO level
Calculate anion gap: Na + - (HCO 3 - + Cl - ): o
Correct anion gap for hypoalbum inem ia:
For every 1 g/dL decrease in album in (from 4.0 g/dL), add 2.5 points to calculated anion gap.
o
Norm al range = 5–12 ± 3 m Eq/L
o
Anion gap >25 m Eq/L is seen only with:
Lactic acidosis
Ketoacidosis
Toxin-associated acidoses
Calculate the degree of com pensation: o
Expected PaCO 2 = 1.5[HCO 3 - ] + 8
o
If PaCO 2 inappropriately high, patient has a concom itant respiratory acidosis and inadequate com pensation
Respiratory acidosis: o
Acute: expected HCO 3 - increased by 1 m Eq/L for every 10 m m Hg increase in PaCO 2
o
Chronic: expected HCO 3 - increased by 4 m Eq/L for
Pa ge 2 3 8
every 10 m m Hg increase in PaCO 2
Evaluate the delta gap: o
For every one-point increase in anion gap, HCO 3 should decrease by 1 m Eq/L in sim ple acid/base disorder.
Evaluate by com paring the change in the anion gap (ΔAG) with the change in the HCO 3 - (ΔHCO 3 - ) from norm al: o
If ΔAG > ΔHCO 3 - , then patient has a concom itant m etabolic alkalosis.
o
If ΔHCO 3 - > ΔAG, then patient has concom itant non-anion gap acidosis.
P.25
Tests Lab
Urinalysis for glucose and ketones
Measure serum osm olality: o
Calculated serum osm olality = 2 Na + glucose/18 + blood urea nitrogen/2.8
Osm olal gap = difference between calculated and m easured osm olality: o
Norm al = 65 years old or Table o f C o ntents > Acute C o ro nary Syndro m e: M yo cardial Infarctio n
Acute Coronary Syndrome: Myocardial Infarction Shamai A. Grossman Leon D. Sanchez
Basics Description
Im balance in m yocardial blood supply and oxygen requirem ent
Acute cardiac ischem ia encom passes a spectrum of disease processes: o
Unstable angina pectoris
o
Acute m yocardial infarction (AMI)
o
ST elevation m yocardial infarction (STEMI)
o
Non-STEMI
Etiology
Atherosclerotic narrowing of coronary vessels
Vasospasm —although this is usually at rest and considered unstable if new onset
Microvascular angina or abnorm al relaxation of vessels with diffuse vascular disease
Plaque disruption
Pa ge 2 6 6
Throm bosis
Arteritis: o
Lupus
o
Takayasu disease
o
Kawasaki disease
o
Rheum atoid arthritis
Prolonged hypotension
Anem ia o
Hem oglobin 55 years
o
Postm enopausal wom en
Diagnosis Signs and Symptoms
Chest pain:
Pa ge 2 6 7
o
Most com m on presentation of m yocardial infarction (MI)
o
Substernal pressure
o
Heaviness
o
Squeezing
o
Burning sensation
o
Tightness
Anginal equivalents (MI without chest pain): o
Abdom inal pain
o
Syncope
o
Diaphoresis
o
Nausea or vom iting
o
Weakness
May localize or radiate to arm s, shoulders, back, neck, or jaw
Associated sym ptom s: o
Dyspnea
o
Syncope
o
Fatigue
o
Diaphoresis
o
Nausea
o
Vom iting
Sym ptom s are usually reproduced by exertion, eating, exposure to cold, or em otional stress.
Sym ptom s com m only last 30 m inutes or m ore.
Sym ptom s m ay occur with rest or during exertion.
Often preceded by crescendo angina
May be im proved or relieved with rest or nitroglycerin
Sym ptom s generally unchanged with position or inspiration
Positive Levine sign or clenched fist over chest is suggestive of angina.
Blood pressure (BP) is usually elevated during sym ptom s.
Pa ge 2 6 8
Physical Exam
Physical exam is usually unrevealing.
Occasional physical findings include: o
S3 or S4 due to left ventricular systolic or diastolic sym ptom s
o
Papillary m uscle dysfunction resulting in m itral regurgitation
o
Dim inished peripheral pulses
Essential Workup History is critical in differentiating MI from noncardiac etiologies.
Tests ECG
Lab
CK-MB and troponin I or T
Hem atocrit
Coagulation profile
Creatinine
Diagnostic Procedures/Surgery See Cardiac Testing
Differential Diagnosis
Anxiety
Aortic dissection
Biliary colic
Costochondritis
Esophageal reflux
Esophageal spasm
Herpes zoster
Hiatal hernia
Mitral valve prolapse
Myocardial infarction
Pa ge 2 6 9
Panic disorder
Peptic ulcer disease
Pneum onia
Psychogenic
Pulm onary em bolus
Unstable angina
Treatment Pre Hospital
IV access
Aspirin
Oxygen
Cardiac m onitoring
Sublingual nitroglycerin for sym ptom relief
12-lead ECG, if possible, with transm ission or results relayed to receiving hospital
Alert
All chest pain should be treated and transported as a possible life-threatening em ergency.
Do not adm inister throm bolytics or heparin if aortic dissection is suspected.
Initial Stabilization
IV access
Oxygen
Cardiac m onitoring
Oxygen saturation
Continuous BP m onitoring and pulse oxim etry
ED Treatment
Pa ge 2 7 0
STEMI requires reperfusion therapy as soon as possible: o
Throm bolytics should be used if percutaneous coronary intervention is not readily available within a 90-m inute tim e fram e (see Reperfusion Therapy, Cardiac).
Patients with non-STEMI, if started on glycoprotein IIb/IIIa inhibitors and if they subsequently receive a stent, benefit from a PCI within a 48-hour tim e fram e.
Aspirin should be adm inistered first to all patients with suspected MI unless the patient has a known allergy.
If BP is >90–100 m m Hg systolic, adm inister sublingual nitroglycerin, nitropaste, or IV nitroglycerin assum ing no ECG criteria of right ventricular infarct: o
Sym ptom s that persist after three sublingual nitroglycerin tablets are strongly suggestive of AMI or noncardiac etiology
Beta-blockers should be adm inistered if no contraindications (e.g., bradyarrhythm ias, heart rate 90 m m Hg
Nitroglycerin: 0.4 m g sublingual
Nitroglycerin: IV drip at 5–10 µg/m in
Nitropaste: 1–2 inches transderm al
Throm bolytics: see Reperfusion Therapy, Cardiac, for dosing
Follow-Up Disposition Admission Criteria
Patients with an AMI require hospital adm ission.
If the diagnosis is unclear, adm ission to the hospital or an ED observation unit m ay be useful for serial cardiac
Pa ge 2 7 3
enzym es, ECGs, and exercise stress testing and/or cardiac catheterization.
Discharge Criteria No patient with an AMI should be discharged from the ED.
Issues for Referral If PCI is unavailable in the treating institution, and particularly if the patient is in cardiogenic shock, patients should be transported to another hospital if PCI can be underway in less than 90 m inutes.
References 1. Braunwald E, Antm an EM, Beasley JW, et al. ACC/AHA guidelines for the m anagem ent of patients with unstable angina and non-ST-segm ent elevation m yocardial infarction. J Am Coll Cardiol. 2000;36:970–1062. 2. Gibson CM. Prim ary angioplasty com pared with throm bolysis: new issues in the era of glycoprotein IIb/IIIa inhibition and intracoronary stenting. Ann Intern Med. 1999;130:841–847. 3. Lieu TA, Gurley RJ, Lundstrom RJ, et al. Prim ary angioplasty and throm bolysis for acute m yocardial infarction: an evidence based sum m ary. J Am Coll Cardiol. 1996;27:737–750. 4. Ryan TJ, Antm an EM, Brooks NH, et al. ACC/AHA practice guidelines for the m anagem ent of patients with acute m yocardial infarction. J Am Coll Cardiol. 1996;28:1328–1428. See also 1999 web update at http://www.acc.org. 5. Schm ig A, Kastrati A, Dirschinger J, et al. Coronary stenting plus platelet glycoprotein IIb/IIIa blockade com pared with tissue plasm inogen activator in acute m yocardial infarction. N Engl J Med. 2000;343:385–391. 6. Sabatine MS, Cannon CP, Gibson CM, et al. CLARITY-TIMI 28 Investigators. Addition of clopidogrel to aspirin and fibrinolytic therapy for m yocardial infarction with ST-segm ent elevation. N Engl J Med. March 24, 2005;352(12):1179–1189. Epub 2005 Mar 9.
Pa ge 2 7 4
Miscellaneous SEE ALSO: Cardiac Testing; Reperfusion Therapy; Unstable Angina
Codes ICD9-CM 410.0
ICD10 I21.9
Pa ge 2 7 5
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Acute C o ro nary Syndro m e: No n†“Q-Wave (No n-ST
Acute Coronary Syndrome:
Elevatio n) M I
Non–Q-Wave (Non-ST Elevation) MI David F. M. Brown Murray J. McLachlan
Basics Description
Non-ST-elevation m yocardial infarction (NSTEMI) is a part of a clinical syndrom e that includes unstable angina.
Probable cause is the generation of a subtotal coronary occlusion or functional collateral circulation: o
Often indicates an incom plete ischem ic event
Coronary plaque disruption: o
Endothelial disruption exposes subendothelial collagen and other platelet-adhering ligands, von Willebrand factor (vWF), and fibronectin.
o
Release of tissue factors activates factor VII and extrinsic pathway
Throm bus generation: o
Platelet adhesion via glycoprotein (GP) Ia/IIa to collagen; GP Ib to vWF:
Pa ge 2 7 6
Platelet activation: release of ADP, throm boxane A 2 , and serotonin alters the platelet GP IIb/IIIa receptor; also causes local vasoconstriction
Platelet aggregation: GP IIb/IIIa receptor binds fibrinogen m olecules, cross-links platelets form ing local platelet plug
o
Platelet stabilization: throm bin converts fibrinogen to fibrin, provides fibrin m esh, stabilizes platelet aggregate
Etiology
Coronary throm bosis
Coronary artery spasm , idiopathic or cocaine induced
In situ throm bosis/hypercoagulable states
Em bolic event
Arteritis
Diagnosis Signs and Symptoms History
Pain: o
Pressure or tightness or heaviness
o
Substernal, epigastric
o
+/- radiation to arm , jaw, back
Nausea, vom iting
Diaphoresis
Cough
Dyspnea
Anxiety
Pa ge 2 7 7
Light-headedness
Syncope
Physical Exam
Hypertension
Hypotension
Arrhythm ias
S4 heart sound
Essential Workup ECG, cardiac m arkers, chest radiograph
Tests Lab
Cardiac m arkers: o
Troponins: specific indicators of m yocardial infarction, positive 3–6 hours after MI, peaks at 9–10 days
o
Creatine kinase (CK): rises following infarction in 4–8 hours, peaks at 18–24 hours, subsiding at 3–4 days; isoenzym e CK-MB m ore specific for cardiac origin
o
Myoglobin: rises within 2–6 hours, returns to baseline within 24 hours, highly sensitive but very nonspecific
o
LDH: rises within 24 hours, peaks at 3–6 days, baseline at 8–12 days
CBC
Serum electrolytes including m agnesium
ESR: nonspecific m arker of inflam m ation, rises within 3 days, elevated for several weeks
PT/PTT/INR for patients on warfarin
Imaging
Pa ge 2 7 8
ECG: o
ST-segm ent depression or transient elevation indicates increased risk
o
T-wave inversion in regional patterns does not increase risk but helps differentiate cardiac pain from non cardiac pain
Chest radiograph: o
To assess heart size, pulm onary edem a/congestion or identify other causes of chest pain
Echocardiography: o
To identify wall m otion abnorm alities and assess left ventricular function
Radionuclide studies: o
Thallium or sestam ibi scanning: identifies viable m yocardium
o
Technetium 99: identifies recently infarcted m yocardium
Differential Diagnosis
ST-elevation m yocardial infarction
Pulm onary em bolus
Aortic dissection
Acute pericarditis
Pneum othorax
Pancreatitis
Pneum onia
Esophageal spasm /gastroesophageal reflux
Esophageal rupture
Musculoskeletal pain (diagnosis of exclusion)
Treatment
Pa ge 2 7 9
Pre Hospital
IV access
Oxygen adm inistration
Cardiac m onitoring and treatm ent of arrhythm ias
Aspirin, analgesia, anxiolytics
Initial Stabilization
Oxygen adm inistration
IV access
Cardiac m onitoring and treatm ent of arrhythm ias
ED Treatment
Anti-ischem ic therapy to reduce m yocardial dem and and increase m yocardial supply of oxygen: o
Beta-blockers
o
Nitrates
o
Oxygen
o
Morphine sulfate
o
Calcium channel blockers (nondihydropyridines—e.g., diltiazem , verapam il) m ay be used in patients with ongoing ischem ia and contraindications to beta-blockade.
Antiplatelet therapy to decrease platelet aggregation: o
Aspirin
o
Clopidogrel
o
GP IIb/IIIa inhibitors (eptifibatide, tirofiban):
When catheterization and PCI is planned
Ongoing ischem ia
Positive initial cardiac m arkers
Antithrom botic therapy to prevent throm bus propagation: o
Low m olecular weight heparin (specifically enoxaparin) preferred over unfractionated heparin
Anxiolytics to suppress sym pathom im etic release
Pa ge 2 8 0
Medication (Drugs)
Aspirin 162–325 m g PO per day
Beta-blockers: o
Atenolol: Start 5 m g IV over 5 m inutes, then 5 m g IV 10 m inutes later, then 50–100 m g PO per day (1–2 hours after IV doses).
o
Esm olol: 100 m cg/kg/m in IV infusion (titrate by increasing 50 m cg/kg/m in q15m in until effect—to m ax dose 300 m cg/kg/m in)
o
Metoprolol: Start 5 m g IV q5m in × 3, after 15 m inutes begin 25–50 m g PO q6h.
o
Propranolol: 0.5–1 m g IV then 40–80 m g PO q6h–q8h
P.35
Calcium channel blockers o
Diltiazem : start 0.25 m g/kg IV bolus, then 0.35 m g/kg IV after 15 m inutes if needed then 30 m g PO q6h
o
Verapam il: start 5–10 m g IV, repeat after 30 m inutes if needed, then 80–160 m g PO q8h
Clopidogrel: 300–600 m g PO × 1, then 75 m g per day
GP IIb/IIIa inhibitors: o
Abcixim ab: (only just prior to PCI): 0.25 m g/kg IV bolus then 0.125 m cg/kg/m in infusion (m ax 10 m cg/m in) for 12–24 hours
o
Eptifibatide: 180 m cg/kg IV bolus then 2 m cg/kg/m in infusion for 72–96 hours
o
Tirofiban: 0.4 m cg/kg/m in IV × 30 m in, then 0.1
Pa ge 2 8 1
m cg/kg/m in infusion for 48–96 hours
Heparins: o
Enoxaparin: 1 m g/kg SC q12h, can give 30 m g IV bolus before SC dose (beware of enoxaparin in patients with renal dysfunction) or
o
Unfractionated heparin: 60–70 units/kg IV bolus then 12–15 units/kg/hr infusion (m ax bolus 5000 units, m ax infusion rate 1000 units/hr (goal is a PTT 50–75 seconds)
Lorazepam : 1–2 m g IV PRN anxiety
Morphine sulfate 1–5 m g IV q5m in–q30m in PRN pain
Nitroglycerin: 0.3–0.6 m g SL or 0.4 m g by spray q5m in followed by IV infusion beginning at 10–20 m cg/m in if pain persists (m ax. dose 200 m cg/m in)
Follow-Up Disposition Admission Criteria
All patients with positive cardiac m arkers or significant clinical probability of acute coronary syndrom e
Intensive care unit for m onitoring unstable patients
Discharge Criteria Only those who are ruled out for acute coronary syndrom e/non–Q-wave infarction can be safely sent hom e.
References 1. Braunwald E, et al. ACC/AHA guideline update for the managem ent of patients with unstable angina and non—ST-segm ent elevation
Pa ge 2 8 2
m yocardial infarction, 2002, http://www.acc.org/clinical/guidelines/unstable/unstable.pdf. 2. Braunwald E. Application of Current Guidelines to the Management of Unstable Angina and Non-ST-Elevation Myocardial Infarction. Circulation; 108(16 Suppl 1): III28–11137, 2003 Oct 21. 3. DeFilippi CR. Evaluating the chest pain patient. Scope of the problem . Cardiol Clin. 1999;17(2):307–326. 4. Harrington RA, Becker RC, Ezekowitz M, Meade TW, O'Connor CM, Vorchheim er DA, Guyatt GH. Antithrom botic therapy for coronary artery disease: the Seventh ACCP Conference on Antithrom botic and Throm bolytic Therapy. Chest.126(3 Suppl):513S–548S, 2004 Sept. 5. Storrow AB. Chest pain centers: diagnosis of acute coronary syndrom es. Ann Em erg Med. 2000;35(5):449–461. 6. Tatum JL. Com prehensive strategy for the evaluation and triage of the chest pain patient. Ann Em erg Med. 1997;29(1):116–125. 7. Zalenski RJ. National Heart Attack Alert Program position paper: chest pain centers and program s for the evaluation of acute cardiac ischem ia. Ann Em erg Med. 2000;35(5):462–471. 8. Zalenski RJ. Evaluation and risk stratification of patients with chest pain in the em ergency departm ent. Predictors of life threatening events. Em erg Med Clin North Am . 1998;16(3):495–517, vii.
Codes ICD9-CM 410.9
ICD10 I21.4
Pa ge 2 8 3
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Acute C o ro nary Syndro m e: Stable Angina
Acute
Coronary Syndrome: Stable Angina Shamai Grossman Tarina Lee Kang
Basics Description
Chest discom fort that is predictable in nature, occurs with exertion, and im proves with rest
Im balance in m yocardial blood supply and oxygen requirem ents
Canadian Cardiovascular Classification—class I: ordinary physical activity does not cause sym ptom s.
Canadian Cardiovascular Classification—class II: sym ptom s that slightly lim it norm al activity such as: o
Walking
o
Clim bing stairs
o
Em otional stress
o
Cold
Etiology
Cardiac risk factors include: o
Hypercholesterolem ia
o
Diabetes m ellitus
Pa ge 2 8 4
o
Hypertension
o
Sm oking
o
Fam ily history
o
Men: age >35 years
o
Postm enopausal wom en
Atherosclerotic narrowing of coronary vessels
Vasospasm , although this is usually at rest and considered unstable if new onset
Microvascular angina or abnorm al relaxation of vessels with diffuse vascular disease
Arteritis: o
Lupus
o
Takayasu disease
o
Kawasaki disease
o
Rheum atoid arthritis
Anem ia: hem oglobin Table o f C o ntents > Acute C o ro nary Syndro m e: Unstable Angina
Acute
Coronary Syndrome: Unstable Angina Shamai A. Grossman Leon D. Sanchez
Basics Description
Im balance in m yocardial blood supply and oxygen requirem ent
Canadian Cardiovascular Classification, Class III: severe lim itations of ordinary physical activity
Class IV: inability to perform any activity without discom fort, sym ptom s m ay be present at rest
Etiology
Atherosclerotic narrowing of coronary vessels
Vasospasm , although this is usually at rest and considered unstable if new onset
Microvascular angina or abnorm al relaxation of vessels with diffuse vascular disease
Plaque disruption
Throm bosis
Pa ge 2 9 2
Arteritis: o
Lupus
o
Takayasu disease
o
Kawasaki disease
o
Rheum atoid arthritis
Anem ia: o
Hem oglobin 55 years
o
Postm enopausal wom en
Diagnosis Signs and Symptoms
Unstable angina is defined by either: o
New-onset sym ptom s
o
Sym ptom s that occur at rest
Pa ge 2 9 3
o
A change in the patient's usual pattern of angina
Chest pain: o
Most com m on presentation of m yocardial infarction
o
Substernal pressure
o
Heaviness
o
Squeezing
o
Burning sensation
o
Tightness
Occasional anginal equivalents: o
Abdom inal pain
o
Syncope
o
Diaphoresis
o
Nausea or vom iting
o
Weakness
May localize or radiate to arm s, shoulders, back, neck, or jaw
May be associated with dyspnea, syncope, fatigue, diaphoresis, nausea, or vom iting
Sym ptom s are usually reproduced by exertion, eating, exposure to cold, or em otional stress.
Sym ptom s com m only last 15 m inutes or m ore.
Usually im proved or relieved with rest or nitroglycerin
Sym ptom s generally unchanged with position or inspiration
Positive Levine sign or clenched fist over chest is suggestive of angina
Blood pressure (BP) is usually elevated during sym ptom s.
Physical Exam
Physical exam is usually unrevealing.
Occasional physical findings include: o
S3 or S4 due to left ventricular systolic or diastolic sym ptom s
o
Papillary m uscle dysfunction resulting in m itral
Pa ge 2 9 4
regurgitation o
Dim inished peripheral pulses
Essential Workup History is critical in differentiating m yocardial infarction (MI) from noncardiac etiologies.
Tests
ECG: o
Will be norm al approxim ately 50% of the tim e
o
ST segm ent changes or T-wave inversions m ost often will be unchanged from previous tracings.
o
Must be com pared to prior tracings if available
o
New ST segm ent changes or T-wave inversions are suspicious for unstable angina.
o
Serial ECG tracings that rem ain unchanged m ay assist in differentiating stable from unstable angina.
o
1-m m depression of the ST segm ent below the baseline, 80 m sec from the J point, is characteristic of angina.
ECG m ay be helpful in diagnosing other etiologies of chest pain: o
Pericarditis is suggested by diffuse ST elevations followed by T-wave inversions and PR depression.
o
Pulm onary em bolism is suggested by an S1, Q3, T3 pattern and unexplained tachycardia.
Lab
CK-MB and troponin I or T
Hem atocrit
Coagulation profile
Creatinine
Imaging
Pa ge 2 9 5
Chest radiograph: o
Usually norm al
o
May show cardiom egaly
o
Congestive heart failure is suggestive of unstable angina.
o
May identify other etiologies of chest pain such as pneum onia
Rest echocardiography m ay establish the diagnosis of acute coronary insufficiency (ACI): o
Has a sensitivity of 70% and specificity of 87% for ACI
Technetium Tc-99 sestam ibi (rest): o
Has a sensitivity of 81% and specificity of 73% for ACI
Exercise stress testing m ay help establish the diagnosis of angina and provide prognostic inform ation when the clinical presentation is equivocal: o
Exercise stress testing with ECG alone has a sensitivity of 68% and specificity of 77%.
o
Exercise stress testing with echocardiography has a sensitivity of 85% and specificity of 77%.
o
Exercise stress testing with thallium -201 or technetium Tc-99m sestam ibi has a sensitivity of 87% and specificity of 64%.
o
1-m m depression of the ST segm ent below the baseline, 80 m sec from the J point, in three consecutive beats and two consecutive leads is characteristic of cardiac ischem ia.
o
Early positive (within 3 m inutes) stress tests are worrisom e for unstable angina.
Diagnostic Procedures/Surgery See Cardiac Testing
Pa ge 2 9 6
Differential Diagnosis
Acute MI
Anxiety
Aortic dissection
Biliary colic
Costochondritis
Esophageal reflux
Esophageal spasm
Herpes zoster
Hiatal hernia
Mitral valve prolapse
MI
Panic disorder
Peptic ulcer disease
Pneum onia
Psychogenic
Pulm onary em bolus
P.39
Treatment Pre Hospital
IV access
Aspirin
Oxygen
Cardiac m onitoring
Sublingual nitroglycerin for sym ptom relief
Alert
Pa ge 2 9 7
All chest pain should be treated and transported as a possible life-threatening em ergency.
Initial Stabilization
IV access
Oxygen
Cardiac m onitoring
Oxygen saturation
Continuous BP m onitoring and pulse oxim etry
ED Treatment
Aspirin should be adm inistered first to all patients with suspected unstable angina
Sublingual nitroglycerin, nitro paste, or IV nitroglycerin; o
Sym ptom s that persist after three sublingual nitroglycerins are strongly suggestive of unstable angina, acute MI, or noncardiac etiology.
Beta-blockers should be adm inistered if no contraindications (e.g., bradyarrhythm ias or obstructive pulm onary disease) are present.
Morphine m ay be given to relieve pain and increase oxygen-carrying capacity.
Enoxaparin or heparin is generally appropriate as the next line of therapy.
If unstable angina is clearly the clinical diagnoses, a glycoprotein IIb/IIIa inhibitor should be started as well.
Medication (Drugs)
Aspirin: 160–325 m g PO
Enoxaparin (Lovenox): 1 m g/kg SC q12h
Glycoprotein IIb/IIIa inhibitors: o
Eptifibatide (Integrilin): 180 µg/kg IV over 1–2
Pa ge 2 9 8
m inutes, followed by continuous infusion of 2 µg/kg/m in up to 72 hours o
Tirofiban (Aggrastat): 0.4 µg/kg/m in for 30 m inutes, then 0.1 µg/kg/m in for 48–108 hours
o
Abcixim ab (ReoPro): for use prior to percutaneous coronary intervention only, 0.25 m g/kg IV bolus
Heparin: 80 units/kg IV bolus, then 18 units/kg/hr
Metoprolol: 5 m g IV q5m in–q15m in followed by 25–50 m g PO starting dose as tolerated (note: beta-blockers contraindicated in cocaine chest pain)
Morphine: 2 m g IV, m ay titrate upward in 2-m g increm ents for relief of pain assum ing no respiratory deterioration and SBP >90 m m Hg
Nitroglycerin: 0.4 m g sublingual
Nitroglycerin: IV drip at 5–10 µg/m in
Nitropaste: 1–2 inches transderm al
Follow-Up Disposition Admission Criteria
Patients with unstable angina require hospital adm ission.
If the diagnosis is unclear, adm ission to the hospital or an ED observation unit m ay be useful for serial cardiac enzym es, ECGs, and exercise stress testing and/or cardiac catheterization.
Discharge Criteria No patient with unstable angina should be discharged from the ED.
References
Pa ge 2 9 9
1. Boden WE, McKay RG. Optim al treatm ent of acute coronary syndrom es: an evolving strategy. N Engl J Med. 2001;344:1939–1942. 2. Braunwald E, et al. ACC/AHA guidelines for the m anagem ent of patients with unstable angina and non ST segm ent elevation m yocardial infarction. J Am Coll Cardiol. 2000;36:970–1062. 3. Cannon CP, et al. Com parison of early invasive and conservative strategies in patients with unstable coronary syndrom es treated with the glycoprotein IIb/IIIa inhibitor tirofiban, the TACTICS-throm bolysis in m yocardial infarction 18 investigators. N Engl J Med. 2001;344:1879–1887. 4. Lau J, Ioannidis JP, Balk EM, et al. Diagnosing acute cardiac ischem ia in the em ergency departm ent: a system atic review of the accuracy and clinical effect of current technologies. Ann Em erg Med. 2001;37(5):453–460. 5. Main C, Palm er S, Griffin S, Jones L, Orton V, Sculpher M, Henderson R, Sudlow C, Hawkins N, Riem sm a R. Clopidogrel used in com bination with aspirin com pared with aspirin alone in the treatm ent of non-ST-segm ent- elevation acute coronary syndrom es: a system atic review and econom ic evaluation. Health Technol Assess. 2004 Oct;8(40):iii–iv, xv–xvi, 1–141.
Miscellaneous SEE ALSO: Cardiac Testing; Myocardial Infarction; Reperfusion Therapy; Stable Angina
Codes ICD9-CM 411.1
ICD10
Pa ge 3 0 0
I20.0
Pa ge 3 0 1
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Adrenal Insufficiency
Adrenal
Insufficiency Rita Cydulka Eva Escatel
Basics Description
Inadequate hydrocortisone secretion to m eet body's stress requirem ent
Adrenal deficiency: o
Inadequate cortisol
o
Unresponsive to stim ulation with adrenocorticotropic horm one (ACTH)
Functional hypoadrenalism : o
Inadequate cortisol
o
Partial responsive to stim ulation with ACTH
Addisonian crisis (acute adrenal insufficiency): o
Life-threatening em ergency
o
Precipitated by intensification of:
Chronic adrenal insufficiency
Acute adrenal hem orrhage
Rapid steroid withdrawal
Treatm ent of hypothyroidism with unrecognized
Pa ge 3 0 2
adrenal disease
Steroid-dependent patient under stress owing to pregnancy, surgery, traum a, infection, or dehydration
Etiology Primary Adrenal Failure
Adrenal dysgenesis/im paired steroidogene: o
Congenital hypoplasia
o
Allgrove syndrom e:
o
ACTH resistance
Achalasia
Alacrim a
Glycerol kinase deficiency:
Psychom otor retardation
Hypogonadism
Muscular dystrophy
o
Congenital hyperplasia
o
Aldosterone synthetase deficiency
o
Mitochondrial disease
Adrenal destruction: o
Autoim m une:
Autoim m une polyglandular syndrom e types 1 and 2 (alopecia universalis, chronic m ucocutaneous candidiasis, hypoparathyroid, thyroid autoim m unity, diabetes, celiac disease, pernicious anem ia)
o
Adrenoleukodystrophy
Infectious:
Granulom atous: tuberculosis
Protozoal and fungal: histoplasm osis, coccidioidom ycosis, candidiasis
Pa ge 3 0 3
Viral: cytom egalovirus, herpes sim plex virus, and HIV
o
Bacterial
Infiltration:
Sarcoid
Neoplasm
Hem ochrom atosis
Am yloidosis
Iron depletion
Postadrenalectom y
Hem orrhage: o
Sepsis: particularly m eningococcem ia, Pseudom onas infection
o
Birth traum a/anoxia
o
Pregnancy
o
Seizures
o
Anticoagulants
o
Rhabdom yolysis
Pharm acologic inhibition: o
Etom idate
o
Herbal m edications
o
Ketoconazole
o
Metyrapone
o
Suram in
Secondary Adrenal Failure Pituitary insufficiency:
Sepsis
Head traum a
Hem orrhage
Infarction (Sheehan syndrom e)
Infiltration: neoplasm , am yloid, sarcoid, hem ochrom atosis
Adrenocorticotropic horm one deficiency
Pa ge 3 0 4
Pharm acologic: glucocorticoid adm inistration, herbal m edications
Tertiary Adrenal Failure
Hypothalam us insufficiency
Sepsis
Infiltrative: neoplasm , am yloid, sarcoid, hem ochrom atosis
Head traum a
Diagnosis Signs and Symptoms
Sym ptom s: o
Depression
o
Lethargy
o
Malaise
o
Myalgias
o
Anorexia
o
Abdom inal pain
o
Nausea
o
Vom iting
o
Dehydration (found in prim ary adrenal insufficiency only)
o
Salt craving
Signs: o
Fever or hypotherm ia
o
Mental status changes
o
Tachycardia
o
Orthostatic blood pressure changes or frank shock
o
Weight loss
o
Goiter
Pa ge 3 0 5
o
Hypogonadism
o
Hyperkalem ia
o
Sodium depletion
o
Eosinophilia
o
Hyperpigm entation (found in prim ary adrenal insufficiency only)
o
Vitiligo
Addisonian crisis: o
Hypotension and shock
o
Hyponatrem ia
o
Hyperkalem ia
o
Hypoglycem ia
Essential Workup
Laboratory confirm ation of diagnosis not possible in em ergency departm ent
Adrenal crisis: life-threatening condition: o
High degree of suspicion should prom pt initiation of therapy before definitive diagnosis.
Plasm a cortisol level Table o f C o ntents > Alkalo sis
Alkalosis
Matthew Robinson
Basics Description Respiratory Alkalosis
Elevated serum pH secondary to alveolar hyperventilation and decreased PaCO 2
Hyperventilation occurs through stim ulation of two receptor types: o
Central receptors—located in the brainstem and respond to decreased CSF pH
o
Chest receptors—located in aortic arch and respond to hypoxem ia
Increased alveolar ventilation secondary to: o
Disorders causing acidosis
o
Hypoxem ia or
o
Nonphysiologic stim ulation of those receptors by CNS or chest disorders
Rarely life threatening with pH typically Table o f C o ntents > Am ebiasis
Amebiasis
Ann P. Nguyen
Basics Description
Invasive parasitic infection with both intestinal and extraintestinal m anifestations
Endem ic in developing countries
Fifty m illion cases and 40,000–100,000 deaths worldwide each year
Fecal-oral transm ission: o
Hum ans are sole reservoir.
o
Up to 90% asym ptom atic carriage
Populations at risk: o
Travelers to and im m igrants from endem ic areas
o
Institutionalized persons
o
Practitioners of anal sexual activity
Risk factors for increased severity of disease and com plications: o
Corticosteroid use
o
Malignancy
o
Malnutrition
o
Pregnancy/postpartum state
o
Extrem es of age
Pa ge 3 6 1
o
HIV disease
Etiology
Entam oeba histolytica, a nonflagellated protozoa
Biphasic life cycle: o
Ingested as cysts
o
Cysts becom e trophozoites, which cause invasive colitis.
o
Create m ultiple flask-shaped ulcers in the colonic m ucosa and m uscularis
o
Extraintestinal spread is hem atogenous.
Diagnosis Signs and Symptoms Intestinal Disease
Onset 1 week to 1 m onth postexposure
Acute diarrhea (80% of cases):
o
1–4 weeks’ duration
o
Afebrile
o
Occult blood in stool
o
Benign abdom inal exam
Classic dysentery: o
1–4 weeks’ duration
o
Bloody m ucoid diarrhea
o
Abdom inal pain
o
Bloating
o
Tenesm us
o
Weight loss
o
Fever (rare)
o
Benign abdom inal exam
Pa ge 3 6 2
Fulm inant colitis: o
Toxic-appearing patient
o
Rigid abdom en (25%)
o
Fever
o
Severe bloody diarrhea
o
Rapid progression to perforated bowel and frank peritonitis
o
>50% m ortality
Toxic m egacolon: o
Toxic-appearing patient
o
Profuse diarrhea (>10 stools per day)
o
Fever
o
Tachycardia
o
Distended, tym panitic abdom en with signs of peritonitis
o
Associated with corticosteroid use
o
High m ortality
Am ebom a: o
Intralum inal granulated m ass
o
Most com m on in the cecum , ascending colon, and rectosigm oid colon
o
Tender palpable m ass on exam
Am ebic strictures: o
Owing to chronic inflam m ation and scarring
o
Most com m on in the anus, rectum , or sigm oid colon
o
Cram py abdom inal pain
o
Nausea and vom iting (m ay be feculent)
o
May lead to partial or com plete bowel obstruction
Chronic am ebic colitis: o
Mild recurrent episodes of bloody diarrhea, abdom inal cram ping, tenesm us
o
Weight loss
Pa ge 3 6 3
o
May persist for years
Extraintestinal Disease
Am ebic liver abscess: o
Most frequent extraintestinal m anifestation (3–9% of cases)
o
Single abscess in right lobe (50–80%)
o
May develop m onths to years postexposure (m edian of 3 m onths)
o
Fever
o
Cough
o
Right upper quadrant pain
o
Hepatom egaly with point tenderness
o
Rales at right lung base
o
Concurrent diarrhea unusual (20–33%)
o
Com plication: rupture into pleural cavity (10–20%), peritoneum (2–7%) or pericardium (rare)
Extrahepatic am ebic abscess: o
Hem atologic spread
o
Brain
o
Lung
o
Perinephric
o
Splenic
o
Vaginal/cervical/uterine
Cutaneous am ebiasis: o
Perineum and genitalia
o
Well-defined, irregularly shaped friable ulcers
o
Purulent exudate
o
Painful
Pediatric Considerations Children m ore likely than adults to present with fulm inant colitis
Pa ge 3 6 4
Pregnancy Considerations Pregnant patients m ore likely to present with fulm inant colitis
Essential Workup
History: o
Possible sources of exposure
o
Mem bership in high-risk group
Physical exam : o
Identify evidence of peritonitis, sepsis, or shock.
o
Tender abdom inal m ass m andates workup for liver abscess or am ebom a.
o
Digital rectal exam shows gross or occult blood in >70% of patients.
Tests Lab
Stool enzym e-linked im m unosorbent assay (ELISA) for E. histolytica–specific antigen: o
74–100% sensitive
o
Stool m icroscopy is insensitive and no longer the test of choice.
Fecal leukocytes and culture: o
Rule out infection owing to enteroinvasive bacteria.
o
Negative in am ebiasis
Serum for anti-E. histolytica antibodies: o
Essential if suspecting liver abscess as these patients rarely shed parasites in their stool
o
90–100% sensitive in am ebic liver abscess
o
70–90% sensitive in am ebic colitis
CBC: o
Leukocytosis in am ebic liver abscess and peritonitis
Alkaline phosphatase and ALT:
Pa ge 3 6 5
o
Elevated in am ebic liver abscess
Serum electrolytes, BUN/creatinine if prolonged diarrhea or evidence of dehydration
Imaging
Abdom inal ultrasound: o
58–90% sensitive
o
Evaluate abscess for increased risk of rupture (>5 cm or located in left lobe)
Abdom inal CT or MRI: o
Equivalent to ultrasound for delineating liver abscesses
o
Superior to ultrasound for detecting abscesses in other organs
Head CT or MRI: o
Suspect am ebic brain abscess if patient with known am ebiasis presents with altered m ental status or focal neurologic findings.
o
Irregular nonenhancing lesions
Chest radiograph: o
Elevated right hem idiaphragm and/or right pleural effusion in liver abscess
Diagnostic Procedures/Surgery
Colonoscopy with biopsy: o
Provides definitive diagnosis of am ebic dysentery, colitis, am ebom a, and am ebic stricture
Percutaneous fine-needle aspiration of liver abscess: o
Indicated to exclude bacterial abscess if high suspicion for this entity (elderly patient, nondiagnostic serology, failure of antiam ebic therapy)
P.53
Pa ge 3 6 6
Differential Diagnosis
Intestinal am ebiasis: o
Enteroinvasive bacterial infection (Staphylococcus, E. coli, Shigella, Salm onella, Yersinia, Cam pylobacter)
o
Inflam m atory bowel disease
o
Ischem ic colitis
o
Arteriovenous m alform ation
o
Abdom inal aortic aneurysm
o
Perforated duodenal ulcer
o
Intussusception
o
Diverticulitis
o
Pancreatitis
o
Colorectal carcinom a
Am ebic abscess: o
Bacterial abscess
o
Tuberculous cavity
o
Echinococcal cyst
o
Malignancy
o
Cholecystitis
Cutaneous am ebiasis: o
Carcinom a
o
Sexually transm itted diseases (condylom a acum inata, chancroid, syphilis)
Treatment Initial Stabilization
Airway, breathing, circulation (ABCs)
Pa ge 3 6 7
IV 0.9 NS if signs of significant dehydration or shock
ED Treatment
Oral fluids for m ild dehydration
Avoid antidiarrheal agents.
Correct any serum electrolyte im balances.
Stool sam ple for E. histolytica–specific antigen plus serology for anti–E. histolytica antibodies
If stool or serum is positive for E. histolytica: o
Metronidazole is first-line drug for system ic am ebiasis.
o
Ninety percent cure rate
Tetracycline for m ild dysentery in m etronidazole-intolerant patients, but will not eradicate hepatic infection
o
Dehydroem etine if m etronidazole fails:
Must adm it all dehydroem etine patients to a m onitored setting because of the potential for cardiac toxicity and dysrhythm ia
o
Always follow system ic therapy with a lum inal am ebicidal agent to eradicate intestinal colonization (diloxanide furoate, parom om ycin, or iodoquinol).
If stool or serum is negative for E. histolytica: o
Refer to gastroenterologist for colonoscopy with biopsy.
o
Repeat serology in 7 days.
o
Consider em piric course of m etronidazole if high suspicion for am ebiasis and patient is critically ill.
If evidence of peritonitis or sepsis: o
Add IV antibiotic directed against anaerobic and gram -negative bacteria.
o
Surgery if toxic m egacolon or colonic perforation
If liver abscess is suspected:
Pa ge 3 6 8
o
Ultrasound of hepatobiliary system with concurrent am ebic serology
o
Abdom inal CT scan if ultrasound is equivocal
o
If im aging dem onstrates an abscess but serology is negative, treat with am ebicidals as above and repeat serology in 7 days.
o
Consult surgery for drainage of >5 cm and left lobe abscesses (risk of rupture).
o
If sym ptom s do not im prove after 5 to 7 days of em piric am ebicidal therapy, consider fine-needle aspiration to rule out bacterial liver abscess or hepatom a.
Pregnancy Considerations
Adm inister m edications with caution in first-trim ester pregnancy, but do not withhold if patient has fulm inant colitis or am ebic abscess.
Erythrom ycin for m ild dysentery in first-trim ester pregnancy
Medication (Drugs)
Dehydroem etine: 90 m g (peds: 1–1.5 m g/kg/24h) IM q24h for 5 days
Diloxanide furoate: 500 m g (peds: 20 m g/kg/24h) PO q8h for 10 days
Erythrom ycin: 500 m g (peds: 30–50 m g/kg/24h) PO q6h for 10 days
Iodoquinol: 650 m g (peds: 30–40 m g/kg/24h) PO q8h for 20 days
Metronidazole: 750 m g (peds: 30–50 m g/kg/24h) PO/IV q8h for 10 days
Pa ge 3 6 9
Parom om ycin: 25–30 m g/kg/24h PO q8h for 7–10 days
Tetracycline: 250 m g PO q8h for 10 days
Follow-Up Disposition Admission Criteria
Shock, sepsis or peritonitis
Hypotension or tachycardia unresponsive to IV fluids
Children with >10% dehydration
Severe electrolyte im balance
Patients unable to m aintain adequate oral hydration: o
Extrem es of age, cognitive im pairm ent, significant co-m orbid illness
Fulm inant colitis or toxic m egacolon
Bowel obstruction
Extraintestinal abscesses
Failure of outpatient regim en
Dehydroem etine therapy
Discharge Criteria
Nontoxic presentation of acute or chronic dysentery
Able to m aintain adequate oral hydration
Dehydration responsive to IV fluids
Issues for Referral Consult surgery if evidence of peritonitis, toxic m egacolon, colonic perforation, or liver abscess >5 cm or located in left liver lobe.
References 1. Blessm an J, Binh HD, Hung DM, et al. Treatm ent of am oebic liver abscess with m etronidazole alone or in com bination with
Pa ge 3 7 0
ultrasound-guided needle aspiration: a com parative, prospective and random ized study. Trop Med Int Health. 2003;8:1030–1034. 2. Elzi L, Laifer G, Sendi P, et al. Low sensitivity of ultrasonography for the early diagnosis of am ebic liver abscess. Am J Med. 2004;117:519–522. 3. Haque R, Huston CD, Hughes M, et al. Current concepts: am ebiasis. N Engl J Med. 2003;348:1565–1573. 4. Hung CC, Deng HY, Hsiao WH, et al. Invasive am ebiasis as an em erging parasitic disease in patients with HIV-1 infection in Taiwan. Arch Int Med. 2005;165:409–415. 5. Petri WA. Therapy of intestinal protozoa. Trends Parasitol. 2003;19:523–526. 6. Stanley SL. Am oebiasis. Lancet. 2003;361:1025–1034. 7. Stauffer W, Ravdin JI. Entam oeba histolytica: an update. Curr Opin Inf Dis. 2003;16:479–485. 8. Tanyuksel M, Petri WA. Laboratory diagnosis of am ebiasis. Clin Microbiol Rev. 2003;16:713–729.
Miscellaneous SEE ALSO: Diarrhea; Gastroenteritis
Codes ICD9-CM 006.0
ICD10 A06.9
Pa ge 3 7 1
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Am eno rrhea
Amenorrhea
Christy Rosa Mohler
Basics Description Absence of m enstruation
Etiology
Prim ary: o
Gonadal dysgenesis
o
Chrom osom al abnorm alities
Secondary: o
Pregnancy, breast-feeding, postpartum
o
Asherm an syndrom e (intrauterine adhesions)
o
Dysfunction of the hypothalam ic-pituitary-ovarian axis
o
Endocrinopathies
o
Obesity, starvation, intense exercise
o
Drugs:
Oral contraceptives, antipsychotics, antidepressants, calcium channel blockers, chem otherapeutic agents, digitalis, m arijuana
o
Autoim m une disorders
o
Ovarian failure
o
Menopause
Pa ge 3 7 2
Diagnosis Signs and Symptoms History
Prim ary am enorrhea: o
No spontaneous uterine bleeding by age 14 years in the absence of the developm ent of secondary sexual characteristics or by age 16 years with otherwise norm al developm ent
Secondary am enorrhea: o
Absence of m enstrual bleeding for 6 m onths in a wom an with prior regular m enses or for 12 m onths in a wom an with prior oligom enorrhea
Physical Exam
Low estrogen: atrophic vaginal m ucosa, m ood swings, irritability
High androgen: truncal obesity, hirsutism , acne, m ale-pattern baldness
Essential Workup Pregnancy test
Tests Lab
If pregnancy test is negative, no further testing is needed em ergently.
May send thyroid-stim ulating horm one (TSH), prolactin, luteinizing horm one (LH), follicle-stim ulating horm one (FSH) for follow-up by gynecology or prim ary care physician
Pa ge 3 7 3
Imaging None needed em ergently
Diagnostic Procedures/Surgery None needed em ergently
Differential Diagnosis Pregnancy P.55
Treatment Pre Hospital If am enorrhea is the result of pregnancy, stabilize patient as appropriate for pregnancy.
ED Treatment Reassurance and referral for follow-up
Medication (Drugs) Defer for gynecology evaluation.
Follow-Up Disposition Admission Criteria No need for adm ission
Pa ge 3 7 4
Discharge Criteria All patients can be discharged with appropriate referral.
Issues for Referral Nonem ergent referral to gynecology
References 1. Prim ary and secondary am enorrhea. In:Stenchever MA, et al., eds. Com prehensive Gynecology. 4th ed. St. Louis, MO: Mosby; 2001:1099–1119. 2. Warren MP, Hagey AR. The genetics, diagnosis and treatm ent of am enorrhea. Minerva Ginecol. 2004;56(5):437–455.
Codes ICD9-CM N/A
Pa ge 3 7 5
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Am phetam ine, Po iso ning
Amphetamine,
Poisoning James W. Rhee
Basics Description
Increased release of norepinephrine, dopam ine, serotonin
Decreased catecholam ine reuptake
Direct effect on α- and β-adrenergic receptors
Etiology
Prescription drugs: o
Am phetam ine (Benzedrine)
o
Dextroam phetam ine (Dexedrine)
o
Diethylpropion (Tenuate)
o
Fenfluram ine (Pondim in)
o
Metham phetam ine
o
Methylphenidate (Ritalin)
o
Phenm etrazine (Preludin)
o
Phenterm ine
“Designer drugs―: o
Variants of illegal parent drugs
o
Often synthesized in underground laboratories
o
“Ice―:
Pa ge 3 7 6
Crystalline m etham phetam ine hydrochloride
Sm oked, insufflated, or injected
Rapid onset; duration several hours
o
“Crank―
o
“Ecstasy― (3,4-m ethylenedioxym etham phetam ine, MDMA, XTC):
Often used at dances and “rave― parties
Dehydration can lead to hypertherm ia, hyponatrem ia, fatality.
o
MDA (3,4-m ethylenedioxyam phetam ine)
o
Methcathinone (“cat,― “Jeff,― “m ulka―):
Derivative of cathinone, found in the evergreen tree Catha edulis
Frequently synthesized in hom e laboratories
Does not show up on urine toxicology screens
Diagnosis Signs and Symptoms
Central nervous system (CNS): o
Agitation
o
Delirium
o
Hyperactivity
o
Trem ors
o
Dizziness
o
Mydriasis
o
Headache
o
Choreoathetoid m ovem ents
o
Hyperreflexia
Pa ge 3 7 7
o
Cerebrovascular accident
o
Seizures and status epilepticus
o
Com a
Psychiatric: o
Euphoria
o
Increased aggressiveness
o
Anxiety
o
Hallucinations (visual, tactile)
o
Com pulsive repetitive actions
Cardiovascular: o
Palpitations
o
Hypertensive crisis
o
Tachycardia or (reflex) bradycardia
o
Dysrhythm ias (usually tachydysrhythm ias)
o
Cardiovascular collapse
Other: o
Rhabdom yolysis
o
Myoglobinuria
o
Acute renal failure
o
Anorexia
o
Diaphoresis
o
Dissem inated intravascular coagulation (DIC)
Essential Workup
Vital signs: o
o
Tem perature >40°C:
Core tem perature recording essential
Peripheral tem perature m ay be cool.
Indication for urgent cooling
Om inous prognostic sign
Blood pressure:
Severe hypertension can lead to cardiac and neurologic abnorm alities.
Pa ge 3 7 8
Late in course, hypotension m ay supervene.
ECG: o
Signs of cardiac ischem ia
o
Ventricular tachydysrhythm ias
o
Reflex bradycardia
Tests Lab
Urinalysis: o
Blood
o
Myoglobin
Electrolytes, BUN/creatinine, glucose: o
Hypoglycem ia m ay contribute to altered m ental status.
o
Acidosis m ay accom pany severe toxicity.
o
Rhabdom yolysis m ay cause renal failure.
o
Hyperkalem ia—life-threatening consequence of acute renal failure
Coagulation profile to m onitor for potential DIC: o
Creatine phosphokinase (CPK): o
INR, PT, PTT, platelets
Markedly elevated in rhabdom yolysis
Urine toxicology screen: o
For other toxins with sim ilar effects (e.g., cocaine)
o
Som e am phetam inelike substances (e.g., m ethcathinone) m ay not be detected.
Aspirin and acetam inophen levels if suicide attem pt a possibility
Arterial blood gas (ABG)
Imaging
Chest radiograph: o
Adult respiratory distress syndrom e
Pa ge 3 7 9
o
Noncardiogenic pulm onary edem a
Head CT for: o
Significant headache
o
Altered m ental status
o
Focal neurologic signs
o
For subarachnoid hem orrhage, intracerebral bleed
Diagnostic Procedures/Surgery Lum bar puncture for:
Suspected m eningitis (headache, altered m ental status, hyperpyrexia)
Suspected subarachnoid hem orrhage and CT norm al
Differential Diagnosis
Sepsis
Thyroid storm
Serotonin syndrom e
Neuroleptic m alignant syndrom e
Pheochrom ocytom a
Subarachnoid hem orrhage
Drugs that cause delirium : o
Anticholinergics:
Belladonna alkaloids
Antihistam ines
o
Tricyclic antidepressants
o
Cocaine
o
Ethanol withdrawal
o
Sedative/hypnotic withdrawal
o
Hallucinogens
o
Phencyclidine
Drugs that cause hypertension and tachycardia: o
Sym pathom im etics
o
Anticholinergics
Pa ge 3 8 0
o
Ethanol withdrawal
o
Phencyclidine
o
Caffeine
o
Phenylpropanolam ine
o
Ephedrine
o
Monoam ine oxidase inhibitors
o
Theophylline
o
Nicotine
Drugs that cause seizures: o
Carbon m onoxide
o
Carbam azepine
o
Cyanide
o
Cocaine
o
Cholinergics (organophosphate insecticides)
o
Cam phor
o
Chlorinated hydrocarbons
o
Ethanol withdrawal
o
Sedative/hypnotic withdrawal
o
Isoniazid
o
Theophylline
o
Hypoglycem ics
o
Lead
o
Lithium
o
Local anesthetics
o
Anticholinergics
o
Phencyclidine
o
Phenothiazines
o
Phenytoin
o
Propoxyphene
o
Salicylates
o
Strychnine
P.57
Pa ge 3 8 1
Treatment Pre Hospital
Patient m ay be uncooperative or violent.
Secure IV access.
Protect from self-induced traum a.
Initial Stabilization
Airway, breathing, and circulation m anagem ent (ABCs)
Establish IV 0.9% norm al saline (NS) access.
Cardiac m onitor
Naloxone, dextrose (or Accu-Chek), and thiam ine if altered m ental status
ED Treatment
Decontam ination: o
Gastric lavage:
Consider if recent (1–2 hours) or life-threatening ingestion.
Instill activated charcoal through large-bore orogastric tube both before and after lavage.
o
Adm inister activated charcoal with sorbitol.
Hypertensive crisis: o
Initially adm inister benzodiazepines if agitated.
o
Alpha-blocker (phentolam ine) as second-line agent
o
Nitroprusside for severe, unresponsive hypertension
o
Avoid beta-blockers, which m ay exacerbate hypertension.
Agitation, acute psychosis:
Pa ge 3 8 2
o
Adm inister benzodiazepines.
Hypertherm ia: o
Benzodiazepines if agitated
o
Active cooling if tem perature >40°C:
o
Tepid water m ist
Evaporate with fan.
Paralysis:
Indicated if m uscle rigidity and hyperactivity contributing to persistent hypertherm ia
Nondepolarizing agent (e.g., vecuronium )
Avoid succinylcholine.
Intubation; m echanical ventilation
o
Adm inister acetam inophen.
o
Apply cooling blankets.
Rhabdom yolysis: o
Adm inister benzodiazepines.
o
Hydrate with 0.9% NS.
o
Maintain urine output at 1–2 m L/m in.
o
Hem odialysis (if acute renal failure and hyperkalem ia occur)
Seizures: o
Maintain airway.
o
Adm inister benzodiazepines.
o
Phenobarbital if unresponsive to benzodiazepines
o
Phenytoin contraindicated
Medication (Drugs)
Activated charcoal slurry: 1–2 g/kg up to 100 g PO
Dextrose: D 5 0 W 1 am p: 50 m L or 25 g (peds: D 2 5 W 2–4 m L/kg) IV
Diazepam (benzodiazepine): 5–10 m g (peds: 0.2–0.5
Pa ge 3 8 3
m g/kg) IV
Lorazepam (benzodiazepine): 2–6 m g (peds: 0.03–0.05 m g/kg) IV
Nitroprusside: 1–8 µg/kg/m in IV (titrated to blood pressure)
Phenobarbital: 15–20 m g/kg at 25–50 m g/m in until cessation of seizure activity
Phentolam ine: 1–5 m g IV over 5 m inutes (titrated to blood pressure)
Sorbitol: 1–2 g/kg to a m ax. of 100 g PO m ixed in the activated charcoal slurry (peds: >1 year old: 1–1.5 g/kg as a 35% solution to a m ax. of 50 g); avoid repeat doses of sorbitol.
Vecuronium : 0.1 m g/kg IVP
Follow-Up Disposition Admission Criteria
Hypertherm ia
Persistent altered m ental status
Hypertensive crisis
Seizures
Rhabdom yolysis
Persistent tachycardia
Discharge Criteria
Asym ptom atic after 6 hours observation
Absence of above adm ission criteria
References
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1. Callaway CW, Clark RF. Hypertherm ia in psychostim ulant overdose. Ann Em erg Med. 1994;24:68–75. 2. Chan P, Chen JH, Lee MH, et al. Fatal and nonfatal m etham phetam ine intoxication in the intensive care unit. Clin Toxicol . 1994;32:147–155. 3. Christophersen AS. Am phetam ine designer drugs—an overview and epidem iology. Toxicol Lett. 2000;112–113:127. 4. Doyon S. The m any faces of ecstasy. Curr Opinion Pediatr. 2001;13:170–176. 5. Kalant H. The pharm acology and toxicology of “ecstasy― (MDMA) and related drugs. Can Med Assoc J. 2001;165:917–928.
Codes ICD9-CM 969.7
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Am putatio n Traum atic/Replantatio n
Amputation Traumatic/Replantation Matthew Solley Jennifer Oman
Basics Description
Partial am putations have tissue connecting the distal and proxim al parts and are treated by revascularization.
Com plete am putations have no connecting tissue and m ay be treated by replantation.
Both of the above are treated the sam e from an em ergency standpoint.
Etiology Traum atic am putations result from m achinery, powered hand tools, household appliances, lawnm owers, getting caught between objects, m otor vehicle collisions, crush injuries, blast injuries, gunshot wounds, knives, degloving injuries to digits (ring avulsions), and m am m alian bites.
Diagnosis Signs and Symptoms
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History
Exact tim e of injury critical, as ischem ia tim e predicts success for replantation: o
Warm ischem ia tim e:
Elapsed tim e since injury without cooling the am putated part
4–6 hours for m ajor am putations; 6 to 8 hours for digits
o
Cold ischem ia tim e:
Elapsed tim e since injury with cooling of am putated part
10–12 hours for m ajor am putations; up to 30 hours or longer for digits
Mechanism of injury: o
Clean am putations (with sharp objects) have better prognosis for replantation than crush or avulsion injuries.
Co-m orbid illnesses that hinder successful replantation: o
i.e., diabetes, peripheral vascular disease, rheum atologic disease
Physical Exam
Assessm ent and docum entation of injured extrem ity is crucial.
Signs of neurologic com prom ise: o
Loss of sensation and two-point discrim ination
o
Loss of active range of m otion
Signs of vascular com prom ise in partial am putations: o
Distal part dusky or cyanotic
o
Delayed capillary refill (>2 seconds)
o
Dim inished or absent pulses (Doppler or palpation)
o
Use Allen test in hand injuries.
Pa ge 3 8 7
o
Pulse oxim etry m ay be helpful.
Soft tissue: Assess skin, m uscle, tendon, and nail bed integrity.
Identify exposed bone and fractures (gross deform ity, tenderness, crepitus).
Essential Workup Em ergency departm ent workup includes obtaining an accurate history and physical, stabilizing the patient and injured part, and consultation or transfer if replantation is an option.
Tests Lab Preoperative lab studies if needed
Imaging Radiographs of both am putated part and stum p are im portant, but should not delay transport.
Diagnostic Procedures/Surgery Determ ined by surgical consultant for replantation
Differential Diagnosis
Involves neurologic, vascular, and soft tissue integrity and potential for replantation/revascularization
Do not m iss other m ajor injuries with concurrent traum a.
Treatment Pre Hospital
Collect all am putated body parts, including pieces of bone, tissue, and skin.
See Initial Stabilization for care of am putated parts during
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transport.
Transport patient and body parts to the nearest m icrovascular replantation center unless other m ajor injuries require transport to the nearest traum a center: o
Air transport from rem ote locations should be considered if ischem ia tim e is of concern.
Initial Stabilization
Consult surgical specialist as early as possible.
Establish IV access.
Lim it blood loss: o
Elevate injured lim b.
o
Direct pressure using bulky pressure dressing or pressure points if ineffective.
o
Use tourniquet if above m ethods fail to give desired hem ostasis (blood pressure cuff 30 m m Hg greater than systolic blood pressure [SBP]).
o
Partial am putations bleed m ore because of lack of both retraction and spasm of blood vessels.
Avoid further dam age to injured part: o
Avoid vascular clam ps, cautery, vessel ligation, or débridem ent.
o
Avoid repeated exam inations of the stum p or am putated part.
Care of am putated part (com plete and partial): o
Rem ove gross contam ination/foreign m aterial.
o
Gently irrigate with saline (avoid antiseptics).
o
Wrap in gauze m oistened with saline.
o
Place in clean, dry plastic bag or specim en cup.
o
Place sealed bag/cup in ice water (half water, half ice) or refrigerate at 4°C.
o
Never place directly onto ice or into ice water.
o
Avoid dry ice to prevent freezing.
Pa ge 3 8 9
Care of the stum p: o
Irrigate with saline and cover with saline dam pened gauze
o
Splint if necessary; keep partial am putations as near anatom ic position as possible.
Maintain norm al blood volum e with intravenous fluids or blood products if necessary.
ED Treatment
Tetanus prophylaxis
Adequate IV analgesia
Patient NPO
Prophylactic antibiotics if devitalized tissue, exposed bone, or contam ination: o
First-generation cephalosporin
All patients are candidates for surgical repair until a specialist deem s otherwise.
Lim it ischem ia tim e of the am putated part (i.e., early transfer if necessary).
Patient considerations in decision to replant: o
Age
o
Occupation/handedness
o
Degree of m otivation
o
General physical condition and underlying diseases
Indications for replantation: o
Thum b, any level (supplies 40% of hand function)
o
Multiple digits
o
Hand am putations through the palm and distal wrist
o
Individual digit distal to flexor digitorum superficialis tendon insertion and proxim al to distal inter-phalangeal joint (DIP)
o
Som e single-digit ring avulsion injuries
o
Arm proxim al to m idforearm (if sharp or m oderately
Pa ge 3 9 0
avulsed) o
Virtually all pediatric am putations (younger patients have lower success rates but better functional outcom es)
Contraindications to replantation: o
Severely crushed or m angled parts
o
Injuries at m ultiple levels
o
Single-digit am putations proxim al to the flexor digitorum superficialis m uscle insertion
o
Am putated parts with tendons avulsed from m usculotendinous junctions
o
Very distal finger am putations (fingertip am putations, see below)
o
Lower extrem ities rarely attem pted and usually in children
o
Unstable patients secondary to other serious injuries or diseases
o
Older patients or those with contraindications to general anesthesia
o
Inappropriately prolonged ischem ia tim e
Fingertip am putations: m ost com m on type of upper extrem ity am putation: o
Distal to DIP joint
o
Prim ary goals of treatm ent:
Early functional recovery (coverage of bone, pain free, and sensate tip)
Minim ize pain
Prom ote healing
Cosm esis
P.59
Pa ge 3 9 1
o
Dorsal better prognosis than ventral
o
No exposed phalanx:
Irrigate with saline, apply petrolatum -soaked gauze and allow to heal by secondary intention (best result in wounds Table o f C o ntents > Anaphylaxis
Anaphylaxis
Sean-Xavier Neath
Basics Description
An acute, widely distributed form of shock that occurs within m inutes of exposure to antigen in a sensitized individual
There are approxim ately 400–800 deaths annually in the United States attributed to anaphylaxis.
Involves release of bioactive m olecules such as histam ine, leukotrienes, and prostaglandins from inflam m atory cells: o
Mediator release results in increased vascular perm eability, vasodilation, sm ooth-m uscle contractions, and increased epithelial secretion
o
Physiologically, this is m anifested in a decrease in total peripheral resistance, venous return, and cardiac output, as well as intravascular volum e depletion.
Etiology
IgE-m ediated: o
Antibiotics, particularly penicillin fam ily
o
Venom s, especially bee and wasp
o
Latex
Pa ge 4 0 7
o
Vaccines
o
Foodstuffs (shellfish, soybeans, peanuts, tree nuts, wheat, m ilk, eggs, nitrates/nitrites)
Non-IgE m ediated: o
Iodine contrast m edia
o
Opiates
o
Vancom ycin
o
Quaternary am m onium m uscle relaxants
Pediatric Considerations In children, foods are an im portant trigger for IgE-m ediated anaphylaxis. Milk, egg, wheat, and soy (MEWS) are the m ost com m on food allergens. Peanut allergies are less com m on but can be m ore potent; children can develop anaphylaxis from residual peanut in a candy bar.
Diagnosis Signs and Symptoms
Sym ptom s begin within seconds to m inutes after contact with an offending antigen.
Anaphylactic reactions alm ost always involve the skin or m ucous m em branes. More than 90% of patients have som e com bination of urticaria, erythem a, pruritus, or angioedem a.
Som e patients m ay have an initial sensation of im pending doom followed by m ore clearly definable sym ptom atology. o
Respiratory: from sneezing and nasal congestion to frank bronchospasm and laryngeal edem a
o
Cardiovascular: hypotension, dysrhythm ias, m yocardial ischem ia
Pa ge 4 0 8
o
Gastrointestinal: nausea, vom iting, diarrhea
o
Ocular: eye itching and tearing, conjunctival injection
o
Hem atologic: activation of intrinsic coagulation pathway som etim es leading to dissem inated intravascular coagulation, throm bocytopenia
o
Neurologic: seizures
Essential Workup
Diagnosis is m ade based on clinical sym ptom s.
It is im portant not to underestim ate the potential severity of an allergic reaction in its early stages.
ECG should be done in patients with previous cardiac history or ischem ic sym ptom s; consider routinely in the elderly.
Tests Lab The diagnosis of anaphylaxis is m ade on clinical grounds; laboratory tests are usually not useful in aiding diagnosis in the acute setting.
Imaging Hyperinflation can be seen on chest radiograph.
Differential Diagnosis
Pulm onary em bolism
Acute m yocardial infarction
Airway obstruction
Asthm a
Tension pneum othorax
NSAID reaction
Vasovagal collapse
Hereditary angioedem a
Serum sickness
System ic m astocytosis
Pa ge 4 0 9
Pheochrom ocytom a
Carcinoid syndrom e
Treatment Pre Hospital
IV access, O2, cardiac and pulse oxim etry m onitoring
Early intubation is param ount as laryngeal edem a and spasm can progress rapidly.
Laryngeal edem a can be m anaged with racem ic epinephrine prior to intubation.
Subcutaneous epinephrine can be adm inistered en route even prior to establishm ent of an IV.
Initial Stabilization
ABCs
Assure adequate ventilation
Orotracheal intubation is the technique of choice.
Difficult because of laryngeal edem a, spasm , or soft tissue swelling; use advanced airway adjuncts if necessary
Consider blind nasotracheal intubation if soft tissue swelling prohibits an oral approach and there is absence of stridor.
Transtracheal jet insufflation or cricothyrotom y m ay be necessary to control the airway.
Epinephrine IV/SC or endotracheal adm inistration
Direct injection into the venous plexus at the base of the tongue is an option.
Volum e resuscitation with crystalloids or colloids
ED Treatment
Continuous cardiac and vital sign m onitoring until stable
Pa ge 4 1 0
Persistent bronchospasm can be treated with β 2 -agonist bronchodilators.
Hypotension should be treated with volum e repletion.
Vasopressors, MAST garm ents, and Trendelenburg positioning are useful adjuncts.
Antihistam ines (both H 1 and H 2 blockers) have been shown to be helpful in preventing histam ine interactions with target tissues.
Corticosteroids help prevent the progression or recurrence of anaphylaxis.
Glucagon is particularly useful in epinephrine-resistant anaphylaxis from β-adrenergic blocking agents.
P.65
Medication (Drugs) Alert
A patient's concom itant use of a beta-blocker m ay antagonize the effects of epinephrine. For these patients consider glucagon as it increases intracellular cyclic adenosine m onophosphate levels by a m echanism that does not depend upon beta-receptors.
Diphenhydram ine: adults—50 m g IV; (peds: 1–2 m g/kg) slow IVP
Epinephrine: 0.3–0.5 m g; use 1:1,000 dilution for SC route and 1:10,000 for IV route (peds: epinephrine 0.01 m g/kg SC/IV)
Racem ic epinephrine: 2.25% solution (0.5 m L placed in a nebulizer in 2.5 m L of norm al saline)
Pa ge 4 1 1
Glucagon: adults—1–2 m g IV/IM/SQ
Hydrocortisone: adults: 500 m g IV (peds: 4–8 m g/kg/dose IV)
Methylprednisolone: adult—125 m g IV (peds: 1–2 m g/kg IV)
Prednisone: adult—60 m g PO (peds: 1 m g/kg PO)
Ranitidine: adult—50 m g IV or cim etidine 300 m g IV
Follow-Up Disposition Admission Criteria
Intubated patients or patients in respiratory distress should be adm itted to an intensive care unit setting.
A m onitored bed m ay be necessary for the patient who has not had substantial response to initial therapy.
Patients with significant generalized reactions and persistent sym ptom s should be adm itted for observation for 24 hours.
Discharge Criteria
Patients with com plete resolution of sym ptom s m ay be discharged after several hours of ED observation.
Patients with allergic reactions should have a follow-up within 48 hours of discharge to evaluate effectiveness of outpatient therapy.
A follow-up visit with an allergist is also recom m ended.
Patients should be advised to carry som e type of treatm ent that can be self-adm inistered in the event of future reactions such as the prefilled syringe EpiPen.
Patients with a known trigger should be counseled on strict
Pa ge 4 1 2
avoidance of that trigger.
Issues for Referral
Consultation with an allergist/im m unologist is appropriate when desensitization to an antibiotic is being considered for the treatm ent of an infectious process.
When a patient at high risk for contrast reaction needs a contrast study, consultation with the radiologist regarding pretreatm ent and choice of contrast agent is appropriate.
Refer patients who are treated and released from the ED after an episode of anaphylaxis, angioedem a, or urticaria to an allergist for follow-up skin testing and consideration for desensitization.
References 1. Barach EM, et al. Epinephrine for the treatm ent of anaphylactic shock. JAMA. 1984;251:2118. 2. Muellem an RL, Tran TP. Allergy, hypersensitivity and anaphylaxis. In: Marx J, et al. eds. Rosen's Em ergency Medicine. St. Louis, MO: Mosby, 2002;1619–1635. 3. Neugut AI, Ghatak AT, Miller RL. Anaphylaxis in the United States: an investigation into its epidem iology. Arch Intern Med. 2001;161:1521. 4. Thom as M, Crawford I. Glucagon infusion in refractory anaphylactic shock in patients on beta-blockers. Em erg Med J. 2005;22:272–273.
Miscellaneous SEE ALSO: Angioedem a; Urticaria
Codes ICD9-CM
Pa ge 4 1 3
995.0
ICD10 T78.2
Pa ge 4 1 4
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Anem ia
Anemia
Paul Allegretti
Basics Description
Reduction below norm al in the m ass of RBCs: o
Measured by one or m ore of the m ajor RBC com ponents
o
Hgb (hem oglobin): concentration of the m ajor oxygen-carrying com ponent in whole blood
o
Hct (hem atocrit): percent volum e of whole blood occupied by intact RBCs
o
RBC count: RBCs contained in a volum e of whole blood
o
Adult fem ale: Hgb Table o f C o ntents > Angio edem a
Angioedema
Sean-Xavier Neath
Basics Description
Nonpruritic, well-dem arcated, nonpitting edem a of the derm is
Prim arily involves the periorbital and perioral regions
Sim ilar in pathologic basis to urticaria except that affected tissue lies deeper: o
Urticaria affects superficial tissue and causes irritation to m ast cells and nerves in the epiderm is leading to intense itching.
o
Angioedem a occurs in deeper layers, which have fewer m ast cells and nerves, therefore causing less itching.
There are two types of angioedem a: the classic hereditary form and the acquired form s: o
Hereditary angioedem a (HAE) is an autosom al dom inant disorder caused by a deficiency of C1 esterase inhibtor (C1-INH), which leads to the form ation of bradykinin resulting in angioedem a.
o
The acquired form s dem onstrate norm al quantities and function of C1-INH, but it becom es bound to
Pa ge 4 2 7
circulating antibodies that inactivate it. o
Absolute or functional deficiency of C1-INH from either type results in unopposed activity of the first com ponent of the com plem ent cascade, resulting in higher levels of bradykinin, which incites the form ation of angioedem a.
Genetics
The prevalence of hereditary angioedem a is estim ated to range from 1:10,000–1:150,000.
More than 100 m utations of the C1-INH gene have been reported.
Etiology Typical trigger include:
Food additives
Food allergies
Drug allergies
Insect stings
Exposure to heat or cold
Exercise
Traum a
Thyroid disease
Diabetes
Lupus
Infections
Contact allergies
ACE inhibitors
NSAIDs, aspirin
Diagnosis
Pa ge 4 2 8
Signs and Symptoms History
A fam ily history or history of recurrent episodes with the use of particular agents can be useful in the diagnosis.
Abdom inal pain associated with nausea, vom iting, and diarrhea
Attacks of hereditary angioedem a are not associated with hives.
Em otional stress or physical traum a can trigger attacks.
Physical Exam
The lesions of angioedem a are large, swollen and nonpitting wheals.
The eyelids and lips are frequently involved.
Involvem ent of the pharynx and larynx m ay cause airway obstruction.
Essential Workup
The diagnosis is m ade of clinical grounds based on the presentation of large nonpitting, nonpruritic wheals.
A fam ily history need not be present to diagnose the disease.
Tests Lab
CBC with differential, ESR, ANA, rheum atoid factor
Skin biopsy if an urticarial lesion is accessible
Diagnostic Procedures/Surgery Measurem ent of C1-INH levels (not routinely available in EDs):
Patients affected with hereditary angioedem a have very low levels; carriers will have half-norm al levels.
C4 and C2 levels are low during attacks in both hereditary
Pa ge 4 2 9
and acquired form s
Differential Diagnosis
Prim ary angioedem a: o
IgE-m ediated allergic reactions
o
Drug reactions
o
Food allergies
o
Inhalation, ingestion, or contact with allergens
o
Panic attacks, globus hystericus
Secondary angioedem a: o
Physical urticaria such as cold, pressure, solar
o
System ic m astocytosis
o
Fam ilial cold urticaria
o
C3b inactivator deficiency
o
Am yloidosis
o
Exercise-induced anaphylaxis
o
Transfusion reaction
o
Collagen vascular disease
o
ACE-inhibitor reaction
Pediatric Considerations Recurrent angioedem a presenting around puberty should raise suspicion of hereditary angioedem a.
Treatment Pre Hospital
Establish IV access
Early intubation m ay be necessary due to the rapid progression of laryngeal swelling.
Initial Stabilization
Pa ge 4 3 0
Active airway m anagem ent and supportive m easures are the prim ary goals of em ergency treatm ent.
Intubation m ay be necessary in severe cases: o
Orotracheal intubation is the technique of choice but m ay be difficult because of laryngeal edem a, spasm , or soft-tissue swelling.
o
Consider advanced airway adjuncts such as the gum elastic bougie to assist in securing endotracheal tube placem ent;
o
Blind nasotracheal intubation if soft tissue swelling prohibits an oral approach
o
Transtracheal jet insufflation or cricothyrotom y m ay be necessary to control the airway.
Epinephrine, antihistam ines, and steroids in obstructive airway swelling, although patient response can be variable.
ED Treatment
Airway m anagem ent as above
Acute angioedem a with features of a type I hypersensitivity reaction m ay be treated sim ilarly to an allergic reaction with H1 and H2 blocker along with corticosteroids.
Subcutaneous epinephrine should be used in refractory cases where the benefits outweigh the risks.
For abdom inal attacks consider the addition of parenteral pain relief, antiem etics and IV fluid replacem ent.
Tranexam ic acid (Cyklokapron), an antifibrinolytic agent, is useful in both acute and prophylactic treatm ent.
Epsilon am inocaproic acid (Am icar) another antifibrinolytic agent is considered to be of questionable efficacy.
A C1-INH concentrate is useful during acute attacks.
Pa ge 4 3 1
Alert P.69
While C1-INH is standard therapy in Europe, the U.S. FDA has not approved its use in the United States. Som e patients with HAE in the United States m ay carry vials of the m edication obtained abroad.
Therapy with fresh frozen plasm a (FFP) (as a source of nonpurifiied C1-HN) is advised with caution as it m ay paradoxically worsen som e attacks due to its high concentration of com plem ent com ponents.
Attenuated androgens, such as the anabolic steroids and gonadotropin inhibitor danazol, are used in the long-term prophylactic treatm ent. They m ay not have any effect for 24–48 hours in the acute setting.
Angioedem a associated with ACE inhibitors occurs in 0.1–0.2% of cases and requires im m ediate withdrawal of the ACE inhibitor and replacem ent with another antihypertensive m edication. ACE inhibitor-related angioedem a usually occurs within a week after starting ACE inhibitor therapy, but m ay occur at any tim e during the use of the m edication.
Medication (Drugs)
C1-INH: concentrate given in 5% dextrose IV over 10–45 m inutes dose: 10 years old 1000 units; additional infusion and reassessm ent if sym ptom s persist for >2h. This m edication is not currently available in the United States.
Pa ge 4 3 2
Cim etidine: 300 m g IV
Danazol 400–600 m g orally up to 1 gm per day Contraindicated in children and pregnancy.
Diphenhydram ine: adult: 50 m g IV.; peds: 1–2 m g/kg slow IVP
Epinephrine: 0.3–0.5 m g (use 1:1,000 dilution for subcutaneous route, and 1:10,000 for IV route); peds: epinephrine 0.01 m g/kg subcutaneous/IV
Racem ic epinephrine: 2.25% solution (0.5 m L placed in a nebulizer in 2.5 m L of norm al saline)
FFP (if C1-INH is unavailable): adult dosage 2 units
Hydrocortisone: adult: 500 m g IV; peds: hydrocortisone 4–8 m g/kg/dose IV.
Methylprednisolone: adult: 125 m g IV.; peds: 1–2 m g/kg IV
Prednisone: adult: 60 m g PO; peds: 1 m g/kg PO
Ranitidine: adult: 50 m g IV
Stanozolol: 2 m g orally up to 16 m g per day
o
Discontinued in the United States
o
Contraindicated in children and in pregnancy
Tranexam ic acid: (Cyklokapron) 1 gm orally every 3–4 hours for up to 48 hours if necessary
Follow-Up Disposition Admission Criteria
Patients with system ic sym ptom s that do not resolve com pletely will need to be hospitalized for observation.
A m onitored bed is recom m ended for those with airway
Pa ge 4 3 3
involvem ent.
Discharge Criteria Patients without system ic sym ptom s who are stable for discharge should been seen in outpatient followup in a few days.
Issues for Referral Patients should be evaluated by an allergist/im m unologist after the initial presentation, especially if there is a fam ily history of angioedem a, or if the angioedem a is accom panied by abdom inal pain, or triggered by traum a.
References 1. Gom pels M, Lock R, Abinun M, et al. C1 inhibitor deficiency: consensus docum ent. Clin Exp Im m . 2005;139:379–408. 2. Grattan C, Powell S, Hum phreys F. Managem ent and diagnostic guidelines for urticaria and angio-oedem a. Br J Derm atol. 2001;144:708–714. 3. Nadel ES, Brown DF. Angioedem a. J Em erg Med. 1988;16(3):477–479. 4. Nzeako UC, Frigas E, Trem aine WJ. Hereditary angioedem a. Arch Intern Med. 2001;161:2417–2429. 5. Zuraw B. Current and future therapy for hereditary angioedem a. Clin Im m . 2005;114:10–16.
Miscellaneous SEE ALSO: Anaphylaxis; Urticaria
Codes ICD9-CM Angioneurotic edem a/Urticaria 995.1 Hereditary angioedem a 277.6
Pa ge 4 3 4
ICD10 Angioedem a T78.3
Pa ge 4 3 5
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Ankle F racture/Dislo catio n
Ankle
Fracture/Dislocation Binh T. Ly
Basics Description Com m on m echanism s and injury patterns of the ankle
Mechanism of Injury
Inversion injury: o
Avulsion fracture of the lateral m alleolus
o
Oblique fracture of the m edial m alleolus
Eversion injury: o
Avulsion fracture of the m edial m alleolus
o
Oblique fracture of the fibula
External rotation injury: o
Disruption of the tibiofibular syndesm osis, or a fibular fracture above the plafond
o
Anterior or posterior tibial fracture with separation of the distal tibia and fibula (unstable fracture)
Inversion and external rotation (Maisonneuve fracture): o
Medial m alleolus avulsion fracture or deltoid ligam ent tear
o
Disruption of the tibiofibular syndesm osis
Pa ge 4 3 6
o
Oblique fracture of the proxim al fibula
Pediatric Considerations
Ankle fractures in children often involve the physis (growth plate): o
May cause chronic deform ity from growth plate injury
o
In children 4 m m and tibiofibular clear space >6 m m .
Consider radiographs for the following special circum stances: o
Altered sensorium or dim inished distal lim b sensation
o
Multiple painful and distracting injuries
o
Injuries that occurred 10 days prior to evaluation
Tests Imaging
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Unstable ankle fractures or dislocations require postreduction radiographs in all three planes after splinting.
AP and lateral radiographs of the tibia and fibula are indicated if a Maisonneuve fracture is suspected clinically.
Stress-testing the ligam ents in a painful ankle is unnecessary in the ED if the patient will be re-exam ined in 3–7 days.
Stress radiographs of the ankle are usually unnecessary acutely.
CT scan or MRI: o
Assess the degree of injury to the tibial plafond.
o
Intra-articular pathology
o
Ligam entous injuries
o
Pediatric epiphyseal injuries
P.71
Differential Diagnosis
Ankle sprain
Achilles tendon injury
Os trigonum fracture
Fifth m etatarsal fracture (Jones fracture)
Peroneal tendon dislocation or injury
Talar fractures
Talar-dom e fracture
Subtalar dislocations
Calcaneal fractures
Foot fractures
Ankle diastasis
Rattlesnake envenom ation
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Pediatric Considerations
Injury to the growth plates m ay not be apparent on plain radiographs.
Consider im m obilization, non–weight-bearing status, and orthopedic referral if clinical suspicion warrants, even in the setting of negative radiographs.
CT scan or MRI m ay be warranted to delineate the extent of the injury.
Inform parents of the possibility of growth abnorm alities in patients with injury to the physis.
Treatment Pre Hospital
Im m obilize with soft splint to reduce pain, bleeding, and further injury.
Cautions: o
Traction devices are usually unnecessary:
o
Contraindicated with open injuries
Protruding bone should not be reduced; the wound should be covered with a clean dressing.
Initial Stabilization
Avoid weight bearing
Ice
Com pression
Elevation
ED Treatment Ankle Fracture
All ankle fractures or dislocations require orthopedic
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consultation or referral.
Open ankle fractures: o
Rem ove contam inants.
o
Apply m oist sterile dressing.
o
Assess tetanus im m unity.
o
Antibiotics
o
Em ergent orthopedic consultation
Closed ankle fractures: o
Closed reduction, if necessary
o
Im m obilize with a posterior splint.
o
Posterior splint im m obilizes the foot at a 90° angle with the application of bulky dressings and covered by volar (posterior) and coaptation (U-shaped stirrup) splinting m aterial.
Stable injury (injury to only one side of the ankle): o
Isolated injury to the lateral m alleolus without m edial involvem ent is virtually always stable.
o
Apply posterior splint.
Unstable injury (both sides of the ankle are injured): o
Urgent orthopedic consultation
o
Posterior splint as in stable injuries
o
May require open reduction and internal fixation (ORIF) em ergently before significant swelling develops
Neurovascular injury requires em ergent orthopedic consultation.
Ankle Dislocations
Closed reduction should be perform ed as rapidly as possible to m inim ize ischem ia to the skin and reduce the risk of avascular necrosis of the talus.
Skin tenting and evidence of neurovascular com prom ise are indications for im m ediate reduction, even prior to
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radiographs.
Most ankle dislocations require ORIF.
After reduction, place a posterior splint.
Medication (Drugs)
Closed fractures: o
Prim arily analgesics (opioids)
Dislocations or displaced fractures requiring closed reduction: o
Short-acting benzodiazepine (m idazolam 0.05–0.1 m g/kg IV) or barbiturate (m ethohexital 1–1.5 m g/kg IV) with opioid analgesic
Open fractures: o
Cefazolin: 2 g loading dose (peds: 50 m g/kg) IV
o
Gentam icin: 5–7 m g/kg (peds: 2.5 m g/kg) IV
o
Vancom ycin: 1 g loading dose (10 m g/kg in children) if penicillin allergic IV
o
Tetanus toxoid if indicated
Follow-Up Disposition Admission Criteria
Unstable ankle fractures require urgent orthopedic consultation and m ay require adm ission.
Open ankle fractures and dislocations should be adm itted for débridem ent, irrigation, and IV antibiotics.
Ankle dislocations that are treated with either open or closed reduction
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Concern for com partm ent syndrom e or neurovascular injury
Discharge Criteria Sim ple nondisplaced stable ankle fractures without neurovascular com prom ise m ay be discharged following splinting.
References 1. Bachm ann LM, Kolb E, Koller MT, et al. Accuracy of Ottawa ankle rules to exclude fractures of the ankle and m id-foot: system atic review. Br Med J. 2003;326:417. 2. Duchesneau S, Fallat LM. The Maisonneuve fracture. J Foot Ankle Surg. 1995;34(5):422–428. 3. Marsh JL, Saltzm an CL. Ankle fractures. In: Bucholz RW, Heckm an JD, eds. Rockwood and Green's Fractures in Adults. 5th ed. Philadelphia: Lippincott William s & Wilkins; 2001: 201–283. 4. Moehring HD, Tan RT, Marder RA, et al. Ankle dislocation. J Orthop Traum a. 1994;8:167–172. 5. Plint AC, Bulloch B, Osm ond MH, et al. Validation of the Ottawa Ankle Rules in children with ankle injuries. Acad Em erg Med. 1999;6:1005–1009.
Codes ICD9-CM 824.8 837.0
ICD10 S82.8 S92.1 S93.0
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Ankle Sprain
Ankle Sprain
Taylor Young Cardall
Basics Description
Injuries to ligam entous supports of the ankle
Ankle joint is a hinge joint com posed of the tibia, fibula, and talus.
Injuries m ay range from stretching with m icroscopic dam age (grade I) to partial disruption (grade II) to com plete disruption (grade III)
Etiology
Forced inversion or eversion of the ankle
Forceful collisions
85–90% of ankle sprains involve lateral ligam ents: o
Anterior talofibular (ATFL)
o
Posterior talofibular (PTFL)
o
Calcaneofibular (CFL)
o
Usually the result of an inversion injury
o
The ATFL is the m ost com m only injured.
o
If the ankle is injured in a neutral position, the CFL is often injured.
o
The PTFL is rarely injured alone.
Injury to the deltoid ligam ent (connecting the m edial
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m alleolus to the talus and navicular bones) is usually the result of an eversion injury: o
Often associated with avulsion at the m edial m alleolus or talar insertion
o
Rarely found as an isolated injury
o
Suspect associated lateral m alleolus fracture or fracture of the proxim al fibula (Maisonneuve fracture).
Syndesm osis sprains (injury to the tibiofibular ligam ents or the interosseous ligam ent of the leg): o
Occur m ost com m only in collision sports
o
Syndesm osis injuries (“high ankle sprains―) have a higher m orbidity and potential for long-term com plications.
Pediatric Considerations
Children younger than age 10 years with traum atic ankle pain and no radiologic evidence of fracture m ost likely have a Salter-Harris I fracture.
The ligam ents are actually stronger than the open epiphysis.
Diagnosis Signs and Symptoms History
History m ay predict the type of injury found and should include: o
Tim e of injury
o
Mechanism
o
The presence of a “pop― or “crack.―
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o
History of previous traum a
o
Relevant m edical conditions (e.g., bone or joint disease)
o
Treatm ents attem pted prior to arrival
o
Ability to bear weight subsequent to the injury at scene and ED
Physical Exam
Aim ed at detecting joint instability and any associated injuries: o
Note the presence or absence of bony tenderness at posterior edge of m edial and lateral m alleoli as well as at the base of the fifth m etatarsal.
Docum ent neurovascular status distal to the injury.
Assess range of m otion and com pare it with the uninjured side.
Stress testing in the ED is often lim ited by pain and m ay im pair detection of ligam ent injury.
The squeeze test helps identify syndesm osis injuries: o
Squeeze tibia and fibula together at the m idcalf; pain felt in the ankle indicates a positive test.
Essential Workup
The Ottawa Ankle Rules, a selective strategy for obtaining ankle radiographs in adults, suggest that foot or ankle radiographs are unnecessary except when any of the following are present: o
Bony tenderness at the posterior edge of the distal 6 cm or tip of either m alleolus
o
Bony tenderness along the base of the fifth m etatarsal or navicular bone
o
Inability to take four unassisted steps both im m ediately after the injury and in the ED
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The rules have been prospectively validated by the original authors as well as independently by groups in the United States, the United Kingdom , France, and other countries.
Tests Imaging
Ankle injuries should be radiographed if there is concern for fracture.
Stress radiographs are rarely useful in the ED and should not be routinely ordered unless requested by a consultant.
Differential Diagnosis
Ankle fracture (lateral, m edial, or posterior m alleolus) or dislocation
Achilles tendon injury
Maisonneuve fracture
Os trigonum fracture
Fifth m etatarsal fracture (Jones fracture)
Transchondral talar dom e fracture
Peroneal tendon dislocation or injury
P.73
Treatment Pre Hospital Im m obilize ankle as necessary.
Initial Stabilization
Prevent further injury; avoid weight bearing if painful.
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RICE (rest, ice, com pression, elevation)
ED Treatment
The goal of treatm ent is reduction of pain and return to norm al activity without long-term pain or joint laxity.
Existing evidence supports early m obilization and functional treatm ent: o
Unstable ankles (i.e., grade III) or those with severe pain m ay benefit from brief im m obilization followed by early return to functional treatm ent.
Grade I or II sprains can be treated with functional support (elastic bandage, air splint, gel splint, etc.): o
Evidence suggests air or gel splints m ay be superior to elastic bandage dressings.
Grade III sprains can be treated by im m obilization (sugar tong with posterior splint or bulky Jones dressing) and early orthopedic consultation or referral.
Crutches m ay be needed initially for com fort, but encourage weight bearing as tolerated for grades I and II.
Once acute pain and swelling have resolved, strengthening exercises and proprioceptive training (e.g., balance board, sm all circle walking) im prove ankle strength and function and prevent reinjury.
Full sports activities m ay be resum ed only when running and turning are pain free.
Ankle taping, air splints, or gel splints reduce the risk of recurrent injury in high-risk sports such as basketball, volleyball, soccer, and running.
Medication (Drugs)
Nonsteroidal anti-inflam m atory drugs (NSAIDs) are useful
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in treating acute pain: o
Ibuprofen: 800 m g (peds: 5–10 m g/kg) PO t.i.d.
Narcotic analgesics m ay be required for severe pain.
Follow-Up Disposition Admission Criteria An isolated ankle sprain should not require adm ission.
Discharge Criteria
Grades I and II sprains should be instructed to follow up with the prim ary care physician in 1–2 weeks.
Grade III sprains and syndesm osis injuries should be referred to an orthopedic surgeon or sports m edicine specialist within 7–10 days.
Issues for Referral Patient copies of any radiographs obtained m ay facilitate early follow-up.
References 1. Ho K, Abu-Laban RB. Ankle and foot. In: Marx JA, ed. Rosen's Em ergency Medicine: Concepts and Clinical Practice. 5th ed. St. Louis, MO: Mosby; 2002:706–735. 2. Renstrom PA, Konradsen L. Ankle ligam ent injuries. Br J Sports Med. 1997;31:11–20. 3. Stiell IG, McKnight RD, Greenberg GH, et al. Decision rules for use of radiography in acute ankle injuries: refinem ent and prospective validation. JAMA. 1993;269:1127–1132. 4. Wedm ore IS, Charette J. Em ergency departm ent evaluation and treatm ent of ankle and foot injuries. Em erg Med Clin North Am .
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2001;18:85–113.
Codes ICD9-CM 845.00
ICD10 S93.4
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Ankylo sing Spo ndylitis
Ankylosing
Spondylitis Paul L. DeSandre
Basics Description
Inflam m atory disorder, prim arily spinal, with sym m etric sacroiliitis in 100%
Onset 15–40 years of age in 90%
Male to fem ale ratio is 3:1.
Inflam m ation at the bony insertions of ligam ents or tendons (entheses)
May have system ic inflam m atory m anifestations such as uveitis
Spondylitis of ankylosing spondylitis (AS) begins at the insertions of the outer fibers of the annulus fibrosus (enthesitis) of the vertebrae: o
Ossification (syndesm ophyte form ation) m ay lead to com plete fusion, ankylosis, of the vertebrae.
o
Extensive spinal involvem ent causes the radiographic appearance of the so-called bam boo spine.
Alert The fused spine is dangerously brittle: significantly increases the
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risks for fracture and paralysis.
Genetics HLA-B27 antigen in 90–95% of AS patients
Etiology Cytokine inflam m atory process triggered by traum a, infection, or neuroendocrine-im m une abnorm alities in patients genetically predisposed
Diagnosis Signs and Symptoms
Spinal: Low back pain with sacroiliitis is the m ost com m on presentation:
o
Paralysis from m inor spinal traum a or m anipulation
o
Cauda equina syndrom e
Ocular: Acute anterior uveitis is the m ost com m on extraspinal m anifestation and m ay precede onset of arthritis.
Enthesitis (inflam m ation at tendon or ligam ent insertion): Achilles tendonitis or plantar fasciitis is com m on.
Pulm onary: restrictive lung disease owing to progressive reduction in chest expansion and upper lobe fibrosis
Joints: asym m etric arthritis of large joints of lower extrem ities occasionally
Genitourinary (GU): prostatitis occasionally
Cardiac: aortic valve regurgitation and cardiac conduction defects occasionally
History
Low back pain, radiating into gluteal areas bilaterally from sacroiliac region, and progressing to involve entire spinal
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region; exacerbated by rest and im proved with m ild activity or stooping forward
Prior history of enthesitis, uveitis, restrictive pulm onary disease, arthritis to lower extrem ity large joints, prostatitis, or aortic valve disease
Physical Exam
Flattening of the norm al lum bar lordosis
Exaggeration of thoracic kyphosis
Lim itation of spinal flexion
Reduction in chest expansion
Possible aortic valve regurgitation m urm ur
Pediatric Considerations
Juvenile ankylosing spondylitis (JAS) m ay m im ic a septic process with fever and system ic signs.
Onset of JAS is late childhood or adolescence (usually before age 16 years); prim arily boys.
JAS m ay initially present as aortic regurgitation with fulm inant aortitis and m ay have an association with Takayasu arteritis.
JAS has a m uch greater predilection for extraspinal joints and entheses of the lower extrem ities; exam ine for: o
Asym m etrical arthritis of the joints of the lower extrem ities, especially hip
o
Enthesitis of the Achilles tendon attachm ent at the heel, the plantar fascia attachm ents to the sole of the foot, the patellar ligam ent attachm ent to the tibial tuberosity, and the quadriceps tendon attachm ents to the patella
Essential Workup
Exclude fracture or nerve injury in any new spinal pain of a patient suspected of AS.
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Exclude sepsis or septic joint.
Evaluate for sacroiliitis with pelvic rock test (com pression) or Patrick test (sacroiliac distraction).
Tests Lab
CBC m ay show m ild leukocytosis with slight to m oderate anem ia and throm bocytosis.
BUN, creatinine, and electrolytes m ay be useful to assess renal involvem ent.
Erythrocyte sedim entation rate (ESR) or C-reactive protein (CRP) m ay be elevated, but are of lim ited use in the ED.
Imaging
Pelvic radiograph: should be done in any adult patient suspected of undiagnosed ankylosing spondylitis: o
Sacroiliitis is essential to the diagnosis of AS; this is seen initially as subchondral bony erosions on the iliac side of the sacroiliac (SI) joint, which later m anifest as bony proliferation and sclerosis.
Lum bar, thoracic, and cervical spine radiographs to exclude fracture for com plaint of new pain to these areas with or without traum a
CT should be perform ed to further evaluate possible fractures on plain radiographs.
MRI should be perform ed em ergently on any patient with neurologic deficit.
Chest radiograph m ay show patchy inflam m atory infiltrates.
Differential Diagnosis
Mechanical low back pain is generally im proved with rest
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and exacerbated by exercise without signs of system ic inflam m atory process.
Infectious low back pain is m ore constant, unrem itting, and associated with fever.
Neoplastic low back pain is m ore typical in patients older than age 40 years and m ore constant and unrem itting: o
Night pain is a characteristic sym ptom .
Septic arthritis should be excluded by arthrocentesis if clinically suspected in single joint involvem ent.
Psoriatic arthritis usually presents in a patient with known psoriasis and has m uch greater predilection for the hands and feet.
Reiter disease: the classic triad of arthritis, urethritis, and conjunctivitis: sym ptom onset about 1 m onth after an episode of urethritis or enteritis
Arthritis associated with inflam m atory bowel disease occurs in patients with Crohn disease or ulcerative colitis: o
Prim arily involves knee, elbow, ankle, or wrist, and usually exacerbated by flares of the bowel disease
P.75
Treatment Pre Hospital Alert
Increased risk of traum atic spinal injury from even m inor injuries
Spinal im m obilization efforts m ust avoid worsening spinal
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injury.
Intubation difficulty (spinal deform ity)
Ventilation difficulty (chest wall restriction)
Initial Stabilization
Traum a: airway, breathing, circulation (ABCs) while m aintaining im m obilization (including in-line spinal stabilization if intubation required)
Acute traum atic paralysis: m ethylprednisolone IV and im m ediate neurosurgical evaluation
ED Treatment
Control pain and inflam m ation with nonsteroidal anti-inflam m atory drugs (NSAIDs); steroids or opioids m ay be useful in severe refractory cases.
Exclude infection by clinical presentation, laboratory analysis, and possibly arthrocentesis.
Exclude spinal fracture (use CT for equivocal findings on plain radiographs).
Medication (Drugs)
Nonselective NSAIDs: o
Ibuprofen: 35 m g/kg/d divided q.i.d., m ax. 50 m g/kg/d (adult: 300–800 m g PO t.i.d. or q.i.d.)
o
Indom ethacin: 1–2 m g/kg/d divided b.i.d. or q.i.d., m ax. 4 m g/kg/d (adult: 25 m g PO b.i.d. or t.i.d.)
o
Naproxen: 10 m g/kg/d divided b.i.d., m ax. 1,000 m g/d (adult: 250–500 m g PO b.i.d)
o
Note: if NSAIDS are poorly tolerated, ineffective, or contraindicated, consider opioid analgesics, m uscle relaxants, or low-dose steroids.
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Alert
Steroids: o
Methylprednisolone: high-dose protocol for acute paralysis: 30 m g/kg bolus, then 5.4 m g/kg/h for 24 hours total
Follow-Up Disposition Admission Criteria
Acute neurologic im pairm ent
Pain is intractable.
Sepsis or septic joint cannot be excluded.
Discharge Criteria
No serious injuries or neurologic deficit
Pain controlled
Issues for Referral
Additional m edical therapy m ay be useful for chronic treatm ent.
Resting splints for inflam ed joints
Orthoses for enthesitis (such as heel cushion inserts to rest Achilles tendon attachm ent)
References 1. Bracken MB, Shepard MJ, Collins WF, et al. A random ized, controlled trial of m ethylprednisolone or naloxone in the treatm ent of acute spinal-cord injury: result of the second National Acute Spinal Cord Injury Study. New Engl J Med. 1990;322:1405–1411. 2. Dougados M, Behier JM, Jolchine I, et al. Efficacy of celecoxib, a cyclooxygenase 2-specific inibitor, in the treatm ent of ankyolsing
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spondylitis: a six-week controlled study with com parison against placebo and against a conventional nonsteroidal anti-inflam m atory drug. Arthritis Rheum . 2001;44(1):180–185. 3. Dougados M, Dijkm ans B, Khan M, et al. Conventional treatm ents for ankylosing spondylitis. Ann Rheum atol Dis. 2002;61(suppl 3):iii40–50. 4. Fleischm ann R, Iqbal I, Slobodin G. Meloxicam . Expert Opin Pharm acother. 2002;3(10):1501–1512. 5. Karasick D, Schweitzer ME, Abidi NA, et al. Fractures of the vertebrae with spinal cord injuries in patients with ankylosing spondylitis: im aging findings. AJR Am J Roentgenol. 1995;165:1205–1208. 6. Nakstad PH, Server A, Josefsen R. Traum atic cervical injuries in ankylosing spondylitis. Acta Radiol. 2004;45(2):222–226. 7. Papadopoulos MC, Chakraborty A, Waldron G. Exacerbating cervical spine injury by applying a hard collar. Br Med J. 1999;319:171–172. 8. Pepm ueller PH, Moore TL. Juvenile spondyloarthropathies. Curr Opin Rheum atol. 2000;12(4):269–273. 9. Seiper J, Braum J, Rudwaleit M, et al. Ankylosing spondylitis: an overview. Ann Rheum atol Dis. 2002;61(suppl 3):iii8–18.
Codes ICD9-CM 720.0
ICD10 M45
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Anterio r C ruciate Ligam ent Injury
Anterior
Cruciate Ligament Injury Moss Mendelson
Basics Description
The anterior cruciate ligam ent (ACL) inserts anterolaterally to the anterior tibial spine and to the posterior aspect of the lateral fem oral condyle: o
Portions are under tension (i.e., at risk) in both flexion and extension.
The ACL prevents excessive anterior m ovem ent, excessive internal rotation of the tibia on the fem ur, or hyperextension of the knee.
Mechanism of injury is often deceleration with flexion and rotation: o
Hyperextension can also occur.
Etiology
The ACL is the m ost com m only injured ligam ent of the knee: o
Most injuries to the ACL are sports related, especially skiing and football.
o
Noncontact injury is com m on: plant-and-pivot or
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stop-and-jum p m echanism . o
Fem ale athletes are m ore susceptible to ACL injury.
Pediatric Considerations
The ACL is the m ost frequently injured knee ligam ent in children.
Tears of the ACL in children often occur at the insertion site of the ligam ent.
Diagnosis Signs and Symptoms History
Feeling knee “give way.―
Hearing a pop, or feeling a tearing sensation at time of injury
Pain m ost com m on com plaint with ACL rupture
Partial injury m ay not be particularly painful owing to paucity of pain fibers in ACL itself.
Most patients report im m ediate knee dysfunction: o
Som e m ay am bulate despite com plete ACL rupture because of stability from supporting structures.
Physical Exam
Im m ediate effusion (hem arthrosis within 2–3 hours) usually indicates a significant intra-articular injury.
About 70% of acute knee hem arthroses are caused by ACL injury.
Lack of hem arthrosis does not rule out ACL injury: o
Capsular disruption m ay allow extravasation of intra-articular blood.
“Locking― m ay occur because of interposition of torn
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cruciate, or associated torn m enisci, or loose body: o
Pseudolocking m ay be present from pain, effusion, or spasm .
Stress testing–always com pare the injured to the uninjured side: o
Asym m etry is m ore reliable than absolute degree of laxity.
o
Lachm an test is m ost reliable:
Knee flexed 20 degrees, patient supine with thigh supported; tibia is brought forward on the fem ur, one hand holding proxim al tibia, the other stabilizing the fem ur just above the patella.
Pain with no m otion is probable grade 1 injury.
Pain with m otion indicates partial tear or disruption.
o
Firm end point of m otion suggests partial tear.
Pivot shift test: m ore specific for ACL injury but unreliable without anesthesia; use cautiously in acutely injured knee:
Patient supine, knee in full extension
Internal rotation of tibia via a hand on foot is applied sim ultaneously with valgus stress from the other hand.
With knee flexion to 20–30°, the exam iner notices a jerk at the anterolateral corner of the proxim al tibia.
o
Anterior drawer sign: not as sensitive or specific as Lachm an test:
Knee flexed 90°, patient supine, hip flexed 45°, foot neutral and stabilized
Anterior m otion is positive.
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Pediatric Considerations
Children and adolescents show m ore laxity on exam than adults.
Ottawa knee rules do not apply to children.
Essential Workup
Neurovascular evaluation
Exclusion of fractures/dislocations
Valgus/varus stress at 20° flexion
Extensor m echanism function
Lachm an test (as described above) is m ost im portant and sensitive test for ACL injury.
Look for signs of associated ligam ent or m eniscus injury: o
Present in about half of patients with ACL injury
Tests Lab
If cause of knee effusion is uncertain, synovial aspirate can be sent for cell count, Gram stain, and culture and crystals: o
Fat globules in aspirate suggest fracture.
Arthrocentesis usually not indicated except to relieve sym ptom s from tense effusion
Imaging
Plain film s have low rate of positive findings: Clinical decision rules lim it num ber of negative plain film s obtained.
Ottawa knee rules (apply to adults): plain film s required for patients with any of five findings: o
Age 55 or older
o
Isolated tenderness of patella
o
Tenderness at head of fibula
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o
Inability to flex 90°
o
Inability to bear weight both im m ediately and in ED (four steps)
Lateral capsular sign is lateral tibial plateau avulsion fracture, just below joint line: o
Diagnostic for ACL rupture, but present in Table o f C o ntents > Antidepressant Po iso ning
Antidepressant
Poisoning Gerald Maloney Jr.
Basics Description
Newer antidepressants, including the atypical antidepressants and selective serotonin reuptake inhibitors (SSRIs), and atypical antipsychotics
Most widely prescribed m edications in the United States
Tricyclic antidepressants (TCAs) covered in separate chapter
Etiology Mechanism
Selective serotonin reuptake inhibitors: o
Inhibit the reuptake of serotonin at the 5HT1A receptor
o
Older agents include fluoxetine (Prozac).
o
Newer agents include citalopram (Celexa) and escitalopram (Lexapro).
Atypical antidepressants: o
Activity on m ultiple receptor sites, including
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serotonin dopam ine and norepinephrine reuptake
Atypical antipsychotics: o
Multiple receptor sites involved; serotonin, norepinephrine, anticholinergic and antihistam inic effects
o
Multiple drug–drug interactions
Cardiotoxicity in these agents is owing to sodium and potassium channel blockade, sim ilar to TCAs but less frequent.
Diagnosis Signs and Symptoms SSRIs
Traditional SSRIs (fluoxetine, paroxetine): o
Seizures
o
Serotonin syndrom e
o
Rarely, QTc prolongation
o
Sedation
Citalopram : o
Seizures
o
Sedation
o
QTc prolongation
o
Active m etabolite is cardiotoxic:
Exhibits delayed cardiotoxicity (up to 12 hours postingestion)
Escitalopram : o
QTc and QRS prolongation
o
Sedation
Atypical Antidepressants
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Venlafaxine: o
Seizures
o
QTc prolongation
Bupropion: o
Sedation
o
Seizures
o
QRS/QTc prolongation
Trazodone: o
Sedation
o
QTc prolongation
o
Hypotension
o
Priapism
Mirtazapine: o
Sedation
o
QTc prolongation
o
Agranulocytosis (usually with chronic dosing)
Atypical Antipsychotics
All have activity at dopam ine receptors.
Fewer extrapyram idal sym ptom s (EPS) and tardive dyskinesias
Clozapine: o
Sedation
o
Agranulocytosis (in up to 1% taking chronically)
o
Anticholinergic toxidrom e
Olanzapine: o
Fluctuating level of consciousness (LOC) with m iosis
o
Pancreatitis
o
Diabetic ketoacidosis (DKA)
o
Only atypical clearly associated with neurologic m alignant syndrom e (NMS)
Quetiapine: o
QTc prolongation
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o
Sedation up to com a
Risperidone: o
Sedation
o
QTc prolongation (rare)
o
Mild anticholinergic toxidrom e
Ziprasidone: o
Sedation
o
QRS/QTc prolongation
Aripiprazole: o
Lim ited data; m ay see sedation
Essential Workup
Determ ine agents ingested, dose, and tim e of ingestion: o
Investigate for coingested drugs.
Rapid bedside glucose (Accu-Chek) if altered m ental status
Tests Lab
Specific drug levels rarely available and usually do not guide clinical m anagem ent
ECG: o
For evaluation of QTc and QRS width
Urine pregnancy: o
In fem ales of childbearing age
Electrolytes, BUN, creatinine, glucose
Serum osm olality: o
Cannot rely on serum osm olality to rule out ingestion of other agents such as toxic alcohols
Routine toxicology screening: o
Rarely alters clinical m anagem ent
Salicylate and acetam inophen levels
Serum EtOH: o
To exclude ethanol intoxication as a cause of altered
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m ental status o
Required if osm oles are m easured
Arterial/venous blood gases (ABG/VBG) o
Check pH.
Imaging
CT of brain for altered m entation
Chest radiograph
Differential Diagnosis
Tricyclic antidepressant overdose
Ethanol overdose
Isoniazid overdose
Hypoglycem ia
Hypoxem ia
Hyponatrem ia
Hypocalcem ia
Withdrawal syndrom es
Serotonin syndrom e
Head traum a
Opioid intoxication
Sedative-hypnotic intoxication
DKA
P.81
Treatment Pre Hospital
In cases of suspected overdose, bring all m edication bottles to hospital with patient.
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Airway, breathing, and circulation m anagem ent (ABCs)
O.9% norm al saline (NS) IV fluids for blood pressure stabilization
Benzodiazepines for seizures
In cases of wide-com plex tachycardia, adm inister sodium bicarbonate IV fluid bolus to standard advanced cardiac life support (ACLS) m easures.
Initial Stabilization
ABCs: o
Adm inister oxygen.
o
Place on cardiac m onitor and m easure pulse oxim etry.
o
Establish IV access with 0.9% norm al saline.
o
Intubation as dictated for airway protection or respiratory status
Rapid bedside glucose determ ination
Naloxone, thiam ine, and D 5 0 W as indicated for altered m ental status: o
Flum azenil is not recom m ended for m ixed-overdose patients, patients with underlying seizure disorder, or patients chronically on benzodiazepines.
ED Treatment
Patient decontam ination: o
Do not attem pt decontam ination in a patient who does not have a stable airway.
o
Intubation solely for decontam ination purposes, however, is not generally indicated.
o
Activated charcoal in a dose of 50–75 g PO or via nasogastric tube (NGT) if the patient is intubated m ay be beneficial in early presenting overdoses.
o
Gastric lavage is not generally indicated for patients
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with an isolated overdose of the agents listed in this chapter.
For QRS widening, adm inister sodium bicarbonate IV bolus.
Treat hypotension unresponsive to IV fluids with norepinephrine rather than dopam ine owing to alpha-1 receptor antagonism .
Treat seizures with: o
Initial therapy: benzodiazepines
o
For refractory seizures: phenobarbital and pyridoxine
Treat sym ptom s of serotonin syndrom e (fever, AMS, tachycardia, rigidity, hyperreflexia) with benzodiazepines, cooling, cyproheptadine.
Medication (Drugs)
Activated charcoal: 50–75 g PO initial dose
D 5 0 W: 25 g (peds: 0.5 g/kg D 5 0 W if 50 kg) IV for hypoglycem ia
Diazepam : 5–10 m g IV bolus (peds: 0.1 m g/kg IV bolus or 0.5 m g/kg rectal)
Lorazepam : 2–4 m g (peds: 0.1 m g/kg) IV bolus
Naloxone: 0.4–2 m g (peds: 0.1 m g/kg) initial bolus; m ay repeat up to a total of 10 m g
Norepinephrine: 0.5–2 µg/kg IV infusion
Phenobarbital: 15–20 m g/kg IV m ax. dose is 2 gm ; caution: see respiratory depression with IV loading doses
Pyridoxine: 5 g (peds: 50–100 m g) initial IV bolus unless known am ount of isoniazid is given, in which case pyridoxine is gram :gram of INH
Sodium bicarbonate: 1 m Eq/kg IV bolus (adult 8.4%; peds: 12 hours postingestion m ay be m edically cleared for psychiatric adm ission
Discharge only asym ptom atic patients >12 hours postingestion who are not suicidal.
References 1. Balit CR, Isbister GK, Hackett LP, et al. Quetiapine poisoning: a case series. Ann Em erg Med. 2003;42(6):751–758. 2. Cuenca PJ, Holt KR, Hoefle JD. Seizure secondary to citalopram overdose. J Em erg Med. 2004;26(2):177–181. 3. Dart RC, et al. Medical Toxicology. 3rd ed. 2003. 4. Isbister GK, Bowe SJ, Dawson A, et al. Relative toxicity of selective serotonin reuptake inhibitors (SSRIs) in overdose. J Toxicol Clin Toxicol. 2004;42(3):277–285. 5. Sarko J. Antidepressants, old and new. A review of their adverse effects and toxicity in overdose. Em erg Med Clin North Am . 2000;18(4):637–654. Review.
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Miscellaneous SEE ALSO: Tricyclic Antidepressant Poisoning
Codes ICD9-CM 969.3 Poisoning by other antipsychotics, neuroleptics, and m ajor tranquilizers
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Ao rtic Dissectio n, Tho racic
Aortic
Dissection, Thoracic Jeffrey I. Schneider Jonathan S. Olshaker
Basics Description
Aortic dissection begins when a jet of blood induces an intim al tear.
Blood then dissects through the m edia under aortic systolic pressure.
It is thought that hypertension is a m ajor factor in the dissection process.
Dissections can start proxim ally at the root and dissect distally to involve any or all branches of the aorta, such as the carotid and subclavian arteries.
The dissection process can also proceed proxim ally to involve the aortic root, the coronary ostia, and the pericardium .
Dissection that progresses proxim ally m ay lead to occlusion of the coronary ostia, aortic valve incom petence, or cardiac tam ponade.
Classification related to portion of aorta involved:
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o
o
Stanford classification:
Type A: ascending aorta
Type B: distal to ascending aorta
DeBakey classification:
DeBakey I: intim al tear in aortic arch or root
DeBakey II: ascending aorta
DeBakey III: distal to takeoff of left subclavian artery
Etiology
Any process that affects the m echanical properties of the aortic wall can lead to dissection: o
Hypertension
o
Congenital heart disease (bicuspid aortic valve, coarctation)
o
Aortic wall connective tissue abnorm alities (cystic m edial necrosis)
o
Connective tissue disease (Marfan disease, Ehlers-Danlos syndrom e)
o
Pregnancy
o
Infectious/inflam m atory conditions of the aorta (lupus, syphilis, endocarditis, giant cell arteritis)
o
Tobacco use
Diagnosis Signs and Symptoms History
Chest pain: o
May be absent in as m any as 15% of patients
o
Substernal if type A dissection
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o
Intrascapular is descending thoracic dissection
o
Lum bar if abdom inal aorta involved
o
Starts abruptly
o
Usually described as sharp
o
Most severe at onset
Back pain: o
Com m only interscapular or lum bar
Com bination of chest, back, and abdom inal pain
Neurologic com plaints: o
Visual changes
o
Stroke sym ptom s
Nausea, vom iting
Peak age for occurrence: o
Proxim al dissection: 50–55 years
o
Distal dissection: 60–70 years
Pregnancy Considerations
Risk of dissection increases in presence of pregnancy: o
In wom an less than 40 years of age, 50% of dissections occur during pregnancy.
Physical Exam
Hypertension: o
35–40% m ay be norm otensive
Pulse deficits: o
Discrepancies in blood pressure (BP) between lim bs
o
Usually in upper extrem ities
Neurologic/spinal cord deficits
Murm ur of aortic regurgitation: o
Occurs in up to 31% of patients
o
Musical, vibrating quality with variable intensity
Essential Workup ECG:
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Useful in ruling in or out ST-elevation m yocardial infarction or ischem ia
Dissection m ay involve coronary ostia and cause m yocardial infarction.
Inferior m yocardial infarction (right coronary artery lesion) is m ore com m on than left coronary artery territory.
Useful for evaluating the presence of left ventricular hypertrophy
A norm al ECG in the presence of severe, acute-onset chest/back pain should heighten one's suspicion of an aortic dissection.
Tests Lab
Leukocytosis
Hem aturia
Elevated blood urea nitrogen and creatinine
Elevated am ylase secondary to bowel ischem ia
Elevated cardiac enzym es due to m yocardial ischem ia
Imaging
Chest radiograph: o
Useful in excluding other etiologies such as pneum othorax and pneum onia
o
In dissection, there m ay be a widened m ediastinum or abnorm al aortic contour.
o
An enlarged heart secondary to pericardial fluid (blood) m ay be present.
o
May be com pletely norm al in as m any as 12%–18% of cases
Echocardiogram —transthoracic or transesophageal: o
Transthoracic:
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Not very helpful in the diagnosis of aortic dissection
May be used to evaluate for com plications of a known dissection, such as tam ponade, valvular incom petence, or m yocardial infarction (from ostial occlusion)
P.83
o
Transesophageal:
May be perform ed in the ED
Patients m ay require intubation.
Provides inform ation regarding extent of dissection and com plications
CT: o
Very useful in defining extent of dissection
o
May also be used in diagnosing clinical entities such as pulm onary em bolism
o
Has a high sensitivity for the diagnosis of aortic dissection and is the diagnostic m odality of choice in m any centers
MRI: o
Highly sensitive and specific
o
Requires patient transport out of ED for extended period of tim e
o
Lack of im m ediate availability m ay be a problem
o
Study of choice in those with renal insufficiency or dye allergy
Aortography: o
High sensitivity and specificity
o
Useful for preoperative planning
o
Difficult to obtain in m any centers
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Cardiac catheterization: o
Due of overlap of sym ptom atology with cardiac ischem ia, som e patients m ay have diagnosis m ade by cardiac catheterization when an intim al flap is visualized.
Differential Diagnosis
Myocardial infarction/ischem ia
Unstable angina
Pneum othorax
Esophageal rupture
Pulm onary em bolism
Pericarditis
Pneum onia
Musculoskeletal pain
Treatment Pre Hospital
Monitor
IV access
Initial Stabilization
Two large-bore IV lines
Continuous cardiac m onitoring
Pulse oxim etry
Oxygen
Type and cross
ED Treatment
BP reduction to reduce shearing forces on aortic wall and slow down the dissection process
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Medications: IV beta-blockade and nitroprusside o
Medications are used to control hypertension and cardiac contractility and decrease shearing forces.
o
Esm olol (IV) or labetalol (IV):
Contraindications: bradycardia, chronic obstructive pulm onary disease, hypotension
o
Nitroprusside (com m only used in conjunction with IV beta-blocker)
o
Caution when using the above together: To prevent an initial increase in shear forces, beta-blocker therapy should be started prior to the addition of nitroprusside therapy
Em ergent surgery: o
Treatm ent of choice for type A dissection
o
Treatm ent for type B dissections in those who have failed m edical therapy
Medical m anagem ent: o
Treatm ent of choice for stable type B dissections
Alert Sym ptom s of aortic dissection m ay be sim ilar to those of cardiac ischem ia/infarction and pulm onary em bolus. Treatm ent with throm bolytics and anticoagulants m ay be harm ful and potentially fatal if aortic dissection is present.
Medication (Drugs)
Esm olol: 500 µg/kg bolus IV, then 25–50 m g/kg/m in drip
Labetalol: 10–20 µg IV every 10–15 m inutes, then 2–4 m g/h drip
Nitroprusside: 0.5 µk/kg/m in IV and titrate upwards to
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desired effect
Follow-Up Disposition Admission Criteria
All patients with aortic dissection should be adm itted to the intensive care unit.
Em ergency cardiothoracic surgery consultation should be obtained, especially in cases of type A dissection.
References 1. Erbel R, et al. Diagnosis and m anagem ent of aortic dissection. Eur Heart J. 2001;22(18):1642–1681. 2. Hagan PG, et al. The international registry of acute aortic dissection: New insights into an old disease. JAMA. 2000;283(7):897–903. 3. Khan IA, Nair CK. Clinical, diagnostic, and m anagem ent perspectives of aortic dissection. Chest. 2002;122(1):311–328. 4. Moore AG, et al. Choice of com puted tom ography, transesophageal echocardiography, m agnetic resonance im aging, and aortography in acute aortic dissection: International registry of acute aortic dissection. Am J Cardiol. 2002;89:1235–1238. 5. Rogers RL, McCorm ack R. Aortic disasters. Em erg Med Clin N Am . 2004;(22):887–908.
Codes ICD9-CM 441.00
ICD10
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171.0
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Ao rtic Rupture, Traum atic (TAI)
Aortic
Rupture, Traumatic (TAI) Kevin J. L. Martens Elizabeth L. Lynch
Basics Description
Most patients with significant traum a to the aorta die im m ediately.
Patients surviving to the ED usually have a contained rupture (pseudoaneurysm ).
Several theories exist: o
Shear forces arise from unequal rates of deceleration of the relatively fixed descending aorta and the m ore m obile arch.
o
“Bending― stress is created by lateral im pact.
o
Twisting of the arch occurs, forcing it superiorly and thus causing it to stretch.
o
Osseous pinch (bony com pression of the thoracic cage) tears m ajor vessels.
o
Water-ham m er pulse wave causes sudden increase in intralum inal pressure.
Most com m on location for rupture (56–95%) is the
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isthm us at the ligam entum arteriosum .
Brachiocephalic vessels m ay also be injured.
Innom inate artery is the m ost com m only injured branch of the aorta.
Most tears are transverse, not longitudinal.
Tears m ay be partially or com pletely circum ferential.
Alert
Rare in patients younger than 15 years; m ay be protected by a m ore com pliant chest wall
Etiology
Most com m only results from m otor vehicle collisions
Other m echanism s: auto versus pedestrian, airplane crashes, falls from heights >10 ft, crush and blast injuries, direct blow to chest
Cause of death in up to 20% of lethal m otor vehicle collisions
Approxim ately 85% of patients with traum atic aortic rupture (TAI) die before reaching the hospital
Of patients with TAI who survive the initial event, 71–84% survive with prom pt diagnosis and treatm ent, 49% die within 24 hours, and 90% die at 4 m onths without treatm ent.
Drivers are 50% m ore likely to sustain TAI than passengers.
Ejection from vehicle doubles the risk.
Diagnosis Signs and Symptoms
Substernal chest pain
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Anterior chest wall contusion
Midscapular pain
Shortness of breath, dyspnea, dysphagia, stridor, hoarseness (owing to expanding hem atom a)
Harsh precordial or m idscapular systolic m urm ur
Acute coarctation syndrom e:
o
Hypertension of upper extrem ity
o
Increased pulse am plitude of upper extrem ities
o
Decreased pulse am plitude in lower extrem ities
o
Cyanosis of lower extrem ities
Paraplegia, anuria, or ischem ic extrem ity pain caused by im paired spinal blood supply
Swelling of neck (extravasation of blood)
Back pain with signs of an acute abdom en
Essential Workup Plain chest radiograph is the prim ary screening tool; high sensitivity and >90% negative predictive value, but low specificity
Tests Lab
Com plete blood count
Electrolytes
Prothrom bin tim e/partial throm boplastin tim e
Type and cross-m atch (6–8 units PRBC)
Imaging
Plain chest radiograph: o
Findings consistent with m ediastinal hem orrhage, hem atom a, or associated injuries:
Widened m ediastinum (>8 cm anteroposterior supine at level of aortic arch, >6 cm posteroanterior upright, or >0.25
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m ediastinum -width to chest-width ratio)
Obliteration of aortic knob
Obscured descending aorta
Opacification of aortopulm onary window
Left apical capping
Deviation of trachea to right
Depression of left m ainstem bronchus
Displacem ent of nasogastric tube to right
Widened paraspinal stripe without spinal fracture
Left hem othorax, pleural effusion, pneum om ediastinum
o
Fracture of sternum or first or second ribs
o
Norm al m ediastinum in up to 12%
o
In pediatric patients: The m ost com m on findings are a left apical cap, pulm onary contusion, aortic obscuration, and m ediastinal widening.
Aortography: still considered diagnostic standard: o
Shows location and extent of injury
o
Also diagnoses nonaortic great vessel injuries
o
Can produce false-negative result with throm bosis of a false lum en
Conventional CT: o
May be considered in hem odynam ically stable patients with low suspicion, but whose chest film findings suggest dam age
o
Angiography indicated with m ediastinal hem atom a
Helical CT-angiography: o
Preferred initial study in stable patients
o
High negative predictive value, but m ay have false-positives
o
Artifact and slice thickness m ay cause a sm all tear to
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be m issed. o
Aortography often needed to confirm findings or for equivocal studies
Transesophageal echocardiography: o
Can be done rapidly in the em ergency departm ent
o
Shows isthm us well
o
May not visualize distal ascending aorta or arch well
o
Patients with cervical fractures, m axillofacial, or esophageal injuries are not candidates.
o
Can detect other cardiac injuries (cardiac contusion, pericardial effusion, etc.)
MRI: o
High accuracy, but m any lim itations
o
Lim ited availability, lengthy study tim e
o
Difficulty m onitoring patients
o
Traum a patients often have support devices that cannot enter the m agnetic field.
o
Not widely used in the diagnosis of traum atic aortic injury
Note: Patients at high risk for traum atic aortic injury by clinical suspicion should undergo aortography even if results of other studies are negative.
Pediatric Considerations Presence of large thym us m ay m ake diagnosis of widened m ediastinum difficult.
Differential Diagnosis
Mediastinal hem atom a owing to other causes
Mediastinal lym phadenopathy
Redundant aorta resulting from hypertension
Ductus diverticulum (norm al variant—bulge at isthm us)
P.85
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Treatment Pre Hospital
Im portant inform ation needs to be gathered from the accident scene:
o
Rate of speed
o
Direction of im pact
o
Dam age to steering wheel
o
Ejection from vehicle
o
Use of safety restraints
o
Driver or passenger affected
Im m ediate transport of any patient with suspected TAI to a level 1 traum a center
Initial Stabilization
Follow traum a care protocols.
Avoid m aneuvers that m ay result in Valsalvalike response (gagging, straining).
ED Treatment
Im m ediate consultation with traum a and chest surgeons is m andatory.
Medical therapy of hypertensive patient should be initiated to lower risk of rupture of pseudoaneurysm : o
Negative inotropes (beta-blockers, such as esm olol or labetalol) to target heart rate 60 ±5 beats per m inute (bpm ); systolic blood pressure, 100–120 m m Hg; m ean arterial blood pressure of 70–80 m m Hg
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o
In patients in whom beta-blockade is contraindicated (sinus bradycardia, second- or third-degree atrioventricular block, congestive heart failure, bronchospasm ), calcium channel blockers m ay be used.
o
Add vasodilators (nitroprusside sodium ) as needed after negative inotropes.
o
For significant hypotension, rapid volum e expansion, including blood, should be given.
o
For refractory hypotension requiring vasopressors, norepinephrine, or phenylephrine are preferred, with dopam ine used to im prove renal perfusion
Central venous catheter
Arterial pressure-m onitoring catheter
Acute coarctation syndrom e is a relative contraindication to antihypertensive therapy.
Peritoneal injuries take precedence.
Concom itant workup of other injuries
TEE m ay be perform ed in OR while correcting abdom inal injuries.
Medication (Drugs)
Diltiazem : 20 m g (0.25 m g/kg) IV over 2 m inutes; second bolus 25 m g (0.35 m g/kg) in 15 m inutes if needed; infusion 5–15 m g/h
Esm olol: 500–1,000 µg/kg (peds: 100–500 µg/kg over 1 m inute) IV load; infusion 50–150 (peds: 25–100 µg/kg/m in; repeat load, increase drip 50) (peds: 25 µg/kg/m in every 5 m inutes; m ax. 300) (peds: 200 µg/kg/m in)
Labetalol: 20 m g IV over 2 m inutes, followed by additional
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doses of 40–80 m g (peds: 0.2–10 m g/kg per dose, m ax. 20 m g per dose) IV every 10–15 m inutes, to 300 m g total; start infusion at 2 m g/m in and titrate up to 10 m g/m in (peds: infusion 0.4–1 m g/kg/h, m ax. 3 m g/kg/h)
Nitroprusside: start at 0.3 µg/kg/m in; m ax. 10 µg/kg/m in
Norepinephrine: 8–12 µg/m in intravenously (peds: start 0.05–0.1 µg/kg/m in, m ax. 2 µg/kg/m in)
Phenylephrine: 50-µg (peds: 5–20-µg/kg per dose) boluses tension every 10–15 m inutes as needed; infusion 100–180 µg/m in IV (peds: 0.1–0.5 µg/kg/m in)
Follow-Up Disposition Admission Criteria All patients with aortic injuries m ust be adm itted to the ICU if not taken directly to the OR.
References 1. Britt LD, Weireter LJ, Cole FJ. Newer diagnostic m odalities for vascular injuries: the way we were, the way we are. Surg Clin North Am . 2001;81:1263–1279. 2. Feliciano DV. Traum a to the aorta and m ajor vessels. Chest Surg Clin North Am . 1997;7:305–323. 3. Gavant ML. Helical CT grading of traum atic aortic injuries. Im pact on clinical guidelines for m edical and surgical m anagem ent. Radiol Clin North Am . 1999;37:553–574. 4. Greenberg MD, Rosen CL. Evaluation of the patient with blunt chest traum a: an evidence based approach. Em erg Med Clin North
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Am . 1999;17:41–62. 5. Lowe LH, Bulas DI, Eichelberger MD, et al. Traum atic aortic injury in children: radiologic evaluation. AJR Am J Roentgenol. 1998;170:39–42. 6. O'Connor CE. Diagnosing traum atic rupture of the thoracic aorta in the em ergency departm ent. Em erg Med J. 2004;21:414–419. 7. Prêtre R, Chilcott M. Blunt traum a to the heart and great vessels. New Engl J Med. 1997;336:626–632.
Codes ICD9-CM 901.0 Injury to thoracic aorta 902.0 Injury to abdom inal aorta
ICD10 S25.0 S35.0
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Aphtho us Ulcers
Aphthous Ulcers
Matthew R. Berkman
Basics Description Ovoid or round ulcerations on the m ucous m em branes of the m outh or genitals
Etiology
Single etiology: unknown
Etiology likely m ultifactorial with som e correlation with: o
Im m unologic dysfunction; activation of cell-m ediated im m unes system
o
Infection
o
Food hypersensitivities
o
Vitam in deficiency
o
Pregnancy
o
Menstruation
o
Psychologic and genetic factors
Risk factors: traum a, stress, vitam in deficiency, im m unodeficiency
Epidem iology: usually occurs in children and young adults (10–30 years old), about 20% of general population
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Diagnosis Signs and Symptoms
Minor aphthous ulcers: o
70–90% of all aphthae
o
Sm aller than 10 m m in diam eter; up to five appear at a tim e
o
Painful, shallow ulcers
o
Necrotic centers
o
Raised m argins and erythem atous halos
o
Gray-white pseudom em brane
o
Found on nonkeratinized m ucosa of anterior oral cavity
o
Labial m ucosa, m axillary and m andibular sulci, nonattached gingiva
o
Floor of m outh
o
Ventral surface of tongue
o
Last for 10–14 days; do not scar
o
Fever rarely associated
Major aphthous ulcers or Sutton disease: o
10–15% of all aphthae
o
Sim ilar in appearance and pain to m inor
o
Larger than 10 m m in diam eter; 1–10 ulcers at a tim e
o
Deeper than m inor form
o
Involve all areas of oropharynx including pharynx, soft palate, tonsillar fauces
o
Last for weeks to m onths, heal with scarring
o
Often underlying disease
o
Fever is rarely associated
Herpetiform aphthous ulcers:
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o
7–10% of all aphthae
o
Multiple sm all clusters
o
Between 1 and 3 m m in diam eter, 10–100 at any tim e, m ay coalesce into plaques
o
Herpetiform in nature, but herpes sim plex virus cannot be cultured from lesions.
o
Last for 7–30 days; scarring could occur.
Tests History
Prodrom e of burning or pricking sensation of oral m ucosa 1–2 days prior to appearance of ulcers
Inquire about fam ily history of system ic lupus erythem atosus (SLE), inflam m atory bowl disease (IBD), Behçet disease.
Inquire about patient m edical history of SLE, HIV, BID, IBD, Behçet disease or CA
Physical Exam
See Signs and Sym ptom s
Look for signs of dehydration: o
Vital signs should be within norm al lim its.
Evaluate for signs of secondary infection.
Essential Workup
Diagnosis is m ade by history and clinical presentation.
Rule out oral m anifestation of system ic disease.
Focus on sym ptom s of eye, m outh, genitalia, skin, gastrointestinal (GI) tract, allergy and diet history.
Tests Lab
Needed only when other etiologies causing ulcers are suspected
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Com plete blood chem istry series
Rapid plasm a reagin test
Fluorescent treponem al antibody-absorption test
Antinuclear antibody test
Tzanck stain: o
Biopsy: o
Inclusion giant cells (herpes virus)
Multinucleated giant cells (Cytom egalovirus)
Fungal cultures: o
Cryptosporidium
Differential Diagnosis
Traum a: o
Biting
o
Dentures
Drug exposure: o
NSAIDs
o
Nicorandil
Infection: o
o
Herpesvirus:
Vesicular lesions
Ulcers on attached m ucosa
Cytom egalovirus:
o
Varicellovirus:
o
o
Characteristic skin lesions
Coxsackievirus:
Ulcers preceded by vesicles
Hand, foot, buttock lesions
Syphilis:
o
Im m unocom prom ised patient
Other skin or genital lesions
Erythem a m ultiform e:
Lip crusting
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Lesions on attached and unattached m ucosa skin lesions
o
Cryptosporidium infection, m ucorm ycosis, histoplasm osis
o
Necrotizing gingivitis
Underlying disease: o
o
o
o
o
Behçet syndrom e:
Genital ulceration
Uveitis
Retinitis
Reiter syndrom e:
Uveitis
Urethritis
HLA-B27-associated arthritis
Sweet syndrom e:
Fever
Erythem atous skin plaques/nodules
In conjunction with m alignancy
IBD:
Bloody or m ucous diarrhea
GI ulcerations
Lupus erythem atosus:
o
Malar rash
Bullous pem phigoid/pem phigoid vulgaris:
Vesiculobullous lesions on attached and unattached m ucosa
o
Cyclic neutropenia:
o
Diffuse skin involvem ent
Periodic fever
Squam ous cell carcinom a:
Chronicity
Head/neck adenopathy
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Im m unocom prom ised patient: o
HIV
o
Agranulocytosis
P.87
Treatment ED Treatment General Measures Sym ptom atic pain relief with analgesics; can use the following for initial pain relief:
Viscous lidocaine 2%: Apply–ulcer as needed q.i.d.
Sucralfate: 10 m L, swish and swallow or swish and spit q.i.d.
Magnesium hydroxide/diphenhydram ine hydrochloride: 5 m g/5 m L in 1/1 m ix swish and swallow q.i.d.
Dyclonine HCL: 1% solution, 5 m L rinse q.i.d.
5-am inosalicylic acid 5% cream : three tim es a day for 2 weeks
Topical over-the-counter preparations (Orabase, Anbesol)
Medication (Drugs)
Analgesia: o
5-am inosalicylic acid 5% cream : three tim es a day for 2 weeks
o
Dyclonine HCL 1% solution: 5 m L rinse q.i.d.
o
Magnesium hydroxide/diphenhydram ine
Pa ge 5 0 8
hydrochloride: 5 m g/5 m L in 1/1 m ix swish and swallow q.i.d. o
Sucralfate: 10 m L, swish and swallow or swish and spit q.i.d.
o
Viscous lidocaine 2%: Apply to ulcer as needed q.i.d.
Prom ote ulcer healing/prevent recurrence (first-line agents): o
Am lexanox 5% paste: 0.5 cm applied to ulcer q.i.d. after m eals
o
Clobetasol 0.05%: 0.5 cm applied to ulcer per day two tim es a day
o
Fluocinonide 0.05% gel: 0.5 cm applied to ulcer up to five tim es a day
o
Triam cinolone 0.1% in Orabase: Apply to ulcer two to four tim es a day until healed.
Second-line agents: o
Prednisone tablets: 40 m g PO per day × 7 days
o
Thalidom ide: 200 m g PO per day × 4 weeks
Follow-Up Disposition Admission Criteria
Unable to eat or drink after appropriate analgesia
Abnorm al vital signs or evidence of dehydration
Discharge Criteria
Tolerating fluids
Adequate analgesia
Norm al vital signs
Issues for Referral
Pa ge 5 0 9
Follow up with prim ary care physician if lesions have not resolved within 2 weeks.
References 1. McBride DR. Managem ent of aphthous ulcers. Am Fam Physician. 2000;62:149–154. 2. Porter S, Scully C: Aphthous ulcers (recurrent). Clin Evid. 2004;12:360–361. 3. Scully C, Gorsky M, Lozada-Nur F. The diagnosis and m anagem ent of recurrent aphthous stom atitis-a consensus approach. Journal of Am erican Dental Association. 2003;134:200–207. 4. Shashy RG, Ridley MB. Aphthous ulcers: a difficult clinical entity. Am J Otolaryngol. 2000;21:389–393. 5. Ship JA, Chavez EM, Doerr PA, et al. Recurrent aphthous stom atitis. Quintessence Int. 2000;31:95–112. 6. Sook BW, Sonis ST. Recurrent aphthous ulcers: a review of diagnosis and treatm ent. J Am Dent Assoc. 1996;127:1202–1213.
Codes ICD9-CM 528.2
Pa ge 5 1 0
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Apnea
Apnea
James M. Stephen MD
Basics Description
Cessation of all respiration
Central apnea: o
Disruption in the generation of propagation of respiratory signals in the brainstem and descending neurom uscular pathways
Obstructive apnea: o
Occluding airway m ass
o
Functional obstruction from airway collapse due to positive pressure inspiration.
The apneic patient m ust be aggressively treated or death is im m inent in 4–6 m inutes
Apparent life-threatening event (ALTE): o
Episode that is of concern to the caregiver and is associated with a com bination of apnea, color change, change in tone, choking, or gagging
Etiology Adults
Drug overdose
Pa ge 5 1 1
Severe hypoglycem ia
Cardiac arrest
Airway obstruction
Head or brainstem injury
Pulm onary failure
Near drowning
Sleep apnea
Pediatric
Central apnea: o
Prem aturity
o
Head traum a
o
Congenital central hypoventilation syndrom e (Ondine curse)
Obstructive apnea: o
Pierre Robin syndrom e
o
Adenotonsillar hypertrophy
o
Foreign body aspiration
o
Laryngom alacia
o
Intralum inal cysts
o
Vocal cord paralysis, central com pression of the abductor vocal cord nerves from hydrocephalus or Chiari type II
o
Bronchiolitis
o
Pneum onia
o
Bronchospasm /Asthm a
o
Seizures
o
Traum a
o
Sepsis/Meningitis
Neonatal: o
Those above plus
o
Apnea of prem aturity
o
Apnea of infancy
Pa ge 5 1 2
o
Suffocation
o
Metabolic abnorm alities
o
Cardiac dysrhythm ias
Diagnosis Alert If the patient is apneic, treatm ent m ust com m ence at once.
Signs and Symptoms Apnea m ay be current, past, or im pending.
History
Past episodes
Com orbidity
Medications (diabetes)
Pediatric Considerations
Must assum e ALTE
Was child awake during the event?
Did the child turn red or blue?
Did he or she have seizure activity?
Did the child require stim ulation and/or rescue breaths to recover?
Were there antecedent sym ptom s such as fever or upper respiratory infection?
Any past history of ALTEs in this patient or siblings?
Physical Exam
Establish unresponsiveness.
Check/Clear out upper airway.
Rem ove or suction any obstruction.
Ensure proper head positioning.
Pa ge 5 1 3
Brief physical assessm ent—look for CNS deficits, toxidrom es, traum a, lung disease, fever
Assess im pending apnea.
Fast or slow respirations
Increased work of breathing
Use of accessory m uscles
Abnorm al vital signs
Decreasing O 2 sat
P.89
Essential Workup
Vital signs with tem perature,
Exam of airway, lung, and heart
Pulse oxim etry
A brief m ental status exam ination
Tests Lab
Dextrostix
CBC
Electrolytes (including calcium )
Blood urea nitrogen, creatinine
Arterial blood gases
Toxicologic screen (including toxic alcohols)
ECG
Urinalysis
Consider liver function tests, am m onia, serum osm olarity
Pediatric Considerations
Consider occult sepsis in the neonate.
Consider occult traum a.
Pa ge 5 1 4
Imaging
Chest radiograph
Upper airway radiographs
Head CT
Diagnostic Procedures/Surgery Endotracheal Intubation
Differential Diagnosis
Breath-holding spells (voluntary apnea): o
Occur from the first to fourth year of life
Ongoing apnea
Interm ittent apnea
Adult sleep apnea
Periodic breathing m ay be seen in neonates: o
Pauses last Table o f C o ntents > Arsenic Po iso ning
Arsenic Poisoning
Gerald Maloney
Basics Description
Acute toxicity: o
May be intentional ingestion, m alicious poisoning, or m edication error
Chronic toxicity: o
May be owing to occupational exposures, contam ination of drinking water or food, or use of folk rem edies containing arsenic
Prim arily owing to ingestion
May also be inhalational toxicity from arsine gas
Etiology
Most arsenic poisonings seen in the ED setting are a result of intentional ingestion or m alicious poisoning.
Sodium arsenate, found in ant killer, m ost com m on acute exposure in United States
Overall, contam inated food/water supplies m ost com m on cause worldwide
Arsenic trioxide has been recently approved as chem otherapy for acute m yelogenous leukem ia (AML).
Melarsoprol used as antitrypanosom al agent in developing
Pa ge 5 2 8
countries
Found in pesticides, certain folk rem edies (herbal balls), preservatives in wood
Also m ay be released as arsine gas from com bustion of zinc- and arsenic-containing com pounds
Mechanism
Arsenic exists in several form s: gas (arsine, or Lewisite), organic, elem ental, and inorganic
Inorganic form s m ost frequently encountered toxic exposure
Inorganic in trivalent (arsenite) or pentavalent (arsenate) form s: o
Most pentavalent arsenic converted to trivalent arsenic in body, which is m ore toxic
Trivalent arsenic binds sulfhydryl groups and interferes in hem oglobin production.
Pentavalent arsenic uncouples oxidative phosphorylation.
Both function as cellular poisons.
Diagnosis Signs and Symptoms
Cardiovascular: o
Prolonged QTc interval
o
Hypotension
o
Dysrhythm ias, prim arily ventricular
o
Nonspecific ST segm ent changes
o
Noncardiogenic pulm onary edem a
Central nervous system : o
Altered m ental status/encephalopathy
Pa ge 5 2 9
o
Peripheral neuropathy:
Acute—sensory neuropathy
Subacute—sensorim otor neuropathy
Peripheral dysesthesias:
o
Muscle weakness up to paralysis
o
Headache
o
Seizures
Gastrointestinal: o
Nausea, vom iting:
Protracted and m ay be refractory to antiem etics at usual doses
Can have hem orrhagic gastroenteritis; corrosive to GI tract
Rice water diarrhea has been described
o
Abdom inal pain
o
Garlic odor to breath, vom it, stools
o
Causes acute hepatitis; chronically, can cause portal hypertension
Miscellaneous: o
Derm atitis (toxic erythroderm a/hyperpigm ented lesions)
o
Mee lines (white bands across the nails owing to growth arrest caused by arsenic)
o
Hem olytic anem ia (m ore pronounced with arsine gas exposure)
o
Leukopenia (after several days)
o
Increased risk of carcinom a (liver/basal cell/squam ous cell of skin/bronchogenic)
o
Acute rhabdom yolysis
o
Hypothyroidism (antagonizes thyroid horm one)
o
Patchy alopecia
Essential Workup
Pa ge 5 3 0
Spot urine arsenic level
CBC
Tests Lab
Spot urine arsenic level >1,000 µg/L m ay confirm diagnostic suspicion: o
Peaks 10–50 hours postingestion
Definitive test is 24-hour urine collection with speciation into organic and inorganic types of arsenic.
Blood levels not routinely helpful owing to short half-life in serum (approxim ately 2 hours)
CBC to check for: o
Anem ia
o
Leukopenia
o
Basophilic stippling
Electrolytes, BUN/creatinine and glucose
Urinalysis to look for evidence of hem olysis/rhabdom yolysis
Liver function tests
Total creatine phosphokinase (CPK) for rhabdom yolysis
Hair and nail arsenic levels: o
Difficult to interpret and not helpful acutely
o
May help determ ine chronicity of exposure in select populations
Imaging
Plain abdom inal radiographs to look for radio-opaque foreign body
Cranial CT/other studies as indicated by patient's condition
Differential Diagnosis
Other heavy m etal intoxications
Pa ge 5 3 1
Cyclic antidepressants
Encephalopathy/Korsakoff syndrom e
Hyperem esis gravidarum
Shock
Guillain-Barré syndrom e
Addison disease
Cholera
Other neuropathies
P.93
Treatment Pre Hospital Alert
If possible to do so safely, bring containers in suspected overdose/poisoning.
Decontam inate skin.
Support airway/breathing/circulation.
Cardiac m onitoring.
Initial Stabilization
Airway, breathing, circulation (ABCs): o
Cardiac m onitor
o
Isotonic crystalloids as needed for hypotension
o
Vasopressors if refractory hypotension is present
Naloxone, thiam ine, and dextrose (D 5 0 W) as indicated for altered m ental status
Cardiovascular: o
Avoid type 1A antidysrhythm ics:
Pa ge 5 3 2
o
Exacerbate QTc prolongation
Continuous m onitoring as QTc prolongation is com m on
Neurologic: o
Treat seizures with benzodiazepines.
o
Assist ventilation as needed for respiratory insufficiency owing to neurom uscular weakness.
Renal: o
Urinary alkalinization for rhabdom yolysis
o
Hem odialysis for renal failure
ED Treatment
Decontam ination: o
If the patient presents within the first hour of ingestion, m ay try orogastric lavage/aspiration
o
Activated charcoal: 75 g
o
If opacities seen on upright abdom inal film , institute whole bowel irrigation at 1–2 L/h of polyethylene glycol until abdom inal film s are clear.
o
If derm al exposure, decontam inate skin as first step in m anagem ent.
Ensure that no one else is contam inated and environm ent is evaluated.
Evaluate need for chelation therapy; based on levels, acuity of exposure, sym ptom s:
o
Consultation with a m edical toxicologist advised
o
Agents:
Dim ercaprol (British Anti-Lewisite)
DMSA (succim er)
Elim ination: o
Hem odialysis not routinely effective
Consider for patient with renal failure
Must continue chelation through hem odialysis
Pa ge 5 3 3
(HD)
Medication (Drugs)
Dim ercaprol (British Anti-Lewisite): 3 m g/kg IM q4h for 24 hours, then q6h for the next 24 hours, then q12h until able to tolerate PO: o
Caution: cannot use if patient has peanut allergy
DMSA (succim er): 10 m g/kg PO q8h for 5 days, then q12h for 14 days
Sodium bicarbonate: 1 m Eq/kg IV bolus, followed by infusion of 150 m Eq in 1 L of D 5 W at 150 m L/h: o
Used to treat rhabdom yolysis
Thiam ine: 100 m g IM or IV (peds: 1 m g/kg)
Naloxone: 0.4–2.0 m g (peds: 0.1 m g/kg) IV, m ay repeat up to 10 m g for suspected opioid intoxication
Dextrose 50%: 25 g (50 m L) (peds: 0.5 g/kg D 2 5 W) IV for hypoglycem ia
Follow-Up Disposition Admission Criteria Sym ptom atic arsenic exposures should be adm itted to an intensive care setting.
Discharge Criteria
Asym ptom atic patients with a spot urinary arsenic level Table o f C o ntents > Arterial G as Em bo lism (AG E)
Arterial Gas
Embolism (AGE) Peter J. Park
Basics Description
Results when air bubbles enter the pulm onary venous return from ruptured alveolae: o
Then propagate through the system ic vasculature
o
Clinical m anifestations dependent on location of air bubbles in system ic vasculature system
Also known as dysbaric air em bolism or cerebral air em bolism
Mechanism
Overpressurization of lung tissue causing pleural tear with air entering the vascular circulation: o
Air bubbles tend to rise and enter the cerebral vessels where they occlude vascular flow.
o
Boyle's law: At a constant tem perature, pressure (P) is inversely related to volum e (V):
o
PV = K (constant) or P 1 V 1 = P 2 V 2
As pressure increases/decreases, volum e decreases/increases.
Pa ge 5 3 6
o
Trapped air (in lungs with closed glottis) expands on diver ascent.
Etiology
Pulm onary atrioventricular (AV) shunts, or as paradoxical em bolism via a patent foram en ovale (up to 30% of the adult population)
Breath-holding during ascent: o
Sym ptom s attributable to a shower of bubbles and m ultiple blood vessel involvem ent
Iatrogenically during placem ent of central venous pressure (CVP) lines, cardiothoracic surgery, or hem odialysis
Penetrating injuries to heart with em ergent repair of cardiac wound
Diagnosis Signs and Symptoms
Cerebral: o
Dive-related stroke
o
Second leading cause of dive-related death (after drowning)
o
o
Two m ain presentations:
Apnea and full cardiopulm onary arrest
Any com bination of neurologic deficits
Presentation depends on arterial distribution of gas em bolism
Change in level of consciousness (40%)
Sensory loss (20%)
Motor deficit (20%)
Paraplegia (10%)
Pa ge 5 3 7
o
o
Seizure (4%)
Visual changes
Aphasia
Paresthesias
Rapid onset:
8.6% during ascent
83.6% Table o f C o ntents > Arthritis, Degenerative
Arthritis,
Degenerative Michael K. Doney
Basics Description
Most com m on progressive joint disease
Found alm ost exclusively in the elderly
Etiology Mechanism
Repetitive stress to synovial joints associated with age
May be seen in younger patients secondary to joint traum a
Destruction of articular cartilage: o
Reactive changes in joint m argin bone and subchondral sclerosis
Risk factors include age, obesity, traum a, genetics, sex, and environm ent.
Diagnosis Signs and Symptoms
Pa ge 5 4 9
Chronic progressive joint pain: o
Worse with weight bearing, im proved with rest
Asym m etric joint involvem ent: o
Involves hands, knees, hips, spine, and m etatarsophalangeal joints
Morning joint stiffness usually Table o f C o ntents > Arthritis, Rheum ato id
Arthritis,
Rheumatoid Hagop Isnar
Basics Description
Chronic system ic inflam m atory disorder that attacks the joints: o
Nonsuppurative, proliferative synovitis
o
Destruction of the articular cartilage
o
Ankylosis of the joint
Involvem ent of knee is com m on.
Baker cysts m ay be seen in chronic disease.
Involvem ent of spine is lim ited to cervical region: o
May cause atlantoaxial subluxation
o
Rarely results in cord com pression
Pediatric Considerations Juvenile rheum atoid arthritis (JRA) is a distinct entity (see Arthritis, Juvenile Idiopathic).
Genetics
Genetic predisposition related to HLA-DR4
Fem ale-to-m ale ratio is 3:1.
Typical age of onset is between 30 and 50.
Pa ge 5 7 2
Etiology
Etiology is unknown.
Possible triggers include infection and autoim m une response.
Prevalence is about 1% of both United States and world population.
Diagnosis Signs and Symptoms
Malaise, fatigue
Generalized m usculoskeletal pain
After weeks to m onths, patients develop swollen, warm , painful joints.
Often worse in m orning
Joint involvem ent usually sym m etric and polyarticular
Starting in sm all joints of hands and feet: o
Later wrists, elbow, and knees
Distal interphalangeal (DIP) joints of hand generally not involved: o
Presence of swelling in these joints should suggest another type of arthritis.
Synovitis is typically gradual.
Classic joint findings in long-standing disease: o
Metacarpophalangeal (MCP) swelling with ulnar deviation
o
Swan neck and boutonniere deform ities
Extra-articular com plications: o
Subcutaneous nodules
o
Vasculitis
Pa ge 5 7 3
o
Pericarditis or m yocarditis
o
Pulm onary fibrosis
o
Pneum onitis
o
Sjögren syndrom e
o
Mononeuritis m ultiplex
Evidence of m ild pericarditis on echocardiogram is found in up to one third of patients.
Patients usually present to ED owing to exacerbations of the disease or com plication in other organ system s: o
Airway obstruction from cricoarytenoid arthritis or laryngeal nodules
o
Heart block, constrictive pericarditis, pericardial effusion with possible tam ponade or m yocarditis
o
Pulm onary fibrosis, pleuritis, intrapulm onary nodules, or pneum onitis
o
Hepatitis
Neurologic findings m ay result from cervical spine subluxation or ocular m anifestations such as scleritis and episcleritis.
Com plications of chronic steroid use: o
Infections
o
Steroid-induced osteopenia and fractures
Patients m ay present with side effects related to chronic salicylate or nonsteroidal antiinflam m atory drug (NSAID) use such as GI bleeding.
Drugs such as m ethotrexate, gold, or d-penicillam ine also have toxic side effects, m ost com m only gastrointestinal.
Essential Workup
Prim ary diagnosis of rheum atoid arthritis (RA) is rarely m ade in the ED.
Synovitis should be present for at least 6 weeks; a m inim um of four of the following seven criteria as
Pa ge 5 7 4
established by the Am erican Rheum atism Association m ust be m et to m ake the diagnosis: o
Stiffness of the involved joints in the m orning for at least 1 hour
o
Arthritis in three or m ore joints with effusion or soft tissue swelling
o
Arthritis of joint in hand (wrist, MCP, or proxim al interphalangeal [PIP] joint)
o
Sym m etric arthritis
o
Rheum atoid nodules on extensor surfaces or juxta-articular surfaces
o
Significantly elevated rheum atoid factor
o
Characteristic radiographic changes include erosions and decalcification (not attributable to osteoarthritis).
Other pertinent history: m alaise, weakness, weight loss, m yalgias, bursitis, tendonitis, fever of unknown cause
Initial workup should focus on dem onstrating that other causes of arthritis are not present, especially septic arthritis, reactive arthritis, or gout.
Arthrocentesis of a joint effusion m ay be required.
Tests ECG, chest radiograph, C-spine or extrem ity radiograph, and hem oglobin testing are helpful if patient presents with com plications of RA.
Lab
CBC: m ild anem ia with leukocytosis and throm bocytosis
Erythrocyte sedim entation rate (ESR): often >30
C-reactive protein
Antinuclear antibodies (ANA) 30–40% positive screening tool
Pa ge 5 7 5
Rheum atoid factor: elevated in about 70% of cases
Joint fluid analysis: o
Typically between 4,000 and 50,000 white cells
o
Neutrophil predom inance
o
Microscopic Gram stain of fluid should show no organism s and no crystals.
ECG: conduction defects are rare, but heart block m ay be seen.
Imaging
Joint radiograph: o
Joint effusion
o
Juxta-articular erosions and decalcification
o
Narrowing of joint space
o
Loss of cartilage
Magnetic Resonance Im aging (MRI) of joints can detect early inflam m ation before plain radiograph
Chest radiographm ay reveal pulm onary fibrosis, pleural changes, nodular lung disease, or pneum onitis: o
Cardiac silhouette m ay show changes related to m yocarditis.
Cervical spine radiograph: o
Atlantoaxial joint subluxation m ay occur.
Differential Diagnosis
Osteoarthritis
Septic arthritis
Reactive arthritis
Gonococcal arthritis
Lym e disease
Gout
Connective tissue disorders
system ic lupus erythem atosus (SLE), derm atom yositis,
Pa ge 5 7 6
polym yositis, vasculitis, Reiter syndrom e, and sarcoid
Rheum atic fever
Malignancy
P.105
Treatment Pre Hospital Cervical spine im m obilization and airway support as indicated
Initial Stabilization
Airway, breathing, and circulation m anagem ent (ABCs): o
Manage airway with attention to C-spine im m obilization during intubation.
Treat com plications of RA as appropriate.
ED Treatment
Salicylates or NSAIDs are first-line treatm ent for RA: o
If one NSAID fails, another NSAID from a different chem ical class m ay work better.
Early treatm ent of RA is im portant as joint changes m ay be m ost progressive during the first 18 m onths.
Medication (Drugs)
Glucocorticoids, m ethotrexate, and other second-line therapies should be initiated by a rheum atologist.
Aspirin (ECASA): adult: 900 m g PO q.i.d. (2.6–5.4 g/d); peds: 60–90 m g/kg/d q.i.d. up to 3.6 g
Pa ge 5 7 7
Auranofin: 3–9 m g/d (peds: 0.15 m g/kg/d up to 9 m g) divided b.i.d.
Celecoxib (Celebrex): 100–200 m g PO b.i.d.; peds: N/A
Hydroxychloroquine: adult: 200–600 m g/d divided b.i.d.; peds: 6 m g/kg/d up to 600 m g/d
Ibuprofen (Ibuprin, Advil, Motrin): 200–800 m g (peds: 10 m g/kg) PO q6h
Leflunom ide (Arava): 100 m g PO daily for 3 days, then m aintenance dose of 10–20 m g PO daily; peds: N/A
Methotrexate (Rheum atrex): 0.2–0.4 m g/kg PO per week single dose
Prednisone: m aintenance: 5–10 m g PO daily; acute exacerbations: 20–50 m g PO daily; peds: m aintenance: 0.1 m g/kg/d PO, acute exacerbations: 2–5 m g/kg/d PO
Rofecoxib (Vioxx; voluntary m anufacturer withdraw: 25 m g PO daily; peds: N/A
Sulfasalazine: adult: 500–1,000 m g PO b.i.d.; peds: 30–60 m g/kg/d q.i.d. up to 2 g
Valdecoxib (Bextra): 10 m g PO daily; peds: N/A
Alert Note: Recent studies have shown possibly increased risk of cardiovascular event with NSAID m edications, particularly with COX-2 inhibitors.
Follow-Up Disposition Admission Criteria
Patients with severe or life-threatening presentations of RA and its com plications should be adm itted to hospital.
Pa ge 5 7 8
Adm ission is warranted when diagnosis is unclear and serious illnesses such as septic joint or system ic vasculitis m ay be present or cannot be ruled out.
Adm ission m ay be required for pain control.
Adm ission m ay be required if patient has inadequate social supports and is unable to m aintain activities of daily living.
Pediatric patients with fever and arthritis should be strongly considered for adm ission.
Discharge Criteria Patients without serious com plications m ay be m anaged as outpatients with appropriate m edications and follow-up.
Issues for Referral All patients should have prim ary physician for further therapy and care as well as appropriate specialty care referral such as rheum atologists, cardiologists, and orthopedics.
References 1. Anaya J, Diethelm L, Ortiz L, et al. Pulm onary involvem ent in rheum atoid arthritis. Sem in Arthritis Rheum . 1995;24(4):242–254. 2. Bingham CO. Developm ent and clinical application of COX-2 selective inhibitors for the treatm ent of osteoarthritis and rheum atoid arthritis. Cleve Clin J Med. 2002;69(suppl 1): SI5–12. 3. Ilowite NT. Current treatm ent of juvenile rheum atoid arthritis. Pediatrics. 2002;109(1):109–115. 4. Jain R, Lipsky P. Treatm ent of rheum atoid arthritis. Adv Rheum . 1997;81(1):57–84. 5. King R. Arthritis, rheum atoid. Available at http://www.em edicine.com 6. Leicht M, Harrington T, Davis D. Cricoarytenoid arthritis: a cause of laryngeal obstruction. Ann Em erg Med. 1987;16(8):885–888. 7. Sanders S, Harisdangkul V. Leflunom ide for the treatm ent of rheum atoid arthritis and autoim m unity. Am J Med Sci.
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2002;323(4):190–193. 8. Sm ith JB, Haynes MK. Rheum atoid arthritis: a m olecular understanding. Ann Intern Med. 2002;136(12):908–922.
Codes ICD9-CM 714.0
ICD10 M06.9
Pa ge 5 8 0
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Arthritis, Septic
Arthritis, Septic
Ziad N. Kazzi A. Antoine Kazzi
Basics Description
Bacteria can be introduced into a joint by: o
Hem atogenous spread (m ost com m on)
o
Invasive procedures
o
Contiguous infection (e.g., osteom yelitis, cellulitis)
o
Direct inoculation such as plant thorns or nails
Acute inflam m atory process results in WBC m igration into joint.
Synovial hyperplasia, cartilage dam age, and form ation of a purulent effusion
Irreversible loss of function in up to 50%
Pediatric Considerations
Hip infections are m ost com m on: o
Com m only in patients with otitis m edia or upper respiratory tract infections
o
Com plications of septic arthritis (SA) of hip in children: avascular necrosis, epiphyseal separation, pathologic dislocation, and arthritis
Fifty percent occur in children younger than 3 years old.
Pa ge 5 8 1
Infants present with irritability, fever, and loss of appetite.
Older children present with a lim p or refusal to bear weight or use joint.
Etiology
Risk factors: o
Old age, infancy
o
Rheum atoid arthritis and degenerative joint disease
o
Intravenous drug user (IVDU), endocarditis
o
Fem ales (gonococcal [GC])
o
Im m unosuppression (AIDS, diabetes, chem otherapy, steroid therapy)
o
Repeated joint injections, pre-existing joint diseases, traum a, or prosthesis
No bacterial pathogen is identified in 10–20%.
Most com m on organism s: o
Staphylococcus aureus in adults, hip infections (80%), and patients with rheum atoid arthritis or diabetes
o
Neisseria gonorrhea (GC) m ost com m on in young, healthy, and sexually active patients (m ost com m on source in the U.S.)
Other pathogens: group A β-hem olytic and group B, C, and G streptococci
o
Gram -negative rods (e.g., P. aeruginosa, E. coli) in 10% of cases:
Com m on in old age, infancy, im m unosuppression, and IVDU (Pseudom onas)
Anaerobes: diabetes, prosthetic joints
Mycobacterial and fungal causes: atypical (e.g., in HIV); m ore indolent course
Pa ge 5 8 2
Diagnosis Signs and Symptoms
Presents abruptly as a single painful, swollen, warm , and tender joint
Com m on findings include: o
Fever
o
A separate source of infection (e.g., skin)
o
Extrem ely painful joint m otion in all planes
o
A joint effusion (less evident in sacroiliac, hip, and shoulder)
Any joint can be involved: o
Typically a single joint is involved.
o
Most com m only knee, then hip, shoulder, and ankle
Com m only seen in IVDU: sacroiliac costochondral and sternoclavicular joints: o
Vertebral involvem ent such as lum bar facets possible
Hum an and anim al bites, local steroid therapy, and traum a m ay lead to infection in atypical locations.
Polyarticular involvem ent in 10–20%: o
Mostly with rheum atoid arthritis; delay in diagnosis from low suspicion and m ore subtle presentations (fever in only 50%)
o
Patients with sepsis
Gonococcal (GC) SA features: o
Develops in 1–3% of untreated gonorrhea and in 42–85% of dissem inated GC infection:
Typically m onoarticular but com m only polyarticular
Migratory polyarthralgia, tenosynovitis (present in 20% of patients with arthritis), and
Pa ge 5 8 3
derm atitis o
Involves sm all joints (e.g., fingers, wrist, elbow, ankle):
Signs of urethral or vaginal GC infection m ay be present.
Painless m aculopapular lesions on trunk, arm s, legs, and around affected joint
Essential Workup Arthrocentesis
Perform joint aspiration in any suspected case.
Send fluid for protein and glucose, cell count, Gram stain, and culture.
Typical SA findings: o
A turbid, purulent, or serosanguinous fluid
o
A leukocytosis (50,000–150,000/m m 3 ) with a polym orphonuclear predom inance (>75%)
o
Often a decreased glucose and elevated protein level
The appearance of crystals does not rule out SA.
Use special stain or culture m edia when indicated (e.g., GC, anaerobes, fungus, m ycobacterium )
Intra-articular lidocaine reduces the sensitivity of subsequent cultures; im m ediate em ptying of aspirated sam ple into a blood culture flask increases the yield.
In non-GC SA, Gram stain and culture are positive in 50% and 90% of cases, respectively: o
Drops to nearly 10% and 50% in GC SA, respectively
Fluoroscopic, sonographic, or CT guidance can be used in technically difficult aspirations.
CT scan and MRI m ay aid in the diagnosis for joints such as the sacroiliac joint.
Arthrocentesis is contraindicated whenever there is an
Pa ge 5 8 4
underlying joint prosthesis or an overlying skin infection: o
If cellulitis present, use an alternate approach through norm al skin.
Tests Lab
Nonspecific serum leukocytosis (m ore com m on in children), left shift, and C-reactive protein (CRP) and erythrocyte sedim entation rate (ESR) elevation are usually present.
Urinalysis and culture can reveal a urologic source for the pathogen.
Blood cultures m ay be useful: positive in 50–70% of non-GC SA
Culture any potential focus of infection (pharynx, urine, cervix, or anus), particularly when suspecting GC.
Imaging
Plain radiographs to identify: o
Effusion
o
Baseline status of the joint
o
Contiguous osteom yelitis
o
Concurrent rheum atologic diseases
o
Fractures or foreign body
o
Joint loosening (a late and nonspecific sign)
Ultrasound, CT, and MRI are m ore sensitive: o
Ultrasound m ay be used to guide aspiration of som e joints (e.g., hip) and to detect joint effusions
Scintigraphic techniques are sensitive and specific in diagnosis of SA: o
Often not available through ED
Other tests: o
Bacterial DNA am plification techniques in early
Pa ge 5 8 5
detection of organism s P.107
Differential Diagnosis
Viral arthritis
Rheum atoid arthritis
Gout or pseudogout
HIV-associated arthritis
Reactive arthritis
Lym e disease
Osteom yelitis
Endocarditis
Traum a
In children: o
Juvenile rheum atoid arthritis
o
Slipped capital fem oral epiphysis
o
Legg-Calvé-Perthes
o
Metaphyseal osteom yelitis
o
Transient synovitis
Pediatric Considerations
Because of vaccine, H. influenzae is no longer m ost com m on.
S. aureus is m ost com m on.
Group B streptococcus, enterobacteria, and gram -negative rods in the newborn
Treatment Pre Hospital
Pa ge 5 8 6
No specific considerations
Initial Stabilization
Patient m ay be septic and require resuscitation.
If patient is toxic, do not delay antibiotics for aspiration results.
ED Treatment
Prom ptly aspirate joint fluid.
Obtain cultures.
Start em piric antibiotics: staphylococcal, streptococcal, and gram -negative coverage; duration of treatm ent recom m ended is 2–4 weeks: o
Com bine β-lactam ase–resistant penicillin (e.g., nafcillin) with an am inoglycoside (e.g., gentam icin) or a third-generation cephalosporin (e.g., ceftriaxone).
o
Use Vancom ycin instead of penicillin when m ethicillin-resistant S. aureus or penicillin resistant pneum ococci are suspected.
o
Initial guidance by Gram stain, patient's age, risk factors, and com orbid illness is appropriate.
o
When suspecting GC, use a third-generation cephalosporin or a quinolone (e.g., ceftriaxone, ciprofloxacin).
o
Treat patients with sickle cell disease using third-generation cephalosporin (ceftriaxone) and an antistaphylococcal drug (nafcillin, cloxacillin, clindam ycin).
o
Intra-articular antibiotics are contraindicated.
Early orthopedic consultation to evaluate eligibility for surgical drainage
Pain-control: narcotics and m oderately flexed splinting
Pa ge 5 8 7
Im m unologic therapies are experim ental.
Prosthesis: som e m ay try to preserve it unless it is loose on plain film s.
Patients should be at rest with joint m aintained in optim al position to prevent dam age.
Medication (Drugs)
Cefotaxim e: 1 g IV q8h; peds: 50 m g/kg q12h
Ceftriaxone: 1 g IV daily; peds: 50 m g/kg
Ciprofloxacin: 400 m g IV q12h
Gentam icin: 2–5 m g/kg IV load
Nafcillin: 2 g IV q4h; peds: 25 m g/kg q6h
Piperacillin: 4 g IV q6h
Tobram ycin: 1 m g/kg IV q8h; peds: 2.5 m g/kg q8h
Vancom ycin: 1 g IV q12h; peds: 10 m g/kg q6h
Pediatric Considerations
Open surgical drainage is the m ethod of choice in pediatric hip SA.
Cover H. influenzae type B if prior im m unization cannot be established.
Follow-Up Disposition Admission Criteria
All patients with suspected SA should be adm itted until SA is ruled out.
May undergo drainage of their joint as indicated, by serial
Pa ge 5 8 8
aspirations, arthroscopy, or arthrotom y
Discharge Criteria Cases where suspected SA has been adequately ruled out.
References 1. Baker D, Schum acher HR. Acute m onoarthritis. N Engl J Med. 1993;329:1013–1019. 2. Deng GM, Tarkowski A. The role of bacterial DNA in septic arthritis. Int J Mol Med. 2000;6:29–33. 3. Donatto KC. Orthopedic m anagem ent of septic arthritis. Rheum Dis Clin North Am . 1998;24(2):275–286. 4. Goldenberg D. Septic arthritis. Lancet. 1998;35:197–202. 5. Greenspan A, Tehranzadeh J. Im aging of infectious arthritis. Radiol Clin North Am . 2001;39(2):267–276. 6. Malleson P. Managem ent of childhood arthritis. Part 1: acute arthritis. Arch Dis Child. 1997;76:460–462. 7. Shetty AK, Gedalia A. Managem ent of septic arthritis. Indian J Pediatr. 2004;71:819–824. 8. Shirtliff ME, Mader JT. Acute septic arthritis. Clin Microbiol Rev. 2002;15(4):527–544.
Codes ICD9-CM 711.00
Core Content Code 10.2.1.1
ICD10 M00.9
Pa ge 5 8 9
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Ascites
Ascites
Paul Allegretti
Basics Description
Pathologic accum ulation of serous fluid in the peritoneal cavity
Portal hypertension (>12 m m Hg) starts fluid retention.
Avid sodium retention state.
Retained sodium and water increases plasm a volum e.
Water excretion becom es im paired.
Increased release of antidiuretic horm one (ADH)
Urinary sodium retention, increased total body sodium , and dilutional hyponatrem ia
Degree of hyponatrem ia correlates with disease severity; prognostic factor.
Decreased plasm a oncotic pressure from hypoalbum inem ia
Peritoneal irritation owing to infection, inflam m ation, or m alignancy
Etiology
Parenchym al liver disease: o
Cirrhosis and alcoholic hepatitis:
o
Eighty percent of adult patients
Fulm inant hepatic failure
Pa ge 5 9 0
Hepatic congestion: o
Congestive heart failure
o
Constrictive pericarditis
o
Veno-occlusive disease and Budd-Chiari syndrom e
Malignancies: o
Peritoneal carcinom atosis
o
Hepatocellular carcinom a or m etastatic disease
Infections: o
Tuberculous, fungal, or bacterial peritonitis
Hypoalbum inem ic states: o
Nephrotic syndrom e
o
Malnutrition; album in 250 cells/m m 3
o
Ascitic fluid protein 250 cells/m m 3 with m ultiple m icro-organism s on Gram stain plus two of the following found with secondary bacterial peritonitis:
Total protein >1 g/dL
Glucose Table o f C o ntents > Asthm a, Pediatric
Asthma, Pediatric
Nathan Shapiro Tarina Lee Kang
Basics Description
2.7 m illion children (90% considered norm al
Tests Lab
Arterial blood gas (ABG) m ay be an adjunct to pulse oxim etry to m easure oxygenation and clinical exam to assess ventilation; not m andatory or routinely done
CBC as a nonspecific m arker of infection
Theophylline level: only for patients on theophylline (not recom m ended)
Imaging Chest radiograph in the following patients:
Younger than 1 year of age to exclude foreign body or atelectasis
First episode of wheezing (suggested)
Increasing respiratory distress or m inim al response to therapy
Respiratory distress/failure
Shortness of breath in the absence of wheezing
Differential Diagnosis
Infection/inflam m ation: o
Bronchiolitis: clinically difficult to differentiate except by age and clinical history
o
Pneum onia: viral, bacterial, chem ical, hypersensitivity
o
Aspiration
o
Lym phadenopathy
o
Anaphylactic reaction
Pa ge 6 1 6
Anatom ic: o
Pneum othorax
o
Foreign body
Vascular disorder: o
Com pression of trachea by vascular anom aly
o
Pulm onary em bolism
o
Congestive heart failure
Congenital disease: o
Cystic fibrosis
o
Tracheoesophageal fistula
o
Bronchogenic cyst
Intoxication: m etabolic acidosis
Neoplasm
Vocal chord dysfunction
Pulm onary edem a
P.113
Treatment Pre Hospital
Oxygen and oxygen saturation m onitoring
Nebulized β-adrenergic agonist: albuterol
Intubate for respiratory failure or severe fatigue.
Rapid transport and good com m unication with ED
Initial Stabilization
Maintain SaO 2 >90–95%.
β-adrenergic nebulizer(s): albuterol
Intubate for respiratory failure.
Pa ge 6 1 7
ED Treatment
Assess patient for signs of potential respiratory failure: o
Cyanosis
o
Severe anxiety or irritability
o
Lethargy, som nolence, fatigue
o
Persistent tachypnea
o
Poor air entry, ventilation
o
Severe retractions
Monitor oxygenation; titrate oxygen saturation to SaO 2 >95% (sea level).
β-adrenergic nebulizer: albuterol: o
Frequent or continuous for severe asthm a
o
Levalbuterol m ay require less frequent dosing.
Ipratropium brom ide m ay be added as adjunct to β-adrenergic agonists.
Steroid therapy: o
Oral for m oderate exacerbations in those able to take oral m eds
o
Intravenous for severe exacerbations or in those unable to take oral m eds
Subcutaneous epinephrine or terbutaline for severe or refractory asthm a (rarely used)
Magnesium sulfate m ay be useful in severe disease following standard therapy.
Intubate for respiratory failure: o
Ketam ine is a useful induction agent.
Medication (Drugs)
Albuterol (0.5% solution or 5 m g/m L): o
Nebulizer: 0.015 m g (0.03 m L)/kg per dose, up to 5
Pa ge 6 1 8
m g per dose, q15m in–q30m in as needed o
Metered-dose inhaler (with spacer) (90 µg/puff): two puffs q5m in–q10m in, m ax. 10 puffs
Epinephrine (1:1,000) (1 m g/m L): 0.01 m g/kg SC, up to 0.35 m L per dose, q20m in for two doses
Ipratropium brom ide: nebulizer (0.02% inhaled sol 500 µg/2.5 m L), 250–500 µg per dose q6h
Ketam ine (for intubation): 1–2 m g/kg IV as induction agent
Levalbuterol (0.63 and 1.25 m g vials): q6h–q8h by nebulizer
Magnesium sulfate: 25 m g/kg per dose IV over 20 m in; m ax. 1.2–2 g per dose
Methylprednisolone: 1–2 m g/kg per dose IV q6h; m ax. 125 m g per dose
Prednisolone: 1–2 m g/kg per dose PO q12h
Prednisone: 1–2 m g/kg per dose PO q6h–q12h; m ax. 80 m g per dose
Terbutaline (0.01%): 0.01 m L/kg SC q15m in–q20m in up to 0.25 m L per dose, q20m in for two doses
(available as 15 m g/5 m L)
Follow-Up Disposition Admission Criteria
Persistent respiratory difficulty: o
Persistent wheezing
o
Increased respiratory rate/tachypnea
o
Retraction and use of accessory m uscles
Pa ge 6 1 9
SaO 2 Table o f C o ntents > Ataxia
Ataxia
Sean P. Kelly
Basics Description
Ataxia is the inability to perform coordinated m ovem ents.
It is a disorder of coordination and rhythm .
May result from dysfunction at several levels of the cerebellar circuit, including sensory or m otor pathways
Sensory ataxia: o
Proprioceptive sensory pathways to the cerebellum are faulty.
Dorsal root ganglia cells
Posterior colum ns of the spinal cord
Lem niscal system in the brainstem
Thalam us
Parietal cortex
Motor ataxia: o
Sensory pathways are intact, but the integration of proprioceptive data is faulty.
Cerebellum
Contralateral frontal lobe
Internal capsule
Motor output to the spinal neurons
Pa ge 6 2 8
Different types of ataxia should be distinguished: o
Vertiginous ataxia due to dizziness
o
Cerebellar ataxia due to im balance
o
Spinal cord and m uscular ataxia due to weakness
Etiology
Acute sym m etric: o
Toxicologic:
Alcohol
Lithium
Diphenylhydantoin
Barbiturates
o
Acute viral cerebritis
o
Meningitis
o
Hydrocephalus
o
Postinfection syndrom e
o
Hyponatrem ia
o
Hypothyroidism
Acute focal: o
Anterior cerebral artery syndrom e
o
Cerebellar infarction
o
Cerebellar hem orrhage
o
Subdural hem atom a of the posterior fossa
o
Cerebellar abscess
Subacute sym m etric: o
Mercury
o
Hydrocarbons
o
Toluene
o
Vitam in B 1 or B 1 2 deficiency
o
Lym e disease
o
AIDS
o
Toxoplasm osis
o
Mycoplasm a
Pa ge 6 2 9
o
Legionella
o
Bacterial abscesses
o
Creutzfeldt-Jakob disease
Subacute focal: o
Cerebellar gliom a
o
Metastatic tum ors
o
Paraneoplastic syndrom es:
Breast cancer
Hodgkin disease
Children with neuroblastom as
o
Multiple sclerosis
o
AIDS-related m ultifocal leukoencephalopathy
o
Lym phom a
o
Cervical spondylosis
o
Syringom yelia
o
Guillain-Barré syndrom e
Chronic: o
Cerebellar degeneration
o
Stable gliosis
o
Inherited and developm ental ataxias:
Friedreich ataxia and other recessive ataxias
Ataxia-telangiectasia
Autosom al-dom inant cerebellar ataxia
Cerebellar hypoplasia: o
Hartnup disease
o
Niem ann-Pick disease
o
Pyruvate decarboxylase deficiency
o
Dandy-Walker and Arnold-Chiari m alform ation
o
Joubert and Gillespie syndrom es
Signs and Symptoms
A careful history and physical are essential to classify the ataxia and determ ine the etiology:
Pa ge 6 3 0
o
Onset:
Hours to days—acute
Weeks to m onths—subacute
Years—chronic
o
Bilateral, sym m etrical, or focal involvem ent
o
Truncal or lim b ataxia
o
Motor or sensory ataxia (see below)
Perform neurological exam ination: o
Mental status
o
Motor sensory
o
Finger-to-nose
o
Heel-to-shin
o
Rom berg
o
Gait (if possible)
o
Speech
o
Cranial nerves
o
Babinski
Assess for associated signs or sym ptom s of acute, life-threatening disorders such as hem orrhage or stroke:
o
Altered m ental status
o
Headache
o
Focal weakness, num bness, tingling
o
Nausea/vom iting
o
Slurred speech
o
Incontinence
Assess for altered hand coordination (bilaterally): o
Finger-to-nose test
o
Rapid alternating hand m ovem ents
Assess for altered coordination in lower extrem ities (bilaterally): o
Abnorm al heel-to-shin coordination
Assess balance:
Pa ge 6 3 1
o
Ataxia usually results from dysfunction of two out of three of vision, vestibular sense, or proprioception.
o
Evaluated by Rom berg test
o
Positive Rom berg test: unsteady with eyes open, worse with eyes closed—sensory ataxia
o
Negative Rom berg test: unsteady with eyes open, no change with eyes closed—m otor ataxia (cause m ay be in cerebellum )
o
Norm al Rom berg test: no ataxia
Assess gait
Assess for intentional trem or
Specific Syndromes
Frontal lobe lesions: o
Wide based gait
o
Tendency to fall backward
o
Motor perseveration
o
Grasp and suck reflexes
o
Urinary incontinence
o
Slowness in thinking
o
Headache
o
Altered m ental status
Subcortical lesions: o
Em otional lability
o
Brisk reflexes
o
Dysarthria
o
Dem entia
Brainstem lesions: o
Crossed m otor or sensory findings
o
Internuclear ophthalm oplegia
o
Nystagm us
o
Dysarthria
Cerebellar lesions:
Pa ge 6 3 2
o
Truncal and gait ataxia if m idline lesions
o
Ipsilateral lim b ataxia if hem ispheric lesions
o
Nystagm us
o
Hypotonia
o
Occipital headache
o
Occipital gaze palsy
Posterior colum n dysfunction: o
Positive Rom berg sign
o
Neck and arm pain
o
Positive Babinski sign
o
Loss of vibration and position sense
Peripheral neuropathy: o
Loss of deep tendon reflexes
o
Decreased strength and sensation peripherally
o
Wernicke encephalopathy
o
Encephalopathy
o
Oculom otor dysfunction
o
Gait ataxia
P.117
Essential Workup
Thorough history and physical exam ination
Tests as described below
Tests Lab
Blood glucose level
Electrolytes
Toxicology screen
Anticonvulsant drug screen
CBC; consider lum bar puncture if infection, abscess
Pa ge 6 3 3
suspected
TSH, free T 4 if hypothyroidism suspected
Imaging
Head CT scan: o
Identifies supratentorial m asses, hem orrhage, or evidence of hydrocephalus
o
If MRI is unavailable, obtain both contrast and noncontrast studies.
o
CT angiogram of the neck can be used to evaluate the neck vessels if MRI/m agnetic-resonance angiography not available
Head MRI: o
Diagnostic study of choice to assess the posterior fossa
o
Excellent study to evaluate for ischem ia, hem orrhage, tum or, edem a or other lesions
o
MR angiogram of the head and neck m ay be indicated if a vertebral basilar artery insufficiency or other vascular abnorm ality is suspected.
Electrom yography: o
Not indicated as part of the em ergency workup
o
Assesses for denervation of peripheral nerves
Diagnostic Procedures/Surgery Lum bar puncture:
Rarely indicated unless fever or m ental status changes suggest an infectious etiology
Indicated in the evaluation for possible Lym e disease although m ay be done in this setting as an outpatient
Differential Diagnosis
Stroke
Hem orrhage
Pa ge 6 3 4
Intoxication
Toxicologic
Infection
Electrolyte abnorm alities
Endocrine abnorm alities
Vertebrobasilar Insufficiency
Congenital ataxias
Benign paroxysm al positional vertigo
Acute labyrinthitis
Ménière disease
Hydrocephalus
Vitam in deficiency
Neoplasm
Paraneoplastic syndrom e: o
Multiple sclerosis
o
Guillain-Barré syndrom e
Syringom yelia
Atypical seizure
Com plicated m igraine
Treatment Pre Hospital Alert
Acute onset of ataxia m ay be due to stroke or hem orrhage: o
Supplem ental oxygen
o
Monitor
o
IV access
o
Observe m ental status carefully; deterioration m ay
Pa ge 6 3 5
warrant field endotracheal intubation
Initial Stabilization
ABCs
IV access, cardiac m onitor if altered m ental status or cerebellar hem orrhage suspected
Naloxone, dextrose (or rapid fingerstick glucose) if altered m ental status
Em piric thiam ine in chronic alcoholics and poorly nourished patients
ED Treatment Treatm ent should be determ ined by the underlying cause.
Medication (Drugs)
Dextrose: D 5 0 W 1 am p (50 m L or 25 g) (peds: D 2 5 W 2–4 m L/kg) IV
Naloxone (Narcan): 2 m g (peds: 0.1 m g/kg up to 2 m g) IV or IM initial dose
Thiam ine (vitam in B 1 ): 100 m g IM or 100 m g thiam ine in 1,000 m L of IV fluid wide open
Follow-Up Disposition Admission Criteria
Acute and subacute ataxia, especially if an underlying etiology cannot be established
Patients who cannot am bulate safely without hom e support
Patients with cerebellar hem orrhage should be adm itted to
Pa ge 6 3 6
the intensive care unit
Discharge Criteria Reversible acute and subacute causes or chronic causes if patient's m ental status is okay and can am bulate without risk of injury:
Most often due to alcohol, m edications, or cerebellar atrophy
References 1. Baloh RW. Approach to the dizzy patient. In: Baloh RW, ed. Neurotology. Baillieres Clin Neurol. 1994;3:453. 2. Huff JS. Ataxia and Gait Disturbances. In: Tintinalli JE, et al., eds. Em ergency m edicine: a com prehensive study guide. 5th ed. New York: McGraw-Hill, 2000:1449–1452. 3. Rosenberg RN. Ataxic disorders. In: Fauci AS, et al., eds. Harrison's principles of internal m edicine. Philadelphia: McGraw-Hill, 1998:2363–2368.
Codes ICD9-CM 334.0 334.2 334.3 334.8
ICD10 R27.0
Pa ge 6 3 7
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Atrial F ibrillatio n
Atrial Fibrillation
Jason K. Wong
Basics Description
Dysrhythm ia characterized by seem ingly disorganized atrial depolarizations without effective atrial contraction
Caused by m ultiple re-entrant waveform s within the atria
Atrial rate ranges from 350–600 beats/m in.
Ventricular rate usually ranges from 160–200 beats/m in secondary to blocking by atrioventricular (AV) node: o
Faster rate suggests bypass tract
o
Slower rate suggests abnorm al AV node or presence of AV nodal blocking m edication
Results in loss of organized atrial contractions and rapid ventricular rate:
o
Decrease in cardiac output
o
Em bolus form ation
Affects 2.2 m illion Am ericans: o
Prevalence increasing with age
Etiology
System ic disease: o
Hypertension
o
Hyperthyroidism
Pa ge 6 3 8
o
Chronic pulm onary disease
o
Pulm onary em bolus
o
Hypoxia
o
Drugs:
Cocaine
Am phetam ines
o
Acute alcohol ingestion (holiday heart syndrom e)
o
Obesity
Underlying cardiac disease: o
Cardiom yopathy
o
Coronary artery disease
o
Valvular disease:
Especially m itral
o
Pericarditis
o
Sick sinus syndrom e
o
Myocardial contusion
o
Congestive heart failure (CHF)
o
Congenital heart disease
Idiopathic: o
Absence of any known etiologic factor
o
No clinical or echocardiographic evidence of heart disease
Diagnosis Signs and Symptoms
Palpitations
Irregularly irregular pulse
Slight variation in intensity of the first heart sound
Absence of a waves in the jugular venous pulse
Pulse deficit with m ore rapid ventricular rates
Pa ge 6 3 9
o
The auscultated or palpated apical rate is faster than the rate palpated at the wrist.
o
Helps differentiate atrial fibrillation (AF) from other supraventricular tachycardias
Decreased cardiac output: o
Weakness
o
Light-headedness
o
Syncope
o
Hypotension
o
Angina
o
Pulm onary edem a
o
Altered m ental status
o
Lower-extrem ity edem a
o
Hepatojugular reflex
Em bolus form ation: o
Acute neurologic injury
o
Mesenteric ischem ia
o
Digit ischem ia
Essential Workup
History and physical exam : o
Assess for instability and need for im m ediate cardioversion
o
Duration of sym ptom s
o
Evidence of system ic disease or underlying cardiac disease
ECG o
Irregularly irregular R-R intervals
o
No identifiable P waves
o
If rate >200 associated with wide-irregular QRS, consider bypass tract.
Tests
Pa ge 6 4 0
Lab
CBC
Electrolytes
Cardiac enzym es
Thyroid function
Digoxin level
Ethanol level
Urine drug screen
Imaging
Chest radiograph
Echocardiogram (ECG)
Differential Diagnosis
Atrial flutter with variable AV block
Multifocal atrial tachycardia
Sinus rhythm with frequent prem ature atrial contractions
Atrial tachycardia with variable AV block
Treatment Pre Hospital
IV access
Monitor
Oxygen
Cardioversion: o
In rare settings where patient is unstable
Initial Stabilization
IV
Oxygen
Monitor
Pa ge 6 4 1
Im m ediate synchronized electrical cardioversion starting at 200 J if the patient is unstable
ED Treatment
Control rate: o
Not necessary if rate 48 hours, delayed cardioversion: anticoagulation (INR 2–3) for at least 3 weeks, then cardioversion with 200–300 J, then anticoagulation for 4 m ore weeks
o
>48 hours, im m ediate cardioversion: IV heparin im m ediately then transesophageal echocardiography to exclude atrial clot then cardioversion then anticoagulation for four m ore weeks; if atrial clot noted on echo, will have to defer to delayed cardioversion protocol
o
60 kg; 0.01 m g/kg IV for patients Table o f C o ntents > Atrio ventricular Blo cks
Atrioventricular
Blocks Colleen N. Roche James Scott
Basics Description
Im paired conduction through the aortic valve (AV) node or His-Purkinje system
First-degree AV block: o
Prolonged conduction through the AV node >0.20 seconds
o
Ventricular im pulses are not lost.
Second-degree AV block: o
Marked by a failure of som e atrial im pulses to reach ventricles
o
Type I (Wenckebach):
Usually secondary to conduction deficit in AV node
Generally benign
Progressive prolongation of the pulse-rate (PR) interval until there is a nonconducted P wave and a dropped QRScom plex
Pa ge 6 5 9
May be a com plication of an inferior wall m yocardial infarction (MI)
o
Type II:
Conduction deficit is usually below the level of the AV node.
PR intervals are constant until a single or m ultiple beats are abruptly dropped.
High likelihood of progression to com plete heart block
Worse prognosis if associated with an acute m yocardial infarction
Less com m on than type I
Third-degree AV block: o
Also known as com plete heart block
o
All atrial im pulses are unable to reach the ventricular conducting system ; a ventricular escape pacem aker then takes over, resulting in AV dissociation.
o
Constant PP and RR intervals with variable PR intervals because PP and RR intervals are independent of each other.
o
More severe sym ptom s occur when the block is lower in the conducting system .
o
If secondary to toxicologic agents, often resolves upon om ission of offending toxin
o
Never a benign condition
Etiology
Essentially due to: o
A structural lesion
o
Increase in inherent refractory period
o
Marked shortening of the supraventricular cycle
MI: o
First-degree block and type I second-degree AV block
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m ay be associated with an inferior wall MI:
10–15% of all inferior wall MIs are com plicated by AV blocks.
AV conduction usually returns to norm al with no increased m orbidity or m ortality.
o
Type II second-degree AV block m ay be associated with an anterior wall MI:
5% anterior wall MIs are associated with AV blocks.
Increased m ortality secondary to ventricular arrhythm ias and left heart failure
Coronary artery disease: o
Chronic ischem ic injury can lead to fibrosis around the AV node
Toxicologic: o
Digoxin
o
Beta-blockers
o
Calcium -channel blockers
o
Am iodarone
o
Procainam ide
o
Class 1C agents: propafenone, encainide, flecainide
o
Clonidine
Congenital
Valvular heart disease
Surgical traum a: o
S/P coronary artery bypass graft or valvular replacem ent
Increased vagal tone
Infectious: o
Syphilis
o
Diphtheria
o
Chagas disease
Pa ge 6 6 1
o
Tuberculosis
o
Toxoplasm osis
o
Lym e disease
o
Myocarditis
o
Endocarditis
o
Rheum atic fever
o
Abscess form ation in interventricular septum
Collagen vascular diseases
Infiltrative diseases: o
Sarcoidosis
o
Am yloidosis
o
Hem ochrom atosis
Cardiom yopathy
Electrolyte disturbances: o
Hyperkalem ia
Myxedem a
Hypotherm ia
Pediatric Considerations
Occurs in children, but is often asym ptom atic
Associated m ortality is highest in the neonatal period.
Associated with: o
Congenitally acquired m aternal antibodies
o
Congenital heart disease
o
Infectious etiologies, such as rheum atic fever or m yocarditis
Be sure to consider potential toxic ingestions in pediatric patients with new AV block
Diagnosis
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Signs and Symptoms History
First-degree AV block: o
Type I second-degree AV block: o
Asym ptom atic
Pulse irregularities
Type II second-degree AV block and third-degree block: o
Exercise intolerance
o
Palpitations
o
Chest pain
o
Presyncope/syncope
o
Altered m ental status
o
Dyspnea, orthopnea
Physical Exam
First-degree AV block: o
Type I second-degree AV block: o
No discrete physical exam findings
Regularly irregular pulse
Type II second-degree AV block and third-degree block: o
Irregular pulse
o
Hypotension
o
Confusion
o
Signs of heart failure:
Rales
Cyanosis
Jugular venous distention
Essential Workup A 12-lead ECG to determ ine the type of block and identify evidence of infarction or drug toxicity:
First-degree AV block:
Pa ge 6 6 3
o
PR interval >0.20 seconds
Second-degree AV block: o
Type I: progressive prolongation of PR interval until there is a nonconducted P wave and a dropped QRS; occurs in repeated cycles; QRS is usually narrow P.123
o
Type II: PR interval rem ains constant; atrial im pulses are not conducted interm ittently, giving the appearance of an occasionally dropped ventricular beat; QRS m ay be prolonged depending on the level of the lesion
Third-degree AV block: o
Com plete electrical dissociation: atria and ventricles beat at separate, unrelated rates; constant PP and RR intervals with variable PR intervals
o
QRS duration depends on the level of the pacem aker: pacem akers above the level of the His-Purkinje system result in narrow QRS com plexes, pacem akers below this level produce wide QRS com plexes
Tests Lab
Electrolytes
Calcium , m agnesium
Cardiac enzym es: o
Especially for type II second-degree and third-degree blocks
Digoxin level
Imaging
Chest radiograph:
Pa ge 6 6 4
o
May identify cardiom yopathy or congestive heart failure
ECG: o
May identify regional wall m otion abnorm alities or valvular dysfunction
Differential Diagnosis
Accelerated junctional rhythm
Idioventricular rhythm
Sinus bradycardia
Treatment Pre Hospital
Transcutaneous pacing for unstable type II second- or third-degree block
Atropine: o
Avoid with type II second-degree block because it m ay precipitate com plete heart block
o
Contraindicated in third-degree heart block with a widened QRS com plex
Attem pts should be m ade at preventing increases in vagal tone.
Initial Stabilization
Transcutaneous pacem aker: o
o
Necessary for the unstable patient:
Profound bradycardia and chest pain
Shortness of breath
Hypotension
Mild sedation is recom m ended beforehand
Atropine:
Pa ge 6 6 5
o
Can be adm inistered in:
Com plete heart block with a narrow QRS
Sym ptom atic bradycardia
ED Treatment
First-degree AV block: o
No treatm ent required
o
Close m onitoring to ensure that it does not progress to higher level AV block
o
Evaluate for associated MI, electrolyte abnorm alities, m edication excess.
Type I second-degree AV block: o
Usually no treatm ent needed
o
If sym ptom atic, atropine will enhance AV conduction
Type II second-degree AV block: o
Tem porary transcutaneous or transvenous pacem aker
o
Atropine and isoproterenol are not effective
Third-degree AV block: o
May transiently respond to atropine
o
Em ergent pacem aker
o
Digoxin-specific antibodies
o
Digoxin overdose with a com plete heart block
o
Glucagon and calcium :
If beta-blocker or calcium -channel overdose
Medication (Drugs)
Atropine: 0.5–1.0 m g (peds: 0.01–0.03 m g/kg) IV every 5 m inutes as necessary
Calcium chloride: 250–500 m g (peds: 20 m g/kg) IV
Digoxin-specific antibodies:
Pa ge 6 6 6
o
Serum level × weight (kg) = num ber of vials to be adm inistered
Glucagon: 5–10 m g (peds: 50 µg/kg IV over 5 m inutes
Isoproterenol: Begin infusion at 2 µg/m in and titrate to a m ax 10 µg/m in IV (peds: infusion at 0.1 µg/kg/m in and titrate to a m ax of 1.5 µg/kg/m in).
Follow-Up Disposition Admission Criteria Monitored bed:
Type II second-degree block
Third-degree block
Discharge Criteria Asym ptom atic first-degree and type I second-degree blocks:
Ensure follow-up for further outpatient workup.
References 1. Barold SS, Serge S, Hayes DL. Second-degree atrioventricular block: a reappraisal. Mayo Clin Proc. 2001;76(1):4457. 2. Bourke JP. Atrioventricular block and problem s with atrioventricular conduction. Clin Geriatric Med. 2002;18(2). 3. Brady WJ, Harrigan RA. Diagnosis and m anagem ent of bradycardia and atrioventricular block associated with acute coronary ischem ia. Em erg Med Clin North Am . 2001;19:371–384. 4. Haushik V, Leon A, Forrester JS, et al. Bradyarrhythm ias, tem porary and perm anent pacing. Crit Care Med 2001;28(10):N121–N128. 5. Kaltm an J. Evaluation of the Child with an arrhythm ia. Pediatr Clin
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North Am . 2004;54(6). 6. Olgin JE, Zipes DP. Specific arrhythm ias: diagnosis and treatm ent. In: Brunwald E, ed. Heart disease: a textbook of cardiovascular m edicine. 6th ed. Philadelphia: WB Saunders, 2001:872–876.
Codes ICD9-CM 426.0 426.1
Pa ge 6 6 8
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Babesio sis
Babesiosis
Philip D. Anderson
Basics Description
Tick-borne, m alarialike disease caused by an intracellular parasite that invades the red blood cells.
Protozoa pass from tick salivary glands to m am m alian bloodstream .
Erythrocytes are penetrated and infected by parasites that m ature and divide.
RBC m em brane dam age and lysis leads to hem olytic anem ia and hem oglobinuria.
Dam aged RBCs becom e less deform able, enhancing rem oval by spleen.
Asplenic patients are less able to clear infected RBCs, leading to m ore severe disease.
Dam aged RBCs m ay result in m icrovascular stasis with secondary ischem ic organ injury.
Subsequent com plications can include renal failure secondary to acute tubular necrosis, shock, cardiac failure, hypotension, acute respiratory distress syndrom e (ARDS), and dissem inated intravascular coagulation (DIC)
Babesiosis in Europe:
Pa ge 6 6 9
o
Often a fulm inate disease in im m unocom prom ised patients
o
40% m ortality in asplenic patients
o
Bovine strain (Babesia divergens)
North Am erica: o
Usually presents as m ild or subclinical disease in im m unocom petent patients (5% m ortality)
o
Rodent strain (Babesia m icroti) in the Northeastern United States
o
Canine strain (Babesia gibsoni) in the Northwestern United States
Incubation period: o
1–4 weeks after tick bite
o
6–9 weeks after transfusion
Geographic distribution in the United States: o
Coastal areas of Northeastern United States
o
Em erging clusters:
Midwest (Minnesota, Wisconsin, Missouri)
West coast (California, Washington)
Seasonal distribution: 80% of hum an cases occur between May and August when tick nym ph populations and hum an outdoor activity are highest.
Risk factors for severe disease: o
Age >40 years
o
Splenectom y
o
Depressed cellular im m unity (HIV, corticosteroid use, other im m unosuppressive drugs)
o
Co-infection with Lym e disease
o
In im m unosuppressed patients, up to 85% of RBCs m ay be infected.
Etiology
Pa ge 6 7 0
Intraerythrocytic protozoa of the genus Babesia
Transm itted to hum ans by the Ixodes tick:
o
Ixodes ricinus in Europe
o
Ixodes scapularis in the United States
o
Anim al reservoirs:
Cattle in Europe
White-footed m ouse in the United States
I. scapularis: o
Requires a blood m eal to develop through each of it's three developm ental stages.
o
Larvae:
o
o
Nym phs:
Feed on hum ans
Nym ph form is 1–2 m m in length
Tan color
Patients m ay not recall being bitten
Adult ticks:
o
Feed on white-footed m ice
Generally feed on white-tailed deer
Also the vector for Lym e disease and ehrlichiosis
Transfusion-associated infections are possible: o
Parasitem ia not always visible on donor blood sm ear.
o
Risk of transm ission in endem ic areas reported to be 0.17%.
Pregnancy Considerations Transm ission can occur in utero and during delivery; youngest reported case was a 4-week old infant.
Diagnosis
Pa ge 6 7 1
Signs and Symptoms Clinical spectrum ranges from m ild to fulm inate with sym ptom s lasting from weeks to m onths.
History
Mild flulike illness
Fatigue
Anorexia
Myalgias
Arthralgias
Cough
Nausea
Vom iting
Headache
Em otional lability
Physical Exam
Conjunctival injection
High-spiking fevers
Shaking chills
Drenching sweats
Rash: o
Uncom m on
o
Petechial or purpuric rash caused by associated throm bocytopenia
o
Erythem a m igrans if concurrent Lym e disease
Respiratory distress
Dark urine
Jaundice
Hepatosplenom egaly
Meningism us
Altered sensorium
Hypotension
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ARDS
DIC
Essential Workup
History of nonspecific febrile illness in any patient with recent outdoor activities or transfusion in an endem ic area during warm weather should prom pt consideration of diagnostic workup for babesiosis, especially if associated with hem aturia, jaundice, anem ia, splenom egaly, and lym phocytosis.
Septic presentation in patients with above history and risk factors (asplenia, im m unocom prom ised, age >40 years) should prom pt consideration of diagnostic workup and em piric treatm ent for babesiosis
Tests Lab
Nonspecific studies: o
CBC (anem ia, throm bocytopenia, m ild leukopenia, atypical lym phocytosis)
o
Liver function studies (elevated alkaline phosphatase, transam inases, lactate dehydrogenase, bilirubin)
o
Urinalysis (hem oglobinuria, proteinuria)
o
Hem olysis profile (elevated reticulocyte count, decreased serum haptoglobin, hyperbilirubinem ia, elevated lactate dehydrogenase, hem oglobinuria)
o
Elevated blood urea nitrogen, creatinine suggests renal insufficiency
o
Elevated serum potassium m ay result from m assive hem olysis
Specific diagnostic studies: o
Peripheral blood sm ear:
Microscopy of Giem sa- or Wright-stained thin
Pa ge 6 7 3
sm ears
Parasites within RBCs can be round, oval, or pear shaped
Most com m on appearance is round (ring form s) to oval (pyriform ) rings with pale blue cytoplasm and red-staining nucleus; extracellular parasites m ay also be seen
Parasites in budding tetrad form ation (Maltese cross) are a rare, but highly suggestive finding of babesiosis.
Level of parasitem ia can range from 85%; higher levels m ore com m on in splenectom ized patients
o
Polym erase chain reaction:
Available for both Babesia m icroti and B. divergens
Higher sensitivity, equal specificity to blood sm ear
Useful in cases with very low levels of parasitem ia
P.125
o
Serology:
Indirect im m unofluorescent antibody assay
Serum antibody titer usually rises within a few weeks of infection; falls off slowly over m onths
Titers of 1:64 or higher considered positive (acute or prior infection); serology m ay rem ain positive for years
Titers of 1:256 or m ore are indicative of acute infections
Pa ge 6 7 4
Blood and urine cultures if presentation consistent with sepsis
Cerebrospinal fluid analysis if presentation suggestive of CNS infection
Imaging
Chest radiograph indicated for respiratory com plaints or evidence of hypoxia
Head CT m ay be indicated in setting of altered m ental status.
Abdom inal CT m ay be indicated in setting of splenom egaly and hypotension.
ECG indicated for ischem ic sym ptom s
Differential Diagnosis
Malaria
Other tickborne diseases:
o
Lym e disease
o
Ehrlichiosis
o
Rocky Mountain spotted fever
o
Colorado tick fever
o
Q fever
o
Tularem ia
o
Relapsing fever
Typhoid fever
Treatment Alert Acute respiratory failure, shock, and m yocardial infarction have been reported as com plications of babesiosis.
Pa ge 6 7 5
Pre Hospital
Ensure a patent airway
Provide supplem ental oxygen and ventilatory assistance as needed
If patient appears to be in shock, establish IV access and adm inister a fluid bolus of 0.9% norm al saline 500 m L (peds: 20 m L/kg) IV
Initial Stabilization
Airway m anagem ent, ventilatory support for patients with acute respiratory failure
Pulse oxim etry: hypoxia m ay be present in patients with severe disease.
IV access should be established in patients with evidence or risk factors for severe disease.
IV fluids
Pressor support for patients in shock
ED Treatment
Start em piric antibiotic therapy with two drug regim en in patients at risk with significant sym ptom s and/or shock
Clindam ycin plus quinine: o
Adverse effects (tinnitus, abdom inal com plaints) or treatm ent failure m ay lim it use.
Atovaquone plus o
Com parable efficacy to clindam ycin-quinine (65% versus 73%) with fewer adverse effects (12% versus 67%) and m ay be used as an alternative
Exchange transfusion as adjunctive therapy in patients with severe sym ptom s or risk factors for severe disease: o
Im m unodeficiency
o
splenia
o
Severe hem olysis
Pa ge 6 7 6
o
B. divergens infection
o
High-level parasitem ia (>10%)
Antibiotic therapy in known m ild or asym ptom atic cases due to risk of transm ission via blood transfusion or recrudescence, especially if risk factors for severe disease are present
Hem odialysis m ay be indicated for patients with acute renal failure
Treat fever with antipyretics
Medication (Drugs)
Acetam inophen: 325–1,000 m g (peds: 40–60 m g/kg/24h) PO/PR q4h–q6h PRN
Atovaquone: 750 m g (peds: 40 m g/kg/24h) PO b.i.d. × 7 days
Azithrom ycin: 500 m g (peds: 10 m g/kg up to m ax. 500 m g) PO on day 1, followed by 250 m g (peds: 5 m g/kg up to m ax. 250 m g) PO per day: 6 days
Clindam ycin: 300–600 m g (peds: 20 m g/kg/24h in 3 div. doses) PO q8h 7–10 days
Ibuprofen: 200–400 m g (peds: 20–40 m g/kg/24h) PO q6h–q8h PRN
Quinine: 650 m g (peds: 25 m g/kg/24h) PO q8h × 7–10 days o
Quinine is contraindicated in pregnancy
Follow-Up Disposition
Pa ge 6 7 7
Admission Criteria
Patients with severe disease: o
Severe, sym ptom atic anem ia
o
Jaundice
o
Renal insufficiency
o
Respiratory distress
o
DIC
o
Shock
Patients at risk of developing severe disease: o
Im m unodeficiency, asplenia
o
Severe hem olysis
o
B. divergens infection
o
High-level parasitem ia (>10%)
Patients requiring exchange transfusion
Discharge Criteria
Patients with asym ptom atic or m ild disease
Intact spleen
Able to tolerate oral m edications
Issues for Referral HIV patients m ore likely to relapse following initial treatm ent; should be referred for infectious disease follow up
References 1. Boustani MR, Gelfand JA. Babesiosis. Clin Infect Dis. 1996;22:611–615. 2. Boustani MR, Lepore TJ, Gelfand JA, et al. Acute respiratory failure in patients treated for babesiosis. Am J Respir Crit Care Med. 1994;149:1689–1691. 3. Dacey MJ, Martinez H, Raim ondo T, et al. Septic shock due to babesiosis. Clin Infect Dis. 2001;33:E37–E38. 4. Dorm an SE, Cannon ME, Telford SR III, et al. Fulm inant babesiosis
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treated with clindam ycin, quinine, and whole-blood exchange transfusion. Transfusion. 2000;40:375–380. 5. Gerber MA, Shapiro ED, Krause PJ, et al. The risk of acquiring Lym e disease or babesiosis from a blood transfusion. J Infect Dis. July 1994;170(1):231–234. 6. Hom er MJ, Aguilar-Delfin I, Telford SR III, et al. Babesiosis. Clin Microbiol Rev. 2000;13:451–469. 7. Krause PJ, Telford SR III, Spielm an A, et al. Concurrent Lym e disease and babesiosis. Evidence for increased severity and duration of illness. JAMA. 1996;275(Jun 5)(21):1657–1660. 8. Krause PJ, Telford SR III, Pollack RJ, et al. Babesiosis: an underdiagnosed disease of children. Pediatrics. June 1992;89(6) Pt 1: 1045–1048. 9. Krause PJ, Lepore T, Sikand VK, et al. Atovaquone and azithrom ycin for the treatm ent of babesiosis. N Engl J Med. 2000;343:1454–1458. 10. New DL, Quinn JB, Qureshi MZ, Sigler SJ. Vertically transm itted babesiosis. J Pediatr. 1997;131:163. 11. Meldrum SC, Birkhead GS, White DJ, et al. Hum an babesiosis in New York State: an epidem iological description of 136 cases. Clin Infect Dis. Decem ber 1992;15(6):1019–1023.
Codes ICD9-CM 08882
ICD10 B60.0
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Back Pain
Back Pain
Eric Legome
Basics Description
Low back pain (LBP): o
Refers to pain in the area between the lower rib cage and the gluteal folds, often with radiation into the thighs
Sciatica: o
Pain in the distribution of the lower lum bar spinal roots
o
Often accom panied by neurosensory and m otor deficits
Pain classification: o
Acute if zero to 6 weeks
o
Subacute if 6–12 weeks
o
Chronic if >12 weeks
Etiology
Nonspecific m usculoligam entous source including m uscle, ligam ent, fascia (great m ajority)
Herniation of the nucleus pulposus
Degenerative joints or discs
Spinal stenosis
Pa ge 6 8 0
Anatom ic abnorm alities—especially spondylolisthesis
Fractures from traum a and osteoporosis
Underlying system ic diseases (m inority): o
Neoplasm
o
Infections
o
Vascular (dissection, aneurysm and thom bosis)
o
Renal
o
Gastrointestinal
o
Pelvic organ pathology
Diagnosis Signs and Symptoms
Musculoligam entous: o
Poorly localized and dull back/gluteal pain without radiation past the knee
o
Usually there are no objective neurologic signs.
o
Back spasm is a variable and poorly reproducible finding.
Sciatica: o
Sharp, shooting, well-localized pain
o
Leg com plaints often greater than back
o
May present with:
Asym m etric deep tendon reflexes
Decreased sensation in a derm atom al distribution
Objective weakness
Massive central disc herniation (cauda equina syndrom e): o
Decreased perineal sensation
o
Urinary retention with overflow incontinence
o
Fecal incontinence
Pa ge 6 8 1
Infectious processes: o
Fever
o
Localized percussion tenderness of the vertebral bodies
Bony lesion: o
Continuous pain that does not change with rest
o
Constitutional sym ptom s
Vascular etiology: o
Severe, often “ripping or tearing― pain
o
May be associated with cold or insensate extrem ities
History
Can assist with focusing and narrowing differential diagnosis. Helps rule out concerning pathology for pain:
o
Intensity
o
Quality
o
Location and radiation
o
Onset
o
Exacerbating or rem itting factors
o
Social or psychological factors
o
Response to previous therapy
Risk factors for serious disease: o
Fever
o
Constitutional sym ptom s
o
Traum a
o
Age >60 years
o
History of cancer:
Especially those that m etastasize to bone
o
Chronic steroid use
o
IV drug use
o
Recent instrum entation or bacterem ia
o
Night pain
Pa ge 6 8 2
Physical Exam
Fever-suggests infectious etiology
Spasm or soft tissue tenderness is a poorly reproducible finding: o
Vertebral tenderness sensitive but nonspecific for infection
Straight leg raise—elevating the leg while supine reproduces sciatic sym ptom s:
o
Ipsilateral raise highly sensitive but not specific
o
Crossed leg raise highly specific but insensitive
Ankle and great toe dorsiflexion and ankle plantar flexion (L5, S1 nerve roots)
Ankle deep tendon reflexes (S1)
Derm atom al sensory exam ination
Essential Workup
Thorough history and physical, including detailed neurologic and vascular exam ination
No specific tests are needed for uncom plicated m usculoligam entous or sciatic pain without com plicating factors
Rapid diagnostic testing and vascular consultation for pain concerning aortic etiology
Tests Lab
Urinalysis for suspected: o
Urinary tract infection (UTI)
o
Pyelonephritis
o
Prostatitis
ESR o
Very sensitive, though nonspecific for infectious or
Pa ge 6 8 3
inflam m atory etiologies o
Used for screening if suspicion exists
Imaging
Lum bosacral radiograph: o
Significant traum a
o
Age >50 years (som e guidelines recom m end >60)
o
History or signs/sym ptom s of cancer
o
Fever
o
IV drug user
o
Pain at rest
o
Suspicion of ankylosing spondylitis or inflam m atory etiology
o
Pain that does not im prove after 4 weeks
MRI: o
Suspicion of abscess
o
Rapidly progressing neurologic sym ptom s
o
Urinary retention or fecal incontinence associated with back pain
Abdom inal CT or bedside ultrasound o
Suspicion of abdom inal aortic aneurysm (AAA)
o
CT secondary m odality for diagnosis of abscess, cancer or m assive disc when MRI unavailable.
o
Test of choice of im aging potential unstable fractures.
Chest CT or transesophageal TEE: o
Suspicion of aortic dissection or aneurysm
Differential Diagnosis
Spinal origins—in the m ajority of patients no precise anatom ic site is discovered: o
Musculoligam entous (m ajority)
o
Discogenic
o
Fracture
Pa ge 6 8 4
o
Spondylolisthesis
o
Ankylosing spondylitis
o
Osteom yelitis
o
Epidural abscess/hem atom a
o
Neoplasm
Nonspinal causes: o
AAA
o
Prostatitis
o
Upper UTI
o
Abdom inal neoplasm
o
Renal colic
o
Aortic dissection
P.127
Treatment Pre Hospital
Traum a patients with acute back pain should be im m obilized on a backboard until an unstable fracture can be ruled out.
Rapid transport with IV access for any patient with concerns of vascular etiology
ED Treatment
NSAIDs for m usculoligam entous pain, renal colic: o
Initial treatm ent of choice, although acetam inophen m ay be preferred due to its preferable side-effect profile.
o
No agent has definitive benefits over others
Pa ge 6 8 5
o
Recom m end using cost and dosing schedules as guide
Muscle relaxants: o
Possible benefits m ust be balanced by side effects, m ostly sedation and dry m outh
o
Cyclobenzaprine
o
Methocarbam ol
o
Carisoprodol
Efficacy of benzodiazepines for back pain is rarely studied: o
No clear evidence of utility.
Lim ited course of narcotic analgesics for severe pain not relieved by anti-inflam m atory agents or renal colic
Spinal m anipulation: o
A short course ( Table o f C o ntents > Barbiturates, Po iso ning
Barbiturates,
Poisoning Sean Patrick Nordt Shaun D. Carstairs David A. Tanen
Basics Description
Class of sedative-hypnotic agents
Derivatives of barbituric acid
Mechanism : o
Enhances activity of γ-am inobutyric acid (gam m a-am inobutyric acid [GABA])
o
At high levels, can directly open GABA-A associated calcium channels
o
May inhibit presynaptic release of excitatory neurotransm itters
o
Direct m yocardial depression
o
Inhibition of vascular sm ooth m uscle tone
Diagnosis
Pa ge 6 9 8
Signs and Symptoms
CNS: o
Lethargy
o
Slurred speech
o
Incoordination
o
Ataxia
o
Com a (can m im ic brain death)
o
Loss of reflexes
Cardiovascular: o
Hypotension
o
Bradycardia
Ophthalm ologic: o
Miosis (generally associated with deep com a)
o
Nystagm us
o
Dysconjugate gaze
Other: o
Respiratory depression
o
Hypotherm ia
o
Bullae or “barb blisters―
Essential Workup
Check vital signs and gag reflex
Finger stick glucose
Oxygen saturation m onitor/ABG
ECG and continuous cardiac m onitoring
Barbiturate poisoning can m im ic brain death: o
Cannot pronounce patient until barbiturate poisoning has been ruled out in patients in whom it is suspected
Tests Lab
Electrolytes, blood urea nitrogen/creatinine, glucose:
Pa ge 6 9 9
o
Calculate anion gap
Urinalysis: o
For m yoglobin
o
For crystalluria (Prim idone)
Creatine phosphokinase for evidence of rhabdom yolysis
Urine toxicology screen
Obtain serum phenobarbital level (if suspected)
Acetam inophen and salicylate levels if suspected suicide attem pt
CBC for other etiologies of altered m ental status
Thyroid function tests
Imaging
CT scan of head for altered m ental status
Chest radiograph for evidence of aspiration
Diagnostic Procedures/Surgery Lum bar puncture for altered m ental status
Differential Diagnosis
Sedative-hypnotic poisoning
Carbon m onoxide poisoning
CNS infections
Space-occupying lesions of the head
Hypoglycem ia
Urem ia
Electrolyte im balance (i.e., hyperm agnesem ia)
Postictal state following seizure
Hypothyroidism
Liver failure
Psychiatric illness
Pa ge 7 0 0
Treatment Pre Hospital
Moderate to severe poisonings require param edic transport.
Intubation often necessary because of respiratory depression or loss of gag reflex
IV access and supplem ental oxygen
Hypotension often requires IV fluids
Initial Stabilization
ABCs: o
Adm inister supplem ental oxygen
o
Severe poisonings usually require endotracheal intubation
0.9% NS: o
Hypotensive patients require 1–2 L IV fluid resuscitation
o
Pressor support m ay be necessary for refractory hypotension
Activated charcoal effectively binds barbiturates and m ay decrease system ic absorption
P.131
ED Treatment
Adm inister one dose of activated charcoal: o
Consider “gut dialysis― with repeated dose activated charcoal (without sorbitol) given q2h–q4h (as long as bowel sounds are present).
Rewarm patient if hypotherm ic (see hypotherm ia chapter).
Treat hypotension resistant to IV fluid bolus with
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vasopressors.
Alkalinize the urine for phenobarbital intoxication to increase excretion (not effective for shorter-acting barbiturates).
Treat hyperkalem ia (from m uscle breakdown) with calcium , sodium bicarbonate, insulin and glucose, and/or potassium -binding agents.
Consider hem odialysis if patient has: o
Decreased or no renal function
o
Prolonged com a
o
Serum phenobarbital level >100 m g/dL
o
Refractory hypotension
Repeat phenobarbital level in 2–4 hours to determ ine whether level is increasing.
Medication (Drugs)
Activated charcoal: 1 g/kg PO
Dopam ine: 5–10 m cg/kg/m in titrating to desired effect (to m ax. of 20 m cg/kg/m in)
Sodium bicarbonate: o
Bolus: 1–3 am pules (44 m Eq/am pule) IV over 20–30 m inutes (peds: 1–2 m Eq/kg/dose)
o
Maintenance: 2–3 am pules (100–150 m Eq) in 1 L D 5 W at 150–200 m L/h (peds: 2x m aintenance fluid requirem ents) to achieve a blood pH of 7.45–7.50 and m aintain urine output of 2 m L/kg/h (m onitor serum potassium closely)
Follow-Up
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Disposition Admission Criteria Intensive care unit adm ission for:
Com a
Respiratory depression
Hypotension
Hypotherm ia
Rhabdom yolysis
Discharge Criteria Asym ptom atic after m inim um of 6 hours of observation with two consecutive subtoxic phenobarbital levels before discharge
References 1. Frenia ML, Schauben JL, Wears RL, et al. Multiple-dose activated charcoal com pared to urinary alkalinization for the enhancem ent of Phenobarbital elim ination. J Toxicol Clin Toxicol. 1996;34:169–175. 2. Lee DC. Sedative-hypnotic agents. In: Goldfrank LR, et al., eds. Goldfrank's Toxicologic Em ergencies., 7th ed. New York: McGraw-Hill, 2002;929–945. 3. Pond SM, Olson KR, Osterloh J, et al. Random ized study of the treatm ent of phenobarbital overdose with repeated doses of activated charcoal. JAMA. 1984;251:3104–3108.
Miscellaneous See Also: Benzodiazepine, Poisoning; Hypotherm ia
Codes ICD9-CM 967.0
ICD10
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T42.3
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Baro traum a
Barotrauma
Peter J. Park
Basics Description Injury resulting from the expansion or contraction of gases in an enclosed space
Etiology Mechanism
Tissue dam age results when a gas-filled space does not equalize its pressure with external pressure.
Boyle's law: At a constant tem perature, pressure (P) is inversely related to volum e (V): o
PV = K (constant) or P 1 V 1 = P 2 V 2
o
As pressure increases/decreases, volum e decreases/increases.
Solid and liquid-filled spaces distribute pressure equally.
Volum e changes experienced during diver ascent are greatest in the few feet nearest the surface.
Gas-filled cavities in the body are subject to expansion/contraction: o
Middle ear:
Barotraum a of descent
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Most com m on type of barotraum as
Seen in 30% of inexperienced divers and 10% of experienced divers
Inadequate equalization of pressure between m iddle ear and external ear canal
Eustachian tube provides sole route of pressure equalization for m iddle ear.
Inadequate clearance via eustachian tube leads to increasingly negative pressure gradient across tym panic m em brane (TM)
o
External ear:
Barotraum a of descent
Pressure cannot equalize throughout canal because of blockage, and relative intracanal vacuum is created as pressure differential across obstruction increases.
o
Inner ear:
Barotraum a of descent
Results from forceful attem pts at equalizing m iddle ear pressure (Valsalva, Frenzel m aneuvers)
Increased m iddle ear pressure can raise intracranial pressure and cause rupture of round or labyrinth windows, allowing perilym ph to enter m iddle ear.
o
Paranasal sinus:
Barotraum a of descent
Nasal ostia act as valves to regulate sinus pressure.
If ostia fail to allow pressure equalization, congestion, edem a, and hem orrhage can occur.
o
External objects:
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Air pockets in dive suit/m ask expand and contract.
o
Teeth;
o
Air trapped inside a filling
GI:
Barotraum a of ascent
Swallowed air in GI tract expands as external pressure decreases.
o
Pulm onary:
Barotraum a of ascent
Lungs expand against closed glottis (breath-holding).
Can lead to pulm onary rupture
Potential arterial gas em bolism (see Arterial Gas Em bolism )
Divers with decreased lung com pliance/increased lung volum es at increased risk (chronic obstructive pulm onary disease [COPD], asthm a)
Diagnosis Signs and Symptoms
Middle ear (barotitis m edia): o
Begins as clogged sensation
o
Increasingly painful as pressure differential increases across TM
o
Progresses to rupture of TM
o
TM appearance:
Progresses from TM congestion to edem a to hem orrhage to TM rupture
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External ear: o
May result from tight-fitting hood, earplug or earwax occluding canal
o
Auditory canal m ucosa becom es edem atous, then hem orrhagic, and ultim ately tears
Inner ear: o
Sudden, severe vertigo
o
Tinnitus
o
Sensineural hearing loss in affected ear
Paranasal sinuses (barosinusitis): o
Sinus congestion
o
Pain
o
Epistaxis
Facial: o
Occlusive dive m ask: conjunctival hem orrhage, facial edem a, and swelling
Extrem ities: o
Tight-fitting dive suit: edem a and erythem a of the skin at locations of air pockets
Teeth (barodontalgia): o
Severe tooth pain: possible air trapped in fillings
GI (aerogastralgia): o
Excessive belching
o
Flatulence
o
Abdom inal distention
Pulm onary (pulm onary barotraum a [PBT], or pulm onary overpressurization syndrom e): o
Dyspnea: “the chokes―
o
Cough productive with frothy red sputum
o
Subcutaneous em physem a
o
Delayed sym ptom s include bull neck appearance, dysphagia, changes in voice character
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Essential Workup
Head, ears, eyes, nose and throat (HEENT) exam with particular attention paid to TM and auditory canal to determ ine if rupture has occurred
Pulm onary exam looking for signs of subcutaneous em physem a and pneum othorax
Neurologic exam looking for signs of inner ear pathology
Tests Lab Arterial blood gas (ABG) for pulm onary sym ptom s
Imaging
Sinus im aging: o
CT
o
Plain film s
Chest radiograph for pneum othorax
Abdom inal series (upright, decubitus) for free air from a ruptured viscus
Differential Diagnosis
Decom pression sickness
Otitis m edia
Otitis externa
Sinusitis
P.133
Treatment
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Pre Hospital
Cautions: o
For barotraum a of descent, unless air-filled cavity has ruptured, no progression of disease on return to norm al atm ospheric pressure is to be expected.
o
If patient requires air evacuation, m aintain air cabin pressure at 1 atm or fly below 1,000 feet to avoid aggravating barotraum as.
Initial Stabilization Airway, breathing, and circulation m anagem ent (ABCs):
One hundred percent oxygen for ill-appearing patients
Intubation for patients with subcutaneous em physem a of neck
Im m ediate needle thoracostom y for evidence of tension pneum othorax
ED Treatment
Establish IV access for unstable patients.
Control bleeding from ear or nose.
Decongestants for m iddle ear or sinus congestion
Antibiotics with TM or sinus rupture
Analgesics
Medication (Drugs)
Am oxicillin: 250–500 m g (peds: 40 m g/kg/24 h) PO t.i.d.
Oxym etazoline 0.05% (Afrin): 2 or 3 drops/sprays per nostril b.i.d. for 3 days
Pseudoephedrine (Sudafed): 60 m g (peds: 6–12 years old, 30 m g; 2–5 years old, 15 m g per dose) PO q4h–q6h
Pa ge 7 1 0
Trim ethoprim -sulfam ethoxazole (Bactrim DS): 1 tablet double strength (160 m g/800 m g) (peds: 40 m g/200 m g per 5 m L, 5 m L/10 kg per dose) PO b.i.d.
Follow-Up Disposition Admission Criteria
Pulm onary barotraum as (PBTs)
Inner ear barotraum a with round window rupture or severe vertigo
Discharge Criteria
Most non-PBT
Ear, nose, and throat (ENT) follow-up for severe TM or sinus pathology
References 1. Becker GD, Parell GJ. Barotraum a of the ears and sinuses after scuba diving. Eur Arch Otorhino. 2001;258(4):159–163. 2. Kizer KW. Diving m edicine and barotraum a. In: Auerbach PA, ed. Wilderness Medicine. 4th ed. St. Louis, MO: Mosby; 2001. 3. Moon RE, Gorm an DF. Treatm ent of decom pression disorders. In: The Physiology and Medicine of Diving. 5th ed. Philadelphia: WB Saunders; 2003. 4. Raym ond LW. Pulm onary barotraum a and related events in divers. Chest. 1995;107:1648–1652. 5. Tetzlaff K, et al. Risk factors for pulm onary barotraum a in divers. Chest. 1997;112(3): 654–659.
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Miscellaneous SEE ALSO: Arterial Gas Em bolus; Decom pression Sickness; Hyperbaric Oxygen Therapy
Codes ICD9-CM 993.2 Barotraum a 993.2 Odontalgia 993.0 Otitic 993.1 Sinus
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Bartho lin Abscess
Bartholin Abscess
Marilyn Althoff Mark Mandell
Basics Description
The Bartholin glands are located inferiorly on either side of vaginal opening: o
Ducts open on sides of labial vestibule.
Obstruction of duct produces a usually painless cyst: o
Infection of cyst results in abscess form ation.
Epidemiology Prevalence Most com m on in wom en aged 20–40 years
Etiology
Anaerobic and aerobic m icroflora norm ally found in vagina:
o
Bacteroides species
o
Peptostreptococcus species
o
Escherichia coli
o
Other Gram -negative organism s
Occasionally Neisseria gonorrhoeae and Chlam ydia trachom atis
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Diagnosis Signs and Symptoms
Swollen, painful labia
Tender, fluctuant m ass on posterolateral m argin of vestibule of vagina
Warm th, erythem a
Essential Workup Diagnosis based on findings of tender, localized, fluctuant m ass in region of Bartholin gland
Tests Lab
Culture m aterial from abscess for gonorrhea and chlam ydia.
Culture cervix for gonorrhea and chlam ydia.
Differential Diagnosis
Bartholin cyst
Carcinom a of Bartholin gland (rare)
Perineal hernia
Treatment ED Treatment
Prom pt incision and drainage using local anesthesia with patient in lithotom y position
Narcotic analgesia for patient com fort
Alternative approaches include:
Pa ge 7 1 4
o
Sim ple incision and drainage
o
Word catheter m ethod
o
Marsupialization
Antibiotics not necessary after incision and drainage: o
If m ild cellulitis present or patient im m unocom prom ised, broad-spectrum coverage m ay be started.
o
If sexually transm itted disease suspected, treat with antibiotics.
Sim ple incision and drainage: o
After local anesthesia, palpate abscess between thum b and index fingers.
o
Spread vulva apart and m ake stab incision on m ucosal surface of abscess, parallel to hym enal ring.
o
When incising abscess, two tissue layers m ust be penetrated:
First the labial m ucosa
Then abscess wall
Free flow of pus indicates penetration of abscess wall.
o
Pack wound with gauze.
o
Follow up in 24–48 hours for rem oval of packing.
o
Start sitz baths after 24 hours.
o
Consider referral for m arsupialization to avoid recurrence.
Word catheter m ethod: o
Use sm all, inflatable, bulb-tipped Word catheter to treat abscess.
o
May avoid recurrence and m ake m arsupialization unnecessary
o
Stab wound is m ade as with sim ple incision and drainage:
Pa ge 7 1 5
It should be just large enough to easily adm it catheter so that balloon does not fall out after inflation.
P.135
o
After inserting bulb tip of catheter, inflate balloon by injecting 2–4 m L water using 25-gauge needle (to m inim ize size of puncture):
Overinflation m ay cause patient discom fort,
Rem edied by withdrawing som e water from balloon
o
Sitz baths m ay be started after 24 hours.
o
Follow-up in 2–4 days.
o
Leave catheter in place for 6–8 weeks until epithelialization is com plete; after device is rem oved, gland resum es norm al function.
o
Com m on for catheter to fall out prem aturely:
If this occurs, catheter m ay be reinserted or abscess can heal as with sim ple incision and drainage.
Marsupialization: o
Procedure allows for a perm anent fistula by suturing wound edges of abscess cavity to edges of labial m ucosa:
Technically m ore challenging in ED and better reserved for specialist.
o
Excise an ellipse of labial m ucosa that overlays cyst cavity.
o
Incision and drainage of abscess
o
Evert edges of abscess and suture them to labial epithelium using absorbable suture:
Pa ge 7 1 6
Opening will shrink but rem ain patent.
Packing is not needed.
o
Start sitz baths in 24–48 hours.
o
Follow-up within 1 week.
Medication (Drugs) Broad-spectrum coverage:
Am oxicillin/clavulanic acid: 875 m g PO b.i.d. for 5 days with m etronidazole 500 m g PO b.i.d. for 5 days
Ciprofloxacin: 500 m g PO b.i.d. for 5 days with m etronidazole 500 m g PO b.i.d. for 5 days
Follow-Up Disposition Admission Criteria
Sepsis
Significant cellulitis
Evidence of necrotizing infection
Discharge Criteria Well-appearing patients m ay be discharged with designated follow-up plan.
References 1. Aghajanian A. Bartholin's duct abscess and cyst: a case control study. South Med J. 1994;87:26–29. 2. Brook I. Aerobic and anaerobic m icrobiology of Bartholin's abscess. Surg Gynecol Obstet. 1989;169:32–34. 3. Van Bogaert LJ. Managem ent of Bartholin's abscess. World Health
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Forum . 1997;18:(2)200–201. 4. Word B. Office treatm ent of cyst and abscess of Bartholin's gland duct. South Med J. 1968;61:514–518. 5. Zeger W, Holt K. Gynecologic infections. Em erg Med Clin North Am . 2003;21(3):631–648.
Codes ICD9-CM 616.3 Abscess of Bartholin gland
ICD10 N75.1 Abscess of Bartholin gland
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Bell's Palsy
Bell's Palsy
Robert F. McCormack Richard S. Krause
Basics Description
Acute, idiopathic peripheral palsy of CN VII (facial nerve)
Com plete recovery in 85% of cases without treatm ent
Degree of deficit correlates with prognosis:
o
Com plete lesions have poorest prognosis.
o
Partial lesions often have excellent results.
Recovery usually begins within 2 weeks (often taste returns first) and is com plete by 2–3 m onths: o
Advanced age and slow recovery are poor prognosticators.
Affects m en and wom en equally
Age predom inance between the third and fifth decade (m ay occur at any age)
Incidence 15–40 per 100,000 per year
Etiology
Innervation to each side of forehead is from both m otor cortices: o
Unilateral cortical processes do not com pletely disrupt m otor activity of forehead.
Pa ge 7 1 9
o
Only peripheral or brainstem lesion can interrupt m otor function of just one side of forehead.
Idiopathic by definition, but viral cause (particularly herpes sim plex) suspected
Lym e disease, infectious m ononucleosis (Epstein-Barr virus [EBV] infection), varicella-zoster infections, and others m ay cause peripheral seventh nerve palsy.
Mechanism : edem a and nerve degeneration within stylom astoid foram en
Diagnosis Signs and Symptoms
Sudden onset of unilateral facial droop, incom plete eyelid closure, and loss of forehead m uscle tone: o
Maxim al deficit by 5 days in alm ost all cases (2 days in 50%)
If forehead m uscle tone is not lost, a central lesion is strongly im plied (i.e., this is not Bell's palsy)
Tearing (68%) or dryness of eye (16%) and less frequent blinking on affected side
The Bell phenom enon (upward rolling of the eye on attem pted lid closure) m ay be seen.
Subjective “num bness― of the affected side
Abnorm al taste, drooling
Hyperacusis (sensitivity to loud sounds)
Fullness or pain behind m astoid
Viral prodrom e frequently reported
Essential Workup
Diagnosis is clinical and based on history and physical
Pa ge 7 2 0
exam .
Motor weakness isolated to seventh nerve distribution: o
Involves both upper and lower face
An otherwise norm al neurologic exam including all cranial nerves and extrem ity m otor function
Tests Lab
Not helpful in diagnosis of Bell's palsy
Lym e titers are useful when Lym e disease is suspected or in endem ic area
Tests for m ononucleosis (CBC, Monospot) if EBV infection suspected
Imaging
Not helpful in diagnosis of Bell's palsy
CNS im aging (CT, MRI) useful if CNS pathology is suspected
Differential Diagnosis
Brainstem events (m ass, bleed, infarct) affecting CN VII alm ost always involve CN VI (abnorm al EOM) and m ay affect long m otor tracts: o
There have been (rare) case reports of isolated CN VII palsy from brainstem disease.
Lym e disease: history of tick bite, erythem a m igrans rash, or endem ic area
Zoster (Ram say-Hunt syndrom e): Look for herpetic vesicles, inquire about tinnitus or vertigo.
Infectious m ononucleosis: look for pharyngitis, posterior cervical adenopathy
Tum ors: parotid, bone, or m etastatic m asses, acoustic neurom a (deafness)
Pa ge 7 2 1
Traum a: Skull fracture or penetrating facial injury m ay dam age CN VII.
Middle ear or m astoid surgery or infection, cholesteatom a
Meningeal infection
Guillain-Barré syndrom e: other neurologic deficits (e.g., ascending m otor weakness or dim inished deep tendon reflexes [DTRs] present)
Basilar artery aneurysm ; other CN deficits should be present.
Bilateral peripheral CN VII palsy: Consider m ultiple sclerosis, sarcoid, leukem ia, and Guillain-Barré idiopathic (Bell's) palsy m ay be bilateral in rare cases.
Bell's palsy m ay reoccur; treatm ent is unchanged.
P.137
Treatment Initial Stabilization Patients with an isolated peripheral CN VII palsy are stable.
ED Treatment
Oral steroids m ay hasten recovery if started within 1 week of onset: o
Com plications of therapy are rare and treatm ent is recom m ended by m any authors.
o
Som e m eta-analyses question efficacy.
Corneal dam age m ay result from incom plete eyelid closure: o
Lubricating and hydrating ophthalm ic preparations is
Pa ge 7 2 2
essential/ o
Eyelid taping at night
Acyclovir with steroids m ay be effective in im proving functional nerve recovery: o
Initiate within 72 hours of sym ptom onset.
Suspected Lym e disease should be treated with doxycycline or am oxicillin.
Surgical decom pression m ay be indicated for com plete lesions that do not im prove; this is controversial.
Medication (Drugs)
Acyclovir: 400 m g five tim es per day PO for 7 days (peds: no data to support its use) or valacyclovir 1 g PO for 7 days
Lacri-Lube: at bedtim e and PRN; dryness/irritation in affected eye (or equivalent)
Prednisone: 30–40 m g PO b.i.d. (or 60 m g PO daily) for 5 days, then taper over 5 days; total 10 days of therapy (peds: 2 m g/kg/d PO [m ax. 60 m g])
Follow-Up Disposition Admission Criteria Isolated peripheral CN VII palsy does not require adm ission.
Discharge Criteria
Isolated peripheral CN VII palsy m ay be treated on outpatient basis.
Follow-up should be within 1 week.
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References 1. Adour K, et al. Bell's palsy treatm ent with acyclovir and prednisone com pared with prednisone alone. Ann Otol Rhinol Laryngol. 1996;105:371–378. 2. Austin JR, et al. Idiopathic facial nerve paralysis: a random ized double blind controlled study of placebo versus prednisone. Laryngoscope. 1993;103:1326–1333. 3. Gilden D. Bell's palsy. N Engl J Med. 2004; 351:1323–1231. 4. Grogan PM, et al. Practice param eter: steroids, acyclovir, and surgery for Bell's palsy (an evidence-based review). Neurology. 2001; 56(7):830–836. 5. Ram sey JR, et al. Corticosteroid treatm ent for idiopathic facial nerve paralysis: a m eta-analysis. Laryngoscope. 2000;110:335–341. 6. Salinas R, Alvarez G, Ferreira J. Corticosteroids for Bell's palsy (idiopathic facial paralysis). Cochrane Database Syst Rev. 2004;4:CD001942.
Codes ICD9-CM 351.0
ICD10 G51.0
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Benz o diaz epine, Po iso ning
Benzodiazepine, Poisoning Sean Bryant
Basics Description
Acts to potentiate activity of γ-am inobutyric acid (GABA; m ajor inhibitory neurotransm itter) by binding to its own specific site
Facilitates GABA binding to its site
Results in chloride influx, m em brane hyperpolarization, and inhibition of cellular excitation: o
Highly protein bound
o
Large V d
o
Hepatic m etabolism
o
Duration of action is inversely proportional to lipophilicity.
o
Duration of lorazepam > diazepam > m idazolam .
Diagnosis Signs and Symptoms
CNS:
Pa ge 7 2 5
o
Sedation/drowsiness
o
Slurred speech
o
Com a
o
Delirium
o
Midposition to sm all pupils
Neurom uscular: o
Incoordination
o
Slowed voluntary m ovem ents
o
Ataxia
o
Hypotension
o
Hyporeflexia/areflexia
Cardiovascular: o
Mild depression
o
Rare fatality
Respiratory: o
Mild depression
o
Less depression versus barbiturates
o
Short acting and IV m ay produce depression.
GI: o
Nausea, vom iting, diarrhea
Other: o
Hypotherm ia
o
Com plications m ay include cerebral hypoxia, rhabdom yolysis, pressure-induced neuropathies.
o
No long-term organ toxicity
Essential Workup Diagnosis based on:
History of ingestion or recent injection
Clinical findings associated with CNS depression
No response to naloxone
Tests
Pa ge 7 2 6
Lab
Pulse oxim etry
Electrolytes, BUN, creatinine, serum glucose
Urinalysis (UA) for m yoglobin when com a present
Core body tem perature
Arterial blood gas (ABG)
Qualitative urine screen: o
Confirm s exposure m any tim es, but does not indicate or m easure intoxication
o
False-negative test results reported
o
Qualitative im m unoassays detect only benzodiazepines (BZs) that are m etabolized to oxazepam .
o
Those that do not produce this m etabolite (clonazepam , lorazepam , m idazolam , alprazolam ) are not detected on qualitative screen.
o
Do not correlate with clinical state
o
Serum levels not acutely practical
o
Clinical signs and sym ptom s m ore im portant than theoretic LD 5 0 or serum levels
Alcohol(s) level
Barbiturate level
Acetam inophen and salicylate levels
Pregnancy test
Imaging
ECG
Chest radiograph for aspiration pneum onia
Differential Diagnosis
Drugs and toxins causing decreased level of consciousness: o
Hypoglycem ics
o
Other sedative-hypnotics (barbiturates)
Pa ge 7 2 7
o
Antidepressant-antipsychotic
o
Narcotics
o
Anticonvulsants
o
Carbon m onoxide/cyanide
o
Alcohols
Nontoxic m edical condition: o
Hypoxem ia
o
Hypotherm ia
o
Head traum a (intracranial bleeding)
o
Infection (m eningitis or encephalitis)
o
Electrolyte and m etabolic disturbances
Treatment Pre Hospital
Attention to airway and breathing
Cardiac m onitor
IV access
Rapid glucose determ ination
Bring in pill bottles/pills in suspected overdose.
Initial Stabilization
Airway, breathing, and circulation m anagem ent (ABCs): o
Secure airway and assist ventilation with supplem ental oxygen to prevent hypoxem ia and shock.
o
IV access with 0.9% norm al saline (NS)
o
Cardiac m onitor
Adm inister naloxone, thiam ine, and dextrose if altered m ental status.
P.139
Pa ge 7 2 8
ED Treatment
Gastric lavage considered only when presents within 1 hour of life-threatening ingestion with protected airway
Activated charcoal (AC) PO or via nasogastric tube (NGT)
No role for diuresis, dialysis, or charcoal hem operfusion
Flum azenil (FZ): o
Com petitive BZ-receptor inhibitor: rapidly reverses BZ-induced com a and respiratory depression
o
Onset within 1–2 m inutes; peak at 6–10 m inutes; duration 1–2 hours (repeated dosing m ay be indicated)
o
Efficacy dependent on dose of BZ being antagonized and dose of FZ used
o
Do not adm inister em pirically as part of any standard protocol therapy or in unknown poisoned patient.
o
Might help avert need of airway intubation
o
May be beneficial in shortening hospital stay or as diagnostic m aneuver
o
Indications include isolated BZ overdose in nonhabituated user.
o
Useful to reverse iatrogenic poisoning (conscious sedation)
o
Contraindications include:
Coingestions that m ight lower seizure threshold (tricyclic antidepressants [TCAs])
Seizure activity
Allergy
Neurom uscular blockade
Do not use if hypotension, hypoxia, dysrhythm ias, or increased intracranial pressure
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May precipitate withdrawal state
Medication (Drugs)
AC: 1–2 g/kg PO/NG (ideal 10:1 ratio)
Dextrose: D 5 0 W one am pule: 50 m L or 25 g (peds: D 2 5 W 2–4 m L/kg) IV
FZ (Rom azicon): o
Initial: 0.2 m g IV over 30 seconds (adult)
o
If no response: 0.3 m g IV after 30 seconds
o
If still no response: 0.5 m g IV and repeat every 1 m inute if needed, to m ax. dose of 3 m g
o
Continuous infusion at 0.2–1.0 m g/h if m ultiple repeated doses required to m aintain response
o
Pediatric dosing not established; recom m ended starting dose is 0.01 m g/kg IV, titrate to m ax. dose of 1 m g, continuous infusion at 0.005–0.01 m g/kg/h
Naloxone (Narcan): 2 m g (peds: 0.1 m g/kg) IV or IV initial dose
Thiam ine (vitam in B 1 ): 100 m g IV/IM
Follow-Up Disposition Admission Criteria
Persistent or profound CNS depression
Cardiovascular or respiratory com prom ise
Coingestants with potential delayed toxicity
Discharge Criteria
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Discharge after 4- to 6-hour observation period if no signs or sym ptom s of BZ poisoning develop.
If FZ used, observe for additional 2–4 hours for recurrent sedation.
Issues for Referral Intentional overdose:
Psychiatry consultation
References 1. Farrell SE. Benzodiazepines. In: Ford MD, Delaney KA, Ling LJ, et al, eds. Clinical Toxicology. Philadelphia: WB Saunders; 2001. 2. Lee DC. Sedative-hypnotic agents. In: Goldfrank LR, ed. Goldfrank's Toxicologic Em ergencies. New York: McGraw-Hill; 2002. 3. Leikin J, Paloucek F. Benzodiazepines, qualitative, urine. In: Poisoning and Toxicology Handbook. Hudson, OH: Lexi-Com p; 2002. 4. Rasanen I, Ojanpera I, Vuori E. Quantitative screening for benzodiazepines in blood by dual-colum n gas chrom atography and com parison of the results with urine im m unoassay. J Anal Toxicol. 2000;24:46–53. 5. Spivey WH. Flum azenil and seizures: analysis of 43 cases. Clin Ther. 1992;14:292. 6. Spivey WH, Roberts JR, Derlet RW. A clinical trial of escalating doses of flum azenil for reversal of suspected benzodiazepine overdose in the em ergency departm ent. Ann Em erg Med. 1993; 22:1813–1821. 7. Weinbroum A, et al. The use of flum azenil in the m anagem ent of acute drug poisoning: a review. Intensive Care Med. 1991;17:32–38.
Codes ICD9-CM 969.4
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ICD10 T42.4
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Beta-Blo cker Po iso ning
Beta-Blocker
Poisoning Janet Eng
Basics Description Normal Physiology Cardiovascular: β 1 -receptors:
ATP converted to cAMP by adenyl cyclase with stim ulation of β-receptors
cAMP activates protein kinase, which phosphorylates proteins of the sarcoplasm ic reticulum .
Sarcoplasm ic reticulum releases calcium .
Excitation-contraction coupling occurs.
Effects of β-Blockers
Cardiovascular: o
Decreased excitation/contraction
o
Mem brane stabilizing activity
o
Sodium channel blockade causes a prolongation of the QRS com plex (with som e agents).
o
Prolongation of QTc interval leading to ventricular dysrhythm ias (with som e agents)
o
Intrinsic sym pathom im etic activity
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o
Partial agonist properties (with som e agents)
Neurologic: o
CNS effects with the lipophilic agents (propranolol, m etoprolol, labetalol)
Diagnosis Signs and Symptoms
Cardiovascular: o
Hypotension
o
Bradycardia
o
Cardiac conduction delays
o
Heart block
o
Heart failure
o
Electrical m echanical dissociation
o
Loss of β-selectivity in overdose settings
Neurologic: o
Com a
o
Seizures
Pulm onary: o
Bronchospasm
o
Pulm onary edem a
Metabolic: o
Hypoglycem ia
Essential Workup
With unknown ingestion: suspect β-blocker poisoning with bradycardia/hypotension
ECG: o
Conduction delays
o
First-, second-, or third-degree heart block
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o
Bradycardia
Tests Lab
CBC
Electrolytes, BUN, creatinine, glucose
Differential Diagnosis
Calcium channel blocker toxicity
Clonidine toxicity
Digoxin toxicity
Acute m yocardial infarction with heart block
Treatment Pre Hospital CAUTIONS:
Transport pills and pill bottles when overdose suspected.
Initial Stabilization
Airway, breathing, circulation (ABCs): o
Airway protection as indicated by m ental status
o
Supplem ental oxygen as needed
o
0.9% norm al saline (NS) IV access
o
Close hem odynam ic m onitoring
Naloxone and thiam ine if altered m ental status
Accu-Chek and treat hypoglycem ia with D 5 0 W.
Treat prolonged seizures with benzodiazepines.
ED Treatment Goals
Heart rate >60 beats per m inute
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Systolic BP >90 m m Hg
Adequate urine output
Im proving level of consciousness
GI Decontamination
Syrup of ipecac is contraindicated in the em ergency departm ent.
Consider lavage with Ewald tube if ingestion within 1 hour: o
Propranolol m ay cause esophageal spasm producing difficulty with passage and rem oval of gastric lavage tube
Activated charcoal helpful especially in the presence of coingestants
Bradycardia/Hypotension
Atropine: o
Initial agent
o
Low success rate
Glucagon: o
Adm inister if atropine does not increase heart rate.
o
Prom otes cAMP production through a receptor site other than the β-receptor
o
May cause nausea and vom iting
o
Mix with NS or D 5 W
IV fluids: o
Adm inister cautiously in the hypotensive patient
o
Swan-Ganz catheter or central venous pressure (CVP) m onitoring to help follow volum e status
Am rinone: o
Use in conjunction with glucagon to treat sym ptom atic sustained bradycardia.
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Pressor agents: o
Initiate when sym ptom atic hypotension/bradycardia persists after atropine/glucagon.
o
Use invasive m onitoring to help guide therapy.
o
Utility m ay be lim ited owing to β-blockade:
o
Isoproterenol (nonselective β-agonist):
o
Higher doses m ay be required.
Titrate for blood pressure (BP) and heart rate
Epinephrine (potent α- and β-receptor agonist):
BP increases as a result of direct m yocardial stim ulation, increase in heart rate, and vasoconstriction
o
Use if no BP response with isoproterenol
High-dose dopam ine
Sodium bicarbonate: o
In theory, this is used if there is evidence of prolongation of QRS >100 m s owing to som e of the β-blockers also causing sodium channel blockade leading to a prolonged QRS.
o
Not routinely adm inistered for all β-blocker toxicities
Electrical pacing: when other treatm ent options have failed
Insulin: o
Prom otes m ore efficient m yocardial m etabolism
o
May be considered as a treatm ent option
Enhanced Elimination Hem odialysis helpful with water-soluble β-blocking agents:
Nadolol
Atenolol
Sotalol
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Medication (Drugs)
Activated charcoal: 1 g/kg PO
Am rinone: loading dose 0.75 m g/kg; m aintenance drip 2–20 µg/kg/m in; titrate for effect
Atropine: 0.5 m g (peds: 0.02 m g/kg) IV; repeat 0.5–1.0 m g IV (peds: 0.04 m g/kg)
Dopam ine: 2–20 µg/kg/m in IV
Dextrose: D 5 0 W 1 am pule (50 m L or 25 g; peds: D 2 5 W 2–4 m L/kg) IV
Epinephrine: 2 µg/m in (peds: 0.1 µg/kg/m in); titrate to effect
Glucagon: 3.5–5 m g IV (peds: 0.03–0.1 m g/kg) bolus followed by 70-µg/kg/h infusion
Isoproterenol: 5 µg/m in IV and titrate for heart rate effect
Naloxone (Narcan): 2 m g (peds: 0.1 m g/kg) IV or IM initial dose
Sodium bicarbonate: 1 m Eq/kg IVP
Thiam ine (vitam in B 1 ): 100 m g (peds: 50 m g) IV or IM
Follow-Up Disposition Admission Criteria
ICU adm ission for decreased level of consciousness or hem odynam ic instability (bradycardia, conduction delays, hypotension)
Observation and m onitoring for 24 hours for long-acting or sustained-release preparations owing to the potential
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delay in sym ptom s
Discharge Criteria Asym ptom atic 8–10 hours after ingestion of short- or im m ediate-release preparation
References 1. DeWitt CR, Waksm an JC. Pharm acology, pathophysiology and m anagem ent of calcium channel blocker and β-blocker toxicity. Toxicol Rev. 2004;23:223–238. 2. Kerns W, Schroeder D, William s C, et al. Insulin im proves survival in a canine m odel of acute beta-blocker toxicity. Ann Em erg Med. 1997;29:748–757. 3. Love J. Acebutolol overdose resulting in fatalities. J Em erg Med. 2000;18:341–344. 4. Love J, Howell J. Glucagon therapy in the treatm ent of sym ptom atic bradycardia. Ann Em erg Med. 1997;29:181–183.
Miscellaneous SEE ALSO: Calcium Channel Blocker, Poisoning
Codes ICD9-CM 977.9
ICD10 T44.7
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Bio lo gic Weapo ns
Biologic Weapons
Ian Greenwald
Basics Description
Defined as naturally occurring organism s or toxins that are purified and prepared for m ass dissem ination with intent of causing m ass m orbidity, m ortality, and social disruption
Over 400 potential or actualized etiologic agents capable of being used as biological weapon: o
Characterized by their relatively low cost com pared with other weapons of m ass destruction (WMD), high potency, and their ability to be delivered in stealth m anner
o
Stealth quality of biologic weapons com es from organism 's natural incubation period.
Easy to conceal and difficult to detect: o
Agents often invisible to naked eye, odorless, and tasteless
Patients typically present to various health care facilities with host of com m on com plaints, adding to delay in recognition of covert release of biologic weapon.
Victim s of biologic warfare agents are exposed either via direct cutaneous contact with agent, respiratory inhalation
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of aerosolized agent, or via GI tract after poisoning of food or water source.
Etiology
Bacteria: o
Anthrax—Bacillus anthracis
o
Plague—Yersinia pestis
o
Cholera—infection from Vibrio cholerae: Presents with severe gastrointestinal sym ptom s and rapidly leads to profound dehydration
o
Tularem ia—Francisella tularensis
o
Brucellosis—organism in the Brucella genus
o
Q fever—Coxiella burnetii
Viruses: o
Sm allpox—variola virus
o
Viral encephalitides—m em bers of Alphavirus genus (Venezuelan equine encephalitis, Eastern equine encephalitis, and Western equine encephalitis)
o
Viral hem orrhagic fevers—from four fam ilies of viruses, includes illnesses such as Ebola, Marburg, Lassa and dengue fever
Diagnosis Signs and Symptoms
Health care providers need to be alert to detect illness patterns and diagnostic clues that indicate biologic weapon release.
Indications of intentional release of agent include: o
Geographic clustering of illnesses with individuals who live, work, or attended event in close proxim ity
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(if m ultiple people who work in sam e office develop pneum onia, it could potentially represent respiratory pathogen release) o
Unusual age distribution for com m on illness (chickenpoxlike illness am ong adult patients could represent sm allpox release)
o
Two or m ore patients presenting with sim ilar unexplained illnesses (two patients presenting with flaccid paralysis could represent botulinum toxin release)
o
Single case of illness caused by uncom m on agent (sm allpox, inhalational anthrax)
o
High volum e of patients with sim ilar presentation of sym ptom s associated with escalating m orbidity and m ortality
Anthrax
Inhalational anthrax: o
Fever
o
Chills
o
Fatigue, m alaise, lethargy
o
Cough, usually dry or m inim ally productive
o
Nausea or vom iting
o
Dyspnea
o
Diaphoresis
o
Chest pain
o
Myalgias
o
Tachycardia
o
Fever
o
Meningeal signs
Cutaneous anthrax: o
Skin lesion:
Painless pruritic papule
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Turning into vesicle that ruptures form ing necrotic ulcer
o
Black eschar
o
Surrounding gelatinous nonpitting edem a
Plague
Abrupt onset
Fever, chills
Cough, hem optysis, dyspnea
Headache
Vom iting
Swollen tender lym ph nodes (buboes)
Skin lesions at site of inoculation (i.e., flea bite)
Confusion
Abdom inal pain
Oliguria
Obtundation
Extensive ecchym osis
Acral gangrene (digits, nose, penis)
Tularemia
See Tularem ia chapter.
Typhoidal: o
Most likely form of disease when weaponized and delivered by aerosol
o
Fever, headache, m alaise
o
Nonproductive cough
o
Thirty-five percent m ortality if untreated
Q fever
Incubation period 10–40 days
Flulike sym ptom s and pleuritic chest pain for 2–10 days
Chest radiograph shows patchy infiltrates.
Definitively diagnosed serologically
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Mortality: o
Less than 1% even if untreated
Smallpox
Incubation period 7–17 days (average is 12 days)
Flulike sym ptom s (fever, fatigue, m yalgias, headache) for about 2–3 days followed by characteristic rash o
Progresses from m acules to papules to pustular lesions and crusted lesions
o
Starts on face and extrem ities (including palm s/soles) and spreads to trunk in 1 week
o
Scabs over in 1–2 weeks
Mortality: o
30% if untreated
Hemorrhagic Fevers
See Hem orrhagic Fever chapter.
Incubation period 1–3 weeks
Starts as flulike syndrom e with fever, m alaise, m yalgias, headache, and sore throat
Afterward, infectious gastroenteritis syndrom e, rash, and renal/hepatic dysfunction
Finally, hem orrhagic sym ptom s develop around the fifth day followed by shock and death: o
Mortality in 50–90% for Ebola if untreated
Essential Workup Suspect bioterrorism if:
Multiple cases of relatively young, healthy patients who present with flulike syndrom e and within days deteriorate rapidly
Typical cutaneous lesions appear.
Tests
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Lab
CBC
Electrolytes, BUN, creatinine
Arterial blood gas (ABG)
Cerebrospinal fluid (CSF): o
Anthrax—50% with inhalation anthrax develop hem orrhagic m eningitis.
Coagulation studies: o
Plague—dissem inated intravascular coagulation (DIC)
Blood cultures
Wound cultures
Alert laboratory personnel to potential concerns of clinicians.
P.143
Imaging Chest radiograph:
Anthrax—m ediastinal widening, pulm onary infiltrate/consolidation, pleural effusion
Plague—bronchopneum onia
Differential Diagnosis
Anthrax: o
Influenza
o
Bacterial pneum onia
o
Bacterial m eningitis
o
Brown recluse spider bite
o
Tularem ia
o
Streptococcal/staphylococcal skin infection
Plague:
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o
Tularem ia
o
Catscratch disease
o
Lym phogranulom a venereum
o
Chancroid
o
Tuberculosis
o
Streptococcal adenitis
o
Meningitis
o
Encephalitis
o
Sepsis
Sm allpox: o
Varicella
o
Rash starts centrally on trunk and spreads outward:
Lesions in different stages of developm ent
Rarely involves palm s or soles
Dissem inated m olluscum contagiosum
o
Monkeypox
o
Drug eruptions
Toxins: o
Staphylococcal enterotoxin B:
Most com m on cause of food poisoning
Can be aerosolized in addition to being placed in food or water reservoir
When inhaled, produces febrile type of illness that can progress to septic shock picture
o
Ricin:
Plant protein derived from castor beans
Causes rapid progression from upper respiratory congestion to cardiopulm onary collapse
Ingestion is less toxic because GI tract does not absorb it well, but it can lead to local cytotoxic death, shock, and death.
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o
Botulinum toxin:
Initially sym ptom s include cranial nerve dysfunction with descending paralysis that leads to respiratory failure.
o
Mycotoxins:
Highly toxic com pounds produced by certain species of fungus
Derm al, respiratory, or GI contact can rapidly, lead to m ultiorgan system failure and death.
Treatment Pre Hospital Universal precautions with N-95 m ask
Initial Stabilization
Airway, breathing, and circulation m anagem ent (ABCs)
0.9% norm al saline (NS) fluid bolus for hypotension
Supplem ental oxygen for hypoxem ia
Vasopressors for persistent hypotension.
Respiratory and contact isolation for suspected cases
ED Treatment
Control fever with acetam inophen.
Initiate therapy for specific disease.
Anthrax
Initiate antibiotics: o
IV for inhalational or severe cutaneous
o
Antibiotic choice depends on susceptibility.
Antibiotic options: o
Ciprofloxacin
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o
Doxycycline
o
Rifam pin
o
Clindam ycin
o
Vancom ycin
Plague
Antibiotics initiated within 24 hours m inim izes m ortality.
First-line agents: streptom ycin or gentam icin
Add chloram phenicol if signs of m eningitis or unstable patient
Prophylaxis: doxycycline or ciprofloxacin
Q fever
Recovery occurs within 2 weeks without treatm ent.
Doxycycline shortens duration of illness.
Smallpox
Supportive therapy
Vaccine given within 4 days of initial exposure decreases chances of contracting sm allpox or developing severe sym ptom s.
Vaccinate m edical staff caring for patient.
Treat secondary bacterial infection.
Tularemia See Tularem ia
Hemorrhagic Fevers See Hem orrhagic Fever
Medication (Drugs)
Chloram phenicol: 25 m g/kg IV q6h
Ciprofloxacin: 400 m g IV q12h or 500 m g PO b.i.d. (peds: 15 m g/kg b.i.d.)
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Clindam ycin: 900 m g IV q12h
Doxycycline: 100 m g (peds: ≥45 kg, 100 m g; if weight ≤45 kg, 2.2 m g/kg IV) PO/IV q12h
Gentam icin: 5 m g/kg IM or IV q24h (peds: 2.5 m g/kg IV/IM q8h)
Rifam pin: 10 m g/kg IV not to exceed 600 m g/d
Streptom ycin: 1 g (peds: 15 m g/kg) IM q12h
Vancom ycin: 1 gm IV q12h
Follow-Up Disposition Admission Criteria
Decision to treat patient as inpatient versus outpatient will have to be m ade in context of overall disaster.
Toxic or hypoxic patients require adm ission.
Respiratory isolation
Discharge Criteria Mild, noncontagious illness
References 1. Dennis DT, Inglesby TV, et al. Tularem ia as a biological weapon. JAMA. 2001;285:2763–2773. 2. Khan AS, Morse S, Lillibridge S. Public-health preparedness for biological terrorism in the USA. Lancet. 2000;356:1179–1182. 3. O'toole T. Em erging illness and bioterrorism : im plications for public health. J Urban Health. 2001;78(2):396–402. 4. Centers for Disease Control and Prevention. Recognition of illness associated with the intentional release of a biologic agent. MMWR Morb Mortal Wkly Rep. 2001;50(41):893–897.
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5. Richards CF, Burstein JL, Waeckerle JF, et al. Em ergency physicians and biological terrorism . Ann Em erg Med. 1999;34(2):183–190.
Useful Web Sites http://www.bt.cdc.gov http://www.hopkins-biodefense.org/index.htm l
Miscellaneous SEE ALSO: Botulism ; Hem orrhagic Fever; Tularem ia
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Bipo lar Diso rder
Bipolar Disorder
Paul H. Desan Gary S. Sachs
Basics Description
Mania: o
Presentation is diverse, from sim ple irritability or cheerfulness to psychosis, delirium , or agitation, which m ay be difficult to recognize as m ania.
o
Full extent of pathology often revealed only by outside inform ants
o
Onset gradual or acute, duration several weeks or m onths; rarely m ay be chronic
Hypom ania: o
Milder sym ptom s without m arked im pairm ent
Mixed m ood: o
Sim ultaneous sym ptom s of m ania and depression
o
Treat in ED as for m ania
Bipolar (form erly m anic depressive) disorder: o
Defined as one or m ore episodes of hypom anic, m anic, or m ixed m ood
o
Possibly with episodes of depressed m ood
o
Bipolar II is used to denote cases where hypom ania
Pa ge 7 5 1
has occurred in the course of the disorder but never m ania. o
Typically begins in the teens or 20s
o
Episodes of abnorm al m ood m ay be m ild or severe, brief or prolonged, infrequent or chronic, chiefly elevated or chiefly depressed in character.
o
Bipolar disorder m ay be readily responsive to treatm ent or nearly intractable.
Schizoaffective disorder also characterized by episodes of altered m ood, but psychotic features present even when m ood is norm al
Etiology Bipolar disorder is typically a prim ary psychiatric disorder with an etiology related to both genetic and environm ental factors; it m ay also present as a secondary disorder, for exam ple, originating after stroke, head traum a, or other neurological process.
Diagnosis Signs and Symptoms History
Psychiatric history: o
Recent sym ptom s of m ania (often collateral sources critical): elevated, expansive, or irritable m ood; increased energy and activity; decreased need for sleep; irresponsibility, disregard for negative consequences of actions; talkativeness; distractibility; fast thoughts; grandiosity, overconfidence
o
Past m ania or depression
Pa ge 7 5 2
o
Noncom pliance with m ood stabilizer
o
Recent initiation or discontinuation of antidepressant m ay trigger elevated m ood
o
Recent substance abuse
o
Bipolar fam ily history
Medical history: o
Especially endocrine, m etabolic, or neurologic disorders
o
Particularly likely to be secondary to m edical condition if it is the first episode, patient is older than 40 years, there is atypical or m ixed presentation, or abnorm al sensorium
o
Current or recent m edications
Physical Exam
Appearance: o
Hyperactive, if not agitated
o
Talkative, often with loud, rapid or, “pressured†• speech
Affect: o
Irritable, argum entative, often m ultiple recent argum ents or fights
o
Less com m only euphoric or expansive
o
Often labile with depressed or tearful intervals (m ay confound diagnosis)
o
Patient likely to describe m ood as tense, irritable, or depressed rather than euphoric
Neurovegetative: o
Increased energy, engaged in m ultiple goal-directed activities m any hours per day
o
Racing thoughts
o
Decreased sleep
Thought process:
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o
Rapid, distractible, m ay be incoherent, delirious
Thought content: o
Psychosis possible, either m ood congruent (e.g., such as delusions of grandeur or power) or m ood incongruent (m ay be indistinguishable from other psychotic disorders)
Judgm ent: o
Inflated self-esteem , perhaps to grandiose or psychotic extent
o
Uncharacteristic, irresponsible behavior, such as financial or sexual indiscretions, with inability to recognize negative consequences of actions
o
Substance abuse is frequent during m ania.
Sensorium : o
Typically norm al
o
Confusion or delirium possible
Essential Workup
Physical and neurologic exam ; vital signs
Mania m ay present as delirium and need workup of full differential diagnosis of delirium .
Tests Lab
Toxicologic screen (urine or serum )
Electrolytes
Blood glucose
CBC
TSH
Lithium , carbam azepine, valproate serum levels, if relevant
Other tests as suggested by history or exam
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Imaging Head im aging only with suspicion of neurologic etiology
Differential Diagnosis
Prim ary m ania of bipolar or schizoaffective disorder
Psychosis
Agitated depression
Personality disorders (borderline, narcissistic, antisocial)
Attention deficit disorder
Conduct or interm ittent explosive disorders
Organic brain syndrom e
Intoxication or withdrawal from alcohol or sedative hypnotics
Intoxication with cocaine, am phetam ines, or phencyclidine
Accidental or deliberate toxic overdose
Treatm ent with antidepressants or electroshock therapy in susceptible individuals
Corticosteroid or thyroid horm ones
Anticholinergics
Sym pathom im etics
Treatm ents of parkinsonism
Cyclobenzaprine (Flexeril)
Recent discontinuation of antidepressant m edication
Endocrine or m etabolic disorders (particularly thyroid disease)
Encephalitis
Meningitis
Postictal states
Multiple sclerosis
Post-cerebrovascular accident
CNS tum ors
CNS vasculitis
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General paresis
P.145
Treatment Initial Stabilization
High violence potential: o
Quiet environm ent
o
Prom pt evaluation
o
Nonconfrontational m anner
o
Adequate security backup
o
Physical restraint and sedation as needed
For cooperative agitated patient: o
PO neuroleptics (e.g., haloperidol, consider olanzapine or chlorprom azine as alternate) or PO benzodiazepines (e.g., lorazepam )
For severe or uncooperative agitated patient: o
Synergistic com bination of IM, IV, or PO haloperidol and lorazepam
o
Benztropine for prevention of acute dystonic reaction to haloperidol is not usually required when concurrent benzodiazepine is given.
o
Consider olanzapine, ziprasidone, chlorprom azine, or lorazepam IM as alternative
ED Treatment Outpatient Management
Neuroleptics for sym ptom atic treatm ent, on tem porary or continuing basis
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Agents for sleep
Discontinuation of antidepressant if related to present hypom ania or m ania
Initiation or restart of m ood-stabilizer therapy: o
Action of m ood-stabilizing agents requires days or weeks, even after full serum level attained
Inpatient Management Sedation or initiation of m ood stabilizer in consultation with adm itting psychiatrist
Medication (Drugs) Acute Agitation
Lorazepam : 2 m g PO/IM (lower dose in m ild agitation or in frail or elderly); m ay repeat every 30 m inutes, generally not to exceed 12 m g/24 hours
Haloperidol: 5 m g PO (lower dose in m ild agitation or in frail or elderly); m ay repeat every 30 m inutes, generally not to exceed 20 m g/24 hours (consider benztropine 1–2 m g PO q12hr prophylaxis of dystonic reaction, particularly in continued neuroleptic treatm ent without benzodiazepine or in patients with history of dystonia); consider olanzapine 5–10 m g PO or chlorprom azine 50–100 m g PO as alternative to haloperidol
Synergistic com bination of haloperidol, 5–10 m g IM/IV/PO plus lorazepam 1–2 m g IM/IV/PO, repeat every 30 m inutes as required (doses m ay be sm aller in elderly or frail patients)
Olanzapine 10 m g IM, ziprasidone 10 m g IM, or chlorprom azine 50 m g IM m ay be useful parenteral alternatives, perhaps at a lower dose in frail or elderly
Pa ge 7 5 7
(avoid chlorprom azine in hypotension; ziprasidone m ay have m ore QT elongating effect than other neuroleptics but the clinical relevance of such effect at this dose is unclear).
Typical Outpatient Medications
Benztropine: 1 m g PO b.i.d.
Carbam azepine: 400–2,000 m g/d (often in div. doses or in sustained release dose form s)
Clonazepam : 0.5–2 m g PO q.h.s. or 0.5–2 m g PO b.i.d.
Haloperidol: 0.5–5 m g PO b.i.d.
Lam otrigine: 25–200 m g/d in 1 or 2 div. doses (typically up to 100 m g/d in patients taking valproate, up to 500 m g/d in patients taking carbam azepine or certain other cytochrom e inducers, but not valproate)
Alert
Lam otrigine m ust be started by a gradual dose escalation schedule specified by m anufacturer to avoid increased risk of severe derm atological reactions; if resum ed after discontinuation for m ore than five half-lives, the gradual dose escalation schedule m ust be used again.
Lithium : 600–3,000 m g/d (often in div. doses or in sustained release dose form s; in acute m ania, initiate at 300 m g PO t.i.d.)
Olanzapine: 1.25–30 m g/d, q.h.s. or in div. doses
Perphenazine: 4–16 m g PO b.i.d.
Risperidone: 0.5–3 m g PO b.i.d.
Valproate (e.g., Depakote): 750–3,000 m g/d (often in div. doses; in acute m ania, initiate at 250 m g PO t.i.d.)
Pregnancy Considerations The safety of psychotropic m edications in pregnancy is a com plex
Pa ge 7 5 8
issue, but valproate and carbam azepine m ay pose particular risks in the first trim ester.
Follow-Up Disposition Admission Criteria
Involuntary hospitalization is required by danger to self: o
Suicidal risk, especially if m ixed or labile m ood or psychotic
o
Unsafe behaviors due to im paired judgm ent
o
Medically unstable
o
Hospitalization diagnostically required
Involuntary hospitalization also required by: o
Risk of behaviors dangerous to others
o
Inability to care for self (unable to obtain basic needs, such as food, clothing, or shelter)
Discharge Criteria
Patients with m ild sym ptom s m ay be discharged on m edications noted above if: o
Necessary supports to ensure safety are in place
o
Patient is com pliant with treatm ent plan
o
Consultation with outpatient psychiatrist is available within 1–3 days
Som e patients who are not legally com m ittable m ay refuse treatm ent; explain availability of future treatm ent to patient and any involved friends or fam ily.
References 1. Allen MH, Currier GW, Hughes DH, et al. The Expert Consensus
Pa ge 7 5 9
Guideline Series: treatm ent of behavioral em ergencies. Postgrad Med . 2001;Spec No: 188. 2. Muller-Oerlinghausen B, Berghofer A, Bauer M. Bipolar disorder. Lancet. 2002;359(9302): 241–247. 3. Sachs GS, Printz DJ, Kahn DA, et al. The Expert Consensus Guideline Series: m edication treatm ent of bipolar disorder 2000. Postgrad Med. 2000; Spec No: 1104.
Codes ICD9-CM 296.4 Mania 296.5 Bipolar depression 296.6 Bipolar m ixed state 296.7 Bipolar unspecified 296.89 Bipolar II 295.7 Schizoaffective disorder
ICD10 F31 Bipolar disorder
Pa ge 7 6 0
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Bite, Anim al
Bite, Animal
Daniel T. Wu
Basics Description
Most bites are from provoked anim als
Dog bite wounds: o
Large dogs inflict the m ost serious wounds (pit bulls cause the m ost hum an fatalities).
o
Most fatalities in children (70%) due to bites to face/neck
o
Dogs of fam ily or friends account for m ost bites.
Cat bite wounds: o
Majority from pets known to victim
o
50% infection rate in those seeking care
o
Puncture wounds m ost frequent due to sharp thin teeth causing deep inoculation of bacteria
Cat-scratch disease: o
Three of the following four criteria:
Cat contact, with presence of scratch or inoculation lesion of the skin, eye, or m ucous m em brane
Positive CSD skin test result
Characteristic lym ph node histopathology
Pa ge 7 6 1
Negative results of laboratory studies for other causes of lym phadenopathy
Rat bite wounds: o
Occur in laboratory personnel or children of low socioeconom ic class
o
Infection rate
o
Rat bites rarely transm it rabies, and prophylaxis not routine
Etiology
Dog and cat bites: o
Pasteurella m ultocida is the m ajor organism in both
Twice as likely to be found in cat bites than dog bites
Gram -negative aerobe found in up to 80% of cat infections
o
Staphylococcus or Streptococcus
o
Infection appears in 24 hours
Other organism s include anaerobes and Capnocytophaga canim orsus (dogs)
Cat-scratch disease: o
Caused by Bartonella henselae
Rat bites: o
Caused by Spirillum m inus and Streptobacillus m oniliform is
Diagnosis Signs and Symptoms
Distribution of m am m alian bites:
Pa ge 7 6 2
o
Dog bites represent 80–90% of all bites.
o
Cat bites represent 5–15% of all bites.
o
Hum an bites represent 2–5% of all bites (see Hum an Bite chapter).
o
Rat bites represent 2–3% of all bites.
Dog bites: o
Appearance
Crush injuries (m ost com m on), tears, avulsions, punctures, and scratches
o
Low rates of infection com pared with cat and hum an bites
o
Infections usually present with:
Cellulitis
Malodorous gray discharge
Fever
Lym phadenopathy
Cat bites: o
o
Appearance
Puncture wounds (m ost com m on)
Abrasions
Lacerations
High infection rates (30–50%) due to deeper puncture wounds
Cat-scratch disease: o
From the bite/scratch of a cat, dog, or m onkey
o
Sm all m acule or vesicle that progresses to a papule
Begins several days (3–10) after inoculation
Resolves within several days or weeks
Regional lym phadenopathy occurs 3 weeks postinoculation
Tender
Nonsuppurative
Pa ge 7 6 3
o
Resolves after 2–4 m onths
Low-grade fever, m alaise, headache
History
Anim al's behavior, provocation, location, ownership
Tim e since attack
Past m edical history: conditions com prom ising im m une function, allergies, and tetanus status
Physical Exam
Record the location and extent of all injuries.
Docum ent any swelling, crush injuries, or devitalized tissue.
Note the range of m otion of affected areas.
Note the status of tendon and nerve function.
Docum ent any signs of infection, including regional adenopathy.
Docum ent any joint or bone involvem ent.
Tests Lab
Aerobic and anaerobic cultures from any infected bite wound
Cultures not routinely indicated if wounds not clinically infected
Cat-scratch disease o
Presence of elevated titers of Bartonella (Rochalim aea) henselae, or
o
Positive reaction to cat-scratch antigen (CSA)
Inject 0.1 m L CSA intraderm ally
Induration at the site 48–72 hours later equal to or exceeding 5 m m is positive
Imaging
Pa ge 7 6 4
Plain radiograph indications:
Fracture
Suspect foreign body, e.g., tooth
Baseline film if a bone or joint space has been violated in evaluating for osteom yelitis
For infection in proxim ity to a bone or joint space
Differential Diagnosis
Hum an bite injuries: hum an teeth cause crush injuries and anim al teeth cause m ore punctures and lacerations.
Bite injuries from other anim als
CSD-caused lym phadenopathy: o
Reactive hyperplasia (leading cause of lym phadenopathy in children younger than 16 years)
o
Infection, chronic lym phadenitis, drug reaction, m alignancy, and congenital conditions
P.147
Treatment Initial Stabilization
Achieve hem ostasis on any bleeding wound.
Airway stabilization if bite located on face or neck
ED Treatment
Wound irrigation: o
Copious volum es of norm al saline irrigation with an 18-gauge plastic catheter tip aim ed in the direction of the puncture
o
Avoid injection of saline through tissue planes due to
Pa ge 7 6 5
force of irrigation
Débridem ent: o
Rem ove foreign m aterial, necrotic skin tags, or devitalized tissues
o
Do not débride puncture wounds
o
Rem ove any eschar present so underlying pus m ay be expressed and irrigated
Wound closure: o
Closing wounds increases risk of infection and m ust be balanced with scar form ation and effect of leaving wound open to heal secondarily.
o
Do not suture infected wounds or wounds >24 hours after injury.
o
Repair of wounds >8 hours: controversial
o
Close facial wounds (warn patient of high risk of infection).
o
Infected wounds, those presenting >24 hours after the event, and deep hand wounds should be left open
o
May approxim ate the wound edges with Steri-Strips and perform a delayed prim ary closure
Antibiotic indications: o
Infected wounds
o
Cat bites
o
Hand injuries
o
Severe wounds with crush injury
o
Puncture wounds
o
Full-thickness puncture of hand, face, or lower extrem ity
o
Wounds requiring surgical débridem ent
o
Wounds involving joints, tendons, ligam ents, or fractures
o
Im m unocom prom ised patients
Pa ge 7 6 6
o
Wounds presenting >8 hours after the event
Elevate injured extrem ity.
Tetanus prophylaxis
Rabies Immunoprophylaxis
Not required if rabies not known or suspected
Rodents (squirrels, ham sters, rats, m ice) and rabbits rarely transm it the disease.
Skunks, raccoons, bats, and foxes represent the m ajor reservoir for rabies.
Recom m ended in following situations: o
Dog or cat in rabies-known area unable to be quarantined for 10 days
o
Previously healthy dog or cat becom es ill while being quarantined (and awaiting results of rabies fluorescent antibody test)
o
An ill dog or cat while awaiting rabies test results (to be continued or halted based on results of rabies test)
Active im m unization: o
Hum an diploid cell vaccine (HDCV): 1 m L IM on days 1, 3, 7, 14, and 28 after exposure
Passive im m unization: o
Hum an rabies im m une globulin (HRIG): 20 IU/kg
o
Up to one half in area around wound with the rest IM
Cat-Scratch Disease
Analgesics
Apply local heat to affected nodes.
Avoid lym ph node traum a.
Disease usually self-lim iting
Antibiotics controversial, consider if severe disease is present or im m unocom prom ised victim
Pa ge 7 6 7
Medication (Drugs)
Am oxicillin/clavulanic acid (Augm entin): 500–875 m g (peds: 40 m g/kg/24 hr) PO b.i.d. (first line for all three anim als)
Am picillin/sulbactam (Unasyn): 1.5–3.0 g IV q6h
Cefoxitin (Mefoxin): 2.0 g IV q8h
Cefuroxim e axetil (Ceftin): 500 m g PO b.i.d.
Clindam ycin (Cleocin): 300 m g PO q6h; 900 m g IV q8h
Ciprofloxacin (Cipro): 500 m g PO b.i.d.; 400 m g IV q12h
Doxycycline (Vibram ycin): 100 m g PO b.i.d.
Im ipenem /cilastatin (Prim axin): 0.5–1.0 g (peds: 50 m g/kg/24h) IV q6h
Piperacillin/tazobactam (Zosyn): 3.375 g IV q6h
Ticarcillin/clavulanic acid (Tim entin): 3.1 g IV q6h
Trim ethoprim -sulfam ethoxazole (Bactrim ): 1 tablet (peds: 6–12 m g TMP, 30–60 m g SMX/kg/24h) PO b.i.d.
Follow-Up Disposition Admission Criteria
All bites: o
Infected wounds at presentation
o
Severe/advancing cellulitis/lym phangitis
o
Signs of system ic infection
o
Infected wounds that have failed to respond to outpatient (PO) antibiotics
Cat-scratch disease:
Pa ge 7 6 8
o
Prolonged fever, system ic sym ptom s, and/or m arked lym phadenopathy
Discharge Criteria
Healthy patient with localized wound infection: discharge on antibiotics with 24-hour follow-up.
48-hour follow-up for noninfected wounds
References 1. Brook I. Microbiology and m anagem ent of hum an and anim al bite wound infections. Prim Care. 2003;30(1):25–39, v. 2. Galloway RE. Mam m alian bites. J Em erg Med. 1998;6:325–331. 3. Griego RD, et al. Dog, cat, and hum an bites: a review. J Am Acad Derm atol. 1995;33: 1019–1029. 4. Klein JD. Cat scratch disease. Pediatr Rev 1994; 15(9):348–353. 5. Pickering L, Red Book: 2003 Report of the Com m ittee on Infectious Diseases. Am er Academ y of Pediatrics 2003. 26th edition. 6. Sm ith PF, et al. Treating m am m alian bite wounds. J Clin Pharm Ther. 2000;25:85–99.
Miscellaneous See also: Rabies
Codes ICD9-CM 879.8
ICD10 T14.1
Pa ge 7 6 9
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Bite, Hum an
Bite, Human
Daniel T. Wu
Basics Description
Third m ost com m on bite (after dogs and cats)
Most bites (up to 75%) occur during aggressive acts
15–20% are related to sexual activity (love nips)
Two types of bites: o
Occlusional bites: laceration or crush injury to affected body part:
o
Occurs when hum an teeth bite into the skin
Sam e risk of infection as other wounds
Clenched-fist injuries: (CFIs; m ost serious type): present as sm all wounds over m etacarpophalangeal joints in dom inant hand (fight bites)
Sustained from a clenched fist striking the m outh and teeth of another person
With joint relaxation from the clenched position: o
Puncture site sealed
o
Oral bacteria inoculated in the anaerobic setting within the joint
o
Bacterial inoculation carried by the tendons deeper into the potential spaces of the hand
Pa ge 7 7 0
o
Increases chances for a m ore extensive infection
Etiology
Aerobic and anaerobic organism s: o
o
Most com m on
Streptococcus
Staphylococcus
Anaerobes (about 50%):
Eikenella corrodens
Haem ophilus influenzae
Neisseria species
Corynebacterium
E. corrodens exhibits synergism with Streptococcus, Staphylococcus aureus, Bacteroides, and gram -negative organism s
Diagnosis Signs and Symptoms
Location: o
Upper extrem ities (60–75%)
o
Head and neck (15–20%)
o
Trunk (10–20%)
o
Lower extrem ities (about 5%)
Frequent com plications: o
Cellulitis
o
Serious deep-space infections (septic arthritis and osteom yelitis)
o
Fractures and tendon injuries
o
Hand bites have highest rates of infection.
History
Pa ge 7 7 1
Tim e of injury
Patient allergies
Relevant m edical history (im m une status)
Last tetanus shot
HIV, Hepatitis B status of person inflicting bite
Physical Exam
Record the location and extent of all injuries.
Docum ent any swelling, crush injuries, or devitalized tissue.
Note the range of m otion of affected areas.
Note the status of tendon and nerve function.
Docum ent any signs of infection, including regional adenopathy.
Docum ent any joint or bone involvem ent.
Tests Lab
Aerobic and anaerobic cultures from any infected bite wound
Cultures not indicated if wounds not clinically infected
Imaging Plain radiograph indications:
Fracture
Suspect foreign body, e.g., tooth
Baseline film if a bone or joint space has been violated in evaluating for osteom yelitis
For infection in proxim ity to a bone or joint space
Differential Diagnosis Bite injuries from anim als:
Sharper teeth cause m ore punctures and lacerations than hum an teeth, which usually cause m ore crush-type injuries
Pa ge 7 7 2
Pediatric Considerations
In suspected sexual abuse: o
Check for a central area of bruising or “hickey― from suction
Linear abrasions or bruises on both the dorsal and palm ar/plantar surfaces of the hand or foot: o
Highly suggestive of bite m arks
o
Lesions on one extrem ity should prom pt a search for lesions on the other extrem ities.
An intercanine distance of >3 cm indicates perm anent dentition (present only if the attacker is older than 8 years)
If abuse suspected: o
Rub a saline-m oistened swab in the wound to collect any saliva and then place in a paper envelope for analysis
o
Obtain photographs.
Treatment Initial Stabilization ABCs: ensure patent airway and adequate peripheral tissue perfusion
ED Treatment
Wound irrigation: o
Copious volum es of norm al saline irrigation with an 18-gauge needle or plastic catheter tip aim ed in the direction of the puncture
o
Care should be taken not to inject fluid into the tissues
Débridem ent:
Pa ge 7 7 3
o
Rem ove any foreign m aterial, necrotic skin tags, or devitalized tissues.
o
Do not débride puncture wounds.
o
Rem ove any eschar present so that underlying pus m ay be expressed and irrigated.
Closed-fist injuries: o
Im m obilize
o
Splint in a position of function that m aintains the m axim al length of ligam ents and intrinsic m uscles.
o
Use a bulky hand dressing.
o
Consultation with hand surgeon regarding operative irrigation/exploration of wound
o
Elevation for several days until any edem a resolved
o
Sling for outpatients
o
Place the hand in a tubular stockinette attached to an IV pole for inpatients.
o
Adm inister antibiotics
Do not perform prim ary repair of avulsion wounds.
Wound closure: o
Closing wounds increases risk of infection and m ust be balanced with scar form ation and effect of leaving wound open to heal secondarily.
o
Do not suture infected wounds or wounds >24 hours after injury.
o
Repair of wounds >8 hours after bite: controversial
o
Close facial wounds up to 24 hours after bite (warn patient of high risk of infection).
o
Infected wounds and those presenting >24 hours should be left open.
o
May approxim ate the wound edges with Steri-Strips and perform a delayed prim ary closure
o
Do not suture closed-first injuries.
Pa ge 7 7 4
Prophylactic antibiotics controversial for low-risk bites P.149
Antibiotics for outpatients with: o
Moderate to severe injuries with crush injury or edem a
o
Involvem ent of the bone or a joint
o
Hand bites
o
Wounds near a prosthetic joint
o
Underlying disease (diabetes, prior splenectom y, or im m unosuppression) that increases the risk of developing a m ore serious infection
Tetanus prophylaxis
Refer for possible testing/surveillance for HIV infection.
Medication (Drugs)
Am oxicillin/clavulanic acid (Augm entin): 500/125 m g (peds: 40 m g/kg/24h) q8h PO
Cefoxitin (Mefoxin): 1–2 g (peds: 80–160 m g/kg/24h) q6h IV
Ciprofloxacin (Cipro): 500–750 m g q12h PO or 400 m g q12h IV o
Poor anaerobic coverage
Clindam ycin (Cleocin): 150–450 m g (peds: 8–20 m g/kg/24h) PO q6h or 600–900 m g (peds: 20–40 m g/kg/24h) IV q8h o
No coverage against E. corrodens
Dicloxacillin (Pathocil): 500 m g (peds: 50 m g/kg/24h) PO q6h
Penicillin (Penicillin VK): 500 m g (peds: 50 m g/kg/24h) PO
Pa ge 7 7 5
q6h
Ticarcillin/clavulanic acid (Tim entin): 3.1 g q4h–q6h
Trim ethoprim -sulfam ethoxazole (Septra DS): 1 tablet q12h (peds: 8 m g/kg trim ethoprim and 40 m g/kg sulfam ethoxazole per day divided into two daily doses) PO o
Poor anaerobic coverage
Follow-Up Disposition Admission Criteria
Infected wounds at presentation
Severe/advancing cellulitis/lym phangitis
Signs of system ic infection
Infected wounds that have failed to respond to outpatient (oral) antibiotics
Discharge Criteria
Healthy patient with localized wound infection: discharge on antibiotics with 24-hour follow-up
48-hour follow-up for noninfected wounds
Geriatric Considerations
Hum an bite m arks rarely occur accidentally; good indicators of inflicted injury.
Consider elder abuse
Pediatric Considerations
Hum an bite m arks rarely occur accidentally; good indicators of inflicted injury
Consider child abuse.
References
Pa ge 7 7 6
1. Brook I. Microbiology and m anagem ent of hum an and anim al bite wound infections. Prim Care 2003;30(1):25–39, v. 2. Broder J, et al. Low risk infection in selected hum an bites treated without antibiotics. Am er Jour of Em erg Med 2004;22(1):10–13. 3. Pickering L, Red Book: 2003 Report of the Com m ittee on Infectious Diseases. Am er Academ y of Pediatrics 2003. 26th edition. 4. Sm ith PF, et al. Treating m am m alian bite wounds. J Clin Pharm Ther. 2000;25:85–99.
Miscellaneous SEE ALSO: Bite, Mam m al
Codes ICD9-CM 879.8
ICD10 T14.1
Pa ge 7 7 7
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Bladder Injury
Bladder Injury
Roneet Lev
Basics Description
Blunt traum a is the m ost com m on m echanism .
10–15% of pelvic fractures have bladder injury.
95% of bladder ruptures have pelvic fracture.
Mortality: 17–22% overall; 60% if com bined intraperitoneal/extraperitoneal rupture
Etiology Mechanism
Traum a, 82%
Blunt traum a: m otor vehicle accident (MVA; 87%), falls (7%), assault (6%)
Penetrating: GSW (85%), stabbings (15%)
Iatrogenic 14%: TURP and urologic procedures, gynecologic procedures, obstetric procedures, abdom inal procedures, hernia repair, intrauterine device (IUD), orthopedic hip procedures, biopsies, indwelling Foley
Intoxication 2.9%
Spontaneous Table o f C o ntents > Bo erhaave Syndro m e
Boerhaave
Syndrome Robert C. Montana
Basics Description
Spontaneous esophageal rupture: o
o
From sudden com bined increase in both:
Intra-abdom inal pressure
Negative intrathoracic pressure
Causes com plete, full-thickness (transm ural), longitudinal tear in distal esophagus at left posterolateral aspect
Esophagus has no serosal layer (which norm ally contains collagen and elastic fibers): o
Results in weak structure vulnerable to perforation and m ediastinal contam ination
o
Esophageal wall is further weakened by conditions that dam age m ucosa (esophagitis of various causes)
Significant m orbidity/m ortality (m ost lethal GI tract perforation): o
Owing to explosive nature of tear
o
Owing to alm ost im m ediate contam ination of
Pa ge 7 9 3
m ediastinum with contents of esophagus
Etiology
Associated with: o
Forceful vom iting and retching
o
Heavy lifting
o
Seizures
o
Childbirth
o
Blunt traum a
o
Induced em esis
o
Laughing
Com m on in m iddle-aged m en
Alcoholism , ingesting large m eals, and peptic ulcer disease
Second m ost com m on cause of esophageal rupture after iatrogenic perforation from instrum entation
Pediatric Considerations Described in fem ale neonates but rarely seen
Diagnosis Signs and Symptoms History
Often no classic sym ptom s
Most com m on sym ptom s: o
Chest or epigastric pain after vom iting/retching
Mackler triad: o
Vom iting/retching
o
Chest pain
o
Subcutaneous em physem a
Retrosternal chest pain present in m ost patients: o
Often pleuritic
Pa ge 7 9 4
o
Radiates to back or left shoulder
o
Worsens with swallowing
Odynophagia
Swallowing m ay precipitate coughing.
Physical Exam
Dyspnea
Diaphoresis
Subcutaneous em physem a in neck and chest wall
Mediastinal crackling on auscultation (Ham m an sign)
Pleural effusions
Tachypnea
Fever
Shock, in m ore severe cases
If untreated, m ediastinitis will develop and abscesses will form .
Not usually associated with bleeding
Essential Workup
Upright chest radiographs (preferably posteroanterior and lateral views if tolerated) evaluating for: o
Pneum om ediastinum
o
Subcutaneous em physem a
o
Pleural effusion (left side)
o
Pneum othorax
o
Widened m ediastinum
o
Hydropneum othorax
o
Em pyem a
o
Free peritoneal air
o
Naclerio “V― sign:
V-shaped radiolucency seen through the heart (air in left lower m ediastinum )
Esophagram identifies leak in esophagus:
Pa ge 7 9 5
o
Initially use water-soluble contrast m aterial
o
If esophagus is intact, use barium contrast for better detail.
o
Aids in decision of which type of surgical approach
o
If negative and high suspicion, repeat with patient in left and right decubitus positions.
Tests Lab
CBC
PT/PTT
Blood cultures
Pleural effusion:
o
Am ylase content
o
pH ( Table o f C o ntents > Bo tulism
Botulism
Philip Shayne
Basics Description
Caused by a polypeptide, heat-labile exotoxin produced by Clostridium botulinum : o
Most potent poison known
Toxin blocks neurom uscular transm ission in cholinergic nerve fibers.
Sym ptom s occur by inhibition of acetylcholine release from presynaptic nerve m em branes: o
Dam age is perm anent.
o
Recovery is by form ation of new synapses through sprouting from the axon.
Onset: 12–36 hours after exposure: o
Death can occur in 24 hours.
Slow recovery; sym ptom s often persist for m onths
Mortality:
o
Untreated: 60–70%
o
With supportive care: 10–15%
Three m ajor types: food-borne botulism , wound botulism , and infantile botulism (see Pediatric Considerations)
Food-borne botulism :
Pa ge 8 0 0
o
Occurs by ingestion of preform ed toxin; im properly canned food facilitates the necessary anaerobic conditions.
o
Conditions required for exposure:
Food product contam inated with C. botulinum bacilli or spores
Proper conditions for germ ination of spores exist.
Tim e and conditions perm it production of toxin before eating.
Food not heated sufficiently to destroy botulism toxin
Toxin-containing food ingested by susceptible host
Wound botulism : o
Clinical evidence of botulism after traum a with a resultant infected wound and no history suggestive of food-borne illness
o
Botulinum isolated in about 50%
o
Wounds usually contam inated with soil
o
Seen rarely in chronic drug abusers
Other types: o
Hidden botulism is an adult variant of infantile botulism seen in com prom ised hosts (rare).
o
Inadvertent botulism seen rarely from reactions to botulism toxin used therapeutically:
Sym ptom s sim ilar to those of classic botulism
Pediatric Considerations
Infantile botulism occurs from the ingestion of C. botulinum spores, which germ inate in the gut and produce the toxin.
Ninety percent occur in children younger than 6 m onths.
Pa ge 8 0 1
Progresses for 1–2 weeks, then stabilizes for 2–3 weeks before receding: o
Usually subacute presentation with low m ortality
Slower onset is attributed to the toxin being produced locally as opposed to being ingested in one dose
C. botulinum spores found in honey: o
Honey not recom m ended for children younger than 6 m onths
Etiology
C. botulinum is a large spore-form ing, usually gram -positive, strictly anaerobic bacilli ubiquitous in nature.
Each strain produces antigenically distinct toxins, designated types A through G: o
Types A, B, and E are responsible for m ost hum an cases.
Diagnosis Signs and Symptoms History
Ingestions
Im m une status (AIDS, cancer, chronic illness)
Physical Exam
Food-borne botulism (classic botulism ): o
Most com m on:
Diplopia
Blurred vision
Bulbar weakness: dysphagia, dysarthria, dysphonia
Pa ge 8 0 2
o
Subsequent sym m etric, descending weakness or paralysis of the extrem ities (hallm ark of the disease)
o
No sensory deficit
o
Patient rem ains awake/alert; m entation unaffected.
o
Ventilatory insufficiency from weakness of respiratory m uscles
o
Autonom ic dysfunction (sym pathetic and parasym pathetic):
Dry m outh
Blurred vision
Orthostatic hypotension
Constipation
Urinary retention
o
Nausea and vom iting with food-borne botulism only
o
Afebrile
Wound botulism : o
Finding sim ilar to food-borne botulism
o
May be febrile
Infantile botulism : o
Constipation
o
Weakness
o
Poor suck
o
Lethargy
o
Hypotonia
o
Flaccid facial expression
o
Respiratory difficulty
Essential Workup
Diagnosis is entirely clinical.
Workup focuses on differentiation from other conditions causing general paralysis.
Notify public health officials of diagnosis.
Pa ge 8 0 3
Tests Lab
CBC
Electrolytes, BUN/creatinine, glucose: o
Arterial blood gas (ABG): o
Check for hypokalem ia.
For signs of respiratory insufficiency
Toxin detection in: o
Blood
o
Feces
o
Gastric contents
o
Suspected food and containers
Anaerobic blood cultures
Imaging CT/MRI of brain:
Norm al
Diagnostic Procedures/Surgery
Cerebrospinal fluid (CSF) testing: o
Norm al
o
Helps differentiate from Guillain-Barré syndrom e
Electrophysiologic studies: o
Norm al nerve conduction with dim inished evoked m uscle action potential
Edrophonium testing m ay be positive, but not to the degree seen in m yasthenia gravis.
P.157
Differential Diagnosis
Myasthenia gravis (less acute)
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Lam bert-Eaton m yasthenic syndrom e (less acute)
Polio (fever and asym m etric)
Guillain-Barré (sim ultaneous sensory findings and elevated spinal fluid protein)
Tick paralysis
Magnesium intoxication
Hypokalem ic periodic paralysis
Diphtheritic neuropathy
Pediatric Considerations Often m isdiagnosed as dehydration, sepsis, or Reye syndrom e
Treatment Alert
Death is invariably from progressive ventilatory failure: o
Intubate as soon as respiratory insufficiency noted.
Initial Stabilization
Early intubation and ventilatory support is the key to survival.
Respiratory difficulties occur rapidly.
ED Treatment
Trivalent ABE antitoxin: o
IV adm inistration as soon as the diagnosis is m ade, without waiting for laboratory confirm ation
o
Use should be preceded by testing for hypersensitivity to horse serum
Nasogastric (NG) suctioning if ileus is profound
With wound botulism , perform wound débridem ent even if it appears to be healing.
Pa ge 8 0 5
Antibiotics for specific infectious com plications
Medication (Drugs) Trivalent botulism antitoxin: two vials (approxim ately 10,000 IU each of types A, B, and E) IV
Pediatric Considerations
Antitoxin is rarely indicated for infantile botulism .
Antibiotics: o
Ineffective in eradicating organism from the intestine
o
Release of toxin in the gut through bacterial cell lysis m ay worsen neurologic sym ptom s.
Follow-Up Disposition Admission Criteria Adm it patients with suspected botulism poisoning to m onitored bed:
ICU adm ission for any respiratory deficiency
Discharge Criteria Clinical course of botulism poisoning is unpredictable; it can becom e rapidly progressive and fatal:
Discharge only patients with a prolonged period of progressive recovery from sym ptom s
References 1. Bleck TP. Clostridium botulinum . In: Mandell GI, Bennett JE, Dolin R, eds. Mandell, Douglas, and Bennett's Principles and Practice of Infectious Diseases. 4th ed. New York: Churchill-Livingstone; 1995. 2. Cherington M. Clinical spectrum of botulism . Muscle Nerve.
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1998;21:701–710. 3. Darling RG, Catlett CL, Huebner, et al. Threats in bioterrorism I: CDC category A agents. Em erg Med Clin N Am . 2002;20:273–309. 4. Hatheway CL. Botulism : the present status of the disease. Curr Top Microbiol Im m unol. 1995;195: 55–75. 5. Mechem CC, Walter FG. Wound botulism . Vet Hum Toxicol. 1994;36(3):233–237. 6. Midura TF. Update: infant botulism . Clin Microbiol Rev. 1996;9(2):119–125. 7. Shapiro RL, Hatheway C, Swerdlow DL. Botulism in the United States: a clinical and epidem iologic review. Ann Intern Med. 1998;129(3):221–228. 8. Wigginton JM, Thill P. Infant botulism : a review of the literature. Clin Pediatr. 1993;32(11):669–674.
Codes ICD9-CM 005.1
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Bo w el Obstructio n
Bowel Obstruction
Jenny Lu
Basics Description
Obstruction of norm al flow of intestinal contents owing to m echanical or nonm echanical causes
Obstruction leads to rapid increase in both anaerobic and aerobic bacteria, with resultant increase in m ethane and hydrogen production.
Distended bowel becom es progressively edem atous, and increased intestinal secretions cause further distention.
Retrograde peristalsis causes vom iting.
Etiology
Sm all bowel: o
Adhesions: m ost com m on
o
Hernias
o
Neoplasm s
o
Strictures: inflam m atory bowel
o
Traum a: bowel wall hem atom a
o
Miscellaneous: (e.g., ascaris infection)
Large bowel: o
Carcinom a
o
Volvulus
Pa ge 8 0 8
o
Diverticular disease
o
Inflam m atory bowel disease
o
Ischem ic colitis
Diagnosis Signs and Symptoms History
Previous surgery, m alignancy, constipation, cathartic use
Abdom inal pain:
o
Interm ittent when early
o
Constant with strangulated obstruction
Vom iting: o
Bile-stained em esis with proxim al obstruction
o
Feculent em esis with distal obstruction
Obstipation
Stool caliber changes
Physical Exam
Vital signs: o
Tachycardia, hypotension with significant volum e depletion
o
Fever with strangulation or perforation
o
Hypotherm ia with sepsis
Abdom inal exam ination: o
Distention
o
Variable tenderness, often diffuse
o
Hyperactive and high-pitched bowel sounds when early; hyperactive when late
o
Ischem ic or gangrenous bowel if pain out of proportion to findings
Pa ge 8 0 9
o
Peritoneal signs indicate strangulation or perforation.
Hernia (ventral, inguinal, fem oral)
Rectal exam : o
Rectal m ass
o
Blood in stool, gross or occult
Geriatric Considerations
Abdom inal pain variable in elderly
Nausea/vom iting and abdom inal pain are com m on sym ptom s in elderly patients with acute m yocardial infarctions: o
Abdom inal distention, obstipation, and colicky pain suggests GI cause.
Pediatric Considerations
Intussusception: o
Leading cause of intestinal obstruction in infants
o
Most com m on between 3 and 12 m onths of age
Incarcerated inguinal/um bilical hernia
Malrotation with volvulus: o
Can occur as early as 3–7 days of age
o
Double bubble sign seen on plain radiograph owing to partial obstruction of duodenum , resulting in air in stom ach and in first part of duodenum
Pyloric stenosis: o
Progressive, projectile, nonbilious, postprandial vom iting
o
Male/fem ale ratio: 5:1 incidence
o
Onset usually 2–5 weeks of age
Other causes include duodenal atresia, Hirschsprung, im perforate anus.
Essential Workup Careful history and physical exam
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Tests Lab
CBC: o
Leukocytosis com m on
Electrolytes, BUN/creatinine, glucose: o
Hypokalem ia
o
Hypochlorem ic m etabolic alkalosis
o
Prerenal azotem ia
Urinalysis
Am ylase/lipase
Stool hem e test
Type and cross-m atch
PT/PTT
ECG in patients at risk of coronary artery disease
Liver panels to exclude hepatic/biliary pathology
Imaging
Upright chest radiograph: o
Evaluate for lung pathology.
o
Check for free air beneath diaphragm .
Plain abdom inal radiographs, flat and upright (75% sensitivity) o
Distended loops of bowel (norm al sm all bowel 13 cm indicates potential rupture.
o
Air fluid levels
o
“String of pearls― sign if sm all bowel loops nearly com pletely fluid filled
P.159
Abdom inal CT for detecting neoplastic causes of
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obstruction (90% sensitivity for SBO):
o
Identify early strangulation
o
Delineate other causes of pain
Ultrasound (US): o
More sensitive and specific than plain film s for sm all bowel obstruction but not as accurate as CT
Diagnostic Procedures/Surgery Upper GI/barium enem a:
If carcinom a or m ass lesion suspected as cause
Differential Diagnosis
Paralytic ileus
Pseudo-obstruction (Ogilvie)
Perforated ulcer
Pancreatitis
Cholecystitis
Colitis
Mesenteric ischem ia
Urem ia
Treatment Initial Stabilization
Airway, breathing, and circulation m anagem ent (ABCs)
0.9% norm al saline (NS) or lactated ringers (LR) IV fluid resuscitation for significant volum e depletion and strangulated or perforated bowel:
o
Adults: 1 L bolus
o
Peds: 20 m L/kg bolus
Correct electrolyte abnorm alities, especially hypokalem ia.
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ED Treatment
Intravenous fluids (IVFs)
Nasogastric tube (NGT)
Foley catheter to m onitor urine output
Surgical consultation
Antibiotics for suspected strangulated/perforated bowel: o
Antibiotic choices to cover gram -negative aerobic and anaerobic organism s:
o
o
Single agent:
Piperacillin/tazobactam
Am picillin/sulbactam
Meropenem or im ipenem
Com bination regim en:
Analgesics o
Metronidazole PLUS ciprofloxacin or ceftriaxone
Morphine sulfate
Antiem etics: o
Odansetron
o
Prom ethazine
Medication (Drugs) Antibiotics:
Piperacillin-tazobactam (Zosyn): 3.375 g (peds: 150–400 m g/kg/24h IV div. q6h–q8h) IV q4h–q6h
Am picillin-sulbactam (Unasyn): 1.5–3 g (peds: 100–400 m g/kg/24h IV div. q6h) IV q6h
Meropenem (Merrem ): Adult: 1 g (peds: 60–120 m g/kg/24h IV q8h) IV q8h
Im ipenem -cilastatin (Prim axin): 250–1000 m g (peds: 50–100 m g/kg/24h IV q6h–q12h) IV q6h–q8h
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Metronidazole (Flagyl): 1 g IV, then 500 m g IV q6h (peds: 7.5–30 m g/kg/24h IV div. q6h–q8h)
Ciprofloxacin (Cipro): 400 m g IV q12h
Ceftriaxone (Rocephin): 1–2 g (peds: 25–75 m g/kg/d IV up to 2 g div. q12h–q24h) IV q24h
Analgesics:
Morphine sulphate: 2–10 m g/dose (peds: 0.1–0.2 m g/kg IV/IM/SC q2h–q4h) IV/IM/SC q2h–q6h PRN
Anti-em etics:
Odansetron (Zofran): 4 m g (peds: 0.1 m g/kg IV div. q8h) IV q4h–q8h PRN OR
Prom ethezine (Phenergan) 12.5–25 m g (peds: >2 yrs: 0.25–1 m g/kg/d IV/IM/PR div. q4h–q6h PRN) IV/IM/SC q4h
Follow-Up Disposition Admission Criteria All patients with suspected/confirm ed intestinal obstruction should be adm itted with early surgical consultation.
References 1. Adam so W. Bowel Obstruction in the Newborn. Em edicine [on-line reference]. Available at http://www.em edicine.com /ped/topic2857.htm . Last updated June 15, 2004. 2. Elsakr R. Antim icrobial treatm ent of intra-abdom inal infections. Dig Dis 1998;16: 47–60. (DOI: 10.1159/000016848) 3. Kim ura K, Loening-Baucke V. Bilious vom iting in the newborn: rapid diagnosis of intestinal obstruction. Am Fam Physician. 2000;61:
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2791–2798. 4. McCabe C. Obstruction, Large Bowel. Em edicine [on-line reference]. Available at http://www.em edicine.com /EMERG/topic65.htm . Last updated April 2005. 5. Nobie B. Obstruction, sm all bowel. Em edicine [on-line reference]. Available at http://www.em edicine.com /em erg/topic66.htm . Last accessed Novem ber 2005. Last updated Septem ber 2005. 6. Quickel R, Hodin RA. Clinical Manifestations and Diagnosis of Sm all Bowel Obstruction. UpToDate [on-line reference]. Available at http://www.uptodate.com . Last updated Februray 2005. 7. Quickel R, Hodin RA. Treatm ent of Sm all Bowel Obstruction. UpToDate [on-line reference]. Available at http://www.uptodate.com . Last updated January 2006. 8. Sanson TG, O'Keefe KP. Evaluation of abdom inal pain in the elderly. Em erg Med Clin North Am . 1996;14:615–627. 9. Sivit C. Gastrointestinal em ergencies in older infants and children. Radiol Clin North Am . 1997;35:865.
Codes ICD9-CM 560.9
ICD10 K57.6
Pa ge 8 1 5
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Bradyarrhythm ias
Bradyarrhythmias
Adam Z. Barkin
Basics Description
Defined as heart rate less than 60
Can be norm al variant
May present without sym ptom s
Etiology
Sinus node dysfunction: o
Sick sinus syndrom e:
Intrinsic disease: o
May alternate with tachycardia
Fibrous tissue replaces pacem aker cell
Extrinsic causes: o
β-blockers
o
Calcium channel blockers
o
Digoxin
o
Anti-arrhythm ics
o
Hypoxia
o
Hypotherm ia
o
Increased intracranial pressure
o
Increased vagal tone
o
Hypothyroid
Pa ge 8 1 6
o
Hyperkalem ia
o
Hypokalem ia
o
Hypoglycem ia
Atrioventricular node dysfunction: o
First degree aortic valve block:
Pulse rate prolongation greater than 0.2 seconds
o
Every P wave conducts a QRS com plex.
May not be bradycardic
Second degree AV block, type I—Mobitz I (Wenckebach):
o
o
Progressive prolongation of PR segm ent
P wave eventually fails to conduct
Often grouped beating
β-blocker or calcium channel blocker toxicity
Digitalis
Inferior wall ischem ia
Increased vagal tone
Myocarditis
Second degree AV block, type II—Mobitz II:
PR segm ents are constant
Interm ittent failure to conduct a QRS com plex
Anteroseptal ischem ia
Sclerodegenerative disease
Risk of third-degree heart block
Third-degree AV block—com plete heart block:
Dissociation of atrial and ventricular activity
Cardiac ischem ia
β-blocker or calcium channel blocker toxicity
Digitalis toxicity
Hyperkalem ia
Junctional bradycardia:
Pa ge 8 1 7
o
Loss of atrial rhythm , atrioventricular pacem aker takes over at 45–60 im pulses per m inute
o
β-blocker or calcium channel blocker toxicity
o
Digitalis toxicity
o
Cardiac ischem ia
Idioventricular bradycardia: o
Loss of both sinoatrial and atrioventricular nodal activity; bundle branch or Purkinje network takes over at 30–40 im pulses per m inute
o
Myocardial infarction
o
Cardiac tam ponade
o
Severe acidem ia
o
Preterm inal rhythm
Pediatric Considerations Hypoxia is the m ost com m on cause.
Pregnancy Considerations Can see bradycardia in setting of ectopic pregnancy
Diagnosis Signs and Symptoms
Asym ptom atic
Weakness
Syncope
Lightheaded/dizzy
Falls
Hypotension
Palpitations
History
Medication changes
Pa ge 8 1 8
Urine output
Traum a related to falls
Physical Exam
Mental status
Perfusion state
Essential Workup
Twelve-lead electrocardiogram and continuous cardiac m onitoring
Pulse oxim etry
Blood pressure m onitoring
Tests Lab
Serum glucose
Serum potassium
Serum electrolytes
Blood urea nitrogen
Creatinine
Cardiac enzym es
Digoxin level, if relevant
Thyroid function tests
Imaging Chest radiograph
Diagnostic Procedures/Surgery
Transcutaneous pacing
Transvenous pacing
Differential Diagnosis
Norm al variant
β-blocker toxicity
Calcium channel blocker toxicity
Pa ge 8 1 9
Digoxin toxicity
Hypoxia
Hypotherm ia
Hyperkalem ia
Hypokalem ia
Hypoglycem ia
Renal failure
Cardiac ischem ia
Increased intracranial pressure
Hypothyroidism
Treatment Pre Hospital
Treat the patient, not the heart rate.
Epinephrine/atropine: o
May increase the rate but lead to increased ischem ia
o
Should be used only in patients with evidence of hypoperfusion
o
Atropine usually does not affect heart rate in third-degree heart block.
Transcutaneous pacing: o
Initiated for poor perfusion that cannot be corrected by other m eans
o
Must obtain ventricular capture, dem onstrated by a palpable pulse
Hypotherm ia: Avoid m edication or pacing.
Pediatrics: Correct hypoxem ia before attem pting to increase the heart rate.
P.161
Pa ge 8 2 0
Initial Stabilization
ABC's
Apply pacing pads
Oxygen therapy
IV access
ED Treatment
Atropine and/or epinephrine for sym ptom atic or unstable bradycardia
Isoproterenol for hem odynam ically unstable bradycardia
D 5 0 for hypoglycem ia
β-blocker or calcium channel blocker overdose o
Calcium gluconate and glucagon
Calcium , D 5 0 , insulin and sodium bicarbonate for hyperkalem ia
Digoxin antibodies for digoxin toxicity
Initiate treatm ent of ischem ia associated with the bradyarrhythm ia.
Correct acid-base disturbances
Tem porary transvenous pacing wire if other therapy is not successful
Medication (Drugs)
Atropine: 0.5–1 m g (peds: 0.02 m g/kg; m in. dose of 0.1 m g) IV q3–5m in; m ax. dose of 0.04 m g/kg
Calcium gluconate: 1,000 m g (40–60 m g/kg) IV
D 5 0 : 25 g (peds: 1 cc/kg) IV
Epinephrine: 0.5–1 m g (peds: 0.01–0.03 m g/kg) IV q3–5m in; 1–4 m cg/m in (peds: 0.1–1 m cg/kg/m in) IV infusion
Pa ge 8 2 1
Glucagon: 0.05–0.15 m g/kg IV; 2–5 m g/h IV infusion
Isoproterenol infusion: 1–4 m cg/m in IV
Follow-Up Disposition Admission Criteria
Intensive care unit: o
Hem odynam ically unstable bradycardia
o
Transvenous pacer
o
Pressor therapy
o
Acute m yocardial infarction or ischem ia
o
After/ongoing em ergent antidote treatm ent
Telem etry: o
Hem odynam ically stable bradycardia
Discharge Criteria Asym ptom atic sinus bradycardia
References 1. Birkhahn RH, Gaeta TJ, Tloczkowski J, et al. Em ergency m edicine-trained physicians are proficient in the insertion of transvenous pacem akers. Ann Em erg Med. 2004;43:469–474. 2. Brady WJ, Harrigan RA. Diagnosis and m anagem ent of bradycardia and atrioventricular block associated with acute coronary ischem ia. Em erg Med Clin North Am . 2001;19:371–384. 3. Kaushik V, Leon AR, Forrester JS, et al. Bradyarrhythm ias, tem porary and perm anent pacing. Crit Care Med. 2000: 28:N121–128. 4. Mangrum JM, DiMarco JP. The evaluation and m anagem ent of bradycardia. NEJM. 2000;342: 703–709.
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Miscellaneous SEE ALSO: Acute Coronary Syndrom e; β-Blocker Overdose; Calcium Channel Blocker Overdose; Digoxin Overdose; Hyperkalem ia
Codes ICD9-CM 427.8
ICD10 I49.8
Pa ge 8 2 3
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Bro nchio litis
Bronchiolitis
Suzanne Schuh
Basics Description Lower respiratory tract infection by airway inflam m ation and bronchoconstriction with wheezes/tachypnea and respiratory distress and upper respiratory prodrom e
Etiology
Respiratory syncytial virus (RSV) in 85–90% of cases
Influenza
Parainfluenza
Adenovirus
Diagnosis Signs and Symptoms
Age younger than 2 years
Nasal congestion
Cough
Wheezing
Crackles
Pa ge 8 2 4
Respiratory distress m anifested by nasal flaring, retractions, grunting
Fever usually Table o f C o ntents > Bundle Branch Blo cks
Bundle Branch
Blocks Keith S. Boniface James Scott
Basics Description
Blockage of intraventricular electrical im pulses through the right and left bundles
Com plete bundle branch block: o
Absence or delay of conduction down one bundle, with norm al conduction down the other bundle
o
Affected ventricle depolarizes from m uscle to m uscle in a slower and m ore disorganized fashion.
o
Quasi-random signal (QRS) com plex at 120 m sec or longer
Incom plete bundle branch block: o
Delayed depolarization, but less than com plete bundle branch block
o
QRS com plex less than 120 m sec and 100 m sec or longer
Right bundle branch block: o
Delayed depolarization of the right ventricle
Pa ge 8 3 9
Left bundle branch block: o
Delayed depolarization of the left ventricle
o
Left bundle branch block can be caused by delay of conduction in m ain left bundle or delay in both fascicles of the left bundle.
o
Causes early activation of the right side of the septum and the right ventricular m yocardium (so explaining loss of “septal Q― on ECG)
o
Left bundle branches into two fascicles:
Left anterior fascicle: Initial septal activation proceeds inferiorly, anteriorly, and to the right.
Left posterior fascicle: rare; activation begins in the m idseptum and finishes in inferior and posterior walls.
Bifascicular block: o
Right bundle branch block with concom itant block of the left anterior or left posterior fascicle
Etiology
Myocardial infarction
Cardiom yopathy
Hypertension
Age-related fibrosis of Purkinje fibers
Valvular disease
Exercise induced
Congenital/atrial septal defect
Brugada syndrom e (right bundle branch block): cause of sudden cardiac death in otherwise healthy patients
Chagas disease (especially Central/South Am erica)
Postoperative, following cardiac surgery
Drugs: o
Beta-blockers
o
Calcium blockers
Pa ge 8 4 0
o
Tricyclic antidepressants
o
Type Ia and Ic antiarrhythm ics
o
Digitalis
Diagnosis Signs and Symptoms
Asym ptom atic
Right bundle branch block: split S 2 that persists with expiration
Left bundle branch block: reversed/paradoxic split S 2
Syncope
Chest pain
Essential Workup Electrocardiography:
Right bundle branch block: o
Com plete: QRS com plex ≥ 0.12 seconds; incom plete: ≤ 0.10 seconds QRS com plex ≤ 0.12 seconds
o
rsr′, rsR′, rSR′ in V 1 or V 2 (M shape)
o
Wide and deep S wave in V 5 through V 6
o
Brugada syndrom e: RBBB and ST-segm ent elevation in V 1 through V 3
Left bundle branch block: o
Broad slurred R waves in leads V 5 through V 6 , aVL, and I
o
Sm all/absent R wave in V 1 through V 2 and deep S waves
o
Absence of norm al q waves in leads V5 through V6 and I
Pa ge 8 4 1
Left anterior fascicular block: o
QRS com plex Table o f C o ntents > Bursitis
Bursitis
Kelly Pettit
Basics Description
Bursae are synovial fluid-filled sacs: o
Approxim ately 150 located between bones, ligam ents, tendons, m uscles, and skin
o
Provide lubrication to reduce friction during m ovem ent
Bursitis is inflam m ation of a bursae caused by traum a (acute or chronic), repetitive use, prolonged pressure, infection, crystal deposition, or system ic disease.
Affected joints: o
Potentially any bursa m ay be affected.
o
Com m only affected joints:
Shoulder
Elbow: usually secondary to traum a
Wrist and hand
Hip: m ore com m on in elderly
Knee: secondary to traum a or arthritis
Foot: calcaneal bursitis is alm ost always secondary to im properly fitting shoes/heels.
Etiology
Pa ge 8 5 7
Traum a (m ost com m on cause): o
Specific traum atic event or repetitive use of associated joints
Infection: m ay be obvious or m icroscopic: o
Higher risk with diabetes, chronic alcohol abuse, urem ia, gout, im m unosuppression
o
90% caused by staphylococci
Crystal deposition: calcium phosphate, urate
System ic disease: rheum atoid arthritis, gout, ankylosing spondylitis, psoriatic arthritis, lupus, rheum atic fever
Diagnosis Signs and Symptoms History
Acute onset, but m ay be chronic (especially in hip)
Elicit history of traum a, overuse, or prolonged pressure.
Screen for system ic disease.
Physical Exam
Localized pain that worsens with m ovem ent of structures adjacent to affected bursae
Often reduced active range of m otion (ROM) with preserved passive ROM
Localized swelling m ay be present with superficial bursal involvem ent.
Overlying erythem a, warm th, or skin traum a m ay be present with infectious bursitis.
May have low-grade tem perature
Essential Workup
Full assessm ent of adjacent m usculoskeletal structures
Pa ge 8 5 8
Any suspicion of infection warrants aspiration of bursae (especially olecranon and prepatellar bursae).
Aspiration of hip and other deep bursae m ay be guided in ED by ultrasound or deferred to interventional radiology, orthopedics, or rheum atology.
Tests Lab
Serum labs: o
Suspected infection: CBC with differential
o
Evaluation of related system ic disease (e.g., uric acid level for gout)
o
Send serum glucose if bursal fluid aspiration is done.
Bursal fluid analysis: o
Send fluid for cell count with differential, glucose, total protein, crystal determ ination, Gram stain, and culture.
o
Because infection and inflam m ation m ay be difficult to differentiate, cultures m ust always be sent.
o
Norm al fluid: Fluid is clear yellow with 0–200 WBCs, 0 RBCs, low protein, and glucose is sam e as serum .
o
Traum atic bursitis: Fluid is bloody/xanthochrom ic with 50,000 WBCs, few RBCs, slightly increased protein, and decreased glucose; bacteria on Gram stain.
o
Rheum atoid and m icrocrystalline inflam m ation: fluid is yellow, can be cloudy, and has 1,000–40,000 WBCs, few RBCs, slightly increased protein, and variable glucose; use polarizing m icroscope to
Pa ge 8 5 9
identify crystals.
Imaging
Radiographs m ay dem onstrate chronic arthritic changes or calcium deposits: o
Recom m ended when traum a is involved to rule out fracture or foreign body
MRI and ultrasound m ay aid in diagnosis of deep bursitis and in defining the extent of infectious bursitis.
Differential Diagnosis
Arthritis, gout
Tendonitis, fasciitis, epicondylitis
Fracture, tendon/ligam ent tear, contusion, sprain
Osteom yelitis
Also in hips: neuritis, lum bar spine disease, sacroiliitis
Treatment Pre Hospital May be difficult to distinguish from fractures; suspicious joints should be im m obilized, particularly in the setting of traum a.
Initial Stabilization Im m obilize joint if pain severe:
Shoulders should not be im m obilized for >2–3 days because of the risk of adhesive capsulitis.
P.171
ED Treatment
Noninfectious bursitis:
Pa ge 8 6 0
o
Rest and rem oval of aggravating factors (e.g., avoid direct pressure and repetitive use)
o
Ice affected areas for 10 m inutes, four tim es a day until im proved; m ay alternate with heat.
o
Nonsteroidal anti-inflam m atory drugs (NSAIDs) for at least 7 days; best if continued for 5 days after im provem ent to help prevent recurrence
o
If no im provem ent within 5–7 days and infection has been ruled out (by culture), injection of lidocaine and steroids m ay be considered:
Mix 2 m L of 2% lidocaine with 20–40 m g of depoglucocorticoid and inject 1–3 m L of this m ixture into the bursae using sterile technique.
Steroid injections should not be repeated until at least 4 weeks have passed, and no m ore than two injections into one joint should be perform ed without rheum atologic or orthopedic consultation.
Septic bursitis: o
Olecranon: Aspiration and antibiotics m ay be sufficient with close follow-up.
o
Other m ajor bursae: antibiotics and drainage of bursae (leaving in perforated drainage catheter can reduce period of treatm ent and avoid eventual bursectom y)
o
Base antibiotic choice on the Gram stain:
Penicillinase-resistant antistaphylococcal drug m ay be used if Gram stain result is negative or shows gram -positive cocci.
If gram -negative organism s are found, blood cultures should be done and another prim ary source for the infection should be sought.
Pa ge 8 6 1
o
Antibiotics should be continued for 5–7 days beyond the sterilization of bursal fluid.
Treat associated diseases as needed (e.g., gout).
Medication (Drugs)
NSAIDs (m any choices; a few are listed here): o
Diclofenac: 50 m g PO b.i.d./t.i.d.
o
Ibuprofen: 600 m g PO q6h (peds: 5–10 m g/kg PO q6h)
o
Ketorolac: 30 m g IV/IM q6h or 10 m g PO q4h–q6h
o
Piroxicam : 20 m g PO daily
Corticosteroids: o
Methylprednisolone acetate: 20–40 m g single intrabursal injection
o
Triam cinolone acetonide: 20–40 m g single intrabursal injection
Follow-Up Disposition
Most patients m ay be treated as outpatients.
Most patients respond to therapy in 3–4 days and m ay follow up within a week.
Septic bursitis requires repeated bursal aspiration every 3–5 days until sterile.
Admission Criteria
Patients with high fevers, chills/rigors, large surrounding cellulitis, unable to take oral antibiotics, failed outpatient therapy, or im m unosuppressed
Pa ge 8 6 2
Unusual organism s, extrabursal prim ary site, or deep bursal involvem ent
Issues for Referral Rheum atology or orthopedic referral is recom m ended for patients who do not respond to intrabursal steroids or recurrent bursitis.
References 1. Butcher JD, et al. Lower extrem ity bursitis. Am Fam Physician. 1996;53(7):2317–2324. 2. Chau CL, Griffith JF. Musculoskeletal infections: ultrasound appearances. Clin Radiol. 2005;60(2):149–159. 3. Greene WB, ed. Essentials of Musculoskeletal Care. 2nd ed. Rosem ont, IL: Am erican Academ y of Orthopedic Surgeons; 2001: 20–23, 335–337, 368–370, 402–403. 4. Gutierrez G, Burroughs M, Poddar S. Clinical inquiries. Does injection of steroids and lidocaine in the shoulder relieve bursitis? J Fam Pract. 2004;53(6):488–492. 5. Larsson L, Baum J. The syndrom es of bursitis. Bull Rheum Dis. 1986;36(1):1–8.
Codes ICD9-CM 727.3
Pa ge 8 6 3
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > C alcium C hannel Blo cker, Po iso ning
Calcium
Channel Blocker, Poisoning Janet Eng
Basics Description Three Classes of Calcium Channel Blockers
Phenylalkylam ines (verapam il): o
Vasodilation resulting in a decrease in blood pressure (BP)
o
Negative chronotropic and inotropic effects: reflex tachycardia not seen with a drop in BP.
Dihydropyridine (nifedipine): o
Decreased vascular resistance resulting in a drop in BP
o
Little negative inotropic effect: reflex tachycardia occurs.
Benzodiazepine (diltiazem ): o
Decreased peripheral vascular resistance leading to a decrease in BP
o
Heart rate (HR) and cardiac output initially increased
o
Direct negative chronotropic effect, which leads to a fall in HR
Pa ge 8 6 4
Effects of Calcium Channel Blockade
Calcium plays key role in cardiac and sm ooth m uscle contractility.
Calcium channel blockers (CCBs) prevent: o
The entry of calcium , resulting in a lack of m uscle contraction
o
The norm al release of insulin from pancreatic islet cells, resulting in hyperglycem ia
Diagnosis Signs and Symptoms
Cardiovascular: o
Hypotension
o
Bradycardia
o
Reflex tachycardia (dihydropyridine)
o
Conduction abnorm alities/heart blocks
Neurologic: o
CNS depression
o
Com a
o
Seizures
Metabolic: o
Hyperglycem ia
Essential Workup ECG:
Bradycardia (tachycardia with nifedipine)
Conduction delays: QRS-com plex prolongation
Heart blocks
Tests
Pa ge 8 6 5
Lab
Ionized calcium level when adm inistering calcium
Digoxin level if patient taking digoxin (dictate safety of calcium adm inistration)
CBC
Electrolytes, BUN, creatinine, glucose: o
Hyperglycem ia/m etabolic acidosis m ay occur.
Toxicology screen if coingestants suspected
Differential Diagnosis
β-Blocker toxicity
Clonidine toxicity
Digitalis toxicity
Acute m yocardial infarction with heart block
Treatment Pre Hospital Cautions:
Transport pill/pill bottles to ED.
Calcium for bradycardic/unstable patient with confirm ed CCB overdose
Initial Stabilization Airway, breathing, circulation (ABCs):
Airway protection as indicated
Supplem ental oxygen as needed
0.9% norm al saline (NS) IV access
Hem odynam ic m onitoring
ED Treatment
Pa ge 8 6 6
Goals
Heart rate >60 beats/m inute
Systolic BP >90 m m Hg
Adequate urine output
Im proving level of consciousness
GI Decontamination
Syrup of ipecac: contraindicated in the ED
Activated charcoal: o
May be helpful, especially in the presence of coingestants
Whole bowel irrigation: o
Beneficial with ingestion of sustained-release preparations
o
Contraindicated in hem odynam ically unstable patients
P.173
Calcium
First-line agent for CCB toxicity
Calcium chloride (10%): o
Contains 1.36 m Eq Ca 2 + /m L (three tim es m ore calcium than calcium gluconate)
o
Can cause tissue necrosis and sloughing with extravasation
o
Very irritating to veins
Calcium gluconate (10%): o
Contains 0.45 m Eq Ca 2 + /m L
o
Does not cause tissue necrosis as calcium chloride does
o
Calcium gluconate: preferred agent in an acidem ic
Pa ge 8 6 7
patient
Follow serum calcium levels if repeated doses of calcium adm inistered.
Contraindicated in digoxin toxicity because calcium can produce serious adverse effects in digoxin toxicity
Bradycardia/Hypotension
IV fluids: o
Adm inister cautiously in the hypotensive patient.
o
Swan-Ganz catheter or central venous pressure (CVP) m onitoring to help follow volum e status
Atropine usually ineffective
Pressor agents: o
No clear evidence that one agent is m ore effective than another
o
Institute invasive m onitoring to help guide treatm ent.
o
Dopam ine:
β 1 -Receptor agonist at low doses, which causes a positive inotropic effect on the m yocardium
α-Receptor agonist at higher doses, which leads to vasoconstriction
o
Epinephrine:
Potent α- and β-receptor agonist
Glucagon: o
Prom otes cAMP production through a receptor site other than the β-receptor
o
May cause nausea and vom iting
o
Mix with NS or 5% dextrose in water.
Am rinone: o
Selective phosphodiesterase III inhibitor
o
Indirectly increases cAMP
Electrical pacing: when other treatm ent options have
Pa ge 8 6 8
failed
Insulin: o
Prom otes m ore efficient m yocardial m etabolism
Hypertonic sodium bicarbonate: o
Potential treatm ent in the future
Medication (Drugs)
Am rinone: loading dose 0.75 m g/kg; m aintenance drip 2–20 µg/kg/m in; titrate for effect
Atropine: 0.5 m g (peds: 0.02 m g/kg) IV; repeat 0.5–1.0 m g IV (peds: 0.04 m g/kg)
Calcium chloride: 10 m L of 10% solution slow IVP (peds: 0.2–0.25 m L/kg; repeat in 10 m inutes if necessary) followed by infusion 20–50 m g/kg/h
Calcium gluconate: 10 m L of 10% solution slow IVP (peds: 1 m L/kg; m ay repeat in 10 m inutes if necessary)
Dopam ine: 2–20 µg/kg/m in; titrate to effect
Epinephrine: 2 µg/m in (peds: 0.1 µg/kg/m in); titrate to effect
Glucagon: 3.5–5 m g (peds: 0.03–0.1 m g/kg) IV bolus followed by 70 µg/kg/h infusion
GoLYTELY WBI: 2 L/h PO or by nasogastric tube (NGT) for 4–6 hours or until rectal effluent is clear (peds: 40 m L/kg/h)
Insulin: 1 IU/kg bolus IV followed by 0.5–1.0 IU/kg/h titrated to clinical response
Follow-Up
Pa ge 8 6 9
Disposition Admission Criteria
Adm it sym ptom atic patients to a m onitored bed for hem odynam ic m onitoring.
Adm it all patients who ingested sustained-release CCBs for 24 hours of observation and m onitoring owing to the potential delay in sym ptom s.
Discharge Criteria Discharge asym ptom atic patients 8 hours after ingestion of im m ediate-release preparation.
References 1. Boyer EW, Shannon MW. Treatm ent of calcium channel blocker intoxication with insulin infusion. New Engl J Med. 2001;344:1721–1722. 2. Kalm an S, Berg S, Lisander B. Com bined overdose with verapam il and atenolol: treatm ent with high doses of adrenergic agonists. Acta Anaesthesiol Scand. 1998;45:379–382. 3. Salhanick SD, Shannon MW. Managem ent of calcium channel antagonist overdose. Drug Safety. 2003;26:65–79. 4. Tanen DA, Ruha AM, Curry SC, et al. Hypertonic sodium bicarbonate is effective in the acute m anagem ent of verapam il toxicity in swine m odel. Ann Em erg Med. 2000;36:547–553.
Miscellaneous SEE ALSO: β-Blocker, Poisoning
Codes ICD9-CM 977.9
Pa ge 8 7 0
ICD10 T46.1
Pa ge 8 7 1
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > C andidiasis, Oral
Candidiasis, Oral
Howard K. Mell Kristine M. Thompson
Basics Description
Infection of oral m ucosa with any species of Candida, m ost com m only Candida albicans
Candida norm ally present as oral flora in 20–60% of the healthy population.
Several variations exist, ranging in severity from superficial and localized to severe system ic disease with 50% m ortality.
In im m unocom petent individuals, a benign course is the norm .
Often recurrent in im m unocom prom ised patients
May represent an early m anifestation of AIDS in HIV-infected patients
Etiology
Usually overgrowth of Candida albicans from alterations in intraoral environm ent
Antim icrobial treatm ent
Changes in salivary flow (anticholinergic m edications, steroid inhalers, psychotropics, and others)
Pa ge 8 7 2
Presence of dentures or other orthodontic appliances
Interruption of epithelial barrier (cheek biting)
Endocrinopathies (diabetes, hypothyroidism )
Im m unosuppression (iatrogenic, congenital, or acquired)
Acute Pseudomembranous Candidiasis (Thrush)
Com m only occurs with other serious underlying conditions (diabetes, leukem ia, AIDS)
Frequently m edication induced in the im m unocom petent
Acute and Chronic Atrophic Candidiasis Occurs in up to 60% of denture wearers
Angular Cheilosis
Often seen with intraoral candidal infection
Loss of skin barrier from repetitive irritation
Often superinfected with Staphylococcus epiderm idis
Hyperplastic Candidiasis
Im m unosuppressed individuals
High incidence of m alignant degeneration in tobacco users
Geriatric Considerations
Candida organism s are norm ally present as oral flora in up to 80% of elderly or those in long-term care facilities.
The presence of dentures or other orthodontic appliances can lead to the overgrowth of candida.
Angular cheilosis is m ore com m on in the elderly secondary to facial wrinkling.
Pediatric Considerations
Acute pseudom em branous candidiasis (thrush) is com m on in infancy likely because of im m aturity of their im m une system and lack of m ature oral flora.
Pa ge 8 7 3
The source of infection is believed to be m aternal birth canal.
Diagnosis Signs and Symptoms Pseudomembranous Candidiasis (Thrush)
Painless white m ucosal plaques
Adherent but rem ovable
Erythem atous base
May becom e confluent and curdlike
Anorexia
Atrophic Candidiasis (Denture Stomatitis)
Burning sensation in m outh or on tongue
Erythem atous with few, if any, white patches
Usually lim ited to the denture-bearing m ucosa
Angular Cheilosis
Cracking and erythem a at the corners of the m outh
Lesion can be asym ptom atic, pruritic, or painful.
Hyperplastic Candidiasis
Chronic, invasive ulcers
Typically on lateral borders of tongue or buccal m ucosa
Essential Workup
Determ ine whether there is a cause for a breakdown of host factors.
If no reason is found, evaluate for possible HIV infection or diabetes.
Exclude a system ic infection.
Pa ge 8 7 4
Tests Lab
CBC if suspect severe infection
Glucose testing
Potassium hydroxide (KOH)/fungal culture
P.175
Differential Diagnosis
Hairy leukoplakia
Hyperkeratosis
Lichen planus
Squam ous cell carcinom a
Adherent food/m ilk
Treatment ED Treatment
Topical antifungal m edications: o
Clotrim azole
o
Itraconazole
o
Nystatin
o
Com bine with topical steroid for angular cheilosis.
System ic agents (should be reserved for those with disease resistant to topical therapy):
o
Fluconazole
o
Itraconazole
o
Ketoconazole
Analgesia:
Pa ge 8 7 5
o
“Magic m outhwash―:
Form ulas vary by institution; one com m only used is equal parts viscous lidocaine, diphenhydram ine elixir, and m agnesium alum inum hydroxide.
Medication (Drugs) Pediatric Considerations
Dissolve troche in nipple of bottle.
Mix suspensions with fruit juice and freeze into popsicle.
Apply suspensions to affected areas with cotton-tipped swab.
Topical
Clotrim azole: 10-m g troche five tim es daily (children >3 years)
Itraconazole: 10 m L solution (peds: 5 m g/kg/d, m ax. 600 m g/d) swish and swallow daily
Nystatin oral suspension: 6 m L (peds: infants 2 m : PO; children 4–6 m L PO) swish and swallow four tim es daily
Nystatin/triam cinolone ointm ent: Apply twice daily.
Nystatin troche: 1 or 2 troches (peds: infants one-half troche, children 1 troche) 4–5 tim es daily
Systemic
Fluconazole: 200 m g day 1, then 100 m g (peds: 14 days old 12 m g/kg, then 6 m g/kg, m ax. 400 m g daily) PO daily
Itraconazole solution: 200 m g (peds: 5 m g/kg/d) PO twice daily
Ketoconazole: 200 m g (peds: 5–10 m g/kg) PO daily
Pa ge 8 7 6
Nystatin: one or two tabs (peds: use oral suspension as above) PO three tim es daily
Follow-Up Disposition Admission Criteria
Inability to tolerate oral intake owing to discom fort
Newly diagnosed im m unocom prom ised state
System ic infection
Discharge Criteria Patients with candidiasis that does not threaten the patient's hydration status m ay be discharged with close follow-up.
References 1. Fotos PG, Lilly JP. Clinical m anagem ent of oral and perioral candidosis. Derm atol Clin. 1996;14:273–280. 2. Glick M. Viral and fungal infections of the oral cavity in im m unocom petent patients. Infect Dis Clin North Am . 1999;13(4):817–831. 3. McGee D. Topical and local anesthesia. In: Roberts JR, Hedges JR, eds. Clinical Procedures in Em ergency Medicine. 4th ed. St. Louis, MO: WB Saunders; 2004. 4. Messadi DV, Waibel JS, Mirowski GW. White lesions of the oral cavity. Derm atol Clin. 2003;21(1):63–78. 5. Patel NJ, Sciubba J. Oral lesions in young children. Pediatr Clin North Am . 2003;50(2):469–486. 6. Shay K, Truhlar MR, Renner RP. Oropharyngeal candidosis in the older patient. J Am Geriatr Soc. 1997;45(7):863–870.
Codes
Pa ge 8 7 7
ICD9-CM 112.0
ICD10 B37.0
Pa ge 8 7 8
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > C arbam az epine, Po iso ning
Carbamazepine, Poisoning James W. Rhee
Basics Description
Therapeutic uses of carbam azepine: o
Anticonvulsant
o
Treatm ent of chronic pain
o
Migraine prophylaxis
o
Mood stabilizer
Mechanism : o
Anticholinergic
o
Sim ilarities to phenytoin and tricyclic antidepressants (TCAs)
o
Sodium channel blocker
o
Decreases synaptic transm ission
Etiology Toxicity m ay occur from :
Suicide attem pt
Accidental ingestion
Supratherapeutic dosing
Drug–drug interaction
Pa ge 8 7 9
Diagnosis Signs and Symptoms
Neurologic m anifestations com m on
Cardiotoxicity rare, except in m assive overdose
CNS:
o
Ataxia
o
Dizziness
o
Drowsiness
o
Nystagm us
o
Hallucinations
o
Com bativeness
o
Com a
o
Seizures
Respiratory system : o
Respiratory depression
o
Aspiration pneum onia
Cardiovascular system : o
Hypotension
o
Conduction disturbances (m ostly in elderly)
o
Supraventricular tachycardia
o
Sinus tachycardia or bradycardia
o
ECG changes:
Prolongation of PR, QRS, and QTc intervals
T-wave changes
Miscellaneous: o
Anticholinergic m anifestations:
Decreased bowel sounds
Mydriasis
Flushing
Urinary retention
Pa ge 8 8 0
o
Neurom uscular changes:
Trem or
Slurred speech
Myoclonus
Choreiform and choreoathetoid m ovem ents
Pediatric Considerations Higher incidence of neurologic m anifestations
Essential Workup
Continuous cardiac m onitor
Serum carbam azepine level: o
Therapeutic, 6–12 µg/L
o
Levels >25–40 µg/m L associated with serious toxicity:
o
Com a
Seizures
Respiratory failure
Conduction defects
Serum levels do not clearly predict clinical toxicity:
Active m etabolite carbam azepine epoxide not m easured
Neurologic m anifestations depend on CNS (not serum ) level.
o
Serial levels m ay be needed owing to erratic absorption of carbam azepine.
ECG: o
Conduction delays:
Increased QRS interval
Increased PR interval
o
Dysrhythm ias
o
Sinus tachycardia (m assive carbam azepine overdose)
o
Bradydysrhythm ia (often seen in elderly with m ild
Pa ge 8 8 1
increase in carbam azepine level)
Serum acetam inophen level (to evaluate for coingestion in a suicide attem pt)
Tests Lab
CBC: o
Leukopenia or leukocytosis
Electrolytes, BUN/creatinine, glucose: o
Hyperglycem ia
o
Hypokalem ia
o
Hyponatrem ia
Arterial blood gases (ABGs)
Urinalysis: o
Glucosuria
o
Ketonuria
Pregnancy test
ALT, AST, bilirubin, alkaline phosphatase: o
May be m ildly elevated
o
Usually not clinically significant
Imaging Chest radiograph:
Aspiration pneum onia
Pulm onary edem a
Differential Diagnosis
Drugs that cause decreased m ental status: o
Alcohol
o
Anticholinergics
o
Barbiturates
o
Benzodiazepines
o
Lithium
Pa ge 8 8 2
o
Opiates
o
Phenothiazines
Drugs that cause seizures: o
Alcohol withdrawal
o
Anticholinergics
o
Cam phor
o
Isoniazid
o
Lithium
o
Phenothiazines
o
Sym pathom im etics
o
Am phetam ine
Cocaine
TCAs
Drugs that cause abnorm al m ovem ent: o
Antihistam ines
o
Butyrophenones
o
Caffeine
o
Cocaine
o
Levodopa
o
Meperidine
o
Phencyclidine
o
Phenothiazines
o
Phenytoin
o
TCAs
Treatment Pre Hospital
Do not adm inister ipecac.
Intubate if significant respiratory depression or airway com prom ise.
Pa ge 8 8 3
Secure IV access.
Get com plete inform ation about all products potentially ingested.
Initial Stabilization
Airway, breathing, and circulation m anagem ent (ABCs)
Intravenous access and fluid resuscitation if hypotensive
Oxygen
Cardiac m onitor
Naloxone, thiam ine, D 5 0 W (or Accu-Chek) if altered m ental status
P.177
ED Treatment
General m anagem ent: o
Gastric lavage:
Consider if recent ingestion (100 m sec):
Sodium bicarbonate (to overcom e sodium channel blockade)
Psychiatric consultation if suicide attem pt
Medication (Drugs)
Activated charcoal (initial bolus): slurry 1–2 g/kg up to 100 g PO m ixed with sorbitol (below)
Dextrose: D 5 0 W 1 am pule: 50 m L or 25 g (peds: D 2 5 W 2–4 m L/kg) IV
Diazepam : 5–10 m g (peds: 0.2–0.5 m g/kg) IV
Multidose activated charcoal: 25 g (peds: 0.25 g/kg) q2h PO after bolus dose (above)
Pa ge 8 8 5
Naloxone (Narcan): 2 m g (peds: 0.1 m g/kg) IV/IM initial dose
Norepinephrine: 4–12 µg/m in (peds: 0.05–0.1 µg/kg/m in) IV titrated to effect
Sodium bicarbonate 1 or 2 am ps IV push (peds: 1–2 m Eq/kg)
Sorbitol: 1–2 g/kg to m ax. 100 g (peds: older than 1 year old, 1–1.5 g/kg as 35% solution to m ax. 50 g) PO m ixed with activated charcoal slurry (first dose only)
Follow-Up Disposition Admission Criteria
Decreased m ental status at any tim e, even if resolving: o
Observe at least 24 hours for late relapse.
Seizures
Cardiac dysrhythm ias
Lack of psychiatric clearance after suicidal ingestion
Discharge Criteria
Asym ptom atic after 6 hours of observation
Norm al m ental status
Norm al or baseline ECG
GI m otility present
Psychiatric clearance (after suicidal ingestion)
Issues for Referral
Suicidal patients need psychiatric evaluation referral.
Supratherapeutic dosing will need ongoing m onitoring by physician treating underlying disorder.
Pa ge 8 8 6
References 1. Bridge TA, Norton RL, Robertson WO. Pediatric carbam azepine overdoses. Pediatr Em erg Care. 1994;10:260–263. 2. Deshpande G, Meert KL, Valentini RP. Repeat charcoal hem operfusion treatm ents in life threatening carbam azepine overdose. Pediatr Nephrol. 1999;13:775–777. 3. Hojer J, Malm lund H, Berg A. Clinical features in 28 consecutive cases of laboratory confirm ed m assive poisoning with carbam azepine alone. J Toxicol Clin Toxicol. 1993;31:449–458. 4. Schm idt S, Schm itz-Buhl M. Signs and sym ptom s of carbam azepine overdose. J Neurol. 1995;242: 169–173. 5. Seym our JF. Carbam azepine overdose: features of 33 cases. Drug Safety. 1993;8:81–88. 6. Wason S, Baker RC, Carolan P, et al. Carbam azepine overdose: the effects of m ultiple dose activated charcoal. J Toxicol Clin Toxicol. 1992;30:39–48.
Codes ICD9-CM 966.3
Pa ge 8 8 7
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > C arbo n M o no xide, Po iso ning
Carbon
Monoxide, Poisoning Trevonne M. Thompson
Basics Description
Carbon m onoxide (CO) is a colorless, odorless, nonirritating gas.
Binds to hem oglobin to form carboxyhem oglobin: o
Decreases oxygen-carrying capacity
o
Decreases oxygen release to tissue owing to shift of oxyhem oglobin dissociation curve to the left
Direct cellular toxin
Binds to other hem e-containing proteins: o
Cytochrom es:
o
Im pairs cellular oxygen utilization
Myoglobin:
Im pairs cardiac and skeletal m uscle function
Etiology
Endogenous: o
Result of norm al m etabolism
Incom plete com bustion of carbonaceous fossil fuel: o
Internal com bustion engines
Pa ge 8 8 8
o
Natural gas
o
Heaters
o
Indoor grills
o
Fireplaces
o
Furnaces
o
Accidental fires
o
Tobacco sm oke
Methylene chloride: o
Found in som e solvents for paint rem oval and furniture stripping
o
Endogenously converted to carbon m onoxide after exposure
o
Peak carboxyhem oglobin levels delayed after exposure
o
Half-life is approxim ately two tim es that of inhaled carbon m onoxide.
Diagnosis Signs and Symptoms History
CNS: o
Headache
o
Dizziness
o
Ataxia
o
Confusion
o
Syncope
o
Seizures
GI: o
Nausea
Pa ge 8 8 9
o
Cardiovascular: o
Chest pain
o
Palpitations
Respiratory: o
Vom iting
Dyspnea
Ophthalm ologic: o
Decreased visual acuity
Physical Exam
CNS: o
Acute encephalopathy
o
Seizures
o
Com a
Cardiovascular: o
Tachycardia
o
Prem ature ventricular contractions
o
Dysrhythm ias
o
Myocardial ischem ia/infarction
Respiratory: o
Tachypnea
o
Noncardiogenic pulm onary edem a
Ophthalm ologic: o
Retinal hem orrhage
Other: o
Respiratory alkalosis
o
Rhabdom yolysis
o
Lactic acidosis
Essential Workup
History: o
Maintain a high index of suspicion.
o
Sym ptom s m ay be m ild, nonspecific.
Pa ge 8 9 0
o
Inquire about the following:
Sim ilar sym ptom s in other household m em bers
Malfunctioning furnaces
Use of space heaters, open ovens for supplem ental heat
Ill pets
Arterial blood gas: o
Norm al PaO 2
o
Norm al calculated oxygen saturation
o
Low m easured oxygen saturation
o
Metabolic acidosis in severe cases
Carboxyhem oglobin level: o
Measure as soon as possible.
o
Level m ay not reflect clinical severity:
Patient m ay be critically ill despite unim pressive carboxyhem oglobin level.
May be m isleadingly low if significant tim e has passed since exposure
Norm al range is 0–3% (up to 10% in sm okers).
Tests Lab
Pulse oxim etry: o
Falsely elevated reading
o
Device cannot distinguish oxyhem oglobin from carboxyhem oglobin.
Electrolytes: o
Metabolic acidosis and elevated anion gap associated with increased clinical severity
Urinalysis: o
Myoglobinuria m ay indicate rhabdom yolysis.
Pa ge 8 9 1
Cardiac enzym es: o
When m yocardial ischem ia/infarction suspected
Pregnancy test
ECG: o
Carbon m onoxide m ay precipitate m yocardial ischem ia/infarction.
o
Dysrhythm ias
o
Nonspecific ST-segm ent and T-wave abnorm alities
P.179
Imaging
Chest radiography: o
Pulm onary edem a
CT scan of the head: o
To evaluate for intracranial causes of altered m ental status when indicated
o
Bilateral globus pallidus low-density lesions m ay be clue to CO poisoning in unclear cases.
Differential Diagnosis
Viral illness/viral syndrom e
Meningitis/encephalitis
Intracranial hem orrhage
Gastroenteritis
Migraine headache
Tension headache
Ethanol intoxication
Sedative-hypnotic overdose
Cyanide poisoning
Salicylate overdose
Toxic alcohol exposure
Pa ge 8 9 2
Treatment Initial Stabilization
Evaluate and m anage airway, breathing, circulation (ABCs).
Establish IV access.
100% oxygen
Cardiac m onitor
Dextrose, naloxone, thiam ine when indicated for altered m ental status
ED Treatment
Oxygen: o
Adm inister 100% norm obaric oxygen:
o
Via face m ask or endotracheal tube
Continue oxygen therapy until carboxyhem oglobin level 40%
Carboxyhem oglobin level 20–70 consult a hyperbaricist
Pregnancy with carboxyhem oglobin level >10%
Pregnancy Considerations
Fetal hem oglobin has higher affinity for CO than adult hem oglobin.
Fetal carboxyhem oglobin levels 10–15% higher than m aternal levels
Delayed clearance of fetal carboxyhem oglobin com pared to m aternal
Treat pregnant patients with 100% norm obaric oxygen for five tim es as long as it takes to reduce m aternal levels below 10%.
Treat with hyperbaric oxygen if level >15%.
Pa ge 8 9 4
Medication (Drugs)
Dextrose: D 5 0 W one am pule (50 m L or 25 g) (peds: D 2 5 W 2–4 m g/kg) IV
Naloxone: 2 m g (peds: 0.1 m g/kg) IV or IM
Thiam ine (vitam in B 1 ): 100 m g (peds: 50 m g) IV or IM
Follow-Up Disposition Admission Criteria
Persistent sym ptom s after 4 hours of treatm ent with 100% oxygen
Evidence of m yocardial ischem ia or cardiac instability
Seizures
Persistent m etabolic acidosis
Syncope
Rhabdom yolysis
Discharge Criteria
Asym ptom atic after 4 hours of observation
Absence of aforem entioned adm ission criteria
Psychiatric clearance if suicidal exposure
Issues for Referral Need for hyperbaric oxygen
References 1. Gorm an D, Drewry A, et al. The clinical toxicology of carbon m onoxide. Toxicology. 2003;187:25–38. 2. Kao LW, Nanagas KA. Carbon m onoxide poisoning. Em erg Med Clin North Am . 2004;22(4): 985–1018. 3. Weaver LK, Hopkins RO, et al. Hyperbaric oxygen for acute carbon
Pa ge 8 9 5
m onoxide poisoning. N Engl J Med. 2002;347:1057–1067.
