1600 John F. Kennedy Blvd. Suite 1800 Philadelphia, PA 19103–2899
ESSENTIAL EMERGENCY MEDICINE: FOR THE HEALTHCARE PRACTITIONER Copyright # 2007 by Saunders, an imprint of Elsevier Inc.
ISBN: 978–1–4160–2971–7
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Notice Knowledge and best practice in this field are constantly changing. As new research and experience broaden our knowledge, changes in practice, treatment and drug therapy may become necessary or appropriate. Readers are advised to check the most current information provided (i) on procedures featured or (ii) by the manufacturer of each product to be administered, to verify the recommended dose or formula, the method and duration of administration, and contraindications. It is the responsibility of the practitioner, relying on their own experience and knowledge of the patient, to make diagnoses, to determine dosages and the best treatment for each individual patient, and to take all appropriate safety precautions. To the fullest extent of the law, neither the Publisher nor the Editor assumes any liability for any injury and/or damage to persons or property arising out or related to any use of the material contained in this book.
Library of Congress Cataloging-in-Publication Data Essential emergency medicine : for the healthcare practitioner / [edited by] Steven W. Salyer. – 1st. p. ; cm. Includes bibliographical references. ISBN 1–4160–2971–0 1. Emergency medicine–Handbooks, manuals, etc. I. Salyer, Steven W. [DNLM: 1. Emergencies–Handbooks. 2. Emergency Medicine–Handbooks. WB 39 E768 2007] RC86.7.E785 2007 616.02'5–dc22
2007000839
Acquisitions Editor: Rolla Couchman Developmental Editor: Mary Beth Murphy Project Manager: Bryan Hayward Design Direction: Steven Stave
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Dedication To my wife Sally, my daughter Laura Emilie, and my son Zachary who gave up so much “daddy” time while I wrote and edited this second book. And to all those Physician Assistants and physicians who have chosen the profession of Emergency Medicine and who still go to work everyday still caring about the lives, hearts, and souls of their patients. And a special prayer for all those men and women on the frontiers of freedom who everyday defend our way of life and keep us all free. God bless all of you!
Contributors GREG A. ABRAHAMIAN, MD Assistant Professor of Surgery, Transplant Center, University of Texas Health Science Center at San Antonio, San Antonio, Texas Chapter 20. Renal Transplantation
JONATHON ALLEN, MD Department of Emergency Medicine, Medical College of Georgia, Augusta, Georgia Chapters 08. Diabetic Ketoacidosis; Hyperglycemic Hypersmolar Nonketotic Coma; 19. Acute Renal Failure
CULLEN ARCHER, MD Department of Obstetrics and Gynecology, University of Texas Health Science Center at San Antonio, San Antonio, Texas Chapter 10. Ectopic Pregnancy; Hypertensive Disorders of Pregnancy (Preeclampsia and Eclampsia)
MICHAEL A. AROCHO, MD,CPT, USAF United States Air Force Chapter 17. Lead; Mercury
SIMEON W. ASHWORTH, DO,CPT, MC, USA Madigan Army Medical Center, Tacoma, Washington Chapter 03.Toxicodendron Dermatitis
DAVE BARRY, MD, MAJ, MC, USA Department of Emergency Medicine, Brooke Army Medical Center, Fort Sam Houston, Texas Chapter 17. Barbituates; Hallucinogens
CHARLES R. BAUER, MD,CPE, FACS, FACPE, FACEP Director, Center for Public Health Preparedness & Biomedical Research, Professor of Surgery & Emergency Medicine, The University of Texas Health Science Center at San Antonio, San Antonio, Texas Chapter 18. Abdominal Trauma; Pelvic Trauma; Thoracic Trauma; Trauma in the Pregnant Patient
ROGER MATTHEW BAUTISTA, MD,CPT, MC, USA Brooke Army Medical Center, Fort Sam Houston, Texas Chapters 07.Tetanus; 10. Ovarian Cysts
MARY ANN BROWNING, FNP Family Nurse Practitioner, Oregon Health & Sciences University, Instructor, Department of Emergency Medicine, Portland, Oregon Chapters 04. Jaundice and Hepatitis; 13. Dehydration in Children; 19. Urinary Tract Infections in Adults
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CONTRIBUTORS
JOHN H.CALHOON, MD Professor, Department of Surgery, Chief, Division of Cardiothoracic Surgery, University of Texas Health Science Center, San Antonio, Texas Chapter 20.Cardiac and Lung Transplantation
JASON CAPRA, MD United States Air Force, Medical Corps Chapter 17.Cyanide
BARBARA A.CARR, MD,CPT, MC, USA Brooke Army Medical Center, Fort Sam Houston, Texas Chapters 06. Spider Bites and Scorpion Stings; 12. Acute Ankle Injuries
ROBERT L.CLOUTIER, MD Oregon Health and Sciences University, Department of Emergency Medicine, Portland, Oregon Chapter 13. Electrolyte and Fluid Management in Pediatric Patients
JIMMY COOPER, MD CAPT, MC, USA Madigan Army Medical Center, Tacoma, Washington Chapter 02. Permanent Pacemakers
STEPHEN A.CRANDALL, MD Division of Emergency Medicine, University of Washington, Madigan Army Medical Center, Tacoma, Washington Chapter 13. Asthma
CHRISTOPHER B.CROWELL, MD University of Washington, Emergency Medicine Residency, Madigan Army Medical Center, Tacoma, Washington Chapter 13. Abdominal Pain
RICHARD L. DAGROSA, MD U.S. Air Force, Medical Corps Chapter 07. Herpes Virus
CHARLES P. DAVIS, MD, PHD Professor, Department of Surgery, Division of Emergency Medicine, University of Texas Health Science Center at San Antonio, San Antonio, Texas Chapter 19.Common Disorders of the Penis
MOHAMUD DAYA, MD Associate Professor of Emergency Medicine, Oregon Health and Science University, Portland, Oregon Chapter 17.Clonidine; Phenytoin
MARC L. DAYMUDE, MD, FACEP United States Army, Brooke Army Medical Center, Fort Sam Houston, Texas Chapter 01. Abdominal Aortic Aneurysm (AAA); Appendicitis; Hernias; Intestinal Obstruction; Thoracic Aortic Dissection
Contributors
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JOHN T. DEEL, MD Transplant Center, University of Texas Health Science Center at San Antonio, San Antonio, Texas Chapter 20.Cardiac and Lung Transplantation
CARRY DEPOLD, PA-C Physician Assistant, University of Texas Health Science Center at San Antonio, San Antonio, Texas Chapters 12. Elbow Injuries; 17. IronToxicity
GERALD D. DEPOLD, PA-C, MPAS Captain, Army Medical Specialist Corps Chapters 06.Thermal Burns; 12. Elbow Injuries
DIANE DEVITA, MD, FACEP Staff Physician, DEM MAMC, Assistant Clinical Professor, University of Washington Chapter 13. Asthma
AMY K. DITZEL, PA-C Family Practice Physician Assistant Chapters 07, Influenza; 10. Emergent Pelvic and Abdominal Pain; Genital Herpes
MARTIN A. DOCHERTY, MD, MAJOR, USAR Clinical Instructor, Division of Emergency Medicine, Washington University School of Medicine, Attending Physician, Barnes-Jewish Hospital, St. Louis, Missouri Chapters 02.Congestive Heart Failure; Hypertensive Emergencies; 07. HIV Infections; 08. Geriatric Emergencies
GARY W. DUFRESNE, DO,CPT, MC, USA Brooke Army Medical Center, Fort Sam Houston, Texas Chapter 09. Seizures and Status Epilepticus
JENNY E. DUNLAVY, MD,CPT, USAF Wilford Hall Medical Center, Lackland Air Force Base, San Antonio, Texas Chapters 06. Snakebite Injuries; 12. Foot Injuries
STEVE DURNING, MD, FACP Director, Department of Medicine, Uniformed Services University of the Health Sciences, Bethesda, Maryland Chapter 02. Mitral Valve Prolapse
TERRY EMANUEL, PA-C, MPAS Faculty Associate, Department of Surgery, Division of Emergency Medicine, University of Texas Health Science Center at San Antonio, San Antonio, Texas Chapters 08. Lactic Acidosis; 19. End-Stage Renal Disease
x CONTRIBUTORS
ALFREDO ESPINOZA, MD Transplant Center, University of Texas Health Science Center at San Antonio, San Antonio, Texas Chapter 20. Liver Transplantation
ROBERT M. ESTERL, MD Professor of Surgery, Transplant Center, University of Texas Health Science Center at San Antonio, San Antonio, Texas Chapter 20. Renal Transplantation
BARBARA M. FISHMAN, MD Associate Professor, Department of Medicine, Department of Emergency Medicine, University of Texas Health Science Center at San Antonio, San Antonio, Texas Chapters 08. Acid^Base Problems; Fluid and Electrolyte Emergencies; 17.Cocaine
JEFF FOXWORTH, PA-C Division of Plastic Surgery, Department of Surgery, University of Texas Health Science Center at San Antonio, San Antonio, Texas Chapter 18.Trauma Overview
MARK S. FUNK, MD Department of Obstetric and Gynecology, University of Texas Health Science Center at San Antonio, San Antonio, Texas Chapter 10. Sexual Assault
RYAN GARNER, MD United States Air Force, Medical Corps Chapter 13. Neonatal Emergencies; Hirschsprung’s Disease or Congenital Aganglionic Megacolon; Pyloric Stenosis; The Abused Child; Tetralogy of Fallot
DAVID GLENDENING, MD Associate Professor, Department of Surgery, Division of Emergency Medicine, University of Texas Health Science Center at San Antonio, San Antonio, Texas Chapter 15. Adult Bacterial Pneumonias
VINITA GOYAL, MD Department of Obstetrics and Gynecology, University of Texas Health Science at San Antonio, San Antonio, Texas Chapter 10. Miscarriage (Abortion)
ROBERT D. GRAYDON, PA-C, MPAS Faculty Associate, Department of Surgery, Division of Emergency Medicine, The University of Texas Health Science Center at San Antonio, San Antonio, Texas Chapters 08. Acute Ethanol Withdrawal; 17.General Principles of the Poisoned Patient; Anticholinergics; Ethanol Intoxication; Ethylene Glycol; Opioids
Contributors
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LEN GRUPPO, PA-C,CPT, SP, USA Brooke Army Medical Center, Fort Sam Houston, Texas Chapter 02. Acute Pericarditis; Cardiac Examination; Evaluation of Cardiac Chest Pain
GLENN HALFF, MD Transplant Center, University of Texas Health Science Center at San Antonio, San Antonio, Texas Chapter 20. LiverTransplantation
BENJAMIN P. HARRISON, MD, FACEP, LTC, MC, USA Madigan Army Medical Center, Tacoma, Washington Chapters 03.Toxicodendron Dermatitis; 08. Adrenal Insufficiency; 12. Hand Injuries
KATHERINE ANNE HARRISON, MD Assistant Professor, Department of Surgery, Division of Emergency Medicine, University of Texas Health Science Center at San Antonio, San Antonio, Texas Chapters 10. Pelvic Inflammatory Disease; Toxic Shock Syndrome; Vulvovaginitis; 12. Shoulder Injuries
GUYON J. HILL, MD,CAPT, MC, USA Department of Emergency Medicine, Brooke Army Medical Center, Fort Sam Houston, Texas Chapters 03.Toxic Epidermal Necrolysis; 06. Lightning Injuries; 17. Hydrocarbons; Isoproponal; Methanol
DAVID A. HNATOW, MD Associate Professor, Department of Surgery, Division of Emergency Medicine, University of Texas Health Science Center at San Antonio, San Antonio, Texas Chapters 04.Gastrointestinal Bleeding; Acute and Chronic Pancreatitis; 06.Chemical Burns
REX L. HOBBS, JR., MPAS, PA-C Assistant Professor, UT Southwestern Medical Center-Dallas, Dallas, Texas Chapters 07. Diphtheria; 09. Bell’s Palsy; Botulism; Multiple Sclerosis; Myasthenia Gravis; Neurological Examination
JULIE HUSLEY, PA-C Faculty Associate, Department of Surgery, Division of Emergency Medicine, University of Texas Health Science at San Antonio, San Antonio, Texas Chapter 13. Bronchiolitis; Constipation; Sudden Infant Death Syndrome and Apparent Life-Threatening Event Syndrome
JENNIFER JAMUL, PA-C Faculty Associate, Department of Surgery, Division of Emergency Medicine, University of Texas Health Science Center at San Antonio, San Antonio, Texas Chapter 07. Foodborne and Waterborne Infections
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CONTRIBUTORS
ROY JOHNSON III, MD Uniformed Services University of the Health Sciences, Andrews Air Force Base Chapters 13. Pediatric Airway Management; Pediatric Analgesia and Sedation; 17. Cyanide; Theophylline
SCOTT B. JOHNSON, MD Transplant Center, University of Texas Health Science Center at San Antonio, San Antonio, Texas Chapter 20.Cardiac and Lung Transplantation
MELISSA KAGARISE, MMS, PA-C Department of Physician Assistant Studies, Saint Francis University, Lorretto, Pennsylvania Chapter 13. Pediatric Pneumonia; Pharyngotonsillitis; 15. Aspiration Pneumonia
SANDEEP J. KHANDHAR, MD Transplant Center, University of Texas Health Science Center at San Antonio, San Antonio, Texas Chapter 20.Cardiac and Lung Transplantation
C.GORDON KING, MD Department of Medicine, University of Texas Health Science Center at San Antonio, San Antonio, Texas Chapter 08. Fluid and Electrolyte Emergencies
JOHN T. KODOSKY, PA-C, MMS Faculty Associate, Department of Surgery, Division of Emergency Medicine, University of Texas Health Science Center, San Antonio, Texas Chapters 04. Peptic Ulcer Disease; 18. Head and Brain Trauma
ADAM CLAY KOERTNER, MD,CAPT United States Air Force, Medical Corps Chapter 08. Hyperthyroidism and Thyroid Storm (Thyrotoxicosis); Hypothyroidism and Myxedema Coma
CHRISTOPHER M. KREBS, MD,CPT, MC, USA Uniformed Services University of the Health Sciences, Andrews Air Force Base, Maryland Chapter 17.Theophylline
DAVID W. KUHNS, MD, FACEP Department of Emergency Medicine, Darnall Army Community Hospital, Fort Hood, Texas Chapters 03. Urticaria; 13. Kawasaki Disease
KHIM K. LAM, MD Department of Obstetrics and Gynecology, University of Texas Health Science at San Antonio, San Antonio, Texas Chapter 10. Abruptio Placentae; Amniotic Fluid Embolism
Contributors
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LINDA L. LAWRENCE, MD, FACEP COL, USAF, MC Chief of Medical Staff, Emergency Medicine Consultant to Air Force Surgeon General Chapter 13. Neonatal Emergencies; Pediatric Airway Management; Hirschsprung’s Disease or Congenital Aganglionic Megacolon; Pyloric Stenosis; The Abused Child; Tetralogy of Fallot; Pediatric Analgesia and Sedation
DEREK R. LINKLATER, MD, FACEP, FAAEM Assistant Program Director, Darnall Army Community Hospital EM Residency Program, Assistant Clinical Professor of Emergency Medicine, Texas A&M School of Medicine, Assistant Clinical Professor of Military and Emergency Medicine, USUHS School of Medicine Chapter 15. Pulmonary Embolism
REENIE LOPEZ, PA-C Department of Surgery, Division of Emergency Medicine, University of Texas Health Science Center at San Antonio, San Antonio, Texas Chapter 13. Febrile Seizures
CLIFFORD C. LUTZ, MD MAJOR, MC, USA Department of Emergency Medicine, Brooke Army Medical Center, Fort Sam Houston, Texas Chapter 06. Hymenoptera Stings
JUSTIN MADILL, DO CPT, MC, USA Department of Emergency Medicine, Madigan Army Medical Center, Tacoma, Washington Chapter 06. Submersion Incidents
ANANTHA K. MALLIA, DO Department of Emergency Medicine, Brooke Army Medical Center, Fort Sam Houston, Texas Chapter 17. AcetaminophenToxicity; Cyclic Antidepressant Toxicity; Digitalis Glycoside Toxicity
MARGARET MANN-ZEBALLOS, MD Department of Surgery, Division of Emergency Medicine, University of Texas Health Science Center at San Antonio, San Antonio, Texas Chapter 19. Prostatitis
DANIEL F. MCBRIDE, MD United States Army, Medical Corps Chapter 13. Otitis Media
SAMUEL TIMOTHY MCILRATH, MD Medical College of Georgia, Augusta, Georgia Chapter 13. Pediatric Bacteremia, Sepsis, and Meningitis; Pediatric Diarrhea
xiv CONTRIBUTORS
JOHN MCMANUS, MD, MCR, FACEP, LTC, MC, USA Clinical Investigator at Army Institute of Surgical Research, Brooke Army Medical Center, San Antonio, Texas; Adjunct Assistant Professor Emergency Medicine, Oregon Health and Science University, Portland, Oregon Chapters 06. Altitude-Related Conditions; Frostbite; Hypothermia; 13.Cardiopulmonary Arrest in Children
CHRISTOPHER R. MCNEIL, MD,CPT, USA Department of Emergency Medicine, Brooke Army Medical Center, Fort Sam Houston, Texas Chapters 02. Automatic Implantable Cardioverter-Defibrillators; Cardiac Arrhythmias; Cardiac Tamponade; Prosthetic Heart Valve Dysfunction; Heart Transplant; 08. Rhabdomyolysis; 13. Pediatric Cardiopulmonary Resuscitation; Pediatric Diabetes and Pediatric Diabetic Ketoacidosis
SUMERU GHANSHYAM MEHTA, MD,CAPT, MC, USA Department of Emergency Medicine, Brooke Army Medical Center, Fort Sam Houston, Texas Chapters 06. Heat Injuries; 10. OvarianTorsion; 19.Torsion of the Testicle
CARL MENCKHOFF, MD, FACEP, FAAEM Associate Professor, Residency Director, Department of Emergency Medicine, Medical College of Georgia, Augusta, Georgia Chapters 01.Wound Management; 12. Injuries to the Forearm and Wrist; Injuries to the Lower Leg
KAZUO MIHATA, MD United States Air Force, Medical Corps Chapter 13. Neonatal Emergencies; Hirschsprung’s Disease or Congenital Aganglionic Megacolon; Pyloric Stenosis; The Abused Child; Tetralogy of Fallot
MICHAEL A. MILLER, MD, LTC, MC, USA Department of Emergency Medicine, Darnall Army Community Hospital, Fort Hood, Texas Chapter 17. Amphetamines; Lithium; Organophosphorus and Carbamate Insecticides Poisoning
JAMES ALAN MORGAN, DO,COL, MC, USA (RET) Assistant Professor, Department of Surgery, Division of Emergency Medicine, University of Texas Health Science Center at San Antonio, San Antonio, Texas Chapters 06. Marine Fauna Evenomations; 15. Acute Respiratory Distress Syndrome; Hemoptysis; 17.Carbon Monoxide
JULIE ANN MORGAN, MD,COL, MC, USA (RET) Brooke Army Medical Center, Fort Sam Houston, Texas Chapters 06. Electrical Injuries; Marine Fauna Evenomations; 15. Acute Respiratory Distress Syndrome; Hemoptysis; 17.Carbon Monoxide
KARI MURPHEY, PA-C Emergency Medicine Physician Assistant, Medical College of Georgia, Augusta, Georgia Chapter 19. Renal Stones
Contributors
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YOKO NAKAMURA, MD Visiting Physician, Department of Emergency Medicine, Oregon Health and Science University, Portland, Oregon Chapter 17.Clonidine; Phenytoin
ALICIA NASIR, RN, BSN Andrews Air Force Base, Maryland Chapter 02. Mitral Valve Prolapse
JAVED M. NASIR Medical Student, Uniformed Services University of the Health Sciences Chapter 13. Acute Rheumatic Fever
ROBERT NOLAN, DO,CPT, MC, USA Chief Resident, Emergency Medicine, Madigan-University of Washington, Tacoma, Washington Chapter 15. Pneumothorax
BRENDA OSWALD, PA-C, MHE Physician Assistant in Emergency Department at Medical College of Georgia, Assistant Emergency Medicine Physician Assistant Residency Director, Clinical Faculty with Physician Assistant Department, Augusta, Georgia Chapter 12, Injuries to the Forearm and Wrist; Injuries to the Lower Leg
STACEY BLACK PEARLMAN, PA-C, MPAS Saint Vincent Hospital at Worcester Medical Center, Worcester, Massachusetts Chapter 15.The Basics of Ventilator Management in the Emergency Department; Ventilator Settings and Ongoing Monitoring of Critical Patients in the Emergency Department; Sedation and Analgesia in the Intubated Patient
JAMES A. PFAFF, MD,COL, MC, USA (RET) Brooke Army Medical Center, Department of Emergency Medicine, Fort Sam Houston, Texas Chapter 05. Dental Emergencies; Maxillofacial Injuries; Ophthalmological Emergencies; Otolaryngolical Emergencies; Pharyngitis; Sialolithiasis; Sinusitis; Dental Trauma
KRISTEN A. PLASTINO, MD Assistant Professor, Program Coordinator, Sex Education Program, Associate Residency Program Director, Department of Obstetrics and Gynecology, University of Texas Health Science Center at San Antonio, San Antonio, Texas Chapter 10. Placenta Previa
ERIC R. PRESSER Transplant Center, University of Texas Health Science Center at San Antonio, San Antonio, Texas Chapter 20.Cardiac and Lung Transplantation
xvi CONTRIBUTORS
LON RAMEY, PA-C Faculty Associate, Division of Neurosurgery, Department of Surgery, University of Texas Health Science Center at San Antonio, San Antonio, Texas Chapter 18. Spinal Cord Injuries
JAKE ROBERTS, DO,CPT Department of Emergency Medicine, Madigan Army Medical Center, Tacoma, Washington Chapter 13. Urinary Tract Infections in Children
DAWN F. RONDEAU, RN, MS, ACNP-CS Acute Care Nurse Practitioner, Washington State University, Pullman, Washington Chapter 13. Upper Respiratory Emergencies in Children
STEVEN W. SALYER, PA-C,CPT, USA (RET) Emergency Medicine Physician Assistant, San Antonio, Texas Chapters 09. Ataxia, Dizziness, and Vertigo; Headaches; 12. Basic Principles of Orthopedic Injuries; Acute Back Pain; 13.The Pediatric Patient: An Overview; Seizures and Status Epilepticus; 15.Chronic Obstructive Pulmonary Disease; 18. Genitourinary Tract Trauma; Pediatric Trauma
KATHLEEN M. SAMSEY, MD,CPT, MC, USA Department of Emergency Medicine, Brooke Army Medical Center, Fort Sam Houston, Texas Chapter 12. Hip Trauma
JOHN ROBERT SCOTT, MD Assistant Professor, Department of Surgery, Division of Emergency Medicine, University of Texas Health Science Center at San Antonio, San Antonio, Texas Chapters 11. Blood Transfusions; 13. Reye’s Syndrome
MICHAEL K. SHAFE´, MD, FACEP, FAAEM Assistant Professor Department of Emergency, Medical College of Georgia, Augusta, Georgia Chapters 08. Disseminated Intravascular Coagulation; 11. Acute Bleeding Diathesis; Hemophilia; Sickle Cell Anemia
MARK S. SHORT, PA-C,CAPT U.S. Army Chapter 12. Hand Injuries
SEAN MICHAEL SILER, DO,CAPT, MC, USA Department of Emergency Medicine, Brooke Army Medical Center, Fort Sam Houston, Texas Chapter 06. Diving Injuries
JACQUELYN L. SIMONDS, PA-C, MPAS Department of Emergency Medicine, Darnall Army Community Hospital, Fort Hood, Texas Chapters 10. Breast Abscesses and Mastitis; 13. Kawasaki Disease
Contributors
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HOWELL J. SMITH III, PA-C,CPT, USA (RET) Orthopedic Physician Assistant, Veterans Administration, Tampa, Florida Chapter 12. Acute Knee Pain
K.VINCENT SPEEG, MD Transplant Center, University of Texas Health Science Center at San Antonio, San Antonio, Texas Chapter 20. LiverTransplantation
RICHARD J. SPITZ, MD Clinical Assistant Professor, Department of Surgery, Department of Emergency Medicine, University of Texas Health Science Center at San Antonio, San Antonio, Texas Chapters 03. Erythema Multiforme; 08. Alcoholic Ketoacidosis
LAURA ANN SPIVAK, MD Medical Toxicology, Oregon Health and Science University, Department of Emergency Medicine, Oregon Poison Center, Portland, Oregon Chapter 17. Arsenic; Beta-Blocker Overdose; Calcium-Channel Blockers; Caustic Ingestions
MARK STEVENS, PA-C,CPT, USA (RET) Faculty Associate, Department of Surgery, Division of Emergency Medicine, University of Texas Health Science Center at San Antonio, San Antonio, Texas Chapter 17. Salicylates
BENJAMIN H.TAYLOR, PHD, PA-C Medical College of Georgia, Augusta, Georgia Chapters 03. Exfoliative Dermatitis; 12. Infections of the Bones and Joints
RALPH TERPOLILLI, MD Associate Professor, Department of Surgery, University of Texas Health Science Center at San Antonio, San Antonio, Texas Chapter 09. Acute Stroke Syndromes
SHAWN M.VARNEY, MD, LTCOL, USAF, MC Flight Commander, 959 MSFS, Wilford Hall Medical Center, Lackland Air Force Base, Texas Chapters 04. Diverticulosis and Diverticulitis; 08. Hypoglycemia
BROOKE ASHLEY VEALE, PA-C Assistant Professor, Department of Physician Assistant Studies, University of Texas Southwestern Medical Center at Dallas, Dallas, Texas Chapters 07. Malaria; 14. Panic Disorder; Generalized Anxiety Disorder; Conversion Disorder; Personality Disorders; Paranoid Personality Disorder; Schizoid Personality Disorder; Schizotypal Personality Disorder; Antisocial Personality Disorder; Borderline Personality Disorder; Histrionic Personality Disorder; Narcissitic Personality Disorder; Avoidant Personality Disorder; Dependent Personality Disorder; Obsessive-Compulsive Personality Disorder; Suicide
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CONTRIBUTORS
SHAWNA WALL, MD Department of Obstetric and Gynecology, University of Texas Health Science Center at San Antonio, San Antonio, Texas Chapter 10. Hyperemesis Gravidarum
KENNETH WASHBURN, MD Transplant Center, University of Texas Health Science Center at San Antonio, San Antonio, Texas Chapter 20. Liver Transplantation
IAN WEDMORE, MD, FACEP, LTC, MC, USA Assistant Chief, Department of Emergency Medicine, Madigan Army Medical Center, Tacoma, Washington Chapter 06. Altitude-Related Conditions; Hypothermia
RYAN WELLS, MD Willford Hall Medical Center, Lackland Air Force Base, San Antonio, Texas Chapters 01.Cholelithiasis and Cholecystitis; 15. Asthma
ALLEN WHITFORD, DO, LTC, MC, USA (RET) Assistant Professor, Department of Emergency Medicine, University of Texas Health Science Center at San Antonio, San Antonio, Texas Chapter 16. Airway Management; Shock
CLAUDIO F. ZEBALLOS, MD Assistant Professor, Department of Surgery, Division of Emergency Medicine, University of Texas Health Science Center at San Antonio, San Antonio, Texas Chapters 04. Anorectal Disorders; 07. Rabies; 19. Epididymitis
DAVID ZINSMEISTER, PA-C Assistant Professor, Department of Orthopedics, University of Texas Health Science Center at San Antonio, San Antonio, Texas Chapter 12. Acute Compartment Syndrome; Open Fractures
Preface When I first walked into an “Emergency Room” in 1987, as a young PA student, CTs were just coming into general use. MRIs were an experimental radiological test, tPA and Streptolinase-plasminogen were still “voodoo” medicine and cardiac catheterization labs were not yet in general use. We had to “practice” medicine! Back then we still examined patients. We had to! We did not have the radiological or laboratory tests we had today. We talked to patients and listened to them. Patients told us what was wrong with them. You didn't have to have three specialty consults before you could get someone admitted. No one got sued! Patients and insurance companies paid their bills. Patient's respected doctors and PAs; we respected patients and their beliefs. We asked about their families. We were able to talk about fishing! Emergency Medicine wasn't yet a business. With that said, things have gotten better. If you diagnosed someone with HIV/AIDS in 1987, it was a death sentence. With the four drug therapies of today, the life expectancy of someone with HIV is normal. Cardiac catheterization and stents save thousands of lives yearly. We have orthopedic replacement parts for just about every joint! On the horizon, stem cell research will “cure” many diseases in our lifetime. Gene splicing will prevent future human beings from ever developing the diseases that kill us today. We will develop a vaccine for HIV. Emergency Medicine will change and evolve just like all other medical specialties. But we will always be the “safety net” of society. Emergency Medicine and the “emergency room” will always be the last refuge of the sick, injured, tired, and lonely. We will still see and treat all comers no matter what their insurance is or what side of town they live on. They probably won't pay us. If they think we messed up, they will find a lawyer on TV and sue us. We will still listen and console. We will be social worker, chaplain, big brother, and the giver of hope at 3 AM. We will still see that one last patient 5 minutes before our shift change, and we will always leave late. This book is a continuum of the evolution of Emergency Medicine. I spent 4 years in the 2nd Armored Calvary Regiment in Germany. I am a veteran of Desert Storm I. I have practiced a lot of emergency medicine during my time in the Army in a tracked vehicle and a tent. Whether in a tent or a modern emergency center, the principles of emergency medicine are the same; care for the individual’s body, save lives, and never forget to care about the person.
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xx PREFACE
The 2nd Calvary Regiment is the longest continuous active-duty unit in the U.S. Army (1832). During WWI in France, the regiment obtained the regimental motto of Toujours Pret (always ready). If Emergency Medicine ever had a motto I believe it would also be Toujours Pret. Steven W. Salyer, PA-C
Introduction This is my second book on Emergency Medicine. I wrote the first book in its entirety. This is not a second edition of the first book. I selected the best emergency medicine physician assistants and emergency medicine physicians in the country to contribute to this book. Many of the chapter's authors were or are faculty at Emergency Medicine residencies. These are the best emergency medicine minds I could find. I also sought the best non-emergency medicine minds to write the complementary chapters to the book. There is no better an example of the quality of their writing than in the transplant chapters. I have expanded the transplant chapter to include topics on heart, lung, liver and kidney transplants. These topics are written by some of the best transplant practitioners in the country. This is a unique book in that the contributing chapter authors are Physician Assistants, Nurse Practitioners and physicians. It is edited by a Physician Assistant. This collaboration of different practitioners is unique in the medical publishing community. The evolution of the “team process” is evident in collaboration in the production of this book. With the business concern over billing and reimbursement, we have added ICD codes to the beginning of each chapter. This addition will help with identification of the illness or disease and hopefully will increase reimbursement. We have also added “Key Points” and “Emergency Actions” at the beginning of each topic. In a busy emergency department, the “Key Points” section will serve as a quick reference to give the practitioner the key points of knowledge about the illness or condition. The “Emergency Actions” section of each topic will act as a quick reference for the practitioner to refer to what emergency actions need to be taken immediately. This book is designed to be used, not to sit on a shelf. In a year's time, its corners should be bent and its pages worn. Please enjoy and use this book.
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Chapter 1
Acute Surgical Abdominal Emergencies Abdominal Aortic Aneurysm (AAA) MARC L. DAYMUDE
ICD Code: 441.4
Key Points/Quick Reference Abdominal aortic aneurysm (AAA) is diagnosed in most patients as an incidental finding on examination or radiologic procedure for another reason. Most patients who present with ruptured AAA, a life-threatening condition, are unaware that they have an AAA. Ruptured AAA should be suspected in all patients at risk who report abdominal pain, back or flank pain, or symptoms of hypotension such as syncope, even if transient. ! Emergency Actions ! If an AAA is suspected, two large-bore intravenous (IV) lines should be started, a cardiac monitor should be placed, emergent abdominal ultrasound and computed tomography (CT) scans should be performed, and an emergent surgical consult should be obtained.
DEFINITION An aneurysm is a permanent, focal dilation of an artery to greater than 1.5 times its expected diameter, involving all layers of the arterial wall (i.e., intima, media, and adventitia). Although any artery can develop an aneurysm, it is most commonly found in the infrarenal aorta. An infrarenal aortic diameter of 3 cm or greater is defining. This is a different entity from dissection, in which blood flows through a tear in the intima, resulting in a false lumen and dilation of the artery. Pseudoaneurysms are localized arterial wall ruptures that are contained by the adventitia and fibrous reaction and result in focal arterial wall expansion. They commonly result from trauma, infection, or previous surgical intervention of the arterial wall.
EPIDEMIOLOGY AAA is a disease primarily of the elderly. Risk factors include atherosclerotic disease, age older than 50 years, and hypertension. Smoking is the most important risk factor. Men are affected twice as often as women. AAA in first-degree relatives represents an 11.6-fold increased risk. Patients with connective tissue disorders such as Ehlers-Danlos or 1
2 ESSENTIAL EMERGENCY MEDICINE FOR THE HEALTHCARE PRACTITIONER
Marfan syndromes may develop AAA at an earlier age. Incidence in the United States is estimated at 2%–4% in patients older than 50 years and increases to 5%–10% in men over the age of 65 years. The majority of AAAs occur distal to the renal arteries. Two percent extend proximally to include the renals and thoracic portion of the aorta. Forty percent extend distally to involve the iliac arteries. The natural progression of AAA is to gradually expand, then rupture, resulting in fatal hemorrhage. The average rate of enlargement is 0.4 cm/yr. The risk of rupture increases with diameter. AAAs less than 4 cm in diameter have very low risk of rupture, whereas the risk for 4- to 5-cm AAAs is 1%–3%/yr, for those 5–7 cm is 6%–11%/yr, and for those greater than 7 cm is 20%/yr. The mortality rate for ruptured AAA is 78%–94%, with only half of patients surviving the journey to the hospital. The operative mortality rate for ruptured AAA is approximately 50%. Ruptured AAA accounts for an estimated 15,000 deaths per year in the United States and is the tenth leading cause of death. Seventy-five percent of patients presenting to the hospital with a ruptured AAA are unaware that they have an AAA. AAA management is aimed at prevention of rupture and usually involves elective surgical repair. Elective surgical mortality is less than 5%. Patients who survive repair have an excellent prognosis, with life expectancy similar to nonaffected cohorts. The cause of death in these patients is usually from cardiac causes.
CLINICAL PRESENTATION Most patients are diagnosed with AAA as an incidental finding during physical examination or radiographic procedure performed for another reason; most patients are asymptomatic at the time of presentation. The triad of abdominal pain, palpable pulsatile abdominal mass, and hypotension is present in only 30%–50% of patients with ruptured AAA. Patients often present with atypical complaints. The majority of ruptures are left retroperitoneal and may result in left lower quadrant pain and tenderness. Flank pain mimicking renal colic is common, and ureterolithiasis is misdiagnosed in 10% of patients with AAA. Expansion of a retroperitoneal hematoma may result in compression of nerve roots, most commonly femoral and obturator. Five percent of patients report neurologic problems, including anterior thigh pain and numbness with hip flexor weakness. Syncope, diaphoresis, nausea, and vomiting may be the only symptoms related to transient hypotension. Twelve percent of AAAs are initially diagnosed as diverticulitis. Five percent present with peripheral microemboli resulting in “blue toe syndrome.” Hypotension and shock may dominate the presentation. Retroperitoneal ruptures may tamponade and have delayed presentations of days to weeks. Free intraperitoneal ruptures that occur in 10%–30% result in rapid exsanguination, and these patients rarely survive long enough to make it to the hospital. The
Abdominal Aortic Aneurysm (AAA)
3
expanding mass of the AAA may erode into adjacent structures. Aortoenteric fistula results from erosion into the duodenum (most common) and can present as massive upper gastrointestinal tract bleeding. Erosion into the inferior vena cava results in aortocaval shunting and high-output heart failure manifested as dyspnea, jugular venous distention, venous distention, and pulmonary edema.
EXAMINATION Physical examination is not a reliable method to exclude AAA in the patients at risk. A pulsatile abdominal mass—especially if it extends to the right of midline—is suggestive. However, only 30% of AAAs 3–4 cm in diameter, 50% of AAAs 4–5 cm, and 75% of AAAs greater than 5 cm are palpable. Abdominal bruits are present in only 5%–10% and may indicate atherosclerotic occlusive disease of other vessels. Femoral pulses usually are normal.
LABORATORY FINDINGS Laboratory findings are not helpful in establishing the diagnosis of AAA and may be misleading. Hematuria may result from compression of the ureters and is common in aortocaval fistula due to increased renal vein pressure. This, in the face of reports of flank pain, may suggest ureterolithiasis.
DIAGNOSIS Ruptured AAA should be in the differential diagnosis of any patient over the age of 50 years who presents with flank or abdominal pain, hypotension, or syncope. In a patient whose condition is unstable, a palpable, pulsatile abdominal mass is all that is needed to obtain emergent surgical consultation for immediate surgery. In other patients, ultrasound or CT scans may be necessary to establish the diagnosis.
RADIOGRAPHS Plain radiography of the abdomen may reveal the “eggshell” appearance of a calcified AAA, but it is not helpful in excluding AAA from the differential diagnosis in patients who are at risk. Multiple studies have demonstrated that ultrasound is 100% sensitive in the detection of AAA and that this can be done at the bedside in the emergency department (ED) by emergency physicians using portable ultrasound devices with the same accuracy. ED bedside ultrasound for AAA has been demonstrated to significantly decrease time to diagnosis and disposition. Obesity and bowel
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gas may limit visualization of the aorta in some patients, making diagnosis difficult. All patients who are at risk for AAA should have bedside ultrasound scanning performed in the ED. Stable patients can undergo a formal ultrasound or CT scan. The advantages of CT over ultrasound are that CT can better define the extent of disease, identify retroperitoneal hemorrhage or rupture, or identify alternative diagnoses in the setting of a normal aorta. The major disadvantage is that the patient must leave the ED to go to receive the CT scan, and resuscitation is often difficult in that setting. Aortography is helpful for preoperative planning in elective repairs but is not indicated for diagnosis in the ED.
TREATMENT AND OUTCOME For patients whose AAA is found incidentally and is truly asymptomatic, outpatient referral to surgery for elective repair is appropriate. These patients should be cautioned to return for any symptoms potentially referable to AAA. Patients who have suspected rupture of AAA require access via two large-bore IV lines. Blood samples should be drawn for baseline complete blood count (CBC), blood urea nitrogen (BUN)/creatinine and electrolyte measurements, coagulation studies, and type and cross-match for 10 units of blood. Definitive treatment requires operative repair. An emergency surgical consultation should be made as soon as the diagnosis of ruptured AAA is suspected. Preoperative hypotension is the most important prognosticator of mortality. Patients whose conditions are unstable require aggressive fluid/blood product resuscitation to maintain a systolic blood pressure of 90–100 mmHg or adequate cerebral (i.e., normal mental status) and cardiac (no ischemic chest pain/electrocardiographic changes) perfusion.
Bibliography Barkin AZ, Rosen CL: Ultrasound detection of abdominal aortic aneurysm, Emerg Med Clin North Am 2004;22(3):675–682. Bessen HA: Abdominal aortic aneurysm. In Marx J (ed): Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 5. Mosby: St Louis, 2002, pp 1176–1186. Lin PH, Bush RL, McCoy SA, et al: A prospective study of a hand-held ultrasound device in abdominal aortic aneurysm evaluation, Am J Surg 2003;186(5):455–459. Rogers RL, McCormack R: Aortic disasters, Emerg Med Clin North Am 2004; 22(4):887–908. Salen P, Mclanson S, Buro D: ED screening to identify abdominal aortic aneurysm in asymptomatic geriatric patients, Am J Emerg Med 2003;21(2):133–135. Zarins CK, Heikkinen MA, Hill BB: Aneurysmal vascular disease. In Townsend CM (ed): Sabiston Textbook of Surgery, ed 17. Elsevier: St Louis, 2004, pp 1969–1981.
Appendicitis
5
Appendicitis MARC L. DAYMUDE
ICD Code: 541
Key Points/Quick Reference Classically acute appendicitis develops as diffuse, periumbilical pain followed by nausea, vomiting, low-grade fever, and anorexia. Over the course of 12^18 hours, the pain localizes to the right lower quadrant with evidence of local peritoneal irritation on examination. The CBC and differential that usually show an elevated white blood cell count (WBC) with a left shift and normal urinalysis results are the most relevant laboratory findings. Diagnosis may be made purely on the basis of history and physical examination in classic cases, or it may require an ultrasound or CT scan in conjunction with surgical consultation. Treatment is primarily surgical. ! Emergency Actions ! Patients who present having experienced 12–18 hours of abdominal pain and the above symptoms should have their fluids replenished; should be treated for their pain, nausea, and vomiting; and should undergo an emergent abdominal CT scan. If an acute appendicitis is present, an emergent surgical consult should be obtained.
DEFINITION The appendix is an appendage off the base of the cecum of uncertain function. It contains lymphoid and mucus-producing tissues. In an adult, its length averages 9 cm but may range from 2 to 22 cm. The location of the tip varies from retrocecal, intraperitoneal in 65% to pelvic in 30% and retroperitoneal in 2%. Acute appendicitis is an inflammatory process of the appendix, usually precipitated by luminal obstruction caused by lymphoid hyperplasia, appendicolith, fecal material, or other foreign body resulting in bacterial overgrowth.
EPIDEMIOLOGY Normal appendiceal lymphoid tissue gradually increases through adolescence then slowly decreases after the third decade, corresponding to peak incidence of appendicitis in the late teens to 20s. The lifetime risk of acute appendicitis is 8.6% in men and 6.7% in women, with a general
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population perforation rate of 17%–20% and a mortality rate of 0.25%. Although appendicitis is less common in young children and elderly persons, perforation rates are as high as 30%–65% in children and 70% in patients older than 60 years. Children also have a higher rate of general peritonitis. The mortality rate in elderly persons is 4%–8%, and the risk of complications and mortality increase with perforation. Annually, 250,000 appendectomies are performed in the United States. Historically, attempts were made to balance the risk of perforation with its higher incidence of complications and mortality in patients with unrecognized appendicitis with the removal of normal appendices. Negative appendectomy rates were accepted at 15%–20% to decrease the chances of missing a case of appendicitis that would go on to perforate.
CLINICAL PRESENTATION The typical history of appendicitis is of generalized abdominal pain followed by nausea and anorexia. Pain is initially most prominent in the epigastrium, then migrating to the periumbilical region, and over a period of hours localizing in the right lower quadrant. Pain typically precedes the onset of nausea and vomiting. As the pain becomes localized, patients may report that activities that jar the abdomen such as jumping, bumps in the road while driving, or coughing exacerbate the pain. Diarrhea is uncommon except in children. Low-grade fever may be present. Because of the varied location of the tip of the appendix, atypical presentations are not uncommon and occur in 20%–33% of affected patients. Atypical presentations are more likely in elderly persons and in young children. The location of the appendix is also affected by pregnancy, with its position becoming more cephalad and lateral as the gravid uterus displaces abdominal contents with the progression of pregnancy; this alters the site of pain, as well. Eighty-three percent of patients present in the first 48 hours of the inflammatory process. Patients who present beyond that time are more likely to have a perforated appendix, fever, and evidence of peritonitis.
EXAMINATION Examination of the abdomen may reveal diminished bowel sounds and localized tenderness in the right lower quadrant. With the progression of inflammation, abdominal muscle spasm may progress from voluntary in response to pain to involuntary guarding. Rebound tenderness may also develop. Signs of peritoneal irritation are often present but are not specific for appendicitis. Psoas sign is elicited by having the patient lie on his or her left side while the right thigh is flexed backward. Pain may indicate an inflamed appendix overlying the psoas muscle. Rovsing sign is pain
Appendicitis
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referred to the right lower quadrant when the left lower quadrant is palpated. A positive obturator sign is pain that is elicited in a supine patient by internally and externally rotating the flexed right hip. Rectal examination may reveal right rectal tenderness or an inflammatory mass. Women require pelvic examination to identify possible gynecologic sources of their pain. With perforation, abdominal pain, tenderness, and guarding may be more pronounced and diffuse.
LABORATORY FINDINGS The total leukocyte count is elevated over 10,000 in 88% of patients with appendicitis. An elevation of the percentage of neutrophils (left shift) is important even in the setting of a normal total WBC. A completely normal WBC and differential is uncommon. The C-reactive protein level may be elevated but is not specific. Urinalysis may reveal pyuria due to the proximity of the ureter to the appendix. Other laboratory tests are neither specific nor helpful in establishing the diagnosis, except to exclude other possible diagnoses. A pregnancy test should be performed on all women of childbearing age.
DIAGNOSIS The diagnosis of appendicitis is made primarily based on history and the results of a physical examination. Corroborative evidence includes elevation of the WBC or left shift. In patients who do not have a typical presentation or physical findings or in whom alternative diagnoses cannot be excluded, radiologic studies can help establish the diagnosis.
RADIOGRAPHY Plain radiographs may reveal an appendicolith but are generally not useful. Ultrasound scanning using graded compression has been shown in multiple studies to have greater than 85% sensitivity and 90% specificity. Sonographic criteria for the diagnosis of acute appendicitis are noncompressible appendix greater than 7 mm in diameter, the presence of an appendicolith, submucosal incontinuity, or periappendiceal fluid or mass. It is less sensitive for perforated appendicitis. Sonography is operator dependent, and patient body habitus can affect performance. CT has essentially supplanted ultrasound scanning, except in specific patient populations such as pregnant women or persons with contrast allergy. The sensitivity and specificity of CT for appendicitis are both around 90%, depending on the clinical study and the use of oral, IV, and rectal contrast. CT criteria for diagnosing appendicitis are an appendix greater than 5–7 mm in diameter, a “target” sign of
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circumferential thickening, and periappendiceal inflammation. CT in conjunction with serial examinations and clinical observation in patients who have atypical presentations or equivocal findings or who are at high risk have lowered the negative appendectomy rate to 2% in some studies without increasing the rate of perforation.
TREATMENT AND OUTCOME When the diagnosis of appendicitis is suspected, urgent surgical consultation is required. Vomiting and anorexia can result in dehydration. Patients should receive replenishing fluids and not receive anything by mouth before possible surgery. Narcotic pain medications have been shown not to significantly change physical examination findings. The patient’s pain should be addressed. If perforation is suspected, treatment with broadspectrum antibiotics that cover coliform and anaerobic bacteria should be initiated. Definitive treatment requires surgical removal of the inflamed appendix, either laparoscopically or by open technique, as determined by the consultant.
Bibliography Cydulka RK: Meta-analysis of the clinical and laboratory diagnosis of appendicitis [abstract], Ann Emerg Med 2005;45(1):105. Jones K, Pena AA, Dunn EL, et al: Are negative appendectomies still acceptable? Am J Surg 2004;188(6):748–754. Lally KP, Cox CS, Andrassy RJ: Appendix, In Townsend CM (ed): Sabiston Textbook of Surgery, ed 17. Elsevier: St Louis, 2004. Lin CJ, Chen JD, Tiu CM, et al: Can ruptured appendicitis be detected preoperatively in the ED? Am J Emerg Med 2005;23(1):60–66. McCollough M, Sharieff GQ: Abdominal surgical emergencies in infants and young children, Emerg Med Clin North Am 2003;21:909–935. Morris KT, Kavanagh M, Hansen P, et al: The rational use of computed tomography scans in the diagnosis of appendicitis, Am J Surg 2002;183(5):547–550. Storm-Dickerson TL, Horattas MC: What have we learned over the past 20 years about appendicitis in the elderly? Am J Surg 2003;185(3):198–201. Wolfe JM, Smithline HA, Phipen S, et al: Does morphine change the physical examination in patients with acute appendicitis? Am J Emerg Med 2004;22(4):280–285.
Cholelithiasis and Cholecystitis
9
Cholelithiasis and Cholecystitis RYAN WELLS
ICD Codes: Calculus of gallbladder with acute cholecystitis 574.0, Calculus of gallbladder with other cholecystitis 574.1, Acute cholecystitis 575.0, Other cholecystitis (without mention of calculus) 575.1
Key Points Cholelithiasis (gallstones) is a very common presenting feature in obese, fertile female patients. Cholecystitis causes prolonged pain in the upper abdomen.The diagnosis of cholelithiasis should be entertained in any diabetic patient with right upper quadrant pain, fever, nausea, and vomiting. ! Emergency Actions ! Any patient who presents with fever, sepsis, and cholelithiasis should be administered IV fluids and antibiotics, and an immediate right upper quadrant ultrasound scan should be performed. An immediate surgical consultation should be sought.
DEFINITION Gallstones are crystalline structures formed from both normal and abnormal bile components. Bile is a pigmented, isotonic fluid that is composed of primarily water and bile acids. Bile is formed in the hepatocytes and is required for the breakdown and absorption of fats in the intestines. The biliary tract consists of the gallbladder, the hepatic bile canaliculi, the intrahepatic bile ducts, the extrahepatic bile ducts, the cystic duct, and the common bile duct. Bile is manufactured in and secreted from hepatocytes before being transported via portions of the biliary tract to the gallbladder for storage. While in the gallbladder, stored bile is concentrated and acidified. Cholelithiasis is the formation of gallstones in any part of the biliary tract. Seventy percent of gallstones are cholesterol stones, and the remainders are pigment stones. The principal cause of biliary tract disorders is related to the formation of gallstones. Gallstones can be asymptomatic, or they can lead to obstruction of the gallbladder and bile ducts, resulting in symptomatic cholelithiasis, cholecystitis, pancreatitis, or cholangitis. Cholecystitis is an acute inflammation of the gallbladder typically caused by gallstone obstruction of the neck of the gallbladder
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or at the cystic duct. However, between 5% and 10% of cholecystitis is acalculous (without gallstones).
EPIDEMIOLOGY An estimated 10%–20% of Americans have gallstones, and as many as one third will develop cholecystitis. Risk factors for the development of cholelithiasis and subsequent cholecystitis include increasing age, obesity, female sex, rapid weight loss, pregnancy, oral contraceptives, medications, chronic intravascular hemolysis, and multiparity. There is also an increased familial tendency for the formation of gallstones. There is an increased incidence in Pima Indians and persons of Scandinavian heritage. Cholelithiasis is less common in children, yet the condition does occur in this age group. Diseases involving hemolytic anemia (e.g., spherocytosis and sickle cell anemia) increase the likelihood of developing gallstones. It is important to note that even patients without classic risk factors develop gallstones and cholecystitis. Therefore, a high index of suspicion should be maintained for anyone presenting with symptoms consistent with gallbladder disease.