Miscellaneous SEE ALSO: Hyperbaric Oxygen
Codes ICD9-CM 986
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > C ardiac Arrest
Cardiac Arrest
Todd C. Rothenhaus
Basics Description
Sudden death: o
Death within 24 hours of sym ptom onset
o
Initial presentation in 50% of patients with cardiovascular disease
Return of spontaneous circulation (ROSC) achieved in 9–65%
1–20% of patients survive to discharge
Factors affecting survival:
o
Initial rhythm
o
Tim e to successful defibrillation
Incidence of re-arrest in neurologically intact survivors: o
30% at 1 year and 60% at 5 years
Etiology
Acute coronary ischem ia: o
Underlying etiology in 50% of arrests
o
Myocardial irritability leads to ventricular fibrillation
Prim ary dysrhythm ia: o
Congenital and acquired electrical abnorm alities
o
Hypertrophic/dilated cardiom yopathy
Pa ge 8 9 7
o
Myocarditis
Cardiac rupture
Pericardial tam ponade
Metabolic abnorm alities
Noncardiac etiologies: o
Consider especially in cases of pulseless electrical activity
o
Tension pneum othorax
o
Hem orrhage
o
Massive pulm onary em bolus
o
Sepsis
o
Severe acidosis
Drugs or toxins: o
Antidysrhythm ics
o
Digoxin
o
Beta-blockers
o
Calcium channel blockers
o
Tricyclic antidepressants
o
Cocaine
o
Heroin
Diagnosis Signs and Symptoms
Unresponsiveness
Pulselessness
Shallow, gasping respirations m ay persist for a few m inutes
Occasionally preceded by: o
Chest pain
o
Dyspnea
Pa ge 8 9 8
o
Palpitations
o
Seizure activity
Im m ediately prior to arrest: o
Shock or hypotension
o
Im paired m entation
Essential Workup
“Quick look― using paddles of a cardiac defibrillator
Determ ine rhythm
Tests Lab Indicated only when successful ROSC is achieved:
Electrolytes
Blood urea nitrogen/creatinine
Creatinine kinase with isoenzym es, cardiac troponin
Arterial blood gas (avoid arterial puncture in throm bolysis candidates).
CBC
Therapeutic drug levels
Toxicological testing
Imaging
ECG: o
Establish or rule out acute coronary syndrom e
Chest radiograph: o
Endotracheal tube position
o
Cardiac silhouette
o
Pneum othorax
ECG: o
Pericardial effusion
o
Wall m otion abnorm ality
o
Valvular dysfunction
Pa ge 8 9 9
Differential Diagnosis Sudden loss of consciousness with a palpable pulse:
Syncope
Seizure
Acute stroke
Hypoglycem ia
Acute airway obstruction
Head traum a
Toxins
Treatment Pre Hospital
Prom pt initiation of standard CPR or active com pression-decom pression CPR (ACD-CPR)
Confirm underlying rhythm
Early defibrillation of ventricular tachycardia (VT) or ventricular fibrillation (VF):
o
Autom ated external defibrillator
o
EMT-D or layperson
Consider CPR before defibrillation in cases of if arrest >5 m inutes.
Secure airway and provide adequate respirations: o
Endotracheal intubation
o
Laryngeal m ask airway
Post-resuscitation care: o
Identify cause of arrest
o
12-lead ECG
o
Monitor vital signs
Transport to the closest facility:
Pa ge 9 0 0
o
If return of spontaneous circulation, consider transport to center equipped for interventional cardiac care.
o
Pediatric critical care center for children
Term ination of resuscitative efforts: o
Persistent, confirm ed asystole
o
Prolonged arrest
Initial Stabilization
Initiate advanced cardiac life support (ACLS).
Perform standard CPR as long as no pulse is palpable.
Consider ACD-CPR: o
Stop CPR only briefly to check cardiac rhythm or intubate.
Secure the airway
Obtain IV access
Cardiac m onitor
Therapy based on the underlying rhythm according to ACLS protocols
P.181
ED Treatment Pulseless VT or VF
Im m ediate defibrillation with up to three countershocks: o
200 J
o
200–300 J
o
360 J
If defibrillation is unsuccessful: o
Epinephrine
o
Vasopressin
If refractory to defibrillation and epinephrine:
Pa ge 9 0 1
o
Am iodarone
o
Lidocaine
o
Procainam ide
o
Magnesium for Torsades de Pointes
Asystole
Dism al prognosis if this is the presenting rhythm
Confirm in two or m ore leads
Epinephrine
Atropine
Consider transcutaneous pacing for severe brady-asystolic rhythm .
Pulseless Electrical Activity
Epinephrine
Atropine
Treat for reversible cause of pulseless electrical activity o
Pneum othorax
o
Cardiac tam ponade
o
Hypoxia
o
Pulm onary em bolus
o
Hypovolem ia (hem orrhage)
Post-Resuscitation
Treat the underlying cause of the arrest.
ECG to establish presence of acute coronary syndrom e: o
Im m ediate catheterization or throm bolysis for ACS
Ventilatory support
Continue antidysrhythm ic therapy.
Correct electrolyte abnorm alities.
Initiate volum e resuscitation and provide inotropic support as needed.
Pa ge 9 0 2
Medication (Drugs)
Am iodarone: 300 m g (peds: 5 m g/kg) IVP
Atropine: 1 m g (peds: 0.02 m g/kg) IV q3–5m in up to 0.04 m g/kg
Epinephrine: 1 m g (peds: 0.01 m g/kg) IVP q3–5m in
Lidocaine: 100 m g (peds 1 m g/kg) IVP, then 2–4 m g/m in (peds: 20–50 µg/m in) IV continuous infusion
Magnesium : 1–2 g (peds: 25–50 m g/kg) slow IV
Procainam ide: 20 m g/m in slow IV to a total of 1 g or until arrhythm ia is suppressed; m aintenance infusion 1–4 m g/m in (peds: 15 m g/kg over 30 m in, then 20–80 µg/kg/m in IV)
Sodium bicarbonate: 1 m Eq/kg slow IV
Vasopressin: 40 U IVP (adults with VT/VF only)
Follow-Up Disposition Admission Criteria Return of spontaneous circulation:
Coronary care unit or intensive care unit
Postresuscitation care
References 1. Am erican Heart Association. Guidelines 2000 for cardiopulm onary resuscitation and em ergency cardiovascular care. Circulation. 2000;102(Suppl): I-1–I-384. 2. Dorian P, Cass D, Schwartz B, et al. Am iodarone as com pared with lidocaine for shock-resistant ventricular fibrillation. N Engl J Med. 2002;346:884–890.
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3. Hallstrom AP, Ornato JP, Weisfeldt M, et al. Public-access defibrillation and survival after out-of-hospital cardiac arrest. N Engl J Med. 2004;351:637–646. 4. Nolan JP, Morley PT, Vanden Hoek TL, et al. Therapeutic hypotherm ia after cardiac arrest: an advisory statem ent by the advanced life support task force of the International Liaison Com m ittee on Resuscitation. Circulation. 2003;108:118–121. 5. Stiel IG, Hebert PC, Wells GA, et al. Vasopressin versus epinephrine for inhospital cardiac arrest: a random ised controlled trial. Lancet. 2001;358:105–109. 6. Wik L, Hansen TB, Fylling F, et al. Delaying defibrillation to give basic cardiopulm onary resuscitation to patients with out-of-hospital ventricular fibrillation: a random ized trial. JAMA. 2003;289:1389–1395. 7. Zoll PM, Linenthal AJ, Gibson W, et al. Term ination of ventricular fibrillation in m an by externally applied electric countershock. N Engl J Med. 1956;254:727–732.
Codes ICD9-CM 798 427.5
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > C ardiac Pacem akers
Cardiac
Pacemakers Susan P. Torrey
Basics Description Equipment
Perm anent, im planted pacem aker has three com ponents o
A battery-powered energy source:
o
Lithium batteries last 7–10 years
Generator:
A sophisticated com puter with m any program m able param eters
o
Leads connected to the right ventricle and/or right atrium :
These typically sense electrical activity and pace the m yocardium .
Pacem aker m agnet: o
Placed over pulse generator
o
Converts pacer to asynchronous m ode
o
Useful if no pacer spikes on presenting rhythm
o
A depleted battery will result in decrease in m agnet rate by 10%.
Pa ge 9 0 5
Pacemaker Terminology
Fixed m ode: o
The pacem aker is set to fire at a set rate regardless of patient's underlying rhythm .
o
Occasionally seen in old pacers
Dem and m ode: o
The pacem aker fires only when necessary.
o
It senses the underlying rhythm .
o
It will only pace the atria or ventricle if the intrinsic rhythm is absent.
Sensing: o
Refers to the pacem aker's ability to determ ine whether the heart is being intrinsically paced
All pacem akers have a five-letter code to describe their function.
For ED purposes, only the first three letters of the code are necessary: o
First letter in code indicates cham ber being sensed by pacem aker:
o
A: atria
V: ventricle
D: dual (both cham bers)
Second letter in code indicates cham ber that can be paced:
o
A: atria
V: ventricle
D = dual (both cham bers)
Third letter in code describes pacem aker's response to sensed intrinsic com plex:
T: trigger (a sensed beat results in a pacing response as when a sensed atrial beat provokes a subsequent ventricular beat)
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I: inhibit (a sensed beat precludes pacem aker function)
D: dual (a pacem aker is capable of both functions)
o
O: no response
The m ost com m on pacem akers are VVI (single lead) and DDD (two leads).
Pacemaker-Associated Complications
Pacem aker-associated infection: o
Infection of pacem aker com ponents often associated with endocarditis
o
Staphylococcus epiderm idis and Staphylococcus aureus account for >90% of infections
o
Transesophageal echo is the preferred diagnostic m ethod.
Venous throm bosis: o
Very com m on (overall incidence 30–50%)
o
Sym ptom atic, acute obstruction is rare (200 beats/m in) with hem odynam ic com prom ise
Diagnosis Signs and Symptoms
Pacem aker failure: o
Bradycardia
o
Syncope
o
Hypotension, progressive to shock and hem odynam ic collapse
o
Fatigue and weakness
o
Dyspnea on exertion or shortness of breath secondary to congestive heart failure
o
Ischem ic chest pain
o
Altered level of consciousness
Pa ge 9 0 8
Pacem aker-induced tachycardia: o
Dyspnea
o
Ischem ic chest pain
o
Lightheadedness
o
Syncope
Pacem aker syndrom e: o
Sym ptom s related to asynchronous aortic valve contractions
o
Lightheadedness
o
Dyspnea
o
Palpitation
o
Syncope
Physical Exam
General cardiac exam ination
Heart exam for m urm urs
Lung exam for congestive heart failure
Chest wall exam at generator site
Tests Lab
Serum potassium
Arterial blood gas
Serum levels of antidysrhythm ic drugs
Imaging Chest radiograph:
Evaluate problem with pacer lead(s) and position.
Fractured lead
Lead dislodgm ent
Perforation
P.183
Pa ge 9 0 9
Essential Workup
12-lead ECG to assess whether there is any obvious evidence of pacem aker failure
Metabolic workup to determ ine whether an acquired m edical condition led to an elevated m yocardial threshold
ECG with pacer m agnet: o
Assess m agnet rate
o
Particularly useful when the baseline ECG does not reveal pacer spikes
o
The m agnet activates asynchronous pacing m ode.
o
Produces pacer spikes at a preprogram m ed rate—regardless of the intrinsic rhythm :
If the m agnet rate equals the preprogram m ed rate set at im plantation, the pacer is okay.
If the m agnet rate is >10% slower than at im plantation, the battery is depleted.
If there are no pacer spikes, there is significant pacem aker m alfunction.
Treatment Initial Stabilization
Oxygen adm inistered via 100% nonrebreather
Intubation as needed
Intravenous access
Advanced cardiac life support drugs as per usual protocol
Defibrillation: Avoid placing paddles over generator.
Transcutaneous pacem aker in hem odynam ically unstable patients with pacem aker failure
Pa ge 9 1 0
ED Treatment
Pacem aker failure: o
Transcutaneous pacem aker
o
Tem porary transvenous pacem aker
Obtain central IV access with a Cortis introducer.
Perform the procedure under fluoroscopy if possible.
Set the pulse generator to asynchronous m ode.
Turn the output dial all the way up.
Advance the catheter through the central venous access Cortis until you see a QRS com plex on the m onitor.
Check the fem oral pulse.
If you have a pulse and see a QRS com plex, the pacer is “capturing.―
Slowly turn the output dial down until you lose the QRS com plex (capture threshold).
Turn the output dial up to 2 or 3 tim es the capture threshold.
Continuous ECG m onitoring facilitates correct placem ent.
Treat hyperkalem ia (see Hyperkalem ia)
Runaway pacem aker: o
AV node blocking or reprogram m ing
o
In extrem e situation, m ay need to disconnect lead from generator surgically
Medication (Drugs) Adenosine: 6 m g IV bolus
Pa ge 9 1 1
Follow-Up Disposition Admission Criteria
Perm anent pacem aker failure
Suspicion of infection involving pacem aker com ponents
Discharge Criteria
Asym ptom atic pacem aker m alfunction
A cardiologist has interrogated the pacem aker
References 1. Cardall TY, Brady WJ, Chan TC, et al. Perm anent cardiac pacem akers: Issues relevant to the em ergency physician, parts I and II. J Em erg Med. 1999;17:479–489, 697–709. 2. Griffin J, Sm ithline H, Cook J. Runaway pacem aker: A case report and review. J Em erg Med. 2000;19:177–181. 3. Kusum oto FM, Goldschlager N. Cardiac pacing. N Engl J Med. 1996;334:89–98. 4. Stone KR, McPherson CA. Assessm ent and m anagem ent of patients with pacem akers and im plantable defibrillators. Crit Care Med. 2004;32:155–165.
Codes ICD9-CM 429.4
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > C ardiac Testing
Cardiac Testing
Shamai A. Grossman Jonathan Fisher
Basics Description
Testing is indicated for em ergency patients at risk for acute cardiac ischem ia (ACI) and heart failure (HF): o
Spectrum of disease processes, including acute m yocardial infraction (AMI) and unstable angina pectoris
o
About 10% of ED visits are cardiac related, m ost with chest pain.
o
10% of ED m alpractice claim s are due to m issed diagnosis of AMI.
o
2–8% of patients presenting to the ED with chest pain are sent hom e with AMI.
o
History, physical exam , and ECG m iss 1–4% of all AMIs.
Various approaches to differentiation of chest pain m ay be em ployed: o
History is the critical com ponent.
o
All m odalities beyond history and ECG are adjuncts to diagnosing the etiology of chest pain.
Pa ge 9 1 3
Etiology
Cardiac risk factors include: o
Hypercholesterolem ia
o
Diabetes m ellitus
o
Hypertension
o
Sm oking
o
Fam ily history
o
Men >35 years old
o
Postm enopausal wom en
Atherosclerotic narrowing of coronary vessels
Vasospasm , although this is usually at rest and considered unstable if new onset
Microvascular angina or abnorm al relaxation of vessels with diffuse vascular disease
Anem ia: hem oglobin 100 pg/m L diagnosed HF with a sensitivity of 90% and specificity of 76%
Unclear significance of elevated BNP in setting of ACI
Pa ge 9 1 7
Imaging
Chest radiograph: o
Usually norm al
o
May show cardiom egaly
o
Congestive heart failure is suggestive of unstable angina.
o
May identify other etiologies of chest pain such as pneum onia
P.185
Echocardiography m ay establish the diagnosis of ACI: o
Rest echocardiography has a sensitivity of 70% and specificity of 87% for ACI.
o
Rest echocardiography has a sensitivity of 93% and specificity of 66% for AMI.
Technetium -99m sestam ibi (rest): o
Has a sensitivity of 81% and specificity of 73% for ACI
o
Has a sensitivity of 92% and specificity of 67% for AMI
Exercise stress testing m ay help establish the diagnosis of angina and provide prognostic inform ation. o
1-m m depression of the ST segm ent below the baseline, 80 m illiseconds from the J point, in three consecutive beats and two consecutive leads is characteristic of cardiac ischem ia.
o
Early positive (within 3 m inutes) stress tests are worrisom e for unstable angina.
o
Six m inutes of exercise using a standard Bruce protocol suggests an excellent prognosis
o
Exercise stress testing with ECG alone has a
Pa ge 9 1 8
sensitivity of 68% and specificity of 77%. o
Exercise stress testing with echocardiography has a sensitivity of 85% and specificity of 77%.
o
Exercise stress testing with thallium -201 or technetium -99m sestam ibi has a sensitivity of 87% and specificity of 64%.
Cardiac catheterization is considered the gold standard: o
A history of a negative catheterization does not exclude AMI.
Differential Diagnosis
Aortic dissection
Anxiety
Biliary colic
Costochondritis
Esophageal spasm
Esophageal reflux
Herpes zoster
Hiatal hernia
Mitral valve prolapse
Myocardial infarction
Peptic ulcer disease
Psychogenic
Panic disorder
Unstable angina
Pneum onia
Pulm onary em bolus
Treatment Pre Hospital
Pa ge 9 1 9
IV access
Oxygen
Cardiac m onitoring
Out-of-hospital ECG: o
Alone has a sensitivity of 76% and specificity of 88% for ACI
o
Alone has a sensitivity of 68% and specificity of 97% for AMI
Sublingual nitroglycerin for sym ptom relief
Caution All chest pain should be treated and transported as a possible life-threatening em ergency.
Initial Stabilization
IV access
Oxygen
Cardiac m onitoring
Oxygen saturation
ED Treatment See Acute Coronary Syndrom e: Stable Angina; Acute Coronary Syndrom e: Unstable Angina; and Acute Coronary Syndrom e: Myocardial Infarction for m ore detail
Guidelines for Cardiac Testing
History suggestive of acute cardiac syndrom e: o
ECG or first set of cardiac enzym es abnorm al: o
Adm it patient; consider cardiology consult,
Ongoing chest pain or pressure: o
Obtain ECG and first set of cardiac enzym es.
Obtain pain sestam ibi or echocardiogram
Pain sestam ibi or echocardiogram abnorm al: o
Adm it patient; consider cardiology consult.
Pa ge 9 2 0
Second set of cardiac enzym es abnorm al: o
Adm it patient; consider cardiology consult.
o
History suggestive of acute cardiac syndrom e, ECG nondiagnostic, enzym es norm al.
o
Ancillary testing
o
Standard exercise testing (ETT)
o
Stress echocardiogram or sestam ibi (abnorm al or uninterpretable ECG)
Pharm acologic ETT (i.e., dobutam ine echocardiogram or dipyridam ole [Persantine] sestam ibi [patient unable to exert])
o
Ancillary testing abnorm al:
Adm it patient or cardiology consult.
Medication (Drugs) Patient should not be started on new antianginal m edication before stress testing in the ED.
Follow-Up Disposition Admission Criteria
History suggestive of cardiac etiology for chest pain
Abnorm al or changed ECG
Positive cardiac enzym es
Positive rest im aging
If the diagnosis is unclear, adm ission to the hospital or an ED observation unit m ay be useful for serial cardiac enzym es, ECGs, and exercise stress testing.
Pa ge 9 2 1
Early positive stress test
If the patient has an otherwise positive stress test, the decision for adm ission should be m ade in consultation with the prim ary care physician or cardiologist.
Discharge Criteria Patients who m eet the following criteria are safe to discharge:
History not suggestive of cardiac etiology for chest pain
Norm al ECG
Norm al cardiac testing
References 1. Braunwald E, Antm an EM, Beasley JW, et al. ACC/AHA 2002 guideline update for the m anagem ent of patients with unstable angina and non-ST-segm ent elevation m yocardial infarction: A report of the Am erican College of Cardiology/Am erican Heart Association Task Force on Practice Guidelines. Circulation. 2002;106(14):1893–1900. 2. Ioannidis JPA, Salem D, Chew PW, et al. Accuracy and clinical effect of out-of-hospital electrocardiography in the diagnosis of acute cardiac ischem ia: a m eta-analysis. Ann Em erg Med. 2001;37:461–470. 3. Ioannidis JPA, Salem D, Chew PW, et al. Accuracy of im aging technologies in the diagnosis of acute cardiac ischem ia in the em ergency departm ent: a m eta-analysis. Ann Em erg Med. 2001;37:471–477. 4. Lau J, Ioannidis JPA, Balk EM, et al. Diagnosing acute cardiac ischem ia in the em ergency departm ent: a system atic review of the accuracy and clinical effect of current technologies. Ann Em erg Med. 2001;37:453–460.
Pa ge 9 2 2
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > C ardiac Transplantatio n C o m plicatio ns
Cardiac
Transplantation Complications Barrett Adams Samuel Keim
Basics Description
Cardiac transplant recipients are a unique population with increased risk for cardiac ischem ia, heart failure, as well as general risks as an im m unocom prom ised host.
2,200 cardiac transplants per year in the United States
1-year survival 85–90%; 5-year survival approxim ately 75%
Typical im m unosuppresive therapy to control rejection is a “triple drug― regim e often including steroids.
Frequent biopsies are used initially to evaluate rejection; echocardiography often used in children.
Com plications occur m ost com m only in the first 6 weeks after cardiac transplantation
Etiology
Rejection: o
Hyperacute rejection:
Occurs within m inutes of transplantation
Pa ge 9 2 3
Rare, due to ABO or other graft/host m ajor incom patibility
o
o
Aggressive and im m ediately fatal to graft
Acute rejection:
Lym phocyte infiltration and m yocyte destruction
Most com m on in first 6 weeks
May occur at any tim e
75% prevalence
Chronic rejection:
Fibrosis and graft vascular disease
Long-term com plication
Incom pletely understood etiology
No effective therapy
Cardiac allograft vasculopathy: o
Analogous to accelerated coronary artery disease in native hearts
o
Lim its long-term survival, leading cause of m ortality after 1 year
o
Im m une-m ediated atherosclerosis, form of chronic rejection
Infections: o
First m onth:
Bacterial infections are m ost com m on cause of m ortality during this high-risk tim e period:
Pneum onia (Pseudom onas, Legionella, other gram -negative organism s)
o
Mediastinitis
Wound infection
Urinary tract infection
First year:
Opportunistic and conventional infections
Cytom egalovirus (CMV)
Pa ge 9 2 4
Herpes sim plex virus (HSV)
Legionella
Fungal infections
Pneum ocystis carinii
Medication toxicity: o
Cyclosporine, Neoral (2nd generation cyclosporine), Tacrolim us:
o
o
o
Nephrotoxicity (30% incidence)
Hepatotoxicity
Neurotoxicity
Hyperlipidem ia, diabetogenic
Azathioprine, Mycophenolate Mofetil:
Bone m arrow suppression
Leukopenia
Sirolim us:
Hyperlipidem ia
Wound healing
Steroids:
Osteoporosis
Cushing's disease
Neoplasm s: o
Secondary to im m unosuppression
o
10–100 tim es m ore com m on versus general population
o
Skin and lip cancer
o
Lym phom as
o
Kaposi sarcom as
o
Solid organ neoplasm s
Pediatric Considerations
If the patient is not on steroids, bacterem ia risk is sim ilar to that in the general population.
High incidence of pneum onia
Pa ge 9 2 5
Patients on steroids m ay not show m eningeal signs.
Diagnosis Signs and Symptoms Acute Rejection
Nonspecific sym ptom s predom inate because the heart is usually denervated: o
Fatigue
o
Dyspnea
o
Low-grade fever
o
Nausea
o
Vom iting
May be difficult to differentiate between infection
Signs of heart failure: o
Tachypnea
o
Rales
o
Hypoxia
o
S3
o
Murm ur
o
Edem a
Allograft Vasculopathy
As early as 3 m onths after transplantation (20–50% incidence by 5 years)
Insidious onset: o
Fatigue
o
Cough
o
Dyspnea
Acute onset: o
Heart failure
Pa ge 9 2 6
o
Sudden death
o
Infarction
Denervated hearts do not present with typical angina.
Infection (Opportunistic and Conventional)
Fever
Skin lesions (zoster)
CMV: o
o
Mild (flu-like illness)
Fever
Nausea
Malaise
Severe:
Pneum onitis (13–50% m ortality)
Hepatitis
Gastroenteritis
Profound leukopenia
Pediatric Considerations
Higher risk for post-transplant lym phoproliferative disease with Epstein-Barr virus seroconversion
Like adults, at risk for allograft vasculopathy and its associated cardiac ischem ia
Essential Workup
Assess for signs of rejection, cardiac dysfunction, and infarction:
o
ECG
o
Cardiac enzym es
o
Chest radiograph
o
Echocardiography
Possible rejection requires biopsy-consult transplant team .
Pediatric Considerations
Pa ge 9 2 7
Norm al fever workup plus chest radiograph and ECG; if on steroids, perform LP
Tests Lab
Electrolytes: o
Cyclosporine effects:
Increased blood urea nitrogen, creatinine
Hyperkalem ia
Metabolic acidosis
Hyponatrem ia
CBC: o
Relative eosinophilia m ay indicate rejection over infection
Blood and urine culture if febrile
Lum bar puncture if seizures, altered m ental status, or severe headache
Consider: o
BNP (expect baseline elevation)
o
CMV titers
o
Urine antigen test
o
Cyclosporine trough level
P.187
Imaging
ECG o
Tachycardia
o
20% decrease in total voltage (nonsensitive)
o
Note that norm al rhythm for denervated heart is sinus 90–110 beats/m in
o
Depending on transplant surgical technique, m ay see
Pa ge 9 2 8
two P waves (native and donor heart):
Native P waves do not correspond to quasi-random signal
Chest radiograph: o
Cardiom egaly
o
Pulm onary edem a
o
Pleural effusions
o
Com pare with previous (healthy donor heart m ay appear large in sm all recipient)
Echocardiography: o
Decreased m itral deceleration tim e
o
Initial diastolic dysfunction
o
Biventricular enlargem ent
o
Mitral/tricuspid regurgitation
Differential Diagnosis
Rejection
Infection
Ischem ia
CMV
Viral illness
Malignancy
Cyclosporine toxicity
Treatment Initial Stabilization ABCs:
IV access
Oxygen
Monitor
Pa ge 9 2 9
Intubation
Defibrillation/pacing
Vasopressors as required
Arrhythm ias: o
Advanced cardiac life support
o
Bradycardia does not respond to atropine; use isoproterenol
ED Treatment
Hem odynam ically significant rejection: o
Methylprednisolone
o
May also require OKT3 or other anti–T-cell antibody therapy
Infarct/vasculopathy: o
Aspirin
o
Heparin
o
Possible angioplasty
o
Likely need retransplantation
CMV: o
HSV: o
Search for CMV infection with culture, serology
Fever without a source: o
Oral or IV acyclovir
Gastroenteritis: o
Em piric IV ganciclovir
Consult infectious disease or transplantation team
Headache: o
Threshold for CT scan and lum bar puncture should be low (m eningitis, abscess)
Serious illness/traum a/operation: o
Steroid burst
Lim it NSAID use because risk for renal insufficiency from cyclosporine and tacrolim us.
Pa ge 9 3 0
Medication (Drugs)
Acyclovir: 5–10 m g/kg IV q6h; genital herpes: 400 m g PO t.i.d. × 7–10 days; varicella: 20 m g/kg up to 800 m g PO q.i.d. for 5 days
Ceftriaxone: 50 m g/kg IV
Cyclosporine, Cellcept, Tacrolim us, Sirolim us, Neoral, Azathioprine, Mycophenolate Mofetil: per transplantation team
Ganciclovir: 5 m g/kg b.i.d. for 2–3 weeks (adjust for renal function)
Isoproterenol: 1–4 m cg/m in, titrate to effect; m ax. 10 m cg/m in
Methylprednisolone: 1 g IV; peds: 10–20 m g/kg IV
OKT3, Daclizum ab or other antibody therapy: per transplant team
Follow-Up Disposition Admission Criteria
Hem odynam ically significant rejection
Vasculopathy/ischem ia
New dysrhythm ia
Poorly controlled hypertension
Congestive heart failure
Dyspnea
Hypoxia
Tem perature >38°C in adult or child on steroids
Pa ge 9 3 1
Suspected CMV (unexplained fever, gastroenteritis, or interstitial pneum onitis)
Not tolerating oral m edicines
Syncope
Discharge Criteria
Mild rejection
Only in consultation with transplantation team
Fever in nontoxic child: o
Do not give children stress dose steroids
References 1. Chinnock R, Sherwin T, Robie S, et al. Em ergency departm ent presentation and m anagem ent of pediatric heart transplant recipients. Pediatr Em erg Care. 1995;11(5):355–360. 2. Deng MC. Cardiac transplantation. Heart. 2002;87:177–184. 3. Johnson MR. Clinical follow-up of the heart transplant recipient. Curr Opin Cardiol. 1995;10:180–192. 4. Massad MG. Current trends in heart transplantation. Cardiology. 2004;101:79–92. 5. Mill MR, Grady MS. Cardiac transplantation. In: Tintinalli JE, Kelen GD, Stapczynski JS, eds. Em ergency m edicine: a com prehensive study guide. 6th ed. San Francisco: McGraw-Hill; 2000:422–428. 6. Miniati DN, Robbins RC, Reitz BA. In:Braunwald E, ed. Heart disease: a textbook of cardiovascular m edicine, 6th ed. Philadelphia: WB Saunders; 2001:615–631. 7. Mueller XM. Drug im m unosuppression therapy for adult heart transplantation. Ann Thorac Surg. 2004;77:363–371. 8. Poston RS, Griffith BP. Heart transplantation. J Intensive Care Med . 2004;19:3–12. 9. Vulsteke A, Wallwork J. The heart-transplanted patient in the intensive care unit: last news before the m illennium . Cur Opinion in Crit Care. 1999;5(5):422–426.
Pa ge 9 3 2
Codes ICD9-CM 996.83 Com plications of transplanted Heart. Transplant failure or rejection—Use additional code to identify nature of com plication, such as: 078.5 Cytom egalovirus [CMV] infection
Pa ge 9 3 3
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > C ardio genic Sho ck
Cardiogenic Shock
Nadeem Al-Duaij
Basics Description
Inadequate tissue perfusion due to cardiac dysfunction
Underlying m echanism s in acute m yocardial infarction (AMI): o
o
o
Pum p failure:
≥40% left ventricle (LV) infarct
Infarct in pre-existing LV dysfunction
Reinfarction
Mechanical com plications:
Acute m itral regurgitation
Ventricular septal defect
LV rupture
Pericardial tam ponade
Right ventricular (RV) infarction
6–7% of patients with AMI develop cardiogenic shock
Cutting-edge: o
Role of a system ic inflam m atory response in the pathophysiology of cardiogenic shock
o
Recent evidence suggests that nitric oxide synthase inhibition m ay reduce m ortality.
Pa ge 9 3 4
Etiology
AMI
Sepsis
Myocarditis
Myocardial contusion
Valvular disease
Cardiom yopathy
Left atrial m yxom a
Drug toxicity: o
Beta-blocker
o
Calcium channel blocker
o
Adriam ycin
Diagnosis Signs and Symptoms
ABCs and vital signs: o
Patent airway (early)
o
Labored breathing and tachypnea (early); respiratory failure (late)
o
Diffuse crackles or wheezing
o
Hypoxia
o
Hypotension:
Systolic blood pressure Table o f C o ntents > C ardio m yo pathy
Cardiomyopathy
Elizabeth Temin James Feldman
Basics Description
Diseases of the m yocardium associated with cardiac dysfunction.
Dilated cardiom yopathy: o
Dilated and im paired contraction of the left or both ventricles
o
Idiopathic dilated cardiom yopathy accounts for 25% of all cases of heart failure.
Hypertrophic cardiom yopathy: o
Left or right asym m etric ventricular hypertrophy
o
Usually involves the interventricular septum
Restrictive cardiom yopathy: o
Restrictive filling and reduced volum e of either or both ventricles
o
Norm al or near-norm al systolic function
Arrhythm ogenic right ventricular cardiom yopathy: o
Progressive fibrofatty replacem ent of the right ventricular m yocardium
o
Relative sparing of the septum
Pa ge 9 6 1
Unclassified cardiom yopathy: o
Disorders such as fibroelastosis that do not fit into a dom inant pattern
Specific cardiom yopathy: o
Heart m uscle disease associated with a system ic disease or condition
Pediatric Considerations
Genetic: 20–30%
Acquired
Idiopathic
Pregnancy Considerations
Onset during last m onth of pregnancy to 5 m onths postpartum
No identifiable cause
Depressed systolic function
Etiology
Dilated: o
Idiopathic
o
Viral
o
Genetic/Toxic
o
Im m une
Hypertrophic: o
Fam ilial disease with autosom al dom inance
Restrictive: o
Idiopathic
o
Am yloid
Arrhythm ogenic right ventricular: o
Fam ilial disease with dom inant and recessive patterns
Specific: o
Infectious
Pa ge 9 6 2
o
Lym e disease
o
Viral
o
Chagas disease
o
HIV
Toxic agents: o
Alcohol
o
Chem otherapeutic agents
Peripartum period
Metabolic
o
Hyperthyroidism
o
Pheochrom ocytom a
o
Am yloid
General system s diseases: o
Lupus
o
Scleroderm a
o
Neurom uscular diseases
Pediatric Considerations
Idiopathic
Genetic:
o
Inborn errors of m etabolism
o
Malform ation syndrom es
o
Neurom uscular disease
o
Fam ilial isolated cardiom yopathy disorders
Acquired: o
Vitam in and/or trace m ineral deficiencies
o
Electrolyte disturbances
o
Endocrine disorders
o
Toxins
o
Collagen vascular disease
o
Im m unologic disease
o
Malignancy
o
Morbid obesity
Pa ge 9 6 3
o
Myocarditis
o
Pulm onary disease
o
Kawasaki disease
o
Infection
o
Radiation
o
Congenital heart disease
o
Asphyxia
Diagnosis Signs and Symptoms History
Antecedent illness or exposure: o
Chem otherapy
o
HIV
o
Lym e disease
o
Viral
Underlying system ic condition: o
Hem ochrom atosis
o
Sarcoidosis
o
Pregnancy
Fam ily history: o
Fam ilial sudden death
o
Exertional com plaints (syncope, dyspnea)
Dilated Cardiomyopathy
General: o
Fatigue
o
Weakness
Respiratory: o
Dyspnea on exertion
Pa ge 9 6 4
o
Cardiac: o
Chest pain
o
S4 gallop is alm ost always present.
o
S3 gallop only after cardiac decom pensation occurs
o
Jugular venous distention (JVD)
o
Dysrhythm ias
o
Mitral or tricuspid regurgitation
Abdom en: o
Enlarged, pulsatile liver
Extrem ities: o
Orthopnea
Peripheral edem a
System ic em boli
Hypertrophic Cardiomyopathy —See Cardiom yopathy, Hypertrophic
Restrictive Cardiomyopathy
General: o
Exercise intolerance
o
Weakness
Respiratory: o
Dyspnea
o
Pulm onary congestion
Cardiac: o
Exertional chest pain is usually absent
o
JVD with Kussm aul sign (rise with inspiration)
o
Apex is usually easily palpated
o
Mitral regurgitation
Abdom inal: o
Increased abdom inal girth
o
Right upper-quadrant pain
o
Ascites
Pa ge 9 6 5
o
Hepatom egaly
Extrem ities: o
Edem a
o
Peripheral edem a
Arrhythmogenic Right Ventricular Cardiomyopathy
Dizziness
Near syncope and syncope
Palpitations
Sudden death
Ventricular arrhythm ias
Congestive heart failure (CHF)
Pediatric Considerations
Irritability
Hepatom egaly
Generalized m uscle weakness
Acute biochem ical crisis
Hypoglycem ia
Metabolic acidosis
Hyperam m onem ia
Cyanosis
Encephalopathy
Dysm orphic features
Pregnancy Considerations See Cardiom yopathy, Peripartum
Tests Lab
CBC
Electrolytes, blood urea nitrogen, creatinine, liver function tests
Pa ge 9 6 6
Cardiac enzym es
Brain (B-type) natriuretic peptide: level >100 pg/m L
Serologies
Not useful in the ED
P.191
Imaging
Chest radiograph: o
o
Dilated cardiom yopathy:
Cardiom egaly
Pulm onary congestion
Pleural effusions
Hypertrophic cardiom yopathy:
o
See Cardiom yopathy, Hypertrophic
Restrictive cardiom yopathy:
Norm al cardiac silhouette
Pulm onary congestion
ECG: o
o
Hypertrophic cardiom yopathy:
Left ventricle (LV) hypertrophy
Abnorm al septal Q waves
Dilated, Lym e, Chagas, and toxic cardiom yopathies:
Atrial fibrillation
Heart block
Conduction abnorm alities
Pseudoinfarct pattern with pathologic Q waves can be seen in anterior and inferior leads without coronary artery disease.
Em ergency transthoracic 2D echocardiogram ; o
Depressed LV ejection fraction
o
Excludes pericardial tam ponade
Pa ge 9 6 7
Form al transthoracic Doppler echocardiography: o
Study of choice in patients with cardiom yopathy
o
Identification of underlying disease
Nuclear scintigraphy: o
Indicated when ECG is indeterm inate
o
Direct determ ination of the thickness of the septum and free wall
o
Alternative assessm ent to echo
CT and MRI distinguish between constrictive pericarditis and restrictive cardiom yopathy.
Diagnostic Procedures/Surgery Cardiac catheterization:
Dilated cardiom yopathy: o
Suspicion of ischem ia
o
Treatable system ic disease
Hypertrophic cardiom yopathy: o
Assessm ent of hem odynam ic abnorm alities
o
Endom yocardial biopsy
o
Evaluation for m yocarditis or define etiology
Pediatric Considerations
Electrolytes
pH
Glucose
Am m onia level
Cardiac output
Dysm orphic evaluation
ECG
Echocardiogram : o
Genetic workup; see individual causes
Differential Diagnosis
Other causes of dyspnea:
Pa ge 9 6 8
o
Chronic obstructive pulm onary disease
o
Anem ia
o
Asthm a
o
Interstitial lung disease
o
Pulm onary em bolism
o
Pericardial tam ponade:
Valvular heart disease
o
Ischem ic heart disease
o
Hypothyroidism
o
Constrictive pericarditis, com m only confused with restrictive cardiom yopathy
Other causes of syncope: o
Hypovolem ia
o
Heat disorder
o
Hypoglycem ia
Treatment Pre Hospital
Monitor
Oxygen
Hypertrophic cardiom yopathy, known or suspicion:
o
Avoid or use a lower dose of nitroglycerine.
o
Cardioversion if deterioration due to atrial fibrillation
LV heart failure: o
Oxygen
o
Nitroglycerine spray
o
Furosem ide
o
Morphine
Initial Stabilization
Pa ge 9 6 9
Airway, breathing, and circulation:
Control airway as needed.
Supplem ental oxygen
Continuous positive airway pressure
ED Treatment
Anticoagulation: o
Dilated cardiom yopathy
o
Standard treatm ent of atrial fibrillation
o
System ic em bolization
Lim ited ED experience with agents effective in hypertrophic cardiom yopathy: o
Disopyram ide to reduce obstruction
o
Am iodarone to convert and m aintain sinus rhythm
Standard treatm ent of CHF
Standard treatm ent of dysrhythm ias
Pediatric Considerations
Keep NPO until inborn errors of m etabolism ruled out.
IV fluids: o
D10 should be given until defects in the protein or fatty acid m etabolism pathways can be ruled out.
o
IV fluids need to be given slowly to avoid rapid fluid shifts to the extravascular space.
Do not give any products with lactate to avoid worsening any m etabolic acidosis or lactic academ ia.
Antioxidants and vitam in cofactors
L-Carnitine to increase m itochondrial energy m etabolism
Standard treatm ent of CHF
Dichloroacetate acutely lowers acetic acid levels in patients with m itochondrial disorders.
Pa ge 9 7 0
Medication (Drugs)
Am iodarone: 5 m g/kg over 10 m inutes
Carnitine: (peds: 50–300 m g/kg/d PO or IV)
Digoxin: start 0.125 m g
Disopyram ide: 100–200 m g PO q6h.
Furosem ide: 20–40 m g IV to a m ax. of 200 m g on subsequent doses (peds: 1 m g/kg IV q12h–q24h)
Heparin: load 80 IU/kg IV.; then 18 IU/kg/h
Milrinone: bolus 50 µg/kg IV over 10 m inutes, then 0.375–0.75 µg/kg/m in IV
Morphine: 2–5 m g IV
Nesiritide: bolus 2 µg/kg IV, then 0.01 µg/kg/m in IV with a m axim um of 0.03 µg/kg/m in
Nitroglycerine: 5 µg/m in IV titrate to SBP
Verapam il: 2.5–10 m g IV over 2 m inutes; m ax. 20 m g (peds: Table o f C o ntents > C arpal Tunnel Syndro m e
Carpal Tunnel
Syndrome Matthew T. Spencer Linda L. Spillane
Basics Description
The m edian nerve, flexor digitorum profundus, flexor digitorum superficialis, and flexor pollicis longus are located in the carpal tunnel.
Area bound by the carpal bones and the transverse carpal ligam ent
Com pression of the m edian nerve causes sym ptom s.
Etiology
Occupational/overuse syndrom es—high im pact, repetitive m otion
Traum a
Pregnancy, birth control pills
Granulom atous disease: tuberculosis, sarcoidosis
Mass lesions with m edian nerve com pression
Osteophytes
Am yloid
Multiple m yelom a
Pa ge 9 7 9
Rheum atoid arthritis
Endocrine disorders: hypothyroidism , diabetes m ellitus, acrom egaly
Chronic hem odialysis
Idiopathic
Pediatric Considerations
Idiopathic cause rare in children; m ost cases have correctable cause including: o
Traum a
o
Mucolipidosis
o
Ham artom a of the m edian nerve
o
Anom alous flexor digitorum superficialis (FDS)
o
Hem ophilia with hem atom a
Diagnosis Signs and Symptoms History
Num bness/paresthesias in m edian nerve distribution: o
Thum b, index, m iddle, and radial aspect of ring finger
Pain: o
Location: wrist or hand, som etim es radiating to elbow, forearm , or shoulder
o
Often worse at night—relieved by “shaking out†• the hand
o
Exacerbated by repetitive wrist m ovem ent and by activities in which the wrist is flexed (e.g., driving)
Physical Exam
Weakness of the abductor pollicis brevis and opponens
Pa ge 9 8 0
m uscles: o
Innervated by the recurrent branch of the m edian nerve
o
Patient m ay com plain of dropping things or having decreased fine m otor control.
o
Sensitivity of 29%; specificity of 80%, on average
Loss of two-point discrim ination: o
Late finding, highly specific
o
Sensitivity of 24%; specificity of 94%
Atrophy of thenar m uscles: o
Late finding, highly specific
o
Sensitivity of 18%; specificity of 94%
Essential Workup
History of characteristic nocturnal pain and paresthesias in the m edian nerve distribution.
Muscle weakness and thenar wasting are later findings.
Provocative testing: o
Phalen test:
Wrist flexion for 60 seconds produces num bness or tingling in the m edian nerve distribution.
o
Sensitivity of 68%; specificity of 73%
Tinel sign:
Gentle tapping over the m edian nerve at wrist produces tingling in the fingers in the m edian nerve distribution.
o
Sensitivity of 50%; specificity of 77%
Carpal com pression test:
Thum b pressure applied over the proxim al carpal ligam ent produces tingling in the fingers in the m edian nerve distribution.
o
Sensitivity of 64%; specificity of 83%
Tourniquet test:
Pa ge 9 8 1
Blood pressure (BP) cuff inflated to just above the patient's systolic blood pressure for 2 m inutes produces paresthesias in the m edian nerve distribution.
Sensitivity of 59%; specificity of 61%
Tests Lab
Not indicated in m ost cases
Thyroid function studies; rheum atoid factor and im m une panel if indicated by history and physical exam
P.199
Imaging
Wrist radiograph if traum a or degenerative arthritis suspected
CT in select cases: o
May show encroachm ent of carpal tunnel
MRI—displays the soft tissues well but m ay not be justified in ED owing to tim e and cost: o
Findings: palm ar bowing of transcarpal ligam ent, flattened m edian nerve, m edian nerve or synovial swelling, fluid in carpal tunnel, signal abnorm ality of m edian nerve
Ultrasound can be diagnostic: o
Findings: m edian nerve swelling at proxim al canal, m edian nerve flattening at distal canal, bowing of transcarpal ligam ent
Diagnostic Procedures/Surgery Nerve conduction studies and electrom yography are criterion
Pa ge 9 8 2
standard tests.
Differential Diagnosis
Cervical nerve root com pression: o
Origin of m edian nerve is at the sixth and seventh cervical roots.
o
Sym ptom s are aggravated by erect posture and neck m ovem ent.
Hand-arm vibration syndrom e: o
Characterized by Raynaud, num bness and tingling in ulnar and m edian nerve distributions when exposed to cold or vibration, weakened grip, and upper extrem ity m yalgias
o
Associated with prolonged exposure to vibration
Thoracic outlet obstruction
Osteoarthritis of the first carpom etacarpal joint
Brachial plexitis
Generalized neuropathy
Syringom yelia
Treatment Initial Stabilization None necessary
ED Treatment
Splint wrist in neutral position (0 degrees).
Aspirin or nonsteroidal anti-inflam m atory drugs (NSAIDs)
Avoidance of repetitive wrist m ovem ent
Wrist splint to be worn at night until follow-up
Apply heat to involved wrists—heating pad, hot water bottle, low-level heat wraps
Pa ge 9 8 3
Referral to occupational m edicine for ergom etric testing if caused by repetitive m otion, and tendon gliding or nerve gliding exercises
May need referral to a hand surgeon for consideration of surgical release of transverse carpal ligam ent using either open or endoscopic technique
Medication (Drugs)
NSAIDs (there are m any choices; a few are listed below): o
Ibuprofen: 600 m g (peds: 5–10 m g/kg) PO q6h
o
Ketorolac: 30 m g IV or IM q6h or 10 m g PO q4h–q6h
o
Diclofenac: 50 m g PO b.i.d. or t.i.d.
o
Piroxicam : 20 m g PO daily
Local corticosteroid injection provides transient relief in two thirds of patients (m any different regim ens): o
Hydrocortisone: 25–100 m g
o
Methylprednisolone: 40 m g
o
Prednisolone suspension: 20–40 m g
o
Triam cinolone: 20 m g
Follow-Up Disposition Discharge Criteria Discharge to hom e with appropriate referral to either patient's prim ary care physician or directly to a specialist in occupational m edicine or hand surgery.
Pa ge 9 8 4
References 1. Al-Qattan MM, Thom pson HG, Clarke HM. Carpal tunnel syndrom e in children and adolescents with no history of traum a. J Hand Surg. 1996;21B(1):108–111. 2. Kanaan N, Sawaya RA. Carpal tunnel syndrom e: m odern diagnostic and m anagem ent techniques. Br J Gen Pract. 2001;51:311–314. 3. MacDerm id JC, Wessel J. Clinical diagnosis of carpal tunnel syndrom e: a system atic review. J Hand Ther. 2004;17(2):309–319. 4. Michlovitz SL. Conservative interventions for carpal tunnel syndrom e. J Orthop Sports Phys Ther. 2004;34(10):589–600. 5. O'Gradaigh D, Merry P. Corticosteroid injection for the treatm ent of carpal tunnel syndrom e. Ann Rheum Dis. 2000;59:918–919. 6. Sternbach G. The carpal tunnel syndrom e. J Em erg Med. 1999;17:519–523. 7. Whitley JM, McDonnell DE. Carpal tunnel syndrom e. A guide to prom pt intervention. Postgrad Med. 1995;97(1):89–96.
Codes ICD9-CM 354.0 G56.0
Pa ge 9 8 5
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > C auda Equina Syndro m e
Cauda Equina
Syndrome Kyan J. Berger
Basics Description Com pression of lum bar and sacral nerve fibers in cauda equina region:
Nerve fibers below conus m edullaris
Fibers end at L1-2 interspace.
Risk Factors
Neoplasm
IV drug use
Etiology
Herniated disc m ost com m on: o
L4–L5 discs > L5–S1 > L3–L4
o
Most com m on in fourth and fifth decades of life
Mass effect from : o
Myelom a, lym phom a, sarcom a, m eningiom a, neurofibrom a, hem atom a
o
Spine m etastases (breast, lung, prostate, thyroid, renal)
Pa ge 9 8 6
o
Epidural abscess (especially in IV drug users)
Blunt traum a
Penetrating traum a
Spinal anesthesia
Diagnosis Signs and Symptoms History
Low back pain
Sciatica/radicular pain (unilateral or bilateral)
Lower extrem ity num bness or weakness
Difficulty am bulating owing to weakness or pain
Bladder or rectal dysfunction: o
Retention or incontinence
Physical Exam
Lum brosacral tenderness
Lower extrem ity sensory or m otor deficits: o
May be asym m etric
o
Decreased foot dorsiflexion strength
o
Decreased quadriceps strength
Decreased deep tendon reflexes
Saddle hypalgesia or anesthesia
Decreased anal sphincter tone
Essential Workup
Neurologic exam m ost essential: o
Straight-leg raise
o
Lasègue sign:
With patient supine, flex hip and dorsiflex foot.
Pain or spasm in posterior thigh indicates nerve
Pa ge 9 8 7
irritation. o
Perineal sensation
o
Rectal tone
o
Anal wink: reflex contraction of external anal sphincter with gentle stroking of skin lateral to anus
Postvoid residual volum e: o
Estim ate by bladder catheterization or using ultrasound.
o
Greater than 50–100 m L is considered abnorm al.
o
Residual increases with age.
o
Diagnosis unlikely if norm al
Tests Lab
Based on differential diagnoses
CBC, urinalysis, erythrocyte sedim entation rate (ESR)
Imaging
Radiographs of lum bosacral (LS) spine
MRI of spine is definitive study.
CT m yelogram if MRI unavailable
Differential Diagnosis
Osteoarthritis, LS strain, sciatica
Vertebral fracture (pathologic and nonpathologic)
Osteom yelitis
Spinal epidural abscess
Conus m edullaris or higher cord com pression
Ankylosing spondylitis, spinal stenosis
Abdom inal aortic aneurysm dissection
Vascular claudication
Hip pathology
Acute transverse m yelitis
Pa ge 9 8 8
P.201
Treatment Pre Hospital
Manage airway and traum atic injuries as indicated.
If evidence of traum a, patient should be transported with full spine im m obilization.
Alert Even in nontraum a patient, consider spinal im m obilization given possibility of unstable lesion.
Initial Stabilization
Spine im m obilization if traum a or unstable spine lesion suspected
Analgesia
NPO until evaluated by neurosurgery
ED Treatment
Repeat neurologic exam inations to detect progression.
For acute spinal cord traum a (48 hours) also benefit from surgical decom pression.
Discharge Criteria Patients with established cauda equina syndrom e with prior com plete evaluation and no new neurologic deficits m ay be discharged with close follow-up with their neurosurgeon.
References 1. Della-Giustina DA. Em ergency departm ent evaluation and treatm ent of back pain. Em erg Med Clin North Am . 1999;27:877–893. 2. Green BA, et al. Spinal cord injury in adults. In: Youm ans JR, et al., eds. Neurological Surgery. 4th ed. Philadelphia: WB Saunders;
Pa ge 9 9 0
1996:1969–1940. 3. Hussain SA, Gullan RW, Chitnavis BP. Cauda equina syndrom e: outcom e and im plications for m anagem ent. Br J Neurosurg. 2003;17(2):164–167. 4. Miller DW, et al. General m ethods of clinical exam ination. In: Youm ans JR, et al., eds. Neurological Surgery. 4th ed. Philadelphia: WB Saunders; 1996:40. 5. Shapiro S. Medical realities of cauda equina syndrom e secondary to lum bar disc herniation. Spine. 2000;25(3):348–352.
Codes ICD9-CM 344.60
ICD10 G83.4
Pa ge 9 9 1
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > C austic Ingestio n
Caustic Ingestion
Paul Kolecki
Basics Description Alkalis
Dissociate in the presence of H 2 O to produce hydroxy (OH ) ions, which leads to liquefaction necrosis
Post-ingestion—m ainly dam ages the esophagus: o
Gastric dam age can occur (see acids).
Esophageal dam age (in the order of increasing dam age) consists of:
o
Superficial hyperem ia
o
Mucosal edem a
o
Superficial blisters
o
Exudative ulcerations
o
Full-thickness necrosis
o
Perforation
o
Fibrosis with resulting esophageal strictures
Do not directly produce system ic com plications
Acids
Dissociate in the presence of H 2 O to produce hydrogen (H + ) ions, which leads to a coagulation necrosis with eschar
Pa ge 9 9 2
form ation
Post-ingestion—dam ages the stom ach because of rapid transit tim e through esophagus: o
Esophageal dam age can occur (see alkalis).
Gastric dam age (in the order of increasing dam age) consists of:
o
Edem a
o
Inflam m ation
o
Im m ediate or delayed hem orrhage
o
Full-thickness necrosis
o
Perforation
o
Fibrosis with resulting gastric outlet obstruction
Well-absorbed and can cause hem olysis of RBCs and a system ic m etabolic acidosis
Etiology
Direct chem ical injuries
Injuries occur secondary to acid and alkali exposures.
Many caustic agents (acids and alkalis) are found in com m on household and industrial products.
Caustic substances: o
Am m onia hydroxide:
o
Form aldehyde:
o
o
Em balm ing agent
Hydrochloric acid:
o
Glass cleaners
Toilet bowel cleaners
Hydrofluoric acid:
Glass etching industry
Microchip industry
Rust rem overs
Iodine:
Antiseptics
Pa ge 9 9 3
o
Phenol:
o
o
Antiseptics
Sodium hydroxide:
Drain cleaners
Drain openers
Oven cleaners
Sodium borates, carbonates, phosphates, and silicates:
o
Detergents
Dishwasher preparations
Sodium hypochlorite
Bleaches
Sulfuric acid:
Car batteries
Diagnosis Signs and Symptoms
Oropharyngeal: o
Pain
o
Erythem a
o
Burns
o
Erosions
o
Ulcers
o
Drooling
o
Hoarseness
o
Stridor
o
Aphonia
o
Absence of visible lesions in the oropharynx does not exclude visceral injuries.
Pulm onary:
Pa ge 9 9 4
o
Tachypnea
o
Cough
o
Pneum onitis if aspirated
Gastrointestinal: o
Pain
o
Em esis or hem atem esis
o
Melena, dysphagia
o
Odynophagia
o
Esophageal or gastric perforation
o
Peritonitis owing to perforation
Cardiovascular: o
Tachycardia
o
Hypotension
o
Orthostatic changes
Hem atologic: o
Acid ingestion can cause RBC hem olysis.
Derm atologic: o
Pain
o
Erythem a
o
First, second, or third-degree burns
Ocular: o
Pain
o
Erythem a
o
Injection
o
Corneal burns
o
Full-thickness corneal dam age
Metabolic: o
Metabolic acidosis
Essential Workup
History of or signs and sym ptom s of an exposure
Absence of oropharyngeal lesions does not exclude visceral injury.
Pa ge 9 9 5
Tests Lab
CBC
Electrolytes, BUN, creatinine, glucose
Arterial blood gas
Blood cultures: o
If m ediastinitis or peritonitis suspected
Type and cross-m atch.
Imaging Chest and abdom inal radiographs for:
Esophageal or gastric perforation
Diagnostic Procedures/Surgery
Esophageal and gastric endoscopy: o
For sym ptom atic patients to determ ine the extent of injury
o
Perform within the first 12–24 hours after ingestion.
o
Not recom m ended in the presence of respiratory distress without proper airway m anagem ent
o
Not recom m ended in the presence of severe pharyngeal dam age
Radiographic oral contrast im aging not recom m ended acutely: o
May be used in follow-up for assessm ent for strictures
Differential Diagnosis
Chem ical injuries from corrosives, acids, alkalis, desiccants, vesicants, and oxidizing and reducing agents
Foreign body ingestion
Upper airway infection or angioedem a
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P.203
Treatment Pre Hospital
For oral burns or sym ptom s: Rinse m outh liberally with water or m ilk.
Water or m ilk can be given to following patients: o
Able to drink
o
Not com plaining of significant abdom inal pain
o
Do not have airway com prom ise or vom iting
Copious irrigation for ocular or derm al exposure
Initial Stabilization
Airway, breathing, circulation (ABCs): o
Prophylactic intubation if there is any evidence of respiratory com prom ise
o
Blind nasotracheal intubation contraindicated
Treat hypotension with 0.9% norm al saline (NS) IV fluid resuscitation.
ED Treatment
Decontam ination: o
Derm al or ocular exposure:
Im m ediate and thorough irrigation with water or 0.9% NS until physiologic pH attained
Alkalis typically require m ore irrigation than acids.
o
Ipecac, activated charcoal, gastroesophageal lavage, and a neutralizing acid or base are all contraindicated
Pa ge 9 9 7
with caustic ingestions.
Dilution: o
Water or m ilk in the first 30 m inutes of ingestion:
Especially useful for solid caustic alkali ingestions
Excessive intake m ay induce vom iting and worsen esophageal dam age.
o
If respiratory distress, intubate before dilution.
o
Contraindicated if esophageal or gastric perforation suspected
Keep patient NPO (nothing by m outh) if oral exposure.
Broad-spectrum antibiotics if m ediastinitis or peritonitis suspected
Antiem etics for nausea and vom iting
Treat derm al exposures according to standard burn recom m endations.
Detailed exam ination for ocular exposures
Intravenous H 2 blockers for sym ptom atic relief
Gastroenterology and surgical consultation
Benefit of corticosteroids following esophageal dam age is controversial: o
May prevent the form ation of esophageal stricture
o
May prom ote bacterial invasion, im m une suppression, and tissue softening
o
The decision to initiate corticosteroids requires input from entire team caring for patient.
o
Initiate broad-spectrum antibiotics if corticosteroids are given.
Laparoscopy or laparotom y for perforation and full-thickness necrosis
Topical hydrofluoric acid exposure (options depend on severity and location):
Pa ge 9 9 8
o
Intraderm al injection of 5% calcium gluconate (0.5 m L/cm 2 of skin with 30-gauge needle)
o
Intra-arterial infusion of 10 m L of 10% calcium gluconate in 40 m L D 5 W over 4 hours
Medication (Drugs)
Methylprednisolone: 40 m g q8h IV (peds: 2 m g/kg/d IV); the course of therapy is 14–21 days followed by a corticosteroid taper
Prochlorperazine (Com pazine): 5–10 m g IV (peds: 0.13 m g/kg per dose IM)
Ranitidine (Zantac): 50 m g IV q6h–q8h
Follow-Up Disposition Admission Criteria
All sym ptom atic patients
Nonaccidental ingestion
Discharge Criteria
Asym ptom atic patients who accidentally ingested and are able to swallow without difficulty
Minim al oropharyngeal pain with a corresponding visible lesion; no drooling; no respiratory com prom ise; no deep throat, chest, or abdom inal pain; and able to swallow without difficulty
References 1. Anderson KD, Rouse TM, Randolph JG. A controlled trial of
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corticosteroids in children with corrosive injury of the esophagus. N Engl J Med. 1990;323:10:637–640. 2. Nagi B, Kochar R, Thapa BR, et al. Radiological spectrum of late sequelae of corrosive injury to upper gastrointestinal tract. A pictorial review. ACTA Radiologica. 2004;1:712. 3. Rao RB, Hoffm an RS. Caustics and batteries. In: Goldfrank LR, Flom enbaum NE, Lewin NA, et al., eds. Goldfrank's Toxicologic Em ergencies. 7th ed. New York: McGraw-Hill; 2002:1323–1340.
Codes ICD9-CM 983.2 983.1
ICD10 T54.9
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > C averno us Sinus Thro m bo sis
Cavernous
Sinus Thrombosis Edward Stettner
Basics Description
Throm bosis of a branch of the m ajor intracerebral venous drainage system
Most com m only infectious
Spreads from odontogenic or sinus infectious source.
Less frequently occurs with hypercoagulable states
Anatomy
Three prim ary sites of throm bosis: o
Cavernous sinus: m ost com m on:
Drainage from superficial venous system
Superolateral to the sphenoid sinus and surrounds the sella
Cranial nerves (CN) III, IV, V1, and V2 traverse the lateral wall of the sinus.
CN VI and the internal carotid artery occupy the m edial portion of the sinus.
o
Can also involve transverse sinus and superficial sagital sinus
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Pathophysiology
Hem atogenous spread of facial, otic, or neck infection into venous drainage system
Bacterial overgrowth leads to inflam m ation and coagulation, resulting in throm bosis.
Venous engorgem ent of cavernous sinus can effect adjacent structures: o
Ophthalm oplegia from inflam m ation of CN III, IV, or VI
o
Pupillary fixation from CN III
o
Sensory deficits or parasthesias of forehead or cheek from CN V1 and V2
Etiology Septic
Cavernous sinus: o
Thirty percent m ortality
o
Midface infection spreads into cavernous sinus
o
Maxillary dental infection and sphenoid sinusitis are m ost com m on.
Lateral: o
Twenty-five percent m ortality
o
Prim arily disease of young children
o
Spread from otogenic source
o
Otitis m edia or m astoiditis
Superior sagital: o
Extrem ely rare, with 80% m ortality
Aseptic
Less com m on
Granulom atous conditions (tuberculosis [TB])
Inflam m atory disorders
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From m ass effect (tum ors at base of skull, aneurysm s)
Hypercoagulable states (postoperation, m alignancy, nephritic syndrom e, pregnancy, oral contraceptives)
Complications
Blindness can result from : o
Central retinal artery occlusion
o
Central retinal vein occlusion
o
Septic em boli
o
Arteritis
o
Ischem ic optic neuritis
o
Glaucom atous optic atrophy
o
Corneal ulceration from loss of corneal reflex
Hearing loss from otic invasion
Local spread can cause m eningitis or intracranial abscess
Pituitary necrosis and insufficiency from local invasion
Sepsis can develop from system ic hem atogenous seeding: o
Septic em boli
o
Adult respiratory distress syndrom e (ARDS)
Pediatric Considerations
Children m ay present with nonspecific sym ptom s such as decreased energy, vom iting, fever.
Have high level of suspicion for any child with recent otitis or pharyngitis with worsening sym ptom s, declining m ental status, or signs of increased intracranial pressure: o
Hypertension, bradycardia, lethargy, vom iting, gait instability
More com m on in the neonatal period where diagnosis can be extrem ely difficult to m ake
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Diagnosis Signs and Symptoms Signs
Headache
Fever if infectious cause
Ocular or retrobulbar pain
Facial swelling
Visual disturbance
Facial dysesthesias
Lethergy and alteration in consciousness
Symptoms
Ptosis
Chem osis with retinal vein engorgem ent
Facial or periorbital edem a
Ophthalm oplegia
Retinal hem orrhage or papilledem a
Altered level of consciousness or com a
Seizures
Sepsis with cardiovascular instability or collapse
Essential Workup Clinical diagnosis based on:
Sym ptom s of venous obstruction
Ophthalm oplegia
Sepsis or m eningitis
Sym ptom s that becom e unilateral and spread to becom e bilateral are diagnostic.
Tests Lab
Neither sensitive nor specific
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CBC: o
Leukocytosis
PT/PTT/INR
Erythrocyte sedim entation rate (ESR) elevated in 50–60%
Lum bar puncture/cerebrospinal fluid (CSF): o
To evaluate fever and altered m ental status
o
CSF with elevated protein and WBC
Imaging
CT scan: o
Can be norm al early in disease course
o
Findings include:
Nonspecific abnorm alities
May identify original source of infection (e.g., sinusitis)
Delayed filling of involved sinus
Filling defect of sinus owing to throm bosis
Dilated superior ophthalm ic vein
Associated intracranial hem orrhage
Signs of increased intracranial pressure (ICP): sm all ventricles, loss of sulci
MRI with m agnetic resonance angiography (MRA)/m agnetic resonance venography (MRV): o
Diagnostic m odality of choice
o
Direct visualization of intracranial vessels and sinuses
o
Capable of visualizing throm bus as any stage
P.205
Differential Diagnosis
Meningitis
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Encephalitis
Intracranial abscess
Periorbital and orbital cellulitis
Bacterem ia
Migraine
Pseudotum or cerebri
Intracranial hem orrhage
Tolosa-Hunt syndrom e: o
Rare granulom atous inflam m ation of cavernous sinus
Alert
This can be an extrem ely difficult diagnosis to m ake.
Maintain a high level of suspicion in toxic-appearing patients with recent ear/nose/throat (ENT) infections, or in patients with refractory headache and risk factors for hypercoagulability or intracranial infection.
Treatment Pre Hospital Alert
Patients can be altered and unstable.
May require rapid assessm ent and stabilization of airway, breathing, and circulation (ABCs)
Initial Stabilization
Careful assessm ent of m ental status with intubation for airway protection as needed
Aggressive fluid resuscitation for cardiovascular instability
ED Treatment
High level of suspicion—difficult diagnosis to m ake
Pa ge 1 0 0
Broad-spectrum antibiotics with m ultiple drug regim ens: o
Cover for gram -positives, gram -negatives, as well as anaerobes.
o
Nafcillin or vancom ycin (for m ethicillin resistant staphlococcal aureus [MRSA]) plus ceftriaxone:
Add m etronidazole or clindam ycin in significant infections.
Surgical consultation for drainage of prim ary site of infection (e.g., dental abscess or sinusitis)
Heparin: o
May im prove m orbidity and m ortality in cavernous throm bosis
o
Controversial in transverse and sagital throm bosis owing to higher risk of subsequent hem orrhage
o
Adm inister only after ruling out bleed on CT scan.
System ic steroids: o
Believed to be of benefit with concom itant pituitary insufficiency
Appropriate m anagem ent of increased ICP as needed
Medication (Drugs)
Ceftriaxone: 2 g (peds: 80–100 m g/kg daily to b.i.d.) IV daily
Clindam ycin: 300–900 m g (neonates: 10–20 m g/kg/24h IV div. q6h–q12h; peds: 25–40 m g/kg/24h div. q6h–q8h) IV q6h–q12h
Metronidazole: 500 m g (neonates: 7.5–30 m g/kg/24h IV div. q12h–q24h; peds: 30 m g/kg/24h IV div. q6h) IV q6h
Nafcillin: 1–2 g (peds: 50–75 m g/kg/24h IV div. b.i.d.–t.i.d. depending on age) IV q4h
Vancom ycin: 1 g (peds: 10–20 m g/kg IV b.i.d.–t.i.d.
Pa ge 1 0 0
depending on age) IV q12h
Follow-Up Disposition Admission Criteria
All patients with sinus throm bosis need adm ission to a m onitored setting.
Consider ICU adm ission.
Neurologic and neurosurgical consultation.
Discharge Criteria None
References 1. Cannon ML, Antonio BL, McCloskey JJ, et al. Cavernous sinus throm bosis com plicating sinusitis. PediatrCcrit Care Med. 2004;5(1):86–88. 2. Carvalho KS, Garg BP. Cerebral venous throm bosis and venous m alform ations in children. Neurol Clin North Am . 2002;20:1061–1077. 3. Eustis HS, Mahm ood FM, Wato C, et al. Im aging in ophthalm ology. I: MR im aging and CT of orbital infections and com plications in acute rhinitis. Radiol Clin North Am . 1998;36(6):1165–1183. 4. Heilpern KL, Lorber B. Infectious disease em ergencies: focal intracranial infections. Infect Dis Clin North Am . 1996;10(4):879–898. 5. Sztajunkrycer M, Jauch EC. The difficult diagnosis: unusual headaches. Em erg Med Clin North Am . 1998;16(4):741–760.
Codes ICD9-CM
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325 Phlebitis and throm bophlebitis of intracranial venous sinuses 671.5 Other phlebitis and throm bosis 437.6 Nonpyogenic throm bosis of intracranial venous sinus
ICD10 S36.4
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > C ellulitis
Cellulitis
John Mahoney Dolores Gonthier
Basics Description
Acute, spreading erythem atous superficial infection of skin and subcutaneous tissues: o
Variety of pathogens
o
Extension into deeper tissues can result in necrotizing soft tissue infection.
Progressive spread of erythem a, warm th, pain, and tenderness
Predisposing factors: o
Lym phedem a
o
Tinea pedis
o
Open wounds
o
Pre-existing skin lesion (furuncle)
o
Prior traum a or surgery
o
Retained foreign body
o
Vascular or im m une com prom ise
o
Injection drug use
Etiology
Sim ple cellulitis:
Pa ge 1 0 1
o
Group A streptococci
o
Staphylococcus aureus—including resistant strains; see below
Extrem ity cellulitis after lym phatic disruption o
Non-group A β-hem olytic streptococci (groups C, B, G)
Cellulitis in diabetics: o
Can be polym icrobial with S. aureus, streptococci, gram -negative bacteria, and anaerobes, especially when associated with skin ulcers
Periorbital cellulitis: o
S. aureus
o
Streptococcal species
Buccal cellulitis: o
Haem ophilus influenzae type B
o
Anaerobic oral flora, associated with intraoral laceration or dental abscess
Nosocom ial m ethicillin-resistant S. aureus: o
Risk factors: recent hospital or long-term care adm ission, surgery, injection drug use, vascular catheter, dialysis, recent antibiotic use, unresponsive infection
o
Resistant to m ost antibiotics (see Treatm ent)
Com m unity-acquired m ethicillin-resistant S. aureus (CA-MRSA): o
No identified risk factor
o
Different antibiotic susceptibility than nosocom ial MRSA:
Trim ethoprim -sulfam ethoxazole (TMP/SMX) and clindam ycin m ay be effective.
o
Variable, rising local prevalence should be considered when starting em piric antibiotic therapy.
Pa ge 1 0 1
o
Suspect in unresponsive infections
Less com m on causes: o
Clostridia
o
Anthrax
o
Pasteurella m ultocida—com m on after cat and dog bites
o
Eikenella corrodens—hum an bites
o
Pseudom onas aeruginosa:
o
Hot-tub folliculitis—self-lim ited
Foot puncture wound
Ecthym a gangrenosum in neutropenic patients
Erysipelothrix species—raw fish, poultry, m eat or hide handlers
o
Aerom onas hydrophila—freshwater swim m ing
o
Vibrio species–seawater or raw seafood
Pediatric Considerations
Facial cellulitis in children: o
Streptococcus pneum oniae
o
H. influenzae type B, although incidence declining since introduction of HIB vaccine
Perianal cellulitis: o
Group A streptococci
o
Associated or antecedent pharyngitis or im petigo
Neonates: o
Group B streptococci
Diagnosis Signs and Symptoms
Com m on to all syndrom es:
Pa ge 1 0 1
o
Pain, tenderness, warm th
o
Erythem a
o
Edem a or induration
o
Fever/chills
o
Tender regional lym phadenopathy
o
Lym phangitis
o
Accom panying subcutaneous abscess possible
o
Superficial vesicles
Buccal cellulitis: o
Odontogenic cases m ore serious:
Toothache, sore throat, or facial swelling
Progressive extension into soft tissues of neck with fever, erythem a, neck swelling, and dysphagia
Pediatric Considerations
Facial cellulitis in children: o
Erythem a and swelling of the cheek and eyelid
o
Rapidly progressive
o
Usually unilateral
o
Upper respiratory tract sym ptom s
o
Risk for cavernous sinus throm bosis and perm anent optic nerve injury
Perianal cellulitis: o
Erythem a and pruritus extending from the anus several centim eters onto adjacent skin
o
Pain on defecation
o
Blood-streaked stools
Essential Workup
Cellulitis is a clinical diagnosis.
Physical exam ination to reveal infection source.
Tests
Pa ge 1 0 1
Lab
White blood count unnecessary
Gram stain and culture to focus antim icrobial selection and reveal resistant pathogens (MRSA): o
Aspirate point of m axim al inflam m ation or punch biopsy.
o
Consider in treatm ent failures.
Blood culture: o
Usually negative in uncom plicated cellulitis
o
May identify organism in patients with:
Lym phedem a
Buccal or periorbital cellulitis
Salt water or freshwater source
Fever or chills
Imaging
Plain radiographs m ay reveal abscess form ation, subcutaneous gas, or foreign bodies: o
Extension to bone (osteom yelitis) not visualized early on plain radiographs
Extrem ity vascular im aging (Doppler ultrasound) can help rule out deep venous throm bosis.
CT or MRI can help rule out necrotizing fasciitis.
Differential Diagnosis
Necrotizing fasciitis
Lym phangitis or lym phadenitis
Throm bophlebitis or deep venous throm bosis (DVT): o
Differentiation from cellulitis:
Absence of initial traum atic or infectious focus
No regional lym phadenopathy
Presence of risk factors for DVT
Insect bite
Pa ge 1 0 1
Allergic reaction
Acute gout or pseudogout
Ruptured Baker cyst
Herpetic whitlow
Neoplasm
Phytophotoderm atitis
Prom inent response to sm allpox vaccination
Erythem a chronicum m igrans lesion of Lym e disease
Sm allpox vaccination, norm al variant of usual reaction to vaccination
Differential diagnosis of facial cellulitis: o
Allergic angioedem a
o
Conjunctivitis
o
Contusion
Pediatric Considerations
Differential diagnosis of perianal cellulitis: o
Candida intertrigo
o
Psoriasis
o
Pinworm infection
o
Child abuse
o
Behavioral problem
o
Inflam m atory bowel disease
P.207
Treatment Initial Stabilization Airway com prom ise possible with deep extension of facial or neck
Pa ge 1 0 1
cellulitis
ED Treatment
General principles: o
Consider local prevalence of MRSA and other resistant pathogens in addition to usual causes.
o
Usual outpatient treatm ent: 7–10 days
o
Cool com presses for com fort
o
Analgesics
o
Extrem ity elevation
o
Treat predisposing tinea pedis with topical antifungal such as clotrim azole.
Sim ple cellulitis: o
Outpatient: oral dicloxacillin; alternatives: oral m acrolide, cephalexin, or levofloxacin
o
Extrem ity cellulitis after lym phatic disruption: o
Inpatient: IV nafcillin or equivalent
Sam e as sim ple cellulitis
Cellulitis in diabetics: o
Outpatient: am oxicillin/clavulanate or clindam ycin
o
Inpatient: IV am picillin/sulbactam or im ipenem cilastatin or equivalent
Periorbital cellulitis in adults: o
Outpatient: oral dicloxacillin or azithrom ycin
o
Inpatient: IV vancom ycin
Buccal cellulitis in adults: o
Outpatient: oral am oxicillin/clavulanate
o
Inpatient: IV ceftriaxone
o
Odontogenic source:
Drainage essential
Coverage for anaerobes: clindam ycin
Facial cellulitis in children: o
IV ceftriaxone
Pa ge 1 0 1
Perianal cellulitis: o
Outpatient: oral penicillin VK
o
Inpatient: IV penicillin G (aqueous)
Anim al or hum an bite: o
Foot puncture wound: o
Oral am oxicillin/clavulanate
Oral or IV ciprofloxacin or IV ceftazidim e
Methicillin-resistant Staphylococcus aureus: o
Nosocom ial MRSA: IV vancom ycin or oral or IV linezolid
o
Com m unity-acquired MRSA:
Add oral TMP/SMX to em piric treatm ent or use oral clindam ycin alone.
More severe: IV clindam ycin or IV vancom ycin
Medication (Drugs)
Am oxicillin/clavulanate: 500–875 m g (peds: 45 m g/kg/24h) PO b.i.d. or 250–500 m g (peds: 40 m g/kg/24h) PO t.i.d.
Am picillin/sulbactam : 1.5–3 g (peds: 100–300 m g/kg/24h up to 40 kg; over 40 kg give adult dose) IV q6h
Azithrom ycin: (adults and peds) 10 m g/kg up to 500 m g PO on day 1, followed by 5 m g/kg up to 250 m g PO daily on days 2–5
Ceftazidim e: 500–1,000 m g (peds: 150 m g/kg/24h; m ax., 6 g/24h; use sodium form ulation in peds) IV q8h
Ceftriaxone: 1–2 g (peds: 50–75 m g/kg/24h) IV daily
Cephalexin: 500 m g (peds: 50–100 m g/kg/24h) PO q.i.d.
Ciprofloxacin: (adult only) 500–750 m g PO b.i.d. or 400 m g IV q8h–q12h
Clindam ycin: 450–900 m g (peds: 20–40 m g/kg/24h)
Pa ge 1 0 1
PO or IV q8h
Dicloxacillin: 125–500 m g (peds: 12.5–25 m g/kg/24h) PO q6h
Erythrom ycin base: (adult) 250–500 m g PO q.i.d.
Im ipenem cilastatin: 500–1,000 m g (peds: 15–25 m g/kg) IV q6h; m ax. 4 g/24h or 50 m g/kg/24h, whichever is less
Levofloxacin: (adult only) 500–750 m g PO or IV daily
Linezolid: 600 m g PO or IV q12h (peds: 30 m g/kg/24h div. q8h)
Nafcillin: 1–2 g IV q4h (peds: 50–100 m g/kg/24h divided q6h); m ax. 12 g/24h
Penicillin VK: 250–500 m g (peds: 25–50 m g/kg/24h) PO q6h
Penicillin G (aqueous): 4 m U (peds: 100,000–400,000 U/kg/24h) IV q4h
Trim ethoprim /sulfam ethoxazole (TMP/SMX): 1 DS tab PO q12h (peds: 6–10 m g/kg/24h TMP div. q12h)
Vancom ycin: 1 g IV q12h (peds: 10 m g/kg IV q6h; dosing adjustm ents required younger than age 5 years); check serum levels
Follow-Up Disposition Admission Criteria
Toxic appearing
Tissue necrosis
History of im m une suppression
Concurrent chronic m edical illnesses
Pa ge 1 0 1
Unable to take oral m edications
Unreliable patients
Discharge Criteria
Mild infection in a non-toxic-appearing patient
Able to take oral antibiotics
No history of im m une suppression or concurrent m edical problem s
No hand or face involvem ent
Has adequate follow-up within 24 to 48 hours
References 1. Givner LB, Mason EO, Barson WJ, et al. Pneum ococcal facial cellulites in children. Pediatrics. 2000;106(5):e61. 2. Moran GJ, Talan DA. Com m unity-acquired m ethicillin-resistant Staphylococcus aureus: is it in your com m unity and should it change practice? Ann Em erg Med. 2005;45:321–322. 3. Padm anabhan R, Fraser T. The em ergence of m ethicillin-resistant Staphylococcus aureus in the com m unity. Cleve Clin J Med. 2005;72(3):235–241. 4. Swartz MN. Cellulitis. New Engl J Med. 2004;350:904–912. 5. Swartz MN, Pasternack, MS. Cellulitis and subcutaneous tissue infections. In: Mandell GL, Bennett JE, Dolin R, eds. Mandell, Douglas and Bennett's Principles and Practice of Infectious Diseases. 6th ed. New York: Elsevier/Churchill Livingstone; 2005:1172–1194.
Miscellaneous SEE ALSO: Abscess, Skin/Soft Tissue; Lym phadenitis; Lym phangitis; Necrotizing Fasciitis
Codes ICD9-CM
Pa ge 1 0 1
682.9
ICD10 L03.9
Pa ge 1 0 2
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > C erebral Aneurysm
Cerebral
Aneurysm Veronique Au Rebecca Smith-Coggins
Basics Description
Abnorm al, localized dilation or outpouching of cerebral artery wall: o
Occurs in 5–10% of population
Rupture of saccular aneurysm s account for 5–15% of strokes.
Of those that rupture: o
Forty percent occur at anterior com m unicating artery (ACA)
o
30% at internal carotid (IC)
o
20% in m iddle cerebral artery (MCA)
o
5–10% in vertebrobasilar artery (VBA) system
Etiology
“Congenital,― saccular, or berry aneurysm s m ost com m on (90%): o
Develop at weak points in arterial wall and bifurcations of m ajor cerebral arteries
Pa ge 1 0 2
o
Incidence increases with age.
o
Multiple in 20–30%
o
Increased incidence: Polycystic kidney disease
Cerebral arteriovenous m alform ation
Type III collagen deficiency
Fibrom uscular dysplasia
Ehlers-Danlos syndrom e
Marfan syndrom e
Pseudoxanthom a elasticum
Neurofibrom atosis
Moyam oya disease
Coarctation of the aorta
Tuberous sclerosis
Sickle cell disease
Osler-Weber-Rendu syndrom e
α1-Antitrypsin deficiency
System ic lupus erythem atosus
Arteriosclerotic, fusiform or dolichoectatic (7%): o
More com m on in peripheral arteries
Inflam m atory (m ycotic): o
Ten percent of patients with bacterial endocarditis
Traum atic, associated with severe closed head injury
Neoplastic, em bolized tum or fragm ents
Pediatric Considerations
Although rare in children, m ore likely to be giant (>25 mm)
Occur in the posterior circulation
Diagnosis
Pa ge 1 0 2
Signs and Symptoms
Com m only asym ptom atic before rupture
Sentinel headaches occur in 30–60% of patients before rupture: o
Can be unilateral
Seizures, syncope, or altered level of consciousness
Com pression of adjacent structures m ay cause neurologic sym ptom s: o
Anterior com m unicating artery aneurysm s:
Optic tract: altitudinal field cut or hom onym ous hem ianopsia
o
Optic chiasm : bitem poral hem ianopsia
Optic nerve: unilateral am blyopia
Aneurysm s at internal carotid–posterior com m unicating artery junction:
Oculom otor nerve: fixed and dilated pupil, ptosis, diplopia, and tem poral deviation of eye with inability to turn eye upward, inward, or downward
o
Aneurysm s in cerebral cortex m ay produce focal deficits, including hem iparesis, hem isensory loss, visual disturbances, aphasia, and seizures.
Rupture results in subarachnoid hem orrhage: o
Headache: severe (“worst headache ever―) with sudden onset (“thunderclap―)
o
Different from prior headaches
Classically without focal deficits
Nuchal rigidity (m ost com m on sign) secondary to blood in cerebrospinal fluid (CSF)
Essential Workup
Com plete neurologic exam ination
Pa ge 1 0 2
Em ergent noncontrast head CT scan will diagnose 90–95% of subarachnoid hem orrhages.
Lum bar puncture with CSF analysis if CT scan is negative
Tests Lab
Coagulation studies
Baseline com plete blood chem istry with platelets and differential
Electrolytes
Renal and liver function tests
Arterial blood gases
Imaging
Chest radiographs for pulm onary edem a
Four-vessel cerebral angiography rem ains gold standard.
Magnetic resonance angiography
Helical CT scanning m ay be useful in detecting aneurysm s >3 m m .
Transcranial Doppler ultrasound m ay be useful in detecting vasospasm .
Differential Diagnosis
Neoplasm
Arteriovenous m alform ation
Optic neuritis
Migraine
Meningitis
Encephalitis
Hypertensive encephalopathy
Hyperglycem ia or hypoglycem ia
Tem poral arteritis
Acute glaucom a
Pa ge 1 0 2
Subdural hem atom a
Epidural hem atom a
Intracerebral hem orrhage
Throm boem bolic stroke
Air em bolism
Sinusitis
Treatment Pre Hospital Cautions:
Neurologic exam ination in the field can be extrem ely helpful.
Assess: o
Level of consciousness
o
Glasgow com a scale score
o
Gross m otor deficits
o
Speech abnorm alities
o
Gait disturbance
o
Facial asym m etry
o
Other focal deficits
Patients with subarachnoid hem orrhage m ay need em ergent intubation for rapidly deteriorating level of consciousness.
Patients m ust be transported to a hospital with em ergent CT scanning and intensive care unit–level treatm ent.
P.209
Initial Stabilization
Pa ge 1 0 2
Managem ent of airway, breathing, and circulation: o
Supplem ental oxygen
o
Rapid-sequence intubation m ay be required for airway protection or for controlled ventilation.
o
Continuous cardiac m onitoring and pulse oxim etry
For altered m ental status, check blood glucose im m ediately, give D 5 0 (if glucose is low), naloxone, and thiam ine.
Managem ent of acute hypertension is essential; this m ay be accom plished with labetalol, nicardipine, nitroprusside, or hydralazine.
Prevention of acute increases in intracranial pressure from vom iting should be accom plished with antiem etics.
Seizures should be m anaged acutely with intravenous benzodiazepines and phenytoin.
ED Treatment Following initial stabilization, the m ajor goals of early treatm ent of ruptured or leaking aneurysm s are to prevent rerupture, cerebral vasospasm , and hydrocephalus (see: Subarachnoid Hem orrhage).
Pediatric Considerations Aneurysm s in children have a high rate of hem orrhage and should be repaired early.
Medication (Drugs)
Diazepam : 5–10 m g IV q10–15m in m ax., 30 m g (peds: 0.2–0.3 m g/kg q5–10m in m ax. 10 m g)
Docusate sodium : 100 m g PO b.i.d.
Hydralazine: 10–20 m g IV q30m in
Labetalol: 20–30 m g/m in IV bolus, then 40–80 m g q10m in m ax. 300 m g; follow with continuous infusion
Pa ge 1 0 2
0.5–2 m g/m in
Lorazepam : 2–4 m g IV q15m in PRN (peds: 0.03–0.05 m g/kg per dose; m ax. 4 m g per dose)
Nicardipine 5 m g/h IV infusion, increase by 2.5 m g/h q5–15m in m ax. 15 m g/h (peds: dosing unavailable)
Nim odipine: 60 m g PO/nasogastric q4h
Nitroprusside: 0.25–10 µg/kg per m inute (adult and peds)
Phenytoin: 15–20 m g/kg IV load at m ax. 50 m g/m in; m ax. 1.5 g (adult and peds); m aintenance 4–6 m g/kg/d IV/IM
Prochlorperazine: 5–10 g IV/IM q6h–q8h (peds: 0.2 m g/kg/d IM in 3 or 4 div. doses); m ax. 40 m g/d
Surgery Optim al tim ing for angiography and surgery rem ain controversial, but trend is toward early surgery to decrease incidence of rebleeding and cerebral vasospasm .
Follow-Up Disposition Admission Criteria
Any patient with acute aneurysm al subarachnoid hem orrhage should be adm itted, preferably to intensive care unit.
Any patient with sym ptom atic unruptured aneurysm should receive adm ission and urgent neurosurgical consultation, given high rate of rupture.
Discharge Criteria
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Patients with incidentally discovered asym ptom atic intracranial aneurysm s m ay be discharged with close neurosurgical follow-up.
Note that overall risk of rupture is 1–2% per year and that critical size at which risk for rupture outweighs risk for surgery is controversial (classically 10 m m , but probably in the 4- to 8-m m range).
References 1. Barrow DL, Reisner A. Natural history of intracranial aneurysm s and vascular m alform ations. Clin Neurosurg. 1993;40:3–39. 2. Barsan WG, Kothari R. Stroke. In: Rosen P, et al. eds. Em ergency Medicine: Concepts and Clinical Practice. 4th ed. St. Louis, MO: Mosby; 1997:2184–2197. 3. Becker KJ. Epidem iology and clinical presentation of aneurysm al subarachnoid hem orrhage. Neurosurg Clin N Am . 1998;9:435–444. 4. Bederson JB, Awad IA, Wiebers DO, et al. Recom m endations for the m anagem ent of patients with unruptured intracranial aneurysm s: a statem ent for healthcare professionals from the Stroke Council of the Am erican Heart Association. Stroke. 2000;31:2742–2750. 5. Edlow JA, Caplan LR. Avoiding the pitfalls in the diagnosis of subarachnoid hem orrhage. New Engl J Med. 2000;1:29–36. 6. Mitchell P, Gholkar A, Vindlacheruvu RR, et al. Unruptured intracranial aneurysm s: benign curiosity or ticking bom b? Lancet Neurol. 2004;3:85–92. 7. Victor M, Ropper AH. Cerebrovascular diseases. In: Adam s RD, Victor M, eds. Principles of Neurology. 5th ed. New York: McGraw-Hill; 1993. 8. Wijdicks EF, Kallm es DF, Manno EM, et al. Subarachnoid hem orrhage: neurointensive care and aneurysm repair. Mayo Clinic Proc. 2005;80:550–559. 9. White PM, Wardlaw JM, Easton V. Can noninvasive im aging accurately depict intracranial aneurysm s? A system atic review.
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Radiology. 2000;217:361–370.
Miscellaneous SEE ALSO: Subarachnoid Hem orrhage
Codes ICD9-CM 437.3 Cerebral Aneurysm , Nonruptured
ICD10 I67.1 Subarachnoid Haem orrhage from Middle Cerebral Artery
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > C erebral Vascular Accident
Cerebral
Vascular Accident Veronique Au Rebecca Smith-Coggins
Basics Description Interruption of blood flow to a specific brain region:
Neurologic findings determ ined by specific area affected
Onset m ay be sudden and com plete, or stuttering and interm ittent
Risk Factors
Diabetes
Sm oking
Hypertension
Coronary artery disease
Peripheral vascular disease
Oral contraceptive use
Polycythem ia vera
Sickle cell anem ia
Deficiencies of antithrom bin III, protein C, or protein S
Etiology
Pa ge 1 0 3
May be ischem ic (throm botic or em bolic) or hem orrhagic (intracranial or subarachnoid hem orrhage)
Throm botic stroke is caused by occlusion of blood vessels: o
Clot form ation at an ulcerated atherosclerotic plaque is m ost com m on.
o
Sludging (sickle cell anem ia, polycythem ia vera, protein C deficiency)
o
Arterial dissection, arteritis (giant cell, Takayasu), or fibrom uscular dysplasia
Em bolic stroke is caused by acute blockage of a cerebral artery by a piece of foreign m aterial from outside the brain, including: o
Cardiac m ural throm bi associated with m itral stenosis, atrial fibrillation, cardiom yopathy, congestive heart failure, or m yocardial infarction
o
Prosthetic heart valves or abnorm al native valves
o
Atherosclerotic plaques in the aortic arch or carotid arteries
o
Atrial m yxom a
o
Ventricular aneurysm s with ventricular throm bi
Global ischem ic or hypotensive stroke is caused by an overall decrease in system ic blood pressure: o
Sepsis
o
Hem orrhage
o
Shock
Pediatric Considerations Usually attributable to underlying disease process such as sickle cell anem ia, leukem ia, or a blood dyscrasia
Diagnosis
Pa ge 1 0 3
Signs and Symptoms
Aphasia
Hem iparesis, hem iplegia
Hem isensory loss
Dysarthria, dysphagia
Facial droop
Ataxia, clum siness
Visual loss, photophobia, diplopia
Headache
Nausea, vom iting
Vertigo, dizziness
Altered level of consciousness, confusion, agitation
Cardiac dysrhythm ias, m urm urs
Cheyne-Stokes breathing, apnea
Hypertension
Transient ischem ic attacks: o
Focal neurologic deficits that com pletely resolve in 130–150 m m Hg on repeated m easurem ents
o
If indicated for other concurrent problem s (m yocardial infarction, aortic dissection, congestive heart failure, hypertensive encephalopathy)
o
Initial goal is systolic BP Table o f C o ntents > C esarean Sectio n, Em ergency
Cesarean
Section, Emergency James Walker Michael Chamales
Basics Alert
The sole indication for ED physician to perform em ergency perim ortem cesarean section is gravid fem ale (>24 weeks’ gestation) in cardiopulm onary arrest who has not responded to initial resuscitative m easures, regardless of cause.
The m ost im portant predictor of fetal survival is length of tim e between m aternal cardiac arrest and cesarean delivery: o
Cesarean section should begin within 4 m inutes of m aternal arrest.
o
Goal is delivering fetus within 1 m inute.
Obtain im m ediate consultations from obstetrics, pediatrics (and surgery, if traum a related): o
Do not defer or delay perform ing procedure until arrival of consultants.
Do not perform em ergent cesarean section if patient is
Pa ge 1 0 4
24 weeks’ gestation determ ined by uterine fundal height) who is in cardiopulm onary arrest
Essential Workup
Physical exam ination for apnea and pulselessness in obviously gravid fem ale
Quickly evaluate for reversible causes of cardiopulm onary arrest: o
Tension pneum othorax
o
Pericardial tam ponade
Pa ge 1 0 5
o
Supine hypotension syndrom e (com pression of inferior vena cava by enlarged uterus)
Assess gestational age by uterine fundal height.
Distance from pubis to fundus in centim eters is roughly equivalent to gestational age in weeks.
Ultrasonography is beneficial if im m ediately available to assess fetus.
Tests Imaging
None necessary to establish cardiopulm onary arrest
Do not waste tim e by attem pting to find fetal heart tone.
Differential Diagnosis Cardiopulm onary arrest is final com m on pathway:
Evaluate for underlying cause.
Treatment Pre Hospital Cautions:
Minim al scene tim e, “scoop and run―
Place the patient in the left lateral decubitus position to avoid com pression of inferior vena cava (supine hypotension syndrom e)
Traum a patient requiring spinal im m obilization o
Uterus can be m anually displaced to left.
o
Backboard can be wedged to keep right hip elevated 45 degrees.
Initial Stabilization
Standard resuscitation m easures:
Pa ge 1 0 5
o
Em ergency intubation
o
High-flow oxygen
o
Cardiac and blood pressure m onitoring
o
Two large-bore peripheral intravenous lines
Fluid resuscitation
O-negative blood if indicated
Fetal survival correlates with m aternal survival and adequacy of initial m aternal resuscitation.
If patient is at 24 weeks’ gestation, use 4-m inute rule: o
Perform advanced cardiac life support or advanced traum a life support for 4 m inutes.
o
If no response, proceed to im m ediate em ergency cesarean section.
o
Goal is to deliver fetus within 1 m inute.
o
If it is obvious there is no chance for m aternal survival, begin perim ortem cesarean section im m ediately.
P.215
ED Treatment
Call for im m ediate obstetric, surgical, and pediatric consultations: o
Do not delay perform ing procedure while waiting for consultants.
Ensure a Foley catheter has been inserted to decom press bladder.
Perform cesarean section:
Pa ge 1 0 5
o
Use linea nigra as landm ark for vertical m idline incision.
o
Incise abdom inal wall from pubic hairline to 5 cm above um bilicus.
o
This incision should pass through fascial and peritoneal layers.
o
Retract urinary bladder inferiorly against pubic sym physis.
o
Make sm all vertical incision in lower uterine segm ent, just cephalad to urinary bladder.
o
Extend incision cephalad with scissors.
Insert your free hand into uterus.
Lift uterine wall away from fetus to avoid fetal injury.
o
Deliver fetus.
o
Clam p um bilical cord in two places and cut between the two clam ps.
o
Manually deliver placenta.
o
Perform neonatal resuscitation as indicated.
o
Im m ediately reassess m aternal vital signs because occasionally spontaneous circulation m ay return.
o
Continue m aternal resuscitation as appropriate.
o
Suture uterus with running lock stitch using no. 0 polyglactin suture.
o
Suture fascia and peritoneum with running stitch using no. 0 polyglactin suture.
o
Close the skin with staples or suture
o
Adm inister broad-spectrum antibiotics.
Follow-Up
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Disposition Admission Criteria
The infant should be adm itted to neonatal ICU.
If m aternal resuscitation is successful, patient should be adm itted to appropriate ICU.
Discharge Criteria Neither infant nor m other should be discharged from ED.
References 1. Boyd R, Teece S. Towards evidence based em ergency m edicine: best BETs from the Manchester Royal Infirm ary. Perim ortem caesarean section. Em erg Med J. 2002;19:324–325. 2. Dildy GA, Clark SL. Cardiac arrest during pregnancy. Obstet Gynecol Clin North Am . 1995;22:303–314. 3. Gianopoulos JG. Em ergency com plications of labor and delivery. Em erg Med Clin North Am . 1994;12:201–217. 4. Katz VL, Dotters DJ, Droegenueller W. Perim ortem caesarean delivery. Obstet Gynecol. 1986;68: 571–576. 5. Lanoix R, Akkapeddi V, Goldfeder B. Perim ortem caesarean section: case reports and recom m endations. Acad Em erg Med. 1995;2: 1063–1067. 6. Stallord TC, Burns B. Em ergency delivery and perim ortem C-section. Em erg Med Clin North Am . 2003;21:679–693.
Codes ICD9-CM 669.7 Cesarean delivery, without m ention of indication
ICD10 O82.1 Delivery by em ergency cesarean section
Pa ge 1 0 5
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > C hancro id
Chancroid
Norbert Elsner
Basics Description
Sexually transm itted genital ulcerative disease: o
Increased risk for HIV infection
A com m on cause of genital ulceration in Africa, southeast Asia, and Latin Am erica: o
Uncom m on in United States where HSV > syphilis >> chancroid, but likely underreported
Etiology Causative agent: Haem ophilus ducreyi:
Highly infectious bacterium
Diagnosis Signs and Symptoms
Begins as single erythem atous papule or pustule: o
Quickly erodes into painful chancres (1–20 m m )
o
Soft and friable with ragged, irregular borders
Prim ary ulcer usually excavated
Pa ge 1 0 5
Moist, granulation tissue at base
Purulent or hem orrhagic exudate
Location: o
Male:
Penile shaft, glans, internal surface of foreskin, anus
o
Fem ale:
Cervix, vagina, vulva, perineum , anus
Occurs 4–7 days (m edian) after exposure
Incubation period 3–10 days (range 1–35 days)
Inguinal adenopathy: o
In approxim ately 50% of m en; less com m on in wom en
o
Appears 3–14 days after initial ulcer
o
Unilateral (usually)
o
Painful
o
Suppurative large nodes (buboes)
o
May rupture and form chronic draining sinuses
Dysuria, dyspareunia secondary to contact with lesions
Variants: o
Phagedenic:
Secondary superinfection (especially fusospirochetal) and rapid extensive tissue destruction
o
Giant chancroid:
o
Very large single ulcer
Serpiginous ulcer:
Rapidly spreading, indolent, shallow ulcers in groin or thigh
o
Follicular:
Multiple sm all ulcers with perifollicular distribution
Pa ge 1 0 5
Essential Workup
Clinical diagnosis based on appearance is often inaccurate, and lab tests difficult or unavailable, so consider:
CDC case definitions: o
Definite: positive culture of H ducreyi
o
Probable: typical signs, sym ptom s of chancroid PLUS negative darkfield exam for T. pallidum PLUS negative syphilis serology PLUS negative culture for HSV (or clinical exam atypical for herpes).
Tests Lab
Gram stain unreliable (positive in 50–80%) o
Gram -negative coccobacilli: linear or “school-of-fish― pattern
Culture extrem ely difficult (positive in 0–80%); requires com plex m edia o
Obtain specim en from
Base of ulcer
Needle aspiration of inguinal node by placing needle through norm al skin (to avoid form ation of fistula)
Polym erase chain reaction (PCR) assay: sensitive and specific, but not widely available
RPR o
Coinfection with syphilis is com m on
o
Part of CDC guidelines for probable clinical diagnosis of chancroid
Herpes sim plex virus (HSV) culture o
Part of CDC guidelines for probable clinical diagnosis of chancroid
HIV testing
Pa ge 1 0 5
Differential Diagnosis Infectious:
Syphilis (T. pallidum ) o
Herpes genitalis (H. sim plex) o
Vesicular, m ultiple, recurrent
Granulom a inguinale or Donovanosis (C. granulom atis) o
chancre usually painless, indurated, clean
Ulcer m argins elevated; + induration
Lym phogranulom a venereum (C. trachom atis) o
Often single lesion; tender, fluctuant, unilateral lym phadenopathy
Non-Infectious:
Drug eruption
Less com m on: o
Pyoderm a gangrenosum ; Behçet's disease
Treatment Initial Stabilization Usual precautions for patient exam and handling of specim ens
ED Treatment Antibiotics:
Ceftriaxone: single IM dose
Azithrom ycin: single PO dose
Ciprofloxacin: PO × 3 days P.217
Pa ge 1 0 5
Erythrom ycin: PO × 7 days o
Recom m ended for HIV positive or pregnant patients
o
Requires m ultiple doses
o
GI side effects
Needle aspiration of suppurative nodes (>5 cm diam eter): o
To prevent chronic sinus drainage from spontaneous rupture
o
Use 18-gauge needle through lateral intact skin.
o
May require repetition
Recom m end concurrent HIV, syphilis, HSV testing and follow-up testing in 3 m onths if initially negative.
Medication (Drugs)
Azithrom ycin: 1 g PO × 1
Ceftriaxone: 250 m g IM × 1
Ciprofloxacin: 500 m g PO b.i.d. for 3 days
Erythrom ycin: 500 m g PO q.i.d. for 7 days
Follow-Up Disposition Discharge Criteria
Sexual abstinence or condom use until lesions healed
Clinical course: o
Sym ptom s im prove within 2 days of treatm ent.
o
Ulcers im prove within 3–7 days.
o
Possible delayed resolution in those HIV-positive or uncircum cised
Issues for Referral
Pa ge 1 0 5
Exam ine and treat sexual partners if contact within 10 days of sym ptom onset
References 1. Centers for Disease Control and Prevention. Sexually Transm itted Diseases Treatm ent Guidelines 2002. Available at http://www.cdc.gov/std/treatm ent. 2. Lewis DA. Chancroid: clinical m anifestations, diagnosis and m anagem ent. Sex Transm Inf. 2003;79:68–71. 3. Schlossberg D. Current Therapy of Infectious Disease. Philadelphia: WB Saunders; 2002. 4. Chancroid. UpToDate Online. 2005;v13.1. Available at http://www.utdol.com .
Codes ICD9-CM 099.0
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > C hem ical Weapo ns Po iso ning
Chemical
Weapons Poisoning Kirk Cumpston
Basics Description Chem ical agents that affect CNS, pulm onary, cardiovascular, derm al, ocular, or GI system s when exposed to victim s
Etiology
Blood agents: cyanide: o
Inhibition of cellular respiration by binding to ferric ion in cytochrom e oxidase a-a3 and uncoupling oxidative phosphorylization
Blister agents: sulfur m ustard, nitrogen m ustard, lewisite, phosgene oxim e: o
Alkylation and cross-linking of purine bases of DNA and am ino acids resulting in change in structure of nucleic acid, proteins, and cellular m em branes
Lacrim ators and riot control agents: 1-chloroacetophenone (CN; Mace), o-chlorobenzilidine m alononitrile (CS), oleoresin capsicin-pepper spray (OC), chloropicrin, adam site (DM) o
Mucous m em brane irritators
Pa ge 1 0 6
Pulm onary irritants (choking agents): o
High water solubility: am m onia:
Mucous m em brane irritation of eyes and upper airway
o
Interm ediate water solubility: chlorine:
Form s hydrochloric acid, hydrochlorous acids, which form free radicals causing upper airway and pulm onary irritation
o
Low water solubility: phosgene:
Mild irritant effects initially, then delayed pulm onary edem a as late as 24 hours
Direct pulm onary dam age after hydrolysis in lungs to hydrochloric acid
Nerve agents o
Anticholinesterase inhibitors—causes cholinergic overstim ulation at m uscarinic, nicotinic, and central nervous system sites
o
Incapacitating agents: 3-quinuclidinyl benzilate (BZ):
Anticholinergic (antim uscarinic)
Diagnosis Signs and Symptoms
Blood agents (cyanide and cyanogens): o
Vital signs:
Tachypnea and hyperpnea (early); respiratory depression (late)
Hypertension and tachycardia (early); hypotension and bradycardia (late)
o
Death within seconds to m inutes
Central nervous system :
Pa ge 1 0 6
o
o
Headache
Mental status changes
Seizures
Pulm onary:
Dyspnea
Noncardiogenic pulm onary edem a
Cyanosis uncom m on
Gastrointestinal:
Odor of bitter alm onds (som etim es)
Burning in m outh and throat
Nausea, vom iting
Blister agents (m ustards, lewisite): o
General:
o
Mortality, 2–4%
Derm atologic:
Skin erythem a, edem a, pruritus can appear 2–24 hours after exposure.
Necrosis and vesiculation appear 2–18 hours after exposure.
o
Head, eyes, ears, nose, and throat (HEENT):
Airway occlusion from sloughing of debris
Laryngospasm , sore throat, sinusitis
Eye pain, photophobia, lacrim ation, blurred vision, blepharospasm , periorbital edem a, conjunctival edem a, corneal ulceration
o
o
Pulm onary:
Bronchospasm , tracheobronchitis
Respiratory failure
Hacking cough
Gastrointestinal:
o
Nausea, vom iting
Hem atologic:
Pa ge 1 0 6
Leukopenia
Lacrim ators and riot control agents (tear gases): o
o
o
HEENT:
Eye pain
Lacrim ation
Blepharospasm
Tem porary blindness
Derm atologic:
Skin irritation
Papulovesicular derm atitis (tear gas)
Superficial burns
Pulm onary:
Cough
Chest tightness
Dry throat
Sensation of suffocation
Pulm onary edem a when exposed to high concentrations without ventilation
Pulm onary irritants (choking agents): o
o
HEENT:
Eye pain, lacrim ation, blepharospasm
Tem porary blindness
Derm atologic:
o
Skin irritation, dry throat, nasal irritation
Pulm onary:
Shortness of breath, cough, bronchospasm
Chest pain
Pulm onary edem a as late as 24 hours from exposure (phosgene)
Nerve agents (sarin, tabun, som an, VX): o
SLUDGEBAM syndrom e
Salivation
Pa ge 1 0 6
Lacrim ation
Urination
Defecation
Gastrointestinal cram ps
Em esis
Bronchorrhea, bronchoconstriction, bradycardia (m ost life threatening)
o
Abdom inal upset
Miosis
HEENT:
Miosis
Hypersecretion by salivary, sweat, lacrim al, and bronchial glands
o
o
o
o
Central nervous system :
Irritability, nervousness
Giddiness
Fatigue, lethargy, depression
Ataxia, convulsions, com a
Pulm onary:
Bronchoconstriction
Bronchorrhea
Gastrointestinal:
Nausea, vom iting, diarrhea
Cram py abdom inal pains
Urinary and fecal incontinence
Musculoskeletal:
Fasciculations, skeletal m uscle twitching
Weakness
Flaccid paralysis
Incapacitating agents (BZ): o
Anticholinergic (antim uscarinic) toxidrom e:
Hot as a hare
Pa ge 1 0 6
Dry as a bone
Red as a beet
Blind as a bat
Mad as a hatter
Hypertension
Tachycardia
Hyperpyrexia
Urinary retention
Decreased bowel sounds
Essential Workup
History and sym ptom s key to type of agent exposure
Physical exam ination: o
Cyanide (bitter alm onds, com atose, hypotensive, m etabolic acidosis)
o
Mustard (faint, sweet odor of m ustard or garlic, blisters, sloughing of skin, dyspnea)
o
Check for SLUDGEBAM syndrom e.
o
Lacrim ators (eye irritation, lacrim ation, blepharospasm )
o
Choking agents (dyspnea, bronchospasm )
Tests Lab
Arterial blood gases: o
Cyanide:
Decreased atrioventricular (AV) oxygen saturation gap
Lactic acidem ia with high anion gap m etabolic acidosis
Arterialization of venous blood
Cyanide levels cannot be perform ed in clinically relevant tim e fram e.
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P.219
CBC: o
Leukopenia, throm bocytopenia, anem ia with significant m ustard exposure
Electrolytes, BUN, creatinine, glucose
Urinalysis
Creatine phosphokinase (CPK)
Lactate for cyanide
Erythrocyte cholinesterase activity for nerve agents
Imaging Chest radiograph for pulm onary edem a
Differential Diagnosis
Asthm a
Chronic obstructive pulm onary disease
Stevens-Johnson syndrom e
Toxic epiderm al necrolysis
Pem phigus vulgaris
Scalded skin syndrom e
Organophosphate or carbam ate pesticide poisoning
Botulism
Radiation poisoning
Reactive airway disease
Congestive heart failure
Anaphylactoid reaction
Other anticholinergic agent
Treatment
Pa ge 1 0 6
Pre Hospital
Avoid contam ination of environm ent and clinicians: o
Use level A or level B personal protective equipm ent.
o
Decontam ination:
Derm al wet decontam ination prim arily for nerve and blistering agents
Dry decontam ination (rem oval of clothing and jewelry) for other agents
Adm inister atropine even if patient is tachycardic because condition m ay result from hypoxia.
Initial Stabilization
Airway, breathing, and circulation m anagem ent (ABCs)
Patient decontam ination: o
Brush off powder from chem ical.
o
Irrigate skin and eyes with copious am ounts of water or saline.
o
Rem ove and dispose of clothing in double bags.
Protection for health care workers: o
Level A or B personal protective suit
o
Chem ical-resistant suit
o
Heavy rubber gloves and boots, neoprene gloves
Adm inister oxygen.
Place on cardiac m onitor and m easure pulse oxim etry.
Establish IV access with 0.9% norm al saline.
ED Treatment
Blood agents: o
One hundred percent oxygen
o
Benzodiazepines for seizures
o
Cyanide antidote kit, m ay be repeated
o
Hydroxocobalam in available in Europe as cyanide antidote
Pa ge 1 0 6
Blister agents: o
Supportive care
o
Standard burn m anagem ent
o
Atropine to relieve eye pain
o
Monitor fluids, electrolytes, com plete blood chem istry.
o
Monitor com plete blood count for nadir.
o
Supportive care for sepsis, anem ia, hem orrhage
o
Granulocyte colony-stim ulating factor (G-CSF) for neutropenia
Choking agents, lacrim ators, riot control agents: o
Supportive care, bronchodilators
o
Eye irrigation
o
Chest radiograph and careful m onitoring for respiratory com plications
o
Phosgenes require m onitoring for delayed pulm onary edem a for 24 hours
Nerve agents: o
o
Supportive care:
One hundred percent oxygen
Frequent airway suctioning
Atropine 2 m g IV every 5 m inutes until reversal of bronchorrhea, bronchoconstriction, and hypoxem ia:
Antagonizes m uscarinic effects and som e central nervous system but no effect on skeletal m uscle weakness or respiratory failure
Pupillary response and heart rate are not useful m easures of adequate atropinization.
Stop atropine after patient regains consciousness and spontaneous ventilation (m ay need for periodic relapses); give as m uch as it takes to reverse respiratory com prom ise.
Pa ge 1 0 6
o
Pralidoxim e chloride (2-PAM or Protopam ):
Regenerates cholinesterase by reversing phosphorylation (unless aging has occurred)
Reduces abnorm al skeletal m uscle m ovem ents, im proves skeletal m uscle weakness, and reverses flaccid paralysis
May repeat first dose or start on continuous infusion
If im provem ent from first dose, repeat 60–90 m inutes later.
o
Diazepam : Give for seizures
Incapacitating agents (BZ): o
Supportive care
o
Aggressive IV fluid hydration
o
Benzodiazepines for agitation and increased m uscular activity
o
Consider physostigm ine in consultation with a poison center.
Medication (Drugs)
Albuterol using nebulizer: 2.5 m g in 2.5 m L norm al saline (peds: 0.1–0.15 m g/kg per dose)
Atropine: 2 m g IM or IV (6 m g in severely intoxicated patients; peds: 0.02–0.08 m g/kg), then q5–10m in titrate to clinical effect
Diazepam : 5–10 m g IV over 3–5 m inutes (peds: 0.2–0.4 m g/kg up to 10 m g over 2–3 m inutes)
Hydroxocobalam in: 5 g IV (available in France)
Cyanide antidote kit: o
Inhale am yl nitrite am pule for 30 seconds every m inute until sodium nitrite given.
Pa ge 1 0 7
o
Sodium nitrite: 10 m L of 3% solution or 300 m g IV over 3–5 m inutes (peds: 0.15–0.33 m L/kg)
o
Monitor m ethem oglobin levels to keep Table o f C o ntents > C hest Pain
Chest Pain
Kelly Corrigan
Basics Description
One of the m ost frequent chief com plaints in the ED
There is a wide differential diagnosis of life-threatening etiologies as well as benign conditions often with m inim al physical findings.
Chest wall pain: o
Inflam m ation of skin and subcutaneous structures of the chest wall
o
Pain is reproduced by:
Palpation
Horizontal flexion of the arm s
Extension of the neck
Vertical pressure on the head
Pleuritic pain: o
Inflam m ation or traum a to the ribs, cartilage, m uscles, nerves, pleural or pericardial surface
o
Pain increased by breathing, laughing, coughing, sneezing
o
Tenderness to palpation m ay be present
o
Diaphragm atic pleurisy:
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Sharp shooting pains in the epigastrium , lower restrosternal area, or shoulder intensified by thoracic m ovem ent
Deep visceral pain: o
Upper thoracic visceral pain:
Pain caused by visceral structures served by sensory fibers originating from T1–T4
May involve the m yocardium , pericardium , the ascending aorta, pulm onary artery, m ediastinum , and esophagus
Pain is generally precordial.
Pain is deep, visceral, and poorly localized.
Characteristics vary from severe and crushing to m ild, burning, or indigestion
o
Lower thoracic visceral pain:
Pain caused by visceral structures served by sensory fibers originating from T5–T6
May involve the descending aorta, diaphragm atic m uscles, the gallbladder, the pancreas, the duodenum , and the stom ach
Pain is generally located to the xiphoid region and in the back.
Etiology Chest Wall Pain
Chest wall hem atom a
Chest wall laceration
Throm bophlebitis of the thoracoepigastric vein
Xiphisternal arthritis
Adiposis Dolorosa
Breast abscess, fibroadenosis, carcinom a
Pleuritic pain:
Pa ge 1 0 7
Chest-wall twinge syndrom e: o
Brief episodes of sharp anterior chest pain lasting 30 seconds to three m inutes, aggravated by deep breathing and relieved by shallow respirations
o
Cause unknown
Costochondritis
Epidem ic pleurodynia: o
Sudden severe pains with shifting of loci associated with fever and headache
o
Caused by a viral infection
Diaphragm atic pleurisy: o
Splenic rupture
o
Subdiaphragm atic abscess
Esophageal rupture
Herpes zoster
Intercostal m yositis
Intercostal neuralgia
Pectoralis m inor strain
Pericarditis
Pleuritis
Pulm onary em bolism
Pneum othorax
Pneum onia
Pneum onitis
Rib fractures
Rib periostitis
Slipping cartilage
Upper Thoracic Visceral Pain
Coronary artery disease
Pericarditis
Myocarditis
Stress-induced cardiom yopathy
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Cardiac syndrom e X: o
Anginalike chest pain, often with signs of cardiac ischem ia in the absence of coronary artery disease.
Thoracic aortic dissection
Esophagitis
Esophageal spasm
Gastroesophageal reflux disease
Esophageal hyperalgesia
Abnorm al m otility patterns and achalasia
Esophageal rupture and m ediastinitis
Lower Thoracic Visceral Pain:
Dissection of the descending aorta
Peptic ulcer disease
Pancreatitis
Cholecystitis
Splenic rupture
Subdiaphragm atic abscess
Diagnosis Signs and Symptoms Coronary Artery Disease
Shortness of breath
Pressure
Squeezing pain
Radiation to arm , jaw
Tachycardia or bradycardia
Diaphoresis
Nausea
Vom iting
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Signs of congestive heart failure (CHF)
Anxiety
Aortic Dissection
Sudden onset of pain with m axim al intensity early
Tearing pain
Radiation to back and/or flank
Hypertension
Differential pulses
Associated neurological changes (i.e., visual changes)
Pulmonary Embolism
Pleuritic pain
Shortness of breath
Anxiety
Diaphoresis
Tachypnea
Tachycardia
Low-grade fever
Localized rales
Wheezing
Acute Pericarditis
Substernal pain
Varies with respiration
Increased with recum bency
Relieved by leaning forward
Anxiety
Anorexia
Fever
Pericardial friction rub
History
The history is the m ost im portant tool to distinguish
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between the various etiologies.
Have the patient define the key features: o
Duration
o
Location:
Retrosternal
Subxiphoid
Diffuse
P.221
o
o
o
Frequency:
Constant
Interm ittent
Sudden versus delayed onset
Precipitating factors:
Exertion
Stress
Food
Respiration
Movem ent
Tim ing:
Context of onset of pain (i.e., at rest, exertional)
o
o
Duration of pain
Quality:
Burning
Squeezing
Dull
Sharp
Tearing
Heavy
Associated sym ptom s:
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Shortness of breath
Diaphoresis
Nausea
Vom iting
Jaw pain
Back pain
Radiation
Palpitations
Change to focal or generalized weakness
Fatigue
Tests Lab
Creatine kinase, with m uscle and brain subunits (CK-MB) and troponin T or I: o
They have a high positive predictive value.
o
If negative initially, they cannot be used to rule out m yocardial infarction (MI).
o
Serial troponin studies rule out MI and significantly decrease the probability of significant ischem ia.
D-Dim er: o
Sensitive but poor specificity for physical exam ination
o
Increased sensitivity with enzym e-linked im m unosorbent assay m ethods
o
Indicated for low risk patient
Serum lipase: o
If an atypical presentation of pancreatitis is suspected
Imaging
Ultrasound: o
Test of choice for pericardial and valvular disease
Pa ge 1 0 7
o
May be helpful in acute ischem ic coronary artery disease by showing wall m otion abnorm alities if there is no prior infarction
o
Transesophageal echocardiography can be used in diagnosis of aortic dissection, especially in unstable patients and those unable to tolerate contrast.
o
Right ventricular dilation and hypokinesia m ay suggest pulm onary em bolus.
Stress echocardiogram : o
Chest pain centers
o
Stable patients in whom MI has been ruled out with serial enzym es and ECGs over 6–12 hours
Helical CT scan: o
Sensitive for aortic dissection
o
Useful in stable patient
o
Som e centers are using in diagnosis of pulm onary em bolus and in stable cardiac effusion
Ventilation/Perfusion scan: o
Useful in pulm onary em bolus
o
Must have norm al chest radiograph
o
Can rule in or out based on high probability or norm al scan in the patient with high or low pretest probability, respectively
o
Angiography: o
Otherwise, further testing based on clinical suspicion
Useful in dissection, especially in stable patients
MRI: o
Mostly used to follow stable dissections or aneurysm s over tim e
ECG
Inexpensive and available
Obtain and interpret within 10 m inutes of arrival
Pa ge 1 0 8
See specific etiologies
Chest radiograph
Pneum othorax
Pneum onia
A com plication of ischem ic heart disease such as CHF
Aortic dissection: o
Widened m ediastinum seen in about 55–62% of patients
o
A pleural effusion is found in about 20% of patients.
o
Apical capping
o
Aortic knob obliteration
o
A norm al chest radiograph is found in 12–15% of patients.
Acute pericarditis: o
Usually norm al unless m assive effusion enlarges cardiac silhouette
Esophageal rupture: o
Usually will show m ediastinal air
o
May have left pleural effusion
Differential Diagnosis See Etiology
Treatment Pre Hospital
IV access
Cardiac m onitoring
Oxygen
Baby aspirin
Pain control:
Pa ge 1 0 8
o
Nitrates
o
Morphine
All chest pain should be treated and transported as a possible life-threatening em ergency.
Initial Stabilization
ABCs
IV
Oxygen
Cardiac m onitoring
ED Treatment
IV, oxygen, and m onitoring
Treatm ent varies based on suspected etiologies:
Medication (Drugs)
Alum inum and m agnesium hydroxide: 15 to 30 m L PO q2h–q4h
Aspirin: 160–325 m g PO
Cim etidine: 300 m g IV or PO q6h
Donnatal: 5–10 m L PO q6h
Esm olol: 50 µg/kg bolus, then 50–200 µg/m in drip
Labetalol: 20 m g IV every 10 m inutes up to 300 m g
Metoprolol: 5 m g IV every two hours up to 15 m g
Morphine sulfate: 2–4 m g every five m inutes
Nitroglycerin: 0.4 m g sublingual, or 1–2 inches of nitro paste, or drip at 5–10 µg/m in and titrate to effect
Nitroprusside: 0.3–10 µg/kg/m in drip
Propranolol: 1–2 m g IV every 2 m inutes
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Follow-Up Disposition Admission Criteria Dependent on the risk for life-threatening cardiopulm onary etiologies
Discharge Criteria Very low risk for untoward event if discharge is planned
References 1. ACC/AHA Guidelines for the Managem ent of Patients with unstable Angina and Non-ST-Segm ent Elevation MI: Executive Sum m ary and Recom m endations. Circulation. 2000;102:1193. 2. Davis K, Aspera G. Exposure to liquid sulfur m ustard. Ann Em erg Med. 2001;37:653–656. 3. Thoracic: Respiratory, Cardiovascular, and Lym phatic Sym ptom s. In: LeBlond RF, DeGowin RL, Brown DD, et al, eds. DeGowin's Diagnostic Exam ination McGraw-Hill Professional. 8th ed. (March 26, 2004). 4. Leikin J, Paloucek F. Leikin and Paloucek's Poisoning and Toxicology Handbook. 3rd ed. Hudson, OH: Lexi-Com p; 2002. Clinical Toxicology. Philadelphia: WB Saunders; 2001.
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > C hest Traum a, Blunt
Chest Trauma,
Blunt Lisa G. Lowe
Basics Description
Significant source of m orbidity and m ortality in the United States
Approxim ately 12 thoracic traum a victim s per m illion population per day
Approxim ately 33% of these injuries require hospital adm ission.
Directly responsible for 20–25% of all deaths attributed to traum a
Contributing cause of death in 25% of patients who die from other traum atic injuries
Etiology
Com m on m echanism s of injury include: o
Motor vehicle collisions (70–80%)
o
Motorcycle collisions
o
Pedestrians struck by a m otor vehicle
o
Falls from great heights
o
Assaults
Pa ge 1 0 8
o
Blast injuries
Injuries can result from direct blunt force to the chest or from forces related to rapid deceleration.
Diagnosis Signs and Symptoms
Obvious contusion, wound, or other defect of the chest wall: o
Paradoxical chest wall m ovem ent suggests flail chest segm ent.
Usually occurs in com bination with other injuries
Hypotension
Som e patients with severe intrathoracic injuries, such as traum atic aortic disruption, m ay have no visible external signs of traum a.
History
Tim e of injury
Mechanism of injury
Estim ates of m otor vehicle accident (MVA) velocity and deceleration
Loss of consciousness
Chest pain
Pain with deep inspiration or cough
Dyspnea
Physical Exam
Unilaterally absent breath sounds
Crepitus or subcutaneous air in the chest wall
Decreased or absent breath sounds
Tenderness to palpation on the chest wall
Pa ge 1 0 8
Jugular venous distention
Hyperresonance to percussion on involved side
Essential Workup
Check airway, breathing, and circulation (ABCs) to determ ine the patient's stability.
Focused exam ination of the chest: o
Respiratory effort and rate
o
Chest wall excursion
o
Crepitus
o
Subcutaneous air
o
Breath sounds and heart sounds
o
Presence of jugular venous distention
Obtain a supine chest radiograph im m ediately: o
Avoid an upright chest radiograph because of the potential for other injuries (especially spinal injuries).
Electrocardiogram and m onitor to detect m yocardial ischem ia or dysrhythm ias
Tests Lab
Baseline hem oglobin
Pulse oxim etry
Arterial blood gas
Serum lactate
Type and cross-m atch
Coagulation profile
Cardiac enzym es if concerned for cardiac contusion
Periodic chem istry panel for patients receiving significant fluid resuscitation
Imaging
Pa ge 1 0 8
Chest radiograph is the initial radiologic study of choice: o
If chest radiograph reveals widened m ediastinum and patient hem odynam ically stable, repeat film in upright position.
Chest CT is m ore specific for pneum othoraces and pulm onary contusions/occult injuries.
Chest CT with contrast, or aortic angiogram , is useful in identifying aortic and large vessel injuries.
Esophagram m ay be useful for possible esophageal injury (e.g., pneum om ediastinum )
Electrocardiogram if sternal tenderness is present or abnorm alities on cardiac m onitor
Diagnostic Procedures/Surgery
If patient's condition is unstable, em ergency thoracotom y m ay be necessary to repair a traum atic aortic disruption.
If there are signs of tam ponade and patient is stable, perform an echocardiogram on an urgent basis.
If there are signs of pericardial tam ponade and patient is unstable, em ergent pericardiocentesis m ay be necessary, followed by im m ediate transport to the OR for a pericardial window.
Bronchoscopy for possible upper airway injuries (e.g., large persistent air leak after chest tube)
Bedside ultrasound is up to 90% sensitive for identifying pericardial injuries or hem othoraces.
Pregnancy Considerations
In pregnant patients, rem em ber to use the least am ount of radiation available and to shield the uterus during im aging when possible.
See Pregnancy, Traum a in, for details.
Differential Diagnosis
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Sim ple pneum othorax
Tension pneum othorax
Open pneum othorax
Hem othorax
Rib fractures
Flail chest
Pulm onary contusion
Myocardial contusion
Myocardial rupture
Pericardial tam ponade
Traum atic aortic disruption
Esophageal injury
Large vascular injury (subclavian, pulm onary artery)
Tracheobronchial injury
Diaphragm atic injury
Pediatric Considerations Rib cage is highly elastic in children and can withstand significant forces without overt signs of external traum a, but such patients m ay have m ajor internal injuries.
Treatment Pre Hospital
All patients with any signs of life in the field should be transported to a traum a center.
Full spinal precautions
Needle decom pression for tension pneum othorax: o
Unilaterally absent breath sounds
o
Hypotension
o
Jugular venous distention
Pa ge 1 0 8
o
Hyperresonance to percussion
If large open pneum othorax exists, tape occlusive dressing on three sides; a totally occlusive dressing m ay produce a tension pneum othorax
Do not delay transport to hospital for intravenous access: o
IV access can be established en route.
Initial Stabilization
ABCs m anagem ent; intubate patient early if signs of respiratory insufficiency, shock, or altered m ental status exist.
Resuscitation attem pts should be initiated only in patients who arrive in the ED with vital signs.
Any patient who presents in blunt traum atic arrest is not likely to survive a thoracotom y in the ED, and is therefore not indicated in this group. P.223
If the patient's condition is unstable and clinically shows signs of a tension pneum othorax, perform needle thoracostom y and place a chest tube im m ediately after: o
Do not wait to obtain a chest radiograph.
o
Place chest tube on the affected side or bilaterally if injury site is unclear.
Oxygen by nonrebreather face m ask for stable patients
Obtain vascular access, preferably two large intravenous lines (>18 gauge).
Maintain spinal im m obilization.
ED Treatment
Tube thoracostom y if pneum othorax or hem othorax is identified:
Pa ge 1 0 8
o
36-French chest tube in an adult
o
In children use the largest tube that the intercostal space will accom m odate.
Provide resuscitation with isotonic fluids and blood products as necessary: o
Aggressive fluid resuscitation m ay be harm ful if severe pulm onary contusions exist.
Workup for associated intra-abdom inal injuries (e.g., with diagnostic peritoneal lavage, abdom inal ultrasound, abdom inal CT scan): o
Patients with chest traum a frequently have concom itant intra-abdom inal injuries.
Medication (Drugs)
Tetanus booster if indicated
Methylprednisolone (for signs of spinal cord injury): 30 m g/kg intravenously over 1 hour, followed by a continuous drip of 5.4 m g/kg/h for next 23 hours
Judicious doses of short-acting analgesics (fentanyl 1–2 µg/kg IV, m orphine 0.1 m g/kg IV) as needed for pain control
Follow-Up Disposition Admission Criteria
Patients with conduction blocks, frequent ectopy, or ischem ic changes visible on ECG should be adm itted to a m onitored setting for possible m yocardial contusion.
Pa ge 1 0 9
Hem odynam ically unstable patients should go to the operating room on an em ergency basis for thoracotom y or laparotom y.
More than 1,000–1,500 m L of blood drawn out of the chest tube on initial insertion indicates need for thoracotom y.
More than 200 m L of blood per hour from chest tube for several hours suggests the need for operative intervention.
Patients with significant rib fractures should be adm itted for pain control: o
Epidural catheter
Patients who lose vital signs in the ED should undergo rapid open thoracotom y.
Discharge Criteria Patients with clinically insignificant chest wall contusions and an initial negative upright chest radiograph m ay be observed for 6 hours in the ED and have a repeat radiograph; if the repeat radiograph reveals no pneum othorax, hem othorax, or pulm onary contusion and the patient is able to breathe deeply and to cough, he or she m ay be discharged.
Issues for Referral
Notify traum a surgeon prom ptly about patients with significant injuries requiring surgical intervention or adm ission.
The following are indications for em ergent surgical referral: o
Traum atic thoracotom y with loss of chest wall integrity
o
Blunt diaphragm atic injuries
o
Massive air leak following chest tube insertion
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o
Massive hem othorax or continued high rate of blood loss via the chest tube (i.e., 1,500 m L on insertion of tube or continued loss of 200–300 m L/h
o
Radiographically or endoscopically confirm ed tracheal, m ajor bronchial, or esophageal injury
o
Gastrointestinal tract contents recovered on chest tube placem ent
o
Cardiac tam ponade
o
Radiographic confirm ation of a great vessel injury
o
Em bolism or m issile into pulm onary artery or heart
References 1. Adam s JE 3rd, Davila-Rom an VG, Bessey PQ, et al. Im proved detection of cardiac contusion with cardiac troponin I. Am Heart J. 1996;131(2):308–12. 2. Fabian TC, Davis KA, Gavant ML, et al. Prospective study of blunt aortic injury: helical CT is diagnostic and antihypertensive therapy reduces rupture. Ann Surg. 1998;227(5):666–676; discussion 676–677. 3. Feliciano DV. The diagnostic and therapeutic approach to chest traum a. Sem in Thorac Cardiovasc Surg. 1992;4:156–162. 4. Karm y-Jones R, Jurkovich GJ. Blunt chest traum a. Curr Probl Surg. 2004;41(3):211–380. 5. Mansour KA. Traum a of the diaphragm . Chest Surg Clin North Am . 1997;7(2):373–383. 6. Sartorelli KH, Vane DW. The diagnosis and m anagem ent of children with blunt injury of the chest. Sem in Pediatr Surg. 2004;13(2):98–105. 7. Sim on BJ, Leslie C. Factors predicting early in-hospital death in blunt thoracic aortic injury. J Traum a. 2001;51(5):906–910; discussion 911.
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Miscellaneous SEE ALSO: Chest Traum a, Penetrating; Flail Chest; Pregnancy, Traum a in; Traum a, Multiple
Codes ICD9-CM 862.8 Multiple and unspecified intrathoracic organs, without m ention of open wound into cavity
ICD10 S29.9 Unspecified injury of thorax
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > C hest Traum a, Penetrating
Chest Trauma,
Penetrating Mamata Kene
Basics Etiology
Gunshot wounds or stab wounds m ost com m on
Im palem ent on a sharp object from a fall can occur.
Diagnosis Signs and Symptoms
Object im paled in the chest wall
Obvious wound in the chest wall with or without bleeding
Chest pain
Dyspnea
Respiratory distress
Altered m ental status from hypoxem ia
Absent or altered breath sounds on one or both sides
Hypotension
Jugular venous distention
Essential Workup
Pa ge 1 0 9
Perform routine assessm ent of airway, breathing, and circulation.
Rapid exam ination: o
Respiratory effort and rate
o
Chest excursion
o
Crepitus
o
Subcutaneous air
o
Breath sounds and heart sounds
Upright chest radiograph is preferred for identifying a pneum othorax: o
Supine chest radiograph should be taken first if spinal precautions m ust be m aintained.
Baseline hem oglobin
Pulse oxim etry
Arterial blood gas
Serum lactate
Type and screen
Tests Lab
Perform echocardiogram if signs of tam ponade present or if wound is close to the heart.
ECG
Imaging
With gunshot wounds, other areas (abdom en, pelvis) should be im aged: o
total num ber of wounds and bullets m ust be the sam e.
Arteriogram of aortic arch, carotid arteries, or subclavian artery if great vessel injury is suspected
Esophageal Gastrografin swallow or endoscopy to identify esophageal perforation
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Bronchoscopy to identify tracheobronchial injuries
Differential Diagnosis
Sim ple pneum othorax
Tension pneum othorax
Open pneum othorax
Hem othorax
Rib fractures
Flail chest
Pulm onary contusion
Myocardial contusion
Myocardial rupture
Pericardial tam ponade
Traum atic aortic disruption
Esophageal injury
Large vessel injury
Tracheobronchial injury
Diaphragm atic injury
Intra-abdom inal injury
Spinal cord injury
Treatment Pre Hospital
Cautions: o
All patients with signs of life in the field according to reports from EMS personnel should be transported to a traum a center.
o
Full spinal im m obilization if spinal injury suspected
o
Never rem ove objects im paled in the chest because exsanguination m ay follow.
Pa ge 1 0 9
o
Needle decom pression m ay be necessary if tension pneum othorax suspected:
Unilaterally absent breath sounds, hypotension, jugular venous distention
o
If large open pneum othorax exists, occlusive dressing taped on three sides:
A totally occlusive dressing m ay produce a tension pneum othorax.
Controversies: o
Do not delay transport to hospital to obtain intravenous access:
Intravenous access m ay be established en route.
Initial Stabilization
Airway, breathing, and circulation m anagem ent: o
Intubate for signs of serious chest injury, obvious respiratory distress, or hypotension.
Oxygen by nonrebreather face m ask for patients in stable condition
Obtain vascular access, two peripheral large-bore intravenous lines (>18 gauge), and fluid resuscitation as needed: o
Two-liter isotonic fluid bolus initially
P.225
For tension pneum othorax, perform a needle thoracostom y and place a chest tube im m ediately: o
Do not wait to get a chest radiograph.
For pericardial tam ponade, perform an em ergency pericardiocentesis: o
Followed by rapid transport to the operating room for
Pa ge 1 0 9
a pericardial window
Maintain spinal im m obilization if indicated.
ED Treatment
Notify traum a surgeon about patient's arrival.
Tube thoracostom y if a pneum othorax or hem othorax is identified: o
36-gauge chest tube in an adult
o
In children use largest tube intercostal space will accom m odate.
Fluid resuscitation as necessary: o
Contused lung parenchym a will have leaky capillary beds, and aggressive crystalloid resuscitation m ay aggravate pulm onary dysfunction.
Any wound with an entry or exit site below the nipple or the posterior tip of the scapula is concerning for an intra-abdom inal injury: o
Work up with a diagnostic peritoneal lavage (DPL), ultrasound, CT scan, exploratory laparotom y, or laparoscopy.
o
DPL positive with 5,000 RBC
Describe the nature of wounds accurately: o
Retain any bullet fragm ents, clothes, or tissue rem oved from the wound.
Probing a chest wound is contraindicated because it can create a pneum othorax or worsen hem orrhage.
Im paled objects should be rem oved only in the operating room .
Tetanus booster if indicated
Medication (Drugs)
Pa ge 1 0 9
Methylprednisolone (for spinal cord injury): 30 m g/kg IV over 1 hour, followed by a continuous drip of 5.4 m g/kg/h for 23 hours
Sm all doses of short-acting analgesics (fentanyl, 1–2 µg/kg IV, m orphine 0.1 m g/kg IV) or sedatives (m idazolam , 0.05 m g/kg intravenously) as needed for pain control and sedation
Treat with intravenous antibiotics if wound grossly contam inated (e.g., cephalexin 1 g IV).
Follow-Up Disposition Admission Criteria
All patients with penetrating chest traum a should be adm itted.
A patient who has signs of life in the field but no blood pressure on arrival in the ED should have an em ergency thoracotom y perform ed by the m ost experienced person present: o
If the source of bleeding is controlled and there are signs of cardiac activity, the patient should go to the operating room for form al operative repair.
Hem odynam ically unstable patients should go im m ediately to the operating room .
Any patient with intrathoracic penetration should have a chest tube placed and should be adm itted to a m onitored setting.
More than 1,000–1,500 m L of blood drawn out of the chest tube on initial insertion indicates the need for
Pa ge 1 0 9
thoracotom y.
More than 200 m L of blood per hour from a chest tube for several hours suggests the need for surgical intervention.
Patients with large, persistent air leaks usually require surgery.
Patients with significant rib fractures should be adm itted and have an epidural catheter placed for pain control and pulm onary toilet.
Discharge Criteria Patients with isolated m inor chest wounds and a norm al chest radiograph can be observed for 6 hours in the ED and have a repeat radiographic study; if no intrathoracic penetration is suspected, the patient can be discharged.
References 1. Baillot R, Dontigny L, Verdant A, et al. Penetrating chest traum a: a 20-year experience. J Traum a. 1987;27:994–997. 2. Degiannis E, Bowley DM, Westaby S. Penetrating cardiac injury. Ann R Coll Surg Engl. 2005;87(1):61–63. 3. Ivatury RR, Cayten CG. The Textbook of Penetrating Traum a. Baltim ore: William s & Wilkins; 1996. 4. Mandavia DP, Joseph A. Bedside echocardiography in chest traum a. Em erg Med Clin North Am . 2004;22(3):601–619. 5. Mansour KA. Traum a of the diaphragm . Chest Surg Clin N Am . 1997;7(2):373–383. 6. Millham FH, Grindlinger GA. Survival determ inants in patients undergoing em ergency room thoracotom y for penetrating chest injury. J Traum a. 1993;34:332–336.
Codes ICD9-CM 862.9 Multiple and unspecified intrathoracic organs, with open wound
Pa ge 1 1 0
into cavity
ICD10 S21.9 Open wound of thorax, part unspecified
Pa ge 1 1 0
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > C ho langitis
Cholangitis
Robert G. Buckley
Basics Description
Partial or com plete obstruction of the com m on bile duct owing to gallstones, tum or, cyst, or stricture
Increased intralum inal pressure in biliary tree
Bacterial m ultiplication results in bacterem ia and sepsis.
Purulent infection of biliary tree, which m ay involve the liver and gallbladder
Mirizzi syndrom e is defined as com m on bile duct obstruction owing to extrinsic com pression from gallbladder or cystic duct edem a or stones.
Etiology
Bacterial sources of infection include: o
Ascending duodenal source
o
Gallbladder infection
o
Portal venous seeding
o
Hem atogenous spread with hepatic secretion
o
Lym phatic spread
Bacterial organism s include: o
Anaerobes (Bacteroides and Clostridium species)
o
Intestinal coliform (Escherichia coli)
Pa ge 1 1 0
o
Enterococcus
AIDS sclerosing cholangitis characterized by: o
Papillary stenosis
o
Sclerosing cholangitis
o
Extrahepatic biliary obstruction
o
Cytom egalovirus (MV), Cryptosporidium , and m icrosporidia isolated, but causal role not established
Diagnosis Signs and Symptoms History
Charcot triad: o
Classic presentation of fever and chills; right upper quadrant (RUQ) pain and jaundice found in only 50–70%
o
Addition of shock and altered m ental status denotes a m ore advanced form of biliary sepsis known as Reynold pentad
Abdom inal pain present in >70%— localizing to RUQ.
AIDS sclerosing cholangitis presents with sim ilar sym ptom s but with m ore chronic indolent course and near-norm al serum bilirubin levels.
Physical Exam
Fever found in >90%
Peritoneal findings found in 30%
Clinically apparent jaundice m ay be absent in up to 40%.
Essential Workup
ECG in patients at risk for coronary artery disease
Pa ge 1 1 0
CBC
Liver function test (LFT)
Am ylase, lipase
Urinalysis
Blood cultures
Gallbladder ultrasound or hepatoim inodiacetic acid (HIDA) scan
Tests Lab
CBC: o
Leukocytosis with left shift unless im m unocom prom ised or severe sepsis
LFTs consistent with cholestasis: o
Elevated direct bilirubin and alkaline phosphatase
o
Minim al elevation of transam inases ( Table o f C o ntents > C ho lelithiasis
Cholelithiasis
Robert G. Buckley
Basics Description
Sym ptom s arise when gallstones pass through the cystic or com m on bile ducts leading to im pedance of norm al bile flow and gallbladder spasm .
Biliary dyskinesia produces sym ptom s identical to biliary colic in the absence of stones.
Etiology
Cholesterol stones: o
Most com m on type of gallstone
o
Form when solubility exceeded
Pigm ent stones: o
20%
o
Com posed of calcium bilirubinate
o
Associated with clinical conditions such as hem olytic anem ias that lead to increased concentration of unconjugated bilirubin
Incidence increases with age and favors fem ales to m ales 2:1.
Gallstones are exceedingly rare in childhood and are m ost com m only associated with sickle cell disease, hereditary
Pa ge 1 1 1
spherocytosis, or other hem olytic anem ias that result in pigm ent stone form ation.
Biliary sludge: o
Nonstone, crystalline, granular m atrix
o
Associated with rapid weight loss, pregnancy, ceftriaxone or octreotide therapy, and organ transplantation
o
May develop sym ptom s identical to cholelithiasis and its com plications
Diagnosis Signs and Symptoms History
Dull, aching epigastric or right upper quadrant (RUQ) pain: o
Arising over 2–3 m inutes, continuous (rather than colicky), and lasting from 30 m inutes to 6 hours before dissipating
o
May radiate to the tip of right scapula, acrom ion, or thoracic spine
o
Often correlated with ingestion of large, fatty m eal
Anorexia
Nausea and vom iting
Afebrile: o
Fever and chills suggest cholecystitis or cholangitis
Physical Exam
Tenderness to deep palpation but without rebound
Murphy sign (inspiratory arrest during deep palpation of the RUQ) m ay be present during the episode of colic, but should resolve when sym ptom s pass.
Pa ge 1 1 1
Essential Workup
Obtain ECG on those whose pain m ay be owing to m yocardial ischem ia.
CBC
Liver function tests (LFTs)
Am ylase, lipase
Urinalysis
Hum an chorionic gonadotropin (hCG)
Tests Lab
CBC: o
White blood cell count (WBC) usually norm al, but m ay elevate after vom iting
o
Leukocytosis suggestive of cholecystitis or cholangitis
LFTs: o
Usually norm al
o
Elevation suggests com m on duct obstruction, cholangitis, cholecystitis, or hepatitis.
Am ylase/lipase: o
Norm al or m inim ally elevated with passage of gallstone
o
Elevation in context of severe persistent epigastric pain suggests pancreatitis.
Urinalysis: o
Exclude nephrolithiasis or pyelonephritis.
o
Bilirubinuria suggests com m on duct obstruction or hepatitis.
Imaging
Ultrasound: o
Detects gallstones with sensitivity and specificity
Pa ge 1 1 1
>90% o
Dilation of com m on bile duct >10 m m indicates obstruction, but m ay be norm al with acute obstruction.
o
Gallbladder wall thickening >5 m m or pericolic fluid 90% sensitive and 80% specific for cholecystitis
o
Accuracy enhanced in fasting patient with noncontracted gallbladder
Radionuclide scanning (HIDA) o
Cannot detect gallstones
o
Passage of tracer into sm all intestine without visualization of gallbladder highly diagnostic of cystic duct obstruction and cholecystitis; sensitivity and specificity roughly 95%
o
Failure of tracer to pass into duodenum suggests com m on bile duct obstruction.
Plain radiographs: o
Not helpful in diagnosing uncom plicated cholelithiasis
o
Exclude intestinal perforation or intestinal obstruction
o
Up to 20% of gallstones radiopaque
o
Reveal rare com plications such as air in gallbladder wall in em physem atous cholecystitis or air-filled gallbladder in biliary-enteric fistula
CT scanning: o
Less sensitive than ultrasound to detect gallstones
o
Most useful to exclude other causes of upper abdom inal pain such as aortic aneurysm , perihepatic abscess, or pancreatic pseudocyst
Differential Diagnosis
Myocardial infarction
Abdom inal aortic aneurysm
Acute cholecystitis, cholangitis, or choledocholithiasis
Pa ge 1 1 2
Renal colic or pyelonephritis
Duodenal ulcer perforation
Acute pancreatitis
Intestinal obstruction
Peptic ulcer disease, gastritis, or gastroesophageal reflux
Right lower lobe pneum onia, pleurisy, or pulm onary infarction
Hepatitis or hepatic abscess
Fitz-Hugh and Curtis syndrom e
P.231
Treatment Initial Stabilization IV access
ED Treatment
IV hydration with 0.9% norm al saline (NS) if vom iting
NPO
Parenteral nonsteroidal anti-inflam m atory drugs (NSAIDs; ketorolac) m ay lessen biliary spasm , but m ay exacerbate peptic causes of pain.
Narcotic analgesics (m eperidine) with antiem etic (prom ethazine): o
Adm inister for refractory pain once diagnosis is reasonably established.
o
Morphine sulfate m ay lead to spasm at sphincter of Oddi (clinical significance not well established).
Anticholinergics (glycopyrrolate) com m only used despite
Pa ge 1 1 2
lack of clinical trials proving benefit
Medication (Drugs)
Glycopyrrolate (anticholinergic): acutely, 0.2 m g intravenous push (IVP) q10m in up to 3 doses until pain relieved, 2 m g PO t.i.d. for recurrent colic
Ketorolac: 60 m g IM or 30 m g (peds: start 0.5 m g/kg for first dose up to 1 m g/kg/24h) IV q6h. In elderly: 30 m g IM or 15 m g IV
Meperidine: 0.5 m g/kg intravenous push (IVP) titrated to pain relief up to 2.0 m g/kg IV
Morphine sulfate: 2–5 m g IV titrated to pain relief
Prom ethazine: 12.5–25 m g (1–2 m g/kg/25h) intravenous push (IVP) q4h to q6h
Follow-Up Disposition Admission Criteria Adm ission and surgical or gastroenterologic consultation for evidence of:
Acute cholecystitis
Acute cholangitis
Com m on duct obstruction
Gallstone pancreatitis
Discharge Criteria
Lack of clinical, laboratory, or radiographic evidence of cholecystitis, cholangitis, com m on duct obstruction, or pancreatitis
Pa ge 1 1 2
Resolution of all pain and tenderness
Ability to tolerate oral fluids
Issues for Referral General Surgery referral for all cases of biliary colic with docum ented cholelithiasis
References 1. Ahrendt SA, Pitt HA. Biliary tract: calculous biliary disease. In: Townsend CM Jr, ed. Sabiston Textbook of Surgery. 17th ed. Philadelphia: WB Saunders; 2004:1597–1642. 2. Elta GH. Motility and dysm otility of the biliary tract and sphincter of Oddi. In: Feldm an, M. Sleisenger & Fordtran's Gastrointestinal and Liver Disease. 7th ed. Philadelphia: WB Saunders; 2002: 1043–1050. 3. Ko CW, Sekijim a JH, Lee SP. Biliary sludge. Ann Intern Med. 1999;130:301–311. 4. Moscati RM. Cholelithiasis, cholecystitis and pancreatitis. Em erg Med Clin North Am . 1996;14:719–737. 5. Silen W. The colics. In: Silen W, ed. Cope's Early Diagnosis of the Acute Abdom en. 20th ed. Oxford, UK: Oxford University Press; 2000:142–149.
Miscellaneous SEE ALSO: Cholangitis; Cholelithiasis
Codes ICD9-CM 572.4
ICD10 K80.2
Pa ge 1 1 2
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > C hro nic Obstructive Pulm o nary Disease
Chronic
Obstructive Pulmonary Disease Adam Z. Barkin
Basics Description
A disease characterized by airflow obstruction due to several processes: o
Em physem a: irreversible alveolar destruction with loss of airway elastic recoil
o
Chronic bronchitis: airway inflam m ation without alveolar destruction
o
Reactive airway disease: reversible bronchospasm , m ucous plugging, and m ucosal edem a
Chronic obstructive pulm onary disease (COPD) affects about 15 m illion people in the United States.
Genetics α 1 -antitrypsin deficiency
Etiology
Sm oking is the overwhelm ing cause: o
COPD develops in 15% of sm okers.
Air pollution
Pa ge 1 1 2
Airway hyperresponsiveness
α 1 -Antitrypsin deficiency
Acute exacerbations: o
Viral or bacterial infections
o
Pollutants
Diagnosis Signs and Symptoms History
Dyspnea on exertion
Cough
Sputum production
Fatigue
Wheezing
Orthopnea
Altered m ental status
Carbon dioxide narcosis
Physical Exam
Wheezing
Retractions
Poor air m ovem ent
Cyanosis
Prolonged expiratory phase
Barrell chest
Lower extrem ity edem a
Jugular venous distension
S3 and S4 gallops
Tests
Pa ge 1 1 2
Lab
CBC: o
Elevated hem atocrit m ay indicate chronic hypoxem ia.
o
Increased neutrophils and elevated WBC m ay indicate infection.
Arterial blood gas: o
Retaining carbon dioxide
o
Acidosis
o
Oxygenation
Beta natriuretic peptide: o
Differentiate between COPD and congestive heart failure (CHF)
Sputum sam ple
Theophylline level as needed
Imaging
Chest radiography: o
Pneum othorax, pneum onia, CHF, lobar collapse
Chest CAT scan: o
When needed to evaluate for pulm onary em bolus or further characterize disease
Diagnostic Procedures/Surgery
Pulse oxim etry
ECG
Pulm onary function tests
Echocardiography: o
To diagnose left or right ventricular failure or strain
Differential Diagnosis
Pneum othorax
CHF
Pneum onia
Pa ge 1 1 2
Pulm onary em bolus
Upper airway obstruction
Asthm a
Restrictive lung disease
Acute respiratory distress syndrom e
Pleural effusions
Acute coronary syndrom e
Pericardial effusion
Metabolic derangem ent
Treatment Pre Hospital
Supplem ental oxygenation: o
100% via nonrebreather
o
Do not withhold for fear of CO 2 retention.
Initiate nebulized bronchodilator therapy.
Initial Stabilization
Oxygen therapy: o
Maintain oxygen saturation >90–92%.
o
Patients at risk for CO 2 narcosis are those with slow respiratory rate.
o
Monitor closely for ventilation suppression.
P.233
Noninvasive ventilation: o
May prevent intubation
o
May help resolve hypercarbia
Intubation for airway control:
Pa ge 1 1 2
o
Indicated if clinical tiring, altered m ental status, or the inability to com ply with em ergent therapy
o
Ineffective ventilation
o
CO 2 narcosis
ED Treatment
Continuous ECG and pulse oxim etry m onitoring
Bronchodilator therapy o
β-agonists:
o
Anticholinergics:
o
Anti-inflam m atory effects
o
Reduce relapses
o
Methylprednisolone or prednisone
Antibiotics: Fever, increased sputum production and/or dyspnea
Methylxanthines: o
Ipratropium brom ide
Corticosteroids:
o
Albuterol
Controversial
Ventilator settings: o
Allow sufficient expiratory tim e to m inim ize air trapping and subsequent barotraum a.
o
Perm issive hypercapnia
Medication (Drugs)
Albuterol: 2.5 m g nebulized q10–30m in
Azithrom ycin: 500 m g PO/IV once then 250 m g PO per day for 4 days
Ceftriaxone: 1 g IV q24h
Ipratropium brom ide: 0.5 m g nebulized q6h
Pa ge 1 1 2
Levofloxacin: 500 m g PO/IV q24h
Methylprednisolone: 125 m g IV q6h
Prednisone: 40–60 (1–2 m g/kg) m g PO per day for 5 days
Terbutaline: 0.25 m g SC q30m in
Follow-Up Disposition Admission Criteria
Intensive care unit adm ission: o
Intubated patients
o
CO 2 narcosis with oxygen saturation 92%
References 1. Mandavia DP, Dailey RH. Chronic obstructive pulm onary disease. In: Marx J, et al. (eds). Rosen's em ergency m edicine: Concepts and clinical practice. 5th ed. St. Louis, MO: CV Mosby; 2002: 956–969. 2. McCullough PA, Hollander JE, Nowak RM, et al. Uncovering heart failure in patients with a history of pulm onary disease: Rationale for the early use of B-type natriuretic peptide in the Em ergency Departm ent. Acad Em erg Med. 2003;10:198–204. 3. Wouters EFM. Managem ent of severe COPD. Lancet. 2004;364:883–895. 4. Sutherland ER, Cherniack RM. Managem ent of chronic obstructive pulm onary disease. New Eng J Med. 2004;350:2689–2697.
Miscellaneous SEE ALSO: Asthm a; Congestive Heart Failure; Dyspnea; Pulm onary Em bolism
Codes ICD9-CM 491.2
ICD10 J44.9
Pa ge 1 1 3
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > C irrho sis
Cirrhosis
Paul Allegretti
Basics Description
Progressive process of inflam m ation, cellular injury and necrosis, diffuse fibrosis, and form ation of regenerative nodules
Loss of lobular and vascular architecture
Irreversible in advanced stages
Intrahepatic portal hypertension owing to increased resistance at the sinusoid, com pression of the central veins, and anastom osis between the arterial and portal system s
Markedly reduced life expectancy
Tenth leading cause of death in the United States
Etiology
Chronic alcohol abuse (m ost com m on cause in U.S.)
Chronic viral hepatitis, B or C (second m ost com m on cause in U.S.)
Autoim m une hepatitis
Biliary cirrhosis, prim ary (PBC) or secondary (sclerosing cholangitis)
Metabolic:
Pa ge 1 1 3
o
Hereditary hem ochrom atosis
o
Wilson disease
o
Porphyria
Drugs: o
Acetam inophen
o
Methotrexate
o
Am iodarone
o
Methyldopa
Hepatic congestion: o
Right-sided heart failure
o
Pericarditis
o
Budd-Chiari syndrom e (hepatic venous outflow obstruction)
Infiltrative: o
Sarcoidosis
o
Am yloidosis
o
Nonalcoholic steatohepatitis (NASH)
Hepatocellular carcinom a, diffusely infiltrating
Infections: o
Brucellosis
o
Echinococcosis
o
Tertiary syphilis
o
Schistosom iasis
Pediatric Considerations
Congenital
Arteriohepatic dysplasia, biliary atresia, cystic fibosis, α 1 -antitrypsin deficiency
Metabolic
Fructosem ia, tyrosinem ia, galactosem ia, glycogen storage diseases
Infectious
Congenital hepatitis B
Pa ge 1 1 3
Diagnosis Signs and Symptoms
May be silent
Insidious onset with nonspecific findings: o
Malaise
o
Fatigue
o
Anorexia
o
Nausea and vom iting
o
Weight loss
o
Pruritus
o
Hyperpigm entation
Jaundice
Fetor hepaticus
Asterixis
Hypotension
Cruveilhier-Baum gartnen m urm ur
Renal insufficiency
Spider telangiectasias
Palm ar erythem a
Dupuytren contractures
Parotid and lacrim al gland enlargem ent
Nail changes
Terry nails
Muehrcke lines
Clubbing
Fem inization: o
Testicular atrophy
o
Im potence
o
Loss of libido
Pa ge 1 1 3
o
Gynecom astia
Ascites
Am enorrhea
Abdom inal collateral circulation including caput m edusae
Hepatom egaly
Splenom egaly
Abdom inal discom fort or tenderness
Fever
Com plications
When com plications develop, patient is considered to have decom pensated disease: o
Ascites
o
Spontaneous bacterial peritonitis (SBP)
o
Hepatic encephalopathy—m ay be precipitated by:
o
GI bleed
Infections
Increased dietary protein
Hypokalem ia
Sedatives
Constipation
Azotem ia
Alkalosis
Variceal hem orrhage:
One third of patients with varicies bleed.
Each bleeding episode carries a 33% m ortality rate.
Hepatic venous pressure gradient >12 m m Hg increases risk of bleed.
o
Portal hypertensive gastropathy or peptic ulcer disease
o
Hepatorenal failure:
Caused by decreased renal perfusion during
Pa ge 1 1 3
severe decom pensated cirrhosis
May be iatrogenic: secondary to diuretics, nonsteroidal anti-inflam m atory drugs (NSAIDs), IV contrast, am inoglycosides, large-volum e paracentesis
o
High m ortality rate
Hepatopulm onary syndrom e:
Intrapulm onary vascular dilation and hypoxia
Results in increased alveolar-arterial gradient
Essential Workup Detailed historical and physical exam search for clues to liver disease
Tests Lab
CBC: o
Anem ia
o
Macrocytosis
o
Leukopenia and neutropenia
o
Throm bocytopenia
Im paired liver function: o
High bilirubin
o
Low album in
o
High globulins
o
Prolonged prothrom bin tim e
o
Varying degrees of dissem inated intravascular coagulation (DIC)
o
Hypoglycem ia
Increased liver enzym es: o
Aspartate alanine am inotransferase (AST, SGOT), alanine am inotransferase (ALT, SGPT)— reflect injury
o
Ratio of AST:ALT ≥2.0 in alcoholic liver disease
Pa ge 1 1 3
o
Alkaline phosphatase and 5′-nucleotidase reflect cholestasis.
o
Gam m a-glutam yltranspeptidase (GGT)
o
May be norm al in inactive cirrhosis
Electrolytes, BUN, and creatinine
Hyponatrem ia: o
Renal dysfunction and hepatorenal syndrom e
Arterial blood gases or pulse oxim eter for: o
Suspected pneum onia
o
Congestive heart failure
o
Hepatopulm onary syndrom e
P.235
Search for cause: o
Hepatitis B surface antigen
o
Hepatitis C antibody
o
Antinuclear antibody (ANA) and anti-sm ooth m uscle antibody (autoim m une hepatitis)
o
Antim itochondrial antibody (prim ary biliary cirrhosis)
o
Serum iron, transferrin saturation, and ferritin (hem ochrom atosis)
o
Ceruloplasm in (Wilson disease)
o
α 1 -Antitrypsin deficiency
o
Serum im m une electrophoresis (high im m unoglobulin M [IgM] in PBC)
o
Cholesterol (chronic cholestasis)
o
Alpha fetoprotein (hepatocellular cancer)
Imaging
Ultrasound for liver architecture, biliary obstruction, ascites, portal vein throm bosis, splenom egaly
CT scan to explore abnorm al finding on ultrasound
Pa ge 1 1 3
MRI role unclear and lim ited
Chest radiograph for pleural effusion, cardiom egaly, and congestive heart failure (CHF)
Diagnostic Procedures/Surgery
Esophagogastroduodenoscopy (EGD) indicated for upper GI bleeding or variceal surveillance
Variceal ligation or endoscopic sclerotherapy
Cholangiogram for suspected biliary obstruction
Liver biopsy to confirm diagnosis
TIPS (transjugular intrahepatic portal system ic shunt)
Differential Diagnosis
Ascites: o
Increased right heart pressure
o
Hepatic vein throm bosis
o
Peritoneal m alignancy/infection
o
Pancreatic disease
o
Thyroid disease
o
Lym phatic obstruction
Upper GI bleeding: o
Peptic ulcer disease (PUD)
o
Gastritis
Encephalopathy: o
Metabolic
o
Toxic
o
Intracranial process
Treatment Pre Hospital
Naloxone, dextrose (or Accu-Chek), and thiam ine for
Pa ge 1 1 3
altered m ental status
Reverse hypotension with IV fluids to prevent acute ischem ic hepatic injury.
Initial Stabilization Treat com plications such as GI bleeding or hepatic encephalopathy.
ED Treatment
For suspected variceal bleed: o
IV octreotide—analog of som atostatin (splanchnic vasoconstrictor)
o
IV vasopressin with sim ultaneous nitroglycerin has been used, but has high com plication rate.
Nitroglycerin decreases vasoconstriction of vasopressin.
o
Reverse coagulopathy:
Fresh-frozen plasm a 1 IU/h until bleeding is controlled
Desm opressin (DDAVP)—im proves bleeding tim e and prolonged partial throm boplastin tim e
o
Balloon tam ponade with Sengstaken-Blakem ore tube or a variant for variceal com pression (rarely used anym ore, prophylactic intubation recom m ended)
o
Em ergent endoscopic sclerotherapy
Initiate broad-spectrum antibiotics in suspected sepsis or spontaneous bacterial peritonitis (SBP):
o
Cefotaxim e
o
Ticarcillin-clavulanate
o
Piperacillin-tazobactam
o
Am picillin-sulbactam
Treat com plicating conditions such as ascites, hepatic encephalopathy, SBP.
Treat pruritus with:
Pa ge 1 1 3
o
Diphenhydram ine 25–50 m g IM/IV q4h
o
Cholestyram ine, ursodeoxycholic acid, or rifam pin
o
Naloxone infusion 0.2 µg/kg/m in for tem porary relief for extrem e cases
For prolonged PT, adm inister vitam in K, 10 m g PO daily for 3 days.
Relieve biliary obstruction (e.g., stricture) by endoscopic, radiologic, or surgical m eans.
Provide nutritious diet; high in calories and adequate in protein (1 g/kg), unless there is com plicating hepatic encephalopathy (HE)
Beta-blocker (propranolol) for large esophageal varices: o
Titrated to pulse rate of 60 or 25% reduction of resting pulse
o
With or without isosorbide dinitrate
o
Decreases rebleeeding rate
o
May delay or prevent occurrence of first bleed
Consult transplantation coordinator whenever post-liver transplantation patient presents to the ED with liver dysfunction, suspected sepsis, or possible treatm ent-related com plication.
Specific Therapy
Hem ochrom atosis: phlebotom y or deferoxam ine (iron-chelating agent)
Autoim m une hepatitis: prednisone with or without azathioprine
Chronic hepatitis B or C: alpha interferon (avoid in decom pensated cirrhosis)
Prim ary biliary cirrhosis: ursodeoxycholic acid
Wilson disease: penicillam ine
The only cure for m ost advanced cirrhosis is liver transplantation.
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Medication (Drugs)
Azathioprine: 1–2 m g/kg PO
Cefotaxim e: 1–2 g q6h–q8h (peds: 50–180 m g/kg/d q6h) IV
Cholestyram ine: 4 g PO one to six tim es per day
Desm opressin (DDAVP): 0.3 µg/kg in 50-m L saline infused over 15–30 m inutes
Dextrose: D 5 0 W 1 am p (50 m L or 25 g; peds: D 2 5 W 2–4 m L/kg) IV
Naloxone (Narcan): 0.2–2 m g (peds: 0.1 m g/kg) IV or IM initial dose
Octreotide: 25–50 µg IV bolus followed by 50 µg/hr IV infusion
Piperacillin-tazobactam : 3.375 g IV q6h (peds: 100–400 m g/kg/d divided q6h–q8h; renal dosing required)
Prednisone: 40 m g (peds: 1–2 m g/kg) PO daily
Propranolol: 40 (initial) to 240 m g (peds: 1–5 m g/kg/d) PO t.i.d.
Rifam pin: 600 m g (peds: 10–20 m g/kg) PO daily
Thiam ine: 100 m g (peds: 50 m g) IV or IM
Ursodeoxycholic acid: 8–10 m g/kg/d t.i.d.
Follow-Up Disposition Admission Criteria
Acute decom pensation or com plicating conditions
First presentation with clinically evident cirrhosis, unless
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close outpatient workup is possible
Advanced grades hepatic encephalopathy, sepsis, active GI bleed, and hepatorenal and hepatopulm onary syndrom es require ICU.
Discharge Criteria Most patients with com pensated cirrhosis can be treated as outpatients.
References 1. Braunwald E, et al. Harrison's Principles of Internal Medicine. 15th ed. New York: McGraw-Hill; 2001. 2. Feldm an M. Sleisenger and Fordtran's Gastrointestinal and Liver Disease. 7th ed. Philadelphia: WB Saunders; 2002. 3. Goldberg, E. Diagnostic Approach to the Patient With Cirrhosis. Wellesley, MA: UpToDate; 2004. 4. Goldberg, E. Overview of Com plications, Prognosis, and Managem ent of Cirrhosis. Wellesley, MA: UpToDate; 2004. 5. Runyon BA. Treatm ent of patients with cirrhosis and ascites. Sem in Liver Dis. 1997;17:249. 6. Sanyal A. Prim ary Prophylaxis against Variceal Hem orrhage in Patients with Cirrhosis. Wellesley, MA: UpToDate; 2004.
Miscellaneous SEE ALSO: Ascites, Varices; Hepatic Encephalopathy; Hepatitis; Spontaneous Bacterial Peritonitis
Codes ICD9-CM 571.5
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > C lavicle F racture
Clavicle Fracture
Sean Patrick Nordt Jeffrey Manko
Basics Description
Clavicle fractures account for 5% of all fractures in all age groups
80% of clavicle fractures involve the m iddle third
15% occur in the distal third
5% occur in the m edial third
Classification
Group I: m iddle-third fractures
Group II: distal-third fractures: o
Type I: coracoclavicular ligam ents are intact (nondisplaced).
o
Type II: severing of the coracoclavicular ligam ents (conoid)
o
Type III: articular surface involvem ent of the acrom ioclavicular joint
Group III: m edial (proxim al)-third fractures
Etiology Mechanism
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Direct traum a to the clavicle
Fall on the lateral shoulder
Fall on the outstretched hand
Pediatric Considerations
Most com m on of all pediatric fractures
May occur in newborns secondary to birth traum a
Diagnosis Signs and Symptoms History
Local pain, tenderness, and swelling over the fracture site
Crepitus is often present owing to the clavicle's subcutaneous position
Arm held in adduction against the chest wall with resistance to m otion
Shoulder displaced anteriorly and inferiorly
Physical Exam
Palpate the clavicle for tenderness, crepitus, and swelling.
Exam ine the hum erus and shoulder joint for other fractures, dislocations, or subluxations.
Determ ine whether the fracture is open or closed.
Evaluate for associated injuries (often serious and life threatening) that m ust be excluded: o
Skeletal injuries:
First rib fracture with underlying aortic injury
Sternoclavicular joint separation/fracture-dislocation
Acrom ioclavicular joint separation/fracture-dislocation
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Cervical spine injuries
Tests Imaging
AP radiographs of both clavicles are m andatory and m ust include:
o
Upper third of the hum erus
o
Shoulder girdle (rule out other fractures)
o
Upper lung fields (rule out pneum othorax)
Oblique and apical lordotic views: o
May be helpful, especially for m edial and distal clavicle fractures that are not easily visualized on the AP view
Stress views (weight-bearing) for distal clavicle fractures are no longer routinely recom m ended.
Angiography: o
Should be perform ed if there is any evidence or suspicion of vascular injuries (m ost com m only subclavian vessels)
Differential Diagnosis
Distal fractures: Consider acrom ioclavicular separation.
Medial fractures: Consider sternoclavicular separation.
Shoulder fracture-dislocation
Treatment Pre Hospital
Ice packs to affected area
Pain m anagem ent using either narcotics or NSAIDs
Im m obilize affected side in a sling.
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Initial Stabilization Airway m anagem ent and resuscitate as indicated
ED Treatment
Open fracture: uncom m on occurrence, but usually requires open débridem ent and internal fixation (obtain im m ediate orthopaedic referral)
Closed fracture: if severely displaced, attem pt closed reduction and im m obilize depending on type of fracture: o
Middle third:
If nondisplaced, a sling or shoulder im m obilizer is enough to provide support
Controversy exists as to whether closed reduction is necessary because the alignm ent is rarely m aintained regardless of splinting technique.
To perform a closed reduction, 1% lidocaine should be injected into the fracture hem atom a. The shoulders are pulled upward, outward, and backward, and the fracture is then m anipulated into place.
Sedation m ay be given to alleviate pain or anxiety.
o
A figure-of-eight splint is then applied.
Ice should be applied for the first 24 hours.
Analgesia (narcotics or NSAIDs) for pain
Distal third type I:
Ice for the first 24 hours.
Im m obilization with a sling or shoulder im m obilizer.
Orthopaedic referral
Analgesia (narcotics or NSAIDs) for pain
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Early range of m otion
P.237
o
Distal third type II:
Ice for the first 24 hours.
Im m obilization with a sling or shoulder im m obilizer.
Orthopaedic referral (m ay require operative repair)
Analgesia (narcotics or NSAIDs) for pain
o
Distal third type III: sam e as type II
o
Medial (proxim al) third:
Ice for the first 24 hours.
Im m obilization in a sling or shoulder im m obilizer for support
Analgesia (narcotics or NSAIDs) for pain
Orthopaedic follow-up
Reassess neurovascular status after all splints are applied.
Pediatric Considerations
Children who do not cooperate with the figure-of-eight splint should be referred to an orthopaedic surgeon for possible shoulder spica placem ent.
Most children will tolerate a shoulder im m obilizer best.
Medication (Drugs)
Acetam inophen: 500–1,000 m g PO q6h PRN, (peds: 15–20 m g/kg PO q6h PRN)
Ibuprofen: 600–800 m g PO q6h PRN with m eals, (peds: 5–10 m g/kg PO q6h PRN)
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Follow-Up Disposition Admission Criteria
Open fracture
Associated injuries that are potentially life threatening
Discharge Criteria
Isolated closed clavicle fracture without other injuries
Appropriate support services at hom e (especially for elderly patients)
Orthopaedic follow-up
Adequate pain m anagem ent
Issues for Referral Open fracture, com plex injury, signs of neurovascular injury require im m ediate orthopaedic referral.
References 1. Anderson K. Evaluation and treatm ent of distal clavicle fractures. Clin Sports Med. 2003;22:319–326. 2. Eiff MP. Managem ent of clavicle fractures. Am Fam Physician. 1997;55:12–128. 3. Heckm an J, Bucholz R. Rockwood and Green's fractures in adults. 5th ed. Philadelphia: Lippincott William s & Wilkins, 2001. 4. Post M. Current concepts in the treatm ent of fractures of the clavicle. Clin Orthop. 1989;245:89–101. 5. Sim on RR, Koenignsknecht SJ. Em ergency orthopedics: the extrem ities. 4th ed. McGraw-Hill.
Codes
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ICD9-CM 810.00
ICD10 S42.0
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > C o caine, Po iso ning
Cocaine,
Poisoning Steven Aks
Basics Description
Sym pathom im etic
Inhibits neurotransm itter reuptake at the nerve term inal
Metabolism : o
Hepatic degradation
o
Nonenzym atic hydrolysis
o
Cholinesterase m etabolism
Etiology
IV, nasal, oral adm inistration of cocaine
Oral ingestion: o
Body stuffers:
Ingest hastily wrapped packets in attem pt to evade police
o
Body packers:
Ingest cocaine packets to sm uggle the drug using couriers’ oral, rectal, and vaginal cavities
Cocaine is wrapped carefully in packets
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containing large am ounts of drug.
Diagnosis Signs and Symptoms
Sym pathom im etic toxidrom e
Cardiovascular:
o
Hypertension
o
Tachycardia
o
Chest pain (angina)
Respiratory: o
Tachypnea
o
Pleuritic chest pain:
o
Pneum om ediastinum
Pneum othorax
Bronchitis
Pulm onary infarction
Cough
Central nervous system (CNS): o
Agitation
o
Trem ulousness
o
Com a
o
Seizures
o
Stroke
Miscellaneous: o
Hypertherm ia (poor prognosis)
o
Lim b ischem ia (inadvertent intra-arterial injection)
o
Corneal ulcerations (heavy crack sm okers):
Owing to local chem ical and therm al irritation that disrupts corneal epithelium
o
Rhabdom yolysis
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Essential Workup
Recognition of the sym pathom im etic toxidrom e caused by cocaine: o
Distinguish from anticholinergic toxidrom e.
Toxidrom e recognition: o
o
o
Sym pathom im etic:
Heart rate (tachycardia)
Blood pressure (increased)
Moist skin
Bowel sounds present
Tem perature (increased)
No urinary retention
Anticholinergic:
Heart rate (tachycardia)
Blood pressure (increased)
Dry skin
Bowel sounds dim inished
Tem perature (increased)
Urinary retention present
History of route of drug ingestion:
If oral ingestion, inquire how the packets were wrapped to determ ine leakage potential.
Tests Lab
CBC
Electrolytes, BUN, creatinine, glucose
Urinalysis dip for m yoglobin
Cardiac enzym es (troponin, creatine phosphokinase) for:
o
Anginal chest pain
o
Abnorm al results on ECG
Creatine phosphokinase (CPK) for evidence of
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m yoglobinuria
Imaging
ECG: o
For anginal chest pain
o
Consider possibility of m yocardial infarction with cocaine-related chest pain.
Chest radiograph: o
For chest pain or shortness of breath
o
Check for pneum om ediastinum , pneum othorax, aortic rupture.
Abdom inal radiograph: o
For body packers/stuffers
o
Usually produces negative result for stuffers because drug is loosely packed in cellophane
o
Positive for packers because drug is densely packed and usually radiopaque
CT of the abdom en with contrast: o
When unreliable history of body packers/stuffers and negative on abdom inal frontal radiograph
CT brain scan: o
For altered m ental status or severe headache
o
Detects cerebral ischem ia or hem orrhage
Differential Diagnosis
Other agents with sym pathom im etic effects
Theophylline
Caffeine
Am phetam ines
Albuterol
Tricyclic antidepressants
Antihistam ines
Phencyclidine (PCP)
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Thyrotoxicosis
Neuroleptic m alignant syndrom e
Hallucinogens
Treatment Pre Hospital
Cautions o
Establish IV access
o
Cardiac m onitor
Chest pain m ay be ischem ic
Benzodiazepine therapy to control agitation
When drug is used as a “speedball― (com bination of heroin and cocaine), adm inister naloxone in increm ents to reverse com a
Initial Stabilization
Check airway, breathing, and circulation (ABCs).
Establish IV access.
Establish cardiac m onitor.
Provide therapy with naloxone (Narcan), thiam ine, dextrose (or Accu-Check) for altered m ental status.
P.239
ED Treatment
Supportive care for m ildly sym ptom atic patients
Benzodiazepines:
o
For agitation and trem or
o
Initial agents for hypertension and tachycardia
Cooling m easures for hypertherm ia:
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o
Evaporative-convective m ethod
Treat rhabdom yolysis: o
Hydrate with 0.9% norm al saline (NS)
o
Alkalinization with IV bicarbonate in severe cases
Cardiac chest pain: o
Aspirin
o
Nitrates
o
Oxygen
o
Opiates
o
Avoid β-blockers because of unopposed α-stim ulation
o
Angiography/angioplasty/throm bolysis for acute m yocardial infarction
Hypertension/tachycardia: o
Benzodiazepine initial agent
o
Use α-blocking agent (phentolam ine) as sole agent or com bine with β-blocker (propranolol, esm olol) if unresponsive to benzodiazepine.
Use labetalol cautiously (does not have equal α- and β-blocking properties).
o
IV nitroglycerin/nitroprusside for severe unresponsive hypertension
Body packer/stuffers: o
Treat asym ptom atic or m inim ally sym ptom atic body packers and body stuffers:
Oral activated charcoal
Whole-bowel irrigation with polyethylene glycol-electrolyte lavage solution
o
Consult with surgeons about sym ptom atic body packers and stuffers:
If toxicity is not easily m anaged with previously suggested pharm acologic therapy, rem ove the
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drug packets intraoperatively.
Medication (Drugs)
Activated charcoal slurry: 1–2 g/kg up to 90 g PO
Dextrose: D 5 0 W 1 am pule (50 m L or 25 g) (peds: D 2 5 W 2–4 m L/kg) IV
Diazepam : 5 m g increm ental doses IV
Esm olol: 50–200 µg/kg/m in IV infusion titrated to effect
Lorazepam : 2 m g increm ental doses IV
Naloxone (Narcan): 2 m g (peds: 0.1 m g/kg up to 2 m g) IV or IM initial dose
Nitroglycerin: 10–100 µg/m in IV infusion
Nitroprusside: 0.3 µg/kg/m in IV (titrate to effect up to 10 µg/kg/m in)
Phentolam ine: 5 m g IV q15–24m in (titrate to clinical effect)
Polyethylene glycol (GoLYTELY): 4 L PO over 4 hours until com plete bowel evacuation
Follow-Up Disposition Admission Criteria
Altered m ental status
Abnorm al vital signs: Heart rate >100 beats per m inute, diastolic blood pressure >120 m m Hg, or hypotension
Hypertherm ia
Cocaine-induced m yocardial ischem ia
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Body stuffers and body packers
Intensive care unit adm ission for m oderate to severe toxicity
Discharge Criteria
Mental status and vital signs norm al after 6 hours of observation
Body packers or stuffers with confirm ed expulsion of packets and no clinical signs of toxicity.
References 1. Hollander JE. The m anagem ent of cocaine-associated m yocardial ischem ia. N Engl J Med. 1995;33:1267. 2. Hollander JE, Hoffm an RS. Cocaine. In: Goldfrank LR, ed. Goldfrank's Toxicologic Em ergencies. 6th ed. Stam ford, CT: Appleton & Lange; 1998: 1071–1089. 3. June R, Aks S, Keys N, et al. Medical outcom e of cocaine bodystuffers. J Em erg Med. 2000;18:221–224. 4. Lange RA, Hillis LD. Cardiovascular com plications of cocaine use. N Engl J Med. 2001;345:351–358.
Codes ICD9-CM 968.5 Surface (topical) and infiltration anesthetics
ICD10 T40.5 Cocaine
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > C o lo n Traum a
Colon Trauma
Rebecca Apollon Blake Spirko
Basics Description
Traum a that perforates the colon inflam es the cavity in which it lies.
Peritoneal inflam m ation from hollow viscus perforation often requires hours to develop.
Mesenteric tears from blunt traum a cause hem orrhage and bowel ischem ia.
Delayed perforation from ischem ic or necrotic bowel m ay occur.
Peritonitis and sepsis m ay develop from the extravasated intralum inal flora.
Ascending and descending colon segm ents are retroperitoneal.
The left colon has a higher bacterial load than the right.
Morbidity and m ortality increase if the diagnosis of colon injury is delayed.
Etiology
Penetrating abdom inal traum a: o
The colon is the second m ost com m only injured organ
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in penetrating traum a.
o
Gunshot wounds have the highest incidence.
o
Transverse colon is m ost com m only injured.
o
Often presents with peritonitis
Blunt abdom inal traum a: o
Colon rarely injured in blunt traum a
o
Burst injury occurs from com pression of a closed loop of bowel.
o
Intestine m ay be squeezed between a blunt object (lap belt) and vertebral colum n or bony pelvis.
o
Sudden deceleration m ay produce bowel-m esenteric disruption and consequent devascularization.
o
With deceleration, the sigm oid and transverse colon are m ost vulnerable.
Transanal injury: o
Iatrogenic endoscopic or barium enem a injury
o
Foreign bodies used during sexual activities m ay reach and injure the colon.
o
Com pressed air under high pressure such as at autom obile repair facilities can perforate the colon even if the com pressor nozzle is not inserted anally.
Swallowed sharp foreign bodies (toothpick) m ay penetrate the colon, particularly the cecum , appendix, and sigm oid: o
Most foreign bodies pass without com plications.
Pediatric Considerations Unlike adults, children have an equal frequency of blunt and penetrating colon injuries.
Diagnosis
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Signs and Symptoms
Colon traum a is generally associated with other intra-abdom inal and extra-abdom inal injuries, com m only to the sm all intestine.
Injuries of significant severity m ay have m inim al early findings.
It is uncom m on to determ ine specific organ injury on physical exam .
Assess on exam ination: o
Abdom en for peritoneal signs
o
Ecchym osis or hem atom a on lower abdom en from lap-belt com pression
o
Ecchym osis on epigastric region from steering-wheel com pression
o
Grey Turner sign (flank hem atom as) resulting from retroperitoneal bleeding.
o
Foreign bodies or blood on digital rectal exam ination (particularly in the presence of pelvic fracture).
o
Note: Abdom inal wall ecchym osis or hem atom a is not always present despite existing injury.
o
Note: Bowel sounds are not helpful.
Essential Workup
Serial abdom inal exam ination because inflam m ation takes tim e to develop.
Abdom inal CT with contrast is the best diagnostic study in stable patients.
Ultrasound and diagnostic peritoneal lavage (DPL) are helpful in the potentially unstable patient.
Tests
No individual test or com bination of currently available diagnostic m odalities is adequate to detect blunt colonic
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injury.
Signs of peritoneal irritation owing to intestinal injury typically develop hours after the event.
Imaging
CT is m ore useful for detecting penetrating versus blunt colon injury.
CT with triple contrast allows intraperitoneal and retroperitoneal visualization.
Oral contrast is not essential in blunt abdom inal traum a CT evaluation.
Although CT m ay m iss colon injuries, abnorm al findings are typical.
CT is only m oderately sensitive at identifying hollow viscus injury.
Hollow viscus injury associated CT findings include extralum inal gas or contrast, m esenteric fat streaking, and free fluid without solid organ injury.
Water-soluble enem a with fluoroscopy is useful if other test results are inconclusive.
Plain abdom inal radiographs can show indirect signs such as intraperitoneal and retroperitoneal free air.
FAST ultrasound exam does not evaluate for enteric injury and retroperitoneal hem orrhage.
See Abdom inal Traum a, Blunt; Abdom inal Traum a, Im aging.
Diagnostic Procedures/Surgery
DPL or ultrasound in addition to CT will increase sensitivity.
In blunt traum a, DPL will often not detect retroperitoneal injuries and enteric injury as intra-abdom inal bleeding is lim ited.
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Fecal or vegetable m aterial on DPL analysis indicates hollow viscus injury.
Lavage white cell response m ay be negative secondary to delayed peritoneal inflam m ation.
In hollow viscus injury, lavage white blood cell count: red blood cell count ratio is higher than that seen with solid-organ injuries.
Differential Diagnosis
Other intra-abdom inal injuries
A fractured pelvis m ay present sim ilarly to intraperitoneal injuries in children.
P.241
Treatment Pre Hospital
Cautions: o
Follow standard prehospital guidelines for traum a treatm ent (airway, breathing, andcirculation [ABCs]).
o
Do not rem ove penetrating foreign bodies.
o
Do not attem pt to replace eviscerated bowel; cover with m oist saline dressings.
o
Obtain history regarding m echanism of injury, vehicular dam age, and seat belt use.
Controversies: o
Use of intravenous crystalloid resuscitation is still considered the standard of care.
Initial Stabilization
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Refer to topic on Abdom inal Traum a.
ABCs should precede abdom inal evaluation.
Aggressive m anagem ent with intravenous crystalloid resuscitation and blood replacem ent as needed.
ED Treatment
Early surgical consultation; surgery is definitive treatm ent.
Cover eviscerated bowel in m oist saline gauze, in a nondependent position.
Adm inister broad-spectrum antibiotics to cover gram -negative aerobic and anaerobic bacteria.
The efficacy of m ultiple-agent and single-agent antibiotic regim ens is sim ilar.
Ensure tetanus prophylaxis.
Medication (Drugs)
Am picillin: 2 g (peds: 50 m g/kg) IV q6h plus gentam icin 2 m g/kg (peds: 2.5 m g/kg) IV q8h plus m etronidazole 500 m g IV q6h (peds: use clindam ycin 25–40 m g/kg IV q24h div. q6h–q8h)
Aztreonam : 2 g IV q8h (peds: 90–120 m g/kg IV q24h div. q6h–q8h) plus clindam ycin 900 m g IV q8h (peds: use clindam ycin 25–40 m g/kg IV q24h div. q6h–q8h)
Cefoxitin: 2 g IV q8h (peds: 40 m g/kg IV q6h)
Piperacillin/tazobactam : 4.5 g (peds: 75 m g/kg) IV q8h
Follow-Up Disposition
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Admission Criteria
Colon injuries require adm ission for surgical repair.
All penetrating foreign bodies m ust be rem oved to prevent sepsis.
Patients with abdom inal ecchym osis require hospital adm ission and observation because of potential for undiagnosed hollow viscus injury.
Discharge Criteria
Patients in whom serious abdom inal injury is not suspected and with com pletely norm al abdom inal exam ination, norm al hem odynam ic status, and no other injury m ay be considered for discharge with appropriate precautions.
If there is any doubt about the possibility of colon injury, the patient should be adm itted and observed.
References 1. ACEP Clinical Policies Com m ittee and Clinical Policies Subcom m ittee on Acute Blunt Abdom inal Traum a. Clinical policy: critical issues in the evaluation of adult patients presenting to the em ergency departm ent with acute blunt abdom inal traum a. Ann of Em erg Med. 2004;43:278–290. 2. Asbun H, Irani H, Roe EJ, et al. Intra-abdom inal seatbelt injury. J Traum a. 1990;30:189–193. 3. Carrillo EH, Som berg LB, Ceballos CE, et al. Blunt traum atic injuries to the colon and rectum . J Am Coll Surg. 1996;183:548–552. 4. Fealk M, Osipov R, Foster K, et al. The conundrum of traum atic colon injury. Am J Surg. 2004;188(6): 663–670. 5. Killeen KL, Shanm uganathanm K, Poletti PA, et al. Helical com puted tom ography of bowel and m esenteric injuries. J Traum a. 2001;51(1):26–36. 6. McCabe C, Warren R. Traum a: an annotated bibliography of the
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literature—2001. Am J Em erg Med. 2002;20(4):352–366. 7. Stokes M, Jones D. ABC of colorectal diseases: colorectal traum a. Br Med J. 1992;305:303–306. 8. William s MD, Watts D, Fakhry S. Colon injury after blunt abdom inal traum a: results of the EAST Multi-Institutional Hollow Viscus Injury Study. J Traum a. 2003;55(5):906–912.
Codes ICD9-CM 863.40 Colon, unspecified site
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > C o m a
Coma
Gregory D. Jay Linda C. Cowell
Basics Description
Light com a: o
Deep com a: o
Responds to noxious stim uli
Does not respond to pain
Unresponsiveness: o
Loss of either arousability or cognition:
Loss of arousal
Arousal is prim arily a brain-stem function.
Im pairm ent of the reticular activating system
Loss of cognition
Requires dysfunction of both cerebral hem ispheres
o
o
Stupor:
Deep sleep, although not unconsciousness
Exhibits little or no spontaneous activity
Awaken with stim uli
Little m otor or verbal activity once aroused
Obtundation:
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Mental blunting with m ild or m oderate reduction in alertness
o
o
Delirium :
Floridly abnorm al m ental status
Irritability
Motor restlessness
Transient hallucinations
Disorientation
Delusions
Clouding of consciousness:
Disturbance of consciousness
Im paired capacity to:
think clearly
perceive, respond to, and rem em ber current stim uli
Etiology
Diffuse brain dysfunction (69%): o
o
Lack of nutrients:
Hypoglycem ia
Hypoxia
Poisoning:
Ethanol
Isopropyl alcohol
Ethylene glycol
Methanol
Salicylates
Sedative-hypnotics
Narcotics
Anticonvulsants
Isoniazid
Heavy m etals
Opiates
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o
o
o
o
o
Anticholinergics
Lithium
Phenylcyclidine
Cyanide
Carbon m onoxide
Infection:
Bacterial/Tuberculous/Syphilitic m eningitis
Encephalitis
Falciparum m eningitis
Typhoid fever
Rabies
Endocrine disorders:
Myxedem a com a
Thyrotoxicosis
Addison disease
Cushing disease
Pheochrom ocytom a
Metabolic disorders:
Hepatic encephalopathy
Urem ia
Porphyria
Wernicke encephalopathy
Am inoacidem ia
Reye syndrom e
Hypercapnia
Electrolyte disorders:
Hypernatrem ia, hyponatrem ia
Hypercalcem ia, hypocalcem ia
Hyperm agnesem ia, hypom agnesem ia
Hypophosphatem ia
Acidosis, alkalosis
Tem perature regulation:
Pa ge 1 1 6
Hypotherm ia
Heat stroke
Neuroleptic m alignant syndrom e
Malignant hypertherm ia
o
Urem ia
o
Postictal state, status epilepticus
o
Psychiatric
o
Shock
o
Fat em bolism
o
Hypertensive encephalopathy
Supratentorial lesions (19%): o
o
o
Hem orrhage (15%):
Intraparenchym al hem orrhage
Epidural hem atom a
Subdural hem atom a
Subarachnoid hem orrhage
Infarction (2%):
Throm botic arterial occlusion
Em bolic arterial occlusion
Venous occlusion
Tum or or abscess (2%):
Hydrocephalus
Herniation
Hem orrhage from erosion into adjacent blood vessels
Subtentorial lesions (12%): o
Infraction
o
Hem orrhage
o
Tum or
o
Basilar m igraine
o
Brain-stem dem yelination
Pa ge 1 1 6
Diagnosis Signs and Symptoms History Ongoing disturbance of consciousness
Physical Exam
No spontaneous eye opening
Lack of response to painful stim uli
No m otor activity
Regular cardiorespiratory function
Glasgow Com a Scale (GCS) scoring: o
o
Eye opening (E)
Spontaneously: 4
To verbal com m and: 3
To pain: 2
No response: 1
Best m otor response (M) to verbal com m and
o
o
Obeys: 6
Best m otor response to painful stim ulus
Localizes to pain: 5
Withdraws to pain: 4
Flexion—abnorm al: 3
Extension—abnorm al: 2
No response: 1
Best verbal response (V):
Oriented and converses: 5
Disoriented and converses: 4
Verbalizes: 3
Vocalizes: 2
No response: 1
Pa ge 1 1 6
o
GCS = E + M + V
Hypotherm ia: o
Infection, hypoglycem ia, m yxedem a com a, alcohol and sedative-hypnotic poisoning
Fever: o
Infection, thyrotoxicosis, anticholinergics, sym pathom im etics, neuroleptic m alignant syndrom e, hypothalam ic hem orrhage
Hypertension: o
Structural lesion, hypertensive encephalopathy
Hypotension: o
System ic disease
o
Sepsis should be highly considered
HEENT
Mydriasis: o
Miosis: o
Narcotics
o
Anticholinergics
o
Pontine lesion
Loss of pupillary reflexes or unequal pupils: o
Organophosphates
Structural lesions
Evidence of head traum a: o
Contusions
o
Hem atom as
o
Lacerations
o
Hem otym panum
P.243
Neck: o
Nuchal rigidity
Pa ge 1 1 7
o
Meningitis
o
Subarachnoid hem orrhage
Neurologic
Decorticate posturing: o
Flexion of elbows and wrists
o
Adduction and internal rotation of shoulders
o
Supination of the forearm s
o
Suggests severe dam age above the m idbrain
Decerebrate posturing: o
Extension of elbows and wrists
o
Adduction and internal rotation of shoulders
o
Pronation of the forearm s
o
Suggests dam age at the m idbrain or diencephalon
Asym m etric m ovem ents: o
Structural lesions
Persistent twitching of an extrem ity: o
Status epilepticus
Essential Workup
Detect and treat reversible causes
Im m ediate exclusion of com alike states: o
Noting resistance to passive opening of eyelids, fluttering of eyelids when stroked, abrupt eyelid closure, eye m ovem ents by saccadic jerks (rather than roving), or finding the eyes rolled back
o
Provocation of nystagm us with ice-water caloric testing
o
Before paralyzing a patient for intubation, an attem pt should be m ade to detect a locked-in syndrom e.
o
Dem onstrating that the patient is able to blink on verbal com m and will establish this diagnosis.
o
Intubation is still indicated to prevent aspiration.
Pa ge 1 1 7
Tests Lab
Dextrostix
CBC
Electrolytes
Imaging Head CT scan:
Diagnosis of hem orrhage and m idline shift
CT angiography for suspected cerebrovascular accident
Diagnostic Procedures/Surgery
Lum bar puncture: o
All patients with com a of unknown etiology, particularly if fever is present
o
Antibiotics m ay be adm inistered for as long as 68 hours before lum bar puncture.
o
CT scan should be perform ed before lum bar puncture if there is evidence of increased intracranial pressure, a m ass lesion, pre-existing traum a, or focal findings.
Risk of tonsillar herniation in patients with a m ass lesion is very sm all.
Electroencephalography: o
Perform ed to rule out suspected seizure activities
o
Little use in the em ergency evaluation
o
Unlike electroencephalogram studies perform ed in a laboratory, lighting will cause artifacts.
Differential Diagnosis
Locked-in syndrom e
Psychogenic unresponsiveness
Stupor
Pa ge 1 1 7
Catatonia
Akinetic m utism
Treatment Pre Hospital
Airway m anagem ent if loss of airway patency
Endotracheal intubation if no response to com a cocktail
IV access
Dextrose or Dextrostix
Narcan
Monitor
Look for signs of an underlying cause: o
Medical alert bracelets
o
GCS
o
Pupils
o
Extrem ity m ovem ents
Initial Stabilization
Airway m anagem ent
Em piric use of naloxone
Em piric dextrose: o
Adm inister if serum glucose cannot be m easured at the bedside
o
Can safely be adm inistered before thiam ine
o
Does not worsen outcom e in patients with stroke
ED Treatment
Specific therapy directed at underlying cause once identified: o
Adm inister glucose, thiam ine, naloxone, flum azenil
Screen for drug overdose
Pa ge 1 1 7
CT scan
Consider em piric use of antibiotics for com a of undeterm ined etiology: o
Broad-spectrum with good cerebrospinal fluid penetration such as ceftriaxone
Adm inister m annitol if clinical or radiographic evidence of im pending herniation
Stop seizure activity with benzodiazepines, phenytoin, and phenobarbital.
Em piric treatm ent for a toxic ingestion: o
Activated charcoal
o
Fom epizole for suspected m ethanol or ethylene glycol ingestion
Spinal tap
Correct body tem perature: o
Aggressive rewarm ing for patients with core tem perature between 32–35°C and invasive rewarm ing for Table o f C o ntents > C o njunctivitis
Conjunctivitis
Jessica Freedman
Basics Description Inflam m ation of the conjunctiva arising from a broad group of clinical causes
Etiology Bacterial
Staphylococcus aureus
Streptococcus pneum oniae
Haem ophilus influenza
Gonococcal: o
Ophthalm ic em ergency
Chlam ydia: o
Transm ission occurs via autoinoculation from genital secretions.
o
Often occurs in newborns
Viral
Adenovirus m ost com m on: o
Frequently associated with upper respiratory infections or exposure to som eone with a red eye
Herpes sim plex virus:
Pa ge 1 2 1
o
Recurrent ocular infection occurs in 25% patients within 2 years.
o
Use of steroids is contraindicated.
Allergic Frequent history of allergy, atopy, nasal sym ptom s
Contact Related
Most vision-threatening cause of “red eye―
May be owing to chem ical irritation, hypersensitivity from preservatives, m edications
Pseudom onas com m only im plicated organism : o
May be found in patients using saliva to clean contact lenses
Diagnosis Signs and Symptoms General
Red eye (conjunctival irritation)
Gritty, foreign body sensation
Discharge
Eyelid sticking (worse on arising)
Conjunctival edem a (chem osis) and eyelid edem a
Bacterial—General Mucopurulent or purulent discharge
Gonococcal
Hyperacute, copious purulent discharge: o
Discharge starts 12 hours after inoculation.
Severe chem osis
Eyelid swelling:
Pa ge 1 2 1
o
Tender preauricular lym phadenopathy
Invades intact conjunctiva and cornea within 24 hours and causes ulcerations, scarring, and perforations leading to blindness
Chlamydia
Lacrim ation
Mucopurulent discharge
With or without photophobia
Concom itant genital infection (>50%)
Transm ission occurs via autoinoculation from genital secretions.
Viral—General
Watery, m ucous discharge, lacrim ation
Gritty feeling or foreign body sensation in eye
Pinpoint subconjunctival hem orrhages: o
Tarsal conjunctiva m ay have a bum py appearance.
Herpes Simplex Virus (HSV)
Acute follicular conjunctival reaction
Skin lesions or vesicles along eyelid m argin or periocular skin
Corneal involvem ent—dendritic lesion
Herpes Zoster Virus (HZV)
Associated with pain or paresthesias of the skin
Rash or vesicles involving the distribution of cranial nerve V1
Dendritic characters on cornea
Rarely vesicles or ulcers form on the conjunctiva.
Allergic
Hallm ark: itching
Red conjunctiva
Pa ge 1 2 1
Watery discharge
Papillary hypertrophy
Frequent history of allergy, atopy, nasal sym ptom s
Contact Related Acute sym ptom s result of corneal ulceration:
Norm al visual acuity and intraocular pressures
Essential Workup
History for: o
Onset of inflam m ation
o
Environm ental or work-related exposure
o
Ill contacts
o
Sexual activity, discharge, rash
o
Use of over-the-counter m edicines or cosm etics
o
System ic diseases
Careful physical exam ination including slit-lam p exam ination including fluorescein staining
Tests Lab
Bacteriologic studies: o
Not indicated in routine cases
o
Indications:
Ophthalm ia neonatorum (except chem ical)
Suspected gonococcal ophthalm ia
Com prom ised host
Signs and sym ptom s of system ic disease
Refractory to treatm ent within 48–72 hours (with good com pliance)
Positive Gram stain for gram -negative intracellular diplococci: o
Sufficient to initiate system ic and topical treatm ent
Pa ge 1 2 2
for gonococcal disease
Rapid plasm a reagent (RPR): o
For suspected cases of sexually transm itted disease
Differential Diagnosis
Dry eye
Foreign body
Corneal abrasion
Allergies or hypersensitivity
Nasolacrim al obstruction
Anterior uveitis
Acute angle-closure glaucom a (m ost serious cause)
Scleritis or episcleritis
Subconjunctival hem orrhage
Treatment Initial Stabilization
Initiate em piric antibiotic therapy with broad-spectrum topical agent.
System ic therapy for gonococcal, chlam ydial, and m eningococcal conjunctivitis, ophthalm ia neonatorum , and all severe infections regardless of cause
Manage herpetic eye infections in consultation with an ophthalm ologist.
ED Treatment
Rem ove discharge from the eye(s): o
Contact lens wearers should discontinue use and throw away affected contact lenses.
o
Contact lens wearers should discontinue use until:
Eye is white.
Pa ge 1 2 2
Antibiotic therapy is com pleted.
No discharge for 24 hours
o
Frequent hand washing
o
No sharing of towels, tissues, cosm etics, linens
Bacterial conjunctivitis: o
Antibiotics—topical:
Can use ointm ent or drops
Continue therapy for 48 hours after clearing of sym ptom s.
Discontinue therapy and obtain cultures if no im provem ent in 48–72 hours (with good com pliance).
o
Antibiotics—system ic:
Parenteral therapy m andatory for gonococcal infection
Chlam ydia requires system ic treatm ent of sexual partners and parents of neonates.
P.253
Viral conjunctivitis: o
No specific antiviral therapy
o
Lim ited use of topical antihistam ine or decongestant
Allergic conjunctivitis (there m ay be a lag tim e of up to 2 weeks for im provem ent with these agents): o
Antihistam ine or decongestant drops (naphazoline [Naphcon-A])
o
Mast cell stabilizer/antihistam ine or nonsteroidal anti-inflam m atory drug (NSAID) ophthalm ic drops as second line
Noninfectious: o
Eye lubricant drops or ointm ent
Pa ge 1 2 2
Em piric treatm ent: o
Topical antibiotic ointm ent or drops
Medication (Drugs)
General: o
All contact lens wearers require pseudom onal coverage.
o
Bacitracin ophthalm ologic ointm ent (no pseudom onal coverage)
o
Ciprofloxacin: 0.35% 1 drop q1h–q6h (has antipseudom onal properties; m ay be used in children)
o
Erythrom ycin: 0.5% ointm ent
o
Gentam icin: 0.3% ointm ent q3h–q4h or drops q1h–q4h (has antipseudom onal coverage)
o
Sulfacetam ide: 10% 1 drop q1h–q6h (lacks pseudom onal coverage)
o
Tobram ycin ointm ent
Chlam ydia: o
Doxycycline: 100 m g PO b.i.d. for 3 weeks
o
Erythrom ycin: 500 m g PO q.i.d. for 3 weeks (peds: 50 m g/kg/d PO in four div. doses for 14 days)
o
Tetracycline: 250–500 m g PO q.i.d. for 3 weeks
Gonococcal: o
Adults:
Ceftriaxone: 1 g IV or IM daily for 3–5 days or as needed
Erythrom ycin: 500 m g PO q.i.d. for 2–3 weeks or doxycycline 100 m g PO b.i.d. for 2–3 weeks
Plus topical antibiotics as above
Pa ge 1 2 2
o
Neonates:
Penicillin G 100,000 IU/kg/d in 4 div. doses for 7 days or ceftriaxone 25–50 m g/kg/d IV for 7 days
Viral o
Artificial tears
o
Naphcon-A or Visine AC 1 or 2 drops q.i.d. PRN for no m ore than 1 week
HSV or HZV: o
Trifluorothym idine: 1% five tim es per day, or
o
Vidarabine: 3% ointm ent five tim es per day
Allergic: o
Naphazoline (Naphcon-A): 1 drop b.i.d.–q.i.d. or Visine AC
o
Acular: 1 or 2 drops b.i.d.
o
Crom olyn sodium 4% (Crolom ): 1 drop q.i.d.
Noninfectious and nonallergic: o
Eye lubricant drops or ointm ent: artificial tears or Lacri-Lube
Em piric treatm ent: o
Erythrom ycin ointm ent 0.5% (half inch q.i.d.)
o
Sulfacetam ide 10% ophthalm ic drops (1 or 2 drops q.i.d.) for 5–7 days
Pediatric Considerations
Often a m anifestation of system ic disease in infants
Neonates becom e infected during passage through the birth canal.
Gonococcal, herpetic, chlam ydial organism s m ost com m on
Ophthalm ia neonatorum is conjunctivitis within the first 4 weeks of life.
Chlam ydia trachom atis is not eradicated by silver nitrate.
Som e newborns treated with erythrom ycin still develop
Pa ge 1 2 2
conjunctivitis.
Ointm ent is preferred over drops because of difficulty with adm inistration of drops.
Follow-Up Disposition Admission Criteria Known or suspected gonococcal infection (any age group)
Discharge Criteria Close follow-up for all cases
References 1. Alteveer JG, McCans KM. The red eye, the swollen eye, and acute vision loss. Em erg Med Pract. 2002;4(6):27. 2. Bertolini J, Pelucio M. The red eye. Em erg Med Clin North Am . 1995; 13(3):561–579. 3. Kunim oto D, Kanitkar K, Makar M. The Wills Eye Manual: Office and Em ergency Room Diagnosis and Treatm ent of Eye Diseases. 4th ed. Philadelphia: Lippincott William s & Wilkins; 2004. 4. Leibowitz HM. The red eye. New Engl J Med. 2000;343:345.
Codes ICD9-CM 372.30
ICD10 H10.9
Pa ge 1 2 2
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > C o nscio us Sedatio n
Conscious
Sedation Christopher Ross
Treatment Initial Stabilization Preparation
Perform a com plete history and physical.
Have patient positioned in area with accessibility to appropriately sized resuscitation equipm ent: o
Breathing m asks, Am bu bag with m ask, oropharyngeal and nasal airways, laryngoscopes, endotracheal tubes, and stylets appropriate for size of patient
o
Defibrillator
o
Em ergency cart with all available m edications necessary to resuscitate the patient including flum azenil and naloxone
Apply cardiorespiratory m onitor, pulse oxim eter, and blood pressure m onitor.
Gather m edicines that will be used in procedure, label, and place at bedside.
Assem ble reversal agents if applicable.
Pa ge 1 2 2
Apply appropriate oxygen delivery device (cannula or m ask) and keep oxygen saturation >95%
Assem ble wall suction unit and catheters
Acquire inform ed consent.
Sedation Agents and Techniques
Can be adm inistered by various m eans (e.g., IV, IM, PO, rectal (PR), sublingual, transm ucosal, and intranasal)
Adm inister m edications and titrate to effect.
Adm inister local or regional anesthesia if applicable.
Perform the procedure.
Closely observe and m onitor patient during entire course of procedure as well as the recovery period afterwards.
Monitor patient until awake, alert, and back to baseline.
Benzodiazepines: o
Provide anxiolysis and am nesia but not analgesia, so that for painful procedures m ust not be the sole agent.
o
Midazolam is a negative inotropic and m ay induce hypotension.
o
Effects m ay be reversed with flum azenil.
o
Midazolam :
Dosage (IV): 0.05–0.15 m g/kg (single m ax. dose, 2 m g) with subsequent increm ental doses at 3-m inute intervals to desired effect or to a total of 0.2 m g/kg
Dosage (IM): 0.05–0.2 m g/kg
Dosage (PO): 0.5–0.75 m g/kg (m ax. of 15 m g)
Dosage (nasal): 0.2–0.5 m g/kg (m ax. of 5 m g)
o
Duration of action: 30–90 m inutes
Diazepam (largely replaced by shorter-acting
Pa ge 1 2 2
m idazolam ):
o
Dosage (IV): 0.1–0.2 m g/kg (m ax. 10 m g)
Dosage (PO): 0.2–0.3 m g/kg
PR: 0.5 m g/kg
Duration of action: 2–6 hours
Cautions for benzodiazepines:
Respiratory depression
Hypotension
Excessive sedation
Effects augm ented by opioids
Sedative-hypnotics: o
Chloral hydrate:
Dosage (PO): 20–100 m g/kg with usual dose of 50–75 m g/kg (m ax. 2 g)
Dosage (PR): Not recom m ended owing to erratic absorption
Duration of action: 2–4 hours (effects up to 24 hours)
Tim e of onset: 30–45 m inutes
Alert
Nausea, vom iting, and paradoxic delirium /excitem ent
Not reversible
Serious effects of airway obstruction and death have been reported. o
No analgesia
Pentobarbital: o
Dosage (IV): 2–5 m g/kg
o
Dosage (IM): 4 m g/kg
o
Duration of action: 30–60 m inutes
o
Onset: IV m ode acts within 30 seconds, and patient is appropriately sedated within 5 m inutes
o
Titrated sm all increm ental dosing:
Pa ge 1 2 2
Central nervous system and respiratory depression
No analgesia
Narcotics: o
Can be adm inistered with an anxiolytic for sedation for painful procedures
o
Fentanyl:
Dosage (IV): 1–3 µg/kg with onset in 1–3 m inutes
Transm ucosal (oral lozenge [Oralet] allows patient to suck on drug, which then can be rem oved by physician or patient when adequate sedation achieved): 10–15 µg/kg with onset in 15–20 m inutes
Duration of action: 30 m inutes
Respiratory depression
Chest wall rigidity
Use less than one-third dose in children younger than 6 m onths.
Em esis with transm ucosal preparation
Nitrous oxide: o
Provides analgesia, anxiolysis, and sedation without the need for IV placem ent
o
Adm inistered in a 50% N 2 O/O 2 concentration by inhalation:
Onset of action: 30–60 seconds and peaks at 5 m inutes
Duration of action: 3–5 m inutes after ceasing inhalation
Side effects rare
Potent sedation if previous narcotic in past 4 hours
Pa ge 1 2 2
Nausea and vom iting
Pregnancy
Pneum othorax or bowel obstruction
P.255
Ketam ine: o
Produces analgesia, am nesia, and sedation owing to its dissociative effect
o
Spontaneous respirations and airway reflexes m aintained:
Dosage (IV): 0.5–1.0 m g/kg (use m idazolam 0.05 m g/kg and atropine 0.01 m g/kg concurrently) with onset of action 5–10 m inutes
Dosage (IM): 2.0–4.0 m g/kg (com bine atropine and m idazolam in sam e syringe) with onset of action 15–25 m inutes
Dosage (PO): 5–10 m g/kg (use m idazolam 0.5 m g/kg and atropine 0.02 m g/kg) with onset of 30–45 m inutes
Duration of action: IV (15–45 m inutes); IM (30–90 m inutes); PO (60–120 m inutes)
o
Causes hypertension and tachycardia, so do not use if hypertension or cardiovascular disease
o
Increases intracranial and intraocular pressure, so do not use with head injury or penetrating globe injury
o
Stim ulates salivary and tracheobronchial secretions, so m ust be adm inistered with an anticholinergic such as atropine
o
Em ergence reactions with hallucinations reported, but are less frequent in children younger than 10
Pa ge 1 2 3
years; the incidence can be reduced by prem edicating the patient with m idazolam . o
Not for use in children younger than 3 m onths old
Propofol: o
Produces am nesia and sedation but not analgesia:
Onset of action: seconds
Dosage: 0.5–1.0 m g/kg bolus (usually given as 20-m g boluses every 10 seconds in adults until desired effect is obtained) followed by infusion of 50–75 µg/kg/m in; effective total dosages for adults range from 20–150 m g
Duration of action: Table o f C o ntents > C o nstipatio n
Constipation
Julia Sone
Basics Description Less than two bowel m ovem ents per week
Pediatric Considerations
Three percent of pediatric outpatient visits are because of defecation disorders.
Children with cerebral palsy often develop functional constipation.
Most com m on cause of fecal retention and soiling in children is functional fecal retention: o
Caused by fears associated with defecation
o
Associated with irritability, abdom inal cram ps, decreased appetite, early satiety
Etiology
Metabolic and endocrine: o
Diabetes
o
Urem ia
o
Porphyria
o
Hypothyroidism
o
Hypercalcem ia
Pa ge 1 2 3
o
Pheochrom ocytom a
o
Panhypopituitarism
o
Pregnancy
Functional and idiopathic: o
Colonic irritable bowel syndrom e
o
Diverticular disease
o
Colonic inertia
o
Megacolon/m egarectum
o
Pelvic intussusception
o
Nonrelaxing puborectalis
o
Rectocele/sigm oidocele
o
Posthysterectom y syndrom e
o
Descending perineum
Pharm acologic: o
Analgesics
o
Anesthetics
o
Antacids
o
Anticholinergics
o
Anticonvulsants
o
Antidepressants
o
Antihypertensives
o
Calcium channel blockers
o
Diuretics
o
Ferrous com pounds
o
Laxative abuse
o
Monoam ine oxidase inhibitors
o
Opiates
o
Paralytic agents
o
Parasym patholytics
o
Phenothiazines
o
Psychotropics
Neurologic:
Pa ge 1 2 3
o
Central Parkinson disease
o
Multiple sclerosis
o
Cerebrovascular accidents
o
Spinal cord lesions/injury
o
Peripheral Hirschsprung disease
o
Chagas disease
o
Neurofibrom atosis
o
Autonom ic neuropathy
Mechanical obstruction: o
Neoplasm
o
Stricture
o
Hernia
o
Volvulus
Diagnosis Signs and Symptoms
Constipation is a sym ptom , not a disease.
Passage of hard stool
Straining/difficulty passing stool
Infrequent bowel m ovem ents
Abdom inal distention/bloating
Firm /hard stool on digital rectal exam : o
May have em pty rectal vault
Diarrhea (liquid stool passes around firm feces)
Essential Workup Thorough history and physical exam :
Medical, surgical, and psychiatric investigation and date of onset
Note abdom inal distention, hernias, tenderness, or m asses
Pa ge 1 2 3
Com plete anorectal exam for anal stenosis, fissure, neoplasm , sphincter tone, perineal descent, tenderness, spasm
Tests Lab
Only necessary when considering m etabolic/endocrine disorders
CBC if inflam m atory or neoplastic origin
Electrolytes and calcium indicated if at risk of:
o
Hypokalem ia
o
Hypocalcem ia
Thyroid function test if patient appears to be hypothyroid
P.257
Imaging
Rarely indicated unless an underlying process suspected
Abdom inal radiograph:
o
Large am ount of feces in colon
o
Dilated colon
Barium enem a study: o
Diverticulosis
o
Megarectum
o
Megacolon
o
Hirschsprung disease
o
Stricture
Differential Diagnosis
See Etiology
Bowel obstruction
Pa ge 1 2 3
Treatment ED Treatment
Clean out colon: o
Enem as, suppositories
o
Manual disim paction of hard stool
o
Laxatives
Maintain bowel regim en: o
Increase noncaffeinated fluids (8–10 cups per day).
o
Increase dietary fiber intake (20 g/d).
o
Stool softeners
o
Exercise
o
Change m edications causing constipation.
Medication (Drugs)
Enem as: o
Fleet: 120 m L (peds: 60–120 m L) per rectum (PR)
o
Mineral oil: 60–150 m L (peds: 5–11 years old, 30–60 m L; older than 12 years, 60–150 m L) PR daily
o
Tap water: 100–500 m L PR
Fiber supplem ents: o
Methylcellulose: 1 tbs in cup water PO daily to t.i.d.
o
Psyllium : 1–2 tsp in cup of water/juice (peds: younger than 6 years, 1/4–1/2 tsp in 2 oz water or juice; 6–11 years, 1/2–1 tsp in 4 oz water or juice; older than 12 years, 1–2 tsp in cup water or juice) PO daily to t.i.d.
Laxatives (osm otic):
Pa ge 1 2 3
o
Lactulose: 15–30 m L (peds: 1 m L/kg) PO daily to b.i.d.
o
Polyethylene glycol: 17 g (peds: 0.8 g/kg/d dissolved in 4–8 oz of liquid) PO daily dissolved in liquid
Laxatives (stim ulant): o
Bisacodyl: 10–15 m g PO daily (peds: younger than 3 years, 5 m g PR daily; 3–12 years, 5–10 m g PO/PR daily; older than 12 years, 5–15 m g PO daily or 10 m g PR daily)
o
Cascara sagrada: 5 m L (peds: infants, 1.25 m L; 2–12 years, 2.5 m L; older than 12 years, 5 m L) PO at bedtim e on an em pty stom ach
o
Castor oil: 15–60 m L (peds: 2–12 years, 5–15 m L) PO daily; do not take at bedtim e
o
Senna: 2–4 tabs PO daily to t.i.d. (peds: 2–6 years, 1/2–1 tab PO daily to b.i.d.; 6–12 years, 1–2 tabs PO daily to b.i.d.; older than 12 years, 2–4 tabs PO daily to b.i.d.)
Stool softeners: o
Docusate sodium : 100 m g (peds: 3–5 m g/kg/d in divided doses) PO daily to b.i.d.
o
Mineral oil: 15–45 m L (peds: 5–15 m L) PO daily
Suppositories: o
Glycerin: 1 adult (peds: infant, 1 infant suppository) PR PRN
Follow-Up Disposition Admission Criteria
Pa ge 1 2 3
Patients with severe abdom inal pain, nausea, and em esis
Neurologically im paired, elderly, m orbidly obese who cannot be cleaned out in the ED or hom e
Bowel obstruction/peritonitis
Discharge Criteria
No co-m orbid illness requiring adm ission
Pain free
Adequately cleaned out
References 1. Prather C, Ortiz-Cam acho C. Evaluation and treatm ent of constipation and fecal im paction in adults. Mayo Clin Proc. 1998;73(9):881–887. 2. Rasquin-Weber A, Hym an PE, Cucchiara S, et al. Childhood functional gastrointestinal disorders. Gut. 1999; 45(suppl II):II60–II68. 3. Talley N. Differentiating functional constipation from constipation-predom inant irritable bowel syndrom e: m anagem ent im plications. Rev Gastroenterol Disord. 2005;5(1):1–9.
Codes ICD9-CM 564.0
ICD10 K59.0
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > C o ntact Derm atitis
Contact
Dermatitis Jeffrey Horton
Basics Description
Irritant: o
Eczem atous eruption (superficial inflam m atory process prim arily in epiderm is)
o
Direct injury to skin resulting in nonim m unologic inflam m atory reaction with erythem a, dryness, cracking, or fissuring
May see vesicles
Usually owing to repeated exposure to m ild irritant (e.g., water, soaps, heat, friction)
o
Lesions itch or burn:
Usually gradual onset with indistinct borders
Most often seen on hands
Allergic: o
Delayed hypersensitivity reaction (requires prior sensitization)
o
Local edem a, vesicles, erythem a, pruritus, or burning:
Pa ge 1 2 4
Usually corresponds to exact distribution of contact (e.g., watchband)
o
Onset usually within 12–48 hours with prior sensitization; m ay take 14–21 days for prim ary exposure
Pediatric Considerations
Allergic contact derm atitis is less frequent in children, especially infants, than in adults.
Major sources of pediatric contact allergy: o
Metals, shoes, preservatives or fragrances in cosm etics, topical m edications, and plants
Circum oral derm atitis: seen in infants and sm all children; m ay result from certain foods (irritant or allergic reaction)
Etiology
Irritant (80% of contact derm atitis), for exam ple: o
Soaps, solvents
o
Chem icals
o
Certain foods
o
Urine, feces
o
Continuous or repeated exposure to m oisture (hand washing)
o
Course paper, glass, wool fibers
Allergic, for exam ple: o
Plants, poison ivy, oak, sum ac (rhus derm atitis):
Com m on form of allergic contact derm atitis
Direct: reaction to oleoresin from plant
Indirect: contact with pet or clothes with oleoresin on surface or fur or in sm oke from burning leaves
Lesions m ay appear up to 3 days after exposure with prior sensitization (12–21 days after
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prim ary exposure) and m ay persist up to 3 weeks.
Fluid from vesicles is not contagious and does not produce new lesions.
o
Cem ent (prolonged exposure m ay result in severe alkali burn)
o
Metals (especially nickel)
o
Solvents, epoxy
o
Chem icals in rubber (e.g., elastic waistbands) or leather
o
Lotions, cosm etics
o
Topical m edications (e.g., neom ycin, hydrocortisone, benzocaine, paraben)
o
Som e foods
Shoe derm atitis: o
Com m on; identify by lesions lim ited to distal dorsal surface of foot usually sparing the interdigital spaces
Photoderm atitis: o
Inflam m atory reaction from exposure to irritant (frequently plant sap) and sunlight
Diagnosis Signs and Symptoms History
Date of onset
Tim e course
Pattern of lesions
Relationship to work
New products (e.g., lotions and cosm etics), m edications,
Pa ge 1 2 4
and jewelry
Physical Exam
Special attention to character and distribution of rash
Acute lesions: skin erythem a and pruritus: o
May see edem a, papules, vesicles, bullae, serous discharge, or crusting
Subacute: vesiculation less pronounced
Chronic lesions: m ay see scaling, lichenification, pigm entation, or fissuring with little to no vesiculation; m ay have characteristic distribution pattern
Tests Lab No specific tests in ED are helpful.
Imaging No specific tests in ED are helpful.
Diagnostic Procedures/Surgery
Patch testing: o
Generally not done in ED; refer to subspecialist.
When tinea is suspected, m ay use Wood lam p for fluorescence
Differential Diagnosis
Atopic derm atitis: associated with fam ily history of atopy
Seborrheic derm atitis: scaly or crusting “greasy― lesions
Num m ular derm atitis: coinlike lesions
Intertrigo: derm atitis in which skin is in apposition
Infectious eczem atous derm atitis: derm atitis with secondary bacterial infection, usually Staphylococcus aureus
Cellulitis: warm , blanching, painful lesion
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Im petigo: yellow crusting
Scabies: intensely pruritic, frequently interdigital with tracks
Psoriasis: silvery adherent, scaling, lesions well delineated, affecting extensor surfaces, scalp, and genital region
Herpes sim plex: groups of vesicles, painful, burning
Herpes zoster: painful, follows derm atom al pattern
Bullous pem phigoid: diffuse bullous lesions
Tinea: m axim al involvem ent at m argins, fluoresces under Wood lam p
Pityriasis alba: discrete, asym ptom atic, hypopigm ented lesions
Urticaria: pruritic raised lesions (wheal) frequently with surrounding erythem a (flare)
Acroderm atitis enteropathica: vesiculobullous lesion of hands and feet, associated with failure to thrive, diarrhea, and alopecia
Letterer-Siwe tum or (Langerhans cell histiocytosis): o
Associated with hepatosplenom egaly and adenopathy
Dyshidrotic derm atitis (eczem a)
P.259
Treatment Initial Stabilization Rarely required in absence of concom itant pathology
ED Treatment
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General
Prim arily sym ptom atic
Wash area with m ild soap and water
Rem ove or avoid offending agent (including washing clothes)
Cool, wet com presses; especially effective during acute blistering phase
Antipruritic agents: o
Topical:
Calam ine lotion, corticosteroids (do not penetrate blisters); avoid benzocaine or hydrocortisone-containing products, which m ay further sensitize skin.
o
System ic: antihistam ines, corticosteroids
Alum inum acetate (Burrows) solution: weeping surfaces
Irritant Dermatitis
Rem ove offending agent
Decrease wet/dry cycles (hand washing)
Bland em ollient
Topical steroids for severe cases (ointm ent preferred) m edium to high potency (hands) b.i.d. for several weeks
Allergic Dermatitis
Topical steroids (ointm ent preferred) b.i.d. 2–3 weeks: o
Face: low potency
o
Arm s, legs, trunk: m edium potency
o
Hands and feet: high potency
Oral steroids for severe cases
Rhus Dermatitis
Follow general m easures plus: o
Aseptic aspiration of bullae m ay relieve discom fort.
Pa ge 1 2 4
o
Severe reaction: system ic corticosteroids for 2–3 weeks with gradual taper:
Prem ature term ination of corticosteroid therapy m ay result in rapid rebound of sym ptom s.
Shoe Dermatitis Follow general m easures plus:
Wear open-toe, canvas, or vinyl shoes.
Control perspiration: change socks, use absorbent powder.
Medication (Drugs) Systemic
Antihistam ine (H 1 -receptor antagonist, first and second generation)
Cetirizine (Zyrtec): adult and children older than 6 years, 5–10 m g PO daily (peds: age 2–6 years, 2.5 m g PO daily to b.i.d.) o
Diphenhydram ine hydrochloride (Benadryl): 25–50 m g IV/IM/PO q6h PRN (peds: 5 m g/kg/24h div. q6h PRN)
o
Fexofenadine (Allegra): 60 m g PO b.i.d. or 180 m g PO daily (peds: age 6–12, 30 m g PO b.i.d.)
o
Hydroxyzine hydrochloride (Atarax): 25–50 m g PO IM up to q.i.d. PRN (peds: 2 m g/kg/24h PO div. q.i.d. or 0.5 m g/kg IM q4h–q6h PRN
o
Loratadine (Claritin): 10 m g PO b.i.d.
o
For refractory pruritus: doxepin: 75 m g daily m ay be effective.
Corticosteroid: o
Prednisone: 40–60 m g PO daily (peds: 1–2 m g/kg/24h, m ax. 80 m g/24h) div. daily/b.i.d.
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Topical
Alum inum acetate (Burrows) solution: Apply topically for 20 m inutes t.i.d. until skin is dry.
Calam ine lotion: q.i.d. PRN
Topical corticosteroid
Triam cinolone: ointm ent 0.025, 0.1%; cream 0.025, 0.1%; lotion 0.025, 0.1% t.i.d. or q.i.d.
Follow-Up Disposition Admission Criteria Rarely indicated unless severe system ic reaction or significant secondary infection
Discharge Criteria
Sym ptom atic relief
Adequate follow-up with prim ary care physician (PCP) or derm atologic specialist
References 1. Habif TP. Skin Disease Diagnosis and Treatm ent. 2nd ed. China: Mosby; 2005. 2. Habif TP. Clinical Derm atology. St Louis, MO: Mosby; 1996: 81–99. 3. Hurwitz S. Clinical Pediatric Derm atology. Philadelphia: WB Saunders; 1993: 68–82. 4. Juckett G. Plant derm atitis. Postgrad Med 1996;100(3):159–171. 5. White IR. Occupational derm atitis. Br Med J. 1996;313:487–489. 6. Wolf R, Wolf D. Contact derm atitis. Clin Derm atol. 2000;18(6):661–666.
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > C o r Pulm o nale
Cor Pulmonale
Jedd E. Roe
Basics Description
Ventricular failure confined to the right ventricle: o
Right ventricular hypertrophy or dilation is an adaptive response to pulm onary hypertension, which predom inately occurs as a result of alveolar hypoxia.
The pulm onary circulation is a low-resistance, low-pressure system : o
The pulm onary arteries are thin walled and distensible.
o
Mean pulm onary arterial pressure is usually 12–15 m m Hg
o
Norm al left-arterial pressure is 6–10 m m Hg.
o
The resulting pressure difference driving the pulm onary circulation is only 6–9 m m Hg.
Three factors affect pulm onary arterial pressure: o
Cardiac output
o
Pulm onary venous pressure
o
Pulm onary vascular resistance
Pulm onary hypertension can arise through a num ber of m echanism s:
Pa ge 1 2 4
o
A m arked increase in cardiac output
o
Left-to-right shunt secondary to congenital heart disease
o
Hypoxia:
Most com m only causes pulm onary vascular resistance to increase
The resulting hypercapnia and acidosis induce additional vasoconstriction.
Pulm onary venous pressure increases.
A com pensatory rise is seen in the pulm onary arterial system so flow is m aintained across the pulm onary vascular bed.
o
Pulm onary em bolus causes a sim ilar change by increasing resistance to pulm onary blood flow.
o
Left ventricular failure achieves the sam e result by directly influencing pulm onary venous pressure.
o
Dram atic rises in blood viscosity or intrathoracic pressure im pede blood flow.
Functional classification of pulm onary arterial hypertension based on New York Heart Association criteria: o
Class I—Pulm onary arterial hypertension without lim itation of physical activity
o
Class II—Pulm onary arterial hypertension resulting in slight lim itation of physical activity (e.g., ordinary activity causes sym ptom s such as dyspnea on exertion)
o
Class III—Pulm onary arterial hypertension resulting in m arked lim itation of physical activity (e.g., less than ordinary activity causes sym ptom s such as dyspnea on exertion)
o
Class IV—Pulm onary arterial hypertension resulting in an inability to carry out any physical activity
Pa ge 1 2 5
without sym ptom s (signs of cor pulm onale are present)
Incidence
Approxim ately 86,000 patients die from chronic obstructive pulm onary disease (COPD) each year: o
Associated right ventricular failure is a significant factor in m any of these cases.
In patients older than 50 years with COPD, 50% develop pulm onary hypertension and are at risk of developing cor pulm onale.
The course of cor pulm onale is generally related to the progression of the underlying disease process.
Once biventricular failure is noted, life expectancy is usually 16–18 m m )
An enlarged right-ventricular silhouette
Shows abnorm alities in >90% of patients in the detection of cor pulm onale, but does not indicate the severity of disease
Pleural effusions do not occur in the setting of cor pulm onale alone.
ECG o
Right-axis deviation
o
Tall, peaked P waves (P pulm onale)
o
Right-ventricular hypertrophy (specific not sensitive)
o
Transient changes due to hypoxia
o
Right precordial T-wave flattening
o
ST-segm ent depression in segm ents II, III, and arteriovenous fistula
Echocardiography—the noninvasive diagnostic m ethod of choice: o
Right ventricular dilation or hypertrophy in the
Pa ge 1 2 5
setting of norm al left ventricular dim ensions o
Assessm ent of tricuspid regurgitation
o
Doppler quantization of pulm onary artery pressure, right ventricular ejection fraction
Ventilation/perfusion scans or pulm onary angiography: o
Useful in the setting of acute cor pulm onale
CT or MRI: o
Delineates size and shape of the ventricles and pulm onary arteries
o
Detection of larger pulm onary em boli
Right heart catheterization: o
The m ost precise estim ate of pulm onary vascular hem odynam ics
o
Gives accurate m easurem ents of pulm onary arterial pressure and pulm onary capillary wedge pressure
Differential Diagnosis
Prim ary disease of the left side of the heart
Congenital heart disease
Hypothyroidism
Cirrhosis
P.261
Treatment Pre Hospital
Supportive therapy: o
Supplem ental oxygen
To an endpoint of 90% arterial saturation:
Pa ge 1 2 5
o
IV access
o
Cardiac m onitoring
o
Pulse oxim etry
Treat bronchospasm from associated respiratory disease: o
β-agonist nebulizers
Caution: o
Vasodilators and diuretics do not have a role in the field.
o
Severely hypoxic patients m ay require ETT intubation
Initial Stabilization ED therapy is directed at the underlying disease process and reducing pulm onary hypertension.
ED Treatment
Supplem ental oxygen sufficient to raise arterial saturation to 90%: o
Im proving oxygenation reduces pulm onary arterial vasoconstriction and right ventricular afterload.
o
The im proved cardiac output enhances diuresis of excess body water.
o
Care m ust be taken to m onitor the patient's ventilatory status and PCO 2 , as hypercapnia m ay reduce respiratory drive and cause an acidosis.
Diuretics, such as furosem ide, m ay be added cautiously to reduce pulm onary artery pressure by contributing to the reduction of circulating blood volum e.
Patients should be m aintained on salt and fluid restriction.
There is no role for digoxin in the treatm ent of cor pulm onale.
Bronchodilator therapy is particularly helpful for those patients with COPD: o
Selective β-adrenergic agents such as subcutaneous
Pa ge 1 2 5
terbutaline 0.25 m g SC o
Bronchodilator affects and reduces ventricular afterload.
o
Theophylline m ay play a role to im prove diaphragm atic contractility and reduce m uscle fatigue.
While controversial, anticoagulation in the form of warfarin has been recom m ended to m aintain a target international norm alized ratio between 1.5–2.5.
In the future, nitric oxide adm inistration for patients with severe disease m ay becom e an adjunctive therapy initiated in the ED.
Acutely decom pensated COPD patients: o
Early steroid therapy
o
Antibiotic adm inistration
In general, im provem ent in the underlying respiratory disease results in im proved right ventricular function.
Medication (Drugs)
Furosem ide: 20–60 m g IV (peds: 1 m g/kg m ay increase by 1 m g/kg/q2h not to exceed 6 m g/kg)
Terbutaline: 0.25 m g SC
Follow-Up Disposition Admission Criteria
New-onset hypoxia
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Anasarca
Severe respiratory failure
Adm ission criteria for the underlying disease process
Discharge Criteria
Patients without hypoxia or a stable oxygen requirem ent
Close follow-up as long as the underlying etiology has responded to acute m anagem ent
References 1. Braunwald E. Heart Failure and Cor pulm onale. In: Kasper D, et al, eds. Harrison's textbook of m edicine. 16th ed. New York: McGraw-Hill, 2005: 1355–1359. 2. Hum bert M, Sitbon O, Sim onneau G. Treatm ent of Pulm onary Arterial hypertension. N Engl J Med. 2004;351:14:1425–1436. 3. Schwam E. B-Type Naturietic Peptide for Diagnosis of Heart failure in Em ergency Departm ent Patients: A Critical Appraisal 4. Weitzenblum E. Chronic Cor Pulm onale. Heart. 2003;89:225–230.
Codes ICD9-CM 415.0 415.1 416 416.0 416.1 416.8 416.9
ICD10 I27.9 I26.0
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > C o rneal Abrasio n
Corneal Abrasion
Kevin Kern
Basics Description
Traum atic desquam ation of portions of corneal epithelium
Focal epithelial loss secondary to rem oval of corneal foreign body
Previous corneal transplant, corneal surgery, or radial keratotom y: o
Predisposes patient to m ore severe injury after m inor traum a to eye
Etiology
Contusive force
Direct contact injury: o
Hum an fingernail
o
Branches
o
Fingers/toes
o
Hairbrushes/com bs
o
Sand/stones
o
Metallic object
o
Snow
o
Pens/pencils
o
Toys
Pa ge 1 2 5
o
Activated charcoal
o
Airbag deploym ent
Mechanical action of eyelid: o
Blinking or rubbing eye with loose foreign body (scratches on windshield)
Projectiles at high speeds (m etal workers): o
Carefully exam ine for globe perforation (Seidel test positive, teardrop pupil)
Poorly fitting contact lens or prolonged contact lens use: o
Extended-wear soft contact lenses increase infection rate 10–15% over daily-wear contact lenses.
Pediatric Considerations
Signs and sym ptom s m ay differ: o
Excessive crying
o
Conjunctival erythem a
o
Tearing
o
Eye rubbing
o
Lid edem a
o
Grunting respiration
Younger than 12 m onths: o
Frequently no history of eye traum a
o
Often no eye signs
Older than 12 m onths: o
More often will have history of m inor eye traum a
o
Positive eye signs
o
No excessive crying
Com pression injuries to cornea associated with birth: o
Localized edem a
o
Corneal clouding
o
Clear within hours
Pa ge 1 2 5
Diagnosis Signs and Symptoms
Severe ocular pain
Tearing/ocular discharge
Blepharospasm
Foreign body sensation
Photophobia
Conjunctival injection
Blurred vision
Headache
Essential Workup
History: o
Past ocular traum a
o
Ocular/periocular surgery
o
Pre-existing visual im pairm ent
o
Glasses
o
Contact lens use (extended wear has increased risk of corneal ulcer)
o
Tim e of onset
o
Associated sym ptom s
o
Treatm ent before visit
o
Use of safety glasses (pounding, drilling, grinding m etal)
o
System ic disease (diabetes, autoim m une disorders)
Com plete eye exam : o
Visual acuity
o
Evert upper lids to check for retained foreign body
o
Bright white light for visual inspection of cornea to rule out infiltrate/edem a/loss of corneal luster
Pa ge 1 2 6
o
Slit-lam p to evaluate anterior segm ent and depth of abrasion
o
Fluorescein to identify area of dam aged corneal epithelium :
Dam aged area appears bright green using blue Wood lam p.
o
Funduscopic exam ination of retina and m acula
Tests Pediatric Considerations Handheld slit-lam p and Wood lam p: helpful in exam ination of pediatric eye
Differential Diagnosis
Herpes sim plex virus keratitis
Recurrent corneal erosion syndrom e
Ultraviolet keratitis (snow blindness)
Corneal ulcer
Corneal dystrophy (inherited)
More extensive injury than corneal abrasion: o
Laceration of cornea
o
Perforation of cornea
o
Hyphem a
o
Iris prolapse
o
Lens disruption
Treatment Initial Stabilization
Instill topical anesthetic (proparacaine/tetracaine).
Consider cycloplegic for intense pain owing to ciliary
Pa ge 1 2 6
spasm (hom atropine 5%).
ED Treatment
Exam ination
Rem oval of superficial foreign body
Pain control (topical/oral):
o
Diclofenac (topical)
o
Ketorolac (topical)
o
Oral narcotics
o
Cool com presses
Cycloplegic (optional): o
Cyclopentolate (m ydriasis 1–2 days)
o
Tropicam ide (m ydriasis 6 hours)
o
Hom atropine 5%
P.263
Antibiotic ointm ent/drop options: o
Ciprofloxacin
o
Erythrom ycin
o
Gentam icin
o
Sulfacetam ide
o
Tobram ycin/TobraDex
o
Contact lens wearers m ust be covered for Pseudom onas:
Use am inoglycoside or quinolone.
Eye patch: o
Controversial regarding efficacy
o
No patch required for sm all abrasions
o
Never patch contact lens-related injury.
o
Never patch infection-prone injury:
Fingernail
Vegetable m atter
Pa ge 1 2 6
o
Rem oval of wood particles
Patch non–contact lens–related abrasions >10 m m 2 only or recurrent corneal erosions
o
Collagen shields/soft bandage contact lenses (currently under investigation)
Disadvantages of patching: o
Rem oves binocular vision/reduces visual field
o
Uncom fortable
o
Increases corneal tem perature
o
Decreases corneal oxygenation
o
Slows re-epithelialization
o
Decreases tear exchange
o
Prolongs healing
Tetanus prophylaxis: o
When contam inants include dirt, fecal m aterial, or saliva
o
Routine tetanus not necessary
Medication (Drugs)
Ciprofloxacin: 0.35% 1 drop q.i.d.
Cyclopentolate: 0.5%, 1.0%, or 2.0% drops (m ydriasis 1 or 2 drops t.i.d.)
Diclofenac: 0.1% drops 1 drop q.i.d.
Erythrom ycin: 0.5% ointm ent q.i.d.
Gentam icin: 0.3% ointm ent q.i.d.
Gentam icin: 0.3% 2 drops q6h
Hom atropine: 5% solution 2 drops b.i.d.
Ketorolac: 0.5% drops 1 drop q.i.d.
Proparacaine: 0.5% 1 drop once
Sulfacetam ide: 10% drops 2 drops q.i.d.
Sulfacetam ide: 10% ointm ent q.i.d.
Pa ge 1 2 6
TobraDex: suspension 0.1%/0.3% 2 drops q4h–q6h
Tobram ycin: 0.3% drops 2 drops q6h
Tobram ycin: 0.3% ointm ent q6h
Tropicam ide: 0.5%, 1.0% drops (m ydriasis 6 hours) 1 drop q4h
Follow-Up Disposition Admission Criteria Associated injuries requiring adm ission
Discharge Criteria
All sim ple corneal abrasions
Follow-up in 24–48 hours with ophthalm ologist for re-exam ination and ongoing care
Follow-up with ED when access to specialist is lim ited
Issues for Referral All corneal burns should be referred to ophthalm ologist within 12–24 hours.
References 1. Alteveer JG, McCans KM, eds. The red eye, the swollen eye, and acute visual loss. Em erg Med Pract. 2002:4(6). 2. Calder LA, Fergusson D. Topical nonsteroidal anti-inflamm atory drugs for corneal abrasions: Meta-analysis of random ized trials. Acad Em erg Med. 2005;12:467–473. 3. Khaw PT, Shah P, Elkington AR. Injury to the eye. Br Med J. 2004;328:36–38. Available at http://www.bm j.com . 4. Le Sage N, Verreault R, Rochette LM. Efficacy of eye patching for traum atic corneal abrasions. Ann Em erg Med. 2001;38:129–134.
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5. Micheal JG, Hug D, Dowd MD. Managem ent of corneal abrasions in children: a random ized clinical trial. Ann Em erg Med. 2002;40:67–72. 6. Mukherjee P, Sivakum ar A, Mackway-Jones K. Tetanus prophylaxis in superficial corneal abrasions. Em erg Med J. 2003;20:62–64. 7. Upadhyay MP, Karm acharya PC, Koirala S, et al. The Bhaktapur eye study: ocular traum a and antibiotic prophylaxis for the prevention of corneal abrasions in Nepal. Br J Ophthalm ol. 2001;85:388–392. 8. Weavers CS, Terrell KM. Evidence based em ergency m edicine. Update: do ophthalm ic nonsteroidal anti-inflam m atory drugs reduce the pain associated with sim ple corneal abrasions without delaying healing? Ann Em erg Med. 2003;41:134–140.
Miscellaneous SEE ALSO: Red Eye
Codes ICD9-CM 918.1 Corneal abrasion 370.00 Corneal ulcer, unspecified 930.9 Eye foreign body, external, unspecified
ICD10 S05.0
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > C o rneal Burn
Corneal Burn
Kevin Kern
Basics Description
Inappropriate exposure of cornea to chem icals, heat, cold, electrical, or radiant energy causing dam age to the cornea and often extending to adjacent structures
Severity of injury related to duration of exposure, type of agent, anion concentration, pH level of solution
Alkalis: o
Cause im m ediate rise in pH level
o
Highly soluble in lipids, so rapidly penetrate the eye, causing severe corneal injury and continue to penetrate over tim e if no intervention undertaken
o
Penetration can occur in Table o f C o ntents > C o rneal F o reign Bo dy
Corneal Foreign
Body David A. Harter
Basics Description
Com m on com plaint: Som ething fell, flew, or otherwise landed in m y eye. o
Hot, high-speed projectiles m ay not produce pain initially.
Corneal epithelium disrupted: o
Abrasion if only epithelium disrupted
o
Scar if deeper layers of cornea involved
Etiology
Poorly tolerated: o
Organic m aterial (plant m aterial, insect parts)
o
Inorganic m aterial that oxidizes (iron, copper)
Well tolerated: o
Inert objects (paint, glass, plastic, fiberglass, nonoxidizing m etals)
Pa ge 1 2 7
Diagnosis Signs and Symptoms
Foreign body sensation
Eye pain
Conjunctiva and sclera injection
Tearing
Blurred or decreased vision
Photophobia
Visible foreign body or rust ring
Iritis
Essential Workup
Injury history to determ ine type of foreign body and likelihood of perforation
Com plete eye exam : o
Visual acuity
o
Visual fields
o
Extraocular m ovem ents
o
Lids and lashes
o
Pupils
o
Sclera
o
Conjunctiva
o
Fundi:
Slit-lam p
Fluorescein exam
Perform Seidel test (visualization of flow of aqueous through corneal perforation during fluorescein slit-lam p exam ination)
Intraocular pressure if no evidence of perforation
Exclude intraocular foreign body: o
Suspect intraocular foreign body with high-speed
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m echanism s such as m achine operated or ham m ering m etal on m etal.
Tests Imaging
Ocular CT or B-m ode ultrasound (US) when suspect intraocular foreign body
Orbital plain radiograph to screen for intraocular m etallic foreign body
Differential Diagnosis
Conjunctival foreign body
Corneal abrasion
Corneal perforation with or without intraocular foreign body
Corneal ulcer
Keratitis
Treatment Pre Hospital Place a Fox shield and position the patient upright.
Initial Stabilization Apply topical anesthetic to stop eye discom fort and assist in exam ination.
ED Treatment
Deep foreign bodies: o
Refer those penetrating the Bowm an m em brane (next layer under epithelium ) to an ophthalm ologist, because perm anent scarring m ay occur.
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Superficial foreign bodies: o
Irrigation rem oval technique:
Apply topical anesthetic
Try to wash foreign body off cornea by directing a stream of 0.9% norm al saline (NS) at an oblique angle to cornea.
o
25-gauge needle or foreign-body (FB) spud rem oval technique:
Using slit-lam p to im m obilize patient's head and allow good visualization.
Hold needle (bevel up) with thum b and forefinger, allowing other fingers to be stabilized on the patient's cheek.
Lift foreign body off cornea, keeping needle parallel to corneal surface.
Rust rings rem oval: o
Within 3 hours, iron-containing foreign bodies oxidize, leaving a rust stain on adjacent epithelial cells.
o
Rem oval recom m ended as rust rings delay healing and act as an irritant focus
o
Rem ove with needle or pothook burr either at sam e tim e as foreign body or delayed 24 hours
P.267
Postrem oval therapy: o
Recheck Seidel test to exclude corneal perforation.
o
Treat resultant corneal abrasion with antibiotic drops.
o
Initiate cycloplegic agent when suspect presence of keratitis.
o
Update tetanus.
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o
Initiate analgesia (nonsteroidal anti-inflam m atory drug [NSAID] or acetam inophen with codeine).
Pediatric Considerations May require sedation to facilitate exam and foreign body rem oval
Medication (Drugs)
Cyclopentolate 1–2%: 1 drop t.i.d. (lasts up to 2 days)
Gentam icin ophthalm ic: 2 drops q6h
Hom atropine 2% or 5%: 1 drop daily (lasts up to 3 days)
Sulfacetam ide 10%: 1 drop q6h
Tobram ycin ophthalm ic: 2 drops q6h
Follow-Up Disposition Admission Criteria Globe penetration
Discharge Criteria
All corneal foreign bodies
Ophthalm ologist follow-up in 24 hours for: o
Rust ring rem oval
o
Vegetative m aterial rem oval owing to risk of ulceration
References 1. Khaw P, Shaw P, Elkington A. ABC of eyes. Injury to the eye. Br Med J. 2004;328:36–38. 2. Levine L. Pediatric ocular traum a and shaken infant syndrom e. Pediatr Clin N Am . 2003;50:137–148.
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3. Rhee D, Pyfer M. The Wills eye m anual: office and em ergency room diagnosis and treatm ent of eye disease. 3rd ed. Philadelphia: Lippincott William s & Wilkins; 1999:24–26. 4. Santen S, Scott J. Ophthalm ologic procedures. Em erg Med Clin North Am . 1995;13(3):681–694.
Codes ICD9-CM 930
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > C o ugh
Cough
Alison K. Sisitsky
Basics Description
A sudden spasm odic contraction of the thoracic cavity resulting in violent release of air from the lungs and usually accom panied by a distinctive sound: o
Deep inspiration
o
Glottis closes
o
Expiratory m uscles contract
o
Intrapulm onary pressures increase
o
Glottis opens
o
Air expiration at high pressure
o
Secretion and foreign m aterial excretion
o
Vocal cord vibration with tracheobronchial walls, lung parenchym a, and secretions
Defense m echanism to clear the airway of foreign m aterial and secretions: o
Voluntary or involuntary
o
Reflex involves respiratory tissue receptor activation of afferent neurons to the central cough center followed by efferent output to the respiratory m uscles.
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o
Mechanical receptors in larynx, trachea, and carina sense touch and displacem ent.
o
Chem ical receptors in larynx and bronchi are sensitive to gases and fum es.
o
Activated by irritants, m ucus, edem a, pus, and therm al stim uli.
Etiology
Acute—8 weeks: o
Postnasal drip
o
Asthm a
o
Gastroesophagal reflux disease (GERD)
o
Chronic bronchitis
o
Bronchiectasis
o
Eosinophilic bronchitis
o
Angeotestin converting enzym e (ACE) inhibitor use
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o
Bronchogenic carcinom a
o
Carcinom atosis
o
Sarcoidosis
o
Left ventricular failure
o
Aspiration syndrom e
o
Psychogenic/habit
Diagnosis Signs and Symptoms History
Sputum production: o
Frothy (pulm onary edem a)
o
Mucopurulent
o
Suggestive of bacterial pneum onia or bronchitis but also seen with viral infections
o
Rust colored (pneum ococcal pneum onia)
o
“Currant jelly― (Klebsiella pneum onia)
o
Hem optysis
Posttussive syncope or em esis (suggests pertussis)
Shortness of breath
Chest pain
Chills/fever
Night sweats
Wheezing
GERD: o
Heartburn
o
Dysphagia
o
Regurgitation
o
Belching
Pa ge 1 2 8
o
Early satiety
Malignancy: o
Weight loss
o
Poor appetite
o
Fatigue
Physical Exam
Vital signs
Abnorm al breath sounds: o
Absence or decreased: reduced airflow vs. overinflation
o
Rales (crackles): popping or rattling when air opens closed alveoli
o
Moist, dry, fine, coarse
Rhonchi: snoringlike sounds when large airways are obstructed
o
Wheezes: high-pitched sounds produced by narrowed airways
o
Stridor: upper airway obstruction
Evidence of respiratory distress: o
Use of accessory m uscles
o
Abdom inal breathing
Essential Workup
Com plete m edical history: o
Duration
o
Associated sym ptom s
o
Sm oking exposure
o
ACE inhibitor use
o
HIV/Im m unocom prom ised state
o
Potential exposure to tuberculosis
ECG: o
History of cardiac disease
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o
Associated chest pain or abnorm al vital signs
o
Lack of infectious sym ptom s
Tests Lab Order according to presenting signs and sym ptom s:
WBC count with differential
Sputum gram stain, cultures, and sensitivities
Acid fast bacilli (AFB) culture
CD4 count
Pertussis titers
D-dim er
Imaging
Chest radiograph: o
For im m unosuppressed patient
o
Abnorm al lung sounds on exam
o
Ill appearing
o
Change in chronic cough
o
Continued cough after discontinuation of ACE inhibitor
CT of chest: o
Abnorm al chest radiograph
o
Assess for pulm onary em bolism
P.269
Diagnostic Procedures/Surgery
Peak flow
Bronchoscopy: o
For unknown m ass on chest radiograph
o
Hem optysis
o
Suspected cancer
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Differential Diagnosis See Etiology
Pediatric Considerations
Most frequent causes: o
Asthm a
o
Sinusitis
o
GERD
Less com m on causes: o
Tracheobronchom alacia
o
Mediastinal tum or
o
Acyanotic congenital heart disease
o
Ventricular septal defect
o
Patent ductus arteriosus
o
Pulm onary stenosis
o
Tetralogy of Fallot
o
Lodged foreign body
o
Chronic aspiration of m ilk
o
Environm ental exposure
Consider: o
Neonatal history
o
Feeding history
o
Growth and developm ental history
o
Allergies
o
Eczem a
o
Sleep disorders
Indications for chest radiograph: o
Suspicion of foreign body ingestion
o
Suspect aspiration
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Treatment Initial Stabilization Assess airway, breathing, and circulation.
ED Treatment Specific treatm ent related to cause:
Respiratory infection: Consider antibiotics, decongestants, and antitussives.
Asthm a: inhaled β 2 -agonist and steroid
GERD: H 2 -blockers, proton pum p inhibitors, and antacids
Malignancy: supportive care
Medication (Drugs)
Antitussives: o
Benzonatate (Tessalon Perles): 100–200 m g PO q6h
o
Codeine: 10–20 m g (peds: 1–1.5 m g/kg/d) PO q4h–q6h
o
Dextrom ethorphan: 10–20 m g (peds: 1 m g/kg/d) PO q6h–q8h
o
Hydrocodone: 5–10 m g (peds: 0.6 m g/kg/d q6h–q8h) PO q6h–q8h
Bronchodilators: o
Albuterol: 2.5 m g in 2.5 NS (peds: 0.1–0.15 m g/kg/dose q20 m in) q20m in inhaled
o
Ipratropium : 0.5 m g in 3 m L NS (peds: nebulizer 250–500 µg/dose q6h) q3h
Decongestants: o
Chlorpheniram ine: 4–12 m g (peds: 2 m g PO q4–6h) PO q4h–q12h
o
Phenylpropanolam ine: 25–50 m g (peds:
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6.25–12.5 m g PO q4h) PO q4h–q8h
Mucolytics: o
Guaifenesin: 5–20 m L (peds: 5–10 m L/dose if older than 6 years; 2.5–5 m L/dose if younger than 6 years) PO q4h
Steroids: o
Dexam ethasone: 2 sprays/nostril b.i.d.
o
Methylprednisolone: 60–125 m g IV (peds: 1–2 m g/kg/dose IV/PO q6h)
o
Prednisone: 40–60 m g (peds: 1–2 m g/kg/d q6h–q12h) PO
Follow-Up Disposition Admission Criteria
Hypoxem ia or critical illness
Suspected tuberculosis with positive chest radiograph result
Im m unocom prom ised with fever
Risk of bacterem ia or sepsis
Discharge Criteria
Oxygenation at baseline for patient
Oral m edications
Safe environm ent at hom e
References 1. Barkin R, Rosen P. Em ergency Medicine: Concepts and Clinical Practice. 4th ed. St. Louis, MO: Mosby-Year Book Inc., 1998. 2. Irwin RS. Managing cough as a defense m echanism and as a
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sym ptom . Chest. 1998;114(2):133S–181S. 3. Irwin RS. Prim ary care: the diagnosis and treatm ent of cough. N Engl J Med. 2000;343(23):1715–1721. 4. http://www.nlm .nih.gov/m edlineplus
Codes ICD9-CM 786.2
ICD10 R05
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > C ro up
Croup
Dale W. Steele
Basics Description
Viral infection of the upper and lower respiratory tract
Most com m only presents in children 6 m onths to 3 years: o
Laryngotracheitis/laryngotracheo-bronchitis
o
Inspiratory stridor owing to extrathoracic airway obstruction
o
Expiratory wheeze suggests lower airway involvem ent.
o
Inflam m atory edem a of subglottic region
o
Narrowest part of pediatric airway
May progress to respiratory failure
Spasm odic croup: o
Sudden onset at night without viral prodrom e
o
Consistent response to m ist or cool night air
o
Often recurrent
o
May represent allergic reaction to viral antigen
Etiology
Parainfluenza types 1, 2, and 3
Influenza A and B
Adenoviruses
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Respiratory syncytial virus
Measles
Mycoplasm a pneum oniae
Herpes sim plex
Diagnosis Signs and Symptoms History
Nonspecific upper respiratory prodrom e with or without fever
Duration of illness: o
Prior airway m anipulation
o
Possibility of foreign body aspiration
Previous episodes
Im m unization status (Haem ophilus influenzae Type b [HIB]; diphtheria, pertussis, and tetanus [DPT])
Physical Exam
Toxic appearing?
Preferred position?
Quality of cry/voice?
Drooling/trism us/lim ited neck extension?
Mental status
Stridor at rest, increased work of breathing?
Hydration status:
Westley croup score (m axim um total points: 17) o
Stridor (inspiratory or biphasic)
0 = None
1 = Audible with stethoscope at rest
2 = Audible without stethoscope at rest
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o
o
o
o
Retractions:
0 = None
1 = Mild
2 = Moderate
3 = Severe
Air entry:
0 = Norm al
1 = Decreased
2 = Severely decreased
Cyanosis:
0 = None
4 = With agitation
5 = At rest
Level of consciousness:
0 = Norm al
5 = Altered
Essential Workup N/A
Tests Lab
Pulse oxim etry
Other tests are not routinely indicated.
Imaging Anteroposterior (AP) and lateral neck radiographs:
Steeple sign indicates narrowing of subglottic trachea.
Not routinely indicated, unless atypical presentation or clinical course
Subject to m isinterpretation
Should not delay definitive visualization and intubation in OR in child with concern for epiglottitis or bacterial
Pa ge 1 2 9
tracheitis
Monitor child during im aging, if done.
Differential Diagnosis
Infection: o
Bacterial tracheitis
o
Retropharyngeal or parapharyngeal abscess
o
Epiglottitis
o
Peritonsillar abscess
o
Diphtheria
Foreign body (airway or esophageal)
Angioedem a
Vocal cord paralysis
Congenital airway anom aly: o
Laryngom alacia
Acquired subglottic stenosis
Therm al injury to upper airway
Hem angiom a
Laryngeal papillom atosis
Vocal cord dysfunction (adolescents)
P.271
Treatment Pre Hospital
Allow child to m aintain position of com fort.
Defer interventions that m ay distress child such as: o
IV access
o
IM injections
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If severe distress: o
Im m ediate nebulized epinephrine with hum idified oxygen
Initial Stabilization
Oxygen (via blowby) for suspected or docum ented hypoxia
Mist therapy often used, but of unproven efficacy
Dexam ethasone: o
Indicated in patients with stridor at rest and those receiving epinephrine
o
Effective even in m ild croup (Westley croup score ≤2)
Nebulized racem ic epinephrine or L-epinephrine if any distress or stridor at rest: o
L-epinephrine containing only the active isom er; has been shown to be therapeutically equivalent to racem ic epinephrine
If poor response to nebulized racem ic epinephrine or L-epinephrine: o
Consider trial of heliox.
Heliox, when available, has been used to decrease the work of breathing in patients with an incom plete response to epinephrine.
If im pending or existing respiratory failure despite aforem entioned therapy: o
Tracheal intubation by m ost experienced person available
o
Use uncuffed endotracheal tube (ETT) 0.5–1.0 m m sm aller than usual size.
If epiglottitis suspected: o
Ideally, to OR for inhalational anesthesia, direct laryngoscopy, and intubation
o
Surgeon standing by for em ergent tracheostom y
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ED Treatment See Initial Stabilization
Medication (Drugs)
Racem ic epinephrine 2.25%: 0.25–0.5 m L nebulized in 2.5 m L norm al saline (NS)
L-epinephrine 1:1,000: 5 m L (5 m g) nebulized
Dexam ethasone: single dose of 0.6 m g/kg (m ax. 10 m g) PO (use crushed tablet with flavored syrup). As effective when given PO, IV, or IM
Heliox (70% helium : 30% oxygen m ixture adm inistered via face m ask or tent house)
Antibiotics: not indicated
Follow-Up Disposition Admission Criteria
Young infants, pre-existing upper airway obstruction
Persistent stridor at rest unresponsive to nebulized epinephrine
Recurrent stridor 3–4 hours after initial treatm ent with epinephrine and dexam ethasone. Children should norm ally be observed for a m inim um of 3 hours after adm inistration of epinephrine.
Pediatric intensive care unit (PICU): o
Persistent severe obstruction
o
Need for frequent epinephrine treatm ents and/or
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heliox o
Tracheal intubation with assisted ventilation
Discharge Criteria
Norm al oxygenation in room air
No stridor at rest after brief observation or
No recurrent stridor 3–4 hours after nebulized epinephrine
Reliable caretaker, com m unication, transport
Issues for Referral Concern for underlying anatom ic abnorm ality
References 1. Bjornson L, Klassen TP, William son J, et al. A random ized trial of a single dose of oral dexam ethasone for m ild croup. N Engl J Med. 2004;351:1306–1313. 2. Ham m er J. Acquired upper airway obstruction. Paediatr Respir Re. 2004;5:25–33. 3. Johnson D. Croup. Clin Evid. 2004;12:401–426. 4. Ledwith CA, Shea LM, Mauro RD. Safety and efficacy of nebulized racem ic epinephrine in conjunction with oral dexam ethasone and m ist in the outpatient treatm ent of croup. Ann Em erg Med. 1995;25:331–337. 5. Neto GM, Kentab O, Klassen TP, et al. A random ized controlled trial of m ist in the acute treatm ent of m oderate croup. Acad Em erg Med. 2002;9:873–879. 6. Rittichier KK, Ledwith CA. Outpatient treatm ent of m oderate croup with dexam ethasone: intram uscular versus oral dosing. Pediatrics. 2000;106:1344–1348. 7. Waism an Y, Klein BL, Boenning DA, et al. Prospective random ized double-blind study com paring L-epinephrine and racem ic epinephrine aerosols in the treatm ent of laryngotracheitis (croup). Pediatrics. 1992;89:302–306.
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8. Weber JE, Chudnofsky CR, Younger JG, et al. A random ized com parison of helium -oxygen m ixture (heliox) and racem ic epinephrine for the treatm ent of m oderate to severe croup. Pediatrics. 2001;107:e96.
Codes ICD9-CM 464.4
ICD10 J05.0
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > C ushing Syndro m e
Cushing
Syndrome Hugh Schuckman
Basics Description
Cushing disease: pituitary adenom a producing excess adrenocorticotropic horm one (ACTH)
Cushing syndrom e: excessive glucocorticoid effects
Genetics
Multiple endocrine neoplasia type I
Carney com plex (pigm ented lentigines, atrial m yxom a, germ -cell tum ors with Cushing disease)
Etiology
Most com m only exogenous adm inistration of glucocorticoids either therapeutically or surreptitiously
Pituitary adenom a secreting ACTH
Adrenal production of cortisol from adenom a, carcinom a, or m icronodular disease
Tum or-producing ectopic ACTH: o
Sm all cell lung carcinom a:
Most com m on
Pa ge 1 2 9
o
Uterine cervical carcinom a
o
Islet cell tum or of pancreas:
Multiple endocrine neoplasia (MEA) I-type syndrom e
o
Medullary thyroid cancer
o
Pheochrom ocytom a
o
Ganglioneurom a
o
Melanom a prostate carcinom a
o
Carcinoid tum or:
Lung
Pancreas
GI tract
Thym us
Ovary
Diagnosis Signs and Symptoms Alert
The m ost im portant aspect of Cushing syndrom e in the ED is recognizing the potential for addisonian (adrenal) crisis during periods of stress.
Although nonem ergent, the early recognition of Cushing syndrom e m ay prevent m orbidity and m ortality.
Pediatric Considerations Suspect if increasing in obesity while falling off in height on the growth chart
Pregnancy Considerations Cushing syndrom e rarely com plicates pregnancy, but has been associated with severe pre-eclam psia and HELLP syndrom e (h
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em olysis, elevated liver function, and low platelets).
History
Cushing disease previously diagnosed
Prior use of corticosteroids
Characteristic appearance should lead to questions concerning change in weight, facial appearance, hirsutism , or psychiatric sym ptom s.
Physical Exam
Diagnosis suggested by: o
Abnorm al fat deposition with m oon facies
o
Buffalo hum p
o
Central obesity with thin extrem ities
o
Supraclavicular fat deposition
o
Above findings raise suspicion in a stressed patient of potentially developing addisonian (adrenal) crisis
Hypokalem ia while not on diuretic therapy
Cardiovascular:
o
Uncontrolled hypertension
o
Myocardial infarction
Neurologic: o
Atherosclerotic or em bolic stroke
o
Pseudotum or cerebri (prim arily with exogenous glucocorticoid adm inistration)
o
Spinal lipom atosis with cord or nerve-root com pression
Gastroenterologic: o
Peptic ulcers
o
GI hem orrhage
o
Pancreatitis (prim arily with exogenous glucocorticoid adm inistration)
o
Fatty liver
Pa ge 1 3 0
Psychiatric: o
Toxic psychosis
o
Mood disorders (40%)
o
Depression
o
Mem ory im pairm ent
o
Euphoria
Musculoskeletal: o
Myopathy (proxim al weakness)
o
Pathologic fractures
o
Osteoporosis
o
Aseptic necrosis hum eral or fem oral heads (prim arily with exogenous glucocorticoid adm inistration)
o
Delayed bone age
Endocrine: o
Glucose intolerance
o
Hyperlipidem ia
o
Am enorrhea, fem ale with m ale pattern balding, or hirsutism
Hem atologic: o
Increased neutrophils
o
Decreased lym phocytes and eosinophils
o
Opportunistic infections
Ophthalm ologic: o
Cataracts (prim arily with exogenous glucocorticoid adm inistration)
o
Glaucom a (prim arily with exogenous glucocorticoid adm inistration)
Derm atologic: o
Purple striae >1 cm in diam eter
o
Hyperpigm entation—especially of buccal m ucosa (from excess ACTH production)
o
Facial plethora
Pa ge 1 3 0
o
Thin skin
o
Im paired wound healing
o
Ecchym oses
o
Acne
o
Hyperhidrosis
Essential Workup
Cannot confirm diagnosis in ED
Anticipate im pending addisonian (adrenal) crisis: o
Most frequent and com m on problem with Cushing syndrom e is its recognition in patient with intercurrent illness to prevent acute addisonian crisis.
Search for life-threatening conditions: o
Myocardial infarction
o
Stroke
o
Sepsis
o
Pathologic fracture
o
Uncontrolled DM
o
Psychiatric em ergency necessitating adm ission
P.273
Tests Lab
Electrolytes, BUN, creatinine, glucose: o
Hypokalem ia
o
10% with m etabolic alkalosis
o
Dim inished glucose tolerance (75%):
50% have glycosuria.
20% overt diabetes m ellitus (DM)
CBC: o
Increased WBCs
Pa ge 1 3 0
o
Decreased eosinophils
Imaging
ECG for m yocardial ischem ia
Chest radiograph for tum or-causing ectopic ACTH
Plain film s if suspect possible pathologic fractures
Diagnostic Procedures/Surgery N/A
Nonemergent Testing
MRI for pituitary tum or
CT for adrenal carcinom a, adenom a, or hyperplasia
Dexam ethasone-suppression test (follow-up study with prim ary physician): o
If suspicion of endogenous Cushing syndrom e exists
o
Low-dose (screening test): 1 m g at 11:00 PM with an 8 AM cortisol level drawn:
Low specificity
Decrease false-positive results by stopping alcohol, estrogens, spironolactone, phenytoin, and barbiturates.
o
High-dose dexam ethasone-suppression test needed to confirm the diagnosis:
2 m g q.i.d. of dexam ethasone with cortisol level 6 hours later
Com pare day 2 urine-free cortisol and 17-hydroxyketosteroids with baseline levels.
Differential Diagnosis
Alcohol-induced pseudo–Cushing syndrom e
Obesity
Psychiatric states: o
Depression
Pa ge 1 3 0
o
Obsessive-com pulsive disorder
o
Panic disorder
Physiologic states: o
Chronic stress
o
Third-trim ester pregnancy
o
Chronic strenuous exercise
Treatment Pre Hospital
Acute addisonian (adrenal) crisis under stress m ay develop with iatrogenic Cushing syndrom e.
Patients m ay have extrem ely labile behavior with violent behavior.
Cause of death in untreated Cushing syndrom e is: o
Infection
o
Stroke
o
Myocardial infarction
Initial Stabilization
Anticipate addisonian (adrenal) crisis.
Initiate treatm ent for associated com plications: o
Myocardial infarction
o
Stroke
o
Psychiatric stabilization
ED Treatment
IV rehydration
Glucose-lowering agents for hyperglycem ia
Appropriate cultures and antibiotics for suspected infection
Antihypertensive agents for uncontrolled blood pressure (BP)
Pa ge 1 3 0
Adm inister steroids (hydrocortisone) with iatrogenic Cushing if patient under stress to prevent addisonian crisis.
Medications to lower cortisol levels (brom ocriptine, ketoconazole, am inoglutam ide, m etapyrone): o
Used rarely with severe sym ptom s in patients awaiting surgery
o
Institute under the direction of an endocrinologist.
Definitive Therapy
Iatrogenic: o
Taper steroids as rapidly as possible,
o
Calcium , vitam in D, and estrogen supplem entation if possible
Pituitary Cushing: o
Transsphenoidal surgery
o
Radiation for surgical failures and a few select patients
Adrenal adenom a/carcinom a: o
Adrenal resection with m edical therapy for m etastatic lesions not resectable
Ectopic ACTH: o
Tum or resection (if possible) with m edical therapy for m etastatic lesions not resectable
Medication (Drugs) Hydrocortisone: 100 m g (peds: 1–2 m g/kg) IV q6h if adrenal crisis
Follow-Up
Pa ge 1 3 0
Disposition Admission Criteria
Com plications that require adm ission such as: o
Myocardial infarction
o
Stroke
o
Sepsis
o
Pathologic fracture
o
Uncontrolled DM
o
Psychiatric em ergency
Im pending addisonian (adrenal) crisis
Discharge Criteria Well-appearing, stable patient without adm ission criteria
Issues for Referral
Any patient suspected of Cushing syndrom e for further evaluation.
Conditions secondary to Cushing requiring treatm ent
References 1. Goldm an L, Bennett JC, eds. Cecil's Textbook of Medicine. 22nd ed. Philadelphia: WB Saunders; 2000. 2. Greenspan FS, Gardner DG. Basic and Clinical Endocrinology. 7th ed. Lange Publishers. 2003. 3. Marx JA, Hockenberger RS, Walls RM, et al., eds. Rosen's Em ergency Medicine. 5th ed. Philadelphia: Mosby; 2002. 4. Wallach J, ed. Interpretation of Diagnostic Tests. 7th ed. Boston: Little, Brown and Com pany; 2000.
Codes ICD9-CM 255.0
ICD10
Pa ge 1 3 0
E24.9
Pa ge 1 3 0
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > C yanide Po iso ning
Cyanide Poisoning
Kirk Cumpston
Basics Description
Toxicity through inhalation, derm al, or GI tract absorption
Intracellular toxin that inhibits aerobic m etabolism through interruption of oxidative phosphorylation: o
Leads to decreased O 2 utilization and ATP production
Inhibits antioxidant defense enzym es; contributes to oxidative dam age
Stim ulates neurotransm itter release in CNS/peripheral nervous system (PNS)
Cyanide Detoxification Rhodanese: hepatic m itochondrial enzym e responsible for the m etabolism :
Com bines cyanide (CN) with sulfur (rate-lim iting step) covalently (irreversible) to form less toxic and water-soluble thiocyanate (T-CN)
Form s less toxic reversible cyanhem oglobin when com bined with hem oglobin (Fe 2 + )
Form s nontoxic cyanocobalam in (B 1 2 ) when com bined with hydroxocobalam in (B 1 2 a )
Rate of CN rem oval requires adequate bioavailability of
Pa ge 1 3 0
sulfur com pounds (thiosulfate [TS]).
Etiology
Fires: o
Com bustion by-product of natural and synthetic products
Vehicle exhaust
Industry:
o
Metal plating, m icrochip m anufacturing
o
Chem ical synthesis
o
Plastic m anufacturing
o
Pesticides
Solvents: o
Artificial nail rem over
o
Metal polishes
By-product of nitroprusside m etabolism (nonenzym atic)
By-product of Pseudom onas aeruginosa and pyocyaneus infections
Am ygdalin (converted by intestinal flora to CN)-containing plants (apricot and peach pits, apple and pear seeds, and cassava)
Jewelry m aking
Diagnosis Signs and Symptoms
Derm al exposure: standard decontam ination
Oral exposure: can be caustic, 50 m g has caused death.
Inhalational exposure: o
50 parts per m inute causes anxiety, palpitations, dyspnea, headache.
Pa ge 1 3 0
o
100–135 ppm 0.5–1 m g/L: toxic
o
Levels 2.5–3.0 m g/L: fatal
Thiocyanate level
Blood gas determ inations: o
Increased arterial saturation gap (calculated direct [m easure] O 2 saturation [cooxim eter])
o
Elevated m ixed venous O 2 : MvO 2 (norm al about 35–40)
o
Elevated m ixed venous O 2 saturation (cooxim eter): Sm vO 2 (norm al about 75%)
o
Decreased arteriovenous O 2 difference: AVO 2 D (norm al about 3–4.8 m L/dL)
Elevated lactate level >8 m m ol/L
Imaging Chest x-ray
Differential Diagnosis
Carbon m onoxide
Hydrogen sulfide
Methem oglobinem ia (MH)
Sulfhem oglobinem ia
Inert gases “asphyxiants―
Causes of high anion gap m etabolic acidosis
Pa ge 1 3 1
Treatment Pre Hospital
Rem ove source of CN.
Prevent others from becom ing contam inated.
Rem ove and bag all contam inated clothing and wash affected areas copiously with soap and water. If vapor contam ination, rem oval of clothing m ay be all that is necessary.
Initial Stabilization
Airway, breathing, and circulation m anagem ent (ABCs): o
Adm inister 100% oxygen:
Even in presence of norm al PaO 2
Acts synergistically with antidotes
Gastric decontam ination for oral ingestions if within 1 hour: o
Perform gastric lavage and adm inister activated charcoal (AC) if ingestion of CN or CN-containing products and no contraindications.
o
Do not induce em esis.
P.275
ED Treatment Cyanide Antidote Kit
Adm inister if m anifesting significant CN toxicity with persistent high anion gap m etabolic acidosis and narrow arteriovenous O 2 difference, and hypotension.
Pa ge 1 3 1
Adm inistration often instituted em pirically; CN levels not im m ediately available
Contents: am yl nitrite pearls, sodium nitrite, and TS
Nitrite action: o
Induce a CN-scavenging MH by oxidizing hem oglobin (Fe 2 + to Fe 3 + ), which attracts extracellular CN away from the m itochondria-form ing CN-MH, which is less toxic.
o
Do not adm inister em pirically or prophylactically.
TS action: o
Substrate for the enzym e rhodanase
o
Com bines with CN to form a less toxic T-CN
o
May adm inister em pirically
Use clinical response and not m ethem oglobin levels to guide nitrite adm inistration.
Side effects of nitrites: o
Hypotension (nitrite-induced vasodilation)
o
MH:
Does not function as O 2 transporter
Im pairs oxygen delivery
Elevated level leads to further tissue hypoxia.
Hydroxocobalamin (B 12a )
Alternate safe antidote
Binds to CN: o
Form s nontoxic cyanocobalam in (B 1 2 ); renally excreted
Advantages: o
No m ethem oglobin induction
o
Does not cause hypotension
Lim itations: o
Large am ount needed to successfully treat poisoned patients (50 g B 1 2 a :1 g CN)
Pa ge 1 3 1
o
Use of TS com bined with B 1 2 a m ay reduce am ount of B 1 2 a required.
o
Available only in Europe
Combined TS and B 12a Therapy
Victim s of sm oke inhalation m ay have com bination of: o
CN toxicity
o
MH
o
CO toxicity
Avoid further reduction in oxygen transport; initially treat with TS and/or B 1 2 a until CO and MH levels are known.
Hyperbaric Oxygen Therapy
Maxim izes tissue oxygenation despite toxic MH level
Use as adjunct to aforem entioned antidotes in severe cases or when antidotes have failed.
Antidote Alternatives
Not yet FDA approved
Do not institute em pirically because of toxicity.
Dicobalt edetate: o
Inactivates CN by chelation
o
Associated with hypertension, dysrhythm ias, and m etabolic acidosis
Dim ethylam inophenol: o
Induces a m uch faster scavenging m ethem oglobinem ia
o
Nephrotoxic
Medication (Drugs)
AC: 1–2 g/kg PO
Hydroxocobalam in (B 1 2 a ): o
Dose equivalent to 50 tim es am ount of CN exposure
Pa ge 1 3 1
infused in 30 m inutes o
Em piric single dose, 4–5 g (50 m g/kg) IV in D 5 W
o
Prophylactic IV infusion at 25 m g/h in Nipride usage
Cyanide Antidote Kit (Eli Lilly Antidote Kit)
Am yl nitrite pearls: o
Crush one or two am pules in gauze and hold close to nose, in lip of face m ask, or within Am bu bag
o
Inhale for 30 seconds to 1 m inute until IV access obtained.
Sodium nitrite (NaNO 2 ): 10 m L (300 m g) (peds: 0.15–0.33 m L/kg) IV as 3% solution over 5–20 m inutes: o
May repeat once at one-half dose within 30–60 m inutes
o
Keep MH level Table o f C o ntents > C yano sis
Cyanosis
Michael S. Murphy
Basics Description
Caused by abnorm al elevations of hem oglobin or hem oglobin derivatives:
o
Reduced hem oglobin >5 g/dL
o
Methem oglobin >1.5 g/dL
o
Sulfhem oglobin >0.5 g/dL
The am ount of oxyhem oglobin does not affect the blood's color.
Cyanosis is m ore com m on in patients with polycythem ia.
Cyanosis is less com m on in patients with anem ia.
Methem oglobinem ia cyanosis presents with norm al PO 2 and chocolate-colored blood.
Etiology Central Cyanosis/Decreased Saturation
Im paired pulm onary function: o
Hypoventilation:
Pneum onia
Chronic obstructive pulm onary disease
Pulm onary edem a
Pa ge 1 3 1
o
o
Ventilation/perfusion m ism atch:
Asthm a
Pulm onary em bolus
Diffusion problem s:
Interstitial lung disease
Anatom ic shunts: o
o
Congenital cardiac causes:
Transposition
Tetralogy
Pulm onary arteriovenous fistula:
o
Hereditary hem orrhagic telangiectasia
High-altitude related, with decreased atm ospheric pressure at 16,000 feet
Low-oxygen affinity hem oglobin m utants: o
Hb Kansas
o
Beth Israel
o
St. Mande
Central Cyanosis/Hemoglobin Abnormalities
Methem oglobinem ia: o
o
Congenital:
Cytochrom e b5 reductase deficiency
Hem oglobin M disease
Most cases are acquired:
Aniline dyes
Chloroquine, prim aquine
Dapsone
Local anesthetic agents such as lidocaine
High doses of m ethylene blue
Naphthalene
Nitrites, nitroglycerine
Sulfonam ides
Sulfhem oglobin:
Pa ge 1 3 1
o
Generally benign
o
Irreversible alteration of hem oglobin
o
Caused by m any m edications:
Dim ethyl sulfoxide
Paint
Phenacetin
Phenazopyridine
Phenylenediam ine
Phenylhydroxylam ine
Sulfanilam ide
Sulfapyridine
Sulfathiazole
Sulfur com pounds
Peripheral Cyanosis
Vasoconstriction to cold air or water
Arterial obstruction seen in em boli or Raynaud
Venous obstruction throm bophlebitis
Decreased cardiac output com pensatory vasoconstriction
Differential Cyanosis
Lower extrem ities involved, but upper extrem ities spared
Patent truncus arteriosus or pulm onary hypertension
Pediatric Cyanosis
Cardiac: o
o
Cyanotic congenital defects:
Tetralogy of Fallot
Transposition of great vessels
Truncus arteriosus
Pulm onary and tricuspid atresia
Ebstein anom aly
Total anom alous pulm onary venous return:
Pulm onary stenosis
Pa ge 1 3 1
Any right-to-left shunting
Respiratory: o
o
Upper airway disorders
Croup:
Bacterial tracheitis
Epiglottitis
Retropharyngeal abscess
Foreign body
Traum a
Lower airway disorders:
Asthm a
Bronchiolitis
Pneum onia
Cystic fibrosis
Pulm onary edem a/congestive heart failure
Pulm onary em bolism
Chest wall injury
Pleural disorders such as pneum othorax or diaphragm atic hernia
Neurologic: o
CNS injury/lesions
o
Infection
o
Seizure
o
Toxins
o
Breath holding
o
Hem oglobinopathy
Diagnosis Signs and Symptoms
A bluish discoloration of the skin and m ucous m em branes:
Pa ge 1 3 2
o
Chocolate color:
o
Slate gray color:
o
Methem oglobinem ia
Methem oglobinem ia or sulfhem oglobin
Varies based on skin thickness or pigm ent
Central or generalized: o
Visible in lips, nailbeds, ears, or m alar regions
o
Peripheral or local cyanosis:
o
Lim ited to extrem ities
Differential cyanosis: o
Lower extrem ities involved, but upper extrem ities spared
o
Clubbing
o
Dyspnea
o
Fatigue
o
Headache
o
Occupational exposure or use of certain chem icals or drugs
Asym ptom atic: o
Suggests m ethem oglobinem ia
Essential Workup
Assess airway and ventilation as first priority: o
Stabilize airway and provide adequate ventilation.
Investigate hypoxem ia causes: o
Cardiac and respiratory m ost com m on
o
Consider m ethem oglobinem ia.
Tests Lab
Pulse oxim etry: o
Does not assess ventilation
o
Results inaccurate with:
Pa ge 1 3 2
Abnorm al hem oglobins
Nail polish
Pigm ented skin
Hypoperfusion
Used of vital dyes
Arterial blood gas: o
Oxygen tension
o
Measured hem oglobin saturation
o
Cyanosis in face of norm al PO 2 , think m ethem oglobinem ia
o
Blood in m ethem oglobinem ia is chocolate color.
o
Methem oglobin level
Com plete blood chem istry: o
Check hem oglobin.
Hyperoxia test for congenital cyanosis of newborn: o
If PO 2 fails to increase to 100 m m Hg after 100% O 2 , suspect congenital heart disease.
P.277
Imaging
Chest radiograph to investigate respiratory or cardiac pathology:
o
Inspiratory/Expiratory views if foreign body
o
Expiratory view if occult pneum othorax suspected
Radiograph of neck for upper airway disorders: o
Foreign body
o
Steeple sign (croup)
o
Prevertebral swelling (retropharyngeal abscess)
o
Epiglottic swelling
ECG: o
Dysrhythm ia, injury, or ischem ia
Pa ge 1 3 2
Echocardiography: o
Bubble study if septal defect/shunt suspected
o
Wall m otion/valvular abnorm alities
o
Pericardial fluid
Differential Diagnosis
Hyperpigm entation: o
Drugs or m etals
o
Chronic high-dose chlorprom azine
o
Minocycline
o
Argyria (silver deposits)
o
Tattoos
Polycythem ia
Treatment Pre Hospital
Assess and establish patent airway.
Correct any airway obstruction.
Recognize an incorrectly placed airway.
One hundred percent O 2 using a nonrebreathing device
Ensure adequate ventilation.
Recognize need to establish definitive airway.
Protect cervical spine if traum a suspected.
IV line, m onitor, pulse oxim etry
Albuterol nebulizer for bronchospasm
Racem ic epinephrine nebulizer for severe croup
Managem ent of pulm onary edem a per protocol
Initial Stabilization
Oxygen supplied through a 100% nonrebreathing device
Im m ediately assess and address airway issues.
Pa ge 1 3 2
ED Treatment General m easures:
Recognize and m anage cardiopulm onary disorders.
Methylene blue for m ethem oglobinem ia exceeding 30%: o
Do not use if patient has G6PD deficiency.
Medication (Drugs)
Albuterol nebulized: 0.03 m L/kg (5 m g/m L)
Dexam ethasone: (for croup) 0.6 m g/kg IV/IM
Furosem ide: 1.0 m g/kg IV q6h
Magnesium : 2.0 g IV over 10 m inutes (40 m g/kg IV over 20 m inutes)
Methylene blue: 1–2 m g/kg IV of 1% solution over 5 m inutes
Methylprednisolone: 1–2 m g/kg IV q6h
Morphine: 2–4 m g IV (0.05–0.1 m g/kg IV g2h PRN)
Nitroglycerine: 0.4 m g sublingually or IV (0.5–5 µg/kg/m in IV)
Prostaglandin E 1 : 0.05–0.1 µg/kg/m in IV; m axim um 0.4 µg/kg/m in
Racem ic epinephrine nebulized: 0.05 m L/kg
Follow-Up Disposition Admission Criteria Most affected patients should be adm itted to hospital:
Intensive care unit adm ission is required for any instability
Pa ge 1 3 2
or cyanosis.
Discharge Criteria Reversible causes of hypoxia:
Reactive airway disease responsive to β-agonists
Pulm onary edem a in patient with known congestive heart failure but no suspicion of m yocardial injury and diuresis
References 1. Braunwald E. Hypoxia, polycythem ia, and cyanosis. In: Harrison's Principles of Internal Medicine. 13th ed. New York, NY: McGraw-Hill; 1994:178–183. 2. Mansouri A, Lurie A. Concise review: m ethem oglobinem ia. Am J Hem atol. 1993;42:7–12. 3. Stack A. Cyanosis. In: Synopsis of Pediatric Em ergency Medicine. 4th ed. Philadelphia, PA: Lippincott William s & Wilkins; 2002:64–67. 4. Wright RO, Lewander WJ, Woolf AD. Methem oglobinem ia: etiology, pharm acology, and clinical m anagem ent. Ann Em erg Med. 1999;34:646–656.
Codes ICD9-CM 782.5 Cyanosis
Pa ge 1 3 2
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > C ystic F ibro sis
Cystic Fibrosis
Roger Barkin
Basics Description
Defect of the cystic fibrosis transm em brane conductance regulator (CFTR)
CFTR functions as an ATP-regulated chloride channel that regulates the activity of chloride and sodium channels on the cell surface: o
Abnorm al electrolyte transport in exocrine glands and secretory epithelia
o
Decreased exocrine pancreatic function with m alabsorption
o
Thickened m ucus, recurrent pulm onary infections, and progressive obstructive dam age to the lungs
Occurs in 1:3,500 live births
More prevalent in white populations (1/2,500)
Diagnosed in the first decade of life in about 70% of cases
Approxim ately 30,000 children and young adults in United States have CF.
Median life expectancy in the United States is about 30 years.
Approxim ately 40% of CF patients are older than 18 years
Pa ge 1 3 2
of age.
10 m illion Am ericans are unknown, asym ptom atic carriers of the defective gene.
Alert An acute or chronic respiratory problem in a patient with CF requires pulm onary consultation.
Genetics Recessively inherited genetic disease, involving the CFTR gene on the long arm of chrom osom e 7:
Different m utations produce variable phenotypes.
Classic disease is hom ozygous for the DF508 m utation.
Etiology Com m on organism s in patients with pneum onia; often m ultiple drug resistance:
Pseudom onas aeruginosa o
Prevalence increases with age; 70% of adults are chronically infected.
Haem ophilus influenzae
Staphylococcus aureus
Burkholderia cepacia:
Prevalence 5%
Associated with rapid clinical deterioration
Aspergillus
Diagnosis Signs and Symptoms
General: o
Failure to thrive
o
Recurrent respiratory tract infections
Pa ge 1 3 2
o
Anasarca in infancy
o
Salty taste of skin
Head, ears, eyes, nose and throat (HEENT): o
Nasal polyps
o
Severe headaches owing to sinusitis
Pulm onary: o
Persistent, dry hacking paroxysm al cough
o
Recurrent pneum onitis or bronchiolitis in the first year of life
o
Wheezing
o
Hem optysis
o
Pneum onia
o
Respiratory distress
o
Pneum othorax
o
Most com m on cause of hospitalization
Cardiac: o
Congestive heart failure (CHF)
o
Cor pulm onale
o
Pulm onary hypertension
GI: o
Abdom inal pain
o
Distal ileal obstructive syndrom e or “m econium ileus equivalent―
o
Cholelithiasis
o
Pancreatitis
o
Ileocecal intussusception
o
Foul sm elling, fatty stools
o
Jaundice
o
Cirrhosis or cholelithiasis
o
Rectal prolapse
o
Hem atem esis
Extrem ities:
Pa ge 1 3 2
o
Bone pain
o
Edem a
o
Joint effusions
Cardiorespiratory failure is m ost com m on cause of death.
Essential Workup
Test patients with chronic or unusual respiratory and GI com plaints.
Prior culture results m ay be helpful in patients with known CF.
Tests Lab
Sweat chloride test: o
Chloride concentration >80 m Eq/L
o
With classic signs and sym ptom s, a positive test result confirm s the diagnosis.
Stool sam ple: o
Trypsin or chym otrypsin absent or dim inished
o
Increased fat in 72-hour fecal fat excretion
Im m unoreactive trypsin (IRT): o
Defines increased risk and/or diagnosis
o
May be falsely positive or negative
Cytogenetic analysis: o
Indicated if sym ptom s are highly suggestive, but sweat test result is negative
o
Positive if two abnorm al genes present
o
Genotyping, however, cannot establish the diagnosis.
o
Detects 70 of 500 CTFR m utations
o
Am eliorating or neutralizing second m utation m ay be present.
CBC: o
Throm bocytopenia
Pa ge 1 3 2
Serum electrolytes: o
Hyponatrem ic, hypochlorem ic alkalosis
Serum glucose: o
Hyperglycem ia and new-onset diabetes occurs prim arily in adolescents and adults; ketoacidosis is rare.
Liver function tests and PT: o
Indicated when CF is com plicated by hem atem esis or signs of liver failure
ABG: o
Hypoxem ia
o
Metabolic alkalosis
Sputum culture: o
Determ ine whether pseudom onal colonization is present.
o
Studies indicated in patients at high risk with a difficult diagnosis
Sem en analysis: o
Azoosperm ia
o
Nasal potential-difference m easurem ents
o
Com plex and tim e-consum ing study
Imaging
Chest radiograph: o
Hyperaeration
o
Peribronchial thickening
o
Atelectasis
o
Hilar lym phadenopathy
o
Possible pneum othorax
o
Bronchiectasis
o
Blebs
o
Com pare with previous chest radiograph for acute pulm onary deterioration.
Pa ge 1 3 3
P.279
Abdom inal radiographs: o
Indicated if abdom inal pain, vom iting, or abdom inal distention
o
Distal ileal obstruction syndrom e
o
Intussusception
Barium enem a: o
Indicated if suspicion of intussusception
Sinus film s: o
Lim ited use because routine sinus film s are always cloudy
o
CT scan is needed to assess sinuses.
Diagnostic Procedures/Surgery Bronchoalveolar lavage:
High percentage of neutrophils and absolute neutrophil count
Unnecessary in patients with obvious pulm onary sym ptom s
Differential Diagnosis
Respiratory: o
Asthm a
o
Recurrent pneum onia
o
Bronchiectasis
o
Pertussis
o
Im m unodeficiency
GI: o
Chronic diarrhea
o
Gastroenteritis
o
Milk allergy
Elevated electrolyte levels in sweat:
Pa ge 1 3 3
o
Fucosidosis
o
Glycogen storage disease type I
o
Mucopolysaccharidosis
o
Hypothyroidism
o
Vasopressin-resistant diabetes insipidus
o
Adrenal insufficiency
o
Fam ilial cholestasis
o
Fam ilial hypoparathyroidism
o
Malnutrition
o
Ectoderm al dysplasia
o
Atopic derm atitis
o
Infusion of prostaglandin E 1
Treatment ED Treatment
Stabilize airway, breathing, and circulation (ABCs): o
Correct fluid, respiratory, electrolyte, and glucose abnorm alities.
Pneum othorax: o
Observe if Table o f C o ntents > Dacryo cystitis
Dacryocystitis
Shari Schabowski
Basics Description
Suppurative infection involving the lacrim al sac which is located below the m edial aspect of the eye and accessed through lacrim al ducts in the inner canthus
Epidemiology
Occurs m ost com m only in infants and postm enopausal wom en
Congenital nasolacrim al obstruction owing to stenosis occurs in approxim ately 2–4% of full-term newborns (presents as acute dacryocystitis).
Etiology
Under norm al conditions, tears drain via pum ping action at lacrim al duct, m oving tears to lacrim al sac and then to m iddle turbinate and into sinuses.
Sym ptom s begin when duct to lacrim al sac becom es partially or com pletely obstructed: o
Stasis in this conduit results in overgrowth of bacteria and infection.
May also occur secondary to traum a, a dacryolith, after
Pa ge 1 3 4
nasal or sinus surgery, or with chronic inflam m ation
Infection m ay be recurrent and m ay becom e chronic.
Most com m on bacteria: ocular and sinus flora
Staphylococcus aureus is m ost com m on organism in acquired acute dacryocystitis.
Pediatric Considerations
Congenital nasolacrim al obstruction owing to stenosis presents as acute dacryocystitis.
Most com m on organism in congenital dacryocystitis: Streptococcus pneum onia
Diagnosis Signs and Symptoms
Unilateral, red, painful, swollen m ass extending inferiorly and m edially from inner canthus
Epiphora or excessive tearing—hallm ark sym ptom
Discharge from punctum
Cellulitis extending to lower lid in som e cases
Low-grade fever m ay be present, but patient rarely appears toxic.
Essential Workup
Apply pressure to m ass: Expression of purulent m aterial from punctum confirm s diagnosis.
Com plete eye exam , including visual acuity, slit-lam p, and funduscopic exam s.
Exam ine nasal passages.
Tests Lab
Pa ge 1 3 4
Tests of expressed m aterial (used to help direct specific antibiotic treatm ent)
Gram stain
Culture and sensitivity
Chocolate agar plating
Imaging CT of orbit/sinus to evaluate deep tissue extension, particularly with recurrent cases
Differential Diagnosis
Insect bite
Traum atic injury
Acute ethm oid sinusitis
Acute m axillary sinusitis
Periorbital (preseptal) cellulitis
Orbital cellulitis
Acute conjunctivitis
Acute blepharitis
Treatment Initial Stabilization
Confirm diagnosis by expressing purulent m aterial.
Begin treatm ent to avoid extension of infection to adjacent structures.
Determ ine whether sym ptom s are recurrent.
ED Treatment
Drainage of infected sac is essential: o
Warm com presses and gentle m assage to relieve obstruction
Pa ge 1 3 4
o
May facilitate outflow from obstructed tract with nasal introduction of vasoconstricting agent
Incision and drainage in severe cases: o
Typically done by ophthalm ology
o
Avoid in ED when possible.
o
May result in fistula form ation
Duct instrum entation to facilitate drainage is not indicated in acute setting (controversial): o
Reserve instrum entation for nonacute setting, if necessary at all.
o
Only 50% of adults show im provem ent after m anipulation.
o
Manipulation while duct is inflam ed m ay cause injury to duct and perm anent obstruction from scarring and stenosis.
Topical ophthalm ic antibiotic drops to prevent secondary conjunctivitis
System ic antibiotics to resolve infection and prevent spread to adjacent structures:
o
Oral for m ild infection
o
Intravenous when febrile or severe infection
Analgesics
P.283
Pediatric Considerations
Newborns respond well to m assage and topical antibiotics in about 95% of cases.
If no resolution in first year of life, m ay require probing of duct by ophthalm ologist
Children Table o f C o ntents > Deep Vein Thro m bo sis
Deep Vein
Thrombosis Jonathan A. Edlow
Basics Description
A constant balance exists between intravascular clot form ation and clot dissolution, clot form ing when the form er overpowers the latter. Clot can be superficial (to the fascia) or deep. The latter is called deep vein throm bosis (DVT). DVT can be upper or lower extrem ity and distal or proxim al (to the popliteal vein).
About 600,000–2,000,000 new cases present annually
Prevalence increases with advancing age in the general population.
Diagnosis is m ore accurate using active surveillance rather than clinical suspicion.
Com m on in both m edical and surgical hospitalized patients
Pulm onary em bolism (PE) and DVT are different ends of the clinical spectrum of the sam e disease process.
Pediatric Considerations DVT in children is unusual, but when cases do occur, search for an underlying reason for hypercoagulability. Also, upper-extrem ity DVT
Pa ge 1 3 5
is associated with central IV lines in children.
Etiology
Three generic factors prom ote clotting
Hypercoagulable states: o
Cancer
o
Nephrotic syndrom e
o
Sepsis
o
Inflam m atory conditions:
o
Ulcerative colitis
Increased estrogen:
Pregnancy
Oral contraceptives
o
Antiphospholipid syndrom e
o
Protein S, C, and antithrom bin III deficiencies, Factor V Leiden, prothrom bin gene m utations, others
Stasis: o
Prolonged bed rest
o
Im m obility (such as from a cast)
o
Long plane, car or train ride
o
Neurologic disorders with paralysis
o
Congestive heart failure
o
Obesity
Vascular dam age: o
Traum a
o
Surgery
o
Central lines:
Especially with upper extrem ity DVT
Multifactorial issues: o
Advancing age:
Prior DVT or PE
Pregnancy Considerations
Pa ge 1 3 5
Pregnancy is a risk factor for DVT, especially in the third trim ester and the two weeks postpartum .
Geriatric Considerations Age in and of itself is a risk for DVT (and PE). As with m any diseases, the presentation m ay be atypical in the elderly.
Genetics Im portant with respect to som e of the risk factors; ask about fam ily history of clotting.
Diagnosis Signs and Symptoms
Leg swelling: o
Greater than 1 cm difference is usually significant.
Leg warm th and redness
Leg pain and tenderness
Palpable cord
In superficial throm bophlebitis, a red pipe cleaner-like cord m ay be visible and palpable.
Arm swelling, warm th, or tenderness: o
Upper extrem ity or subclavian vein involved
Phlegm asia cerulea dolens: o
Cold, tender, swollen, and blue leg (secondary arterial insufficiency)
In phlegm asia alba dolens: o
Cold, tender, and white leg (secondary arterial insufficiency)
Essential Workup
Determ ination of a patient's clinical (pretest) risk is a key step in a workup for DVT.
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A careful history and physical exam , interpreted in the context of the risk factor profile, is the m ost im portant driver of subsequent diagnostic evaluation.
Tests Lab
D-dim er testing: o
D-dim er, a byproduct of endogenous clot form ation, is becom ing increasingly used in evaluation of patients for DVT and PE.
o
Only useful when the result is negative (to exclude DVT). Positive D-dim er does not m ake the diagnosis; it only m andates further testing.
o
Methods of m easuring D-dim er levels:
Latex agglutination (first generation tests) are not sufficiently sensitive and should not be used.
Microlatex agglutination tests (2nd generation test) show som e prom ise but rem ain insufficiently tested as com pared with other m ethods.
Whole-blood latex agglutination (Sim pliRED) is valuable if negative in low probability patients (using Well criteria).
Enzym e-linked im m unosorbent assay testing gives a quantitative result and has been validated in large clinical studies in ED patients.
Imaging
Contrast venography: o
Once the im aging test of choice; now rarely perform ed because it is invasive, is expensive, and has com plications.
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o
Involves injection of contrast m edium into a leg vein, the inflam m ation from which can cause throm bophlebitis in several percent of patients undergoing the procedure.
o
Reactions to the contrast dye m ay also cause reaction.
Radionuclide venography: o
Radionuclide venous im aging is under investigation.
o
This test is not com m only used in routine clinical practice.
Im pedance plethysm ography: o
Another uncom m only used test, which can m iss sm aller distal clots
Com pression ultrasound: o
Standard first-line diagnostic test
o
It exam ines the veins. Norm al veins com press; those with clots do not.
o
Color Doppler can be useful for identifying the vein but does not add substantially to accuracy.
o
Duplex scanning refers to the com bination of com pression B-m ode ultrasound and color Doppler.
o
Has a sensitivity in the high 90% range
o
Should be repeated (or followed up with contrast venography) in high-risk patients with negative ultrasounds
P.287
Differential Diagnosis
Superficial throm bophlebitis
Cellulitis
Torn m uscle and/or ligam ents (including plantaris and
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gastrocnem ius tears)
Ruptured Baker cyst
(Bilateral) edem a secondary to heart, liver, or kidney disease
(Unilateral) edem a from abdom inal m ass (gravid uterus or tum or) or lym phedem a
Postphlebitic syndrom e (from prior throm bophlebitis)
Treatment Initial Stabilization In cases of phlegm asia cerulean, or alba dolens:
IV access
Supplem ental oxygen
Surgical or vascular consultation
ED Treatment
System ic anticoagulation: o
In patients without contraindications
o
Use either unfractionated heparin or low-m olecular-weight heparin (LMWH)
o
Carefully selected patients can be prim arily treated with LMWH as outpatients.
Warfarin: o
Started shortly after a heparin has been adm inistered
o
Not before heparin because of the theoretic risk for inducing a transient hypercoagulable state
o
Xim elagatran, a direct oral throm bin inhibitor, is effective, but not FDA-approved at the present tim e because of concern about hepatotoxicity.
Vena cava filters:
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o
Indications:
Contraindications to system ic anticoagulation
New throm boem bolic event while on adequate anticoagulation
o
Vena cava filters (or um brellas) can be placed transcutaneously, usually by a vascular surgeon or radiologist.
o
Em piric filter placem ent m ay be useful in certain settings:
Ongoing risk such as cancer
Risk for a recurrent PE could be fatal because of poor cardiopulm onary reserve or a recent PE.
o
Random ized data suggest that filter placem ent is no m ore effective than anticoagulation.
o
Filters can also be deployed in the superior vena cava in the setting of upper-extrem ity DVT.
Throm bolysis: o
Rarely indicated
o
Roughly a threefold increase in bleeding com plications
o
Catheter-adm inistered lytic therapy is used m ore com m only in upper extrem ity DVT.
Throm bectom y: o
Occasionally recom m ended for patients with extensive disease
o
Consult a vascular surgeon.
Septic throm bophlebitis: o
Surgical excision of the vein or IV antibiotics
Medication (Drugs)
Enoxaparin: 1 m g/kg SQ b.i.d. for outpatients (or
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inpatients); a dose of 1.5 m g/kg SQ per day is FDA-approved for inpatients.
Heparin (unfractionated): 80 U/kg bolus followed by an 18 U/kg/h drip, with the activated partial throm boplastin tim e (aPTT) titrated 2–2.5 tim es norm al
Tinzaparin: 175 IU/kg SQ per day
Warfarin: 5 m g/d with a prothrom bin tim e being checked on the third day
Follow-Up Alert When the clinical suspicion is high but the ultrasound is negative, rem em ber to advise the patient to follow-up with his or her prim ary care physician, and to have a follow-up ultrasound in 5–10 days.
Disposition Admission Criteria
Patients with DVT unable to receive LMWH as an outpatient
Patients with concom itant PE or other serious diseases
Patients thought to be at especially high bleeding risk
Patients with phlegm asia
Discharge Criteria
Outpatient treatm ent with a LMWH: o
No serious concom itant disease that requires hospitalization
o
Patient has m eans of com m unication and transportation to return to the hospital if needed.
o
Patient (or fam ily m em ber) is willing and able to
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inject the m edication. o
Patient needs hem atocrit, platelet count, and international norm alized ratio (INR) checked in two to three days.
o
aPTT does not need to be checked.
o
Heparin-induced throm bocytopenia is less com m on with the LMWH but still occurs.
o
INR needs to be checked at about day three.
Patients with superficial or distal throm bophlebitis can be discharged with close follow-up.
Issues for Referral
Consult vascular surgery if there is any question about arterial insufficiency.
Consider need for inferior vena cava filter in patients who have contraindications to full anticoagulation or form new clots on adequate anticoagulation.
References 1. Brown DFM. Treatm ent options for DVT. Em erg Med Clin North Am . 2001;19:913–923. 2. Decoussis MN, et al. A clinical trial of vena cava filters in the prevention of pulm onary em bolism in patients with proxim al deep-vein throm bosis. N Engl J Med. 1998;333:409–415. 3. Hirsh J, Hoak J. Managem ent of DVT and PE. Circulation. 1996;93:2212–2245. 4. Kelly J, Hunt BJ. Role of D-dim ers in diagnosis of venous throm boem bolism . Lancet. 2002;359(9305):456–458. 5. Levine M, et al. A com parison of LMWH adm inistered prim arily at hom e with unfractionated heparin adm inistered in the hospital for proxim al DVT. N Engl J Med. 1996;334:677–681. 6. Kyrle PA and Eichinger, S; Deep venous throm bosis. Lancet 2005;365(9465):1163–74.
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7. Tracy JA and Edlow, JA; Ultrasound diagnosis of DVT. Em erg Med Clin North Am . 2004;22:775–796.
Codes ICD9-CM 451.9
ICD10 I80.2
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Defibrillato rs, Im plantable
Defibrillators,
Implantable Robert Sidman Lawrence S. Rosenthal
Basics Description
Therapy related (im plantable cardioverter defibrillator [ICD] fires):
o
Appropriate
o
Inappropriate
Device/site related: o
Wound infection
o
Pocket hem atom a
o
Vascular occlusion
Etiology
Therapy related: o
Appropriate therapies:
Ventricular fibrillation (VF): Consider acute coronary syndrom e
Ventricular tachycardia (VT): Consider prior infarct
o
Inappropriate therapies:
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o
Atrial fibrillation
Atrial flutter
Other supraventricular tachycardias (SVT)
Lead related
Phantom shocks:
Patient awakened from sleep by a perceived shock
Device/site related: o
Wound infection:
Staphylococcus aureus (m ost aggressive and seen early)
Staphylococcus epiderm idis (m ore indolent and later)
Escherichia coli, Pseudom onas species, and Streptococcal species (less com m on)
o
Pocket hem atom as
o
Vascular (venous throm bosis/em bolism secondary to im pedance of venous flow as a result of the ICD lead[s])
Diagnosis
Therapy related: o
Based on sym ptom s before shock
o
Based on device interrogation
o
12-lead ECG:
Ongoing ischem ia
Cardiac enzym es
Device/site related: o
Exam ination of surgical wound
o
Exam ination of upper extrem ities
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Signs and Symptoms
Therapy related: o
o
Appropriate ICD therapies:
Syncope or near syncope
Lightheadedness or dizziness
Shortness of breath
Palpitations (non-SVT)
Chest discom fort or pain
Diaphoresis
Inappropriate therapies:
Palpitations (SVT)
Lead related fractures, inappropriate sensing
Device/site related: o
o
o
Wound infection:
Purulent drainage
Warm th
Erythem a
Pain
Fluctuance
Skin erosion
Fever
Hem atom a at the insertion site (pocket hem atom a):
Pain (m ild)
Swelling
Vascular (throm boem bolic phenom ena):
Unilateral swelling in upper extrem ity
Superficial varicosities
History
Therapy related: o
Recent angina, heart failure
Device related:
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o
Recent im plant ( Table o f C o ntents > Delirium
Delirium
Arthur Sanders
Basics Description
Syndrom e caused by m ultiple m edical disorders
Delirium is caused by underlying m edical condition.
Pathophysiology unknown: o
Diffuse derangem ents of cerebral acetylcholine
o
CNS dopam ine, γ-am inobutyric acid, and serotonin m ay be involved.
Etiology
Life threats: o
Withdrawal from barbiturates
o
Wernicke encephalopathy
o
Hypoxia and hypoperfusion of the brain
o
Hypertensive crisis
o
Hypoglycem ia
o
Hypertherm ia or hypotherm ia
o
Intracranial bleed or m ass
o
Acute coronary syndrom es
o
Meningitis or encephalitis
o
Poisoning or m edications
o
Status epilepticus
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o
Sepsis
General categories of disorders causing delirium : o
Medications
o
Drug abuse
o
Intoxication
o
Withdrawal
o
Metabolic abnorm alities
o
CNS pathology
o
Hypoperfusion from cardiovascular disease
o
Hypoxem ia
o
Vitam in deficiencies
o
Endocrinopathies
o
Infections
o
Toxins
o
Collagen vascular illnesses
Geriatric Considerations
Com m on presentation in older ED patients
Up to 10% of older ED patients m ay have delirium .
Many patients will present with subtle sym ptom s and vague chief com plaints: o
Fall, dizzy, or not feeling well
Waxing and waning sym ptom s
Cause m ay be life-threatening condition.
Diagnosis Signs and Symptoms
Disturbed consciousness: o
Hyperalert
o
Lethargic
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o
Stupor
o
Com a
Cognitive changes: o
Disorientation
o
Im paired m em ory
o
Disorganized thinking and speech
o
Misperceptions, illusions, delusions, and hallucinations
Tim e course: o
Hours to days
o
Fluctuating course
Reduced awareness of environm ent
Inattention: o
Difficulties in focusing, shifting, and m aintaining attention
o
Restlessness
o
Distractibility
o
Lability
Essential Workup
Awareness of delirium as syndrom e is key.
Confusion assessm ent m ethod: o
Acute onset or fluctuating course
o
Inattention
o
Disorganized thinking
o
Altered level of consciousness
Vital signs and physical exam ination
Neurologic exam ination with careful attention to changes in m ental status
Ancillary studies to determ ine underlying cause
Tests Lab
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Electrolytes, calcium
BUN and creatinine
Glucose
CBC
Toxicology screens
Further studies based on signs and sym ptom s: o
Arterial blood gases
o
Liver function tests
o
Thyroid tests, thyroid-stim ulating horm one m easurem ent
o
Cardiac enzym es
Imaging
ECG
Head CT scan
Lum bar puncture
Chest radiograph
P.291
Differential Diagnosis
Cardiovascular diseases producing hypoperfusion
Pulm onary diseases causing hypoxia
Metabolic abnorm alities
Infections
Environm ental illness
Adverse drug event
Drug or alcohol withdrawal
Psychiatric illness
Dem entia
CNS disorders
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Treatment Pre Hospital
Intravenous access: o
Pulse oxim etry to m onitor respiratory status
Glucose m easurem ent
ECG m onitoring
Naloxone (Narcan) if associated respiratory insufficiency
Monitor patient: o
Advanced life support (ALS) transport with all m edications
Look for signs of an underlying cause: o
Medications
o
Medical alert bracelets
Docum ent basic neurologic exam ination: o
Glasgow com a scale score
o
Pupils
o
Extrem ity m ovem ents
Initial Stabilization
Most patients with delirium do not need m edications acutely.
Treatm ent is based on cause of delirium .
Chem ical sedation in severely agitated patients: o
Benzodiazepines
o
Neuroleptics
o
If withdrawal is likely, consider lorazepam .
ED Treatment
Diagnosis and treatm ent of underlying m edical condition
Thiam ine is adm inistered to alcoholic and m alnourished patients.
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For patients who are significantly agitated, treatm ent of agitation m ay help facilitate ED workup: o
Benzodiazepines
o
Neuroleptics
Medication (Drugs)
Alprazolam : 0.25–0.5 m g PO
Haloperidol: 5–10 m g IV or IM
Lorazepam : 0.5–2 m g IV, IM, or PO
Thiam ine: 100 m g IV, IM, or PO
Follow-Up Disposition Admission Criteria
When cause is unclear, adm it.
If delirium has not resolved, adm it.
Discharge Criteria
Treatable cause is found and treated.
Mental status clears while in the ED: o
Reliable caregivers and follow-up
References 1. Am erican College of Em ergency Physicians. Clinical policy for the initial approach to patients presenting with altered m ental status. Ann Em erg Med. 1999;33:251–280. 2. Hustey FM, Meldon SW. The prevalence and docum entation of im paired m ental status in elderly em ergency departm ent patients. Ann Em erg Med. 2002;39:248–253.
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3. Inouye SK, van Dyck CH, Alessi CA, et al. Clarifying confusion: the confusion assessm ent m ethod: a new m ethod for detection of delirium . Ann Intern Med. 1990;113:941–948. 4. Kalbfleisch N. Altered m ental status. In: Em ergency Care of the Elder Person. St. Louis, MO: Beverly Cracom Publications, 1996:119–142. 5. Murphy BA. Delirium . Em erg Med Clin North Am . 2000;18:243–252.
Codes ICD9-CM 780.09
ICD10 F05.9
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Delivery, Unco m plicated
Delivery,
Uncomplicated James Walker
Basics Etiology
Delivery in ED is rare: o
Incidence of ED deliveries in United States is not known.
o
Health care system s in which patients have little prenatal care tend to have greater incidence of ED deliveries.
ED deliveries usually occur in one of following three scenarios: o
Multiparous patient with history of prior rapid labor
o
Nulliparous patient who does not recognize sym ptom s of labor
o
Patients with lack of prenatal care, lack of transportation, or prem ature labor
Diagnosis
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Signs and Symptoms
True labor presents as uterine contractions occurring at least every 5 m inutes and lasting 30–60 seconds.
Signs and sym ptom s of im pending delivery: o
Ruptured m em branes (am niotic sac)
o
Bloody show (loss of m ucous plug)
o
Urge to push or to have bowel m ovem ent
Signs of im m inent delivery: o
Fully effaced and dilated cervix (about 10 cm in term infant)
o
Palpable fetal parts
o
Bulging of perineum
o
Widening of vulvovaginal area
Significant vaginal bleeding with labor dem ands im m ediate assessm ent for placenta previa or abruption.
Essential Workup
Bim anual pelvic exam is m ost useful tool to assess presence of labor and possibility of im m inent delivery: o
Assess dilation, station, and effacem ent.
o
Bim anual exam should not be done with vaginal bleeding until ultrasound can rule out placenta previa.
Fetal heart tones (FHTs) should be obtained by Doppler.
Tests Lab
If patient is in active labor, CBC, blood typing, and Rh screen should be sent: o
Kleihauer-Betke testing should be ordered after delivery if Rh-negative m other gives birth to Rh-positive child.
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o
Rh im m unoglobulin can be adm inistered to m other within 72 hours of delivery.
Urinalysis if there is concern about urinary tract infection or pre-eclam psia
Imaging
Im aging studies are not needed for uncom plicated vaginal deliveries.
Third-trim ester vaginal bleeding should have em ergent ultrasound to evaluate for placental abruption or placenta previa.
Differential Diagnosis
Braxton Hicks contractions: o
Irregular uterine contractions that do not result in cervical dilation or effacem ent
Muscular low back pain
Round uterine ligam ent pain
Other causes of abdom inal pain, such as torsion of the ovary, appendicitis, nephrolithiasis
Treatment Pre Hospital
Place patients in left lateral recum bent position.
Em ergency m edical services (EMS) personnel should be adequately trained and have proper equipm ent available for delivery.
EMS transportation of high-risk obstetric patients before delivery: o
Lower neonatal m orbidity and m ortality
o
Faster and less expensive when com pared with
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transportation of neonate after delivery
Use of air transport for obstetric patients has been shown to be safe and effective: o
If altitude during flight can result in hypoxia for fetus, pregnant patients should be placed on supplem ental oxygen.
Initial Stabilization
Im m ediate pelvic exam ination to assess for cervical dilation, effacem ent, station, or presenting parts
Patients in active labor should be transferred to Labor and Delivery im m ediately unless delivery is im m inent.
If patient is com pletely dilated and fetal parts are on perineal verge, prepare for ED delivery.
ED Treatment
Obstetrician should be notified that delivery will be occurring in ED.
If patient is high risk or fetus is Table o f C o ntents > Depressio n
Depression
Kathy Sanders
Basics Description Major depression:
Psychiatric illness with depressed m ood and neurovegetative signs and sym ptom s lasting two weeks or m ore
Significant associated m orbidity and m ortality
Clinician should try to recognize this disorder in the m edically ill.
Etiology
Major depression with suicidal ideations: o
Biological illness associated with derangem ents in several neurotransm itter system s of the brain, including serotonin
Causes of neurobiological derangem ent include: o
Genetic predisposition
o
Medical illness
o
Effects of m edications
o
Chronic unrem itting stressors in a predisposed individual
Wom en are twice as likely to have m ajor depression than
Pa ge 1 4 2
m en: o
Men are m ore likely to com plete suicide successfully
Pediatric Considerations
Depressed children and adolescents are difficult to diagnose because the criteria are not as easily recognized
Indicators of m ajor depression in children: o
Irritability
o
Changes in school, hom e, and social functioning
o
Social withdrawal
o
Substance abuse
Consultation with a child psychiatrist is crucial in further assessm ent and disposition
Diagnosis Signs and Symptoms
Wide variety of presentations: o
Dram atically in suicidal crisis
o
Quietly with som atic com plaints, panic attacks, or psychosocial distress
Vague som atic com plaints: o
Weakness, m alaise
o
Weight loss
o
Headache
o
Back pain
Dim inished sense of self-esteem
Loss of interest in or lack of enjoym ent of pleasurable activities
Loss of energy
Poor appetite
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Sleep disturbance
Decreased attention span
Irritability
Essential Workup
Eliciting the signs and sym ptom s of m ajor depression is key to m aking the diagnosis.
DSM-IV diagnostic criteria include: o
The presence of depressed m ood or loss of interest or pleasure for two weeks or longer accom panied by at least five of the following criteria:
Weight loss or gain
Insom nia or hypersom nia
Psychom otor agitation or retardation
Fatigue or loss of energy
Feelings of excessive guilt or worthlessness
Dim inished thinking or concentration or indecisiveness
Suicidal ideation or preoccupation with death
Tests Lab
May be needed for m edical screening based on the initial presentation
CBC
Electrolytes, blood urea nitrogen, creatinine, glucose
Liver function tests
Thyroid screen
Differential Diagnosis Depressivelike Psychiatric Illnesses Dysthym ia:
Adjustm ent reactions
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Bereavem ent
Acute reactions to stress
Medical Causes of Depression
Drug induced: o
Antihypertensives
o
Oral contraceptives
o
Steroids
o
Cim etidine and ranitidine
o
Sedative-hypnotics
o
Cocaine and am phetam ine
o
Beta-blockers
o
Metoclopram ide
Endocrine disorders: o
Thyroid
o
Adrenal
o
Diabetes m ellitus
o
Hyperparathyroid
Tum ors: o
Pancreatic
o
Lung
o
Brain
Neurologic disorders: o
Dem entia (early phase)
o
Epilepsy
o
Huntington's disease
o
Multiple sclerosis
o
Parkinson's disease
o
Stroke
o
Subdural hem atom a
o
Syphilis
Infections: o
Hepatitis
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o
Influenza
o
Mononucleosis
Nutritional disorders: o
Folate deficiency
o
Pellagra
o
Vitam in B 1 2 deficiency
Electrolyte disturbances
End-stage renal pulm onary and cardiovascular disease
Chronic pain syndrom es
Treatment Initial Stabilization One-to-one nursing, or restrain any potentially suicidal patient for patient safety
ED Treatment Psychological Management
Em pathetic listening to understand the stressors involved in the depression helps focus and encourage patients.
Em phasizing that depression is a treatable condition is reassuring as well as helpful in developing a treatm ent alliance.
Initiation of Psychotropic Medications
Use for diagnosed neurovegetative, m ajor depression
Decision to initiate antidepressant m edication should be for patients with established follow-up and only with enough m edication given until the next appointm ent.
Low-dose benzodiazepines or neuroleptics m ay be used for associated agitation, insom nia, or psychosis.
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Usually takes weeks for antidepressant m edications to resolve m ajor depression.
Choice of drug for the initiation of antidepressant therapy depends on:
o
Efficacy
o
Side-effect profile of the agent
o
Potential lethality if used to overdose
o
Com pliance factors
Selective serotonin reuptake inhibitors (citalopram , escitalopram , fluoxetine, sertraline, paroxetine) o
Well tolerated
o
Side effects include
Mild nausea
Decreased appetite
Agitation
Som nolence
Sexual dysfunction
Minim al overdose potential
o
Starting dose is often final dose
o
Sertraline better tolerated in the m edically ill but m ay be titrated to 150–200 m g
P.301
Tricyclic antidepressants (am itriptyline, im ipram ine, nortriptyline): o
Side effects include:
Anticholinergic effects
Postural hypotension
Sedation
Decreased seizure threshold
Overdoses of as little as 1 g of tricyclic
Pa ge 1 4 2
antidepressant can be fatal o
Nortriptyline is best tolerated and effective
Monoam ine oxidase inhibitors (phenelzine, tranylcyprom ine): o
Dietary restrictions to avoid hypertensive crisis
o
Best prescribed by psychiatrist
Medication (Drugs)
Am itriptyline: initial 25–50 m g PO per day
Citalopram 20–40 m g PO per day
Escitalopram 10 m g PO per day
Fluoxetine: 20 m g PO per day
Im ipram ine: initial 25–50 m g PO per day
Nortriptyline: initial 25 m g PO per day
Paroxetine: 20 m g PO per day
Phenelzine: 15 m g PO TID
Sertraline: 50 m g PO per day
Tranylcyprom ine: 10 m g PO t.i.d.
Follow-Up Disposition Admission Criteria
Patient is suicidal or at high risk for suicide o
See Suicide, Risk Evaluation
Minim al or unreliable social supports
Previous history of suicide or poor treatm ent response
Sym ptom s so severe that continual observation or nursing supportive care is required
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Psychotic features
Civil com m itm ent for psychiatric hospitalization is necessary if the patient is refusing treatm ent and is suicidal or otherwise judged to be at-risk to harm self or others.
Discharge Criteria
Low suicide risk
Adequate social support
Close follow-up available
Issues for Referral
Insurance carrier determ ines inpatient disposition.
Options for any level of care are specified by the patient's insurance coverage
Outpatient followup appointm ents with m ental health provider are im portant if discharging rather than adm itting. Waiting tim es for appointm ents m ay m ake this difficult
Use of case m anagem ent or social services in ED for disposition issues
References 1. APA practice guidelines for the treatm ent of patients with m ajor depressive disorder, 2nd ed. Washington DC: APPI, 2000. 2. Cassem NH et al. Mood disordered patients. In: Stern TA, Fricchione GL, Cassem NH, Jellinek MS, Rosenbaum JR, eds. MGH Handbook of general hospital psychiatry. 5th ed. St. Louis, MO: Mosby, 2004. 3. Rosenbaum JF, Arana GW, Hym an SE, Labbate LA, Fava M. Drugs for the Treatm ent of Depression. In: Rosenbaum JF, Arana GW, Hym an SE, Labbate LA, Fava M, eds. Handbook of psychiatric drug therapy. 5th ed. Philadelphia, PA: Lippincott William s & Wilkins, 2005:55–120.
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4. Stern TA, Herm an JB, Slavin PL, eds. MGH Guide to Prim ary Care Psychiatry, 2nd ed. New York: McGraw-Hill, 2004.
Codes ICD9-CM 311
ICD10 F32.9
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Derm ato m yo sitis/Po lym yo sitis
Dermatomyositis/Polymyositis Sean-Xavier Neath
Basics
DM/PM is a system ic inflam m atory m yopathy.
Progression of m uscle weakness over weeks to m onths
Respiratory insufficiency from respiratory m uscle weakness
Aspiration pneum onia owing to a weak cough m echanism , pharyngeal m uscle dysfunction, and esophageal dysm otility
Cardiac m anifestations include m yocarditis and congestive heart failure (CHF).
Arthralgias of the hands, wrists, knees, and shoulders
Ocular m uscles are not involved, and facial m uscle weakness m ay be seen in advanced cases.
Etiology
The exact cause is unknown, although an autoim m une m echanism is thought to be largely responsible.
Incidence about 1:100,000 with a fem ale preponderance
Association with HLA-B8 and HLA-DR3
There m ay be an association between PM and viral, bacterial, and parasitic infections.
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DM/PM occurs with collagen vascular disease about 20% of the tim e.
Deposition of com plem ent is the earliest and m ost specific lesion, followed by inflam m ation, ischem ia, m icroinfarcts, necrosis, and destruction of the m uscle fibers.
Pediatric Considerations
Although DM is seen in both children and adults, PM is rare in children.
Juvenile form m ay include vasculitis, ectopic calcifications (calcinosis cutis), and lipodystrophy.
The juvenile form m ay be associated with coxsackievirus.
Diagnosis Signs and Symptoms History
Polym yositis (PM) is distinguished from derm atom yositis (DM) by the absence of rash.
Patients with PM present with m uscle pain and proxim al m uscle weakness.
DM presents with skin rash, m uscle pain, and weakness.
Constitutional sym ptom s include weight loss, fever, anorexia, m orning stiffness, m yalgias, and arthralgias.
Often note fatigue doing custom ary tasks: o
Brushing hair, clim bing stairs, reaching above the head, rising from a chair
o
May also com plain of dysphagia, dyspnea, and cough
Progressive weakness of the proxim al lim b and girdle m uscles is seen early; distal m uscle weakness can occur late in the disease.
Pa ge 1 4 3
Physical Exam Skin findings of DM:
Skin rash occurs with or precedes m uscle weakness.
Heliotrope rash (lilac discoloration) on the upper eyelids associated with edem a
Gottron sign: violaceous or erythem atous papules over the extensor surfaces of the joints, particularly knuckles, knees, and elbows
Shawl sign: a V-shaped erythem atous rash occurring on the back and shoulders
Periungual telangiectasias: nail-bed capillary changes that include thickened irregular and distorted cuticles
“Machinist hands―: darkened horizontal lines across the lateral and palm ar aspects of the fingers
Tests
Serum m uscle enzym es: o
Creatine phosphokinase (CPK)
o
Lactate dehydrogenase (LDH), aldolase, aspartate transam inase (AST), and serum glutam ic-oxaloacetic transam inase (SGOT)
ECG and urinalysis
Diagnostic criteria established in 1975 by Bohan and Peter: o
Sym m etric proxim al m uscle weakness with dysphagia and respiratory m uscle weakness
o
Elevation of serum m uscle enzym es
o
Electrom yographic features of m yopathy
o
Muscle biopsy showing features of inflam m atory m yopathy
o
Confidence lim its for diagnosis (typical rash m ust be seen for diagnosis of DM)
Definite diagnosis: three or four criteria
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Probable diagnosis: two criteria
Possible diagnosis: one criterion
Newer diagnostic criteria using the MHC/CD8 com plex m ay prove to be m ore specific for this diagnosis.
Imaging
Chest radiograph m ay show interstitial lung disease, evidence of aspiration pneum onia, CHF, or cardiom yopathy.
Electrom yogram (EMG) studies show m yopathic potentials that are not specific for DM/PM.
Pulm onary function tests are useful in following the progression of interstitial lung disease.
Renal biopsies of patients m ay show focal proliferative glom erulonephritis.
Muscle biopsy is the definitive test: o
In PM, inflam m atory infiltrates are often endom ysial, although they m ay be perivascular.
o
In DM, inflam m atory infiltrates are m ostly perivascular and include a high percentage of B cells.
P.303
Differential Diagnosis
Collagen vascular diseases
Muscular dystrophies, spinal m uscular atrophy, m yasthenia gravis, am yotrophic lateral sclerosis, poliom yelitis, Guillain-Barré syndrom e
Hypothyroidism , hyperthyroidism , Cushing syndrom e
Drug-induced: colchicine, zidovudine (AZT), penicillam ine, ipecac, ethanol, chloroquine, corticosteroids
Toxoplasm osis, trichinosis, coxsackievirus, HIV, influenza,
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Epstein-Barr virus
Hypokalem ia, hypercalcem ia, hypom agnesem ia, vasculitis, paraneoplastic neurom yopathy, hypereosinophilic m yalgia syndrom e
Treatment Initial Stabilization
Intubation and m echanical ventilation as required
Nasogastric (NG) suction to prevent aspiration
Pneum othorax has been described as a rare occurrence in childhood DM.
ED Treatment
Elevate head of the bed to prevent aspiration.
Begin high-dose corticosteroids to suppress inflam m ation and im prove m uscle weakness.
Avoid triam cinolone and dexam ethasone because there is an associated m yopathy.
Efficacy of prednisone determ ined by objective increase in m uscle strength
Im m unosuppressive m edications
Azathioprine is lim ited by GI intolerance and bone m arrow suppression.
Cyclosporine has been used but with lim ited success.
Methotrexate
Do not treat CPK level.
Medication (Drugs)
Azathioprine: 3 m g/kg/d PO for 4–6 m onths
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Methotrexate: 15–25 m g PO per week; (peds: 0.5–1 PO m g/kg per week–not to exceed adult dose)
Prednisone: 60 m g/d PO (peds: 1–2 m g/kg/d PO)
Intravenous im m unoglobulin (IVIG), m ycophenolate, cyclosporine, cyclophospham ide are increasingly used by rheum atologists.
Follow-Up Disposition Admission Criteria Respiratory insufficiency, aspiration pneum onia, m uscle weakness, weakened cough m echanism s, and pharyngeal dysfunction, CHF
Discharge Criteria
Well-appearing patients with no respiratory dysfunction and no risk for aspiration
Patients who can take oral corticosteroids and im m unosuppressive agents as outpatients
Issues for Referral Consultation with a rheum atologist should be m ade when the diagnosis is suspected for assistance with definitive diagnosis and further treatm ent.
References 1. Bohan A, Peter JB. Polym yositis and derm atom yositis. N Engl J Med. 1975;292:344–347. 2. Caro I. Derm atom yositis as a system ic disease: collagen vascular diseases. Med Clin North Am . 1989;73(5):1181–1191. 3. Dalakas M. Inflam m atory disorders of m uscle: progress in polym yositis, derm atom yositis and inclusion body m yositis. Curr Opin
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Neurol. 2004;17:561–567. 4. Pachm an L. Juvenile derm atom yositis: im m unogenetics, pathophysiology, and disease expression. Rheum Dis Clin North Am . 2002;28(3):579. 5. Shearer P, Jagoda A. Derm atom yositis. In: Marx JA, ed. Rosen's Em ergency Medicine: Concepts and Clinical Practice. 5th ed. St. Louis, MO: Mosby; 2002:1525–1526.
Miscellaneous SEE ALSO: Hypokalem ia; Hypothyroidism ; Myasthenia Gravis; System ic Lupus Erythem atosus
Codes ICD9-CM 710.4 710.3
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Diabetes Insipidus
Diabetes Insipidus
Rahul Patwari
Basics Description
Excessive urinary loss of solute-free water (polyuria)
Often characterized by excessive fluid intake (polydipsia)
Two types: o
Central DI (CDI; failure or deficiency of arginine vasopressin [AVP] release):
Four types:
No AVP to release (loss or m alfunction of posterior pituitary neurons)
Defective osm oreceptors—release AVP only in response to severe dehydration
o
Elevated threshold for AVP release
Subnorm al am ount of AVP released
Nephrogenic DI (lack of renal response to AVP):
Differentiate from prim ary polydipsia.
Genetics
Central DI: Fam ilial cases have been reported (autosom al dom inant).
Nephrogenic DI: usually X-linked recessive in m ales
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Etiology
Central DI: o
Any condition that disrupts the osm oreceptor-hypothalam us-hypophyseal axis:
Traum a (skull fractures, hem orrhage)
CNS neoplasm —DI can be considered a tum or m arker.
Pituitary adenom as
Craniopharyngiom as
Germ inom as
Pinealom as
Metastatic tum ors
Leukem ia
Histiocytosis X
Sarcoidosis
o
Congenital CNS defects
o
Pituitary or hypothalam ic surgery
o
CNS infections (e.g., m eningitis, encephalitis)
o
Pregnancy (Sheehan syndrom e)
o
Idiopathic (autoantibodies, occult tum or)
o
Wolfram syndrom e (DI, diabetes m ellitus, optic atrophy, deafness)
Nephrogenic DI: o
Congenital renal disorders
o
Obstructive uropathy
o
Renal dysplasia
o
Polycystic kidney disease
o
System ic disease with renal involvem ent
o
Sickle cell disease
o
Sarcoidosis
o
Am yloidosis
o
Drugs:
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o
Am photericin
Phenytoin
Lithium (persists past discontinuation of drug)
Am inoglycosides
Methoxyflurane
Dem eclocycline
Electrolyte disorders:
Hypercalcem ia
Hypokalem ia
Pregnancy Considerations
Sheehan syndrom e
Release of placental vasopressinase
Desm opressin (dDAVP) resists this vasopressinase.
Diagnosis Signs and Symptoms History
Polyuria (up to 16–24 L/d of urine): o
Polydipsia (often craves cold fluids): o
Note the voiding frequency.
Note the am ount of PO fluid intake per day.
Signs and sym ptom s of hypothalam ic tum ors: o
Headache
o
Visual disturbances
o
Growth disturbances
o
Cachexia
o
Obesity
o
Hyperpyrexia
o
Sleep disturbances
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o
Sexual precocity
o
Em otional disturbances
Drug intake
Physical Exam
Signs of dehydration
Signs of traum a
Pediatric Considerations
Polyuria and polydipsia m ay not be recognized by caregivers until sym ptom s of dehydration develop.
Neonatal diabetes insipidus: o
Often present at birth
o
If unrecognized, dehydration and hypernatrem ia m ay cause perm anent CNS dam age.
In infants: o
Irritability
o
Poor feeding
o
Growth failure
o
Interm ittent high fever
o
Abnorm al behavior (hyperactivity, restlessness)
In children: o
Enuresis
Essential Workup
Clinical diagnosis in the ED: o
Elevated serum sodium concentration
o
Copious am ounts of dilute urine
History: o
Am ount of PO fluid intake per day
o
Voiding frequency
o
Medication use history
Physical exam : o
Signs of dehydration
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o
Signs of traum a
Tests Lab
Serum and urine osm olality: o
High serum osm olality
o
Low urine osm olality
Electrolytes, BUN, creatinine, and glucose: o
Hypernatrem ia
o
Hypercalcem ia
o
Hypokalem ia
CBC: o
Anem ia m ay be a sign of a neoplasm .
Serum and urine AVP tests are expensive and unnecessary in the ED.
Imaging
As needed to evaluate for traum a or search for neoplasm s
Chest radiograph
CT of brain
MRI of pituitary axis
Diagnostic Procedures/Surgery N/A
Dehydration Test
Unnecessary in the em ergency setting
Can be dangerous in cases of hypotension or sm all children
Perform ed as a confirm atory test for those receiving treatm ent
Method: o
No PO fluids for 3 hours or until urine osm olality stabilizes
o
Determ ine plasm a osm olality.
Pa ge 1 4 4
o
Should be >288 m m ol/kg
o
AVP 5 units (or desm opressin 1 µg SC or 10 µg intranasally)
o
Check urine osm olality at 0 m inutes, 30 m inutes, and 60 m inutes afterward.
Interpretation: o
In norm al patients:
Osm olality will not change >9%.
Endogenous AVP will increase osm olality to m axim um .
o
Exogenous AVP has no effect.
In central DI:
Osm olality rises >9%.
No or little endogenous AVP
Exogenous AVP has significant concentrating effect.
o
In nephrogenic DI:
Osm olality does not change.
Renal tubules are insensitive to AVP.
Differential Diagnosis
Prim ary water deficit: o
Inadequate access to free water
o
Increased insensible water loss (e.g., prem ature infants)
o
Inadequate breast-feeding
Prim ary sodium excess: o
Excessive sodium bicarbonate during resuscitation
o
Hypernatrem ic enem as
o
Ingestion of seawater
o
Hypertonic saline adm inistration
o
Accidental substitution of salt (sodium chloride [NaCL]) for glucose in infant form ulas
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o
Intentional salt poisoning
o
High breast m ilk sodium
Prim ary polydipsia (psychogenic polydipsia): o
Solute-induced polyuria
o
Diuretic use
o
Resolving acute renal failure
o
Uncontrolled diabetes m ellitus
P.305
Treatment Pre Hospital
Manage airway, breathing, and circulation (ABCs).
IV access and fluids if signs of dehydration exist
Initial Stabilization
Manage ABCs.
Manage traum atic injuries accordingly.
High index of suspicion for head traum a
ED Treatment
Correction of hypotension: o
Use of 0.9% NaCl is indicated for shock.
o
Intravascular losses represent only about one twelfth of total water losses.
Correction of initial water deficit: o
Sym ptom atic hypertonicity (seizures, com a):
P o s m should be corrected aggressively 1 to 2 m Osm /kg/h to about 330 m Osm /kg
To a level of Na = 160 or until asym ptom atic
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o
Asym ptom atic hypertonicity with Na Table o f C o ntents > Diabetes M ellitus, Juvenile
Diabetes
Mellitus, Juvenile Madeline M. Joseph
Basics Description
Decrease in effective circulating insulin
Increase in counterregulatory horm ones including glucagon, catecholam ines, cortisol, and growth horm one
Hyperglycem ia owing to: o
Decreased peripheral glucose utilization
o
Increased hepatic gluconeogenesis
Hyperosm olality and osm otic diuresis
Ketoacidosis produced by increased lipolysis, with ketone body (β-hydroxybutyrate, acetoacetate) production, causes ketonem ia and m etabolic acidosis.
Potassium deficit: o
Intracellular shifts into extracellular space owing to hydrogen ion exchange.
o
Loss from osm otic diuresis
Etiology Mechanism
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Im m une-m ediated pancreatic islet β-cell destruction
Precipitating events leading to diabetic ketoacidosis (DKA): o
Infection
o
Stress
o
Pregnancy
o
Psychiatric disorders, including eating disorders
o
Medication noncom pliance, inappropriate interruption of insulin pum p therapy, or treatm ent error
Risk factors for cerebral edem a: o
Attenuated rise in m easured serum sodium during DKA therapy (unrelated to the volum e or sodium content of intravenous fluid or rate of change in serum glucose)
o
Bicarbonate treatm ent for acidosis correction
o
Hypocapnia
o
Increased serum urea nitrogen
o
No association with degree of hyperglycem ia
Diagnosis Signs and Symptoms
Polydipsia
Polyuria
Polyphagia
Weight loss, unexplained
Diabetic ketoacidosis (DKA): o
Initial presentation in 20–40% of patients
o
Nausea
o
Vom iting
o
Abdom inal pain, often resolving with reduction in
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ketosis
o
Hyperpnea
o
Ketotic breath
o
Dehydration
o
Shock
Cerebral edem a: o
The incidence ranges from 0.87–1.1%.
o
Cerebral edem a accounts for 57–87% of all DKA deaths.
o
Headache
o
Gradual decrease or deterioration in level of consciousness
o
Inappropriate slowing in pulse rate
o
Increase in blood pressure
Essential Workup
For DKA: o
Hourly vital signs and neurologic checks
o
Frequent blood chem istries
o
ECG m onitoring (in severe DKA) to assess T waves for evidence of hyperkalem ia/hypokalem ia
o
Accurate fluid input and output. Consider urinary catheterization in patients with im paired level of consciousness.
Tests Lab
For DKA: o
Glucose, serum , and bedside hyperglycem ia
o
Urinalysis:
Glycosuria
Ketonuria
Exclude urinary tract infection.
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o
Blood chem istries every 2–4 hours until acidosis has resolved (m ore frequent as clinically indicated in the m ore severe cases)
o
Electrolytes and venous pH
o
Anion gap m etabolic acidosis:
Potassium —high or norm al (artifactual owing to extracellular shift)
Sodium —low or norm al (m ay be artifactual owing to hyperglycem ia)
Bicarbonate—low
o
Serum ketones—elevated
o
Serum osm olality
o
CBC:
White blood cell count often elevated owing to stress or infection
o
Calcium
o
Phosphate
o
Cultures as indicated
Differential Diagnosis
Infection: o
Urinary tract infection
o
Gastroenteritis
o
Appendicitis
o
Sepsis
Ingestion (salicylates, alcohols, glycols)
Diabetes insipidus
P.307
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Treatment Pre Hospital For DKA:
Monitor airway, breathing, and circulation (ABCs).
Airway protection
Establish intravenous access and initiate fluid therapy.
Initial Stabilization For DKA:
Oxygen
Cardiac m onitor
Intravenous access and volum e resuscitation
ED Treatment For DKA
Fluid replacem ent: o
Assum e fluid deficit of 10% of body weight
o
Initial volum e expansion with 10–20 m L/kg of 0.9% NaCl; m ay repeat to achieve hem odynam ic stability
o
Correct 50% of fluid deficit over first 8 hours, rem ainder over 24–48 hours.
o
Do not give >3 L/m 2 over first 24 hours.
Begin intravenous insulin infusion after ketoacidosis confirm ed: o
Initial rate of continuous infusion (regular insulin) 0.1 U/kg/h
o
Adjust rate to drop serum glucose m axim um of 100 m g/dL/h.
o
Add dextrose to infusion fluid when serum glucose 320
CBC: o
Leukocytosis m ay be present without infection.
o
If left shift in differential, suspect infection.
Other lab tests: o
Am ylase—elevation is nonspecific in DKA.
o
Lipase—elevation specific for pancreatitis
o
Calcium , Mg, Phosphate: all usually decreased as is K +
Imaging
CT head—to rule out other causes of altered m ental status
Chest radiograph—if pneum onia suspected as precipitant or hypoxia present
ECG—to rule out ischem ia as a precipitant, and look for signs of hyper/hypo K +
Differential Diagnosis
Other causes of anion gap acidosis
Use ACAT MUD PILES m nem onic: o
Alcoholic ketoacidosis
o
Carbon m onoxide/cyanide
o
Aspirin
o
Toluene
o
Methanol
o
Urem ia
o
Diabetic ketoacidosis
o
Paraldehyde
o
Iron/isoniazid
o
Lactic acidosis
o
Ethylene glycol
o
Starvation/sepsis
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Hyperglycem ic hyperosm olar nonketotic syndrom e
P.309
Treatment Pre Hospital
Fluid bolus often initiated in field
Quantify am ount given by param edics to guide further ED fluids
Initial Stabilization
Airway, breathing, and circulation (ABCs) for patients with altered m ental status
Com a cocktail for AMS: naloxone, thiam ine, Accu-Chek
0.9% norm al saline (NS) bolus for hypotension/tachycardia
ED Treatment
Cardiac m onitor and pulse oxim etry for patients with abnorm al vitals
Fluids: o
Average adult water deficit is 100 m L/kg (5–10 L).
o
Initial 1- to 2-L bolus of 0.9% NS to restore intravascular volum e over first hour.
o
If corrected serum sodium is low, continue with 0.9% NS, giving 1–2 m ore liters over the next 2–4 hours.
o
If corrected serum sodium is norm al or elevated, use 0.45% NS giving 1–2 m ore liters over next 2–4 hours.
o
Be careful to avoid fluid overload in patients with
Pa ge 1 4 6
cardiac disease. o
Avoid precipitous falls in serum sodium /osm olality as this m ay contribute to cerebral edem a.
o
Total fluid replacem ent should take 24–36 hours.
Insulin: o
Reverses ketogenic state and downregulates counterregulatory horm ones
o
Adm inistered as continuous IV infusion of regular insulin at 0.1 units/kg/h:
Adjust infusion in response to changes in glucose and anion gap
o
Continue until pH >7.3 and resolution of anion gap.
o
Serum glucose will fall sooner than resolution of acidosis and should be kept >250 m g/dL with glucose-containing fluids such as D 5 , 45% NS.
Potassium : o
Adm inistration is essential.
o
Total body deficit of 3–5 m Eq/kg
o
Will drop precipitously with adm inistration of fluid and insulin
o
Adm inister KCl, 10 m Eq/h IV once renal function is established and K + is known to be 10 years, but recent studies dem onstrate safety in infants as well
o
Consider oral agent if concurrent cutaneous or oral candidiasis is present or in recalcitrant case because stool m ay be colonized with C. albicans.
Antibacterials: o
Typically concurrent with other therapies
o
Mupirocin (Bactroban) applied after diaper changes
o
System ic antibiotics rarely needed
Medication (Drugs)
Ciclopirox 0.77% cream , gel, or suspension: applied topically twice daily after diaper change
Clotrim azole 1% cream : applied topically twice daily after diaper change
Hydrocortisone 0.5–1% topical cream : applied three or four tim es daily
Miconazole topical 2% cream : applied twice daily after diaper change
Mupirocin 2% ointm ent or cream (Bactroban): applied topically three to five tim es daily after diaper changes (for infants >3 m onths of age)
Nystatin 100,000 U/g cream , powder, or ointm ent: apply twice daily after diaper change.
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Follow-Up Disposition Admission Criteria
Evidence of child abuse or neglect
Evidence of sepsis
References 1. Gupta AK, Skinner AR. Managem ent of diaper derm atitis. Int Soc Derm . 2004;43:830–834. 2. Sires UL, Mallory SB. Diaper derm atitis: how to treat and prevent. Postgrad Med. 1995;98:79–84. 3. Ward DB, Fleischer AB Jr, Feldm an SR, et al. Characterization of diaper derm atitis in the United States. Arch Pediatr Adolesc Med. 2000;154(9): 943–946. 4. Wolf R, Wolf D, Tuzun B, et al. Diaper derm atitis. Clin Derm atol. 2000;18(6):657–660.
Codes ICD9-CM 691.0
ICD10 L22
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Diaphragm atic Traum a
Diaphragmatic
Trauma Robert S. Hamilton
Basics Description
Penetrating injury: o
Violation of the diaphragm by penetrating object (knife and gunshot wounds)
o
May involve any portion of diaphragm
Blunt injury: o
Increased intra-abdom inal or intrathoracic pressure is transm itted to diaphragm , causing rupture.
o
Injuries are typically in radial orientation:
Posterolateral area of the left side of the diaphragm
Em bryologic point of weakness
Injuries are frequently between 5 cm and 15 cm in length.
Diaphragm atic defects do not heal spontaneously because of pleuroperitoneal pressure gradient: o
May exceed 100 cm H 2 O during m axim al respiratory effort
Pa ge 1 4 8
o
Prom otes herniation of abdom inal contents through rent in diaphragm and into chest
Epidemiology Incidence Estim ated to be 1–6% in all patients sustaining m ultiple-system traum a
Etiology
Lateral torso im pact is three tim es m ore likely to result in ipsilateral diaphragm atic rupture than frontal im pact.
Suspect diaphragm atic injury: o
Penetrating traum a to thoracoabdom inal area
o
Injuries that cross plane of the diaphragm
Diagnosis Alert
In acute phase, there m ay be no abdom inal visceral herniation: o
This injury m ay even be m issed on initial laparotom y or laparoscopy.
Signs and Symptoms
Vary depending on whether phase is acute, latent, or obstructive: o
Acute:
Tachypnea
Hypotension
Absence of breath sounds
Abdom inal distention
Bowel sounds in chest
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o
Latent:
Abdom inal discom fort from interm ittent herniation of abdom inal contents into thorax
o
Abdom inal pain that is worse postprandially
Exacerbated by lying supine
Pain radiating to left shoulder
Nausea, vom iting, or belching
Obstructive:
Severe abdom inal pain
Obstipation
Nausea, vom iting
Abdom inal distention
Strangulated abdom inal organs m ay perforate and spill abdom inal contents into chest.
Respiratory com prom ise, sepsis, and death
Essential Workup Chest radiograph m ay reveal herniated loops of bowel or other abdom inal viscera in thorax:
Pathognom onic finding is presence of nasogastric tube above diaphragm .
Findings are often nonspecific: o
Unilaterally elevated diaphragm
o
Mediastinal shift away from affected side
o
Unilateral pleural thickening
o
Areas of atelectasis or consolidation at bases
o
Sm all hem othorax or pneum othorax
50% of initial chest radiographs m ay be norm al.
Diagnosis m ay be difficult in latent phase because of interm ittent nature of herniation.
Contrast studies of gastrointestinal tract m ay be helpful.
Tests
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Lab
If diagnostic peritoneal lavage (DPL) is perform ed: o
Red blood cell count of 5,000 RBC/m m 3 is considered positive.
No laboratory studies confirm or rule out presence of diaphragm atic injury.
Imaging
Gastrointestinal contrast studies are the m ost useful in diagnosing chronic herniation of abdom inal contents through diaphragm .
Ultrasound m ay be used, particularly on right side with accom panying hepatic herniation.
Conventional CT is rarely diagnostic and has poor sensitivity.
New m ultidetector CT (MDCT) has had m uch better success at diagnosing subtle diaphragm atic injuries.
MRI m ay be useful.
P.315
Diagnostic Procedures/Surgery
Diagnostic pneum operitoneography: o
Air is injected through DPL catheter.
o
Pneum othorax on subsequent chest radiograph is diagnostic of diaphragm atic injury.
o
Poorly tolerated by unstable patients and m ay require chest tube placem ent
Thoracoscopy and laparoscopy are potentially valuable tools, both diagnostically and therapeutically.
Differential Diagnosis
Pa ge 1 4 8
Atelectasis
Hem othorax
Pneum othorax
Pulm onary contusion
Gastric dilation, intra-abdom inal fluid
Traum atic pneum atocele
Subdiaphragm atic abscess
Intrathoracic cyst
Em pyem a
Congenital eventration of the diaphragm
Treatment Alert
Herniation of abdom inal contents into chest wall m ay m im ic hem othorax or tension pneum othorax: o
Bowel sounds in chest m ay help distinguish.
o
Be suspicious of diaphragm atic injury with lateral com pression of chest:
Be cautious in placem ent of needle or tube thoracostom ies.
o
Fecal thorax has been reported with bowel rupture.
Initial Stabilization
Follow advanced traum a life support (ATLS) protocols
If respiratory distress is present, im m ediate placem ent of a nasogastric tube m ay decom press herniated abdom inal contents.
ED Treatment
Palpate within the chest wall com pletely for visceral organs before placing chest tube.
Pa ge 1 4 8
Patients with visceral perforations are septic and need aggressive resuscitation and antibiotic therapy.
Early surgical intervention is param ount.
Thoracoscopy or laparoscopy is useful in selected injuries and patients.
Em piric broad-spectrum antibiotics are indicated in the case of perforated viscera.
Medication (Drugs)
Gram -negative aerobes: o
Gentam icin: Adults/peds: 2–5 m g/kg IV initial dose
Gram -negative anaerobes: o
Clindam ycin: 900 m g (peds: 20–40 m g/kg/24h) IV q8h
o
Metronidazole: 1 g (peds: 15 m g/kg) IV load, then 500 m g (peds: 7.5 m g/kg) IV q6h
Both aerobic and anaerobic: o
Am picillin/sulbactam : 1.5–3 g (peds: 100–400 m g/kg/24h) IV q6h
o
Cefotetan: 2 g (peds: 40–80 m g/kg/24h) IV q12h
o
Cefoxitin: 2 g (peds: 80–160 m g/kg/24h) IV q12h
o
Ticarcillin/clavulanate: 3.1 g (peds: 50 m g/kg per dose) IV q6h
Follow-Up Disposition Admission Criteria
Patients with suspicion for diaphragm atic injury m ust be
Pa ge 1 4 8
adm itted to traum a surgeon.
Patients should be adm itted to m onitored or intensive care unit setting.
Discharge Criteria Patients with diaphragm atic injury or any significant suspicion for it m ust not be discharged from ED.
References 1. Blaivas M, Brannam L, Hawkins M, et al. Bedside em ergency ultrasonographic diagnosis of diaphragm atic rupture in blunt abdom inal traum a. Am J Em erg Med. 2004;22(7):601–604. 2. Kanowitz A, Markovchick V. Esophageal and diaphragm atic traum a. In: Rosen's Em ergency Medicine: Concepts and Clinical Practice. 4th Ed. St. Louis, MO: Mosby; 1998:546–554. 3. Mansour KA. Traum a to the diaphragm . Chest Surg Clin North Am . 1997;7(2):373–383. 4. Mirvis SE. Diagnostic im aging of acute thoracic injury. Sem in Ultrasound CT MR. 2004;25(2): 156–179. 5. Rosati C. Acute traum atic injury of the diaphragm . Chest Surg Clin North Am . 1998;8(2):371–379. 6. Shah R, Sabanathan S, Mearns AJ, et al. Traum atic rupture of the diaphragm . Ann Thorac Surg. 1995;60(5):1444–1449. 7. Sharm a OP, Duffy B. Transdiaphragm atic intercostals hernia: review of the world literature and presentation of a case. J Traum a. 2001;50(6): 1140–1143. 8. Vallina VL, Norwood S, McAuley C, et al. Laparoscopic diaphragm rupture repair. Surg Endosc. 2002;16(5):869.
Codes ICD9-CM 862.0 Injury to other and unspecified intrathoracic organs
ICD10
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S27.8
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Diarrhea, Adult
Diarrhea, Adult
Isam Nasr Harminder Brar
Basics Description Bowel m ovem ents characterized as frequent (m ore than three per day), loose and watery owing to an infectious or toxin exposure
Etiology N/A
Infectious
Viruses: o
50–70% of all cases
Invasive bacteria: o
Cam pylobacter:
Contam inated food or water, wilderness water, birds, and anim als
o
Most com m on bacterial diarrhea
Gross or occult blood is found in 60–90%.
Salm onella:
Contam inated water, eggs, poultry, or dairy products
Typhoid fever (Salm onella typhi) characterized
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by unrem itting fever, abdom inal pain, rose spots, splenom egaly, and bradycardia o
Shigella:
o
Vibrio parahaem olyticus:
o
Fecal or oral route
Raw and undercooked seafood
Yersinia:
Contam inated food (pork), water, and m ilk
May present as m esenteric adenitis or m im ic appendicitis
Bacterial toxin: o
Escherichia coli:
Major cause of traveler's diarrhea
Ingestion of food or water contam inated by feces
o
o
o
Staphylococcal aureus:
Most com m on toxin-related disease
Sym ptom s 1–6 hours after ingesting food
Bacillus cereus:
Classic source—fried rice left on steam tables
Sym ptom s within 1–36 hours
Clostridium difficile:
Antibiotic-associated enteritis linked to pseudom em branous colitis
Incubation period within 10 days of exposure or initiation of antibiotics
o
o
Aerom onas hydrophila:
Aquatic sources prim arily
Affects children younger than 3 years of age
Fecal leukocytes absent
Cholera:
Caused by enterotoxin produced by Vibrio
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cholerae
Profuse watery stools with m ucus (classic appearance of rice-water stools)
Protozoa: o
Giardia lam blia:
Most com m on cause of parasite gastroenteritis in North Am erica
High-risk groups: travelers, children in day care centers, institutionalized people, hom osexual m en, and cam pers who drink untreated m ountain water
o
Cryptosporidium parvum :
o
Com m only carried in patients with AIDS
Entam oeba histolytica (entam ebiasis):
5–10% extraintestinal m anifestations (hepatic am ebic abscess)
Pediatric Considerations
Most are viral in origin and self-lim ited.
Rotavirus accounts for 50%.
Shigella: infections associated with seizures
Focus evaluation on state of hydration.
Diagnosis Signs and Symptoms History
Loose, watery bowel m ovem ents
Bloody stools with m ucus
Abdom inal pain and cram ps, tenesm us, flatulence
Fever, headache, m yalgias
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Nausea, vom iting
Dehydration, lethargy, and stupor
Physical Exam
Dry m ucous m em branes
Abdom inal tenderness
Perianal inflam m ation, fissure, fistula
Essential Workup
Digital rectal exam ination to determ ine presence of gross or occult blood
Fecal leukocyte determ ination: o
Present with invasive bacteria
o
Absent in protozoal infections, viral, toxin-induced food poisoning
Tests Lab
CBC—indications: o
Significant blood loss
o
System ic toxicity
Electrolytes, glucose, BUN, creatinine—indications: o
Lethargy, significant dehydration, toxicity, or altered m ental status
o
Diuretic use, persistent diarrhea, chronic liver or renal disease
Stool culture—indications: o
Presence of fecal leukocytes
o
Historical m arkers: im m unocom prom ised, travel, hom osexual
o
Public health: food handler, day care or health care worker, institutionalized
Blood cultures—indications:
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o
Suspected bacterem ia or system ic infections
o
Ill patients requiring adm ission
o
Im m unocom prom ised
o
Elderly patients and infants
Imaging Abdom inal radiographs:
No value unless obstruction or toxic m egacolon suspected
Differential Diagnosis
Ulcerative colitis
Crohn disease
Mesenteric ischem ia
Diverticulitis, anal fissures, hem orrhoids
Irritable bowel syndrom e
Milk and food allergies
Malrotation with m idgut volvulus
Meckel diverticulum
Intussusception
Appendicitis
Drugs and toxins: o
Mannitol
o
Sorbitol
o
Phenolphthalein
o
Magnesium -containing antacids
o
Quinidine
o
Colchicine
o
Mushroom s
o
Mercury poisoning
P.317
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Treatment Pre Hospital
Difficult IV access with severe dehydration
Avoid exposure to contam inated clothes or body substances.
Initial Stabilization
Airway, breathing, and circulation m anagem ent (ABCs)
IV fluid with 0.9% norm al saline (NS) resuscitation for severely dehydrated
ED Treatment
Oral fluids for m ild dehydration (Gatorade/Pedialyte)
IV fluids for: o
Hypotension, nausea and vom iting, obtundation, m etabolic acidosis, significant hypernatrem ia or hyponatrem ia
o
0.9% NS bolus: 500 m L–1 L (peds: 20 m L/kg) for resuscitation, then 0.9% NS or D 5 W 0.45% NS (peds: D 5 W 0.25% NS) to m aintain adequate urine output
Bism uth subsalicylate (Pepto-Bism ol): o
Antisecretory agent
o
Effective clinical relief without adverse effects
Kaolin-pectin (Kaopectate): o
Reduces fluidity of stools
o
Does not influence course of disease
Antim otility drugs: diphenoxylate (Lom otil), loperam ide (Im odium ), paregoric, and codeine o
Appropriate in noninfectious diarrhea
o
Initial use of sparse am ounts to control sym ptom s in infectious diarrhea
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o
Avoid prolonged use in infectious diarrhea—m ay increase duration of fever, diarrhea, and bacterem ia and m ay precipitate toxic m egacolon
Antibiotics for Infectious pathogens: o
Cam pylobacter: quinolones or erythrom ycin
o
Salm onella: quinolones or trim ethoprim -sulfam ethoxazole (TMP-SMX)
o
Typhoid fever: ceftriaxone
o
Shigella: quinolone, TMP-SMX, or am picillin
o
Vibrio parahaem olyticus: tetracycline or doxycycline
o
Clostridium difficile: vancom ycin
o
Escherichia coli: quinolones or TMP-SMX
o
Giardia lam blia: m etronidazole or quinacrine
o
Entam oeba histolytica (entam ebiasis): iodoquinol or m etronidazole
Medication (Drugs)
Am picillin: 500 m g (peds: 20 m g/kg/24 h) PO or IV q6h
Bactrim DS (TMP-SMX): 1 tab (peds: 8–10 m g TMP/40–50 m g SMX/kg/24h) PO or 4–5 m g/kg TMP IV b.i.d.
Ceftriaxone: 1 gram (peds: 50–75 m g/kg/12h) IM or IV b.i.d.
Ciprofloxacin (quinolone): 500 m g PO or 400 m g IV b.i.d. (older than 18 years)
Doxycycline: 100 m g PO or 100 m g IV b.i.d.
Erythrom ycin: 500 m g (peds: 40–50 m g/kg/24h) PO q.i.d.
Iodoquinol: 650 m g (peds: 30–40 m g/kg/24h) PO t.i.d.
Metronidazole: 250 m g (peds: 35 m g/kg/24h) PO t.i.d. (older than 8 years)
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Quinacrine: 100 m g (peds: 6 m g/kg/24h) PO t.i.d.
Tetracycline: 500 m g PO or IV q6h
Vancom ycin: 500 m g (peds: 10–50 m g/kg/24h) IV q.i.d.
Follow-Up Disposition Admission Criteria
Hypotension, unresponsive to IV fluids
Significant bleeding
Signs of sepsis or toxicity
Intractable vom iting or abdom inal pain
Severe electrolyte im balance or m etabolic acidosis
Altered m ental status
Children with >10–15% dehydration
Discharge Criteria
Mild cases requiring oral hydration
Dehydration responsive to IV fluids
References 1. Dupont HL. What's new in enteric infectious diseases at hom e and abroad. Curr Opinion Infect Dis. 2005;18:407–412. 2. Gough JE, Clem ent PA. Diarrhea. In: Marx JA, Hockberger RS, Walls RM, et al., eds. Rosen's Em ergency Medicine: Concepts and Clinical Practice. 5th ed. St. Louis, MO; 2002:200–208. 3. Hogan D. The em ergency departm ent approach to diarrhea. Em erg Med Clin North Am . 1996;14(4): 673–694. 4. Reisdorff E, Pflug V. Infectious diarrhea: beyond supportive care. Em erg Med Rep. 1996;17(14): 141–150. 5. Surawicz CM. Infectious causes of chronic diarrhea. Gastroenterol
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Clin North Am . 2001; 30(3):679–692.
Miscellaneous SEE ALSO: Gastroenteritis
Codes ICD9-CM 787.91
ICD10 A09
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Diarrhea, Pediatric
Diarrhea,
Pediatric Richard Lichenstein
Basics Description
One of the m ost com m on pediatric com plaints; second only to respiratory infections in overall disease frequency
Leading cause of illness and death in children worldwide
Acute infectious enteritis (AIE): o
Vom iting and diarrhea
o
Children Table o f C o ntents > Digo xin, Po iso ning
Digoxin, Poisoning
Kirk Cumpston
Basics Description Acute Digitalis Effects (Elevated Levels in Children and Intentional Overdose)
Inhibits sodium -potassium ATPase pum p in cell m em branes
Allows m ore calcium ions to enter cell and cardiac cells to contract m ore strongly
Increases K + extracellularly
Increases vagal tone
Slows atrioventricular (AV) node conduction (vagotonic)
Increases autom aticity and conduction system refractory period
Bradydysrhythm ias
Chronic Digitalis Effects (Therapeutic to Toxic Levels in Elderly Patients)
Inhibits sodium -potassium ATPase pum p in cell m em branes
Increases intracellular calcium
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Increases vagal tone
Increases autom aticity
Usually hypokalem ic secondary to diuretic use
Tachydysrhythm ias
Etiology
Digoxin/digitoxin pharm aceuticals
Plants and anim als containing cardiac glycosides: o
Foxglove
o
Oleander
o
Lily of the valley
o
Dogbane
o
Red squill
o
Cane toad, Colorado River toad
Diagnosis Signs and Symptoms
Toxicity onset: 2 hours after PO ingestion and 15 m inutes following IV
Toxicity: o
Occurs with norm al digoxin levels (chronic)
o
May be absent with elevated digoxin levels (acute)
Cardiovascular
Dysrhythm ias: o
Paroxysm al atrial tachycardia (PAT) with AV block
o
Bidirectional ventricular tachycardia is pathognom onic:
o
Classic dysrhythm ia
Uncom m on
Prem ature ventricular contractions (PVCs) m ost
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com m on o
Nonparoxysm al accelerated junctional tachycardia
o
Ventricular tachycardia (VT)
o
Atrial fibrillation
o
Bigem iny
o
Bradycardia
o
Nonparoxysm al atrial tachycardia
o
AV blocks
o
Sinus arrhythm ia
o
Prem ature atrial contraction
Congestive heart failure (CHF) exacerbation
Hypotension
Shock
Cardiovascular collapse
Syncope
CNS
Mental status changes: o
Agitation
o
Lethargy
o
Psychosis
Visual perception: o
Blurred
o
Scotom a
o
Green to yellow halo
o
Photophobia
o
Hallucinations
o
Color perception changes
GI
Anorexia
Nausea and vom iting
Diarrhea
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Abdom inal pain
General
Headache
Weakness
Light-headedness
Essential Workup
ECG: o
For dysrhythm ia
Digoxin level: o
Norm al range: 0.5–2.0 ng/m L
o
Distribution after oral intake not com plete until 6 hours; therefore, a 6-hour level is m ost accurate steady state concentration.
o
False elevations possible with spironolactone use, pregnancy, hyperbilirubinem ia, chronic renal failure, liver failure, congestive heart failure
o
May be falsely elevated after digoxin Fab fragm ents given
Tests Lab
Electrolytes, BUN, creatinine, glucose: o
Hypokalem ia contributes to digitalis toxicity.
o
Hyperkalem ia seen in acute toxicity and correlates with acute digitalis m ortality better than digoxin serum levels.
o
Follow K + serially.
Calcium , m agnesium
Serum digoxin concentration should not be obtained after digoxin-specific antibody Fab fragm ents have been adm inistered because it will be inaccurate.
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Differential Diagnosis
Overdoses: o
Calcium channel blockers
o
Beta-blockers
o
Quinidine, procainam ide
o
Clonidine
o
Organophosphates
o
Antidysrhythm ics
o
Other antihypertensives
Prim ary cardiac dysrhythm ias
Acute gastroenteritis
Treatment Pre Hospital Alert
If cardioversion is necessary for tachydysrhythm ias, use low levels (50 J): o
May precipitate refractory tachydysrhythm ias
Initial Stabilization Airway, breathing, and circulation m anagem ent (ABCs):
IV, oxygen, m onitor: o
IV fluid bolus if hypovolem ic
Adm inister naloxone, thiam ine, dextrose, for altered m ental status.
ED Treatment Cardiac Arrest Resuscitation
Defibrillate for ventricular fibrillation, pulseless VT.
Standard advanced cardiac life support (ACLS) protocol
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Adm inister digoxin-specific antibody Fab fragm ents (Digibind), up to 20 vials IV push (IVP).
MgSO 4 , 2 g IVP
Continue resuscitation for 30 m inutes after digoxin-specific antibody Fab fragm ents.
General Measures
Gastric lavage if 4.0 m Eq/L in chronic overdose: o
Use with caution if bradycardia or AV block.
Replenish m agnesium .
Treat hyperkalem ia with insulin, dextrose, bicarbonate, sodium polystyrene sulfonate: o
Calcium contraindicated
Dysrhythmia Management
First choice is digoxin-specific antibody Fab fragm ents. If these are not im m ediately available, initiate the following: o
o
o
Lidocaine:
For ventricular dysrhythm ias without AV block
Not harm ful but not very effective
For bradydysrhythm ias:
Atropine
Pacing for sym ptom atic bradydysrhythm ia
Beta-blockade (propranolol, esm olol) for
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supraventricular tachycardia:
Avoid with AV block, bradycardia.
P.321
o
MgSO 4 for ventricular dysrhythm ias
o
Quinidine, procainam ide contraindicated
Cardioversion is last resort for severe, life-threatening tachydysrhythm ia: o
Start at low energy 10–50 J, then increase to high levels if ineffective.
o
Safe if digoxin level 10 m g in adults or 0.2 m g/kg or 4 m g in children
o
Hyperkalem ia >5.0–5.5 m Eq/L
o
Hem odynam ically unstable or life-threatening dysrhythm ias
o
Ventricular tachycardia, ventricular fibrillation
o
Atrial tachycardia
o
Variable AV block
o
Bradycardia with no response to atropine
o
Hypotension
Onset: 20–30 m inutes
Digoxin levels m ay increase, decrease, or stay in therapeutic range after therapy owing to Fab digoxin
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com plexes.
Renal clearance of drug–antibody com plexes: o
Too large to be rem oved by dialysis
Second dose if rebound toxicity
Com plications: o
Exacerbation of CHF
o
Hypokalem ia
o
Afibrillation with rapid ventricular response
Medication (Drugs)
Activated charcoal slurry: o
1 m g/kg if within 1 hour
Atropine: 0.5 m g (peds: 0.02 m g/kg) IV; repeat 0.5–1.0 m g IV (peds: 0.04 m g/kg)
Dextrose: D 5 0 W 1 am p: 50 m L or 25 g (peds: D 2 5 W 2–4 m L/kg) IV
Digoxin-specific antibody Fab fragm ents: o
40-m g vial neutralizes 0.6 m g of digoxin.
o
If am ount ingested known:
Num ber of vials needed equals am ount ingested m g/0.6.
o
If steady serum level known:
Num ber of vials needed equals serum digoxin level m ultiplied by patient's weight in kg/100.
o
If neither am ount ingested or serum level known:
Acute toxicity: 10–15 vials adults or children
Chronic toxicity: 2–3 vials adults
o
Bolus for cardiac arrest
o
Additional doses as needed
Insulin and glucose: 10 U (peds: 0.25 U/kg) regular insulin plus 50 m L 50% (peds: 1 g/kg) dextrose IV
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Lidocaine: 1 m g/kg IV, then 0.5 m g/kg q10m in to m ax. 3 m g/kg
Magnesium sulfate: 2 g (peds: 25–50 m g/kg per dose) IVPB
Naloxone: 2 m g (peds: 0.1 m g/kg) IV or IM
Propranolol: 1 m g (peds: 0.01–0.1 m g/kg) IV
Sodium polystyrene sulfonate (Kayexalate):
o
Oral: 15 g m ixed with water or 50 m L of sorbitol
o
Rectal enem a: 50 g in 200 m L of sorbitol
o
Peds: 1.0 g/kg PO or per rectum (PR)
Sorbitol: 1–2 g/kg to m ax. 100 g (peds: >1 year old: 1–1.5 g/kg as 35% solution to m ax. 50 g) PO
Thiam ine: 100 m g (peds: 50 m g) IV or IM
Follow-Up Disposition Admission Criteria
ICU: o
Unstable cardiovascular status in acute or chronic toxicity
Telem etry: o
Asym ptom atic or m ildly sym ptom atic dysrhythm ia
o
High risk for developing toxicity
Discharge Criteria
Acute/chronic ingestion: o
Digoxin level Table o f C o ntents > Diverticulo sis
Diverticulosis
Robert C. Montana
Basics Description
Single (diverticulum ) or m ultiple (diverticula) colonic wall outpouchings from colonic m uscle dysfunction
Sequence: o
Insufficient am ounts of dietary fiber cause dim inished stool bulk.
o
Increased colonic contractions to propel stool through colon cause increase in intralum inal pressure.
o
Increased pressure forces m ucosa and subm ucosa to herniate through m uscularis propria at its weakest point of artery (vasa recta) penetration site.
Etiology
Occurs anywhere in GI tract, although generally a colonic disease:
o
Left sided m ore than right sided
o
Sigm oid colon is m ost com m on site.
Pseudodiverticula: o
Outpouchings of m ucosa and subm ucosa only
o
Most com m on form of colonic diverticula
o
True congential diverticula (uncom m on) contain all
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bowel wall layers.
Incidence directly related to increase in age
Com m on in Western society, owing to refined diet and low fiber intake
Com plications: o
Massive arterial bleeding usually from right colon:
Fecalith (dry, hard stool) erodes through arterial branch.
o
Inflam m ation (diverticulitis)
Diagnosis Signs and Symptoms History
Thorough history and physical exam ination essential to avoid excessive workup
Clinical patterns: o
Asym ptom atic (70–85%)
o
Sym ptom atic (painful)
o
Hem orrhagic (5–15%)
Chronic or interm ittent left lower quadrant pain: o
Often precipitated by eating
o
Som etim es relived by flatulence or bowel m ovem ent
Painless brisk hem atochezia (m aroon stools or bright red blood)
Constipation (or diarrhea)
Dyspepsia
Diverticulitis and diverticular bleeding are separate entities and rarely coexist.
Physical Exam
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Abdom inal palpation: o
Tenderness in left lower quadrant
o
Firm sigm oid colon in left lower quadrant
Rectal exam : o
Predom inantly reveals hem e-negative stool
o
Bleeding typically m ild
Fever: absent
Essential Workup Thorough history and physical exam ination essential to avoid excessive workup
Tests Lab
Asym ptom atic diverticulosis: o
Requires no testing
Uncom plicated painful disease (no peritoneal signs) with known history: o
Requires no workup
Uncom plicated painful disease (no peritoneal signs) without previous history: o
Requires workup to rule out carcinom a (if weight loss, anorexia, hem e-positive stool)
o
CBC for leukocytosis or anem ia
o
Urinalysis to exclude hem aturia or pyuria
Hem orrhagic diverticulosis: o
CBC
o
Electrolytes, BUN, creatinine, glucose, calcium
o
Type and cross for 4 U of packed red blood cells (PRBCs)
o
Prothrom bin tim e (PT), partial throm boplastin tim e (PTT), international norm alized ratio (INR)
o
ECG
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Imaging
Uncom plicated painful diverticulosis—outpatient options: o
Flexible sigm oidoscopy, then barium enem a:
Sigm oidoscopy: Rule out carcinom a (before barium studies for optim al visualization).
Barium enem a: Search for classic diverticula and exclude carcinom a or polyps.
o
Colonoscopy
Hem orrhagic diverticulosis: o
Anoscopy:
o
If m ild bleeding, to rule out hem orrhoids
Proctosigm oidoscopy:
If no blood in stool above rectum , assum e rectal bleed.
o
Colonoscopy:
Bleeding cannot be excessive (difficult to visualize pathology).
Allows for therapeutic intervention
Usually done prior to radionuclide im aging or angiography
o
Radionuclide im aging:
Safe, no bowel prep needed
Poor localization of bleeding site
Ideal for detecting interm ittent bleeding, owing to long half-life of radioisotope (24–36 hours)
o
Angiography:
No bowel prep needed
Localizes site of bleeding (m ore exact after radionuclide scanning)
o
Allows for therapeutic intervention
Barium enem a:
Rarely indicated
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Identifies diverticula but not bleeding (can hinder visualization of other im aging techniques)
P.329
Differential Diagnosis
Painful diverticulosis: o
Irritable bowel syndrom e (alm ost identical clinical presentation)
o
Diverticulitis
o
Colon carcinom a
o
Crohn disease
o
Urologic (renal colic)
o
Gynecologic (ruptured or torsed ovarian cyst)
Hem orrhagic diverticulosis: o
Hem orrhoids
o
Anal fissure
o
Proctitis
o
Colitis
o
Carcinom a
o
Polyps
o
Ischem ic enteritis
o
Angiodysplasia
o
Am yloidosis
o
Vascular-enteric fistula
o
Upper GI source
Treatment
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Pre Hospital
Avoid opiates in abdom inal pain when underlying cause is uncertain.
Establish two large-bore intravenous lines with 0.9% norm al saline (NS) if significant rectal bleeding/hem odynam ic instability.
For hypotension: o
1–2 L (20 m L/kg) bolus 0.9% NS intravenously
o
Trendelenburg position
Initial Stabilization Hem orrhagic diverticulosis (m assive):
Airway control (100% oxygen or intubate if unresponsive)
Intravenous access with at least one large-bore catheter or two if unstable
0.9% NS bolus 1–2 L (20 m L/kg) for hypotension
Central catheter placem ent if unstable following initial fluid resuscitation for m ore efficient delivery of fluids and m onitoring of central venous pressure
Nasogastric tube to rule out upper GI bleed
Bladder catheter to m onitor urine output
Transfuse O-negative red blood cells im m ediately if im pending arrest.
Consult surgeon (m ost diverticular bleeding stops spontaneously).
ED Treatment
Uncom plicated sym ptom atic diverticulosis: o
High-fiber diet and/or hydrophilic bulk laxative (e.g., psyllium )
o
Warm com presses to abdom en
o
Reassurance
o
Avoid cathartic laxatives.
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o
No evidence to support use of antispasm odic (dicyclom ine)
Hem orrhagic diverticulosis (m assive): o
Initial stabilization (see above)
o
Monitor fluid status (input/output).
o
Prepare for radionuclide scan followed by angiography if necessary.
o
Surgical intervention for segm ental colectom y if bleeding on radionuclide scan
o
Consider selective angiography with injection of vasopressin to control bleeding.
o
Em bolization not recom m ended for colonic hem orrhage
Medication (Drugs) Dicyclom ine: 20 m g PO/IM q.i.d. (not for IV use)
Follow-Up Disposition Admission Criteria
ICU if unstable with m assive hem orrhagic diverticulosis
Mild or interm ittent hem orrhagic diverticulosis that is otherwise stable, to determ ine site of bleeding and to evaluate need for definitive treatm ent
Discharge Criteria
Uncom plicated, sym ptom atic diverticulosis
Stable with trace hem e-positive stool, negative gastric aspirate, no anem ia, and no other com plaints
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References 1. Bono MJ. Gastrointestinal em ergencies. Part I: lower gastrointestinal tract bleeding. Em erg Med Clin North Am . 1996;14(3):547–556. 2. Kim YI, Marcon NEl. Injection therapy for colonic diverticular bleeding. A case study. J Clin Gastroenterol. 1993;17(1):46–48. 3. Kohler L, Sauerland S, Neugebauer E. Diagnosis and treatm ent of diverticular disease: results of a consensus developm ent conference. The Scientific Com m ittee of the European Association for Endoscopic Surgery. Surg Endosc. 1999;13(4):430–436. 4. McGuire HH. Bleeding colonic diverticula: a reappraisal of natural history and m anagem ent. Ann Surg. 1994;220(5):653–656.
Miscellaneous SEE ALSO: Diverticulitis; Gastrointestinal Bleeding
Codes ICD9-CM 562.10 Diverticulosis of colon
ICD10 K57.9 Diverticular disease of intestine, part unspecified, without perforation or abscess
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Diz z iness
Dizziness
Mitchell Adelstein Jonathan Edlow
Basics Description
Nonspecific feeling that m ay define a whirling sensation, a tendency to fall, feeling faint, weakness, or feeling confused
May be caused by a num ber of problem s: o
o
o
Vertigo:
Vestibular dysfunction
Cerebellar disease
Disequilibrium :
Suggests a structural CNS disorder
Multiple sensory deficits
Near syncope/syncope:
Cardiovascular insufficiency
Faintness that is postural or paroxysm al suggests a cardiovascular disorder
o
Weakness
o
Psychiatric illness:
Constant, ill-defined dizziness unrelated to posture suggests a psychogenic etiology
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Etiology Vertigo
Peripheral (85%): o
Benign paroxysm al positional (m ost com m on)
o
Acute labyrinthitis
o
Ménière disease
o
Vestibule neuritis
o
Acoustic neurom a
o
Ototoxic drugs:
Am inoglycosides
Antim alarials
Erythrom ycin
Furosem ide
o
Otitis m edia and serous otitis with effusion
o
Foreign body in ear canal
Central (15%): o
Cerebellar hem orrhage
o
Vertebral basilar artery insufficiency
o
Cerebellar traum a
o
Cerebellopontine angle tum or
o
Tem poral lobe epilepsy
o
Vertebral basilar m igraines
o
Multiple sclerosis
o
Subclavian steal syndrom e
o
Drugs suppressing the reticular activating system :
Sedative hypnotics
Anticonvulsants
Disequilibrium
Multiple sensory defects
Frontal lobe disorder: o
Tum ors:
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Meningiom a
Gliom a
Metastatic tum or
o
Anterior cerebral artery syndrom e
o
Hydrocephalus
Subcortical disorders: o
Multiple strokes
o
Ataxic hem iparesis
Brainstem disorders: o
Stroke
o
Multiple sclerosis
Cerebellar disorders: o
Cerebellar hem orrhage, infarct, tum or
o
Spinocerebellar degeneration
o
Alcoholism
o
Acute cerebellitis
Cardiac and Vascular Insufficiency
Hypovolem ia
Orthostatic hypotension
Anem ia
Myocardial ischem ia
Structural cardiac or valvular disease
Cardiac dysrhythm ias: o
Preexcitation
o
Prolonged QT syndrom e
o
Hypokalem ia
o
Supraventricular tachycardia
o
Ventricular dysrhythm ia
Pulm onary em bolism :
Subarachnoid hem orrhage
Hypoglycem ia
Hypoxia
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Hypercarbia
Hyperventilation syndrom e
Vasovagal episode
Other
Psychogenic: o
Anxiety
o
Hyperventilation syndrom e
o
Depression
Chronic fatigue syndrom e
Fam ilial periodic paralysis
Hypothyroidism
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Diagnosis Signs and Symptoms
Dizziness is used to describe a wide range of sym ptom s: o
Abnorm al sensation of m otion
o
Feeling faint or fainting
o
Lightheadedness
o
Unsteadiness
Classify dizziness into one of four categories by asking the patient to explain the sensation without using the word dizzy: o
Vertigo:
Abnorm al sensation of m ovem ent and position in space
Nystagm us
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Alert
Vertical nystagm us is abnorm al and should elicit concern for a central etiology:
o
Nausea
o
Vom iting
o
Diaphoresis
Disequilibrium : o
Disorder of coordination and rhythm
o
Loss of equilibrium
o
May include sensory deficits such as peripheral neuropathy
Near syncope/syncope: o
Diaphoresis
o
Palpitations
o
Pallor during the episode
Other: o
Depression
o
Fatigue
o
Weakness
o
Hyperventilation
Essential Workup Must be tailored to each individual patient's signs and sym ptom s
Tests Lab
Hem atocrit, if suspected anem ia/blood loss
Glucose in setting of DM
Electrolytes in setting of volum e depletion
Toxicologic screen, if suspected exposure/ingestion
Imaging
CT scan if central vertigo or ataxia is present
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Magnetic-resonance angiogram if vertebral basilar insufficiency is suspected
Diagnostic Procedures/Surgery ECG to detect cardiac causes of near syncope and weakness
Differential Diagnosis See Etiology
Treatment Initial Stabilization
Supplem ental oxygen
Stabilization should be determ ined by m ore specific classification of dizziness based on the history, physical exam ination, and ancillary studies.
ED Treatment Treatm ent should be determ ined by the underlying cause.
Medication (Drugs)
Diazepam : 2.5–5 m g IV. q8h or 2–10 m g PO q8h
Diphenhydram ine: 25–50 m g IV, IM, or PO q6h
Meclizine: 25 m g PO q6h PRN
Prom ethazine: 12.5 m g IV q6h or 25–50 m g PO, IM, or PR q6h
Follow-Up Disposition
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Admission Criteria Adm ission or discharge of patients with dizziness should be based on the underlying etiology or associated sym ptom s.
Issues for Referral Referral for com pletion of workup as an outpatient to a prim ary-care physician or a neurologist
References 1. Baloh RW. Approach to the dizzy patient. In: Baloh RW, ed. Neurotology. Baillieres Clin Neurol. 1994;3:453. 2. Brown JJ. A system atic approach to the dizzy patient. Neurol Clin. 1990;8:209–224. 3. Herr RD, Zun L, Mathews JJ. A directed approach to the dizzy patient. Ann Em erg Med. 1989;18:664. 4. Olshaker S. Vertigo. In: Marx J, et al., eds. Rosen's em ergency m edicine: concepts and clinical practice. St Louis: Mosby; 2002:123–131. 5. Pigott DC, Rosco CJ. The dizzy patient: an evidence-based diagnosis and treatm ent strategy. Em erg Med Pract. 2001;3(3):120. 6. Walker JS, Barnes SB. Dizziness. Em erg Med Clin North Am . 1998;16(4):845–875.
Miscellaneous SEE ALSO: Vertigo
Codes ICD9-CM 386 780.2
ICD10
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R42
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Do m estic Vio lence
Domestic Violence
Jim Comes
Basics Description
Intim ate partner violence and abuse is the infliction or the threat of physical harm against an intim ate partner.
Occurs in dating, m arried, cohabiting, or separated relationships
Intim ate partner violence and abuse is a pattern of assaultive and coercive behaviors that include physical, sexual, and psychologic attacks against the victim .
The perpetrator uses these tactics to attain com pliance from and to control the victim .
Tactics used by perpetrators to gain power and control over their partners include: o
Pushing
o
Shoving
o
Slapping
o
Punching
o
Kicking
o
Choking
o
Holding
o
Tying down
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Verbal abuse: o
Threatening harm (including toward children or pets), intim idation, or destruction of property
o
Isolating the victim physically or socially
o
Degrading or hum iliating behavior
o
Attem pting to force or forcing the victim to perform sexual acts against his or her will or without protection against pregnancy
o
Causing physical harm during sex or assaulting genitalia
Etiology
Most victim s are wom en, and m ost perpetrators are m en.
Partners in sam e-sex relationships and m en m ay also be victim s.
Most rapes and assaults of wom en are by known assailants.
Diagnosis
Diagnosis and recognition in the ED, clinic, or office rem ains difficult and problem atic.
Signs and Symptoms
Traum atic injuries: o
Sm all subset of presenting com plaints
o
Fractures
o
Contusions
o
Lacerations
o
Penetrating and blunt traum a to body
Psychiatric: o
Chronic pain syndrom es
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o
Physical sym ptom s related to stress
o
Anhedonia
o
Insom nia
o
Anorexia
o
Som atic com plaints
o
Anxiety
o
Depression and suicidal ideation
Alert
Clinical clues: o
History not com patible with exam
o
Repeat visits for the sam e chief com plaint
o
Delay in seeking care
o
Any injury during pregnancy
o
Interaction between wom an and partner that suggests interpersonal problem s
o
Evidence of traum a not attributable to a m otor vehicle accident
o
Multiple sym ptom s without obvious physical findings
History
Short screening questions of all fem ale patients m ay be an effective m eans of identifying victim s of dom estic violence.
Screening should be direct, nonjudgm ental, supportive, and private.
Differential Diagnosis
Partner violence m ay be the acute precipitant of the patient's reason for presenting to the ED, or it m ay be part of the patient's past or present social history.
There is no traum atic or nontraum atic presentation that is pathognom onic for intim ate partner violence.
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Treatment Initial Stabilization
Provide tim ely and appropriate m edical attention.
Maintain advocacy by expressing m essages of support and validating victim 's dilem m a.
P.333
ED Treatment
Docum ent in the chart the victim 's allegations in his or her own words.
Diagram or photograph injuries (after consent) and incorporate them into the clinical record.
Address the patient's safety in returning to the sam e hom e environm ent: o
Im portant determ inants in predicting future danger include violence that is increasing in frequency and severity, threats of hom icide or suicide by the partner, or the availability of a lethal weapon.
With the aid of social services or dom estic violence advocates, review the patient's options:
o
Outpatient victim services
o
Em ergency shelter inform ation
o
Hotlines
o
Restraining order inform ation
o
Legal services
Mandatory reporting requirem ents vary am ong states: o
Som e states require the health-care practitioner to m ake a verbal and written report if he or she
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suspects wound or physical injury results from assaultive and abusive conduct. o
Determ ine how local authorities respond to reports of intim ate partner violence and abuse from health-care practitioners.
o
Recognize that m andatory reporting requirem ents m ay place the victim in m ore danger and create ethical dilem m as for the physician when the victim does not want the case reported to police or social service agencies.
Medication (Drugs)
Acetam inophen: 650–975 m g PO
Meperidine: 1.0–1.8 m g/kg/dose IV or IM
Morphine sulfate: 0.1 m g/kg/dose IV or IM
Follow-Up Disposition Admission Criteria
A victim whose life is in im m inent danger and who cannot be safely discharged (to his or her hom e, fam ily, friends, or shelter) m ay need to be adm itted to the hospital (under an assum ed nam e).
Use appropriate adm ission guidelines depending on degree of traum a sustained.
Discharge Criteria A victim whose safety is ensured and whose injuries can be m anaged as an outpatient m ay be discharged.
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References 1. Abbott J. Injuries and illnesses of dom estic violence. Ann Em erg Med. 1997;29:781–785. 2. Hayden SR, Barton ED, Hayden M. Dom estic violence in the em ergency departm ent: how do wom en prefer to disclose and discuss the issues? J Em erg Med. 1997;15:1–5. 3. Hym an A, Schillinger D, Lo B. Laws m andating reporting of dom estic violence: do they prom ote well-being? JAMA. 1995;273:1781–1787. 4. Salber PR, Taliaferro E.Intim ate partner violence and abuse. In: Rosen's Em ergency Medicine Concepts and Clinical Practice 5th ed. St. Louis, MO.: Mosby; 2002:863–875. 5. Salber PR, Taliaferro E. The Physician's Guide to Dom estic Violence. Volcano, Calif.: Volcano Press; 1995.
Codes ICD9-CM V15.49 Other V15.41 History of Physical Abuse
ICD10 R45.6 Physical Violence
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Duo denal Traum a
Duodenal Trauma
Hagop Isnar
Basics Description
Characteristics of duodenum : o
12 inches long
o
C shaped
o
Divided into four sections:
o
Last three sections intraperitoneal
Lies m ostly over first three lum bar vertebrae
Second section is m ost com m only injured.
Types of injury:
o
Duodenal wall hem atom a
o
Wall perforation
o
Hem orrhage
Incidence of duodenal injury is about 5% of all intra-abdom inal injuries.
Penetrating traum a accounts for 85% of duodenal injuries: o
Mortality ranges from 13–28%.
o
Associated with exsanguination
Blunt duodenal injuries have higher m ortality: o
If injury is diagnosed in 24 hours has passed, m ortality rate approaches 40%.
o
Late m ortality usually from sepsis
Pediatric Considerations
Most duodenal injuries are secondary to recreational injuries (e.g., bicycle handlebar injuries).
Intram ural duodenal hem atom as m ay occur in nonaccidental traum a: o
If suspected, then prom pt referral to appropriate child protective agencies is required along with m edical treatm ent.
In children, hem atom a is m ost com m only seen in first portion of duodenum .
Diagnosis Signs and Symptoms
Com plaints m ay be m inim al with vague abdom inal, flank, and back pain.
High gastrointestinal obstruction m ay be seen with duodenal hem atom as.
History Penetrating or blunt abdom inal traum a
Physical Exam Elicit tenderness or ecchym osis of upper abdom en or penetrating wounds to right upper quadrant or lower chest.
Tests Lab
Laboratory tests are of little value.
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Fifty percent of patients with duodenal injuries have elevated serum am ylase.
Imaging
Upright chest and abdom inal radiographs m ay show: o
Intraperitoneal air
o
Retroperitoneal air
o
Air in biliary tree
o
Scoliosis to right
o
Loss of psoas shadow
o
Air around right kidney
o
Injecting air into nasogastric tube m ay dem onstrate retroperitoneal air m ore clearly.
o
Intram ural hem atom as without leakage m ay have coiled spring appearance.
CT with contrast: o
Perhaps best diagnostic test that shows sm all am ounts of retroperitoneal gas and extravasated contrast m aterial
o
Sausage-shaped m ass in duodenal wall strongly suggests hem atom a.
Diagnostic Procedures/Surgery Diagnostic peritoneal lavage (DPL):
Often positive for blood, bile, or bowel content
Negative lavage does not exclude injury.
Differential Diagnosis
Injury to hollow organs (stom ach, sm all and large intestines)
Liver and biliary tree injuries
Vascular injuries (aortic and m esenteric arteries as well as venous injuries)
Postoperative com plications from prior duodenal surgery
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or injury repair such as infection and suture line dehiscence
Treatment Pre Hospital
Follow traum a protocols.
Im portant to have prehospital personnel provide clear description of m echanism of injury and to transport to appropriate facility
Initial Stabilization
Airway m anagem ent, resuscitation as needed
Aggressive fluid therapy with warm ed norm al saline or lactated Ringer solution if patient hypotensive
Central line m ay be needed for unstable patients.
Nasogastric decom pression
Early traum a surgical consultation
ED Treatment
Tetanus and antibiotic prophylaxis for penetrating wounds
Definitive treatm ent involves laparotom y with exploration of duodenum for injuries.
Broad-spectrum antibiotics to prevent sepsis in patients with perforation
P.335
Medication (Drugs)
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Cefoxitin: 2 g (peds: 40 m g/kg) IV plus gentam icin: 2 m g/kg IV loading dose (adult and peds) or
Cefotetan: 2 g (peds: 20 m g/kg) IV plus gentam icin: 2 m g/kg IV loading dose (adult and peds) or
Clindam ycin: 600 m g IV (peds: 20–40 m g/kg/d IV in 3–4 div. doses) plus gentam icin: 2 m g/kg IV loading dose (adult and peds) or
Ceftriaxone: 1–2 g IV (peds: 50–75 m g/kg/d in 2 div. doses, not to exceed 2 g) plus m etronidazole: 15 m g/kg IV
Follow-Up Disposition Admission Criteria
All patients with duodenal injuries need adm ission to traum a surgical service.
Minor duodenal hem atom as that do not require im m ediate surgery m ay require nasogastric decom pression for obstruction (up to 7 days) and observation for possible expansion or rupture of the hem atom a.
Discharge Criteria No patient with identified traum atic duodenal injury should be discharged from the Em ergency Departm ent without Traum a Surgical consultation.
References 1. Carrillo EH, Richardson JD, Miller FB, et al. Evolution in the m anagem ent of duodenal injuries. J Traum a. 1996;40:1037–1046. 2. Cogbill TH, Moore EE, et al. Conservative m anagem ent of duodenal traum a: a m ulticenter perspective. J Traum a.
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1990;30:1469–1475. 3. Degiannis E, Boffard K. Duodenal injuries. Br J Surg. 2000;87:1473–1479. 4. Ivatury RR, Nassoura ZE, Sim on RJ, et al. Com plex duodenal injuries. Surg Clin North Am . 1996;76:797–812. 5. Tyburski JG, Dente CJ, Wilson RF, et al. Infectious com plications following duodenal and/or pancreatic traum a. Am Surg. 2001;67:227–230.
Codes ICD9-CM 863.21 Duodenum
ICD10 S36.4
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Dysfunctio nal Uterine Bleeding
Dysfunctional Uterine Bleeding Christy Rosa Mohler
Basics Description Excessive (>80 m L) or prolonged vaginal bleeding without dem onstrable organic cause
Etiology
Unopposed estrogen stim ulation of proliferative endom etrium
Anovulatory (m ost com m on): o
Alteration of neuroendocrinologic function
o
Obesity
o
Very low calorie diets, rapid weight change, intense exercise
o
Psychologic stress
o
Most com m on in postm enarchal, prem enopausal wom en
Ovulatory
Pediatric Considerations Anovulatory bleeding com m on in adolescence owing to im m aturity of the hypothalam ic-pituitary-ovarian axis
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Diagnosis Signs and Symptoms History
Vaginal bleeding that is significantly changed from a patient's norm al pattern
Abnorm al uterine bleeding in the absence of system ic or structural disease: o
Includes bleeding between norm al m enstrual cycles, change in norm al pattern of m enstrual cycle, increased or decreased am ount of m enstrual bleeding
Physical Exam
Mild to m oderate bleeding on pelvic exam
Pallor, tachycardia, hypotension, orthostasis in severe cases
Alert It is rare for wom en to be hem odynam ically unstable sim ply from dysfunctional uterine bleeding; if such instability is present, concern is for ectopic pregnancy or other cause for hem orrhage.
Essential Workup Pregnancy test
Tests Lab
CBC, prothrom bin tim e (PT), partial throm boplastin tim e (PTT), bleeding tim e
May send iron studies, thyroid-stim ulating horm one (TSH), luteinizing horm one (LH), follicle-stim ulating horm one
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(FSH), prolactin level, cervical cultures for routine follow-up by prim ary m edical doctor (PMD)/gynecology
Imaging Pelvic ultrasound m ay show uterine, tubal, or ovarian abnorm ality; m ay be needed to rule out differential diagnoses.
Diagnostic Procedures/Surgery
Dilation and curettage (D & C) m ay be required for heavy bleeding unresponsive to other interventions.
Refer for endom etrial biopsy if older than 35 years of age
Differential Diagnosis
Pregnancy com plications: o
Threatened, incom plete, or spontaneous abortion; ectopic or m olar pregnancy
Infectious: o
Vaginitis, cervicitis, pelvic inflam m atory disease (PID)
Coagulopathies: o
Von Willebrand disease, idiopathic throm bocytopenic purpura, platelet defects, thalassem ia
Medications: o
Warfarin, aspirin, oral contraceptives, tricyclic antidepressants, m ajor tranquilizers
System ic illness: o
Adrenal, hepatic, renal or thyroid dysfunction, diabetes m ellitus, other endocrinopathies
Anatom ic lesions: o
Fibroids, endom etriosis, polyps, endom etrial hyperplasia, neoplasm
Intrauterine devices
Traum a
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Treatment Pre Hospital IV crystalloid boluses as needed for hypotension, tachycardia secondary to heavy bleeding
Initial Stabilization Airway, breathing, and circulation (ABCs):
Packed RBCs for significant bleeding unresponsive to crystalloids
ED Treatment
Observation usually adequate if bleeding m ild
IV crystalloid, packed red blood cells for continued bleeding or hem odynam ic instability
Gynecology consultation if bleeding is severe and unresponsive to crystalloids, m edications o
D & C m ay be necessary for hem odynam ic instability.
o
Hysteroscopy or hysterectom y for continued heavy bleeding unresponsive to other m easures
Medication (Drugs)
Conjugated estrogen (Prem arin) for heavy bleeding, hem odynam ic instability: o
2.5 m g PO q.i.d.
o
25 m g IV, repeat in 3 hours if needed:
Intravenous dosing has not been shown to be
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superior to oral route. o
Medroxyprogesterone acetate (Provera) 10 m g PO per day is added when bleeding subsides.
Oral contraceptive pills o
Ethinyl estradiol 35 µg and norethindrone 1 m g PO q.i.d. for 1 week
Medications m ay be deferred in m ild cases with referral to gynecology.
Follow-Up Disposition Admission Criteria
Significant blood loss
Continued bleeding
Unresponsive hem odynam ic instability for D & C or operative treatm ent
Discharge Criteria Most patients can be discharged with gynecology referral once bleeding is controlled and patient is hem odynam ically stable.
References 1. Abnorm al uterine bleeding. In: Stenchever MA, et al., eds. Com prehensive Gynecology. 4th ed. St. Louis, MO: Mosby; 2001:1079–1098. 2. Albers JR, Hull SK, Wesley RM. Abnorm al uterine bleeding. Am Fam Phys. 2004;69(8):1915–1927. 3. Bradford JC, Kyriakedes CG. Vaginal bleeding. In: Marx JA, et al., eds. Rosen's Em ergency Medicine: Concepts and Clinical Practice. 5th ed. St. Louis, MO: Mosby–Year Book; 2002:226–233.
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4. Morrison LJ, Spence JM. Obstetrics and gynecology: vaginal bleeding and pelvic pain in the non pregnant patient. In: Tintinalli JE, ed. Em ergency Medicine: a Com prehensive Study Guide. 6th ed. New York: McGraw-Hill; 2004: 647–653.
Codes ICD9-CM 626.8
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Dysphagia
Dysphagia
Timothy J. Mader Allison V. Brewer
Basics Description Dysphagia:
Difficulty swallowing
Im paired passage of solids or liquids from the oral cavity to the stom ach
Etiology
Mechanism : o
Can be neurom uscular or m echanical
o
Frequency and severity increase with advancing age
Classification: o
Oropharyngeal (transfer) dysphagia:
Difficulty transferring from the oropharynx to the proxim al esophagus (difficulty initiating a swallow)
Easier to swallow solids versus liquids
Im m ediate, within seconds of swallowing
Sensation of the bolus not passing below the cervical esophagus
Nasal or oral regurgitation
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Coughing or choking (indicating aspiration)
Gurgling noise after swallowing (suggests Zenker diverticulum )
Vocal quality changes
Usually a neurom uscular disorder resulting in bulbar m uscle weakness or im paired coordination
o
Esophageal (transport) dysphagia:
Failure of norm al transit through the esophagus
Retrosternal sticking sensation 10–15 seconds after swallowing
Nocturnal regurgitation
Drooling or regurgitation of undigested food and liquid (characteristic of esophageal obstruction)
Usually obstructive but consider m otility disorders
o
Functional dysphagia:
Diagnosis of exclusion
Full workup without evidence of m echanical or neurom uscular pathology
Sym ptom s >12 weeks
Odynophagia: o
Pain with swallowing
o
Separate, but often related, entity
Pain pattern: o
Voluntary striated m uscle in the upper one-third transitions to involuntary nonstriated m uscle in the lower two-thirds
o
Som atic nerve fibers in the upper esophagus—excellent pain localization
o
Afferents, from the vagus nerve along with the cervical and thoracic sym pathetic ganglia, innervate
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the lower esophagus—poor pain localization o
Visceral pain from the lower esophagus m ay be difficult to distinguish from that of acute coronary syndrom e.
Pediatric Considerations
Pediatric dysphagia: o
Wide range of feeding and swallowing difficulties
o
Multifactorial pathophysiology:
o
Neurom uscular developm ent
Anatom ical changes from infancy to childhood
Esophageal disorders m ost com m on etiology
Classification: o
Oral phase:
Im paired ingestion/m astication and transfer to posterior pharynx
o
Pharyngeal phase:
Im paired swallow m echanism and transport of m aterial through pharynx with appropriate airway closure (requires intact sensory and m otor m echanism s to prevent aspiration)
o
Esophageal phase:
Im paired transport of m aterial from esophagus to stom ach
Diagnosis Signs and Symptoms History Three im portant questions:
What causes sym ptom s?
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o
Solids and liquids suggests a neurom uscular disorder.
o
Solids only or progression from solids to liquids suggests a m echanical abnorm ality.
Are sym ptom s interm ittent or progressive? o
Interm ittent sym ptom s suggest rings or webs.
o
Progressive sym ptom s suggest peptic or m alignant strictures.
o
Motility disorders can be interm ittent or progressive.
Are there concom itant sym ptom s? o
Odynophagia or chest pains
o
Chronic cough or nocturnal wheezing
o
Nasopharyngeal regurgitation
o
Weight loss
o
Chronic heartburn
o
Hem atem esis
Physical Exam
Often unrem arkable
Oropharyngeal inspection
Pulm onary and cardiac auscultation
Neurologic exam with em phasis on cranial nerves
Tests ECG
Consider cardiac etiology for chest discom fort
Heart and esophagus share a com m on neural pathway.
Lab No specific studies are indicated.
Imaging
Chest radiograph: o
Food dilating the esophagus
o
Aspiration pneum onitis
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o
Extrinsic com pressing m ass
Soft tissue lateral neck radiograph
Cineradiography barium swallow (liquid or bread soaked):
o
Defines esophageal anatom y
o
Assesses function
o
Do not perform if endoscopy anticipated
CT of the head: o
Indicated for new-onset neurom uscular dysphagia
Diagnostic Procedures/Surgery
Endoscopy: o
Indicated to relieve obstruction and inspect the esophageal anatom y
Esophageal m anom etry
Fiberoptic endoscopic evaluation of swallowing
Electrom yography
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Differential Diagnosis
Oropharyngeal: o
o
o
Infectious:
Derm atom yositis
Infectious pharyngitis
Lym e disease
Botulism
Mechanical:
Malignancy
Pharyngeal pouch
Congenital
Medications:
Anticholinergics
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o
o
Metoclopram ide
Am inoglycosides
Am iodarone
Phenothiazines
Procainam ide
Penicillam ine
HMG-CoA reductase inhibitors
Potassium
Ferrous sulfate
Aspirin and NSAIDs
Neurom uscular:
Cerebrovascular accident
Multiple sclerosis
Am yotrophic lateral sclerosis
Parkinson disease
Huntington chorea
Myasthenia gravis
Cranial nerve palsy
Cricopharyngeal spasm
Psychological/Behavioral
Esophageal: o
o
Mechanical:
Foreign body
Peptic esophageal stricture
Neoplasm
Schatzki ring
Esophageal webs
Diverticula
Radiation injury
Motor:
Scleroderm a
Achalasia
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o
o
Diffuse esophageal spasm
Nutcracker esophagus
Nonspecific m otor disorders
Inflam m atory:
Eosinophilic esophagitis
Pill esophagitis
Extrinsic:
Cardiovascular abnorm alities (vascular rings, thoracic aneurysm , left atrial enlargem ent, aberrant subclavian artery)
Mediastinal m ass
Cervical osteophytes
Treatment Pre Hospital
Vigilant airway attention
Position of com fort with suction available
Initial Stabilization
Vigilant airway attention
Position of com fort with suction available
NPO
0.9% NS 500 m L (peds: 20 m L/kg) IV fluid bolus for significant dehydration
ED Treatment
Nitroglycerin for esophageal spasm
Glucagon for im pacted foreign body
Treat com plications: o
Airway obstruction
o
Aspiration, pneum onia, lung abscess
Pa ge 1 5 8
o
Dehydration, m alnutrition
Dietary m odifications: o
Thickened liquids for neurom uscular disorder
o
Thin liquids for m echanical disorders
Medication (Drugs)
Glucagon: 1 m g IV followed by second dose of 1 m g after 5 m inutes if there is no im provem ent in sym ptom s
Nitroglycerin: 0.4 m g SL q5m in repeated up to 3 tim es
Follow-Up Disposition Admission Criteria
Esophageal obstruction
Com prom ised fluid or nutrition status
Inability to protect airway
Sym ptom s cannot be distinguished from cardiac ischem ia.
Discharge Criteria
Well-hydrated patient
Urgent neurology, otolaryngology, or gastroenterology referral arranged for further evaluation and treatm ent
References 1. Baker BM. Sym ptom s, diagnosis, and m anagem ent of dysphagia. J Ky m ed Assoc. 1998;96(9):362–367. 2. Cefalu CA. Diagnosing and treating dysphagia. Provider. 1999;25(11):7172–7475. 3. Miller CK, Willging JP. Advances in the evaluation and
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m anagem ent of pediatric dysphagia. Cur Op in Otolaryn and Head and Neck Surg. 2003;11(6):442–446. 4. Owen W. Dysphagia (Clinical review: ABC of the upper gastrointestinal tract). Brit Med J. 2001;323(7317):850–853. 5. Rothstein RD. A system atic approach to the patient with dysphagia. Hosp Pract. 1997;32(3):169–175. 6. Swann LA, Munter DW. Esophageal em ergencies. Em erg Med Clin North Am . 1996;14(3):557–570.
Codes ICD9-CM 787.2
ICD10 R13
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Dyspnea
Dyspnea
Elizabeth L. Mitchell
Basics Description
Dyspnea com es from the Greek word for “hard breathing.―
Often described as “shortness of breath―
Usually an unconscious activity, dyspnea is the subjective sensation of breathing, from m ild discom fort to feelings of suffocation.
Etiology
Dyspnea usually reflects an im pairm ent in ventilation, perfusion, m etabolic function, or CNS drive.
Mechanism s that control breathing: o
Control centers:
Brainstem and cerebral cortex affect both autom atic and voluntary control of breathing.
o
Chem o, stretch, and irritant sensors:
CO 2 receptors located centrally and PO 2 receptors located peripherally
Mechanoreceptors lie in respiratory m uscles and respond to stretch.
Intrapulm onary m echanoreceptors respond to
Pa ge 1 5 9
chem ical irritation, engorgem ent, and stretch. o
Effectors of respiratory center output are in the respiratory m uscles and respond to central stim ulation to m ove air in and out of the thoracic cavity.
o
Motor-sensory control of the diaphragm and m uscles of respiration are controlled by C-3–C-8 nerves and T-1–T-12 nerves
Derangem ents of any of these neurosensory pathways produces dyspnea: o
Many etiologies for the sensation of dyspnea are due to the com plex nature of m echanism s that control breathing.
Diagnosis Signs and Symptoms
Difficult, labored, or uncom fortable breathing
Upper airway:
o
Stridor
o
Upper-airway obstruction
Pulm onary: o
Tachypnea
o
Accessory m uscle use
o
Wheezing
o
Rales
o
Asym m etric breath sounds
o
Poor air m ovem ent
Cardiovascular: o
S3 gallop
o
Murm ur
Pa ge 1 5 9
o
CNS: o
Jugular venous distention
Altered levels of consciousness
General o
Diaphoretic/cool versus hot/dry skin
o
Pallor
o
Upright patient position
o
Clubbing
o
Cyanosis
o
Edem a
o
Ketotic breath odor
Essential Workup
Pulse oxim etry: o
May be falsely elevated due to increased ventilation or carbon m onoxide
Chest radiograph: o
For diagnosis of pulm onary conditions
o
Assess heart size and evidence of congestive heart failure (CHF)
Arterial blood gas: o
Oxygenation
o
Calculate arterial-alveolar gradient:
o
A-a (at sea level) = 150 - (PO 2 - PCO 2 )/0.8
Norm al = 5–20
Assess degree of acidosis.
Tests Lab
CBC: o
Evaluation of anem ia
o
Neutrophil count helpful in evaluation of infectious processes
Pa ge 1 5 9
Electrolyte, blood urea nitrogen, creatinine, glucose: o
Consider when specific m etabolic derangem ents are suspected
o
B-natriuretic peptide May be elevated in CHF
Toxicology screen
Methem oglobin/Carboxyhem oglobin level
Thyroid function tests
D-dim er (ELISA): o
Useful for excluding pulm onary em bolus if norm al
Imaging
ECG for suspected m yocardial ischem ia, CHF
Ventilation-perfusion scan or CT pulm onary angiogram for suspected pulm onary em bolism
Soft-tissue neck radiograph or fiberoptic visualization for suspected upper airway obstruction
Echocardiography for suspected pericardial effusion/tam ponade
Peak expiratory flow/spirom etry to assess for reactive-airway disease
Tensilon test for suspected m yasthenia gravis
P.341
Differential Diagnosis
Upper airway: o
Epiglottitis
o
Laryngeal obstruction
o
Tracheitis or tracheobronchitis
o
Angioedem a
Pulm onary: o
Airway m ass
Pa ge 1 5 9
o
Asthm a
o
Bronchitis
o
Chest wall traum a
o
CHF
o
Drug-induced conditions (e.g., crack lung, aspirin overdose)
o
Effusion
o
Em physem a
o
Metastatic disease
o
Pneum onia
o
Pneum othorax
o
Pulm onary em bolism
o
Pulm onary hypertension
o
Restrictive lung disease
Cardiovascular: o
Arrhythm ia
o
Coronary artery disease
o
Intracardiac shunt
o
Left ventricular failure
o
Myxom a
o
Pericardial disease
o
Valvular disease
Neurom uscular: o
CNS disorders
o
Myopathy and neuropathy
o
Phrenic nerve and diaphragm atic disorders
o
Spinal cord disorders
o
System ic neurom uscular disorders
Other: o
Acidosis
o
Altitude
o
Anaphylaxis
Pa ge 1 5 9
o
Anem ia
o
Thyroid disorders
o
Psychogenic
o
Sepsis
Pediatric Considerations
Unique conditions in differential diagnosis for age 40
Medical condition requiring hospital therapy
Discharge Criteria
Adequate oxygenation
Stable m edical illness that can be m anaged as outpatient
References 1. De Peuter S, Van Diest I, Lem aigre V, et al. Dyspnea: the role of psychological processes. Clin Psychol Rev. 2004;Sep24(5):557–581. 2. Manning HL, Mahler DA. Pathophysiology of dyspnea. Monaldi Arch Chest Dis. 2001;Aug56(4):325–30. 3. Michelson E, Hollrah S. Evaluation of the patient with shortness of breath: an evidence based approach. Em erg Med Clin North Am . 1999;17(1):221–237. 4. Schwartzstein RM, Manning HL. Pathophysiology of dyspnea. N Engl J Med. 1995;12(3):1547–1552. 5. Tobin MJ. Dyspnea: pathophysiologic basis, clinical presentation, and m anagem ent. Arch Intern Med. 1990;8:1604–1612. 6. Weism an IM, Zeballos RJ. Clinical evaluation of unexplained dyspnea. Cardiologia. 1996;41(7):621–634.
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Miscellaneous SEE ALSO: Respiratory Distress
Codes ICD9-CM 786.09
ICD10 R06.0
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Dysto nic Reactio n
Dystonic Reaction
Kenneth Jackimczyk
Basics Description
Norm al pattern of CNS neurotransm ission m aintained by balance between dopam inergic and cholinergic receptors: o
Certain drugs disrupt this balance, leading to involuntary m uscle spasm s.
Although the spasm s are uncom fortable and frightening, they are not life threatening.
Etiology
Usually occur after patient has taken antipsychotic, antiem etic, or antidepressant drug
Incidence of dystonic reactions in patients taking neuroleptics is 2–25%, depending on the agent.
Neuroleptic agents: o
Phenothiazine (Thorazine, Mellaril, Prolixin, Com pazine, Stelazine, Phenergan)
o
Thioxanthenes (Navane)
o
Butyrophenones (Haldol, Droperidol)
o
Indole (Moban)
o
Dibenzoxipine (Loxitane)
Antiem etic agents:
Pa ge 1 5 9
o
Metoclopram ide (Reglan)
o
Trim ethobenzam ide (Tigan)
Other agents: o
Cyclic antidepressants
o
Antihistam ines
o
Doxepin
o
Cim etidine
o
Prozac
o
Cocaine
o
Ketam ine
o
Chloroquine
o
Lithium
o
Phencyclidine
Pediatric Considerations Children are particularly vulnerable to dystonic reactions when dehydrated or febrile.
Diagnosis Signs and Symptoms General
Usually occurs within hours of ingestion: o
Alm ost always within first week after exposure to offending drug
Age: o
Twice as com m on in m ales
o
Uncom m on in older patients
o
Children are m ore susceptible.
Difficulty with vocalization
Com pletely alert and able to answer questions
Pa ge 1 5 9
Involuntary m uscle spasm s usually involving the face, neck, and trunk (see Physical Exam )
History Ingestion of antipsychotic, antiem etic, or other drug within week of sym ptom onset
Physical Exam
Characteristic m otor spasm s occur.
Oculogyric crisis: o
Involves eye and periorbital m uscles
o
Starts as blepharospasm
o
Evolves into painful upward or lateral deviation of eyes
Buccolingual crisis: o
Involves facial m uscles and tongue
o
Bizarre grim acing
o
Trism us
o
Tongue protrusion
o
Dysphagia
o
Dysarthria
o
Rarely causes spasm of pharynx and larynx that can be severe enough to cause stridor
Torticollic crisis: o
Tortipelvic crisis: o
Twisting of neck
Abdom inal wall m uscle spasm
Opisthotonos: o
Involves m uscles of trunk and back
o
Twisting and arching of spine
Essential Workup
Clinical diagnosis is based on characteristic signs and sym ptom s with history of possible drug exposure.
Pa ge 1 6 0
Diagnosis is confirm ed by response to treatm ent.
Differential Diagnosis
Tardive dyskinesia: o
Com plication of chronic antipsychotic therapy
o
Usually choreiform m ovem ents
Akathisia: o
Involuntary m otor restlessness
o
May appear agitated
Seizure: o
History of prior seizures
o
Not responsive to verbal stim uli
o
Tonic-clonic-type m otor m ovem ents rather than spasm
Hysteria or pseudoseizure: o
History of precipitating em otional event
o
Tonic-clonic m otor activity rather than sustained spasm
Tetanus
Strychnine poisoning
Chronic dystonias: o
Cerebral palsy, fam ilial choreas
o
Usually history of dystonia is associated with chronic neurologic process.
Scorpion envenom ation: o
Oculogyric crisis and opisthotonos are com m on m anifestations of scorpion envenom ation.
o
Patient lacks history of drug exposure.
Meningitis and encephalitis m ay present with atypical seizures that m im ic dystonic reaction.
P.343
Pa ge 1 6 0
Treatment Pre Hospital
Rarely life threatening
Direct attention toward spasm of larynx and tongue to be sure dystonic reaction is not causing respiratory com prom ise
Ask fam ily and friends about ingestions of antipsychotic m edications, antiem etics, and recreational drugs.
Transport pill bottles.
Initial Stabilization Stabilize airway to prevent spasm of larynx or tongue from causing respiratory com prom ise.
ED Treatment
Adm inister diphenhydram ine (Benadryl) or benztropine m esylate (Cogentin): o
Rapid resolution of m uscular spasm by restoring cholinergic-dopam inergic balance in CNS
o
IV adm inistration is preferred route of treatm ent.
o
Onset of relief in 2–5 m inutes
o
Com plete resolution of sym ptom s in 15 m inutes
o
IM adm inistration is alternate route of treatm ent.
o
Begins to work in 15–30 m inutes
o
Continue oral adm inistration for 3 days to prevent redevelopm ent of sym ptom s.
Diazepam (Valium ): o
Adm inister in cases of dystonia unresponsive to adequate doses of anticholinergic m edications.
o
Failure to respond to standard treatm ent should lead
Pa ge 1 6 0
physician to consider other diagnoses.
Medication (Drugs)
Benztropine m esylate (Cogentin): 1–2 m g either IV (over 2 m inutes) or IM followed by 1–2 m g PO b.i.d. for 3 days: o
Not to be used in children 3 years old: 0.02 m g/kg IV (over 2 m inutes) or IM followed by 0.02 m g/kg PO b.i.d. for 3 days
Diphenhydram ine (Benadryl): 1–2 m g/kg up to 100 m g either IV (over 2 m inutes) or IM followed by 25–50 m g (peds: 1–2 m g/kg) PO q6h–q8h for 3 days, or
Diazepam : 5–10 m g IV followed by 5 m g PO q4h–q6h as necessary for 3 days
Follow-Up Disposition Admission Criteria None
Discharge Criteria
Discharge after resolution of sym ptom s.
Patient should not drive or perform tasks that require full alertness while taking sedating m edications.
References 1. Diederich NJ, Goetz CG. Drug-induced m ovem ent disorders. Neurol Clin. 1998;16:125–139.
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2. Gallagher EJ. Neurologic principles. In: Goldfrank LR, ed. Goldfrank's Toxicologic Em ergencies. New York: McGraw-Hill, 2002:282–301. 3. Manognerra AS. Dystonic reactions. In: Harwood-Nuss A, ed. The Clinical Practice of Em ergency Medicine. Philadelphia: Lippincott William s & Wilkins; 2005:1622–1624. 4. Van Harten PN, Hoek HW, Kahn RS. Acute dystonia induced by drug treatm ent. Br Med J. 1999;319:623–626.
Codes ICD10 G24.0
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Eating Diso rder
Eating Disorder
David B. Herzog Hope W. Levin Safia C. Jackson
Basics Description Anorexia Nervosa (AN)
Refusal to m aintain body weight at or above a m inim ally norm al weight for age and height
Failure to m ake expected weight gain during a period of growth
Intense fear of gaining weight or becom ing fat, even though underweight
Disturbance in the way body weight or shape is experienced
Undue influence of body weight and shape on self-evaluation
Denial of seriousness of low body weight
In postm enarchal fem ales, am enorrhea for three consecutive cycles
Bulimia Nervosa (BN)
Recurrent episodes of binge eating characterized by:
Pa ge 1 6 0
o
Eating a larger than usual am ount of food in a discrete period of tim e
o
A sense of loss of control over eating during the episode
Recurrent inappropriate com pensatory behaviors used to prevent weight gain: o
Self-induced vom iting
o
Misuse of laxatives
o
Diuretics
o
Enem as or other m edications
o
Fasting
o
Excessive exercise
Binge Eating Disorder (BED)
Recurrent episodes of binge eating characterized by: o
Eating a larger than usual am ount of food in a discrete period of tim e
o
A sense of loss of control over eating during the episode
Binge-eating episodes associated with three or m ore of the following: o
Eating m uch m ore rapidly than norm al
o
Eating until feeling uncom fortably full
o
Eating large am ounts of food when not feeling physically hungry
o
Eating alone because of being em barrassed by how m uch one is eating
o
Feeling disgusted with oneself, depressed, or very guilty after overeating
o
Marked distress regarding binge eating
Prevalence: o
AN: 0.5% of the United States fem ale population
o
BN: 2% of the United States fem ale population
Pa ge 1 6 0
o
BED: 2% of the United States fem ale population
Etiology
Eating disorders result from a com bination of genetic, neurochem ical, developm ental, psychological, and sociocultural factors.
Typical age of onset for AN is bim odal at 13–14 years and 17–18 years.
AN com m only onsets in a teenager whose initial dieting behavior escalates into an obsessive preoccupation with weight and thinness.
BN and BED com m only onset in late adolescence or early adulthood.
BN com m only onsets in an individual who: o
Has attem pted m any diets and failed
o
May have learned purging behaviors from a friend or fam ily m em ber
BED is associated with a history of obesity, weight cycling, and dieting.
Diagnosis Signs and Symptoms
Endocrine/m etabolic com plications: o
Electrolyte im balances
o
Hypotherm ia
o
Am enorrhea
o
Sleep disturbance
o
Growth retardation
o
Osteoporosis
o
Nutritionally based osteoporosis
Pa ge 1 6 0
Cardiovascular problem s: o
Arrhythm ias
o
Bradycardia
o
Hypotension
o
QTC prolongation
o
Ipecac cardiom yopathy
Renal com plications: o
Hypokalem ia
o
Edem a
Hem atologic com plications: o
Anem ia
o
Leukopenia
o
Throm bocytopenia
Gastrointestinal com plications: o
Decreased m otility
o
Intestinal dilatation
Neurological com plications: o
Potentially irreversible structural brain changes
Physical Exam
Weight, body m ass index [weight in kg/(height in m eters) 2 ]
Vital signs
Dry skin
Lanugo: o
A soft, downy body hair that develops on the chest and arm s
Breast atrophy
Parotid swelling, subm andibular swelling
Hypercarotenem ia
Abnorm al dentition
Abrasions of dorsum of hand
Pa ge 1 6 0
Essential Workup
Clinical diagnosis
Medical evaluation
Physical exam ination
Nutritional assessm ent
Psychiatric interview:
o
Concurrent psychiatric illness
o
Suicide risk assessm ent
o
Explore psychosocial context
Fam ily evaluation when patient lives with her or his fam ily
Tests Lab
Com plete blood count
Electrolytes, blood urea nitrogen, creatinine, glucose
Liver function tests
Calcium , m agnesium , phosphorus
Am ylase
Consider checking thyroid-stim ulating horm one
ECG
Consider cardiac ECHO if substantial weight loss
Differential Diagnosis
Mood disorders
Obsessive-com pulsive disorder
Borderline personality disorder
Medical conditions o
Crohn disease
o
Diabetes m ellitus
o
Thyroid disease
o
Cancer
Pa ge 1 6 0
Treatment Initial Stabilization
ABCs
IV 0.9% NS 1 L bolus (peds: 20 m L/kg) for severe dehydration
Accu-Chek, correct hypoglycem ia with dextrose
Correct hypokalem ia
Warm ing blankets for severe hypotherm ia
ED Treatment Labs, physical exam ination, psychiatry consultation (including assessm ent of suicide risk), and m edical stabilization P.345
Medication (Drugs)
Escitalopram (Lexapro): 10–20 m g q.i.d. daily for BN
Fluoxetine (Prozac): 20–60 m g every AM for treatm ent of BN and relapse prevention in AN
Olanzapine (Zyprexa): 2.5–10 m g q.i.d. daily for AN
Sertraline (Zoloft): 50–200 m g q.i.d daily for BN
Follow-Up Disposition Admission Criteria
Pa ge 1 6 1
Medical risk: o
Extrem ely low weight
o
Rapid weight loss
o
Serum electrolyte im balance
o
Cardiac disturbance
o
Marked orthostatic hypotension
o
Bradycardia 110
o
Hypotherm ia Table o f C o ntents > Ecz em a/Ato pic Derm atitis
Eczema/Atopic
Dermatitis Jon Ludwig James Nelson
Basics Description
Chronic disease with acute flares
Superinfection with bacteria (especially Staphylococcus aureus) com m on
Altered cell-m ediated im m unity predisposes to infection with herpes sim plex virus (eczem a herpeticum ), m olluscum contagiosum , com m on warts, and fungi.
Genetics Fam ily history of atopy (asthm a, allergic rhinitis) 30–70% of the tim e:
If both parents are atopic, the incidence of atopic derm atitis (AD) in their child is 79%.
Etiology Allergic etiology; preferential T helper 2 (TH2)–m ediated production of IL-4, which increases IgE and circulating eosinophils
Pa ge 1 6 2
Diagnosis Signs and Symptoms History
Itching
Distribution varies with age: o
Infancy: tends to be m ore widespread with facial and scalp involvem ent; from 8–12 m onths, extensor surface involvem ent
o
Childhood: wrists, ankles, antecubital and popliteal fossae
o
Adolescents/adults: flexor areas, hands, feet, face, and neck
Physical Exam
Chronic disease: hyperpigm entation, hypopigm entation, lichenification, and scaling
Acute flares: o
Mild/m oderate: erythem atous, scaly patches with crusting and excoriation
o
Severe: diffuse, exfoliative erythroderm a
Other exam findings com m only associated with AD include: o
Dennie-Morgan folds (infraorbital grooves)
o
Pityriasis alba (dry, white patches to the face and upper body)
o
Hyperlinear palm s
o
Follicular accentuation
o
Keratosis pilaris (flesh-colored, keratotic papules on upper arm s, thighs, buttocks)
o
Derm atographism
Pediatric Considerations
Pa ge 1 6 2
Occurs in 10–15% of children 2 years of age: 0.03%) apply to affected areas b.i.d.
Triam cinolone 0.1% ointm ent: apply to affected areas of body b.i.d. (m id potency).
Follow-Up
Pa ge 1 6 2
Disposition Follow-up with prim ary physician or derm atology referral for problem atic cases
Admission Criteria Severe secondary infection
Discharge Criteria Nearly all patients m ay be discharged with appropriate follow-up instructions.
References 1. Boguniewicz M, Eichenfield LF, Hultsch T. Current m anagem ent of atopic derm atitis and interruption of the atopic m arch. J Allergy Clin Im m unol. 2003;112(6 suppl):S140–150. 2. Hanifin J, Ling M, Langley R, et al. Tacrolim us ointm ent for the treatm ent of atopic derm atitis in adult patients Part I: efficacy. J Am Acad Derm atol. 2001;44(1 suppl):S28–38. 3. Leung DY, Bieber T. Atopic derm atitis. Lancet. 2003;361:151–60. 4. Odom RB, Jam es WD, Berger TG, eds. Andrews’ Diseases of the Skin. 9th ed. Philadelphia: WB Saunders; 2001 (8th ed. 2000:69–95). 5. Paller A, McCalister R, Doyle J, et al. Atopic derm atitis in pediatric patients: perceptions of physicians and parents. Paper presented at: Annual Meeting of the Am erican Academ y of Derm atology; March 2000; San Francisco, CA. 6. Sieberry G, Iannone R, eds. The Harriet-Lane handbook. 15th ed. St. Louis, MO: Mosby; 2001 (14th ed. 2000:908–909).
Codes ICD9-CM 619.8
Pa ge 1 6 2
ICD10 L30.9 L20.9
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Edem a
Edema
Laura Macnow
Basics Description
Clinically apparent accum ulation of extravascular fluid due to a derangem ent in the balance of oncotic and hydrostatic forces: o
Increase in venous hydrostatic pressure:
System ically, as with congestive heart failure
Locally, as with deep vein throm bosis
o
Increase in lym phatic hydrostatic pressure
o
Decrease in oncotic pressure:
o
System ically from hypoalbum inem ia
Locally from increased capillary perm eability
Increased venous hydrostatic pressure or decreased oncotic pressure results in pitting edem a
o
Protein-rich extravasated fluid results in nonpitting edem a
Lym phedem a
Increased capillary perm eability
In certain disorders, there is no clear relation to Starling forces: o
Myxedem a
Pa ge 1 6 3
o
Idiopathic (cyclic) edem a
Worsened with heat
More com m on in wom en
Not necessarily related to m enses
Etiology Generalized
Right heart failure
Constrictive pericarditis
Acute glom erulonephritis
Renal failure
Salt retention: o
Steroids/estrogens/progestins
o
NSAIDs
o
Antihypertensives (especially vasodilators)
o
Lithium
o
Cyclosporine
o
Insulin
o
Acute withdrawal of diuretics
Idiopathic (cyclic) edem a
Cirrhosis
Nephrotic syndrom e
Protein-losing enteropathy
Starvation
Pregnancy
Localized
Throm bophlebitis
Chronic lym phangitis
Cellulitis
Baker cyst
Vasculitis
Angioedem a:
Pa ge 1 6 3
o
Allergic
o
Acquired
Hypothyroidism (m yxedem a)
Mechanical traum a
Therm al injuries
Radiation injuries
Chem ical burns
Hem iplegia
Com pressive or invasive tum or
Postsurgical resection of lym phatics
Postirradiation
Filariasis
Diagnosis Signs and Symptoms
Weight gain of several kilogram s
Discom fort in the affected areas
Swelling
Tenderness
Pitting edem a: o
Increased venous hydrostatic pressure or decreased oncotic pressure
Nonpitting edem a: o
Protein-rich extravasated fluid
Generalized Edema (Anasarca)
Edem a is m ost prom inent in dependent areas: o
Feet
o
Sacrum
o
Bilateral lower extrem ities
Pa ge 1 6 3
o
Face/periorbital (especially in the m orning)
Cardiac: o
Dyspnea
o
Orthopnea
o
Paroxysm al nocturnal dyspnea
o
Increased jugular venous pressure
o
Rales
o
S3 gallop
Renal: o
Anorexia
o
Puffy eyelids
o
Frothy urine
o
Oliguria
o
Dark urine
o
Hem aturia
o
Hypertension
Hepatic: o
Jaundice
o
Spider angiom as
o
Palm ar erythem a
o
Gynecom astia
o
Testicular atrophy
Localized
Ascites
Hydrothorax
History of traum a: o
Mechanical, therm al, radiation
Infectious/Inflam m atory: o
Chills
o
Fever
o
Erythem a
o
Increased warm th
Pa ge 1 6 3
Allergic: o
Pruritus
o
Hives
o
Involvem ent of the lips and the oral m ucosa
Myxedem a: o
Pretibial nonpitting edem a
o
Dry waxy swelling of skin and subcutaneous tissues
o
Periorbital m ost com m on (puffy eyes)
o
Nondependent areas
o
Fatigue
o
Cold intolerance
o
Weight gain
o
Constipation
o
Slowed deep-tendon reflex relaxation
Idiopathic: o
Diurnal weight gain/loss
Pregnancy Considerations
Com m on secondary to horm onally m ediated fluid retention
When involving hands and face, m ay be early sign of pre-eclam psia
Dependent edem a: o
Usually in late pregnancy
o
From im pedance of venous return
Diuretics contraindicated
Essential Workup Diagnostic studies should be directed by the underlying etiology suggested by the history and physical exam ination. P.351
Tests
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Lab
Renal etiology suspected: o
Electrolytes
o
Blood urea nitrogen and creatinine
o
Urinalysis
o
Urine electrolytes and protein
Hepatic etiology suspected: o
Serum album in
o
Liver function tests
o
Prothrom bin tim e and partial throm boplastin tim e
Myxedem a suspected: o
Thyroid function tests
Imaging
Cardiac etiology suspected: o
ECG
o
Chest radiograph
o
Echocardiography
Localized edem a to an extrem ity: o
Ultrasound (duplex scanning) or contrast venography
Differential Diagnosis
Cellulitis
Contact derm atitis
Diffuse subcutaneous infiltrative process
Lym phedem a
Obesity
Treatment Initial Stabilization
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See ED Treatm ent.
ED Treatment
Treatm ent should be directed toward the underlying cause.
Diuretics are indicated in cases of generalized edem a but are not required em ergently.
Medication (Drugs)
Am iloride: 5–20 m g PO q.i.d.
Captopril: 12.5–100 m g PO t.i.d. (m ax. 450 m g/d)
Furosem ide: 20–80 m g IV/PO q.i.d. (m ax. 600 m g/d)
Hydrochlorothiazide: 25–200 m g PO q.i.d.
Spironolactone: 25–200 m g PO q.i.d.
Follow-Up Disposition Admission Criteria
Base the decision to adm it the patient on the underlying etiology.
Inability to am bulate without adequate hom e support
Hypoxia
Discharge Criteria
Patient should be advised to decrease salt intake.
Elastic support stockings
References 1. Brater DC. Diuretic therapy. N Engl J Med. 1998;339:387–395. 2. Braunwald E. Edem a. In: Braunwald E., et al., eds. Harrison's principles of internal m edicine. 16th ed. New York: McGraw-Hill,
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2005. 3. Chertow GM: Approach to the patient with edem a. In: Braunwald E, Goldm an L, eds. Prim ary Cardiology. 2nd ed. Philadelphia: Saunders, 2003. 4. Kay A, Davis DL. Idiopathic edem a. Am J Kidney Dis. 1999;34:405–423.
Codes ICD9-CM 782.3
ICD10 R60.9
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Ehrlichio sis
Ehrlichiosis
Jonathan A. Edlow
Basics Description
Relatively recently described tick-borne hum an infection that presents as a nonspecific febrile illness
Several form s of ehrlichiosis, but two predom inate in North Am erica.: o
Hum an m onocytic ehrlichiosis (HME), first described in 1987
o
Hum an granulocytic ehrlichiosis (HGE), first described in 1994
o
Both are tick-borne, but have different vectors and geographical ranges. Other species have been reported, but presently, HME and HGE are the im portant ehrlichial hum an pathogens.
HME: o
Vector tick: Am blyom m a am ericanum (Lone Star tick)
o
Geographical range: central, southern, and m id-Atlantic states with range expanding to parts of New England
HGE:
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o
Vector tick: Ixodes scapularis (deer tick)
o
Geographical range: east coast, m id-central states, and Pacific Northwest (sam e area as Lym e disease)
Etiology Two distinct species of obligate intracellular organism s:
The taxonom y of these pathogens has changed in recent years as m ore DNA and ribosom al RNA data becom e available.
HME is caused by the organism Ehrlichia chaffeensis.
HGE is caused by Anaplasm a phagocytophila (a new nam e as of 2002).
Diagnosis
Signs and sym ptom s of HME and HGE are sim ilar.
Since both of these are new diseases: o
Many patients who are infected undergo asym ptom atic seroconversion.
o
The spectrum reported m ay overrepresent the m ore severely affected patients.
With any tick-borne infection, patients can be coinfected by m ore than one pathogen from the sam e tick bite: o
May have com plicated presentation of two different diseases
Signs and Symptoms History
The season and other epidem iologic context are im portant in diagnosing tick-borne diseases: o
Most com m only present from April through October
o
Variability is likely owing to changes in weather
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patterns from year to year and from region to region.
Sym ptom onset between 1 and 2 weeks (m edian 9–10 days) following the tick bite: o
Bite of the larger Lone Star tick is m ore likely to be recalled by the patient than that of the sm aller deer tick.
Abrupt onset of: o
Fever
o
Chills
o
Headache
o
Myalgias
o
Malaise
Rash: o
HME (35–40% of cases)
o
HGE (approxim ately 5% of cases)
o
Often delayed
Sym ptom s m ay relate to com plications of ehrlichiosis such as: o
Adult respiratory distress syndrom e
o
Renal failure
o
Hypotension and shock
o
Rhabdom yolysis
o
GI disturbances
o
CNS or peripheral nervous system (PNS) involvem ent
Physical Exam
Fever
Rash: o
May be m acular, m aculopapular, or petechial
o
May be absent during first week of illness
Lym phadenopathy
Hepatosplenom egaly
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Neurologic findings: o
Abnorm al m ental status
o
Meningism us
o
Nystagm us
Pulm onary findings (rales, rhonchi) depending on pulm onary com plications.
Alert
Ehrlichiosis is a potentially fatal tick-borne illness that is usually diagnosed clinically.
Consider diagnosis in all patients with nonspecific febrile illnesses, especially during the warm m onths of the year, and definitely if there is a history of tick bite.
Tests Lab
CBC: o
Leukopenia
o
Throm bocytopenia
o
Anem ia
Hepatic transam inases: o
Often elevated 2–6 norm al
Indirect im m unofluorescence antibody test: o
Usual test available
o
Threshold for a positive test is usually m ade by the individual lab testing the serum .
Wright stain of peripheral blood: o
Morula m ay be seen:
Sm all intracytoplasm ic ehrlichial DNA inclusion bodies
Diagnostic
Sensitivity of seeing m orulae depends on who is looking, for how long, and the im m unologic
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com petence of the patient.
Found m ore com m only in HGE (approxim ately 50%) than in HME (approxim ately 10–15%).
Culture and polym erase chain reaction test (PCR): o
Not routinely available
Antibody titer tests: o
Not available in real tim e
Imaging
Head CT for encephalopathy
Chest radiograph for fever/dyspnea
Differential Diagnosis
Most tick-borne illnesses: o
Rocky Mountain spotted fever
o
Lym e disease
o
Babesiosis
Many viral and bacterial infections, and num erous other infectious diseases, especially early in their course, can initially present with an undifferentiated febrile illness sim ilar to ehrlichiosis.
Mononucleosis
Throm botic throm bocytopenia purpura
Hem atologic m alignancy
Cholangitis
Pneum onia
P.353
Treatment
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Initial Stabilization Airway, breathing, and circulation (ABCs)
ED Treatment
Initiate antibiotics: o
Doxycycline:
Drug of choice
Children who are severely affected should also receive doxycycline.
o
Rifam pin for:
Pregnant patients
Allergy to doxycycline
Mildly affected children younger than 9 years of age
Patients who are pregnant, allergic to doxycycline, or who are m ildly affected can be given rifam pin for 7–10 days.
Initiate therapy for other tick-borne diseases that m ay have been cotransm itted
Medication (Drugs) Doxycycline:
Adults: 100 m g IV/PO q12h
Children: (severely affected) 3 m g/kg q12h if less than 45 kg; older children can be dosed as adults.
Pediatric Considerations Despite the fact that doxycycline is generally contraindicated in patients younger than 9 years old, it is the drug of choice in young children who are severely affected by ehrlichiosis. In less affected children, rifam pin has been used successfully.
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Pregnancy Considerations Rifam pin can be used to treat pregnant wom en with ehrlichiosis.
Follow-Up Disposition Admission Criteria
Significant com orbidities/severely affected
Cannot take PO antibiotics
Im m unosuppressed
Discharge Criteria Healthy appearing
References 1. Edlow JA. Bull's Eye: Unraveling the Medical Mystery of Lym e Disease. New Haven, CT: Yale University Press; 2004. 2. Olano JP, Walker DH. Hum an ehrlichioses. Med Clin North Am . 2002;86:375–392. 3. Ram sey AH, Belongia EA, Gale CM, et al. Outcom es of treated HGE cases. Em erg Infect Dis. 2002;8(4):398–401. 4. Stone JH, Kerry D, Aram G, et al. Hum an m onocytic ehrlichiosis. JAMA. 2004;292:2263–2270.
Miscellaneous SEE ALSO: Lym e Disease; Rocky Mountain Spotted Fever; Tick-Borne Diseases
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Elbo w Injuries
Elbow Injuries
Christian M. Sloane
Basics Description Bony Injuries
Supracondylar fracture: o
Most com m on in children
o
Peak ages 5–10 years, rarely occurs after age 15 years
o
Extension type (98%): FOOSH (fall on out stretched h and) with fully extended or hyperextended arm :
Type 1: m inim al or no displacem ent
Type 2: slightly displaced fracture; posterior cortex intact
Type 3: totally displaced fracture; posterior cortex broken
o
Flexion type: blow directly to flexed elbow:
Type 1: m inim al or no displacem ent
Type 2: slightly displaced fracture; anterior cortex intact
Type 3: totally displaced fracture; anterior cortex broken
Radial head fracture:
Pa ge 1 6 4
o
Usually indirect m echanism , i.e., FOOSH
o
Radial head driven into capitellum
Soft Tissue Injuries
Elbow dislocation: o
Second only to shoulder as m ost dislocated joint
o
Most are posterior.
Medial/lateral epicondylitis: o
Overuse injuries usually related to rotary m otion at elbow
o
Involving attachm ent points of hand and wrist flexor/extensor groups to elbow
o
Plum bers, carpenters, tennis players, golfers
o
Pain m ade worse by resisted contraction of particular m uscle groups
Pediatric Considerations
Subluxed radial head (nursem aid's elbow): o
Twenty percent of all upper extrem ity injuries in children
o
Peak age 1–4 years; occurs m ore frequently in fem ales than m ales
o
Sudden longitudinal pull on forearm with forearm pronated
Etiology
Mechanism aids in determ ining expected injury.
Traum a predom inates.
Most elbow injuries caused by indirect traum a transm itted through bones of forearm (FOOSH)
Direct blows account for very few fractures or dislocations.
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Diagnosis Signs and Symptoms How patient carries arm m ay give clues to diagnosis.
Bony Injuries Supracondylar fracture:
Flexion type: o
Patient supports injured forearm with other arm and elbow in 90° flexion.
o
Loss of olecranon prom inence
Extension type: o
Patient holds arm at side in S-type configuration.
Soft Tissue Injuries
Elbow dislocations: o
Posterior: abnorm al prom inence of olecranon
o
Anterior: loss of olecranon prom inence
Radial head subluxation: o
Elbow slightly flexed and forearm pronated, resists m oving arm at elbow
Medial/lateral epicondylitis: o
Gradual onset of dull ache over inner/outer aspect of elbow referred to forearm
o
Pain increases with grasping and twisting m otions.
Essential Workup
Radiographs
Assess wrist and shoulder for associated injury.
Evaluate neurovascular status of lim b.
Assess skin integrity.
Exam ine for com partm ent syndrom e, which is m ore com m on in supracondylar fractures.
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Alert
Injuries to ipsilateral upper lim b, particularly fractures to m idshaft hum erus and distal forearm , are com m on.
Evaluate for associated neurovascular injuries (up to 20%).
Tests Lab None specific for elbow injuries
Imaging
Not usually necessary if overuse injury suspected
Routine anteroposterior (AP) and lateral; add oblique for assessm ent of subtle injuries to radial head/distal hum erus.
Fat pad sign: o
Seen with intra-articular injuries
o
Norm ally, anterior fat pad is narrow radiolucent strip anterior to hum erus.
o
Posterior fat pad is norm ally not visible.
o
Anterior fat pad sign indicates joint effusion/injury when raised and becom es m ore perpendicular to anterior hum eral cortex (sail sign).
o
Posterior fat pad sign indicates effusion/injury:
In adults, posterior fat pad sign im plies radial head fracture.
In children, it im plies supracondylar fracture.
Pediatric Considerations
Fractures in children often occur through unossified cartilage, m aking radiographic interpretation confusing.
A line drawn down anterior surface of hum erus should always bisect the capitellum in lateral view.
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If any bony relationships appear questionable on radiographs, obtain com parison view of uninvolved elbow.
Suspect nonaccidental traum a if history does not fit injury.
Ossification centers: first appears: o
Capitellum : 3–6 m onths
o
Radial head: 3–5 years
o
Medial epicondyle: 5–7 years
o
Trochlea: 9–10 years
o
Olecranon: 9–10 years
o
Lateral epicondyle: 9–13 years
Differential Diagnosis
Sprain/strain
Effusion
Contusion
Bursitis
Arthritis
P.355
Treatment Pre Hospital Appropriate splinting
Initial Stabilization Im m obilization to prevent further injury before taking radiographs is essential.
ED Treatment
Orthopedic consultation is recom m ended for all but
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nondisplaced, stable fractures that can generally be splinted with 24- to 48-hour orthopedic follow-up.
Fractures generally requiring orthopedic consultation: o
Transcondylar, intercondylar, condylar, epicondylar fractures
o
Fractures involving articular surfaces such as capitellum or trochlea
Supracondylar fractures: o
Type 1 can be handled by ED physician with 24- to 48-hour orthopedic follow-up.
o
Elbow m ay be flexed and splinted with posterior splint.
o
Types 2 and 3 require im m ediate orthopedic consult.
o
Reduce these in ED when fracture is associated with vascular com prom ise.
Anterior dislocation: o
Reduce im m ediately if vascular structures com prom ised.
o
Then flex to 90° and place posterior splint.
Posterior dislocation: o
Reduce im m ediately if vascular structures com prom ised.
o
Then flex to 90° and place posterior splint.
Radial head fracture: o
Minim ally displaced fractures m ay be aspirated to rem ove hem arthrosis; instill bupivacaine (Marcaine) and im m obilize.
o
Other types should have orthopedic consult.
Radial head subluxation: o
In one continuous m otion, supinate and flex elbow while placing slight pressure on radial head.
o
Often will feel click with reduction
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o
If exam suggests fracture but radiograph is negative, splint and have patient follow up in 24–48 hours for re-evaluation.
Medial/lateral epicondylitis: o
Severe cases can be splinted.
o
Rest, heat, anti-inflam m atory agents
Alert
Neurovascular injuries to num erous structures that pass about the elbow, including anterior interosseus nerve, ulnar and radial nerve, brachial artery
Volkm ann ischem ic contracture is com partm ent syndrom e of forearm .
Medication (Drugs)
Conscious sedation is often required to achieve reductions; see Conscious Sedation.
Ibuprofen: 600–800 m g (peds: 5–10 m g/kg) PO t.i.d.
Naprosyn: 250–500 m g (peds: 10–20 m g/kg) PO b.i.d.
Tylenol with codeine no. 3: 1 or 2 tabs (peds: 0.5–1 m g/kg codeine) PO q4h–q6h
Morphine sulfate: 0.1 m g/kg IV q2h–q6h
Follow-Up Disposition Admission Criteria
Vascular injuries, open fractures
Fractures requiring operative reduction or internal fixation
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Adm it all patients with extensive swelling or ecchym osis for overnight observation and elevation to decrease risk for com partm ent syndrom e.
Discharge Criteria
Stable fractures or reduced dislocations with none of above features
Splint and arrange orthopedic follow-up in 24–48 hours.
Uncom plicated soft tissue injuries
References 1. Anderson BC. Office Orthopedics for Prim ary Care: Diagnosis and Treatm ent. 2nd ed, Philadelphia: WB Saunders; 1999. 2. McCarty LP, Ring D, Jupiter JB. Managem ent of distal hum erus fractures. Am J Orthop. 2005;34(9):430–438. 3. Minkowitz B, et al. Supracondylar hum erus fractures: current trends and controversies. Orthop Clin North Am . 1994;25:4. 4. Nicholson DA, et al. ABC of em ergency radiology: the elbow. Br Med J. 1993;307:23. 5. Sim on R, Koenigsknecht S. Em ergency Orthopedics: The Extrem ities. 4th ed. East Norwalk, CT: Appleton & Lange; 1996.
Codes ICD9-CM 959.3
ICD10 S59.9
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Electrical Injury
Electrical Injury
Scot Hill
Basics Description
Ohm 's law: Voltage (V) = current (I) × resistance (R): o
Am perage (electron flow or current) is proportional to voltage (potential difference) and inversely proportional to resistance.
Levels of electrical exposure in voltage: o
Telephone lines: 65 V
o
Household circuits: 110 V
o
Electrical range or dryer: 220 V
o
Household power lines: 220 V
o
Subway third rail: 600 V
o
Residential trunk line: 7,620 V
Alternating current (AC): o
Has periodic reversal of electron flow (60 Hz in U.S.)
o
Found in residential power supply
o
Can produce tetanic m uscle contraction, prolonging contact
o
More likely to result in ventricular fibrillation at household current level
Direct current (DC):
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o
Continuous electron flow in one direction
o
Defibrillators and pacem akers, industrial sources
o
Single forceful contraction, tends to throw patient from source
o
More likely to result in asystole
Factors that increase severity of injury: o
High voltage (>600 V considered high voltage)
o
Higher current (am perage)
o
Lower resistance (wet skin 10 tim es less resistant than dry skin) allows m ore penetration.
o
Higher resistance m ay m ean m ore conversion of electricity to heat, m ore necrosis.
o
Longer tim e of contact with source (AC >DC)
o
Current pathway through susceptible vital organs (brain, spinal cord, heart)
Trim odal distribution of electrical injuries: o
Toddlers (household outlets and cords)
o
Teenagers (risk-taking behavior)
o
Adults (work-related injuries)
Etiology
Types of electrical injury: o
o
Prim ary electrical phenom ena:
Cardiac arrhythm ias
Muscle contractions and tetany
Tissue destruction:
Electrotherm al burn m ay cause skin or deep tissue coagulation necrosis.
Burns from noncontact arcing
Burns from burning cloths or equipm ent
Minor visible injuries m ay be m isleading for extensive deep tissue injury.
o
Secondary injury from traum a:
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Supraphysiologic m uscle contraction
Fall or being thrown
Tissue resistance: o
Blood and nerves least resistant
o
Fat and bone m ost resistant
o
Skin interm ediate resistance:
o
Wet skin 10 tim es less resistant
More resistance m eans less flow, m ore conversion to heat.
Diagnosis Signs and Symptoms
Sym ptom s and effects of electricity: o
0.2–2 m A AC: tingling sensation
o
1–4 m A AC: pain
o
6–22 m A AC: unable to let go/local tetany
o
30–50 m A AC: diaphragm /intercostal tetany
o
100 m A AC: ventricular fibrillation
o
1,000 m A AC: ventricular standstill
Severity ranges from m inor cutaneous burns to crush-type traum a involving deep tissues: o
Minor skin burns m ay m ask m ajor deep injury.
Cardiac: o
Cardiac standstill/asystole is leading cause of death from DC and high-voltage AC.
o
o
Ventricular fibrillation:
Most com m on lethal dysrhythm ia
Induced by AC at household current 60 Hz
Other dysrhythm ias: sinus tachycardia, atrial fibrillation, and prem ature ventricular contractions
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o
Usually resolve spontaneously
Myocardial dam age occurs rarely:
Generally epicardial, not transm ural
Dam age does not follow distribution of coronary arteries.
ECG will not show standard injury patterns.
Respiratory com prom ise m ay occur from : o
Brain injury causing respiratory center inhibition
o
Tetanic contraction of chest wall/diaphragm m uscles
o
Prolonged paralysis of respiratory m uscles
o
Postcardiac arrest respiratory arrest
o
Traum atic lung injury
o
Lung tissue itself appears resistant to electrical injury, probably owing to air content
Neurologic: o
o
Acute:
Respiratory arrest
Am nesia
Altered m ental status, seizures, com a
Localized paresis up to/including quadriplegia
Delayed:
Ascending paralysis
Transverse m yelitis
Am yotrophic lateral sclerosis
Reflex sym pathetic dystrophy
Vascular: o
Throm bosis in slow-m oving venous system owing to coagulation
o
Intim al injury in fast-m oving arterial system m ay lead to acute or delayed arterial m alfunction.
o
Com partm ent syndrom es secondary to edem a
Renal failure secondary to m yoglobinuria
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Orthopedic injuries result from : o
Supraphysiologic m uscle contraction from electrostim ulation
o
Secondary injury from traum a
o
Classically described injuries:
Vertebral colum n fracture
Posterior shoulder dislocation
Fem oral neck fracture
Ophthalm ologic: o
Corneal burns
o
Intraocular hem orrhage
o
Uveitis
o
Retinal injuries
o
Delayed effects:
Optic nerve atrophy
Cataracts (onset 4–6 m onths postinjury)
Derm atologic: o
Burns from current, arcing, or clothes burning
o
Contact/ground wounds—hands, feet, and head m ost com m on sites
o
Kissing burns from current exit and re-entry on flexor surfaces
P.357
Pediatric Considerations
Oral com m issure burn: o
Results from child biting electrical cord
o
Associated with bleeding from labial artery 3–5 days after injury
o
May heal with significant contractures
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Pregnancy Considerations
Fetus m uch less resistant to electrical shock than m other: o
All pregnant patients m ust undergo period of fetal m onitoring.
Essential Workup
ECG
Urinalysis for m yoglobin
Cardiac m onitor: o
Prolonged m onitoring is probably not necessary in asym ptom atic patients with norm al ECG, no dysrhythm ias, and exposure to 7.45
Furosem ide: 0.5 m g/kg IV
Mannitol: 25 g (peds: 0.25–0.5 m g/kg) IV bolus, then 12.5 m g/kg/h IV titrated to urine flow >1 m L/kg/h
Follow-Up Disposition Admission Criteria
Docum ented loss of consciousness
Dysrhythm ias, abnorm al ECG, or evidence of m yocardial dam age
Suspicion of deep tissue dam age
Myoglobinuria or acidosis
Burn criteria for adm ission
Traum atic injuries requiring adm ission
Discharge Criteria
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Minor, low-voltage injury ( Table o f C o ntents > Encephalitis
Encephalitis
Arunchalam Einstein
Basics Description
Acute infectious inflam m ation of the brain
20,000 cases in United States annually
Mortality 10%
Inflam m atory reaction occurs within brain parenchym a with destruction of neurons, parenchym al edem a, and petechial hem orrhages.
Route of CNS infection usually hem atogenous; search for another site
Neural m igration occurs with rabies, herpes sim plex virus (HSV), and varicella-zoster encephalitis.
Etiology
Viral is m ost com m on.
50% of cases have no identifiable cause.
Specific Viruses
HSV: o
10–20% of all encephalitides
o
Prim ary or reactivation
o
Early treatm ent im proves prognosis.
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Arbovirus: o
10–15% of all encephalitides
o
Zoonotic transm ission (m osquitoes, ticks) in warm m onths
o
o
Eastern equine causes fulm inant encephalitis:
Tropism for the hippocam pus
Abrupt onset of headache, fever, vom iting
Western equine occurs m ostly in the western two thirds of the United States:
Often preceded by nonspecific upper respiratory/GI tract sym ptom s
o
Japanese—m ost prevalent arboviral encephalitis worldwide:
Indolent course of fever, headache, m yalgias, and fatigue followed by confusion, delirium , m asklike facies, and parkinsonism s, seizures, brainstem dysfunction, com a, and death
Flavivirus: o
West Nile virus—increased incidence in North Am erica:
Found in m osquitoes and birds
Febrile illness, often with rash
Headache
Lym phadenopathy
Polyarthropathy
Increased m orbidity/m ortality in elderly patients
Enteroviral: o
Occurs m ainly in children Table o f C o ntents > Endo carditis
Endocarditis
Michael S. Murphy
Basics Description
A m icrobial infection of the endothelial surface of the heart
Characterized by the vegetation (a throm bus with superim posed m icroorganism s)
Older population
Frequently affects m en
Fewer patients at present dem onstrate the classic signs once noted by Osler
Risk factors: o
Poor dental hygiene
o
IV drug abuse (IVDA):
Greater risk than rheum atic heart disease or prosthetic valves
o
Predilection for right-sided heart valves
Risk factor for recurrent endocarditis
Structural heart disease serves as com m on vegetative site due to altered intracardiac flow:
o
Mitral valve prolapse
Aortic valve dysfunction
Congenital heart disorders in the pediatric
Pa ge 1 6 7
populations:
Tetralogy of Fallot
Aortic stenosis
Patent ductus arteriosus
Ventricular septal defects
Aortic coarctation
o
Prosthetic valves
o
Indwelling catheters
o
Any m echanical devices m ay serve as a portal of entry or attachm ent for m icroorganism s.
Etiology
Major categories: o
Bacterial endocarditis
o
Prosthetic valve endocarditis
o
Nonbacterial throm botic endocarditis:
Malignancy
Urem ia
Burns
System ic lupus erythem atosus
Com m on organism s: o
Streptococcus viridans
Found in oropharynx, com m on agent in native valve endocarditis
o
Streptococcus bovis:
Com m on association with colonic polyps or gastrointestinal m alignancy
o
Streptococcus pneum oniae:
Causes rapid valvular destruction, abscess, and congestive heart failure (CHF)
Risk factor: alcoholism
o
Staphylococcus epiderm idis
o
Staphylococcus aureus
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Seen in all populations, especially IVDA and toxic illness
o
Som etim es m etastatic
Enterococci:
Seen in young wom en and old m en following instrum entation or infection
o
Candida and Aspergillus
Found in IVDA, prosthetic valves, or im m unocom prom ised patients
o
HACEK (Haem ophilus species)
o
Culture-negative endocarditis (Q fever, psittacosis, Bartonella, brucellosis)
Diagnosis Signs and Symptoms General
Fever: o
Most com m on sym ptom
o
Often absent in certain settings:
Elderly
CHF
Severe debility
Chronic renal failure
Flulike illness
Chills
Sweats
Rigors
Malaise
Head, Eyes, Ears, Nose, and Throat
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Retinal hem orrhages or Roth spots
Respiratory
Dyspnea
Cough
Cardiac A new or changing m urm ur in 80–85% of patients
Abdominal
Abdom inal or back pain
Splenom egaly (15–50%)
Extremities
Myalgias
Arthralgias
Digital clubbing
Neurologic Septic em bolization (stroke or m ycotic aneurysm )
Skin Cutaneous vasculitic lesions:
Mucosal and conjunctival petechiae
Splinter hem orrhages
Osler nodes: o
Erythem atous, painful tender nodules
Janeway lesions: o
Erythem atous or hem orrhagic, m acular or nodular lesions, a few m illim eters in diam eter on the hands and feet
Essential Workup
Identify risk factors for endocarditis in patients with fever of unknown etiology.
Blood cultures
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Echocardiography is needed to confirm the diagnosis.
Tests Lab
CBC: o
Anem ia (som etim es hem olytic)
o
Leukocytosis (with granulocytosis and bandem ia)
Blood cultures: o
Multiple sets (three sets over a tim e period) should be obtained before antibiotic adm inistration.
Elevated sedim entation rate and C-reactive protein (lacks specificity)
Urinalysis: o
Microscopic hem aturia
Imaging
Chest radiography: o
CHF
o
Septic pulm onic em boli, which m ay be seen in right-sided endocarditis
ECG: o
Arrhythm ia, new heart block
Echocardiography: o
Acute valvular pathology
o
Abscess
o
Vegetations
o
Transesophageal echocardiography provides greater sensitivity.
Differential Diagnosis
Rheum atic fever
Atrial m yxom a
Acute pericarditis
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Myocardial infarction
Aortic dissection with regurgitant valve
Throm botic throm bocytopenic purpura
System ic lupus erythem atosus
Occult neoplasm with m etastasis
Septicem ia
P.361
Treatment Initial Stabilization
Monitor for signs of heart failure
Operative repair if:
o
Severe valvular dysfunction causing failure
o
Unstable prosthesis
o
Perivalvular extension with intracardiac abscess
o
Antim icrobial therapy failure
o
Large or fungal vegetations
Antibiotic therapy: o
IV, bactericidal, and em piric, pending culture results
o
Native valve or congenital abnorm ality:
o
Penicillin G + nafcillin + gentam icin
Vancom ycin + gentam icin
Prosthetic valve or history of IVDA:
Vancom ycin + gentam icin + rifam pin
Nafcillin + gentam icin + rifam pin (if m ethicillin-resistant S. aureus [MRSA] is not suspected)
If MRSA vancom ycin failure/intolerant consider
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daptom ycin or quinupristin-dalfopristin
Vancom ycin-resistant enterococcus faecium consider quinupristin-dalfopristin
o
Fungal:
o
Am photericin B
HACEK:
Ceftriaxone
Medication (Drugs)
Am photericin B: o
Test dose 0.1 m g/kg up to 1 m g slow IV.
o
Wait 2–4 hours.
o
If tolerated, begin 0.25 m g/kg IV and advance to 0.6 m g/kg IV q.i.d.
Ceftriaxone: 2 g IV q.i.d.
Daptom ycin 4 m g/kg IV q.i.d.
Gentam icin: 1 m g/kg IV q8h
Nafcillin: 2 g IV q4h
Penicillin G: 20 m illion IU IV q.i.d.
Quinupristin-dalfopristin: 7.5 m g/kg IV q12h
Rifam pin: 600 m g PO q.i.d.
Vancom ycin: 15 m g/kg IV q12h
Follow-Up Disposition Admission Criteria
Patients with risk factors who exhibit pathologic criteria or clinical findings
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All IV drug users with fever
Adm it patients with cardiovascular instability to an intensive care unit/m onitored setting.
Discharge Criteria None
Expected Course Most patients will defervesce within 1 week.
Complications
Cardiac: CHF, valve abscess, pericarditis, fistula
Neurologic: em bolic stroke, abscess, hem orrhage
Em bolization: CNS, pulm onary, ischem ic extrem ities
Mycotic aneurysm s: cerebral or system ic
Renal: infarction, nephritis, abscess
Metastatic abscess: kidney, spleen, tissue
References 1. Berbari E, Cockerill F, et al. Infective endocarditis due to unusual or fastidious m icroorganism s. Mayo Clin Proc. 1997;72:532–542. 2. Hogevik H, Alestig K. Fungal endocarditis: a report on seven cases and a brief review. Infection. 1996;24(1):17–21. 3. Karchm er A, Alestig K. Infective endocarditis. In: Braunwald E, ed. Heart disease: a textbook of cardiovascular m edicine. 5th ed. Philadelphia: WB Saunders, 1996;1997:1077–1104. 4. Mylonakis E, Calderwood S. Infective endocarditis in adults. N Engl J Med. 2001;345(18):1318–1330. 5. Salm an L, Prince A, et al. Pediatric infective endocarditis in the m odern era. J Pediatr. 1993;122:847–853.
Codes ICD9-CM 421
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ICD10 I38
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Endo m etrio sis
Endometriosis
Christy Rosa Mohler
Basics Description Ectopic endom etrial tissue with cyclic horm onal responsiveness
Etiology
Theories include retrograde m enstruation, im m unologic factors, and m etaplastic transform ation.
Invades tissues, spreads locally and hem atogenously
Pediatric Considerations Not seen before m enarche
Genetics Fam ilial disposition suggested by clinical, population, and twin studies
Diagnosis Signs and Symptoms History
Pelvic or back pain, usually cyclic
Dysm enorrhea m ay be severe.
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Dyspareunia
Infertility
Physical Exam
Pelvic exam nonspecific: o
Rarely im m obile tender uterus or nodular m asses are present.
Abdom inal exam typically benign unless ruptured endom etriom a produces peritoneal signs
Endom etriosis has been found in the lungs, brain, and m any nonperitoneal sites; signs and sym ptom s can vary greatly depending on location of lesions.
Essential Workup
Pregnancy test
Rule out other, life-threatening diagnoses, as directed by history and physical exam .
Tests Lab Pregnancy test
Imaging Pelvic ultrasound, CT, and MRI m ay show ovarian endom etriom as, but rarely reveal im plants.
Diagnostic Procedures/Surgery Laparoscopy usually required for definitive diagnosis
Differential Diagnosis
Appendicitis
Ectopic pregnancy
Ovarian cysts
Ovarian torsion
Pelvic inflam m atory disease/tubo-ovarian abscess
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Menstrual cram ps/m ittelschm erz
Inflam m atory bowel disease
Irritable bowel disease
Sm all bowel obstruction
Diverticulosis
Gastroenteritis
P.363
Treatment Initial Stabilization
Manage hypotension initially with isotonic IV fluid.
For severe bleeding not responsive to IV fluid, m ay need transfusion of packed red blood cells (PRBC)
ED Treatment
Analgesia
Gynecology consultation for large or ruptured endom etriom as
Oral contraceptives, gonadotropin-releasing horm one agonists (e.g., leuprolide [Lupron]), or other horm onal treatm ent m ay be started in consultation with the prim ary care physician or gynecologist.
Medication (Drugs)
Acetam inophen: 650 m g to 1 g PO
Ibuprofen: 400–800 m g PO
Ketorolac: 30 m g IM/IV
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Morphine: 4–8 m g IM/IV or equivalent analgesic
Follow-Up Disposition Admission Criteria
Intractable pain
Unclear diagnosis to follow serial exam s or for further workup and treatm ent
Ruptured endom etriom a with peritoneal signs
Discharge Criteria Most patients with a clear exacerbation of endom etriosis can be discharged with gynecology referral once pain is controlled.
References 1. Dart R. Acute pelvic pain. In: Marx JA, et al, eds. Rosen's Em ergency Medicine: Concepts and Clinical Practice. 5th ed. St. Louis, MO: Mosby–Year Book; 2002:219–226. 2. Giudice LC, Kao LC. Endom etriosis. Lancet. 2004;364:1789–1799. 3. Morrison LJ, Spence JM. Gynecology and obstetrics: abdom inal and pelvic pain in the non pregnant patient. In: Tintinalli JE, ed. Em ergency Medicine: A Com prehensive Study Guide. 6th ed. New York: McGraw-Hill; 2004:655–657.
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Epididym itis/Orchitis
Epididymitis/Orchitis Matthew D. Cook
Basics Description Epididymitis
Definition: inflam m ation or infection of the epididym is
Rare in prepubertal boys
Pathogenesis: o
o
Initial stages:
Cellular inflam m ation begins in vas deferens
Descends to lower pole of epididym is
Acute phase:
Epididym is is swollen and indurated in upper and lower poles.
o
Sperm atic cord thickened
Testis m ay becom e edem atous owing to passive congestion or inflam m ation.
o
Resolution:
May be com plete without sequelae
Peritubular fibrosis m ay develop, occluding ductules
Com plications:
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o
Two thirds of m en have atrophy due to partial vascular throm bosis of testicular artery.
o
Abscess and infarction rare (5%)
o
Incidence of infertility with unilateral epididym itis unknown:
50% with bilateral epididym itis
Orchitis
Definition: inflam m ation or infection of the testicle: o
Usually from direct extension of the sam e process within the epididym is
o
Isolated testicular infection is rare:
Can result from hem atogenous spread of bacteria or following m um ps infection
Categories: o
Pyogenic bacterial orchitis secondary to bacterial involvem ent of epididym is
o
Viral orchitis:
Most com m only due to m um ps
Rare in prepubertal boys; occurs in 20–30% of postpubertal boys with m um ps.
Occurs 4–6 days after parotitis but can occur without parotitis.
Unilateral in 70% of patients
Usually resolution in 6–10 days
30–50% of testes involved have residual atrophy; rarely affects fertility.
o
Granulom atous orchitis:
Syphilis
Mycobacterium and fungal diseases
Usually occurs in im m unocom prom ised host
Etiology
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Epididymitis
Children: o
Coliform or pseudom onal urinary tract infections
o
Sexually transm itted diseases rare in prepubertal m ales
o
Associated with predisposing abnorm alities of lower urinary tract
Young m en, age 35 years: o
Com m only associated with underlying urologic pathology (benign prostatic hypertrophy, prostate cancer, strictures)
o
May have acute or chronic bacterial prostatitis
o
Coliform bacteria m ore com m on (23–67%), especially after instrum entation
o
Chlam ydia trachom atis (8–80%)
o
Klebsiella and Pseudom onas species
o
Neisseria gonorrhoeae (15%)
o
Gram -positive cocci
Drug related: o
Am iodarone-induced epididym itis:
Usually with am iodarone levels higher than
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therapeutic levels
Granulom atous: o
Syphilis or m ycobacterial and fungal causes:
May be presenting feature of Mycobacterium tuberculosis in high prevalence regions
Urine cultures often negative for M. tuberculosis
Vasculitis: o
Polyarteritis nodosa
o
Behçet disease
o
Henoch-Schönlein purpura
Orchitis
Pyogenic bacterial orchitis: o
Escherichia coli
o
Klebsiella pneum oniae
o
Pseudom onas aeruginosa
o
Staphylococci
o
Streptococci
Viral orchitis: o
Mum ps:
20% m ay develop epididym oorchitis
Rarely associated with live-attenuated m um ps vaccine
o
Coxsackie A and lym phocytic choriom eningitis virus
Granulom atous orchitis: syphilis and m ycobacterial and fungal diseases
Fungal orchitis: o
Blastom ycosis in endem ic regions
o
Invasive candidal infections in im m unosuppressed hosts
Posttraum atic orchitis: inflam m ation
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Diagnosis Signs and Symptoms History
Gradual onset of m ild to m oderate testicular or scrotal pain, usually unilateral
Progressive scrotal swelling
Dysuria (30%):
o
Recent urinary tract infection
o
History of abnorm al bladder function
Urethral discharge: o
Of patients with gonococcal epididym itis, 21–30% did not com plain of urethral discharge
o
No dem onstrable urethral discharge in 50%
Fever (14–28%)
Recent urethral instrum entation or catheterization
Physical Exam
Tenderness in groin, lower abdom en, or scrotum
Scrotal skin com m only erythem atous and warm (60%)
Early: o
May feel swollen, indurated epididym is
Later: o
May not be able to distinguish epididym is from testis
Sperm atic cord m ay be edem atous.
Intact crem asteric reflex and Prehn sign: o
Pain relief with testicular elevation
o
Com m only observed but not specific
Coexistent prostatitis is rare (8%)
Pyogenic bacterial orchitis: o
Patients usually are acutely ill.
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o
Fever
o
Intense discom fort
o
Swelling of testicle
o
Often reactive hydrocele
Essential Workup
Must differentiate from testicular torsion
Early consultation with urologist if strong suspicion of testicular torsion
Tests Lab
CBC: o
Often leukocytosis in range of 10,000–30,000/m m 3
Urinalysis and culture: o
15–50% of patients with epididym oorchitis have pyuria
o
24% of patients have positive urine bacterial cultures
o
Urine chlam ydial enzym e im m unoassay low sensitivity (50–70%)
Urethral swab (50–73% have dem onstrable urethritis despite m inority of sym ptom s): o
Gram stain and culture
o
Chlam ydia testing
o
Avoid bladder em ptying within two hours of tests (lowers sensitivity)
o
Especially for postpubertal and sexually active
Blood culture if system ically ill
P.365
Imaging
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Ultrasonography: color Doppler im aging: o
82–100% sensitivity, 100% specificity in detecting testicular torsion or decreased blood flow
o
o
Epididym oorchitis:
Hyperem ia
Increased vascularity and blood flow
Advantages:
Can evaluate for epididym itis or other causes of scrotal pain
o
70% sensitivity, 88% specificity for epididym itis
Disadvantages:
Highly exam iner dependent
Difficult in infants or children
Testicular scintigraphy: o
Radionuclide study to assess perfusion
o
90–100% sensitivity, 89–97% specificity in detecting testicular torsion
o
Inflam m atory processes have increased flow and uptake
o
o
False-positive scans:
Large fluid collections in scrotum
Abscess
Hydrocele, hem atocele
Bowel herniation
False-negative scans:
Early torsion
Spontaneous detorsion
Sm all children or infants
Diagnostic Procedures/Surgery Surgical indications:
Scrotal abscess
If another scrotal problem , such as torsion, cannot be
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excluded
Suspected or proved ischem ia caused by severe epididym itis
Patient with solitary testicle
Scrotal fixation: indicates severe inflam m ation and potential suppuration
Differential Diagnosis
Testicular torsion
Testicular tum or
Torsion of testicular appendages
Traum a to scrotum
Acute hernia
Acute hydrocele
Treatment Pre Hospital
IV access
IV fluids, especially if system ically ill
Initial Stabilization
IV access
IV fluids, especially if system ically ill
ED Treatment
Antibiotics: o
Cover for chlam ydial and gonococcal etiologies if adult or presum ed sexually transm itted
o
Cover for coliform etiology:
Child, or adult >35 years of age
Insertive partner in anal intercourse
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Presum ed nonsexually transm itted
o
Adjust according to culture and sensitivity
o
Treat sexual partners
Bed rest and scrotal support
Ice packs
Analgesics and ant inflam m atories
Medication (Drugs) Age 35 Years or Insertive Partners in Anal Intercourse
Prim ary: ciprofloxacin 500 m g PO b.i.d. or 400 m g IV b.i.d. (or ofloxacin 300 m g PO b.i.d. or levofloxacin 750 m g PO/IV per day) for 10–14 days
Alternative: am picillin/sulbactam 3 g IV q6h or cefotaxim e 2 g IV q8h or ceftriaxone 2 g IV per day
Children
Azithrom ycin: 10 m g/kg PO day 1, 5 m g/kg PO per day 2 through 10 or TMP-SMX 4 m g/kg TMP and 20 m g/kg SMX b.i.d. for 10–14 days
Avoid quinolones and tetracyclines in children.
Follow-Up
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Disposition Admission Criteria
Surgical indications present
Older age group if it is the only way to ensure appropriate workup: o
Many will have underlying urologic pathology.
System ically ill, fever, nausea, vom iting
Scrotal abscess
Intractable pain
Discharge Criteria
Fails to m eet adm ission criteria
Patient with good follow-up
Able to take oral antibiotics
Issues for Referral Urologic consultation and follow-up:
Children need workup for urologic abnorm alities: o
Voiding cystourethrography
o
Renal ultrasound
If bacteriuria present, exam ination of lower tract with cystoscopy after treatm ent com pleted
References 1. Herberner TE. Ultrasound in the assessm ent of the acute scrotum . J Clin Ultrasound. 1996;24:405–421. 2. Kass EJ, Lundak B. The acute scrotum . Pediatr Clin North Am . 1997;44:1251–1266. 3. Luzzi GA, O'Brien TS. Acute epididym itis. Br J Urol Int. 2001;87:747–755. 4. Marcozzi D, Suner S. The nontraum atic acute scrotum . Em erg Med Clin North Am . 2001;19:547–568.
Codes
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ICD9-CM 604.90
ICD10 N45.9
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Epidural Abscess
Epidural Abscess
Richard S. Krause
Basics Description
Pyogenic infection of epidural space
Most com m on in thoracic spine, followed by lum bar and cervical areas
Etiology
Focus of infection is present followed by either hem atogenous spread (approxim ately 50%) or direct extension.
Most com m on source is skin infection: o
Staphylococcus aureus accounts for >50% of cases: o
Any pyogenic infection m ay be source.
Streptococcus is second m ost com m on.
Haem ophilus influenzae, gram -negative bacilli, m ycobacteria, anaerobic and m ixed infections also occur.
May occur after lum bar puncture (usually follows m ultiple attem pts)
Pediatric Considerations
Children present sim ilar to adults with back pain, fever, and neurologic signs as well as nonspecific system ic
Pa ge 1 6 9
sym ptom s.
Infants m ay exhibit only fever, irritability, and associated m eningitis.
Sphincter disturbance is frequently seen.
Most cases are secondary to hem atogenous spread.
Location and bacteriology sim ilar to adults
Diagnosis Fever and severe back pain represent “red flag― for potentially serious condition:
If pain is radicular or there is neurologic disturbance, likelihood of epidural abscess is increased.
Signs and Symptoms
Classic presentation: o
Severe, progressive back pain (often radicular)
o
Fever
o
Neurologic deficit:
Weakness or paralysis
Sensory level
Sphincter disturbance
May present with signs and sym ptom s of sepsis without prom inent back pain
Occurs at all ages including infants: o
Peak is at ages 60–70 years
Most patients have predisposing condition: o
IV drug abuse
o
Diabetes
o
Malignancy
o
Chronic steroids
o
Chronic alcoholism
Pa ge 1 6 9
o
Instrum entation or spinal surgery
May occur in absence of identifiable predisposing factors
Essential Workup
History should include predisposing conditions when this diagnosis is suspected.
Physical exam for source of infection, localized spinal tenderness, and neurologic findings:
o
Especially decreased sphincter tone
o
Saddle anesthesia
o
Lower extrem ity weakness
Voided urine followed by postvoid catheterization: o
Younger adults should have Table o f C o ntents > Epiglo ttis, Pediatric
Epiglottis,
Pediatric Beverly Bauman
Basics Description
Inflam m ation of the epiglottis and surrounding supraglottic region, which is potentially life threatening owing to airway obstruction
Children are at greater risk of upper airway obstruction owing to: o
Decreased cross-sectional area of the upper airway (resistance is proportional to the inverse of the radius to the fourth power)
o
Loose attachm ent of m ucosal surface and increased vascularity of m ucosa allows for edem a
o
Dynam ic collapse of the airway
A precipitous decline in the incidence of childhood epiglottitis since the introduction of the Haem ophilus influenzae vaccination, although vaccine failure m ay result in rare cases am ong children who have been im m unized
In the post-Hib vaccine era, the m ean age for this disease has increased, and it is now m ore com m only seen in
Pa ge 1 7 1
adolescents and adults than in toddlers or young school-aged children.
May occur throughout the year
Alert All patients with suspected epiglottis require intensive m onitoring and intervention. Rapid progression of airway obstruction m ay occur.
Etiology
Infection: o
H. influenzae type B
o
S. pneum oniae
o
Group A β-hem olytic Streptococcus
o
Staphylococcus aureus
o
Viruses
o
Less com m on infections include Klebsiella, Pseudom onas, Candida
Caustic
Therm al
Traum atic
Posttransplant lym phoproliferative disorder
Diagnosis Signs and Symptoms History
Usually fulm inant presentation without prodrom al illness
General: o
Irritability, throat pain, fever, noisy breathing
o
Progressive toxicity and respiratory distress
Physical Exam
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General: o
Toxic appearing
o
High fever is typical.
Throat: o
Drooling
o
Dysphagia
o
Muffled “hot potato― voice
Respiratory: o
Rapidly progressive respiratory distress (dyspnea in only one third of adults)
o
Children usually prefer to sit upright, leaning forward with open m outh (“tripod sniffing position―) to m axim ize air entry.
o
Subtle stridor that m ay progress to severe stridor (stridor in only 10% of adults)
Com plications: o
Airway obstruction is the m ost severe com plication.
o
Epiglottic abscess
o
Associated pneum onia and atelectasis
Essential Workup
Epiglottitis is a clinical diagnosis.
Indirect laryngoscopy or any attem pts to directly visualize the epiglottis are not indicated in children with suspected epiglottis unless perform ed in a controlled environm ent (In adolescents or adults, use of fiberoptic nasopharyngoscope m ay be indicated for patients without im pending airway obstruction).
If infection is suspected, obtain cultures of the epiglottis during laryngoscopy after airway is secure.
Tests Lab
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Avoid laboratory tests until airway is controlled.
Throat cultures after control of airway
Blood cultures after airway is secure: o
Often positive if H. influenzae is the pathogen
Imaging Radiographs of the soft tissue lateral neck:
Usually not necessary to m ake the diagnosis
Create additional risk by delaying stabilization of the airway, prom oting airway obstruction by agitating the patient, and often rem oving the child from the ED to an uncontrolled environm ent
Variable findings: o
Norm al
o
Swelling of the epiglottis (“thum bprint sign―) and often supraglottic region
o
Ballooned hypopharynx
o
Obliteration of vallecula
o
EW/C3W (epiglottic width to third cervical vertebral body width) ratio of >0.5
Diagnostic Procedures/Surgery Laryngoscopy:
In a controlled environm ent whenever possible
Cultures of the epiglottis during laryngoscopy after the airway is secured m ay help identify pathogens and direct treatm ent.
Epiglottis will appear swollen, inflam ed, reddened.
Differential Diagnosis
Other infectious processes: o
Bacterial tracheitis
o
Mononucleosis
o
Diphtheria
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o
Pertussis
o
Croup or laryngotracheobronchitis (prim arily in younger children, but there is a significant overlap in the ages of presentation)
o
Ludwig angina
o
Peritonsillar infection
o
Retropharyngeal abscess
Anaphylactic reaction with angioedem a
Foreign body in upper airway
Laryngeal traum a
Laryngospasm
Inhalation or aspiration of toxins (e.g., hydrocarbons)
Airway burns (have been related to crack cocaine)
Hyperventilation
CNS disorders
Treatment Pre Hospital Degree and m ode of intervention m ust reflect degree of obstruction, tim e and m eans of transport, capability of care providers, etc. Consult and notify receiving hospital.
Initial Stabilization Airway m anagem ent if patient is in extrem is:
Bag-valve-m ask ventilation with 100% O 2 with cricoid pressure often provides adequate ventilation and tim e to prepare for intubation and m ove to a controlled setting such as the OR.
Oral intubation: o
Use an endotracheal tube (ETT) size that is one or
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two sizes sm aller than indicated by age or length. o
Direct com pression of the anterior neck in the glottic region m ay help visualize air bubbles at the opening of the swollen glottis.
If oral intubation fails: o
Em ergent cricothyrotom y or needle cricothyrotom y if age older than 10–12 years
o
Needle cricothyrotom y if age younger than 10–12 years
P.373
ED Treatment
One hundred percent O 2 as tolerated by patient
Allow child to rem ain in position of com fort and do not force child to lie down, which m ay worsen airway obstruction.
Although not proven, racem ic epinephrine or L-epinephrine by nebulizer m ay tem porize sym ptom s while plans for a definitive airway are rapidly arranged. It m ust be done with caution to avoid agitating the child.
Avoid procedures that agitate the child such as IV access and blood draws.
Em piric invasive airway m anagem ent m ay be indicated: o
Patients with rapidly progressive respiratory difficulty, tachypnea, worsening throat pain, tachycardia, or hypoxem ia
o
Patients at high risk of acute obstruction (e.g., children with im m unodeficiency disorders)
Intubate in OR or controlled environm ent by m ost skilled person.
Use inhalational anesthesia before intubation.
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Have appropriate various diam eters of endotracheal tubes available to accom m odate the inflam ed supraglottic region.
Surgical backup is required in case intubation is not possible; then em ergency tracheotom y or cricothyrotom y can be perform ed.
Equipm ent for intubation and for a surgical airway or needle cricothyrotom y m ust be available at the bedside.
Adm inister IV antibiotics: Second- or third-generation cephalosporins are active against β-lactam ase–producing H. influenzae.
Steroids are controversial but frequently adm inistered, particularly in patients with chem ical or therm al epiglottitis.
Medication (Drugs)
Am picillin/Sulbactam : 100–200 m g/kg/24h q6h IV
Am picillin: 100–200 m g/kg/24h q6h IM/IV; given with chloram phenicol
Cefotaxim e: 150 m g/kg/24h q8h IV
Ceftriaxone: 100 m g/kg/24h q12h IV
Chloram phenicol: 75–100 m g/kg/24h q6h IV
Decadron: 0.6 m g/kg/d (m ax. 10 m g) IV
Epinephrine, racem ic: 0.05 m L/kg (m ax. 0.5 m L) q30m in in 2.5 m L norm al saline (NS) via nebulizer
L-Epinephrine, 1:1,000: 0.5 m L/kg (m ax. 5 m L) q30m in via nebulizer
Rifam pin for contact prophylaxis: 20 m g/kg (m ax. 600 m g) daily for 4 days
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Follow-Up Disposition Admission Criteria Patients with suspected or proven epiglottitis should be adm itted to ICU after stabilization of airway and adm inistration of antibiotics and fluids.
Discharge Criteria
Rifam pin prophylaxis m ay be indicated for close contacts of H. influenzae epiglottitis. If the household has children younger than 12 m onths of age or children who are unim m unized, incom pletely im m unized, or im m unosuppressed, prophylaxis is indicated for nonpregnant household contacts. Child care center contacts should receive prophylaxis when two or m ore cases of Hib invasive disease have occurred within 60 days.
All cases of invasive H. influenzae disease should be reported to the local or state public health departm ent.
Issues for Referral Critical care or pulm onary consult on all patients
References 1. Am erican Academ y of Pediatrics. Haem ophilus influenzae infections. In: Pickering LK, ed. Red Book: 2003 Report of the Com m ittee on Infectious Diseases. 26th ed. Elk Grove Village, IL: Am erican Academ y of Pediatrics; 2003:293–301. 2. Dam m M, Eckel HE, Jungehulsing M, et al. Managem ent of acute inflam m atory childhood stridor. Otolaryngol Head Neck Surg. 1999;121(5):633–638.
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3. Frantz T, Ragson B, Quesenberry C. Acute epiglottitis in adults: analysis of 129 cases. JAMA. 1994;272:1358–1360. 4. Rothrock S, et al. Radiologic diagnosis of epiglottitis: objective criteria for all ages. Ann Em erg Med. 1990;19:978–982. 5. Shah RK, Roberson DW, Jones DT. Epiglottitis in the Hem ophilus influenzae type B era: changing trends. Laryngoscope. 2004;114:557–560. 6. Stroud RH, Friedm an NR. An update on inflam m atory disorders of the pediatric airway: epiglottitis, croup and tracheitis. Am J Otolaryngol. 2001;22(4):268–275.
Miscellaneous SEE ALSO: Bacterial Tracheitis; Epiglottis, Adult
Codes ICD9-CM 464.3 464.30 464.31
ICD10 J05.1
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Epiglo ttitis, Adult
Epiglottitis, Adult
Jonathan Fisher Owen Landers
Basics Description Rapidly progressive inflam m ation of the epiglottis and surrounding tissues leading to airway com prom ise
Alert Patients with respiratory distress are at high risk for com plete airway obstruction. Surgical airway m anagem ent m ay be required.
Mechanism
Inflam m ation of supraglottic structures: o
Epiglottis:
Involvem ent of this is of prim ary airway concern.
May be prim ary or secondary from adjacent structures
o
Vallecula
o
Arytenoids
Uncom m on: o
Incidence is rising in adults, while decreasing in children.
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o
Unclear whether this is true incidence versus im proved diagnosis
Im m une com prom ised patients m ay be particularly fulm inant, with m inim ally associated sym ptom s and unusual pathogens, such as candida.
Com plications: o
Total airway obstruction
o
Retropharyngeal abscess
o
Acute respiratory distress syndrom e
o
Pneum onia
o
Em pyem a
Etiology
Infectious causes: o
Haem ophilus influenzae B, also type A and nontypable strains
o
Haem ophilus parainfluenzae
o
Streptococcus pneum oniae
o
Staphylococcus aureus
o
Group A strep
o
Herpes sim plex
o
Neisseria m eningitis
o
Cytom egalovirus
o
Num erous other uncom m on agents
Physical agents: o
Chem ical burns
o
Therm al burns
o
Toxic or illicit drug inhalation
Traum a, instrum entation
Diagnosis
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Signs and Symptoms
General: o
Fever
o
Upper respiratory tract infection sym ptom s
Prodrom e absent in significant num ber of cases
o
Toxic appearance
o
Drooling
Head, eyes, ears, nose, throat: o
Dysphagia
o
Muffled voice
o
Voice change:
“Hot potato― voice
Hoarseness
o
Foreign body sensation in throat
o
Associated tonsillar, peritonsillar, uvula findings
o
“Cherry red― epiglottis is classic, m ay be pale and edem atous in up to 50 percent.
o
Hyoid/thyroid cartilage tender to gentle palpation
o
Lym phadenopathy
Respiratory: o
Respiratory com prom ise
o
Subjective sense of obstructed airway
o
Stridor
o
Sudden loss of airway
o
May be m ore indolent in adults than pediatrics; rapid progression to total airway occlusion still seen in adults
Essential Workup
If significant respiratory distress: o
Avoid invasive diagnostic procedures
o
Manage em pirically with antibiotics and control of
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airway
Portable lateral soft-tissue x-ray
Pediatric Considerations
Children with a high suspicion of epiglottitis are at risk of com plete airway obstruction and should be quickly transferred to a setting where the airway can be definitively m anaged in a surgical setting.
Staff capable of m anaging the airway should accom pany the child until the airway has been secured.
IV insertion, adm inistration of antibiotics, and obtaining blood work should follow airway m anagem ent.
A needle cricothyrotom y m ay be required in extrem e situations in young children.
Tests Lab
CBC with differential
Blood cultures
Cultures of pharynx: o
Only if no signs of respiratory distress
Imaging
Portable lateral soft-tissue x-ray: o
Epiglottic “thum b― sign:
o
Thickening of the epiglottis
“Vallecula― sign:
The vallecula is norm ally well delineated, deep, and roughly parallel to the pharyngotracheal air colum n.
Absence of a deep and well-defined vallecula, approaching the level of the hyoid bone
o
Swelling of the arytenoids and aryepiglottic folds
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o
Prevertebral soft-tissue swelling
o
Significant false-negative with im aging
o
If suspected with negative film results, rule out with indirect visualization
CT: o
Indicated when a laryngoscopic evaluation cannot be perform ed or if coexistent soft-tissue com plications are suspected
Diagnostic Procedures/Surgery
Avoid prior to airway m anagem ent if any signs of respiratory distress are present, including stridor
Nasopharyngoscopy (m ini-fiberoptic scope)
Indirect laryngoscopy
Differential Diagnosis
Croup
Airway foreign body
Anaphylaxis
Paradoxic vocal cord dysfunction
Angioedem a
Laryngitis
Pharyngitis
Oropharyngeal abscess (peritonsillar or retropharyngeal)
Bacterial tracheitis
Congenital anom aly
P.371
Treatment
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Pre Hospital
Transport patients in position of com fort
Supplem ental oxygen as tolerated; avoid increasing anxiety
Intubation indicated only if patient is in severe respiratory distress: o
Likely difficult airway and significant chance of exacerbating com prom ise with laryngoscopy attem pts
Inhaled agents, racem ic epinephrine, and β-agonists have no dem onstrated value.
Initial Stabilization
ABCs
Be prepared with all equipm ent on hand for definitive airway m anagem ent, including a surgical airway, from presentation until diagnosis is ruled out or transport to intensive care setting.
Exam ination of the airway can trigger airway obstruction.
Orotracheal intubation in patients with signs of obstruction or significant respiratory distress: o
Respiratory distress/airway failure m ay develop precipitously.
o
Consider ear-nose-throat/surgical consult if patient's condition perm its for possible difficult/surgical airway.
Needle jet insufflation m ay be a life-saving tem porizing m easure if a surgical airway is not im m ediately attainable with failed intubation.
ED Treatment
Hum idified oxygen support
IV access, hydration as indicated
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Begin antibiotic coverage em pirically: o
o
o
First line:
Cefotaxim e
Ceftriaxone
Second line:
Am picillin/sulbactam
Trim ethoprim -sulfam ethoxazole
Consider adding increased coverage against Staph Aureus:
Nafcillin
Vancom ycin
Corticosteroids controversial
Medication (Drugs)
Am picillin/sulbactam : 3 g IV initially, then 200–300 m g/kg/d in 4 div. doses
Cefotaxim e: 1–2 g IV initially, then 180 m g/kg/d in 4 div. doses
Ceftriaxone: 1–2 g IV initially, then 100 m g/kg/d in 2 doses
Trim ethoprim -sulfam ethoxazole: 320 m g IV initially, then 4–5 m g/kg IV q12h
Nafcillin: 150–200 m g/kg IV per day in 4 div. doses
Vancom ycin: 40–60 m g/kg IV per day in 3 div. doses if concern for MRSA
Rifam pin prophylaxis: o
Adults: 600 m g PO per day for 4 days
o
>1 m onth of age: 20 m g/kg PO per day for 4 days
o
Table o f C o ntents > Epiphyseal Injuries
Epiphyseal
Injuries Steven F. Fisher Daniel L. Savitt
Basics Description
Occur m ost frequently in distal radius, phalanges, and distal tibia
More com m on than sprains in children: o
Physis relatively weak com pared with ligam ents or m etaphyseal bone
o
Ligam ents often insert into epiphyses.
Com m on m echanism s: o
Shearing
o
Tension
o
Com pression
Most com m on during peak growth
More com m on in m ales
Salter-Harris classification: o
Type I:
Fracture line confined to physis
Epiphyseal separation from m etaphysis
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o
No growth disturbance
Type II:
Fracture propagates along physis, and fragm ent from m etaphysis accom panies displaced epiphysis.
o
Periosteum torn opposite m etaphyseal fragm ent
Most com m on epiphyseal fracture
No growth disturbance
Type III:
Fracture through a portion of physis extending through epiphysis and articular surface
Phalanges and distal tibia m ost com m only affected
Requires anatom ic alignm ent owing to displacem ent of both physis and articular surface
Growth disturbance m ay occur despite anatom ic reduction.
o
Type IV:
Fracture originates at articular surface.
Extends through physis and into m etaphysis
Distal hum erus and distal tibia m ost com m only affected
Anatom ic reduction essential and frequently requires surgical intervention
o
Growth arrest is com m on.
Type V:
Results from crush injuries to physis
No im m ediately visible radiographic alteration
Often found in retrospect with prem ature physeal closure
Usually involves knee or ankle
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o
Growth arrest is com m on.
Type VI (not described in original Salter-Harris classification):
Involves periosteum surrounding physis
Reactive form ation of bone external to growth plate causing tethering of epiphysis to m etaphysis and restricting further expansion at physis
May result from ligam entous avulsion or therm al injuries
o
Type VII (not described in original Salter-Harris classification): involves epiphysis only
Etiology Traum atic injury, often without specific history in young children
Diagnosis Signs and Symptoms
Pain and localized, often pinpoint, tenderness
Lim ited m obility of affected joint
Swelling
Ecchym osis
Bony deform ities
Complications Long-term com plications:
Overreduction
Bone growth disturbances
Reduced joint m obility
Essential Workup
Assess pulses and capillary filling distal to injury.
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Evaluate distal m otor and sensory function.
Verify integrity of skin overlying injury.
Address and m anage coexisting injuries.
Tests Imaging
Plain radiography of injured extrem ity: o
Type I fractures:
May appreciate a slightly separated physis or an associated joint effusion; usually unrem arkable radiograph
Consider com parison views of contralateral joint to detect sm all defects.
Callus m ay be present on subsequent follow-up film s.
o
Types II through IV: film s diagnostic of fracture
o
Types V and VI:
Initial film often norm al
Subsequent radiographs m ay reveal prem ature bone arrest.
Radionuclide bone scan: o
Rarely necessary
o
Fractures m ust be ≥24–48 hours old.
o
Valuable adjunct if child abuse is suspected.
CT scan: helpful in assessing integrity of articular surfaces in type III and IV fractures
MRI: o
If diagnosis rem ains equivocal and identification of a specific fracture would alter m anagem ent
o
Allows for early detection of growth arrest
Differential Diagnosis
Strain
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Sprain
Contusion
P.375
Treatment Pre Hospital
Im m obilize lim b in position found.
Apply ice or cold packs to injury.
Assess injured extrem ity for neurologic and vascular function.
Consider concom itant injuries.
Initial Stabilization
Control hem orrhage.
Apply sterile dressings to open wounds.
Analgesia
ED Treatment
Reduction/alignm ent required: o
Displacem ent to achieve anatom ic alignm ent
o
Vascular or neurologic com prom ise distal to injury requires intervention.
Im m obilization: o
Splint m ust im m obilize joints proxim al and distal to injury in anatom ic alignm ent.
o
Elevate injured lim b.
Open fractures: o
Intravenous antibiotics for Staphylococcus aureus, group A streptococcus, and potentially anaerobes
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after culture
o
Copious irrigation with saline
o
Sterile dressing
o
Orthopedic consultation
Consultation: o
Types III and higher
Medication (Drugs)
Cefazolin: 25–50 m g/kg/d IV/IM q6h–q8h
Clindam ycin: 20–40 m g/kg/d IV q6h–q8h
Fentanyl: 2–3 µg/kg IV; transm ucosal lollipops 5–15 µg/kg, m ax. 400 m g, contraindicated if Table o f C o ntents > Epistaxis
Epistaxis
Christopher M. McCarthy II
Basics Description
Anterior epistaxis (90% of cases): o
Source: Kiesselbach plexus of anterior inferior nasal septum
o
Generally unilateral
Posterior epistaxis (10% of cases): o
Source: posterolateral branch of sphenopalatine artery
Etiology
Local factors: o
Traum a (including postoperative, facial traum a from MVC)
o
Nose picking (especially com m on in children)
o
Dry nasal m ucosa (low hum idity)
o
Environm ental irritants (am m onia, gasoline, sulfuric acid, glutaraldehyde)
o
Inflam m ation and local hyperem ia from allergic or infectious rhinitis
o
Neoplasia (e.g., papillom a and polyp)
o
Nasal foreign body
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System ic factors: o
Atherosclerosis of nasal vasculature
o
Barotraum a
o
Hypertension (data supporting association is controversial)
o
Coagulopathy (fam ilial): hem ophilia A or B, von Willebrand disease
o
Coagulopathy (acquired): throm bocytopenia, liver disease, renal failure/urem ia
o
Drug induced (salicylates, NSAIDs, heparin, coum adin)
o
Diabetes m ellitus
o
Alcoholism
o
Hereditary hem orrhagic telangiectasia (Osler-Weber-Rendu disease)
Diagnosis Signs and Symptoms History
Intensity and am ount of bleeding from nare(s)
Com plaints of vom iting or coughing blood
Recurrence of epistaxis
Known tum ors or coagulopathy
Presence of system ic disease exacerbated by blood loss (coronary artery disease, chronic obstructive pulm onary disease)
Physical Exam
Anesthetize nasopharynx prior to exam with cotton swab soaked in anesthetic and vasoactive agent (lidocaine,
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cocaine, oxym etolazine, etc.—see below).
Attem pt to identify bleeding source with nasal speculum (i.e., Kiesselbach plexus versus posterior source).
Blood in m outh or oropharynx
Tachycardia
Hypotension
Airway com prom ise
Essential Workup
Assess stability: airway com prom ise, hypovolem ia.
Determ ine source (anterior versus posterior).
Consider underlying coagulopathy.
Tests Lab Consider for severe bleeding or suspected coagulopathy:
Type and cross-m atch, hem atocrit, PT, PTT, blood urea nitrogen
Imaging Direct visualization of nasal m ucosa with nasal speculum :
Pretreat with topical vasoconstricting agent and anesthetic
Ensure adequate lighting (i.e., headlam p) and suction
Differential Diagnosis
Hem atem esis
Hem optysis
Pediatric Considerations
Posterior epistaxis is rare in children; consider further workup for bleeding diatheses.
Consider nasal foreign bodies or neoplasm such as juvenile angiofibrom a or papillom a.
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Treatment Pre Hospital
Stable patients: Patient should bend forward at the waist, pinch nares closed, and spit out blood rather than swallow it.
Unstable patients: o
Intubation, if airway is com prom ised
o
IV access
o
Crystalloid resuscitation, if signs of hypovolem ia
Initial Stabilization
Secure the airway in patients who are unconscious, have m ajor facial traum a, or are otherwise at risk of obstruction or aspiration.
Treat hypotension with crystalloids and blood products, if necessary, and ensure adequate IV access.
ED Treatment
Universal precautions against blood/fluid contam ination
Anterior source: o
Instruct patient to bend forward at waist, pinch nares closed for 15 m inutes, and spit out blood rather than swallow it.
o
If bleeding persists, use bayonet forceps to place cotton pledgets soaked in vasoconstricting and anesthetic agents (see list below) into affected nares.
o
Visualize source of bleeding and cauterize lim ited area with silver nitrate or trichloroacetic acid.
o
Consider Gelfoam or Surgicel packing over cauterized site.
o
Consider anterior packing with Vaseline ribbon gauze
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coated with Bacitracin if cautery is unsuccessful, ensuring that both ends protrude from nares and that the strip is rem oved by 48 hours. o
Merocel synthetic sponge tam pon is an alternative to ribbon gauze packing.
o
After anterior packing, persistent new bleeding m ay be a sign of inadequate packing or posterior source.
o
All patients with nasal packing in place should be prescribed an anti-Staphylococcal antibiotic (am oxicillin-clavulanate, cephalexin, trim ethoprim -sulfam ethoxazole) for the duration that the packing rem ains in place for prevention of both acute sinusitis and toxic shock syndrom e.
P.377
Posterior source: o
Posterior packing with balloon device such as Nasostat, Epistat; these are not left in for m ore than 3 days, with antibiotic prophylaxis for anterior packing
o
If com m ercial packs are unavailable, a Foley catheter m ay be directed into posterior nasopharynx until the tip visible in m outh. The balloon is then inflated and the catheter retracted until the balloon is lodged in the posterior nasopharynx. The catheter is then held in place by um bilical clam p.
Com plications of posterior packing: o
Pressure necrosis of posterior oropharynx (do not overfill balloon)
o
Nasal traum a
o
Vagal response
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o
Aspiration
o
Infection
o
Hypoxia
o
Endoscopic cautery by otolaryngology is also useful and m ay obviate need for adm ission.
Medication (Drugs)
Vasoactive solutions: o
4% cocaine
o
1:1 m ixture of 2% tetracaine and epinephrine (1:1,000)
o
1:1 m ixture of oxym etazoline 0.05% (Afrin) and lidocaine solution 4%
o
Phenylephrine (Neo-Synephrine)
Am oxicillin-clavulanate potassium : 250 m g PO q8h
Cephalexin: 250 m g PO q6h
Clindam ycin: 150 m g PO q6h
Trim ethoprim -sulfam ethoxazole: 160/800 m g PO q12h
Follow-Up Disposition Admission Criteria
Severe blood loss requiring transfusion
Severe coagulopathy that places the patient at risk of further blood loss
Posterior nasal packing: otolaryngology consult and adm ission for supplem ental oxygen, sedation, and observation; possible further surgical intervention (e.g.,
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arterial ligation or em bolization)
Patients with packing who cannot be relied upon to follow up in a tim ely m anner
Discharge Criteria
Stable patients: o
Use Afrin nasal spray for 2 days
o
Lubricate nares with an antibiotic ointm ent
o
Hum idify air
o
Avoid nose picking
Return to ED for bleeding not controlled by pressure, fever, difficulty breathing, or vom iting.
Issues for Referral Refer all patients with packing to a specialist within 48 hours.
References 1. Evans JA, Rothenhaus TC. Epistaxis. In: Wolfson AB et al, eds. Harwood-Nuss’ Clinical Practice of Em ergency Medicine. 4th ed. Philedelphia: Lippincott William s & Wilkins, 2005:185–190. 2. Frazee TA, Hauser MS. Nonsurgical m anagem ent of epistaxis. J Oral Maxillofac Surg. 2000;58:419–424. 3. Kucik C, Klenny T. Managem ent of Epistaxis. Am erican Fam ily Physician. 2005;71:305–377. 4. Middleton P. Episaxis. Em ergeny Medicine Australasia. 2004;16:428–440. 5. Pfaff JA, Moore GP. Otolaryngology. In: Marx J, Hockberger R, Walls R, eds. Em ergency m edicine: concepts and clinical practice. 5th ed. St. Louis: Mosby, 2002:933–935. 6. Tan LS, Calhoun KH. Epistaxis. Med Clin North Am . 1999;83:43–56.
Codes ICD9-CM
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784.7
ICD10 R04.0
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Erysipelas
Erysipelas
Irving Jacoby
Basics Description Superficial cellulitis of the skin with prom inent lym phatic involvem ent
Pediatric Considerations
Hem ophilus influenza Type b causes facial cellulitis in children that m ay appear sim ilar to erysipelas: o
Should be considered in unim m unized children
o
Many will be bacterem ic and require adm ission.
o
Cefuroxim e or other appropriate Hem ophilus influenza coverage is im portant.
o
Hem ophilus influenza is m uch less com m on with the vaccine.
Group B streptococci can cause erysipelas in the newborn.
Can develop from infection of um bilical stum p
Etiology
Group A β-hem olytic streptococcus is the causative organism (uncom m only, group C or G streptococci).
Portals of entry are com m only skin ulcers, local traum a or abrasions, psoriatic or eczem atous lesions, or fungal infections.
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Diagnosis Signs and Symptoms
Most com m on sites of involvem ent are the face (5–20% of cases), lower legs (70–80% of cases), and ears.
Skin has an intense fiery red color, earning the nam e “Saint Anthony's fire.―
Predilection for infants, children, and the elderly
System ic sym ptom s m ay include m alaise, fever, chills, nausea, and vom iting.
Traum atic portal of entry on skin is not always apparent.
Rarely there m ay be an associated periorbital cellulitis or cavernous sinus involvem ent.
History
Facial erysipelas m ay follow an upper respiratory tract infection.
Predilection for areas of lym phatic obstruction
Thirty percent recurrence rate within 3 years, owing to lym phatic obstruction caused by an episode of erysipelas
Physical Exam
The involved skin is an edem atous, indurated (peau d'orange), painful, well-circum scribed plaque with sharp, clearly dem arcated edge.
Classical butterfly rash on cheeks and across nose when affecting face
Vesicles and bullae m ay be present in m ore serious infections.
Essential Workup
The diagnosis is clinical based on the characteristic skin
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findings and the clinical setting.
Needle-aspirate wound cultures are seldom positive and not indicated.
Positive blood cultures in 3–5%; leukocytosis is com m on; when com plicating infected ulcers, cultures are positive in 30%.
Tests Lab
Swabs of the skin are not indicated for culture, as they will show only skin organism s.
CBC, differential blood cultures should be perform ed in diabetics and other high-risk populations. o
Check glucose in diabetics as infection m ay disrupt control.
Differential Diagnosis
Allergic inflam m ation
Cellulitis
Contact derm atitis
Fam ilial Mediterranean fever
Herpes zoster, second division of fifth central nerve
Im petigo
Viral exanthem
Diffuse inflam m atory carcinom a of the breast
P.379
Treatment
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Pre Hospital Wearing gloves, followed by hand washing when m anaging patients, to decrease risk of transm ission of streptococcal carriage
Initial Stabilization Patients m ay be toxic and in need of intravenous fluid resuscitation or pressure support.
ED Treatment Appropriate antibiotic therapy, treatm ent should be for 10 days:
Patients with extensive involvem ent should be adm itted for parenteral antibiotic treatm ent.
When parenteral antibiotics used, can switch to oral m edication when patient is stable and showing signs of response
Mild cases: patients can be discharged on oral therapy if nontoxic appearing, good com pliance, and close follow-up can be ensured.
Penicillin is the drug of choice when clearly the sym ptom s are consistent with erysipelas.
If there is difficulty in distinguishing from cellulitis, staphylococcal coverage should be added. o
Use penicillinase-resistant penicillin or first-generation cephalosporin
o
If in com m unity with high incidence of m ethicillin-resistant S. aureus (MRSA), use vancom ycin or other anti-MRSA coverage.
Medication (Drugs)
Cefuroxim e: peds: 50–100 m g/kg/d PO div. q8h
Cephalexin: adult: 500 m g PO q6h (peds: 40 m g/kg/d PO
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div. q8h)
Dicloxacillin: adult: 500 m g PO q6h (peds: 30–50 m g/kg/d PO div. q6h)
Erythrom ycin ethylsuccinate: adult: 250–500 m g PO q6h (peds: 40 m g/kg/d PO in div. doses q6h)
Penicillin G: adult: 2 m illion U q4h IV (peds: 25,000 U/kg IV q6h)
Penicillin G, procaine: 600,000 U q12h IM
Penicillin V: adult: 500 m g PO q6h (peds: 25–50 m g/kg/d div. q6h–q8h)
Follow-Up Disposition Admission Criteria
Patients with extensive involvem ent, fever, toxic appearance, or those who live alone will require adm ission for IV antibiotics.
Children m ore often require adm ission. Blood cultures, intravenous antibiotics, including coverage for H. influenza , should be initiated for patients who have not been im m unized.
Discharge Criteria
Minim al facial involvem ent
Nontoxic appearing
Not im m unosuppressed
Able to tolerate and com ply with oral therapy
Adequate follow-up
References
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1. Bisno Al, Stevens DL. Streptococcal infections of skin and soft tissues. N Engl J Med. 1996;334:240–244. 2. Kahn RM, Goldstein EJ. Com m on bacterial skin infections. Postgrad Med. 1993;93(6):175–182. 3. Morris A. Cellulitis and erysipelas. Clin Evid. 2004 Dec;(12):2271–2277.
Codes ICD9-CM 035
Core Content Code 3.2.1.3
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Erythem a Infectio sum
Erythema
Infectiosum Kathlene Bassett Alec Tuan Huynh
Basics Description
Characteristic viral exanthem also known as fifth disease: o
Based on historical order of com m on exanthem s described
o
Measles (first disease), scarlet fever (second), rubella (third), Duke disease (fourth), roseola (sixth)
School-aged children age 3–12 years typically infected
Etiology
Caused by hum an parvovirus B19
Incubation period typically 4–14 days
Seasonal predilection for late winter and spring
Spreads via respiratory transm ission
Sixty percent of adults have serologic evidence of prior infection.
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Diagnosis Signs and Symptoms History
Mild constitutional sym ptom s (fever, headache)
Contagious only until appearance of facial rash
Rash begins within 1 week.
Physical Exam
Three stages: o
o
o
Stage 1:
Malar blush (“slapped cheek―) in 75%
Warm , erythem atous, and nontender
Asym ptom atic
Contagious
Stage 2:
Nonspecific m aculopapular eruption
1–4 days after facial rash
More prom inent on extrem ities than trunk
Usually spares palm s and soles
May be pruritic
Stage 3:
Fading rash on sixth day
Usually with central clearing leaving characteristic lacy reticulated pattern
Can last up to several weeks
Rash m ay recur secondary to cutaneous vasodilation, especially during periods of stress, exercise, sun exposure, and bathing.
Com m on com plications: o
Arthritis or hypersensitivity derm atitis in adults
o
Transient aplastic crisis in patients with hem olytic
Pa ge 1 7 5
anem ias (classically sickle cell disease):
Fever, pallor, lethargy, hepatosplenom egaly, heart failure
Pregnancy Considerations
Nonim m une hydrops fetalis in pregnancy: o
About 60% pregnant wom en are susceptible to infection.
o
30% risk of transplacental infection when infected
Essential Workup Clinical diagnosis based on characteristic signs and sym ptom s
Tests Lab
Usually no workup necessary
CBC if concern for aplastic crisis
IgM antibody assay rarely available, but confirm s acute infection
Differential Diagnosis
Scarlet fever
Rubella
Roseola
Infectious m ononucleosis
Echovirus
Coxsackie virus
Drug eruptions
P.381
Pa ge 1 7 5
Treatment Initial Stabilization Airway, breathing, and circulation (ABCs) for septic or ill-appearing infant
ED Treatment
No specific antiviral treatm ent or vaccine is available.
Sym ptom atic treatm ent with fluids and acetam inophen
Hospitalization and respiratory isolation for aplastic crisis
Follow-Up Disposition Admission Criteria
Aplastic crisis
Hydrops fetalis
Toxic appearance
Severe arthritis
Discharge Criteria
Nearly all patients
Patients are no longer contagious following facial rash and m ay return to school or day care.
References 1. Adam s DM, Ware RE. Parvovirus B19: how m uch should you worry? Contem p Pediatr. 1996;13(4): 85–96. 2. Anderson MJ, Higgins PG, Davis LR, et al. Experim ental parvoviral infection in hum ans. Infect Dis. 1985;152:257–265. 3. Hurwitz S. Clinical Pediatric Derm atology. 2nd ed. Philadelphia: WB Saunders; 1993.
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4. Ussery X, Dem m ler G. Hum an parvovirus B19. Sem in Pediatr Infect Dis. 1996;7(2):89–96. 5. Young NS, Brown KE. Parvovirus B19. New Engl J Med. 2004;350:586–597.
Codes ICD9-CM 057.9
Pa ge 1 7 5
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Erythem a M ultifo rm e
Erythema
Multiforme Gregory W. Hendey Thomas A. Utecht
Basics Description
A rash caused by a hypersensitivity reaction: o
May occur in response to various m edications, infections, or other illness
Divided into m ajor and m inor types: o
Erythem a m ultiform e m ajor: separate disease pattern that includes m ore severe disorders (see Toxic Epiderm al Necrolysis and Stevens-Johnson syndrom e)
o
Erythem a m ultiform e m inor is characterized by a benign, self-lim ited rash, generally not associated with acute, serious illness; sim ply referred to as erythem a m ultiform e
Most often affects children and young adults (>50% younger than 20 years)
Males are affected m ore often than fem ales.
Etiology
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Hypersensitivity reaction, probably transient autoim m une defect
Herpes sim plex virus is the m ost com m on precipitant (>70%).
Other causes include idiopathic, m edications (antibiotics: penicillin, sulfur-based, phenytoin, and others), m alignancy, and Mycoplasm a infections.
Diagnosis Signs and Symptoms History
Prodrom e: infrequent system ic sym ptom s (m ild fever/m alaise), antecedent (within 3 weeks) herpes sim plex virus (HSV) in m ost cases
Usually not associated with severe system ic illness
Physical Exam Characteristic rash:
Lesions: sym m etric dull red m acules and papules, evolving into round, well-dem arcated target lesions with central clearing
Multiform e refers to the evolution of the rash through various stages at different tim es.
Distribution: extrem ities, dorsal hands and feet, extensor surfaces, especially elbows and knees. It is one of the few rashes that involve palm s and soles.
Spread: from extrem ities toward trunk
Mucosal involvem ent: often involves m ild blistering or erosions on the lips or m outh
Duration: usually 1–4 weeks, but m ay becom e chronic or
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recurrent
Essential Workup Com plete history and physical exam , with special attention to the skin, genitourinary system , recent infectious sym ptom s, and recent m edications
Tests Lab No specific laboratory tests needed
Imaging No specific im aging is helpful.
Diagnostic Procedures/Surgery
Skin biopsy reveals m ononuclear cell infiltrate around upper derm al blood vessels, without leukocytoclastic vasculitis and necrosis of epiderm al keratinocytes.
Biopsy is not necessary in m ost cases.
Differential Diagnosis
System ic lupus erythem atosus
Fixed drug eruption
Pityriasis rosea
Secondary syphilis
Erythem a m igrans
Urticaria
P.383
Treatment
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Pre Hospital Not contagious and does not require isolation or postexposure prophylaxis for exposed personnel
Initial Stabilization Generally benign and self-lim ited, requiring no initial stabilization
ED Treatment
Attem pt to identify, treat, or rem ove underlying cause or precipitant.
Sym ptom atic: cool com presses, antipruritics
Medication (Drugs)
Antipruritic agents: o
Cetirizine (Zyrtec): 10 m g PO daily (peds: 2.5–5 m g)
o
Diphenhydram ine: 25–50 m g (peds: 5 m g/kg/24h) PO q6h–q8h
o
Hydroxyzine: 25 m g PO q6h to q8h (peds: 2 m g/kg/24h)
Antiviral therapy: o
If HSV infection is present, see Herpes for specific treatm ent options.
Follow-Up Disposition Admission Criteria Adm ission is not needed unless required for another concurrent disorder.
Pa ge 1 7 5
Discharge Criteria Erythem a m ultiform e is a benign disorder that does not require adm ission.
References 1. Assier H, Bastuji-Garin S, Revuz J, et al. Erythem a m ultiform e with m ucous m em brane involvem ent and Stevens-Johnson syndrom e are clinically different disorders with distinct causes. Arch Derm atol. 1995;131:539–543. 2. Foster J. Erythem a m ultiform e. Available at http://www.em edicine.com , updated January 5, 2005. 3. Kerob D, Assier-Bonnet H. Recurrent erythem a m ultiform e unresponsive to acyclovir prophylaxis and responsive to valacyclovir continuous therapy. Arch Derm atol. 1998;134:877–878. 4. Leaute-Labreze C, Lam ireau T, Chawki D, et al. Diagnosis, classification, and m anagem ent of erythem a m ultiform e and Stevens-Johnson syndrom e. Arch Dis Child. 2000;83:347–352. 5. Weston WL. What is erythem a m ultiform e? Pediatr Ann. 1996;25(2):106–109.
Miscellaneous SEE ALSO: Stevens-Johnson Syndrom e; Toxic Epiderm al Necrolysis
Codes ICD9-CM 695.1
ICD10 L51.8
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Erythem a No do sum
Erythema
Nodosum Herbert G. Bivins Theresa Schwab
Basics Description
Characterized by m ultiple sym m etric, nonulcerative tender nodules on the extensor surface of the lower extrem ities typically in young adults
Peak incidence in third decade, m ore com m on in wom en (4:1)
Nodules are round with poorly dem arcated edges and vary in size from 1–10 cm .
Skin lesions are initially red, becom e progressively ecchym otic appearing as they resolve over 3–6 weeks.
Lesions are caused by inflam m ation of the septa between SC fat nodules (septal panniculitis).
Spontaneous regression of lesions within 3–6 weeks
Major disease variants include: o
Erythem a nodosum m igrans (usually m ild unilateral disease with little or no system ic sym ptom s)
o
Chronic erythem a nodosum (lesions spread via
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extension, and associated system ic sym ptom s tend to be m ilder)
Etiology
Im m une-m ediated response; 30–50% of the tim e etiology is idiopathic.
Often a m arker for underlying disease; specific etiologies include: o
Drug reactions (oral contraceptives, sulfonam ides, penicillins)
o
Infections including streptococcal, m ycobacterium tuberculosis (TB), atypical m ycobacteria, and coccidioidom ycosis, hepatitis, syphilis, chlam ydia, Rickettsia, Salm onella, Cam pylobacter, Yersinia, parasites, and leprosy
o
System ic diseases such as sarcoidosis, inflam m atory bowel disease, Behçet, and connective tissue disorders
o
Malignancies such as lym phom a and leukem ia
o
Catscratch disease
o
HIV infection
o
Rarely can be caused by vaccines for hepatitis and TB (BCG)
Typically erythem a nodosum begins 2–3 weeks after the onset of pharyngitis in children.
Diagnosis Signs and Symptoms
Tender erythem atous nodules sym m etrically distributed on extensor surface of lower legs
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Lesions occasionally occur on fingers, hands, arm s, calves, and thighs.
In bedridden patients, dependent areas m ay be involved.
Fever, m alaise, leukocytosis, arthralgias, arthritis, and unilateral or bilateral hilar adenopathy with any form of the disease
Essential Workup Careful history and physical exam directed at detecting precipitating cause
Tests Lab CBC, erythrocyte sedim entation rate (ESR), appropriate chem istry tests; TB and coccidioidom ycosis skin tests m ay be useful initial screening tests for lym phom a, leukem ia, TB, and cocci.
Imaging
Chest radiograph can serve as initial screen for sarcoidosis.
Definitive diagnosis m ade by deep elliptical biopsy and histopathologic evaluation (punch biopsy m ay be inadequate)
Differential Diagnosis
Erythem a nodosum m igrans and chronic erythem a nodosum
Any type of panniculitis can resem ble erythem a nodosum .
Differences can be determ ined histopathologically.
Other disorders include periarteritis nodosum , m igratory throm bophlebitis, superficial varicose throm bophlebitis, scleroderm a, system ic lupus erythem atosus, α 1 -antitrypsin deficiency, Behçet syndrom e, lipodystrophies, leukem ic infiltration of fat, and
Pa ge 1 7 6
panniculitis associated with steroid use, cold, and infection.
Treatment Pediatric Considerations
Rare in children, streptococcal pharyngitis is the m ost likely etiology.
Catscratch disease should be considered.
Initial Stabilization Airway, breathing, and circulation (ABCs); IV, oxygen, m onitoring as appropriate
ED Treatment
Treatm ent should be directed at underlying disease.
Supportive therapies including analgesics
Treatm ent of the underlying pathology and disappearance of the lesions within 1–2 m onths
Specific therapies such as potassium iodide and system ic corticosteroids are used only when the underlying process is known.
System ic corticosteroids are contraindicated in presence of certain underlying infections such as TB or coccidioidom ycosis, which m ay dissem inate with their use.
P.385
Medication (Drugs)
Pa ge 1 7 6
Aspirin: 650 m g PO q4h–q6h PRN (peds: contraindicated)
Ibuprofen: 300–800 m g PO q8h (peds: 5–10 m g/kg PO q6h)
Indom ethacin: 25–50 m g PO q8h
Potassium iodide/SSKI (used for resistant disease; contraindicated in hyperthyroidism ): 900 m g PO daily for 3–4 weeks
System ic corticosteroids (prednisone): 40 m g PO daily—duration determ ined by prim ary physician
Follow-Up Disposition Admission Criteria Dictated by the severity of sym ptom s and the etiologic agent
Discharge Criteria
Nontoxic patients, able to take oral fluids without difficulty
Scheduled follow-up should be arranged.
References 1. Barbier SC, Faucher R. Erythem a nodosum and adenopathy in a 15-year-old boy: uncom m on signs of cat scratch disease. Arch Pediatr . 2005;12(3):295–297. 2. Gonzalez-Gay MA. Erythem a nodosum : a clinical approach. Clin Exp Rheum atol. 2001;19:365–368. 3. Myerson MS. Erythem a nodosum leprosum . Int J Derm atol. 1996;35(6):389–392. 4. Psychos DN, Voulgari PV. Erythem a nodosum : the underlying conditions. Clin Rheum atol. 2000;19:212–216.
Codes
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ICD9-CM 695.2
ICD10 L52
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Eso phageal Traum a
Esophageal
Trauma Susan Dufel
Basics Description
Adult esophagus is approxim ately 25–30 cm in length.
It begins at hypopharynx posterior to larynx at level of cricoid cartilage.
On either side of this slit are piriform recesses: o
May be site for foreign body to lodge
Sites of esophageal narrowing: o
Cricopharyngeal m uscle (upper esophageal sphincter)
o
Crossover of left m ain stem bronchus and aortic arch
o
Gastroesophageal junction (lower esophageal sphincter)
o
Areas of disease (cancer, webs, or Schatzki ring)
Upper third of esophagus is striated m uscle: o
Initiates swallowing
Middle portion is m ixture of striated and sm ooth.
Distal portion is sm ooth m uscle.
It is fixed structure, but can becom e displaced by other organs:
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o
Goiter
o
Enlarged atria
o
Mediastinal m asses
Etiology Mechanism
External forces or agents (30%): o
Penetrating:leading to tears:stab wounds, m issile wounds
o
Perforation:
Foreign bodies via direct penetration
Pressure necrosis
Chem ical necrosis
Instrum entation
o
Blunt: m otor vehicle accident
o
Caustic ingestions/burns:
Acid pH 12 accidental or intentional
Alkali: liquefaction necrosis causing burns, airway edem a or com prom ise, perforation, chronic stricture, and cancer
Acid: coagulation necrosis, therm al injury, and dehydration causing perforation, ulceration, and infection, m ore likely to perforate than alkali
o
Swallowed foreign bodies: coins, bones, buttons, m arbles, pins, button batteries
o
Food bolus im paction:
Most com m on type is m eat
In adults, often associated with prisoners, psychiatric patients, intoxicated patients, or edentulous patients
Iatrogenic (55%):
Pa ge 1 7 6
o
Perforation secondary to instrum entation, endoscopy m ost com m on cause
o
Nasotracheal intubation/nasogastric tube m ost com m on cause in em ergency departm ent
Increased gastric pressure (15%): o
Large pressure differences between thorax and intra-abdom inal cavity
o
May lead to lacerations or perforation
Mallory-Weiss syndrom e
Longitudinal tears in distal esophageal m ucosa with bleeding
o
Boerhaave syndrom e:
Spontaneous esophageal rupture
Full thickness rupture of distal esophagus
Classically after alcohol or large m eals and vom iting
Pediatric Considerations
Accounts for 75–80% of swallowed foreign bodies: o
Typically in infants ages 18–48 m onths
Entrapm ent usually at upper esophageal sphincter
Diagnosis Signs and Symptoms
General: o
Dysphagia: difficulty swallowing
o
Odynophagia: pain with swallowing
o
Chest pain: angina like, often pleuritic, severe, and unrelenting
o
Hoarseness
Pa ge 1 7 6
o
Dyspnea
Tears or perforations: o
Bleeding
o
Hem atem esis
Ingestions/foreign bodies: o
Drooling or excessive salivation
o
Choking, gagging, vom iting, stridor, or wheezing
o
Inability of food or liquid to pass
Caustic ingestions: o
Oral pain
o
Abdom inal pain
o
Vom iting
o
Drooling
Esophagus injury scale: o
I: contusion/hem atom a; partial thickness
o
II: laceration ≤50% circum ference
o
III: laceration >50% circum ference
o
IV: segm ental loss or devascularization 2 cm
History
History of ingestions (type, tim e, am ount)
History of protracted vom iting
History of inability to swallow after eating, foreign body sensation in throat
History of penetrating traum a
Physical Exam
Tears or perforations: o
Subcutaneous air at base of neck
o
Ham m an crunch:
Systolic crunching sound secondary to air in m ediastinum
Pa ge 1 7 6
o
Shock
o
Septicem ia
o
Peritonitis
Penetrating traum a: o
Associated neck, chest, or abdom inal injury with traum a:
Most com m only trachea
Associated with penetrating/blunt traum a
Caustic ingestions: o
Airway edem a leading to stridor
o
Oral burns
Essential Workup High level of suspicion and early diagnosis are key:
Mortality Table o f C o ntents > F ailure to Thrive
Failure to Thrive
David A. Listman
Basics Description
Not a single disease, but a description of a group of sym ptom s
Inadequate physical growth: o
Usually diagnosed earlier than age 2 years
o
Broadly divided into:
Organic (underlying m edical condition)
Nonorganic (no underlying m edical condition)
o
Found in all socioeconom ic groups
o
Poverty increases risk of failure to thrive (FTT).
o
May result in long-term growth, behavioral, and developm ental difficulties
Genetics Many genetic syndrom es can contribute
Etiology Many diseases with unique causes resulting in one or m ore of:
Inadequate caloric intake
Inadequate caloric absorption
Excessive caloric expenditure
Pa ge 1 8 1
Diagnosis Signs and Symptoms
Failure to achieve or m aintain a growth rate appropriate for age
Weight less than two standard deviations below norm al for age (corrected for prem aturity)
Weight that crosses downward through two m ajor percentiles (m ajor percentiles are 5th, 10th, 25th, 50th, 75th, and 90th percentiles) on standard growth chart (see References below) o
Weight loss initially followed by im paired growth in length/height and finally head circum ference
Can m anifest as: o
Reduced m uscle m ass
o
Loss of subcutaneous fat
o
Alopecia
o
Derm atitis
o
Chronic disease
o
Marasm us
o
Kwashiorkor
History
Detailed feeding history: o
o
Breast-feeding:
Prior breast-feeding experience
Frequency of feedings
Length of feedings
Fam ily support for breast-feeding
Form ula:
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Type of form ula (m ilk, soy, elem ental, prem ie follow-up)
How form ula is prepared (ready to feed, powder, liquid concentrate)
Frequency of feedings
Volum e per feeding
o
Solid foods
o
Vom iting associated with feeds
o
Urine and stool output
Gestational history: o
Maternal m edical com plications
o
Drug or alcohol use
Birth history: o
Com plications
o
Birth weight
Developm ental history: o
Achievem ent of appropriate m ilestones
o
Child's perceived tem peram ent
Psychosocial history: o
Fam ily com position
o
Fam ily/social support
o
Stresses
o
Maternal depression
o
Abuse or neglect
Physical Exam
Weight, length/height, head circum ference: o
Plotted on appropriate growth chart:
Include as m any prior growth points as possible.
Dysm orphic features: o
Cardiac disorders
o
Pulm onary disorders
o
Gastrointestinal disorders
Pa ge 1 8 1
Skin exam to include signs of child abuse
Essential Workup
Detailed history and physical exam
Growth param eters plotted on appropriate growth charts
Observation of fam ily–child interaction
Direct observation of feeding
CBC, electrolytes, urinalysis, lead level
Tests Lab
CBC
Infections:
o
Anem ia
o
Leukem ia/m alignancy
o
Lead level
o
Lead poisoning
Chem istry panel (electrolytes, BUN, creatinine, glucose, liver function, protein, album in, calcium , phosphate, m agnesium ):
o
Hydration and acidosis
o
Metabolic disorders
o
Diabetes m ellitus
o
Renal disease
o
Blood gas analysis
o
Renal tubular acidosis
o
Inborn errors of m etabolism
Urinalysis with culture: o
Renal disease
o
Infection
HIV
Imaging
Pa ge 1 8 1
Chest radiograph:
Tuberculosis
Pneum onia
Cardiom egaly
Diagnostic Procedures/Surgery
pH probe: o
Sweat chloride test: o
Gastroesophageal reflux
Cystic fibrosis
Tuberculin skin testing
P.397
Differential Diagnosis Organic Causes
GI: o
Malabsorption syndrom es
o
Celiac disease
o
Cystic fibrosis
o
Food allergy
o
Inflam m atory bowel disease
o
Hepatobiliary disease
o
Hepatitis
o
Cirrhosis
o
Biliary Atresia
o
Obstructive disease
o
Pyloric stenosis,
o
Malrotation
o
Hirschsprung disease
o
Gastroesophageal reflux
Cardiac
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o
Congenital heart disease
o
Cyanotic
o
Congestive
o
Acquired heart disease
Pulm onary o
Bronchopulm onary dysplasia
o
Obstructive sleep apnea
o
Chronic lung disease
o
Cystic fibrosis
Hem atologic/oncologic: o
Iron deficiency anem ia
o
Thalassem ia
o
Lead poisoning
o
Leukem ia
Renal: o
Chronic renal insufficiency
o
Renal tubular acidosis
o
Recurrent urinary tract infections (UTIs)
Neurologic/CNS o
Hydrocephalus
o
Hypertonia/hypotonia
o
Generalized weakness (i.e., spinal m uscular atrophy)
Im m unologic o
AIDS
Endocrine: o
Diabetes m ellitus
o
Thyroid/parathyroid disease
o
Adrenal disease
o
Growth horm one deficiency
o
Hypopituitarism
o
Hypophosphatem ic rickets
Infectious:
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o
Tuberculosis
o
Parasite
Genetic/congenital o
Fetal alcohol syndrom e
o
Sm ith-Lem li Opitz syndrom e
o
Cleft lip/palate
o
Inborn errors of m etabolism
Toxic
Nonorganic Causes Parent–child dysfunction:
Mother–infant bonding problem s
Maternal m ental illness/substance abuse
Inexperienced m other
Breast-feeding difficulties
Im proper form ula preparation
Chaotic fam ily environm ent
Child abuse or neglect
Münchhausen syndrom e by proxy
Treatment Initial Stabilization
Check for hypoglycem ia
Fluid resuscitation when dehydrated
Supportive/nonjudgm ental environm ent
ED Treatment
Recognize/identify child with FTT.
Rule out organic abnorm alities: o
Organic causes m ay have specific treatm ents.
Social services consult
Pa ge 1 8 1
Breast-feeding consult: o
Advise on appropriate feeding.
Medication (Drugs) Dependent on underlying cause
Follow-Up Disposition Admission Criteria
Organic cause requiring m edical adm ission
Nonorganic causes to observe caregiver–child interaction
Nonorganic causes to observe weight while m onitoring oral intake
Child abuse/neglect
Severe dehydration, m alnutrition, or electrolyte im balance
Discharge Criteria
Case appropriately m anaged by prim ary care physician
Follow-up is ensured.
Issues for Referral Subspecialty referral depending on cause
References 1. Bithoney WG, Dubowitz H, Egan H. Failure to thrive/growth deficiency. Pediatr Rev. 1992;13:453–460. 2. Gahagan S, Holm es R. A stepwise approach to evaluation of undernutrition and failure to thrive. Pediatr Clin North Am . 1998;45(1):169–187. 3. Shah MD. Failure to thrive in children. J Clin Gastroenterol.
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2002;35(5):371–374.
Miscellaneous SEE ALSO: Centers for Disease Control and Prevention, National Center for Health Statistics: Growth charts. Available at http://www.cdc.gov/growthcharts. Accessed April 23, 2005.
Codes ICD9-CM 783.41
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > F atigue
Fatigue
Matthew Mostofi
Basics Description
A subjective state of overwhelm ing, sustained exhaustion and decreased capacity for physical and m ental work, which is not relieved by rest
Fatigue occurs with or without objective findings on physical exam .
Fatigue is a com m on com plaint in people with and without system ic disease, which m akes this com plaint a challenge to practicing physicians.
Etiology
The specific m echanism s of fatigue are unknown.
Hem atological:
o
Anem ia
o
Leukem ia
Endocrine: o
Thyroid disorders
o
Adrenal insufficiency
o
Diabetes
o
Pregnancy
Malignancy:
Pa ge 1 8 1
o
Paraneoplastic syndrom es
Psychiatric: o
Chronic pain
o
Em otional distress
o
Depression
o
Eating disorders
o
Chem ical dependency
o
Withdrawal syndrom es
Sleep disorders: o
Insom nia
o
Sleep apnea
Cardiac and pulm onary disorders
Infections acute and chronic
Rheum atic and autoim m une disorders
Nutritional deficiencies including electrolyte abnorm alities
Physical inactivity and deconditioning
Medications
Chronic fatigue syndrom e: o
Sym ptom com plex which is defined by the Centers for Disease Control and Prevention
o
Severe fatigue lasting greater than 6 m onths
o
No definable organic disease
o
Presence of associated physical sym ptom s:
Headache,
Arthralgias
Sleep disturbances
Lym phadenopathy
Exercise intolerance
Myalgias
Pa ge 1 8 2
Diagnosis Signs and Symptoms
Fatigue is a subjective com plaint of exhaustion or tired sensation that interferes with norm al activities of life, and sym ptom s do not resolve with sleep.
There are no specific signs of fatigue, but frequently physical signs m ay hint at the underlying cause of com plaint.
History
Onset, pattern, duration of fatigue
Associated sym ptom s: fever, night sweats, weakness, dyspnea, weight loss/gain, sleep patterns
Past m edical and surgical history
Psychiatric history: em otional and m ental stressors, depression
Social history: alcohol, drug use, m ajor life events
Medications
Full review of system s
Essential Workup
Because fatigue is a subjective com plaint, the essential workup is directed at identification of an underlying cause.
Vital signs review, including pulse oxim etry
Tests Lab
Lab evaluation should be directed by findings of history and physical exam .
CBC: o
Screen for anem ia or leukem ia
Serum glucose:
Pa ge 1 8 2
o
Both hyperglycem ia and hypoglycem ia can present with fatigue.
Pregnancy test
Electrolytes with blood urea nitrogen/creatininer
Thyroid-stim ulating horm one: o
Screen for hypothyroidism
Urine drug screen
Imaging Im aging/special test: special tests are reserved for evaluation of abnorm al physical exam findings or history suggesting further evaluation.
Differential Diagnosis
Infection: o
Bacterem ia
o
Urosepsis
o
Pneum onia
o
Viral syndrom es
o
Abscess
o
Epstein-Barr virus, Monospot
o
Cytom egalovirus
o
HIV
o
Hum an herpes virus-6
Im m unologic/connective tissue: o
Rheum atologic (rheum atoid arthritis, system ic lupus erythem atosus, juvenile rheum atoid arthritis)
o
Osteoarthritis
o
Fibrom yalgia
o
Myasthenia gravis
o
Lam bert-Eaton syndrom e
Neoplastic: o
Solid or hem atologic cancers
Pa ge 1 8 2
Metabolic: o
Electrolyte abnorm alities
o
Mitochondrial diseases
o
Brom ism
Hem atologic: o
Anem ia
o
Hypovolem ia
o
Hem oglobinopathy
Endocrine: o
Hyperthyroid or hypothyroid
o
Adrenal insufficiency
o
Diabetes
o
Hypoglycem ia
Neurologic: o
Multiple sclerosis
o
Cerebrovascular accident
o
Am yotrophic lateral sclerosis
Cardiovascular: o
Myocardial infarction
o
Cardiom yopathy
o
Congestive heart failure
P.399
Pulm onary: o
Pneum onia
o
Chronic obstructive pulm onary disease
o
Asthm a
o
Sleep apnea
Gastrointestinal: o
Reflux
o
Peptic ulcer disease
Pa ge 1 8 2
o
Liver disease
Autonom ic dysfunction
Lifestyle:
o
Excessive or insufficient exercise
o
Obesity
Psychiatric: o
Major depression
o
Anxiety
o
Grief
o
Stress
Medication related: o
Drug interactions
o
Com m only caused by blood pressure, cardiovascular, psychiatric, and narcotic m edications
Dehydration
Treatment Initial Stabilization
ABCs
Adm inister supplem ental oxygen for hypoxia
IV fluid bolus for signs of dehydration
ED Treatment
Treatm ent should be directed to correction of the underlying cause of fatigue: o
Identify and treat any infectious process.
o
Correct m etabolic and hem atologic disturbances.
o
Diagnose progressive neurologic disease and acute psychiatric crisis.
o
Initiate workup for endocrine and neoplastic disease.
Pa ge 1 8 2
o
Stop any offending m edications or toxins.
Most cases will not have identifiable cause, so reassurance and close follow up is required.
Recom m end appropriate diet, exercise regim en, and consistent sleep cycles.
Follow-Up Disposition Admission Criteria
Underlying disease requiring IV m edication or m onitoring
Failure to thrive as outpatient
Unable to provide for self
Discharge Criteria
Able to care for self
Serious disturbances have been excluded.
Adequate follow-up is arranged.
References 1. Buchwald D, Wener MH, Pearlm an T, et al. Markers of inflam m ation and im m une activation in chronic fatigue and chronic fatigue syndrom e. J Rheum atol. 1997;24(2):372–376. 2. Dickinson CJ. Chronic fatigue syndrom e etiological aspects. Eur J Clin Invest. 1997;27(4):257–267. 3. Fukuda K. The chronic fatigue syndrom e: a com prehensive approach to its definition and study. International Chronic Fatigue Syndrom e Study Group. Ann Intern Med. 1994;121(12):953–959. 4. Maul AC. Chronic fatigue syndrom e. Im m unol Invest. 1997;26(1–2):269–273. 5. Morrison RE, Keating HJ. Fatigue in prim ary care. Obstet Gynecol
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Clin. 2001;28(2). 6. Manzullo EF, Escalante CP. Research into Fatigue. Hem /Onc Clinics of North Am . 2002;16(3).
Codes ICD9-CM 780.7
ICD10 R53
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > F eeding Pro blem s, Pediatric
Feeding
Problems, Pediatric Niels Rathlev Fernando G. Mendoza
Basics Description
Feeding requires coordinated series of actions involving several com ponents: o
Getting food into oral cavity: appetite, food-seeking behavior, ingestion
o
Swallowing food: oral and pharyngeal phases
o
Ingestion and absorption: esophageal swallowing, gastrointestinal phase
Infant requires m inim um of 100–120 calories/kg/d; form ula and hum an breast m ilk provide 20 calories/oz.
Minor feeding difficulties reported in 25–50% of norm al children
Etiology
Behavioral issues: o
Poor environm ental stim ulation
o
Dysfunctional feeder–child interaction
o
Selective food refusal
Pa ge 1 8 2
o
Rum ination
o
Phobias
o
Conditioned em otional reactions
o
Depression
o
Poverty (inadequate food available)
Conditioned dysphagia: o
Gastroesophageal reflux
o
Aspiration
o
Fatigue (heart or lung disease)
Structural abnorm alities of the oropharynx, larynx, and trachea: o
Retrognathic jaw
o
Cleft lip/palate
o
Choanal atresia
o
Posterior tongue placem ent
o
Macroglossia
o
Ankyloglossia
o
Pierre Robin sequence
o
Esophageal strictures or stenosis
o
Tonsillar hypertrophy
o
Retropharyngeal m ass or abscess
o
Laryngeal cleft
o
Laryngom alacia
o
Tracheotom y
o
Laryngeal cyst
o
Subglottic stenosis
o
Tracheom alacia
o
Tracheoesophageal cleft
o
Tracheoesophageal com pression from vascular ring/sling
o
Tracheoesophageal fistula
o
Esophageal stricture, web, or ring
Pa ge 1 8 2
o
Esophageal m ass or tum or
o
Foreign body
o
Vascular ring
Neurologic conditions: o
Cerebral palsy
o
Muscular dystrophies
o
Myasthenia gravis
o
Cranial nerve dysfunction
o
Arnold-Chiari m alform ation
o
Mental retardation/developm ental disabilities
o
Brainstem injury
o
Pervasive developm ental disorder
o
Infant botulism
o
Brainstem gliom a
o
Polym yositis/derm atom yositis
Cardiorespiratory problem s: o
Congestive heart failure
o
Cyanotic heart disease
Metabolic dysfunction: o
Hereditary fructose intolerance
o
Organic acidem ias
o
Urea cycle disorders
o
Dum ping syndrom e
Diagnosis Signs and Symptoms
Sym ptom s: o
Food refusal
o
Failure to thrive
o
Oral aversion
Pa ge 1 8 2
o
Recurrent pneum onia
o
Chronic lung disease
o
Recurrent em esis
Signs: o
Vital signs variable
o
Hydration variable
o
Growth (especially weight) velocity slow; im paired nutritional status
o
Cough, tachypnea, color change
o
Oropharyngeal inflam m ation, infection, or anatom ic abnorm ality
o
Chest: evidence of aspiration
o
Neurologic status: abnorm al m uscle tone, reflexes, m ental status
History
Define nature of problem s: o
Frequency, duration, and quantity of feeding
o
Onset, duration, and severity
o
Findings during feeding: cough, dyspnea, color change, vom iting, spitting
Variability in feeding patterns is typical; parental im pression of norm al feeding for their infant is best guide: o
Full-term healthy infant usually has 2–3 oz of form ula every 2–3 hours.
o
Breast-fed baby eats 10–20 m inutes on each breast every 2–3 hours.
o
One-m onth-old norm ally eats 4 oz every 4 hours.
Poor weight gain
Irritability
Physical Exam
Observation of feeding: neurom uscular tone, posture,
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position; patient m otivation; oral structure and function; efficiency of oral intake
Ability to handle oral secretions
Pace of feeding
Tongue and jaw m ovem ents
Num ber of swallows to clear a bolus
Noisy airway sounds after swallowing
Gagging, coughing, or em esis during feeding
Essential Workup
Medical and dietary history
Observation: o
Caretaker feeding child
o
Parent–child interactions
Tests Lab
Initial assessm ent if child failing to thrive or dehydrated: o
CBC, urinalysis, electrolytes, BUN, glucose
o
Consider erythrocyte sedim entation rate (ESR) and thyroid functions.
Oxim etry if suspected cardiopulm onary concerns
Chest radiograph if suspect aspiration or respiratory cause
Cultures of blood, urine, and CSF if concern of infection
Urine for organic acids if concern for m etabolic disorders
P.401
Imaging
Chest x-ray film if suspected cardiopulm onary concerns
Fluoroscopy, contrast radiographs, endoscopy, and ultrasonography m ay be needed on an individual basis to
Pa ge 1 8 3
define nature of swallowing, reflux, and associated conditions.
Direct visualization with nasopharyngeal scope or GI endoscopy
MRI if concerns for brainstem , skull base, or spinal problem s
Diagnostic Procedures/Surgery May need a m ultidisciplinary swallow study involving speech pathologist, pediatrician, and potentially an otolaryngologist
Differential Diagnosis
Fam ily dysfunction, stress leading to potential neglect
Difficulty getting food into oral cavity: o
Depression or other behavioral issues
o
Deprivation
o
Infection of oropharynx (e.g., herpes or aphthous ulcers)
o
CNS or endocrine disease:
Thyroid dysfunction
Adrenal dysfunction
o
Sensory deficit
o
Neurom uscular disease
o
Continued dysphagia and fatigue because of overwhelm ing infection (sepsis, m eningitis, urinary tract infection)
o
Anem ia
o
Cardiopulm onary disease:
Congestive heart failure (CHF)
Congenital heart disease
Bronchopulm onary dysplasia
Bronchiolitis
Pneum onia
Pa ge 1 8 3
Difficulty swallowing: o
Anatom ic abnorm alities of oropharynx or esophagus: congenital or acquired
o
Cardiopulm onary disease
o
Neurom uscular disorder
o
Disorder of esophagus:
Peristaltic abnorm ality
Mucosal inflam m ation
Esophagitis
Reflux
Treatment Pre Hospital Assess vital signs and hydration; resuscitate as necessary.
Initial Stabilization Resuscitation as required
ED Treatment Observe feeding session with prim ary caretaker. Note:
Gagging
Coughing
Em esis
Noisy airway sounds
Ability to handle secretions
General Measures
Speech pathologist m ay be helpful.
Behavioral therapy m ay be needed.
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Follow-Up Disposition Admission Criteria
Suspected system ic infection
Moderate to severe dehydration
Significant failure to thrive, particularly in infants Table o f C o ntents > F em ur F racture
Femur Fracture
Colleen J. Buono
Basics Description Fractures classified according to:
Location: o
Proxim al third (subtrochanteric region)
o
Middle third
o
Distal third (distal m etaphyseal-diaphyseal junction)
Geom etry: o
Spiral
o
Transverse
o
Oblique
o
Segm ental
Extent of soft tissue injury: o
Open
o
Closed
Degree of com m inution: Winquist and Hansen classification: o
Grade I: fracture with sm all fragm ent 50% width of fem oral shaft; unstable lengthwise and rotationally
o
Grade IV: circum ferential loss of cortex; unstable lengthwise and rotationally
Etiology
Usually requires m ajor, high-energy traum a
Patients are m ostly young adults with high-energy injuries (m otor vehicle accidents [MVAs], gunshot wounds [GSWs], falls): o
Spiral fractures with falls from height
Consider pathologic fracture if m inor m echanism
Can occasionally be due to stress fracture from repetitive activity
Com plications include com partm ent syndrom e, fat em bolism , adult respiratory distress syndrom e (ARDS), hem orrhage
Pediatric Considerations
Seventy percent of fem oral fractures in children 6 m onths 1–2 m cg/kg IV once)
Ketam ine: not recom m ended in adults due to em ergence reaction (peds: 1.0–2 m g/kg IV, 4 m g/kg IM once)
Methohexital: 1–1.5 m g/kg IV once (peds: not recom m ended) Midazolam : 0.07 m g/kg IM or 1 m g slowly q2–3m in up to 5 m g m ax. (peds: 0.25–1.0 m g/kg PO once to a m ax.) of 20 m g PO; 6 m o to 5 yr: 0.05–0.1 m g/kg IV titrate to m ax. of 0.6 m g/kg 6–12 yr: 0.025–0.05 m g/kg IV titrate to m ax. of 0.4 m g/kg
Propofol: 40 m g IV q10sec until induction; 5–60 m cg/kg/m in IV continuous infusion
Pain Control
Hydrom orphone: 0.5–2.0 m g IM/SC/slow IV q4h–q6h PRN; titrate for pain control (peds: 0.015 m g/kg per dose IV q4h–q6h PRN)
Morphine: 2–10 m g IV q4h; titrate for pain control (peds: 0.1 m g/kg IV q4h; titrate for pain control to m ax. 15 m g/dose)
Pediatric Considerations
Assess m arkers for nonaccidental traum a: o
Delay in presentation
o
History of m echanism inconsistent with the injury
o
Isolated traum a to the thigh, associated burns, bruises, or linear abrasions
Assess for dislocation of the fem oral capital epiphysis.
Depending on the age of the patient and the fracture type, pediatric fem oral fractures m ay not require operative treatm ent.
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Follow-Up Disposition Admission Criteria
All fem ur fractures m ust be adm itted except as noted below in Discharge Criteria.
Any suspicion of nonaccidental traum a in children
Discharge Criteria In certain rare circum stances of pathologic fracture or fem ur fractures in patients who are not am bulatory and would not undergo operative fixation, discharge can be considered in consultation with orthopedics if adequate pain control can be achieved and proper follow-up ensured.
References 1. Abarbanell N. Prehospital m idthigh traum a and traction splint use: recom m endations for treatm ent protocols. Am J Em erg Med. 2001;19:137–140. 2. Brien W, et al. Managem ent of gunshot wounds to the fem ur. Orthop Clin North Am . 1995;26(1):133–138. 3. Buckley S. Current trends in the treatm ent of fem oral shaft fractures in children and adolescents. Clin Orthop. 1997;338:60–73. 4. The Harriet Lane Handbook. Fifteenth Edition. 2000, Mosby, Inc. Saint Louis, Mo. 5. Rockwood C, et al. Fractures of the fem oral shaft. In: Rockwood and Green's Fractures in Adults and Children. Philadelphia: Lippincott–Raven Publishers; 1991: Chapter 19. 6. Rudm an N, McIlm ail D. Em ergency departm ent evaluation and treatm ent of hip and thigh injuries. Em erg Med Clin North Am . 2000;18:29–66.
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7. Tarascon Pocket Pharm acopoeia 2006 Edition. Tarascon Publishing, Lom poc, CA. 8. Ward K, Yealy D. System ic analgesia and sedation in m anaging orthopedic em ergencies. Em erg Med Clin North Am . 2000;18:141–166.
Miscellaneous SEE ALSO: Hip Injury
Codes ICD9-CM 821.00
Core Content Code 18.4.13.1.7
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > F ever, Adult
Fever, Adult
Henry J. Grazioso
Basics Description
Fever represents an elevation in the body's set therm oregulatory point.
Core tem perature is regulated by the anterior hypothalam us at 37°C ± 2°C.
Fever is caused by increased prostaglandin E 2 (PGE 2 ) synthesis in the hypothalam us.
Autonom ic discharge from hypothalam us raises core tem perature through shivering and derm al vasoconstriction.
Norm al circadian variation in core tem perature occurs with nadir in early m orning and peak in late afternoon.
Both exogenous and endogenous factors can raise the body's set therm oregulatory point: o
Endogenous factors include IL-1 and IL-6, tum or necrosis factor, and IFN-γ
o
Exogenous factors include endotoxin (lipopolysaccharide) and other toxins and m etabolites produced by infectious organism s.
Etiology
Pa ge 1 8 5
Any infectious process m ay present with fever: o
Cardiac (endocarditis, pericarditis)
o
Respiratory (pneum onia, upper respiratory tract infection, sinusitis)
o
Genitourinary (urinary tract infection, pyelonephritis, prostatitis)
o
Gastrointestinal (infectious diarrhea, gastroenteritis, hepatitis, pancreatitis, appendicitis)
o
CNS (m eningitis, encephalitis)
o
Skin and connective tissue (cellulitis, abscess, osteom yelitis)
o
Gynecologic (pelvic inflam m atory disease)
o
System ic (Epstein-Barr virus, cytom egalovirus, HIV, sepsis, insect vector-borne disease, biological weapons)
o
Iatrogenic (indwelling catheters, prostheses)
Drugs: Nearly all drugs m ay cause fever: o
Antiarrhythm ics (procainam ide, quinidine)
o
Antibiotics (penicillins, sulfonam ides, erythrom ycin, isoniazid, nitrofurantoin)
o
Anticonvulsants (barbiturates, carbam azepine, phenytoin)
o
Antidepressants (TCAs, m onoam ine oxidase inhibitors)
o
Antihistam ines (H 1 and H 2 antagonists)
o
Antihypertensives (nifedipine, hydralazine, m ethyldopa, captopril, hydrochlorothiazide)
o
Drugs of abuse (cocaine, am phetam ines)
o
NSAIDs
o
Others (allopurinol, heparin, m eperidine)
System ic inflam m atory: o
Collagen vascular diseases
Pa ge 1 8 5
o
Rheum atic fever
o
Rheum atoid arthritis
o
System ic lupus erythem atosus
o
Vasculitis
o
Polym yalgia rheum atica
o
Tem poral arteritis
o
Granulom atous diseases
o
Sarcoidosis
o
Inflam m atory bowel disease
o
Sickle cell disease
o
Hem olytic anem ia
Neoplastic disease: o
Lym phom as and leukem ias
o
Hepatom a
o
Metastatic carcinom as
o
Atrial m yxom as
Endocrine: o
Hyperthyroidism or thyrotoxicosis
o
Pheochrom ocytom a
Pulm onary em bolus
Fam ilial Mediterranean fever
CNS lesions
Fever of unknown origin: o
Defined as fever >38.3°C for at least 3 weeks as an outpatient and 3 days of inpatient evaluation or three outpatient visits without determ ining etiology
o
A diagnosis of exclusion is rarely m ade in the ED.
Diagnosis Signs and Symptoms
Pa ge 1 8 5
History
Chills, shivering, and rigors: o
Mechanism s to raise body core tem perature
Fatigue
Malaise
Myalgias
Night sweats: o
Suggestive of lym phom a, solid tum or, chronic inflam m atory disease, or tuberculosis (TB)
Anorexia
Specific fever patterns: o
Relapsing fevers: febrile episode with alternating afebrile intervals
o
Seen in m alaria, Borrelia infections, rat-bite fever, and lym phom a (Pel Ebstein fevers)
o
Rem ittent fever: tem perature falls daily but does not return to norm al
o
Seen in TB and viral diseases
o
Interm ittent fevers: exaggerated circadian rhythm
o
Seen in system ic infections, m alignancy, and drug fever
o
Reversal of norm al circadian patterns
o
Som etim es seen in typhoid fever and dissem inated TB
Physical Exam
Elevated core tem perature: o
Tem perature >38°C (100.4°F) rectally or 37.5°C (99.5°F) orally
o
Lower thresholds in patients older than 65 years, as the febrile response is not as strong
Diaphoresis:
Pa ge 1 8 5
o
Absence of diaphoresis with severe hypertherm ia suggests anticholinergic poisoning or heat stroke.
Muscle rigidity: o
Found in patients with neuroleptic m alignant syndrom e or serotonin syndrom e
Changes in heart rate: o
Tachycardia is com m only seen.
o
Tem perature pulse dissociation (relative bradycardia) is seen in typhoid, brucellosis, psittacosis, leptospirosis, Legionnaire disease, Lym e disease, and factitious fevers.
Changes in m ental status: o
Can range from irritability to frank delirium and obtundation
Rash: o
Type of lesions and distribution can offer im portant clues to diagnosis.
o
Petechial rashes concerning for m eningococcem ia and Rocky Mountain spotted fever
Signs of hyperthyroidism : o
Goiter
o
Exophthalm os
Essential Workup
Core tem perature is m ost acutely m easured rectally.
Careful history and physical exam (PE) necessary to determ ine need for further diagnostic testing: o
History should elicit any sick contacts, previous infections, recent travel, m edications, anim al exposure, and im m unization status.
Tests Lab
Pa ge 1 8 5
CBC: o
Com m only perform ed, but rarely helpful in m anagem ent of fever in the ED
o
Im portant in determ ining neutropenia in patients with risk factors
o
Differential WBC count is unreliable but m ay give clues to certain etiologies.
o
Neutrophilia and bandem ia suggestive of bacterial infection
o
Lym phocytosis suggestive of typhoid, TB, brucellosis, and viral disease
o
Atypical lym phocytosis seen in m ononucleosis, cytom egalovirus, HIV, rubella, varicella, m easles, and viral hepatitis
o
Monocytosis suggestive of TB, brucellosis, viral illness, and lym phom a
o
Platelet count 41°C m ore com m on in these states
o
Neuroleptic m alignant syndrom e
o
Malignant hypertherm ia
o
Serotonin syndrom e
o
Heat stroke
Factitious fever
Treatment Pre Hospital
No specific field interventions required
Monitoring and IV access should be obtained in the field for unstable patients or patients with altered m ental status.
Pa ge 1 8 6
Initial Stabilization
Im m ediate treatm ent rarely required
Airway control, breathing and circulatory support for unstable patients
Initiate broad-spectrum antibiotic treatm ent im m ediately for im m unocom prom ised patients and patients with unstable vital signs or profound m ental status changes.
ED Treatment
Antipyretics: o
Acetam inophen, NSAIDs, or salicylates:
Inhibit the cyclooxygenase enzym e, thereby blocking synthesis of prostaglandins.
o
Most febrile patients do not require antipyretic m edication other than for com fort.
o
Selected patients require m ore aggressive antipyretic interventions:
Pregnant wom en
Patients with history of seizure disorders
Patients with significant cardiac disease
Hem odynam ically unstable patients
Patients with altered m ental status
Glucocorticoids: o
Inhibit phospholipase A 2 blocking prostaglandin synthesis.
o
Indicated only in chronic inflam m atory conditions; contraindicated in infectious etiologies
Em piric antibiotics for unstable or im m unocom prom ised patients
External cooling m echanism rarely indicated
Pa ge 1 8 6
Medication (Drugs)
Antipyretics: o
Acetam inophen (B): 650 to 1,000 m g PO/PR q4–6h
o
Aspirin (D): 650 m g PO q4h
o
Ibuprofen (B): 800 m g PO q6h
Em piric antibiotics (dosage, interval assum e norm al renal function): o
Unstable, nonneutropenic patients with unidentified source of fever:
Gentam icin (D) or tobram ycin (D): 2 m g/kg IV load then 1.7 m g/kg q8h plus piperacillin/tazobactam (B) 3.375 g IV q4h or ticarcillin/clavulanate (B) 3.1 g IV q4h
Im ipenem /cilastatin (C): 500 to 1,000 m g IV q8h
o
Meropenem (B): 1 g IV q8h
If asplenic:
Consider Cefotaxim e (B) 2 g IV q8h or Ceftriaxone (B) 2 g IV q12h
o
If neutropenic and low risk (24/7 access to hospital; no focal findings, structural lung disease, fungal infection, or dehydration; hem odynam ically stable; 16 Table o f C o ntents > F ever, Pediatric
Fever, Pediatric
Nathan Mick David Peak
Basics Description
Fever is defined as a tem perature of 38°C (100.4°F) rectally: o
Oral and tym panic tem peratures are generally 0.6–1.0°C lower.
Tym panic tem peratures are not accurate in children younger than 6 m onths.
Axillary tem peratures are generally unreliable.
After 3 m onths of age, significant fever is defined as a tem perature of 39°C.
Children who are afebrile but have a reliable history of docum ented fever should be considered to be febrile to the degree reported.
Etiology
Bacterem ia (Haem ophilus influenzae type B and Streptococcus pneum oniae vaccines have decreased incidence of invasive Haem ophilus and pneum ococcal disease), viral exanthem (varicella, roseola, rubella), coxsackievirus (hand-foot-m outh disease), abscess.
Pa ge 1 8 6
CNS: m eningitis, encephalitis
Head, eyes, ears, neck and throat (HEENT): otitis m edia, facial cellulitis, orbital/periorbital cellulitis, pharyngitis (group A β-hem olytic streptococcus, herpangina, adenovirus pharyngoconjunctival fever), viral gingivostom atitis (herpes and coxsackievirus), cervical adenitis, sinusitis, m astoiditis, conjunctivitis, peritonsillar/retropharyngeal abscess
Respiratory: croup (param yxovirus), epiglottitis, bronchiolitis (respiratory syncytial virus [RSV]), pneum onia, em pyem a
Cardiovascular: purulent pericarditis, endocarditis, m yocarditis
Genitourinary (GU): cystitis, pyelonephritis
GI: bacterial diarrhea, intussusception, appendicitis, hepatitis
Extrem ity: osteom yelitis, septic arthritis, cellulitis
Miscellaneous: Kawasaki disease, vaccine (DPT) reaction, heat exhaustion/stroke, factitious, fam ilial dysautonom ia, thyrotoxicosis, collagen vascular disease, vasculitis, rheum atic fever, m alignancy, drug induced, overbundling (recheck 15 m inutes after unbundling)
Diagnosis Signs and Symptoms
Clinical appearance m ust be evaluated.
Toxicity associated with lethargy, poor perfusion, hypoventilation/hyperventilation, weak cry, decreased PO intake; purpuric or petechial rash
Altered m ental status:
Pa ge 1 8 6
o
Lethargy presenting with decreased level of consciousness
o
Irritability
o
Im paired interaction with environm ent, parents, physician, toys
Physical exam (PE) to search for underlying condition
Febrile seizures
Tem peratures >42°C often have a noninfectious cause.
Serious infection m ay occur in the absence of fever.
Antipyretics m ay change findings without im pacting underlying disease.
Approxim ately 20% of children will have fever without source after history and PE.
Essential Workup
Oxygen saturation as m andatory 5th vital sign
Resuscitate as appropriate.
Determ ine duration of illness, degree and level of fever, use of antipyretics, past m edical history, drug allergies, vaccination status, recent m edications/antibiotics, birth history if younger than 6 m onths of age, exposures, feeding, activity, urine/bowel habits, travel history, and relevant review of system s.
Search for underlying condition.
Initiate antipyretic therapy.
Tests Lab
CBC with differential
Urinalysis and culture in all m ale infants younger than 6 m onths, uncircum cised infants younger than 12 m onths, and fem ales younger than 2 years
Blood culture:
Pa ge 1 8 6
o
The developm ent of autom ated blood culture system s has led to m ore rapid detection of bacterial pathogens.
Cerebrospinal fluid (CSF) for cell counts/culture for children toxic or 0–28 days of age; consider for non–toxic-appearing children 28–90 days of age as well as older in whom m eningitis m ust be excluded.
Stool for WBCs and culture when diarrhea present
Imaging
Chest radiograph to exclude pneum onia if patient tachypneic or hypoxic
Lum bar puncture as indicated
Other studies as indicated to evaluate for underlying infection
Differential Diagnosis See Etiology
Treatment Pre Hospital
Resuscitate as appropriate.
Begin cooling with antipyretics or tepid towels.
Initial Stabilization
Treat any life-threatening conditions.
Antipyretic therapy
Evaporative cooling techniques such as sponge bath have m inim al role.
P.409
Pa ge 1 8 6
ED Treatment
Focal infections require evaluation and treatm ent.
Toxic children require prom pt septic workup and appropriate antibiotics.
All potential life-threatening conditions m ust be excluded before treating a m inor acute illness, which is m ore com m on.
Infants 0–28 days old need a full septic workup: CBC, urinalysis (UA), cultures (blood, urine, CSF), lum bar puncture, chest radiograph:
o
Antibiotics: cefotaxim e and am picillin
o
Adm it
Nontoxic infants 28–90 days old need workup, selective antibiotic use (ceftriaxone), and re-evaluation within 24 hours of adm ission: o
H. influenzae type B and S. pneum oniae incidence has declined significantly with widespread vaccination.
o
It is currently reasonable to perform blood culture and urine culture with selective lum bar puncture, coupled with ceftriaxone IM in low-risk patients (see definition under Disposition) if re-evaluation in 24 hours is ensured.
o
Lum bar puncture is optional in this setting, but should be done if em piric antibiotics (ceftriaxone) are given to ensure that subsequent re-evaluation is not com prom ised.
o
Presence of respiratory syncytial virus in this age group decreases the risk of bacterem ia and m eningitis, but the rate of urinary tract infections is still appreciable.
Pa ge 1 8 6
Children 3 m onths to 3 years of age are evaluated selectively; antibiotic use is individualized for specific identifiable infections and pending appropriate cultures: o
Nontoxic children with tem peratures >39°C and no identifiable infection receive urinalysis/culture as indicated, chest radiograph as indicated, CBC/blood culture, and selective em piric antibiotics.
o
Children with WBC >15,000/m m 3 and no identifiable infection m ay benefit from em piric antibiotics pending culture results, especially if not vaccinated with H. influenzae type B and pneum ococcal vaccines.
Im m unocom prom ised children need aggressive evaluation, as do children with fever and petechiae/purpura.
Medication (Drugs)
Acetam inophen: 15 m g/kg per dose PO/PR (per rectum ) q6h
Am oxicillin: 50 m g/kg/d PO t.i.d.
Am picillin: 150 m g/kg/d IV q4h–q6h
Cefotaxim e: 100 m g/kg/d IV q6h–q8h
Ceftriaxone: 50–100 m g/kg/d IV/IM q12h
Ibuprofen: 10 m g/kg per dose PO q6h
Penicillin V: 25–50 m g/kg/d PO b.i.d.–q.i.d.
Follow-Up Disposition Admission Criteria
All toxic patients
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Infants 0–28 days of age with tem perature >38°C
Nontoxic infants 28–90 days of age with tem perature >38°C who do not m eet low-risk criteria (see definition under Discharge Criteria)
Poor com pliance or follow-up
Discharge Criteria
Infants 28–90 days of age m eeting low-risk criteria: o
No prior hospitalizations, chronic illness, antibiotic therapy, prem aturity
o
Reliable, m ature parents with hom e phone, available transport, therm om eter, and living in relative proxim ity to ED
o
No evidence of focal infection (except otitis m edia); non-toxic appearing; norm al activity, perfusion, and hydration with age-appropriate vital signs
o
Norm al WBC (5–15,000/m m 3 ), urine (negative Gram stain of unspun urine or leukocyte esterase or Table o f C o ntents > F ibro m yalgia
Fibromyalgia
Jennifer S. Johnson
Basics Description
Nonarticular, noninflam m atory form of m uscular rheum atism :
o
Widespread pain
o
Tender points (not trigger points)
o
Fatigue
o
Sleep disturbance
o
Lim ited physical findings
Not diagnosis of exclusion, m ay occur with other rheum atic diseases
Painful sym ptom s believed to be m uscular in origin
Abnorm alities identified as possible m echanism : o
Decreased ATP/phosphocreatine level
o
Prolonged m uscle ischem ia/tension
o
Low blood flow in exercise m uscles of patients with fibrom yalgia
Muscle biopsies from tender points have shown no reproducible abnorm alities.
Genetics Genetic predisposition m ay play role when sym ptom s triggered by
Pa ge 1 8 8
exposure to environm ental stressors.
Etiology Mechanism
Unknown
May involve neuroendocrine system or com bination of peripheral and central m echanism s, such as: o
Physiologic im balance in hypothalam ic-pituitaryadrenal axis with decreased free cortisol production
o
Low serum levels of insulin growth factor
o
Elevated levels of substance P (enhances pain perception) in cerebrospinal fluid (CSF)
o
Reduced serotonin levels
o
Sleep disturbance of norm al stage 3 and 4 phases (non-REM):
Results in nonrestorative sleep and im m unologic dysfunction
Psychologic distress
Central hyperexcitability of nociceptive system
Diagnosis Signs and Symptoms History
Generalized m usculoskeletal pain and m orning stiffness
Weakness and fatigue
Sleep disturbance
Tension or m igraine headaches
GI com plaints (e.g., irritable bowel syndrom e)
Genitourinary (GU) com plaints (e.g., interstitial cystitis)
Mood disturbances (e.g., depression, anxiety)
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Paresthesias
Sensation of swollen hands and joints
Skinfold tenderness
Postexertional pain
Cold intolerance
Physical Exam Derm atographism
Essential Workup
History and characteristic physical findings are key to m aking diagnosis.
Use classification criteria established by Am erican College of Rheum atology (ACR) for fibrom yalgia: o
Absence or less than num ber of required tender points does not exclude syndrom e.
o
Widespread pain present for at least 3 m onths on both left and right side of body:
Pain above and below waist
Axial skeletal pain m ust be present (cervical or anterior chest or thoracic spine or low back pain).
o
Eleven of 18 specific tender points on digital palpation with force of 4 kg/cm (am ount of pressure required to blanch thum bnail)
o
The nine paired (bilateral) tender points are located at the:
Occiput: suboccipital m uscle insertions
Low cervical: anterior aspects of C-5, C-7 intertransverse spaces
Trapezius: m idpoint of upper border
Supraspinatus: above m edial border of scapular spine
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Second rib: second costochondral junction about 3 cm lateral to sternal border
Lateral epicondyle: about 2 cm below bony prom inence
Gluteal: upper outer quadrant of buttocks
Greater trochanter: posterior to trochanteric prom inence
Knee: m edial fat pad proxim al to joint line
Tests Lab
Evaluate for alternative diagnoses: o
CBC
o
Blood chem istries
o
Erythrocyte sedim entation rate (ESR)
o
Muscle enzym es
o
Thyroid function tests
No specific laboratory abnorm alities are characteristic of fibrom yalgia.
Imaging No specific radiographic abnorm alities are characteristic.
Differential Diagnosis
Myofascial pain syndrom e (trigger points present, not tender points)
Chronic fatigue syndrom e
Major depression
Polym yalgia rheum atica
Lym e disease
Hypothyroidism
Collagen vascular disease
Electrolyte im balance
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Myopathies (m etabolic and drug induced)
Osteom alacia
Psychogenic rheum atism
Eosinophilia-m yalgia syndrom e
P.413
Treatment ED Treatment
Patient education and reassurance: o
Em phasize that fibrom yalgia is not life threatening and does not reduce life expectancy.
o
Disorder is chronic but not crippling or deform ing.
o
Goal is to m anage pain and im prove functional disability.
Patients with poor coping skills m ay require psychiatric intervention.
Pharmacologic Therapy
Pharm acotherapy for im proving pain, relaxing m uscles, and im proving sleep quality has been m ost successful with CNS agents.
Com binations of m edications (e.g., am itriptyline and fluoxetine or am itriptyline and cyclobenzaprine) m ay be m ore beneficial than either m edication alone.
Tricyclic antidepressants (TCAs; am itriptyline, nortriptyline)
Muscle relaxants (cyclobenzaprine)
Selective serotonin reuptake inhibitors (fluoxetine)
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Serotonin norepinephrine reuptake inhibitors (duloxetine, m ilnacipran)
Tram adol with or without acetam inophen
Anticonvulsants (pregabalin)
Benzodiazepines (clonazepam ) are of no benefit other than their role in sleep disturbances.
Nonsteroidal anti-inflam m atory drugs (NSAIDs) and corticosteroids have not been shown to be effective.
Steroids or local anesthetic (lidocaine) injection into tender points is controversial: o
No studies available to prove efficacy
Opioids: no data showing benefit in long term
Medication (Drugs)
Am itriptyline: 10–50 m g PO at bedtim e
Clonazepam : 0.5 m g PO at bedtim e
Cyclobenzaprine: 10–30 m g/d PO at bedtim e
Duloxetine: 60 m g PO b.i.d
Fluoxetine: 20–80 m g PO daily
Pregabalin: 450 m g PO daily
Tram adol: 200–300 m g PO daily
Lifestyle Modifications
Physical exercise should be encouraged: o
Exercise program should be gradual to avoid overexertion and discouragem ent.
o
Aerobic exercise is m ore beneficial than sim ple stretching.
o
Efficacy not m aintained if exercise stops
Good sleep pattern should also be discussed: o
Establishing nightly ritual in preparation for sleep
Pa ge 1 8 8
o
Avoiding caffeine-containing beverages or foods in afternoon or evenings
Encourage stress m anagem ent and coping strategies.
Participation in educational program s (e.g., cognitive-behavioral therapy): o
Im provem ent is often sustained for m onths.
Follow-Up Disposition Admission Criteria
Patients with serious underlying disease, intractable pain, or im m unocom prom ised
Patients with suicidal ideation
Discharge Criteria Patients with uncom plicated fibrom yalgia can be m anaged as outpatients.
References 1. Arnold LM, et al. A double-blind, m ulticenter trial com paring duloxetine with placebo in the treatm ent of fibrom yalgia patients with or without m ajor depressive disorder. Arthritis Rheum . 2004;50:2974–2984. 2. Arthritis Foundation. Prim er on the Rheum atic Diseases. 12th ed. Atlanta, GA; 2001:188–193. 3. Crofford LJ, et al. Pregabalin for the treatm ent of fibrom yalgia syndrom e: results of a random ized, double-blind, placebo-controlled trial. Arthritis Rheum . 2005;52:1264–1263. 4. Desm eules JA, et al. Neurophysiologic evidence for a central sensitization in patients with fibrom yalgia. Arthritis Rheum .
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2003;48:1420–1429. 5. Goldenberg DL, et al. Managem ent of fibrom yalgia syndrom e. JAMA. 2004;292:2388–2395.
Codes ICD9-CM 729.1
ICD10 M79.0
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > F lail C hest
Flail Chest
Gregory W. Lampe
Basics Description
Free floating segm ent of chest wall: o
Three or m ore adjacent ribs are fractured in two or m ore places.
o
Rib fractures in conjunction with sternal fractures or costochondral separations
The free-floating segm ent of chest wall paradoxically m oves inward during inspiration and outward during expiration.
The principle pathology associated with flail chest is the associated pulm onary contusion: o
Not alteration in ventilatory m echanics owing to the free-floating segm ent
Etiology
Blunt thoracic traum a
Fall from a height
Motor vehicle accident
Assault
Missile injury
Ribs usually break at the point of im pact or posterior
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angle: o
Weakest region structurally
Transfer of kinetic energy to the lung parenchym a adjacent to the injury: o
Disruption of the alveolocapillary m em brane and developm ent of pulm onary contusion
o
Arteriovenous shunting
o
Ventilation/perfusion m ism atch
o
Hypoxem ia
o
Respiratory failure m ay result
Pediatric Considerations Relatively elastic chest wall m akes rib fractures less com m on in children.
Diagnosis Signs and Symptoms History
Blunt thoracic traum a by any m echanism
Mechanism as described by patient, parent or prehospital personnel:
o
Seat belt usage
o
Steering wheel dam age
o
Air bag deploym ent
Localized chest wall pain increases with deep inspiration, coughing, m oving
Pleuritic chest pain
Dyspnea
Hem optysis
Physical Exam
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Flail chest paradoxically m oves inward during inspiration and outward during expiration: o
Initially this m ay not be seen because of m uscle spasm and splinting respirations.
o
Inspection under tangential light m ay m agnify paradoxical m otion of the chest wall.
Multiple rib fractures: o
Bony stepoffs
o
Ecchym osis
o
Crepitus
o
Edem a
o
Erythem a and tenderness associated with
Splinting respirations
Intercostal m uscle spasm
Dyspnea, tachypnea: o
Onset m ay be insidious, increasing over tim e.
Cyanosis, tachycardia, hypotension
Auscultation with initially norm al breath sounds progressing to wet rales or absent breath sounds.
Essential Workup Diagnosis is initially m ade on clinical grounds.
Tests Lab Arterial blood gas analysis:
May reveal hypoxem ia
Elevated alveolar-arterial gradient
Imaging
Chest radiograph aids diagnosis, revealing m ultiple rib fractures: o
May reveal associated intrathoracic pathology:
Pa ge 1 8 9
o
Pneum othorax, hem othorax
Pneum om ediastinum
Pulm onary contusion
Widened m ediastinal silhouette
Pulm onary contusion appears within 6–12 hours after injury:
Ranges from patchy alveolar infiltrates to frank consolidation
Thoracic CT is useful in detecting associated intrathoracic injuries not identified on chest radiograph.
Differential Diagnosis
Chest wall contusion or intercostal m uscle strain
Costochondral separation
Sternal fracture and dislocation
Radiographic differential diagnosis includes: o
Acute respiratory distress syndrom e
o
Pulm onary laceration, infarction or em bolism
o
Congestive heart failure
o
Pneum onia, abscess, other infectious process
o
Noncardiogenic causes of pulm onary edem a
Treatment Pre Hospital
Positioning the patient injured side down can stabilize the involved chest wall: o
Im prove ventilation in noninjured hem ithorax.
Thoracic traum a with significant m echanism or com bined with pre-existing pulm onary disease should be routed to the nearest traum a center.
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Initial Stabilization
Manage airway and resuscitate as indicated
IV line, O 2 , continuous cardiac m onitoring and pulse oxim etry
Control airway: o
Endotracheal intubation
o
Indicated for patients with severe hypoxem ia (PaO 2 Table o f C o ntents > F o o t F racture
Foot Fracture
Colleen Campbell
Basics Description Injury to tarsal bones or m etatarsals including calcaneus, talus, navicular, cuboid, cuneiform , and m etatarsals
Etiology
Most com m on foot injuries are of the m etatarsals and phalanges.
The calcaneus is the m ost com m only fractured of the tarsal bones.
Calcaneus fractures: com pression injury from sudden high-velocity im pact to heel: o
Seventy-five percent are intra-articular; 50% have associated injuries:
10% spine fractures
25% with associated lower extrem ity traum a
5% bilateral, 5% open
Metatarsal fractures: divided into stress fractures, twisting injuries, or direct traum a: o
First m etatarsal: direct applied force
o
Second and third m etatarsals are m ost often involved in stress fractures and twisting injuries.
Pa ge 1 8 9
o
Fifth m etatarsal: Avulsion fracture (dancer's fracture) of proxim al apophysis is m ost com m on injury.
o
Jones fracture: transverse fracture of the m etaphyseal-diaphyseal junction of fifth m etatarsal; results from twisting while foot inverted
Talus: caused by dorsiflexion with axial load, com m on snowboarder's injury
Navicular: results from axial com pression or stress fractures
Cuboid and cuneiform fractures are rare and occur in conjunction with other injuries, often with tarsal-m etatarsal injuries.
Tarsal-m etatarsal injuries (Lisfranc injuries): high-energy injuries: o
Axial load on plantar-flexed foot, or hindfoot fixed with forced foot eversion
o
Unstable forefoot on hindfoot
o
20% go undiagnosed on initial visit.
Pediatric Considerations
Metatarsal fractures account for 90% of foot fractures in children: o
Avulsion fractures of the fifth m etatarsal are m ost com m on.
o
Physeal injury m ay occur with proxim al first m etatarsal fractures.
Other com m on injuries include phalangeal fractures (17%) and navicular fractures (5%).
Diagnosis
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Signs and Symptoms History
History of preceding traum a m ost com m on
Stress fractures m ay present with increasing pain in setting of repetitive activities
Physical Exam
Ecchym osis, pain, swelling, or deform ity of foot
Pain with weight bearing
Joint instability
Essential Workup
Physical exam of extrem ity is necessary to assess neurovascular status, skin integrity, gross swelling, deform ity, or loss of function.
Exam ination of spine is also essential in suspected calcaneus fractures, as there is a 10% incidence of coexistent injury.
Anterior-posterior/lateral and oblique views are necessary for all foot fractures.
Com plications: o
Com partm ent syndrom e m ost com m only presents as severe pain in a swollen foot:
Pressures >35 m m Hg require opening of all m ajor foot com partm ents.
o
Nonunion and avascular necrosis are com m on com plications with talar neck fractures owing to distal blood supply.
o
Calcaneus fractures m ay be accom panied by sural nerve injury; test sensation along lateral aspect of foot.
Tests
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Imaging Special views m ay be needed for som e fractures:
Lisfranc fractures m ay require stress views with weight bearing.
Talar fractures m ay require a 45-degree internal oblique view.
Midfoot fractures m ay require an external oblique foot view.
Calcaneus fractures require an axial view and m ay require CT: o
Boehler angle 6 feet.
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Initial Stabilization Manage coexisting traum a as indicated. P.417
ED Treatment
Airway, breathing, and circulation m anagem ent
Assess for neurovascular com prom ise distal to fracture site.
Dislocations m ust be reduced as quickly as possible with assessm ent of neurovascular status before and after procedure: o
Procedural sedation usually required
Im m obilize, ice, and elevate in a bulky splint: o
Application of circum ferential cast should be delayed until swelling subsides.
Crutches
Pain m anagem ent: o
If large am ount of swelling and pain with toe m ovem ent, suspect com partm ent syndrom e.
Orthopedic consult indicated early for displaced fractures: o
Many injuries require repair within 6 hours of injury to prevent delay of open reduction with internal fixation for 6–10 days owing to swelling.
Medication (Drugs)
Cefazolin: 1 g IV/IM (peds: 25 m g/kg IV/IM)
Diprivan: 40 m g IV q10s until sedation
Etom idate: 0.1–0.2 m g/kg IV
Fentanyl: 50–250 µg IV titrated (peds: 2 µg/kg IV)
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Ibuprofen: 800 m g PO (peds: 10 m g/kg PO)
Meperidine: 25–100 m g IV/IM titrated (peds: 1–1.75 m g/kg IV/IM)
Methohexital: 1.0–1.5 m g/kg IV
Morphine: 2–10 m g IV/IM titrated (peds: 0.1 m g/kg IV)
Follow-Up Disposition Admission Criteria
Open fracture
Evidence of com partm ent syndrom e or neurovascular injury
Open reduction internal fixation required im m ediately
Discharge Criteria Most patients with m etatarsal fractures can be discharged with orthopedic follow-up.
Issues for Referral All open fractures, as well as all m idfoot/Lisfranc injuries and displaced fractures that are not successfully reduced, should be seen in ED by an orthopedic specialist.
References 1. Ribbans WJ, Natarajan R, Alavala S. Pediatric foot fractures. Clin Orthop Relat Res. 2005;432:107–115. 2. Steele PM, Bush-Joseph C, Bach B Jr. Managem ent of acute fractures around the knee, ankle, and foot. Clin Fam Pract. 2000;2(3):661–705. 3. Wedm ore IS, Charette J. Em ergency departm ent evaluation and treatm ent of ankle and foot injuries. Em erg Med Clin North Am .
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2000;18(1):85–113.
Codes ICD9-CM 825 Fracture of one or m ore tarsal and m etatarsal bones
ICD10 S92.9 Fracture of foot, unspecified
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > F o rearm F racture, Shaft/Distal
Forearm
Fracture, Shaft/Distal Trevor J. Mills Peter DeBlieux
Basics Description
Shaft fractures (single and paired) often displaced by contraction of m uscles of arm ; som etim es associated with dislocations o
Galeazzi fracture:
Distal radius fracture with distal radioulnar dislocation
o
Monteggia fracture:
Proxim al ulnar fracture with dislocation of radial head
Distal fractures include extension, flexion, and intra-articular classifications: o
Colles fracture:
Hyperextension fracture of distal radius
Distal fragm ent displaced dorsally
Radial deviation
May also involve ulnar styloid and distal
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radioulnar joint o
o
Sm ith fracture:
Hyperflexion fracture of distal radius
Distal fragm ent displaced volarly
Barton fracture:
Intra-articular fracture of dorsal rim of distal radius
o
Often associated with dislocation of carpal bones
Hutchinson fracture:
Intra-articular fracture of radial styloid
Pediatric Considerations
Shaft fractures: o
Torus fracture:
Com pression (buckling) of cortex on one or both sides
o
Greenstick fracture:
Distraction of one side of cortex with opposite side intact
o
Plastic deform ity:
Bowing of radius or ulna without apparent disruption of cortex
Multiple m icrofractures
Distal fractures: o
Salter-Harris–type fractures (see Salter-Harris classification)
Etiology
Direct blow to forearm
Longitudinal com pression load:
o
Fall on outstretched hand (FOOSH)
o
Horizontal force
Excessive pronation, supination, hyperextension, or
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hyperflexion
Diagnosis Signs and Symptoms History
Associated events and concurrent injuries
Past history of bone disease or old fractures
History of repetitive stress of forearm m ovem ent
Occupation
Hand dom inance
Physical Exam
Physical exam with special attention to skin integrity, deform ity, and neurovascular status
Forearm pain, crepitus, tenderness to palpation, deform ity, shortening of forearm
Forearm edem a, ecchym osis, elbow or wrist joint effusions
Abnorm al m obility or loss of function at elbow/wrist/hand
Neurologic abnorm alities
Vascular com prom ise
Essential Workup Suspected forearm fractures require anteroposterior (AP) and lateral radiographs, including wrist and elbow.
Tests
Com partm ent pressures should be m easured for suspected com partm ent syndrom e.
Som e intra-articular fractures m ay require CT im aging.
Differential Diagnosis
Upper extrem ity m uscle, ligam entous injury
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Elbow or wrist dislocations, including pediatric nursem aid's elbow
Forearm contusions, hem atom as
Cellulitis, abscesses, soft tissue m asses
Forearm osteogenic tum ors
Osteom yelitis
Upper extrem ity vascular or neurologic injuries
Elbow or wrist arthritis, joint effusions
Pediatric growth plates, nutrient vessels m ay be m istaken for fractures
Treatment Pre Hospital
All suspected forearm fractures should be elevated, splinted, and im m obilized, including elbow and wrist joints.
All open fractures should be wrapped with sterile dressing before im m obilization: o
Do not reduce open fractures back under skin in the field.
o
In patients with isolated extrem ity traum a, analgesia m ay be adm inistered.
ED Treatment
Shaft fractures, nondisplaced: o
Long-arm splint
o
Orthopedic referral
Shaft fractures, displaced: o
Orthopedic consultation
o
Often require open reduction, internal fixation
Pa ge 1 9 0
Distal fractures, nondisplaced o
Forearm sugar-tong or AP splint
o
Orthopedic referral
Distal fractures: Colles/Sm ith: o
Sim ple, noncom m inuted, extra-articular Colles and Sm ith fractures m ay be reduced in ED:
o
Splint (long-arm sugar-tong splint)
Sling
Referred to orthopedics
Com plicated Colles and Sm ith fractures require orthopedic consultation.
Distal fractures: Barton/Hutchinson: o
o
Uncom plicated Barton and Hutchinson fractures
Splint (AP or sugar-tong splint)
Place in sling
Referred to orthopedics
Com plicated fractures require orthopedic consultation.
Open fractures: o
Cover with sterile dressings.
o
IM/IV antibiotics
o
Tetanus im m unization (if indicated)
o
Splint
o
Im m ediate orthopedic consultation
Forearm fractures associated with com partm ent syndrom e or neurovascular com prom ise require im m ediate orthopedic consultation.
P.419
Pediatric Considerations
Torus and Greenstick fractures with Table o f C o ntents > F o reign Bo dy, Ear
Foreign Body, Ear
Kathleen Nasci Charles V. Pollack Jr.
Basics Description
Foreign bodies lodged in the external auditory canal
Typical foreign bodies in children:
o
Stones
o
Sm all beads
o
Paper
o
Toys
o
Seeds and popcorn kernels
o
Beans and other food and organic m aterials
Typical foreign bodies in com petent adults: o
Cotton-swab tips
o
Earplugs
o
Insects
Inanim ate foreign objects are often associated with delayed presentations.
Most objects tend to becom e trapped in outer two-thirds of external auditory canal.
Children and psychiatric patients m ay insert anything sufficiently sm all to enter the external auditory canal.
Pa ge 1 9 1
Ear foreign bodies are m ost com m on in children younger than 8 years.
Com plications: o
Canal laceration
o
Perforation of tym panic m em brane, which is m ore likely to result from rem oval procedure
o
Otitis externa
Sym ptom s usually resolve within a few days after foreign body rem oval.
Diagnosis Signs and Symptoms
Decreased hearing
Unilateral ear pain
Fullness
Loud noises
Buzzing sound (with live insects)
Nausea
Dizziness
Ipsilateral tearing
Purulent discharge from the external ear
Itching
Bleeding
Essential Workup
Always seek to identify the nature of the foreign body before trying to rem ove it: o
Live insect
o
Vegetable
o
Inanim ate object
Pa ge 1 9 1
Careful otoscopic exam ination: o
Minim ize pain.
o
Gain the patient's trust.
o
Achieve optim al visualization by having an assistant exert gentle, steady traction on the patient's lobule.
o
Perform a bilateral exam ination; especially im portant in children and psychiatric patients, and prevents overlooking a quiescent foreign body in the contralateral ear.
o
Repeat exam after rem oval to assess possible traum a of external canal or tym panic m em brane.
Tests Imaging
Operating m icroscope: o
Use if em ergency departm ent rem oval fails
Radiographs are not indicated.
Differential Diagnosis
Cerum en im paction
Granulom a
Hem atom a
Injury
Otitis externa
Perforated tym panic m em brane
Residual otitis externa after self-extraction of the foreign body
Tum or
Treatment
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Pre Hospital
Cautions: o
Severe ear pain, sensation of m ovem ent, and loud, buzzing sound:
Typical signs of a live insect in external auditory canal
Instill warm lidocaine or m ineral oil into affected ear to kill insect.
Controversies: o
Attem pts at rem oval in the field are not indicated:
Lack of appropriate equipm ent
Prior failed attem pts m ay m ake future attem pts m ore difficult.
Initial Stabilization For a patient in distress because of a live insect:
Drown or im m obilize insect before any rem oval attem pts.
Instill warm solution into the external auditory canal:
o
Mineral oil
o
Viscous lidocaine
o
Ether
o
2% lidocaine
o
Microscope im m ersion oil
Cold fluids should not be used so as to avoid a caloric response.
ED Treatment
Appropriate instrum ents: o
Otoscope
o
Alligator forceps
o
Cupped forceps: num bers 3, 5, and 7 suction tips, preferably with Frazier suction cups
o
A wire loop
Pa ge 1 9 1
o
Ear curettes
o
A right-angled blunt hook
Achieve proper head im m obilization
Vegetable m atter rem oval: o
Visualize
o
Attem pt rem oval with forceps.
o
Be certain to delineate clearly between foreign body and inflam ed external auditory canal tissue.
o
Do not irrigate the external auditory canal if the foreign body is of such a nature that it m ight swell.
Nonvegetable inanim ate foreign body rem oval: o
Visualize
o
If easily grasped, attem pt rem oval with forceps.
o
If not accessible, attem pt rem oval with irrigation.
o
Perform careful visualization.
o
Place an Angiocath catheter adjacent to, or preferably distal to, the foreign body.
o
Inject warm water or sterile saline through catheter via a syringe.
o
Backwash the foreign body out.
o
Never attem pt rem oval by irrigation when the foreign body is a button battery.
P.421
Polished or sm ooth object extraction: o
Visualize
o
Direct suction
o
Blunt right-angled probe: pass beyond the foreign body; rotate 90°; rem ove it with the foreign body
o
Fogarty catheter: carefully pass beyond the foreign body and inflate and withdraw; this approach puts
Pa ge 1 9 1
the tym panic m em brane at particular risk of inadvertent injury o
Cyanoacrylate glue (superglue): place on the tip of a blunt probe, place on the foreign body for 10 seconds, and then pull; quick bonding m ay allow foreign body rem oval with the probe
Insect rem oval: o
Once killed, rem ove with forceps or by irrigation
o
Re-exam ine to ensure that all insect parts are rem oved
Sharp objects: o
Rem ove with operating m icroscope
o
Consider otolaryngologic referral if there is evidence of traum a or if patient is uncooperative,
Anesthesia or analgesia: o
None needed in adults for sim ple foreign body rem oval
o
Four-quadrant local anesthetic block
o
1–2% lidocaine, with or without epinephrine
o
Infiltrate around the external auditory canal.
o
Procedural sedation
o
Indicated for children and uncooperative adults
o
Use before attem pts, as unsuccessful efforts m ay produce bleeding, edem a, or injury to the tym panic m em brane
o
Ketam ine for children
o
Benzodiazepines for older patients
o
Consider fentanyl if analgesia is indicated during rem oval.
Medication (Drugs)
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Fentanyl: 1 µg/kg
Ketam ine: 1–2 m g/kg IV or 4 m g/kg IM
Midazolam : 1 m g IV slowly every 2–3 m inutes up to 5 m g (peds: 6 m onths to 5 years, 0.05–0.1 m g/kg, titrate to m axim um of 0.6 m g/kg; 6–12 years, 0.025–0.05 m g/kg, titrate to m ax. of 0.4 m g/kg)
Follow-Up Disposition Admission Criteria Hospital adm ission is usually not necessary.
Discharge Criteria
Patient should be instructed not to place any objects in ear.
A short course of analgesics after traum atic foreign body rem oval
Otitis externa: o
Topical antim icrobial such as Cortisporin suspension
Im m unocom prom ised patients m ay require oral antibiotics.
Perforated tym panic m em brane: o
Prophylaxis with antibiotics
o
Follow-up with ear/nose/throat specialist
Avoid subm ersion in water until follow-up if traum a or infection present.
References 1. Ansley JF, Cunningham MJ. Treatm ent of aural foreign bodies in children. Pediatrics. 1998;101:638–641.
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2. Balbani AP, Sanchez TG, Butugan O, et al. Ear and nose foreign body rem oval in children. Int J Pediatr Otorhinolaryngol. 1998;46:37–42. 3. Bressler K, Shelton C. Ear foreign body rem oval: a review of 98 consecutive cases. Laryngoscope. 1993;103:367–370. 4. Brown L, Denm ark TK, Wittlake WA, Vargas EJ, Watson T, Crabb JW. Procedural sedation use in the ED: m anagem ent of pediatric ear and nose foreign bodies. Am J Em erg Med. 2004;22(4):310–314. 5. Davies PH, Benger JR. Foreign bodies in the nose and ear: a review of techniques for rem oval in the em ergency departm ent. J Accid Em erg Med. 2000;17:91–94. 6. Kum ar S, Kum ar M, Lesser T, Banhegyi G. Foreign bodies in the ear: a sim ple technique for rem oval analysed in vitro. Em erg Med J. 2005;22(4):266–268.
Codes ICD9-CM 931 Foreign body in ear
ICD10 T16 Foreign body in ear
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > F o reign Bo dy, Eso phageal
Foreign Body,
Esophageal Jason J. Prystowsky
Basics Description
Esophageal foreign bodies typically lodge at three sites of physiologic constriction: o
Cricopharyngeal m uscle—63%, m ost com m on (C6)
o
Gastroesophageal junction—20% (T11)
o
Aortic arch—10% (T4)
90% of ingested foreign bodies pass spontaneously.
10–20% are rem oved endoscopically, and 1% or less require surgery.
Etiology
Most com m on adult and adolescent foreign bodies are food boluses and bones: o
Esophageal pathology alm ost always underlies food im pactions.
o
Esophageal stricture, esophageal spasm , achalasia, esophageal m otor disorder
Increased risk: o
Edentulous adults
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o
Intoxicated patients
o
Patients with underlying esophageal disease
Pediatric Considerations
Eighty percent of foreign body ingestions occur in pediatric age group, particularly younger than 2 years.
Coins: o
Most com m on: 80% of esophageal foreign bodies
Predisposing factor: esophageal strictures
Diagnosis Signs and Symptoms
Acute ingestion: o
Dysphagia
o
Odynophagia
o
Drooling
o
Vom iting
o
Choking
o
Gagging
o
Blood-stained saliva
Chronically retained foreign body: o
Respiratory sym ptom s predom inate (paraesophageal tissue swelling com prom ises adjacent trachea):
Cough
Stridor
Hoarseness
o
Chest pain
o
Site of foreign body sensation usually corresponds to esophageal level of foreign body
o
Esophageal perforation:
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o
Redness
Swelling
Crepitus in the neck
Less than 20% asym ptom atic
Pediatric Considerations
Infants: signs/sym ptom s: o
Refusal to eat
o
Stridor
o
Upper respiratory tract infection
o
Neck/throat pain
Essential Workup
History about object ingested: type, when, and how
Physical exam focused by degree of distress exhibited: o
o
o
Esophagus for:
Obstruction
Perforation
Hem orrhage
Oropharynx:
Red, irritated throat
Palatal abrasions
Lung:
o
Abdom en:
Stridor and wheezing
Peritonitis or bowel obstruction
Direct or indirect laryngoscopy can be useful.
Tests Imaging
Biplane chest radiograph including all of neck for foreign body localization: o
Need for additional radiographs dictated by clinical
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situation o
Those with food bolus need no radiographs usually.
o
Esophageal foreign bodies usually align them selves in coronal plane.
o
Esophageal perforation is noted by air in retropharyngeal space, in soft tissues of neck, or by pneum om ediastinum .
Esophageal contrast studies for nonradiopaque foreign bodies: o
Radiolucent objects (sm all pieces of glass, bone fragm ents, alum inum , plastic, pieces of wood)
o
Thin barium esophagogram : changes in contour of barium colum n localize foreign body.
o
Passage of contrast solution into stom ach: partial versus com plete obstruction
o
Cautions:
Oral contrast in high-grade esophageal obstructions can increase risk of aspiration, and barium m ay coat m ucosa, lim iting subsequent endoscopy.
Traditional water-soluble contrast can cause severe tissue reaction in perforations because of its hyperosm olality.
Metal detectors have been used in localizing ingested m etal, particularly coins in pediatric population.
Endoscopy: o
Method of choice for localizing and m anaging m ost esophageal foreign bodies
o
Ability to inspect surrounding esophageal m ucosa for pathology
o
Both diagnostic and therapeutic
CT can often detect foreign bodies not identified by other
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m eans, especially if use 3D reconstruction.
Differential Diagnosis
Globus hystericus phenom enon (“lum p in throat―)
Esophagitis
Croup
Epiglottitis
Upper respiratory tract infection
Retropharyngeal abscess
Treatment Pre Hospital Cautions:
Airway m aintenance and prevention of aspiration param ount
Oxygen for patients in distress
Place patient in whatever position gives m ost com fort.
Ipecac and cathartics contraindicated
Initial Stabilization
Airway, breathing, and circulation m anagem ent first priority
Prevent aspiration
ED Treatment
Foreign bodies lodged in upper or m id-esophagus: o
Extraction required
Asym ptom atic patients with coins or sm ooth objects (not button batteries) in distal esophagus: o
Observe up to 24 hours after ingestion to see whether it will pass into stom ach.
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o
Danger of perforation increases after 24 hours.
Im pacted food bolus obstructing esophagus: o
Em ergent rem oval indicated
o
Digestion with proteolytic enzym es (papain) not recom m ended because of serious m orbidity including esophageal perforation, hypernatrem ia, and aspiration
Extricate sharp or pointed esophageal foreign bodies regardless of their location: o
Perforation incidence ranges from 15–35%
o
Objects m ost com m only associated with com plications are:
o
Chicken and fish bones
Straightened paper clips
Toothpicks
Needles
Bread bag clips
Dental bridgework
Direct laryngoscopy can be perform ed if above cricopharyngeus.
o
Objects that reach stom ach and are shorter than 5 cm and 3–4 days should be rem oved.
Large-diam eter batteries (>20 m m ) should be rem oved from stom ach after 48 hours.
o
Once past duodenal sweep, 85% are passed within 72 hours.
Narcotic/am phetam ine packets: o
Body packing seen in regions of high drug traffic
o
Packets usually seen on radiographs
o
Rupture or leakage of contents can be fatal.
Rem oval techniques: o
Fluoroscopically guided Foley catheter extraction:
Successful and safe in experienced hands
Foley catheter (10–16 French) placed nasally, passed into esophagus, tip and balloon pushed beyond foreign body under fluoroscopic control
Foley balloon inflated with contrast and catheter slowly withdrawn
Contraindicated in chronic ingestions, uncooperative patients, sharp-pointed objects
o
Foley catheters m ay also be used to push distal foreign body into stom ach.
Endoscopy: o
Preferred m ethod to rem ove acute or chronic foreign bodies
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o
Always used with im pactions of long duration (>2–4 days) because of associated esophageal irritation/edem a
o
General endotracheal anesthesia needed in difficult cases: infants, psychiatric patients, difficult foreign body
o
Bougienage: using dilator to push foreign body into stom ach
IV glucagon: o
Decreases lower esophageal sphincter tone without interfering with esophageal contractions
o
Often perm its distal food boluses to pass into the stom ach
o
For im pactions Table o f C o ntents > F o urnier G angrene
Fournier
Gangrene Gary M. Vilke
Basics Description
Inadequate hygiene leads to skin m aceration and excoriation: o
Portal of entry for bacteria in tissue
Once skin barrier is broken, polym icrobial flora spread along fascial planes of perineum .
Colles fascia fuses with urogenital diaphragm , slowing propagation posteriorly and laterally.
Anteriorly, Buck and Scarpa fascia are continuous, allowing rapid extension to anterior abdom inal wall and laterally along fascia lata.
Testes and urethra are usually spared.
Three anatom ic origins account for m ost cases: o
Lower urinary tract (40%): urethral strictures, indwelling catheters
o
Penile or scrotal (30%): condom catheters, hydradenitis, and balanitis
o
Anorectal (30%): fistulas, perirectal infections, and
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hem orrhoids
Rarely, intra-abdom inal sources such as perforating appendicitis, diverticulitis, or pancreatitis have produced Fournier gangrene by dependent contiguous spread.
Etiology
Infection by polym icrobial flora (m ixed aerobic and anaerobic organism s)
Mixed bacteria exert synergistic tissue-destructive effect.
End arterial throm bosis in subcutaneous tissues produces anaerobic environm ent.
Bacterial toxins and tissue necrosis factors m ay contribute to clinical presentation.
Risk factors: o
Traum a
o
Diabetes
o
Alcoholism
o
Other im m unocom prom ised states
o
Morbid obesity
o
Abdom inal surgery
Diagnosis Signs and Symptoms
Rapidly progressive necrotizing infection of perineum involving subcutaneous and fascial tissues and often m uscle layers: o
Usually seen in diabetics or im m unocom prom ised patients
Patients are often toxic in appearance with nausea, vom iting, fever, chills, and pain.
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Sources of infection m ay be flora from genitourinary, rectal, or penile/scrotal regions.
Skin findings: o
Bronze or violaceous discoloration of skin
o
Thin brown watery discharge
o
Ulceration, bullous vesicles
o
Crepitance, subcutaneous air
o
Frank necrosis and eschar form ation
Pain is out of proportion to exam ination in early phases, but eventually dead tissue becom es insensate.
Lethargy and inappropriate indifference to the illness are com m on.
Pediatric Considerations
Though unusual in children, >50 cases have been described.
Most often are com plications of burns, circum cision, balanitis, severe diaper rashes, or insect bites
Organism s are m ore frequently Staphylococcus or Streptococcus.
Pediatric patients have m ore local disease and are less toxic.
Essential Workup
Fournier gangrene is a clinical diagnosis.
History and physical exam with special attention to perineum
Evaluate for signs of sepsis.
Early surgical consultation for em ergent débridem ent is essential.
Other workup directed toward relevant co–m orbid factors such as diabetes or im m unocom prom ised status
Tests
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Lab
Other than Gram stain of tissue and associated drainage, there are no specific laboratory tests that are diagnostic of Fournier gangrene.
Urinalysis should be perform ed.
Leukocytosis, anem ia, electrolyte im balances, acidosis, and renal failure are com m on.
Dissem inated intravascular coagulation (DIC) m ay be present; PT, PTT, fibrin-split products, and fibrinogen levels help identify.
If patient is suspected of or known to have diabetes, glucose, electrolytes, and serum ketones to evaluate for diabetes and diabetic ketoacidosis (DKA)
Culture of blood, urine, and tissue (when available)
Imaging
Plain film s of the pelvis m ay reveal subcutaneous em physem a and ileus.
CT scanning helps if intra-abdom inal or ischiorectal source is suspected.
Ultrasound (US) m ay be useful in differentiating from other causes of acute scrotum .
Retrograde urethrography, anoscopy, proctosigm oidoscopy, and barium enem as m ay be helpful to localize anatom ic sources of infection.
Differential Diagnosis
Testicular torsion
Scrotal cellulitis
Epididym itis/orchitis
Tinea cruris
Scrotal abscess/inguinal abscess
Perirectal infections
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Insect and hum an bites
P.429
Treatment Pre Hospital Cautions:
Patients m ay be hypotensive from septic shock and require aggressive fluid resuscitation and pressor support.
Initial Stabilization
Manage airway and resuscitate as indicated.
Central venous access, aggressive fluid resuscitation, and pressure support as indicated: o
Avoid fem oral access, fem oral venipuncture, and lower extrem ity venous access
Early goal-directed therapy if septic
Foley catheter placem ent or suprapubic access if indicated
ED Treatment
Em piric broad-spectrum antibiotics
Early em ergent aggressive surgical débridem ent
Adjunctive hyperbaric oxygen therapy coordinated with surgical care
Treat dehydration and correct electrolytes.
Blood products as needed for DIC or anem ia; oxygen debt can be m inim ized by keeping hem atocrit >30%
Tetanus prophylaxis as indicated
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Medication (Drugs)
Antibiotic regim ens: o
Multidrug regim en:
Am picillin: 2 g IV q6h (peds: 50 m g/kg) and
Clindam ycin: 900 m g IV q8h (peds: 10 m g/kg) and
o
Gentam icin: 5 m g/kg daily load IV q8h
Single-drug regim ens (peds: safety not established)
Am picillin/sulbactam : 3 g IV initial ED dose
Im ipenem : 1 g IV initial ED dose
Piperacillin/tazobactam : 3.375 g IV initial ED dose
Ticarcillin/clavulanate: 3.1 g IV initial ED dose or
Blood products as indicated
Dopam ine or dobutam ine IV drips starting at 5 µg/kg/m in titrating to effect if hypotensive after aggressive hydration
Insulin adjusted to control glucose and acidosis
Pediatric Considerations
More conservative surgical approach
Adequate staphylococcal coverage
Follow-Up Disposition Admission Criteria
All patients with Fournier gangrene require adm ission and surgical ICU care.
Mortality estim ates of 3–38% em phasize need for early
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aggressive care.
Consider early transfer to facility capable of providing adjunctive hyperbaric oxygen therapy if stable for transport.
Discharge Criteria No patients with Fournier gangrene should be discharged.
References 1. Corm an JM, Moody JA, Aronson WJ. Fournier's gangrene in a m odern surgical setting: im proved survival with aggressive m anagem ent. Br J Urol. 1999;84:85–88. 2. Jallali N, Withy S, Butler PE. Hyperbaric oxygen as adjuvant therapy in the m anagem ent of necrotizing fasciitis. Am J Surg. 2005;189:462–466. 3. Morpurrgo E, Galandiuk S. Fournier's gangrene. Surg Clin N Am . 2002;82:1213–1224. 4. Norton KS, Johnson LW, Perry T, et al. Managem ent of Fournier's gangrene: an eleven year retrospective analysis of early recognition, diagnosis, and treatm ent. Am Surg. 2002;68:709–713.
Codes ICD9-CM 608.83
ICD10 N49.8
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > F racture, Open
Fracture, Open
Christy Rosa Mohler
Basics Description
Continuity between skin violation and fracture site, ranging from a puncture wound to grossly exposed bone
Surgical em ergency as delays in care increase risk of infection and rate of com plications
Predisposition to com plications in certain patients: o
Massive soft tissue dam age
o
Severe wound contam ination
o
Com prom ised vascularity
o
Fracture instability
o
Com prom ised host (diabetes, vascular disease)
Diagnosis Signs and Symptoms
Deform ity with nearby violation in skin integrity
Neurovascular com prom ise m ay occur.
Other significant injuries m ay be present: o
Thirty percent of patients with open lower extrem ity
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fractures are m ultiple-traum a victim s.
Essential Workup
Com plete neurologic and vascular exam ination
Plain radiographs including joints above and below the affected area
Tests Lab
CBC, chem istry panel, coagulation studies for large-bone (fem ur, pelvis) fractures or m ultiple-traum a victim s
Type and screen or type and cross-m atch for potential of significant blood loss.
Imaging Doppler or angiography if vascular dam age suspected:
Posterior knee dislocation
Ischem ic extrem ity
Massive soft tissue injury in high-risk areas
Diagnostic Procedures/Surgery
Measurem ent of com partm ent pressures if concern for com partm ent syndrom e
Consider arthrogram by intra-articular injection of saline or m ethylene blue if joint involvem ent suspected.
Angiography if noninvasive techniques inadequate for ruling out vascular com prom ise
Differential Diagnosis Noncontinuous laceration/abrasion
Treatment
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Pre Hospital
Sterile dressings over open wound
Im m obilize joints above and below fracture; splint lim b.
Longitudinal traction of involved extrem ity if distal pulses absent
Traction splint for pain control if prehospital tim e prolonged
Initial Stabilization
Airway, breathing, and circulation m anagem ent
Reduction and im m obilization of fracture with steady, longitudinal traction
ED Treatment
Intravenous access
Keep patient NPO for conscious sedation or OR
Tetanus vaccination, if needed
Parenteral antibiotics within 3 hours of injury
Minim ize num ber of tim es dressing is rem oved to avoid secondary contam ination.
Exam ine regularly for com partm ent syndrom e and neurovascular status.
Early orthopedic consultation for form al irrigation, débridem ent, and operative fixation (if needed): o
Irrigation and treatm ent is optim ally perform ed within 6 hours to reduce likelihood of infection.
Vascular surgery consultation for injuries with vascular dam age
P.431
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Medication (Drugs)
Cefazolin: 1–2 g (peds: 20 m g/kg IM/IV)
Add gentam icin: 6 m g/kg IV, for m ore extensive injuries (peds: 2.5 m g/kg IV)
Add penicillin G: 4–5 m illion U IV, in farm yard injuries and wounds at risk of contam ination with Clostridium or with vascular injury (peds: 50,000 U/kg IV)
Tetanus booster: 0.5 m L IM
Tetanus im m unoglobulin: 250 IU IM if not previously im m unized against tetanus
Morphine sulfate: 2–10 m g (peds: 0.05–0.1 m g/kg per dose IV or equivalent analgesic)
Pediatric Considerations Diphtheria-pertussis-tetanus booster for children younger than 7 years
Follow-Up Disposition Admission Criteria Most patients will be adm itted for irrigation and IV antibiotics and possibly débridem ent or operative fixation.
Discharge Criteria Sim ple open fractures m ay be washed out and im m obilized in the em ergency departm ent after consultation with an orthopaedic surgeon. The patient should be discharged with oral antibiotics and follow-up in 24 hours.
References 1. Behrens FF, Sirkin MS. Fractures with soft tissue injuries. In:
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Browner BD, et al., eds. Skeletal Traum a: Basic Science, Managem ent and Reconstruction. 3rd ed. Philadelphia: WB Saunders; 2003:293–319. 2. Geiderm an JM. General principles of orthopaedic injuries. In: Marx JA, et al., eds. Rosen's Em ergency Medicine: Concepts and Clinical Practice. 5th ed. St. Louis, MO: Mosby–Year Book; 2002:467–492. 3. Menkes JS. Injuries to the bones, joints and soft tissues: initial evaluation and m anagem ent of orthopaedic injuries. In: Tintinalli JE, ed. Em ergency Medicine: A Com prehensive Study Guide. 6th ed. New York: McGraw-Hill; 2004:1651–1665. 4. Zalavras CG, Patzakis MJ. Open fractures: evaluation and m anagem ent. J Am Acad Orthop Surg. 2003;11(3):212–219.
Codes ICD9-CM 829.1 Unspecified bone, open
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > F ractures, Pediatric
Fractures,
Pediatric Adam Z. Barkin
Basics Description
Anatom y: o
Diaphysis: physis to physis; bone shaft
o
Epiphysis: cartilaginous center at or near end of bone that is site of bone growth
o
Physis (equals epiphyseal or m etaphyseal growth plate): radiolucent line between epiphysis and m etaphysis; cartilaginous
o
Metaphysis: region of rapidly growing trabecular bone underlying base of cartilaginous growth plate; between diaphysis and epiphysis
Bones are highly resilient, elastic, and springy
Allow for fractures not seen in adults: o
Greenstick fracture:
Incom plete fracture through cortex on opposite side of im pact
o
Torus (buckle) fracture:
Usually at junction of m etaphysic and diaphysis
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o
Plastic deform ity:
o
Com pression of bone of one cortex
Bowing without disruption of cortex
Fractures involving the physis
Cartilaginous growth plates are potential areas of injury.
Ligam ents m ore resistant to injury than growth plates
Salter-Harris classification: o
Risk of growth disturbance increases from type I to type V.
o
Type I:
Separation of epiphysis from m etaphysis without displacem ent or injury to the growth plate
o
o
Tenderness and pain at point of growth plate
Radiograph typically norm al
Growth disturbance is rare.
Type II:
Metaphyseal fracture extending to physis
Most com m on
Growth disturbance is rare.
Type III:
Intra-articular fracture extending through the epiphysis into the physis
o
Most com m on site is distal tibial epiphysis.
Growth disturbance possible
Type IV:
Epiphyseal, physeal, and m etaphyseal fracture
Intra-articular
Lateral condyle of hum erus is m ost com m on site.
o
Growth disturbance highly likely
Type V:
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Crush injury to epiphyseal plate, producing growth arrest
Usually occurs in joints that m ove in only one plane such as knee or ankle
Fractures often accom pany dislocations.
Nonaccidental traum a (NAT) if history inconsistent with findings
Etiology
Mechanism is useful in defining the potential and type of injury: o
Falls, m otor vehicle accidents, blunt traum a, NAT
Obesity and rapid growth spurts are risk factors.
Com m on fractures include lower forearm , clavicle, tibia or fibula, supracondylar fracture of hum erus.
Nonaccidental traum a (NAT): o
Any fracture in a child younger than 1 year of age in whom history is not consistent with injury
o
Metaphyseal “corner― fractures are pathognom onic.
o
Posterior rib fractures
o
Spiral fem ur fracture
o
Fractures at different stages of healing
o
Skull fractures crossing suture lines, especially in children younger than 1 year
o
Unusual behavior in child or parent
Diagnosis Signs and Symptoms
Decreased lim b m ovem ent, unwilling to use
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Swelling
Tenderness
Deform ity
Ecchym oses
Crepitus
Lim p
Abnorm al neurovascular status of extrem ity
Com partm ent syndrom e:
o
Severe pain, especially in forearm , calf, foot
o
Pain with passive stretching of fingers or toes
o
Sensory deficit in the distal extrem ity
Open fracture m ay be obvious or subtle (collection of blood with fat globules under skin)
History
Mechanism of injury: o
Velocity of car, bike, and so on
o
Height of fall
Neurologic com prom ise
Events surrounding injury
Other injuries
Physical Exam
Thorough secondary survey looking for deform ities, bruising, other injuries
Assess neurovascular status: o
Motor/sensation
o
Distal pulses
o
Capillary refill
Range of m otion of all joints involved
Exclude concurrent injuries
Ensure that history consistent with injury
Essential Workup
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Prom pt im m obilization
Im aging as below
Tests Lab
Required only if concom itant injuries, surgery anticipated, or m ultiple/m ajor bone involvem ent
CBC, erythrocyte sedim entation rate (ESR) if infection suspected
Imaging
Anteroposterior (AP), lateral, and oblique radiographs as necessary, including the joint above and below the fracture
Com parison views m ay be useful if growth plates involved.
Follow-up radiographs at 7–10 days m ay be required to exclude avascular necrosis or Salter I fractures.
Bone scan/CT/MRI m ay be useful to exclude fractures if plain radiographs are unhelpful or to evaluate for infection.
Diagnostic Procedures/Surgery Arthrocentesis if infection is suspected
Differential Diagnosis
Sprain or strain
Contusion
Infection
Tum or
Neurologic deficits
Subtle dislocations such as radial head subluxation (nursem aid's elbow)
NAT
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Treatment Pre Hospital Im m obilization
Initial Stabilization
Resuscitation for concurrent injuries
Im m obilization
ED Treatment
Managem ent of life-threatening concurrent injuries
Pain control
Dislocations require im m ediate assessm ent and attention to neurovascular com prom ise: o
Mechanism helps in understanding the direction of the force required to reduce.
Alignm ent is essential, particularly when fracture involves a joint surface.
Open fractures: o
Require em ergent orthopedic consultation for irrigation and débridem ent
o
IV antibiotic therapy
P.433
Appropriate reporting of NAT
Salter-Harris fractures: o
Type I and type II fractures require im m obilization and orthopedic follow-up.
o
Type II distal fem ur fractures, type III, and type IV require urgent orthopedic consultation for anatom ic reduction.
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o
Type V fractures require im m obilization and consultation.
o
Anatom ic reduction does not elim inate possibility of growth disturbance.
Clavicle fracture: o
Figure-of-eight splint or sling for com fort
o
Distal third clavicle fractures should be referred with initial sling and swathe or shoulder im m obilizer.
Supracondylar hum erus fracture: o
May present with only posterior effusion on lateral radiograph
o
Orthopedic consultation because of potential neurovascular com plications
o
Brachial artery injury, m edian nerve injury possible
o
Volar com partm ent syndrom e of forearm (results in Volkm ann contracture)
o
Epiphyseal injury with long-term growth abnorm alities
Distal radius and ulna fractures: o
Rotational deform ities m ust be elim inated.
o
Reduce angulated fractures >15°
o
Im m obilize for 4–6 weeks.
Colles fracture: o
Reduce by traction in the line of deform ity to disim pact the fragm ents, followed by pressure on the dorsal aspect of the distal fragm ent and volar aspect of the proxim al fragm ent.
o
Correct radial deviation.
o
Im m obilize the hand in ulnar deviation, wrist in neutral, and forearm in full pronation.
o
Orthopedic consultation
Torus fracture (incom plete fracture; buckling or angulation
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on the com pression side of the bone only: o
Most often in distal forearm
Greenstick fracture (incom plete fracture of diaphysis of long bone with fracture on tension side of cortex): o
Im m obilize in long-arm splint for 4–6 weeks.
o
Reduction if angulation >30° in infants, >15° in children
Tibia or fibula fracture: o
Isolated fibular fractures: short-leg walking cast
o
Nondisplaced tibial fracture: long-leg posterior splint, non-weight bearing
o
Displaced tibial fracture and com plex fractures require consultation.
Toddler's fractures: o
Nondisplaced, oblique, distal tibia fracture
o
May need tangential view radiograph or bone scan to diagnose
o
Splint if concern and repeat radiograph in 7–10 days.
Radial head subluxation (nursem aid's elbow): o
Infant or preschooler
o
Longitudinal traction on wrist or hand
o
Radiograph if bony tenderness
o
Reduce with supination and elbow flexion.
o
Follow-up in 24–72 hours.
Slipped capital fem oral epiphysis: o
Disruption though capital fem oral epiphysis
o
Overweight adolescent boys
o
May have referred pain to knee, thigh, or groin
o
Non-weight bearing with prom pt orthopedic follow-up
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Medication (Drugs)
Acetam inophen: 10–15 m g/kg PO/PR (per rectum ) q4h–q6h
Hem atom a block: 1% lidocaine without epinephrine (m ax. 3–5 m g/kg)
Ibuprofen: 10 m g/kg PO q6h–q8h
Morphine: 0.05–0.2 m g/kg SC/IM/IV q2h–q4h
Follow-Up Disposition Admission Criteria
NAT (or per social services)
Potential neurovascular com prom ise/com partm ent syndrom e: o
Condylar or supracondylar hum erus fracture
o
Fem oral shaft
o
Com plete patella
Discharge Criteria
Uncom plicated fracture: no concurrent injury or neurovascular/com partm ent com prom ise
Follow-up arranged and parents understand injury and m anagem ent
Issues for Referral
All Salter-Harris fractures should have orthopedic follow-up.
References 1. Chew FS. Skeletal Radiology: The Bare Bones. 2nd ed. Baltim ore, MD: William s & Wilkins; 1997.
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2. Della-Giustina K, Della-Giustina DA. Em ergency departm ent evaluation and treatm ent of pediatric orthopedic injuries. Em erg Med Clin North Am . 1999;17:895–922. 3. Marx JA. Rosen's Em ergency Medicine Concepts and Clinical Practice. 5th ed. St. Louis, MO: Mosby; 2002. 4. Musgrave DS, Mendelson SA. Pediatric orthopedic traum a: principles in m anagem ent. Crit Care Med. 2002;30:S431–443. 5. Rodriguez-Merchan EC. Pediatric skeletal traum a: a review and historical perspective. Clin Orthop Relat Res. 2005;432:8–13.
Miscellaneous SEE ALSO: Conscious Sedation; C-spine Fractures, Pediatric; Fractures, Open; Nursem aid's Elbow; Shoulder Dislocation; Slipped Capital Fem oral Epiphysis
Codes ICD9-CM 829.0
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > F ro stbite
Frostbite
Paul Arnold
Basics Description Tissue dam age caused by cold tem perature exposure
Mechanism
Tissue dam age results from : o
Direct cell dam age: owing to intracellular ice crystal form ation
o
Indirect cell dam age: extracellular ice crystal form ation leads to intracellular dehydration through osm osis.
o
Microvascular stasis and throm bosis: erythrocyte sludging leads to hypoxia, then vasospasm , ischem ia, tissue necrosis.
o
Progressive derm al ischem ia: m ediated by throm boxane and prostaglandins in blisters
o
Reperfusion injury: occurs after thawing; is caused by edem a, then throm bosis, inflam m atory leukocyte infiltration, and necrosis
o
Therm al shock: direct cell death owing to the extrem e cold
Devitalized tissue dem arcates as the injury evolves over
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weeks to m onths, hence the expectant m anagem ent of severe frostbite
Etiology
Cold exposure
Vulnerability increased owing to: o
Extrem es of age
o
Poor self-care:
o
Intoxication
Altered m ental status
Im m obility
Poor circulatory status
Diagnosis Signs and Symptoms
Extrem ities (fingers, toes) and head (ears, nose) m ost com m only affected
Initial appearance of an injury often fails to predict eventual depth or outcom e
Superficial Frostbite
Only skin structures involved: o
No tissue loss
Frozen skin loses touch, pain, or tem perature sensation.
Stinging, num bness, burning
Appearance: o
Initially white/waxy/m ottled
o
Becom es hyperem ic and edem atous as warm ing progresses
Rewarm ing leads within 3 hours to hyperem ia, swelling, and pain, which resolve within 2–3 days.
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Deep Frostbite
Subcutaneous, m uscle, nerve, or bone involved: o
Tissue loss inevitable
Initially insensate, injuries develop severe pain/burning on rewarm ing.
Tissue feels hard, woody to the touch.
Postrewarm ing appearance:
o
Edem a within 3 hours and lasts 5 days
o
Large clear blebs within 6–24 hours
o
Sm all, hem orrhagic blebs form after 24 hours,
o
Eschar form s in 9–15 days,
o
Mum m ification in 3–6 weeks
Reduced m obility, persistent m ottling, anesthesia despite edem a after rewarm ing are unfavorable prognostic indicators.
Devitalized tissue dem arcates as the injury evolves over weeks to m onths.
Essential Workup
Diagnosis is based on the clinical presentation.
Look for underlying factors contributing to cold exposure and co-m orbid conditions requiring em ergency m anagem ent: o
Intoxication
o
Head injury
o
Traum a
o
Hypoglycem ia
o
Cardiac or neurologic problem s
Tests Lab
None indicated in m ild cases
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For severe frostbite: o
CBC
o
Electrolytes, BUN/creatinine, glucose
o
Urinalysis for evidence for m yoglobinuria
Cultures and Gram stains from open areas when infection suspected
Imaging Technetium -99 scintigraphy:
Helpful in early identification of unsalvageable bone
Perm its earlier decision about am putation
Perform 2–7 days after cold injury.
Differential Diagnosis
Frostnip: o
Superficial, reversible ice crystal form ation without tissue destruction
o
Transient num bness and paresthesia resolve after rewarm ing.
Trench foot: o
Exposure to wet cold for prolonged periods
o
Neurovascular dam age without ice crystal form ation
o
Pallor, m ottling, paresthesias, pulselessness, paralysis, and num bness
o
Hyperem ia with rewarm ing lasting up to 6 weeks
Chilblains: o
Chronic repeated exposure to dry cold
o
Localized erythem a, cyanosis, plaques, and vesicles
Treatment Pre Hospital
Pa ge 1 9 6
Protect and im m obilize frostbitten area during transport.
Rem ove restrictive or wet garm ents.
Avoid dry rewarm ing of the frostbitten lim b if there is a likelihood of refreezing of the injury during transport.
If evacuation will be delayed and suitable facilities are available, field rewarm ing in warm (40–42°C) water can be attem pted.
Rubbing, m anipulating the lim b, or applying snow while it is still frozen is contraindicated.
P.435
Alert
Hypotherm ia: o
Com m on in frostbite victim s
o
In the severely hypotherm ic patient, avoid rough handling to m inim ize risk of cardiac dysrhythm ias.
Initial Stabilization
Airway, breathing, and circulation (ABCs) m anagem ent
Identify and correct hypotherm ia.
IV fluid volum e expansion with 0.9% norm al saline (NS) for severe frostbite
Protect frostbitten areas from excessive handling or dry warm ing during resuscitation.
ED Treatment
If the injury is Table o f C o ntents > G allsto ne Ileus
Gallstone Ileus
Edward A. Stettner
Basics Description
Mechanical intestinal obstruction secondary to im paction of a gallstone within bowel lum en
Stone is usually larger than 2.5 cm
1–5% of all intestinal obstructions
Most cases occur in patients older than 65 years: o
25% of bowel obstructions in patients older than 65 years
5:1 fem ale to m ale predom inance
Mortality 15–18%
Etiology
Chronic gallbladder inflam m ation causes adhesions between gallbladder and adjacent bowel wall.
Cholecystenteric fistula develops, perm itting stone passage into intestine: o
Duodenum is m ost com m on site of fistula form ation, followed by colon.
o
Gastric fistulas are rare.
Site of im paction: o
Term inal ileum m ost com m on (54–65%):
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Narrowest part of sm all intestine
o
Jejunum (27%)
o
Duodenum (1–3%):
Gastric outlet obstruction caused by duodenal im paction referred to as Bouveret syndrom e
o
Colonic obstruction is rare.
Stones spilled intraperitoneally during cholecystectom y—open or laparoscopic—m ay also lead to bowel obstruction: o
Can have recurrent obstruction from subsequent gallstones
Diagnosis Signs and Symptoms
“Tum bling― abdom inal discom fort: o
Episodic abdom inal pain as stone lodges and dislodges throughout the intestines
o
Com plete im paction leads to severe, often acute abdom inal pain.
Nausea
Vom iting: o
Can be bilious or feculent
Obstipation
Abdom inal distention and tym pany
Abdom inal tenderness: o
Peritoneal findings late
Abnorm al bowel sounds
Occasional jaundice
Only 50–60% of patients have history of biliary colic or disease.
Pa ge 1 9 7
Essential Workup Evaluation for intestinal obstruction
Tests Lab
Electrolytes, BUN/creatinine, glucose since decreased oral intake and vom iting leads to: o
Hypochlorem ia
o
Hypokalem ia
o
Hyponatrem ia
o
Alkalosis
o
Pre–renal azotem ia
Liver function panel and bilirubin m ay be elevated.
Am ylase: o
Elevated in late obstructions
CBC/hem atocrit: o
Hem oconcentration secondary to dehydration
o
Elevated WBC nonspecific
Imaging
Flat and upright abdom inal radiographs: o
Multiple air fluid levels and distended bowel consistent with bowel obstruction
o
Rigler triad: 2 of 3 pathognom onic (present in 30–50%)
Air in the biliary tree (pneum obilia)
Partial or com plete bowel obstruction
Ectopic stone visualized within the intestinal tract
Chest radiograph: o
Evaluate for pneum operitoneum
Abdom inal CT scan:
Pa ge 1 9 7
o
Increasing use in evaluating sm all bowel obstruction
o
Can directly visualize and localize stone within intestinal lum en
Abdom inal ultrasonography: o
Can identify pneum obilia and gallstones, but lower yield in locating obstructing stone
Differential Diagnosis
Paralytic ileus
Extrinsic bowel obstruction: o
Adhesions
o
Volvulus
o
Hernia
o
Intussusception
Gastrointestinal m alignancy
Diverticulitis
Bezoar
Inflam m atory bowel disease
Pseudo-obstruction
Cholecystitis
Ascending cholangitis
Pancreatitis
P.437
Treatment Initial Stabilization IV fluid resuscitation
ED Treatment
Pa ge 1 9 7
Nasogastric suction to decom press the stom ach and intestine
Nothing PO
Electrolyte replacem ent
Monitor urine output.
Analgesics
Broad-spectrum antibiotics to cover bowel flora: o
Piperacillin/tazobactam
o
Am picillin/sulbactam
o
Ticarcillin/clavulanate
o
Alternatives include im ipenem , m eropenem , third-generation cephalosporins plus m etronidazole.
Surgical consultation
Medication (Drugs)
Am picillin/sulbactam : 3 g (peds: 100–200 m g/kg/24h) IV q6h
Piperacillin/tazobactam : 3.375 g (peds: 240–400 m g/kg/24h) IV q6h
Ticarcillin/clavulanate: 3.1 g IV q4h–q6h
Follow-Up Disposition Admission Criteria
Adm it all patients with gallstone ileus.
Surgical evaluation for em ergent operative intervention
Discharge Criteria None
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References 1. Bennett G, Balthazar E. Ultrasound and CT evaluation of em ergent gallbladder pathology. Radiol Clin North Am . 2003;41:1203–1216. 2. Delabrousse E, Bartholom ot B, et al. Gallstone ileus: CT findings. Eur Radiol. 2000;10:938–940. 3. Lobo D, Jobling J, et al. Gallstone ileus: diagnostic pitfalls and therapeutic successes. J Clin Gastroenterol. 2000;30(1):72–76. 4. Marschall J, Hayton S. Bouveret's syndrom e. Am J Surg. 2004;187:547–548 5. Rosenberg M, Parsiak K. Vom iting gravel. Am J Em erg Med. 2004;22(2):131–132.
Codes ICD9-CM 560.31 Gallstone ileus
ICD10 K56.3 Gallstone ileus
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > γ-G HB, Po iso ning
γ-GHB, Poisoning
Amy V. Kontrick Mark B. Mycyk
Basics Description
Naturally occurring analog of γ-am inobutyric acid (GABA)
Used m edically for narcolepsy
Nonm edical uses: o
Bodybuilding agent
o
Euphoric agent
o
Date-rape/predatory agent
Onset of activity: 15–30 m inutes after ingestion
Duration of effect: 2–6 hours
Etiology Deliberate or accidental ingestion of γ-hydroxybutyrate (GHB)
Diagnosis Signs and Symptoms
Central nervous system : o
CNS depression
Pa ge 1 9 7
o
Ataxia/dizziness
o
Im paired judgm ent
o
Aggressive behavior
o
Clonic m ovem ents of the extrem ities
o
Com a
o
Seizures
Pulm onary: o
Respiratory depression
o
Apnea
o
Laryngospasm (rare)
Gastrointestinal: o
Nausea
o
Vom iting
Cardiovascular: o
Bradycardia
o
Atrioventricular block
o
Hypotension
Other: o
Nystagm us
o
Hypotherm ia
Withdrawal sym ptom s: o
Hypertension
o
Tachycardia
o
Hypertherm ia
o
Agitation
o
Diaphoresis
o
Trem ors
o
Nausea, vom iting, and abdom inal cram ping
o
Hallucinations, delusions, and psychosis
Essential Workup
Diagnosis based on clinical presentation and an accurate history
Pa ge 1 9 8
Exclude coingestants if signs and sym ptom s inconsistent with GHB intoxication.
Tests Lab
Confirm atory GHB screen is typically a send-out lab and does not change ED m anagem ent.
Urine toxicology screen to exclude coingestants
Serum alcohol level
Urinalysis and creatine kinase (CPK) if suspected rhabdom yolysis from prolonged im m obilization or agitation
Imaging
ECG: o
Sinus bradycardia
o
Atrioventricular block
Chest radiograph: o
Aspiration pneum onia
Head CT if suspected occult head traum a
Differential Diagnosis
Alcohol intoxication
Barbiturate overdose
Benzodiazepine overdose
Neuroleptic overdose
Opiate overdose
Withdrawal: o
Alcohol withdrawal
o
Sedative-hypnotic withdrawal
Treatment
Pa ge 1 9 8
Pre Hospital
Transport all pills/bottles and drug paraphernalia involved in overdose for identification in em ergency departm ent.
γ-Hydroxybutyrate (GHB) precursors (γ-butyrolactone [GBL], 1,4 butanediol [1,4-BD], GHV [γ-hydroxyvalerate], and GVL) have sam e effects as γ-hydroxybutyrate.
Initial Stabilization
ABCs (airway, breathing, circulation): o
Airway control essential
o
Adm inister supplem ental oxygen.
o
Intubate if indicated.
Adm inister thiam ine, dextrose (or Accu-Chek), and naloxone for depressed m ental status.
ED Treatment
Supportive care
Bradycardia:
o
Atropine
o
Tem porary pacing
Hypotension: o
0.9% norm al saline IV fluid bolus
o
Trendelenburg
o
Dopam ine titrated to pressure
Seizures: o
Treat initially with benzodiazepine.
o
Treat refractory seizures with phenobarbital.
Withdrawal: o
Treat aggressively with benzodiazepine.
o
Treat with phenobarbital or propofol if large doses of benzodiazepines unsuccessful.
P.451
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Medication (Drugs)
Dextrose: 50–100 m L D 5 0 (peds: 2 m L/kg of D 2 5 over 1 m inute) IV; repeat if necessary
Diazepam : 5–10 m g (peds: 0.2–0.5 m g/kg) IV q10–15m in
Dopam ine: 2–20 µg/kg/m in with titration to effect
Lorazepam : 2–4 m g (peds: 0.03–0.05 m g/kg) IV q10–15m in
Naloxone: 0.4–2 m g (peds: 0.1 m g/kg; neonatal: 10–30 µg/kg) IV or IM
Phenobarbital: 10–20 m g/kg IV (loading dose)
Propofol: 0.5–1.0 m g/kg IV (loading dose), then 5–50 µg/kg/m in (m aintenance dose)
Thiam ine (vitam in B 1 ): 100 m g (peds: 50 m g) IV or IM
Follow-Up Disposition Admission Criteria
Intubated patient
Patient with hypotherm ia or other hem odynam ic instability
Coingestion prolonging duration of intoxication
Discharge Criteria
Asym ptom atic after 6 hours of observation
No clinical evidence of withdrawal syndrom e
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Issues for Referral Consider substance abuse referral for patients.
References 1. Caldicott DG, Chow FY, Burns BJ, et al. Fatalities associated with the use of gam m a- hydroxybutyrate and its analogues in Australasia. Med J Aust. 2004;181(6):310–313. 2. Dyer JE, Roth B, Hym a BA. Gam m a- hydroxybutyrate withdrawal syndrom e. Ann Em erg Med. 2001;37:147–153. 3. Gahlinger PM. Club drugs: MDMA, gam m a- hydroxybutyrate (GHB), Rohypnol, and ketam ine. Am Fam Physician. 2004;69(11):2619–2926. 4. Li J, Stokes SA, Wockener A. A tale of novel intoxication: a review of the effects of γ-hydroxybutyric acid with recom m endations for m anagem ent. Ann Em erg Med. 1998;31:729–736. 5. Shannon M, Quang LS. Gam m a-hydroxybutyrate, gam m a-butyrolactone, and 1,4-butanediol: a case report and review of the literature. Pediatr Em erg Care. 2000;16:435–440.
Codes ICD9-CM 967.8 Poisoning by sedatives and hypnotics, other
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > G angrene
Gangrene
Karen B. Van Hoesen
Basics Description
Gas gangrene or clostridial m yonecrosis
An acute, rapidly progressive, gas-form ing necrotizing infection of m uscle and subcutaneous tissue
Can be seen in posttraum atic or postoperative situations
Etiology
Clostridial organism s: o
Facultative anaerobic, spore-form ing, gram -positive bacillus
o
Produce a num ber of toxins; the m ost prevalent and lethal is α-toxin
Clostridium perfringens is the m ost com m on bacteria; found in 80–90% of wounds
Other clostridial bacteria include Clostridium novyi, Clostridium septicum , Clostridium histolyticum , Clostridium biferm entans and Clostridium fallax.
Two distinct m echanism s for introduction of clostridial organism s: o
Traum atic and postoperative
o
Nontraum atic associated with diabetes m ellitus,
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peripheral vascular disease, alcoholism , IV drug abuse, and m alignancies
Diagnosis Signs and Symptoms
Sudden severe pain of extrem ity or involved area
Low-grade fever
Tachycardia out of proportion to fever
Bronzing of the skin over involved area
Crepitus
Form ation of blebs and bullae
Thin, serosanguineous exudate and sweet odor
Rapid local extension
Obtunded sensorium
System ic toxicity
Essential Workup
History and physical exam with special attention to clinical evidence of crepitus in soft tissue
Soft tissue x-rays of involved area to detect gas dissecting along fascial planes: o
The absence of gas does not rule out significant disease.
Stat gram stain of wound exudate for gram -positive bacillus with paucity of leukocytes
Tests Lab
CBC with differential, electrolytes, blood urea nitrate, and creatinine
Coagulation studies
Pa ge 1 9 8
Evaluate for hem olysis
Stat gram stain of wound exudate
Anaerobic cultures of wound or tissue biopsy
Imaging
Radiographs m ay reveal soft tissue gas.
CT if area involves abdom en or flank
Diagnostic Procedures/Surgery All patients with gas gangrene m ust undergo surgical debridem ent.
Differential Diagnosis
Cellulitis
Necrotizing fasciitis
Nonclostridial m yositis and m yonecrosis
Other causes of gas in tissues, as from dissection from respiratory or gastrointestinal tracts
Treatment Initial Stabilization Manage airway and resuscitate as indicated:
Rapid sequence intubation as needed
Supplem ental oxygen: o
Cardiac and oxygen saturation m onitors should be placed
IV access; consider central venous pressure m onitoring
Aggressive volum e expansion, including crystalloid, plasm a, packed RBCs, and album in if septic shock
ED Treatment
Parenteral antibiotic therapy: o
Prim ary: penicillin G plus clindam ycin
Pa ge 1 9 8
o
Alternative: ceftriaxone or erythrom ycin
o
If m ixed infection: penicillin plus clindam ycin, m etronidazole, or vancom ycin and gram -negative coverage with gentam icin
Surgical consultation: o
Débridem ent, am putation, or fasciotom y are required.
Hyperbaric oxygen as adjunctive therapy: o
Early transfer to hyperbaric facility m ay be life saving
Tetanus prophylaxis
Observe for m ajor com plications including acute respiratory distress syndrom e, renal failure, m yocardial irritability, and dissem inated intravascular coagulation
Polyvalent antitoxin is not m ade in the United States, and studies have not dem onstrated efficacy: o
Because of the unacceptable hypersensitivity reactions, it is not routinely recom m ended.
P.439
Medication (Drugs)
Ceftriaxone: 2.0 g (peds: 100 m g/kg/24h m ax. 4 g) IV q24h
Clindam ycin: 900 m g (peds: 40 m g/kg/d q6h) IV q8h.
Gentam icin: 2.0 m g/kg (peds: 2.0 m g/kg IV q8h) IV q8h
Metronidazole: 500 m g (peds: safety not established) IV q8h
Penicillin G: 24 m illion IU/24 hours (peds: 250,000 IU/kg/24h) IV q4h–q6h
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Tetanus im m une globulin: 500 IU IM
Tetanus toxoid: 0.5 m g IM
Follow-Up Disposition Admission Criteria
All patients with gas gangrene and evidence of m yonecrosis m ust be adm itted for surgical débridem ent and IV antibiotics.
Use of hyperbaric oxygen therapy is an im portant adjunct.
Discharge Criteria No patient with acute gangrene should be discharged.
Issues for Referral After stabilization with antibiotics and surgical debridem ent, consider referral for hyperbaric oxygen treatm ent as an adjunct.
References 1. Brook I. Microbiology and m anagem ent of m yositis. Int Orthop. 2004;28(5):257–260. 2. Clark LA, Moon RE. Hyperbaric oxygen in the treatm ent of life-threatening soft-tissue infection. Respir Care Clin North Am . 1999;5(2):203–219. 3. Headley AJ. Necrotizing soft tissue infections: a primary care review. Am Fam Physician. 2003 15;68(2):323–328. 4. Langhan M, Arnold L. Clostridial m yonecrosis in an adolescent m ale. Pediatrics. 2005;116(5):e735–737. 5. Perry BN, Floyd WE 3rd. Gas gangrene and necrotizing fasciitis in the upper extrem ity. J Surg Orthop Adv. 2004;13(2):57–68.
Codes
Pa ge 1 9 8
ICD9-CM 040.0
ICD10 R02
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > G astric Outlet Obstructio n
Gastric Outlet
Obstruction Jenny Lu
Basics Description
Mechanical obstruction that im pedes gastric em ptying, resulting from any disease process
Benign and m alignant causes: o
Edem a, scarring, stricture or hyperplasia of pylorus or duodenum
o
Intrinsic or extrinsic m ass, causing com pression at pylorus or at proxim al duodenum
Etiology
Peptic ulcer disease
Pyloric stenosis (m ost com m on in pediatric population)
Neoplasm s (pancreatic m ost com m on)
Inflam m ation/edem a
Strictures/webs
Caustic ingestions
Gallstone obstruction
Pa ge 1 9 9
Diagnosis Signs and Symptoms History
Interm ittent sym ptom s until obstruction becom es com plete
Vom iting, usually nonbilious
Abdom inal pain variable
Early satiety and epigastric fullness
Epigastric discom fort relieved with em esis
Physical Exam
Vital signs: o
Usually norm al
o
Tachycardia, hypotension with significant volum e depletion
Weight loss in chronic, and with m alignancy
Abdom inal exam ination:
o
Variable epigastric distention
o
Tym pany
o
Succession splash >4 hours after eating
Malnutrition in chronic or late obstruction
Pediatric Considerations
Abdom inal pain, nausea/vom iting: very com m on in elderly patients with acute m yocardial infarctions o
Obtain ECG in elderly/at risk of coronary artery disease
Pediatric Considerations
Pyloric stenosis: o
Most com m on cause in pediatric population
o
Early as first week up to age 3 m onths
Initially occasional nonprojectile postprandial vom iting,
Pa ge 1 9 9
progressing to projectile (nonbilious) vom iting
Midepigastric peristaltic wave prior to vom iting m ay be seen.
Epigastric “olive― m ass palpable in 80% to 90% of patients
Essential Workup
Careful history and physical exam
Abdom inal ultrasound (US) in pediatric patients: o
Reveals elongated hypertrophic pyloric sphincter
Tests Lab
CBC: o
Anem ia if blood loss from ulcer
o
High hem atocrit indicates hem oconcentration.
Electrolytes, BUN/creatinine, glucose: o
Hypokalem ia
o
Hypochlorem ic m etabolic alkalosis
o
Hypoglycem ia
o
Prerenal azotem ia
Urinalysis
Am ylase/lipase
Liver function tests, if m alignancy suspected
Helicobacter pylori, if peptic ulcer disease (PUD) suspected
Imaging
Plain abdom inal radiographs (obstructive series): o
Dilated stom ach
o
Absence of air in bowel distally
Abdom inal CT for detecting neoplastic causes of obstruction
P.441
Pa ge 1 9 9
Diagnostic Procedures/Surgery
Upper GI: o
To dem onstrate site of obstruction
Upper endoscopy: o
To visualize gastric outlet
Differential Diagnosis
Proxim al bowel obstruction
Exacerbation of peptic ulcer disease
Gastroenteritis
Cholelithiasis
Cholecystitis
Acute pancreatitis
Diabetic gastroparesis
Psychogenic vom iting
Treatment Initial Stabilization
0.9% norm al saline (NS) IV fluid resuscitation for prolonged obstruction and significant volum e depletion:
o
Adults: 1 L bolus
o
Peds: 20 m L/kg bolus
Correct electrolyte abnorm alities, especially hypokalem ia.
ED Treatment
Nasogastric tube (NGT)
Foley catheter to m onitor urine output
Surgical consultation/intervention:
Pa ge 1 9 9
o
Balloon dilatation of benign strictures
o
Enteral stent placem ent (m alignant causes)
o
Gastrojejunostom y (m alignant causes)
o
Vagotom y and antrectom y or pyloroplasty or gastrojejunostom y or other variation (benign causes)
Medication (Drugs)
Fam otidine: adults: 20 m g (peds: 0.6–0.8 m g/kg/24h div. q6h–q8h) IV q12h or
Ranitidine: adults: 50 m g (peds: 2–4 m g/kg/24h div. q6h–q8h) IV q8h
Pantoprazole: adults: 40 m g IV daily (also H. pylori treatm ent as needed)
Follow-Up Disposition Admission Criteria All patients with gastric outlet obstruction require adm ission for fluid resuscitation and possible surgical intervention.
References 1. Castellanos, Andres E. Gastric Outlet Obstruction. Available at http://www.em edicine.com /m ed/topic2713.htm . Last updated July 27, 2005. 2. Feldm an M, Friedm an LS, Sleisenger MH, eds. Feldm an, Sleisenger & Fordtran's Gastrointestinal and Liver Disease. 6th ed. Philadelphia: WB Saunders; 1998:666–668. 3. Lam Y, et al. Endoscopic balloon dilatation and Helicobacter pylori
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eradication in the treatm ent of gastric outlet obstruction. Gastrointest Endosc. 1997;46(4):379–380. 4. Marx, JA. Rosen's Em ergency Medicine: Concepts and Clinical Practice. 5th ed. St. Louis, MO: Mosby; 2002:1243. 5. Shaffer H. Perforation and obstruction of the gastrointestinal tract. Radiol Clin North Am . 1992;30:405. 6. Sivit C. Gastrointestinal em ergencies in older infants and children. Radiol Clin North Am . 1997;35:865. 7. Thom as M. Enteral Stents for the Palliation of Gastroduodenal Obstruction. Available at http://www.uptodate.com . Last updated Novem ber 15, 2005.
Codes ICD9-CM 537.0
ICD10 K31.1
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > G astritis
Gastritis
Jason M. Lebwohl
Basics Description
Inflam m atory response of gastric m ucosa to injury
Three lines of defense of gastric m ucosa: o
Mucous layer that form s protective pH gradient
o
Surface epithelial cells that can repair sm all defects
o
Postepithelial barrier that neutralizes any acid that has traversed first two layers
No definite link between histologic gastritis and dyspeptic sym ptom s
Etiology Acute Gastritis
Stress (sepsis, burns, traum a): o
Decrease in splanchnic blood flow leading to decreased m ucus production, bicarbonate secretion, and prostaglandin synthesis
o
Results in m ucosal erosions and hem orrhage
Alcohol: o
Induces production of leukotrienes that cause m icrovascular stasis, engorgem ent, and increased
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vascular perm eability o
Leads to hem orrhage
Nonsteroidal anti-inflam m atory drugs (NSAIDs), including aspirin: o
Interfere with prostaglandin synthesis, leading to sim ilar cascade as induced by alcohol
o
Results in m ucosal erosions
Steroids
Chronic Gastritis
Produced by Helicobacter pylori
Mechanism of H. pylori unclear: o
Gram -negative spiral bacteria found in gastric m ucous layer
o
Contains enzym e urease that allows it to change pH level (alkaline) of its m icroenvironm ent
Diagnosis Signs and Symptoms History
Dyspepsia
Epigastric pain or discom fort (episodic and chronic)
Bloating, indigestion, eructation, flatulence, and heartburn
Anorexia, nausea/vom iting
Dehydration, tachycardia, and electrolyte disturbances (with vom iting)
Hem atem esis, m elena, pallor, and signs of volum e depletion (hem orrhagic gastritis)
Physical Exam
Careful physical exam including stool Hem occult testing
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and vital signs with orthostatics
Nasogastric tube (NGT) when history of hem atem esis or unstable vital signs
Abdom inal exam nonspecific
Essential Workup
Airway, breathing, and circulation m anagem ent (ABCs)
Hem atocrit determ ination
Evaluation for dehydration/shock
Tests Lab
Norm al laboratory values in uncom plicated gastritis
CBC: o
Anem ia with acute hem orrhagic gastritis
o
Leukocytosis: infection
Electrolytes, BUN, creatinine, glucose
Am ylase/lipase for pancreatitis in differential
Urinalysis: o
Assess dehydration/ketosis (starvation)
o
Bilirubin present with hepatitis
Imaging No specific im aging studies
Diagnostic Procedures/Surgery
ECG: o
For elderly patients
o
Myocardial ischem ia in differential
Endoscopy: o
Outpatient unless significant hem orrhage
o
Allows for visualization of bleeding sites, histologic confirm ation of m ucosal inflam m ation, and detection of H. pylori
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Noninvasive H. pylori testing: o
13
C and
14
C urea breath tests
o
Stool antigen test
o
Serology to detect antibodies to H. pylori
Differential Diagnosis
Peptic ulcer disease (PUD)
Nonulcer dyspepsia (sym ptom s without ulcer on endoscopy)
Gastroesophageal reflux
Biliary colic
Cholecystitis
Pancreatitis
Hepatitis
Abdom inal aortic aneurysm
Aortic dissection
Myocardial infarction
Treatment Pre Hospital
ABCs
IV fluid resuscitation
Initial Stabilization
ABCs with acute erosive or hem orrhagic gastritis that presents with hem odynam ic instability
IV fluid resuscitation with lactated Ringer solution or 0.9% norm al saline (NS) via two large-bore catheters
NGT for gastric decom pression and lavage
Foley catheterization to assess volum e replacem ent
P.443
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ED Treatment Pain control with:
Antacids
GI cocktail: o
30 m L antacids plus 10–20 m L viscous lidocaine
H 2 antagonists
Sucralfate
Avoid narcotics—m ay m ask serious illness
Acute Hemorrhagic Gastritis
IV fluid resuscitation
Blood transfusion if low hem atocrit
Reverse causes (alcohol, sepsis, NSAIDs, or traum a)
Prevent acute or erosive gastritis in critically ill: o
Antacids hourly or IV proton pum p inhibitors (PPI) or H 2 antagonists
o
Goal is to keep pH level at >4.
Chronic Gastritis
Treatm ent of H. pylori infection: o
Invasive or noninvasive testing to confirm infection
o
Oral (PO) eradication antibiotic therapy options:
Most com m on regim en consists of PPI (om eprazole 20 m g or lansoprazole 30 m g) plus clarithrom ycin 500 m g and am oxicillin 1 g, all taken b.i.d. for 2 weeks.
For penicillin-allergic patients: PPI plus clarithrom ycin 500 m g b.i.d. plus m etronidazole 500 m g b.i.d. for 14 days
H 2 blocker, bism uth subsalicylate (Pepto-Bism ol) plus either am oxicillin 1,000 m g
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b.i.d. or tetracycline 500 m g q.i.d. in com bination with either m etronidazole 250 m g q.i.d. or clarithrom ycin 500 m g b.i.d. for 14 days o
Resistance:
Increasing antibiotic resistance to m etronidazole (30–48%), and clarithrom ycin (>10%)
Uncom m on resistance to am oxicillin and tetracycline
No resistance to bism uth
Treatm ent controversial for asym ptom atic or nonulcer dyspepsia gastritis
Vitam in B 1 2 supplem entation for atrophic gastritis
Medication (Drugs)
Bism uth subsalicylate: 525-m g tabs 2 PO q.i.d.
Cim etidine (H 2 -blocker): 800 m g PO at bedtim e nightly (peds: 20–40 m g/kg/24h) for 6–8 weeks
Fam otidine (H 2 -blocker): 40 m g PO at bedtim e nightly (peds: 0.5–0.6 m g/kg q12h) for 6–8 weeks
Lansoprazole (PPI): 30 m g PO b.i.d. for 2 weeks
Maalox plus: 2 to 4 tablets PO q.i.d.
Misoprostol: 100–200 µg PO q.i.d.
Mylanta II: 2–4 tablets PO q.i.d.
Nizatidine (H 2 -blocker): 300 m g PO at bedtim e nightly for 6–8 weeks
Om eprazole (PPI): 20 m g PO b.i.d. (peds: 0.6–0.7 m g/kg q12h–q24h) for 2 weeks
Pantoprazole (PPI): 40 m g PO/IV daily for 2 weeks
Ranitidine (H 2 -blocker): 300 m g PO at bedtim e nightly
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(peds: 5–10 m g/kg/24h given q12h) for 6–8 weeks
Sucralfate: 1 g PO q.i.d. for 6–8 weeks
Follow-Up Disposition Admission Criteria
Acute hem orrhagic or erosive gastritis that presents with upper GI tract bleeding, tachycardia, and hypotension
Uncontrolled pain or vom iting
Coagulopathy from m edication or liver disease
Discharge Criteria
Unrem arkable physical exam with norm al CBC and hem e-negative stools
If hem e-positive stools, discharge if stable vital signs, norm al hem atocrit, and negative NGT aspiration for upper GI tract hem orrhage: o
Outpatient evaluation for endoscopy
Issues for Referral Outpatient referral for endoscopy and H. pylori testing
References 1. Czinn SJ. Helicobacter pylori infection: detection, investigation, and m anagem ent. J Pediatr. 2005;146:S21–26. 2. Eswaran S, Roy MA. Medical m anagem ent of acid-peptic disorders of the stom ach. Surg Clin North Am . 2005;85:895–906. 3. Leung WK, et al. Ulcer and gastritis. Prim Care. 2001;28(3):487–503. 4. McGuirk TD, et al. Upper gastrointestinal tract bleeding. Em erg Med Clin North Am . 1996;14(3):530–533.
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5. Sm oot DT, Go MF, Cryer B. Peptic ulcer disease. Prim Care. 2001;33(1):8–15. 6. Sung JJ, Chung SC, et al. Antibacterial treatm ent of gastric ulcers associated with Helicobacter pylori. N Engl J Med. 1995;332:139–142.
Miscellaneous SEE ALSO: Gastrointestinal Bleeding; Gastroesophageal Reflux Disease; Peptic Ulcer Disease
Codes ICD9-CM 535.5
Pa ge 2 0 0
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > G astro enteritis
Gastroenteritis
Isam Nasr Harminder Brar
Basics Description Inflam m ation of stom ach and intestines associated with diarrhea and vom iting; often result of infectious or toxin exposure
Etiology Infectious
Viruses: o
50–70% of all cases
Invasive bacteria: o
Cam pylobacter: contam inated food or water, wilderness water, birds and anim als:
o
Most com m on cause
Gross or occult blood is found in 60–90%.
Salm onella: contam inated water, eggs, poultry, or dairy products:
Typhoid fever (Salm onella typhi) characterized by unrem itting fever, abdom inal pain, rose spots, splenom egaly, and bradycardia
Im m unocom prom ised susceptible
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o
Shigella: fecal-oral route
o
Vibrio parahaem olyticus: raw and undercooked seafood
o
Yersinia: contam inated food (pork), water, and m ilk:
May present as m esenteric adenitis or m im ic appendicitis
Specific food-borne disease (food poisoning): o
o
o
Staphylococcus aureus:
Most com m on toxin-related disease
Sym ptom s 1–6 hours after ingesting food
Bacillus cereus:
Classic source is fried rice left on steam tables.
Sym ptom s within 1–36 hours
Cholera: profuse watery stools with m ucous (rice-water stools)
o
Ciguatera:
Fish intoxication
Onset 5 m inutes to 30 hours (average 6 hours) after ingestion
Paresthesias, hypotension, peripheral m uscle weakness
o
Am itriptyline m ay be therapeutic.
Scom broid:
Caused by blood fish: tuna, albacore, m ackerel, and m ahi m ahi
Flushing, headache, erythem a, dizziness, blurred vision, and generalized burning sensation
Sym ptom s last 10–15% dehydration
Discharge Criteria
Mild cases requiring oral hydration
Dehydration responsive to IV fluids
References 1. Bitterm an R. Acute gastroenteritides. In: Marx JA, Hockberger RS, Walls RM, et al. eds. Rosen's Em ergency Medicine: Concepts and Clinical Practice. 5th ed. St. Louis, MO: Mosby; 2002: 1301–1325. 2. Blacklow NR, Greenberg HB. Viral gastroenteritis. N Engl J Med. 1991;325:252.
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3. Dupont HL. What's new in enteric infectious diseases at hom e and abroad. Curr Opinion Infect Dis. 2005;18:407–412.
Miscellaneous SEE ALSO: Diarrhea, Adult; Diarrhea, Pediatric
Codes ICD9-CM 558.9
ICD10 A06
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > G astro eso phageal Reflux Disease
Gastroesophageal Reflux Disease Jason M. Lebwohl
Basics Description
Spectrum of pathology in which gastric reflux causes sym ptom s and dam age to esophageal m ucosa
Reflux esophagitis versus nonerosive reflux disease
Approxim ately 40% of general population experience sym ptom s m onthly.
Etiology
Incom petent reflux barrier allowing increase in frequency and duration of gastric contents into esophagus
Transient lower esophageal sphincter relaxations (TLESRs): o
Occur with higher frequency in gastroesophageal reflux disease (GERD) patients
o
Exposed esophageal m ucosa becom es acidified and with tim e necroses.
o
Main antireflux barrier
Lower esophageal sphincter (LES): o
Crural diaphragm attachm ent (diaphragm atic sphincter)
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o
Contributes to pressure barrier at gastroesophageal junction
o
Esophageal acid clearance via peristalsis and esophageal m ucosal resistance are additional barriers.
o
Most healthy individuals have brief episodes of reflux without sym ptom s.
Decreased LES tone: o
Sm oking
o
Foods: alcohol, chocolate, onion, coffee, tea
o
Drugs: calcium channel blockers, m orphine, m eperidine, barbiturates, theophylline, nitrates
Delayed gastric em ptying, increased body m ass, and gastric distention contribute to reflux.
Hiatal hernias associated with GERD: o
Significance varies in any given individual
o
Most persons with hiatal hernias do not have clinically evident reflux disease.
Acid secretion is sam e in those with or without GERD.
Associated m edical conditions: pregnancy, chronic hiccups, cerebral palsy, Down syndrom e, autoim m une diseases, diabetes m ellitus (DM), hypothyroidism
Diagnosis Signs and Symptoms History
Typical signs and sym ptom s: o
Heartburn (pyrosis):
Retrosternal burning pain
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Radiates from epigastrium through chest to neck and throat
o
Dysphagia:
Dysphagia suggests esophageal spasm or stricture.
o
Odynophagia:
Odynophagia suggests ulcerative esophagitis.
o
Regurgitation
o
Water brash
o
Belching
o
Esophageal strictures, bleeding
o
Barrett esophagus (esophageal carcinom a)
o
Early satiety, nausea, anorexia, weight loss
o
Sym ptom s worse with recum bence or bending over
o
Sym ptom s usually relieved with antacids, although tem porarily
Atypical signs and sym ptom s: o
Noncardiac chest pain
o
Asthm a
o
Persistent cough, hiccups
o
Hoarseness
o
Pharyngeal/laryngeal ulcers and carcinom a
o
Frequent throat clearing
o
Recurrent pneum onitis
o
Nocturnal choking
o
Upper GI tract bleeding
Physical Exam Nonspecific
Pediatric Considerations
Regurgitation is com m on in infants: o
Incidence decreases from twice daily in 50% of those
Pa ge 2 0 1
age 2 m onths to 1% of 1-year-olds.
Signs: o
Frequent vom iting, irritability, cough, crying, and m alaise
o
Arching the body (hyperextension) at feeding and refusals of feedings
Failure to thrive
Form ula intolerance
Sepsis
Essential Workup
Differentiate GERD from m ore em ergent conditions such as ischem ic heart pain, esophageal perforation, or aortic pathology.
History: typical
Physical exam : vital signs, head, ears, eyes, nose, throat (HEENT), chest and abdom inal exam s
Tests No gold standard
Lab
CBC: o
Chronic anem ia from esophagitis
Stool testing for occult bleeding
Imaging
No routine Im aging
Chest radiograph: o
Evidence of esophageal perforation, hiatal hernia, aortic disease
Diagnostic Procedures/Surgery
Diagnostic trial of antacid: o
Those with persistent sym ptom s should be referred
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for endoscopy. o
90% of GERD patients respond to proton pum p inhibitor (PPI) therapy.
Barium esophagram for prom inent dysphagia
Esophageal pH m onitoring: o
Correlate sym ptom s to acid reflux,
Esophageal m anom etry (poor sensitivity): o
Evaluate LES resting pressure and esophageal peristaltic contractions.
Esophagogastroduodenoscopy (EGD)—detects reflux esophagitis and com plications (Barrett's esophagus, hiatal hernia, stricture, ulcers, m alignancy)
Differential Diagnosis
Ischem ic heart disease
Asthm a
Peptic ulcer disease
Gastritis
Hepatitis/pancreatitis
Esophageal perforation
Esophageal foreign body
Esophageal infection
Cholecystitis/cholelithiasis
Mesenteric ischem ia
P.447
Treatment Pre Hospital
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Esophageal pain m ay m im ic angina.
Airway m ay need active control secondary to vom iting.
Initial Stabilization
Airway, breathing, and circulation (ABCs) need to be evaluated.
IV fluid resuscitation for blood loss or shock
ED Treatment
Sym ptom atic relief: o
Antacids
o
Antacids with viscous lidocaine
o
Sublingual nitroglycerine for esophageal spasm
o
Analgesics
Lifestyle m odifications: o
Avoid late-night or heavy/fatty m eals.
o
Minim ize tim e in supine position after eating.
o
Elevation of head of bed
o
Weight loss
o
Elim inate sm oking and alcohol intake.
Avoid direct esophageal irritants such as citric juices and coffee
Avoid foods that decrease LES pressures such as fatty foods, chocolate, and coffee.
Avoid drugs that lower LES tone.
Antacids (Maalox, Mylanta, etc.): o
Treatm ent of m ild and infrequent reflux sym ptom s
o
Not effective for healing esophagitis
o
Alginic acid slurry floats on surface of gastric contents, providing m echanical barrier
Sucralfate: o
Binds to exposed proteins on surface of injured m ucosa to form protective barrier
Pa ge 2 0 1
o
May also directly stim ulate m ucosal repair
Metoclopram ide (prokinetic drug): o
Im proves peristalsis
o
Accelerates gastric em ptying
o
Increases LES pressure
H 2 -blockers: o
Effective for m ild to m oderate disease
o
Severe disease requires greater dosage than that used for peptic ulcer disease
Proton pum p inhibitors: o
More potent long-acting inhibitors of gastric acid secretion
o
Faster healing than other drug therapies
o
More efficacious in severe GERD and frank esophagitis
Endoscopic therapy: o
Suturing (plication), therm al injury, chem ical injection
Antireflux surgery (goal: increase LES pressure): o
Chronic reflux, younger patients, nonhealing ulceration, severe bleeding
o
Fundoplication can be m ore effective than m edical therapy in selected cases
Pregnancy Considerations
Pyrosis present in 30–50% of pregnancies
Increased intra-abdom inal pressure, horm onal fluctuations lead to increased TLESRs.
EGD reserved for severe presentations
H 2 -blockers—first-line therapy (longer safety record)
PPIs—lim ited safety history in pregnancy
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Medication (Drugs)
Antacids: 30 m L plus viscous lidocaine, 10 m L, PO q6h
Cim etidine: 400 m g PO b.i.d., 300 m g IM/IV q6h–q8h
Esom eprazole: 20–40 m g PO daily
Fam otidine: 20 m g PO/IV b.i.d. (peds: 0.5–1.0 m g/kg/d div. q8h–q12h, m ax. 40 m g/d)
Lansoprazole: 15–30 m g daily
Metoclopram ide: 10–15 m g PO/IV/IM q6h before m eals and nightly at bedtim e
Nizatidine: 150 m g PO b.i.d.
Om eprazole: 20–40 m g PO daily
Pantoprazole: 40 m g PO/IV daily
Rabeprazole: 20 m g PO daily
Ranitidine: 150 m g (peds: 5–10 m g/kg q12h) PO b.i.d. or 300 m g PO nightly at bedtim e
Sucralfate: 1 g PO 1 hour before m eals and nightly at bedtim e
Follow-Up Disposition Admission Criteria
Seriously ill patients
Significant esophageal bleeding
Uncontrolled reactive asthm a
Dehydration
Starvation and failure to thrive
Discharge Criteria Uncom plicated GERD: Refer to patient's prim ary care physician (PCP)
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or gastroenterologist for further evaluation.
Issues for Referral Extraesophageal m anifestations (asthm a, laryngitis, etc.)
References 1. Cappell, MS. Clinical presentation, diagnosis, and m anagem ent of gastroesophageal reflux disease. Med Clin North Am . 2005;89(2):243–291. 2. Klinkenberg-Knol EC, Nelis F, Dent J, et al. Long-term om eprazole treatm ent in resistant gastroesophageal reflux disease: efficacy, safety and influence on gastric m ucosa. Gastroenterology. 2000;118:661–669. 3. Lundell L, Miettinen P, Myrvold HE, et al. Long-term m anagem ent of gastro-esophageal reflux disease with om eprazole or open antireflux surgery: results of a prospective, random ized clinical trial. Eur J Gastroenterol Hepatol. 2000;12:879–887. 4. Spechler SJ, Lee E, Ahnen D, et al. Long-term outcom e of m edical and surgical therapies for gastroesophageal reflux disease. JAMA. 2001;205:2331–2338.
Miscellaneous SEE ALSO: Gastritis; Peptic Ulcer Disease
Codes ICD9-CM 530.81
Pa ge 2 0 2
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > G astro intestinal Bleeding
Gastrointestinal Bleeding Adit A. Ginde
Basics Description
Active or recent bleeding arising from the gastrointestinal (GI) tract
Two categories: o
o
Upper GI tract
Proxim al to the ligam ent of Treitz
Arises from esophagus, stom ach, or duodenum
Lower GI tract:
Distal to the ligam ent of Treitz
Arises from jejunum , ileum , colon, or rectum
Mortality rate: o
10% overall
o
Increases as age increases
o
Ranges from 7
GI source:
Dark red or brown blood
Accom panied by gastric contents
Worsens in setting of nausea/vom iting
PH 90 m m Hg.
o
Attem pt second IV line while transporting patient.
Pa ge 2 0 2
o
Do not rem ain at the scene for a second IV line.
Initial Stabilization
Adm inister 100% oxygen
Control airway in patients with m assive GI bleeding with unstable vital signs and altered m ental status.
Place cardiac, pulse oxim etry, and noninvasive blood pressure m onitors.
Initiate two large-bore (at least 16 gauge) IV lines: o
Consider central venous cordis catheter if unable to establish adequate peripheral venous access.
o
Adm inister 1 L NS bolus (peds: 20 cc/kg). Repeat once if necessary.
o
Transfuse packed RBCs if still unstable after NS boluses.
Crossm atched or type specific blood if available. Otherwise use O negative for prem enopausal wom en and O positive for others
Adm inister fresh frozen plasm a (FFP) and Vitam in K if coagulopathic.
ED Treatment Treatment for All GI Bleeding Patients
Consult gastroenterology for any significant GI bleeding
Consider surgical consult and/or interventional radiology (if available) for m assive ongoing bleeding, unstable patient, or evidence of perforation.
Follow serial hem atocrits, as levels m ay take hours to reflect blood loss.
Place Foley catheter to m onitor urine output.
Blood transfusion for: o
Unstable vital signs despite crystalloid infusion
o
Ongoing chest pain or ischem ic ECG changes
Pa ge 2 0 3
o
Significant anem ia, especially with ongoing bleeding
Treatment for Upper GI Bleeding
IV proton pum p inhibitor (i.e., pantoprazole)
Octreotide (som atostatin analog) for suspected variceal bleeding: o
Decreases portal and intravariceal pressures
Consider vasopressin for suspected variceal bleeding: o
Potent vasoconstrictor
o
Adm inister concurrently with IV nitroglycerin to prevent tissue necrosis/m yocardial ischem ia.
Em ergent endoscopy: o
Indications:
Active bleeding that does not clear with saline lavage
Hem odynam ic instability in setting of liver disease
o
Therapeutic options:
Cauterization of bleeding ulcers or vessels
Injection sclerosis of visible vessels
Endoscopic sclerotherapy for varices (m ost effective)
Balloon tam ponade for varices (if refractory)
Spontaneous resolution: o
60% from variceal bleeding
o
80% from other upper GI tract sources
Treatment for Lower GI Bleeding
Consider angiography for m assive, active bleeding
Consider bowel resection for m assive, active bleeding that is refractory to m edical m anagem ent.
Spontaneous resolution: o
80% of the tim e
Pa ge 2 0 3
o
25% rate of rebleeding
Medication (Drugs)
Nitroglycerin: 5–50 m cg/m in (peds: 0.25–1 m cg/kg/m in) IV
Octreotide: 50 m cg (peds: 1–2 m cg/kg) IV bolus, then 50 m cg/hr (peds: 1–2 m cg/kg/hr) IV
Pantoprazole (Protonix): 40–80 m g (peds: dosing not approved) IV q24h
Vasopressin: 0.2–0.4 IU/m in (peds: 2–5 m U/kg/m in) IV, titrate up as needed. When no bleeding for 12 hours, taper over 24–48 hours.
Vitam in K: 10 m g (peds: 1–5 m g) PO/SC q24h. IV use is controversial and m ust be given slowly.
Follow-Up Disposition Admission Criteria
Unstable vital signs at any tim e
Decreased hem atocrit with recent GI bleeding
Coagulopathy
Advanced age/com orbid conditions
Active upper GI bleeding
Lower GI bleeding: o
Large am ount of initial blood loss
o
Significant, active bleeding
Discharge Criteria
Resolution of upper GI bleeding with negative nasogastric
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lavage and EGD
Minor or resolved lower GI bleeding
Stable vital signs
Stable hem atocrit >30
Norm al coagulation
Otherwise healthy patient
Issues for Referral Consider referral to gastroenterologist for outpatient colonoscopy and/or EGD.
References 1. Barkun A, Bardou M, Marshall JK. Consensus recom m endations for m anaging patients with nonvariceal upper gastrointestinal bleeding. Ann Intern Med. 2003;139:843. 2. Bounds BC, Friedm an LS. Lower gastrointestinal bleeding. Gastroenterol Clin North Am . Decem ber 2003;32(4):1107–1125. 3. D'Am ico G, Criscuoli V, Fili D, et al. Meta-analysis of trials for variceal bleeding. Hepatology. 2002;36:1023. 4. Jensen DM, Machicado GA, Jutabha R, et al. Urgent colonoscopy for the diagnosis and treatm ent of severe diverticular hem orrhage. N Engl J Med. 2000;342(2):78–82. 5. McGuirck TD, Coyle WJ. Upper gastrointestinal tract bleeding. Em erg Med Clin North Am . 1996;14(3):523–539. 6. Sharara AI, Rockey DC. Medical progress: gastroesophageal variceal hem orrhage. N Engl J Med. 2001;345(9):669–681. 7. Van Dam J, Brugge WR. Medical progress: endoscopy of the upper gastrointestinal tract. N Engl J Med. 1999;341(23):1738–1748. 8. Zuccaro, G. Managem ent of the adult patient with acute lower gastrointestinal bleeding. Am J Gastroenterol. 1998;93:1202.
Codes ICD9-CM
Pa ge 2 0 3
578.9
Pa ge 2 0 3
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > G iardia
Giardia
Ann P. Nguyen
Basics Description
Noninvasive diarrhea
Found worldwide
5% of all travelers’ diarrhea
Most com m on intestinal parasite in the United States: o
Highest incidence in sum m er m onths
o
Highest incidence in children aged 1–9 years and adults aged 30–39 years
A Centers for Disease Control nationally reportable disease as of 2002
Fecal-oral transm ission: o
Hum ans are m ajor reservoir.
o
Zoonotic reservoir in dom estic (dogs, cats, sheep, cattle) and wild anim als (beavers, deer, rodents)
o
Reservoir in contam inated surface water
Populations at risk: o
Travelers to endem ic areas (developing countries, wilderness areas of U.S.)
o
Children in day care centers and their close contacts
o
Institutionalized persons
Pa ge 2 0 3
o
Practitioners of anal sexual activity
Etiology
Giardia lam blia: o
A protozoan flagellate
Also called Giardia intestinalis or Giardia duodenalis
Biphasic life cycle of Giardia: o
Ingested as cysts
o
As few as 10 cysts shown to produce infection
o
Cysts becom e trophozoites in the duodenum and attach to intestinal villi.
o
Trophozoites re-encyst in the ileum and cysts are shed in the feces.
Alters the intestinal brush-border enzym es, im pairing digestion of lactose and other saccharides
No toxin produced
Diagnosis Signs and Symptoms History
Onset 1–2 weeks postexposure
Infection m ay be asym ptom atic (m ost com m on).
Diarrhea of acute onset (90% of sym ptom atic patients): o
Foul-sm elling stools
o
Steatorrhea
o
Nonbloody
o
Self-lim iting within 2–4 weeks
o
More severe in im m unocom prom ised patients and patients with underlying bowel disease
Flatulence and bloating (70–75%)
Pa ge 2 0 3
Abdom inal cram ping (70%)
Nausea (70%)
Vom iting (30%)
Malaise (86%)
Anorexia (66%)
Weight loss (60–70%)
Fever is rare (15%).
30–50% of acute cases progress to chronic giardiasis (>4 weeks): o
Fat m alabsorption
o
Severe m acrocytic anem ia secondary to folate deficiency
o
Secondary lactase deficiency (in 20–40% of patients)
Infection is m ore severe and harder to eradicate in im m unosuppressed patients.
Pediatric Considerations
With acute infection: o
Severe dehydration
With chronic infection: o
Failure to thrive
o
Growth retardation and cognitive im pairm ent owing to nutrient m alabsorption
Physical Exam
Abdom inal exam is benign.
Extraintestinal m anifestations (10% of patients): o
Polyarthritis
o
Urticaria
o
Aphthous ulcers
o
Maculopapular rash
o
Biliary tract disease
Pa ge 2 0 3
Essential Workup
History: o
Possible sources of exposure
o
Mem bership in high-risk group
Physical exam : o
If gross or occult blood on digital rectal exam , unlikely to be Giardia
Tests Lab
Stool sam ple for m icroscopy (ova and parasites): o
50–70% sensitive if one sam ple
o
85–90% sensitive if three sam ples taken at 2-day intervals (ideal)
o
100% specific
o
Ability to detect other parasites
Stool enzym e-linked im m unosorbent assay (ELISA) or im m unofluorescent antibody (IFA) assay for Giardia antigen:
o
95% sensitive, 95–100% specific
o
Unlike m icroscopy, cannot rule out other parasites
Stool polym erase chain reaction (PCR): o
100% sensitive and 100% specific
o
Not yet widely available
Fecal leukocytes and stool culture unnecessary unless enteroinvasive organism s suspected (fever, bloody stool)
Serology for antiGiardia antibodies not helpful in the ED setting
Electrolytes, BUN/Cr, glucose o
If prolonged diarrhea or evidence of dehydration
CBC: o
Macrocytic anem ia in chronic giardiasis
Pa ge 2 0 3
o
Nondiagnostic in acute giardiasis
Imaging Abdom inal radiographs or CT of no value
Diagnostic Procedures/Surgery
Duodenal sam pling: o
Entero-Test (patient swallows a weighted string, which is later retrieved and exam ined for Giardia)
Endoscopy: o
Duodenal aspiration
o
Endoscopic duodenal biopsy
Differential Diagnosis
Viral gastroenteritis: o
Norwalk virus
o
Rotavirus
o
Hepatitis A
Bacterial infections: o
Staphylococcus
o
E. coli
o
Shigella
o
Salm onella
o
Yersinia
o
Cam pylobacter
o
Clostridium difficile
o
Vibrio cholerae
Other protozoa: o
Cryptosporidium
o
Microsporidia
o
Cyclospora
o
Isospora
o
Entam oeba
Inflam m atory bowel disease
Pa ge 2 0 3
Irritable bowel syndrom e
Lactase deficiency
Tropical sprue
Drugs and toxins:
o
Antibiotics
o
Calcium channel blockers
o
Magnesium antacids
o
Caffeine
o
Alcohol
o
Sorbitol
o
Laxative abuse
o
Quinidine
o
Colchicine
o
Mercury poisoning
Endocrine: o
Addison disease
o
Thyroid disorders
Malignancy: o
Colorectal carcinom a
o
Medullary carcinom a of the thyroid
P.453
Treatment Initial Stabilization
ABCs: airway, breathing, circulation
IV 0.9 norm al saline (NS) if signs of significant dehydration
Pediatric Considerations
Pa ge 2 0 4
For severe dehydration (>10%): o
IV bolus with 0.9% NS at 20 m L/kg
o
Cardiac m onitor
o
Blood glucose determ ination
ED Treatment
Oral fluids for m ild dehydration
Correct any serum electrolyte im balances.
Stool sam ple for m icroscopy
If stool sam ple is positive for Giardia: o
Metronidazole is first-line antiparasitic drug in United States:
o
80–95% cure rate
Albendazole or furazolidone if m etronidazole unsuccessful
o
Quinacrine and tinidazole highly effective but not available in United States
If stool sam ple negative for Giardia: o
Refer to gastroenterologist for further specialized testing.
o
Consider em piric course of m etronidazole if high suspicion for Giardia.
Im m unocom prom ised patients at risk for disease that is refractory to standard drug regim ens: o
Try drug of a different class or m etronidazole plus quinacrine for at least 2 weeks
Pediatric Considerations
Metronidazole is first line therapy (80–95% efficacy)
Alternatives: o
Furazolidone (80–95% efficacy)
o
Nitazoxanide (60–80% efficacy)
Pregnancy Considerations
Pa ge 2 0 4
Metronidazole contraindicated in first trim ester: o
Parom om ycin (55–90% efficacy) or furazolidone instead
Medication (Drugs)
Albendazole: 400 m g (peds: 10–15 m g/kg/24h) PO daily for 5–7 days
Furazolidone: 100 m g (peds: 6–8 m g/kg/24h) PO q6h for 7–10 days
Metronidazole: 250 m g (peds: 30–40 m g/kg/24h) PO q8h for 5–7 days
Nitazoxanide: 500 m g (peds: 100 m g for ages 2–3 years, 200 m g for ages 4–11 years) PO b.i.d. for 3 days
Parom om ycin: 500 m g (peds: 25–30 m g/kg/24h) PO q8h for 5–10 days
Quinacrine: 100 m g (peds: 6 m g/kg/24h) PO q8h for 5–7 days
Tinidazole: 2,000 m g (peds: 50–75 m g/kg) PO once
Follow-Up Disposition Admission Criteria
Hypotension or tachycardia unresponsive to IV fluids
Severe electrolyte im balance
Children with >10% dehydration
Signs of sepsis/toxicity (rare in isolated giardiasis)
Patients unable to m aintain adequate oral hydration: o
Extrem es of age, cognitive im pairm ent, significant
Pa ge 2 0 4
co-m orbid illness
Discharge Criteria
Able to m aintain adequate oral hydration
Dehydration responsive to IV fluids
Issues for Referral Gastroenterology referral for diagnostic endoscopy if sym ptom s persist for >4 weeks despite drug therapy
References 1. Ali SA, Hill DR. Giardia intestinalis. Curr Opin Infect Dis. 2003;16:453–460. 2. Bailey JM, Erram ouspe J. Nitazoxanide treatm ent for giardiasis and cryptosporidiosis in children. Ann Pharm acother. 2004;38:634–640. 3. Gardner TB, Hill DR. Treatm ent of giardiasis. Clin Microbiol Rev. 2001;14:114–128. 4. Hlavsa MC, Watson JC, Beach MJ. Giardiasis surveillance—United States, 1998–2002. MMWR Surveillance Sum m aries. 2005;54(SS01):9–16. 5. Katz DE, Taylor DN. Parasitic infections of the gastrointestinal tract. Gastroenterol Clin North Am . 2001;30:797–815. 6. Lebwohl B, Deckelbaum RJ, Green PHR. Giardiasis. Gastrointest Endosc. 2003;57:906–913. 7. Nash TE, Ohl CA, Thom as E, et al. Treatm ent of patients with refractory giardiasis. Clin Infect Dis. 2001;33:22–28. 8. Petri WA. Therapy of intestinal protozoa. Trends Parasitol. 2003;19:523–526. 9. Verweij JJ, Blange RA, Tem pleton K, et al. Sim ultaneous detection of Entam oeba histolytica, Giardia lam blia, and Cryptosporidium parvum in fecal sam ples by using m ultiplex real-tim e PCR. J Clin Microbiol. 2004;42:1220–1223.
Pa ge 2 0 4
Miscellaneous SEE ALSO: Am ebiasis; Diarrhea, Adult
Codes ICD9-CM 007.1
ICD10 A07.1
Pa ge 2 0 4
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > G lauco m a
Glaucoma
Yasuharu Okuda
Basics Description Disease characterized by elevation of intraocular pressure, optic neuropathy, and progressive loss of vision
Etiology
Prim ary glaucom a: o
Open-angle glaucom a:
Norm al anterior cham ber angle
Insidious onset with persistent rise in intraocular pressure
Most com m on type accounting for 90% of glaucom as in United States
Leading cause of blindness in African Am ericans
Risk factors include: African Am erican, age >40, fam ily history, m yopia, diabetes, and HTN
o
Angle-closure glaucom a:
Narrowing or closing of anterior cham ber angle precluding natural flow of aqueous hum or from posterior to anterior cham ber of eye and through its filtering portion of trabecular m eshwork
Pa ge 2 0 4
Usually abrupt onset with sudden increase in intraocular pressure
Risk factors include: Asians and Eskim os, hyperopia, fam ily history, increased age, and fem ale gender
Secondary glaucom a occurs from other diseases, including diseases of eye, traum a, and drugs: o
Can be either open or closed angle
o
Drugs: steroids
o
Diseases: neurofibrom atosis, uveitis, neovascularization, and intraocular tum ors
o
Traum a
Diagnosis Signs and Symptoms History
Prim ary open-angle glaucom a: o
Gradual reduction in peripheral vision or night blindness
o
Typically bilateral
o
Painless
Prim ary angle-closure glaucom a: o
Severe deep eye pain and headache often associated with nausea and vom iting
o
Decrease in visual acuity often described as visual clouding with halos surrounding light sources
o
Associated abdom inal pain, which m ay m isdirect diagnosis
o
Concurrent exposure to dim ly lit environm ent such as
Pa ge 2 0 4
m ovie theater o
Use of precipitating m edications:
Mydriatic agents: scopolam ine, atropine
Sym pathom im etics: pseudoephedrine, albuterol
Antihistam ines: Benadryl, Antivert
Antipsychotics: Haldol
Phenothiazines: Com pazine, Phenergan
Tricyclic antidepressants: Elavil
Physical Exam
Prim ary open-angle glaucom a: o
Decreased visual acuity
Prim ary angle-closure glaucom a: o
Decreased visual acuity
o
Pupil is m iddilated and nonreactive.
o
Corneal edem a with hazy appearance
o
Conjunctival injection
o
Firm globe to palpation
Essential Workup
Detailed ocular exam ination
Visual acuity
Tonom etry: o
Norm al pressures are between 10 and 21 m m Hg.
o
Prim ary open-angle glaucom a:
Degree of elevation can vary, but 25% to 30% of patients m ay have norm al intraocular pressures.
o
Prim ary angle-closure glaucom a:
Any elevation is abnorm al, but usually seen in ranges >40 m m Hg.
Slit-lam p exam : o
Evaluation of anterior cham ber angle
Pa ge 2 0 4
o
Used to elim inate other possibilities in differential including corneal abrasion and foreign body
Tests Lab Directed toward workup of differential
Imaging Directed toward workup of differential
Differential Diagnosis
Cavernous sinus throm bosis
Acute Iritis and uveitis
Retinal artery or vein occlusion
Tem poral arteritis
Retinal detachm ent
Conjunctivitis
Corneal abrasion
P.455
Treatment Initial Stabilization Initiate steps to lower intraocular pressure in acute closed-angle glaucom a.
ED Treatment
Prim ary open-angle glaucom a: o
Recognition and prom pt ophthalm ologic referral
Prim ary angle-closure glaucom a (ophthalm ologic
Pa ge 2 0 4
em ergency): o
Intraocular pressure reduction:
Topical beta-blocker, tim olol m aleate, to decrease aqueous hum or production
Topical α 2 -agonist, apraclonidine, to decrease aqueous hum or production
Carbonic anhydrase inhibitor, acetazolam ide, for reduction of form ation of aqueous hum or
Hyperosm otic agent, m annitol, to draw aqueous hum or from vitreous cavity into blood. (Indicated for severe attacks)
o
Movem ent of iris away from trabecular m eshwork:
Topical parasym pathom im etic, pilocarpine hydrochloride, to constrict pupil once intraocular pressure is Table o f C o ntents > G lo be Rupture
Globe Rupture
Alexander T. Limkakeng Jr.
Basics Description
A full-thickness corneal or scleral injury owing to traum a
Blunt traum a: o
Causes an abrupt rise in intraocular pressure diffusely
o
Subsequent rupture of the eye either opposite the point of im pact or at the weakest points:
Extraocular m uscle insertion
Corneoscleral junction
Penetrating injury: o
Occurs with sharp objects or projectiles injuring the sclera or anterior eye directly
o
Most com m only anterior—the bony orbit protects the globe laterally and posteriorly
o
Posterior injury can occur with fracture of the bony orbit or with penetrating injuries of the eyelid or eyebrow.
Prognosis worse with: o
Larger lacerations
o
Injury posterior to the rectus insertion
Pa ge 2 0 5
o
Blunt injury
o
Intraocular foreign body, especially if m ade of organic m aterial
o
Vitreous extrusion
o
Lens dam age
o
Hyphem a
o
Retinal Detachm ent
o
Poor visual acuity at presentation
o
Afferent pupillary defect
o
Increased tim e to OR
Etiology
Falls, im pact injuries
Sport-related injuries (e.g., elbow, ball im pacts, arrows, etc.)
Indirect concussive injuries (explosions)
Sharp instrum ent/stabbing injuries, accidental or intentional
Projectile injuries (industrial, firearm s, BB pellets, blast explosion shrapnel—glass, etc.)
Diagnosis Signs and Symptoms
Pain
Localized ecchym osis and swelling
Scleral or corneal laceration
Extrusion of intraocular contents
Markedly decreased visual acuity
Lim ited extraocular m otion
Hyphem a
Pa ge 2 0 5
Severe subconjunctival hem orrhage and edem a, especially if circum ferential bloody chem osis
Abnorm ally deep or shallow anterior cham ber
Low intraocular pressure: o
Note: do not perform tonom etry if there is obvious rupture.
Irregular pupil (points toward lesion)
Subluxed lens
Com m otio retinae—gray-white discoloration of the retina
History
Mechanism of injury: o
Assess for possibility of retained intraocular foreign body
History of previous eye surgery
Preinjury visual acuity
Assess tetanus status
Ascertain tim e of last PO intake
Physical Exam
Penlight or slit-lam p exam ination observing for signs of globe rupture
If the diagnosis of ruptured globe is m ade, defer further ocular exam ination until the tim e of surgical repair: o
Prevents placing any undue pressure on the eye and risking extrusion of the intraocular contents
If no evidence of globe rupture on initial survey, proceed with thorough ophthalm ologic exam ination: o
Visual acuity
o
Slit-lam p exam ination:
Cornea
Anterior cham ber
Iris
Pa ge 2 0 5
o
Sclera
Fluorescein:
Seidel test: observe if fluorescein m oves away as contents (which appear yellow-green) leak out at site of rupture.
o
Visualize fundus/retina.
o
Measure intraocular pressure:
Perform only if globe rupture is definitely not present.
Tests Lab Preoperative labs:
CBC
Electrolytes
Coagulation studies
Imaging
Orbital radiograph (anteroposterior/lateral) for m etallic intraocular foreign body
CT scan of the orbits (axial and coronal views)
MRI scan of the orbits after retained m etallic foreign body is ruled out
B-scan ultrasound of the eye
Diagnostic Procedures/Surgery
Slit-lam p
Fluorescein
Differential Diagnosis
Intraocular foreign body
Hyphem a
Severe subconjunctival hem orrhage and chem osis
Partial corneal laceration
Pa ge 2 0 5
Partial scleral laceration
P.457
Treatment Pre Hospital
Place a shield (not patch) over eye with no pressure on the globe.
Use a Styrofoam cup if no shield available.
Initial Stabilization
Keep m anipulation of the eye to a m inim um if ruptured globe is suspected.
Try to prevent any activity that will cause an increase in intraocular pressure such as straining, coughing, or vom iting.
ED Treatment
Em ergent ophthalm ologic consultation
Bed rest
No food or drink (NPO)
Adm inister antiem etic for nausea/vom iting: o
Prochlorperazine (Com pazine)
Update tetanus status.
Adm inister prophylactic antibiotics IV:
o
Cefazolin (Ancef)
o
Gentam icin or clindam ycin
Succinylcholine is relatively contraindicated: o
However, with a defasciculating dose of a nondepolarizing agent and sufficient anesthesia, it
Pa ge 2 0 5
m ay be used.
Pregnancy Considerations
Because of risk of extrusion of intraocular contents, straining should be avoided.
If necessary, delivery by cesarean section or tocolysis should be considered in conjunction with obstetric consultation.
Medication (Drugs)
Cefazolin (Ancef): 1 g (peds: 25–50 m g/kg/24h) IV q6h–q8h
Clindam ycin: 450 m g (peds: 25–40 m g/kg/24h div. q6h–q8h) IV q8h
Gentam icin: 1 m g/kg (peds: 2–2.5 m g/kg) IV q8h
Prochlorperazine (Com pazine): 5–10 m g IV/IM
Follow-Up Disposition Admission Criteria
All patients with globe rupture/penetrating eye injuries
Early enucleation for severe injury
Discharge Criteria Globe penetration excluded
Issues for Referral
Em ergent ophthalm ologic consultation in the ER m ay be needed to definitively rule out globe rupture owing to difficulty with exam and the desire to m inim ize
Pa ge 2 0 5
m anipulation of the eye.
Speed is of the essence since the risk of infection increases with prolonged tim e to operative repair.
If appropriate, patient should be counseled on use of protective eyewear to prevent recurrence.
References 1. Anesthesia. In: Miller RD, ed. Anesthetic Agents. Philadelphia: Churchill Livingstone; 2000:473. 2. Dunya IM, Rubin PAD, Shore JW. Penetrating orbital traum a. Int Ophthalm ol Clin. 1994;34:25–36. 3. Klystra JA, Lam kin JC, Runyan DR. Clinical predictors of scleral rupture after blunt ocular traum a. Am J Ophthalm ol. 1993;115(4):530–535. 4. Linden JA, Renner GS. Traum a to the globe. Em erg Med Clin North Am . 1995;13(3):581–605. 5. Navon SE. Managem ent of the ruptured globe. Int Ophthalm ol Clin. 1994;34:71–91. 6. Sabaci G, Bayer A, Mutlu M, et al. Endophthalm itis after deadly-weapon-related open-globe injuries. Am J Ophthalm ol. 2002;133:62–69.
Miscellaneous SEE ALSO: Blowout Fracture; Corneal Abrasion; Corneal Foreign Body; Hyphem a; Retinal Detachm ent; Visual Loss
Codes ICD9-CM 871.0
ICD10 S05.3
Pa ge 2 0 5
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > G lo m erulo nephritis
Glomerulonephritis Scott A. Miller
Basics Description
Syndrom e characterized by: o
Hem aturia
o
Red blood cell casts
o
Proteinuria
o
Hypertension
o
Renal insufficiency
Accounts for 10–15% of End-Stage Renal Disease (ESRD)
Com m on pathway of m ultiple diseases resulting in intraglom erular inflam m ation and cellular proliferation
Contributing factors: o
Genetics
o
Antibody deposition:
Antibody attaches to glom erular antigen (native or im planted).
o
Circulating antigen-antibody com plex deposited
Influx and activation of inflam m atory m ediators:
Leukocytes, com plem ent, cytokines
Cell-m ediated im m une m echanism s
Pa ge 2 0 5
Results in glom erular dysfunction
Persistent inflam m ation can lead to scarring and perm anent dam age.
Etiology
Postinfectious: o
Poststreptococcal glom erulonephritis (PSGN)
Occurs 7–21 days after streptococcal pharyngitis or skin infection
Most com m on in children and m en
Ranges from asym ptom atic hem aturia to oliguric renal failure
o
Can follow other bacterial, fungal, viral, or parasitic infections
IgA nephropathy: o
Most com m on in m en in the third and fourth decades of life
o
Possibly related to increased production of IgA after infection
Rapidly progressive glom erulonephritis (RPGN): o
Can destroy renal function in days
o
Crescentic deposits in glom eruli destroy function.
o
Pauci-im m une (sm all vessel vasculitides):
Often antineutrophil cytoplasm ic antibody (ANCA)-positive
o
Can involve other areas (i.e., lungs, skin)
Wegener granulom atosis
Microscopic polyangiitis
Im m une com plex deposits:
Postinfectious
System ic disease (i.e., system ic lupus erythem atosus [SLE], Henoch-Schönlein purpura [HSP])
Pa ge 2 0 6
o
Antiglom erular basem ent m em brane deposits:
Goodpasture disease with pulm onary involvem ent
Mem branoproliferative glom erulonephritis (MPGN): o
Com plem ent deposits in basem ent m em brane
o
Hepatitis C
Diagnosis Signs and Symptoms
Cardinal signs: o
Hem aturia
o
Proteinuria
Edem a: o
Owing to renal salt and water retention
o
Periorbital
o
Ascites
o
Pleural effusion
Hypertension
Oliguria
Azotem ia
Congestive heart failure
Renal failure
Nonspecific m anifestations:
o
Fatigue
o
Weight loss
o
Abdom inal pain
o
Nausea/vom iting
Autoim m une disorders: o
Arthralgias
o
Arthritis
Pa ge 2 0 6
o
Rash
o
Fever
Essential Workup Urinalysis for:
Hem aturia, proteinuria, and RBC casts
Tests Lab
Electrolytes, BUN, Cr: o
Renal function
o
Hyperkalem ia
Album in, total protein: o
Varying degrees of hypoalbum inem ia depending on clinical process
CBC: o
Anem ia secondary to chronic renal disease, neoplasm , Goodpasture disease
o
PT, PTT: o
With or without elevated WBC in infections
Coagulation factors consum ed in certain types of GN
Labs to be considered for consultants: o
Cultures—throat, skin, blood
o
24-hour urine collection—protein, urine electrolytes
o
Streptozym e or antistreptolysin O titer
o
Com plem ent levels (C1, C3, C4, CH 5 0 )—reduced in PSGN, MPGN, SLE
o
ANA, rheum atoid factor—connective tissue diseases
o
Anti—glom erular basem ent m em brane (GBM)—Goodpasture
o
ANCA—Wegener
Imaging
Pa ge 2 0 6
Renal ultrasound o
Kidney size predictor of potential reversibility of disease, alternative diagnosis (i.e., neoplasm , stone)
Chest radiograph (CXR): heart size, pulm onary edem a, or hem orrhage
Diagnostic Procedures/Surgery Renal biopsy: Discern prim ary glom erulopathies versus other causes. P.459
Differential Diagnosis
Hem atologic: o
Sickle cell disease
o
Coagulopathy
Renal: o
Infectious
o
Malform ation
o
Neoplasm
o
Ischem ic
o
Traum a
o
Vasculitis
Postrenal: o
Mechanical (i.e., stones, reflux, obstruction, catheterization)
o
Inflam m atory (i.e., cystitis, prostatitis, epididym itis, endom etriosis, periurethritis)
o
Neoplasm
Factitious: o
Food
o
Drugs
o
Pigm enturia (i.e., m yoglobin, porphyria, hem oglobin)
Pa ge 2 0 6
o
Vaginal bleeding
Treatment Initial Stabilization ABCs: airway, breathing, circulation
ED Treatment
Treatm ent m ainly supportive care: o
o
Blood pressure control:
Loop diuretics
ACE inhibitor for m aintenance
Treat hypertensive em ergencies.
Dialysis:
Fluid overload
Hyperkalem ia
Urem ia
PSGN: o
Usually resolves spontaneously
o
No benefit to antibiotics
IgA Nephropathy: o
Supportive care
o
Im m unosuppressives if inflam m ation on biopsy
o
Variable course, but m ost recover
RPGN: o
Can irreversibly destroy renal function in days
o
Em ergently consult nephrologist to discuss starting potentially toxic therapies.
o
Im m unosuppressives and high-dose steroids:
Methylprednisolone and prednisone
Cyclophospham ide
Pa ge 2 0 6
Plasm apheresis for anti-GBM antibody
MPGN: o
Treat underlying disease if known.
Medication (Drugs)
Benazepril: 5–40 m g PO daily (or any other ACE inhibitor)
Cyclophospham ide: dose in conjunction with nephrology
Diazoxide: 1–3 m g/kg IV, m ax. 150 m g, repeat q15m in
Furosem ide: 20–80 m g IV; m ax. 2 m g/kg/d
Methylprednisolone: 30 m g/kg IV on alternative days for 3 doses, followed by oral prednisone (dose in conjunction with nephrology)
Nitroprusside: 0.3–10 µg/kg/m in IV
Prednisone: 0.5–2 m g/kg/d
Follow-Up Disposition Admission Criteria
Unstable vital signs
Oliguria, anuria
Urem ia
Acute renal failure
Electrolyte abnorm ality
Hypertensive em ergency
Congestive heart failure
Infectious cause of GN
Discharge Criteria
Pa ge 2 0 6
Healthy patients with no com orbid illness who present with m ild hem aturia and proteinuria with:
Stable vital signs
No signs of infection
Otherwise norm al lab work
Close follow-up recom m ended
Issues for Referral All patients with glom erulonephritis should follow up with nephrology.
References 1. Couser WG. Glom erulonephritis. Lancet. 1999;353(9163):1509–1515. 2. Glassock RJ. Managem ent of rapidly progressive glom erulonephritis. Hosp Pract. (office ed). 2000;35(2):59–62, 65–66, 69–70. 3. Hricik DE, Chung-Park M, Sedor JR. Glom erulonephritis. N Engl J Med. 1998;339(13):888–899. 4. Madaio MP, Harrington JT. The diagnosis of glom erular diseases: acute glom erulonephritis and the nephrotic syndrom e. Arch Intern Med. 2001;161(1):25–34. 5. Vinen CS, Oliveira DB. Acute glom erulonephritis. Postgrad Med J. 2003;79:206–213.
Miscellaneous SEE ALSO: Nephritic Syndrom e; Nephrotic Syndrom e; Renal Failure
Codes ICD9-CM 583.9
ICD10
Pa ge 2 0 6
N05
Pa ge 2 0 6
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > G o no co ccal Disease
Gonococcal
Disease JiWon E. Lee
Basics Description
Infection of upper genital tract
Second m ost com m on com m unicable disease in United States:
o
Often seen with chlam ydia
o
600,000 new cases per year
Major cause of urethritis in m en, cervicitis/PID in wom en: o
Rising resistance to penicillin (up to 25%)
o
Hum ans only known host
o
Increasing incidence in wom en and m en who have sex with m en (MSM):
Extragenital infections (pharynx, rectum ) occur m ore com m only in MSM.
Etiology Neisseria gonorrhoeae:
Gram -negative aerobic diplococci
Pa ge 2 0 6
Diagnosis Signs and Symptoms Female
Cervicitis: o
Most com m on m ucosal site of infection
o
Fifty percent asym ptom atic rate
o
Vaginal pruritis, m ucopurulent discharge
o
Cervical edem a, congestion, friability:
Abnorm al vaginal bleeding
Abdom inal pain, dysparenuria
Pelvic inflam m atory disease (PID): o
10–40% occurrence rate
o
Pelvic/abdom inal pain, abnorm al vaginal bleeding, and dysparenuria
o
Sym ptom s often occur at onset of m enses.
o
Fever (50%)
o
Uterine tenderness, bilateral adnexal or cervical m otion tenderness:
Nausea/vom iting
Fitz-Hugh Curtis syndrom e: o
Ten percent occurrence rate
o
Perihepatitis
o
Right upper quadrant pain/tenderness
Vaginal itching
Dysuria
Thirty percent to 40% asym ptom atic carriers
Proctitis: o
May self-inoculate
Male
Incubation period 3–7 days
Pa ge 2 0 6
Sym ptom s occur in 10–14 days
Urethritis: o
Penile discharge or dysuria
o
Yellow-white thick discharge:
Indistinguishable from nongonococcal urethritis (chlam ydia)
Prostatitis
Epididym itis: o
Acute, unilateral testicular pain and swelling:
Rule out torsion/traum a.
Proctitis: o
Often asym ptom atic
o
One percent to 2% with tenesm us, pruritis ani, rectal bleed
o
Only site of infection in 40% of MSM
o
Threefold increase in HIV infection risk
Urinary tract infection (UTI): o
Dysuria
Disseminated
One percent to 3% occurrence rate
Com m on cause of polyarthralgias, polyarthritis, or oligoarthritis in young, healthy patients
Fem ale > Male, 3:1: o
1 week postm enses
Triad: tenosynovitis, derm atitis, polyarthralgias: o
Fever, chills, m alaise
o
Migratory tenosynovitis at wrist, fingers, ankles, toes:
o
Flexor tendon sheath of wrist/Achilles tendon
Derm atitis, few painless lesions:
Pustular or vesiculopustular
Hem orrhagic, necrotic pustules on
Pa ge 2 0 7
erythem atous base
Begin distally
Resem ble m eningococcus
Healing crust in 4 days
Purulent arthritis without skin lesions: o
Knees, wrists, and ankles:
Asym m etric, polyarthritis
Swollen, warm joint effusion
Arthralgia: o
Usually fewer than three joints
Endocarditis
Meningitis
Osteom yelitis
Other Pharyngitis:
Oropharyngeal exudates or cervical lym phadenitis
Conjunctival injection/irritation
Essential Workup
Clinical diagnosis in m ale gonorrhea: o
Gram stain 95% sensitive
Cervical culture in fem ale gonorrhea
Tests Lab
Cultures (gold standard): o
Thayer-Martin m edium :
Urethral/cervical culture
Gram stain: o
Intracellular gram -negative diplococci
Sixty percent sensitive in sym ptom atic wom en
Ninety-five percent sensitive in sym ptom atic
Pa ge 2 0 7
m en
Enzym e im m unoassay (EIA): o
Cervical swab or urine specim en
DNA probe: o
FDA approved
o
Cervical swabs
DNA am plification techniques: o
Nucleic acid am plification tests (NAATs)
DNA or RNA sequences using polym erase chain reaction (PCR)
Pharyngeal/rectal cultures for local sym ptom s in high-risk individuals
Dissem inated gonococcal infection (DGI): o
Synovial fluid analysis:
Neutrophilic leukocytosis, >50,000 cells/m m 3
Positive cultures when >80,000 cells/m m 3
o
Two or m ore sets of blood cultures
o
Synovial, skin, urethral or cervical, and rectal cultures:
Thayer-Martin m edia
PID/lower abdom inal pain in fem ale: o
CBC
o
Urinalysis
o
Pregnancy test
Rapid plasm a reagin (RPR) o
For associated syphilis
P.461
Differential Diagnosis
Urethritis: o
Chlam ydia
Pa ge 2 0 7
o
Trichom onas
o
UTI
o
Syphilis
DGI: o
Bacterial arthritis:
Meningococcus (rash)
o
Hepatitis B
o
Connective tissue disease:
o
Reiter syndrom e
Rheum atoid arthritis
Psoriatic arthritis
Acute rheum atic fever:
Poststreptococcal arthritis
o
Infective endocarditis
o
Others:
HIV
Secondary syphilis
Viral infection
Lym e disease (rash)
Gout (arthritis)
Treatment ED Treatment
Hydration (0.9% NS) for nausea/vom iting
Cervical, urethral, and anorectal infection: o
Ceftriaxone 125 m g IM once
o
Cefixim e 400 m g PO once
o
Ciprofloxacin 500 m g PO once
o
Ofloxacin 400 m g PO once
o
Avoid quinolones in pregnancy, nursing, and age 15,000/m m 3
Pa ge 2 0 7
o
Intractable nausea/vom iting
o
Conjunctivitis requiring IV antibiotics
Discharge Criteria
Uncom plicated genital, pharyngeal, or conjunctival infection
Mild DGI in nontoxic patient: o
Without arthritis in weight-bearing joint
Issues for Referral
Infertility
Recurrent infection despite m ultiple therapy
References 1. Cook RL, et al. System atic review: noninvasive testing for Chlam ydia trachom atis and Neisseria gonorrhoeae. Ann Int Med. 2005;142(11):914–925. 2. Fox KK. et al. Gonorrhea in the HIV era: a reversal in trends am ong m en who have sex with m en. Am J Public Health. 2001;91:959. 3. Hopkins RS, et al. Sum m ary of notifiable diseases—United States, 2003. MMWR Morb Mortal Wkly Rep. 2005;52(54):1–85. 4. Khan A, et al. The prevalence of chlam ydia, gonorrhea, and Trichom onas in sexual partnerships. Sex Transm Dis. 2005;32(4):260–264.
Miscellaneous SEE ALSO: Chlam ydia; Urethritis
Codes ICD9-CM 98.0
Pa ge 2 0 7
ICD10 A54.9
Pa ge 2 0 7
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > G o ut/Pseudo go ut
Gout/Pseudogout
Delaram Ghadishah
Basics Description
Uric acid deposition into tissues affecting m ainly m iddle-aged m en and postm enopausal wom en: o
Most com m on crystalline diseases
o
Four phases:
Asym ptom atic hyperuricem ia (serum urate >7 m g/dL)
o
Acute gout
Intercritical gout: quiet intervening periods
Tophaceous gout (up to 45% of cases)
Risk factors:
Age >40
Male/fem ale ratio 2:1 to 6:1 ankle; tarsal area; knee > hand; wrist
Pseudogout: o
Typically involves larger joints than with gout
o
Most com m on: knee > wrist > m etacarpals; shoulder; elbow; ankle > hip; tarsal joints
Pa ge 2 0 8
o
Monoarticular (25%)
o
Asym ptom atic (25%)
o
Pseudo-osteoarthritis (45%): progressive degeneration, often sym m etric
o
Pseudorheum atoid arthritis (in elderly):
Polyarticular variant with fever and confusion
Essential Workup
Arthrocentesis and aspiration of tophi: o
Exam ine aspirant for crystals, Gram stain, cultures, leukocyte count, and differential
o
Fluid is typically thick pasty white:
Gout: 20,000–100,000 WBC/m m 3 ; poor string and m ucin clot; no bacteria
Pseudogout: up to 50,000 WBC/m m 3 ; no bacteria
Microscopic exam ination of crystals under polarized light: o
o
Gout:
Needle shaped
Strong birefringence
Negative elongation
Pseudogout:
Rhom boid
Weak birefringence
Positive elongation
Tests Lab
CBC often shows leukocytosis.