PATHOPHYSIOLOGY Bile is formed in the hepatocytes and is transported via the biliary tree to the gallbladder. The gallbladder stores approximately 50 ml of bile at any one time. When the stomach receives food (especially fatty food), both vagal responses and secretion of cholecystokinin cause the gall bladder to contract. Bile is released into the duodenum for digestion of a meal. The purpose of the gallbladder is to concentrate and acidify the bile. When this process is increased or rapidly reproduced and when rising cholesterol levels are present, lecithin and bile acids act to solubilize cholesterol. While cholesterol levels rise and lecithin and bile acids decline, cholesterol comes out of solution and forms crystals or stones. Gallstones can consist of three types: cholesterol, pigmented, and mixed. Between 70% and 80% of gallstones are cholesterol stones. Pigmented gallstones come in two types: brown and black. Black gallstones occur in the gallbladder and contain high concentrations of calcium bilirubinate. Black gallstones are found more often in elderly persons and in those with sickle cell disease and hereditary spherocytosis. Brown gallstones are found in the gallbladder, intrahepatic duct, and extrahepatic duct. Brown gallstones are more often associated with infection. Gallstones may migrate into either the cystic or common bile duct and become lodged, leading to symptomatic cholelithiasis. The consequent obstruction leads to increased intraluminal pressure and distention of the gallbladder, causing pain in the right upper quadrant or epigastric region of the abdomen, nausea, and vomiting.
Cholelithiasis and Cholecystitis
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If the obstruction persists, acute cholecystitis may develop. This often occurs when a gallstone is lodged in either the cystic duct or the infundibulum of the gallbladder. Gallstones are found in 95% of the patients with cholecystitis. Duct obstruction can also occur from external causes such as tumor, parasites, fibrosis, or kinking of the duct. The inflammatory response may be complicated by infection and bacterial organisms can be isolated in 50%–75% of patients with a diagnosis of cholecystitis. The infection is often polymicrobial, but the most common individual pathogens include Escherichia coli and Klebsiella species. Although bacteria are often isolated from inflamed gallbladders, it is unclear what role infection plays in cholecystitis. The small amount of cholecystitis not associated with gallstones is called acalculous cholecystitis. Acalculous cholecystitis makes up approximately 5%–10% of cases of cholecystitis. Conditions associated with acalculous cholecystitis include major surgery, severe trauma, debilitation, sepsis, long-term total parenteral nutrition, prolonged fasting, sickle cell disease, Salmonella infections, cardiac events, and other microbial infections in patients with acquired immunodeficiency syndrome. A very small percentage of patients will develop serious complications associated with cholecystitis, including gallbladder empyema and emphysematous (i.e., gangrenous) cholecystitis. These patients are often elderly and diabetic. The patient typically presents in extremis with fever, septic shock, and right upper quadrant pain.
CLINICAL PRESENTATION Gallbladder disease can produce a wide range of symptoms. Patients may have asymptomatic cholelithiasis or they may experience biliary colic (i.e., symptomatic cholelithiasis) or acute cholecystitis. Biliary colic is the right upper quadrant or epigastric abdominal pain associated with gallstones. The classic presentation for symptomatic cholelithiasis or cholecystitis is biliary colic associated with nausea and vomiting. This often follows ingestion of foods (typically fatty foods) by about 30–60 minutes. However, it is important to note that gallstone pain is not related to meals in at least one third of patients. This pain is typically present in the right upper quadrant and may initially be colicky but often becomes constant. The pain may radiate to the right shoulder or scapula. The patient may be in severe discomfort and diaphoretic. Patients with cholecystitis may also have fever. If the patient has known gallstones or a history of similar episodes, this will aid in diagnosis. Differentiating the clinical presentation of symptomatic cholelithiasis from cholecystitis may be difficult, especially early in the presentation. Cholecystitis is more likely if the symptoms persist longer than 4–6 hours or if fever is present.
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EXAMINATION Patients with biliary colic may be in severe discomfort. On examination, they may be tachycardic and diaphoretic. Abdominal examination reveals tenderness in the right upper quadrant or epigastric region. If the patient has cholecystitis, he or she may have fever and a Murphy’s sign. Murphy’s sign is the inspiratory arrest that occurs upon palpation of the right upper quadrant during a deep breath. Fever makes the diagnosis of acute cholecystitis much more likely than simple biliary colic. However, in a retrospective chart review by Gruber et al, 71% of patients with pathologically diagnosed cases of acute nongangrenous cholecystitis were afebrile. Physicians should be cautious in considering lack of fever a comforting finding in a patient with possible cholecystitis.
LABORATORY FINDINGS Unfortunately, no single laboratory test or combination of tests will catch all cases of acute cholecystitis. Laboratory test values are expected to be normal with cholelithiasis and are often normal in cholecystitis. Nonetheless, a multitude of laboratory tests are often ordered for these patients. A CBC, urinalysis, urine pregnancy test, and measurements of electrolytes, aspartate aminotransferase (AST), alanine aminotransferase (ALT), bilirubin, international normalized ratio, alkaline phosphatase, and lipase may be ordered. The most important lab tests—clinically and diagnostically— are the urine pregnancy test and the lipase analysis. With cholecystitis, one may find an elevated CBC, AST, ALT, and alkaline phosphatase depending on the location of the gallstone in the biliary tract and the disease progression. If the lipase is elevated, the patient likely has pancreatitis. Of note, however, no lab test will make or break the diagnosis of cholecystitis.
DIAGNOSIS A diagnosis is made using a history, physical examination, and imaging study. Ultrasound, CT, and hepatobiliary scintigraphy (hepatobiliary iminodiacetic acid [HIDA] scans) are imaging options. Symptomatic cholelithiasis is differentiated from cholecystitis by complete resolution of symptoms and an ultrasound scan that reveals no evidence of cholecystitis. The differential diagnosis of gallbladder pain includes pancreatitis, cholangitis, gastritis, peptic ulcer disease, hepatitis, hepatic abscess, pyelonephritis, renal colic, right lower lobe pneumonia, pleural effusion, appendicitis, atypical myocardial infarction, pelvic inflammatory disease, and ectopic pregnancy.
Cholelithiasis and Cholecystitis
13
RADIOGRAPHS Plain radiographs can be useful if one is looking for another cause of the pain. In general, plain radiographic films will not help one to diagnose gallbladder problems. Ultrasound has become the imaging modality of choice in the ED. Ultrasound provides greater than 95% sensitivity and specificity for the diagnosis of gallstones more than 2 mm in diameter. Ultrasound is also 90%–95% sensitive for cholecystitis. Ultrasound findings consistent with acute cholecystitis include gallstones, sonographic Murphy’s sign, thickened gallbladder wall, and pericholecystic fluid. HIDA has been found to have a sensitivity approaching 100% and a specificity of 90% for diagnosing acute cholecystitis. Many believe that the HIDA scan is the gold standard imaging study. However, it is a difficult study to attain from most EDs. CT and magnetic resonance imaging (MRI) have recently been advocated for diagnosing gallbladder pathology. There are reports of significantly improving capabilities in diagnosing gallbladder disease in newergeneration CT scanners. CT is preferred over MRI in the ED because it is much quicker and more accessible than MRI. CT has an advantage over ultrasound in that it can make other diagnoses if the gallbladder is not the cause of the symptoms.
TREATMENTS AND OUTCOMES Some patients may be quite ill, especially elderly persons. The ABCs of life support (i.e., airway, breathing, and circulation) must be evaluated and treated. Oxygen administration and cardiac monitoring should be used at least until a cardiac cause is ruled out. The treatment of biliary colic consists of the administration of IV fluids, analgesics, and antiemetics and, rarely, nasogastric suctioning for intractable vomiting. Analgesia can be accomplished with ketorolac or ibuprofen (if tolerating oral) and narcotics. Some practitioners prefer meperidine over morphine because it is thought to cause less spasm to the sphincter of Oddi. However, many authorities feel this is not clinically relevant. Antiemetics include promethazine (Phenergan), prochlorperazine (Compazine), metoclopramide (Reglan), or ondansetron (Zofran). Treatment and time will cause symptoms of symptomatic cholelithiasis/biliary colic to resolve, usually within 4–6 hours. If symptoms are initially thought to be due to symptomatic cholelithiasis but they do not resolve, early acute cholecystitis should be considered. Treatment of acute cholecystitis consists of all of the above plus antibiotic coverage and immediate surgical evaluation. Ampicillin/sulbactam, ticarcillin/clavulanic acid, or piperacillin/tazobactam is a good option. One may also use clindamycin with gentamicin in a penicillin-allergic
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patient. If intra-abdominal sepsis is a concern, a regimen of ampicillin, gentamycin, and metronidazole can be used. All patients with cholecystitis should be admitted to the hospital. Their definitive care will require surgery and a cholecystectomy. The timing of surgery is not universally accepted, however. Some surgeons perform the cholecystectomy on the same day, whereas others wait 24–72 hours for the gallbladder to “cool off.” Patients with acalculous cholecystitis tend to have a more aggressive course with a mortality rate as high as 41%. Emphysematous cholecystitis is a rare form of cholecystitis. Gas-producing organisms likely invade the mucosa, and gas will be found in the gallbladder wall. Treatment in the ED is the same, but surgery is performed emergently.
DISPOSITION Patients with symptomatic cholelithiasis who have complete resolution of symptoms can be discharged home. They should have close follow-up with a surgeon because definitive care for gallstone-related pain is surgery. Other less common options include medical dissolution therapy and gallstone lithotripsy. Patients may be discharged with a prescription for ibuprofen and oral narcotics to treat further episodes of biliary colic. The patient should be instructed to return to the ED immediately if fever or worsening or persistent pain (greater than 2–3 hours) occurs, if the patient is unable to tolerate food or liquids, or if a change in his or her symptoms occurs. If a patient with gallstones has persisting symptoms, he or she should not be discharged without a surgical evaluation. This is true even if the laboratory test results are all normal and possibly even if an ultrasound scan has shown gallstones, as long as no evidence of acute cholecystitis exists. Remember that none of our diagnostic studies are 100% sensitive. All patients with acute cholecystitis should be admitted to the hospital.
Bibliography Aufderheide TP, Brady WJ, Tintinalli JE: Cholecystitis and biliary colic, In Tintinalli JE (ed): Emergency Medicine: A Comprehensive Study Guide, ed 5. McGraw-Hill: New York, 2000, pp 576–580. Gladden D, Clinton B, Wolf J, et al: Cholecystitis Emedicine online journal. August 2004. Available at www.emedicine.com. Gruber PJ, Silverman RA, Gottesfeld S, Flaster E: Presence of fever and leukocytosis in acute cholecystitis, Ann Emerg Med 1996;28(3):273–277. Guss DA: Cholelithiasis and cholecystitis, In Marx J (ed): Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 5. Mosby: St Louis, 2002, pp 1265–1272. Riviello RJ, Brady WJ: Presentation and management of acute biliary tract disorders in the emergency department: Optimizing assessment and treatment of cholelithiasis and cholecystitis, Emergency Medicine Reports 2002 Aug 12:23(17). Rosen P, Barkin RM, Braen GR, et al: Cholelithiasis and cholecystitis, In Schaider J, Hayden SR, Wolfe R, et al (eds): The 5 Minute Emergency Medicine Consult. Lippincott, Williams & Wilkins: Philadelphia, 1999, pp 226–229.
Hernias
15
Shea JA, Berlin JA, Escarce JJ, et al: Revised estimates of diagnostic test sensitivity and specificity in suspected biliary tract disease, Arch Intern Med 1994;154(22):2573–2581. Singer AJ, McCracken G, Henry MC, et al: Correlation among clinical, laboratory, and hepatobiliary scanning findings in patients with suspected acute cholecystitis, Ann Emerg Med 1996;28(3):267–272.
Hernias MARC L. DAYMUDE
ICD Codes: Femoral 553, Inguinal 550.9, Umbilical 553.1, Incisional 553.21
Key Points/Quick Reference A hernia represents an abnormal protrusion of an organ or tissue through a defect in its surrounding wall. A hernia that cannot be reduced, an incarcerated hernia, is a surgical urgency because of its contents risk loss of blood flow, which is known as a strangulated hernia. ! Emergency Actions ! Any hernia that is suspected to be incarcerated or strangulated and cannot be reduced should be considered a medical emergency. Two large-gauge IV lines should be placed, the patient’s fluids should be replenished, an emergent CT scan should be obtained, and an emergent surgical consult should be sought.
DEFINITION The most common hernias involve the abdominal wall and are inguinal, femoral, umbilical, and incisional. Inguinal hernias occur in the groin superior to the inguinal ligament through a defect in processus vaginalis. A direct inguinal hernia protrudes through the muscle and fascia of the abdominal wall, whereas an indirect inguinal hernia protrudes through the internal inguinal ring into the inguinal canal. Femoral hernias protrude inferior to the inguinal ligament through a defect in the transversalis fascia into the femoral canal. Umbilical hernias pass through the fibromuscular ring of the umbilicus and can be present at birth or acquired in adulthood due to increased abdominal pressure from obesity, ascites, or
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pregnancy. Incisional hernias protrude through areas of postincisional weakness after abdominal surgery. A hernia is considered reducible if, when the abdominal muscles are relaxed and the patient is supine, the hernia contents either spontaneously or under gentle pressure return to an intra-abdominal position. An incarcerated hernia does not reduce with the above measures. A strangulated hernia is an incarcerated hernia in which the blood supply to the hernia contents is compromised by the narrow hernia defect and/or swelling. This can lead to ischemia, bowel obstruction, or perforation.
EPIDEMIOLOGY The lifetime risk of developing a hernia is 5% for males and 2% for females. Approximately 75% of all hernias are inguinal, and two thirds of these are indirect. Incisional hernias account for 15%–20% of hernias. Ten percent are ventral or umbilical, and 5% are femoral. Men are 25 times more likely to have an inguinal hernia, though this is still the most common hernia in women. Women are 10 times more likely to have a femoral hernia and twice as likely to have an incisional hernia. Femoral hernias have the highest rate of strangulation at 15%–20%. Strangulation is more common at either extreme of age.
CLINICAL PRESENTATION Asymptomatic hernias present as a painless lump or bulge at the site. Less commonly, pain may be part of the reported symptoms caused by the compression of local nerves or the hernia defect by the contents as it slides in and out. Incarcerated hernias present with progressive pain and swelling, often at the site of a known hernia. A strangulated hernia may involve features suggestive of bowel obstruction with pain, swelling, nausea, vomiting, and obstipation. The strangulated hernia may become blue or purple and have significant tenderness. There may also be clinical evidence of perforation with fever, shock, and peritoneal tenderness.
EXAMINATION A complete examination must include examination of the suspected hernia in positions that place it both dependent and not dependent to the pull of gravity. For most abdominal hernias, this could be the standing position in which gravity would pull hernia contents through the defect and the supine position, which would allow gravity to pull the hernia contents back into the intraperitoneal cavity. These can be augmented by having the patient perform a Valsalva maneuver to increase intra-abdominal pressure and thereby demonstrate the hernia. Direct palpation over the areas of
Hernias
17
concern during position changes and resultant changes in the hernia mass help to differentiate hernias from other causes of a “lump” and may demonstrate the actual abdominal wall defect.
LABORATORY FINDINGS In hernias found to be uncomplicated by examination, laboratory testing is not necessary. In patients with suspected incarcerated or strangulated hernias, CBC, electrolyte measurements, and renal function tests may reveal an elevated WBC with left shift and evidence of volume depletion. In patients in whom the diagnosis is not clearly hernia, laboratory values may help differentiate other causes of a lump, especially in the inguinal region where adenopathy or genital pathology may mimic a hernia.
DIAGNOSIS The diagnosis of hernias is primarily clinical, with the demonstration on examination of a mass that protrudes when under increased pressure, such as with gravity or a Valsalva maneuver, and recedes when the pressure is decreased or with gentle palpation. Incarcerated or strangulated hernias or “bulges” that are not clearly hernias may require radiologic evaluation.
RADIOGRAPHS Plain supine and upright films of the abdomen may demonstrate free air from perforation or evidence of bowel obstruction in cases of suspected incarceration or strangulation, but these are generally not useful in the evaluation of hernias. Ultrasound is highly sensitive and specific in the diagnosis of inguinal and femoral hernias. CT may be useful in detecting less common hernias and in identifying ischemic hernia contents.
TREATMENT AND OUTCOME Patients with hernias that are easily reduced in the ED may be discharged home with outpatient surgical consultation and precautions to return if they experience increased pain, fever, nausea and vomiting, or irreducibility of the hernia mass. Reduction of hernias may require adequate pain management to relax the abdominal wall and putting the patient into Trendelenburg’s position and applying gentle pressure. Hernias should not be forced back in because of the risk of reducing necrotic bowel into the peritoneal cavity and inducing diffuse peritonitis. Patients with
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suspected incarcerated or strangulated hernias require urgent surgical evaluation in the ED. If there is evidence of strangulation and bowel obstruction or perforation, fluid resuscitation and treatment with broadspectrum antibiotics should be initiated while surgical consultation is awaited.
Bibliography Blaivas M: Ultrasound-guided reduction of a Spigelian hernia in a difficult case: An unusual use of bedside emergency ultrasonography, Am J Emerg Med 2002;20(1):59–61. Fitzgibbons RJ, Jonasson O, Gibbs J: The development of a clinical trial to determine if watchful waiting is an acceptable alternative to routine herniorrhaphy for patients with minimal or no hernia symptoms, J Am Coll Surg 2003;196(5):737–742. Frager D: Intestinal obstruction: Role of CT, Gastroenterol Clin 2002;31(3):777–799. Malangoni MA, Gagliardi RJ, Hernias. In Townsend CM: Sabiston Textbook of Surgery, ed 17. Elsevier: St Louis, 2004, pp 1199–1217. Manthey DE: Abdominal hernia reduction. In Roberts JR, Hedges JR: Clinical Procedures in Emergency Medicine, ed 4. Elsevier: St Louis, 2004, pp 860–866. Perrott CA: Inguinal hernias: Room for a better understanding, Am J Emerg Med 2004;22 (1):8–50.
Intestinal Obstruction MARC L. DAYMUDE
ICD Code: 560.9
Key Points/Quick Reference In adults the most common cause of small bowel obstruction (60%^75%) are adhesions from previous abdominal surgery. Malignancy, from primary or secondary metastatic lesions, is the second most common cause of obstructions in adults. In infants aged 2^3 weeks, pyloric stenosis is the most likely cause of obstruction. In children aged 3 months to 6 years, intussusception is the most likely cause of bowel obstruction. ! Emergency Actions ! Any patient who is suspected to have an intestinal bowel obstruction should have two large-gauge IV lines placed, and aggressive fluid resuscitation should be started. Upright and flat plain radiographs should be obtained. If an intestinal bowel obstruction is suspected, an abdominal CT scan and an emergent surgical consult should be obtained.
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DEFINITION Bowel obstruction represents a mechanical interruption in the flow of intraluminal intestinal contents. The etiology and treatment of the obstruction vary widely depending on whether the interruption occurs in the small or large bowel. The terms pseudo-obstruction, ileus, or Ogilvie's syndrome represent a functional decrease in bowel motility and progressive dilation that is thought to result from autonomic imbalance from multiple causes.
EPIDEMIOLOGY In adults, the most common cause of small bowel obstruction (60%–75%) is adhesion after abdominal surgery, especially lower abdominal and pelvic surgeries such as appendectomy, hysterectomy, and colectomy. Malignancy, primarily metastatic with peritoneal implants, account for approximately 20%. The third most common cause of small bowel obstruction in adults, representing 10%, is incarcerated hernia, most commonly inguinal or ventral. Crohn’s disease accounts for 5% either by acute inflammation or chronic scarring and strictures. The remaining 2%–3% are from intraluminal obstruction from intussusception, gallstones that pass through a cholecystoduodenal fistula, enteroliths, foreign bodies, and bezoars. Rarely, intra-abdominal inflammatory masses such as from diverticulitis can cause small bowel obstruction. Large bowel obstruction in adults is predominantly caused by primary malignancy, representing 60% of obstructions. Volvulus (sigmoid 60% and cecal 40%) make up 10%–13% of large bowel obstruction. Sigmoid volvulus usually occurs in an elderly patient with debilitating diseases or in patients with severe psychiatric or neurologic diseases. A common history is of long-standing constipation. Diverticular disease with inflammatory masses or chronic scarring accounts for almost all other cases of large bowel obstruction in the United States. In children, the most common causes of bowel obstruction are age dependent. In the first 2–3 weeks of life, pyloric stenosis causes gastric outlet obstruction in 1 in 150 males and 1 in 750 females. From 3 months to about 6 years, the most common cause of small bowel obstruction is intussusception. The second most frequent cause is incarcerated hernias, especially in the younger age group. Less common causes are postsurgical adhesions, sigmoid volvulus, and Meckel’s diverticula. Pseudo-obstruction or ileus has multiple etiologies to include common medications, intra-abdominal processes, or severe stresses to the body. Common precipitants include narcotic medications, medications with anticholinergic effects, withdrawal of laxative abuse, intra-abdominal surgeries, sepsis, severe burns, pelvic or lumbar trauma or surgeries, spinal cord injuries, and retroperitoneal hematomas.
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CLINICAL PRESENTATION The classic symptoms of bowel obstruction are progressive abdominal distention, colicky abdominal pain, nausea and vomiting, and obstipation or inability to pass flatus or stool. Vomiting is a more prominent symptom the more proximal the obstruction. The crampy abdominal pain tends to occur in paroxysms 4–5 minutes apart as the bowel peristalses against the obstruction. Obstipation is a late finding. The early course may actually be marked by diarrhea due to the increased peristaltic activity both proximal and distal to the obstruction. Later in the course of obstruction, the vomitus may become feculent due to bacterial overgrowth of pooled intestinal contents proximal to the obstruction. Bowel obstruction causes the loss of absorptive properties of the bowel, leading to accumulation of fluids in the lumen, bowel wall edema with third-space fluid losses, and marked intravascular depletion. This can progress to hypotension and shock.
EXAMINATION The patient’s vital signs may reflect the severity of volume depletion with tachycardia and hypotension. Tachypnea may reveal an attempt to compensate a metabolic acidosis. Fever may suggest bowel strangulation and perforation. The abdominal examination typically reveals diffuse distention, tenderness, and tympany to percussion. Early in the course of obstruction, bowel sounds are high pitched and hyperactive with “rushes” and “tinkles.” As the obstruction progresses and the bowel becomes more distended, the abdomen may become quiet. A complete physical examination is essential to identify possible causes of the obstruction. In adults, the abdomen likely will reveal surgical scars from previous surgeries. Incarcerated hernias should be sought, especially inguinal, femoral, or incisional. A rectal examination may reveal an obstructing mass of colon cancer. Similarly, a bimanual pelvic examination may identify ovarian masses. Infants may have an epigastric “olive” of pyloric stenosis or the “sausage” mass of intussusception. “Current jelly” stools of intussusception are a late finding indicative of bowel mucosal sloughing. Focal tenderness or peritoneal signs suggest bowel strangulation, necrosis, or perforation.
LABORATORY FINDINGS Laboratory findings in bowel obstruction are nonspecific and not helpful with the diagnosis. There often will be an elevated WBC with left shift. Elevation of BUN and creatinine levels give evidence of volume depletion. Electrolyte level abnormalities—especially hypokalemia, hypochloremia, and metabolic alkalosis from vomiting—are not uncommon. Lactic acidosis may be present.
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DIAGNOSIS Diagnosis is made primarily based on history and physical examination with the support of plain upright and supine abdominal radiographs. The diagnostic accuracy of plain radiographs for small bowel obstruction is 60%. Characteristic findings include dilated loops of small bowel without colonic gas. Upright radiographs reveal multiple layers of air-fluid levels that resemble stacked coins. Cecal volvulus may have a dilated kidney-bean–shaped dilated loop of colon in the left upper quadrant. Radiographs in sigmoid volvulus reveal dilated sigmoid colon with a tapered end pointing to right upper quadrant resembling a bent inner tube. On equivocal cases, CT is 90% sensitive and specific in the diagnosis of small bowel obstruction and helpful in identifying extrinsic causes of obstruction such as internal hernias, tumors, or inflammatory masses. Barium enema may be both diagnostic and therapeutic for intussusception and sigmoid volvulus. Enteroclysis, in which contrast is instilled directly into the small bowel by a nasogastric tube then followed fluoroscopically through the bowel, may be necessary to diagnose partial or intermittent obstruction.
RADIOGRAPHS For most cases of bowel obstruction, supine and upright radiographs are the only radiographs needed to establish the diagnosis. These may also reveal some causes of obstruction such as foreign bodies or gallstones. CT, barium enema, and enteroclysis increase the diagnostic accuracy in less certain cases or in cases of partial or intermittent obstruction.
TREATMENT AND OUTCOME Emergency management hinges on establishment of the diagnosis, volume resuscitation, and prevention of further distention of the bowel. In the case of small bowel obstruction more so than large bowel obstruction, third-space fluid losses can be substantial and patients will require isotonic crystalloid fluid boluses to restore intravascular volume. Correction of electrolyte abnormalities should be initiated. A urinary catheter may aid in managing fluid resuscitation. All patients should have a nasogastric tube placed at low, intermittent suction to decompress the bowel and prevent further accumulation of fluids and swallowed air. Antibiotics are indicated for patients who have evidence of bowel strangulation, necrosis, or perforation. All patients will require surgical consultation and admission. Many patients with ileus or partial obstruction may be managed conservatively with fluid resuscitation, bowel decompression, and rest. Patients with complete obstruction or evidence of strangulation, necrosis, or perforation will require operative management.