Chem istry panel to assess for renal im pairm ent
Magnesium and calcium , thyroid-stim ulating horm one (TSH), and serum iron
Uric acid level has lim ited value.
Pa ge 2 0 8
If infectious arthritis is suspected: o
Blood and urine cultures
o
Urethral, cervical, rectal, or pharyngeal gonococcal cultures
Imaging
Plain radiographs to assess the presence of: o
Effusion
o
Joint space narrowing
o
Baseline status of joint
o
Contiguous osteom yelitis
o
Fractures or foreign body
Acute gout: soft tissue swelling; norm al m ineralization; joint space preservation
Chronic gout: calcified tophi; asym m etric bony erosions; overhanging edges; bony shaft tapering
Pseudogout: chondrocalcinosis; subchondral sclerosis or cysts (wrist); radiopaque calcification of cartilage, tendons, and ligam ents; radiopaque osteophytes
Diagnostic Procedures/Surgery
Arthrocentesis
Aspiration of tophi
P.463
Differential Diagnosis
Infectious arthritis
Traum a
Osteoarthritis
Reactive arthritis
Miscellaneous crystalline arthritis
Aseptic necrosis
Pa ge 2 0 8
Rheum atoid arthritis
System ic lupus erythem atosus
Sickle cell
Osteom yelitis
Treatment Initial Stabilization
Relieve pain.
Rule out infectious cause.
ED Treatment
Nonsteroidal anti-inflam m atory drugs (NSAIDs) are first-line treatm ent.
If NSAIDS ineffective or contraindicated: o
Steroids (oral, intravascular, intram uscular, intra-articular)
o
Colchicine (lim ited by toxicity)
Joint aspiration
Avoid aspirin.
Reduction of hyperuricem ia and long-term m anagem ent of gout and pseudogout are not within usual scope of ED care. o
Careful withdrawal of gout-producing agent
o
Uricosurics (e.g., probenecid, sulfinpyrazone)
o
Allopurinol to reduce uric acid synthesis
o
Increased fluid intake and urine alkalization to prevent renal stones
o
Long-term colchicine or NSAIDs prophylactically
Pa ge 2 0 8
Medication (Drugs)
Allopurinol: 50–100 m g PO daily, m ax. 200–300 m g daily:
o
Adjust for kidney disease.
o
Discontinue with rash or fever.
o
Treatm ent of choice with uric acid kidney stones
Colchicine: 0.5 m g/h PO up to pain relief, 8 m g total, or GI toxicity: o
Can cause bone m arrow suppression at high doses
o
Not dialyzable
o
Long-term use m ay cause m yopathy.
o
Adjust dose for liver or kidney disease.
o
Does not prevent m onosodium urate deposition or joint dam age of chronic gout
Corticosteroids: o
Corticotropin: 40 Units IM, q8h, up to 3 doses
o
Methylprednisolone: 40 m g (peds: 1–2 m g/kg) IM or IV daily for 3–4 days
o
Prednisone: 40 m g (peds: 1–2 m g/kg) PO daily for 3–4 days; taper over 7–14 days
o
Triam cinolone: 10–40 m g plus dexam ethasone 2–10 m g intra-articularly
NSAIDs in m axim al doses initially for 3 days, then taper over 4 days: o
Ibuprofen: 800 m g (peds: 10 m g/kg) PO q.i.d.
o
Indom ethacin: 25–50 m g PO t.i.d.–q.i.d. (peds: 2 m g/kg/d t.i.d.–q.i.d.; not for children younger than 14 years old)
o
Ketorolac: 15–30 m g IM/IV in ED, m ay repeat for 1 dose (peds: 1 m g/kg to m ax. 30 m g IM or 0.5 m g/kg to m ax. 15 m g IV) IM
o
Naproxen: 500 m g PO t.i.d. (peds: 5 m g/kg PO
Pa ge 2 0 8
b.i.d.) o
Sulindac: 200 m g PO t.i.d.
Probenecid: 250–500 m g PO t.i.d., m ax. 3 g daily: o
Not effective or less effective with renal disease or aspirin or diuretic use
o
Relatively contraindicated with presence of uric acid kidney stones
Sulfinpyrazone: 50 m g t.i.d., m ax. 800 m g daily
Geriatric Considerations NSAIDs m ay worsen renal function, fluid retention, gastropathy, hepatotoxicity, and cognitive function, particularly in the elderly.
Pediatric Considerations Gout not usually seen in children although possible during chem otherapy treatm ent for cancer
Follow-Up Disposition Admission Criteria
Suspected infectious arthritis
Acute renal failure
Intractable pain
Discharge Criteria
No evidence of infection
Adequate pain relief
Issues for Referral
Septic arthritis
Renal failure
Pa ge 2 0 8
References 1. Agudelo CA, Wise CM. Crystal-associated arthritis in the elderly. Rheum Dis Clin North Am . 2000;26(3):527–546. 2. Buckley TJ. Radiologic features of gout. Am Fam Physician. 1996;54(4):1232–1238. 3. Harris MD, Siegel LB, Alloway JA. Gout and hyperuricem ia. Am Fam Physician. 1999;59(4):925–934. 4. Joseph J, McGrath H. Gout or “pseudogout―: how to differentiate crystal-induced arthropathies. Geriatrics. 1995;50(4):33–39. 5. Rott KT, Agudelo CA. Gout. JAMA. 2003;289:2857–2860. 6. Terkeltaub RA. Gout. New Engl J Med. 2003: 349:1647–1655. 7. Winklerprins VJ, Vincent J, Weism antel AM. How effective is prophylactic therapy for gout in people with prior attacks? J Fam Pract. 2004: 53(10):837–838.
Codes ICD9-CM 274.9 275.49
ICD10 M10.9
Pa ge 2 0 8
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > G ranulo cyto penia
Granulocytopenia
Elicia Sinor Kennedy
Basics Description
Less than norm al num ber of polym orphonuclear leukocytes
Num ber of polym orphonuclear + bands Table o f C o ntents > Hallucino gen Po iso ning
Hallucinogen
Poisoning Brandon K. Wills
Basics Description
Predom inantly alters perception, cognition, and m ood
All hallucinogens potentiate neurotransm itter release or bind directly to receptors: o
Serotonin (5-hydroxytryptam ine; 5-HT): Many hallucinogens are agonists or antagonists at 5-HT receptor subtypes.
o
Norepinephrine, N-m ethyl-D-aspartate (NMDA), dopam ine
Etiology
Most exposures are intentional.
Com m on hallucinogens: o
Indoleam ine:
Lysergic acid diethylam ide (LSD) (duration 6–12 hours)
o
Morning glory (Ipom oea spp.)
Tryptam ines:
Psilocybin (Psilocybe m ushroom s); frequently
Pa ge 2 1 0
adulterated with LSD
N,N-dim ethyltryptam ine (DMT); 5-MeO-DMT (“foxy-m ethoxy―), and other tryptam ine congeners
o
Phenylethylam ines (hallucinogenic am phetam ines):
Methylenedioxyam phetam ine (MDA)
Methylenedioxyetham phetam ine (MDEA)
Methylenedioxym etham phetam ine (MDMA; “ecstasy―; duration 8–12 hours)
Param ethoxyam phetam ine
Dim ethoxyam phetam ine
Mescaline (peyote cactus); frequently adulterated with LSD (duration 6–12 hours)
o
o
o
Arylcycloalkylam ines:
Phencyclidine (PCP)
Ketam ine
Anticholinergic:
Deadly nightshade (Atropa belladonna)
Jim sonweed (Datura stram onium )
Other:
Piperazines: benzyl piperazine (BZP) and trifluorom ethylphenylpiperazine (TFMPP)
Dextrom ethorphan (DXM)
Marijuana
Diagnosis Signs and Symptoms
Considerable individual variation; effects m ay last 4–12 hours depending on agent/dose.
Sym ptom s characterized by sym pathetic arousal
Pa ge 2 1 0
Usually oriented and able to give history of exposure, even while having delusions
Initial sym ptom s: o
Nausea, flushing, chills, trem or
Neurologic sym ptom s: o
Restlessness and dizziness early after ingestion
o
Affective lability
o
Desire to laugh (especially with Psilocybe m ushroom s)
o
Anxiety, despair, helplessness, dread
o
Intensified perceptions, visual distortions/intensification
o
Tactile distortions (especially with m escaline)
o
Synesthesia (blending of sensory m odalities, e.g., seeing sounds)
o
Religious or m ystical experiences
o
Sleep disruption
Neurologic signs: o
Unusual/bizarre behavior
o
Speech disruption
o
Mydriasis
o
Piloerection
o
Hyperreflexia
o
Com a with m assive exposure
o
Convulsions:
Hallucinogenic am phetam ines
Children who becom e hyperpyrexic after Psilocybe m ushroom ingestion
Pulm onary: o
Mild tachypnea
o
Respiratory arrest (with m assive exposure)
Cardiovascular:
Pa ge 2 1 0
o
Tachycardia
o
Hypertension (with hallucinogenic am phetam ines)
o
Dysrhythm ia (with hallucinogenic am phetam ines)
o
Intracerebral hem orrhage (with hallucinogenic am phetam ines)
Gastrointestinal: o
Nausea/vom iting (especially with m escaline)
Metabolic: o
Hyperpyrexia:
Especially with MDMA use at “rave― clubs
Hepatic failure, renal failure, and dissem inated intravascular coagulopathy m ay follow.
o
May be lethal
Hyponatrem ia: has been reported with MDMA use
Hem atopoietic: o
Coagulopathies and hem orrhage at high doses owing to disruption of platelet serotonin function
Essential Workup
Core tem perature m easurem ent
Determ ination of risk of rhabdom yolysis: o
Creatine kinase level
o
Urine dip or m yoglobin level
Tests Lab
Electrolytes, blood urea nitrogen, creatinine, glucose levels
Urine toxicology screen: o
Rarely indicated
o
Distinguishing between hallucinogens is of little value.
o
Most hallucinogenic substances are not tested for on
Pa ge 2 1 0
routine drug screens. o
Am phetam ine screen is frequently negative for hallucinogenic am phetam ines (e.g., MDMA).
Differential Diagnosis
Meningitis
Intracranial bleeds or lesions
Withdrawal (ethanol, sedative-hypnotic, baclofen)
Serotonin syndrom e (especially with concom itant serotonergic agents involved)
Psychiatric illnesses: o
LSD associated with prolonged psychoses resem bling schizoaffective disorders
o
Chronic am phetam ine/cocaine abuse
o
Steroids
Infectious/febrile seizures in hyperpyretic child
Pediatric Considerations Assess parent-child relationships for possibility of neglect or abuse.
Treatment Pre Hospital
Controversies: o
Sedation with benzodiazepines versus haloperidol versus physical restraints:
Benzodiazepines are generally preferred.
Sedation m asks sym ptom s and m ay lim it history.
Cautions: o
Sedate or restrain patient to ensure safe transport.
o
For hypertherm ic patient:
Pa ge 2 1 0
Sedation rather than physical restraint
Begin cooling m easures.
P.469
Initial Stabilization
Airway, breathing, and circulation m anagem ent (ABCs)
Aggressive cooling if hypertherm ic
Intravenous access/rehydration with isotonic fluids for significant fluid loss or evidence of rhabdom yolysis
Naloxone, Accu-Chek, dextrose, and thiam ine if patient has altered m ental status
ED Treatment
Cooling m easures: o
Cool m ist and fans
o
Benzodiazapines, if agitated
o
Paralytics with intubation, if needed (generally not succinylcholine)
Sedate for agitation or autonom ic signs: o
Benzodiazapines
o
Rarely neuroleptics:
May intensify hallucinogenic experience
Possibly lower seizure threshold
Activated charcoal (AC) is not expected to be helpful for m ost agents owing to rapid absorption and delayed patient presentation: o
Consider AC for oral ingestions within 2–3 hours in patients with intact protective airway reflexes; especially for anticholinergics or seeds owing to delayed GI m otility/absorption.
Place in a quiet, calm environm ent.
Pa ge 2 1 0
Maintain urine output of 2–3 m L/kg/h and consider urine alkalinization for treatm ent of rhabdom yolysis.
Medication (Drugs)
Dextrose D 5 0 W for hypoglycem ia: 1 am pule: 25 g/50 m L (peds: D 2 5 W, 0.5–1 g/kg or 2–4 m L/kg) IV
Benzodiazepine (Diazepam ): 5–10 m g (peds: 0.2–0.5 m g/kg) IV
Haloperidol (Haldol): 2.5–5 m g IV or IM; not recom m ended for children
Naloxone (Narcan): initial dose: 2 m g (peds: 0.01–0.1 m g/kg) IV or IM
Sodium bicarbonate drip for rhabdom yolysis: 3 am pules in 1 L of D 5 W; infuse at 1.5–2 tim es m aintenance rates (keep urine pH >7.5)
Thiam ine (vitam in B 1 ): 100 m g (peds: 25 m g) IV or IM
Follow-Up Disposition Admission Criteria
Severely intoxicated
Atypical presentation
Prolonged sym ptom s (>12 hours after exposure)
Prolonged periods of agitation and hypertherm ia: o
Risk of rhabdom yolysis or organ dam age
Discharge Criteria Most patients can be discharged after receiving supportive therapy and observation once they are asym ptom atic.
Pa ge 2 1 0
Pediatric Considerations Suspected cases of child abuse or neglect require referral to child protective services.
References 1. Abraham HD, Aldridge AM, Gogia P. The psychopharm acology of hallucinogens. Neuropsychopharm acology. 1996;14:285–298. 2. Acute reactions to drugs of abuse. Med Lett Drugs Ther. 2002;44:21–24. 3. Graem e KA. New drugs of abuse. Em erg Med Clin North Am . 2000;18:625–636. 4. Kalant H. The pharm acology and toxicology of “ecstasy― (MDMA) and related drugs. Can Med Assoc J. 2001;165:917–928. 5. Wilson JM, McGeorge F, Sm olinske S, et al. A foxy intoxication. Forensic Sci Int. 2005;148(1):31–36.
Codes ICD9-CM 969.6 Psychodysleptics (hallucinogens)
ICD10 T40.9 Other and unspecified psychodysleptics (hallucinogens)
Pa ge 2 1 0
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Hand Infectio n
Hand Infection
Chet Shermer
Basics Description
Hand infections are com m only seen in the ED.
The range of pathology is broad and m ay include acute and chronic conditions.
Alert Hand infections are potential liability issues and m ust be handled with extrem e caution. Referral to hand surgeon is alm ost always indicated.
Etiology
Bacterial infection of the hand is associated with skin pathogens:
o
Staphylococcus or Streptococcus species
o
History of a puncture wound
Anaerobes are identified in 75% of paronychia in children owing to thum b sucking and nail biting.
Chronic paronychia m ay be caused by Candida albicans.
Herpetic whitlow is caused by type 1–2 herpes sim plex virus.
Clenched fist injuries involve a variety of pathogens,
Pa ge 2 1 0
including anaerobic Streptococcus and Eikenella sp.
Diagnosis Signs and Symptoms
Paronychia: o
Localized edem a, erythem a, and pain in proxim al portion of lateral nail fold
o
Fluctuance m ay be present and m ay extend beneath the nail m argin.
o
System ic signs and sym ptom s are usually not present.
Felon: o
Erythem a and tense swelling of the distal pulp space that does not extend proxim al to the proxim al interphalangeal (PIP) joint
o
Aching pain early, severe throbbing pain late
o
System ic signs are usually not present.
Herpetic whitlow: o
Distal pulp space is swollen, but rem ains soft.
o
Lateral nail folds m ay be affected.
o
Throbbing pain of the distal pulp space
o
Vesicles containing nonpurulent fluid are present and m ay form bullae.
o
System ic sym ptom s m ay be present:
Fever
Lym phadenopathy
Constitutional sym ptom s
Flexor tenosynovitis: o
Kanavel signs:
Severe pain and sym m etric edem a of the digit
Pa ge 2 1 0
Tenderness over the course of tendon sheath
Flexed position of the finger at rest
Pain on passive extension of the finger—m ay be the only finding in early infection
Clenched fist injury: o
Laceration over the m etacarpophalangeal (MCP) joint from striking an object with a clenched fist
o
Any laceration over the MCP m ust be assum ed to be a hum an bite wound until proven otherwise.
Web space abscess: o
Pain and edem a of the affected web space and adjacent palm
o
Fingers are held abducted.
Palm ar space infections: o
Thenar space infection:
Pain, tenderness, tense edem a of thenar em inence
Dorsal edem a without tenderness
Thum b is held abducted and flexed, and passive adduction is painful.
o
Midpalm ar space infection:
Pain, edem a, and tenderness of the m idpalm ar space
o
Dorsal edem a without tenderness
Motion of m iddle and ring fingers is painful.
Hypothenar space infection:
Pain and fullness over hypothenar em inence
No lim itation of finger m ovem ent
Essential Workup Most hand infections are diagnosed by history and physical exam ination with special attention to neurovascular status.
Pa ge 2 1 1
Tests Lab
Although usually not necessary, herpetic whitlow m ay be confirm ed by Tzanck test.
Gram stain and culture m ay guide antibiotic choice in felons.
Blood cultures, CBC are not routinely indicated.
Imaging
Radiographs are usually not helpful unless there has been traum a or a suspected foreign body.
With felon, flexor tenosynovitis, and palm ar space infection, radiograph m ay identify osteom yelitis or foreign body.
Radiographs in clenched fist injury m ay reveal a fracture.
Differential Diagnosis
Paronychia should be differentiated from herpetic whitlow and felon.
The differential for palm ar space infection includes flexor tenosynovitis, cellulitis, and web space infection.
Treatment
Paronychia: o
Early paronychia/sim ple cellulitis without purulence present m ay be m anaged with oral antibiotics and rest:
Cephalexin, dicloxacillin
Clindam ycin or erythrom ycin if associated with nail biting or oral contact
Pa ge 2 1 1
o
Superficial infections are drained by inserting a No. 11 blade between nail and eponychium and lifting the eponychium from the nail.
o
If necessary, the lateral nail fold m ay be incised tangential to the curvature of the nail.
o
When pus is present under the adjacent nail, one fourth of the nail should be rem oved.
o
When pus is present under the dorsal roof of the proxim al nail, rem ove one third of the proxim al nail.
P.471
Felon: o
A lateral incision avoiding the neurovascular bundle is preferred.
o
More extensive felons are drained through a unilateral longitudinal incision that does not cross the distal interphalangeal (DIP) flexor crease.
o
Disruption of fibrous septa is no longer recom m ended:
o
Results in an unstable fingertip
Loculations m ay need to be broken up.
Give oral antibiotics to cover skin pathogens, place a drain, and recheck in 48 hours:
Cephalexin, dicloxacillin
Herpetic whitlow: o
Usually self-lim ited; do not incise and drain.
o
Oral acyclovir m ay be given to patients with system ic involvem ent.
Flexor tenosynovitis, web space abscess, palm ar space infection: o
Elevation, IV antibiotics, and pain control:
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Am picillin/sulbactam , cefoxitin, ticarcillin/clavulanate
o
All of these infections require im m ediate consultation with a hand surgeon.
Clenched fist injury: o
Elevation, IV antibiotics, tetanus prophylaxis, and pain control in the ED:
Am picillin/sulbactam , cefoxitin, ticarcillin/clavulanate
o
All bite wounds with evidence of infection or joint involvem ent require em ergent consultation with a hand surgeon.
o
If there are no signs of infection and no joint penetration, patients m ay be considered for outpatient treatm ent with oral antibiotics after appropriate irrigation and wound care:
Am picillin/clavulanate or penicillin V plus cephalexin or dicloxacillin
Do not prim arily close lacerations associated with a hum an bite; delayed prim ary closure or healing by secondary intention is appropriate.
Medication (Drugs)
Acyclovir: 400 m g PO t.i.d. for 10 days (peds: not recom m ended for herpetic whitlow)
Am picillin/clavulanate: 875/125 m g PO b.i.d. (peds: 40 m g/kg/d PO div. q6h)
Am picillin/sulbactam : 1.5–3.0 g IV q6h (peds: safety not established)
Cefoxitin: 2 g IV q8h (peds: 80–160 m g/kg/d IV or IM div. q6h)
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Cephalexin: 500 g PO q.i.d. for 7 days (peds: 40 m g/kg/d PO div. q6h)
Clindam ycin: 300 m g PO q.i.d. for 7 days (peds: 20–40 m g/kg/d div. q6h PO IV or IM)
Dicloxacillin: 500 m g PO q.i.d. for 7 days (peds: 12.5–50 m g/kg/d PO div. q6h)
Erythrom ycin: 500 m g PO q.i.d. for 7 days (peds: 40 m g/kg/d div. q6h PO)
Penicillin V: 250 m g PO q.i.d. (peds: 40 m g/kg/d PO div. q6h)
Ticarcillin/clavulanate: 3.1 g IV q4h–q6h (peds: safety not established)
Follow-Up Disposition Admission Criteria
Flexor tenosynovitis, web space abscess, palm ar space infections: o
All these infections require adm ission for IV antibiotics and drainage.
Clenched fist injury with signs of infection: o
Requires adm ission for surgical débridem ent and IV antim icrobials
Discharge Criteria
Paronychia and felons: o
Patients with uncom plicated paronychia or felon m ay be discharged from the ED with a recheck and drain rem oval in 48 hours.
Herpetic whitlow:
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o
Patients with herpetic whitlow m ay be discharged from the ED with appropriate follow-up.
Clenched fist injury without infection: o
May be discharged on oral antibiotics with follow-up in 24 hours
References 1. Antosia RE, Lyn E. The hand. In: Rosen P, et al., eds. Em ergency Medicine: Concepts and Clinical Practice. 4th ed. St. Louis, MO: Mosby; 1997;1998:625–668. 2. Hausm an MR, Lisser SP. Hand infections. Orthop Clin North Am . 1992;23(1):171–185. 3. Tintinalli JE, Kelen GD, Stapcynski JS, eds. Em ergency m edicine: a com prehensive study guide. Hand Infect. 1999;277–280.
Codes ICD9-CM 136.9
ICD10 L08.9 L70.8 M70.1
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Haz m at
Hazmat
Moses S. Lee
Basics Description Hazm at refers to exposure to hazardous m aterials causing local or system ic toxicity.
Pathophysiology
Acids cause coagulation necrosis with eschar, usually lim iting penetration to deeper tissue.
Alkalis cause liquefaction necrosis and soluble com plexes that penetrate into deep tissues.
Dam age also occurs through oxidation, protein denaturation, cellular dehydration, local ischem ia, and by m etabolic com petition/inhibition.
Etiology Hazardous m aterials are encountered in household, industry, agriculture, and transportation accidents and in crim inal/terrorist activities.
Associated Conditions Related to toxic agent and its effects
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Diagnosis Signs and Symptoms
Skin: o
Chem ical burns; m ay appear deceptively m ild at first
o
Visible liquid or powder on skin
o
Absorption through skin m ay cause system ic toxicity.
Mucous m em branes (eyes, nasopharynx; see Corneal Burn): o
Ranges from subjective irritation to serious m ucosal burns
o
Potential airway com prom ise
Pulm onary: o
Cough
o
Pleuritic chest pain
o
Bronchospasm
o
Dyspnea
o
Pulm onary edem a (im m ediate or delayed)
System ic (after skin or pulm onary absorption): o
Altered m ental status
o
Seizures
o
Tachy/brady dysrhythm ias
o
Hypotension/hypertension
o
Gastrointestinal sym ptom s
o
Electrolyte disturbances
o
Carboxyhem oglobinem ias and m ethem oglobinem ias
o
Cholinergic syndrom e (see Chem ical Weapons Poisoning, Nerve Agents)
Essential Workup
Attem pt to identify substance using prehospital providers,
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Material Safety Data Sheet, and Chem trec (Chem ical Tr ansportation Em ergency Center).
Material Safety Data Sheet (MSDS): o
Identifies chem icals
o
Differentiates vapor versus skin hazard
o
Determ ines need for decontam ination
o
Lim ited treatm ent data
Determ ine route and duration of exposure.
Inhalation injury m ore likely in an enclosed space
Determ ine toxicity using poison control, com puterized databases such as POISINDEX or TOXNET, or standard toxicology text.
Observe as needed for system ic toxicity.
Tests Lab
Depends on substance
Electrolytes, BUN, creatinine, and glucose levels
Liver function tests
Calcium level
Magnesium level
Phosphorus level
Arterial blood gases: o
Metabolic acidosis
o
Carboxyhem oglobinem ias and m ethem oglobinem ias
o
Respiratory failure
Imaging Chest radiograph for pulm onary edem a
Differential Diagnosis
Skin: o
Hypersensitivity reaction
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o
Therm al burns
Pulm onary: o
Pneum onia
o
Pulm onary em bolism
o
Anaphylaxis
System ic: o
Status epilepticus
o
Overdose
o
Psychiatric illness
o
Myocardial infarction
Treatment Pre Hospital
Recognize a Hazm at situation: o
Accident at industrial/agricultural site
o
Accident involving transport of hazardous m aterials
o
Suspected terrorist m ass casualty incident
o
Cholinergic syndrom e
o
Irritant m ucous m em brane sym ptom s
o
Chem ical burns
Protect yourself: o
Approach from upwind.
o
Do not enter scene until safety of m aterial is determ ined.
o
Use level A protective gear if safety not established
o
Anyone able to walk and talk is m inim ally contam inated.
Personal chem ical protective equipm ent: o
Level A: positive-pressure self-contained breathing apparatus (SCBA), fully encapsulated
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chem ical-resistant suit, double chem ical-resistant gloves, chem ical-resistant boots, and airtight seals between suit, gloves, boots o
Level B: SCBA, nonencapsulated chem ical suit, double gloves, boots
o
Level C: air-purification device, suit, gloves, boots
o
Level D: Com m on work clothes
Identify substance: o
Departm ent of Transportation (DOT) placard, Material Safety Data Sheet (MSDS), shipping papers, hazard labels
o
If unsuccessful, call Chem ical Transportation Em ergency Center (Chem trec: 1[800] 424-9300) to determ ine substance and toxicity.
o
Determ ine toxicity and need for decontam ination: o
Poison control
o
Chem trec
Decontam inate: o
Hazm at team s can do chem ical testing.
Hazm at team
Treat: o
Provide basic life support and advanced life support care as indicated.
o
Generally basic list support only in a “hot zone†•
o
Irrigate skin and ocular burns im m ediately and continue until arrival at hospital.
P.473
Initial Stabilization
Protect em ergency departm ent personnel:
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o
Secondary contam ination can occur from derm al contact or through inhalation of volatile gases/particles.
Keep patients outside in designated hot zones until decontam inated.
When in doubt, decontam inate.
Expect contam inated patients to arrive via em ergency m edical services or private vehicle.
If treatm ent is required before/during decontam ination: o
Use m inim um necessary staff in appropriate personal protection gear.
o
Focus on life- and lim b-saving care only.
Decontam ination: o
Security to enforce hot zone
o
Rem ove, label, and double-bag clothing (including contact lens).
o
Copious irrigation with soap and water for 10–15 m inutes with special attention to obviously contam inated areas, wounds, and exposed eyes
o
Recapture water to prevent contam ination of the sewer and downstream areas:
In an em ergency or m ass casualty situation, it is acceptable to let water drain into sewer.
o
Hydrotherapy:
Mainstay of therapy for chem ical burns
Contraindicated only for elem ental m etals (sodium and potassium )
o
Allow patient to decontam inate him self or herself or use trained decontam ination team .
o
Decontam inate children, dependent elderly, m entally/physically challenged and their appliances (e.g., wheelchairs) with caregivers.
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o
Gloves, m asks, goggles, and disposable gowns provide som e protection.
o
Rem ove/replace bandages, tourniquets, airway adjuncts, intravenous sets.
o
Retriage after decontam ination.
ED Treatment
Provide supportive care as needed.
Determ ine if antidotal treatm ent would be effective and available.
Hazm at incidents provoke extrem e fear: o
Expect casualties suffering from collective hysteria.
o
Knowledge of toxicologic profile can exclude contam ination in these patients.
Em ergency departm ent staff m ay becom e sym ptom atic even if chem ical concentrations in the air are below toxic levels and m ay need to be escorted to fresh air.
Chem ical burns: o
Irrigation should be started as soon as possible and, if owing to a strong alkali, m ay need to be continued for hours.
o
Aggressive fluid resuscitation 2–4 m L/kg lactated Ringer solution per total burn surface area (TBSA) percent over 24 hours with one half given over the first 8 hours
o
Pain control
Pulm onary sym ptom s: o
Bronchodilators, oxygen, intubation, and m echanical ventilation
Selected special treatm ents: o
Hydrofluoric acid burns:
Calcium gluconate via topical cutaneous gel, subcutaneous or intra-arterial
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For system ic toxicity: intravenous calcium gluconate and m agnesium
o
Phenol burns:
Rem ove phenol from skin with polyethylene glycol 300 or 400 or with isopropyl alcohol.
o
Nitrates:
Ingested or extensive burns m ay cause m ethem oglobinem ia.
Treat levels >30% with high-flow oxygen and intravenous m ethylene blue.
o
Elem ental m etals (sodium /potassium ):
Water lavage is contraindicated and dangerous.
Cover with oil until substance can be débrided from skin.
o
Organophosphates/carbam ate insecticides (see: Chem ical Weapons Poisoning)
Medication (Drugs)
Albuterol: 2.5–5.0 m g nebulized
Calcium gluconate: 10 m L of 10% solution
Magnesium : 2 g IV over 20 m in
Methylene blue: 1–2 m g/kg slow IV (peds: not recom m ended for 6 years old: 1 m g/kg IV/IM over 5 m in)
Follow-Up Disposition Admission Criteria
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Airway com prom ise, respiratory difficulty (hypoxia)
Significant system ic sym ptom s
Adm it patients with chem ical burns to burn center.
Discharge Criteria
Patients who are well after a period of observation and consultation with poison control
Superficial chem ical burns owing to a toxin without potential for system ic toxicity (weak acid/alkali)
References 1. Burgess JL, Kirk M, Borron SW, et al. Em ergency departm ent hazardous m aterials protocol for contam inated patients. Ann Em erg Med. 1999;34:205–212. 2. Goldfrank LR, Flom enbaum NE, Lewin NE. Goldrank's Toxicologic Em ergencies. 6th ed. New York: McGraw-Hill; 1998. 3. Greenberg MI, Cone DC, Roberts JR. Material Safety Data Sheet: a useful resource for the em ergency physician. Ann Em erg Med. 1996;27:347–352. 4. Waeckerle JF. Dom estic preparedness for events involving weapons of m ass destruction. JAMA. 2000;283:252–254. 5. Yeung R. Em ergency departm ent Hazm at decontam ination contingency plan. J Prehospital Med. Disaster Med. 2001;16.
Miscellaneous SEE ALSO: Chem ical Weapons Poisoning; Radiation Injury
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Head Traum a, Blunt
Head Trauma,
Blunt Gary M. Vilke
Basics Description Blunt traum a to head resulting in a variety of injuries ranging from closed head injury to death
Etiology Blunt traum a to head m ay cause several types of closed head injuries:
Concussion: transient loss of consciousness or am nesia with norm al head CT
Subdural hem atom a: tearing of subdural bridging veins and bleeding into the subdural space
Epidural hem atom a: dural arterial injury, especially the m iddle m eningeal artery often associated with a skull fracture: o
Classically, transient loss of consciousness followed by a lucid interval, then rapid dem ise
Subarachnoid hem orrhage: bleeding into the subarachnoid space following traum a
Cerebral contusion: focal injuries to the brain
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characterized as coup (beneath area of im pact) or contrecoup (area rem ote from im pact)
Intracerebral hem orrhage: m ass intracranial lesion with bleeding into the brain parenchym a
Diffuse axonal injury: m icroscopic injuries scattered throughout the brain in a patient in deep com a
Diagnosis Signs and Symptoms
Evidence of traum a to head includes: o
Scalp laceration, cephalohem atom a, or ecchym osis
o
Raccoon eyes: bilateral ecchym osis of orbits associated with basilar skull fractures
o
Battle sign: ecchym osis behind the ear at m astoid process associated with basilar skull fracture
o
Hem otym panum
o
Cerebral spinal fluid rhinorrhea or otorrhea
Evidence of increasing intracranial pressure includes: o
Decreasing level of consciousness, falling Glasgow com a scale score
o
Cushing response, bradycardia, hypertension, and dim inished respiratory rate
o
Dilated pupils associated with decorticate or decerebrate posturing
Tests Lab
Rapid check of blood glucose level
Com plete blood count, platelet count, and coagulation param eters
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Type and cross-m atch for surgical candidates.
Baseline electrolytes, blood urea nitrogen, and creatinine levels
Blood alcohol level if indicated
Imaging
Cervical spine radiographs or helical CT when indicated
Head CT should be perform ed in patients with any of the following:
o
Loss of consciousness or am nesia of events
o
Progressive headache
o
Alcohol or drug intoxication
o
Unreliable history or dangerous m echanism
o
Posttraum atic seizure
o
Repeated vom iting
o
Signs of basilar skull fracture
o
Possible skull penetration or depressed skull fracture
o
Glasgow com a scale score age 60–65 years) and alcoholics are at higher risk of intracranial hem orrhage: o
Have a low threshold for obtaining CT scan
Differential Diagnosis
Penetrating head traum a
Any condition that alters m ental status that m ay have produced a fall and caused external evidence of head traum a (e.g., hypoglycem ic episode, seizure)
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Treatment Pre Hospital
Blunt head traum a patients with risk for intracranial lesion m ust go to a traum a center: o
High-risk patients include those with depressed consciousness, focal neurologic signs, m ultiple traum a, or palpable depressed skull fractures.
Moderate-risk patients should go to a hospital with availability of prom pt neurosurgical consultation: o
Moderate-risk patients include those with progressive headache, alcohol or drug intoxication, unreliable history, posttraum atic seizure, repeated vom iting, posttraum atic am nesia, signs of basilar skull fracture.
Protect and m anage the airway including intubation: o
Routine hyperventilation without signs of cerebral herniation should be avoided.
If evidence of cerebral herniation (see Signs and Sym ptom s) or progressive neurologic deterioration, then initiate m easures to decrease intracranial pressure: o
o
Mild hyperventilation to keep PaCO 2 about 35:
16–20 breaths per m inute in adults
20–24 breaths per m inute in children
24–26 breaths per m inute in infants
Elevating head of bed 20–30°
Cervical spine precautions m ust be m aintained in all patients.
Cautions: o
Avoid hypotension (systolic blood pressure 30%.
Avoid hypotherm ia, which will increase risks of coagulopathy during surgery.
Maintain NPO status.
Surgery: o
Surgical procedure based on findings of CT scan and neurosurgical consultation
Medication (Drugs)
Etom idate: 0.2–0.3 m g/kg IV
Fentanyl: 3–5 µg/kg IV if systolic blood pressure >100 m m Hg
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Mannitol: 0.25–1 g/kg IV bolus
Morphine sulfate: 2–20 m g IV (peds: 0.1 m g/kg IV up to adult doses)
Phenytoin: 15–20 m g/kg IV up to 1,000 m g
Rocuronium : 0.6 m g/kg IV
Succinylcholine: 1–2 m g/kg IV
Vecuronium brom ide: 0.1 m g/kg IV; m inidose pretreatm ent: 0.01 m g/kg IV
Follow-Up Disposition Admission Criteria
Patients with m ass lesion associated with head traum a m ust be adm itted to the intensive care unit or undergo surgery.
Patients with subarachnoid hem orrhage and diffuse axonal injury should be initially adm itted to the intensive care unit.
Patients with ongoing sym ptom s including repetitive questioning, anterograde am nesia, or disorientation should be adm itted to a m onitored unit for neurologic evaluation.
Discharge Criteria
Patients with resolved sym ptom s, negative findings on head CT, and no other co-m orbid factors (e.g., intoxication, additional traum a needing treatm ent) m ay be discharged.
Patients with m inor head traum a, no loss of consciousness or am nesia, and norm al neurologic exam findings m ay be discharged hom e with a friend or fam ily m em ber and head
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injury instructions.
Pediatric Considerations Cases of suspected nonaccidental traum a m ust be reported to the appropriate legal agency.
References 1. Brain Traum a Foundation. Guidelines for Prehospital Managem ent of Traum atic Brain Injury. New York: Brain Traum a Foundation; 1999. 2. Brain Traum a Foundation. Managem ent and Prognosis of Severe Traum atic Brain Injury. New York: Brain Traum a Foundation; 2000. 3. Chestnut RM, Marshall LF, Klauber MR, et al. The role of secondary brain injury in determ ining outcom e from severe head injury. J Traum a. 1993;34:216–222. 4. Com m ittee on Traum a. Head traum a: Advanced Traum a Life Support. 7th ed. Chicago: Am erican College of Surgeons; 2002. 5. King BS, Gupta R, Narayan RK. The early assessm ent and intensive care unit m anagem ent of patients with severe traum atic brain and spinal cord injuries. Surg Clin North Am . 2000;80(3):855–870.
Codes ICD9-CM 959.01 Head injury, unspecified
ICD10 S09.90 Unspecified injury of head
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Head Traum a, Penetrating
Head Trauma,
Penetrating Gary M. Vilke
Basics Description Penetrating injury to intracranial contents:
High-velocity penetration: usually bullets, which cause traum a directly to brain tissue, but also have a “shock wave― injury to local surrounding brain
Low-velocity penetration: usually knives, picks, or other sharp objects, with direct local traum a to brain tissue
Etiology
Direct penetration of the skull into the intracranial cavity by foreign object: o
Direct or local dam age to brain tissue
o
Intracranial hem orrhage, including subdural, epidural, and intraparenchym al bleeds
A bullet that hits the skull, ricochets off, and does not fracture the skull can still cause significant traum a to the underlying brain tissue.
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Diagnosis Signs and Symptoms
Alteration in level of consciousness and neurologic exam varies based on object and location.
Evidence of increasing intracranial pressure: o
Decreasing level of consciousness
o
Falling Glasgow com a scale score
o
Cushing response: bradycardia, hypertension, and dim inished respiratory rate
o
Blown pupil associated with decorticate or decerebrate posturing
Evidence of penetrating injury to head or basilar skull fracture, or object still rem aining in head: o
Raccoon eyes: bilateral ecchym osis of orbits associated with basilar skull fractures
o
Battle sign: ecchym osis behind the ear at m astoid process associated with basilar skull fracture
o
Hem otym panum
o
Cerebral spinal fluid rhinorrhea or otorrhea
Essential Workup
Determ ine the weapon type or caliber of weapon at scene.
Thorough exam to assess extent of injuries
Neurologic exam : o
Alteration in level of consciousness and neurologic exam varies based on object and location.
o
Evidence of penetrating injury to head
Tests Lab
Com plete blood count
Platelet count
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Coagulation perim eters
Type and cross-m atch.
Electrolytes, blood urea nitrogen, and creatinine baseline levels
Imaging
CT of head depicts location of lesion and extent of dam age.
Skull radiographs m ay reveal depth of im palem ent, location of bone fragm ents, and presence of fragm ents within the cranium .
Cervical spine evaluation (when indicated): o
Helical CT scanning or anteroposterior, lateral, and odontoid views plain radiographs
Differential Diagnosis
Blunt head traum a
Basilar skull fracture
Any condition that alters m ental status that m ay have induced a fall and caused secondary penetrating traum a
Treatment Pre Hospital
Stabilize, but do not rem ove, foreign object (e.g., knife).
Determ ine the weapon type or caliber of weapon at scene.
Protect and m anage the airway to avoid hypoxem ia.
Avoid hyperventilation.
Maintain cervical spine precautions.
Transport to traum a center.
Avoid hypoxia (oxygen saturation 30%.
If definitive neurosurgical care is not im m ediately available, a single burr hole m ay preserve life until neurosurgical intervention can be attained: o
Perform only in com atose patients with decerebrate or decorticate posturing on the side of a known m ass lesion/hem atom a who have not responded to initial treatm ent.
Avoid hypotherm ia, which will increase risks of coagulopathy during surgery.
Maintain NPO status.
Surgery: o
Based on clinical and radiologic findings and neurosurgical consultation
Medication (Drugs)
Etom idate: 0.2–0.3 m g/kg IV
Fentanyl: 3–5 µg/kg IV: o
If systolic blood pressure >100 m m Hg
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Mannitol: 0.25–1 g/kg IV bolus
Morphine sulfate: 2–20 m g IV (peds: 0.1 m g/kg up to adult doses)
Phenytoin: 15–20 m g/kg IV up to 1,000 m g
Rocuronium : 0.6 m g/kg IV
Succinylcholine: 1–2 m g/kg IV
Vecuronium brom ide: 0.1 m g/kg IV: o
Pretreatm ent m inidose: 0.01 m g/kg IV
Follow-Up Disposition Admission Criteria Adm it all patients to intensive care unit or transport directly to surgery.
Discharge Criteria Do not discharge.
References 1. Brain Traum a Foundation. Guidelines for Prehospital Managem ent of Traum atic Brain Injury. New York: Brain Traum a Foundation; 1999. 2. Brain Traum a Foundation. Managem ent and Prognosis of Severe Traum atic Brain Injury. New York: Brain Traum a Foundation; 2000. 3. Chestnut RM, Marshall LF, Klauber MR, et al. The role of secondary brain injury in determ ining outcom e from severe head injury. J Traum a. 1993;34:216–222. 4. Com m ittee on Traum a. Head traum a: Advanced Traum a Life Support. 7th ed. Chicago: Am erican College of Surgeons; 2002. 5. King BS, Gupta R, Narayan RK. The early assessm ent and
Pa ge 2 1 3
intensive care unit m anagem ent of patients with severe traum atic brain and spinal cord injuries. Surg Clin North Am . 2000;80(3):855–870.
Codes ICD9-CM 959.01 Head injury, unspecified
ICD10 S01.9 Open wound of head, part unspecified
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Headache, C luster
Headache, Cluster
Gary Johnson
Basics Description
Not clearly understood, but m ay be result of vasoactive substances released from m ast cells
May have m any clinical and pathophysiologic sim ilarities with m igraine and variants
Etiology
Cause is unclear at present.
Affects 0.1% of the population
Diagnosis Signs and Symptoms History
Occurs predom inantly in m iddle-aged m en
Episodes are often nocturnal and are m ore com m on in spring and fall.
Headaches occur in clusters, several tim es per day for weeks or m onths at a tim e.
Pa ge 2 1 4
Attacks are m ore likely after ingestion of alcohol, nitroglycerine, or histam ine-containing com pounds.
More likely in tim es of stress, prolonged strain, overwork, and upsetting em otional experiences
No prodrom e or aura
Unilateral, excruciating, nonthrobbing, incapacitating headache
Pain is ocular or retrobulbar
Rarely lasts longer than 2 hours; often lasts a few m inutes
Physical Exam
Com plete neurologic exam
Nasal congestion, lacrim ation, rhinorrhea, conjunctival injection, or facial flushing on the sam e side as headache
Horner syndrom e m ay be seen.
Essential Workup
An accurate history and physical exam ination should confirm the diagnosis.
Life-threatening alternatives need to be ruled out.
Tests Lab
Lum bar puncture (if m eningitis or subarachnoid hem orrhage is suspected)
Erythrocyte sedim entation rate (ESR; if tem poral arteritis is suspected)
Imaging CT scan/MRI (to rule out hem orrhage, tum or)
Differential Diagnosis
Migraine headache
Trigem inal neuralgia
Meningitis
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Tem poral arteritis
Intracerebral m ass lesion
Herpes zoster
Intracerebral bleed
Dental causes
Orbital/ocular disease (acute glaucom a)
Tem poral m andibular joint syndrom e
Treatment Pre Hospital
Recognize m ore severe life-threatening causes of headache.
Adm inistration of oxygen by face m ask m ay alleviate sym ptom s.
Initial Stabilization
Rule out life-threatening causes of headache.
Adm inistration of supplem ental oxygen
Medication (Drugs)
Ergots: DHE 1 m L IV; repeat in 1 hour if necessary
Fentanyl: 2–3 µg/kg IV
Meperidine: 50–75 m g IM or IV
Morphine: 2–4 m g IV or IM, m ay repeat q10m in
Nonsteroidal anti-inflam m atory drugs (NSAIDs): ketorolac 15–30 m g IM or IV
Oxygen: 100% via face m ask
Prochlorperazine: 10 m g IM or IV
Sum atriptan: 6 m g SC, m ay repeat in 1 hour (m ax. of 2
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doses in 24 hours) P.481
Follow-Up Disposition Admission Criteria
Persistent headache unresponsive to usual m easures
Unclear headache diagnosis
Discharge Criteria
Patients with m oderate to com plete pain relief, a norm al neurologic exam , and with a confident diagnosis of cluster headache
Issues for Referral Follow-up with a neurologist should be arranged.
References 1. Diener HC. Advances in the field of headache 2003/2004. Curr Opinion Neurol. 2004;17(3):271–273. 2. Diam ond S. The m anagem ent of m igraine and cluster headaches. Com pr Ther. 1995;21(9):492–498. 3. Kum ar KL. Recent advances in the acute m anagem ent of m igraine and cluster headaches. J Gen Intern Med. 1994;9(6):339–348.
Codes ICD9-CM 346.20
Pa ge 2 1 4
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Headache, M igraine
Headache,
Migraine Gary Johnson
Basics Description
Poorly understood. May involve vasoconstriction, cortical excitation, or both
May begin with intracranial artery vasoconstriction: o
Results in reduced cerebral blood flow and aura; type of which is dependent on the area of reduced flow
o
Followed by rebound vasodilation of arteries during which headache occurs
o
Arterial dilation, plasm a leak m ay cause pain.
Trigem inal nerve activation m ay account for headache.
Pediatric Considerations Migraines do present in the pediatric age group, but are less com m on.
Etiology
Idiopathic
May be precipitated by chocolate, cheese, nuts, alcohol, sulfites, m onosodium glutam ate (MSG), stress, or puberty.
Pa ge 2 1 4
Fam ily history of m igraines in 60% of cases
Affects 5–15% of the population: o
Wom en 3 tim es m ore than m en
Diagnosis Signs and Symptoms History
Com m on m igraine: o
Headache is recurrent, throbbing, and frequently unilateral.
o
Usually associated with photophobia, phonophobia, nausea, and vom iting
Classic m igraine: o
Sim ilar to com m on m igraine except it is preceded by a prodrom e; often visual sym ptom s such as bright lights, selective field defects, or jagged lines
Com plex m igraine: o
Migraine headache with associated focal neurologic sym ptom s such as num bness, weakness, paralysis, or aphasia
Essential Workup
An accurate history and physical exam should confirm the diagnosis.
Patients with new onset of headache syndrom e need an objective evaluation to rule out m ore serious causes of severe headaches: o
Com plete neurologic exam ination
o
Im aging m ay be appropriate in ED.
Tests
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Not needed for classic m igraine or established m igraines with typical sym ptom s
Lum bar puncture (LP) if m eningitis, subarachnoid hem orrhage, or pseudotum or cerebri is suspected
Erythrocyte sedim entation rate (ESR) if tem poral arteritis is suspected
Carbon m onoxide (CO) level if there is history or suspicion of CO exposure
Intraocular pressure m easurem ents if suspect glaucom a
Imaging CT or MRI of the head
Diagnostic Procedures/Surgery Lum bar puncture (LP)
Differential Diagnosis
Meningitis/encephalitis
Subarachnoid/intracranial hem orrhage
Cerebral ischem ia (if com plex m igraine)
Hypertension
Brain tum or
Carbon m onoxide intoxication
Tem poral m andibular joint (TMJ) syndrom e
Glaucom a
Pseudotum or cerebri
Tem poral arteritis
P.483
Treatment
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Pre Hospital
It is im portant to recognize life-threatening causes of headache and transport rapidly: o
Sudden onset of sym ptom s, altered m ental status, neck stiffness, fever, or neurologic deficit is a useful sign that suggests a m ore serious cause of headache.
o
Prior history of sim ilar headache, absence of above sym ptom s, or strong fam ily history is m ore suggestive of m igraine.
Allow patients with m igraine headache to be in a calm , dark environm ent.
Initial Stabilization Patients with convincing evidence of increased intracranial pressure m ay need rapid-sequence intubation and controlled ventilation.
ED Treatment
Abortive therapy and pain m anagem ent are the prim ary issues for patients in whom life-threatening causes of headache have been ruled out.
Generally, abortive therapy options should be attem pted first.
Narcotic pain m edications m ay be adm inistered as rescue therapy.
Intravenous saline hydration is often a helpful adjunct for m igraine headaches.
Medication (Drugs)
Abortive therapy in ED: o
Sum atriptan: 6 m g SC or nasally; m ay repeat in 1 hour (m ax. 2 doses per 24 hours). Newer triptans
Pa ge 2 1 4
have also shown efficacy. o
Ergot alkaloids: DHE 1 m g IM or IV, then repeat in 1 hour if necessary.
o
Droperidol (if ECG norm al): 0.625–2.5 m g IM/IV
o
Metoclopram ide: 10 m g IV
o
Prochlorperazine: 10 m g IV
o
Valproic acid: 250–1000 m g IV
Rescue pain m edication: o
Hydrom orphone: 1–2 m g IM/IV per dose
o
Morphine: 2–10 m g IM/IV per dose
o
Nonsteroidal anti-inflam m atory drugs (NSAIDs): ketorolac 15–30 m g IM/IV
Prophylactic therapy: o
Beta-blockers: propranolol 40 m g PO b.i.d.
o
Ca 2 + channel blockers: verapam il 40 m g PO t.i.d.
o
Cyclic antidepressants: am itriptyline 25 m g PO t.i.d.
o
Topiram ate: 50–200 m g PO daily
Follow-Up Disposition Admission Criteria
Severe intractable headache pain
Intractable vom iting, electrolyte im balance, or inability to take oral food or fluid
Unresolved com plex m igraines
Discharge Criteria Patients with m oderate to com plete pain relief, a norm al neurologic exam , and a confident diagnosis of m igraine
Issues for Referral
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Rapidly evolving therapeutic options suggest neurologic follow-up is im portant.
References 1. Diener HC. Advances in the field of headache 2003/2004. Curr Opinion Neurol. 2004;17(3):271–273. 2. Green MW. The em ergency m anagem ent of headaches. Neurologist . 2003;9(2):93–98.
Codes ICD9-CM 346.90
Pa ge 2 1 4
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Headache
Headache
Richard Wolfe Jonathan A. Edlow
Basics Description
Prolonged pain in the cranial vault, orbits, or nape of the neck
Intracranial and extracranial pain-sensitive structures project pain to the cranial surface. o
o
Intracranial:
Circle of Willis blood vessels
Medium -size arteries and m ajor branches
Large veins
Dura
Meninges
Extracranial:
Skin, scalp, fascia, m uscles
Mucosal linings of the sinuses
Arteries
Tem porom andibular joints
Teeth
Pain is transm itted via the 5th cranial nerve.
Pain m ay be caused by a num ber of m echanism s:
Pa ge 2 1 5
o
Nerve irritation
o
Traction on pain-sensitive vessels
o
Vasodilatation of pain-sensitive vessels:
Hypoxia, hypercapnia, fever, histam ine injection, nitroglycerin ingestion, or a sudden rise in blood pressure
o
Prolonged contraction of cranial m uscles
o
Inflam m ation of pain-sensitive structures
o
Nonorganic pain
2–4% of all ED visits have a chief com plaint of headache o
95% have a benign etiology
o
Life-threatening etiologies are rare but difficult to diagnose and often m issed.
Etiology
Vascular: o
Intra/extracranial vasodilatation and constriction of pain-sensitive blood vessels
o
Severe, throbbing headache
o
Divided into m igraine (the m ajority) and vascular nonm igrainous
o
Triggered by stress, horm one fluctuations, lack of sleep, certain foods
Tension: o
Unknown (possibly serotonin im balance, decreased endorphins)
o
Most com m on type of chronic recurring headache
o
Secondary to sustained contraction of head and neck m uscles
o
Triggered by poor posture, stress, anxiety, depression, cervical osteoarthritis
Cluster headaches: o
Triggered by alcohol, certain foods, altered sleep
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habits, strong em otions
Intracranial (traction): o
Mass lesions inside the calvarium stretching arteries and other pain-sensitive structures
Extracranial: o
Pathology from an extracranial site causing pain in a peripheral nerve of the head and neck
Unassociated with a structural lesion: o
Idiopathic stabbing headache
o
Cold stim ulus headache
o
Benign cough headache
o
Benign exertional headache
Other headaches: o
Multiple etiologies depending on cause (see differential diagnosis)
Diagnosis Signs and Symptoms History
Attributes of the pain—PQRST: o
Provocative and palliative features:
Position of the head, effect of coughing, straining, and m ovem ent
o
Quality:
Throbbing or continuous
Deep or superficial
Change com pared with any prior headaches
o
Region
o
Severity:
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o
Tim ing:
Is this the worst headache of the patient's life?
Is the onset sudden or gradual?
Associated findings: o
Visual sym ptom s
o
Dizziness
o
Nausea or vom iting
Historical factors indicating testing beyond the history and physical exam ination: o
o
New onset:
Over the age of 50 years
In an HIV patient
In a cancer patient
Severe headache or “worst headache of m y life†•
o
Persistent vom iting
Risk factors for cerebral sinus throm bosis: o
Malignancy
o
Pregnancy
o
Protein S or C deficiency
o
Oral contraceptive
o
Ulcerative colitis
o
Behçet syndrom e
Physical Exam
Factors indicating testing beyond the history and physical exam ination: o
Abnorm al vital signs:
Diastolic blood pressure >130 m m Hg
Fever
o
Altered level of consciousness
o
Papilledem a
o
Abnorm al neurologic findings or m eningism us
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Tension: o
Most com m on recurrent pain syndrom e:
o
Bilateral
o
Nonpulsatile
o
Bandlike
o
Mild to m oderate intensity
o
4- to 13-hour duration
Cluster: o
Requires 10 or m ore attacks of a specific nature
See Headache, Cluster
Migraine: o
See Headache, Migraine
Essential Workup
Detailed history and CNS, head, eyes, ears, nose, and throat and neck exam ination
Dependent on the clinical differential diagnosis
Tests Lab
Lab tests should be ordered only when the history or physical exam ination suggests threatening etiologies.
Erythrocyte sedim entation rate: o
If tem poral arteritis or other inflam m atory disorders suspected
See Tem poral Arteritis
Imaging
Head CT scan: o
Indications:
Unclear diagnosis based on history and physical exam ination
Signs of increased intracranial pressure
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Worst or first headache
Abrupt onset
Focal neurologic abnorm alities
Papilledem a
Recurrent m orning headache
Persistent vom iting
Headache associated with fever, rash, and nausea without system ic illness
Head traum a with loss of consciousness, focal neurologic findings, or lethargy
o
Altered m ental status, m eningism us
> 95% sensitive for subarachnoid hem orrhage (SAH) Table o f C o ntents > HELLP Syndro m e
HELLP Syndrome
Michael J. Bono
Basics Description
HELLP syndrom e: hem olysis, elevated liver enzym es, and l ow platelets
Signs/sym ptom s of hem olysis, abnorm al liver function tests, and throm bocytopenia were recognized 100 years ago.
Weinstein coined the term HELLP syndrom e in 1982.
Liver involvem ent is hallm ark: o
Other organs m ay be involved (e.g., brain, kidneys).
HELLP syndrom e recently divided into three groups, representing severity of the disease; severity is directly related to the platelet count: o
Class 1: m ost severe form ; platelet nadir 140/90 is abnorm al)
Im m ediate com plete blood count with platelet count and sm ear, blood urea nitrogen, creatinine, liver function tests, coagulation profile, and m agnesium level
Urinalysis for protein; screen for urinary tract infections.
Obstetric history:
o
Parity
o
Deliveries
o
Outcom es
Weigh patient to determ ine recent weight gain.
Tests Lab
Com plete blood count: o
Anem ia
o
Throm bocytopenia
o
Peripheral sm ear dem onstrates m icroangiopathic hem olytic anem ia (burr cells or schistocytes).
o
Other hem olysis m arkers are elevated lactate dehydrogenase (LDH) levels, increased reticulocyte count, and elevated bilirubin levels.
Platelet count and sm ear: o
Less than 100,000 cells per µL
Dissem inated intravascular coagulation screen
Coagulation profile: o
Prothrom bin tim e
o
Partial throm boplastin tim e
Blood urea nitrogen, creatinine, and m agnesium levels
Liver function tests to assess hem olysis m arkers and hepatic dysfunction: o
Elevated aspartate am inotransferase level: >40 IU/L
Pa ge 2 1 7
o
Elevated alanine am inotransferase level: >40 IU/L
o
Elevated lactate dehydrogenase: >600 IU/L
Imaging
Chest radiograph: o
CT of head: o
Suspected pulm onary edem a
Mental status changes (cerebral edem a)
Ultrasound of the pelvis (transabdom inal or transvaginal): o
Im age fetus and placenta
Alert Determ ination of gestational age and fetal viability is critical in HELLP.
Differential Diagnosis
Gastrointestinal: o
Cholecystitis
o
Cholelithiasis
o
Biliary colic
o
Pancreatitis
o
Hepatitis
o
Ulcer disease
o
Acute fatty liver of pregnancy
o
Acute gastritis
o
Hiatal hernia
o
Severe gastroesophageal reflux
Hem atologic: o
Pre-eclam psia-associated throm bocytopenia
o
Gestational throm bocytopenia
o
Idiopathic throm bocytopenic purpura
o
Throm botic throm bocytopenic purpura
o
Hem olytic urem ic syndrom e
Neurologic:
Pa ge 2 1 7
o
Epilepsy
o
Encephalitis
o
Meningitis
o
Encephalopathy
o
Brain tum or
o
Intracranial hem orrhage
Other: o
Drug abuse
o
Pyelonephritis
o
Sepsis
P.487
Treatment Pre Hospital Cautions:
Transport patient in left lateral decubitus position to prevent inferior vena cava syndrom e.
Venous access for anticipated seizure activity
Routine seizure m anagem ent (preferably with m agnesium sulfate) if the patient seizes
Alert Transport to a facility capable of providing high-risk obstetric care.
Initial Stabilization
Airway, breathing, and circulation m anagem ent
Left lateral decubitus position to prevent inferior vena cava syndrom e
One hundred percent oxygen via face m ask
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Maternal m onitoring: o
Cardiac
o
Pulse oxim etry
o
Tocography
Fetal m onitoring
ED Treatment
Control hypertension with antihypertensives (see Medications): o
Avoid angiotensin-converting enzym e inhibitors because of fetal side effects.
Heparin should be avoided because of bleeding com plications.
Treat pre-eclam psia or eclam psia with intravenous m agnesium sulfate: o
Magnesium sulfate is not given to treat hypertension.
Order type and screen for possible transfusion.
Call for em ergent obstetric consult, consider neonatology consult: o
Consider em ergent delivery.
o
Early plasm a exchange therapy has shown prom ise in postpartum patients with severe disease.
Discuss adm inistration of glucocorticoid with consultant: o
Helps fetal lung m aturity
o
Intravenous dexam ethasone m ore effective than intram uscular betam ethasone
o
Depends on gestational age of fetus
o
Does not reduce disease severity or duration
Lim it intravenous fluid adm inistration unless clinical evidence of dehydration: o
Excess fluids prom ote further capillary leak
o
Lactated Ringer or norm al saline at 60 m L per hour (no m ore than 125 m L per hour)
Pa ge 2 1 7
o
Monitor urine output with Foley catheter.
General Measures Diet As indicated
Activity Com plete bed rest
Special Therapy Blood products:
Correct throm bocytopenia by platelet transfusion in wom en with platelet counts 40,000 cells/µL are safe for vaginal delivery.
Correct throm bocytopenia to platelet counts >50,000 cells/µL if cesarian delivery planned.
If coagulation dysfunction is present, transfusion with fresh frozen plasm a and packed red blood cells in consultation with obstetrics
Transfusion with packed red blood cells for hem oglobin Table o f C o ntents > Hem o philia
Hemophilia
Steven H. Bowman
Basics Description
Caused by deficiency of factor VIII or factor IX
Absence of factors causes partial inactivation of coagulation cascade and im paired hem ostasis.
Two types: o
Hem ophilia A: factor VIII deficiency
o
Hem ophilia B (Christm as disease): factor IX deficiency
Severity varies am ong different individuals reflecting available natural factor activity: o
Seventy percent of type A hem ophiliacs are severe.
Sym ptom s dependent on factor availability: o
5–30% factor activity (m ild hem ophilia):
o
1–5% factor activity:
o
Bleeding alm ost exclusively with traum a:
Occasional spontaneous hem orrhages
Less than 1%:
Frequent spontaneous hem orrhages
Genetics
Sex-linked recessive occurring in m ales
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Rare disease: o
Hem ophilia A occurs in approxim ately 1 in 10,000 m ales.
o
Hem ophilia B occurs in approxim ately 1 in 30,000 m ales
Diagnosis Signs and Symptoms Bleeding:
Hem arthrosis (m ost com m on): o
Knee (m ost com m on) > elbow > ankle > shoulder > wrist (least com m on)
Muscle hem orrhage
Postextraction or oral m ucosal bleeding
Epistaxis (only in severe disease)
Hem aturia
Sustained from m inor traum a
Intracranial hem orrhage
Gastrointestinal bleeding
Pseudotum ors (blood cysts)
Essential Workup
Thorough physical exam ination
Factor-specific assays (see below)
Tests Lab
CBC
Platelet count: norm al
PT/PTT: o
PT: norm al
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o
PTT: increased
Bleeding tim e: norm al
Urinalysis: o
Asym ptom atic hem aturia is com m on finding.
Specific factor assays: o
Factor VIII:Ag (m easures factor VIII quantity): decreased
o
Factor VIII:c (m easures factor VIII activity): decreased
o
vWF (m easures von Willebrand factor activity): norm al
o
vWF:Ag (m easures von Willebrand factor quantity): norm al
Imaging Radiographic studies m ay be required in certain circum stances:
Head CT to evaluate or exclude intracranial bleed
Renal ultrasound/intravenous pyelograph (US/IVP) to evaluate excessive hem aturia or renal traum a
Abdom inal CT to evaluate or exclude retroperitoneal bleeding
Differential Diagnosis
Von Willebrand disease
Anticoagulant drugs
Antiplatelet agents
Throm bocytopenia
Hepatic dysfunction
Treatment Initial Stabilization
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Control bleeding.
Establish IV access.
ED Treatment General
Abort current bleeding episode by raising factor level.
Prevent additional m orbidity.
Coordinate ED care with prim ary provider (hem atologist).
Patients generally have excellent understanding of their disease.
Determ ine desired factor level based on risk of bleeding and location/system : o
Factor VIII required (in units) = wt (kg) × 0.5 × (% factor activity desired).
o
One IU factor VIII/kg raises activity approxim ately 2%.
o
Factor IX required (in units) = wt (kg) × 1.0 × (% factor activity desired).
o
One IU factor IX/kg raises activity approxim ately 1%.
May need to increase dose if inhibitors (antibodies to factor) are present or use special factor replacem ent
Patient/prim ary care provider or hem atologist usually has this inform ation.
Alert
Avoid all IM injections.
Avoid aspirin and aspirin-containing products.
Approach to Factor Replacement
Low to m oderate risk of bleeding: o
Soft tissue injury
o
Joint or m uscle bleeding
Pa ge 2 1 9
o
Desired hem ostatic factor level:
o
Thirty percent to 50%
Em pirical factor VIII therapy:
25–50 IU/kg
P.491
Moderate to severe risk of bleeding: o
GI or genitourinary (GU) bleeding
o
Desired hem ostatic factor level:
o
Em pirical factor VIII therapy:
50–100%
25–50 IU/kg
Severe risk of bleeding: o
CNS injury
o
Major traum a
o
Desired hem ostatic factor level:
o
100%
Em pirical factor VIII therapy:
50 IU/kg
Factor Replacement Options
Cryoprecipitates: o
Obtained from fresh frozen plasm a (FFP) after thawing at 4°C
o
Contains m ultiple proteins but high in VIII, vWF, and fibrinogen
o
Use only if purified factor not available.
o
Not useful in hem ophilia B; does not contain factor IX
Factor VIII concentrates: o
Mainstay of m odern hem ophilia therapy
o
Choice based on patient's profile, prior agents, cost
Interm ediate-purity products:
Pa ge 2 1 9
o
Low factor VIII specific activity
o
Contain fibronectin, fibrinogen, other proteins
o
Viruses killed by solvent detergent extraction or pasteurization
o
Indicated for older hem ophiliacs, patients with prior exposure to blood products
o
Exam ples: Hum ate-P, Profilate
High-purity products: o
High factor VIII specific activity
o
Contain fewer plasm a proteins
o
Exam ple: Alphanate
Very high purity products: o
Highest factor VIII specific activity
o
Contain no plasm a proteins
o
Either plasm a derived and m onoclonal antibody purified or produced using recom binant DNA technology
o
Indications: pediatric patients; those with lim ited prior exposure to blood products
o
Very expensive
o
Exam ple: Monoclate-P
Factor IX concentrates: o
Fewer options
Low-purity products also known as prothrom bin com plex concentrates (PCCs): o
Plasm a derived; contain factors VII, X, and prothrom bin
o
May be activated, i.e., able to initiate coagulation cascade (APCCs)
o
If adm inistered at frequent or prolonged intervals, m ay cause dissem inated intravascular coagulation (DIC) or throm bosis
Pa ge 2 1 9
o
Exam ples: Profilnine (PCC); Autoplex (APCC)
High-purity concentrates o
Plasm a derived; purified either using chrom atography or im m unoaffinity
o
Expensive
o
Exam ple: Alphanine
Adjuncts o
DDAVP:
Synthetic analogue of the antidiuretic horm one L-arginine vasopressin
Raises factor VIII level two to four tim es in patients with activity >5%
Not useful in patients with hem ophilia B
Maxim al effect occurs 15–30 m inutes after infusion.
Side effects: m ild flushing, headache, tachycardia, hypotension, hyponatrem ia
Dose 0.3 µg/kg of DDVAP diluted in 50 m L 0.9% norm al saline (NS) given over 15–30 m inutes
o
Am icar:
Only for m ucosal bleeding
Do not use in children.
Do not use in hem arthrosis or hem aturia.
Specific Management Considerations
Hem arthrosis: o
Replace factor prom ptly.
o
Splint
o
Ace, ice
o
Avoid aspirin.
o
Arthrocentesis rarely indicated
Muscle hem orrhage:
Pa ge 2 1 9
o
Replace factor prom ptly.
o
Forearm /calf—consider com partm ent syndrom e.
o
Avoid cylindrical casts.
o
Psoas hem atom a—groin pain, fem oral nerve paresthesias
Postextraction or oral m ucosal bleeding: o
Treat locally with Avitene or m icrofibrillar collagen.
o
Replace factor if severe.
o
Am icar m ay be useful.
Hem aturia: o
Generally m ild
o
Replace factor if sym ptom s >2 days (50–100%)
o
Hydrate.
o
Avoid Am icar and cryoprecipitate.
Intracranial hem orrhage: o
All head injuries should be considered significant, especially in children.
o
Do not delay therapy for diagnostic testing.
o
Replace factor to 100%.
o
CT scan aggressively.
Gastrointestinal bleeding: o
Secondary to ulcers, polyps, hem orrhoids
o
Replace factor prom ptly (50–100%).
o
Replace factor prior to endoscopy.
Follow-Up Disposition Admission Criteria
Low threshold for adm ission
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Generally observe 23 hours for resolution of bleeding.
Bleeding episodes m ay require m ultiple infusions.
Severe com plications
Head traum a
Discharge Criteria
Minor bleeding with resolution
If subjective sym ptom s only
References 1. Cohen AJ, Kessler CM. Treatm ent of inherited coagulation disorders. Am J Med. 1995;99:675. 2. DiMichele D. Hem ophilia 1996: new approach to an old disease. Pediatr Clin North Am . 1996;43:709. 3. Friedm an K, et al. Inherited coagulation disorders. In: Lee G, et al., eds. Wintrobe's Clinical Hem atology. 11th ed. Philadelphia: Lippincott William s & Wilkins; 2004:1619–1667. 4. Furie B, Lim entani SA, Rosenfield C. A practical guide to the evaluation and treatm ent of hem ophilia. Blood. 1994;843. 5. Roberts HR, et al. Hem ophilia A and Hem ophilia B. In: Beutler E, et al., eds. William s’ Hem atology. 6th ed. New York: McGraw-Hill; 2001:1639–1657.
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Hem o ptysis
Hemoptysis
Christian Young Peter Pang
Basics Description
Expectoration of blood, originating from the tracheobronchial tree
Mortality: o
If bleeding rate >1000 m L/24 hours, m ortality increases significantly: 58% (80% if m alignancy present).
o
If bleeding rate 7
Gastrointestinal (GI) source: o
Dark red or brown blood
o
Accom panied by gastric contents
o
Worsens in setting of nausea/vom iting
o
PH 8 Fr endotracheal tube to facilitate suctioning and subsequent bronchoscopy
o
Selective intubation of non-bleeding lung with single
Pa ge 2 2 0
or double lum en endotracheal tubes m ay be required
o
Supplem ental oxygen as needed
o
Continuous pulse oxim etry and cardiac m onitoring
Massive Hem optysis o
Principle risk to life is asphyxiation, not exsanguination
o
Maintain dual large-bore IV access
o
Volum e resuscitation with crystalloid or type specific blood as needed
ED Treatment
Respiratory and droplet precautions for ED staff
Antibiotic therapy if infiltrate present on chest radiograph
Correct hypoxem ia and/or coagulopathy
If m assive hem optysis o
Large bore IV or central access with volum e resuscitation as needed
o
Early involvem ent of pulm onary, anesthesiology, interventional radiology and/or thoracic surgery
o
Pt should be positioned upright, or with side of hem orrhage in m ost dependent position
o
Adm inister blood products as needed
o
Intubation for airway protection, im pending respiratory failure, or to facilitate bronchoscopic evaluation
o
Endobronchial tam ponade with Foley or Fogarty ( Table o f C o ntents > Hem o rrhagic Sho ck
Hemorrhagic
Shock Theodore C. Chan
Basics Description
Loss of effective circulating blood volum e resulting in inadequate organ perfusion
Com pensated shock: o
Patient's physiologic reserve prevents significant alteration in vital signs.
Decom pensated shock: o
Loss of circulating volum e overcom es patient's physiologic reserve, resulting in signification alteration in vital signs.
Blood loss estim ate: o
Multiply 70 m L/kg (adult blood volum e) tim es body weight (kg) tim es percentage loss as determ ined by class of hem orrhage.
Risk Factors
Traum a
Chronic or acute illness
Physical anom alies
Pa ge 2 2 1
Genetics
Arteriovenous m alform ations
Other genetic anom alies
Pathophysiology In hem orrhagic shock, blood loss exceeds the body's ability to com pensate and provide adequate tissue and organ perfusion. At the tissue level, hypoperfusion leads to inadequate oxygenation, anaerobic m etabolism , cellular injury, and death.
Etiology
Traum a—penetrating and blunt: o
o
o
Abdom inal:
Splenic injury (40% of abdom inal hem orrhage)
Liver injury (20% of abdom inal hem orrhage)
Chest:
Hem othorax
Aorta or great vessel injury
Pelvis:
Pelvic fracture with vascular injury
Abortion: com plete, partial, or inevitable
Aneurysm s m ay lead to thoracic, retroperitoneal, or intraperitoneal bleeding: o
Abdom inal aortic aneurysm m ost com m on
o
Mycotic aneurysm secondary to endocarditis
Aortogastric fistula
Arteriovenous m alform ations m ay lead to thoracic, retroperitoneal, or intraperitoneal bleeding.
Ectopic pregnancy
Epistaxis
Fractures (especially pelvis and long bones)
Gastrointestinal (GI) bleeding
Hem optysis
Pa ge 2 2 1
Malignancies
Mallory-Weiss tear
Placenta previa
Postpartum hem orrhage
Retroperitoneal bleeds
Splenic rupture
Vascular injuries
Associated Conditions Dependent on cause of hem orrhage
Diagnosis Signs and Symptoms
Class I hem orrhage: loss of up to 15% of blood volum e (up to 750 m L in 70-kg adult):
o
Heart rate (HR) 100
o
BP norm al
o
RR 20–30
o
Decreased pulse pressure
o
Mild anxiety
o
Sm all decrease in urine output
Class III hem orrhage: loss of 30–40% of blood volum e (1,500–2,000 m L)
Pa ge 2 2 2
o
HR >120
o
BP decreased
o
RR 30–40
o
Decreased pulse pressure
o
Significant change in m ental status: anxiety or confusion
o
Marked decrease in urine output
Class IV hem orrhage: loss of >40% of blood volum e (m ore than 2,000 m L): o
HR >140
o
BP decreased
o
RR >35
o
Very narrow pulse pressure
o
Depressed m ental status: confusion, lethargy, loss of consciousness
o
Negligible urine output
o
Cold and pale skin
Pediatric Considerations
Children often have greater physiologic reserve than adults and can preserve norm al vital signs longer.
System ic responses to blood loss in the pediatric patient include: o
Volum e loss 40%: hypotension, tachycardia, or bradycardia; com atose; pale, cold skin; no urine
Pa ge 2 2 2
output
Pregnancy Considerations Physiologic m aternal hypervolem ia requires greater blood loss to m anifest m aternal perfusion abnorm alities which m ay result in decreased fetal perfusion.
Geriatric Considerations Underlying disease and m edications m ay alter responses to hem orrhage and blood loss.
Essential Workup
Thorough health history
Description of events preceding and/or causing onset of sym ptom s
Com plete physical exam , including rectal exam , to determ ine shock category
Nasogastric tube: o
For undifferentiated hypovolem ic shock to rule out GI hem orrhage
Blood type and cross-m atch
Hem oglobin and hem atocrit levels
Insert Foley catheter: o
Monitor urine output.
Measure urine specific gravity.
Tests Lab
Coagulation studies: o
Prothrom bin tim e
o
Partial throm boplastin tim e
o
International norm alized ratio
Other m easures of shock and tissue hypoperfusion: o
Arterial blood gas
Pa ge 2 2 2
o
Base deficit
o
Serum lactate level
o
Serum electrolytes
Imaging
Chest radiograph: o
Blunt chest injuries
Thoracic arteriovenous m alform ation
Pelvic radiograph: o
Hem othorax:
Pelvic fracture
Focused Abdom inal Sonography for Traum a (FAST exam ): o
Abdom inal traum a
o
Possible abdom inal aortic aneurysm : Perform bedside evaluation.
o
Nontraum atic intraperitoneal hem orrhage
o
Fluid in Morison's pouch im plies significant hem orrhage or ascites.
o
Negative findings do not rule out intraperitoneal hem orrhage.
Endovaginal ultrasound: o
Positive pregnancy test
o
Fluid in the cul-de-sac
o
Ectopic pregnancy
Abdom inal CT scan: o
Detects both intraperitoneal and retroperitoneal hem orrhage
o
Perform ed once the patient has been stabilized
o
Abdom inal aortic aneurysm
P.497
Pa ge 2 2 2
Diagnostic Procedures/Surgery
Diagnostic peritoneal lavage: o
For unstable traum a patients when ultrasound fails to show intraperitoneal hem orrhage
o
Detects intraperitoneal bleeding only
o
Aspiration of 10 m L of blood defines the need for em ergent laparotom y in unstable patients.
Endoscopy: o
In the setting of upper or lower GI bleeding
Angiography: o
Pelvic fracture
o
Retroperitoneal hem orrhage
o
Lower GI bleeding
Em bolization therapy for bleeding from arterial sources can be perform ed.
Pathologic Findings Dependent on causative factor
Differential Diagnosis See Shock
Treatment Pre Hospital
Rapid assessm ent and transport to appropriate care center
IV access and fluid resuscitation are standard, but controversial.
Overaggressive fluid resuscitation to norm alize in field hypotension associated with increased m ortality in penetrating traum a
Pa ge 2 2 2
Initial Stabilization
Airway and breathing: o
Intubation as indicated by patient's respiratory and m ental status
o
100% oxygen via face m ask should be adm inistered.
Circulation: o
Two large-bore peripheral intravenous lines (16-gauge or larger)
o
Venous cutdown (saphenous) m ay be necessary.
o
Aggressive crystalloid resuscitation
o
Three-to-one rule: For one unit volum e of blood loss, give three volum es of crystalloid.
Early blood transfusion with evidence of class III or IV hem orrhage: o
Type-specific and cross-m atched blood is preferred when tim e perm its, often 1 hour.
o
Type-specific blood is usually available within 10–15 m inutes.
Type O blood can be used in im m ediate, life-threatening situations (type O Rh-negative blood only for wom en of child-bearing age).
ED Treatment
Control hem orrhage (direct pressure, pelvic fixation/stabilization, etc.).
Place patient on continuous m onitor.
Central venous access m ay be indicated for central vena cava m onitoring, but placem ent of such lines should not interfere with resuscitation m easures.
Continually reassess patient for clinical response or deterioration: o
Monitor vital signs, m ental status, and urine output.
Pa ge 2 2 2
o
Follow serial blood gas, lactate level, and hem oglobin/hem atocrit m easurem ents.
o
Maintain urine output at 50 m L per hour.
Response to initial fluid resuscitation is the key to determ ining subsequent therapy: o
Rapid response to fluid adm inistration indicates m inim al (less than 20%) blood loss.
o
Transient response to volum e resuscitation indicates ongoing hem orrhage or inadequate resuscitation; continue fluid and blood adm inistration and rapidly obtain necessary studies and consultations.
o
Minim al or no response to volum e resuscitation indicates ongoing severe blood loss; im m ediate angiography or surgical intervention is warranted.
Use fluids warm ed (approxim ately 39°C [102.2°F]) by m icrowave ovens, warm -water baths, or fluid warm ers.
Transfuse platelets and coagulation factors as indicated.
Consider autotransfusion devices with tube thoracostom y treatm ent and decom pression of large hem othoraces
Pediatric Considerations
Access m ay be obtained by intraosseous route after one or two unsuccessful attem pts at peripheral access.
Maintain urine output at 1 m L/kg per hour for children and 2 m L/kg per hour for infants.
Pregnancy Considerations Optim izing perfusion and treatm ent of the m other is treatm ent of choice for fetus
General Measures Diet Nothing by m outh
Pa ge 2 2 2
Activity Strict bed rest
Special Therapy
Blood products: cross-m atched, type-specific, O-positive or O-negative: o
O-negative should be reserved for wom en of child-bearing age
o
Adult: Initiate with four to six units of packed red blood cells.
o
Pediatric: 10 m L/kg of packed red blood cells
Other blood products: o
Platelets
o
Coagulation factors, such as fresh frozen plasm a (large transfusions of packed red blood cells as opposed to whole blood m ay lead to significant dilution of platelet and coagulation factors)
Hem oglobin substitutes: o
Under study, but of no proven benefit
IV Fluids
Crystalloids: norm al saline or lactated Ringer IV
Adults: 1- to 2-L bolus: o
Reassess for perfusion.
Pediatric: 20 m L/kg bolus
Surgery As indicated for causative factor after patient is stabilized
Follow-Up Disposition
Pa ge 2 2 2
Admission Criteria All patients with hem orrhage should be adm itted to the appropriate service.
Discharge Criteria Do not discharge.
References 1. Am erican College of Surgeons, Com m ittee on Traum a. Advanced Traum a Life Support for Doctors. 7th ed. Chicago: Am erican College of Surgeons, 2004. 2. Bickell WH, Wall MJ Jr, Pepe PE, et al: Im m ediate versus delayed fluid resuscitation for hypotensive patients. New Eng J Med. 1994;331:2205–2209. 3. Kline JA. Shock. In: Marx J, et al. Rosen's Em ergency Medicine: Concepts and Clinical Practice. 5th ed. St. Louis, MO: Mosby; 2001: 33–47. 4. Stainsby D, MacLennan S, Ham ilton PJ. Managem ent of m assive blood loss: a tem plate guideline. Br J Anaesth. 2000;85:487–491. 5. Wilson M, Davis DP, Coim bra R: Diagnosis and m onitoring of hem orrhagic shock during the initial resuscitation. J Em erg Med. 2003;24:413–422.
Codes ICD9-CM 958.4 Traum atic shock 785.59 Shock without m ention of traum a, other
ICD10 R57.1 Hypovolem ic shock
Pa ge 2 2 2
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Hem o rrho id
Hemorrhoid
Julia Sone
Basics Description
No precise definition exists.
Abnorm al vascular cushions of anal canal
Do not cause pain unless throm bosed/strangulated
Discrete m asses of thick subm ucosa contain: o
Blood vessels
o
Sm ooth m uscle
o
Elastic and connective tissue
Sliding down of part of anal canal lining
External hem orrhoids:
o
Vessels situated below dentate line
o
Covered by skin/anoderm
o
Drain to internal iliac veins
Internal hem orrhoids: o
Subm ucosal vessels above dentate line
o
Drain to portal system
o
Usually at left lateral, right posterolateral, and right anterolateral positions
o
Grade 1: painless, bleeding
o
Grade 2: prolapse with bowel m ovem ent (BM),
Pa ge 2 2 2
spontaneously reduce o
Grade 3: prolapse with BM, require m anual reduction
o
Grade 4: chronically prolapsed, not reducible
Etiology
Exact cause unknown
Associated with straining and irregular bowel habits: o
Hard, bulky stools or diarrhea cause tenesm us/straining.
o
Push anal cushions out of anal canal
o
Weaken subm ucosal tissue
Higher resting anal pressures
Erect posture
Heredity: o
Absence of valves in veins
Increased intra-abdom inal pressure: o
Ascites
o
Pregnancy
Portal hypertension
Diagnosis Signs and Symptoms
Painless, rectal bleeding with defecation
Blood on stool or toilet paper
Blood drips into toilet bowel
Severe pain if: o
Internal hem orrhoids prolapse and strangulate.
o
External hem orrhoids throm bose.
Pruritus ani
May also have fissure
Pa ge 2 2 3
History
Length of bleeding: o
Pain?
o
Duration?
Any new lum ps or m asses by rectum ?
Physical Exam
Exam ination of perianal area: o
Gently spread buttocks.
o
Discrete, dark blue, tender m ass covered with skin: throm bosed external hem orrhoid:
o
Can have internal com ponent
Purplish, tender m ucosal covered m ass: prolapsed, strangulated internal hem orrhoid:
Usually associated with enlarged, throm bosed external hem orrhoid
o
Have patient bear down to check for prolapsing hem orrhoids.
o
Digital rectal exam m andatory to rule out cancer
Anoscopy to visualize anal canal: o
Identify bleeding internal hem orrhoids.
Tests Lab
Hem atocrit (Hct) if history of significant blood loss
Platelets and PT/PTT/INR if patient on anticoagulants or severe co–m orbid condition
Differential Diagnosis
Rectal prolapse
Anal fissure
Perirectal abscess
Pa ge 2 2 3
Treatment Initial Stabilization Direct digital pressure to control bleeding
ED Treatment
Conservative therapy for all: o
Hot sitz baths for 15 m inutes t.i.d. and after each bowel m ovem ent
o
High-fiber diet—30 g/d:
Eat m ore fresh fruits and vegetables.
Increase bran intake.
o
10–12 glasses of water per day
o
Stool softeners
o
Bulk-form ing laxatives
Excise throm bosed external hem orrhoid if severe pain and if the hem orrhoid is 1,000 m L): restlessness, anxiety, pallor, pleuritic pain, hem optysis, dyspnea, or air hunger
Tachycardia, tachypnea, hypotension
Chest inspection: asym m etric expansion, paradoxical wall m ovem ent, abrasion, contusion
Chest wall palpation: tenderness or crepitus over ribs, clavicles, scapulae, or the sternum ; subcutaneous em physem a, dullness to percussion
Auscultation: ipsilateral decreased breath sounds
Essential Workup
Pa ge 2 2 3
Chest radiography is the single best diagnostic tool; fluid collections >200–300 m L can usually be seen on upright, decubitus chest radiograph: o
In the supine position, up to 1,000 m L of blood m ay not be readily apparent.
o
Hem othorax appears as a slight haziness over the involved hem ithorax on the anteroposterior (AP) radiograph.
o
In the hem odynam ically stable patient, the optim al technique is an upright posteroanterior (PA) projection at full inspiration.
Pulse oxim etry, arterial blood gas
Tests Lab
Hem atocrit m ay be helpful if it shows a drop or changes on serial evaluations.
Type and cross-m atch.
Imaging
Ultrasound diagnostic im aging is a valuable tool in the evaluation of intrapleural fluid collection.
CT is useful in detecting sm all am ounts of intrapleural fluid not visible on the chest radiograph.
Differential Diagnosis
Hem opneum othorax
Pneum othorax
Pulm onary contusion
Treatment
Pa ge 2 2 3
Pre Hospital Cautions:
Difficult to differentiate hem othoraces from pneum othoraces clinically: o
All m ay present with dyspnea, pleuritic chest pain, decreased breath sounds, and hem odynam ic instability.
o
Certain clues aid in m aking the diagnosis such as subcutaneous em physem a for pneum othorax and dullness to percussion for hem othorax
Perform needle thoracostom y for potential tension pneum othorax if the patient hem odynam ically unstable.
Initial Stabilization Manage airway, breathing, circulation:
Control airway as needed; endotracheal intubation for patients with im pending respiratory failure
Supplem ental oxygen
Intravenous access to restore circulating blood volum e
Needle thoracostom y should be perform ed in patients with hem odynam ic instability unless chest tube kit is im m ediately available.
ED Treatment
Hem othorax is treated by evacuating accum ulated blood in the intrapleural space.
Tube thoracostom y evacuates blood; allows for re-expansion of the lung as well as constant m onitoring of blood loss.
Tube thoracostom y: o
Use a large-bore chest tube (36–40 French).
o
Insert in the fourth or fifth intercostal space at the m idaxillary line aim ing posteriorly and superiorly.
Pa ge 2 2 3
o
Tube is then connected to underwater-seal drainage and suction (20–30 m L H 2 O)
P.501
Autotransfusion should be used if available to replace blood loss.
Indications for thoracotom y: o
Initial tube drainage >20 m L/kg of blood (or 1,000 m L of blood for adults from the pleural cavity)
o
Persistent bleeding at a rate >7 m L/kg/h (or 200 m L/h for 4 hours)
o
Increasing hem othorax seen on chest radiography
o
Patient rem ains hypotensive despite adequate blood replacem ent and other sites of blood loss have been ruled out.
o
Patient decom pensates after initial response to resuscitation.
Indications for ED thoracotom y: o
Penetrating traum a:
Traum atic arrest at any point with initial signs of life in the field
Blood pressure Table o f C o ntents > Hepatic Encephalo pathy
Hepatic
Encephalopathy Matthew N. Graber
Basics Description
Changes in behavior and consciousness associated with hepatic insufficiency and the accum ulation of substances norm ally m etabolized by the liver. This accum ulation occurs when the liver is unable to perform its norm al m etabolic activity secondary to either hepatocellular dysfunction or portal system ic shunting: o
Accum ulation of am m onia from :
Protein degradation by colonic bacteria
Deam ination of glutam ine in sm all bowel
Accum ulated am m onia crosses blood–brain barrier and allows for form ation of elevated levels of cerebrospinal fluid (CSF) glutam ine.
Am m onia levels correlate poorly with degree of hepatic encephalopathy (HE).
o
Other neurotoxins
Short-chain fatty acids
Phenols
Pa ge 2 2 5
Mercaptans
Am ino acids such as tryptophan
Increased levels of inhibitory neurotransm itters: o
Benzodiazepines
o
γ-Am inobutyric acid (GABA)
o
Serotonin
Decreased levels of excitatory neurotransm itters: o
Glutam ate
o
Dopam ine
o
Aspartate
o
Catecholam ines
Other contributing factors to HE: o
CSF glutam ine levels correlate closely with degree of HE.
o
Decreased cerebral blood flow and oxygen
o
Increased glucose consum ption and possible hypoglycem ia
o
Zinc deficiency
Genetics Inherited errors of the urea cycle
Etiology
Advanced cirrhosis or fulm inant hepatic failure with hepatocellular dysfunction often in association with portal hypertension
Precipitating events: o
GI bleeding (m ore com m on in elderly)
o
Hypokalem ia
o
Alkalosis
o
Sepsis (e.g., spontaneous bacterial peritonitis)
o
Constipation
o
Noncom pliance with treatm ent regim en in chronic
Pa ge 2 2 5
liver failure o
High-protein diet
o
Hypoglycem ia
o
Hypovolem ia (e.g., post-large-volum e paracentesis)
o
Azotem ia (e.g., diuretic induced)
o
Narcotics or sedatives, including alcohol
o
Zinc deficiency as m ultiple urea cycle enzym es are zinc dependent
o
Hepatocellular injury
o
Viral- or drug-induced hepatitis
o
Post portosystem ic shunt placem ent
o
Recurrent encephalopathy can occur without precipitating factors.
Diagnosis Signs and Symptoms
Wide range of m ental status changes affecting behavioral, intellectual, neurom uscular function and level of consciousness
Signs and sym ptom s of associated chronic liver disease, portal hypertension, or fulm inant hepatic failure (FHF): o
Ascites
o
Spider angiom ata
o
Testicular atrophy
o
Muscle wasting
o
Easy bruising
o
Palm ar erythem a
o
Gynecom astia
Asterixis with m ild to m oderate encephalopathy
Fetor hepaticus—peculiar sweet odor associated with
Pa ge 2 2 5
severe HE
Grading (West Haven Criteria)
Stage 0: o
No apparent clinical changes
o
Abnorm al neurophysiologic and neuropsychologic tests
Stage I: o
Personality changes, irritability, depression or euphoria
o
Reversal of norm al sleep pattern
o
Im pairm ent of writing, drawing, addition, subtraction
Stage II: o
Significant behavioral changes, often inappropriate
o
Lethargy
o
Slow responses
o
Asterixis
o
Slurred speech
o
Ataxia
Stage III: o
Disorientation to tim e and place
o
Am nesia
o
Paranoia
o
Nystagm us
o
Hypoactive reflexes
o
Positive Babinski reflex
o
Sem istupor to stupor
Stage IV: o
Dilated pupils
o
Stupor or com a
Essential Workup
Elicit history of liver disease and prior episodes of HE.
Pa ge 2 2 5
Clinical diagnosis—altered m ental status with evidence of liver failure or portal hypertension
Search for precipitating cause (particularly GI bleeding and infection).
Check for electrolyte abnorm alities: o
Even m inim al abnorm alities m ay m anifest as significant clinical changes.
Tests Lab
Blood am m onia level: o
Increased in HE
o
Level correlates poorly with the degree of HE.
o
Helpful in detecting HE in cases of altered m ental status of unknown cause
o
Norm al am m onia level with suspected HE warrants search for other causes of altered m ental status.
o
Level affected by:
Dehydration/hypovolem ia
Infusion of am ino acid solution
Massive tissue breakdown
Hem occult testing and nasogastric lavage to rule out GI bleeding
CBC to search for anem ia
Cultures of blood, urine, and ascitic fluid to search for infectious cause
Electrolytes, BUN, creatinine, glucose
PT/INR with elevations suggesting significant liver failure
Liver profile/liver enzym es
Urinalysis
Toxicology screen for alternate cause of altered level of consciousness:
Pa ge 2 2 5
o
Acetam inophen and alcohol level as necessary
Additional labs as clinical scenario dictates: o
Thyroid-stim ulating horm one (TSH)
o
Arterial blood gas (ABG)
o
Magnesium
o
Zinc level
o
Viral serology
Diagnostic Procedures/Surgery
Chest radiograph for pneum onia and signs of congestive heart failure (CHF)
ECG for arrhythm ia and electrolyte im balance
Head CT scan: o
For new-onset altered m ental status, focal neurologic deficit, or suspected traum a
o
Cerebral edem a and atrophy associated with HE
CSF exam ination: o
For new-onset or unexplained worsening of HE
o
CSF glutam ine level correlates with severity of HE.
Paracentesis for spontaneous bacterial peritonitis (SBP) workup and culture of ascitic fluid
EEG is usually abnorm al, m ost com m only with generalized slowing and other nonspecific changes.
P.505
Differential Diagnosis
Alcohol withdrawal syndrom es including delirium trem ens
Asterixis seen in other m etabolic encephalopathies: o
Urem ia
o
CO 2 narcosis
o
CHF
Pa ge 2 2 5
o
Sedative overdose
o
Toxic confusional states secondary to:
Medications
Illicit drugs (e.g., am phetam ines, cocaine, etc.)
o
Metabolic encephalopathy
o
Hypokalem ia
o
Hypocalcem ia and hypercalcem ia
Urem ia
Hypoglycem ia
Sedative use including alcohol intoxication
Head traum a with concussion or intracranial bleed
Cerebrovascular accident and neuropsychiatric disorders
Meningitis or encephalitis
Pediatric Considerations
Consider Reye syndrom e early (m ost com m on cause of FHF in children) even if PT is only m ildly prolonged.
Consider fatty acid β-oxidation disorder: o
Freeze serum and urine sam ple for subsequent testing.
Treatment Initial Stabilization For advanced stages of HE:
Oxygen and airway protection
Cardiac m onitor
Fluid resuscitation
Usual initial altered m ental status treatm ent of naloxone, D 5 0 W (or bedside glucose) and thiam ine
ED Treatment
Pa ge 2 2 5
Identification and rem oval of precipitating factors is key and m ay im prove clinical picture alone.
Alert
Liver failure predisposes patients to both hypoglycem ia and HE, and these can be additive to the clinical picture; therefore, frequent glucose checks are of absolute im portance.
Treatm ent of com plicating conditions: o
Acute GI bleeding
o
Sepsis
o
Electrolyte abnorm alities
o
Coagulopathy
o
Renal and electrolyte disturbances
Avoid sedative/narcotics if possible: o
If necessary, use agents not m etabolized by the liver.
Increase nitrogen elim ination: o
Bowel cleansing with laxatives and nonabsorbable sugars (i.e., lactulose, sorbitol PO or per rectum [PR])
Decrease am m onia-producing intestinal flora (in com bination with lactulose): o
Neom ycin (nephrotoxic and ototoxic)
o
Metronidazole
Correct zinc deficiency with zinc acetate or sulfate.
Short-term restriction of protein intake in diet
Flum azenil in patients who have received benzodiazepines m ay provide m oderate, short-term im provem ent.
Alert
Avoid flum azenil unless you are sure that the patient is not a chronic alcoholic or benzodiazepine user as resultant
Pa ge 2 2 5
seizures m ay occur.
Precautions to prevent bodily harm to the confused patient with HE
Liver transplantation provides cure for severe, spontaneous, or recurrent HE.
Possibly of benefit: o
L-carnitine
o
Album in dialysis
o
Brom ocriptine
o
Broad-spectrum antibiotic coverage
o
N-acetylcysteine
o
Lactobacillus acidophilus supplem entation
o
Ornithine aspartate
o
Benzoate
o
Branched-chain am ino-acid supplem entation
o
Chelation of m anganese with edatate calcium disodium
Medication (Drugs)
Dextrose: 1 am p (25 g) of 50% dextrose 1–2 m L/kg (child: 2 m L/kg D 2 5 W) IV
Lactulose: 30 m L (peds: 0.3 m L/kg) PO or via nasogastric (NG) tube q6h titrated to produce 2 or 3 soft stools per day and stool pH Table o f C o ntents > Hepato renal Syndro m e
Hepatorenal
Syndrome Anwer Hussain
Basics Description
Renal failure (RF) in patients with acute or chronic liver disease with no other identifiable cause of renal pathology
Hepatorenal syndrom e (HRS) represents significant decline in renal perfusion due to severe liver disease: o
Type I hepatorenal syndrom e:
Acute form with spontaneous RF in patients with liver disease
Rapidly progressive
Decrease in creatinine clearance (CrCl) by 50% or doubling of Cr in 2 weeks (>2.5)
80% m ortality within 2 weeks
Seen with acute liver failure or alcoholic hepatitis
o
Oliguric or anuric
Type II hepatorenal syndrom e:
Slow course of RF
Seen in patients with diuretic resistant ascites
Pa ge 2 2 7
Lower m ortality rate than type I HRS
Hallm arks of HRS: o
Prerenal disease
o
Reversible renal vasoconstriction and m ild system ic hypotension
o
Kidneys have norm al histology and structure.
o
Lack of im provem ent in renal function after volum e expansion
Liver disease causes system ic vasodilation with decrease in arterial blood volum e: o
Reflex activation of sym pathetic nervous system
o
Activation of renin-angiotensin–aldosterone system (RAAS)
o
Stim ulation of num erous vasoactive substances:
Nitric oxide
Prostacyclin
Atrial natriuretic peptide (ANP)
Arachidonic acid m etabolites
Platelet-activating factor
Endothelins
Catecholam ines
Angiotensin II
Throm boxane
Action of vasoconstrictors prevails over vasodilator effects: o
Renal hypoperfusion ensues due to renal cortical vasoconstriction.
o
Decrease in renal blood flow and glom erular filtration rates
Decreased urine sodium excretion (U Na Table o f C o ntents > Herpes Sim plex
Herpes Simplex
Joanne Davis Mark Richmond
Basics Description
Viral disease characterized by recurrent painful vesicular lesions of m ucocutaneous area
Lips, genitalia, rectum , hands, and eyes m ost com m only involved
Characterized by latency in sensory ganglia and reactivation
Incubation period is approxim ately 4 days from exposure.
Viral shedding occurs from 7–10 days (up to 23 days) in prim ary infection and 3–4 days in recurrent infections.
Neonatal infections can occur in utero, intrapartum (m ost com m on), or postnatal; occur in 1/3,500 births per year in the United States
Hum an-to-hum an transm ission; 60–90% of population is infected with HSV-1 or HSV-2.
More com m on in blacks than whites in ages HSV-1
Infection of pulp and lateral aspect of finger with single or m ultiple vesicles
May occur from autoinoculation with prim ary oral or genital infection or from direct inoculation from occupational exposure
o
Can last 3–4 weeks
Recurrence possible
Traum atic herpes:
Can occur following cosm etic procedures of face, surgical and dental interventions, sun exposure or burns
o
Herpes gladiatorum :
Mucocutaneous infection of chest, face, and hands in wrestlers transm itted through traum atized skin
o
Eczem a herpeticum :
HSV-1 > HSV-2
Occurs in children and young adults with atopic derm atitis
Higher risk if on steroids or infected with HIV
Varicelliform eruption with spread to
Pa ge 2 2 9
surrounding skin
Fever, headache, and fatigue
HSV-associated erythem a m ultiform e
Usually presents on palm s and soles
Lasts 2–3 weeks
Eye: o
Most com m on cause of corneal blindness
o
Caused by extension of facial lesions or direct inoculation
o
Acute onset of pain and photophobia
o
Periauricular adenopathy, blurry vision, chem osis, and conjunctivitis
o
May be unilateral or bilateral
o
Dendritic lesions of cornea noted on fluorescein exam
o
Different from herpes varicella zoster as derm atom e not involved
CNS/encephalitis: o
Most com m on cause of severe sporadic encephalitis in the western world
o
Usually from HSV-1 reactivation disease
History May or m ay not have known history of exposure to HSV-1 or HSV-2
Physical Exam Vesiculoulcerative lesions in orofacial or genital area
Pediatric Considerations
Up to 60–80% of babies who develop neonatal HSV are born to m others without history of genital herpes.
Vesicular skin lesions m ay or m ay not be present on initial exam .
Prim ary genital disease of the m other increases risk of transm itting virus to fetus.
Pa ge 2 2 9
Most prim ary infections occur during childhood; sym ptom atic in only 5–10% of children
Orofacial disease is m ost likely to present as gingivostom atitis in children younger than 5 years of age.
Whitlow m ay be caused by thum b-sucking children with oral herpes.
Tests
Orofacial: o
Presum ptive diagnosis m ade by history and exam
o
If definitive diagnosis is necessary (e.g., system ic disease, child abuse):
Viral culture of vesicles
Fluorescent antibody detection of antigen; serum antibody studies
Scrapings for Tzanck sm ear or Papanicolaou stain
Skin biopsy if hyperkeratotic or lichenoid lesions
Eye: o
Dendritic corneal lesions by fluorescein exam
o
Swab of affected area for viral culture or fluorescent antibody detection
CNS/encephalitis: o
Lum bar puncture with cerebrospinal fluid (CSF) pleocytosis and negative bacterial antigens
o
CSF polym erase chain reaction (PCR) test
o
MRI/CT
o
EEG diagnostic if spike and waves in tem poral region
Lab
Lesion scrapings
Virus isolation by tissue culture of fluorescent antibody provides isolate that can be typed, but has lim ited
Pa ge 2 2 9
reliability depending on lab.
Tzanck sm ear dem onstrating m ultinucleated giant cells, atypical keratinocytes, and large nuclei
Serum testing has lim ited ED use.
Enzym e-linked im m unosorbent assay (ELISA) testing m ay dem onstrate HSV antibodies, determ ining past exposure only.
Requires from 2 weeks to >3 m onths to detect seroconversion
P.517
Differential Diagnosis
Orofacial and skin: o
Bacterial pharyngitis
o
Mycoplasm a pneum oniae pharyngitis
o
Stevens-Johnson syndrom e
o
Herpes zoster
o
Varicella
o
Pem phigus
o
Contact or chem ical derm atitis
o
Im petigo
Eye: o
Conjunctivitis: viral, bacterial, or allergic
o
Herpes zoster ophthalm icus
o
Scleritis/episcleritis
o
Angle-closure glaucom a
Treatment
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Pre Hospital
Maintain universal precautions.
Pain control
Initial Stabilization Protect airway in com atose or obtunded patients with suspected CNS disease.
ED Treatment
Orofacial/gingivostom atitis: o
Prim ary disease in healthy children is generally not treated.
o
Prim ary disease in norm al host with m ild disease
o
Supportive treatm ent with hydration and topical anesthetics (viscous lidocaine, diphenhydram ine elixir)
o
Oral acyclovir:
Severe disease or im m unocom prom ised patients: IV or oral acyclovir, valacyclovir, or fam ciclovir
If recurrent disease, oral acyclovir m ost helpful if started with prodrom e or at first sign of lesion
Reduces lesions and sym ptom s by 1–2 days
Topical antivirals generally ineffective for prophylaxis
Consider prophylaxis in patients with m ore than six episodes per year; history of herpes associated erythem a m ultiform e or herpes gladiatorum ; upcom ing intense sun exposure or stress; perioral/intraoral surgery; cosm etic facial procedures
Reduces frequency and severity of herpes labialis and m ay help decrease asym ptom atic
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shedding, leading to decreased transm ission
Does not cure or term inate the disease
When prophylaxis stopped, m ost patients have recurrences
Skin (other than orofacial or genital): o
May be treated with oral acyclovir
o
Antibiotics if secondary bacterial infection
o
Do not incise and drain: m ay lead to spread of infection.
Eye: o
Topical antiviral therapy with trifluridine or vidarabine
o
Vidarabine ointm ent for children
o
Do not treat with steroids: m ay cause increased viral replication
o
Suppressive therapy with oral acyclovir
o
Ophthalm ology consult
Pregnancy Considerations Acyclovir has been used to suppress genital herpes near end of pregnancy and appears safe, but is not FDA approved.
Medication (Drugs)
Acyclovir: o
Orofacial 400 m g PO t.i.d. for 10–24 days or 5 m g/kg IV (5–10 m g/kg) q8h for 7–14 days
o
Peds: prim ary infection: 15 m g/kg PO 5 tim es per day for 7 days
o
Skin (not orofacial or genital): 400 m g (20 m g/kg) PO t.i.d. for 10 days
o
Eyes for suppression therapy: 400 m g PO b.i.d.
Pa ge 2 3 0
o
Encephalitis: 10–15 m g/kg (20 m g/kg) IV q8h for 14–21 days
Fam ciclovir: o
Orofacial/im m unocom prom ised host: 250–500 m g PO t.i.d. for 5 days
Fluocinonide: o
Adults: topical 0.05% gel q8h for 5 days
Penciclovir: o
Adults and unapproved peds: topical 1% cream applied q2h while awake for 4 days
Trifluridine: o
Adults and peds older than 6 years: one drop of 1% ophthalm ic ointm ent to eye q2h while awake (m ax. nine drops per day) for 14–21 days
Valacyclovir: o
Adults: 500–1,000 m g PO b.i.d. for 7 days (not FDA approved)
Vidarabine: o
Adults or peds older than 2 years: topical 0.5-inch ribbon of 3% ophthalm ic ointm ent to eye 5 tim es per day
Suppressive therapy: o
Acyclovir: 200 m g PO 5 tim es per day for 5 days
o
Fam ciclovir: 125 m g PO daily for 3–5 days
o
Valacyclovir: 500 m g PO b.i.d. for 3–5 days
Long-term prophylaxis: o
Acyclovi: 400 m g PO b.i.d.
o
Valacyclovir: 500–1,000 m g PO daily
o
Fam ciclovir: 250 m g PO b.i.d.
Alert Antiviral dosing m ay need adjustm ent for renal failure.
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Follow-Up Disposition Admission Criteria
Encephalitis, dissem inated disease, dehydration
Severe local or dissem inated disease in im m unocom prom ised host
Neonatal HSV
ICU versus ward based on toxicity and need for airway support
Discharge Criteria Uncom plicated local disease
Issues for Referral
Neonatal herpes infection
Suppressive treatm ent options
Herpes infection during pregnancy
References 1. Brady RC, Bernstein DI. Treatm ent of herpes sim plex virus infections. Antiviral Res. 2004;61:81–94. 2. Nikkels AF, Pierard GE. Treatm ent of m ucocutaneous presentations of herpes sim plex virus infections. Am J Clin Derm atol. 2002;3:475–487. 3. Spruance SL, Kriesel JD. Treatm ent of herpes sim plex labialis. Herpes. 2002;9:64–69. 4. Waggoner-Fountain LA, Grossm an LB. Herpes sim plex virus. Pediatr Rev. 2004;25:86–93.
Miscellaneous
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SEE ALSO: Genital Herpes
Codes ICD9-CM 054.2 Herpetic gingivostom atitis 054.3 Herpes encephalitis/m eningitis 054.42 Herpes keratitis 054.6 Herpetic whitlow 054.9 Herpes labialis 646.8 Herpes gestationis 771.2 Congenital herpes
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Herpes Zo ster
Herpes Zoster
Michelle E. Pyka Mark G. Richmond
Basics Description
Com m only known as shingles or derm atom al zoster
Most com m on in patients with decreased cell- m ediated im m unity:
o
Older than 50 years of age
o
Neoplastic diseases (lym phoproliferative cancers)
o
Im m unosuppressive drugs
Dissem inates in 1–2% of norm al hosts and frequently in im m unocom prom ised hosts
Ram say Hunt syndrom e is characterized by zoster oticus, peripheral facial palsy, regional adenopathy, vertigo, and anesthesia of anterior two thirds of hem itongue: o
From 7th and 8th cranial nerve involvem ent
Postherpetic neuralgia (PHN) is a com plication of zoster: o
Described as pain that persists at site of zoster lesions for >1 to 3 m onths after cutaneous disease has healed
o
10–70% of patients will have pain after resolution of lesions.
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o
Incidence increases with age older than 50 years, severe rash, and severe pain.
Syndrom e of herpes zoster occurring without rash is called zoster sine herpete.
Etiology
Caused by varicella-zoster virus (VZV), a DNA virus in the Herpesviridae fam ily
Mostly in individuals who previously had chickenpox and very rarely in vaccinated individuals
Reactivation of a virus that lies dorm ant in dorsal root ganglia
Pregnancy Considerations Extrem ely low rate of fetal com plications; no need to consider term ination
Pediatric Considerations Childhood zoster is m ost com m on when varicella occurred in utero or within 6 m onths of life.
Diagnosis Signs and Symptoms
Prodrom e of pain and paresthesias in derm atom al distribution: o
Character of pain m ay be sharp, dull, tingling, burning, or intense pruritus.
o
Pain precedes rash by 1–10 days.
o
Prodrom e less likely in young patients
o
Classical rash is grouped vesicles on erythem atous base.
o
Initially are patches of erythem a and then vesicles
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o
Progress to scab and crust form ation over 10–12 days
o
Crusts fall off in 2–3 weeks.
o
Lesions evolve synchronously.
o
One derm atom e typically affected, rarely crosses m idline
o
Most com m on nerve distributions are thoracic and lum bar, followed by trigem inal and cervical.
Ocular involvem ent occurs in half of cases involving ophthalm ic division of trigem inal nerve: o
Closely associated with disease occurring at tip of nose (Hutchinson sign)
o
Corneal involvem ent begins as punctate keratitis, which m ay coalesce to form pseudodendritic or stellate pattern.
Dissem inated disease m ay cause signs and sym ptom s of m eningoencephalitis, m yelitis, peripheral neuropathy, hepatitis, and pneum onitis.
Im m unosuppressed patients are m ore likely to have severe disease and visceral involvem ent.
Essential Workup
Clinical presentation is sufficient for diagnosis in m ost patients.
If definitive diagnosis is necessary, tissue culture is recom m ended.
Herpes zoster ophthalm icus (HZO) is diagnosed by slit-lam p exam : o
The pseudodendrites of HZO are elevated and plaquelike, sitting on top of epithelium , and stain brighter with rose bengal.
o
Is less ulcerative than HSV and stains less brightly with fluorescein
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Tests Lab
Cell yields are highest if base of vesicular lesions are scraped.
Num erous rapid im m unofluorescence assays exist to detect VZV in vesicular fluid and are preferred m ethod: o
Can distinguish between HSV and VZV
Tzanck sm ear dem onstrates giant cells and intranuclear inclusions.
IgM and IgG are m ost com m only m easured by enzym e-linked im m unosorbent assay (ELISA): o
Antibody titers rise 2 weeks after acute infection.
Polym erase chain reaction (PCR) m ay be useful in cerebrospinal fluid (CSF) analysis or verrucous lesions in which cultures are otherwise negative.
Differential Diagnosis
Zosteriform herpes sim plex
Varicella
Herpes sim plex (HSV)
Nonherpetic conjunctivitis
Enteroviral infections (e.g., hand-foot-and-m outh disease)
Insect bites
Bullous im petigo
Molluscum contagiosum
Treatment Pre Hospital
Zoster is potentially contagious and m ay cause varicella in
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nonim m une health care workers: o
Lesions should be covered.
Maintain universal precautions.
Initial Stabilization
Rarely necessary
IV access to adm inister fluids and antiviral therapy
Dissem inated disease to CNS or lungs m ay require airway support.
P.519
ED Treatment
Goal of treatm ent is to treat acute viral infection, decrease pain, and prevent postherpetic neuralgia.
Acyclovir, valacyclovir, or fam ciclovir is recom m ended: o
Should be instituted within 72 hours of rash form ation
o
Valacyclovir and fam ciclovir are recom m ended over acyclovir in prevention of PHN.
Foscarnet recom m ended for acyclovir-resistant VZV in im m unocom prom ised patients
Ocular involvem ent: o
Necessitates ophthalm ologic consultation
o
Oral (norm al host) or intravenous (im m unocom prom ised host) acyclovir is best started within 72 hours; m ay be beneficial up to 1 week after sym ptom onset.
Oral corticosteroids in acute zoster are controversial: o
May reduce pain
o
Do not help prevent PHN
o
If not contraindicated, recom m ended in patients >50 years old, severe disease (>21 lesions), or severe
Pa ge 2 3 1
pain
Long-acting narcotics and topical lidocaine patches are recom m ended for m oderate to severe pain.
Over-the-counter analgesia for m ild pain
Postherpetic neuralgia (PHN) is difficult to m anage: o
Early use of antiviral drugs m ay prevent it.
o
Lidocaine patch or lidocaine and prilocaine cream provides short-term relief.
o
Topical capsaicin is controversial and should not be initiated in ED.
o
Sustained-release oxycodone useful for analgesia
o
Tricyclic antidepressants recom m ended:
Nortriptyline and desipram ine have fewer side effects than am itriptyline.
o
Gabapentin is safe and effective.
Medication (Drugs)
Acyclovir: adults: 800 m g PO 5 tim es per day for 7–10 days; im m unocom prom ised with severe disease 10–12 m g/kg IV infused over 1 hour q8h (peds: 20 m g/kg PO q.i.d. for 5 days, 10 m g/kg IV q8h)
Fam ciclovir: adults: 500 m g PO t.i.d. for 7 days (peds: not approved)
Foscarnet: 40 m g/kg IV q8h for 14–26 days
Gabapentin: 100–300 m g nightly at bedtim e increasing 100–300 m g every 3 days until adequate response or m ax. 3,600 m g/d div. t.i.d.
Lidocaine patch 5%: apply up to 3 patches for Table o f C o ntents > Hiccups
Hiccups
Carrie Tibbles James L. Smith Jr.
Basics Description
Sudden, involuntary, contraction of the diaphragm (usually unilateral) and other inspiratory m uscles term inated by abrupt closure of the glottis.
Usually occur with a frequency of 4–60 per m inute
Occurs as a result of stim ulation of one or m ore lim bs of the hiccup reflex arc: o
Involves irritation of the vagus and phrenic nerves
o
The “hiccup center― is located in the upper spinal cord.
Male-to-fem ale ratio is 4:1: o
In m en, m ore than 90% of cases have an organic basis.
o
In wom en, a psychogenic cause is m ore likely.
Etiology
Idiopathic
Gastrointestinal: o
Gastric distention
o
Esophageal lesions
Pa ge 2 3 2
o
Reflux esophagitis
o
Achalasia
o
Candida esophagitis
o
Carcinom a
o
Obstruction
o
Gastric lesions
o
Ulcer
o
Cancer
o
Hepatic lesions
o
Hepatitis
o
Hepatom a
o
Pancreatic lesions
o
Pancreatitis
o
Pseudocysts
o
Cancer
o
Inflam m atory bowel disease
o
Cholelithiasis
o
Cholecystitis
o
Appendicitis
o
Abdom inal aortic aneurysm
o
Postoperative, abdom inal procedure
Diaphragm atic irritation: o
Hiatal hernia
o
Tum ors
o
Pericarditis
o
Eventration
o
Splenom egaly
o
Hepatom egaly
o
Peritonitis
CNS lesions: o
Encephalitis
o
Ventriculoperitoneal shunt
Pa ge 2 3 2
o
Stroke
o
Subarachnoid hem orrhage
o
Arteriovenous m alform ations
o
Parkinson disease
o
Multiple sclerosis
Mediastinal and other thoracic lesions: o
Pneum onia
o
Aortic aneurysm
o
Tuberculosis
o
Myocardial infarction
o
Lung cancer
o
Mediastinal adenopathy
Metabolic causes: o
Urem ia
o
Hyponatrem ia
o
Gout
o
Hypocalcem ia
o
Diabetes
Toxic/drug-induced: o
α-Methyldopa
o
Benzodiazepines
o
Steroids
o
Barbiturates
o
General anesthesia
Psychogenic causes: o
Stress/excitem ent
o
Grief
o
Malingering
o
Conversion disorder
Head and neck: o
Otic foreign body irritating the tym panic m em brane
o
Pharyngitis
Pa ge 2 3 2
o
Laryngitis
o
Goiter
o
Retropharyngeal/peritonsillar abscess
Diagnosis Signs and Symptoms
Characteristic sound abruptly ending an inspiratory effort
Attacks usually occur at brief intervals and last only a few seconds or m inutes.
Attacks lasting m ore than 48 hours or persisting during sleep suggest an underlying disorder.
Described as persistent if duration longer than 48 hours; intractable if greater than 1 m onth
Essential Workup
Targeted history and review of system s to determ ine likelihood of potential underlying etiology:
o
Severity and duration of current episode
o
History of previous episodes and treatm ent attem pts
Careful physical exam ination in search of an underlying cause
Consider further diagnostic testing, dictated by history and physical, if hiccups are persistent or chronic
Tests Lab
CBC with differential
Electrolytes, blood urea nitrogen, creatinine
Imaging
Chest radiography
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Further im aging m ay be indicated depending on clinical suspicion of a particular etiology; this can often be perform ed on an outpatient basis.
Differential Diagnosis Eructation P.521
Treatment ED Treatment
Treat specific causes when identified: o
Rem ove foreign bodies from the ear
o
Relieve gastric distention with a nasogastric tube
Nonpharm acologic m aneuvers: o
Catheter stim ulation of the posterior pharynx
o
Direct stim ulation of the uvula with a cotton swab
o
Supraorbital pressure
o
Carotid sinus m assage
o
Digital rectal m assage
Pharm acologic treatm ent: o
Chlorprom azine
o
Haloperidol
o
Baclofen
o
Nebulized lidocaine
o
Am itriptyline
o
Phenytoin
o
Metoclopram ide
Pa ge 2 3 2
Medication (Drugs)
Am itriptyline: 10 m g PO t.i.d.
Baclofen: 10 m g PO t.i.d.
Chlorprom azine: 25–50 m g IV/IM, 25–50 m g PO t.i.d.
Haloperidol: 2–5 m g IM
Lidocaine (4%): 3 m L nebulized, repeat if necessary
Metoclopram ide: 10 m g IV/IM, 10–20 m g PO q.i.d.
Phenytoin: 200 m g IV
Follow-Up Disposition Admission Criteria Adm ission is not indicated for uncom plicated cases of hiccups.
Discharge Criteria Rem edies that can be tried at hom e in case of recurrence:
Swallowing a spoonful of sugar
Sucking on a hard candy or swallowing peanut butter
Breath holding/Valsalva m aneuver
Tongue traction
Lifting the uvula with a cold spoon
Drinking from the far side of a glass
Inducing fright
Sm elling salts
Rebreathing into a paper bag
Issues for Referral Referral in cases of intractable hiccups for investigation into underlying cause and m ore definitive therapeutic m easures:
Pa ge 2 3 2
Phrenic nerve block of dom inant diaphragm
Phrenic nerve crush or transection
Psychiatric interventions
Hypnosis
Behavioral m odification
References 1. Kolodzik PW, Eilers MA. Hiccups (singultus): review and approach to m anagem ent. Ann Em erg Med. 1991;20:565–573. 2. Launois S. Hiccup in adults: an overview European Respiratory Journal. 1993;Apr;6(4):563–575. 3. Lewis JH. Hiccups: reasons and rem edies. In: Lewis JH, ed. A pharm acologic approach to gastrointestinal disorders. Baltim ore: William s & Wilkins, 1994:116. 4. Rosseau P. Hiccups. South Med J. 1995;88(2):175–181.
Codes ICD9-CM 786.8
ICD10 R06.6
Pa ge 2 3 3
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > High Altitude Illness
High Altitude
Illness Christopher B. Colwell
Basics Description
Incidence dependent on: o
Rate of ascent
o
Final altitude
o
Sleeping altitude
o
Duration at altitude
Acute m ountain sickness (AMS) incidence: o
Up to 67% incidence with rapid ascent (1–2 days) to >14,000 feet
o
Twenty-two percent incidence for skiers visiting resorts and sleeping at 7,000–9,000 feet, 40% at 10,000 feet
AMS risk factors: o
Previous history of high altitude illness
o
Exertion
o
Younger persons ( Table o f C o ntents > Hip Injury
Hip Injury
Colleen Buono
Basics Description Hip Fracture
Fracture of proxim al fem ur
Classified by: o
Location
o
Displacem ent/angulation
o
Open/closed
o
Com m inution
o
Fracture lines
o
Neurovascular state
Femoral Head/Neck Fracture (Intracapsular)
Minor m echanism in eldery, high-energy m echanism in young
Patient m ay or m ay not be am bulatory.
Associated with hip dislocations (anterior > posterior)
Nondisplaced head/neck fractures difficult to visualize; increased m orbidity when fracture goes from nondisplaced to displaced
Fem oral neck is occasional site of stress fracture in
Pa ge 2 3 4
runners and m ilitary recruits (repetitive activity)
Intertrochanteric Fracture (Extracapsular)
Often due to fall in elderly patients
Nonam bulatory with significant pain
Extrem ity often shortened, externally rotated
Can be site of significant blood loss
Subtrochanteric Fracture
Usually due to direct, significant traum a in young patients or lesser traum a in elderly
Com m on site for pathologic fracture
Extrem ity shortened, displacem ent of proxim al fragm ent
Can be site of significant blood loss
Greater/Lesser Trochanter Fractures In young patients; usually apophyseal avulsion
Hip Dislocation
Disarticulation of fem oral head
Posterior dislocation (m ost com m on): o
Often from m otor vehicle accident (MVA) in which knees strike dashboard
o
Ten percent associated with sciatic nerve injury
Anterior dislocation: o
Often due to traum a with sudden abduction of thigh
o
Associated fem oral head fractures, fem oral nerve injury
Central dislocation with acetabular fracture: o
Usually from direct im pact to greater trochanter
o
Associated significant blood loss, sciatic nerve injury
Pediatric Considerations
Usually have posterior hip dislocation: o
Trivial force required for posterior hip locations in
Pa ge 2 3 4
children Table o f C o ntents > Ho rdeo lum and C halaz io n
Hordeolum and
Chalazion Shari Schabowski
Basics Description Result from inflam m atory processes involving the glands of the eyelid along the lash line:
Hordeolum —acute glandular obstruction resulting in inflam m ation
Chalazion—end result of a chronic granulom atous inflam m ation
Hordeolum
Develops owing to outflow obstruction in one or m ore of the glands of the eyelid
The eyelid has m any secretory glands: o
o
External hordeolum :
Glands of Zeis—superficial sebaceous glands
Glands of Moll—superficial sweat glands
Internal hordeolum :
Meibom ian glands—deeper m odified sebaceous glands
May evolve into chalazion
Pa ge 2 3 7
Obstructed glands m ay becom e secondarily infected.
May progress to localized abscess form ation or cellulitis
Chalazion Chronic granulom atous inflam m ation in the m eibom ian gland:
Originates from inspissated secretions
Blockage of the gland's duct at the eyelid m argin m ay result in release of the contents of the gland into the surrounding eyelid soft tissue.
A lipogranulom atous reaction ensues.
Occasionally, chalazia becom e secondarily infected.
May evolve from incom pletely drained internal hordeolum
Etiology Hordeolum May becom e secondarily infected:
Staphylococcus aureus m ost com m only
Diagnosis Signs and Symptoms Hordeolum
Develops acutely when glandular outflow is obstructed
Red, tender, painful, swollen m ass within the distal eyelid m argin
Typically solitary, but m ay be m ultiple
Nontoxic-appearing patient
Presentation depends on which gland is affected: o
External hordeolum :
Originates from obstruction of the superficial sebaceous or sweat glands whose ducts are
Pa ge 2 3 7
located between the eye lashes
Exquisitely tender sm all m ass that points anteriorly
o
Internal hordeolum :
Originates from obstruction of the sebaceous glands whose ducts are located on the inner aspect of the lid m argin
Painful sm all m ass that is palpable through the eyelid
May cause a foreign body sensation in the eye
Typically m ore inflam ed, larger, and m ore painful
Most com m only drains through the conjunctival surface after 1 week of treatm ent, but m ay drain through the skin
Associated with localized inflam m ation in the surrounding tissue: o
May lead to preseptal cellulitis
Tender preauricular lym ph nodes m ay be present.
Chalazion
Firm , circum scribed, nontender, or m inim ally tender nodule
Noninflam ed
Typically long-standing
Sym ptom s m ost com m only owing to physical properties: o
Disrupts natural contour of eye
o
Obstructs visual field/peripheral vision
o
Pressure on globe
Essential Workup Com plete ophthalm ologic exam ination
Hordeolum
Pa ge 2 3 7
Identify the origin of the abscess.
Determ ine extent of surrounding inflam m ation/cellulitis.
Chalazion Determ ine whether physical properties of chalazion result in corneal exposure and injury.
Differential Diagnosis
Hordeolum
Chalazion
Blepharitis
Dacryocystitis
Dacryoadenitis
Preseptal cellulitis
Pyogenic granulom a
Sebaceous cell carcinom a
P.531
Treatment ED Treatment Hordeolum
Relieve obstruction and prevent abscess form ation: o
Warm com presses for 15 m inutes 4–6 tim es per day
o
Gently m assage the nodule to express obstructed m aterial.
o
Rarely, in severe cases, incision and drainage of internal hordeolum m ay be necessary:
Pa ge 2 3 7
Typically done by ophthalm ologist
If pointed toward the conjunctiva, vertical incision is m ade to avoid injury to the m eibom ian glands.
o
Prophylactic topical antistaphylococcal antibiotic ointm ent is applied in the cul-de-sac and m assaged along the lid m argin to stim ulate duct and prevent secondary conjunctivitis.
Chalazion For chalazion, com plaints typically reflect nonem ergent aesthetic and cum bersom e physical properties of the m ass:
Referral to ophthalm ology for incision and curettage or steroid injection
Lubricating eyedrops m ay provide sym ptom atic relief
Medication (Drugs)
Lacri-Lube ophthalm ologic drops: as needed for com fort
Sulfacetam ide ophthalm ologic ointm ent: applied every 2–4 hours until 24 hours after sym ptom s resolve com pletely
Gentam icin ophthalm ologic ointm ent: applied every 2–4 hours until 24 hours after sym ptom s resolve com pletely
Follow-Up Disposition Admission Criteria Secondary cellulitis or deep tissue infection develops
Pa ge 2 3 7
Discharge Criteria
All uncom plicated cases m ay be discharged.
If incision and drainage is necessary, follow-up with ophthalm ology within 1–2 days
Sym ptom s are expected to resolve com pletely within 3–4 weeks; m ore typically com plete resolution is seen within 7–10 days.
References 1. Cullom R. The Will's Eye Manual: Office and Em ergency Room Diagnosis and Treatm ent of Eye Disease. Philadelphia: Lippincott–Raven Publishers; 1998. 2. Kanski JJ. Clinical Ophthalm ology. London: Butterworth-Heinem ann; 1994:24. 3. Lederm an C, Miller M. Disorders of the lacrim al system apparatus. Hordeola and chalazia. Pediatr Rev. 1999;20(8):283–284. 4. Prochazka MD, MSc, Allan V. Diagnosis and treatm ent of red eye. Prim ary Care Case Rev. 2001;4(1)23–31. 5. Rubin S, Hallagan L. Lids, lacrim als and lashes. Em erg Clin North Am . 1995;13(3):631–647.
Codes ICD9-CM 373.2 373.11
ICD10 H00.1 H00.0
Pa ge 2 3 7
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Ho rner Syndro m e
Horner Syndrome
Richard S. Krause
Basics Description Unilateral sym pathetic denervation produces signs of Horner syndrom e:
Relaxation of retracting m uscles in upper and lower lids: o
Loss of pupillary dilator innervation: o
Ptosis
Miosis (unopposed pupillary constriction)
Loss of sym pathetic stim ulation of sweat glands: o
Anhidrosis
Etiology
Tum ors of lung or m etastases to cervical nodes: o
May interrupt preganglionic sym pathetic fibers (between thoracic sym pathetic trunk and superior cervical ganglion)
Traum a: penetrating neck wounds
Pneum othorax: o
Tension pneum othorax m ay cause traction on sym pathetic fibers owing to shift of m ediastinal structures.
Infiltration or infection of cervical nodes:
Pa ge 2 3 7
o
Sarcoidosis, tuberculosis
Vascular disorders: o
Migraine or cluster headaches, carotid artery dissection
Pediatric Considerations
Hereditary Horner syndrom e: o
Blue iris (or irregular coloration) on affected side
o
Brown on unaffected side (heterochrom ia iridis)
Birth traum a: o
May cause dam age to sym pathetic chain
Diagnosis Signs and Symptoms
Horner syndrom e is characterized by: o
Ptosis: drooping of eyelid on affected side, usually slight
o
Miosis: decrease in pupillary size on involved side (pupillary asym m etry = 1 m m )
o
Anhidrosis: lack of sweating on involved side of face
The im portance of Horner syndrom e is its association with certain disease states.
Essential Workup
History and physical exam focused on neurologic findings
Chest radiograph to screen for tum or or pneum othorax
Tests Provocative Testing
Pharm acologic (cocaine) testing confirm s diagnosis of sym pathetic ocular lesion:
Pa ge 2 3 7
o
One drop of 5% ocular cocaine solution is instilled into each eye.
o
Failure of pupil on involved side to dilate as m uch as other pupil (increase in am ount of anisocoria) in 1 hour is confirm atory (positive test).
Imaging
CT or MRI of head, neck, or chest m ay be indicated depending on signs and sym ptom s.
Other
Ocular tonom etry for suspected glaucom a
Carotid Doppler ultrasound (US) m ay be indicated to evaluate for carotid dissection (usually painful)
Differential Diagnosis
Increased intracranial pressure (ICP): alm ost always associated with altered level of consciousness (LOC), headache
Sim ple anisocoria (pseudo-Horner syndrom e): 15–20% of the population have anisocoria and 3–4% also have m iosis and ptosis. o
Cocaine test is negative (both pupils dilate equally).
o
Inspect photo ID for pre-existing anisocoria.
Topical m edications or exposures
Migraine or cluster headache
Glaucom a, inflam m atory ocular diseases, or ocular traum a
Pediatric Considerations
Birth traum a in newborns
Hereditary Horner syndrom e
P.533
Pa ge 2 3 7
Treatment Pre Hospital Cautions:
The im portance of Horner syndrom e is its association with m ore serious underlying conditions.
Patients with increased ICP or tension pneum othorax m ust be recognized im m ediately.
Initial Stabilization
If increased ICP is suspected, initiate m easures to control ICP: o
Intubation, osm otic diuretics
Tension pneum othorax: o
Needle thoracostom y followed by chest tube
ED Treatment Horner syndrom e per se requires no ED treatm ent.
Medication (Drugs) Cocaine: 5% (adult), 2.5% (peds:) ophthalm ic solution: One drop in each eye is diagnostic.
Follow-Up Disposition Admission Criteria Adm ission for isolated Horner syndrom e is not needed:
Pa ge 2 3 8
Adm ission m ay be needed for underlying condition.
Discharge Criteria Patients with isolated Horner syndrom e m ay be discharged with appropriate follow-up arranged for continued workup as outpatient.
References 1. Arcasoy S, Jett J. Current concepts: superior pulm onary sulcus tum ors and Pancoast's syndrom e. New Engl J Med. 1997;337:1370–1376. 2. Fields C, Barker F. Review of Horner's syndrom e and a case report. Optom Vis Sci. 1992;69(6):481–485. 3. Thanvi B, et al. Carotid and vertebral artery dissection syndrom es. Postgrad Med. 2005;81:383–388. 4. Wilheim H, et al. Horner's syndrom e: a retrospective analysis of 90 cases and recom m endations for clinical handling. Ger J Ophthalm ol. 1992;1(2):96–102.
Codes ICD9-CM 337.9
ICD10 G90.2
Pa ge 2 3 8
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Hum erus F racture
Humerus Fracture
Julie Marmon
Basics Description
Proxim al hum erus fractures involve: o
Hum eral head
o
Lesser tuberosity
o
Greater tuberosity
o
Bicipital groove
o
Account for 5% of all fractures
o
Typically seen in adults over the age of 45 years and the elderly
o
>70% of patients with a proxim al hum erus fracture are 60 years and older
o
Neer classification: A system that identifies the num ber of fragm ents and their location
Fractures consist of 2- to 4-part fractures, and the locations include the anatom ic neck, the surgical neck, the greater and lesser tuberosity.
Fracture-dislocation and hum eral head splitting also part of Neer classification
Hum eral shaft fractures o
Hum eral shaft fractures are of three types:
Pa ge 2 3 8
Nondisplaced,
Displaced or angulated
Severely displaced or associated with neurovascular com prom ise
o
Hum eral shaft fractures account for 3% of all fractures
Etiology
Most often a history of a fall
Fall onto an outstretched hand
High-energy direct traum a
Excessive rotation of the arm in the abducted position
Electrical shock or seizure
Pathologic fracture from m etastatic disease
Ball throwing
Pregnancy Considerations Discuss need for operative treatm ent with orthopaedics and weigh benefits against possible risks to fetus.
Diagnosis Signs and Symptoms
Pain, swelling, and tenderness
Difficulty in initiating active m otion
Arm often closely held against the chest
Crepitus m ay be present
Ecchym osis within 24 to 48 hours at area of fracture
Dim inished peripheral pulses
Decreased sensation over the deltoid m uscle (axillary nerve), or forearm /first web space (radial nerve)
Essential Workup
Pa ge 2 3 8
Assessm ent of neurovascular status:
Assess individual nerves: o
Radial (radial nerve palsy m ost com m on with m iddle and m iddle-distal transverse and spiral fractures)
o
Median
o
Ulnar
o
Axillary (sensation to the lateral aspect of the shoulder)
o
Musculocutaneous nerve (sensation to the extensor aspect of the forearm )
Presence of radial, ulnar, and brachial pulses, and good capillary refill in all digits
Diagnosis is confirm ed by x-ray.
Pediatric Considerations
Salter-Harris I fractures are seen in children Table o f C o ntents > Hydro carbo n Po iso ning
Hydrocarbon
Poisoning James W. Rhee
Basics Description
Main com plication from hydrocarbon exposure is aspiration: o
Hydrocarbon aspiration prim arily affects central nervous and respiratory system s.
Physical properties determ ine type and extent of toxicity: o
Viscosity (resistance to flow):
Higher aspiration risk from products with lower viscosity
o
Volatility (ability of a substance to vaporize):
Hypoxia from arom atic hydrocarbons displacing alveolar air
o
Surface tension (ability to adhere to itself at liquid's surface):
Low surface tension allows easy spread from oropharynx to trachea, prom oting aspiration (e.g., m ineral oil, seal oil).
Volatile substance abuse:
Pa ge 2 4 0
o
Com m on solvents abused:
Typewriter correction fluid
Adhesive
Gasoline
Cigarette-lighter fluid
o
Sniffing: product inhaled directly from container
o
Huffing: product inhaled through a soaked rag held to face
o
Bagging: product poured into bag and m ultiple inhalations taken from bag
Major classes of hydrocarbons: o
Aliphatics:
Include kerosene, m ineral oil, seal oil, gasoline, solvents, and paint thinners
Pulm onary toxicity via aspiration
Asphyxiation from gaseous m ethane and butane by displacem ent of alveolar oxygen
o
o
Halogenated hydrocarbons:
Include carbon tetrachloride and trichloroethane
Found in industrial settings as solvents
Well absorbed by lungs and gut
High toxicity
Liver and renal failure associated with ingestion
Cyclics or arom atic com pounds include toluene and xylene:
Highly volatile and well absorbed from gut
Death from benzene reported with 15-m L ingestion
o
Terpenes or wood distillates include turpentine and pine oil:
Significant gastrointestinal tract absorption
Significant central nervous system depression
Pa ge 2 4 0
Etiology
Accidental exposures typical in young children
Inhalation abuse of volatile hydrocarbons
Suicide attem pts in adolescents and adults
Diagnosis Signs and Symptoms
Often asym ptom atic at presentation
Odor of hydrocarbons on breath
Early: euphoria: o
Disinhibition
Late: dysphoria: o
Ataxia
o
Confusion
o
Hallucination
Sudden sniffing death: o
Cardiac arrest in volatile substance abusers secondary to hypersensitization of m yocardium leading to m alignant dysrhythm ias on adrenergic stim ulation
Pulm onary: o
Mild to severe respiratory distress
o
Cyanosis
o
Aspiration (prim ary com plication)
Central nervous system : o
Intoxication
o
Euphoria
o
Slurred speech
o
Lethargy
Pa ge 2 4 0
o
Com a
Gastrointestinal tract: o
Local m ucosal irritation
o
Gastritis
o
Diarrhea
Cardiac: o
Tachycardia
o
Dysrhythm ias (volatile substance abuse)
Derm al: o
Local erythem a
o
Maculopapular or vesicular eruptions
o
Defatting derm atitis from chronic skin exposure
o
Huffer face rash in chronic abusers
Essential Workup Obtain inform ation on the following:
Product: exact nam e on label, m anufacturer, and ingredients
Nature of ingestion or exposure: accidental or intentional
Estim ated am ount ingested
In industrial settings, Material Safety Data Sheets (MSDSs)
Tests ECG for intoxicated volatile substance abusers
Lab
Pulse oxim etry: o
If abnorm al, follow with arterial blood gases.
Electrolytes; BUN, creatinine, and glucose levels; and liver function tests: o
For halogenated and arom atic hydrocarbon exposure
o
Metabolic acidosis
o
Hypokalem ia
Pa ge 2 4 0
Carboxyhem oglobin levels for m ethylene chloride exposure: o
Methylene chloride m etabolized to carbon m onoxide in vivo
Imaging Chest radiograph:
Abnorm alities visible 20 m inutes to 24 hours after exposure
Increased bronchovascular m arking and bibasilar and perihilar infiltrates (typical)
Lobar consolidation (uncom m on)
Pneum othorax, pneum om ediastinum , and pleural effusion (rare)
Pneum atoceles resolve over weeks.
Differential Diagnosis
Caustic, pesticide, or toxic alcohol ingestions
Accidental versus intentional: o
Psychiatric evaluation for all intentional ingestions
Child neglect: o
Poor supervision or unsafe hom e environm ent
P.539
Treatment Pre Hospital
Decontam inate clothes, skin, and hair of any hydrocarbon exposure
Do not induce em esis.
Pa ge 2 4 0
Ipecac contraindicated owing to increased risk of aspiration
Keep volatile-substance abusers calm and avoid interventions that cause anxiety or distress.
Managem ent of accidental hydrocarbon exposures at hom e controversial: o
Fewer than 1% require physician intervention.
o
For asym ptom atic or quickly asym ptom atic after ingestion with reliable observer available
o
Applies only when exact product and its com ponents are known and there is no indication for gastric decontam ination or possibility for delayed organ toxicity
Initial Stabilization
Airway, breathing, and circulation m anagem ent (ABCs)
Intravenous access and fluid resuscitation if hypotensive or ongoing fluid losses
Oxygen
Cardiac m onitor
Naloxone, thiam ine, D 5 0 W (or Accu-Chek) if altered m ental status
ED Treatment
Supportive care
Treat respiratory sym ptom s: o
Oxygen
o
Nebulized β 2 -agonist for bronchospasm (albuterol)
o
Endotracheal intubation and m echanical ventilation for respiratory failure
o
Steroids not indicated for bronchospasm
o
Avoid using epinephrine in volatile substance abusers as it m ay precipitate dysrhythm ias
Pa ge 2 4 0
Gastric evacuation not indicated for vast m ajority of hydrocarbon ingestions: o
Aspiration risk higher than risk of system ic absorption for aliphatic hydrocarbon m ixtures, which account for m ost ingestions
o
Contraindicated if spontaneous em esis has occurred
o
Sm all-bore nasogastric tube aspiration of stom ach contents m ay be indicated for som e hydrocarbon (CHAMP) ingestions that have system ic toxicity:
CHAMP: cam phor, halogenated hydrocarbons, a rom atic hydrocarbons, m etals (e.g., lead, m ercury), pesticides
Only for very recent ingestions
Benefit of doing this procedure needs to be weighed heavily against risk of aspiration and subsequent pneum onitis.
Cuffed-tube endotracheal intubation for airway protection during lavage if no gag reflex or altered m ental status
Activated charcoal not indicated except for significant coingestants
Cathartics not indicated: o
Diarrhea com m on with hydrocarbon
Medication (Drugs)
Dextrose: D 5 0 W 1 am pule of 50 m L or 25 g (peds: D 2 5 W 2–4 m L/kg) IV
Naloxone (Narcan): 2 m g (peds: 0.1 m g/kg) IV or IM initial dose
Thiam ine (vitam in B 1 ): 100 m g (peds: 50 m g) IV or IM
Pa ge 2 4 0
Follow-Up Disposition Admission Criteria
Sym ptom atic patients
Patients with potential delayed organ toxicity (carbon tetrachloride or other toxic additives)
Discharge Criteria
Observe for 6 hours, then discharge: o
Asym ptom atic patients with norm al chest radiograph and pulse oxim etry findings
o
Asym ptom atic patients with abnorm al chest radiograph and norm al oxygenation and respiratory rate m ay be discharged if reliable follow-up is ensured.
o
Sym ptom atic patients on presentation who quickly becom e asym ptom atic
Observe volatile-substance abusers until m ental status clears.
Issues for Referral Psychiatry consult as needed
References 1. Anas N, Nam asonthi V, Ginsburg C. Criteria for hospitalizing children who have ingested products containing hydrocarbons. JAMA. 1981;246:840–843. 2. Dice WH, Ward G, Kelly J, et al. Pulm onary toxicity following gastrointestinal ingestion of kerosene. Ann Em erg Med. 1982;11:138–142. 3. Esm ail A, Meyer L, Pottier A, et al. Deaths from volatile substance
Pa ge 2 4 0
abuse in those under 18 years: results from a national epidem iological study. Arch Dis Child. 1993;69:356–360. 4. Klein BL, Sim on JE. Hydrocarbon poisonings. Pediatr Clin North Am . 1986;33:411. 5. Machado B, Cross K, Snodgrass WR. Accidental hydrocarbon ingestion cases telephoned to a regional poison center. Ann Em erg Med. 1988;17:804–807.
Codes ICD9-CM 987.1
Pa ge 2 4 0
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Hydro cele
Hydrocele
Sean O. Henderson
Basics Description
Com m unicating hydrocele: o
Patent processus vaginalis
o
Scrotum fills and em pties with peritoneal fluid depending on body position
Noncom m unicating hydrocele is owing to production of serous fluid by a disease process
Etiology
Im balance between production and resorption of fluid within space between tunica vaginalis and tunica albuginea
Disease processes causing adult noncom m unicating hydrocele include: o
Epididym itis
o
Hypoalbum inem ia
o
Tuberculosis
o
Traum a
o
Mum ps
o
Sperm atic vein ligation
o
In Third World, hydrocele is prim arily caused by infections such as Wuchereria bancrofti or Loa Loa.
Pa ge 2 4 1
o
Rarely m alignancy (first-degree testicular neoplasm or lym phom a)
Rare etiology is the abdom inoscrotal hydrocele that m ay cause hydroureter or unilateral lim b edem a owing to com pression: o
Ultrasound reveals single sac extending from scrotum into abdom inal cavity via the deep inguinal ring
Pediatric Considerations
Congenital in 6% of newborn boys
Usually diagnosed in newborn nursery
Caused by patent processus vaginalis, a structure that rem ains patent in 85% of newborns
May vary in size owing to position or crying: o
Patients m ay present with history of scrotal m ass that has resolved.
Most close by age of 2 years
Diagnosis Essential Workup
History and exam ination with special attention to identifying torsion of testicle
Initial diagnostic test is transillum ination of affected side: o
This is rapidly being replaced as diagnostic test of choice by bedside ultrasound.
o
Bedside ultrasound:
Allows visualization of hydrocele as well as of testicle
Especially in cases of m assive fluid collection, bedside ultrasound should be diagnostic test of
Pa ge 2 4 1
choice.
Because of possibility in adults that a hydrocele m ay be owing to a prim ary neoplasm , the testicle m ust be palpated in its entirety.
Tests Lab No specific laboratory testing is indicated unless underlying cause dem ands it.
Imaging Ultrasound is diagnostic and allows visualization of testicular anatom y:
Appears as large fluid-filled space surrounding the testicle
Differential Diagnosis
Testicular neoplasm
Testicular torsion
Epididym itis
Orchitis
Indirect inguinal hernia
Treatment Initial Stabilization Stabilization should focus on underlying cause (e.g., trauma).
ED Treatment Appropriate exam ination of testicle to exclude prim ary neoplasm and referral P.541
Pa ge 2 4 1
Medication (Drugs) Treat underlying cause.
Pediatric Considerations See Disposition below.
Follow-Up Disposition Admission Criteria Patients with secondary hydrocele m ay need adm ission for further evaluation of underlying pathology (e.g., neoplasm , traum a).
Discharge Criteria
Otherwise healthy patients without co-m orbid illness m ay be referred for further evaluation to urologist.
Hydrocele is usually repaired if cosm esis is a factor or in cases where it causes discom fort.
Repair can be: o
Surgical:
Aspiration or sclerotherapy are alternatives to open hydrocelectom y.
o
Medical:
Aspiration of hydrocele contents and sclerotherapy to prevent recurrence
Pediatric Considerations
Most hydroceles in infant population will spontaneously resolve by 12 m onths of age:
Pa ge 2 4 1
o
Referral and observation are appropriate once diagnosis is m ade.
After age of 12–18 m onths, refer for surgical repair as com m unicating hydroceles usually have hernia that needs repair.
References 1. Akin EA, Khati NJ, Hill MC. Ultrasound of the scrotum . Ultrasound Q. 2004;20:181–200. 2. Beiko DT, Kim D, Morales A. Aspiration and sclerotherapy versus hydrocelectom y for treatm ent of hydroceles. Urology. 2003;61:708–712. 3. Kaplan GW. Scrotal swelling in children. Pediatr Rev. 2000;21:311–314. 4. Lau MW, Taylor PM, Payne SR. The indications for scrotal ultrasound. Br J Radiol. 1999;72:833–837. 5. Rabinowitz R, Hulbert WC. Acute scrotal swelling. Urol Clin North Am . 1995;22:101–105. 6. Rubenstein RA, Dogra VS, Seftel AD, et al. Benign intrascrotal lesions. J Urol. 2004;171:1765–1772.
Codes ICD9-CM 603.9
ICD10 N43.3
Pa ge 2 4 1
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Hydro cephalus
Hydrocephalus
Richard S. Krause
Basics Description
Increased fluid in cranium
Obstructive hydrocephalus is m ost com m on form : o
Obstruction is within ventricular system or in subarachnoid space.
Acute obstructive hydrocephalus m ay cause rapid rise in intracranial pressure (ICP), rapidly leading to death or perm anent cerebral dam age.
Nonobstructive hydrocephalus causes subacute sym ptom s and is a potentially treatable form of dem entia.
Etiology
Obstructive hydrocephalus: o
Obstruction of:
Foram en of Monro
Third ventricle, fourth ventricle
Aqueduct of Sylvius
Foram ina of Luschka and Magendie (tum or or other m asses)
Subarachnoid space around brainstem (postinfectious or postsubarachnoid hem orrhage
Pa ge 2 4 1
[post-SAH]) o
Acute presentations usually secondary to cerebrospinal fluid (CSF) shunt blockage, SAH, or severe head traum a
Nonobstructive hydrocephalus: o
Norm al pressure hydrocephalus:
Increased intracranial volum e without intracranial hypertension
o
Increased ventricular size on CT
Pediatric hydrocephalus: o
Congenital hydrocephalus owing to neonatal hem orrhages, congenital m alform ations, or acquired postm eningitis secondary to subarachnoid scarring around brainstem
Diagnosis Signs and Symptoms Obstructive (Noncommunicating) Hydrocephalus
Headache
Nausea and vom iting
Decreased level of consciousness
Urinary incontinence
Ocular palsies
Papilledem a, decreased vision
Pupillary dilation
Cushing response: o
Raised systolic pressure and bradycardia
Pediatric patients:
Pa ge 2 4 1
o
Full fontanelle, irritability, and lethargy
May present like nonobstructive hydrocephalus if obstruction develops slowly
Nonobstructing (Communicating) Hydrocephalus
Progressive dem entia, som nolence
Gait disturbance
Urinary incontinence
Im paired upward gaze
Generalized weakness and lethargy
Dem entia is often insidious with subacute onset of progressive intellectual deterioration.
No headache or papilledem a
Pediatric patients increase CSF volum e slowly: o
Craniom egaly
o
Retardation
o
Prom inent scalp veins
o
Im paired upward gaze (setting sun sign)
Essential Workup CT scan of the head will allow assessm ent of ventricular size and sym m etry:
Aid in diagnosis of cerebral edem a, m ass lesions, and hem orrhage
Tests Lab Lum bar puncture (LP) is typically perform ed after head CT (for nonobstructive causes):
Opening pressure on LP will reflect increased ICP in nonobstructive hydrocephalus.
CSF should be sent for routine tests if infection is
Pa ge 2 4 1
suspected. o
Gram stain, culture, protein, and glucose
Imaging MRI of brain reveals ventricular size and sym m etry and m ay allow for better visualization of m asses than CT.
Differential Diagnosis
Acute cerebral infarction or hem orrhage
Intracranial infection
Mass effect from fast-growing tum or or hem atom a
Dem entia or delirium of other cause
Toxic or m etabolic encephalopathies
Pediatric Considerations
Suspect hydrocephalus in infant whose head circum ference is increasing excessively.
Congenital anom alies: o
Constitutional m acrocrania
o
Megalencephaly
o
Dandy-Walker m alform ation
o
Arnold-Chiari m alform ation
o
Meningom yelocele
o
Choroid plexus papillom a
o
Hypoplasia/dysfunction of arachnoid villi
Infections: o
Rubella
o
Cytom egalovirus (CMV)
o
Toxoplasm osis
o
Syphilis
o
Bacterial m eningitis
o
Reye syndrom e
Tum ors, especially posterior fossa tum ors: o
Medulloblastom a, astrocytom a, ependym om a
Pa ge 2 4 1
Hem orrhage: o
Intraventricular bleed and fibrosis, subarachnoid bleed
P.543
Treatment Pre Hospital Cautions:
Elevated ICP cannot be definitively diagnosed in the field.
When it is suspected, supplem ental O 2 and aggressive airway m anagem ent are indicated.
If not contraindicated, patients should be transported with head elevated at 30°.
Initial Stabilization
Signs of im pending herniation: o
Rapid-sequence intubation (RSI)
Thiopental or etom idate for induction
Paralytic choice is controversial.
Depolarizing agents (succinylcholine) m ay increase ICP, although this effect m ay not be clinically significant.
Nondepolarizing agents (rocuronium , vecuronium ) m ay be preferable.
o
Controlled ventilation to m aintain PaCO 2 at approxim ately 35 m m Hg
o
Maintain systolic blood pressure (BP) >100 m m Hg (adult) with fluids or pressors.
Pa ge 2 4 1
o
Mannitol
If a CSF shunt is present and there are signs of im pending herniation: o
Forced pum ping of shunt cham ber:
Flush device with 1 m L saline to rem ove distal obstruction.
Slow drainage of CSF from reservoir to achieve pressure Table o f C o ntents > Hypercalcem ia
Hypercalcemia
Jeffrey King
Basics Description
Severity depends on level of serum calcium and rate of its rise
0.1–1% of patients on routine screening
Most cases m ild (14 m g/dL, associated with serious signs and sym ptom s
Calcium in bloodstream in three form s: o
Ionized: 45%
o
Bound to protein (prim arily album in): 40%
o
Bound to other anions: 15%
Ionized calcium —only physiologically active form
Etiology
Prim ary hyperparathyroidism
Malignancy
Miscellaneous
Diagnosis
Pa ge 2 4 2
Signs and Symptoms History
Neurologic: o
Headache
o
Fatigue
o
Weakness
o
Difficulty concentrating
o
Confusion
Renal: o
Polyuria, polydipsia
o
Com plaints related to oliguric renal failure
o
Chronically: com plaints related to renal calculi, nephrocalcinosis, interstitial nephritis
Gastrointestinal: o
Anorexia
o
Nausea
o
Vom iting
o
Abdom inal pain
o
Constipation
o
Com plaints related to intestinal ileus
o
Chronically: com plaints related to increased risk of peptic ulcer disease and pancreatitis
Derm atologic: o
Pruritus
Pediatric Considerations
Failure to thrive
Slow developm ent
Mental retardation m ay ensue
Physical Exam
Neurologic:
Pa ge 2 4 3
o
Irritability
o
Lethargy
o
Stupor
o
Com a
o
Hyporeflexia
Cardiovascular: o
Hypotension, if severely volum e depleted, or hypertension
o
Sinus bradycardia, cardiac arrest with severe hypercalcem ia (rare)
Renal: o
Signs of dehydration
Derm atologic: o
Band keratopathy
o
Ectopic calcification
Pediatric Considerations
Characteristic facies: pug nose, fat nasal bridge, “cupid's bow― upper lip
Hypotonia
Essential Workup
Ionized and total serum calcium levels, album in levels: o
Norm al total calcium level is 14 m g/dL or signs or sym ptom s
o
First-line drug therapy:
Bisphosphonates: pam idronate (m ore potent and possibly less toxic), etidronate
Calcitonin: rapid onset but m odest decrease in levels
o
Other potential drug therapy:
Plicam ycin: efficacious but num erous side effects
Hydrocortisone: especially useful with m alignancies, granulom atous disorders, or vitam in D intoxication
o
Encourage am bulation in appropriate patients.
Underlying disorder: o
Prepare to treat underlying cause.
Pa ge 2 4 3
o
Parathyroidectom y for prim ary hyperparathyroidism resulting in sym ptom atic or severe hypercalcem ia
o
Treat tum or for m alignancy.
o
Discontinue m edication if cause.
Medication (Drugs)
Calcitonin: 4 IU/kg IM/SC q12h
Etidronate: 7.5 m g/kg over 4 hours daily for 3–7 days IV
Furosem ide: 10–40 m g q6h–q8h (peds: 1–2 m g/kg) IV
Gallium nitrate: continuous infusion of 200 m g/m 2 /d for 5 days IV
Hydrocortisone: 200–400 m g/d IV for 3–5 days (peds: consult pediatrician)
Pam idronate: single 24-hr infusion of 60–90 m g IV (peds: consult pediatrician)
Plicam ycin: 25 µg/kg/d over 4–6 hours IV for 3–8 doses
Follow-Up Disposition Admission Criteria
Corrected total calcium level >13.0 m g/dL
Signs or sym ptom s attributed to hypercalcem ia
Monitored bed or ICU for corrected level >14 or serious signs and sym ptom s
Discharge Criteria Corrected calcium level 5% of total body weight
o
Laboratory findings: increased urine specific gravity, ketonuria, electrolyte disturbances, ketonem ia
Essential Workup
History and physical exam ination with special attention to state of hydration and abdom inal exam for other diagnoses associated with vom iting (appendicitis, cholecystitis, etc.)
The only m andated test is an uncontam inated urinalysis.
If patient has unrem itting vom iting for >24 hours, obtain a CBC, electrolytes, renal function, liver enzym es, bilirubin, and lipase.
Tests Lab
Urinalysis: o
Increased specific gravity and ketonuria
o
Presence of glucose m andates checking serum glucose to rule out diabetes.
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o
Presence of bilirubin m andates a search to rule out hepatobiliary cause for the vom iting.
CBC: o
May have an elevated hem atocrit owing to dehydration
o
White blood cell count is usually norm al.
Electrolytes: o
Elevated blood urea nitrogen indicating volum e depletion
o
Hyponatrem ia, hypokalem ia, hypochlorem ia, and m etabolic alkalosis from loss of HCl in em esis
Liver function tests: o
Mild increases in bilirubin m ay occur, but should be 100 IU/L
Am ylase/lipase: o
In one study, am ylase was elevated in 24% of patients with hyperem esis gravidarum ; however, the am ylase was not pancreatic in origin; thus, use lipase rather than am ylase to evaluate for pancreatitis.
Differential Diagnosis
Pyelonephritis; m ost com m only m issed
Gastroenteritis
Hepatobiliary disease; hepatitis, cholecystitis, fatty liver of pregnancy
Pancreatitis
Appendicitis
Diabetic ketoacidosis
Hyperthyroidism
Urem ia; persistent nausea and vom iting are seen with severe renal dysfunction.
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Treatment Initial Stabilization IV hydration using a crystalloid with dextrose (D 5 LR or D 5 NS)
ED Treatment
IV hydration using up to 3 L of D 5 LR or D 5 NS
Dextrose is added to help break cycle of ketosis.
Treat until patient is no longer sym ptom atic from hypovolem ia.
Antiem etics adm inistered IV are given to break vom iting cycle. P.549
Most com m only used m edications: o
Phenothiazines (prom ethazine and prochlorperazine):
Both Food and Drug Adm inistration (FDA) category C, m eaning have not been adequately studied
o
Metoclopram ide:
o
Selective 5-HT3 receptor antagonist (ondansetron):
o
FDA category B
FDA category B
These m edications have been used extensively in pregnancy, and there is little or no evidence that these antiem etics are associated with an increased risk of congenital anom alies.
o
Parenteral antiem etics are preferable to the risk of prolonged ketosis and the associated hypovolem ia.
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Oral rehydration in the ED after the initial fluid resuscitation and antiem etics are given
Thiam ine 100 m g IV or IM in the patient who has a protracted course of sym ptom s: o
There are case reports of patients developing Wernicke encephalopathy owing to hyperem esis gravidarum .
Methylprednisolone m ay be effective for patients with hyperem esis gravidarum : o
Two studies dem onstrated relief in sym ptom s and decreased need for adm ission for hyperem esis.
Medication (Drugs)
Methylprednisolone (category C): 48 m g IV or PO
Metoclopram ide (category B): 10–20 m g IV
Ondansetron (category B): 8 m g IV
Prochlorperazine (category C): 5–10 m g IV not to exceed 40 m g/d
Prom ethazine (category C): 12.5–25 m g IV
Discharge m edications: o
Use first-line m edications and elevate to the second-line agents for repeated visits.
o
Meclizine (category B): 25 m g PO q6h PRN, first line
o
Metoclopram ide (category B): 10 m g PO q6h–q8h PRN, second line
o
Prochlorperazine (category C): 5–10 m g PO q6h or 25 m g PR q12h PRN, second line
o
Prom ethazine (category C): 12.5–25 m g PO or PR q4h–q6h PRN, second line
o
Pyridoxine (vitam in B 6 ; category A): 25 m g PO t.i.d., first line (over-the-counter)
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Follow-Up Disposition Admission Criteria
Inability to tolerate oral intake after treatm ent
Inability to control the em esis despite treatm ent
Severe electrolyte or m etabolic disturbances
Discharge Criteria
Most patients can be discharged as long as they are able to tolerate oral intake and have adequate follow-up.
Correction of dehydration and associated sym ptom s
Decreased ketonuria
Patients should be reassured that their sym ptom s are com m on and alm ost always self-lim ited.
Patients should be counseled to eat frequent, sm all m eals: o
Meals should contain sim ple carbohydrates and be low in fats.
o
Avoid irritant or spicy foods.
Hom e IV therapy can be arranged if indicated.
References 1. Broussard C, Richter J. Nausea and vom iting of pregnancy. Gastroenterol Clin North Am . 1998;27:123–151. 2. Einarson A, Maltepe C, et al. The safety of ondansetron for nausea and vom iting of pregnancy: a prospective com parative study. Br J Obstet Gynaecol. 2004;111(9):940–943. 3. Eliakim R, Abulafia O, Sherer D. Hyperem esis gravidarum : a current review. Am J Perinatol. 2000;17(4):207–218. 4. Goodwin T. Hyperem esis gravidarum . Clin Obstet Gynecol.
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1998;41(3):597–605. 5. Safari H, Alsulym an O, Gherm an R, et al. Experience with oral m ethylprednisolone in the treatm ent of refractory hyperem esis gravidarum . Am J Obstet Gynecol. 1998;178(5):1054–1058.
Codes ICD9-CM 643.00
ICD10 O21
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Hyperkalem ia
Hyperkalemia
Christopher B. Colwell
Basics Description
Potassium distribution: o
Extracellular space: 2%
o
Intracellular space: 98%
Potassium excretion: o
Renal: 90%
o
GI: 10%
Renal and extrarenal m echanism s m aintain norm al plasm a concentration between 3.5 and 5.0 m m ol/L.
Renal excretion of potassium affected by: o
Dietary intake
o
Distal renal tubular function
o
Acid-base balance
o
Mineralocorticoids
Regulation between intracellular and extracellular potassium balance affected by: o
Acid-base balance
o
Insulin
o
Mineralocorticoids
o
Catecholam ines
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o
Osm olarity
o
Drugs
Etiology Decreased Potassium Excretion
Most com m on cause: renal failure (acute or chronic)
Distal tubular diseases:
o
Acute interstitial nephritis
o
Renal transplant rejection
o
Sickle cell nephropathy
o
Renal tubular acidosis (diabetes)
Mineralocorticoid deficiency: o
Addison disease
o
Hypoaldosteronism
Drugs: o
Angiotensin-converting enzym e (ACE) inhibitors/angiotensin receptor blockers
o
Beta-blockers
o
Potassium -sparing diuretics
o
Nonsteroidal anti-inflam m atory drugs (NSAIDs)
o
Cyclosporine
o
High-dose trim ethoprim
o
Lithium toxicity
Intracellular to Extracellular Potassium Shifts
Metabolic acidosis: o
Serum K + rises 0.2–1.7 m m ol/L for each 0.1 unit fall in arterial pH.
Hyperosm olar states
Insulin deficiency
Cell necrosis
Rhabdom yolysis
Hem olysis
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Chem otherapy
Drugs:
o
Digitalis toxicity
o
Depolarizing m uscle relaxants (e.g., succinylcholine)
o
Beta-blockers
o
α-Agonists
Hyperkalem ic periodic paralysis
Excess Exogenous Potassium Load
Cellular breakdown: o
Traum a
o
Tum or lysis
Salt substitutes
Oral potassium
Potassium penicillin G
Rapid transfusions of banked blood
Pseudohyperkalemia
Traum atic venipuncture with hem olysis
Postvenipuncture release of potassium can occur in setting of:
o
Throm bocytosis (platelets >800,000/m m 3 )
o
Extrem e leukocytosis (WBC >100,000/m m 3 )
Prolonged tourniquet tim e
Diagnosis Signs and Symptoms History
Neurom uscular sym ptom s, predom inantly weakness, which can progress to paralysis
Dyspnea owing to respiratory m uscle weakness
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Cardiac dysrhythm ias can be initial m anifestation, so patients could also present with chest pain, palpitations, or syncope.
Physical Exam
Muscular weakness (rare except in severe cases)
Cardiac dysrhythm ias (see ECG Changes)
Essential Workup
Serum potassium >5.0 m m ol/L
Collect in heparinized tube if pseudohyperkalem ia suspected.
Tests Lab
Electrolytes, BUN, creatinine, glucose: o
Elevated BUN, creatinine in renal failure
o
Hyponatrem ia with m ineralocorticoid deficiency
o
Mild m etabolic acidosis with type IV renal tubular acidosis
Arterial blood gases: o
Assess acid-base status
Creatinine kinase
Ca 2 +
For hyperkalem ia in face of norm al renal function, calculate transtubular potassium gradient (TTKG): o
TTKG = urine K × Posm /Plasm a K × Uosm
o
Posm , plasm a osm olality; Uosm , urine osm olality
o
TTKG >8 suggests extrarenal cause; TTKG 7.0) or Moderate (6.0–7.0) with ECG Changes (Heightened T waves or loss of P wave): Shift Potassium Intracellularly
Adm inister com bination of insulin and glucose: o
Onset 20–30 m inutes
o
2–4-hour duration
IV sodium bicarbonate: o
Much m ore effective in patient who is acidotic
o
Onset 20 m inutes
o
2-hour duration
o
Caution in patients at risk for volum e overload
o
Worsens concom itant hypocalcem ia
Inhaled albuterol: o
Onset within 30 m inutes
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o
2–4-hour duration
Enhanced Excretion for K + >6.0 without ECG Changes Adm inister cation exchange resin:
Calcium or sodium polystyrene sulfonate PO or per rectum (PR)
Avoid in patients with suspected ileus or bowel obstruction.
All Patients
Lim it exogenous potassium and potassium -sparing drugs.
Treat underlying cause.
Special Situations
Renal failure: o
Arrange for dialysis.
o
Hem odialysis im m ediately effective at rem oving potassium
Furosem ide: o
Effective in absence of oliguric renal failure
o
Causes potassium -losing diuresis
Cardiac arrest: o
Adm inister CaCl 2 and NaHCO 3 with known or suspected hyperkalem ia.
Digoxin toxicity: o
Avoid calcium :
When necessary, adm inister sm all doses extrem ely slowly.
o
Consider Digibind for K + >5.5 m m ol/L.
Mineralocorticoid deficiency: o
Hydrocortisone
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Medication (Drugs)
Albuterol: 10–20 m g (peds: 2.5 m g if Table o f C o ntents > Hypero sm o lar Syndro m e
Hyperosmolar
Syndrome Matthew Robinson
Basics Description
Results from a relative insulin deficiency in the undiagnosed or untreated diabetic
Sustained hyperglycem ia creates an osm otic diuresis and dehydration: o
Extracellular space m aintained by the osm otic gradient at the expense of the intracellular space
o
Eventually profound intracellular dehydration occurs.
Total body deficits of H 2 O, Na + , Cl - , K + , PO 4 - , Ca 2 + and Mg 2 +
In contrast to diabetic ketoacidosis (DKA), significant ketoacidosis does not occur: o
Circulating insulin levels are higher.
o
The elevation of insulin counterregulatory horm ones is less m arked.
o
The hyperosm olar state itself inhibits lipolysis (the release of free fatty acids) and subsequent generation of ketoacids.
Geriatric Considerations
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Most com m only seen in elderly type II diabetics who experience a stressful illness that precipitates worsening hyperglycem ia and reduced renal function
In the elderly, 30–40% of cases are associated with the initial presentation of diabetes.
Pediatric Considerations Hyperosm olar syndrom e (HHS) rare in pediatric patients
Etiology
Hyperosm olar state precipitated by factors that: o
Im pair peripheral insulin action
o
Increase endogenous or exogenous glucose
o
Decrease patient's ability to replace fluid loss
Infection is m ost com m on precipitating factor in 32–60% of cases.
Other precipitating causes include: o
Inadequate diabetes therapy
o
Medication om ission
o
Diet indiscretion
o
Infections
o
Pneum onia
o
Urinary tract infection
o
Sepsis
o
Medications/drugs
o
Diuretics
o
Beta-blockers
o
Calcium channel blockers
o
Phenytoin
o
Cim etidine
o
Am phetam ines
o
Ethanol
o
Coexisting illness
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o
Myocardial infarction
o
Stroke
o
Renal failure
o
Heat stroke
o
Pancreatitis
o
Intestinal obstruction
o
Endocrine disorders
o
Burns
o
Heat stroke
Diagnosis Signs and Symptoms History
Progression of signs and sym ptom s occurs over days to weeks.
Polyuria/polydipsia/weight loss
Dizziness/weakness/fatigue
Blurred vision
Leg cram ps
Physical Exam
Dehydration
Tachycardia
Sunken eyes
Hypotension
Orthostasis
Dry m ucous m em branes
Decreased skin turgor
Collapsed neck veins
Com a/lethargy/drowsiness
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Urinary output m aintained until late
Seizures/focal neurologic deficits
Concurrent precipitating m edical illness
Essential Workup
Diagnostic criteria: o
Serum glucose ≥600 m g/dL (usually >1,000 m g/dL)
o
Minim al ketosis
o
pH ≥7.30, HCO 3 ≥15 m Eq/L
o
Effective serum osm olality >320 m Osm /kg:
Effective serum osm olality = 2 × Na + + glucose/18
Blood urea nitrogen not included because it is freely perm eable between fluid com partm ents
Tests Lab
Broad testing indicated to evaluate hyperosm olar syndrom e and for precipitating causes
Electrolytes: o
K + m ay be elevated even in presence of total body deficit owing to shift from intracellular space to extracellular space.
o
Mild anion gap m etabolic acidosis owing to lactic acid, β-hydroxybutyric acid, or renal insufficiency
o
Increased sodium —Correct for hyperglycem ia: Corrected [Na + ] = [Na + ] + 1.6 × [(glucose in m g/dL) – 100]/100
BUN, creatinine: o
Azotem ia with elevated BUN/creatinine ratio owing to prerenal and intrarenal causes
Venous blood gas (VBG) or arterial blood gas (ABG) to
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rapidly determ ine pH: o
ABG necessary to evaluate m ixed acid base disorders
Serum ketones, β-hydroxybutyrate, and lactate level if pH < 7.3 or significantly elevated anion gap to evaluate m ixed acid-base disorder
Serum osm olarity
CBC: o
Leukocytosis owing to infection, stress, or hem oconcentration
o
Increased hem oglobin and hem atocrit owing to hem oconcentration
Lipase and am ylase: o
Pancreatitis com m on
o
Elevated am ylase and lipase with no evidence of pancreatitis com m on
o
May be owing to increased salivary secretion, hem oconcentration, or decreased renal clearance
Urinalysis: o
Check for ketones/glucose.
o
Assess for urinary tract infection (UTI).
Magnesium , calcium , phosphate
Blood cultures in sepsis
Creatine kinase for rhabdom yolysis: o
Incidence as high as 17%
Urine pregnancy test in fem ales of childbearing years
Cardiac enzym es and troponin for m yocardial infarction
Diagnostic Procedures/Surgery
ECG
Chest radiograph
Head CT: indicated if com atose or with a focal neurologic deficit
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Differential Diagnosis Differentiate from DKA:
If acidosis or significant anion gap present, m ust determ ine cause (i.e., ketosis, [DKA], lactic acidosis, [hypoperfusion, sepsis, or postictal], or other cause of m etabolic acidosis
Mixed disorder of HHS and DKA present in up to 33% of patients
Treatment Initial Stabilization Airway, breathing, and circulation m anagem ent (ABCs):
Secure airway in com atose patients.
Cardiac m onitor and 18-gauge IV
Naloxone, thiam ine, and blood glucose for com a of unknown cause
Restore hem odynam ic stability with IV fluids.
0.9% norm al saline (NS) 1–2 L over the first hour
Larger volum es of fluid m ay be needed to norm alize the vital signs and establish urine output.
P.555
ED Treatment
General strategy: o
Frequent reassessm ent of volum e and m ental status
o
Electrolyte assessm ent difficult
Serum levels of Na + , K + , PO 4 - do not accurately reflect the total body solute deficits or the
Pa ge 2 4 6
intracellular environm ent. o
Repeat electrolyte and glucose levels hourly.
Search for a precipitating illness.
Fluids: o
Begin resuscitation with 0.9% saline 1–2 L over 1–2 hours to restore intravascular volum e and achieve hem odynam ic stability.
o
Use 0.45% saline after initial resuscitation
o
Calculate total body water (TBW) deficit using corrected serum sodium :
TBW deficit = 0.6 × weight (Kg) × (1 140/corrected Na + )
o
Average fluid deficit is 9 L.
o
Replace 50% of the fluid deficit over the next 12 hours.
o
Add D 5 to intravenous fluids when serum glucose 5.5 m Eq/L.
If the initial K + is norm al (3.5–5.5 m Eq/L), give 20–30 m Eq KCl in the first liter of fluids, then give 20 m Eq/h.
If the initial K + is low ( Table o f C o ntents > Hypertherm ia
Hyperthermia
Michelle Canham
Basics Description
Continuum of increasingly severe illnesses secondary to overwhelm ing heat stress
Begins with dehydration and electrolyte abnorm alities and progresses to therm oregulatory dysfunction and m ultisystem organ failure
Body tem perature is m aintained within a narrow range by balancing heat load with heat dissipation.
Tem perature elevation is accom panied by an increase in oxygen consum ption and m etabolic rate.
Oxidative phosphorylation becom es uncoupled and a variety of enzym es cease to function above 42°C (108°F).
Heat Stroke
Core body tem p >105°F (40.5°C)
Loss of therm oregulatory function, severe CNS dysfunction, and m ultisystem organ failure
Classic heat stroke (nonexertional): o
Occurs in those with com prom ised therm oregulation or an inability to rem ove them selves from a hot
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environm ent (extrem es of age, debilitated)
o
Develops over days to weeks
o
Severe dehydration, skin warm and dry
Exertional heat stroke: o
Occurs in younger, athletic individuals with a com bined environm ental and exertional heat stress
o
Develops over hours
o
Internal heat production overwhelm s dissipating m echanism s.
o
May be sweating
Heat Exhaustion
Core tem p: Table o f C o ntents > Hyperthyro idism
Hyperthyroidism
Rita Cydulka Danielle A. Hoover
Basics Description
Excessive thyroid horm one production results in a continuum of disease: o
Mild hyperthyroidism
o
Thyrotoxicosis
o
Thyroid storm or thyrotoxic crisis with life-threatening m anifestations
1–2% of patients with hyperthyroidism progress to thyroid storm .
Genetics
Interplay between genetics and environm ent is likely.
Graves disease is associated with HLA-B8 and HLA-DR3.
Autosom al dom inant inheritance seen in som e fam ilies with nontoxic goiter: o
Chrom osom e 14q, MNG1, and
o
Chrom osom e Xp22, MNG2
Etiology
Toxic diffuse goiter (Graves disease)
Pa ge 2 5 0
Toxic m ultinodular or uninodular goiter
T 3 toxicosis
Hashim oto thyroiditis
Malignancy
Hypothalam ic hyperthyroidism
Thyroid-stim ulating horm one (TSH)–producing pituitary tum or
Postpartum thyroiditis
Radiation thyroiditis
Ingestion of excessive iodine (Jodbasedow disease)
Drug induced: o
Am iodarone
o
Lithium
o
Iodine
o
Excessive thyroid horm one (factitious thyrotoxicosis)
Diagnosis Alert
Thyroid storm is a life-threatening condition which m ay be precipitated by: o
Infection
o
Traum a
o
Diabetic ketoacidosis
o
Myocardial infarction
o
Cerebrovascular accident
o
Abrupt withdrawal or acute ingestion ofthyroid m edication
Thyroid storm s involves exaggerated signs and sym ptom s of thyrotoxicosis: o
Hyperpyrexia
Pa ge 2 5 0
o
Extrem e tachycardia/dysrhythm ias
o
Congestive heart failure
o
Shock
o
Disorientation/m ental status changes
Signs and sym ptom s reflect end organ responsiveness to thyroid horm one: o
o
Signs:
Fever
Tachycardia disproportional to fever
Hyperhidrosis
Wide pulse pressure
Congestive heart failure (CHF)
Shock
Trem or
Disorientation/psychosis
Com a
Goiter
Thyrotoxic stare/exophthalm os
Thyrom egaly
Jaundice/tender liver
Sym ptom s:
Weight loss
Dysphagia or difficulty breathing secondary to obstruction by a goiter
Rash/pruritus/hyperhidrosis
Palpitations/chest pain
Dyspnea
Abdom inal pain
Diarrhea/hyperdefecation
Myalgias
Weakness
Nervousness/anxiety
Pa ge 2 5 0
Menstrual irregularities
Heat intolerance
Insom nia
Geriatric Considerations
Apathetic hyperthyroidism : o
Seen in the elderly
o
Owing to m ultinodular goiter
o
Subtle clinical findings:
Often reflecting single-organ dysfunction (CHF)
Weight loss
Depressed m entation
Trem or
Hyperactivity
Signs and Symptoms History Gradual onset of aforem entioned signs and sym ptom s
Physical Exam
Vital signs: o
Fever
o
Tachycardia
o
Elevation of systolic blood pressure
o
Tachypnea/hypoxia
Alopecia
Exophthalm os
Thyrom egaly or goiter
Thyroid bruit
Fine, thin, diaphoretic skin
Irregularly irregular heartbeat
Lung rales (CHF)
Abdom inal/right upper quadrant (RUQ)
Pa ge 2 5 0
tenderness/jaundice
Muscular atrophy/weakness
Trem or
Mental status changes/com a
Essential Workup
Search for the underlying cause.
Plasm a thyroid-stim ulating horm one (TSH) assay is the initial test of choice in the ED: o
Norm al level usually excludes hyperthyroidism .
o
If TSH levels are not available, strong clinical picture should prom pt initiation of therapy.
Tests Lab
Thyroid function tests for: o
Sym ptom s of hyperthyroidism
o
Elderly patient with new-onset CHF
o
New atrial fibrillation/supraventricular tachycardia (AFib/SVT)
TSH (usually decreased)
Free T 4 (usually elevated) o
CBC: o
If free T 4 is unavailable, total T 4 and resin T 3 uptake
Anem ia
Electrolytes, BUN, creatinine, glucose: o
Elevated BUN, creatinine, secondary dehydration
o
Hypokalem ia
Calcium
Liver function tests
Urinalysis
Arterial blood gases for hypoxem ia
Cardiac m arkers
Pa ge 2 5 0
ECG: o
Tachydysrhythm ias
o
Atrial fibrillation
Imaging Chest radiograph (in CHF)
Differential Diagnosis
Pheochrom ocytom a
Sepsis
Sym pathom im etic ingestion (e.g., cocaine, am phetam ines)
Psychosis
Heat stroke
Delirium trem ens
Malignant hypertherm ia
Neuroleptic m alignant syndrom e
Hypothalam ic stroke
Hypothyroidsim (m ay m im ic apathetic hyperthyroidism )
Factitious thyrotoxicosis
P.563
Treatment Initial Stabilization
Airway, breathing, and circulation m anagem ent (ABCs)
Cardiac m onitor
Supplem ental oxygen to m eet m etabolic needs
Initiate cooling m easures: o
Acetam inophen for fever:
Avoid aspirin (aspirin displaces thyroid horm one
Pa ge 2 5 0
from thyroglobulin). o
Cooling blanket
ED Treatment
Identify and treat the precipitating event.
For thyroid storm , initiate treatm ent sequence outlined below.
Inhibit horm one synthesis using thioam ides: o
Propylthiouracil (PTU):
Drug of choice
Decreases horm one synthesis and reduces peripheral conversion of T 4
o
Methim azole
Block horm one release: o
Potassium iodide, or
o
Oral Lugol solutions, or
o
Sodium iodide
o
Adm inister iodine therapy at least 1 hour after thioam ides to prevent organification of the iodine.
Prevent peripheral conversion of T 4 –T 3 : o
PTU or
o
Dexam ethasone
Block the peripheral effects of thyroid horm one: o
Beta-blockade:
Contraindicated/caution advised with CHF, diabetes m ellitus, and reactive airway disease
o
Propranolol
Esm olol
When beta-blocker is contraindicated, use:
Reserpine
Guanethidine
Treatm ent of thyrotoxicosis, secondary thyroiditis: o
Beta-blockade
Pa ge 2 5 1
o
Anti-inflam m atory m edications
General support: o
Acetam inophen for hyperpyrexia
o
Control congestive heart failure with digitalis and diuretics.
o
Manage dehydration
o
Hydrocortisone
Medication (Drugs)
Dexam ethasone: 2 m g IV q6h (peds: 0.15 m g/kg)
Esm olol: 500 µg/kg IV over 1 m inute followed by m aintenance dose of 50 µg/kg/m in IV; titrate to effect
Guanethidine: 30–40 m g PO q6h
Hydrocortisone: 100 m g IV q8h
Lugol solutions: 8–10 drops PO q6h
Methim azole: 40 m g PO initially, then 25 m g PO q6h
Potassium iodide (SSKI): 5 drops PO q6h
Propranolol: 1–2 m g IV, repeated q10–15m in as needed
Propylthiouracil (PTU): 600–1000 m g initially, then 200–250 m g PO q4h (peds: 5–7 m g/kg/24h)
Reserpine: 1–5 m g IM q4h–q6h, up to 15 m g/24h
Sodium iodide: 1 g IV q8h–q12h
Pregnancy Considerations
Physiologic changes associated with pregnancy m ay resem ble m any sym ptom s of hyperthyroidism , thus causing a delay in diagnosis.
Poorly controlled hyperthyroidism during pregnancy m ay result in: o
Prem ature labor
Pa ge 2 5 1
o
Pre-eclam psia
o
Low birth weight
o
Spontaneous abortion
o
Stillbirth
Thyroid storm often precipitated by stress, including infection or birth
Treatm ent: o
Initial stabilization as in the nonpregnant patient (ABCs, supportive m easures)
o
PTU considered the safest drug in inhibiting horm one synthesis
o
Propranolol m ay be safely used to treat the peripheral effects of excess thyroid horm one.
o
Radioactive iodine absolutely contraindicated during pregnancy or while nursing
Postpartum thyroiditis: o
Occurs in 5–10% of patients within 6 m onths of delivery
o
May require antithyroid m edications tem porarily
o
Half of those affected becom e euthyroid within 1 year
o
Transient hypothyroidism m ay follow; however, 40% of those affected go on to develop thyroid failure.
Follow-Up Disposition Admission Criteria
Thyroid storm
Requiring IV m edications to control heart rate (HR)
Sym ptom atic patients (tachycardia, fever)
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Discharge Criteria Minim ally sym ptom atic individuals who respond well to oral therapy
References 1. Larsen R, et al. William s’ Textbook of Endocrinology. 10th ed. Philadelphia, PA: WB Saunders; 2003. 2. Mestm an J. Hyperthyroidism in pregnancy. Clin Obstet Gynecol. 1997;40:45. 3. Tietgens ST, Leinung MC. Thyroid storm . Med Clin North Am . 1995;79:169–184. 4. Wogan JM. Selected endocrine disorders. In: Marx J, et al. Rosen's Em ergency Medicine: Concepts and Clinical Practice. 5th ed. St. Louis, MO: Mosby; 2001.
Codes ICD9-CM 242.9
ICD10 E05.9
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Hyperventilatio n
Hyperventilation
Robert F. McCormack
Basics Description
Hyperventilation syndrom e describes a constellation of sym ptom s (m ost com m only: dyspnea, chest pain, lightheadedness, and paresthesias) produced by a nonphysiologic increase in m inute ventilation. Minute ventilation m ay be increased by increasing respiratory rate or tidal volum e (sighs).
Pathologic or physiologic causes of hyperventilation m ust be excluded before the diagnosis of hyperventilation syndrom e can be assigned.
Prevalence
10–15% in the general population
More com m on in wom en (m ay be related to progesterone)
Etiology
Usually a response to psychological stressors
Etiology of sym ptom s is unclear; sym ptom s m ay be related to hypocapnia, hypophosphatem ia, or hypocalcem ia, but significant controversy exists in the literature.
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Diagnosis Signs and Symptoms
Cardiac: o
Chest pain
o
Dyspnea
o
“Air hunger―
o
Palpitations
Neurologic: o
Dizziness
o
Light-headedness
o
Syncope
o
Paresthesias
o
Headache
o
Carpopedal spasm
o
Tetany
Psychiatric: o
Intense fear, anxiety
o
Giddiness
o
Feeling of unreality
General: o
Fatigue
o
Weakness
o
Malaise
Clinical signs are rare and varied: o
Tachypnea m ost com m on
o
However, tachypnea m ay not be present. Patient m ay increase tidal volum e rather than respiratory rate.
Carpopedal spasm :
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o
May be dram atic
o
Chvostek sign m ay be present.
Essential Workup
Diagnosis of exclusion: o
Prim ary pathologic or physiologic causes of hyperventilation m ust be investigated and excluded.
Clinical diagnosis based on the history and physical exam
Vital signs including pulse oxim etry
Hyperventilation syndrom e will not result in hypoxia.
Tests
Hyperventilation provocation test after resolution of sym ptom s: o
Forced overbreathing for 3 m inutes m ay be attem pted to reproduce the sym ptom s.
o
Diagnostic accuracy is controversial.
o
Reproducibility of the sym ptom s m ay help the patient understand the role of overbreathing and help m anage future attacks.
ECG if chest pain present
Lab
Consider an arterial blood gas in any hypoxic patient.
Electrolytes, blood urea nitrogen, creatinine, and glucose levels for suspected acidosis/diabetic ketoacidosis
Imaging Chest radiograph of any patient with hypoxia or focal findings on lung exam ination
Differential Diagnosis
Pathologic
Hypoxia: o
Asthm a
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o
Congestive heart failure
o
Pulm onary em bolus
o
Pneum onia
Severe pain
CNS lesions
Acidosis (DKA)
Pulm onary hypertension
Pulm onary em bolus
Hypoglycem ia
Mild asthm a
Drugs: o
Aspirin intoxication
o
Withdrawal syndrom e (e.g., alcohol, benzodiazepines)
Physiologic
Pregnancy
Pyrexia
Altitude
P.565
Treatment Pre Hospital
Patients with abnorm al vital signs require IV access and pulse oxim etry.
Supplem ental oxygen if hypoxic
Initial Stabilization
Patients with abnorm al vital signs require IV access and
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pulse oxim etry
Initiate therapy for pathologic or physiologic cause of hyperventilation.
ED Treatment
Initiate treatm ent of hyperventilation syndrom e for the following:
Initial workup does not support a pathologic or physiologic cause.
History and physical exam findings suggest the diagnosis of hyperventilation syndrom e.
Reassurance, calm ing, and explanation of the voluntary com ponent of the patient's sym ptom s often have im m ediate dram atic results.
Do not use paper bag rebreathing to increase the PCO 2 . This has not been supported in the literature.
It m ay be dangerous in patients with hypoxia or a pathologic or physiologic cause for hyperventilation.
Clarification of the psychologic stressors helps the patient avoid further attacks.
Assess for need of psychiatric evaluation (i.e., suicidal ideation)
Anxiolytics
Short course of anxiolytics m ay benefit patients with definable tem porary stressors.
Medication (Drugs)
ED treatm ent: o
Benzodiazepine if sym ptom s persist to break the cycle of anxiety and hyperventilation
o
Lorazepam : 1–2 m g PO or IV
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o
Valium : 2–5 m g PO or IV
Outpatient treatm ent: o
Buspirone: 5 m g PO t.i.d.
o
Valium : 2–5 m g PO or IV
Follow-Up Disposition Admission Criteria Hyperventilation syndrom e does not require adm ission.
Discharge Criteria
Exclusion or successful treatm ent of prim ary pathologic or physiologic causes of hyperventilation
No acute psychiatric issues
Adequate follow-up with a prim ary care physician
References 1. Saisch S, Wessely S, William N. Patients with Acute Hyperventilation Presenting to an Inner–City Em ergency Departm ent. Chest. 1996;110(4):952–957. 2. Gardner W. The pathophysiology of hyperventilation disorders. Chest. 1996;109:516–534. 3. Block M, Szidon P. Hyperventilation syndrom es. Com pr Ther. 1994;20:306–311. 4. Hanashiro PK. Hyperventilation: benign sym ptom or harbinger of catastrophe? Postgrad Med. 1990;88:191–193. 5. Gardner WN, Bass C. Hyperventilation in clinical practice. Br J Hosp Med. 1989;41:73–81. 6. Callaham M. Hypoxic hazards of traditional paper bag rebreathing in hyperventilating patients. Ann Em erg Med. 1989;18:622–628.
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Codes ICD9-CM 306.1
ICD10 R06.4
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Hypervisco sity Syndro m e
Hyperviscosity
Syndrome Matthew B. Mostofi
Basics Description
Clinical consequences of increased blood viscosity
Viscosity is the resistance a m aterial has to change in form .
The higher the blood viscosity, the m ore internal resistance to blood flows.
Increased cardiac output is required to provide adequate perfusion of hyper viscous blood.
Oxygen delivery is im paired as transit through the m icrocirculatory system slows.
Etiology
The m ost com m on cause (85–90%) of hyperviscosity is increased concentration of gam m a globulins: o
Monoclonal gam m opathies: in m alignant diseases like Waldenstrom m acroglobulinem ia and m ultiple m yelom a
o
Polyclonal gam m opathies: usually rheum atic diseases (very rare)
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Increased num bers of red blood cells, as in polycythem ia vera
Increased concentration (>100,000) of WBC, as in acute and chronic leukem ia
Diagnosis Signs and Symptoms
Classic triad: o
Mucosal bleeding
o
Visual disturbances
o
Neurological
Hem atological: o
Bleeding is the m ost com m on m anifestation.
o
Epistaxis
o
Gingival, rectal, uterine bleeding
o
Prolonged postprocedural bleeding
o
Blood dyscrasias
o
Pruritus owing to red cell breakdown products
o
Splenic enlargem ent
Ocular: o
o
Change in visual acuity
Blurring
Diplopia
Visual loss
Characteristic “link-sausage effect― on funduscopy
o
Alternating bulges and constrictions within the retinal veins
o
Retinal hem orrhage, detachm ent
o
Exudate, m icroaneurysm form ation
Pa ge 2 5 2
o
Papilledem a
Renal: o
Nephritic or nephrotic syndrom e
o
Hem aturia
o
Sterile pyuria
Neurological: o
Headache
o
Ataxia
o
Mental status changes/com a
o
Dizziness/vertigo
o
Nystagm us
o
Tinnitus, hearing loss
o
Paresthesia, peripheral neuropathy
o
Seizure
Cardiovascular: o
Angina or m yocardial infarction
o
Dysrhythm ias
o
Congestive heart failure
Derm atologic: o
Raynaud phenom enon
o
Livedo reticularis
o
Palpable purpura
o
Eruptive spider nevuslike lesions
o
Digital infarcts
o
Peripheral gangrene
Essential Workup
Evaluate end-organ ischem ia and bleeding.
Measure serum or whole blood viscosity.
Suspect diagnosis if the laboratory evaluation is ham pered by serum stasis and increased viscosity causing analyzer blockage
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Tests Lab
CBC with WBC differential: o
Anem ia or erythrocytosis can be seen in hyperviscosity syndrom e.
o
Anem ia usually norm ocytic and norm ochrom ic
o
Rouleaux of erythrocytes on the peripheral sm ear im portant diagnostic clue
o
WBC for leukem ia
Electrolyte, blood urea nitrogen, creatinine, and glucose levels: o
Renal dysfunction is com m only noted in hyperviscosity syndrom e.
o
Hypercalcem ia and pseudohyponatrem ia in m ultiple m yelom a
Urinalysis: o
Proteinuria
o
Hem aturia
o
Sterile pyuria
Coagulation profile
Serum and urine protein electrophoresis
Measurem ent of serum viscosity (not routinely available in ED setting): o
Ostwald viscosim eter
o
Norm al range for the serum viscosity relative to water is 1.4–1.8.
o
Minim al viscosity at which sym ptom s develop is 4.0 centipoise (cp).
Elevated leukocyte alkaline phosphatase, lactate dehydrogenase, and serum vitam in B 1 2 levels
Differential Diagnosis
Pa ge 2 5 2
Bleeding and clotting disorders:
Platelet disorders (qualitative and quantitative)
Hereditary factor deficiencies
Acquired disorders (vitam in K deficiency, liver disease)
Dissem inated intravascular coagulation
P.567
Treatment Pre Hospital IV fluid resuscitation with hem orrhage
Initial Stabilization
Rehydrate with 0.9% norm al saline IV fluid.
Bleeding or end-organ ischem ia m ay not be controlled by any treatm ent except plasm apheresis.
In patients with anem ia and a leukem ic picture, avoid blood transfusion until pheresis is perform ed to avoid exacerbation of hyperviscosity syndrom e.
ED Treatment
Plasm apheresis/leukapheresis: o
In stable patients: 40 m L/kg of body weight
o
In critical patients: 60 m L/kg of body weight
o
Side effects include hypocalcem ia with use of a citrate-containing anticoagulant and dysrhythm ia (rare).
Phlebotom y: o
Useful in acute severe cases if plasm apheresis not readily available
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o
Blood (100–200 m L) can be withdrawn and replaced with isotonic saline.
Special Therapy Plasm apheresis:
Many patients require m ore than one plasm apheresis.
Follow-Up Disposition Admission Criteria
Evidence of end-organ ischem ia or hem orrhage
Intensive care unit adm ission for the following: o
Hem orrhage
o
Altered m ental status
o
Acute m yocardial infarction
Discharge Criteria Discharge after definitive treatm ent of the underlying disorder.
References 1. Forconi S, Pieragalli D, Guerrini M, et al. Prim ary and secondary blood hyperviscosity syndrom es and syndrom es associated with blood hyperviscosity. Drug. 1987;33(suppl 2):19–26. 2. Geraci JM, Hansen RM, Kueck BD. Plasm a cell leukem ia and hyperviscosity syndrom e. South Med J. 1990;83:800–805. 3. Gertz MA. Hyperviscosity Syndrom e. J Intensive Care Med. 1995;10:128–141. 4. Pim entel L. Medical com plications of oncologic disease. Em erg Med Clin North Am . 1993;22:407–419. 5. Som er T, Meiselm an HJ. Disorders of blood viscosity. Ann Med. 1993;25:31–39.
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6. Stolz JF, Donner M, Larcan A. Introduction to hem orheology: theoretical aspects and hyperviscosity syndrom es. Int Angiol. 1987;6:119–132.
Codes ICD9-CM 273.3
ICD10 C88.0
Pa ge 2 5 2
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Hyphem a
Hyphema
Jamil D. Bayram Sami H. Uwaydat
Basics Description
Blood in anterior cham ber (AC) of eye (between iris and cornea)
Hyphem a: grossly visible layering of blood
Microhyphem a: suspended RBCs visible by slit-lam p only
Genetics Genetic predisposition is related to hereditary blood dyscrasias (see below).
Etiology
Blunt traum a: m ost com m on (70–80%).
Anteroposterior com pression of globe with sim ultaneous equatorial globe expansion causing rupture of iris strom al/ciliary body vessels
Penetrating traum a: direct injury to strom al vessels or sudden ocular decom pression
Spontaneous: less com m on, lower incidence of com plications: o
Tum ors:
Pa ge 2 5 2
o
Melanom a
Retinoblastom a
Xanthogranulom a
Metastatic tum ors
Blood dyscrasias:
Hem ophilia
Leukem ia
Throm bocytopenia
Von Willebrand disease
o
Blood thinners: aspirin, Coum adin, heparin
o
Neovascularization of iris: in proliferative diabetic retinopathy, retinal vein occlusion, carotid stenosis
o
Postsurgical: cataract extraction, trabeculectom y, pars plana vitrectom y
Alert In children with no history of traum a, suspect child abuse.
Diagnosis Signs and Symptoms
Photophobia
Blurring of vision
Decreased visual acuity
Ocular pain
Nausea/vom iting
History
Previous visual acuity
Prior eye surgery
Prior glaucom a treatm ent
Past m edical history (blood disorders including sickle cell
Pa ge 2 5 2
disease)
Mechanism of traum a
Exact tim e of injury and of visual loss
History of excessive tearing after injury
Alert History of excessive tearing m ay indicate open globe injury.
Physical Exam
General physical exam with em phasis on associated bodily injuries
Periorbital ecchym osis
Eyelid lacerations
Enophthalm os (depression of the globe within the orbit)
Lim ited ocular m ovem ent with diplopia (m ay indicate orbital floor fracture)
Proptosis (m ay indicate retro-orbital hem orrhage)
Ocular exam o
Visual acuity
o
Rule out open globe (positive Seidel sign, corneal laceration, prolapse of intra-ocular structures)
o
Pupillary reaction to light (check for afferent pupillary defect prior to using dilating drops)
o
Tonom etry for intraocular pressure (IOP) m easurem ent
Alert
Exclude globe perforation before m easuring intraocular pressure (IOP); low pressure can indicate globe perforation.
Slit-lam p exam ; look for layer of blood in AC: o
Four grades of hyphem a depending on percentage of anterior cham ber occlusion by blood:
Grade I: less than one third
Pa ge 2 5 3
Grade II: one third to one half
Grade III: greater than one half
Grade IV: total (called 8-ball hyphem a; blood is dark and filling 100% of AC)
o
High-grade hyphem as are:
More likely to rebleed (25% of grade I com pared with 67% of grade III)
More likely to develop glaucom a and corneal staining
o
Less likely to recover visual acuity
Dilated fundus exam (avoid pressure on globe)
Tests Lab
Laboratory tests should be individualized depending on case.
Platelet count, PT/PTT, bleeding tim e if bleeding disorder is suspected
BUN, creatinine, and pregnancy test if am inocaproic acid is to be used (see below)
Factor VIII assay if fam ily history of hem ophilia
Sickle cell screen especially in African Am ericans and Mediterranean descent
Imaging
CT orbits (1-m m cuts) if open globe injury, intraocular foreign body, or orbital wall fracture are suspected
Ultrasound biom icroscopy (B scan) if total hyphem a and intraocular structures cannot be visualized
Alert Do not perform B scan if open globe injury is suspected (pressure applied during this procedure m ay cause extrusion of intraocular
Pa ge 2 5 3
contents).
Differential Diagnosis
Uveitis
Endophthalm itis
Treatment Pre Hospital Place eye shield in case of corneal perforation.
Initial Stabilization
Keep head upright to allow blood in AC to settle down.
Lim it activity, avoid bending, straining or exertion.
Place m etal or plastic shield over involved eye until integrity of globe is confirm ed.
Do not patch affected eye (if eye is patched, patient cannot notice sudden loss of vision).
Note that m etal and plastic shields have holes that let patient see through whereas patch com pletely blocks patient's vision.
ED Treatment
Mild analgesics (avoid nonsteroidal anti-inflam m atory drugs [NSAIDs] because of antiplatelet effect)
Antiem etics (associated N/V m ay worsen hyphem a by increasing IOP)
Cycloplegics decrease pain from iritis: o
Atropine 1% eyedrops 2–3 tim es per day until hyphem a resolves
Topical steroids m ay decrease inflam m ation from iritis: o
Prednisolone acetate 1% eyedrops (or equivalent)
Pa ge 2 5 3
4–8 tim es per day until hyphem a resolves (usually 7–10 days)
Am inocaproic acid (antifibrinolytic): o
Use in consultation with ophthalm ologist:
Not com m only used because of frequent system ic side effects
o
Stabilizes fibrin clot in AC and decreases incidence of rebleed, but has no effect on final visual outcom e
o
50 m g/kg PO q4h for total of 5 days (do not exceed 30 g/d). Dose should be adjusted in renal failure.
o
May cause postural hypotension, nausea, vom iting, diarrhea
o
New topical form is not yet FDA approved.
o
Do not use in pregnant wom en or in patients prone to throm bosis. It can also cause acute renal failure in patients with hem ophilia.
P.569
Prednisone: o
o
Indications:
Hem ophilia
Uncooperative children
Total hyphem a
History ofthrom botic disease
Dose: 0.6–0.75 m g/kg/24h in div. doses, up to 60 m g/d for 5 days
For increased IOP: o
For non-sickle cell patients, treat if IOP >30 m m Hg.
o
For sickle cell patients, treat if IOP >24 m m Hg.
o
Treat until IOP is controlled as indicated above.
o
Always start with one m edication. Add another if
Pa ge 2 5 3
unsuccessful in controlling pressure.
B-blockers—drug of choice: tim olol or levobunolol 0.5% b.i.d.
Alpha agonist: apraclonidine 0.5% or brim onidine 0.2% t.i.d.
Topical carbonic anhydrase inhibitors (CAI): dorzolam ide 2% or brinzolam ide 1% t.i.d.
Oral CAI: acetazolam ide 500 m g PO q12h (peds: 8–30 m g/kg/24h q6h–q8h) or m ethazolam ide 50 m g q8h
Mannitol (1–2 m g/kg IV over 45 m inutes q24h) when all other eyedrops fail to lower IOP to acceptable level
Avoid CAI and m annitol in sickle cell patients, as they m ay cause acidosis and induce sickling.
o
Allow 25–30 m inutes for each eyedrop to work. If after using all the drops and m annitol, IOP is still high, then surgical evacuation of blood clot is warranted (AC tap or washout).
Drugs to avoid: o
Pilocarpine: constricts pupil and prevents visualization of lens and retina
o
Prostaglandin eyedrops (e.g., latanoprost): increase inflam m atory response
Follow-Up Disposition
Discharge patient on atropine, prednisolone, and any appropriate IOP-lowering m edications.
Continue am inocaproic acid if decision was m ade to start it
Pa ge 2 5 3
in em ergency departm ent.
Antiem etics if needed
Stool softeners to m inim ize straining during bowel m ovem ents
Arrange for follow-up with ophthalm ologist: o
Daily slit-lam p exam daily for 3 days after initial traum a, to m onitor for rebleeding, corneal staining, and increased IOP
o
Follow-up exam will determ ine length of treatm ent with atropine, prednisone acetate, and IOP-lowering eyedrops.
Note that hyphem a size is not criterion for discharge or adm ission; IOP control is m ost im portant.
Admission Criteria
Medically uncontrolled IOP requiring surgical intervention
Ruptured globe
Noncom pliant patients
Associated ocular or orbital injuries
Children Table o f C o ntents > Hypo G lycem ia
HypoGlycemia
Matthew N. Graber
Basics Description
Deficiency in counterregulatory horm ones (glucagon, epinephrine, cortisol, growth horm one) or excessive insulin response
Serum glucose Table o f C o ntents > Hypo glycem ic Po iso ning
Hypoglycemic
Poisoning Mark B. Mycyk
Basics Description
Oral or parenteral agents that m ay cause hypoglycem ia or other m etabolic im balances
Hypoglycem ic poisoning m ay be intentional or unintentional (accidental).
Etiology
Insulin: o
Enhances glucose uptake into cells
o
Lim its glucose availability to the brain (m ost sensitive to hypoglycem ia)
o
Influences potassium redistribution
Sulfonylurea agents: o
Enhance insulin release from β cells, reduce hepatic glucose production, and increase peripheral insulin sensitivity
o
Hypoglycem ic effect enhanced by polypharm acy, alcohol use, hepatic dysfunction, and renal insufficiency
Pa ge 2 5 5
Biguanide agents (m etform in): o
Antihyperglycem ic agents
o
Decrease elevated serum glucose concentrations, but generally do not cause hypoglycem ia on their own
o
In the presence of insulin, biguanides do the following:
Increase glucose uptake into cells
Lim it glucose availability to the brain (m ost sensitive to hypoglycem ia)
Influence potassium redistribution
Decrease gastrointestinal glucose absorption
Decrease hepatic gluconeogenesis
Metabolize glucose to lactate in intestinal cells, which m ay accum ulate and lead to lactic acidosis
Thiazolidinediones: o
In the presence of insulin, thiazolidinediones increase glucose uptake and use and decrease gluconeogenesis
α-Glucosidase inhibitors: o
Lower system ic glucose by decreasing gastrointestinal absorption of carbohydrates
Diagnosis Signs and Symptoms
Insulin or sulfonylureas: o
Overdose causes hypoglycem ia.
o
Sym ptom s m ost often occur when glucose Table o f C o ntents > Hypo natrem ia
Hyponatremia
Linda Mueller
Basics Description
Sodium 120 mEq/L
Headache
Nausea
Vom iting
Weakness
Anorexia
Muscle cram ps
Rhabdom yolysis
Moderate: Na + between 110 and 120 mEq/L
Im paired response to verbal stim uli
Decreased response to painful stim uli
Visual/Auditory hallucinations
Bizarre behavior
Pa ge 2 5 7
Incontinence
Hyperventilation
Gait disturbance
Severe: Na + 120–125 m Eq/L over 6 hours with adm inistration of hypertonic saline
Calculate sodium deficit: o
Na + deficit = 0.6 (weight in kg)(140 – Na + )
250 m L of 3% or 5% saline solution in adult over 4–6 hours will raise serum sodium by 10–15 m Eq/L
Pa ge 2 5 7
o
OR m ay dose 1–2 m L/kg/h of 3% saline solution
Sodium contents: o
1 L 0.9% NS = 154 m Eq of sodium
o
1 L 3% saline = 513 m Eq of sodium
Hypovolemic Hyponatremia
Correct underlying cause.
Replete volum e with 0.9% NS IV.
Prim ary goals to restore: o
Extracellular fluid
o
Cardiac output
o
Organ perfusion
Hypervolemic/Euvolemic Hyponatremia
Water restriction to less than 1 L per day with high dietary salt intake
For faster correction of sodium : o
Adm inister IV 0.9% NS with loop diuretic (furosem ide).
Maxim um rate of correction = 0.5 m Eq/L/h
Medication (Drugs)
Furosem ide: 20–40 m g IV push
Sodium replacem ent: o
Calculate Na + deficit
o
Replace no m ore than half of requirem ent over 8–12 hours
Follow-Up Disposition
Pa ge 2 5 8
Admission Criteria
Sym ptom atic hyponatrem ia
Sodium 60.
Imaging Tooth roots m ay be absent.
Pa ge 2 5 8
Diagnostic Procedures/Surgery ECG:
Prolonged QT interval: o
Owing to ST-segm ent prolongation from hypocalcem ia
Differential Diagnosis
Must differentiate from variety of causes of hypocalcem ia
Lab artifact: o
Low total calcium that is norm al when corrected for album in level with no sym ptom s of hypocalcem ia
Alkalosis: o
Sym ptom atic hypocalcem ia with a norm al total calcium
Hypom agnesem ia (needed for PTH secretion)
PTH resistance (congenital)
PTH suppression by ethanol, chem otherapeutics, or cim etidine P.581
Vitam in D deficiency (low Ca 2 + + low PO 4 ): o
Anticonvulsant use (decreased vitam in D absorption)
o
Liver disease
o
Resistance to vitam in D
o
Malabsorption or dietary deficiency
Gram -negative sepsis
Renal failure or nephrotic syndrom e
Chelation: o
Pancreatitis (fatty acids chelate calcium )
o
Am m onium bifluoride (tire cleaner spray)
o
Hydrofluoric acid
Pa ge 2 5 8
o
Citrated blood
o
Acute hyperphosphatem ia:
Fleet enem as
Rhabdom yolysis
Acute renal failure
Treatment Pre Hospital
Adm inister calcium in refractory VFib or status epilepticus in addition to usual m edications if known hypoparathyroidism or suspected hypocalcem ia.
Stridor m ay herald laryngospasm .
Initial Stabilization
Airway, breathing, and circulation m anagem ent (ABCs): o
Manage airway if laryngospasm .
Adm inister IV calcium bolus (chloride or gluconate) if unstable cardiac rhythm or tetany: o
Slow infusion m uch safer unless patient m arkedly sym ptom atic
Prepare for ventricular dysrhythm ias including ventricular fibrillation.
Seizure precautions
ED Treatment
Calcium replacem ent: o
Ten percent calcium chloride (27.2 m g elem ental Ca 2+
/m L)
For life-threatening conditions: 1 am p (10 m L) over 3–5 m in IV or 10%
o
Calcium gluconate (9 m g elem ental Ca 2 + /m L)
Pa ge 2 5 8
For life-threatening conditions: 1–3 am p (10 m L/am p) over 5–10 m in/am p
o
For non-life-threatening conditions, adm inister calcium via slow infusion of 500–1,000 m g elem ental Ca 2 + over 6–24 hours (peds: 100 m g elem ental Ca 2 + /kg/24h)
o
Continuous cardiac m onitoring
o
Stop infusion if bradycardia develops.
o
Perform frequent checks of serum Ca 2 + levels.
o
Calcium adm inistration m ay precipitate digitalis toxicity.
o
Supplem ent to lowest possible Ca 2 + level keeping the patient asym ptom atic, then switch to oral replacem ent.
Soft tissue calcification m ay occur with calcium /phosphorus product of 60 (Ca × PO 4 ).
Replace m agnesium if low.
Bind phosphorus: o
Alum inum hydroxide–containing antacids (Maalox, Mylanta, or Gelusil) if creatinine 2
Vitam in D supplem entation
Avoid carbonated beverages (high in phosphorus).
Assess for associated endocrinopathies.
Medication (Drugs)
Calcium acetate (Phos-lo 167 m g elem ental Ca): 1 or 2 tabs with m eals
Calcium carbonate 500 m g (elem ental Ca): 1 or 2 tabs q.i.d. (2–4 g/d) (peds: 45–65 m g/kg/d)
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Calcium chloride 10% (27.2 m g elem ental Ca 2 + /m L): one am p over 3–5 m in IV if life-threatening condition; otherwise, slow infusion
Calcium gluconate 10% (9 m g elem ental Ca 2 + /m L): 1–3 am p over 5–10 m in per am p if life-threatening condition; otherwise, slow infusion
Magnesium oxide 400 m g: 1 or 2 tabs daily
Magnesium sulfate: 2 g IV (peds: 25–50 m g/kg up to 2 g) over 2 hours—if severe, 6 g over 6 hours
Vitam in D: 400 IU/d
Follow-Up Disposition Admission Criteria
Sym ptom atic hypocalcem ia
Abnorm al ECG
Inability to take vitam in D or calcium orally
Corrected calcium Table o f C o ntents > Hypo therm ia
Hypothermia
Jordan Moskoff
Basics Description Body tem perature Table o f C o ntents > Hypo thyro idism
Hypothyroidism
Rita Cydulka Jessica R. Goldstein
Basics Description
Decreased levels of effective circulating thyroid horm one and sensitivity to catecholam ines lead to decreased m etabolic rate, com pensatory vasoconstriction, reduced blood volum e, heart rate, and cardiac output.
Myxedem a com a is a rare extrem e form of hypothyroidism characterized by altered m ental status and defective therm oregulation triggered by a precipitating event or illness.
Results from a deficiency of thyroid horm one
Prim arily owing to thyroid disease caused by: o
Autoim m une process, e.g., Hashim oto thyroiditis, postpartum thyroiditis
o
Iatrogenic failure, e.g., radiation, thyroidectom y, drugs
Pituitary disease or secondary failure accounts for less than 4% of cases.
Usually follows an indolent course with decom pensation after specific stress factors
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Myxedem a com a caused by further stress on patient with hypothyroidism , which results in failure of com pensatory m echanism s. Stressors include: o
Hypoxia
o
Hypotherm ia
o
Hypotension
o
Hypoglycem ia
o
Hyponatrem ia
o
Adrenal insufficiency
o
Sedative hypnotic drugs
Etiology
Prim ary: o
Congenital
o
Autoim m une:
Thyroiditis
Hashim oto disease
o
Idiopathic
o
Iatrogenic:
o
Postsurgical
External radiation
Radioiodine therapy
Antithyroid drugs (iodides, lithium )
Inherited defect:
Aplasia
Hypoplasia
Enzym atic defect
Treatm ent of m aternal hyperthyroidism
o
Ingestion of drugs or goitrogens during pregnancy
o
Neoplasm : prim ary (carcinom a) or secondary (infiltration)
o
Infection: viral (rarely aerobic or anaerobic bacteria)
o
Traum a: neck injury
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Secondary: o
Pituitary tum or
o
Infiltrative disease (sarcoid) or tum or
o
Traum a
Diagnosis Signs and Symptoms History
Weakness/fatigue/drowsiness
Cold intolerance
Headaches
Myalgias
Menorrhagia
Constipation
Weight gain
Em otional lability
Mental status changes
Physical Exam
Puffy eyelids
Sparse pubic, axillary hair
Absent lateral one-third eyebrows
Prolonged relaxation phase deep tendon reflexes (DTRs)
Yellow tinged/dry skin
Pallor
Goiter
Myxedem a—dry, waxy swelling of skin/subcutaneous tissues
Swelling of hands/feet
Huskiness of voice
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Galactorrhea
Myxedema Coma
Extrem e form of hypothyroidism (see above) triggered by stress or illness
Hypotherm ia
Bradycardia
Hypotension
Altered m ental status
Geriatric Considerations Suspect m yxedem a com a in decom pensated elderly wom en with history of chronic or untreated hypothyroidism .
Pregnancy Considerations
Postpartum thyroiditis occurs in up to 5% of wom en.
Usually occurs 3–6 m onths postpartum
Com plain of depression, weakness, fatigue
Pediatric Considerations
Neonatal Graves disease occurs in about 10% of wom en with Graves during pregnancy regardless of treatm ent.
Thyroid-stim ulating horm one (TSH) antibodies and propylthiouracil (PTU) cross placenta.
PTU excreted in sm all quantities in breast m ilk
Essential Workup Laboratory confirm ation of the diagnosis of hypothyroidism /m yxedem a com a is usually not possible in the ED.
Tests Search for the underlying cause of m yxedem a com a.
Lab
Thyroid function studies: o
Free T 4 (low)
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o
High-sensitivity TSH (increased)
o
If free T 4 unavailable—total T 4 (decreased) and resin T 3 uptake (increased)
CBC: o
Anem ia
Electrolytes, BUN, creatinine, glucose: o
Hyponatrem ia
o
Hypoglycem ia
AST, lactate dehydrogenase (LDH), creatine phosphokinase (CPK)
Arterial blood gases: o
Hypoxem ia/hypercapnia
o
Acidosis
Imaging ECG:
Profound bradycardia
Differential Diagnosis
Nephrotic syndrom e
Chronic nephritis
Hypoalbum inem ia
Chronic renal disease
Sepsis
Depression
Congestive heart failure (CHF)
Treatment Initial Stabilization
Airway, breathing, and circulation m anagem ent (ABCs): o
Intubation and ventilation m ay be necessary.
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Cardiac m onitor
Blood pressure support
Supplem ental oxygen to m eet m etabolic needs
Correct hypotherm ia: o
Initiate passive warm ing m easures.
o
Aggressive rewarm ing m ay precipitate hypotension from vasodilation.
P.585
ED Treatment Mild hypothyroidism —refer for oral thyroid replacem ent as an outpatient.
Myxedema Coma
Life-threatening condition
Initiate thyroid horm one replacem ent therapy if a high index of suspicion: o
Prom pt IV replacem ent im proves survival.
o
L-thyroxine (LT 4 ) or liothyronine (LT 3 ):
Som e experts advocate LT 4 over LT 3
o
Reassess 4 hours after initial dose.
o
Use sm aller doses of thyroid horm one in the elderly or patients with cardiac disease.
Hydrocortisone to prevent Addisonian crisis
Dextrose for hypoglycem ia
IV fluid bolus for hypotension: o
Avoid pressors, if possible, as they m ay precipitate dysrhythm ias.
o
Response to pressors is poor until thyroid replacem ent initiated.
o
Thyroid horm one augm ents action of pressors.
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Correct the underlying precipitant.
Medication (Drugs)
Dextrose: 50–100 m L D 5 0 (peds: 2 m L/kg of D 1 0 over 1 m in) IV
Hydrocortisone: 100 m g (peds: 4 m g/kg) IV q6h–q8h
L-thyroxine (LT 4 ): 300–600 µg load IV followed by 50–100 µg IV daily
Liothyronine (LT 3 ): 10–20 µg load IV followed by 10 µg IV q4h for 24h, then 10 µgIV q6h for 24–48h.
Follow-Up Disposition Admission Criteria ICU adm ission for m yxedem a com a
Discharge Criteria Hypothyroid patients should be referred to a prim ary caretaker for initiation of oral thyroid horm one replacem ent therapy.
References 1. Fliers E, Wiersinga WM. Myxedem a com a. Rev Endocr Metab Disord. 2003;4:137–141. 2. Holm es L, Lakshm anan M. The patient with chronic endocrine disease. In: Herr RD, Cydulka RK, eds. Em ergency Care of the Com prom ised Patient. Philadelphia: Lippincott–Raven Publishers; 1994:123–133. 3. Jordan RM. Myxedem a com a. Pathophysiology, therapy, and factors affecting prognosis. Med Clin North Am . 1995;79:185–194.
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4. Larson R, Davies TF, Hay ID. The thyroid. In: Wilson JD, ed. William s’ Textbook of Endocrinology. 9th ed. Philadelphia, PA: WB Saunders; 2001:389–516. 5. Pim entel L, Hansen KN. Thyroid disease in the em ergency departm ent: a clinical and laboratory review. J Em erg Med. 2005;28(2):201–209. 6. Sarlis NJ, Gourgiotis L. Thyroid em ergencies. Rev Endocr Metab Disord. 2003;4(2):129–136. 7. Wogan JM. Endocrine disorders. In: Marx JA, Hockenberger RS, Walls RM, et al., eds. Rosen's Em ergency Medicine. 5th ed. St. Louis, MO. Mosby; 2002.
Codes ICD9-CM 244.9
ICD10 E03.9
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Idio pathic Thro m bo cyto penic Purpura
Idiopathic
Thrombocytopenic Purpura Michael Schmidt Amer Aldeen
Basics Description
Idiopathic throm bocytopenic purpura (ITP) is throm bocytopenia without apparent cause or abnorm alities in other cell lines.
Incidence is approxim ately 10/100,000 per year—m ay be an underestim ate owing to subclinical cases of throm bocytopenia.
Acute ITP: o
Half of cases involve children.
o
90% of children recover within 8 weeks with or without therapy.
o
Adult recovery is delayed and requires specific therapy to achieve rem ission.
Chronic ITP: o
Occurs m ostly in adults
o
Young wom en are m ost susceptible
o
Characterized by variable response to corticosteroids
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and other im m une suppressants
Genetics ITP appears to run in fam ilies, as do variations in response to corticosteroids for treatm ent.
Etiology
Autoantibodies cause im m une-m ediated destruction of circulating platelets, prim arily in the spleen.
Som e patients do not possess autoantibodies, suggesting a role for T-cell-m ediated cytotoxicity.
Eradication of H. pylori can som etim es be associated with platelet recovery (unclear m echanism ).
Diagnosis Signs and Symptoms History
Up to 28% of patients are asym ptom atic and diagnosed on routine CBC.
Bleeding is the m ost com m on com plaint: o
Com m on:
Mucous m em brane: gingiva, epistaxis, conjunctival, m enorrhagia
o
Rare (m ore com m on in coagulopathies):
GI bleeding, hem arthrosis, hem aturia, and hem atom as
84% of pediatric cases of ITP follow recovery from a viral illness.
Physical Exam
Petechiae
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Nonpalpable nature of purpura distinguishes ITP from Henoch-Schönlein purpura (HSP).
Neurologic deficits from intracranial hem orrhage (ICH): o
ICH is the m ost com m on cause of death in ITP.
o
Risk of ICH in ITP increases with age:
Age 60 years: 48%
Essential Workup Diagnosis of exclusion—other causes of throm bocytopenia m ust be ruled out.
Tests Lab
CBC with differential and peripheral sm ear: o
Throm bocytopenia
o
Norm al platelet size
o
Norm al WBC and RBC m orphology and size
HIV testing
Electrolytes, BUN, creatinine: to evaluate kidney function for TTP/HUS (hem olytic urem ic syndrom e)
Imaging CT head to evaluate for ICH
Diagnostic Procedures/Surgery Bone m arrow biopsy:
All adults >60 years
Atypical sym ptom s
Patients considering splenectom y
Children with persistent throm bocytopenia >6 m onths
Children unresponsive to intravenous im m unoglobulin (IVIG)
Children before steroids to evaluate for acute leukem ia
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Differential Diagnosis
Im paired bone m arrow production: o
Bone m arrow fibrosis
o
Bone m arrow infiltration owing to m alignancy
o
Cytotoxic drugs used in chem otherapy
o
Congenital/acquired bone m arrow abnorm alities
Splenic sequestration: o
Portal hypertension
o
Neoplastic infiltration
o
Sickle cell disease
Accelerated destruction of platelets: o
Vasculitis
o
TTP/HUS
o
Dissem inated intravascular coagulation (DIC)
o
Cardiac valvular disease
Drug induced: o
o
Decreased platelet production:
Chem otherapy
Thiazide diuretics
Ethanol
Estrogen
Increased destruction of platelets:
Aspirin
Heparin
Chlorpropam ide
Chloroquine
Gold salts
Sulfonam ides
Insecticides
P.587
Pa ge 2 6 1
Treatment Initial Stabilization
Airway, breathing, and circulation m anagem ent (ABCs)
Stabilize life-threatening bleeding: o
o
Intracranial hem orrhage:
Airway control
Cautious hyperventilation or m annitol
Neurosurgery consultation
Hem orrhagic shock:
Two large-bore IVs
Direct pressure for hem ostasis
Blood transfusions
Platelet transfusions: 2–3 tim es the norm al am ount
o
IV glucocorticoids
IVIG
Mucous m em brane bleeding:
Apply topical collagen sponge.
ED Treatment
Initial treatm ent options for ITP are based on: o
Degree of throm bocytopenia
o
Severity of illness
o
Duration of sym ptom s
o
Age
o
Risk factors for bleeding (hypertension, peptic ulcer disease, vigorous lifestyle)
o
Hem atologist preference
Efficacy of treatm ent is dem onstrated in term s of platelet
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recovery tim e and not m orbidity or m ortality.
Specific treatm ent options: o
Observation is recom m ended for children without bleeding com plications or profound throm bocytopenia (40.5°C unexplained by other cause
Severe local reaction involving the circum ference of the injected lim b unless owing to inadvertent subcutaneous injection
o
Encephalopathy within 7 days of vaccine:
severe acute neurologic illness with prolonged seizures and/or unconsciousness and/or focal signs
o
Progressive neurologic disease excluding epilepsy
o
Im m unocom prom ised hosts should not receive the varicella vaccine.
o
Severely im m unocom prom ised patients (non-HIV related) should not receive the MMR vaccine.
o
Pregnant patients should not receive the varicella vaccine, and the hepatitis A vaccine should be used with caution. Live virus vaccines are not routinely recom m ended during pregnancy.
Vaccines m ay be given with the following: o
Mild acute illness with or without fever
o
Mild to m oderate local reaction (i.e., swelling, redness, soreness), low-grade or m oderate fever after previous dose
o
Lack of previous physical exam ination in well-appearing person
o
Current antim icrobial therapy
o
Convalescent phase of illness
o
Prem ature birth (hepatitis B vaccine is an exception)
o
Recent exposure to an infectious disease
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o
History of penicillin allergy, other nonvaccine allergies, relative with allergies, receiving allergen extract im m unotherapy
o
HIV-infected children who are either asym ptom atic or not severely im m unocom prom ised should be vaccinated.
Review the tim ing of the patient's im m unizations and determ ine if catch-up im m unizations are necessary.
Specific discussion with the parents is required to review the risks and benefits of tetanus, particularly given the frequent occurrence of traum a and the need to provide both passive and active im m unity at that tim e: o
Generally, an inform ed consent is required or at a m inim um , docum entation in the chart that the risks and benefits have been thoroughly discussed.
o
In addition, The National Childhood Vaccine Injury Act requires that all health care providers provide parents or patients with copies of Vaccine Inform ation Statem ents before adm inistering each dose of the vaccines listed in the schedule.
Treatment
Route and tim ing of vaccine adm inistration: See Reference 1.
Prophylaxis with acetam inophen at the tim e of injection and again at 4 and 8 hours postvaccination m ay reduce the incidence of fever and local reactions:
Children who receive varicella vaccine should avoid salicylates for 6 weeks postvaccination because of the association of varicella infection and salicylates to Reye
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syndrom e.
Follow-Up Disposition Admission Criteria
Patients with serious adverse reactions following im m unization should be adm itted.
Patients with anaphylaxis and encephalopathy m ay require adm ission to a pediatric intensive care unit.
Unexpected adverse events should be reported to the Vaccine Adverse Event Reporting System (VAERS).
Discharge Criteria Patients m ay be discharged hom e after routine im m unizations unless an im m ediate adverse reaction occurs.
References 1. Advisory Com m ittee on Im m unization Practices of the CDC: Available at http://www.cdc.gov/nip. 2. Am erican Academ y of pediatrics (http://www.aap.org). 3. Am erican Academ y of Pediatrics. Red Book 2003: Report of the Com m ittee on Infectious Diseases. 26 th ed. Elk Grove Village, IL: Author; 2003. 4. Am erican Academ y of Pediatrics. Thim erosal in vaccines–Joint statem ent of the Am erican Academ y of Fam ily Physicians, The Am erican Academ y of Pediatrics, The Advisory Com m ittee on Im m unization Practices, and the United States Public Health Service. Available at: http://www.aap.org/policy/jointthim .htm l. 5. Black S, Shinefield H, Firem an B, et al. Efficacy, safety, and im m unogenicity of heptavalent pneum ococcal vaccine in children.
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Pediatr Infect Dis J. 2000;19:187–195. 6. Black SB, Shinefield HR, Hansen J, et al. Postlicensure evaluation of the effectiveness of seven valent pneum ococcal conjugate vaccine. Pediatr Infect Dis J. 2001;20:1105–1107. 7. Halsey NA, Hym an SL. Measles-m um ps-rubella vaccine and autistic spectrum disorder: report from the New Challenges in Im m unization Conference. Pediatrics. 2001;107:e84. 8. National im m unization hotline ([800] 232-2522). 9. Recom m ended Childhood and Adolsecent Im m unization Schedule, by Vaccine and Age—United States, 2006. Available at http://www.cdc.gov/nip/recs/child-schedule.htm
Miscellaneous SEE ALSO: Anaphylaxis; Encephalitis; Hepatitis; Influenza; Measles; Mum ps; Pertussis; Polio; Seizure, Adult; Seizure, Pediatric; Tetanus; Varicella
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Im m uno suppressio n
Immunosuppression Lara K. Kulchycki Larry A. Nathanson
Basics Description Deficiency in the ability to fight infection:
Antibody (B cell)
Cellular (T cell)
Phagocytic dysfunction
Com plem ent deficiency
Breach of skin/m ucosal barriers
Congenital versus acquired
Etiology
Aging: o
Im m unosenescence
o
Poor circulation and wound healing
o
Nosocom ial infections:
o
Recent or frequent hospitalizations
Nursing hom e residents
Blunted fever and inflam m atory responses
IV drug abuse
HIV infection:
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o
CD4 count determ ines susceptibility to particular pathogens
Diabetes: o
Hyperglycem ia im pairs im m une system
o
Large and sm all vessel vascular disease
o
Decreased sensation from peripheral neuropathy
Malnutrition: o
Poverty and hom elessness
o
Alcoholism
Asplenia: o
Functional asplenia (sickle cell disease)
o
Surgical rem oval of the spleen
Organ transplant recipients: o
Im m unosuppressive m edications
o
At risk for viral infections with cytom egalovirus, Epstein Barr virus, and hum an herpes viruses
Cancer and cytotoxic chem otherapy: o
Neutropenia defined as absolute neutrophil count (ANC) Table o f C o ntents > Inbo rn Erro rs o f M etabo lism
Inborn Errors
of Metabolism David A. Perlstein
Basics Description
Defect in the type, am ount, and toxicity of m etabolites that accum ulate owing to an inherited abnorm al pathway in children; results in a variety of clinical findings. More than 400 hum an diseases caused by inborn errors of m etabolism
Epidem iology: o
Incidence:
Variable: 1:10,000–1:200,000 births
Genetics Com m on inherited m etabolic diseases:
Urea cycle defects
Organic acidem ias
Disorders of am ino acid m etabolism
Defects in fatty-acid oxidation
Mitochondrial disorders
Carbohydrate disorders
Mucopolysaccharidoses
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Sphingolipidoses
Peroxisom al disorders
Pathophysiology Related to defect in m etabolic pathway
Etiology Diverse group of disorders involving genetic deficiency of an enzym e of an interm ediary m etabolite or a m em brane transport system
Diagnosis Signs and Symptoms
Rapid decom pensation m ay occur.
Neonates, initial presentation: o
Asym ptom atic
o
Hypotherm ia (m itochondrial defects)
o
Hypotonia/hypertonia (peroxisom al disorders)
o
Apnea (urea cycle defects, organic acidosis)
o
Seizures (peroxisom al disorders, glucose transporter defects)
o
Com a (num erous)
o
Vom iting (num erous)
o
Poor feeding, growth (num erous)
o
Jaundice (galactosem ia, Niem ann-Pick C)
o
Hypoglycem ia (galactosem ia, m aple syrup urine
o
Dysm orphic features (lysosom al storage disorders, congenital adrenal hyperplasia, Sm ith-Lem li-Opitz)
Older children, untreated: o
Failure to thrive (urea cycle defects)
o
Dehydration (organic acidosis)
o
Vom iting (urea cycle defects and others)
Pa ge 2 6 4
o
Diarrhea (num erous)
o
Food intolerance (lipid defects, am ino acid defects)
o
Lethargy (urea cycle defects)
o
Ataxia (urea cycle defects)
o
Seizures (num erous)
o
Mental retardation (phenylketonuria [PKU] and others)
History Com plete history of current and concom itant illness:
Newborn screening
Dietary
Fam ily
Consanguinity
Other
Physical Exam
Abnorm al odor
Altered m ental status
Tachypnea
Abnorm al facies
Cataract
Cardiom yopathy
Hepatom egaly
Splenom egaly
Derm atitis
Jaundice
Essential Workup Key is to consider in differential diagnosis:
Deteriorating neurologic status
Unexplained failure to thrive with dehydration, persistent vom iting, or acidosis
Shock unresponsive to conventional resuscitative
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m easures
Tests Lab
Bedside glucose determ ination
Electrolytes, BUN/creatinine, glucose
CBC with differential
Calcium level
Liver function tests, fractionated bilirubin, prothrombin tim e
Arterial or venous blood gas
Uric acid
Urinalysis
Chem istries, as indicated:
o
Am m onia level
o
Quantitative serum am ino acids
o
Urine organic and am ino acids
o
Lactate and pyruvate levels
Cultures: o
Blood
o
Cerebrospinal fluid
Imaging
CT scan of head for altered m ental status
Chest radiograph
Diagnostic Procedures/Surgery Spinal tap
Differential Diagnosis
Often m isdiagnosed as sepsis, dehydration, failure to thrive, toxic ingestion, or nonaccidental traum a
Infection: o
Sepsis
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o
Meningitis
o
Encephalitis
Metabolic: o
Reye syndrom e
o
Hepatic encephalopathy
o
Hyperinsulinem ia
o
Horm onal abnorm ality
Renal: o
Renal failure
o
Renal tubular acidosis
Toxic ingestion
Central nervous system m ass lesions
Nonaccidental traum a
Treatment Pre Hospital Alert
Careful assessm ent of airway, breathing, circulation
Bedside glucose, if possible
Intravenous glucose infusion takes precedence over fluid boluses unless patient in shock. Correction can occur concurrently.
Avoid lactated Ringer solution.
Keep child NPO.
Initial Stabilization For altered m ental status, adm inister Narcan, glucose (ideally after Accu-Chek and thiam ine.) P.595
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ED Treatment
Initiate IV glucose at rate of 8–10 m g/kg/m in to prevent catabolism : o
Corresponds to D 1 0 at 1.5 tim es m aintenance
o
Do not delay glucose infusion to give a “bolus― of isotonic saline; m ay be given concurrently in a child in shock.
o
If patient is severely hypoglycem ic, give IV glucose bolus of D 2 5 .
Rehydrate if patient is hypoglycem ic: o
Restore norm al acid-base balance.
Adm inister bicarbonate if pH is Table o f C o ntents > Inflam m ato ry Bo w el Disease
Inflammatory
Bowel Disease Shayle Miller
Basics Description
Idiopathic, chronic inflam m atory diseases of intestines, which can involve extraintestinal sites as well.
Differentiation between ulcerative colitis (UC) and Crohn's not always clear; interm ediate form s of inflam m atory bowel disease (IBD) exist.
May present as initial onset of disease or exacerbation of existing disease.
Maintain high index of suspicion owing to frequent, subtle presentation of Crohn's disease
Pediatric considerations: o
Can occur in first few years of life.
o
Extraintestinal m anifestations m ay predom inate.
Differences between Crohn's and UC: o
Rectum is alm ost always involved in UC with continuous inflam m ation proxim ally in colon.
o
Sm all intestine is not involved in UC.
o
Crohn's can occur anywhere from m outh to anus,
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often with norm al GI tract segm ents between affected areas. o
Crohn's involves transm ural inflam m ation, whereas UC is confined to subm ucosa.
Sim ilarities between Crohn's and UC: o
Higher rate of colon cancer with disease >10 years
o
Pain of exacerbation rem ission
o
Bim odal age distribution with early peak between teens and early 30s and second peak about age 60
Crohn's disease clinical pattern: o
Ileocecal: approxim ately 40%
o
Sm all bowel: approxim ately 30%
o
Colon: approxim ately 25%
o
Other: approxim ately 5%
UC clinical pattern on presentation: o
Pancolitis: 30%:
o
Proctitis or proctosigm oiditis: 30%:
o
Most severe clinical course
Relatively m ild clinical course
Left-sided colitis (up to splenic flexure): 40%:
Between two above in severity
Etiology
Unknown
Two diseases—these are separate entities with com m on genetic predisposition.
A positive fam ily history very com m on.
Multifactorial origin involving interplay am ong following factors:
o
Genetic
o
Environm ental
o
Im m une
Pathogenesis:
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o
Gut wall becom es unable to downregulate its im m une responses, ultim ately resulting in chronic inflam m ation.
There is no definitive evidence for etiologic role of infectious agent
Psychogenic factors m ay play role in som e sym ptom atic exacerbations.
Diagnosis Signs and Symptoms
Crohn's disease can present with any clinical correlates of chronic inflam m atory, fibrostenotic, or fistualizing illness.
Ulcerative colitis m ay begin subtly or as catastrophic illness.
Constitutional, gastrointestinal, and extraintestinal m anifestations are com m on with both Crohn's and UC.
History
Constitutional: o
o
Crohn's:
Low-grade fever
Night sweats
Weight loss
Fatigue
UC:
Fever usually only in fulm inant disease
Weight loss
Fatigue
Gastrointestinal: o
Abdom inal pain/tenderness—Crohn's disease:
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Episodic
Perium bilical; m ay localize to right lower quadrant (RLQ) with ileal disease
Generalized with m ore diffuse intestinal involvem ent
Can localize to area of intra-abdom inal abscesses or fistulous involvem ent
Tenderness and distension suggest obstruction or toxic m egacolon
o
Abdom inal pain/tenderness—UC:
More generalized than Crohn's disease
Often lim ited to predefecatory period
Tenderness with distension—suspect toxic dilation
Stool: o
o
Crohn's disease:
Mild loose stool
Rarely m ore than four or five per day
About 50% bloody
UC:
Diarrhea variable, can be severe
Vast m ajority are bloody, som etim es with severe hem orrhage
Mucus
Tenesm us and urgency com m on
Nausea/vom iting: o
Crohn's disease:
o
Obstruction com m on with ileocolonic disease
UC:
Obstruction rare
Dim inished bowel sounds with toxic dilation
Liver:
Pa ge 2 6 5
o
Sclerosing cholangitis can be seen.
o
Cholelithiasis can be seen in 35–60% of Crohn's.
Renal: o
Nephrolithiasis
o
Obstructive hydronephrosis
Musculoskeletal: o
Peripheral arthritis/arthralgias—follows disease activity
o
May be confused with juvenile rheum atoid arthritis, idiopathic growth failure, anorexia nervosa
Physical Exam
Perianal: o
Crohn's disease:
Perianal abscesses
Fissures—characteristically painless
Fistulas—seen in up to half of patients with colonic disease
o
May present prior to other m anifestations
UC:
No perianal involvem ent
RLQ pain/m ass often m istaken for appendicitis
Extraintestinal: o
o
Eye:
Uveitis
Episcleritis
Keratitis
Oral:
o
Aphthous stom atitis
Derm atologic:
Erythem a nodosum
Pyoderm a gangrenosum
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Essential Workup
It m ay present as initial onset of disease or exacerbation of existing disease.
Maintain high index of suspicion because of subtle presentation of Crohn's disease.
Tests Lab
Nothing diagnostic
CBC: o
Anem ia secondary to chronic or acute blood loss
Electrolytes, BUN/creatinine, glucose
Stool exam : o
Occult blood
o
Clostridium difficile
o
Fecal leukocytes m ay be present.
o
O & P and culture to rule out infectious cause of enteritis
Erythrocyte sedim entation rate (ESR) is always elevated.
Newer, investigational, serologic tests m ay have use as adjunctive diagnostic aides, screening testing, or predictors in therapy.
Imaging
Upright chest and abdom inal radiographs for: o
Toxic m egacolon (>6 cm dilation)
o
Obstruction
o
Air in wall of colon (m ay indicate im pending perforation)
o
Perforation—subdiaphragm atic air or free air outlining liver or gall bladder
CT abdom en:
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o
Distinguish abscess from localized inflam m atory m ass in Crohn's
P.597
Colonoscopy with biopsy can confirm diagnosis of UC or Crohn's: o
Can be withheld with severe sym ptom s owing to perforation risk.
Contrast im aging of sm all bowel, especially term inal ileum , m ay confirm diagnosis of Crohn's.
Differential Diagnosis
Infectious enteritis
Pseudom em branous colitis (C. difficile)
Appendicitis
Diverticulitis
Diverticulosis
Functional bowel disease
Lym phom a involving bowel
Ischem ic colitis
Gonococcal or chlam ydial proctitis
HIV
Colon cancer
Vasculitis
Am yloidosis
Treatment Initial Stabilization
IV 0.9% norm al saline (NS) volum e replacem ent if
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dehydrated
Transfusion if significant blood loss
ED Treatment General Measures
Nasogastric (NG) suction if obstruction or toxic dilation suspected
Broad-spectrum antibiotics for fulm inant UC or suspected perforation
Consider steroid replacem ent if stress doses required for those recently on oral steroids
Surgical evaluation indications: o
Free perforation
o
Intestinal obstruction
o
Massive, unresponsive hem orrhage
o
Toxic dilation:
Not an absolute indication for surgical intervention
Intensive m edical m anagem ent with sm all bowel decom pression and close radiographic m onitoring and surgical consultation
Walled off perforation with abscess: o
Usually not indication for em ergent surgery
o
Careful observation for peritonitis
Medical therapy: o
Treatm ent is usually not initiated unless diagnosis already established.
o
Refill or restart m edications in patient with known disease.
o
ED prescribed m edical regim en should be individualized, and consultation with gastroenterologist strongly recom m ended:
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Am inosalicylate (sulfasalazine m esalam ine) is used for m ild to m oderate disease.
Antidiarrheal agent (diphenoxylate) is used—but withhold if severe disease or suspect toxic m egacolon.
Steroid (prednisone, budesonide or hydrocortisone enem a, ACTH) is used for m oderate to severe disease.
Antibiotics (m etronidazole and/or ciprofloxacin) aid in treatm ent of Crohn's with colon/perineal involvem ent.
Im m unosuppressive agents (azathioprine, m ethotrexate) are used in severe disease.
Monoclonal antibodies neutralize cytokine tum or necrosis factor (TNF)-alpha and inhibit binding to TNF-alpha receptors (inflixim ab [Rem icade]). Used as parenteral therapy in disease unresponsive to other m odalities. Not ED drug, but be aware of potential severe adverse reactions, infusion reactions, autoim m une diseases and infections.
Pediatric Considerations If nonaccidental traum a is suspected, prom pt referral to appropriate child protective agencies is required along with m edical treatm ent.
Medication (Drugs)
ACTH: 80–120 IU/24h IM or IV
Ciprofloxacin: 500 m g PO q12h
Hydrocortisone enem a: 60 m g
Mesalam ine enem as: 1–4 g retention enem a—retain
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overnight
Mesalam ine suppository: 500 m g per rectum (PR) b.i.d.
Mesalam ine tablets (Asacol sustained release 400 m g; Pentasa 250 m g): 800 m g PO t.i.d; 1,000 m g PO q.i.d.
Metronidazole: 250–500 m g (peds: 30 m g/kg/24h) PO t.i.d.
Prednisone: 40–60 m g PO daily
Sulfasalazine (Azulfidine): 500 m g PO q.i.d.
Follow-Up Disposition Admission Criteria
Surgical indication: o
Massive, unresponsive hem orrhage
o
Perforation
o
Toxic dilation
o
Obstruction
Severe flare-up: o
Electrolyte im balance
o
Severe dehydration
o
Severe pain
o
High fever
o
Significant bleeding
Discharge Criteria
Initial presentation of diarrhea, m ild pain, without toxicity, with close follow-up
Mild to m oderate exacerbation of known disease without obstruction, severe bleeding, severe pain, dehydration, with close follow-up, on renewed therapy or with addition
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of steroid
References 1. Chang JC, Cohen RD. Medical m anagem ent of severe ulcerative colitis. Gastroenterol Clin North Am . 2004;33(2):235–250, viii. 2. Lim WC, Hanauer SB. Controversies with am inosalicylates in inflam m atory bowel disease. Rev Gastroenterol Disord. 2004;4(3):104–117. 3. Sanborn WJ. New concepts in anti-tum or necrosis factor therapy for inflam m atory bowel disease. Rev Gastroenterol Disord. 2005;5(1):10–18. 4. Sanborn WJ. Serologic m arkers in inflam m atory bowel disease. Rev Gastroenterol Disord. 2004;4(4):167–174.
Codes ICD9-CM 555.9 556.9
ICD10 K50.9 K51.9
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Influenz a
Influenza
Philip Shayne
Basics Description
Acute, usually self-lim ited, viral infection
Transm ission: by dispersion in sm all-particle aerosols created by sneezing, cough, and talking
Virus deposited on respiratory tract epithelium and absorbed
Incubation period: 1–2 days
Duration: 3 days: o
Severity of sym ptom s in proportion to height of the fever
Outbreaks usually occur during winter m onths.
Com plications: o
Prim ary influenza viral pneum onia
o
Secondary bacterial pneum onia
o
Exacerbations of chronic obstructive pulm onary disease (COPD)
o
Rare com plications: m yositis, m yocarditis, pericarditis, and aseptic m eningitis
Key features: o
Epidem ic nature of the disease
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o
Mortality results largely from pulm onary com plications.
Pediatric Considerations
Children exhibit m ore lower-respiratory involvem ent (croup, bronchitis, bronchiolitis, pneum onitis) and higher tem peratures than adults.
Myalgias in the calf m uscle
Febrile convulsions occur in approxim ately 10% of children younger than 5 years of age with influenza infection.
Reye syndrom e: o
Influenza m ay be predisposing factor.
o
Rare and severe com plication
o
Characterized by fatty degeneration of the liver and cerebral edem a
o
o
Sym ptom s:
Nausea
Vom iting
Stupor
Strong correlation with salicylates: Avoid aspirin products in children with influenza.
Etiology
Most caused by three genera of the Orthom yxoviridae fam ily: influenza virus types A, B, and C
Epidem ics: o
Every 1–3 years
o
Caused by antigenic drift—new variants from m inor changes in surface protein
o
Most cases occur in 2–3 weeks.
o
Duration of the epidem ic 65 years
o
Residents of nursing hom es and long-term care facilities
o
Children age 6–23 m onths
o
Children 6 m onths to 18 years old on chronic aspirin therapy
o
High-risk individuals (COPD, cardiovascular disease, im m unocom prom ised, diabetics)
o
Health care workers
o
Caretakers of children 65 years old, decrease am antadine dosage to 100 m g/d
Oseltam ivir: 75 m g PO b.i.d. for 3–4 days
Rim antadine: 200 m g PO initially, then 100 m g PO b.i.d. for 3–5 days
Zanam ivir: 10 m g nasal insufflation b.i.d. for 3–5 days
Follow-Up Disposition Admission Criteria
Hypoxia (pneum onia)
Severe dehydration
Alteration in m ental status
Discharge Criteria Most patients will have a short, self-lim ited course provided they are able to tolerate fluids and antipyretics.
References
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1. Antiviral drugs for prophylaxis and treatm ent of influenza. Med Lett. 2004;46(1194):85–86. 2. Arruda E, Hayden FG. Update on therapy of influenza and rhinovirus infections. Adv Exp Med Biol. 1996;394:174–187. 3. Call SA, Vollenweider MA, et al. Does this patient have influenza? JAMA. 2005;293:987–997. 4. CDC. Notice to readers: considerations for distinguishing influenza-like illness from inhalational anthrax. MMWR Morb Mortal Wkly Rep. 2001;50(44):984–986. 5. Flem ing DM. Managing influenza: am antadine, rim antadine and beyond. Int J Clin Pract. 2001;55(3):189–195. 6. Influenza vaccine 2004–2005. Med Lett. 2004;46(1193):83–84. 7. Mossad SB. Prophylactic and sym ptom atic treatm ent of influenza. Current and developing options. Postgrad Med. 2001;109(1):97–105.
Miscellaneous SEE ALSO: Anthrax
Codes ICD9-CM 487
ICD10 J11.1
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Intracerebral Hem o rrhage
Intracerebral
Hemorrhage Atul Gupta Rebecca Smith-Coggins
Basics Description Hem orrhage into brain parenchym a:
Com pression of brain tissues
Secondary injury results from cerebral edem a, increased intracranial pressure, and the possibility of brain herniation.
Etiology Intracerebral hem orrhage can occur spontaneously or from traum a:
Uncontrolled or acute hypertension (m ost com m on)
Vascular m alform ations: o
Arteriovenous m alform ation
o
Venous angiom as
o
Ruptured cerebral aneurysm s
Neoplasm (particularly m elanom a and gliom a)
Anticoagulant therapy (Coum adin, heparin)
Throm bolytic agents
Illicit drugs (cocaine, am phetam ines)
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Bleeding disorders (hem ophilia)
Cerebral am yloid angiopathy
Traum atic hem orrhage secondary to blunt or penetrating injury
Diagnosis Signs and Symptoms History
Severe headache, typically sudden in onset
Hypertension
Seizures
Evidence of head injury
Meningism us
Vom iting
Altered level of consciousness (m ay be com atose): o
Altered m ental status m ay occur as late as 24–48 hours after head injury.
Physical Exam Variable neurologic deficits depending on site of intracerebral hem orrhage:
Putam en hem orrhage (35%): contralateral hem iparesis and hem isensory loss, with occasional dysphagia or neglect
Lobar hem orrhage (30%): variable signs depending on involved area
Cerebellar hem orrhage (15%): vom iting, ataxia, and nystagm us
Thalam ic hem orrhage (10%): sim ilar to putam en, but m ay also have eye m ovem ent abnorm alities
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Caudate hem orrhage (5%): confusion, m em ory loss, hem iparesis, gaze paresis
Pontine hem orrhage (5%): quadriplegia, pinpoint pupils, ataxia, sensorim otor loss
Essential Workup Im m ediate noncontrast head CT:
Acute hem orrhage appears as high-density lesion.
Tests Lab Check coagulation studies (PT/PTT, INR, platelets).
Imaging
CT as above
New-generation MRI m ay be useful but currently not as available or rapid as CT.
Differential Diagnosis
Seizure
CNS infection
CNS m ass
Electrolyte or acid-base abnorm ality
Intoxication/Wernicke encephalitis
Migraine headache
Transient ischem ic attack (TIA):
o
Todd paralysis
o
Air em bolism
Differential diagnosis once bleed is seen on CT: o
Spontaneous hem orrhage (hypertensive, arteriovenous m alform ation [AVM], neoplasm , etc.)
o
Traum atic hem orrhage
o
Subarachnoid hem orrhage
o
Subdural hem atom a
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o
Epidural hem atom a
Pediatric Considerations
Additional differential diagnoses include: o
Moyam oya disease
o
Acute infantile hem iplegia
P.601
Treatment Pre Hospital
C-spine precautions if head or neck injury is suspected
Elevation of head with C-spine control
Initial prehospital responder m ust ascertain neurologic defect to be able to note progression of sym ptom s.
Initial Stabilization
Manage airway and resuscitate as needed: o
Patients with depressed level of consciousness should be intubated im m ediately for controlled ventilation.
Early neurosurgical consultation
ED Treatment Blood pressure (BP) m anagem ent:
Must use caution in blood pressure control because acute lowering of BP to norm al in setting of increased intracranial pressure (ICP) could reduce cerebral perfusion to ischem ic levels
Use nitroprusside, esm olol, or labetalol to slowly lower diastolic blood pressure initially by 10%.
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Norm otensive levels should be achieved over 12–24 hours.
May use hydralazine as an alternative
Treatm ent of elevated intracranial pressure
Controlled ventilation to PaCO 2 of 35 torr
Fluid restriction; elevate head of bed 30°
Mannitol—osm otic diuresis
Use furosem ide as an alternative.
Correct coagulopathies if present.
Consider anticonvulsants: phenytoin.
Medication (Drugs)
Esm olol: 0.5–1 m g/kg initial bolus IV, followed by 50–150 µg/kg/m in infusion
Furosem ide: 20–40 m g (peds: 0.5–1.0 m g/kg per dose) IV; m ay repeat as necessary
Hydralazine: 10–40 m g (peds: 0.1–0.2 m g/kg per dose) IV; m ay repeat as necessary
Labetalol: 20 m g (peds: 0.3–1.0 m g/kg per dose) IV; m ay give additional 40–80 m g IV q10m in to m ax. 300 mg
Mannitol: 1 g/kg IV
Nitroprusside: 0.5 µg/kg/m in IV initially and titrate to effect
Phenytoin: 15–20 m g/kg per dose (peds: 0.5–1.0 m g/kg/m in) at rate of 40–50 m g/h
Follow-Up
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Disposition Admission Criteria
To OR if surgical intervention is indicated
To ICU if intubated; altered level of consciousness; or on IV infusion for blood pressure control
Adm it to neurologic observation unit if norm al neurologic exam without evidence of progression of bleed, and hem odynam ically stable
Discharge Criteria All patients with intracerebral hem orrhage should be adm itted.
References 1. Broderick JP, Adam s HP Jr, Barsan W. Guidelines for the m anagem ent of spontaneous intracerebral hem orrhage: a statem ent for healthcare professionals from a special writing group of the stroke council, Am erican Heart Association. Stroke. 1999;30:905–915. 2. Diringer MH. Intracerebral hem orrhage: pathophysiology and m anagem ent. Crit Care Med. 1993;21:1591–1603. 3. Heiskanen O. Treatm ent of spontaneous intracerebral and intracerebellar hem orrhages. Stroke. 1993;24(12 suppl):I94–95. 4. MacKenzie JM. Intracerebral hem orrhage. J Clin Pathol. 1996;49(5):360–364. 5. Ojem ann RG, Heros RC. Spontaneous brain hem orrhage. Stroke. 1983;14:468–475. 6. Panagos PD. Intracerebral hem orrhage. Em erg Med Clin North Am . 2002;20:631–655.
Codes ICD9-CM 431
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Intussusceptio n
Intussusception
Roger Barkin
Basics Description
The proxim al bowel invaginates into the distal bowel, producing infarction and gangrene of the inner bowel: o
Greater than 80% involve the ileocecal region.
Often occurs with a pathologic lead point in children >2 years: o
Hypertrophied lym phoid patches m ay be present in infants.
o
Children >2 years, one third of patients have pathologic lead point.
o
Children >6 years, lym phom a is the m ost com m on lead point.
o
Adults usually have a pathologic lead point.
The m ost com m on cause of intestinal obstruction within the first 2 years of life
Epidem iology in the United States: o
Most frequently between 5 and 9 m onths of age
o
The incidence is 2.4 cases per 1,000 live births.
o
Male > fem ale predom inance of 2:1
o
Mortality is Table o f C o ntents > Iritis
Iritis
Jessica Freedman
Basics Description
Inflam m ation of anterior uveal tract
Iritis and anterior uveitis are synonym ous.
Uveitis secondary to traum a is also called traum atic iritis.
Etiology
Most cases are idiopathic, but m ay be traum atic or associated with num erous infectious and noninfectious system ic diseases.
May be acute or chronic
Noninfectious system ic diseases include the following: o
Ankylosing spondylitis
o
Reiter syndrom e
o
Sarcoidosis
o
Behçet disease
o
Inflam m atory bowel disease
o
Juvenile rheum atoid arthritis
o
Kawasaki syndrom e
o
Interstitial nephritis
o
IgA nephropathy
o
Drug reactions
Pa ge 2 6 8
o
Sjögren syndrom e
o
Psoriatic arthritis
Infectious conditions include the following: o
o
o
Viral:
Rubella
Measles
Adenovirus
Herpes sim plex virus
Herpes zoster virus
HIV
Mum ps
Varicella
Cytom egalovirus
West Nile virus
Bacterial:
Tuberculosis
Syphilis
Pertussis
Brucellosis
Lym e disease
Chlam ydia
Rickettsia
Gonorrhea
Leprosy
Fungal
Malignancies include the following: o
Leukem ia
o
Lym phom a
o
Multiple sclerosis
o
Malignant m elanom a
Other causes include the following: o
Cocaine use
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o
Exposure to pesticides
o
Corneal foreign body
o
Blunt traum a
Diagnosis Signs and Symptoms
Acute presentation: o
Ocular pain, red eye
o
Photophobia (consensual)
o
Lacrim ation
o
Decreased visual acuity (usually m ild)
o
Cells and flare in anterior cham ber; hypopyon
o
Posterior synechiae (adhesions of iris to lens)
o
Miosis
o
Low intraocular pressure (occasionally m ay be high)
o
Injection of perilim bal vessels (ciliary flush)
Chronic presentation: o
Recurrent episodes
o
Few or no acute sym ptom s
Essential Workup
History and review of system s: o
Up to 50% m ay be associated with system ic disease.
Slit-lam p exam : o
Inflam m atory cells (leukocytes) or “flare― in the anterior cham ber are diagnostic.
o
Flare is a hom ogeneous fog secondary to protein leakage into aqueous hum or.
o
Use short, wide beam to best appreciate cells and flare.
Pa ge 2 6 9
o
Cellular deposits with m ore severe inflam m ation
Intraocular pressure
If topical anesthesia relieves pain, probably not iritis
Tests
None usually indicated
Tailored outpatient workup if history, signs, and sym ptom s point strongly to a certain cause (with referral to ophthalm ology, rheum atology, or internal m edicine)
Lab
Tuberculosis: o
Sarcoidosis: o
o
Erythrocyte sedim entation rate
o
HLA-B27
Inflam m atory bowel disease:
o
HLA-B27
o
Cultures of conjunctiva and urethra
Psoriatic arthritis:
HLA-B27
Lym e disease: o
HLA-B27
Reiter syndrom e:
o
PPD
Ankylosing spondylitis:
o
Purified protein derivative (PPD)
Im m unoassays
Juvenile rheum atoid arthritis: o
Antinuclear antibody
o
Rheum atoid factor
Sarcoidosis: o
Angiotensin-converting enzym e
o
Serum lysozym e level
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Sexually transm itted disease: o
Rapid plasm a reagin or VDRL test
o
Fluorescent treponem al antibody absorption (FTA-ABS) test
o
Appropriate cultures
Imaging
Ankylosing spondylitis: o
Sarcoidosis: o
Sacroiliac spine radiograph
Chest radiograph
Tuberculosis: o
Chest radiograph
Differential Diagnosis
Conjunctivitis
Keratitis
Acute angle-closure glaucom a
Episcleritis
Corneal abrasion
Corneal foreign body
Intraocular foreign body
Posterior segm ent tum or
P.605
Treatment Initial Stabilization
Goal: o
Reduce inflam m ation and prevent com plications
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Cycloplegic agent (short-acting): o
Decreases pain, photophobia
o
Prevents developm ent of posterior synechiae
ED Treatment
Cycloplegia
Topical steroids if indicated: o
Use with caution, in consultation with ophthalm ologist.
o
May cause significant com plications (i.e., progression of herpes sim plex virus keratitis)
Treat secondary glaucom a.
Supportive m easures:
o
Warm com presses
o
Dark glasses
o
Analgesia
Identification of cause: o
Ankylosing spondylitis: o
System ic anti-inflam m atory agents
o
Physical therapy
Inflam m atory bowel disease: o
System ic steroids
o
Sulfadiazine
o
Vitam in A
Reiter syndrom e: o
Treat urethritis (and sexual contacts).
Behçet disease: o
Initiate appropriate m anagem ent.
System ic steroids or im m unosuppressive agents
Infectious causes: o
Appropriate m anagem ent of underlying infection
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Medication (Drugs)
Cycloplegic: o
Cyclopentolate 1–2% for m ild to m oderate inflam m ation: 1 drop t.i.d. for (lasts up to 24 hours)
o
Hom atropine 2 or 5% for m oderate inflam m ation: 1 drop t.i.d. (lasts up to 3 days)
o
Atropine 1% for m oderate to severe inflam m ation: 1 drop t.i.d. (lasts 7–14 days)
Topical steroid: o
Prednisolone acetate 1%: 1 drop q1h–q6h, depending on severity
Analgesic: o
Tylenol or Tylenol with codeine
Pediatric Considerations
Cycloplegics not recom m ended in children younger than 6 years: o
May cause system ic anticholinergic toxicity with blurred vision, flushing, tachycardia, hypotension, and hallucinations
Follow-Up Disposition Admission Criteria Not indicated unless significant system ic illness
Issues for Referral
Iritis: o
Refer to ophthalm ologist within 24 hours for follow-up care and possible steroid therapy.
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Inflam m atory bowel disease: o
Reiter syndrom e: o
Rheum atology consult
Psoriatic arthritis: o
Gastroenterology consult
Rheum atology consult
Juvenile rheum atoid arthritis: o
Rheum atology consult
References 1. Bertolini J, Pelucio M. The red eye. Em erg Med Clin North Am . 1995;13:561–579. 2. Kunim oto D, Kanitkar K, Makar M. The Wills Eye Manual: Office and Em ergency Room Diagnosis and Treatm ent of Eye Diseases. 4th ed. Philadelphia: Lippincott William s & Wilkins; 2004. 3. Leibowitz HM. The red eye. New Engl J Med. 2000;343:345. 4. Weinberg RS. Uveitis. Ophthalm ol Clin North Am . 1999;12:71–79.
Codes ICD9-CM 364.3
ICD10 H20.9
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Iro n Po iso ning
Iron Poisoning
Sean Bryant
Basics Description
Peak concentrations are 2–4 hours postingestion.
Serum concentrations not reliable if obtained m ore than 4–6 hours after ingestion: o
Enteric coated or sustained release—erratic and m ay warrant serial levels
Postabsorption: Iron redistributes into tissues and fall in serum iron occurs as free iron then causes dam age at cellular level.
Injury patterns: o
Corrosive injury to intestinal m ucosa results in profound fluid loss (shock), hem orrhage, and perforations.
o
Liver receives largest load of iron because of portal venous circulation—has highest injury (hem orrhagic periportal necrosis)
Free iron: o
Concentrates in m itochondria, disrupting oxidative phosphorylation; catalyzes lipid peroxidation and free radical form ation, resulting in cell death, and
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increases anaerobic m etabolism and acidosis o
Causes m yocardial depression, venodilation, and cerebral edem a
Hydration of ferric form yields three protons, resulting in acidem ia.
Etiology
Elem ental iron ingestion: o
Nontoxic 40 m g/kg
o
Lethality possible >60 m g/kg
o
Elem ental iron equivalents:
o
Ferrous sulfate—20% (325 m g = 65 m g Fe)
Ferrous gluconate—12%
Ferrous fum arate—33%
Prenatal vitam ins vary from 60–90 m g elem ental iron per tablet.
o
Children's vitam ins m ay contain 5–18 m g elem ental iron per tablet.
Pediatric Considerations
Historically highest m ortality rate am ong pediatric accidental exposures (adult iron products)
Children's chewable iron products have been shown to be safe.
Diagnosis Signs and Symptoms
Classically divided into five stages: o
Stage 1: gastrointestinal (0.5–6 hours):
Abdom inal pain
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o
o
o
o
Vom iting
Diarrhea
Hem atem esis
Hem atochezia
Stage 2: latent/quiescent (6–24 hours):
Resolution of GI sym ptom s
Deceptive phase
Possible hypotension and acidosis
Stage 3: shock and organ failure (6–72 hours):
Hypoperfusion
Metabolic acidosis
Com a
Coagulopathy
Stage 4: hepatic failure (2–3 days):
Coagulopathy
Hypoglycem ia
Jaundice
Elevated liver function tests (LFTs) and bilirubin
Stage 5: obstruction (2–4 weeks):
Gastric outlet and sm all bowel obstruction
Abdom inal pain, vom iting
Patient m ay present in or skip any of the five stages.
If onset of stage 1 does not occur within 6 hours, likely not significant ingestion
Essential Workup Acute iron poisoning is clinical diagnosis, regardless of laboratory results.
Tests Lab
Serum iron levels (µg/dL) o
Peak absorption between 2 and 6 hours
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o
Four hours m ost com m on tim e for peak level
o
Delayed peak with enteric coated/sustained release
Electrolytes, BUN/creatinine, glucose: o
Anion gap m etabolic acidosis
o
Hyperglycem ia early
o
Hypoglycem ia late
Arterial blood gas (ABG): o
Metabolic acidosis
CBC: o
Anem ia with significant hem orrhage
o
Leukocytosis
Liver function
Coagulation profile
Lactate level
Type and screen if hem orrhage
Total iron-binding capacity (TIBC) is not useful.
Imaging Abdom inal radiograph check for:
Tablets (children's chewables rarely visible)
Absence of pill fragm ent interpretation: o
Patient did not ingest iron.
o
Iron was in solution or has already dissolved.
o
Patient ingested pediatric m ultivitam in product.
o
Absence of radiopacities does not rule out significant or lethal ingestion.
Perforation
Differential Diagnosis
Sepsis
Acetam inophen toxicity
Toxic ingestions causing anion gap acidosis: o
Salicylate
Pa ge 2 6 9
o
Cyanide
o
Methanol
o
Ethylene glycol
Mushroom s
Heavy m etals
Theophylline toxicity
GI bleed from other causes (alcoholic liver disease)
P.607
Treatment Initial Stabilization
Airway, breathing, and circulation m anagem ent (ABCs): o
Airway if needed
o
Venous access and fluids for hypotension
o
Cardiac m onitor and pulse oxim etry
Narcan, thiam ine, dextrose (or Accu-Chek) as needed for altered m ental status
ED Treatment Decontamination
Iron is poorly adsorbed to activated charcoal.
Gastric lavage has not been shown to change outcom e.
NaHCO 3 , phospho soda, and oral deferoxam ine are not recom m ended.
If pill fragm ents are visualized or history of significant ingestion: o
Adm inister whole bowel irrigation (WBI) with adm inistration of Go-Lytely (peds: 10–15 m L/kg/h;
Pa ge 2 7 0
adult: 1–2 L/h) while m onitoring progression with kidneys, ureters, and bladder (KUBs) radiograph. o
Caution with GI bleed
Endoscopy or gastrotom y can rem ove bezoar form ation after m assive ingestions (>240 m g/kg).
Chelation with Deferoxamine (DFO)
DFO is highly specific chelator of parenteral iron.
IV infusion results in m ore constant DFO levels and is route of choice: o
Must be given as soon as possible ( Table o f C o ntents > Irritable Infant
Irritable Infant
Stacey A. Suecoff David H. Rubin
Basics Description
Most children have som e period of the day when they are m ost irritable, usually toward the evening: o
Norm al infant crying ranges from 1–4 hours by 6 weeks of age.
Irritability based on a com parison with the child's norm al pattern
Colic is the m ost com m on cause of inconsolable crying in infants, occurring in as m any as 25% of healthy children: o
Episodes of scream ing accom panied by drawing up knees and passage of flatus
o
Usually begins at 2–3 weeks and m ay continue through 12 weeks
o
Diagnosis of exclusion
Etiology
Infection/inflam m ation: o
Minor acute infections (upper respiratory infection, otitis m edia, thrush, gingivostom atitis)
o
Urinary tract infection
Pa ge 2 7 1
o
Meningitis
o
Osteom yelitis
o
Pneum onia
o
Gastroenteritis
o
Gastroesophageal reflux, esophagitis
Colic
Teething
Constipation
Parental anxiety
Traum a: o
Foreign body, fracture, tourniquet (hair around digit or penis)
o
Hem atom a—subdural, epidural
o
Corneal abrasion
o
Child abuse
o
Diaper pin
o
Splinter
o
Anal fissure
Sickle cell crisis
Incarcerated hernia, testicular torsion
Intussusception
Medications: o
Diphtheria, pertussis, and tetanus (DPT) vaccine reaction
o
New prescription
o
Hom e rem edy
o
Vitam in use/overdose
Deficiency: o
Malnutrition
o
Iron deficiency/anem ia
Hypoxia—cardiopulm onary disorder: o
Supraventricular tachycardia
Pa ge 2 7 1
o
Endocrine/m etabolic: o
Congestive heart failure
Hypoglycem ia
Vascular
Diagnosis Signs and Symptoms History Obtain com plete history (including neonatal history) and inform ation regarding routine feeding, crying.
Physical Exam
Assess vital signs including rectal tem perature and pulse oxim etry.
Measure and plot for percentiles: height, weight, and head circum ference.
Perform a thorough physical exam with infant com pletely undressed.
Tests Lab
CBC, urinalysis, chem istries, and cultures as indicated by history and physical exam ination
Stat blood glucose at bedside if indicated.
Imaging
Fluorescein eye exam
Chest radiograph to exclude cardiopulm onary disease
ECG
CT scan of the head
Contrast radiograph studies such as barium enem a for
Pa ge 2 7 1
specific indications
Diagnostic Procedures/Surgery
Skeletal survey
Stool hem occult test
Differential Diagnosis See Etiology above. P.611
Treatment Initial Stabilization
Manage underlying conditions; stabilize airway, breathing, and circulation (ABCs).
Im m ediate rem oval of hair tourniquets, splinters, and so on.
ED Treatment
Initial evaluation of the child focusing on parent–child interaction and then on potential underlying conditions
Colic responds to soothing, rhythm ic activities, avoiding stim ulants (coffee, cola), m inim izing daytim e sleep: o
Soy or hydrolyzed casein form ula m ay be transiently beneficial.
o
Parents m ust reduce stress:
o
No proven pharm acologic therapy
Support, em pathy, close follow-up
Prolonged observation of the child is usually appropriate.
Pa ge 2 7 1
Medication (Drugs) Dependent on the underlying condition
Follow-Up Disposition Admission Criteria
Life-threatening underlying condition
Significant parental stress secondary to crying infant
Discharge Criteria
No serious condition
Functional and supportive fam ily
Excellent follow-up is essential; parents m ust feel that their observations and concerns are not being ignored; close follow-up and ongoing observation will occur.
References 1. Barnett RM. Psychiatric and behavioral disorders. In: Barkin RM, ed. Pediatric Em ergency Medicine. 2nd ed. St. Louis, MO: Mosby; 1997:1042–1055. 2. Barr RG. Colic and crying syndrom es in infants. Pediatrics. 1998;102(5 suppl E):1282–1286. 3. Chalabi R, Matre WM, Greene MK. Infant with irritability, feeding problem s, and progressive developm ent abnorm alities presenting repeatedly to a pediatric em ergency departm ent. Pediatr Em erg Care . 1997;13(2):123–126. 4. Garrison MM, Christakis DA. A system atic review of treatm ents for infant colic. Pediatrics. 2000;106(1 pt 2):184–190. 5. Hiscock H, Jordan B. 1. Problem crying in infancy. Med J Aust.
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2004;181(9):507–512. 6. Hyam s JS. Functional gastrointestinal disorders. Curr Opin Pediatr. 1999;11(5):375–378. 7. Ruiz-Contreras J, Urquia L, Bastero R. Persistent crying as predom inant m anifestation of sepsis in infants and newborns. Pediatr Em erg Care. 1999;15(2):113–115. 8. Swischuk LE. Irritable infant and left lower extrem ity pain. Pediatr Em erg Care. 1997;13(2):123–126. 9. Trocinski DR, Pearigen PD. The crying infant. Em erg Med Clin North Am . 1998;16:895–910.
Codes ICD9-CM 799.2
ICD10 R68.1
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Irritant G as Expo sure
Irritant Gas
Exposure Sean Bryant
Basics Description
An irritant is any noncorrosive substance that on im m ediate, prolonged, or repeated contact with respiratory m ucosa will induce a local inflam m atory reaction.
Respiratory irritants are inhaled as gases, fum es, particles, or liquid aerosols.
Inhaled irritants: o
Pulm onary toxicity determ ined prim arily by its water solubility
Inhalation accidents frequently involve a m ixture of irritant gases as well as chem ical asphyxiants: o
Carbon m onoxide
o
Hydrogen cyanide
o
Hydrogen sulfide
o
Oxides of nitrogen
Risk Factors Exposure to potential irritants:
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Occupational
Leisure
Intentional
Accidental
Pathophysiology Cellular injury through interaction with respiratory m ucosal water with subsequent form ation of acids, alkalis, and free radicals
Etiology
Settings: o
Industrial: chem ical m anufacturing, m ining, plastics, and petroleum industries
o
Hom e: im proper use or storage of cleaning chem icals
o
Fires: Com bustion yields toxic gases.
Im m ediate onset of upper airway inflam m ation with highly water-soluble irritant gases or with aerodynam ic diam eter >5 µm : o
Am m onia (fertilizers, refrigerants, dyes, plastics, synthetic fibers, cleaning agents):
Im m ediate sym ptom s range from m ild edem a and erythem a to full-thickness burns and airway obstruction.
o
Sulfur dioxide (fum igants used on produce, bleaching, tanning, brewing, wine m aking, com bustion of coal, and sm elting of sulfide-containing ores):
o
Com bines with water, form ing sulfuric acid
Hydrogen chloride (form ed during com bustion of chlorinated hydrocarbons such as polyvinyl chloride):
o
Com bines with water, form ing hydrochloric acid
Chloram ine (generated when am m onia and bleach are m ixed):
When exposed to m oist surfaces, releases
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hydrochlorous acid o
Acrolein (production of plastics, pharm aceuticals, synthetic fibers; form ed during com bustion of petroleum products, cellulose, wood, paper):
May cause protein dam age via free radical production and sulfhydryl binding
o
Form aldehyde (production of plywood, particle board, insulation; com bustion product of gas stoves and heaters):
Com bines with water to form sulfuric acid and form ic acid
o
Hydrogen fluoride (com bustion of fluorinated hydrocarbons):
Depletes calcium stores, resulting in cell death
Latent period of m inutes to hours before onset of sym ptom s with irritant gases of interm ediate water solubility or aerodynam ic diam eter of 1–5 µm : o
Chlorine (product of chlorinated chem icals; bleaching agent):
Upper and lower airway dam age after reacting with water to form hydrochloric and hydrochlorous acids
Delayed onset of sym ptom s up to 24 hours after inhalation with irritant gases of poor water solubility or aerodynam ic diam eter 40 m g/dL, Cr values rise at approxim ately 1 m g Cr/100 m g/dL acetone.
Cr returns to baseline following acetone m etabolism .
CBC: o
Decreased hem atocrit with significant hem orrhagic gastritis
Arterial blood gas (ABG): o
Acidosis rare unless owing to hypoperfusion or coingestant
Urinalysis: o
Ketones present
Serum ketones present
Isopropanol level: o
Com a with level >150 m g/dL
Serum osm olarity: o
Osm olar gap—difference between m easured and calculated osm olarity
o
Calculated osm olarity = 2 Na + BUN/2.8 + glucose/18 + ethanol/4.3.
o
Osm olar gap present if m easured m inus calculated osm olality >10
o
Gap increases by 1 m Osm /kg for each 5.9 m g/dL of isopropanol and 5.5 m g/dL of acetone.
Imaging
Chest radiograph: for aspiration pneum onia with altered m eatal status (AMS) and vom iting
Pa ge 2 7 3
CT head: concom itant head injury occurs.
Differential Diagnosis For CNS depression and elevated osm olar gap includes:
Ethanol
Ethylene glycol
Methanol
Glycerol
Mannitol
Pediatric Considerations Prone to hypoglycem ia following exposure P.617
Treatment Initial Stabilization
Airway, breathing, and circulation m anagem ent (ABCs) o
Maintain airway and assist in ventilation if necessary.
Hypotension: o
Treat initially with 0.9% norm al saline (NS) IV fluid bolus.
o
Initiate dopam ine or norepinephrine infusion if hypotension persists.
o
Packed red blood cells with significant hem orrhagic gastritis
Naloxone, thiam ine, dextrose (or Accu-Chek) if altered m ental status
ED Treatment
Pa ge 2 7 3
Prim arily supportive therapy—no specific antidote
Irrigate skin/eyes for derm al or ocular exposure.
Consider activated charcoal: o
For coingestants
o
Large doses can absorb significant am ounts of isopropanol.
Do not treat with ethanol infusion or 4-m ethylpyrazole.
Hem odialysis: o
Effectively rem oves isopropanol and acetone
o
Most m anaged with supportive care alone
o
Indications:
Hem odynam ic instability despite fluid replacem ent and use of pressors
Levels >400 m g/dL (associated with severe hypotension and prolonged com a)
Medication (Drugs)
Activated charcoal slurry: 1–2 g/kg up to 90 g PO
Dextrose: D 5 0 W 1 am p: 50 m L or 25 g (peds: D 2 5 W 2–4 m L/kg) IV
Dopam ine: 2–20 µg/kg/m in IV
Naloxone (Narcan): 2 m g (peds: 0.1 m g/kg) IV or IM initial dose
Sorbitol: 1–2 g/kg to m ax. 150 g (peds >1 year old: 1–1.5 g/kg as 35% solution to m ax. 50 g) PO m ixed in activated charcoal slurry
Thiam ine (vitam in B 1 ): 100 m g (peds: 50 m g) IV or IM
Follow-Up
Pa ge 2 7 4
Disposition Admission Criteria Moderate to severe isopropanol toxicity (altered m ental status, hypotension)
Discharge Criteria
Observe asym ptom atic patients following ingestion for 2–4 hours before discharge.
Mild intoxication that resolves over 4–6 hours
References 1. Burkhart KK, Kulig K. The other alcohols. Methanol, ethylene glycol, and isopropanol. Em erg Med Clin North Am . 1990;8:913–928. 2. Sharm a AN. Toxic Alcohols. In: Goldfrank LR, Flom enbaum NE, Lewin NA, et al., eds. Goldfrank's Toxicologic Em ergencies. 7th ed. New York: McGraw-Hill; 2002:980–990.
Codes ICD9-CM 980.2
ICD10 T55.2
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Jaundice
Jaundice
Andrew Chang
Basics Description Yellow pigm entation of tissues and body fluids due to elevated serum bilirubin
Etiology
Unconjugated hyperbilirubinem ia: Unconjugated bilirubin is the direct breakdown product of hem e, water insoluble, and m easured as indirect bilirubin: o
Hem olytic:
o
o
Hepatic:
Decreased conjugation of bilirubin
Gilbert syndrom e
Decreased uptake:
Excessive production of unconjugated bilirubin
Physiologic jaundice
Conjugated hyperbilirubinem ia: o
Conjugated bilirubin is water soluble and m easured as direct bilirubin.
o
In conjugated hyperbilirubinem ia, bilirubin is returned to the bloodstream after conjugation in the liver instead of draining into the bile ducts.
Pa ge 2 7 4
o
Hepatocellular dysfunction:
Hepatitis
Cirrhosis
Tum or invasion
Toxic injury
o
Intrahepatic (nonobstructive) cholestasis
o
Extrahepatic (obstructive) cholestasis
Diagnosis Signs and Symptoms History
Cholestasis: o
Pruritus
o
Pale stools
o
Dark urine
Malignancy: o
Anorexia
o
Weight loss
o
Malaise
Abdom inal pain
Physical Exam
Right upper quadrant tenderness: o
Courvoisier's rule:
Painless jaundice and a palpable, nontender gallbladder represent m alignant com m on duct obstruction.
Stigm ata of cirrhosis: o
Abdom inal collateral circulation including caput m edusae, hepatosplenom egaly, or hepatic atrophy
Pa ge 2 7 4
o
Ascites
o
Spider telangiectasis
o
Palm ar erythem a
o
Dupuytren contractures
Palpable gallbladder
Hepatom egaly
Splenom egaly
Abdom inal m ass
Evidence of cachexia
Kayser-Fleischer rings: o
Wilson disease
Essential Workup
History and physical exam ination, together with routine laboratory tests, will suggest the diagnosis in about 80% of patients with jaundice.
Bilirubin level—severity m ay suggest cause of obstruction: o
Malignancy causes highest levels (10–30 m g/dL).
o
Choledocholithiasis rarely exceeds 15 m g/dL.
Tests Lab
Alkaline phosphatase: o
If no bone disease and not pregnant, then elevation suggests im paired biliary tract function.
o
2×: hepatitis and cirrhosis
o
3×: extrahepatic biliary obstruction (i.e., choledocholithiasis) and intrahepatic cholestasis (i.e., drug-induced and biliary cirrhosis)
Am inotransferases—provide evidence of hepatocellular dam age: o
Alanine am inotransferase (ALT, SGPT): prim arily in
Pa ge 2 7 4
the liver o
Aspartate am inotransferase (AST, SGOT): liver, heart, kidney, skeletal m uscle, and brain
GGTP (γ-glutam yl transpeptidase)—throughout hepatobiliary system , pancreas, heart, kidneys, and lungs: o
May be the m ost sensitive indicator of biliary tract disease
5′-Nucleotidase—widespread tissue distribution: o
Confirm s hepatic origin of an elevated alkaline phosphatase level
Album in: decreased with severe liver disease
Prothrom bin tim e: Prolonged level is an im portant prognostic indicator in patients with acute hepatitis.
Imaging
Ultrasound: m ost effective initial im aging technique: o
More than 90% effective in identifying cholelithiasis
o
Ductal dilation is a reliable indicator of extrahepatic obstruction:
A dilated com m on bile duct (CBD) and gallbladder suggest distal obstruction, whereas dilation of the intrahepatic ducts (without CBD dilation) suggests proxim al obstruction.
o
Tum ors of the liver and head of pancreas usually well visualized
o
Distinguishes solid liver tum ors from cystic structures
Plain radiographs: o
May show evidence of hepatic and splenic enlargem ent or biliary calcifications
Hepatic nuclear scan (HIDA): o
Accurate m ethod of diagnosing acute cholecystitis or cystic duct obstruction
o
Tim e consum ing (usually several hours)
Pa ge 2 7 4
CT: o
Superior to ultrasound in detecting pancreatic and intra-abdom inal tum ors
o
Can help differentiate fluid-containing structures
Diagnostic Procedures/Surgery Endoscopic retrograde cholangiopancreatography (ERCP):
Diagnostic: o
Stones seen as filling defects within bile duct lum en.
o
Malignancies seen as strictures
Therapeutic: o
Extraction of com m on bile duct stones and insertion of stents to bypass m alignant obstructions
o
Biopsy under direct vision.
Differential Diagnosis
Prehepatic: o
Hem olysis (sickle cell, other hem oglobinopathies)
o
Ineffective erythropoiesis
o
Drugs
o
Gilbert syndrom e: usually benign inherited form of unconjugated hyperbilirubinem ia
o
Crigler-Najjar syndrom e
o
Prolonged fasting
Hepatocellular: o
Hepatitis (infectious, alcoholic, autoim m une, toxin, drug induced)
o
Cirrhosis
o
Postischem ia
o
Hem ochrom atosis
P.619
Pa ge 2 7 4
Intrahepatic cholestasis: o
Pregnancy
o
Drugs
o
Dubin-Johnson syndrom e
o
Rotor syndrom e
o
Benign recurrent cholestasia
o
Fam ilial syndrom es
o
Sepsis
o
Postoperative jaundice
o
Lym phom a
Extrahepatic obstruction: o
Com m on duct stone
o
Biliary stricture
o
Bacterial cholangitis
o
Sclerosing cholangitis
o
Carcinom a (am pulla, gallbladder, pancreas), cholangiosarcom a
o
Pancreatitis, pancreatic pseudocyst
o
Hem obilia
o
Duodenal diverticula
o
Ascariasis
o
Post–laparoscopic cholecystectom y com plications
o
Congenital biliary atresia
o
Congenital choledochal cyst
Pediatric Considerations
Intrahepatic cholestasis: o
Cardiovascular (congenital heart disease, congestive heart failure, shock, asphyxia)
o
Metabolic or genetic (α l -antitrypsin deficiency, trisom y 18 and 21, cystic fibrosis, Gaucher's disease, Niem ann-Pick disease, glycogen storage disease type IV)
Pa ge 2 7 4
o
Infectious (bacterial sepsis, cytom egalovirus [CMV], enterovirus, herpes sim plex virus [HSV], rubella, syphilis, tuberculosis, varicella, viral hepatitis)
o
Hem atologic (severe isoim m une hem olytic disease)
Treatment Initial Stabilization
Isotonic IV fluid therapy if dehydrated
Toxic-appearing patients: o
Supplem ental oxygen, cardiac m onitoring
o
Nasogastric suction and bladder catheterization
ED Treatment
For bacterial cholangitis/sepsis, obtain blood cultures and adm inister parenteral antibiotics:
o
Am picillin, gentam icin, and m etronidazole or
o
Ticarcillin, or piperacillin, and m etronidazole or
o
Cefoxitin and tobram ycin
Obstructive extrahepatic jaundice: o
Surgical consult
Choledocholithiasis: o
ERCP papillotom y, balloon or basket retrieval, or open surgery
Obstructive intrahepatic or nonobstructive jaundice: o
Medical m anagem ent:
Withdraw causative drug, ethanol
Interferon for chronic hepatitis B and C
Penicillam ine and phlebotom y for Wilson disease and hem ochrom atosis
Corticosteroids for chronic hepatitis of
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autoim m une origin
Pediatric Considerations
Exchange transfusion: o
Em ergent treatm ent of m arkedly elevated bilirubin (>20 m g/dL in full-term infants) and for correction of anem ia caused by isoim m une hem olytic disease
Phototherapy—for neonatal jaundice when bilirubin = 17 m g/dL: o
Measure bilirubin once to twice daily and stop when bilirubin has been reduced by about 4–5 m g/dL
Phenobarbital: in sepsis and drug-induced causes; decreases conjugated bilirubin
Metalloporphyrins: investigational inhibitors of hem e oxygenase
Medication (Drugs)
Am picillin: 2 g IV q6h (peds: 25 m g/kg IV q6h–q8h)
Cefoxitin: 2 g IV q6h (peds: 40–160 m g/kg/d div. q6h–q12h)
Gentam icin: 2–5 m g/kg IV q8h (peds: sam e)
Metronidazole: 1 g IV q12h (peds: 30 m g/kg/d div. q12h)
Piperacillin/TZ: 3 g IV q6h (peds: 300 m g/kg/d div. q6h [>2 m onths of age])
Ticarcillin/CL: 3 g IV q6h (peds: 75–100 m g/kg/d div. q6h)
Tobram ycin: 2–5 m g/kg IV q6h (peds: sam e)
Follow-Up
Pa ge 2 7 4
Disposition Admission Criteria
Bacterial cholangitis
Intractable pain
Intractable em esis
Associated pancreatitis
Elevated prothrom bin tim e
Discharge Criteria
No evidence of infection (evaluate as outpatient)
Tolerating liquids
References 1. Dennery PA, Seidm an DS, Stevenson DK. Neonatal hyperbilirubinem ia. N Engl J Med. 2001;344:581–590. 2. Faust TW, Reddy KR. Postoperative jaundice. Clin Liver Dis. 2004;8:151–166. 3. Frank BB. Clinical evaluation of jaundice: a guideline of the Patient Care Com m ittee of the Am erican Gastroenterological Association. JAMA. 1989;262(21):3031–3034. 4. Gartner LM, Herschel M. Jaundice and breastfeeding. Pediatr Clin North Am . 2001;48:389–399. 5. Roche SP, Kobos R. Jaundice in the adult patient. Am Fam Physician. 2004;69:299–304. 6. Rossi RL, Traverso LW, Pim entel F. Malignant obstructive jaundice. Surg Clin North Am . 1996;76:63–70. 7. Stevenson DK, Wong RJ, DeSandre GH, et al. A prim er on neonatal jaundice. Adv Pediatr. 2004;51:263–288.
Codes ICD9-CM 782.4
Pa ge 2 7 5
ICD10 R17
Pa ge 2 7 5
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Kapo si Sarco m a
Kaposi Sarcoma
Adam Wos
Basics Description
A m esenchym al tum or involving blood and lym phatic vessels
Associated with hum an herpesvirus 8 (HHV-8) also known as Kaposi sarcom a herpesvirus (KSHV)
Lesions are typically found on the skin, m ucous m em branes, GI and respiratory tracts, lym phatic system , and visceral organs.
Tum ors consist of spindle-shaped cells between collagen bundles, neovascular spaces, extravasated erythrocytes, and an infiltrate of lym phocytes.
Staging based on AIDS Clinical Trials Group (ACTG) classification o
Characterizes patients as good or poor based on:
Tum or burden
Im m une function
Presence or absence of system ic illness
Four epidem iologic m anifestations: o
Classic Kaposi sarcom a (KS):
Initially described in 1872 in m ales in
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Mediterranean region and Eastern Europe
Prim arily cutaneous disease, occurring after sixth decade of life, with a typically indolent course
o
Endem ic African KS:
High prevalence up to 12% in sub-Saharan Africa
Clinical pattern ranges from benign cutaneous disease to fulm inant lym phadenopathic disease.
o
Iatrogenic im m unosuppressive KS:
Occurring in organ transplant recipients or patients receiving chronic im m unosuppressive therapy
o
AIDS-related KS:
The m ost com m on HIV-associated m alignancy
Incidence has declined significantly in the United States in the era of highly active antiretroviral therapy (HAART)
Decreased incidence as an AIDS-defining illness
Unpredictable clinical course, even in patients with well-controlled HIV disease
Etiology Mechanism
HHV-8 is found in all KS lesions, yet not all those infected with HHV-8 have KS: o
HHV-8 is felt to be necessary but not sufficient by itself to cause KS.
Host genetic factors likely contribute.
HHV-8 genom e codes for viral cyclins, cytokines, and antiapoptotic factors: o
Thought to disrupt m itosis, interrupt apoptosis, and
Pa ge 2 7 5
increase angiogenesis
Spindle cells thought to originate from peripheral blood hem atopoietic precursors: o
First invade derm is and progress from m acular to plaque to tum or stage
Risk of developing KS increases with degree of im m unosuppression: o
Measured by lower CD4 counts and higher HHV-8 and HIV viral loads
AIDS-KS lesions tend to flare during opportunistic infections.
Survival for patients with HIV-related KS is influenced m ore heavily by the depth of im m unosuppression and the control of the underlying HIV disease than by tum or burden.
Modes of transm ission of HHV-8: o
Sexual contact, especially am ong hom osexual m ales, who have m uch higher risk of KS than other HIV patients
o
Vertical transm ission from m other to child
o
Saliva appears to be m ost frequent form of transm ission in endem ic African form .
o
Blood products
o
Donated transplanted organs
Diagnosis Signs and Symptoms
Cutaneous: o
Lesions m ay arise quickly within a few days.
o
Red, pink, purple, or brown m acular lesions with
Pa ge 2 7 5
occasional yellow halos o
Irregularly shaped, ranging from several m illim eters to few centim eters in size
o
Frequently lesions are sym m etric and arranged along lines of skin tension.
o
Painless and nonpruritic
o
Com m on sites include face, especially adnexal structures of eyes and nose, trunk, and lower extrem ities.
o
Lym phatic obstruction can lead to severe edem a, pain, and ulceration, especially in lower extrem ities, groin, and periorbital areas.
Oral: o
Most com m on site of initial involvem ent
o
Purplish lesions on palate and gingiva
o
Can be easily traum atized from norm al chewing, causing bleeding, ulceration, and secondary infection
Visceral: o
Gastrointestinal:
Com m on, but usually asym ptom atic
Does not typically affect prognosis
Can occur anywhere in GI tract but m ost com m only in stom ach
Lesions begin as m acular and subm ucosal.
Lesions m ay progress to becom e nodular and bulky with central ulceration.
Advanced disease m ay present with pain, obstipation, and bleeding.
o
Respiratory:
Found in about one third of KS patients
Lesions in tracheobronchial tree, pulm onary parenchym a, or pleura
Pa ge 2 7 5
Presents at the lower range of CD4 counts
Eighty-five percent of patients have evidence of cutaneous disease.
Frequently presents concom itantly with opportunistic infections
Sym ptom s: dyspnea, nonproductive cough
Chest pain, fever, and hem optysis are less com m on.
Sym ptom s m ay persist for weeks, then progress rapidly to pulm onary failure.
Lung sounds often clear, but m ay have crackles, wheezes, or signs of pleural effusion
System ic: o
Lym phatic obstruction is m ost com m on cause of m orbidity; can occur in absence of cutaneous involvem ent.
o
Solid organs such as liver, spleen, heart, bone m arrow, and urogenital tract are less com m only affected.
Essential Workup
History should focus on sym ptom s by system , and exam iner should assess degree of im m une com prom ise.
Physical exam ination: o
Careful exam ination of skin, oral m ucosa for lesions
o
Fecal occult blood in patients with suspected GI bleed
o
Lung exam for signs of crackles or dullness to percussion that m ay suggest a pleural effusion
Tests Lab
Punch biopsy of skin lesions with histologic exam ination is the gold standard of diagnosis:
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o
Not usually perform ed in ED
o
Dem onstrates angioproliferation with spindle cells, cleftlike spaces, and extravasation of RBCs
CBC m ay show leukopenia, throm bocytopenia from AIDS, anem ia in setting of GI bleed.
Arterial blood gas (ABG) in setting of respiratory distress m ay dem onstrate hypoxem ia or respiratory alkalosis.
Electrolytes, liver panel, blood cultures, sputum sm ear and culture, lactate dehydrogenase (LDH) in setting of fever and respiratory sym ptom s to rule out other causes
Thoracentesis in setting of pleural effusion typically exudative, or frankly bloody
P.621
Imaging
Chest radiograph: o
Bilateral opacities in a central or perihilar distribution
o
Nodular densities
o
Pleural effusions
o
Intrathoracic adenopathy
Thallium /gallium scan: o
KS lesions are thallium avid and gallium negative.
o
Opposite pattern of opportunistic infections and non-Hodgkin lym phom a
Chest CT can guide biopsy of extrabronchial lesions.
Kidneys, ureters, and bladder (KUB) radiograph or CT of abdom en to look for sm all bowel obstruction if suspected
Diagnostic Procedures/Surgery
Bronchoscopy with lesional biopsy: o
Gold standard for diagnosis of pulm onary KS
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o
Dem onstrates cherry red nodules
GI endoscopy to evaluate source of bleeding or upper GI obstruction
Differential Diagnosis
Cutaneous disease: o
Bacillary angiom atosis (Bartonella species infection of the skin)
o
Purpura
o
Hem atom a
o
Hem angiom a
o
Arteriovenous m alform ation
o
Angiosarcom a
o
Derm atofibrom a
o
Nevi
Gastrointestinal disease: o
Peptic ulcer disease
o
Pancreatitis
o
Hepatobiliary tract disease
o
Carcinoid tum or
o
Stom ach cancer
o
Variceal disease
Pulm onary disease: o
Com m unity acquired pneum onia
o
Active tuberculosis
o
Opportunistic infections such as Pneum ocystis carinii, aspergillosis, Coccidioides
o
Lung carcinom a
o
Non-Hodgkin or Hodgkin lym phom a
Treatment
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Pre Hospital Determ ination of the existence of any advanced directives for patients with advanced AIDS
Initial Stabilization
Protection for health care workers: o
Universal precautions
Adm inister oxygen.
Place on cardiac m onitor and m easure pulse oxim etry.
Establish IV access with 0.9% norm al saline.
Endotracheal intubation and m echanical ventilation if respiratory failure evident
Resuscitation with intravenous crystalloid, blood products as needed if hypotensive from GI bleed
ED Treatment
Care of KS m ust take into account type of KS, extent of tum or, and organs involved.
ED care focused on stabilizing acute m anifestations of disease and appropriate referral for m anagem ent of nonem ergent lesions
Goal of treatm ent for AIDS-KS is palliation of sym ptom s: o
Cosm etically disfiguring lesions
o
Problem atic oral lesions
o
Pain and edem a from lym phadenopathy
Intensification of HAART m edications is first line of treatm ent in AIDS-KS.
Local therapy of cutaneous lesions: o
Cryotherapy
o
Radiation therapy
o
Laser therapy
o
Local excision surgery for troublesom e lesions at carefully selected sites
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o
Topical treatm ent with alitretinoin gel
o
Intralesional chem otherapy with vinblastine or vincristine
System ic therapy: o
Liposom al anthracyclines (pegylated liposom al doxorubicin):
First-line therapy for advanced KS
Higher response rates with fewer adverse events than previous standard of bleom ycin and vincristine
o
Paclitaxel:
High response rate in patients who have failed anthracyclines
o
Interferon alpha:
Indicated for HIV-related KS if CD4 count is >400 and KS in early stages
o
Experim ental:
Thalidom ide
Angiogenesis inhibitors
Anti-HHV-8 therapy with ganciclovir, cidofovir, or foscarnet
Medication (Drugs)
Vinblastine: 0.1–0.5 m g/cm 2 of lesion intralesional, up to 2 m g; repeat once in 3 weeks
Interferon alpha: 30 m illion U/m 2 body area SC three tim es weekly
Pegylated liposom al doxorubicin: 20 m g/m 2 body area IV every 3 weeks
Paclitaxel: 100 m g/m 2 body area IV every 2 weeks
Thalidom ide: 100 m g PO daily for 8 weeks
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Follow-Up Disposition Admission Criteria
Respiratory failure
Unstable GI bleed
Bowel obstruction
Secondary infection of lesion or sepsis
Discharge Criteria Patients with uncom plicated KS lesions m ay be discharged with referral to a hem atologist/oncologist or HIV specialist.
Issues for Referral Uncom plicated m ucocutaneous lesions for local therapy as indicated for palliation
References 1. Belleza WG, Browne B. Pulm onary considerations in the im m unocom prom ised patient. Em erg Med Clin North Am . 2003;21(2):499–531, x–xi. 2. Hengge UR, et al. Update on Kaposi's sarcom a and other HHV8 associated diseases. Part 1: epidem iology, environm ental predispositions, clinical m anifestations, and therapy. Lancet Infect Dis. 2002;2(5):281–292 3. Huang L, Stansell JD. Pulm onary com plications of hum an im m unodeficiency virus infection. In: Murray J, Nadel J, eds. Textbook of Respiratory Medicine. 3rd ed Philadelphia: WB Saunders; 2000:2204–2206. 4. Levine AM, Hancock BW, MacPhail P, et al. The treatm ent of AIDS-related cancer. Lancet Oncol. 2003;4(9):576–581.
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5. Mbulaiteye SM, Parkin DM, Rabkin CS. Epidem iology of AIDS-related m alignancies: an international perspective. Hem atol Oncol Clin North Am . 2003;17(3):673–696. 6. VonRoenn JH. Clinical presentations and standard therapy of AIDS-associated Kaposi's sarcom a. Hem atol Oncol Clin North Am . 2003;17(3):747–762.
Codes ICD9-CM 176.9
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Kaw asaki Disease
Kawasaki Disease
Adam Z. Barkin
Basics Description
Acute inflam m atory process involving m ultiple organs
Vasculitis m ost severe in m edium -sized arteries, including coronary arteries
Stages: o
Acute (lasts 1–2 weeks):
Fever, oral m ucosal erythem a, conjunctival injection, erythem a and edem a of hands and feet, cervical adenopathy, aseptic m eningitis, hepatic dysfunction, diarrhea
Myocarditis, pericardial effusion, no aneurysm s by echocardiography
o
Subacute (when fever, rash, and lym phadenopathy resolve until about 4 weeks):
Anorexia, irritability, desquam ation of hands and feet, throm bocytosis
Coronary artery aneurysm s visible on echocardiography
o
Risk for sudden death is highest.
Convalescent phase (about 6–8 weeks):
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Clinical signs are absent.
Erythrocyte sedim entation rate (ESR) norm alizes.
Epidem iology: o
Eighty percent of cases occur in children 38.5°C (often spiking) for at least 5 days: o
Begins abruptly and m ay last >2 weeks
Cardiac: o
Shortness of breath
o
Chest pain
HEENT: o
Eyes:
Conjunctivitis
Photophobia
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o
Mouth:
Erythem a, dry and fissured lips, strawberry tongue, pharyngeal erythem a
Skin rash
Musculoskeletal: o
Neurologic: o
Arthralgia, arthritis
Extrem e irritability
Gastrointestinal: o
Diarrhea
o
Vom iting
o
Abdom inal pain
Physical Exam
Cardiac: o
Evidence of congestive heart failure
o
Evidence of pericarditis
o
Rub
o
Myocarditis
o
Evidence of valvular disease
o
Murm ur
HEENT: o
Eyes:
Bilateral conjunctival injection without exudates
Bulbar conjunctiva is m ore frequently involved than palpebral conjunctiva.
Usually within 2 days of onset of fever and lasting 1–2 weeks
o
Photophobia, uveitis, iritis
Mouth:
Erythem a, dry and fissured lips, strawberry tongue, pharyngeal erythem a
o
Lym ph:
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Cervical lym phadenopathy (node diam eter >1.5 cm )
Neurologic: o
Irritability
o
Meningism us
Skin: o
Rash, prim arily on the trunk
o
May be m aculopapular, scarlatiniform , or erythem a m ultiform e–like; erythroderm a
o
Changes in the hands or feet—erythem a, edem a (acute phase); unwilling to bear weight
o
Desquam ation (subacute phase) of the tips of fingers and toes 2–3 weeks after onset of illness
Genitourinary: o
Urethritis
o
Meatitis
Gastrointestinal: o
Hydrops of the gallbladder
Essential Workup
Diagnostic criteria: o
Fever for 5 days plus four of the five following criteria:
o
Bilateral conjunctival injection
o
Changes in oral m ucosa
o
Polym orphous erythem atous rash
o
Changes in hands or feet—edem a, erythem a, desquam ation
o
Cervical lym phadenopathy >1.5 cm
Atypical cases can be seen without m eeting diagnostic criteria.
Experienced clinicians can m ake the diagnosis before 5 days of fever.
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P.623
Tests Lab
CBC: o
WBC—norm ally elevated with shift to left in acute phase
o
Norm ocytic anem ia
o
Throm bocytopenia if m yocardial infarction or severe coronary disease
o
Throm bocytosis usually in second to third week
Urinalysis: o
Sterile pyuria
o
Proteinuria
Erythrocyte sedim entation rate (ESR) elevated from first week until 4–6 weeks
Increased C-reactive protein
Cerebrospinal fluid (CSF) pleocytosis
Cultures: negative blood, urine, CSF, throat
Increased transam inases and bilirubin
Imaging
Echocardiogram : o
Acute phase (baseline)
o
2–3 weeks
o
6–8 weeks
Chest radiograph
Diagnostic Procedures/Surgery
ECG if concern about m yocardial infarction or pericarditis
Slit-lam p exam —uveitis
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Differential Diagnosis
Viral infections: o
Adenovirus
o
Enterovirus
o
Measles
o
Epstein-Barr virus
o
Rubella
o
Rubeola
Bacterial infection: o
Scarlet fever (responds rapidly to penicillin)
o
Staphylococcal scalded skin syndrom e
o
Rickettsial disease, including Rocky Mountain spotted fever and leptospirosis
Drug reaction: o
Stevens-Johnson syndrom e
o
Erythem a m ultiform e
Treatment Pre Hospital
Airway, breathing, and circulation m anagem ent (ABCs)
Oxygen
Initial Stabilization ABCs with focus on cardiovascular system
ED Treatment
Initiate intravenous gam m aglobulin (IVIG) and aspirin therapy: o
Do not generally need to m onitor salicylate levels because decreased absorption and increased
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clearance
Treatm ent within the first 10 days of illness reduces cardiac sequelae from range of 20–25% to range of 2–4%
Cardiology consultation
Treatm ent of m yocardial infarctions as in adults
Corticosteroids are controversial.
Medication (Drugs)
IVIG: 2 g/kg IV over 10–12 hours; retreatm ent m ay be required for persistent (>48–72 hours) or recrudescent fever
Aspirin: 80–100 m g/kg/d PO q6h until about day 14 when fever has resolved; then 3–5 m g/kg/d PO daily for 6–8 weeks
Follow-Up Disposition Admission Criteria
Adm it all patients who fulfill diagnostic criteria for Kawasaki disease.
Adm it toxic-appearing patients who do not yet m eet the criteria for Kawasaki disease.
Discharge Criteria
Nontoxic children who do not fulfill diagnostic criteria
Close follow-up is required.
Issues for Referral
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Cardiology consultation for all patients
References 1. Burns JC. Kawasaki disease. Adv Pediatr. 2001;48:157–177. 2. Muta H, Ishii M, Egam i K, et al. Early intravenous gam m a-globulin treatm ent for Kawasaki disease: the nationwide surveys in Japan. Pediatrics. 2004;114:751–754. 3. Newburger JN, Takahashi M, Gerber MA, et al. Diagnosis, treatm ent, and long-term m anagem ent of Kawasaki disease: a statem ent for health professionals from the Com m ittee on Rheum atic Fever, Endocarditis, and Kawasaki Disease, Council on Cardiovascular Disease in the Young, Am erican Heart Association. Pediatrics. 2004;114:1708–1733. 4. Yam am oto LG. Kawasaki disease. Pediatr Em erg Care. 2003;19:422–424.
Codes ICD9-CM 446.1
ICD10 M30.3
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Knee Dislo catio n
Knee Dislocation
Kelly Anne Foley
Basics Description
Defined by the position of the tibia in relation to the distal fem ur: o
Anterior dislocation:
Most com m on dislocation, accounts for 60%
Hyperextension of the knee
Rupture of the posterior capsule at 30°
Rupture of the posterior cruciate ligam ent (PCL) and popliteal artery (PA) occurs at 50°
o
Posterior dislocation
o
Direct blow to the anterior tibia with the knee flexed at 90°, “dashboard injury―
Anterior cruciate ligam ent (ACL) is usually spared.
o
Medial dislocation:
Varus stress causing tear to the ACL, PCL, and lateral collateral ligam ent (LCL)
o
Lateral dislocation:
Valgus stress causing tear to the ACL, PCL and m edial collateral ligam ent (LCL)
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Associated injuries: o
Popliteal artery (PA) injury
PA occurs in 35% of dislocations.
Failure to revascularize within 6–8 hours: Am putation rate approaches 90%.
Anterior dislocations place traction on PA and cause contusion or intim al injury, which m ay result in delayed throm bosis.
Posterior dislocations cause direct intim al fracture and transection of the artery with im m ediate throm bosis.
o
Peroneal nerve injury:
Less com m on than PA injury
If present, m ust rule out concom itant arterial insult
Hypesthesia of first web space, inability to dorsiflex foot
Poor prognosis for recovery
Medial dislocation causes injury by traction of the nerve.
Rotary injuries have a high incidence of traction and transection.
Etiology High-energy injuries such as m otor vehicle crashes, auto–pedestrian accidents, and athletic injuries (football m ost com m on)
Diagnosis Signs and Symptoms
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Grossly deform ed knee
Grossly unstable knee in AP plane or on varus/valgus stress
Lack of distal pulse: o
Popliteal artery injury is prim ary concern.
Signs of distal ischem ia: o
Pallor, paresthesias, pain, paralysis
Essential Workup
History of m echanism of injury
Com plete and careful physical exam : o
Pulses—palpation, Doppler, ankle-brachial index (ABI), and cap refill
o
Neurologic—sensation to first web space and great toe, m ovem ent of toes, dorsiflexion of foot
AP and lateral knee radiographs
Docum ented repeat exam if any closed reduction is attem pted
Tests Imaging
AP/lateral radiograph of knee
MRI within 1 week of injury to define ligam entous injury
P.625
Diagnostic Procedures/Surgery
ABI—likelihood of significant arterial injury requiring surgery low if ≥0.9
Peripheral vascular ultrasonography
Arteriogram should be considered: o
High suspicion of PA injury
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o
Poor pulses or distal perfusion after reduction
o
Peroneal nerve injury
o
Ischem ic sym ptom s despite norm al pulses
Differential Diagnosis
Tibial plateau fracture
Supracondylar fem oral fracture
Ligam entous/tendonous avulsion fracture
Treatment Pre Hospital
Airway, breathing, and circulation m anagem ent (ABCs)
Docum entation of pulses and m otor response essential
Splint knee in slight flexion to prevent PA traction or com pression.
Initial Stabilization
ABCs especially when m otor vehicle crash or auto–pedestrian accident
Fluid resuscitation, hypotension m ay alter distal pulses and perfusion.
Closed reduction im m ediately for any lim b ischem ia
Early surgical consult in an open injury or high suspicion or arterial injury
ED Treatment
Closed reduction by longitudinal traction and lifting fem ur into norm al alignm ent without placing pressure on popliteal fossa
Posterior leg splint/knee im m obilizer with knee in 15–20° flexion
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Repeat neurovascular exam after m anipulation and frequent intervals.
IV analgesia for patient com fort
Surgical consult: open injury, PA injury, or unable to reduce
Follow-Up Disposition Admission Criteria All patients require adm ission for observation of lim b perfusion and PA repair if necessary.
Discharge Criteria All patients should be adm itted.
Issues for Referral Eventual repair of ligam entous injuries:
Usually at 3 weeks
Arthroscopic surgery contraindicated for 2 weeks after injury to prevent com partm ent syndrom e
References 1. Browner, ed. Skeletal Traum a: Basic Science, Managem ent, and Reconstruction. 3rd ed.: Elsevier; 2003:Chapter 55. 2. Green JR, Cam bize S, Owens BD, et al. Knee dislocation. Em ed J [serial online]. 2005. Available at http://www.em edicine.com /orthoped/topic409.htm . 3. Mills JW. The value of ankle-brachial index for diagnosing arterial injury after knee dislocation: a prospective study. J Traum a. 2004;56(6):1261–1265. 4. Miranda, FE. Confirm ation of the safety and accuracy of physical
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exam in the evaluation of knee dislocation for injury of the popliteal artery: a prospective study. J Traum a. 2002;52(2):247251.
Codes ICD9-CM 836.50
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Labo r
Labor
James Walker
Basics Labor denotes the sequence of physiologic occurences that result in a fetus being transported from the uterus through the birth canal.
Description
Labor brings about changes in cervix to allow passage of fetus through birth canal
Synchronous, coordinated contractions of uterus
Contractions progress in m agnitude, duration, and frequency to produce dilation of cervix and ultim ate delivery.
Labor is divided into three stages: o
Stage 1: From onset of uterine contractions to full dilation of cervix
o
Stage 1 is further divided into latent and active phases:
In latent phase; uterine contraction with little change in cervical dilation or effacem ent; contractions are m ild, short (45 seconds). o
Stage 2: From onset of com plete cervical dilation to tim e of delivery of infant
o
Stage 3: From tim e of delivery of baby to tim e of placental delivery
Total duration of labor varies with each wom an.
Generally, lengths of first and second stages of labor are significantly longer for nulliparous wom an: o
Nulliparous: Mean length for first stage of labor is 14.4 hours and 1.0 hours for second stage of labor.
o
Parous: Mean length of first stage of labor is 7.7 hours and 0.2 hours for second stage of labor.
Length of second stage of labor is greatly influenced by “three Ps―:
o
Passenger (infant size and presentation)
o
Passageway (size of bony pelvis and soft tissues)
o
Powers (uterine contractions)
Problem s with any of these three Ps can cause abnorm al progression of labor: o
Fetal m alposition, uterine dysfunction, cephalopelvic disproportion
False labor (Braxton-Hicks contractions): o
Irregular, nonsynchronous contractions of uterus several weeks to days before onset of true labor, and does not cause cervical dilation
Etiology
Prem ature labor occurs in 8–10% of pregnancies.
About 30–40% of prem ature labor is caused by uterine, cervical, or urinary tract infections.
Prem ature rupture of m em branes is defined as rupture of am niotic/chorionic m em branes at least 2 hours before
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onset of labor in patient before 37 weeks’ gestation. o
This occurs in only 3% of pregnancies, but accounts for 30–40% of all prem ature births.
Diagnosis Signs and Symptoms
Sym ptom s of labor: o
Interm ittent low abdom inal pain with or without low back pain
o
Occurring regularly at least every 5 m inutes
o
Lasting 30–60 seconds
Preterm labor is of sufficient frequency and intensity to bring about changes in dilation or effacem ent of cervix before 37 weeks.
Labor is not associated with vaginal bleeding: o
Patients with third-trim ester abdom inal pain or vaginal bleeding should raise suspicion of placenta previa or placental abruption.
Sudden release of clear fluid from vagina or feeling of constant perineal wetness can represent rupture of m em branes: o
This is not always associated with labor, but often leads to onset of labor.
Essential Workup
All patients presenting in possible labor should have im m ediate sterile pelvic exam to assess dilation, effacem ent of cervix, and possibility of im m inent delivery.
Bim anual pelvic exam should not be done in third-trim ester patient with vaginal bleeding until
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ultrasound can be done to assess for placenta previa or placental abruption.
Patients with suspected rupture of m em branes should have sterile speculum exam with visual exam ination of cervix and collection of fluid from vaginal area.
Suggestive of rupture of m em branes: o
Presence of ferning when fluid is allowed to dry on a slide
o
Presence of pooling of fluid in vagina
o
Change of color of litm us paper from yellow to blue
Patients with preterm labor and with cervical changes should have urinalysis with culture and cervical cultures.
Fetal m onitoring should be initiated.
Tests Lab
If patient is in labor, CBC, type, and screen should be sent.
Urinalysis for proteinuria
In patients with no prenatal care, obtain Rh factor and antibody screen.
Cervical cultures and urine culture in patients with preterm labor
Imaging
Not generally needed
Third-trim ester patients with abdom inal pain and vaginal bleeding should have em ergent ultrasound to evaluate for placenta previa or abruption.
Differential Diagnosis
Braxton-Hicks contractions are irregular uterine contractions without associated cervical changes.
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Round uterine ligam ent pain, m usculoskeletal back pain
Other com m on causes of abdom inal pain, such as appendicitis
P.627
Treatment Pre Hospital
Em ergency m edical services (EMS) personnel should place patients in labor on oxygen and in left lateral recum bent position to m axim ize delivery of oxygen to uterus.
Maternal transport of high-risk obstetric patients before delivery results in im proved outcom es instead of transfer of neonate after delivery.
Air transport of high-risk obstetric patients has been shown to be beneficial and cost effective.
Patients in labor who are transported by aircraft should have high-flow oxygen available in the event of cabin decom pression at high altitudes.
Initial Stabilization If delivery is im m inent (presenting part visible), prepare for im m ediate vaginal delivery in ED (see Delivery, Uncom plicated).
ED Treatment
Unless delivery is im m inent, patient should be sent directly to labor and delivery unit.
If transport to labor and delivery will be delayed, or if transfer to another facility is necessary, these steps should be taken:
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o
IV hydration with 1 L of norm al saline or D-5-LR over 30–60 m inutes
o
Maternal m onitoring and, if available, fetal m onitoring
o
If labor needs to be arrested (prem ature fetus), begin tocolytic such as β-agonist terbutaline or MgSO 4 .
Magnesium toxicity is suggested by loss of deep tendon reflexes.
High doses of m agnesium can cause cardiac dysrhythm ias and respiratory depression.
Medication (Drugs)
Magnesium sulfate: 4–6 g IV over 30 m inutes, followed by 2–6 g/h
Terbutaline: 0.25 m g SC; m ay repeat sam e dose in 30 m inutes
Follow-Up Disposition Admission Criteria
All patients in labor who are not at risk for im m inent delivery should be adm itted to labor and delivery departm ent.
Preterm patients in labor dem and im m ediate obstetric consultation and should be adm itted to labor and delivery departm ent for further treatm ent.
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References 1. Gianopoulos JG. Em ergency com plications of labor and delivery. Em erg Med Clin North Am . 1994;12:201–217. 2. Liao JB, Buhim schi CS, Norwitz ER. Norm al labor: m echanism s and duration. Obstet Gynecol Clin North Am . 2005;32:145–164.
Codes ICD9-CM 650.0
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Labyrinthitis
Labyrinthitis
Paul A. Andrulonis Charles V. Pollack
Basics Description
An inflam m ation that decreases afferent firing from the labyrinth
The CNS interprets this decreased signal as head rotation away from the diseased labyrinth.
The resulting im balance in firing from the labyrinth results in spontaneous nystagm us with the fast phase away from the pathologic side.
The three m ost com m on causes of peripheral vertigo are: o
Benign paroxysm al positional vertigo (BPPV)
o
Ménière disease
o
Labyrinthitis
Etiology
Labyrinthitis: o
Serous—viral or bacterial
o
Suppurative—bacterial
o
Chronic
BPPV: o
Dislodgem ent of otoconia debris:
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o
Idiopathic—49%
o
Posttraum atic—18%
o
Sequela of labyrinthitis—15%
o
Sequela of ischem ic insult
Pediatric Considerations
Suppurative and serous labyrinthitis: o
Usually secondary to acute otitis m edia, m astoiditis, or m eningitis
BPPV: o
Onset between 1 and 5 years of age
o
Sym ptom s: abrupt onset of crying, nystagm us, diaphoresis, em esis, ataxia
o
Recurrences for up to 3 years
o
Migraine–BPPV com plex is the m ost com m on etiology of pediatric vertigo.
Ménière disease: o
Rare before 10 years of age
Diagnosis Signs and Symptoms History
Sensation of m ovem ent or spinning
Nausea and vom iting
No auditory com plaints
Physical Exam
Pallor
Diaphoresis
Nystagm us: o
Augm ented by head m ovem ent or rapid head shaking
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o
Acute onset
o
Positional
o
Horizontal, frequently with rotational com ponent
o
Direction is constant.
o
Attenuates with fixation
o
Fatigable
Caloric testing: o
Irrigate external ear canal with cold water for 20 seconds.
o
Norm al response causes horizontal nystagm us with the fast phase away from the irrigated ear.
o
Labyrinthitis produces partial or com plete loss of response.
Dix-Hallpike m aneuver o
Tests for evidence of BPPV.
o
The patient's head is rotated 45°.
o
The patient is then brought from a sitting position to a supine position with the head extending 20° below the exam table.
o
Observe for 5–15 second latent torsional nystagm us directed at the downward ear.
o
Clockwise torsional nystagm us with the left ear down
o
Counterclockwise torsional nystagm us with the right ear down
o
The m aneuver is then repeated with the head turned to the opposite side.
o
Reverse nystagm us m ay occur when patient returns to sitting position.
o
Fatigable with repeat testing
Labyrinthitis: o
No consensus on definition
o
Peripheral vertigo
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o
Single episode of prolonged vertigo lasting days to weeks
o
Peak onset 30–60 years old
o
Recent upper respiratory tract infection in 50% of patients
o
Sym ptom s predom inantly with head m ovem ent but also persist at rest
o
Recovery phase gradual over weeks to m onths
BPPV: o
Positional peripheral vertigo
o
Precipitated by directional specific head m ovem ents (e.g., rolling over in bed, looking up, sham pooing in beauty saloon basin)
o
Recurrent episodes usually last less than 5 m inutes.
o
May take m onths to resolve com pletely
o
Recurrence is not uncom m on.
Essential Workup
Careful neurologic exam to exclude focal findings
Exclude underlying infections: o
Acute otitis m edia
o
Meningitis
o
Ram say Hunt syndrom e (herpetic lesions on the tym panic m em brane)
Orthostatics
Auditory evaluation
Tests
Indicated only if evaluating patients for central vertigo or m ore unusual etiologies of peripheral vertigo
Rarely helpful in the routine em ergency evaluation of labyrinthitis
Once perform ed, ensure appropriate follow-up for delayed
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lab results, such as syphilis screening.
Lab
Finger-stick glucose
Syphilis screening
Rheum atoid factor
Pediatric Considerations Lum bar puncture if clinical suspicion of m eningitis
Imaging
Indications: o
Findings suggestive of central nystagm us
Acute or gradual onset
Not positional but m ay be exacerbated by head m ovem ents
Pure direction—vertical, horizontal, or torsional
Direction m ay change
Nonfatigable
Minim al effect with fixation:
o
High cardiovascular risk factors
o
Focal neurologic findings
Head CT: o
Fine cuts through the cerebellum
MRI and MRA o
Evaluates the posterior fossa, the eighth cranial nerve and the vestibulobasilar circulation
o
Im aging study of choice in patients suspected of central vertigo
Alert Consider brain im aging in patients older than 45 years, children, and patients with cardiovascular risk factors. P.629
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Differential Diagnosis
Peripheral vertigo: o
Acoustic neurom a
o
Autoim m une inner-ear disease
o
BPPV
o
Cholesteatom a
o
Ménière disease (associated tinnitus, “fullness― or hearing loss)
o
Otosyphilis
o
Ototoxic drugs (loop diuretics, am inoglycosides, streptom ycin, salicylates, ethanol)
o
Perforated tym panic m em brane
o
Perilym ph fistula (sym ptom s accentuated with valsalvae)
o
Posttraum atic vestibular concussion
o
Suppurative labyrinthitis (toxic appearance)
o
Tem poral bone fracture
Central vertigo—often presents with sym ptom s indistinguishable from peripheral vertigo because the labyrinth has a m onosynaptic connection to the brainstem : o
Brainstem ischem ia
o
Cerebellar hem orrhage (high risk of herniation requires intensive care unit [ICU] adm ission)
o
Inferior cerebellar ischem ia (high risk of herniation requires ICU adm ission)
o
Multiple sclerosis (paresthesias, optic neuritis)
o
Partial seizures of tem poral lobe
o
Vestibular-m asseter syndrom e (associated m asseter m uscle weakness)
o
Vestibular m igraine (30% have vertigo independent
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of headaches) o
Wallenberg syndrom e (associated Horner syndrom e, crossed sensory signs)
Cardiac arrhythm ia (presyncopal sym ptom s)
Hypoglycem ia (gradual onset, not positional)
Hypotension (exacerbated with standing)
Cervicogenic disease (onset with rotational neck m ovem ent)
Hypothyroidism
Treatment Pre Hospital
Antiem etics for nausea and vom iting
IV fluids for dehydration
Fall precautions
Assessm ent for acute stroke
Telem etry for arrhythm ia
Finger-stick glucose to exclude hypoglycem ia
Blood pressure check for hypotension
ED Treatment
Medications are m inim ally beneficial for BPPV.
Avoid chronic use to encourage developm ent of vestibular com pensation.
Medications for sym ptom atic relief: o
Vestibular suppressants: diazepam , m eclizine, scopolam ine
o
Antiem etics: prochlorperazine, prom ethazine
o
Corticosteroids: poor evidence for efficacy
Debris repositioning is prim ary therapy for BPPV. Effective
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relief in 50–80% of patients.
Epley m aneuver: o
While sitting, turn head 45° to the left.
o
Lie back quickly with shoulders on a pillow and head reclined onto the bed.
o
Wait for 30 seconds.
o
Turn head 90° to the right (without raising it) and wait again for 30 seconds.
o
Turn body and head another 90° to the right and wait for another 30 seconds.
o
Sit up on the right side.
Sem ont m aneuver: o
From a sitting position, the patient is quickly forced to lie down on the affected side.
o
The patient should rem ain in position for 4 m inutes.
o
Then turn to the other side, always keeping the ear downwards.
o
The patient is again m aintained in the position for 4 m inutes.
Brand-Daroff exercises
Vestibular enhancem ent exercises
Surgery for failed m edical and physical therapy: o
Posterior canal plugging to occlude canal
o
Nerve section
Medication (Drugs)
Diazepam (benzodiazepine): 2–10 m g IV; 5–10 m g (0.1–0.3 m g/kg/24h) PO q6h–q12h
Meclizine (antihistam ine): 25 m g (50 m g/24h older than 12 years) PO q6h
Prochlorperazine: 5–10 m g (0.3 m g/kg/24h IM or PO
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over 2 years old) IV, IM, or PO q6h–q8h
Prom ethazine: 12.5–25 m g (1.5–2.0 m g/kg/24h) IV or PO q4h–q6h
Scopolam ine (anticholinergic, not approved in pediatrics): 0.6 m g PO q4h–q6h; 1.5 m g transderm al patch q3d
Pediatric Considerations
Dim enhydrinate: 5 m g/kg/24h PO, IM, IV, or PR
Bacterial labyrinthitis: o
Antibiotics IV
o
Surgical débridem ent
Pregnancy Considerations Class D m edication: Diazepam
Follow-Up Disposition Admission Criteria
Intractable nausea and vom iting
Severe dehydration
Unsteady gait
Sym ptom s concerning for an acute stroke or central etiology of vertigo
Discharge Criteria
Tolerate oral fluids
Steady gait
Norm al neurological exam
Avoid driving, heights, and operating dangerous equipm ent.
Fall precautions
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Arrange neurology or otolaryngology follow-up.
For BPPV, patient should perform Epley m aneuver three tim es/day
Issues for Referral
Recurrent sym ptom s
Concern for cholesteatom a
References 1. Baloh RW. Vestibular neuritis. N Engl J Med. 2003;348:1027–1032. 2. Goebel JA. Managem ent options for acute versus chronic vertigo. Otolaryngol Clin North Am . 2000;33(3):483–493. 3. Hilton M, Pinder D. The Epley m anoeuvre for benign paroxysm al positional vertigo. Cochrane Database Syst Rev. 2004;(3):CD003162. 4. Korres SG, Balatsouras DG. Diagnostic, pathophysiologic, and therapeutic aspects of benign paroxysm al positional vertigo. Otolaryngology—Head and Neck Surgery. 2004;131(4):438–444. 5. Teach SJ. Dizziness. In: Fleisher GR, Ludwig S, eds. Pediatric em ergency m edicine. 4th ed. Philadelphia, Pa.: Lippincott William s & Wilkins. 2000;217–222. 6. Tusa RJ. Vertigo. Neurol Clin. 2001;19(1):23–55.
Miscellaneous SEE ALSO: Dizziness; Vertigo
Codes ICD9-CM 386.30
ICD10 H83.0
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Laceratio n M anagem ent
Laceration
Management Gordon Chew
Basics Description
A laceration is a disruption in skin integrity m ost often resulting from traum a.
May be single or m ultiple layered
Diagnosis Signs and Symptoms Lacerations m ay be accom panied by:
Bleeding
Tissue foreign bodies
Hem atom a
Pain or num bness
Loss of m otor function
Dim inished pulses, delayed capillary refill
History
Mechanism and circum stances of injury
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Tim e of injury
History of foreign body (glass, splinter, teeth)
Tetanus im m unization
Co-m orbid condition that m ay im pede wound healing
Physical Exam
Evaluate nerve and m otor function.
Docum ent associated neurovascular injury.
Assess presence of devitalized tissue, debris from foreign m aterials, bone or joint violation, tendon injury: o
Avoid digital exploration if the object is believed to be sharp.
Essential Workup
Consider repair in operating room if unable to be perform ed safely within the em ergency departm ent, especially for children requiring deep sedation.
Consider surgical consultation for com plex lacerations, especially involving eyes, face.
Pediatric Considerations Assess for possible nonaccidental traum a.
Tests Imaging
Evaluation for possible foreign bodies
Plain radiography: o
Soft tissue views m ay aid in visualization.
o
Objects with the sam e density as soft tissue m ay not be seen (wood, plants).
Ultrasonography
CT scan
MRI with m etal precautions
Differential Diagnosis
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Skin avulsion
Contusion
Abrasion
Treatment Pre Hospital
Obtain hem ostasis, or control of bleeding with direct pressure.
Straighten any flaps of skin whose blood supply m ay be strangulated.
Application of splint if needed
Universal precautions
Initial Stabilization
Airway, breathing, and circulation m anagem ent (ABCs)
Control of hem ostasis
ED Treatment
Tim e of onset: o
Lacerations m ay be closed prim arily ≤8 hours old in areas of poorer circulation.
o
Lacerations m ay be closed ≤12 hours old in areas of norm al circulation.
o
On face, lacerations m ay be closed ≤24 hours if clean and well irrigated.
o
If not closed, wound m ay heal by secondary intention or by delayed prim ary closure (DPC) in 3–5 days.
Analgesia and conscious sedation: o
Adequate analgesia is crucial for good wound m anagem ent.
o
Conscious sedation m ay be required (see Conscious
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Sedation).
Local anesthetics: o
o
Topical:
TAC (tetracaine, adrenaline, cocaine)
EMLA (eutectic m ixture, lidocaine, prilocaine)
Local/regional:
Lidocaine, bupivacaine
Epinephrine will cause vasoconstriction and im prove duration of action of anesthetic.
Avoid epinephrine in the penis, digits, toes, ears, eyelids, tip of nose, skin flaps (necrosis), and severely contam inated wounds (im pairs defense).
For patient com fort, inject slowly with sm all-gauge needle; buffer every 9 m L of 1% lidocaine with 1 m L 8.4% sodium bicarbonate.
Consider a 1% diphenhydram ine solution in the lidocaine-allergic patient.
Exploration and rem oval of foreign body: o
Indications for rem oval of a foreign body include:
Potential or actual injury to tendons, nerves, vasculature
Toxic substance or reactive agent
Continued pain
Irrigation and débridem ent: o
Surrounding intact skin m ay be cleaned with an antiseptic solution (povidone-iodine).
Do not use antiseptic solution within the wound itself because it m ay im pair healing.
o
Scrub with a fine-pore sponge only if significant contam ination or particulate m atter.
o
Irrigation with 200 m L or m ore of norm al saline
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(NS):
Optim al pressure (5–8 psi) generated with 30-m L syringe through 18- to 20-gauge needle
Débride devitalized and contam inated tissue.
Wound repair: o
Universal precautions
o
Wounds that cannot be cleaned adequately should heal by secondary intention or DPC.
o
Reapproxim ate all anatom ic borders carefully (e.g., skin–verm ilion border of lip)
o
Consider tissue adhesive for wounds with clean borders, low tension.
Single-layered closure: o
Sim ple interrupted sutures:
o
Avoid in lacerations under tension.
Horizontal m attress sutures (running or interrupted):
Edem atous finger and hand wounds
Ideal in skin flaps where edges at risk for necrosis
o
Vertical m attress:
For wounds under greater tension
Multiple-layered closure: o
Closes deep tissue dead space
o
Lessens tension at the epiderm al level, im proves cosm etic result
o
Buried interrupted absorbable suture, sim ple or running nonabsorbable sutures for epiderm is
Dressing: o
Dress wound with antibiotic ointm ent and nonadherent sem iporous dressing.
o
Inform patient about scarring and risk for infection, use of sunscreen.
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o
Apply splint if needed.
Antim icrobial agents: o
Uncom plicated lacerations do not need prophylactic antibiotics.
o
If antibiotics are used, initiate before wound m anipulation or as early as possible.
o
Lacerations with high likelihood of infection:
Anim al, hum an bites, especially to hand (see Hand Infection)
o
Contam inated with dirt, bodily fluids, feces
Tetanus im m unization
P.631
Medication (Drugs)
See Conscious Sedation.
Tetanus (Td adults, DT peds): 0.5 m L IM
Local anesthetics: o
Topical, applied directly to wound with cotton, gauze:
EMLA (eutectic m ixture, 5% lidocaine, and prilocaine): apply for 60 m inutes.
TAC (0.5% tetracaine, 1:2,000 adrenaline, 11.8% cocaine): Apply for 20–30 m inutes.
o
Injected:
Bupivacaine (m ax.: 2 m g/kg; duration 3–10 hours)
Lidocaine (m ax.: 4.5 m g/kg; duration 1.5–3.5 h)
Suture Materials
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Absorbable: o
For use in m ucous m em branes and buried m uscle/fascial layer closures:
Natural—dissolve Table o f C o ntents > Larynx F racture
Larynx Fracture
Diane Devita David Della-Giustina
Basics Description Disruption of any of the cartilaginous structures between the pharynx and trachea:
Epiglottis, thyroid, arytenoid, cricoid, corniculate, and cuneiform cartilages
Etiology
Rare injury, incidence appears to be decreasing.
Blunt traum a to the anterior neck associated with m otor vehicle or m otorcycle crash, assault, or recreational activities
Typical m echanism is hyperextension of neck with a direct blow to the exposed anterior neck.
“Clothesline― injury is a classic m echanism (victim struck in neck by cord, wire, or branch hung across path of travel).
Pediatric Considerations
Bicycle handlebars: o
Extended neck hits the bar, com pressing structures
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between the bar and vertebral colum n.
Diagnosis Signs and Symptoms
May be subtle or delayed for hours
Neck tenderness
Bruising or abrasions over the anterior neck
Hoarseness or voice changes
Hem optysis
Dysphonia
Stridor
Subcutaneous em physem a
Dyspnea
Loss of norm al cartilaginous landm arks of neck
Essential Workup
Cervical spine radiograph: o
Exam ine for concom itant spinal injury as well as soft-tissue swelling and subcutaneous em physem a.
Chest radiograph: o
Identify pneum othorax, pneum om ediastinum , and subcutaneous em physem a.
CT scan of larynx: o
¾Recom m ended unless the patient is going directly to surgery
o
Useful even in cases of apparently less severe sym ptom s and m inor abnorm alities on indirect laryngoscopy
Pulse oxim etry
Tests
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Lab Arterial blood gas if the patient is having respiratory difficulty:
Identifies hypoxia, hypercarbia
Diagnostic Procedures/Surgery
Fiberoptic laryngoscopy: o
Allows visualization of injuries involving the airway, vocal cords
Arteriography: o
Only when concerned with possible vascular injuries
Fiberoptic bronchoscopy and esophagoscopy
Surgical exploration
Surgery: o
As indicated by severity of injury
o
Em ergent surgical repair if necessary
Differential Diagnosis Associated injuries:
Hyoid fracture
Thyroid cartilage disruption
Recurrent laryngeal nerve disruption
Carotid artery injury
Phrenic nerve injury
Cervical spine injury
Hypoxic cerebral injury
Airway edem a
Aspiration pneum onitis
Air em bolism
Pediatric Considerations
Pediatric larynx located higher in the neck, m ore cartilaginous and m obile than adults; thus, pediatric patients are m ore resistant to laryngeal fractures.
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Loosely attached subm ucosal tissue allows for greater soft tissue traum a, m assive edem a, and hem atom a form ation: o
With sm aller airway diam eters, rapid airway com prom ise can occur.
Neck tenderness is a m ore com m on com plaint than dysphagia or dyspnea.
Treatment Pre Hospital
Cautions: o
Aggressive airway m anagem ent is necessary: oxygen, suction.
o
Cervical spine im m obilization
o
Injury m ay be overlooked if intubated prehospital for other injuries owing to loss of subjective com plaints.
Controversies: o
Elective intubation not advocated
Initial Stabilization Airway m anagem ent is of prim ary concern:
Severe injuries m ay require operative m anagem ent.
Early intubation to preclude respiratory em barrassm ent
Form al tracheostom y under local m ay be required rather than endotracheal intubation when m ore severe neck injury is present.
Avoid repeated intubation attem pts: o
Proceed to surgical airway.
Cricothyrotom y for severe m axillofacial injuries and injury is superior to cricothyroid cartilage.
Avoid cricothyrotom y if hem atom a present over the
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cricothyroid m em brane or evidence of cricotracheal disruption.
Em ergent tracheostom y m ay be the only option to secure an airway.
P.635
Pediatric Considerations
Elective intubation is potentially dangerous.
Mandatory flexible fiberoptic laryngoscopy
CT scan if m anagem ent course in doubt
ED Treatment
Supplem ental hum idified oxygen
Elevate head of bed to decrease cerebral and neck soft tissue edem a.
Intravenous access
Consult otolaryngologist for surgical evaluation.
Positive end expiratory pressure and volum e-controlled ventilation for severe pulm onary injury associated with acute respiratory distress syndrom e or aspiration pneum onitis
Medication (Drugs)
For laryngeal injury with subcutaneous em physem a: o
Assum e that the m ucosa of the upper airway has com m unicated with the deep tissue of the neck:
Am picillin/sulbactam : 1.5–3.0 g (peds: 50 m g/kg) IV q6h
Clindam ycin: 600–900 m g IV q8h (peds: 25–40 m g/kg/24h IV)
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Histam ine 2 blockers to prevent irritation to m ucosal injuries (e.g., ranitidine 150–300 m g IV; peds: 2–4 m g/kg/d div. q6h IV)
For laryngeal edem a, the following m ay be used: o
Steroids:
Controversial, but m ay be used for m assive edem a. If used, m ost effective within a few hours of injury
Dexam ethasone: 4 m g (peds: 0.15–0.6 m g/kg per dose) IV
Pediatric Considerations If stridor present, consider nebulized racem ic epinephrine: 2.25% 0.25–0.5 m L in 2.5 m L norm al saline (NS).
Follow-Up Disposition Admission Criteria
Patients with true laryngeal injuries m ust be adm itted to a m onitored setting for observation and airway m anagem ent; prepare for em ergent surgical repair of laryngeal defect.
Patients with suspected laryngeal injury or highly suspicious m echanism m ust be adm itted to a m onitored setting for observation and serial flexible fiberoptic laryngoscopic exam inations.
Pediatric Considerations Mandatory adm ission recom m ended in all patients for oxim etry, oxygen, and serial fiberoptic laryngoscopy exam inations
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Discharge Criteria Patients without evidence of serious laryngeal injury, airway edema, or com prom ise after an appropriate period of observation in the em ergency departm ent (usually 6 hours):
Patients can appear deceptively norm al for several hours after injury; if there is any doubt, adm it to a m onitored setting.
References 1. Atkins Z, Abbate S, Fisher S, et al. Current m anagem ent of laryngotracheal traum a: case report and literature review. J Traum a. 2004;56:185–190. 2. Francis S, Gaspard D, Rogers N, et al. Diagnosis and m anagem ent of laryngotracheal traum a. J Natl Med Assoc. 2002;94:21–24. 3. Gold SM, Gerber ME, Hott SR, et al. Blunt laryngotracheal traum a in children. Arch Otolaryngol Head Neck Surg. 1997;123:83–87. 4. Ikram M, Naviwala S. Case report: acute m anagem ent of external laryngeal traum a. Ear Nose Throat J. 2000;79:802–804. 5. Kleinsasser NH, Priem er FG, Schulze W, et al. External traum a to the larynx: classification, diagnosis, therapy. Eur Arch Otorhinolaryngol. 2000;257:439–444. 6. Muniz A, Foster R, Ram iah V. Laryngeal traum a m im icking croup. J Traum a. 2001;51:565–567. 7. O'Mara W, Hebert AF. External laryngeal traum a. J La State Med Soc. 2000;152:218–222.
Codes ICD9-CM 959.09
ICD10 S12.8
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Lead Po iso ning
Lead Poisoning
Gerald Maloney Jr.
Basics Description
Lead has m ultiple m echanism s: o
Binds sulfhydryl groups and affects m ultiple enzym atic processes
o
Resem bles Ca ++ and therefore can interfere with Ca ++ -dependent processes, including cell signaling
o
Mutagenic potential—not known to be a hum an carcinogen
Distribution: o
Up to 99% of lead is bound to erythrocytes after initial absorption.
o
o
Ultim ately redistributed into bone
Ninety-five percent of total body lead in adults
Seventy percent of total body lead in children
High lead levels in the serum will com prom ise the blood–brain barrier and result in lead entry into the CNS and neurotoxicity.
Often coexists with iron deficiency; this allows for increased lead absorption in the gut.
Im pairs hem e synthesis, leading to elevated erythrocyte
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protoporphyrin; this com plexes with zinc, causing elevated zinc protoporphyrin (ZPP).
Etiology
Acute toxicity: o
Most often owing to environm ental exposure or ingestion of substance containing high lead levels
o
Pottery glaze
o
Certain folk rem edies
o
Jewelry
o
Weights
o
Hom e-distilled alcoholic beverages
Chronic toxicity: o
o
Occupational exposures:
Most com m on via inhalation route
Sm elting
Deleading
Bridge painting
Hom e exposures:
Lead paint ingestion by children
o
Contam ination of drinking water or food
o
Use of folk rem edies containing high lead concentrations
In the United States, lead intoxication is prim arily owing to ingestion of leaded paints and m ost frequently affects children age 1–6 years.
May also be seen when a retained bullet enters synovium or other body cavity where it is system ically absorbed
Diagnosis
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Signs and Symptoms
Neurologic: o
Seizures (m ay be prolonged and refractory)
o
Encephalopathy
o
Learning disabilities/decreased intelligence
o
Cerebral edem a
o
Peripheral neuropathy (wrist drop), classic (but rarely seen) finding with chronic toxicity
Gastrointestinal: o
Colicky abdom inal pain (lead colic)
o
Ileus
o
Nausea/vom iting
o
Lead lines in gum s (Burton lines) appear as bluish tint to gingival line
o
Hepatitis/pancreatitis
Cardiovascular: o
Hypertension (generally secondary to renal failure)
o
Myocarditis and conduction defects
Renal: o
Chronic renal insufficiency with long-term exposure
o
Saturnine gout
Hem atologic: o
Anem ia (owing to interference with globin chain synthesis)
o
Elevated ZPP
o
Increases RBC fragility so decreased RBC life span
Musculoskeletal: o
Lead lines from increased Ca ++ deposition (not actually lead itself)
o
May lead to decreased bone strength and growth
Essential Workup
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Lead level
Tests Lab
Whole blood lead level: o
Norm al Table o f C o ntents > Legg-C alvé-Perthes Disease
Legg-Calvé-Perthes Disease Brandon H. Backlund
Basics Description Avascular necrosis of all or part of fem oral head in children
Genetics Association with factor V Leiden m utation and anticardiolipin antibodies
Etiology
Multiple episodes of infarction causing characteristic findings
Disruption of vascular supply to fem oral head with exact underlying cause unknown
Growing evidence im plicating hypercoagulable states; m ay be m ultifactorial
Risk factors include growth horm one therapy, exposure to secondhand sm oke, and low birth weight
Progression through four stages of disease: o
Synovitis: brief duration (weeks), reaction to ischem ia
o
Necrosis and collapse of fem oral head
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o
Fragm entation: resorption of avascular bone; deform ation of fem oral head often occurs at this stage.
o
Reconstitution: form ation of new bone
More com m on in boys with m ale-to-fem ale ratio of 4:1
Most com m only occurs between ages of 3 and 9 years: o
Range, 2–18 years of age
Bilateral in 10–15% of cases
Associated with short stature and delayed skeletal m aturation
Diagnosis Signs and Symptoms History
Frequently insidious onset
Lim p often presenting com plaint
Pain: o
Aching in hip, groin, anterom edial thigh, or anterom edial knee
o
May be m ild
o
Aggravated by activity, relieved by rest
o
Muscle spasm com m on com plaint early in course of disease
Physical Exam
Tenderness over anterior aspect of hip joint
Joint stiffness:
o
Lim itation of internal rotation seen earliest
o
Lim ited abduction
Muscle atrophy and shortening of leg on affected side late
Pa ge 2 8 2
findings
Otherwise well-appearing and afebrile
May be asym ptom atic
Essential Workup
Radiographs of hip m ost im portant study for diagnosis in em ergency room
Consider and exclude septic arthritis (usually an acute febrile illness).
Tests Lab CBC, erythrocyte sedim entation rate (ESR) if septic arthritis a concern
Imaging
Hip radiographs: o
Anteroposterior and frog-leg views of hip
o
Early findings:
Coxa m agna: cartilaginous overgrowth of fem oral head, m ay see joint space widening or lateral shift of fem oral head in acetabulum
Subchondral fracture (Caffey sign): crescentic subchondral radiolucency
Minim al joint effusion, prom inence of soft tissues over capsule
o
Over subsequent weeks:
Increased opacity of fem oral head
Fragm entation of fem oral head
May see m etaphyseal “cysts― (also known as physeal bridge): radiolucent areas in m etaphysis representing ingrowth of cartilage from growth plate
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Flattening of fem oral head (coxa plana)
Ultrasound: o
Evaluate for effusion.
o
Evaluate articular cartilage for thickening and enlargem ent.
o
Evaluate deform ity and containm ent of fem oral head.
Technetium -99m bone scan: o
Detects changes in fem oral head earlier than plain radiographs
o
Shows decreased uptake in fem oral head on affected side
Magnetic resonance im aging: o
Shows decreased signal in fem oral head
P.639
Diagnostic Procedures/Surgery Hip joint aspiration if concern for septic arthritis; m ay need orthopedic consultation
Differential Diagnosis
Unilateral involvem ent: o
Transient (or toxic) synovitis
o
Septic arthritis
o
Osteom yelitis
o
Juvenile rheum atoid arthritis
o
Rheum atic fever
o
Traum a:
o
Fem oral neck fracture
Hip dislocation
Slipped capital fem oral epiphysis
Tuberculosis:
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o
Tum or
Bilateral involvem ent: o
Hypothyroidism
o
Epiphyseal dysplasia
o
Gaucher disease
Treatment ED Treatment
Pain control m ain ED intervention
May need crutches to avoid weight bearing
Medication (Drugs)
Diazepam : 0.1–0.2 m g/kg per dose (m ax. 5 m g) PO q6h–q8h PRN m uscle spasm
Ibuprofen: 10 m g/kg per dose PO q6h–q8h PRN pain
Follow-Up Orthopedic consultation to determ ine m anagem ent; m ay be outpatient
Disposition Admission Criteria Need for adm ission rare, indicated for:
Severe pain or m uscle spasm not controlled by oral m edications
Social considerations; bedrest/care at hom e not possible
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Discharge Criteria
Adequate pain control with oral m edications
Orthopedic follow-up arranged
Issues for Referral
Very young or m inim al involvem ent usually good outcom e with m inim al intervention
For m ore severe disease, range of treatm ent options including conservative treatm ent, orthotics, traction, and surgical osteotom y, determ ined by consulting orthopedist
References 1. Balasa V, et al. Legg-Calve-Perthes disease and throm bophilia. J Bone Joint Surg Am . 2004;86-A(12):2642–2647. 2. Docquier P, et al. Orthopaedic concerns in children with growth horm one therapy. Acta Orthop Belg. 2004;70(4):299–305. 3. Gordon JE. et al. Sm oking and socio-econom ic status in the etiology and severity of Legg-Calve-Perthes’ disease. J Pediatr Orthop B. 2004;13(6):367–370. 4. Lappin K, et al. Does low birthweight predispose to Perthes’ disease? Perthes’ disease in twins. J Pediatr Orthop B. 2003;12(5):307–10. 5. Staheli L. Practice of Pediatric Orthopedics. Philadelphia: Lippincott William s & Wilkins; 2001:146–151. 6. Szepesi K, et al. The m ost severe form s of Perthes’ disease associated with the hom ozygous factor V Leiden m utation. J Bone Joint Surg Br. 2004;86(3):426–429. 7. Tachdijan M. Clinical Pediatric Orthopedics. Norwalk, CT: Appleton & Lange; 1997:210–223. 8. Wall E. Legg-Calve-Perthes disease. Curr Opin Pediatr. 1999;11(1):76–9. 9. Yilm az D, et al. Evaluation of anticoagulant system in Turkish children with Perthes disease. Pediatr Int. 2005;47(1):43–48.
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Codes ICD9-CM 732.1
ICD10 M91.1
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Leukem ia
Leukemia
Linda Mueller
Basics Description
Neoplasm s of white blood cells (WBCs) that have undergone a m alignant transform ation
Hyperleukocytosis: o
Occurs with WBC >100,000/m m 3
o
Leads to occlusions of sm all vessels prim arily in brain or lungs
o
Present with confusion, stupor, or shortness of breath
Chronic Myelogenous Leukemia (CML)
Overproduction of granulocytic WBCs (neutrophils): o
Neutrophil function preserved
Throm bocytosis
Basophilia
Philadelphia chrom osom e present in bone m arrow of >95%
Chronic Lymphocytic Leukemia (CLL)
Most com m on leukem ia in adults
Overproduction of m onoclonal lym phocytes
Cells accum ulate in lym ph nodes, bone m arrow, liver,
Pa ge 2 8 3
spleen
Particularly prone to herpes virus infections
Acute Leukemias
Proliferation of undifferentiated im m ature cells: o
Acute m yelogenous leukem ia (AML)—im m ature m yeloid cells
o
Acute lym phocytic leukem ia (ALL)—im m ature lym phoid cells (blasts)
Rapidly fatal
Etiology
Cause unknown
Fam ilial clustering in CLL
Increased incidence of AML, ALL, and CML with ionizing radiation
Pediatric Considerations
Usually have ALL: o
Most com m on pediatric cancer
Sixty percent to 80% rem ission in those who are standard risk
Better overall prognosis, except if younger than 1 year of age
May develop leukostasis at lower levels
Diagnosis Signs and Symptoms Chronic Myelogenous Leukemia
Asym ptom atic
Fatigue
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Weight loss
Left upper quadrant pain, tenderness
Abdom inal fullness
Splenom egaly (m ost com m on)
Later stage: o
Headaches
o
Bone pain
o
Arthralgias
o
Fever
o
Leukotactic sym ptom s:
Dyspnea
Drowsiness
Confusion
Chronic Lymphocytic Leukemia
Asym ptom atic
Fatigue
Lethargy
Weight loss
Lym phadenopathy
Splenom egaly
Hepatom egaly
Acute Lymphocytic Leukemia (ALL); Acute Myelogenous Leukemia (AML)
Fever
Fatigue
Pallor
Headache
Angina
Congestive heart failure, dyspnea on exertion
Bone pain
Granulocytic sarcom a (isolated m ass of leukem ic blasts)
Pa ge 2 8 3
Easy bleeding (throm bocytopenia): o
Petechiae
o
Ecchym osis
o
Epistaxis
o
Hem orrhage
Infections (granulocytopenic)
Organ involvem ent with advanced ALL: o
Lym phadenopathy
o
Hepatom egaly
o
Splenom egaly
o
Leukem ic m eningitis:
Headache
Nausea
Seizures
Essential Workup CBC/platelets:
CML: o
WBC range, 10,000–1 m illion/m m 3
o
Neutrophils predom inate.
o
Throm bocytosis in 50%
CLL: o
Absolute lym phocytosis >5,000
o
WBC range, 40,000–150,000/m m 3
Acute leukem ia (AML/ALL): o
Anem ia
o
Throm bocytopenia
o
Elevation/depression of WBC
Tests Lab
Electrolytes, BUN, creatinine, glucose, calcium
Uric acid level:
Pa ge 2 8 3
o
Lactate dehydrogenase: o
Frequently elevated, especially in ALL
Increased in acute leukem ias
Coagulation profile: o
Prothrom bin tim e (PT), partial throm boplastin tim e (PTT), fibrinogen, fibrin-split products
o
If dissem inated, suspect intravascular coagulation.
Blood/urine cultures if fever
Arterial blood gases/pulse oxim etry for shortness of breath
Imaging
Bone m arrow biopsy: o
Required to m ake diagnosis
o
CML—hypercellular with m yeloid hyperplasia
o
CLL—lym phocytosis (30–100%)
o
Acute leukem ia—hypercellular with blast cells, which replace norm al m arrow
Leukocyte alkaline phosphatase test: o
Decreased in neutrophils in CML
Ph1 chrom osom e present in CML
Chest radiograph
P.641
Differential Diagnosis
CML: o
Lym phom a
o
Myeloproliferative syndrom es
o
System ic lupus erythem atosus
o
Infection—bacterial, fungal, m ycobacterial
CLL: o
Pertussis
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o
Infectious lym phocytosis
o
Cytom egalovirus
o
Epstein-Barr virus/m ononucleosis
o
Hepatitis
o
Rubella
Acute leukem ia: o
Aplastic anem ia
o
Leukem oid reactions to infections
Treatment Initial Stabilization
One hundred percent oxygen for hypoxia/shortness of breath
IV access with 0.9% norm al saline (NS)
Initiate platelet transfusion for severe bleeding from throm bocytopenia.
Begin broad-spectrum antibiotics for fever and granulocytopenia.
Treat dissem inated intravascular coagulation (see Dissem inated Intravascular Coagulation).
ED Treatment
Treat leukostasis: o
Rehydrate with 500-m L bolus (20 m L/kg) IV 0.9% NS
o
Adm inister acetazolam ide to alkalinize urine.
o
Initiate allopurinol.
o
Arrange for leukapheresis.
o
Whole-brain radiation for CNS effects
o
Adm inister hydroxyurea for CML: 20–30 m g/kg single dose daily
Pa ge 2 8 3
Transfuse packed RBCs for sym ptom atic anem ia: o
May require irradiated, filtered, and HLA-type specific blood
Post ED Treatment
CLL: o
Chem otherapy
o
Prednisone for im m une-m ediated throm bocytopenia
o
Radiation to localized nodular m asses/enlarged spleen
CML: o
Interferon therapy
o
Chem otherapy
o
Bone m arrow transplantation
ALL: o
Chem otherapy
o
CNS prophylaxis with intrathecal m ethotrexate/cranial radiation
o
Bone m arrow transplantation
AML: o
Chem otherapy
o
Bone m arrow transplantation
Follow-Up Disposition Admission Criteria
Newly diagnosed leukem ia with: o
Sym ptom atic anem ia
o
WBC >30,000
o
Throm bocytopenia
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ICU adm ission for unstable patients with dissem inated intravascular coagulation, blast crisis, or bleeding
Discharge Criteria Asym ptom atic patients without significant laboratory abnorm alities
References 1. Abram son N. Leukocytosis: basics of clinical assessm ent. Am Fam Physician. 2000;62:2053–2060. 2. Lowenberg B. Acute m yeloid leukem ia. N Engl J Med. 1999;341:1051–1062. 3. Pui C. Acute lym phoblastic leukem ia. N Engl J Med. 1998;339:605–614. 4. Sawyers C. Chronic m yeloid leukem ia. N Engl J Med. 1999;340:1330–1340. 5. Tsiodras S. Infection and im m unity in chronic lym phocytic leukem ia. Mayo Clin Proc. 2000;75:1039–1054.