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Bibliography Bitterman R, Peterson M: Large intestine, In Marx J (ed): Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 5. Mosby: St Louis, 2002, pp 1327–1342. Evers BM: Small intestine. In Townsend CM (ed): Sabiston Textbook of Surgery, ed 17. Elsevier: St Louis, 2004, pp 1323–1375. Frager D: Intestinal obstruction: Role of CT, Gastroenterol Clin North Am 2002; 31(3):777–799. Garcia EA: Intestinal obstruction in infants and children, Center Pediatr Emerg Med 2002;3(1):14–21. Kahi CJ, Rex DK: Bowel obstruction and pseudo-obstruction, Gastroenterol Clin North Am 2003;32(4):1229–1247. Nagle A, Ujiki M, Denham W, et al: Laparoscopic adhesiolysis for small bowel obstruction, Am J Surg 2004;187(4):464–470.
Thoracic Aortic Dissection MARC L. DAYMUDE
ICD Code: 441.01 (thoracic)
Key Points/Quick Reference Aortic dissection represents a splitting between the three layers of the aortic arterial wall: the intima, media, and adventitia. This separation of the media allows blood to flow through a false lumen and can result in rupture of the weakened arterial wall.The most common symptom is sudden, sharp chest pain that radiates to the back. Dissection, a potentially lethal condition, should be on the differential diagnosis of any patient with chest or upper back pain. ! Emergency Actions ! Any patient suspected of having an aortic dissection should immediately have two large-gauge IV lines placed, should be placed on the cardiac monitor, and should have an immediate CT angiogram and blood pressure control. If an aortic dissection is present, immediate surgical consult should be obtained.
DEFINITION Aortic dissection is a separation between the layers of the aorta caused by the shear forces of blood flow. This results from a weakening or
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degeneration of the middle layer of the aorta (i.e., the media). A tear in the arterial lining (i.e., the intima) allows blood to flow between the layers of the wall of the aorta, creating a false lumen. The weakened aortic wall can dilate and rupture. The dissection may involve arterial branches off the aorta, resulting in decreased blood flow distal to the involved area and causing additional symptoms due to ischemia. The dissection may propagate both distally and proximally from the intimal tear. Dissection is termed acute if it is diagnosed within 14 days of symptom onset and chronic if diagnosed after 14 days. Aortic dissection is distinctly different in pathogenesis, prognosis, and management from aortic aneurism, which represents a diffuse expansion of all three layers of the aortic wall to 50% or more than the normal diameter. There are two major classification systems based on the site of dissection that correlate with prognosis and guide treatment decisions: Stanford and DeBakey.
Stanford A: Involves the ascending aorta Stanford B: Does not involve the ascending aorta DeBakey I: Involves the ascending and descending thoracic aorta DeBakey II: Involves only the ascending aorta DeBakey IIIA: Does not involve the ascending aorta and is proximal to the diaphragm DeBakey IIIB: Does not involve the ascending aorta and extends distal to the diaphragm
EPIDEMIOLOGY Acute aortic dissection is the most common aortic disaster. It occurs more commonly in men and the incidence increases with age, rarely occurring before the age of 40 years. Mortality rates from dissection are 1 to 5/100,000 per year. Seventy-five percent of untreated patients with dissection die within 2 weeks of symptom onset. The most common risk factor is hypertension. Atherosclerosis is not a contributing factor in most cases. Connective tissue disorders and congenital heart syndromes such as Marfan syndrome, Ehlers-Danlos syndrome, Turner’s syndrome, giantcell arteritis, polycystic kidney disease, bicuspid aortic valve, and coarctation of the aorta contribute to increased risk of dissection at an earlier age. Pathophysiology is theorized to be due to degeneration of the media as part of the aging process that is exacerbated by hypertension. Accumulated stresses from the shear forces of blood flow and flexion of the aorta with every contraction of the heart induce a tear in the intima that allows blood to flow into the medial layer. The depth and distance of dissection is related to the degree of medial degeneration and magnitude of shear forces caused by hypertension. Dissections involving the ascending aorta are more lethal and are more often associated with complications of the aortic branch arteries than those confined to the descending aorta.
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CLINICAL PRESENTATION Pain is the most common symptom named at presentation and is present in 90% of patients with dissection. It is typically described as sharp and of sudden onset, with maximal pain from the start. The pain is sometimes described as tearing or ripping. It may involve the anterior chest with or without radiation to the neck and jaw, the interscapular region of the back, or the lumbar and abdominal areas; alternatively, it may migrate through those regions with progression of the dissection from the ascending to descending aorta. Vagal symptoms of nausea and vomiting, diaphoresis, lightheadedness, and anxiety are commonly associated. Syncope, representing acute hemorrhage and hypotension, rupture into the pericardium and tamponade or involvement of the carotid arteries interrupting cerebral blood flow occurs in 9%. Involvement of the carotid arteries may also result in stroke-like neurologic symptoms in 6%. The coronary arteries, most commonly the right coronary artery, may be occluded by the dissection and result in acute myocardial infarction, most commonly an inferoposterior myocardial infarction, when the right coronary artery is involved.
EXAMINATION Most patients will appear apprehensive, pale, and diaphoretic. Patients may be hypertensive from acute catecholamine release or hypotensive due to rupture, tamponade, or impaired blood flow through the subclavian arteries (pseudohypotension). With ascending dissections, involvement of the subclavian arteries may result in pulse deficits and blood pressure discrepancies between the upper extremities. This is evident in 24% of patients with ascending dissection. Involvement of the carotid arteries can result in cerebral ischemia and stroke-like findings of hemiparesis and altered mental status. Ascending dissections can propagate proximally, resulting in aortic valve regurgitation or rupture into the pericardium. Aortic regurgitation (occurs in 18%–50%) is evidenced by a loud pansystolic murmur and can result in congestive heart failure. Rupture into the pericardium can result in cardiac tamponade with muffled heart sounds, distended neck veins, and hypotension. Extension of dissection distally can cause spinal paraparesis, mesenteric ischemia, renal failure, femoral pulse deficits, and lower extremity ischemia.
LABORATORY FINDINGS Laboratory testing is not helpful in establishing the diagnosis of aortic dissection. However, sending blood samples for CBC, electrolyte panel, BUN/creatinine measurement, cardiac enzyme analysis if indicated by presentation, and type and cross-match for 6–10 units packed red blood cells and fresh frozen plasma will aid in management.
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DIAGNOSIS Thoracic aortic dissection must be included in the differential diagnosis of all patients presenting with chest pain, upper back pain, or ischemic symptoms. Confirmation is made with radiography.
RADIOGRAPHS The findings on chest radiograph are abnormal in 80%–90% of patients with aortic dissection, with findings of widened mediastinum (75%), localized bulge in the aorta, obliteration of the aortic knob, displacement of the trachea or nasogastric tube to the right, inferior displacement of the right main bronchus, or calcium sign. Calcium sign is a collection of aortic calcium deposits that are separated from the outer wall of the aorta by more than 5 mm. Transesophageal echocardiography (TEE) is highly sensitive for diagnosing dissection and is helpful in detecting aortic regurgitation and pericardial effusion. The advantage of TEE is that it can be performed at the bedside in the ED, thought it may not be available at every institution. CT angiography is the diagnostic method of choice in most institutions. This method can identify an intimal flap, true and false lumens, and associated dilation of the aorta. Aortography, once the gold standard, has largely been supplanted by TEE and CT. MRI is highly specific and diagnostic, but it may be more appropriate in monitoring chronic, nonoperative dissections rather than making an initial diagnosis.
TREATMENT AND OUTCOME Emergency management revolves around resuscitation, limiting the extension of dissection, and securing emergent surgical consultation. Patients with suspected aortic dissection require two large-bore IV lines with isotonic crystalloid, continuous cardiac and blood pressure monitoring, and oxygen. An arterial line for continuous blood pressure monitoring optimizes control. Pain control with opiates will help decrease catecholamine release. Control of blood pressure and the rate of arterial pulse rise with each heartbeat will decrease the shear forces in the dissection. This is best accomplished initially with beta blockers. Labetalol 20 mg IV can be administered as a bolus every 5–10 minutes, increasing to 80-mg boluses to a target blood pressure of 100–120 systolic and pulse rate 60–80 beats/min or total of 300 mg. This can be followed by 1- to 2-mg/hr continuous drip. Alternatively, esmolol can be titrated with 500 mg/kg boluses every 5 minutes and an initial drip rate of 50 mg/kg/min up to 200 mg/kg/min. If additional blood pressure control is required, nitroprusside can be added and titrated at 0.3–5.0 mg/kg/min. Definitive management of ascending thoracic aortic dissections requires operative repair. Descending dissections often are managed medically with blood pressure control. Twenty
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percent of descending dissections will require operative management for persistent pain, uncontrolled hypertension, occlusion of major arterial branches, aortic leaking or rupture, or localized dilation. New methods of endovascular stenting are being tested and may provide an alternative to medical management for patients at high surgical risk of mortality due to comorbidities. All patients diagnosed with dissection in the ED will require admission to an intensive care unit. Long-term survival rates in treated patients at 1, 5, 10, and 15 years are 56%, 48%, 29%, and 11%, respectively.
Bibliography Ankel F: Aortic dissection, In Marx J (ed): Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 5. Mosby: St Louis, 2002; pp 1171–1176. Huyah T, Estrera A, Miller C, et al: Thoracic vasculature (with emphasis on thoracic aorta), In Townsend CM (ed): Sabiston Textbook of Surgery, ed 17. Elsevier: St Louis, 2004; pp 1905–1929. Lee JT, White RA: Current status of thoracic aortic endograft repair, Surg Clin North Am 2004;84(5):1295–1318. Nienaber CA, Zannetti S, Barbieri B, et al: Investigation of stent grafts in patients with type B aortic dissection: Design of the INSTAD trial—a prospective, multicenter, European randomized trial, Am Heart J 2005;149(4):592–599. Rogers RL, McCormack R: Aortic disasters, Emerg Med Clin North Am 2004;22 (4):887–908.
Wound Management CARL MENCKHOFF
ICD or CPT Code: See particular wounds for codes
Key Points/Quick Reference All wounds should be evaluated for infection, potential for infection, bleeding with threat of loss of limb or life, retained foreign bodies, and viability of soft tissue with consideration for underlying bony structures of organ injury and viability.
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EPIDEMIOLOGY Over 12 million traumatic wounds are treated each year in U.S. EDs. The most commonly affected group is young males aged 15–44 years, and the most commonly affected areas are the head (face and scalp) and the upper extremities (hands and fingers). The most common mechanism of injury is blunt trauma, although other causes include glass, sharp implements, wooden objects, and mammalian bites.
WOUND HEALING Wound healing can be divided into five stages: coagulation, inflammation, collagen synthesis, wound contraction, and epithelialization. Coagulation starts immediately after the injury, along with smooth muscle contraction to control bleeding. Inflammation is stimulated by factors released from platelets and by the complement cascade. Vascular permeability is increased with the influx of neutrophils and monocytes, which act as scavengers of debris and bacteria. Monocytes change into macrophages, which provide wound defense and also release chemotactic substances and stimulate fibroblast replication and neovascularization. Collagen synthesis starts as early as 48 hours after the injury and peaks at day 7 as tensile strength increases. The wound has its greatest mass at 3 weeks but only 20% of its tensile strength. The wound then remodels itself over the next 6–12 months. Collagen fibers are unable to form without ascorbic acid and oxygen. Wound contraction is the movement of full-thickness skin toward the center of the wound. Immediately after the injury, the skin edges retract. Over the next 3–4 days, the wound edges move toward the center (independent of epithelialization). The wound then continues to remodel itself over the next 6–12 months. Epithelialization is the process of epithelial cells migrating across the wound. In a repaired laceration, epithelialization will bridge the defect in 48 hours.
MEDICAL HISTORY Because a wound is usually visually obvious, a good history is sometimes overlooked and can lead to serious complications. There are several pieces of information that need to be ascertained to determine the risk of infection and the best way to approach wound repair. The time that has passed since the injury has occurred will influence the decision whether to close a wound primarily, with the risk of infection increasing as the time from injury to closure increases. Most wounds should be closed within 8–12 hours of injury, though some authors
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advocate closure of low-risk wounds on the face up to 24 hours after the injury. Other factors that increase the risk of infection include crush injury, retained foreign body, dirty wound (e.g., saliva, feces, organic material), and puncture or deep penetrating wounds Lastly, one needs to determine the immunocompetence and general health of the patient, any allergies to anesthetics, latex, or antibiotics, and tetanus vaccination status.
PHYSICAL EXAMINATION The physical examination should begin with an assessment of the neurologic, sensory, and motor function distal to the laceration. The wound should then be explored to look for injured structures and foreign bodies. In most cases, anesthesia will be required for adequate wound exploration. In wounds over tendons, the tendon should be examined in its full range of motion. For example, a laceration sustained in flexion during a fistfight may not be readily apparent when the fingers are extended.
ANESTHESIA After an appropriate physical examination, the area can be anesthetized (neurologic exam should always be performed before anesthesia). This can be accomplished by systemic, regional, or local anesthesia. Systemic analgesia may be necessary for some large wounds or in some children. It can be accomplished with a number of different agents, including ketamine, benzodiazepines, narcotics, or etomidate. Regional anesthesia is preferred when applicable because it usually requires less anesthetic, can cover multiple wounds in the same area, and does not distort the wound. However, local anesthesia is simple to perform and appropriate for many wounds. Anesthetic agents can be divided into two classes—the amides and the esters. There is no cross-reactivity between the groups, so an allergy to an amide does not mean an allergy to an ester. Examples of the amides are lidocaine, mepivacaine, and bupivacaine. The esters include procaine, tetracaine, and benzocaine. The two most commonly available local anesthetics in the United States are lidocaine and bupivacaine. Both come with and without epinephrine. Epinephrine causes vasoconstriction, which helps control bleeding and decreases the speed of systemic absorption (thereby allowing for higher doses to be administered). Epinephrine has also been shown to delay healing and increase the risk of infection and, because of the small risk of necrosis, it should not be used where there are distal-end arteries such as in the fingers, nose, penis, and toes. Those looking for alternative local anesthetics may want to consider aqueous Benadryl 1%, LET (lidocaine, epinephrine, tetracaine), or EMLA
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(lidocaine and prilocaine). Aqueous Benadryl is diluted to 1% solution and injected locally. In some studies, it has been found to be equivalent to lidocaine as a local anesthetic. LET is used in gel form and is placed over the wound, then covered with an occlusive dressing. It should not be used near mucous membranes or distal-end arteries due to its epinephrine component. EMLA is also used as a gel and placed over the wound with an occlusive dressing. Both lidocaine and bupivacaine can be toxic, especially when used to close large lacerations on patients with less body mass. Lidocaine toxicity can cause a metallic taste, dizziness, tinnitus, disorientation, dysarthria, seizures, coma, and death. The toxic dose of lidocaine (or bupivacaine) should always be calculated before usage (Table 1-1).
WOUND PREPARATION Hemostasis can be accomplished most of the time with direct pressure alone. Other techniques to assist include gravity, vasoconstriction (epinephrine, ice), completion of partial incisions (so vessels can contract), cautery, tourniquets (maximum time, 30 minutes on the fingers and 1 hour elsewhere), and suture ligature of a bleeding vessel. Skin disinfection can be accomplished with povidone-iodine (Betadine), which is effective against gram-positive bacteria, gram-negative bacteria, fungi, and viruses. However, it is toxic to wound defenses and may increase wound infection, so care should be taken not to spill it into the wound itself. Hair can be prepared with Betadine and should not be shaved because surgical studies show that this increases wound infection by exposing wounded follicles to bacteria. If visualization of the wound is difficult, hair can be clipped short without damaging the follicle. Irrigation is one of the most important determinants of wound prognosis. Three questions should be answered to determine effective irrigation: Table 1-1 Calculating Toxic Dosage of Lidocaine and Bupivacaine TOXIC DOSE
Lidocaine Bupivacaine
ONSET
DURATION
NO EPI
EPI
Seconds to minutes Seconds to minutes
½–1 hr >6 hr
5 mg/kg 2 mg/kg
7 mg/kg 3 mg/kg
Epi, Epinephrine. Example: A 1-year-old boy (weight, 10 kg) presents to the ED with 25 cm of lacerations to the right thigh. How much lidocaine can be used? 1% lidocaine equals 1 g/100 ml ¼ 1000 mg/100 ml ¼ 10 mg/ml 10-kg boy 7 mg/kg (with epi) ¼ maximum dose of 70 mg of lidocaine with epi 70-mg maximum dose/10 mg/ml ¼ 7 ml of lidocaine One can see that 7 ml of lidocaine is not very much for 25 cm of lacerations, and regional or systemic anesthesia may be necessary.
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how much pressure do I need, what solution should I use, and how much volume do I need? Irrigating with pressures of about 8 psi is recommended. This can be accomplished with a 19-gauge Angiocath catheter (or equivalent) and a 60-ml syringe. Low pressures are not as effective at cleaning out debris and bacteria, whereas very high pressures can cause tissue damage. Normal saline is the recommended irrigant. Studies have been done looking at other more expensive solutions but have not shown them to be superior. One study examined the use of tap water, which appeared to be as effective as normal saline. The volume of irrigant that should be used has not been well established. Some authors recommend 50–60 ml/cm of wound. Others recommend that the wound should be irrigated until clean (with a minimum of 200 ml). Debridement of devitalized tissue is important to decrease the risk of infection and to improve overall wound healing. Only devitalized tissue should be debrided. Jagged edges should be preserved when possible because this increases the surface area of the wound and decreases the skin tension.
WOUND CLOSURE The first decision to be made is how the wound should be closed. Primary closure is the traditional immediate closure. In secondary closure, the wound is left open and heals on its own. Cosmetic outcome is the worst with secondary closure. In tertiary (delayed primary) closure, the wound is prepared as with primary closure but then is packed open. If not infected, the wound can be closed 4 days after injury with the same cosmetic outcome as primary closure. Closing a wound loosely is never indicated. Loose closure allows the wound to seal itself within 48 hours without the cosmetic advantage of primary or tertiary closure. Skin tape is quick and inexpensive and has a low rate of infection, but it also has low tensile strength and a higher rate of wound dehiscence. It may be useful in small, linear superficial lacerations without tension. Benzoin should be used on the surrounding skin to help with adhesion. Tissue adhesives are quick and comfortable and do not require removal, but they also do not have the tensile strength of sutures. The octylcyanoacrylates are the most flexible and strongest of the group, and a study comparing octyl-cyanoacrylate to sutures found the cosmetic outcomes to be comparable after 3 months and a year. Tissue adhesives are best used in uncomplicated lacerations in low-tension areas, but they can also be used in combination with subcutaneous sutures. Staples are quick to apply but do not permit a closure quite as accurate, and they are somewhat less comfortable for the patient. Sutures enable the most cosmetic closure of all the techniques. However, a large closure can take time and, with the introduction of foreign
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material, sutures have the greatest amount of tissue reactivity. If sutures are to be used, the next questions to be answered are as follows: what type, what size, and what needle? Suture types can be divided into absorbable and nonabsorbable, defined by whether the tensile strength is maintained for less than or greater than 60 days (Table 1-2). Nonabsorbable sutures are usually used for cutaneous closures and tendon repairs, whereas absorbable sutures are used for deep structures such as fascia and dermis. For cutaneous closures, nylon and polypropylene (Prolene) sutures are the most commonly used and have good strength and low infectivity. Fast-absorbing plain gut or polyglactin (Vicryl Rapide) sutures may be considered for closures requiring tensile strength for a week or less or in cases in which suture removal is difficult (e.g., on a child’s face) or may be doubtful (e.g., in a homeless patient). Silk is comfortable and may be preferred around the lips or nipples. For deep sutures, Vicryl has low reactivity and good strength and is an appropriate choice for most uses. Suture size should be tailored to the amount of tension and the need for cosmesis (Table 1-3). In general, the face should be closed with 6–0 and the body with 5–0. One size larger may be used for deep layers and one size larger should be used for areas of increased tension. For example, this means that deep fascia over the knee can be closed Table 1-2 Suture Type NONABSORBABLE
BRAID (B) VS MONO (M) DURABILITY
Silk
B
Mersilene Nylon
B M
Prolene
M
Ethibond
B
Staples/steel
M
Absorbable Fast-absorbing plain gut Vicryl Rapide
M
3–5 days
B
5–7 days
Plain gut
M
7 days
Chromic gut Vicryl
M B
10–14 days 30 days
Polydioxanone (PDS)
M
45–60 days
COMMENTS Comfortable; use around lips, nose, nipples Use for fascia and tendons Common, strong, low infectivity, tendons Common, strong, low infectivity, tendons Costly, more comfortable, easier workability Fast, low infectivity, strong, uncomfortable, poor cosmesis Can be handy for children's faces; no removal necessary Handy when no removal is desired Rarely used; consider in homeless patients Primarily used intraorally Good for subcutaneous suturing and in mucous membranes Synthetic
32 ESSENTIAL EMERGENCY MEDICINE FOR THE HEALTHCARE PRACTITIONER Table 1-3 Suture Size ANATOMICAL LOCATION Face Body
SIZE FOR SKIN SUTURE
SIZE FOR DEEP SUTURE
6–0 skin 5–0 skin
5–0 deep 4–0 deep
Sutures one size larger should be used for increased tension (e.g., over joints).
with 3–0, deep fascia on the forearm with 4–0, skin on the thigh with 5–0, and skin on the face with 6–0. Needles are available in a wide variety of shapes and sizes. Most wounds in the ED can be closed using a conventional cutting needle. The main exception is closure of fascia and repair of tendons, which should be done with a tapered needle
Suture Techniques Several suture techniques can be used to optimize cosmetic outcome (Fig. 1-1). Wound tension should be minimized by undermining the wound edges or by placing subcutaneous sutures. Wound edges should be everted so that the germinating layers of the skin will be in contact with one another. This can be accomplished by ensuring that the needle enters and exits the skin perpendicularly. The suture should be tied just tightly enough to bring the wound edges together. With uneven wounds, care should be taken that the depth of bite should be the same on both sides of the wound. Jagged margins of a wound should be preserved if viable. A better scar will result due to increased surface area and therefore decreased tension. Simple interrupted percutaneous sutures are the most common method of laceration repair in the ED. The needle enters the skin perpendicularly on one side of the wound and crosses subdermally to the other side, where it exits perpendicularly and the knot is tied. Continuous percutaneous sutures are useful in linear lacerations with low tension. They are placed like the interrupted sutures above except that after the first knot is tied, the suture is not cut and the needle is reintroduced on the opposite side of the wound. Inverted intradermal sutures are used primarily to reduce tension on the wound edges. They are placed by introducing the needle deep in the wound and emerging just below the skin’s surface. The needle then enters (at the same level) just below the skin surface on the other side and exits deep in the wound, where the knot is tied. Horizontal mattress sutures are used primarily in areas of tension to help disperse the tension. This author also finds them useful in some elderly patients with paper-thin skin, where simple interrupted sutures may tear through. These begin like a simple interrupted suture, but rather than tying the knot, the needle reenters the skin on the same side
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Needle holder rolled
33
More tissue in depth than at surface Skin edge retracted
Direction of needle Simple interrupted percutaneous
Dermis Subcutaneous layer Grasp this loop and pull through to form knot
Inverted intradermal Continuous percutaneous
A Figure 1-1. Suture techniques. A, Simple interrupted percutaneous, continuous percutaneous, and inverted internal techniques.
(Continued)
of the wound approximately 0.5 cm adjacent to where it emerged. It then exits on the other side of the wound about 0.5 cm from where the stitch began, and the ends are tied. Vertical mattress sutures are useful for forced wound edge eversion as well as for closing deep and superficial layers with one stitch. The needle is introduced and a large bite is taken through to the other side of the wound. The direction of the needle is then reversed and a smaller bite is taken in the reverse direction. Half-buried horizontal mattress sutures (flap stitch) are ideal for closing the tips of wound flaps because they minimize suture-induced ischemia to an already tenuous area. The needle is inserted through the skin on one side of the wound level with the apex of the flap corner. The needle then passes intradermally through the tip of the flap and out through the skin on the other side of the wound. Care should be taken that the needle enters and exits at the same level on each bite so that the flap is not drawn deeper into the wound, causing an uneven scar to develop.
34 ESSENTIAL EMERGENCY MEDICINE FOR THE HEALTHCARE PRACTITIONER
Only a small bite of the skin edge taken here
Horizontal mattress
Begin here with deep bite of tissue
Vertical mattress
1
2
B Half-buried horizontal mattress (flap stitch)
Figure 1-1. cont’d, Suture techniques. B, Horizontal, vertical, and half-buried horizontal mattress techniques.
DRESSINGS The ideal dressing should be nonadherent and gas permeable, should keep the wound from getting too moist or too dry, and should be impermeable to bacteria and dirt. An adequate dressing for the majority of lacerations is antibiotic ointment applied over the wound and covered with a microporous
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dressing. Antibiotic ointment should not be used over tissue adhesives because it will loosen the adhesive.
ANTIBIOTIC PROPHYLAXIS Irrigation and debridement are the biggest factors in decreasing wound infection. Routine antibiotic use for lacerations is not recommended, and prophylaxis should be tailored to the individual patient and based on the risk of infection. Some wounds that are considered higher risk, and therefore candidates for antibiotics, are crush injuries, those with gross contamination, those in immunocompromised patients (e.g., persons with diabetes, transplant recipients, HIV-positive persons), puncture wounds, wounds with retained foreign bodies, cat or human bites, dog bites (on the hand or if difficult to clean), open fractures, and exposed joints or tendons. A first-generation cephalosporin such as cephalexin or an antistaphylococcal penicillin such as dicloxacillin is appropriate for most wounds. Penicillin can be used for oral wounds. Alternatively, amoxicillin-clavulanate can be used for oral wounds or mammalian bites. The usual antibiotic course is 5 days.