Codes ICD9-CM 208.9
ICD10 C95.9
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Lightning Injuries
Lightning Injuries
Paul Arnold
Basics Description Constellation of problem s caused by lightning strikes
Mechanism
Lightning is a stream of negative current that proceeds downward from cloud to ground.
Because of the brief duration (1–100 m illiseconds) of lightning: o
Current tends to pass over the skin rather than through the body (flashover).
o
Deep tissue injuries are rare.
Mechanism s of injury—electrical: o
Direct strike
o
Side splash injury:
Current jum ps from another object to the victim .
o
Contact strike:
Current passes to victim through an object he or she is touching.
o
Ground strike:
Current m oves through ground surface and m ay
Pa ge 2 8 4
injure m ultiple victim s. o
Hypothetically, an upward stream er of positive current from the ground can also cause injury.
Mechanism s of injury—other: o
Blunt injury owing to atm ospheric shock wave, or fall
o
Therm al burning
Etiology Exposure to lightning:
Usually during outdoor activity
Lightning can strike indoor victim s who are handling ungrounded electrical equipm ent or telephones.
Diagnosis Signs and Symptoms History
Consider lightning strike in unwitnessed falls, cardiac arrests, or unexplained com a in an outdoor setting.
Conscious patients m ay report: o
Pain
o
Neurologic deficits including:
Num bness or paraesthesias
Weakness
Visual disturbance
Headache
Confusion
o
Chest pain
o
Respiratory distress
Physical Exam
Cardiorespiratory injuries:
Pa ge 2 8 4
o
Cardiac asystole:
Due to direct current injury
May resolve spontaneously as the heart's intrinsic autom aticity resum es
o
Respiratory arrest
Caused by paralysis of m edullary respiratory center
May persist longer than cardiac asystole and lead to hypoxia-induced ventricular fibrillation
o
Acute m yocardial infarction (rare)
o
Shock:
o
Neurogenic (spinal injury)
Hypovolem ic (traum a)
Mottled or cold extrem ities:
Caused by autonom ic vasom otor instability
Usually resolves spontaneously in a few hours
Neurologic injuries: o
Confusion, cognitive or m em ory defects
o
Altered level of consciousness (>70% of cases)
o
Flaccid m otor paralysis
o
Seizures
o
Fixed dilated pupils owing to either serious head injury or autonom ic dysfunction
Traum atic injuries: o
Blunt traum a:
To the head or spine
Fractures, dislocations, m uscle tears, and com partm ent syndrom es
o
Ruptured tym panic m em brane with ossicular disruption (up to 50%)
o
Burns:
Discrete entrance and exit wounds uncom m on
Pa ge 2 8 4
Direct therm al injury is uncom m on owing to the brevity of electrical currents.
Therm al burns can arise from evaporation of water on skin, ignited clothing, heated m etal objects (buckles/jewelry).
o
Feathering pattern of fernlike “burns―:
Cutaneous im prints from electron showers that track over skin
Pathognom onic of lightning injury
Resolve within 24 hours
Ophthalm ologic injuries: o
Cataracts occur days to years after injury
o
Corneal lesions
o
Intraocular hem orrhages
o
Retinal detachm ent
Essential Workup Confirm atory history from bystanders or rescuers of the circum stances of the injury
Tests Lab
CBC for baseline hem atocrit
Urinalysis for m yoglobin
Electrolytes for acidosis
BUN, creatinine for renal function
Troponin, creatine kinase (CK), and cardiac enzym es for m uscle/cardiac dam age
Imaging
Chest radiograph
Cervical spine radiograph
Head CT for altered m ental status or significant head
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traum a
Relevant im aging for specific injuries
Diagnostic Procedures/Surgery ECG:
Nonspecific ST changes com m on
Acute m yocardial infarction rare
Differential Diagnosis Other causes of com a, cardiac dysrhythm ia, or traum a:
Hypoglycem ia
Intoxication
Drug overdose
Cardiovascular disease
Cerebrovascular accident (CVA)
Treatment Pre Hospital
Field triage should rapidly focus on providing ventilatory support to unconscious victim s or those in cardiopulm onary arrest: o
Prevents reversible asystolic cardiac arrest from degenerating into hypoxia-induced ventricular fibrillation
o
Conscious victim s are at lower risk for im m inent dem ise.
Spine im m obilization for: o
Cardiopulm onary arrest (suspected traum a)
o
Significant m echanical traum a
o
Suspected loss of consciousness at any tim e
Cover superficial burns with sterile saline dressings.
Pa ge 2 8 4
Im m obilize injured extrem ities.
Rapid extrication to decrease risk for repeat lightning strikes
P.643
Initial Stabilization
Airway, breathing, and circulation m anagem ent (ABCs)
Standard advanced cardiac life support (ACLS) m easures for cardiac arrest
Diligent prim ary and secondary survey for traum atic injuries and other causes of collapse/injury: o
Maintain cervical spine precautions until cleared.
Treat altered m ental status with glucose, naloxone, or thiam ine as indicated.
Hypotension requires volum e expansion and pressor agents.
ED Treatment
IV access for m edication adm inistration
Clean and dress burns.
Tetanus prophylaxis
Treat m yoglobinuria if present:
o
Diuretics, such as furosem ide or m annitol
o
Alkalinize urine to a pH of 7.45
o
Maintain urine output with IV fluid adm inistration.
Volum e expansion: o
Do not follow burn treatm ent form ulas because flashover burns are rarely the cause of fluid loss.
o
Occult deep burn injury is rare when com pared with other types of electrical current injury.
o
Titrate volum e adm inistration to urine output:
Pa ge 2 8 4
Fluid loading m ay be dangerous if patient also has head injury.
Com partm ent syndrom e: o
Must be distinguished from vasospasm , autonom ic dysfunction, and paralysis, which are usually self-lim ited phenom ena
o
Delay fasciotom y if possible because it will rarely be necessary.
Nonsteroidal anti-inflam m atory drugs (NSAIDs) and high-dose steroids have been proposed to reduce long-term neurologic and corneal dam age.
Medication (Drugs)
Furosem ide: 1 m g/kg IV slow bolus q6h
Mannitol: 0.5 m g/kg IV, repeat PRN
Sodium bicarbonate: 1 am p IV push (peds: 1 m Eq/kg) followed by 2–3 am ps/L D 5 W IV fluid
Follow-Up Disposition Admission Criteria
Seriously injured and postcardiac arrest victim s
History of change in m ental status/altered level of consciousness
Myoglobinuria
Acidosis
History of dysrhythm ias or ECG changes: o
May not resolve spontaneously
Pa ge 2 8 4
o
24- to 48-hour observation period to identify potentially unstable cases
Discharge Criteria
Asym ptom atic patients with no injuries
Close follow-up required owing to the risk for delayed sequelae: o
Neurologic
o
Ophthalm ologic
o
Psychologic
References 1. Cooper MA. A fifth m echanism of lightning injury. Acad Em erg Med. 2002;9(2):172–174. 2. Cooper MA. Lightning injuries. In: Marx JA, Hockenberger RS, Walls RM, et al., eds. Rosen's Em ergency Medicine. 5th ed. Philadelphia: Mosby; 2002. 3. O'Keefe Gatewood M, Zane RD. Lightning injuries. Em erg Med Clin North Am . 2004;22(2):369–403.
Miscellaneous SEE ALSO: Electrical Injury
Codes ICD9-CM 994.0
ICD10 T75.0
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Lithium Po iso ning
Lithium Poisoning
Sean Bryant
Basics Description
GI absorption is rapid: o
Regular release: peak serum levels 2–4 hours
o
Sustained release: peak serum levels 4–12 hours
Half-life 24 hours
Slow distribution
Volum e of distribution (V d ): 0.6–0.9 L/kg
Elim ination: o
Not m etabolized
o
Excreted renally unchanged
o
Reabsorbed in the proxim al tubules by sodium transport m echanism
o
Elim ination half-life (therapeutic) is 20–24 hours and prolonged in chronic users.
Therapeutic and toxic indices: o
Therapeutic and toxic effects occur only when lithium is intracellular.
o
Narrow toxic-to-therapeutic ratio
o
Therapeutic level 0.6–1.2 m Eq/L (after intracellular/extracellular equilibration)
Pa ge 2 8 5
o
Because of its size, renal handling sim ilar to sodium , potassium , and m agnesium
Risk Factors
Acute conditions increasing risk of toxicity: o
Dehydration (greater percent reabsorbed)
o
Overdose
Chronic conditions increasing risk of toxicity: o
Hypertension
o
Diabetes m ellitus
o
Renal failure
o
Congestive heart failure
o
Advanced age
o
Dose change
o
Drug interactions
o
Lithium therapy
o
Low-salt diet
The following increase serum lithium levels owing to decreased renal clearance or exacerbated effects: o
Nonsteroidal anti-inflam m atory drugs
o
Thiazides
o
Angiotensin-converting enzym e inhibitors
o
Dilantin
o
Tricyclic antidepressants
o
Phenothiazines
Etiology
Acute or chronic conditions affecting lithium clearance
Overdose
Diagnosis
Pa ge 2 8 5
Signs and Symptoms Acute Toxicity
Less com m on and less serious than chronic toxicity
Neurologic (m ild):
o
Weakness
o
Fine trem or
o
Light-headedness
Neurologic (m oderate): o
Ataxia
o
Slurred speech
o
Blurred vision
o
Tinnitus
o
Profound weakness
o
Coarse trem or
o
Fasciculations
o
Hyperreflexia
o
Apathy
Neurologic (severe): o
Confusion
o
Com a
o
Clonus
o
Extrapyram idal sym ptom s
o
Seizure
Gastrointestinal: o
Very com m on
o
Nausea/vom iting
o
Diarrhea
o
Abdom inal pain
Cardiac: o
Prolonged QT, ST depression
o
T-wave flattening m ost com m on ECG abnorm ality
Pa ge 2 8 5
o
U waves
o
Serious arrhythm ia (rare)
Chronic Toxicity
Neurologic: o
Most com m on
o
Sam e sym ptom s as acute
o
Severe toxicity includes Parkinson-type sym ptom s, psychosis, and m em ory deficits.
Renal: o
Nephrogenic diabetes insipidus
o
Interstitial nephritis
o
Distal tubular acidosis
o
Direct cellular dam age
Derm atologic: o
Derm atitis
o
Ulcers
o
Localized edem a
Endocrine: o
Hypothyroidism
Hem atologic: o
Leukocytosis
o
Aplastic anem ia
Essential Workup
Lithium level: o
Obtain history of tim e of ingestion or last dose.
o
Because of prolonged distribution, repeat every 2 hours to detect trend.
Stratify patient into one of three categories of toxicity to interpret level and predict toxicity: acute, acute on chronic, chronic: o
Acute toxicity:
Pa ge 2 8 5
Intentional overdose in patient not previously taking lithium
Poor correlation between lithium level and sym ptom s because intracellular distribution has not yet occurred
Toxic levels m ay appear in asym ptom atic patients.
Lithium level >4 m Eq/L is toxic because clearance is slow and com plications are possible.
o
Acute on chronic toxicity:
Intentional or accidental overdose in patient on lithium therapy
Lithium level >3 m Eq/L usually associated with sym ptom s.
o
Chronic toxicity:
Patients on lithium therapy who progressively develop toxicity secondary to factors other than acute ingestion
Stronger correlation between lithium level and sym ptom s
Lithium level >1.5 m Eq/L m ay be toxic.
Tests Lab
Electrolytes, BUN, creatinine, and glucose levels to determ ine electrolyte disturbances/renal function
Aspirin and/or acetam inophen levels as indicated
Urinalysis: o
Specific gravity
Differential Diagnosis
Consider lithium toxicity with altered m ental status and
Pa ge 2 8 5
fasciculations.
Endocrine: o
Hypoglycem ia
Toxicologic: o
Organophosphates
o
Cholinergic substances
o
Heavy-m etal poisoning
o
Neuroleptic overdose
o
Black widow/scorpion envenom ation
o
Strychnine poisoning
P.645
Treatment Pre Hospital
Transport all appropriate pill bottles to hospital.
Intravenous access, oxygen, and cardiac m onitoring
Initial Stabilization
Airway, breathing, and circulation m anagem ent (ABCs)
Secure intravenous access with 0.9% norm al saline.
Cardiac m onitor
Naloxone, thiam ine, dextrose (or Accu-Chek) if altered m ental status
Benzodiazepine (diazepam ) for seizures
ED Treatment
Prevent absorption: o
Consider gastric lavage only if patient presents within 1 hour of acute life-threatening ingestion and has
Pa ge 2 8 5
protected airway. o
Activated charcoal:
Lithium not absorbed by charcoal
Consider one dose of activated charcoal if possible coingestants
o
Whole-bowel irrigation:
Polyethylene glycol solution (PEG/GoLytely)
Indicated with sustained-release products
Flushes lithium through gut
Adm inister (2 L/h per nasogastric [NG] tube) until rectal effluent is clear.
Contraindications include bowel obstruction or perforation, ileus or hypotension, and unprotected airway in obtunded or seizing patient.
Enhance elim ination: o
Intravenous fluids:
Rapidly correct any pre-existing fluid deficit with 0.9% norm al saline at 150–300 m L/h.
Saline hydration im proves glom erular filtration and decreases proxim al tubule reabsorption of lithium .
Maintain urine output between 1 and 2 m L/kg/h.
Lim ited value once glom erular filtration rate m axim ized
Sodium bicarbonate offers no additional advantage.
o
Loop, thiazide, and osm otic diuretics not recom m ended:
Dehydration m ay result in worsening toxicity.
No direct effect on renal reabsorption, because lithium is reabsorbed in proxim al tubules
Pa ge 2 8 5
o
Kayexalate (sodium polystyrene sulfonate):
Anim al studies indicate reduced lithium levels.
Only very large doses studied
Com plications m ay include hypokalem ia, hyperkalem ia, fluid overload, and dysrhythm ias.
Dialysis: o
Peritoneal dialysis not recom m ended
o
Hem odialysis recom m ended for augm enting elim ination (below)
General Measures
Correct electrolyte abnorm alities.
Continuous cardiac m onitoring
Maintain well-hydrated state.
Observe for neurologic changes.
Special Therapy
Hem odialysis recom m ended for severe cases or acute ingestions with high levels indicating im m inent toxicity
Controversial indications (valid criteria not established): o
Severe and progressive neurologic abnorm alities
o
Renal failure
o
Altered m ental status
o
Ventricular arrhythm ia/cardiogenic shock
o
History of congestive heart failure or pulm onary edem a
o
Acute ingestions with levels >4 m Eq/L
o
Chronic ingestions with levels >2.5 m Eq/L
Standard end point is lithium level 2 m Eq/L despite em ergency departm ent intervention
Moderate to severe sym ptom s with chronic levels >4 m Eq/L warrant adm ission to intensive care unit.
Intentional ingestion
Discharge Criteria Decreasing lithium levels every 2–4 hours in asym ptom atic patient and serum lithium level Table o f C o ntents > Ludw ig's Angina
Ludwig's Angina
Paul Blackburn
Basics Description
A life-threatening infection of the floor of the m outh
Rapidly spreading gangrenous cellulitis, necrotizing fasciitis of subm axillary, sublingual, subm andibular spaces
First described by von Ludwig in 1836
Mortality exceeded 50% in preantibiotic era.
Most deaths due to respiratory obstruction
Im proved dental care, antibiotics reduce incidence
Four cardinal aspects: o
Bilateral involvem ent of m ore than one deep-tissue space
o
Gangrene with serosanguineous, putrid infiltration; little or no frank pus
o
Involvem ent of connective tissue, fasciae, and m uscles; not glandular structures
o
Spread by fascial space continuity, not lym phatics
Brawny, painful induration of suprahyoid neck results in woody edem a of the floor of the m outh; tongue, soft tissues forced superiorly, posteriorly.
Rapid respiratory obstruction (asphyxia) can occur.
Pa ge 2 8 6
Etiology
Odontogenic—50–90% of reported cases: o
Most com m only second, third m andibular m olars
o
Children less likely to have an odontogenic source
Less com m only: o
IV drug injections into neck veins
o
Mandibular fractures
o
Oral lacerations
o
Sialadenitis
o
Peritonsillar abscess
o
Tongue piercing
Invariably polym icrobial, oral flora: o
Most com m on pathogens Strep viridans, Staph aureus, Staph epiderm idis
o
Anaerobes: m ost com m only Bacteroides species
Diagnosis Signs and Symptoms
Subm andibular pain
Tongue elevation, protrusion
Trism us: o
Difficult to exam ine m outh, pharynx
Dysphonia
Odynophagia
Stridor
Anxiety
Salivary incontinence
Fever
Tachypneic, tachycardic
Pa ge 2 8 6
Patient will prefer sitting/“sniffing― position.
Subm andibular area hard, “woody,― painful
Essential Workup Diagnosis apparent from the history, physical exam ination
Tests Lab
WBC count
Blood cultures
Imaging
Soft tissue film s of neck: o
Edem a, presence of gas
CT, MRI detects severe cellulitis, abscesses, intrathoracic extension.
Panorex detects odontogenic abscesses.
Chest radiograph: o
Intrathoracic extension
Ultrasound detects abscesses.
Differential Diagnosis
Cellulitis
Peritonsillar abscess
Salivary gland abscess
Lym phadenitis
Angioneurotic edem a
Lingual carcinom a
Sublingual hem atom a secondary to anticoagulation
Treatment
Pa ge 2 8 6
Pre Hospital
Transport in sitting position: o
Supplem ental oxygen, suction secretions as needed
Early, aggressive airway protection
Initial Stabilization
Airway com prom ise is the prim ary concern
Expect difficulty: altered anatom y, swollen tissue, trism us
Rapid-sequence intubation m ay result in loss of supporting structures; loss of visualization, patent airway
Sedation-assisted orotracheal intubation is preferred: o
Short-acting agents (etom idate, thiopental)
Awake, fiberoptic laryngoscopic intubation is recom m ended as a first-line approach
Avoid blind nasotracheal intubation: o
Distorted anatom y
o
Risk of inducing bleeding or perforating an abscess
Cricothyrotom y, jet ventilation m ay be difficult.
Tracheostom y is the “gold standard― m anagem ent: o
Risk of secondary intrathoracic spread
ED Treatment
Initiate broad spectrum antibiotics: o
Aerobic/anaerobic/polym icrobial infection
o
Clindam ycin or penicillin G + m etronidazole; also cefoxitin, ticarcillin/clavulanate, piperacillin/tazobactam , am picillin/sulbactam
Steroids of no proven benefit
Hyperbaric oxygen if m ediastinitis, necrotizing fasciitis of the chest wall
P.647
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Medication (Drugs)
Antibiotics: o
Am picillin/SB: 3 g IV q6h
o
Cefoxitin: 2 g IV q8h
o
Clindam ycin: 900 m g IV q8h
o
Metronidazole: 500 m g IV q6h
o
Penicillin G: 4 m IU IV q4h–q6h Piperacillin/TZ: 3.375 g IV q6h
o
Ticarcillin/CL: 3.1 g IV q4h–q6h
General anesthetics: o
Etom idate: 0.2–0.3 m g/kg IV
o
Thiopental: 3–5 m g/kg IV
Follow-Up Disposition Admission Criteria
All are adm itted
Intensive care unit or m onitored setting; airway com prom ise can be precipitous
References 1. Barakate MS, Jensen MJ, Hem li JM, et al. Ludwig's angina: report of a case and review of m anagem ent issues. Ann Otol Rhinol Laryngol . 2001;110(5 Pt 1):453–456. 2. Britt JC, Josephson GD, Gross CW. Ludwig's angina in the pediatric population: report of a case and review of the literature. Int J Pediatr Otorhinolaryngol. 2000;52(1):79–87.
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3. Busch RF, Shah D. Ludwig's angina: im proved treatm ent. Otolaryngol—Head Neck Surg. 1997;117(6):S172–S175. 4. Chandradeva K, Palin C, Ghosh SM, Pinches SC. Percutaneous transtracheal jet ventilation as a guide to tracheal intubation in severe upper airway obstruction from supraglottic oedem a. Br J Anaesth. 2005;May;94(5):683–686. 5. Ovassapian A, Tuncbilek M, Weitzel EK, Joshi CW. Airway m anagem ent in adult patients with deep neck infections: a case series and review of the literature. Anesth Analg. 2005;Feb100(2):582–589. 6. Spitalnic SJ, Sucov A. Ludwig's angina: case report and review. J Em erg Med. 1995;13(4):499–503.
Codes ICD9-CM 528.3 Cellulitis and abscess
ICD10 K12.2 Cellulitis and abscess of m outh M72.6 Necrotizing fasciitis
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Lunate Dislo catio n
Lunate Dislocation
Mary Anne Fuchs Alec Tuan Huynh
Basics Description
Dislocation of the lunate relative to the radius and distal row of m etacarpals, either dorsally or volarly
In perilunate dislocation, relationship of lunate to radius is m aintained and lunate is dislocated relative to capitate.
Usually from high-energy hyperextension with ulnar deviation of the wrist
Etiology
Im plies disruption of all four perilunate ligam ents and radiocarpal ligam ent
In volar dislocations, m edian nerve injury occurs in the carpal tunnel.
Associated fractures of the radial styloid, scaphoid, capitate, and triquetrum are com m on and, if present, should raise suspicion of an occult perilunate ligam entous injury.
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Diagnosis Signs and Symptoms Frequently m issed injury
History
Often from fall or m otor vehicle accident
Pain and tenderness in the wrist
Physical Exam
Mass or swelling in the wrist, either dorsally or volarly depending on direction of dislocation
Gross deform ity often m asked by swelling
May display signs of m edian nerve injury
Essential Workup
Clinical exam is frequently not diagnostic.
Assess skin integrity and neurovascular status, including two-point discrim ination.
Radiographs as outlined below
Tests Imaging
Radiographic im aging to include three views of the wrist
Lateral view m ost useful: o
Disruption of the norm al im aginary longitudinal line through the centers of the radius, lunate, and capitate indicates dislocation or subluxation.
o
In volar dislocations, the lunate is frequently tilted with the opening of the “cup― toward the palm (spilled teacup sign)
Posteroanterior (PA) view: o
The dislocated lunate has a triangular (as opposed to the usual quadrangular) appearance.
Pa ge 2 8 6
o
Disruption of a sm ooth and continuous arc form ed by the radiocarpal row suggests lunate dislocation.
Pediatric Considerations Radiograph can be difficult to interpret unless full ossification is present. P.649
Geriatric Considerations Other fractures are com m on.
Differential Diagnosis
Lunate fracture
Perilunate dislocation
Scapholunate dissociation
Scaphoid fracture
Treatment Pre Hospital
Dress open wounds.
Im m obilize in neutral position.
Initial Stabilization Im m obilize in position of com fort with a volar or “sugar tongs― splint.
ED Treatment
Identify m ultiple traum a or other injuries.
Contact a hand surgeon for im m ediate reduction and possible operative intervention.
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Closed reduction can be difficult or unstable
Open reduction and internal fixation are frequently required.
Pediatric Considerations Although serious injury is unusual, children with wrist pain should be splinted and referred for ongoing evaluation of possible occult fractures.
Follow-Up Disposition Admission Criteria
Adm ission is often necessary for definitive care.
Open fracture, presence of m ultiple traum a, or other m ore serious injuries m andates adm ission.
Discharge Criteria Patients with closed dislocations or fractures that have been adequately reduced and im m obilized in the ED m ay be discharged with orthopedic follow-up.
References 1. Am erican Society for Surgery of the Hand. The Hand: Prim ary Care of Com m on Problem s. 2nd ed. New York: Churchill Livingstone; 1990:637–649. 2. Eisenhauer MA. Forearm and wrist. In: Rosen P, et al., eds. Em ergency Medicine: Concepts and Clinical Practice. 4th ed. St. Louis, MO: Mosby-Year Book; 2002:535–542. 3. Mital RC. The wrist and forearm . In: Schwartz D, et al. Em ergency Radiology. New York: McGraw-Hill; 2000:48–63. 4. Perron AD. Orthopedic pitfalls in the ED: lunate and perilunate
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injuries. Am J Em erg Med. 2001;19(2):157–162. 5. Sim on RR, Koenigsknecht SJ, eds. Em ergency Orthopedics: The Extrem ities. 4th ed. New York: McGraw-Hill; 2001:176–180. 6. Uehara DT. The hand in em ergency m edicine. Em erg Clin North Am . 1993;11(3):781–796.
Codes ICD9-CM 833.00
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Lym e Disease
Lyme Disease
Moses S. Lee
Basics Description
Most com m on tickborne illness in North Am erica
Endem ic in northeastern, upper m idwestern, and northwestern California
Etiology
Peak between April and Novem ber; 80–90% in sum m er m onths
Spirochete Borrelia burgdorferi introduced by Ixodes tick: o
Ixodes dam m ini (deer tick) m ost com m on
Fewer than 50% of patients recall tick bite.
Pathogenesis—com bination of:
o
Organism -induced local inflam m ation
o
Cytokine release
o
Autoim m unity
No person-to-person transm ission
Diagnosis
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Signs and Symptoms Stage I (Early)
Onset few days to m onth after tick bite (arthropod transm ission)
30–50% of patients recall tick bite.
Erythem a chronicum m igrans (ECM): o
Pathognom onic finding:
o
Bull's-eye rash
Maculopapular, irregular expanding annular lesion:
Single or m ultiple
Central clearing with red outer border
Diam eter >5 cm
Regional adenopathy
Low-grade, interm ittent fever
Headache
Myalgia
Arthralgias
Fatigue
Malaise
Stage II (Secondary, Disseminated)
Days to weeks after tick bite
Interm ittent and fluctuating sym ptom s with eventual disappearance
Triad of aseptic m eningitis, cranial neuritis, and radiculoneuritis:
o
Facial (Bell) palsy m ost com m on cranial neuritis
o
May present without rash
o
Prognosis generally good
Cardiac: o
Tachycardia
o
Bradycardia
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o
Atrioventricular block
o
Myopericarditis
Stage III (Tertiary, Late)
Onset >1 year after disease onset
Acroderm atitis chronica atrophicans: o
Extensor surfaces of extrem ities, especially lower leg
o
Initial edem atous infiltration evolving to atrophic lesions
o
Resem bles scleroderm a
Arthritis: o
Brief arthritis attacks
o
Monoarthritis
o
Oligoarthritis
o
Occasionally m igratory
o
Most com m on joints (descending order):
Knee
Shoulder
Elbow
Other
Gastrointestinal: o
Hepatitis
o
Right upper quadrant pain
Ocular: o
Keratitis
o
Uveitis
o
Iritis
o
Optic neuritis
Jarisch-Herxheim er reaction: o
Worsening of sym ptom s a few hours after treatm ent initiated
o
More com m on in patients with m ultiple ECM lesions
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Babesiosis occurs sim ultaneously in endem ic areas.
Persistent Lyme Disease Articular and neurologic sym ptom s despite treatm ent:
Chronic axonal polyneuropathy or encephalopathy
Recurrent Lyme Disease
Relapse despite treatm ent
Second episodes less severe
Pediatric Considerations
More likely than adults to be febrile
Only 50% of children with arthralgias have history of ECM.
Facial palsy accom panied by aseptic m eningitis in one third
Asym ptom atic cardiac involvem ent with abnorm al ECGs
Appropriately treated children have excellent prognosis for unim paired cognitive functioning.
Untreated children m ay have keratitis, joint pain, or chronic encephalopathy.
Essential Workup
Clinical diagnosis: o
Presence of ECM obviates serologic tests.
Careful search for tick
Lum bar puncture when m eningeal signs
Arthrocentesis for acute arthritis
ECG
Tests Lab
CBC: o
Leukocytosis
o
Anem ia
o
Throm bocytopenia
Erythrocyte sedim entation rate (ESR):
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o
Greater than 30 m m /h
o
Most com m on laboratory abnorm ality
Electrolytes, BUN, creatinine, glucose
Liver function tests: o
Elevated liver enzym es (gam m a-glutam yl transferase [GGT] m ost com m on)
Culture: o
Low yield
o
Not indicated
Cerebrospinal fluid (CSF): o
Pleocytosis
o
Elevated protein
o
Obtain CSF spirochete antibodies.
P.651
Special Tests
Serology: o
Obtain enzym e-linked im m unosorbent assay (ELISA), im m unofluorescence assay (IFA), and Western blot when disease suggested without ECM lesion.
o
Antibodies m ay persist for m onths to years.
o
Positive serology or previous Lym e disease does not ensure protective im m unity.
Polym erase chain reaction assay: o
Highly specific and sensitive
o
Not available for routine use
Joint fluid: o
Cryoglobulin increased fivefold com pared with serum
Joint film s m ay show soft tissue, cartilaginous, osseous changes.
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Differential Diagnosis
Other tickborne illnesses: o
Deer tick usually larger (1 cm ) than ixodid ticks (1–2 m m )
o
Rocky Mountain spotted fever
o
Tularem ia
o
Relapsing fever
o
Colorado tick fever
o
Tick-bite paralysis
Rheum atic fever: o
Rash of erythem a m arginatum
o
Tem porom andibular joint arthritis m ore com m on than in Lym e disease
o
Valvular involvem ent rather than heart block
o
Chorea m ay be isolated finding.
Viral m eningitis
Syphilis
Septic arthritis
Parvovirus B19 infection—polyarticular arthritis
Infectious endocarditis
Juvenile rheum atoid arthritis
Reiter syndrom e
Brown recluse spider bite
Fibrom yalgia
Chronic fatigue syndrom e
Treatment Initial Stabilization
500 m L (20 m L/kg) 0.9% norm al saline (NS) IV fluid bolus
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fluids for dehydration
IV access for neurologic and cardiac involvem ent
Cardiac m onitoring
Tem porary pacem aker for heart block
ED Treatment
Rem ove tick: o
Disinfect site.
o
With blunt instrum ent, grasp tick close to skin and pull upward with gentle pressure.
Adm inister: o
Aspirin as adjunctive therapy for cardiac involvem ent
o
Nonsteroidal anti-inflam m atory drugs (NSAIDs) for arthritis and arthralgias
Vaccine (LYMErix) for prevention of disease: o
A recom binant surface protein
o
For persons in high/m oderate risk areas
o
For travelers to endem ic areas
o
Three doses (0 to 1 m onth to 12 m onths)
Stage I
Am oxicillin, doxycycline, or cefuroxim e (21 days)
Azithrom ycin (14–21 days)
Parenteral therapy in pregnant patients
Stage II
Oral therapy for isolated Bell palsy and m ild involvem ent: o
Am oxicillin with probenecid (30 days) or doxycycline (avoid if pregnant or Table o f C o ntents > Lym phangitis
Lymphangitis
John Mahoney
Basics Description
Lym phangitis is infection of lym phatics that drain focus of inflam m ation.
Histologically, lym phatic vessels are dilated and filled with lym phocytes and histiocytes: o
Inflam m ation frequently extends into perilym phatic tissues and m ay lead to cellulitis or abscess form ation.
Etiology
Acute lym phangitis: o
Likely caused by bacterial infection
o
Most com m only group A β-hem olytic streptococcus
o
Less com m only owing to other strep groups, and occasionally Staphylococcus aureus
o
Other organism s:
Pasteurella m ultocida (cat or dog bite)
Spirillum m inus (rat-bite fever)
Wuchereria bancrofti (filariasis):
Consider in im m igrants from Africa, Southeast Asia/Pacific, and tropical South
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Am erica
o
Mosquitoborne
Usually involves lower extrem ities
Com m unity-acquired m ethicillin-resistant S. aureus (CA-MRSA):
No single identified risk factor
Different antibiotic susceptibility than nosocom ial MRSA; trim ethoprim -sulfam ethoxazole (TMP/SMX) and clindam ycin m ay be effective.
Variable, rising local prevalence should be considered when starting em piric antibiotic therapy.
Suspect in unresponsive infections, m ultiple or recurrent abscesses.
Chronic lym phangitis: o
Usually caused by m ycotic, m ycobacterial, and filarial infections
o
Sporothrix schenckii (m ost com m on cause of chronic lym phangitis in U.S.)
Inoculation occurs while gardening or farm ing (rose thorn).
Organism is present on som e plants and in sphagnum m oss.
Multiple subcutaneous nodules appear along course of lym phatic vessels.
Typical antibiotics and local treatm ent fail to cure lesion.
o
Mycobacterium m arinum :
Atypical m ycobacterium
Grows optim ally at 25–32°C in fish tanks and swim m ing pools
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May produce a chronic nodular, single wartlike or ulcerative lesion at site of abrasion
Additional lesions m ay appear in distribution sim ilar to sporotrichosis.
o
Nocardia brasiliensis
o
Mycobacterium kansasii
o
Wuchereria bancrofti
Diagnosis Signs and Symptoms
Acute lym phangitis: o
Warm , tender erythem atous streaks develop and extend proxim ally from source of infection.
o
Regional lym ph nodes often becom e enlarged and tender (lym phadenitis).
o
Peripheral edem a of involved extrem ity
o
System ic m anifestations:
Fever
Rigors
Tachycardia
Headache
Chronic (nodular) lym phangitis: o
Erythem atous nodule, chancriform ulcer, or wartlike lesion develops in subcutaneous tissue at inoculation site.
o
Often presents without pain or evidence of system ic infection
o
Multiple lesions possible along lym phatic chain
History
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History and physical directed at discovering source of infection
Physical Exam
Fever
Erythem atous streaks from source of infection proceeding toward regional lym ph nodes
Essential Workup Lym phangitis is clinical diagnosis.
Tests Lab
White blood count unnecessary but often elevated
Gram stain and culture of initial lesion to focus antim icrobial selection and reveal resistant pathogens (MRSA): o
Aspirate point of m axim al inflam m ation or punch biopsy.
o
Essential if treatm ent failure
If sporotrichosis or M. m arinum infection is suspected, diagnosis should be confirm ed by culture of organism from wound.
Blood culture m ay reveal organism .
Imaging
Im aging not com m only perform ed
Plain radiographs m ay reveal abscess form ation, subcutaneous gas, or foreign bodies if these are suspected.
Extrem ity vascular im aging (Doppler ultrasound) can help rule out deep venous throm bosis.
Differential Diagnosis
Throm bophlebitis; deep venous and superficial: o
Differentiation from lym phangitis:
Pa ge 2 8 9
Absence of initial traum atic or infectious focus
No regional lym phadenopathy
Intravenous line infiltration
Sm allpox vaccination, norm al variant of usual reaction to vaccination
Phytophotoderm atitis: o
Linear inflam m atory reaction, m im ics lym phangitis
o
Lim e rind, lim e juice, and certain plants can act as photosensitizing agents.
P.655
Treatment Initial Stabilization If patient septic, m anage airway and resuscitate as indicated.
ED Treatment
Antim icrobial therapy should be initiated with first dose in ED.
General principles: o
Consider local prevalence of MRSA and other resistant pathogens in addition to usual causes.
o
Usual outpatient treatm ent: 7–10 days
o
Elevation
o
Application of m oist heat
Acute lym phangitis, em piric coverage: o
Outpatient: oral dicloxacillin or cephalexin; alternatives: oral m acrolide or levofloxacin
o
Inpatient: IV nafcillin or equivalent
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Lym phangitis after dog or cat bite: IV am picillin/sulbactam
Methicillin-resistant S. aureus: o
Nosocom ial MRSA: IV vancom ycin or oral or IV linezolid
o
Com m unity-acquired MRSA:
Add oral TMP/SMX to em piric treatm ent or use oral clindam ycin alone.
Oral doxycycline or com bination of oral TMP/SMX and rifam pin m ay be effective for cases not responding to above.
More severe: IV clindam ycin or IV vancom ycin
Sporotrichosis: o
Itraconazole or saturated solution of potassium iodide (SSKI)
Mycobacterium m arinum : o
Localized granulom as are usually excised.
o
Antim icrobial therapy is usually reserved for m ore severe infections:
Lim ited data on what com bination of agents should be used
Rifam pin and etham butol m ay be best choice.
Medication (Drugs)
Am picillin/sulbactam : 1.5–3 g (peds: 100–300 m g/kg/24h up to 40 kg; >40 kg, give adult dose) IV q6h
Cephalexin: 500 m g (peds: 50–100 m g/kg/24h) PO q.i.d.
Clindam ycin: 450–900 m g (peds: 20–40 m g/kg/24h) PO or IV q8h
Dicloxacillin: 125–500 m g (peds: 12.5–25 m g/kg/24h) PO q6h
Doxycycline: 100 m g PO b.i.d. for adults
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Erythrom ycin base: (adult) 250–500 m g PO q.i.d.
Itraconazole (adult): 100–200 m g PO daily, continue until lesions resolve (6–12 weeks); peds: not approved for use
Levofloxacin: (adult only) 500–750 m g PO or IV daily
Linezolid: 600 m g PO or IV q12h (peds: 30 m g/kg/24h div. q8h)
Nafcillin: 1–2 g IV q4h (peds: 50–100 m g/kg/24h div. q6h); m ax. 12 g/24h
Rifam pin: 600 m g PO b.i.d. for adults
Saturated solution of potassium iodide (SSKI): 5–10 drops, increase to 40–50 drops (peds: 5–10 drops, increase to 25–40) PO t.i.d. Take in m ilk, juice, or carbonated beverage to avoid bitter taste.
Trim ethoprim /sulfam ethoxazole (TMP/SMX): 1 DS tab PO q12h (peds: 6–10 m g/kg/24h TMP div. q12h)
Vancom ycin: 1 g IV q12h (peds: 10 m g/kg IV q6h, dosing adjustm ents required under age 5 years); check serum levels.
Follow-Up Disposition Admission Criteria
Toxic appearing
History of im m une suppression
Concurrent chronic m edical illnesses
Unable to take oral m edications
Unreliable patients
Discharge Criteria
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Mild infection in a non–toxic-appearing patient
Able to take oral antibiotics
No history of im m une suppression or concurrent m edical problem s
Adequate follow-up within 24–48 hours
References 1. Rex JH, Okhuysen PC. Sporothrix schenckii. In: Mandell GL, Bennett JE, Dolin R, eds. Mandell, Douglas and Bennett's Principles and Practice of Infectious Diseases. 6th ed. New York: Elsevier/Churchill Livingstone; 2005:2984–2988. 2. Sm ego RA, Castiglia M, Asperilla MO. Lym phocutaneous syndrom e: a review of non-sporothrix causes. Medicine. 1999;78(1):38–63. 3. Swartz MN, Pasternack MS. Lym phadenitis and lym phangitis. In: Mandell GL, Bennett JE, Dolin R, eds. Mandell, Douglas and Bennett's Principles and Practice of Infectious Diseases. 6th ed. New York: Elsevier/Churchill Livingstone; 2005:1204–1214.
Miscellaneous SEE ALSO: Cellulitis; Lym phadenitis
Codes ICD9-CM 457.2 682.9
ICD10 I89.1
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Lym pho granulo m a Venereum
Lymphogranuloma Venereum Joel Kravitz
Basics Description Also known as strum a, tropical bubo, Nicolas-Favre-Durand disease
Etiology Chlam ydia trachom atis—serotypes L1, L2, and L3
Diagnosis Signs and Symptoms History Prim ary genital lesions:
Incubation: 3–30 days after sexual exposure to Chlam ydia trachom atis
Painless genital chancre lasts 2–3 days (rarely, a papule or vesicle) o
Initial lesion is rarely noticed.
Physical Exam
Inguinal adenopathy:
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o
Occurs 1–3 weeks after initial inoculation
o
Adenopathy is unilateral in two thirds of cases.
o
Buboes (large inguinal lym ph nodes) form in inguinal and fem oral chains.
o
Groove sign: scarred or coalescent buboes above and below inguinal ligam ent give a linear depression parallel to the inguinal ligam ent (seen in 30%).
o
Anal-receptive patients m ay develop hem orrhagic proctocolitis.
o
Perirectal lym phatic inflam m ation causes fistulae and strictures.
o
System ic sym ptom s (absent with chancroid) m ay include fever, m yalgias, headache, erythem a nodosum , nausea, and vom iting:
Meningoencephalitis is rare
Chronic com plications: o
Genital strictures, perineal and perianal fistulae, and elephantiasis of the ipsilateral leg
Tests Lab
Standard chlam ydia DNA probes do not test for lym phogranulom a venereum (LGV) strain.
False-positive VDRL in 20%
Serologic testing and culture are the standard.
Com plem ent fixation titers >1:64 are consistent with LGV infection.
Diagnostic Procedures/Surgery Bubo aspiration—specific but expensive and im practical
Differential Diagnosis
Genital herpes (ulcers usually not seen in LGV)
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Syphilis—nodes are nontender, longer incubation.
Chancroid—m ultiple ulcers, no system ic sym ptom s
Granulom a inguinale—lesions are painless and bleed easily.
P.657
Treatment Initial Stabilization No field or ED stabilization required
Medication (Drugs) Antibiotics:
First line—doxycycline: 100 m g PO b.i.d. for 3 weeks
Alternative—erythrom ycin: 500 m g PO q.i.d. for 3 weeks
Pregnancy Considerations Pregnant patients receive erythrom ycin.
Follow-Up Disposition Admission Criteria Hospitalization rarely needed (i.e., severe system ic sym ptom s)
Discharge Criteria Im m unocom petent patient without system ic involvem ent
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Issues for Referral
Outpatient follow-up required to confirm diagnosis and cure
Rectal infection m ay require retreatm ent.
References 1. Borchardt KA, Noble MA. Sexually Transm itted Diseases. Boca Raton, FL: CRC Press; 1997. 2. Centers for Disease Control and Prevention: 2002 guidelines for treatm ent of sexually transm itted diseases. MMWR. 2002;47:RR. 3. Ernst AA, Marvez-Valls E, Martin DH. Incision and drainage versus aspiration of fluctuant buboes in the em ergency departm ent during an epidem ic of chancroid. Sex Transm Dis. 1995;22(4):217–220. 4. Goens JL, Schwartz RA, DeWolf K. Mucocutaneous m anifestations of chancroid, lym phogranulom a venereum and granulom a inguinale. Am Fam Physician. 1994;49(2):415.
Codes ICD9-CM 099.1
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > M alaria
Malaria
Jordan Moskoff
Basics Description
Protozoan infection transm itted through the anopheles m osquito
Incubation period 8–16 days
Periodicity of disease owing to life cycle of protozoan: o
Exoerythrocytic phase: Im m ature sporozoites m igrate to liver where they rapidly m ultiply into m ature parasites (m erozoites)
o
Erythrocytic phase: m ature parasites released into circulation and invade RBC
o
Replication within RBC followed 48–72 hours later by RBC lysis and release of m erozoites into circulation, repeating cycle
o
Fever corresponds to RBC lysis.
Plasmodium Falciparum
Most cases and alm ost all deaths
Usually presents as an acute, overwhelm ing infection
Able to infect red cells of all ages: o
Results in greater degree of hem olysis and anem ia
Causes widespread capillary obstruction:
Pa ge 2 9 0
o
Results in end organ hypoxia and dysfunction
More m oderate infection in people who are on or who have recently stopped prophylaxis with an agent to which the falciparum is resistant
Posttraum atic im m unosuppression m ay cause relapse of m alaria in patients who have lived in endem ic areas.
Plasmodium Vivax and Ovale
May present with an acute febrile illness
Dorm ant liver stages (hypnozoites) that m ay cause relapse 6–11 m onths after the initial infection
Plasmodium Malariae May persist in the bloodstream at low levels up to 30 years
Etiology
Transm ission usually occurs from the bite of infected fem ale anopheles m osquito.
North Am erican transm ission possible: o
Anopheles m osquitoes on the east and west coasts of the United States
o
Transm ission m ay also occur through infected blood products and shared needles.
Pediatric Considerations
Sickle cell trait protective
Cerebral m alaria m ore com m on in children
In highly endem ic areas with m inim al lab capability, all children presenting with febrile illness m ay be treated.
Pregnancy Considerations Pregnant patients especially prim igravid at higher risk
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Diagnosis Signs and Symptoms Timing
P. falciparum —exhibits within 8 weeks of return
P. vivax—delayed several m onths
Most sym ptom atic within 1 year
General
Malaise
Chills
Fever—usually >38°C: o
Classic m alaria paroxysm :
Fifteen m inutes to 1 hour of chills
Followed by 2–6 hours of nondiaphoretic fever ≤39–42°C
Profuse diaphoresis followed by defervescence
Pattern every 48 hours (vivax and ovale) or every 72 hours (falciparum )
o
Fever pattern m ay be varied—rare to have classical fever.
Orthostatic hypotension
Myalgias/arthralgias
Hematology
Hem olysis: o
Blackwater fever—nam ed from the dark color of the urine partially owing to hem olysis in overwhelm ing falciparum infections
Jaundice
Splenom egaly: o
More com m on in chronic infections
o
May cause splenic rupture
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CNS—Cerebral Malaria
Headache
Focal neurologic findings
Mental status changes
Com a
Seizures
GI
Em esis
Diarrhea
Abdom inal pain
Pulmonary
Shortness of breath
Rales
Pulm onary edem a
Severe Malaria One or m ore of the following:
Greater than 20% m ortality even with optim al m anagem ent
Prostration—unable to sit up by oneself
Im paired consciousness
Respiratory distress or pulm onary edem a
Seizure
Circulatory collapse
Abnorm al bleeding
Jaundice
Hem oglobinuria
Severe anem ia
Essential Workup Oil em ersion light m icroscopy of a thick-sm ear Giem sa stain:
Dem onstrates intraerythrocytic m alaria parasites
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Cannot exclude diagnosis without three negative sm ears in 48 hours
Only high degrees of parasitem ia will be evident on a standard CBC sm ear.
Tests Lab
CBC: o
Anem ia—25%
o
Throm bocytopenia—70% 40°C
Acetam inophen
Mist/cool-air fans
Naloxone, D 5 0 W (or Accu-Chek), and thiam ine if altered m ental status
ED Treatment
Dependent on identifying the type of m alaria present and geographic area of acquisition
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Assum e drug resistant until proven otherwise.
Plasm odium vivax, Plasm odium ovale, Plasm odium m alariae, and non–chloroquine-resistant P. falciparum : o
Treated with oral chloroquine in both adults and children:
o
Chloroquine—safe in pregnant wom en
Chloroquine-sensitive for falciparum , including Central Am erica, Caribbean, and Middle East
o
Eradicate persistent hypnozoites in vivax and ovale with prim aquine beginning after com pletion of course of chloroquine.
Chloroquine-resistant falciparum infection—PO treatm ent options: o
Quinine, plus
Doxycycline (avoid in pregnant wom en and children 8 years only, 1.5–2 m g/kg (m ax. 100 m g) b.i.d. for 5–7 days
Malarone (atovaquone/proguanil): o
Prophylaxis: 250 m g/100 m g PO per day
o
Treatm ent: 1,000 m g/400 m g (4 tablets) PO per day for 3 days
Mefloquine: 1250-m g single dose (peds: 25-m g/kg single dose)
Naloxone (Narcan): 2 m g (peds: 0.1 m g/kg) IV or IM initial dose
Prim aquine phosphate: 15-m g base (peds: 0.3-m g base/kg/24h) PO for 14 days
Pyrim etham ine-sulfadoxine (Fansidar): three tablets PO on last day of quinine treatm ent
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Quinidine gluconate: 10 m g/kg loading dose (m ax. 600 m g) in norm al saline infused slowly over 1–2 hours, followed by continuous infusion of 0.02 m g/kg/m in until patient is able to begin oral therapy
Quinine: 650 m g PO t.i.d. for 3–7 days
Quinine dihydrochloride: 20 m g salt/kg loading dose in 5% dextrose over 4 hours, followed by 10 m g salt/kg over 2–4 hours q8h (m ax. 1,800 m g/d) until patient is able to begin oral treatm ent
Thiam ine (vitam in B 1 ): 100 m g (peds: 50 m g) IV or IM
Follow-Up Disposition Admission Criteria
ICU adm ission for severe P. falciparum infection
Suspected acute P. falciparum infection
Severe dehydration
Inability to tolerate oral solution/m edication
More than 3% of RBC containing parasites
Discharge Criteria
Non–P. falciparum infection
Able to tolerate oral m edications
References 1. Stanley J. Malaria. Em erg Med Clin North Am . 1997;15:113–155. 2. Suh K. Malaria. Can Med Assoc J. 2004;170(4):1693–1702. 3. White NJ. The treatm ent of m alaria. N Engl J Med. 1996;335:800–806.
Codes
Pa ge 2 9 1
ICD9-CM 84.6
ICD10 B54
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > M algaigne F racture
Malgaigne
Fracture Theodore Chan
Basics Description
Am ong m ost unstable pelvic fractures: o
Displacem ent or potential displacem ent of entire hem ipelvis
Vertical shear forces result in anterior and posterior disruption of hem ipelvis.
Malgaigne fracture indicates that significant forces were applied to pelvic bones.
Fractures often occur from vehicular traum a, pedestrian struck by autom obile, or falls from heights.
Incidence As m any as 20% of all vehicular traum a fatalities have associated Malgaigne fracture.
Etiology
Involves at least two breaks in continuity of pelvic ring
Tile type C pelvic fracture: o
Resulting in rotational and vertical instability in
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pelvic ring (see Pelvic Fracture)
Both anterior and posterior disruption with real or potential displacem ent of intervening fragm ents or hem ipelvis o
Anterior disruption of sym physis pubis; 2–4 pubic ram i fractures
Posterior displacem ent and instability through sacrum , sacroiliac joint, or ileum
Pediatric Considerations
Children can have proportionately greater blood loss with pelvic fractures.
Nonaccidental traum a should always be considered.
Associated Conditions Pelvic hem orrhage and hem orrhagic shock:
Intra-abdom inal
Genitourinary and urinary tracts
Gynecologic, including uterine and vaginal
Neurologic
Major vessel
Diagnosis Signs and Symptoms
Gross pelvic instability, often with anterior iliac crest displaced or m obile
Shortening of legs from m igration of hem ipelvis
Ecchym oses, swelling, abrasions, and open wounds involving hips, groin, buttocks, perineum , pelvis
Severe pain on pelvic m ovem ent, tilt, and com pression
Often presents in setting of m ultiple traum a
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Evidence of perineal, urethral, rectal, and vaginal injuries
In hem orrhagic shock: o
Tachycardia, hypotension, narrowed pulse pressure
o
Altered m ental status
o
Cool and pale extrem ities
Essential Workup
Pelvic radiography is m ost valuable initial diagnostic test.
Single anteroposterior (AP) view of pelvis should be done early for any m ajor traum a victim in whom pelvic fracture is suspected: o
Most m algaigne fractures will be seen on AP view of pelvis.
Inlet projection (30° caudal angulation) allows visualization of posterior pelvis: o
May aid in assessm ent of posterior displacem ent
Other radiographic signs suggesting presence of Malgaigne fracture include the following: o
Pubic sym physis disruption with diastasis >15 m m
o
Sym physis disruption associated with overlapping of pubis
o
Sym physis disruption associated with unilateral fracture of both ram i
o
Bilateral breaks of both pelvic ram i or m arkedly displaced unilateral fractures of both ram i
o
Vertical fracture of sacrum (these fractures rarely occur as isolated pelvic fractures)
o
Asym m etry of iliac wings
o
Avulsion of ischial spine or L-5 transverse process associated with hem ipelvis m igration
Tests Lab
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Type and cross-m atch.
Hem oglobin/hem atocrit, platelet count, and coagulation studies (PT/PTT)
Imaging
Com puted tom ography scan: o
To delineate Malgaigne fracture and retroperitoneal hem atom a
Magnetic resonance im aging m ay be indicated with evidence of neurologic injury.
Abdom inal ultrasound and diagnostic peritoneal lavage are rapid bedside evaluations for intraperitoneal hem orrhage: o
Avoid false-positive results (higher m ortality rate in victim s with pelvic fractures who undergo negative laparotom y)
Diagnostic Procedures/Surgery
Diagnostic peritoneal lavage: o
Supraum bilical open approach for diagnostic peritoneal lavage for Malgaigne fracture
Surgery as indicated
Differential Diagnosis
Other pelvic fractures: o
Straddle fracture
o
Open-book fracture
o
Severe m ultiple pelvic fractures; see Pelvic Fracture
Intra-abdom inal injury and hem orrhage
Treatment Pre Hospital
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Controversy: o
Pneum atic antishock garm ent (PASG) as alternative in victim s suspected of having pelvic fracture:
Particularly when faced with prolonged transport tim e or hem odynam ic instability
Caution: o
Aggressive fluid resuscitation m ust occur before deflation of PASG abdom inal com partm ent if it has been used.
P.661
Initial Stabilization Airway, breathing, and circulation m anagem ent (ABCs) of traum a care:
Avoid using lower extrem ity IV sites.
Aggressive resuscitation with blood or crystalloid: o
O-negative or type-specific blood if hem odynam ically unstable
Im m obilize pelvis to prevent further injury and decrease bleeding.
PASG: Use in ED is controversial, but allows rapid pelvic im m obilization and pelvic com pression to slow bleeding.
External fixator requires m ore tim e to place than PASG, but “splints― pelvis in sim ilar m anner. o
Contraindicated in severely com m inuted Malgaigne fracture
Placem ent of stabilization device should not interfere with further workup and care (e.g., ultrasound [US], diagnostic peritoneal lavage [DPL]).
Diagnostic Procedures/Surgery
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Pelvic hem orrhage:
Angiography and selective vessel em bolization: o
Particularly for sm all-vessel arterial bleeding
Direct operative control of pelvic bleeding; m ost likely necessary for large vessels
ED Treatment
Im m ediate traum a surgery and orthopedics consultation
Nothing by m outh
Prioritization of studies: com puted tom ography, angiography, or surgery: o
In hem odynam ically unstable patient, rapidly perform ed US or DPL can determ ine treatm ent course.
o
If US or DPL aspirate is positive for bleeding, patient should undergo celiotom y with external pelvic fixation followed by selective angiography.
o
If DPL or US is negative, patient should undergo external fixation as appropriate, followed by selective angiography.
o
Hem odynam ically stable patient m ay undergo com puted tom ography evaluation of abdom en, pelvis, and retroperitoneum with external fixation as appropriate.
Special Therapy Blood products:
Cross-m atched, type specific, or O-negative
Four to 6 IU (peds: 10 m L/kg initial transfusion)
IV Fluids Crystalloid fluids, norm al saline, or lactated Ringer solution:
2-L IV bolus (peds: 20 m L/kg bolus)
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Surgery
As indicated on basis of clinical findings and orthopedic/surgical consult
Pelvic hem orrhage: o
Direct operative control of pelvic bleeding; m ost likely necessary for large vessels
o
Angiography and selective vessel em bolization, particularly for sm all-vessel arterial bleeding
Follow-Up Disposition Admission Criteria
All patients with Malgaigne fractures because of the m agnitude of the insult, instability of fracture, and likelihood of hem orrhage and concom itant injury.
Adm it to intensive care unit or m onitored setting.
Discharge Criteria Stable patients without Malgaigne fracture
References 1. Allen CF, Goslar PW, Barry M, et al. Managem ent guidelines for hypotensive pelvic fracture patients. Am Surg. 2000;66:735–738. 2. Am erican College of Surgeons, Com m ittee on Traum a. Advanced Traum a Life Support for Doctors. 7th ed. Chicago: Am erican College of Surgeons; 2004. 3. Coppola PT, Coppola M. Em ergency departm ent evaluation and treatm ent of pelvic fractures. Em erg Med Clin North Am . 2000;18:127. 4. Lashutka MK, Bahner D, Werm an H. Adult pelvic fractures. Traum a
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Rep. 2002;3:1–12
Miscellaneous SEE ALSO: Hem orrhagic Shock; Pelvic Fracture
Codes ICD9-CM 808.43 808.8
ICD10 S32.7
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > M allo ry-Weiss Syndro m e
Mallory-Weiss
Syndrome Robert C. Montana
Basics Description
Partial-thickness intralum inal longitudinal m ucosal tear of distal esophagus or proxim al stom ach
Sudden increase in intra-abdom inal and/or transgastric pressure causes: o
Mild to m oderate subm ucosal arterial and/or venous bleeding:
May be related to underlying pathology
“Mushroom ing― of stom ach into esophagus during retching has been observed endoscopically.
Etiology
Associated with: o
Seizures
o
Forceful coughing/laughing
o
Lifting
o
Straining
o
Blunt abdom inal traum a
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o
Childbirth
o
Cardiopulm onary resuscitation
Risk factors: o
Alcoholics:
Especially after recent binge
o
Patients with hiatal hernia
o
Hyperem esis gravidarum
Greater bleeding associated with: o
Portal hypertension
o
Esophageal varices
o
Coagulopathy
Diagnosis Signs and Symptoms History
Multiple bouts of nonbloody vom iting and/or retching followed by hem atem esis: o
Most bleeding is sm all and resolves spontaneously.
o
Massive life-threatening hem orrhage can occur.
Epigastric pain
Back pain
Dehydration: o
Dizzy, light-headed; syncope
Physical Exam
Hem atem esis
Melena
Postural hypotension
Shock
Essential Workup
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CBC
Rectal exam for occult blood
Tests Lab
Prothrom bin tim e (PT), partial throm boplastin tim e (PTT), INR
Electrolytes, BUN, creatinine, glucose
Am ylase/lipase if abdom inal pain
Type and cross-m atch: o
At least four units of packed red blood cells (PRBCs) if bleeding is severe
ECG if elderly or with cardiac history
Imaging
Upright chest radiograph for free air from esophageal or gastric perforation
Upper endoscopy (esophagogastroscopy): o
Procedure of choice to locate, identify, and treat source of bleeding
Differential Diagnosis
Nasopharyngeal bleeding
Hem optysis
Esophageal rupture (Boerhaave syndrom e)
Esophagitis
Gastritis
Gastroenteritis
Duodenitis
Ulcer disease
Varices
Carcinom a
Vascular-enteric fistula
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Hem angiom a
Treatment Pre Hospital
Airway control: o
One hundred percent oxygen or intubate if unresponsive or airway patency in jeopardy
If hem odynam ically unstable or m assive hem orrhage: o
Initiate two large-bore IV catheters.
o
One-liter bolus (20 m L/kg) lactated Ringer (LR) solution or 0.9% norm al saline (NS)
o
Trendelenburg position
P.663
Initial Stabilization
Airway, breathing, and circulation m anagem ent (ABCs): o
Intravenous access with at least one large-bore catheter; m ore if unstable
o
Central catheter placem ent if unstable for m ore efficient delivery of fluids and m onitoring of central venous pressure
o
IV fluids of either 0.9% NS (or LR) at 250 m L/h if stable; wide open if hem odynam ically unstable
o
Dopam ine for persistent hypotension unresponsive to aggressive fluid resuscitation
Large-bore Ewald tube placem ent with evidence of large am ount of bleeding: o
Safe
Pa ge 2 9 2
o
Will not aggravate Mallory-Weiss tear
o
Lavage blood from stom ach with water while patient is on side in Trendelenburg position.
Nasogastric (NG) tube placem ent to check for active bleeding
Transfuse O-negative red blood cells im m ediately if hypotensive and not responsive to 2 L of crystalloid.
Most bleeding stops spontaneously with conservative therapy.
ED Treatment
NPO
Transfuse PRBCs if unstable or lowering hem atocrit with continued hem orrhage.
Bladder catheter to m onitor urine output
Monitor fluid status closely.
With continuing hem orrhage, arrange for im m ediate endoscopy: o
Control bleeding endoscopically via:
Electrocoagulation
Injection therapy (epinephrine)
Band ligation
Hem oclips
Application of blood-clotting agents
Intravenous vasopressin in m assive bleeding and unavailable endoscopy
In persistent/unresponsive hem orrhage, angiographic infusion of vasopressin
Surgery—last but definitive treatm ent m odality using techniques to oversew bleeding site or perform gastrectom y
Failure of above m ay require gastric arterial em bolization in patients of poor surgical risk.
Pa ge 2 9 2
Avoid Sengstaken-Blakem ore tubes (especially in presence of hiatal hernia).
Antiem etics, antacids, and H 2 blockers are helpful.
Medication (Drugs)
Dopam ine: 2–20 µg/kg/m in IV piggyback (IVPB)
Vasopressin: 0.1–0.5 IU/m in IVPB titrating up to 0.9 IU/m in as necessary
Follow-Up Disposition Admission Criteria
ICU adm ission for: o
Continued or m assive hem orrhage
o
Hem odynam ic instability
o
Extrem e age
o
Poor underlying m edical condition
o
Com plications
General floor adm ission if never unstable and m inim al bleed that has since cleared
Discharge Criteria
History of m inim al bleed that has stopped
Hem odynam ically stable
Norm al/stable hem atocrit
Negative or trace hem e-positive stool
Negative or trace gastric aspirate
References
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1. Hastings PR, et al. Mallory-Weiss syndrom e: review of 69 cases. Am J Surg. 1981;142(5);560–562. 2. Michel L, et al. Mallory-Weiss syndrom e: evolution of diagnostic and therapeutic patterns over two decades. Ann Surg. 1980;192:716–721. 3. Sugawa C, et al. Mallory-Weiss syndrom e: a study of 224 patients. Am J Surg. 1983;145(1):30–33. 4. Younes Z, et al. The spectrum of spontaneous and iatrogenic esophageal injury: perforations, Mallory-Weiss tears, and hem atom as. J Clin Gastroenterol. 1999;29(4):306–317.
Miscellaneous SEE ALSO: Gastrointestinal Bleeding
Codes ICD9-CM 530.7
ICD10 K22.6
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > M alro tatio n
Malrotation
Andrea Bracikowski Sally Santen
Basics Description
Incom plete rotation and fixation of intestine during em bryogenesis during transition from extracolonic position during 10th week of gestation
Risk factor: o
Congenital defect
Associated conditions: o
o
Gastrointestinal anom alies:
Duodenal stenosis/atresia/web
Meckel diverticulum
Intussusception
Gastroesophageal reflux
Om phalocele or gastroschisis
Congenital diaphragm atic hernia
Hirschsprung disease
Metabolic acidosis
Etiology
Duodenojejunal junction rem ains right of m idline.
Cecum rem ains in the upper left abdom en with abnorm al
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m esenteric attachm ents.
Abnorm al anatom y predisposes to obstruction and other conditions.
Usually found in com bination with other congenital anom alies (70%): cardiac, esophageal, urinary, anal
Epidemiology
1 in 500 live births
Incidence: o
In neonates, m ale-to-fem ale ratio 2:1
o
40% of patients present within first year
o
50% diagnosed by age 1 m onth
o
75% diagnosed by age 1 year of life
Diagnosis Signs and Symptoms
Neonates: o
Bilious em esis
o
Abdom inal distention
o
Bloody stools
o
Constipation/obstipation
o
Difficulty feeding
o
Poor weight gain
Older than 1 year: abdom inal pain followed by bilious em esis
Older children and adolescents: o
Chronic vom iting
o
Interm ittent colicky abdom inal pain
o
Diarrhea
o
Hem atem esis
Pa ge 2 9 2
o
Constipation
o
May not exhibit abnorm al physical findings at tim e of presentation (50–75%)
Adults: sym ptom s vague and nonspecific
General: o
Dehydration, acidosis
o
Peritonitis
o
Ischem ic bowel
o
Sepsis, shock
History
Bilious vom iting is hallm ark.
Other pertinent history—acute or chronic abdom inal pain, poor feeding, lethargy
Physical Exam
Abdom inal exam ination
Evaluate for congenital anom alies.
Essential Workup Diagnosis is suggested by history and physical exam findings and is delineated by contrast radiography.
Tests Lab
CBC
Electrolytes, BUN, creatinine, glucose; hypoglycem ia in infants with poor feeding and em esis
Urinalysis
Imaging
Plain abdom inal radiographs: o
Diagnostic in Table o f C o ntents > M astitis
Mastitis
Marco Coppola Timothy Stallard
Basics Etiology
Staphylococcus aureus m ost com m on
Coagulase-negative Staphylococcus, Streptococcus species, Escherichia coli, Haem ophilus influenzae
Diagnosis Signs and Symptoms
Fever usually >39°C
Chills, rigors, m alaise
Tachycardia
Breast pain, induration, erythem a, warm th; usually unilateral
Onset typically 2–3 weeks to m onths postpartum while breast-feeding
Rare during first postpartum week
More com m on in advanced m aternal age and patients with diabetes
Pa ge 2 9 5
Essential Workup Physical exam ination with special attention to detecting abscess:
Abscess is frequently difficult to detect, but is m ore com m on in periareolar area.
Purulent nipple discharge with palpation
Tests Lab Breast m ilk culture usually not required
Imaging Consider breast ultrasound if abscess is suspected:
Mam m ography is not indicated acutely.
Differential Diagnosis
Breast engorgem ent: o
Transient fever Table o f C o ntents > M easles
Measles
Austen Chai
Basics Etiology
Negative-strand param yxovirus
Hum ans are only known reservoir.
Highly contagious; outbreaks seen in nonim m unized or underim m unized
Diagnosis Signs and Symptoms Incubation (8–14 days)
Transm ission via direct contact or inhalation of infectious droplet
Prodrome (2–8 days)
Mild respiratory illness
Koplik spots: o
Sm all white to grayish-blue specks on buccal m ucosa
o
Pathognom onic for rubeola
o
Transient and disappear within 48 hours after onset
Pa ge 2 9 7
of rash
Active Disease
Cough, coryza, conjunctivitis with fever and rash
Rash begins on head and neck and spreads centrifugally downward: o
Initially pale, then discrete and m aculopapular, and ultim ately, confluent
o
Clinical im provem ent seen in 48 hours of appearance of rash
o
Rash clears in 3–4 days and m ay desquam ate as rash fades.
Complications
Respiratory: o
Cough m ay persist for 1–2 weeks after m easles infection.
o
Pneum onia seen m ost com m only in im m unocom prom ised
o
Most com m on cause of fatality
o
Laryngotracheobronchitis in patients Table o f C o ntents > M edial M eniscus Injury
Medial Meniscus
Injury Charles S. Graffeo
Basics Description
Am ong m ost com m on adult knee injuries
Medial m eniscus injury 10 tim es m ore com m on than lateral
Sudden rotary m otion of knee associated with squatting, pivoting, turning, and bending.
Com m on in those sports with low stance positions: o
Wrestling and football
o
Occupations such as carpet installers and plum bers
Etiology
Medial m eniscus is m ore firm ly attached to the joint capsule: o
Less m obile than the lateral m eniscus
o
Predisposing it to injury when tensile/com pressive forces are applied
Tears are the result of tensile or com pressive forces between the fem oral and tibial condyles: o
With knee flexion, the fem ur rotates internally on the
Pa ge 2 9 9
flexed tibia, displacing the m edial m eniscus toward the center of the joint. o
With rapid forceful extension, the m eniscus m ay be trapped centrally, resulting in peripheral segm ent stretching or tear.
o
Extension of the tear m ay result in a free segm ent that m ay becom e displaced into the joint, resulting in a true locked joint.
Diagnosis Signs and Symptoms
Usually present within 24 hours of acute injury
May report hearing a pop, feeling a tear, catch, lock, or a click
Usually occurs with rotational force, often when knee is flexed
History
Patient m ay recall the knee “giving way.―
Inability to fully extend knee is com m on.
Effusion found in 50% and usually occurs over 6–12 hours
Pain often interm ittent/localized to the joint line
Unlike ligam entous injury, patients often report com pletion of activities at tim e of injury.
Physical Exam
Physical exam ination with special attention to joint line tenderness: o
High predictive value of 75–85% and neurovascular system
Pa ge 2 9 9
Effusion is found in 50% and is typically delayed in onset.
Inability to extend the joint at 20–45° secondary to true or pseudo locking is a com m on finding.
Essential Workup
Lim itation of extension owing to severe pain from m uscle spasm /effusion suggests pseudo locked joint
True locked joint from torn fragm ent within the joint occurs in only 30%.
Provocative testing should be deferred until severe pain resolves: o
McMurray, Apley, Steinm ann, Childress, and Helfet
Recent system atic review concludes that physical diagnostic tests have low diagnostic accuracy.
Tests Lab If arthrocentesis perform ed, send joint fluid for cell count, protein and glucose, gram stain, culture, and crystals, as indicated.
Imaging
Plain radiograph m ay dem onstrate effusion or associated bony abnorm alities.
MRI has replaced arthrography: o
Diagnostic accuracy greater than 90–98%, depending on type of injury
Diagnostic Procedures/Surgery
Arthroscopy the standard for diagnostic accuracy
Arthrocentesis: o
May afford significant sym ptom atic relief when effusion is present
o
Aspiration of bloody fluid suggests cruciate ligam ent tear or injury to peripheral vascular part of
Pa ge 2 9 9
m eniscus.
Differential Diagnosis
Osteochondral fractures
Osteochondritis dessicans
Patellofem oral joint syndrom es
Anterior and posterior cruciate ligam ent injury
Medial/lateral collateral ligam ent injury
Iliotibial band syndrom e
Lum bar radiculopathy
Gout and other inflam m atory arthropathies
P.683
Treatment Pre Hospital
Application of ice packs
Im m obilization in a position of com fort
Careful neurovascular exam ination
Assess for dislocations and associated injuries.
Initial Stabilization Assess for significant associated injuries.
ED Treatment
Arthrocentesis m ay afford relief with large effusions and assist in reducing locked joint.
Arthrocentesis should be followed by application of com pressive dressing.
Reduction of locked joint should be perform ed within first
Pa ge 2 9 9
24 hours after injury: o
With patient seated, hang extrem ity off edge of exam ination table at 90°.
o
This alone m ay reduce locked joint.
Applying gentle traction and rotation of tibia usually result in reduction of the locked joint.
Nonsteroidal anti-inflam m atory drugs, both parenteral and oral
Weight bearing and range of m otion are perm itted as tolerated.
Individuals unable to bear weight or those with severe restriction of range of m otion m ay be placed in a knee im m obilizer or crutches as needed.
Definitive treatm ent by orthopedic consultant: o
Operative vs. nonoperative treatm ent is dependent on m ultiple factors.
Medication (Drugs)
Nonsteroidal anti-inflam m atory m edications
Supplem ent with narcotic analgesia for breakthrough pain
Follow-Up Disposition Admission Criteria
Intractable pain is suggestive of true locked joint and m ay require em ergent orthopedic consult.
Evidence of potential for neurovascular com prom ise
High-risk elderly patients unable to m anage splinting
Pa ge 2 9 9
devices
Discharge Criteria
Patients capable of following a structured discharge plan
No com orbid conditions likely to negatively im pact outcom e
Issues for Referral Refer all patients for close orthopedic follow-up
References 1. Antosia RE, Lyn E, Marx J. Rosen's Em ergency Medicine: Concepts and Clinical Practice. 5th ed. St. Louis, MO: Mosby; 2002. 2. Koski JA. Meniscal injury and repair: clinical status [Review]. Orthop Clin North Am . 2000;31:419–436. 3. Sim on RR, Koenigsknecht SJ, Em ergency Orthopedics the Extrem ities. 4th ed. McGraw-Hill2001. 4. Scholten RJ. The accuracy of physical diagnostic tests for assessing m eniscal lesions of the knee: a m eta-analysis. J Fam Pract. 2001;50:938–944. 5. Solom on DH. The rational clinical exam ination: does this patient have a torn m eniscus or ligam ent of the knee? JAMA. 2001;286:1610–1620.
Codes ICD9-CM 959.7
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > M éniè re Disease
Ménière
Disease Charles V. Pollack Jr.
Basics Description
Episodic vertigo, hearing loss, tinnitus, and aural fullness sensation, although all sym ptom s m ay not be present sim ultaneously
Estim ated to affect about 0.1% of United States. population
Affects m en and wom en equally
Fam ily history in greater than 7%
May develop at any age: o
Peak incidence between the ages of 20 and 50 years
Classically unilateral, but m ay be bilateral in up to 40% of cases
Characterized by recurrent, interm ittent attacks or rotatory vertigo, decreased hearing, tinnitus, and sensation of aural pressure
Attacks occur with little or no warning
Persists from 5 m inutes to several hours
Close clustering of attacks m ay occur
Pa ge 2 9 9
Hearing loss is progressive over tim e, sensorineural in nature, and initially involves lower frequencies.
Etiology
Endolym phatic hydrops: o
Progressive dilation of the endolym phatic space
o
Thought to be overproduction or reduced absorption of endolym phatic fluid
o
Long-term therapy directed at decreasing production or enhancing drainage of endolym ph
Im m une m echanism : o
Im m une com plex deposition in endolym phatic sac in patients with Ménière disease
o
Autoantibodies directed against endolym phatic sac in sera of Ménière patients
Diagnosis A diagnosis of exclusion
Signs and Symptoms History
Unilateral ear fullness and pressure
Decreased hearing
Tinnitus
Vertigo: o
Intense and whirling in nature
o
Reaching m axim um intensity within m inutes, slowly subsides over hours
Horizontal nystagm us, often with a rotational com ponent
Nausea and vom iting
Physical Exam
Pa ge 3 0 0
Patient typically lies with the affected ear up and avoids looking toward the norm al side because doing so exaggerates the nystagm us and dizziness.
Must exclude central CNS lesion, peripheral pathology in ear (ruptured TM, cholesteatom a, cerum en im paction, etc)
Essential Workup
Com plete history and neurologic exam
Patients with central vertigo or focal neurologic findings require neuroim aging
Focal findings include new unilateral hearing loss, usually with tinnitus
Tests Lab None routinely helpful
Imaging CT or MRI of brain:
Indicated for any patient with focal neurologic findings or central vertigo
The m ost im portant diagnosis to exclude is acoustic neurom a
Diagnostic Procedures/Surgery Patients with Ménière disease require audiom etry and electronystagm ography (ENG) testing, but these tests are not necessary to the ED evaluation.
Differential Diagnosis
Otologic: o
Chronic suppurative otitis m edia
o
Benign positional vertigo
o
Acoustic neurom a
o
Vestibular neuronitis
Pa ge 3 0 0
o
Otosclerosis
o
Otic capsule dysplasia
System ic: o
Vertebrobasilar insufficiency or stroke
o
Basilar m igraine
o
Epilepsy
o
Multiple sclerosis
o
Paget disease
o
Thyroid disease
o
Drugs/m edications
o
Autoim m une disorders
o
Syphilis
o
Head injury
o
CNS lesion
P.685
Treatment Pre Hospital
Vertigo and neurologic sym ptom s can represent a stroke: o
Rapid transport to ED
Protect patient from falling
Maintain in com fortable position
IV isotonic fluids for patients with vom iting
Monitor for dysrhythm ia
Initial Stabilization
IV hydration with isotonic fluids
Benzodiazepines
Pa ge 3 0 0
Antiem etics, benzodiazepines
ED Treatment Supportive therapy
Medication (Drugs)
Sym ptom atic: o
Diazepam : 5–10 m g PO, PR, or IV
o
Lorazepam : 0.5–2.0 m g PO, IV, or IM
o
Meclizine: 12.5–25 m g PO q8h
o
Metoclopram ide: 10 m g IV or IM
o
Prom ethazine: 10–25 m g PO, PR, IV or IM.
Therapeutic (patients with established diagnosis of Ménière disease): o
Acetazolam ide: 250 m g PO daily
o
Furosem ide: 20 m g PO daily
o
Hydrochlorothiazide (HCTZ): 25–50 m g PO daily
o
Triam terene: 100 m g PO daily
Follow-Up Disposition Admission Criteria
Central cause of vertigo
Patients refractory to ED therapy
Discharge Criteria
Patient with norm al neurologic exam ination
Sym ptom s adequately controlled in ED
Refer to neurology or ear-nose-throat clinic for outpatient
Pa ge 3 0 0
audiom etry and ENG testing.
Recurrent attacks are typical.
Restrict sodium , tobacco, caffeine, and alcohol intake.
Avoid driving, operating dangerous equipm ent, and working at heights until attacks have resolved and sedating m edications have been withdrawn.
Issues for Referral
Persistent sym ptom s
Concern for ear pathology
References 1. Jam es A: Ménière's disease. Clin Evid. 2004;11:664–672. 2. Kim HH. Trends in the diagnosis and m anagem ent of Ménière's disease. Otolaryngol Head Neck Surg. 2005;132:722–726. 3. Knox GW, McPherson A. Ménière's disease: differential diagnosis and treatm ent. Am Fam Physician. 1997;55:4:1185–1190. 4. Saeed SR. Diagnosis and treatm ent of Ménière's disease. Br Med J. 1998;316:368–372. 5. Thai-Van, et al. Ménière's disease pathophysiology and treatm ent. Drugs. 2001;61:8:1089–1102.
Miscellaneous SEE ALSO: Dizziness
Codes ICD9-CM 388.31 386.00 386.10 386.20
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ICD10 H81.0
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > M eningitis
Meningitis
Austen Chai Patricia Shipley
Basics Description CNS infection
Etiology
Bacterial: o
Neonates: group B streptococcus, gram -negative bacilli, Listeria species infection
o
Children/adults: Streptococcus pneum oniae, Neisseria m eningitides, Haem ophilus influenzae (now rare owing to vaccination)
o
Elderly/alcoholic: S. pneum oniae, gram -negative bacilli, Listeria species infection
o
Neurosurgical patients: staphylococcus- and gram -negative organism s
o
Transplant recipients and dialysis patients: rising incidence of Listeria species infection
o
AIDS: as above, plus tuberculosis, syphilis
Viral
Fungal
Chem ical, drug, or toxin induced
Pa ge 3 0 0
Pediatric Considerations
Pneum ococcus m ost com m on cause of bacterial m eningitis
Pneum ococcal vaccine now part of childhood im m unization schedule
Dexam ethasone reduces sensorineuronal hearing loss caused by H. influenzae.
Meningitis does not present as uncom plicated febrile seizure.
Diagnosis Signs and Symptoms General
Fever
Meningism us: o
Kernig: flexed knee resists extension (bilateral).
o
Brudzinski: flexion of neck produces flexion at hips.
Confusion/altered m ental state
Headache
Photophobia
Papilledem a
Focal CNS abnorm alities
Seizures
Petechial rash (m eningococcal)
Associated infections: sinusitis, otitis, pneum onia
Infant/Pediatric
Fever or hypotherm ia
Lethargy
Weak suck
Vom iting/dehydration
Pa ge 3 0 0
Respiratory distress
Irritability
Bulging fontanel
Meningism us: com m only absent when 80% PMNs
Protein >200 m g/dL
Glucose 3 m onths old and adults
Vancom ycin plus (aztreonam or chloram phenicol) plus Bactrim : o
Consider only for severe penicillin allergy (i.e., anaphylaxis).
o
Do not delay therapy for lesser allergy history.
o
Consult infectious disease specialist.
Aztreonam : o
May use in place of cephalosporins in patients allergic to penicillin
Pa ge 3 0 1
Medication (Drugs)
Am ikacin: (peds: 7.5 m g/kg IV q8h)
Am picillin: 2 g (peds: 50–100 m g/kg q6h–q8h) IV q4h
Aztreonam : 2 g (peds: 30 m g/kg) IV q6h–q8h
Bactrim : 4–5 m g/kg TMP IV q12h
Cefotaxim e: 75 m g/kg IV q8h
Ceftazidim e: 2 g IV q8h
Ceftriaxone: 2 g (peds: 50–100 m g/kg) q12h
Chloram phenicol: 1 g (peds: 25 m g/kg) IV q6h
Dexam ethasone: 0.4 m g/kg IV q12h for 2 days
Gentam icin: (peds: 2.5 m g/kg IV q8h)
Hydrocortisone: 100–300 m g IV
Meropenem : 40 m g/kg q8h
Tobram ycin: (peds: 2.5 m g/kg IV q8h)
Vancom ycin: 1 g (peds: 15 m g/kg q6h) q6h–q12h
Follow-Up Disposition Admission Criteria
All known or suspected cases of bacterial infections
Im m unocom prom ised host
Any toxic-appearing patient
Discharge Criteria
Clear viral infection with well-controlled sym ptom s
Thorough and specific discharge instructions
Careful follow-up plan discussed with prim ary care physician
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References 1. De Gans J, van de Beek D. Dexam ethasone in adults with bacterial m eningitis. N Engl J Med. 2002;347:1549–1556. 2. Goldm an L, ed. Cecil Textbook of Medicine. 21st ed. Philadelphia: WB Saunders; 2000: 1645–1654. 3. Hasbun R, et al. Com puted tom ography of the head before lum bar puncture in adults with suspected m eningitis. N Engl J Med. 2001;345:1727–1733. 4. Pong A, Bradley JS. Bacterial m eningitis and the newborn infant. Infect Dis Clin North Am . 1999;13:711–733. 5. Preventing pneum ococcal disease am ong infants and young children. Recom m endations of the Advisory Com m ittee on Im m unization Practices (ACIP). MMWR Recom m Rep. 2000;49(RR-9):1–35. 6. Tunkel AR, et al. Practice guidelines for m anagem ent of bacterial m eningitis. Clin Infect Dis. 2004;39:1267–1284.
Codes ICD9-CM 320 047.9
ICD10 G03.9
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > M eningo co ccem ia
Meningococcemia
Ann Buchanan
Basics Description
Acquired from close contact with an infected individual or an asym ptom atic carrier by inhalation of airborne nasopharyngeal droplets carrying the bacteria
Bacteria attach to and enter nasopharyngeal epithelial cells.
Bacteria spread from the nasopharynx through the bloodstream via entry of vascular endothelium .
Most circulating m eningococci are elim inated by the spleen—som e penetrate endothelial cells at other sites to cause infection (m eninges, synovium , conjunctivae).
Meningococci produce an endotoxin (lipooligosaccharide): o
involved in pathogenesis of the skin, adrenal m anifestations, and vascular collapse
Hum an oropharynx/nasopharynx—only reservoir
Carrier usually has developed im m unity to serotype-specific antibody (not im m une to all serotypes): o
Age Table o f C o ntents > M etacarpal Injuries
Metacarpal
Injuries David Palafox
Basics Description
Most m etacarpal injuries are caused by crush injuries, a direct blow with hand versus object, orburn.
Most com m on fracture is boxer's fracture of distal fifth m etacarpal neck.
Diagnosis
Pain or swelling at the site of injury
Deform ity at the site of injury
Malalignm ent of the distal tip of the finger on flexion indicates rotational deform ity.
Lines drawn down the longitudinal axis of each digit in flexion norm ally should converge on the scaphoid volarly.
Lim itation of m ovem ent secondary to pain and anatom ic deform ity
Alert
Pa ge 3 0 4
Have a high suspicion for “fight bite.― This injury is the direct blow of a closed fist against a hum an tooth: o
Concern is violation of the extensor sheath, m etacarpophalangeal (MCP) joint, or m etacarpal head by a tooth with subsequent infection by oral flora.
Signs and Symptoms History Not all patients are truthful as to cause of injury.
Essential Workup Exam ination should pay specific attention to skin integrity and alignm ent of the distal phalanges in flexion and extension.
Tests Imaging
Hand radiographs when fracture suspected and/or to rule out opaque foreign body
Special radiographic views (CT) of the proxim al m etacarpals and the carpom etacarpal joints m ay be necessary for patients with a suggestive physical exam and no definite fracture on a standard three-view series.
Differential Diagnosis Fracture of the m etacarpal m ay be accom panied by dislocation of adjacent phalanges or carpal bones.
Treatment Pre Hospital
Most do not require EMS transport solely for m etacarpal
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injury.
Cautions: o
Metacarpal injuries should be splinted in position of com fort.
Initial Stabilization
Other, m ore serious injuries should be treated first.
Im m obilize hand pending evaluation.
Lacerations should be cleaned as soon as possible, and consideration should be given to the possibility of foreign body.
Therm al burns are treated with early analgesia.
ED Treatment
Elevation, rest, and interm ittent application of ice for the first 24 hours are appropriate treatm ent for all hand injuries (RICE).
Boxer's fractures usually have som e volar flexion of the distal fragm ent: o
Reduction should be attem pted for volar angulation of 40° or m ore.
o
Fractures of the fourth and fifth m etacarpals that are stable and with no significant rotational com ponent can be treated with a padded ulnar gutter splint.
Fractures of the index and m iddle finger m etacarpals are m ore difficult to stabilize: o
Radial gutter splint and early orthopedic referral
Thum b m etacarpal fractures are uniform ly com plicated and should all be referred early to a hand surgeon or orthopedist: o
Place in thum b spica splint.
Dislocations should be reduced im m ediately and splinted; m etacarpal dislocations are rare and frequently need open
Pa ge 3 0 4
reduction and pinning. P.695
Appropriate splinting position for the MCP joint is the intrinsic plus, or “cobra― position (20–30° wrist extension): o
MCP joint as close to 90° of flexion as possible
o
Proxim al interphalangeal (PIP) and distal interphalangeal (DIP) joints in extension
Antibiotics for oral flora should be started early for any open injury to the m etacarpals suspicious for injury against a tooth and m ay require curettage of the im paction site in the operating room .
Sim ple torus (buckle) fractures m ay be splinted and m ay be followed by a prim ary care physician.
Medication (Drugs)
Check for tetanus status and vaccinate per im m unization schedule.
Silvadene cream or bacitracin ointm ent is appropriate for therm al burn injury.
Analgesics m ay be necessary; nonsteroidal anti-inflam m atory drug (NSAID) or hydrocodone is usually sufficient.
For hum an bites or dirty wounds, adm inister am oxicillin/clavulanate (Augm entin), or o
A cephalosporin or other penicillinase-resistant antibiotic given parenterally is appropriate.
Pa ge 3 0 4
Follow-Up Disposition Admission Criteria
Open fractures or dislocations require urgent surgical intervention and should be adm itted.
All thum b m etacarpal fractures or dislocations should be seen by an orthopedist or hand surgeon because of the special im portance of the thum b in all activities of the hand.
Infection from a bite wound requires prom pt orthopedic consultation, adm ission for irrigation, débridem ent, and intravenous antibiotics.
Discharge Criteria
Patients with a stable transverse or oblique fracture in a good splint m ay be discharged for early orthopedic follow-up.
Metacarpal-carpal dislocations are usually unstable enough to require surgery even if reduction is achieved, but this m ay be sem iurgent rather than em ergent.
If a m etacarpal fracture produces im paired range of m otion or m isalignm ent of the finger, the patient will require surgical repair in the first several days after injury.
Pediatric Considerations Epiphyseal injuries m andate orthopedic referral.
References 1. Am erican Society for Surgery of the Hand. The Hand: Exam ination and Diagnosis. 3rd ed. New York: Churchill Livingstone; 1990.
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2. Am erican Society for Surgery of the Hand. The Hand: Prim ary Care of Com m on Problem s. 2nd ed. New York: Churchill Livingstone; 1990. 3. Am erican College of Radiology, Expert Panel on Musculoskeletal Im aging. Acute Hand and wrist traum a. 2001. 4. Harrison B, Holland P. Diagnosis and m anagem ent of hand injuries in the ED. Em erg Med Pract. 2005;7(2):.
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > M ethano l Po iso ning
Methanol
Poisoning Kirk Cumpston
Basics Description
Colorless, volatile liquid
Absorbed in 30–60 m inutes
Metabolized by liver
Half-life 4–8 hours
Mechanism : o
Inebriating
o
Nontoxic
o
Metabolites of form aldehyde and form ic acid produce toxic effects.
o
Uncouples oxidative phosphorylation
Form ic acid level determ ines degree of acidosis, visual sym ptom s, and m ortality.
Form ic acid—directly toxic to retinal and optic nerve tissue
Methanol m etabolism : o
Step 1: m ethanol converted to form aldehyde by liver enzym e alcohol dehydrogenase
Pa ge 3 0 4
o
Step 2: form aldehyde then rapidly converted by aldehyde dehydrogenase to form ic acid
o
Step 3: form ic acid is degraded to carbon dioxide and water by folate-dependent m echanism .
o
Steps 1 and 3 are rate-lim iting steps.
Etiology
Com m on sources of m ethanol: o
Wood alcohol
o
Windshield washer fluid
o
Inhalational abuse of carburetor cleaners
Fuel antifreeze solutions: o
Form alin
o
Gasoline
o
Paint solvents
o
Household cleaners
Sterno cans
Moonshine
Diagnosis Signs and Symptoms
GI: o
Anorexia
o
Nausea/vom iting
o
Abdom inal pain
CNS: o
Headache
o
Dizziness
o
Confusion
o
Inebriation
Pa ge 3 0 5
o
Com a
o
Seizures
Ophthalm ologic: o
Blurry vision
o
Photophobia
o
“Snow fields―
o
Mydriasis
o
Blindness
o
Optic disc:
Hyperem ia or pallor
Papilledem a
Essential Workup
History of all substances ingested
Inquire about visual sym ptom s.
Funduscopic exam ination
Drawn sim ultaneously: o
Arterial blood gas (ABG)
o
Serum m ethanol, ethylene glycol, isopropyl alcohol, and ethanol levels
o
Electrolytes, BUN, creatinine, and glucose
o
Measured serum osm olality (by freezing-point depression is preferred)
Tests Lab
Calculate anion gap = (Na + ) – (Cl - + HCO 3 - ): o
Norm al = 8–12.
Determ ine serum osm ol gap: o
Osm ol gap = m easured osm olality - calculated osm olarity:
Calculated osm olarity = 2(Na + ) + glucose/18 + BUN/2.8 + ethanol (in m g/dL)/4.6.
Pa ge 3 0 5
Traditionally an osm ol gap >10 is considered indication for ruling out occult m ethanol ingestion. However, potentially toxic serum concentrations of m ethanol can be present with osm ol gap 1 hour.
Ipecac-induced em esis not recom m ended
Activated charcoal: o
For potential coingestants
o
Poorly adsorbs m ethanol
Prevent Methanol Conversion to Toxic Metabolites
Pa ge 3 0 5
4-Methylpyrazole (4-MP, fom epizole, Antizol): o
Com petitive inhibitor of alcohol dehydrogenase
o
FDA approval for use in m ethanol poisoning
o
Indications for fom epizole therapy:
Intentional m ethanol ingestion
Accidental m ethanol ingestion of m ore than a sip
Altered m ental status or visual sym ptom s associated with unexplained osm ol gap and/or elevated anion gap m etabolic acidosis
P.697
o
Initiate before serum m ethanol concentration returns if intentional ingestion or m ore than a sip.
o
Advantages:
No need for continuous infusion
No inebriation/CNS depression
Ease of dosing
No hypoglycem ia, no hyponatrem ia, no hyperosm olality
No checking serum concentrations
Reduced nursing care and m onitoring
Occult m ethanol exposure can often be ruled out before second dose is needed.
o
Class C in pregnancy
Disadvantages:
Initial cost of product
Blurry vision
Transient elevation of LFTs
Ethanol therapy: o
Not FDA approved for treatm ent of m ethanol
Pa ge 3 0 5
o
Initiate before m ethanol level returns if potentially toxic ingestion is highly suspected or confirm ed by history.
o
Ethanol has greater affinity than m ethanol for alcohol dehydrogenase.
o
Slows m etabolism to form aldehyde and form ic acid by com petitive inhibition
o
Indications for ethanol therapy:
Intentional m ethanol ingestion
Accidental m ethanol ingestion of m ore than a sip
Altered m ental status or visual sym ptom s associated with unexplained osm ol gap and or elevated anion gap m etabolic acidosis
o
Therapeutic range is 100–150 m g/dL.
o
Continue until m ethanol level is 1 m L/kg of 100% m ethanol
Ophthalm ologic m anifestations
Severe m etabolic acidosis unresponsive to bicarbonate therapy
o
Persistent electrolyte or fluid im balance
Renal insufficiency
Serum m ethanol level >25 m g/dL
Continue hem odialysis until m ethanol level approaches zero.
Folic acid and folinic acid (leucovorin): o
Folic acid: cofactor required for conversion of form ic acid to carbon dioxide and water
o
Folinic acid: activated form of folic acid, used only for initial dose
o
Supplem ental folate im portant in m alnourished individuals (alcoholics)
Correct Acid-Base Abnormalities Sodium bicarbonate for severe acidosis (pH Table o f C o ntents > M o lluscum C o ntagio sum
Molluscum
Contagiosum Guy Tarleton Jeffrey A. Bush
Basics Description
Molluscum contagiosum (MC) is a generally benign hum an disease characterized by m ultiple sm all, painless, pearly lesions.
MC appears on epithelial surface, spreads through close contact or autoinoculation.
Etiology
MC is caused by a double-stranded DNA poxvirus.
Transm ission in children is by direct skin-to-skin contact, fom ites, pool or bath water.
Transm ission in adults is m ost often by sexual contact; autoinoculation com m on at any age.
Diagnosis Signs and Symptoms
Pa ge 3 0 7
History
Incubation period: 14–50 days
Patients usually asym ptom atic, with occasional pruritus or tenderness
10–25% of patients m ay have eczem atous reaction surrounding the lesions.
Untreated lesions in im m unocom petent hosts usually resolve within several m onths, but can last up to 5 years.
Physical Exam
Lesions are sm ooth-surfaced, firm , spherical papules, 3–5 m m in diam eter.
May be flesh colored, white, translucent, or light yellow
Distinctive central um bilication in 25%
Distribution in children: face, trunk, and extrem ities; healthy adults: genitals and lower abdom en; occasionally perioral; rarely on palm s and soles
MC is com m only seen with HIV infection, causing atypical involvem ent of face, neck, and trunk, lesions to 1.5 cm , and a progressive course.
Occasional intraocular or periocular involvem ent presenting as trachom a or chronic follicular conjunctivitis
Essential Workup
History and careful skin exam ination
Skin biopsy for confirm ation
Tests Lab If anogenital, consider testing for HIV, syphilis, hepatitis B.
Differential Diagnosis
Basal cell carcinom a, histiocytom a, keratoacanthom a, intraderm al nevus
Pa ge 3 0 7
Darier disease, nevoxanthoendotheliom a, syringom a, epithelial nevi, sebaceous adenom a
Atopic derm atitis, derm atitis herpetiform is, m ycosis fungoides, Jessner lym phocytic infiltration
Treatment Pre Hospital Maintain universal precautions.
Initial Stabilization Not applicable in routine cases
ED Treatment
Treatm ent is aim ed at destruction or rem oval of virus-infected epithelial cells and is indicated to prevent autoinoculation and transm ission: o
Avoid being overly aggressive: Lesions are self-lim ited in im m unocom petent hosts.
Physical treatm ent m odalities generally m ost effective: o
Curettage after local anesthesia with EMLA (eutectic m ixture, lidocaine, prilocaine) or ethyl chloride
o
Cryotherapy with liquid nitrogen
o
Podophyllin, trichloroacetic acid, cantharidin, and tretinoin applied topically are variably effective.
Griseofulvin and m ethisazone orally for extensive disease have given m ixed results.
Highly active antiretroviral therapy (HAART) has been effective in reducing incidence in HIV-infected patients.
Topical im iquim od has shown effectiveness in several sm all studies.
Exam ine sexual partners for MC and other sexually
Pa ge 3 0 8
transm itted diseases: o
Patients should avoid contact sports, swim m ing pools, shared baths and towels, scratching, and shaving until lesions have resolved.
Re-exam ine treated patients for recurrence every 2–4 weeks; two to four treatm ents often needed to clear lesions com pletely.
P.703
Medication (Drugs)
Cantharidin 0.9% solution with equal parts acetone and flexible collodion: apply topically one to three treatm ents every 7 days or until resolution.
Podophyllin (podofilox 0.5%): apply topically q12h for 3 days, withhold for 4 days; repeat 1-week cycle up to four tim es until resolved.
Trichloroacetic acid (50–80%): apply and cover with bandage 5–6 days.
Tretinoin 0.1%: apply topically q12h for 10 days or until resolution of lesions.
Im iquim od 2%: apply topically b.i.d. for 3–5 consecutive days for 16 weeks.
Follow-Up Disposition Admission Criteria
Pa ge 3 0 8
Widespread disease with extensive superinfection in an im m unocom prom ised host
Discharge Criteria Patients without extensive superinfection m ay be safely treated as outpatients.
References 1. Allen AL, Siegfried EC. Managem ent of warts and m olluscum in adolescents. Adolesc Med. 2001;12(2):vi, 229–242. 2. Lewis EJ, Lam M, Crutchfield CE 3rd. An update on m olluscum contagiosum . Cutis. 1997;60(1):29–34. 3. Ordoukhanian E, Carrington D. Warts and m olluscum contagiosum : beware of treatm ents worse than the disease. Postgrad Med. 1997;101(2):223–226, 229–232, 235. 4. Sladden MJ, Johnston GA. Com m on skin infections in children. Br Med J. 2004;329:403. 5. Sm ith KJ, Yeager J, Skelton H. Molluscum contagiosum : its clinical, histopathologic, and im m unohistochem ical spectrum . Int J Derm atol. 1999;38(9):664–672.
Codes ICD9-CM 078.0
ICD10 B08.1
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > M o no am ine Oxidase Inhibito r, Po iso ning
Monoamine Oxidase Inhibitor, Poisoning James W. Rhee
Basics Description
Monoam ine oxidase inhibitors (MAOI) are prescribed prim arily for depression.
Selegiline, a selective m onoam ine oxidase B inhibitor, is som etim es used to treat Parkinson disease.
MAOI pharm acologic actions: o
Disruption of equilibrium between endogenous m onoam ine synthesis and degradation resulting in:
Increased neural norepinephrine levels
Downregulation of several receptor types
o
Inhibition of irreversible (noncom petitive) enzym e
o
Inhibition of other B 6 -containing enzym es
Monoam ine oxidase (MAO): principal inactivator of neural bioactive am ines: o
MAO A:
Present in the gut and liver
Protects against dietary bioactive am ines
Pa ge 3 0 8
o
MAO B:
Present in neuron term inals and platelets
Sym pathom im etic am ines: type of bioactive am ines
Etiology
MAOI overdose: o
Toxicopharm acology poorly understood
o
MAO inhibitors: am phetam inelike in structure:
Early: indirect sym pathom im etic effect
Late: sym patholytic response (hypotension seen here)
MAOI hypertensive crisis syndrom e: o
Results from im paired norepinephrine degradation, com bined with m assive norepinephrine release precipitated by exposure to an indirect- or m ixed-acting sym pathom im etic agent
o
Com m on precipitants: tyram ine, cocaine, am phetam ines
Serotonin syndrom e: o
Com m only results from exposure to com binations of agents that affect serotonin m etabolism or action
o
Agents that increase serotonin synthesis:
o
Tryptophan
Agents that increase serotonin release:
Indirect- and m ixed-acting sym pathom im etic agents
o
Dopam ine receptor agonists
Agents that decrease serotonin reuptake:
Selective serotonin reuptake inhibitors (SSRI)
Tricyclic antidepressants
Newer antidepressants: trazodone, nefazodone, venlafaxine
Pa ge 3 0 8
o
Meperidine, dextrom ethorphan, tram adol
Agents with direct serotonin receptor agonist:
Buspirone, sum atriptan, lysergic acid diethylam ide (LSD)
o
Agents that decrease serotonin breakdown:
o
MAOIs
Agents that increase nonspecific serotonin activity:
Lithium
Diagnosis Signs and Symptoms
MAOI overdose: o
Delayed onset (12 hours)
o
Initial hypertension with headache
o
Hyperadrenergic activity:
o
Tachycardia
Hypertension
Mydriasis
Agitation
Neurom uscular excitation:
Nystagm us
Hyperreflexia
Trem or
Myoclonus
Rigidity
Seizures
o
Hypertherm ia
o
Associated com plications:
Rhabdom yolysis
Renal failure
Pa ge 3 0 8
Dissem inated intravascular coagulation (DIC)
Acute respiratory distress syndrom e (ARDS)
MAOI hypertensive crisis syndrom e (MAOI interaction with drug or food):
o
Hypertension
o
Tachycardia or bradycardia
o
Hypertherm ia
o
Headache, usually occipital
o
Altered m ental status
o
Intracranial hem orrhage
o
Seizures
Serotonin syndrom e (SS): o
Increased neurom uscular activity
o
Increased deep tendon reflexes:
Lower extrem ity m ay be greater than upper
o
Trem or
o
Myoclonus
o
Rigidity (when severe)
o
Autonom ic nervous system hyperactivity:
o
Hypertherm ia
CNS:
Agitation
Hallucinations
Delirium
Com a
o
Diarrhea
o
SS versus neuroleptic m alignant syndrom e (NMS):
Both present along a spectrum of severity (m ild to severe)
Onset: several hours (SS) versus days (NMS)
Gastrointestinal sym ptom s: m ay be present (SS) versus absent (NMS)
Pa ge 3 0 8
Only drug/m edication history m ay differentiate in m any cases.
Essential Workup
History of ingested substances
Rectal tem perature m onitoring as indicated
Blood pressure/cardiac m onitoring
Tests Lab
Urinalysis: o
Blood
o
Myoglobin
Electrolytes, blood urea nitrogen/creatinine, glucose: o
Hypoglycem ia m ay contribute to altered m ental status.
o
Acidosis m ay accom pany severe toxicity.
o
Rhabdom yolysis m ay cause renal failure.
o
Hyperkalem ia—life-threatening consequence of acute renal failure
Coagulation profile to m onitor for potential DIC: o
International norm alized ration, prothrom bin tim e test, partial throm boplastin tim e test, platelets
Creatinine Kinase (CPK): o
Markedly elevated in rhabdom yolysis
Urine toxicology screen: o
May be positive for am phetam ines given the structural sim ilarities between som e MAOIs and am phetam ines
Aspirin and acetam inophen levels if suicide attem pt a possibility
Arterial blood gas
Pa ge 3 0 8
Imaging
Chest radiograph: o
ARDS
Head CT for: o
Significant headache
o
Altered m ental status
o
Focal neurologic signs
o
For subarachnoid hem orrhage, intracerebral bleed
Diagnostic Procedures/Surgery Lum bar puncture for:
Suspected m eningitis (headache, altered m ental status, hyperpyrexia)
Suspected subarachnoid hem orrhage and CT norm al
Differential Diagnosis
Hypertherm ia: o
Infection
o
Hyperthyroidism
o
Heat stroke
o
Anatom ic thalam ic dysfunction
o
Neuroleptic m alignant syndrom e
o
Malignant hypertherm ia
o
Malignant catatonia
o
Ethanol or drug withdrawal
o
Anticholinergic toxicity
o
Sym pathom im etic overdose
o
Cocaine-associated delirium /rhabdom yolysis
o
Salicylate toxicity
o
Theophylline toxicity
o
Nicotine toxicity
Hypertension: o
Hypoglycem ia
Pa ge 3 0 8
o
Carcinoid syndrom e
o
Pheochrom ocytom a
o
Accelerated renovascular hypertension
o
Ethanol or drug withdrawal
o
Sym pathom im etic toxicity
P.705
Treatment Pre Hospital
Patient m ay be uncooperative or violent.
Secure IV access.
Protect from self-induced traum a.
Initial Stabilization
ABCs
IV access and fluid resuscitation if hypotensive
Oxygen
Cardiac m onitor
Naloxone, thiam ine, D 5 0 W (or Accu-Chek) if altered m ental status
ED Treatment
Gastrointestinal decontam ination: o
Gastric lavage if within one hour of ingestion or if clinical condition m andates endotracheal intubation
o
Adm inister activated charcoal.
Hypertherm ia: o
Benzodiazepines if agitated
o
Active cooling if tem perature >40°C
Pa ge 3 0 8
o
Tepid water m ist
Evaporate with fan
Paralysis:
Indicated if m uscle rigidity and hyperactivity contributing to persistent hypertherm ia
Nondepolarizing agent (e.g., vecuronium )
Avoid succinylcholine
Intubation; m echanical ventilation
o
Adm inister acetam inophen.
o
Apply cooling blankets.
Severe, m alignant hypertension: o
Nitroprusside (for MAOI overdose)
o
Calcium -channel blocker or phentolam ine (for MAOI/food interaction)
o
Use short-acting IV agent that can be rapidly “turned off.―
o
Phentolam ine contraindicated in MAOI overdose (results in unopposed beta agonist)
Hypotension: o
Initially bolus with isotonic crystalloid solution
o
If no response, adm inister norepinephrine.
o
Dopam ine theoretically contraindicated
Dysrhythm ias (prem orbid sign in MAOI overdose): o
Treat with lidocaine or procainam ide.
Seizures: o
Benzodiazepines
o
Barbiturates if benzodiazepines unsuccessful
o
Pyridoxine for refractory seizures
Rigidity: o
Benzodiazepines
o
Paralysis with vecuronium , endotracheal intubation and m echanical ventilation
Pa ge 3 0 9
ARDS: o
Oxygen
o
Intubation and positive end-expiratory pressure (PEEP) as indicated
DIC: o
Fresh-frozen plasm a
o
Platelets
o
Whole-blood transfusions
Rhabdom yolysis: o
IV isotonic crystalloid solution
o
Maintain hydration.
o
Maintain adequate urine output.
Specific treatm ent for serotonin syndrom e: o
Hum an data lim ited to case reports and series
o
Mainstay: supportive care, discontinuation of offending agents
o
Nonselective serotonin antagonists:
Cyproheptadine
Medication (Drugs)
Activated charcoal: 1–2 g/kg PO
Cyproheptadine: 4–8 m g PO/per NGT q1h–q4h until therapeutic response; m axim um daily dose: 0.5 m g/kg (peds: 0.25 m g/kg/d; m ax. 12 m g/d; safety not established age Table o f C o ntents > M ultiple M yelo m a
Multiple Myeloma
Maggie Ferng
Basics Description
Norm al cells transform into m yelom a cells at the hem atopoietic stem cell level.
Pathologic derangem ents: o
Tum or cells within m arrow lead to bone destruction and cytopenia.
o
Im m unodeficiency develops secondary to suppression of norm al im m une functions.
o
Myelom a proteins lead to hyperviscosity and am yloidosis.
o
Multifactorial renal failure
Plasm a cell secretions activate osteoclasts, leading to: o
Bone lysis, pathologic fractures, and neurologic im pairm ent
o
Hypercalcem ia (exacerbated by im paired renal function)
Anem ia owing to m arrow infiltration and renal insufficiency
Im m unocom prom ised owing to: o
Decrease in the num ber of norm al im m unoglobulins
o
Qualitative and quantitative defects in T- and B-cell
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subsets
o
Granulocytopenia
o
Decreased cell-m ediated im m unity
Hyperviscosity secondary to protein accum ulation: o
Leads to high-output congestive heart failure
Myelom a light chains accum ulate in the renal epithelial cells and destroy the entire nephron.
Etiology
Incidence: 4 cases per 100,000 population: o
1% of all cancers
o
15% of all hem atopoietic m alignancies
o
10,000 deaths per year
Mean age at diagnosis is 62 years
Slightly higher incidence in wom en and African Am ericans (reason unknown)
Pediatric Considerations
Multiple m yelom a (MM) is rarely seen in children.
Less than 2% in patients younger than 40 years of age
Diagnosis Signs and Symptoms
Bone pain predom inates (with secondary disuse or neurologic sequelae): o
Ribs/sternum
o
Spine
o
Clavicle
o
Skull
o
Shoulder
o
Hip
Pa ge 3 1 0
o
Constitutional sym ptom s: o
Anem ia
o
Weakness
o
Fatigue
o
Recurrent infection
o
Weight loss
Asym ptom atic (20%): o
Back
MM found on follow-up of routine blood screening
Multiple bouts of sepsis secondary to the encapsulated organism s (Streptococcus pneum oniae, Haem ophilus influenzae, and Staphylococcus
Essential Workup
Official diagnosis requires: o
Dem onstrating pathologic cells in the bonem arrow
o
Monoclonal gam m opathy on electrophoresis
o
Clinical signs such as anem ia, renal insufficiency, or lytic bone lesions
Com plications: o
Pathologic fractures
o
Hypercalcem ia
o
Renal failure
o
Recurrent infection
o
Anem ia
o
Spinal cord com pression (10% of all MM patients)
Tests Lab
CBC: o
Norm ochrom ic, norm ocytic anem ia
o
Throm bocytopenia
o
Leukocytosis
Pa ge 3 1 0
Rouleaux form ation on peripheral blood sm ear
Electrolytes, BUN, creatinine, glucose: o
Serum calcium : o
Renal insufficiency
Hypercalcem ia owing to bone resorption
Urinalysis: o
Dipstick selects for album in and not light-chain proteinuria.
o
False-negative screening urinalysis for protein com m on
Elevated erythrocyte sedim entation rate (ESR)
P.709
Imaging
Plain radiographs dem onstrate: o
Lytic bone lesions
o
Pathologic fractures
Urinary and serum electrophoresis: show a m onoclonal protein spike: o
Quantitative screening for light chain is diagnostic.
Technetium pyrophosphate bone scan: o
Lights up bone deposition
o
False-negative scan with MM owing to an uncoupling of bone absorption and deposition that results in a negative bone scan even when lytic lesions present
Bone m arrow biopsy: increase in plasm a cells
Cytogenetic screening m ay offer prognostic significance.
Differential Diagnosis
Monoclonal gam m opathy
Chronic lym phocytic leukem ia
Pa ge 3 1 0
Non-Hodgkin lym phom a
Waldenström m acroglobulinem ia
Bone m arrow plasm acytosis includes collagen vascular disease, cirrhosis, im m une com plex disease, viral illness, papular m ucinosis.
Treatment Pre Hospital Im m obilize appropriately patients with MM who present with back pain or neurologic sym ptom s:
Presum e to have a pathologic spinal fracture
Initial Stabilization Recognition and treatm ent of:
Hypercalcem ia
Renal failure
Sepsis
Spinal cord com pression
Anem ia
ED Treatment
Analgesics m ainstay of therapy in ED
Splint pathologic fracture; im m obilize pathologic spine fractures.
Chem otherapy—adm inister on inpatient/outpatient basis: o
Early or asym ptom atic stages do not need treatm ent.
o
Chem otherapy in early stage shows no benefit.
o
Melphalan and prednisone com bination chem otherapy the m ost com m on treatm ent:
Sym ptom relief and decrease in M protein levels in up to 70% of patients
Pa ge 3 1 0
o
Alternative chem otherapy includes cyclophospham ide with or without prednisone or VAD (vincristine, doxorubicin [Adriam ycin], and dexam ethasone).
Prolonged m elphalan use m ay lead to a secondary leukem ia.
High-dose chem otherapy with stem cell transplantation has shown prom ise.
Thalidom ide is useful for salvage therapy.
Follow-Up Disposition Admission Criteria
Refractory pain requiring system ic analgesics
Life-threatening com plications of MM, including acute renal failure, hypercalcem ia, sepsis, spinal cord com pression, hyperviscosity, neutropenia, and cardiac tam ponade
Discharge Criteria Pain controlled with oral analgesics
Miscellaneous SEE ALSO: Anem ia; Hypercalcem ia; Renal Failure; Sepsis
References 1. Altundag K, Altundag O, Gundeslioglu O, et al. Multiple m yelom a. N Engl J Med. 2005;352:840–841. 2. Bortezom ib com pared with dexam ethasone in treating patients with relapsed or refractory m ultiple m yelom a. Paper presented at: Annual Meeting of the Am erican Society of Clinical Oncology (ASCO);
Pa ge 3 1 0
June 5, 2004; New Orleans, LA. 3. Hideshim a T, Chauhan D, Podar K, et al. Novel therapies targeting the m yelom a cell and its bone m arrow m icroenvironm ent. Sem in Oncol. 2001;28:607–612. 4. Kyle RA, Rajkum ar SV. Multiple m yelom a. N Engl J Med. 2004;351:1860–1873.
Codes ICD9-CM 203.0
ICD10 C90.0
Pa ge 3 1 0
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > M ultiple Sclero sis
Multiple Sclerosis
Richard S. Krause
Basics Description
Recurrent episodes of CNS dem yelinization: o
Signs and sym ptom s depend on location of lesions.
Multiple sclerosis (MS) occurs in distinct patterns: o
Relapsing recurring m ultiple sclerosis: two or m ore episodes lasting ≥24 hours separated by ≥1 m onth
o
Prim ary progressive m ultiple sclerosis: slow or stepwise progression over at least 6 m onths
o
Secondary progressive m ultiple sclerosis: initial exacerbations and rem issions followed by slow progression over at least 6 m onths
o
Stable m ultiple sclerosis: no progression (without treatm ent) over at least 18 m onths
Etiology
MS is chronic dem yelinating disease of CNS: o
Etiology is not well understood.
Presum ed to be T-cell–m ediated autoim m une disease
There is evidence for viral trigger.
Plaques in white m atter:
Pa ge 3 1 0
o
Characterized by infiltrate of T-cells and m acrophages
Persons of northern European origin m ost often affected (in United States)
Increased prevalence is seen m oving away from equator.
Diagnosis Signs and Symptoms
Initial attacks of MS usually represent single lesion, are abrupt in onset, and are seen in characteristic patterns (in order of decreasing frequency): o
Optic neuritis:
Eye pain exacerbated by m ovem ent progressing to visual loss
o
Paresthesias (or changed sensory level) in one lim b
o
Lim b (usually leg) weakness
o
Diplopia:
Internuclear ophthalm oplegia from lesion of m edial longitudinal fasciculus
Results in unilateral or bilateral paralysis of adduction of eye on horizontal gaze
o
Trigem inal neuralgia
o
Urinary retention
o
Vertigo
o
Transverse m yelitis:
Acute onset of m otor and sensory findings at specific spinal cord level
Often associated with bladder or bowel incontinence
Can be early m anifestation of MS
Pa ge 3 1 1
Sym ptom s typically develop abruptly (m inute to hours) and last 6–8 weeks.
Most com m on in young wom en of northern European descent:
o
Increased risk in first-degree relatives
o
Peak age: 30 years
o
Fem ale-to-m ale ratio, 2:1
Pain is uncom m on sym ptom in MS: o
Exceptions: trigem inal neuralgia, early optic neuritis
Essential Workup
MS is suspected based on history and physical exam .
Definitive diagnosis is not m ade in ED and requires observation over tim e and confirm atory testing.
Physical exam : focused on “hard― neurologic signs: o
Afferent pupillary defect
o
Internuclear ophthalm oplegia
o
Sensory level or sphincter disturbance (transverse m yelitis)
o
Physical exam should reveal objective evidence of neurologic dysfunction.
MRI is sensitive but not specific: o
May see plaques (m ay also see on CT)
Lum bar puncture m ay show “oligoclonal bands― on cerebrospinal fluid (CSF) electrophoresis.
Differential Diagnosis
Signs and sym ptom s of MS usually focal; diffuse sym ptom s (seizures, syncope, and dem entia) seldom owing to MS
System ic lupus erythem atosus: o
CNS involvem ent usually in setting of known disease and usually nonfocal
Sarcoid:
Pa ge 3 1 1
o
CNS m anifestations usually with known disease and lung involvem ent and nonfocal
Lym e disease: o
May m im ic MS
o
Seek history of rash and tick exposure in geographic areas of high risk.
o
Lym e titers m ay aid in diagnosis.
Psychiatric illness is diagnosis of exclusion.
Postinfectious or postim m unization dem yelination m ay m im ic MS, usually in children.
MS unlikely in patients with: o
Norm al neurologic exam
o
Abrupt hem iparesis
o
Aphasia
o
Pain predom inating
o
Very brief sym ptom s (seconds to m inutes)
o
Age 50 years
P.711
Treatment Initial Stabilization Fever in MS patients should be treated aggressively because it can worsen neurologic m anifestations of MS.
ED Treatment
Acute optic neuritis or transverse m yelitis: o
High-dose parenteral steroids possibly effective
o
Oral steroids contraindicated (oral prednisone has
Pa ge 3 1 1
been reported to exacerbate sym ptom s)
Exacerbations: o
High-dose IV m ethylprednisolone (up to 1 g/d) or other parenteral corticosteroid regim en
Sym ptom atic treatm ent: o
Spasticity: baclofen
o
Trem or: clonazepam
o
Urinary sym ptom s:
Treat infection.
Self-catheterization for increased postvoid residual (PVR)
Oxybutynin m ay prom ote continence between catheterizations.
o
Trigem inal neuralgia: carbam azepine
o
Fatigue, general weakness: no specific treatm ent
Medication (Drugs)
Baclofen: 10 m g PO t.i.d. initially; m ay increase to 25 m g t.i.d.
Carbam azepine: 100 m g PO b.i.d.–200 m g q.i.d.
Clonazepam : 0.5 m g/d PO, increase in 0.5-m g increm ents and up to three tim es a day
Methylprednisolone: 1 g IV
Oxybutynin: 5 m g PO b.i.d. or t.i.d.
Follow-Up Disposition Admission Criteria
Pa ge 3 1 1
Acute exacerbation that requires IV therapy
Patients unable to care for them selves owing to severity of their illness or in whom another condition requiring inpatient treatm ent cannot be effectively ruled out
Discharge Criteria
Suspected MS: Patients m ay be referred for outpatient evaluation if their general condition perm its and other serious conditions requiring adm ission have been effectively ruled out.
Com plication of known MS: Discharge if effective outpatient treatm ent available for condition.
References 1. Antel JP: Multiple sclerosis—em erging concepts of disease pathogenesis. J Neuroim m unol. 1999;98(1):45–48. 2. Brod SA, Lindsey JW, Wolinsky JS. Multiple sclerosis: clinical presentation, diagnosis, and treatm ent. Am Fam Physician. 1996;54:1301–1311. 3. Leary S, Porter B, Thom pson A. Multiple sclerosis: diagnosis and the m anagem ent of acute relapses. Postgrad Med J. 2005;81:302–308. 4. Poser CM. The epidem iology of m ultiple sclerosis: a general overview. Annals of Neurology. 1994;36(suppl 2):S180–S199. 5. Rolak LA. The diagnosis of m ultiple sclerosis. Neurol Clin. 1996;14(2):27–43.
Codes ICD9-CM 340
ICD10 G35
Pa ge 3 1 1
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > M um ps
Mumps
Austen Chai
Basics Etiology
Param yxovirus, single-stranded RNA virus
Hum an reservoir
Pediatric Considerations
May present as lower respiratory tract infection
System ic sym ptom s and serious com plications less com m on
Mum ps vaccine with m easles and rubella (MMR) should be adm inistered to all children on or after 12 m onths of age.
Adm itted patients should be isolated from unim m unized.
Diagnosis Signs and Symptoms Incubation (12–25 days)
Viral transm ission via respiratory droplets and saliva
Replication in nasopharynx and regional lym ph nodes
Virem ia to m eninges and glands; salivary, pancreas,
Pa ge 3 1 1
testes, and ovaries
Active Illness (1 to 10 days)
Nonspecific prodrom al sym ptom s
May include low-grade fever, headache, m alaise, m yalgia, anorexia, otalgia, jaw pain
Up to 20% of infections are asym ptom atic but still contagious.
Up to 50% of cases have nonspecific sym ptom s of upper respiratory tract infection, fever, m alaise, anorexia, and headache.
Contagious 3 days before and up to 6 days after sym ptom s end
Parotitis (30–40% of patients): o
Most com m on m anifestation of m um ps
o
Painful and tender unilateral or bilateral enlargem ent of parotid gland
o
May begin as earache or pain at angle of jaw
o
Any salivary gland m ay be affected
o
Skin overlying swollen gland is nonerythem atous.
o
Sym ptom s decrease after 1 week and resolve by 10th day.
o
Contagious until swelling resolves
Orchitis (20–50% of postpubertal m ales): o
Most com m on com plication in postpubertal m ales
o
May occur alone, before, during, but m ost com m only, after parotitis
o
Unilateral or bilateral (up to 30%)
o
Abrupt, painful, tender swelling with nausea, vom iting, and fever
o
Pain and swelling resolve in 1 week.
o
Testicular atrophy in up to 50% of patients
o
Sterility rare
Pa ge 3 1 1
Oophoritis (5% of postpubertal fem ales): o
May m im ic appendicitis if right sided
o
Fertility not im paired
Pancreatitis (2–5%): o
May occur without any other m anifestations of m um ps
o
Fever, nausea, vom iting, and epigastric pain
o
May see transient hyperglycem ia
o
May be com plicated by pseudocyst form ation and shock
CNS involvem ent: o
Aseptic m eningitis (10–15% of patients)
o
Usually resolves without sequelae in 3–10 days
o
Encephalitis (very rare)
o
Deafness (80% unilateral) with perm anent hearing im pairm ent
Other: o
Myocarditis (rarely with sym ptom atic involvem ent)
o
Glom erulonephritis
o
Polyarthralgia and arthritis
o
Throm bocytopenic purpura
o
Ocular com plaints
Essential Workup Diagnosis based on clinical findings P.713
Tests Lab
Laboratory tests as needed
Cerebrospinal fluid (CSF) for sym ptom atic CNS
Pa ge 3 1 1
involvem ent
Hyperam ylasem ia usually owing to parotitis
Viral cultures: o
Provides definitive diagnosis
o
From blood, throat swab, salivary gland secretions, CSF, or urine
o
Not indicated unless need to confirm diagnosis in absence of parotitis
Enzym e im m unoassay: o
Rapid detection
o
Not indicated unless need to confirm diagnosis in absence of parotitis
Differential Diagnosis
Bacterial parotitis: o
Com m only Staphylococcus aureus
o
Erythem atous and tender parotid gland
o
Usually in elderly or im m unocom prom ised
Calculus parotid: o
Stone m ay be palpable or be seen on sialogram .
Cervical adenitis
Tum ors: o
Older patients
o
History of indolent course
Testicular torsion
Bacterial epididym o-orchitis
Treatment Pre Hospital Nonim m unized prehospital care personnel exposed to m um ps should
Pa ge 3 1 1
be advised of potential risks.
Initial Stabilization IV fluids for vom iting/dehydration
ED Treatment
Prevention with m um ps vaccination is cornerstone of therapy: o
MMR at 1 year of age
o
Second MMR at 4–6 years of age, no later than 12 years of age
Supportive and sym ptom atic: o
Antipyretics
o
Analgesia:
Acetam inophen, nonsteroidal anti-inflam m atory drugs (NSAIDs), narcotics (for severe pain)
o
IV fluids for vom iting and dehydration
o
Ice pack
o
Scrotal support
Follow-Up Disposition Admission Criteria
Seriously ill who m ay require supportive care
Severe vom iting and dehydration
Encephalitis
Severe pancreatitis
Isolate adm itted patients.
Discharge Criteria
Virtually all patients
Pa ge 3 1 1
Contagious until about 9 days after onset of sym ptom s
References 1. Am erican Academ y of Pediatrics. Mum ps. In: Pickering LK, ed. 2000 Red Book: Report of the Com m ittee on Infectious Diseases. 25th ed. Elk Grove Village, IL: Author; 2000:405–408. 2. Centers for Disease Control and Prevention. Measles, m um ps, and rubella: vaccine use and strategy for elim ination of m easles, rubella, and congenital rubella syndrom e and control of m um ps. Recom m endations of the Advisory Com m ittee on Im m unization Practices (ACIP). MMWR Recom m Rep 1998;47(RR-8):1–57. 3. Goldm an L, ed. Cecil Textbook of Medicine, 21st ed. Philadelphia: WB Saunders; 2000:808–810. 4. Mandell GL, ed. Principles and Practice of Infectious Disease. 5th ed. Philadelphia: Churchill Livingstone; 2000:1776–1780.
Codes ICD9-CM 72.9
ICD10 B26.9
Pa ge 3 1 2
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > M unchausen's Syndro m e
Munchausen's
Syndrome J. C. Huffman T. A. Stern
Basics Description Intentional production/feigning of physical sym ptom s m otivated by a need to assum e the sick role
Etiology
No universal etiology
Patients often have a history of gaining support/attention via illness during childhood and of abusive or neglectful upbringing.
Diagnosis Difficult to m ake a definitive diagnosis but several com m on features exist
Signs and Symptoms
Frequent visits to EDs for what appears to be an acute illness
Pa ge 3 1 2
Num erous hospital adm issions (often prolonged)
A plausible, but dram atic, case history
Escalating dem ands for diagnostic testing and therapeutic interventions
Hostility/bullying m anner and evasiveness regarding specifics
Arrival with num erous m edical reports, hospital cards, or insurance form s
Masochistic acceptance of painful procedures
Use of m edically sophisticated language
Em ploym ent in a m edically related field
A paucity of verifiable history
Pseudologia fantastica (the telling of wild, untrue stories)
Vast array of possible presenting m edical com plaints and signs
Social History
Frequent hom elessness and significant wandering between cities and states
An absence of close interpersonal relationships
A history of sadistic and rejecting parents
A history of chronic childhood illness
Gastrointestinal
Vom iting
Diarrhea
Abdom inal pain
Hematologic
Dizziness
Weakness associated with bleeding
Anem ia (from self-phlebotom y or abuse of anticoagulants)
Neurologic
Pa ge 3 1 2
Feigned seizures
Loss of consciousness
Musculoskeletal
Self-induced wounds
Multiple scars
Cardiac
Com plaints of chest pain
Palpitations
Dysrhythm ias
Renal
Renal colic
Dysuria
Hem aturia
Endocrine
Hypoglycem ia (from self-adm inistration of insulin)
Hyperthyroidism :
o
Secondary to exogenous adm inistration of thyroxine
o
See Hyperthyroidism
Hyperdynam ic states (from use of epinephrine): o
Tachycardia
o
Hypertension
o
Diaphoresis
Infectious
From injection of sputum or feces
Factitious fever from m anipulation of therm om eters
Pulmonary Shortness of breath
Pediatric Considerations
Munchausen syndrom e by proxy
Pa ge 3 1 2
A form of child abuse
A parent provides a m isleading history or induces illness in their child to obtain m edical attention.
Essential Workup
The diagnosis is suggested by inconsistencies in the history or the pattern of illness and by the recognition of the above patterns of behavior.
Diligent detective work, including obtaining records from other hospitals and calling on fam ily m em bers who can provide evidence of sim ilar prior presentations
Direct observation of the patient and a search of the patient's room /belongings that m ay reveal their m ethod of deception (e.g., insulin vials and syringes)
Critical to perform tests/workup that focus on objective findings of illness on exam
Tests Depend on organ system involved and on objective findings
Lab
Testing stool for phenolphthalein m ay detect laxative abuse.
Testing blood for C3 peptide reveals exogenous insulin adm inistration.
Imaging Do not rely on im aging brought by the patient to m ake diagnoses or treatm ent plans. P.715
Diagnostic Procedures/Surgery Avoid unless clear objective findings indicate the necessity of a
Pa ge 3 1 2
procedure
Differential Diagnosis
True prim ary physical illness: o
Munchausen patients often with co-m orbid prim ary m edical illness
True illness secondary to self-destructive acts or surgical interventions: o
Sm all bowel obstruction, infection, dehydration
Malingering: o
Also has intentional sym ptom production
o
In this case, a clear-cut secondary gain (e.g., m eals/room , disability benefits) is present.
o
The patient is usually m uch less willing to undergo painful procedures.
Conversion disorder: o
Sym ptom s not consciously/intentionally produced
o
Typically with neurologic sym ptom s
o
Blindness
o
Hem iparesis
o
Seizures
Som atization disorder o
Sym ptom s not consciously produced
o
Multiple som atic com plaints
o
Multiple organ system involvem ent
Treatment Initial Stabilization Treat obvious threats to life or lim b:
Hypoglycem ia, bleeding, or wounds
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ED Treatment
Identify objective physical illness and treat as appropriate.
Docum ent history/findings suggestive of factitious illness.
Flag chart or create list to identify such patients.
Refer for psychiatric care if the patient accepts referral.
Report Munchausen syndrom e by proxy to child protective services.
Be aware of your em otional reaction to avoid inappropriate abandonm ent or treatm ent.
Follow-Up Disposition Admission Criteria
Often requires m edical adm ission to treat or stabilize physical conditions
Psychiatric adm ission m ay be of benefit, but is rarely accepted by patient.
Discharge Criteria
Medical stability
Not an active threat to harm self
Appropriate referral for m edical and psychiatric follow-up arranged
Issues for Referral
May offer psychiatric referral as a m ethod of dealing with stress caused by illness
Psychiatric providers located directly in m edical settings (e.g., prim ary care physician office) m ay be m ore accepted.
Pa ge 3 1 2
Overall, this is a chronic illness with poor prognosis.
References 1. Feldm an MD, Ford CV. Factitious disorders. In: Sadock BJ, Sadock VA, eds. Kaplan and Sadock's Com prehensive Textbook of Psychiatry. 7th ed. Philadelphia, PA: Lippincott William s & Wilkins, 2000:1533–1543. 2. Robertson MM, Cervilla JA. Munchausen's syndrom e. Br J Hosp Med . 1997;58(7):308–312. 3. Souid AK, Keith DV, Cunningham AS. Munchausen syndrom e by proxy. Clin Pediatr. 1998;37(8):497–503. 4. Stern TA. Munchausen's syndrom e revisited. Psychosom atics. 1980;21:329–336. 5. Walker EA. Dealing with patients who have m edically unexplained sym ptom s. Sem in Clin Neuropsychiatry. 2002;7:187–195.
Codes ICD9-CM 301.51
ICD10 F68.1
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > M ushro o m , Po iso ning
Mushroom,
Poisoning Adam Black Timothy Erickson
Basics Description Amanitin/Phalloidin
Species: o
Am anita phalloides (“death cap―)
o
Am anita virosa/verna (“destroying angel―)
o
Galerina m arginata; Galerina venenata
Mechanism : o
Cyclopeptide toxins inhibit RNA polym erase 2, which kills GI epithelium , hepatocytes, nephrocytes
Gyromitrin
Species: o
Gyrom itra esculenta (“false m orels―)
o
Other Gyrom itra species
Mechanism : o
Inhibits pyridoxal phosphate
o
Dam age to RBCs, hepatocytes, neurons
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Muscarine
Species: o
Inocybe (several species)
o
Clitocybe (several species)
Mechanism : o
Parasym pathom im etic
Coprine
Species: o
Coprinus atram entarius (“inky caps―)
Mechanism : o
Blocks acetaldehyde dehydrogenase
Causes disulfiram like reaction if m ixed with alcohol
Ibotenic Acid/Muscimol
Species: o
Am anita pantherina (“the panther―)
o
Am anita m uscaria (“fly agaric―)
Mechanism : o
GABA agonists
Psilocin/Psilocybin
Species: o
Psilocybe and Panaeolus species as well as others
Mechanism : o
Sim ilar structure to lysergic acid diethylam ide (LSD)
Gastric Irritants Many various m ushroom s including those norm ally considered edible
Orellanine
Species: o
Cortinarius (several species)
Mechanism :
Pa ge 3 1 2
o
Direct renal toxicity
Diagnosis Signs and Symptoms Amanitin/Phalloidin
Nausea
Vom iting
Abdom inal cram ps
Bloody diarrhea
Clinical course: o
Onset of sym ptom s 6–36 hours
o
Transient latent phase m ay last 2 days (no pain)
o
Can progress to hepatic or renal failure and death in 4–7 days
o
Most lethal m ushroom toxins
Gyromitrin
First 6 hours: o
Abdom inal cram ps
o
Vom iting
o
Watery diarrhea
Later sym ptom s: o
Weakness
o
Cyanosis
o
Confusion
o
Seizures
o
Com a
Muscarine
Cholinergic sym ptom s include: o
Miosis
Pa ge 3 1 3
o
Salivation
o
Lacrim ation
o
Sweating
o
Diarrhea
o
Flushed skin
o
Nausea
o
Bradycardia
o
Bronchoconstriction
Onset usually within 1 hour (m ay be delayed)
Coprine
Disulfiram like reaction when com bined with alcohol: o
Flushing
o
Sweating
o
Nausea
o
Vom iting
o
Palpitations
o
Chest pain
Begins m inutes after com bining this toxin with ethanol
Ibotenic Acid/Muscimol
Anticholinergic sym ptom s include: o
Hallucinations
o
Dysarthria
o
Ataxia
o
Muscle cram ps
o
Vom iting
o
Seizures
o
Com a
Clinical course: o
Relatively rapid onset of 30–60 m inutes
Psilocin/Psilocybin
Visual hallucinations
Pa ge 3 1 3
Alteration of perception
Nausea
Mydriasis
Tachycardia
Fever and seizures in children: o
Rarely fatal (case report of m yocardial infarction in 18 year old)
Gastric Irritants
Group of toxins that cause nausea, vom iting, intestinal cram ps, and watery diarrhea
Onset 30 m inutes to 2 hours, usually resolved in 6–12 hours
Orellanine
Nausea
Headache
Sweating
Chills
Low-back pain
Thirst
Clinical course o
May progress to oliguria and acute renal failure
o
Markedly delayed onset of sym ptom s (2–14 days)
Essential Workup
Mushroom description: o
Fewer than 3% of cases result in an exact m ushroom identification.
Careful history and physical exam : o
Special detail to tim ing of sym ptom onset
Tests Lab
Pa ge 3 1 3
CBC
Prothrom bin tim e (PT), partial throm boplastin tim e (PTT)
Electrolytes, BUN, creatinine, glucose
Urinalysis
Liver function tests (LFTs), creatine phosphokinase (CPK)
Differential Diagnosis
Sym ptom s with late onset (>6 hours) indicate m ore lethal toxins.
Always entertain possibility of m ultiple species ingestion.
Com bination with ETOH m ay suggest coprine (disulfiram reaction).
Consider other illicit drugs with visual hallucinations.
Fertilizers, insecticides, fungicides, if m ushroom s were found in a public place
Botulism if canned m ushroom s
Treatment Pre Hospital Bring any unconsum ed m ushroom s or m ushroom pieces to hospital to aid in diagnosis:
Refrigerate specim ens if possible, place in brown paper bag.
P.717
Initial Stabilization
Airway, breathing, and circulation m anagem ent (ABCs)
Establish IV 0.9% norm al saline (NS)
Monitor
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Naloxone, D 5 0 W (or Accu-Chek) and thiam ine for altered m ental status
ED Treatment General
Decontam ination: o
Activated charcoal (50–100 g)
o
Gastric decontam ination if early after ingestion and:
Patients have not yet vom ited.
Norm al m ental and respiratory status
Not undergoing hallucinations
Fluid rehydration and electrolyte replacem ent as necessary
Call local poison control center and request m ycologist—digital picture m ay be electronically sent for identification.
Obtain specim ens (vom itus if needed) for identification.
Toxin-Specific Therapy
Am anitin/phalloidin: o
Ewald oral gastric tube aspiration of m ushroom fragm ents if 1–2 hours postingestion
o
Adm inister charcoal orally every 2–4 hours
o
Hypoglycem ia and elevated PT:
Signs of liver failure
Adm inister fresh frozen plasm a and vitam in K for coagulation disorders with active bleeding.
o
Adm inister calcium in presence of hypocalcem ia.
o
Liver transplant for severe hepatic necrosis
o
Consider N-acetylcysteine, high-dose penicillin G, or silibinin if available (thioctic acid controversial)
Gyrom itrin: o
Adm inister pyridoxine (vitam in B 6 ) in severely
Pa ge 3 1 3
sym ptom atic patients. o
Treat seizure with benzodiazepines.
o
Treat liver dysfunctions as outlined for am anitin/phalloidin group.
o
Muscarinic: o
Dialysis for renal failure
Adm inister atropine in severe cases.
Coprine: o
Self-lim ited toxicity—supportive care
o
Avoid syrup of ipecac (contains alcohol).
o
Beta-blockers for cardiac dysrhythm ias
Ibotenic acid/m uscim ol: o
Usually self-lim ited toxicity
o
Provide supportive care.
o
Monitor for hypotension.
o
Treat m oderate anticholinergic sym ptom s with benzodiazepines, severe sym ptom s with physostigm ine.
Psylocin/psilocybin: o
Self-lim ited toxicity
o
Monitor if tachycardic.
o
Dark, quiet room and reassurance
o
No aggressive oral decontam ination if hallucinating
o
External cooling m easures if needed in children
GI Irritants: o
When poisoning from above groups not suspected:
Adm inister fluids and antiem etics.
Supportive care
Orellanine and Am anita sm ithiana: o
Closely m onitor BUN, creatinine, electrolytes, and urine output.
o
Forced diuresis with Lasix contraindicated:
Pa ge 3 1 3
o
Accelerates nephrotoxicity in rats
Diuresis with alkalinization of urine with NaHCO 3 if signs of rhabdom yolysis
o
Hem odialysis/renal transplantation m ay be needed.
o
Monitor LFTs in cases in which cyclopeptide-containing m ushroom s are suspected.
o
Monitor CPK, urine output: Tricholom a equestre (“m an on horse―) m ushroom s can lead to acute rhabdom yolysis.
Medication (Drugs)
Activated charcoal slurry: 1–2 g/kg up to 100 g PO
Atropine: 0.5 m g (peds: 0.02 m g/kg) IV; repeat 0.5–1.0 m g IV (peds: 0.04 m g/kg) q10m in if secretions recur, to m ax. 1 m g/kg in children and 2 m g/kg in adults
Dextrose: D 5 0 W 1 am p: 50 m L or 25 g (peds: D 2 5 W 2–4 m L/kg) IV
Diazepam (benzodiazepine): 5–10 m g (peds: 0.2–0.5 m g/kg) IV
Lorazepam (benzodiazepine): 2–6 m g (peds: 0.03–0.05 m g/kg) IV
Naloxone (Narcan): 2 m g (peds: 0.1 m g/kg) IV or IM initial dose
Physostigm ine: 0.5–2 m g IM or IV in adults
Propranolol: 1 m g (peds: 0.01–0.1 m g/kg) IV
Pyridoxine: 25 m g/kg over 30 m inutes
Sorbitol: 1–2 g/kg to m ax. of 150 g. Avoid in very young children (peds: >2 years: 1–1.5 g/kg as 35% solution to m ax. 50 g) PO m ixed in activated charcoal slurry
Thiam ine (vitam in B 1 ): 100 m g (peds: 50 m g) IV or IM
Pa ge 3 1 3
Follow-Up Disposition Admission Criteria
All sym ptom atic patients: o
Protracted vom iting, dehydration, liver or renal toxicity, or seizures
Transfer to tertiary m edical center for early signs of renal or hepatic failure.
Sym ptom atic infants and young children found with m ushroom s: o
Assum e ingestion.
ICU adm ission for known ingestion of an am anitin-containing m ushroom : o
Early liver service consultation
Discharge Criteria Asym ptom atic during 6–8 hours with 24 hours of close hom e observation available
References 1. Bedry R, Baudrim ont I, Deffieux G, et al. Wild m ushroom intoxication as a cause of rhabdom yolysis. N Engl J Med. 2001;345:798–802. 2. Berger KJ, Guss DA. Mycotoxins revisited. Part I. J Em erg Med. 2005;28(1):53–62. 3. Berger KJ, Guss DA. Mycotoxins revisited. Part II. J Em erg Med. 2005;28(2):175–183. 4. Diaz JH. Evolving global epidem iology, syndrom ic classification, general m anagem ent, and prevention of unknown m ushroom ingestion. Crit Care Med. 2005;33(2):419–426.
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5. Fischbein C, Aks S, Mueller GM. Mushroom poisoning. In: Erickson T, Ahrens W, Aks S, et al., eds. Pediatric Toxicology. New York: McGraw-Hill; 2005:533–540. 6. Fischbein C, Mueller G, Leacock P, et al. Digital im aging: a prom ising tool for m ushroom identification. Acad Em erg Med. 2003;10:808–811. 7. Ganzert M, Felgenhauer N, Zilker T. Indication of liver transplantation following am atoxin intoxication. J Hepatol. 2005;42(2):202–209. 8. Goldfrank LR. Mushroom s. In: Goldfrank LR, Flom enbaum NE, Lewin NA, et al., eds. Goldfrank's Toxicologic Em ergencies. 7th ed. New York: McGraw-Hill; 2002:. 9. McPartland JM, Vilgalys RJ, Cubeta MA. Mushroom poisoning. Am Fam Physician. 1997;55:1797–1800, 1805–1809. 10. O'Donnel M, Flem ing S. The renal pathology of m ushroom poisoning. Histopathology. 1997;30(3):280–282. 11. Satora L, Pach D, Butryn B, et al. Fly agaric (Am anita m uscaria) poisoning, case report and review. Toxicon. 205;45:941–943. 12. Warden CR, Benjam in DR. Acute renal failure associated with suspected Am anita sm ithiana m ushroom ingestions: a case series. Acad Em erg Med. 1998;8:808–812.
Codes ICD9-CM 988.1
ICD10 T62.0
Pa ge 3 1 3
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > M yasthenia G ravis
Myasthenia Gravis
Angela Loh
Basics Description
Antibody-m ediated condition that results in painless, fatigable weakness
Bim odal distribution: o
One peak in second and third decades affecting m ostly wom en
o
Second peak in sixth and seventh decades
Ocular or generalized: o
Ocular m uscle weakness:
Most com m on initial sym ptom (60%)
Alm ost all patients with m yasthenia gravis will have ocular involvem ent within 2 years.
o
Generalized:
Usually affects proxim al lim bs, axial m uscle groups such as neck, face, bulbar m uscles
Acute or subacute, with relapses and rem issions
Associated with thym om a in 20% and with thym ic hyperplasia in 70%
Myasthenic crisis: o
Respiratory failure resulting from m yasthenic
Pa ge 3 1 3
weakness o
Triggers: infection, surgery, traum a, m edication changes (e.g., rapid tapering of steroids)
o
Difficult to distinguish from cholinergic crisis resulting from excessive doses of acetylcholinesterase (AChE) inhibitors
Etiology
Antibody-m ediated attack on nicotinic acetylcholine receptors
Som e patients m ay be acetylcholine receptor antibody (AChR Ab) negative
Medications that worsen m yasthenic weakness: o
Am inoglycosides, am picillin, ciprofloxacin, erythrom ycin
o
Local anesthetics
o
Antidysrhythm ics (propafenone, quinidine, procainam ide)
o
Beta-blockers
o
Phenytoin
o
Neurom uscular blocking agents
o
Penicillam ine can cause m yasthenia gravis as well as other autoim m une conditions.
Diagnosis Signs and Symptoms History
Weakness worse with repeated or sustained m uscular activity
Im proves with rest
Pa ge 3 1 4
Ocular weakness: o
Diplopia
o
Ptosis while driving or reading
Bulbar and facial m uscle weakness: o
Trouble chewing, speaking, swallowing
o
Inability to keep jaw closed after chewing
o
Slurred, nasal speech
Lim b weakness: o
Difficulty clim bing stairs, rising from chair, reaching up with arm s
Physical Exam
Ocular findings: o
Ptosis, diplopia
o
Inability to keep eyelid shut against resistance
o
No pupillary changes
Bulbar and facial findings: o
Ask patient to count to 100; look for changes in speech.
o
Decreased facial expression
o
Head droop
Lim b findings: o
Repetitively test proxim al m uscles or sm all m uscles of hand.
o
Reflex and sensory exam are norm al.
Essential Workup
Search for secondary triggers.
Assess for respiratory com prom ise.
Tests Lab
CBC
Pa ge 3 1 4
Electrolytes
Liver function tests
Thyroid function tests
Search for infectious source; consider chest radiograph
Anti-AChR Ab:
o
Positive in 90% with generalized disease
o
Positive in 50% with ocular disease
Other tests for initial diagnosis: o
Antistriated m uscle antibody
o
Antinuclear antibody (ANA)
o
Rheum atoid factor
o
Erythrocyte sedim entation rate (ESR)
Imaging
Head CT or MRI to rule out com pressive lesions causing cranial nerve findings
Chest CT with contrast to look for associated thym om a
Diagnostic Procedures/Surgery
Edrophonium (Tensilon) test: o
Short-acting acetylcholinesterase inhibitor
o
Produces rapid, short-lived (2 to 5 m inutes) im provem ent in strength
o
Positive in 90% of m yasthenia gravis patients
o
Keep patient on cardiac m onitor during test.
o
Atropine at bedside for possible bradycardia
Ice test: o
Place ice on eyelid for 2 m inutes.
o
Im provem ent in ptosis suggests m yasthenia gravis.
Differential Diagnosis
Hyperthyroidism
Electrolyte abnorm alities
Graves disease
Pa ge 3 1 4
Botulism
Lam bert-Eaton syndrom e
Am yotrophic lateral sclerosis
Guillain-Barré syndrom e
Inflam m atory m uscle disorders
Multiple sclerosis
Periodic paralysis
Intracranial m ass lesions
P.719
Treatment Pre Hospital Attention to airway m anagem ent
Initial Stabilization
Myasthenic crisis: o
Most im portant is early intubation and m echanical ventilation.
o
Though no single param eter can predict need for respiratory support; consider following forced vital capacity or m ean inspiratory pressure
o
Considerations regarding paralytics
Decreased sensitivity to depolarizing agents m ay necessitate higher dose; consider doubling the usual dose of succinylcholine
Nondepolarizing agents can cause extended paralysis; consider halving the usual dose of vecuronium
Pa ge 3 1 4
Others recom m end m idazolam , etom idate, or thiopental instead.
ED Treatment
Treat infections aggressively.
Search for and rem ove triggers.
Atropine for AChE inhibitor effects (bradycardia, GI sym ptom s, increased bronchial or oral secretions)
Myasthenic crisis m ay require plasm apheresis or intravenous gam m aglobulin.
Steroids and im m unosuppressive therapies are not used in acute m anagem ent.
Medication (Drugs)
Atropine: 0.4–0.5 m g IV or IM
Edrophonium (Tensilon): 2 m g IV over 15–30 seconds; if no effect after 45 seconds, can give second dose of 8 m g IV slowly
Pyridostigm ine (Mestinon): for m yasthenic crisis, infusion at 1–2 m g/h
Other m edications that m ay be initiated by neurologist: o
Prednisone, azathioprine, m ycophenolate m ofetil, cyclosporine, tacrolim us, rituxim ab
Follow-Up Disposition Admission Criteria
Myasthenic crisis or questionable respiratory status
Pa ge 3 1 4
m andates adm ission to intensive care unit (ICU).
Myasthenic patients with worsening sym ptom s
New-onset m yasthenic sym ptom s
Diagnosis unclear, but m yasthenia a possibility
Discharge Criteria Myasthenic patients who are im proving can be considered for discharge in consultation with neurology.
References 1. Bedlack RS, Sanders DB. How to handle m yasthenic crisis. Postgrad Med. 2000;107(4):211–214. 2. Berrouschot J, Baum ann I, Kalischewski P, et al. Therapy of m yasthenic crisis. Crit Care Med. 1997;25:1228–1235. 3. Drachm an DB. Myasthenia gravis. N Engl J Med. 1994;330:1797–1810. 4. Kothari M. Myasthenia gravis. J Am Osteopath Assoc. 2004;104(9):377–384. 5. Sanders DC, Scoppetta CS. Treatm ent of patients with m yasthenia gravis. Neurol Clin North Am . 1994;12(2):343–365. 6. Thom as CE, et al. Myasthenic crisis: clinical features, m ortality, com plications, and risk factors of prolonged intubation. Neurology. 1997;48:1253–1260. 7. Vincent A, Palace J, Hilton-Jones D. Myasthenia gravis. Lancet. 2001;357:2122–2128.
Codes ICD9-CM 358.0
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > M yo cardial C o ntusio n
Myocardial
Contusion Robert S. Hamilton
Basics Description
Pathologically characterized by discrete and well-dem arcated area of hem orrhage
Usually subendocardial
May extend in pyram idal transm ural fashion
Most com m only involves anterior wall of right ventricle or atrium
Etiology
Blunt traum a to chest: o
High-speed deceleration accidents
o
May occur in accidents with speeds as low as 20–35 m ph
Auto–pedestrian injuries
Falls
Prolonged closed-chest cardiac m assage
Heart m ay be com pressed between sternum and vertebrae.
Strike sternum during deceleration
Pa ge 3 1 4
Dam aged by abdom inal viscera upwardly displaced by force on abdom en
Associated Conditions
Life-threatening dysrhythm ias
Cardiogenic shock/congestive heart failure
Hem opericardium with tam ponade
Valvular/m yocardial rupture
Intraventricular throm bi
Throm boem bolic phenom ena
Coronary artery occlusion from intim al tearing or adjacent hem orrhage and edem a m ay rarely occur.
Diagnosis Signs and Symptoms
Clinical picture is varied and nonspecific: o
Excruciating chest pain
o
Cardiogenic shock
o
Subtle ECG changes without clinical sym ptom s
Most com m on sign is tachycardia out of proportion to degree of traum a or blood loss.
Friction rub m ay occur rarely.
Retrosternal chest pain unrelieved by nitroglycerin:
o
Often delayed up to 24 hours
o
May respond to oxygen
Evidence of significant thoracic traum a: o
Contusions, abrasions
o
Palpable crepitus
o
Sternal fracture
o
Visible flail segm ents
Pa ge 3 1 4
Other injuries m ay m ask signs and sym ptom s of m yocardial contusion.
Essential Workup
No single diagnostic study (other than autopsy findings!) confirm s presence of m yocardial contusion.
Only abnorm al ECG and creatine phosphokinase (CPK)-MB have been shown to correlate directly with com plications requiring treatm ent.
ECG: o
Best initial screening tool
o
Most com m on rhythm is sinus tachycardia (70%).
o
Norm al ECG does not rule out m yocardial dam age.
o
ECG changes m ay be subtle or include nonspecific findings such as right bundle branch block.
o
At least one repeat ECG is recom m ended because changes m ay occur over tim e.
o
Serious dysrhythm ias m ay result in hem odynam ic instability:
Atrial fibrillation
Ventricular tachycardia
Ventricular fibrillation
Echocardiography should be perform ed on all patients with any ECG changes, elevated CPK-MB, or elevated troponin-I or troponin-T.
Tests Lab
CPK-MB, troponin: o
Levels should be sent on all patients being adm itted.
o
Sensitivity varies from 11–85%.
o
Specificity decreased in m ultiple traum a.
Cardiac troponin and m yoglobin assays have not been as
Pa ge 3 1 4
well studied.
Imaging
Radiographs, CT, MRI detect associated injuries: o
Pulm onary contusion
o
Rib or sternal fractures
o
Acute pulm onary edem a
o
No specific findings in cardiac contusion
Echocardiography: o
Generally regarded as best im aging study for detecting cardiac contusion
o
Detects wall-m otion abnorm alities and effusions
o
Allows direct visualization of cardiac cham bers and valves
o
May not visualize sm all (possibly clinically insignificant) contusions
o
Transesophageal echocardiography (TEE) m ay be used in patients with painful chest wall injuries.
o
May also visualize great vessels
Radionuclide ventriculography: o
Has been largely abandoned owing to wide availability of echocardiography
Thallium -201 scintigraphy (single photon em ission com puted tom ography [SPECT]): o
Sensitive and specific to left ventricular injury
o
Unable to evaluate right ventricle, which is m ost com m only injured
Differential Diagnosis
Cardiac rupture
Tam ponade
Valvular dam age
Other traum atic chest wall injury
Pa ge 3 1 4
Angina or m yocardial infarction
P.721
Treatment Pre Hospital Prehospital personnel should convey accurate inform ation to em ergency departm ent personnel:
Mechanism of injury
Motor vehicle status
Steering wheel and dashboard dam age
Use of restraint devices
Vehicle speed
Patient position
Initial Stabilization Manage airway and resuscitate as indicated:
Oxygen
Intravenous access
Cardiac m onitoring
ED Treatment
Dysrhythm ias m ay be treated with sam e pharm acologic agents used for nontraum atic dysrhythm ias: o
Supraventricular tachycardia:
Adenosine or calcium channel blocker if patient not hypovolem ic
o
Bradycardia:
Atropine
Pacing
Pa ge 3 1 5
o
o
o
Ventricular dysrhythm ias:
Electrical conversion
Am iodarone
Lidocaine
Procainam ide
Cardiac arrest:
Epinephrine
Atropine
Other interventions as appropriate
Rapid atrial fibrillation or flutter:
Diltiazem , or digoxin if patient not hypotensive
Prophylactic treatm ent of dysrhythm ias is not indicated.
Cardiogenic shock caused by m yocardial contusion: o
Judicious fluid adm inistration
o
Inotropic support (dopam ine or dobutam ine)
o
Intra-aortic balloon counterpulsation m ay be necessary.
Medication (Drugs)
Medications used in cardiac contusion are supportive for dysrhythm ias or hem odynam ic com prom ise secondary to injury.
There is no prim ary therapy for cardiac contusion.
Adenosine: 6 m g rapid IVP (peds: 0.1–0.2 m g/kg rapid IVP), m ay repeat 12 m g q1–2m in twice if no response
Am iodarone: load 150 m g IV over 10 m inutes (peds: 5 m g/kg), then 1 m g/m in for 6 hours, then 0.5 m g/m in (peds: 5 µg/kg/m in)
Atropine: 0.5–1.0 m g (peds: 0.02 m g/kg per dose, m inim um 0.1 m g) IV or endotracheal tube (ET)
Digoxin: Load 0.5 m g (peds: 0.02 m g/kg) IV, then 0.25
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m g (peds: 0.01 m g/kg) IV q6h for 2 m ore doses
Diltiazem : 10–20 m g (peds: 0.25 m g/kg) IV over 2 m inutes, m ay rebolus 0.35 m g/kg (adult and peds) 15 m inutes later
Dobutam ine: 2–15 µg/kg/m in (adult and peds)
Dopam ine: 2–20 µg/kg/m in (adult and peds)
Epinephrine: 1 m g (peds: 0.01 m g/kg) IV or ET for cardiac arrest (1:10,000 solution)
Lidocaine: load 1 m g/kg IV, then 0.5 m g/kg q8–10m in to m ax. 3 m g/kg (adult and peds); infusion 1–4 m g (peds: 20–50 µg/kg) per m inute IV
Procainam ide: 100 m g (peds:15 m g/kg per dose) IV q10m in up to 17 m g/kg
Verapam il: 0.1–0.3 m g/kg up to 5–10 m g IV over 2 m inutes (not approved in children)
Follow-Up Disposition
Adverse outcom es, particularly dysrhythm ias, are uncom m on but generally occur within first 24 hours.
No single test or com bination of tests will accurately predict which patients can be discharged safely from ED: o
All patients in whom diagnosis is seriously being entertained should be adm itted.
Admission Criteria
ECG abnorm alities
Cardiac enzym e abnorm alities
Hem odynam ic instability
Other studies suggesting cardiac contusion
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Adm it to m onitored unit for close observation.
Discharge Criteria Asym ptom atic patients with no ECG abnorm alities or dysrhythm ia and with norm al cardiac enzym es after 4- to 6-hour period m ay be discharged.
References 1. Chu WW, Dieter RS, Stone CK. Evolving clinical applications of cardiac m arkers: a review of the literature. WMJ. 2002;101(3):49–55. 2. Kaye P, O'Sullivan I. Myocardial contusion: em ergency investigation and diagnosis. Em erg Med J. 2002;19:8–10. 3. Maenza RL, Seaberg D, D'Am ico F. A m eta-analysis of blunt cardiac traum a: ending m yocardial confusion. Am J Em erg Med. 1996;14:237–241. 4. Roxburgh JC. Myocardial contusion. Injury. 1996;27:603–605. 5. Sybrandy KC, Cram er MJ, Burgersdijk C. Diagnosing cardiac contusion: old wisdom and new insights. Heart. 2003;89(5):485–459.
Codes ICD9-CM 861.01
ICD10 S28.8
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > M yo carditis
Myocarditis
Liudvikas Jagminas
Basics Description
An inflam m atory change in the heart m uscle which is characterized by m yocyte necrosis and subsequent m yocardial destruction
May result in a dilated cardiom yopathy
Direct cytotoxic effect of causative agent followed by a secondary im m une response o
Over 4–14 days m acrophage activation and cytokine expression
o
Surviving cells develop the classic histologically apparent infiltration of m ononuclear cells
o
Natural killer cells target m yocardium expressing viral RNA and continue m yocyte necrosis
o
T lym phocytes infiltrate the m yocardium with direct lysis of cardiocytes
o
Often results in cardiac dysfunction and heart failure
o
40–50% of patients report recent antecedent viral illness
True incidence is unknown because m any cases are asym ptom atic.
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Autopsy studies have dem onstrated evidence of m yocarditis in 0.5–1% of cases
Male to Fem ale ratio is 1.5:1
Average age of patients with m yocarditis is 42 years
Etiology
Viral: o
Enteroviruses (coxsackie B)
o
Adenovirus
o
Herpesvirus (including cytom egalovirus [CMV])
o
Hepatitis C
o
Influenza
o
Echovirus
o
Herpes sim plex virus
o
Varicella-zoster
o
Epstein-Barr virus
o
Cytom egalovirus
o
Mum ps
o
Rubeola
o
Variola/vaccinia
o
Yellow fever
o
Rabies
o
HIV
Bacteria: o
Diphtheria
o
Tuberculosis
o
Brucellosis
o
Psittacosis
o
Meningococcus
o
Mycoplasm a
o
Group A streptococcus
Protozoa: o
Leishm aniasis
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o
Malaria
o
Toxoplasm osis in the im m unocom prom ised host
o
Treponem a cruzi (Chagas disease):
Most com m on cause of heart failure and m yocarditis worldwide
20 m illion persons infected Central and South Am erica
o
Trichinosis
o
Trypanosom iasis
Spirochetes: o
Borrelia burgdorferi, the spirochete agent in Lym e disease
o
Syphilis
Rickettsial: o
Scrub typhus
o
Rocky m ountain spotted fever
o
Q fever
Fungal: o
Candidiasis
o
Aspergillosis
o
Cryptococcosis
o
Histoplasm osis
o
Actinom ycosis
o
Helm inthic
o
Trichinosis
o
Echinococcosis
o
Schistosom iasis
o
Cysticercosis
Drugs: o
Acetam inophen
o
Am picillin
o
Chem otherapeutic agents (anthracyclines)
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o
Cocaine
o
Hydrochlorothiazide
o
Lithium
o
Methyldopa
o
Penicillin
o
Sulfam ethoxazole
o
Sulfonam ides
o
Zidovudin
o
Radiation
o
Hypersensitivity
o
Heavy m etals
o
Hydrocarbons
o
Carbon m onoxide
o
Arsenic
Autoim m une disorders: o
System ic lupus erythem atosus (SLE)
o
Wegener granulom atosis
o
Kawasaki disease
o
Giant cell arteritis
o
Sarcoidosis
Peripartum cardiom yopathy
Bites/stings: o
Scorpion
o
Snake
o
Black widow venom
Diagnosis Signs and Symptoms History
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Fatigue
Myalgias/arthralgias
Malaise
Fever
Chest pain: o
Reported in 35%
o
Most com m only pleuritic, sharp, stabbing, precordial
Dyspnea on exertion is com m on.
Orthopnea and shortness of breath if congestive heart failure (CHF) is present
Palpitations are com m on
Syncope: o
May signal high-grade aortic valve block or risk for sudden death
Physical Exam
Fever
Tachypnea
Tachycardia: o
Often out of proportion to fever
Cyanosis
Hypotension: o
Due to left ventricular dysfunction
o
Uncom m on in the acute setting and indicates a poor prognosis when present
Bibasilar crackles
Rales
Jugular venous distention (JVD)
Peripheral edem a
Hepatom egaly
Ascites
S 3 or a sum m ation gallop if significant biventricular involvem ent
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Intensity of S 1 m ay be dim inished
Murm urs of m itral or tricuspid
Pericardial and pleural friction rub
Pediatric Considerations
Particularly infants, present with nonspecific sym ptom s: o
Fever
o
Respiratory distress
o
Poor feeding or, in cases with CHF, sweating while feeding
o
Cyanosis in severe cases
Essential Workup
Physical exam ination
ECG
Chest radiograph
Tests Lab
Cardiac enzym e levels: o
Levels are only elevated in a m inority of patients.
o
Norm ally there is a slow elevation and fall over a period of days.
o
More abrupt rise observed with acute m yocardial infarction.
o
Cardiac troponin I m ore sensitive because it is present for longer periods after m yocardial dam age
Erythrocyte sedim entation rate (ESR) is elevated in 60% during the acute phase.
Leukocytosis is present in 25%.
Viral titers; cultures rarely positive
Mycoplasm a, antistreptolysin titers
Hepatitis panels
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Monospot testing
CMV serology
Blood cultures
P.723
Imaging
ECG: o
Sinus tachycardia m ost frequent finding
o
Transient, nonspecific ST- and T-wave changes
o
Atrial and ventricular dysrhythm ias
o
Heart block and conduction defects com m on:
20% have a conduction delay, including Mobitz I, Mobitz II, or com plete heart block
20% have a left bundle branch block
Chest radiograph: o
Norm al cardiac silhouette
o
Pericarditis or overt clinical CHF is associated with cardiom egaly
o
Pulm onary edem a
o
Vascular redistribution
o
Interstitial and alveolar edem a
o
Pleural effusion
Echocardiography: o
Im pairm ent of left ventricular systolic and diastolic function
o
Segm ental wall m otion abnorm alities
o
Im paired ejection fraction
o
Pericardial effusion
o
Ventricular throm bus has been identified in 15% of patients
Gallium -67- and indium -111-labeled antim yosin antibody
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scans
Gadolinium -enhanced MRI: o
Indicate cardiac inflam m ation and m yocyte necrosis
Diagnostic Procedures/Surgery
Right ventricular endom yocardial biopsy: o
Appropriate in heart transplant recipients
o
Polym erase chain reaction am plification of viral genom e in endom yocardial tissue
Polym erase chain reaction (PCR) identification of a viral infection from pericardial fluid, or other body fluid sites
Differential Diagnosis
Acute m yocardial infarction
Acute and chronic pulm onary em bolus
Aortic dissection
Adrenal insufficiency
Environm ental challenges
Esophageal perforation/rupture/tear
Hyperpyrexia
Hypotherm ia
Kawasaki Disease
Pericarditis
Pneum onia
Viral
Bacterial
Sepsis
Severe hypothyroidism and hyperthyroidism
Toxin-m ediated disease
Treatment
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Alert
Avoid sym pathom im etic and beta-blocker drugs because they increase the extent of m yocardial necrosis and m ortality.
Patients presenting with Mobitz II or com plete heart block require pacem aker placem ent.
Initial Stabilization
ABCs
Supplem ental oxygen
Cardiac m onitor
Pulse oxim etry
IV access
ED Treatment
Sam e as for acute CHF/pulm onary edem a (see Congestive Heart Failure)
Treat dysrhythm ias if present.
Transthoracic or transvenous pacing for sym ptom atic heart block
Supplem ental oxygen
ACE inhibitors (captopril)
Reduce afterload and inflam m ation.
Digoxin
CHF or atrial fibrillation
Diuretics (furosem ide, bum etanide)
Im m unosuppressive therapy (e.g., cyclosporine, prednisone) are of unproved benefit except in patients with im m une m ediated disease (e.g., SLE).
Hyperim m unoglobulin therapy im proves cardiac function in CMV-associated m yopericarditis.
NSAIDs contraindicated in early and acute-phase m yocarditis because they increase m yocardial dam age.
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Heparin and warfarin decrease risk for throm boem bolic events in patients with depressed LV function or intracardiac throm bus
Pediatric Considerations
IV im m unoglobulin is an effective treatm ent option in pediatric viral m yocarditis
Im proved LV function and trend toward better survival
Medication (Drugs)
Captopril: o
Adult dose: initial dose 6.25 m g; can titrate to 50 m g/dose
o
Pediatric dose:
Infants: 0.15–0.3 m g/kg/dose (m ax. 6 m g/kg)
Digoxin: o
Adult dose:
o
o
Children: 0.5–1.0 m g/kg/24h
0.125–0.375 m g PO per day
Pediatric dose:
Infants: 12.5 to 20.0 m cg/kg IV or PO
2–10 years old: 7.5–15.0 m cg/kg IV or PO
5–10 years: 20–35 m cg/kg PO
>10 years: 10–15 m cg/kg PO
Maintenance dose: use 25–35% of PO loading dose
Furosem ide: o
Adult dose:
20–80 m g/d PO/IV/IM; titrate up to 600 m g/d for severe edem atous states
o
Pediatric dose:
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1–2 m g/kg PO; not to exceed 6 m g/kg; do not adm inister >q6h 1 m g/kg IV/IM slowly under close supervision; not to exceed 6 m g/kg
Im m une globulin IV (Gam im une, Gam m agard, Gam m ar-P, Sandoglobulin): o
Adult dose:
o
2 g/kg IV over 2–5 d
Pediatric dose:
Not established
Follow-Up Disposition Admission Criteria Sym ptom atic patients with m yocarditis:
New-onset
CHF
Dysrhythm ia
Mobitz II or com plete heart block
Em bolic events
Cardiogenic shock
Discharge Criteria Asym ptom atic patient with no evidence of dysrhythm ia or cardiac dysfunction
References 1. Brady WJ, Ferguson JD, Ullm an EA, Perron AD: Myocarditis: em ergency departm ent recognition and m anagem ent. Em erg Med Clin North Am . 2004 Nov; 22(4):865–885. 2. D'Am brosio A, Patti G, Manzoli A. The fate of acute m yocarditis
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between spontaneous im provem ent and evolution to dilated cardiom yopathy: a review. Heart. 2001;85:499–504. 3. Feldm an AM, McNam ara D. Myocarditis. N Engl J Med. 2000;343(19):1388–1398. 4. Fuse K, Kodam a M, Okura Y, et al. Predictors of disease course in patients with acute m yocarditis. Circulation. 2000;102(23):2829–2835. 5. Gajarski RJ, Towbin JA. Recent advances in the etiology, diagnosis and treatm ent of m yocarditis and cardiom yopathies in children. Curr Opin Pediatr. 1995;7(5):587–594. 6. Liu PP, Mason JW: Advances in the understanding of m yocarditis. Circulation. 2001 Aug 28;104(9):1076–1082. 7. Oakley CM. Myocarditis, pericarditis and other pericardial diseases. Heart. 2000;84(4):449–454.
Codes ICD9-CM 429.0
ICD10 109.0 151.4
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Nasal F ractures
Nasal Fractures
David W. Munter
Basics Description
Fractures of nasal skeleton are m ost com m on body fractures.
Most nasal fractures are result of blunt traum a, frequently from m otor vehicle crashes, sports injuries, and altercations.
Lateral forces are m ore likely to cause displacem ent than are straight-on blows.
Characteristics that suggest associated injuries: o
History of traum a with significant force
o
Loss of consciousness
o
Findings of facial bone injury
o
Frontal bone crepitus
o
Cerebrospinal fluid (CSF) leak
Etiology
The vast m ajority of nasal fractures are from direct traum a
Altercations account for m ost nasal fractures in adults
Direct blows, especially sports, account for m ost nasal fractures in children
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Diagnosis Signs and Symptoms
Nasal deform ity, asym m etry, swelling, or ecchym osis
Epistaxis
Periorbital ecchym osis (“raccoon eyes―) from dam age to branches of ethm oidal artery: o
May indicate nasofrontoethm oid com plex injury
Palpable sharp edges, depressions, or other irregularities suggest nasal fracture.
Crepitus or m obility of skeletal parts on palpation
Septal hem atom a:
o
Bluish fluid-filled sac overlying nasal septum
o
Critical to detect because it m ust be drained
Flattening of nasal root and widening of intercanthal distance (telecanthus): o
Indicative of serious nasofrontoethm oid com plex injury
Clear rhinorrhea indicates possible CSF leak: o
Rhinorrhea m ay be delayed.
Loss of sense of sm ell suggests significant injury.
Tear duct injuries m ay be present with abnorm al tearing.
Associated eye injuries: o
Subconjunctival hem orrhage
o
Hyphem a
o
Retinal detachm ents
History
Direct blow
Associated injuries or sym ptom s
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Presence of epistaxis
Changes in vision or sm ell
Physical Exam
Physical exam ination with visual inspection and palpation is m ost im portant.
It is critical to identify a septal hem atom a: o
Bluish bulging m ass on nasal septum
Exam ine closely for telecanthus: o
Intercanthal width >30–35 m m
o
Wider than width of one eye
o
May indicate nasofrontoethm oid fracture
o
Usually associated with depressed nasal bridge
CSF rhinorrhea: o
Indicates m ore serious underlying facial bone or skull fracture
o
CSF m ixed with blood will cause double ring sign when placed on filter paper.
Essential Workup
Evaluate nasolacrim al duct for patency: o
Instill fluorescein into eye and look for it in nasopharynx under inferior turbinate.
o
Absence im plies duct injury.
Eyelash traction test: o
Grasp eyelashes on eyelid and pull laterally:
o
If eyelid m argin does not becom e taut or “bow string,― then m edial portion of tendon has been disrupted.
o
This test is perform ed on both upper and lower eyelids.
Possible for only one portion of tendon to be selectively injured
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Tests Imaging
Nasal radiographs are rarely indicated: o
Norm ally do not alter initial or subsequent m anagem ent
o
Gross deform ities will need referral.
o
Fractures without deform ity will be treated conservatively regardless of radiographic findings.
o
Patients with associated facial bone deform ity, crepitus, or tenderness m ay require radiographs.
CT is test of choice if facial bone, nasofrontoethm oid, or depressed skull fractures are suspected.
Differential Diagnosis
Other facial injuries such as orbital, frontal sinus, m axillary sinus, or cribriform plate fractures
Nasofrontoethm oid fracture
Treatment Pre Hospital
Managem ent of airway takes precedence.
Nasotracheal intubation is contraindicated.
Consider orotracheal intubation or cricothyroidotom y if definitive airway control is needed.
Cervical spine precautions are indicated if there is associated traum a.
Epistaxis can norm ally be controlled with direct pressure; pinch nares together.
Initial Stabilization
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Airway m anagem ent with orotracheal intubation or cricothyroidotom y: o
Nasotracheal intubation is contraindicated.
Cervical spine precautions
Other injuries take precedence.
P.725
ED Treatment
Abrasions and lacerations: o
Proper cleansing of facial wounds is essential.
o
Lacerations m ay be sutured.
Epistaxis m ust be controlled if it does not stop spontaneously: o
Anesthetize/vasoconstrict with topical cocaine, lidocaine, or neosynephrine spray.
o
Identify bleeding source; cauterize anterior source if necessary.
o
Pack nares with petroleum jelly–im pregnated gauze or any num ber of com m ercial packs.
o
Posterior packs are rarely needed.
o
Prophylactic antibiotics to prevent sinus infection are indicated if packed.
o
Displaced fractures do not need reduction in ED unless airway is com prom ised.
o
Generally recom m ended to let swelling go down and reduce fracture in 3–5 days
Septal hem atom a m ust be drained im m ediately in ED: o
Anesthetize with topical cocaine or lidocaine and vascular constriction with neosynephrine.
o
Attem pt to aspirate with 18- to 20-gauge needle on 3-m L syringe.
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o
Rolling cotton swab down septum m ay facilitate drainage.
o
Holding m ucosa down against cartilage m ust be done to prevent reaccum ulation.
o
This can be done with petroleum jelly gauze packing.
o
Both nares should be packed to ensure adequate pressure:
Packing is left in place for 3–5 days or until follow-up with ear, nose, and throat (ENT).
o
Prophylactic antibiotics are prescribed.
Medication (Drugs)
Am oxicillin: 500 m g PO t.i.d. (peds: 40 m g/kg PO divided t.i.d.)
Am oxicillin/clavulanate: 500/125–875/125 m g PO b.i.d. (peds: 40 m g/kg/d of am oxicillin PO b.i.d.
Cocaine: topical 4%
Lidocaine: 1–2% without epinephrine
Neosynephrine nasal spray
Trim ethoprim -sulfam ethoxazole: double strength (DS) PO b.i.d. (peds: 40 m g/kg/d sulfam ethoxazole PO b.i.d.)
Follow-Up Disposition Admission Criteria
Most nasal fractures do not require adm ission.
Adm it patients with nasoethm oid fractures or m ore significant craniofacial injuries.
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Discharge Criteria
No evidence of significant head, neck, or other injuries
Follow up with ENT, plastic surgery, or oral m axillofacial (OMF) surgeon in 3–5 days for m anagem ent: o
Patients with septal hem atom a should follow up in 24 hours for re-evaluation after drainage.
Return for signs of clear rhinorrhea, difficulty breathing, fever, or signs associated with head injury.
Pediatric Considerations
Follow up with specialist sooner because fibrous union begins in only 3–4 days.
Consider contacting child protective services if any suspicion of nonaccidental traum a: o
History does not fit injury.
o
Always consider nonaccidental traum a as potential m echanism of injury.
Fractures are rare in children; nasal injuries in children are m ore likely to be cartilaginous.
Significant injuries in children are not always fully appreciated.
References 1. Cox AJ. Nasal fractures—the details. Facial Plast Surg. 2001;16:87–94. 2. Druelinger L, Guenther M, Marchand EG. Radiographic evaluation of the facial com plex. Em erg Med Clin North Am . 2000;18:393–410. 3. Ellis E, Scott K. Assessm ent of patients with facial fractures. Em erg Med Clin North Am . 2000;18:411–447. 4. Fedok FG. Com prehensive m anagem ent of naso-ethm oidorbital injuries. J Craniom axillofac Surg. 1995;1(4):36–48. 5. Hegtvedt AK, Larsen PE. Isolated nasal fractures. Atlas Oral Maxillofac Surg Clin North Am . 1994;2:1–18.
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6. Kucik CJ, Clenney T, Phelan J. Managem ent of acute nasal fractures. Am Fam Physician. 2004;70:1315–1320. 7. Staffel JG. Optim izing treatm ent of nasal fractures. Laryngoscope. 2002;112:1709–1719.
Codes ICD9-CM 802.0
ICD10 S02.2
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Near Dro w ning
Near Drowning
Janet Poponick
Basics Description Definitions
Drowning: o
Death by suffocation after subm ersion in a liquid
o
Death within 24 hours of the accident
Near drowning: o
Survival beyond 24 hours of subm ersion accident
Scenario of Drowning
Unexpected subm ersion with struggle
Aspiration of sm all am ount of water
Laryngospasm
Hypoxia
Pathophysiology
Aspiration: o
Sm all volum e of water
o
No significant electrolyte changes
o
Grossly contam inated water: risk for pulm onary infection
Hypoxem ia:
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o
Metabolic lactic acidosis
o
Multisystem organ dysfunction
o
Myocardial dysfunction
o
Coagulation abnorm alities (dissem inated intravascular coagulation [DIC])
o
Renal failure
o
CNS dysfunction
Pediatric Considerations
Hypotherm ia: o
More com m on in young children
o
Larger body surface-to-m ass ratio
o
Decreases the m etabolic rate
o
Survival with full recovery possible (neuroprotective)
Diving reflex: o
Young children m ore susceptible
o
Potentiated by fear
o
Triggered by subm ersion of face in cold water
o
Bradycardia ensues: redistribution of blood flow to the heart and brain
Diagnosis Signs and Symptoms
Cardiopulm onary arrest
Cyanosis
Dyspnea
Copious pulm onary secretions
Loss of consciousness
Cerebral edem a/injury
Evidence of traum a:
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o
Cervical spine injury
Hypotherm ia
Essential Workup
Inform ation from witnesses or em ergency m edical services (EMS) personnel at the scene
Rectal tem perature for hypotherm ia
Tests Lab
Arterial blood gas
CBC
Electrolytes, BUN, creatinine, glucose:
o
Usually norm al
o
Hyperkalem ia
o
Hypernatrem ia or hyponatrem ia
Alcohol and toxicology screen
Imaging
Chest radiograph: o
Diffuse or focal infiltrates
o
May be norm al initially
Cervical spine series
ECG: o
Long QT interval
Differential Diagnosis Consider reason for subm ersion
Dysrhythm ia (long QT syndrom e)
Myocardial infarction
Seizure
Syncope
Traum a
Pediatric Considerations
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Consider child abuse/neglect: o
Especially infants in bathtub near drowning
Treatment Pre Hospital
Attention to airway, breathing, and circulation (ABCs): o
Avoid further aspiration.
o
Apply cricoid pressure during bag-to-m ask ventilation.
o
Secure airway—intubate.
Strict cervical spine precautions
Ninety percent survival with appropriate intervention
Controversies Abdom inal thrusts to rem ove water:
Increases risk for aspiration
Useful if foreign body in airway
Initial Stabilization
ABCs
Core tem perature: o
Initiate rewarm ing (see Hypotherm ia).
o
Rem ove wet clothing.
ED Treatment
Correct hypoxem ia: o
Titrate to oxygen saturation.
o
Intubate and provide m echanical ventilation with positive end expiratory pressure.
Evaluate and treat traum atic injuries.
Correct acidosis:
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o
Adm inister sodium bicarbonate if pH 32°C or until spontaneous pulse and respirations return.
Poor prognostic signs: o
Severe acidosis (pH ≤7.0)
o
Ventricular fibrillation
o
Low oxygen saturation
P.727
Medication (Drugs)
Atropine: 1 m g (peds: 0.02 m g/kg) IV
Epinephrine: 1 m g (peds: 0.01 m g/kg) IV
Lidocaine: 1 m g/kg IV
Sodium bicarbonate: 1 m Eq/kg IV
Pediatric Considerations
Hypotherm ia m ay be protective: o
Aggressive rewarm ing
o
Aggressive resuscitation
Evaluate for child abuse/neglect:
Fam ily history: sudden death, sim ilar episode: o
Long QT syndrom e
Prevention is key to treatm ent: o
Supervision around water
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o
Em pty pails and buckets
Follow-Up Disposition Delayed sym ptom atology occurs:
Pulm onary edem a (12 hours later)
Neurologic abnorm alities
Admission Criteria
ICU: o
Patients who required cardiopulm onary resuscitation (CPR) or artificial ventilation
o
Abnorm al chest radiograph
o
Arterial blood gas abnorm alities
o
Glascow com a scale (GSC) 1 m inute
o
History of cyanosis or apnea
o
Patients who required brief assisted ventilation
o
GCS ≥13
Discharge Criteria
Questionable history of subm ersion: o
Observe in ED for 6–8 hours
o
No respiratory distress
o
No neurologic im pairm ent
Discharge to reliable hom e.
Hom e-going instructions: o
Return for shortness of breath or m ental status changes.
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References 1. Causey AL, Tilelli JA, Swanson ME. Predicting discharge in uncom plicated near-drowning. Am J Em erg Med. 2000;18:9–11. 2. Choi G, Kopplin LJ, Tester DJ, et al. Spectrum and frequency of cardiac channel defects in swim m ing-triggered arrhythm ia syndrom es. Circulation. 2004;1102:2119–2124. 3. Harries M. Near drowning. Br Med J. 2003;327:1336–1338. 4. Zuckerm an GB, Gregory PM, Santos-Dam iant SM. Predictors of death and neurologic im pairm ent in pediatric subm ersion injuries. Arch Pediatr Adolesc Med. 1998;152:134–140.
Codes ICD9-CM 994.1
ICD10 W74
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Neck Injury by Strangulatio n/Hanging
Neck
Injury by Strangulation/Hanging Patrick Cline Holland David Della-Giustina
Basics Description
Hanging: o
Com plete: victim 's entire body is suspended off the ground.
o
Incom plete: som e part of victim 's body contacts the ground.
o
Typical: the point of suspension is placed centrally over the occiput.
o
Atypical: the point of suspension is in any position other than over the central occiput.
o
Intentional: suicide, hom icide, autoerotic
o
Accidental: often children or clothing caught in m achinery
Strangulation: o
Ligature: m aterial used to com press structures of neck
o
Manual: physical force used to com press structures of
Pa ge 3 1 8
neck o
Postural: airway obstruction from body weight (over an object) or position (typically in infants)
Etiology
Hanging or strangulation: o
External neck pressure causes cerebral hypoxia secondary to either arterial or venous obstruction or m ore likely a com bination of both.
o
Pressure on neck structures m ay cause airway, soft tissue, and vascular injuries.
o
Cervical spine injuries are rare except with judicial-type hanging.
Judicial: o
Victim is dropped a distance at least equal to his or her height:
o
Forceful distraction of head from torso results in a decapitation type of injury (fracture of cervical spine and transection of spinal cord).
Death: o
Secondary to m echanical closure of blood vessels or airway
o
Secondary to cardiac arrest from extrem e bradycardia secondary to increased vagal tone from carotid sinus pressure
o
Secondary to direct neurologic injury to the spinal cord
o
Secondary to cerebral hypoxia
Associated Conditions
Larynx fracture
Hyoid fracture o
Most com m only seen in m anual strangulation
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Thyroid cartilage disruption
Vascular disruption: o
Arterial or venous
Phrenic nerve injury
Cervical spine injury
Hypoxic cerebral injury
Airway edem a
Aspiration pneum onitis (m ay be late m anifestation)
Neurogenic pulm onary edem a (m ay be late m anifestation)
Air em bolism : o
Consider when subcutaneous air and vascular injuries are present.
Diagnosis Signs and Symptoms
Airway disruption: o
Neck ecchym osis or em physem a
o
Dyspnea
o
Dysphonia or stridor
o
Loss of norm al cartilaginous landm arks
Neurologic injury: o
Hoarseness
o
Dysphagia
o
Altered m ental status
o
Neurologic deficit
Vascular injuries: o
Expanding hem atom a
o
Pulse deficits or bruits
o
Evidence of cerebral infarction
o
Subconjunctival or skin petechiae
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Cervical spine injury: o
Respiratory arrest
o
Paralysis
Pediatric Considerations
Structures of neck are m ore cartilaginous and m obile than in adults.
More resistant to crush injuries and fractures
Rapid airway com prom ise can occur with relatively little edem a of soft tissues secondary to sm aller airway diam eter.
Essential Workup
Plain radiography: o
Cervical spine/soft tissue neck to evaluate for bony injuries as well as soft tissue swelling and subcutaneous em physem a
o
Chest to evaluate for subcutaneous em physem a as well as aspiration pneum onitis
Pulse oxim etry
Tests Lab
Arterial blood gas: o
Evaluate for evidence of hypoxia or respiratory com prom ise.
Hem atocrit: o
Check for evidence of significant blood loss.
Type and cross-m atch: o
In anticipation of transfusion for vascular injuries
Imaging
Arteriography: o
Definitive evaluation for potential vascular injuries
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CT scan of neck: o
Further defines soft tissue injuries
Carotid duplex im aging with flow studies
CT scan of the brain for suspected cerebral injury or ischem ia
Diagnostic Procedures/Surgery
Fiberoptic endoscopy: o
Allows direct visualization for evaluation of endolaryngeal injury
o
May aid in intubation
Surgical exploration
P.729
Treatment Pre Hospital
Early and aggressive airway m anagem ent: oxygen, suction, intubation
Cervical spine stabilization
Initial Stabilization
Aggressive airway m anagem ent with cervical spine precautions is param ount: o
Early intubation to preclude respiratory com prom ise
Supplem ental hum idified oxygen
Control bleeding with application of direct pressure: o
Do not explore in the ED.
Em ergent tracheostom y m ay be required.
Cricothyrotom y if severe m axillofacial injuries are
Pa ge 3 1 8
present: o
Avoid if hem atom a over cricothyroid m em brane or evidence of cricotracheal disruption is seen.
o
Arrange for em ergent tracheostom y (see Larynx Fracture).
ED Treatment
IV access
Consult otolaryngologist in m anagem ent of neck soft tissue injuries.
Elevate head of bed to decrease cerebral edem a.
Monitoring of intracranial pressure if evidence of severe hypoxic cerebral injury
Neck injury with subcutaneous em physem a: o
Assum e that m ucosa of upper airway com m unicates with deep tissues of neck.
o
Adm inister antibiotics.
Laryngeal edem a: o
Consider steroids.
Medication (Drugs)
Hypoxic brain injury: o
Mannitol: 0.25–1 g/kg IV (for cerebral edem a; not routinely used in pediatric cases)
o
Phenytoin: 15 m g/kg IV as needed for seizures
Neck injury with subcutaneous em physem a: o
Am picillin/sulbactam : 3 g (peds: 100–400 m g/kg/d) IV q6h
o
Clindam ycin: 600 m g (peds: 25–40 m g/kg/d) IV q8h
Laryngeal edem a:
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o
Dexam ethasone: 4 m g (peds: 0.25–0.5 m g/kg) IV q6h
Follow-Up Disposition Admission Criteria
Adm it patients with strangulation or hanging-m echanism injuries to a m onitored setting: o
To observe for airway com prom ise (m ay have delayed onset)
Prepare for em ergent surgical correction of laryngeal injuries.
All patients with suspected suicidal or hom icidal strangulation injury should have psychiatric or social work consultation.
Discharge Criteria Only patients proven not to have strangulation or hanging injuries m ay be discharged after appropriate observation in the ED for the developm ent of any airway com prom ise or m ental status changes.
References 1. Iserson KV. Strangulation: a review of ligature, m anual and postural neck com pression injuries. Ann Em erg Med. 1984;13:179–185. 2. Kaki A, Crosby ET, Lui AC. Airway and respiratory m anagem ent following non-lethal hanging. Can J Anesth. 1997;44:445–450. 3. McClane GE, Strack GB, Hawley D. A review of 300 attempted strangulation cases. Part II: clinical evaluation of the surviving victim . J Em erg Med. 2001;21:311–315.
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4. Sabo RA, Hanigan WC, Flessner K, et al. Strangulation injuries in children. Part I: clinical analysis. J Traum a. 1996;40:68–72. 5. Wahlen BM, Thierbach AR. Near-hanging. Eur J Em erg Med. 2002;9:348–350.
Codes ICD9-CM 959.09 Injury of face and neck
ICD10 W84
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Neck Traum a, Blunt, Anterio r
Neck Trauma,
Blunt, Anterior Tamaki Kimbro
Basics Description Blunt anterior neck traum a m ay result in various injuries:
Vascular injuries: o
Carotid or vertebral artery injury
o
Intram ural hem atom a, intim al tear, throm bosis, and pseudoaneurysm
o
Laryngotracheal injuries: o
Tracheal hem atom a or transection
o
Fracture of thyroid cartilage
o
Vocal cord disruption
Pharyngoesophageal injuries: o
Hem orrhage or neck hem atom a
Hem atom a or perforation of pharynx or esophagus
Nervous system injuries: o
Ischem ic or throm boem bolic events
o
Direct injury to recurrent laryngeal nerve or stellate ganglion resulting in Horner syndrom e
Cervical spine injury
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Etiology
Motor vehicle accidents: o
Unrestrained occupants involved in frontal collisions m ay strike neck on dashboard or steering wheel.
o
Shoulder harness can also cause shearing injury to anterior neck.
Assault: blows to anterior neck from fists, weapons, or other objects
“Clothesline injury―: o
Motorcycle, snowm obile, or all-terrain vehicle
o
Drivers strike neck on cord or wire suspended between two objects.
Strangulation
Pediatric Considerations Head is proportionally larger in children, increasing risk of acceleration-deceleration injury to neck.
Diagnosis Signs and Symptoms
Presentation varies depending on m echanism of injury and structures involved: o
o
Vascular injury:
Hem orrhage, ecchym osis, edem a
Loss of character of lateral neck profile
Carotid bruit or thrill
Neurologic deficits (often delayed)
Laryngotracheal injury:
Voice changes, hoarseness, aphonia
Dyspnea, inspiratory stridor, labored breathing
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Subcutaneous em physem a, tenderness to palpation
o
o
Pharyngoesophageal injury:
Dysphagia, odynophagia, hem atem esis
Tenderness to palpation
Infection, sepsis (delayed presentation)
Neurologic injury:
Central or peripheral nervous system deficits
Physical Exam
Ensure adequate airway.
Inspection of neck for hem orrhage, ecchym osis, edem a, or distortion of anatom y
Auscultation for carotid bruits
Palpation to detect tenderness or subcutaneous em physem a
Neurologic exam ination to detect evidence of ischem ic event, spinal cord injury, or peripheral nerve dam age
Tests Lab
Type and cross-m atch.
Baseline CBC and chem istry panel
Imaging
Cervical spine radiographs
Chest radiograph to rule out associated injury to thorax
Carotid duplex ultrasound is noninvasive, rapid screening test for arterial injury.
CT m ay be used in stable patient to evaluate laryngotracheal injury, cartilage disruption, or cervical spine injury.
Angiography is still considered standard for evaluation of
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arterial injury.
Indications for angiography: o
Presence of carotid bruit
o
Pulse deficit
o
Expanding hem atom a
o
Neurologic abnorm ality unexplained by intracranial injuries
Diagnostic Procedures/Surgery
Unstable patients m ust go directly to surgery.
Endoscopy to detect internal soft tissue defects in larynx and trachea
Indications for esophagram or rigid esophagoscopy: o
Odynophagia
o
Hem atem esis
o
Subcutaneous em physem a
Differential Diagnosis
Peripheral or central nervous system injury
Cervical spine injury
Associated head or thoracic traum a
P.731
Treatment Pre Hospital
Airway m ust be vigilantly m onitored: o
Edem a or expanding hem atom a can progress to airway com prom ise.
Early oral intubation indicated for clinical signs of
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respiratory distress:
o
Stridor
o
Air hunger
o
Labored breathing
o
Expanding neck hem atom a
Blind nasotracheal intubation should be avoided: o
Owing to anatom y distortion and risk of hem atom a rupture
Cervical spine m ust be stabilized.
Initial Stabilization Airway m anagem ent with cervical spine control:
Im m ediate intubation indicated for patients with signs of airway com prom ise or im pending com prom ise
Orotracheal intubation initial m ethod of choice
Cricothyroidotom y or em ergent tracheostom y m ay be needed if oral intubation is unsuccessful.
Care should be taken to avoid puncturing neck hem atom a during invasive procedures.
Bleeding into pharynx can be reduced by packing throat with heavy gauze after airway is secured by intubation.
Unstable patients m ust go directly to OR.
General Measures
Surgical consultation should be obtained for patients with suspicion of vascular, tracheal, or esophageal injury.
Im m ediate surgical repair required for sym ptom atic vascular injury, tracheal injury, pharyngeal or esophageal injury
Laryngeal injury m ay not require im m ediate surgical repair.
Once airway is secured, patient should be placed on voice rest, hum idified oxygen, and prophylactic antibiotics.
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Medication (Drugs) Prophylactic antibiotics recom m ended in presence of laryngotracheal or pharyngoesophageal injury:
Cefoxitin: 2 g (peds: 80–160 m g/kg/d div. q6h) IV q8h or
Clindam ycin: 600–900 m g (peds: 25–40 m g/kg/d div. q6h–q8h) IV q8h or
Penicillin G: 24 m IU (peds: 150,000–250,000 IU/kg/d div. q4h–q6h) IV per day div. q4h–q6h plus
Metronidazole: 1 g load, then 500 m g (peds: 30 m g/kg/d div. q12h) IV q6h
Follow-Up Disposition Admission Criteria
Patients who are sym ptom atic, have abnorm al studies, or have significant blunt traum a m echanism m ust be adm itted and observed for at least 24 hours.
Patients with suspicion of airway or vascular injury m ust be adm itted to ICU.
Discharge Criteria Only patients with m ost trivial injuries who have negative studies m ay be discharged from ED after thorough evaluation.
References 1. Fuhrm an GM, Stieg FH, Buerk CA. Blunt laryngeal traum a. J Traum a. 1990;30:87.
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2. McKevitt EC, Kirkpatrick AW, Vertesi L, et al. Blunt vascular neck injuries: diagnosis and outcom es of extracranial vessel injury. J Traum a. 2002;53(3):472–476. 3. Miller PR, Fabian TC, Croce MA, et al. Prospective screening for blunt cerebrovascular injuries: analysis of diagnostic m odalities and outcom es. Ann Surg. 2002;236(3):386–393. 4. Newton K. Neck traum a. In: Marx J, ed. Em ergency Medicine: Concepts and Clinical Practice. 5th ed. St. Louis, MO: Mosby; 2002: 371. 5. Sweeney TA, Marx JA. Blunt neck injury. Em erg Med Clin North Am . 1993;11:71–79.
Codes ICD9-CM 959.09 Injury of face and neck
ICD10 S19.8
Pa ge 3 1 9
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Neck Traum a, Penetrating, Anterio r
Neck
Trauma, Penetrating, Anterior Tamaki Kimbro
Basics Description
Wound that penetrates platysm a m uscle
Neck is divided into three zones based on superficial landm arks: o
Zone I lies below cricoid cartilage:
Penetrating traum a in this zone carries highest m ortality owing to injury to thoracic structures.
o
Zone II lies between cricoid cartilage and angle of m andible:
Zone II wounds have lower m ortality because hem orrhage can be controlled with direct pressure.
Structures m ore easily accessible for surgical exploration
o
Zone III lies above angle of m andible.
Pediatric Considerations Larynx is located higher in neck and receives better protection from m andible and hyoid bone.
Pa ge 3 1 9
Etiology
Gunshot wounds
Stab wounds
Miscellaneous (e.g., glass shards, m etal fragm ents, anim al bites)
Diagnosis Signs and Symptoms
Vary depending on specific structures injured
Vascular injury: o
Active hem orrhage or hem atom a
o
Tracheal deviation, loss of norm al anatom ic landm arks
o
Pulse deficits in upper extrem ities
o
Thrills or bruits in neck
Laryngotracheal injury: o
Respiratory distress
o
Hoarseness, voice changes
o
Hem optysis
o
Neck pain or tenderness
o
Crepitus
Pharyngoesophageal injury: o
Dysphagia
o
Odynophagia
o
Hem atem esis
Neurologic injury: o
Central or peripheral nervous system deficits
Physical Exam
Careful exam ination of wound to determ ine extent of
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injury and whether it penetrates platysm a
Wounds should never be probed blindly: o
May result in uncontrolled hem orrhage
Essential Workup
Lateral neck radiograph to evaluate soft tissue injury and detect foreign bodies
Chest radiograph to detect hem opneum othorax, m ediastinal air, or bleeding that extends into upper m ediastinum
Tests Lab
Type and cross-m atch.
Baseline CBC and chem istry panel
Imaging
Angiography: o
Considered standard for evaluating arterial injury
o
Indicated for penetrating wounds in zone I or zone III
CT angiography can be used in stable patients to screen for vascular, cervical spine, or laryngotracheal injury.
Color duplex ultrasound: noninvasive, rapid screening test for arterial injury
Esophagram with water soluble contrast or dilute barium : o
Low sensitivity
o
Com bine with esophagoscopy to exclude injury.
o
Indications: Wound approaches/crosses m idline, subcutaneous air.
Diagnostic Procedures/Surgery Bronchoscopy can be helpful in evaluating tracheal injury.
Differential Diagnosis
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Peripheral or central nervous system injury
Cervical spine injury
Associated head or thoracic traum a
Treatment Pre Hospital
Frequent suctioning to clear airway of blood, secretions, or vom itus
Lateral decubitus or prone positioning m ay be required to prevent aspiration.
Airway m ust be vigilantly m onitored, as edem a or expanding hem atom a can progress to airway com prom ise.
Indications for early oral intubation: o
Clinical signs of respiratory distress
o
Stridor
o
Air hunger
o
Labored breathing
o
Expanding neck hem atom a
Alert
Nasotracheal intubation should be avoided: o
Potential rupture of expanding hem atom a
o
Distortion of anatom y.
Occlusive dressings should be applied to lacerations over m ajor veins to prevent air em bolism .
Initial Stabilization
Airway m anagem ent with cervical spine control: o
Patients who are in respiratory distress or com atose require im m ediate intubation.
o
Patients who are stable without evidence of
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respiratory distress m ay be m anaged aggressively with prophylactic intubation or observed closely with airway equipm ent at bedside. o
Orotracheal intubation with rapid-sequence induction is m ethod of choice for securing airway in penetrating neck traum a.
o
Blind nasotracheal intubation is contraindicated with apnea, severe facial injury, or airway distortion.
o
Endoscopic intubation is contraindicated with active bleeding that m ay obscure scope.
o
Percutaneous transtracheal ventilation m ay be useful when oral or nasotracheal intubation fails:
This is contraindicated in cases of upper airway obstruction.
May cause barotraum a
P.733
o
Cricothyroidotom y, tracheostom y, or intubation via penetrating wound m ay be required in cases of severe facial injury, laryngotracheal injury, or uncontrolled upper-airway hem orrhage.
Breathing: o
Zone I injury can cause pneum othorax or subclavian vein injury and hem othorax:
May require needle decom pression and tube thoracostom y
Circulation: o
External hem orrhage:
Control with direct pressure.
Blind clam ping of vessels is contraindicated owing to risk of further neurovascular injury.
Pa ge 3 2 0
o
Uncontrolled bleeding or hem odynam ic instability: Send directly to OR.
o
After intubation, throat can be packed with heavy gauze to tam ponade bleeding.
o
Hem othorax: tube thoracostom y
General Measures
Nasogastric tube should not be placed because of risk of rupturing pharyngeal hem atom a.
Prophylactic antibiotics are recom m ended (cefoxitin, clindam ycin, penicillin G plus m etronidazole).
Tetanus prophylaxis
Medication (Drugs)
Cefoxitin: 2 g (peds: 80–160 m g/kg/d div. q6h) IV q8h or
Clindam ycin: 600–900 m g (peds: 25–40 m g/kg/d div. q6h–q8h) IV q8h or
Penicillin G: 2.4 m IU (peds: 150,000–250,000 IU/kg/d div. q4h–q6h) IV per day div. q4h–q6h plus
Metronidazole: 1 g load, then 500 m g (peds: 30 m g/kg/d div. q12h) IV q6h
Surgery
Surgical consult for all wounds that penetrate platysm a m uscle
Controversy exists regarding m andatory versus selective surgical exploration in stable patients: o
Mandatory approach:
Surgical exploration is indicated in all cases of penetrating neck traum a because significant injury m ay not m anifest outward signs or
Pa ge 3 2 0
sym ptom s. o
Selective approach:
Surgical exploration for specific indications
Expanding or pulsatile hem atom a
Active bleeding
Absence of peripheral pulses
Hem optysis
Horner syndrom e
Bruit
Subcutaneous em physem a
Respiratory distress
Air bubbling through wound
Follow-Up Disposition Admission Criteria
All patients with penetrating neck traum a should be adm itted and observed for at least 24 hours.
Observation m ust take place in facility capable of providing definitive surgical care.
Patients with injuries suggesting airway or vascular injury m ust be adm itted to ICU.
Discharge Criteria Asym ptom atic patients who have negative studies m ay be discharged after 24 hours of observation.
References 1. Carducci B, Lowe RA, Dalsey W. Penetrating neck traum a: consensus and controversies. Ann Em erg Med. 1986;15:208.
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2. Kendall JL, Anglin D, Dem etriades D. Penetrating neck traum a. Em erg Med Clin North Am . 1998;16:85–105. 3. Munera F, Cohn S, Rivas LA. Penetrating injuries of the neck: use of helical com puted tom ographic angiography. J Traum a. 2005;58(2):413–418. 4. Newton K. Neck traum a. In: Marx J, ed. Em ergency Medicine: Concepts and Clinical Practice. 5th ed. St. Louis, MO: Mosby; 2002: 371. 5. Rathlev NK. Penetrating neck traum a: m andatory versus selective exploration. J Em erg Med. 1990;8:75–78.
Codes ICD9-CM 959.09 Injury of face and neck
ICD10 S19.8
Pa ge 3 2 0
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Necro tiz ing So ft Tissue Infectio ns
Necrotizing
Soft Tissue Infections Karen B. Van Hoesen
Basics Description
Necrotizing soft-tissue infections are usually caused by toxin-producing, virulent bacteria.
Characterized by widespread fascial and m uscle necrosis with relative sparing of the skin
Crepitant anaerobic cellulitis: o
Necrotic soft-tissue infection with abundant connective tissue gas
Progressive bacterial gangrene: o
Slowly progressive erosion affecting the total thickness of skin but not involving deep fascia
Nonclostridial m yonecrosis (synergistic necrotizing cellulitis): o
Aggressive soft-tissue infection of skin, m uscle, subcutaneous tissue and fascia
Necrotizing fasciitis: o
Progressive, rapidly spreading infection with extensive dissection and necrosis of the superficial
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and deep fascia
Fournier gangrene: o
Mixed aerobic-anaerobic soft-tissue necrotizing fasciitis of the skin of the scrotum and penis in m en and the vulvar and perianal skin in wom en
Etiology
Conditions that lead to the developm ent of necrotizing soft-tissue infections: o
Local tissue traum a with bacterial invasion
o
Local ischem ia and reduced host defenses:
More frequently in diabetics, alcoholics, im m unosuppressed patients, IV drug users, and patients with peripheral vascular disease
Polym icrobial etiology including: o
Group A β-hem olytic streptococcus (GABHS); group B streptococcus, staphylococci, enterococci, bacillus, pseudom onas, Enterobacter, Bacteroides, clostridia, and Vibrio species
Possible relationship between the use of NSAIDs and severe invasive GABHS infections has been suggested.
Diagnosis Signs and Symptoms
Rapid progression of pain and swelling of involved area
Pain out of proportion to physical findings
In first 24 hours, rapid developm ent of local swelling, heat, erythem a, and tenderness
24–48 hours: purple and blue discoloration, blisters and bullae develop (often hem orrhagic)
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Necrosis of fascia and fat produces a watery, thin, foul-sm elling fluid.
System ic toxicity with fever, tachycardia, and depressed m entation
Pediatric Considerations
Neonates: Om phalitis and circum cision are predisposing factors
Children: surgery, traum a, varicella, and congenital and acquired im m unodeficiencies are m ajor factors for the developm ent of necrotizing fasciitis: o
GABHS necrotizing fasciitis as a com plication of varicella has been reported
Physical Exam
Skin: erythem a, tense edem a, grayish or other discolored wound drainage, vesicles or bullae, necrosis, ulcers or crepitus
Pain that extends past m argin of infection
General: fever, tachycardia, diaphoresis, toxic delirium
Essential Workup
Diagnosis can be difficult.
Careful exam ination for the aforem entioned signs and sym ptom s in high-risk patients
Necrotizing soft-tissue infections m ust be suspected in patients who appear very ill and have pain out of proportion to physical findings.
Diagnosis requires incision and probing of tissue.
Tests Lab
CBC with differential, electrolytes, blood urea nitrogen, and creatinine, dissem inated intravascular coagulation
Pa ge 3 2 0
panel
Calcium level: hypocalcem ia can develop from extensive fat necrosis.
Gram stain and aerobic/anaerobic cultures of wound or tissue biopsy
Imaging
X-rays to detect soft-tissue gas
CT scan or MRI can delineate extent of spread of the infection
Diagnostic Procedures/Surgery All patients with suspected necrotizing soft tissue infections m ust undergo surgical debridem ent.
Differential Diagnosis
Cellulitis
Gas gangrene
Treatment Pre Hospital IV fluid resuscitation
Initial Stabilization Manage airway and resuscitate as indicated:
Rapid sequence intubation as needed
Supplem ental oxygen, m onitor, evaluate for acid-base disturbances
IV access, CVP line m ay be needed
Aggressive volum e expansion including crystalloid, plasm a, packed RBCs, and album in
Pa ge 3 2 0
ED Treatment
Antibiotics: broad coverage of aerobic gram -positive and gram -negative organism s and anaerobes: o
Penicillin or cephalosporin, an am inoglycoside, and anaerobic coverage with either clindam ycin or m etronidazole
o
Penicillin G if strep or clostridia
o
Im ipenem cilastatin or m eropenem if polym icrobial
o
Am picillin-sulbactam (Unasyn)
o
Piperacillin-tazobactam (Zosyn)
P.735
Surgical consultation: o
Early débridem ent of all necrotic tissue with fasciotom y and drainage of fascial planes is param ount
Hyperbaric oxygen as an adjunct: o
Early transfer to hyperbaric facility m ay result in greater tissue salvage
Observe for m ajor com plications including acute respiratory distress syndrom e, renal failure, m yocardial irritability, and DIC
Medication (Drugs)
Am picillin-sulbactam (Unasyn): 1.5–3 g (peds: 100–400 m g/kg/d of am picillin div. q6h) IV q6h
Ceftriaxone: 2 g (peds: 100 m g/kg/24h; m ax. 4 g) IV q24h
Clindam ycin: 900 m g (peds: 40 m g/kg/d q6h) IV q8h
Gentam icin: 2.0 m g/kg (peds: 2.0 m g/kg IV q8h) IV q8h
Pa ge 3 2 0
Im ipenem -cilastatin: 250–1,000 m g IV q6h–q8h
Meropenem 1 g (peds: 20–40 m g/kg up to 2 g/dose) IV q8h
Metronidazole: 500 m g (peds: safety not established) IV q8h
Penicillin G: 24 m IU/24 h (peds: 250,000 IU/kg/24h) IV q4h–q6h
Piperacillin-tazobactam 3.375–4.5 g (peds: 240 m g/kg/d pf piperacillin div. q8h) IV q6h
Follow-Up Disposition Admission Criteria
All patients with a necrotizing soft-tissue infection m ust be adm itted for surgical débridem ent and IV antibiotics.
Early hyperbaric oxygen therapy is an im portant adjunct.
Discharge Criteria No patient with necrotizing soft tissue infection should be discharged.
Issues for Referral After stabilization with antibiotics and surgical débridem ent, consider referral for hyperbaric oxygen treatm ent as an adjunct.
References 1. DiNubile MJ, Lipsky BA. Com plicated infections of skin and skin structures: when the infection is m ore than skin deep. J Antim icrob Chem other. 2004 Jun;53 Suppl 2:ii37–50. 2. Headley AJ. Necrotizing soft tissue infections: a primary care review. Am Fam Physician. 2003 Jul 15;68(2):323–328. 3. Legbo JN, Shehu BB. Necrotizing fasciitis: a com parative analysis
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of 56 cases. J Natl Med Assoc. 2005 Dec;97(12):1692–1697. 4. Perry BN, Floyd WE 3rd. Gas gangrene and necrotizing fasciitis in the upper extrem ity. J Surg Orthop Adv. 2004 Sum m er;13(2):57–68. 5. Wilkinson D, Doolette D. Hyperbaric oxygen treatm ent and survival from necrotizing soft tissue infection. Arch Surg. 2004 Dec;139(12):1339–1345.
Codes ICD9-CM 709.8
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Necro tiz ing Ulcerative G ingivitis
Necrotizing
Ulcerative Gingivitis Stephen K. Epstein Laura B. Glicksman
Basics Description
Periodontal disease
Characterized by the “punched out― appearance of the gingival papillae
Synonym (s): o
Acute necrotizing ulcerative gingivitis
o
Trench m outh
o
Vincent disease
o
Fusospirochetal gingivitis
Not contagious
Occurs m ost often in children in developing nations.
Occurs m ost often in young adults in developed countries.
Males affected m ore than fem ales
Can progress to m ore advanced disease:
o
Necrotizing ulcerative periodontitis
o
Orofacial gangrene (nom a)
Mainly occurs in sub-Saharan Africa
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Rare; seen m ostly in severely im m unocom prom ised patients
Etiology
Caused by an overgrowth of oral flora
Prevotella interm edia
Spirochetes
Predisposing factors (not required for diagnosis): o
Em otional and physical stress
o
Poor oral hygiene/gingivitis
o
Sm oking
o
Im m unodeficiencies (e.g., HIV)
o
Im m unosuppression
o
Malnutrition
Diagnosis Signs and Symptoms Essential Clinical Features
Painful gingival lesions
“Punched-out,― craterlike ulcers of the papillae
Ulcers bleed easily or spontaneously
Non-Essential Clinical Features
“Pseudom em brane― of necrotic debris covering the ulcerated area
Foul breath
Fever/m alaise
History
Acute, generalized oral pain
Bleeding gum s:
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o
Spontaneous or with m inim al m anipulation
Foul breath
Malaise
Low-grade fever
Physical Exam
Loss of interdental papillae (key clinical feature)
“Punched-out,― craterlike ulcers of the papillae
Necrotic debris often present over ulcerated surfaces
“Pseudom em brane― of inflam m atory and necrotic cells
Covers ulcerative lesions
Leaves a bleeding surface when rem oved
Lym phadenopathy, particularly subm andibular
Foul breath
Low-grade fever
Essential Workup
Consider system ic disease: o
Neutropenia
o
HIV
Other reasons for im m unosuppression or im m unocom prom ise
Rule out com plications: o
Progression to necrotizing ulcerative periodontitis
o
Lesions extending to periodontal ligam ent and alveolar bone
o
Alveolar bone destruction
o
Progression to orofacial gangrene (nom a)
Tests Lab Laboratory tests not clinically helpful
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Differential Diagnosis
Other diseases rarely have the essential clinical feature of “punched-out― interdental papillae with ulcerations
Infectious diseases: o
Acute herpetic gingivostom atitis:
Affects entire gingival, not just papillae
Low grade fever com m only present
Contagious
Viral: o
Viral infections: Epstein-Barr, Varicella Zoster virus
o
Thrush
o
Actinom ycosis
o
Streptococcal/gonococcal gingivitis/stom atitis
o
Secondary syphilis
o
Diphtheria
o
Vesiculobullous disease
o
Pem phigoid
o
Pem phigus
o
Oral lichen planus
o
System ic lupus erythem atosus
Traum a: o
Toothpicks
o
Vigorous toothbrushing/flossing
Im m unocom prom ise: o
Leukem ia
o
Agranulocytosis (m alignant neutropenia)
o
HIV
P.737
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Treatment Initial Stabilization IV fluids for dehydration
ED Treatment
Adm inister system ic and topical pain m anagem ent: o
Narcotics rarely necessary
o
Viscous lidocaine
Débride pseudom em brane: o
Use gauze or cotton-tip applicator soaked in diluted H 2
O2 .
Antibiotics (penicillin/m etronidazole or clindam ycin) when indicated:
o
Fever
o
Lym phadenopathy
Institute outpatient therapy: o
Rem ove predisposing factors.
o
Dilute hydrogen peroxide rinses.
o
Chlorhexidine gluconate (Peridex)
o
Antibiotics if indicated
o
Avoid irritants (spicy foods, hot beverages).
o
Analgesics for pain control
o
Im prove oral hygiene with daily brushing and flossing of teeth.
Medication (Drugs)
Oral rinses: o
Chlorhexidine gluconate (Peridex): 15 m L swish/spit b.i.d.
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o
Hydrogen peroxide (3% solution diluted in half): rinse up to 12 tim es daily
Metronidazole: 250–750 m g (peds: 30 m g/kg/q24h) PO q.i.d. ×7 days
Penicillin VK: 500 m g (peds: under age 12, 25–50 m g/kg q24h) PO q.i.d. ×10 days
Clindam ycin: 300 m g PO (peds: 6–8 m g/kg q24h) t.i.d.
Follow-Up Disposition Admission Criteria
Extensive disease with system ic signs
Severe dehydration/inability to tolerate PO fluids
Evidence of orofacial gangrene (nom a): infection of m outh/face: o
70% m ortality with no treatm ent
Discharge Criteria Able to m aintain hydration
Issues for Referral Urgent referral to a dentist or periodontist for deep scaling and debridem ent
References 1. Am erican Academ y of Periodontology. Param eter on acute periodontal diseases. J Periodont. 2000;71(5 suppl):863–866. 2. Am erican Academ y of Periodontology. Treatm ent of Plaque-Induced Gingivits, Chronic Periodontitis, and Other Clinical Conditions. J Periodontol. 2001;72:1790–1800. 3. Am erican Academ y of Periodontology. Periodontal Diseases of
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Children and Adolescents. J Periodontol. 2003;74:1696–1704. 4. Corbet EF. Diagnosis of acute periodontal lesions. Periodontol. 2000. 2004;34:204–216. 5. Berm ejo-Fenoll A, Sanchez-Perez A. Necrotising periodontal diseases. Med Oral Patol Oral Cir Bucal. 2004;9(Suppl):S108–19. 6. Enwonwu CO, Falkler WA, Idigbe EO. Oro-facial gangrene (nom a/cancrum oris): pathogenetic m echanism s. Crit Rev Oral Biol Med. 2000;11(2):159–171. 7. Musa NJ, Kum ar V, Hum prheys L, et al. Oral Pem phigoid Masquerading as Necrotizing Ulcerative Gingivitis in a Child. J Periodontol. 2002;73:657–663. 8. Rowland RW. Necrotizing Ulcerative Gingivitis. Ann Periodontol. 1999;4:65–73. 9. Periodontal Em ergencies, in The Periodontic Syllabus (Fedi PF editor). Phildelphia: Lea & Febinger, 1985.
Codes ICD9-CM 523.0
ICD10 A69.1
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Needle Stick
Needle Stick
Gordon Chew
Basics Description Mechanism s of exposure to blood or body fluid:
Percutaneous
Mucous m em brane
Skin
General Prevention
Universal precautions
Avoid recapping of needles
Wear gloves: decreases am ount of blood exposure by 50%
Double gloving
Follow body–substance isolation protocols.
Hepatitis B virus vaccination
Risk Factors
Risk of seroconversion from a single needle-stick exposure without prior im m unization: o
Hepatitis B virus: 37–62% from HBsAg-positive and HBeAg-positive source, 23–37% from HBsAg-npositive and HBeAgnegative source
o
Hepatitis C virus: 1.8%
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o
HIV: blood 0.3%, m ucous m em brane 0.09%
Infectiousness of various body fluids for HIV: o
Plasm a/serum : 10–5,000 ppm
o
Cerebrospinal fluid: 10–1,000 ppm
o
Sem en: 10–50 ppm
o
Vaginal secretions, urine, saliva, tears, breast m ilk: Table o f C o ntents > Neo natal Jaundice
Neonatal Jaundice
Michele Chetham
Basics Results from a transient im balance between rates of bilirubin production and bilirubin elim ination:
Newborns have higher rates of bilirubin production than adults because of increased RBC m ass and shorter RBC life span.
Newborns, especially preterm infants, have rate lim itations in hepatic conjugation and biliary excretion of bilirubin, increased enterohepatic circulation, and dim inished bilirubin binding to album in- and bilirubin-binding protein.
Alert Although norm ally benign, significantly elevated bilirubin can cause significant injury and reflect a potentially life-threatening underlying condition.
Description
In the vast m ajority of newborns, this represents physiologic jaundice and is not pathologic: o
Bilirubin norm ally increases from 1.5 m g/dL in cord blood to a m ean of 6.5 m g/dL on day 3, followed by a gradual decline to norm al adult levels of 1.5 m g/dL
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by day 10 or 12 of life:
However, serum bilirubin levels m ay rise to dangerous levels exceeding neuroprotective defenses causing bilirubin toxicity to the basal ganglia, hippocam pus, brainstem nuclei and cerebellum .
o
Acute bilirubin encephalopathy (ABE) describes the acute m anifestations of bilirubin toxicity seen in the first weeks after birth.
o
Kernicterus is the chronic form of bilirubin encephalopathy, resulting in significant m ortality; survivors m ay have serious neurologic consequences including a choreoathetoid type of cerebral palsy, gaze abnorm alities, hearing loss, and dental dysplasia.
o
Bilirubin-induced neurologic dysfunction (BIND) refers to the wide spectrum of disorders caused by increasingly severe hyperbilirubinem ia from m ild dysfunction to ABE and kernicterus.
o
Rate of progression of BIND depends on rate of increase of bilirubin levels, duration of hyperbilirubinem ia, album in-binding reserves, unbound bilirubin level, host susceptibility, com orbidities.
o
Death is owing to respiratory failure and progressive com a, or intractable seizures.
Neurotoxic effects of hyperbilirubinem ia are seen m ore com m only with hem olytic disease, less com m only in healthy newborns.
Severe hyperbilirubinem ia m ay be caused by pathologic conditions.
Risk factors for hyperbilirubinem ia:
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o
Hem olytic disease
o
Gestation 35–38 weeks
o
Low birth weight
o
Large weight loss after birth
o
Breast-feeding
o
Ethnicity: Asian, Native Am erican, Greek Islander
o
Siblings with hyperbilirubinem ia
o
Fam ily history of G6PD deficiency or hereditary spherocytosis
o
Maternal diabetes
o
Perinatal factors: polycythem ia, birth traum a, infection
Early discharge of newborns has resulted in m ore problem atic jaundiced newborns owing to delayed diagnosis and increased breast-feeding.
Etiology Unconjugated Hyperbilirubinemia
Physiologic jaundice
Jaundice in breast-fed infants: o
Breast-feeding jaundice—exaggeration of physiologic jaundice owing to inadequate ingestion of breast m ilk in the first week of life; prolongation up to 8 weeks m ay be caused by factors in breast m ilk that inhibit hepatic conjugation of bilirubin.
Specific hem olytic conditions: o
Blood group isoim m unization owing to ABO, Rh, and m inor blood group incom patibility; ABO is m ost com m on: Rh disease is unusual (RhoGAM prevents).
o
Red cell m em brane defects: hereditary spherocytosis
o
Red cell enzym e deficiencies: G6PD deficiency
Sepsis: bacterial, viral, or protozoal
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Birth traum a: o
Increased hem e load from resolving cephalohem atom a or ecchym osis
Polycythem ia: o
Caused by m aternal-fetal transfusion
o
Fetal-fetal transfusion
o
Infants of diabetic m others
Congenital hypothyroidism
Defective hepatic conjugation: o
Gilbert syndrom e (fam ilial partial defect in glucuronyl transferase activity) is a com m on benign condition.
o
Crigler-Najjar syndrom e (congenital absence of glucuronyl transferase causes lifelong unconjugated hyperbilirubinem ia)
o
Lucy-Driscoll syndrom e (severe unconjugated hyperbilirubinem ia thought to be owing to inhibition of infant's glucuronyl transferase by unidentified m aternal serum factors)
Conjugated Hyperbilirubinemia
Failure of hepatic excretion of conjugated bilirubin
Causes include neonatal hepatitis, congenital biliary atresia, extrahepatic biliary obstruction, shock liver from neonatal asphyxia, neonatal hem osiderosis
Diagnosis Signs and Symptoms History
Sleepiness, poor intake, and inadequate urine output m ay be present.
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Early phase of acute bilirubin encephalopathy (ABE): o
Feeding difficulties with poor suck
o
Fussiness and irritability
o
Lethargy with altered awake-sleep pattern
o
Hypotonia
Interm ediate Phase of ABE: o
High-pitched cry, irritability
o
Increased tone with backward arching of neck (retrocollis) and trunk (opisthotonos) alternating with hypotonia
o
Fever
Signs of advanced ABE: o
Pronounced retrocollis-opisthotonos
o
Sem icom a, seizures
o
Bicycling m ovem ents
Physical Exam
Yellowish discoloration of skin, tissues such as sclerae, and body fluids in the newborn infant
Indicates an elevated serum bilirubin level
Increasing levels of bilirubin affect skin color progressing from the face downward: o
Blanch skin with digital pressure to reveal underlying skin color—only approxim ates level
o
Face—bilirubin levels >6–8 m g/dL
o
Feet—bilirubin levels >12–15 m g/dL
Physical exam clues to som e causes: o
Sepsis: lethargy, tem perature instability, poor feeding, vom iting, apnea or tachypnea
o
Hem olytic disease: pallor, hepatosplenom egaly
o
Extravascular hem olysis: birth traum a associated with cephalohem atom a or bruising
o
Polycythem ia: ruddy com plexion
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o
Cholestatic jaundice: persistent jaundice for >3 weeks, dark urine, or light-colored stool
Visual diagnosis of jaundice is unreliable, especially in darkly pigm ented infants.
Essential Workup
Clinical diagnosis
Total serum bilirubin (TSB) m andatory in any infant with suspected or obvious jaundice
Direct (conjugated) and indirect (unconjugated) bilirubin levels
Interpret TSB according to infant's age in hours, not days, to determ ine risk and need for treatm ent.
Determ ine if TSB level drawn prior to birth hospitalization discharge.
Transcutaneous m easurem ent of bilirubin (TcB) correlates well with TSB and is available in som e centers.
Further evaluation is recom m ended for these newborns with jaundice: o
Occurs in the first 24 hours of life
o
Persists beyond the first week of life
o
TSB levels reach level to initiate intensive phototherapy.
o
Bilirubin is >10% or >2 m g/dL conjugated.
o
Any signs of ABE
Tests Lab
Serum album in, electrolytes, calcium
CBC with differential and sm ear for RBC m orphology
Reticulocyte count
Maternal and infant blood type
Direct Coom bs test on cord blood:
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o
Hospital routines vary: Som e will test newborns from all type O m others.
o
If not available, direct Coom bs test on infant's blood
Further workup is directed at suspected cause.
Red cell enzym e assay
Liver function tests
Sepsis evaluation
Urine-reducing substance
P.741
Imaging Evaluation for obstructive liver disease (direct hyperbilirubinem ia): consultation and im aging studies
Differential Diagnosis
See Etiology.
Essential to differential unconjugated from conjugated
Treatment Initial Stabilization 0.9% norm al saline (NS) 20 m L/kg, bolus if signs of dehydration
ED Treatment
Treatm ent guidelines for infants ≥35 weeks gestation based on TSB plotted versus age in hours for infants at lower, m edium , or higher risk.
Higher risk are 35–37 6/7 weeks plus risk factors.
Medium risk are ≥38 weeks plus risk factors, or 35–37 6/7 weeks and well.
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Lower risk are ≥38 weeks and well.
Risk factors: isoim m une hem olytic disease, G6PD deficiency, asphyxia, significant lethargy, tem perature instability, sepsis, acidosis, album in 0.5 m g/dL/h.
Indications for exchange transfusions are also determ ined by age in hours and risk stratification: o
For exam ple, at 48 hours, exchange transfusion recom m ended if higher risk with TSB ≥16 m g/dL, m edium risk with TSB ≥19 m g/dL, and low risk with TSB ≥22 m g/dL.
Im m ediate exchange transfusion is recom m ended regardless of TSB level if infant shows signs of acute bilirubin encephalopathy: o
Type and cross-m atch for 170 m L/kg of blood for double-volum e exchange transfusion.
o
Album in infusion 1 gm /kg if serum album in is low ( Table o f C o ntents > Neo natal Sepsis
Neonatal Sepsis
Lazaro Lezcano
Basics Description
Life-threatening infection of the newborn, rarely occurring as late as 3 m onths of age
Overwhelm ingly bacterial: o
Rarely viral or fungal infection
o
Organism s usually present in the m aternal perineal flora.
Occurs in 3–5 newborns per 1,000 live births
Risk factors: o
o
Perinatal:
History of recent fever (>37.5°C)
Urinary tract infection
Chorioam nionitis
Prolonged rupture of m em branes (>18 hours)
Foul lochia
Uterine tenderness
Intrapartum asphyxia
Neonatal:
Prem aturity
Fetal tachycardia (>180 beats/m in)
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Male
Twinning (especially second twin)
Developm ental or congenital im m une defects
Adm inistration of intram uscular iron
Galactosem ia
Congenital anom aly (urinary tract, asplenia, m yelom eningocele, sinus tract)
Om phalitis
Etiology Sepsis
Bacterial: o
Group B streptococcus
o
Escherichia coli
o
Listeria m onocytogenes
o
Coagulase-negative Staphylococcus
o
Treponem a pallidum
Viral: o
Herpes sim plex is a com m on viral cause
o
Enterovirus
o
Adenovirus
Fungi: o
Candida species
Protozoa: o
Malaria
o
Borrelia
Meningitis
Bacterial: o
Group B streptococcus
o
E. coli type K1
o
L. m onocytogenes
o
Other streptococci
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o
Nontypeable Haem ophilus influenzae
o
Coagulase-positive and coagulase-negative
o
Staphylococcus
o
Less com m only: Klebsiella, Enterobacter,
o
Pseudom onas, T. pallidum , and Mycobacterium tuberculosis
o
Citrobacter diversus (im portant cause of brain abscess)
o
Additional pathogens: Mycoplasm a hom inis and
o
Ureaplasm a urealyticum
Viral: o
Enteroviruses
o
Herpes sim plex virus (type 2 m ore com m only)
o
Cytom egaloviruses
o
Toxoplasm a gondii
o
Rubella
o
HIV
Fungi: o
Candida albicans and other fungi
Diagnosis Signs and Symptoms History
Nonspecific history: o
“Not acting norm al―
o
Feeding poorly
o
Irritable or lethargic
General: o
Toxic appearing
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o
Altered m ental status—irritable or lethargic
o
Apnea or bradycardia
o
Mottled, ashen, cyanotic, or cool skin
Physical Exam
Vital signs: o
Hypertherm ia/hypotherm ia
o
Tachypnea
o
Tachycardia
o
Prolonged capillary refill tim e
Abdom inal distention
Jaundice
Bruising or prolonged bleeding
Sepsis syndrom e in the neonate: o
Septic shock
o
Hypoglycem ia
o
Seizures
o
Dissem inated intravascular coagulation (DIC)
o
If untreated, cardiovascular collapse and death
Essential Workup
Sepsis evaluation followed by em piric antibiotics and support
Determ ine a source for the infection.
Identify m etabolic abnorm alities.
Tests Lab
Bedside glucose determ ination
CBC: o
WBCs elevated or suppressed
o
Shift to the left
o
Throm bocytopenia
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Urinalysis
Cultures as soon as the diagnosis is entertained: o
Blood, cerebrospinal fluid (CSF), catheterized or suprapubic urine, stool
Lum bar puncture: o
May need to delay if hem odynam ically unstable
o
Cell count, protein, glucose, culture
Serum glucose needed to exclude hypoglycem ia
ABG and oxim etry: o
Metabolic acidosis is com m on.
Electrolytes and calcium : o
Hyponatrem ia
o
Hypocalcem ia
DIC panel: o
Coagulopathy is a late com plication.
o
Monitor PT, PTT, and fibrinogen-split products.
P.743
Imaging Chest radiograph to rule out pneum onia
Differential Diagnosis
Heart disease: o
Hypoplastic left heart syndrom e
o
Myocarditis
Metabolic disorders: o
Hypoglycem ia
o
Adrenal insufficiency (congenital adrenal hyperplasia)
o
Organic acidoses
o
Urea cycle disorders
Intussusception
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Child abuse
CNS: o
Intracranial hem orrhage
o
Perinatal asphyxia
Neonatal jaundice
Hem atologic em ergencies: o
Neonatal purpura fulm inans
o
Severe anem ia
o
Methem oglobinem ia
o
Malignancy (congenital leukem ia)
Treatment Pre Hospital Cautions:
Ventilatory support if obtunded, apneic, or respiratory distress
IV access
Continuous m onitoring
Initial Stabilization
Airway m anagem ent indicated if obtundation, apnea, or respiratory distress
IV access to adm inister fluids and pressors as needed
Continuous m onitoring
ED Treatment
Im plem ent em piric treatm ent for neonatal sepsis if presentation at all consistent, particularly if any risk factors are present.
Adm inister antibiotics: o
Am picillin and gentam icin
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o
Add vancom ycin if the patient's condition continues to deteriorate or any suggestion of Streptococcus pneum oniae.
o
Cefotaxim e m ay be substituted for gentam icin.
Support for septic shock if present
Medication (Drugs)
Am picillin: 200 m g/kg/d q6h IV/IM for infants >2 kg birth weight and older than 2 weeks; 150 m g/kg/d q8h if younger than 7 days
Cefotaxim e: 150 m g/kg/d q6h IV/IM for infants >2 kg birth weight and older than 1 week; 150 m g/kg/d q8h IV/IM if 8–28 days of age; 100 m g/kg/d IV/IM q12h if 0–7 days of age
Gentam icin: 2.5 m g/kg per dose q8h IV/IM if postconceptual age >37 weeks and older than 7 days; 2.5 m g/kg per dose q12h if younger than 7 days
Vancom ycin: 15 m g/kg per dose IV q8h if postconceptual age >37 weeks and older than 7 days; 15 m g/kg IV q12h if younger than 7 days
Follow-Up Disposition Admission Criteria All patients with suspected sepsis are adm itted to the hospital for supportive care, IV antibiotic therapy, and close m onitoring.
References
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1. Anderson MR, Blum er JI. Advances in the therapy for sepsis in children. Pediatr Clin North Am . 1997;44:179–205. 2. Edwards MS. Postnatal bacterial infections. In: Fanaroff AA, Martin RJ, eds. Neonatal-Perinatal Medicine. Diseases of the Fetus and Infant. 7th ed. St. Louis, MO: Mosby; 2002:706–722. 3. Polin RA, Parravicini E, Regan JA, et al. Bacterial sepsis and m eningitis. In: Taesch HW, Ballard RA, Gleason CA. Avery's Diseases of the Newborn. 8th ed. Philadelphia: Elsevier Saunders, 2005: 551–568. 4. Shapiro NI, Zim m er GD, Barkin AZ. Sepsis syndrom e. In: Marx JA, Hockberger RS, Walls RM, eds. Rosen's Em ergency Medicine: Concepts and Clinical Practice. 5th ed. St. Louis, MO: Mosby; 2002.
Codes ICD9-CM 771 790.7
ICD10 P36.9
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Nephritic Syndro m e
Nephritic
Syndrome Anwer Hussain
Basics Description
Acute glom erulonephritis (AGN) is acute inflam m atory dam age to glom erulus, associated with: o
Abrupt onset of hem aturia with or without RBC casts
o
Acute renal failure m anifested by edem a, hypertension, azotem ia
o
Variable proteinuria
o
Active urine sedim ent (RBC casts)
Exact m echanism of AGN unclear: o
Com bination of autoim m une reactivity to specific antigens at renal glom eruli
o
Glom erulonephritis com prises 25–30% of end-stage renal disease (ESRD)
Etiology Postinfectious Causes of Acute Nephritic Syndrome (PIGN) N/A
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Poststreptococcal Glomerulonephritis (PSGN)
Occurs between the ages of 3 and 15 years but can occur at any age
Due to group A β-hem olytic streptococci
Incidence of GN is 5–10% in pharyngitis and 25% in skin infections.
Consider PIGN in new onset proteinuria, RBC casts, and any recent infection.
Latent period between infection and onset of nephritis helps differentiate between PSGN and IgA nephropathy: o
1–3 weeks in pharyngeal infection
o
2–4 weeks in cutaneous infection
Renal biopsy usually not necessary for diagnosis.
Hum p-shaped subepithelial deposits due to antigen-antibody reaction
Low com plem ents for 6–8 weeks (C3, CH50)
Progresses to severe renal failure if infection persists
Treat with antibiotics
Prognosis: o
Excellent; >95% recover spontaneously with norm alization of renal function within 6–8 weeks, even with dialysis
o
Hem aturia usually resolves in 3–6 m onths
o
Transient nephrotic phase in 20% of patients during resolution of illness
o
ESRD occurs Table o f C o ntents > Neuro leptic Po iso ning
Neuroleptic
Poisoning Mark B. Mycyk
Basics Description
Neuroleptics (antipsychotics) used for m anagem ent of: o
Psychotic disorders
o
Depressive neurosis
o
Dem entia in the elderly
o
Behavioral problem s in children
o
Antiem etic
Peak plasm a levels within 4 hours
Dystonia occurs within hours to days of ingestion.
Akathisia occurs within days to weeks of increased dosing.
Etiology
Typical neuroleptics (phenothiazines, butyrophenones) strongly antagonize dopam inergic receptors: o
Haloperidol (Haldol)
o
Chlorprom azine (Thorazine)
o
Thioridazine (Mellaril)
o
Fluphenazine (Prolixin)
o
Prom ethazine (Phenergan)
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o
Droperidol (Inapsine)
Atypical neuroleptics have weaker dopam inergic antagonism and m oderate serotonergic antagonism : o
Clozapine (Clozaril)
o
Risperidone (Risperdal)
o
Olanzapine (Zyprexa)
o
Quetiapine (Seroquel)
o
Ziprasidone (Geodon)
Both exhibit strong α-adrenergic antagonism .
Both exhibit anticholinergic activity.
Diagnosis Signs and Symptoms
Overdose: o
Toxic effects are typically m ild to m oderate.
o
CNS sym ptom s predom inate.
Neurologic: o
Slurred speech
o
CNS depression
o
Agitation
o
Com a
o
Seizures
o
Extrapyram idal sym ptom s (dystonia, akathisia)
Cardiovascular: o
Hypotension
o
Tachycardia
o
Prolonged QRS or QTc
o
Torsades de pointes
Respiratory: o
Respiratory depression
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Gastrointestinal: o
Constipation
o
Dry m outh
Genitourinary: o
Urinary retention
Hypertherm ia:
Ocular: m iosis or m ydriasis
Hem atologic: anem ia, agranulocytosis (clozapine)
Neuroleptic m alignant syndrom e (NMS): o
Hypertherm ia
o
Skeletal m uscle rigidity
o
Altered m ental status
o
Autonom ic dysfunction
Alert
Chronic use: o
New-onset diabetes m ay occur with atypical neuroleptic use.
Essential Workup
Monitor vital signs with significant ingestions.
Cardiac m onitor
Pulse oxim etry
Tests Lab
Electrolytes, BUN, creatinine, glucose
CBC for clozapine overdose
Urinalysis: o
Dip for m yoglobin if rhabdom yolysis suspected
Creatine phosphokinase (CPK) levels if NMS suspected, agitation, or prolonged im m obilization
Urine toxicologic screen to exclude coingestants
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Quantitative levels are rarely helpful.
Imaging ECG:
QTc/QRS prolongation
Conduction disturbances
Differential Diagnosis
Antidepressant overdose
Antihistam ine overdose
Cocaine overdose
Am phetam ine overdose
MDMA overdose
Opioid overdose
Occult head injury
Endocrine disorder
Sepsis
P.751
Treatment Initial Stabilization Airway, breathing, and circulation m anagem ent (ABCs):
Adm inister supplem ental oxygen.
Adm inister naloxone, thiam ine, D 5 0 (or Accu-Chek) for altered m ental status.
Intubate if respiratory depression.
ED Treatment
Supportive care
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Decontam ination: o
Adm inister single dose of activated charcoal if recent ingestion.
Hypotension: o
0.9% norm al saline (NS) IV fluid bolus
o
Trendelenburg
o
Treat resistant hypotension with norepinephrine or phenylephrine.
o
Dopam ine m ay be ineffective.
Ventricular dysrhythm ias: o
Avoid class 1a antidysrhythm ics: potential exacerbation of neuroleptic cardiotoxicity.
o
Magnesium for prolonged QTc
o
Cardioversion if hem odynam ically unstable
Dystonic reactions: o
Adm inister diphenhydram ine or benztropine m esylate.
Hypertherm ia: o
Rapid cooling
o
Adm inister dantrolene and brom ocriptine.
Seizures: o
Treat initially with diazepam or lorazepam .
o
Phenobarbital for persistent seizures
Medication (Drugs)
Activated charcoal: 1–2 g/kg PO
Benztropine m esylate: 1–2 m g IV or PO
Brom ocriptine: 2.5–10 m g q8h PO
Dantrolene: 1–2 m g/kg q10m in IV (10 m g/kg m ax.)
Diazepam : 5–10 m g IV q10–15m in (0.2–0.5 m g/kg)
Diphenhydram ine: 25–50 m g IV (1 m g/kg)
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Lorazepam : 2–4 m g (peds: 0.03–0.05 m g/kg) IV q10–15m in
Magnesium sulfate: 1–2 g IV over 5–15 m inutes
Norepinephrine: 1–2 µg/kg/m in IV titrate to blood pressure (BP)
Phenobarbital: 10–20 m g/kg IV (loading dose)
Phenylephrine: 40–80 µg/m in IV titrate to BP
Disposition Admission Criteria
Adm it overdose with CNS sedation, agitation, dysrhythm ias, or vital sign abnorm alities to m onitored bed.
Adm it if neuroleptic results in new-onset diabetes with severe hyperglycem ia and/or ketoacidosis.
Discharge Criteria
Asym ptom atic after 6 hours of observation
Patients successfully treated for acute dystonia should be given 3-day course of diphenhydram ine to prevent recurrence.
Issues for Referral
Patients with unintentional (accidental) poisoning require poison prevention counseling.
Patients with intentional (e.g., suicide) poisoning require psychiatric evaluation.
New-onset diabetes requires prim ary care/endocrine follow-up.
References 1. Burns MJ. The pharm acology and toxicology of atypical antipsychotic agents. J Toxicol Clin Toxicol. 2001;39(1):1–14. 2. De Roos FJ. Neuroleptics. In: Ford MD, Delaney KA, Ling LJ, et al.,
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eds. Clinical Toxicology. Philadelphia: WB Saunders, 2001:539–545. 3. Leslie DL, Rosenhek RA. Incidence of newly diagnosed diabetes attributable to atypical antipsychotic m edications. Am J Psychiatry. 2004;161:1709–1711. 4. Trenton A, Currier G, Zwem er F. Fatalities associated with therapeutic use and overdose of atypical antipsychotics. CNS Drugs. 2003;17(5):307–324.
Codes ICD9-CM E853.0
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > No ncardio genic Pulm o nary Edem a
Noncardiogenic Pulmonary Edema David Jerrard
Basics Description
Functional disruption of the capillary–alveolar m em brane from a noncardiac source
Diffuse injury to either the alveolar epithelium or to the vascular endothelium
Pulm onary parenchym al changes m im ic congestive heart failure (CHF): o
Cephalad redistribution of blood flow, pulm onary effusions, and cardiom egaly do not develop.
Typically, onset of this edem a is within 1–2 hours of noxious insult.
First described by William Osler in 1889 in a patient “poisoned― by m orphine.
Approxim ately 250,000 cases occur each year in the United States.
Etiology
Cause of capillary leak or alveolar m em brane dam age is uncertain.
Proposed m echanism s include hypoxia, im m unologic
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effects, or direct toxic effects.
Major causes: o
Sm oke inhalation
o
Salicylate intoxication
o
Toxic gas inhalation
o
Transfusion reaction
o
Near drowning
o
Dissem inated intravascular coagulation
o
High-altitude pulm onary edem a (HAPE)
o
Radiation pneum onitis
o
Narcotic abuse
o
Urem ia
o
Cardiopulm onary bypass
o
Major traum a
o
Aspiration
o
Bacterial pneum onia
Diagnosis Signs and Symptoms
Fatigue
Weakness
Anxiety
Shortness of breath
Cough
Malaise
Physical Exam
Tachycardia: o
Characteristically seen secondary to decreasing PO 2 levels
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Scattered rhonchi and rales
Dyspnea
Tachypnea
Cyanosis
Pink, frothy sputum
The stigm as of left- and right-sided heart failure will not be found
Essential Workup
History and physical to identify severity and determ ine underlying etiology
The chest radiograph is essential in confirm ing the diagnosis and in assessing severity.
Tests Lab
General lab abnorm alities are not specific to noncardiogenic pulm onary edem a.
Serum protein levels: o
Hypoproteinem ia m ay be useful for differentiating perm eability-induced pulm onary edem a (noncardiogenic) from cardiogenic pulm onary edem a.
Interleukin-8 level in lung lavage washings: o
Rapid increase in the early stages of acute lung injury before full developm ent of acute respiratory distress syndrom e
Imaging Chest radiograph:
Initially norm al
Classic butterfly pattern of pulm onary edem a
Unilateral patchy infiltrates resem bling pneum onia
Lack of cardiom egaly
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Diagnostic Procedures/Surgery Pulm onary artery catheter:
Pulm onary capillary wedge pressures norm al or near-norm al in contrast to elevated pressures with cardiogenic pulm onary edem a
Differential Diagnosis
Cardiogenic pulm onary edem a
Chronic obstructive pulm onary disease exacerbation
Pulm onary em bolus
Restrictive lung disease
Pneum onia
P.753
Treatment Pre Hospital
Patent airway
Adequate oxygenation
Cautions —Patients will not typically respond to usual m easures to treat CHF
Initial Stabilization
Supplem ental oxygen (high-flow oxygen)
IV catheter
Continuous cardiac m onitor
Continuous pulse oxim etry
ED Treatment
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The treatm ent of noncardiogenic pulm onary edem a (NCPE) is supportive
NCPE associated with drug overdose usually responds to high-flow O 2
Diuretics are not used
Rem oval of trigger that m ay have caused NCPE o
Noxious gas
o
Having patient descend from elevation in cases of HAPE
Noninvasive ventilatory support (BiPAP, CPAP) m ay be used if im m ediately available o
Measure blood gases frequently
o
If unable to provide adequate oxygenation or ventilation, intubation is required
o
Useful in NCPE caused by drug overdose
Endotracheal intubation is often necessary o
Positive end-expiratory pressure (PEEP) of 5–10 cm H2O
NCPE of a neurogenic etiology has a worsened prognosis when PEEP is em ployed
o
Im proved oxygenation
o
Decrease work of breathing
o
To reduce the likelihood of atelectasis, tidal volum es should be on order of 12–15 m L/kg
o
Initially place on 100% O 2
Measure PO 2 and decrease FIO 2 accordingly
Steroids and cyclooxygenase inhibitors have not been proven effective
Follow-Up
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Disposition Admission Criteria All sym ptom atic patients should be adm itted to ICU
Sym ptom s m ay worsen at any point for up to 3 days after noxious insult
Discharge Criteria Asym ptom atic patients (especially narcotic overdose, HAPE, or aspiration)
Observe in ED for 6–12 hours and then discharge with close follow-up scheduled if no evidence of pulm onary edem a is present and adequate oxygenation is dem onstrated
References 1. Macias DJ, Brillm an JC. Adult respiratory distress syndrom e. In: Harwood-Nuss A, Linden C, Luten R, et al, eds. The clinical practice of em ergency m edicine. 2nd ed. Philadelphia: JB Lippincott Co, 1996:640–643. 2. McIntyre RC Jr. Thirty years of clinical trials in acute respiratory distress syndrom e. Crit Care Med. 2000;28(9):3314–3331. 3. Perina DG. Noncardiogenic pulm onary edem a. Em erg Med Clin North Am . 2003;21(2):385–393
Codes ICD9-CM 518.4
ICD10 J81
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > No nstero idal Anti-inflam m ato ry Po iso ning
Nonsteroidal Anti-inflammatory Poisoning Michele Zell-Kanter
Basics Description
Inhibit cyclo-oxygenase (COX) that blocks the conversion of arachidonic acid to prostaglandin
Typically, ingestion of an nonsteroidal anti-inflam m atory drug (NSAID) is benign.
Fatalities reported with large ingestions
Greater potential for toxicity with underlying congestive heart failure (CHF) or renal failure: o
NSAIDs cause sodium and water retention and decrease renal blood flow
o
Very little overdose experience with the COX-2 inhibitors (celecoxib); treatm ent should be the sam e as for the traditional NSAIDs
o
Patients m ay ingest rofecoxib and valdecoxib from stored supplies even though both are no longer available.
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Diagnosis Signs and Symptoms Gastrointestinal
Nausea
Vom iting
Epigastric pain
CNS
Drowsiness
Dizziness
Lethargy
Seizures
Cardiovascular
Hypotension
Tachycardia
Pulmonary
Eosinophilic pneum onia
Apnea
Hyperventilation
Renal
Acute renal failure
Acute tubular necrosis
Acute interstitial nephritis
Liver
Hepatocellular injury
Cholestatic jaundice
Metabolic Mild, short-lived m etabolic acidosis
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Hypersensitivity
Aseptic m eningitis
Asthm a exacerbation
Essential Workup
Generally, NSAID ingestion results in only m ild toxicity.
Exact identification of drug helpful: o
Subtle toxicologic differences am ong the NSAIDs
Tests Lab
Electrolytes, BUN/creatinine, glucose: o
Baseline renal function
o
Check for m etabolic acidosis.
CBC
Arterial blood gas (ABG) for large overdoses
PT/PTT: o
False-positive bilirubin/ketone dipstick with etodolac ingestion
NSAID difficult to detect on toxicology screens
Differential Diagnosis Agents causing m etabolic acidosis, altered m ental status, and GI irritation:
Salicylates
INH
Ethylene glycol
Methanol
Isopropanol
P.755
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Treatment Pre Hospital Collect prescription bottles/m edications for identification in the ED.
Initial Stabilization
ABCs
Naloxone, thiam ine, dextrose (or Accucheck) for altered m ental status
ED Treatment
Supportive care and GI decontam ination
Gastric lavage: o
If the patient presents within 1 hour of ingestion with an intact gag reflex
o
If no gag reflex is present, protect airway with a cuffed endotracheal tube before lavage.
Avoid syrup of ipecac because NSAIDs m ay cause CNS depression and seizures in the overdose setting.
Adm inister activated charcoal and sorbitol early (after lavage com pletion).
Extracorporeal m ethods to enhance elim ination are not beneficial owing to high degree of plasm a protein binding.
Medication (Drugs)
Activated charcoal slurry: 1–2 g/kg up to 90 g PO
Dextrose: D 5 0 W 1 am p (50 m L or 25 g; peds: D 2 5 W 2–4 m L/kg) IV
Naloxone (Narcan): 2 m g (peds: 0.1 m g/kg) IV or IM initial dose
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Naloxone (Narcan): 2 m g (peds: 0.1 m g/kg) IV or IM initial dose
Sorbitol: 1–2 g/kg to a m ax. of 100 g (peds: older than 1 year, 1–1.5 g/kg as a 35% solution to a m ax. of 50 g) PO m ixed in the activated charcoal slurry; use only for first dose.
Thiam ine (vitam in B 1 ): 100 m g (peds: 50 m g) IV or IM
Pediatric Considerations Piroxicam , naproxen, ketoprofen, and m efenam ic acid have caused seizures in children.
Follow-Up Disposition Admission Criteria
Protracted vom iting, hem atem esis
CNS depression, seizure activity
Metabolic acidosis
CHF, hypotension, hypertension
Renal failure
Discharge Criteria Nontoxic ingestion in a patient who is asym ptom atic 6–8 hours after ingestion
References 1. Paloucek FP, Rynn KO. Nonsteroidal anti-inflam m atory drugs (NSAIDs). In: Ford MD, Delaney KA, Ling LJ, et al., eds. Clinical Toxicology. Philadelphia: WB Saunders; 2001:281–284. 2. Seifert SA, Bronstein AC, McGuire TH. Massive ibuprofen ingestion with survival. J Toxicol Clin Toxicol. 2000;38:55–57.
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3. Zuckerm an GB, Uy CC. Shock, m etabolic acidosis, and com a following ibuprofen overdose in a child. Ann Pharm acother. 1995;29:869–871.
Codes ICD9-CM 965.6
ICD10 T39.3
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Nursem aid's Elbo w
Nursemaid's
Elbow Daren D. Girard Daniel L. Savitt
Basics Description
One of the m ost com m on injuries of the upper extrem ity in children younger than 5 years: o
Caused by longitudinal traction on an extended, pronated arm
o
Typical history is a sharp pull on the child's outstretched arm such as lifting the child by the wrist.
o
Alternatively, caregiver m ay report history of a fall.
Subluxation of the radial head: o
Annular ligam ent slips or tears and becom es interposed between the radial head and the capitellum
Diagnosis
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Signs and Symptoms
Child refuses to use arm .
Elbow slightly flexed with forearm held close to trunk
Pain with flexion of the elbow
Pain with forearm supination or pronation
Absence of point tenderness
Minim al to no swelling
Essential Workup
Clinical diagnosis: o
Classic history, passive position of arm , and physical exam are sufficient for diagnosis.
Radiographs: o
Not routinely indicated
o
Obtain to exclude or diagnose other injuries if any of the following are present:
Point tenderness
Soft tissue swelling
Deform ity
Ecchym osis of the elbow
Failed reduction
Child continues to favor after reduction.
Differential Diagnosis
Hum erus or radius fracture
Elbow dislocation
Joint infection
Osteom yelitis
Tum or
Treatment
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Pre Hospital Cautions:
Place ice on the injured elbow to reduce pain and swelling.
Im m obilize in a sling or splint to facilitate transport and prevent further injury.
Assess distal neurovascular status.
Initial Stabilization Assess distal m otor, sensory, and vascular function.
ED Treatment
Two com m on reduction techniques
Supination/flexion technique: o
Grasp child's hand in handshake position.
o
Stabilize injured elbow with the other hand.
o
In a sm ooth, swift m otion, fully supinate the forearm and flex the elbow.
Hyperpronation technique: o
Grasp child's hand in handshake position.
o
Stabilize injured elbow with the other hand.
o
Hyperpronate and extend the forearm .
P.757
Palpable click m ay accom pany successful reduction, but is not essential.
Child m ay cry during the reduction, but is frequently pain free and using the arm shortly thereafter.
Second reduction attem pt if the child does not use arm 15 m inutes after first attem pt
Consider opposing technique for second reduction attem pt.
Radiographic studies indicated if the second reduction attem pt is unsuccessful
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Perform postreduction neurovascular assessm ent.
Medication (Drugs) Acetam inophen: 15 m g/kg PO q4h:
Ibuprofen 10 m g/kg PO q6h–q8h
Follow-Up Disposition Admission Criteria None
Discharge Criteria
Discharge to hom e after child regains full, unrestricted use of the arm .
Patient instructions: o
Inform parents not to pull or lift the child by the hand, wrist, or forearm .
o
Warn fam ily of increased incidence of recurrence until the child reaches 5–6 years of age.
Splint with prom pt orthopedic referral for any injury of the elbow with a radiographic abnorm ality; condylar, supracondylar, or displaced fractures need orthopedic evaluation expedited.
Posterior splint with orthopedic follow-up in 24–48 hours, if reduction attem pts fail and no radiographic abnorm alities can be identified
Warn fam ily to observe for neurovascular com prom ise.
References
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1. Kaufm an D. Evaluation of the patient with extrem ity pain: an evidence based approach. Em erg Med Clin North Am . 1999;17(1):77–95. 2. Macias CG, Bothner J, Wiebe R. A com parison of supination/flexion to hyperpronation in the reduction of radial head subluxations. Pediatrics. 1998;102(1):e10. 3. Macias CG, Wiebe R, Bothner J. History and radiographic findings associated with clinically suspected radial head subluxations. Pediatr Em erg Care. 2000;16(1):22–25. 4. McDonald J, Whitelaw C, Goldsm ith LJ. Radial head subluxation: com paring two m ethods of reduction. Acad Em erg Med. 1999;6(7):715–718.
Codes ICD9-CM 832.0
ICD10 S59.9
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Oculo m o to r Nerve Palsy
Oculomotor
Nerve Palsy James M. Leaming
Basics Description
Com plete: o
Com pressive lesions such as aneurysm s or tum ors
o
Brainstem herniation with com pression of third cranial nerve
Increased intracranial pressure
Incom plete: o
Vascular infarction of vasa nervorum of third cranial nerve
Etiology
Intracranial or orbital tum or
Aneurysm (particularly posterior com m unicating artery)
Traum a
Intracranial hem orrhage
Diabetes m ellitus
Migraine headache
Infection, m eningitis
Arteriovenous m alform ation or fistula
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Cavernous sinus throm bosis
Neuropathy (e.g., m yasthenia gravis, Guillain-Barré)
Collagen vascular diseases (e.g., sarcoidosis)
Pediatric Considerations
Traum a is m ost com m on cause of acquired oculom otor nerve palsies.
Other causes less com m on than in adult population: o
Diabetes
o
Posterior com m unicating artery aneurysm s
o
Metastatic tum or
o
Pituitary lesions
Diagnosis Signs and Symptoms
Diplopia, with involved eye deviated laterally and downward
Com plete: o
Mydriasis of involved eye
Incom plete: o
Reactive m idpoint pupil of involved eye
History History is of utm ost im portance in determ ining cause:
History of long-standing diabetes m ellitus
Head traum a, either recent or distant
Unintentional weight loss
Recent infection involving the upper respiratory tract, eyes, or ears
Severe headache (classic thunderclap or chronic and worsening)
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Constitutional sym ptom s: nausea, vom iting, fever
Physical Exam Ophthalm ologic exam ination:
Extraocular m ovem ents
Exophthalm us
Funduscopic exam ination to dem onstrate papilledem a
Direct and consensual pupillary reaction
Essential Workup CT/MRI of brain, orbit, sinuses
Tests Lab
CBC with differential
Erythrocyte sedim entation
Antinuclear antibodies, rheum atoid factor to evaluate for vasculitis
Lum bar puncture
Imaging
Doppler im aging for arteriovenous m alform ations, dural sinus throm bosis
Cerebral arteriogram rarely useful as m ost aneurysm s are seen on CT or MRI
Differential Diagnosis
Infection
Malignancy
Vasculitis
Pediatric Considerations Consider congenital oculom otor nerve palsy.
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Treatment Pre Hospital Without associated traum a, no specific prehospital care issues exist.
Initial Stabilization
Initial stabilization of posttraum atic patient should concentrate on underlying traum atic condition.
Airway m anagem ent and resuscitation as indicated
Any patient with evidence of herniation should have the following m easures to control intracranial pressure: o
Intubation using rapid-sequence induction and controlled ventilation to a PCO 2 level of 35–40 m m Hg
o
Elevate head of bed 30°.
o
Mannitol
P.759
ED Treatment General Measures
Crucial to differentiate between aneurysm and other com pressive lesions early in ED evaluation
Differentiation between incom plete and com plete oculom otor nerve palsy guides focus of ED treatm ent.
Medication regim en determ ined by cause: o
Aneurysm :
Control severe hypertension with nitroprusside.
Decrease intracranial pressure with intubation.
Controlled ventilation
Elevation of head
Mannitol
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o
Intracranial tum or: control increasing intracranial pressure as above.
o
Inflam m ation and edem a: decrease with intravenous steroids.
o
Meningitis:
Rapid adm inistration of intravenous antibiotics
Intravenous steroids m ay be useful to decrease inflam m atory response and edem a.
o
Vasculitis and collagen vascular diseases: Decrease inflam m atory cell infiltration with intravenous steroids.
o
Neuropathy: m yasthenia gravis—edrophonium chloride test
Medication (Drugs)
Ceftriaxone: 1–2 g (peds: 50–100 m g/kg) IV
Dexam ethasone: 10 m g IV (peds: 0.15–0.5 m g/kg IV single dose in ED)
Edrophonium Cl: 5–8 m g IV (peds: 0.15 m g/kg IV; 1/10 test dose given first)
Mannitol: 1 g/kg IV (peds: not routinely recom m ended)
Methylprednisolone: adults/peds: 1–2 m g/kg IV single dose in ED
Follow-Up Disposition Admission Criteria
Com plete oculom otor nerve palsy of any cause requires
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adm ission and em ergency neurosurgical evaluation.
Incom plete oculom otor nerve palsy with abnorm al CT or MRI, abnorm al laboratory studies, or other focal neurologic or constitutional sym ptom s
Discharge Criteria Incom plete oculom otor nerve palsy with negative CT or MRI, norm al laboratory studies, and no other sym ptom s can be referred for urgent outpatient neurologic evaluation.
References 1. Chen CC, Pai YM, Wang RF, et al. Isolated oculom otor nerve palsy from m inor head traum a. Br J Sports Med. 2005;39(8):e34. 2. Ing EB, Sullivan TJ, Clarke MP, et al. Oculom otor nerve palsies in children. J Pediatr Ophthalm ol Strabism us. 1992;29:331–336. 3. Kodsi SR, Younge BR. Acquired oculom otor, trochlear, and abducent cranial nerve palsies in pediatric patients. Am J Ophthalm ol . 1992;114:568–574. 4. Richards BW, Jones FR Jr, Younge BR. Causes and prognosis in 4,278 cases of paralysis of the oculom otor, trochlear, and abducens cranial nerves. Am J Ophthalm ol. 1992;113:489–496. 5. Tiffin PA, MacEwen CJ, Craig EA, et al. Acquired palsy of the oculom otor, trochlear, and abducens nerves. Eye. 1996;10(pt 3):377–384.
Codes ICD9-CM 378.81 Palsy of conjugate gaze
ICD10 G58.8
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Opiate Po iso ning
Opiate Poisoning
Amy V. Kontrick Mark B. Mycyk
Basics Description
Bind to µ, κ, and δ opiate receptors in CNS and PNS
Physical and psychologic dependence occurs.
Peak plasm a levels: o
PO: 1–2 hours
o
Intram uscular: 0.5–1 hour
o
Intravenous or intranasal: seconds to m inutes
Etiology
Overuse or abuse of oral prescription analgesics for m oderate to severe pain
Street preparations of narcotic analogs m ay contain adulterants: o
Cocaine
o
PCP
o
Strychnine
o
Dextrom ethorphan
o
Quinine
o
Scopolam ine
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Diagnosis Signs and Symptoms
CNS: o
CNS depression
o
Com a
o
Seizures
Gastrointestinal: o
Nausea
o
Vom iting
o
Constipation
Cardiovascular: o
Hypotension
o
Bradycardia
o
Palpitations
Pulm onary: o
Respiratory depression
o
Bronchospasm
o
Pulm onary edem a
o
Apnea
Other: o
Miosis
o
Hypotherm ia
Withdrawal: o
Hypertension
o
Tachycardia
o
Tachypnea
o
Abdom inal cram ps
o
Diarrhea
o
Piloerection
o
Yawning
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Pediatric Considerations
Neonatal withdrawal: o
Infants born to addicted m others
o
Onset: 12–72 hours after birth
o
Irritability, trem ors, poor feeding, and dehydration
Diphenoxylate (Lom otil): toxicity m ore severe in children than adults and m ay be fatal
Essential Workup Monitor vital signs and pulm onary status with significant exposure:
Pulse oxim etry or arterial blood gases
Chest radiograph if persistent hypoxia or possible aspiration
Abdom inal radiograph if body packing suspected
Tests Lab
Plasm a opiate levels not clinically useful: o
Treatm ent based on clinical presentation, not opiate level
Urine toxicity screen for opioids m ay not identify som e synthetic opioids (e.g., m ethadone).
Acetam inophen level for overuse or abuse of oral prescription analgesic products
Differential Diagnosis
Clonidine overdose
Barbiturate overdose
Benzodiazepine overdose
γ-Hydroxybutyrate (GHB) overdose
Neuroleptic overdose
Occult head injury
Pa ge 3 3 0
Treatment Pre Hospital
Transport all pills/pill bottles involved in overdose for identification in ED.
Provide respiratory support.
Adm inister naloxone.
Initial Stabilization
Check airway, breathing, and circulation (ABCs): o
Airway control essential
o
Adm inister supplem ental oxygen.
Adm inister naloxone: o
Reverses respiratory depression and com a in opiate overdoses
o
Intubate if naloxone does not reverse respiratory depression.
P.761
ED Treatment
Naloxone adm inistration: o
Start with low doses for opiate-habituated patients.
o
High doses (10 m g) m ay be required to reverse the effects of propoxyphene, m ethadone, and fentanyl.
o
Adm inister repeated doses that reversed sym ptom s, as needed every 20–60 m inutes.
o
For long-acting opioids, consider an hourly infusion of two thirds the dose needed to reverse sym ptom s.
Decontam ination: o
Adm inister activated charcoal for oral ingestion.
Pa ge 3 3 0
o
Adm inister whole bowel irrigation with polyethylene glycol for asym ptom atic body packers.
Treat opiate withdrawal with clonidine or m ethadone.
Hypotension:
o
0.9% norm al saline IV fluid bolus
o
Trendelenburg test
o
Initiate dopam ine for resistant hypotension.
Seizures: o
Treat initially with diazepam .
o
Adm inister phenobarbital for persistent seizures.
Medication (Drugs)
Activated charcoal: 1–2 g/kg PO
Clonidine: 0.1–0.3 m g PO b.i.d. for 10 days; 0.1–0.2 m g/kg/d transderm al patch
Diazepam : 5–10 m g IV (peds: 0.2–0.5 m g/kg IV) q10–15m in
Dopam ine: 2–20 µg/kg/m in; titrate to effect
Methadone: 15–40 m g/d
Naloxone: 0.4–2 m g (peds: 0.1 m g/kg; neonates: 10–30 µg/kg) IV or IM
Phenobarbital: 10–20 m g/kg IV (loading dose)
Polyethylene glycol: 2 L/h until clear rectal effluent and/or passage of packets
Follow-Up Disposition Admission Criteria
Pa ge 3 3 0
Sym ptom atic after oral overdose
Repeated naloxone dosing or infusion needed to reverse sym ptom s
Children younger than 5 years postdiphenoxylate ingestion should be observed for 24 hours.
Opiate body packers
Discharge Criteria
Asym ptom atic 6 hours after oral overdose
Asym ptom atic 4 hours after naloxone adm inistration
Com plete elim ination of opiate packets
Issues for Referral Consider substance abuse referral for patients.
References 1. Dietze P, Jolley D, Cvetkovski S, et al. Characteristics of non-fatal opioid overdoses attended by am bulance services in Australia. Aust N Z J Public Health. 2004;28(6):569–575. 2. Kelly AM, Kerr D, Dietze P, et al. Random ised trial of intranasal versus intram uscular naloxone in prehospital treatm ent for suspected opioid overdose. Med J Aust. 2005;182(1):24–27. 3. Kleinschm idt KC, Wainscott M, Ford MD. Opioids. In: Ford MD, Delaney KA, Ling LJ, et al., eds. Clinical Toxicology. Philadelphia: WB Saunders; 2001:637–639. 4. Sporer KA. Acute heroin overdose. Ann Intern Med. 1999;130:584–590.
Codes ICD9-CM 850.0
ICD10 T460.6
Pa ge 3 3 0
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Oppo rtunistic Infectio n
Opportunistic
Infection Elicia Sinor Kennedy
Basics Description Unusual infections that occur when host suffers a decrease in resistance against norm ally nonpathogenic organism s
Etiology
Occurs in HIV patients when the CD4 T-lym phocyte count falls below 200 cells/m m 3 or less than 14% of the total lym phocyte count: o
Pneum ocystis jiroveci pneum onia
o
Cryptococcal infection
o
Dissem inated tuberculosis
o
Cryptosporidiosis
o
Isosporiasis
o
Toxoplasm osis
o
Histoplasm osis
o
Cryptococcosis
o
Mycobacterium avium com plex
o
Tuberculosis pericarditis or m eningitis
o
Cytom egalovirus
Pa ge 3 3 0
Cell-m ediated deficiency: o
Hem atologic m alignancies
o
Lym phom a
o
High-dose glucocorticoid therapy
o
Autoim m une disorders
o
Viral infections
o
Cytotoxic drugs/chem otherapy
o
Radiation therapy
o
Associated with:
Legionella
Nocardia
Salm onella
Mycobacteria
Neutrophil im pairm ent/depletion: o
Cytotoxic drugs
o
Aplastic anem ia
o
Drug reactions:
Dapsone
o
Neoplastic invasion of bone m arrow
o
Arsenic
o
Penicillin
o
Chloram phenicol
o
Procainam ide
o
Vitam in deficiencies
o
Associated with:
Staphylococcus and α-hem olytic Streptococcus
Enteric organism s and anaerobes
Diagnosis Signs and Symptoms
Pa ge 3 3 0
New or worsening fatigue
Confusion
Tachypnea
Fever
Chills
Pulm onary source of infection:
o
Cough
o
Congestion
o
Rales
Genitourinary source of infection: o
Dysuria
o
Increased frequency
o
Urinary retention
Gastrointestinal (GI) source of infection: o
Vom iting
o
Diarrhea
o
Bleeding
Physical Exam
Signs of system ic inflam m atory response syndrom e: o
Tem perature >38°C or 90 beats per/m inute
o
Respiratory rate >20 breaths per m inute or PCO 2 12,000 is a criteria for the system ic inflam m atory response score
o
Neutropenia:
Num ber of polym orphonuclear + bands Table o f C o ntents > Optic Artery Occlusio n
Optic Artery
Occlusion Yasuharu Okuda
Basics Description
Obstruction of the central retinal artery associated with sudden painless loss of vision
Occurs in older population, 50–70 years of age
Risk factors include hypertension, sickle cell disease, vasculitis, valvular heart disease, lupus, traum a, and coronary artery disease.
Etiology
Em bolic: o
Occlusion by intravascular m aterial from a proxim al source:
Atherosclerotic disease (m ajority)
Valvular heart disease
Atrial m yxom a
Dissection of the ophthalm ic artery in the region of the cribriform plate (rare)
Throm botic: o
Obstruction of flow from the rupture of a pre-existing
Pa ge 3 3 1
intravascular atherosclerotic plaque
Inflam m atory: o
Inflam m ation from diseases such as tem poral arteritis and lupus
Arterial spasm : o
Associated with m igraine headaches
Decreased perfusion o
Low flow conditions such as in severe hypotension or high pressure situations seen in acute angle closure glaucom a or retrobulbar hem orrhage.
Diagnosis Signs and Symptoms History
Sudden, painless, m onocular loss of vision
Prior episodes of sudden visual loss: o
Lasts a few seconds to m inutes (am aurosis fugax)
o
Caused by transient em bolic phenom ena or decreased ocular blood flow
Partial field deficits: o
Only if branch of central retinal artery involved
Physical Exam
Significantly decreased visual acuity with loss of afferent pupillary reflex
Retinal appearance: o
Em boli visualized within vascular tree of the retina
Appears as glinting white or yellow flecks (Hollenhorst plaques) within the vessels
o
Ischem ic edem a visible within 15–20 m inutes of
Pa ge 3 3 1
occlusion o
Affected arteries em pty or showing dark red stationary or barely pulsatile segm ented rouleaux (“box carring―)
o
Within one to two hours:
Opacification of the usually transparent infarcting retinal nerve layer occurs.
“Cherry-red spot― rem ains over the fovea (only area where there is very thin retina allowing the vascular choroids to show through).
Tests Visual acuity
Lab
Directed towards evaluating underlying etiology of occlusion
CBC with differential and platelet count
Prothrom bin tim e/partial throm boplastin tim e test (PTT)
Electrolytes, blood urea nitrogen/creatinine, glucose
Electronic spin resonance for giant cell arteritis (in patients >55 years old)
ANA
Rheum atoid factor
Rapid plasm a reagin
Hem oglobin electrophoresis
Serum protein electrophoresis
Imaging
Directed toward evaluating underlying etiology of occlusion
Carotid artery evaluation by ultrasound and Doppler
Cardiac evaluation: o
ECG
Pa ge 3 3 1
o
Echocardiography
o
Holter m onitoring
Fluorescein angiography or electroretinography to confirm the diagnosis
Differential Diagnosis
Central retinal vein occlusion
Retinal detachm ent
Giant cell arteritis (tem poral arteritis)
Acute angle closure glaucom a
Optic neuritis
P.765
Treatment Initial Stabilization
Initiate treatm ent im m ediately because irreversible visual loss occurs at 90 m inutes: o
Only im m ediate treatm ent m ay help to salvage or restore sight to the affected eye
Goals of therapy include dislodging or dissolving the em bolus, arterial dilation to im prove forward flow, and reduction of intra-ocular pressure to im prove the profusion gradient.
ED Treatment
Im m ediate global m assage in an attem pt to dislodge the em bolus: o
Lay patient flat and apply digital global m assage bolus.
Pa ge 3 3 1
o
On closed eyelid, apply constant pressure for 15 seconds and rem ove for 15 seconds. Repeat for 5 cycles.
Increase PCO 2 to dilate retinal vessels: o
Have patient breath into paper bag for 10 m inutes each hour or use inhaled Carbogen.
Adm inister IV acetazolam ide to decrease intra-ocular pressure.
Apply topical tim olol m aleate to reduce intra-ocular pressure.
Adm inister aspirin and IV heparin for prevention of clot propagation.
Obtain em ergent ophthalm ology consultation for: o
Anterior cham ber paracentesis to help reduce intraocular pressure
o
Possible intra-arterial fibrinolysis for clot lysis
Adm inister high dose system ic steroids in suspected cases of inflam m atory arteritis.
Medication (Drugs)
Acetazolam ide: 500 m g IV or PO
Aspirin: 325 m g PO
Carbogen: inhalation of 95% oxygen and 5% carbon dioxide m ixture.
Heparin: 80 U/kg IV bolus then 18 U/kg/hr continuous infusions (rate adjusted based on PTT level)
Methylprednisolone: 250 m g IV in suspected cases of inflam m atory arteritis
Tim olol m aleate 0.5% solution: one drop topically to affected eye
Pa ge 3 3 2
Follow-Up Disposition Admission Criteria Acute central retinal artery occlusion for workup for source of em bolic phenom ena or throm bosis
Discharge Criteria Chronic retinal artery occlusion with no evidence of active disease can be worked up as an outpatient.
Issues for Referral All suspected cases warrant em ergent ophthalm ology consultation.
References 1. Arnold M, Koerner U, Rem onda L, et al. Com parison of intra-arterial throm bolysis with conventional treatm ent in patients with acute central retinal artery occlusion. J Neurol Neurosurg Psychiatry. Feb 2005;76(2):196–199. 2. Fraser S, Siriwardena D. Interventions for acute non-arteritic central retinal artery occlusion. Cochrane Database Syst Rev. 2002;(1):CD001989. 3. Morgan A, Hem phill R. Acute visual change. Em erg Med Clin North Am . Nov 1998;16(4):825–843.
Codes ICD9-CM 362.30
Pa ge 3 3 2
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Optic Neuritis
Optic Neuritis
Alexander T. Limkakeng Jr.
Basics Description
Optic nerve dysfunction owing to an inflam m atory process, com m only associated with m yelin destruction
Grouped by site of inflam m ation: o
Papillitis: inflam m ation of the optic disk
o
Retrobulbar neuritis: inflam m ation of the optic nerve proxim al to the globe
Five-year risk for clinically definite m ultiple sclerosis following optic neuritis: o
Norm al MRI—16%
o
More than 3 lesions on MRI—51%
Genetics High prevalence of A23, B7, and DR2 HLA alleles in patients with optic neuritis:
Especially those that progress to clinically definite m ultiple sclerosis
Etiology
Idiopathic: o
Most com m on
Pa ge 3 3 2
o
Multiple sclerosis (MS): o
Single isolated events
20–50% of patients with optic neuritis
Viral infections: o
Chicken pox
o
Measles
o
Mononucleosis
o
Herpes zoster
o
Encephalitis
Postviral optic neuritis: o
Usually occurs 4–6 weeks after a nonspecific viral illness
Granulom atous inflam m ation: o
Tuberculosis
o
Syphilis
o
Sarcoidosis
o
Cryptococcal infection
System ic lupus erythem atosus
HIV: o
Cytom egalovirus
o
Toxoplasm osis
o
Histoplasm osis
o
Cryptococcus
Lym e disease
Contiguous inflam m ation of m eninges, orbit, sinuses, and intraocular inflam m ation
Drug induced: o
Etham butol
o
Tam oxifen
Pa ge 3 3 2
Diagnosis Signs and Symptoms
Visual loss occurring over days (rarely over hours): o
Adults usually unilateral
o
Bilateral visual loss m ore com m on in children
Retrobulbar pain: increased with m ovem ent of the affected eye
Light, color vision, and depth perception loss m ore pronounced than visual acuity loss
Afferent pupillary defect occurring in unilateral cases
Visual field defects: o
Central scotom a
Funduscopic exam usually reveals either swollen (papillitis) or norm al disk:
Uhthoff sign: o
Visual deficit occurring with exercise or increased body tem perature
o
Unusual sign seen occasionally
History
Age (typically wom en age 18–45 years)
Pain on eye m ovem ent
Speed of onset of sym ptom s
Associated sym ptom s
Previous episodes
Fam ily history of optic neuritis, MS
Physical Exam
Check blood pressure (BP)
Com plete ophthalm ologic and neurologic exam ination, especially assessm ent of: o
Pupillary function
Pa ge 3 3 2
o
Afferent pupillary defect
o
Visual field defect
o
Color vision (Ishihara color plates)
o
Evaluation of the vitreous body for cells
o
Dilated retinal exam (swollen optic disk)
Tests Lab
CBC
Erythrocyte sedim entation rate (ESR)
RPR, FTA–ABS
Lym e titer
Antinuclear antibody (ANA)
Purified protein derivative (PPD) testing
HIV testing
Imaging
Chest radiograph for tuberculosis, sarcoid
CT scan or MRI of brain and orbits: o
Inflam m ation of the retrobulbar optic nerve during the acute phase m ay appear as enlargem ent, thus falsely raising the issue of an optic nerve m ass.
o
Visual field testing (preferably autom ated testing, such as Octopus or Hum phrey)
P.767
Differential Diagnosis
Acute papilledem a
Ischem ic optic neuropathy
Severe system ic hypertension
Intracranial tum or com pressing the afferent visual
Pa ge 3 3 2
pathway
Orbital m ass com pressing the optic nerve
Toxic or m etabolic neuropathy:
o
Heavy m etal poisoning
o
Anem ia
o
Malnutrition
o
Alcohol
o
Chloroquine
o
Etham butol
o
INH
Leber hereditary optic atrophy
Treatment ED Treatment
Early ophthalm ologic and neurologic consultations
IV steroid pulse followed by oral steroids: o
Recom m ended for those with two or m ore dem yelinating lesions on MRI without a prior history of MS or optic neuritis
o
Decreases recurrence, progression to MS over 2 years, and shortens duration of visual im pairm ent, but does not affect rate of progression at 5 years or visual outcom e at 1 year.
o
Treatm ent should be individualized for those with one lesion on MRI.
Medication (Drugs) Methylprednisolone: 250 m g IV q6h for 3 days
Pa ge 3 3 2
Follow-Up Disposition Admission Criteria
Bilateral vision loss
If other sources of acute vision loss cannot be ruled out
IV steroid pulse treatm ent needed
Discharge Criteria
Unilateral visual im pairm ent
Good hom e support system s
Neurology and ophthalm ology follow-up arranged
Issues for Referral Referral for interferon beta 1a treatm ent as outpatient for those with two or m ore dem yelinating lesions on MRI:
Reduces progression to MS
References 1. Balcer LJ, Galetta SL. Treatm ent of acute dem yelinating optic neuritis. Sem in Opthalm . 2002;17(1):4–10. 2. Beck RW, Cleary PA, Anderson MM, et al. Optic Neuritis Study Group. A random ized controlled trial of corticosteroids in the treatm ent of acute optic neuritis. N Eng J Med. 1992;326:581–588. 3. Beck RW, Cleary PA, Anderson MM, et al. Optic Neuritis Study Group. Visual function 5 years after optic neuritis: experience of the ONTT. Arch Opthalm . 1997;115(12):1545–1552. 4. Jacobs LD, Beck RW, Sim on JH, et al.CHAMPS Study Group. Interferon beta-1a for optic neuritis patients at high risk for m ultiple sclerosis. Am J Ophthalm . 2001;132:463–471. 5. Kunim oto DY, Kanitkark KD, Makar MS, eds. Wills Eye Manual. 4th
Pa ge 3 3 2
ed. Philadelphia: Lippincott William s & Wilkins; 2004.
Miscellaneous SEE ALSO: Visual Loss
Codes ICD9-CM 377.3
ICD10 H46
Pa ge 3 3 2
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Organo pho sphate Po iso ning
Organophosphate Poisoning Sean Bryant
Basics Description
Organophosphates (pesticides and nerve agents) irreversibly bind to cholinesterases, causing deactivation of acetylcholinesterase.
Initial accum ulation of acetylcholine at neural synapse results in cholinergic overdrive (central and peripheral).
Predom inate effects (m uscarinic, nicotinic, CNS) m ay vary and can overlap.
Death usually secondary to respiratory failure resulting from weakness of respiratory m uscles, pulm onary edem a, and central depression of respiratory drive.
Pediatric Considerations
Sym ptom s are difficult to differentiate in toddlers.
Com m on sym ptom s: m iosis, salivation, and m uscle weakness
Seizures found in 25% (3% of adults).
Etiology
Exposure to insecticides (organophosphorus com pounds)
Pa ge 3 3 2
Exposure to chem ical nerve agents (Sarin, Som an, VX, Tabun)
Diagnosis Signs and Symptoms
Classic presentation—cholinergic toxidrom e: o
DUMBELS:
Diarrhea/diaphoresis
Urination
Miosis/m uscle fasciculations
Bradycardia, bronchorrhea, bronchospasm
Em esis
Lacrim ation
Salivation
Chronic interm ittent exposure, nonspecific sym ptom s: o
Weakness
o
Fatigue
o
Malaise
o
Anorexia
Mild Exposure
Visual: o
Miosis
o
Decreased visual acuity
CNS: o
Headache
o
Dizziness
o
Trem ors of tongue and eyelids
o
Anxiety
o
Weakness
Pa ge 3 3 3
Gastrointestinal (GI): o
Anorexia
Moderate Exposure
CNS: o
Muscle fasciculation followed by flaccid paralysis
o
Respiratory m uscle weakness
o
Incoordination
GI: o
Nausea
o
Vom iting
o
Abdom inal cram ps
Exocrine glands: o
Salivation
o
Lacrim ation
Severe Exposure
Visual: o
Pinpoint nonreactive pupils
Respiratory: o
Respiratory difficulty
o
Pulm onary edem a
Cardiovascular o
Bradycardia
o
Heart block
CNS: o
Convulsion
o
Com a
o
No sphincter tone
GI: o
Diarrhea
Muscarinic Manifestations
Respiratory:
Pa ge 3 3 3
o
Bronchoconstriction
o
Wheezing
o
Dyspnea
o
Increased bronchial secretion
o
Cough
o
Pulm onary edem a
Cardiovascular: o
Bradycardia (tachycardia m ay follow pulm onary edem a and hypoxia)
o
GI: o
Nausea, vom iting
o
Abdom inal pain
o
Diarrhea
o
Tenesm us
o
Fecal incontinence
Exocrine glands: o
Diaphoresis
o
Salivation
o
Lacrim ation
Pupils: o
Miosis, occasionally anisocoria
Ciliary body: o
Cyanosis
Blurred vision
Bladder: o
Frequency
o
Urinary incontinence
Nicotinic Manifestations
Striated m uscle: o
Fasciculation
o
Weakness including respiratory m uscles
Sym pathetic ganglia:
Pa ge 3 3 3
o
Mydriasis
o
Tachycardia
o
Hypertension
o
Bronchodilation
CNS: o
Agitation
o
Restlessness
o
Trem ors
o
Confusion
o
Depression
o
Ataxia
o
Weakness
o
Com a
o
Seizures
o
Death
Essential Workup
Inquire about possible exposure, occupation, recent insecticide in hom e, m islabeled, or poorly stored insecticides: o
Obtain original container if suicide attem pt.
Look for parasym pathetic and CNS signs with m uscle weakness or paralysis.
Tests Lab
RBC and plasm a cholinesterase levels to confirm diagnosis: o
RBC (true) cholinesterase level is best reflection of synaptic inhibition (a send-out lab)
o
Plasm a (pseudo) cholinesterase level not as reliable but m ore tim ely
o
Cholinesterase levels
Pa ge 3 3 3
o
Latent exposure: >50% of norm al value
Mild exposure: 20–50% of norm al value
Moderate exposure: 10–20% of norm al value
Severe exposure: Table o f C o ntents > Osgo o d-Schlatter Disease
Osgood-Schlatter Disease Raj J. Patel
Basics Description
Inflam m ation at bone–tendon junction of patellar tendon into ossification center of tibial tuberosity: o
Repetitive stress
o
Partial avulsion injuries
o
Fragm entation m ay lead to heterotopic ossification anterior to tibial tuberosity.
Fusion of tubercle to tibia norm ally occurs by 18 years of age: o
Elim inates any further sym ptom s
Etiology Active adolescent boys between 10 and 15 years of age and girls between 8 and 13 years of age:
Two to three tim es m ore com m on in boys
Fivefold incidence in very athletic children
Diagnosis
Pa ge 3 3 4
Signs and Symptoms
Pain and swelling over tibial tuberosity: o
Often bilateral, but unilateral cases m ore sym ptom atic
Pain exacerbated by running, jum ping, and kneeling activities
Increased pain while sitting with knees flexed
Essential Workup Clinical diagnosis:
Typically pain, swelling, and tenderness localized over tibial tubercle
Exam ination of knee joint unrem arkable
Tests Imaging Knee radiographs in unilateral cases to exclude potentially serious pathology only if presentation not typical for Osgood-Schlatter disease
Differential Diagnosis
Fracture
Legg-Calvé-Perthes disease: o
Referred hip pain
Osteochondritis desiccans
Osteom yelitis
Patellofem oral syndrom e
Septic joint
Sinding-Larsen-Johansson syndrom e: o
Slipped-capital fem oral epiphysis: o
Apophyseal injury at inferior pole of patella
Referred hip pain
Stress fracture
Pa ge 3 3 4
Tendinitis or bursitis
P.771
Treatment Initial Stabilization
Place leg in position of com fort.
Im m obilize if necessary to m inim ize pain.
ED Treatment
Mainstay of therapy: o
Nonsteroidal anti-inflam m atory drugs (NSAIDs)
o
Lim ited activity for 2–4 m onths is recom m ended.
o
Ice to affected area after activity
o
Com press painful area with elastic bandage.
o
Elevate leg.
o
Avoid corticosteroid injections.
Mild cases: o
Avoid overuse until sym ptom atic im provem ent.
o
Apply protective padding.
o
Reassurance of benign, self-lim ited course
o
Stretching and strengthening exercises of quadriceps and ham strings
Severe cases: o
Surgical excision of prom inent tibial tubercle or ossicle under patellar tendon only after com plete skeletal m aturity
Pa ge 3 3 4
Medication (Drugs) Ibuprofen: 10 m g/kg PO q6h; m ax. 50 m g/kg/d
Follow-Up Disposition Discharge Criteria Discharge all patients.
Issues for Referral Repeat visits after reasonable conservative approach (pediatric orthopedics)
References 1. Bloom OJ, Mackler L, Barbee J. What is the best treatm ent for Osgood-Schlatter disease? J Fam Pract. 2004;53(2):153–156. 2. Greene WB, ed. Essentials of Musculoskeletal Care. 2nd ed. Rosem ont, IL: Am erican Academ y of Orthopedic Surgeons; 2001:684–685. 3. Morrissy RT, Weinstein SL, eds. Lovell and Winter's Pediatric Orthopaedics. 5th ed. Philadelphia: Lippincott William s & Wilkins; 2001:1280–1281. 4. Orava S, Malinen L, Karpakka J, et al. Results of surgical treatm ent of unresolved Osgood-Schlatter lesion. Ann Chir Gynaecol. 2000;89(4):298–302. 5. Peck DM. Apophyseal injuries in the young adult. Am Fam Physician. 1995;51:1891–1895.
Codes ICD9-CM 732.4
Pa ge 3 3 4
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Osteo genesis Im perfecta
Osteogenesis
Imperfecta Daniel Davis
Basics Description
Inherited abnorm ality of procollagen am ino acid sequence
Bone hypom ineralization and incom plete ossification result in brittle bones.
Abnorm al collagen affects all connective tissue to varying degrees.
Tim e course is variable: o
Most cases involve fractures during childhood followed by quiescence during adolescence and early adulthood.
Etiology
Procollagen defects result in bone and connective tissue m atrix abnorm alities.
Defects in different sites on procollagen protein chain result in m ore severe form s.
Defects are inherited, either autosom al recessive (generally m ilder) or autosom al dom inant (m ore severe).
Lethal cases involve sporadic or new m utations.
Pa ge 3 3 4
Ehlers-Danlos syndrom e involves m utations of sam e procollagen protein in different location.
Pediatric Considerations
Most cases involve pathologic fractures during childhood.
Multiple fractures often initiate evaluation for abuse, but possibility of pathologic fractures also should be considered.
Diagnosis Signs and Symptoms Multiple heritable defects that lead to brittle bones:
Often associated with other connective tissue abnorm alities
Bones
Multiple recurrent fractures (especially in long bones) are hallm ark of this disease.
Fractures m ay be present at birth or m ay recur in the elderly.
All bones are affected to som e extent (see Im aging/Special Tests).
Eyes
Blue sclera are another hallm ark of this disease.
No visual changes are reported.
Ears
Hearing loss usually begins in adolescence; >90% of patients have som e deficit by age 30 years.
Hearing loss is generally sensorineural, although som e m iddle ear abnorm alities have been dem onstrated.
Pa ge 3 3 4
Other
Yellow-brown or blue-gray discoloration and abnorm al shape of teeth
Shares several features with Ehlers-Danlos syndrom e: o
Loose joints
o
Valve problem s
o
Vascular abnorm alities
Thyroid abnorm alities m ay be seen.
Extrem e cases m ay result in perinatal death.
Essential Workup
Diagnosis is usually m ade as com bination of clinical and radiographic findings.
History of repeated fractures or fractures with unim pressive m echanism
Thorough search for other tender areas and evaluation of eyes, teeth, and joints is im portant for diagnosis.
Careful exam ination of neurovascular status distal to fracture
Tests Lab
Evaluate for m etabolic derangem ents such as hyperparathyroidism , vitam in C or D deficiencies, and calcium /phosphate abnorm alities.
DNA studies m ay be indicated for fam ilial analysis, prenatal testing, and genetic counseling.
Tissue biopsy is controversial, but m ay help differentiate from tum ors.
Imaging
Radiographs of fracture sites: o
May reveal osteopenia (usually m ild)
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o
Crum pled long bones (“accordion fem ora―)
o
Incom plete ossification at physes
Skeletal survey is m andatory, especially in children.
Skull film s m ay show worm ian appearance of irregular ossification.
Popcornlike deposits on long-bone ends is poor prognostic finding.
Form al audiologic testing as outpatient is required in older patients.
P.773
Differential Diagnosis
Nonaccidental traum a in children
Ehlers-Danlos syndrom e
Hypophosphatasia
Achondroplasia
Scurvy
Congenital syphilis
Celiac disease
Treatment Pre Hospital Personnel should obtain inform ation about m echanism or social factors that point toward pathologic fracture versus nonaccidental traum a.
Initial Stabilization
Airway m anagem ent and resuscitation as indicated
Fracture im m obilization/splinting
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ED Treatment
Specific fracture m anagem ent dictated by type and location of injury
Orthopedic consultation regarding need for traction or operative fixation
No specific treatm ent for osteogenesis im perfecta exists at present.
Medication (Drugs)
Pain m edications as indicated
Elderly wom en m ay benefit from calcium (1–1.5 g/d) and estrogen replacem ent (0.625 m g/d).
Follow-Up Disposition Admission Criteria
Adm ission is determ ined by m ultiple traum a or operative needs for fracture repair.
Pediatric patients m ay need adm ission to investigate possibility of nonaccidental traum a.
Discharge Criteria
Patients m ay be considered for outpatient m anagem ent if isolated fracture is present and appropriate hom e resources are available.
Most patients should be discharged with orthopedic and prim ary physician follow-up.
References
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1. Chandrasom a P, Taylor CR. Concise Pathology. East Norwalk, CT: Appleton & Lange, 1991. 2. Cole WG. Advances in osteogenesis im perfecta. Clin Orthop Relat Res. 2002;(401):6–16. 3. McKusick VA. Heritable Disorders of Connective Tissue. 4th ed. St. Louis, MO: Mosby; 1972. 4. Prockop DJ. Heritable disorders of connective tissue. In: Wilson JD, et al., eds. Harrison's Principles of Internal Medicine. 12th ed. New York: McGraw-Hill; 1991:1860.
Codes ICD9-CM 756.51
ICD10 Q78.0
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Osteo m yelitis
Osteomyelitis
Anthony J. Medak Irving Jacoby
Basics Description
Osteom yelitis (OM): infection of bone with ongoing inflam m atory destruction
Usually bacterial, but fungal OM does occur.
Etiology Hematogenous OM
Prim arily in children, elderly, IV drug abuse (IVDA) patients
Seeding of bacteria to bone from rem ote site of infection via bloodstream
Children have acute OM and adults subacute or chronic.
Hem atogenous OM of long bones rarely occurs in adults.
Most children with acute hem atogenous OM have no preceding illness.
One third have history of traum a to affected area.
Staphylococcus aureus is m ost com m on cause of OM in all ages.
Neonates: S. aureus, Enterobacteriaceae, group A and B
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streptococci, and Escherichia coli
Children: S. aureus, group A streptococci, Haem ophilus influenzae, Enterobacteriaceae
Salm onella: com m on in sickle cell disease
Adults: S. aureus, Enterobacteriaceae, Pseudom onas, gram -negative rods, Staphylococcus epiderm idis, gram -positive anaerobes, esp peptostreptococcus
Illicit drug users: Candida, Pseudom onas, Serratia m arcescens
Prolonged neutropenia: Candida, Aspergillus, Rhizopus, Blastom yces, Coccidioidom ycosis
Hematogenous Vertebral OM
Uncom m on
Most prevalent in adults older than 45 years
Involves the disk and vertebra above and below
Often in setting of long-term urinary catheter placem ent, IVDA, cancer, hem odialysis, or diabetes
IVDA: OM of pubic sym physis, sternoclavicular, and sacroiliac (S-I) joints
Lum bar vertebrae m ost com m on, followed by thoracic, then cervical
Posterior extension leads to epidural/subdural abscess or m eningitis.
Anterior extension m ay lead to paravertebral, retropharyngeal, m ediastinal, subphrenic, retroperitoneal, or psoas abscess.
Direct or Contiguous OM
Organism (s) directly seeded in bone due to traum a, esp following open fractures: o
Spread from adjacent site of infection or from surgery
Pa ge 3 3 5
More com m on in adults and adolescents
S. aureus, Enterobacteriaceae, Pseudom onas
Norm al vascularity o
S. aureus and S. epiderm idis, gram -negative bacilli, and anaerobic organism s
Vascular insufficiency/diabetes o
Sm all bones of feet are com m on sites.
o
Infection resulting from m inor traum a, infected nail beds, cellulitis, or skin ulceration
o
If ulcer size >2 cm 2 and >3 m m in depth, bone involvem ent is likely.
o
Polym icrobial including anaerobes
o
If bone palpated, high correlation with OM
Puncture wound through tennis shoe: S. aureus, Pseudom onas
Clavicular OM can occur as com plication of subclavian vein catheterization.
Chronic OM
Osteom yelitis that persists or recurs
Distinguishing characteristic is necrotic bone (sequestrum ) that m ust be débrided.
S. epiderm idis, S. aureus, Pseudom onas aeruginosa, Serratia m arcescens, and E. coli
Diagnosis Signs and Symptoms Vary with duration of disease
History
Pain: localized, deep, dull, and throbbing; occurs with and
Pa ge 3 3 5
without m ovem ent
Fever and chills
Malaise, nausea, vom iting
Reluctance to use extrem ity
Consider OM as a cause of fracture nonunion
Physical Exam
Tenderness to palpation, warm th, erythem a, edem a, decreased range of m otion
Drainage of sinus tract
Essential Workup
CBC
ESR and C-reactive protein
Radiographs
Blood and wound cultures and sensitivities
Tests Lab
CBC; WBC m ay be elevated but often norm al
ESR and C-reactive protein (usually elevated)
Blood cultures (positive in ~50% of cases)
Imaging
Plays a central role in evaluation
Start with plain film s; other tests often required
Radiographs
May be norm al for the first 2–3 weeks of sym ptom s
Earliest finding is periosteal elevation, followed by cortical erosions, then new bone form ation
40–50% of focal bone loss needed to detect lucency on radiograph; fewer than one third of cases have diagnostic findings at 10 days
Obtain chest radiograph if tuberculosis (TB) suspected
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Bone scan
Technetium -99m m ethylene diphosphonate ( 9 9 m Tc-MDP)
Measures increase in bone m etabolic activity
~95% sensitive but less specific than MRI
Bone scan abnorm al after 2–3 days of sym ptom s
Negative study 24 hours after onset of sym ptom s rules out acute OM
Leukocyte Scintigraphy
Indium -111–labeled WBCs
More specific but less sensitive than bone scan
Difficult to distinguish bone inflam m ation from soft-tissue inflam m ation (i.e., cellulitis, tum ors, inflam m atory arthritis)
False negative in chronic infection
CT
Reveals bone edem a, cortical destruction, periosteal reaction, sm all foci of gas or foreign bodies, joint surface dam age, and soft-tissue involvem ent when plain film s not helpful
Useful in vertebral OM
MRI 99m
As sensitive as
Tc-MDP scan but m ore specific
Reveals bone edem a, cortical destruction, periosteal reaction, joint surface dam age, and soft-tissue involvem ent before x-rays
Effective in early detection (diagnosis m ay be evident by MRI before scintigraphy)
Test of choice to identify vertebral OM and OM in diabetic foot ulcers
Occasional false-positive results in traum a, previous
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surgical procedures, or neuropathic joint disease P.775
Ultrasound
An em erging m odality for OM
Periosteal elevation or thickening, fluid collections adjacent to bone often seen
May show findings of OM days prior to plain film s
Diagnostic Procedures/Surgery
Gold standard for diagnosis is open biopsy with histology and tissue gram stains, including culture and sensitivities
Needle aspiration has lower sensitivity than open biopsy
Culture of sinus or drainage from wound can be m isleading; correlates well with S. aureus, but not as reliable for other organism s.
Pediatric Considerations
70–85% of children have fever higher than 38.5°C.
Neonates com m only afebrile
Only approxim ately one in three of children will have leukocytosis
Blood cultures positive in ~50%
Differential Diagnosis
Cellulitis
Paronychia/felon
Bursitis, toxic synovitis, septic arthritis
Extrem ity fracture
Bone infarction in sickle cell patients
Acute leukem ia, m alignant bone tum ors
Mechanical back pain
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Spinal epidural abscess
Brucellosis, esp in S-I joint
TB, m ore com m on in thoracic spine (Pott's disease)
Treatment Initial Stabilization Em ergent stabilization if septic or if neurologic deficits from spine involvem ent
ED Treatment
Em piric antibiotic treatm ent in ED
Cultures should guide subsequent antibiotic regim en
Antibiotics: depend on patient's age and organism (see Medications section)
Orthopaedic and infectious disease consultation
Surgical intervention m ay be needed to optim ize treatm ent (e.g., infected fracture, bone necrosis)
Parenteral antibiotic treatm ent for 4–6 weeks
Medication (Drugs)
Newborn to 4 m onths: penicillinase-resistant synthetic penicillin (e.g., nafcillin: 37 m g/kg IV q6h) plus a third-generation cephalosporin (e.g., ceftriaxone: 50–75 m g/kg IV per day); if suspect m ethicillin-resistant Staphylococcus aureus (MRSA) then vancom ycin (40–60 m g/kg IV q6h) plus a third-generation cephalosporin. (note: doses are based on age >28 days)
Children (>4 m onths): penicillinase-resistant synthetic penicillin (e.g., nafcillin: 37 m g/kg IV q6h to m ax. 8–12
Pa ge 3 3 5
g/d). If suspect MRSA, then vancom ycin (40–60 m g/kg IV q6h to m ax. 2–4 g/d). Add third-generation cephalosporin if suspicion for gram negative rods, or presence on gram stain noted (e.g., ceftriaxone: 50–75 m g/kg IV per day to m ax. 2–4 g/d)
Adult: penicillinase-resistant synthetic penicillin (e.g., nafcillin: 2 g IV q4h); if suspect MRSA, vancom ycin (15 m g/kg IV q12h)
Sickle cell anem ia with OM: ciprofloxacin 400 m g IV q12h, or levofloxacin 750 m g IV q24h (not in children); alternative: third-generation cephalosporin
Post–nail puncture through tennis shoe: ciprofloxacin 750 m g PO b.i.d. or levofloxacin 750 m g PO q24h; alternative: ceftazidim e 2 g IV q8h
Involving orthopaedic prosthesis or hardware: add rifam pin (10 m g/kg PO/IV per day to m axim um of 600 m g/d) to regim en for S. aureus. Hardware rem oval generally required.
Post-traum atic OM: vancom ycin and ceftazidim e
If vancom ycin resistant enterococcus present: linezolid 600 m g IV q12h × 6 weeks
Pediatric Considerations Children with hem atogenous OM m ay undergo short-course IV antibiotics and then be changed to oral for additional 1–2 months.
Follow-Up Disposition Admission Criteria
Patients with acute OM should be adm itted.
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Patients with chronic osteom yelitis usually require adm ission for surgical procedures, debridem ent, and obtaining bone cultures and histology.
Discharge Criteria Subacute or chronic OM patients m ay be considered for outpatient m anagem ent if hom e IV antibiotics arranged, bone specim ens obtained, and necrotic bone débrided.
Issues for Referral
Cases refractory to debridem ent and antibiotics benefit from hyperbaric oxygen as an adjunct to standard treatm ent.
Approxim ately two thirds of these cases will dem onstrate benefit.
References 1. Carek PJ, Dickerson LM, Sack JL. Diagnosis and m anagem ent of osteom yelitis. Am Fam Physician. 2001;63(12):2413–2420. 2. Ghiorzi T, Mackowiak P. Diagnosis of osteom yelitis. In: Rose BD, ed. UpToDate. Waltham , MA: UpToDate, 2005. 3. Lew DP, Waldvogel FA. Osteom yelitis. Lancet. 2004;364:369–379. 4. Santiago Restrepo C, Gim enez CR, McCarthy K. Im aging of osteom yelitis and m usculoskeletal soft tissue infections: current concepts. Rheum Dis Clin North Am . 2003;29(1):89–109. 5. Shuford JA, Steckelberg JM. Role of oral antim icrobial therapy in the m anagem ent of osteom yelitis. Curr Opin Infect Dis. 2003;16:515–519.
Codes ICD9-CM 730.20
Pa ge 3 3 5
ICD10 M86.9
Pa ge 3 3 5
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Osteo po ro sis
Osteoporosis
Daniel Davis
Basics Description
Overall decrease in skeletal m ass, generally diffuse
Trabecular bone (especially vertebrae and fem ur) affected m ore com m only and earlier
Disease begins in adolescence, but fractures do not usually m anifest until age 50 or older.
Fem ales affected m uch m ore com m only than m ales, especially postm enopause
Etiology
Overall increase in resorption over form ation of new bone
Advanced age is m ost im portant risk factor.
Inadequate dietary calcium im portant factor, especially early in life
Sedentary lifestyle is risk factor (weight bearing on bone favors new bone form ation).
Decrease in estrogen with m enopause is key factor in wom en.
Other causes include long-term steroid use, alcoholism , m ethotrexate.
May be fam ilial or hereditary factor as well
Pa ge 3 3 6
Pediatric Considerations Although disease appears to start in adolescence, pediatric patients are asym ptom atic.
Diagnosis Signs and Symptoms
Usually asym ptom atic until pathologic fractures occur
Fractures with insignificant m echanism or recurrent fractures are hallm ark.
Vertebral colum n m ost com m only involved
Multiple com pression fractures of vertebral colum n often lead to kyphosis and scoliosis.
Hip fractures (fem oral neck and intertrochanteric fractures) also com m on
Essential Workup
Fracture without significant m echanism and identification of risk factors is m ost im portant.
Careful neurovascular exam ination distal to fem ur or other extrem ity fracture
Rectal tone and postvoid residual determ ination should be done in patients with vertebral fractures.
Radiographs of suspected fracture m ay show osteopenia (late finding in disease).
Spine film s m ay show old com pression fractures.
CT scan should be perform ed to better evaluate vertebral fractures: o
Retropulsion, spinal canal com prom ise is not always apparent on plain film s.
o
Make sure CT cuts extend full level above and below
Pa ge 3 3 6
injuries on spine radiographs.
Tests Lab Serum chem istries, such as calcium , parathyroid horm one, and alkaline phosphatase, m ay help differentiate between other illnesses.
Imaging
Plain film s can identify fractures; however, age of each fracture m ay be difficult to determ ine.
Bone scan or CT help determ ine age of fractures, especially in spine.
Bone densitom etry can provide prognostic inform ation and help guide therapy.
Differential Diagnosis
Multiple m yelom a or other m etastatic tum or
Osteogenesis im perfecta (usually apparent in childhood)
Hyperparathyroidism
Other dem ineralizing bone diseases
Treatment Pre Hospital Cautions:
Obtain prehospital inform ation on m echanism to help diagnose pathologic fracture.
Avoid aggressive m anipulation or m ovem ent of patient, as this m ay exacerbate bony injury.
Initial Stabilization Im m obilize fractures
Pa ge 3 3 6
P.777
ED Treatment
Fractures are treated with expectation of delayed or incom plete healing.
Prevention is far m ore effective than treatm ent.
Long-term therapy is beneficial (see Medications).
Use of orthotic back braces and vests should be arranged in conjunction with orthopedic spine consultation.
Exercise is also helpful.
Balance m ust be achieved between osteoporosis risk and steroid or m ethotrexate therapy.
Medication (Drugs)
Alendronate: 10 m g/d
Calcitonin: 0.5 m g/d SC of hum an, 100 IU/d SC of salm on; alternative: nasal spray (100 IU) one spray per day in alternate nostrils
Calcium supplem entation (often with vitam in D): 1–1.5 g/d
Estrogen: 0.625 m g/d (with or without m edroxyprogesterone)
Etidronate: 400 m g/d for 2-week cycles every 15 weeks
Raloxifene (selective estrogen receptor m odulator): 60 m g PO daily
Sodium fluoride: 25 m g b.i.d. with calcium
Pediatric Considerations Ensure adequate calcium in diet from early age.
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Follow-Up Disposition Admission Criteria
Per norm al orthopedic protocols, with special considerations for age and social situation
Com pression fractures are generally stable, but possibility of burst fracture with cord com pression m ust be ruled out.
Any cervical fracture or fracture with neurologic sym ptom s requires adm ission with em ergent consultation with neurosurgery or orthopedics.
Adm ission m ay be necessary for pain control and because of decreased am bulation.
Discharge Criteria
Per norm al orthopedic protocols with special considerations for age and social situation
Patients with m inim al injuries, able to care for them selves at hom e, or with appropriate assistance, and adequate postoperative pain control m ay be discharged with orthopedic follow-up
References 1. Chandrasom a P, Taylor CR. Concise Pathology. East Norwalk, CT: Appleton & Lange, 1991. 2. Krane SM, Holick MF. Metabolic bone disease. In: Wilson JD, et al., eds. Harrison's Principles of Internal Medicine. 12th ed. New York: McGraw-Hill; 1991:19–21. 3. North Am erican Menopause Society. Managem ent of postm enopausal osteoporosis: position statem ent. Menopause. 2002;9(2):84–101.
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4. Papaioannou A, et al. Diagnosis and m anagem ent of vertebral fractures in elderly adults. Am J Med. 2002;113(3):220–228.
Codes ICD9-CM 733.00
ICD10 M81.9
Pa ge 3 3 6
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Otitis Externa
Otitis Externa
Assaad J. Sayah
Basics Description
Inflam m ation or infection of the auricle, auditory canal, or external surface of the tym panic m em brane (TM): o
Spares the m iddle ear
Also called “swim m er's ear― due to the usual history of recent swim m ing: o
Occasional cases after norm al bathing
Necrotizing otitis externa: o
Infection starts at ear canal and progresses through periauricular tissue toward base of skull
o
Occurs in elderly, diabetic, or other im m unocom prom ised patients
o
Caused by Pseudom onas aeruginosa
o
Can lead to cellulitis and osteom yelitis
Etiology
Often precipitated by an abrasion of the ear canal or m aceration of the skin from persisting water or excessive dryness
Predisposing factors include: o
History of ear surgery or TM perforation
Pa ge 3 3 6
o
Narrow or abnorm al canal
o
Hum idity
o
Allergy
o
Traum a
o
Abnorm al cerum en production
P. aeruginosa, Staphylococcus aureus, Streptococcal species, and rarely fungi.
Diagnosis Signs and Symptoms History
Itching of the external ear canal is usually the first sym ptom
1–2 day history of progressive pain
Ear drainage
Decreased auditory acuity
Clogged sensation in ear
Physical Exam
Pain in ear or with m otion of pinna/tragus
Swollen, erythem atous external ear canal
Ear drainage
Decreased auditory acuity
Pain/swelling in preauricular area
Necrotizing (Malignant) Otitis Externa
Pain, tenderness, swelling in periauricular area
Headache
Otorrhea
Cranial nerve palsy o
Facial nerve m ost affected
Pa ge 3 3 6
Essential Workup Clinical diagnosis with typical signs/sym ptom s:
Pain in ear or with m otion of pinna/tragus
Otoscopic exam ination
Swollen, erythem atous external ear canal
Ear drainage
Cheesy white or gray green exudate
Tests Lab
None usually indicated except when possibility of necrotizing otitis externa: o
Signs of system ic toxicity or local spread of infection should be checked
WBC count
ESR
Glucose (check for diabetes)
Cultures
Imaging CT/MRI to exclude osteom yelitis if the patient has signs of toxicity or bony involvem ent
Diagnostic Procedures/Surgery
Rem ove debris with a soft plastic curette or gentle irrigation with peroxide/water m ix.
Wick placem ent m ay be needed to facilitate m edication delivery.
Differential Diagnosis
Necrotizing otitis externa
Otitis m edia
Folliculitis from obstruction of sebaceous glands
Otic foreign bodies
Pa ge 3 3 6
Herpes zoster infection of the geniculate ganglion
Parotitis
Periauricular adenitis
Mastoiditis
Dental abscess
Sinusitis
Tonsillitis
Pharyngitis
Tem porom andibular joint pain
Pediatric Considerations Consider ear canal foreign bodies in children with purulent drainage from edem atous, painful ear canals. P.779
Treatment ED Treatment
Clean external ear canal: o
Rem ove the inflam m atory debris by gentle curettage with a cotton-tipped wire applicator.
o
Occasional suction with a Fraser suction tip m ay be necessary.
Insert a cotton or gauze wick 10–12 m m into the canal after cleansing, if the ear canal is very edem atous.
Medication (Drugs)
Most cases respond well to topical treatm ent:
Pa ge 3 3 6
o
Antiseptic, anti-inflam m atory, and drying otic drops elim inate the pathogenic bacteria and allow for rapid healing of the canal.
o
Acetic acid solutions such as Dom eboro otic (2% acetic acid): 4–6 drops q4h–q6h.
o
Corticosporin otic (hydrocortisone 1%, polym yxin + neom ycin) suspension: 4 drops to ear canal q.i.d. (use suspensions and not solutions with suspected tym panic m em brane perforation)
o
Ofloxacin: 5 drops b.i.d. (drug of choice in perforated tym panic m em brane)
Oral antibiotics: o
Adm inister to patients with cellulitis of the face or neck, severe edem a of the ear canal, concurrent otitis m edia, or when the tym panic m em brane cannot be visualized.
o
Treat diabetics and other im m unocom prom ised patients with oral ciprofloxacin and follow closely for sym ptom s of m alignant otitis externa.
o
Am oxicillin: 500 m g (peds: 40 m g/kg/d) PO t.i.d.
o
Ciprofloxacin: 500 m g PO b.i.d.
IV antibiotics for patients with necrotizing otitis externa, severe cellulitis, or septic looking
Prophylaxis: o
Apply rubbing alcohol or acetic acid (2%) to keep the external ear canal dry and prevent recurrence of infection
Follow-Up Disposition
Pa ge 3 3 7
Admission Criteria
Necrotizing otitis externa
Significant involvem ent of the pinna
Signs of system ic illness
Discharge Criteria
Most patients
Close follow-up for patients at risk of otitis externa
Ear-nose-throat follow-up for perforated tym panic m em brane, worsening of sym ptom s or failure of initial m anagem ent
Patient instructions: o
Avoid swim m ing and keep ears com pletely dry for 3–4 weeks.
o
Apply m edications as directed
o
Return if worse pain, fever, hearing loss develops, or there is any change in m ental or neurologic status.
o
Follow-up if sym ptom s are not im proved within 2–3 days
References 1. Beers SL, Abram o TJ. Otitis externa review. Pediatr Em erg Care. 2004;20(4):250–256. 2. Schapowal a. Otitis externa: a clinical overview. Ear Nose Throat J . 2002;81(8 Suppl 1):21–22. 3. Rutka J. Acute otitis externa: treatm ent perspectives. Ear Nose Throat J. 2004;83(9 Suppl 4):20–21; discussion 21–22. 4. Hughes E, Lee JH. Otitis externa. Pediatr Rev. 2001;22(6):191–197. 5. Sander R. Otitis externa: a practical guide to treatm ent and prevention. Am Fam Physician. 2001;61(5):927–936, 941–942.
Codes
Pa ge 3 3 7
ICD9-CM 380.10
ICD10 H60.9
Pa ge 3 3 7
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Otitis M edia
Otitis Media
Assaad J. Sayah
Basics Description
Infection of the m iddle ear
Most com m only occurs in children 6–36 m onths of age
Etiology
Usually associated with (or as a result of) upper respiratory tract infections
Viral: o
Parainfluenza
o
Respiratory syncytial virus
o
Influenza
o
Adenovirus
o
Rhinovirus
Bacterial: o
Staphylococcus pneum oniae
o
Moraxella catarrhalis
o
Haem ophilus influenzae
o
Streptococcus pyogenes
o
Mycoplasm a pneum oniae
Associated with blockage of eustachian tube
Predisposing factors:
Pa ge 3 3 7
o
Deficient m ucus, cilia, or antibodies
o
Intubation, especially nasotracheal
o
Am erican Indians, Eskim os
o
Down syndrom e
o
Cleft palate
Diagnosis Signs and Symptoms History
Ear pain
Irritability
Rhinitis
Vom iting, diarrhea
Poor feeding
Fever
Sensation of plugged ear
Pulling at ear
Vertigo, tinnitus
Conjunctivitis
Physical Exam
Tym panic m em brane inflam m ation, bulging and lim ited m obility
Decreased visibility of the landm arks of the m iddle ear
Essential Workup
Exclude associated conditions.
Otoscopic exam ination for appearance and m obility of tym panic m em brane o
Full visualization essential
o
Increased vascularity, erythem a, purulence
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o
Obscured landm arks—bony, light reflex
o
Pneum atic otoscopy—m obility, bulging, retracted
Tests Lab Cultures unhelpful unless done by tym panocentesis
Imaging CT scan if associated m astoiditis is suspected.
Diagnostic Procedures/Surgery
Tym panocentesis—indications: o
Severe pain or toxicity
o
Failure of antim icrobial therapy
o
Suspicion of suppurative com plication
o
Sick neonate
o
Im m unocom prom ised patient
Tym panom etry and acoustic otoscopy m ay be useful with difficult exam inations.
Differential Diagnosis
Infection: o
Otitis externa
o
Mastoiditis
o
Dental abscess
o
Peritonsillar abscess
o
Sinusitis
o
Lym phadenitis
o
Parotitis
o
Meningitis
Traum a: o
Perforation of the tym panic m em brane
o
Foreign body in ear
o
Barotraum a
Pa ge 3 3 7
o
Instrum entation
Serous otitis m edia or eustachian tube dysfunction
Im pacted ear cerum en
Im pacted third m olar
Tem porom andibular joint dysfunction
P.781
Treatment ED Treatment
Most m ild cases could resolve without antibiotics
Antibiotics are indicated for all infants younger than 6 m onths and older children with certain diagnosis or severe illness.
Considerations should include recurrent nature of otitis m edia, lack of clinical response, and resistance patterns in com m unity.
Parenteral antibiotics indicated in febrile toxic children younger than 1 year or with im m unocom prom ise.
Antihistam ines, decongestants, and steroids have no proven efficacy.
Antipyretics and analgesics are im portant (avoid local analgesics in perforated tym panic m em branes).
Medication (Drugs)
Am oxicillin: 500 m g PO t.i.d (peds: 80 m g/kg/d PO t.i.d) for 7–10 days
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Am oxicillin-clavulanic acid: 500 m g PO t.i.d. (peds: 80 m g/kg/d PO t.i.d) for 7–10 days
Azithrom ycin: 10 m g/kg PO day 1, then 5 m g/kg/d PO days 2–5
Cefuroxim e: 500 m g PO b.i.d. (peds: 30m g/kg PO b.i.d)
Trim ethoprim (TMP)-sulfam ethoxazole: 8 m g of TMP/kg/d PO b.i.d.
Follow-Up Disposition Admission Criteria Febrile toxic children who are:
Younger than 1 year, im m unocom prom ised
Moderately or severely dehydrated
Unable to tolerate oral fluids or m edications
Suspected or proven associated significant infection
Suspected abuse
Unreliable caretaker
Discharge Criteria
Children without any of the aforem entioned criteria
Follow-up in 10–14 days to ensure resolution
Indications for earlier follow-up: o
Child does not get better in 24–48 hours
o
Any progression of signs or sym ptom s
o
New problem s develop including a rash
o
Any concerns arise
Complications
Recurrent otitis m edia: o
Three episodes within 6 m onths or 4 or m ore
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episodes within 1 year
Perforated tym panic m em brane
Serous otitis m edia
Conductive hearing loss
Facial nerve injury
Mastoiditis
Cholesteatom a
Meningitis
Subdural em pyem a
Venous sinus throm bosis
References 1. Rosenfeld RM, Lous J, Bluestone CD et al. Recent advances in otitis m edia. 9. Com plications and sequelae. Ann Otol Rhinol Laryngol. Suppl 2005; 194:140–160. 2. Jung TT, Hunter ll, Alper CM et al. Recent advances in otitis m edia.8. Treatm ent. Ann Otol Rhinol Laryngol. 2005;194(suppl):114–139 3. Bauchner H. Ear, ears, and m ore ears Arch Dis Child. 2001:84(2):185–186. 4. Am erican Academ y of Pediatrics: Diagnosis and m anagem ent of acute otitis m edia. Pediatrics. 2004;113(5):1451–65.
Codes ICD9-CM 382.9
ICD10 H66.9
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Oto lo gic Traum a
Otologic Trauma
Shan Liu
Basics Description
Ear cartilage has no blood supply and is nutritionally dependent on perichondrium .
Hem atom as often disrupt perichondrium and cartilage leading to ischem ia, possible perichondritis, necrosis, and cauliflower ear.
Penetrating injuries or anim al bites m ay lead to infection of cartilage.
Etiology
Blunt traum a (often contact sports)
Penetrating traum a (e.g., tym panic m em brane perforation from cotton swabs)
Blast injury
Lightning injury; both tym panic-m em brane and ossicular disruption occur in 50% of lightning strikes.
Chem ical exposure
Therm al injury
Diving injuries: o
Inner-ear barotraum as
o
Tym panic m em brane rupture
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Pediatric Considerations Consider nonaccidental traum a
Diagnosis Signs and Symptoms
Severe ear pain
Bleeding
Auricular deform ity:
o
Edem a
o
Hem atom a
o
Laceration
o
Am putation
Decreased hearing: o
Partial loss suggests tym panic m em brane rupture.
o
Com plete hearing loss suggests additional injuries to ossicles or inner ear.
Hem otym panum
Purulent or bloody discharge from ear canal
Tinnitus
Vertigo: o
Inner ear injury
o
Tym panic m em brane perforation in water
History
Mechanism
Associated injuries
Allergies
Medications
Past otologic history
Physical Exam
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Search for concom itant injury; exam ine:
Head
Cranial nerves
Vascular structures
Tem poral bone
Pinna
External ear canal
Tym panic m em brane
Hearing
Tests Lab Wound culture if signs of infection
Differential Diagnosis
Infection
Hem angiom a
Foreign body in ear
Treatment Pre Hospital If auricle is am putated, wrap in m oist gauze and place in plastic bag.
Initial Stabilization
Check airway, breathing, and circulation; full traum a evaluation; resuscitation as appropriate
Sterile dressing to injured site
General Measures
All injury types: o
Anesthesia:
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Local anesthesia via nerve block to auriculotem poral branch of m andibular nerve, lesser occipital nerve, greater auricular nerve, and auricular branch of vagus nerve; use 1% lidocaine or 0.25% m arcaine.
Alternative: inject ring of anesthetic around base of pinna.
Managem ent of tym panic m em brane perforation
Tetanus prophylaxis if necessary
For hum an and anim al bites, use both penicillin and Ceftazidim e or Augm entin.
Specific injury types: o
Hem atom a: drainage im perative to reapproxim ate perichondrium to cartilage to prevent cartilage necrosis, ideally within 72 hours. However, no clearly defined best treatm ent based on m eta-analysis. Treatm ent traditional is as follows:
Antistaphylococcal antibiotics for 7–10 days
Aspiration: preferred alterative if clot not yet form ed. Use 18–20-gauge needle for aspiration; m ilk hem atom a until totally evacuated. P.783
Incision and drainage: m ore effective with larger and/or clotted hem atom as. Incise along curvature of pinna with no. 15 scalpel, evacuate, and irrigate; apply pressure dressing for 3–7 days to prevent reaccum ulation.
Vaseline gauze: place to fill crevices of pinna. Place over and behind pinna; wrap soft gauze
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firm ly around head.
Alternatively, suture dental rolls into place over incised area.
Therm oplastic splints, if available, can be used.
If patient presents again with reaccum ulation, reaspirate, consider wick placem ent.
Laceration: o
Prophylactic antibiotics are controversial.
o
Clean and débride wound, anesthetize as necessary.
o
Superficial abrasions: clean, dress with antibiotic ointm ent.
o
Sim ple lacerations: 5.0 or 6.0 m onofilam ent nylon or polypropylene suture, then pressure dressing. May use absorbable suture on m edial skin lacerations to avoid having to bend ear for suture rem oval.
o
Exposed auricular cartilage: carefully débride jagged edges; com pletely cover cartilage to prevent perichondritis. Can rem ove sm all am ount of cartilage to allow skin coverage. Approxim ate cartilage first with absorbable sutures at m ajor landm arks; include anterior and posterior perichondrium in stitch.
o
Avulsions: 2 cm : consult or urgently refer to otolaryngologist or plastic surgeon; save in subcutaneous pocket.
Medication (Drugs)
Augm entin (am oxicillin-clavulanate): o
Adults: 875/125 m g PO t.i.d. (peds: 40 m g/kg per day PO t.i.d.
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Dicloxacillin: 250 m g PO q.i.d.
Erythrom ycin: 250 m g PO q.i.d.
Penicillin VK: 250 m g PO q.i.d.
Follow-Up Disposition Admission Criteria
Concom itant serious traum atic injuries
Need for IV antibiotics
Im m unosuppressed persons with serious infections, perichondritis, or chondritis
Discharge Criteria
Able to tolerate oral antibiotics
Follow up wound suture repair.
Follow up hem atom as after 24 hours to determ ine whether re-accum ulation of fluid.
References 1. Cantrill ST. Facial traum a. In: Rosen P, et al., eds. Em ergency Medicine: Concepts and Clinical Practice. 4th ed. St. Louis, MO: Mosby; 1998. 2. Henderson JM, Salam a AR, Blanchaert RH. Managem ent of Auricular Hem atom a Using a Therm oplastic Splint. Arch Otolaryngol Head Neck Surg. 2000;126(7):888–890. 3. Jones SEM, Mahendran S. Interventions for Acute Auricular Haem atom a. The Cochrane Database of System atic Reviews. 2005, Vol (2). 4. Lam m ers RL, Trott AT. Methods of wound closure. In: Rogers JR, Hedges J, eds. Clinical Procedures in Em ergency Medicine. 3rd ed.
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Philadelphia: WB Saunders; 1998. 5. Manthey DE, Harrison BP. Otolaryngologic procedures. In: Rogers JR, Hedges J, eds. Clinical Procedures in Em ergency Medicine. 3rd ed. Philadelphia: WB Saunders; 1998. 6. Spring PM, Am edee RG. Ear pain and drainage. In: Calhoun KH, ed. Expert Guide to Otolaryngology. Philadelphia: Am erican College of Physicians; 2001. 7. Turbiak TW. Ear traum a. Em erg Med Clin North Am . 1987;5:243–251.
Miscellaneous SEE ALSO: Tym panic Mem brane Perforation
Codes ICD9-CM 959.09 Injury of face and neck
ICD10 S09.9
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Ovarian C yst/To rsio n
Ovarian
Cyst/Torsion Kyan J. Berger
Basics Description
Ovarian cysts: o
Generally asym ptom atic until com plicated by hem orrhage, torsion, rupture, or infection
o
Follicular cysts:
Most com m on
Occur from fetal life to m enopause
Unilocular; diam eter 3–8 cm
Thin wall predisposes to rupture, which usually causes m inim al or no bleeding.
Rupture during ovulation at m idcycle known as m ittelschm erz
o
Corpus luteal cysts:
Most significant
Diam eter 3 cm
Rapid bleeding from intracystic hem orrhage causes rupture.
Rupture m ost com m on just before m enses
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begins
Can cause severe intraperitoneal bleeding
Gradual bleeding into cyst or ovary distends capsule and m ay cause pain without rupture.
Adnexal torsion: o
Twisting of vascular pedicle of ovary, fallopian tube, or paratubal cyst
o
Causes adnexal ischem ia leading to necrosis
o
Occlusion of lym phatics and venous drainage lead to rapid enlargem ent of adnexa.
Risk Factors Adnexal torsion:
Highest frequency in reproductive-age wom en, especially m id-20s
Ovarian cysts
Ovarian hyperstim ulation
Tum ors:
o
Serous cystadenom a m ost com m on
o
Teratom as
Pelvic surgery: o
Tubal ligation
o
Hysterectom y
Pregnancy
History of pelvic inflam m atory disease
Alert
Anticoagulated patients at increased risk of: o
Hem orrhagic corpus luteal cyst
o
Significant bleed from ruptured cyst, including with ovulation
Etiology
Ovarian cyst:
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o
Follicular, corpus luteal, theca lutein, cystic teratom a, endom etriom a (chocolate cyst)
o
Follicular cysts result from nonrupture of m ature follicle or failure of atresia of im m ature follicle.
o
Corpus luteal cysts result from norm al intracystic hem orrhage 2–4 days after ovulation.
Adnexal torsion: o
Right > left
o
Highest frequency in reproductive fem ales
Alert Cysts found in postm enopausal wom en suggests carcinom a.
Diagnosis Signs and Symptoms History
Ovarian cyst: o
Lower-quadrant abdom inal pain:
Sudden, sharp, unilateral
Onset often with exercise, intercourse, traum a, or pelvic exam
o
Dizziness, syncope
o
Fever rare
Adnexal torsion: o
Lower-quadrant abdom inal pain:
Sudden, sharp, colicky
Unilateral
Radiation to back, flank, or groin
May be chronic or recurrent with torsion-detorsion
Pa ge 3 3 8
o
Nausea, vom iting
o
Occasional signs/sym ptom s:
Fever
Vaginal bleeding
Urinary tract infection sym ptom s
Physical Exam
Ovarian cyst: o
Abdom inal tenderness (m ild to severe with peritonitis)
o
Adnexal tenderness
o
Pelvic m ass
o
Hem orrhagic shock possible:
Usually from corpus luteal cyst rupture
Orthostasis, hypotension, tachycardia
Adnexal torsion: o
Abdom inal tenderness (m ild to severe)
o
Adnexal tenderness
o
Adnexal m ass
o
Leukocytosis (occasional)
Essential Workup
Pregnancy test essential to rule out ectopic pregnancy
Rapid hem oglobin determ ination
Tests Lab
Urine or serum hum an chorionic gonadotropin (HCG) determ ination
CBC
Urinalysis
If significant hem orrhage, type and cross packed red blood cells.
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Imaging
Ultrasound, to reveal: o
Adnexal cysts and m asses:
Cystic m asses 15% suggests significant hem operitoneum .
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Laparoscopy is gold standard for torsed adnexa and definitive diagnosis.
Differential Diagnosis
For pelvic pain: o
Ectopic pregnancy
o
Pelvic inflam m atory disease
o
Round ligam ent pain
o
Endom etriosis
o
Neoplasm
o
Torsion of uterus
o
Appendicitis
o
Diverticulitis
o
Inflam m atory bowel disease
o
Renal colic
For adnexal m ass: o
Benign tum ors
o
Malignant tum ors
o
Polycystic ovaries
Treatment Pre Hospital Alert Patients m ay becom e hem odynam ically unstable, so intravenous access is im portant.
Initial Stabilization Airway m anagem ent and resuscitation as indicated:
Provide supplem ental oxygen and intubation as needed for respiratory failure.
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Intravenous access and volum e replacem ent with norm al saline or lactated Ringer solution or blood transfusion when indicated
ED Treatment
Focus on stabilizing patient and providing analgesia.
Uncom plicated cyst rupture:
o
Analgesia
o
Observation
Unstable patients and patients with significant hem orrhage: o
Keep NPO.
o
Arrange im m ediate gynecologic consultation and adm ission.
o
Unstable patients and patients with torsion require im m ediate adm ission to OR.
Medication (Drugs)
Acetam inophen: 325–650 m g PO/PR (peds: 15 m g/kg PO/PR, m ax. 650 m g) q4h
Ibuprofen: 400–600 m g (peds: 5–10 m g/kg) PO q6h
Morphine sulfate: 2–4 m g (peds: 0.1 m g/kg) IV/SC q5m in
Follow-Up Disposition Admission Criteria
Significant hem orrhage ascertained by serial hem atocrits, orthostasis, culdocentesis, or evidence of shock
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Culdocentesis fluid hem atocrit >15%
All patients with torsion
Discharge Criteria Stable patients with ruptured cyst and without coagulopathy or evidence of significant hem orrhage can be discharged with close follow-up with gynecologist.
References 1. Beaunoyer M, Chapdelaine J, Bouchard S, et al. Asynchronous bilateral ovarian torsion. J Pediatr Surg. 2004;39:746–749. 2. Copeland LJ, Jarrell JF. Textbook of Gynecology. 2nd ed. Philadelphia: WB Saunders; 2000. 3. Houry D, Abbott JT. Ovarian torsion: a fifteen-year review. Ann Em erg Med. 2001;38:156–159. 4. Pena JE, Ufberg D, Cooney N, et al. Usefulness of Doppler sonography in the diagnosis of ovarian torsion. Fertil Steril. 2000;73:1047–1050. 5. Tanos Scheaher JG. Ovarian cysts: a clinical dilem m a. Gynecol Endocrinol. 1994;8:59–67. 6. White M, Stella J. Ovarian torsion: 10-year perspective. Em erg Med Australas. 2005;17(3):231–237.
Codes ICD9-CM 620.2 Other and unspecified ovarian cyst 620.5 Torsion of ovary, ovarian pedicle, or fallopian tube
ICD10 N83.2
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Paget's Disease
Paget's Disease
Daniel Davis
Basics Description
Occurs in approxim ately 3% of patients older than 40 years
Starts with resorptive or osteolytic phase, during which osteoclasts rem ove healthy bone
Hypervascularity begins in resorptive phase: o
Predisposes to hem atom a and fracture
Resorbed bone is eventually replaced by irregular, dense, disorganized trabecular bone in sclerotic or osteoplastic phase.
Malignant transform ation is rare: o
Osteosarcom a is m alignancy of concern.
o
Usually m alignant transform ation occurs in 1%.
Etiology
Unknown
May represent vascular hyperplasia with subsequent inflam m ation
Presence of nucleocapsids from m easles, canine distem per, or respiratory syncytial virus m ay im plicate viral cause.
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Fam ilial or genetic com ponent
Pediatric Considerations
Generally not seen in children
Diagnosis Signs and Symptoms
Paget disease involves resorption of norm al bone and its replacem ent with fibrous and sclerotic tissue.
It is also known as osteitis deform ans.
Usually focal, bones m ost frequently involved include:
o
Pelvis
o
Fem ur
o
Skull
o
Tibia
o
Spine
o
Flat bones
Many patients are asym ptom atic, with disease discovered by incidental radiographs or elevated alkaline phosphatase levels.
Acute (resorptive/osteolytic) phase: o
Pathologic fractures
o
Pain from acute lysis, pathologic fracture, or resultant arthritis
o
Hypercalcem ia or renal stones
o
Hypervascularity m ay result in significant bleeding if affected bone is fractured.
o
Widespread disease:
Increased vascularity and blood flow m ay result in high-output cardiac failure.
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Secondary (sclerotic/osteoplastic) phase: o
Long-bone involvem ent m ay present with swelling or deform ity and gait abnorm ality.
o
Skull involvem ent m ay lead to headaches or abnorm al skull contours (change in hat size).
o
Severe skull or spine involvem ent m ay result in CNS com pression.
o
Hearing loss m ay result from nerve com pression or ossicle involvem ent.
o
Sarcom a occurs in Table o f C o ntents > Pancreatic Pseudo cyst
Pancreatic
Pseudocyst Trevor Lewis
Basics Description
Cystic collection of fluid with high content of pancreatic enzym es lacking true epithelial lining
Localized in parenchym a of pancreas or adjacent abdom inal spaces (lesser peritoneal sac)
Requires 4 or m ore weeks to form from onset of acute pancreatitis
Etiology
Ethanol abuse accounts for 70–80% cases.
Other causes include traum a, biliary tract disease, hypertriglyceridem ia, and recent surgery.
Average age at diagnosis is 45 years.
Occurs m ore frequently in m en than in wom en
Com plication in 2% of acute pancreatitis; up to 10% of chronic pancreatitis
Pediatric Considerations
Greater than 60% result from blunt traum a.
Pa ge 3 4 0
Usually can palpate a m ass
Signs and Symptoms Frequency:
Abdom inal pain: 86%
Nausea/vom iting: 72%
Palpable m ass: 49%
Weight loss: 35%
Pleural effusion: 15%
Jaundice: 13%
Ascites: 11%
Internal hem orrhage: 7%
Gastrointestinal
In chronic pancreatitis, pseudocyst heralded by change in typical pain pattern
Sym ptom s reflecting structural com pression by pseudocyst: o
Nausea, vom iting, weight loss—duodenal or gastric outlet obstruction
o
Jaundice—com m on bile duct com pression
Respiratory Left lung pleural effusion com m on
Cardiac
Com m only occurs with pseudocyst rupture or hem orrhage
Tachycardia
Hypotension
Shock (depending on fluid losses)
Infected Pseudocyst
Fever
Chills
Leukocytosis
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Pseudocyst Hemorrhage
Hypotension
Expanding abdom inal m ass
Usually erodes into splenic or gastroduodenal arteries
Ruptured Pseudocyst Abdom inal rigidity, severe pain:
Occurs when cyst ruptures into peritoneal cavity
Essential Workup
Laboratory tests not helpful in diagnosis
Useful to anticipate com plications
Tests Lab
Am ylase: o
Norm al value in up to 50% of pseudocysts
CBC: o
Leukocytosis suggests infected pseudocyst
o
Low hem atocrit with pseudocyst hem orrhage
Electrolytes, BUN, creatinine, glucose: o
Hypocalcem ia
o
Hypokalem ia with extensive fluid losses
o
Hypom agnesem ia with underlying ethanol abuse
o
Hyperglycem ia
Imaging
CT scan: o
Im aging test of choice
o
Indicated for all cases of newly suspected pseudocyst
Ultrasound: o
Useful for follow-up of previously diagnosed pseudocyst to assess pseudocyst dim ensions
Angiography:
Pa ge 3 4 0
o
Helpful in cases of pseudocyst hem orrhage
o
Usually im practical owing to instability of patient
Differential Diagnosis
Pancreatic abscess
Neoplastic pancreatic cysts
Perforated ulcer
Ruptured abdom inal aortic aneurysm (pseudocyst hem orrhage)
Myocardial infarction
Biliary colic
Intestinal obstruction
Treatment Pre Hospital
Initiate IV access in cooperative patients.
Apply cardiac m onitor.
Initial Stabilization
Airway, breathing, and circulation m anagem ent (ABCs)
Supplem ental oxygen
Cardiac m onitor
IV fluids
P.789
ED Treatment
Fluid resuscitation: o
Fluid losses m ay necessitate large fluid volum es.
o
Continuously assess vitals, urine output, and
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electrolytes to ensure rapid and adequate replacem ent of intravascular volum e.
Correct electrolytes abnorm alities (hypocalcem ia, hypokalem ia, hypom agnesem ia)
Blood products: o
Transfuse im m ediately in cases of pseudocyst hem orrhage pending definitive surgical treatm ent.
Analgesia (opiate analgesia drug of choice)
Nasogastric suction if intractable nausea/vom iting
Antiem etics (prom ethazine)
Geriatric Considerations Consider central venous pressure (CVP) m onitoring in elderly.
Medication (Drugs)
Calcium gluconate 10%: 10 m L IV over 15–20 m inutes
Magnesium sulfate: 16 m Eq (2 g) in 50 m L D 5 W over 20 m inutes
Meperidine (Dem erol): 25–50 m g IV; 50–75 m g IM q3h–q4h
Morphine: 2–4 m g IV
Potassium chloride: 10 m Eq/h IV
Prom ethazine: 12.5–25 m g PO/IM/IV or by rectum (PR)
Follow-Up Disposition Admission Criteria
All newly diagnosed pseudocysts >6 cm
Pseudocysts 6 weeks): o
Observation (no acute intervention):
o
Surgical excision:
o
Used infrequently
External drainage:
o
Usually reserved for asym ptom awtic patients
CT- or ultrasound-guided percutaneous drainage
Internal drainage:
Open versus endoscopic technique
References 1. Aguilar M, Jones RS, Sanfey H. Pseudocysts of the pancreas: a review of 97 cases. Am Surg. 1994;60:661–668. 2. Baillie J. Pancreatic pseudocysts. Gastrointest Endosc. 2004;59:873–879. 3. Cooperm an AM. An overview of pancreatic pseudocysts: the em peror's new clothes revisited. Surg Clin North Am .
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2001;81:391–397. 4. Maule W, Reber H. Diagnosis and m anagem ent of pancreatic pseudocysts, pancreatic ascites, and pancreatic fistulas. In: Go V, et al., eds. The Pancreas. New York: Raven Press; 1993:71–78. 5. Werner J, Warshaw AL. Pseudocysts, postinflam m atory cystic fluid collections, and other non-neoplastic cysts. In: Trede M, et al., eds. Surgery of the Pancreas. New York: Churchill Livingstone; 1997:405–410.
Miscellaneous SEE ALSO: Pancreatitis
Codes ICD9-CM 577.2
ICD10 K86.3
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Pancreatic Traum a
Pancreatic
Trauma Beth Anne Joseph
Basics Description
Direct epigastric blow com pressing pancreas against vertebral colum n
Injury to pancreas from penetrating object
Pediatric Considerations
Traum a affects proportionately larger areas leading to m ultisystem injuries.
Children have less protective m uscle and subcutaneous tissue.
Children will less often present with hypotension.
Etiology
Penetrating traum a: m ost com m on m echanism
Blunt traum a: deep location of pancreas requires significant force to cause injury: o
Steering wheel or bicycle handlebars to abdom en
o
In children, evaluate for nonaccidental traum a
Associated Conditions
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Ninety percent of pancreatic injuries associated with injuries to adjacent structures:
Liver, stom ach
Major arteries and veins
Spleen, kidney
Duodenum , colon, sm all bowel
Com m on bile duct, gallbladder
Diagnosis Alert Extent of pancreatic injury m ay not be apparent on initial evaluation.
Signs and Symptoms
Abdom inal pain: o
Diffuse or epigastric
o
Often out of proportion to physical exam and vital signs
Soft-tissue contusion in upper abdom en
Injury to lower ribs or costal cartilage
Acute abdom en, often associated with other intra-abdom inal injuries
Hypotension
Grey-Turner sign: o
Flank ecchym osis
Cullen sign: o
Perium bilical ecchym osis
History Concise; details of incident especially im portant for blunt traum a
Physical Exam
Inspection for abrasions, contusions, penetrating wounds:
Pa ge 3 4 0
o
Must logroll patient for full inspection
Auscultation for presence or absence of bowel sounds
Palpation to determ ine location and severity of pain, presence of guarding, and rebound tenderness
Rectal exam for occult blood, vaginal exam , or penile exam
Serial physical exam inations and vital signs for unidentified injuries
Essential Workup
Pace of workup dictated by patient condition and other injuries
Abdom inal CT with IV contrast essential to evaluate for pancreatic traum a
Tests Lab
Blood type, screen, or cross-m atch
Hem atocrit, WBC with differential
Am ylase: o
Not a reliable indicator of pancreatic traum a
o
Serial levels m ay increase sensitivity, but specificity still poor.
o
Elevated am ylase m ay be early indicator of potential pancreatic injury.
o
Norm al am ylase does not rule out pancreatic injury.
Lipase
Urinalysis
Pregnancy test
Alcohol and drug screening if indicated
Prothrom bin tim e/partial throm boplastin tim e, blood urea nitrogen, and creatinine
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Imaging Note that all im aging tests m ay m iss pancreatic injury:
Cervical spine, chest radiograph film s, and pelvis film s as for all blunt traum a patients
Bedside ultrasound
CT scan with IV contrast, helical CT if available: o
Shows better contrast enhancem ent of pancreatic parenchym a than standard scanning
Endoscopic retrograde cholangiopancreatography: o
Useful for patients with persistent hyperam ylasem ia
o
Unexplained abdom inal sym ptom s
Diagnostic Procedures/Surgery Diagnostic peritoneal lavage to identify intraperitoneal injuries:
Check fluid for am ylase level.
May still m iss significant pancreatic injury
Differential Diagnosis Other abdom inal traum atic injuries P.791
Treatment Pre Hospital Transport to closest traum a center.
Initial Stabilization
Airway m anagem ent, resuscitation as indicated
Nasogastric-tube suction m ay be especially helpful in setting of pancreatic traum a.
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General Measures
Follow standard traum a treatm ent for blunt abdom inal traum a.
Penetrating traum a: o
Tetanus prophylaxis and broad spectrum antibiotic therapy.
Intra-abdom inal injury requiring operative intervention: o
Broad spectrum antibiotic therapy
Must cover for colonic bacteria: o
Aerobic: Escherichia coli, Enterobacter, Klebsiella, Enterococcus
o
Anaerobic: Bacteroides fragilis, Clostridium , Peptostreptococcus
Medication (Drugs)
Adults: o
Cefotetan: 2g IV plus gentam icin 2 m g/kg IV or
o
Cefoxitin: 2 g IV plus gentam icin 2 m g/kg IV or
o
Ceftriaxone: 1–2 g IV plus Flagyl 15 m g/kg IV or
o
Clindam ycin: 600 m g IV plus gentam icin 2 m g/kg IV
Children: o
Cefotetan: 20 m g/kg IV plus gentam icin 2 m g/kg IV or
o
Cefoxitin: 40 m g/kg IV plus gentam icin 2 m g/kg IV or
o
Ceftriaxone: 50 m g/kg per dose IV plus Flagyl 15 m g/kg IV
Follow-Up
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Disposition Admission Criteria
All patients with pancreatic injuries m ust be adm itted.
Abdom inal pain after blunt traum a requires serial exam ination and observation for 24 hours.
Intoxicated traum a patient requires adm ission and serial exam inations for unidentified injury.
Discharge Criteria Only for very m inor traum a and with no evidence of pancreatic or any other intra-abdom inal injury
References 1. Beckingham IJ. ABC of diseases of liver, pancreas and biliary system : liver and pancreatic traum a. BMJ. 2001;322:783–785. 2. Bradley EL, Young PR, Chang MC, et al. Diagnosis and initial m anagem ent of blunt pancreatic traum a. Ann Surg. 1998;6:861–869. 3. Em m ick RH Jr, Peterson SR. Evaluation of pancreatic injury after blunt abdom inal traum a. Ann Em erg Med. 1996;27:658–661. 4. Jurkovich J. Injury to the duodenum and pancreas. In: Feliciano DV, Mattox KL, Moore EE, eds. Traum a. 3rd ed. Norwalk, CT: Appleton & Lange; 1996:473–494. 5. Novelline RA, Rhea JT, Bell T. Helical CT of abdom inal traum a. Radiol Clin North Am . 1999;37:591–612.
Codes ICD9-CM 863.84 Pancreas, m ultiple and unspecified sites
ICD10 S36.2
Pa ge 3 4 1
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Pancreatitis
Pancreatitis
Trevor Lewis
Basics Description
Inflam m ation of pancreas owing to activation, interstitial liberation, and digestion of gland by its own enzym es
Acute pancreatitis: o
Exocrine and endocrine function of gland im paired for weeks to m onths
o
Glandular function will return to norm al.
Chronic pancreatitis: o
Exocrine and endocrine function progressively deteriorate with resultant steatorhea and m alabsorption.
o
Dysfunction progressive and irreversible
Etiology
Gallstones and alcohol abuse m ost com m on causes of acute pancreatitis (75–80%)
Alcohol abuse accounts for 70–80% of chronic pancreatitis.
Acute: o
Biliary tract disease
o
Chronic alcoholism
Pa ge 3 4 1
o
Obstruction pancreatic duct
o
Ischem ia
o
Drugs
o
Infectious
o
Postoperative
o
Metabolic diseases
o
After renal transplant
o
Scorpion venom
o
Penetrating peptic ulcer
o
Hereditary
Chronic o
Chronic alcoholism
o
Obstruction pancreatic duct
o
Tropical
o
Hereditary
o
Shwachm an disease
o
Enzym e deficiency
o
Idiopathic
o
Hyperlipedem ia
Pediatric Considerations Cause m ainly viral, traum a, and drugs
Diagnosis Signs and Symptoms
Frequency: o
Abdom inal pain: 95–100%
o
Epigastric tenderness: 95–100%
o
Nausea and vom iting: 70–90%
o
Low grade fever: 70–85%
Pa ge 3 4 1
o
Hypotension: 20–40%
o
Jaundice: 30%
o
Grey Turner/Cullen Sign: 200 m g/dL
o
Serum lactate dehydrogenase (LDH) >350 IU/L
o
AST >250 IU/L
Criteria during first 48 hours: o
Hem atocrit fall >10%
o
BUN increase > 5 m g/dL
o
Serum calcium 6 L
Essential Workup Laboratory tests confirm physical diagnosis.
Tests Lab
Am ylase: o
Rise within 6 hours of pain onset
o
More than five tim es upper lim it is highly specific for
Pa ge 3 4 1
pancreatitis. o
More than 1,000 IU suggests biliary pancreatitis.
o
May be norm al during acute inflam m ation owing to significant pancreatic destruction
o
Secreted from various sources
Lipase: o
Rise within 4–8 hours pain onset
o
More reliable indicator of pancreatitis than am ylase
Electrolyte, BUN, creatinine, glucose: o
Hypokalem ia occurs with extensive fluid losses.
o
Hyperglycem ia
CBC: o
Increased hem atocrit with fluid losses
o
Hem atocrit >47% at risk for pancreatic necrosis
o
Decreased hem atocrit with retroperitoneal hem orrhage
o
WBC count >12,000 unusual
P.793
Calcium /m agnesium : o
Hypocalcem ia indicates significant pancreatic injury.
o
Hypom agnesem ia occurs with underlying alcohol abuse.
Liver function tests: o
Useful for prognostic indicators if suspected biliary cause
Pregnancy test
Arterial blood gases (ABGs): o
Indicated if hypoxic (assess PO 2 ) or toxic appearing (assess base deficit)
ECG:
Pa ge 3 4 1
o
Assess electrolyte im balances, ischem ia.
Imaging
Abdom inal series radiograph: o
Excludes free air
o
May visualize pancreatic calcifications
o
Most com m on finding is isolated dilated bowel loop (sentinel loop) near pancreas.
Chest radiograph: o
Pleural effusion
o
Atelectasis
o
Infiltrate
Ultrasound (US): o
Useful if gallstone pancreatitis suspected
Abdom inal CT indications: o
High-risk pancreatitis (>three Ranson criteria)
o
Hem orrhagic pancreatitis
o
Suspicion pseudocyst
o
Diagnosis in doubt
Diagnostic Procedures/Surgery Endoscopic retrograde cholangiopancreatography (ERCP):
Indicated for severe pancreatitis with cholangitis or biliary obstruction
Differential Diagnosis
Mesenteric ischem ia/infraction
Myocardial infarction
Biliary colic
Intestinal obstruction
Perforated ulcer
Pneum onia
Ruptured aortic aneurysm
Ectopic pregnancy
Pa ge 3 4 1
Treatment Pre Hospital
Initiate IV access in cooperative patients.
Apply cardiac m onitor.
Initial Stabilization
Airway, breathing, and circulation m anagem ent (ABCs)
Supplem ental oxygen
Cardiac m onitor
IV fluids
ED Treatment
Airway m anagem ent: o
Pulm onary com plaints necessitate supplem ental oxygen.
o
Endotracheal intubation for adult respiratory distress syndrom e (ARDS) or severe encephalopathy
Fluid resuscitation: o
Large fluid volum es (up to 5–6 L in first 24 hours) owinge to fluid losses
o
Continuously assess vitals, urine output, and electrolytes to ensure rapid and adequate replacem ent of intravascular volum e.
Geriatric considerations: o
Consider central venous pressure (CVP) m onitoring when fluid overload is concern.
Correct electrolyte abnorm alities if present: o
Hypocalcem ia (calcium gluconate)
o
Hypokalem ia occurs with extensive fluid losses.
o
Hypom agnesem ia occurs with underlying alcohol
Pa ge 3 4 2
abuse.
Blood products: o
In hem orrhagic pancreatitis, transfuse to hem atocrit level of 30%.
o
Fresh frozen plasm a and platelets if coagulopathic and bleeding
Analgesia: o
Opiate analgesia is drug of choice.
Nasogastric suction: o
Not useful in cases of m ild pancreatitis
o
Beneficial in severe pancreatitis or intractable vom iting
Antiem etics
Antibiotics: o
Indicated it pancreatic necrosis >30% on abdom inal CT
Medication (Drugs)
Calcium gluconate 10%: 10 m L IV over 15–20 m inutes
Meperidine (Dem erol): 25–50 m g IV, 50–75 IM q3h–q4h
Morphine: 2–4 m gIV
Im ipenem : 500 m g IV q6h
Potassium chloride: 10 m Eq/h IV
Prom ethazine: 12.5–25 m g PO/IM/IV or by rectum (PR)
Follow-Up Disposition
Pa ge 3 4 2
Admission Criteria
Acute pancreatitis with significant pain, nausea, vom iting
ICU adm ission for hem orrhagic/necrotizing pancreatitis
Discharge Criteria
Mild acute pancreatitis without evidence of biliary tract disease and able to tolerate oral fluids
Chronic pancreatitis with m inim al abdom inal pain and able to tolerate oral fluids
Issues for Referral Surgical consultation for ERCP in severe pancreatitis with cholangitis or biliary obstruction
References 1. Banks PA. Practice guidelines in acute pancreatitis. Am J Gastroenterol. 1997;92(3):377–386. 2. Go V, et al, eds. The Pancreas. New York: Raven Press; 1993:575–535. 3. Heinisch A, Scholm erich J, Leser H. Diagnostic approach to acute pancreatitis: diagnosis, assessm ent of etiology and prognosis. Hepatogastroenterology. 1993;40(6):531–537. 4. Mayerle J, et al. Medical treatm ent of acute pancreatitis. Gastroenterol Clin N Am . 2004;855–869. 5. Tenner S. Initial m anagem ent of acute pancreatitis: critical issues during the first 72 hours. Am J Gastoenterol. 2004;99:2489–2494.
Miscellaneous SEE ALSO: Pancreatic Pseudocyst
Codes ICD9-CM
Pa ge 3 4 2
577.0 577.1
ICD10 K85
Pa ge 3 4 2
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Panic Attack
Panic Attack
B. J. Beck
Basics Description
Characteristic, acute episodes of physical sym ptom s and intense fear that rapidly peak within 10 m inutes and resolve in about 20 m inutes
There m ay be a nonfearful variant in m edical patients.
Panic Disorder
Recurrent, unexpected panic attacks with one or m ore m onths of persistent: o
Concerns about having another attack
o
Worry about the im plications or consequences of the attacks
o
Behavioral change, such as phobic avoidance, related to the attacks
Episodic, recurrent, or chronic attacks
Frequently com orbid with depression, substance abuse, disability, suicidal tendency
Genetics Probably genetic:
Fam ily history of panic or anxiety is com m on.