TETANUS IMMUNIZATION Tetanus toxoid should be given to all patients who received their last dose more than 5 years previous, with the exception of clean minor wounds. Tetanus toxoid should be given even for clean minor wounds if the patient’s last dose was received more than 10 years previous. Passive immunization with tetanus immune globulin (immunoglobulin G) as well as active immunization with tetanus toxoid is recommended for those without a history of primary tetanus vaccination (series of three injections).
DISPOSITION Patients should be discharged with adequate pain control as well as explicit instructions for wound care and signs of infection. The wound should be kept dry for about 8 hours, after which the patient should cleanse it daily. Showering is a sufficient method, but submersion (e.g., in a bath, hot tub, or lake) is not. Patients should return immediately if they experience any redness, swelling, pus, fever, red streaks, or increasing pain. Wound checks should be done after 48 hours for high-risk wounds, and patients should return in 5–14 days for suture removal (Table 1-4).
36 ESSENTIAL EMERGENCY MEDICINE FOR THE HEALTHCARE PRACTITIONER Table 1-4 Suture Removal ANATOMICAL LOCATION Face Scalp/trunk Arms/legs Joints
DURATION OF USE 3–5 days 7–10 days 10–14 days 14 days
RADIOGRAPHS Radiography may sometimes be required to rule out fractures or retained foreign bodies. Fluoroscopy may also be used to locate foreign bodies, and ultrasound has been used to detect tendon injuries or retained foreign bodies. CT may be used for foreign bodies that are difficult to visualize.
Bibliography Bowman MJ: Animal bites in infants and children: An approach to diagnosis and treatment, Emergency Medicine Reports 1999;4(6)53–62. Capellan O: Management of lacerations in the emergency department, Emerg Med Clin North Am 2003;21(1):205–231. Freeman L: Update on wound management: Evidence-based strategies for optimizing outcomes, Emergency Medicine Reports 2002;23(26):315–328. Hals G: The facial trauma patient in the emergency department: Review of diagnosis and management, part II, Emergency Medicine Reports 2004;25(28):217–232. Hollander JE, Singer AJ: Laceration management [review], Ann Emerg Med 1999; 34(3):356–367. Lionelli GT: Wound dressings, Surg Clin North Am 2003;83(3):617–638. Marx JA, Hockberger RS, Walls RM, eds: In Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 5. Mosby: St Louis, 2002, pp 737–751. Pearson AS: Management of skin trauma, Prim Care 2000;27(2):475–492. Roberts JR, Hedges JR: Clinical Procedures in Emergency Medicine, ed 4. Saunders; Philadelphia, 2004, pp 655–693. Singer AJ, Hollander JE, Quinn JV: Current concepts: Evaluation and management of traumatic lacerations, N Engl J Med 1997;337(16):1142–1148. Sells L: Topical anesthetics and tissue adhesives: A new generation in pediatric wound, Pediatric Emergency Medicine Reports 1999. Tintinalli JE, Kelen GD, Stapczynski JS, eds: In Emergency Medicine: A Comprehensive Study Guide, ed 6. McGraw-Hill: New York, 2004, pp 287–331.
Chapter 2
Cardiology Acute Pericarditis LEN GRUPPO
ICD Code: 420
Key Points Chest pain is positional; it is worse when a patient is supine and diminished or relived when he or she is sitting or leaning forward. A friction rub is common and very helpful diagnostically, but it is frequently difficult to appreciate. Life-threatening causes of chest pain and life-threatening etiologies of pericarditis should be ruled out before idiopathic or presumptive viral pericarditis are diagnosed. ! Emergency Actions ! If a cardiac tamponade is suspected and the patient’s condition is rapidly decompensating, an urgent pericardiocentesis should be performed. If fever or persistent tachycardia disproportionate to the fever are present, myocarditis should be considered and the suspected underlying etiology treated.
DEFINITION Pericarditis is an inflammation of the pericardium, the fibrous sack surrounding the heart. It is frequently idiopathic and benign, but several pathologic conditions can be associated with this condition.
EPIDEMIOLOGY Cardiac tamponade is more common in males than in females. It is most common in adolescents and young adults. Cardiac tamponade occurs in up to 20% of patients after acute myocardial infarction (AMI). Myocarditis is frequently associated with pericarditis; however, the reverse is not as common. Common causes include the following:
Idiopathic Infectious, viral, bacterial, fungal Malignancy Drug-induced 37
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Systemic rheumatic disease Radiation AMI (2–4 days post-AMI) Dressler’s syndrome (2–10 weeks post-AMI) Uremia Myxedema Traumatic (occurring in the posttraumatic period)
CLINICAL PRESENTATION Patients present with precordial or retrosternal chest pain. The pain will be positional in nature; it tends to be worse when the patient is supine and diminished or relived when the patient sits or leans forward. The pain will frequently be sharp or stabbing but may be described as pressure or squeezing. The pain can be gradual or sudden onset and aggravated by inspiration, movement, or exertion. Patients will often have a low-grade fever, but this symptom may be intermittent. Patients can present with dyspnea resulting from increased pain with inspiration and dysphagia resulting from esophageal irritation.
EXAMINATION Patients will present with a pericardial friction rub. This is best heard at lower left sternal border or the apex of the heart. It is frequently audible only during certain phases of respiration. The rub is frequently intermittent— there now, but not in the next hour.
ELECTROCARDIOGRAPHIC FINDINGS Electrocardiographic (ECG) findings in a patient with acute pericarditis include the following:
In V5, V6, or I, calculate the ratio of ST-segment elevation (i.e., baseline to J point) to the height of the T wave. Suspect pericarditis if this measurement is >0.25; the condition is unlikely if it is 0.04 sec or > one third the height of the QRS complex Large R wave in V1 (consider as a Q wave from the posterior myocardium)
Figure 2-27. Rhythm strip showing ECG abnormalities in cardiac chest pain: ischemia.
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Figure 2-28. Rhythm strip showing ECG abnormalities in cardiac chest pain: infarction.
Nonspecific ST- or T-wave changes Arrhythmias Serial ECGs very helpful
LABORATORY FINDINGS Useful laboratory test results include the following:
Cardiac enzymes Helpful for patients with nondiagnostic ECG findings. Perform serial cardiac enzyme measurements; repeat every 6 hours for three times (i.e., initial, plus two more). These tests are essential to be reasonably certain that an AMI has not occurred. Troponin I: This test is 90%–100% sensitive and 83%–96% specific. Troponin I rises in 2–4 hours, has a maximum sensitivity in 8–12 hours, and remains elevated for 7–10 days. Creatine kinaseMB isoenzyme: This test of a component of total CK is 71%–86% sensitive and 95%–97% specific. Creatine kinaseMB rises in 3–4 hours, has a maximum sensitivity in 8–12 hours, and remains elevated for 2–4 days. Myoglobin: This test is 80%–94% sensitive and 80%–92% specific. The level rises in 1–2 hours, has a maximum sensitivity in 4–8 hours, and remains elevated 0.5–1 day. BNP: This test is helpful in diagnosing CHF. BNP is a hormone produced by the heart that is increased in the blood when the heart workload increases.
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CBC: This test assists in recognition of bleeding disorders and infection. Chemistries: Electrolyte imbalances can cause arrhythmias, MI can precipitate diabetic ketoacidosis, and hypoglycemia/hyperglycemia can complicate management. Lipid profile: This test helps risk-stratify ambiguous cases and aids cardiologists with in-hospital and discharge management.
RADIOGRAPHS Portable chest x-ray helps to rule out other causes of chest pain and dyspnea. Radiographs can also assist with the identification of cardiomegaly, calcified heart valves, CHF, pneumonia, pneumothorax, pulmonary embolism, and aortic dissection. If chest radiography is available, it should be performed before lytics or heparin are given to rule out aortic dissection.
DIAGNOSIS History is frequently most important component of diagnosis. Symptoms of more than 15 minutes’ duration are concerning and may signify acute coronary syndrome or AMI. Physical examination provides valuable clues. An ECG is critical to the determination of which treatment pathway to take. Cardiac enzyme analyses can also be helpful in ambiguous cases.
TREATMENT AND OUTCOME Appropriate treatment is as follows:
Use the acronym and aphorism: “‘MONA’ greets all patients.” This stands for the administration of morphine, oxygen, nitroglycerin, and aspirin. Administer sublingual nitroglycerin unless the diastolic blood pressure is less than 60 mmHg or the heart rate is less than 60 or greater than 120 beats/min. Consider a diagnosis of right-sided MI if marked hypotension occurs. Always establish the minimum of one intravenous line to deliver NS before administration of nitroglycerin in the event the nitroglycerin causes hypotension. Provide analgesia with morphine: 3–5 mg given intravenously every 5 minutes as needed to control pain. If systolic blood pressure falls to less than 90 mmHg or the heart rate falls below 60 beats/min, discontinue morphine use. Administer aspirin (162.5–325 mg PO).
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If there is ST segment elevation of 1 millivolt (1 mV) or more, in two anatomically contiguous leads, or if there is a newly confirmed left bundle branch block, consider emergent fibrinolysis or percutaneous coronary intervention (PCI). Treatment will be dependent on the availability of an interventional cardiologist at your institution. The goal from the time the patient is received at the emergency department door to the time the patient is receiving PCI is 30 to 60 minutes. Administer beta blockers: metoprolol (Lopressor) at a loading dose of 5 mg intravenous every 5 minutes (3) if systolic blood pressure is greater than 90 mmHg and the heart rate is greater than 60 beats/ min; then give 50 mg PO. Low-molecular-weight heparin (Lovenox) should be given at 1 mg/kg subcutaneously once, unless the patient’s condition meets criteria for lytics or PCI; in that case, use unfractionated heparin. A heparin loading dose of 60 IU/kg up to 4000 IU should be given, followed by 12 IU/kg/hr up to 1000 IU/hr. If CHF is present, a diuretic agent should be given. If the patient is in shock, consider using an intra-aortic balloon pump and catheter with PCI or coronary artery bypass graft. The administration of angiotensin-converting enzyme (ACE) inhibitors is generally not started in the ED. However, this treatment should be initiated within 24 hours. Aspirin and beta blockers are the only class I agents used. (Class I indicates that studies show definite benefit of the agents.)
Fibrinolytic and Unfractionated Heparin Contraindications
Absolute contraindications include the following: Active internal bleeding Suspected aortic dissection Known intracranial neoplasm History of any hemorrhagic cerebrovascular accident (i.e., stroke) ever occurring, or history of other cerebrovascular event within the past year Relative contraindications include the following: Severe hypertension on presentation (blood pressure >180/110 mmHg) History of chronic severe hypertension History of prior cerebrovascular accident or other intracranial pathology Recent major trauma (in the past 2–4 weeks) or major surgery (in the past 3 weeks) Prolonged or traumatic cardiopulmonary resuscitation (lasting >10 minutes)
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Noncompressible vascular punctures Recent internal bleeding (in the past 2–4 weeks) For prior exposure or allergy to anisoylated plasminogen-streptokinase activator complex drugs (APSAC), use tissue plasminogen activator or Tenecteplase. APSAC drugs include Abbokinase (urokinase), Abbokinase Open-Cath (urokinase), Activase (recombinant alteplase), Eminase (anistreplase), Retavase (recombinant reteplase), and Streptase (streptokinase) Known bleeding diathesis or current international normalized ratio greater than 2–3
Special Considerations
Right ventricular MI should be considered as a diagnosis. Suspect right-sided ventricular MI in patients with hypotension, shock, clear breath sounds, or JVD. Right ventricular preload is essential to maintain blood pressure. A right-sided MI rarely occurs as an isolated event. Right-sided MI can be associated up to 30% of the time with an inferior MI. There will be ST-segment elevation in the inferior leads and leads II, III, and AVF. If an acute right-sided MI is suspected, perform an ECG. If a rightsided MI is present, it will show ST-segment elevation in V4R. This is 90% sensitive. ECG shows ST-segment elevation in V4R. This is 90% sensitive (move only the V4 lead to its mirror position, placing on the right and repeat the ECG). Fifty percent of posterior MIs have some degree of right ventricular involvement. Look for ST-segments depression in V1, V2, or V3. Treatment includes the following: Maintain right ventricular preload. Administer fluids (e.g., normal saline) and inotropic agents (e.g., norepinephrine or dobutamine) if the patient is hypotensive. Use nitroglycerin and morphine with extreme caution! These may cause profound hypotension.
Bibliography Hazinski MF, Cummins RO, Field JM, (eds): 2000 Handbook of Emergency Cardiovascular Care for Healthcare Providers, ed 4. American Heart Association: Dallas, 2000. Hollander JE: Acute coronary syndromes: Acute myocardial infarction and unstable angina, In Tintinalli JE, Kelen GD, Stapczynski JS (eds): Emergency Medicine: A Comprehensive Study Guide, ed 5. McGraw-Hill: New York, 2000, pp 343–352. The Merck Manual of Diagnosis and Therapy, ed 2 online, 16.202. Available at: http://www.merck.com/mrkshared/mmanual/section16/chapter202/202d.jsp. Accessed on: July 4, 2005.
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Hypertensive Emergencies MARTIN A. DOUCHERTY
ICD Codes: 401–405
Key Points It is very important to evaluate the patient’s underlying cause of his or her hypertension. The healthcare provider must establish whether the hypertension is constituted by persistent elevated blood pressure, hypertensive emergency, or hypertensive urgency. It is dangerous to lower the blood pressure too fast. A goal of 20% decrease in the mean arterial pressure is safe. ! Emergency Actions ! Initial resuscitative treatment includes establishing the minimum of two IV lines and providing oxygen. An emergency EKG should be performed and the patient should be placed on a cardiac monitor. An immediate chest radiograph should be performed.
DEFINITIONS Hypertension is defined as a persistently elevated blood pressure. The term hypertensive emergency defines a condition in which an elevated blood pressure leads to a rapid deterioration of end-organ function. Hypertensive urgency defines a condition in which a patient may be in danger of developing end-organ damage as a result of his or her elevated blood pressure. It should be noted that though blood pressure readings of 180/ 110 mmHg have been used in the past to mandate treatment, no good evidence exists to support a rapid reduction of blood pressure in patients who are otherwise asymptomatic and showing no evidence of end-organ damage. The “at-risk” organs affected by markedly elevated blood pressure are the brain, heart, and kidneys. Physical examination, history, and tests should be directed toward evaluating organ function to guide ED therapy.
EPIDEMIOLOGY
Hypertensive encephalopathy: This entity results from a loss of normal vascular autoregulation in the brain resulting from severe hypertension. The most common presenting history is headache, seen in 85% of patients. Altered mental status, nausea and vomiting, and confusion or
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lethargy may be reported. Physical examination findings may include neurological deficits, papilledema, retinal hemorrhages, and exudates. Hypertensive cardiac disease: Patients may present with chest pain associated with markedly elevated blood pressure. Myocardial ischemia is the most common cause; however, the possibility of an aortic dissection should always be considered. In addition, signs and symptoms of CHF should be noted because therapy may differ. Hypertensive renal disease: This is a laboratory diagnosis for the most part. Findings include azotemia, hematuria, and proteinuria.
EXAMINATION A comprehensive history should be obtained, with emphasis on signs and symptoms of acute end-organ damage. In addition, a past medical history of CHF, angina, renal insufficiency, or poorly controlled hypertension should alert the practitioner to patients at higher risk of developing endorgan damage. The use of recreational drugs, stimulants, or monoamine oxidase inhibitors should also be noted.
PHYSICAL EXAMINATION The physical examination should proceed as follows: 1. Measure blood pressure initially and every 5–15 minutes. Check blood pressure in both arms. 2. Evaluate the patient’s mental status for signs of confusion or encephalopathy. 3. Perform a funduscopic examination to look for papilledema or retinal exudates. 4. Check for carotid bruits, distended neck veins, or a goiter. 5. Evaluate for pulses in all extremities and signs of edema. 6. Perform a cardiac examination to look for tachycardia, murmurs, cardiomegaly, and extra heart sounds. 7. Perform a pulmonary examination to evaluate for rales and wheezes. 8. Perform an abdominal examination to evaluate for bruits and pulsatile aortic masses. 9. Perform a neurological examination to evaluate for deficits.
LABORATORY FINDINGS 1. Order a urinalysis to look for proteinuria, hematuria, or casts. 2. Measure serum electrolytes and BUN/creatinine levels to evaluate renal function. 3. Analyze cardiac enzymes and BNP in patients with signs of CHF or angina.
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4. Perform a CBC to evaluate for microangiopathic hemolytic anemia. 5. Use an ECG to evaluate for signs of infarction, ischemia, or ventricular hypertrophy.
RADIOGRAPHS A chest radiograph can be used to evaluate for CHF and a widened mediastinum associated with thoracic aortic dissection. CT of the brain should be undertaken in patients with any signs or symptoms of encephalopathy.
TREATMENT Hypertensive Emergency The presence of end-organ damage constitutes a hypertensive emergency. Most guidelines recommend treatment to drop the mean arterial pressure by 20% over the course of 1 hour. Several agents are available; the most commonly used are as follows:
Sodium nitroprusside 1. Sodium nitroprusside is a rapidly acting agent that reduces preload by venous dilation and afterload by arteriolar dilation. 2. This agent may produce tachycardia and can increase myocardial contractility and oxygen demand. It should be used in conjunction with a beta blocker in cases of aortic dissection. 3. The recommended starting dose is 0.25–0.5 mg/kg/min and can be titrated for effect up to a dose of 10 mg/kg/min. 4. Prolonged use can lead to cyanide and thiocyanate toxicity, especially in patients with underlying renal insufficiency. Labetalol: 1. Labetalol is a combination alpha and beta blocker. 2. This agent decreases heart rate and is a venous and arterial dilator. 3. It should be avoided in patients with CHF, reactive airways disease, and significant bradycardia. 4. Labetalol can be given as an intravenous bolus of 20–80 mg every 10 minutes to a total dose of 300 mg. Alternatively, an infusion of 0.5–2 mg/min may be used. 5. The onset of action is approximately 15 minutes. Nitroglycerin 1. Nitroglycerin is a more potent venodilator than arterial dilator. 2. This is the drug of choice in patients with myocardial ischemia complicated by severe hypertension. 3. Headache, hypotension, and reflex tachycardia are the main adverse effects. 4. The starting dose is 5 mg/min with titration for effect up to 200 mg/min.
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Esmolol 1. Esmolol is a short-acting cardioselective beta-1 blocker. 2. This drug has a rapid onset of action. 3. It is most useful in the treatment of hypertension in perioperative patients. 4. Esmolol is also useful in patients with myocardial ischemia. 5. Use of this drug should be avoided in patients with CHF or reactive airways disease. 6. Appropriate dosage is 200–500 mg/kg bolus over 1 minute and an infusion of 50–300 mg/kg/min. Hydralazine 1. Hydralazine acts as a direct arteriolar vasodilator. 2. This agent can cause reflex sympathetic stimulation. 3. It is contraindicated in patients with angina, myocardial infarction, and aortic dissection. 4. Safe in pregnant patients, hydralazine is considered a drug of choice for treatment of pregnancy-related hypertension. 5. The appropriate dosage is 10 mg given as an intravenous bolus up to a maximum of 20 mg.
Hypertensive Urgency Patients who have asymptomatic hypertension without evidence of endorgan damage should be treated with care. Ischemic complications have been reported with overzealous treatment of such patients. Treatment in the ED should be reserved for those patients at risk for complications of hypertension due to serious comorbid conditions. Selected oral medications for treatment of hypertensive urgencies include the following:
Clonidine 1. Clonidine is an alpha-2 blocker. 2. The appropriate dosage is 0.05–0.2 mg PO. 3. Sedation and orthostatic hypotension are the most common side effects. Labetalol 1. Labetalol is a combined alpha and beta blocker. 2. Dosage is 300 mg PO. 3. Avoid use of this agent in the presence of CHF, reactive airways disease, and significant bradycardia. Nifedipine 1. Nifedipine is a calcium-channel blocker. 2. The appropriate dosage is 5–10 mg PO. 3. Reflex tachycardia, angina, and profound hypotension are side effects.
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Captopril 1. Captopril is an ACE inhibitor. 2. Dosage is 25 mg PO. 3. Adverse effects include angioedema, and use of this drug should be avoided in patients with known renal artery stenosis.
Bibliography Chiang WK, Jamshahi B: Asymptomatic hypertension in the ED, Am J Emerg Med 1998;16:701. Kaplan NM: Management of hypertensive emergencies, Lancet 1994;344:1335. Varon J, Marik P: The diagnosis and management of hypertensive crises, Chest 2000;118:214. Zanchetti A: Impact of hypertension and antihypertensive treatment on organ damage, Am J Cardiol 1999;84:18.
Mitral Valve Prolapse ALICIA NASIR AND STEVE DURNING
ICD Code: 424.0
Key Points/Quick Reference MVP is usually seen in young women and is usually easily managed. MVP is a diagnosis of exclusion. A simple echocardiogram can diagnose or exclude the condition.
DEFINITION Mitral valve prolapse is the billowing of one or both of the mitral valve leaflets into the left atrium during ventricular systole.
EPIDEMIOLOGY MVP is the most common valvular heart disease, affecting approximately 2%–6% of the U.S. population. The high prevalence of MVP reported in the past among asymptomatic young women may be due to inappropriate echocardiographic diagnoses. Although MVP typically occurs with little or no mitral regurgitation, it is the leading cause mitral regurgitation in
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the United States. MVP can be familial or associated with connective tissue disorders or with bony abnormalities of the thoracic cavity (i.e., pectus excavatum, a straight thoracic spine, or scoliosis).
PATHOLOGY The term mitral valve prolapse is typically used to characterize primary myxomatous degeneration of one or both leaflets of the mitral valve. The pathogenesis of MVP is not known, but changes in valvular tissue can usually be seen under histological examination. Functional prolapse can also occur in patients with anatomically normal valves in several conditions: ischemic injury to papillary muscles, rheumatic heart disease, conditions that cause stretching of the mitral annulus (e.g., dilated cardiomyopathy), or diseases causing a small left ventricular cavity (e.g., hypertrophic cardiomyopathy, atrial septal defect, or volume depletion). The term mitral valve prolapse, however, usually refers only to primary myxomatous degeneration and not these causes of functional prolapse.
CLINICAL PRESENTATION Most patients with MVP are asymptomatic. Patients with MVP may also present with palpitations, atypical chest pain, fatigue, and dyspnea unrelated to exertion. Some studies have shown that these symptoms are no more prevalent in MVP than in the rest of the population.
PHYSICAL EXAMINATION The most important auscultatory finding in MVP is a mid to late (nonejection) systolic slick. This is likely generated by the sudden tensing of the chordae tendineae. There may be multiple clicks, and it may be followed by a high-pitched late systolic crescendo-decrescendo murmur heard best at the apex of the heart. The click or murmur occurs earlier in systole with maneuvers that decrease venous return to the heart (e.g., standing or Valsalva); the click or murmur will occur later or even disappear with maneuvers that increase venous return to the heart (e.g., squatting or isometric exercise). Bony abnormalities of the thoracic wall, as described earlier, may also be detected in a patient with MVP.
DIAGNOSIS The diagnosis of MVP is usually made by cardiac auscultation in asymptomatic patients or as an incidental finding on an echocardiogram. Patients with MVP or suspected MVP should receive an echocardiogram. This allows risk stratification and identification of patients who will require antibiotic prophylaxis with procedures.
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LABORATORY AND ANCILLARY FINDINGS No routine laboratory tests or studies are needed for the workup of MVP in the ED. An ECG is frequently obtained in patients presenting with MVP symptoms and typically appears normal. The ECG can also show nonspecific ST-T wave changes, T-wave inversion, U waves, or prolongation of the QT interval. Chest radiographs are also frequently obtained and occasionally show bony abnormalities such as pectus excavatum, a straight thoracic spine, or scoliosis, as mentioned previously. Echocardiography should be performed on an outpatient basis.
TREATMENT The treatment for most patients with asymptomatic MVP is reassurance. Most patients with a definitive diagnosis of MVP will require antibiotic prophylaxis for infective endocarditis before certain procedures. Patients who present with symptoms such as palpitations or chest pain can have resolution of their symptoms with the cessation of use of cigarettes, caffeine, and alcohol. Beta blockers are also effective treatments for this type of chest pain. In patients experiencing focal neurological events, anticoagulation with aspirin therapy or warfarin therapy is indicated.
Bibliography ACC/AHA Practice Guidelines for Management of Patients with Valvular Heart Disease, J Am Coll Cardiol 1998;32:1486–1588. Braunwald E: Valvular heart disease, In Harrison’s Principles of Internal Medicine, ed 15. McGraw-Hill: New York, 2001, pp 1348–1349. Ling LH, Enriquez-Sarano M, Seward JB, et al: Clinical outcome of mitral regurgitation due to flail leaflet, N Engl J Med 1996;335:1417–1423. Cline DM, Valvular emergencies. In Tintinalli JE, Kelen GD, Stapczynski JS (eds): Emergency Medicine: A Comprehensive Study Guide, ed 6. McGraw-Hill: New York, 2004, p 375. Winkle RA, Lopes MG, Goodman DJ, et al: Propranolol for patients with mitral valve prolapse, Am Heart J 1977;93:422–427.