Pa ge 3 4 2
Etiology Mechanism Lim bic system , norepinephrine release, other neurotransm itters (e.g., serotonin) im plicated
Risk Factors
Major life events in year preceding onset
Fam ily history of panic or anxiety
Childhood shyness or separation anxiety
May develop in the course of predisposing physical illness or cocaine abuse: o
May persist after the illness or substance use has resolved
Diagnosis Signs and Symptoms
Multiple system s suggest autonom ic arousal
Cardiac:
o
Palpitations
o
Tachycardia
o
Chest pain
Respiratory: o
Shortness of breath
o
Sm othering
o
Choking
Neurologic: o
Trem or
o
Dizziness
o
Light-headedness
o
Feeling faint
Pa ge 3 4 2
o
Num bness
o
Tingling
o
Sweating
o
Chills
o
Flushing
o
Feelings of unreality or detachm ent
Gastrointestinal: o
Nausea
o
Cram ps
o
Abdom inal pain
Intense fears: o
Autom atic, stereotypic
o
Im m inent death
o
Having a heart attack
o
Hum iliation
o
Loss of control—“going crazy―
History
Known m edical conditions
All m edications, including over the counter
Herbal supplem ents
Recreational drugs/alcohol use
Caffeine consum ption
Age at onset
Fam ily history of panic, anxiety
Initiating life events
Childhood antecedents
Resultant avoidance
Response to previous m edication trials
Physical Exam
Thorough physical and neurological exam
Guided by particular sym ptom s
Pa ge 3 4 2
Tests Lab
Toxicology screen
CBC
Electrolytes, blood urea nitrogen/creatinine, glucose
Thyrotropin
Imaging ECG for suspected m itral valve prolapse (MVP)
Diagnostic Procedures/Surgery
ECG o
Age >40 years
o
Cardiac sym ptom s
Sleep-deprived EEG if seizure suspected
Differential Diagnosis
Consider organic causes if: o
Panic presents late in life (>50 years old)
o
No childhood antecedents or fam ily history
o
No initiating or m ajor life events
o
Without avoidance or significant fear
o
With a history of poor response to previous trials of antipanic or antidepressant m edication
Medications: o
Neuroleptics (akathisia)
o
Bronchodilators
o
Digitalis
o
Anticholinergic agents
o
Psychostim ulants
o
Diet pills
Respiratory: o
Chronic obstructive pulm onary disease
Pa ge 3 4 2
o
Pulm onary em bolus
Cardiovascular: o
Angina
o
Arrhythm ia
o
Anem ia
o
MVP m ay be com orbid with panic.
Substances: o
Stim ulant abuse
o
Withdrawal (alcohol, sedative-hypnotics)
o
Excessive caffeine intake
Endocrine: o
Hyperthyroidism
o
Hypoglycem ia
o
Parathyroid disorders
o
Pheochrom ocytom a
Neurologic: o
Com plex partial, or lim bic seizures (fear, physical sym ptom s, perceptual distortions)
o
Transient ischem ic attack
Psychiatric: o
Other anxiety, stress, or phobic disorders; for exam ple, obsessive-com pulsive disorder, posttraum atic stress disorder, or social phobia
P.795
Treatment Initial Stabilization
Be calm and reassuring.
Pa ge 3 4 2
Most panic attacks resolve within 20–30 m inutes without any treatm ent.
Fear m ay trigger another panic attack.
ED Treatment
High-potency benzodiazepines:
Drugs of choice o
Clonazepam :
Slow for em ergency use
Long-acting without rapid onset/offset phenom ena
Best choice in this class for m aintenance therapy of recurrent panic attacks
o
Alprazolam :
Rapid onset
Rebound anxiety occurs due to short duration and rapid offset.
o
May lead to escalating doses with continued use
Lorazepam :
Quick onset
Advantage of sublingual use
Longer effect and less abrupt offset than alprazolam
Avoid low-potency benzodiazepines: o
Diazepam
o
Chlordiazepoxide
Treat recurrent panic attacks and panic disorder with SSRI (or TCA) antidepressants, with or without clonazepam : o
Will not work im m ediately
o
Do not need to be started em ergently, especially if there is not clear, established access to follow-up m anagem ent
Prelim inary case reports on the efficacy of olanzapine for
Pa ge 3 4 2
treatm ent resistant panic disorder
Discharge therapy: o
Several clonazepam tablets in case of repeated attacks:
Do not prescribe alprazolam —withdrawal m ay trigger further attacks.
Medication (Drugs)
Alprazolam : 0.5 m g PO
Clonazepam : 0.5 m g PO in the ED; 0.25–0.5 m g PO b.i.d. for initial outpatient therapy
Lorazepam : 1 m g PO or SL
Follow-Up Disposition Admission Criteria
As m edically indicated to rule out organic cause
Meets criteria for psychiatric adm ission (suicidal, hom icidal)
Discharge Criteria Most panic attacks do not require inpatient level of care.
Issues for Referral
Managed care m ental health carve-outs
Psychopharm acological and cognitive behavioral therapy evaluation for repeated attacks, or interepisode fear or avoidance
Stigm a
Pa ge 3 4 3
Prim ary care follow-up m ay be an acceptable alternative to specialty, m ental health/psychiatry referral.
References 1. Fleet RP, Martel J-P, Lavoie KL, et al. Non-fearful panic disorder: a variant of panic in m edical patients? Psychosom atics. 2000;41:311–320. 2. Huffm an JC, Pollack MH. Predicting panic disorder am ong patients with chest pain: an analysis of the literature. Psychosom atics. 2003;44:222–236. 3. Roy-Byrne PP, Clary CM, Miceli RJ, et al. The effect of selective serotonin reuptake inhibitor treatm ent of panic disorder on em ergency room and laboratory resource utilization. J Clin Psychiatry . 2001;62:678–682. 4. Wulsin L, Liu t, Storrow A, et al. A random ized, controlled trial of panic disorder treatm ent initiation in an em ergency departm ent chest pain center. Ann Em erg Med. 2002;39:139–143. 5. Khaldi S, Korreich C, Dan B, Pelc I. Usefulness of olanzapine in refractory panic attacks. J Clin Psychopharm . 2003;23:100–101. 6. Mago R, Berlin M. Olanzapine and panic attacks. Am J Psychiatry. 2000;157:659–660. 7. Rayburn NR, Otto MW. Cognitive-behavioral therapy for panic disorder: a review of treatm ent elem ents, strategies, and outcom es. CNS Spectr. 2003;8:356–362.
Codes ICD9-CM 300.01
ICD10 F41.0
Pa ge 3 4 3
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Paraphim o sis
Paraphimosis
Daniel Firestone
Basics Description
Paraphim osis is a urologic em ergency.
It is the entrapm ent of the retracted foreskin proxim al to the glans of the penis.
Leads to lym phatic congestion, venous obstruction, which m ay result in arterial com prom ise to the glans
Etiology
A num ber of conditions of the foreskin m ay predispose to paraphim osis, including:
o
Phim osis
o
Inflam m ation
o
Traum a
Com m only iatrogenic, from failure to replace the foreskin after exam ination, catheterization, or cleaning
Diagnosis Signs and Symptoms
Pa ge 3 4 3
Retracted foreskin
Pain
Swollen, edem atous glans
Local cellulites
Necrosis of glans in untreated cases
Essential Workup
Paraphim osis is a clinical diagnosis with the clinical findings described earlier.
Exam ination should include a search for constricting foreign bodies, constricting bands.
Treatm ent m ust not be delayed pending diagnostic laboratory or radiographic studies.
Tests Imaging If history suggests penile foreign body, radiographs m ay be obtained once the vascular com prom ise has been relieved.
Differential Diagnosis
Foreign bodies constricting the penile shaft m ay m im ic paraphim osis; these include: o
Hair tourniquets
o
Wire, string, or other m aterial used for sexual enhancem ent or punishm ent
Balanoposthitis
Traum a (zipper injuries)
Acute idiopathic penile edem a
Treatment Pre Hospital
Pa ge 3 4 3
Patients should be transported prom ptly; do not attem pt reduction in the field.
Pre hospital personnel can be advised to apply an ice pack to the glans with adequate protection of the skin.
Initial Stabilization
Ice can be applied to the glans while preparing to reduce the prepuce: o
Use the thum b of a glove as an ice-filled condom to aid in direct application.
The incarcerated foreskin m ust be released as soon as possible to prevent ischem ia and necrosis of the glans.
The pain associated with reduction techniques m ust be m anaged with som e com bination of conscious sedation, adequate analgesia, and local anesthesia.
P.797
ED Treatment
The following sequence of procedures should be followed: o
Paraphim osis can m ost frequently be reduced using a penile block and com pressing the glans m anually while applying traction on the foreskin.
o
Penile block is perform ed by infiltrating 5 m L of 1% lidocaine without epinephrine in the angle between the inferior ram i of the sym physis pubis.
Then use another 5 m L to infiltrate a wheel along the sides of the penis.
o
This produces a block after 5 m inutes.
In children, conscious sedation will usually be required.
o
If m anual reduction is unsuccessful, then the
Pa ge 3 4 3
technique of m ultiple punctures m ay facilitate reduction:
One m akes m ultiple holes in the swollen foreskin with a sm all sterile needle (26 g), allowing expression of edem a fluid.
o
If this fails to return the foreskin to its original position, it will be necessary to incise the constricting ring of tissue with a dorsal longitudinal slit in the foreskin after sterile preparation.
If the incision has been on the long side, after reduction it m ay be necessary to suture the incision transversely with 3.0 absorbable sutures.
If a delay is likely before the paraphim osis can be treated (e.g., NPO status), then applying a gauze swab soaked in 50% dextrose will reduce edem a by osm osis and facilitate reduction.
Medication (Drugs)
Appropriate analgesics or anesthetics as required
It appears that prophylactic antibiotics following the m ultiple puncture technique are not routinely indicated: o
Their role in paraphim osis reduction by incision is not well studied.
Follow-Up Disposition Admission Criteria
Pa ge 3 4 3
Necrosis or cellulitis of the penis
Discharge Criteria
Successful reduction with relief of sym ptom s
Close urologic follow-up
Issues for Referral
Urologic consultation is required.
Subsequent circum cision to prevent recurrence is an area of clinical debate; historically, it has been com m on practice.
References 1. Little B, White M. Treatm ent options for paraphim osis. Int J Clin Pract. 2005 May; 59(5):591–593. 2. Barone JG, Fleisher MH. Treatm ent of paraphim osis using the “puncture― technique. Pediatr Em erg Care. 1993;9(5):298–299. 3. O'Donnell JA II. Phim osis and paraphim osis. In: Barkin RM, et al, eds. Pediatric em ergency m edicine. 2nd ed. St. Louis, MO: Mosby, 1997:1152–1153. 4. Pontari MA. Phim osis and paraphim osis. In: Seidm an, Hanno PM, eds. Current urologic therapy. 3rd ed. Philadelphia, PA: WB Saunders, 1994:392–397. 5. Raveenthwan V. Reduction of paraphim osis: a technique based on pathophysiology. Br J Surg. 1996;83(9):1247.
Miscellaneous SEE ALSO: Phim osis
Codes ICD9-CM
Pa ge 3 4 3
605
Pa ge 3 4 3
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Parkinso n's Disease
Parkinson's
Disease James M. Leaming
Basics Description
Gradually progressive disorder of m iddle or late life
Aggregates of m elanin-containing nerve cells in the brainstem : o
Substantia nigra locus ceruleus
Reactive gliosis with nerve cell loss
Lewy bodies: o
Eosinophilic intracytoplasm ic inclusions
Decreased dopam ine in the caudate nucleus and putam en
Accelerated cortical atrophy
Can begin unilaterally, but generalizes to sym m etric
Etiology
Sporadic or idiopathic, degenerative
Type A Encephalitis of von Econom o
CNS viral infections
Vascular infarction
Intoxications: o
Phenothiazine
Pa ge 3 4 3
o
Butyrophenones
o
Metoclopram ide
o
Illicit drugs
o
Carbon m onoxide:
o
Bilateral infarctions of the globus pallidus
Manganese
Diagnosis Signs and Symptoms
“Pill-rolling― resting trem or
“Cog-wheel― rigidity due to increased m uscular tone
Stooped posture and instability of posture
Stiffness and slowness of m ovem ent
“Masked face― appearance
Depression and dem entia
Sudden change in baseline m otor function or m ental status: o
May be the only indication of system ic disease such as infection
Essential Workup
History is of prim ary im portance: o
Diagnosis is m ade based on clinical findings.
Im portant historical inform ation includes: o
Onset of sym ptom , whether gradual or sudden
o
History of encephalitis, herpes virus infection, or carbon m onoxide exposure
o
Patients with established Parkinson disease:
Sudden change in baseline m otor function
Change in m ental status
Pa ge 3 4 3
Should prom pt workup for infectious process such as urinary tract infection
Tests Lab
No specific or recom m ended laboratory studies necessary to confirm the diagnosis
Nonidiopathic Parkinson disease m ay require directed laboratory studies.
Urinalysis, CBC, chest radiograph, and other appropriate workup for occult infection in patients with established disease
Imaging
CT scan/MRI are not required to diagnose Parkinson disease but are often elem ents of evaluation for dem entia.
Chest radiograph m ay be indicated for any signs of respiratory tract infection.
Differential Diagnosis
Benign fam ilial trem or
Major depression
Wilson disease
Huntington disease
Alzheim er disease
Creutzfeldt-Jacob disease
Carbon m onoxide poisoning
B 1 2 deficiency
Hydrocephalus
Multi-infarct dem entia
Essential trem or disorders
P.799
Pa ge 3 4 4
Treatment ED Treatment
Treatm ent with anti-Parkinsonian m edications can be initiated in the ED to alleviate sym ptom s.
Consultation with neurology for recom m ended m edication regim ens and ongoing support and m onitoring is prudent.
For patients with m ild disease, no m edication m ay be required.
For m oderate disease anticholinergic m edications and dopam inergic m edications should be used.
Treat underlying infection, if present.
Medication (Drugs)
Am antadine: 100 m g b.i.d.
Benztropine: 0.5–1 m g t.i.d.
Brom ocriptine: 15 m g every day
Levodopa/Dopa carboxylase inhibitor (carbidopa) com bination: 25/100 m g every day
Trihexyphenidyl: 1–2 m g q.i.d.
Follow-Up Disposition Admission Criteria
Pa ge 3 4 4
Patient with intercurrent infections, dehydration, or other m edical problem s
Depression with intent to do self-harm
Medication regim en adjustm ent
Discharge Criteria
Mild to m oderate disease without m edications
Moderate to severe disease with m edications and urgent neurologic outpatient follow-up
References 1. Flint MB, Beal M, Richardson EP, et al. Parkinson's disease. In: Isselbacher KJ, et al, eds. Harrison's principles of internal m edicine. New York: McGraw-Hill, 1994. 2. Freidm an JH and Factor SA: Atypical antipsychotics in the treatm ent of drug-induced psychosis in Parkinson's disease. Mov Disord. 2000;15:201. 3. Lieberm an, A. Managing the neuropsychiatric sym ptom s of Parkinson's disease. Neurology. 1998;50[6 Suppl 6]:533–538. 4. Obeso JA, et al. Levodopa m otor com plications in Parkinson's disease. Trends Neurosci. 2000;23(Suppl):S2. 5. Rajput A, et al. Epidem iology of parkinsonism : Incidence, classification, and m ortality. Ann Neurol. 1984;16:178. 6. Richard IH and Nutt J. Worsening of m otor function in Parkinson's disease: A ‘typical’ response to ‘atypical’ antipsychotic m edications. Neurology. 2000;55:748. 7. Shulm an LM, et al. The use of dopam ine agonists in very elderly patients with Parkinson's disease. Mov Disord. 2000;15:664.
Codes ICD9-CM 332.0
ICD10
Pa ge 3 4 4
G20
Pa ge 3 4 4
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Paro nychia
Paronychia
Gene Ma
Basics Description
Disruption of the seal between the nail plate and the nail fold m ay allow entry of bacteria into the eponychial space.
Inflam m ation of the nail folds surrounding the nail plate
Etiology
Acute paronychia: predom inantly Staphylococcus aureus but also streptococci, Pseudom onas, and anaerobes
Chronic paronychia: predom inantly Candida albicans, but m ay also be other fungi, atypical m ycobacteria; com m only coexisting with Staphylococcus species
Diagnosis Signs and Symptoms History
Acute paronychia: nail biting, finger sucking, aggressive m anicuring or m anipulation, and traum a predispose to developm ent.
Pa ge 3 4 4
Chronic paronychia: occupations with persistent m oist hands; dish washers, bartenders; also increased in patients with peripheral vascular disease
Pediatric Considerations Frequently anaerobic m outh flora in children from nail biting
Physical Exam
Begins as swelling, pain, and erythem a in the dorsolateral corner of the nail fold bulging out over the nail plate
Progresses to subcuticular abscess
Essential Workup
History and physical exam with special attention to evaluating for concom itant infections such as felon or cellulitis
Assess tetanus status.
Tests Lab
No specific tests are useful.
Cultures not routinely indicated
Imaging Soft tissue radiographs if foreign body is suspected; routine film s if osteom yelitis suspected
Differential Diagnosis
Felon
Herpetic whitlow
Traum a or foreign body
Prim ary squam ous cell carcinom a
Metastatic carcinom a
Osteom yelitis
Pa ge 3 4 4
Treatment ED Treatment Acute Paronychia
Early paronychia without purulence present m ay be m anaged with warm -water soaks four tim es a day with or without oral antibiotics.
Early superficial subcuticular abscess: o
Elevation of the eponychial fold by sliding the flat edge of a no. 11 blade (18-gauge needle or sm all clam ps m ay be used) gently between the proxim al nail fold and the nail plate near the point of m axim al tenderness
o
A digital nerve block or local anesthesia m ay be necessary.
Partial nail involvem ent: o
If the lesion extends beneath the nail, rem ove a longitudinal section of the nail.
o
Vaseline or iodoform gauze packing for 24 hours
Runaround abscess: o
If the lesion extends beneath the base of the nail to the other side, rem ove one quarter to one third of the proxim al nail with two sm all incisions at the dorsolateral edges of the nail fold and pack eponychial fold with petroleum or iodoform gauze to prevent adherence.
P.801
Extensive subungual abscess:
Pa ge 3 4 4
o
Rem ove entire nail.
Early paronychia without purulence present m ay be m anaged with warm soaks alone, but beyond that, antibiotics are recom m ended if there is any apparent cellulitis, abscess, or system ic signs of infection.
Cephalexin, dicloxacillin, and am oxicillin-clavulanate are appropriate first-line agents, with treatm ent regim ens ranging from 5–10 days, depending on severity.
Clindam ycin, erythrom ycin, or am oxicillin-clavulanate if associated with nail biting or oral contact or allergy
Chronic Paronychia
Avoidance of predisposing exposures
Eponychial m arsupialization involving rem oval of a crescentic piece of skin just proxim al to the nail fold including all thickened tissue down to, but not including, germ inal m atrix: o
Topical steroids with a topical antifungal agent have been used with success.
o
Antistaphylococcal treatm ent should also be adm inistered.
o
Oral antifungal therapy is rarely necessary.
Medication (Drugs)
Am oxicillin-clavulanate: 875 m g PO b.i.d. for 7 days (peds: 25 m g/kg/d PO q12h)
Cephalexin: 500 g PO q.i.d. for 7 days (peds: 40 m g/kg/d PO q6h)
Clindam ycin: 300 m g PO q.i.d. for 7 days (peds: 20–40 m g/kg/d div. q6h PO, IV, IM)
Dicloxacillin: 500 m g PO q.i.d. for 7 days (peds: 12.5–50
Pa ge 3 4 4
m g/kg/d PO q6h)
Erythrom ycin: 500 m g PO q.i.d. for 7 days (peds: 40 m g/kg/d PO q6h)
Follow-Up Disposition Admission Criteria Adm ission is not needed for paronychia alone.
Discharge Criteria
Patients with uncom plicated paronychias m ay be discharged with appropriate follow-up instructions.
Patients with packings should be re-evaluated in 24 hours.
Issues for Referral Chronic paronychias refractory to treatm ent
References 1. Canales FL, Newm eyer WL, Kilgore ES. The treatm ent of felons and paronychias. Hand Clin. 1989;5(4):515–523. 2. Hochm an LG. Paronychia: m ore than just an abscess. Int J Derm atol. 1995;34(6):385–386. 3. Jebson PJ. Infections of the fingertip. Paronychias and felons. Hand Clin. 1998;14:547–55, viii. 4. Moran GJ, Talan DA. Hand infections. Em erg Med Clin. 1993;11(3):601–619. 5. Rockwell PG. Acute and chronic paronychia. Am Fam Physician. 2001;63(6):1113–1116.
Codes ICD10
Pa ge 3 4 4
L03.0
Pa ge 3 4 4
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Patellar Injuries
Patellar Injuries
Francis L. Counselman
Basics Description Dislocation
Usually caused by sudden flexion and external rotation of tibia on fem ur, with sim ultaneous contraction of quadriceps m uscles
Lateral dislocation of patella m ost com m on, with patella displaced over the lateral fem oral condyle
Uncom m on dislocations include superior, m edial, and rare intraarticular dislocation.
Direct traum a to patella
Fracture
Direct traum a: o
Most com m on m echanism of injury
o
Secondary to direct blow or fall on patella
o
Usually results in com m inuted or m inim ally displaced fracture
Indirect forces: o
Avulsion injury secondary to contraction of the quadriceps tendon
Pa ge 3 4 5
o
Usually results in transverse or displaced fracture (often both)
Types of patellar fractures: o
Transverse: 50–80% (usually m iddle or lower third of patella)
o
Com m inuted (or stellate): 30–35%
o
Longitudinal: 25%
o
Osteochondral
Patellar Tendon Rupture
Usually caused by forceful eccentric contraction on a flexed knee (e.g., jum p landing and weight lifting)
Often occurs in m iddle-aged athlete
Patellar Tendinitis Overuse syndrom e from repeated acceleration, deceleration, jum ping, landing
Etiology Dislocation
Risk factors for patellar dislocation: o
Genu valgum (knock-knee)
o
Genu recurvatum (hyperextension of knee)
o
Shallow lateral fem oral condyle
o
Deficient vastus m edialis
o
Lateral insertion of patellar tendon
o
Shallow patellar groove
o
Patella alta (high-riding patella)
o
Deform ed patella
o
Pes planus (flatfoot)
Com m on injury in adolescents, especially girls
The younger the patient at tim e of initial dislocation, the greater the risk of recurrent dislocation.
Pa ge 3 4 5
Fracture
Direct traum a
Indirect forces caused by forcible quadriceps tendon contraction
Male-to-fem ale ratio of 2:1
Highest incidence in 20- to 50-year-old age group
Patellar Tendon Rupture
Peak incidence in third and fourth decades: o
Often athletically active individual
Risk factors: o
History of patellar tendinitis
o
History of diabetes m ellitus, previous steroid injections, rheum atoid arthritis, gout, system ic lupus erythem atosus
o
Previous m ajor knee surgery
Patellar Tendinitis
Microtears of tendon m atrix from overuse
Seen in high jum pers, volleyball and basketball players, and runners
Diagnosis Signs and Symptoms Dislocation
History of feeling knee “go out―; popping, ripping, or tearing sensation
Pain
Inability to bear weight
Obvious lateral deform ity of patella
Pa ge 3 4 5
Mild to m oderate swelling
Often reduced spontaneously before ED evaluation
Tenderness along patella
Positive apprehension or Fairbanks sign: o
Attem pts to push the patella laterally elicit patient apprehension.
Fracture
Pain over anterior knee
Difficulty am bulating
Increased pain with m ovem ent of patella
Tenderness and swelling over patella
Difficulty or inability to extend knee
Palpable defect, crepitus, or joint effusion/hem arthrosis
Patellar Tendon Rupture
Abrupt onset of severe pain
Decreased ability to bear weight
Occasionally hem arthrosis
Proxim ally displaced patella
Incom plete extensor function
Unable to m aintain knee extension against force
Patellar Tendinitis
“Jum per's knee―
Pain in area of patellar tendon
Pain worse from sitting to standing or going up stairs
Point tenderness at distal aspect of patella or proxim al patellar tendon
Essential Workup
Radiographs essential: o
Anteroposterior (AP) and lateral views of knee should be obtained.
Pa ge 3 4 5
o
Postreduction radiographs should include AP, lateral, and sunrise (or skyline, axial) views to exclude osteochondral fracture (in patellar dislocations).
o
Bipartite patella (patella with accessory bony fragm ent connected to m ain body by cartilage) m ay be m istaken for fracture; com parison view m ay help differentiate.
For patellar tendon rupture, a high-riding patella (i.e., patella located superior to level of intercondylar notch) observed
For patellar tendinitis, radiographic findings unlikely with sym ptom s of 4 m m , if patient unable to raise extended leg off bed, or if articular step-off >3 m m .
All open fractures require débridem ent and irrigation and should be adm itted.
For patellar tendon rupture, discuss case with orthopedics.
Discharge Criteria
Patients with successful reduction of lateral patellar dislocation and norm al postreduction radiographs m ay be discharged with knee im m obilization, crutches, and orthopedic follow-up.
Fracture is displaced 5% has a sensitivity of 5% for identifying intra-abdom inal injuries.
An initial hem atocrit of Table o f C o ntents > Pediculo sis
Pediculosis
Danielle J. Douglas
Basics Etiology
Infestation by Pediculus capitis (head louse), Pediculus corporis (body louse), or Pthirus pubis (pubic louse)
Bites are painless.
Signs and sym ptom s result from host response to saliva and anticoagulant injected during feeding.
Transm itted by direct contact and fom ites; pubic lice are transm itted by sexual contact, use of contam inated objects like com bs, clothing, bed linen, hats.
Obligate hum an parasites cannot survive away from hosts m ore than 7–10 days.
Diagnosis Signs and Symptoms
Head lice: o
Scalp and posterior neck erythem a, scaling, and excoriated papules
o
Nits (egg casings) attached to hair shafts
Pa ge 3 4 7
o
Excoriations m ay lead to pyoderm a, posterior cervical lym phadenopathy, and febrile episodes.
o
Most often found in postauricular and occipital areas
o
Not an indicator of poor hygiene
Body lice: o
Linear excoriations of neck and trunk
o
Pus or serum stains on clothing
o
Nits found in seam s of clothing
o
Often an indicator of poor hygiene
Pubic lice: o
Intense pruritus, particularly at night
o
Occasional urticaria with typical flare/wheal form ation
o
May infest eyelashes and scalp in children
o
Characteristic bluish m acules (m aculae caeruleae) appear infrequently on trunk and thighs.
o
Prefer the perineum and pubic areas
o
Inguinal adenopathy
Physical Exam
Exam ine hair for adult lice and nits.
Nits are cem ented on hair shafts and are not easily rem oved.
Head lice and pubic lice infestation is confirm ed by differentiating nits from scales, hair casts, and other easily brushed-off artifacts.
Em pty nits are not diagnostic of active infection.
Body lice are observed only in very heavy infestation; infestation is confirm ed by finding nits in clothing seam s.
Tests Lab
Nits m ay be visualized under low-power m icroscopy along
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hair shafts. They are 131°F (55°C) for >5 m inutes kills eggs, nym phs, and m ature lice.
Pubic lice: o
Topical pediculicide applied to hairy areas of chest, axilla, and groin
o
Rem ove nits with fine-toothed com b. P.809
o
Treat sexual contacts sim ultaneously.
o
Wash and dry bedding and clothing using hot cycles.
o
Treat eyelash involvem ent with topical petrolatum twice daily for 9 days.
Body lice: o
Wash and dry bedding and clothing using hot cycles.
o
Apply topical pediculicide cream or lotions from chin to toes.
o
Oral antihistam ines and topical steroids m ay help pruritic sym ptom s of all lice infestations.
Medication (Drugs)
Antipruritics: o
Cetirizine (Zyrtec): age older than 12 years, 5–10 m g PO (peds: ages 6–11 years, 5–10 m g PO;
Pa ge 3 4 7
ages 2–5 years, 2.5 m g PO) daily o
Diphenhydram ine (Benadryl): 25–50 m g PO (peds: 5 m g/kg/d) q6h
o
Hydroxyzine (Atarax): 25 m g PO q8h (peds: 12.5 m g per dose q6h)
Pediculicides: o
Lindane (γ-benzene hexachloride) 1% sham poo: lather for 4 m inutes, then rinse; third-line agent after Perm ethrin or Rid given side effects.
Lotion: apply chin to toes, wash off after 8 hours; avoid use in children, lactation, pregnancy, or seizure disorder.
o
Perm ethrin 1% cream rinse (Nix): apply to scalp and hair, rinse after 10 m inutes; reapply in 7–10 days if needed.
o
Pyrethrin/piperonyl butoxide (Rid): apply to scalp and hair, wash after 10 m inutes; repeat in 7–10 days; avoid in patients with ragweed allergies.
o
Mercuric oxide ophthalm ic ointm ent 1%: use for louse infestation of eyelids: apply q.i.d. for 14 days.
o
Trim ethoprim -sulfam ethoxazole: 8 m g/kg/d of TMP in divided doses is effective for head lice in patients who have previously failed treatm ent.
Follow-Up Disposition Admission Criteria Extensive bacterial superinfection; system ic hypersensitivity reaction with cardiorespiratory com prom ise
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Discharge Criteria
Mild to m oderate infestation with absence of significant superinfection or hypersensitivity reaction
Children m ay return to school after initial treatm ent if repeat therapy is adm inistered in 7–10 days.
Pubic lice are often associated with sexually transm itted diseases; prudent screening is recom m ended. Pubic lice m ay also indicate sexual abuse in children.
References 1. Angel TA, Nigro J, Levy ML. Infestations in the pediatric patient. Pediatr Clin North Am . 2000;47(4):921–935, viii. 2. Chosidow O. Scabies and pediculosis. Lancet. 2000;355:819–826. 3. Elston DM. Controversies concerning the treatm ent of lice and scabies. J Am Acad Derm atol. 2002;46(5):794–796. 4. Potts J. Eradication of ectoparasites in children. How to treat infestations of lice, scabies, and chiggers. Postgrad Med. 2001;110(1):57–59, 63–64. 5. Roberts RJ. Head lice. N Engl J Med. 2002;346:1645.
Codes ICD9-CM 132.9
ICD10 B85.2
Pa ge 3 4 8
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Pelvic F racture
Pelvic Fracture
Theodore C. Chan
Basics Description
3% of all bony fractures
Pelvis is m ade up of sacrum and two innom inate bones: o
The innom inate bones consist of the ilium , ischium , and pubis.
Boney structures are stabilized by network of ligam ents, m usculature, and other soft tissues in the pelvic area.
Anterior stability and support are provided by the sym physis pubis and pubic ram i.
Posterior stability and support are provided by the sacroiliac com plex and pelvic floor.
Pelvis provides protection for lower urinary tract; gastrointestinal tract; gynecologic, vascular, and nervous structures contained in the region: o
Pelvic fractures have a high associated m ortality rate and require urgent diagnosis and therapy.
Etiology
Sixty-five percent of pelvic fractures caused by vehicular traum a, including pedestrians struck by autom obiles
Ten percent caused by falls
Pa ge 3 4 8
Ten percent caused by crush injuries
The rem ainder caused by athletic, penetrating, or nontraum atic injuries
Mortality rate from pelvic fractures is 6–19%: o
Increases to 30% with open fractures
o
Increases to 50% with hem orrhagic shock
Significant pelvic hem orrhage can occur in unstable, high-energy pelvic fractures (Tile type B and C fractures): o
Bleeding m ost com m only from posterior injuries involving the venous plexuses
o
Retroperitoneal hem atom a that m ay tam ponade in the enclosed pelvic space
Tile Classification System
Includes stable single bone and avulsion fractures as well as pelvic ring fractures
Predicts need for operative repair
Type A: stable pelvic ring injuries: o
A1: avulsion fractures of the innom inate bone (ischial tuberosity, iliac crest)
o
A2-1: iliac wing fractures
o
A2-2: isolated ram i fractures; m ost com m on pelvic fracture
o
A2-3: four-pillar anterior ring injuries
o
A3: transverse fractures of sacrum or coccyx
Type B: partially stable pelvic ring injury (rotationally unstable, but vertically stable): o
B1: unilateral open-book fracture
o
B2: lateral com pression injury
B2-1: ipsilateral double ram i fractures and posterior injury
B2-2: contralateral double ram i fractures and posterior injury (bucket-handle fracture)
Pa ge 3 4 8
B2-3: bilateral type B injuries
Type C: unstable pelvic ring injury—rotationally and vertically unstable, Malgaigne fracture: o
Anterior disruption of sym physis pubis or two to four pubic ram i with posterior displacem ent and instability thru sacrum , SI joint, or ileum
C1: unilateral vertical shear fracture
C2: unilateral vertical shear com bined with contralateral type B injury
C3: bilateral vertical shear fracture
Acetabular fractures (posterior lip, central/transverse, anterior colum n, or posterior colum n fractures)
Young Classification System
Based on m echanism of injury
Only fractures that result in disruption of pelvic ring included; no single bone, avulsion, or acetabular fractures
Predicts chance of associated injuries and m ortality risk: o
LC: lateral com pression
o
APC: anteroposterior com pression
o
VS: vertical shear
o
CM: com bination of injury patterns
Pediatric Considerations
Children can have proportionately greater hem orrhage.
Nonaccidental traum a is a concern.
Pregnancy Considerations Gravid uterus m ay be at risk for injury, including uterine rupture.
Diagnosis Signs and Symptoms
Pa ge 3 4 8
Localized pain, swelling, ecchym oses, tenderness over hips, groin, perineum , and lower back
Lower extrem ities m ay be shortened or rotated.
Pain on hip m ovem ent, am bulation, sitting, standing, defecation
Tenderness on lateral com pression of pelvis, palpation of sym physis pubis or sacroiliac (SI) joints
Often presents with other traum atic injuries including neurologic, intra-abdom inal, genitourinary, perineal, rectal, vaginal, and vascular injury
Gross pelvic instability, deform ity, asym m etry in lower extrem ity
Evidence of hem orrhagic shock
Inability to actively or passively perform range of m otion of involved hip
Essential Workup
Pelvic radiograph is m ost valuable initial test.
A single AP view of the pelvis can confirm diagnosis in 90% of cases and should be obtained as early as possible when fracture suspected: o
Most significant unstable pelvic fractures will be seen on the single AP view.
o
Other views include:
Inlet projection: 30-degree caudal view; allows visualization of posterior arch
Outlet projection: 30-degree cephalic angulation; allows visualization of sacrum
Judet oblique views: allow evaluation of acetabulum
Tests Lab
Pa ge 3 4 8
Type and cross-m atch.
Hem oglobin/hem atocrit, platelet count, and coagulation studies (PT/PTT)
Imaging
CT scan m ay further delineate pelvic fracture(s), retroperitoneal hem atom a, visceral injuries.
MRI indicated with evidence of neurologic injury
Diagnostic peritoneal lavage (DPL) is a rapid bedside evaluation for intraperitoneal hem orrhage: o
In the setting of pelvic fracture, the supraum bilical open approach for DPL should be used.
Abdom inal ultrasound (US) m ay be used in place of DPL, but differentiation of intraperitoneal from extraperitoneal hem orrhage from pelvic fracture can be difficult.
Differential Diagnosis
Norm al variants (i.e., os acetabuli epiphyseal line, can m im ic type I fracture on radiograph)
Ligam entous injury
Spinal injury
Intra-abdom inal injury and hem orrhage
P.811
Treatment Initial Stabilization Airway, breathing, and circulation (ABCs) of traum a care:
Avoid using lower extrem ity IV sites.
Aggressive resuscitation with blood or crystalloid,
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O-negative or type-specific blood if hem odynam ically unstable
Im m obilize the pelvis to prevent further injury and decrease bleeding.
PASG: Use in ED is controversial, but allows rapid pelvic im m obilization and pelvic com pression to slow bleeding.
External fixator requires m ore tim e to place than PASG but “splints― pelvis in a sim ilar m anner; contraindicated in severely com m inuted pelvic fracture.
Placem ent of a stabilization device should not interfere with further workup and care (e.g., US, DPL).
ED Treatment
Determ ine which pelvic fractures are stable and which are unstable.
Type A fractures are generally stable.
Type B and C fractures are unstable.
Type A fractures: o
Treated conservatively with bed rest, analgesics, and com fort m easures; m anagem ent decisions m ay be m ade in conjunction with orthopedics.
o
For four-pillar anterior ring injuries, a CT scan should be obtained to evaluate the posterior pelvis.
o
Ensure that there are no other breaks in the pelvic ring.
Type B and C fractures: o
Im m ediate orthopedics consultation; patient should rem ain NPO.
o
May require ED pelvic stabilization m easures
o
Assess for pelvic hem orrhage (see Pelvic Hem orrhage).
Acetabular fractures: o
Im m ediate orthopedics consultation; patient should
Pa ge 3 4 8
rem ain NPO.
Pelvic hem orrhage: o
Mechanical stabilization of unstable pelvic fractures (usually by application of external pelvic fixation)
o
Angiography and selective vessel em bolization
o
Direct operative control of pelvic bleeding
Prioritization of studies: CT, angiography, or surgery: o
In the hem odynam ically unstable patient:
Open B and C fractures: surgical exploration
Closed fractures: DPL or US can help determ ine m anagem ent in term s of need for surgical exploration or selective angiography.
o
In the hem odynam ically stable patient, the patient can go to CT scan for evaluation of the abdom en, pelvis, and retroperitoneum with external fixation as appropriate.
Medication (Drugs)
Blood products: 4–6 U cross-m atched, type specific, or O negative (peds: 10 m L/kg)
Crystalloid fluids: 2-L IV bolus of norm al saline (NS) or lactated Ringer (peds: 20 m L/kg)
Follow-Up Disposition Admission Criteria
Hem odynam ic instability, and pelvic hem orrhage to the ICU
Pa ge 3 4 8
Type B or C pelvic fracture
Acetabular fracture
Other related injuries (e.g., genitourinary, intra-abdom inal, neurologic)
Intractable pain
Discharge Criteria Type A pelvic fracture; hem odynam ically stable with no evidence of other injuries
References 1. Allen CF, Goslar PW, Barry M, et al. Managem ent guidelines for hypotensive pelvic fracture patients. Am Surg. 2000;66:735–738. 2. Am erican College of Surgeons, Com m ittee on Traum a. Advanced Traum a Life Support for Doctors. 7th ed. Chicago: Am erican College of Surgeons; 2004. 3. Coppola PT, Coppola M. Em ergency departm ent evaluation and treatm ent of pelvic fractures. Em erg Med Clin North Am . 2000;18(1):127. 4. Lashutka MK, Bahner D, Werm an H. Adult pelvic fractures. Traum a Rep. 2002;3:1–12.
Codes ICD9-CM 808.8
ICD10 S32.8
Pa ge 3 4 8
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Pelvic Inflam m ato ry Disease
Pelvic
Inflammatory Disease Erich Salvacion
Basics Description
Pelvic inflam m atory disease (PID) is an acute, com m unity-acquired, sexually transm itted infection of the upper genital tract, including the uterus, fallopian tubes, ovaries, or adjacent structures.
Most frequent gynecologic cause for ED visits (350,000 per year)
Represents a spectrum of infection: o
No single diagnostic gold standard
o
Requires low clinical threshold for considering the diagnosis and starting em piric antibiotic therapy
Progressive disease can lead to tubo-ovarian abscess (TOA)
Fitz-Hugh-Curtis syndrom e is a capsular inflam m ation of the liver associated with PID: o
Sharp right upper quadrant abdom inal pain
o
Worse with inspiration, m ovem ent, or coughing
Etiology
Pa ge 3 4 9
Risk factors: o
Age younger than 35 years
o
Multiple or sym ptom atic sexual partners
o
Previous episode of PID
o
Nonbarrier contraception
o
Oral contraception
o
African Am erican ethnicity
Most com m on causes of PID are Chlam ydia trachom atis and Neisseria gonorrhea.
Other organism s include groups A and B streptococci, staphylococci, gram -negative rods (com m only Klebsiella species, Escherichia coli, and Proteus species), and anaerobes.
Diagnosis Signs and Symptoms
Lower abdom inal pain, usually bilateral
Vaginal discharge
Abnorm al uterine bleeding
Dysm enorrhea
Dysuria
Dyspareunia
Nausea and vom iting
Fever and chills
Proctitis
Lower abdom inal tenderness
Decreased bowel sounds
Bilateral adnexal tenderness
Cervical m otion tenderness
Purulent endocervical discharge
Pa ge 3 4 9
Adnexal m ass or fullness
Right upper quadrant tenderness
Essential Workup
History and physical exam including pelvic exam ination
Pregnancy test to rule out ectopic pregnancy or com plications of an intrauterine pregnancy
Cervical culture for N. gonorrhea and C. trachom atis
Minim um criteria for clinical diagnosis:
o
Lower abdom inal tenderness or
o
Uterine/adnexal tenderness or
o
Cervical m otion tenderness
Supportive criteria for diagnosis: o
Fever >38.3°C (101°F)
o
Abnorm al cervical/vaginal discharge
o
Intracellular gram -negative diplococci on endocervical Gram stain
o
Leukocytosis >10,000/m m 3
o
Elevated erythrocyte sedim entation rate (ESR) or C-reactive protein
o
WBCs or bacteria in peritoneal fluid obtained by culdocentesis or laparoscopy
Tests Lab
CBC
Gram stain of endocervix
Urine polym erase chain reaction (PCR)
Microscopic exam of vaginal discharge in saline
Liver enzym es m ay be elevated in Fitz-Hugh-Curtis syndrom e.
Positive urinalysis (UA) or occult blood in stool decrease the probability of PID.
Pa ge 3 4 9
ESR or C-reactive protein m ay be elevated, but not routinely recom m ended.
Imaging
Patients with adnexal fullness or an adnexal m ass on exam should have im m ediate transvaginal ultrasound (US) to exclude a tubo-ovarian abscess.
Consider obtaining a pelvic US in patients who use an intrauterine device, fail outpatient antibiotic therapy for PID, or who have inadequate pelvic exam s due to pain or obesity.
Diagnostic Procedures/Surgery Laparoscopy m ay be useful in confirm ing PID in a patient with high suspicion of com peting diagnosis, or patients who have failed outpatient treatm ent for PID.
Differential Diagnosis
Ectopic pregnancy (m ust be excluded with a pregnancy test in any wom an suspected of having PID)
Acute appendicitis
Adnexal torsion
Endom etriosis
Cystitis
Urolithiasis
Ovarian tum or
Adenom yosis uteri
Chronic pelvic pain
Benign ovarian cyst
Diverticulitis
Inflam m atory bowel disease
Mesenteric vascular disease
Irritable bowel syndrom e
Pa ge 3 4 9
Treatment Pre Hospital
No specific pre hospital considerations
Appropriate pain m anagem ent
Initial Stabilization
Resuscitation rarely indicated
Pain control
ED Treatment
Outpatient: o
Regim en A (for patients not sexually active):
Ofloxacin or levofloxacin; with m etronidazole when anaerobes are a particular concern
o
Regim en B (for sexually active patients):
Ceftriaxone or cefoxitin/probenecid plus doxycycline; with m etronidazole when anaerobes are a particular concern
Ceftriaxone or cefixim e plus azithrom ycin; single dose indicated for cervicitis only
o
Must evaluate and treat sex partner as appropriate
Inpatient: o
Doxycycline plus cefoxitin or cefotetan
o
Alternatives include gentam icin plus clindam ycin; or m etronidazole plus levofloxacin or ofloxacin; or am picillin/sulbactam plus doxycycline.
o
Continue parenteral antibiotic adm inistration for 24 hours after clinical im provem ent, followed by oral doxycycline or clindam ycin for a total of 14 days.
o
TOAs m ay require drainage or surgical intervention in addition to antibiotics.
Pa ge 3 4 9
o
Laparoscopy can be used to lyse adhesions in the acute and chronic stages of Fitz-Hugh-Curtis syndrom e.
Add m etronidazole when anaerobes are a particular concern.
P.813
Medication (Drugs)
Am picillin/sulbactam : 3 g IV q6h
Azithrom ycin: 1 gPO single dose (cervicitis only)
Cefixim e: 400 m g PO single dose (cervicitis only)
Cefotetan: 2 g IV q12h
Cefoxitin: 2 g IM single dose (outpatient); 2 g IV q6h (inpatient)
Ceftriaxone: 250 m g IM single dose
Clindam ycin: 450 m g PO q.i.d. for 14 days (outpatient); 900 m g IV q8h (inpatient)
Doxycycline: 100 m g PO b.i.d. for 14 days (outpatient); 100 m g IV or PO q12h (inpatient)
Gentam icin: 2 m g/kg loading dose followed by 1.5 m g/kg IV q8h
Levofloxacin: 500 m g PO daily for 14 days (outpatient); 500 m g IV q24h (inpatient)
Metronidazole: 500 m g PO b.i.d. for 14 days (outpatient); 500 m g IV q8h (inpatient)
Ofloxacin: 400 m g PO b.i.d. for 14 days (outpatient); 400 m g IV q12h (inpatient)
Probenecid: 1 g PO single dose
Pa ge 3 4 9
Follow-Up Disposition Admission Criteria
Uncertain diagnosis and toxic appearance
Suspected pelvic abscess, including TOA
Pregnancy
Im m unodeficiency
Severe illness (e.g., vom iting or severe pain)
Failure of outpatient therapy
Probable noncom pliance with outpatient therapy (e.g., adolescents)
Consider adm ission if appropriate clinical follow-up cannot be arranged.
Discharge Criteria
Patients who do not m eet adm ission criteria m ay be treated as outpatients.
Recent studies have shown that in wom en with m ild to m oderate PID, there was no difference in reproductive outcom es between wom en random ized to inpatient versus outpatient treatm ent.
References 1. Centers for Disease Control and Prevention. 2002 guidelines for treatm ent of sexually transm itted diseases. MMWR Morb Mortal Wkly Rep. 2002;51(RR-6):1. 2. Drugs for sexually transm itted infections. Treat Guidel Med Lett. 2004;2:67. 3. Grim es DA. Intrauterine device and upper-genital-tract infection. Lancet. 2000;356:1013.
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4. McCorm ack WM. Pelvic inflam m atory disease. N Engl J Med. 1994;330:115–119. 5. Ness RB, et al. Effectiveness of inpatient and outpatient treatm ent strategies for wom en with pelvic inflam m atory disease: results from the Pelvic inflam m atory disease Evaluation And Clinical Health (PEACH) random ized trial. Am J Obstet Gynecol. 2002;186(5):929–937. 6. Pastorek JG. Pelvic inflam m atory disease and tubo-ovarian abscess. Obstet Gynecol Clin North Am . 1989;16:347–361. 7. Peipert JF, Ness RB, Blum e J, et al. Clinical predictors of endom etritis in wom en with sym ptom s and signs of pelvic inflam m atory disease. Am J Obstet Gynecol. 2001;184:856. 8. Ross J. Pelvic inflam m atory disease. Br Med J. 2001;322:658–659.
Codes ICD9-CM 614.9
ICD10 N73.9
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Pem phigus
Pemphigus
James T. Steen James T. Vandenberg Christopher S. Kang
Basics Description
Autoantibody (IgG)-m ediated blistering disease of the skin and m ucous m em brane: o
Characterized by loss of cell-to-cell adhesion.
Acquired blistering diseases include those caused by drugs (e.g., toxic epiderm al necrolysis) and idiopathic (e.g., bullous diabeticorum ).
Pem phigoid: a term describing the group of syndrom es that cause a separation of the epiderm is from the derm is
If untreated, m ortality rates average >75% at 5 years.
Pem phigus is a rare disease with a worldwide incidence of 0.1–0.5 cases per 100,000.
Incidence equal for m ales and fem ales
Two m ajor subtypes exist: o
Vulgaris; m ore serious with deeper involvem ent:
Affects m ost races in m iddle age and elderly Jewish patients
o
Foliaceus; m ilder and m ore superficial:
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No preference for Jewish persons
o
Vulgaris accounts for 80% of all cases.
o
Seventy percent of patients with vulgaris present with oral lesions.
o
Superficial pem phigus (foliaceus) often lacks oral lesions and has better prognosis.
Pem phigus is m ost com m on in individuals 40–60 years old, but has been reported in people ranging from neonates to 89 years of age.
Pediatric Considerations
Pem phigus is rare in children.
Neonates m ay develop the disease secondary to transplacental transfer of IgG.
Neonatal pem phigus spontaneously resolves in several weeks as the m aternal antibodies are catabolized.
Etiology/Genetics
IgG autoantibodies are directed against pem phigus antigens found in all keratinocytes.
Autoantibodies cause acantholysis: o
Separation of the keratinocytes from each other and loss of cell–cell adhesion
o
Leads to blistering
Im m unogenetic predisposition secondary to higher frequencies of specific HLA haplotypes
Drugs m ay induce or trigger pem phigoid reactions: o
Penicillam ine, captopril, rifam pin, piroxicam , and phenobarbital
Pem phigoid reactions m ay occur in association with a neoplasm , usually lym phom a (paraneoplastic pem phigus).
Endem ic pem phigus foliaceus (fogo selvagem ) m ay be triggered or transm itted by bites from flying insects.
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Diagnosis Signs and Symptoms
Generalized or focal flaccid bullae (blisters) of the skin and m ucosa
Painful skin erosions with shreds of detached epithelium
Painful nonhealing oral erosions
Crusting, partially healing skin erosions from ruptured bullae
Hypertrophic, hyperplastic erosive plaques with pustules in intertriginous areas (pem phigus vegetans)
Moist, edem atous, exfoliative erosions in seborrheic areas (pem phigus foliaceus)
Erythem atous, scaly, crusting skin lesions in a m alar distribution (pem phigus erythem atosus)
History
Typically features m ucocutaneous blisters followed by erosions
Often appear first in m ucous m em branes and several m onths later appear cutaneously
Skin lesions are painful flaccid blisters that m ay appear anywhere.
Physical Exam Nikolsky sign (separation of the epiderm is with lateral pressure) is characteristic but not diagnostic.
Essential Workup
Suspected based on clinical presentation
Biopsy with histologic and im m unofluorescence testing is essential for definitive diagnosis (arrange with a
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derm atologist).
Tests Lab Serum antibody titers, detected by indirect im m unofluorescence, are often used as a m arker of disease activity; however, the ED physician usually does not order these titers.
Imaging No diagnostic im aging test exists.
Diagnostic Procedures/Surgery Biopsy
Differential Diagnosis
Bullous pem phigoid
Derm atitis herpetiform is
Erythem a m ultiform e
Toxic epiderm al necrolysis
Epiderm olysis bullosa
Hand, foot, and m outh disease
System ic lupus erythem atosus
System ic vasculitis
Oral candidiasis
Herpes sim plex gingivostom atitis
Erosive lichen planus
Seborrheic derm atitis
P.815
Treatment
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Pre Hospital If severe disease, IV access, pulse oxim etry m onitor, and cardiac m onitor
Initial Stabilization
If sym ptom s of hypotension or sepsis are present, IV fluid resuscitation should be guided by the Parkland burn form ula: o
4 m L of crystalloid/kg body weight per percentage of body surface area involved per 24 hours
o
Give half of the total calculated fluid over the course of the first 8 hours, the rem ainder over the next 16 hours.
o
Adjust fluids to keep urine output >0.5 m L/kg/h
If signs or sym ptom s of sepsis are present, initiate broad-spectrum antibiotic coverage.
In steroid-dependent patients, adm inister stress-dose steroids.
ED Treatment
System ic corticosteroids are the m ainstay of therapy.
Severe disease: conventional high-dose corticosteroids: o
If severe sym ptom s are unresponsive to high-dose PO corticosteroids, consider pulse IV corticosteroids and adm ission for plasm apheresis.
Mild to m oderate disease should receive PO prednisone, and intralesional triam cinolone acetonide m ay be used.
Adjuvant im m unosuppressive therapy m ay also be added to decrease the sym ptom s associated with high-dose system ic corticosteroids or in patients with contraindications to steroid therapy: o
Dapsone, gold, azathioprine, cyclophospham ide, cyclosporine, m ethotrexate, m ycophenolate, and IV
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im m unoglobulins
Medication (Drugs)
Hydrocortisone: 100–300 m g IV stress-dose steroids
Methylprednisolone (pulse IV therapy; adults): 1 g IV over 3 hours daily
Prednisone: 20–400 m g PO daily (adults); severe disease, 200–400 m g PO daily for 5–10 weeks, then taper; m ild to m oderate disease, 20–80 m g PO daily
Triam cinolone acetonide: 20 m g/m L 0.1-m L injection into each superficial lesion
Follow-Up Disposition Admission Criteria
Adm it to the ICU or burn unit if any signs and sym ptom s of shock or sepsis are present, because aggressive fluid resuscitation, wound care, and m ultiple m edications will be required.
Adm it to a floor bed if pulse parenteral steroid therapy or plasm apheresis is indicated.
Adm it first-tim e presentations of disease to facilitate treatm ent and definitive diagnosis.
Discharge Criteria
Discharge if m ild to m oderate disease will not require aggressive steroid m anagem ent or plasm apheresis.
A follow-up evaluation is essential to m onitor the course of the disease and to adjust treatm ent.
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References 1. Ahm ed AR. Intravenous im m unoglobulin therapy in the treatm ent of patients with pem phigus vulgaris unresponsive to conventional im m unosuppressive treatm ent. J Am Acad Derm atol. 2001;45(5):679–690. 2. Ahm ed AR, Sam i N. Intravenous im m unoglobulin therapy for patients with pem phigus foliaceus unresponsive to conventional therapy. J Am Acad Derm atol. 2002;46(1):42–49. 3. Bystryn JC, Steinm an NM. The adjuvant therapy of pem phigus. Arch Derm atol. 1996;132:203–212. 4. Cotell S, Robinson ND, Chan LS. Autoim m une blistering skin diseases. Am J Em erg Med. 2000;18(3):288–299. 5. Korm an NJ. New im m unom odulating drugs in autoim m une blistering diseases. Derm atol Clin. 2001;19(4):637–648. 6. Odom RB, Jam es WD, Berger TG, et al. Andrews’ Diseases of the Skin: Clinical Derm atology. Philadelphia: WB Saunders; 2000. 7. Udey MC, Stanley JR. Pem phigus—diseases of antidesm osom al autoim m unity. JAMA. 1999;282(6):572–576. 8. Usatine RP, Sauret J. Rupturing bullae not responding to antibiotics. J Fam Pract. 2004;53(12):981–983.
Codes ICD9-CM 694.4
ICD10 L10.9
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Penile Shaft F racture
Penile Shaft
Fracture Ian R. Grover
Basics Description
Traum atic rupture of the corpus cavernosum and the encom passing tunica albuginea
May involve the corpus spongiosum and urethra
Hem atom a form ation occurs at rupture site.
Injury is usually unilateral and transverse.
Most com m on fracture site is the proxim al shaft of the penis.
During erection, pressure within corpus cavernosum is m axim al, close to arterial pressure, increasing volum e in each corpus to m axim um , which thins tunica albuginea, m aking it susceptible to rupture.
Penile erection stretches spongiosum to the lim it, which will lim it m ovem ent vertically while still allowing lateral m ovem ents; this form s a bend at base of penis, m aking it vulnerable to lateral swing and rupture of corpus cavernosum .
Twenty-five percent to 30% have associated urethral
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injury, which m ay be partial or com plete.
Caused by blunt traum a to erect penis during: o
Sexual intercourse
o
Manipulation
o
Fall on erect penis
o
Entanglem ent in clothing
Etiology
Peyronie's disease
Urethritis in past
Surgical procedure on corpus cavernosum or traum a to corpus cavernosum resulting in weak scar tissue
Diagnosis Signs and Symptoms History
Sudden painful sensation in erect penis during sexual intercourse or soon after with loss of erection: o
May hear cracking or crunching sound at the tim e of traum a
May have dysuria, inability to void, or an increase in size of the swelling with voiding owing to extravasation of urine
Problem s with poor erections after the injury
Blood at the urethral m eatus after intercourse
Penile deviation with erection
Urinary retention or weak urinary stream
Physical Exam
Swelling and blue-black discoloration at base of penis, usually on one side
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Ecchym osis m ay also involve scrotum .
Penis flaccid and edem atous with angulation away from the side of tear
Defect in the penile shaft m ay be palpable at the site of the tear.
Blood at tip of penis or frank hem aturia suggests an associated urethral injury.
Tests Lab Urinalysis to evaluate urethral traum a:
May have frank blood or m icroscopic hem aturia
PT/PTT if patient is on coum adin or has a history of bleeding disorder
Imaging
Retrograde urethrography—recom m ended in all cases of suspected urethral traum a: o
Should be done with low pressure during injection, before urethral catheterization
Cavernosography and MRI of penis m ay be needed to confirm diagnosis and site of tear.
Ultrasonography m ay also be done to confirm a suspected tear.
Diagnostic Procedures/Surgery Diagnostic exploration of the penis is recom m ended when cavernosography is negative but clinical suspicion of a fracture is high.
Differential Diagnosis
Cellulitis of penis
Contusion of penis
Lym phangitis of penis
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Neoplasm of penis
Paraphim osis
Traum a because of constrictive ring or other structure
Urethral injury
Vasculature rupture, especially superficial or deep dorsal vein or dorsal artery
P.817
Treatment Pre Hospital
Other injuries take precedence in the setting of m ultiple traum a.
Local treatm ent: ice packs locally to penis; splinting with tongue blade
Elevate the area to reduce swelling.
Initial Stabilization
Pain control
Needle suprapubic cystotom y in patients with urethral traum a and full bladder to relieve patient discom fort
ED Treatment
Com bined efforts of ED physician and urologist are aim ed toward restoration of norm al shape of penis and sexual and urinary functions.
ED treatm ent directed to reduce hem orrhage, prevent further com plications
Prophylactic antibiotic use is unnecessary.
Urethral catheterization in all cases after excluding
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urethral traum a
Urologic evaluation and early surgical treatm ent are essential to prevent com plications such as erectile dysfunction, im potence, penile deform ity, urethral stenosis.
All patients with suspected or definite diagnosis m ust have early urologic evaluation.
Medication (Drugs)
Diazepam : 2–5 m g IV
Fentanyl: 0.05–0.2 m g IV
Hydrom orphone: 0.5–1.0 m g IV
Lorazepam : 0.5–1.0 m g IV
Morphine sulfate: 0.1 m g/kg IV
Follow-Up Disposition Admission Criteria All patients with penile fracture m ust be hospitalized for prom pt surgery.
Discharge Criteria N/A
Issues for Referral If im m ediate urologic consultation and treatm ent unavailable, patient m ay be transferred to a suitable hospital after initial stabilization and transfer criteria have been m et
References
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1. Asgari MA, et al. Penile fractures: evaluation, therapeutic approaches and long-term results. J Urol. 1996;155:148–149. 2. Eke N. Fracture of the penis. Br J Surg. 2002;89(5):555–565. 3. Ekwere PD, Al Rashid M. Trends in the incidence, clinical presentation, and m anagem ent of traum atic rupture of the corpus cavernosum . J Natl Med Assoc. 2004;96(2):229–233. 4. Fedel M, et al. The value of MRI in diagnosis of suspected penile fracture with atypical clinical findings. J Urol. 1996;155(6):1924–1927. 5. Haas CA, et al. Penile fracture and testicular rupture. World J Urol. 1999;17(2):101–106. 6. Kervancioglu S, et al. Color Doppler sonographic findings in penile fracture. J Clin Ultrasound. 2005;33(1):38–42. 7. Koifm an L, et al. Penile fracture experience in 56 cases. Int Braz J Urol. 2003;29(1):35–39. 8. Muentener M, et al. Long-term experience with surgical and conservative treatm ent of penile fracture. J Urol. 2004;172(2):576–579.
Codes ICD9-CM 959.1
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Peptic Ulcer
Peptic Ulcer
Jason M. Lebwohl
Basics Description
Produced by breakdown in gastric or duodenal m ucosal defenses
Im balance exists between production of acid and ability of m ucosa to prevent dam age.
Etiology
Helicobacter pylori: o
Gram -negative spiral bacteria that live in m ucous layer
o
Responsible for 90–95% of duodenal ulcers and 80% of gastric ulcers
o
Increases antral gastrin production and decreases m ucosal integrity
NSAIDs: o
Interfere with prostaglandin synthesis
o
Lead to break in m ucosa
Aspirin
Cigarette sm oking
Alcohol
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Diagnosis Signs and Symptoms
Epigastric pain or tenderness (80–90%): o
Burning, gnawing, aching pain
o
Location: m idline, xiphoid, or um bilicus
Duodenal ulcers: o
Pain occurs 90 m inutes to 3 hours after m eals.
o
Usually awakens patient at night
o
Food and antacids relieve pain.
Gastric ulcers: o
Pain worsens after m eals.
o
Nausea and anorexia
Difficult to differentiate clinically between gastric and duodenal ulcers
Relief of pain with antacids
Hem e-positive stools
Com plications of peptic ulcer disease (PUD): o
o
Acute perforation:
Rigid boardlike abdom en
Generalized rebound tenderness
Pain radiation to back or shoulder
Obstruction:
Pain with vom iting
Succussion splash from retained gastric contents and abdom inal distention
o
Hem orrhage:
Hem atem esis
Melena
Hypotension
Tachycardia
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Skin pallor
Orthostatic changes
Essential Workup
Careful physical exam ination including Hem occult testing and vital signs with orthostatics
For stable patients, oral GI cocktail typically relieves pain: o
Antacid: 30 m L
o
Viscous lidocaine: 10 m L
Tests Lab
Norm al lab values in uncom plicated ulcer disease
CBC:
o
Low hem atocrit with bleeding
o
Leukocytosis with perforation/penetration
Am ylase/lipase: o
Elevated with perforation/penetration
o
Pancreatitis in differential diagnosis
Electrolytes, BUN/creatinine, glucose for critically ill
Type and cross-m atch: o
For significant blood loss
Imaging Chest radiograph/abdom inal series:
Evaluate for perforations/obstructions
Diagnostic Procedures/Surgery
ECG: o
For elderly patients
o
Myocardial ischem ia in differential diagnosis
Endoscopy: o
Procedure of choice
o
Outpatient unless significant hem orrhage
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o
Allows for biopsies of gastric/duodenal ulcers for presence of H. pylori
o
Detects m alignant gastric ulcers
Upper GI series: o
Single contrast barium diagnoses 70% to 80%.
o
Double contrast diagnoses 90%.
Gastrin level is elevated in Zollinger-Ellison syndrom e.
Differential Diagnosis
Gastroesophageal reflux
Biliary colic
Cholecystitis
Pancreatitis
Gastritis
Abdom inal aortic aneurysm
Aortic dissection
Myocardial infarction
Subset with sym ptom s and no ulcer on endoscopy called nonulcer dyspepsia
Treatment Pre Hospital
Airway, breathing, and circulation m anagem ent (ABCs)
IV fluid resuscitation for hypotensive/shock patients
Initial Stabilization
ABCs
Identify ulcer com plications (hem orrhage, perforation, obstruction)
Treat hypotension with LR/norm al saline (NS) fluid bolus via two large-bore IVs
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Type and cross early.
Nasogastric tube (NGT) for gastric decom pression/check for hem orrhage
P.819
ED Treatment
Pain control with antacids (GI cocktail) or IV H 2 antagonists
Avoid narcotics—m ay m ask serious illness.
Prom otion of ulcer healing: o
Antacids
o
H 2 antagonists (cim etidine, fam otidine, ranitidine, nizatidine)
o
Sucralfate
o
Prostaglandin congers (m isoprostol)
o
Protease pum p inhibitors (PPIs; om eprazole, lansoprazole, or pantoprazole)
Gastric outlet obstruction: o
Decom press stom ach with NGT.
o
IV hydration
Gastric hem orrhage o
IV fluid resuscitation
o
Blood transfusion depending on loss/hem atocrit
o
Foley catheter to m onitor volum e status
o
GI consultation
Perforation: o
IV hydration
o
Foley catheter
o
Preoperative antibiotics
o
Em ergency surgical consultation
Treatm ent of H. pylori infection:
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o
Invasive or noninvasive testing to confirm infection
o
Oral eradication antibiotic therapy options:
Proton pum p inhibitor (om eprazole 20 m g b.i.d.) or lansoprazole 30 m g PO b.i.d. and two antibiotics (clarithrom ycin 500 m g b.i.d. plus m etronidazole 500 m g b.i.d.) for 14 days
H 2 blocker, bism uth subsalicylate (Pepto-Bism ol) plus either am oxicillin 1,000 m g b.i.d. or tetracycline 500 m g q.i.d. in com bination with either m etronidazole 250 m g q.i.d. or clarithrom ycin 500 m g b.i.d. for 14 days
Most com m on regim en: om eprazole 20 m g or lansoprazole 30 m g plus clarithrom ycin 500 m g and am oxicillin 1 g, all taken twice a day for 2 weeks
Medication (Drugs)
Bism uth subsalicylate: two 525-m g tabs PO q.i.d.
Cim etidine (H 2 blocker): 800 m g PO nightly at bedtim e (peds: 20–40 m g/kg/24h) for 6–8 weeks
Fam otidine (H 2 blocker): 40 m g PO nightly at bedtim e (peds: 0.5–0.6 m g/kg q12h) for 6–8 weeks
Lansoprazole (PPI): 30 m g PO b.i.d. for 2 weeks
Maalox plus: 2–4 tablets PO q.i.d.
Misoprostol: 100–200 µg PO q.i.d.
Mylanta II: 2–4 tablets PO q.i.d.
Nizatidine (H 2 blocker): 300 m g PO nightly at bedtim e for 6–8 weeks: 20 m g PO b.i.d. (peds: 0.6–0.7 m g/kg q12h–q24h) for 2 weeks
Pantoprazol (PPI): 40 m g PO daily for 2 weeks
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Ranitidine (H 2 blocker): 300 m g PO nightly at bedtim e (peds: 5–10 m g/kg/24h given q12h) for 6–8 weeks
Sucralfate: 1 g PO q.i.d. for 6–8 weeks
Follow-Up Disposition Admission Criteria
Gastric obstruction
Perforation
Active upper GI bleed
Melena
Uncontrolled pain
Anem ia
Discharge Criteria
Unrem arkable physical exam ination with norm al CBC and hem e-negative stools
If hem e-positive stools, discharge if stable vital signs, norm al hem atocrit, and negative NGT aspiration for upper GI hem orrhage
Issues for Referral Outpatient GI evaluation and endoscopy
References 1. Louw JA, Marks IN. Peptic ulcer disease. Curr Opinion Gastroenterol. 2004,20(6);533–537. 2. McGuirk TD, et al. Upper gastrointestinal tract bleeding. Em erg Med Clin North Am . 1996;14(3):530–533. 3. Sm oot DT, et al. Peptic ulcer disease. Prim Care. 2001;28(3):487–503.
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Miscellaneous SEE ALSO: Gastroesophageal Reflux Disease; Gastritis; Gastrointestinal Bleeding
Codes ICD9-CM 533.9
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Perfo rated Visco us
Perforated
Viscous Ingrid D. Carter
Basics Description Perforation of viscous structure into peritoneal cavity:
Inflam m ation
Ulceration
Shearing/crushing or bursting forces in traum a
Obstruction
Chem ical peritonitis occurs as result of disruption of gastric or intestinal lining into peritoneal cavity.
Etiology
Peptic ulcer disease
Appendicitis
Inflam m atory bowel disease
Diverticular disease
Colon carcinom a
Foreign body ingestion
Traum a
Radiation enteritis
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Pediatric Considerations
Blunt traum a m ore com m on cause of bowel rupture than penetrating traum a
Jejunum is m ost com m on site of rupture.
Diagnosis Signs and Symptoms
Sudden severe abdom inal pain: o
Initially local
o
Rapidly becom ing diffuse
Rigidity
Guarding
Rebound tenderness
Absent bowel sounds
Hypovolem ic shock: o
Tachycardia
o
Hypotension
Essential Workup Upright chest radiograph:
Best dem onstrates pneum operitoneum
When in upright position for 5–10 m inutes, m ay detect as little as 1–2 m L of free air under diaphragm
Tests Lab
CBC
Electrolytes, BUN/creatinine, glucose
Lipase
Urinalysis
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Liver function test
Imaging
Abdom inal radiographs: o
Left lateral decubitus film
o
Supine abdom en
o
Double wall
o
Air in intestinal lum en and peritoneal cavity allows for visualization of both serosal (not norm ally seen) and m ucosal surfaces of intestine.
Abdom inal CT: o
Detects sm all am ounts of free air from perforated viscous
ECG
Differential Diagnosis
Intra-abdom inal abscess
Pneum om ediastinum with peritoneal extension
Pancreatitis
Peptic ulcer disease
Inferior wall m yocardial infarction
Cholecystitis
P.821
Treatment Initial Stabilization Treat hypotension/tachycardia with 0.9% norm al saline:
Adults: 500 m L to 1 L bolus
Pediatric: 20 m L/kg bolus
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ED Treatment
Nasogastric tube
Foley catheter
Adm inister broad-spectrum antibiotics:
o
Cephalosporin
o
Am inoglycoside plus clindam ycin
Im m ediate surgical consultation for operative intervention
Medication (Drugs)
Am ikacin: 15 m g/kg/24h IV q8h
Cefoxitin: 2 g (peds: 1 week, 80–160 m g/kg IV q6h) IV q6h
Clindam ycin: 600–900 m g (peds: 20 to 40 m g/kg/24h) IV q8h
Morphine sulfate: 2–4 m g (peds: 0.1 m g/kg) IV q2h–q3h
Follow-Up Disposition Admission Criteria Suspected or confirm ed perforation requires adm ission and im m ediate surgical consultation.
Discharge Criteria None
References 1. Graff LG, Robinson D. Abdom inal pain and em ergency departm ent evaluation. Em erg Med Clin North Am . 2001;19:123–136.
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2. Shaffer H. Perforation and obstruction of the gastrointestinal tract. Radiol Clin North Am . 1992;30:405–426. 3. Sivit C. Gastrointestinal em ergencies in older infants and children. Radiol Clin North Am . 1997;35:865–877.
Codes ICD9-CM 799.8 K63.1
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Pericardial Effusio n/Tam po nade
Pericardial
Effusion/Tamponade Sandra S. Yoon Teriggi J. Ciccone Carlo L. Rosen
Basics Description
Pericardial effusion: o
Accum ulation of fluid in the pericardial sac
o
Occurs in 10% of cancer patients
Pericardial tam ponade: o
Accum ulation of pericardial fluid with elevation of pressure in the pericardial space that results in im pairm ent of ventricular filling and decreased cardiac output.
o
Potentially lethal
o
Rapid accum ulation of 50–200 m L of fluid in the pericardial sac causes hem odynam ic com prom ise and pericardial tam ponade.
o
Occurs in 15% of patients with idiopathic pericarditis
o
Occurs in 2% of patients with penetrating chest traum a
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Etiology
Medical causes: o
Idiopathic
o
Bacterial, viral, fungal, and parasitic infections
o
Tuberculosis
o
HIV
o
Malignancy
o
Urem ia, dialysis
o
Autoim m une/collagen vascular diseases
o
System ic lupus erythem atosus
o
Rheum atoid arthritis
o
Rheum atic fever
o
Scleroderm a
o
Radiation therapy
o
Myxedem a
o
Drug toxicity (isoniazid, doxorubicin, procainam ide, hydralazine, phenytoin)
o
Postm yocardial infarction (Dressler syndrom e)
Surgical causes: o
Penetrating chest traum a
o
Blunt traum a rarely causes pericardial effusion
o
Thoracic aortic dissection
o
Iatrogenic (cardiac catheterization, post–cardiac surgery, central line placem ent)
Diagnosis Signs and Symptoms
Most are asym ptom atic
Pleuritic chest pain:
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o
Relieved by sitting forward
Dyspnea
Cough
Fatigue
Malaise
Pericardial friction rub
Signs of shock or right heart failure
Fever >38°C is uncom m on; if present, consider purulent pericarditis
Pulsus paradoxus: o
Fall in systolic blood pressure >10 m m Hg with inspiration
o
Sensitive but not specific
Dressler syndrom e: o
Fever
o
Chest pain
o
Pericardial friction rub
o
Seen several weeks after a m yocardial infarction
Beck triad: o
Classic presentation of cardiac tam ponade
o
Only present in one third of patients
o
Hypotension
o
Muffled heart sounds
o
Jugular venous distention (JVD):
JVD m ay be absent in hypovolem ic patients
Essential Workup
ECG: o
Low voltage:
o
Electrical alternans
Alternating beat-to-beat variation of QRS am plitude
Rare in patients with traum atic pericardial
Pa ge 3 5 2
effusion or tam ponade
Chest radiograph: o
Enlarged cardiac silhouette only in cases of pericardial effusion/tam ponade that develop over tim e
Echocardiography: o
Fluid in pericardial sac
o
Transthoracic echo is accurate for penetrating cardiac injury and effusions or tam ponade.
o
Right ventricular or atrial diastolic collapse-characteristic finding suggestive of tam ponade.
o
“Sniff― test:
Inferior vena cava will not collapse in patients with tam ponade.
Suggestive of increased central venous pressure (CVP)
Tests Lab
CBC
Electrolytes, blood urea nitrogen/creatinine, glucose for renal failure in suspected urem ic pericarditis
Cardiac enzym es m ay be elevated
Blood cultures if an infectious source is suspected
Imaging
Chest CT for detecting hem opericardium
Transesophageal echocardiography
MRI with gadolinium
Diagnostic Procedures/Surgery
Pericardiocentesis and fluid analysis:
Pa ge 3 5 2
o
Further work-up of m edical causes of pericardial effusion with determ ination of the etiology of the pericardial fluid
CVP determ ination: o
May be used in penetrating chest traum a patients
o
CVP >15 cm H 2 O suggests tam ponade, but m ay be norm al in the hypovolem ic patient.
Differential Diagnosis
Other causes of shock
Myocardial infarction
Myocardial ischem ia
Congestive heart failure
Pulm onary em bolus
Sepsis
Tension pneum othorax
Hem othorax
Air em bolism
Aortic dissection
Gastrointestinal tract bleeding
Ruptured abdom inal aortic aneurysm
P.823
Treatment Pre Hospital Insert two large-bore IV lines in all cases of suspected cardiac tam ponade.
Initial Stabilization
Pa ge 3 5 2
IV fluid resuscitation with NS or blood
Pericardiocentesis for unstable patients to decom press the tam ponade
ED thoracotom y with pericardiotom y for patients in cardiac arrest after penetrating thoracic traum a or those who rem ain unstable after volum e replacem ent and pericardiocentesis
ED Treatment
Bacterial pericardial effusion: o
Initiate antibiotic therapy to cover gram -negative and anaerobic organism s and Staphylococcus aureus.
o
May require partial surgical resection of the pericardium
Urem ic pericardial effusion: o
Dressler syndrom e and postirradiation pericardial effusion: o
Arrange urgent dialysis
Initiate NSAIDs
Medical causes of tam ponade in patients who are unstable: o
Perform pericardiocentesis with placem ent of an indwelling catheter for continued drainage
Traum atic pericardial tam ponade: o
Consult traum a surgeon im m ediately.
o
Definitive therapy is thoracotom y in the OR.
Aortic dissection: o
Im m ediate surgical consultation for operative repair
Medication (Drugs)
Aspirin: 650 m g PO q4h
Ibuprofen: 800 m g PO q8h
Indom ethacin: 25–75 m g PO b.i.d.
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Follow-Up Disposition Admission Criteria
Intensive care unit adm ission for acute, sym ptom atic pericardial effusion/tam ponade
New pericardial effusion
Discharge Criteria Known sm all effusion in asym ptom atic stable patient
References 1. Braunwald E. Pericardial diseases. In: Fauci AS, Braunwald E, Isselbacher KJ, et al. eds. Harrison's principles of internal m edicine. 14th ed. New York: McGraw-Hill, 1998:1334–1341. 2. Ciccone TJ, Grossm an SA. Cardiac Ultrasound. Em er Med Clin of N Am erica. 2004;23(3):621–640. 3. Jouriles NJ. Pericardial and m yocardial disease. In: Marx JA, et al, eds. Rosen's em ergency m edicine: concepts and clinical practice, 5th ed. St. Louis, MO: Mosby, 2002:1130–1149. 4. Lange RA, Hillis LD. Acute Pericarditis. N Eng J Med. 2004;351:2195–2202. 5. Rosen CL, Wolfe RE. Blunt chest traum a. In: Ferrera PC, et al. eds. Traum a m anagem ent, an em ergency m edicine approach. St. Louis, MO: Mosby, 2001:232–258. 6. Soler-Soler J, Sagrista-Sauleda J, Perm anyer-Miralda G. Managem ent of pericardial effusion. Heart. 2001;86(2):235–240. 7. Tsang TSM, Oh JK, Seward JB. Diagnosis and m anagem ent of cardiac tam ponade in the era of echocardiography. Clin Cardiol. 1999;22:442–446.
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Miscellaneous SEE ALSO: Cardiogenic Shock
Codes ICD9-CM 429.0
ICD10 131.3 131.9
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Pericarditis
Pericarditis
Wende R. Reenstra
Basics Description
Inflam m ation, infection, or infiltration of the pericardial sac, which surrounds the heart: o
Pericardial effusion m ay or m ay not be present
Acute pericarditis: o
Rapid in onset
o
Potentially com plicated by accum ulation of pericardial fluid leading to cardiac tam ponade
Constrictive pericarditis: o
Results from chronic inflam m ation causing thickening and adherence of the pericardium to the heart
Etiology
Idiopathic (m ost com m on)
Viral: o
Echovirus
o
Coxsackie
o
Adenovirus
o
Varicella
o
Epstein-Barr virus
o
Cytom egalovirus
Pa ge 3 5 3
o
Hepatitis B
o
AIDS
Bacterial: o
Staphylococcus
o
Streptococcus
o
Haem ophilus
o
Salm onella
o
Legionella
o
Tuberculosis
Fungal: o
Candida
o
Aspergillus
o
Histoplasm osis
o
Coccidioidom ycosis
o
Blastom ycosis
o
Nocardia
Parasitic: o
Am ebiasis
o
Toxoplasm osis
o
Echinococcosis
Neoplastic: o
Lung
o
Breast
o
Lym phom a
o
Leukem ia
o
Melanom a
Urem ia
Myxedem a
Myocardial infarction: o
Dressler syndrom e
Connective tissue disease o
System ic lupus erythem atosus
Pa ge 3 5 3
o
Rheum atoid arthritis
o
Scleroderm a
Radiation
Chest traum a
Postpericardiotom y
Aortic dissection
Pancreatitis
Inflam m atory bowel disease
Am yloidosis
Drugs: o
Procainam ide
o
Crom olyn sodium
o
Hydralazine
o
Dantrolene
o
Methysergide
o
Mesalam ine
Diagnosis Signs and Symptoms History
Chest pain: o
Retrosternal or precordial
o
Usually sharp
o
Pleuritic
o
Radiating to the shoulder or the trapezial ridge
o
Worsened with cough or inspiration
o
Increased with recum bency
o
Im proved with leaning forward
Fever
Pa ge 3 5 3
Mild dyspnea
Cough
Hoarseness
Nausea
Anorexia
Physical Exam
Tachypnea
Tachycardia
Odynophagia
Friction rub: o
Heard best at lower left sternal border
o
Any of three com ponents:
o
Presystolic
Systolic
Early diastolic
Interm ittent and exacerbated by leaning forward
Beck triad with the accum ulation of pericardial fluid: o
Muffled heart sounds
o
Increased venous pressure (distended neck veins)
o
Decreased system ic arterial pressure (hypotension)
Ewart sign: o
Dullness and bronchial breathing between the tip of the left scapula and the vertebral colum n
Pulsus paradoxus: o
Exaggerated decrease (>10 m m Hg) in systolic pressure with inspiration
Constrictive pericarditis: o
Signs of both right- and left-sided heart failure
o
Pulm onary and peripheral edem a
o
Ascites
o
Hepatic congestion
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Essential Workup
ECG: o
Stage: 1
ST-segm ent elevation diffusely except aVR and V1
ST segm ents concave up
No reciprocal ST-segm ent depression in other leads (in contradistinction to the changes seen in acute m yocardial infarction)
o
o
Stage 2:
ST segm ents return to norm al
T waves flatten
PR segm ents m ay becom e depressed
Stage 3:
o
T-wave inversion
Stage 4:
Eventual resolution of all changes
Differentiation from m yocardial infarction
No Q waves form ed
T-wave inversion occurs after the resolution of the ST-segm ent changes
P.825
Tests Lab
CBC
Leukocytosis
Erythrocyte sedim entation rate m ay be elevated
Cardiac enzym es: o
Helpful in distinguishing pericarditis from m yocardial
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infarction o
Reported elevated with the inflam m ation of pericarditis
Imaging
Chest radiograph: o
Can be norm al
o
May show enlargem ent of the cardiac silhouette
o
No change in heart size until >250 m L of fluid has accum ulated in the pericardial sac
Echocardiography: o
Diagnostic m ethod of choice for the detection of pericardial fluid
o
Can detect as little as 15 m L of fluid in the pericardial sac
Chest CT: o
Useful for the detection of calcifications or thickening of the pericardium
Diagnostic Procedures/Surgery Pericardiocentesis:
Indicated when a pericardial effusion is present and fluid is needed to determ ine the underlying etiology
Used to obtain fluid for protein, glucose, culture, cytology, gram and acid-fast stains, and fungal sm ears
Differential Diagnosis
Acute m yocardial infarction
Pulm onary em bolism
Pneum othorax
Aortic dissection
Pneum onia
Em pyem a
Cholecystitis
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Pancreatitis
Treatment Pre Hospital
ABCs, IV access, O 2 , m onitor
Consider fluid bolus if no crackles.
Initial Stabilization
ABCs
Pericardiocentesis: o
For hem odynam ic com prom ise secondary to cardiac tam ponade
o
Rem oval of even a sm all am ount of fluid can lead to a dram atic im provem ent.
o
Guided by ultrasound is the safest technique.
ED Treatment
Treatm ent dependent on the underlying etiology
Idiopathic, viral, rheum atologic, and posttraum atic:
o
NSAID regim ens effective
o
Corticosteroids reserved for refractory cases
Bacterial: o
Aggressive treatm ent with IV antibiotics along with drainage of the pericardial space
o
Search for prim ary focus of infection.
o
Therapy guided by determ ination of pathogen from pericardial fluid tests
Neoplastic: o
Treat underlying m alignancy.
Urem ia: o
Intensive 2- to 6-week course of dialysis
Pa ge 3 5 3
o
Caution should be used if using nonsteroidal m edications.
Expected course/prognosis: o
Most patients will respond to treatm ent within 2 weeks.
o
Most have com plete resolution of sym ptom s:
Few progress to recurrent bouts with eventual developm ent of constrictive pericarditis or cardiac tam ponade.
Medication (Drugs)
Aspirin: 350–650 m g PO q3h–q4h
Ibuprofen: 400–800 m g PO q6h–q8h
Indom ethacin: 25–50 m g PO q6h
Follow-Up Disposition Admission Criteria Intensive care unit:
Hem odynam ic instability
Cardiac tam ponade
Associated m alignant dysrhythm ia
Any suspicion of m yocardial infarction
Severe pain unresponsive to oral m edications
Suspicion of bacterial etiology
Patients having undergone pericardiocentesis due to the relatively high incidence of com plications
Discharge Criteria
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Mild sym ptom s in patients without any hem odynam ic com prom ise
Close follow-up
Able to tolerate a regim en of oral m edication
References 1. Bessen HA and Byyny R, Acute Pericarditis and Cardiac Tam ponade. In: Wolfson AB et al eds. Harwood-Nuss’ Clinical Practice of Em ergency Medicine. 4th ed. Philadelphia: Lippincott William s and Wilkins 2005:294–297. 2. Jourilles NJ. Pericardial and m yocardial disease. In: Rosen P, et al. eds. Em ergency m edicine: Concepts and clinical practice, 5th ed. St. Louis, MO: Mosby YearBook, 2002:1130–1138. 3. Maisch B. The classification of pericardial disease in the age of m odern m edicine. Curr Cardiol Rep. 2002;4(1):1321. 4. Maisch B. Pericardial diseases, with a focus on etiology, pathogenesis, pathophysiology, new diagnostic im aging m ethods, and treatm ent. Curr Opin Cardiol. 1994;9:379–388. 5. Pankuweit S, Ristic AD, Seferovic PM, Maisch B. Bacterial pericarditis: diagnosis and m anagem ent. Am J Cardiovasc Drugs. 2005;5(2):103–112. 6. Ristic AD, Seferovic PM, Maisch B. Managem ent of pericardial effusion the role of echocardiography in establishing the indications and the selection of the approach for drainage. Herz. February 2005;30(2):144–150. 7. Yazdani K, Maraj S, Am anullah AM. Differentiating constrictive pericarditis from restrictive cardiom yopathy. Rev Cardiovasc Med. Spring 2005;6(2):61–71.
Miscellaneous SEE ALSO: Pericardia Effusion/Tam ponade
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Codes ICD9-CM 423.9
ICD10 I31.9
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Perilunate Dislo catio n
Perilunate
Dislocation John MacKay
Basics Description Dislocation of carpal bones (usually capitate) volar or dorsal from lunate
Etiology
Fall on outstretched hand usually dorsiflexed
Motor vehicle accidents bracing hands on steering wheel
Associated Conditions Scaphoid is frequently fractured with perilunate dislocation.
Diagnosis Signs and Symptoms
Pain in wrist
Swelling or palpable deform ity in wrist
Physical Exam
Diagnosis often m issed by clinical exam
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Pay special attention to skin integrity and neurovascular status, including two-point discrim ination.
Essential Workup Im aging of wrist
Tests Imaging
Radiographic im aging that includes three views of wrist
Perilunate dislocation visualized best on true lateral view: o
Distal carpal row, capitate seen dorsal or volar to lunate
o
Lunate in its norm al relationship to radius
CT and MRI are not generally needed for diagnosis, but som e orthopedists m ay request them for preoperative planning.
Pediatric Considerations
Wrists are rarely sprained in children, and radiograph is difficult to interpret.
Com parison view of other wrist m ay be helpful.
Differential Diagnosis
Lunate fracture
Lunate dislocation: o
Dislocation occurs between lunate and distal radius.
Scapholunate dissociation and other sim ilar ligam entous disruptions
Pediatric Considerations Consider nonaccidental traum a
Pa ge 3 5 4
Treatment Alert
Concern is for other, m ore serious, injuries.
Dress open wounds.
Im m obilize in neutral position.
Elevation, cold to reduce swelling
Age-appropriate social m anagem ent
Initial Stabilization
Im m obilize, ice, elevate, pending definitive evaluation.
Identify other, m ore serious, associated injuries.
P.827
General Measures Reduction of dislocation:
Operative fixation to reduce and m aintain fracture is frequently required.
Consultation with orthopedist before first attem pt at reduction recom m ended
Give patient appropriate procedural sedation.
Place hand in finger traps and use counterweights.
Place finger pressure at level of dislocation and gently exaggerate injury, then bring to appropriate position, m aintaining pressure over dislocated segm ent.
Im m obilize wrist using thum b-spica or sugar-tong splint in neutral position.
Pain control
Pediatric Considerations
Wrists are rarely sprained in children, and radiograph is difficult to interpret.
Pa ge 3 5 4
Although perilunate dislocation is unusual in pediatric patients, children with wrist pain should be splinted and referred for ongoing evaluation: o
Wrist should be splinted with thum b-spica sugar tong splint.
Consider nonaccidental traum a.
Follow-Up Disposition Admission Criteria
Open dislocation, presence of m ultiple traum a, or other, m ore serious, injuries
Inability to reduce dislocation or m aintain reduction
Preference of consulting orthopedist
Neurovascular com prom ise
Discharge Criteria
Closed injuries
Adequate reduction
No neurovascular involvem ent
Orthopedic follow-up within 2 days
References 1. Am erican Society for Surgery of the Hand. The Hand: Prim ary Care of Com m on Problem s. 2nd ed. New York: Churchill Livingstone; 1990:637–649. 2. Eisenhauer MA. Wrist and forearm . In: Rosen P, et al., eds. Em ergency Medicine: Concepts and Clinical Practice. 5th ed. St Louis, MO: Mosby; 2002:535–542. 3. Escarza R, Chin HW. Wrist injuries. In: Hart RG, Uehara DT,
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Wagner MJ, eds. Em ergency and Prim ary Care of the Hand. Dallas, TX: Am erican College of Em ergency Physicians; 2001:139–160. 4. Uehara DT, Wolanyk D, Escarza RH. Wrist injuries. In: Am erican College of Em ergency Physicians. Em ergency Medicine: A Com prehensive Study Guide. 6th ed. New York: McGraw-Hill; 2004: 1675–1684.
Codes ICD9-CM 833.00
ICD10 S63.0
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Perio do ntal Abscess
Periodontal
Abscess John Sullivan
Basics Description
Collection of pus in supporting structures of teeth: o
Periodontal ligam ent
o
Alveolar bone
Periodontal pockets result from progression of periodontal disease and resultant bone loss: o
Food and debris accum ulate in periodontal pockets.
o
Coronal epithelial tissues can reattach to tooth while bacteria and food debris rem ain trapped in pocket, im pairing drainage.
o
Food and debris becom e secondarily infected in setting of im paired drainage.
Com plications: o
Osteom yelitis
o
Dentocutaneous fistula
o
Cavernous sinus throm bosis
o
Ludwig angina
o
Maxillary sinusitis
Pa ge 3 5 4
o
Tooth loss
Pediatric Considerations
Periodontal abscess rare in children.
Periapical abscess com m on: o
Originates in pulp
o
Associated with caries
Etiology Anaerobic and Gram negative pathogens:
Usually polym icrobial
Diagnosis Signs and Symptoms Periodontal abscess is a clinical diagnosis.
History
Dental pain
Malaise
Fever
Physical Exam
Focal swelling or fluctuance of gum s and or face
Tenderness to palpation
Increased tooth m obility
Parulis: o
Pim plelike lesion on gingival, representing term inal aspect of a sinus tract
o
May be seen in chronic abscess
Expression of pus from sinus tract
Heat sensitivity
Lym phadenopathy
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Trism us generally absent, unless infection has spread to m uscles of m astication
History Necessary
Tests Ancillary testing not essential to m ake diagnosis
Lab Anaerobic culture of pus:
Com plicated abscess
Im m unocom prom ised patients
Imaging Panoram ic, periapical, or occlusal radiographs:
Not essential to m ake diagnosis
Can confirm and help define extent of abscess
Diagnostic Procedures/Surgery Electric pulp testing:
Perform ed by dental consultant to verify viability of tooth
Differential Diagnosis
Periapical abscess
Aphthous ulcers
Oral herpes
Salivary gland tum ors
Mum ps
Blocked salivary gland due to siladenitis or dehydration
Localized adenopathy due to oral infections
Facial cellulitis
Maxillary sinusitis
Acute otitis m edia
Peritonsillar abscess
Pediatric consideration: Periapical abscess
Pa ge 3 5 4
For asym ptom atic parulis: o
Fibrom a
o
Pyogenic or peripheral ossifying granulom a
o
Kaposi's sarcom a
Treatment Pre Hospital Rarely associated with airway em ergencies, but if any signs of airway com prom ise are present:
Intubation equipm ent at bedside
Transport in sitting position
Supplem ental oxygen
Suction secretions as needed
Initial Stabilization
Assess for airway patency.
Establish definitive airway via endotracheal intubation or cricothyrotom y/tracheostom y in presence of: o
Respiratory distress
o
Inability to handle secretions
o
Oropharyngeal tissue swelling that im pairs or threatens airway
ED Treatment
Analgesia with NSAIDs or opiates m ay be required
Incision and drainage: o
Anesthetize gingiva superficially with 2% lidocaine with 1:100,000 epinephrine until blanching occurs.
o
Make a 1-cm stab incision using a scalpel blade toward alveolar bone.
o
Blunt dissection using m osquito hem ostat
Pa ge 3 5 5
o
Irrigate cavity with saline.
o
If abscess cavity sufficiently large, place one quarter–inch iodoform gauze drain or fenestrated Penrose drain for 24–48 hours; to prevent its aspiration, secure gauze or drain with silk suture.
Antibiotics: o
Indicated if abscess extensive or if system ic signs present
o
Penicillin considered first-line em piric therapy
o
Erythrom ycin, azithrom ycin, clindam ycin for penicillin-allergic patients
o
Clindam ycin for penicillin-allergic patients or patients not responding to penicillin
o
Am picillin/sulbactam for severe infections
Warm saltwater rinses hourly while awake for 24–48 hours.
P.829
Medication (Drugs)
Penicillin G: 4 m illion Units (peds: 16–66 m U/kg) IM/IV q4h
Penicillin VK: 250–500 m g (peds: 6–12 m g/kg) PO q.i.d.
Am picillin/sulbactam IV: 1.5–3.0 g (peds: 15–30 m g/kg) IV/IM q6h
Azithrom ycin PO: 500 m g (peds: 10 m g/kg) PO first day then 250 m g (peds: 5 m g/kg) PO per day × 4 days
Clindam ycin PO: 150–450 m g (peds: 2.5–7.5 m g/kg) PO q.i.d.
Pa ge 3 5 5
Clindam ycin IV: 300–900 m g (peds: 8.3–13.3 m g/kg) IV q8h
Erythrom ycin PO: 250–500 m g (peds: 10–17 m g) PO q6h–q8h
Follow-Up Disposition Admission Criteria
Severe infection or com plication requiring parenteral antibiotics
Necrosis or cellulitis involving areas with potential airway com prom ise
Cavernous sinus throm bosis
Osteom yelitis
Outpatient therapy failure
Im m unocom prom ised patients: o
Neutropenia
o
Uncontrolled diabetes
o
Advanced HIV
o
Cancer patients undergoing chem otherapy
Ludwig angina
System ic involvem ent with significant dehydration
Patients unable to handle secretions
Patients unable to m anage infection at hom e because of physical or m ental disability or psychosocial factors
Discharge Criteria
Uncom plicated cases
Dental follow-up available in 24–48 hours
Pa ge 3 5 5
References 1. Am sterdam JT. Oral Medicine. In: Marx ed. Rosen's Em ergency Medicine; Concepts and Clinical Practice. 5th ed. St. Louis, MO: Mosby, 2002;892–908. 2. Benko K, Em ergency Dental Procedures. In: Roberts J, Hedges J, eds. Clinical Procedures in Em ergency Medicine. 4th ed. Philadelphia: W.B. Saunders, 2004;1317–1340. 3. Clerehugh V, Tugnait A. Diagnosis and m anagem ent of periodontal diseases in children and adolescents. Periodontol 2000. 2001;26:146–168. 4. Douglas AB, Douglas JM. Com m on Dental Em ergencies. Am Fam Phys. 2003. 5. Herrera D, et al. The Periodontal Abscess, Short-term clinical and m icrobiological efficacy of 2 system ic antibiotic regim es. J. Clin. Periodontol 2000 Jun; 27(6):387–404. 6. McLeod DE, Lainson PA, Spivey JD. Tooth loss due to periodontal abscess: a retrospective study. J Periodontol. 1997 Oct: 68(10):963–966. 7. Mulut M, et al. Fatal Descending Necrotizing Mediastinitis. Em erg Med J. 2004 Jan; 21(1):122–123. 8. Pappa H, Jones DC. Mediastinitis from odontogenic infection: A case report. Br Dent J. May 14, 2005;198(9):547–548. 9. Robert A. Bacteria in the m outh. Dent Update. April 2005;32(3):134–136, 39–140, 142. 10. Sawalha W, Ahm ad M. Case Report: Bilat Pleural em pyem a following periodontal abscess. Eastern Med Health J. 2001;(7):846–851. 11. Van Winkelhoff AJ, Ram s TE, Slots J. System ic antibiotic therapy in periodontics. Periodontol 2000. 1996;10:45–78. 12. Wayne DB, Trajtenberg CP, Hym an DJ. Periodontal disease: a review for the prim ary care physician. South Med J. 2001;94:925–932.
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Miscellaneous SEE ALSO: Toothache
Codes ICD9-CM 523 Gingival and periodontal diseases
ICD10 K05.2
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Perio rbital and Orbital C ellulitis
Periorbital
and Orbital Cellulitis Shari Schabowski
Basics Description Periorbital Cellulitis
Periorbital cellulitis is anatom ically distinguished by its location isolated to the tissues anterior to the orbital septum : o
Orbital septum is the connective tissue extension of the orbital periosteum that is reflected into the upper and lower eyelids.
o
Extension into the tissues deep to the orbital septum is rare because the septum represents a nearly im penetrable barrier.
Most com m only presents as a com plication of upper respiratory tract infection (URTI) and sinusitis: o
Swelling owing to inflam m atory edem a from vascular and lym phatic congestion
o
Not infected tissue
May occur as a com plication of a localized inflam m ation/infection in the eyelid or adjacent structures:
Pa ge 3 5 5
o
Blepharitis
o
Hordeolum
o
Dacryocystitis
o
Surrounding skin disruptions:
Insect bites
Minor traum a
Im petigo or other derm atologic disorders
Orbital Cellulitis
Inflam m atory process in the structures posterior to the orbital septum
Occurs secondary to extension from an adjacent structure: o
Sinusitis:
Most com m only ethm oid
o
Dental abscess
o
Retained foreign body in the orbit
o
Puncture wounds
o
Orbital fracture
o
Postoperative infection
o
Hem atogenous spread from a rem ote source
o
Rare cause—extension of periorbital cellulitis
Etiology Periorbital Cellulitis
Streptococcus pneum oniae
Staphylococcus aureus
Streptococcus pyogenes
Moraxella catarrhalis
H. influenzae (children younger than 5 years)
Gonococcus: o
May extend from conjunctivitis or dacryoadenitis
Consider nonbacterial cause.
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Orbital Cellulitis
S. pneum oniae
S. pyogenes: o
Currently streptococcal infections are the m ost com m on cause.
S. aureus: o
Com m on in puncture wounds
S. pyogenes
Staphylococcus epiderm idis
Anaerobes
Bacteroides
Gram -negative: o
Associated with traum a
Fungal infection—cerebrorhino-orbital phycom ycosis (CROP): o
Life-threatening disease presenting with orbital cellulitis
o
Rapidly fatal in 75% of cases
o
Presentation:
Eighty percent of cases occur in diabetic patients with a recent episode of diabetic ketoacidosis (DKA).
Predisposing factor: severe m etabolic acidosis
Toxic appearance
All age groups
More com m on in im m unocom prom ised patients
Begins in the paranasal sinuses
Proliferates in the blood vessels and causes throm bosis and necrosis
Bloody nasal discharge
Frequently presents with evidence of necrosis of the palate and/or nasal m ucosa
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Pediatric Considerations
In children younger than 2 years, H. influenzae is an im portant cause of bacterem ic periorbital cellulitis: o
Toxic appearance
o
Tem perature >39°C
o
Erythem atous and violaceous swollen eyelids
o
Dram atic decrease (80%) since Hib vaccine:
Incidence decreases significantly after two im m unizations.
o
Preceded by upper respiratory infection
Diagnosis Signs and Symptoms Periorbital Cellulitis/Orbital Cellulitis
Both will present with a unilateral, red, swollen eye.
Differences include: o
Anatom ic location
o
Extent of deep tissue involvem ent
o
Cause and m echanism of infection
o
Associated com plications
Periorbital Cellulitis
Periorbital erythem a, warm th, tenderness, and swelling
Often preceded by URTI o
Typically unilateral and involving the upper or the lower lid, rarely involving both
o
Gradual onset
o
Swelling m ay becom e predom inant sym ptom leading to obscured vision in affected eye.
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Orbital Cellulitis
Orbital involvem ent: o
Blurred vision or diplopia
o
Photophobia
Typically involves upper and lower lid: o
About 95% unilateral
Swelling m ay obscure vision in the affected eye.
Headache
Periorbital Cellulitis
Associated with low-grade fever usually 39°C:
o
Restricted, painful extraocular m ovem ents
o
Afferent pupillary defect
o
Conjunctival injection
o
Chem osis
o
Proptosis
Meningism us
Essential Workup
Physical exam to rule out orbital involvem ent: o
Orbital involvem ent m ay lead to serious com plications.
o
High level of suspicion:
Patients who appear toxic
Orbital pain
Painful restriction of eye m ovem ent
Proptosis swelling of upper and lower lids
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Com plete neurologic exam ination to rule out CNS involvem ent: o
High level of suspicion for CNS penetration:
Altered m ental status
Meningism us
Visual loss
Identify com plicating m edical problem s: o
Im m unocom prom ise
o
Diabetes
Tests Lab
Supportive but not diagnostic
CBC: o
WBC 15,000 m ay suggest bacterem ic periorbital cellulitis.
Blood culture
Gram stain and culture of tissue aspirate or swab of draining purulent m aterial: o
Chocolate agar plate should be used when gonorrhea suspected.
P.831
Imaging CT scan orbits:
Indicated if: o
Suspect orbital cellulitis or traum atic penetration of the orbital septum
o
Failure to respond to parenteral antim icrobial therapy
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Dem onstrates extent: o
Orbital cellulitis
o
Sinusitis
o
Orbital em physem a
o
Subperiosteal abscess
o
Presence of foreign body
Diagnostic Procedures/Surgery Lum bar puncture:
Rule out CNS involvem ent.
Consider in patients with: o
Signs or sym ptom s of m eningism us
o
Toxic appearance
o
Patients at risk of H. influenzae type B: younger than 4 years and non–Hib vaccinated
Differential Diagnosis Periorbital Cellulitis
Lack of fever and leukocytosis suggests noninfectious cause: o
Insect bite
o
Allergy
Dacryoadenitis
Dacryocystitis
Hordeolum
Orbital cellulitis
Orbital Cellulitis
Periorbital cellulitis
Contusion
Dacryoadenitis
Dacryocystitis
Hordeolum
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Retrobulbar hem orrhage
Cavernous sinus throm bosis
Cranial nerve palsy
Inflam m atory orbital pseudotum or
Graves disease
Orbital rhabdosarcom a
Treatment Initial Stabilization
IV fluids for vom iting/dehydration/sepsis
0.9% norm al saline (NS) 500-m L bolus (20 m L/kg children) for hydration and resuscitation
ED Treatment Periorbital Cellulitis
Antibiotics: o
Typically responds to oral antibiotics unless appears bacterem ic or toxic
o
IV antibiotics for severe infections/treatm ent failures
Antipyretics and pain m edication as needed
Orbital Cellulitis
Antipyretics
Pain m edication
Early adm inistration of parenteral antibiotics
Ophthalm ologic consultation
If sinusitis is the source, consider ear, nose, and throat (ENT) consultation.
Em ergent surgical intervention m ay be necessary.
If Bacteroides is suspected organism :
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o
Surgical débridem ent
o
Vancom ycin
Tetanus toxoid when appropriate
If proptosis leaves the cornea exposed: o
Lubricating drops (Lacri-Lube: 2 drops q2h–q4h PRN)
Suspect CROP: o
Am photericin B IV at highest tolerated dose
o
Topical am photericin B (1 m g/m L) irrigation or nasal packing
o
Local débridem ent
Medication (Drugs) Periorbital Cellulitis
Augm entin: 500 m g (peds: 45 m g/kg/24h) PO t.i.d.
Cephalexin: 500 m g (peds: 100 m g/kg/24h) PO q.i.d.
Cefazolin: 1 g (peds: 100 m g/kg/24h) IV q6h–q8h
Cefotaxim e: 1–2 g (peds: 150 m g/kg/24h) IV q6h–q8h
Clindam ycin: 600 m g (peds: 40 m g/kg/24h) IV q6h; 300 m g (peds: 20 m g/kg/24h) PO q.i.d.
Dicloxacillin: 500 m g (peds: 100 m g/kg/24h) PO q.i.d.
Vancom ycin: 500 m g (peds: 40 m g/kg/24h) IV q6h
Orbital Cellulitis
Ceftriaxone: 1–2 g (peds: 100 m g/kg/24h) IV q12h–q24h
Erythrom ycin ophthalm ologic ointm ent: applied q4h to lower cul-de-sac
Gentam icin: 5 m g/kg/24h IV
Metronidazole: 15 m g/kg IV load, then 7.5 m g/kg q6h
Nafcillin: 1–2 g (peds: 100 m g/kg/24h) IV q4h
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Vancom ycin: 1 g (peds: 40 m g/kg/24h) q12h
Follow-Up Disposition Periorbital Cellulitis
Toxicity
Progression of infection on oral antibiotics
Unable to arrange follow-up within 24–48 hours
High risk H. influenzae type B
Orbital Cellulitis
IV antibiotics
Observation for progression: o
Without visual findings or restriction
Surgical incision and drainage
Periorbital Cellulitis
Localized infection and inflam m ation
Tolerating oral antibiotics
Good follow-up
Orbital Cellulitis Adm it all:
High risk of CNS penetration and ophthalm ologic com plications
References 1. Chang CH, et al. Antibiotic treatm ent of orbital cellulitis: an analysis of pathogenic bacteria and bacterial susceptibility. J Ocul Pharm acol Ther. 2000;16(1):75–79. 2. Danter EM, Jolly BT. Pediatric ophthalm ology. Em erg Med Clin North Am . 1995;13(3):669–680.
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3. Ghosh C. Periorbital and orbital cellulitis after H. influenzae B vaccination. Ophthalm ology. 2001;108:1514–1515. 4. Jain A, Rubin PA. Orbital cellulitis in children. Int Ophthalm ol Clin. 2001;41(4):71–86.
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Peripheral Neuro pathy
Peripheral
Neuropathy Minh V. Le
Basics Description Peripheral neuropathy is a general term for peripheral nerve disorders of any cause.
Diagnosis Signs and Symptoms
Sensory nerve dysfunction: o
Num bness, localized tingling, paresthesias, dysesthesias
o
Vibration and position sensations decreased with large-fiber neuropathy
o
Pain and tem perature sensation decreased with sm all-fiber neuropathy
o
Deep tendon reflexes decreased secondary to decrease sensation of afferent lim b
Motor nerve dysfunction:
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o
o
Weakness
Distal greater than proxim al
Occasionally fasciculations
Muscle atrophy, dim inished tone with long-standing m otor nerve involvem ent
o
Loss of reflexes secondary to slowing of conduction along m otor nerve efferent lim b
Autonom ic nerve dysfunction: o
Orthostasis, constipation, urinary retention, or im potence
Essential Workup
Studies based on acuteness, severity of neuropathy, and m ost likely diagnosis
Neurologic consult early if acute and severe sym ptom s
Tests Lab
Basic m etabolic panel
CBC
Liver function tests
Urinalysis
Thyrotropin-stim ulating horm one
HIV, or vitam in B 1 2 based on individual presentations
ECG
Imaging Chest radiograph if indicated
Diagnostic Procedures/Surgery
Electrom yographic studies, nerve conduction studies, and nerve biopsy per neurologic consult on adm ission or outpatient follow-up
Lum bar puncture as appropriate
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Differential Diagnosis
Focal: o
Entrapm ent
o
Com m on sites of com pression:
Carpal, ulnar tunnel
Tarsal tunnel
Peroneal
Myxedem a
Rheum atoid arthritis
Am yloidosis
Acrom egaly
o
Com pressive neuropathies
o
Traum a
o
Ischem ic lesions
o
Diabetes m ellitus (DM), vasculitis
o
Leprosy
o
Sarcoidosis
o
Neoplastic infiltration or com pression
Multifocal (m ononeuropathy m ultiplex): o
DM
o
Vasculitis:
Polyarteritis nodosa
System ic lupus erythem atosus
Sjögren syndrom e
o
Sarcoid
o
Leprosy
o
Malignancy related
o
HIV/AIDS
o
Hereditary predisposition to pressure palsies
Sym m etric: o
Endocrine:
Most com m on is DM
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Hypothyroidism
P.833
o
o
Medications:
Isoniazid
Lithium
Metronidazole
Phenytoin
Cim etidine
Hydralazine
Am itriptyline
Am iodarone
Nutritional diseases:
Alcoholism
B 1 2 /folate deficiency
Thiam ine
o
Critical illness neuropathy
o
Hypophosphatem ia
o
Guillain-Barré syndrom e
o
Toxic neuropathy:
o
Carbon m onoxide
Acrylam ide
Carbon disulfide
Ethylene oxide
Organophosphate esters
Lead
Myelopathy m im icking peripheral neuropathy:
Back pain
Saddle anesthesia
Lower extrem ity weakness
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Treatment Pre Hospital
Pain control as needed
Airway protection as indicated
Initial Stabilization Establish airway protection with severe acute peripheral neuropathy, such as Guillain-Barré syndrom e.
ED Treatment Variable depending on acuity of sym ptom s
Medication (Drugs)
Variable depending underlying diagnosis
Neurontin is often effective: 300 m g PO t.i.d. up to 1800 m g/d.
Follow-Up Disposition Admission Criteria
Respiratory distress or acute gait disturbance
Intractable pain
Discharge Criteria Stable respiratory and gait status with outpatient follow-up
References 1. England JD, Asbury AK. Peripheral Neuropathy. Lancet.
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2004;2151–2161. 2. Morgenlander JC. Recognizing peripheral neuropathy. Postgrad Med. 1997;102:71–80. 3. Pascuzzi RM, Fleck JD. Acute peripheral neuropathy in adults. Neurol Clin. 1997; 15(3):529–547. 4. Poncelelet AN. An algorithm for the evaluation of peripheral neuropathy. Am Fam Physician. 1998;57:755–764.
Codes ICD9-CM 356.9
ICD10 G62.9
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Peripheral Vascular Disease
Peripheral
Vascular Disease Sally Santen
Basics Description
Peripheral arterial vascular disease (PAD) consists of three inter-related m anifestations:
o
Chronic arterial insufficiency
o
Acute arterial insufficiency
o
Atheroem bolism
Atherosclerosis causes PAD: o
Patients with PAD m ay also have coronary artery and cerebrovascular disease.
Chronic arterial insufficiency (CAI): o
Progressive obstructing atherosclerotic disease causing subacute ischem ia and pain (claudication). Fifteen percent develop critical leg ischem ia.
o
Risks factors:
Age
Sm oking
Diabetes
Hyperlipidem ia
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o
Hypertension
Associated with m orbidity and m ortality of other form s of atherosclerosis (coronary artery disease, stroke)
o
Com plications:
Aneurysm
Throm bosis
Ulceration
Lim b loss
Acute arterial insufficiency (AAI): o
Caused by either arterial throm bosis (50%) or em bolism
o
Causes acute lim b ischem ia with signs and sym ptom s of the 6 Ps
Atheroem bolism : o
Caused by rupture or partial disruption of an atherosclerotic plaque (aorta, fem oral, iliac)
o
Gives rise to cholesterol em boli showers and obstructing arteriolar networks
o
May be precipitated by invasive arterial procedures such as cardiac catheterization
Etiology
Obstruction by atherosclerotic plaques (CAI)
Arterial throm bosis
Arterial em boli: o
Cardiac em boli from dysrhythm ias, valvular heart disease, or cardiom yopathy (80%)
o
Aneurysm s
o
Infection
o
Tum or
o
Vasculitides or foreign body
o
Throm bosis of plaques from preexisting CAI
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Atheroem bolism
Diagnosis Signs and Symptoms Chronic Arterial Insufficiency
Claudication: o
Aching pain in the calves (fem oropopliteal occlusion) or buttocks and thighs (aortoiliac region)
o
Occurs with activity and slowly relieved by rest
o
Classic claudication present in about half of patients with PVD
Severe disease presents with lim b pain at rest: o
Usually starting in the foot
o
Rapidly progressive claudication or ulceration
Physical Exam
Absent or decreased peripheral pulses
Delayed capillary refill with cool skin
Increased venous filling tim e
Bruits
Pallor and dependent rubor of the leg
Muscle and skin atrophy
Thickened nails and loss of dorsal hair
Ulcerations (especially toes or heels) or gangrene with severe disease
Acute Arterial Insufficiency Sudden onset of pain and pallor in extrem ity
Physical Exam
Six Ps:
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o
Pain (first sym ptom )
o
Pallor
o
Pulselessness
o
Poikilotherm ic
o
Paresthesias (late finding)
o
Paralysis (late finding)
Identification of a source of a possible em bolic process is crucial (atrial fibrillation, cardiom egaly).
Atheroembolism
Com plaint of cold and painful fingers or toes
Sm all atherosclerotic em boli m ay effect both extrem ities: o
Ischem ic and painful digits
o
“Blue toe syndrom e―
o
Livedo reticularis
Essential Workup
CAI: o
Ankle-brachial index (ankle systolic blood pressure [BP] divided by arm systolic BP)
o
Bedside test to determ ine whether CAI is present.
o
Ratio of 80–90% for occlusion of vessels proxim al to the popliteal vessels
Plethysm ography/Segm ental pressure m easurem ents: o
Uses m easurem ents of the volum e and character of blood flow to detect areas of CAI
o
Less widely available than US, therefore requires an experienced technician
o
Approxim ates US in sensitivity and specificity
Angiography: o
Determ ines details about the anatom y, including the level of occlusion, stenosis, and collateral flow
o
Useful where the diagnosis of AAI is uncertain or before em ergent bypass grafting
o
Advantage is intervention (atherectom y, angioplasty, or intralum inal throm bolytics) can be done at the
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tim e of diagnosis.
CT angiogram : o
CT is useful for diagnosis of occlusive aortic disease or dissection.
o
Rapidly available and reliable
o
Many centers have m oved to CT angiogram as the first-line diagnostic tool. The decision for operative or angiographic intervention is based on the CT angiogram .
o
Requires contrast, therefore m ay not be first line for patients with renal insufficiency
P.835
MRI: o
MRI is sensitive for evaluation of CAI and dissection.
o
Disadvantages are that MRI is tim e consum ing and expensive.
Operative revascularization: o
Depending on the location of the lesion and severity of disease, peripheral arterial disease can be treated by angiographic intervention (atherectom y, angioplasty, or intralum inal throm bolytics) or by operative revascularization.
Differential Diagnosis
Acute throm bosis or em boli
Arterial dissection
Deep venous throm bosis
Massive venous insufficiency
Com partm ent syndrom e
Buerger disease
Spinal stenosis
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Neuropathy
Bursitis
Arthritis
Reflex sym pathetic dystrophy
Treatment Pre Hospital
Maintain hem odynam ic stability with fluids.
Apply cardiac m onitor.
Place the ischem ic lim b at rest and in a dependent position.
Provide oxygen if low oxygen saturation or pulm onary sym ptom s.
Initial Stabilization
IV fluid bolus for hypotension
ECG, m onitor, pulse oxim etry
Supplem ental oxygen
ED Treatment
CAI: o
Antiplatelet and anticoagulant drugs m ay help but have not been definitively shown to prevent progression of CAI.
o
Clopidogrel m ay be used as first-line treatm ent.
Given that other form s of atherosclerosis are com m only present in patients with CAI, other m edications for m edical m anagem ent of CAI are cilostazol and pentoxifylline
o
Invasive therapy depending on the severity of obstruction:
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o
Atherectom y
Bypass grafting
Balloon angioplasty
Initiate m easures to prevent disease progression:
Tobacco cessation
Aggressive m anagem ent of hyperlipidem ia
Exercise therapy
AAI: o
Lim it further clot propagation with heparin.
o
Do not anticoagulate patients suspected of having an aortic dissection or sym ptom atic aneurysm .
o
Em ergent consultation with a vascular surgeon:
To determ ine which diagnostic study to best m ake the diagnosis
To begin arrangem ents for possible operative therapy or other intervention
o
Options for operative therapy include throm bectom y, em bolectom y, regional arterial throm bolysis, or bypass grafting.
o
Blood flow to the affected lim b m ust be re-established within 4–6 hours after onset of ischem ic sym ptom s.
o
Com plications of AAI include:
Com partm ent syndrom e
Irreversible ischem ia requiring am putation
Rhabdom yolysis, renal failure
Electrolyte disturbances
Atheroem bolism : o
Treat conservatively if a lim ited am ount of tissue is involved and renal function is not significantly com prom ised.
o
No available therapy for the ischem ic digits besides
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supportive wound care and analgesia o
Am putation for irreversibly necrotic toes
o
Vascular surgeon referral within 12–24 hours of ED visit
o
Prevent further em bolic events by a thorough investigation and correction of the source of atheroem boli.
Medication (Drugs)
Aspirin: 81–325 m g/d
Cilostazol: 100 m g b.i.d.
Clopidogrel: 75 m g/d
Heparin: 80 U/kg bolus IV followed by 18 U/h IV
Pentoxifylline: 400 m g t.i.d.
Follow-Up Disposition Admission Criteria
All patients with AAI are adm itted for evaluation and revascularization.
CAI: consider adm ission for rapidly progressive claudication or ischem ic pain at rest: o
To undergo heparinization and angiography to rule out an acute throm bosis
Atheroem bolism with large areas involved, significant pain, infection, or renal com prom ise
Discharge Criteria
Atheroem bolism :
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o
If they have sm all lesions, adequate pain controls, no evidence of renal com prom ise or superinfection, and follow-up within 24 hours.
CAI: o
No evidence of rapid progression, critical leg ischem ia, gangrene, or infection
Issues for Referral
CAI will need urgent referral to vascular surgery.
Atheroem bolism , depending on the origin of the em boli, m ay need referral to vascular surgery or to cardiology.
References 1. Belch JJ, Topol EJ, Agnelli G, et al. Critical issues in peripheral arterial disease detection and m anagem ent. Arch Intern Med. 2003;163:884–892. 2. Dorm andy JA, Rutherford RB. Managem ent of peripheral arterial disease. J Vasc Surg. 2000;31:S1–S296. 3. Halperin JL. Evaluation of patients with peripheral vascular disease. Throm bosis Res. 2002;106:V303–311. 4. Hiatt WR. Drug therapy: m edical treatm ent of peripheral arterial disease and claudication. N Engl J Med. 2001;344:1608–1621. 5. Mukherjee D, Yadav JS. Update on peripheral vascular diseases: from sm oking cessation to stenting. Cleve Clin J Med. 2001;68:723–733.
Miscellaneous SEE ALSO: Arterial Occlusion
Codes ICD9-CM 414.0
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ICD10 173.9
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Perirectal Abscess
Perirectal Abscess
Scott A. Miller
Basics Description Localized infection and accum ulation of purulent m aterial adjacent to anus or rectum
Genetics No genetic link has been described.
Etiology
Predom inant theory is anal crypt gland infection, with subsequent spread of infection to adjacent areas separated by m uscle and fascia: o
o
Perianal:
Most com m on
Usually with red bulge near anus
Ischiorectal:
Large potential space
May becom e very large before diagnosed
Can com m unicate posteriorly with other side form ing “horseshoe― abscess
o
Intersphincteric:
Contained at prim ary site of origin between
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internal and external sphincters o
May be difficult to diagnose
Supralevator:
Very deep above levator ani
Needs operative débridem ent under general anesthesia
Often system ic sym ptom s before diagnosis is m ade
Rarely caused by surgery, episiotom ies, traum a, or hem orrhoids
Bacterial cause is typically a m ix of stool pathogens: o
Escherichia coli
o
Bacteroides species
o
Peptostreptococcus species
o
Streptococcal species
o
Staphylococcus species
Associated diseases: o
Diabetes
o
Inflam m atory bowel disease
o
Malignancy
o
Im m unocom prom ised host
Diagnosis Signs and Symptoms History
Perianal pain: o
Constant
o
Aggravated by defecation, sitting, coughing, or sneezing
Pa ge 3 5 8
o
Perianal abscesses or ischiorectal abscesses that extend to perineum
Dull deep pelvic or rectal pain: o
More likely to have system ic toxicity owing to delayed diagnosis and spread of infection
o
Ischiorectal and supralevator abscesses
Rectal or perirectal drainage
Fever/chills
Constipation
Difficult urination
Physical Exam
Perianal swelling, erythem a, induration, fluctuance, tenderness: o
Intra-anal and intrarectal swelling: o
Intersphincteric and supralevator abscesses
o
May be only clue to abscess
Pelvic exam : o
Perianal and large ischiorectal abscesses
Thickened rectovaginal septum or tenderness
Hypotension or signs of dehydration if system ic infection present
Local anesthesia insufficient for thorough rectal exam ination and determ ination of extent of abscess on all but sm all, superficial abscesses (m ostly perianal)
Essential Workup
Careful history and physical param ount in m aking diagnosis
Have high index of suspicion for any constant perirectal pain.
Alert
Factors associated with significant m orbidity and
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m ortality: o
Delay in diagnosis or treatm ent:
Hem orrhoid m ost com m on m isdiagnosis
o
Inadequate initial exam ination or treatm ent
o
Associated system ic disease
Tests No labs or im aging routinely indicated
Lab
CBC: o
Wound culture: o
Leukocytosis with left shift
Consider if giving antibiotics.
Blood cultures: o
If concern for sepsis exists
Imaging
CT
MRI
Ultrasound: o
May be helpful in diagnosis and delineating extent of abscess
Diagnostic Procedures/Surgery
Incision and drainage is the definitive m anagem ent.
Barium enem a or anoscopy/proctoscopy m ay be helpful to diagnose supralevator or intersphincteric abscess bulging into rectum .
Differential Diagnosis
Anal fissure
Sentinel pile in the posterior m idline or anterior m idline
Throm bosed or inflam ed hem orrhoids
Anal ulcer (i.e., HIV)
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Proctitis (i.e., gonococcal)
Anorectal carcinom a
Pediatric Considerations Rectal duplication in children
Treatment Initial Stabilization
IV fluids if septic or dehydrated
Pain m eds
P.837
ED Treatment
Antibiotics alone without drainage is contraindicated: o
Infection m ay worsen, leading to extensive soft tissue destruction, sepsis, or death.
o
Adm inister prior to surgery with valvular heart disease.
Incision and drainage (I&D) for all abscesses
Bedside drainage under local anesthetic: o
Sm all visible abscess, nontoxic patient (m ostly perianal and sm all superficial ischiorectal abscesses)
o
May attem pt needle aspiration initially to localize, but I&D m ust be done.
o
Radial incision close to anal verge:
Facilitates surgical excision of potential subsequent fistula
o
Elliptical or cruciate incision:
Ensure ongoing adequate drainage.
Pa ge 3 5 8
o
Explore cavity breaking any loculations.
o
Pack with iodoform gauze:
Rem ove/replace at 48-hour intervals.
Follow up with surgeon in 24–48 hours (evaluate for fistula).
Operative exam ination and débridem ent under anesthesia: o
All supralevator and intersphincteric abscesses
o
Ischiorectal abscesses that are large or have extensive necrosis
o
Unable to drain under local anesthetic
o
Im m unosuppressed (i.e., HIV, diabetics, transplant recipients, patients on chem otherapy)
Antibiotic adm inistration: o
Rarely necessary:
Marked cellulitis
Im m unosuppression
Valvular heart disease
System ic infection
Prosthetic device
o
If required, often need IV antibiotics and adm ission
o
Oral:
o
Am oxicillin clavulanate or ofloxacin
Intravenous:
Cefoxitin
Am picillin sulbactam
Com bination therapy with am picillin, gentam icin, and clindam ycin or m etronidazole
Postoperative care: o
Sitz baths t.i.d. 24 hours after I&D
o
High-fiber diet or bulking agent
o
Analgesic
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Alert
Large ischiorectal abscesses: o
Do not I&D if drainage already occurring inside the rectum .
o
I&D of draining abscess m ay result in high extrasphincteric fistula.
Medication (Drugs)
Am picillin: 500 m g IV q6h
Am picillin sulbactam : 1.5–3 g IV q6h
Am oxicillin clavulanate: 875 m g PO q12h or 500 m g PO q8h
Cefoxitin: 1–2 g IV q6h–q8h
Clindam ycin: 600 to 2,700 m g/d IV div. q6h–q12h
Gentam icin: 3–6 m g/kg/d IV div. q8h
Metronidazole: 7.5 m g/kg IV q6h
Ofloxacin: 400 m g PO q12h
Follow-Up Disposition Admission Criteria
Need for operative drainage
System ic toxicity/signs of sepsis
Discharge Criteria
Adequate I&D with return of discernible pus
Ability to am bulate and care for wound
Issues for Referral
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All should be referred to surgeon to evaluate for fistula:
Fistulas develop in 25% to 50% of anorectal abscesses.
References 1. Billingham RP, Isler JT, et al. The diagnosis and m anagem ent of com m on anorectal disorders. Curr Probl Surg. 2004;41(7):586–645. 2. Janicke DM, Pundt MR. Anorectal disorders. Em erg Med Clin North Am . 1996;14:757–788. 3. Marcus RH, Stine RJ, Cohen, MA. Perirectal Abscess. Ann Em erg Med. 1995;25(5):597–603. 4. Nelson R. Anorectal abscess fistula: what do we know?. Surg Clin N Am . 2002;82:1139–1151.
Miscellaneous SEE ALSO: Abscess; Anal Fissure; Hem orrhoid
Codes ICD9-CM 566
ICD10 K61.0
Pa ge 3 5 9
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Perito nsillar Abscess
Peritonsillar
Abscess Lee Shockley Kurt Whitaker
Basics Description
Consists of suppuration outside the tonsillar capsule
Most com m on deep infection of the head and neck
Occurs in all ages, m ost frequently from 10–40 years of age
Peritonsillar abscess (PTA) m ay be life threatening.
Com plications o
Airway com prom ise (uncom m on)
o
Sepsis (uncom m on)
o
Recurrence (2–22%)
o
Extension to lateral neck or m ediastinum
o
Spontaneous perforation and aspiration
o
Jugular vein throm bosis (“Lem ierre disease―)
Etiology Two theories explain the developm ent of PTA:
Direct bacterial invasion into deeper tissues in the patient with acute pharyngitis
Pa ge 3 5 9
Acute obstruction and bacterial infection of sm all salivary glands in the superior tonsil:
Most com m on pathogens o
α-hem olytic streptococcus
o
β-hem olytic streptococcus
o
Staphylococcal species
o
Anaerobes
o
Mixed organism s
Diagnosis Signs and Symptoms History
Sore throat (100%)
Fever (26–97%)
Voice change
Dysphagia
Drooling
Headache
Pain radiating to the ear
Decreased PO intake
Malaise
Physical Exam
Fever
Trism us (55–100%)
“Hot potato― voice
Tonsils/soft palate erythem atous
Suppuration
Unilateral peritonsillar bulge on soft palate
Uvular deviation away from affected side
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Halitosis
Tests
Usually a clinical diagnosis m ade by visually exam ining oropharynx
May be difficult with severe trism us
Lab
Throat culture and m onospot
CBC and culture of the abscess contents m ay be useful in som e cases.
Imaging
Bedside intraoral ultrasound (US): o
High-frequency endocavity US transducer with a lubricated latex cover is used.
o
Can aid identification and localization of abscess in the hands of em ergency physicians
o
A cooperative patient can be instructed to place the transducer at the point of m axim al tenderness.
Soft tissue lateral neck: o
If suspicion for epiglotitis or retropharyngeal abscess exists
Chest radiograph o
With severe respiratory sym ptom s or draining abscess
CT scan of neck: o
If suspicion exists for other deep space infection of the neck, CT m ay be indicated.
Diagnostic Procedures/Surgery Needle aspiration is diagnostic and often curative.
Differential Diagnosis
Peritonsillar cellulitis
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Epiglottitis
Retropharyngeal abscess
Peripharyngeal abscess
Tracheitis
Meningitis
Retropharyngeal hem orrhage
Dystonic reactions
Cervical osteom yelitis
Cervical adenitis
Epidural abscess
Other deep space infection of the neck
Treatment Pre Hospital
Rarely associated with airway em ergencies, but diagnosis is likely to be uncertain in transport, so suction and intubation equipm ent should be at the bedside,
Pulse oxim etry, supplem ental oxygen
Cardiac m onitor
IV access
Pediatric Considerations
PTA occurs in children (younger than 18 years) in 24–39% of reported cases.
Young children m ay need sedation or general anesthesia if incision and drainage (I&D) or aspiration of the abscess is attem pted.
Obtain soft-tissue lateral neck radiograph before oral exam ination in young children with sym ptom s of upper airway obstruction.
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Initial Stabilization
Sam e as for pre hospital
Airway m anagem ent m ay be necessary.
Equipm ent for intubation and cricothyroidotom y should be available
ED Treatment
Antibiotics should be adm inistered.
A single dose of steroids m ay im prove sym ptom s.
Adequate anesthesia prior to aspiration or I&D procedures is im portant.
No clear benefit has been found of one drainage technique over another: o
Needle drainage:
Successful 87–93%
Should be perform ed by person experienced in drainage procedure and adept at advanced airway techniques
Less painful, less invasive than I&D
The internal carotid artery lies about 2.5 cm posterolaterally to the tonsil; sheathing the aspiration needle to prevent introduction of the needle to Table o f C o ntents > Phalangeal Injuries, F o o t
Phalangeal
Injuries, Foot Taylor Young Cardall
Basics Description
The phalanges of the foot are prone to injury.
Fifth (or sm all) toe m ost com m only affected
Etiology
Usually the result of direct traum a
Stubbing the toe, kicking a hard surface, or dropping a heavy object onto toes m ost com m on m echanism s of injury
Diagnosis Signs and Symptoms History History m ay predict the type of injury found and should include:
Tim e of injury
Mechanism
Pa ge 3 6 0
History of previous traum a
Status of tetanus im m unization if laceration is present
Physical Exam
Tenderness, swelling, crepitus, and ecchym osis of affected digit
Subungual hem atom as are often present.
Lacerations or crush-type wounds
Docum ent neurovascular status of the affected digit.
Essential Workup Radiographs of involved digit
Tests Imaging
Radiographs of involved digit
Lateral view m ay be m ost sensitive.
Differential Diagnosis
Fracture
Contusion
Abrasion/laceration
Dislocation
Treatment Pre Hospital
Ice to affected digit
Direct pressure and dressing to any wounds
Initial Stabilization
Ice to affected digit
Direct pressure and dressing to any wounds
Pa ge 3 6 0
ED Treatment
Fractures involving the proxim al phalanx and interphalangeal (IP) joint of the hallux: o
Nondisplaced, nonintra-articular fractures m ay be placed in a short-leg walking cast with toe extension for com fort.
o
Displaced, nonintra-articular fractures:
Closed reduction with digital block anesthesia
Longitudinal traction
Placem ent in short-leg walking cast with toe extension
o
Intra-articular fractures of the hallux m erit orthopedic consult:
Frequently treated with open reduction and internal fixation
Fractures involving the proxim al phalanx and IP joint of the lesser toes: o
Rarely cause long-term disability
o
Nondisplaced fractures:
Treat with splinting or buddy taping
Gauze padding between the taped toes to prevent skin breakdown
o
Displaced fractures:
Closed reduction by digital block anesthesia
Longitudinal traction
Buddy taping or splinting
o
Hard-sole shoe, weight bearing as tolerated
o
Oral analgesics for pain
o
Pain usually resolved by two to three weeks
IP joint dislocations: o
Closed reduction by digital block anesthesia
o
Longitudinal traction with gentle downward pressure
Pa ge 3 6 0
on distal phalanx o
Buddy tape to adjacent toe
o
Unstable or unsuccessful reductions require orthopedic consultation
o
Oral analgesics for pain
Distal tuft fractures: o
Subungual hem atom as should be drained.
o
Nail-bed laceration repair m ay be necessary. P.843
o
Buddy tape digit to adjacent toe.
o
Weight bearing as tolerated
o
Oral analgesics for pain
o
Pain usually resolved in two to three weeks
Open fractures: o
Orthopedic consultation
o
Prophylactic antibiotics
Medication (Drugs)
NSAIDS are useful treating acute pain: o
Ibuprofen 800 m g (peds: 5–10 m g/kg) PO t.i.d.
Narcotic analgesics m ay be required for severe pain:
Cephalexin: 1 g IM/IV in ED (peds: 50–100 m g/kg IM/IV in ED) for open fractures
Follow-Up Disposition
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Admission Criteria
Intra-articular fractures involving the proxim al phalanx of the great toe
Unstable or blocked dislocations
Open fractures require orthopedic consultation in the ED.
Discharge Criteria All other fractures m ay be discharged with orthopedic follow-up in 2–3 weeks to evaluate healing.
Issues for Referral Patient copies of any radiographs obtained m ay facilitate early follow-up.
References 1. Ho K, Abu-Laban RB. Ankle and foot. In: Marx JA, ed. Rosen's Em ergency m edicine: concepts and clinical practice. 5th ed. St. Louis, MO: Mosby, 2002:706–735. 2. Kensinger DR, Guille JT, Horn BD, et al. The stubbed great toe: im portance of early recognition and treatm ent of open fractures of the distal phalanx. J Pediatr Orthop. 2001;21:31–34. 3. Wedm ore IS, Charette J. Em ergency departm ent evaluation and treatm ent of ankle and foot injuries. Em erg Med Clin North Am . 2001;18:85–113.
Codes ICD9-CM 959.7
ICD10 S93.4
Pa ge 3 6 1
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Phalangeal Injuries, Hand
Phalangeal
Injuries, Hand David Palafox
Basics Description
The fingers are body part m ost frequently injured in athletic or occupational accidents.
Children usually present with crush injuries.
Hyperextension injuries m ost com m only cause ligam entous injury or chip fractures.
Hyperflexion injury to the tip of digits m ay cause m allet finger injury with avulsion fracture at the insertion of the extensor tendon on the distal phalanx.
Crush injuries m ost com m only cause fractures and diffuse soft tissue injury.
Alert
Indications for reim plantation in am putation: o
Thum b
o
Single digit between proxim al interphalangeal (PIP) and distal interphalangeal (DIP) joint
o
Multiple digits
o
Am putation in child
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Pediatric Considerations
Injuries m ay be m ore difficult to diagnose in children who are unable to cooperate for a full exam ination.
Open epiphyses m ake radiographic interpretation less sensitive.
Careful repeated exam ination and protective splinting are necessary.
Etiology Accident
Diagnosis Signs and Symptoms
Pain in the area of injury
Swelling and ecchym osis
Deform ity, laceration, burn, or am putation of the digit
Loss of m otion in the digit involved
Alert High-presure injection injury requires im m ediate consult to orthopedic hand surgeon.
Essential Workup
Careful history and com plete physical: o
Explore all wounds fully to identify tendon injury or foreign body and perform two-point discrim ination testing.
o
Radiographic series of the affected hand if there is any suggestion of m ore than a m inor superficial injury
Special attention directed at assessing individual tendon
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status, neurovascular integrity, and identifying rotational deform ity
Exam ination conducted first to assess function, then under anesthesia, and finally with tourniquet if needed to allow a bloodless field for better exam ination of lacerated areas o
For distal digits, an elastic band can be used at the base of the digit.
Tests Imaging Plain radiography of involved digits including true lateral and oblique views
Differential Diagnosis
Tendon laceration/rupture; partial/com plete
Com plicated open injuries m ay include several injuries, and the entire hand should be exam ined carefully.
Beware of lacerations over dorsal m etacarpal-phalangeal areas, which m ay be “fight bites― (hum an bites).
Pediatric Considerations Many fractures in children are torus (buckle) fractures of the phalanges.
Treatment
Most phalangeal dislocations are dorsal or dorsolateral: o
These m ay be reduced under digital block.
o
Gentle distraction, hyperextension, and guiding the base of the dislocated phalanx into proper position with m ild pressure
o
Always check for stability postreduction by having
Pa ge 3 6 1
patient perform active range of m otion (ROM).
Sim ple im pacted transverse or sm all corner fractures not exceeding 25% of a joint surface and dislocations: o
Treated with “buddy― splinting in functional position or padded splint in neutral position
o
Splint for several days, with arrangem ents for appropriate follow-up within a week.
P.845
Unstable fractures (rotational deform ity, oblique fractures, fractures involving larger portion of a joint, angulated fractures, or significant epiphyseal injuries): o
Splinted and referred for urgent orthopedic care
Subungual hem atom a: o
Blood released by using a heated paper clip, electric cautery, or a hole drilled in the nail with an 18-gauge needle
o
This injury does not have to be treated as open injury just because of subungual hem atom a.
Nail avulsions: o
Repair of nail bed lacerations
o
Splinting of the eponychium and germ inal m atrix to avoid adhesions
o
The avulsed nail can be used or a sm all piece of gauze or foil can be inserted in the area.
Many other lacerations can be left open with protective cover and allowed to heal secondarily.
Pre Hospital
Most patients do not require em ergency m edical services (EMS) transport solely for phalangeal injury.
Cautions:
Pa ge 3 6 1
o
Prehospital personnel should not attem pt to reduce a phalangeal dislocation at the scene unless there will be an unusually long transport tim e or there is vascular or neurologic com prom ise:
Reduction m ay be successful but prom pt the physician to m iss significant ligam entous injuries.
Alert
Am putated digits or tissue should be placed in clean m oist saline gauze, placed in plastic bag, and then placed in a separate bag with ice. Do not place digit in direct contact with ice!
Bleeding should be treated with appropriate direct pressure dressings.
Initial Stabilization
Assess for other, m ore serious injuries.
Rem ove all rings from injured hand.
Im m obilize the involved areas by proxim al-to-distal splinting.
Interm ittent ice pack application with constant elevation for the first 24 hours
Dislocations or severely deform ed fractures producing vascular com prom ise should be reduced im m ediately to a neutral position and im m obilized.
Medication (Drugs)
Evaluate tetanus status and vaccinate per im m unization schedule.
Mild analgesics should be offered, with nonsteroidal anti-inflam m atory drugs (NSAIDs) or hydrocodone usually
Pa ge 3 6 1
sufficient.
Antibiotics are not indicated for sim ple noncontam inated wounds: o
Indicated for high-risk wounds such as bite wounds or grossly contam inated injury
Follow-Up Disposition Patients with a stable fracture in an appropriate splint m ay be discharged for orthopedic follow-up.
Pediatric Considerations
Sim ple fractures can be treated with splinting if no significant rotational deform ity.
Epiphyseal fractures (Salter-Harris injuries) m andate orthopedic referral
Admission Criteria
Open joint injuries or fractures usually adm itted for irrigation, débridem ent, and early repair
Closed injuries requiring surgical m anagem ent m ay be adm itted for early operative intervention: o
Acceptable to wait a day or two for sem ielective repair of clean injuries
References 1. Am erican College of Radiology, Expert Panel on Musculoskeletal Im aging. Acute Hand and wrist traum a. 2001. 2. Am erican Society for Surgery of the Hand. The Hand: Exam ination and Diagnosis. 3rd ed. New York: Churchill Livingstone; 1990. 3. Am erican Society for Surgery of the Hand. The Hand: Prim ary
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Care of Com m on Problem s. 2nd ed. New York: Churchill Livingstone; 1990.
Codes ICD9-CM 959.5
ICD10 S60.9
Pa ge 3 6 1
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Pharyngitis
Pharyngitis
David A. Vitberg Brian J. Browne
Basics Description
Inflam m ation/infection of the pharynx
Third m ost com m on com plaint for physician visits
200 visits per 1,000 population annually in the United States
$300 m illion annually to diagnose and treat
Strep throat: o
15–30% childhood pharyngitis
o
5–10% adult pharyngitis
o
Unusual in children younger than 3 years
o
Peak ages 4–11 years
o
Peak m onths January through May; also start of school year
Etiology
Viral: o
Most com m on cause of infectious pharyngitis
o
Rhinovirus (20%)
o
Coronavirus (>5%)
o
Adenovirus (5%)
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o
Herpes sim plex virus (4%)
o
Parainfluenza virus (2%)
o
Influenza virus (2%)
o
Coxsackievirus ( Table o f C o ntents > Pheo chro m o cyto m a
Pheochromocytoma David N. Zull
Basics Description
Catecholam ine-producing tum or arising from the chrom affin tissues of the sym pathetic nervous system
Origin from the adrenal m edulla or sym pathetic ganglia: o
80% solitary adrenal (usually the right side)
o
10% bilateral (usually inherited form )
o
10% extra-adrenal in location
Location: o
Abdom inal, within m esenteric ganglia (86%)
o
Thorax (10%)
o
Neck (3%)
o
Urinary bladder (1%)
o
10% m alignant (usually inherited form )
Incidence
Incidence ranges from 0.05–0.2% of hypertensive patients, but higher proportion of patients with severe hypertension.
2 per m illion population per year
Peaks in the 3rd to 5th decade, 10% in children
Pa ge 3 6 4
Male = Fem ale
In about half of cases, the diagnosis is m ade postm ortem .
Ten percent are asym ptom atic, found incidentally by CT scanning.
Genetics
Inherited form in 25%
Autosom al dom inant trait with pheochrom ocytom a (Pheo) alone or in com bination with other endocrine tum ors
Usually associated with m ultiple endocrine neoplasia (MEN), less so with von Hippel-Lindau (VHL) disease: o
MEN 2A (m edullary thyroid carcinom a [CA], Pheo, and hyperparathyroidism )
o
MEN 2B (m edullary thyroid CA, Pheo, oral m ucosal neurom as, skeletal and bony abnorm alities)
o
VHL (hem angiom as of the retina, cerebellum , and brainstem , with renal tum ors)
Other associated diseases include neurofibrom atosis, tuberous sclerosis, Sturge-Weber syndrom e, and paragangliom as of the neck.
Etiology
The tum or synthesizes and stores catecholam ines in the sam e m anner as the norm al adrenal m edulla.
Most secrete norepinephrine and epinephrine, but m ay secrete predom inantly one or the other.
Paroxysm al release of catecholam ines
Spontaneously owing to changes in blood flow or tum or necrosis
Direct pressure on the gland from external forces (traum a, exercise)
Precipitation of release (opiates, glucagons, m etoclopram ide, histam ine)
Pa ge 3 6 4
Augm entation of catecholam ine effect (tricyclic antidepressants [TCAs], beta-blockers, and sym pathom im etics)
Diagnosis Signs and Symptoms History
Hypertension—m oderate to severe, refractory to treatm ent
40%—paroxysm s with norm al blood pressure (BP) between episodes
30%—sustained hypertension with paroxysm s
30%—sustained hypertension without paroxysm s
Classic features of paroxysm s: o
Sudden onset
o
Duration: m inutes to hours
o
Intervals: days to m onths
o
Increasing frequency, duration, and severity with tim e
Clinical characteristics: o
Hypertensive crisis or urgency
o
Headache
o
Tachycardia/palpitations
o
Profuse diaphoresis
o
Apprehension/anxiety
o
Precipitants (see Etiology)
o
Other clinical m anifestations
o
Hypotension (decreased plasm a volum e and blunted sym pathetic reflexes)
Pa ge 3 6 4
o
Orthostasis
o
Shock associated with traum a or surgery
Associated sym ptom s: o
Chest pain (m yocardial ischem ia, dissection)
o
Syncope (arrhythm ia, hypotension)
o
Abdom inal pain, vom iting (tum or necrosis, m esenteric ischem ia)
o
Trem ors, sweating, increased heart rate
o
Weight loss/fevers (increased m etabolic rate)
o
Diarrhea (if vasoactive intestinal peptide [VIP] producing tum or)
o
Flushing or pallor
o
Lethargy, confusion (hypertensive encephalopathy)
o
Focal neurologic findings (cerebral vascular accident [CVA])
o
Acute hem orrhagic tum or necrosis
o
Acute abdom en
o
Marked hypertension followed by declining BP leading to hypotensive shock
Physical Exam
Moderate to severe hypertension, often with orthostatic changes
Tachycardic, diaphoretic, evidence of weight loss
No palpable m asses (tum ors tend to be sm all)
Essential Workup
Accurate BP determ ination
ECG: o
Ischem ia
o
Dysrhythm ias
Tests
Pa ge 3 6 4
Lab
CBC: o
Elevated hem oglobin owing to dim inished plasm a volum e
o
Indicated when abdom inal pain/infection
Electrolytes, BUN, creatinine, glucose: o
Lactic acidosis
o
Renal failure secondary to hypertension/renal dam age
o
Hyperglycem ia owing to im paired response to insulin and effect of catecholam ines
o
Hypercalcem ia owing to excess parathyroid horm one (PTH)
Urinalysis: proteinuria and hem aturia
Diagnostic Studies
Fractionated plasm a m etanephrine: o
Ninety-nine percent sensitive, 85% specific—excellent screening, but false-positives
o
Least likely to be interfered by m edications or stress
Clonidine suppression test if diagnosis uncertain (levels not suppressed if Pheo)
Provocative testing with glucagon is not recom m ended.
Twenty-four-hour urine collection for free catecholam ines, m etanephrine (total and fractionated), and vanillylm andelic acid test (VMA): o
Ninety-eight percent com bined specificity
o
Must include creatinine to verify adequate collection
o
Medications that interfere: levodopa, m ethyldopa, MAO inhibitors, labetalol, propanolol, radiographic contrast m edia, sym pathom im etics, benzodiazepines, TCAs, caffeine, nicotine
Pa ge 3 6 4
o
May require several collections
o
Should be done at the tim e of a paroxysm
Imaging
CT scanning sensitive for adrenal m asses >1 cm
MRI or positron em ission tom ography (PET) scanning useful in identifying extra-adrenal tum ors
Metaiodobenzylguanidine scan (MIBG) radionuclear scintiscan—high specificity for localization, but not sensitive enough to exclude Pheo
Chest radiograph for pulm onary edem a
CT head for CVA/intracranial bleed
Diagnostic Procedures/Surgery
Fine-needle aspiration is contraindicated.
Laparoscopic resection is feasible in m any cases.
P.853
Differential Diagnosis
Panic attack
Thyrotoxicosis
Cocaine or am phetam ine intoxication
MAO inhibitor reaction
Hypertensive crisis
Alcohol withdrawal
Severe m igraine
Treatment Initial Stabilization
Pa ge 3 6 4
IV access
Continuous cardiac/blood pressure m onitoring
ED Treatment
Hypertensive crisis: o
Alpha-blockade with phentolam ine—first-line agent
o
Nitroprusside for uncontrolled hypertension
o
Vigorous fluid resuscitation required as vasoconstriction is relieved
Beta-blockade (labetalol or esm olol): o
For further BP control
o
If tachycardia develops during induction of alpha-blockade
o
Never use alone: institution of beta-blockade without prior α-adrenergic blockade m ay exacerbate hypertension by antagonizing β-m ediated vasodilatation in sm ooth m uscle.
Ventricular tachydysrhythm ias: o
Beta-blockade
o
Am iodarone
o
Lidocaine
Medication (Drugs) Management of Hypertensive Paroxysm
Phentolam ine: o
2.5–5.0 m g IV bolus at 1 m g/m in
o
Repeat bolus q5m in to response.
o
Infusion: 100 m g in 500 m L D 5 W (dose as for nitroprusside)
Nitroprusside: o
0.5–10 µg/kg/m in IV infusion
Pa ge 3 6 4
Beta-blockade: o
Esm olol: load 500 µg/kg over 1 m inute, followed by 50 µg/kg/m in for 4 m inutes; if adequate therapeutic effect not achieved within 5 m inutes, repeat loading dose and increase infusion to 100 µg/kg/m in; repeat loading dose and titrate infusion rate upward at 50 µg/kg/m in q4–q5m in as needed; om it further loading doses once nearing therapeutic target.
o
Labetalol: begin with 10–20 m g IV; BP falls within 5 m inutes, m ax. effect at 10 m inutes; can double IV dose q15–q30m in until target reached.
o
Metoprolol: 5 m g IV q15m in until response
Mild to Moderate Hypertension
Doxazosin: 1–8 m g/d orally
Nicardipine: 5–15 m g IV over the first hour, then 3–5 m g/h infusion
Prophylaxis of hypertensive paroxysm (preoperative): o
Phenoxybenzam ine—start at 10 m g b.i.d. orally, titrate up 10 m g every other day until desired effect
o
Beta-blocker to control reflex tachycardia
Follow-Up Disposition Admission Criteria
Suspicion of pheochrom ocytom a in an ill patient m andates alpha-blockade and aggressive volum e expansion in a closely m onitored setting.
Hypertensive urgency or crisis
Cardiac arrhythm ias
Pa ge 3 6 5
End organ com prom ise: congestive heart failure (CHF), m yocardial infarction (MI), renal insufficiency, CVA, abdom inal pain
Discharge Criteria Stable patient with m ild hypertension m ay be referred for prom pt outpatient evaluation.
References 1. Brouwers FM, Lenders JWM, Eisenhofer G, et al. Pheochrom ocytom as as an endocrine em ergency. Rev Endocr Metab Disord. 2003;4:121–128. 2. Kercher KW, Novitsky YW, Park A, et al. Laparoscopic curative resection of Pheochrom ocytom as. Ann Surg. 2005;241(6):919–928. 3. Lenders JW, et al. Biochem ical diagnosis of pheochrom ocytom a: which test is best? JAMA. 2002;287:1427–1434. 4. Manger WM, Eisinhofer G. Pheochrom ocytom a: diagnosis and m anagem ent update. Curr Hypertens Rep. 2004;6:477–484. 5. Schifferdecker B, Kodali D, Hausner E, et al. Adrenergic shock—an overlooked clinical entity? Cardiol Rev. 2005;13(2):69–72. 6. Westphal SA. Diagnosis of a pheochrom ocytom a. Am J Med Sci. 2005;329(1):18–21.
Codes ICD9-CM 227.0
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Phim o sis
Phimosis
Daniel Firestone
Basics Description
True phim osis is the inability to retract the foreskin over the glans of the penis as a result of scarring.
The inability to retract a norm al, supple foreskin is not true phim osis.
The foreskin is rarely retractable at birth due to norm al adhesions between the glans and the inner prepuce.
Approxim ately 90% are retractable by three years of age, and 99% are retractable by age 17, as the epithelial cells that com prise sm egm a are shed.
Parents should be instructed not to forcibly retract the foreskin.
Etiology Possible causes of true phim osis include:
Traum a from forcible retraction of the foreskin
Repetitive bouts of diaper derm atitis
Recurrent balanoposthitis
Poor hygiene
Poorly perform ed circum cision
Congenital anom alies
Pa ge 3 6 5
Diagnosis Signs and Symptoms
Whitish, narrowed preputial opening of the foreskin
Dysuria, hem aturia
Poor urinary stream
Edem a, erythem a, and tenderness of prepuce
Balanoposthitis (inflam m ation of the glans and foreskin)
Ballooning of foreskin on urination in severe cases
Essential Workup
In the m ajority of cases, no workup is necessary.
In patients with severe stenosis, the com plication of an obstructive uropathy m ay occur.
This should be investigated by: o
Evaluation of kidney function:
o
Blood urea nitrogen and creatinine
Renal sonogram
Phim osis secondary to recurrent balanoposthitis should prom pt a workup for diabetes m ellitus: o
Urinalysis, serum glucose, or glycosylated hem oglobin (Hgb A1C)
Differential Diagnosis
Preputial adhesions are norm al in young children.
Balanoposthitis without phim osis
Treatment
Pa ge 3 6 5
Pre Hospital
Pre hospital personnel and fam ily m em bers should be instructed not to attem pt retraction of the foreskin prior to m edical evaluation.
Unwarranted attem pts m ay traum atize a norm al, nonretractable prepuce, or convert the situation to a m ore em ergent paraphim osis.
Initial Stabilization
None required in m ost cases
Exam ination should include an evaluation for potential com plications: o
Obstruction and vascular com prom ise of glans
These occur only in the m ost extrem e cases.
P.855
ED Treatment
Relieve obstructive uropathy, if present, with urethral catheterization or suprapubic aspiration.
If vascular flow to the glans is com prom ised, a dorsal slit m ust be m ade in the foreskin: o
Perform ed after achieving adequate penile block (see paraphim osis section for m ore detailed description of procedure)
o
This is rarely necessary in phim osis.
Potent topical steroids for a m ultiweek course have been reported to successfully reduce phim osis: o
Decision to prescribe should only be m ade in conjunction with a urologist
Pediatric Considerations
Pa ge 3 6 5
For foreskin incision, procedural sedation will likely be needed in place of penile-block.
Medication (Drugs) Pain control as required
Follow-Up Disposition Admission Criteria
Obstructive uropathy
Severe balanoposthitis with ischem ia or necrosis
Discharge Criteria
Ability to urinate
Adequate urologic follow-up
Issues for Referral
In uncom plicated cases, provide patients with urologic follow-up for conservative trial of topical steroids, elective dilation of the preputial opening, operative repair, or elective circum cision as necessary.
References 1. Webster TM, Leonard MP: Topical steroid therapy for phim osis. Can J Urol. 9:1492,2002. 2. Dewan PA, Tieu HC. Phim osis: Is circum cision necessary? J Pediatr Child Health. 1996;32(4):285–289. 3. Pontari MA. Phim osis and paraphim osis. In: Seidm an EJ, Hanno PM, eds. Current urologic therapy. 3rd ed. Philadelphia, PA: WB Saunders, 1994:392–397.
Pa ge 3 6 5
4. Super DM. Phim osis. In: Hoekelm an R, et al., eds. Prim ary pediatric care. St. Louis: CV Mosby, 1987: 1232–1234.
Miscellaneous SEE ALSO: Paraphim osis
Codes ICD9-CM 605
Pa ge 3 6 5
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Pityriasis Ro sea
Pityriasis Rosea
Nate Rudman
Basics Description
A com m on papulosquam ous rash of unknown etiology
Classically m anifests by a herald patch involving the trunk and proxim al extrem ities
Etiology
Unknown; weak evidence exists for an infectious (viral) cause
Herpes virus 6 and 7 have been suggested
Medications have been associated with a pityriasislike eruption: o
Barbiturates
o
Captopril
o
Clonidine
o
Gold
o
Isotretinoin
o
Metronidazole
o
Penicillam ine
Pa ge 3 6 5
Diagnosis Signs and Symptoms
Herald patch: o
Solitary, erythem atous, slightly raised papule 2–10 cm in diam eter
o
Seen in 50–90% of cases
Secondary eruption: o
Widespread salm on colored, elliptic, finely scaling 1-cm m acular or papular lesions
o
Longest axis along lines of skin tension (a “fir tree― distribution)
o
Generally follows herald patch by seven to 14 days
o
Lesions are concentrated on the trunk and proxim al extrem ities.
Pruritus accom panies rash in up to 75% of cases
Prodrom al sym ptom s m ay be seen in 5%:
o
Fever
o
Headache
o
Malaise
o
Arthralgias
o
GI sym ptom s
Atypical presentations including oral involvem ent and inverse pityriasis rosea are m ore com m on in children.
Oral lesions: o
Punctate hem orrhages
o
Ulcerations
o
Erythem atous m acules, and vesicles
Lesions concentrated on the face and distal extremities with m inim al trunk involvem ent characterize inverse pityriasis: o
Atypical form s of individual lesions occasionally occur
Pa ge 3 6 5
including papular, urticarial, pustular, and purpuric
Essential Workup
Syphilis testing: o
Secondary syphilis can m im ic pityriasis rosea
o
RPR or VDRL is required if the diagnosis is in question.
o
Especially with history of chancre or absence of herald patch
KOH preparation m ay be needed to differentiate the herald patch from tinea corporis: o
Atypical form s of individual lesions occasionally occur including papular, urticarial, pustular, and purpuric.
P.857
Differential Diagnosis
Herald patch: o
Num m ular eczem a
o
Tinea corporis
Generalized eruption: o
Secondary syphilis
o
Drug eruption
o
Guttate psoriasis
o
Kaposi sarcom a
o
Lichen planus
o
Occult m alignancy
o
Scabies
o
Seborrheic derm atitis
o
Tinea versicolor
Pa ge 3 6 5
Treatment Initial Stabilization None required
ED Treatment Pityriasis is treated sym ptom atically.
Medication (Drugs)
Diphenhydram ine: adult: 50 m g PO q.i.d.; peds: 5 m g/kg/d div. q.i.d.
Hydrocortisone: adult: 1% cream t.i.d.; peds: 1% cream t.i.d.
Prednisone: adult: 15–40 m g per day; peds: 0.25–0.5 m g/kg per day
Ultraviolet B (UVB): five daily erythem ogenic doses
Follow-Up Disposition Discharge Criteria Pityriasis rosea is a self-lim ited disease; adm ission is not required.
References 1. Allen R, Janniger CK, Schwartz RA. Pityriasis rosea. Cutis. 1995;56(4):198–202. 2. Bjornborg A. Epiderm al-derm al inflam m atory conditions of unknown etiology. In: Fitzpatrick TB, et al., eds. Derm atology in general m edicine. 4th ed. New York: McGraw-Hill,1993:1117–1123. 3. Gonzalez LM, Allen R, Janniger CK, Schwartz RA. Pityriasis rosea:
Pa ge 3 6 6
an im portant papulosquam ous disorder. Int J Derm atol. 2005 Sep;44(9):757–64. 4. Hartley AH. Pityriasis rosea. Pediatr Rev. 1999;20(8):266–269.
Codes ICD9-CM 696.3
ICD10 L42
Pa ge 3 6 6
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Placenta Previa
Placenta Previa
Roneet Lev
Basics Description
Im plantation of placenta over the internal cervical os
Uterine enlargem ent and cervical dilation cause placental vessels near the cervix to tear, resulting in vaginal bleeding
Placenta previa seen on ultrasound before 28 weeks frequently “m igrates― and does not end up as placenta previa at term .
Twenty percent of all antepartum hem orrhage
Classifications: o
Total placenta previa: cervical os is com pletely covered by placenta.
o
Partial placenta previa: cervical os is partially covered by placenta.
o
Marginal placenta previa: edge of placenta is at m argin of cervical os.
o
Low-lying placenta: placenta edge is close to cervical os—60% chance of vaginal birth.
Etiology
Unknown
Pa ge 3 6 6
Incidence: 1/300 births = 0.33% of pregnancies
Maternal m ortality: 0.03%
Perinatal m orbidity and m ortality: Triple increase: o
Associated with preterm delivery and fetal anom alies
Factors affecting location of im plantation: o
Abnorm al endom etrial vascularization
o
Delayed ovulation
o
Prior traum a to endom etrium
Risk Factors
Multiparity (1/20 grand m ultiparous patients versus 1/1,500 nulliparous)
Multifetal gestations (40% increase)
Prior C-section (up to 6 tim es increase; increases with num ber of prior C-sections; 1.9–4.1%)
Increased m aternal age (triple increase if age >30 years com pared with age 20 weeks’ gestation
First episode of bleeding typically occurs at 27–32 weeks.
Inciting factors—usually no cause; recent intercourse or heavy exercise m ay contribute.
Initial bleeding is often self-lim ited and not lethal.
Many cases are discovered on routine ultrasound, and patients are asym ptom atic.
Physical Exam
Never do a digital exam ination or instrum ent probing of the cervix in second-trim ester vaginal bleeding until placenta previa is ruled out.
If obstetric (OB) consult is not readily available, do a partial speculum insertion to identify if blood is from the os or vaginal lesion.
Blood seen at patient's feet is a sign of heavy bleeding.
Hypotension and tachycardia m ay indicate hem orrhagic shock.
Fetal heart tones should be m onitored along with other vital signs.
Essential Workup
Ultrasonogragraphy is diagnostic procedure of choice.
Placental edge at 5 m L of fetal cells in m aternal circulation (it takes only 0.1 m L to sensitize m other if Rh negative)
If coagulopathy suspected (rare): PT/PTT, fibrin-split products (FSP), fibrinogen (24 weeks should be transported to a facility that can handle high risk and prem ature delivery.
Place patient in left lateral recum bent position if hypotensive in second half of pregnancy.
O 2 and IV as with other patients
Initial Stabilization
Airway, breathing, and circulation m anagem ent (ABCs)
Two large-bore IVs with norm al saline (NS) or lactated Ringers (LR)
Left lateral recum bent position if hypotensive in second half of pregnancy
Fluid resuscitation
Blood transfusion for hem atocrit (Hct) 15 m L of fetal RBS
Follow-Up Disposition Admission Criteria Adm it all patients >20 weeks gestation with vaginal bleeding caused by placenta previa.
Discharge Criteria
Incidental finding of placenta previa by ultrasound at Table o f C o ntents > Pneum o m ediastinum
Pneumomediastinum Jennifer De La Pena Leon D. Sanchez
Basics Description
Presence of air or gas within the m ediastinum
May occur spontaneously or as result of traum a or other pathologic processes
Spontaneous pneum om ediastinum : o
Caused by extrapleural tracheobronchial tears:
Increased alveolar pressure or overdistension
Term inal alveolar rupture into the lung interstitium
Dissection of air into the hilum and subsequently the m ediastinum along a pressure gradient
Mediastinal air then dissects into the fascial planes m ost com m only into the tissues of the neck
o
Often in setting of a Valsalva m aneuver, in association with bronchospasm or inhalational drug use
Pa ge 3 6 9
o
Most com m only in young m en
Relatively rare, occurs in one in 30,000–40,000 hospital adm issions
Etiology
Prim ary or spontaneous pneum om ediastinum : o
o
Associated with forced Valsava m aneuvers:
Illicit inhalation drug use (cannabis, cocaine)
Childbirth
Forceful straining during exercise
Straining at stool
Coughing
Sneezing
Vom iting
Inflation of party balloons
Pulm onary function testing
Has been rarely described after dental extraction/procedures.
Secondary pneum om ediastinum : o
Secondary to thoracic barotraum a
o
Positive-pressure ventilation
o
Esophageal rupture (Boerhaave syndrom e)
o
In association with m ediastinal infection caused by gas-form ing organism s
Rarely develops into a tension pneum om ediastinum : o
Life-threatening event
o
Usually in patients on positive pressure ventilation
Diagnosis Signs and Symptoms
Pa ge 3 7 0
Chest pain: o
Sharp
o
Pleuritic
o
Often positional
Dyspnea
Neck pain: o
Occurs in association with dissection of air into soft tissues of neck
o
Often described as “neck swelling,― “neck pain,― “throat pain,― or “difficulty swallowing―
Subcutaneous em physem a o
Most com m only located to the supraclavicular area and anterior neck
Ham m an crunch: Presence of a crinkling or crepitant sound that varies with heartbeat
Essential Workup
Exclude secondary causes, notably esophageal rupture
Chest radiography
Tests Lab CBC if there is suspicion of m ediastinitis
Imaging
Chest radiograph: o
Most valuable initial test
o
Im portant to include lateral view because m ediastinal air is often m issed on posterior-anterior view
o
Excludes pneum othorax
o
Identification of a pleural effusion or parenchym al infiltrate suggests an esophageal rupture.
Pa ge 3 7 0
o
Negative in up to 30% of cases
Chest CT: o
Im aging test of choice if suspicion is high but chest radiograph is negative
Esophagram with Gastrografin: o
Study of choice to exclude diagnosis of esophageal rupture
Differential Diagnosis
Pericarditis
Pneum othorax
Pulm onary em bolus
Pneum onia
Coronary ischem ia
Aortic dissection
Treatment Initial Stabilization
IV line
Oxygen
Cardiac m onitoring
Pulse oxim etry
P.867
ED Treatment
Spontaneous pneum om ediastinum : o
Does not require specific treatm ent
o
Efforts should focus on pain relief and reassurance once diagnosis is confirm ed.
Pa ge 3 7 0
o
High-flow oxygen will facilitate the reabsorption of nitrogen and provide com fort.
o
Condition is self-lim iting and m ay be expected to resolve over two to five days
Secondary pneum om ediastinum : direct therapy toward underlying cause
Follow-Up Disposition Admission Criteria
Secondary pneum om ediastinum
Associated pneum othorax
Possibility of esophageal rupture has not been excluded
Abnorm al vital signs
Discharge Criteria
Spontaneous pneum om ediastinum
Norm al vital signs
No pneum othorax
Period of observation in the ED with im provem ent in sym ptom s
Close outpatient follow-up
References 1. Brody S, Anderson G, Gutm an J. Pneum om ediastinum as a com plication of “crack― sm oking. Am J Em erg Med. 1988;6:241–243. 2. Chen SC, Lin FY, Chang KJ. Subcutaneous em physem a and pneum om ediastinum after dental extraction. Am J Em erg Med. 1999;17(7):678–680.
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3. Dekel B, Paret G, Szeinberg A, et al. Spontaneous pneum om ediastinum in children: clinical and natural history. Eur J Pediatr. 1996;155:695–697. 4. Gerazounis M, Athanassiadi K, Kalantzi N, et al. Spontaneous Pneum om ediastinum : a rare benign entity. 5. Jougin JB, Ballester M, Delcam bre F, et al. Assessm ent of spontaneous pneum om ediastinum : experience with 12 patients. Ann Thorac Surg. 2003;75(6):1711–1714. 6. Newcom b AE. Spontaneous pneum om ediastinum : a benign curiosity or a significant problem ? Chest. 2005;128(5):3298–3302. 7. Panacek E, Singer A, Sherm an B, et al. Spontaneous pneum om ediastinum : clinical and natural history. Ann Em erg Med. 1992;21:1222–1227.
Codes ICD9-CM 518.1 Interstitial em physem a
ICD10 J98.2 Interstitial em physem a
Patient Teaching Prevention Caution against use of inhalational drugs or any activity associated with Valsalva-type or breath-holding m aneuvers.
Pa ge 3 7 0
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Pneum o nia, Adult
Pneumonia, Adult
Jason Imperato
Basics Description
6th leading cause of death in the United States o
Num ber-one infectious cause
o
5 m illion cases per year
o
500,000 hospital adm issions per pear
o
Most deaths occur in the elderly or im m unosuppressed.
Com orbid conditions: o
Advanced age
o
Cigarette sm oking
o
Chronic obstructive pulm onary disease (COPD)
o
Diabetes m ellitus
o
Alcoholism
o
Malnutrition
o
Im m unosuppression
o
Sickle cell disease
o
Congestive heart failure
o
HIV/AIDS
Com plications: o
Sepsis
Pa ge 3 7 0
o
Lung abscess
o
Em pyem a
o
Extrapulm onary com plications (e.g. m eningitis)
o
Respiratory failure
Etiology
Classification based on the setting of initial infection
Com m unity acquired: o
Streptococcus pneum oniae
o
Haem ophilus influenzae
o
Klebsiella pneum oniae
o
Moraxella catarrhalis
o
Staphylococcus aureus
o
“Atypicals―:
o
Mycoplasm a pneum oniae
Chlam ydia pneum oniae
Legionella pneum ophila
Viruses:
Influenza virus
Parainfluenza virus
Nosocom ial acquired (Includes above plus the following): o
Pseudom onas aeruginosa
o
Staphylococcus aureus
o
Aneorobes
o
Aspiration pneum onias are typically polym icrobial
Diagnosis Signs and Symptoms History
Cough
Pa ge 3 7 0
Sputum production
Fever
Chills
Rigors
Shortness of breath
Pleuritic chest pain
“Atypical― pneum onia is often present differently: o
Viral prodrom e
o
Gradual onset
o
Nonproductive cough
o
Low-grade fever
o
Absence of pleurisy and rigors
Physical Exam
Abnorm al vital signs: o
Tachypnea
o
Tachycardia
o
Hypoxia
o
Fever
Pulm onary exam ination: o
Dullness to percussion
o
Increased tactile frem itus
o
Egophony
o
Coarse rales
o
Rhonchi
o
However, pneum onia m ay be present in the absence of consolidation
Geriatric Considerations
Elderly patients have a higher m orbidity and m ortality from pneum onia.
Often present with atypical features.
Essential Workup
Pa ge 3 7 0
Pneum onia is both a clinical as well as a radiographic diagnosis.
Tests Lab
Nonspecific for identifying the etiology of the pneum onia
CBC with differential: o
WBC count >15,000/m m 3 suggests a bacterial cause.
o
A very high or very low WBC count predicts increased m orbidity.
Serum chem istries
Pulse oxim etry
Arterial blood gas
Sputum gram stain and culture
Blood cultures
Imaging Chest radiograph:
Chest radiograph findings are nonspecific for predicting a particular infectious etiology
May be deferred in young, healthy patients
The absence of chest radiograph findings should not preclude antim icrobial therapy in those with clinical pneum onia.
Findings suggestive of pneum onia include: o
Segm ental or subsegm ental infiltrate
o
Air bronchogram s
o
Abscess
o
Cavitation
o
Em pyem a
o
Pleural effusion
Diagnostic Procedures/Surgery Diagnostic thoracentesis:
Pa ge 3 7 0
Perform ed for large effusions, enigm atic pneum onia, and patients who fail to respond to standard therapy
Differential Diagnosis
Bronchitis
Pneum othorax
COPD
Asthm a
Congestive heart failure
Pulm onary em bolism
Foreign body aspiration
Occupational or environm ental exposure
Tum or
Treatment Pre Hospital
Supplem ental oxygen
IV access
Consider inhaled bronchodilators.
Consider endotracheal intubation in patients with severe respiratory distress.
Initial Stabilization
Supplem ental oxygen
IV access
Consider inhaled bronchodilators.
Consider endotracheal intubation in patients with severe respiratory distress.
IV fluid resuscitation
P.869
Pa ge 3 7 0
ED Treatment
Em piric antim icrobial therapy is necessary before definitive etiology is established.
The Am erican Thoracic Society has set guidelines for em piric therapy
Outpatient m anagem ent—no cardiopulm onary disease: o
Advanced generation m acrolide (azithrom ycin)
o
OR doxycycline
Outpatient m anagem ent—cardiopulm onary disease: o
Second or third generation cephalosporin (cefuroxim e)
o
OR β-lactam ase inhibitor com bination (am oxicillin/clavulanate)
o
PLUS m acrolide (azithrom ycin)
o
Alternatively, extended spectrum fluoroquinolone (levofloxacin) as a single agent
Inpatient m anagem ent—noncritical care setting o
Second generation cephalosporin (cefuroxim e) OR third generation cephalosporin (ceftriaxone) OR β-lactam and β-lactam ase inhibitor com bination (am picillin-sulbactam )
o
PLUS m acrolide (azithrom ycin or clarithrom ycin)
o
Alternatively, extended spectrum fluoroquinolone (levofloxacin) as a single agent
o
May add clindam ycin or m etronidazole if aspiration is suspected
Inpatient m anagem ent—critical care setting: o
Third generation cephalosporin with antipseudom onal activity (ceftazidim e)
o
May add vancom ycin for drug-resistant S. pneum oniae
Pa ge 3 7 1
Medication (Drugs)
Am oxicillin-clavulanate (Augm entin): 500 m g PO q12h
Am picillin-sulbactam (Unasyn) 1.5–3.0 g IV q6h
Azithrom ycin: 500 m g PO on day one and 250 m g PO on days 2 through 5
Ceftazidim e: 1 g IV q8h
Ceftriaxone: 1–2 g IV every day
Cefuroxim e: 0.75 and 1.5 g IV q8h
Clindam ycin: 150 and 450 m g PO q.i.d. or 300–600 m g IV q.i.d.
Levofloxacin: 500 m g PO/IV every day
Vancom ycin: 1 g q12h
Follow-Up Disposition Admission Criteria
Decision to adm it is based on a scoring system based on age, com orbid illnesses, physical exam , and laboratory findings.
Good clinical judgm ent should supersede a strict interpretation of the scoring system .
Age >50 years old
Significant com orbid illnesses o
COPD
o
Diabetes m ellitus
o
Chronic renal failure
o
Chronic liver failure
Pa ge 3 7 1
o
Congestive heart failure
o
Neoplastic disease
o
Cerebrovascular disease
o
Post-splenectom y
o
Im m unosuppression
o
Chronic alcohol abuse
o
Malnutrition
o
Pregnancy
Physical exam ination findings: o
Altered m ental status
o
Respiratory rate >30
o
Systolic blood pressure 125
Laboratory findings: o
Arterial pH < 7
o
.35
o
BUN >30 m g/dL
o
Sodium 250 m g/dL
o
Hem atocrit Table o f C o ntents > Pneum o nia, Pediatric
Pneumonia,
Pediatric Gary D. Zimmer Karen P. Zimmer
Basics Description
Mechanism is often unknown.
Sources are oropharyngeal aspiration (m ost com m on) or hem atogenous.
Distribution depends on the organism : interstitial ( Mycoplasm a pneum onia, virus), lobar (Streptococcus pneum oniae), abscesses (Staphylococcus aureus), or diffuse (Pneum ocystis carinii)
Etiology
Haem ophilus influenza type b is becom ing rare secondary to m ass im m unization.
Less than 2 weeks: o
Group B Streptococcus species
o
Enteric gram -negative organism s
o
Respiratory syncytial virus (RSV)
o
Herpes sim plex virus
o
S. aureus
Pa ge 3 7 1
2 weeks to 3 m onths: o
Chlam ydia trachom atis
o
Parainfluenza virus
o
RSV
o
S. pneum oniae
o
S. aureus
o
H. influenza
o
Bordetella pertussis
3 m onths to 8 years: o
Viral (predom inate):
RSV
Parainfluenza virus
Influenza virus
Adenovirus
o
S. pneum oniae
o
H. influenza in unim m unized children
o
Group A streptococci
o
S. aureus
o
B. pertussis
Older than 8 years: o
M. pneum oniae m ost com m on
o
Viral
o
S. pneum oniae
Recent im m igrants from developing countries: o
Mycoplasm a tuberculosis
o
H. influenza
o
B. pertussis
Im m unocom prom ised (e.g., HIV, cancer): o
P. carinii
o
Mycoplasm a avium com plex
o
M. tuberculosis
o
Klebsiella pneum oniae
Pa ge 3 7 1
o
Pseudom onas aeruginosa
Less com m on: o
Fungal (coccidioidom ycosis, histoplasm osis)
o
Rickettsia (Q fever)
Diagnosis Signs and Symptoms
General (in all ages): o
Fever
o
Hypoxia
o
Tachycardia
o
Tachypnea, retractions
o
Rash (up to 10% of cases); usually m aculopapular
o
Nonspecific sym ptom s of toxicity
o
Pulm onary
o
Cough
o
Decreased breath sounds, ventilation
o
Dullness to percussion
o
Rales
Infants younger than 6 m onths: o
Altered behavior: listless, irritable
o
Apnea
o
Conjunctivitis (Chlam ydia 9,000)
o
Much overlap between viral and bacterial findings
o
Viral and M. pneum oniae tend to show interstitial infiltrates, often perihilar and peribronchial
o
Bacterial pneum onias m ay show focal lobar consolidation, focal alveolar infiltrates, and possibly effusion or pneum atocele.
o
Round pneum onia pathognom onic of S. pneum onia
o
Lateral decubitus film s m ay aid in dem onstrating effusion.
Tests Lab
CBC with differential: o
Patients with bacterem ia tend to have leukocytosis with left shift.
o
Sensitivity and specificity are poor.
o
Patients with WBC ≥20,000 or ANC >9,000 are at
Pa ge 3 7 1
increased risk of pneum ococcal bacterem ia. o
B. pertussis usually has elevated WBC with lym phocytosis.
Blood culture: o
Low yield ( Table o f C o ntents > Po iso ning, Antido tes
Poisoning,
Antidotes Suzan Mazor
Treatment N-Acetylcysteine (NAC)
Indications: o
Acetam inophen overdose
Warnings: o
Unpleasant odor, nausea, vom iting
o
Most effective if given in first 8 hours postingestion
Dose: o
PO: 140 m g/kg, then 70 m g/kg q4h for 17 doses
o
IV: (consult poison center) 150 m g/kg in 200 m L D 5 W over 15 m inutes, then 50 m g/kg in 500 m L D 5 W over 4 hours, then 100 m g/kg in 1,000 m L D 5 W over 16 hours
Pediatric Considerations This volum e of D 5 W m ay need to be reduced in dosing pediatric patients to avoid fluid overload/hyponatrem ia.
Atropine
Indications:
Pa ge 3 7 3
o
Bradycardia owing to drugs
o
Organophosphate insecticides
Warnings: o
Myasthenia gravis, narrow-angle glaucom a, hypertension, coronary ischem ia, and urinary obstruction
Dose: o
Adult: 0.5–1.0 m g IV
o
Pediatric: 0.02 m g/kg (m in. 0.1 m g) IV
o
Large repeated doses needed in organophosphate poisoning
Benztropine (Cogentin)
Indications: o
Acute dystonic reactions
Warnings: o
Carbam ates, m yasthenia gravis, narrow-angle glaucom a, hypertension, coronary ischem ia, and urinary obstruction
Dose o
Adult: 1–2 m g IV (for acute reaction) or PO (to prevent reaction)
o
Pediatric: 0.02 m g/kg IV (for acute reaction) or PO (to prevent reaction)
Benzodiazepine
Indications: o
Warnings: o
Agitation, stim ulant drugs, seizures
Respiratory/CNS depression
Dose: o
Midazolam :
Adult: 1 m g IV/IM every 2–3 m inutes PRN
Pa ge 3 7 3
o
Pediatric: 0.1 m g/kg IV/IM
Diazepam :
Adult: 2–5 m g IV/IM, repeat in 10–15 m inutes
Pediatrics: 0.1 m g/kg IV/IM
Bicarbonate, Sodium
Indications: o
Cyclic antidepressant poisoning, m etabolic acidosis, urinary alkalinization
Warnings: o
May cause congestive heart failure (CHF), excessive alkalosis, hypokalem ia
Dose: o
Serum alkalinization:
o
1 m Eq/kg IVP
Urine alkalinization:
100–150 m Eq in 1 L DW at 2–3 m L/kg/h IV, goal urine pH 7–8
Black Widow Spider Antivenin (Lactrodectus Mactans)
Indications: o
Severe hypertension, m uscle spasm s not alleviated by analgesics and m uscle relaxants; consider in extrem es of age (65 years), pregnant wom en with threatened abortion
Warnings: o
Equine serum derived—im m ediate hypersensitivity, serum sickness 10–14 days
o
Prem edicate for anaphylaxis if know equine serum hypersensitivity.
Dose:
Pa ge 3 7 3
o
1–2 vials IV slowly over 15–30 m inutes
Botulin Antitoxin Trivalent A,B,E
Indications: o
Clinical botulism , prior to onset of paralysis
Warnings: o
Binds only free toxins
o
Not for infant botulism
o
Equine serum derived—im m ediate hypersensitivity, serum sickness 10–14 days
o
Prem edicate for anaphylaxis if know equine serum hypersensitivity.
o
Adm inister slow IV push.
Dose: o
1–2 vials IV q4h for 4 or 5 doses
Calcium
Indications: o
Hyperkalem ia with cardiac toxicity
o
Hydrofluoric acid burn
o
Calcium channel blocker overdose
o
Citrate, oxalate, phosphate poisoning
Warnings: o
Avoid in digoxin toxicity, hypercalcem ia.
o
Calcium chloride (CaCl) corrosive to skin, SC tissue
o
Incom patible with certain IV solutions
o
Adm inister slow IV push
Dose: o
Adult: 5–10 m L of 10% Ca chloride, or 10–20 m L of 10% Ca gluconate
o
Pediatric: 0.1–0.2 m L/kg of 10% Ca chloride, or 0.2–0.3 m L/kg of 10% Ca gluconate
Calcium Edta (Edetate Disodium)
Pa ge 3 7 3
Indications: o
Lead, chrom ium , nickel, m anganese, zinc toxicity
Warnings: o
Nausea, vom iting, chill, nephrotoxicity, hypercalcem ia
Dose: o
20–30 m g/kg over 24 hours as six divided doses or continuous IV infusion, follow lead (Pb) level
P.877
Coral Snake Antivenin (Micrurus Fulvius)
Indications: o
Eastern or Texas coral snake
Warnings: o
Equine serum derived—im m ediate hypersensitivity, serum sickness 10–14 days
o
Prem edicate for anaphylaxis if know equine serum hypersensitivity.
Dose: o
4–10 vials IV over 15–30 m inutes
Cyanide Antidote Kit
Indications: o
Warnings: o
Cyanide poisoning
Hypotension, m ethem oglobinem ia
Dose: o
Am yl nitrite: 1–2 am p crushed, inhaled
o
Sodium nitrite:
Adult: 300 m g in 10 m L IV over 5 m inutes
Pediatric: 0.3 m L/kg of 3% solution IV
Pa ge 3 7 3
o
Sodium thiosulfate:
Adult: 12.5 g IV, m ay repeat in 1 hour
Pediatric: 50 m g/kg IV
Dantrolene
Indications: o
Malignant hypertherm ia
o
Neuroleptic m alignant syndrom e
o
Serotonin syndrom e
o
Muscle rigidity
Warnings: o
Muscle weakness, respiratory depression, hepatitis
Dose: o
1–2 m g/kg IV bolus, repeat q10–15 m in PRN, m ax. 10 m g/kg
Deferoxamine (Desferal)
Indications: o
Iron toxicity
Warnings: o
Do not treat for >24 hours, risk for delayed adult respiratory distress syndrom e (ARDS).
o
Hypotension if >15 m g/kg/h, flushing, urticaria
Dose: o
10–15 m g/kg/h IV, m ay increase in severe iron (Fe) poisoning
Digoxin Antibody (Digibind)
Indications: o
Digoxin, digitoxin toxicity
Warnings: o
Falsely elevated digoxin levels after use
o
Developm ent of CHF/atrial fibrillation in patients requiring digoxin
Pa ge 3 7 3
Dose: o
One vial (40 m g) binds 0.6 m g digoxin.
o
Num ber of vials = digoxin level (ng/m L) × weight (kg)/100
o
Dose estim ate: acute overdose 10–20 vials, chronic overdose 4–6 vials
Dimercaprol (Bal)
Indications: o
Arsenic, gold, m ercury, lead-induced encephalopathy
Warnings: o
Renal toxicity, fever, nausea, vom iting, urticaria, cholinergic sym ptom s
Dose: o
3 m g/kg deep IM q4h for 2 days, then q12h for 7 days; follow m etal levels
o
For Pb level >100 µg/dL: 4–5 m g/kg IM q4h until Pb 25%
Pa ge 3 7 4
Warnings: o
G6-PD deficiency
Dose: o
1–2 m g/kg slow IV as 1% solution, repeat in 1 hour
Narcan
Indications: o
Warnings: o
Opiate poisoning, em piric treatm ent of com a
Acute opiate withdrawal, severe agitation
Dose: o
Adult: 0.4–2.0 m g IV or IM, repeat to 10 m g
o
Pediatric: 0.1 m g/kg IV or IM
Octreotide
Indications: o
Warnings: o
Sulfonylurea overdose with hypoglycem ia
Use with caution in diabetic patients.
Dose: o
Adult: 50 µg SC q6h
o
Pediatric: 4–5 µg/kg/d SC div. q6h
Oxygen, Hyperbaric
Indications: o
Carbon m onoxide (CO) poisoning
Warnings: o
Tym panic m em brane (TM) perforation, seizures owing to oxygen toxicity
o
Difficulty m onitoring patient
Dose: o
100% oxygen at 2–3 atm
Penicillamine
Pa ge 3 7 4
Indications: o
Arsenic, copper, lead, m ercury with/following BAL or EDTA
Warnings: o
Contraindicated in penicillin allergy, renal insufficiency
Dose: o
o
Lead:
Adult: 250–500 m g per dose PO q8h–q12h
Pediatric: 25–40 m g/kg/d PO in 3 div. doses
Arsenic:
100 m g/kg/d PO divided in four doses for 5 days (m ax. 1 g/d)
o
Mercury:
Adult: 250 m g PO q.i.d.
Pediatric: 20–30 m g/kg/d PO in 4 div. doses
Phentolamine
Indications: o
Hypertensive crisis: stim ulants, sym pathom im etics, MAO-tyram ine reaction, and extravasated pressors
o
Warnings: o
Reversal of cocaine-m ediated vasospasm
Hypertension, tachycardia, dysrhythm ias
Dose: o
o
Hypertension (HTN):
Adult: 1–5 m g IV bolus
Pediatric: 0.02–0.1 m g/kg bolus
Extravasation:
Adult: 5 m g diluted in 10–15 m L saline SC
Pediatric: 0.1 m g/kg diluted in 10–15 m L saline SC
Pa ge 3 7 4
Physostigmine
Indications: o
Warnings: o
Severe anticholinergic syndrom e
Contraindicated in TCA overdose
Dose: o
Adult: 0.5–1.0 m g IV, repeat in 10 m in PRN
o
Pediatric: 0.02 m g/kg IV, repeat in 10 m in PRN
P.879
Pralidoxime (2-PAM, Protopam)
Indications: o
Organophosphate toxicity
o
Reversal of nicotinic effects
o
Reactivates enzym e
o
Use in conjunction with atropine
Warnings: o
Myasthenic crisis if m yasthenia gravis
o
Nausea, headache, dizziness, laryngospasm , m uscle rigidity
Dose: o
Adult: 1–2 g in 100 m L NaCl over 15 m inutes, repeat in 1 hour PRN, repeat in 6 hours if nicotinic sym ptom s return
o
Pediatrics: 25–50 m g/kg over 15 m inutes, repeat in 1 hour PRN, repeat in 6 hours if nicotinic sym ptom s return
Protamine
Indications: o
Reversal of heparin anticoagulation
Pa ge 3 7 4
Warnings: o
Hypersensitivity in patients with fish allergy
o
Avoid benzyl alcohol diluent in neonates.
Dose: o
1 m g for each 100 IU heparin, half dose if 30–60 m inutes, and quarter dose if 2 hours after heparin bolus
Pyridoxine (Vitamin B 6)
Indications: o
Isoniazid-induced seizures
o
Gyrom itra m ushroom
Warnings: o
None, nontoxic
Dose: o
Isonicotinic acid hydrazide (INH)–induced seizures:
Unknown ingested am ount: 5 g for adult or 1 g for pediatrics
Dose (m g) = am ount INH ingested (m g)
Gyrom itra: 25 m g/kg IV over 30 m inutes to 1 hour
Digoxin Antibody (Digibind)
Indications: o
Significant envenom ation by Crotaline species: rattlesnake, cottonm outh, water m occasin, pit viper
Warnings: o
Equine or ovine derived products—im m ediate hypersensitivity, serum sickness 10–14 days
o
Prem edicate for anaphylaxis if know equine/ovine serum hypersensitivity.
Dose: o
Equine-derived (Wyeth-Ayerst polyvalent):
Pa ge 3 7 4
o
Mild: 5 vials—infuse slowly
Moderate: 10 vials—infuse slowly
Severe: 15 vials—infuse slowly
Ovine-derived (Crofab):
4–6 vials slowly; m ay repeat dose of 4–6 vials if control of envenom ation not achieved, then 2 vials q6h for 3 doses
Vitamin K (Phytonadione, Aqua Mephyton)
Indications: o
Warnings: o
Reversal of Coum adin anticoagulation
Hypersensitivity from IV adm inistration
Dose: o
2–10 m g IM/SC/slow IV, m ay repeat in 8 hours
o
2–10 m g PO, m ay repeat in 12–48 hours
Pa ge 3 7 4
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Po iso ning, G astric Deco ntam inatio n
Poisoning,
Gastric Decontamination Frank LoVecchio
Basics Description Modalities to decontam inate the GI tract of poisons
Treatment Pre Hospital Alert
Ipecac contraindicated in am bulance setting
Controversies: o
Hom e use of ipecac in general is not recom m ended.
In extrem ely rare cases (e.g., very prolonged transit tim es, protecting airway), consider ipecac adm inistration only after consultation with regional poison control center.
o
Decreased tim e to activated-charcoal adm inistration when given in pre hospital setting
Pa ge 3 7 4
o
Decreased drug absorption in a sim ulated ingestion while volunteers were lying in left lateral versus right lateral decubitus position
Initial Stabilization
Airway, breathing, and circulation m anagem ent (ABCs): o
Secure airway for decreased m ental status/inability to protect airway.
o
Intravenous access
o
Cardiac m onitor
With altered m ental status from overdose: o
Naloxone
o
Thiam ine
o
Dextrose (or Accu-Chek)
ED Treatment
Ipecac: o
General:
Derived from the roots of the plant Cephaelis acum inata
Exerts em etic action by direct gastric irritation and centrally m ediated chem oreceptive trigger-zone stim ulation
Delays adm inistration of activated charcoal
Offers no advantage over activated charcoal alone when both treatm ents potentially effective
o
Dosage:
Older than 12 years: 30 m L
Ages 1 through 12 years: 15 m L
Ages 6 m onths to 1 year: 5–10 m L plus 15 m L clear fluid
o
Indications:
Pa ge 3 7 5
o
No utility in ED
Adverse effects:
Vom iting m ay com plicate and worsen clinical presentation.
Delay to adm inistration of activated charcoal or oral antidotes
o
Contraindications:
Caustics (acids and alkali) ingestion
Hydrocarbon ingestion
Ingestion of agents that rapidly depress m ental status
Patients actively vom iting
Orogastric lavage: o
General:
Placem ent of large-bore tube (32–36 Fr) in stom ach for rem oval of ingested toxins
Effectiveness of orogastric lavage depends on tim e interval since ingestion, tim ing of last m eal, and toxin ingested.
Protected airway essential prior to any attem pts at orogastric lavage
o
Indications:
Presentation within 1 hour of taking a potentially lethal ingestion with no known antidote
o
o
Poisoned intubated patient
Adverse effects:
Intubation of respiratory tree
Esophageal or gastric perforation
Charcoal aspiration
Patient discom fort
Contraindications:
Pa ge 3 7 5
Large pills (lim ited by lavage-tube port size) ingestion
Caustics (acids and alkali) ingestion
Hydrocarbon ingestion
Ingestion of agents that rapidly depress m ental status
Unprotected airway
P.881
o
Pediatric considerations:
Avoid in children
Unlikely to result in any clinically significant pill extraction secondary to sm aller-bore orogastric tube (i.e., 18 Fr)
o
Risk of aspiration increased in children
Controversies:
Several random ized, controlled trials have docum ented no benefit when lavage plus activated charcoal is com pared with activated charcoal alone.
Activated charcoal: o
General:
Prepared by treating heated wood pulp, which creates a large surface area to bind toxins
Mainstay of gastric decontam ination
Effective when contents have reached sm all intestine
o
Dose:
1–2 g/kg of body weight or an activated charcoal-to-drug ratio of 10:1; often m ixed with sorbitol (see below)
Pa ge 3 7 5
o
Oral or nasogastric-tube adm inistration
Indications:
Adm inister in every toxic ingestion (see below for exceptions).
Optim al for toxic ingestions presenting within 1 hour of ingestion
o
Adverse effects:
Vom iting and constipation
Charcoal aspiration and subsequent charcoal pneum onitis
o
o
o
Contraindications:
Caustic ingestions
Unprotected airway
Bowel obstruction or ileus
Drugs not effectively bound to charcoal:
Metals (borates, brom ide, iron, lithium )
Alcohols
Potassium
Potassium cyanide (poorly absorbed)
Hydrocarbons
Caustics
Pediatric considerations:
Mix with palatable substance (cola or juice) to facilitate intake or adm inister via gastric tube.
o
Controversies:
Random ized, controlled trials have shown a slightly worse outcom e and higher com plication rate when asym ptom atic patients received charcoal versus nothing.
An extrem ely sm all m inority of patients are likely to benefit from gastric lavage.
Multiple-dose activated charcoal:
Pa ge 3 7 5
o
General:
Used in toxic ingestions that are well absorbed by charcoal and undergo enterohepatic circulation
o
Dose:
1 g/kg followed by 0.5 g/kg q2h–q6h
Never use cathartics in conjunction with m ultiple-dose activated charcoal.
o
Indications:
Theophylline
salicylates
Multiple-dose activated charcoal m ay decrease area under the curve for such drugs as phenobarbital, phenytoin, and carbam azepine, but has not been proven to im prove outcom e.
Cathartics: o
General:
Used in com bination with activated charcoal to prevent constipation and to enhance gastrointestinal transit tim e
Lim ited data available to dem onstrate any decreased absorption when a cathartic (sorbitol) is added to activated charcoal
Cathartics alone are of no proven benefit and should be avoided.
Never use cathartics in conjunction with m ultiple-dose activated charcoal.
o
Dose:
Magnesium citrate: 10% solution: 250 m L (peds: 4 m L/kg)
Magnesium sulfate: 15–20 g (peds: 250 m g/kg)
Pa ge 3 7 5
Sorbitol: 0.5–1 g/kg to a m ax. 100 g of 70% solution (peds: >1 year old: 0.5–1 g/kg as a 35% solution to a m ax. 50 g) PO m ixed in the activated charcoal slurry—use only in first dose.
o
o
Adverse effects:
Dehydration
Hyperm agnesem ia
Diarrhea
Abdom inal discom fort
Contraindications:
Pre-existing dehydration
Renal disease (cathartics containing m agnesium )
o
Avoid in children
Controversies:
No proven benefit with som e cases of harm reported
Whole-bowel irrigation: o
General: cleansing of bowel
o
Indications:
Toxins not well absorbed by charcoal such as toxic iron and lithium ingestions
Toxins in sealed containers (body packers) without signs of gastrointestinal perforation
o
Toxic, sustained-release product ingestions
Dose:
Polyethylene glycol (Colyte, Go-Lytely)
Solution at 2 L/h in adults (0.5 L/h in children) until rectal excretions clear
Adm inister via nasogastric tube with activated charcoal via continuous or bolus m ethod as
Pa ge 3 7 5
indicated. o
o
Adverse effects:
Bloating
Rectal irritation
Frequent bowel m ovem ents
Contraindications:
Mechanical or pharm acologic ileus
Bowel obstruction
Intestinal perforation
Unprotected airway
Follow-Up N/A
References 1. Am erican College of Em ergency Physicians. Clinical policy for the initial approach to patients with acute toxic ingestions or derm al or inhalation exposure. Ann Em erg Med. 1995;25:570–585. 2. Ellenhorn MJ, Schoonwald S, Ordog G, et al. Gut decontam ination. In: Ellenhorn MJ, ed. Ellenhorn's Medical Toxicology. 2nd ed. Baltim ore: William s & Wilkins; 1997:66–78. 3. Perrone J, Hoffm an RS, Goldfrank LR. Special considerations in gastric decontam ination. Em erg Med Clin. 1994;12:285–299. 4. Pond SM, Lewis Driver DJ, William s GM, et al. Gastric em ptying in acute overdose: a prospective random ized controlled trial. Med J Aust . 1995;163:345–349.
Miscellaneous SEE ALSO: Poisoning; Poisoning, Toxidrom es; Poisoning, Antidotes
Pa ge 3 7 5
Codes ICD9-CM 977.9 Unspecified drug or m edicinal substance
ICD10 T47.6 Antidiarrheal drugs
Pa ge 3 7 5
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Po iso ning, To xidro m es
Poisoning,
Toxidromes Kirk Cumpston
Basics Etiology N/A
Mechanism
Anticholinergic: o
Adrenergic im balance results from inhibition of acetylcholine at receptors.
Cholinergic: o
Excess parasym pathetic stim ulation and cholinergic crisis result from inhibition of acetylcholinesterase or increased activity at acetylcholine receptor.
Opiates: o
Differ in their agonist and antagonist properties at various opioid receptor sites
o
µ-Receptor stim ulation—full agonist
o
K and δ receptors share partial agonist and antagonist properties.
Sym pathom im etic: o
Stim ulation of sym pathetic effector organs
Pa ge 3 7 5
(particularly CNS)
Withdrawal: o
Hyperactivity of sym pathetic nervous system predom inates.
Diagnosis Signs and Symptoms
Toxicologic m nem onics: o
Use the following m nem onics to rem em ber the substances and drugs that can present each sign or sym ptom :
Anion gap acidosis: A CAT MUD PILES: o
AKA
o
CO/cyanide
o
Acetam inophen in fulm inant hepatic failure
o
Toluene
o
Methanol
o
Urem ia
o
DKA
o
Paraldehyde, phenform in/m etform in, prophylene glycol
o
Iron/INH
o
Lactic acidosis
o
Ethylene glycol
o
Salicylates, Starvation ketosis
Increased osm olar gap: ME DIE: o
Methanol
o
Ethylene glycol
o
Diuretics (m annitol, glycerol, sorbital) Diluents (propylene glycol)
Pa ge 3 7 5
o
Isopropyl alcohol
o
Ethanol
Seizures: OTIS CAMPBELL: o
Organophosphates
o
Tricyclic antidepressants
o
INH/insulin
o
Sym pathom im etics, salicylates
o
Cam phor/cocaine/citalopram
o
Am phetam ines, anticholinergic agents
o
Methylxanthines (theophylline, caffeine), m ushroom s (m onom ethyl hydrazine group)
o
PCP, pethidine (Dem erol), propoxyphene, plants (nicotine, water hem lock)
o
Benzodiazepine withdrawal, bupropion
o
Ethanol withdrawal
o
Lithium , lidocaine
o
Lead, lindane
Mydriasis: AAAS: o
Antihistam ines
o
Antidepressants
o
Anticholinergics/atropine
o
Sym pathom im etics
Miosis: COPS: o
Cholinergic/clonidine
o
Opiates/organophosphates/olanzapine
o
Phenothiazines/pilocarpine/pontine bleed
o
Sedative hypnotics
Hypertension: CT SCAN: o
Cocaine
o
Theophylline
o
Sym pathom im etics
o
Caffeine
Pa ge 3 7 6
o
Anticholinergics/am phetam ines
o
Nicotine
Hypotension: CRASH: o
Cocaine/calcium channel blockers
o
Reserpine/antihypertensives/beta-blockers
o
Antidepressants/am inophylline
o
Sedative-hypnotics
o
Heroin/other opioids
Bradycardia: PACED: o
Propranolol (beta-blockers)
o
Anticholinesterase inhibitors drugs
o
Clonidine/calcium channel blockers
o
Ethanol/alcohols
o
Digoxin
Tachycardia: FAST: o
Free base (cocaine)
o
Anticholinergic/antihistam ines/am phetam ines
o
Sym pathom im etics/solvent abuse
o
Theophylline
Hypotherm ia: COOLS: o
Carbon m onoxide
o
Opiates
o
Oral hypoglycem ics
o
Liquor
o
Sedative hypnotics
Hypertherm ia: NASA o
Neuroleptic m alignant syndrom e, nicotine
o
Antihistam ines/Alcohol withdrawal
o
Salicylates, sym pathom im etics, serotonin toxicity
o
Anticholinergics, antidepressants
Rapid respiration: PANT: o
PCP, paraquat, pneum onitis
Pa ge 3 7 6
o
ASA (acetylsalicylic acid)
o
Noncardiogenic pulm onary edem a
o
Toxin-induced m etabolic acidosis
Slow respiration: SLOW: o
Sedative-hypnotics (γ-hydroxybutyrate [GHB])
o
Liquor
o
Opiates
o
Weed
Diaphoresis: SOAP: o
Sym pathom im etics
o
Organophosphates
o
Acetylsalicylic acid
o
PCP
Drugs that cause pulm onary edem a: MOPS: o
Meprobam ate, m ethadone
o
Opiates, organophosphates
o
Phenobarbital, propoxyphene, phenothiazines
o
Salicylates, sm oke inhalation, solvents
Toxidromes
Cholinergic: SLUDGE BAM: o
Salivation
o
Lacrim ation
o
Urination
o
Diarrhea
o
Em esis
o
Bronchorrhea, bronchospasm , bradycardia
o
Abdom inal discom fort
o
Miosis
Anticholinergic: o
Hypertherm ia (“Hot as a hare, red as a beet―)
o
Dry skin (“Dry as a bone―)
o
Dilated pupils (“Blind as a bat―)
Pa ge 3 7 6
o
Delirium (“Mad as a hatter―)
o
Tachycardia
o
Hypertension
o
Hypertherm ia
o
Urgency retention
o
Decreased bowel sounds
P.883
Sym pathom im etic: o
Diaphoresis
o
Mydriasis
o
Tachycardia
o
Hypertension
o
Hypertherm ia
o
Seizures
Opiate: o
Miosis
o
Hypovolem ia
o
Com a
o
Bradycardia
o
Hypotension
Withdrawal (alcohol, benzodiazepine, barbiturates): o
Mydriasis
o
Tachycardia
o
Hypertension
o
Hypertherm ia
o
Trem or
o
Agitation
o
Hallucinations
o
Seizures
Withdrawal (opioid):
Pa ge 3 7 6
o
Nausea
o
Vom iting
o
Diarrhea
o
Abdom inal cram ps
o
Mydriasis
o
Piloerection
o
Tachycardia
o
Lacrim ation
o
Salivation
o
Hypertension
o
Yawning
o
Cram ps
Dermatologic
Dry skin: o
Antihistam ines
o
Anticholinergics
Bullae: o
Barbiturates/carbon m onoxide
Acneiform rash: o
Dioxins
o
Brom ides
o
Chlorinated
o
Hydrocarbons
Flushed or red appearance: o
Anticholinergics
o
Disulfiram reactions
o
Niacin
o
Boric acid
o
Scom broid poisoning
o
Monosodium glutam ate
o
Carbon m onoxide (frequently postm ortem )
o
Cyanide (rare)
Pa ge 3 7 6
o
Vancom ycin
Cyanosis: o
Ergotam ines
o
Methem oglobinem ia form ing:
Nitrite
Nitrate
Dapsone
Aniline dye
Phenazopyridine
Benzocaine (caines)
Chloroquine
Odors: o
Bitter alm onds: cyanide
o
Carrots: cicutoxins
o
Fruity: diabetic ketoacidosis (DKA), isopropanol
o
Garlic: organophosphates, arsenic
o
Gasoline: petroleum distillates
o
Mothballs: naphthalene, cam phor
o
Pears: chloral hydrate
o
Pungent odor: ethchlorvynol
o
Oil of wintergreen: m ethyl salicylate
o
Rotten eggs: hydrogen sulfide
o
Peanut butter: Vacor
Treatment Initial Stabilization Airway, breathing, and circulation m anagem ent (ABCs)
ED Treatment Depends on ingested substance (see related chapter)
Pa ge 3 7 6
References 1. Erickson TB. Toxicology update: a rational approach to managing the poisoned patient. Em erg Med Pract. 2001;3(8). 2. Keyes DC, Dart RC. Initial diagnosis and treatm ent of the poisoned patient. In Dart RC, ed. Medical Toxicology. 3rd ed. Philadelphia: Lippincott William s & Wilkins; 2004:21–31.
Miscellaneous SEE ALSO: Poisoning; Poisoning Antidotes; Poisoning, Gastric Decontam ination
Pa ge 3 7 6
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Po iso ning
Poisoning
Mark B. Mycyk
Basics Description
Poisoning m ay be intentional or unintentional.
Patients with change in m ental status without clear cause should have poisoning (intoxication, overdose) considered in differential diagnosis.
Etiology
Intentional: o
Depression
o
Suicide
o
Hom icide
o
Recreational drug abuse
Unintentional (accidental): o
Com m on cause in children
o
Therapeutic error (e.g., double dose)
o
Recreational drug experim entation
Pediatric Considerations
Accidental ingestions—typically young children (ages 1–5 years)
Consider child abuse if inconsistent or suspicious history.
Pa ge 3 7 6
Diagnosis Signs and Symptoms
Neurologic: o
Lethargy
o
Agitation
o
Com a
o
Hallucinations
o
Seizures
Respiratory: o
Tachypnea/bradypnea/apnea
o
Inability to protect airway
Cardiovascular: o
Dysrhythm ias
o
Conduction blocks
Vital signs: o
Varies depending on toxic substance
o
Hypertherm ia/hypotherm ia
o
Tachycardia/bradycardia
o
Hypertension/hypotension
Selected Toxidromes (see Poisoning, Toxidromes)
Anticholinergic: o
Altered m ental status (confusion, delirium , lethargy)
o
Dry skin and m ucous m em branes
o
Fixed dilated pupils
o
Tachycardia
o
Hypertherm ia
o
Flushing
Pa ge 3 7 6
o
Urinary retention
Cholinergic: o
Secretory overdrive (salivation, lacrim ation, urination, diaphoresis)
o
Miosis
o
Bronchospasm /wheezing
Opiate: o
CNS and respiratory depression
o
Pinpoint pupils
Sym pathom im etic: o
CNS excitation
o
Seizures
o
Tachycardia
o
Hypertension
o
Diaphoresis
Essential Workup
Accurately identify ingestant(s).
Send som eone to patient's hom e to obtain product(s) if necessary.
Accurately identify tim e of ingestion.
Call poison control center or toxicologist for help.
Tests Lab
Electrolytes, BUN/creatinine, glucose
Calculate anion gap: Na - (Cl+HCO 3 ) o
Norm al anion gap: 8–12
o
Use m nem onic A CAT MUD PILES for elevated anion gap acidosis:
Alcoholic ketoacidosis
Cyanide, carbon m onoxide
ASA, other salicylates
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Toluene
Methanol, m etform in
Urem ia
Diabetic ketoacidosis
Paraldehyde, phenform in
Iron, INH
Lactic acidosis from other causes
Ethylene glycol
Starvation ketosis
Serum osm ol gap: o
Calculate osm ol gap if elevated anion gap acidosis from potential toxic alcohol.
o
Most sensitive early in poisoning
o
Norm al osm ol gap does not com pletely rule out toxic alcohol ingestion.
o
Calculated osm olality = 2(Na + ) + glucose/18 + BUN/2.8 + ethanol (in m g/dL)/4.6.
o
Osm ol gap = m easured osm olality – calculated osm olality.
o
Use m nem onic ME DIE A when osm ol gap >10
Methanol
Ethanol
Diuretics (m annitol, glycerin, sorbitol)
Isopropyl alcohol
Ethylene glycol
Acetone
Pregnancy test
Acetam inophen level for suicidal ingestions
Toxicology screen
Imaging
ECG for dysrhythm ias or QRS/QT changes
CT of head for altered m ental status not clearly owing to
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toxin
Chest radiograph if suspected aspiration or pneum onia
Differential Diagnosis Causes of Altered Mental Status
Intracranial m ass, bleeding
Infection, sepsis
Endocrine abnorm alities
Hypotherm ia
Hypoxia
Metabolic abnorm alities
Psychogenic
Treatment Pre Hospital
Search for clues at scene: o
Pills/pill bottles
o
Drug paraphernalia
o
Witnesses
o
Transport all drugs and pill bottles for identification.
Restrain uncooperative patients for patient and health care giver protection.
Consider co-m orbid conditions: o
Traum a
o
Medical illness
o
Environm ental exposure
Pre hospital adm inistration of activated charcoal m ay optim ize decontam ination if prolonged transport tim e.
Initial Stabilization
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Airway, breathing, and circulation m anagem ent (ABCs): o
Endotracheal intubation as needed for airway protection, oxygenation, ventilation, and orogastric lavage
o
Supplem ental oxygen for hypoxia
o
Pulse oxim etry
o
Cardiac m onitor
o
IV access
Hypotension: o
Adm inister 0.9% norm al saline (NS) IV fluid bolus.
o
Trendelenburg
o
Vasopressors for persistent hypotension
Bradycardia: o
Atropine
o
Cardiac pacing
If altered m ental status, adm inister com a cocktail: thiam ine, D 5 0 W (or Accu-Chek), naloxone
P.875
ED Treatment Decontamination
See Poisoning, Gastric Decontam ination.
Prevents system ic absorption of ingested toxin
Orogastric lavage: o
Consider in potentially lethal ingestions without known antidote within 1 hour of ingestion.
o
Protected airway essential prior to lavage
Activated charcoal: o
Most effective within a few hours of m ost toxic ingestions
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o
Contraindicated if caustic ingestion, unprotected airway, or bowel obstruction
o
Drugs not effectively bound to charcoal: m etals (borates, brom ide, iron, lithium ), alcohols, potassium
Whole-bowel irrigation: o
Polyethylene glycol (Colyte, Go-Lytely) evacuates bowel without causing electrolyte disturbances.
o
Consider in toxins not well adsorbed by charcoal (e.g., iron and lithium ), body packers/stuffers, sustained release ingestions.
o
Contraindicated if bowel obstruction, perforation, or hypotension
Enhanced Elimination Enhances rem oval of system ically absorbed toxin:
Multiple-dose activated charcoal: o
Theophylline
o
Carbam azepine
o
Phenobarbital
Urinary alkalinization: o
Salicylates
o
Phenobarbital
Hem odialysis/hem operfusion: o
Lithium
o
Salicylates
o
Theophylline
o
Toxic alcohols
Seizures
Treat initially with diazepam or lorazepam .
For persistent seizures, consider phenobarbital.
Phenytoin not indicated in toxicologic seizures: o
Indicated only if seizures secondary to idiopathic
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epilepsy, posttraum atic, or status epilepticus
Antidotes
See Poisoning, Antidotes.
Acetam inophen: N-acetylcysteine
Anticholinergic: physostigm ine
Benzodiazepines: flum azenil
Beta-blockers: glucagon
Calcium channel blockers: calcium chloride/gluconate, insulin
Carbon m onoxide: oxygen, hyperbaric oxygen
Coum adin: vitam in K 1
Cyanide: cyanide antidote kit
Digoxin: Digibind
Ethylene glycol: ethanol, 4-m ethylpyrazole
Iron: deferoxam ine
Isoniazid (INH): pyridoxine (vitam in B 6 )
Methanol: ethanol, 4-m ethylpyrazole
Methem oglobinem ia: m ethylene blue
Opiates: naloxone
Organophosphates: atropine, pralidoxim e
Tricyclic antidepressants: NaHCO 3
Medication (Drugs)
Activated charcoal slurry: 1–2 g/kg PO
Dextrose: D 5 0 W one am p: 50 m L or 25 g (peds: D 2 5 W 2–4 m L/kg) IV
Diazepam : 5–10 m g (peds: 0.2–0.5 m g/kg) IV every 10–15 m inutes
Lorazepam : 2–6 m g (peds: 0.05–0.1 m g/kg) IV every 10–15 m inutes
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Naloxone (Narcan): 0.4–2 m g (peds: 0.1 m g/kg) IV or IM initial dose
Thiam ine (vitam in B 1 ): 100 m g (peds: 50 m g) IV or IM
Follow-Up Disposition Admission Criteria
Altered m ental status
Cardiopulm onary instability
Suicidal
Laboratory abnorm alities
Potential for decom pensation from delayed acting substance
Discharge Criteria
Psychiatrically clear
Detoxified
Hem odynam ically stable
Issues for Referral
Patients with unintentional (accidental) poisoning require poison prevention counseling.
Patients with intentional (e.g., suicide) poisoning require psychiatric evaluation.
Consider substance abuse referral for patients.
References 1. Dem orest RA, Posner JC, Osterhoudt KC, et al. Poisoning prevention education during em ergency departm ent visits for childhood poisoning. Pediatr Em erg Care. 2004;20(5):281–284. 2. Ford MD, Delaney KA. Initial approach to the poisoned patient. In:
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Ford MD, Delaney KA, Ling LJ, et al., eds. Clinical Toxicology. Philadelphia: WB Saunders; 2001:14. 3. Goldfrank LR, Flom enbaum NE, Lewin NA, et al. Vital signs and toxic syndrom es. In: Goldfrank LR, Flom enbaum NE, Lewin NA, et al., eds. Goldfrank's Toxicologic Em ergencies. 7th ed. Norwalk, CT: Appleton & Lange, 2002:37–40. 4. Hoffm an RS, Goldfrank LR. The poisoned patient with altered consciousness. JAMA. 1995;274:562–569. 5. Kulig K. Initial m anagem ent of toxic substances. N Engl J Med. 1992;326:1678–1682.
Miscellaneous SEE ALSO: Poisoning, Antidotes; Poisoning, Gastric Decontam ination; Poisoning, Toxidrom es
Codes ICD9-CM 977.9
ICD10 T65.9
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Po lio
Polio
Philip Shayne
Basics Description
Caused by poliovirus infection
Incubation period 9–12 days
Duration Table o f C o ntents > Po stpartum Hem o rrhage
Postpartum
Hemorrhage Marco Coppola Clyde Turner
Basics Description
Im m ediate: hem orrhage occurring within 24 hours after delivery
Delayed: hem orrhage occurring m ore than 24 hours after delivery: o
Often 1–2 postpartum
Etiology
Im m ediate: o
Uterine atony
o
Lower genital lacerations
o
Retained placental tissue
o
Placenta accreta
o
Uterine rupture
o
Uterine inversion
o
Puerperal hem atom a
o
Coagulopathies
Delayed:
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o
Retained products of conception
o
Postpartum endom etritis
o
Withdrawal of exogenous estrogen
o
Puerperal hem atom a
Coagulopathies: o
Pre-existing idiopathic throm bocytopenic purpura
o
Throm botic throm bocytopenic purpura
o
Von Willebrand disease
o
Dissem inated intravascular coagulation (DIC)
Associated Conditions If bleeding is present at other sites, consider coagulopathy
Diagnosis Signs and Symptoms
Ongoing blood loss, usually painless
Significant hypovolem ia, resulting in:
o
Tachycardia
o
Tachypnea
o
Narrow pulse pressure
o
Decreased urine output
o
Cool, clam m y skin
o
Poor capillary refill
o
Altered m ental status
Maternal tachycardia and hypotension m ay not occur until blood loss >1,500 m L.
Essential Workup
Abdom en and pelvic exam ination to assess for uterine atony, retained products, or other anatom ic abnorm ality
Type and cross-m atch for packed RBC
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Rapid hem oglobin determ ination
Tests Lab
CBC, platelets
Prothrom bin tim e, partial throm boplastin tim e
Fibrinogen level
Type and cross-m atch
Imaging Ultrasound m ay be helpful to evaluate for retained products in delayed postpartum hem orrhage.
Differential Diagnosis Consider puerperal hem atom as if perineal, rectal, or lower abdom inal pain in conjunction with tachycardia and hypotension.
Treatment Alert
Patients with postpartum hem orrhage m ay be hem odynam ically unstable.
IV access and fluid resuscitation is im portant.
Initial Stabilization
Attem pt to sim ultaneously control bleeding and stabilize hem odynam ic status.
Manage airway and resuscitate as indicated: o
Supplem ental oxygen
o
Cardiac m onitor
IV fluid resuscitation with norm al saline or lactated Ringer solution
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Foley catheter
P.889
ED Treatment
Managem ent of uterine atony: o
Bim anual m assage
o
Oxytocin (Pitocin) adm inistered IV/IM
o
Methylergonovine (Methergine) or ergonovine (Ergotrate) IM if oxytocin fails
o
Avoid if known hypertensive
Onset in m inutes
15-Methyl prostaglandin F 2 Î ± (PGF 2 Î ± ; Hem abate) intram uscularly if above fails:
o
Relatively contraindicated in asthm a
Surgery if m edical intervention fails
Inspect closely for genital tract laceration: o
Repair required if ≥2 cm
o
Use 00 or 000 absorbable suture; continuous, locked recom m ended.
Managem ent of uterine inversion (acute): o
Reposition uterus using Johnson m aneuver or Harris m ethod.
o
Use left hand on abdom inal wall to stabilize fundus of uterus.
o
Place right hand with fingers spread into vagina and push steadily on inverted part to reduce.
o
If unsuccessful, give terbutaline IV or m agnesium sulfate to produce cervical relaxation, and reposition.
o
Surgery if unsuccessful or if subacute or chronic inversion
Managem ent of coagulopathies:
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o
Fresh frozen plasm a, platelets, cryoprecipitate as indicated
o
Careful attention to volum e status
o
Continuous reassessm ent
Medication (Drugs)
Uterotonics—stim ulate uterine contraction to control bleeding: o
Ergonovine (Ergotrate): 0.2 m g IM; avoid if known hypertensive
o
Methylergonovine (Methergine): 0.2 m g IM; 0.2 m g PO q6h; avoid if known hypertensive
o
15-Methyl PGF 2 Î ± (Hem abate): 0.25 m g IM; m ay repeat in 15–60 m inutes
o
Oxytocin (Pitocin): 20–40 IU in 1 L norm al saline at 200 m L per hour; do not use for resuscitation
Cervical relaxation agents facilitate uterine inversion reduction: o
Magnesium sulfate 20%: 2 g IM bolus over 10 m inutes
o
Terbutaline: 0.25 m g IV; avoid if hypotensive
Follow-Up Disposition Admission Criteria
All patients with im m ediate postpartum hem orrhage require adm ission to a closely m onitored setting.
Early obstetrics consultation recom m ended
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Early surgical intervention dependent on cause
Intensive care unit setting if DIC or evidence of hem odynam ic com prom ise
Patients with endom etritis should be adm itted for parenteral antibiotics.
Discharge Criteria
Delayed postpartum hem orrhage that is easily controlled without excessive bleeding
Outpatient m anagem ent with m ethylergonovine 0.2 m g PO every 6 hours m ay be considered in consultation and close follow-up with obstetrician
References 1. Druelinger L. Postpartum em ergencies. Em erg Med Clin North Am . 1994;12:219–237. 2. Gilstrap LC, Ram in SM. Postpartum hem orrhage. Clin Obstet Gynecol. 1994;37:824–830. 3. Mallon W, Henderson S. Labor and delivery. In: Marx JA, Hockberger RS, Walls RM, eds. Rosen's Em ergency Medicine: Concepts and Clinical Practice. 5th ed. St. Louis, MO: Mosby; 2002: 2479–2481. 4. Roberts WE. Em ergent obstetric m anagem ent of postpartum hem orrhage. Obstet Gynecol Clin North Am . 1995;22:283–302.
Codes ICD9-CM 666.10 Other im m ediate postpartum hem orrhage, unspecified as to episode of care or not applicable
ICD10 O46.8 Other antepartum hem orrhage
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Po stpartum Infectio n
Postpartum
Infection Timothy Stallard Marco Coppola
Basics Description
Early postpartum endom etritis (PPE): o
Develops within 48 hours
o
Most often com plicating cesarean section
Late PPE: o
Develops after three days to six weeks
o
Usually following vaginal delivery
Septic pelvic throm bophlebitis is a diagnosis of exclusion with two distinct clinical presentations, either of which m ay present with postpartum pulm onary em bolus: o
Acute throm bosis: m ost com m on right ovarian vein, usually occurring in first 48 hours as acute, progressive lower abdom inal pain
o
Enigm atic fever: “picket fence― spiking fevers and tachycardia
Etiology
Polym icrobial infection result of ascending spread from
Pa ge 3 8 0
lower genital tract
Anaerobic (up to 80%) and aerobic (~70%): o
o
o
o
Gram -positive aerobes:
Group A, B streptococcus
Enterococci
Gardnerella vaginalis
Gram -negative aerobes:
Escherichia coli
Enterobacter
Anaerobes:
Bacteroides
Peptostreptococcus
Other genital m ycoplasm as com m on in late PPE:
Ureaplasm a urealyticum
Mycoplasm a hom inis
Chlam ydia trachom atis
Diagnosis Signs and Symptoms
Persistent fever and chills
Localized pain and swelling
Lower abdom inal pain
Foul-sm elling lochia
Cervical m otion tenderness, uterine tenderness
Absence of other sources of infection: o
Genital tract infection should be assum ed until ruled out
Essential Workup
Abdom inal and pelvic exam ination
Pa ge 3 8 0
Cervical cultures for chlam ydia
Transcervical endom etrial cultures
Tests Lab
CBC
Urinalysis and culture
Blood cultures
Imaging
CT or MRI for ovarian vein throm bosis
Ultrasound is sensitive for abscess
Differential Diagnosis Fever from other sources:
Table o f C o ntents > Pre-excitatio n Syndro m es
Pre-excitation
Syndromes Richard Wolfe Eric Glasser
Basics Description
A group of conditions characterized by antegrade ventricular activation or retrograde atrial activation via an accessory pathway distinct from the norm al cardiac conduction system : o
Connects the atria and the ventricles by bypassing the atrioventricular (AV) node
o
Conduction is faster and the refractory period is shorter.
o
Sum of vectors allows for shorter pulse rate intervals
Accessory pathways are sm all bands of tissue that failed to separate during developm ent: o
Kent bundle connects atrium to ventricle bypassing the AV node
Results in delta waves and the Wolff-Parkinson-White (WPW) syndrom e
o
Jam es fiber connects atrium to his bundle or lower AV
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node o
Mahain fibers:
Allows a range of connections
Atrium to distal right bundle
Atrium to the right ventricle near the AV annulus
AV node to the ventricle
His bundle to ventricle
Allows for early depolarization of the ventricles generating rapid supraventricular tachycardias
WPW syndrom e: o
Syndrom e caused by ventricular pre-excitation via an accessory AV pathway, the bundle of Kent
o
Conduction m ay be anterograde, retrograde, or both
o
Type A, or orthodrom ic, is the m ost com m on (70%).
Im pulse travels down the AV node and then up the retrograde pathway.
A circuit is created that potentiates reentrant tachycardia.
o
Type B or antidrom ic:
Less com m on than Type A
The circuit operates in the opposite direction
Lown-Ganong-Levine syndrom e: o
Rare pre-excitation syndrom e with an accessory pathway in the AV node, usually Jam es fiber
Com plications: o
Atrial flutter (5%)
o
Atrial fibrillation (10–20%)
o
Paroxysm al SVT (40–80%)
The m ajority of patients with accessory pathways never becom e sym ptom atic.
Risk of death is very low (0.1–4%).
Pa ge 3 8 1
Pre-excitation with wide com plex tachycardia is m ost at risk for ventricular dysrhythm ias.
Prevalence is estim ated at 0.1–0.3% of the population.
Males are affected twice as often as fem ales.
Most are young and healthy.
Pediatric Considerations
Most supraventricular tachycardias in children are the result of AV nodal reentry.
10% are the result of an identified pre-excitation syndrom e.
Genetics
Recent m olecular genetic investigations indicate that pre-excitation disorders m ay have a substantial genetic com ponent.
Pre-excitation disorders are som etim es inherited as single gene disorders.
Etiology
Idiopathic
In association with structural heart disease: o
Cardiom yopathy
o
Transposition of the great vessels
o
Mitral valve prolapse
o
Ebstein anom aly
Diagnosis Signs and Symptoms History
Asym ptom atic
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Palpitations: o
Fast or irregular
Chest Pain
Dyspnea
Dizziness
Nausea
Diaphoresis
Physical Exam
Tachycardia up to 250 bpm : o
Rapid and regular
o
Supraventricular tachycardia
o
Irregular (atrial fibrillation)
Signs of instability: o
Chest pain
o
Hypotension
o
Change in m ental status
o
Rales
o
Cyanosis
Essential Workup
The diagnosis is m ade on the 12-lead ECG
Pre-existing history
Stable patients m ust be carefully m onitored and reassessed for signs of instability.
Tests Lab
Cardiac enzym es only if signs of ischem ia
Consider electrolytes
Imaging ECG:
Com plications of the pre-excitation syndrom e:
Pa ge 3 8 1
o
Atrial fibrillation
o
Atrial flutter
o
SVT
WPW syndrom e o
Short pulse rate (PR) 0.10 seconds
o
Delta wave: Sm all slurred upstroke at the beginning of the QRS
Lown-Ganong-Levine syndrom e: o
PR interval less than 0.12 seconds
o
Norm al QRS upstroke and duration
o
Absence of a delta wave
Mahaim tachydysrhythm ia: o
QRS axis between 0 and –75°
o
QRS duration of 0.15 seconds or less
o
R-wave in lead 1
o
rS com plex in lead V1
o
Precordial transition in lead V4 or later
o
Cycle length between 220 and 450 m secs
Diagnostic Procedures/Surgery Radiofrequency catheter ablation:
Definitive diagnosis and therapeutic procedure for accessory pathways that is not perform ed on an em ergent basis
P.895
Differential Diagnosis
AV nodal re-entry SVT
Ventricular tachycardia
Pa ge 3 8 1
Treatment Pre Hospital
Supplem ental oxygen
Monitor
Synchronized cardioversion: o
Signs of instability
o
Atrial fibrillation with WPW- wide com plex tachycardia
Pre hospital use of adenosine: o
Stable patients do not require em ergent conversion.
o
Unstable patients should undergo cardioversion not adenosine.
Initial Stabilization
Unstable patients: o
Synchronized cardioversion starting with 50 J-m in
o
Increase increm entally until sinus rhythm is restored
Stable patients with wide com plex tachycardia: o
Procainam ide
ED Treatment
Vagal m aneuvers such as a Valsalva: o
Right carotid artery m assage for no m ore than 10 seconds
o
Auscultate the artery first for a bruit that would contraindicate this procedure
Fluid replacem ent and Trendelenburg if the patient has m ild hypotension
Pharm acologic conversion if carotid m assage fails: o
Adenosine
o
Verapam il
Pa ge 3 8 1
Irregular wide com plex tachycardia: o
Procainam ide or m agnesium is effective
o
Never use calcium -channel blockers, beta-blockers, or digoxin
These m edications block the AV node.
Conduction occurs exclusively down the faster accessory pathway.
Precipitation of ventricular dysrhythm ias
Pediatric Considerations
Children m ay develop ventricular rates up to 320 bpm that are poorly tolerated.
Cardiovert unstable children with 0.5–2 J/kg.
Vagal m aneuvers and adenosine are safe in stable children.
Medication (Drugs)
Adenosine: 6 m g rapid IV bolus over 1–2 seconds; if ineffective, repeat with 12 m g (peds: 0.1 m g/kg rapid IV push, repeat with 0.2 m g/kg)
Magnesium : 2 g IV bolus
Procainam ide: 6–13 m g/kg IV at 0.2–0.5 m g/kg/m in until either arrhythm ia controlled, QRS widens 50%, or hypotension, then 2–6 m g/m in, m ax. dose of 1,000 m g
Only to be used in stable narrow com plex tachycardia o
Diltiazem : 0.25 m g/kg IV over 2 m in followed in 15 m in by 0.35 m g/kg IV over 2 m in
o
Esm olol: 0.5 m g/kg over 1 m in; m aintenance infusion at 0.05 m g/kg/m in over 4 m in, then 0.1–0.2 m g/kg/m in continuously
o
Verapam il: 2.5–5 m g IV bolus over 2 m in; m ay
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repeat with 5–10 m g q5–30m in to m ax. 20 m g
Follow-Up Disposition Admission Criteria
Patients with signs of instability require adm ission to a m onitored bed.
Failure of outpatient therapy for continuous pharm acologic control or ablation
Discharge Criteria
The m ajority of patients will be stable and can be discharged once converted to sinus rhythm
Consider low-dose verapam il prophylaxis
Issues for Referral
Follow-up should be arranged with a cardiologist.
Electrophysiologic studies with possible ablative therapy during the outpatient workup
References 1. Rosner MH, Brady WJ Jr, Kefer MP, Martin ML, Electrocardiography in the patient with the Wolff-Parkinson-White syndrom e: diagnostic and initial theraputic issues. Am J Em erg Med. Nov 1999;17:705–714. 2. Stahm er SA, Cowan R, Tachydysrhythm ias. Em erg Med Clin North Am 2006;24(1):11–40 3. Wellens HJ, Brugada P, Penn OC, The Managem ent of Preexcitation Syndrom es. JAMA, 1987 May;257(17):2325–2333. 4. Xie B, Thakur RK, Shah CP, Hoon VK, Clinical differentiation of narrow QRS com plex tachycardia, Em erg Med Clin North Am . 1998
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May;16(2):295–330. 5. Redfearn DP, Krahn AD, Skanes AC, Yee R, Klein GJ Use of m edications in Wolff-Parkinson-White syndrom e. Expert Opin Pharm acother. 2005;6(6):955–963.
Codes ICD9-CM 426.7
ICD10 I45.6
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Pregnancy, Traum a in
Pregnancy,
Trauma in A. Antoine Kazzi Ziad N. Kazzi
Basics Description
Fetal and m aternal injury specific to pregnancy is evident after the first trim ester: o
Increased rate of fetal loss, but not m aternal m ortality
Likelihood of fetal injury increases with the severity of m aternal insult.
Physiologic hypervolem ia of pregnancy m ay lead to an underestim ation of blood loss: o
Clinical shock m ay be apparent only after a 30% m aternal blood loss.
Abdom inal findings are less evident in the gravid patient.
Minor traum a can also lead to fetal injuries (at least 50% of fetal losses).
Less frequent bowel injury
More frequent retroperitoneal hem orrhage due to the engorgem ent of pelvic organs and veins
Pa ge 3 8 2
Increased m orbidity and m ortality with pelvic fractures due to pelvic and uterine engorgem ent
Fetal or uterine traum a includes o
Placental abruption
o
Fetal m aternal hem orrhage
o
Prem ature labor
o
Uterine contusion or rupture (prior C section)
o
Fetal dem ise
o
Prem ature m em brane rupture
o
Hypoxem ic or anatom ic fetal injury (skull fracture)
Abruption occurs in up to 50% of severe traum a and 1–5% of m inor injuries: o
Accounts for up to 50% of fetal loss
o
May occur with no external bleeding (20%)
o
Occurs after 16 weeks of gestation
o
Early sym ptom s of vaginal bleeding, uterine contractions, or abdom inal/uterine tenderness had a sensitivity of 52% and specificity 48% for a preterm delivery or adverse outcom e.
o
Hallm ark is uterine contractions
Fetal/m aternal hem orrhage (FMH) occurs in m ore than 30% of severe traum a: o
Isoim m unization of Rh-negative m others (with as little as 0.03 cc of FMH)
Penetrating traum a results in direct injury to fetus, m aternal shock, and prem ature delivery
Etiology
Traum a occurs in about 7% of all pregnancies
Most com m on cause of nonobstetric m orbidity and m ortality in pregnancy
Rate of fetal loss varies between 3.4 and 38%
Motor vehicle accidents (48–84%)
Pa ge 3 8 2
Falls
Dom estic violence
Direct abdom inal traum a
Penetrating (stab or gunshot)
Electrical or burn
Diagnosis Signs and Symptoms
Abdom inal pain
Uterine contraction
Vaginal bleeding, leakage of fluid
Contusion, lap belt m arks
Essential Workup
Identify m aternal condition first o
Airway m anagem ent and resuscitate as indicated
Determ ine the gestational age (EGA) to assess viability o
Estim ate LMP
o
Fundal height (FH); EGA = FH (cm ) × 8/7 after week 16
o
Doppler fetal heart tones
o
Sonography (m ay m iss sm all abruptions)
Fetal/m aternal m onitoring for >4–6 hours o
Only m onitor viable fetuses (typically with an EGA > 24 weeks)
o
Abruption does not occur if no contractions during first 4 hours of m onitoring
o
More than 8 contractions per hour over 4 hours is associated with an adverse outcom e
o
If m ore than 1 contraction every 10 m in, there is a
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20% incidence of abruption o
The occurrence of bradycardia, poor beat-to-beat variability, or type II “late― deceleration indicates fetal distress.
o
An abnorm al tracing has a sensitivity and specificity of 62, and 49% of predicting adverse fetal outcom es.
o
A norm al tracing com bined with a norm al physical exam has a negative predictive value of nearly 100%.
Tests Lab
CBC, urinalysis
Blood gas and electrolyte panel
Type, Rh, and screening of blood
The Kleihauer-Betke (KB) stain: o
Identifies FMH in vaginal fluid or blood
o
Indicated when quantification of FMH is im portant
Imaging
Shield the uterus if possible, but obtain necessary m aternal radiographs.
Less than 1% of traum a victim s are exposed to m ore than 3 radiation-absorbed doses (rad).
No adverse effects are expected with exposure to radiation up to 10 rads
In a large retrospective study, there was no increase in the relative risk of adverse effects in neonates exposed to radiation in utero.
The rad exposure is estim ated at the following: o
C-spine and chest x-rays: Table o f C o ntents > Priapism
Priapism
David Barlas
Basics Description
Penile erection (engorgem ent of corpora cavernosa) in the absence of sexual arousal that is prolonged and frequently painful
Low-flow priapism : o
Most com m on m echanism
o
Poor venous outflow
o
Usually painful
o
Ischem ia and throm bosis from stagnant, hypoxic blood can occur after a few hours.
o
Fibrosis and im potence are late sequelae.
High-flow priapism : o
Rare
o
Penile arterial laceration with uncontrolled inflow of arterial blood
o
Usually painless
o
Presentation m ay be later than in low-flow priapism .
o
Ischem ia and im potence are uncom m on.
Etiology
Idiopathic
Pa ge 3 8 3
Pharm acologic agents: o
Intracavernosal injectables for the treatm ent of im potence:
o
o
o
PGE-1
Papaverine
Phentolam ine
Psychotropics:
Phenothiazines
Butyrophenones
Trazodone
Sedative-hypnotics
Selective serotonin uptake inhibitors (SSRIs)
Antihypertensives:
Prazosin
Hydralazine
Phenoxybenzam ine
Guanethidine
Rarely im plicated agents:
Sildenafil (Viagra)
Anticoagulants
Cocaine
Marijuana
Ethanol
Androstenedione
Hem atologic disorders predisposing to sludging of blood: o
Sickle cell anem ia
o
Leukem ia
o
Multiple m yelom a
o
Polycythem ia
Penile and perineal traum a can result in arterial laceration and high-flow priapism .
Spinal traum a m ay cause priapism from loss of inhibitory
Pa ge 3 8 4
adrenergic tone.
Rare causes: o
Pelvic neoplasm s and infections
o
Dialysis
o
Parenteral nutrition solutions containing a fat em ulsion
Pediatric Considerations Sickle cell anem ia is the cause of m ost priapism in children.
Diagnosis Signs and Symptoms History Type of priapism m ay be determ ined by history:
Low-flow priapism : o
Painful
o
Predisposing condition or m edication
High-flow priapism : o
Painless
o
Penile traum a
Physical Exam
Diagnosis is clinically apparent.
Penile im plants
Traum a
Urinary retention
Tests Lab
Com plete blood count
Coagulation studies
Pa ge 3 8 4
Sickle cell evaluation m ay be indicated.
Imaging
Duplex Doppler ultrasound can verify and localize the arterial laceration in high-flow priapism .
Angiography enables localization and em bolization of the arterial laceration in high-flow priapism .
Diagnostic Procedures/Surgery Intracavernosal blood gas analysis:
Can help differentiate type of priapism
Because of the possibility of penile arterial injury, a urologist should perform this procedure.
High-flow priapism : near-norm al values
Low-flow priapism : acidosis and hypoxia (O 2 Table o f C o ntents > Pro statitis
Prostatitis
Robert S. Hamilton
Basics Description Five categories:
Prostatic abscess: o
Once com m on after acute prostatitis, now rare except in im m unocom prom ised patients
o
Fever, rectal pain, and leukocytosis despite treatm ent
o
Fluctuant m ass on rectal exam
Acute (bacterial) prostatitis: o
Acute febrile illness
o
System ic sym ptom s m ay appear days before localizing urinary sym ptom s appear.
o
Patients m ay appear toxic and usually have a concurrent cystitis.
Chronic bacterial prostatitis: o
About 10% of cases of prostatitis
o
Most com m on cause of recurrent urinary tract infection in m en
o
WBC and bacteria m ay be present in expressed prostatic secretions (EPS)
Pa ge 3 8 4
Chronic nonbacterial prostatitis (also called prostatosis): o
Sam e sym ptom s as chronic bacterial prostatitis but unable to culture organism s from urine or EPS
Prostatodynia: o
Sym ptom s referable to the prostate
o
No inflam m atory cells are found
o
No bacteria cultured from the urine or EPS
Etiology
Usually a single organism bacterial infection of the prostate
Acute prostatitis: o
Age Table o f C o ntents > Pso riasis
Psoriasis
Stephen R. Hayden
Basics Description
Chronic skin condition presents with erythem atous plaques with silver scaling
Caucasians and atopics m ost affected
Majority of cases are diagnosed between 10 and 30 years of age.
Equal num ber of adult m ale and fem ale cases
Occurs as the result of defective inhibition of epiderm al proliferation
Several clinical presentations: o
Chronic plaque psoriasis:
Most com m on form with classic lesions on the extensor surfaces (elbows, kness, occipital scalp, back)
o
Guttate psoriasis:
Red drop like lesions usually on the trunk
Occurs m ore com m only in children and often after streptococcal infections
o
Pustular psoriasis:
Collections of pustules on one area of the body,
Pa ge 3 8 7
usually palm s or soles o
Erythroderm ic psoriasis:
Sim ple confluent erythroderm a or the patient m ay exhibit pustules
o
Light-sensitive psoriasis:
o
Response to sunburning (Koebner phenom enon)
Inverse flexural psoriasis:
A variant that causes lesions in flexural areas that don't exhibit scaling due to m oisture in these areas
o
HIV-induced psoriasis:
May be the first m anifestation of AIDS with an explosive presentation
o
Keratoderm a blennorrhagicum :
Psoriasis of the penis seen with Reiter syndrom e with a distinctive winding pattern to the lesion (balanitis circinata)
Genetics Autosom al-dom inant inheritance pattern
Etiology
Affects approxim ately 1–2% of people in the United States
Triggers include: o
Drugs:
Lithium
Beta-blockers
Antim alarials
Steroids
NSAIDs
Alcohol
Tetracycline
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o
o
Penicillin
Am iodarone
Morphine
Procaine
Potassium iodide
Sulfapyridine, and sulfonam ides
Infections:
Streptococcal pharyngitis
HIV
Viral URI
Local traum a:
Frostbite
Sunburn
Routine skin breaks (Koebner phenom enon)
o
Stress: em otional and physical
o
Winter:
Low light exposure
Dry weather
o
Cigarette sm oking
o
Horm onal changes such as puberty or m enopause
Diagnosis Signs and Symptoms History
Patients usually com plain of skin lesions that are not intensely pruritic but m ay itch or burn.
May give a history of previously diagnosed psoriasis
May relate one of the above triggers
Age at first appearance of lesions
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Specific location of lesions
Fam ily history of the disease
History of im provem ent with sun exposure, or if recurrent, success of prior regim ens
System ic sym ptom s like fevers or joint pains
Physical Exam
The classic skin lesion is a round red patch with central plaque of silvery white scale that appears on extensor surfaces: o
The lesions not intensely pruritic, but do itch.
Positive Auspitz sign: o
Erythem a and punctuate bleeding when scales are rem oved.
Scalp lesions m ay be confused with seborrhea: o
Lesions that extend beyond the hair borders indicate psoriasis.
Stippling and pitting of nail and oncolysis: o
Yellow or brown band across the nail will help differentiate psoriasis (+ band) from onychom ycosis (– band)
Approxim ately 10% of patients with plaque psoriasis have concom itant psoriatic arthritis: o
Often affects the DIP joints of the hands and feet.
Asym m etric oligoarticular arthritis: o
Present in 70% of these patients
o
Swelling of the juxtaarticular tissue
o
“Sausage-shape― to the affected digits
Essential Workup
The diagnosis is clinical.
Rarely a biopsy is necessary.
Skin biopsies can confirm the diagnosis or rule out other
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conditions in unusual cases.
Tests Lab
Elevated sedim entation rate and uric acid
Decreased serum album in
Anem ia with vitam in B 1 2 , folate, and iron deficiency
Positive streptococcal cultures and titers
Hypocalcem ia and leukocytosis in pustular disease
Negative rheum atoid factor
Key biopsy traits: o
Dilated tortuous capillaries (Auspitz sign)
o
Hyperkeratosis
o
Epiderm al hyperplasia
o
Munro m icroabscesses
Imaging Plain radiographs of the hands or feet m ay show osteoporosis and bone loss at the distal phalanx:
Pencil-in-cup deform ation at the MTP or MCP joints
Sacroiliitis and ankylosing spondylitis m ay also be seen on radiographs.
Differential Diagnosis
Best thought of by region: o
Scalp: seborrhea
o
Flexure creases:
Candidiasis
Intertrigo
Eczem a
o
Nails: onychom ycosis
o
Trunk and extrem ities:
Num m ular eczem a
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Pityriasis rosea or rubra pilaris
Tinea
System atic lupus erythem atosus
Syphilis
Drug eruption
Atopy
Mycosis fungoides
Squam ous cell carcinom a
Treatment Initial Stabilization
General resuscitation efforts aim ed at correcting fluid and electrolyte abnorm alities
Treating sepsis if present: o
Cultures of lesions, blood, and urine
Soothing m oist com presses are appropriate
System ic steroids should not be used as they m ay predispose to severe com plications
P.909
ED Treatment
There are three basic types of treatm ent for psoriasis: o
Topical therapy
o
System ic therapy
o
Phototherapy
Topical therapy is the m ost com m only prescribed treatm ent m odality from the ED.
System ic therapy is usually em ployed only after patients
Pa ge 3 8 7
have failed topical and phototherapy.
Exceptions where system ic therapy m ay be used: o
Generalized pustular psoriasis
o
Very active psoriatic arthritis
o
Psoriasis which is considered severely disabling
Phototherapy is not an ED treatm ent m odality.
Derm atology consult should be obtained in all severe cases.
Medication (Drugs)
Mild to m oderate disease: o
Usually topical treatm ent only
o
No single topical agent works best for all people.
o
Em ollients:
Hydrates and softens plaques
Greasier choices work best, but are poorly tolerated by patients
o
Keratolytics:
Help to rem ove plaques
Salicylic acid (2–10%) is the m ainstay of treatm ent (caution m ust be used in applying near the eyes)
o
Coal-tar preparations:
Usually used with topical steroids
Ointm ents and sham poos are available
o
Anthralin
o
May be used in com plex treatm ent regim ens with other topical agents and ultraviolet light
o
Topical corticosteroids:
Mainstay of treatm ent in the United States
Best results are obtained by rotating drugs and
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using occlusive dressings.
Sm all lesions m ay be treated with intralesional Kenalog as m ay psoriatic nails.
Steroids have been im plicated in serious relapses and pustular psoriasis.
o
Vitam in D derivatives:
o
Topical retinoids (Tazarotene):
Calcipotriene is applied to lesions twice daily
Particularly useful for scalp lesions
Moderate to severe disease: o
The above-nam ed agents m ay be em ployed along with phototherapy and system ic m edications.
o
Phototherapy:
Indicated in patients with very large areas of skin involvem ent or refractory to topical treatm ents.
Proper facilities are required for this form of treatm ent.
Ultraviolet B light is usually com bined with one or m ore topical agents and has reports of 80% rem ission.
Ultraviolet B m ay be used alone in guttate psoriasis.
Ultraviolet A light (PUVA) is com bined with a system ic agent (psoralen) which sensitizes the skin to UVA light.
Therapy is usually given two to three tim es per week.
o
System ic agents: m ay be used in various com binations with the above m odalities:
Methotrexate (im m unosuppressant); assess renal, liver, and hem atologic function prior to
Pa ge 3 8 8
therapy and not to be used during pregnancy
Etretinate: a retinoid, it causes dryness, scaling, redness, and tenderness of the skin
System ic corticosteroids: not in favor due to iatrogenic Cushing syndrom e; it m ay have a role in acute erythroderm ic psoriasis if patient is extrem ely ill
Cyclosporine: use in conjunction with derm atology consult
o
Psoralens (see above): have no effect unless com bined with UVA light therapy
o
Etanercept (Enbrel): injectable agent that works with the im m une system to reduce inflam m ation
o
Alefacept (Am evive): im m unosuppressant given as injection once per week
Follow-Up Disposition Admission Criteria Acute erythroderm a and acute pustular psoriasis warrant adm ission for supportive therapy and system ic treatm ent as noted above.
Discharge Criteria
Patients without the above-m entioned form s m ay be discharged.
Advise patients the disease is not contagious.
Warn against excessive scrubbing to loosen scale, as it m ay worsen the disease.
Educate the patient on avoiding m edications that trigger relapses.
Pa ge 3 8 8
Refer patients to the National Psoriasis Foundation (telephone 503-244-7404) for further inform ation
Pediatric Considerations
37% of all psoriasis cases occur before age 20.
The younger the patient at onset of disease, the worse the course.
The em otional side of this chronic disease m ay be param ount in children whose body im age is being form ed.
In general, topical agents are well tolerated, but PUVA and system ic agents are generally avoided in children.
Pregnancy Considerations Many of the drugs used to treat psoriasis are contraindicated in pregnancy.
References 1. Cam isa C. Psoriasis: a clinical update on diagnosis and new therapies. Cleve Clin J Med. 2000;67(2):105–106,109–113,117–119, S193. 2. Habif T. Psoriasis. In: Habif T, ed. Clinical derm atology. 3rd ed. St. Louis: CV Mosby,1996: 190–212. 3. Rogers M. Childhood psoriasis. Curr Opin Pediatr. 2002;14(4):404–409. 4. Wood J. Treatm ent of psoriasis. N Engl J Med. 1995;332:581–588.
Codes ICD9-CM 696.1
ICD10 L40.9
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Psychiatric C o m m itm ent
Psychiatric
Commitment Jennifer M. Park Lawrence Park
Basics Description Com m itm ent criteria (check specific laws in your state):
Individual is m entally ill.
Failure to hospitalize or discharge from hospital creates likelihood of serious harm .
Likelihood of serious harm defined as: o
Substantial risk of physical harm to self: threats or attem pts at suicide
o
Substantial risk of physical harm to other persons: hom icidal or violent behaviors, or others are placed in reasonable fear of violent behaviors
o
Very substantial risk of physical im pairm ent owing to inability to protect self resulting from im paired judgm ent; reasonable protection not available in com m unity
No less-restrictive alternative to hospitalization would attenuate risk.
Pa ge 3 8 8
Physician usually m ust sign form attesting that patient m eets one of above criteria.
(1) Often leads to 72-hour m andatory hospitalization, which m ay be followed by petition for psychiatric com m itm ent (2) once the patient is adm itted involuntarily, psychiatrist petitions the court for psychiatric com m itm ent.
If court does not grant petition for com m itm ent, patient m ust be released from psychiatric facility.
Diagnosis Signs and Symptoms
Civil com m itm ent: confinem ent of an individual
Involuntary com m itm ent: confinem ent against patient's will
Basis of civil com m itm ent: danger to self or others
Psychiatric (civil) com m itm ent: o
Refers to order by judge for continued hospitalization of inpatient in a m ental health facility for treatm ent of psychiatric disease against patient's wishes
o
Based on danger to self or others by reason of m ental illness
Psychiatric com m itm ent not indicated for other causes of dangerous behavior:
o
Anger
o
Antisocial behavior
o
Substance abuse
o
Medical illness
Psychiatric com m itm ent usually involves two steps: o
Initial involuntary hospitalization in psychiatric
Pa ge 3 8 8
facility, m ost com m only initiated by a psychiatrist o
Petition to court for psychiatric com m itm ent
Essential Workup
Psychiatric evaluation through history/m ental status exam : o
History of psychiatric illness
o
Recent change in behavior or thinking
o
Medication dosages
o
Drugs of abuse: am ount and tim e of last use
o
Disabling thought patterns: hallucinations, delusions, disorganization
Assessm ent of com m itm ent criteria: o
Threat of violence toward self
o
Threat of violence toward others
o
Inability to care for self or severe deficits in judgm ent
Rule out crim inal behavior.
Com plete physical and neurologic exam
Rule out m edical causes for m ental status change, com m only delirium or substance intoxication/withdrawal.
Tests
Labs as indicated by history and physical: o
Electrolytes, blood urea nitrogen, creatinine, glucose
o
Liver function tests
o
CBC and differential
o
Toxicology screens and m edication levels
o
Urinalysis if infection suspected
Im aging: o
CT of head if injury or structural CNS pathology suspected
Differential Diagnosis
Pa ge 3 8 8
Intoxication or withdrawal
Delirium
Dem entia
Traum atic brain injury
Antisocial behavior
P.911
Treatment Pre Hospital Controversies/ethical considerations:
Involuntary adm ission leads to loss of basic rights.
Parens patriae power: State's authority to care for citizen who cannot care for self
Police power: State's authority to detain citizen who is danger to self or som eone else
Initial Stabilization
Initial containm ent by police
Transport patient to facility for psychiatric evaluation.
Ensure patient and staff safety
ED Treatment
Restrain dangerous patients as needed: o
Nurse or security guard standing outside room
o
Physical restraints
o
Medications given PO, intram uscularly, or intravenously
o
Closely observe patients when using physical restraints or involuntary m edications.
Pa ge 3 8 8
Determ ine if patient requires psychiatric hospitalization.
Medication (Drugs) May be necessary for extrem ely agitated patient
Disposition Discharge Criteria Patients m ay be discharged after initial psychiatric evaluation if they:
Can care for them selves adequately and
Have no intention of harm to self or others
References 1. Behnke SH, Hilliard JT. The Essentials of Massachusetts Mental Health Law. New York: WW Norton; 1998. 2. Folstein MF, Folstein FE, McHugh PR. The “m ini-m ental state†•: a practical m ethod for grading the cognitive state of patients for the clinician. J Psychiatr Res. 1975;12:189. 3. Gutheil TG, Appelbaum PS. Clinical Handbook of Psychiatry and the Law. 3rd ed. Philadelphia: Lippincott William s & Wilkins; 2000. 4. LaFond JQ. Law and the delivery of involuntary m ental health services. Am J Orthopsychiatry. 1994;64:209–222. 5. Nickens HW. Assessm ent and m anagem ent of the violent patient. In: Dubin WR, Hom ke N, Nichory H, eds. Clinics in Em ergency Medicine: Psychiatric Em ergencies. Vol 4. Edinburgh, Scotland: Churchill Livingstone; 1984:101–111. 6. Schouten R. Psychiatry and the law I: inform ed consent, com petency, treatm ent refusal, and civil com m itm ent. In: Stern TA, Herm an JB, eds. Psychiatry Update and Board Preparation. New York: McGraw-Hill; 2000:415–419.
Codes
Pa ge 3 8 8
ICD9-CM V70.2 General psychiatric exam ination, other and unspecified
ICD10 Z00.4 General psychiatric exam ination
Pa ge 3 8 8
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Psycho sis, Acute
Psychosis, Acute
Richard Wolfe Robert Vissers
Basics Description
A severe m ental disorder characterized by derangem ent of personality and loss of contact with reality causing gross disorganization of a person's m ental capacity
The psychosis m ay be secondary to functional (psychiatric) or organic (m edical) causes.
Medical psychoses are generally secondary to system ic or neurologic diseases or neuroactive m edications.
Neurodevelopm ental abnorm alities in the dopam inergic and serotonergic system s are im plicated in functional psychosis.
Etiology Organic
Autoim m une disease
CNS: o
Alzheim er disease
o
Cerebritis:
Autoim m une disorders
Pa ge 3 8 9
o
Cerebrovascular accident
o
Encephalitis
o
Encephalopathy
o
Head injury
o
Huntington chorea
o
Migraine
o
Multiple sclerosis
o
Neoplasm s
o
Norm al pressure hydrocephalus
o
Parkinson disease
o
Seizure
Endocrine: o
Addison disease
o
Cushing disease
o
Thyroid dysfunction
o
Parathyroid dysfunction
o
Postpartum psychosis
o
Recurrent m enstrual psychosis
o
Sydenham chorea
Metabolic: o
Intoxication or withdrawal
o
Hypercarbia
o
Hypoglycem ia
o
Hypoxia
o
Porphyria
o
Electrolyte im balance
Nutritional deficiencies: o
Niacin
o
Thiam ine
o
Vitam in B 1 2 and folate
Organ failure: o
Hepatic encephalopathy
Pa ge 3 8 9
o
Renal failure
Pharmacologic
Psychoactive agents
Benzodiazepines
Chlordiazepoxide
Antidepressants
Antiepileptics
Antibiotics:
o
Isoniazid
o
Rifam pin
Cardiovascular agents: o
Captopril
o
Digoxin
o
Methyldopa
o
Procainam ide
o
Propranolol
o
Reserpine
Drugs of abuse: o
Alcohol
o
Am phetam ines
o
Cocaine
o
Opioids
o
Hallucinogens
Other: o
Steroids
o
Heavy m etals
o
Antihistam ines
o
Cim etidine
o
Disulfiram
Functional
Brief psychotic disorder:
Pa ge 3 8 9
o
Usually secondary to acute em otional stress
Schizophreniform disorder: o
Sym ptom s present 1–6 m onths
Schizophrenia
Mood disorder with psychotic features or schizo-affective disorder
Diagnosis Signs and Symptoms
Delusions are erroneous beliefs that: o
Involve a m isinterpretation of perceptions
o
Are clearly im plausible
o
Are often persecutory, religious, or som atic in nature
Hallucinations: o
Sensory experiences that exist only in the m ind of the patient
o
Can involve any sense; auditory and visual are m ost com m on.
Disorganized speech: o
Loose associations
o
Neologism s
o
Perseverations
o
Poverty of content
o
Word salad
Disorganized or catatonic behavior: o
Unable to perform goal-directed behavior
o
Unaware of the environm ent
Negative sym ptom s: o
Flattened affect
o
Poverty of speech
Pa ge 3 8 9
o
Avolition:
Unable to m aintain goal-directed activities
Features suggesting an organic etiology: o
Sudden onset
o
>40 years old
o
Fluctuating course
o
Confusion
o
Headaches
o
Loss of consciousness
o
Focal neurologic sym ptom s
o
Speech difficulties
o
Abnorm al vital signs
o
Disorientation
o
Psychom otor retardation
o
Visual hallucinations
o
Global im pairm ent of attention and cognitive function
o
Delusions are disorganized.
o
Labile affect
o
Incoherent speech
o
Social im m odesty
Essential Workup
The workup is case specific and prim arily based on the suspected etiology.
Functional and organic etiologies are generally distinguished by features of the history and physical exam ination described below.
Collateral history is im portant, as the patient history is often unreliable.
Com plete physical exam ination with particular attention to the neurologic exam ination, vital signs, and m ental status exam ination
Mental status exam ination:
Pa ge 3 8 9
o
Orientation
o
Mem ory (short- and long-term )
o
Attention (or calculation)
o
Recall
o
Language
o
Thoughts
o
Perception
o
Mood/Affect
o
Judgm ent
P.913
Tests Lab Laboratory evaluation is needed in patients at risk for an organic etiology:
Routine “screening labs― not helpful
Specific studies should be guided by the suspected underlying etiologies.
Serum glucose
Toxicologic screen
Serum electrolytes
Urinalysis
Imaging Head CT scan indicated in patients at risk for a neurologic etiology
Diagnostic Procedures/Surgery Lum bar puncture indicated if signs and sym ptom s suggest delirium
Differential Diagnosis See Etiology
Pa ge 3 8 9
Treatment Pre Hospital
Prevention of violent behavior m ust be established before transport.
Consider police backup to reduce risk of violence and to place restraints.
Controversies Chem ical restraints are rare in field protocols; m ay be an adjunct to physical restraints.
Initial Stabilization Prevention of violence:
See Violence, Managem ent of
ED Treatment
Antipsychotic agents are sym ptom specific and therefore useful in both organic or functional psychoses.
High potency, IV antipsychotics, such as haloperidol, are m ost com m only utilized in the ED setting.
Rapid tranquilization m ay be achieved with the addition of a benzodiazepine.
If a specific organic etiology is identified, therapy should be directed toward the treatm ent of the m edical condition.
Treatm ent of adverse effects from antipsychotic m edications: o
Extrapyram idal sym ptom s, dystonia, akathisia, pseudoparkinsonism , and tardive dyskinesia:
o
Treat with diphenhydram ine or benztropine.
Neuroleptic m alignant syndrom e is a life-threatening com plication:
Pa ge 3 8 9
Characterized by hypertherm ia, m uscle rigidity, autonom ic instability, and altered consciousness
Treat with supportive m easures and dantrolene.
Droperidol has been reported to cause QT prolongation and dysrhythm ias.
Medication (Drugs)
Antipsychotics: o
Droperidol: 2.5–5.0 m g IV or IM
o
Haloperidol: 2–5 m g IV or IM or PO; 0.5–2.0 m g for elderly
o
Benzodiazepines o
Risperidone: 1–2 m g PO
Lorazepam 1.0–2.0 m g IV or IM or PO
Treatm ent of m edication side effects o
Benztropine: 2 m g IM or IV
o
Dantrolene: 1 m g/kg IV repeated to sym ptom resolution or total of 10 m g/kg
o
Diphenhydram ine: 50 m g IV, IM, or PO
Follow-Up Disposition Admission Criteria
If the cause is determ ined to be m edical in origin, adm ission to the appropriate m edical service is indicated.
Acute psychosis of psychiatric etiology requires adm ission to a psychiatric service.
Safety of staff and patient m ust be m aintained in the
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hospital after disposition from the ED, including possible chem ical and physical restraint or a one-on-one sitter.
If the patient is felt to be a danger to either self or others, the patient cannot be discharged.
Involuntary com m itm ent is required if patient is uncooperative and a threat to self or others.
Discharge Criteria
If the psychotic behavior was caused by a tem porary, reversible organic cause (e.g., drug intoxication) and the patient is now deem ed to be in control, com petent, and not a danger to self or others, the patient m ay be discharged.
Psychiatric consultation prior to discharge is recom m ended.
References 1. Battaglia J, Moss S, Rush J, et al. Haloperidol, lorazepam , or both for psychotic agitation? A m ulticenter, prospective, double-blind em ergency departm ent study. Am J Em erg. 1997;15:335–340. 2. Hutzler JC, Rund DA. Behavioral disorders: Em ergency assessm ent and stabilization. In: Tintinalli JE, Kelen GD, Stapczynski JS, eds. Em ergency m edicine: a com prehensive study guide. 5th ed. New York, NY: McGraw-Hill, 2000. 3. Richards CF, Gurr DE. Psychosis. Em erg Med Clin North Am . 2000;18:253–262. 4. Lukens TW, Wolf SJ, Edlow JA, et al. Clinical policy: critical issues in the diagnosis and m anagem ent of the adult psychiatric patient in the em ergency departm ent. Ann Em erg Med. 2006;47(1):79–99.
Codes ICD9-CM 297
Pa ge 3 8 9
298 299
ICD10 F23.9
Pa ge 3 8 9
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Psycho sis, M edical vs. Psychiatric
Psychosis,
Medical vs. Psychiatric Kathy Sanders
Basics Description
Wide variety of m edical and neurological illnesses have psychosis as one of their presenting m anifestations or psychosis em erges during the course of the illness.
Difficult to determ ine whether m edical or psychiatric illness is the cause of psychotic behavior
Nature of im pairm ent determ ines whether a prim arily psychiatric disorder or a secondary psychosis based on a m edical, neurologic, or toxic etiology
Evaluation for underlying m edical or neurologic condition essential for patients with psychotic presentation without previous history of psychosis
Etiology
Age factor: o
Late adolescence/early adulthood presentation m ore likely to be schizophrenia
o
Middle- to late-life presentation m ore likely to be m edical cause.
Pa ge 3 9 0
Etiology of the CNS im pairm ent that results in a psychotic presentation include: o
Neurological disorders
o
Metabolic conditions
o
Toxic or drug effects
o
Nonorganic or psychiatric
Diagnosis Signs and Symptoms
Psychosis characterized by: o
Im paired reality testing
o
Inappropriate affect
o
Poor im pulse control
o
Regressive or inappropriate behavior
Hallucinations: o
Auditory
o
Visual
o
Olfactory
o
Tactile
Delusions: o
False beliefs held strongly by the patient even in the face of reasonable evidence to the contrary
Affective sym ptom s include m ania and catatonic states.
Focal and diffuse CNS im pairm ent result in derangem ents of:
o
Thinking
o
Com m unicating
o
Perceiving
Responding inappropriately
Pa ge 3 9 0
Essential Workup
Careful history and physical exam ination
Laboratory investigation for new or previously undiagnosed psychosis
Use history and physical to guide workup.
Tests Lab
CBC
Electrolytes, blood urea nitrogen/creatinine, glucose
Toxicology screen
Am m onium level
Urinalysis
Thyroid function tests
Imaging CT head
Diagnostic Procedures/Surgery Lum bar puncture/cerebrospinal fluid analysis
Differential Diagnosis
Neurological: o
Head traum a
o
Space-occupying lesions
o
Cerebrovascular disease
o
Postanoxic encephalopathy
o
Seizure disorders
Degenerative diseases: o
Alzheim er
o
Pick
o
Huntington's
o
Parkinsonism
o
Hydrocephalus
Pa ge 3 9 0
CNS infections:
Viral
Herpetic
Nonherpetic (e.g., rabies, m um ps, influenza)
Cerebral m alaria
Syphilis
Toxoplasm osis
Trypanosom iasis
Schistosom iasis
Myelin diseases
Multiple sclerosis
Leukodystrophies
Marchiafava-Bignam i disease
Narcolepsy
Endocrine
Thyroid disorders
Parathyroid disorders
Diabetes m ellitus
Pituitary abnorm alities
Adrenal abnorm alities
Postpartum psychosis
Metabolic: o
Electrolyte im balance
End-organ failure: o
Respiratory cardiac
o
Renal
o
Hepatic
o
Pancreatic
Ketoacidosis
Porphyria
Wilson disease
Deficiency diseases:
Pa ge 3 9 0
o
Pernicious anem ia
o
Beriberi, Wernicke-Korsakoff syndrom e
o
Pellagra
o
Pyridoxine deficiency
System ic illnesses: o
Carcinom atosis
o
Infections, sepsis
Viral syndrom es: o
Hepatitis
o
Mononucleosis
Collagen and autoim m une disorders
Postoperative states:
o
Delirium
o
Psychosis
o
Depression
Intoxicants: o
Alcohol
o
Barbiturates
Stim ulants
Hallucinogens
Opiates
Heavy m etals
Brom ide
Organic phosphates
Anticholinergic com pounds
Carbon m onoxide
Industrial agents
Withdrawal states:
o
Alcohol withdrawal (delirium trem ens)
o
Barbiturate withdrawal
Medication side effects: o
Antipsychotics
Pa ge 3 9 0
o
Steroids
o
Sedative-hypnotics
o
Antidepressants
o
Lithium carbonate
o
Cim etidine
o
Disulfiram
o
Belladonna alkaloids
o
Levodopa
o
Anticonvulsants
o
Antituberculous drugs
o
Antiinflam m atory drugs
o
Antihypertensive agents
o
Cardiac drugs digitalis lidocaine propranolol procainam ide
o
Idiosyncratic drug reaction of any m edication
Psychiatric: o
Schizophrenia
o
Manic-depressive illness
o
Stress reactions including posttraum atic stress disorder (PTSD)
o
Interm ittent explosive disorder
o
Im pulse control disorder
P.915
Treatment Initial Stabilization
ABCs of psychiatric assessm ent: o
Safety
Pa ge 3 9 0
o
Evaluation
o
Managem ent
If uncooperative and dangerous, control behavior with neuroleptics or benzodiazepines.
ED Treatment
Determ ine if a m edical cause for psychosis
Treat underlying m edical illness or substance abuse disorder
Psychiatric evaluation for true psychosis
Control psychotic behavior with psychotropic m edications: o
Treatm ent approach based on the severity of the psychotic features of the m edical or psychiatric illness
o
Severe behavioral disturbance of m edical psychosis requires sedating the patient to adequately attend to the m edical workup and treatm ent.
o
The m ore behaviorally unstable the patient, the m ore difficult it is to stabilize m edical derangem ents.
Haloperidol in com bination with lorazepam : o
Safest, fastest, and least disruptive of the ongoing m ental exam ination of the patient
o
Effectively calm s and sedates the behaviorally agitated, psychotic, m edical patient
o
Atypical neuroleptics (olanzapine, risperidone, ziprasidone):
Targets the lim bic dopam ine neuroreceptors
Im proves both positive and negative sym ptom s of schizophrenia
Few extrapyram idal side effects
Better tolerated than typical neuroleptics
Sedation, weight gain
Olanzapine and ziprasidone can be given
Pa ge 3 9 0
parenterally
Olanzapine zydus and risperidone m -tab are a dissolving wafer preparation
Medication (Drugs)
Neuroleptics. o
Haloperidol: 2.5–10 m g IM or IV
o
Atypical neuroleptics used in em ergency:
olanzapine 5–10 m g PO or Zydis or IM
risperidone 1–2 m g PO or Zydis
ziprasidone 10–20 m g IM
Benzodiazepines: o
Diazepam : 5–10 m g IV
o
Lorazepam : 0.5–2 m g IV or IM
o
Midazolam : 1–5 m g IV
Follow-Up Disposition Admission Criteria
Psychosis prim arily psychiatric (i.e., schizophrenia/m anic depressive)
Adm ission sam e as for involuntary com m itm ent: o
Suicidal/hom icidal behavior
o
Inability to care for self
o
Deranged thought pattern that can be threat to self or others
Psychosis prim arily m edical etiology
Adm ission dictated by specific m edical condition and
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behavior
Discharge Criteria
Stable m edical condition
Not suicidal/hom icidal
Able to care for self
Capable of m aking m edical decisions
Issues for Referral
Patient's insurance coverage determ ines inpatient psychiatric disposition options.
Case m anagem ent or social services are necessary for psychiatric disposition.
References 1. Cum m ings JL. Secondary psychoses, delusions, and schizophrenia. In: Cum m ings JL, ed. Clinical neuropsychiatry. Orlando, FL: Grune & Stratton, 1985:163–182. 2. Goff D, Freudenreich O, Henderson DC. Psychotic patients. In: Stern TA, Fricchione GL, Cassem NH, Jellinek MS, Rosenbaum JR, eds. MGH Handbook of general hospital psychiatry. St. Louis: Mosby, 2004:155–174. 3. Sanders KM. Aggressive and im pulsive patients. In: Stern TA, Fricchione GL, Cassem NH, Jellinek MS, Rosenbaum JR, eds. MGH Handbook of general hospital psychiatry. St. Louis: Mosby, 2004: 501–512.
Codes ICD9-CM 289.9
ICD10 F29
Pa ge 3 9 0
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Pulm o nary C o ntusio n
Pulmonary
Contusion Gregory W. Lampe
Basics Description Transfer of kinetic energy to the lung parenchym a adjacent to traum atic injury:
Causes disruption of the alveolocapillary m em brane
Developm ent of pulm onary contusion
Microhem orrhage, localized pulm onary edem a, and extravasation of blood into the interstitial and alveolar spaces: o
Arteriovenous shunting
o
Ventilation-perfusion m ism atch
o
Decreased lung com pliance
o
Hypoxem ia
o
Respiratory failure
Etiology
Blunt or penetrating thoracic traum a
Sudden deceleration
Fall from height
Motor vehicle accident
Pa ge 3 9 0
Assault
Missile
Pediatric Considerations Relatively m ore elastic chest wall m ay transm it greater force to the thoracic contents in children.
Diagnosis Signs and Symptoms History
Blunt or penetrating thoracic traum a by any m echanism
Mechanism as described by patient, parent or prehospital personnel: o
Seat belt usage
o
Steering wheel dam age
o
Air bag deploym ent
Pleuritic chest pain
Dyspnea
Hem optysis
Physical Exam
Auscultation: o
Initially norm al or dim inished breath sounds
o
Progresses to wet rales, absent breath sounds
Localized ecchym osis, edem a, erythem a and tenderness of chest wall
Bony stepoffs, crepitus, point tenderness associated with rib fractures
Ecchym osis from seat belt, aka “seat belt sign―
Ecchym osis from steering wheel im pact
Splinting respirations
Pa ge 3 9 1
Cyanosis, tachycardia, hypotension
Dyspnea, tachypnea
Alert Insidious onset increasing 6–12 hours post injury
Essential Workup Chest radiograph:
Radiographic findings m ay not appear until 6–12 hours post injury.
Patchy alveolar infiltrates to frank consolidation.
Associated intrathoracic injury: o
Rib fractures
o
Pneum othorax, hem othorax
o
Widened m ediastinal silhouette
Tests Lab Arterial blood gas m ay reveal hypoxem ia and elevated alveolar-arterial gradient.
Imaging Thoracic CT is useful in detecting pulm onary injury and associated intrathoracic injuries not identified on chest radiograph.
Differential Diagnosis
Adult respiratory distress syndrom e
Pulm onary laceration, infarction or em bolism
Congestive heart failure
Pneum onia, abscess or other infectious process
Noncardiogenic causes of pulm onary edem a
P.917
Pa ge 3 9 1
Treatment Pre Hospital Thoracic traum a with significant m echanism or pre-existing pulm onary disease should be routed to the nearest available traum a center.
Initial Stabilization
Manage airway and resuscitate as indicated.
IV line, O 2 , continuous cardiac m onitoring and pulse oxim etry
Control airway: o
Endotracheal intubation indications:
Severe hypoxem ia (PaO 2 Table o f C o ntents > Pulm o nary Edem a
Pulmonary Edema
Shamai Grossman Seric Cusick
Basics Description
Im balance in Starling forces causes an increase in lung fluid secondary to leakage from pulm onary capillaries into the interstitium and alveoli of the lung.
If capacity of lym phatic drainage is exceeded, liquid accum ulates in interstitial spaces surrounding bronchioles and lung vasculature, creating congestive heart failure (CHF).
If increased fluid and pressure tracks into the interstitial space around the alveoli and disrupts the alveolar m em brane, the alveoli are flooded causing pulm onary edem a.
Systolic dysfunction is characterized by a dilated left ventricle with im paired contractility.
Diastolic dysfunction occurs in a norm al or intact left ventricle with im paired ability to relax and receive as well as eject blood.
New York Heart Association classification of CHF: o
Class I: not lim ited in norm al physical activity by
Pa ge 3 9 1
sym ptom s o
Class II: ordinary physical activity results in fatigue, dyspnea, or other sym ptom s
o
Class III: m arked lim itation in norm al activity
o
Class IV: sym ptom s at rest or with any activity
Epidem iology: o
400,000 new cases present yearly.
o
Prevalence is 1–2% of the general population.
o
Incidence is greater in m ales than in fem ales for patients aged 40–75 years.
o
No sex predilection exists for patients older than 75 years.
o
Incidence of CHF increases with increasing age and affects 10% of population older than 75.
o
30–40% of patients with CHF are hospitalized every year.
o
Five-year m ortality after diagnosis was reported as 60% in m en and 45% in wom en.
o
Median survival of 3.2 years for m ales and 5.4 years for fem ales
o
Sudden death accounts for up to 45% of all deaths.
o
In-hospital m ortality rate: 19%
o
African Am ericans are 1.5 tim es m ore likely to die of CHF than whites.
o
Mortality approxim ately 50–60% for noncardiogenic pulm onary edem a and up to 80% for cardiogenic shock
Etiology
Six categories: o
Pulm onary edem a secondary to altered capillary perm eability
o
Pulm onary edem a secondary to increased pulm onary
Pa ge 3 9 1
capillary pressure: pulm onary venous throm bosis, stenosis or veno-occlusive disease, and volum e overload o
Pulm onary edem a secondary to decreased oncotic pressure found with hypoalbum inem ia
o
Pulm onary edem a secondary to large negative pleural pressure with increased end expiratory volum e
o
Pulm onary edem a secondary to lym phatic insufficiency
o
Pulm onary edem a secondary to m ixed or unknown m echanism s
Specific etiologies: o
Cardiogenic/altered capillary perm eability:
Left heart failure
Ischem ic heart disease
Acute m yocardial infarction
Aortic and m itral valvular disease
Hypertensive heart disease
Cardiom yopathy
Volum e overload
Arrhythm ias
Endocarditis
Myocarditis
Congenital heart disease
Acute rheum atic fever and rheum atic heart disease
o
o
Septal defects
High cardiac output states:
Thyrotoxicosis
Beriberi
Urem ia
Pa ge 3 9 1
Respiratory/adult respiratory distress syndrom e/altered capillary perm eability:
o
Pneum onia
o
Inhaled toxins
o
Circulating foreign substances
o
Snake venom
o
Endotoxins
o
Aspiration
o
Acute radiation pneum onitis
o
Dissem inated intravascular coagulation
o
Hypersensitivity pneum onitis
o
Shock lung in association with nonthoracic traum a
o
Acute hem orrhagic pancreatitis
o
Near drowning
Hypoalbum inem ia/decreased oncotic pressure: o
Renal failure
o
Hepatic failure
o
Protein-losing enteropathic
o
Severe derm atologic disease with high protein losses
o
Starvation
Increased negativity of interstitial pressure: o
Rapid decom pression of a pneum othorax
o
Asthm a
Lym phatic obstruction: o
Post–lung transplant
o
Lym phangitic carcinom atosis
o
Fibrosing lym phangitis
Mixed or unknown m echanism : o
High-altitude pulm onary edem a
o
Neurogenic pulm onary edem a
o
Narcotic overdose
o
Pulm onary em bolism
Pa ge 3 9 1
o
Eclam psia
o
Postcardioversion
o
Postanesthesia
o
Post–cardiopulm onary bypass
o
Postextubation
Diagnosis Signs and Symptoms History
General: o
Weakness
o
Fatigue
o
Anxiety
Respiratory: o
Dyspnea with exertion is the single m ost sensitive test.
o
Dyspnea at rest is also com m on.
o
Orthopnea, paroxysm al nocturnal dyspnea
o
Cough
o
Pink, frothy sputum
o
Noisy respirations
Cardiovascular: o
Nocturnal angina
o
Presence of valvular heart disease
Physical Exam
General: o
Diaphoresis
o
Cold, ashen, or cyanotic skin
Respiratory:
Pa ge 3 9 1
o
Tachypnea
o
Wheezing, rhonchi, gurgles
o
Moist, crepitant rales noted initially at bases and progressing to apices
o
Dilated alae nasi
o
Inspiratory retraction of the intercostal spaces or supraventricular fossae
o
Cheyne-Stokes respirations
Cardiovascular: o
Tachycardia
o
Jugular venous distention
o
Abnorm al heart sounds
o
Increased P 2 , S 3 , S 4
o
Pulsus alternans—alternating weak and strong pulses
Essential Workup A careful history and physical should determ ine if the underlying etiology is cardiogenic.
Tests Lab
B-type natriuretic peptide (BNP): o
A proteohorm one secreted by the left ventricle in response to wall tension
o
Laboratory param eter for the detection and follow-up of heart failure:
500 pg/m L—m ost consistent with CHF
BNP is available for point of care testing with 10- to 15-m inute turnaround tim e.
Pa ge 3 9 2
o
May be helpful in determ ining whether dyspnea is secondary to chronic obstructive pulm onary disease or CHF
N-term inal pro-BNP: o
B-natriuretic peptide precursor
o
Can be used concom itantly with Nesiritide
P.919
Serum electrolytes, blood urea nitrogen, creatinine, urinalysis o
Hyperkalem ia with severe low output states
o
Increased creatinine and dilutional hyponatrem ia are observed in severe cases.
o
Mild azotem ia and proteinuria are observed in early and m ild-to-m oderate disease.
Elevated alanine am inotransferase, aspartate am inotransferase, or bilirubin suggests congestive hepatopathy
Cardiac enzym es m ay be useful if ischem ia or infarction is presum ed to be the underlying cause.
Serum lipase if pancreatitis is suspected as the underlying cause
Arterial blood gas m ay help evaluate hypoxem ia, ventilation/perfusion m ism atch, hypercapnia, and acidosis.
Imaging
Chest radiograph: o
Three phases of pulm onary findings
o
Pulm onary redistribution:
o
Cephalization of vessels
Interstitial edem a:
Effusions
Pa ge 3 9 2
o
Kerley B lines
Classic butterfly infiltrate
Frank alveolar infiltrates:
May be asym m etric and m istaken for pneum onia
ECG: o
Assess for underlying cardiac disorders.
Echocardiography: o
Excludes acute valvular pathology
o
Assessm ent for focal or global left ventricle dysfunction
o
Measurem ent of cardiac output
Differential Diagnosis
Pneum onia
Asthm a
COPD exacerbation
Pulm onary em bolism
Hyperventilation syndrom e
Pericardial tam ponade
Pneum othorax
Pleural effusion
Treatment Pre Hospital
IV access
Supplem ental oxygen
100% nonrebreather m ask
Cardiac m onitor
Pulse oxim etry
Pa ge 3 9 2
Sublingual nitrates
Furosem ide
Endotracheal intubation m ay be required in severe cases
Initial Stabilization
IV access
Supplem ental oxygen
Place patient in an upright position.
Cardiac m onitor
Pulse oxim etry
Control airway as needed
Noninvasive ventilation or endotracheal intubation for im pending respiratory failure
ED Treatment
Norm otensive or hypertensive patients with cardiogenic pulm onary edem a: o
Rapid-acting nitrates preferably sublingual or Nitrospray
o
IV nitroglycerin
o
Morphine sulfate
o
IV diuretics:
o
Lasix or Bum ex
IV BNP (Nesiritide) is a balanced vasodilator with no inotropic or chronotropic properties.
Com pared to dobutam ine, BNP is not proarrhythm ic and has no effect on heart rate and is particularly useful in patients already taking nitrates, as tolerance to Nesritide has not been described.
o
Sodium nitroprusside for afterload reduction can be helpful for severe persistent hypertension but is not recom m ended if cardiac ischem ia m ay be concurrent.
Pa ge 3 9 2
o
Noninvasive ventilatory support: continuous or bilevel positive airway pressure (CPAP or Bi-PAP) m ay decrease the need for intubation, although Bi-PAP m ay be associated with a higher incidence of acute m yocardial infarction.
o
Endotracheal intubation for im pending respiratory failure
Hypotensive patients: o
Avoid nitrates, m orphine, and diuretics
o
Use agents that increase m yocardial contractility:
Dopam ine
Dobutam ine
Am rinone
Milrinone
Renal dialysis patients: o
Em ergent renal dialysis is the treatm ent of choice.
o
If rapid dialysis cannot be rapidly achieved:
IV nitroglycerin
IV enalapril or oral captopril m ay be useful
Medication (Drugs)
Bum ex: 0.5–1 m g IV
Captopril: 25–50 m g PO t.i.d.
Dobutam ine: begin at 2 m cg/kg/m in IV; titrate to BP, cardiac output, and pulm onary capillary wedge pressure
Enalapril: 1.25 m g IV q6h over 5 m inutes
Furosem ide: 20–80 m g IV
Morphine sulfate: 2–5 m g IV
Nesiritide: IV bolus of 2 m cg/kg followed by a continuous infusion of 0.01 m cg/kg/m in
Nitroglycerin:
Pa ge 3 9 2
o
Sublingual or Nitrospray: 0.4 m g m ay give repeatedly as SBP tolerates q5m in
o
Paste: 1–2 inches
o
IV infusion: begins at 5 m cg/m in and increases by 5–10 m cg/m in every few m inutes; titrate to BP
Nitroprusside: begin drip at 10 m cg/m in and increasing by 5–10 m cg/m in every few m inutes
Follow-Up Disposition Admission Criteria
Intensive care unit: o
Intubated patients
o
Patients on Bi-PAP
o
Adult respiratory distress syndrom e
Monitored unit: o
New-onset pulm onary edem a
o
Electrocardiographic changes
Observation: o
Known CHF with m ild to m oderate disease
Discharge Criteria
Patients with known CHF presenting with m ild pulm onary edem a no concom itant com plaints suggestive of ischem ia: o
Com plete resolution of sym ptom s after ED m anagem ent
o
Norm al oxygenation on room air at the tim e of discharge
o
No new electrocardiographic changes
Follow-up arranged within the next 48 hours
Pa ge 3 9 2
Low-salt diet
Serial weights to assess fluid accum ulation
References 1. Braunwald E. Pulm onary edem a. In: Braunwald E, ed. Heart disease: a textbook of cardiovascular m edicine. 6th ed. Philadelphia: WB Saunders, 2001:503–614. 2. Evaluation and m anagem ent of chronic heart failure in the adult: ACC/AHA practice guidelines. J Am Coll Cardiol. 2001;38:2101–2113. 3. Ketai LH, Godwin JD. A new view of pulm onary edem a and acute respiratory distress syndrom e. J Thorac Im aging. 1998;13:147–171. 4. McCullough PA, Nowak RM, McCord J, et al: B-type natriuretic peptide and clinical judgm ent in em ergency diagnosis of heart failure: analysis from Breathing Not Properly (BNP) Multinational Study. Circulation. 2002 Jul 23;106(4):416–422. 5. Pang D, Keenan SP, Cook DJ, et al. The effect of positive pressure airway support on m ortality and the need for intubation in cardiogenic pulm onary edem a. A system atic review. Chest. 1998;114:1186–1192. 6. Wright SP, Doughty RN, Pearl A, et al: Plasm a am ino-term inal pro-brain natriuretic peptide and accuracy of heart-failure diagnosis in prim ary care: a random ized, controlled trial. J Am Coll Cardiol. Nov 19,2003;42(10):1793–1800.
Miscellaneous SEE ALSO: Congestive Heart Failure
Codes ICD9-CM
Pa ge 3 9 2
518.4
ICD10 J81
Pa ge 3 9 2
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Pulm o nary Em bo lism
Pulmonary
Embolism Alan M. Kumar
Basics Description
The m ajority of cases arise from throm bi in the deep veins of the lower extrem ities and pelvis.
Throm bi also originate in renal and upper extrem ity veins.
After traveling to lungs, size of throm bus determ ines signs and sym ptom s.
Etiology
Most with pulm onary em bolism (PE) have identifiable risk factor: o
Recent surgery
o
Pregnancy
o
Previous deep vein throm bosis (DVT)/PE
o
Stroke or recent paraplegia
o
Malignancy
o
Age >50 years
o
Obesity
o
Sm oking
o
Oral contraceptives
Pa ge 3 9 2
o
Major traum a
o
Hem atologic risk factors:
Factor 5 Leiden
Protein C or S deficiency
Antithrom bin III deficiency
Antiphospholipid antibody syndrom e
Lupus Anticoagulant
Pediatric Considerations
Throm boem bolic disease is quite rare.
Risk factors in children: o
Presence of central venous catheter
o
Im m obility
o
Heart disease
o
Traum a
o
Malignancy
o
Surgery
o
Infection
Diagnosis Signs and Symptoms
Most com m on: o
Dyspnea
o
Pleuritic chest pain
o
Tachypnea
General: o
Fevers (rarely >102.0°F)
o
Diaphoresis
Pulm onary: o
Cough
Pa ge 3 9 2
o
Hem optysis (rarely m assive)
o
Rales
Cardiovascular: o
Tachycardia
o
Syncope
o
Murm ur
Extrem ities: o
Cyanosis
o
Evidence of throm bophlebitis
o
Lower extrem ity edem a
Abdom inal pain
Sym ptom s sim ilar in elderly but typically m ore subtle if age Table o f C o ntents > Pylo ric Steno sis
Pyloric Stenosis
Roger Barkin
Basics Description
Postnatal hypertrophy and hyperplasia of the circular sm ooth m uscle cell layer causing a thickened pylorus and antrum leads to worsening gastric outlet obstruction.
Neuronal nitric oxide synthase (NOS-1) m ay be a genetic susceptibility locus.
Adm inistration of erythrom ycin in infants m ay increase risk of hypertrophic pyloric stenosis.
Jaundice due to transient glucuronyl transferase deficiency
Adult: caused by peptic ulcer disease
Etiology
Most com m on cause of gastrointestinal obstruction in infants with an incidence of 1 in 150 m ales and 1 in 750 fem ales (average: 3 in 100 live births)
Males affected 5 tim es m ore com m only than fem ales; firstborn m ost com m on
Fam ilial, 15%: o
Child of affected parent has 7% incidence.
o
Recurrence risk in subsequent m ale children is 10%; 2% in fem ales.
Pa ge 3 9 5
Diagnosis Signs and Symptoms History
Vom iting: o
Gradual onset, usually beginning at around 3 weeks of age
o
Progressive, usually becom ing projectile
o
Nonbilious
o
May be blood tinged (secondary to esophagitis, gastritis, gastric ulceration)
o
Progressively worsening
o
Postprandial
Represents the hypertrophied pylorus: o
Confirm s diagnosis
Constipation or sm all am ount of stools
“Lean and hungry― infant early in course; dehydrated and uninterested in feeding late in course; failure to thrive
Variable dehydration and wasting depending on duration of sym ptom s
Jaundice in 8% of children
Adult presents with vom iting, anorexia, early satiety, and epigastric pain.
Physical Exam
Often norm al unless a relaxed abdom en
May feel olive-shaped m ass at lateral m argin of the right rectus abdom inis m uscle in the right upper quadrant (80% of patients), often after vom iting:
Pa ge 3 9 5
o
Best felt im m ediately after vom iting or after the stom ach is em ptied via gastric suction as the dilated body of the stom ach overlies the pylorus
o
Represents the hypertrophied pylorus:
Helps confirm diagnosis
Peristaltic waves m oving from the left to right in the left upper quadrant, seen best after feeding or just prior to vom iting
Essential Workup If “olive― palpable, further diagnostic evaluation is unnecessary and surgical consultation should be sought; otherwise, im aging studies are indicated.
Tests Lab
Electrolytes, BUN/creatinine, glucose: o
Hypokalem ic, hypochlorem ic m etabolic alkalosis
o
Norm al electrolytes do not exclude the diagnosis.
Bilirubin elevated
CBC if blood in em esis
Urinalysis for hydration
Imaging
Abdom inal ultrasound: o
Study of choice
o
Ultrasonic diagnosis hinges on identification and m easurem ent of pyloric m uscle m ass (3-m m ring thickness with 1.5-cm pylorus channel) and observation of fluid m ovem ent through the pylorus
o
Positive predictive value approaches 100%; 19% false-negatives
o
Serial ultrasounds for equivocal or negative study
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Upper GI series: o
String sign representing contrast passing through a narrowed gastric outlet
o
95% accurate
o
Rem ove contrast from the stom ach after the study to prevent aspiration.
Supine abdom inal film : o
Not diagnostic; rarely helpful
o
Dilated stom ach and no air distal to the pylorus
o
Most useful with other views to begin evaluation for other abdom inal pathology
Differential Diagnosis
GI anatom ic/functional disorder: o
Gastroesophageal reflux (GER)
o
Hiatal hernia
o
Obstruction/atresia
o
Gastric or duodenal web
Infection: o
Gastroenteritis
o
Urinary tract infection
o
Sepsis
Metabolic: o
Adrenal insufficiency
o
Inborn error of m etabolism
Feeding problem s: o
Psychosocial: poor m aternal interaction or stress
o
Chalasia
o
Form ula intolerance
o
Overfeeding
Drug withdrawal
Increased intracranial pressure
P.927
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Treatment Pre Hospital Fluid resuscitation if significant volum e deficit
Initial Stabilization
IV access
Rapid bedside glucose test to exclude hypoglycem ia
Correct volum e deficit with 20 m L/kg bolus of 0.9% norm al saline (NS) IV; m ay repeat.
ED Treatment
Correct electrolyte abnorm alities.
Hydrate with dextrose-containing solution after fluid resuscitation at 1–1.5 tim es m aintenance rate: o
Add potassium after ensuring adequate urine output.
Insert nasogastric tube to decom press the stom ach.
Restrict oral intake.
Consult pediatric surgeon for pylorom yotom y.
Adult: proton pum p antagonist (lansoprazole or om eprazole)
Medication (Drugs)
Lansoprazole: 30 m g daily PO
Om eprazole: 20 m g daily PO
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Follow-Up Disposition Admission Criteria
All pediatric patients should be adm itted to the hospital for rehydration and surgical correction with either an um bilical pylorom yotom y or laparoscopic pylorom yotom y.
Adult patients: Adm it as necessary for rehydration; m ay be scheduled for elective pylorotom y if proton pum p inhibitors fail to im prove this condition.
Discharge Criteria None
References 1. Bishop HC. Diagnosis of pyloric stenosis by palpation. Clin Pediatr. 1973;12(4):226–227. 2. Heller RM, Hernanz-Schulm an M. Application of new im aging m odalities to the evaluation of com m on pediatric conditions. J Pediatr . 1999;135:632–639. 3. Majon BE, Rosenm an MG, Kleinm an MB. Maternal and infant use of erythrom ycin and other m acrolide antibiotics as rick factors for infantile hypertrophic pyloric stenosis. J Pediatr. 2001;13:380. 4. Najm aldin A, Tan HL. Early experience with laparoscopic pylorom yotom y for infantile hypertrophic pyloric stenosis. J Pediatr. 1995;30–37. 5. Feldm an H, Friedm an LS, Sleisenger MH, eds. Sleisenger and Fordtran's Gastrointestinal and Liver Disease. 6th ed. Philadelphia: WB Saunders; 1998. 6. Touloukian RJ, Higgins E. The spectrum of serum electrolytes in hypertrophic pyloric stenosis. J Pediatr Surg. 1983;18(4):394–397.
Codes
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ICD9-CM 537.0
ICD10 K31.1
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > QT Syndro m e, Pro lo nged
QT Syndrome,
Prolonged Jason A. Tracy
Basics Description
Alteration in cardiac sodium , potassium or calcium -channel m echanics
Prolonged ventricular repolarization results in lengthening of QT interval on surface ECG: o
“Pause-dependent― lengthening due to short-long-short sequence in which a sinus beat is followed by an extrasystole (short), then a post-extrasystolic pause (long), concluding with a ventricular extrasystole (short)
o
“Adrenergic-dependent― pauses found in congenital cases
Sym ptom s preceded by vigorous exercise, em otional stress, or loud noise.
Nocturnal bradycardia can lengthen QT interval causing sleep-related sym ptom s.
Re-entrant rhythm can lead to torsades de pointes, ventricular tachycardia, and ventricular fibrillation.
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Hem odynam ic com prom ise following dysrhythm ia leads to syncope or death.
Genetics
Six genetic loci identified with sporadic cases due to spontaneous m utations: o
Autosom al-recessive form associated with deafness (Jervell and Lange-Nielsen syndrom es)
o
Autosom al-dom inant form not associated with deafness (Rom ano-Ward syndrom e)
o
Adrenergic stim ulation (fright, exertion, delirium trem ens, and loud auditory stim ulus) becom es prodysrhythm ic in certain genotypes while sleep-related sym ptom s found in others.
10–15% of carriers have baseline norm al QTc.
Death occurs in 1–2% of untreated patients per year.
o
Drug-induced QT prolongation m ay also have a genetic background.
o
Congenital form occurs in one in 3,000–5,000 with m ortality of 6% by age 40 years.
Pediatric Considerations
Diagnosis suspected in the young with syncope, cardiac arrest, or sudden death
Syncope following em otional stress or exercise suggestive
Death occurs without preceding sym ptom s in 10% of pediatric patients.
Etiology Drugs:
Com plete list at http://www.QTDrugs.org
Class Ia antidysrhythm ics—quinidine, procainam ide, disopyram ide
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Class III antidysrhythm ics—sotalol, ibutilide, am iodarone
Antibiotics—erythrom ycin, pentam idine, chloroquine, trim ethoprim -sulfam ethoxazole
Antifungal agents—ketoconazole, itraconazole
Psychotropic drugs—phenothiazines, haloperidol, risperidone, STCAs
Cisapride
Antihistam ines
Organophosphates
Electrolyte abnorm alities
Hypokalem ia
Hypom agnesem ia
Hypocalcem ia
Cardiac
Bradyarrhythm ias
Arteriovenous block
Mitral valve prolapse
Myocarditis
Myocardial ischem ia
CNS
Subarachnoid hem orrhage
Stroke
Congenital (idiopathic)
Other
Protein-sparing fasting
Anorexia nervosa
Hypothyroidism
Hypotherm ia
Diagnosis
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Signs and Symptoms History
Syncope
Near syncope
Light-headedness
Dizziness
Seizure
Sudden death
Essential Workup
A detailed history: o
Medications
o
Congenital deafness
o
Syncope or sudden death:
Fam ily history of syncope or sudden death
Cardiac m onitor: o
ECG
o
QTc (QT corrected for heart rate) >0.44 seconds in m en and >0.46 seconds in wom en
o
QT m easured from beginning of quasi-random signal to end of T wave:
Measured best in the lim b leads and should be averaged over three to five beats
There is no expert consensus on best heart rate correction (QTc) form ula.
Bazett form ula (QT divided by square root of RR interval) is m ost com m only used
Increase in QT variability
o
T-wave abnorm alities (T-wave alternans, biphasic)
o
Appearance of U waves
o
Ventricular tachycardia
o
Ventricular fibrillation
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o
Torsades de pointes
Tests Lab
Full electrolytes including calcium and m agnesium
Toxicology screen
Imaging Echocardiography to exclude other cardiac causes
Diagnostic Procedures/Surgery
ECG stress testing to induce a prolonged QT interval in suspected cases
Holter m onitoring of QTc
Genetic counseling/testing in suspected congenital form s
Fam ilial ECG testing
Differential Diagnosis
Myocardial infarction
Hypertrophic cardiom yopathy
Valvular defect
P.929
Treatment Pre Hospital
Supplem ental oxygen
IV access
Monitor
Alert
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Stable patients with prolonged QT interval transported without intervention
Cardioversion for unstable patients with confirm ed torsades de pointes
Magnesium sulfate for stable patients with evidence of torsades de pointes
Initial Stabilization
IV access
Monitor
Determ ine hem odynam ic stability
Unstable patients require im m ediate cardioversion
ED Treatment
IV m agnesium sulfate for torsades de pointes
IV potassium to serum levels of 4.5–5 m Eq/L
Tem porary transvenous cardiac pacing (rates between 90 and 110 beats/m in) for recurrences of torsades de pointes refractory to m agnesium sulfate therapy (shortens QTc)
IV isoproterenol for refractory cases of hem odynam ically unstable patients with acquired long QT (ineffective in congenital cases) and inability to transvenous pace
Rem ove any offending m edications and correct m etabolic derangem ents
Consultation with cardiology in those with sym ptom atic long QT as β-blockers at m axim um doses are to be started
No ED treatm ent needed (in consultation with cardiology) for those with suspected idiopathic long QT and no history of syncope, fam ily history of sudden cardiac death or ventricular arrhythm ias
Pacem aker or defibrillator placem ent with or without cervicothoracic stellectom y (to reduce adrenergic
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stim ulation) m ay be required in high-risk patients.
Beta-blockers prevent 70% of cardiac events in congenital cases.
Medication (Drugs)
Isoproterenol: 1µg/m in (peds: 0.1–1.0 µg/kg/m in) IV continuous infusion, titrate for effect, up to 10 µg/m in
Magnesium sulfate: 2 g (peds: 25–50 m g/kg) IV bolus over 2–3 m inutes followed by IV infusion at 2–4 m g/m in
Propanolol: 2–3 m g/kg/d (peds: 2–3 m g/kg/d) PO (in consultation with cardiology)
Follow-Up Disposition Admission Criteria
Sym ptom atic prolonged QT
Syncope
Cardiac dysrhythm ia
Possible cardiac or ischem ic event
Metabolic abnorm ality
Discharge Criteria Asym ptom atic prolonged QT in consultation with cardiology
References 1. Al-Khatib SM, LaPointe NM, Kram er JM, et al. What clinicians should know about the QT interval. JAMA. 2003;289:2120–127. 2. Khan IA. Clinical and therapeutic aspects of congenital and
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acquired long QT syndrom e. Am J Med. 2002;112:58–66. 3. Meyer JS, Mehdirad A, Salem BI, et al. Sudden arrhythm ia death syndrom e: Im portance of the long QT syndrom e. Am Fam Phys. 2003;68:483–488. 4. Olgin JE, Zipes DP. Specific arrhythm ias: diagnosis and treatm ent. In: Braunwald E, Zipes DP, Libby P, eds. Braunwald: Heart disease: a textbook of cardiovascular m edicine. 6th ed. Philadelphia: WB Saunders 2001:867–870. 5. Vincent GM. Ventricular arrhythm ias: long QT syndrom e. Cardiol Clin. 2000;18:309–325.
Miscellaneous SEE ALSO: http://www.QTDrugs.org
Codes ICD9-CM 427
ICD10 I49.9
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Rabies
Rabies
Matthew Kippenhan
Basics Description CNS infectious disease of m am m als caused by the rabies virus:
Negative-stranded RNA genom e, fam ily Rhabdoviridae, genus Lyssavirus
Etiology
Epidem iology: o
30,000–70,000 hum an cases worldwide per year:
Especially com m on in southeast Asia, Philippines, Africa, South Am erica, and the Indian subcontinent
o
Dogs and foxes are m ain reservoirs.
United States has two to three hum an cases per year:
Most clinical cases in the United States com e from foreign travel and bat exposures.
Wild anim als account for 93% of cases, dom estic anim als for 6.8%.
Raccoons, skunks, bats, foxes, woodchucks, groundhogs are reservoirs.
Lasionycteris (Silver haired) and Pipistrellus
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(Eastern pipistrelle) bats are associated with m ost cases.
Thought not enough to constitute exposure, squirrel, rat, m ouse, ham ster, guinea pig, gerbil, chipm unk, rabbit are also reservoirs.
Mode of transm ission: o
Infected saliva of host passed to uninfected anim al
o
Bite: m ost com m on
o
Nonbite: scratch, abrasion, m ucous m em brane contact with saliva, bat aerosol exposure
o
Corneal and solid organ transplant procedures
o
Not considered transm ission risk: petting rabid anim al; contact with blood, urine, or feces of rabid anim al
Progression after infection: o
Virus m ultiplies in local tissue (i.e., m uscle)
o
Virus taken up into peripheral nerves through acetylcholine receptors
o
Virus transported to CNS via retrograde axoplasm ic flow
o
Once in CNS, rapid replication and dissem ination causes encephalitis.
o
Centrifugal spread of virus to peripheral nerves, including salivary glands
Diagnosis Signs and Symptoms
Five stages—latent period, prodrom e, encephalitis, com a, death (or recovery) o
Latent period: 1–3 m onths (range 10 days to >6
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years):
o
Virus incubation in peripheral tissues
Shorter period for head or neck bite
Prodrom e—duration 1–7 days:
Fever, headache, m alaise, m yalgias, anorexia, sore throat, nausea, and vom iting
Paresthesias or fasciculations around bite site give clue to diagnosis.
o
Encephalitis—duration 2–7 days:
Anxiety, agitation, hallucinations, confusion or delirium , m uscle spasm s, seizure, persistent high fever
Aerophobia—pharyngeal spasm from draft of air
Hydrophobia—violent involuntary m uscle contraction of diaphragm , pharyngeal, laryngeal and accessory respiratory m uscles when attem pting to swallow (seen in two thirds of cases)
Autonom ic instability, dysrhythm ias, m yocarditis
Brainstem involvem ent—diplopia, facial paralysis
o
Com a:
Apnea from respiratory center involvem ent, vascular collapse, flaccid paralysis, adult respiratory distress syndrom e, syndrom e of inappropriate diuretic horm one
o
Most die within 2 weeks
Death (or recovery):
Fatal if no pre- or postexposure prophylaxis given
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Single case report in 2004 of survival without prophylaxis
Residual neurologic deficits likely persist.
Three m anifestations of disease: o
Classic (encephalitic) accounts for about 80% of cases.
o
Dum b rabies (Paralytic) accounts for about 20%: ascending paralysis m im icking Guillain-Barré.
o
Nonclassic (atypical) rabies (100 rad exposure; sooner with higher exposures
Vom iting within 1 hour of exposure indicates potentially lethal injury (>600 rad).
o
Confusion and weakness (>200 rad)
o
Fever:
o
Acutely, from inflam m ation
During m anifest illness, from infection
Hair loss, hem orrhage, diarrhea m ay develop with doses >300 rad.
Derm al exposure: o
Initial erythem a
o
Blistering and ischem ic necrosis m ay follow.
Essential Workup
Survey for radiation using a Geiger counter, which can be
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found in any nuclear m edicine or radiation therapy departm ent: o
Any probe style is okay for survey.
o
Cover probe with exam glove:
Prevents contam ination of probe
Blocks alpha radiation, but will detect beta/gam m a
o
Measure background radiation away from patient.
o
Move probe slowly over patient's skin:
1–2 cm from skin
Move probe only 2–3 cm /s.
Contam ination is greater than two tim es background.
Note any contam inated areas.
Follow system atic pattern to avoid m issing areas.
Rem em ber to survey palm s, soles, hair.
Absolute lym phocyte count is best indicator of severity of ARS: o
m ucous m em branes > intact skin
o
Use fenestrated drapes to shield adjacent skin.
o
Use soap and water; no harsh chem icals.
o
Diaper wipes work well for intact skin; wipe from edges of area to center, then lift away.
o
Irrigate wounds—collect and survey runoff, avoid splashing.
o
Resurvey frequently to assess effectiveness of decontam ination.
o
Do not abrade skin.
o
If contam ination cannot be rem oved, cover area to prevent spread and m ove on—residual contam ination can be controlled.
Treat vom iting and dehydration: o
Antiem etics (5-HT3 antagonist, e.g., ondansetron 4 m g IV)
o
IV fluids
Decorporation agents for internal decontam ination are specific to each radionuclide: o
Contact REAC/TS for guidance.
Potassium iodide is useful only to prevent thyroid uptake of radioactive iodine (found in nuclear reactors), and only
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if given within a few hours after contam ination; see VA/DOD Pocket Guide for dosage (see References).
Cytokines and transfusions m ay be needed with doses >200 rad.
RDD: o
Necessary surgery m ust be done im m ediately (36–48 hours), or else delayed 1–2 m onths, with exposure >200 rad.
o
Any bom bing victim m ust be assessed for radioactive contam ination until RDD ruled out by assessm ent of scene.
o
Preserve evidence for crim inal investigation.
Medication (Drugs) Potassium iodide:
Adults: 130 m g PO
Peds: o
3–18 years: 65 m g PO
o
1 m onth to 3 years: 32 m g PO
o
100 rad
Tolerating oral fluids
Issues for Referral
Internal contam ination: Contact REAC/TS for guidance.
External contam ination that cannot be rem oved
Any patient with radiation exposure will require dose assessm ent and risk counseling.
Skin injuries m ay require m onths of treatm ent and require expert consultation to guide débridem ent.
References 1. Arm ed Forces Radiobiology Research Institute. Medical Managem ent of Radiological Casualties. 2nd ed. 2003. Available at http://www.afrri.usuhs.m il/. 2. Managem ent of Terrorist Events Involving Radioactive Material. NCRP Reportno. 138. Bethesda, MD: National Council on Radiation Protection; 2001. 3. Medical Radiobiology Advisory Team (MRAT): Call (301)295-0530. 4. Potassium iodide dosing: inform ation available at http://www.fda.gov/cder/guidance/4825fnl.htm . 5. Radiation Em ergency Assistance Center/Training Site (REAC/TS). Inform ation available at http://www.orisa.orav.gov/reacts/guides/m anage.htm 6. Step-by-step guidance for radiation incident m anagem ent: available at http://www.orau.gov/reacts/guidance.htm . 7. 24-hour em ergency line: (865) 576-1005 (ask for REACTS). 8. VA/DOD. Terrorism with Ionizing Radiation General Guidance Pocket Guide. Available at http://www.oqp.m ed.va.gov/cpg/cpg.htm
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Miscellaneous SEE ALSO: Chem ical Weapons Poisoning
Codes ICD9-CM NEC 990
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Rapid Sequence Intubatio n
Rapid
Sequence Intubation Christopher Ross
Treatment Initial Stabilization
Preparation: o
Have patient in appropriately m onitored area where resuscitation m ay be instituted.
o
Assem ble appropriate m edicines.
o
Apply cardiorespiratory m onitor, pulse oxim eter, and blood pressure (BP) m onitor.
o
Test laryngoscope blade:
Adult: nos. 3 or 4 Macintosh (curved) blade
Child 8 years
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and adults. o
Use uncuffed endotracheal tube for children Table o f C o ntents > Rash, Pediatric
Rash, Pediatric
Bruce Webster
Basics
Lesion m orphology: o
Macule:
Localized nonpalpable changes in skin color
Purpura or petechiae (nonblanching with pressure)
Maculopapule
Slightly elevated lesions with localized changes in skin
o
o
o
Papule:
Solid, elevated lesions 5 m m in diam eter
Often results from a confluence of papules
Nodule:
Solid, elevated lesions extending deep into the derm is or subcutaneous tissue >5 m m in diam eter
Pa ge 4 0 0
o
Wheal:
Circular, irregular lesions varying from red to pale
o
Vesicle:
o
Bullae:
o
Clear, fluid-filled lesions >5 m m in diam eter
Pustules:
Clear, fluid-filled lesions Table o f C o ntents > Rash
Rash
Owen Lander J. Scott Goudie
Basics Description Abnorm al skin lesions that can be classified into broad categories:
Erythem a/Red m acular lesions from dilatation of superficial vasculature
Vesicobullous lesions form ed by disruption of epiderm al/derm al integrity and filling with exudative fluid, com m only allergic/infectious/system ic inflam m atory response
Purpura and petechiae from failure of norm al vascular integrity/hem ostatic m echanism s
Nodules from prolonged inflam m atory response
Urticaria from contact/system ic allergic response, histam ine release
Etiology
Maculopapular: o
Infections:
Viral
Bacterial
Rickettsial
Pa ge 4 0 1
Fungal
Parasitic
o
Allergic reaction
o
Autoim m une disease
Purpura/petechiae: o
Clotting pathway dysfunction
o
Platelet dysfunction, qualitative or quantitative
o
Vasculitis
o
System ic infection, sepsis
Vesicobullous: o
Localized:
Allergic reaction
Mechanical/physical traum a: heat, radiation, sunburn
o
Infections
Generalized (system ic):
Infections
Allergic reaction/anaphylaxis
Autoim m une
Diagnosis Signs and Symptoms History
Age
Im m une status (HIV, chem otherapy, diabetes, steroids)
Previous episodes/prior history of lesions/reactions
Sick contacts
Chronologic and physical evolution
Associated sym ptom s, pruritus, fever, abdom inal pain,
Pa ge 4 0 1
m yalgias/arthralgias
Prodrom e: fever, headache, cough, odynophagia, rhinorrhea
Environm ental exposure: tick bite, unusual flora, diet, travel
Recent change in m edication
Fam ily history
Physical Exam
Prim ary lesion appearance: o
Macule:
Nonraised areas of distinct coloration
Blanching lesions are inflam m atory; nonblanching lesions are either altered pigm entation or petechiae/purpura.
o
Papule:
Raised, palpable lesions 5 m m seated in deeper layer of skin and tissue
Secondary changes: o
Scaling, lichenification, excoriation, fissuring all result from m anipulation/scratching or
Pa ge 4 0 1
proliferation/shedding of epiderm al cells o
Erosions/ulcers from varying degrees of tissue loss (superficial to deep) from loss of vascular supply/tissue integrity
Distribution: o
Characterized as central/peripheral, confluent/scattered, m ucosal/nonm ucosal, presence of palm /sole involvem ent
Associated signs/sym ptom s: o
Pruritus associated with allergic reactions, system ic and contact
o
Fever with infection/drug reaction/system ic inflam m atory response, viral exanthem a com m on in children
Vital signs: o
Abnorm al vital signs, airway com prom ise, respiratory distress, hem odynam ic instability present in severe disease.
Essential Workup
Identify system ic illness: o
Fever
o
Abnorm al vital signs
o
Nausea, vom iting, abdom inal pain, generalized distribution, altered m ental status
o
Signs/Sym ptom s of local infectious source:
Pharyngitis, abscess, foreign body, m eningism us signs
Categorize the lesions: o
Maculopapular
o
Vesicobullous
o
Petechial
Pa ge 4 0 1
Tests Lab
Presence of fever, system ic sym ptom s, or possible infection warrants blood work: o
CBC with differential, electrolytes, blood urea nitrogen/creatinine
o
Blood cultures, viral cultures
o
Gram stain and culture of purulent lesions
o
Tzanck sm ear for suspected herpetic lesions
o
Venereal disease research laboratory/rapid plasm a reagin for suspected syphilis
Suspected autoim m une disorders (Lupus, rheum atoid arthritis, juvenile rheum atoid arthritis, Sjogren syndrom e) o
CBC, ESR, particular assays in consultation with rheum atologist (ANA, antineutrophil cytoplasm ic antibody, etc.)
Petechiae/Purpura warrant com plete coagulation evaluation: o
CBC with platelets
o
Partial throm boplastin tim e, prothrom bin tim e, international norm alized ratio
o
Dissem inated intravascular coagulation (DIC) screen: fibrinogen, fibrin split products, haptoglobin, LDH
Imaging Chest radiograph indicated for respiratory sym ptom s, possible infectious/autoim m une etiology.
Diagnostic Procedures/Surgery
Lum bar puncture for altered m ental status, m eningeal signs, suspected m eningococcus
Biopsy under derm atologic consultation to differentiate
Pa ge 4 0 1
allergic/autoim m une/infectious processes.
Nikolsky test: expansion of bullous lesion with lateral stress at m argin indicates epiderm al/derm al disruptive process
Scrapings: Indicated to rule out topical fungal infections and parasites o
Potassium hydroxide preparation from edge of lesion reveal hyphae
o
Plain m ineral oil to rule out scabies in pruritic linear lesions of hands
Differential Diagnosis
Diffusely erythem atous rashes: o
Toxic shock syndrom e (TSS): exotoxin, 90% Staphylococcus aureus, desquam ation 2 weeks after early rash, end organ involvem ent
o
Toxic epiderm al necrolysis (TEN): constitutional sym ptom s, adults, drug related, positive Nikolsy test result, full-thickness desquam ation, oral lesions prom inent
o
Staphylococcal scalded skin syndrom e (SSSS): exotoxin, fever, m alaise, flaccid bullae later, superficial desquam ation, oral lesions rare, children
o
Kawasaki syndrom e
o
Generalized exfoliative erythroderm a
o
Lupus
o
Cutaneous T-cell lym phom a
Vesicobullous lesions: o
Anaphylaxis
o
Stevens-Johnson syndrom e: continuum with TEN, drug related, constitutional sym ptom s, m ucous m em branes involved, sym m etric blistering P.937
Pa ge 4 0 2
o
Toxic epiderm al necrolysis
o
Pem phigus vulgaris: fulm inant, usually 40–65 years, painful, flaccid bullae, positive Nikolsky test result, oral lesions, antiepithelial antibody by biopsy
o
Bullous pem phigoid: m ore elderly population, oral lesions less com m on, positive Nikolsky test result, basem ent m em brane antibody by biopsy
o
Sm allpox
o
Dissem inated herpes sim plex, zoster/varicella, vaccinia
Maculopapular and local lesions: o
Gonococcem ia: sexually active, polyarthritis, tenosynovitis, hem orrhagic pustules with erythem atous base
o
Secondary syphilis
o
Erysipelas
o
Pustular psoriasis
o
Ecthym a gangrenosum : with gram -negative sepsis, discrete lesions, few in num ber, peripheral, evolve from m acule to pustule to an erythem atous base
o
Envenom ations
o
Malignancy
Petechial/purpuric lesions: o
Meningococcem ia
o
Gonococcem ia
o
Pneum ococcem ia
o
DIC
o
Rocky Mountain spotted fever (RMSF): pronounced prodrom e of fever, headache, m yalgia, rash, peripheral m oves to palm s/soles, system ic
Pa ge 4 0 2
o
Babesiosis: sim ilar to RMSF, rash less often, frequent co-infection with Lym e
o
Henoch-Schönlein purpura
o
Multiple system ic illnesses (see Purpura)
Nonlethal diagnoses: o
Maculopapular lesions:
Psoriasis
Tinea
Pityriasis rosea
Seborrheic derm atitis
Intertrigo
Lichen planus
Lym e disease
Phototoxic and photoallergic reactions
Viral exanthem s (m ostly in children, see Rash, Pediatric)
o
Contact derm atitis
Scabies
Eczem a
Im petigo
Candidiasis
Urticaria
Nevi
Hypopigm entation
Warts
Vesicobullous lesions:
Herpes sim plex
Zoster
Vaccinia
Contact allergic derm atitis
Coxsackie (hand, foot, m outh)
Echovirus
Pa ge 4 0 2
o
Scabies
Insect bites
Petechial/purpuric lesions:
Usually reflect system ic infection/inflam m ation/vasculitis
o
Few trivial causes
Actinic purpura in elderly
Traum atic
Pustular lesions:
Trivial causes m ust be localized, have no associated sym ptom s, and no petechial com ponent.
Folliculitis
Candidiasis
Acne
Treatment Pre Hospital
Managem ent is dictated by presence of hem odynam ic instability, airway com prom ise, and concern for infectious exposure.
Alert Universal precautions, m asks if infectious etiology suspected
Initial Stabilization
Aggressive, presum ptive m anagem ent of potentially lethal presentations: o
Petechial lesions
o
Fever
o
Dissem inated erythem atous or vesicobullous lesions
Pa ge 4 0 2
Treat for anaphylaxis if acute, urticarial, known exposure, or respiratory distress.
Treat resuscitation of dissem inated bullous or exfoliative disease as a severe therm al burn.
ED Treatment
Treatm ent directed for underlying cause
Antibiotics if life threatening infectious em ergency suspected: o
SSSS: nafcillin/oxacillin
o
TSS: penicillin G and clindam ycin:
Rem oval of the offending agent, supportive care, if any clinical suspicion treat as infectious
o
RMSF: doxycycline or chloram phenical
o
Meningococcem ia: ceftriaxone or penicillin G
If varicella or dissem inated herpes is suspected, initiate acyclovir.
Sym ptom atic treatm ent of pruritus (diphenhydram ine or hydroxyzine)
Steroid therapy reserved for clear allergic reactions, relapse of known steroid responsive disease, or in consultation with derm atologist
Allergic reactions treated aggressively: o
Diphenhydram ine
o
H2-blocker
o
Steroids
o
Epinephrine if respiratory com prom ise
Medication (Drugs)
Acetam inophen: 625 m g PO/PR q4h–q6h (peds: 60 m g/kg/24h)
Pa ge 4 0 2
Acyclovir: 10 m g/kg/dose IV q8h
Cefotaxim e: 1–2 g IV q6h (peds: 100–200 m g/kg/24h)
Ceftriaxone: 1–2 g IV q12h (peds: 100–200 m g/kg/24h)
Chloram phenicol: 50 m g/kg/24h IV divided q6h (peds: sam e)
Clindam ycin: 900 m g IV q8h (peds: 40 m g/kg/24h)
Diphenhydram ine: 50 m g PO/IM/IV q6h (peds: 5 m g/kg/24h)
Doxycycline: 100 m g PO q12h (peds: 4.4 m g/kg/24h divided, m ax. 100 m g; not recom m ended Table o f C o ntents > Reactive Arthritis
Reactive Arthritis
Christine Yang-Kauh
Basics Description
Culture-negative arthritis after extra-articular infection, usually enteritis or venereal disease
System ic disease with widely varying extra-articular sym ptom s
“Reiter syndrom e― is the classic triad of: o
Arthritis
o
Nongonoccocal urethritis/cervicitis
o
Conjunctivitis
Num ber-one cause of inflam m atory arthritis in young m en
Men >wom en by 5–10:1 in venereal infection
Men = wom en in enteric infection
Peak onset 15–35 years of age
First episode of arthritis usually resolves in 3–6 m onths
10–20% Recurrence or chronic disease
1% severe or fatal disease o
Keratoderm a blenorrhagica is a predictor of poor outcom e
Rate of chronic disease varies with etiologic organism and presence of HLA-B27.
Pa ge 4 0 2
Genetics
Genetic predisposition plays a strong role.
HLA-B27 seen in 70–80% of patients
Etiology
Different m echanism s m ay be used depending on the infectious agent.
Infection-triggered aseptic arthritis: o
Ongoing im m une response to persistent bacterial antigen
o
Autoim m une response or antigenic cross-reactivity with HLA-B27 (i.e., enteric organism s)
Chronic infection with a sm all am ount of a slow-growing, difficult to culture organism : o
Chlam ydia, m ycoplasm a, borrelia
First episode of arthritis typically occurs 1–6 weeks after infection with: Salm onella, Shigella, Yersinia, Cam pylobacter, and Chlam ydia
Case reports of m any other agents, including HIV, C. Difficile and intravesicular BCG
Diagnosis Signs and Symptoms
History of dysentery, urethritis, or cervicitis 1–6 weeks prior
Musculoskeletal: o
o
Asym m etric oligoarthritis
Usually lower extrem ities
May be m igratory
Dactylitis: “sausage― digits
Pa ge 4 0 2
o
Enthesitis: inflam m ation of the tendinous insertions into bone
o
Low back pain
Alternating buttock pain
o
Achilles tendonitis
o
Plantar fasciitis
General: o
Fever
o
Weight loss
o
Malaise
Eyes: o
Conjunctivitis with m ild nonpurulent discharge
o
Uveitis, iritis,
Mouth: o
Oral ulcers: erythem atous, painless, transient
o
Often unnoticed
Cardiovascular: o
Rare dysrhythm ia
o
Pericarditis or aortic regurgitation in chronic disease
Gastrointestinal o
Sacroiliitis:
Diarrhea 1–6 weeks prior
Genitourinary: o
Nonpurulent urethritis:
Dysuria, urinary frequency
Occasional hem aturia
o
Cervicitis
o
Balanitis circinata:
Shallow, painless, red penile lesions
Skin, nails: o
Keratoderm a blennorrhagica:
Clear vesicles on an erythem atous base that
Pa ge 4 0 2
evolve to hyperkeratotic lesions
Com m only on soles, palm s
Associated with severe disease
o
Onycholysis
o
Nail yellowing and hyperkeratosis
Neurologic: o
Rare transient neurologic dysfunction:
Nerve palsies, hem iplegia
Essential Workup
Includes a search for the etiologic infection by history and exam ination, especially in wom en where cervicitis is often asym ptom atic
Joint aspiration should be perform ed to rule out septic arthritis or crystal arthropathy.
Tests Lab
Urethral or cervical swab for Chlam ydia infection: o
Preferably direct fluorescent antibody or DNA probes for chlam ydial ribosom al RNA
CBC with differential m ay show a m oderate neutrophilic leukocytosis and anem ia.
ESR m ildly elevated
C-reactive protein and C3/C4 levels m ildly elevated
Rheum atoid factor, ANA and HLA-B27 m ay be considered for further rheum atologic work-up.
Stool cultures if ongoing dysentery
HIV testing should be considered, especially if use of im m unosuppressive therapy is contem plated
Imaging
Radiograph of affected joints:
Pa ge 4 0 3
o
Usually norm al
o
Soft tissue swelling and effusion m ay be seen.
o
Enthesitis (periosteal spurs with indistinct m argins and fluffy periostitis at the sites of tendinous insertions) m ay be noted, especially of the lower extrem ities.
Radiograph of lum bar spine, sacroiliac joints: o
Unilateral sacroiliitis in early disease (10%)
o
Bilateral in chronic disease (70%)
o
Asym m etric spondylitis
o
Syndesm ophytes
P.941
Diagnostic Procedures/Surgery Arthrocentesis with fluid analysis should be perform ed:
Synovial fluid shows inflam m ation (usually between 2–50,000 cells/m L) with neutrophilia.
Fluid glucose is norm al.
Fluid is gram stain and culture negative
Differential Diagnosis
Gonococcal arthritis
Ankylosing spondylitis
Psoriatic arthritis
Arthritis related to inflam m atory bowel disease
Occult celiac disease
Undifferentiated spondyloarthropathy
Lym e disease
Behçet syndrom e
Rheum atoid arthritis
Still's disease
Pa ge 4 0 3
Sarcoid arthritis
Gout/pseudogout
Rheum atic fever
Viral arthropathy
Treatment Initial Stabilization
Supportive care
IV fluids if hypovolem ia due to dysentery
Ice to inflam ed joints
ED Treatment
High-dose NSAIDs are the m ainstay of therapy: o
A m inim um of 1 m onth of NSAID treatm ent at m axim um dosage is m andatory before evaluating effectiveness
Sulfasalazine for NSAID failure or contraindication
Treat urethritis/cervicitis if present or suspected: o
Doxycycline or azithrom ycin
o
Prolonged (up to 3 m onths) of antibiotic treatm ent for chlam ydia-associated arthritis m ay im prove recovery.
o
Partners should also be treated.
Antibiotics are not indicated for enteric disease.
Local corticosteroids injections m ay be helpful for severe arthritis or enthesitis.
In persistent or aggressive disease, im m unom odulating therapies m ay be initiated in consult with a rheum atologist: o
System ic corticosteroids
Pa ge 4 0 3
o
Azathioprine
o
Methotrexate
Medication (Drugs)
Azathioprine: 1–2.5 m g/kg/d PO q12h–q24h
Azithrom ycin: 1 g (peds: 10 m g/kg) PO for 1 day
Doxycycline: 100 m g (peds: 5 m g/kg/d, div.) PO q12h for 10 days (consider prolonged therapy)
Ibuprofen: 2,400 m g/d, div. (peds: 20–40 m g/kg/d) PO q6h–q8h
Indom ethacin: 75–200 m g/d (peds: 1–2 m g/kg/d) PO q6h–q12h
Methotrexate: 7.5–25 m g (peds: 0.5–1 m g/kg; m axim um , 15–25 m g) PO per week for aggressive unrem itting disease
Sulfasalazine: 1–3 g (peds: 30–60 m g/kg/d; m ax., 2 g) PO q6h, for NSAID failure or contraindication
Pregnancy Considerations
Doxycycline is contraindicated in pregnancy.
Azithrom ycin m ay be safe.
Am oxicillin: 500 m g PO t.i.d. for 7 days
Erythrom ycin: base 500 m g PO q6h × 7 days
Follow-Up Disposition Admission Criteria
Concom itant disease(s) that require adm ission
Pa ge 4 0 3
Unrem itting pain or inability to am bulate
Discharge Criteria Most patients can be discharged.
Issues for Referral
Close follow-up with a rheum atologist or a prim ary care physician is required.
Physical therapy and vocational counseling m ay help.
References 1. Am or B. Reiter's syndrom e: diagnosis and clinical features. Rheum Dis Clin North Am . 1998;24(4):677–695. 2. Flores DF, Marquez J, Garza M, Espinoza LR. Reactive arthritis: newer developm ents. Rheum Dis Clin N Am . 2003;29:37–59. 3. Kataria RK, Brent LH. Spondyloarthropathies. Am Fam Physician. 2004;69:2853–2860. 4. Sibilia J, Lim bach FX. Reactive arthritis or chronic infectious arthritis? Ann Rheum Dis. 2002;61:580–587.
Codes ICD9-CM 716.80
ICD10 M02.9
Pa ge 4 0 3
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Rectal Pro lapse
Rectal Prolapse
Scot Hill
Basics Description Three types of rectal prolapse:
Full-thickness rectum protrudes through anus; by far m ost com m on.
Partial thickness or m ucosal prolapse: o
Only m ucosal layer protrudes through anus.
Internal or occult prolapse: o
May be partial or full thickness
o
Never protrudes through anus
o
May be difficult to diagnose
Etiology
Cause unclear and m ultifactorial: o
Chronic constipation/straining at stool
o
Laxity of sphincter:
Pelvic floor traum a/weakness
Neurologic disease
More com m on in wom en, peak in seventh decade.
Pediatric Considerations
Very rare after age 4 years
Pa ge 4 0 3
True rectal prolapse unusual in children; m ore likely partial or intussusception
Consider chronic diarrhea, parasites, cystic fibrosis (CF) as contributing causes.
Diagnosis Signs and Symptoms
Protruding rectum
Mucous or bloody discharge
Sensation of rectal m ass
Tenesm us
Constipation or incontinence
History History with em phasis on bowel obstruction and duration of prolapse:
Often progressive sym ptom s over tim e with self-reducing prolapse initially
Physical Exam Rectal exam ination—m ust differentiate prolapse, hem orrhoids, or intussusception:
True prolapse shows circum ferential circular folds in beefy m ucosa of protruding rectum .
Mucosal prolapse rarely m ore than a few centim eters of protrusion; will not contain m uscular layer
Internal hem orrhoids identified by folds of m ucosa radiating out like spokes in wheel
Intussusception identified by placing exam ining finger between protruding rectum and anus
Essential Workup Careful physical exam ination
Pa ge 4 0 3
Tests Lab
No lab test necessary for uncom plicated prolapse
Preoperative testing for incarcerated, going to OR
Imaging No im aging is necessary for uncom plicated prolapse.
Differential Diagnosis
Prolapsed internal hem orrhoids
Prolapsed polyp
Other rectal m ass
Treatment Pre Hospital
Position of com fort
Prevent m ucosal desiccation with m oist gauze.
Avoid traum a to m ucosa.
Initial Stabilization Stabilization generally not needed in sim ple prolapse P.943
Incarcerated or ischem ic prolapse: o
NPO
o
IV fluids
o
Prepare for surgery.
ED Treatment
Reduce prolapse:
Pa ge 4 0 3
o
Gentle steady pressure
o
Invert m ucosa through lum en from distal.
o
Sedation as needed to relax sphincter
If prolapse incarcerated or ischem ic: o
Adm ission for reduction and surgical correction before swelling creates full-thickness necrosis
Alert
Constriction of blood flow to rectum by anal sphincter can lead to ischem ia, possible loss of gut.
Tim ely reduction decreases risk.
Surgical intervention required for ischem ic m ucosa.
Medication (Drugs) Sedation and pain m edication only as needed
Follow-Up Disposition Admission Criteria
Necrotic or ischem ic m ucosa
Inability to reduce acute prolapse
Discharge Criteria
Reduced rectal prolapse
Stable and tolerating PO
Instructions to reduce pressure on rectum : o
Correct constipation:
Stool softeners
Increase fluid intake.
Pa ge 4 0 3
o
Avoid prolonged sitting or straining.
Issues for Referral Refer for workup including:
Search for leading lesion.
Refer for definitive surgical repair of recurrent prolapse.
Testing for CF in children
References 1. Heine JA, Wong WD. Rectal prolapse. In: Mazier PW, et al., eds. Surgery of the colon, rectum , and anus. Philadelphia: WB Saunders; 1995:515–537.
Miscellaneous SEE ALSO: Hem orrhoid
Codes ICD9-CM 569.1
ICD10 K62.3
Pa ge 4 0 3
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Rectal Traum a
Rectal Trauma
Elaine Sapiro
Basics Description
Injury to rectal m ucosa
Sim ple contusion to full-thickness laceration with extension into peritoneum or perineum
Two thirds of rectum is extraperitoneal.
Etiology
Penetrating traum a: o
Gunshot wounds account for 80%.
o
Knife wounds
o
Im palem ent injuries
Blunt traum a; less frequent cause of rectal injury: o
Motor-vehicle collision
o
Motorcycle accident
o
Waterskiing and watercraft accidents:
o
Falls and crush injuries
o
Pelvic fractures:
Hydrostatic pressure injury
Bony fragm ents penetrate rectum
Foreign body: o
Autoeroticism
Pa ge 4 0 4
o
Anal intercourse
o
Assault
o
Ingestion of sharp objects
Iatrogenic traum a is m ost com m on cause of rectal injury: o
Barium enem a:
Perforation occurs in 0.04% patients; 50% m ortality.
o
Colonoscopy:
0.2% perforation rate; increased risk with polypectom y
o
Urologic and obstetric-gynecologic procedures
o
Episiotom y
Pediatric Considerations
Rectal injury m ay result from therm om eter insertion.
Any rectal traum a in young children should raise the suspicion of nonaccidental traum a.
Diagnosis Signs and Symptoms
Perineal, anal, or lower abdom inal pain
Signs of perforation or peritonitis: o
Guarding
o
Rebound tenderness
o
Fever
Pelvic fracture
Rectal bleeding
Obstipation
History of anal m anipulation, foreign body insertion, sexual abuse
Pa ge 4 0 4
Essential Workup
History: o
Tim e and m echanism of injury
o
Suspect rectal injury in all patients with gunshot wound, stab wound, or im palem ent injury to trunk, buttocks, perineum , or upper thigh.
o
Consider in any patient with history of anal m anipulation com plaining of lower abdom inal or pelvic pain
Physical exam ination: o
Inspect and palpate thoroughly the buttocks, anus, and perineum .
o
Identify entrance and exit wounds if penetrating traum a.
o
Perform digital rectal exam ination to assess for gross blood or guaiac-positive stool; note position of prostate.
o
Assess perineal integrity: speculum and bim anual exam in all fem ale patients, thorough genitourinary exam in all m ale patients.
Anoscopy and sigm oidoscopy: o
Must be perform ed if rectal injury is suspected by history or exam
o
Irrigate and suction feces and blood.
o
Avoid insufflating large am ount of air during sigm oidoscopy:
Can force stool into peritoneum if proxim al bowel perforation exists
Evidentiary exam required in cases of sexual assault.
Tests Lab
Pa ge 4 0 4
CBC
Type and screen
Urinalysis
Imaging
Supine/Upright abdom inal film s, pelvic radiographs: o
Evaluate for pneum operitoneum or extraperitoneal and extrarectal densities suggesting perforation.
o
Identify location, size, and shape of foreign body.
o
Identify pelvic fracture or diastasis of sym physis pubis, which m ay accom pany rectal injury.
Retrograde urethrogram if high-riding prostate noted on rectal exam .
Contrast enem a helpful only in situations where perforation is unclear: o
Use water-soluble contrast (e.g., gastrografin)
Differential Diagnosis
Colon injuries
Genitourinary injuries
Treatment Alert
Airway m anagem ent and resuscitation as indicated
Spinal precautions if blunt traum a
Fluid resuscitation if blood loss, hypotension
Prehospital personnel should not attem pt to rem ove foreign body from rectum .
Initial Stabilization In penetrating or blunt abdom inal traum a, follow traum a protocols:
Pa ge 4 0 4
Prim ary survey
Resuscitation
Secondary survey
Treatm ent
P.945
ED Treatment
Adm inister tetanus prophylaxis if needed.
Adm inister broad-spectrum antibiotics if significant m ucosal disruption or signs of peritonitis are present (see Medications).
Place Foley catheter after excluding urethral injury.
Obtain surgical consultation for: o
Peritonitis
o
All traum atic rectal m ucosal lacerations
o
Objects >10 cm from anal verge
o
Sharp objects whose rem oval m ay provoke m ucosal injury
o
Inability to extract foreign body in ED
Rectal foreign body rem oval in ED: o
Determ ine location and type of foreign object.
o
Provide adequate IV sedation and use gentle digital sphincter dilation to increase likelihood of successful ED extraction.
o
Adm inister local anesthesia to m axim ize anal sphincter dilation.
o
Place patient in lithotom y position:
Use obstetric, ring, or biopsy forceps, tenaculum , or suctioning device to aid extraction.
Apply suprapubic pressure.
Pa ge 4 0 4
o
Have patient bear down during procedure.
Other m ethods:
Pass Foley catheter above foreign body, inflate balloon and apply gentle traction to release suction and perm it extraction.
Plaster of Paris: Fill hollow object and insert gauze or instrum ent to serve as “handle― ; place above or adjacent to foreign body; when hard, pull on inset handle to perm it extraction.
o
Sigm oidoscopy to evaluate m ucosal injury following extraction
Medication (Drugs)
Antibiotics with coverage against gram -negative and anaerobic organism s: o
Am picillin/sulbactam :
o
Cefotetan:
o
Adults: 3.1 g IV (peds: 75 m g/kg IV)
Additional anaerobic coverage: o
Clindam ycin:
o
Adults: 600–900 m g IV (peds: 10 m g/kg IV)
Metronidazole:
Adults: 3.375 g IV (peds: 75 m g/kg IV)
Ticarcillin/clavulanate:
Adults: 2 g q6h IV (peds: 80 m g/kg q6h IV)
Piperacillin/tazobactam :
o
Adults: 2 g q12h IV (peds: 40 m g/kg IV)
Cefoxitin:
o
Adults: 3 g q6h IV (peds: 50 m g/kg IV)
Adults: 1 g IV (peds: 15 m g/kg IV)
Com bination therapy:
Pa ge 4 0 4
o
Adults: Am picillin 500 m g IV q6h, gentam icin 1–1.7 m g/kg IV, and m etronidazole 1 g IV
o
Peds: Am picillin 50 m g/kg IV q6h, gentam icin 1–1.7 m g/kg IV, and m etronidazole 15 m g/kg IV
Sedation and analgesia: o
Fentanyl: 2–3 µg/kg IV (peds and adults)
o
Midazolam : 0.01–0.2 m g/kg IV (peds and adults)
Surgery
Rectal foreign body rem oval in operating room .
General anesthesia is required to rem ove high-riding or sharp object.
Laparotom y is last resort.
Follow-Up Disposition Admission Criteria
Perforation
Significant bleeding
Unstable vital signs
Abdom inal pain
Torn anal sphincter
Foreign body that requires extraction in operating room
Broken glass or other sharp object in rectum requiring surgical rem oval
Discharge Criteria
Stable vital signs
No abdom inal pain
Norm al sigm oidoscopy/anoscopy exam
Pa ge 4 0 4
References 1. Carrillo EH, Som berg LB, Ceballos CE, et al. Blunt traum atic injuries to the colon and rectum . J Am Coll Surg. 1996;183:548–552. 2. Coates WC. Anorectum . In: Marx J, ed. Em ergency Medicine: Concepts and Clinical Practice. 5th ed. St. Louis, MO: Mosby; 2002:1343–1359. 3. Cohen JS, Sackier JM. Managem ent of colorectal foreign bodies. J R Coll Surg Edinb. 1996;41:312–315. 4. Fry RD. Anorectal traum a and foreign bodies. Surg Clin North Am . 1994;74:1491–1505. 5. Janicke DM, Pundt MR. Anorectal disorders. Em erg Med Clin North Am . 1996;14:757–788.
Codes ICD9-CM 863.45 Injury to gastrointestinal tract without m ention of open wound into cavity, rectum
ICD10 S36.6 Injury of rectum
Pa ge 4 0 4
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Red Eye
Red Eye
Camie J. Sorensen
Basics Description
May be caused by alm ost any eye disorder
Often benign, though m ay represent system ic disease
Red eye is due to vascular engorgem ent of conjunctiva.
Main causes include inflam m atory, allergic, infection, or traum a.
Inflam m atory etiology includes uveitis (anterior and posterior), episcleritis (70% are idiopathic), scleritis (50% associated with system ic disease).
Allergic etiology is due to histam ine release and increased vascular perm eability, resulting in swelling of conjunctiva (chem osis), watery discharge, and pruritis; usually bilateral involvem ent.
Infectious etiology is either bacterial (purulent m ucous discharge), viral (watery or no discharge), or fungal.
Traum atic causes of red eye include corneal abrasions, conjunctival hem orrhage, and foreign bodies.
Etiology
Anterior uveitis, iritis (perilim bic injection)
Posterior uveitis
Pa ge 4 0 4
Pinguecula
Pterygium
Hem orrhage
Episcleritis
Scleritis
Bacterial conjunctivitis (diffuse injection)
Viral conjunctivitis (diffuse injection)
Blepharitis
Dry eye syndrom e
Acute angle closure glaucom a
Endophthalm itis
Allergic reaction
Ophthalm ia neonatorum
Dacryocystitis
Canaliculitis
Conjunctival tum or
Foreign body
Corneal ulcer/abrasion/erosion
Occult perforation
Acute angle closure glaucom a
Endophthalm itis
Orbital cellulites
System ic inflam m atory reactions (see list in Differential Diagnosis Section)
Diagnosis Signs and Symptoms
Discharge
Pruritis
Pain
Pa ge 4 0 4
Foreign body sensation
Ectropion, entropion
Eyelash against globe (trichiasis)
Conjunctival injection
Corneal abrasion, ulcer, or opacity
Anterior cham ber cells or flare
Photophobia (from m ovem ent of an inflam ed iris)
Proptosis
Preauricular (viral conjunctivitis) lym phadenopathy
Subm andibular lym phadenopathy
Rosacea (m ay cause blepharitis)
Facial or skin lesions (herpes)
Sinusitis
Otitis
Pharyngitis
History
Obtain tim e of onset
Patient's occupation (i.e., m etal worker)
Associated signs and sym ptom s (headache, blurring vision)
Other com orbidities
Physical Exam
Thorough physical exam ination
Ophthalm ologic: o
Visual acuity
o
Pupil exam ination
o
Confrontational visual field exam
o
Extraocular m uscle function
o
Slit-lam p exam ination with fluorescein
o
Lid eversion
o
Funduscopy and tonom etry when applicable
Essential Workup
Pa ge 4 0 5
Address and rule-out system ic causes of red eye.
Com plete full physical exam as described above.
Tests
Tests should be directed toward the suspected etiology of red eye: o
Dacryocystitis: culture discharge
o
Corneal ulcers: ophthalm ologist m ay scrape the cornea for cultures.
o
Bacterial conjunctivitis:
Moderate discharge: obtain conjunctival swab for routine culture and sensitivity (usually Staphylococcus aureus, Streptococcus, and Haem ophilus influenzae in children); however, not always needed as conjunctivitis is often treated presum ptively
Severe discharge: Neisseria gonorrhoeae and Chlam ydia
Lab
Often not indicated
Useful if etiology is thought to be system ic disease
If bilateral, recurrent, granulom atous uveitis is suspected, send CBC, ESR, ANA, venereal disease research laboratory, FTA Ab, purified protein derivative, ACE level, CXR (sarcoidosis and tuberculosis [TB]), Lym e titer, and HLA-B27, toxoplasm a, and cytom egalovirus (CMV) titers
Imaging Obtain plain film s and/or CT scan of the orbits if suspect foreign body, orbital disease, or traum a.
Differential Diagnosis
Local: infection, allergy, traum a (also see list in Etiology
Pa ge 4 0 5
section)
System ic (generally an inflam m atory reaction): o
Arthritic disease
o
Ankylosing spondylosis
o
Ulcerative colitis
o
Reiter syndrom e
o
TB
o
Herpes
o
Syphilis
o
Sarcoidosis
o
Toxoplasm a
o
CMV
Treatment Initial Stabilization N/A
ED Treatment
Treatm ent is based on cause of red eye.
Direct therapy toward specific etiology.
Medication as indicated (See Medication Section)
Special rem inders: o
Differentiate between a corneal abrasion and a corneal ulcer.
o
Eye patching is no longer routinely recom m ended for abrasions and is contraindicated for corneal ulcers or abrasions with high infection risk (contact lens wearers, abrasions from tree branches or fingernails).
o
Update tetanus im m unization for corneal injury.
Pa ge 4 0 5
o
Do not wear contact lenses.
o
Do not spread infection from the affected eye to the unaffected eye.
o
Diagnosis of conjunctivitis caused by neisseria gonorrhea or chlam ydia requires treatm ent of system ic infection for the individual as well as treatm ent of all sexual partners.
o
Always include work-up and treatm ent of system ic disease if this is suspected.
Special Topics Corneal Abrasion
Non–contact lens wearer: o
Ointm ent or drops:
Erythrom ycin ointm ent every 4 hours
Polytrim drops four tim es a day
Contact lens wearers need pseudom onal coverage: o
Tobram ycin ointm ent every 4 hours
o
Tobram ycin, ofloxacin, or ciprofloxacin drops four tim es a day
Dilate eyes with cyclopentolate 1–2%, 2–4 drops daily to prevent pain from iritis.
Abrasions will heal without patching.
P.947
Corneal Ulcer
Non–contact lens wearer: o
Polytrim ointm ent four tim es a day
o
Ofloxacin, ciprofloxacin drops q2h–q4h
Contact lens wearers need pseudom onal coverage: o
Tobram ycin, ofloxacin, or ciprofloxacin drops
Pa ge 4 0 5
q2h–q4h o
Tobram ycin or ciprofloxacin ointm ent every hour as needed (optional)
Severe or vision-threatening corneal ulcers: o
Central, larger than 1.5 m m or with significant anterior cham ber reaction
o
Treat as aforem entioned and add increased frequency of antibiotic drops such as one drop every 15 m inutes for 3 doses then every 15 m inutes for 2–6 hours then every 30 m inutes around the clock
o
Ophthalm ology consult for further recom m endations, which m ay include ciprofloxacin 500 m g PO b.i.d. or fortified antibiotic drops m ade by pharm acist
Ulcers from herpes sim plex or zoster: o
Add trifluridine (Viroptic) 1%, 2 gtt 9 tim es/day or vidarabine 3% ointm ent 5 tim es/day (ointm ent preferred for children).
Traum a or uveitis: Rule out foreign body.
Medication (Drugs)
Antibiotic drops: o
Ciprofloxacin 0.3%: 1–2 gtt q1h–q6h
o
Gentam ycin 0.3%: 1–2 gtt q4h
o
Ofloxacin 0.3%: 1–2 gtt q1h–q6h
o
Levofloxacin 0.5%: 1–2 gtt q2h
o
Polytrim : 1 gtt q3–6h
o
Sulfacetam ide 10%: 0.3% 1–2 gtt q2h–q6h
o
Tobram ycin 0.3%: 1–2 gtt q1h–q4h
o
Trifluridine 1%: 1 gtt q2h–q4h
Antibiotic ointm ents: o
Bacitracin: 500 U/g one half-inch ribbon of ointm ent
Pa ge 4 0 5
q3h–q6h o
Ciprofloxacin 0.3%: one half-inch ribbon of ointm ent q6h–q8h
o
Erythrom ycin 0.5%: one half-inch ribbon of ointm ent q3h–q6h
o
Gentam ycin 0.3%: one half-inch ribbon of ointm ent q3h–q4h
o
Neosporin: ½-inch ribbon of ointm ent q3h–q4h
o
Polysporin: one half-inch ribbon of ointm ent q3h–q4h
o
Sulfacetam ide 10%: one half-inch ribbon of ointm ent q3h–q8h
o
Tobram ycin 0.3%: one half-inch ribbon of ointm ent q3h–q4h
o
Vidarabine: one half-inch ribbon of ointm ent 5 tim es/day
Mydriatics and cycloplegics: o
Atropine 1%, 2%: 1–2 gtt per day to q.i.d.
o
Cyclopentolate 0.5%, 1%, 2%: 1–2 gtt p.r.n. dilation
o
Hom atropine 2%: 1–2 gtt b.i.d.–t.i.d.
o
Phenylephrine 0.12%, 2.5%, 10%: 1–2 gtt t.i.d.–q.i.d.
o
Tropicam ide 0.5%, 1%: 1–2 gtt PRN dilation
Corticosteroid antibiotic com bination drops (use only with ophthalm ology consultation):
o
Blepham ide: 1–2 gtt q1h–q8h
o
Cortisporin: 1–2 gtt q3h–q4h
o
Maxitrol: 1–2 gtt q1h–q8h
o
Pred G: 1–2 gtt q1h–q8h
o
TobraDex: 1–2 gtt q2h–q6h
Glaucom a agents (always use with ophthalm ology
Pa ge 4 0 5
consultation): o
Acetazolam ide: 250–500 m g PO per day to q.i.d.
o
Betaxolol 0.25%, 0.5%: 1–2 gtt b.i.d.
o
Carteolol 1%: 1 gtt b.i.d.
o
Levobunolol 0.25%, 0.5%: 1 gtt per day to b.i.d.
o
Dipivefrin 1%: 1 gtt b.i.d.
o
Mannitol: 1–2 g/kg IV over 45 m inutes
o
Pilocarpine 0.25%, 0.5%, 1%, 2%, 3%, 4%, 6%, 8%, 10%: 1–2 gtt t.i.d.–q.i.d. (use only if m echanical closure is ruled out)
o
Tim olol 0.25%, 0.5%: 1 gtt b.i.d.
Follow-Up Disposition Admission Criteria
Endophthalm itis
Perforated corneal ulcers
Orbital cellulites
Concurrent injuries (i.e., traum a)
New or suspected diagnosis of system ic disease
Issues for Referral
Dacryocystitis
Corneal ulcer
Scleritis
Angle closure glaucom a
Uveitis
Proptosis
Orbital cellulitis
Vision loss
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Uncertain diagnosis
Gonorrheal or Chlam ydia conjunctivitis
References 1. Kunim oto DY, Kanitkar KD, Makar MS. The Wills Eye Manual: Office and Em ergency Room Diagnosis and Treatm ent of Eye Disease. 4th ed. Lippincott William s & Wilkins, 2004. 2. Leibowitz HM. “Prim ary Care: The Red Eye.― New Eng J Med . 2000;343(5).
Miscellaneous SEE ALSO: Chalazion; Conjunctivitis; Corneal Abrasion; Corneal Burn; Corneal Foreign Body; Dacryocystitis; Globe Rupture; Hordeolum; Hyphem a; Iritis; Optic Artery Occlusion; Optic Neuritis; Orbital Cellulitis; Ultraviolet Keratitis; Visual Loss; Vitreous Hemorrhage
Codes ICD9-CM 077.9 Viral conjunctivitis NOS 372.01 Serous conjunctivitis
ICD10 H10 Conjunctivitis
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Renal C alculus
Renal Calculus
Jennifer Kolodchak
Basics Description
Urinary tract obstruction
Interm ittent distention of the renal pelvis of proxim al ureter produces pain.
Kidney stones: o
Most com m on cause of renal colic
o
Theories of stone form ation:
Urinary supersaturation of solute followed by crystal precipitation
Decrease in the norm al urinary proteins inhibiting crystal growth
Urinary stasis from a physical anom aly, catheter placem ent, neurogenic bladder, or the presence of a foreign body
o
Stone com position:
75%: calcium in conjunction with phosphate and/or oxalate
15%: m agnesium phosphate (struvite)
Associated with infections caused by urea-splitting organism s (e.g., Pseudom onas,
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Proteus, Klebsiella) along with an alkalotic urine
5% uric acid
90% of urinary calculi radiopaque
Etiology
1% of the population
Three tim es m ore com m on in m en than wom en
Pediatric Considerations
Rare in children
When present, indication of an overt m etabolic or genetic disorder
Painless hem aturia com m on presentation (up to 30%)
Pediatric patients younger than 16 years com prise approxim ately 7% of all cases of renal stones.
1:1 sex distribution
Causes of stone form ation: o
Metabolic abnorm alities (50%)
Most com m on etiologies of stone form ation in the pediatric population
o
Urologic abnorm alities (20%)
o
Infection (15%)
o
Im m obilization syndrom e (5%)
Diagnosis Signs and Symptoms History
Sudden onset of severe pain in the costovertebral angle, flank, and lateral abdom en
Colicky or constant pain: o
Patient cannot find a com fortable position.
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Hem aturia
Nausea/Vom iting
Restlessness
Diaphoresis
History of prior stone form ation
Abdom inal tenderness is not generally present.
Physical Exam
Obtain vital signs: o
Fever suggests an occult infection.
o
Hypotension with an altered m ental status is suggestive of urosepsis.
Abdom inal exam : o
Pain on palpation, rebound tenderness, and or guarding suggests a m ore serious intraabdom inal process.
o
Palpate the abdom inal aorta for tenderness or pulsatile enlargem ent suggestive of an aneurysm .
Genitourinary exam : o
Exam ine the genitalia for evidence of epididym itis, torsion, or testicular m asses.
Essential Workup Urinalysis:
Microscopic hem aturia present in >80%
Gross hem aturia
Absent urinary blood in 10%
No correlation between the am ount of hem aturia and the degree of urinary obstruction
WBC/Bacteria suggestive of infection
Tests Lab
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CBC: o
WBC >15,000 suggestive of concom itant infection
Urine culture
Electrolytes, glucose, blood urea nitrogen, and creatinine
Pregnancy test when suggestive
Imaging
CT: o
Helical CT has replaced IV pyelogram (IVP) as test of choice.
o
Detect calculi as sm all as 1 m m in diam eter
o
Directly visualizes com plications, such as hydroureter, hydronephrosis, and ureteral edem a
o
Advantages over IVP:
Perform ed rapidly
Does not require IV contrast m edia
Detects other nonurologic causes of sym ptom s, such as abdom inal aortic aneurysm s (AAA)
o
Nonenhanced helical CT in the evaluation of renal colic:
o
Sensitivity of 97%
Specificity of 96%
Accuracy of 97%
Indications:
First-tim e diagnosis
Persistent pain
Clinical confusion with pyelonephritis
IVP: o
Establishes diagnosis in 95%
o
Dem onstrates the severity of obstruction
o
Scout film prior m ay localize stones that would otherwise be obscured by the dye.
o
Postvoiding film
Pa ge 4 0 6
Useful to identify stones at the ureteral vesicular junction or distal ureter that are obscured by a full bladder.
Kidney, ureter, and bladder (KUB) radiograph: o
Indicated when allergy to IVP dye and when renal scanning and ultrasound (US) not available
o
Assists in locating radiopaque stones and the exclusion of other pathologies in nonpregnant patients
o
Difficult to distinguish radiopaque body:
Phlebolith
Bowel contents
Obstruction within the urinary tract on the KUB
Oblique film s assist in localizing suspicious calcifications
P.949
US: o
For patients who are not candidates for IV contrast
o
Useful in the detection of larger stones and hydronephrosis
o
Provides anatom ic inform ation only
o
Helpful in diagnosing obstruction and localizing stones in the proxim al and distal portions of the ureter
o
o
Ability to detect hydronephrosis:
Sensitivity of 85–94%
Specificity of 100%
Lim itations:
May m iss stones 65 years or Table o f C o ntents > Renal F ailure
Renal Failure
Matthew N. Graber
Basics
Acute renal failure (ARF): o
Deterioration of renal function over hours to days resulting in the inability to excrete nitrogenous waste products and to m aintain fluid and electrolyte hom eostasis
o
May be reversible or lead to chronic renal failure
Chronic renal failure: o
Deterioration of renal function over an extended period of tim e that results in:
The accum ulation of nitrogenous waste products
The inability to m aintain fluid and electrolyte hom eostasis
o
Acidosis
Anem ia
Less likely to be reversible than acute renal failure
Description
Decline in glom erular filtration
Disrupts the extracellular fluid volum e, electrolyte, and acid-base status
Results in accum ulation of nitrogenous waste
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Etiology
Prerenal failure: o
Caused by renal hypoperfusion
o
Renal tissue rem ains norm al unless severe/prolonged hypoperfusion.
Intrarenal failure: o
Postrenal failure: o
Caused by diseases of the renal parenchym a
Due to acute obstruction of the urinary tract
Iatrogenic causes include: o
Am inoglycoside antibiotics
o
Radiocontrast m aterial adm inistration
o
NSAIDs
o
Angiotensin converting enzym e inhibitors
Diagnosis Signs and Symptoms Acute Renal Failure (ARF)
Often asym ptom atic and com m only diagnosed with incidental laboratory findings
Oliguria (1.018
o
Osm olality >500 m m ol/kg
o
Sodium 20
Pa ge 4 0 7
Rapid recovery of renal function when renal perfusion norm alized
Intrarenal
BUN/Cr ratio 100 m g/dL
o
Cr >10 m g/dL:
Chronic renal failure patients on regular dialysis m ay have a baseline elevated creatinine that by itself is not an indication for em ergent dialysis.
o
Metabolic acidosis (pH 5.5 m Eq/L
o
For K + >6.5 m Eq/L or ECG abnorm alities consistent with hyperkalem ia
Albuterol via nebulizer
Glucose and insulin: onset 30–60 m inutes, duration several hours
Furosem ide if patient not anuric
Sodium bicarbonate: onset Table o f C o ntents > Reperfusio n Therapy, C ardiac
Reperfusion
Therapy, Cardiac Shamal Grossman
Basics Description
Throm bolytic therapy: o
Reduces m orbidity and m ortality in ST-segm ent elevation m yocardial infarction (MI)
o
Maxim um benefit is achieved when started within 6 hours after infarct.
o
The earlier throm bolytics are started, the m ore m yocardium salvaged.
Percutaneous coronary intervention (PCI): o
Balloon inflation results in overstretching of vessel wall and partial disruption of intim a, m edia, and adventitia, resulting in enlargem ent of lum en and outer diam eter of diseased vessel.
o
Stent placem ent decreases early and late loss in lum inal diam eter seen with percutaneous translum inal coronary angioplasty (PTCA).
o
PCI provides greater coronary patency and throm bolysis in MI III flow than do throm bolytics.
Pa ge 4 0 8
o
Lower risk of bleeding than with throm bolytics
o
Im m ediate knowledge of extent of disease
o
Meta-analysis suggests im proved survival with PCI for ST-segm ent elevation MI when com pared with throm bolytic therapy (6.5% vs. 4.4%); however, im proved outcom es m ay be contingent on operator and institutional expertise.
o
Particularly useful when throm bolytic therapy is contraindicated
o
PTCA has a 30% restenosis rate in first 6 m onths.
o
Stents reduce restenosis rate to 20%.
o
Medication coated stents m ay reduce to 5% or less.
o
PCI should be strongly considered within first 48 hours after a non–ST-segm ent elevation MI with concom itant use of glycoprotein IIb/IIIa inhibitors.
Glycoprotein IIb/IIIa inhibitors: o
Antiplatelet agents that bind to platelet receptor glycoprotein IIb/IIIa and inhibit platelet aggregation
o
Reduce m ortality and reinfarction rate in patients in whom PCI is planned
o
Recent data suggest reduced m ortality in all patients with unstable angina and non–Q-wave infarction.
o
Not indicated for patients with ST-elevation MI, unless also undergoing PCI
Unfractionated heparin and low m olecular weight heparin: o
Adjuncts in treatm ent with throm bolytics, glycoprotein IIb/IIIa inhibitors, and PCI
o
Low m olecular weight heparin has been associated with less re-occlusion, enhanced late patency, and reduced reinfarction rates when com pared with unfractionated heparin.
Clopidogrel m ay be of benefit acutely when added to
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standard therapy by reducing the odds of acute MI patients having another occluded artery, or a second heart attack or death by 36% after one week of hospitalization
Statin therapy reduces clinical events in patients with stable coronary artery disease. This m ay also extend to patients experiencing an acute ischem ic coronary event.
Etiology Ischem ic MI is caused by occlusion of a coronary artery, usually as a result of a throm botic event.
Diagnosis Signs and Symptoms
Chest pain, heaviness, or pressure feeling
Shortness of breath
Arm , neck, or back pain
Weakness or fatigue
Nausea, vom iting
Diaphoresis
Palpitations
Dizziness or syncope
Essential Workup
History is critical in assessing window for use of both throm bolytics and PTCA.
ECG: o
Will be norm al approxim ately 50% of tim e
o
Must be com pared with prior tracings if available
o
New ST-segm ent changes or T-wave inversions are suspicious for unstable angina or non–Q-wave infarct.
Pa ge 4 0 9
o
1 m m depression of the ST segm ent below the baseline, 80 m s from the J point, is characteristic of unstable angina or non–Q-wave infarct.
o
New left bundle branch block, or new ST-segm ent elevation 1 m m in two contiguous lim b leads or 2 m m in two contiguous precordial leads suggests Q-wave infarct.
Chest radiograph: m ay be helpful if aortic dissection is being considered
Hem e stool test: helpful in establishing baseline
Tests Lab
Cardiac enzym es
Baseline creatinine, hem atocrit, and coagulation profile are all appropriate in initial work-up.
Differential Diagnosis
Aortic dissection
Anxiety
Biliary colic
Costochondritis
Esophageal spasm
Esophageal reflux
Herpes zoster
Hiatal hernia
Mitral valve prolapse
Peptic ulcer disease
Psychogenic sym ptom s
Panic disorder
Pericarditis
Pneum onia
Pulm onary em bolus
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Treatment Pre Hospital
IV access
Oxygen
Cardiac m onitoring
Sublingual nitroglycerin for sym ptom relief
Aspirin
Controversies: o
Whether to bypass closer EDs in favor of hospitals capable of prim ary PTCA; follow local em ergency m edical service protocols.
Alert
All chest pain should be treated and transported as a possible life-threatening em ergency.
Therapy with throm bolytics and glycoprotein IIb/IIIa inhibitors in the field is not currently standard of care.
Initial Stabilization
Place patient on m onitor.
Obtain IV access.
Oxygen
Nitrates
P.955
ED Treatment
Aspirin
Clopidogrel m ay be of benefit acutely
Pa ge 4 0 9
Throm bolytics: o
Unless contraindicated
o
If PCI is not readily available within 90 m inutes
PCI is preferred for both diagnostic and therapeutic options.
PCI and throm bolytic therapy m ust be used with either unfractionated heparin or a low m olecular weight heparin, such as enoxaparin.
Low m olecular weight heparin: o
Kinetics m ore predictable
o
Requires no m onitoring
o
Less potential for platelet activation
o
Lower bleeding rate
o
Is at least as effective as unfractionated heparin in treatm ent of acute coronary syndrom es
Glycoprotein IIb/IIIa inhibitors
Medication (Drugs)
Aspirin: 80–325 m g PO
Enoxaparin (Lovenox): 1 m g/kg SQ q12h
Clopidogrel (Plavix): 300 m g PO load, 75 m g PO per day
Glycoprotein IIb/IIIa inhibitor: o
Abcixim ab (ReoPro): for use before PCI only; 0.25 m g/kg IV bolus
o
Eptifibatide (Integrilin): 180 µg/kg IV over 1–2 m inutes, followed by continuous IV infusion of 2 µg/kg per m inute up to 72 hours
o
Tirofiban (Aggrastat): 0.4 µg/kg per m inute for 30 m inutes, then 0.1 µg/kg per m inute for 48–108 hours
Heparin: 80 U/kg IV bolus, then 18 U/kg per hour
Pa ge 4 0 9
Metoprolol: 5 m g IV bolus and/or 25–50 m g PO
Throm bolytics: o
Anisoylated plasm inogen streptokinase activator com plex: 30 m g IV over 2–5 m inutes; patients should also receive m ethylprednisolone 250 m g IV.
o
Recom binant tissue plasm inogen activator (Reteplase): 10 m illion-unit IV bolus, repeat dose after 30 m inutes; patients should also receive heparin 5,000 IU IV bolus, then infuse 1,000 IU per hour for 48 hours, keeping activated partial throm boplastin tim e (aPTT) 1.5–2.5.
o
Streptokinase: 1.5 m illion units over 60 m inutes; patients should also receive m ethylprednisolone 250 m g IV.
o
Tissue plasm inogen activator: 15 m g IV bolus, then 0.75 m g/kg (m ax. 50 m g) over 30 m inutes, then 0.5 m g/kg (m ax. 35 m g) over 60 m inutes; patients should also receive heparin 5,000 IU IV bolus, then infuse 1,000 IU per hour for 48 hours keeping aPTT 1.5–2.5
o
Urokinase: 1.5 IU IV over 2 m inutes, then 1.5 IU IV over next 90 m inutes
o
Contraindications:
Active internal bleeding
History of cerebrovascular accident in past 6 m onths
History of a hem orrhagic cerebrovascular accident
Recent (within 2 m onths) intracranial or intraspinal surgery or traum a
Intracranial neoplasm , arteriovenous m alform ation, or aneurysm
Pa ge 4 0 9
Known bleeding diathesis
Severe, uncontrolled hypertension
Pregnancy
Head traum a within past m onth
Traum a or surgery within past 2 weeks that m ay result in closed-space bleed
Follow-Up Disposition Admission Criteria All patients being considered for reperfusion therapy should be adm itted to a telem etry or intensive care unit setting.
Discharge Criteria No patient being considered for reperfusion therapy should be discharged hom e from ED.
References 1. Braunwald E, Antm an EM, Beasley JW, et al. ACC/AHA guidelines for the m anagem ent of patients with unstable angina and non–ST-segm ent elevation m yocardial infarction. J Am Coll Cardiol. 2000;36:970–1062. 2. Gibson CM. Prim ary angioplasty com pared with throm bolysis: New issues in the era of glycoprotein IIb/IIIa inhibition and intracoronary stenting. Ann Intern Med. 1999;130:841–847. 3. Lieu TA, Gurley RJ, Lundstrom RJ, et al. Prim ary angioplasty and throm bolysis for acute m yocardial infarction: An evidence based sum m ary. J Am Coll Cardiol. 1996;27:737–750. 4. Ryan TJ, Antm an EM, Brooks NH, et al. ACC/AHA practice guidelines for the m anagem ent of patients with acute m yocardial
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infarction. J Am Coll Cardiol. 1996;28:1328–1428. (See also 1999 Web update at http://www.acc.org.) 5. Schöm ig H, Kastrati A, Dirschinger J, et al. Coronary stenting plus platelet glycoprotein IIb/IIIa blockade com pared with tissue plasm inogen activator in acute m yocardial infarction. N Engl J Med. 2000;343:385–391.
Miscellaneous SEE ALSO: Acute Coronary Syndrom e: Myocardial Infarction
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Reperfusio n Therapy, C erebral
Reperfusion
Therapy, Cerebral Kama Guluma
Basics Description
Cerebrovascular accident (CVA) or stroke is a focal interruption of blood supply to the brain:
o
Onset m ay be sudden and com plete or gradual.
o
Course m ay be progressive or stuttering.
o
Transient ischem ic attack (TIA):
Sym ptom s that resolve within 24 hours
May predict m ore com plete throm botic CVA
The National Institutes of Health Stroke Scale (NIH-SS) can be used to delineate severity of a CVA (by com puting the total of subcategory scores, to a m axim um of 42) as follows: o
1a. Level of consciousness (LOC): alert = 0; drowsy = 1; stuporous = 2; com a = 3
o
1b. LOC questions: answers both correctly = 0; one correctly = 1; none correct = 2
o
1c. LOC com m ands: obeys both correctly = 0; one correctly = 1; none correctly = 2
Pa ge 4 0 9
o
2. Best gaze: norm al = 0; partial gaze palsy = 1; forced deviation = 2
o
3. Visual: no visual loss = 0; partial hem ianopia = 1; com plete hem ianopia = 2; bilateral hem ianopia = 3
o
4. Facial palsy: norm al, sym m etric = 0; m inor paralysis = 1; partial paralysis = 2; com plete paralysis = 3
o
5 to 8. Best m otor (com puted for each arm and leg): no drift = 0; drift = 1; som e effort against gravity = 2; no effort against gravity = 3; no m ovem ent = 4; untestable (e.g., am putation or joint fusion) = 9
o
9. Lim b ataxia: absent = 0; present in 1 lim b = 1; present in two lim bs = 2
o
10. Sensory (pinprick): norm al = 0; partial loss = 1; dense loss = 2
o
11. Best language: no aphasia = 0; m ild to m oderate aphasia = 1; severe aphasia = 2; m ute = 3
o
12. Dysarthria: norm al articulation = 0; m ild to m oderate dysarthria = 1; unintelligible = 2
o
13. Neglect/inattention: no neglect = 0; partial neglect = 1; com plete neglect = 2
Cerebral reperfusion therapy involves the IV adm inistration of a throm bolytic agent: o
To effect rapid dissolution of an acute cerebrovascular throm boem bolic occlusion
o
Interventional endovascular techniques enable site-specific intra-arterial throm bolysis or m echanical rem oval of the occlusion.
Etiology
Ischem ic CVA is caused by occlusion of a cerebral artery: o
Prim arily from a throm botic or em bolic event
Throm botic CVA is caused by in situ occlusion:
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o
Clot form ation at an ulcerated atherosclerotic plaque or other prothrom botic endothelial abnorm ality
o
Hypercoagulable states:
Antithrom bin III, protein C or protein S deficiencies
o
Sludging:
Sickle cell disease
Polycythem ia vera
Em bolic CVA is caused by acute obstruction by an intravascular em bolus from : o
Cardiac m ural throm bus form ed in:
Fibrillating atrium
Hypokinetic ventricle (m yocardial infarction, cardiom yopathy, failure)
o
Ventricular aneurysm
A prosthetic cardiac valve or an abnorm al native valve
o
Aortic, carotid, or cerebrovascular atherosclerotic plaques
Other occlusive events include: o
Vascular dissection of the aorta, cerebral, vertebral, carotid, or innom inate arteries
o
Cerebral vasospasm induced by:
Subarachnoid hem orrhage (SAH)
Vasoconstrictive agents (e.g., cocaine)
Diagnosis Signs and Symptoms History
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Occlusive event that m ight benefit from em ergent reperfusion therapy with IV throm bolysis: o
Acute focal neurological deficits presenting within 3 hours of onset
Tim e of sym ptom onset is critical: o
If tim e of onset cannot be firm ly established, the tim e the patient last felt norm al or was last seen norm al should be a surrogate.
Historical elem ents that m ay suggest an etiology other than routine throm boem bolic stroke: o
Severe, sudden headache in SAH
o
Acute neck strain in vertebral dissection
o
Injury to the anterior neck in carotid dissection
o
Tearing back pain in aortic dissection
o
Recent or concom itant drug abuse in vasospastic occlusions
Physical Exam Abnorm al neurological exam findings warrant consideration for cerebral reperfusion therapy:
Especially sym ptom s within a distinct vascular supply territory of the brain (see below)
Middle Cerebral Artery
Contralateral hem iplegia (upper > lower)
Contralateral hem isensory deficits
Contralateral hom onym ous hem ianopia
Expressive or receptive aphasia (dom inant hem isphere)
Contralateral neglect
Posterior Cerebral Artery
Cortical blindness in half the visual field
Visual agnosia
Third nerve palsy
Pa ge 4 1 0
Thalam ic syndrom es: o
Abnorm al m ovem ents (chorea or hem iballism us)
o
Hem isensory deficit
Vertebrobasilar System
Im paired vision, visual field defects
Nystagm us, vertigo, dizziness
Facial paresthesia, dysarthria
Cranial nerve palsies
Contralateral sensory deficits (pain and tem perature)
Lim b ataxia, abnorm al gait
Anterior Cerebral Artery
Contralateral hem iplegia (lower >upper)
Hem isensory loss
Apraxia
Confusion, im paired judgm ent
Lacunar (deep subcortical)
Pure m otor hem iplegia (m ost com m on), or pure sensory hem iplegia
Dysarthria and contralateral hand ataxia (clum sy hand), or dysarthria with facial weakness
Ataxic hem iparesis
Essential Workup
STAT bedside blood glucose testing
Im m ediate noncontrast head CT scan: o
Can differentiate between ischem ic and hem orrhagic CVA
o
Can reveal other etiologies
o
May be norm al in the first 24 hours of an ischem ic CVA:
Very likely norm al in the first 3 hours
Pa ge 4 1 0
Early signs of ischem ia (e.g., edem a) should prom pt a re-evaluation of tim e of onset.
ECG to assess for dysrhythm ia, pericarditis or m yocardial infarction
Tests Lab
CBC, serum electrolytes and glucose, blood urea nitrogen, creatinine, prothrom bin tim e (PT)/partial throm boplastin tim e (PTT)
Urine pregnancy test
Urine toxicology screen
Liver function tests in selected patients, such as those prone to liver dysfunction
Imaging
Multim odal MRI (with perfusion- and diffusion-weighted protocols): o
Can detect ischem ic CVA alm ost im m ediately after onset
Perfusion brain CT can reveal a perfusion deficit im m ediately after onset.
Carotid ultrasound
Chest radiograph
Diagnostic Procedures/Surgery Cerebral angiography m ay be a useful diagnostic and therapeutic adjunct:
Considered in consultation with a neurologist and interventional radiologist
Differential Diagnosis
Intracranial hem orrhage (ICH)
Seizure
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Com plex m igraine
Bell palsy or other focal neuropathies
Hypoglycem ia and other m etabolic abnorm alities
Dural sinus throm bosis
Intracranial neoplasm
Intracranial traum a
Meningitis, encephalitis, or brain abscess
Vasculitis
Air em bolism or decom pression illness
Spinal cord lesion
Psychogenic
P.957
Treatment Pre Hospital
Screening for CVA: o
o
Assessing for deficits:
Dysarthria, facial weakness
Arm or leg weakness
Notification and pre-arrival m obilization of ED and hospital resources
Blood-glucose testing should be perform ed: o
Hypoglycem ia can cause focal neurological sym ptom s that m im ic a CVA.
o
Treat with adm inistration of dextrose.
Initial Stabilization
Supplem ental oxygen to correct hypoxia
Pa ge 4 1 0
IV access and norm al saline bolus to correct hypotension
Cardiac m onitoring and pulse oxim etry
Naloxone, thiam ine, and dextrose (if hypoglycem ic) for altered m ental status
Rapid sequence intubation if airway protection is warranted or ventilatory insufficiency is evident
ED Treatment
Exclude other diagnoses in the differential, especially vascular dissection and ICH.
Throm bolytic therapy should be reserved for patients with ischem ic strokes caused by throm bosis or em bolism .
Inclusion criteria for IV throm bolytic therapy: o
Age ≥18 years of age
o
Clearly defined onset of sym ptom s within 3 hours
o
Noncontrast head CT without evidence of hem orrhage
Absolute contraindications to IV throm bolytic therapy: o
ICH on pretreatm ent head CT scan
o
Prior ICH
o
Clinical presentation consistent with SAH
o
Known arteriovenous m alform ation or aneurysm
o
CVA, serious brain injury or intracranial surgery within previous 3 m onths
o
Active internal bleeding
o
Major surgery within previous 14 days
o
Pregnancy
o
Pericarditis
o
Known bleeding diathesis:
Platelet count 1.7, PT >15 seconds
Prolonged PTT
Current anticoagulant use
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Use of heparin within 48 hours
o
Systolic blood pressure (SBP) >185 m m Hg
o
Diastolic blood pressure (DBP) >115 m m Hg
Relative contraindications to IV throm bolytics: o
Rapid im provem ent of neurological sym ptom s
o
Mild CVA
o
Gastrointestinal or genitourinary bleeding with 21 days
o
Recent lum bar puncture
o
Recent arterial puncture at a noncom pressible site
o
Seizure at the tim e stroke was observed
o
Blood-glucose level 400 m g/dL
Treat BP >185/110 m m Hg with nitropaste or 1–2 doses of labetalol, or nicardipine: o
Do not aggressively norm alize BP.
o
Stroke patient m ay be dependant on an elevated m ean arterial pressure for cerebral perfusion.
o
Avoid throm bolytic therapy if BP cannot be reduced with m inim al intervention
Adm inister IV tissue plasm inogen activator (TPA).
Avoid antiplatelet agents and anticoagulants for 24 hours.
Monitor arterial BP during the first 24 hours after treatm ent with TPA and aggressively treat a S BP >180 or a DBP >105: o
Check BP every 15 m inutes for 2 hours, then every 30 m inutes for 6 hours, then every hour for 24 hours.
o
Keep BP 140 m m Hg.
Monitor for signs of ICH:
Pa ge 4 1 0
o
Up to a 6% increased risk with TPA:
Prim arily in patients with a NIH-SS >20
o
Decreased LOC
o
Increased weakness
o
Headache
o
Acute hypertension or tachycardia
o
Nausea or vom iting
If ICH suspected, obtain em ergent head CT to confirm diagnosis:
If present, treat as follows: o
Discontinue TPA.
o
Obtain blood sam ples for PT, PTT, platelet count, fibrinogen level.
o
Prepare cryoprecipitate, fibrinogen and platelets, and infuse as needed.
o
Obtain neurosurgical consultation
Patients who have presented after 3 hours but within 6 hours of sym ptom onset: o
Consider intra-arterial throm bolysis or m echanical recanalization if available.
Medication (Drugs)
Nitropaste: 1–2 inches to anterior chest wall
Labetalol: 10 m g IV over 1–2 m inutes; then, if needed: o
repeat or double dose q10m in–q20m in up to a m ax. of 300 m g, or
o
start a drip at 2–8 m g/m in
Nicardipine: 5 m g/hr as a drip; titrate upwards in 2.5 m g/hr increm ents q5m in, up to a m ax. of 15 m g/hr
Nitroprusside: 0.5–1.0 m g/kg/m inute, continuous IV drip, titrated to BP param eters
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TPA: 0.9 m g/kg IV, m ax. 90 m g: o
Give 10% of dose as a bolus.
o
Followed im m ediately by the rem ainder infused over the subsequent 60 m inutes
Cryoprecipitate and fibrinogen: 6–8 U IV
Platelets: 6–8 U IV
Follow-Up Disposition Admission Criteria All patients given throm bolytic or other reperfusion therapy for a CVA should be adm itted to an intensive care setting for frequent neurological checks and vital sign assessm ents.
Discharge Criteria N/A, see Adm ission Criteria
References 1. Adam s HP, Adam s RJ, Brott T, et al. Guidelines for the early m anagem ent of patients with ischem ic stroke; a scientific statem ent from the Stroke Council of the Am erican Stroke Association. Stroke. 2003;34:1056–1083. 2. Albers GW. Advances in intravenous throm bolytic therapy for treatm ent of acute stroke. Neurology. 2001;57(S2):S77–S81. 3. Furlan A, Higashida R, Wechsler L, et al. Intraarterial pro-urokinase for acute ischem ic stroke (PROACT II). JAMA. 1999;282:2003–2011. 4. Leary M, Saver JL, Gobin PY, et al. Beyond tissue plasm inogen activator: Mechanical intervention in acute stroke. Ann Em erg Med. 2003;41:838–846.
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5. The NINDS rt-PA Stroke Study Group. Tissue plasm inogen activator for acute ischem ic stroke. New Eng J Med. 1995;333:1581–1587.
Codes ICD9-CM ICD-9 for total body throm bolysis: 39.96 ICD-9 for infusion therapy: 99.29 CPT: 907.84
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Respirato ry Distress
Respiratory
Distress Erik D. Barton
Basics Description Respiratory distress, shortness of breath, or dyspnea is a com m on com plaint for patients presenting to the ED.
Etiology
Upper airway obstruction: o
Epiglottitis
o
Croup syndrom es
o
Laryngotracheobronchitis
o
Foreign body
o
Angioedem a
o
Retropharyngeal abscess
Cardiovascular: o
Pulm onary edem a/congestive heart failure (CHF)
o
Dysrhythm ias
o
Cardiac ischem ia
o
Pulm onary em bolus
o
Pericarditis
o
Tam ponade
Pa ge 4 1 0
o
Air em bolism
Pulm onary: o
Asthm a
o
Chronic obstructive pulm onary disease (COPD)/em physem a
o
Pneum onia
o
Bronchiolitis
o
Aspiration
o
Adult respiratory distress syndrom e (ARDS)
o
Pulm onary edem a
o
Pleural effusion
o
Toxic inhalation injury
Traum a: o
Pneum othorax
o
Tension pneum othorax
o
Rib fractures
o
Pulm onary contusion
o
Fat em bolism with long bone fractures
Neurom uscular: o
Guillain-Barré syndrom e
o
Myasthenia gravis
Metabolic/System ic/Toxic
Anaphylaxis
Anem ia
Acidosis
Hyperthyroidism
Sepsis
Septic em boli from IV drug use or infected indwelling lines
Salicylate intoxication
Drug overdose
Am phetam ines
Cocaine
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Sym pathom im etic
Obesity
Psychogenic: o
Anxiety disorder
o
Hyperventilation syndrom e
Pediatric Considerations
Respiratory failure is m ost com m on cause of cardiac arrest in infants.
Croup syndrom es include: o
Viral
o
Spasm odic
o
Bacterial
o
Congenital defects
o
Noninflam m atory causes (foreign body, gastroesophageal reflux, traum a, tum ors)
Most com m on cause of upper airway obstruction: o
Younger than 6 m onths: congenital laryngom alacia
o
Older than 6 m onths: viral croup
Epiglottitis: o
Highest incidence at ages 2–4 years
o
Abrupt onset
o
Fever
o
Respiratory distress and stridor
o
Difficulty swallowing oral secretions
o
Restlessness and anxiety
Pregnancy Considerations
Am niotic fluid em bolism during or after delivery
Septic em bolism from septic abortion or postpartum uterine infection
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Diagnosis Signs and Symptoms
Tachypnea
Dyspnea
Tachycardia
Anxiety
Diaphoresis
Cough (“barking,― productive)
Stridor
Hoarse voice
Difficulty swallowing or handling oral secretions
Upper airway rhonchi (wheezes)
Lower airway crackles (rales)
Increased work of breathing
Accessory and intercostal m uscle use
Hypoxem ia
Hypocapnia or hypercapnia if severe
Respiratory acidosis
Cyanosis
Lethargy, then obtundation
History
Previous history of asthm a, COPD, cardiac disease, or dysrhythm ia, CHF, foreign body aspiration
Recent fever or upper respiratory tract infection, cough, sputum production, sore throat, system ic disease, anxiety disorder
Recent chest or long bone traum a
IV drug use or indwelling catheters
Physical Exam
Observe: m ental status, level of distress, work of
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breathing, jugular venous pressure, skin color
Feel/Palpate: distal pulses, heart perioperative m yocardial infarction, chest wall, peripheral edem a
Percuss: lungs for dullness or resonance, abdom inal distention or hepatom egaly
Auscultate: heart sounds, m urm urs, lung wheezes or crackles, neck for upper airway stridor, abdom en bowel sounds
Pediatric Considerations
Evaluate retractions, behavior, respiratory rate, breath sounds, and skin color.
Weak cry, expiratory grunting, nasal flaring, tachypnea and tachycardia, retractions, and cyanosis in neonates
Essential Workup
Pulse oxim etry
Cardiac and blood pressure (BP) m onitoring
ECG if suspected cardiac etiology
Tests Lab
ABG for severity and acid-base determ ination
CBC
Electrolytes, blood urea nitrogen/creatinine, glucose
Blood, sputum , urine cultures for fever or sepsis
Brain natriuretic peptide for undifferentiated shortness of breath or CHF severity
Urinary output m onitoring for CHF
Toxicology screen or salicylate level if suspected
Imaging
Chest radiograph for: o
Pneum onia
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o
Pneum othorax
o
Hyperinflation
o
Atelectasis
o
CHF/Pulm onary edem a
Spirom etry (peak expiratory flow rates) for asthm a, COPD
Neck radiographs to assess epiglottis and soft tissue spaces, foreign body
Fiberoptic laryngoscopy to assess epiglottis, vocal cords, and pharyngeal space
CT angiography or ventilation/perfusion scan for pulm onary em bolus
Pediatric Considerations
Chest/neck radiograph m ay show foreign body or “steeple sign― in croup syndrom es.
Chest fluoroscopy m ay be used to assess inspiratory and expiratory excursions if foreign body is suspected.
Diagnostic Procedures/Surgery
Bronchoscopy for foreign body in trachea or bronchus
Pulm onary artery (Swan-Ganz) catheter for severe CHF, ARDS, pulm onary edem a
Differential Diagnosis See Etiology P.959
Treatment Pre Hospital
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Assum e a position of com fort for patient
100% oxygen: o
Assisted bag-valve m ask (BMV) ventilation if obtunded
Airway adjunct devices (oral or nasal) to m aintain patency if tolerated
Intubation for severe respiratory distress
Needle aspiration of suspected tension pneum othorax
Initial Stabilization
ABCs
Ensure patent airway; BVM assist or intubate for severe distress or arrest
IV fluids if hypotensive
100% oxygen by face m ask: o
Use cautiously in patients with severe COPD or chronic CO 2 retention.
Monitor BP, heart rate, respirations, pulse oxim etry
Advanced cardiac life support for dysrhythm ias or arrest
ED Treatment
Treat underlying etiology as appropriate.
CHF or pulm onary edem a: o
Diuretics
o
Nitroglycerin
o
Nitroprusside if hypertensive
o
Pulm onary artery catheter if severe
o
Noninvasive positive-pressure ventilation (NPPV) or intubation if severe
Asthm a, bronchiolitis, COPD: o
Bronchodilators
o
Steroids
o
Antibiotics for infection
Pa ge 4 1 1
o
ARDS, aspiration, toxic lung injury: o
Mechanical ventilation as needed
o
Steroids controversial
Pneum onia: o
NPPV or intubation if severe
Antibiotics
Pneum othorax: o
Im m ediate decom pression if suspected tension pneum othorax
o
Aspiration or tube thoracostom y (see Pneum othorax)
Pleural effusion: o
Determ ine etiology
o
Diagnostic and sym ptom atic thoracentesis
Croup: o
Cool, m isted air or oxygen
o
Steroids
o
Racem ic epinephrine
o
Antibiotics for bacterial infection
Epiglottitis: o
Im m ediate airway stabilization with intubation or tracheostom y in operating room if possible
o
Antibiotics for Haem ophilus influenzae
Anaphylaxis, angioedem a: o
IV steroids
o
H 1 /H 2 -blockers
o
SQ or IV epinephrine
o
Early intubation
Retropharyngeal abscess o
Drainage
o
IV antibiotics
o
Ear/Nose/Throat consult
Cardiac:
Pa ge 4 1 1
o
Treat dysrhythm ias or ischem ia
o
Anticoagulation or throm bolysis for PE
o
Pericardiocentesis for tam ponade
o
NSAIDs or aspirin for pericarditis
Neurom uscular: o
Support ventilation
o
Pyridostigm ine brom ide or neostigm ine for m yasthenia gravis
Metabolic/toxic: o
Treat underlying cause
Psychogenic: o
Anxiolytics
Pediatric Considerations
Transtracheal jet ventilation if unable to intubate (cricothyrotom y not recom m ended in children younger than 10 years)
Bronchiolitis: o
Bronchodilators
o
Antivirals for respiratory syncytial virus
o
Antibiotics for infection
Spasm odic croup: o
Very sensitive to m isted air
Bacterial croup (m em branous laryngotracheobronchitis): o
Treat Staphylococcus aureus
Pregnancy Considerations
Supportive oxygen therapy and heparin for PE or am niotic fluid em bolism
IV antibiotics for septic em bolism
Medication (Drugs)
Pa ge 4 1 1
Refer to specific etiologies
Follow-Up Disposition Admission Criteria
Continued supplem ental oxygen requirem ent
Cardiac or hem odynam ic instability: o
Requiring IV therapy or hydration
o
Requiring close airway observation or repeated treatm ents
As required by underlying cause or significant com orbid disease
Discharge Criteria
Correction of underlying disease
Stable airway
Acute supplem ental oxygen not required
Issues for Referral Refer to specific etiologies
References 1. Ausiello D, Goldm an L. Eds. Cecil Textbook of Medicine. 22nd ed., Philadelphia, PA: WB Saunders, 2004:492–583,1523–1524. 2. Sigillito RJ, DeBlieux PM. Evaluation and initial m anagem ent of the patient in respiratory distress. Em erg Med Clin North Am . 2003;21(2):239–258. 3. William s SA, Hutson HR, Speals HL. Dyspnea. In: Em ergency m edicine: Concepts and clinical practice. 4th ed. St. Louis, MO: Mosby, 1998: 1460–1469.
Codes
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ICD9-CM 786.09 Respiratory Distress 770.89 peds Table o f C o ntents > Reye Syndro m e
Reye Syndrome
Brian D. Euerle
Basics Description
Reversible clinicopathologic syndrom e of unknown etiology
Prim ary m itochondrial injury
Decreased enzym e activity:
o
Krebs cycle
o
Gluconeogenesis
o
Urea biosynthesis
Fatty infiltration: o
Liver:
Hyperam m onem ia due to decreased conversion from am m onia to urea
o
Hepatorenal syndrom e m ay be the end result.
Rapid recovery of liver function in survivors
Brain:
Encephalopathy of unclear etiology
Cytotoxic edem a
Deteriorating level of consciousness reflects increasing intracranial pressure.
Herniation is the m ost com m on cause of death.
Norm al recovery of neurologic function in
Pa ge 4 1 5
survivors
o
Skeletal and m yocardial m uscle
o
Fatty infiltration and distorted m itochondria
Fewer than 10% of cases occur before the age of 1 year: o
Average age is 7 years.
o
Peak age is 4–11 years.
Regional differences: o
Highest incidence in the m idwestern states
o
Lower incidence in the states of the southeast and far west
More com m on in whites than in blacks
Peak incidence is in winter and early spring.
Reyelike syndrom e: o
Describes conditions resulting in defects in urea and fatty acid m etabolism , toxicologic injury, and im paired gluconeogenesis
Etiology
Not known with certainty
Multifactorial causes have been epidem iologically im plicated: o
Antecedent viral syndrom e
o
Influenza A or B
o
Varicella
o
Diarrhea illness
o
Genetic predisposition
o
Exposure to salicylates
o
Other undefined factors
Diagnosis
Pa ge 4 1 5
Signs and Symptoms
Usually the patient is afebrile.
Tachycardia
Hyperventilation
History
Biphasic history m arked by an infectious phase (viral illness or prodrom e) followed by an encephalopathic stage
Profuse and repeated vom iting: o
Typically 4–5 days after the start of the viral illness
Marked behavioral changes, including delirium and com bativeness, disorientation, and hallucination
Physical Exam
No focal neurologic signs
Hepatom egaly in 40% of cases
Pancreatitis
Clinical staging of Reye syndrom e with Lovejoy classification: o
Stage 0:
o
o
o
Wakeful
Stage I:
Vom iting
Lethargy
Sleepiness
Stage II:
Disorientation
Delirium
Com bative/stuporous
Hyperventilation
Hyperreflexia
Appropriate response to noxious stim uli
Stage III:
Pa ge 4 1 5
o
Obtunded
Com a
Hyperventilation
Inappropriate response to noxious stim uli
Decorticate posturing
Preservation of pupillary light reflexes
Preservation of oculovestibular light reflexes
Stage IV:
Deeper com a
Decerebrate rigidity
Loss of oculovestibular reflexes
Dilated, fixed pupils
Dysconjugate eye m ovem ents in response to caloric stim ulation
o
Stage V:
Seizures
Absent deep tendon reflexes
Respiratory arrest
Flaccid paralysis
No papillary response
Infants—atypical presentation: o
Tachypnea
o
Apnea
o
Irritability
o
Seizures
o
Hypoglycem ia
Essential Workup
Establish the presence of encephalopathy and liver abnorm alities
Laboratory testing to assess for characteristic biochem ical abnorm alities
Liver biopsy confirm s the diagnosis.
Pa ge 4 1 5
Tests Lab
Liver function tests: o
A threefold or greater rise in AST, ALT
o
Serum am m onia level greater than 1.5–3 tim es norm al:
Transient 24–48 hours after m ental status changes
Level >300 µg/dL associated with poor prognosis
o
Serum bilirubin should be norm al or slightly elevated.
Hypoglycem ia m ay be present, especially in infants.
Elevated blood urea nitrogen
Ketonuria
The prothrom bin tim e m ay be prolonged due to decreased liver-dependent clotting factors (II, VII, IX, X).
Norm al platelet count and blood sm ear
Negative toxicology screen
Imaging
Head CT scan: o
May show diffuse cerebral edem a
Lum bar puncture: o
Perform after head CT
o
Edem a is diffuse and lum bar puncture is not contraindicated.
o
Measure opening pressure.
o
Less than 8 leukocytes/m m 3
Percutaneous liver biopsy: o
Useful in patients with atypical presentation (1 year old, recurrent, fam ilial)
Pa ge 4 1 5
o
Gastroenterology consult
P.969
Differential Diagnosis
Inborn errors of m etabolism : o
Disorders of the urea cycle
o
Disorders of fatty acid oxidation
o
System ic carnitine deficiency
o
Organic acidem ias
o
Disorders of the electron transport chain
Hypoglycem ia
Toxin exposure: o
Toxic encephalopathy without liver dysfunction (Gall syndrom e)
o
Lead
o
Hydrocarbons
Drug intoxication: o
Acetam inophen
o
Salicylates
o
Ethanol
Infection: o
Sepsis
o
Meningitis
o
Encephalitis
o
Varicella hepatitis
Traum a, head
Treatment
Pa ge 4 1 5
Pre Hospital
Decreased m ental status: o
Glucose
o
Narcan
Com a: o
Assist respirations with bag-valve m ask.
Initial Stabilization
Place on a cardiorespiratory m onitor.
Supplem ental oxygen
Rapid-sequence intubation if airway m anagem ent required
Glucose if m ental status is altered: o
10% glucose solution IV
o
Rate of two thirds m aintenance requirem ent after dehydration is corrected.
o
Follow serum glucose hourly; m aintain glucose between 125–175 m g/dL.
Avoid early overhydration.
ED Treatment
Institute treatm ent before the liver biopsy.
Vitam in K: o
Indicated if prothrom bin tim e is elevated.
Fresh-frozen plasm a: o
To control bleeding
o
To correct a severe coagulopathy
Interventions aim ed at lowering intracranial pressure (ICP): o
Stage III or greater
o
Stage II with serum am m onia >300 µg/L:
Intubation using rapid-sequence protocol
Hyperventilation
Fluid restriction
Pa ge 4 1 5
Barbiturate com a
Osm otically active agents:
Mannitol
Furosem ide
Monitor ICP:
Subarachnoid bolt
Intraventricular cannula
Medication (Drugs)
D 5 0 W: 1–2 m L/kg/dose (0.5–1.0 g/kg) IV over the age of 3 years
D 2 5 W: 2–4 m L/kg/dose (0.5–1.0 m g/kg) IV under the age of 3 years; m aintenance infusion 10% dextrose solution at a rate of two-thirds m aintenance
Fresh-frozen plasm a: 10 m L/kg/dose q12h–q24h IV or PRN
Lasix: 1 m g/kg IV
Mannitol: 0.25–1.0 g/kg IV q4h–q6h
Pentobarbital: 3–20 m g/kg IV slowly while m onitoring blood pressure; m aintenance infusion 1–2 m g/kg/h; m aintain level at 25–40 µg/dL
Vitam in K: 1–2 m g/dose (infants and children); 2–10 m g/dose (adolescents)
Follow-Up Disposition Admission Criteria
All children with suspected Reye syndrom e should be
Pa ge 4 1 5
adm itted to the intensive care unit.
Hospital capable of ICP m onitoring
References 1. Arrowsm ith JB, Kennedy DL, Kuritsky JN, Faich GA. National patterns of aspirin use and Reye syndrom e reporting, United States, 1980 to 1985. Pediatrics. 1987;79:858–863. 2. Belay ED, Bresee JS, Holm an RC, et al. Reye's syndrom e in the United States from 1981 through 1997. N Engl J Med. 1999;340:1377–1382. 3. Bhutta AT, Savell VH, Schexnayder SM. Reye's syndrom e: down but not out. South Med J. 2003;96:43–45. 4. Boenning DA. Reye syndrom e. In: Barkin RM, ed. Pediatric em ergency m edicine. 2nd ed. St. Louis, MO: Mosby YearBook,1997:845–847. 5. Chow EL, Cherry JD, Harrison R, et al. Reassessing Reye syndrom e. Arch Pediatr Adolesc Med. 2003;157:1241–1242. 6. Kaufm an RE. Reye's syndrom e and salicylate use, by Karen M. Starko, MD, et al. Pediatrics. 1980;66:859–864. 7. Arrowsm ith, J, et al. National patterns of aspirin use and Reye Syndrom e reporting, United States, 1980 to 1985. Pediatrics. 1987;79:858–863. Pediatrics 1998; 102. 259–62. 8. National Institutes of Health Consensus Conference. Diagnosis and treatm ent of Reye's syndrom e. JAMA. 1981;246:2441–2444. 9. Orlowski JP, Hanhan UA, Fiallos MR. Is aspirin a cause of Reye's syndrom e? A case against. Drug Saf. 2002;25:225–231.
Codes ICD9-CM 331.81
ICD10 G93.7
Pa ge 4 1 5
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Rhabdo m yo lysis
Rhabdomyolysis
Marcelo Sandoval
Basics Description Syndrom e associated with m uscle injury and system ic release of creatine phosphokinase (CPK), m yoglobin, potassium , phosphate, urate com plicated by:
Myoglobin-induced renal failure in 30%
Hyperkalem ia m ay lead to sudden death.
Hypocalcem ia and acidosis also dangerous
Volum e loss due to fluid sequestration in injured or necrotic m uscle
Dehydration due to underlying illness
Com partm ent syndrom e in individual m uscle groups due to traum a and IV hydration fluid sequestration in dam aged tissue
Hepatic dysfunction in 25%
Dissem inated intravascular clot (DIC)
Etiology
Often m ultiple causes in sam e patient
Muscle injury, such as traum a/crush, burn, electrical shock
Muscle exertion: o
Strenuous exercise
Pa ge 4 1 5
o
Marathon running
o
Exercise in hot hum id conditions
o
Exercise by individuals with an inherited m yopathy or with poor physical training
o
Status epilepticus, delirium trem ens
o
Tetanus
o
Psychotic agitation
Muscle ischem ia: o
Extensive throm bosis
o
Multiple em bolism
o
Generalized shock
o
Sickle cell crisis
Surgery: o
Im m obilization
o
Hypotension
o
Ischem ia due to vessel clam ping
Massive blood transfusion
Hypotherm ia, hypertherm ia
Prolonged im m obile state without traum a
Drugs/toxins: o
Alcohols
o
Cocaine, am phetam ines and analogues (m etham phetam ine and ecstasy)
o
Toluene
o
Opiates
o
LSD, PCP
o
Caffeine
o
Carbon m onoxide
o
Snake or bee/hornet venom
o
Hem lock
o
Buffalo fish
o
Tetanus toxin
Pa ge 4 1 6
o
Mushroom poisoning (Tricholom a equestre)
Medications: o
HMG-CoA reductase inhibitors (statin) and other cholesterol-lowering agents
o
Propofol, succinylcholine, halogenated anesthetic gases
o
INH, zidovudine, antim alarials
o
Methylxanthines
o
Colchicine
o
Corticosteroids
o
Itraconazole
o
Erythrom ycin
o
Diuretics
o
Haloperidol, phenothiazines
o
Cyclosporine
o
Antihistam ines
o
Barbiturates
Neuroleptic m alignant syndrom e
Metabolic disorders:
o
Hypokalem ia
o
Hypophosphatem ia
o
Hyper and hyponatrem ia
o
Diabetic ketoacidosis, hyperosm olar state
o
Hypoxia
o
Hyperthyroid state (rare)
o
Pheochrom ocytom a (rare)
Infections: o
Viral:
Coxsackievirus
Herpesviruses
HIV
Influenza B
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Cytom egalovirus, Epstein-Barr virus, adeno/echovirus
o
o
Bacterial:
Legionnaires’ disease
Pyom yositis
Salm onellosis
Shigellosis
Staph, Strep species
Listeria
Tetanus
Toxic shock syndrom e
Tularem ia
Gas gangrene
Bacillus cereus
Parasitic (m alaria falciparum ), protozoan (leptospirosis), rickettsial
Genetic disorders: o
McArdle disease
o
Tarui disease
o
CPT deficiency
o
These inherited m yopathies can exacerbate any other cause.
Im m unologic disorders: derm atom yositis, polym yositis
Idiopathic
Diagnosis Signs and Symptoms History
Can vary dram atically, reflect underlying disease process
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Crush, traum a, exercise, drug/alcohol use, recent surgery, im m obilization, m edications, infections, fever are all com m on and im portant to ask about.
Ask about reddish brown urine and decreased urine output.
Physical Exam
Hypotherm ia/hypertherm ia
Alert/obtunded
Muscle pain (only 50%), tenderness, swelling; diffuse or localized
Neurovascular status of involved m uscle groups if suspect com partm ent syndrom e
Hypovolem ic state, dry m ucous m em brane, poor skin turgor, tachycardia, hypotension
Decreased urine output
Change in urine color
Essential Workup
History and physical are insensitive in m aking the diagnosis.
Serum and urine m yoglobin levels often norm al due to rapid m etabolism and excretion
Serum CPK level is criterion standard and m ust be sent if any clinical suspicion exists.
CPK level not always predictive of renal failure but m ost often associated with level >15,000.
Early ECG to look for signs of severe hyperkalem ia or hypocalcem ia before serum levels available.
Urine dipstick test positive for hem e but absent for RBCs suggests rhabdom yolysis.
Microscopic urinalysis to look for pigm ented tubular casts
Because of rapid urinary excretion of m yoglobin, up to 26% of patients with rhabdom yolysis have negative urine
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dipstick test.
Serum electrolytes (potassium , calcium , m agnesium , phosphorus, bun, creatinine, uric acid, bicarbonate)
Measure com partm ent pressure if com partm ent syndrom e suspected.
Tests Lab In addition to above consider:
ABG
Urine/Serum m yoglobin, but m ay be too transient to be useful
Serum glucose
Liver function tests, including GGTP, LDH, album in
Toxicology screen in absence of physical injury
Prothrom bin tim e/partial throm boplastin tim e, platelet count, fibrinogen, fibrin-split products if DIC is suspected
P.971
Imaging
Renal ultrasound to evaluate for renal failure (sm all shrunken kidneys) or renal obstruction (hydronephrosis)
MRI is 90–95% sensitive in visualizing m uscle injury but does not change initial ED treatm ent.
Differential Diagnosis The following conditions m ay present with elevated serum CPK but m ay not lead to com plications of rhabdom yolysis:
Nontraum atic m yopathies including m uscular dystrophies
Chronic renal failure
Intram uscular injections
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Myocardial injury
Stroke
Treatment Pre Hospital
Need for rapid extrication in case of crush injury
Early IV norm al saline before extrication: o
Prevents com plications of restored blood flow to injured lim b (hypovolem ia, acute renal failure [ARF], hyperkalem ia, etc.)
“Crush injury cocktail― during extrication is 1.5 L 0.9% NS/hr; consider adding 1 am p (40 m eq) bicarbonate and 10 g of m annitol to each liter (controversial).
Initial Stabilization
Airway m anagem ent and resuscitate as indicated
Im m obilization of traum a/crush injuries
IV saline for hypovolem ia at rate of 1 L–1.5 L per hour until volum e restored: o
Restoration of volum e within 6 hours helps prevent renal failure.
Even if the patient is not dehydrated, aggressively hydrate with saline to keep urine flow and protect tubules from dam age due to m yoglobin precipitation.
Avoid furosem ide and other loop diuretics, as they m ay worsen renal failure.
Mannitol supported by anim al studies and retrospective clinical studies, but not prospective
Bicarbonate infusion to alkalinize urine (pH 6.5) also controversial:
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o
A retrospective study suggests use when CPK level >30,000, but not prospectively studied.
ED Treatment
Directed toward treating or reversing the cause of rhabdom yolysis and com plications
Prevent ARF: IV fluid, keep urine output >300 cc/hr with or without m annitol.
Hyperkalem ia: IV fluid, dextrose, insulin, sodium polystyrene sulfonate (Kayexalate), calcium gluconate, hem odialysis, m onitor/ECG
Acidosis: bicarbonate IV (keep urine pH >6.5)
Overdose: activated charcoal, lavage, antidote
Infection: broad-spectrum antibiotics
Com partm ent syndrom e: fasciotom y (com partm ent pressure >35 m m Hg)
Neuroleptic m alignant syndrom e: dantrolene, brom ocriptine
Need for hem odialysis: refractory to treatm ent, hyperkalem ia, hyperphosphatem ia, hyperuricem ia, volum e overload, overdose
Medication (Drugs)
Bicarbonate: 50–100 m L of 8.4% solution IV (peds: 1 m Eq/kg up to 50–100 m Eq); do not continue if urine pH fails to go above 6.5.
Mannitol: 10 g in first liter of one-half isotonic saline; continue only if able to achieve diuresis of >300 cc/hr.
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Follow-Up Disposition Admission Criteria
Because it is im possible to predict which patients will develop com plications, all patients with significant elevated CPK or with sym ptom s suggestive of rhabdom yolysis m ust be adm itted.
Adm it to m onitored bed patients with electrolyte abnorm alities.
Adm it to intensive care unit bed patients who m ight require hem odialysis or closer fluid and electrolyte m onitoring.
Discharge Criteria No patients suspected of having rhabdom yolysis should be discharged from the ED.
References 1. Bhanushali MJ. The evaluation and m anagem ent of patients with neuroleptic m alignant syndrom e. Neurol Clin. 2004;22(2):389–411. 2. Brown CV, Rhee P, Chan L. Preventing renal failure in patients with rhabdom yolysis: do bicarbonate and m annitol m ake a difference? Jrnl of Tr-Inj Inf & Crit Care. 2004;56(6):1191–1196. 3. Cheney P. Early m anagem ent and physiologic changes in crush syndrom e. Crit Care Nurs Q. 1994;17(2):62–73. 4. Gonzalez D. Crush syndrom e. Crit Care Med. January 2005;33(1 Suppl):S34–S41. 5. Pina EM, Mehlm an CT. Rhabdom yolysisa prim er for the orthopaedist. Orthop Rev. 1994;23(1):28–32. 6. Prendergast BD, George CF. Drug-induced rhabdom yolysis m echanism s and m anagem ent Postgrad Med J. 1993;69(811):333–336.
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7. Rosenbaum HK. Malignant hypertherm ia and m yotonic disorders. Anesthesiol Clin North Am erica. 2002;20(3):623–664. 8. Sauret JM, Marinides G, Wang GK. Rhabdom yolysis. Am Fam Physician. 2002;65: 907–912. 9. Sinert R, Kohl L, Rainone T, et al. Exercise-induced rhabdom yolysis. Ann Em erg Med. 1994;23(6):1301–1306. 10. Vanholder Sever, Erek, et al. Rhabdom yolysis. J Am Soc Nephrol. 2000;11(8):1553–1561. 11. Viswswaran, Jayaram a. Rhabdom yolysis. Crit Care Clin. 1999;15(2):415–428. 12. Walsh RJ. Toxic m yopathies. Neurol Clin. 2005;23(2):397–428. 13. Zager RA. Rhabdom yolysis and m yohem oglobinuric acute renal failure [Editorial Review]. Kidney Int. 1996;49(2):314–326.
Codes ICD9-CM 728.89
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Rheum atic F ever
Rheumatic Fever
Jon D. Mason
Basics Description
Constellation of sym ptom s and signs (Jones Criteria)
Follows group A Streptococcal infection (GAS).
Recent resurgence in the western United States
Rem ains a m ajor cause of cardiac m orbidity and m ortality worldwide.
Rheum atic fever (RF) is m ost com m on in the 5- to 15-year age range.
Etiology
GAS infection
Inflam m atory, autoim m une response following GAS infection
Diagnosis Two m ajor or one m ajor and two m inor elem ents of the Jones criteria plus evidence of a recent GAS infection
Signs and Symptoms
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Major Manifestations (Jones Criteria)
Migratory polyarthritis in 60–75% of initial attacks: o
Can involve knees, ankles, elbows, and wrists
o
Lower extrem ities joints m ore com m only involved
o
Rheum atic arthritis generally responds to salicylates.
Carditis occurs in one third of new cases; prednisone used in severe cases: o
Pericardium , m yocardium , and endocardium m ay be affected (pancarditis).
o
Myocarditis m ay lead to heart failure but is frequently asym ptom atic.
o
Valvular disease and endocarditis are m ost serious sequelae of acute renal failure (ARF).
o
Carditis heralded by a new m urm ur, tachycardia, gallop rhythm , pericardial friction rub, or congestive heart failure (CHF)
Chorea occurs in 10% of cases: o
Sydenham chorea predom inantly affects teenage girls.
o
Purposeless, uncoordinated m ovem ents of the extrem ities
o
Movem ents m ore apparent during periods of anxiety and disappear with sleep.
o
Chorea m ay be the sole m anifestation of ARF.
Erythem a m arginatum occurs in 38°C)
o
Arthralgia
Laboratory: o
Elevated acute-phase reactants
o
Prolonged pulse rate interval
Supporting Evidence of Recent GAS Throat Infection
Positive throat culture or rapid antigen test
Elevated or increasing antibody test—antistreptolysin-O (ASO) titer
History Fever, sore throat, joint pains, or unusual m ovem ents of extrem ities
Physical Exam Heart m urm ur consistent with m itral or aortic disease
Tests Lab
Rapid antigen strep test
Throat culture
ASO titer
ECG
CBC
Erythrocyte sedim entation rate or C-reactive protein
Other rheum atic serology tests to rule out other diseases
Imaging
Chest radiograph
Echocardiogram
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Differential Diagnosis
Juvenile rheum atoid arthritis
Infective endocarditis
Reiter syndrom e
System ic lupus erythem atosus
Postgonococcal arthritis
Other infectious causes of arthritis and carditis o
Coxsackie B virus and Parvovirus
P.973
Treatment Initial Stabilization Som e patients in CHF will need airway m anaged.
ED Treatment
Pericardial effusions m ay need drainage.
In severe carditis, start steroids.
In case of severe chorea, start haloperidol.
Penicillin IM, IV, or PO
Nonsteroidal anti-inflam m atory agents
Medication (Drugs)
Aspirin: 4–8 g/d (peds: 100 m g/kg/d) PO q4h–q6h
Digoxin: 0.25–0.5 m g (peds: 0.04 m g/kg) IV
Erythrom ycin: 250 m g (peds: 30–50 m g/kg/d) q6h PO for 10 days
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Furosem ide: 20–80 m g (peds: 1 m g/kg/dose) IV
Haloperidol: 2–10 m g (peds: 0.01–0.03 m g/kg/d) q6h IM or PO
Penicillin (benzathine benzylpenicillin): 1.2 m illion U (peds: 600,000 U for under 27 kg) IM acutely and m onthly thereafter (prophylaxis)
Penicillin VK: 500 m g (peds: 250 m g) PO q8h for 10 days (acute treatm ent)
Prednisone: 1–2 m g/kg/d for 14 days with taper for the next 2 weeks
Follow-Up Disposition Most patients with a new diagnosis should be adm itted for stabilization and further evaluation of the severity of the heart disease.
Admission Criteria
CHF
New diagnosis
Uncontrolled chorea
Uncontrolled pain
Pericardial effusion
Discharge Criteria
Control of pain
Stable cardiovascular status
Issues for Referral All patients need close follow up with their prim ary physician and a cardiologist.
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References 1. Bisno AL et al. Practice guidelines for the diagnosis and m anagem ent of group A streptococcal pharyngitis. (Infectious Disease Society of Am erica.) Clin Infec Dis. 2002;35:113. 2. Kaplan EL. Rheum atic Fever. In: Kasper DL, et al, eds. Harrison's principles of internal m edicine. 16th ed. New York, NY: McGraw Hill, 2005: 1977–1979. 3. Lennon D. Acute rheum atic fever in children: recognition and treatm ent. Pediatr Drugs. 2004;6(6):363–373. 4. Pinals RS. Polyarthritis and fever. N Engl J Med. 1994;330(11):769–774. 5. Stollerm an GH. Rheum atic fever in the 21st century. Clin Infect Dis. 2001;806–814. 6. Tani LY et al. Rheum atic fever in children younger than 5 years: is the presentation different? Pediatrics. 2003;112:1065–1068.
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Rib F racture
Rib Fracture
Gregory W. Lampe
Basics Description
Result of m ajor or m inor thoracic traum a
Can be classified as traum atic or pathologic
Etiology
Blunt thoracic traum a: o
Sim ple fall, fall from height
o
Motor vehicle accident
o
Assault
o
Missile
Penetrating traum a is a less likely cause.
Ribs usually break at the point of im pact or the posterior angle: o
Structurally weakest region
Pathologic fractures associated with m inor traum a or significant underlying disease: o
Coughing or sneezing
o
Advanced age
o
Osteoporosis
o
Neoplasm
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Pediatric Considerations
Relatively elastic chest wall m akes rib fractures less com m on in children.
Consider nonaccidental traum a for infants and toddlers without appropriate m echanism .
Diagnosis Signs and Symptoms History
Blunt thoracic traum a by any m echanism
Mechanism as described by patient, parent or prehospital personnel:
o
Seat belt usage
o
Steering wheel dam age
o
Air bag deploym ent
Localized chest wall pain that increases with deep inspiration, coughing, m oving
Pleuritic chest pain
Dyspnea
Physical Exam
Point tenderness
Pain referred to fracture site with palpation of the involved rib elsewhere
Bony stepoff
Crepitus
Localized edem a
Erythem a
Ecchym osis: o
Ecchym osis from seat belt, a.k.a. “seat belt
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sign― o
Ecchym osis from steering wheel im pact
Intercostal m uscle spasm
Splinting respirations
Hypoxia, tachypnea, respiratory distress
Auscultation shows norm al or dim inished breath sounds.
Essential Workup
Diagnosis is initially m ade on clinical grounds.
Alert
The first three ribs are relatively protected and require significant im pact to fracture, indicating possible intrathoracic injury.
Ribs 9 through 12 are relatively m obile and their fracture suggests possible intraabdom inal injury.
Multiple rib fractures m ay be associated with flail chest and pulm onary contusion.
Tests Lab Arterial blood gas m ay reveal hypoxem ia and elevated alveolar-arterial gradient:
Not indicated for sim ple, uncom plicated rib fractures
May consider in patients with m ultiple rib fractures or preexisting pulm onary disease
Imaging
Chest radiography is indicated to rule out associated intrathoracic injury but m isses up to 50% of rib fractures: o
May reveal associated intrathoracic pathology:
Pneum othorax
Hem othorax
Pneum om ediastinum
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o
Pulm onary contusion
Widened m ediastinal silhouette
Pulm onary contusion appears within 6 to 12 hours after injury:
Ranges from patchy alveolar infiltrates to frank consolidation
Indications for rib radiograph series: o
Suspected fractures of ribs 1 through 3 or 9 through 12
o
Multiple rib fractures
o
Elderly patients with preexisting pulm onary disease or suspected pathologic fractures
CT of the chest m ay be required to rule out intrathoracic injuries.
CT or ultrasound of the abdom en m ay be required to rule out associated intraabdom inal injuries.
Differential Diagnosis
Rib contusion or intercostal m uscle strain
Costochondral separation
Sternal fracture and dislocation
Nontraum atic causes of chest pain: o
o
o
Cardiovascular:
Myocardial ischem ia or infarction
Pericarditis
Aortic dissection
Pulm onary em bolism
Pulm onary:
Infections
Inflam m ation
Barotraum a
Musculoskeletal:
Costochondritis
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o
o
Cervical or thoracic spine disease
Gastrointestinal:
Esophageal reflux or spasm
Mallory-Weiss tear
Biliary or renal colic
Peptic ulcer disease
Gastritis, pancreatitis, hepatitis
Derm atologic:
Herpes zoster
Chest wall tum or
P.975
Treatment Initial Stabilization
For sim ple fractures, generally no significant stabilization is required.
Multiple fractures, elderly patients or significant underlying lung disease: o
Manage airway and resuscitate as indicated.
o
Control airway:
Endotracheal intubation indicated for patients with severe hypoxem ia (PaO 2 Table o f C o ntents > Ring/C o nstricting Band Rem o val
Ring/Constricting Band Removal Carl K. Hsu Bradley Peckler
Basics Description
Prim ary constricting band: A band tightened around an appendage causes swelling and pain (e.g., a hair knotted around a toddler's toe).
Secondary constricting band: Injury or disease process that causes swelling and edem a as a result of tightness against the band (e.g., im pacted ring with an underlying fracture of the finger)
Untreated, the constricting band m ay becom e em bedded and interrupt skin integrity.
Pediatric Considerations In the preverbal child, a constricting band m ay be a m anifestation of child abuse or neglect.
Geriatric Considerations The cognitively im paired nursing hom e resident or Alzheim er patient m ay be unable to give an indication of injury or pain.
Etiology
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Tourniquet syndrom e m ay result from allergic, derm atologic, iatrogenic, endocrinologic, infectious, m alignant, m etabolic, physiologic, or traum atic conditions, or related to pregnancy.
Diagnosis Signs and Symptoms
A constricting band with swollen tissue and skin, m ost com m only a finger
Other locations include wrist, ankle, toe, um bilicus, ear lobe, nipple, septum or nares of nose, penis, scrotum , vagina, labia, uvula or tongue.
Pain on m anipulation of the appendage or constricting band
Essential Workup
Prim ary constricting band: Diagnosis m ade by history and physical exam with special attention to neurovascular status.
Secondary constricting band: Diagnosis of underlying pathology m ay depend on results of im aging and laboratory test results.
Tests Lab
Usually not indicated for acute treatm ent
Measurem ent of electrolytes, blood urea nitrogen, and creatinine; thyroid function tests; and Tzanck sm ear of vesicular lesions m ay be useful in identifying the underlying diagnosis.
Imaging
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Plain film s for evaluation of underlying fracture or foreign body after band rem oval
Differential Diagnosis Any condition causing m arked swelling and edem a predisposing to the tourniquet syndrom e
Treatment Pre Hospital Rem ove rings and other potential constricting bands before developm ent of tourniquet syndrom e:
Particularly in regions of extrem ity traum a
Initial Stabilization Pain m anagem ent or procedural sedation as needed
ED Treatment
Rem oval of the constricting band either by advancing the band distally or by division
The m ost benign m ethods should be attem pted first.
These adjuvant m ethods m ay be used alone or in com bination: o
Elevation of the affected extrem ity m ay decrease vascular congestion.
o
Cooling the extrem ity with ice or cold water m ay reduce edem a and erythem a.
o
Lubrication with soap or m ineral oil m ay allow slippage over an inflam ed or edem atous area.
o
Digital block with 1–2% lidocaine without epinephrine decreases the discom fort of rem oval and m anipulation of an underlying injury.
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o
A digital block m ay, however, increase local swelling.
o
Gauze or a needle holder m ay be used to m anipulate the band.
The distal swollen finger, especially the proxim al interphalangeal, is an im portant obstacle in constricting band rem oval.
Distal to proxim al edem a reduction by sequential com pression: o
Self-adherent tape is wrapped from distal to proxim al to form a sm ooth and decom pressed area over which the band is advanced.
o
A Penrose surgical drain or a finger cut from a sm all glove is stretched to fit over the distal swelling before attem pted rem oval.
o
With lubrication, the proxim al end of the drain is pulled under the ring to form a cuff around the ring; the cuff with distal traction applied advances the band over the decom pressed area.
o
Suture m aterial (no. 0 silk, dental floss, or um bilical tape) is wrapped under tension in a tight layer advancing over the edem a in a distal to proxim al direction; the proxim al tail of the suture m aterial or floss is tucked under the ring; with lubrication, the tail under tension is pulled distally and unwound, forcing the ring over the layered suture m aterial and decom pressed area.
P.977
Constricting band rem oval by division: o
Scissors m ay be used to first lift and then cut the offending fibrous band constricting a toddler's toe or
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penis. o
A no. 11 scalpel blade with cutting edge up m ay be sufficient to cut constricting bands form ed by hair, fibers, or plastic ties.
o
A topical com m ercially available depilatory agent m ay be used to divide a tourniquet form ed by a suspected hair obscured by local edem a.
o
A handheld wire cutter/stripper m ay divide sm all-girth m etallic rings with m inim um discom fort to the underlying injury; this type of rem oval m ay, however, im part a crush defect to the ring, m aking repair difficult.
o
A long-handled bolt cutter, available in m ost operating room s or hospital engineering departm ents, m ay be used to divide large-girth or broad-sized rings:
Long handles provide significant m echanical advantage needed to cut large rings.
The reinforced cutting blades m ay not easily fit through a constricting band with adjacent swollen tissue and skin.
o
A standard hand-powered, m edically approved ring cutter (Steinm ann pin cutter with a MacDonald elevator) m ay be used to divide sm all-girth m etallic constricting bands m ade of soft m etals (gold/silver):
This m ethod has the advantage of a cleaner cut for subsequent repair of the ring.
The disadvantage is that the handheld ring cutter is labor intensive and m ay aggravate the pain of an underlying injury.
o
A m otorized high-revolution-per-m inute cutting device m ay be used to rapidly divide constricting
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bands irrespective of girth and size of the ring; it m ay be AC powered or pneum atically driven in the operating suite.
Cutting procedure: o
The initial cut is m ade on the band on the volar aspect of the extrem ity.
o
A tenaculum m ay be used to spread the band in softer m etals.
o
For a second cut, the band should be rotated 180°on the extrem ity, allowing the second cut on the band over the volar aspect of the extrem ity.
Motorized cutting: o
Rem ove flam m able solvents from the work area.
o
Protective eyewear should be worn by everyone present, including the patient.
o
Place a thin alum inum splint (shaped to the curvature of the ring) between the patient's skin and the ring as a shield to protect underlying tissue.
o
Cool splint and cutting surface with ice water irrigations before and during the cutting procedure.
o
Lim it cutting with m otorized device to 5 seconds during 60–90 second intervals between ice water irrigations to avoid producing local excessive heat.
Postdivision care: o
Underlying injuries should be irrigated thoroughly to rem ove m etallic dust to avoid foreign body reaction and granulom a form ation.
o
Tetanus prophylaxis should be provided if indicated.
Follow-Up
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Disposition Admission Criteria
Neurovascular com prom ise or injury requiring surgical repair
Concom itant infection or necrosis
Discharge Criteria Successful band rem oval with restoration of circulation
References 1. Cresap CR. Rem oval of a hardened steel ring from an extrem ity swollen finger. Am J Em erg Med. 1995;13:318–320. 2. Fasano FJ Jr, Hansen RH. Foreign body granulom a and synovitis of the finger: a hazard of ring rem oval by the sawing technique. J Hand Surg. 1987;12:621–623. 3. Hsu CK, Neblett M, Mansur M and Mok S. Hair tourniquet syndrom e: division by a topical depilatory agent. Unpublished data. 4. Krishna S, Paul RI. Hair tourniquet of the uvula. J Em erg Med. 2003;24(3):325–326. 5. Peckler B, Hsu CK. Tourniquet syndrom e: a review of constricting band rem oval. J Em erg Med. 2001;20(3):253–262. 6. Roberts JR, Hedges JR. Clinical Procedures in Em ergency Medicine. 3rd ed. Philadelphia, PA: WB Saunders; 1997. 7. Rosen P, Chan TC, Vilke GM, et al. Atlas of Em ergency Procedures. St. Louis, MO: Mosby; 2001.
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Ro cky M o untain Spo tted F ever
Rocky
Mountain Spotted Fever Moses S. Lee
Basics Description Rickettsial invasion of sm all blood vessels:
Causes direct vascular dam age
Superim posed vascular dam age owing to im m unologic phenom ena
Etiology Acute infection by Rickettsia rickettsii via tick vector:
Derm acentor andersoni (wood tick) in the western states
Derm acentor variabilis (dog tick) in the eastern states
Diagnosis Signs and Symptoms
Fever in nearly all cases
Tick bite reported within 14 days of rash in 60–70%
Rash: o
Initial rash (3–5 days)
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o
Macular, red, and flat
Blanches under pressure
1–4 m m diam eter
In hours to days:
o
o
Becom es darker, papular, dusky, and palpable
In 2–3 days:
Petechial or purpuric
Positive Rum pel-Leede test
May coalesce or ulcerate
In severe disease, necrosis of dependent peripheral parts m ay occur.
o
Location:
Begins in flexor surfaces of wrist and ankles
Spreads centripetally
Fifteen percent with centrifugal spread to palm s and soles
Triad of fever, headache, and rash in 50%: o
Often not identified when patient initially presents for care
Pulm onary: o
Nonproductive cough
o
Chest pain
o
Dyspnea
o
Rales
Gastrointestinal: o
Associated with fatal Rocky Mountain spotted fever
o
Secondary to vasculitis
o
Nausea/vom iting
o
Abdom inal pain/distention
o
Ileus
o
Hepatosplenom egaly
Neurologic:
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o
Focal or generalized neurologic m anifestation in two thirds
o
Meningism us
o
Severe, unrem itting headache
o
Encephalitis
Other: o
Generalized edem a
o
Dehydration
o
Malaise
o
Myalgia
o
Retinal hem orrhage and conjunctivitis
Com plications: o
Dissem inated intravascular coagulation (DIC)
o
Noncardiogenic pulm onary edem a
o
Acute renal failure
o
Severe or fatal in advanced age, m ale sex, African Am erican, chronic alcohol abuse, G6PD deficiency
Essential Workup Clinical diagnosis
Tests Lab
Serology: o
Diagnose by single titer >1:64 or fourfold increase
o
Methods:
Im m unofluorescent antibody
Com plem ent fixation
Indirect hem agglutination test
Indirect im m unofluorescence assay (IFA) is reference standard.
CBC: o
Norm al WBC count
Pa ge 4 1 9
o
Throm bocytopenia
o
Anem ia
Electrolytes, BUN/creatinine, glucose: o
Hyponatrem ia Table o f C o ntents > Ro seo la
Roseola
Moses S. Lee
Basics Description
Incubation period of 5–15 days
Mode of acquisition unknown: o
Horizontal spread by oral shedding suggested
o
It is spread person to person, but not very contagious.
Pathophysiology: o
Com plex im m une response (cytokines, antibody responses, T-cell reactivity)
Etiology
Exanthem subitum
Hum an herpesvirus 6 (HHV-6):
o
Large, double-stranded DNA
o
Closely related to hum an cytom egalovirus
Peak incidence at 6–12 m onths; 90% occurrence within first year
Highest incidence in late spring and early sum m er
Pa ge 4 1 9
Diagnosis Signs and Symptoms
Sudden, high fever 39.4–41.2°C (103–106°F)
Febrile seizures in 5–35%
Absence of physical findings: o
Child looks well
Tem perature norm alizes in 3–4 days
Maculopapular eruption from trunk to arm s and neck after tem perature norm alization: o
Rash fades within 3 days.
Enlarged lym ph nodes
Diarrhea
Irritability
Erythem atous papules in pharynx (Nakayam a spots)
Rarely causes severe or fatal dissem inating diseases: o
Infectious m ononucleosis syndrom e of hepatitis
Reactivation in im m unocom prom ised individuals
Pediatric Considerations
Most newborns are seropositive for HHV-6 owing to transplacental antibodies.
By age 1–2 years, >90% of infants seropositive
Essential Workup Clinical diagnosis:
High fever in well-appearing child
Tests Lab
CBC: o
Initial increase in WBC, then norm alization with lym phocytosis
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HHV-6 DNA: o
Detected by polym erase chain reaction (PCR)
o
Available at research level
IgM appears early and declines as IgG is produced.
P.981
Differential Diagnosis Fever of unknown origin
Scarlet fever: o
“Sandpaper― rash, Pastia lines, and strawberry tongue
Measles (rubeola): o
Rocky Mountain spotted fever: o
Koplik spots, cough, coryza, conjunctivitis, and fever
Rash begins at ankles and wrists.
Rubella: o
Fever after rash
Fifth disease (erythem a infectiosum )
Dengue fever
Pneum ococcal bacterem ia
Meningitis
Treatment Initial Stabilization Airway, breathing, and circulation m anagem ent (ABCs)
ED Treatment
Supportive
Antipyretics:
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o
Acetam inophen
o
Ibuprofen
Medication (Drugs)
Acetam inophen: 650 m g (peds: 15 m g/kg) PO q4h
Ibuprofen: 200–600 m g (peds: 5–10 m g/kg; suspension 100 m g/5 m L; oral drops 40 m g/m L) PO q6h
Follow-Up Disposition Admission Criteria Fever in child who is toxic and does not respond to initial supportive care
Discharge Criteria Usually, all patients m ay be discharged.
References 1. Asano Y, Yoshikawa T, Suga S, et al. Clinical features of infants with prim ary hum an herpesvirus 6 infection (exanthem subitum , roseola infantum ). Pediatrics. 1994;93:104–108. 2. Hall CB, Long CE, Schnabel KC, et al. Hum an herpesvirus-6 infection in children: a prospective study of com plications and reactivation. N Engl J Med. 1994;331:482–438. 3. Nelson WE, ed. Textbook of Pediatrics. Philadelphia: WB Saunders; 1996:890–892. 4. Stoeckle MY. The spectrum of hum an herpesvirus 6 infection: from roseola infantum to adult disease. Annu Rev Med. 2000;51:423–430.
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Codes ICD9-CM 57.8
ICD10 B09
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Rubella
Rubella
Moses S. Lee
Basics Description
Transm ission via droplets from respiratory secretions
Moderately contagious: o
Especially during rash eruption and infants with congenital rubella syndrom e (CRS)
Up to 50% m ay be subclinical.
Infants with congenital rubella shed large quantities of virus for several m onths.
Infectious period 7 days before to 5 days after appearance of rash
Incubation period: 14–21 days
Etiology
Also known as Germ an m easles or 3-day m easles
Rubella virus (fam ily: Togaviridae, genus: Rubivirus)
Live, attenuated virus vaccine indications: o
All children older than 12 m onths and entering school
o
All wom en of childbearing age
Pa ge 4 2 0
Diagnosis Signs and Symptoms
Acute viral disease
Low-grade fever
Malaise
Headache
Upper respiratory tract sym ptom s
Rash: o
Rash is fainter than m easles rash and does not coalesce.
o
Red m acular rash evolving to pink-red m aculopapules with occasional pruritus
o
Begins in face with rapid caudal spread
o
Com pleted in first day and disappears in 3 days
o
May have hem orrhagic m anifestations
Lym phadenopathy: o
Postauricular
o
Occipital
o
Posterior cervical
Com plications: o
Uncom m on, tend to occur m ore in adults
o
Congenital rubella syndrom e (CRS)—infected wom en in first trim ester
o
o
Arthritis:
More com m on in wom en (up to 79%)
Chronic arthritis is rare.
Begins after 2–3 days of illness
Knees, wrists, fingers affected
Hem orrhagic m anifestations:
Secondary to throm bocytopenia
More com m on in children
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o
Neurologic sequelae:
Encephalitis m ost com m on in adults
Essential Workup Clinical diagnosis
Tests Lab
CBC: o
Decreased WBC, platelets (m ore com m on in children)
Urinalysis (UA): o
Hem aturia
Reverse transcriptase polym erase chain reaction (PCR)
Enzym e-linked im m unosorbent assay (ELISA) to detect rubella IgM
Rubella antibody titer: o
Acute and convalescent serum specim ens
o
Hem agglutination-inhibition test m ost com m on
o
Definitive diagnosis in acute infection
o
Com pare infant with m aternal sera for CRS.
o
False positives in parvovirus, infectious m ononucleosis, rheum atoid factor
Pharynx: o
Virus m ay be isolated from pharynx 1 week before and until 2 weeks after rash onset (valuable epidem iologic tool).
Cerebrospinal fluid (CSF): o
Few WBCs (m onocytes) in encephalitis
Differential Diagnosis
Scarlet fever: o
“Sandpaper― rash, Pastia lines, and strawberry tongue
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Measles (rubeola): o
Roseola infantum : o
Spring and fall
Rocky Mountain spotted fever: o
Koplik spots, cough, coryza, conjunctivitis, and fever
Rash begins at ankles and wrists.
Rheum atoid arthritis
P.983
Treatment Pre Hospital Use N95 filter m ask for potential respiratory transm ission.
Initial Stabilization Airway, breathing, and circulation m anagem ent (ABCs)
ED Treatment
Sym ptom atic therapy
Antipyretics and antiinflam m atory agents:
o
Acetam inophen
o
Ibuprofen
Isolate rubella patients from susceptible persons (e.g., pregnancy).
Vaccine: o
Measles-m um ps-rubella (MMR) vaccine
o
Rubella vaccine is live attenuated virus.
o
Indications:
Older than 12 m onths and entry to school
Susceptible postpubertal fem ales
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High-risk groups (colleges, m ilitary, places of em ploym ent)
Unim m unized contacts
Health care workers and wom en of childbearing age born before 1957
o
Contraindicated in pregnant wom en
o
Avoid pregnancy for 3 m onths after vaccination.
o
One dose confers probable lifelong protection.
o
Com m on com plaints are fever, lym phadenopathy, and arthralgia.
Im m une globulin: o
Will not prevent virem ia, but m ay m odify sym ptom s
Medication (Drugs)
Acetam inophen: 650 m g (peds: 15 m g/kg) PO q4h
Ibuprofen: 200–600 m g (peds: 5–10 m g/kg; suspension 100 m g/5 m L; oral drops 40 m g/m L) PO q6h
Im m une globulin: 0.5 m L reconstituted vial SC (0.25–0.50 m L/kg)
Follow-Up Disposition Admission Criteria
Congenital rubella syndrom e
Encephalitis
Discharge Criteria
Most patients m ay go hom e.
Inquire regarding vaccination status of fam ily m em bers.
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References 1. Banatvala JE, Brown DW. Rubella. Lancet. 2004;363:1127–1137. 2. Centers for Disease Control. Rubella and congenital rubella United States, 1984–1986. MMWR Morb Mortal Wkly Rep 1987(b);36:664–675. Available at http://www.cdc.gov/nip/publications/pink/rubella.pdf. 3. Maldonado Y. Rubella virus (Germ an or three-day m easles). In: Behrm an RE, Kliegm an R, Jensen HB, eds. Nelson Textbook of Pediatrics. 16th ed. Philadelphia: WB Saunders; 2000:951–953. 4. Reef SE, Frey TK, Theall K, et al. The changing epidem iology of rubella in the 1990s. JAMA. 2002;287:464–472.
Codes ICD9-CM 56.9
ICD10 B06.9
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Sacral F racture
Sacral Fracture
Jaime B. Rivas
Basics Description
Sacral fractures are rarely isolated injuries (80–100 m g/dL in acute ingestion.
Lower threshold to dialyze patients with chronic overdose
Medication (Drugs)
Activated charcoal slurry: 1–2 g/kg up to 90 g PO
Dextrose: D 5 0 W 1 am p (50 m L or 25 g) (peds: D 2 5 W 2–4 m L/kg) IV
Naloxone (Narcan): 2 m g (peds: 0.1 m g/kg) IV or IM initial dose
Sorbitol: 1–2 g/kg to m ax. 100 g (peds: >1 year old: 1–1.5 g/kg as 35% solution to m ax. 50 g) PO m ixed in
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activated charcoal slurry—use only with first dose
Thiam ine (vitam in B 1 ): 100 m g (peds: 50 m g) IV or IM
Follow-Up Disposition Admission Criteria
Monitor patients with salicylate levels >25 m g/dL until level drops below 25 m g/dL and sym ptom s abate.
ICU adm ission for altered m ental status, m etabolic acidosis, pulm onary edem a
Discharge Criteria Salicylate level Table o f C o ntents > Scabies
Scabies
James Hwang
Basics Description
Mites m ate on skin surface and gravid fem ale burrows into strateum corneum to lay eggs: o
Anim al scabies burrow but cannot reproduce.
Sym ptom s result from delayed type IV hypersensitivity reaction to m ite, eggs, saliva, and feces: o
Inflam m atory reaction is responsible for intense pruritus, which is the hallm ark of the disease.
o
Norwegian scabies (crusted scabies) is an atypical, highly contagious form of severe scabies:
Seen in disabled, im m unocom prom ised, and institutionalized patients
General Prevention Despite m ore than 2,500 years existence, an effective way to prevent scabies is still not known.
Epidemiology Over the past two decades, the num ber of patients with scabies is increasing.
Etiology
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Produced by the hum an scabies m ite, Sarcoptes scabiei var. hom inis, or from anim al m ites
It is transm itted by direct skin-to-skin contact or, less frequently, by infected bedding or clothing.
Mites subsist on a diet of dissolved hum an tissue (do not feed on blood) and can live up to 4 days off a host's body.
On average, the num ber of m ites on a host at any tim e is approxim ately 10–15: o
Main difference between Norwegian scabies and regular scabies is the num ber of m ites present on the host—patients with Norwegian scabies are infected with thousands of m ites.
Diagnosis Signs and Symptoms History
Generalized, intensely pruritic eruption: o
Pruritus is intensified at night.
Onset 10–30 days after exposure and infestation; re-infestation provokes im m ediate (within 1–4 days) pruritus: o
Patients with Norwegian scabies are usually im m unocom prom ised, have a decreased inflam m atory response, and have less pruritus.
Physical Exam Often m inim al cutaneous findings:
Prim ary lesion: linear, elevated, white-gray burrow (up to 1-cm long, width of a hum an hair) with sm all vesicle containing black dot at the end (m ites barely visible to
Pa ge 4 2 2
naked eye)
Found sym m etrically in web spaces of fingers, flexor surfaces of wrists and elbows, waistline, axillary folds, penis, scrotum , vulva, and areola
Head and neck rarely affected in adults but m ore com m only in infants and children
Secondary lesions: crusted papules, nodules, excoriations, and secondary im petigo or folliculitis seen on back, shoulders, axilla, waist, buttocks, and flexor aspects of elbows
Secondary lesions usually m ore num erous and prom inent than burrows but also m ay be few if topical steroids used o
Norwegian scabies produce gross scaling with hyperkeratotic plaques on hands, feet, scalp, and pressure-bearing areas.
Pediatric Considerations
Eruption m ay be seen from head to toe.
Distribution typically involves the proxim al half of the foot and heel.
Neonatal scabies is associated with poor feeding, poor weight gain, and frequent super infection.
Essential Workup
Careful history and skin exam for characteristic lesions
The diagnosis is easily m issed and should be considered in any patient with persistent generalized pruritus.
Tests Lab May be indicated in im m unocom prom ised patients or in patients with system ic infection
Diagnostic Procedures/Surgery
Pa ge 4 2 2
Scrape skin with no. 15 blade and m ineral oil (adheres scraped m aterial to blade) and observe under low-power m icroscope for m ites, eggs, or fecal m aterial.
A negative scraping does not exclude infestation.
Differential Diagnosis
Atopic derm atitis, derm atitis herpetiform is, papular urticaria folliculitis, lichen planus
Pruritic urticarial papules and plaques of pregnancy
Adult linear IgA bullous derm atosis
Syphilis, pediculosis, pityriasis rosea, im petigo, seborrheic derm atitis, and lym phom a
Treatment Pre Hospital Maintain universal precautions.
Initial Stabilization No specific stabilization necessary in routine cases
ED Treatment
Treat patient and all persons in im m ediate contact with topical scabicide.
Perm ethrin is 89–92% effective and is best tolerated.
Less than 2% of perm ethrin is absorbed into the skin, m aking its potential toxicity low. P.991
Crotam iton is 50–60% effective and used when other scabicides are not tolerated.
Pa ge 4 2 3
Iverm ectin has shown excellent results, particularly with resistant or crusted scabies, though is not yet FDA approved for oral use.
Lindane is slightly less effective and is potentially toxic to the CNS: o
Lindanes absorption is about 10%, with side effects of seizure, nausea, headache, vertigo, am blyopia, and irritability.
o
Don't use in pediatric patients.
o
Its use is prohibited in states such as California.
Sulfur is the oldest known treatm ent of scabies and is the drug of choice for infants younger than 2 m onths and for pregnant or lactating wom en.
Crusted scabies first require rem oval of hyperkeratotic scale with 6% salicyclic acid in petroleum jelly to facilitate entry of scabicide.
Treatm ent failures: o
Treatm ent failures are frequent in Norwegian scabies, and use of several agents including oral m edications is often necessary.
o
Machine wash and dry in hot cycles (60°C) or dry clean all clothes and bedding worn within 2 days of treatm ent; vacuum household floors, carpets, m attresses, and furniture.
o
Em phasize that itching m ay continue for 1 to 4 weeks after m ites are killed due to skin inflam m atory reaction.
o
Topical steroids and oral antihistam ines reduce pruritic sym ptom s.
o
Relapses can occur from untreated areas such as the scalp and subungal regions.
o
Re-evaluate after 2 weeks for recurrence; retreat if
Pa ge 4 2 3
live m ites found. o
Treatm ent failures tend to arise from poor patient understanding.
Medication (Drugs) Scabicides
Crotam iton 10% lotion or cream : Apply topically from neck down in adults and entire skin surface in children qhs for 2 nights, then rinse off 48 hours after last application.
Iverm ectin 3 m g tablets: Single oral dose of 200 m cg/kg provides antiscabietic activity for 6 weeks (pregnancy category C).
Lindane 1% lotion or cream : Apply topically from neck down and rinse off after 8–12 hours; contra-indicated in infants, pregnancy, lactation, excessive excoriations, or seizure disorder.
Perm ethrin 5% cream (Elim ite): Apply topically from neck down in adults and entire skin in children qhs, rinse off after 8–14 hours (pregnancy class B, unknown safety in breastfeeding): o
Sulfur 5% or 10% precipitated in petrolatum : Apply topically nightly for 3 consecutive nights and wash off 24 hours later.
Antipruritics Low Sedating/Selective Antihistamines:
Certirizine (Zyrtec): adults and peds >6 years old: 5–10 m g PO per day; 6–12 m onths: 2.5 m g PO per day; 12–24 m onths: 2.5 m g PO per day to b.i.d.; 2–6 years old: 2.5–5 m g PO per day
Pa ge 4 2 3
Fexofenadine (Allegra): adult and peds >12 years old: 180 m g PO per day or 60 m g PO b.i.d.; 6 m onths to 5 years old: 15–30 m g PO b.i.d.; 6–11 years old: 30 m g PO b.i.d. o
Loratadine (Claritin): adults and peds >6 years old: 10 m g PO per day; 2–5 years old: 5 m g PO per day
Sedating/Nonselective Antihistamines:
Diphenhydram ine (Benadryl): adults and peds >12 years old: 25–50 m g PO q4h–q6h; 2–6 years old: 6.25 m g PO q4h–q6h; 6–12 years old: 12.5–25 m g PO q4h–q6h
Doxepin: 25–50 m g PO b.i.d., peds: dosing currently unavailable
Hydroxyzine HCl (Atarax): adults and peds >12 years old: 25–100 m g PO q6h–q8h; Table o f C o ntents > Schiz o phrenia
Schizophrenia
Joshua L. Roffman Donald C. Goff
Basics Description
A chronic psychotic disorder characterized by delusions, hallucinations, disorganization, and negative sym ptom s
Onset typically early in adulthood
Com orbid substance abuse (alcohol and stim ulants) is com m on.
Approxim ately 10–15% of patients com m it suicide.
Violence m ay result from im paired judgm ent, paranoia, and com m and hallucinations.
Patients with schizophrenia can have abnorm ally high pain thresholds that can com plicate the detection of m edical illness.
Prem orbid phase: o
Developm ent of negative sym ptom s with deterioration of personal, social, and intellectual functioning
Active phase: o
Precipitated by a stressful event
o
Developm ent of active delusions, hallucinations, and
Pa ge 4 2 4
bizarre behavior
Residual phase: o
Patients are left with im paired social and cognitive ability.
Etiology
Genetic com ponent (concordance rate of 50% in m onozygotic twins)
Specific genes rem ain uncertain.
Stressors during pregnancy m ay increase risk.
Influenza during second trim ester
Birth com plications
Diagnosis Signs and Symptoms The Diagnostic and Statistical Manual of Mental Disorders (DSM) criteria require the presence of at least two of the following sym ptom s for m ore than 6 m onths:
Delusions (fixed, false beliefs) o
Bizarre, paranoid, or grandiose:
o
Often involve the conviction that others are tam pering with one's m ind or body
Hallucinations: o
Typically hearing voices
o
May involve any sensory m odality
Thought disorder: o
Disorganized speech ranging from odd, idiosyncratic logic to incoherence
Grossly disorganized or catatonic behavior
Negative sym ptom s
Pa ge 4 2 4
o
Apathy
o
Flat affect
o
Social isolation
o
Anhedonia
Essential Workup
Obtain history from additional sources: o
Friends or fam ily
o
Assists in establishing the diagnosis
Evaluate potential dangerousness to self or others: o
The content of delusions and the nature of auditory hallucinations should be explored to assess safety.
Medical and neurologic screening o
Assessm ent for drug-induced psychosis (see Psychosis, Medical vs. Psychiatric)
o
Evaluate for acute delirium :
Schizophrenia does not affect orientation or m em ory.
Tests Lab
Toxicology screen
Electrolytes, blood urea nitrogen, creatinine, glucose, calcium
Thyroid panel (see Psychosis, Medical vs. Psychiatric)
Imaging Head im aging only with suspicion of neurologic etiology
Differential Diagnosis
Delirium
Drug-induced psychosis
Huntington disease
Tem poral lobe epilepsy
Pa ge 4 2 4
Bipolar (m anic depressive) disorder
Psychotic depression
Delusional disorder
Schizotypal personality:
Brief psychotic episode o
Sim ilar sym ptom s that occur with duration of less than 1 m onth
Schizophreniform disorder: o
Sim ilar sym ptom s that occur with duration between 1 and 6 m onths
P.995
Treatment Pre Hospital
Pre hospital personnel m ust protect them selves from harm .
Patients can display unpredictable and violent behavior toward them selves and others.
Patients m ay require restraints to protect them selves or em ergency m edical services crew.
Know local laws as they apply to involuntary restraint.
Initial Stabilization
Safety of health care workers and patient is param ount.
Patient m ay require a quiet room .
Presence of security staff
Physical or chem ical restraints as appropriate
Agitation m ay be treated with a high-potency antipsychotic
Pa ge 4 2 4
and benzodiazepine: o
Haloperidol com bined with lorazepam is synergistic.
o
Ziprasidone and olanzapine m ay be adm inistered IM for agitation.
Negative sym ptom s tend to be less responsive to pharm acotherapy than psychotic sym ptom s.
ED Treatment
Psychiatric consultation after m edical evaluation is com pleted
High-potency conventional antipsychotic agents (haloperidol, fluphenazine): o
Minim al cardiovascular effects (droperidol and thioridazine affect QT interval)
o
Oral and IM adm inistration can produce extrapyram idal sym ptom s:
o
Dystonia
Parkinsonism
Akathisia (restlessness of lower extrem ities)
IV haloperidol associated with fewer extrapyram idal sym ptom s
Low-potency conventional agents (chlorprom azine, thioridazine):
o
Fewer extrapyram idal sym ptom s
o
More sedating
o
Orthostatic hypotension
o
Anticholinergic side effects
Atypical antipsychotic agents (risperidone, olanzapine, quetiapine, ziprasidone, aripiprazole): o
Better tolerated with fewer extrapyram idal sym ptom s
o
Risperidone and quetiapine can cause orthostatic hypotension
Pa ge 4 2 4
o
Ziprasidone delays cardiac repolarization (QT interval)
o
Clozapine is the only agent that is clearly m ore effective for psychotic sym ptom s:
Requires weekly m onitoring of WBC due to agranulocytosis
Highly sedating, anticholinergic, hypotensive
Risperidone Consta, haloperidol decanoate, and fluphenazine decanoate are long-acting depot preparations.
If a conventional antipsychotic agent is adm inistered, patients younger than age 40 should be started on benztropine (Cogentin) 2 m g b.i.d. for 10 days to reduce the risk of dystonic reactions.
Medication (Drugs)
Aripiprazole (Abilify): 5–30 m g/d
Olanzapine (Zyprexa): 10–30 m g/d
Risperidoxe (Risperdal): 4–8 m g/d
Thioridazine (Mellaril): 50–800 m g/d
Chlorprom azine (Thorazine): 300–800 m g/d
Clozapine (Clozaril): 200–900 m g/d
Fluphenazine (Prolixin): 5–20 m g/d
Haloperidol (Haldol): 5–20 m g/d, acute agitation; 5–20 m g IV/IM repeat q30m in–q60m in
Lorazepam (Ativan): acute agitation; 2–4 m g IV/IM repeat q30m in–q60m in
Olanzapine (Zyprexa): 10–20 m g/d
Quetiapine (Seroquel): 250–750 m g/d
Risperidone (Risperdal): 4–12 m g/d
Thioridazine (Mellaril): 5–30 m g/d
Pa ge 4 2 4
Ziprasidone (Geodon): 80–160 m g/d
Follow-Up Disposition Admission Criteria
Adm it if patient is a danger to self or others or is gravely disabled.
Criteria for involuntary hospitalization vary by state.
Patients with new-onset psychosis should also be adm itted for evaluation and stabilization.
Discharge Criteria
Patients not a danger to self or others and able to perform activities of daily living
Psychiatric follow-up is arranged.
Psychotic sym ptom s m ay persist at tim e of discharge.
References 1. Goff D. A 23 year old m an with schizophrenia. JAMA. 2002;287:3249–3257. 2. Goff D, Heckers S, Freudenreich O. Schizophrenia. In: Nemeroff C, ed. Med Clin North Am . 2001;85:663–689.
Miscellaneous SEE ALSO: Psychosis, Acute
Codes ICD9-CM 295.90
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ICD10 F20
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Sciatica/Herniated Disc
Sciatica/Herniated Disc Ruth Granlund
Basics Description Pain that radiates from the back into buttocks and lower extrem ity distal to knee, with or without sensory or m otor deficits:
95% sensitive, 88% specific for herniated disc (HD)
Peaks fourth to fifth decade
2–10% of low back pain
95% L5 or S1 nerve root
50–80% im prove with conservative m anagem ent
5–10% require surgery
Etiology
Protrusion of colloidal gel (nucleus pulposus) through weakened surrounding fibrous capsule (annulus fibrosis)
Risk factors: o
Sm oking
o
Repetitive lifting/twisting
o
Vehicular/m achinery vibration
o
Obesity
o
Sedentary lifestyle
Pa ge 4 2 4
Diagnosis Signs and Symptoms History
Low back pain precedes onset of leg pain
Leg pain predom inates with tim e
Sharp, well localized, radiates distal to knee
Exacerbated by activities that increase intradiscal pressure:
o
Valsalva m aneuver
o
Cough
o
Nerve-root tension (sitting, straight leg raise)
Relieved by decreasing pressure/tension: o
Lying supine
o
Walking
Physical Exam
Neurologic exam (m otor; sensory; DTRs) o
o
o
L4 root/L3-4 disc:
Knee extension/hip adduction
Anterom edial leg/knee/m edial m alleolus
Patella reflex
L5 root/L4-5 disc:
Great toe and foot dorsiflexion
Dorsom edial foot/first web space
No reflex
S1 root/L5-S1 disc:
Foot plantarflexion
Posterior leg/lateral m alleolus/dorsolateral foot
Achilles reflex
Rectal exam (tone, sensation)
Pa ge 4 2 4
Straight leg raise: o
Elevate ipsilateral leg by heel 30–60 degrees with or without dorsiflex foot.
o
Reproduces radicular pain past knee
o
80% sensitive for HD
Crossed straight leg raise test (pathognom onic): o
Elevate contralateral leg
o
Pain in involved leg
o
Less sensitive but very specific for HD
Essential Workup
Com plete history and physical exam
See below for test indications.
Tests Lab Indicated if clinical suspicion for differential diagnoses (DDX), not lim ited to:
CBC
ESR/CRP
Urine analysis
Imaging N/A
PA/Lateral of LS spine
Helps to rule out som e DDX
Indications: o
Extrem es of age (55 years)
o
Unresolved back pain (>4–6 weeks) despite conservative treatm ent
o
Red flags on history and physical exam :
Traum a
Constitutional sym ptom s (fever, unexplained
Pa ge 4 2 5
weight loss, m alaise)
History of cancer
Im m unocom prom ised
IV drug abuse
Recent bacterial infection
Worse at night/awakens patient from sleep
Fever
Midline point tenderness
Neurologic deficits
MRI (Criterion Standard)
Indications: o
Acute severe neurologic deficits (order from ED)
o
Suspicion of infectious etiology of back pain:
o
Epidural abscess
Osteom yelitis
Discitis
Six weeks failed conservative therapy (order on outpatient basis)
Disc disease (>25%): o
Incidental finding on MRI in asym ptom atic patients
o
No relationship between extent of protrusion and degree of sym ptom s
CT Myelogram
Rarely used alternative for MRI
CT better at bone details
Diagnostic Procedures/Surgery Postvoid residual (PVR):
Overflow incontinence
PVR >100 m L
Differential Diagnosis
Pa ge 4 2 5
Low Back Pain/Referred Pain
Pneum onia, pulm onary em bolus
Pancreatitis
Pyelonephritis, renal calculi
Ectopic pregnancy, pelvic inflam m atory disease
Abdom inal aortic aneurysm (AAA)
Peripheral vascular disease (claudication)
Lum bosacral strain
Hip/SI joint (infection, fracture, bursitis)
Degenerative joint disease
Herpes zoster
Psychologic: o
Functional
o
Secondary gain (drug seeking, disability)
Sciatica Irritating lesion affecting a lum bosacral nerve anywhere along its route:
Thalam us/Spinothalam ic tum or/Hem orrhage
Spinal cord (m yelopathy): o
Intraspinal tum or/hem atom a/infection (epidural abscess, discitis, osteom yelitis)
Root (radiculopathy): o
Intradural: tum or, infection
o
Extradural: HD, lum bar spine/foram inal stenosis (pseudoclaudication), spondylolisthesis, cyst, tum or, infection
Plexus (plexopathy): tum or, AAA, infection (iliopsoas abscess), hem atom a (retroperitoneal)
Peripheral nerve(neuropathy): toxic/m etabolic/nutritional, infection, traum a, ischem ia, infiltration, com pression, entrapm ent
Pa ge 4 2 5
Pediatric Considerations
Usually secondary to traum a or serious underlying m edical disease (i.e., leukem ia); consider com plete workup
Table o f C o ntents > Seiz ure, Adult
Seizure, Adult
Atul Gupta Rebecca Smith-Coggins
Basics Description
Generalized seizures: o
Classically tonic-clonic (grand m al)
o
Begins as m yoclonic jerks followed by loss of consciousness
o
Sustained generalized skeletal m uscle contractions
o
Nonconvulsive generalized seizures:
Absence seizures (petit m al); brief episodes of sudden im m obility and blank stare
Partial seizures: o
Sim ple:
Brief sensory or m otor sym ptom s without loss of consciousness (i.e., jacksonian)
o
Com plex:
Mental and psychological sym ptom s
Affect changes
Confusion
Autom atism s
Hallucinations
Pa ge 4 2 6
Associated with im paired consciousness
Status epilepticus: o
Seizure lasting longer than 1 hour
o
Serial seizures that produce an enduring epileptic condition for longer than 1 hour
o
Life-threatening em ergency with m ortality rate of 10–12%
Pediatric Considerations
Febrile seizure is a generalized seizure occurring between 3 m onths and 5 years of age: o
Typically lasts less than 15 m inutes
o
Associated with a rapid rise in tem perature
o
Without evidence of CNS infection or other definitive cause
Etiology
Meningitis, abscess, encephalitis
Ischem ic or hem orrhagic stroke
Prim ary or m etastatic neoplasm
Metabolic abnorm alities
Electrolytes (hypernatrem ia, hyponatrem ia, hypocalcem ia)
Hypo/hyperglycem ia
Hypoxia
Urem ia
Toxins/Drugs: o
Lidocaine
o
TCAs
o
Cocaine
o
Alcohol withdrawal
Eclam psia
Hypertensive encephalopathy
Traum a
Pa ge 4 2 6
Congenital abnorm alities
Idiopathic
Diagnosis Signs and Symptoms
Altered level of consciousness
Involuntary, repetitive m uscle m ovem ents: o
Seizures have abrupt onset: o
Tonic posturing or clonic jerking
Aura m ay precede a focal seizure
Duration is usually 90–120 seconds: o
Im paired m em ory of the event
o
Postictal state is a brief period of confusion and som nolence following a seizure.
Evidence of recent seizure activity: o
Confusion or som nolence
o
Acute intraoral injury
o
Urinary incontinence
o
Posterior shoulder dislocation
o
Tem porary paralysis (Todd paralysis)
Other findings m ay suggest etiology of seizure: o
Fever and nuchal rigidity (CNS infection)
o
Needle tracks; stigm ata of liver disease (drugs and alcohol)
o
Head traum a:
Papilledem a (increased intracranial pressure)
Lateralized weakness, sensory loss, or asym m etric reflexes
Essential Workup
Pa ge 4 2 6
A thorough history is the m ost valuable part of the workup:
o
Witness accounts
o
History of prior seizures
o
Presence of acute illnesses
o
Past m edical problem s
o
History of substance use
Patients with chronic seizure disorder and typical seizure pattern m ay need to have only serum glucose and anticonvulsant levels checked.
New-onset seizure m andates workup: o
Electrolytes including calcium , phosphorus
o
Head CT
o
Search for specific underlying cause.
o
Patient's condition and resources for follow-up determ ine whether all these tests need to be done in the ED.
Pediatric Considerations
Children with first febrile seizure should receive fever workup as dictated by clinical condition.
Frequently, there is a fam ily history of febrile seizure.
CBC, blood culture, urinalysis, chest radiograph if any signs of respiratory distress
Lum bar puncture for first febrile seizure: o
Consider strongly if age Table o f C o ntents > Seiz ure, Pediatric
Seizure, Pediatric
John Santamaria
Basics Description Sudden, abnorm al discharges of neurons resulting in a change in behavior or function
Etiology
Febrile seizures
Infection
Idiopathic
Traum a
Toxicologic:
o
Ingestion
o
Drug action
o
Drug withdrawal
Metabolic: o
Hypoglycem ia
o
Hypocalcem ia
o
Hypo/Hypernatrem ia
o
Inborn errors of m etabolism
Perinatal hypoxia
Intracranial hem orrhage
CNS structural anom aly or m alform ation
Pa ge 4 2 8
Degenerative disease
Diagnosis Signs and Symptoms Neonates
Subtle abnorm al repetitive m otor activity: o
Facial m ovem ents
o
Eye deviations
o
Eyelid fluttering
o
Lip sm acking/sucking
Respiratory alterations
Apnea
Seizure activity:
o
Focal or generalized tonic seizures
o
Focal or m ultifocal clonic seizure
o
Myoclonic m ovem ents
Generalized problem s (m etabiolic, infection, etc) m ay present with focal seizures.
Older Infants and Children
Generalized seizures: o
Tonic-clonic
o
Tonic
o
Clonic
o
Myoclonic
o
Atonic (“drop―)
o
Absence
Partial or focal seizures: o
Sim ple:
Consciousness m aintained
Pa ge 4 2 8
o
Sim ple partial seizures:
Motor, sensory, and/or cognitive sym ptom s
Motor activity is focal: one part or side.
Paresthesias, m etallic tastes, and visual or auditory hallucinations
o
o
Com plex:
Consciousness im paired
Com plex partial seizure
Siim ple partial seizure progresses with im paired consciousness:
Aura precedes altered consciousness; auditory, olfactory, or visual hallucination
May generalize
Status epilepticus: o
Generalized is m ost com m on.
o
Sustained partial seizures
o
Absence seizures
o
Persistent confusion; postictal period
History
Determ ine whether seizures are febrile or afebrile.
Determ ine type of seizure: o
Partial versus generalized
o
Presence of eye findings, aura, m ovem ents, cyanosis
o
Duration
o
State of consciousness, postictal state
o
Predisposing conditions/history/fam ily history (syndrom es with a genetic com ponent)
A careful neurologic exam should be perform ed: o
Ophthalm oscopic evaluation
o
Skin evaluation to identify neurocutaneous diseases such as tuberous sclerosis
Rapid glucose testing for those in status epilepticus
Pa ge 4 2 8
Tests Lab
Bedside glucose test
Perform ed in young infants and those in status epilepticus
Select studies in other children reflecting history and physical exam ination:
o
Electrolytes
o
Blood urea nitrogen
o
Creatinine
o
Glucose
o
Calcium
o
Magnesium
o
CBC
o
Toxicologic screen
Patients on anticonvulsant therapy: o
Drug levels
Febrile seizure: o
Laboratory studies to evaluate for a serious underlying bacterial infection, if suspected
Imaging
Head CT: o
Focal seizure
o
New focal neurologic abnorm ality
o
Suspected intracranial hem orrhage or m ass lesion
o
New-onset status epilepticus without identifiable cause
o
Not routinely indicated for first afebrile seizure
Lum bar puncture: o
Suspicion of m eningitis or encephalitis
o
CT first if suspect increased intracranial pressure
MRI:
Pa ge 4 2 8
o
Rarely urgently indicated for seizures
EEG: o
Generally indicated in children with an afebrile seizure as a predictor of risk of recurrence and classify the seizure type/epilepsy syndrom e
o
Postictal slowing seen within 24–48 hours of a seizure and m ay be transient; delay EEG if possible.
o
Rarely helpful in the acute setting
P.1005
Differential Diagnosis
Neonates: o
Apnea due to other causes
o
Jitters or trem ors
o
Gastroesophageal reflux
Infants and toddlers: o
Breath-holding spells
o
Night terrors
Children and adolescents: o
Migraine headache
o
Syncope
o
Tics
o
Pseudoseizures
o
Hysteria
Treatment Pre Hospital Cautions:
Pa ge 4 2 8
Many conditions m ay be m istaken for seizures (see Differential Diagnosis, below).
Im m obilize cervical spine if traum a suspected.
Check fingerstick glucose or adm inister dextrose as appropriate.
Initial Stabilization
Airway, breathing, and circulation support if actively seizing
Airway: o
Oxygen/Monitor pulse oxim etry.
o
Nasopharyngeal airway preferred over oral airway
o
Bag valve–m ask support, if hypoventilating or persistently hypoxic
o
Intubation if seizures are refractory and bag valve–m ask support is unsuccessful
IV access
If hypoglycem ic, dextrose
Maintain spine precautions if traum a suspected.
Alert Airway and breathing m ust be stabilized concurrent with m anagem ent of ongoing seizures, if present.
ED Treatment Status Epilepticus
Benzodiazepine: o
Lorazepam is preferred due to its longer duration of action.
o
Valium is acceptable.
o
If IV access is not available:
Diazepam m ay be given per rectum ; use a TB syringe or 14-gauge Angiocath catheter or
Pa ge 4 2 8
feeding tube.
Midazolam IM is also effective if IV access is not available.
Phenytoin: o
If benzodiazepines fail
o
For longer-term control
o
Fosphenytoin easier to adm inister
Phenobarbital: o
Use if benzodiazepines and phenytoin fail to break the seizure.
o
Risk of respiratory depression greatly increases if a benzodiazepine has also been given.
Alternative therapies in the event of refractory status epilepticus
Consultation appropriate: o
Paraldehyde (per rectum )
o
Barbiturate com a:
Barbiturate (pentobarbital) com a requires intubation and EEG m onitoring to be sure the seizure is suppressed
o
Associated hypotension
General anesthesia:
A final resort
Continuous EEG is needed to be sure the seizure is abolished.
Neonates: o
Phenobarbital is acceptable first-line therapy.
o
Preferred m aintenance drug
Alert Note: Aggregate response to second- and third-line agents is less than 10%.
Pa ge 4 2 8
Medication (Drugs)
D 1 0 : 5 m L/kg IV for neonates
D 2 5 : 2 m L/kg IV for children
Diazepam : 0.2–0.3 m g/kg IV; 0.5 m g/kg PR
Fosphenytoin: 20 m g/kg IV over 20 m inutes
Lorazepam : 0.1 m g/kg IV
Midazolam : 0.1 m g/kg IV, 0.2 m g/kg IM
Paraldehyde: 0.3 m L/kg PR m ixed 1:1 with cottonseed or olive oil, m ax. dose is 5 m L
Pentobarbital: 10–15 m g/kg IV over 1–2 hours; m aintenance: 1–3 m g/kg/h IV
Phenobarbital: 20 m g/kg IV over 20 m inutes
Phenytoin: 20 m g/kg IV over 30–45 m inutes
Follow-Up Disposition Admission Criteria
Intensive care unit: o
Active status epilepticus, intubated, or persistent m ental status changes
Inpatient unit: o
Status epilepticus resolved in the ED
o
Underlying cause of seizure not resolved or controlled
o
Intracranial hem orrhage
o
Mass lesion
o
Meningitis/Encephalitis
o
Drug
o
Toxin ingestions
Pa ge 4 2 9
Discharge Criteria
The child is alert with norm al m ental status and neurologic exam .
No evidence of an underlying cause requiring hospitalization
Reliable parent or caregiver
Hom e telephone
Provide seizure precautions and aftercare instructions
Follow-up with a prim ary care physician or pediatric neurologist
References 1. Appleton R, Choonara I, Martland T, et al. The treatm ent of convulsive status epilepticus in children. The Status Epilepticus Working party. Arch Dis Child. 2000;83:415–419. 2. Barata I, Pediatric Seizures. Critical Decisions in Em ergency Medicine. 2005;19:1–10. 3. Bleck TP, Managem ent Approaches to Prolonged Seizures and Status Epilepticus. Epilepsia. 1999;40:S59–S63. 4. Cantor RM, Santam aria JP, eds. Pediatric em ergency guide. Dallas, TX: Am erican College of Em ergency Physicians, 1997. 5. Hirtz D, et al. Practice param eter: evaluating a first nonfebrile seizure in childrenreport of the Quality Standards Subcom m ittee or the Am erican Academ y of Neurology, the Child Neurology Society, and the Am erican Epilepsy Society. Neurology. 2000;55:616–623. 6. Vining EPG. Pediatric seizures. Em erg Med Clin North Am . 1994;12:973–988.
Miscellaneous SEE ALSO: Seizures, Febrile
Pa ge 4 2 9
Codes ICD9-CM 780.31
Pa ge 4 2 9
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Sepsis
Sepsis
Richard Wolfe Nathan Shapiro
Basics Description
System ic inflam m atory response triggered by an infection in the host and m ediated by chem ical m essengers: o
Decreased peripheral vascular resistance
o
Elevated cardiac output in response to vasodilatation
o
Later in septic shock, m yocardial depression, and reduced cardiac output (due to injury at the cellular level or m ediators acting on the heart)
o
Multiple organ dysfunction syndrom e (MODS) if sepsis is ineffectively treated
Adult respiratory distress syndrom e (ARDS)
Acute tubular necrosis and kidney failure
Hepatic injury and failure
Dissem inated intravascular coagulation
Sepsis is classified by the system ic inflam m atory response syndrom e (SIRS): o
Tem perature >38°C or 90 beats/m inute
o
Respiratory rate >20/m inute or PaCO 2 12,000/m m 3 , 10% band form s
Sepsis: two or m ore of the SIRS criteria with an underlying infection
Severe sepsis: o
Sepsis with organ dysfunction as m anifested by one of the following:
Acidosis
Renal dysfunction
Acute change in m ental status
Pulm onary dysfunction
Hypotension
Throm bocytopenia or coagulopathy
Liver dysfunction
Septic shock: o
Sepsis-induced hypotension despite fluid resuscitation
o
Systolic blood pressure (BP) 40 m m Hg from baseline
Etiology
Gram -negative bacteria m ost com m on: o
Escherichia coli
o
Pseudom onas aeruginosa
o
Rickettsiae
o
Legionella species
Gram -positive bacteria: o
Enterococcus species
o
Staphylococcus aureus
o
Streptococcus pneum oniae
Fungi (Candida species)
Viruses
Pediatric Considerations
Pa ge 4 2 9
Children with a m inor infection m ay have m any of the findings of SIRS.
Major causes of pediatric bacterial sepsis o
Neisseria m eningitis
o
Streptococcal pneum oniae
o
Haem ophilus influenzae
Diagnosis Signs and Symptoms Physical Exam
General: o
Fever
o
Tachycardia
o
Tachypnea
o
Hypotherm ia (poor prognosis)
o
Hypoxem ia
o
Diaphoresis
Cardiovascular: o
BP
o
Norm al early in sepsis
o
Hypotension when septic shock occurs
o
Poor perfusion with septic shock:
Prolonged capillary refill
Cool and clam m y extrem ities
Gastrointestinal/Genitourinary: o
Abdom inal pain
o
Nausea, vom iting
o
Diarrhea
o
Dysuria/Frequency
Pa ge 4 2 9
o
Reduced urine output
o
Abdom inal tenderness:
Diffuse
Localized to right upper quadrant (liver or gallbladder source)
Right lower quadrant (appendicitis with or without abscess)
Suprapubic area or lower quadrants (urinary tract or pelvic source or diverticulitis)
o
Flank pain:
With pyelonephritis or retroperitoneal abscess
Pulm onary: o
Shortness of breath
o
Tachypnea:
Present even when the lungs are not the source of sepsis
o
Productive cough
Derm atologic: o
Any rash is im portant.
o
Localized erythem a with lym phangitis (streptococcal or staphylococcal cellulitis)
o
Rash involving palm s of hands and soles of feet (rickettsial infection)
o
Petechiae scattered on the torso and extrem ities (m eningococcem ia)
o
Ecthym a gangrenosum (pseudom onas septicem ia)
o
Round, indurated, painless lesion with surrounding erythem a and central necrotic black eschar
o
Decubitus ulcers
o
Indwelling catheter:
Surrounding skin erythem atous with or without purulent drainage
Pa ge 4 2 9
CNS: o
Change in m ental status
o
Confusion
o
Delirium
o
Com a
o
Neck stiffness (m eningitis)
Essential Workup
Careful history and physical exam ination
Guides further evaluation and initiation of appropriate antibiotic therapy
Tests Lab
Serum lactate: o
>4 m m ol/L defines severe sepsis
CBC with differential: o
Leukocytosis is insensitive and nonspecific.
o
Neutrophil count 5% bands on a peripheral sm ear is an im perfect indicator of infection.
o
Hem atocrit:
Needed to determ ine whether adequate oxygen delivery can be achieved
Patients should be m aintained with a hem atocrit >30% and hem oglobin >10 g/dl.
o
Platelets:
May be elevated in the presence of infection or sepsis-induced volum e depletion
Low platelet count is a significant predictor of bacterem ia and death.
Pa ge 4 2 9
Electrolytes, blood urea nitrogen, creatinine, glucose: o
Low bicarbonate suggests inadequate perfusion.
o
Renal dysfunction or failure indicates a worse prognosis.
Ca, Mg, Ph
C-reactive protein
Cortisol level
International norm alized ratio/prothrom bin tim e/partial throm boplastin tim e
Type and screen
Liver function tests
Arterial blood gas: o
Mixed acid–base abnorm alities: respiratory alkalosis with m etabolic acidosis
Blood cultures: o
From two different sites
o
One m ay be drawn through an indwelling central line (i.e., Broviac).
Urine analysis and culture
Imaging
Chest radiograph: o
Determ ine whether pneum onia is the infectious source.
o
Fluffy, bilateral infiltrates m ay indicate that ARDS is already present.
o
Free air under the diaphragm indicates the source of the infection in intraperitoneal and a surgical intervention.
Soft tissue plain film s: o
Indicated if extrem ity erythem a or severe pain
o
Air in the soft tissues associated with necrotizing or gas-form ing infection
Pa ge 4 2 9
P.1007
CT scan of the abdom en and pelvis o
Suspicion of abdom inal source of infection:
Diverticulitis, appendicitis, necrotizing pancreatitis, m icroperforation of the stom ach or bowel, or form ation of an intra-abdom inal abscess
Abdom inal ultrasound: o
Pelvic ultrasound: o
Indicated for suspected cholecystitis
Tubo-ovarian abscess or endom etritis
Transesophageal echo: o
When endocarditis is suspected to detect the presence of any valvular vegetations
MRI: o
May be useful to identify soft tissue infections or epidural abscess
Diagnostic Procedures/Surgery
Lum bar puncture: o
Indicated when m eningeal signs are present or altered m ental status without a source of infection
o
Cerebrospinal fluid analysis:
Cell count and differential, tube 1
Total protein and glucose, tube 2
Culture and gram stain, tube 3
Cell count and differential, tube 4
Depending on the clinical situation: cytology, venereal disease research laboratory, AFB stain/culture, fungal stain
Central venous access:
Pa ge 4 2 9
o
Central venous pressure (CVP) and ongoing m easurem ent of central venous oxim etry catheter m ay be helpful in guiding resuscitation.
Differential Diagnosis
Pancreatitis
Traum a
Toxic shock syndrom e
Anaphylaxis
Adrenal insufficiency
Drug or toxin reactions
Heavy m etal poisoning
Hepatic insufficiency
Neurogenic shock
Treatment Pre Hospital Aggressive fluid resuscitation for hypotension
Initial Stabilization
ABCs
Supplem ental oxygen to m aintain PaO 2 >60 m m Hg
Intubation and m echanical ventilation if shock or hypoxia are present
Adm inister 0.9% NS IV
ED Treatment
Early goal-directed therapy: o
500 cc boluses of 0.9% saline up to 1–2 liters em pirically
o
Place central line
Pa ge 4 3 0
o
Continue 500 cc saline boluses until CVP >8 cm H 2 O
o
If the m ean arterial pressure 8, then initiate pressors:
Dopam ine or norepinephrine to raise blood pressure
Norepinephrine is preferred if tachycardia or dysrhythm ias are present.
Phenyl epinephrine for cases where shock is refractory to other pressors
If the ScvO 2 30, then add dobutam ine.
Adm inister antibiotics early based on the m ost likely organism s or site of infection.
If no source identified after initial assessm ent: o
Norm al im m une function:
Second- or third-generation cephalosporin and gentam icin
Nafcillin and gentam icin
Add vancom ycin if there is a history of m ethicillin resistant staphylococcus aureous or the patient resides in a nursing facility or there is a history of recent hospitalizations.
o
Im m unocom prom ised host:
Piperacillin and gentam icin
Ceftazidim e and either nafcillin or vancom ycin and gentam icin
If source identified, or highly suspected, treat the m ost likely organism s: o
Pulm onary source:
Second- or third-generation cephalosporin and gentam icin, and possibly erythrom ycin
o
Intra-abdom inal source:
Pa ge 4 3 0
o
Am picillin and m etronidazole and gentam icin
Cefoxitin and gentam icin
Urinary tract source:
Am picillin or piperacillin and gentam icin
Pediatric Considerations
Antibiotic therapy based on age: o
6 m onths: 5–10 m g/kg) q6h–q8h
Prednisone: 0.052 m g/kg PO (peds: 12 m g/kg) per day, 2-week taper
Follow-Up Disposition
Pa ge 4 3 0
Admission Criteria
Involvem ent of the airway
Relapse of sym ptom s and signs after initial steroids
Im m unosuppression
Concom itant serious disease
Sociologic considerations
Discharge Criteria Stable; m ost cases are self-lim iting in 23 weeks.
References 1. LoVecchio F, Curry SC, Welch S, et al. Incidence of im m ediate and delayed hypersensitivity to Centruroides antivenom . Ann Em erg Med. 1999;34:615–619. 2. Piessens WF. System ic im m une com plex disease. In: Ruddy S, ed. Kelley's textbook of rheum atology. 6th ed. Philadelphia, PA: WB Saunders, 2001. 3. Poley GE, Slater JE. Drug and vaccine allergy. Im m unol Allergy Clin North Am . 1999;19:409–419. 4. Rosenwasser LJ. The vasculitic syndrom es. In: Goldm an L, ed. Cecil textbook of m edicine. 21st ed. Philadelphia, PA: WB Saunders, 2000:1525–1527. 5. Winkelstein JA, Fries LF. The com plem ent system and im m unopathology. In: Middleton E, ed. Allergy: principles and practice. 5th ed. St. Louis, MO: Mosby Year Book, 1998:63–64.
Codes ICD9-CM 999.5
ICD10 T80.6
Pa ge 4 3 0
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Sexual Assault
Sexual Assault
Ingrid D. Carter
Basics Description Specific legal definition varies from state to state:
Defined as forced sexual contact without consent
Any unwanted touching or fondling via force, threat of force, or if person is unable to give consent
Continuum from unwanted touching and fondling to forced penetration of vagina, anus, oral cavity
Etiology
78–82% of fem ale rape victim s are raped by som eone they know.
50% of rape victim s older than 30 years old are assaulted by intim ate partner.
Am ong wom en suffering physical abuse by partner, 33–46% report being sexually assaulted.
Age distribution of fem ale rape victim s: o
11–17 years old: 32%
o
18–24 years old: 22%
o
50 years old: 22%
Pa ge 4 3 1
Diagnosis Signs and Symptoms
Victim s m ight not disclose assault: o
Approxim ately 70% of rape victim s do not tell their doctors.
o
Most will reveal history only in response to direct questions.
Tachycardia or pounding heart beat
Headaches
Nausea
Back pain
Skin problem s
Menstrual sym ptom s
Sudden weight change
Sleeping disorders
Abdom inal pain
Trouble breathing
Associated injuries: o
Of those with injuries, 70% report no injury at presentation.
o
Lacerations of perineum
o
Vulvar traum a
o
Laceration of vaginal wall (m ore com m on in younger patients near introitus)
o
Multiple contusions
o
Abrasions
o
Hum an bite
o
Lacerations or puncture wound to extrem ity
o
Burns
o
Depressed skull fracture
Pa ge 4 3 1
Pediatric Considerations
Must follow local laws regarding child abuse
Patient m ost likely never had pelvic exam previously; if possible, involve specialist.
Use sm allest speculum possible.
Use toys and dolls to have child explain what happened.
Early psychiatric intervention necessary
Essential Workup
Obtain written consent prior to any exam , test, or treatm ent.
Allow patient to pause and proceed at com fortable pace.
Allow advocate to stay with patient during exam with patient's consent.
History
Obtain com plete history even if patient does not wish to file charges, including: o
Tim e and place of assault
o
Physical description of assailants
o
Num ber of assailants
o
Types of penetration: vaginal, oral, rectal
o
Assailant ejaculation, if assailant used condom
o
Any bodily fluid exchange
o
Use of force, weapons, restraints, drugs or alcohol
o
If victim has m em ory loss or loss of consciousness
o
Victim 's activity since assault:
Changed clothes
Douched
Bathed
Urinated
Defecated
Ate
Pa ge 4 3 1
Tam pon use
o
Full gynecologic history
o
Last voluntary intercourse
o
Sperm m ay be m obile up to 5 days in cervix and 12 hours in vagina.
Address all physical com plaints.
Physical Exam
Use local evidence kit even if victim unsure if reporting to police.
Fem ale chaperone required if m ale physician
If clothes soiled, photograph prior to undressing with patient's consent.
Note em otional state of victim .
Note general appearance of clothes: o
Staining
o
Tears
o
Mud
o
Leaves
o
Wood lam p for sem inal stains
o
Have patient disrobe while standing on sheet and place all clothes in paper bag.
Plastic causes m old and increases bacteria counts.
o
Have only patient handle clothing.
o
Arrange for change of clothes.
Com plete physical should be done with em phasis on: o
Abrasions
o
Lacerations
o
Bites
o
Scratches
o
Foreign bodies
o
Ecchym oses
Pa ge 4 3 1
o
Dried sem en on skin
P.1011
Forensic collection: o
Fingernail scrapings
o
Scalp or pubic hair sam ples
o
If oral penetration, swab between teeth for acid phosphatase (assay for sem en) and sperm .
o
Throat culture for gonorrhea/chlam ydia if oral sex
Gynecologic exam : o
Explain all steps and allow patient to pace exam .
o
Com b and collect pubic hair per local protocol.
o
Lubricate speculum with water.
o
Look for genital traum a even in asym ptom atic patients.
o
May use toluidine blue to identify sm all pelvic lacerations from traum atic intercourse:
o
Best applied to vaginal m ucosa at introitus
Special attention to hym en as one of m ost com m on places for traum a
o
Lacerations to vaginal wall near introitus m ore com m on in younger patients
o
Aspirate secretions pooled in posterior fornix and place in sterile container to be exam ined for sperm and acid phosphates:
If no secretions in posterior fornix, wipe with cotton tip.
Swab and m icroscopically exam ine for sperm and acid phosphates.
o
Swabs for gonorrhea and chlam ydia:
Controversial; evidence can be used by defense
Pa ge 4 3 1
to show prom iscuity. o
Colposcope allows visualization of sm all lesions and ability to photograph findings.
o
Rectal exam and cultures for gonorrhea and chlam ydia if penetration or attem pted penetration
Tests Lab
Syphilis serology
Hepatitis band C panel
HIV testing and counseling
Drug testing (if suspect victim was drugged, can be used against victim if other agents detected)
Blood type
Pregnancy test
Gonorrhea culture
Chlam ydia culture
Other labs as needed based on injuries
Imaging As indicated by injuries
Diagnostic Procedures/Surgery As indicated by injuries
Treatment Initial Stabilization Treat life-threatening injuries.
ED Treatment
Place patient in quiet, private room .
Pa ge 4 3 1
Assure patient of confidentiality regarding nam e and reason for visit.
Regularly assure patient of safety.
Enforce nonjudgm ental behavior by staff.
Designate nursing and m edical provider for entire stay who is fam iliar with evidence collection kit.
Have sexual assault nurse exam iner (SANE) perform exam if available.
Contact com m unity or in-hospital advocate to stay with patient while in ED.
Alert hospital security to possibility of assailant presenting to ED.
Contact police if patient consents or local law requires.
Collect evidence as outlined above and according to local law.
Adm inister pregnancy prophylaxis if not currently pregnant: o
Estim ated risk of pregnancy is 2–4% if wom an not using contraceptives.
o
Horm onal therapy if within 72 hours:
Levonorgestrel 0.75 m g stat and repeat in 12 hours (preferred) or
Ethinyl estradiol 100 µg stat and repeat in 12 hours
o
72 hours to 7 days post-assault
Consult obstetrics and gynecology (ob/gyn) for possible intrauterine device (IUD) placem ent.
Adm inister prophylactic therapy for gonorrhea, chlam ydia, trichom onas: o
Ceftriaxone 125 m g IM
o
Doxycycline 100 m g PO b.i.d. for 7–10 days or
o
Azithrom ycin 1 g PO (single dose)
Pa ge 4 3 1
o
Flagyl 2 g PO (single dose)
Consider prophylactic therapy for HIV.
Consider prophylactic therapy or vaccine for Hepatitis B.
Follow-Up Disposition Admission Criteria Serious traum atic injury
Discharge Criteria
Medical follow-up for culture and HIV test results
Offer m ental health services and counseling.
Safe place for patient to go to
References 1. Burgess AW, Fawcett J. The com prehensive sexual assault assessm ent tool. Nurse Pract. 1996;21:66. 2. Dunn SFM, Gilchrist VJ. Sexual assault. Prim Care. 1993;20:359–373. 3. Dupre AR, Ham pton HL, Morrison H, et al. Sexual assault. Obstet Gynecol Surv. 1993;45:640–648. 4. Levine DL, Kaufm an LE. Rape and sexual violence: the adult and adolescent fem ale victim . In: Bernstein E, Bernstein J, eds. Case Studies in Em ergency Medicine and the Health of the Public. Boston: Jones & Bartlett; 1996:100–112.
Codes ICD9-CM V71.5
ICD10
Pa ge 4 3 1
T74.2
Pa ge 4 3 1
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Sho ck
Shock
Nathan Shapiro Christopher Fischer
Basics Description
Inadequate supply of blood flow to tissues to m eet the dem ands of the tissues
Nutrient requirem ents are not fulfilled.
Toxic m etabolites are not rem oved.
If untreated, inevitable progression from inadequate perfusion to organ dysfunction and ultim ately to death.
Main com ponents of blood flow: o
Cardiac output
o
Blood volum e
o
Peripheral resistance of arteriolar and venous system (system ic vascular resistance [SVR])
Major categories of shock: o
Hypovolem ic shock:
Decreased blood volum e
Suspect hem orrhage if acute onset
Severe dehydration if progressive onset and elevated hem atocrit, blood urea nitrogen, and creatinine
Pa ge 4 3 1
Decrease in cardiac output leads to com pensatory increase of the SVR in an attem pt to norm alize perfusion pressure.
o
Obstructive (cardiogenic) shock:
Decreased cardiac output and tissue hypoxia with adequate intravascular volum e and m yocardial dysfunction
Venous congestion with increase in central venous pressure
o
Com pensatory increase in SVR
Causes of decreased cardiac output
Cardiac dysfunction with reduced contractility
Obstruction to inflow of blood to the heart
Obstruction to outflow of blood from the heart
Septic shock:
An initial infectious insult overwhelm s the im m une system .
Biochem ical m essengers (leukotrienes, histam ines, prostaglandins) cause vessel dilatation.
Capillary endothelium becom es disrupted and the vessels leak.
Drop in SVR leads to inadequate tissue perfusion.
Secondarily, decreased cardiac output from “cardiac stun― resulting in cold septic shock
o
Neurogenic shock:
Spinal chord insults disrupt sym pathetic stim ulation to vessels.
Loss of sym pathetic tone causes arteriodilating and vasodilatation.
Pa ge 4 3 2
Lesions proxim al to T4 disrupt sym pathetic, spares vagal innervation causing bradycardia.
o
Anaphylactic shock:
An antigen stim ulates the allergic reaction.
Mast cells degranulate.
Histam ine releases along with autocoids stim ulate an anaphylaxis cascade.
o
Vascular sm ooth m uscle relaxes.
Capillary endothelium leaks.
Drop SVR leads to inadequate tissue perfusion.
Pharm acologic agents m ay cause shock through sm ooth m uscle dilation or m yocardial depression.
Etiology See differential diagnosis.
Diagnosis Signs and Symptoms
Generalized shock: o
Hypotension
o
Decreased peripheral pulses
o
Tachycardia
o
Tachypnea
o
Decreased urine output
o
Diaphoresis
o
Obtundation
o
Lethargy
Hypovolem ic shock: o
Cold and clam m y extrem ities
o
Pallor
Pa ge 4 3 2
o
Flattened neck veins
o
Decreased capillary refill
o
Narrowed pulse pressure
Cardiogenic shock: o
Chest pain/pressure
o
Dyspnea
o
Orthopnea
o
Jugular venous distention
o
Cool, clam m y, sweaty extrem ities
o
Rales
o
Wheezes
o
Dullness at lung bases
o
S3 gallop
Septic shock: o
Warm flushed extrem ities
o
Strong pulses
o
Hypertherm ia
o
Hypotherm ia
o
Purpura or petechial rash
Anaphylactic shock: o
Warm flushed extrem ities
o
Urticaria
o
Stridor
o
Throat tightness
o
Hoarseness
o
Wheezing
Neurogenic shock: o
Flaccid paralysis
o
Loss of rectal tone
o
Hypotension with bradycardia
Essential Workup
Identify type or types of shock present.
Pa ge 4 3 2
Identify underlying cause of shock.
Tests Lab
Hem oglobin/Hem atocrit: o
Low hem oglobin and hem atocrit—hem orrhage
o
Very high hem atocrit—dehydration
o
Poor m arker with acute hem orrhage
WBC: o
High—nonspecific m arker of infection
o
Low—neutropenic infections
Electrolytes: o
Low CO 2 —acidosis
o
Increased blood urea nitrogen (gastrointestinal hem orrhage)
o
Increased Na, K, Cl, blood urea nitrogen/creatinine (dehydration)
Blood glucose: o
High (diabetic ketoacidosis or septic shock)
o
Low (pediatric sepsis)
Prothrom bin tim e/partial throm boplastin tim e o
Increased in dissem inated intravascular co-agulation, septic shock, and liver disease
Cardiac enzym es
Urinalysis:
o
High glucose/ketones (DKA or septic shock)
o
WBCs and bacteria in urosepsis
Beta-hum an chorionic gonadotropin: o
Wom en of childbearing age at risk for a ruptured ectopic pregnancy
Lactic acid level: o
Anaerobic m etabolism , cell dysfunction, and organ
Pa ge 4 3 2
dam age leads to release of lactic acids when organ dem ands exceed nutrient supply. o
Good surrogate m arker of shock state
Imaging
ECG: o
Assess for ischem ia and other disorders of cardiac m uscle:
Electrical alternans or low voltage with cardiac tam ponade
Right heart strain with pulm onary em bolism
Chest radiograph: o
Pneum onia
o
Pulm onary edem a
o
Pneum othorax
o
Hem othorax
o
Pulm onary infarction
o
Traum atic injuries
Echocardiography: o
Tam ponade
o
Wall m otion abnorm alities (m yocardial ischem ia)
o
Right ventricle strain (pulm onary em bolus)
o
Aortic dissection
Abdom inal ultrasound: o
Intraperitoneal hem orrhage
o
Ectopic pregnancy
CT abdom en: o
Requires that the patient first be stabilized
o
In the setting of abdom inal traum a and in search for suspicion of abdom inal infection
Differential Diagnosis
Hypovolem ic shock:
Pa ge 4 3 2
o
Abdom inal traum a, blunt or penetrating
o
Abortion—com plete, partial, or inevitable
o
Anem ia—chronic or acute
o
Aneurysm s—abdom inal, thoracic, dissecting
o
Aortogastric fistula
o
Arteriovenous m alform ations
o
Blunt traum a
o
Burns
o
Diabetes
o
Diarrhea P.1013
o
Diuretics
o
Ruptured ectopic pregnancy
o
Epistaxis
o
Fractures (especially long bones)
o
Hem optysis
o
Gastrointestinal bleed
o
Mallory-Weiss tear
o
Penetrating traum a
o
Placenta previa
o
Postpartum hem orrhage
o
Retroperitoneal bleed
o
Severe ascites
o
Splenic rupture
Toxic epiderm al necrolysis: o
Vascular injuries
o
Vom iting
Cardiogenic shock: o
Cardiom yopathy
o
Conduction abnorm alities and arrhythm ias
Pa ge 4 3 2
o
Myocardial infarction
o
Myocardial contusion
o
Myocarditis
o
Pericardial tam ponade
o
Pulm onary em bolus
o
Tension pneum othorax
o
Valvular insufficiency
o
Ventricular septal defect
Vasogenic shock: o
Acute respiratory distress syndrom e
o
Bacterial infection
o
Bowel perforation
o
Cellulitis
o
Cholangitis
o
Cholecystitis
o
Endocarditis
o
Endom etritis
o
Fungem ia
o
Infected indwelling prosthetic device
o
Intraabdom inal infection or abscess
o
Mediastinitis
o
Meningitis
o
Myom etritis
o
Pelvic inflam m atory disease
o
Peritonitis
o
Pyelonephritis
o
Pharyngitis
o
Pneum onia
o
Septic arthritis
o
Throm bophlebitis
o
Tubo-ovarian abscess
o
Urosepsis
Pa ge 4 3 2
Anaphylactic: o
Drug reaction (m ost com m only to aspirin, beta-lactam antibiotics)
o
Exercise (rare)
o
Food allergy (peanuts, tree nuts, shellfish, fish, milk, eggs, soy, and wheat account for 90% of food related anaphylaxis)
o
Insect sting
o
Latex
o
Radiographic contrast m aterials
o
Synthetic products
Pharm acologic: o
Antihypertensives
o
Antidepressants
o
Benzodiazepines
o
Cholinergics
o
Digoxin
o
Narcotics
o
Nitrates
Neurogenic: o
Spinal chord injury
Treatment Initial Stabilization
Large-bore IV access: o
When possible, central venous access and m onitoring
Fluid resuscitation in noncardiogenic shock patients
Control bleeding with direct pressure m easures.
Long bone traction
Stabilization of pelvis with sheet or com m ercial device or
Pa ge 4 3 2
external fixation
ED Treatment
Hypovolem ic shock: o
Identify source of volum e depletion
o
Aggressive fluid resuscitation keeping systolic blood pressure (SBP) >100 m m Hg until definitive treatm ent
o
2–3 L crystalloid initially
o
Packed red blood cells if 2–3 L crystalloids do not im prove SBP
o
Identify source of bleeding and rapidly m ove toward definitive treatm ent.
o
Dopam ine and epinephrine in refractory shock after m axim al fluid and blood product resuscitation with delayed hem orrhage control
o
Thoracotom y and aortic cross-clam ping in refractory shock with penetrating torso traum a
Cardiogenic shock: o
Ease work of breathing with intubation
o
Insult-specific therapy (e.g., throm bolytics for MI, pericardiocentesis for pericardial tam ponade)
o
Treat dysrhythm ias.
Septic shock: o
Aggressive crystalloid fluid resuscitation
o
Titrate fluid to urine output >30 cc/h
o
Blood product transfusion to m aintain HCT 30–35%
o
Early antim icrobial therapy
o
Inotropic support as needed
o
Dopam ine or norepinephrine infusion
Anaphylactic shock: o
Intubation for airway com prom ise
o
Epinephrine
Pa ge 4 3 2
o
Subcutaneous in noncritical settings
o
Intravenous drip for im m ediate life threats or refractory hypotension
o
H-1 blockers (diphenhydram ine)
o
H-2 blockers (cim etidine)
o
Corticosteroids (hydrocortisone or m ethylprednisolone)
o
Nebulized β 2 -antagonists for bronchospasm
o
Patients taking beta-blockers m ay be m ore likely to experience severe sym ptom s of anaphylaxis that m ay m anifest as paradoxical bradycardia, profound hypotension, and severe bronchospasm .
Pharm acologic shock: o
Supportive therapy
o
Decontam ination of overdoses with charcoal
o
Inotropic agents as needed
o
Drug specific antidotes
Neurogenic shock: o
Supportive therapy
o
Traction and fracture stabilization
o
Corticosteroids
Medication (Drugs)
Albuterol: 2.5 m g/2.5 cc nebulizer PRN
Calcium gluconate: 100–1,000 m g IV
Cim etidine: 300 m g IV
Diphenhydram ine: 50–100 m g IV over 3 m inutes
Dobutam ine—5–40 µg/kg/m in IV: o
Dopam inergic: 1–3 µg/kg/m in IV
o
Beta effects: 3–10 µg/kg/m in IV
o
Alpha/Beta effects: 10–20 µg/kg/m in IV
Pa ge 4 3 2
o
Alpha effects: 20 µg/kg/m in IV
Epinephrine: o
1–4 µg/m in IV infusion
o
SQ/IM 1:1000 0.1–0.3 m g repeat q5m in–q20m in × 3 PRN
o
IV 1:10,000 10 m L (1 m g) over 10 m in IV
Glucagon: 1–5 m g IV bolus initial, then 1–20 m g/h infusion
Hydrocortisone: 5–10 m g/kg IV
Methylprednisolone: 1–2 m g/kg IV
Naloxone: 0.01 m g/kg IV initial, titrate to effect
Norepinephrine start: 2–4 µg/m in IV, titrate up to 1–2 µg/kg/m in IV
Phenylephrine: 40–180 µg/kg/m in IV
Follow-Up Disposition Admission Criteria
All patients in shock need to be adm itted.
Intensive care unit (ICU) criteria: o
All patients with persisting shock need ICU m onitoring.
Patients with shock definitively reversed m ay be adm itted to non-ICU setting (e.g., tension pneum othorax that has been decom pressed and chest tube placed).
Discharge Criteria Patients who are in shock should not be discharged hom e from the ED.
Pa ge 4 3 3
References 1. Kline JA. Shock. In: Marx J, et al. eds. Rosen's em ergency m edicine: concepts and clinical practice. St. Louis, MO: Mosby Year Book, 2002: 33–47. 2. Rivers E, Nguyen B, Havstad S, et al. Early goal directed therapy in the treatm ent of severe sepsis and septic shock. N Engl J Med. 2001;345:1368–1377. 3. Shapiro NI, Howell M, Talm or D. “A Blueprint for a sepsis protocol. Academ ic Em ergency Medicine. 2005;12:4:352–359.
Codes ICD9-CM 785.5 785.51
ICD10 R57.9
Pa ge 4 3 3
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Sho ulder Dislo catio n
Shoulder
Dislocation Doodnauth Hiraman Wallace Carter
Basics Description
Shoulder very dynam ic joint prone to injury
Anterior dislocation (90–96%): o
Injury is from direct or indirect forces on the abducted and externally rotated arm .
o
Injury m ay also result from a direct blow to posterior lateral aspect of shoulder.
Posterior dislocation: o
Often m issed
o
Forces on the adducted and internally rotated arm result in posterior dislocation of hum eral head in relation to glenoid fossa.
o
Most com m on m echanism is seizure and sudden contraction of all the posterior m uscle groups.
o
Other m echanism s include electrocution and direct blow to anterior shoulder.
Inferior dislocation (rare):
Pa ge 4 3 3
o
Luxatio erecta
o
Hyperabduction of arm , tear of rotator cuff, and rotation of arm 180° above head
o
Com m only seen after a fall from a height:
Arm has struck object on descent and is thrust above the head.
o
Often accom panied by neurovascular injury and fracture
Pediatric Considerations
Dislocation is rare in children: o
Epiphysial fractures m ust be suspected.
Geriatric Considerations Dislocation is often accom panied by fracture.
Etiology
Falls from height
Im pact injuries
Distraction injuries of upper arm
Seizures
Electrocution
Diagnosis Signs and Symptoms
Severe pain in the affected shoulder
Anterior dislocation: o
Shoulder is squared off.
o
Prom inent acrom ion process and palpable anterior fullness
o
Arm is held in slight abduction and external rotation.
Posterior dislocation:
Pa ge 4 3 3
o
Coracoid process is prom inent, with a palpable posterior bulge.
o
Arm is held in slight adduction and internal rotation.
Inferior dislocation (luxatio erecta): o
Rare but easy to identify
o
Arm is shortened and fixed above head as if raised to ask a question.
Head of hum erus m ay be palpable on the lateral chest wall.
Essential Workup
Evaluate neurovascular status of distal arm .
Retest neurovascular status after any m anipulation.
Dislocation requires prom pt treatm ent: o
Incidence of posttraum atic arthritis increases with tim e dislocation is untreated.
o
Plain film s of the shoulder should be obtained im m ediately.
o
Even in clinically obvious cases, film s should be obtained before m anipulation unless a significant delay will result.
o
An im pacted hum eral head fracture m ay be converted to a displaced hum eral head fracture if m anipulated.
Tests Imaging
At least two views should be obtained: o
Anteroposterior:
o
Trans-scapular Y or axillary view:
To visualize dislocation or fracture
To visualize if anterior or posterior
Anterior dislocation:
Pa ge 4 3 3
o
Posterolateral com pression fracture of the hum eral head (Hills-Sachs deform ity)
o
Corresponding lesion on anterior glenoid rim is the Bankart lesion:
o
These do not require treatm ent.
Fractures of the greater tuberosity of the hum eral head are seen in 15–35%:
If there is >1-cm displacem ent after reduction, surgical intervention m ay be necessary.
Posterior dislocation: o
Often m issed on anteroposterior film
Degree of overlap on radiographic film is sm aller and displaced superiorly, producing the m eniscus sign.
Rotated hum erus yields “light bulb on a stick― finding on anteroposterior view.
o
Reverse Hill-Sachs deform ity from com pression fracture of the anterior m edial hum eral head m ay also be seen.
Differential Diagnosis
Fracture of the hum eral head
Fracture of the hum eral shaft
Acrom ioclavicular injury
Septic shoulder joint
Hem arthrosis in shoulder joint
Scapular fracture
Cervical spine injury
P.1015
Pa ge 4 3 3
Treatment Pre Hospital Neurovascular injury should be identified and the arm splinted in the position of m ost com fort.
Initial Stabilization
Airway m anagem ent and resuscitate as indicated.
Exclude m ore serious injuries especially in m ultitraum a patient.
Ensure no injury to axillary nerve or vessels.
ED Treatment
Adequate analgesia and m uscle relaxation are essential for successful reduction: o
Procedural sedation with a short-acting opioid and a benzodiazepine or
o
Methohexital or etom idate alone
o
In the co-operative patient, intra-articular block only (20 cc of lidocaine 1% or bupivacaine 0.5%) into shoulder joint
Anterior dislocation reduction techniques: o
Scapular m anipulation:
Patient seated, traction to arm in horizontal plane, countertraction with other hand on clavicle
Second person adducts tip of scapula m edially, m oving glenoid fossa
o
Stim son:
Patient in prone position with arm dangling over side, hang 10–15 lb around wrist; m uscle fatigued over 20–30 m inutes
Pa ge 4 3 3
o
Can concurrently use scapular m anipulation
Only one person required
Traction/Countertraction:
Patient in supine position with continuous longitudinal traction to affected arm
Countertraction from sheet wrapped around chest
Arm internally or externally rotated if unsuccessful after several m inutes
o
External rotation:
Patient supine; elbow at 90°; gentle, slow external rotation of arm
Should be done slowly and with cooperative patient
Posterior dislocation reduction techniques: o
May use Stim son or traction/countertraction techniques with m anipulation of hum eral head anteriorly
Inferior dislocation (luxatio erecta) reduction techniques: o
Patient in supine position; gentle longitudinal traction to distract hum eral head
o
Gentle countertraction with sheet draped over trapezius and chest
o
Arm slowly rotated from 180–0°
Postreduction care: o
Post reduction film s
o
Place in sling and swath or shoulder im m obilizer im m ediately after reduction.
o
Shoulder should rem ain im m obilized for 2–3 weeks in young patients.
o
Im m obilization tim e should be less in older patients to avoid frozen shoulder.
Pa ge 4 3 3
Medication (Drugs)
Bupivacaine 0.5%: 20 cc intra-articular to shoulder
Diazepam : 5–10 m g IV (peds: 0.2 m g/kg)
Etom idate: 0.2 m g/kg IV (adult and peds)
Fentanyl: 50–100 µg IV (peds: 2–4 µg/kg)
Lidocaine 1%: 20 cc intra-articular to shoulder
Methohexital: 1–1.5 m g/kg IV (peds: not routinely used)
Midazolam : 2–5 m g IV (peds: 0.035–0.1 m g/kg)
Morphine: 2–8 m g IV (peds: 0.1 m g/kg)
Propofol: 1–2 m g/kg IV
Follow-Up Disposition Admission Criteria
Failure to reduce shoulder m ay require adm ission for reduction under general anesthesia or open reduction.
Patients with neurovascular com prom ise
Discharge Criteria
Patients with successful reductions, confirm ed by plain film s, m ay be discharged with shoulder in appropriate im m obilizer and with orthopaedic follow-up.
Recurrent dislocation m ay require elective surgery.
Patients with residual neuropraxia from injury or m anipulation m ay be safely discharged with instructions that m ost sym ptom s will resolve, but should have neurology follow-up.
Pa ge 4 3 3
Issues for Referral
Patients with residual neuropraxia should be advised to see a neurologist.
Routine orthopaedic consultation should be advised with all successful reductions.
References 1. Hendey GW. Necessity of radiographs in the em ergency departm ent m anagem ent of shoulder dislocations. Ann Em erg Med. 2000;36(2):108–113. 2. Kahn J. The Role of Post-Reduction X-rays after Dislocation. Acad Em erg Med. 2001;8(5):521. 3. McNam ara RM: Reduction of anterior shoulder dislocations by scapular m anipulation. Ann Em erg Med. July 1993;22(7):1140–1144. 4. Perrron AD, et al. Acute com plications associated with shoulder dislocation at an academ ic Em ergency Departm ent. J Em erg Med. 2003;24(2):141–145. 5. Quillen DM, et al. Acute Shoulder Injuries. Am Fam ily Physician. 2004;70(10):1947–1954. 6. Ufberg JW, et al. Anterior Shoulder Dislocations: Beyond Traction-Countertraction. J Em erg Med. 2004;27(3):301–306.
Codes ICD9-CM 831.00 S43.0
Pa ge 4 3 3
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Sick Sinus Syndro m e
Sick Sinus
Syndrome David F. M. Brown Jennifer L. Chan
Basics Description Definition Dysfunction of the sinus node's autom aticity and conductivity to the atria
Mechanism
Caused by progressive degeneration of the cardiac conduction system
Characterized by periods of unexplained sinus node dysfunction leading to bradyarrhythm ias often without appropriate atrial or junctional escape rhythm s
Dysfunction from failure of im pulse generation or conduction to atrial tissue
Syndrom e includes: o
Chronic sinoatrial (SA) nodal dysfunction
o
Frequently depressed pacem akers
o
Arteriovenous nodal conduction disturbances
o
Sluggish return of SA nodal activity after DC
Pa ge 4 3 4
cardioversion
Etiology Intrinsic Causes
Sinus node fibrosis
Coronary artery or SA nodal artery disease
Cardiom yopathy
Hypertensive heart disease
Infiltrative cardiac or collagen vascular disease
Surgical traum a
Inflam m atory diseases: o
Rheum atic heart disease
o
Chagas
o
Pericarditis
Extrinsic Causes
Drugs: o
Beta-blockers, calcium -channel blockers, clonidine
o
Digoxin, am iodarone
o
Lithium , phenytoin
Autonom ically m ediated syndrom es
Hyperkalem ia/Hypokalem ia
Ischem ia
Hypothyroidism
Hypotherm ia
Hypoglycem ia
Sepsis/Infection
Pediatric Considerations Associated with m ajor cardiovascular surgical interventions (e.g., repair of transposition of the great vessels)
Pa ge 4 3 4
Diagnosis Signs and Symptoms History
Asym ptom atic
Palpitations/Fatigue
Syncope/Presyncope
Chest pain
Shortness of breath
Sudden death
Physical Exam
Bradycardia
Alternating bradycardia and atrial tachycardia
Altered m ental status
Cyanosis
Transient ischem ic attack/stroke
Tachypnea
Essential Workup
Ascertaining etiology
12-lead ECG
Chest radiograph
Tests Lab
Serum electrolytes (including m agnesium and calcium )
Cardiac m arkers
Digoxin level, if appropriate
Thyroid function testing
Imaging ECG:
Inappropriate sinus bradycardia
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Sinus pauses or sinus exit block
Atrial fibrillation with slow ventricular response
Prolonged pauses after cardioversion or carotid m assage
Bradyarrhythm ias m ay alternate with supraventricular tachydysrhythm ia.
Differential Diagnosis
Other bradyarrhythm ias
Electrolyte derangem ents
Medication toxicity: beta-blockers, calcium -channel blockers, clonidine, digoxin
Excessive vagal tone
P.1017
Treatment Pre Hospital
Advanced life support transport
Oxygen supplem entation
Cardiac m onitoring
Atropine if bradycardic and hem odynam ically unstable
Transcutaneous pacing for unstable patients
Initial Stabilization
Atropine if a bradydysrhythm ia is causing unstable signs/sym ptom s: angina, m ental confusion, or hypotension
Transcutaneous pacing if atropine unsuccessful
If this fails, em ergent transvenous pacing
ED Treatment
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Supraventricular tachydysrhythm ia alternating with bradycardia: o
Unstable:
Cardiovert
Anticipate subsequent profound bradycardia
o
Stable patients:
o
Cardiac m onitoring
Digoxin, diltiazem , verapam il, or m agnesium can be used
Any m edication m ay cause profound bradycardia.
Bradycardias: o
Discontinuation of m edications that alter sinus node function
o
Identifying other rem ediable causes of SA nodal depression
o
Warm ing in the setting of hypotherm ia as atropine m ay cause m yocardial instability
Anticoagulation patients with atrial fibrillation and bradycardia/tachycardia syndrom e.
Medication (Drugs)
Atropine: 0.5–1.0 m g IV/ET: o
Repeat q5m in as necessary, m ax. dose of 0.04 m g/kg (peds: 0.02 m g/kg, m inim um , 0.1 m g)
Diltiazem : 0.25 m g/kg IV over 2 m inutes followed in 15 m inutes by 0.35 m g/kg IV over 2 m inutes
Verapam il: 2.5–5 m g IV bolus over 2 m inutes o
May repeat with 5–10 m g q15–30m in m ax. 20 m g
o
Peds: Table o f C o ntents > Skin C ancer
Skin Cancer
Michael K. Doney
Basics Description
Basal cell carcinom a: o
Cells arise from epiderm is.
o
Most com m on skin cancer m ore than 75% of total
o
Most im portant risk factor is sun exposure.
o
Locally invasive without risk of distant m etastasis
Squam ous cell carcinom a: o
Second m ost com m on skin cancer
o
Most arise from precancerous actinic keratoses lesions.
o
Most im portant risk factor is sun exposure, especially sunburn.
o
Risk of regional lym ph node and distant m etastasis
Melanom a: o
Arises from m elanin-producing cells
o
Most im portant risk factor is sun exposure, especially sunburn.
o
Additional risk factors:
Multiple com m on m elanocytic nevi
Atypical nevi
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Im m unosuppression
Positive fam ily history
History of nonm elanom a skin cancer (basal cell or squam ous cell carcinom a)
o
Risk of regional lym ph node and distant m etastasis
Etiology Sun exposure
Diagnosis Signs and Symptoms
Basal cell carcinom a: o
Papule or nodule with waxy or pearly appearance
o
Central depression or erosion often present
o
May be single or m ultiple
o
Pigm ented form m ay be brownish or stippled
o
Usually painless
o
Rarely m etastasizes
o
May be locally invasive
o
Usually appears in sun-exposed areas of skin
Squam ous cell carcinom a: o
Characteristic lesion is raised, firm , keratotic papule or plaque.
o
Usually asym ptom atic but m ay be ulcerated and painful.
Melanom a: o
Pigm ented skin lesion
o
Features suggestive of m elanom a (the ABCDs of m elanom a):
Asym m etry (not regularly round or oval)
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Border irregularity (notched or poorly defined); Bleeding (spontaneous)
Color variegation (shades or com binations of brown, tan, red, white, or blue-black)
Diam eter exceeding 6 m m
o
Lesions rarely sym ptom atic unless ulcerated
o
Malignant m elanom a
Presentation related to affected organ system
Lym phangitic spread with local to regional lym phadenopathy
Typical visceral sites of hem atogenous spread include liver, lung, bone, and brain.
Essential Workup Suspicious lesions require biopsy, a procedure rarely done in ED.
Tests Lab
No specific testing is required.
Tests of liver enzym es and function are ordered if suspicion of m etastatic m elanom a exists.
Imaging
Chest radiograph m ay show pulm onary involvem ent by m etastatic m elanom a.
Head or body CT scan m ay show visceral involvem ent by m etastatic m elanom a.
Differential Diagnosis
For basal cell carcinom a: o
Squam ous cell carcinom a
o
Bowen disease
o
Actinic keratosis
o
Paget disease
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o
Benign nevus
o
Melanom a
P.1023
For squam ous cell carcinom a: o
Actinic keratosis
o
Basal cell carcinom a
o
Keratoacanthom a
o
Wart
For m elanom a: o
Atypical nevus
o
Com m on nevus
o
Actinic keratosis
o
Pigm ented basal cell carcinom a
o
Squam ous cell carcinom a
Treatment ED Treatment
No specific ED treatm ent
Treat com plications of visceral involvem ent by m etastatic m elanom a or locally invasive basal cell carcinom a.
Follow-Up Disposition Admission Criteria
Usually adm ission occurs only because of visceral
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involvem ent or invasive spread.
Adm ission is rarely required because of the lesions them selves.
Discharge Criteria Patients are generally discharged with advice on seeking additional consultation.
Issues for Referral Discharged patients should be advised to consult a derm atologist or experienced prim ary care physician.
References 1. Bernstein SC, Lim KK, Brodland DG, Heidelberg KA. The m any faces of squam ous cell carcinom a. Derm atol Surg. 1996;22(3):243–254. 2. Lear JT, Sm ith AG. Basal cell carcinom a. Postgrad Med J. 1997;41:538–542. 3. Marks R. An overview of skin cancers: incidence and causation. Cancer. 1995;75:607–612. 4. Rivers JK. Melanom a. Lancet. 1996;347:803–807. 5. Rubin AI, Chen EH, Ratner D. Basal-cell carcinom a. N Engl J Med. Novem ber 24, 2005;353(21):2262–2269.
Codes ICD9-CM 172.9 Malignant m elanom a of skin, site unspecified 173.9 Other m alignant neoplasm of skin, site unspecified
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Sleep Apnea
Sleep Apnea
Mark Sagarin
Basics Description
Airway closing at the level of nasopharynx or oropharynx during sleep: o
Decreased tone during REM sleep
o
Affects about 3% of m iddle-aged m en and about 1.5% of m iddle-aged wom en
o
Most patients are undiagnosed.
Groups at risk: o
Obese
o
Men
o
Age older than 40 years
o
Upper airway anom alies
o
Hypertrophy
o
Myxedem a (hypothyroidism )
o
Alcohol/Sedative abuse
o
Long-distance truck drivers
Associated illness: o
Various dysrhythm ias, particularly atrial fibrillation
o
Right and left heart failure
o
Myocardial infarction
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o
Stroke
o
Motor vehicle accidents
o
Hypertension poorly controlled by m edical therapies
Genetics Unknown
Etiology
Excessive soft tissue obstructs airway during sleep.
Sleep is disrupted, resulting in daytim e drowsiness.
Diagnosis Signs and Symptoms
Snoring in com bination with observed apnea
Daytim e drowsiness
Sleep disturbance
Irritability
Physical Exam
Hypertension, hypoxem ia
Obesity
Craniofacial anom alies
Enlarged tonsils
Elevated jugular veins (secondary to pulm onary hypertension)
Essential Workup
Pulse oxim etry
ECG
Chest radiograph
Sleep study (polysom nogram ): o
Required for diagnosis
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Never indicated as part of the em ergency evaluation
Tests Lab Consider arterial blood gas.
Imaging
Consider lateral neck soft-tissue radiograph to rule out other etiologies of upper airway obstruction.
Chest radiograph to assess other etiologies of hypoxem ia
Chest CT rarely indicated; consider prim arily to rule out pulm onary em bolism .
Diagnostic Procedures/Surgery
Polysom nogram establishes diagnosis: o
Not a consideration for ED m anagem ent
Various operative interventions have been tried: o
Most intend to reduce or bypass the excessive pharyngeal/airway resistance that occurs during sleep.
o
Varying levels of success; no good random ized trials
o
Not a consideration for ED m anagem ent.
Differential Diagnosis
Central sleep apnea: o
Neurologic, rather than obstructive, cause of apnea during sleep
Chronic obstructive pulm onary disease
Asthm a
Left heart failure
Prim ary pulm onary hypertension
Narcolepsy
Idiopathic hypersom nia
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Treatment Initial Stabilization Chin lift/jaw thrust m aneuver, oxygen as needed, oral or nasal airway devices
ED Treatment
Supplem ental oxygen as needed
Bag-valve m ask ventilation m ay be difficult.
Consider using two nasals and one oral airway, and a two-person technique to ensure a good seal. P.1025
Noninvasive ventilation with continuous positive airway pressure
May obviate need for intubation in setting of hypoxem ia or hypercarbia
Alert
Endotracheal intubation: o
Most patients have redundant soft tissue in the oropharynx and upper airway and thus m ay be difficult to intubate.
o
Consider and plan several possible m ethods of definitive airway control.
o
Have alternative laryngoscope blades and devices (laryngeal m ask airway, bougie) available.
o
Be prepared to perform cricothyroidotom y if necessary.
o
Use neurom uscular blockade only if successful oral intubation is reasonably likely and bag ventilation is
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easy. o
Sweep the tongue out of the way when perform ing laryngoscopy.
Positive end-expiratory pressure for ventilated patients
Medication (Drugs)
No specific m edications useful in ED to treat this chronic disorder
See Airway Managem ent for details on induction agents and neurom uscular blockade.
Follow-Up Disposition Admission Criteria
Ventilatory failure, especially if intubation was necessary
Hem odynam ic instability
Discharge Criteria
Maintenance of O 2 saturation >85% for several hours using oxygenation or ventilation equipm ent available to the patient at hom e
Very low likelihood of decom pensation overnight
Patients with sleep apnea who present after m otor-vehicle crashes: o
Manage initially like other blunt traum a patients.
o
Later, consider the increased risk with sleep apnea and intervene to prevent future accidents.
Issues for Referral
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Consider referral of patients with suspected sleep apnea to a pulm onologist.
Encourage weight loss and refer to a prim ary care physician for assistance with this.
Cardiology referral is appropriate when sleep apnea is com plicated by heart failure or dysrhythm ias.
References 1. Am erican Thoracic Society. Sleep apnea, sleepiness, and driving risk. Am J Respir Crit Care Med. 1994;150[Suppl 5, Pt 1]:1463–1473. 2. Caples SM, Gam i AS, Som ers VK. Obstructive sleep apnea. Ann Intern Med. Febraury 1, 2005;142(3):187–197. 3. den Herder C, Schm eck J, Appelboom DJ, de Vries N. Risks of general anaesthesia in people with obstructive sleep apnea. BMJ. 2004;329(7472):955–959. 4. Fuchs BD, McMaster J, Sm ull G, et al. Underappreciation of sleep disorders as a cause of m otor vehicle crashes. Am J Em erg Med. 2001;19(7):575–578. 5. Gibson GJ. Obstructive sleep apnea syndrom e: underestim ated and undertreated. Br Med Bull. 2005;72:49–65. 6. Hillm an DR, Loadsm an JA, Platt PR, Eastwood PR. Obstructive sleep apnea and anaesthesia. Sleep Med Rev. Decem ber 2004;8(6):459–471. 7. Hudgel DW. Treatm ent of obstructive sleep apnea. Chest. 1996;109:1346–1358. 8. Hung J, Whitford EG, Parsons RW, et al. Association of sleep apnoea with m yocardial infarction in m en. Lancet. 1990;336(8710):261–264. 9. Man GCW. Obstructive sleep apnea: diagnosis and treatm ent. Med Clin North Am . 1996;80(4):804–820. 10. McDonald JP. A review of surgical treatm ent for obstructive sleep apnoea/hypopnoea syndrom e. Surgeon. October
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2003;1(5):259–264. 11. Obenza Nishim e E, Liu LC, Coulter TD, et al. Heart failure and sleep-related breathing disorders. Cardiol Rev. 2000;8(4):191–201. 12. Parish JM, Som ers VK. Obstructive sleep apnea and cardiovascular disease. Mayo Clin Proc 2004;79(8):1036–1346. 13. Strollo PJ, Rogers RM. Obstructive sleep apnea. N Engl J Med. 1996;334(2):99–101. 14. Victor LD. Obstructive sleep apnea. Am Fam Physician. 1999;60(8):2279–2286. 15. Wright J, White J. Continuous positive airways pressure for obstructive sleep apnoea. Cochrane Database Syst Rev. 2000;(2):CD001106. 16. Young T, Peppard PE, Gottlieb DJ. Epidem iology of obstructive sleep apnea: a population health perspective. Am J Respir Crit Care Med. 2002;165(9):1217–1239. 17. Young T, Skatrud J, Peppard PE. Risk factors for obstructive sleep apnea in adults. JAMA. 2004;291(16):2013–2016.
Codes ICD9-CM 780.57
ICD10 G47.3
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Slipped C apital F em o ral Epiphysis
Slipped
Capital Femoral Epiphysis Judd L. Glasser
Basics Description
Fem oral epiphysis translates, or “slips,― relative to the fem oral head/neck.
Classified: o
Degree of displacem ent:
(Mild, grade 1) one-half translation
Tem poral:
Acute (3 weeks of sym ptom s)
Peak age at onset 13–15 years for boys and 11–13 years for girls
Most patients are obese.
Male patients predom inate (8:3).
Approxim ately one third of cases involve bilateral joint.
Etiology
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True etiology rem ains elusive.
Association with endocrine abnorm alities: o
Especially hypothyroidism and treatm ent with growth horm one
Diagnosis Signs and Symptoms
Presents with lim p or exertional lim p
Pain in the knee, thigh, groin, or hip (referral of pain along the obturator nerve): o
Vague and dull for weeks in chronic slipped capital fem oral epiphysis (SCFE)
o
Severe and sudden onset in an acute SCFE
Com m only presents with the leg externally rotated
Flexion is restricted (cannot touch thigh to abdom en).
History
May present with chronic hip pain with exertion
May have acute pain following m inor traum a
May have acute on chronic pain
Physical Exam
Observe resting position of the leg.
If suspicion of SCFE, do not am bulate the patient.
Tests Lab Without diagnostic radiographic abnorm ality, the practitioner should consider the following tests to help risk stratify possible alternative diagnoses:
CBC with differential
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Sedim entation rate
C-reactive protein
Imaging
Anteroposterior and frog-leg lateral radiograph film s of both hips should be obtained: o
Widened or irregular physis
o
Bird's beak appearance of the actual slipping of the epiphysis off of the fem oral head
Klein line (line drawn parallel lateral fem oral neck does not transect epiphysis)
Differential Diagnosis
Legg-Calve-Perthes: o
Typically seen in 4–9-year-old age range
Septic arthritis of hip
Osteom yelitis
Toxic Synovitis
Fem ur or pelvic fractures
P.1027
Treatment Pre Hospital Patient should be im m obilized for transport, as with suspected hip fracture or dislocation.
Initial Stabilization
Im m obilize hip.
Keep non–weight-bearing.
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Do not attem pt reduction.
ED Treatment
SCFE is an urgent orthopaedic condition; delay in diagnosis m ay lead to chronic irreversible hip joint disability.
Consult orthopaedics im m ediately for definitive im m obilization or operative intervention.
Medication (Drugs) Pain m anagem ent is appropriate; avoid PO m edications, as often acute SCFE m ay be m anaged with em ergent surgical fixation.
Follow-Up Disposition Admission Criteria
Patients with acute or acute on chronic (unstable) SCFE require orthopaedic adm ission for urgent operative fixation (usually single central pinning).
Chronic SCFE m ay be m anaged with delayed operative fixation.
Discharge Criteria
None
It is too difficult to achieve com plete non–weight-bearing status, which is required to prevent further slippage, avascular necrosis, and chondrolysis
References 1. Aronsson DD, Loder RT. Treatm ent of the unstable (acute) slipped capital fem oral epiphysis. Clin Orthop Related Res. 1996;322:99110.
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2. Causey AL, Sm ith ER, Donaldson JJ, et al. Missed slipped capital fem oral epiphysis: illustrative cases and a review. J Em erg Med. 1995;13(2):175–189. 3. Loder RT. Slipped capital fem oral epiphysis. Am Fam Physician. 1998;57(9):2135–2142 4. Uglow MG, Clarke NMP. The m anagem ent of slipped capital fem oral epiphysis. J Bone and Joint Sur. 2004;86-B:631–635.
Codes ICD9-CM 732.2
ICD10 M93.9
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Sm all-Bo w el Injury
Small-Bowel
Injury Barry J. Knapp II
Basics Description
Penetrating: visceral injury (96% gunshot wound, 50% stabbing)—serosal tear, bowel wall hem atom a, perforation, bowel transection, m esenteric hem atom a/vascular injury
Blunt: o
Mortality rate from sm all bowel injury is 33%.
o
Deceleration injury at fixed points (e.g., ligam ent of Treitz)
o
Shearing m echanism s near fixed points (e.g., ileocecal junction, adhesions)
o
Com pressive force against anterior spine
o
Bursting or “blowout― at antim esenteric m argin from sudden closed-loop intralum inal pressure rise
o
Mesenteric tears m ay initially be asym ptom atic.
Associated injuries: o
Liver and splenic lacerations; thoracic and pelvic
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fractures o
Seatbelt syndrom e: abdom inal wall ecchym osis, sm all bowel injury; chance fracture of L1, L2
Etiology
Penetrating: o
Sm all bowel is the second m ost com m only injured organ (32%) in anterior abdom inal stabbing.
o
Sm all-bowel injury is m ost com m on in gunshot wounds (49%).
o
About 80% of sm all-bowel injuries are caused by gunshot wounds, 60% by stab wounds.
Blunt: o
Third m ost com m only injured organ (5–10% of all blunt traum a victim s)
o
Lap belts
o
Motor vehicle accidents
o
Nonvehicular traum a: abuse/assault, bicycle handlebars, large-anim al kick
Pediatric Considerations
Penetrating: air-gun accidents at close range (100,000/m m 3
o
Lavage am ylase >20 IU/L and leukocyte count >500/m m 3 (late m arkers of sm all-bowel injury)
o
Lavage m icroscopy for succus/vegetable m atter/feces is specific for sm all-bowel injury but not sensitive.
o
Lavage alkaline phosphatase (>3 IU/L) is reported to be a useful im m ediate m arker of sm all-bowel injury.
Laparoscopy: plays a key role in diagnosing sm all-bowel injury in stable patients with progressive signs or sym ptom s
P.1029
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Differential Diagnosis
Hem operitoneum owing to vascular insult
Solid visceral organ injury or gastric/colon/rectum perforation
Vertebral injury and associated ileus
Pediatric Considerations Delay in diagnosis of 1–2 days is com m on and m ay increase m orbidity.
Treatment Pre Hospital Alert
Patients should be transported to the nearest traum a center.
Do not attem pt to replace eviscerated abdom inal contents; cover with m oist gauze, blanket, and transport.
Do not rem ove im paled objects in the abdom en; stabilize the object with gauze and tape and transport.
Initial Stabilization
Standard advanced traum a life support protocols, including airway, breathing, and circulation m anagem ent
Aggressive fluid resuscitation, central line suggested with pressure infusion of warm ed intravenous fluid (lactated Ringer solution or norm al saline)
Decom pression using a nasogastric tube, then CT contrast adm inistration, as indicated
Cover eviscerated sm all bowel with m oist gauze; do not rem ove im paled foreign body in ED.
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ED Treatment
Im m ediate transfer to operating room is required for patients with an indication for laparotom y: o
Evisceration
o
Abdom inal pain with hypotension
o
Positive diagnostic peritoneal lavage or abdom inal CT
o
Thoracic abdom inal herniation visualized on chest radiograph
o
Im paled foreign body
o
Penetrating gunshot wound to the abdom en
o
Tetanus and antibiotic prophylaxis for penetrating abdom inal wounds and blunt injury requiring surgical exploration
Local wound exploration is safe for abdom inal stab wounds.
Serial abdom inal exam inations and observation for otherwise stable patients
Judicious analgesia as blood pressure perm its after diagnosis is established
Medication (Drugs)
Cefotetan (Cefotan): 1–2 g (peds: 20 m g/kg) IV or
Cefoxitin (Mefoxin): 1–2 g (peds: 40 m g/kg) IV or
Ceftizoxim e (Cefizox): 1–2 g (peds: 50 m g/kg) IV plus
Flagyl: 500 m g (peds: 7.5 m g/kg) IV
Follow-Up Disposition
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Admission Criteria
Indication for laparotom y
Abnorm al m ental status/intoxication with abdom inal injury
Presence of abdom inal pain, tenderness (even with a negative work-up) m andates adm ission for observation and serial exam s.
Stab and gunshot wounds that violate the abdom inal fascia, positive diagnostic peritoneal lavage, or worsening findings on clinical exam
Discharge Criteria
Minim al m echanism blunt traum a in a sober patient with norm al exam result who has no abdom inal pain and will receive adequate follow-up
Explicit discharge instructions to return for worsening signs/sym ptom s are im portant to identify those with unsuspected injury.
Penetrating wounds that do not violate abdom inal fascia
References 1. ACEP Policies Com m ittee. Critical Issues in the evaluation of adult patients presenting to the em ergency departm ent with acute blunt abdom inal traum a. Ann Em erg Med. 2004;43(2):278–290. 2. Fakhry SM, Brownstein M, Watts DD, et al. Relatively short diagnostic delays ( Table o f C o ntents > Sm o ke Inhalatio n
Smoke Inhalation
Trevonne M. Thompson
Basics Description
Suspect sm oke inhalation in anyone involved in a fire within a closed space or with a history of loss of consciousness.
May cause direct injury to the upper (supraglottic) airway structures
May cause chem ical/irritant effect to lower airway structures
May cause system ic toxicity from inhaled substances
Etiology
Direct heat injury from heated gases/sm oke: o
Lim ited to supraglottic structures because of the heat dissipating properties of the upper airway
Irritant effect from sm oke com ponents: o
Acid and aldehyde gases
o
Oxidants
System ic toxicity from inhaled cellular toxins: o
Carbon m onoxide
o
Hydrogen cyanide
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Alert
Inhalation of steam can be rapidly fatal: o
Steam has approxim ately 4,000 tim es the heat-carrying capacity of hot air.
o
Can rapidly cause obstructive glottic edem a, therm ally induced tracheitis, and hem orrhagic edem a of the bronchial m ucosa
Diagnosis Signs and Symptoms History Exposure to a fire or heavy sm oke
Typically in a confined space
Maintain high index of suspicion with history of loss of consciousness
Physical Exam
May have a norm al physical exam ination with sym ptom s developing during the 24-hour interval following exposure
Upper airway (supraglottic): o
Nasopharyngeal irritation
o
Hoarseness
o
Stridor
o
Cough
Lower airway: o
Chest discom fort
o
Hem optysis
o
Bronchospasm
o
Bronchorrhea
May have sym ptom s and signs of carbon m onoxide and/or
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cyanide toxicity
Alert
The following signs are suggestive of significant inhalation injury: o
Facial and upper cervical burns
o
Carbonaceous sputum
o
Singed eyebrows and nasal vibrissae
Essential Workup
Pulse oxim etry: o
May be falsely elevated in cases of carbon m onoxide exposure
Arterial blood gas m easurem ent: o
Hypoxia
o
Metabolic acidosis in cases of carbon m onoxide or hydrogen cyanide
Chest radiography: o
Initial radiograph typically norm al
o
May show signs of pulm onary injury over the next 24 hours
Tests Lab
Electrolytes, blood urea nitrogen, creatinine, glucose
CBC
Coagulation profile
Creatine phosphokinase: o
Carboxyhem oglobin: o
When clinically indicated in burn patients
To evaluate for potential carbon m onoxide exposure
Cyanide level: o
In suspected cases of cyanide exposure, do not wait
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for the level before initiating therapy. o
May send lactate level as a m arker of cyanide toxicity
Pregnancy test
Imaging Bronchoscopy and radionuclide scanning m ay be done to evaluate extent of injury:
Typically not done in the ED
P.1031
Diagnostic Procedures/Surgery
Peak expiratory flow rate: o
Low peak flow associated with m ore severe injury
PaO 2 /FiO 2 ratio: o
A ratio of Table o f C o ntents > Spider Bite, Black Wido w
Spider Bite,
Black Widow Paul Arnold
Basics Description Syndrom es caused by envenom ation by black widow spider bite
Mechanism
Venom s contain potent neurotoxins: o
Disrupt presynaptic nerve term inal m em branes causing neurotransm itter release at the neurom uscular junction (acetylcholine) and in autonom ic and cortical tissues (norepinephrine)
o
Initially, postsynaptic term inals are overstim ulated, then blockaded, and neurotransm itters rapidly becom e depleted.
Morbidity and m ortality are dose dependent.
Severity of envenom ation depends on: o
Prem orbid health of victim :
Hypertension or cardiovascular disease increase risk
o
Size and age of victim :
Children (i.e., sm aller size for a given dose of
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venom ) are at greater risk of m orbidity and m ortality. o
Num ber of bites
o
Location of bite wounds
o
Size and condition of spider
Etiology Black widow spider features:
Appearance: o
Black with red m arkings shaped like an hourglass or a pair of spots on the ventral aspect of the globular abdom en
o
Fem ales have 25- to 50-m m leg spans and 15-m m -long bodies.
Found throughout North Am erica, except the far north and Alaska
Prefer dark, cozy hideaways outdoors and close to the ground
Most bites occur during the warm er m onths when spiders are defending their webs and egg clutches.
Fem ales are responsible for hum an envenom ations.
Diagnosis Signs and Symptoms History
History of spider bite very unreliable and species usually not identified
Local com plaints: o
Pain:
Sharp or burning at the site
Pa ge 4 4 1
Onset within m inutes of the bite
Usually resolves spontaneously after a few m inutes or hours
May becom e worse and spread proxim ally from the bite
System ic com plaints: o
Onset within 20–30 m inutes of bite
o
Neurologic:
Painful m uscle cram ps and spasm s
Entire body m ay becom e progressively involved or sym ptom s m ay rem ain regional.
Arm bites m ay lead to arm and chest m uscle tightness and dyspnea.
Leg bites m ay lead to abdom inal pain and leg spasm s.
o
Cutaneous dysesthesia and hyperesthesia
o
Perspiration, nausea, vom iting, tachycardia
o
Abdom inal pain
o
Restlessness, headache, agitation, and a sense of im pending death
Physical Exam
Skin findings: o
Often there is nothing to see or palpate at the wound site but any or all of the following m ay be observed:
Two pinpricks from the spider's fangs
Tender and blanched skin with surrounding erythem a (“target lesion―)
Urticaria
Piloerection
Swelling
Local sweating
Neurologic findings:
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o
Tetanic contractions of extrem ities with trem ors
o
Spasm and rigidity in the thighs and abdom en
o
Autonom ic instability with diaphoresis, nausea, vom iting, tachycardia or bradycardia
Less com m on system ic findings: o
Fever
o
Hypertension
o
Arrhythm ias
o
Dyspnea
o
Pulm onary edem a
o
Seizures
o
Shock
o
Acute toxic psychosis
Course
Rarely fatal
In m ost untreated patients, sym ptom s peak after 2–3 hours and then begin to resolve, occasionally recurring episodically over the following few days.
In otherwise healthy adults, com plete resolution of sym ptom s occurs within 2–3 days.
Persistent neurologic sym ptom s can last weeks to m onths: o
Fatigue
o
Generalized weakness or m yalgias
o
Paresthesias
o
Headache
o
Insom nia
o
Im potence
o
Polyneuritis
Essential Workup Diagnosis is based on:
Clinical presentation
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Careful inquiry to elicit the spider bite history
Identification of the spider (if it has been caught)
Tests Lab
No specific blood tests for black widow spider venom
WBC can be m ildly elevated but is usually norm al.
Electrolytes, glucose, calcium , blood urea nitrogen, creatinine, am ylase, liver function tests, creatinine kinase, troponin, pregnancy test, and prothrom bin tim e/partial throm boplastin tim e tests o
Appropriate to assess abdom inal or chest pain and rule out alternative diagnoses
o
Usually norm al
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ABGs in rare cases with pulm onary edem a
ECG and cardiac m onitoring for: o
Elderly
o
Presence of chest pain, unstable vital signs or dysrhythm ias
Imaging
Chest radiograph for respiratory com plaints
Abdom inal im aging to rule out other causes of pain
Diagnostic Procedures/Surgery Calcium gluconate infusion considered by som e to be a good diagnostic test due to dram atic but tem porary relief it provides
Differential Diagnosis
A high fever and WBC count should prom pt consideration of alternatives to spider bites (e.g., infection).
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Acute surgical abdom en (e.g., appendicitis, cholecystitis, pancreatitis): o
Black widow spider victim s are restless instead of quiet (the posture favored by m ost patients with peritoneal irritation).
o
The abdom inal wall rigidity is also unexpectedly nontender.
Sym pathom im etics (e.g., cocaine, am phetam ines): o
Tetanic m uscle contractions uncom m on in conscious, nonseizing sym pathom im etic toxicity patients
Muscular injury or strain
Hypertensive em ergency
Myocardial infarction
Treatment Pre Hospital
Im m obilize the wound site and apply cool com presses or ice for com fort during transport to hospital.
Supportive m easures (analgesics, anxiolytics) m ay be required for patients with system ic sym ptom s.
Venom extraction devices (e.g., Sawyer extractor) have been recom m ended anecdotally but are probably ineffective if >10 m inutes has elapsed since the bite.
Alert Every effort should be m ade by caregivers at the scene to find and bring in the responsible spider for identification.
Initial Stabilization
ABCs: o
Support airway and respiration if pulm onary edem a
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is present o
Stabilize dysrhythm ias
Control seizures
ED Treatment
Cleanse the bite site thoroughly.
Tetanus prophylaxis
Benzodiazepines for agitation and restlessness
Antiem etics for nausea and vom iting
Analgesics
Muscle cram ps/spasm therapy—com binations of the following work synergistically: o
Benzodiazepines
o
Narcotics
o
Calcium gluconate:
Com m only advocated but consensus is lacking on its utility
May provide dram atic but tem porary relief
Effects m ay be transient and m ultiple doses m ay be required
Antihypertensive agents for sym ptom atic hypertension
Specific antivenin: o
Indications:
Younger than 16 years or older than 65 years or prem orbid com prom ised health status
Sym ptom s do not respond to sym ptom atic m easures.
Significant hypertension
Respiratory distress
Sym ptom atic and pregnant
Consider using for persistent sym ptom s even several days after envenom ation.
o
Always perform a skin test for sensitivity to horse
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serum first (test kit included in the antivenin package). o
Watch for hypersensitivity reaction in first 20 m inutes:
o
Consider pretreatm ent with antihistam ines.
Due to the sm all quantity of antivenin used, if serum sickness reactions occur, they are usually m ild.
o
Effectiveness is usually apparent within 2 hours of the first treatm ent and repeated doses are rarely necessary.
o
Antivenin probably helps to prevent persistent neuropathic sym ptom s and m ay be worth considering for that indication even if the acute stage illness is m ild.
Medication (Drugs)
Antivenin: 1 am pule (2.5 m L) diluted into 50 m L NS (peds: sam e dose) IV over 1 hour
Calcium gluconate: 10–20 m L of 10% solution IV q2h–q4h PRN
Morphine sulfate: 2–10 m g (peds: 0.1 m g/kg) IV or IM PRN (titrate to patient response)
Follow-Up Disposition Admission Criteria
Elderly, pregnant or sym ptom atic young patients
Significant cardiovascular sym ptom s and signs, or severe
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hypertension, particularly in presence of prem orbid cardiac disease or chronic hypertension
Respiratory distress or pulm onary edem a
Persistent sym ptom s not responding to aggressive m anagem ent and specific antivenin
Discharge Criteria
Asym ptom atic patients with no positive identification of a black widow spider can be released after observation for 1 to 2 hours.
Asym ptom atic patients with no com orbid illness with a positive identification of the black widow spider should be observed for a m inim um of 4 to 6 hours and discharged if their condition does not change.
All discharged patients m ust be instructed about what to watch for in term s of relapsing sym ptom s and to seek appropriate follow-up if needed.
Discharged patients who received antivenin should be instructed to watch for signs of serum sickness.
References 1. Allen C. Arachnid envenom ations. Em erg Med Clin North Am . 1992;10(2):288–291. 2. Boyer Hassen LV, McNally JT. Spider bites. In: Auerbach PS, ed. Wilderness m edicine: m anagem ent of wilderness and environm ental em ergencies. 3rd ed. St. Louis, MO: Mosby Year Book, 1995:769–786. 3. Clark MD, et al. Clinical presentation and treatm ent of black widow spider envenom ation: a review of 163 cases. Ann Em erg Med. 1992;21(7):782–787. 4. Isbister GK, White J. Clinical consequences of spider bites: recent advances in our understanding. Toxicon. 2004;43:477–492.
Codes
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ICD9-CM 989.5
ICD10 T63.3
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Spider Bite, Bro w n Recluse
Spider Bite,
Brown Recluse Paul Arnold
Basics Description Local or system ic illness caused by brown recluse spider bite envenom ation
Etiology Brown recluse spider features:
Appearance: o
Delicate body and legs spanning 10 to 25 m m
o
Light- to m edium -brown with darker violin-shaped m arking visible on the upper aspect of the head
o
Three pairs of eyes
Found widely throughout the southern half of North Am erica
Habitat: typically any warm and dry location indoors or outdoors such as wood piles, bundles of rags, cellars, or attics
Spider not aggressive
Hum ans are bitten when they disturb a spider in its habitat.
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Mechanism
Venom is a com plex cocktail of enzym es and peptides: o
Causes hem olysis and tissue necrosis
o
Triggers com plem ent cascades, platelet aggregation, throm bosis, and release of inflam m atory m ediators.
o
Result is direct cytotoxic effects, coupled with indirect toxicity due to inflam m ation and vascular com prom ise.
System ic toxicity is due to an inflam m atory or allergic response to venom antigenic properties.
Toxicity proportional to: o
The am ount of venom and
o
The am ount of venom relative to the size of patient
Pediatric Considerations Children are m ore vulnerable to a given am ount of venom than healthy adults.
Diagnosis
Rem em ber the lim ited range of brown recluse spiders and the rarity of arachnidism as a cause of necrotic skin wounds.
Diagnosis m ust be based not only on the clinical presentation but also on a reliable history of spider bite.
In the absence of a reliable spider bite by history, other possible diagnoses m ust be carefully sought and excluded.
Signs and Symptoms History
Local wound sym ptom onset: o
Typically delayed 1–24 hours after bite
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o
Usually asym ptom atic but m ay experience m inor stinging and burning sensation
System ic features: o
Rare com plication
o
Develop during the first 1–3 days after the bite
o
Severity is proportional to the am ount of venom injected.
o
Patient m ay report:
Fever, chills, m alaise
Nausea, vom iting, diarrhea
Myalgias, m uscle cram ps, arthralgias
Petechial or urticarial rash
Physical Exam
Bite wound: o
Usually no visible injury if exam ined within first 1–3 days
o
Less com m only, there m ay be pinprick, local blanching and induration, or erythem a.
o
Tissue injury m ay develop at bite site:
Blister m ay form in the center of the blanched area with circum ferential erythem a.
Blister m ay gradually enlarge and darken with the developm ent of skin and subcutaneous fat necrosis over 3–4 days.
Necrosis develops m ost extensively where subcutaneous fat is greatest.
Lower extrem ity blisters spread distally under the influence of gravity.
Local response is not dependent on the extent of envenom ation and cannot be used to predict the severity of subsequent system ic illness.
Other:
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o
Exam ination is otherwise usually unrem arkable.
o
Patient m ay have petechial or urticarial rash.
Course
Skin lesions: o
Vast m ajority of patients recover fully with no sequelae.
o
Lesions rarely evolve into ulcerative necrosis over the following days or weeks.
o
Healing by secondary intention m ay take weeks to m onths.
o
Ulcers can recur even years later.
Rare com plications include: o
Hem olysis, which m ay lead to hem oglobinuria and acute renal failure
o
Dissem inated intravascular coagulation
o
Shock
Essential Workup Careful inquiry required to elicit the spider bite history
Tests Lab
Spider venom can be detected in skin lesions, but widespread clinical testing is not available yet.
CBC, electrolytes, blood urea nitrogen, creatinine, prothrom bin tim e/partial throm boplastin test for baseline m onitoring
Urinalysis for evidence of system ic hem olysis
Imaging Soft-tissue radiograph of bite site is indicated if the differential includes suspected gas-form ing organism , infection of ulcers.
Differential Diagnosis
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Necrotic ulcers: o
Soft-tissue infection
o
Neoplastic lesion
o
Lym e disease
o
Cutaneous anthrax
o
Other arachnid envenom ation
o
Stevens-Johnson syndrom e
o
Erythem a nodosum
o
Diabetic ulcer
o
Bed sore
o
Lower-lim b vascular insufficiency with secondary ulcer
o
Chem ical burn
Other etiologies of hem olytic anem ia, DIC, anaphylactoid reactions
P.1037
Treatment Pre Hospital
Im m obilize wound site.
Cover bite with cool com presses.
Transport to hospital when patient experiences im m ediate onset of sym ptom s.
Supportive m easures for patients with system ic sym ptom s
Venom extraction devices (e.g., Sawyer extractor) have been recom m ended anecdotally but are probably ineffective if >10 m inutes has elapsed since bite.
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Alert Every effort should be m ade by caregivers at the scene to find and bring in the responsible spider for identification.
Initial Stabilization IV fluids, oxygen, cardiac m onitoring if the patient is experiencing system ic collapse
ED Treatment
Cleanse the bite site thoroughly
Tetanus prophylaxis
Antibiotics: o
Appropriate if wound appears infected
o
Not indicated prophylactically
o
Antistaphylococcal (first-generation cephalosporin or penicillinase-resistant penicillins)
Controversial and unproven m easures include: o
Topical or system ic steroids
o
Hyperbaric therapy
o
Topical nitroglycerin
o
Local electric shock
o
Dapsone:
Screen for G6PD deficiency before initiating
Monitor for m ethem oglobinem ia, hem olysis, and leukopenia during therapy.
o
Excision of necrotic wound:
Not indicated in the first 8 weeks because m ay cause m ore severe ulcer form ation
o
Can be considered at a later date
Specific antivenin is of proven benefit if system ic toxicity develops but is of debatable value if only a skin lesion is present.
System ic problem m anagem ent:
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o
Standard supportive care and interventions should be em ployed for shock, seizures, DIC, and com a
o
Analgesics for pain control
o
Hem oglobinuria:
Treated with IV fluids and alkalinization
Monitor renal, fluid, and electrolyte status
Transfusion for significant anem ia
o
Dialysis in the event of acute renal failure
o
Specific antivenin:
Therapeutic value reduced if given >4 to 6 hours after envenom ation (m ost cases present m ore than 6 hours after presum ed bite)
Before use, weigh low m ortality of brown recluse bites against risk of side effects of antivenin.
Always perform a skin test for sensitivity to horse serum beforehand.
Watch for hypersensitivity reaction in first 20 m inutes.
Pretreat with antihistam ines.
Due to sm all dose of antivenin, risk of serum sickness is low.
Medication (Drugs)
Antivenin: 1 am pule (2.5 m L) diluted into 50 m L NS (peds: sam e dose) IV over 1 hour
Dapsone: progressive dosage of 50–500 m g b.i.d. for 2 weeks (peds: 2 m g/kg/24 h PO for 2 weeks)
Methylprednisolone: 125 m g IV bolus followed by prednisone 30–50 m g/d for 5 days (peds: m ethylprednisolone 1–2 m g/kg IV, prednisone 1–2
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m g/kg PO)
Morphine sulfate: 2–10 m g (peds: 0.1 m g/kg) IV or IM PRN
Pediatric Considerations
Use dapsone only in severe cases because of potential for side effects such as: o
Hepatitis
o
Methem oglobinem ia
o
Hem olytic anem ia
o
Leukopenia
Follow-Up Disposition Admission Criteria
Significant local reaction, signs of system ic toxicity, reaction to antivenin
Lower threshold for children, patients with com orbidities
Discharge Criteria
No evidence of system ic toxicity or severe progression of local wound necrosis after envenom ation
Daily reassessm ent, including blood work, until 3 to 4 days after envenom ation to guard against the risk of system ic toxicity.
Patients should be advised about prolonged course for skin healing with consideration for surgical excision after 8 weeks.
Pediatric Considerations Longer observation period before disposition of asym ptom atic cases
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because of the higher m ortality in this population
References 1. Henrique da Silva P, et al. Brown spiders and loxoscelism . Toxicon . 2004;44:693–709. 2. Isbister GK, White J. Clinical consequences of spider bites: recent advances in our understanding. Toxicon. 2004;43:477–492. 3. Krywko DM, Gom ez HF. Detection of Loxosceles Species Venom in Derm al Lesions: A Com parison of 4 Venom Recovery Methods. Ann Em erg Med. 2002;39:475–480. 4. Mold JW, Thom pson DM. Managem ent of Brown Recluse Spider Bites in Prim ary Care. J Am Board Fam Pract. 2004;17:347–352. 5. Swanson DL, Vetter RS. Bites of Brown Recluse Spiders and Suspected Necrotic Arachnidism . New Eng J Med. 2005;352:700–707. 6. Vetter RS, Bush SP. The Diagnosis of Brown Recluse Spider Bite Is Overused for Derm onecrotic Wounds of Uncertain Etiology. Ann Em erg Med. 2002;39:544–546.
Codes ICD9-CM 989.5
ICD10 T14.0
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Spinal C o rd Syndro m es
Spinal Cord
Syndromes Judd L. Glasser
Basics Description
Anterior cord syndrom e: o
Results from flexion or axial loading m echanism or direct cord com pression from vertebral fractures, dislocations, disc herniation, tum or, or abscess
o
Rarely caused by laceration or throm bosis to the anterior spinal artery
Brown-Séquard syndrom e: o
Hem isection of the spinal cord classically as a result of a penetrating wound
o
Rarely unilateral cord com pression
Central cord syndrom e: o
Most com m only occurs in elderly patients who have pre-existing cervical spondylosis and stenosis
o
Forced hyperextension causes buckling of the ligam entum flavum , creating a shearing injury to the central portion of the spinal cord.
Dorsal cord syndrom e:
Pa ge 4 4 2
o
Associated with hyperextension injuries
Com plete cord syndrom e: o
Blunt or penetrating traum a that results in com plete disruption of spinal cord
o
Sym ptom s that rem ain >24 hours generally are perm anent.
Etiology Spinal cord syndrom es result from localized disruption of neurotransm ission and exhibit m ixed m otor and sensory deficits. The m ost com m on m echanism is traum a:
Patients with arthritis, osteoporosis, m etastatic disease, or other chronic spinal disorders are at risk of developing spinal injuries as the result of even m inor traum a.
Diagnosis Signs and Symptoms History Acute loss of m otor and or sensory function usually following a traum atic event
Physical Exam
Anterior cord syndrom e: o
Bilateral spastic paralysis and loss of pain and tem perature sensation below the level of the lesion
o
Preservation of dorsal colum n function (proprioception and position sense)
Brown-Séquard syndrom e (lateral cord syndrom e): o
Ipsilateral spastic paresis and loss of dorsal colum n function (proprioception and position sense)
o
Contralateral loss of pain and tem perature sensation
Pa ge 4 4 3
o
Deficits usually begin two levels below the injury
Central cord syndrom e: o
Loss of m otor function affects upper extrem ities m ore severely than lower extrem ities.
o
Most profound deficits occur in the distal upper extrem ities.
o
Sensory loss is m ore variable.
Dorsal cord syndrom e: o
Loss of proprioception, position sensation, and coordination below the level of the lesion
Com plete cord syndrom e: o
Flaccid paresis below the level of the injury
o
Low blood pressure and heart rate, flushed skin, priapism m ay be present (loss of sym pathetic tone).
Sensory deficit levels: o
C-2—occiput
o
C-4—clavicular region
o
C-6—thum b
o
C-8—little finger
o
T-4—nipple line
o
T-10—um bilicus
o
L-1—inguinal region
o
L-5—dorsum of the foot
o
S-5—perianal area
Motor deficit levels: o
C-5—elbow flexion
o
C-7—elbow extension
o
C-8—finger flexion
o
T-1—finger abduction
o
L-2—hip flexion
o
L-3—knee extension
o
L-4—ankle dorsiflexion
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o
S-1—ankle plantar flexion
Tests Lab
Basic pre-operative laboratory studies are indicated.
Consider sed rate and C-reactive protein to risk-stratify other potential diagnoses.
Imaging
All areas of clinical suspicion should be im aged with plain radiographs.
CT of the spine when plain film s are norm al or am biguous: o
CT allows assessm ent of the spinal canal and any im pingem ent by bone fragm ents.
MRI is the im aging m odality of choice for detection of spinal cord dam age; in the acute setting, the indications for MRI are: o
Neurologic deficits not explained by plain film s or CT
o
Clinical progression of a spinal cord lesion
o
Determ ination of acute surgical candidacy
o
Disadvantages of MRI include the inability to adequately m onitor the patient while undergoing the study and the incom patibility with certain m etal devices.
Diagnostic Procedures/Surgery
Myelography is used with CT when MRI is not available or cannot be perform ed.
A lum bar puncture m ay be required if considering Guillain-Barré.
Differential Diagnosis
Dorsal root injury
Peripheral nerve injury
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Guillain-Barré syndrom e
Multiple sclerosis
Transverse m yelitis
Epidural abscess
P.1039
Treatment Pre Hospital
Full spinal im m obilization
IV access should be established for fluid resuscitation in the setting of neurogenic shock.
Patients should be transported to the nearest traum a center.
Pediatric Considerations Cervical collars m ust be the appropriate size for the child; splinting the head and body with towels and tape is a reasonable alternative.
Initial Stabilization
Spinal im m obilization m ust be m aintained at all tim es.
Intubation m ust proceed with in-line spinal im m obilization.
IV fluids should be adm inistered at m aintenance levels unless shock is present: o
Spinal traum a m ay cause hypotension due to loss of sym pathetic tone; fluid adm inistration is first-line treatm ent.
o
Other causes of hypotension (e.g., hem orrhage) should be sought before being attributed to SCI.
o
Generally hypovolem ic shock causes tachycardia,
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whereas neurogenic shock results in bradycardia. o
If BP does not im prove after a fluid challenge and no other cause for hypotension can be found, vasopressor use m ay be necessary; α-agonist is preferred.
ED Treatment
Other injuries m ust be treated as indicated.
Level of spinal cord injury (SCI) should be determ ined as a baseline to follow for im provem ent or deterioration.
A neurosurgeon m ust be consulted once an SCI is suspected even when plain film s are norm al; early surgical decom pression or im m obilization m ay reduce m orbidity.
The patient with an SCI should be m anaged at an appropriate regional traum a or spinal center: o
If necessary, transfer should occur as soon as m anagem ent of other injuries allow.
High-dose m ethylprednisolone (MP) is started as soon as possible in the patient with SCI: o
The greatest benefit is reported when infusion is begun within 8 hours of injury.
o
MP has not been established as having a definitive clinically significant benefit, and high-dose steroids do increase the likelihood of im m une system com prom ise and gastrointestinal (GI) tract bleeding; however, MP is still considered standard of care in m ost practice settings
o
To prevent GI tract bleeding with steroid use, concurrently start the patient on IV H2 blockade.
IV antibiotics and tetanus prophylaxis are given to patients with a penetrating injury.
IV vasopressor support m ay be required to treat neurogenic shock.
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Medication (Drugs)
MP: 30 m g/kg IV loading dose given over 15 m inutes in the first hour followed by a 5.4 m g/kg/h continuous infusion for the next 23 hours (adults and peds)
Fam otidine: 20 m g IV (peds: 0.6–0.8 m g/kg/24h q8h–q12h)
Phenylephrine: 0.5–2 µg/kg bolus then 50–100 µg/m in drip
Follow-Up Disposition Admission Criteria All patients with spinal cord syndrom e m ust be adm itted to an intensive care unit setting.
Discharge Criteria No patient with sym ptom s suggestive of SCI should be discharged.
References 1. Am erican College of Surgeons, Com m ittee on Traum a. Advanced traum a life support course for physicians. Chicago: College of Surgeons, 1993: 193–203. 2. Bracken MB, et al. A random ized controlled trial of m ethylprednisolone or naloxone in the treatm ent of acute spinal cord injury. N Engl J Med. 1990;322(20):1405–1411. 3. Dum ont RJ, Verm a S, Okonkwo DO, et al. Acute spinal cord injury, part II: contem porary pharm acotherapy. Clin Neuropharm acol. 2000;24(5):265–279.
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4. Gerling MC, Davis DP, Ham ilton RS, Hayden SR. Effects of cervical spine im m obilization technique and laryngoscope blade selection on an unstable cervical spine in a cadaver m odel of intubation. Ann Em erg Med. 2000;36(4):293–300. 5. Hockberger RS, Kirshenbaum KJ. Spinal traum a. In: Marx JA, et al, eds. Rosen's em ergency m edicine: concepts and clinical practice. 5th ed. St. Louis, MO: CV Mosby, 2002:329–370.
Codes ICD9-CM 952.00-952.19
ICD10 T09.3
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Spinal Injury: Lum bar
Spinal Injury:
Lumbar Bret Ginther
Basics Description
Flexion com pression fracture: o
Wedge com pression:
If 20°
o
Translation >2 m m
o
Vertebral body height loss >50%
o
Articular process fracture
Radiographs m ay not help diagnose burst fractures in 25% of cases.
If a fracture is identified, entire spine should be im aged to evaluate potential associated spinal injuries.
Spinous process fracture, transverse process fracture, or sim ple transverse sacral fracture require lum bar flexion-extension film s if patient is neurologically intact and there is no evidence of unstable injury.
CT or MRI should be perform ed for further evaluation of suspected fractures or fractures identified on plain films to assess spinal cord integrity.
Differential Diagnosis
Contusion
Pathologic fracture (m etastatic cancer)
Osteoporosis
Pelvic fracture
Traum atic herniated disc
Low posterior rib fracture
Tuberculous spondylitis (Pott disease)
Ankylosing spondylitis
Osteogenesis im perfecta (pediatric)
Congenital scoliosis with hem ivertebra (m istaken for lateral wedge fracture)
Child abuse
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P.1047
Treatment Pre Hospital It is difficult to determ ine whether an injury is stable in the field; any patients with suspected spinal injuries should be im m obilized to prevent further injury.
Initial Stabilization
Im m obilization while tending to im m ediate life-threatening conditions
Airway, breathing, and circulation m anagem ent
ED Treatment
Maintain spinal im m obilization.
High-dose m ethylprednisolone protocol for any neurologic deficit
Consultation with orthopaedic spine or neurosurgery service
Appropriate analgesia
The following stable injuries m ay be treated conservatively if CT confirm s stability of injury and patient is neurologically intact:
o
Isolated spinous process, transverse process fracture
o
Chance fracture
o
Anterior wedge com pression ( Table o f C o ntents > Spine Injury: C o ccyx
Spine Injury:
Coccyx Gary Schwartz
Basics Description
Often from a fall with the victim in sitting position
Fall usually occurs from standing height.
Can occur during childbirth
More com m on in wom en
Etiology See Description
Diagnosis Signs and Symptoms
Tenderness localized over the coccyx
Ecchym osis over the gluteal fold
Pain with sitting, leaning forward, and with defecation
History Obtain history of accident:
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Including earlier events that m ight influence m echanism of fall or insult
Physical Exam Diagnosis can often be m ade on physical exam ination:
Rectal exam to assess tenderness or m obility of coccyx
Isolated coccyx fractures should have no neurologic deficits.
Essential Workup
Most often isolated injury
If other spinal injury is suspected, spinal im m obilization should be instituted.
Tests Imaging Routine radiographic im aging unnecessary:
Concern about unnecessary radiation to gonads when diagnosis can be m ade clinically
Im aging is indicated if concern for other spine injuries.
Radiographs can be hard to interpret because coccyx has norm al variant positions that can be confused with fracture.
Lateral radiograph is best view for fracture or dislocation.
Differential Diagnosis
Coccygodynia
Levator ani syndrom e
Pilonidal cyst
Perirectal abscess
P.1045
Pa ge 4 4 6
Treatment Initial Stabilization
Usually none required
Spinal im m obilization as indicated
If patient unstable, consider other diagnoses.
Medicate for pain
ED Treatment
Pain m edication
Reduce displaced coccyx fracture, but rarely necessary
General Measures Recom m end donut-shaped seat cushion for com fort.
Medication (Drugs) First Line
Medication for pain if needed
Stool softener
Surgery Reduction m ay be attem pted if displaced coccygeal fracture evident:
Rarely needed or successful
Follow-Up Disposition Admission Criteria Adm ission is generally not required.
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Discharge Criteria Coccygeal fracture can be m anaged as an outpatient unless other injury m akes adm ission necessary.
References 1. Cwinn, AA. Pelvis. In: Marx J. Rosen's Em ergency Medicine: Concepts and Clinical Practice. 5th ed. St. Louis, MO: Mosby; 2002:632–633. 2. Gutierrez PR, Mas Martinez JJ, Arenas J. Salter-Harris type I fracture of the sacro-coccygeal joint. Pediatr Radiol. 1998;28:734.
Codes ICD9-CM 805.6 Fracture of vertebral colum n without m ention of spinal cord injury, sacrum and coccyx, closed
ICD10 S39.9
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Spine Injury: Tho racic
Spine Injury:
Thoracic Richard D. Zane
Basics Description
The following forces account for m ost thoracic fractures and dislocations:
o
Axial com pression
o
Flexion-rotation
o
Shear
o
Flexion-distraction
o
Extension
Three anatom ically distinct colum ns; if two of the three colum ns are disrupted, the spinal colum n is unstable: o
Posterior colum n: posterior bony arch and interconnecting ligam entous structures
o
Middle colum n: posterior aspects of the vertebral bodies, posterior annulus fibrosis, and the posterior longitudinal ligam ent
o
Anterior colum n: anterior longitudinal ligam ent, anterior annulus fibrosis, and anterior vertebral body
Major vs. Minor Fractures
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Minor: o
Isolated articular fracture
o
Transverse process fracture
o
Spinous process fracture
o
Pars interarticularis fracture
Major: o
Com pression fracture
o
Burst fracture
o
Seat-belt injury
o
Fracture-dislocation
Com pression fracture (anterior or lateral flexion): o
Fracture of anterior portion of vertebral body with intact m iddle colum n
o
May be posterior colum n disruption
o
Type A: fracture through both end plates
o
Type B: fracture through superior end plate
o
Type C: fracture through inferior end plate
o
Type D: both end plates intact
Burst fracture (axial loading): o
Fracture through m iddle colum n of spine
o
May have spreading of posterior elem ents and lam ina fractures with possible retropulsion into the spinal canal and potential neurologic com prom ise
o
Type A: fracture through both end plates
o
Type B: fracture through superior end plate
o
Type C: fracture through inferior end plate
o
Type D: burst in m iddle colum n with rotational injury leading to subluxation
o
Type E: burst in m iddle colum n with asym m etric com pression of anterior colum n
Seat-belt injury (flexion-distraction): o
Distraction of posterior and m iddle colum ns with
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anterior colum n intact o
Typically caused by lap belts used without shoulder harness
o
Type A: through bone
o
Type B: prim arily ligam entous
o
Type C: disruption of bone through m iddle colum n
o
Type D: through ligam ents and disc with no m iddle colum n fracture
Fracture-dislocations: o
Failure of all three colum ns following com pression, tension, rotation, or shear forces
o
Type A: flexion-rotation; fall from height
o
Type B: shear—violent force across long axis of trunk
o
Type C: flexion-distraction; bilateral facet dislocation
Etiology
Thoracic spine is rigid due to the rib cage and the costovertebral articulations: o
The spinal canal is narrowest in the thoracic spine.
Because traum atic thoracic spine fractures require enorm ous forces, m otor-vehicle accidents or falls from height account for m ost fractures: o
A sm all percentage is caused by penetrating injuries (see Spinal Cord Syndrom es).
o
50% of all spinal fractures and 40% of all spinal cord injuries occur at the thoracolum bar junction (T11-L2).
Diagnosis Signs and Symptoms
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Significant force is required to produce thoracic vertebral fractures.
Pain at the fracture site or im pingem ent of nearby structures by bone fragm ents
Because of the stabilizing influence of the rib cage, a trem endous am ount of force is needed to cause thoracic spine dislocations: o
Concom itant internal injury should be suspected.
o
Thoracic spine fracture-dislocation is less com m on than thoracolum bar fracture-dislocation but has higher incidence of neurologic im pairm ent.
Com m on signs and sym ptom s: o
Localized soft-tissue defect
o
Pain or tenderness
o
Localized—pain and tenderness over spinous process
o
Referred—paraspinal, anterior chest, or abdom en
o
Paraspinal m uscle spasm
o
Paresthesia or dysesthesia
o
Weakness (focal or global)
o
Distal areflexia, flaccid plegia
o
Bowel or bladder incontinence
o
Priapism
o
Loss of tem perature control
o
Spinal shock—hypotension with bradycardia
Essential Workup
Rapid evaluation of airway, breathing, and circulation
Prim ary and secondary traum a survey
Detailed neurologic exam , including rectal tone and perianal sensation
Thorough spine exam for deform ity or tenderness
Any m idline tenderness elicited on exam ination,
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distracting injury, or intoxication m andates plain film spine radiography.
If fracture present, determ ine whether it is stable or unstable.
Assess for bulbocavernous reflex in spinal shock.
P.1049
Tests Imaging
Midline pain or tenderness, severe m otor-vehicle accident, or falls from height are indications for anteroposterior and lateral plain film views of the spine.
Thin-cut CT scanning is indicated in any patient with evidence of spinal fracture on plain film s to assess spinal canal integrity or in patients with norm al plain film s and significant pain or tenderness and m echanism for severe injury.
Any finding of a fracture anywhere in the thoracic spine m andate im aging of the entire spine with plain radiograph.
Differential Diagnosis
Arthritis (degenerative and rheum atoid)
Ankylosing spondylitis
Spina bifida
Congenital m alform ation
Neoplasm
Pathologic fracture
Treatment
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Pre Hospital
If the patient's positioning initially prevents placem ent of a long spinal board, then a short board should be placed until the patient is fully extricated.
Patients with neurologic deficit should be transported directly to a traum a center.
Initial Stabilization
Manage airway and resuscitate as indicated.
Airway intervention should be done with in-line cervical im m obilization.
Preserve residual spinal cord function and prevent further injury by stabilizing the spine.
ED Treatment
Perform all needed resuscitation and diagnostic tests with the patient in full spinal im m obilization
If spinal cord injury is suspected, consider the adm inistration of high-dose steroids and consult a spine surgeon.
If spinal fracture or ligam entous injury is suspected without neurologic im pairm ent, arrange CT or MRI scanning while consulting neurosurgery or orthopaedic surgery.
Pain control should be adm inistered as soon as possible; NSAIDs, opiates, and benzodiazepines are the m ainstays of treatm ent.
Neurogenic hypotension presents with bradycardia or norm al heart rate, rather than the tachycardia seen with hypovolem ic shock: o
Neurogenic hypotension should be treated with crystalloid bolus but m ay require vasopressors.
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Medication (Drugs)
High-dose steroid protocol
Solu-Medrol: 30 m g/kg IV bolus followed im m ediately by an infusion of 5.4 m g/kg/h for the next 23 hours if started within 3 hours of injury; continue for 48 hours if started 3–8 hours after injury; not recom m ended >8 hours after injury
Follow-Up Disposition Admission Criteria
Patients with significant spinal cord or colum n injury should be treated in a regional traum a center.
Unstable spinal colum n injury
Cord or root injury
Ileus
Pain control
Concom itant traum atic injury
Discharge Criteria Stable m inor fractures after orthopaedic or neurosurgical evaluation
References 1. Bagley LJ, et al, Im aging of spinal traum a. Radiol Clin North Am . January 1, 2006;44(1):1–12, vii. 2. Block BE, et al. Thoracic and lum bar spine injuries in children. Contem p Orthop. 1994;29(4):243–555. 3. Brandser EA, El-Khoury GY. Thoracic and lum bar spine traum a. Radiol Clin North Am . 1997;35(3):533–557.
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4. Chiles BW III, Cooper PR. Acute spinal injury. N Engl J Med. 1996;334(8):514–520. 5. El-Khoury GY, Whitten CG. Traum a to the upper thoracic spine: anatom y, biom echanics, and unique im aging features. Am J Roentgenol. 1993;160:95–102. 6. Hockberger RS, et al. Spine. In: Rosen P, et al, eds. Em ergency m edicine: concepts and clinical practice. 5th ed. St. Louis, MO: Mosby, 2002: 329–369. 7. Rivas LA, et al, Multislice CT in thoracic traum a. Radiol Clin North Am . May 1, 2003;41(3):599–616.
Codes ICD9-CM 952.10
ICD10 S24.2
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Splenic Injury
Splenic Injury
Albert Jin
Basics Description
The spleen is form ed by reticular and lym phatic tissue and is the largest lym ph organ.
The spleen lies in the left upper quadrant between the fundus of the stom ach and the diaphragm .
Etiology
The spleen is the m ost com m only injured intraabdom inal organ: o
In nearly two thirds of cases, it is the only dam aged intraperitoneal structure
Motor-vehicle accidents (auto-auto, pedestrian-auto) are the m ajor cause (50–75%), followed by blows to the abdom en (15%) and falls (6–9%)
Mechanism of injury and kinem atics are im portant factors in evaluating patients for possible splenic injury.
Splenic injuries are graded by type and severity of injury: o
Grade I: superficial laceration
o
Grade II: m ore extensive laceration or subcapsular hem atom a
o
Grade III: laceration >3 cm involving trabecular
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vessels o
Grade IV: laceration involving segm ental or hilar vessels
o
Grade V: shattered spleen
Pediatric Considerations
Poorly developed m usculature and relatively sm aller anteroposterior diam eter increase the vulnerability of abdom inal contents to com pressive forces.
Rib cage is extrem ely com pliant and less prone to fracture in children but provides only partial protection against splenic injury.
Splenic capsule in children is relatively thicker than that of an adult; parenchym a of spleen seem s to contain m ore sm ooth m uscle than in adults.
Significant abdom inal injury occurs in only about 5% of child abuse cases but is the second m ost com m on cause of death after head injury.
Diagnosis Signs and Symptoms History
In blunt traum a, note the type and direction (horizontal or vertical) of any deceleration or com pressive forces: o
Injuries are caused by com pression of the spleen between the anterior abdom inal wall and the posterior thoracic cage or vertebra (e.g., lap-belt restraints).
In penetrating traum a, note the characteristic of the weapon (type and caliber), distance from the weapon, or
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the type and length of knife or im paling object: o
Injuries result from a com bination of the kinetic energy and shear forces of penetration.
Physical Exam
System ic signs from acute blood loss: o
Syncope, dizziness, weakness, confusion
o
Hypotension or shock
Local signs: o
Left upper quadrant (LUQ) abdom inal tenderness
o
Palpable tender m ass in LUQ (Balance sign)
o
Referred pain to the left shoulder (Kehr sign)
o
Abdom inal distention, rigidity, rebound tenderness, involuntary guarding
Contusions, abrasions, or penetrating wounds to the chest, flank, or abdom en m ay indicate underlying spleen injury.
Fractures of lower left ribs are com m only seen in association with splenic injuries.
Pediatric Considerations Age-related difficulties in com m unication, fear-induced uncooperative behavior, or a concom itant head injury m ake clinical exam ination less reliable.
Essential Workup
Physical exam is neither specific nor sensitive for splenic injury.
Adjunctive im aging studies are required.
Tests Lab
No hem atologic laboratory studies are specific for diagnosis of injury to the spleen.
Obtain baseline hem oglobin, type and cross-m atch, and
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chem istries.
Imaging
Plain abdom inal radiographs: o
Too nonspecific to be of value
o
Chest radiograph findings suggestive for splenic injury include left lower rib fracture(s), elevation of left hem idiaphragm , or left pleural effusion
Ultrasound (US; FAST exam ): o
Can be done at bedside, especially if the patient is too unstable to go to CT
o
Prim ary role is detecting free intraperitoneal blood, which m ay suggest splenic injury.
o
Does not im age solid parenchym al dam age well
o
Technically com prom ised by uncooperative patient, obesity, substantial bowel gas, and subcutaneous air
CT scan: o
Procedure of choice in stable patient
o
Depicts the presence and extent of splenic injury and adjacent organs, including the retroperitoneum
o
Provides the m ost specific inform ation in patients stable enough to go to the CT scanner
Diagnostic Procedures/Surgery Diagnostic peritoneal lavage (DPL):
Extrem ely sensitive for the presence of hem operitoneum although nonspecific for source of bleeding and does not evaluate retroperitoneum
Differential Diagnosis
Intraperitoneal organ injury, especially liver
Injury to retroperitoneal structures
Thoracic injury
P.1051
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Treatment Pre Hospital
Obtain details of injury from prehospital providers.
Insert two large-bore IVs.
Penetrating wounds or evisceration should be covered with m oist, sterile dressings.
Initial Stabilization
Airway m anagem ent (including C-spine im m obilization)
Standard traum a resuscitation m easures: o
Adequate IV access, including central lines and cutdowns, as dictated by the patient's hem odynam ic status
o
Fluid resuscitation, initially with 2 L of crystalloid (NS or lactated Ringer solution), followed by blood products as needed
ED Treatment
Im m ediate laparotom y m ay be appropriate in the acutely injured patient who is hem odynam ically unstable with presum ed hem operitoneum and splenic injury.
Most patients with acute splenic injury either are hem odynam ically stable or stabilize rapidly with relatively sm all am ounts of fluid resuscitation.
Adjunctive diagnostic procedures supplem enting the physical exam should be perform ed early in the evaluation, followed by laparotom y when indicated by positive diagnostic findings.
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Gunshot wounds to the anterior abdom en are routinely explored in operating room .
Stab wounds can be m anaged by local wound exploration, followed by US or DPL when intraperitoneal penetration is suspected.
Operative versus nonoperative m anagem ent: o
Patients with signs and sym ptom s of intraperitoneal hem orrhage, those with operative indications based on im aging/diagnostic procedures, and those who fail nonoperative m anagem ent should undergo laparotom y.
o
Splenectom y versus splenic salvage depends on the grade of splenic injury.
o
Patient selection for nonoperative m anagem ent includes hem odynam ic stability, no evidence of other intraabdom inal injury, isolated splenic injury confirm ed by im aging study (m ost com m only CT scan).
Geriatric Considerations Patients older than 55 years should be considered for operative m anagem ent due to decreased physical tolerance to traum atic insult and reduced physiologic reserve.
Pediatric Considerations
Nonoperative m anagem ent of splenic injuries is considered safe: o
Concerns for overwhelm ing postsplenectom y infection/sepsis
Follow-Up
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Disposition Admission Criteria All patients with splenic injury require hospitalization for definitive laparotom y or observation with serial abdom inal exam inations, serial hem atocrit determ inations, and bed rest.
Discharge Criteria Only asym ptom atic patients objectively dem onstrated not to have splenic or other traum atic injury m ay be discharged.
References 1. Dupuy DE, Raptopoulos V, Fink MP. Current concepts in splenic traum a. J Intens Care Med. 1995;10:76–90. 2. Esposito T, Gam elli R. Injury to the spleen. In: Felicano D, et al, eds. Traum a. 3rd ed. Norwalk, CT: Appleton & Lange, 1996:525–550. 3. Jurkovich Gregory J. and C. Jam es Carrico. Managem ent of the Acutely Injured Patient. In:Sabiston Textbook of Surgery. 15th ed. Philadelphia, PA: W.B. Saunders Com pany, 1997: 320V323. 4. Marx J. Abdom inal traum a. In: Rosen P, et al, eds. Em ergency m edicine: concepts and clinical practice. 5th ed. St. Louis, MO: CV Mosby, 2002: 415–436. 5. Peitzm an A, et al. Injury to the spleen. Curr Probl Surg. 2001;38(12):932–1008.
Codes ICD9-CM 865.00
ICD10 S36.0
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Spo ndylo lysis/Spo ndylo listhesis
Spondylolysis/Spondylolisthesis Joel Kravitz
Basics Description Spondylolysis
Bony defect at the pars interarticularis (the isthm us of bone between the superior and inferior facets): o
Can be unilateral or bilateral
Type 1—dysplastic: congenital defect of the neural arch or intra-articular facets
Type 2—isthm ic: stress fracture from repetitive m icrotraum a through the neural arch
Type 3—degenerative: long-standing segm ental instability
Type 4—traum atic
Type 5—pathologic: generalized or focal bone disease
Spondylolisthesis
The slipping forward of one vertebra upon another
Spondylolysis can contribute to spondylolisthesis, which is noted in approxim ately 5% of the population.
Of those with spondylolysis, 50% will have som e degree of
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spondylolisthesis develop during their lifetim e, and 50% of those will be sym ptom atic: o
Literature does not associate athletic activity with increased slippage.
Spondylolisthesis predisposes to sciatica.
Spondylolisthesis is divided into four grades based on degree of slippage (Meyerding grading system ):
o
Grade I: up to 25% of the vertebral body width
o
Grade II: 26–50% of vertebral body width
o
Grade III: 51–75% of vertebral body width
o
Grade IV: 76–100% ofvertebral body width
The m ost com m on location for spondylolisthesis is L-5 displaced on the sacrum (85–95%), followed by L-4 on L-5.
Pediatric Considerations
Spondylolysis is one of the m ost com m on causes of serious low back pain in children, although it is m ost often asym ptom atic.
Sym ptom s m ost often present during adolescent growth spurt between ages 10 and 15 years.
Seen com m only in athletic teens; particularly in sports involving back hyperextension (e.g., gym nastics, diving, football).
Acute sym ptom s are related to traum a.
Etiology Unknown; theories include congenital pars anom alies, bone-density alterations, and recurrent subclinical stress injury.
Diagnosis
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Signs and Symptoms History
Onset often gradual, unless traum atic
Often associated with feeling of stiffness or spasm in paravertebral m uscles
Pain in the back and proxim al legs that is aggravated by standing and walking
Sitting or forward bending relieves pain
Pain occurs after varying am ounts of exercise, with standing, or with coughing: o
Aggravating/Alleviating factors: for exam ple, repetitive hyperextending m ovem ents
Relief of pain with rest is variable and slow and usually requires sitting or stooping.
System ic/Neurologic sym ptom s: m inim al, unless significant traum a or “slip―
Physical Exam
Hyperlordotic posture: o
Trunk m ay appear shortened.
o
Rib cage approaches iliac crests.
Ham string tightness: o
Knees flexed to allow patient to stand upright
Only “typical― finding is one-legged hyperextension: o
Standing on one leg and leaning backward reproduces pain on ipsilateral side.
Palpation m ay reveal step-off with a prom inent spinous process of L-5 in significant spondylolisthesis.
Neurologic exam is usually norm al: o
If abnorm al, pain and sensorim otor loss is in a derm atom al distribution.
o
Consider herniation or spondylolisthesis.
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Pediatric Considerations
Spondylolysis in a child younger than 10 years is rare; these patients should be watched for: o
Constant pain lasting several weeks
o
Pain occurring spontaneously at night
o
Pain that interferes repeatedly with school, play, or sports
o
Pain associated with m arked stiffness, lim itation of m otion, fever, or neurologic signs
o
Pain at the lum bosacral junction
Tests Imaging
Lum bosacral spine radiographs: o
Lateral and oblique radiographs of spine m ost helpful
Spondylolysis will m anifest as a radiolucent defect in the pars interarticularis, visible as a “collar― or “broken neck― on the oblique view “Scottie dog―: o
Majority (85–95%) found at L5-S1 level
Spondylolisthesis will m anifest as forward slipping of one vertebral body on another (on lateral).
SPECT scanning—better specificity for linking back pain to spondylolysis
CT scan: o
Pathology m ore clearly dem onstrated than plain film s
o
Can identify other spinal pathology
o
Plays an im portant role for orthopaedics in m anagem ent decisions through identification of new stress fractures and healing of old stress fractures
Outpatient evaluation unless history of recent traum a
MRI—exact role not yet clarified in literature:
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o
Useful for defining root im pingem ent and foram inal narrowing
Pediatric Considerations
Lower threshold for ordering im aging studies
Progressive slipping m ore likely to occur than in adults.
Differential Diagnosis
Tuberculosis
Discitis
Bone or spinal cord tum or
Pyelonephritis
Retroperitoneal infection
Injury to m uscles or joints of back
Congenital hip dislocation
Rickets
Ruptured intervertebral disc
Vascular claudication
P.1053
Treatment Pre Hospital Spinal precautions are not needed unless there is a history of recent traum a.
Initial Stabilization Vigorous attem pts at traction should not be pursued.
ED Treatment
Pain control and m uscle relaxants as clinically needed
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Supportive therapy if sym ptom s are m ild
Restrict activities if repetitive traum a is likely aggravating cause (e.g., sports) for 3–6 weeks, followed by re-introduction of activity when asym ptom atic.
Consider antilordotic braces (controversial) or physical therapy
Orthopaedic consult or referral if sym ptom s are m oderate to severe or unresponsive to supportive care
Surgical intervention typically consists of spinal fusion in the flexed position: o
50% of sym ptom atic patients with spondylolisthesis m ay require surgery.
All sym ptom atic patients with grade III or IV spondylolisthesis should probably undergo surgery.
Exercises are not of proven benefit.
Pediatric Considerations
Activity restriction is not necessary if m inim al or no sym ptom s.
Literature suggests good outcom e for young athletes with conservative treatm ent.
Medication (Drugs)
Muscle relaxants: o
Exam ple—m ethocarbam ol: 1,000–1,500 m g PO q.i.d. (peds: safety and effectiveness for children younger than 12 years not established)
NSAIDs: o
Exam ple—ibuprofen: 200–800 m g PO t.i.d.–q.i.d. (peds: 5–10 m g/kg PO q6h)
Opioids:
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o
Exam ple—m orphine sulfates: 0.1 m g/kg up to 2–4 m g increm ents IV.
Follow-Up Disposition Admission Criteria
Inability to walk
Inability to cope at hom e due to pain or social situation
Progressive neurologic deficit
Discharge Criteria
Orthopaedic follow-up arranged
Social support system in place
Pain control
Patient education
Pediatric Considerations Close follow-up is m andatory.
References 1. Congeni J, McCulloch J, Swanson K. Lum bar spondylolysis. A study of natural progression in athletes. Am J Sports Med. 1997;25(2):248–253. 2. Debnath UK, Freem an BJ et al. Clinical outcom e and return to sport after the surgical treatm ent of spondylolysis in young athletes. J Bone Joint Surgery. March 2003;85(2);244. 3. Iwam oto J, Takeda T, Wakano K. Returning athletes with severe low back pain and spondylolysis to original sporting activities with conservative treatm ent. Scand J Med Sci Sports. Decem ber 2004;14(6);337. 4. Miller SF, Congeni J, Swanson K. Long-term functional and
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anatom ical follow-up of early detected spondylolysis in young athletes. Am Jour Sports Med. June 2004;32(4);928. 5. Nachem son A. Newest knowledge of low back pain. Clin Orthop. 1992;279:8. 6. Satndaert CJ. Spondylolysis. Phys Med Rehab Clin North Am . 2000;11(4):785–801. 7. Skinner H. Disorders, diseases and injuries of the spine. In: Current diagnosis and treatm ent in orthopedics. Norwalk, CT: Appleton & Lange,1995:206–211. 8. Vitek G. Spine conference spondylolysis and spondylolisthesis. Ortho News Magazine. May 1995. Available at: http://www.nm is.com /onm /htm l/sponconf-spon.htm .
Codes ICD9-CM 721.90 756.12
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Spo ntaneo us Bacterial Perito nitis
Spontaneous Bacterial Peritonitis Michael Schmidt Amer Aldeen
Basics Description
Infection of ascites fluid without an evident intra-abdom inal surgically treatable source: o
Ascites polym orphonuclear leukocyte count >250 cells/m m 3 with a positive bacterial ascites culture
Must be distinguished from secondary bacterial peritonitis: o
Nonsurgical m anagem ent of secondary bacterial peritonitis carries 100% m ortality.
o
Surgical m anagem ent of spontaneous bacterial peritonitis (SBP) carries 80% m ortality.
Etiology Mechanism
Portal hypertension causes translocation of bacteria through edem atous gut m ucosa to lym ph nodes to the peritoneal cavity.
Transient bacterem ia with low serum com plem ent
Im paired activity of reticuloendothelial system
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phagocytosis and opsonization
Patients with a total protein concentration 37.8°C or >100.4°F) is m aintained for cirrhotic patients due to baseline hypotherm ia
Altered m ental status
Ascites: o
Only clinically obvious ascites (shifting dullness and fluid wave) is associated with developm ent of SBP.
Abdom inal tenderness: o
Developm ent of a rigid abdom en does not occur because of the separation of visceral and parietal pleura due to ascites.
Essential Workup Paracentesis is the m ainstay of diagnosis:
Procedure: o
Location (with patient supine):
4 cm cephalad and m edial to anterior superior iliac spine
2 cm caudad to the um bilicus (ensure bladder em ptying beforehand)
o
Total 40 m L should be aspirated:
10 m L for each culture bottle
10 m L for cell count and chem istries (red top, purple top EDTA, and sterile container)
o
Inoculate culture bottles with ascitic fluid im m ediately at the bedside.
o
Coagulopathy does not need to be corrected before the procedure (except for platelets 250 cells/m m 3 )
o
Total protein 1.1 g/dL is consistent with portal hypertension)
o
Am ylase
o
Culture and gram stain
o
Glucose >50 m g/dL
o
Ascites leukocyte esterase on dipstick has excellent negative predictive value for SBP.
CBC with differential
Basic m etabolic panel
Prothrom bin tim e/partial throm boplastin tim e
Liver function tests (including album in)
Blood cultures
Urinalysis and culture
Imaging
Abdom inal ultrasound: o
Confirm s presence of ascites
o
Helps guide paracentesis
Chest radiograph
Abdom inal radiographs: flat plate and upright to evaluate for perforation or obstruction
Differential Diagnosis
Alcohol hepatitis: o
Fever, leukocytosis, abdom inal pain +/- ascites
o
Ascites PMN 1 g/dL
o
Ascites glucose 250 cells/m m 3
o
Ascites culture negative
o
Can be due to tuberculosis or m alignancy
Monom icrobial nonneutrocytic bacterascites: o
PMN Table o f C o ntents > Staphylo co ccal Scalded Skin Syndro m e
Staphylococcal Scalded Skin Syndrome Timothy J. Mader Laura A. Matzkin
Basics Description
Results from the actions of a soluble epiderm olytic exotoxin produced by Staphylococcus aureus: o
Produced at a distant site of infection or colonization
o
Dissem inates hem atogenously
o
Lyses desm osom es of granular cells in the superficial epiderm is
o
Results in generalized intraderm al exfoliation
Disease of infants and children younger than 6 years: o
Adults have specific staph antibodies allowing them to localize, m etabolize, and excrete the staph toxins.
o
Infants, children, and som e im m unocom prom ised are unable to m etabolize and excrete toxin efficiently.
Presentation determ ined by age and extent of the rash: o
Classic staphylococcal scalded skin syndrom e
o
Pem phigus neonatorum
Pa ge 4 5 0
o
Bullous im petigo
Typically, coagulase positive phage group II Staphylococcus: o
Group I and group III also im plicated
Etiology
Colonization often without overt infection
Concurrent infection or break of skin barrier:
o
Minor skin abrasions
o
Circum cision site
o
Conjunctivitis
o
Um bilicus/Om phalitis
o
Im petigo
o
Endocarditis and septicem ia
Often no focus identified
Diagnosis Signs and Symptoms
Constitutional sym ptom s: o
Malaise
o
Fever
o
Irritability
Diffuse tender scarlatiniform erythem atous rash (sandpaperlike) resem bling a “sunburn―— erythroderm a
Areas of prom inence: o
Around the flexor areas of the neck
o
In intertriginous areas, especially axilla and groin
o
Near the eyes and m outh
Increased erythem a in skin creases
Pa ge 4 5 0
Facial edem a with radial crusting fissures around the eyes, nose, and m outh
Child m ay appear well, ill, or overtly toxic.
Flaccid bullae: o
Within 1–3 days after onset of cariniform rash
o
Initially over flexures (axillae, groin, body orifices)
o
Bullae m igrate through epiderm is with light lateral pressure; epiderm is separates with m inor pressure (Nikolsky sign).
o
Rupture within hours
o
Epiderm is separates with m inor traum a.
o
Epiderm is is shed in sheets.
o
Denuded areas are m oist, sensitive, and painful.
o
Com plete healing within 2 weeks, no scarring
Purulent conjunctivitis
Mucous m em branes are not affected
Com plications are rare: o
Hypotherm ia
o
Fluid and electrolyte im balance
o
Secondary infection
o
Pneum onia
o
Septicem ia
o
Cellulitis
o
Osteom yelitis
Essential Workup
Clinical presentation is diagnostic.
Determ ine location/source of toxin producing Staphylococcus.
Tests
Lab
CBC and urinalysis:
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o
Electrolytes: o
Assess for sepsis if source is not obvious.
Indicated if signs of dehydration or extensive rash
Blood cultures: o
Rarely positive
Diagnostic Procedures/Surgery
Fluid aspirated from bullae: o
Sterile in staphylococcal scalded skin syndrom e
o
Consistent with hem atogenous dissem ination of the toxin
Isolation of staphylococci from a site other than the blisters: o
Com m only conjunctivae, nasopharynx, or blood
Skin biopsy or frozen histologic section: o
Determ ine level of epiderm al/derm al separation (cleavage is in granular layer of derm is).
o
Indicated for children on m edications, those older than 6 years and in cases of m ixed presentation
P.1059
Differential Diagnosis
Infection: o
o
Scarlet fever:
Involves the m ucous m em branes
Strawberry tongue:
Painful desquam ation does not occur.
Bullous im petigo:
o
Turbid or cloudy bullae fluid
Bullous varicella:
Tzanck prep or viral base reveals giant cells.
Pa ge 4 5 0
o
5 days after the onset of varicella
Toxic shock syndrom e:
Rapid developm ent of clinical signs and sym ptom s
Mucous m em brane and m ultiorgan involvem ent
Toxic epiderm al necrolysis or drug eruption: o
Much m ore com m on in adults
o
Severely afflicted m ucous m em branes
o
Full thickness epiderm al necrosis
Derm atologic: o
Erythem a m ultiform e
o
Epiderm olysis hyperkeratosis
o
Epiderm olysis bullosa
o
Pem phigus vulgaris
Scald injury
Secondary rash of an underlying disorder: o
Lym phom a
o
Aspergillosis
o
Irradiation
o
Graft-versus-host reaction
o
Kawasaki disease
Treatment Initial Stabilization
Managem ent is sim ilar to an extensive second-degree burn: o
Large total body-surface area involvem ent will require IV fluids.
Provide adequate analgesia.
Undress and place child on sterile linen.
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Lim it handling of child.
Apply m oist sterile dressings.
Avoid excess heat loss.
ED Treatment
Topical burn cream s are of no proven benefit.
Steroids are contra-indicated.
IV antibiotics effective against penicillinase-resistant S. aureus:
o
Cefazolin
o
Nafcillin
Oral antibiotics for m ild involvem ent: o
Dicloxacillin
o
Erythrom ycin
o
Cephalexin
Medication (Drugs)
Cefazolin: 50–100 m g/kg/24h IV div. q.i.d.
Cephalexin: 25–100 m g/kg/24h PO div. q.i.d.
Dicloxacillin: 12–25 m g/kg/24h PO div. q.i.d.
Erythrom ycin: 30–50 m g/kg/24h PO div. q.i.d.
Nafcillin: 1–2 g IV q6h (peds: newborns, 50–100 m g/kg/24h IV div. q6h; children, 100–200 m g/kg/24h IV div. q6h)
Follow-Up Disposition Admission Criteria
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Children younger than 1 year
All toxic-appearing children
Widespread skin involvem ent
Dehydration and/or electrolyte derangem ent
Discharge Criteria
Older well-appearing children with m ild involvem ent
Oral antibiotics for 7 days
Follow-up within 48 hours
References 1. Feigin RD, Cherry JD, eds. Textbook of pediatric infectious diseases. Philadelphia, PA: WB Saunders, 1998:1055–1057. 2. Freedberg Irwin M, et al. Fitzpatrick's Derm atology in General Medicine. McGraw-Hill. 6th ed., 2003: Ch 195. 3. Gem ell CG. Staphylococcal scalded skin syndrom e. J Med Microbiol . 1995;43(5):318–327. 4. Ladhani L. Recent developm ents in staphylococcal scalded skin syndrom e. Clin Microbiol Infect. 2001;7(6):301–307.
Codes ICD9-CM 695.1
ICD10 L00
Pa ge 4 5 0
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Sterno clavicular Jo int Injury
Sternoclavicular Joint Injury Robert S. Chang Wallace Carter
Basics Description
Sternoclavicular joint (SCJ) is the only joint that connects the upper lim b to the trunk.
Am ong least frequently injured joints in the body
Traum a from vehicular or athletic injuries through direct or indirect m echanism
Congenital or atraum atic dislocation rarely seen
Etiology
Injury to the SCJ can be from sprains, subluxations, and dislocations.
The SCJ can dislocate anteriorly or posteriorly.
Anterior dislocation is m ore com m on: o
Caused by a posteriorly directed force to the anterolateral aspect of the shoulder
o
Reciprocal anterior displacem ent of the m edial clavicle
o
May be associated with pneum othorax, hem othorax, pulm onary contusion, and rib fractures
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Posterior dislocation results from : o
Anterior-to-posterior blow to the m edial clavicle
o
Anteriorly directed force to the posterolateral aspect of the shoulder
o
Reciprocal posterior displacem ent of the m edial clavicle
Posterior dislocation is a surgical em ergency: o
Indications for im m ediate reduction:
Com pression/Tear of trachea, esophagus, or great vessels
Recurrent laryngeal nerve
Brachial plexus in the m ediastinum
Pediatric Considerations
The m edial epiphyseal growth plates of the clavicles are last to ossify and fuse between ages 22 and 25 years: o
Up until fusion, growth plate weakest part of the joint
Fractures through the m edial epiphysis m im ic SCJ dislocations: o
Classified as Salter-Harris type I or II fractures
o
True dislocations of the SCJ are extrem ely rare in children because of the strong ligam entous attachm ents.
Diagnosis Signs and Symptoms
Pain localized to the m edial clavicle and SCJ
Affected arm supported across the chest by the contralateral arm
Inability to abduct or externally rotate arm
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If the SCJ is dislocated, shoulder appears shortened: o
Head tilts toward injured side due to sternocleidom astoid m uscle spasm
In anterior dislocation, m edial end of the clavicle is visibly prom inent and palpable.
In posterior dislocation, there m ay be a sulcus of the SCJ area through which the lateral border of the m anubrium m ay be palpated. o
Dislocation m ay be m asked by significant swelling over the sternoclavicular region.
o
Venous congestion in the neck or upper extrem ities
o
Asym m etric upper extrem ity pulses
o
Neuropraxia
o
Shortness of breath, hoarseness, dysphagia
o
Signs of shock:
Suggest life-threatening im pingem ent of the posteriorly displaced clavicle upon structures in the m ediastinum
If subluxed or sprained, the SCJ is tender on direct palpation and with shoulder m ovem ent: o
No deform ity or significant AP m obility
Essential Workup
Com plete traum a evaluation for other life-threatening injuries
Special attention to respiratory, neurologic, and vascular status
Appropriate analgesia for patient com fort
Tests Imaging
Routine plain chest radiographs difficult to evaluate SCJ injury:
Pa ge 4 5 1
o
May dem onstrate asym m etry of the SCJ com pared with contralateral side
o
More useful to assess co-existing bony, pulm onary, and m ediastinal injury
Rockwood or serendipity view: o
Radiograph beam aim ed at m anubrium at 40° cephalic tilt allows view of both SCJs.
Ultrasound can reliably dem onstrate posterior SCJ dislocations: o
Currently used in operating room setting to evaluate reduction and vascular structures
o
Advantage of being noninvasive, portable, and sim ple to use
o
May be useful in the initial ED evaluation of unstable patients with chest traum a
MRI provides superior soft tissue (ligam ent and cartilage) detail of the SCJ and sternum : o
Lim ited utility in the ED setting
CT scan is best to evaluate the SCJ: o
Useful when plain film s are inconclusive
o
Accurately differentiates fractures from dislocations
o
Dem onstrates the position of the m edial end of the clavicle
o
Shows detailed anatom y of the thoracic outlet and m ediastinum
Differential Diagnosis
Sternoclavicular sprain/subluxation
Medial clavicle fracture
Septic joint
Osteoarthritis
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Treatment Pre Hospital
Attention to airway and vital signs, and neurovascular status of the affected extrem ity
The affected arm should be splinted in the position of com fort before transport to the ED.
Initial Stabilization
Endotracheal intubation if indicated: o
Then im m ediate m edial clavicular reduction
Em ergent SCJ reduction for: o
Hoarseness
o
Dysphagia
o
Sensation of throat tightness
o
Neurovascular com prom ise:
Upper extrem ity weakness
Paresthesia
Dim inished pulses
Signs of shock
Orthopaedic and thoracic surgical consults
Analgesia and sedation as needed
P.1061
ED Treatment
Anterior dislocations m ay be reduced in the ED: o
Procedural sedation for adequate pain control and m uscle relaxation
o
Rolled towel placed between the shoulder blades in the supine position:
Pa ge 4 5 1
Longitudinal traction applied to the extended arm with shoulder abducted 90°
Assistant applies gentle inward pressure over the displaced end of the clavicle.
After reduction, im m obilize using a well-padded figure-of-eight dressing.
o
Many anterior dislocations rem ain unstable after reduction.
o
Surgery rarely indicated as deform ity is m ainly cosm etic
Posterior dislocations require urgent reduction best achieved in the operating room under general anesthesia: o
If surgeon not im m ediately available, em ergent reduction in the ED m ay be necessary:
Relieve serious airway, neurologic, or vascular com prom ise.
After airway secured, sm all incision is m ade directly over the m edial clavicle.
A sterile towel clam p used to grasp m edial clavicular head and gentle anterior traction applied to reduce the dislocation.
Medication (Drugs)
Procedural sedation
Atropine: used in pediatric patients in conjunction with ketam ine to decrease hypersalivation (peds: 0.02 m g/kg IM/IV., m inim um dose of 0.1 m g)
Etom idate: 0.1 m g/kg IV
Fentanyl: 1–2 µg/IV q2m in–q3m in
Ketam ine: 1–2 m g/kg IV
Midazolam : 0.01 m g/kg (peds: 0.05–0.1 m g/kg) IV
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q2m in–q3m in
Follow-Up Disposition Admission Criteria
All posterior dislocations of the SCJ require adm ission for prom pt reduction in the OR and evaluation for potential intrathoracic com plications.
Co-existing injury significant enough to warrant hospitalization
Discharge Criteria
SCJ sprains
Anterior dislocations of the SCJ without neurovascular com prom ise or other significant injury
Appropriate outpatient orthopaedic follow-up arranged
References 1. Doss A, Lang IM, Roberts I, et al. Posterior Sternoclavicular joint dislocation in children—Role of spiral com puted tom ography. Pediatr Em erg Care. 2005;21(5):325–326. 2. Ferrera PC, Wheeling HM. Sternoclavicular joint injuries. Am J Em erg Med. 2000;18(1):58–61. 3. Gobet R, Meuli M, Alterm att S, et al. Medial clavicular epiphysiolysis in children: the so-called sterno-clavicular dislocation. Em erg Radiol. 2004;10(5):252–255. 4. Medvecky MJ, Zuckerm an JD. Sternoclavicular joint injuries and disorders. AAOS Instructional Course Lectures. 2000;49:397–406. 5. Salgado RA, Ghysen D. Posttraum atic posterior sternoclavicular dislocation: case report and review of the literature. Em erg Radiol.
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2002;9:323–325. 6. Yeh GL, William s GR. Conservative m anagem ent of sternoclavicular injuries. Orthop Clin North Am . 2000;31(2):189–203.
Codes ICD9-CM 810.01
ICD10 S49.9
Pa ge 4 5 1
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Stevens-jo hnso n Syndro m e
Stevens-johnson Syndrome James Comes Herbert G. Bivins
Basics Description
Stevens-Johnson syndrom e (SJS) is a severe m ucocutaneous disease: o
Blistering of less than 10% of the body surface area
o
95% of patients have m ucous m em brane lesions.
o
85% have conjunctival lesions.
o
Lesions often involving face, neck, and central trunk regions becom e confluent over hours to days.
Erythem a m ultiform e (EM), SJS, and toxic epiderm al necrolysis (TEN) m ay be considered variants of the sam e disease.
Etiology
The m ost com m on causes include m edications and infections: o
Dam age to the skin is thought to be m ediated by cytotoxic T lym phocytes and m ononuclear cells aim ed at keratinocytes expressing (drug-related) antigens.
o
Cytokines from activated m ononuclear cells probably
Pa ge 4 5 1
contribute to cell destruction and system ic sym ptom atology.
Causative m edications: Antibiotics (e.g., Penicillin, Sulfonam ides), anticonvulsants, oxicam s, NSAIDs, and allopurinol have been associated with these severe cutaneous drug reactions.
Infections: Mycoplasm a pneum onia and herpes sim plex are well-recognized causes of erythem a m ultiform e and SJS.
Diagnosis Signs and Symptoms History
Prodrom e: fever, headache, m alaise, upper respiratory infection (URI) sym ptom s, arthritis, arthralgias, and m yalgias prior to m ucocutaneous lesions
Skin: m ild to m oderate skin tenderness followed by skin pain, burning sensation, and paresthesias
Eye: conjunctival burning or itching
Mucous m em branes: painful m icturition, painful swallowing
Physical Exam
Rash: target lesions, erythem atous or purpuric m acules with or without confluence, and raised flaccid blisters or bullae with skin detachm ent that spread with lateral pressure (Nikolsky sign) on erythem atous areas
Mucous m em brane: erythem atous tender erosions of the m outh, pharynx, trachea, genitalia, or anus; possibly pseudom em brane form ation
Eye: m ild to severe conjunctivitis with possible form ation of pseudom em branes and corneal ulcers
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Essential Workup A com plete history and physical exam ination with careful attention to m ucous m em branes, percentage of blistering, and identification of likely etiology
Tests Lab
Electrolytes
Liver enzym es
CBC
Urinalysis
Imaging Chest radiography if pneum onia is a consideration
Diagnostic Procedures/Surgery Skin biopsy of lesions and m ucous m em branes dem onstrates necrosis of the entire epiderm al layer with form ation of subepiderm al split above basem ent m em brane.
Differential Diagnosis
EM m ajor:
Overlapping SJS and TEN (skin detachm ent between 10% and 30% of the body surface area plus widespread m acules or flat atypical target lesions)
Toxic epiderm al necrolysis (skin detachm ent greater than 30% of the body surface area plus widespread m acules or flat atypical targets)
Therm al burns
Phototoxic reactions
Exfoliative derm atitis
Bullous fixed drug eruptions
Graft-versus-host disease in bone m arrow transplant patients
Pa ge 4 5 2
Pediatric Considerations Staphylococcal scalded skin syndrom e is in the pediatric differential diagnosis of severe blistering m ucocutaneous diseases. P.1063
Treatment Initial Stabilization
Endotracheal intubation and ventilatory support m ay be required for im pending respiratory failure (m ore com m only associated with TEN).
IV fluids
ED Treatment Recognize and treat underlying infections:
Sepsis is the prim ary cause of death, frequently from gram -negative pneum onia.
Secondarily infected cutaneous lesions can be treated with débridem ent of blisters, com presses, and system ic antibiotics.
Corticosteroids are controversial.
Prophylactic antibiotics m ay be indicated if system ic steroids are given.
Mild system ic sym ptom s m ay be treated with acetam inophen or NSAIDs, provided they are not the cause of the m ucocutaneous reaction.
Mucous m em brane lesions are extrem ely painful and m ay require parenteral analgesics.
Large extensive bullae should be débrided, ideally in a
Pa ge 4 5 2
burn unit.
Medication (Drugs)
Acetam inophen: 650–975 m g PO/PR (peds: 15 m g/kg/dose)
Acyclovir: 5–10 m g/kg IV q8h (for herpes sim plex virus infections)
Ibuprofen: 300–800 m g PO (peds: 5–10 m g/kg/dose)
Morphine sulfate: 0.1 m g/kg/dose IV
Follow-Up Disposition Admission Criteria
Patients with SJS should be adm itted to the hospital.
Patients with extensive epiderm al detachm ent should be adm itted to a burn center or a specialized intensive care unit.
Discharge Criteria Patients with erythem a m ultiform e m inor m ay be discharged with appropriate and tim ely follow-up.
Issues for Referral Patients m ust be m ade aware of the likely offending drug (and its class) and that it m ust never be adm inistered to them again.
References 1. Fritsch PO, Sidoroff A. Drug-induced Stevens-Johnson syndrom e/toxic epiderm al necrolysis. Am J Clin Derm at. 2000;1(6):349–360.
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2. Roujeau JC, Kelly JP, Naldi L, et al. Medication use and the risk of Stevens-Johnson syndrom e or toxic epiderm al necrolysis. N Engl J Med. 1995;333:1600–1607. 3. Wolff K, Johnson RA, Suurm ond D. Stevens- Johnson Syndrom e and Toxic Epiderm al Necrolysis. In: Fitzpatrick's Color Atlas & Synopsis of Clinical Derm atology. 5th ed. Mc Graw-Hill; 2005: 144–147.
Codes ICD9-CM 695.1
Pa ge 4 5 2
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Sting, Bee
Sting, Bee
Daniel T. Wu
Basics Description
Injection of hym enoptera venom causes: o
Release of biologic am ines
o
Local or system ic allergic reactions
Reactions are: o
Usually IgE-m ediated type I hypersensitivity reactions
o
Rarely type III (Arthrus) hypersensitivity reactions
Etiology
Hym enoptera—order of the phylum Arthropoda
Includes bees, wasps, hornets, and fire ants
Diagnosis Signs and Symptoms History History and physical exam —keys to diagnosis
Physical Exam
Pa ge 4 5 2
N/A
Five Types of Reactions to Stings
Local reaction: o
Most com m on type of reaction
o
Local pain, erythem a, and edem a at sting site
o
Sym ptom s occur im m ediately and resolve within 1–2 hours
Large local reaction: o
Sim ilar to local reaction, but affects larger area or entire lim bs
o
Peaks at 48 hours and can last several days
o
Mild to m oderate fever
System ic reaction: o
Includes anaphylaxis
o
Can be fatal (usually owing to respiratory failure)
o
Respiratory:
o
o
Wheezing
Coughing
Stridor
Shortness of breath
Hoarseness
Angioedem a
Gastrointestinal:
Nausea
Vom iting
Diarrhea
Abdom inal pain
Cardiovascular:
Hypotension
Chest pain
Tachycardia
Shock
Pa ge 4 5 2
o
o
Other:
Urticaria
Pruritus
Flushing
Sym ptom s occur within 15–20 m inutes and last up to 72 hours
Toxic reaction: o
Result of m ultiple stings and large doses of venom
o
Sym ptom s sim ilar to anaphylaxis
Unusual reactions: o
Owing to unusual im m une response
o
Vasculitis
o
Nephrosis
o
Serum sickness
o
Neuritis
o
Encephalitis
o
Reaction delayed (days to weeks after sting)
Essential Workup
History and physical key to diagnosis
No radiologic or laboratory test will confirm hym enoptera envenom ation or anaphylaxis.
Tests Lab CBC, electrolytes, BUN, creatinine, glucose, arterial blood gases (ABGs):
Not routine
Consider when significant system ic effects present
Diagnostic Procedures/Surgery ECG
When significant system ic effects in patients at risk for
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cardiovascular disease
Differential Diagnosis
Insect bites som etim es cause pain; stings always cause pain.
Cellulitis: o
Difficult to distinguish between large local reactions and cellulitis
o
Infections of hym enoptera envenom ations are rare and usually caused by wasp envenom ations.
o
Local reaction can resem ble periorbital cellulitis.
Gout
Soft tissue traum a
System ic/toxic reactions: o
Pulm onary em bolus
o
Anaphylaxis from different agent
o
Hyperventilatory syndrom e/anxiety
o
Acute coronary syndrom e
Treatment Pre Hospital Most deaths occur within first hour owing to either respiratory obstruction or anaphylaxis causing cardiovascular and respiratory collapse.
Initial Stabilization Acute Severe Systemic Reaction/Anaphylaxis
Airway, breathing, and circulation m anagem ent (ABCs): o
Intubation/ventilation with rapidly increasing signs of laryngeal com prom ise
Pa ge 4 5 2
o
Oxygen
o
0.9% norm al saline (NS) IV access
Epinephrine SC/IV
Antihistam ines IV
When signs of system ic reactions: o
Assess for patent airway.
o
Establish IV access.
ED Treatment
System ic reactions: o
Epinephrine for respiratory sym ptom s/hypotension
o
Antihistam ines—H 1 (diphenhydram ine) and H 2 (cim etidine) blockers
o
Steroids (prednisone, m ethylprednisolone)
o
Inhaled β-agonist for wheezing/shortness of breath
o
For persistent hypotension:
0.9% NS IV fluid resuscitation
Vasopressor (epinephrine/α-adrenergic) for hypotension resistant to IV fluids
Rem oval of rem nants of stinger at site of envenom ation (bees m ay leave stingers with venom sacs) by scraping, not squeezing
Local reactions: o
Cool com press
o
Elevation
o
Rem ove constrictive clothing or jewelry
o
Topical antihistam ine/topical steroidal cream as needed
o
Oral antihistam ine or steroids as needed
P.1065
Pa ge 4 5 2
Medication (Drugs)
Albuterol, β-agonist (inhaled): 3 m g in 5 m L solvent (peds: 0.1 m g/kg of 5 m g/m L concentration) via nebulization
Cim etidine: 300 m g (peds: 5 m g/kg) IV, IM, or PO
Diphenhydram ine: o
50–100 m g (peds: 1 m g/kg) IV for severe reactions
o
25–50 m g (peds: 1 m g/kg) PO q.i.d. for severe local reactions
Epinephrine: o
0.1 m g: 1 m L of 1:10,000 dilution (peds: 0.01 m g/kg = 0.1 m L/kg of 1:10,000 dilution up to 1 m L) IV over 5 m inutes for shock
o
0.3–0.5 m g (0.3 m L–0.5 m L of 1:1,000 dilution; peds: 0.01 m g/kg up to 0.5 m g) SC for severe reactions but not in shock
Methylprednisolone: 125 m g (peds: 1–2 m g/kg) IV
Norepinephrine: 4–12 µg/m in (peds: 0.1 µg/kg/m in) titrated continuous infusion
Prednisone: 60 m g (peds: 1–2 m g/kg) PO
Follow-Up Disposition Admission Criteria
Worsening sym ptom s, airway com prom ise
Persistent unstable vital signs require ICU adm ission.
Life-threatening reaction requires 24-hour observation.
System ic reaction requires m inim um of 6 hours of
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observation.
Discharge Criteria
Minim al isolated local reaction
System ic reactions that resolve and do not recur during 6-hour observation period
Issues for Referral Follow-up:
Provide patients with life-threatening reactions em ergency anaphylaxis kits (EpiPen; peds: EpiPen Jr. if Table o f C o ntents > Strepto co ccal Disease
Streptococcal
Disease Scott Sherman
Basics Description
In the late 1980s, an increase was seen in the frequency of an aggressive streptococcal infection that afflicted otherwise healthy patients aged 20–50 years who did not have underlying predisposing diseases.
Dubbed “flesh-eating bacteria― in British press
Rapid progression of shock and m ultiorgan dysfunction, with death occurring in m any afflicted patients within 1–2 days
Streptococcal toxic shock syndrom e (Strep TSS): o
o
Portal of entry for streptococci:
Vagina
Pharynx
Mucosa
Skin
In 50% of cases, the site of entry is unknown.
Nonsteroidal anti-inflam m atory drugs appear to m ask or predispose patients to streptococcal toxic shock
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syndrom e. o
Most cases occur sporadically.
o
Occasional outbreaks in long-term care facilities and hospitals
Necrotizing fasciitis: o
Mortality rate 30–70%
o
Infection of the subcutaneous tissue with progressive destruction of the fascia and fat
o
Often fatal over a course of 24–96 hours
o
Described by Meleney in 1924, but progression in his patients was slower (over 7–10 days) with lower m ortality rate (20%).
Streptococcal m yositis: o
A rare group A beta-hem olytic streptococcal infection was reported only 21 tim es from 1900–1985.
o
Swelling and erythem a develop late.
o
Difficult to differentiate from gas gangrene secondary to Clostridium species infection
o
Mortality rate 80–100%
o
Aggressive surgical débridem ent is essential.
Streptococcal Toxic Shock Syndrome Case Definition Isolation of group A beta-hem olytic streptococcus from sterile or nonsterile body site, and:
Hypotension
Two or m ore of the following: o
Renal im pairm ent
o
Coagulopathy
o
Liver abnorm alities
o
Acute respiratory distress
o
Extensive tissue necrosis (necrotizing fasciitis)
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o
Erythem atous rash
Etiology
Streptococci: o
Catalase-negative spheric cocci
o
Divided into two groups: alpha and beta:
On ability to lyse erythrocytes on an agar plate
Beta-hem olytic streptococci fully lyse erythrocytes
o
Further divided into Lancefield groups by variations in an antigen in the cell wall (C carbohydrate)
o
Group A beta-hem olytic streptococcus:
Possesses another antigen, the M protein, which is associated with the virulence of the bacteria
Strep TSS: o
Occurs when a susceptible host is infected with a virulent strain
o
M protein types 1, 3, and 28 are m ost com m on.
o
Possesses pyrogenic exotoxins (e.g., A, B, and C)
o
Produces fever and shock via activation of tum or necrosis factor and interleukins
o
Risk factors for developm ent of strep TSS:
Patients generally younger than 10 years or older than 60 years of age
Cancer
Renal failure
Leukem ia
Severe burns
Corticosteroids
Necrotizing fasciitis: o
Group A beta-hem olytic streptococcus is causative in 10% of cases.
o
Mixed anaerobic and aerobic organism s are found in
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70% of cases. o
Staphylococcus aureus, Clostridium species, and other enteric organism s
Diagnosis Signs and Symptoms
Presents as: o
Strep TSS
o
Necrotizing fasciitis/m yositis
Pain is the m ost com m on initial sym ptom : o
Often abrupt in onset and severe
o
Occurs in 85% of cases
o
Often requiring palliative IV narcotics
o
Usually involves an extrem ity
o
May m im ic peritonitis, pelvic inflam m atory disease, pneum onia, acute m yocardial infarction, or pericarditis
Fever is the m ost com m on sign: o
Can present with hypotherm ia, especially if patient is in shock
Altered m ental status is present in 55% of patients.
Soft-tissue infection (erythem a and swelling) present in 80% of patients: o
70% progress to necrotizing fasciitis or m yositis:
Indistinct borders, blisters, bullae
No lym phangitis or lym phadenopathy
Most patients will require surgical procedure (e.g., fasciotom y, surgical débridem ent, exploratory laparotom y, intra-ocular aspiration, am putation, or hysterectom y).
Pa ge 4 5 4
Influenzalike syndrom e in 20%: o
Fever
o
Chills
o
Myalgias
o
Nausea, vom iting
o
Diarrhea
Shock: o
Present at adm ission or within 4–8 hours in all patients
o
Persists despite fluids, antibiotics, and pressors in all but 10%
Renal failure: o
Precedes onset of shock in m any cases
o
Dialysis often necessary
o
Kidney function returns to norm al within 4–6 weeks in survivors.
Adult respiratory distress syndrom e: o
Occurs in 55% of patients and develops after hypotension
o
Mechanical ventilation required in 90% of patients with adult respiratory distress syndrom e
P.1069
Essential Workup
Suspect necrotizing fasciitis when pain is out of proportion to exam ination.
Rapid adm inistration of broad-spectrum antibiotics
Early surgical consultation
Tests Lab
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CBC with differential: o
Mild leukocytosis with left shift initially
Electrolytes, blood urea nitrogen, and creatinine
Calcium level: o
Hypocalcem ia in association with fat necrosis from necrotizing fasciitis
Urinalysis: o
Hem oglobinuria if renal involvem ent
Serum creatine phosphokinase level that is elevated or rising correlates with necrotizing fasciitis or m yositis
Aerobic and anaerobic blood cultures
Wound cultures
Prothrom bin tim e/partial throm boplastin tim e/international norm alized ratio and dissem inated intravascular coagulation (DIC) panel
Imaging
Plain film s: o
Gas in soft tissues in 25–75% of cases of necrotizing fasciitis
o
Not com m only associated with group A beta-hem olytic streptococcal infection
o
More com m on in m ixed anaerobic infections
CT scan: o
Asym m etric thickening of deep fascia
o
Gas
MRI: o
High signal intensity of the fascia in T2-weighted im ages
Differential Diagnosis
Sepsis
Cellulitis
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Erysipelas
Necrotizing fasciitis/m yositis secondary to infection by another pathogen
Treatment Initial Stabilization
Maintain airway, breathing, and circulation.
Treat shock with fluids and pressors as needed: o
Hypotension is often intractable, and up to 10–20 L per day m ay be required.
Intubation and m echanical ventilation for: o
Adult respiratory distress syndrom e
o
Severe shock
o
Ventilatory failure
ED Treatment
Broad-spectrum antibiotics im m ediately after cultures: o
Penicillin (or a cephalosporin)
o
Anaerobic coverage (clindam ycin or m etronidazole)
o
Gram -negative coverage (am inoglycoside, third-generation cephalosporin, or ciprofloxacin)
Early surgical consultation for débridem ent: o
Im m ediate surgery indicated if:
Extensive necrosis or gas
Com partm ent syndrom e
Profound system ic toxicity
Aggressive group A beta-hem olytic streptococcal infections do not respond well to penicillin.
Clindam ycin has been found to be a potent suppressor of bacterial toxin synthesis and inhibits M-protein synthesis.
Pa ge 4 5 4
Reports of successful use of IV im m unoglobulin
Hyperbaric oxygen therapy rem ains controversial.
Medication (Drugs) Invasive Streptococcal Disease
Clindam ycin: 900 m g (peds: 40 m g/kg per day) q6h–q8h IV, and Penicillin G: 4 m illion units (peds: 250,000 IU per day) IV q4h–6h, or
Vancom ycin: 15 m g/kg q12h (peds: 10 m g/kg q6h) IV if patient has penicillin allergy
Polymicrobial Necrotizing Fasciitis and Fournier Gangrene
Metronidazole: 15 m g/kg IV loading dose, then 7.5 m g/kg IV q6h, and Ticarcillin/clavulanic acid: 3.1 g (peds: 200 m g/kg per day) IV q6h, or
Am picillin/sulbactam : 3 g (peds: 200 m g/kg per day) IV q6h, or
Piperacillin/tazobactam : 3.375 g IV q6h
Follow-Up Disposition Admission Criteria Intensive care unit adm ission for all patients with suspected invasive streptococcal infection
Discharge Criteria None
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References 1. Ahm ed S, Ayoub E. Severe, invasive group A streptococcal disease and toxic shock. Pediatr Ann. 1998;27:287–292. 2. Am erican Academ y of Pediatrics, Com m ittee on Infectious Disease. Severe invasive group A streptococcal infections: a subject review. Pediatrics. 1998;101:136–140. 3. Stevens DL. The flesh-eating bacterium : What's next? J Infect Dis. 1999;179:(suppl 2)S366–374. 4. Stevens DL. Invasive group A streptococcus infections. Clin Infect Dis. 1992;14:2–13.
Codes ICD9-CM 038.0 Streptococcal septicem ia
ICD10 B95.5
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Strido r
Stridor
Gregory Ciottone
Basics Description Im pedance of air m ovem ent through the upper airway, which causes high-pitched audible wheezing and vibratory harsh sounds evident on auscultation over larynx during inspiration.
Etiology
Congenital: o
Laryngom alacia
Ectopic thyroid: o
Laryngeal webs/rings
o
Vocal cord dysfunction
Infection: o
Bacterial tracheitis
o
Epiglottitis
o
Viral croup
o
Peritonsillar abscess
o
Retropharyngeal abscess
o
Supraglottitis
o
Uvulitis (e.g., Quincke disease)
o
Ludwig angina
o
Diphtheria
Pa ge 4 5 4
o
Tetanus
Extrinsic com pression: o
Traum a
o
Hem atom a
o
Vascular anom alies (e.g., rings)
Intralum inal obstruction of the trachea: o
Foreign body
o
Cyst
o
Invasive tum ors
o
Squam ous cell
o
Lym phom as
o
Thyroid carcinom as
o
Laryngeal or tracheal papillom a
Subglottic stenosis: o
Postoperative scarring
o
After radiation therapy
Angioedem a
Vocal cord dysfunction: o
Congenital
o
Surgical injury
o
Postintubation traum a
o
Thyroid m alignancy
o
Mediastinal m ass
Diagnosis Signs and Symptoms
Anxiety
Audible wheezing or grunting with inspiration
Increased respiratory rate
Effort required for inspiration:
Pa ge 4 5 4
o
Nasal flaring
o
Use of accessory m uscles
Intercostal retractions
Paradoxic diaphragm atic m ovem ent (late finding)
Dyspnea
Cough
Fever
Drooling
Sore throat
“Hot potato― voice in adults
Trism us: o
Peritonsillar abscess, retropharyngeal abscess, Ludwig angina
Respiratory distress: o
Agitation
o
Diaphoresis
o
Cyanosis
o
Decreased respiratory rate
o
Som nolence
Essential Workup Visualization of the upper airway:
Radiographic if sym ptom s very m ild; be careful!
Direct visualization in operating room with a surgeon prepared to perform a cricothyrotom y or tracheostom y is the safest approach.
Tests Lab These tests are not helpful and thus avoidable; m ay upset child even m ore.
Imaging
Pa ge 4 5 4
Radiograph of lateral neck:
Not essential
Only done in extrem ely m ild cases
Diagnostic Procedures/Surgery
Fiberoptic laryngoscopy: o
Should be perform ed with an intubating fiberoptic laryngoscope in a setting where a rapid surgical airway can be obtained
Direct laryngoscopy: o
Diagnostic study of choice
o
Should be perform ed in a setting where a rapid surgical airway can be obtained
Differential Diagnosis
Bronchospasm
Malingering (patient breathing against a closed glottis)
P.1071
Treatment Pre Hospital
Keep child calm , with m other if possible.
Supply blow-by oxygen.
Maintain adequate airway.
Use bag-valve m ask (BVM) if respiratory status deteriorates.
Intubate if BVM ineffective.
Provide rapid transport with ED notification.
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Initial Stabilization
In children: Avoid agitation. Supply blow-by oxygen.
Use 100% nonrebreathing-type face m ask
Pediatric Considerations
Avoid agitating child.
Watch for rapid deterioration of respiratory status.
ED Treatment
Airway m anagem ent: o
Stridor com prises a difficult airway passage:
Be prepared to create an airway surgically before intubation.
If tim e perm its, perform intubation in OR with surgeon and pediatric anesthesiologist present.
Intubate with tube one or two sizes sm aller than would be norm ally used.
Oral awake intubation: o
Ketam ine induction
o
Patient is sedated but continues to ventilate during procedure.
Avoid blind nasotracheal intubation.
Provide surgical airway if intubation fails or sudden deterioration in respiratory status occurs.
Postintubation ceftriaxone in cases of infectious cause
Sedation/Paralysis for duration of intubated status after airway is secured.
Medication (Drugs)
Atropine: 0.02 m g/kg IV
Ceftriaxone: 1–2 g IV
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Diazepam : 2–10 m g IV (peds: 0.2–0.3 m g/kg)
Etom idate: 0.3 m g/kg IV
Fentanyl: 3 µg/kg IV
Ketam ine: 1–2 m g/kg IV or 4–7 m g/kg IM
Lidocaine: 1.5 m g/kg IV
Midazolam : 1–5 m g IV (0.07–0.30 m g/kg for induction)
Vecuronium : 0.1 m g/kg IV
Controversies
Heliox therapy
Racem ic epinephrine therapy
Early intubation
Follow-Up Disposition Admission Criteria All cases of stridor m andate adm ission of patient to hospital.
Discharge Criteria N/A
References 1. Beckm an DB. Diagnostic dilem m a: vocal cord dysfunction. Am J Med. 2001;110:731–741. 2. Chang AB. A review of cough in children. J Asthm a. 2001;38:299–309. 3. Gupta VK. Heliox adm inistration in the pediatric intensive care unit: an evidence based review. Pediatri Crit Care Med. 2005;6(2):204–211. 4. Konarzewski W. Adult epiglottitis: an under-recognized, life
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threatening condition. Br J Anaesth. 2001;86:456–457. 5. Levy RJ. Pediatric airway issues. Crit Care Clin. 2000;16:489–504. 6. McGahey-Oakland PR. A wheezing toddler. J Pediatr Healthcare. 2005;19(3):176–177. 7. Nakam ura H. Acute epiglottitis: a review of 80 patients. J Laryngol Otol. 2001;115:31–34. 8. Verghese ST. Pediatric otolaryngologic em ergencies. Anesthesiol Clin North Am . 2001;19:237–256.
Codes ICD9-CM 786.1 Stridor
ICD10 R06.1
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Subarachno id Hem o rrhage
Subarachnoid
Hemorrhage John W. Morehouse Rebecca Smith-Coggins
Basics Description Bleeding into the subarachnoid space and cerebrospinal fluid (CSF):
Spontaneous or traum atic
Spontaneous m ost often results from cerebral aneurysm rupture
If traum atic, represents severe head injury
Epidemiology
Incidence is 6–10 per 100,000 individuals.
Affects 30,000 in North Am erica annually
Results in death or severe disability in 40–60%.
Uncom m on prior to third decade; incidence peaks in sixth decade
Risk Factors
Fam ily history
Hypertension
Sm oking
Pa ge 4 5 5
Alcohol abuse
Cocaine, m etham phetam ine, and ecstasy (MDMA) use
Gender (fem ale:m ale = 1.6:1)
African Am erican and Japanese ethnicity
Genetics
Three- to seven-fold increased risk with first degree relatives with subarachnoid hem orrhage (SAH)
Autosom al dom inant polycystic kidney disease: o
Strongest genetic association, but represents only 2% of SAH patients
Pediatric Considerations
Most often due to arteriovenous m alform ation in children
Although rare in children, SAH is a leading cause of pediatric stroke.
Aneurysm s that occur are m ore likely to rupture and to be giant (>25 m m ).
Etiology
“Congenital,― saccular, or Berry aneurysm rupture (80–90%) o
Occur at bifurcations of m ajor arteries
o
Incidence increases with age.
o
Aneurysm s m ay be m ultiple in 20–30%.
Nonaneurysm al perim esencephalic hem orrhage (10%)
Rem aining 5% of causes include: o
Mycotic (septic) aneurysm due to syphilis or endocarditis
o
Arteriovenous m alform ations
o
Vertebral or carotid artery dissection
o
Intracranial neoplasm
o
Pituitary apoplexy
Severe closed head injury
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Diagnosis Signs and Symptoms History
Classically a severe, sudden headache: o
Often described as “thunderclap― or “worst headache of life―
o
Headache is often occipital or nuchal, but m ay be unilateral.
o
Usually develops within seconds and peaks within m inutes
o
Distinct from prior headaches
o
Headache often m axim al at onset
Sentinel headaches and m inor bleeding occur in 20–50%: o
May occur days to weeks prior to presentation and diagnosis
Seizures, transient loss of consciousness, or altered level of consciousness occur in m ore than 50% of patients.
Vom iting occurs in 70%.
Syncope, diplopia, and seizure are particularly high-risk features for SAH.
Physical Exam
Focal neurological deficits occur at the sam e tim e as the headache in one third: o
Third cranial nerve (CN) palsy (the “down and out― eye) occurs in 10–15%.
o
Isolated CN VI palsy or papillary dilation m ay also occur.
Pa ge 4 5 5
Nuchal rigidity develops in 25–70%.
Retinal hem orrhage m ay be only clue in com atose patient.
Essential Workup
Com plete neurologic exam ination and funduscopic exam
Em ergent noncontrast head CT scan: o
Diagnoses 93–98% of SAH if perform ed within 12 hours
o
Thin cuts (3 m m ) through base of brain im prove diagnostic yield.
o
CT is less sensitive after 24 hours or if hem oglobin is less than 10 g/l.
Lum bar puncture (LP) and CSF analysis m ust be perform ed if CT negative and history suggests possibility of SAH,
Pregnancy Considerations
Incidence slightly increased in pregnancy
Workup should include CT scan and LP.
Tests Lab
Baseline CBC, platelets, and differential
Electrolytes, renal and liver function tests
Co-agulation studies
Cardiac m arkers: o
Troponin-I elevated in 10–40%
CSF analysis (see below)
Imaging
Chest radiograph for pulm onary edem a: o
Occurs in up to 40% with severe neurological deficit
Four-vessel digital subtraction cerebral angiography is traditional im aging standard.
Spiral CT angiography m ore sensitive and m ore useful for
Pa ge 4 5 5
operative planning.
Magnetic resonance angiography: o
MRI is less sensitive for hem orrhage.
Transcranial Doppler ultrasound m ay be useful in detecting vasospasm .
Diagnostic Procedures/Surgery
LP: o
Presence of erythrocytes in CSF indicates SAH or traum atic tap.
o
If traum atic tap suspected, LP should be perform ed one interspace higher.
o
Dim inishing erythrocyte count in successive tubes suggests but does not firm ly establish a traum atic tap.
o
Xanthochrom ia is diagnostic of SAH if perform ed 12 hours after onset.
o
An elevated opening pressure m ay indicate SAH, cerebral venous sinus throm bosis, or pseudotum or cerebri.
ECG: o
ST-segm ent elevation or depression
o
QT prolongation
o
T-wave abnorm alities
o
Often m im ics ischem ia or infarction
o
Sym ptom atic bradycardia, ventricular tachycardia, and ventricular fibrillation
Differential Diagnosis
Neoplasm
Arterial dissection
Aneurysm (unruptured)
Arteriovenous m alform ation
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Migraine
Pseudotum or cerebri
Meningitis
Encephalitis
Hypertensive encephalopathy
Hyperglycem ia or hypoglycem ia
Tem poral arteritis
Acute glaucom a
Subdural hem atom a
Epidural hem atom a
Intracerebral hem orrhage
Throm boem bolic stroke
Sinusitis
Seizure disorder
Cerebral venous sinus throm bosis
P.1073
Treatment Pre Hospital
Initial assessm ent and history is helpful: o
Level of consciousness
o
Glasgow Com a scale score
o
Gross m otor deficits
o
Other focal deficits
Patients with SAH m ay need em ergent intubation for rapidly deteriorating level of consciousness.
IV access should be established.
Provide supplem ental oxygen.
Pa ge 4 5 5
Monitor cardiac rhythm .
Patients should be transported to a hospital with em ergent CT scan and intensive care unit capability.
Initial Stabilization
Manage airway, resuscitate as indicated: o
Rapid sequence intubation
o
Pretreat with lidocaine, fentanyl and de-fasciculating dose of nondepolarizing paralytic to blunt increase in intracranial pressure (ICP) during intubation.
o
Cardiac m onitoring and pulse oxim etry
o
Establish adequate IV access.
Obtain urgent neurosurgical consultation.
ED Treatment
Major goals: o
Prevent rebleeding.
o
Manage ICP, cerebral vasospasm .
Blood pressure (BP) control: o
Goal m ean arterial pressure 100–120 m m Hg, systolic BP 8 m m Hg and urine output >50 m L/h
o
Labetalol, hydralazine, nitroprusside or nicardipine for hypertension
o
Treat hypotension with volum e expansion.
o
Elevate head of bed to 30°
o
Prevent increases in ICP from vom iting and defecation with antiem etics and stool softeners.
o
Treat increased ICP with controlled ventilation and m annitol.
Pa ge 4 5 5
Cerebral vasospasm m ay cause secondary ischem ia and infarction after SAH: o
Nim odipine im proves outcom e:
o
Should start within 96 hours of SAH
Monitor with transcranial Doppler.
Seizures should be m anaged with IV benzodiazepine or diazepam and phenytoin: o
Prophylactic anticonvulsants not indicated
Correct tem perature, electrolyte, glucose, or pH abnorm alities.
Treat coagulopathy, throm bocytopenia, and severe anem ia.
Maintain norm al pO 2 and pCO 2 with controlled ventilation if necessary.
Monitor for and correct pulm onary edem a and cardiac arrhythm ias.
No current indication for use of glucocorticoid or antifibrinolytic therapies
When stable, expedited transfer to hospital with neurosurgical capabilities is m andatory.
Medication (Drugs)
Diazepam : 5–10 m g (peds: 0.2–0.3 m g/kg) IV/IM q10–15 m inutes PRN; m ax. 30 m g (peds: 10 m g)
Fentanyl:1–3 m cg/kg (adults and peds) IV q1h–q4h PRN
Fosphenytoin:15–20 phenytoin equivalents (PE) per kg (adults and peds) IV × 1; m aintenance 4–6 m g/kg/d IV
Hydralazine: 10–20 m g (peds: 0.1–0.5 m g/kg IV) q30m in–q4h PRN
Labetalol: 20 m g IV bolus, then 40–80 m g q10m in; m ax.
Pa ge 4 5 6
300 m g; follow with IV continuous infusion 0.5–2 m g/m in (peds: 0.4–1 m g/kg/h IV continuous infusion; m ax. 3 m g/kg/h)
Lidocaine: 1–1.5 m g/kg IV × 1 (adults and peds)
Lorazepam : 2–4 m g (peds: 0.03–0.05 m g/kg per dose; m ax. 4 m g per dose) IV q15m in PRN
Midazolam : 1–2 m g (peds: 0.15 m g/kg IV × 1) IV q10m in PRN
Morphine: 2–10 m g (peds: 0.05–0.2 m g/kg IV) q2h–q4h PRN
Nicardipine: 5–15 m g/h IV continuous infusion (peds: safety not established)
Nim odipine: 60 m g PO/NGT q4h; (peds: safety not established)
Nitroprusside: 0.25–10 m cg/kg/m in IV continuous infusion (adults and peds)
Ondansetron: 4–8 m g (peds: 0.1–0.15 m g/kg m ax. 4 m g) PO/IM/IV t.i.d. PRN
Phenytoin: 15–20 m g/kg IV load at m ax. 50 m g/m in; m ax. 1.5 g; m aintenance 4–6 m g/kg/d IV; (adult and pediatric)
Prom ethazine:12.5–25 m g (peds >2 years old: 0.25–1 m g/kg; m ax. 25 m g/dose) PO/IM/IV q4h–q6h hours PRN
Surgery
Per neurosurgical consultant
Early operative intervention m ay prevent vasospasm and im prove outcom e.
Follow-Up
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Disposition Admission Criteria
All patients with SAH should be adm itted to an intensive care unit.
Patients with negative CT findings and equivocal LP findings should be adm itted.
Discharge Criteria
Patients with negative CT and LP findings and onset of sym ptom s less than 2 weeks
Outpatient follow-up for headache treatm ent and further evaluation
Prognosis
Mortality is 12% before arrival to hospital.
Ultim ately fatal in m ore than 50%.
In cases of “sentinel bleed― or early detection of aneurysm al rupture, outcom es are im proved with early surgical or interventional approaches.
References 1. Claassen J, Vu A, Kreiter KT, et al. Effect of acute physiologic derangem ents on outcom e after subarachnoid hem orrhage. Crit Care Med. March 2004;32(3):832–838. 2. Edlow JA. Diagnosis of subarachnoid hem orrhage in the em ergency departm ent. Em erg Med Clin North Am . February 2003;21(1):73–87. 3. Edlow JA, Caplan LR. Avoiding pitfalls in the diagnosis of subarachnoid hem orrhage. N Engl J Med. January 6, 2000;342(1):29–36. 4. Shah KH, Richard KM, Nicholas S, Edlow JA. Incidence of traum atic lum bar puncture. Acad Em erg Med. February 2003;10(2):151–154. 5. Uysal E, Yanbuloglu B, Erturk M, Kilinc BM, Basak M. Spiral CT
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angiography in diagnosis of cerebral aneurysm s of cases with acute subarachnoid hem orrhage. Diagn Interv Radiol. June 2005;11(2):77–82.
Codes ICD9-CM 430 Subarachnoid hem orrhage, Meningeal hem orrhage Ruptured: Berry aneurysm (Congenital) Cerebral aneurysm NOS
ICD10 I60 Subarachnoid haem orrhage I60.9 Subarachnoid haem orrhage, unspecified I69.0 Sequelae of subarachnoid haem orrhage S06.6 Traum atic subarachnoid haem orrhage
CPT 62270 Lum bar puncture, diagnostic
Pa ge 4 5 6
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Subdural Hem ato m a
Subdural
Hematoma Colleen Campbell
Basics Description
Classification of subdural hem atom a (SDH): o
Acute: diagnosis within the first 3 days
o
Subacute: diagnosis 3 days to 3 weeks
o
Chronic: diagnosis after 3 weeks
CT description: o
Rarely crosses m idline
o
Does cross suture lines
o
Inner m argins are often seen to be irregular.
Acute
Most com m only due to acceleration-deceleration forces and less com m only from direct traum a
Sagittal m ovem ent of the head causes stretch of parasagittal bridging veins.
Other bleeding sites include: o
Laceration of dura
o
Venous sinus injury
o
Cortical arteries
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o
Nontraum atic injuries:
Intracerebral aneurysm rupture
Arteriovenous m alform ation
Co-agulation disorder
Arterial hypertension
Drug or alcohol abuse
Chronic Encapsulated hem atom a m ost likely caused by repeated sm all hem orrhages of bridging veins.
Etiology Acute
Most com m on type of intracranial hem atom a (66–70%)
Represents 26–63% of blunt head injury
Motor vehicle crash (MVC) is m ost com m on cause overall.
Falls and assault m ore com m only result in isolated SDH (72%) than do MVCs (24%).
Elderly patients and those with seizure disorders are at increased risk.
Mortality is related to presenting signs and sym ptom s as well as com orbidities: o
Less than one half present as sim ple extra-axial collection—22% m ortality rate
o
About 40% of patients will have com plicated SDH:
Parenchym al laceration or intracerebral hem atom a): m ortality rate >50%
o
Third group associated with contusion—30% m ortality rate with functional recovery of 20%
Chronic
Most com m on in babies or old people with atrophy: o
Associated with infarction in underlying brain
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75% of patients are >50 years old.
Less than one half have history of traum a.
50% are alcoholic.
Epilepsy, shunting procedures, and coagulopathy are also associated.
Pediatric Considerations
May occur secondary to traum a at birth
Nonaccidental traum a m ore com m on
Diagnosis Signs and Symptoms Acute
One fifth has diagnosis discovered at autopsy.
Most com m only m isdiagnosed as intoxication or cerebrovascular accident (CVA)
Headache and altered m ental status: o
50% unconscious at discovery
Subacute/Chronic
Headaches, nausea, vom iting, and seizures are frequent sym ptom s.
Presentation varied: o
Fluctuating m ental status
o
Unsteady gait
o
Slow progression of deficits
Pediatric Considerations Im aging is necessary in infants with persistent vom iting, new seizures, lethargy, irritability, bulging or tense fontanels.
Physical Exam
Pa ge 4 5 6
N/A
Acute
Headache and altered m ental status
Most com m on clinical signs are hem iparesis or hem iplegia:
o
Seen in 40–65%
o
SDH opposite m otor deficit in 60–85%
Pupillary abnorm ality seen in 28–79%: o
SDH will be on sam e side of pupillary abnorm ality in 70–90%.
Seizures m ay be seen in about 10% initially.
Papilledem a in less than one third
Chronic Presentation is varied and m im ics other diseases.
Essential Workup
Obtain directed history: o
Mechanism of injury kinetics
o
Neurologic status: baseline and at-scene
o
Com plicating factors:
Past m edical history, m edications
Allergies, drug use
Rapid neurologic assessm ent: o
Glasgow Com a scale ([GCS] after fluid resuscitation m ost im portant)
o
Brainstem reflexes:
Anisocoria
Pupillary light reflex
Corneal, gag, oculocephalic/oculovestibular
Head im aging
Tests Lab
Pa ge 4 5 6
Arterial blood gas, CBC, electrolytes with glucose, prothrom bin tim e (PT), partial throm boplastin tim e (PTT)
Blood ethyl alcohol, drug screen
Imaging Head CT in co-ordination with other necessary traum a workup
Acute
Characteristic CT finding is crescent-shaped clot overlying hem ispheric convexity.
Most (60%) associated with other intracranial lesions
Chronic
MRI is the test of choice as lesion m ay be isodense on CT from 2–3 weeks.
CT m ay show hypodense lesion after 3 weeks.
Spinal radiographs
Pediatric Considerations Ultrasound can be used to visualize cerebral structures if fontanelles are patent.
Differential Diagnosis Acute
Diffuse axonal injury
Cerebral contusion
Intracerebral bleed
Subdural hygrom a
Epidural hem atom a
Shaken baby/battered child syndrom e
Chronic
Pseudotum or cerebri
Brain tum or
Dem entia
Pa ge 4 5 6
Meningitis
CVA/Transient ischem ic attack
Cerebral atherosclerosis
Toxic, m etabolic, respiratory, or circulatory causes
P.1075
Treatment Initial Stabilization
Manage airway and resuscitate as indicated: o
Hypoxia is a strong predictor of outcom e.
o
Maintain SAO 2 >95%
o
Rapid sequence intubation (RSI) is indicated for GCS 60 years (highest rates of any age group, increasing incidence with age)
Risk Factors for Suicidal Behavior
Alcohol or drug abuse
History of physical or sexual abuse
History of head injury or neurologic disorder
Cigarette sm oking
Positive fam ily history of suicide attem pt
Prior psychiatric diagnosis: o
90% of patients who com m it suicide
o
Depression (bipolar or unipolar)
o
Substance abuse
o
Anxiety/Panic disorders
o
Schizophrenia
o
Personality disorders
o
Chronic severe m edical illness
o
Epilepsy
o
AIDS
o
Huntington disease
o
Stroke
o
Traum atic brain injury
o
Cancer
o
Multiple sclerosis
o
Spinal cord injuries
o
Hypertension
o
Cardiopulm onary disease
o
Peptic ulcer disease
o
Chronic renal failure
Pa ge 4 5 8
o
Cushing disease
o
Rheum atoid arthritis
o
Porphyria
Gender: o
Wom en are three tim es m ore likely to attem pt suicide.
o
Men are three tim es m ore likely to com plete suicide.
Psychological: o
Im pulsivity/Aggression
o
Depression
o
Anxiety
o
Hopelessness
o
Self-consciousness/social disengagem ent
o
Poor problem -solving abilities
o
Social
o
Widowed
o
Divorced
o
Separated
o
Lack of social supports
o
Recent loss of relationship
o
Anniversary of loss
Environm ental: o
Rural areas
o
Access to firearm s
o
Poverty
o
Unem ploym ent
Risk Factors for Completed Suicide
Male
Age >60 years
White or Native Am erican
Widowed/Divorced
Living alone
Pa ge 4 5 8
Unem ploym ent/Poverty
Past suicide attem pt
Methods of Suicide
Firearm s (m ost com m on am ong m en and wom en, three of five com pleted suicides)
Overdose (second m ost com m on am ong wom en); m ost com m on m eans of suicide attem pt (70% of failed attem pts are by overdose)
Hanging (second m ost com m on am ong m en)
Populations at Highest Risk for Completing Suicide
Depression—especially psychotic depression
Anxiety and panic disorder
Alcohol or drug intoxication
Schizophrenia
Adolescents
Others at Risk for Completing Suicide
Recent discharge from psychiatric facility
Past history of suicidal ideation or suicide attem pt
Serious physical illness is present up to 70% of all suicides, particularly in elderly patients.
Prisoners
Doctors
Victim s of violence/abuse
Persons expecting secondary gain through attem pt
Decreased Risk for Suicide
Patients with m ood disorders (m ajor depression and bipolar disorder) treated with lithium
Patient with m ajor depression treated with electroconvulsive therapy
Pa ge 4 5 8
Patients with schizophrenia treated with clozapine
Patients with m ajor depression treated with selective serotonin reuptake inhibitors (SSRI) not shown to decrease suicide rates
Diagnosis Signs and Symptoms
Depressed m ood
Verbalization of suicidal ideation
Hopelessness
Helplessness
Anger/Aggression
Im pulsivity
Psychotic sym ptom s (com m and auditory hallucinations)
Essential Workup
Obtain history to assess risk: o
Asking about suicide does not increase risk for attem pt
Degree of suicidal ideation
Plan: im m ediate risk of self-injury? o
Means available to com plete plan
o
Activity toward initiating plan
o
Patient's expectations of lethality of plan
Intent: reasons, goal
Risk-to-rescue ratio
Plan or intent to harm others?
Presence of acute precipitants: o
Recent losses, lack of social supports
Risk factors:
Pa ge 4 5 8
o
History of past suicide attem pts
o
Psychiatric review of sym ptom s: depression, psychosis, panic/anxiety
o
Chronic m edical illness
o
Alcohol or drug abuse
Serial assessm ent of m ental status, consistency of responses
“Why didn't you attem pt suicide?―
Collateral inform ation from outpatient treaters, fam ily, friends
Safety Plan
Would the patient im m ediately seek help if suicidal ideation recurred?
Elim ination of m eans of suicide
Access to other m eans of suicide
Support and supervision in the outpatient setting
Prom pt outpatient follow-up with psychiatric therapy
Patient investing in not attem pting suicide
Reasons for living?
Safety contracts are not useful
Tests
Blood alcohol level
Serum toxicology screen: aspirin, acetam inophen, and other m edications
Urine drug screen: o
Many psychiatric facilities require toxicology screen before placem ent.
ECG, carbon m onoxide (as indicated)
Im aging not routinely indicated
P.1079
Pa ge 4 5 8
Differential Diagnosis
Norm al despondency
Bereavem ent
Adjustm ent disorder with depressed m ood
Major depressive disorder
Bipolar disorder
Organic m ental disorder (head injury, dem entia, delirium )
Schizophrenia
Panic and anxiety disorders
Alcohol or drug abuse
Borderline personality disorder
Antisocial personality disorder
Accidental death
Attem pted hom icide
Pediatric Considerations
Suicide is third leading cause of death am ong young people 15–24 years of age.
More than 5,000 adolescents com m it suicide every year.
Rapidly increasing in young black m ales, ages 10–14 years
Less evidence available to link suicide in youth to overt psychiatric illness
Stresses: o
Prior attem pts
o
Fam ily disruption
o
History of psychiatric disorder
o
Depression
o
Disciplinary crisis
o
Broken rom ance
o
School difficulties
Pa ge 4 5 9
o
Bereavem ent
o
Rejection
o
History of physical or sexual abuse
Early warning signs: o
Progressive declining schoolwork
o
Multiple physical com plaints
o
Substance abuse
o
Disrupted fam ily relations
Geriatric Considerations
Suicide rates highest in age >65 years
Com pleted suicide: 83% m en
Risk factors: divorced, widowed, m ale, social isolation
Tend to use m ore lethal m ethods
Lower ratio of attem pts to com pletions
Treatment Pre Hospital
Restraint of potentially dangerous patient who refuses transport to treatm ent facility; involve police.
Risk to m edics on the scene in cases of firearm s or other weapons
Know state and local laws, availability of m obile crisis units, and when to involve the police departm ent.
Initial Stabilization
Prevent any ability to elope.
Search the patient. o
Rem ove sharp objects, belts, shoelaces, and other articles that could be use for self-injury.
Appropriate supervision
Pa ge 4 5 9
ED Treatment
Voluntary adm ission to psychiatric facility
Involuntary adm ission if patient refuses voluntary
For involuntary psychiatric adm ission, patient m ust have psychiatric disorder and one of the following: o
Risk for danger to self
o
Risk for danger to others
o
Unable to care for self owing to extrem ely poor judgm ent
Medication (Drugs) Treat underlying psychiatric disorder.
Follow-Up Disposition Admission Criteria
If patient endorses suicidal ideation with plan and intent, then adm ission m ay be needed for safety.
If im pulsivity, anger, or aggression hinder ability to control behavior
Discharge Criteria
Patient has no suicidal ideation.
Patient agrees to return to ED im m ediately or seek psychiatric help if suicidal ideation recurs.
Patient has passive suicidal ideation without plan or intent.
Good support network or placem ent in appropriate crisis housing
Pa ge 4 5 9
Appropriate outpatient psychiatric follow-up ensured
In som e cases, patients who express suicidal ideation while intoxicated m ay be discharged if no longer suicidal once they are sober.
Som e patients with borderline personality disorder and chronic suicidal ideation are discharged after careful psychiatric evaluation, in consultation with long-term outpatient caregivers.
References 1. Connor KR, Duberstein PR, Conwell Y, et al. Psychological vulnerability to com pleted suicide: a review of em pirical studies. Suicide and Life-Threatening Behavior. 2001;31(4):367–385. 2. Harwitz D, Ravizza L. Suicide and depression. Em erg Med Clin North Am . 2000;18(2):263–71, ix 3. Lagom asino IT, Stern TA. Approach to the suicidal patient. In Stern TA, Herm an JB, Slavin PL, eds. The MGH guide to psychiatry in prim ary care. New York, NY: McGraw-Hill, 1998:1522. 4. Mann JJ. A current perspective of suicide and attem pted suicide. Ann Intern Med. 2002;136(4):302–311.
Codes ICD9-CM 300.9
ICD10 Z91.5
Pa ge 4 5 9
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Supraventricular Tachycardia
Supraventricular Tachycardia James Adams Jason Liebzeit
Basics Description
Rhythm that originates ectopically above the His bundle
Heart rate of 100 beats/m in or greater
Irregular narrow com plex supraventricular tachycardia (SVT): o
Most com m on form of SVT seen in the ED
10% of people over 75 years of age have AF.
o
Atrial flutter
o
Multifocal atrial tachycardia
Regular narrow com plex SVT: o
o
Atrial fibrillation (AF):
Arteriovenous nodal re-entry:
60% of SVT
Typically present age 30–40 years
70% are wom en.
AV re-entry involving an accessory pathway
Wide com plex SVT: o
Aberrant conduction or a bundle branch block is
Pa ge 4 5 9
present. o
Conduction is outside of the norm al His-Purkinje system .
o
More com m on in younger patients without structural disease
o
Always suspect a ventricular rhythm with a wide com plex rhythm
Etiology
Atrial tachycardia: o
Precipitated by a prem ature atrial or ventricular contraction
o
Electrolyte disturbances
o
Drug toxicity
o
Hypoxia
Junctional tachycardia: o
AV nodal re-entry
o
Myocardial ischem ia
o
Structural heart disease
o
Pre-excitation syndrom es:
o
Wolff-Parkinson-White (WPW) syndrom e
Drug and alcohol toxicity
AF: o
Hypertension
o
Coronary artery disease
o
Hypothyroidism
o
Heavy alcohol intake
o
Mitral valve disease
o
Chronic pulm onary disease
o
Pulm onary em bolus
o
WPW syndrom e
o
Hypoxia
o
Digoxin toxicity
Pa ge 4 5 9
o
Chronic pericarditis
o
Idiopathic AF
Atrial flutter: o
Ischem ic heart disease
o
Valvular heart diseases
o
Congestive heart failure
o
Myocarditis
o
Cardiom yopathies
o
Pulm onary em bolus
o
Other pulm onary disease
Diagnosis Signs and Symptoms
Palpitations (m ost com m on)
Lightheadedness, pressure in the head
Dyspnea
Diaphoresis
Dizziness
Weakness
Chest discom fort
Syncope
Prom inent neck veins
Signs of instability: o
Mental status changes
o
Chest pain/ischem ia
o
Acute pulm onary edem a
o
Hypotension
History
Abrupt onset of palpitations, lightheadedness, weakness,
Pa ge 4 5 9
chest pain
Insidious onset of generalized weakness and m alaise
Physical Exam
Vital signs: o
Tachycardia
o
Blood pressure norm al or hypotensive
o
Respiratory rate norm al or tachypneic
Cardiac: o
Regular or irregularly irregular rhythm
o
JVD m ay be present in setting of heart failure
Pulm onary: o
Rales m ay be present in setting of heart failure.
Essential Workup
ABCs, assess stable vs. unstable
History: o
Current sym ptom s
o
Previous episodes
o
Prior cardiac history
o
Medications:
o
Over-the-counter, decongestants
Illicit drug use
ECG: o
Regular or irregular?
o
Quasi random signal com plex narrow or wide?
o
P waves present or absent:
Regular or irregular?
Tests ECG
Atrial flutter: o
Regular atrial rate usually greater than 300
Pa ge 4 5 9
o
Beat-to-beat uniform ity of cycle length, polarity, and am plitude
o
Sawtooth flutter waves directed superiorly and m ost visible in leads II, III, aVF
o
AV block, usually 2:1, but occasionally greater or irregular
Multifocal atrial tachycardia: o
Three distinctly different P waves with varying pulse rate intervals
Atrial tachycardia: o
Rate of 100–200 beats/m in
o
P wave precedes QRS and is m orphologically different from the sinus P wave.
Junctional tachycardia: o
There is usually 1:1 conduction, with ventricular rates equaling the atrial rate.
o
May be either paroxysm al or sustained
o
Ventricular rates faster than 200 beats/m in in an adult suggest an accessory pathway syndrom e such as WPW syndrom e.
o
Absence of preceding P waves
o
Often retrograde P waves buried in the QRS
o
Paroxysm al junctional tachycardia rates range from 120–200 beats/m in.
o
Nonparoxysm al junctional tachycardia rates rarely exceed 130 beats/m in.
Lab Studies are indicated when underlying m etabolic abnorm alities or ischem ia is considered:
CBC
Electrolytes
Cardiac enzym es
Pa ge 4 5 9
Thyroid function
Imaging Chest radiograph:
Assess cardiac size
Evaluate for pulm onary process
More useful in AF/flutter
Differential Diagnosis
Sinus tachycardia: o
Sepsis
o
Hypovolem ia
o
Pericardial tam ponade
o
Acute m yocardial infarction
o
Drug intoxication
o
Infection
Wide com plex tachycardias: o
Distinguish between supraventricular with aberrancy or ventricular origins.
P.1081
Treatment Pre Hospital
Supplem ental oxygen
IV access
Monitor
Initial Stabilization
IV access
Pa ge 4 5 9
Oxygen
Monitor
Determ ination of unstable versus stable patient m ade by determ ining whether the patient has organ perfusion (if patient is awake and talking, there is usually tim e to try other m ethods before cardioversion even with low BP).
ED Treatment
AF: o
Most likely diagnosis when the rhythm is irregular
o
When unstable, then im m ediate cardioversion
o
When stable, rate control is a priority:
Beta-blockers or calcium -channel blockers, am iodarone, and digoxin
Cardioversion in stable patients should not be attem pted unless the dysrhythm ia is known to be acute ( Table o f C o ntents > Synco pe
Syncope
Sam Keim Amy Baldwin
Basics Description
Transient loss of consciousness associated with loss of postural tone
Ultim ately, it is the lack of oxygen to the brainstem reticular-activating system , which results in a loss of consciousness and postural tone.
Most com m only, an inciting event causes a drop in cardiac output.
Cerebral perfusion is re-established by autonom ic regulation as well as the reclined posture, which results from the event.
Accounts for 3% of ED visits
Geriatric Considerations
Elderly with highest incidence as well as increased m orbidity
>One third will have num erous potential causes.
Etiology
Neurally m ediated syncope:
Pa ge 4 6 1
o
Reflex response causing vasodilatation and bradycardia with resulting hypoperfusion
o
Vasovagal (com m on faint):
Often incited by pain or fear
Prodrom al findings are usually present.
Typically lasts less than 20 seconds
Tilt-table testing is the gold standard to diagnose.
o
Carotid sinus syncope:
Cough, sneeze
Gastrointestinal stim ulation (e.g., defecation)
Micturition
Orthostatic: o
Positional changes cause abrupt drop in venous return to heart.
o
Volum e depletion:
Severe dehydration (e.g., vom iting, diarrhea, diuretics)
o
Hem orrhage (see Hem orrhagic Shock)
Autonom ic failure:
Diabetic or am yloid neuropathy
Parkinson disease
Drugs (e.g., beta blockers) and alcohol
Cardiac arrhythm ias: o
Typically sudden and without prodrom al sym ptom s
o
Tachydysrhythm ia or bradydysrhythm ia
o
Inherited syndrom es (e.g., long QT syndrom e, Brugada syndrom e)
o
Pacem aker/im plantable cardioverter defibrillator m alfunction
Structural cardiac or cardiopulm onary disease: o
Valvular disease (especially aortic stenosis)
Pa ge 4 6 1
o
Hypertrophic cardiom yopathy
o
Acute m yocardial infarction
o
Aortic dissection
o
Pericardial tam ponade
o
Pulm onary em bolus
Neurologic: o
Transient spike in intracranial pressure that exceeds cerebral perfusion pressure
o
Postsyncopal headache is alm ost universal.
o
May be presentation of a subarachnoid hem orrhage
Cerebrovascular steal syndrom es
Diagnosis Signs and Symptoms History
Prodrom al sym ptom s: o
Lightheadedness
o
Diaphoresis
o
Dim m ing vision
o
Nausea
o
Weakness
The following findings suggest an underlying life threat: o
Sudden event without warning
o
Chest pain or palpitations
Six Ps of a syncope history: o
Pre-Prodrom e activities
o
Prodrom e sym ptom s—visual sym ptom , nausea
o
Predisposing factors—age, chronic disease, fam ily history of sudden death
Pa ge 4 6 1
o
Precipitating factors—stress, postural sym ptom s
o
Passerby witness—what did they see?
o
Postictal phase, if any—suggests seizure
Physical Exam
Evaluate for traum a.
Orthostatic vital signs
Check for difference in blood pressure in both arm s suggesting aortic dissection or subclavian steal syndrom e.
Careful cardiovascular exam ination, including m urm urs, bruits, and dysrhythm ias
Rectal exam ination to check for gastrointestinal (GI) bleeding
Urine pregnancy test in reproductive age fem ale
Careful neurologic exam ination
Pediatric Considerations
Warning signs of a potential serious underlying disease: o
Syncope during exertion
o
Syncope to loud noise, fright, extrem e stress
o
Syncope while supine
o
Fam ily history of sudden death at young age (125 m Eq/L
No unstable com orbid factors
Known diagnosis of SIADH
References 1. Adrogue HJ, Madias NE. Prim ary care: Hyponatrem ia. New Eng J Med. May 25, 2000;342:1581–1589. 2. Fried LF, Palevsky PM. Hyponatrem ia and hypernatrem ia. Med Clin North Am . 1997;81(3):585–609. 3. Miller M. Syndrom e of excess antidiuretic horm one release. Crit Care Clin. 2001;17(1):1123. 4. Sorensen JB, Anderson MK, Hansen HH. Syndrom e of inappropriate secretion of antidiuretic horm one (SIADH) in m alignant disease. J Intern Med. 1995;238(2):97–110. 5. Spigset O, Hedenm alm K. Hyponatrem ia and the syndrom e of inappropriate antidiuretic horm one secretion (SIADH) induced by psychotropic drugs. Drug Saf. 1995;12(3):209–225.
Miscellaneous SEE ALSO: Hyponatrem ia
Codes ICD9-CM 253.6
ICD10 E22.2
Pa ge 4 6 3
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Syno vitis, To xic
Synovitis, Toxic
James E. Colletti Dick Kuo
Basics Description
Acute inflam m ation of the hip joint in children associated with joint effusion
Disease process is self-lim iting.
Num ber-one cause of hip pain in children younger than 10 years of age
Also referred to as transient synovitis and irritable hip syndrom e.
Age group m ost affected is 3–6 years.
2:1 m ale predom inance
Right hip is affected m ore than the left.
Etiology
Cause of toxic synovitis (TTS) is unknown.
Infectious etiology is suspected because there is a preceding upper respiratory illness in a large num ber of cases.
Pa ge 4 6 3
Diagnosis Signs and Symptoms History
Unilateral hip pain, acute onset
Painful lim p
Pain in anterom edial thigh and knee
Refusal or inability to bear weight
Recent or current upper respiratory infection
Physical Exam
Low-grade fever
Nontoxic appearing
Lim itation of hip m edial rotation and abduction
Preferred external rotation, abduction, and flexion
Pain over anterior portion of hip with palpation
Tests Lab
CBC, erythrocyte sedim entation rate (ESR), C-reactive protein (CRP): o
Norm al or elevated
One investigation concluded that if two out of following four criteria are present, there is a 95% sensitivity and 91% specificity for septic arthritis (SA):
o
Severe pain and spasm
o
Tem perature >38°C
o
ESR >20 or CRP >1
o
Tenderness on palpation
An investigation by Kocher et al. utilized the following clinical data to differentiate TTS from SA: o
History of fever
o
Non-weight bearing
Pa ge 4 6 3
o
ESR ≥40 m m /hr
o
WBC >12,000 cell/m m 3
An elevated CBC or ESR alone does not differentiate TTS from SA or osteom yelitis: o
If both CBC and ESR/CRP are norm al, m ore serious causes of hip pain are less likely.
Imaging
Plain hip film s (anteroposterior and frog-leg view): o
Usually norm al
o
May detect an effusion or other causes of hip pain
MRI (rarely indicated): o
Very useful in diagnosing Legg-Calvé-Perthes (LCP) disease
o
Can detect abnorm alities in TTS
o
An investigation by Lee suggested that signal intensity alteration in the bone m arrow of the affected hip m ight differentiate TTS from SA.
Bone scan: o
Used to differentiate LCP disease from TTS
o
Can detect osteom yelitis
o
The increased radiation is usually reserved for recurrent cases or cases in which the diagnosis is still in question.
o
Negative bone scan decreases the likelihood of infection, fracture, or tum or.
Ultrasound to rule out joint effusion if high suspicion for septic arthritis
If a joint effusion is present, an ultrasound-guided joint aspiration should be perform ed to rule out septic arthritis.
Diagnostic Procedures/Surgery Joint aspiration:
Pa ge 4 6 3
Not necessary if the patient is afebrile with a norm al CBC and ESR/CRP
Abnorm al joint fluid analysis indicates SA (see Arthritis, Septic)
Differential Diagnosis
SA
Osteom yelitis
Soft-tissue infection
LCP disease
Slipped capitol fem oral epiphysis
Juvenile rheum atoid arthritis
Rheum atic fever
Chondrolysis
Gaucher disease
Osteosarcom a
Ewing sarcom a
Osteoid osteom a
Leukem ia
Tuberculosis of the hip
Fracture
Lym e disease
Psoas abscess
Sickle cell crisis
P.1089
Pediatric Considerations
Second event m ay occur in 4–17% within 6 m onths of initial event
Association of TTS with LCP disease
2–10% of patients with TTS later develop LCP disease:
Pa ge 4 6 3
o
Suggested that TTS m ay represent an early stage of LCP disease.
Treatment ED Treatment
Conservative treatm ent
Bed rest in position of com fort—flexion and external rotation
Initiate NSAIDs.
Antibiotics and steroids are not indicated.
Som e authors recom m end no weight-bearing for 7–10 days following im provem ent and return of norm al hip function, citing increased risk for recurrence.
Close follow-up essential with repeat radiographs due to association with LCP
Medication (Drugs)
Ibuprofen: 200–600 m g (peds >6 m onths old: 5–10 m g/kg/dose) PO q6h
An investigation by Fink dem onstrated that ibuprofen decreased sym ptom s duration.
Disposition Admission Criteria Patients with severe joint pain or a large effusion m ay require hospitalization for bed rest and analgesics.
Discharge Criteria All patients who have been excluded for m ore serious diagnosis of hip
Pa ge 4 6 3
pain and diagnosed with toxic synovitis can be discharged from the hospital with good follow-up.
References 1. Della-Giustina K, Della-Giustina D. Em ergency departm ent evaluation and treatm ent of pediatric orthopedic injuries. Em erg Med Clin North Am . 1999;17(4):895–922. 2. Do T. Transient synovitis as a cause of painful lim ps in children. Curr Opin Pediatr. 2000;12:48–51. 3. Eich G, et al. The painful hip: evaluation of criteria for clinical decision-m aking. Eur J Pediatr. 1999;158:923–928. 4. Hoffer FA, Zawin JK, Rand FF, et al. Joint effusion in children with an irritable hip: US diagnosis and aspiration. Radiology. 1993;187:459–463. 5. Kerm ond S, Fink M, Graham K, Carlin JB, Barnett P. A random ized clinical trial: should the child with transient synovitis of the hip be treated with nonsteroidal anti-inflam m atory drugs? Ann Em erg Med. Septem ber 2002;40(3):294–299. 6. Kocher MS, Mandiga R, Zurakowski D, Barnewolt C, Dasser JR. Validation of a clinical prediction rule for the differentiation between septic arthritis and transient synovitis of the hip in children. J Bone Joint Surg. 2004;86:1629–1635. 7. Koop S, Quanbeck D. Three com m on causes of childhood hip pain. Pediatr Clin North Am . 1996;43:1053–1066. 8. Lee S, et al. Septic arthritis versus transient synovitis at MR im aging: prelim inary assessm ent with signal intensity alterations in bone m arrow. Radiology. 1999;211:459–465. 9. Spock A. Transient synovitis of the hip joint in children. Pediatrics. 1959;24:1042. 10. Tachidjian MS. Acute transient synovitis of the hip. In: Tachidjian MS, ed. Pediatric orthopedics. Philadelphia, PA: WB Saunders, 1990:1461–1465.
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Syphilis
Syphilis
JiWon E. Lee
Basics Description
Sexually transm itted disease
One hundred thousand new cases per year in United States
Acquired via m ucous m em branes/disrupted skin
Spirochetes m ultiply at site of inoculation and spread via lym phatics and bloodstream : o
Prim ary syphilis:
o
Secondary syphilis:
o
Focal enarteritis, prim ary pathologic lesion
Replication and hem atogenous spread
Secondary/tertiary syphilis:
Granulom atous reaction
Infectious during prim ary and secondary stages
Cofactor transm ission of HIV
Etiology Treponem a pallidum :
Spirochete bacteria
Pa ge 4 6 3
Diagnosis Signs and Symptoms Primary (Early) Syphilis
Two- to three-week incubation period
Chancre: o
Painless papule at site of inoculation
o
Clean-based, circular, sharply defined borders:
o
Solitary lesions
Com m only on penis, vulva, and rectum
Bilateral regional lym phadenopathy
Heal spontaneously in 3–6 weeks
Rectal chancre: o
Painful or painless
o
Rectal irritation/discharge
o
Painless enlargem ent of lym ph nodes
Secondary (Early) Syphilis
Twenty-five percent with untreated infection
Weeks to m onths after initial infection
Rash (m ost com m on):
o
Sym m etric, diffuse, m aculopapular rash
o
Starts on trunk and flexor extrem ities
o
Classic involvem ent of palm s and soles:
Discrete, red/reddish-brown
0.5–2 cm in diam eter
Condylom a lata: o
Large, raised, gray/white lesions
o
Warm , m oist areas:
Mucus m em branes in m outh and perineum
Intertriginous areas
Flat rectal warts
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System ic sym ptom s: o
Fever, headache, m alaise, anorexia, sore
o
throat, m yalgias, and weight loss
Diffuse lym phadenopathy: o
Palpable nodes at inguinal, axillary, posterior cervical, fem oral, and/or epitrochlear regions
o
Painless, firm , and rubbery
Less com m on: o
“Moth-eaten― alopecia
o
Syphilitic m eningitis
Loss of lateral third of eyebrows
Painless m ucosal lesions (m ucous patches)
Heal spontaneously in 1–2 m onths
Latent Syphilis
Period of no sym ptom s but positive serology: o
Cerebrospinal fluid (CSF) is norm al.
Late latent not infectious except for fetal transm ission in pregnant wom en
Persists for lifetim e or develops into tertiary syphilis
Tertiary (Late) Syphilis
Years after initial infection (up to 20 years): o
Destructive stages of disease
Neurosyphilis (m ost com m on): o
o
Asym ptom atic:
Positive CSF-VDRL
CSF pleocytosis (10–100 lym phocytes)
Elevated CSF protein at 50–100 m g/dL
Meningitis:
Aseptic; CSF with positive VDRL, higher protein, and lower glucose (com pared with above)
Cranial nerve palsy, including isolated eighth
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nerve palsy o
General paresis:
Progressive dem entia
Loss of cortical function
Argyll Robertson pupils (sm all fixed pupils that do not react to strong light, but do react to accom m odative convergence)
o
Tabes dorsalis (neuropathy):
Degeneration of posterior colum ns/posterior or dorsal roots of spinal cord
Paresthesias, abnorm al gait, and lightning (sudden, severe) pain of extrem ities/trunk
Progressive loss of reflexes, vibratory/position sensation
Positive Rom berg sign
Vision: optic atrophy
Pupils: Argyll Robertson pupils
Urinary incontinence
Gum m as: o
Late benign syphilis of cutaneous skin/viscera:
o
Bone, brain, abdom inal viscera, and so on
Granulom atous, cellular hypersensitivity Reaction:
Round, irregular, or serpiginous shape
“Great pox―
Cardiovascular: o
Thoracic aneurysm (ascending m ost com m on):
Dilated aorta and aortic valve regurgitation
o
Aortic insufficiency
o
Coronary throm bosis
Destructive lesions of skeletal structures or skin
HIV infected: o
Strong association with syphilis
Pa ge 4 6 4
o
Increased incidence of neurosyphilis
Congenital Syphilis In utero infection:
Age 45 m g/dL
Differential Diagnosis
Genital ulcer: o
Chancroid (painful)
o
Genital herpes:
Vesicular, m ultiple lesions
o
Lym phogranulom a venereum
o
Granulom a inguinale
o
Superficial fungal infection
o
Carcinom a
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Secondary syphilis: o
Pityriasis rosea
o
Drug-induced rash
o
Acute febrile exanthem s
o
Psoriasis
o
Lichen planus
o
Scbies
o
Infectious m ononucleosis
Treatment Initial Stabilization Lower blood pressure and establish IV access for aortic dissection.
ED Treatment
Treatm ent other than penicillin with increased relapse rate: o
Desensitize those allergic to penicillin.
Pregnancy: o
Teat with penicillin even in latent syphilis.
o
If patient allergic to penicillin, adm it for desensitization.
Jarisch-Herxheim er reaction: o
Transient febrile reaction to therapy
o
May be owing to antigen liberation from spirochetes or com plem ent cascade activation
o
Peaks at 8 hours, resolves in 24 hours
o
Sym ptom s:
Fever, headache, m alaise, worsening rash
o
Treat with antipyretics.
o
No serious sequelae
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Recom m ended testing: o
Sexual partners
o
Concom itant sexually transm itted diseases Including HIV
o
Repeat serology test in 6 and 12 m onths.
Medication (Drugs)
Early prim ary, secondary, latent (1 year) except neurosyphilis: o
Benzathine penicillin G: 2.4 m illion U IM weekly for 3 weeks
o
Doxycycline: 100 m g PO b.i.d. for 4 weeks
o
Tetracycline: 500 m g PO q.i.d. for 4 weeks
Neurosyphilis: o
Penicillin G: 3–4 m illion U IV q4h for 10–14 days
o
Procaine penicillin: 2.4 m illion U IM daily plus Probenecid: 500 m g PO q.i.d. for 10–14 days
Congenital syphilis: o
Penicillin G: 50,000 µg/kg IM q8h–q12h for 10–14 days or
o
Procaine penicillin: 50,000 µg/kg IM daily for 10–14 days
Follow-Up Disposition
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Admission Criteria
Neurosyphilis requiring IV antibiotics
Pregnant wom en allergic to penicillin requiring desensitization
Discharge Criteria Follow-up care:
Measure for falling titers in 6 m onths and 1 year after treatm ent.
Tertiary/latent (>1 year): o
Measure for falling titers in 3, 6, 12, and 24 m onths after treatm ent.
References 1. Hook EW. Syphilis control: a continuing challenge. N Eng J Med. 2004;351:122. 2. McKinzie J. Sexually transm itted disease. Em erg Med Clin North Am . 2001;19:723–743. 3. Centers for Disease Control and Prevention (CDC). Prim ary and secondary syphilis in United States, 2002. MMWR Morb Mortal Wkly Rep. 2003;52:1117. 4. Schacter J. Classification of latent syphilis. Sex Transm Dis. 2005;32:143. 5. Tim m erm ans M. Neurosyphilis in the m odern era. J Neurol Neurosurg Psychiatry. 2004;75:1727.
Codes ICD9-CM 97.0 (090–099)
ICD10 A53.9
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > System ic Lupus Erythem ato sus
Systemic
Lupus Erythematosus Steven Furer
Basics Description
Lupus is a chronic autoim m une disease with a peak onset between the ages of 15 and 40 years characterized by flares and rem issions.
It is a m ultisystem disease with diverse clinical m anifestations: o
Arthritis
o
Cardiac:
o
o
Endocarditis
Myocarditis
Congestive heart failure
Conduction abnorm alities
Atherosclerosis
Myocardial infarction
Renal:
Glom erulonephritis
Renal failure
Pulm onary:
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o
Pleural effusion (usually exudative)
Pneum onitis
Pulm onary hem orrhage
Pulm onary em bolism
Pneum onia
Pleuritis
Pulm onary edem a
Pulm onary hypertension
Neurologic:
o
o
Lupus cerebritis
Vascular:
Vasculitis
Throm bosis
Atherosclerosis
Gastrointestinal (GI):
Peritonitis
Mesenteric vasculitis and ischem ia
Pancreatitis
Pediatric Considerations
Neonatal lupus m ay occur when m aternal autoantibodies cross the placenta.
Congenital heart block is the m ost serious com plication.
Geriatric Considerations
Ten tim es greater risk of m yocardial infarction due to atherosclerosis
High incidence of osteoporosis related to chronic steroid use
Genetics
More com m on in fem ales than m ales (ratio, 9:1)
More com m on in African Am ericans
Higher frequency of system atic lupus erythem atosus and
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other autoim m une diseases am ong first-degree relatives
Etiology
Autoantibody production against cell nucleus and cytoplasm ic structures leading to inflam m atory changes, vasculitis, and im m une com plex deposition in m ultiple organ system s
A significant percentage of patients have an associated antiphospholipid syndrom e: o
Characterized by antibodies against cellular phospholipid com ponents
o
Tendency toward recurrent vascular throm bosis
Lupus is a chronic disease with exacerbating factors: o
Infection
o
Sun exposure
o
Traum a
o
Medications
o
Stress
o
Diet
Drug-induced lupus is a m ilder disease that eventually resolves once the m edication is discontinued: o
Chlorprom azine
o
Methyldopa
o
Procainam ide
o
Hydralazine
o
Isoniazid
o
Quinidine
Diagnosis
Four of the 11 criteria from the following list are needed to m ake the diagnosis:
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o
Malar rash
o
Discoid rash
o
Photosensitivity rash
o
Oral ulcers
o
Arthritis
o
Serositis
o
Neurologic disorders
o
Hem atologic disorders
o
Im m unologic disorders
o
Renal disorders
o
Antinuclear antibodies
Signs and Symptoms
System ic: o
Fatigue
o
Fever
o
Weight loss
o
Dyspnea
Skin: o
Malar rash (butterfly facial)
o
Discoid rash (raised red patches)
o
Photosensitivity rash (subacute cutaneous lupus)
Musculoskeletal: o
Myalgias
o
Joint pain
o
Arthritis:
Defined as two or m ore peripheral joints with warm th, tenderness, or effusion
Polyarthritis, sym m etric, or m igratory
Heart: o
Chest pain
o
Pericardial rub
o
Murm ur
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Vascular: o
Vasculitis
o
Throm bosis
o
Atherosclerosis
o
Peripheral vascular disease
Lungs: o
Dyspnea
o
Tachypnea
o
Pleural rub
o
Rales
Nervous system : o
Psychosis
o
Depression
o
Headache
o
Seizures
o
Peripheral neuropathies
o
Stroke
o
Cranial nerve deficits
GI: o
Painless oral ulcers
o
Abdom inal pain
o
Guarding or rebound tenderness
o
Positive stool guaiac suggests m esenteric ischem ia
Essential Workup
Thorough history and physical exam needed to distinguish between m ajor and m inor flare-ups
Major flare-ups: o
CBC
o
Electrolytes, blood urea nitrogen, creatinine, glucose
o
Urinalysis
o
Erythrocyte sedim entation rate (ESR)
o
Chest radiograph, ECG, and pulse oxim etry for
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cardiorespiratory sym ptom s P.1093
Tests Lab
CBC: o
Leukopenia, throm bocytopenia
o
Degree of hem atologic disorders suggests degree of disease activity.
ESR: o
May be elevated during acute exacerbations, but this test tends to rem ain high m onths after a flare-up has ceased.
Partial throm boplastin tim e: o
May be elevated in patients with lupus anticoagulant
Urinalysis: o
Protein
o
Casts
o
Hem aturia
o
WBCs
Am ylase is elevated in m esenteric ischem ia and pancreatitis.
Send antinuclear antibody, rheum atoid factor (RF), anti-streptolysin O (ASO) titer if diagnosis unclear.
Anti-Sm and anti-dsDNA are diagnostic.
A false-positive venereal disease research laboratory (VDRL) is supportive of the diagnosis.
Joint aspirate typically shows fluid with fewer than 3,000 WBCs.
Imaging
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Chest radiograph: o
Pneum onitis
o
Pneum onias
o
Pleural effusion
o
Cardiom egaly
ECG
Echocardiogram
Differential Diagnosis
Hypotension m ay be due to shock secondary to a m ajor flare-up or secondary to acute steroid withdrawal in the known lupus patient.
Other autoim m une diseases: o
Rheum atic fever
o
Rheum atoid arthritis
o
Derm atom yositis
o
Overlap syndrom es
Skin changes: o
Urticaria
o
Erythem a m ultiform e
Idiopathic throm bocytopenic purpura
Multiple sclerosis
Epilepsy
Treatment Initial Stabilization ABCs
ED Treatment
Mainstays include nonsteroidal anti-inflam m atory drugs (NSAIDs), antim alarials, corticosteroids, and
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im m unosuppressive drugs.
Special attention m ust be given to CNS and renal involvem ent as well as infections; these are the m ain determ inants of m orbidity: o
Atherosclerosis is a leading cause of death in the older lupus patients.
Mild flare-ups—arthralgias, m yalgias, and fatigue, rash: o
NSAIDs, acetyle salicylic acid (ASA), topical steroids for rash, sunscreen
o
If not sufficient, begin low-dose prednisone.
Major flare-ups—life- or organ-threatening: o
Methylprednisolone
o
Anticoagulation for throm bosis; give blood products early if needed.
o
Psychotropics for neuropsychiatric sym ptom s
o
Anticonvulsants for seizures
o
If poor response, consult rheum atology before starting cytotoxic m edications such as azathioprine or cyclophospham ide.
Chronically: o
Prednisone taper
o
NSAIDs
o
Rheum atologist initiated:
o
Antim alarials; quinacrine, chloroquine
Cyclophospham ide
Azathioprine
Methotrexate
Horm onal therapy, thalidom ide, and m onoclonal antibodies are under investigation.
Medication (Drugs)
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Methylprednisolone: 15 m g/kg/d IV up to 1 g; consult rheum atologist for peds dosing
Prednisone 5–30 m g (peds: 50% or m ax. 17 m g/kg, then 1–4 m g/m in IV
o
SVT: 15–17 m g/kg IV at 20–30 m g/m in OR 100 m g IV q5m in slow IV push until rhythm resolves or m ax. dose 1000 m g (peds: 3–6 m g/kg IV over 5 m inutes, m ax. 100 m g/dose, m ay repeat q5–10m in as needed to total dose 15 m g/kg)
Vasopressin: 40 units (peds: not recom m ended) IV push once
Follow-Up Disposition Admission Criteria
VT or VF
Possible cardiac ischem ic event
Persistent SVT
Underlying m etabolic abnorm alities
Discharge Criteria
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Term inated supraventricular rhythm without organ hypoperfusion
Issues for Referral Electrophysiologic testing:
Diagnostic but not required em ergently
Determ ines therapy for accessory pathways
References 1. Am erican Heart Association. ACLS guidelines. 2000. 2. Atkins DL, Dorian P, Gonzalez ER. Treatm ent of tachyarrhythm ias. Ann Em erg Med. 2001;37:S91–S109. 3. Connors S, Dorian P. Managem ent of supraventricular tachycardia in the em ergency departm ent. Can J Cardiol. 1997;13(Suppl A):19A–24A. 4. Dagres N, Gutersohn A, Wieneke H, Sack S, Erbel R. A new hereditary form of ectopic atrial tachycardia with autosom al dom inant inheritance. Int J Cardiol. February 2004;93(2-3):311–313. 5. Obel OA, Cam m AJ. Supraventricular tachycardia: ECG diagnosis and anatom y. Eur Heart J. 1997;18(Suppl C):C2–C11.
Codes ICD9-CM 427.0–427.9 785.0
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Tem po ral Arteritis
Temporal Arteritis
Andrew A. Aronson
Basics Description
Chronic vasculitis of large- and m edium -size vessels that occurs am ong individuals over 50 years of age
Tem poral arteritis m ost com m only causes inflam m ation of arteries originating from the arch of the aorta.
Other vessels, including veins, are som etim es involved.
Although usually clinically silent, involvem ent of the thoracic aorta occurs in a significant m inority of patients, and aortic aneurysm m ay result.
Thoracic aortic aneurysm is a late m anifestation with an incidence 17 tim es those without tem poral arteritis.
Abdom inal aortic aneurysm is about twice as com m on in those with tem poral arteritis.
Pathologic specim ens feature patchy m ononuclear granulom atous inflam m ation resulting in a m arkedly thickened intim a and occlusion of the vessel lum en.
Occlusive arteritis m ay involve throm bosis of the ophthalm ic artery resulting in ischem ic optic neuritis and visual loss.
Inflam m ation of arteries supplying the m uscles of
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m astication results in jaw claudication.
Hepatic involvem ent is seen in about 25% of cases.
Age is the greatest risk factor: o
Rare in patients 90% are >60 years old
Increased prevalence in Northern latitude
Two to four tim es m ore com m on in wom en
Rare in African Am erican patients, com m on in whites
Genetics
Genetic predisposition is linked to HLA-DR4—60% prevalence.
There is a strong association with polym yalgia rheum atica.
Etiology Unknown
Diagnosis Presence of any three or m ore of the following in patients with vasculitis:
Erythrocyte sedim entation rate greater than 50
Age greater than 50 years
New onset of headache, or change in quality of headache
Tenderness or decreased pulsation of tem poral artery
Abnorm al artery biopsy
Signs and Symptoms
May present with acute, subacute, or chronic sym ptom s: o
Headache is the single m ost frequent sym ptom .
o
Often boring or lancinating in quality
o
Often described as unilateral over a tem ple
Tongue or jaw claudication upon m astication is com m on
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sym ptom s.
Constitutional sym ptom s: o
Fatigue
o
Malaise
o
Anorexia
o
Weight loss
o
Weakness
o
Arthralgias
o
Low-grade fever
Visual findings: o
Findings are usually in one eye.
o
Develop weeks to m onths after the onset of other sym ptom s
o
May fluctuate, but visual im pairm ent does not usually im prove over tim e, even with treatm ent
o
Diplopia
o
Ptosis
o
Extraocular m uscle weakness
o
Scotom ata
o
Blurred vision
o
Am aurosis fugax
o
Blindness
Sore throat, dysphagia, and cough
Scalp tenderness, especially over the tem poral artery
Pulsations over tem poral artery:
o
Increased pulsations early in disease
o
Decreased pulsations late in the disease
Erythem a, warm th, swelling, or nodules over scalp arteries
Bruits or decreased pulses over large arteries
Rare findings: o
Respiratory sym ptom s
Pa ge 4 6 7
o
Ischem ic chest pain
o
Congestive heart failure
Neurologic problem s: o
Occurs in up to one third of patients
o
Neuropathies
o
Transient ischem ic attacks
o
Cerebral vascular accidents
Occult m anifestations include: o
Glossitis
o
Lingual infarction
o
Tongue infarction
o
Raynaud phenom enon
o
Tum orlike lesions:
Breast
Ovarian
Uterine m ass
40% do not present with the classic features of headache, scalp tenderness, visual changes, or jaw claudication.
Frequently associated with polym yalgia rheum atica (up to 50%):
o
Stiffness
o
Aching pain in the proxim al m uscles
o
Worse in the m orning and decreasing with exercise
Associated synovitis, especially in the knees, is com m on.
Essential Workup
Focused physical exam ination with em phasis on: o
Tem poral artery and scalp abnorm alities
o
Com plete neurologic exam ination
o
Ophthalm ic exam ination including visual acuity and visual field testing
P.1099
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Funduscopy: o
Often norm al initially
o
Iritis and fine vitreous opacities m ay be early findings.
o
Optic nerve edem a
o
Hyperem ia of the disk
o
Pallor
o
Hem orrhage
o
Scattered cotton-wool spots
o
Vessel engorgem ent and exudates are seen later.
Any pulse differences in the extrem ities or bruits over large arteries should be noted.
Tests Lab
Elevated erythrocyte sedim entation rate, usually greater than 100 m m /h
C-reactive protein above 2.45 m g/dL
A m ild norm ochrom ic anem ia is typical; platelets tend to be elevated, white cell count can be norm al or slightly elevated and differential is usually norm al.
Liver function tests and prothrom bin tim e m ay be elevated; creatine phosphokinase, tests of renal function and urinalysis are generally norm al.
Elevation in interleukin-6 (IL-6) is seen during flares.
Imaging
Doppler ultrasound: o
Decreased blood flow in tem poral, facial, and ophthalm ic arteries
o
Presence of a halo is highly suggestive of active tem poral arteritis.
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Angiogram : o
Sm ooth, tapered occlusions or stenosis
MRI: o
Indicated for exam ination of large arteries
Diagnostic Procedures/Surgery Tem poral artery biopsy:
Multiple sections should be done in 24–48 hours and no longer than 96 hours after initiation of steroids.
Gold standard for diagnosis
Differential Diagnosis
Vasculitides: o
Polyarteritis nodosa
o
Hypersensitivity vasculitis
o
System ic lupus erythem atosus
o
Takayasu arteritis
o
Wegener granulom atosis
Throm bosis of retinal, ophthalm ic, or tem poral arteries
Lym e disease
Treatment Pre Hospital
Sym ptom s m ay be confused with stroke.
Initiate appropriate m onitoring and oxygen.
Patients m ay be hypotensive from one of the rare sequelae (aortic dissection, abdom inal aortic aneurysm , or m yocardial infarction).
Initial Stabilization Although rare, patients m ay present with vascular catastrophe such
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as aortic dissection or m yocardial infarction and need appropriate aggressive early m anagem ent.
ED Treatment
Steroids: o
Strong clinical indications are required if started before tem poral artery biopsy.
o
Early treatm ent significantly reduces the incidence of blindness.
o
Steroids effectively control system ic and local sym ptom s within days to weeks.
o
Treatm ent with prednisone m ay continue for years—usual disease length is 3–4 years.
o
Sustained steroid therapy m ay accelerate osteopenia, cause cataracts, and potentiate hyperglycem ia and hypertension.
Sym ptom atic pain m anagem ent with NSAIDs or salicylates
Medication (Drugs)
Ibuprofen: 400 m g PO every 4 hours
Methylprednisolone (Solu-Medrol): 125 m g IV
Prednisone: 60–100 m g PO per day that is not tapered for several weeks
Follow-Up Disposition Admission Criteria
Patients with im pending vascular com plications
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Patients with associated acute visual loss
Discharge Criteria
Less sym ptom atic patients without evidence of end-organ involvem ent
Able to be seen in follow-up within 1–2 days
Issues for Referral
Rheum atology
Ophthalm ology if associated with visual sym ptom s
References 1. Calvo-Rom ero JM. Giant cell arteritis. Postgrad Med J. 2003;79:5115115. 2. Levine SM, Hellm ann DB. Giant cell arteritis. Curr Opin Rheum atol . 2002;14:310. 3. Nordberg E, Noirberg C. Giant cell arteritis: strategies in diagnosis and treatm ent. Curr Opin Rheum atol. 2004;16:25–30.
Codes ICD9-CM 446.5
ICD10 M31.6
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Tem po ral M andibular Jo int Injury/Syndro m e
Temporal Mandibular Joint Injury/Syndrome Timothy J. Mader Gregory R. Murphy
Basics Description
Myofacial pain causing tem porom andibular dysfunction
Tem porom andibular joint (TMJ) pain: o
Originates from the joint (capsulitis, traum atic arthritis, acute disk displacem ent) or m uscles of m astication (spasm )
TMJ clicking: o
Highly correlated with disk displacem ent
o
May be norm al finding; present as a transient finding in 30–40% of the population
TMJ m otion: o
Typical range is 42–55 m m (m axillary to m andible incisors).
o
Lim ited by adhesions within the joint or disk displacem ent or trism us from m uscle spasm
TMJ locking:
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o
Open locking (dislocation): typically from yawning consequent to joint laxity and easily reduce
o
Closed locking: results from disk displacem ent and is difficult to correct
Etiology TMJ dysfunction is poorly understood:
Multifactorial: bruxism , traum a, m alocclusion
Diagnosis Signs and Symptoms History
Preauricular pain: o
Constant
o
Dull and aching
o
May be referred to the ipsilateral ear, head, or neck
o
Exacerbated by m andible m ovem ent (pathognom onic)
o
More conspicuous at night and m ay cause insom nia
o
Often worsens through the day
Tongue, lip, or cheek biting
Physical Exam
Joint sounds: o
Popping or clicking sensation with TMJ articulation
o
A palpable or audible click with opening and closing
Malalignm ent and lim ited range of m otion: o
Dentoskeletal m alocclusion or lateral deviation
o
Open or closed locking of the jaw
Tenderness over the m uscles of m astication and TMJ: o
Masseter m uscle m ost com m only painful
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Essential Workup
Diagnosis based on clinical presentation
Exclude other causes of headache and facial pain.
Tests Lab No specific laboratory tests are indicated. P.1101
Imaging Panorex is the screening radiograph of choice:
May dem onstrate fracture or intra-articular pathology (i.e., tum or, or degenerative joint disease) but usually unrem arkable
Differential Diagnosis
Acute coronary syndrom e
Carotid artery dissection
Intracranial hem orrhage (subarachnoid hem orrhage)
Tem poral arteritis
Trigem inal or glossopharyngeal neuralgia
Vascular headache
Intraoral and dental pathology
Herpes zoster
Salivary gland disorder, otitis, and sinusitis
Elongated styloid process pain
Treatment
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Pre Hospital Provide com fort and reassurance
ED Treatment
Acute therapeutic options: o
Patient reassurance and education—“usually m ild and self-lim ited―
o
Analgesics and anxiolytics
o
Urgent reduction of open or closed locking (Montgom ery 2000)—m ay require procedural sedation
o
Physical therapy—m oist heat or ice packs
Outpatient m anagem ent: o
Com bination pharm acotherapy
o
Hom e physical therapy—m oist heat or ice packs and m echanically soft diet
o
Occlusal appliance worn during sleep
o
Referral to dentist or oral-m axillofacial surgeon
Medication (Drugs)
Narcotic analgesics
NSAIDs
Anxiolytics
Muscle relaxants
Sedative-hypnotics
Follow-Up Disposition
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Discharge Criteria
Treat as outpatients with pain m edication, m uscle relaxants, and warm com presses.
Referral to Otolaryngologist
References 1. Gray RJM, Davies SJ. Em ergency treatm ent of acute tem porom andibular disorders: part I. Dent Update. 1997;24:170–173. 2. Gray RJM, Davies SJ. Em ergency treatm ent of acute tem porom andibular disorders: part II. Dent Update. 1997;24:186–189. 3. Montgom ery MT. Extraoral facial pain. Em erg Med Clin North Am . 2000;18(3):577–600.
Codes ICD9-CM 524.60
ICD10 K07.6
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Tendo n Laceratio n
Tendon Laceration
Robert Marsan Jr. Elisa Aumont Verena Valley
Basics Alert Tendons near lacerations m ust be explored through com plete range of m otion to rule out injury.
Description Based on m echanism
External traum a: o
o
Penetrating traum a:
Gunshot wounds
Glass
Knives
Foreign bodies
Blunt traum a:
Crushing force or avulsion from hyperextension of a joint
Internal traum a: o
Entrapm ent/Laceration from bony fracture (rare)
Etiology
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Tendon injuries grossly categorized into those affecting upper versus lower extrem ities:
Upper-extrem ity injuries frequently related to the workplace, hom e, an assault, or attem pted suicide
Lower-extrem ity injuries m ost often associated with work or m otor vehicle accident
Diagnosis Signs and Symptoms
Pain is the cardinal sym ptom
Functional deficit
Soft-tissue dam age:
o
Swelling
o
Ecchym osis
o
Lacerations
o
Hem orrhage
Abnorm al resting position of the extrem ity or large joint instability increases suspicion for tendon injury.
Essential Workup
A careful history: o
Mechanism , tim e of injury
o
Hand position during injury
o
Hand dom inance
o
Drug allergies
o
Medications
o
Past m edical history
o
Tetanus-vaccination status
Physical exam should follow the orthopaedic schem e of look, feel, m ove:
Pa ge 4 6 8
o
Perform neurovascular exam before local anesthesia is instilled.
o
Exam ine each digit separately.
Flexor digitorum profundus injuries: o
Present with inability to flex the distal interphalangeal joint
o
Exam involves stabilizing the proxim al interphalangeal joint in full extension while the patient attem pts to flex distal interphalangeal joint.
Flexor digitorum superficialis injuries: o
Present with inability to flex the proxim al interphalangeal joint of a digit
o
Usually established by m eans of standard superficialis tendon test:
While holding the uninjured digits in full extension, the patient attem pts to flex the affected finger at the proxim al interphalangeal joint.
o
Falsely negative if profundus is functional
The distal interphalangeal joint extension test:
May m ake this diagnosis m ore apparent
Patient is asked to m ake a precision pinch between the thum b and the injured finger.
Then asked to flex the proxim al interphalangeal joint so that the distal interphalangeal joint is hyperextended
Confirm s the integrity of the flexor digitorum superficialis
Forearm and wrist flexor injuries: o
Present with inability to flex ulnar or radial side of wrist or to flex the wrist while opposing the thum b to the little finger
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Extensor tendon injuries: o
Found by weakness or lack of extension of the distal phalanx against resistant
o
Indicates partial or com plete disruption
o
Best determ ined with patient placing palm on flat surface and asking the patient to attem pt to extend the fingers individually
o
Palpate each tendon.
o
Loss of norm al tension indicates injury
Further explore tendons and wounds after local anesthesia (1% lidocaine or 0.5% bupivacaine) in a bloodless, well-lit surgical field: o
Tendons near lacerations m ust be explored through com plete range of m otion.
o
Best elucidates tendon injuries distal or proxim al to a skin wound
Pediatric Considerations
More difficult to get an adequate exam ination
The healing process is usually quicker and m ore often associated with com plete return to pre-injury function.
Tests Lab Wounds first exam ined >12 hours after injury or wounds with evident infection should be cultured.
Imaging
Radiographs are frequently needed to identify radiopaque foreign bodies or fractures.
High-frequency ultrasound can be used to identify com plete tendon lacerations: o
Partial tendon lacerations difficult to im age
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o
A water bath m ay help when attem pting to im age a painful extrem ity.
Ultrasound guidance m ay help to guide rem oval of foreign bodies.
Differential Diagnosis
Always rule out an associated foreign body or fracture.
Partial lacerations are com m on but m ore difficult to diagnosis than com plete disruptions because they m ay dem onstrate intact function: o
Alterations of the norm al resting hand position m ay indicate partial laceration.
Lacerations over the m etacarpophalangeal joint should be considered the result of a hum an bite until proven otherwise: o
Look for associated extensor tendon injury while m etacarpophalangeal joint flexed.
Lacerations over the proxim al interphalangeal joint m ay involve the lateral bands or the central slip of the extensor m echanism : o
Boutonnière deform ity from im proper repair
Disruption of the extensor tendon distal to the central slip results in a m allet finger deform ity.
Avulsion of the flexor digitorum superficialis distally m ay be present with or without an associated avulsion fracture: o
Suspect when a grasping finger is hit by a fast-m oving object (jam m ed finger).
P.1103
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Treatment Pre Hospital
Do not rem ove foreign m atter from the patient in the field.
Im m obilize and transport patient.
Apply direct pressure to control hem orrhage.
Assess distal neurovascular status for signs of com prom ise.
Contact m edical control before any attem pted reduction.
Initial Stabilization
Evaluate extrem ity and control hem orrhage with direct pressure.
Rem ove all jewelry or constricting bands.
ED Treatment
Pain control as required
Adm inister tetanus toxoid as needed.
Copious irrigation with 1 L norm al saline
Broad-spectrum antibiotic, such as a first-generation cephalosporin (Cefazolin)
Tendon lacerations associated with hum an bites: o
Must be copiously irrigated
o
Place on IV antibiotics with coverage of oral anaerobes (am picillin/sulbactam )
o
Im m obilized and elevate the hand
Rem ove all foreign bodies and provide debridem ent of avascular tissue.
Partial tendon lacerations that involve m ore than 20% of the cross-sectional area of the tendon m ust be repaired.
Sim ple extensor tendon lacerations m ay be repaired in the ED:
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o
Use a 4-0 or 5-0 nonabsorbable suture in a figure-of-eight or a m odified Kessler stitch.
All suspected flexor tendon, wrist, and distal forearm tendon lacerations require consultation by a hand surgeon, ideally within 12 hours.
Tendon lacerations over the proxim al interphalangeal joint m ay result in a boutonnière deform ity: o
Refer to a hand surgeon.
The superficial nature of m ultiple tendons, nerves, and vessels on the volar aspect of the wrist renders them easily vulnerable to penetrating traum a: o
“Spaghetti wrist― or “full house―
Volar wrist laceration with at least 10 structures involved
Requires prom pt consultation with a hand surgeon
Tendon lacerations associated with fractures require referral for operative repair.
If a surgeon is not prom ptly available: o
Irrigate copiously.
o
Close skin without repair of tendon.
o
Im m obilize injured hand with a bulky volar dressing and splint
o
Wrist in 20–30°of flexion
o
Metacarpal joint in 60–70°of flexion
o
Interphalangeal joints in 10–15°of flexion
Medication (Drugs)
Am picillin/sulbactam : 3 g IV q6 (peds: 200 m g/kg per day IM or IV div. q6h)
Cefazolin: 1 g IV piggyback (peds: 100 m g/kg per day IM
Pa ge 4 6 8
or IV div. q6h, followed by 40 m g/kg per day PO q.i.d. for 5–7 days)
Tetanus toxoid: 0.5 m L IM (peds: younger than 7 years—diphtheria-pertussis-tetanus vaccine preferred; in those older than 7 years, adult dose tetanus toxoid if im m unization series not com pleted), tetanus im m une globulin, as required, 250 IU adm inistered IM
Follow-Up Disposition Admission Criteria
Patients with infected tendon lacerations m ust be adm itted for operative debridem ent.
Any patients with tendon injury secondary to hum an bite m ust be adm itted for operative debridem ent and IV antibiotics.
Any patients with significant flexor tendon laceration m ay be adm itted for tim ely operative repair or transferred to the nearest hand surgeon.
Discharge Criteria
Patients with an extensor tendon laceration that is not infected, nor associated with other significant injury or underlying fracture, which was repaired by the ED physician and is now properly splinted, m ay be discharged with tim ely surgical follow-up.
Patients with an extensor tendon laceration requiring surgeon referral for repair (wrist, forearm , proxim al interphalangeal joint), which has been properly treated and splinted, with the patient placed on antibiotics, m ay
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be discharged for tim ely surgical follow-up.
References 1. Blaivas M, Lyon M, Brannam L, et al. Water bath evaluation technique for em ergency ultrasound of painful superficial structures. Am J Em erg Med. 2004;22:589–593. 2. Dogan T, Celebiler O, Gorungluoglu R, et al. A new test for superficialis flexor tendon function. Ann Plast Surg. 2000;45:93–96. 3. Hudson DA, de Jager LT. The spaghetti wrist: sim ultaneous laceration of the m edian and ulnar nerves with flexor tendons at the wrist. J Hand Surg (Br). 1993;18:171–173. 4. Jozsa LG, Kannus P. Hum an Tendons: Anatom y, Physiology and Pathology. Cham paign, IL: Hum an Kinetic, 1997. 5. Lee DH, Robbin ML, Galliott R, et al. Ultrasound evaluation of flexor tendon lacerations. J Hand Surg (Am ). 2000;25:236–241. 6. Perron AD, Brady WJ, Keats TE, et al. Orthopedic pitfalls in the em ergency departm ent: Closed tendon injuries of the hand. Am J Em erg Med. 2001;19:76–80. 7. Stahl S, Kaufm an T, Bialik V. Partial lacerations of flexor tendons in children: prim ary repair versus conservative treatm ent. J Hand Surg (Br). 1997;22B:377–380.
Codes ICD9-CM 848.9 Other and ill-defined sprains and strains, unspecified site of sprain and strain 880.2 Open wound of shoulder and upper arm – With tendon involvem ent 881.2 Open wound of elbow, forearm , wrist – With tendon involvem ent 882 Open wound of hand except finger(s) alone 883 Open wound of finger(s) 894 Multiple and unspecified open wound of lower lim b
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ICD10 T14.6
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Tendo nitis
Tendonitis
James Killeen
Basics Description
Overuse syndrom e: o
Synovial cells increase in thickness
o
Excess synovial fluid collection
o
Constant irritation
If no further injury occurs, the process m ay last from 48 hours to 2 weeks.
Continuous irritation causes fibrosis with tendon thickening and stenosing tenosynovitis.
Etiology
Mechanical overload or repetitive m icrotraum a to the m usculotendinous unit: o
o
Intrinsic factors:
Inflexibility
Muscle weakness or im balance
Extrinsic factors:
Excessive deviation, frequency, or activity
Chem otactive and vasoactive chem ical m ediators are released: o
Vasodilatation and cellular edem a increasing the
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num ber and activity of PMNs
Diagnosis Signs and Symptoms History
Repetitive stress and m echanical overload
The classic inflam m atory signs include pain, warm th, erythem a, and swelling.
Pain will resolve quickly after initial m ovem ent only to becom e a throbbing pain after exercise.
Physical Exam
Defined as inflam m ation of the tendon only
There is a poor distinction between tendonitis and tenosynovitis (degree of inflam m ation).
Clinical findings: o
Warm th
o
Presence of an effusion
o
Decreased range of m otion
o
Instability
o
Pain on m otion
o
Tenderness over tendon site
Specific Conditions Supraspinatus Tendonitis
Supraspinatus and other rotator cuff tendons: o
Com pressed between hum erus and acrom ion
Overuse of the extrem ity m ay lead to m icrotraum a of the tendons fibers.
Neer classification: o
Stage 1:
Age Table o f C o ntents > Testicular To rsio n
Testicular Torsion
Edward Newton
Basics Description
Rotation of the testicle around the sperm atic cord and vascular pedicle
Congenital abnorm ality of the genitalia: o
High insertion of the tunica vaginalis on the sperm atic cord
o
Redundant m esorchium
o
Perm its increased m obility and twisting of the testicle on its vascular pedicle
The anatom ic abnorm ality is generally bilateral, so both testicles are susceptible to torsion.
Rotation often occurs m edially (two thirds of cases): o
Ranges from incom plete (90–180°) to com plete (360–1080° degrees) torsion
o
Depending on the degree of torsion:
Vascular occlusion occurs
Infarction of the testicle after m ore than 6 hours ofwarm ischem ia
Testicular salvage: o
73–100% with less than 6 hours ischem ia
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o
Up to 70% at 6–12 hours
o
Less than 20% after 12 hours
o
It is still worthwhile to attem pt to salvage the testicle up to 24 hours after the onset.
Testicular infarction leads to atrophy and m ay ultim ately decrease fertility.
Bim odal distribution of torsion: o
Peak incidences in infancy and adolescence
o
85% of cases of occur between ages 12 and 18 years, with a m ean of 13 years.
o
Torsion is rare after age 30 but still possible.
Diagnosis Signs and Symptoms History
Sudden onset of unilateral testicular pain
Scrotal swelling and erythem a
Less com m only, torsion m ay present with pain in the inguinal or lower abdom inal area.
Up to 40% of patients m ay describe previous sim ilar episodes that rem itted spontaneously: o
Represents spontaneous torsion and detorsion
Nausea and vom iting occur in 50% of cases.
Low-grade fever occurs in 25%.
Often a history of m inor traum a to the testicle preceding the onset of pain.
Sym ptom s of urinary infection (dysuria, frequency, and urgency) are absent.
Physical Exam
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In distinguishing torsion from epididym itis, localized tenderness is helpful early; however, once significant scrotal swelling occurs, the anatom y becom es indistinct.
The affected testicle m ay lie transversely as opposed to the norm al vertical lie.
Crem asteric reflex is frequently absent on the affected side with testicular torsion.
Prehn sign: o
Relief of pain on elevation of the testicle in epididym itis
o
Worsening or no change in the pain with torsion
o
Considered unreliable
Essential Workup
The presentation of an “acute scrotum ― in a child or adolescent requires rapid assessm ent and im m ediate consultation with an urologist.
These patients require noninvasive flow studies or surgical exploration to confirm torsion.
25–30% of these patients ultim ately prove to have testicular torsion.
Tests Lab
Elevated WBC count with a left shift is present in 50% of cases.
Urinalysis is usually norm al, but up to 20% of cases of torsion have pyuria.
There are no laboratory tests specific for testicular torsion.