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Permanent Pacemakers JIMMY COOPER
ICD Code: 996.01
Key Points/Quick Reference Pacemaker complications can be categorized as failure to pace, failure to capture, failure to sense, and inappropriate rate (tachyarrhythmias). Failure to sense is the most common cause of pacemaker malfunction. Failure to pace is usually due to oversensing. Magnet application converts the pacemaker to a fixed rate pacing mode (‘‘magnet rate’’); it does not turn off the pacemaker. Indications to use the magnet include failure to pace, pacemaker-mediated tachycardia, and the runaway pacemaker. Defibrillation is safe in patients with pacemakers. It should be placed at least 10 cm away from the device (or in the anterior-posterior position). ! Emergency Actions ! The runaway pacemaker is a true potential pacemaker emergency that may require acute intervention. Magnet application can be lifesaving in these patients. Pacemaker-mediated tachycardias can also be terminated by magnet application. Unstable bradycardias may improve with magnet application if the problem is failure to pace and oversensing. It may not improve with the failure to sense or capture patients.
DEFINITION Electrical cardiac pacing has been used since the 1950s. These early devices used external power sources. The first implantable permanent pacemaker was clinically used in 1958. Through the years, advances in technology have allowed pacemakers to become individualized to the person. The modern day pacemaker is a microcomputer with multiple programmable features enabling adjustments to activity level. Despite the increasing complexity of programmable features, the pacemaker is composed of three basic components: the pulse generator, the lead system, and the programming or circuitry. Emergency providers must understand these components to manage related complications. The pulse generator consists of the battery, the reed switch, and the radiopaque marker. Most pacemakers use a lithium battery, which has a slow and steady decay rate. The life of the lithium battery is 4 to 10 years. Voltage output is gradually lost, so that abrupt failure is rare. The reed switch is used to assess pacemaker function. It is activated when placed
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under a magnetic field, which results in inhibition of the sensing circuit. This turns the pacemaker into a fixed-rate pacing mode, also known as the magnet rate. This mechanism is critical to both assessing and managing pacemaker complications. Radiopaque markers are visible with standard chest radiographs. Most patients carry identification cards; however, if they are not available, these markers will identify the pacemaker manufacturer and model. Most pacemakers use endocardial leads that are transvenously placed into the right ventricle, right atrium, or both (dual-chamber devices). Leads can also be implanted on the epicardium during open-heart surgery. Complications associated with leads include infection, thrombosis, cardiac perforation, dislodgement, and lead fracture. Lead fracture is estimated to be 2% per patient-year. Lead displacement is 2%–5% for endocardial leads. There are many different types of pacemaker circuitry. The North American Society of Pacing and Electrophysiology and the British Pacing and Electrophysiology Group have developed a five-letter code scheme to describe them (Table 2-1). The first three letters are most useful in understanding the type of pacemaker. Pacemakers are usually inhibited by intrinsic cardiac depolarization (VVI or DDD). Using the pacemaker code and the patient’s ECG, the provider can determine whether there is a malfunction in the circuitry. Programming complications include failure to pace, failure to capture, failure to sense, and inappropriate rates.
EPIDEMIOLOGY Approximately 200,000 pacemakers are placed or replaced in the United States each year, and about 1 million Americans have pacemakers. Indications include symptomatic bradycardias, heart blocks, syncope, heart failure, cardiomyopathies, and congenital heart malformations. The widespread use of pacemakers guarantees that emergency providers will encounter them and their malfunctions. Pacemaker complications are infrequent, occurring in fewer than 6% of patients. They most commonly occur in the first few months after implantation. Most are due to failure to sense, which accounts for 32%–57% pacemaker problems.
CLINICAL PRESENTATION Patients with pacemaker malfunctions can present with chest pain, dyspnea, syncope, near syncope, orthostasis, palpitations, light-headedness, weakness, or fatigue. These may be similar to the patient’s index
Table 2-1 Five-Letter Pacemaker Code LETTER 1
LETTER 2
LETTER 3
LETTER 4
LETTER 5
CHAMBER PACED
CHAMBER SENSED
SENSING RESPONSE
PROGRAMMABILITY
ANTITACHYCARDIA FUNCTIONS
A ¼ atrium V ¼ ventricle D ¼ dual
A ¼ atrium V ¼ ventricle D ¼ dual
P ¼ simple M ¼ multiprogrammable R ¼ rate adaptive
P ¼ pacing S ¼ shock D ¼ dual (shock þ pace)
O ¼ none
O ¼ none
T ¼ triggered* I ¼ inhibited D ¼ dual (A and V inhibited) O ¼ none
C ¼ communicating O ¼ none
Permanent Pacemakers
From Niemann JT: Implantable cardiac devices. In Marx JA (ed): Rosen's Emergency Medicine, ed 5. Mosby: St Louis, 2002, p 1100. * In the triggered response mode, the pacemaker discharges or fires when it recognizes an intrinsic depolarization. As a result, pacemaker spikes occur during inscription of the QRS complex. Because this mode results in high-energy consumption and a shortened battery life, and because the sensing response can be misinterpreted as pacemaker malfunction, this sensing mode is not used with modern pacemakers.
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symptoms before pacemaker placement. Loss of pacemaker function leaves the patient with his or her underlying condition, which is usually a bradydysrhythmia. Fortunately, this is rarely immediately life threatening. Patients with pacemakers can also present with tachydysrhythmias, as in the case of pacemaker-mediated tachycardia or a “runaway” pacemaker. This may present emergently with profound hypotension and cardiovascular collapse. Runaway pacemaker is a rare complication caused by an extreme inappropriate increase in the pacing rate. Pacemakermediated tachycardia is seen in conjunction with dual-chamber devices, usually from an endless-loop reentry tachycardia. Retrograde conduction through the AV node is sensed as atrial depolarization, causing repeated pacing of the ventricle. Infectious complications should be considered in patients with pacemakers who present with fever of unclear etiology. These may be localized to the skin or pockets, but they may also be more complicated, involving leads or endocarditis. Initial treatment consists of broadspectrum antibiotics to cover Staphylococcus aureus. The pacemaker often needs to be removed.
EXAMINATION The pacemaker identification card should be obtained. It will provide information on the pacing modality and the indication for the pacemaker. Pulses less than 60 or greater than 100 beats/min are suggestive of altered pacing parameters. Pacemakers are usually programmed with a rate between 60 and 80 beats/min. Hypotension may be present. The general appearance is dependent on the patient’s intrinsic heart rhythm and stability. There may be signs of shock and CHF. The chest wall should be inspected for signs of infection. Cardiac examination may reveal a new murmur suggestive of infective endocarditis.
ECG FINDINGS An appropriately paced ECG will have a left bundle branch pattern because the pacing lead is in the right ventricle. Using the pacemaker code and the patient’s ECG, the provider can determine whether there is a malfunction in the circuitry. Pacemaker malfunctions can be separated into three categories: 1. Failure to pace: The ECG shows a complete absence of pacemaker spikes in a patient whose intrinsic rhythm is slower than the programmed rate. This is most commonly due to oversensing. The pacemaker detects electrical activity other than atrial and ventricular depolarizations that suppresses impulse generation. Other etiologies (rarely) include wire fracture and battery depletion.
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2. Failure to capture: Pacemaker spikes are appropriately present, but without associated QRS complexes. Causes include lead dislodgement, battery depletion, and exit block (e.g., fibrosis, infarction, hyperkalemia, antiarrhythmia drugs). 3. Failure to sense (undersensing): The ECG shows constant pacemaker spikes despite intrinsic cardiac activity. Pacemaker spikes occur at inappropriate times due to the inability to sense the patient’s intrinsic cardiac depolarization. They typically occur earlier than the programmed rate. A paced complex may or may not follow, depending on the cardiac refractory period. This is most common after right ventricular infarctions and with the fibrosis of cardiomyopathies. Lead dislodgment and maturation can also cause undersensing. ECGs may also show tachydysrhythmias as previously described in pacemaker-mediated tachycardia.
RADIOGRAPHS Standard chest radiographs should be obtained and compared with old films. Pacemaker type can be ascertained by radiopaque markers. Lead wires should be examined for fracture, displacement, and perforation.
TREATMENT The approach to pacemaker complications is similar to that of other cardiac symptoms. This basic evaluation includes history, examination, ECG, and chest x-ray, as outlined previously. Key historical information should include the pacemaker identification card, which explains the pacing modality and the reason why the pacemaker was placed. Laboratory studies (i.e., chemistry) need to be performed to assess for metabolic abnormalities. All of these patients should be receiving cardiac monitoring and oxygen administration and should have intravenous access. By analyzing the ECG, the pacemaker complication can usually be identified. Failure to sense and failure to capture requires only the basic evaluation and then “pacemaker interrogation” by cardiology. There is usually no ED intervention for these patients. They have pacemaker activity, although it is inappropriate or without effect. Unless battery depletion is suspected, magnet application is usually not necessary. Battery depletion is a rare cause of pacemaker failure and is diagnosed with a lower than programmed rate with magnet application. Failure to pace problems can further be evaluated with magnet testing to determine whether the malfunction is oversensing, component failure, or battery depletion. Standard ring magnets are typically used for this procedure. Some pacemakers may require specific magnets. Place the magnet directly on the chest wall over the pacemaker. This closes the reed switch
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and converts the pacemaker to an asynchronous or fixed-rate pacing mode. Expect the pacemaker to pace at the programmed rate (60–80 beats/min). If this occurs, then the problem was oversensing and the pacemaker was inappropriately inhibited. Causes of oversensing include atrial depolarizations, muscle activity, and external electrical interference. Component failure should be suspected if there are no spikes on magnet application. Battery depletion is indicated by the presence of a pacemaker rate less than the program med rate. All of these conditions require further evaluation by cardiology. The magnet should be left in place if it corrects the underlying bradydysrhythmia. Certain pacemaker complications require acute interventions. Pacemakermediated tachycardia can present with cardiovascular collapse. A magnet should be applied to terminate the arrhythmia, and it should be left in place if it is successful. If this fails, then isometric pectoral exercises should be attempted. The cooperative patient can flex the pectoral muscles surrounding the pacemaker generator. Alternatively, a transcutaneous pacemaker can be applied to stimulate the pectoral muscle. Low outputs in the range of 5–20 mA should be used. The muscle activity may be interpreted as ventricular activity and inhibit the pacemaker. If the patient is unstable, the healthcare provider should consider delivering a precordial thump. The last resort for an unstable patient is to sterilely cut the pacer leads and connect them to an external temporary pacemaker. Pacemakers are complicated devices, and most emergency providers do not have the expertise to fully evaluate them. If pacemaker malfunction is suspected, the patient’s cardiologist should be consulted. These patients will usually be admitted to a monitored setting for further “interrogation.”
Bibliography Bernstein AD, Camm AJ, Fletcher RD, et al: The NASPE/BPEG generic pacemaker code for antibradyarrhythmia and adaptive-rate pacing and antitachyarrhythmia devices, Pacing Clin Electrophysiol 1987;10:794. Braunwald E, Zipes DP, Libby P (eds): Heart Disease: A Textbook of Cardiovascular Medicine, ed 6. WB Saunders: Philadelphia, 2001. Copeland LL, Mace SE: Pacemaker emergencies, Crit Decis Emerg Med 2005;19(7): 13–21. Greenberg RM, Greenspon AJ, Bridenbaugh A, Brest AN: Pacemaker-mediated tachycardia: A complication of atrioventricular universal (DDD) pacemakers, Arch Intern Med 1984;144:1061. Hayes DL, Vliestra RE: Pacemaker malfunction, Ann Intern Med 1993;119:828. Marx J, Hockberger R, Walls R: Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 5. Mosby: St Louis, 2002. Mickley H, Anderson C, Nielsen IH: Runaway pacemaker: A still existing complication and therapeutic guidelines, Clin Cardiol 1989;12:412–416. Roberts JR, Hedges JR (eds): Clinical Procedures in Emergency Medicine, ed 4. WB Saunders: Philadelphia, 2004.
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Prosthetic Heart Valve Dysfunction CHRISTOPHER R. MCNEIL
ICD Code: 394
Key Points/Quick Reference Prosthetic heart valves are classified into two general groups: mechanical and bioprosthetic. Complications of prosthetic heart valves include thrombosis, embolic events, endocarditis, hemolytic anemia, and primary valve failure.Thromboembolic events are the most common complication of prosthetic heart valves. Prosthetic valve endocarditis must be considered in any patient who presents with a fever of unknown origin, sepsis, a change in the murmur, or evidence of peripheral emboli. ! Emergency Actions ! Initial resuscitative treatment includes establishing the minimum of two IV lines and providing oxygen. An emergency EKG should be performed and the patient should be placed on a cardiac monitor. An immediate chest radiograph should be performed.
DEFINITION Prosthetic heart valves are classified into two general groups: mechanical and bioprosthetic. Most mechanical valves consist of three basic designs: the ball and cage, the tilting disk, and the bileaflet hinged disk. Mechanical valves carry a large risk of thrombosis and the ensuing embolic events, thus requiring lifelong anticoagulation. Risks associated with anticoagulation led the way for development of bioprosthetic valves. These most commonly consist of porcine valves or are synthesized from pericardial tissue. Although the need of long-term anticoagulation is unnecessary, bioprosthetic valves are less durable and usually require replacement after 10 years. Complications of prosthetic heart valves include thrombosis, embolic events, endocarditis, hemolytic anemia, and primary valve failure. Thromboembolic events are the most common complication of prosthetic heart valves. Thrombosis can result in improper valve function, obstruction of valve outlet, or systemic emboli. Valve thrombosis can present acutely with CHF, hypotension, and loss of the metallic valvular click on examination. Patients with chronic thrombosis may develop gradually worsening weakness, shortness of breath, and exercise intolerance. These conditions occur more commonly in mechanical valves
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than in bioprosthetic ones. Typically, thrombosis results from inadequate anticoagulation. Prosthetic valve endocarditis must be considered in any patient who presents with a fever of unknown origin, sepsis, a change in the murmur, or evidence of peripheral emboli. Within the first 2 months after valve replacement, the predominant infecting organisms are Staphylococcus epidermidis and other hospital-acquired organisms. After 2 months, the causative organism mimics those that cause native valve endocarditis. Chronic hemolytic anemia is caused by trauma to the turbulent blood flow through the valve. Severe or acute hemolytic events should raise the suspicion for a paravalvular leak. Valve failure occurs much more commonly in bioprosthetic valves. Failure results from cusp tears, perforations, and calcifications of leaflets. Rarely, artificial valves have also been reported to fail. Fracture of the strut mechanism in certain Björk-Shiley valves have led to embolization of the tilting disk. Although most of these have been replaced, there is still a significant population with these valves in place. Mechanical valves are not void of failure.
EPIDEMIOLOGY Prosthetic heart valves are implanted in nearly 400,000 patients annually. Embolic events occur at a rate of approximately 1% per year among patients taking warfarin. Emboli and thrombosis are more common on the mitral valve. The incidence of bacterial endocarditis in patients with prosthetic valves is approximately 0.5% per patient-year. The 5-year mortality for prosthetic valve endocarditis is 20%–60%.
CLINICAL PRESENTATION The patient may present with a variety of symptoms, depending on the complication he or she is experiencing. Thrombosis can present with hypotension, shortness of breath, orthopnea, paroxysmal nocturnal dyspnea, and chest pain. Systemic emboli may present as acute stroke, seizure, or vision loss, or with dermatological findings. Endocarditis presents with fever, weakness, malaise, and with evidence of systemic emboli, as well. Hemolytic anemia presents with weakness and dark-colored urine.
EXAMINATION A complete physical examination should be performed. The healthcare provider should look for signs of pulmonary edema, peripheral edema, and JVD as evidence of CHF. Heart sounds should be auscultated to identify the mechanical click of the valve and any evidence of a diastolic or other new murmur. A funduscopic examination should be performed to
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identify hemorrhages and Roth’s spots. A complete skin examination should be performed to identify petechia, Osler’s nodes, Janeway lesions, and peripheral embolic phenomenon.
LABORATORY FINDINGS A CBC, urine analysis, and lactate dehydrogenase measurement may be required to evaluate for hemolysis. A coagulation panel is necessary to evaluate the patient’s anticoagulation status. A sedimentation rate and multiple blood culture results are useful to diagnose endocarditis.
DIAGNOSIS The diagnosis of prosthetic valve dysfunction is based on a thorough history, physical examination results, and high clinical suspicion. Echocardiography is used to diagnose valve thrombosis, paravalvular leaks, and vegetations (Box 2-1).
RADIOGRAPHS Chest radiography is useful in determining the position of the prosthetic heart valve and in identifying any evidence of pulmonary edema.
TREATMENT Thromboembolic complications require immediate anticoagulation. Patients will also require echocardiography to ultimately diagnose their Box 2-1 Duke Criteria Must meet two major criteria, or one major and three minor criteria, or five minor criteria. Major Criteria: At least two positive blood cultures Endocardial vegetation by echocardiography Paravalvular abscess by echocardiography New partial dehiscence of prosthetic valve by echocardiography New valvular regurgitation by echocardiography Minor Criteria: Predisposition: predisposing heart condition or IV drug use Fever Vascular phenomenon: arterial emboli, septic pulmonary infarction, mycotic aneurysms, conjunctival hemorrhages, Janeway lesions Immunological phenomenon: Osler's nodes, Roth's spots, rheumatoid factor Microbiological evidence: single positive blood culture Echocardiographic findings: consistent with endocarditis but does not meet criteria
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condition. These patients may require surgical thrombectomy or valve replacement. There is a new surge in the use of thrombolytics for the treatment of prosthetic thrombus, but these should be reserved for the intensive care setting. Endocarditis requires intravenous antibiotic therapy. Either vancomycin plus gentamycin or ceftriaxone plus gentamycin is appropriate to administer initially while culture results and sensitivity results are pending. Rarely do these patients require acute valve replacement. Patients with primary valve failure typically experience acute and dramatic onset of CHF and hypotension. These patients require emergent cardiology and cardiothoracic surgery consultation. Their hypotension may not tolerate nitrates or afterload reduction. They may require intubation and positive-pressure ventilation for their pulmonary edema as well as inotropic support. Chronic hemolytic anemia generally responds well to iron replacement. Acute or severe hemolysis may necessitate blood transfusion and requires echocardiography to identify a possible paravalvular leak. Prosthetic heart valves require antibiotic prophylaxis against endocarditis for procedures with high risk for bacteremia. The following common procedures require prophylaxis:
Prophylactic cleaning of teeth Bronchoscopy (with rigid bronchoscope only) Endoscopic retrograde cholangiopancreatography Cystoscopy Urethral dilation
Bibliography Braunwald E, Zipes DP, Libby P (eds): Heart Disease: A Textbook of Cardiovascular Medicine, ed 6. WB Saunders: Philadelphia, 2001. Cannegieter SC, Rosendaal FR, Wintzen AR, et al: Optimal oral anticoagulant therapy in patients with mechanical heart valves, N Engl J Med 1995;333:11–17. Dajani AS, Taubert KA, Wilson W, et al: Prevention of bacterial endocarditis: Recommendations by the American Heart Association, Circulation 1997;96:358–366. Gherli T, Colli A, Fragnito C, et al: Comparing warfarin with aspirin after biological aortic valve replacement: a prospective study, Circulation 2004;110:496–500. Goldman L, Ausiello D: Cecil Textbook of Medicine, ed 22. WB Saunders: Philadelphia, 2004. Marx J, Hockberger R, Walls R: Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 5. Mosby: St Louis, 2002. Stein PD, Alpert JS, Bussey HI, et al: Antithrombotic therapy in patients with mechanical and biological prosthetic heart valves [erratum appears in Chest;120(3):1044], Chest 2001;119:220S–227S. Tintinalli JE, Kelen GD, Stapczynski JS (eds): Emergency Medicine: A Comprehensive Study Guide, ed 5. McGraw-Hill: New York, 2000.
Heart Transplant
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Heart Transplant CHRISTOPHER R. MCNEIL
ICD Code: Heart transplant V42.1
Key Points The surgical procedure causes denervation of their vagus nerve, rendering it void of parasympathetic stimulation. Baseline tachycardia is common and even expected after transplant, with a basal rate of 100^ 110 beats/min. ! Emergency Actions ! Any heart transplant recipient presenting with sepsis, CHF, fever, shortness of breath, hypoxia, hypotension, poorly controlled hypertension, or new dysrhythmia should be admitted to the hospital.
DEFINITION Human heart transplantation was first successfully performed in 1967, and currently more than 2000 transplants are done each year in the United States. Advances in immunosuppressive therapy have established transplantation as an accepted treatment for end-stage heart disease over the last 20 years. Patients are typically discharged from the hospital within 2–3 weeks, and nearly 40% make at least one visit to the ED over the next 3 years. Heart transplant recipients have a 60% ED admission rate after transplant due to an appropriately high concern for rejection or localized or systemic infections. Several important factors must be considered when heart transplant recipients present for medical treatment. The surgical procedure causes denervation of the vagus nerve, rendering patients void of parasympathetic stimulation. Baseline tachycardia is common and expected after transplant with a basal rate of 100–110 beats/min. The ECG typically demonstrates two distinct p waves. The native sinoatrial node remains intact in the posterior wall of the right atrium with the vena caval connections. The donor heart also has a sinoatrial node and maintains action potential conduction to the ventricles as usual. The myocardium upregulates adrenergic receptors in the graft and has an enhanced response to endogenous and exogenous catecholamines. Cardioactive medications have similar effects in the posttransplant heart, with the exception of atropine because of the denervation. The denervation also renders the patient
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void of the typical anginal symptoms that other patients experience. Finally, immunosuppressive agents that heart transplant recipients are prescribed have the potential for significant drug toxicities as well as the increased incidence for both typical and opportunistic infections.
EPIDEMIOLOGY Currently, more than 2000 heart transplants are performed annually in the United States. The 5-year survival rate for adults is now as high as 70%. Acute rejection occurs in 75%–85% within the first 3 months after transplant. Patients experience an annual rate of infection of nearly 20% after the first 3 months. Almost 25% of deaths after transplant result from an infection.
CLINICAL PRESENTATION The most common presenting symptoms are fever, shortness of breath, GI symptoms, and chest pain. Chest pain is rarely related to cardiac ischemia because of the denervation. Infection, rejection, and drug toxicity are the leading causes of morbidity and mortality in the first year after transplant. These conditions need to be strongly considered in the differential diagnosis.
EXAMINATION All patients should be given a complete physical examination to identify any focus of infection. Any evidence of CHF, new murmur, a new S3 heart sound, or dysrhythmia should prompt concerns for rejection and graft CAD.
LABORATORY FINDINGS A CBC, chemistry panel, coagulation panel, liver function tests, cardiac enzymes, BNP, blood cultures, viral cultures, stool cultures, and lumbar puncture should be considered for all patients.
DIAGNOSIS Infection Although many patients will have a major infection in the first year after transplant, life-threatening infections are rare after the first year. All heart transplant recipients with fever should have an aggressive diagnostic workup performed. Typical infections include pneumonia and urinary tract infections. Skin problems typically manifest as herpes zoster. Pneumocystis carinii
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pneumonia and cytomegalovirus (CMV) infection are common pulmonary complications. GI tract symptoms include CMV infection, and abdominal pain may result from diverticulitis. Central nervous system symptoms may include headache, meningitis, or infection with Listeria, Cryptococcus, Toxoplasma, Nocardia, or Aspergillus species.
Rejection Manifestations of rejection include decreased QRS voltage on ECG, a new S3 heart sound, CHF, atrial dysrhythmias, hypotension, and syncope. Most episodes of mild rejection are asymptomatic. Accelerated atherosclerosis of the graft vessels is the hallmark of chronic rejection; however, ischemia presents as congestive heart failure (CHF), ventricular tachycardia (VT) hypotension, and sudden cardiac death (SCD). Patients with these conditions need admission for consideration of myocardial biopsy and increased immunosuppressive therapy.
Drug Toxicity Complications stemming from drug toxicity include the following:
Cyclosporine: nephrotoxicity, hypertension, hyperlipidemia, gout Tacrolimus: nephrotoxicity, neurotoxicity, hyperglycemia, hyperkalemia, not compatible with macrolides Azathioprine: neutropenia, hepatic dysfunction, GI tract disturbance Prednisone: osteoporosis, cataracts, GI tract bleeding, hyperglycemia, adrenal suppression Mycophenolate mofetil: thrombocytopenia, GI tract disturbance OKT3 (muromonab-CD3): increased risk of CMV and opportunistic pathogens, lymphoproliferative disease
RADIOGRAPHS All patients should undergo a chest x-ray to identify evidence of CHF or pneumonia. Patients with abdominal pain should be considered for a CT of the abdomen and pelvis. Patients with headache or CNS symptoms should be considered for a CT scan of the head, with the aim of looking for evidence of infection or brain abscess.
TREATMENT Any heart transplant recipient presenting with sepsis, CHF, fever, shortness of breath, hypoxia, hypotension, poorly controlled hypertension, or new dysrhythmia should be admitted to the hospital.
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SPECIAL TREATMENT Heart transplant recipients are at risk for endocarditis. They require antibiotic prophylaxis for invasive procedures likely to cause bacteremia such as abscess incision and drainage and dental procedures. Varicella-zoster virus immune globulin is recommended for those patients who have had exposure to chickenpox or herpes zoster.
Bibliography Braunwald E, Zipes DP, Libby P (eds): Heart Disease: A Textbook of Cardiovascular Medicine, ed 6. WB Saunders: Philadelphia, 2001. Deng MC: Orthotopic heart transplantation: Highlights and limitations, Surg Clin North Am 2004;84(1):243–255. Goldman L, Ausiello D: Cecil Textbook of Medicine, ed 22. WB Saunders: Philadelphia, 2004. Marx J, Hockberger R, Walls R: Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 5. Mosby: St Louis, 2002. Shanewise J: Cardiac transplantation, Anesthesiol Clin North Am 2004;22(4):753–765.