Imaging Alert
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There are lim itations of all flow studies: o
Reflect only the current state of perfusion
o
Spontaneously detorsed testicle m ay show norm al or even increased flow.
o
Still at high risk for recurrent torsion
Traditional criterion standard has been technetium -99m radionuclide scans: o
Decreased flow in the torsed testicle com pared with the unaffected side
o
Frequent tim e delays in obtaining scans
Doppler ultrasound: o
Assess testicular blood flow.
o
Has replaced nuclear scanning:
o
Less invasive
More readily available test
Com parable results
Overall sensitivity and specificity of 98% and 100%, respectively
o
Epididym itis will reveal increased flow due to inflam m ation.
o
Torsion will reveal decreased or no blood flow.
o
Color-flow Doppler is the m ost com m only available.
o
Use of Doppler contrast m aterial m ay enhance the accuracy.
Pediatric Considerations
All im aging techniques have technical lim itations when in infants: o
Testicular vessels are very sm all.
o
Am ount of blood flow to the testicle under norm al conditions is m inim al.
Scrotal exploration m ay be required.
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Diagnostic Procedures/Surgery
Scrotal exploration can be done rapidly under local anesthesia to diagnose and treat torsion.
The “bell-clapper― deform ity of both testicles should be corrected by orchiopexy.
Differential Diagnosis
Testicular neoplasm
Epididym itis/Orchitis
Torsion of the appendix testis
Testicular traum a or rupture of the testicle
Incarcerated inguinal hernia
Testicular tum or
Acute hydrocele
Henoch-Schönlein purpura
Other intraabdom inal conditions: o
Appendicitis
o
Pancreatitis
o
Renal colic
P.1109
Treatment Pre Hospital
There is no definitive treatm ent that can be rendered in the field.
Prehospital personnel need to recognize the urgency of acute testicular pain in young patients.
These patients should be transported to the ED
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im m ediately.
Initial Stabilization IV fluid, analgesics as appropriate
ED Treatment
Exam ination of testicle to exclude prim ary neoplasm
Establish the diagnosis and m obilize appropriate urologic care.
Applying an ice pack to the scrotum relieves pain: o
Can prolong the viability of the ischem ic testicle
If definitive care is likely to be delayed beyond 4–5 hours from the onset of torsion, m anual detorsion m ay be attem pted: o
Externally rotate the affected testicle opposite the usual m edial direction of torsion.
o
Continue until pain is relieved or norm al anatom y is restored.
o
All patients who undergo m anual detorsion m ust be surgically explored.
Medication (Drugs) Analgesia
Follow-Up Disposition Admission Criteria
Patients with confirm ed torsion m ust be adm itted for scrotal exploration and bilateral orchiopexy.
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Flow studies that are inconclusive and technical failures m andate further investigation by surgical exploration of the scrotum .
Adm ission for urgent surgical exploration of an acute scrotum is m andatory if there is any potential delay in obtaining a flow study: o
Patients in whom apparent spontaneous detorsion has occurred should undergo exploration for bilateral orchiopexy.
Discharge Criteria
Patients with negative scrotal exploration and those with norm al flow studies can be discharged with appropriate urologic follow-up.
Param eters for return to ED m ust be discussed because of the possibility of recurrent torsion.
Patients with an obvious diagnosis other than testicular torsion can be referred for care.
References 1. Al Mufti RA, Ogedegbe AK, Laferty K. The use of Doppler ultrasound in the clinical m anagem ent of acute testicular pain. Br J Urol. 1995;76:625–627. 2. Arce JD, Cortes M, Vargas JC: Sonographic diagnosis of acute sperm atic cord torsion. Rotation of the cord: a key to the diagnosis Pediatr Radiol. 2002;32:485–491. 3. Burgher SW. Acute scrotal pain. Em erg Med Clin North Am . 1998;16:781–809. 4. Kafla N, Veyrac C, Baud C et al: Ultrasonography of the sperm atic cord in children with testicular torsion: im pact on the surgical strategy. J Urol. 2004;1721692-5. 5. Sessions AE, Rabinowitz R, Hulbert WC et al: Testicular torsion: direction, degree, duration and disinform ation. J Urol.
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2003;169:663–665. 6. Sidhu PS. Clinical and im aging features of testicular torsion: role of ultrasound. Clin Radiol. 1999;54:343–352.
Codes ICD9-CM 608.2
ICD10 N44
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Tetanus
Tetanus
Daniel T. Wu
Basics Description
Rare disease in the United States but still prevalent in third world countries
About 40 cases per year in the United States
500,000–1,000,000 cases worldwide
Incubation period: o
o
Inoculation to the appearance of the first sym ptom s:
48 hours to 3 weeks or m ore
7 years and adults.
Clinical tetanus does not confer im m unity.
For clean wounds o
Td should be given if unknown prior vaccination history or greater than 10 years since last booster.
For tetanus prone wounds o
Td should be given if unknown vaccination history or >5 years since last booster.
o
TIG should be given if unknown vaccination or has never received the prim ary series.
Medication (Drugs)
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Benztropine: 1–2 m g IV
Chlorprom azine 10–50 m g IM
Diazepam (benzodiazepine): 5–10 m g (peds: 0.2–0.4 m g/kg) IV
Diphenhydram ine: 50 m g IV
Dobutam ine: 2.5–15 µg/kg/m in IV
Dopam ine: 2–20 µg/kg/m in IV
Doxycycline: 100 m g IV q12h
Erythrom ycin: 500 m g IV q6h
Labetalol: 20 m g (peds: 0.3–1 m g/kg/dose) IV q10m in up to 300 m g PRN—start infusion 2 m g/m in (peds: 0.4–1 m g/kg/hr m ax. 3 m g/kg/hr as needed)
Metronidazole: 1.0 g (peds: 15 m g/kg) load, followed by 500 m g (7.5 m g/kg) IV q6h
Penicillin G potassium : 1.2 m IU (peds: 100,000 IU/kg/24h) IV q6h for 10 days
Propranolol 0.5–1 m g (peds: 0.01–0.1 m g/kg) IV
TIG (tetanus im m une globulin): o
250 IU IM
o
Adm inister in separate site from Td toxoid
o
For unim m unized or incom pletely im m unized in presence of tetanus prone wound
Td 0.5 m L IM
Follow-Up Disposition Admission Criteria All patients should be adm itted to an intensive care setting.
Discharge Criteria
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None for suspected generalized tetanus
References 1. CDC Tetanus Surveillance—United States 1998–2000. MMWR. 2003;52(ss-3):1–7. 2. CDC. Tetanus. Epidem iology and prevention of Vaccine—Preventable Diseases. 8th ed. (The Pink Book) 3. Hsu SS, Tetanus in the Em ergency Departm ent: a current review. J Em erg Med. 2001;20:357–365. 4. McQuillan GM, Serologic im m unity to diphtheria and tetanus in the United States. Ann Intern Med. 2002;136:660–666. 5. Pickering L, Ed 2003: Report of the com m ittee on infectious diseases. 26th ed. Am erican Academ y of Pediatrics, 2003. 6. Thawaites CL. Preventing and treating tetanus. Brit Med J. 2003;326:188–119.
Codes ICD9-CM 37.0
ICD10 A35
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Theo phylline Po iso ning
Theophylline
Poisoning Gerald Maloney
Basics Description
Acute overdose: o
Ingestion within 8-hour interval in patient with no prior theophylline use
Acute-on-chronic overdose: o
Single excessive dose in patient previously receiving usual therapeutic doses for ≥24 hours
Chronic intoxication: o
Accum ulation of theophylline >20 m g/L associated with prior therapeutic use for ≥24 hours secondary to:
Drug–drug, drug–diet, or drug–disease interactions
Use of serial excessive doses
Electrolyte shifts and hypotensive effects occur only in acute overdoses: o
Tachyphylaxis to these effects occurs with m aintenance therapy.
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o
As result of cellular shifts between extracellular and intracellular fluids
Etiology
Acute ingestions require larger concentrations to achieve specific toxic effects than acute-on-chronic or chronic overdoses.
Drug–drug interactions: o
o
Inhibiting theophylline m etabolism :
H 2 -receptor antagonists
Macrolide antibiotics
Fluoroquinolones
Allopurinol
Influenza vaccine
Interferons
Enhances theophylline m etabolism (leads to toxicity when discontinued):
Carbam azepine
Barbiturates
Sm oking
Rifam pin
Chronic theophylline accum ulation: o
Uncontrolled congestive heart failure
o
Liver disease (cirrhosis or severe hepatitis)
o
Acute viral infections
Diagnosis Signs and Symptoms
Cardiovascular: o
Sinus or supraventricular tachycardias:
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o
Multifocal atrial tachycardia
Caused by β 1 -receptor stim ulation
Hypotension:
In acute or acute-on-chronic ingestions only
Associated with theophylline >35 m g/L
Owing to vasodilatation induced by β 2 -receptor stim ulation
May be refractory to fluids, positioning, and conventional vasopressors
Central nervous system : o
Trem or
o
Mental status changes
o
Seizures with theophylline level:
Greater than 100 m g/L in acute overdose
Greater than 30 m g/L in acute-on-chronic intoxication
As low as 20 m g/L in chronic intoxication
Seizures are seen in 14% of chronic intoxications and 5% of acute intoxications.
Gastrointestinal: o
Nausea, vom iting:
Protracted and m ay be refractory to antiem etics at usual doses
o
Abdom inal pain
o
Pharm acobezoar:
From sustained-release dosage form s in acute ingestions
Delays peak concentrations
Miscellaneous: o
Hypokalem ia:
As low as 1.5 m Eq/L
Owing to β-receptor stim ulation
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o
Hyperglycem ia
o
Leukocytosis
o
Hypercalcem ia, hypophosphatem ia, hypom agnesem ia
Essential Workup
Serum theophylline concentration: o
Finding of ≥20 m g/L confirm s diagnosis.
Detailed history to differentiate acute from acute-on-chronic from chronic intoxication
Tests Lab
Theophylline level: o
Repeat every 2 hours until decreasing to confirm im m ediate absorption is com plete and peak value has occurred.
o
Serious m orbidity in acute overdose if ≥100 m g/L
o
Massive caffeine ingestions can yield detectable or toxic theophylline determ inations with conventional lab testing.
CBC
Electrolytes: o
Transient hypokalem ia
Serum acetam inophen level (for intentional ingestions)
Imaging
KUB (kidneys, ureters, bladder): o
Undissolved sustained-release tablets or pharm acobezoars m ay appear as radiopacities.
o
Bead-filled capsules m ay appear as radiolucencies.
Ultrasound of stom ach m ay detect intact sustained-release dosage form s.
Differential Diagnosis
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Caffeine/β-agonist bronchodilator overdose
Am phetam ines
Sym pathom im etics
Anticholinergic agents
Drug withdrawal syndrom es
Pheochrom ocytom a
Thyrotoxicosis
P.1113
Treatment Pre Hospital Alert Bring pill bottles/pill sam ples in suspected overdose.
Initial Stabilization
Airway, breathing, and circulation m anagem ent (ABCs): o
Cardiac m onitor
o
Isotonic crystalloids as needed for hypotension
Naloxone, thiam ine, and dextrose (D 5 0 W) as indicated for altered m ental status
Cardiovascular: o
Initiate beta-blockers or calcium channel blockers for rate control with supraventricular tachyarrhythm ia:
Adenosine is antagonized by theophylline and will not be effective.
o
Adm inister isotonic crystalloid intravenous fluid resuscitation for hypotension:
With treatm ent failure, consider beta-blocker to
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reverse theophylline-induced β 2 -receptor–stim ulated vasodilation.
If vasopressors are needed, choose pressor that is not a β-agonist, such as phenylephrine.
o
Treat ventricular dysrhythm ias conventionally.
Seizures: o
Adm inister benzodiazepines.
o
Phenytoin is contraindicated; it is usually ineffective and m ay paradoxically worsen seizures in theophylline intoxications.
ED Treatment Decontamination
Perform gastric lavage for severe (≥50 m g/kg) acute overdoses presenting within 1 hour of ingestion: o
Ensure airway is adequately m aintained prior to initiating lavage.
Adm inister activated charcoal.
Adm inister cathartics with first dose only of activated charcoal.
Multidose charcoal: o
Especially with sustained-release products
o
Binds theophylline, which back-diffuses to sm all intestine
o
For m ild to m oderate toxicity
o
25 g q2h until theophylline level ≤20 m g/L
Initiate whole-bowel irrigation with sustained-release products: o
Adm inister until a clear, colorless rectal effluent or serum theophylline 100 g
Diazepam : 0.1 m g/kg IV q5–10m in until seizures controlled, up to 30 m g
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Diltiazem : 0.25 m g/kg IV bolus; m ay repeat after 15 m inutes, then 5–15 m g/h infusion for control of heart rate in patients with contraindication to beta-blockade
Esm olol: 500 µg/kg IV bolus, followed by 50 µg/kg/m in infusion; increase by 50 µg/kg/m in increm ents to m ax. of 200 µg/kg/m in
Metoclopram ide: 10 m g IV bolus; m ay repeat to m ax. of 1 m g/kg
Ondansetron: 0.15 m g/kg IV bolus up to m ax. of 32 m g total
Polyethylene glycol (high m olecular weight): 1–2 L/h via nasogastric tube
Follow-Up Disposition Admission Criteria
Acute overdoses with serum theophylline concentrations >100 m g/L
Acute-on-chronic or chronic theophylline with either serum concentration >60 m g/L or patient >60 years old
Seizures, or fluid and vasopressor refractory hypotension in a patient with serum theophylline concentration >30 m g/L
Unchanged or rising serial serum theophylline concentrations (two or m ore) >30 m g/L in acute or acute-on-chronic ingestion of sustained-release theophylline
Discharge Criteria
Two consecutive (≥2 hours apart) decreasing serum
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theophylline concentrations with m ost recent concentration Table o f C o ntents > Thro m bo tic Thro m bo cyto penic Purpura
Thrombotic Thrombocytopenic Purpura Timothy Pavek
Basics Description
Throm botic throm bocytopenic purpura (TTP) is a severe disorder of abnorm al clotting affecting m ultiple organ system s.
Classically characterized by pentad of: o
Throm bocytopenia
o
Hem olytic anem ia
o
Mild renal dysfunction
o
Neurologic signs
o
Fever
Associated with acquired or congenital deficiency of plasm a von Willebrand factor–cleaving protease (VWFcp).
Classic Course
Acute onset
Fulm inant course lasting days to a few m onths
Nearly always fatal outcom e without treatm ent:
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o
Greater than 90% m ortality without treatm ent
o
Reverses to >90% survival with m odern treatm ent
Clinical presentations include: o
Idiopathic
o
Fam ilial, chronic or relapsing
o
Drug-induced:
Allergic or im m une m ediated (quinine, ticlopidine, clopidogrel)
Dose-related toxicity (m itom ycin C, cyclosporine)
o
Pregnancy, postpartum associated:
10–25% of cases
o
Bone m arrow transplantation associated
o
Infection
More com m on in the 3rd–6th decades of life
Uncom m on in pediatric or geriatric populations
Wom en affected about twice as frequently as m en
Etiology
Unknown prim ary stim ulant; possibly system ic endothelial cell dam age results inactivation of coagulation pathway
Platelet aggregation and fibrin deposition occurring in arterioles and capillaries leading to m icrothrom bi and obstruction to blood flow
Platelet aggregation leads to: o
Consum ption of platelets in excess of bone m arrow's ability to respond, producing throm bocytopenia
o
Widespread m icrovascular hyaline throm botic lesions
Microvasculature obstruction with platelet aggregates leads to: o
Red cell hem olysis
o
Accum ulation of hem e breakdown products
o
Anem ia
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End organ ischem ia results from diffuse throm bosis in sm all vessels: o
Most com m on in heart, brain, kidney, pancreas, and adrenal glands
o
Lungs and liver relatively spared
Deficiency of vWF-cleaving protease causes failure of control of coagulation pathway.
Genetics
Som e cases are genetic/fam ilial.
VWFcp was recently identified as new m em ber of ADAMTS fam ily and designated ADAMTS13.
Mutations in ADAMTS13 gene cause autosom al recessive form of chronic relapsing TTP.
Diagnosis Signs and Symptoms Five Major Clinical Features: Classic Pentad
Throm bocytopenia: o
Microangiopathic and hem olytic anem ia: o
Platelet count Table o f C o ntents > Thum b F racture
Thumb Fracture
John MacKay Jr.
Basics Description
Distal phalangeal fractures: o
Blunt traum a, hyperextension of the thum b, axial loading of the thum b
o
Tuft fracture is a fracture sim ilar to that in other digits in which the distal phalanx is crushed and fragm ented.
o
It m ay be open or closed and associated with nailbed injury.
o
It is treated as a soft tissue injury.
Proxim al phalangeal fractures and thum b m etacarpal fractures: o
Blunt traum a to the thum b:
Axial loading of the thum b with the m etacarpal phalangeal (MP) joint flexed, hand closed or the thum b MP joint otherwise stabilized
o
Bennett fracture:
Oblique intra-articular fracture of the ulnar aspect of the base of the thum b m etacarpal with the larger distal fragm ent displaced
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o
Rolando fracture:
Com m inuted Y-shaped intra-articular fracture of the ulnar base of the thum b m etacarpal with the large distal fragm ent displaced
Etiology
Falls
Motor vehicle accidents
Sports, especially downhill or alpine skiing
Basketball
Baseball
Football
Rugby
Diagnosis Signs and Symptoms
Pain, swelling, and deform ity of the thum b
Exam should include the thenar em inence for pain or deform ity.
The thum b m ay be rotated distal to the fracture site.
The base of the thum b m ay appear radially deviated relative to the rest of the hand in the resting position.
Occasionally, there m ay be dam age to the thum b digital nerves.
Pediatric Considerations
Fractures to the thum b som etim es occur in children. o
Consider nonaccidental traum a.
o
Do not neglect appropriate pain m anagem ent in children.
Physical Exam
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Im m obilize thum b pending definitive evaluation.
Essential Workup Radiography as noted below
Tests Imaging
Plain radiography of affected areas
Avoid testing stress of thum b m etacarpophalangeal joint, as in testing for gam ekeeper thum b, until all plain radiography is com plete.
Differential Diagnosis
Extra-articular fracture of the base of the thum b m etacarpal
Scaphoid fracture
Gam ekeeper thum b
P.1119
Treatment Pre Hospital
Dress open wounds.
Im m obilization in neutral position
Elevation and cold to reduce swelling
Age-appropriate social m anagem ent
Initial Stabilization Im m obilize thum b pending definitive evaluation.
ED Treatment
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Thum b spica splint with the thum b in neutral position, as if holding a beverage can
Splint instructions should be provided to patient.
Medication (Drugs) Pain control with oral analgesic preparations
Surgery
72-hour orthopedic referral
Counsel patient that there is a strong likelihood of the need for operative repair.
Follow-Up Disposition Admission Criteria Open fracture, presence of m ultiple traum a, or other m ore serious injuries
Discharge Criteria Closed injuries, referral, and explain frequent need for operative fixation
Issues for Referral 72-hour orthopaedic referral
References 1. Am erican Society for Surgery of the Hand. The Hand: Exam ination and Diagnosis. 2nd ed. New York, NY: Churchill Livingstone; 1983. 2. Am erican Society for Surgery of the Hand. The Hand: Prim ary Care of Com m on Problem s. 2nd ed. New York, NY: Churchill
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Livingstone; 1990. 3. Antosia RE, Lyn E. Hand. In: Marx J, et al. Rosen's Em ergency Medicine: Concepts and Clinical Practice. 5th ed. St. Louis, Mo: Mosby–Year Book; 2002: 493–506. 4. Chaffin TH. Phalangeal fractures. In: Hart RG, Uehara DT, Wagner MJ, et al., eds. Em ergency and Prim ary Care of the Hand. Dallas, Tex: ACEP; 2001:111–122. 5. Sullivan JH, Tsonis GD. Metacarpal fractures. In: Hart RG, Uehara DT, Wagner MJ, et al., eds. Em ergency and Prim ary Care of the Hand . Dallas, Tex: ACEP; 2001:99–110.
Codes ICD9-CM 816.00 Fracture of one or m ore phalanges of hand, closed
ICD10 S62.5
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Tibial Plateau F racture
Tibial Plateau
Fracture Binh T. Ly
Basics Description
Synonym : tibial condylar fracture
Fracture or depression of the proxim al tibial articulating surface
Valgus or varus force applied in com bination with axial loading: o
Lateral plateau fractures:
Occurs classically after pedestrian struck by a vehicle bum per
Lateral aspect of the knee with a m edially directed force
o
Medial plateau fractures are m uch less com m on and require significant force.
Younger patients are m ore resistant to depressed plateau fractures.
Elderly patients are m ore prone to depression-type fractures.
Schatzki Classification of Plateau Fractures
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Type 1: o
Split fracture of the lateral tibial plateau without depression of the plateau
o
Occurs in younger patients
o
Cancellous bone of the plateau resists depression.
o
Usually occurs from a valgus force in com bination with axial load
Type 2: o
Com bination of split fracture and depression of lateral plateau
o
The m echanism is sim ilar to type 1 injury.
o
Patients tend to be in their fourth decade of life or older.
o
Have weaker subchondral bone
Type 3: o
Local depression of the lateral plateau
o
Injuries m ay be unstable.
Type 4: o
Fracture/Depression of the m edial plateau
o
Requires m uch m ore force (varus and axial loading)
o
Be suspicious for associated injuries.
o
Dam age to other structures:
Popliteal artery
Peroneal nerve
Lateral collateral ligam ent
Medial m eniscus
Cruciate ligam ents
Type 5: o
Bicondylar fracture
o
High-energy injury
o
Associated injuries:
Popliteal vessel injury
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Peroneal nerve injury
Com partm ent syndrom e
Type 6: o
Bicondylar, grossly com m inuted fracture of the plateau
o
Diaphyseal-m etaphyseal dissociation
o
Violent force, usually a fall from a height
o
Associated neurovascular injuries and com partm ent syndrom e
Etiology Mechanism of Injury
Fall from a height causing fem oral condyles to im pact on tibial surface
Vehicle bum per injury (forces directed lateral to m edial)
Violent twisting force (e.g., skiing)
Associated injuries include: o
Ligam entous (collaterals, cruciates)
o
Meniscal
o
Neurovascular (peroneal nerve and popliteal vessels)
Pediatric Considerations
Tibial plateau fractures are rare in children: o
Dense cancellous bone of the tibial plateau
Diagnosis Signs and Symptoms
Painful, swollen knee
Inability to bear weight
Knee effusion (hem arthrosis)
Lim ited active and passive range of m otion of the knee
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Tenderness along the proxim al tibia and joint line
Possible varus or valgus deform ity of the knee
Possible joint instability due to associated ligam entous injury
Physical Exam Decision aids for the use of radiography:
Ottawa knee rule—knee radiographs are indicated if any of the following are present: o
Age >55 years
o
Tenderness of the fibular head
o
Isolated patellar tenderness
o
Inability to flex to 90°
o
Inability to transfer weight for four steps both im m ediately after the injury and in the ED
o
Lim ping is allowed.
Pittsburgh knee rule—knee radiographs are indicated in fall or blunt traum a and the following are present: o
Age 55 years
Pittsburgh knee rule should be applied with caution to patients 30 m m Hg are an indication for em ergent orthopaedic consultation.
Differential Diagnosis
Knee dislocation
Proxim al fibula fracture
Fem oral condyle fracture
Patella fracture
Tibial subcondylar fracture
Tibial tuberosity fracture
Tibial spine fracture
Cruciate ligam ent tears
Collateral ligam ent tears
Meniscal tears
Pediatric Considerations Include oblique views as part of routine radiography.
Treatment
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Pre Hospital Cautions:
In high-energy m echanism s, associated m ajor injuries take precedence.
Im m obilize to prevent further neurological or vascular injury.
Initial Stabilization
Stabilization of the m ultiple-injury traum a patient
Long-leg splint
Ice
Elevation
Frank dislocations with vascular com prom ise m ay need im m ediate reduction in ED.
ED Treatment
Non–weight-bearing
Pain control
Nondisplaced fractures or m inim ally displaced ( Table o f C o ntents > Tibial/F ibular Shaft F racture
Tibial/Fibular
Shaft Fracture Tyler F. Vadeboncoeur Seth K. Williams
Basics Description Fracture Description
Tibia
Open versus closed
Extent of soft tissue dam age
Gustilo-Anderson classification of open fractures: o
o
o
Type I:
Wound 1 cm
Moderate soft-tissue dam age
Little or no devitalized soft tissue
Type III—severe soft-tissue injury:
A—adequate soft-tissue coverage of bone
B—tissue loss/periosteal stripping
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C—neurovascular injury requiring surgery
Anatom ic location: o
Proxim al, m iddle, or distal third
o
Articular extension
Displacem ent
Degree of shortening
Angulation
Configuration: o
Spiral, transverse, or oblique
o
Com m inuted, with butterfly fragm ent or m ultiple fragm ents
Fibula: o
Proxim al:
Associated with peroneal nerve injury
Disruption of ankle syndesm osis (Maisonneuve fracture)
o
Middle
o
Distal
Pediatric Considerations
Nonphyseal fracture patterns: o
Com pression (torus)
o
Incom plete tension-com pression (greenstick)
o
Plastic/Bowing deform ity of fibula m ay occur.
o
Com plete fractures
Physeal fracture patterns: o
Tibial shaft fractures m ay extend to the physis in Salter-Harris II pattern.
Etiology
High-energy versus low-energy injury
Am ount of soft-tissue injury is prognostic and is determ ined by the degree of energy involved.
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Indirect force—frequently low-energy traum a: o
Rotary and com pressive forces often result in oblique and spiral fractures.
Skiing, fall, child abuse
Direct force—high-energy traum a: o
Direct blow to leg often results in transverse and com m inuted fractures.
Pedestrian versus auto, m otor vehicle crash (MVC)
o
Bending force over a fulcrum often produces com m inution with a wedge-shaped butterfly fragm ent.
Skier's boot top, football tackle, MVC
Pediatric Considerations
Bicycle spoke injury: o
Foot and lower leg get caught between fram e and wheel spoke.
o
Crush injury is the prim ary problem .
o
Initial benign appearance of the soft tissues is often deceiving:
o
Full-thickness skin loss can occur in days.
Orthopaedic surgery consultation should be obtained on all spoke-injury patients with associated fractures.
Toddler fracture: o
Spiral fracture involving the distal third of the tibia with intact fibula secondary to rotational force (turning on planted foot)
o
Age range is 9 m onths to 6 years, m ost often when learning to walk.
o
Fractures in m idshaft or m ore transverse are suspicious of nonaccidental traum a.
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Diagnosis Signs and Symptoms History
History of traum a
Pain usually im m ediate, severe, and well localized to the fracture site
Physical Exam
Visible or palpable deform ity at the fracture site
Significant soft-tissue dam age with high-energy traum a
Inability to bear weight if tibia involved: o
May be able to walk if isolated fibula fracture
Foot drop on affected leg from peroneal nerve injury as it wraps around fibular head
Com partm ent syndrom e
Pediatric Considerations
Rely on parents for historical inform ation.
Child m ay present lim ping with no obvious deform ity.
Essential Workup
Careful assessm ent of soft tissues
Careful neurovascular exam ination (com pare with contralateral side)
Exam ine for associated injuries.
Com pletely expose patient and put into gown.
Assessm ent for com partm ent syndrom e
Alert Compartment Syndrome
Relatively com m on com plication of tibia fractures and m ay
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not appear until 24 hours after injury
Pain disproportionate from that expected
Swollen, tight com partm ent, with pain on palpation of com partm ent
Pain on passive stretch of foot, toes
Sensory deficit
Motor weakness is late finding.
Pulselessness is not a sign of com partm ent syndrom e: o
Palpable pulses are alm ost always present in com partm ent syndrom e unless there is underlying arterial injury.
Four leg com partm ents: anterior, lateral, deep posterior, and superficial posterior
Anterior com partm ent: o
Deep peroneal nerve
o
Sensation of first web space
o
Ankle and toe dorsiflexion
o
Anterior tibial artery feeds dorsalis pedis artery
Lateral com partm ent: o
Superficial peroneal nerve
o
Sensation of dorsum of foot
o
Foot eversion
Deep posterior com partm ent: o
Tibial nerve
o
Sensation to sole of foot
o
Ankle and toe plantarflexion
o
Posterior tibial and peroneal arteries
P.1123
Superficial posterior com partm ent: o
Branch of sural cutaneous nerve
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o
Sensation to lateral foot
Tests Imaging Anteroposterior and lateral views of the leg, knee, and ankle
Diagnostic Procedures/Surgery Com partm ent pressures:
Pressures >30 m m Hg are an indication for orthopaedic consultation and fasciotom y.
Pediatric Considerations Oblique radiograph to detect nondisplaced fractures
Differential Diagnosis
Stress fracture
Pathologic fracture
Osteom yelitis
Pediatric Considerations
Sarcom a
Pathologic fracture
Osteom yelitis
Nonaccidental traum a
Treatment Pre Hospital
Look for associated injuries in high-energy m echanism s.
Assess for neurologic or vascular com prom ise.
Adequate im m obilization is essential to prevent further injury.
Initial Stabilization
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Manage airway and resuscitate as indicated.
Life-threatening injuries take precedence.
Elevate and im m obilize extrem ity.
Apply ice.
Strict NPO
Pain control
ED Treatment
Closed fractures: o
Gentle attem pt at reduction if fracture displaced (do not attem pt m ultiple reductions)
o
Well-padded long-leg posterior splint
Knee in 10–20° of flexion
o
Avoid circum ferential cast.
o
If pain persists after im m obilization, suspect:
o
Im m obilization:
Com partm ent syndrom e
Nerve com pression
Crutches
Open fractures: o
Rem ove contam inants and cover wound with m oist sterile dressing.
o
Antibiotics
o
Tetanus prophylaxis
o
Im m obilization with well-padded long-leg posterior splint
o
Im m ediate orthopaedic surgery consultation for débridem ent and fracture fixation
Isolated fibula fracture: o
Usually treated sym ptom atically:
Padded splint
Elevation
Ice
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o
Non–weight-bearing until swelling resolves
Crutches if non–weight-bearing
Medication (Drugs)
Open fractures gram -positive cocci coverage: Cefazolin 2 g loading dose then 1 g (peds: 50 m g/kg/day) IV/IM q8h
Gustilo-Anderson type III add gram -negative rod coverage: Gentam icin 3–5 m g/kg (peds: 2.5 m g/kg) IV q8h
Farm ing accident add Clostridium species coverage: Penicillin G 10 m illion IU (peds: 250,000–400,000 IU/kg/d) IV q6h
Tetanus toxoid 0.5 m L IM and tetanus im m une globulin 250 U IM as indicated by the type of wound and the num ber of prim ary im m unizations
If penicillin allergy: Vancom ycin 1 g (peds: 10 m g/kg) IV q12h
Follow-Up Disposition Admission Criteria
Multiple traum a
High-energy m echanism
Soft-tissue involvem ent
Risk for com partm ent syndrom e
All open fractures
Displaced, angulated, transverse, shortened, com m inuted, and otherwise unstable fractures
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Intra-articular involvem ent
Neurovascular com prom ise
Inadequate pain control
Pathologic fracture
Nonaccidental traum a in children
Discharge Criteria
Minim ally displaced fracture with low-energy injury m echanism
Close orthopaedic follow-up
Return param eters for com partm ent syndrom e in a reliable patient
If fracture is m ore than 24 hours old, com partm ent syndrom e is unlikely if it has not occurred; discharge criteria m ay be m ore liberal.
References 1. Court-Brown CM. Fractures of the tibia and fibula. In: Bucholz RW, Heckm an JD, eds. Rockwood and Green's fractures in adults. 5th ed. Philadelphia, PA: Lippincott William s & Wilkins, 2001: 1939–2000. 2. Trafton PG. Tibial shaft fractures. In: Browner BD, Jupiter JB, Levine AM, et al., eds. Skeletal traum a: basic science, m anagem ent and reconstruction, 3rd ed. Philadelphia, PA: WB Saunders, 2003: 2131–2255. 3. Watson JT. Treatm ent of unstable fractures of the shaft of the tibia. J Bone Joint Surg. 1994;76A(10):1575–1584.
Codes ICD9-CM 823.80 823.81
ICD10 S82.2
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Tick Bite
Tick Bite
Jonathan A. Edlow
Basics Description
Tick bite patient concerns: o
Tick rem oval
o
Local effect of the bite
o
Possibility of acquiring a tickborne illness:
Often fear contracting Lym e disease
Want to be tested or treated for Lym e
Tickborne diseases in North Am erica: o
Lym e disease
o
Babesiosis
o
Ehrlichiosis
o
Rocky Mountain spotted fever
o
Relapsing fever
o
Tularem ia
o
Colorado Tick fever
o
Q-fever
o
Tickborne encephalitis (Powassan fever)
o
Tick paralysis
Additional tickborne diseases found in Europe: o
Tickborne encephalitis
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o
Boutonneuse fever (R. connori)
o
Other spotted fever rickettsiae
Etiology
Specific tickborne infections are discussed in other chapters.
Tick bite can be from different species of ticks of two m ajor types: o
Soft ticks (Ornithodoros):
Cause tickborne relapsing fever
Only feed for m inutes and therefore alm ost never provoke a visit to the ED
o
Hard ticks—especially Ixodes and Derm acentor:
Feed for several days to a week and therefore m ay lead to an ED visit.
Lym e disease transm ission: o
Species of tick, stage of developm ent, duration of attachm ent, and geography m ay all play a role in the possibility of developing Lym e disease.
o
Most cases of Lym e are associated with bites from nym phal I. scapularis ticks.
o
Most cases are transm itted only after the tick has been attached for 24–48 hours:
Degree of engorgem ent is a m arker for duration of attachm ent.
Diagnosis Signs and Symptoms History
The patient has usually m ade the diagnosis them selves,
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although som etim es they m istake the tick for skin tags or other skin lesions.
Ask regarding duration of tick attachm ent, as this m ay influence the decision to prescribe antibiotic prophylaxis.
Physical Exam Directly exam ine the skin and the tick:
Try to identify the tick species.
Estim ate degree of engorgem ent.
Alert
Som e of the tickborne infections are potentially fatal and m ust be diagnosed based on history, physical and epidem iological context.
Because the drug of choice for som e of these infections—doxycycline—is not usually prescribed for em piric therapy for acutely ill febrile patients: o
Ask about the potential for tick bites in the history of febrile patients and consider using this drug in the appropriate settings.
Essential Workup Accurate history and physical exam searching for presence of tick
Tests Lab Testing for Lym e disease is not indicated:
Such antibody testing would only reflect prior exposure to Borrelia burgdorferi
No treatm ent im plications whatsoever for the current bite
Diagnostic Procedures/Surgery
Testing of the tick itself is not recom m ended.
See treatm ent for tick rem oval.
P.1125
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Treatment Initial Stabilization Rem ove tick:
Early rem oval reduces the likelihood of transm ission of tickborne infections.
ED Treatment
Tick rem oval m ethod: o
Grasp the tick with very fine forceps, as close to the skin as possible, and gently lift up over 30–120 seconds.
Most ticks will com e out.
Do not to squeeze the tick, which could inject infectious m aterials.
If m outhparts are left in the skin, although this could lead to local infection or foreign body reaction, it has no im plications for transm ission of tickborne diseases.
o
Another described m ethod:
Inject an intraderm al wheal of lidocaine with epinephrine beneath the tick.
o
Tick m ay crawl out of its own accord.
Methods not to use include:
Burning the tick with a m atch
Covering it with petroleum jelly or other noxious agents
Lym e disease prophylaxis:
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o
Indicated if the tick is an engorged Ixodes scapularis nym ph, or if the physician decides to prophylax
o
Doxycycline 200 m g for one dose
o
For children, there is no studied single-dose regim en:
Prescribe am oxicillin (25–50 m g/kg) for 10 days in divided doses.
No data supporting prophylactic antibiotics for other tickborne diseases.
Pediatric Considerations
Several studies used 10 days of am oxicillin in children for prevention of Lym e disease: o
No patients in the treated groups developed Lym e or seroconverted.
Pregnancy Considerations Although there are no high quality data on antibiotic prophylaxis for Lym e disease in pregnant wom en, som e authors recom m end having a very low threshold for treating pregnant wom en with tick bites (using am oxicillin).
Follow-Up Disposition Admission Criteria
Tick bite and sym ptom s or signs of tick paralysis
Tick bite leading to a soft tissue infection sufficiently severe to require adm ission
Discharge Criteria All other patients, the vast m ajority, are safely discharged.
Issues for Referral
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Follow-up with prim ary care physicians if there are issues regarding local bacterial infection from the bite (cellulites) or subsequent sym ptom s and signs of one of the tickborne infections listed above.
Seek m edical attention in the event of a febrile illness and to report the history of the tick bite to that physician.
References 1. Edlow JA. Erythem a m igrans. Med Clin North Am . 2002;86:239–260. 2. Edlow JA. Introduction to tick-borne diseases; 1997, updated 2005. Em ergency Medicine on-line Textbook. Boston Medical Publishing Corporation. 3. Needham GR. Evaluation of 5 popular m ethods for tick rem oval. Pediatrics. 1985;75:997–1002. 4. Fix AD, Strickland T and Grant J. Tick bites and Lym e disease in an endem ic setting. JAMA. 1998;279:206–210. 5. Nadelm an, RB et al; Prophylaxis with single dose doxycycline for the prevention of Lym e disease after an Ixodes scapularis tick bite. New Eng J Med. 2001;245:79–84. 6. Sood SK, et al. Duration of tick attachm ent as a predictor of the risk of Lym e disease in an area in which Lym e disease is endem ic. J Infect Dis. 1997;175:996–999.
Miscellaneous SEE ALSO: Lym e Disease; Rocky Mountain Spotted Fever
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Tinea Infectio ns, C utaneo us
Tinea
Infections, Cutaneous Timothy Young Mark Richmond
Basics Description
Superficial fungal infections of the hair, skin, or nails: o
Usually confined to the stratum corneum layer
Tinea requires keratin for growth, so does not involve m ucosa.
Etiology
Derm atophytes: o
Microsporum
o
Trichophyton
o
Epiderm ophyton
o
Malassezia furfur, a yeast, is the etiologic agent of tinea versicolor (not a true tinea).
Traum a or m aceration of the skin m ay allow fungal entry into skin.
Pediatric Considerations
Fungi can be spread from toys and brushes.
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Tinea unguium is rare in children and is associated with Down syndrom e, im m unosuppression, and tinea pedis or capitis.
Diagnosis Signs and Symptoms
Tinea capitis: o
Children are predom inately affected.
o
Most contagious derm atophytosis
o
Alopecia, dandrufflike scaling
o
Kerion:
Boggy, inflam m atory m ass that exudes pus and causes cervical lym phadenopathy
o
“Black dots― from infected hairs broken off at the scalp
Tinea corporis (“ringworm ―): o
Arm s, legs, and trunk
o
Sharply m arginated, annular lesion with raised m argins and central clearing
o
Hair follicle involvem ent m ay produce indurated papules and pustules
o
Lesions m ay be single, m ultiple, or concentric.
o
Pets are often a vector.
Tinea cruris (“jock itch―): o
Erythem atous, scaly, m arginated patches involving the perineum , thighs, and buttocks
o
Associated with heat, hum idity, and tight-fitting undergarm ents
o
Unlike candidiasis, scrotum and penis are spared.
Tinea pedis (“athlete's foot―):
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o
Scaling, m aceration, fissuring between the toes
o
Risk factors:
Advanced age
Im m unocom prom ised status
Hot and hum id clim ates
Infrequent changing of socks
o
More com m on in adults than children
o
“Trichophytid― reaction:
Vesicular eruption rem ote from the infection
Involving hands, m im ics dyshidrotic eczem a
Tinea unguium : o
One type of onychom ycosis
o
Yellow or brown discoloration with thickening and debris under the nails
o
Onycholysis: loosening of the nail from its bed
o
May involve the plantar surface of the foot
Tinea versicolor: o
Most com m on in warm m onths
o
Round or oval superficial brown, yellow, or hypopigm ented m acules that m ay coalesce
o
Upper trunk, arm s, and neck
o
Facial involvem ent is com m on in children.
Essential Workup
Diagnose by clinical exam .
If diagnosis is in doubt, confirm with m icroscopy before starting oral antifungals because of possible side effects.
Tests Lab Fungal cultures are slow-growing and should not be routinely done.
Diagnostic Procedures/Surgery
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Wood lam p is insensitive: o
Not all fungi fluoresce
o
Trichophyton, the m ost com m on cause of tinea infections, does not fluoresce.
o
Microsporum fluoresces green
o
Malassezia (tinea versicolor) fluoresces yellow to yellow-green.
o
Erythrasm a (nontinea corynebacterial infection) will fluoresce coral red.
Microscopy: o
Cleanse area with 70% ethanol.
o
Scrape active m argin of lesion with #10 or #15 scalpel blades.
o
Place scrapings on a glass slide, add a drop of 10–20% potassium hydroxide solution, and cover with a coverslip.
o
The presence of septate hyphae confirm s derm atophyte infection.
o
Budding yeasts and short hyphae (“spaghetti and m eatballs―) confirm s Malassezia.
Pediatric Considerations
Methods to obtain fungal elem ents for culture or m icroscopy: o
Brushing the hair with a toothbrush
o
Rolling a m oistened cotton swab
o
Collecting skin cells with transparent tape
Differential Diagnosis
Tinea capitis: im petigo, pediculosis, alopecia areata, seborrheic derm atitis, and psoriasis
Tinea corporis: im petigo, herpes sim plex, Lym e disease, verruca vulgaris, psoriasis, num m ular eczem a, granulom a
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annulare, herald patch of pityriasis rosea, erythem a m ultiform e, urticaria, seborrheic derm atitis, and secondary syphilis
Tinea cruris: im petigo, seborrheic derm atitis, psoriasis, candidal infection, irritant and allergic contact derm atitis, and erythrasm a
Tinea pedis: scabies, erythrasm a, candida, allergic and contact derm atitis, and psoriasis
Tinea unguium : psoriasis, derm atitis, lichen planus, and congenital nail dystrophy
Tinea versicolor: vitiligo, secondary syphilis
Treatment Initial Stabilization None required except in im m unocom prom ised or septic patients
ED Treatment
Topical antifungals do not penetrate hair or nails: o
Use in conjunction with system ic agent for tinea capitis or unguium .
Tinea capitis: o
Griseofulvin has traditionally been first line.
o
Newer oral antifungals, including terbinafine, itraconazole, and fluconazole, are preferred.
Retained in tissues longer
Allows for shorter treatm ent courses without a decrease in efficacy
o
Terbinafine is now considered the drug of choice by m ost.
o
Pill form m ay be crushed in food.
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o
Selenium sulfide or ketoconazole sham poo reduces transm issibility.
o
Kerion m ay respond m ore rapidly with addition of prednisone.
Tinea corporis, cruris, and pedis: o
Topical terbinafine or im idazoles (ketoconazole, m iconazole, and clotrim azole) are first line.
o
Topical terbinafine has been shown to be as effective as or m ore effective than the im idazoles with a shorter course. P.1127
o
Oral therapy m ay be necessary for cases resistant to topical treatm ent or for im m unocom prom ised patients.
o
Keep the area dry (talc powders) and frequently change socks and underclothes
Tinea unguium : o
Requires oral therapy and longer course than other tinea infections
o
Terbinafine had a slightly higher cure rate than im idazoles or griseofulvin in a m eta-analysis.
o
Ciclopirox 8% nail lacquer approved for treatm ent but low cure rates:
May enhance oral therapy
Tinea versicolor: o
Topicals are first line therapy:
Selenium sulfide 2.5% sham poo was as effective as topical ketoconazole
o
Oral ketoconazole, itraconazole, or fluconazole have been used with cure rates up to 97% but are not as
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safe as topicals.
Medication (Drugs)
Ciclopirox 8% nail lacquer: Apply to affected nails daily, m ax. 48 weeks; rem ove with alcohol every 7 days (peds: sam e).
Clotrim azole: Apply 1% cream to affected area b.i.d. for 2–4 weeks (peds: sam e).
Fluconazole: tinea unguium —150–300 m g/wk pulse therapy for 3–6 m onths for fingernails, 6–12 m onths for toenails; tinea corporis, cruris, and pedis: 150 m g PO weekly for 2–4 weeks; tinea versicolor: 400 m g PO single dose (peds: 6 m g/kg/d for 3–6 weeks for tinea capitis)
Griseofulvin: tinea capitis—500 m g PO per day for 4–6 weeks (peds: 10–20 m g/kg up to 500 m g PO per day until hair regrows, usually 6–8 weeks)
Itraconazole: tinea capitis: adults and peds: 3–5 m g/kg PO per day for 2–4 weeks; tinea unguium : 200 m g PO per day for 3 m onths; tinea versicolor: 400 m g PO per day for 3–7 days; contraindicated in congestive heart failure
Ketoconazole: 2% topical cream per day for 2 weeks; tinea capitis, corporis, cruris, pedis—200 m g PO per day for 4 weeks (peds: 3.3–6.6 m g/kg PO per day for 4 weeks); tinea versicolor—400 m g PO × 1 or 200 m g per day for 7 days (contraindicated with terfenadine and astem izole); soda increases absorption 65%
Miconazole: Apply cream to affected area b.i.d. for 2–4 weeks (peds: sam e)
Prednisone: adults—none (peds: 1 m g/kg PO per day for 2 weeks)
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Selenium sulfide: 2.5% sham poo to affected area for 10 m inutes for 1–2 weeks (peds: sam e)
Terbinafine: 1% topical cream b.i.d. for 2–3 weeks; tinea unguium —250 m g PO daily for 6 weeks for fingernails, 12 weeks for toenails (peds: 40 kg 250 m g/d at sam e interval as adult; tinea pedis: 250 m g PO daily for 2 weeks; tinea capitis: 250 m g/d for 4 weeks [dose by weight as for tinea unguium for 4 weeks])
Tolnaftate: Apply 1% cream /powder/solution to affected area b.i.d. for 2–3 weeks (peds: sam e)
Alert
The oral antifungals m ay rarely cause hepatotoxicity: o
Consider checking liver transam inases prior to initiating therapy.
Pediatric Considerations Topical preparations are preferred when possible.
Pregnancy Considerations
There are few studies addressing the use of antifungal m edications during pregnancy in hum ans.
The im idazoles have shown adverse effects in anim als.
Risk-to-benefit ratio m ust be considered; elective antifungal therapy is generally not recom m ended in pregnancy.
Topical clotrim azole m ay be used.
Follow-Up Disposition
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Admission Criteria
Invasive disease in im m unocom prom ised host
Kerion with secondary bacterial infection
Discharge Criteria
Most patients m ay be m anaged as outpatients.
Children m ay return to school once appropriate treatm ent has been initiated.
Issues for Referral Patients started on oral antifungals should be referred for follow up to m onitor therapy and advised regarding sym ptom s of hepatitis.
References 1. Gupta AK, Ryder JE, Johnson AM. Cum ulative m eta-analysis of system ic antifungal agents for the treatm ent of onychom ycosis. Br J Derm atol. 2004 Mar;150(3):537–544. 2. Gupta AK, Ryder JE, Nicol K, Cooper EA. Superficial fungal infections: an update on pityriasis versicolor, seborrheic derm atitis, tinea capitis, and onychom ycosis. Clin Derm atol. Septem ber to October, 2003;21(5):417–425. 3. Huang DB, Ostrosky-Zeichner L, Wu JJ, Pang KR, Tyring SK. Therapy of com m on superficial fungal infections. Derm atol Ther. 2004;17(6):517–522. 4. Schwartz RA. Superficial fungal infections. Lancet. Septem ber 25, 2004;364(9440):1173–1182. 5. Sladden MJ, Johnston GA. Com m on skin infections in children. Brit Med J. July 10, 2004;329(7457):95–99.
Codes ICD9-CM 110.9
ICD10
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B35.9
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > To luene Po iso ning
Toluene Poisoning
Kirk Cumpston
Basics Etiology
Volatile hydrocarbon
Abused for its euphoric effect
Used as organic solvent—found in: o
Glue
o
Coolants
o
Paints and paint thinners
o
Petroleum products
o
Aerosolized household products
o
Correction fluid
Pediatric Considerations
Prevalent in adolescent age group: o
Inexpensive “high― with readily available sources
o
Many psychosocial problem s
Develop chronic neurologic dysfunction
Mechanism
Rapidly absorbed by inhalation
Readily crosses blood–brain barrier, reaching high
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concentrations in brain
Alveolar excretion and liver m etabolism
Methods of intoxication: o
Sniffing—sim ple inhalation of substance directly from container
o
Huffing—vapors inhaled through cloth saturated with substance
o
Bagging—vapors inhaled from bag containing substance
Toxic range: o
100 ppm —im pairm ent of psychom otor and perceptual perform ance
o
500–800 ppm —headache, drowsiness, nausea, weakness, and confusion
o
>800 ppm —convulsions, ataxia, staggering gait for several days
o
10,000–30,000 ppm —anesthesia within 1 m inute
Diagnosis Signs and Symptoms Acute
Neurologic: o
Depression
o
Euphoria
o
Ataxia
o
Seizures
Cardiac: o
Fatal dysrhythm ias
Pulm onary
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o
Chem ical pneum onitis
Electrolytes
Hypokalem ia
Gastrointestinal:
o
Abdom inal pain
o
Nausea, vom iting
o
Hem atem esis
Renal: o
Renal tubular acidosis
o
Hem aturia
o
Proteinuria
Musculoskeletal: o
Diffuse weakness
o
If high anion gap m etabolic acidosis, hippuric acid
Electrolytes o
Hypocalcem ia
o
Anion gap m etabolic acidosis
Chronic
Neurologic: o
Peripheral neuropathies
o
Encephalopathy
o
Optic atrophy
o
Clonus
Cardiac: o
Dysrhythm ias
o
Dilated cardiom yopathy
Renal: o
Distal renal tubular acidosis
o
Renal failure
o
Fanconi's syndrom e
Musculoskeletal: o
Rhabdom yolysis
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Essential Workup Physical clues to diagnosis:
Presence of agent on lips, nose, or clothes (gold paint has highest concentration)
Perioral eczem atous derm atitis from chronic huffing or bagging can be covered by beard.
Odor of agents
Tests Lab
Arterial blood gas (ABG): o
Acidosis
o
Hypoxia if chem ical pneum onitis
Electrolytes, BUN, creatinine, glucose: o
Hypokalem ia
o
Norm al or high anion gap m etabolic acidosis
o
Hyperchlorem ia
o
Im paired renal function
Calcium and phosphorus: o
Severe hypocalcem ia/hypophosphatem ia com m on
Urinalysis: o
Check for m yoglobin (rhabdom yolysis)
o
Hem aturia and protein often present
Creatinine kinase if suspect rhabdom yolysis
Alcohol level—often coingestant
Liver enzym es, prothrom bin tim e (PT), partial throm boplastin tim e (PTT), INR, if hepatic dysfunction suspected
Urine for hippuric acid (m etabolite of toluene)
Imaging
ECG:
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o
For atrial and ventricular dysrhythm ias
Chest radiograph: o
Indicated if dyspnea or low oxygen saturation
o
Chem ical pneum onitis
CT: o
For altered m ental status/chronic exposure
o
Cerebral/cerebellar atrophy
P.1129
Differential Diagnosis
Alcohol intoxication
Methanol
Ethylene glycol
Salicylate
Heavy-m etal exposure
Guillain-Barré syndrom e
Other hydrocarbon exposure
Metabolic abnorm alities
Treatment Pre Hospital
Rapid onset of toxicity
Death possible with sudden cardiac dysrhythm ias
Forced em esis is not indicated: o
Aspiration is possibility owing to decreased level of consciousness.
Initial Stabilization
Airway, breathing, and circulation m anagem ent (ABCs)
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Cardiac m onitor
0.9% norm al saline (NS) IV access
Naloxone, thiam ine, and check glucose if altered m ental status
ED Treatment
Treat cardiac dysrhythm ias in standard fashion.
Correct m etabolic abnorm alities: o
Potassium
o
Calcium
o
Phosphate
Acidosis resolves with IV fluids.
If rhabdom yolysis: o
Maintain high urine output.
Gastric decontam ination for oral ingestion: o
Charcoal does not bind hydrocarbons well.
Medication (Drugs)
Dextrose: D 5 0 W, one am p: 50 m L or 25 g (peds: D 2 5 W, 2–4 m L/kg) IV
Naloxone (Narcan): 2 m g (peds: 0.1 m g/kg) IV or IM initial dose
Thiam ine (vitam in B 1 ): 100 m g (peds: 50 m g) IV or IM
Follow-Up Disposition Admission Criteria
Altered m ental status
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Dysrhythm ias
Hepatic dysfunction
Renal failure
Rhabdom yolysis
Severe m etabolic derangem ents
Refractory hypokalem ia
Discharge Criteria After 4–6 hours of observation:
Mental status at baseline
No evidence of cardiac, m etabolic, or neurologic derangem ent
References 1. Filley C, Kleinschm idt-Dem asters B. Toxic leukoencephalopathy. N Engl J Med. 2001;345:425–432. 2. Horowitz R. Arom atic hydrocarbons. In: Ford MD, Delaney KA, Ling LJ, et al., eds. Clinical Toxicology. Philadelphia: WB Saunders; 2001:803–812. 3. Leikin J, Paloucek F. Leikin and Paloucek's Poisoning and Toxicology Handbook. 3rd ed. Hudson, OH: Lexi-Com p; 2002:1195–1196. 4. Tang HL, Chu KH, Cheuk A, et al. Renal tubular acidosis and severe hypophosphataem ia due to toluene inhalation. Hong Kong Med J. 2005;11(1):50–53.
Codes ICD9-CM 982.0
ICD10 T52.2
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > To o thache
Toothache
Franklin D. Friedman
Basics Description Pain caused by irritation of the root nerves located in pulpal tissue (the pulp is the tooth's center and its neurovascular supply).
Etiology
Dental: o
Dental caries (hard structures dem ineralized by bacteria)
o
Pulpitis (inflam ed pulp secondary to infection)
o
Reversible pulpitis is m ild inflam m ation of the tooth pulp caused by caries encroaching on the pulp.
o
Irreversible pulpitis is the result of an untreated carious lesion causing severe inflam m ation of the pulp and to severe, persistent and poorly localized discom fort.
o
Periapical abscess (necrotic pulp and subsequent abscess)
o
Postextraction pain (dry socket, infection)
o
Root canal pain
o
Cracked-tooth syndrom e (pain, cold sensitivity, crack difficult to visualize)
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Periodontal disease: o
Gingivitis and periodontitis (gingivitis with loss of periodontal ligam ent attachm ent)
o
Periodontal abscess (gum boil)
o
Pericoronitis (gingival inflam m ation from m alerupted tooth)
o
Acute necrotizing ulcerative gingivitis (gingival pain, ulcers with/without pseudom em branes)
o
Denture stom atitis
o
Herpetic gingivostom atitis
o
Aphthous ulcers (canker sores)
o
Traum atic ulcers
Diagnosis Signs and Symptoms
Tooth pain: o
May be referred to jaw, ear, face, eye, and neck (sensory distribution of fifth cranial nerve)
o
Pain often associated with chewing, changes in tem perature, and recum bency
Malodorous breath
Fever and chills
Foul taste in m outh
Dental caries
Pain on percussion/palpation of tooth and gum s
Abscess
Facial swelling or erythem a
Cervical adenopathy
Trism us: o
Decreased m axim al interincisal opening (norm al
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opening, 35–50 m m )
Essential Workup
Obtain full m edical and dental history.
Ask about drug allergies, especially antibiotics and analgesics.
Assess need for pre–dental-procedure antibiotic prophylaxis:
o
Rheum atic fever
o
Cardiac valve replacem ents
o
Orthopaedic joint replacem ents
o
Mitral valve prolapse or valvular heart disease
Physical exam ination: o
Inspect and palpate lips, salivary glands, floor of the m outh, lym ph nodes of the neck.
o
Identify periodontal abscess.
o
Evaluate for deep-space infection.
o
Teeth should be percussed for tenderness and m obility.
o
Dental num eric system used in adults:
Maxillary: right to left 1–16; m andibular: left to right 17–32 (peds: A-J and K-T)
Alternatively identifying teeth by their location is also appropriate (i.e., left, rear-m ost, upper m olar, or right, center lower incisor).
If physical exam conflicts with patient's history and intra-oral source of pain is not apparent consider other sources of pain.
Nonodontogenic etiologies of pain
Factitious pain/drug-seeking behavior
Tests Lab
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No such tests needed except in patients with signs of system ic toxicity and those patients with perceptible deep fascial space infection.
Imaging
Panoram ic and periapical radiograph views if suspicion exists about dental infection or fracture
CT or MRI to evaluate deeper infections
Differential Diagnosis
Sinusitis
Otitis m edia
Pharyngitis
Peritonsillar abscess
Tem porom andibular joint syndrom e, which usually presents with pain around the ear
Trigem inal neuralgia
Vascular headache
Herpes zoster
Cardiac ischem ia
Pediatric Considerations
Tooth eruption in a child or infant m ay cause oral pain, irritability, low-grade fever, diarrhea, and decreased food intake.
Facial swelling with fever and leukocytosis >15,000 cells/m m 3 suggests a nonodontogenic source
Children have a m axim um of 20 deciduous teeth, ten upper and ten lower.
Treatment
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Pre Hospital
Maintain patent airway in patients with severe facial swelling or trism us.
The patient should be kept in a sitting position if possible.
Initial Stabilization
Airway m anagem ent for deep-space infection and airway com prom ise
Early pain m anagem ent as indicated
ED Treatment
Appropriate analgesia
Nonsteroidal anti-inflam m atory pain m edication is the first-line therapy for uncom plicated dental pain.
Opiate analgesics are an alternative therapy.
Dental anesthetic field block: o
Injected along the buccal surface of the affected tooth
o
Specific nerve block for m ultiple teeth
o
Long-acting anesthetic (e.g., bupivacaine)
Antibiotics if dental infection is present: o
Penicillin is the antibiotic of choice, if patient is not allergic.
o
Erythrom ycin or clindam ycin for patients with penicillin allergy or for predom inance of anaerobes
Localized periapical and periodontal abscesses should be incised, drained, and irrigated: o
Drain m ay be placed for 24 hours.
Saline rinses at hom e four tim es a day and dental referral in 24 hours
P.1131
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Medication (Drugs)
Antibiotics: o
Clindam ycin: 150–450 m g PO q6h (ped: 25–30 m g/kg/24h [m ax. 2 g] q6h)
o
IV dose 300–900 m g (peds: 6–10 m g/kg)
Erythrom ycin: 500 m g PO q6h (peds: 30–50 m g/kg/24h [m ax. 2 g] q6h)
o
Penicillin VK: 500 m g PO q6h (peds: 25–50 m g/kg/24h [m ax. 3 g] q6h
o
Penicillin G potassium aqueous: 4 m U IM/IV q4h (peds: 250,000–400,000 U/kg/d IM/IV div. q4h–q6h, m ax: 24 m U/d)
Analgesics: o
Acetam inophen: 650–1,000 m g PO q4h (peds: 15 m g/kg/dose q4h)
o
Acetam inophen and codeine #3: 1–2 tablets PO q4–6h (peds: elixir—codeine 12 m g/5 m L)
o
Acetam inophen and oxycodone: 1 or 2 tablets PO q6h (peds: 0.05–0.15 m g/kg/dose [m ax. 10 m g])
o
Ibuprofen: 400–800 m g PO q8h (peds: 10 m g/kg PO q6h)
o
Ketorolac: 30 m g IV, 60 m g IM q6h (peds: 1 m g/kg per dose IM)
o
Morphine sulfate: 2–8 m g SC or IV q2h (peds: 0.1 m g/kg per dose SC or IV q2h)
Pediatric Considerations Teething infants m ay be helped by over-the-counter topical anesthetics and oral analgesics.
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Follow-Up Disposition Admission Criteria
Suspicion of deep fascial space infections (e.g., Ludwig angina, retropharyngeal abscess)
Facial cellulitis proxim al to the eye
Extensive trism us
Inability to m aintain nutrition and hydration stasis
Evidence of system ic toxicity
Discharge Criteria Patients with toothache and localized dental infections can be discharged from the ED.
Issues for Referral Patients treated in the ED should be referred to a dentist or dental surgeon prom ptly.
References 1. Am sterdam JT. Dental disorders. In Marx JA, et al. Rosen's Em ergency Medicine: Concepts and Clinical Practice. 5th ed. St. Louis, Mo: Mosby; 2002:892–908. 2. Annino DJ, Goguen LA. Pain from the oral cavity. Otolaryngol Clin of North Am . 2003:6;1127–1135. 3. Dodson TB, Kaban LB. Special considerations for the pediatric em ergency patient. Em erg Med Clin North Am . 2000:18;539–548. 4. Douglass AB. Com m on dental em ergencies. Am Fam Physician. 2003:67;511–516. 5. Klokkevold P. Com m on dental em ergencies: Evaluation and m anagem ent for em ergency physicians. Em erg Med Clin North Am . 1989;7:29–63.
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Codes ICD9-CM 521.0 Dental caries, unspecified 522.0 Pulpitis 525.9 Unspecified disorder of the teeth and supporting structures 528.3 Cellulitis and abscess (of oral soft tissue) 873.63 Tooth (broken)
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > To rtico llis
Torticollis
Andrew Chang
Basics Description
“Twisted neck―
A fixed or dynam ic posturing of the head and neck
Synonym : cervical dystonia
Etiology Local
Acute wry neck: o
Develops overnight without provocation
o
Most prevalent
o
Self-lim ited, sym ptom s resolve in 1 to 2 weeks
Cervical spine: o
Fracture
o
Dislocation, subluxation
o
Infections
o
Spondylosis
o
Tum or
o
Scar tissue–producing injuries
o
Ligam entous laxity in atlantoaxial region
Inflam m atory disease causing m uscular dam age:
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o
Myositis
o
Lym phadenitis
o
Tuberculosis
Infections of surrounding soft tissues: o
Nasopharyngeal abscess
o
Retropharyngeal abscess
o
Cervical adenitis
o
Tonsillitis
o
Meningitis
o
Mastoiditis
o
Sinusitis
o
Posttraum a
Compensatory
Tilt with essential head trem or (patient tilts head to suppress trem or)
Ocular m uscle palsy
Central
Idiopathic spasm odic torticollis: o
Fem ale > Male
o
Onset 31–60 years old
Dystonias: o
Torsion dystonia
o
Generalized tardive dystonia
o
Wilson disease
o
L-Dopa therapy
o
Acute (neuroleptic drugs)
Pediatric Considerations Local
Congenital: o
Odontoid hypoplasia
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o
Hem ivertebrae
o
Spina bifida
o
Arnold-Chiari syndrom e
o
Pseudotum or of infancy
o
Hypertrophy or absence of cervical m usculature
Otolaryngologic: o
Vestibular dysfunction
o
Otitis m edia
o
Cervical adenitis
o
Pharyngitis
o
Retropharyngeal abscess
o
Pharyngitis
o
Mastoiditis
Esophageal reflux
Syrinx with spinal cord tum or
Traum a:
o
Cervical fracture/dislocation
o
Clavicular fractures
Juvenile rheum atoid arthritis
Compensatory
Strabism us (fourth cranial nerve paresis)
Congenital nystagm us
Posterior fossa tum or
Central Dystonias:
Torsion dystonia
Drug induced
Cerebral palsy
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Diagnosis Signs and Symptoms
Interm ittent painful spasm s of sternocleidom astoid (SCM), trapezius, and other neck m uscles
Head is rotated and twisted to one direction.
Pure flexion (anterocollis) or extension (retrocollis) is rare: o
Represents sym m etric involvem ent of m uscles
Neck m ovem ents vary from jerky to sm ooth.
Sym ptom s usually aggravated by standing, walking, or stressful situations
Usually does not occur with sleep
Congenital form : o
First sign m ay be a firm , nontender enlargem ent of the SCM m uscle visible at birth.
Psychological factors (e.g., depression, anxiety) m ay play a role.
History
Interm ittent painful spasm s of SCM, trapezius, and other neck m uscles
Although the m ajority of antipsychotic m edication–induced dystonic reactions occur between 12 and 23 hours, one case report described torticollis 26 hours after IM haloperidol.
Pure flexion (anterocollis) or extension (retrocollis) is rare: o
Represents sym m etric involvem ent of m uscles
Sym ptom s usually aggravated by standing, walking, or stressful situations.
Usually does not occur with sleep
Psychological factors (e.g., depression, anxiety) m ay play
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a role.
Physical Exam
Head is rotated and twisted to one direction.
Neck m ovem ents vary from jerky to sm ooth.
Congenital form : o
First sign m ay be a firm , nontender enlargem ent of the SCM m uscle visible at birth.
Essential Workup
Geared toward diagnosing life-threatening etiologies above
Distinguish torticollis from other causes of neck stiffness (m eningism us)
Good m edication/ingestion history
Cervical spine film s to evaluate for fracture except patients with chronic paroxysm al episodes
Tests Lab No specific tests helpful
Imaging CT or MRI of cervical spine if retropharyngeal abscess or tumor suspected
Diagnostic Procedures/Surgery Som e patients who do not respond to m edical therapy (such as botulinum toxin injections) m ay benefit from elective surgical treatm ent, such as selective peripheral denervation.
Differential Diagnosis
CNS infections
Tum ors of soft tissue or bone
Basal ganglia disease
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Abscess of cervical glands
Myositis of cervical m uscles
Cervical disk lesions
P.1133
Treatment Pre Hospital
Ensure patent airway.
Cervical spine precautions for any history of traum a
Support head
Initial Stabilization
Cervical spine im m obilization if fracture is suspected
If airway m anagem ent is necessary, rapid sequence intubation is the m ethod of choice.
ED Treatment
Drug (e.g., phenothiazine) induced: o
Diphenhydram ine or benztropine
Acquired: o
If less than 1 week in duration, recom m end soft collar and rest.
o
If less than 1 m onth in duration, consider outpatient orthopaedic referral for possible traction.
Miscellaneous: o
Physical therapy
o
Massage
o
Local heat
o
Analgesics
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o
Sensory biofeedback
o
Transepiderm al neurostim ulation
o
Surgery
Medication (Drugs)
Benztropine (for drug-related dystonia): 1–2 m g IM or slow IV, followed by 3–5 days PO
Botulinum toxin A (used for failed drug therapy): 50–200 IU IM
Clonazepam (second-line drug): 0.5 m g PO t.i.d.
Diphenhydram ine (for drug-related dystonia): 25–50 m g IV or IM, followed by 3–5 days PO (peds: 5 m g/kg/24h div. q6h IV, IM, or PO)
Trihexyphenidyl (a first-line drug): 2–5 m g/d PO, advance to 30 m g/d
Valium : 2–5 m g IV, 2–10 m g PO t.i.d. (peds: 0.1–0.2 m g/kg/dose IV or PO q6h)
Follow-Up Disposition Admission Criteria
Cervical spine fracture
Diagnosis is in doubt
Infectious causes
Toxic appearance
Unable to m aintain adequate fluid intake
No support system
Discharge Criteria
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None of the above and sym ptom s adequately controlled with oral m edications
Issues for Referral
Many non-drug induced patients with torticollis m ay need to be referred for possible therapy, such as with botulinum toxin.
Som e patients who fail m edical treatm ent m ay benefit from surgical treatm ent.
References 1. Braun V, Richter HP. Selective peripheral denervation for spasm odic torticollis: 13-year experience with 155 patients. J Neurosurg Spine. 2002;97:207–212. 2. Dauer WT, Burke RE, Greene P, et al. Current concepts on the clinical features, aetiology and m anagem ent of idiopathic cervical dystonia. Brain. 1998;121:547–560. 3. Duane DD. Spasm odic torticollis. Adv Neurol. 1988;49:135–150. 4. Jhee SS, Zarotsky V, Mohaupt SM, et al. Delayed onset of oculogyric crisis and torticollis with intram uscular haloperidol. Ann Pharm acother. 2003;37:1434–1437. 5. Kahn ML, Davidson R, Drum m ond DS. Acquired torticollis in children. Orthop Rev. 1991;20:667–674. 6. Sm ith DL, DeMario MC. Spasm odic torticollis: a case report and review of therapies. J Am Board Fam Pract. 1996;9:435–441.
Codes ICD9-CM 723.5
ICD10 M43.6
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > To xic Epiderm al Necro lysis
Toxic
Epidermal Necrolysis Andrew Chang Hong K. Choi
Basics Description
One of the m ost fulm inant and potentially fatal of all derm atologic disorders
Skin sloughing at the derm al-epiderm al interface results in the equivalent of a second-degree burn; can affect up to 100% of total body surface area.
May extend to involve gastrointestinal (GI) m ucosa (esophagitis, GI bleeding), respiratory m ucosa (dyspnea, bronchial hypersecretion, respiratory failure), and renal epithelium (glom erulonephritis)
Hypothesized to be a type IV hypersensitivity reaction
Current classification system proposes three categories within the spectrum of Stevens-Johnson syndrom e (SJS) and toxic epiderm al necrolysis (TEN) based on percentage of total body surface area (BSA): o
SJS: Less than 10% of BSA
o
Overlap SJS-TEN: 10–30% of BSA
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o
TEN: m ore than 30% of BSA
More com m on in older patients (m ore m edications), HIV patients (m ore m edications, im m unocom prom ised), system atic lupus erythm atosus patients, and bone m arrow transplant recipients
Mortality rate is about 30%, usually due to secondary sepsis from S. aureus and P. aeruginosa
Synonym s: o
Lyell syndrom e
o
Fixed drug necrolysis
o
Epiderm olysis necroticans com bustiform is
o
Epiderm olysis bullosa
Etiology
Dose-independent drug reactions are the usual cause of toxic epiderm al necrolysis: o
Drugs introduced within previous 1–3 weeks are m ost likely candidates.
o
Frequently im plicated drugs include sulfonam ide antibiotics, anticonvulsants (phenytoin, phenobarbital, carbam azepine, lam otrigine), nonsteroidal anti-inflam m atory drugs (oxicam s, pyrazolones, sulindac), allopurinol, and the antiretroviral drug nevirapine.
Others: severe m ycoplasm al infections, graft versus host disease, idiopathic cases (com bined less than 4%).
Diagnosis Signs and Symptoms History
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Prodrom e: 1 to several days of fever, conjunctivitis, pharyngitis, cough, m alaise, pruritis, cutaneous tenderness, erythem a, anorexia, m yalgias, arthralgias, dysuria, vom iting, or diarrhea
Mucous m em branes are com m only affected 1–3 days before skin lesions appear (oropharynx, eyes, genitalia, anus, esophageal and intestinal m ucosa, respiratory epithelium ).
Physical Exam
Skin: o
Rash usually begins on face (scalp usually spared) and trunk as erythem atous m acules, irregular targetlike bullae, or diffuse ill-defined erythem a.
o
Widespread epiderm olysis, denuding of skin surfaces, flaccid bullae, and sheetlike sloughing of epiderm is generally progress over 3–4 days but can progress rapidly over hours.
o
Nikolsky sign: with lateral pressure the skin denudes and sloughs from separation of epiderm is from derm is
Oral m ucosa: initial swelling and erythem a followed by blistering and ulceration of the lips and oral m ucosa
Ocular lesions (pseudom em branes, synechiae or adhesions, keratitis, corneal erosions)
Essential Workup
Diagnosis is m ade clinically: o
Based on history and characteristic skin and m ucous m em brane lesions
Ophthalm ology consultation is required for eye involvem ent (evaluation and rem oval of pseudom em branes and adhesions).
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Tests Lab
No confirm atory laboratory tests exist.
CBC: norm ocytic anem ia, leukocytosis, lym phopenia/neutropenia, and throm bocytopenia m ay be present.
Erythrocyte sedim entation rate m ay be elevated as a result of system ic inflam m ation.
Serum chem istry: electrolyte derangem ents if extensive fluid losses: o
Prerenal azotem ia.
Urinalysis m ay show hem aturia (urethral m ucosal erosion, glom erulonephritis) or casts (acute tubular necrosis).
Bacterial sam pling of skin, and blood cultures
SCORTEN: prognostic score including m ortality: o
Age above 40 years
o
Malignancy
o
Tachycardia above 120/m in
o
Initial percentage of epiderm al detachm ent above 10%
o
Blood urea nitrogen above 27 m g/dL
o
Serum glucose level above 252 m g/dL, 7 serum bicarbonate level below 20 m Eq/L
Imaging Chest radiograph should be done if pneum onitis or Mycoplasm a pneum oniae is suspected.
Diagnostic Procedures/Surgery Biopsy by consulting derm atologist to rule out autoim m une bullous diseases, staphylococcal scalded skin syndrom e, and other diagnoses.
Results not im m ediately available to ED physician.
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Differential Diagnosis
SJS
Erythem a m ultiform e m ajor (EMM) o
Differentiation of TEN from EMM:
o
Etiology: TEN is m ainly drug induced; EMM occurs m ainly after herpes sim plex virus (HSV) infection
o
Lesions:
TEN: widely distributed, m ainly on the trunk and face, nonspecific, targetlike lesions that often are confluent and too num erous to count
EMM: lim ited in num ber, sym m etric and acral distribution, typical target type (at least three concentric rings) with or without blisters
o
Prognosis: EMM is usually benign; recurrence of disease is com m on (30%); therapeutic prevention of EMM due to HSV is prevention of HSV recurrence
Staphylococcal scalded skin syndrom e (SSSS): o
Differentiation of TEN from SSSS:
o
Age: TEN: prim arily adults (but m ay occur in children); SSSS: prim arily affects children.
o
Etiology:
TEN m ost often represents an idiosyncratic, drug-induced, dose-independent reaction and hence does not require treatm ent with antibiotics.
SSSS results from infection and requires antibiotics.
P.1135
o
Pain: painful in TEN; painless in SSSS
o
Mucous m em branes: involved with TEN; usually
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spared with SSSS o
Skin cleavage: derm al-epiderm al junction in TEN; intraepiderm ally in SSSS (both can produce a positive Nikolsky sign).
Autoim m une bullous diseases (pem phigus vulgaris, bullous pem phigoid)
Scarlet fever
Toxic shock syndrom e
Chem ical or therm al scalds
Kawasaki syndrom e
Treatment Pre Hospital
Transport to facility with burn center.
Care during transport should be gentle to avoid skin traum a.
IV catheter should be avoided for short transport if hem odynam ically stable (m ore sterile conditions in ED).
Avoid using adhesive m aterials.
Initial Stabilization
If intubation is required, gentle technique m ust be used to m inim ize m ucosal dam age.
Meticulous sterile technique
Peripheral IV line is preferred over central line to decrease risk of sepsis.
Cardiac m onitor, pulse oxim eter, nasogastric tube, Foley catheter
ED Treatment
Identify and stop any causative m edication.
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Aggressive fluid resuscitation with lactated Ringer solution as in burn care (Parkland form ula): o
Urine output should be m aintained at a rate of at least 0.5 m L/kg per hour.
Pain should be controlled with IV opiates.
Warm ing m easures and frequent core tem perature evaluation are im portant.
Antibiotics are usually withheld because toxic epiderm al necrolysis is often drug induced.
If available, cover with biologic dressings (e.g., Biobrane): o
Reduces pain, decreases caloric and evaporative losses, and facilitates healing.
Antibiotic drops for eyes
Petroleum jelly application to lips
Prevention of peptic stress ulcers
Topical antibiotics are unproven, but m ay be applied with the exception of silver sulfadiazine (sulfonam ide derivative).
Tim ely adm ission to burn unit/intensive care unit
Tim ely derm atologic and ophthalm ologic consultation
System ic corticosteroids are no longer recom m ended: o
Retrospective studies show no benefit and suggest greater risk of death from infection.
Medication (Drugs) There are no established treatm ent regim ens; however, the following experim ental therapies are under investigation:
Cyclosporin A: 3 m g/kg/d
Cyclophospham ide: 300 m g/d
Intravenous im m unoglobulin: 0.4–1 g/kg/d
Anti-TNF-α Antibodies: inflixim ab 5 m g/kg/dose
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Follow-Up Disposition Admission Criteria All patients with suspected toxic epiderm al necrolysis should be adm itted to a burn unit (if burn unit is unavailable and transfer is not possible, then adm it to intensive care unit).
Issues for Referral Transfer to facility with burn unit has been shown to improve patient outcom e.
References 1. Bachot N, Roujeau JC. Differential Diagnosis of Severe Cutaneous Drug Eruptions. Am J Clin Derm atol. 2003;4:561–572. 2. Bastuji-Garin S, et al. SCORTEN: A Severity-of-Illness Score for Toxic Epiderm al Necrolysis. J Invest Derm atol. 2000;115(2):149–153. 3. Becker DS. Toxic epiderm al necrolysis. Lancet. 1998;351:1417–1420. 4. Ghislain PD, Roujeau JC. Treatm ent of severe drug reactions: Stevens-Johnson Syndrom e, Toxic Epiderm al Necrolysis and Hypersensitivity syndrom e. Derm atol Online J. 2002;8(1):5. 5. Nassif A, et al. Toxic epiderm al necrolysis: Effector cells are drug-specific cytotoxic T cells. J Allergy Clin Im m unol. 2004;114(5):1209–1215. 6. Paquet P, et al. Novel Treatm ents for Drug-Induced Toxic Epiderm al Necrolysis (Lyell's Syndrom e). Int Arch Allergy Im m unol. 2005;136(3);205–216. 7. Prendiville J. Stevens-Johnson Syndrom e and Toxic Epiderm al
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Necrolysis. Adv Derm atol. 2002;18:151–173. 8. Prins C, et al. Treatm ent of Toxic Epiderm al Necrolysis with High-Dose Intravenous Im m unoglobulins. Arch Derm atol. 2003;139:26–32. 9. Wolkenstein P, Revuz J. Toxic epiderm al necrolysis. Derm atol Clin. 2000;18(3):485–495.
Codes ICD9-CM 695.1 Necrolysis, toxic epiderm al
ICD10 L51.2
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > To xic Sho ck Syndro m e
Toxic Shock
Syndrome Michelle Canham
Basics Description
Toxic shock syndrom e (TSS) is a severe, acute life-threatening illness caused by toxin-producing strains of Staphylococcus aureus or, to a lesser extent, by group A streptococci (GAS, Streptococcal TSS).
S. aureus produces an exotoxin, toxic shock syndrom e toxin (TSST-1): o
Produced by 20% of S. aureus isolates
GAS produces pyrogenic exotoxins—m ost com m only exotoxins A (SPEA) and B (SPEB).
The exotoxins are superantigens, a significant factor in the production of sym ptom s associated with TSS.
Biologic properties of superantigens include the ability to: o
Activate up to 20% of T-cells at one tim e resulting in m assive cytokine production
o
Induce fever directly on the hypothalam us or indirectly via interleukin-1 (IL-1) and tum or necrosis factor (TNF) production
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o
Enhance delayed hypersensitivity
o
Suppress neutrophil m igration and im m unoglobulin
o
Enhance host susceptibility to endotoxins
Massive vasodilation occurs: o
Causes rapid m ovem ent of serum proteins and fluids from the intravascular to the extravascular space, causing hypotension.
Etiology
Initially TSS was a disease of young, healthy m enstruating fem ales due to highly absorbent tam pons: o
Changes were m ade to reduce the absorbency and com position of tam pons.
Approxim ately one half of reported TSS cases are nonm enstrual including:
o
Surgical wounds
o
Postpartum wound infections
o
Mastitis
o
Septorhinoplasty
o
Sinusitis
o
Osteom yelitis
o
Arthritis
o
Burns
o
Nasal packing (nasal tam pons)
o
Cutaneous and subcutaneous lesions
30–50% of healthy adults and children carry S. aureus in the nasal vestibule, vagina, and rectum and/or on the skin.
GAS infections often begin within 24–72 hours at the site of m inor traum a, often without a visible break in the skin.
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Diagnosis Signs and Symptoms Criteria for Diagnosis—CDC Case Definition
Fever >38.9°C (102.0°F)
Hypotension (systolic blood pressure [BP] Table o f C o ntents > To xo plasm o sis
Toxoplasmosis
Ann Buchanan
Basics Description
Toxoplasm a gondii—intracellular protozoan parasite: o
Three form s:
Tachyzoite: asexual invasive form
Tissue cyst: persists in tissues of infected hosts during chronic phase
Oocyst: contains sporozoites and produced during sexual cycle in cat intestine
Transm ission: o
Ingesting tissue cysts or oocysts:
Ingesting undercooked m eat
Vegetables contam inated with oocysts
Contact with cat feces, through cat or soil
o
Transplacental
o
Blood product
o
Organ transplantation
Etiology
70% of adults seropositive
Asym ptom atic in m ost im m unocom petent patients
Chorioretinitis:
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o
Usually secondary to congenital transm ission
o
Does not becom e sym ptom atic until 20–30 years of age
Diagnosis Signs and Symptoms Four types of infection
Immunocompromised Host
CNS: o
Subacute presentation (90%)
o
Encephalitis
o
Headache
o
Altered m ental status
o
Fever
o
Seizures
o
Cranial nerve palsies
o
Spinal cord lesions
o
Cerebellar signs
o
Meningitislike sym ptom s
o
Movem ent disorders
o
Neuropsychological sym ptom s:
Psychosis
Paranoia
Dem entia
Anxiety
Agitation
Pulm onary: o
Pneum onitis
o
Prolonged febrile illness
Pa ge 4 8 3
o
Nonproductive cough
o
Dyspnea
Immunocompetent Host
10% with sym ptom s
Lym phadenopathy
Fever
Malaise
Headache
Sore throat
Night sweats
Maculopapular rash
Urticaria
Self-lim ited process; resolves in 2–12 m onths
Rarely presents with pneum onitis or encephalitis
Ocular Toxoplasmosis
Blurred vision
Scotom a
Pain
Photophobia
Retina: o
Sm all clusters of yellow-white, cottonlike patches
Congenital Toxoplasmosis
Results from an asym ptom atic acute infection during pregnancy
First trim ester: o
Spontaneous abortion
o
Stillbirth
o
Severe disease up to 25% of the tim e
Second or third trim ester: o
50–60% chance of acquiring congenital toxoplasm osis
Pa ge 4 8 4
o
2% fatal
Most asym ptom atic at birth
Delayed onset: o
CNS disease
o
Ocular disease (blindness m onths to years later)
o
Lym phadenopathy
o
Hepatosplenom egaly
Essential Workup
Diagnose via: o
Isolation of organism :
Blood
Cerebrospinal fluid (CSF) for encephalitis
Bronchoalveolar lavage for pneum onitis
Am niotic fluid
Aqueous hum or
o
Detection of tachyzoites in tissues or body fluids
o
Dem onstrating characteristic lym ph node pathology
Thorough ocular exam ination: o
Retinal exam ination
o
Visual acuity
Tests Lab
LDH >600/UL associated with toxoplasm osis
CBC: o
Atypical lym phocytes
Arterial blood gas/pulse oxim etry for pulm onary sym ptom s
IgG antibodies: o
High num ber of false-positive and false-negative results
o
Com m on tests:
Sabin-Feldm an dye test
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Indirect fluorescent antibody
Agglutination
Enzym e-linked im m unosorbent assay test
Im m unoglobulin M (IgM) antibodies: o
Absence excludes diagnosis in im m unocom petent host
o
Diagnoses acute infection
o
Appear in 5 days
o
Disappear in weeks to m onths
o
Neonatal testing differentiates from m aternal infection.
Imaging
Chest radiograph for pulm onary sym ptom s: o
CT head with contrast: o
Pneum onitis associated with reticulonodular pattern
Multiple bilateral hypodense ring enhancing lesions
MRI brain: o
High signal abnorm alities on T2-weighted im ages
Diagnostic Procedures/Surgery Brain biopsy for encephalitis—definitive diagnosis P.1139
Differential Diagnosis
Cryptococcal m eningitis
CNS lym phom a
Pneum ocystis carinii pneum onia
Cytom egalovirus retinitis
Treatment
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Initial Stabilization
Treat seizures in standard fashion with diazepam and phenytoin.
Initiate oxygen if hypoxia due to pneum onitis.
ED Treatment Immunocompetent
Toxoplasm ic lym phadenitis: o
No antibiotics unless sym ptom s severe and persistent
o
Treat sym ptom atic patients with Pyrim etham ine and folinic acid plus sulfadiazine or clindam ycin for 2–4 weeks.
o
Reassess to determ ine if longer therapy needed.
Immunocompromised
Confirm ed acute infection by serology/sym ptom s: o
Treat with pyrim etham ine and folinic acid plus sulfadiazine or clindam ycin for 4–6 weeks after resolution of sym ptom s.
o
Alternative m edications:
Trim ethoprim -sulfam ethoxazole
Pyrim etham ine and folinic acid plus dapsone
CNS sym ptom s plus a lesion on CT or MRI: o
Treat em pirically with pyrim etham ine and folinic acid plus sulfadiazine or clindam ycin.
o
Brain biopsy or CSF to confirm diagnosis
o
Adm inister anticonvulsants only if confirm ed prior seizures:
Poorer outcom e for patients on anticonvulsants
Chronic asym ptom atic infection: o
No therapy required
o
Prophylaxis options for toxoplasm osis in AIDS
Pa ge 4 8 4
patients:
Trim ethoprim -sulfam ethoxazole: 1 tablet daily or 2 tablets twice a week
Pyrim etham ine (75 m g/week) and dapsone (200 m g/week)
Fansidar (pyrim etham ine-sulfadoxine) 3 tablets every 2 weeks
Ocular
Treat with pyrim etham ine and sulfadiazine for 1 m onth: o
May add clindam ycin
Adm inister system ic steroids with m acula or optic nerve involvem ent.
Acute Acquired Infection in Pregnancy
Initially treat with spiram ycin pending confirm atory tests.
After the infection is docum ented, initiate treatm ent with:
o
Sulfadiazine in the first 16 weeks
o
Pyrim etham ine and sulfadiazine after 16 weeks
Studies suggest m aternal-fetal transm ission is rapid and treatm ent m ay have little effect.
Treat congenital infection with sulfadiazine, pyrim etham ine, and folinic acid for 12 m onths.
Medication (Drugs)
Clindam ycin: o
600 m g (peds: 20–40 m g/kg/24h) IV q6h
o
300 m g (peds: 8–20 m g/kg/24h) PO q6h
Dapsone: 100 m g PO daily
Folinic acid: 5–10 m g PO daily in conjunction with pyrim etham ine
Pyrim etham ine: 100 m g b.i.d. on first day loading dose,
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then 25–50 m g PO daily (peds: 1 m g/kg/24h PO b.i.d. for 1–2 days, then 0.5 m g/kg/24h)
Sulfadiazine: 500 m g–2 g (peds: 100–200 m g/kg/24h) PO q6h
Trim ethoprim -sulfam ethoxazole: 5 m g/kg of trim ethoprim com ponent IV or PO q6h
Follow-Up Disposition Admission Criteria
Acute infection with severe system ic sym ptom s
Im m unocom prom ised patients with: o
Toxoplasm osis encephalitis
o
Pneum onitis
o
Sepsis
Discharge Criteria
Im m unocom petent patients with: o
Mild sym ptom s
o
Ocular
Maternal/Congenital infection with m ild sym ptom s
References 1. Chang HR. The potential role of azithrom ycin in the treatm ent of prophylaxis of toxoplasm osis. Int J STD AIDS. 1996;(Suppl 1):18–22. 2. Fung HB, Kirschenbaum HL. Treatm ent regim ens for patients with toxoplasm ic encephalitis. Clin Ther. 1996;18:1037–1056. 3. Ram sey RG, Bean AD. Neuroim aging of AIDS. I. Central nervous system toxoplasm osis. Neuroim aging Clin North Am .
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1997;7:171–186. 4. Rodriguez JC, Martinez MM, et al. Evaluation of different techniques in the diagnosis of toxoplasm a encephalitis. J Med Microbiol. 1997;46:597–601. 5. Sciam m arella J. 2002 July 6. Toxoplasm osis. http://www.em edicine.com /em erg/topic601.htm . Accessed 2005 April 15.
Codes ICD9-CM 130.9
ICD10 B58.9
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Transfusio n C o m plicatio ns
Transfusion
Complications Jason Prystowsky
Basics Epidemiology
Som e type of transfusion reaction occurs in 2% of units given during or within 24 hours of use.
Febrile nonhem olytic: 0.5–6% (1–38% in platelets)
Allergic: 1–3%
Anaphylaxis: 0.002–0.005%
Acute hem olytic reaction: 0.0026–0.00142%
Delayed hem olytic reaction: 0.02–0.009%
Circulatory overload: 100 RBC units
Infectious agent: o
Bacteria: RBC 1:1,000, platelets 1:2,000
o
Hepatitis C: 1:1,935,000
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o
Hepatitis B: 1:205,000
o
HTLV I and II: 1:2,993,000
o
HIV: 1:2,135,000
o
HAV: 1:1,000,000
o
B19 Parvovirus: 1:40,000
o
Parasites: Babesia and m alaria: 90%
Im m unologically com petent lym phocytes transfused into im m unocom petent host
Host unable to destroy new WBCs
Donor WBCs recognize host as foreign and attack host's tissues.
o
Anaphylactic reaction:
Can occur with Table o f C o ntents > Transient G lo bal Am nesia
Transient
Global Amnesia Kama Guluma
Basics Description
Transient global am nesia (TGA) has the following features: o
Episode of am nesia with abrupt onset
o
No focal neurological signs or sym ptom s
o
Tem porary, severe, anterograde am nesia:
o
Acute inability to form new m em ories
Perm anent m em ory gap after the episode
Tem porary long-ranging retrograde am nesia:
More recent m em ories at m ore risk
Previously encoded m em ories are only tem porarily unavailable
o
Gradually shrinks, until only rem aining m em ory deficit is the m em ory gap induced by the anterograde am nesia
Incidence between 3.4–10 per 100,000 people: o
23.5 per 100,000 in people over age 50
The average age of patients is 61: o
TGA is rare before age 40.
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The m ajority of attacks last between 1 and 8 hours (range 15 m inutes to 7 days).
Etiology
The exact etiology of TGA is unknown.
Speculated causes: o
Migraine
o
Transient ischem ic attack
o
Seizure
o
Psychogenic hyperventilation in setting of age-related cerebrovascular autoregulatory dysfunction
SPECT and PET have shown som e abnorm alities of regional cerebral blood flow.
Recent studies using MRI and internal jugular vein ultrasonography suggest transient cerebral venous congestion: o
Specifically in the setting of internal jugular vein incom petence
o
Resulting in dysfunction of selectively vulnerable hippocam pal structures
Diagnosis Signs and Symptoms History
Often precipitated by stressful condition: o
Cough, valsalva
o
Physical exertion
o
Sexual intercourse
o
Extrem e fright or shock
o
Intense heat or cold
Pa ge 4 8 5
Patient will likely feel that som ething is wrong: o
May ask “how did I get here?―
o
Will be generally aware of attack
May have other subtle transient sym ptom s at onset, such as headache, dizziness, nausea
Historical features that are helpful in excluding other diagnoses are: o
Onset of attack witnessed, with no seizure activity or epileptiform features noted
o
No history of seizures in prior 2 m onths
o
No history of recent traum atic brain injury
o
Acute anterograde am nesia with relatively preserved rem ote m em ory
Physical Exam
Marked anterograde am nesia
Most cases (up to 90% in case series) will dem onstrate repetitive questioning.
The neurological and general exam norm al
The TGA patient will not have findings of an acute confusional state or dem entia. The patient will not: o
Be som nolent, inattentive or globally confused
o
Confabulate
o
Be disoriented to nam e, birth date, address, phone num ber, date
o
Have problem s perform ing com plex tasks and following com plex com m ands
Aphasia, apraxia, and agnosia are not findings consistent with TGA.
Essential Workup
True TGA can be diagnosed with a careful history and physical alone.
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If clinical diagnosis is certain, no other workup is essential.
Tests Testing is only indicated when the diagnosis is uncertain.
Lab
CBC, com prehensive chem istries including glucose, liver function tests, NH3, thyroid studies, and urine analysis for organic m etabolic etiologies where im plicated
Tox screen, alcohol level for toxicological etiologies where suspected
Imaging Head CT for intracranial m ass or bleed
Diagnostic Procedures/Surgery
Lum bar puncture and cerebrospinal fluid analysis for encephalitis
Electrocardiogram for seizure if indicated
Differential Diagnosis
Since TGA is a unique and very characteristic entity: o
There is little in the way of a differential diagnosis to consider.
Other entities m ay present som ewhat sim ilarly, but will have historical or exam features that readily distinguish them from TGA: o
Acute confusional state/Korsakoff syndrom e/m etabolic disorder:
Alcohol, m edication, or toxin ingestion
Decreased attention or other findings of an encephalopathy
Ability to lay down new m em ory if allowed tim e to encode
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o
Com plex partial seizures/epileptic am nestic attacks:
Witnessed epileptiform activity or features
Short duration (typically less than 30 m inutes)
No repetitive questioning
Frequent and rapid recurrences
P.1143
o
Psychogenic am nesia:
Younger patient with a known psychiatric stressor
Psychiatric history, or history of personality changes
Typically no anterograde am nesia (only a retrograde gap)
Psychogenic m em ory loss for personal identification, nam e, birthdate, etc.
o
Tem poral lobe brain lesion or encephalitis affecting the tem poral lobe:
Typically with other associated neurological sym ptom s (e.g., visual field cut)
o
Progressive and perm anent am nesia
Previously unrecognized Alzheim er dem entia:
Mem ory loss for personal inform ation such as date, phone num ber, address
Signs of additional global cognitive im pairm ent
Treatment ED Treatment
TGA is a self-lim ited, relatively benign entity.
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Observe the patient for im provem ent.
Assum ing a true diagnosis of TGA, no acute treatm ent, beyond reassurance of the patient and fam ily, is indicated.
Follow-Up Disposition Admission Criteria
Adm ission for further observation for patients without significant im provem ent at the tim e of disposition
Patients with uncertain diagnosis
Patients showing a trend towards resolution, but who have suboptim al social support at hom e
Discharge Criteria
A clear diagnosis of TGA
Resolving or resolved am nesia
Good social support
Issues for Referral
Refer patients with recurrent episodes of TGA to a neurologist.
Selected case series have revealed that patients in this subgroup have a different prognosis: o
May have sustained focal cerebral blood flow abnorm alities on specialized im aging
o
More likely to go on to develop clinical epilepsy
References 1. Brown J. ED Evaluation of Transient Global Am nesia. Ann Em erg Med. 1997;30:522–526. 2. Fredericks JAM. Transient Global Am nesia. Clin Neurol Neurosurg.
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1993;95:265–283. 3. Lam pl Y, Sadeh M, Lorberboym M. Transient global am nesia—not always a benign process. Acta Neurol Scand. 2004;110:75–79. 4. Lewis SL. Aetiology of transient global am nesia. Lancet 1998;352:397–399. 5. Pantoni L, Lam assa M, Inzitari D. Transient global am nesia: a review em phasizing pathogenic aspects. Acta Neurol Scand. 2000;102:275–283. 6. Sander D, Winbeck K, Etgen T, Knapp R, Klingelhöfer J, Conrad B. Disturbance of venous flow patterns in patients with transient global am nesia. Lancet. 2000;356:1982–1984. 7. Schreiber SJ, Doepp F, Klingebiel R, Valdueza JM. Internal jugular vein incom petence and intracranial venous anatom y in transient global am nesia. J Neurol Neurosurg Psych. 2005;76;509–513.
Codes ICD9-CM 437.7
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Transient Ischem ic Attack
Transient
Ischemic Attack Renee Hsia Rebecca Smith-Coggins
Basics Description
Classically a tem porary neurologic deficit that resolves within 24 hours due to transient decrease in blood supply: o
80% resolve in less than 30 m inutes.
Modern definitions m ore tissue-based rather than tim e-based: o
Infarction can occur if sym ptom s last m ore than an hour.
Contrasts with other ischem ic neurologic conditions: o
Stroke in evolution—neurologic deficits that continue to worsen over m inutes to hours
o
Com pleted stroke—persistent deficit after 3 weeks despite im provem ent
Etiology Mechanism Transient hypoperfusion of portion of brain from :
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Low flow state from atherosclerotic lesions of large arteries (e.g., internal carotid origin, m iddle cerebral artery stem , junction of vertebral and basilar artery)
Em bolus from heart or proxim al atherosclerotic plaque
Throm bus form ation in involved vessel
Vasculopathies—carotid or vertebral dissection, Takayasu, Moyam oya disease
Diagnosis Signs and Symptoms
The vessel and extent of involvem ent dictate neurologic deficits.
Carotid artery (anterior circulation): o
Manifests signs and sym ptom s of both anterior cerebral artery (ACA) and m iddle cerebral artery (MCA)
ACA: o
Motor and sensory—contralateral leg >arm , ± face
o
Speech—anarthria (speechlessness), dysarthria, perseveration
o
Vision—am aurosis fugax, or blurred vision on one side of field of vision of both eyes opposite to side of diseased artery
o
Contralateral neglect
MCA: o
Motor or sensory—contralateral arm and face greater than leg
o
If dom inant hem isphere involved, receptive or expressive aphasia, or both
o
Mentation—inattention, neglect, apraxia
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o
Vision—hom onym ous hem ianopsia, gaze preference to side of infarct
Vertebrobasilar artery (posterior circulation): o
Hallm ark
o
Vision—diplopia or hom onym ous field defect
o
Other features: dizziness, vertigo, and dysphagia
o
Wallenberg syndrom e—ipsilateral cranial nerve deficits, contralateral m otor weakness, gait and lim b ataxia, and incom plete Horner syndrom e (anhydrosis usually absent)
o
“Drop attack―—sudden onset of inability to walk, often with vertigo, headache, neck pain, and nausea/vom iting
Lacunes/Subcortical areas: o
Pure m otor or sensory deficits
o
Motor deficit is unilateral and equal in face/arm /leg.
o
Ataxic hem iparesis
o
Dysarthria
Essential Workup
Neurologic evaluation that assesses level of consciousness, vision, cranial nerves, m otor and sensory, coordination, speech, and signs of neglect
Noncontrast head CT to rule out hem orrhage
Cardiac m onitoring and ECG to diagnose atrial fibrillation, acute m yocardial infarction, or other cardiac abnorm alities
Glucose level
Tests Lab
CBC: Assess for anem ia or signs of hyperviscosity (elevated hem atocrit or throm bocytosis).
Electrolytes: Rule out hyponatrem ia or other abnorm alities
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that can m im ic stroke
Coagulation studies ± throm bophilic studies (if throm bophilia suspected): o
Investigate for hypercoagulable state or as baseline for possible anticoagulation therapy.
Tox screen: particularly in younger sym ptom atic patients for cocaine or am phetam ine-induced ischem ia
Arterial blood gases
Blood cultures and erythrocyte sedim entation rate: if bacterial or nonbacterial endocarditis suspected
Imaging
Noncontrast head CT: o
Prim arily to assess for hem orrhage
o
Sensitivity of greater than 90% for subarachnoid bleed
o
Ischem ic evidence on CT often does not appear unless im aged >6 hours after sym ptom onset.
Carotid duplex scan: o
Indicated when a high-grade carotid obstruction is suspected or with crescendo transient ischem ic attacks
o
Can detect stenosis of >60% but cannot distinguish 95% from 100% occlusion
o
Positive findings would suggest candidacy for urgent carotid endarterectom y or anticoagulation.
Echo—m ay dem onstrate cardioem bolic phenom enon (m ural throm bus, tum or, or valvular vegetation)
MRI—Identifies and distinguishes ischem ia and infarcts earlier than CT but is less sensitive for hem orrhage: o
Better study for posterior circulation (m agnetic resonance angiography)
o
Detects posterior bleeding better
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Angiography—gold standard for detection of both stenosis and aneurysm of cerebral blood vessels: o
Cost, availability, and invasiveness m ay preclude its use.
Differential Diagnosis
Subarachnoid/Intracerebral hem orrhage
Subdural/Epidural hem atom a
Brain aneurysm or arteriovenous m alform ation
Giant cell arteritis
Air em bolism
Migraine headache
Todd's paralysis
Ménière disease
Benign positional vertigo
Vestibular neuronitis
Epilepsy
Brain tum or/m ass
Syncope
Peripheral nerve or nerve root com pression
Dem entia
Encephalopathy
Wernicke encephalopathy
Carotid dissection after neck traum a
Hypoglycem ia
Diabetic ketoacidosis/hyperosm olar com a
Multiple sclerosis
Hyperventilation
Pediatric Considerations
Severe dehydration with associated hypernatrem ia
Congenital heart disease
Sickle cell anem ia
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Meningitis
Acute and congenital hem iplegia of childhood
Moyam oya disease: o
Rare prim ary vascular disease defined by diffuse cerebral arterial narrowing that m anifests as reoccurring TIAs
P.1145
Treatment Pre Hospital Cautions:
Initial assessm ent of neurologic deficits crucial because they m ay com pletely resolve before arrival at ED
Avoid glucose-containing fluids unless low glucose level confirm ed.
Initial Stabilization
Airway: support as needed
Breathing: oxygen
Circulation: careful hydration avoiding cerebral edem a and decreased cerebral blood flow (CBF)
ED Treatment
Hypertension: o
Only patients suspected to have neurologic findings from hypertension (e.g., hypertensive encephalopathy) should be treated acutely with agents such as nitroprusside, nicardipine, or labetalol.
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o
Avoid precipitous drops in blood pressure because stroke requires m aintaining perfusion to brain.
Early evaluation to prevent transient ischem ia becom ing infarct
Neurology consult
Antiplatelet therapy with aspirin
Full anticoagulation of heparin m ay be used with atrial fibrillation or with neurology consultation if patient is having recurrent sym ptom s or m inor stroke.
Transition to warfarin with target international norm alized ratio of 2.5 for patients with atrial fibrillation
Patients with aspirin failure can be started on clopidogrel, ticlopidine, or aspirin-dipyridam ole.
Patients with TIA and high-grade carotid stenosis (>70%) benefit from carotid endarterectom y (tim ing controversial but within 1–2 weeks at latest).
Medication (Drugs)
Aspirin: 50–325 m g PO daily
Aspirin-dipyridam ole: 25/200 m g PO b.i.d.
Clopidogrel: 75 m g PO daily
Heparin: 5000 IU SC q8h–q12h, or 5,000–7,500 IU IV bolus; 1,000 IU/h infusion
Labetalol 20 m g/m in IV bolus, then 20–80 m g q10m in; m ax. 300 m g; infusion 0.5–2 m g/m in IV
Nicardipine: 5 m g/h IV infusion, increase by 2.5 m g/h q5m in–q15m in; m ax. 15 m g/h, pediatric dosing unavailable
Nitroprusside (adults and peds): 0.25–10 µg/kg/m in IV
Ticlopidine: 250 m g PO b.i.d.
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Follow-Up Disposition Admission Criteria
Controversial, disposition decisions are best m ade in conjunction with neurology.
Work-up should include evaluation for a surgically reversible cause and m edical treatm ent with anticoagulants.
Consider adm ission for TIAs when appropriate im aging studies are not available or in high-risk populations: o
Patients already taking aspirin, clopidogrel, aspirin-dipyridam ole, ticlopidine, or warfarin
o
Possible cardioem bolic stroke (e.g., atrial fibrillation),
o
“Crescendo― TIAs (m ore than three ischem ic events in a 72-hour period that increase in frequency, duration, or severity of sym ptom s)
o
Johnston's “high-risk― group (>60 years, diabetes, duration >10-m inutes, weakness with TIA, speech im pairm ent with TIA)
Discharge Criteria
Com pletely asym ptom atic patients with extensively investigated condition or patients presenting with TIAs greater than 1 week before ED visit m ay be discharged as long as appropriate follow-up is ensured.
Patients with contraindications to antiplatelet therapy or surgery m ay be discharged if stable.
Prognosis: o
5–20% of those who experience a TIA will have a
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stroke in 1 m onth and 50% within 1 year, o
High risk for recurrence: known high-grade lesion, cardioem bolic source, crescendo TIA (three TIAs in 72 hours), and TIAs despite antiplatelet therapy
o
30–325 m g of aspirin daily reduces risk of stroke by 20% after prior stroke or TIA.
Pediatric Considerations All children with TIA require adm ission for close m onitoring of blood pressure, fluid status, and neurologic status in pediatric intensive care.
References 1. Albers GW, et al. Supplem ent to the guidelines for the m anagem ent of transient ischem ic attacks: a statem ent from the Ad Hoc Com m ittee on Guidelines for the Managem ent of Transient Ischem ic Attacks, Stroke Council, Am erican Heart Association. Stroke . 1999;30:2502–2511. 2. Albers GW. A review of published TIA treatm ent recom m endations. Neurology. 2004;62:S26–S28. 3. Scott PA, Barsan WG. Stroke, transient ischem ic attack, and other central focal conditions. In: Tintinalli JE, et al., eds. Em ergency m edicine. 5th ed. New York, NY: McGraw-Hill; 2000: 1430–1439. 4. Shah KH, Edlow JA. Transient ischem ic attack: review for the em ergency physician. Ann Em erg Med. 2004;43:592–604.
Codes ICD9-CM 435.9
ICD10 G45.9
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Transplant Rejectio n
Transplant
Rejection Richard Wolfe Mark Langdorf
Basics Description
A transplant recipient's im m une response to a graft's genetically dissim ilar antigens resulting in rejection of the transplanted organ
The diagnostic challenge is differentiating rejection from infection, surgical com plications, and the side effects of m edication.
(HLA) incom patibility: o
MHC antigens are tissue cell surface antigens that m ost often lead to transplant rejection of solid organ transplants.
Antibodies blood group incom patibility: o
Of m uch less im portance than HLA com patibility in graft survival
o
May result in hyperacute rejection of prim arily vascularized grafts, such as kidney and heart
Three phases of rejection:
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o
Hyperacute:
Occurs in the im m ediate postoperative period
Antibody reaction to red cells or HLA antigens
Endothelial dam age occurs, probably as a result of enzym es released from polym orphonuclear leukocytes.
Platelets accum ulate, throm bi develop, and tissue necrosis occurs.
o
Rare with careful donor-recipient m atching
Acute:
Usually occurs within the first m onths after transplantation but m ay happen at any tim e if im m unosuppressants are stopped
T cell-dependent process whereby inflam m atory cells infiltrate the allograft releasing cellular and hum oral factors that destroy the graft
Presents with constitutional sym ptom s and signs of transplant organ insufficiency.
o
Chronic:
Occurs over years
Results in the gradual failure of the transplanted organ
Genetics
MHC antigens: o
Encoded by the HLA com plex
o
MHC class I genes:
Encoded by genes of the HLA-A, HLA-B, or HLA-C loci on chrom osom e 6
o
Present on all nucleated cells
MHC class II genes:
Encoded by genes of the HLA-D region
Expressed only on B lym phocytes, activated T
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lym phocytes, m onocytes, m acrophages, Langerhans cells, dendritic cells, endothelium , and epithelial cells o
MHC class III genes:
Located between the HLA-B and HLA-D loci
Determ ines the structure of three com ponents of the com plem ent system : C2, C4, and factor B
Etiology
Reduction or noncom pliance with m edication
Medication interactions with cyclosporine, tacrolim us or sirolim us m ay lead to rejection because of lower blood levels: o
Phenobarbital, phenytoin, carbam azepine, rifam pin, isoniazid
Kidney transplant rejection: o
Early rejection caused by T and B lym phocytes, which attack m icrovasculature and im pair graft perfusion
o
Chronic rejection from progressive nephrosclerosis of renal vessels
Cardiac transplant rejection: o
Acute rejection occurs in 75–85% of patients within the first 3 m onths.
o
Accelerated atherosclerosis is the hallm ark of chronic rejection and presents as congestive heart failure (CHF), ventricular dysrhythm ias, hypotension, syncope, or sudden death.
Lung transplant rejection: o
Rejection develops early
o
Only 25–40% develop chronic rejection.
Liver transplant rejection: o
Com m only follows reduction in im m unosuppression regim en
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Bone m arrow transplant rejection: o
Acute graft-versus-host disease (im m une attack of donor m arrow on lung tissue)
o
Chronic graft-versus-host disease (incidence, 25–50% of patients)
o
Marrow rejection:
Destruction of the graft by im m unologically active cells in the host
Most frequent in patients with aplastic anem ia who do not receive total body radiotherapy or in patients receiving m ism atched or unrelated transplants
Diagnosis Signs and Symptoms
Renal transplant rejection: o
Progressive system ic hypertension
o
Fever
o
Swelling
o
Tenderness over the allograft
o
Decreased urine output
Heart transplant rejection: o
Fever: tem perature >38°C
o
Shortness of breath
o
Rales
o
Nausea, vom iting
o
Chest pain:
Not related to ischem ia because the heart is denervated
o
Hypotension or poorly controlled hypertension
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o
New arrhythm ias
Lung transplant rejection: o
Cough
o
Dyspnea
o
Fever
o
Rales
o
Rhonchi
Liver transplant rejection: o
Fever
o
Right upper quadrant pain
o
Jaundice
Bone m arrow transplant rejection: o
Fever
o
Generalized wasting
o
Dyspnea
o
Cough
o
Hypoxia
o
Chest pain
o
Rash
o
Mucositis
o
Keratoconjunctivitis
o
Dysphagia
o
Abdom inal pain
o
Diarrhea
o
Jaundice
o
Encephalopathy
o
Seizures
Tests Lab
General: o
CBC
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o
Blood levels of im m unosuppressant m edications (see Medications):
Levels m ay not represent trough if patient took m edication prior to ED visit.
o
Blood cultures
Renal transplant rejection: o
Electrolytes, blood urea nitrogen, creatinine
o
Urinalysis:
Presence of leukocytes m ay be seen during rejection as well as with infection.
Fractional excretion of sodium to help differentiate rejection from iatrogenic causes
Heart transplant rejection: o
Lung transplant rejection: o
Cardiac troponin T
ABG
Liver transplant rejection: o
Liver function tests:
Late acute rejection presents with elevated bilirubin and transam inases.
Bone m arrow transplant rejection: o
Arterial blood gas
o
Liver function tests
P.1147
Imaging
General: o
Chest radiograph:
Diffuse infiltrates are seen in early acute lung rejection, but when rejection occurs >1 m onth after transplantation, radiographs m ay be
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norm al or unchanged.
Bone m arrow transplant rejection: interstitial infiltrates, pleural effusion, pulm onary edem a
Renal transplant rejection: o
Renal ultrasound
Dem onstration of hydronephrosis im plies obstructive uropathy and warrants urgent percutaneous nephrostom y.
Heart transplant rejection: o
ECG:
Com m only dem onstrates two P waves because the native sinus node is left in place
Decreased quasi-random signal voltage, new S3, or new CHF or atrial arrhythm ias suggest rejection.
o
Echocardiogram
Liver transplant rejection: o
Ultrasound
o
CT
Diagnostic Procedures/Surgery
Renal transplant rejection: o
Heart transplant rejection: o
Allograft biopsy
Endom yocardial biopsy
Lung transplant rejection: o
Pulm onary function tests
o
Bronchoscopy/Biopsy
Differential Diagnosis
Infections: o
Wide variety of bacterial, m ycobacterial, fungal, viral, and parasitic pathogens can cause opportunistic
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infections in transplant patients.
Im m unosuppressant toxicity
Drug interactions with im m unosuppressant m edication
Renal transplant rejection: o
Any disorder that can affect the native kidneys can also occur in the transplant recipient.
o
o
Iatrogenic nephrotoxicity:
Cyclospine, Tacrolim us
May be exacerbated by other m edication
Urinary tract infection/pyelonephritis:
Classic organism s as with native kidney infections
Tubulointerstitial nephritis caused by the BK-polyom a virus (incidence 3–5%)
o
Acute occlusion of the transplant renal artery or vein:
Acute occlusion usually occurs within the first posttransplant week (incidence 0.5–8%) and causes oligoanuria and acute renal failure.
o
Peritransplant hem atom a
o
Urinary leak
o
Lym phocele
o
Obstructive uropathy
o
Bleeding after renal graft biopsy
Lung transplant rejection: o
Cytom egalovirus pneum onia is the m ost com m on pathogen in transplanted lungs.
o
Aspergillus is the m ost com m on fungal infection.
o
Upper respiratory infection or bronchitis:
o
Mim ic chronic lung rejection
Medication-induced pneum onitis
Liver transplant rejection: o
Ascending cholangitis
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Occurs because the biliary stent is left in place for m onths after surgery and can be colonized
o
Cholestatic hepatitis from Azathioprine
o
Methotrexate-induced hepatotoxicity
Treatment Pre Hospital Avoid aggressive fluid resuscitation.
Initial Stabilization
ABCs
Shock state treated with IV fluids and pressor agents
Treat hypertensive crisis like other hypertensive em ergencies.
ED Treatment
For kidney, heart, lung and liver rejection, adm inister IV m ethylprednisolone: o
Stress-dose corticosteroid coverage is also indicated in any ill-appearing transplant patient.
Avoid blood transfusions because these need special screening to prevent transm ission of disease.
Heart transplant rejection: o
Pressors and inotropics work as usual in the transplanted heart.
o
Atropine will have no effect on bradycardia because there is no vagal innervation.
o
Use dopam ine, epinephrine drips, or external pacing to increase heart rate if bradycardia is sym ptom atic.
Com m on im m unosuppressive regim ens are cyclosporine, prednisone, and azathioprine or tacrolim us (form erly
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known as FK506), and prednisone.
Mycophenolate m ofetil: o
May reduce incidence of chronic allograft nephropathy, with less hypertension and hyperuricem ia than earlier regim ens
Medication (Drugs)
Cyclosporine: 5–6 m g/kg PO q12h; m aintenance dose determ ined by blood level: 250–400 ng/m L (initial) 125–200 ng/m L (long term )
Cyclosporine m icroem ulsion: 4–5 m g/kg PO q12h; m aintenance dose determ ined by blood level: 250–400 ng/m L (initial) 125–200 ng/m L (long term )
Tacrolim us: 0.1 m g/kg PO q12h; m aintenance dose determ ined by blood level 10–20 ng/m L (initial) 5–10 ng/m L (long term )
Azathioprine: 1.5–2.5 m g/kg PO per day (adjusted for blood counts); blood-level m onitoring not used in clinical practice
Mycophenolate m ofetil: 1.0–1.5 g PO q12h (adjusted according to gastrointestinal adverse effects and blood counts); blood-level m onitoring not used in clinical practice
Prednisone: 0.5 m g/kg/day (initial) 0.1 m g/kg/d (long term )
Sirolim us: 2–5 m g PO per day (adjusted according to level); blood level:10–20 ng/m L (initial) 5–15 ng/m L (long term )
Disposition Admission Criteria
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Adm it transplant recipients with fever, shortness of breath, signs or sym ptom s of rejection, abdom inal pain, or other signs of organ infection.
Adm it to the intensive care unit patients who are septic or have cardiopulm onary com prom ise.
Discharge Criteria Nontoxic patients in whom rejection or serious infection has been excluded m ay be discharged with close follow-up.
Issues for Referral Treatm ent decisions should be m ade in consultation with the patient's oncologist, transplant surgeon, or organ specialist.
References 1. Andrews PA. Renal transplantation. Br Med J. 2002;324:530–534. 2. Buckley RH. Transplantation im m unology: Organ and bone m arrow. Journal of Allergy and Clinical Im m unology. 2003;111(2): 3. Deng MC. Cardiac transplantation. Heart. 2002;87:177–184. 4. Jain A, Khanna A, Molm enti EP, et al. Im m unosuppressive therapy. Surg Clin North Am . 1999;79:59–76. 5. Yen KT. Pulm onary com plications in bone m arrow transplantation: a practical approach to diagnosis and treatm ent. Clin Chest Med. 2004;25(1):189–201. 6. Noble-Jam ieson G, Barnes N. Diagnosis and m anagem ent of late com plications after liver transplantation. Arch Dis Child. 1999;81:446–451. 7. Sternbach GL, et al. Em ergency departm ent presentation and care of heart and heart/lung transplant recipients. Ann Em erg Med. 1992;21:1140. 8. Suthanthiran M, Strom TB. Mechanism s and m anagem ent of acute renal allograft rejection. Surg Clin North Am . 1998;78:77–94. 9. Venkat KK, Venkat A. Care of the renal transplant recipient in the
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em ergency departm ent. Ann Em erg Med. 2004;44(4):330–341
Codes ICD9-CM 996.52
ICD10 T86.9
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Traum a, M ultiple
Trauma, Multiple
Daniel Davis
Basics Description
Standardized approach for rapid assessm ent of the traum a patient
Although presented as a sequential m ethod for gathering inform ation, m any of these steps can be perform ed sim ultaneously: o
Life-threatening injuries m ust be im m ediately addressed and treated before going on to the next level of care.
With any change in the patient's status, the prim ary survey should be repeated.
Etiology Variety of causes such as:
Motor vehicle/m otorcycle crashes
Falls from heights
Assault
Airplane crashes
Train derailm ents
Results of m ass-casualty weapons
Terrorism
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Diagnosis
Triage to a m ajor traum a center is determ ined by local protocols.
Injured patients with a need for surgical, neurosurgical, or orthopaedic intervention should be transported to a m ajor traum a center.
Prim ary survey should be perform ed at the scene and en route.
Signs and Symptoms
Prim ary survey (ABCDE): o
Airway, cervical spine:
Look, listen, and palpate from nose/m outh to trachea/bronchial tree.
Assess airway patency.
Evaluate gag reflex.
Cervical spine m ust be im m obilized.
Ability to speak or effective m ovem ent of air with respiration indicates patency.
Gurgling, stridor, wheezing, snoring, choking, or absence of air m ovem ent requires im m ediate intervention.
Manage airway com prom ise before next step in prim ary survey.
o
Breathing:
Awake, alert patient with norm al speech and good air m ovem ent suggests effective breathing.
Sym m etric chest wall rise/fall, equal breath sounds, norm al respiratory rate, and oxygen
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saturation at 95% or m ore suggest effective breathing.
Asym m etric chest m ovem ent, unequal breath sounds, abnorm al respiratory rate, decreased oxygen saturation, inadequate air m ovem ent, or an obtunded patient suggests ineffective breathing.
Decreased unilateral breath sounds, tracheal shift, hyperexpansion, hyperresonance to percussion, subcutaneous air, hypoxia, or hem odynam ic com prom ise raises concerns about tension pneum othorax.
Decreased breath sounds with dullness to percussion suggest hem othorax.
Manage patients im m ediately with needle thoracostom y followed by tube thoracostom y.
o
Circulation:
Adequate circulating blood volum e m ust be m aintained.
Prim ary assessm ent includes blood pressure, heart rate, pulse quality, and end organ function (e.g., m entation, urine output, capillary refill).
Tachycardia and oliguria indicate early shock; hypotension is a late finding.
o
Disability:
Assess level of consciousness, gross m otor function, and pupil size/reactivity.
Glasgow com a scale is m ost com m only used; score of 8 or lower indicates severe head injury/com a.
Spinal cord injuries are grossly assessed by
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observing m ovem ent of all extrem ities.
Pupil size and reactivity to light m easure brainstem function.
o
Exposure:
Patient should be undressed com pletely.
Secondary survey: o
After the prim ary survey has been com pleted
o
Patient stabilized at each level
o
Com plete physical exam from head to toe is perform ed.
o
“Tubes and fingers in every body cavity―
Physical Exam Initial stabilization should begin sim ultaneously with essential workup.
Essential Workup
Prim ary and secondary survey
Cervical spine and chest radiographs are m andatory for m ajor traum a patients.
Pelvic radiographs should be perform ed with clinical suspicion of pelvic traum a or with hem odynam ic instability.
Hem oglobin/Hem atocrit, arterial blood gas, blood type
Urine dip for blood
Urinalysis if dip positive result
Urine-based pregnancy test for any fem ale patient of child-bearing age
Tests Lab Baseline co-agulation and chem istry studies with m assive injury or hem orrhage
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Imaging
Loss of consciousness, posttraum atic am nesia (anterograde or retrograde), or persistent altered level of consciousness is indication for head CT.
Significant blunt and penetrating chest traum a requires objective evaluation of the heart and great vessels with echocardiography, CT scan, angiography, or direct visualization.
Blunt abdom inal traum a requires objective evaluation using ultrasound, abdom inal CT or diagnostic peritoneal lavage, depending on patient's condition: o
Hem odynam ically stable patients should have an abdom inal CT with IV contrast.
o
Unstable patients should have an abdom inal ultrasound (FASTexam ) or diagnostic peritoneal lavage.
Extrem ity injury: o
Radiographs
o
Suspected vascular dam age requires angiography or duplex ultrasound.
P.1149
Treatment Initial Stabilization
The initial treatm ent should parallel the prim ary survey with injuries treated before addressing the next assessm ent level.
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Airway with cervical spine control: o
Jaw thrust, suctioning, and oropharyngeal or nasopharyngeal airways provide initial airway support.
o
Rapid sequence intubation is the airway m anagem ent option of choice for m ultiple traum a patients:
Insertion of a Com bitube or laryngeal m ask airway (LMA) or cricothyroidotom y m ay be necessary.
Breathing: o
100% oxygen and respiratory m onitoring
o
Tension pneum othorax should be diagnosed clinically and decom pressed on an em ergency basis with a needle thoracostom y below the axilla or above the second rib in the m idclavicular line:
o
Tube thoracostom y should follow.
Open chest wounds should be covered with an adherent dressing and a tube thoracostom y perform ed.
o
Respiratory distress from flail segm ent or pulm onary contusion should prom pt early intubation with m echanical ventilation and positive end expiratory pressure.
o
Hyperventilation should be avoided except with im pending herniation or intracranial hypertension resistant to other therapies; end-tidal carbon dioxide m onitoring should be strongly considered, especially with m anual ventilation.
Circulation: o
Two large-bore IV lines with constant hem odynam ic and cardiac m onitoring should be placed:
Alternatives include central lines, venous
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cutdowns (e.g., saphenous or fem oral), or intraosseous lines. o
Aggressive fluid replacem ent with three parts fluid for every one part circulatory volum e loss rem ains the standard of care; adjust fluids based on ongoing assessm ent.
2 L initial bolus in adults, 20 m L/kg in children
Whole blood, or autotransfused blood, for hem orrhagic shock or uncontrolled bleeding
o
Pericardial tam ponade requires em ergent pericardiocentesis/pericardial window.
o
External bleeding should be m anaged with direct pressure.
Disability: o
Head injury with Glasgow com a scale of 8 or lower should initiate treatm ent for elevated intracranial pressure with m annitol or hypertonic saline, rapid-sequence intubation, oxygenation, and controlled ventilation to a Pco 2 of 35 m m Hg.
o
Elevate head 20–30°, m aintaining spine im m obilization.
ED Treatment
Definitive treatm ent is often surgical.
Prom pt stabilization, early recognition of the need for operative intervention, and appropriate traum a surgical consultation are param ount.
Medication (Drugs) Dictated by need for specific interventions
Pediatric Considerations
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Intraosseous lines are an alternative to IV lines for fluids and m edications.
Follow-Up Disposition Admission Criteria
Most m ajor traum a patients should be adm itted for observation, m onitoring, and further evaluation.
Patients with significant injuries or hem odynam ic instability should be adm itted to an intensive care unit.
Patients requiring frequent assessm ents should be adm itted to a m onitored setting.
Discharge Criteria Minor traum a patients with negative objective work-up/im aging m ay be observed in the ED for several hours and then discharged.
References 1. Com m ittee on Traum a, Am erican College of Surgeons. Advanced Traum a Life Support. St. Louis, MO: Mosby; 1997. 2. Gin Shaw SL, Jordan RC. Multiple traum as. In: Marx J, et al., eds. Rosen's Em ergency Medicine: Concepts and Clinical Practice. 5th ed. St. Louis, Mo: Mosby; 2002:242–255. 3. Krantz BE. Initial assessm ent. In: Feliciano DV, et al., eds. Traum a. Stam ford, CT: Appleton & Lange; 1996:123.
Codes ICD9-CM 959.80 Injury to other specified sites, including m ultiple
ICD10
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T07
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Tricho m o nas
Trichomonas
JiWon E. Lee
Basics Description
Sexually transm itted disease
Causes urogenital infections:
o
May cause prem ature rupture of m em brane or
o
preterm labor in pregnancy
Prevalence: o
Five m illion cases per year in United States
o
Fifteen percent of wom en seen in sexually transm itted disease (STD) clinics
May facilitate transm ission of HIV
Etiology Trichom onas vaginalis:
Flagellated protozoan: o
Com m only found in urethra, bladder, and Skene gland
Diagnosis
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Signs and Symptoms Female
Vaginitis: o
Often asym ptom atic (25%):
50% develop sym ptom s within 6 m onths.
o
Vaginal discharge (50–75%), pruritis (50%),
o
dysuria (25%), and dyspareunia:
Discharge yellow-green, to gray/white frothy
Inflam m ation of vaginal walls
If chronic, scant discharge and m ild pruritis
Cervix: o
Diffuse erythem a (10–33%)
o
Punctate hem orrhage known as colpitis m acularis or strawberry cervix (2%)
Abdom inal pain
Elevated vaginal pH (>5.5)
Male
Usually asym ptom atic (90%)
Urethritis: o
Twenty percent of nonspecific urethritis
o
Scant discharge
o
Dysuria
Prostatitis
Epididym itis
Reversible sterility
Essential Workup “Hanging-drop― slide test:
80–90% sensitive in sym ptom atic patients
Saline wet m ount on cervical sm ears (from vaginal vault) or spun urine:
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o
Many polym orphonuclear leukocytes (PMNs)
o
Motile, pear-shaped flagellated trichom onas (slightly larger than leukocytes, seen in 60%)
Tests Lab
Culture: o
95% percent sensitivity:
Prostate m assage before collection Increases sensitivity in m ales.
Im m unofluorescence and/or Im m unoassay: o
Available but expensive
Differential Diagnosis
Urinary tract infection (UTI)
Gonorrhea
Chlam ydia
Candidal vaginitis
Nonspecific vaginitis
P.1151
Treatment ED Treatment
Fem ale: o
Metronidazole 2 g PO once:
o
90–95% cure rate
Resistant infections:
Metronidazole 500 m g PO b.i.d. for 7 days or
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o
Metronidazole gel (less effective)
o
If refractory to m etronidazole:
o
Metronidazole 375 m g PO b.i.d. for 7 days
Treat sexual partner to prevent re-exposure.
If allergic, m ay have to desensitize to m etronidazole
Pregnant: o
First trim ester:
Clotrim azole 100 m g vaginal suppository for 7 days (70% effective)
o
After first trim ester:
Metronidazole as above
Males (urethritis): o
Metronidazole 2 g PO once
o
Tinidazole 2 g PO once
o
Metronidazole 500 m g PO b.i.d. for 7 days or
o
Metronidazole 375 m g PO b.i.d. for 7 days
Avoid concom itant alcohol use with m etronidazole: o
Precipitate Antabuse reaction
Test and treat sexual partners.
Test for concom itant sexually transm itted diseases, syphilis, and HIV.
Follow-Up Disposition Discharge Criteria All patients
References 1. Centers for Disease Control and Prevention. Sexually transm itted diseases treatm ent guidelines 2002. MMWR Recom m Rep.
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2002;51(RR-6):1–78. 2. Das S. Treatm ent failure of vaginal trichom oniasis in clinical practice. Int J STD AIDS. 2005;16(4):284–286. 3. Mam m en-Tobin A. Managem ent of m etronidazole-resistant Trichom onas vaginalis. Int J STD AIDS. 2005;16(7):488–490.
Miscellaneous SEE ALSO: Urethritis
Codes ICD9-CM 131.9
ICD10 A59.9
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Tricyclic Antidepressant, Po iso ning
Tricyclic
Antidepressant, Poisoning Steven Aks
Basics Description
Prim ary m echanism of tricyclic antidepressant (TCA) toxicity:
o
Sodium channel blocking effect (quinidinelike effect)
o
Inhibition of norepinephrine reuptake
o
Alpha blockade
o
Anticholinergic effect
Selective serotonin reuptake inhibitors (SSRIs): o
Wider m argin of safety than TCA
o
Less CNS/cardiovascular toxicity
Nonselective serotonin reuptake inhibitors: o
Serotonin and norepinephrine reuptake inhibitors (SNRIs)
o
Can cause cardiac dysrhythm ias or seizures
o
Venlafaxine (Effexor)
o
See Antidepressants, Poisoning
Etiology
Tricyclic antidepressants:
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o
Am itriptyline
o
Nortriptyline
o
Im ipram ine
o
Doxepin
Newer-generation antidepressants (nontricyclic): o
Have different toxic profile than TCAs
o
See Antidepressants, Poisoning
Diagnosis Signs and Symptoms
Rapid deterioration m ay occur.
Classic tricyclic antidepressant (TCA) com pounds (im ipram ine, am itriptyline, nortriptyline)—greatest cardiovascular toxicity
Newer agents (serotonergic agents)—less overall toxicity in overdose
Central Nervous System (CNS)
Stim ulation or depression
Stim ulation: o
Trem ulousness
o
Agitation
o
Fasciculation
o
Seizures (resulting acidem ia m ay lead to worsening cardiovascular toxicity)
Depression: o
Drowsiness
o
Lethargy
o
Com a
Cardiovascular System
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Hypotension
Tachycardia (early; owing to blockade of norepinephrine reuptake and anticholinergic effects)
Bradycardia (late; owing to catecholam ine depletion state)
ECG changes: o
QRS widening (>100–120 m illiseconds)
o
Rightward shift in term inal 40 m illiseconds in frontal plane axis (r wave >3 m m in aVR)
Dysrhythm ias: o
Supraventricular tachycardia (SVT)
o
Ventricular arrhythm ias
Anticholinergic Effects (Less Common)
Dilated pupils
Decreased bowel sounds
Urinary retention
Essential Workup
ECG: factors associated with TCA poisoning: o
Sinus tachycardia (alm ost always present at som e tim e after poisoning)
o
QRS widening:
Greater than 100 m illiseconds associated with seizure
Greater than 160 m illiseconds associated with ventricular dysrhythm ia
o
QT prolongation
o
PR prolongation
o
Rightward shifting of term inal 40 m illiseconds QRS axis
o
R-wave am plitude in aVR >3 m m
Continuous cardiac m onitor
Tests
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Lab
CBC
Electrolytes, BUN, creatinine, glucose
Arterial blood gas (ABG)
Urine toxicology screen: o
Rule out other toxins.
TCA levels: o
Not useful
o
Do not correlate well with degree of toxicity
o
Qualitative screen appropriate to confirm ingestion if necessary
Imaging Chest radiograph for aspiration pneum onia/pulm onary edem a
Differential Diagnosis Drugs That Cause Coma
Alcohols
Alcohol withdrawal
Anticholinergics
Lithium
Phencyclidine (PCP)
Opioids
Phenothiazines
Sedative hypnotics
Salicylates
Cardiotoxic Drugs
Antidysrhythm ics (category IA)
Digoxin toxicity
Sym pathom im etics
Anticholinergics
Drugs That Cause Seizures
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Alcohol withdrawal
Anticholinergics
Cam phor
Isoniazid
Lindane
Lithium
Phenothiazines
Sym pathom im etics
Toxic alcohols
Treatment Pre Hospital
Do not be lulled into false sense of security with well-appearing patient: o
Rapid onset of altered m ental status, seizures, and dysrhythm ias occur.
Perform endotracheal intubation if any evidence of com prom ise.
Secure IV access.
Adm inister sodium bicarbonate if any evidence of QRS widening (>100–120 m illiseconds):
o
One am pule in adults
o
1–2 m Eq/kg in children
Ipecac contraindicated (risk for aspiration with developm ent of depressed m ental status, or seizure)
P.1153
Initial Stabilization
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Airway, breathing, and circulation m anagem ent (ABCs): o
Low threshold to intubate patients with altered m ental status
IV 0.9% norm al saline (NS)
Oxygen
Cardiac m onitor: o
For wide com plex rhythm (QRS >100–120 m illiseconds) bolus sodium bicarbonate
Naloxone, thiam ine, glucose (Accu-Chek) for altered m ental status
Flum azenil contraindicated in com bined TCA/benzodiazepine overdose
ED Treatment Cardiac Toxicity
QRS widening (>100–120 m illiseconds): o
Bolus with one am p (peds: 1–2 m Eq/kg) of sodium bicarbonate; repeat if sudden increase in QRS width
o
Maintain arterial pH of 7.45–7.5 with hyperventilation.
o
Initiate sodium bicarbonate infusion if hyperventilation alone does not reach target pH.
Dysrhythm ia: o
Sinus tachycardia requires no treatm ent.
o
Bolus 1–2 am ps of sodium bicarbonate (1–2 m Eq/kg in children) for sudden change in rhythm
o
Follow advanced cardiac life support (ACLS) protocol with addition of sodium bicarbonate boluses:
Lidocaine is second-line agent after sodium bicarbonate.
o
Use of class IA (procainam ide) and IC agents and physostigm ine contraindicated
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Hypotension
0.9% NS fluid bolus
Norepinephrine: o
Preferred pressor (over dopam ine)
o
Counters alpha blockade better
o
Dopam ine requires higher doses.
Decontamination
Gastric lavage: o
For recent ingestion (1 year old: 1–1.5 g/kg as 35% solution to m ax. of 50 g) PO m ixed in activated charcoal slurry this is unnecessary
Follow-Up Disposition Admission Criteria
Sym ptom atic patients observed >6 hours
Altered m ental status
Dysrhythm ia or conduction delay
Seizure
Heart rate >100 beats/m in 6 hours after ingestion
Coingestion requiring prolonged observation
Discharge Criteria
Asym ptom atic after 6 hours observation
No alteration in m ental status
Norm al ECG with heart rate Table o f C o ntents > Tuberculo sis
Tuberculosis
Vittorio J. Raho
Basics Description Infection with Mycobacterium tuberculosis, an aerobic acid-fast bacillus, resulting in disease
Mechanism
Most com m on route of infection is by droplet nuclei inhaled through the respiratory tract.
Prim ary tuberculosis: o
Initial infection occurs when organism s enter the alveoli, becom e engulfed by m acrophages, and spread via regional lym ph nodes to the bloodstream .
o
Patients are usually asym ptom atic.
o
May be progressive/fatal in im m unocom prom ised hosts
o
Positive reaction to purified protein derivative (PPD) indicates past exposure or infection.
Reactivation tuberculosis: o
Latent infection becom es active tuberculosis.
o
System ic (15%) and pulm onary (85%) sym ptom s
o
Characterized by a chronic wasting disease
o
Tuberculosis affects about one third of the world's
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population (90 m illion new cases in past decade worldwide, with about 30 m illion deaths). o
Estim ated 10–15 m illion people infected in the United States alone
Etiology
Three tuberculosis epidem ics: o
Global resurgence
o
HIV-infected patients
o
Multidrug-resistant tuberculosis
Conditions that predispose the individual to developing tuberculosis include: o
HIV infection and other im m unocom prom ised states
o
Drug and alcohol abuse
o
Poverty
o
Hom elessness
o
Institutionalization
o
Im m igration from a high-prevalence area
Diagnosis Signs and Symptoms
Pulm onary tuberculosis: o
Fever
o
Malaise
o
Weight loss
o
Night sweats
o
Chronic cough
o
Hem optysis
o
Pleuritic chest pain
o
Shortness of breath
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Extrapulm onary tuberculosis: o
CNS infections:
Meningeal irritation and cranial nerve defects
Malaise
Interm ittent headache
Low-grade fever
Confusion
Meningism us
Diplopia
Hyponatrem ia (due to syndrom e of inappropriate antidiuretic horm one)
o
Pericarditis:
o
o
o
o
Acute ischem ic stroke
Pleuritic chest pain increased with recum bency
Renal infection:
Fever
Flank pain
Sterile pyuria
Spinal tuberculosis (Pott disease):
Back pain/stiffness
Fever
Point tenderness
Decreased range of m otion
Cervical lym phadenitis:
Known as Scrofula
Draining sinus tracts m ay form .
Miliary tuberculosis:
Multi-organ system involvem ent
Diffuse adenopathy
Hepatom egaly
Splenom egaly
Weight loss
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Fever
Essential Workup
Diagnosis difficult due to the variety of clinical presentations
Chest radiography: o
Most valuable test for diagnosing active pulm onary tuberculosis
Skin testing
Tests Lab
CBC
Electrolytes, blood urea nitrogen, creatinine, glucose
Arterial blood gas for oxygenation/ventilation assessm ent
Sputum staining for acid-fast bacilli (Ziehl-Neelsen stain):
o
Provides a quick presum ptive diagnosis
o
Not im m ediately available
Sputum , cerebrospinal fluid (CSF), blood, urine, or peritoneal fluid culture:
o
Gold standard for diagnosis of tuberculosis
o
Average tim e for positive culture is 3–6 weeks.
Lum bar puncture with CSF analysis: o
For suspected tuberculous m eningitis
o
WBC range 0–1,500/m m 3 with lym phocyte predom inance
o
Elevated protein
o
Low to norm al glucose
Imaging
Chest radiograph: o
In prim ary disease, parenchym al infiltrates with unilateral hilar adenopathy are the classic findings.
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o
Reactivation tuberculosis typically appears as cavitary lesions with or without calcification usually in upper lung segm ents.
o
Miliary tuberculosis shows bilateral nodules throughout lungs.
o
Chest radiograph m ay be nondefinitive in AIDS patients.
o
Unilateral pleural effusion in both prim ary and reactivation tuberculosis
o
Tracheal deviation with scarring or atelectasis
o
Ghon focus—calcified scar/healed prim ary focus of infection
o
Ghon com plex—prim ary infiltrate with associated unilateral hilar adenopathy
Spine radiographs for Pott disease: o
May be norm al
o
Anterior wedging of two involved vertebral bodies and destruction of disk
CT chest: o
Better define extent of disease
Diagnostic Procedures/Surgery
Skin testing: o
Inject 0.1 m L of PPD subcutaneous in the forearm .
o
Positive test indicates prior or current infection with m ycobacterium .
o
Test results read between 48 and 72 hours after adm inistration.
o
Interpretation of positive:
>5 m m induration
Close contacts with tuberculosis
Positive chest radiographs
HIV
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Organ transplant or other im m unosuppression
>10 m m induration
IV drug users
Im m igrants from high-prevalence countries
Underlying disease (diabetes, renal failure, m alignancies)
Health care workers
Prison inm ates
Institutionalized (nursing hom e, hom eless shelters)
>15 m m induration
Low-risk individuals
P.1157
Differential Diagnosis
Bacterial pneum onia
Pneum ocystis Carinii pneum onia
Lung carcinom a
Bronchiectasis
Lung abscess
Lym phom a
Sarcoidosis
Coccidiom ycosis
Histoplasm osis
Treatment Pre Hospital Cautions:
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Place patient in respiratory isolation (negative flow).
Place a m ask on the patient to prevent respiratory spread of the disease.
Initiate treatm ent with an IV, oxygen, and pulse oxim etry.
Endotracheal intubation m ay be required in patients with severe hem optysis or respiratory com prom ise.
Providers should wear subm icron-particulate filter m asks (N-95 designation).
Inform close contacts.
Initial Stabilization
ABCs: o
Control airway as needed.
o
Adm inister oxygen as needed.
o
Place on cardiac m onitor and m easure pulse oxim etry.
o
Establish IV access with 0.9% norm al saline.
Isolate patients in negative pressure room s with at least six air exchanges per hour.
Protection for health care workers (N-95 m asks)
ED Treatment
Isolation and strict respiratory precautions
Treatm ent is augm ented due to increasing m ulti-drug resistance.
Any regim en m ust contain at least two drugs to which the tuberculous bacillus is susceptible.
CDC currently recom m ends initial therapy that includes four drugs.
Initial treatm ent is continued for 2 m onths and then tailored depending on culture susceptibilities.
Consult infectious disease specialists when treating HIV patients on antiretroviral therapies.
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Directly observed therapy m ay be necessary to ensure com pliance in certain populations.
Medication (Drugs)
Etham butol: 15–20 m g/kg, m ax. 1600 m g (peds: 15–20 m g/kg, m ax. 1 g) PO per day
Isoniazid: 5 m g/kg, m ax. 300 m g (peds: 10–15 m g/kg, m ax. 300 m g) PO per day
Pyrazinam ide: 15–30 m g/kg, m ax. 2 g (peds: 15–30 m g/kg, m ax. 2 g) PO per day
Rifam pin: 10 m g/kg, m ax. 600 m g (peds: 10–20 m g/kg, m ax. 600 m g) PO per day
Rifabutin: 5 m g/kg, m ax. 300 m g (peds: unknown) PO per day
Follow-Up Disposition Admission Criteria
Respiratory com prom ise as in other pulm onary infections
Suspicion of diagnosis
Inability to com ply with outpatient therapy
Unavailable outpatient resources (no prim ary care physician)
Involuntary adm ission for noncom pliant outpatients occurs o
Be aware of respective state laws concerning involuntary adm ission (consult infectious disease specialist).
Discharge Criteria
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Without respiratory com prom ise
Hom e isolation procedure com pliance
Ability and willingness to com ply with long-term therapy
Appropriate outpatient follow-up and treatm ent available
Notification of the public health authorities is m andatory
References 1. Am erican Thoracic Society. Diagnostic standards and classification of tuberculosis. Am Rev Respir Dis. 1990;142:725. 2. Am erican Thoracic Society. Treatm ent of tuberculosis and tuberculosis infection in adults and children. Am J Respir Crit Care Med. 1994;149:1359. 3. Centers for Disease Control and Prevention. Treatm ent of Tuberculosis, Am erican Thoracic Society, CDC, and Infectious Diseases Society of Am erica. MMWR 2003;52(RR11):1–77. 4. Isem an MD. Treatm ent of m ultidrug-resistant tuberculosis. N Engl J Med. 1993;329:784. 5. Isem an MD. Tuberculosis. In: Bennett JC, et al., eds. Cecil's textbook of m edicine, 20th ed. Philadelphia, PA: WB Saunders, 1996: 1683–1689. 6. Moran GJ, Talan DA. Tuberculosis. In Wolfson AB, et al., eds. Harwood Nuss’: Clinical Practice of Em ergency Medicine. 4th ed. Philadelphia, PA. Lippincott William s and Wilkins, 2005:751–756. 7. Neville K, Brom berg A, Brom berg R, et al. Escalating threat from tuberculosis: the third epidem ic. Thorax. 1995;50(Suppl 1):537–542.
Codes ICD9-CM 011.9
ICD10 A16.9
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Acknowledgement Thanks to the previous edition chapter author, Kathleen A. Raftery.
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Tularem ia
Tularemia
Ian Greenwald
Basics Description
Tularem ia is an acute febrile illness caused by the sm all aerobic gram negative coccobacillus Francisella tularensis: o
Organism is highly infectious.
o
Person-to-person transm ission has not been reported.
Hum ans becom e infected through different environm ental exposures: o
Wounds inflicted by infected arthropods
o
Direct contact with infectious anim al tissue or fluid
o
Contact or ingestion of contam inated food, water or soil
o
Inhalation of infected aerosols (e.g., cutting grass with power m owers, which m ay aerolize the organism ).
The four m ajor strains of the bacteria have different virulence and geographic location: o
North Am erican strain is the m ost virulent.
Natural hosts: o
Lagom orphs and other rodents
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Natural vectors: o
Ticks
o
Biting flies
o
Mosquitoes
o
Wild rabbits.
Weaponization of tularem ia accom plished during the cold war: o
Because of its infectivity and ability to be aerosolized, it rem ains a potential biological agent for m ass destruction.
Laboratory technicians handling culture specim ens are at high risk: o
F. tularensis cultures should only be m anipulated in a Biosafety Level 3 facility.
Etiology
Individuals that spend tim e outdoors in endem ic areas at highest risk: o
Farm ers
o
Hunters
o
Forest workers
o
Those that handle anim al carcasses are at highest risk (taxiderm ist and butchers).
Although tularem ia can occur worldwide, it is endem ic in the northern hem isphere: o
Reported nationwide except Hawaii
o
States with the highest incidence include Missouri, Arkansas, South Dakota and Oklahom a.
Pediatric Considerations
Children in rural areas are at risk because tim e spent outdoors in endem ic areas.
Recent case report in the United States of a child who
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developed tularem ia from a com m ercially purchased pet ham ster after sustaining a superficial bite.
Diagnosis Signs and Symptoms
Tularem ia has different presentations based on route of entry: o
Prim ary route of entry is through skin and m ost often a cutaneous ulcer develops.
Six form s of illness: o
Ulceroglandular:
Most com m on presentation (70–80% of cases).
Inoculated cutaneously through as few as 50 organism s
Initially, a local cutaneous papule
Followed by tender regional adenopathy and constitutional sym ptom s to include fever, chills, m yalgias, and headaches
o
Glandular:
Rare form
Tender regional lym phadenopathy with no local lesions
o
Ocular:
Rare form
Organism enters through a splash of infected blood/fluid to the eye or is introduced by eye rubbing after handling infectious m aterials (e.g., rabbit carcass).
Edem a, conjunctivitis, injection, chem osis with
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periauricular, subm andibular or cervical lym phadenopathy o
Pharyngeal:
Rare form
From contam inated food or water.
Severe throat pain with exudative pharyngitis and regional lym phadenitis.
o
Typhoidal (aka septicem ic):
Unapparent point of entry.
Fever develops along with severe diarrhea, bowel necrosis and pneum onia.
Occurs in 10–15% of cases and is m ost lethal if not recognized early and treated with antibiotics
o
Pulm onic:
Secondary to inhalation
Seen in sheep shearers, farm ers, landscapers, and lab technicians
Fever, dry cough and pleuritic chest pain develop
Pneum onia can occur in 10–15% of patients with Ulceroglandular tularem ia and up to 50% of patients with Typhoidal tularem ia.
Physical Exam
Fever
Tender, well-dem arcated cutaneous ulcer
Tender regional lym phadenopathy; lym ph nodes can develop fluctuance and spontaneously drain.
Exudative pharyngitis (with pharyngeal tularem ia)
Ulcerations of the conjunctiva with pronounced chem osis (with oculoglandular tularem ia)
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Tests Lab
No rapid diagnostic test available
Routine lab studies nonspecific:
o
CBC can be norm al.
o
ESR m ight be slightly elevated.
Gram stains, cultures and tissue biopsies: o
Often negative
Blood cultures
Enzym e-linked im m unosorbent assay and polym erase chain reaction are available through reference laboratories.
Serum antibody titers: o
Typically do not obtain diagnostic levels until 10 or m ore days after the onset of the illness
o
A single titer of at least 1:160 for tube agglutination is diagnostic for tularensis infection.
Imaging
Chest radiograph for: o
Consolidative process, pleural effusions and hilar adenopathy
CT scan of chest for: o
Severe pulm onary sym ptom s
o
Other possible etiologies of atypical pneum onia
Differential Diagnosis
Ulceroglandular tularem ia m im ics include: o
Tuberculosis
o
Cat-scratch disease
o
Syphilis
o
Chancroid
Pa ge 4 9 2
o
Lym phogranulom a venereum
o
Toxoplasm osis
o
Sporotrichosis
o
Rat-bite fever
o
Anthrax
Ocular glandular tularem ia m im ics include: o
Adenoviral infection
Pharyngeal tularem ia m im ics include: o
Diphtheria
o
Bacterial pharyngitis
o
Infectious m ononucleosis
o
Adenoviral infection.
Typhoidal tularem ia m im ics include: o
Salm onella
o
Brucellosis
o
Legionella
o
Q fever
o
Malaria
o
Dissem inated fungal or m ycobacterial infections.
Pulm onary tularem ia m im ics include: o
Mycoplasm a
o
Legionella
o
Chlam ydia
o
Tuberculosis.
P.1159
Treatment Pre Hospital
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Universal precautions
Airway, breathing, and circulation m anagem ent.
Treat dehydration/hypotension with NS fluid boluses.
Initial Stabilization
ABCs
Supplem ental oxygen for hypoxia
Fluid resuscitation with norm al saline for intravascular volum e depletion or septic shock
Central line access for unstable patients
Vasopressors for persistent hypotension
ED Treatment
Fever control with acetam inophen
Early adm inistration of antibiotic therapy after obtaining cultures.
Antibiotic options: o
First-line agents:streptom ycin or gentam icin continued for 10 days.
o
Ciprofloxacin if diagnosis of com m unity-acquired pneum onia in differential diagnosis
o
Tetracyclines or chloram phenicol:
Continue for 14 days since only bacteriostatic.
Associated with a higher rate of treatm ent failures than the previously m entioned antibiotics.
Pediatric Considerations Streptom ycin or gentam icin are recom m ended as the first-line agents.
Medication (Drugs)
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Chloram phenicol: 15 m g/kg IV q6h (adult and peds)
Ciprofloxacin: 400 m g (peds: 15 m g/kg) IV q12h
Doxycycline: 100 m g (peds: if weight ≥45 kg, 100 m g; if weight ≤45 kg, 2.2 m g/kg) IV q12h
Gentam icin: 5 m g/kg IV or IM q24h (peds: 2.5 m g/kg IV or IM q8h)
Streptom ycin: 1 g IM (peds: 15 m g/kg, not to exceed 2 g/d) q12h
Follow-Up Disposition Admission Criteria
Intensive care unit adm ission for advanced age, neutropenia, severe hypoxem ia, hem odynam ic instability or patients presenting with Typhoidal tularem ia
In-patient floor bed adm ission for m ild to m oderate illness: o
Isolation bed required only for the purpose of ruling out other etiology (e.g., tuberculosis)
Discharge Criteria Outpatient therapy oral or IM therapy for m ild illness with close follow-up
References 1. Brief report: Tularem ia Associated with a Ham ster Bite—Colorado, 2004. MMWR. 2005;53:1202–1203. 2. Centers for Disease Control; Sum m ary of notifiable diseases, United States, 1998. MMWR. 1998;46:ii–vii, 3–87. 3. Centers for Disease Control; Tularem ia — United States,
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1990–2000. MMWR. 2002;51:181–184. 4. Dennis DT, Inglesby TV, et al. Tularem ia as a Biological Weapon. JAMA. 2001;285:2763–2773. 5. Hopla CE: The ecology of tularem ia, Adv Vet Sci Com p Med 1974;18:25. 6. Spach DH, et al. Tick-borne diseases in the United States. N Engl J Med. 1993;329:936–947.
Codes ICD9-CM 21.0
ICD10 A21.9
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Tum o r C o m pressio n Syndro m es
Tumor
Compression Syndromes Richard Wolfe Martin J. Carey
Basics Description
Com plications arising from the com pression or direct infiltration of solid tum ors on neural and vascular structures
Spinal cord com pression: o
Affects over 20,000 patients each year
o
Occurs in 5–14% of cancer patients
o
More than 50% of cases are m etastases from lung, breast, or prostate cancer.
Other neurologic tum or com pression: o
Brachial plexus
o
Recurrent laryngeal nerve com pression by m ediastinal lym ph nodes
Superior vena cava syndrom e (SVC): o
Obstruction of returning blood flow in the superior vena cave by com pression, infiltration, or throm bosis
o
Venous hypertension within the area ordinarily
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drained by the SVC o
In severe cases, gradual elevation of the intracranial pressure (ICP) with altered m ental status and com a
o
85% caused by m alignancy
Etiology
Spinal cord com pression: o
Prostate cancer
o
Breast cancer
o
Lung cancer
o
Renal cancer
o
Multiple m yelom a
o
Melanom a
o
Thyroid cancer
o
Lym phom a
o
Sarcom a
Brachial plexus com pression: o
Lung cancer
o
Breast cancer
SVC syndrom e from tum or com pression: o
Lung cancer (m ost com m on):
Sm all cell lung cancer prim arily
o
Postirradiation fibrosis
o
Lym phom a
o
Breast cancer
o
Testicular cancer
o
See differential diagnosis for nontum oral causes of the SVC syndrom e
Pediatric Considerations In children with spinal cord com pression, com m on causes are sarcom a, neuroblastom a, germ cell tum ors, and lym phom a.
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Diagnosis Signs and Symptoms History
Spinal cord com pression: o
History of m alignancy
o
Back or neck pain:
Prolonged
Worse with rest
o
Paresthesias
o
Difficulty am bulating
o
Constipation
o
Urinary retention
o
Urinary or fecal incontinence
o
Weight loss
Brachial Plexus com pression: o
Neuropathic pain involving the m edial aspect of the upper extrem ity
Intrathoracic vagal nerve com pression: o
Ipsilateral aching facial pain around the ear
SVC syndrom e: o
Orthopnea
o
Dyspnea
o
Tightness of the shirt collar
o
Cough
o
Chest pain
o
Headache
o
Blurred vision
o
Dizziness
o
Syncope
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Physical Exam
Spinal cord com pression: o
Loss of rectal tone
o
Loss of anal wink
Laryngeal nerve com pression: o
Hoarseness
o
Vocal cord paralysis
Brachial plexus: o
Ulnar paresthesias
o
Weakness and wasting of intrinsic hand m uscles
o
Pan-plexopathy
o
Horner syndrom e
SVC syndrom e: o
Periorbital edem a
o
Conjunctival suffusion
o
Facial swelling
o
Facial plethora
o
Upper extrem ity edem a
o
Findings exacerbated by recum bent or stooped-over position
o
Usually worse in the early m orning hours
o
ICP m ay be elevated in severe cases:
Altered m ental status
Com a
Papilledem a
Tests Imaging
Chest radiograph: o
Spinal cord com pression:
May identify a prim ary lung tum or
Helpful in excluding Tuberculous spondylitis
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o
SVC com pression:
Mass present in 10%
Pleural effusion in 25%
Plain spinal radiography: o
Will show 85% of m etastases causing com pression
o
A norm al spine (or one showing just degenerative changes) on plain radiology does not exclude the diagnosis of possible cord com pression.
CT: o
More sensitive and specific than plain radiography and radionucleotide im aging in distinguishing benign from m alignant disease in spinal com pression syndrom e
o
To identify m ass and im pingem ent in vena cava obstruction
MRI: o
Study of choice for spinal cord com pression
o
Indicated in patients with back or neck pain and:
History of cancer
Bowel or bladder dysfunction
Lower extrem ity weakness
Sensory loss
P.1161
Venography: o
Relative contraindication in SVC syndrom e because of possible bleeding
Diagnostic Procedures/Surgery
CT m yelography: o
Indicated for spinal cord com pression when MRI is unavailable or contraindicated (pacem aker, severe
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claustrophobia).
An invasive procedure is required to obtain a tum or biopsy in patients with SVC syndrom e: o
Bronchoscopy
o
Mediastinoscopy
o
Scalene node biopsy
o
Lim ited thoracotom y
Differential Diagnosis Spinal Cord Compression
Intervertebral disk disease
Osteoporotic vertebral fractures
Spondylosis
Spondylitis
Epidural abscess
Prim ary bone tum ors
Arteriovenous m alform ations
Neurologic diseases
Multiple sclerosis
Am yotrophic lateral sclerosis
Transverse m yelitis
Spinal infarction
Superior Vena Cava Syndrome
Pericardial tam ponade
Nephrotic syndrom e
Cor pulm onale
Cirrhosis: o
Nonm alignant etiologies of SVC syndrom e:
Goiter
Pericardial constriction
Prim ary throm bosis
Idiopathic sclerosing aortitis
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Tuberculous m ediastinitis
Fibrosing m ediastinitis
Histoplasm osis
Indwelling central venous catheters
Treatment Initial Stabilization
Early diagnosis and treatm ent are the keys to an im proved outcom e.
Level of neurologic dysfunction on presentation is a key factor in the prognosis for spinal cord com pression.
Avoid IV line placem ent in upper extrem ities if severe SVC com pression present.
ED Treatment Spinal Cord Compression
Corticosteroids (dexam ethasone): o
Adm inister in ED.
o
Higher doses alleviate the pain m ore rapidly, but studies indicate no significant difference in outcom e with regard to sphincter function or am bulation between the dose schedules.
Radiotherapy: o
Definitive treatm ent m odality
Pain m edication with narcotics
Oncology, radiotherapy, and neurosurgical consultation for further m anagem ent of tum or/m alignancy
Consider em piric broad spectrum antibiotics prior to the MRI if an epidural abscess is being considered.
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SVC Compression
Manage the underlying m alignancy with either radiotherapy or chem otherapy.
Elevation of the head of the bed
Judicious use of diuretics will transiently im prove sym ptom s.
Adm inister steroids if respiratory com prom ise.
Urgent oncology referral
Intravascular stents m ay relieve the obstruction m ore rapidly.
Medication (Drugs)
Dexam ethasone: 1 m g/kg loading dose, followed by 4–24 m g q6h
Furosem ide (Lasix): no prior use—40 m g IVP; prior use—double 24h dose (80–180 m g IV)
Hydrocodone/Acetam inophen: 5/500 m g PO q4h–q6h
Oxycodone/Acetam inophen: 5/500 m g PO q4h–q6h
Follow-Up Disposition Admission Criteria Adm ission is advisable for all patients presenting with a tum or-com pression syndrom e.
Discharge Criteria None
Issues for Referral
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Radiation oncology should be consulted in patients presenting with tum or com pression.
Early neurosurgical consultation for patients with spinal cord com pression
References 1. Boogerd W, van der Sande JJ. Diagnosis and treatm ent of spinal cord com pression in m alignant disease. Cancer Treat Rev. 1993;19:129–150. 2. Byrne TN. Spinal cord com pression from epidural m etastases. N Engl J Med. 1992;327:614–619. 3. Johnston RA. The m anagem ent of acute spinal cord com pression. J Neurol Neurosurg Psychiatry. 1993;56:1046–1054. 4. Jordan JE, Donaldson SS, Enzm ann DR. Cost effectiveness and outcom e assessm ent of m agnetic resonance im aging in diagnosing cord com pression. Cancer. 1995;75:2579–2586. 5. Stock KW, Jacob AL, Proske M, et al. Treatm ent of m alignant obstruction of the superior vena cava with the self-expanding Wallstent. Thorax. 1995;50:1151–1156. 6. Wen PY, Schiff D. Neurologic com plications of solid tum ors. Neurologic Clinics. 2003;21(1).
Codes ICD9-CM 336.9
ICD10 T79.5
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Tym panic M em brane Perfo ratio n
Tympanic
Membrane Perforation Andrew Chang
Basics Description
Perforations can be classified in several ways: o
o
o
Duration:
Acute (3 m onths)
Site:
Pars tensa
Pars flaccida
Extent:
Lim ited to one quadrant ( Table o f C o ntents > Urinary Retentio n
Urinary Retention
Anthony Huynh
Basics Description
Norm al m icturition sequence: o
As the bladder fills, sensory stretch signals conducted to sacral cord through pelvic nerves and then back through parasym pathetics, supplying the body and neck of the bladder
o
Once m icturition reflex becom es powerful enough, an inhibitory reflex through som atic pudendal nerves from S-2–S-3 causes relaxation of external urethral sphincter.
o
Urination occurs if inhibition is m ore powerful than voluntary constriction signals.
Acute urinary retention (AUR): o
Sudden inability to void urine, resulting in bladder distention
More com m on in m en with advancing age than wom en, less com m on in children
Atonic bladder: o
More com m on in wom en
o
Decom pensated bladder that has resulted from years
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of infrequent voiding o
Destruction of sensory nerve fibers from the bladder to spinal cord that prevents transm ission of stretch signals and prevents m icturition reflex contractions
o
Loss of bladder control occurs despite intact neurogenic connections to the brain.
o
Bladder fills to capacity and overflows a few drops at a tim e (overflow incontinence).
Autom atic bladder: o
From dam age of the spinal cord above the level of S-2–S-3
o
Micturition inhibited due to “spinal shock― from the sudden loss of facillatory im pulse from the brainstem and cerebrum
o
Interm ittent straight catheterization facilitates the return of the excitability of m icturition reflex by preventing physical bladder injury.
Neurogenic bladder: o
From partial dam age in spinal cord or brainstem that interrupts inhibition
o
Sacral centers are in a constant state of excitation that even a sm all quantity of urine results in frequent and relatively uncontrollable m icturition.
Etiology
Benign prostatic hypertrophy: m ost com m on in m en
Multiple sclerosis and diabetes: Most com m on in wom en and m ay be an early m anifestation of neurologic disease in children.
Bladder outlet obstruction: o
Benign prostatic hypertrophy
o
Prostate
o
Cancer
Pa ge 4 9 6
o
Acute prostatitis
o
Stones
o
Blood clots
o
Prostatic congestion
Detrusor m uscle failure: o
Acute spinal cord injury
o
Elderly patients
o
Sym pathom im etics
Neurologic causes: o
Detrusor hyperactivity with im paired contractility
o
Multiple sclerosis
o
Parkinson disease
o
Stroke
o
Herniated disk
o
Diabetes m elitis
o
Dem entia
o
Myasthenia gravis
o
Brain tum or
o
Landry-Guillain-Barré syndrom e
o
Bladder neck dysfunction
Urethral stricture: o
Meatal stenosis
o
Phim osis
o
Paraphim osis
o
Foreign body constriction
Gynecologic: o
Posturethropexy
o
Postvaginal delivery
o
Infectious
o
Periurethral abscess
o
Urinary tract infection
o
Constipation
Pa ge 4 9 6
Medications that cause AUR: o
β-Agonists
o
α-Adrenergic stim ulator
o
Narcotics
o
Anticholinergics
o
Musculotropic relaxants
Diagnosis Signs and Symptoms
History of chronic voiding hesitancy: o
Decreased size and force of urine stream
o
Difficulty holding or initiating urinary stream
o
Feeling of incom plete bladder em ptying or postvoid residual
o
Interruption of urinary stream
Lower abdom inal pain
Distended and tender bladder
History Obtain a thorough history focusing on the size and force of urine stream , feeling of incom plete bladder em ptying, dribbling, and interruption of urinary stream .
Physical Exam Perform a through physical exam focusing on the neurological exam , abdom inal exam checking the bladder size, and prostate exam in m en.
Essential Workup
Thorough history and physical exam ination
Urinalysis
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Tests Lab
Electrolytes, blood urea nitrogen, creatinine, and glucose
Urinalysis
For renal failure: o
Prostate-specific antigen
o
Urine culture
Imaging
Ultrasound
CT scan
IV pyelography
P.1171
Treatment Initial Stabilization
Urinary drainage by catheterization
Caution with history of urethral stricture or traum atic catheter insertion
Defer catheterization in patient with pelvic fracture, prostate displacem ent on rectal exam ination, or blood at the urethral m eatus until retrograde urethrogram .
Suprapubic catheter if urethral catheterization contraindicated or im possible
Palpable bladder essential
ED Treatment
Drain bladder and m onitor urine output.
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Place leg Foley bag before discharge if Foley is to rem ain indwelling.
Initiate therapy for underlying cause of AUR: o
Rapid decom pression following catheter placem ent m ay result in transient gross hem aturia in the chronically distended edem atous bladder.
Postobstructive diuresis: o
Com plication of AUR in the catheterized patient
o
Occurs from a com bination of factors, including osm otic diuresis, involvem ent of natriuretic and diuretic factors, disorder nephron function, altered tubular perm eability, and disturbance of sodium -regulating horm ones
o
Hypovolem ic or hypotensive m ay result in severe cases.
Observe for 4–6 hours all patients with chronic or insidious obstructive voiding sym ptom s and urinary retention with particular attention to hourly intake, urinary output, and vital signs.
Medication (Drugs)
Baclofen (Lioresal) for external sphincter em ptying: 5 m g PO t.i.d., m ax. 80 m g/d (peds: 2–7 years old: 10–15 m g/24h div. q8h; titrate to m ax dose 40 m g/24h; >8 years old: m ax. dose 60 m g/d div. q8h)
Belladonna and opium (B and O) suppositories to alleviate the constant urge to urinate secondary to bladder spasm , frequently accom panying an indwelling catheter: 1 PO q4h–q6h
Bethanechol (Urecholine) acts on the detrusor to em pty the bladder: 10–50 m g PO b.i.d./q.i.d.; SC: 5 m g (peds:
Pa ge 4 9 7
PO 0.6 m g/kg/24h div. q6h–q8h; SC: 0.15–0.2 m g/kg/24h div. q6h–q8h)
Dantrolene (Dantrium ) for external sphincter em ptying: initial 25 m g PO per day, increase frequency to t.i.d.–q.i.d., then increase dose by 25 m g/dose at 4- to 7-day intervals (peds [not indicated 5 years old: initial 0.5 m g/kg/dose PO b.i.d.; increm ent—increase frequency to t.i.d.–q.i.d. at 4- to 7-day intervals, then increase doses by 0.5 m g/kg)
Diazepam (Valium ) for external sphincter em ptying: IM or IV to 10 m g/dose q3h–q4h PRN, PO: 2–10 m g/dose q6h–q8h PRN (peds: IM OR IV 0.04–0.2 m g/kg/dose q2–4h (m ax. 0.6 m g/kg within an 8-hour period; PO: 0.12–0.8 m g/kg/24h div. q6–8h)
Doxazosin m esylate (Cardura) for vesical outlet em ptying: initial 1 m g PO per day, after 24 hours, increase to 2 m g PO per day then to 4, 8, 16 m g per day
Meperidine HCl (Dem erol) for external sphincter relaxation: PO, IM, IV: 50–150 m g/dose q3–4h PRN (peds: PO, IM, IV: 1.0–1.5 m g/kg/dose q3h–q4h PRN, m ax. 100 m g)
Oxybutynin (Ditropan) for storage: 5 m g PO b.i.d.–t.i.d.
Phenoxybenzam ine HCl (Dibenzyline) for vesical outlet em ptying: 10 m g PO, increase dosage every other day, usually to 20–40 m g, b.i.d.–t.i.d.
Prazosin HCl (Minipress) for vesical outlet em ptying: initially 1 m g PO b.i.d. to t.i.d., slowly increase to 20 m g/d in divided doses
Tam sulosin (Flom ax) im press irritative and obstructive voiding sym ptom s: 0.4 m g PO every day initially; m ay increase to 0.8 m g PO every day
Alfuzosin (Uroxatral) for vesical outlet em ptying: 2.5 m g
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PO t.i.d.
Pseudoephedrine (Sudafed) for vesical outlet storage: 30–60 m g/dose PO q6h–q8h, m ax. 240 m g/24h (peds: Table o f C o ntents > Urinary Tract F istula
Urinary Tract
Fistula Anthony Huynh
Basics Description
Fistulae can form between any part of the urinary tract and contiguous structures.
Com m unications between the urinary and gastrointestinal tracts, external perineum , and fem ale reproductive organs are m ost com m on.
Urinary fistulae: o
Typically not owing to prim ary urologic disease
o
Caused by a com plication of gynecologic surgery, childbirth, and gastrointestinal disorders
Etiology
Vesicointestinal fistulae: o
Com plication of prim ary gastrointestinal disease
o
Diverticulitis: 50–60% of cases
o
Colon cancer: 20–25% of cases
o
Crohn disease: 10% of cases
o
Radiation enteritis: 7% of cases
o
Pelvic traum a: 5% of cases
Pa ge 4 9 7
o
Bladder cancer: 4% of cases
o
Other causes:
Appendicitis
Gynecologic cancers
Tuberculosis
Vesicovaginal, urethrovaginal, and ureterovaginal fistulae: o
Gynecologic surgery: 80% of cases
o
Occurs 10–14 days after surgery
o
Obstetric com plication: 8–10% of cases
o
Pelvic irradiation: 6% of cases
o
Pelvic traum a: 4% of cases
Vesicocutaneous fistulae: o
Cervical or uterine cancer
o
Bladder cancer
o
Advanced prostatic cancer
Diagnosis Signs and Symptoms
Vesicointestinal fistulae: o
Chronic or recurrent urinary tract infections
o
Most infections are caused by Escherichia coli.
o
Mixed organism s account for one third of infections.
o
Pneum aturia: 60% occurrence rate
o
Fecaluria: 40% occurrence rate
o
Abdom inal pain
o
Change in bowel habits
Vesicovaginal, urethrovaginal, and ureterovaginal fistulae: o
Constant leakage of urine from the vagina; described as watery vaginal discharge
o
Malodorous urine
Pa ge 4 9 7
o
Perineal derm atitis and m aceration
o
Severe perineal pain if fistula is a com plication of radiation therapy
o
Ureterovaginal fistula:
Abdom inal pain
Flank tenderness
Fever
Drainage of urine through the operative site
Vesicocutaneous fistulae: o
Constant leakage of urine from bladder through fistula to skin
o
Usually located in perineal region:
Perineal derm atitis and m aceration at site of leakage
History Thorough history points to diagnosis for urinary tract fistulae.
Physical Exam
Vesicovaginal, urethrovaginal, and ureterovaginal fistulae: o
Clinical diagnosis is usually the key.
o
Speculum exam m ay reveal a sm all, reddened area of granulom atous tissue at site of fistula opening.
o
If uncertain whether vaginal discharge contains urine, give phenazopyridine (Pyridium ), 200 m g orally, and perform speculum exam 1 hour later.
o
Orange discoloration of discharge confirm s fistula.
Vesicocutaneous fistula: o
Clinical diagnosis with thorough physical exam ination
Tests Lab
Urinalysis:
Pa ge 4 9 7
o
Undigested food residue with vesicointestinal fistulae
o
Bacteria with vesicovaginal, urethrovaginal, and ureterovaginal fistulae
o
Bacteria and WBC with vesicocutaneous fistula
o
Detect charcoal in urine with the Bourne test after orally ingesting charcoal.
Urine culture: o
E. coli m ajor pathogen with vesicointestinal fistulae
o
One third infected with m ultiple organism s
o
Mixed organism s with vesicovaginal, urethrovaginal, and ureterovaginal fistulae
o
To exclude infection with vesicocutaneous fistula
Imaging
Cystoscopy with or without fistulography is a reliable m eans of diagnosis.
CT scan has sensitivity close to 100% in diagnosing vesicointestinal fistulae.
Multidetector row CT urography
P.1173
Differential Diagnosis
Vesicointestinal fistulae: o
Recurrent UTI
o
Other causes of pneum aturia
o
UTI with gas-form ing organism such as clostridia
o
Ferm entation of glucose in urine
o
Recent urinary tract instrum entation
Vesicovaginal, urethrovaginal, and ureterovaginal fistulae: o
Urinary incontinence
o
Copious vaginal discharge
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Vesicocutaneous fistula: o
Urinary incontinence
Treatment Initial Stabilization Treat urosepsis with IV fluid bolus and IV antibiotics.
ED Treatment
Vesicointestinal fistulae: o
Rule out com plications from patient's prim ary disease.
o
Obtain cultures if signs of UTI.
o
Initiate broad-spectrum antibiotic if infection found.
o
Antibiotic resistance is com m on.
o
Most patients have received m ultiple antibiotics for recurrent or chronic UTI.
o
Urologic referral for definitive surgical therapy
Vesicovaginal, urethrovaginal, and ureterovaginal fistulae: o
Place Foley catheter for any patient suspected of having a genitourinary fistula.
o
Initiate broad-spectrum antibiotics if a UTI is present
o
Third-generation cephalosporin, fluoroquinolone, or am oxicillin/clavulanate
o
Prom pt referrals to urologist and gynecologist
Vesicocutaneous fistula: o
Place Foley catheter.
o
Initiate broad-spectrum antibiotics if a UTI is present
o
Treat derm atitis and skin m aceration with:
Antifungal cream s such as nystatin, clotrim azole, or m iconazole
Pa ge 4 9 7
Protective ointm ent applied to protect skin from m oisture
o
Third-generation cephalosporin, fluoroquinolone, or am oxicillin/clavulanate acid
o
Prom pt urology referral
Medication (Drugs)
Am oxicillin/clavulanate: 875 m g PO b.i.d. or 500 m g PO t.i.d.
Am picillin/sulbactam : 3 g IV q6h
Cefaclor: 500 m g PO t.i.d.
Cefixim e: 400 m g PO per day
Ceftriaxone: 2 g IV per day
Ciprofloxacin: 400 m g IV or 500 m g PO b.i.d.
Levofloxacin (Levaquin): 500 m g PO per day
Follow-Up Disposition Admission Criteria
Presence of urosepsis or septic shock
Unable to take oral antibiotics
Dehydration
Com plications from prim ary gastrointestinal disease or pelvic m alignancies
Bowel obstruction
Malnutrition
Discharge Criteria
No evidence of urosepsis or shock
Pa ge 4 9 7
Able to adm inister oral antibiotics if urinary tract infections present
Able to care for Foley catheter
References 1. Caoili EM, Cohan RH, Korobkin M: Urinary tract abnorm alities: initial experience with m ulti-detector row CT urography. Radiology. February 2002;222(2):353–360. 2. Davits RJ, Miranda SI: Conservative treatm ent of vesicovaginal fistulas by bladder drainage alone. Br J Urol. August 1991;68(2):155–156. 3. Driver CP, Anderson DN, Findlay K, et al. Vesico-colic fistulae in Gram pian region: presentation, assessm ent, m anagem ent, and outcom e. J R Coll Surg Edinb. 1997;42:182–185. 4. Lee RA, Sym m onds RE, William s TJ. Current status of genitourinary fistula. Obstet Gynecol. 1988;72:313–319. 5. McVay KT, Marshall FF. Urinary fistulas. In: Gillenwater J, et al., eds. Adult and Pediatric Urology. 3rd ed. St. Louis, MO: Mosby; 1996. 6. Moos RL, Ryan JA. Managem ent of enterovesical fistulas. Am J Surg. 1990;159:514–517. 7. Shobeiri SA, Chesson RR, Echols KT. Cystoscopic fistulography: a new technique for the diagnosis of vesicocervical fistula. Obstet Gynecol. 2001;98:1124–1126.
Codes ICD9-CM 599.1 Urethral fistula
ICD10 N36.0
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Urinary Tract Infectio ns, Adult
Urinary Tract
Infections, Adult Paul A. Szucs Barnet Eskin
Basics Description
Colonization of urine with uropathogens and invasion of genitourinary tract (GU)
Defined as urinary sym ptom s with ≥102–105 × 10 5 CFU/m l of uropathogen and ≥10 WBC/m m 3
Uncomplicated Cystitis
Fem ales aged 13–50
Sym ptom s than 5 days or hom eless are risk factors for upper tract infection
Elderly: o
Altered m ental status
o
Anorexia
o
Decreased social interaction
o
Abdom inal pain
o
Nocturia
o
Incontinence
o
Syncope or dizziness
Essential Workup
Urinalysis (dipstick test, m icroscopy)
Fem ales: pregnancy test
Fem ales: rule out urethritis, vaginitis, pelvic inflam m atory disease (PID)
Males: rule out urethritis, epididym itis, prostatitis.
Males: inquire about anal intercourse and HIV.
Urologic evaluation in young healthy m ales with first UTI is not routinely recom m ended.
Tests Lab
Pa ge 4 9 8
Rapid Urine Screen o
Dipstick (leukocyte esterase + nitrite) m ost effective when urine contains 10 5 CFU/m l
o
Laboratory specim en unnecessary if pyuria and bacteriuria confirm ed by dipstick
o
o
Leukocyte esterase:
Sensitivity 75–96%
Specificity 94–98%
Nitrite:
Sensitivity 35–85%
Specificity 92–100%
Both tests have excellent negative predictive values.
Urinalysis/Microscopy: o
Obtain if rapid urine screen is unavailable or negative in patients with presum ed UTI.
o
10 WBC/m m 3 in clean catch m idstream urine indicates infection.
o
Bacteria detected in unspun urine indicates >10 5 CFU/m l.
Indications for urine culture: o
Com plicated UTIs
o
Negative rapid urine screen or m icroscopy in patients with presum ed UTI
o
Persistant signs and sym ptom s after 2–3 days of treatm ent
o
Recurrence (relapse versus reinfection)
o
Recently hospitalized patients
o
Nosocom ial infections
o
Pyelonephritis
o
Additional labs dictated by clinical setting
Imaging
Pa ge 4 9 8
Indicated for com plicated upper tract disease (see chapter: Pyelonephritis)
Helical CT, IV pyelogram or renal ultrasound if concom itant stone or obstruction suspected
Diagnostic Procedures/Surgery Patients with significant hem aturia, recurrent UTI with sam e uropathogen, or sym ptom s of obstruction need urologic evaluation to identify structural or functional abnorm ality. P.1175
Differential Diagnosis
Pyelonephritis
Urethritis
Vulvovaginitis
PID/cervicitis
Prostatitis
Epididym itis
Nephrolithiasis
Appendicitis
Diverticulitis
Treatment Initial Stabilization
Urosepsis/septic shock: o
Manage airway and resuscitate as indicated
o
IV crystalloid
o
Vasopressors as needed
Antibiotics:
Pa ge 4 9 8
o
Fluoroquinolone
o
Antipseudom onal penicillin with am inoglycoside
o
Carbapenem s
o
Third-generation cephalosporin with antipseudom onal activity
ED Treatment Stable Patients
Prevalence of uropathogens resistant to trim ethoprim -sulfam ethoxazole (TMP/SMX) is increasing (up to 30%).
Antibiotics of choice: o
Fluoroquinolones (95% susceptibility rates)
o
TMP/Sulfam ethoxazole (SMX) (10–20% resistance)
o
Nitrofurantoin:
o
15–20% resistance
Bacteriostatic
Fluoroquinolones first-line treatm ent in wom en:
Sulfonam ide intolerance
High frequency of antim icrobial resistance related to recent treatm ent
Live in areas with significant resistance to TMP/SMX (>10–20%)
Live in areas with unknown TMP/SMX resistance rates
o
Second or third-generation oral cephalosporins m ay be reasonable alternates (cefuroxim e, cefixim e) in specific circum stances.
o
require 7-day treatm ent regim ens
Asym ptom atic bacteriuria occurs in 20% of wom en >65 years, 50% of wom en >80 years, and generally should not be treated.
Pa ge 4 9 8
o
Diabetic wom en have increased risk of bacteriuria with Klebsiella spp.
o
Treat dysuria with phenazopyridine.
o
Treat pain with appropriate analgesics.
o
Cranberry juice:
May prevent the recurrence of UTI
Prevents E. coli from adhering to uroepithelial cells
o
Treatm ent of upper tract disease—rule of 2s
2 L of IV fluid
2 tablets of Tylenol #3
2 g of ceftriaxone or 2 m g/kg of gentam icin
If fever drops by 2°C and patient can retain 2 glasses of water
Discharge with fluoroquinolone for 2 weeks.
Follow up in 2 days.
Pregnancy Considerations
Asym ptom atic bacteriuria in pregnancy
Treat with 3- to 7-day course of antibiotics: o
Cephalexin
o
Nitrofurantoin
o
TMP/SMX:
SMX should not be used late in pregnancy as kernicterus can result.
o
Am oxicillin
Fosfom ycin also safe and effective in pregnancy
Nitrofurantoin contraindicated in pregnancy if patient G6PD-deficient
Quinolones not recom m ended during pregnancy: o
CNS reactions
o
Blood dyscrasias
o
Effects on collagen form ation
Pa ge 4 9 8
Medication (Drugs)
Am oxicillin: 500 m g PO q12h or 875 m g PO q12h
Cefixim e: 400 m g PO per day or 200 m g PO q12h
Ceftazidim e: 1–2 g IV q8h–q12h
Ceftriaxone: 1–2 g IV/IM q24h
Cefuroxim e: 250–500 m g PO q12h
Cephalexin: 250–500 m g PO q6h
Ciprofloxacin: 100–500 m g PO q12h
Fosfom ycin: 3 g single dose
Gentam icin: 2 m g/kg IV or IM q8h
Levofloxacin: 250 m g PO q24h
Nitrofurantoin: 100 m g PO q12 (sustained release)
Norfloxacin: 400 m g PO q12h or 800 m g PO q24h
Ofloxacin: 200 m g PO q12h or 400 m g IV q12h
Phenazopyridine: 200 m g PO t.i.d. for 2 days
o
For sym ptom atic treatm ent of dysuria
o
May turn urine and contact lenses orange
TMP/SMX: 160 m g/800 m g PO q12h or q8h–q10h m g/kg IV q12h
Follow-Up Disposition Admission Criteria
Inability to com ply with oral therapy
Unstable vital signs
Toxic appearance
Pyelonephritis
Pa ge 4 9 8
o
Intractable sym ptom s
o
Extrem es of age
o
Im m unosuppression
o
Urinary obstruction
o
Consider if coexisting urolithiasis
o
Significant com orbid disease
o
Outpatient treatm ent failure
o
Late in pregnancy
Discharge Criteria
Well appearing
Stable vital signs
Can m aintain oral hydration
Can com ply with oral therapy
No significant com orbid disease
Adequate follow-up (48–72 hours) as needed
Healthy patients with uncom plicated pyelonephritis who respond to treatm ent in ED according to rule of 2s
Pyelonephritis in early pregnancy with good follow-up m ay be treated as outpatients
References 1. Hooton TM. Practice guidelines for urinary tract infection in the era of m anaged care. Int J Antim icrob Agents. 1999;11:241–245. 2. Hooton TM, Stam m WE. Diagnosis and treatm ent of uncom plicated urinary tract infection. Infect Dis Clin North Am . 1997;11(3):551–581. 3. McLaughlin SP, Carson CC. Urinary tract infections in wom en. Med Clin North Am . March 2004;88(2):417–429. 4. Stam m WE, Hooton TM. Managem ent of urinary tract infections in adults. N Engl J Med. 1993;329(18):1328–1334. 5. Warren JW, Abrutyn E, Hebel JR, et al. Guidelines for antim icrobial treatm ent of uncom plicated acute bacterial cystitis and acute
Pa ge 4 9 9
pyelonephritis in wom en. Clin Infect Dis. 1999;103(4):843–852.
Miscellaneous SEE ALSO: See Urinary Tract Infection, Pediatric
Codes ICD9-CM 599.0
ICD10 N39.0
Pa ge 4 9 9
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Urinary Tract Infectio ns, Pediatric
Urinary
Tract Infections, Pediatric Suzanne Z. Barkin
Basics Description
Bacteria colonize via retrograde contam ination of rectal or perineal flora:
o
Infants—often hem atogenous spread
o
Older children—vesicoureteral reflux m ajor risk
Urinary tract infection (UTI) is defined by culture with >10,000 organism s/m L on a catheterized or suprapubic specim en.
In infants 0–3 m onths old, UTI is associated with a 30% incidence of sepsis.
Predisposing factors: o
Poor perineal hygiene
o
Short urethra of fem ale
o
Fem ale > Male
o
Infrequent voiding
o
Constipation
o
Sexual activity
o
Circum cision probably reduces risk
Pa ge 4 9 9
Etiology
UTI found in 4–7% of febrile infants
Bacterial agents: o
Escherichia coli accounts for 90%.
o
Klebsiella pneum oniae
o
Staphylococcus aureus
o
Enterobacter species
o
Proteus species
o
Pseudom onas aeruginosa
o
Enterococcus species
Diagnosis Alert UTIs in children m ay be difficult to diagnosis without laboratory confirm ation.
Signs and Symptoms
Often nonspecific
Neonates:
o
Manifestations of sepsis
o
Feeding difficulties
o
Irritability, listlessness
o
Fever, hypotherm ia
1 m onth to 3 years of age: o
Fever
o
Irritability
o
Vom iting, diarrhea
o
Abdom inal pain
o
Poor feeding, failure to thrive
Hem aturia
Pa ge 4 9 9
In girls Table o f C o ntents > Vaginal Bleeding in Pregnancy
Vaginal
Bleeding in Pregnancy Paul Ishimine
Basics Description
Leading cause of m aternal/fetal m orbidity and m ortality
Early pregnancy hem orrhage (≤20 weeks):
o
Occurs in 30% of all pregnancies
o
50% lead to spontaneous abortion.
Late pregnancy hem orrhage (>20 weeks): o
Occurs in 3–5% of all pregnancies
Risk factors: o
Risk factors differ for each underlying cause of vaginal bleeding:
Advanced m aternal age
Substance abuse (e.g., cocaine, tobacco)
Pelvic inflam m atory disease (PID)
Previous cesarean section
Previous term ination of pregnancy
Dilation and curettage (D&C)
Previous ectopic pregnancy
Increased parity
Pa ge 5 0 1
Multiple gestation
Pre-eclam psia
Hypertension
Traum a
Genetics 50–60% of m iscarriages due to chrom osom al abnorm alities
Etiology
Structural lesions: o
Vaginal
o
Cervical
o
Uterine
o
Uterine-placental interface
Hem atologic dysfunction
Diagnosis Signs and Symptoms History
Intensity and duration of bleeding: o
Am ount
o
Color (dark or bright red)
o
Painful or painless
o
Watery, blood-tinged m ucus, clots or tissue:
Spontaneous abortion: classically cram py, diffuse pelvic pain
Ectopic pregnancy: classically sharp pelvic pain with lateralization
Placenta previa: classically painless, bright red hem orrhage
Placental abruption: classically painful, dark red
Pa ge 5 0 1
hem orrhage o
Life-threatening conditions m ay present with only m inim al vaginal bleeding
Last m enstrual period
Estim ated duration of gestation
Parity
Fever
Last intercourse
Previous obstetric-gynecologic com plications
Physical Exam
Vital signs: o
Tachycardia
o
Hypotension
o
Orthostatic changes in pulse or blood pressure
o
Signs of hem odynam ic instability m ay be absent due to pregnancy-related physiologic increase in blood volum e.
Fetal heart tones: o
Fetal cardiac activity seen on transvaginal ultrasound at 6.5 weeks
o
Auscultated with Doppler past 10 weeks’ gestation
Abdom inal exam ination: o
Uterine size
o
Peritoneal signs
o
Firm or tender uterus in late pregnancy suggests abruption
Pelvic exam —only in early pregnancy: o
Evaluate source and intensity of bleeding.
o
Determ ine patency of cervical os (perform this with a finger and only in the first trim ester):
Threatened abortion: os closed
Pa ge 5 0 1
o
Inevitable abortion: os open
Incom plete abortion: os open or closed
Com plete abortion: os closed
Em broynic dem ise (m issed abortion): os closed
Products of conception m ay be noted in incom plete or com pleted abortion:
Products of conception in the cervical os can result in profuse bleeding.
o
Evaluate uterine size, tenderness.
o
Evaluate for uterine fibroids or adnexal m asses.
o
Late pregnancy: Do not perform pelvic exam unless in controlled operating room setting:
Severe hem orrhage m ay ensue.
Placenta previa or vasa previa m ust be ruled out by sonography prior to pelvic exam .
Essential Workup
CBC
Type and screen
Quantitative HCG in early pregnancy
Urinalysis
Ultrasound: o
Transvaginal ultrasonography provides m ore inform ation than transabdom inal ultrasonography, especially early pregnancy.
Tests Lab
CBC: o
Dilutional “anem ia― is a norm al physiologic change in pregnancy:
Blood volum e expands by 45%
Quantitative β-hum an chorionic gonadotropin (β-hCG):
Pa ge 5 0 1
o
Useful to correlate with ultrasound findings
o
Detectable 9–11 days following ovulation
o
β-hCG doubles every 48 hours in norm al early pregnancy until 10 weeks of gestation.
Blood typing and Rh: o
Cross-m atch if significant bleeding
Prothrom bin tim e, partial throm boplastin tim e, and dissem inated intravascular coagulation panel in em bryonic dem ise, placental abruption
Blood cultures with septic abortion
Suspected products of conception to lab for identification of chorionic villi
Imaging
Ultrasound: o
Essential to the evaluation of bleeding in pregnancy
Transvaginal ultrasound is m ore helpful than transabdom inal ultrasound in early pregnancy bleeding.
Confirm s intrauterine pregnancy (IUP)
Detects gestational sac at 5 weeks or β-hCG = 1000–2000 IU, yolk sac at 6 weeks, and cardiac activity at 5–6 weeks of gestation
Essentially rules out ectopic pregnancy by showing IUP (except in wom en using assisted reproductive technology)
Proves ectopic pregnancy by showing fetal pole outside uterus
Suggests ectopic pregnancy by detecting free fluid in cul de sac or adnexal m ass
Detects retained products of conception
Diagnostic Procedures/Surgery
Pa ge 5 0 1
Culdocentesis: o
Lim ited use with ultrasound available
o
Identifies free fluid in cul-de-sac
Suction D&C o
Indicated if suspected incom plete or septic abortion or em bryonic dem ise, gestational trophoblastic disease, blighted ovum to evacuate retained products of conception
Laparoscopy/laparotom y o
Indicated for unstable patients not responsive to resuscitation m aneuvers
o
Definitive diagnosis and treatm ent of ectopic pregnancy
Differential Diagnosis
Early pregnancy (20 weeks): o
Abruptio placenta (30%)
o
Placenta previa (20%)
o
Bloody show
o
Vasa previa
Pa ge 5 0 1
o
Cervical/vaginal traum a or pathology
o
Uterine rupture (uncom m on)
o
Bleeding disorders
P.1183
Treatment Pre Hospital
Unstable vital signs warrant aggressive resuscitation and continuous cardiac m onitoring.
In late pregnancy, position patient on left side to decrease uterine com pression of vena cava.
Consider preferential transport of a wom an greater than 23–24 weeks gestation with vaginal bleeding to a facility with obstetric capabilities.
Initial Stabilization
Airway m anagem ent, resuscitation as indicated
Oxygen
Pulse oxim etry
Cardiac m onitor
Two large-bore IV lines with norm al saline or lactated Ringer solution infusion
Blood transfusion as indicated
ED Treatment
All wom en with early pregnancy vaginal bleeding m ust be evaluated for ectopic pregnancy, (preferably by transvaginal ultrasound).
Adm inister anti-Rh im m une globulin if patient is
Pa ge 5 0 1
Rh-negative.
Suspected ectopic pregnancy: o
Unstable: consider bedside US with em ergent OB consultation for laparoscopy/laparotom y
o
Stable: perform US; if confirm s or suggestive of ectopic pregnancy, obtain OB consultation for surgery or m ethotrexate therapy
Threatened abortion:
Em ergent OB/gyn consultation for heavy/uncontrolled bleeding
Arrange OB/gyn follow-up for m inim al bleeding
Inevitable/incom plete/m issed (em bryonic dem ise) abortion: o
Products of conception in the cervical os can result in profuse bleeding:
If products of conception cannot be rem oved with gentle traction, obtain em ergent OB/GYN consultation.
o
Arrange follow-up with OB/GYN if bleeding m inim al.
Com plete abortion: o
Em ergent OB/GYN consultation for heavy/uncontrolled bleeding
o
Arrange follow-up with OB/GYN if bleeding m inim al.
Septic abortion: o
Initiate broad-spectrum antibiotic therapy.
o
Em ergent OB/GYN consultation for D&C
Late pregnancy vaginal bleeding: o
Hem odynam ic stabilization:
Fluid resuscitation
Positioning of patient onto left side or displacem ent of uterus laterally to relieve com pression of the inferior vena cava
Pa ge 5 0 1
Because of com pensatory hem odynam ic changes during pregnancy, significant hypovolem ia m ay exist with m inim al vital sign abnorm alities.
o
Dissem inated intravascular coagulation:
Associated with late pregnancy bleeding
Especially with placental abruption
Treated with blood, coagulation factors and platelets
o
Obstetric consultation and rapid transfer to obstetric unit
Medication (Drugs)
Anti-Rh 0 (D) im m une globulin: 12 weeks—300 m cg IM
Septic abortion: o
Multiple acceptable antibiotic regim ens
o
Must provide polym icrobial coverage
Follow-Up Disposition Admission Criteria
Early pregnancy vaginal bleeding with: o
Unstable vital signs or significant hem orrhage
o
Ruptured ectopic pregnancy
o
Incom plete abortion (open os)
o
Septic abortion
All patients with late pregnancy vaginal bleeding need to be adm itted to a labor and delivery unit.
Pa ge 5 0 1
Discharge Criteria
Threatened abortion (closed os) with stable sym ptom s
Com plete abortion, em bryonic dem ise, blighted ovum with stable sym ptom s
Asym ptom atic, hem odynam ically stable patient with sm all, unruptured ectopic (or suspected ectopic) pregnancy after OB consultation
Controlled bleeding from local vaginal/cervical source
Discharge Instructions
No strenuous activity, tam pon use, douching, or intercourse
Seek m edical advice for increased pain, bleeding, fever, or passage of tissue
Issues for Referral
Wom en with known ectopic pregnancy or in whom ectopic pregnancy is suspected need to have beta-HCG levels checked in 48 hours.
Patients with em bryonic dem ise, blighted ovum , or gestational trophoblastic disease need to be referred for uterine evacuation if D&C not perform ed in ED.
Wom en with threatened, inevitable, com plete, or m issed (em bryonic dem ise) abortion should have OB/GYN follow-up with 24–48 hours
References 1. Am erican College of Em ergency Physicians Clinical Policies Com m ittee and the Clinical Policies Subcom m ittee on Early Pregnancy: crucial issues in the initial m anagem ent of patients presenting to the em ergency departm ent in early pregnancy. Ann Em erg Med. 2003;41:123–133. 2. Coppola PT, Coppola M. Vaginal bleeding in the first 20 weeks of
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pregnancy. Em erg Med Clin N Am . 2003;21:667–677. 3. Dyne PL. Vaginal bleeding and other com m on com plaints in early pregnancy. In: Pearlm an MD, et al. eds. Obstetric & gynecologic em ergencies: diagnosis and m anagem ent. New York, NY: McGraw-Hill. 2004:39–55. 4. Reardon RF, Jehle DVK. Pelvic ultrasonography. In: Tintinalli JE, et al. eds. Em ergency m edicine: a com prehensive study guide. New York, NY: McGraw-Hill. 2004:715–726. 5. Rehm an KS, Johnson TRB. Bleeding after 20 weeks’ gestation: m aternal and fetal assessm ent. In: Pearlm an MD, et al. eds. Obstetric & gynecologic em ergencies: diagnosis and m anagem ent. New York, NY: McGraw-Hill. 2004: 117–136.
Miscellaneous SEE ALSO: Abortion, Spontaneous; Abruptio Placenta; Ectopic Pregnancy; Hydatidiform Mole; Placenta Previa; Postpartum Hem orrhage
Pa ge 5 0 2
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Vaginal Bleeding
Vaginal Bleeding
Carla Valentine
Basics Description
Com m on presenting com plaint in EDs
Most cases have benign etiology.
Som e patients m ay have potentially life-threatening conditions.
Most im portant principles in evaluating wom en with vaginal bleeding: o
All wom en capable of childbearing m ight be pregnant.
o
Menstrual and sexual histories do not rule out pregnancy.
Etiology Pregnancy Related
Early pregnancy: o
Ectopic pregnancy (occurs in 2% of pregnancies)
o
Abortion:
Threatened
Incom plete
Com plete
Missed
Pa ge 5 0 2
Inevitable
Septic
o
Molar pregnancy
o
Traum a
Later pregnancy: o
Placenta previa
o
Placental abruption
o
Molar pregnancy
o
Labor
o
Traum a
Im m ediate postpartum period: o
Postpartum hem orrhage
o
Uterine inversion
o
Retained placenta
o
Endom etritis
Nonpregnant Patients
Dysfunctional uterine bleeding
Structural abnorm alities
Uterine fibroids
Cervical/Endom etrial polyps
Pelvic tum ors
Atrophic endom etrium : o
Most com m on cause of postm enopausal bleeding
Rare for system ic disorders to present solely with vaginal bleeding:
o
Von Willebrand disease
o
Idiopathic throm bocytopenic purpura
Traum a
Diagnosis
Pa ge 5 0 2
Signs and Symptoms
Vaginal bleeding: o
Variable am ounts:
Average tam pon holds approxim ately 5 cc of blood
Average pad holds approxim ately 5–15 cc of blood
o
May be associated with fetal tissue/blood clots
Light-headedness
Fatigue
Weakness
Thirst
Acute hypotension and tachycardia: o
Significant vaginal bleeding due to ectopic pregnancy or ruptured ovarian cyst:
o
May produce altered m entation
Abdom inal distention or tenderness
Essential Workup
Qualitative pregnancy test: o
Point-of-care urine-based pregnancy test preferred
Pelvic exam ination: o
Essential for all wom en with vaginal bleeding
o
Speculum /bim anual exam
o
Assess whether cervical os open or closed.
Delay pelvic exam ination pending ultrasound result in late pregnancy:
Evaluate for placenta previa as the etiology of vaginal bleeding.
o
Defer exam if patient is near term with possible rupture of fetal m em branes.
Pregnancy test m andatory for all patients with
Pa ge 5 0 2
childbearing potential
Early pregnancy: o
Blood type and Rh
o
Ultrasound to confirm intrauterine pregnancy (IUP)
o
Quantitative β-hum an chorionic gonadotropin (HCG)
o
Hem atocrit
o
Type and cross-m atch:
o
Ectopic pregnancy
Low hem atocrit levels
Hem odynam ic instability
Urinalysis
Later pregnancy: o
Type and Rh
o
Fetal heart tones
o
Ultrasound indications:
No fetal heart tones
No docum ented intrauterine pregnancy
Unknown placental lie
o
Hem atocrit if significant bleeding
o
Type and cross-m atch if placenta previa/abruption or low hem atocrit levels
o
Dissem inated intravascular co-agulation panel if placental abruption:
Platelets, prothrom bin tim e (PT), partial throm boplastin tim e (PTT)
Fibrinogen, fibrin-split products
Early postpartum : o
Ultrasound for retained products
o
Hem atocrit
o
β-Hum an chorionic gonadotropin if concerned about retained tissue
Tests
Pa ge 5 0 2
Lab
Hem atocrit for wom en with significant bleeding
Platelet count for suspected throm bocytopenia
PT/PTT for suspected coagulopathy
Imaging
Send any passed tissue or clot for pathology evaluation.
Endom etrial sam pling required if patient older than 35–40 years: o
Risk for endom etrial cancer
Treatment Pre Hospital
Establish IV 0.9% norm al saline with 1-L fluid bolus for significant bleeding or hypotension.
Adm inister high-flow oxygen in pregnant or unstable patients.
In later pregnancy: o
Place patient in left-lateral recum bent position to prevent occlusion of inferior vena cava by uterus.
Initial Stabilization
Manage airway and resuscitate as indicated.
Place cardiac/pulse oxim eter m onitors.
Oxygen for significant bleeding or unstable patient
Establish two large-bore IV lines and initiate fluid bolus (1–2 L) for hypotensive patients: o
Transfuse blood if continued hypotension from blood losses despite IV fluid resuscitation.
ED Treatment
Pa ge 5 0 2
If unstable with surgical condition, arrange for transfer of the patient to the operating room as soon as possible.
RhoGAM for vaginal bleeding, pregnancy, and Rh-negative m other: o
RhoGAM: 300 µg IM if >13 weeks pregnant
o
MICRhoGAM 50 µg IM if 13 weeks pregnant
MICRhoGAM 50 µg IM if 100.4°F, syncope, or dizziness. Patients should not be left alone until the diagnosis of ectopic pregnancy can be safely ruled out. Fam ily and friends should also be instructed on the warning signs and sym ptom s of ruptured/bleeding ectopic pregnancies.
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Vaginal Discharge/Vaginitis
Vaginal
Discharge/Vaginitis Donna Felsenstein
Basics Description
Vaginal discharge
Som e am ount of vaginal discharge is norm al.
Glands in the cervix produce a clear m ucus that m ay turn white or yellow when exposed to air.
Abnorm al discharge is defined by an increased am ount or change in color or o
Vaginitis
o
Irritation or inflam m ation of the vagina
o
Change in the vaginal flora
o
Loss of norm al lactobacillus (e.g., antibiotics)
o
Inability to m aintain norm al vaginal pH ( Table o f C o ntents > Varices
Varices
John Bailitz
Basics Description
Increased portal venous pressure results in portal-system ic shunts.
Shunts at gastroesophageal junction result in fragile subm ucosal esophageal varices.
Etiology
10–30% of all cases of upper gastrointestinal (GI) bleeding
90% of upper GI bleeding in patients with cirrhosis
Variceal hem orrhage occurs in 30% of patients with cirrhosis:
o
30% m ortality per episode
o
70% have recurrent bleeding.
In adults: o
Cirrhosis due to alcoholism or chronic hepatitis
o
Storage disease: Wilson or hem ochrom atosis
o
Middle East: Schistosom iasis
In children: o
Intrahepatic obstruction from biliary cirrhosis
o
α 1 -antitrypsin deficiency
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o
Hepatitis
Diagnosis Signs and Symptoms General
Weakness and fatigue
Tachycardia
Tachypnea
Hypotension
Cool, clam m y skin; prolonged capillary refill
Abdominal
Significant active upper GI bleeding: o
Hem atem esis
o
Hem atochezia
o
Melena
o
20–40% of total blood volum e loss possible
Abdom inal pain
Stigm ata of severe hepatic dysfunction:
o
Jaundice
o
Spider angiom ata
o
Palm ar erythem a
o
Pedal edem a
o
Hepatosplenom egaly
o
Ascites
History of portal hypertension: o
Most com m only alcoholic cirrhosis
o
Others, including:
Prim ary biliary cirrhosis
Schistosom iasis
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Budd-Chiari syndrom e
Severe congestive heart failure
Sarcoidosis
Cardiovascular Chest pain/shortness of breath
CNS
Syncope
Confusion and agitation initially
Lethargy and obtundation later
Pediatric Considerations
Massive hem atem esis: typical initial presentation: o
Hypotension m ay be a late finding.
Essential Workup
Gastric tube placem ent: o
Determ ines whether patient is actively bleeding
o
Facilitates endoscopic exam
o
Will not increase or cause esophageal variceal bleeding
Em ergent endoscopy
Tests Lab
Type and cross-m atch—6–8 units: o
Significant transfusion requirem ents
ABG for: o
Acidosis
o
Hypoxem ia
CBC: o
Hem atocrit is an unreliable indicator of early rapid blood loss.
Electrolytes, blood urea nitrogen, creatinine, glucose:
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o
Evaluate renal function.
o
BUN/Creatinine greater then 30 suggest significant blood in GI tract.
Prothrom bin tim e/partial throm boplastin tim e/international norm alized ratio and platelets: o
Coagulopathy
o
Prolonged bleeding tim es
o
Throm bocytopenia
Imaging
Chest radiograph (portable) for aspiration/perforation
ECG for m yocardial ischem ia
Differential Diagnosis
Bleeding/perforated peptic ulcer
Erosive gastritis
Mallory-Weiss syndrom e
Boerhaave syndrom e
Aortoenteric fistula
Gastric varices
Treatment Pre Hospital
Airway stabilization
Treat hypotension 0.9% norm al saline infusion bolus through two large-bore 16-gauge or large IV lines.
Cardiac and pulse oxim etry m onitoring
P.1191
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Initial Stabilization
ABCs with early aggressive airway control/intubation: o
Early intubation = easier intubation
o
For AMS or m assive hem optysis
o
Facilitates em ergency endoscopy
Establish central IV access with invasive intravascular m onitoring for hypotension not responsive to initial fluid bolus.
Replace lost blood as soon as possible: o
Initiate with O-negative blood until type-specific blood available.
o
10 m L/kg bolus in children
o
Fresh-frozen plasm a and platelets m ay be required.
Place gastric tube nasally (awake) or orally (intubated)
Controversy: o
Overly aggressive volum e expansion m ay lead to rebound portal hypertension, rebleeding, and pulm onary edem a.
Pediatric Considerations
Initiate intra-osseous access if peripheral access unsuccessful in unstable patient.
Most bleeding in children stops spontaneously.
Vital signs changes m ay be a late finding in children: o
Subtle changes in m ental status, capillary refill, m ild tachycardia, or orthostatic changes m ay indicate significant blood loss.
o
Overaggressive correction in infants can quickly lead to significant electrolyte abnorm alities.
ED Treatment Em ergent endoscopy required, used pharm acologic and tam ponade devices as tem porizing m easures
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Endoscopy
Em ergent with active bleeding in nasogastric tube
Procedure of choice in acute esophageal bleeding
Esophageal band ligation equivalent to sclerotherapy with fewer com plications: o
May be difficult to visualize in cases of m assive bleeding
Sclerotherapy with m assive bleeding
Adm inister antibiotics at tim e of procedure to decrease risk for spontaneous bacterial peritonitis: o
Cefotaxim e or ceftriaxone
Pharmacological Therapy
Octreotide is first-line therapy: o
Com plications include hyperglycem ia and abdom inal cram ping.
Vasopressin replaced by octreotide secondary to high incidence of vascular ischem ia
Balloon Tamponade
Initiate in m assive uncontrollable bleed.
Sengstaken-Blakem ore and Minnesota tubes
Applies direct pressure but risks esophageal perforation and ulceration
Tem porary benefit only with m assive uncontrolled bleeding in hands of experienced clinician
Refractory Bleeding Therapy
Interventional radiology: o
Transjugular intrahepatic portosystem ic shunt procedure
Surgical options: o
Portacaval shunt
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o
Variceal transection
o
Stom ach devascularization
o
Liver transplantation
Medication (Drugs)
Cefotaxim e: 2 g (peds: 50–180 m g/kg/24h) IV q8h
Ceftriaxone: 2 g (peds: 50–75 m g/kg/24h) IV q24h
Octreotide: 50 µg bolus, then 50 µg/h infusion for 5 days
Follow-Up Disposition Admission Criteria
Intensive care unit adm ission for actively bleeding varices
Recent history of variceal bleeding
High risk for early rebleeding: o
Age >60 years, renal failure, initial hem oglobin count Table o f C o ntents > Veno us Insufficiency
Venous
Insufficiency Calvin A. Brown III
Basics Description A chronic condition of lower extrem ity vascular incom petence
Etiology
Norm al venous flow is from the superficial to deep veins.
Unidirectional flow is m aintained by m uscular contractions and bicuspid valves.
Valvular incom petence leads to regurgitant blood flow, elevated venous pressures, and distention of superficial veins.
Venous hypertension and endothelial dysfunction results in leakage of protein, red blood cells, and water into extracellular m atrix.
Fibrosis and dim inished oxygen diffusion produces sclerosis, skin breakdown, and ulcer form ation.
Diagnosis
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Signs and Symptoms History
Asym ptom atic phase: o
Venous dilation ranging from venous flares to sm all varicosities
Sym ptom atic phase: o
Ankle and calf swelling
o
Itching
o
Profuse bleeding
o
Hyperpigm entation
o
Lipoderm atosclerosis
o
Ulcer form ation
Physical Exam
Varicosities
Dependent ankle/calf edem a
Skin changes:
o
Induration
o
Sclerosis
Venous ulcers: o
Over either m alleoli or m edial portion of the calf with preserved peripheral pulses
Bacterial infection: o
Surrounding cellulitis
o
Rapidly growing ulcer
o
Increased pain
o
Lym phangitis
Leg edem a and ulcers with ascites, periorbital edem a, orthopnea, or an abnorm al cardiac exam suggests other etiologies.
Essential Workup
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Clinical features usually enough to m ake the diagnosis.
Tests Lab
Lab tests are of little value.
Cardiac m arkers, brain natriuretic, album in, and tests of renal function can be sent if considering other causes of leg edem a.
Imaging Im aging:
Duplex ultrasonography: o
Assess for DVT or valvular incom petence.
Venography: o
Gold standard
o
Expensive and invasive
Ankle-brachial index: o
If arterial insufficiency is suspected
Diagnostic Procedures/Surgery
Im m ediate surgical procedures are not required for varicose veins.
Vein stripping, vein ligation, and sclerotherapy are options for cases refractory to m edical m anagem ent: o
Does not im prove healing but reduces ulcer recurrence
Differential Diagnosis
Leg edem a: o
Congestive heart failure
o
Nephrotic syndrom e
o
Liver failure
o
Lym phatic obstruction
o
Deep venous throm bus
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P.1195
Leg ulcers: o
Venous insufficiency
o
Arterial insufficiency
o
Soft-tissue infection
o
Polyarteritis
o
Pyoderm a gangrenosum
Treatment Initial Stabilization
Leg elevation
Control bleeding with direct pressure.
ED Treatment
Leg elevation
Com pression stockings
Anticoagulants for confirm ed deep vein throm bosis (DVT)
Steroids for stasis derm atitis
Aspirin
Antibiotics for signs of infection
Astringents: o
Dom eboro solution
Antihistam ines for pruritus
Medication (Drugs)
Aspirin: 325 m g/d PO
Augm entin: 875 b.i.d. PO
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Benadryl: 12.5–25 m g q.i.d. PO
Cephalexin: 500 m g q.i.d. PO
Dicloxacillin: 500 m g q.i.d. PO
Coum adin: dose per prothrom bin tim e/international norm alized ratio
Lovenox: 1 m g/kg SC b.i.d.
Follow-Up Disposition Admission Criteria Evidence of cellulitis, lym phangitis, or osteom yelitis m ay require adm ission.
Discharge Criteria
Bleeding under control
DVT has been ruled out.
No evidence of bacterial infection requiring adm ission
Appropriate follow-up/referral arranged
Hom e services for dressing changes
References 1. Barwell JR, Davies CE, Deacon J, et al. Com parison of surgery and com pression with com pression alone in chronic venous ulceration (ESCHAR study): random ised controlled trial. Lancet. 2004;363(9424):1854–1859. 2. Guyton AC, Hall JE. Textbook of Medical Physiology. 10th ed. Philadelphia, PA: WB Saunders; 2000:158–159. 3. Marx JA, Hockberger RS, Walls RM Rosen's Em ergency Medicine: Concepts and Clinical Practice. Mosby, 2002:1228. 4. Tintinalli JE, Kelen GD, Stapczynski JS. Em ergency Medicine: A
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Com prehensive Study Guide. McGraw-Hill, 2004:1529–1530.
Codes ICD9-CM 459.81
ICD10 I87.2
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Ventilato r M anagem ent
Ventilator
Management Owen Lander
Basics Description
Ventilation provided by a m achine that generates a controlled flow of gas into a patient's airways
There are several different m odes and strategies of positive pressure ventilation.
Delivery m odes: o
Pressure-cycled:
Each breath at the set rate is delivered to a set a m axim um pressure.
Markedly reduces the risk of barotraum a
Markedly variable tidal volum es and m inute ventilation as a result of changes in patient chest wall and lung com pliance and spontaneous respiratory efforts
o
Volum e-cycled:
Each breath at the set rate is delivered to a set volum e.
Provides a consistent and reliable m inute
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ventilation, appealing in the initial m anagem ent setting
Can generate excessive peak pressures, particularly if patient chest wall or lung com pliance decreases
In m ost cases, can be lim ited by protective peak pressure cut-off lim its
Support m odes: o
Control m ode:
Each breath, triggered or preset, is delivered as a “full breath,― whether volum e- or pressure-cycled.
o
Support m ode:
Relies solely on supplying set support pressure to patient initiated breaths, term inating when expiratory effort is detected
o
Continuous m andatory ventilation (CMV):
A control m ode that delivers breaths only at the set respiratory rate.
Rarely used because it frequently results in severe air hunger and asynchrony between the patient and the ventilator
In the paralyzed or apneic patient, assist control (AC) is equivalent to CMV.
o
AC:
Delivers a full breath at the preset respiratory rate
In addition, any inspiratory effort by the patient will also trigger the delivery of full breath at the set volum e or pressure.
Ensures adequate m inute ventilation while avoiding asynchrony in the nonapneic patient.
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Can result in over ventilation, hypocarbia and alkalosis in patients with significant spontaneous respiratory effort secondary to pain or agitation
Can result in excessive peak pressures, barotraum as, and breath stacking, particularly in patients with obstructive airway disease requiring prolonged exhalation phases
o
Interm ittent m andatory ventilation (IMV):
Delivers full breaths at the set respiratory rate
Spontaneous respirations by the patient are allowed but not supported.
Rarely used due to the subjective discom fort of m ixing fully supported breaths with unsupported breaths against the resistance of ventilator tubing and the possibility of delivering a full breath to a patient who has already spontaneously inhaled or is trying to exhale
o
Synchronous interm ittent m andatory ventilation (SIMV):
Designed to fit a set num ber of full breaths per m inute around any spontaneous respirations of the patient
Will not deliver a preset full breath when the patient is actively breathing
Spontaneous respirations are aided by an adjustable am ount of pressure support.
Has replaced IMV due to m arked increase in patient com fort and synchrony with the ventilator and reduced risk of barotraum as
o
Pressure support ventilation (PSV):
Provides a set am ount of pressure support whenever inspiratory effort is detected,
Pa ge 5 0 9
term inating when the flow rate of delivered air drops below a certain point indicating that the patient is ready to exhale
Com fortable for the patient, allowing the patient to breath as m uch and as often as desired with sufficient support
Requires nonapneic patient who have an adequate and appropriate respiratory drive
May be augm ented on som e ventilators with a fail-safe set IMV rate if the patient becom es apneic
Noninvasive positive pressure ventilation (NIPPV): o
Increasingly available
o
Tight-fitting m ask delivers respiratory support without intubation.
o
Essentially a PSV m ode of ventilation with variable positive end expiratory pressure (PEEP)
o
May avoid intubation in m ild to m oderate reversible respiratory failure
Congestive heart failure
Chronic obstructive pulm onary disease (COPD)
An awake, responsive patient m andatory
Adequate respiratory drive required
Titrated to the sam e goals as full m echanical ventilation.
Diagnosis Signs and Symptoms Indications for m echanical ventilation:
Apnea
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Respiratory distress with altered m entation
Clinically apparent increased work of breathing
Obtundation
Controlled hyperventilation required
o
Head injury
o
Tricyclic overdose
o
Metabolic acidosis
Severe circulatory shock
Tests Lab Aterial blood gas (ABG):
Within 15 m inutes of initial intubation
Repeat as clinically indicated: o
Changes in clinical status
o
Changes in ventilator settings
o
Significant changes of or inability to obtain noninvasive SaO 2 or ETCO 2 values
PaO 2 >60 m m Hg and saturation > 90%
pH should be 7.20–7.5 initially: o
Avoid overly rapid changes in pH via abrupt changes in ventilation.
o
Acutely pH is m ost easily m anaged via changes in the PaCO 2 .
Imaging Chest radiograph:
Confirm ation of correct placem ent of endotracheal tube
Differential Diagnosis Problem s in providing effective m echanical ventilation:
Pneum othorax
Hyperinflation
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Decreased venous return
Bronchospasm
Pulm onary edem a
Mucous plugging/secretions
Abdom inal distention
Ventilator problem s
Patient asynchrony
P.1197
Treatment Initial Stabilization
Cardiac m onitor
Blood pressure m onitoring
Pulse oxim etry to ensure SaO 2 >90%
Continuous core tem perature via esophageal or rectal probe if available: o
Critically ill patients because of the risk of hypotherm ia (especially if paralyzed)
End-tidal CO 2 m onitoring when available: o
Can reduce the frequency of serial ABG m easurem ents
ED Treatment
Ventilator settings should be adjusted to the patient's specific requirem ents:
Mode: o
Volum e-cycled m odes are the first choice, pressure cycled m odes are rarely used except in PSV.
Pa ge 5 0 9
o
SIMV or AC are the initial m odes of choice in the em ergently intubated patient.
o
PSV can be considered in patients with less severe respiratory failure and a robust respiratory drive.
Respiratory rate: o
Initial rate of 8–14 breaths per m inute
o
Higher rates for increased ventilation m ust be balanced against increased risk of air trapping and barotraum as.
o
Rates as low as 4–6 breaths per m inute m ay be required in severe asthm a to allow for exhalation.
Tidal volum e: o
Traditional volum es of 10–12 m L/kg are based on m aintaining norm al pH in patients with norm al lung parenchym a.
o
Increasing evidence of negative effects of higher volum es, especially in patients with prim ary lung pathology support an initial volum e of 8–10 m L/kg.
o
Lower volum es of 5–8 m L/kg are indicated in patients with severe asthm a/COPD or the presence of acute respiratory distress syndrom e
PEEP: o
3–5 cm H 2 O
Positive inspiratory pressure (PIP): o
Should be set if possible, or m onitored, to ensure they rem ain at or below 35 cm H 2 O
All patients should be adequately sedated to tolerate m echanical ventilation: o
Benzodiazepines are the drug of choice due to m uscle relaxing, am nestic, and anxiolytic effects.
Provide analgesia, optim ally m orphine or fentanyl.
Continued paralysis postintubation m ay be required:
Pa ge 5 0 9
o
Reduce the work of breathing in severe shock.
o
Tolerance of hypercapnia and prolonged I:E ratios in severe obstructive lung disease
Bronchodilators should be used in patients with obstructive lung disease.
Meeting the Goals of Ventilation
Oxygenation: o
Titrate FIO 2 to m aintain SaO 2 >90% and PaO 2 >60 m m Hg
o
Patients with high m etabolic dem and m ay benefit from slightly increased oxygenation.
o
PaO 2 >110 using FIO 2 >0.50 offers no significant benefit and increases the risk of oxygen toxicity.
o
FIO 2 1.0 refractory hypoxia:
Increm ental increase in PEEP
1–2 cm H 2 O at a tim e
Maxim um 10 cm H 2 O
Increased risk of hyperinflation, barotraum a, decreased venous return
Ventilation: o
Titrate m inute ventilation (RR × TV) to achieve pH >7.20 and 35 m m Hg and Table o f C o ntents > Ventricular F ibrillatio n
Ventricular
Fibrillation Ra'ed Hijazi
Basics Description
Ventricular fibrillation (VF) is com pletely disorganized depolarization and contraction of sm all areas of the ventricle without effective cardiac output.
Cardiac m onitor displays absence of quasi-random signal (QRS) com plexes and T waves with the presence of high-frequency, irregular undulations that are variable in both am plitude and periodicity.
Etiology
Initial rhythm in approxim ately 50–70% of patients sustaining sudden cardiac death in the prehospital setting: o
Most often a result of severe m yocardial ischem ia or infarction
Com plication of cardiom yopathy: o
Up to 50% of patients with dilated cardiom yopathy suffer an episode of VF.
o
In hypertrophic cardiom yopathy, unexpected sudden death occurs with reported frequency of up to 3% per
Pa ge 5 1 0
year.
Other less com m on causes of VF: o
Blunt chest traum a
o
Hypotherm ia
o
Iatrogenic m yocardial irritation form pacem aker placem ent or pulm onary artery catheter
VF is often preceded by ventricular tachycardia (VT). Conditions predisposing to VT: o
Drug toxicities (cyclic antidepressants, digitalis)
o
Congenital and acquired prolonged QT syndrom es.
o
Short QT syndrom e
o
Brugada syndrom e
o
Idiopathic VF (5–10%)
Pediatric Considerations
Prim ary ventricular dysrhythm ias are extrem ely rare in children.
VF usually results from a respiratory arrest, hypotherm ia, or near drowning.
Diagnosis Signs and Symptoms
Loss of consciousness, seizure, transient gasping followed by apnea
Absent pulse and heart sounds
Death if the rhythm rem ains untreated
Essential Workup Cardiac m onitor
Tests
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Lab
Laboratory tests are not useful during resuscitation.
After successful resuscitation, electrolytes including calcium and m agnesium , cardiac enzym es, troponin, and toxicologic screen
Differential Diagnosis Asystole: Fine VF m ay m im ic asystole in a single lead. Check rhythm in another lead for fine fibrillations.
Treatment Alert
Early defibrillation of VF is the m ost im portant determ inant of survival, and each m inute without defibrillation reduces survival by 7–10%.
Supraventricular tachycardia or VT with a pulse m ay degenerate into VF if cardioverted without synchronization.
In a hypotherm ic cardiac arrest (core tem perature less than 30°C), if the patient rem ains in VF after the delivery of the first three shocks, rewarm the patient first before further attem pts of defibrillation.
Do not defibrillate any conscious patient.
The subm ission of this chapter precedes the release of the 2005 Am erican Hospital Association guidelines; therefore, som e discrepancies m ay exist following their release.
Controversies
Biphasic autom atic external defibrillation (AED): o
Multicenter study showed that low-energy (150 J)
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biphasic AED resulted in superior defibrillation rate com pared to the m onophasic AED, resulting in return of spontaneous circulation in a greater percentage of patients. The rates of survival to hospital adm ission and discharge did not differ between the two groups.
There is no conclusive evidence supporting nonescalating over escalating biphasic defibrillation.
The optim al energy level of biphasic defibrillation has not yet been agreed upon.
CPR before defibrillation for prolonged VF (>5 m in)
Pre Hospital
ABCs
Follow initial stabilization according to respective prehospital policies and procedures.
Initial Stabilization
Im m ediate defibrillation with three stacked shocks: o
Monophasic 200 J, 200–300 J, 360 J
o
Biphasic escalating 120 J, 150 J, 200 J
o
Biphasic nonescalating 150 J, 150 J, 150 J
Initiate CPR and airway m anagem ent including endotracheal intubation.
Establish IV access.
Adm inister Vasopressin 40 units IV single dose; can be given one tim e only as first drug before Epinephrine or
Adm inister Epinephrine 1 m g IV bolus or 2–2.5 m g via endotracheal tube (ETT).
After Vasopressin or Epinephrine, repeat defibrillation with 360 J (or equivalent biphasic joules) within 30–60 seconds o
If VF persists, consider antiarrhythm ics: Am iodarone,
Pa ge 5 1 0
Lidocaine, Magnesium , and/or Procainam ide. P.1199
Epinephrine can be initiated 10–20 m inutes after Vasopressin.
Follow each m edication with defibrillation within 30–60 seconds at the last energy level used.
Consider sodium bicarbonate for patients with prolonged arrest.
If the patient is successfully resuscitated, start a continuous infusion of the last antiarrhythm ic agent adm inistered to the patient.
If the patient was successfully resuscitated prior to antiarrhythm ic adm inistration, give: o
Am iodarone 150 m g in 100 m L D 5 W over 10 m inutes followed by a m aintenance infusion or
o
Lidocaine 1–1.5 m g/kg IV bolus followed by a m aintenance infusion
Begin an evaluation for the cause of the VF arrest recognizing that the m ost likely cause is m yocardial ischem ia.
Pediatric Considerations
Defibrillation sequence: m onophasic 2 J/kg, 2–4 J/kg, 4 J/kg
Currently, there are no recom m endations for biphasic energy levels for pediatrics.
Medication (Drugs)
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Vasopressin: 40 units IV bolus single dose
Epinephrine—1:10,000 concentration; 1 m g IV bolus, repeat dose q3m in–q5m in: o
Epinephrine via ETT: 1:1,000 concentration; 2–2.5 m g diluted in 10 m L NS via ETT
Am iodarone—300 m g in 20–30 m L NS/D 5 W IV bolus, repeat 150 m g in 20–30 m L NS/D 5 W IV bolus q3m in–q5m in: o
Am iodarone infusion: 1 m g/m in for first 6 hours then 0.5 m g/m in for 18 hours, additional 150 m g in 100 m l D 5 W over 10 m in; repeat q10m in as needed. Max. cum ulative dose 2.2 g/24h
Lidocaine: 1–1.5 m g/kg IV bolus, repeat 0.5–.75 m g/kg IV bolus. Max. IV bolus dose is 3 m g/kg: o
Lidocaine via ETT: 2–4 m g/kg
o
Lidocaine infusion: 1–4 m g/m in (30 to 50 µg/kg/m in)
Magnesium sulfate: 1–2 g in 10 m L D 5 W IV bolus
Procainam ide: 20–50 m g/m in until arrhythm ia suppressed, hypotension, QRS widens by 50%, or a total of 17 m g/kg is reached: o
Procainam ide infusion: 1–4 m g/m in
Sodium bicarbonate: 1 m Eq/kg IV bolus
Follow each m edication with a 20 m L NS flush.
Pediatric Considerations
Epinephrine: 0.01 m g/kg (0.1 m L/kg of 1:10,000) IV/IO repeat with sam e dose q3m in–q5m in or give 0.1–0.02 m g/kg (or 0.1–0.02 m L/kg of 1:1000): o
Epinephrine via ETT: 0.1 m g/kg (0.1 m L/kg of 1:1000)
Am iodarone: 5 m g/kg IV/IO, m ay repeat 5 m g/kg; m ax. cum ulative dose 15 m g/kg/d
Pa ge 5 1 0
Lidocaine: 1 m g/kg IV/IO: o
Lidocaine infusion 20–50 µg/kg/m in
Magnesium sulfate: 25–50 m g/kg IV/IO up to 2 g
Follow each m edication with a 3–5 m L NS flush.
Follow-Up Disposition Admission Criteria All patients who survive need adm ission to the intensive/coronary care unit.
Discharge Criteria No patient who suffers a VF arrest m ay be discharged from the ED.
References 1. Am erican Heart Association Guidelines 2000 for Cardiopulm onary Resuscitation and Em ergency Cardiovascular Care. Circulation. 2000;102. 2. ArKern KG, Halperin HR, Field J. New Guidelines for Cardiopulm onary Resuscitation and Em ergency Cardiac Care. JAMA. 2001;285. 3. Blum FC. Adult Medical Resusciation. In: Howell J. et al. eds. Em ergency Medicine. Philadelphia, PA: WB Saunders, 1997 4. Cum m ins RO, ed. ACLS Provider Manual. Dallas, TX: Am erican Heart Association, 2001 5. Hazinski, MF, ed. PALS Provider Manual. Dallas, TX: Am erican Heart Association, 2002 6. Ewy GA. Cardiocerebral Resuscitation: The New Cardiopulm onary Resuscitation. Circulation. 2005;111:2134–2142. 7. Vilke GM, et al., The three-phase m odel of cardiac arrest as
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applied to ventricular fibrillation in a large, urban em ergency m edical services system . Resuscitation. March 2005;64(3):341–346.
Codes ICD9-CM 427.41
ICD10 149.1
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Ventricular Perito neal Shunts
Ventricular
Peritoneal Shunts Richard S. Krause
Basics Description
Obstruction: Shunt m alfunction im pairs drainage of cerebrospinal fluid (CSF): o
Increases intracranial pressure (ICP)
Rate of increase in ICP determ ines severity.
Overdrainage syndrom e:
o
Assum ing upright posture increases CSF outflow
o
Decreases ICP
o
Produces post-lum bar puncture like headache
Infection: o
A shunt is a foreign body.
o
Conduit between CSF and the peritoneal cavity
o
Staphylococcus epiderm idis and other staphylococcal species in 75% of infections
Slit ventricle syndrom e: o
Prolonged overdrainage causes decreased ventricular size.
o
Interm ittent increases in ICP owing to proxim al
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obstruction
Pediatric Considerations
If cranial sutures are open, CSF m ay accum ulate without m uch ICP increase: o
Produces relatively nonspecific signs and sym ptom s
Etiology
Genetic causes
Cerebral lesion or stroke
Post head traum a
Aneurysm
Meningitis.
Diagnosis Signs and Symptoms
Shunt obstruction: o
Headache, nausea
o
Malaise, general weakness, irritability
o
Decreased level of consciousness or com a
o
Increased head size or bulging fontanelle
o
New-onset seizures, increased seizure frequency
o
Autonom ic instability, decreased upward gaze
o
Apnea/Respiratory arrest
o
Papilledem a: rare
Overdrainage syndrom e: o
Severe headache, focal neurologic signs, m alaise, seizures, com a:
o
Signs and sym ptom s often postural
Rapid overdrainage m ay cause upward shift of the brainstem :
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Apnea, bradycardia
Syncope, hypotension
Laryngospasm
o
Subdural hygrom a or hem atom a
o
Chronic overdrainage
o
Pneum ocranium
Shunt infections: o
Fever (m ay be absent)
o
Meningeal signs
o
Local signs of infection (erythem a, swelling, tenderness)
o
Peritonitis
o
Infections usually occur soon after shunt placem ent (about 80% within 6 m onths).
Slit ventricle syndrom e: o
Episodic headache
o
Alternating periods of norm al behavior and lethargy
o
Headache, nausea, and vom iting
Essential Workup
Suspected shunt m alfunction: o
Manipulation of the pum ping cham ber:
Cham ber should com press easily and refill within 3 seconds.
Failure to com press easily im plies distal obstruction.
Failure to fill im plies proxim al obstruction.
Up to 40% of m alfunctioning shunts com press/fill norm ally.
o
Head CT
o
Shunt series:
Radiographs of skull, chest, abdom en
Aids in diagnosis of disconnection, m alposition,
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or kinking of shunt com ponents
Suspected infection: o
Aspiration of CSF from shunt reservoir (consultation with neurosurgeon):
May be perform ed using sterile technique and 23-gauge butterfly needle
Slowly aspirate 5–10 m L CSF for the studies noted below in the next section.
Tests Lab
Electrolytes, renal function, and glucose
Anticonvulsant levels
CBC
Suspected infection: o
Analysis of CSF from the shunt reservoir:
Send culture, cell count, gram stain, glucose, and protein levels.
CSF analysis m ay have norm al early result, especially with prior antibiotic treatm ent.
o
Blood cultures
Imaging
Cranial CT: o
Evaluate catheter position, ventricular size.
o
Subdural hem atom a or hygrom a
o
Other causes of elevated ICP:
Enlarged ventricles: shunt m alfunction
Sm aller ventricles: overdrainage
Ultrasound m ay be used to assess ventricular size and position of catheter tip.
Shunt m anom etry: o
High pressure >20 cm H 2 O im plies distal shunt
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obstruction
Differential Diagnosis
Seizure disorder (idiopathic, toxic, m etabolic)
Infections:
o
CNS infection not related to the shunt
o
System ic infections
Metabolic abnorm alities: o
Hypoglycem ia
o
Hyponatrem ia
o
Hypoxia
Intoxication/Poisoning
Head traum a
P.1201
Treatment Pre Hospital
Patients with shunt m alfunction are at risk for apnea and respiratory arrest.
Oxygen should be applied with close m onitoring of respiratory status.
If increased ICP is suspected, transport patient with head elevated to 30°.
Initial Stabilization Signs of im pending herniation:
Rapid-sequence intubation and controlled ventilation to Pco 2 about 35 m m Hg o
Pretreat with lidocaine (pediatric: plus atropine).
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o
Thiopental/Etom idate for induction
o
Succinylcholine m ay increase ICP a few m m Hg, although this m ay not be clinically significant.
o
Use only pretreatm ent dose of nondepolarizing agent if depolarizing agent chosen.
o
Nondepolarizing agents (vecuronium , rocuronium ) m ay be preferable.
Forced pum ping of shunt cham ber: o
Flush the device with 1-m L saline solution to rem ove distal obstruction.
o
Allow slow drainage of CSF from the reservoir to achieve pressure Table o f C o ntents > Ventricular Tachycardia
Ventricular
Tachycardia Daniel C. McGillicuddy
Basics Description
A wide-com plex tachydysrhythm ia with a quasi-random signal (QRS) >120 and a rate >100
Rapid and regular depolarization of the ventricles independent of the atria and the norm al conduction system
Re-entry: o
Structural heart disease m ost com m on
o
Seen in dilated cardiom yopathy, ischem ia, and infiltrative heart disease, previous m yocardial infarction, scarring
o
May be pharm acologically induced
o
Usually produces a regular and m onom orphic rhythm
Triggered autom aticity: o
Minority of ventricular tachycardia (VT)
o
Caused by repetitive firing of a ventricular focus
Torsades de pointes: o
Polym orphic form of VT
o
Alternating electrical polarity and am plitude
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o
Prolongation in repolarization necessary
o
Usually pharm acologically induced
Regardless of the m echanism , all VT m ay degenerate to ventricular fibrillation (VF).
Etiology
Wide com plex tachycardia: o
80% likelihood of being VT
o
20% supraventricular tachycardia (SVT) with a baseline left bundle branch block (LBBB) or aberrancy
Wide com plex tachycardia and a history of m yocardial infarction:
o
>98% likelihood of being VT
o
Age >35 years 80% risk of VT
o
Age 120 m illiseconds
Torsades de pointes: o
Polym orphic VT that rotates its axis every 10–20 beats
Criterion to determ ine VT: o
Atrial ventricular (AV) dissociation (present in 60–75%)
o
Fusion beats (P wave partially activates ventricle in advance of next VT cycle), capture beats (P wave totally activates ventricle)
o
Uniform m orphology (except in the case of torsades)
o
Extrem e axis deviation (–90 to +180 degrees)
o
QRS >140 m illiseconds, with right bundle branch block (RBBB) m orphology; or QRS >160 m illiseconds, with LBBB m orphology, but >160 suggests VT regardless of bunch branch m orphology
o
QRS concordance in the precordial leads
o
RBBB pattern with R> R’ is VT 50:1.
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o
LBBB pattern with Q or QS pattern is VT 50:1.
o
Brugada's criteria: (99% sensitivity, 97% specificity)
R-S interval absent in all precordial leads
R-S interval >100 m illiseconds in any precordial lead
o
AV dissociation
V-1 R wave >30 m illiseconds; R-S interval >70 m illiseconds, slurred, notched S
o
Wide QRS with LBBB in precordium
Indicators of SVT with aberrancy include: o
Norm al-axis QRS 140 m m Hg, systolic BP >220 m m Hg, diastolic BP >130 m m Hg) or
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hem orrhage/aneurysm /dissection, m yocardial or other end-organ dysfunction
Gastrointestinal: o
NPO
o
Antiem etics
Consultation: o
Neurology
o
Vascular interventional radiology for neuroangiography
Medication (Drugs)
Aspirin: 325 m g PO
Clopidogrel: 75 m g PO
Coum adin (dose for atrial fibrillation): 2–5 m g PO loading dose
Diphenhydram ine: 25–50 m g PO/IV q6h–q8h
Dopam ine (vasopressor dose): 5–10 m cg/kg/m in
Heparin (dose for atrial fibrillation): 50–60 U/kg IV bolus, then IV infusion at 12–18 U/kg/h for target PTT 50–70 seconds
Labetalol: 20–40 m g IV over 2 m inutes, then 40–80 m g IV q10m in (m ax. 300 m g IV)
Meclizine: 25 m g PO q8h–q12h
Nitroprusside: 0.25–10 m cg/kg/m in IV infusion (m ax. 10 m cg/kg/m in IV)
Ondansetron: 4 m g IV
Prom ethazine: 12.5–25 m g PO/PR/IV q6h–q8h
Ticlopidine: 250 m g PO
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Follow-Up Disposition Admission Criteria
Intensive care unit adm ission for: o
Altered m ental status with airway issues
o
Concurrent hem odynam ic instability
o
Malignant cardiac arrhythm ias
Adm it to hospital to identify or exclude etiologies of VB ischem ia and to prevent recurrence or progression to VB circulation cerebrovascular accident, especially in the following populations: o
Elderly
o
Inability to am bulate
o
Inability to tolerate oral intake
o
Inability to arrange (expeditious) outpatient follow-up
o
New or changing neurological deficit
o
Persistent dizziness
o
Syncope
o
Vascular risk factors
Discharge Criteria Consider discharge with outpatient follow-up in populations with the following:
None of above indications to consider adm ission
Alternative explanation for sym ptom atology
References 1. Caplan LR. Vertebrobasilar disease. In: Barnett HJM, Bogousslavsky J, Meldrium H, eds. Advances in Neurology. Philadelphia, PA: Lippincott William s & Wilkins, 2003;92:131–140. 2. Lang E, Afilalo M. Vertebrobasilar atherothrom botic disease.
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eMedicine. Updated July 2004. Available at http://www.em edicine.com /em erg/topic834.htm Accessed May 28, 2005 3. Love BB, Biller J. Neurovascular system . In: Goetz CG, ed. Textbook of Clinical Neurology. 2nd ed. Philadelphia, PA: Elsevier, 2003:395–423. 4. Savitz SI, Caplan LR. Vertebrobasilar Disease. N Engl J Med. 2005;352:2618–2626.
Codes ICD9-CM Transient cerebral ischem ia, 435 Vertebral artery syndrom e, 435.1 Acute, but ill-defined, cerebrovascular disease, 436 Other generalized ischem ic cerebrovascular disease, 437.1
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Vertigo
Vertigo
Jonathan S. Olshaker
Basics Description
“Dizzy― describes a variety of experiences, including:
o
Sensations of m otion
o
Weakness, fainting
o
Lightheadedness
o
Unsteadiness
o
Depression
o
True vertigo
Sensation of disorientation in space com bined with a sensation of m otion
Hallucination of m ovem ent either of the self or the external environm ent
Most patients have an organic basis for these sym ptom s.
Maintenance of equilibrium depends on interaction of three system s: visual, proprioceptive, and vestibular. Any disease that interrupts the integrity of above system s m ay give rise to vertigo.
Peripheral vertigo: o
Sudden onset
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o
Severe sym ptom s
o
Interm ittent episodes lasting seconds to m inutes, occasionally hours
o
Horizontal or horizontorotary nystagm us (also positional, fatigues, and suppressed by fixation)
o
Norm al neurologic exam
o
Som etim es associated hearing loss or tinnitus
Central vertigo: o
Gradual onset
o
Mild continuous sym ptom s
o
All varieties of nystagm us (horizontal, vertical, rotatory)
o
Absence of hearing loss
o
No positional association
o
Presence of neurologic findings m ost of the tim e
Etiology Peripheral
Benign paroxysm al positional o
Uncertain etiology
o
Dependent on head position
o
Fatigues
Acute labyrinthitis: o
Associated with hearing deficit
o
Sudden onset
o
May be serous, acute suppurative, toxic, or chronic
Ototoxic drugs: o
Am inoglycosides
o
Antim alarials
o
Erythrom ycin
o
Furosem ide
Mèniére disease
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o
Episodic vertigo, hearing loss, and tinnitus
o
Vestibular neuronitis
o
Severe vertigo and sym ptom s resolving over days to weeks
o
No hearing deficits
o
Highest incidence in third to fifth decade
Acoustic neurom a: o
Tum or of Schwann cells enveloping the eighth cranial nerve (CN VIII)
o
Develops into central cause
o
Progressive unilateral hearing deficits and tinnitus
o
May also involve CN V, VII, or X
Traum a: o
Rupture of tym panic m em brane, round window, labyrinthine concussion, or developm ent of perilym phatic fistula can all have severe sym ptom s.
Otitis m edia and serous otitis with effusion
Foreign body in ear canal
Central
Cerebellar hem orrhage: o
Neurosurgical em ergency
o
Sudden onset of headache, vertigo, vom iting, and ataxia
o
Visual paralysis to affected side
o
Ipsilateral CN VI paralysis
Vertebrobasilar artery insufficiency: o
Dysarthria
o
Ataxia
o
Num bness of the face
o
Hem iparesis, headache
o
Diplopia/Visual disturbances
o
Disturbances m ay be transient or exacerbated by
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m ovem ent of the neck. o
Consider in elderly patients with isolated new-onset vertigo without an obvious cause.
o
Can som etim es rapidly progress in the first 24–72 hours
Cerebellar infarction: o
Nausea
o
Vom iting
o
Ipsilateral nystagm us
o
Ataxia
Traum a: o
Vertiginous sym ptom s com m on after whiplash injury
o
Postconcussive syndrom e or dam age to labyrinth or CN VIII secondary to basilar skull fracture
o
Vertebral artery injury has been seen after chiropractic m anipulation.
Tem poral lobe epilepsy: o
Associated with hallucinations, aphasia, trancelike states, or convulsions
o
More com m on in younger patients
Vertebrobasilar m igraines: o
Prodrom e of vertigo, dysarthria, ataxia, visual disturbances, or paresthesias followed by headache
o
Often a fam ily history of m igraines or sim ilar attacks
Tum or
Multiple sclerosis: o
Onset between 20 and 40 years of age
o
All form s of nystagm us
o
May have abrupt onset of severe vertigo and vom iting
o
History of other vague and varying neurologic signs or sym ptom s
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Subclavian steal syndrom e: o
Exercise of an arm causing shunting of blood from vertebral and basilar arteries into the subclavian artery, resulting in vertigo or syncope
o
Secondary to a stenotic subclavian artery
o
Dim inished unilateral radial pulse or differential systolic blood pressure between arm s
Hypoglycem ia: o
Suspect in diabetic patient or any other patient with unexplained sym ptom s or m ental status change
Diagnosis Signs and Symptoms History
Does true vertigo exist?
Tim e of onset and the duration of vertigo
Are auditory sym ptom s present?
Are there associated neurologic sym ptom s?
Has there been head or neck traum a?
Past m edical history
Medication history
P.1207
Physical Exam
Auscultation of the carotid and vertebral arteries for bruits
Pulses and pressures in both arm s
Inspection of the ears: o
Evaluation of hearing (Weber and Rinne tests)
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o
Ocular assessm ent (pupils, fundi, visual acuity, nystagm us)
Cardiac auscultation
Full neurologic exam ination
Essential Workup
Ask patient to describe the sensation without using the word “dizzy.―
Determ ine whether the cause is a peripheral or a central process using patient's clinical presentation (see above).
Tests Lab Electrolytes, blood urea nitrogen, creatinine, glucose
Imaging
ECG for any suspicion of cardiac etiology
Head CT/MRI for evaluation of suspected tum or, central cause, or posttraum atic cause
MRI or angiography for suspected vertebrobasilar insufficiency
Differential Diagnosis
More likely when “dizziness― actually is lightheadedness or m alaise.
Diabetes m ellitus
Hypothyroidism
Drugs (e.g., alcohol, barbiturates, salicylates)
Hyperventilation
Cardiac (i.e., arrhythm ia, m yocardial infarction, or other etiologies of syncope); peripheral vascular disease (i.e., hypertension, orthostatic hypotension, vasovagal)
Infection/sepsis
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Treatment Initial Stabilization
ABCs
IV access for dehydration/vom iting
Monitor
Traum a evaluations as indicated
Finger-stick blood glucose
ED Treatment
Based on accurate diagnosis: o
Central etiologies require m ore aggressive workup than peripheral.
o
Neurosurgical intervention for cerebellar bleed
o
Sym ptom atic treatm ent for peripheral vertigo with appropriate follow-up
Adm inister m edication to control vertiginous sym ptom s—options:
o
Diphenhydram ine
o
Meclizine
o
Prom ethazine
o
Diazepam
Initiate IV antibiotics for acute bacterial labyrinthitis.
Medication (Drugs)
Diazepam (Valium ): 2.5–5 m g IV q8h or 2–10 m g PO q8h
Diphenhydram ine (Benadryl): 25–50 m g IV, IM, or PO q6h
Meclizine (Antivert): 25 m g PO q6h PRN
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Prom ethazine (Phenergan): 12.5 m g IV q6h or 25–50 m g IM, PO, or PR q6h
Follow-Up Disposition Admission Criteria
Cerebellar infarct/hem orrhage
Vertebrobasilar insufficiency
Acute suppurative labyrinthitis
Intractable nausea/vom iting
Inability to am bulate
Discharge Criteria
Patient with peripheral etiology and stable
Issues for referral o
Prim ary care or otolaryngology follow-up for all
o
Otolaryngology follow-up for suspected acoustic neurom a or perilym phatic fistula
References 1. Derebery MD. The diagnosis and treatm ent of dizziness. Med Clin North Am . 1999;83:10. 2. Gizzi M, Riley E, Molinari S. The diagnostic value of im aging the patient with dizziness. Arch Neurol. 1996;53:1299–1304. 3. Gom ez CR, et al. Isolated vertigo as a m anifestation of vertebrobasilar ischem ia. Neurology. 1996;47:94–97. 4. Herr R, Zun L, Mathews JJ. A directed approach to the dizzy patient. Ann Em erg Med. 1989;18:6:664–672. 5. Olshaker S. Vertigo. In: Marx J, et al., eds. Rosen's em ergency m edicine: concepts and clinical practice. St. Louis, MO: CV Mosby,
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2006: 142–149. 6. Rathore S et al. Characterization of Incident Stroke Signs and Sym ptom s: findings from the Atherosclerosis Risk in Com m unities Study. Stroke. Novem ber 2002;33(11):2718–2721. 7. Wolf JS, et al. Success of the m odified Epley m aneuver in treating benign paroxysm al/vertigo. Laryngoscope. 1999;109:900.
Miscellaneous SEE ALSO: Dizziness; Labyrinthitis
Codes ICD9-CM 780.4
ICD10 R42
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Vio lence, M anagem ent o f
Violence,
Management of Richard Wolfe Robert Vissers
Basics Description
ED is likely to be scene of violent episodes owing to 24-hour access.
First contact of victim s and perpetrators of violence
High prevalence of intoxicated patients and psychiatric patients
Only reliable predictors: o
Male gender
o
Alcohol or drug abuse
No difference exists in: o
Ethnicity
o
Language
o
Age
o
Education
o
Em ploym ent status
o
Medical diagnosis
Etiology
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Functional: o
Psychiatric
o
Schizophrenia
o
Affective
o
Antisocial
o
Borderline
o
Paranoid
o
Adjustm ent disorders
o
Antisocial behavior
Organic: o
CNS related
o
Delirium
o
Dem entia
o
Infection
o
Seizures
o
Cerebrovascular accident
o
Head injury
o
Metabolic
o
Hypoglycem ia
o
Hypoxia
o
Hypotherm ia or hypertherm ia
o
Endocrine disorders
o
Drugs
o
Alcohol and sedatives (withdrawal, intoxication)
o
Cocaine
o
LSD
o
Phencyclidine
o
Anticholinergics
o
Steroids
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Diagnosis Alert
Restrain potentially violent patients.
Seek police aid in control of violent or dangerous patients.
Signs and Symptoms Behaviors suggesting im pending violence:
Provocative behavior
Anger
Pacing
Loud speech
Tense posture
Pounding, clenching of fists
Essential Workup
Identify prodrom es of violence: o
Begins with anxiety
o
Then defensiveness
o
Then physical aggression
History: o
Previous threats and violence
o
Psychiatric history
o
Substance abuse
o
Self-m utilation
o
Verbal threats
o
Plans of violence
Physical: o
Focus on identifying and distinguishing associated functional and m edical conditions.
o
Pay careful attention to findings during neurologic and m ental status exam s and note vital signs.
o
Must often be perform ed with the patient under
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restraints
Tests Lab
Com plete blood chem istry if suspected infectious cause for behavior.
Electrolytes, blood urea nitrogen, creatinine, glucose if m etabolic or toxic etiology suspected.
Drug screen if ingestion likely.
Imaging CT head for altered m ental status or head traum a
Treatment Pre Hospital Restrain violent patients and seek police assistance if necessary.
Initial Stabilization
Prevention of violence: o
o
Deterrence:
Signs stating weapons not perm itted
Visible security personnel
Metal detectors
Secure single public entrance
Triage to an appropriate assessm ent room :
Sparse, solid walls
Lockable
Visible
Exits clear of obstruction
Equipm ent free
Panic button
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o
Never underestim ate the potential for violence.
o
ED protocols for violent situations
o
Educate staff on preventing, recognizing, and dealing with potentially violent situations.
Approaching the potentially violent patient: o
Im m ediately assess safety.
o
Call security and em ploy physical or chem ical restraint if the patient is violent or threatening, or if there is an im m ediate perceived danger.
o
Rem ove any potential weapons before interview.
o
Maintain open exit for patient and physician.
o
Maintain distance of 6–8 feet.
o
Allow patient to ventilate.
o
Develop therapeutic alliance.
o
Be nonjudgm ental; m ake peace offering.
o
Use subm issive posture:
o
Avoid eye contact.
Leave im m ediately and initiate seclusion or restraint if there is any destabilization of situation or patient behavior.
ED Treatment Verbal de-escalation:
Situation can be verbally controlled, particularly if situational precipitant can be identified.
Isolation:
Tem porarily isolate patient in an appropriate room before m ore definitive restraint, or to prevent leaving.
Physical restraints: o
Required for patient's safety, the safety of others, and to allow physical exam ination
o
Perform ed by several trained personnel, by protocol, with clear docum entation of indications and rechecks
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Chem ical restraint: o
Least restrictive and potentially therapeutic P.1209
o
Before applying physical restraints, patients should be offered voluntary chem ical sedation.
o
Cooperative patients should receive a com bination of an oral benzodiazepine (lorazepam ) and an oral antipsychotic (risperidone).
o
If uncooperative, patients often require physical restraint first.
o
Initial treatm ent should be a m onotherapy using one of the following:
Benzodiazepines (lorazepam , m idazolam )
Conventional antipsychotic (droperidol, haloperidol)
Consider droperidol instead of haloperidol if rapid sedation desired.
o
May use com bination if single agent ineffective
o
Adm inister every 15–30 m inutes until desired effect reached.
o
Side effects of neuroleptics include:
Dystonic reactions (treat with diphenhydram ine or benztropine)
Neuroleptic m alignant syndrom e (rare)
QT prolongation and torsades de pointes (rare)
Duty to warn:
Doctor can owe a duty to warn a third party when that third party is in danger because of the m edical or psychologic condition of the patient.
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Medication (Drugs)
Benztropine: 2 m g IM or IV
Diphenhydram ine: 50 m g IV, IM, or PO
Droperidol: 2.5–5 m g IV or IM
Haloperidol: 5–10 m g IV or IM; 0.5–2 m g for elderly people
Lorazepam : 1–2 m g IV, IM, or PO
Midazolam : 1–2 m g IV, IM, or PO
Risperdal: 1–m g PO
Follow-Up Disposition Admission Criteria
Violence secondary to an associated organic cause that is not tem porary or reversible in the ED
Psychiatric adm ission: o
Violent psychiatric patient requires psychiatric consultation.
o
Patient is considered to be a danger to either self or others.
o
Involuntary com m itm ent if uncooperative
Discharge Criteria Violent behavior was caused by a tem porary, reversible organic cause (drug or alcohol intoxication), and the patient is now deem ed to be in control, com petent, and not a danger to self or others:.
Psychiatric consultation before discharge recom m ended
If violent act is owing to antisocial behavior, rather than an organic or psychiatric condition, patient m ay be
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discharged into police custody, with the warning that the patient m ay be a danger to self or others.
References 1. Blanchard JC, Curtis KM. Violence in the em ergency departm ent. Em erg Med Clin North Am . 1999;17:717–731. 2. Hill S, Petit J. The violent patient. Em erg Med Clin North Am . 2000;18:301–315. 3. Lukens TW, Wolf SJ, Edlow JA, et al. Clinical policy: critical issues in the diagnosis and m anagem ent of the adult psychiatric patient in the em ergency departm ent. Ann Em erg Med. 2006;47(1):79–99. 4. Spivak HR, Prothrow-Stith D. Addressing Violence in the Em ergency Departm ent. Clinical Pediatric Em ergency Medicine. 2003;4(2):135–140.
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Visual Lo ss
Visual Loss
Camie J. Sorensen Pascal Juang
Basics Description
Decrease in visual function (i.e., visual acuity, visual fields, blurry vision)
Visual loss has m any etiologies and can be caused by m ultiple body system s.
Etiology
Visual system : o
Eyelid or tear film abnorm ality
o
Anterior segm ent (cornea, anterior cham ber, iris, lens)
o
Posterior segm ent (vitreous, retina, optic nerve)
o
Posterior to the eye (optic nerve, chiasm , radiations)
Neurologic: o
Cerebral (cerebrovascular accident [CVA]) or intracranial pathology (m ass lesion)
o
Multiple sclerosis
o
Optic neuritis
o
Migraine
Cardiovascular system :
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o
Em bolic
o
Throm botic
o
Ischem ic
o
Hypertensive events
Im m unologic system : o
Infectious including HIV optic neuropathy or cytom egalovirus (CMV) retinitis
o
Autoim m une causes (uveitis, tem poral arteritis)
Endocrine: o
Diabetic retinopathy
o
Thyroid disease m ay cause diplopia (m uscle hypertrophy) or corneal erosions.
Toxic: o
Methanol (acute severe loss, subacute optic atrophy)
o
Licorice (transient loss, self-lim ited)
o
Digitalis (flashing lights, color changes)
o
Am iodarone (rare cause of optic neuropathy)
Diagnosis
Categorize visual loss by the properties associated with the decrease in visual function.
Transient (24 hours): o
o
o
Sudden and painless:
Artery or vein occlusion
Vitreous hem orrhage
Retinal detachm ent
Optic neuritis
Tem poral arteritis
Gradual and painless (weeks to years):
Cataract
Presbyopia
Refraction errors
Open-angle glaucom a
Chronic retinal disease
Macular degeneration
Diabetic retinopathy
CMV retinopathy
CNS tum or
Painful:
Corneal abrasion or ulcer
Angle closure glaucom a
Optic neuritis
Iritis/uveitis
Keratoconus with hydrops
Monocular: pathology anterior to optic chiasm
Binocular: pathology posterior to optic chiasm
Associated with system ic neurologic sym ptom s of visual field defects: o
CVA (especially posterior or occipital circulation)
o
Mass lesion (pituitary adenom as, aneurysm , m eningiom a, other tum ors)
Malingering
Signs and Symptoms
Pa ge 5 1 5
Flashing lights
New floaters
Decreased vision
Afferent papillary defect
Visual field defects
Eye pain
Lim itation or pain with eye m ovem ents
Conjunctival injection or discharge
Corneal opacity
Cataract
Optic nerve head swelling
Pale retina with a cherry-red spot
Carotid bruits
Neurologic sym ptom s consistent with intracranial or vascular process
Heart m urm ur
History Key elem ents to determ ine:
Acute or gradual onset?
Length of sym ptom s?
Transient vision loss or perm anent?
Binocular or m onocular?
Degree of vision loss?
Painful or painless? o
Other com orbidities
Physical Exam
Ophthalm ologic: o
Visual acuity
o
Pupil exam
o
Confrontational visual field exam
o
Extra-ocular m uscle function
Pa ge 5 1 5
o
Slit-lam p exam ination
o
Funduscopy
o
Tonom etry
Cardiovascular: o
Murm urs
o
Carotid bruits
Neurologic exam : o
Optic chiasm and intracerebral lesions
o
Occipital and posterior circulation lesions
General: o
Manifestations of im m une, endocrine, or toxic disorders
Essential Workup Thorough history and physical exam ination as already discussed
Tests Lab May be obtained to determ ine extent of other com orbidity in association with vision loss (i.e., diabetes, cardiovascular disease)
Imaging
Tests should be directed toward the suspected etiology of visual loss.
Dilated fundus exam m ay be perform ed to assess for posterior segm ent disease.
Erythrocyte sedim entation rate and tem poral artery biopsy m ay be obtained if tem poral arteritis is suspected.
Brain CT, MRI, MR angiography and transcranial Doppler m ay be used to evaluate neurologic sym ptom s and vertebrobasilar artery flow.
Carotid and carotid ultrasound should be obtained urgently if a retinal artery occlusion is diagnosed.
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Differential Diagnosis
Traum a
Neurologic lesion
Infectious
Cardiovascular
Toxic/Metabolic
Autoim m une
P.1211
Treatment
Direct therapy toward cause of visual loss.
Ophthalm ology consultation for visual loss with an uncertain diagnosis
Two conditions for which treatm ent m ust begin in m inutes: o
Central retinal artery occlusion
o
Chem ical burn
Central Retinal Artery Occlusion
Clinical criteria: o
Unilateral, painless, acute loss of vision
o
Afferent papillary defect
o
Pale fundus with a cherry-red spot
o
Counting fingers to light perception in 94% of patients
Therapy: o
Im m ediate ophthalm ology consultation
o
Maneuvers and m edications to lower intra-ocular pressure, allowing the em bolus to m ove to the
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periphery o
Ocular m assage: direct pressure to eye for 5–15 seconds then sudden release, repeat for 15 m inutes
o
Acetazolam ide: 500 m g IV or PO
o
Topical beta-blocker (tim olol or levobunolol 0.5%) b.i.d.
o
Anterior cham ber paracentesis by an ophthalm ologist
o
Referral for cardiac and carotid artery work-up
o
Rule-out tem poral arteritis.
Chemical Burn
Clinical criteria: o
Alkali worse than acids
o
White eye worse than red eye (white eye indicates that vessels have already sloughed while red eye m eans vessels are intact)
o
Treat m ace, cem ents, plasters, solvents.
Therapy: o
Copious irrigation of the eyes with LR or NS (nonsterile water is acceptable if others not available); irrigate for m inim um of 30 m inutes
o
Do not try to neutralize acids with alkalis or vice versa.
o
Moist cotton-tipped applicator to sweep furnaces of residual chem ical precipitants
o
Dilate with cycloplegic (atropine, cyclopentolate, tropicam ide).
o
Do not use phenylephrine; it will vasoconstrict already ischem ic conjunctival blood vessels.
o
Erythrom ycin ointm ent every 1–2 hours while awake
o
Artificial tears every 1 hour
o
Check intra-ocular pressure.
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Medication (Drugs)
Antibiotic drops: o
Ciprofloxacin 0.3%: 1–2 gtt qh1–q6h
o
Gentam icin 0.3%: 1–2 gtt q4h
o
Ofloxacin 0.3%: 1–2 gtt q1h–q6h
o
Levofloxacin 0.5%: 1–2 gtt q2h
o
Polym yxin (Polytrim ): 1 gtt q3h–q6h
o
Sulfacetam ide 10%, 0.3%: 1–2 gtt q2h–q6h
o
Tobram ycin 0.3%: 1–2 gtt q1h–q4h
o
Trifluridine 1%: 1 gtt q2h–q4h
Antibiotic ointm ents: o
Bacitracin: 500 units/g ½-inch ribbon of ointm ent q3h–q6h
o
Ciprofloxacin 0.3%: ½-inch ribbon of ointm ent q6h–q8h
o
Erythrom ycin 0.5%: ½-inch ribbon of ointm ent q3h–q6h
o
Gentam icin 0.3%: ½-inch ribbon of ointm ent q3h–q4h
o
Neosporin: ½-inch ribbon of ointm ent q3h–q4h
o
Polym yxin (Polysporin): ½-inch ribbon of ointm ent q3h–q4h
o
Sulfacetam ide 10%: ½-inch ribbon of ointm ent q3h–q8h
o
Tobram ycin 0.3%: ½-inch ribbon of ointm ent q3h–q4h
o
Vidarabine: ½-inch ribbon of ointm ent 5 tim es/day
Mydriatics and cycloplegics: o
Atropine 1%, 2%: 1–2 gtt per day to q.i.d.
o
Cyclopentolate 0.5%, 1%, 2%: 1–2 gtt PRN dilation
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o
Hom atropine 2%: 1–2 gtt b.i.d.–t.i.d.
o
Phenylephrine 0.12%, 2.5%, 10%: 1–2 gtt t.i.d.–q.i.d.
o
Tropicam ide 0.5%, 1%: 1–2 gtt PRN dilation
Corticosteroid–antibiotic com bination drops (with ophthalm ology consultation): o
Blepham ide (prednisolone): 1–2 gtt q1h–q8h
o
Cortisporin (hydrocortisone; neom ycin sulfate; bacitracin zinc; polym ysin B sulfate): 1–2 gtt q3h–q4h
o
Maxitrol (dexam ethasone; neom ycin sulfate; polym yxin B sulfate): 1–2 gtt q1h–q8h
o
Pred-G (prednisolone acetate; gentam icin sulfate): 1–2 gtt q1h–q8h
o
TobraDex (dexam ethasone; tobram ycin; chlorobutanol): 1–2 gtt q2h–q26h
Glaucom a agents (always with ophthalm ology consultation): o
Acetazolam ide: 250–500 m g PO per day to q.i.d.
o
Betaxolol 0.25%, 0.5%: 1–2 gtt b.i.d.
o
Carteolol 1%: 1 gtt b.i.d.
o
Dipivefrin 1%: 1 gtt b.i.d.
o
Levobunolol 0.25%, 0.5%: 1 gtt per day to b.i.d.
o
Mannitol: 1–2 g/kg IV over 45 m inutes
o
Pilocarpine 0.25%, 0.5%, 1%, 2%, 3%, 4%, 6%, 8%, 10%: 1–2 gtt t.i.d.–q.i.d.
Only if m echanical closure is ruled out o
Tim olol 0.25%, 0.5%: 1 gtt b.i.d.
Follow-Up
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Disposition Admission Criteria
Ruptured globe
Hyphem a (depending on severity)
Significant cardiac, carotid, or neurologic disease
Unexplained, progressive vision loss
Discharge Criteria If the diagnosis is certain and visual loss will not progress
References 1. Kunim oto DY, Kanitkar KD, Makar MS. The Wills Eye Manual: Office and Em ergency Room Diagnosis and Treatm ent of Eye Disease. 4th ed. Lippincott William s and Wilkins, 2004. Website: http://www.eyeatlas.com
Miscellaneous SEE ALSO: Chalazion; Conjunctivitis; Corneal Abrasion; Corneal Burn; Corneal Foreign Body; Dacryocystitis; Globe Rupture; Hordeolum; Hyphem a; Iritis; Red Eye; Optic Artery Occlusion; Optic Neuritis; Orbital Cellulitis; Ultraviolet Keratitis; Vitreous Hem orrhage
Codes ICD9-CM 369.9
ICD10 H54.7
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Vitreo us Hem o rrhage
Vitreous
Hemorrhage David Harter
Basics Description Vitreous hem orrhage is a secondary diagnosis; identification of a specific cause is necessary for successful treatm ent:
Retinal vessel tear secondary to vitreous separation
Sudden tearing of vessels owing to traum a
Spontaneous bleeding owing to neovascularization
Etiology
Blunt or penetrating traum a
Retinal break/tear/detachm ent
Any proliferative retinopathy
Diabetes m ellitus
Sickle cell disease
Retinal vein occlusion
Eales disease
Senile m acular degeneration
Retinal angiom atosis
Retinal telangiectasia
Peripheral uveitis
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Subarachnoid or subdural hem orrhage
Intra-ocular tum or
Diagnosis Signs and Symptoms
Sudden painless unilateral loss or decrease in vision
Appearance of dark spots (floaters) in visual axis: o
Above findings som etim es accom panied by flashing lights; floaters m ove with head m ovem ents.
Blurred vision, decreased visual acuity
Loss of red reflex
Inability to visualize fundus
Mild afferent papillary defect
Essential Workup
History with special attention to pre-existing system ic disease and traum a
Com plete ocular exam including: o
Slit lam p
o
Tonom etry
o
Dilated funduscopic exam
Tests Lab
CBC
Prothrom bin tim e/partial throm boplastin tim e/international norm alized ratio if indicated
Electrolytes, blood urea nitrogen, creatinine, glucose
Imaging
B-scan ultrasound when no direct retinal view is possible
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to rule out retinal detachm ent or intraocular tum or
Fluorescein angiography to define the cause
CT scan/anteroposterior/lateral orbital film s to rule out intra-ocular foreign body
Differential Diagnosis
Vitreitis (leukocytes in the vitreous)
Retinal detachm ent without hem orrhage
P.1213
Treatment Initial Stabilization
Bed rest with head of bed elevated
No activity resem bling Valsalva m aneuvers (lifting, stooping, or heavy exertion)
ED Treatment
Urgent ophthalm ologic consultation is needed with treatm ent based on the cause of the hem orrhage; an exam ination is carried out by the consultant: o
Laser photocoagulation or cryotherapy for proliferative retinal vascular diseases
o
Repair retinal detachm ents.
Avoid nonsteroidal anti-inflam m atory drugs, aspirin, and other anticlotting agents.
Delayed vitrectom y is needed for blood that does not clear with tim e.
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Follow-Up Disposition Admission Criteria Retinal break or detachm ent
Discharge Criteria Retinal break or retinal detachm ent m ust be excluded as cause of hem orrhage.
References 1. Duguid G. Managing ocular flashes and floaters. Practitioner. 1998;242:302–304. 2. Ferrone PJ, de Juan E. Vitreous hem orrhage in infants. Arch Ophthalm ogy. 1994;112:1185–1189. 3. Hutcheson K, Nguyen A, Preslan M. et. al. Vitreous Hem orrhage in Patients with High-risk Retinopathy of Prem aturity. Am J Optham ol. 2003;136:258–263 4. Rhee DJ, Pyfer MF. The Wills Eye Manual: Office and Em ergency Room Diagnosis and Treatm ent of Eye Disease. 3rd ed. Philadelphia, PA: Lippincott William s & Wilkins; 1999. 5. Shingleton BJ, O'Donoghue MW. Blurred vision.N Engl J Med. 2000;343:556–562.
Codes ICD9-CM 379.23 Vitreous hem orrhage
ICD10 H43.1
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Vo lvulus
Volvulus
Ann Buchanan
Basics Description
Axial twist of a portion of the gastrointestinal (GI) tract around its m esentery causing partial or com plete obstruction of the bowel
Anatom ic predisposition: redundant/freely m obile segm ent, with close approxim ation of points of fixation of bowel
Precipitated by pathologic distention of the colon
Blood supply com prom ised by venous congestion, leading to gangrene of the bowel and potential infarction due to arterial obstruction
Etiology
Third m ost com m on cause of colonic obstruction (10–15%) following tum or and diverticular disease
Sigm oid (75%): o
Due to redundant sigm oid colon with narrow m esocolon base
o
Most com m on in:
Elderly
Institutionalized
Pa ge 5 1 6
o
Chronic bowel m otility disorders
Psychiatric diseases
Associated with chronic constipation and concom itant laxative use
Cecal volvulus (22%): o
More com m on in young adults
o
Due to im proper congenital fusion of the m esentery with the posterior parietal peritoneum , causing the cecum to be freely m obile in varying degrees
o
Associated with increased gas production (m alabsorption and pseudoobstruction)
o
Can be seen in pregnancy and after colonoscopy
Transverse colon and splenic flexure (3%)
Gastric volvulus (rare) associated with diaphragm atic defects
Pediatric Considerations
Midgut volvulus: o
Due to congenital m alrotation in which the m idgut fails to rotate properly in utero as it enters the abdom en
o
Entire m idgut from the descending duodenum to the transverse colon rotates around its m esenteric stalk, including the superior m esenteric artery.
o
Com m on in neonates (75% 1 year old)
o
Sudden onset of bilious em esis (97%) with abdom inal pain
o
May have previous episodes of feeding problem s/bilious em esis
o
In children >1 year old, associated with failure to thrive, alleged intolerance to feedings, chronic interm ittent vom iting, bloody diarrhea
Pa ge 5 1 6
o
Constipation
o
Mild distention since obstruction higher in GI tract
o
May not appear toxic based on degree of ischem ia
Diagnosis Signs and Symptoms History
Bowel obstruction: o
Colicky, cram ping abdom inal pain (90%)
o
Abdom inal distention (80%)
o
Obstipation (60%)
o
Nausea and vom iting (28%)
Cecal volvulus: o
Sudden onset of pain and distention
o
Asym m etric abdom inal distention
Sigm oid volvulus: o
More insidious onset
Gastric volvulus: o
Triad of Brochard: severe epigastric distension, intractable wretching, inability to pass nasogastric tube (NGT, 30% of patients)
Physical Exam
Presence of gangrenous bowel: o
Increased pain
o
Peritoneal signs: guarding, rebound, and rigidity
o
Fever
o
Blood on digital rectal exam
o
Tachycardia and hypovolem ia
Cecal volvulus:
Pa ge 5 1 6
o
Often a palpable m ass in the left upper quadrant/m id-abdom en
Essential Workup Plain abdom inal radiograph:
Suggestive but often inconclusive
Diagnostic finding present in 20,000) suggests strangulation with infection/peritonitis.
Electrolytes, blood urea nitrogen, creatinine, glucose: o
Anion gap acidosis due to lactic acidosis
o
Prerenal azotem ia due to dehydration
Urinalysis: o
Elevated specific gravity and ketones
Imaging
Barium enem a o
“Bird's beak― deform ity at the site of torsion
o
Perform cautiously owing to perforation risk.
o
May be therapeutic
Upper GI series: o
Abrupt ending or corkscrew tapering of contrast seen
Pa ge 5 1 7
CT scan: o
“Whirl― sign in cecal volvulus
o
May be useful in sigm oid volvulus to determ ine extent of obstruction
Ultrasound: o
Abnorm al position of the superior m esenteric vein
o
“Whirlpool― sign of volvulus: vessels twirled around the base of the m esentery
Pediatric Considerations
Diagnosis of m idgut volvulus: o
Duodenum lies entirely to the right of the spine on plain film s.
o
“Double-bubble― sign on an upright film due to distended stom ach and proxim al duodenal loop
o
Established by upper GI swallow: coiled spring/corkscrew appearance of jejunum in the right upper quadrant
Pediatric Considerations
Colic
Henoch Schönlein purpura
Necrotizing enterocolitis
P.1215
Alert
Evaluate any child with signs/sym ptom s of obstruction (including bilious vom iting and abdom inal pain) for m alrotation, even if they appear nontoxic.
Delay in diagnosis >1–2 hours results in gangrenous bowel necessitating large resection and leading to perm anent parenteral nutrition with its associated
Pa ge 5 1 7
com plications.
Differential Diagnosis
Obstruction due to colonic tum or or diverticulitis
Sm all bowel obstruction
Ileus
Intussusception
Appendicitis, pelvic inflam m atory disease and salpingitis, especially for cecal volvuli
Ovarian torsion
Treatment Initial Stabilization
ABCs
Aggressive fluid resuscitation with 0.9% NS bolus of 20 m L/kg (peds) or 2 L bolus (adult)
NGT
Foley catheter
ED Treatment
Obtain surgical consultation.
Prepare patient for the operating room .
Correct hypovolem ia and electrolyte abnorm alities.
Preoperative broad-spectrum antibiotics, if suspected sepsis or perforation
Definitive Therapy Sigmoid Volvulus
Nontoxic patient: o
Reduce volvulus nonoperatively with sigm oidoscopy:
60% successful
Pa ge 5 1 7
o
40–50% recurrence
Follow with elective sigm oid resection and prim ary anastom osis ( Table o f C o ntents > Vo m iting, Pediatric
Vomiting,
Pediatric Mark A. Hostetler
Basics Description
Forceful retrograde expulsion of gastric contents through the m outh; characterized by nausea, retching, and em esis; no gastric contents are expelled during retching.
Em esis results from sustained contraction of abdom inal m uscles and diaphragm ; at the sam e tim e, the pylorus and antrum contract.
Etiology Mechanism
Gastrointestinal (GI)/Mechanical: gastroesophageal reflux (GER), m econium ileus, necrotizing enterocolitis, hypertrophic pyloric stenosis, intussusception, m alrotation with m idgut volvulus, Hirschsprung disease, congenital obstructions (atresias, stenoses, and webs), hernia, foreign body/bezoar, paralytic ileus
Metabolic/Endocrine: inborn errors of m etabolism (am ino acidurias, fatty acid oxidation disorders, urea cycle
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defects), urem ia, congenital adrenal hyperplasia, kernicterus
Neurologic: CNS bleeding (often due to traum a), tum or, hydrocephalus
Infectious: otitis m edia, urinary tract infection (UTI), pneum onia, sepsis, m eningitis/encephalitis
Feeding problem s: chalasia, im proper technique (overfeeding, im proper position), m ilk allergy
Other: toxicologic, nonaccidental traum a
Diagnosis Signs and Symptoms
General: o
Appearance variable depending on the underlying cause
o
Signs of dehydration, including tachycardia, tachypnea, pallor, decreased perfusion, and shock
o
Altered m ental status m ay occur secondary to shock, hypoglycem ia, or extra-abdom inal conditions (sepsis, inborn error of m etabolism , increased intracranial pressure, toxicologic poisoning)
Vom iting characteristics: o
Assess color, com position, onset, progression, and relationship to intake and position.
o
Nonbilious em esis is caused by a lesion proxim al to the pylorus.
o
Bilious (green) em esis indicates obstruction below the am pulla of Vater; in infants, bilious em esis is associated with a m ore serious underlying condition (m alrotation, volvulus, intussusception, bowel
Pa ge 5 1 8
obstruction); m ay also be due to adynam ic ileus or sepsis. o
Bloody em esis involves a lesion proxim al to the ligam ent of Treitz; bright red bloody em esis has little or no contact with gastric juices due to an active bleeding site at or above cardia.
o
“Coffee-ground― em esis results from reduction of hem e by gastric juices.
o
Feculent odor suggests lower obstruction or peritonitis.
o
Undigested food in em esis suggests an esophageal lesion or one at or above the cardia.
o
GER: begins shortly after birth, rem ains relatively constant, usually with norm al weight gain
o
Hypertrophic pyloric stenosis: begins insidiously at 3–4 weeks and progresses, becom ing increasingly forceful (projectile) after feedings
o
Obstruction and/or ischem ic bowel (m alrotation with m idgut volvulus, intussusception, necrotizing enterocolitis): sudden onset associated with rapid progression to appearing ill out of proportion to the duration of illness; abdom en distended and tender.
Abdom inal: o
Distention suggests obstruction.
o
Peritoneal signs suggest perforation.
Com plications: o
Aspiration
o
Mallory-Weiss tear
o
Boerhaave syndrom e
Essential Workup Exclude life-threatening causes of vom iting.
Pa ge 5 1 8
Tests Lab As indicated by differential considerations:
Metabolic assessm ent (glucose, electrolytes)
Infection assessm ent (CBC, culture—urine)
Pregnancy tests for fem ales of childbearing age
Imaging
Evaluation/Treatm ent of hypovolem ia and hypoglycem ia
As indicated by differential considerations
Abdom inal radiographs (flat plate, upright and decubitus) helpful for evaluation of obstruction or perforation
Pelvic and abdom inal ultrasound for evaluation of hypertrophic pyloric stenosis, intussusception, appendicitis as well as pelvic pathology
Abdom inal CT scan helpful for evaluation of appendicitis, m ass/tum or often requiring contrast
Differential Diagnosis
Neonate/infant: o
GI/Mechanical: GER, m econium ileus, necrotizing enterocolitis, hypertrophic pyloric stenosis, intussusception, m alrotation with m idgut volvulus, Hirschsprung disease, congenital obstructions (atresias, stenoses, and webs), hernia, foreign body/bezoar, paralytic ileus
o
Metabolic/Endocrine: inborn errors of m etabolism (am ino acidurias, fatty acid oxidation disorders, urea cycle defects), urem ia, congenital adrenal hyperplasia, kernicterus
o
Neurologic: CNS bleeding (often due to traum a), tum or, hydrocephalus
Pa ge 5 1 8
o
Infectious: otitis m edia, UTI, pneum onia, sepsis, m eningitis/encephalitis
o
Feeding problem s: chalasia, im proper technique (overfeeding, im proper position), m ilk allergy
o
Other: toxicologic, nonaccidental traum a
Child/adolescent: o
GI: gastroenteritis, obstruction (hernia, adhesions, intussusception, foreign body, bezoar), pancreatitis, appendicitis, peritonitis, paralytic ileus, traum a (duodenal hem atom a)
o
Metabolic/Endocrine: diabetic ketoacidosis, urem ia, adrenal insufficiency
o
Infectious: gastroenteritis, UTI, sinusitis, upper respiratory infection, sepsis, m eningitis, encephalitis, pneum onia, hepatitis
o
Neurologic: CNS m ass/tum or, CNS bleeding (often due to traum a), cerebral edem a, concussion, m igraine, kernicterus
o
Other: toxicologic, (nonaccidental) traum a, pregnancy, bulim ia
P.1219
Treatment Pre Hospital Not applicable
Initial Stabilization
Fluid resuscitation with 0.9% NS IV; caution if concern
Pa ge 5 1 8
about increased intracranial pressure
Determ ine bedside finger-stick glucose.
ED Treatment
Continue fluid resuscitation and correction of electrolyte im balance if present.
Decom press stom ach with nasogastric or orogastric tube if abdom en distended or vom iting persistent.
Continue evaluation for underlying cause.
Consider antiem etic m edications.
Surgical consultation if acute abdom en; antibiotics if peritonitis or other system ic infection present
Medication (Drugs)
Antiem etics helpful once the underlying cause of vom iting has been determ ined; less frequently used in young children.
Antiem etic options in children: o
Metoclopram ide: 10 m g (0.1 m g/kg/dose) PO q6h
o
Ondansetron: 4–8 m g (0.1 m g/kg/dose) IV q6h
o
Prochlorperazine: 2.5–5 m g (0.1 m g/kg/dose) IV, IM, or PR q6h
o
Prom ethazine: 12.5–25 m g (0.25 m g/kg/dose) PO, PR, or IM q6h
Follow-Up Disposition Admission Criteria
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Unstable vital signs, including persistent tachycardia or other evidence of hypovolem ia
Serious etiologic condition
Inability to exclude serious etiologic conditions
Intractable vom iting or inability to take oral fluids
Inadequate social situation or follow-up
Discharge Criteria
Stable; able to tolerate oral fluids
Benign etiology considered m ost likely
Serious or potentially im portant etiologies excluded
Parental understanding of instructions to advance clear liquids slowly and return for continued vom iting, abdom inal distention, decreased urination, fever, lethargy, or unusual behavior
References 1. Hostetler MA, Bracikowski A. Gastrointestinal disorders. In: Marx JA, Hockerberger RS, Walls RM, et al., eds. Em ergency m edicine: concepts and clinical practice. 5th ed. St. Louis, MO: Mosby, 2000:2296–2315. 2. Hostetler MA, Schulm an M. Necrotizing enterocolitis presenting in the em ergency departm ent: case report and review of differential considerations for vom iting in the neonate. J Em erg Med. 2001;21(2):165–170. 3. Irish MS, Pearl RH, Caty MG, et al. The approach to com m on abdom inal diagnoses in infants and children. Pediatr Clin North Am . 1998;45(4):729–772. 4. Kim ura K, Loening-Baucke V. Bilious vom iting in the newborn: rapid diagnosis of intestinal obstruction. Am Fam Physician. 2000;61(9):2791–2798. 5. Pearl RH, Irish MS, Caty MG, et al. The approach to com m on abdom inal diagnoses in infants and children. Part II. Pediatr Clin
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North Am . 1998;45(6):1287–1326.
Codes ICD9-CM 787.03
ICD10 P92.0
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Vo n Willebrand Disease
Von Willebrand
Disease Matthew Kippenhan
Basics Description
Coagulopathy caused by deficiency or dysfunction of von Willebrand Factor (vWF)
vWF functions: o
Mediates platelet-endothelial cell adhesion
o
Carrier protein for factor VIII
Genetics
Majority of cases are inherited—m ultiple genetic defects identified.
Type 1—quantitative defect of vWF: o
70% of cases
o
Autosom al dom inant
o
vWF deficiency results from decreased synthesis and increased clearance of protein.
o
Manifestation ranges from asym ptom atic to m oderate bleeding.
Type 2—qualitative defect of vWF: o
10–15% of cases
Pa ge 5 1 9
o
Divided into types 2A, 2B, 2M, 2N—all are autosom al dom inant except 2N.
o
Decrease in interm ediate and high m olecular weight m ultim er
o
2N—decreased binding to factor VIII:
Leads to decreased levels of VIII and thus m ore serious coagulopathy
Type 3—absent or severe deficiency in am ount of vWF: o
Rare disease—one per m illion cases
o
Autosom al dom inant
o
Severe coagulopathy
vWD genetically associated with sickle cell disease, hem ophilia A, factor XII deficiency, hereditary hem orrhagic telangiectasia, and throm bocytopenia
Etiology
In addition to genetic causes, acquired form s exist.
Multiple m echanism s:
o
vWF antibody production
o
Decreased synthesis
o
Proteolysis
o
Increased clearance from binding to tum or cells
Seen in association with the following: o
Malignancy:
Wilm s tum or
Multiple m yelom a
Chronic lym phocytic leukem ia
Non-Hodgkin lym phom a
Chronic m yelogenous leukem ia
Waldenstrom m acroglobulinem ia
Monoclonal gam m opathy of uncertain significance
o
Im m unologic:
Pa ge 5 1 9
o
o
System atic lupus erythem atosus
Rheum atoid arthritis
Medication induced:
Valproic acid
Ciprofloxacin
Hetastarch
Griseofulvin
Miscellaneous:
Hypothyroidism
Urem ia
Hem oglobinopathies
Cirrhosis
congenital heart disease
Dissem inated intravascular coagulation
Diagnosis Signs and Symptoms
Sym ptom s vary dependent on type of disease.
Many type 1 and som e type 2 are asym ptom atic, severe type 2 and type 3 are sym ptom atic: o
Easy bruising
o
Menorrhagia
o
Recurrent epistaxis
o
Gum bleeding
o
Gastrointestinal bleeding
o
Soft-tissue bleeds and hem arthroses
o
Prolonged or excessive procedural bleeding
Pregnancy Considerations
Pregnancy causes increased vWF levels in patients with
Pa ge 5 1 9
types 1 and 2 disease.
Pregnancy, labor, and delivery are usually uncom plicated.
vWF levels fall quickly after delivery: o
Patients m ay suffer postpartum bleeding 10–28 days after delivery.
History
Most often diagnosed in pediatric and adolescent populations
Fam ily history
Minor/Moderate recurrent m ucosal bleeding m ost com m on historical clue
Physical Exam
Most will have norm al exam .
Multiple, large bruises
Deep-tissue hem atom as, hem arthroses
Essential Workup
Screen and refer for testing if historical concerns or consistent physical findings.
For type 1 diagnosis, patient m ust have significant m ucocutaneous bleeding, laboratory confirm ation, and fam ily history of type 1 disease.
Tests Lab
CBC: norm al platelet count
Prothrom bin tim e: norm al
Partial throm boplastin tim e: o
Mildly prolonged in 50%
o
Due to low factor VIII levels or co-existent factor deficiency
Measurem ent of vWF level and activity:
Pa ge 5 1 9
o
Ristocetin activity—uses platelet agglutination to determ ine vWF function
o
vWF antigen—tests for vWF level in serum using rabbit antibodies
Bleeding tim e: o
May be norm al in type 1 (50%); prolonged in types 2 and 3
o
Not specific and hard to reproduce; has fallen out of favor for diagnosis
Differential Diagnosis
Hem ophilia A, B
Platelet defects
Use of antiplatelet drugs—aspirin, NSAIDS
Platelet-type pseudo vWD
Bernard-Soulier syndrom e
P.1221
Treatment Pre Hospital Direct pressure for control of hem orrhage
Initial Stabilization Resuscitation with crystalloid and packed RBCs as needed
ED Treatment
Desm opressin acetate (DDAVP): o
Prom otes release of vWF from endothelial cells, increases factor VIII levels
Pa ge 5 1 9
o
Maxim al levels obtained at 30–60 m inutes, with duration of 6–8 hours
o
Effective for type 1; variable effectiveness for type 2; not indicated for type 3
o
Patients m ay use intranasal spray at hom e before m enses or m inor procedures.
vWF replacem ent therapy: o
Hum ate—P Factor VIII concentrate with vWF:
Treated to reduce virus transm ission risks
Indicated for type 3 vWD and severe bleeding in all types
Doses, length of treatm ent depend on severity of bleeding.
o
Fresh frozen plasm a, cryoprecipitate:
Less desirable because they carry infection risk
Antifibrinolytic therapy: o
Am inocaproic acid (Am icar) and trasexam ic acid (Cyklokapron)
o
Block plasm in form ation to prevent clot degradation
Topical agents—applied directly to bleeding site: o
Gelfoam or Surgicel soaked in throm bin
o
Micronized collagen
o
Fibrin sealant
Avoid antiplatelet agents.
Medication (Drugs)
Am inocaproic acid—50–60 m g/kg PO/IV q4h–q6h
Cryoprecipitate—10–12 units initial dose or 2–4 bags/10 kg
DDAVP—desm opressin: o
0.3 m cg/kg IV, m ax. 20 m cg
Pa ge 5 1 9
o
0.3 m cg/kg SQ, m ax. 20 m cg
o
300 m cg intranasal
o
Peds: Table o f C o ntents > Warfarin/C o um adin Overdo se
Warfarin/Coumadin Overdose John Bailitz
Basics Description
Most com m only prescribed oral anticoagulant: o
Inhibits regeneration of vitam in K cofactor required for hepatic carboxylation of factors II, VII, IX, and X
o
Blocks the coagulation cascade's extrinsic system and com m on pathway
o
Com m only used for venous throm boem bolism and prevention of em bolism with prosthetic heart valves or atrial fibrillation
o
Adjustm ents based on the international norm alization ratio (INR)
Typical therapeutic range 2.0–3.0
2.5–3.5 for m echanical valves and antiphospholipid syndrom es:
o
Contraindications include any condition in which the risk of hem orrhage or adverse reaction outweighs clinical benefit.
Prior hypersensitivity
Skin reactions
Pa ge 5 2 0
Recent surgeries
Active or potential gastrointestinal (GI), intracerebral, or genitourinary (GU) bleeding
Fall risk
Etiology
Many factors including age, other drugs, diet, and com orbidities affect INR/bleeding versus throm boem bolism : o
o
Increase INR:
Multiple antibiotics
NSAIDs
Propranolol
Prednisone
Cim etidine
Influenza vaccine
Gingko biloba
Garlic
Cancer
Collagen vascular disease
Congestive heart failure
Age
Liver disease
Decrease INR:
Carbam azepine
Haloperidol
St. John Wart
Hereditary Coum adin resistance
Hyperlipidem ia
15% of patients have bleeding com plications/year; 4.9% m ajor, up to 0.8% fatal, m ost com m only intracranial hem orrhage (ICH): o
Risk of bleeding directly related to INR
Pa ge 5 2 0
Increases dram atically above 4.0
Inversely related to tim e spent in therapeutic range:
o
Risk factors for bleeding:
Age >75 years
Past GI bleeding
Hypertension, cerebrovascular disease, severe heart disease
Renal insufficiency
Alcoholism
Occult GI and GU m alignancies
Pregnancy Considerations
Warfarin: o
Pregnancy class X
o
Crosses the placenta causing spontaneous abortion and birth defects
Diagnosis Signs and Symptoms
Presentation m ay be occult or dram atic: o
High index of suspicion required to detect potentially life-threatening com plications
Com plications occur in sub- and supratherapeutic INR range
Subtherapeutic/Low INR: breakthrough throm bosis
Therapeutic and Supratherapeutic: GI, CNS, retroperitoneal bleeding
Skin necrosis: o
Classic lesions of coum adin skin necrosis begin on the
Pa ge 5 2 0
third to eighth day of therapy resulting from capillary throm bosis in subcutaneous fat. o
Associated with protein C deficiency, but m ay occur with protein S deficiency and in patients with norm al levels
o
Eschar in center differentiates lesions from ecchym osis due to excess coum adin therapy
Essential Workup
Thorough history: o
Many chief com plaints are com plicated by anticoagulation.
Reason for anticoagulation, recent dose changes, com pliance, recent INR testing, other prescriptions, over the counter, and alternative m edicines
Subtle changes in m ental status, recent “m inor falls,― or bleeding
Exam ine for vital sign abnorm alities: o
Early hem orrhagic shock
o
Hypertension and bradycardia m ay be secondary to Cushing response in ICH.
o
Cardiac m eds often m ask im portant changes in vital signs.
Exam ine carefully for: o
Pallor, contusions, abrasions, ecchym osis, and skin lesions
o
Check stool for blood.
Tests Lab
Prothrom bin tim e/partial throm boplastin tim e/INR: o
Significant bleeding m ay occur even in INR
Pa ge 5 2 0
therapeutic range. o
PTT also elevated with toxicity
CBC: o
HCT inaccurate m easure of acute rapid bleeding
o
Platelets
Aspirin and ADP inhibitors/Plavix result in norm al platelet levels but qualitative deficits.
Electrolytes, blood urea nitrogen (BUN), creatinine, glucose:
o
Evaluate renal function.
o
Elevated BUN m ay indicate blood in GI tract.
Type and cross-m atch
Imaging Low threshold for CT im aging to detect occult but life threatening bleeding:
Head CT: o
Minor m echanism s of blunt head traum a without loss of consciousness
o
Detect ICH presenting with only m ild sym ptom s of headache and nausea before the classic gradual progression of sym ptom s to focal deficits and com a
Abdom inal CT: o
Blunt abdom inal traum a without significant tenderness
o
For retroperitoneal hem orrhage
Differential Diagnosis
All causes of bleeding: o
GI, retroperitoneal, CNS, and traum atic
Skin lesions—hem orrhagic skin disorders: o
Hem ostatic deficits such as platelet disorders
o
Vascular purpuras including glucocorticoid use,
Pa ge 5 2 0
vitam in C deficiency, purpura fulim nans, dissem inated intravascular coagulation, Henoch-Schönlein purpura, protein C deficiency P.1223
Treatment Pre Hospital
ABCs
Treat hypotension with two large-bore IV lines and 0.9% NS infusion.
Cardiac and pulse oxim etry m onitoring
Initial Stabilization
Establish central IV access for hypotension not responsive to initial fluid bolus: o
Com pressible sites only
Replace lost blood as soon as possible: o
Initiate with O-negative blood until type-specific blood available.
o
10 m L/kg bolus in children
ED Treatment
Specific m anagem ent depends on the INR, presence of bleeding, reason for anticoagulation, and reliability of patient: o
o
INR 9 without significant bleeding:
Hold Coum adin and give vitam in K 5–10 m g PO; INR will be substantially lowered in 24–48 hours
o
INR >20 with m inor or life-threatening bleeding:
Hold Coum adin
Vitam in K 10 m g by slow IV infusion
Fresh frozen plasm a (FFP) 3–4 units, or prothrom bin com plex concentrate or recom binant factor VIIa depending on volum e status and availability
In the setting of controlled bleeding, m aintain the INR at the lower level of therapeutic efficacy: o
1.5–2.0 for atrial fibrillation
o
2.0–2.5 with a m echanical heart valves
Medication (Drugs)
Vitam in K1 Phytonadione: o
Side effects:
Anaphylaxis with IV > IM or PO
Subcutaneous absorption unpredictable
IM adm inistration m ay result in hem atom a form ation.
Breakthrough throm boem bolism with com plete correction
High-dose vitam in K1 risks prolonged warfarin
Pa ge 5 2 0
resistance and m ay precipitate throm boem bolism for up to 1 week o
10 m g IV infusion over 10 m inutes is recom m ended for life threatening active bleeding with effects beginning in 1–2 hours
FFP: o
Traditionally 3–4 units of FFP (1 L) are given to control continued bleeding in the short term without excessive risk of throm boem bolism .
o
Patient response is variable and m ay not correlate with correction of the INR.
o
Side effects:
Virus transm ission
Fluid overload
Prothrom bin com plex concentrate (PCC): o
PCC is a fractionation product of FFP containing equal am ounts of factors II, VII, IX, and X.
o
Long shelf life and easy reconstitution into a highly concentrated volum e (500–1,000 U/20 cc versus 1 L of FFP per dose)
o
Rapid and quick reversal without volum e overload where available
o
o
Side effects:
Throm bosis
Less virus transm ission then FFP
For patients with an INR of 2.0–3.9, adm inister 25 U/kg, 4.0–5.9, 35 U/kg, and >6.0, 50 U/kg
Recom binant factor VIIa: o
Produces a rapid “throm bin burst― reducing INR and bleeding
o
No risk of virus transm ission
o
Sm all volum e
Pa ge 5 2 0
o
Single bolus of 15–90 µg/kg bodyweight
o
Side effects:
Throm bosis rare
Expensive
Follow-Up Disposition Admission Criteria
Active GI, retroperitoneal, or CNS bleeding
Anticoagulated traum a patient with evidence of active bleeding requires: o
Reversal of anticoagulation and blood replacem ent
o
Early surgical consultation for operative intervention
o
Transport to a level one-traum a center after initial stabilization for definitive care.
Skin necrosis requires adm ission for anticoagulation with alternative agents in consultation with a hem atologist.
Subtherapeutic patient m ay require adequate anticoagulation with inpatient heparin or low m olecular weight heparin to prevent a breakthrough throm boem bolism : o
Outpatient Lovenox therapy followed by increased coum adin with close follow-up prevents unnecessary hospitalization
o
Daily average risk or throm boem bolism low for m ost indications
Discharge Criteria
Asym ptom atic reliable patient with a supratherapeutic INR after consideration of:
Pa ge 5 2 0
o
Indication for anticoagulation, reason for supratherapeutic level, underlying com orbidities, overall risk of bleeding, fall risk, social situation, reliability, and availability of follow up
Asym ptom atic anticoagulated patient with m inor traum a, therapeutic INR, stable hem oglobin, norm al im aging studies, and reliable caretakers, discharge with close follow up.
References 1. Ansell J, Hirsh J. Pharm acology and m anagem ent of the Vitam in K antagonists. Chest. 2004;204S–233S. 2. Deveras RA, Kessler K. Reversal of warfarin induced excessive anticoagulation with recom binant factor VIIa concentrate. Ann Intern Med. 2002;137:884–889 3. Levine MN, Raskob G. Hem orrhagic Com plications of Anticoagulant Treatm ent. Chest 2004;126;287S–310S.
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Warts
Warts
Gary M. Vilke
Basics Description
Condylom a acum inata, also known as genital warts or venereal warts
Self-lim iting benign epithelial tum ors lasting m onths to years
Etiology
Hum an papillom avirus (HPV), usually subtypes 6 and 11
May produce laryngeal papillom atosis in infants from viral exposure at birth
Transm itted by direct sexual contact, contact with contam inated objects, and autoinoculation
Linked to carcinom a of the penis, vulva, anus, and cervix
Diagnosis Signs and Symptoms
Pedunculated growths, often with cauliflowerlike appearance
Pa ge 5 2 1
Flesh-colored to slightly pigm ented or red
In m en, usually on glans penis, shaft, scrotum , or anus
In wom en, found on labia, vagina, cervix, or anus
May extend into urethra, bladder, or rectum
Can develop in m outh or throat if oral sexual contact
Essential Workup
Diagnosis m ade by characteristic appearance of lesions: o
If difficult to see, add acetic acid to suspected area, which will cause infected areas to whiten and becom e m ore visible.
o
Biopsy and viral typing not recom m ended for typical lesions.
o
Biopsy indicated if failing therapy, patient im m unocom prom ised, warts are pigm ented, indurated, fixed, or ulcerated
Screen for other sexually transm itted diseases.
Tests Lab Pregnancy test for fem ales
Differential Diagnosis
Condylom a latum (secondary syphilis)
Herpes sim plex
Prom inent glands around head of penis
Benign or m alignant neoplasm
Molluscum contagiosum
Treatment Initial Stabilization
Pa ge 5 2 1
None required
ED Treatment
If available m ay use im iquim od, podofilox, podophyllin, trichloroacetic acid, or alternative therapies listed below.
Alternative treatm ents: o
Cryotherapy with liquid nitrogen or dry ice
o
Electrocautery
o
Laser therapy
o
Surgical excision
o
Interferon for use by subspecialists
Provide appropriate referral.
P.1225
Medication (Drugs)
Im iquim od cream : apply three tim es/week for up to 16 weeks: o
Cream m ay weaken diaphragm s and condom s.
Podofilox 0.5% gel or solution: o
Apply twice daily for 3 days, then rest 4 days; m ay repeat for four cycles
o
Do not use on perianal, rectal, urethral or vaginal lesions.
Podophyllin 15–25% in benzoin: weekly topical application: o
Protect surrounding norm al tissue with petroleum jelly.
o
Wash off 1–4 hours later
o
Do not use in pregnancy—highly toxic and
Pa ge 5 2 1
teratogenic. o
Do not use on cervix, vagina, or anal canal as m ay cause dysplastic changes.
Trichloroacetic acid, topical 60–90%: o
Wash off 6–10 hours later.
o
May be repeated weekly
Follow-Up Disposition Admission Criteria
Dissem inated cases in im m unocom prom ised patients m ay require adm ission.
Discharge Criteria Most patients can be treated as outpatients.
References 1. Centers for Disease Control and Prevention. Sexually transm itted diseases treatm ent guidelines. MMWR. 2002;51:1–78. 2. Kodner CM, Nasraty S. Managem ent of genital warts. Am Fam Physician 2004;70:2335–2342. 3. Maw R. Critical appraisal of com m only used treatm ent for genital warts. Int J of STD & AIDS. 2004;15:357–364.
Codes ICD9-CM 078.19
ICD10 B07
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Weakness
Weakness
Jason Imperato
Basics Description
Defined as a decrease in physical strength or energy
Often m ultifactorial
Distinguish neurom uscular disorder versus nonneurom uscular disorder
Categories of neurom uscular disorders: o
o
o
Upper m otor neuron (UMN) lesions:
Deep tendon reflexes (DTR) increased
Plantar reflexes upgoing
Increased m uscle tone
Muscle atrophy absent
Lower m otor neuron (LMN) lesions:
DTRs decreased to absent
Plantar reflexes absent or norm al
Decreased m uscle tone
Muscle atrophy present
Fasciculations
Neurom uscular junction (NMJ) lesions:
DTRs norm al
Plantar reflexes norm al or absent
Pa ge 5 2 1
Decreased m uscle tone
Categories of nonneurom uscular disorders: o
Infectious
o
Endocrine
o
Metabolic
o
Cardiac
o
Rheum atologic
o
Toxic
o
Psychiatric
Etiology Neuromuscular Disorders
UMN lesions: o
Multiple sclerosis
o
Am yotrophic lateral sclerosis
o
Transverse m yelitis
o
Poliom yelitis
LMN lesions: o
Guillain-Barre syndrom e
o
Toxic neuropathies
o
Im pingem ent syndrom es
o
Diphtheria
o
Porphyria
o
Seafood toxins
NMJ lesions: o
Myasthenia gravis
o
Lam bert-Eaton syndrom e
o
Botulism
o
Periodic paralysis
o
Tick paralysis
o
Electrolyte im balances
Nonneuromuscular Disorders
Pa ge 5 2 1
Dehydration
Anem ia
Malignancy
Cerebrovascular accident
Head or neck traum a
Myocardial ischem ia
Infection/sepsis:
o
Urinary tract infection
o
Pneum onia
o
Meningitis
o
Mononucleosis
o
HIV
Endocrine abnorm alities: o
Hypothyroidism
o
Adrenal crisis
o
Periodic paralyses
Rheum atologic disorders: o
System ic lupus erythem atosus
o
Polym yalgia rheum atica
Toxins: o
Medications
o
Environm ental
o
Carbon m onoxide poisoning
o
Cocaine
o
Alcohol
Psychiatric: o
Sim ple fatigue
o
Chronic fatigue syndrom e
o
Fibrom yalgia
o
Anxiety
o
Malingering
Pa ge 5 2 1
Diagnosis Signs and Symptoms Altered Physical Strength
Assessm ent of strength: o
1: No contraction
o
2: Active m ovem ent with gravity elim inated
o
3: Active m ovem ent against gravity
o
4: Active m ovem ent against gravity and resistance
o
5: Norm al power
Change in m uscle tone: o
Flaccidity
o
Spasticity
o
Rigidity
Abnorm al DTRs
Abnorm al plantar reflexes
Muscle atrophy: o
Difference of >1 cm in the leg and thigh and >0.5 cm in the forearm and arm
Systemic Findings
Weakness
Fatigue
Dizziness
Paresis
Paresthesias
Hoarse voice
Dysphagia
Visual changes
Confusion
Associated sym ptom s:
Pa ge 5 2 1
o
Fever
o
Chest pain
o
Dyspnea
o
Cough
o
Weight loss
o
Rash
o
Dysuria
o
Upper respiratory infection sym ptom s
Essential Workup Clinical suspicion gathered through history and physical exam guides further testing:
Generalized versus focal
Acute versus chronic
Proxim al versus distal
Ascending versus descending
Sym m etric versus asym m etric
Im proved versus worsened with activity
Tests Diagnostic testing should be broad unless history and physical exam identify the cause of weakness.
Lab
Serum glucose
CBC
Electrolytes
Blood urea nitrogen and creatinine
Toxin screen
Urinalysis
Thyroid function tests (r/o hypothyroidism )
Erythrocyte sedim entation rate (r/o rheum atologic cause)
Carboxyhem oglobin (r/o CO poisoning)
P.1227
Pa ge 5 2 1
Imaging
EKG (r/o acute coronary syndrom e)
Chest radiograph (r/o pneum onia)
CT head or MRI head (r/o intracranial pathology)
Diagnostic Procedures/Surgery
Bedside spirom etry: o
Forced vital capacity, negative inspiratory force, peak expiratory flow rate
o
May identify those with im pending ventilatory failure
Lum bar puncture: o
In suspected Guillain-Barré syndrom e:
Album in-cytologic dissociation in cerebrospinal fluid (protein >400, WBC Table o f C o ntents > West Nile Virus
West Nile Virus
Malik Mamta
Basics Description Infectious agent is arbovirus that is m em ber of the Flaviviridae fam ily.
Etiology
Vector-borne virus
Transm itted by infected m osquitoes late sum m er/early fall
Wild birds are prim ary reservoir hosts.
Introduced to Western Hem isphere 1999
Infection after blood transfusion and solid organ transplant can occur.
Case reports of occupational exposure and infection of lab workers via percutaneous inoculation exist.
Pregnancy Considerations Infection via transplacental transm ission and breast-feeding has been reported.
Diagnosis
Pa ge 5 2 2
Variable severity of illness: o
80% asym ptom atic
o
20% m ild sym ptom s, flulike illness
o
Approxim ately 1/150 with CNS involvem ent (encephalitis, m eningitis)
Incubation period is usually 2–6 days, but can be up to 14 days in average patient, up to 21 days in im m unocom prom ised patients.
Sym ptom s are sudden onset and last 38°C, 100°F
Hepatosplenom egaly
Musculoskeletal:
Pa ge 5 2 2
o
Hem atologic: o
Nuchal rigidity
Lym phadenopathy
Derm atologic: o
Rash (m aculopapular or m orbilliform on neck, trunk, extrem ities)
Cardiovascular: o
Myocarditis (rare)
Ophthalm ologic: o
Optic neuritis
o
Vitritis
o
Chorioretinitis
Essential Workup Most sensitive screening test is serologic testing of cerebrospinal fluid (CSF) and serum for IgM antibody-capture enzym e-linked im m unosorbent assay [ELISA] and culture:
Can be detected during first 4 days of illness, and nearly all tests are positive by day 7–8; m ay rem ain positive up to 1 year after infection
Procedures for subm itting sam ples vary by state.
Refer to local public health departm ent for guidelines.
Tests Lab
CSF: o
Pleocytosis with lym phocyte predom inance
o
Elevated protein
o
Norm al glucose
CBC: o
WBC m ay be m ildly elevated (50%) or norm al.
o
Leukopenia m ay be present (15%).
o
Anem ia can occur.
Pa ge 5 2 2
Chem istry: o
Hyponatrem ia som etim es seen:
Cause uncertain, possibly syndrom e of inappropriate antidiuretic horm one (SIADH) when CNS involvem ent exists
o
Pancreatitis (rare)
o
Fulm inant hepatitis (rare)
Imaging
CT head usually norm al
MRI can be useful to identify CNS inflam m ation: o
One third of patients show abnorm ality.
o
Im aging findings generally nonspecific, but m ay include enhancem ent of leptom eninges and/or periventricular white m atter or can m im ic dem yelinating process
Diagnostic Procedures/Surgery Lum bar puncture P.1229
Differential Diagnosis
Other causes of m eningitis: o
Bacterial
o
Viral
o
Tuberculous
o
Fungal
Other causes of viral encephalitis: o
Other arboviruses, especially St. Louis encephalitis virus
o
Enterovirus, particularly in patients 16 years and younger
Pa ge 5 2 2
o
Herpes sim ple virus (HSV)
o
Cytom egalovirus (CMV)
o
Epstein-Barr virus (EBV)
o
Mum ps virus
o
Varicella-zoster virus
o
Rabies virus
Intracranial abscess
CNS vasculitis
Nonspecific viral syndrom e
Gastroenteritis
Treatment Initial Stabilization
ABCs
Seizure precautions
ED Treatment
Supportive care
IV fluids for signs of dehydration
For signs of m eningitis, adm inister antibiotics pending results of CSF.
Consider acyclovir if index of suspicion for only treatable cause of viral encephalitis, HSV, is high.
Adm inister antipyretics and pain m edications.
No known effective antiviral therapy or vaccine
No controlled studies proving effectiveness of Interferon-α2b, ribavirin, corticosteroids, anticonvulsants, or osm otic agents
Pa ge 5 2 2
Follow-Up Disposition Admission Criteria
Neurologic sym ptom s
Dehydration
Concerning risk factors (advanced age, im m unocom prom ise)
Discharge Criteria
No signs of CNS involvem ent (encephalitis, m eningitis)
Able to tolerate oral solutions
References 1. Hayes EB, O'Leary DR. West Nile virus infection: a pediatric perspective. Pediatrics. 2004;113:1375–1381. 2. Nash D, Mostashari F, Fine A, et al. The outbreak of West Nile virus infection in the New York City area in 1999. N Engl J Med. 2001;344:1807–1814. 3. Petersen LR, Marfin AA, Gubler DJ. West Nile virus. JAMA. 2003;290:524–528. 4. Ravindra KV, Freifeld AG, et al. West Nile virus-associated encephalitis in recipients of renal and pancreas transplants: case series and literature review. Clin Infect Dis. 2004;38:1257–1260. Epub 2004 Apr 14. 5. Solom on T, Ooi MH, et al. West Nile encephalitis. Br Med J. 2003;326:865–869. 6. West Nile Virus: Inform ation and Guidance for Clinicians. Available at http://www.cdc.gov/ncidod/dvbid/westnile/clinicians. 7. Zak I, Altinok D, et al. West Nile virus infection. AJR Am J Roentgenol. 2005 Mar;184(3):957–61. Review
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Miscellaneous SEE ALSO: Meningitis; Encephalitis
Codes ICD9-CM 066.4
Pa ge 5 2 2
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Wheez ing
Wheezing
Stephen K. Epstein
Basics Description
Result of turbulent airflow: o
High-pitched sound with dom inant frequency at 400 Hz:
Gas flowing through constricted airways analogous to a vibrating reed
o
Resonant vibration of the bronchial walls when airflow velocity reaches critical values
Caused by airway narrowing between 2 and 5 m m : o
Wheezing is very low pitched with airway diam eters of 5 m m .
o
Airways of Table o f C o ntents > Wilm s†™ Tum o r
Wilms’ Tumor
Joseph H. Kahn
Basics Description
Solid tum or (nephroblastom a) of the kidney, accounting for 6–8% of childhood solid tum ors in the United States
Incidence: 7 cases per m illion children per year
Mean age at diagnosis: 3.2 years (m edian: 2.6 years; range: 3 m onths to 16 years)
Equal m ale-to-fem ale ratio
Overall 5-year survival: 89.5%
Relapse rate: 22%
Stages (10-year survival):
o
I: Lim ited to kidney (94%)
o
II: Spread by direct extension (86%)
o
III: Spread via lym phatic drainage (71%)
o
IV: Spread via hem atogenous m etastasis (36%)
o
V: Involves both kidneys
Favorable versus unfavorable histology: o
10-year survival with unfavorable histology is 36%
Genetics
Denys-Drash syndrom e (pseudoherm aphroditism , severe glom erulopathy, Wilm s tum or)
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WAGR syndrom e (Wilm s tum or, aniridia, genitourinary m alform ation, m ental retardation)
5–10% of Beckwith-Wiedem ann syndrom e (hem ihypertrophy, m acroglossia, om phalocele, viscerom egaly) has Wilm s tum or.
Etiology Abnorm al proliferation of m etanephric blastem a without norm al differentiation into tubules and glom eruli
Diagnosis Signs and Symptoms History
Abdom inal pain
Gross hem aturia
Physical Exam
Abdom en: o
Abdom inal m ass that is usually sm ooth and 5–10 cm in size
Usually does not cross m idline
Vital signs: o
Hypertension (60%) due to renal ischem ia from tum or pressure on the renal artery
o
Uncom m only, hypertension m ay be due to renin-secreting Wilm s tum or.
Cardiac/Pulm onary: o
Congestive heart failure (CHF) m ay be present.
Alert
Com plications:
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o
Before surgery: m assive bleeding from ruptured tum or, “acute abdom en,― bowel obstruction
o
After nephrectom y: bowel obstruction (5.1%), urinary tract infection (UTI), pneum onia, hem orrhage (1.9%), vascular injury (1.5%)
o
During and after chem otherapy: neutropenia with fever, renal insufficiency, anem ia, throm bocytopenia, hepatotoxicity, venoocclusive disease of liver (VOD)
o
VOD seen in 4.9% of patients receiving vincristine and actinom ycin-D
o
Associated with throm bocytopenia
o
Can cause liver failure with ascites and elevated international norm alized ratio (INR)
o
Acquired von Willebrand syndrom e is rarely associated with Wilm s tum or.
Essential Workup
Urinalysis: hem aturia in 25% of patients
Ultrasound can identify m ass and distinguish cystic from solid tum or.
Tests Lab
Renal function tests
CBC
INR/partial throm boplastin tim e
Imaging
CT or MRI scan of abdom en to diagnose and stage the disease
Chest radiograph and chest CT scan evaluating for m etastases
Diagnostic Procedures/Surgery
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See Treatm ent
Differential Diagnosis
Infection: UTI
Anatom ic: urinary tract anom aly, hydronephrosis, renal cyst
Neoplasm : neuroblastom a, renal cell carcinom a, sarcom a, lym phom a
Treatment Initial Stabilization Resuscitation as appropriate, including m anagem ent of hypertension, CHF, anem ia, renal failure
ED Treatment Pediatric oncologic/genitourinary referrals after initiating diagnostic evaluation P.1233
Definitive Treatment Surgical rem oval of affected kidney m ay consider partial nephrectom y for sm all tum ors with favorable histology:
Chem otherapy reflecting type and stage: o
Stage I with favorable histology: vincristine or vincristine plus actinom ycin D
o
Stage II with favorable histology: sam e agents with longer course than stage I
o
Stages III and IV with favorable histology and any stage with unfavorable histology: radiation and
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vincristine and actinom ycin D plus doxorubicin
Follow-Up Disposition Admission Criteria
Hypertension, CHF
Renal insufficiency
Significant anem ia
Pulm onary findings
Poor com pliance
Lack of tim ely follow-up
Discharge Criteria
Norm al blood pressure
Norm al renal function
Near-norm al hem atocrit
Norm al cardiac and pulm onary exam ination
Reliable parents
Rapid follow-up available
Issues for Referral
Pediatric oncology referral
Pediatric genitourinary referral
References 1. Czauderna P, Katski K, Kowalczyk J, et al. Venoocclusive liver disease (VOD) as a com plication of Wilm s’ tum our m anagem ent in the series of consecutive 206 patients. Eur J Pediatr Surg. 2000;10:300–303. 2. Grundy RG, Hutton C, Middleton H, et al. “Outcom e of patients with stage III or inoperable Wilm s’ Tum or treated on the second
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United Kingdom Wilm s’ Tum or protocol (UKWT2).― Pediatric Blood and Cancer. 2004;42:311–319. 3. Haecker FM, von Schweinitz D, Harm s D, et al. “Partial nephrectom y for unilateral Wilm s tum or: results of study SIOP 93-01/GPOH.― J Urol. 2003;170:943–944. 4. Hartm an DJ, MacLennan GT. “Wilm s Tum or.― The Journal of Urology. 2005;172:21–47. 5. Ritchey ML, Sham berger RC, Haase G, et al. Surgical com plications after prim ary nephrectom y for Wilm s’ tum or: report from the National Wilm s’ Tum or Study Group. J Am Coll Surg. 2001;192:63–68. 6. Wong W, Mauger D. “Treatm ent of Wilm s tum or-related hypertension with losartan and captopril.― Pediatric Nephrology. 2004;19:805–807.
Codes ICD9-CM 189.0
ICD10 C64
Pa ge 5 2 4
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins
Withdrawal,
> Table o f C o ntents > Withdraw al, Alco ho l
Alcohol Lee Shockley
Basics Description
Chronic alcohol use “down-regulates― gam m a-am inobutyric acid (GABA) receptors, leading to tolerance (increasing doses or frequency of alcohol use is necessary to achieve the sam e effects).
Tolerance is necessary for withdrawal to occur.
Alcohol dependence is the altered physiologic state induced by chronic alcohol use; associated with inhibition of excitatory glutam atergic pathways and up-regulation of N-m ethyl-D-aspartate (NMDA) receptors.
Dependence is necessary for withdrawal to occur.
Characterized by a hyperadrenergic state that develops 6–8 hours after the cessation of drinking and m ay last up to 5 days.
Enhanced excitatory neurotransm ission: o
Increased levels of plasm a and urine catecholam ines (glutam ate effects)
o
Decreased inhibitory activity of presynaptic α2
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receptors (GABA effects) o
Increased dopam inergic activity (hallucinogenic effects)
Genetics Alcoholism is related to inherited functional variants of genes that alter the m etabolism of alcohol and alter the neurobiologies of reward, executive cognitive function, anxiety/dysphoria, and neuronal plasticity:
Functional alleles: o
Com m on alcohol dehydrogenase 1B and aldehyde dehydrogenase 2 variants (flushing reaction)
o
Catechol-O-m ethyltransferase (COMT) Val158Met (executive cognitive function, stress/anxiety response, and opioid function)
o
Opioid receptor m icro1 (OPRM1) Asn40Asp (gatekeeper m olecule in the action of naltrexone)
o
5-HT transporter gene-linked polym orphic region (5-HTTLPR) alters serotonin transporter function (stress response and anxiety/dysphoria)
Geriatric Considerations
Alcoholism is not uncom m on am ong older adults.
Age-related increase in alcohol sensitivity
Alcohol-related problem s m ay be m isdiagnosed as norm al consequences of aging.
Pediatric Considerations Newborns whose m others are intoxicated during delivery can experience withdrawal sym ptom s, such as trem ors and even seizures.
Pregnancy Considerations Alcohol withdrawal m ay exacerbate the adverse effects of chronic
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alcohol abuse on the fetus, particularly neuronal developm ent.
Etiology
The m ost com m on withdrawal syndrom e seen in the ED
Predisposing factors: acute, prolonged, and chronic ethanol ingestion; m alnutrition
Dose dependence
Am ount and chronicity of alcohol intake related to the severity of the syndrom e: o
“Kindling― hypothesis: withdrawal episodes becom e progressively m ore severe
Diagnosis There are four alcohol withdrawal syndrom es:
Trem ulousness: o
Hypersym pathetic state (norepinephrine storm ): sim ilar to hypothyroidism
o
Withdrawal of anticonvulsant properties of ethyl alcohol
o
Hypom agnesem ia
Hallucinosis: o
Otherwise clear sensorium
Seizures
Delirium trem ens (DT)
These withdrawal syndrom es m ay occur in isolation or com bination.
Signs and Symptoms History
Withdrawal is typically seen in patients who are daily drinkers for 3 m onths or m ore or binge drinkers (large quantities for at least 1 week).
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Trem ulousness: o
Onset 6–8 hours after last drink, duration 2–3 days
o
Intention trem or
o
Nausea and vom iting
o
Anxiety
o
Agitation
o
Sleep disturbance
Hallucinosis: o
Onset 7–48 hours, duration 1–3 days
o
Seen in up to 25% chronic alcoholics
o
Visual hallucinations: five tim es m ore com m on than auditory
o
Auditory hallucinations m ore benign
o
May becom e perm anent
Seizures: o
Onset 7–48 hours after last drink (95% first 12 hour
o
Generalized, tonic-clonic
o
3–20% have som e focality
o
No aura
o
40% single seizure
o
90% have less than five in a 6-hour period
o
Only 3% develop status epilepticus; should prom pt a search for other etiologies
DTs: o
Onset 3–5 days after last drink (up to 14 days), duration 4–5 days
o
Global confusion, trem or, agitation, anxiety, delusions, delirium , sleep disturbances, and gastrointestinal distress (nausea, vom iting)
o
Hallucinosis does not necessarily precede DTs.
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Physical Exam
Autonom ic lability: o
Tachycardia
o
Tachypnea
o
Hypertension
o
Low-grade hypertherm ia
o
Diaphoresis
o
Flushing
o
Hyperreflexia
Stigm ata of chronic alcohol abuse: o
Spider angiom ata
o
Rhinophym a
o
Parotid swelling
o
Flushed facies
o
Hepatom egaly, caput m edusae, ascites
o
Cirrhosis
o
Muscle wasting
o
Peripheral neuropathy
Extraocular m uscles paralysis or nystagm us m ay be seen in Wernicke encephalopathy.
Essential Workup
Com plete vital signs, including rectal tem perature
Rapid blood glucose
Pulse oxim etry
Tests Lab
Electrolytes, blood urea nitrogen, creatinine, glucose, m agnesium
CBC
Alcohol level (Breathalyzer or serum sam ple)
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Urinalysis
Creatine kinase (if the patient has been agitated or struggling)
Drug screen if co-ingestion suspected
Consider coagulation studies.
Imaging
Electrocardiography: o
o
Adrenergic storm :
Increased m yocardial dem and
May precipitate ischem ia or infarction
Prolonged QTc interval; possibly related to hypom agnesem ia
CT scan of the brain: o
Abnorm al m ental status
o
Head traum a
o
First-tim e seizure (3–6% incidence of unsuspected intracranial pathology)
o
Focal or status seizures
Chest radiograph for suspected traum a or aspiration
Diagnostic Procedures/Surgery Lum bar puncture and cerebrospinal fluid analysis if m eningitis suspected
Differential Diagnosis
Withdrawal from sedative-hypnotic drugs
Head traum a
Epilepsy
Encephalopathy
Hypoglycem ia
Hyperthyroidism
Sepsis
Meningitis
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Encephalitis
Sym pathom im etic overdose
Pheochrom ocytom a
Anticholinergic poisoning
Psychosis
Electrolyte disorders
Mercury poisoning
Lithium overdose
Cyclic antidepressant overdose
Phenytoin overdose
P.1235
Treatment Pre Hospital
Cardiac m onitoring
Blood glucose determ ination
IV glucose if necessary: o
Concerns over precipitating Wernicke syndrom e should not delay glucose adm inistration. Thiam ine should be adm inistered where there is a concern; however, thiam ine takes several hours to enter into cells.
Physical or chem ical restraints for agitation
Seizure precautions
Initial Stabilization
ABCs
Oxygen
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Correct hypoglycem ia
IV fluids
Initiate tranquilization to prevent the progression of the syndrom e to m ore severe levels and to relieve the sym ptom s
Adm inister thiam ine
ED Treatment Restore inhibitory tone to the CNS:
Benzodiazepines: o
Standard therapy
o
High doses required owing to cross-tolerance with chronic ethanol ingestion
o
Sym ptom s-triggered therapy is preferred (over fixed-schedule therapy).
o
Large doses m ay be necessary.
Barbiturates: o
Alternatives to benzodiazepines
o
May also have a synergistic effect in patients with apparent “benzodiazepine resistance―
Propofol: o
Last-resort drug in refractory DT and status epilepticus
o
Directly activates GABA receptors and inhibits NMDA receptors.
Butyrophenone antipsychotics: o
Haloperidol (low doses)
o
Indicated as adjuncts in the hallucinating patient but do not replace treatm ent with adequate quantities of benzodiazepines or barbiturates
o
Best avoided in the nonhallucinating patient
Beta-blockers: o
Propranolol and atenolol
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o
Used to relieve som e of the signs and sym ptom s
o
Considered adjunctive therapy (especially in patients with existing coronary artery disease [CAD]), but do not replace treatm ent with adequate quantities of benzodiazepines or barbiturates.
o
Avoid in patients with contraindications (asthm a, bradycardia, or CHF).
Clonidine: o
Adjunct to treat the hyperadrenergic signs and sym ptom s of alcohol withdrawal, but do not replace treatm ent with adequate quantities of benzodiazepines or barbiturates.
Anticonvulsive prophylaxis: o
Phenytoin is not useful in alcohol-withdrawal patients who do not also have an underlying seizure disorder that is not alcohol related. Identify and correct fluid, electrolyte, and nutritional deficiencies:
Adm inister glucose for hypoglycem ia or alcoholic ketoacidosis.
Treat hypovitam inosis syndrom es due to m alnutrition with thiam ine and folate.
Correct electrolyte abnorm alities.
Replete m agnesium : o
25% of chronic alcoholic patients are total-body m agnesium depleted owing to m alnutrition and increased renal losses.
o
Hypom agnesem ic state m akes replenishm ent of potassium difficult and m ay lower patient's seizure threshold.
Bed rest, m inim al physical stim ulation
Minim al use of physical restraints after adequate sedation
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to decrease the risk for rhabdom yolysis associated with agitation and struggling
Medication (Drugs)
Chlordiazepoxide: 25–100 m g PO for m ild reactions; 25 m g IV in repeated doses as necessary for m ore severe reactions
Clonidine: 0.1–0.2 m g PO q4h–q6h
Clorazepate: 15–30 m g PO q8h–q12h
Diazepam : 5–20 m g PO for m ild reactions; 5–10 m g IV
Folate: 1–4 m g IV or PO
Glucose: 5% solution in IV fluids; 25 g IV bolus in hypoglycem ic patients
Haloperidol: 2–10 m g PO, IV, or IM, q60m in–q120m in
Lorazepam : 2 m g PO, repeat q2h–q4h as necessary for m ild reactions; 2 m g IV in repeated doses as necessary for m ore severe reactions
Magnesium sulfate: 2–6 g in IV solutions, except in renal failure
Pentobarbital: 260 m g IV loading dose followed by 130 m g in repeated doses q30m in. titrated to light sedation
Propranolol: 0.5–1 m g IV; 10–40 m g PO for cardiac risk pts: add propranolol 10–40 m g PO q6h
Propofol: Loading dose: 0.2 m g/kg IV; m aintenance: 0.1–0.2 m g/kg/m in (6–12 m g/kg/h) IV: o
Titrated up to 90 m cg/kg/m in IV
Thiam ine: 100 m g IV
Trazodone 50–150 m g PO PRN qHS for sleep (m ay repeat once)
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Follow-Up Disposition Admission Criteria
Moderate to severe sym ptom s or persistent sym ptom s
Im pending DTs, DTs, or patients who fail to resolve their sym ptom s with m oderate am ounts of m edication should be adm itted to an intensive care unit.
Consider adm ission or observation for: o
Age >60 years old
o
First episode of ethanol withdrawal
o
Dehydration
o
Patients with com orbidities
Discharge Criteria Mild to m oderate sym ptom s that can be controlled with oral m edications:
Having patients self-adm inister their m edications is strongly discouraged.
Consider a detoxification facility
Issues for Referral Patients identified as having alcohol withdrawal should be referred to detoxification centers, addiction specialists, or counselors.
References 1. Bayard M, McIntyre J, Hill KR, et al. Alcohol withdrawal syndrom e. Am Fam Physician. March 15, 2004;69(6):1443–1450. 2. Bouchard NC, Meltzer A, Hoffm an RS. Treatm ent of delirium trem ens. Arch Intern Med. March 14 2005;165(5):587; author reply 587. 3. Chang PH, Steinberg MB. Alcohol withdrawal. Med Clin North Am .
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Septem ber 2001;85(5):1191–1212. 4. DeBellis R, Sm ith BS, Choi S, et al. Managem ent of delirium trem ens. J Intensive Care Med. May/June 2005;20(3):164–173. 5. Holbrook AM, Crowther R, Lotter A, et al. Diagnosis and m anagem ent of acute alcohol withdrawal. Cm aj. March 9 1999;160(5):675–680. 6. Lappin R. Propofol in delirium trem ens. Ann Em erg Med. Aug 1998;32(2):271–272. 7. Polycarpou A, Papanikolaou P, Ioannidis J, et al. Anticonvulsants for alcohol withdrawal. Cochrane Database Syst Rev. 2005(3):CD005064. 8. William s D, McBride AJ. The drug treatm ent of alcohol withdrawal sym ptom s: a system atic review. Alcohol. March/April 1998;33(2):103–115.
Codes ICD9-CM 291.81
ICD10 F10.3
Pa ge 5 2 5
Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Withdraw al, Drug
Withdrawal, Drug
Lee Shockley Maria Moreira
Basics Description
Gam m a-am inobutyric acid (GABA)—m inergic withdrawal: o
Requires physical dependence
o
Characterized by a hyperadrenergic state that develops in 3–7 days after the cessation of the drug
o
Enhanced excitatory neurotransm ission
o
Increased levels of plasm a and urine catecholam ines
o
Decreased inhibitory activity of presynaptic α2 receptors
o
Sym ptom severity determ ined by the am ount of endogenous norepinephrine released during withdrawal
o
Severe withdrawal can be life-threatening.
Opiate withdrawal: o
Requires physical dependence
o
Decrease in the exogenous opioid binding causes a catecholam ine release in the locus ceruleus.
o
Syndrom e m ay be tem porarily disabling and very
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uncom fortable. o
Not life-threatening
o
Onset within 4–8 hours for heroin, 36–72 hours for m ethadone
o
Opiate antagonists adm inistration (e.g., naloxone) can precipitate withdrawal (usually only lasting 20–60 m inutes).
Sym pathom im etic postexcitation syndrom e: o
Causes tiredness, depression, and dysphoria
o
Neurotransm itter depletion
o
No serious m etabolic or neurologic com plications
o
May be associated with an increased suicide risk and cravings for the drug, which often result in cycles of binges and transient abstinence
Diagnosis Signs and Symptoms
GABA-am inergic (benzodiazepines, barbiturates, alcohol): o
Anxiety
o
Depression
o
Agitation
o
Trem ulous
o
Anorexia
o
Nausea, vom iting
o
Confusion
o
Hallucinations
o
Seizures
o
Sleep disturbances (insom nia and nightm ares)
o
Physical signs:
Diaphoresis
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Flushing
Tachycardia
Hypertension
Orthostatic hypotension
Tachypnea
Fever
Hyperreflexia, m yoclonus
Seizures, delirium , and autonom ic instability
Markers of severe withdrawal
Opiates: o
o
Mild withdrawal:
Drug craving
Lacrim ation
Rhinorrhea
Yawning
Diaphoresis
Anxiety
Restlessness
Myalgias, arthralgias
Dysphoria
Mydriasis
Piloerection
More severe withdrawal:
Nausea, vom iting
Diarrhea
Abdom inal pain
Mild increase in blood pressure, pulse, and respiratory rate
o
Concurrent benzodiazepine withdrawal exacerbates opiate withdrawal sym ptom s.
Sym pathom im etics: o
Postexcitation syndrom e, not true withdrawal
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because continuous use of the drug does not prevent the syndrom e o
Crash (extrem e exhaustion that follows binge usage):
Lethargy
Psychom otor retardation
Increased appetite or anorexia
Sleep disturbances
Muscle twitching
Depression
Fatigue and dysphoria m ay last 6–18 weeks in the abstinent patient
Extinction (episodically evoked cravings that can last for m onths to years after abstinence)
Essential Workup
Thorough physical exam ination to determ ine nature of withdrawal
Blood glucose
Tests Lab
Electrolytes, blood urea nitrogen, creatinine, glucose
Drug screens m ay be useful if polysubstance abuse is suspected.
Imaging
Lum bar puncture and cerebrospinal fluid analysis for withdrawal patients in whom m eningitis suspected
CT scan of the brain for: o
Abnorm al m ental status
o
Head traum a
o
Focal seizures
o
Status seizures
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Differential Diagnosis
GABA-am inergic: o
Ethanol withdrawal
o
Head traum a
o
Epilepsy
o
Encephalopathy
o
Hypoglycem ia
o
Hyperthyroidism
o
Sepsis, m eningitis
o
Encephalitis
o
Sym pathom im etic overdose
o
Pheochrom ocytom a
o
Anticholinergic poisoning
o
Psychosis
o
Electrolyte disorders
Opiates: o
Sedative-hypnotic and ethanol withdrawal
o
Gastrointestinal diseases
Sym pathom im etics: o
Alcohol or sedative-hypnotic intoxication
o
Acute psychiatric disease (depression or psychosis)
o
Head traum a
o
CNS infection
Treatment Pre Hospital
Initiate cardiac m onitoring.
Determ ine blood glucose if abnorm al m ental status.
Physical or chem ical restraints for agitated patients
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Initial Stabilization
ABCs
Correct hypoglycem ia with glucose
Initiate IV fluid for dehydration
P.1237
ED Treatment
Sedative-hypnotic withdrawal: o
Reinstitution of therapy or the substitution of a sedative-hypnotic drug with a long half-life to facilitate detoxification
o
Beta-blocking agents
o
Adjuncts to lessen the adrenergically m ediated sym ptom s
Opiate withdrawal: o
Phenothiazines and butyrophenones for nausea and vom iting
o
Clonidine reduces the signs and sym ptom s of opiate withdrawal.
o
Com bination therapy with clonidine and the long half-life antagonist naltrexone m ay shorten the withdrawal duration by as m uch as 50% without increasing the severity of sym ptom s.
o
Benzodiazepines:
o
May help ease som e of the sym ptom s
Rapid opiate detoxification or ultra-rapid opiate detoxification protocols (high-dose naloxone treatm ent while under general anesthesia) followed by antiem etics, sedatives, clonidine, and naltrexone; the safety and efficacy of these protocols have not
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been proved.
Sym pathom im etics withdrawal: o
Supportive therapy
Medication (Drugs)
Buprenorphine 8 m g SL on day 1, 15 m g SL on day 2. Maintenance 15 m g SL per day
Chlordiazepoxide: 25–100 m g PO for m ild reactions; 25 m g IV in repeated doses as necessary for m ore severe reactions
Clonidine: 0.1–0.2 m g PO q4h–q6h
Clorazepate: 15–30 m g PO q8h–q12h
Diazepam : 5–20 m g PO for m ild reactions; 5–10 m g IV in repeated doses as necessary for m ore severe reactions
Glucose: 5% solution in IV fluids; 25 g IV bolus in hypoglycem ic patients
Haloperidol: 2–10 m g PO or IV
Lorazepam : 2 m g PO, repeat q2h–q4h as necessary for m ild reactions; 2 m g IV in repeated doses as necessary for m ore severe reactions
Methadone: 5–20 m g/d PO—only designated m ethadone clinics m ay dispense to outpatients
Naltrexone: 50 m g/d PO
Pentobarbital: 100 m g IV in repeated doses as necessary for m ore severe reactions
Prom azine: 25 m g IM q30m in as needed, up to 125 m g
Propranolol: 0.5–1.0 m g IV; 10–40 m g PO
Pediatric Considerations
Treatm ent with opioids is the preferred initial therapy for neonates with neonatal abstinence syndrom e:
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Medications: o
Chlorprom azine 0.55 m g/kg q6h IM or PO:
Lim ited usefulness in neonate secondary to side effects of cerebellar dysfunction, decreased seizure threshold, and hem atological problem s
o
Clonidine 0.5–1.0 m g/kg single dose followed by m aintenance dose of 3–5 m g/kg/d div. q4h–q6h
o
Methadone 0.05–0.1 m g/kg q6h
o
Paregoric 0.1 m L/kg or 2 drops/kg with feedings q4h:
Lim ited usefulness secondary to side effects
o
Phenobarbital 16 m g/kg per 24 hours
o
Tincture of opium (diluted solution) 0.1 m L/kg or 2 drops/kg with feedings q4h
Follow-Up Disposition Admission Criteria
Sedative-hypnotic: o
Moderate severe or persistent sym ptom s
o
Seizures
o
Psychosis during withdrawal
o
Severe autonom ic instability or delirium should be adm itted to an intensive care unit
Opiates: o
Medical conditions that m ay com plicate withdrawal
o
Intractable vom iting
Sym pathom im etics: o
Extrem ely lethargic or m inim ally responsive m ust be adm itted.
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o
Suicidal patients require psychiatric evaluation and possible adm ission.
Discharge Criteria
Able to tolerate oral solutions
Not suicidal
References 1. Am erican Academ y of Pediatrics Com m ittee on Drugs. Neonatal Drug Withdrawal. Pediatrics. June 1998;101(6):1079–1088. Erratum in: Pediatrics. Septem ber 1998;102(3 Pt 1):660. 2. de Wet C, Reed L, Glasper A, Moran P, Bearn J, Gossop M. Benzodiazepine co-dependence exacerbates the opiate withdrawal syndrom e. Drug Alcohol Depend. October 2004;5;76(1):31–35. 3. Ham ilton RJ, Olm edo RE, Shah S, Hung OL, Howland MA, Perrone J, Nelson LS, Lewin NL, Hoffm an RS. Com plications of ultrarapid opioid detoxification with subcutaneous naltrexone pellets. Acad Em erg Med. January 2002;9(1):63–68. 4. Lintzeris N, Bell J, Bam m er G, Jolley DJ, Rushworth L. A random ized controlled trial of buprenorphine in the m anagem ent of short-term am bulatory heroin withdrawal. Addiction. 2002 Nov;97(11):1395–1404. 5. O'Connor PG, Kosten TR. Rapid and ultrarapid opioid detoxification techniques. JAMA. January 21, 1998;279(3):229–334. 6. Olm edo R, Hoffm an RS. Withdrawal syndrom es. Em erg Med Clin North Am . May 2000;18(2):273–288. 7. Upthegrove RA, Naik PC. Pharm acological m anagem ent of opiate withdrawal. Hosp Med. May 2001;62(5):277,280–281. 8. William s H, Salter M, Ghodse AH. Managem ent of substance m isusers on the general hospital ward. Br J Clin Pract. March 1996;50(2):94–98. 9. William s H, Salter M, Ghodse AH. Managem ent of substance m isusers on the general hospital ward. Br J Clin Pract.
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1996;50(2):948. 10. Woods JH, Winger G. Current benzodiazepine issues. Psychopharm acology (Berl). 1995;118(2):107–115; discussion, 118, 1201.
Codes ICD9-CM 292.0
ICD10 F11.3 Narcotic withdrawal F13.3 Sedative and hypnotic withdrawal
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Wo lff-Parkinso n-White Syndro m e
Wolff-Parkinson-White Syndrome Mitchell Adelstein
Basics Description
Syndrom e caused by ventricular pre-excitation via an accessory atrioventricular (AV) pathway, the bundle of Kent
Conduction m ay be anterograde, retrograde, or both.
Type A or orthodrom ic is the m ost com m on (70%).
Im pulse travels down the AV node and then up the retrograde pathway: o
A circuit is created that potentiates reentrant tachycardia.
Type B or antidrom ic: o
Less com m on than type A
o
The circuit operates in the opposite direction.
Diagnosis Signs and Symptoms
Asym ptom atic
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Palpitations
Dyspnea
Dizziness
Nausea
Abnorm al heart rate: o
Rapid and regular (supraventricular tachycardia [SVT])
o
Irregular (atrial fibrillation)
Signs of instability: o
Hypotension
o
Change in m ental status
o
Rales
Essential Workup
Wolff-Parkinson-White (WPW) syndrom e should be considered the underlying etiology in all cases of tachydysrhythm ia.
The diagnosis should be based on the characteristic ECG findings once the patient has converted to a sinus rhythm .
Tests Diagnostic Procedures/Surgery
ECG in sinus rhythm : o
Short pulse rate, 0.10 seconds
o
Delta wave:
Sm all slurred upstroke at the beginning of the QRS
o
ECG m orphology will depend on the degree of preexcitation
Differential Diagnosis
AV nodal reentry SVT
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Ventricular tachycardia
Treatment Initial Stabilization Unstable patients:
Synchronized cardioversion starting with 50 J/m in
Increase increm entally until sinus rhythm is restored.
ED Treatment
Stable patients with narrow com plex, regular tachycardia: o
Vagal m aneuvers such as Valsalva
o
Right carotid artery m assage for no m ore than 10 seconds:
Auscultate the artery first for a bruit, which would contraindicate this procedure.
o
Fluid replacem ent and Trendelenburg position if the patient has m ild hypotension
o
Pharm acologic conversion if carotid m assage fails
o
Adenosine
Stable patients with irregular wide com plex tachycardia: o
Procainam ide is the drug of choice.
Alert
Never use calcium -channel blockers, beta-blockers, or digoxin: o
These m edications prolong the refractory period of the AV node, increasing the rate of transm ission through the accessory pathway, and m ay result in fatal ventricular dysrhythm ias.
P.1239
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Medication (Drugs)
Adenosine: 6 m g rapid IV bolus over 1–2 seconds; if ineffective, repeat with 12 m g (peds: 0.1 m g/kg rapid IV push, repeat with 0.2 m g/kg)
Procainam ide: 6–13 m g/kg IV at 0.2–0.5 m g/kg/m in until either arrhythm ia controlled, QRS widens 50%, or hypotension, then 2 to 6 m g/m in, m ax. of 1,000 m g
Follow-Up Disposition Admission Criteria
Patients with signs of instability require adm ission to a m onitored bed.
Failure of outpatient therapy for continuous pharm acologic control or ablation
Discharge Criteria
Most patients will be stable and can be discharged once converted to sinus rhythm .
Follow-up should be arranged with a cardiologist.
Issues for Referral Electrophysiology studies to assess for radioablation or surgery m ay be perform ed on outpatient basis.
References 1. Al-Khatib SM, Pritchett EL. Clinical features of Wolff-Parkinson-White syndrom e. Am Heart J. 1999;(3 Pt
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1):403–413. 2. Donald M. Dysrhythm ias. In: Marx J, et al., eds. Rosen's em ergency m edicine: concepts and clinical practice. St Louis, MO: CV Mosby, 2002:1053–1099. 3. Keating L. Electrocardiographic features of Wolff-Parkinson-White syndrom e. Em ergency Medicine Journal. 2003;20(5):491–493. 4. Rosner MH. Electrocardiography in the patient with Wolff Parkinson White syndrom e: diagnostic and initial therapeutic issues. Am er J Em er Med. 1999;17(7):705–714. 5. Shah CP. Clinical approach to wide QRS com plex tachycardias. Em erg Med Clin North Am . 1998;16:331–360. 6. Xie B, Thakur RK, Shah C, et al. Em ergency m anagem ent of cardiac arrhythm ias: clinical differentiation of narrow QRS com plex tachycardias. Em erg Clin North Am . 1998;16:295–330. 7. Zipes DP. Specific arrhythm ias: diagnosis and treatm ent. In: Braunwald E, ed. Heart disease: a textbook of cardiovascular m edicine. 5th ed. Philadelphia, PA: WB Saunders, 1997: 667–675.
Miscellaneous SEE ALSO: Pre-excitation Syndrom e
Codes ICD9-CM 426.7
ICD10 I45.6
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Table o f C o ntents > Wo und Ballistics
Wound Ballistics
Brian K. Snyder
Basics Description The physical forces that determ ine the wounding potential of gunshot and other penetrating wounds
Etiology
Wounding potential of bullet is determ ined by m ass and velocity.
The type and severity of a wound is determ ined by: o
Wounding potential
o
Construction and shape of the bullet
o
Orientation upon striking body
o
Deform ity or fragm entation
o
What tissues the bullet traverses
Traditional distinction between low and high m uzzle velocity does not differentiate kind and severity of wounding: o
A civilian hunting rifle or a large caliber handgun with a hollow point bullet m ay produce a m ore severe wound than a round with a full m etal jacket from a “high-velocity― m ilitary rifle.
Bullets wound by two m ain m echanism s—crush and
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stretch: o
Sonic pressure wave that precedes bullet has no role in wounding.
o
Bullet crushes tissue it directly passes through, form ing perm anent cavity.
o
Stretch is produced by radial energy transferred from bullet as it slows down in tissue, form ing tem porary cavity.
o
A bullet is stabilized in flight by spin transm itted from rifling in the barrel.
o
Spin m inim izes yaw, which is angle between long axis of the bullet and its flight vector.
o
Without spin, a bullet would yaw to its m ost stable flight configuration, which is base and center of m ass forward:
o
Not aerodynam ically efficient
As bullet enters tissue, spin of bullet is reduced and bullet will yaw.
o
When yaw is 90°, a bullet crushes m axim al am ount of tissue, slows down the m ost, and m axim al stretch injury occurs.
Bullets designed to deform in tissue (soft point, hollow point) will expand on im pact:
o
Increases am ount of crush injury
o
Moves bullet center of m ass forward
Jacketed bullets prevent lead stripping in the barrel that occurs at high m uzzle velocities: o
Jacketed bullets do not deform but m ay fragm ent.
o
Fragm entation increases surface area and crush injury.
Bullets striking bone often fragm ent and m ay cause bone fragm ents to becom e secondary projectiles.
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Wound severity also dependent upon tissue composition and thickness: o
Minim ally elastic tissues, near water-density tissue (brain, liver), fluid-filled (heart, bowel) and dense organs (bone) m ay be injured by the tem porary cavity.
o
More elastic tissue such as lung and skeletal m uscle m ay absorb the energy from tem porary cavity form ation and sustain m inim al dam age.
o
Extrem ities are often not thick enough for the bullet to fully yaw:
Tem porary cavity form ation is m inim al.
Most dam age is caused by direct crush injury of the bullet, its fragm ents, or secondary projectiles.
Short-range shotgun blasts produce severe wounds with com prom ise of the blood supply: o
In short-range shotgun injuries, pellets m ay be greatly scattered in tissue secondary to the pellets striking each other.
Stab wounds with knives and other sharp instrum ents are low-energy wounds with tissue injury from direct weapon contact.
Diagnosis Signs and Symptoms
Severe underlying tissue dam age and life-threatening injury m ay occur with even sm all entrance wounds.
A knowledge of how different kinds of weapons and bullets wound, the trajectory of the bullet through the body, and
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the effect on different body tissues will allow the physician to carefully evaluate gunshot and stab wounds and their potential m orbidity and m ortality.
History Field personnel can provide inform ation about weapon type and size, distance and angle between the weapon and victim :
This inform ation m ay not be available or m ay be inaccurate.
Physical Exam Evaluate for entrance and exit wounds:
May estim ate trajectory and potential for tissue dam age
Exit wounds are often stellate and larger than entranced wounds unless energy is dissipated at skin surface by special bullet type (hollow point, etc.).
With high-velocity projectiles, exit wound m ay be m uch m ore extensive than entrance wound.
Because of elasticity of the skin, bullet can often be palpated subcutaneously.
It is not always possible to differentiate entrance from exit wounds; clinicians do this poorly, so wounds should be only described fully in the m edical record; classification as entrance or exit wounds should be avoided.
Tests Imaging
Anteroposterior and lateral radiographs help localize bullet: o
With placem ent of m arker at the entrance, wound trajectory can be estim ated
o
Fragm ents, fractures, pneum othoraces, or hem othoraces can be identified.
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CT scanning: o
Identify location of projectile.
o
Location and am ount of tissue dam age (especially to the head and brain)
Angiography m ay be necessary if patient has potential vascular injury and surgical exploration not otherwise warranted.
Diagnostic Procedures/Surgery Extent of tissue injury often only apparent on surgical exploration
Treatment Pre Hospital
Gunshot and stab wounds to chest with unstable vital signs warrant a needle thoracostom y in the side of the chest with entrance wound: o
Relieves tension pneum othorax
o
If no im provem ent, a needle thoracostom y should be placed in the contralateral hem ithorax.
P.1241
Im paled objects or projectiles should not be rem oved: o
Im m obilize with tape and gauze and transport.
Clothing should be preserved if possible: o
Clothing should be cut around holes m ade by the projectiles to preserve evidence.
Patient should be transported to the closest traum a center.
Hypotensive patient m ay be taken directly to the
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operating room .
Initial Stabilization Stabilize airway, breathing, and circulation.
ED Treatment
Im paled objects should be rem oved only in operating room .
In the ED, estim ate tissue injury based on above principles.
Wound care includes appropriate exploration, irrigation, and débridem ent of devitalized tissue.
All bullets are contam inated with bacteria and are not sterilized by being fired: o
All nongrazing bullet wounds warrant em piric antibiotics.
Early traum a, orthopaedic, and vascular surgery consultation is necessary.
Medication (Drugs) Prophylactic antistaphylococcal antibiotics should be prescribed for several days:
Cefazolin: 1 g IV q6h
Cephalexin: 500 m g PO q6h–q8h
For penicillin allergic patients or patients at risk for m ethicillin-resistant S. aureus then vancom ycin 1 g IV q12h or clindam ycin 300 m g PO q6h can be prescribed
Intra-abdom inal wounds require broader coverage (m any regim ens available) such as cefotetan 1 g IV q6h or the com bination of ciprofloxacin 500 m g IV q12h with m etronidazole 500 m g IV q8h
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Follow-Up Disposition Admission Criteria
Patients with neurovascular com prom ise and extensive tissue dam age m ust be adm itted for appropriate surgical intervention.
Patients with injury to the head, neck, torso, or abdom en should be adm itted.
Patients with injury from high-velocity projectiles or gunshot wounds should be adm itted to a m onitored setting for observation of neurovascular status.
Discharge Criteria Patients with m inor penetrating extrem ity traum a or stabbing victim s found not to have significant injury m ay be discharged with appropriate follow-up.
Issues for Referral Em ergent consultation of appropriate surgical specialists should be obtained in patients with potential injuries to vascular or nervous structures.
References 1. Fackler, ML. Gunshot wound review. Ann Em erg Med. 1996;28:194–203. 2. Santucci, RA and Chang Y. Ballistics for physicians: Myths about wound ballistics and gunshot injuries. J Urology. 2004;171:1408–1414. 3. Swan KG, Swan RC. Principles of ballistics applicable to the treatm ent of gunshot wounds. Surg Clin Am er. 1991;71:221–239.
Codes
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ICD9-CM E922.9 Unspecified firearm m issile (Gunshot wound NOS, Shot NOS)
ICD10 W43
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Editors: Schaider, Jeffrey; Hayden, Stephen R.; Wolfe, Richard; Barkin, Roger M.; Rosen, Peter Title: Rosen & Barkin's 5-Minute Emergency Medicine Consult, 3rd Edition Copyright ©2007 Lippincott William s & Wilkins > Back o f Bo o k > Appendix > Appendix
Appendix
Emergency Medications Pediatric (Pediatric dose should not generally exceed Drug
Adult
adult dose)
Abcixim ab
0.25 m g/kg IV, then 0.125 N/A
(ReoPro)
m g/kg/m in infusion
Adenosine
6m g IV (rapid) Give 12 m g 0.1 m g/kg IV (rapid);
(Adenocard) (3
IV if no response after 2
give 0.2 m g/kg if no
m g/m L)
m in
response after 2 m in
Albuterol
2.5 m g (0.5 m L) by
0.03 m L (0.15
(Ventolin,
inhalation; m ay repeat;
m g/kg/dose) by
Proventil) (0.5%
MDI available.
inhalation; m ay
soln: 5m g/m L)
repeat
Alteplase (t-PA,
15 m g IV bolus, then 0.75 N/A
Activase)
m g/kg (m ax 50 m g) over 30 m in, then 0.5 m g/kg (m ax 35 m g) over next 60 m in
Am iodarone
Cardiac arrest: 300 m g IV Cardiac arrest: 5 push
m g/kg IV push
Wide com plex tachycardia: Wide com plex 150 m g IV over 10 m in
tachycardia: 5/m g/kg
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IV over 20–60 m in Am rinone,
0.75 m g/kg over 10–15
0.75 m g/kg over
inam rinone
m in; Infusion: 5–10
10–15 m in;
µg/kg/m in
Infusion: infants & children: 5–10 µg/kg/m in; neonates 3–5 µg/kg/m in
Anistreplase
30 IU IV over 2–5 m in
N/A
5 m g IV q5 m in to 10 m g
N/A
(APSAC) Atenolol
total Atropine (0.1,
0.5–1.0 m g IV/ET
0.4, 1 m g/m L)
0.02 m g/kg IV/ET (m in 0.1 m g/dose)
Bicarbonate,
1 m Eq/kg/dose IV q10m in 1 m Eq/kg/dose IV q10
sodium 44, 50
PRN (per ABG)
m Eq/50 m L
m in PRN (per ABG); dilute
Calcium chloride
500 m g/dose IV slowly
20 m g/kg/dose IV
(10% soln: 100
q10m in PRN
slowly q10 m in PRN
m g/m L, 1.36 m Eq Ca µ/m L Crystalloid (0.9% Flush: 1–2 liters IV over Flush: 20 m L/kg IV NS, LR)
20–30 m in
over 20–30 m in
Defibrillation
200 joules/dose; double for 2 joules/kg/dose; subsequent dose;
double for subsequent
synchronized: 50–100
dose; synchronized:
joules
0.5–1.0 joules/kg/dose
Dexam ethasone
5–10 m g IM/IV
(Decadron) (4, 24
0.15–0.60 m g/kg/dose IM/IV
m g/m L) Dextrose
25–50 g IV
0.5–1.0 g (2–4 m L
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(D-50-W: 25 g/50
D-25-W)/kg/dose IV
m L) Diazepam
5–10 m g IV
0.2–0.3 m g/kg/dose
(Valium ) (5
IV q2–5m in slowly;
m g/m L)
0.2–0.5 m g/kg/dose PR q5m in
Digibind (40-m g
3–5 vials for
Dose (in no. of vials)
vial binds 0.6 m g chronicoverdose;10–20
= [(serum digitoxin
dig)
concentration in
vials for acute over dose
ng/m L) (weight in kg)] ÷ 100 Digoxin
Load: 0.5 m g IV initially
Initial loading dose:
followed by 0.25 m g q6h Ã