Chapter 3
Acute Dermatologic Emergencies Erythema Multiforme RICHARD J. SPITZ
ICD Code: 695.1
Key Points Patients present with a symmetrical skin lesion that has a target appearance.
DEFINITION Erythema multiforme (EM) is a mild, self-limited skin disorder that tends to have abrupt onset and is sometimes recurrent. It is recognized by its characteristic target or iris lesion and is usually associated with infection, particularly with herpes simplex virus infection. Previously, EM was grouped with two other skin disorders: Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN). Current thinking separates EM from these other two disorders, which have a distinctly different histopathology. In contrast to the relatively mild nature of EM characterized by target lesions and associated with infection, SJS and TEN are severe, have a poor prognosis, and are associated with drug exposures. Some authors feel that, in actuality, both SJS and TEN are a continuum of the same disorder, with TEN being the more widespread and severe form.
EPIDEMIOLOGY The true occurrence of the disease is unknown due to overlap with other diseases, its benign self-limited nature, and lack of adherence to a uniform definition.
PATHOLOGY Disease is theorized to result from deposition of immune complexes in skin and oral mucous membranes.
CLINICAL PRESENTATION Patients present with a symmetrical skin lesion that has the appearance of a target. The rash is most common on the hands, feet, and extensor 97
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aspects of the forearms and legs, though severe cases can progress to involvement the trunk.
EXAMINATION The patient should be examined to distinguish EM from more severe diseases such as Kawasaki disease, SJS, TEN, meningococcemia, secondary syphilis, toxic shock syndrome, collagen vascular disease, septic emboli in bacterial endocarditis, and Rocky Mountain spotted fever.
DIAGNOSIS A patient is diagnosed by the presence of the classic target lesion in a nontoxic-appearing patient. Skin biopsies would show mononuclear infiltrate, but due to the benign course of the disease, these are not performed.
LABORATORY FINDINGS There are no laboratory findings suggestive of the skin lesions themselves.
TREATMENT The disease is usually self-limited with lesions resolving within several weeks without any residual manifestations. Recurrent episodes can be treated with herpes simplex virus medication (e.g., valacyclovir, acyclovir, or famciclovir). Other agents such as nonsteroidal anti-inflammatory drugs, steroids, and antihistamines do not appear to affect the disease course.
Bibliography Assier H, Bastuji-Garin S, Revuz J, Roujeau JC: Erythema multiforme with mucous membrane involvement and Stevens-Johnson syndrome are clinically different disorders with distinct causes, Arch Dermatol 1995;131:539. Bastuji-Garin S, Rzany B, Stern RS, et al: Clinical classification of cases of toxic epidermal necrolysis, Stevens-Johnson syndrome, and erythema multiforme, Arch Dermatol 1993;129:92. Behrman RE, Kliegman RM, Jenson HB: Nelson Textbook of Pediatrics, ed 17. WB Saunders: Philadelphia, 2004. Ferri FF: Practical Guide to the Care of the Medical Patient, ed 7. Mosby: St Louis, 2007. Habif TP: Clinical Dermatology, ed 4. Mosby: St Louis, 2004. Leaute-Labreze C, Lamireau T, Chawki D, et al: Diagnosis, classification, and management of erythema multiforme and Stevens-Johnson syndrome, Arch Dis Child 2000;83:347. Long SS, Pickering LK, Prober CG: Principles and Practice of Pediatric Infectious Diseases, ed 2. Churchill Livingstone: New York, 2003.
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Mandell GL, Bennett J, Dolin R: Principles and Practice of Infectious Diseases, ed 5. Churchill Livingstone: New York, 2000. Marx J, Hockberger R, Walls R (eds): In Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 5. Mosby: St Louis, 2002. Noble J: Textbook of Primary Care Medicine, ed 3. Mosby: St Louis, 2001. Paquet P, Pierard GE: Erythema multiforme and toxic epidermal necrolysis: A comparative study, Am J Dermatopathol 1997;19:127. Rakel RE: Conn’s Current Therapy, ed 57. WB Saunders: Philadelphia, 2005. Roujeau JC, Revuz J: Toxic epidermal necrolysis: an expanding field of knowledge, J Am Acad Dermatol 1994;31:301. Roujeau JC, Stern RS: Severe adverse cutaneous reactions to drugs, N Engl J Med 1994;331:1272. Schofield JK, Tatnall FM, Leigh IM: Recurrent erythema multiforme: Clinical features and treatment in a large series of patients, Br J Dermatol 1993;128:542. Weston WL, Morelli JG: Herpes simplex virus-associated erythema multiforme in prepubertal children, Arch Pediatr Adolesc Med 1997;151:1014. Weston WL, Morelli JG, Rogers M: Target lesions on the lips: Childhood herpes simplex associated with erythema multiforme mimics Stevens-Johnson syndrome, J Am Acad Dermatol 1997;37:848.
Exfoliative Dermatitis BENJAMIN H.TAYLOR
ICD Code: Exfoliative dermatitis 695.89
Key Points Exfoliative dermatitis is usually caused by an underlying disease or illness or is drug induced. ! Emergency Actions ! Any patient suspected to have exfoliative dermatitis should be admitted to a surgical intensive care unit (SICU) or a burn center for evaluation and treatment.
DEFINITION Exfoliative dermatitis and erythroderma are synonymous terms used to define a common clinical syndrome characterized by widespread scaling, often with itching (i.e., pruritus), skin redness with desquamation (i.e., erythroderma), and hair loss.
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EPIDEMIOLOGY Exfoliative dermatitis occurs in all races and accounts for about 1% of all hospital admissions for dermatological conditions. Although the disease affects both men and women, it is more common in men, with an average male-to-female ratio of 2:1. The average age at onset is older than 40 years, although it may occur at any time.
PATHOLOGY Exfoliative dermatitis may occur in response to drug therapy, systemic disease, or an idiopathic entity (Box 3-1). More than half of all cases are due to aggravation of a preexisting skin disease that often has diagnostic findings. Approximately 10% of cases are the result of drug reactions (more than 60 drugs have been implicated), and 40% of all cases are caused by some underlying systemic disease. The remaining cases are idiopathic. Malignancies are a major cause of exfoliative dermatitis. Reticuloendothelial neoplasms, as well as internal visceral malignancies, can produce erythroderma, with the former being the more predominant cause. Cutaneous T-cell lymphomas are the lymphomas most commonly associated with exfoliative dermatitis. The most notable member of this group is mycosis fungoides. Acute and chronic leukemia may also cause exfoliative dermatitis. The relative risk of leukemia inducing exfoliative dermatitis is highly variable, ranging from 11% to 50%.
CLINICAL PRESENTATION The general clinical presentation may be altered according to the nature of the underlying disease and the patient’s general physical condition. Patients often present with generalized erythema in the first stage of the disorder, beginning as single or multiple pruritic patches and involving the head, trunk, and genital region. These patches tend to spread for days, and they may last for weeks when most of the skin surface
Box 3–1 RED MAN: A Mnemonic for Identifying Possible Causes of Exfoliative Dermatitis Radiation (sunburn) or photosensitive eczema Eczema, atopic dermatitis, psoriasis, and other inflammatory skin disorders Drugs Malignancy (most commonly lymphoma, such as mycosis fungoides) AIDS No known cause (idiopathic)
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becomes covered with an erythematous, pruritic eruption. Pruritus commonly results in excoriations and present in varying stages of healing. In some cases, the palms of the hands, the soles of the feet, and the mucous membranes are spared. Exfoliative dermatitis may persist for weeks and becomes a chronic entity. Patients’ hair may shed and their nails may become ridged and thickened. Periorbital skin may be inflamed and edematous, resulting in ectropion (with consequent epiphora). Pigmentary disturbances (especially in darker-complexion patients, resembling vitiligo) has become commonplace. Other signs and symptoms with which patients may present include any of the following:
Gynecomastia is a common finding in almost all patients with a chronic history of exfoliative dermatitis. It is believed to result from hyperestrogenism, but the precise mechanism is unknown. Patients may present tachycardic and febrile, with temperatures higher than 38 C. Lymphadenopathy, referred to as dermatopathic lymphadenitis, is common. Hepatomegaly and splenomegaly is present in approximately 30% of patients and may represent lymphoma. Steatorrhea may develop and tends to resolve when exfoliative dermatitis clears. Patients with exfoliative dermatitis have increased cutaneous blood flow, transcutaneous fluid losses, and radiation and convective heat losses. Hypothermia has been reported in some patients. Cardiac output is increased as a result of fluid shifts causing dyspnea, dependent edema, and, in some patients, cardiac failure. Prostate or thyroid glands may be enlarged or nodular.
EXAMINATION A complete physical examination should include a cardiac examination as well as skin biopsy of representative areas.
DIAGNOSIS AND LABORATORY FINDINGS A detailed history of the sequence of events leading to the development of exfoliative dermatitis is required in all patients. Laboratory evaluation of patients with exfoliative dermatitis is generally not very helpful in determining a specific diagnosis. Typical laboratory values to be obtained include mild anemia, leukocytosis, eosinophilia, elevated erythrocyte
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sedimentation rate, abnormal serum protein electrophoresis with a polyclonal elevation in the gamma globulin region, and elevated immunoglobulin E levels when the condition is caused by atopic dermatitis or drug reactions. Blood counts and bone marrow studies may reveal an underlying leukemia. Analysis for circulating Sézary cells may be helpful—but, only if the Sézary cells are identified in unequivocally large numbers. In most patients, skin biopsies show nonspecific histopathologic features, such as hyperkeratosis, parakeratosis, acanthosis, and a chronic perivascular inflammatory infiltrate, with or without eosinophils. Even patients with clear histories of preexisting dermatoses tend to have biopsy results that are not diagnostic.
TREATMENT Every attempt must be made to determine the underlying cause of exfoliative dermatitis. A history or signs of a primary dermatitis may be helpful. All patients who present with acute exfoliative dermatitis must be hospitalized in the intensive care unit or burn center for supportive care, fluid replacement, laboratory studies, and contact isolation for protection against secondary bacterial and fungal infections. Dermatological consultation is indicated in most cases to ensure that the necessary cutaneous, laboratory, and radiological investigations and monitoring are performed. The administration of all drugs should be stopped or, if essential, should be changed to chemically dissimilar medications. In the acute phase of exfoliative dermatitis, before determination of the etiology, treatment consists of measures to soothe the inflamed skin, including bed rest, lukewarm soaks or baths, bland emollients, and oral antihistamines for pruritus. Petrolatum applied after tap-water baths gives temporary relief. A high-protein diet with folic acid supplementation is required since protein losses may be increased as much as 30% above normal. Exfoliative dermatitis commonly resists therapy until the underlying disease is treated. The outcome is unpredictable, and the course is usually marked by multiple exacerbations. Prolonged glucocorticoid therapy is often necessary. Appropriate inpatient/outpatient medications are influenced by the underlying etiology. Systemic steroids may be helpful in some cases but should be avoided in suspected cases of psoriasis and staphylococcal scalded skin syndrome.
Bibliography Fitzpatrick TB, Johnson RA, Wolff K: Exfoliative dermatitis. In Color Atlas and Synopsis of Clinical Dermatology, ed 4. McGraw-Hill: New York, 2001, pp 152–157. Freeberg IM: Exfoliative dermatitis, In Fitzpatrick TB, Eisen AZ, Wolff K, (et al): Dermatology in General Medicine, ed 4. McGraw-Hill: New York, 1993, pp 527–530.
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Papadakis MA, McPhee SJ: Exfoliative dermatitis. In Current Consult Medicine. McGraw-Hill, 2005, pp 302–303. Sehgal IN, Srivastava G, Sardana K: Erythroderma/exfoliative dermatitis: A synopsis, Inter J Dermatol 2004;43(1):39–52. Thestrup-Pederson K, Sorenson HC, Sogaard H: The red man syndrome: Exfoliative dermatitis of unknown origin. A description and follow-up of 38 patients, J Am Acad Dermatol 1988;18:1307–1312.
Toxic Epidermal Necrolysis GUYON J. HILL
ICD Code: 695.1
Key Points Toxic epidermal necrolysis is a rare skin disorder resulting from a severe hypersensitivity reaction. Up to 100% of the epidermis may separate from the dermis and be shed in sheets. The precipitating factors are usually medications. The disease has a high mortality rate, and patients should be treated in similar fashion to burn patients and transferred to a dedicated burn unit. ! Emergency Actions ! The patient should be stabilized and resuscitated following current advanced cardiac life support guidelines. Use of adhesives should be avoided while intravenous lines are being placed, if possible. Intubation and mechanical ventilation may be necessary if the upper airway or the pulmonary tree is involved. Any sources of skin trauma should be avoided, as should central lines, if possible, due to the risk for infection.
DEFINITION Toxic epidermal necrolysis is a severe hypersensitivity reaction frequently precipitated by medications. The process is thought to be a combination of type III and IV hypersensitivity reactions and can result in a loss of up to 100% of the full thickness of the epidermis. TEN is in the same family of disorders as EM and SJS. Although it is generally accepted that SJS is a more severe form of EM, debate exists as to whether TEN is a further
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point on this spectrum or its own clinical entity. What is known is that the precipitating factors for all three disorders are similar. Medications can be implicated in up to 77% of cases. Common offending medications that are implicated in the etiology of this disorder include sulfa drugs, nonsteroidal anti-inflammatory drugs, and phenytoin and other convulsants. Other possible inciting drugs are allopurinol, penicillins, and barbiturates. A relationship has also been found between the disease and patients with either human immunodeficiency virus (HIV) infection or active malignancy. The rate is also higher in elderly persons (who are often taking more medications) and bone marrow transplant recipients. TEN has occurred after immunization for smallpox, tetanus, diphtheria, measles, and poliomyelitis. Often the etiology is unknown. No association has been found with viral illness.
EPIDEMIOLOGY TEN is an extremely rare condition and accounts for only 1.3% of cutaneous drug eruptions. It occurs in 0.2 cases per million users of penicillins and 4.5 cases per million users of sulfonamides. The overall frequency in the United States is 0.22–1.23 cases per 100,000. There is a female predominance, with the gender ratio of 1.6:1 for infection.
CLINICAL PRESENTATION Early in the course of the disease, patients with TEN usually present with a nonspecific prodrome that may include fever, malaise, arthralgias, anorexia, conjunctivitis, and symptoms of an upper respiratory tract infection. These symptoms occur before skin involvement. As a general rule, mucous membrane involvement precedes skin involvement. Initially affected organs include the eyes, nose, and mouth. The genitalia may also be involved. The painful rash usually begins on the face but may also start on the upper trunk. Blisters form and become confluent, resulting in the sloughing of sheets of epidermis similar to that which occurs in the case of thermal burns. The reaction of the body includes shedding of up to 100% of the epidermis in sheets. This results in substantial fluid loss and a greatly increased risk of secondary bacterial infection. The average onset from exposure to symptoms is 2 weeks, and the range is 1–3 weeks.
EXAMINATION Nikolsky’s sign is present (i.e., gentle traction placed on a blister or rubbing will result in lateral expansion, implying separation of the epidermis from the dermis). The pigment is lost, a phenomenon that does not
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occur with staphylococcal scalded skin syndrome. Other systems such as gastrointestinal, ocular, pulmonary, and renal systems may be involved to varying degrees.
LABORATORY FINDINGS Useful laboratory studies include a complete blood count and electrolyte analysis. Blood and urine cultures should be performed if there is suspicion for a secondary infection.
DIAGNOSIS The diagnosis is primary made on the basis of clinical presentation and an exposure to an offending agent. There is no direct confirmatory test, and the definitive diagnosis is made from a skin biopsy. The differential diagnosis of TEN includes toxic shock syndrome, staphylococcal scalded skin syndrome (although TEN is usually in adults), other exfoliative drug eruptions, Kawasaki syndrome, and primary blistering disorders such as pemphigus or pemphigoid.
TREATMENT AND OUTCOME The cornerstone of treatment is supportive care. This, combined with prevention of secondary infection and proper wound care, will have the greatest impact on survival. Patients with TEN should be treated as burn patients would, with admission to a dedicated burn center. Laboratory results and fluid status should be monitored, and any electrolyte abnormalities should be corrected. Sufficient potassium may be lost from the skin to cause significant hypokalemia. To monitor urine output, a Foley catheter should be placed. The provide should discontinue any newly instituted medications or other medications that may be responsible for the condition. No tests can be used to identify the precipitant, so any nonessential medications should be stopped. TEN is an extremely painful condition, and pain should be treated appropriately. The use of corticosteroids is controversial because there is little effect on the disease and their use may interfere with the early diagnosis of sepsis. Plasmapheresis is experimental. The administration of intravenous immunoglobulin should be considered, in consultation with a dermatologist. Antibiotics should be withheld if there is no suspicion for secondary infection. The condition carries up to a 50% overall mortality rate, with the major source being sepsis from either Staphylococcus aureus or Pseudomonas aeruginosa. Survival is primarily dependent on treatment at a burn center. The next likely cause of death is hypovolemia with associated electrolyte
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disorders. Mortality may be as low as 4% if this occurs within 7 days but as high as 8% if greater than 7 days. Blindness may result from ocular sequelae such as purulent conjunctivitis and erosions. Ocular involvement often portends permanent disability to some degree.
Bibliography Mangione S: Physical Diagnosis Secrets, Hanley and Belfus: Philadelphia, 2000, pp 54–56. Marx J, Hockberger R, Walls R (eds): Rosen’s Emergency Medicine Concepts and Clinical Practice, ed 5. Mosby: St Louis, 2002, pp 1643, 1729. Salyer S: The Emergency Medicine Physician Assistant Handbook, WB Saunders: Philadelphia, 1997, pp 62–64. Schaider J, Hayden SR, Wolfe R, et al (eds): Rosen and Barkin’s 5-Minute Emergency Medicine Consult, ed 2. Lippincott, Williams & Wilkins: Philadelphia, 2003, pp 1140–1141. Stone C, Humphries RL (eds): Current Emergency Diagnosis and Treatment, ed 5. Lange Medical Books/McGraw-Hill: New York, 2004, p 1014. Tierney LM (eds): Current Medical Diagnosis and Treatment, Lange Medical Books/ McGraw-Hill: New York, 2003, pp 144, 1544. Tintinalli JE, Kelen GD, Stapczynski JS (eds): Emergency Medicine: a Comprehensive Study Guide, ed 5. McGraw-Hill: New York, 2000, pp 1595–1596.
Toxicodendron Dermatitis SIMEON W. ASHWORTH AND BENJAMIN P. HARRISON
ICD Code: 696.6
Key Points Toxicodendron dermatitis is the most common cause of contact dermatitis in the United States.
DEFINITION Poison ivy, oak, and sumac, members of the plant genus Toxicodendron, cause an allergic contact dermatitis (i.e., allergic phytodermatitis) that occurs from direct exposure to the plants and their oils. This type of contact dermatitis is often called “Rhus.”
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DEMOGRAPHICS AND EPIDEMIOLOGY Toxicodendron dermatitis is the most common cause of contact dermatitis in the United States. Toxicodendron species are found in every state except for Alaska and Hawaii and in all regions except for the desert areas and the higher elevations. Poison oak is most common west of the Rocky Mountains, poison ivy to the east, and poison sumac in the southeast. Approximately 70% of the U.S. population is susceptible, with 15% of the population being extremely sensitive. There is no clear gender or racial difference in susceptibility, but elderly persons appear to have reduced sensitivity.
NOMENCLATURE AND PLANT IDENTIFICATION Poison ivy and oak have eastern (Atlantic) and western (Pacific) variations: Toxicodendron radicans and Toxicodendron rydbergii for the ivy variations and Toxicodendron pubescens and Toxicodendron diversilobum oak variations, respectively. Poison sumac comes in a single and rarer species of Toxicodendron vernix Kuntze. The leaves of poison oak and ivy are alternate, with trifoliate leaflets. The leaves are shiny green in the spring and turn yellow and deep red in the fall. The flowers grow in axillary panicles and are yellow-green. The fruit is globe shaped, resembling small pumpkins, and turns yellow or light brown when mature. Poison sumac has 7–13 leaflets per leaf, bearing the same kind of fruit as poison oak and ivy.
PATHOPHYSIOLOGY The allergic reaction is to the oil, not the plant itself, so one can react by touching objects that have come in contact with the plant such as tools, pets, and footwear. A delayed type IV hypersensitivity reaction occurs from the antigenic oleoresins that are found in the Toxicodendron species. When the oleoresin evaporates, the solvent—urushiol—remains and produces a dermatitis. Other urushiol-containing plants include the cashew nut tree, mango tree, and ginkgo tree. More resin is contained in younger plants; therefore, exposure to these often causes a more severe reaction. Exposure can come from the roots and other parts of the plant, not exclusively from the leaves, and may even cause a more severe reaction due to higher concentrations of the oleoresins.
CLINICAL PRESENTATION Within 48 hours of exposure to the resin, the reaction occurs in those who are sensitive and can last up to 3 weeks. The integument is primarily
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affected; however, the airway, eyes, and lungs can be involved if exposed to smoke produced from burning plants. Patients can develop erythema, papules, vesicles, bullae, pruritus, and redness, and the lesions often present in crusty, weeping linear configurations. In severe cases, edema, induration, and thickening of the dermis may occur. The dermatitis is usually self-limited and disappears without scarring. Occasionally hyperpigmentation remains and, in severe cases, EM can develop. The dermatitis is not spread by ruptured vesicles. The fluid in the vesicles contains no antigen; thus, the dermatitis cannot be spread by the rupturing of vesicles.
DIAGNOSIS Diagnosis is made primarily based on history and physical examination findings.
LABORATORY FINDINGS AND TESTING Laboratory testing is not needed for diagnosis. Allergenic patch testing is generally discouraged for toxicodendron dermatitis because it might sensitize an unsensitized person.
TREATMENT Treatment is based on the level of severity, the location of the eruption, and the presence of rare secondary infection. Removal of urushiol before it binds to membrane lipids (within 20 minutes) can prevent reaction. This is best performed with copious water irrigation. Soaps may spread the urushiol oil around the skin and worsen the dermatitis, so washcloths should be used with soap, and this washing should be followed by copious irrigation of all contacted skin. Domeboro, calamine, oatmeal baths, and Burrow’s solution (aluminum acetate) are topical solutions that have been proven to reduce the irritation in toxicodendron dermatitis. Recently Zanfel, an over-the-counter topical scrub, has been released for the treatment and prevention of dermatitis after exposure. The manufacturer’s claim that it binds the urushiol resin and clears mild cases of dermatitis, however, is unproven. Systemic steroids are beneficial in the treatment of moderate to severe toxicodendron dermatitis. These can be given orally (e.g., prednisone or methylprednisolone) or intramuscularly (e.g., dexamethasone). Oral medications are most reliable and should be tapered off for at least 10–14 days, with a warning to the patient that early withdrawal might cause the dermatitis to recur. Pre-made dose packs of steroids often have inadequate initial doses or too short of a course of prednisone. Ideally, a
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good starting dose is approximately 1 mg/kg of prednisone tapered over a 10- to 14-day period. Low-dose steroids and topical antihistamines have not been shown to have any beneficial effect but may be used in mild, localized cases. Oral antihistamines are helpful in relieving pruritus. Oral analgesics are occasionally required for pain relief in very severe cases. Oral antibiotics are indicated for secondary infections only. Initial treatment of toxicodendron dermatitis includes education and prevention using barriers to prevent exposure and washing the affected area soon after exposure. Vinyl gloves will not absorb the urushiol as readily as fabric gloves and should be used by patients with a history of severe reactions. Patients should be instructed to clean their clothes and any other objects that might have been in contact with the oils, including pets. Copious irrigation and cleansing of exposed skin should occur immediately after exposure.
Bibliography Davila A, Laurora M, Fulton J: A new topical agent, Zanfel, ameliorates urushiol-induced toxicodendron allergic contact dermatitis, [abstract no 364], Ann Emerg Med 2003;42 (4 suppl 1):s98. Isnar H: Plant poisoning, resins. Available at http://www.emedicine.com. Accessed on May 24, 2005. Stephanides S: Plant poisoning: toxicodendron. Available at http://www.emedicine.com. Accessed on May 19, 2005.
Urticaria DAVID W. KUHNS
ICD Codes: Urticaria 708.9, Angioedema 995.1
Key Points/Quick Reference Urticaria may be minor or can rapidly progress to a life-threatening condition. Rapid progression should prompt early and aggressive treatment. ! Emergency Actions ! Early administration of epinephrine and institution of intravenous access may be lifesaving for patients with urticaria. H1 and H2 blockers are generally recommended. Steroids are also frequently used in the treatment of this disorder.
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DEFINITION Urticaria (also known as hives) and a related condition, angioedema, are the cutaneous manifestations of the release of histamine and other mediators by mast (and other) cells in response to various stimuli. Most frequently, urticaria is self-limited in nature or responds readily to simple therapy. Occasionally, the activation of mast cells can proceed systemically to cause the life-threatening syndrome of anaphylaxis, manifested by hypotension, wheezing, and throat swelling. It is critical to recognize when simple urticaria may be progressing to a more serious condition. Anaphylaxis is dealt with in Chapter 16.
ETIOLOGY Cutaneous mast cells are located primarily around capillaries, lymphatics, and nerves in the skin. Erythema occurs due to vasodilation, the wheal is caused by fluid leakage, and the pruritus is caused by activation of dendritic itch receptors on nonmyelinated C fibers in the epidermis. Urticaria due solely to histamine typically resolves within an hour. Urticaria lasting longer than 1 hour is generally caused by the activity of additional mediators. Angioedema is a result of mediator release in the deeper dermis and leads to swelling that is most frequently nonpruritic. Angiotensin-converting enzyme inhibitor usage is one of the more common causes of angioedema, with an incidence of between 0.1% and 0.7%. Angioedema causing swelling in airway tissues necessitates aggressive treatment. Simple angioedema can be treated similarly to urticaria.
EPIDEMIOLOGY Between 15% and 23% of the population will experience urticaria sometime in their lifetimes. The majority of patients with urticaria do not have increased numbers of mast cells, but instead have mast cells that are more easily triggered to release their mediators. One exception is the clinical entity known as mastocytosis, in which there is a transient increase in the number of mast cells as well as a tendency for these to be easily triggered.
PATHOPHYSIOLOGY The primary cause of urticaria is the release of histamine—and less commonly, other mediators—by activated mast cells and other cells. Other mediators that can be responsible for hives include prostaglandin D2, bradykinin, various leukotrienes, and platelet-activating factor. Urticaria may be a response to exposures such as dust, molds, animal dander, and foods. Urticaria may also occur due to recent viral illnesses, amebiasis, malaria, diabetes, chronic renal insufficiency, primary biliary
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cirrhosis, systemic lupus erythematosus, rheumatoid arthritis, polymyositis, amyloidosis, polycythemia vera, carcinoma and lymphoma, fungal infections, mycoplasma, HIV infection, and pregnancy. Urticaria may also occur as a response to cold, exercise, or vibration.
CLINICAL PRESENTATION Angioedema usually affects the genitals, eyelids, lips, ear lobes, and mucous membranes. The affected area is not ecchymotic, is minimally tender, and is less pruritic than urticaria. Angioedema is often asymmetrical. Hereditary angioedema is a variant that is caused by a deficiency in C1 esterase inhibitor. This type of angioedema is more likely to affect airway tissues.
EXAMINATION The characteristic lesion of hives is a raised, erythematous, pruritic lesion known as a wheal. These lesions may coalesce to become giant wheals. They are often migratory and evanescent.
DIAGNOSIS Diagnosis is based on an appropriate history of exposure to an offending agent and by the presence of the characteristic lesions.
LABORATORY FINDINGS Laboratory evaluation is not generally useful in the emergency department (ED) evaluation of hives. Laboratory evaluation to look for the specific clinical conditions mentioned previously may be helpful in individual circumstances but rarely changes the ED treatment.
TREATMENT Aggressiveness of treatment is based on the severity of the urticaria, the rapidity of progression, and the presence or absence of systemic symptoms. In all cases, further exposure to the offending agent should be avoided. Hypotension, severe respiratory distress, and altered mental status should be treated as anaphylaxis. Any explosive, generalized urticaria should be treated with aqueous epinephrine 0.2 ml of 1:1000 SQ (not IV, because IV epinephrine is a 1:10,000 concentration and this can be a deadly mistake). An intravenous line should be started with preparation for the potential development of anaphylaxis. Intravenous Benadryl should be administered in a dose of
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1 mg/kg. If there is any delay in obtaining intravenous Benadryl, oral Benadryl elixir in the same dose is absorbed almost as rapidly. H2 blockers can be given intravenously as well. Zantac (ranitidine hydrochloride) can be given intravenously, 0.5 mg/kg over the course of 5 minutes. Cimetidine is given intravenously as a dose of 4–8 mg/kg. Intravenous Solu-Medrol (methylprednisolone) in a dose of 1–2 mg/kg up to 125 mg should also be given. Hydrocortisone can be given intravenously in a dose of 5–10 mg/kg up to a maximum dose of 500 mg. Patients with any severe reaction should be admitted to the hospital or at least should undergo prolonged observation in the ED until their conditions are clearly improved and stable. Patients with a severe or progressive episode of urticaria and a history of known hereditary angioedema frequently require C1 esterase inhibitor concentrate. Fresh frozen plasma can be used when C1 esterase inhibitor is unavailable. Mild urticaria (and non–life-threatening angioedema) can be treated with oral antihistamines. Oral Benadryl elixir is frequently given at triage in a dose of 0.5–1.0 mg/kg. Hydroxyzine (0.5–1 mg/kg) can be used as an alternative. Failure of the condition to resolve within an hour should prompt the addition of an H2 blocker and a steroid to the treatment regimen. Commonly used H2 blockers are ranitidine (Zantac) and cimetidine (Tagamet). In mild urticaria, these may be given orally. The oral dose of ranitidine is 1–2 mg/kg every 12 hours. The oral dose of cimetidine is 5–10 mg/kg/day divided twice or three times per day. If these are given for the treatment of the urticaria, they should be continued after discharge. Steroids are not believed to be effective in preventing degranulation of cutaneous mast cells in acute urticaria. They have, however, been shown to prevent a biphasic reaction that may occur 4–8 hours later in 20% of persons. The fact that this reaction cannot be predicted at the initial presentation prompts many ED providers to give steroids to prevent “bounce-backs.” Prednisone is given in an oral dose of 1–2 mg/kg daily. Intravenous steroids have little advantage over oral steroids in terms of effect or time of onset. Patients with minor urticarial eruptions are frequently sent home with a prescription for oral antihistamines. Traditionally, Benadryl or hydroxyzine were used. Newer, less-sedating agents have been developed that deliver various degrees of antihistaminic activity. Some clinicians use a regimen that includes a nonsedating agent during the day and a more sedating agent at bedtime. Various options include the following:
Benadryl 1 mg/kg taken every 6 hours for 4 days may be used in children for whom sedation is less of an issue. Zyrtec (cetirizine) 10 mg daily can be given to adults, 2.5 mg of syrup can be given to children aged 2–5 years, and 5-mg tablets or syrup can be given to children 6–11 years old. (This is less sedating.) Many other agents are available.
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As discussed previously, patients who have been treated with H2 blockers or steroids in the ED should also be sent home with a prescription for these agents. Since leukotrienes have been shown to be partially responsible for persistent or delayed urticaria, leukotriene antagonists have been used with some anecdotal success. These agents are not yet recommended in the treatment of urticaria. Patients with a significant urticarial reaction may be at risk for a more serious reaction in the future. Consideration should be given to providing them with a prescription for an EpiPen (epinephrine) autoinjector for use in case of future attacks that prove to be serious. These patients should be given instructions for administration and should be told to present to the ED if this therapy is required.
Bibliography Beltrani VS: Urticaria and angioedema, Dermatol Clin 1996;14(1):171–198. Beltrani VS: Urticaria, angioedema, and anaphylaxis, ACP Medicine 2003; Ch 6 (Immunology) XIII:1–6. Bensch G, Borish L: Leukotriene modifiers in chronic urticaria, Ann Allergy Asthma Immunol 1999;83(4):348. Heymann WR: Chronic urticaria and angioedema associated with thyroid autoimmunity: Review and therapeutic implications, J Am Acad Dermatol 1999;40(2 Pt 1):229–232. Joint Task Force on Practice Parameters, The diagnosis and management of urticaria: A practice parameter. Part I: Acute urticaria/angioedema. Part II: Chronic urticaria/ angioedema, Ann Allergy Asthma Immunol 2000;85(6 Pt 2):521–544. Tharp MD: Chronic urticaria: Pathophysiology and treatment approaches, J Allergy Clin Immunol 1996;98(6 Pt 3):S325–S330.
Chapter 4
Acute Gastrointestinal Emergencies Anorectal Disorders CLAUDIO F. ZEBALLOS
ICD or CPT Codes: Hemorrhoids 455.0, Anorectal abscess 566.0, Pilonidal 685.0, Proctalgia fugax 546.6, Pruritus ani 698.0, Rectal prolapse 569.1
Key Points/Quick Reference Anorectal disorders include hemorrhoids, anal fissures, anorectal abscesses and fistulas, pilonidal disease, proctalgia fugax, pruritus ani, and rectal prolapse. ! Emergency Actions ! Any patient who has diabetes, fever, chills, an elevated glucose level, and an anal disorder should be thoroughly evaluated for sepsis along with the anorectal disorder.
DEFINITIONS Hemorrhoids are varicosities of the veins of the hemorrhoidal plexus that can become inflamed, thrombose, and bleed. External hemorrhoids are located below the dentate line and are covered by squamous epithelium. Internal hemorrhoids are located above the dentate line. Anal fissures are superficial linear tears in the anal canal that can develop into a chronic ulcer. Anorectal abscess is a localized collection of pus that develops due to an infected anal crypt gland in the intersphincteric space. An anorectal fistula is a communication between the anal canal and, usually, perianal skin that can drain. Pilonidal disease is an acute or recurrent chronic abscess that drains from sinuses located in the midline sacrococcygeal area in the gluteal fold. Hidradenitis suppurativa is a localized infection of the apocrine sweat glands that develops a network of sinus tracts and is associated with hair follicles found along the perineum, groin, or axillae. Proctalgia fugax is a severe painful spasm of the muscles of the pelvic floor and rectal area that can occur spontaneously and usually lasts less than 30 minutes. Rectal prolapse (i.e., procidentia) is a condition in which the rectum protrudes through the anus. Pruritus ani is defined as anal and perianal itching. 114
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EPIDEMIOLOGY Hemorrhoids are common, affect both sexes, and have a 4.4% incidence in the U.S. population with a peak prevalence between the ages of 45 and 65 years and increased incidence among persons with higher socioeconomic status. Anal fissures are most common in persons 30–50 years of age. This is also the most common anorectal problem encountered in infants. Anorectal abscesses and fistulas most commonly affect males aged 30–50 years. Prevalence in the general population is likely higher than is seen in clinical practice because the majority of patients do not seek medical care. Anorectal fistulas develop in 30%–60% of patients with anorectal abscesses. Rectal prolapse tends to affect persons at the extremes of age and has a higher incidence in women with a history of excessive straining. Pilonidal disease usually affects young hirsute males and is associated with obesity. It is rarely found past the fourth decade of life. Pruritus ani is more common in older men and during the summer months, with exacerbation of symptoms at night.
PATHOLOGY Hemorrhoids Hemorrhoids are vascular cushions in the anal submucosa that normally become engorged during defecation to protect the anal canal. With aging and stressors the muscle layer, muscularis submucosa breaks down and the vascular cushions become overdistended with venous blood. These overdistended vascular cushions are prone to bleed, thrombose, or ulcerate. External hemorrhoids are located below the dentate line, whereas internal hemorrhoids are located above.
Anal Fissures An anal fissure is a tear in the lining of the anal canal, usually in the posterior midline, caused by local trauma such as passage of large hard stool. Anal fissures can also be seen in patients with Crohn’s disease, tuberculosis, and leukemia. The tear can reoccur with subsequent bowel movements. The exposed internal sphincter muscle—below the fissure— spasms, pulling apart the edges of the fissure and preventing healing. This cycle leads to the development of a chronic anal fissure.
Anorectal Abscesses and Fistulas Anal glands that are located circumferentially within the anal canal at the level of dentate line become blocked and infected develop into abscesses.
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These can progress into fistulas. Because these glands are located in several different planes, four different kinds of abscesses can present clinically. The four types are perianal (40%–45%), ischiorectal (20%–25%), intersphincteric (2%–5%), and supralevator (>5%). Anorectal fistulas usually develop after either surgical or spontaneous drainage of a chronic perianal abscess, but they can also result from trauma/postoperative and chronic anal fissure, radiation, and leukemia.
Rectal Prolapse Rectal prolapse is caused by weakening of the pelvic floor muscles, creating a laxity in the pelvic structures and may be seen with uterine prolapse.
Pilonidal Disease Debate surrounding the etiology of pilonidal disease centered on the theory that a pilonidal sinus develops in the gluteal fold during embryogenesis. This is in contrast to the concept that disease is caused by a simple bacterial infection of sterile hair follicle that occludes drainage, forming an ever-enlarging cavity that invades the subcutaneous fat and developing an epithelium-lined tract to the skin.
Pruritus Ani Pruritus ani can have many causes, but most commonly carries the benign etiology of poor hygiene and fecal irritation. Other etiologies include pinworms, hemorrhoids, anal fissure or fistulas, and systemic disease such as iron or vitamin deficiencies, psoriasis, lichen simplex, and sexually transmitted diseases. Contact dermatitis can also cause this condition as a result of the use of a new cream or toiletry item.
CLINICAL PRESENTATION Hemorrhoids Because most patients use the term hemorrhoid loosely to describe a myriad of anorectal problems, a thorough patient history should be obtained, including symptoms, bleeding and its association to defecation, pain, itching, protrusion, discharge, color of stool, systemic disease such as human immunodeficiency virus (HIV) infection or Crohn’s disease, polyps, cancer, and anal sexual intercourse. A patient with hemorrhoids most commonly present reporting of rectal bleeding particularly with defecation, and the bleeding described as bright red. Bright red blood seen on toilet paper suggests anal fissure or external hemorrhoids. Drops of blood in the toilet bowl suggest internal
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hemorrhoids. Both internal and external hemorrhoids are usually painless unless the hemorrhoid is thrombosed, at which point it becomes painful. A prolapsed or thrombosed hemorrhoid can present as a gradual-onset, persistent pain.
Anal Fissures Anal fissures commonly present with acute-onset, tearing, intense pain associated with rectal bleeding during bowel movements. The blood is usually bright red and found on surface of stool but not mixed with stool. The pain lasts several hours and subsides until the next bowel movement.
Anorectal Abscesses and Fistulas A patient with an anorectal abscess usually reports severe rectal pain that is constant and not associated with bowel movements. He or she may also report rectal drainage and fever. In the case of anorectal fistulas, the patient will report recurrent perianal intermittent discharge, which is usually painless unless the fistula becomes occluded.
Rectal Prolapse A patient with rectal prolapse will present reporting a painless protruding anal mass or fullness with Valsalva maneuver, walking, or standing. Rectal bleeding may occasionally occur, and incontinence is frequent.
Pilonidal Disease A patient with pilonidal disease reports tender fluctuant nodule midline in the gluteal fold region of sacrococcygeal area.
Pruritus Ani Patients with pruritus ani report uncontrollable anal itching. A thorough history should be obtained, including diet, systemic diseases, use of topical agents, and sexual practices.
EXAMINATION Hemorrhoids Hemorrhoids are usually visualized by performing anoscopy to assess the type and degree. It is useful to have the patient perform the Valsalva maneuver during the examination. Internal hemorrhoids are classified as
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first-degree if they protrude into the anal canal but do not prolapse and can present as a feeling of fullness, whereas second-degree hemorrhoids prolapse with stress but spontaneously reduce. Third-degree hemorrhoids prolapse but require manual reduction, and fourth-degree are not reducible and require surgery. External hemorrhoids usually do not cause any symptoms unless they become thrombosed/clotted. Thrombosed external hemorrhoids presents as a firm bluish-purple and are painful with palpation and defecation.
Anal Fissure Usually found in the posterior midline, anal fissure can also be seen in the anterior midline in women. Fissures found in other areas should make the practitioner consider Crohn’s disease, leukemia, HIV infection, or tuberculosis. Chronic fissure may exhibit the triad of a deep ulcer, an external skin tag (i.e., sentinel pile) at the lower end, and a papillae at the superior end. Rectal examination during an acute painful episode can be difficult because of sphincter spasm and pain.
Anorectal Abscesses and Fistulas In the presence of anorectal abscess or fistula, a fluctuant or indurated mass may be palpated. Purulent drainage may be visualized. Perianal abscess is the most common form and will be visualized and palpated in the perineum. Ischiorectal abscess may present as a fluctuant mass within the buttock. Intersphincteric abscess can be seen as fluctuant mass protruding in the lumen and can be confused with thrombosed internal hemorrhoid. Supralevator abscess usually has no external evidence of disease, which makes the diagnosis difficult. Patients will report buttock pain, fever, and sometimes urinary retention. Computed tomography (CT) scan may aid in this diagnosis. A fistula will often be visualized as a secondary cordlike tract in the perineum. Practitioner should avoid probing the tract because this may create other fistulas.
Rectal Prolapse The patient should be examined while in a standing position or while performing a Valsalva maneuver. A moist reddish protruding mass will often be visualized extruding the anal canal.
Pilonidal Cysts Pilonidal cysts are tender fluctuant nodules midline in the gluteal fold region of sacrococcygeal area.
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Pruritus Ani In examining for pruritus ani, the healthcare provider should carefully examine the anus for tears, lesions, hygiene, excoriations, masses, or any evidence of abscesses. Pinworms can be identified by using transparent tape on the anus then transferring the specimen to glass slide to be viewed for eggs under the microscope at 10 magnification.
LABORATORY FINDINGS A complete blood count (CBC) may be useful if the practitioner is concerned about the amount bleeding or is looking for leukocytosis. Clotting studies can be helpful if the patient is taking Coumadin (warfarin) or has a bleeding disorder. A digital rectal examination should be performed to document the color, quality, and hemoccult status of stool.
DIAGNOSIS Careful history and physical examination with an anoscope is necessary to make a diagnosis.
IMAGING STUDIES, RADIOGRAPHS, AND GRAPHS The American Gastroenterology Society recommends that all patients with bright red rectal bleeding should have an anoscopy, at minimum, and should be scheduled for flexible sigmoidoscopy. CT scanning may aid in the diagnosis of supralevator abscess.
TREATMENT AND OUTCOMES Hemorrhoids Hemorrhoid treatment varies with degree. First-, second-, and most thirddegree nonthrombosed hemorrhoids can be managed with “WASH” regimen consisting of warm water/sitz baths, analgesia (oral), stool softeners, and a high-fiber diet. The use of topical steroids, anesthetics, and suppositories remain controversial for the treatment of hemorrhoids; however, all of these are readily available over the counter. There are data to support the theory that long-term topical steroids use can cause tissue atrophy. Patients with third-degree hemorrhoids will need referral for surgery, whereas acute, gangrenous, or fourth-degree hemorrhoids will require emergent hemorrhoidectomy. Thrombosed external hemorrhoids can be excised within the first 48 hours to provide relief of symptoms. An
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elliptical excision with evacuation of the blood clot should be cautiously performed only by experienced practitioners with prior experience.
Anal Fissures Anal fissures often respond to conservative measure, including “WASH” regimen of warm sitz bath post-defecation for 15 minutes, analgesia (i.e., topical anesthetic cream), stool softeners (e.g., Fiberall or Metamucil), and a high-fiber diet. A topical agent like glycerin trinitrate ointment or nifedipine 0.2% gel given twice a day aid in lubricating the anal canal and decreasing sphincter tone. Steroid suppositories have not been shown to be useful and can actually hinder healing. Most anal fissures will resolve in 2–4 weeks. Cases of chronic anal fissure should be referred to a surgeon.
Anorectal Abscesses and Fistulas Abscesses should be drained in a timely manner in consultation with a surgeon. Antibiotics should be given if perianal abscess involves evidence of cellulitis, if the patient has diabetes, and for all other types of abscesses. Patients with anorectal fistula should be referred to a surgeon for operative repair.
Rectal Prolapse Rectal prolapse should be manually reduced immediately as prolonged prolapse can cause tissue necrosis. Stool softeners should be administered after reduction, along with surgical referral. If the practitioner is unable to reduce the prolapse, the condition becomes an emergent surgical issue.
Pilonidal Disease Pilonidal disease management involves drainage via a lateral incision off midline. Recurrence is common, and definite treatment will often involve surgical consultation.
Pruritus Ani Treatment should be aimed at underlying cause. Appropriate anodermal hygiene is recommended if fecal irritation is identified as the cause. The anus area should be kept clean and dry, and excessive wiping of the anus should be avoided. After defecation, the patient should bathe and pat dry the area. Hydrocortisone cream 1% should be applied twice a day for 1 week; this can help relieve symptoms and promote healing. Oral
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antihistamine such as diphenhydramine can help ease symptoms. Pinworms can be treated with mebendazole 1 g taken once PO. Scabies are treated with lindane 1% or permethrin 5% lotion. Lindane is not recommended in children because it can cause seizures in epileptics or, if overused or misused in children, there is an increased risk of seizures. Lindane is contraindicated for use in infants. If the pruritus is related to sexually transmitted disease, the condition should be treated with appropriate antibiotics. Irritants should be avoided.
Bibliography American Gastroenterology Society, Diagnosis and care of patients with anal fissure, Gastroenterology 2003;124:233. American Gastroenterology Society, Diagnosis and treatment of hemorrhoids, Gastroenterology 2004;126:1461. Barnett JL, Raper SE: Anorectal diseases, In Yamada T, Alpers D, Qwayng C, et al (eds): Yamada Textbook of Gastroenterology, ed 2. JB Lippincott: Philadelphia, 1995, p 2027. Beers MH, Berkow R (eds): Gastrointestinal disorders. Anorectal Disorders, Online Medical Library, www.merck.com. Merck Research Laboratories DIVISION OF Merck & Co, Whitehouse Station, NJ. Breen E, Bleday R: Anal fissures 2005. Available at: http://www.uptodate.com. Burgess BE, Bouzoukis JK: Anorectal disorders. In Tintinalli JE: Emergency Medicine: A Comprehensive Study Guide, ed 6. McGraw-Hill: New York, 2004. Gorfine SR: Topical nitroglycerin therapy for anal fissures and ulcers [letter], N Engl J Med 1995;333:1156. Johanson JF, Sonnenberg A: The prevalence of hemorrhoids and chronic constipation: An epidemiologic study, Gastroenterology 1990;98(2):380–386. Lund JN, Scholefield JH: A randomised, prospective, double-blind, placebo-controlled trial of glyceryl trinitrate ointment in treatment of anal fissure, Lancet 1997;349 (9044):11–14. Marx J, Hockberger R, Walls R: Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 5. Mosby: St Louis, 2002. Noble J (ed): Textbook of Primary Care Medicine, ed 3. Mosby: St Louis, 2001. Ramanujam P, Venkatesh KS: Fibrin glue application in the treatment of recurrent anorectal fistulas, Dis Colon Rectum 1999;42:1136. The role of endoscopy in the patient with lower gastrointestinal bleeding, Guidelines for clinical application, Gastrointest Endosc 1988;34:23S. Smith LE, Henrichs D, McCullah RD: Prospective studies on the etiology and treatment of pruritus ani, Dis Colon Rectum 1982;25:358. The Society for Surgery of the Alimentary Tract: Surgical management of hemorrhoids. Available at: http://www.ssat.com/cgi-bin/hemorr.cgi. Accessed on August 11, 2003.
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Diverticulosis and Diverticulitis SHAWN M.VARNEY
ICD Codes: Diverticulosis 562.10, Diverticulitis 562.11, Diverticular hemorrhage 562.12
Key Points/Quick Reference Diverticulitis and lower gastrointestinal (GI) bleeding resulting from diverticulosis are clinically important complications of diverticular disease. ! Emergency Actions ! Volume resuscitation and broad-spectrum antibiotics address the emergent complications of diverticulitis and diverticulosis.
DEFINITION Diverticulosis refers to small outpouchings from the colonic lumen formed by herniation of the mucosa and submucosa at sites of vascular penetration. The sigmoid colon is affected most commonly (90%–98%), with the right colon involved only about 15% of the time. Nevertheless, diverticula may affect any portion of the GI tract from the duodenum to the sigmoid and may be solitary or multiple, numbering in the hundreds. Symptomatic diverticular disease is diverticulosis with clinical symptoms (e.g., abdominal pain or change in bowel habits) but no signs of inflammation (e.g., fever, leukocytosis, or peritoneal signs). Diverticulitis is diverticulosis with clinical symptoms and evidence of inflammation.
EPIDEMIOLOGY Diverticular disease is largely an ailment of industrialized Western societies and is found equally in males and females. In the United States, diverticular disease is uncommon (1.5) or thrombocytopenia (50 lesions) is correlated with older age, severe pain, and greater number of affected dermatomes. Severe rash also is a risk factor for prolonged pain and postherpetic neuralgia. Herpes zoster ophthalmicus represents 10%–25% of all cases of zoster.
Epstein-Barr Virus Between 90% and 95% of the adult population has developed antibodies to EBV. Approximately half of the population will seroconvert as young children, with a second peak incidence during the teen and young adult years. The virus is spread by contact with oral secretions.
Cytomegalovirus CMV is present in approximately 1% of newborns and in 40%–100% of adults. There are two peaks of seroconversion: the first occurs in the perinatal period and the second during young adulthood, presumably due to sexual contact. CMV is transmitted through milk, saliva, urine, semen, and cervical secretions. Virus may be present in milk, saliva, blood, or urine. The virus is not spread by casual contact but rather by prolonged exposure.
CLINICAL PRESENTATION There are a variety of infections associated with herpes viruses. The clinical manifestations of each type are listed later; however, human herpes viruses 6 and 7, both of which cause roseola, and human herpes virus 8, implicated in Kaposi sarcoma, will not be discussed here.
Oral HSV Both HSV-1 and HSV-2 can cause identical oral lesions. HSV-1 is a more common cause of oral lesions than HSV-2. The primary lesion of HSV-1 is often mild. In young children, it may present solely as a pharyngitis or gingivostomatitis and have associated fever or cervical adenopathy. For primary outbreaks, gingivostomatitis and pharyngitis are the most common presenting symptoms, and herpes labialis is most commonly seen in recurrent outbreaks. Lesions are typically distributed throughout the mouth. Primary lesions last 1–2 weeks, on average. Recurrent oral lesions occur in 60%–90% of infected persons, are usually milder, and generally occur
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on the lower vermillion border of the lip. Recurrences may be triggered by local trauma, sunburn, or stress. Prodromal symptoms of local adenopathy, pain, or tingling may precede the outbreaks. The lesions usually present within 48 hours of the prodrome and may last up to 10 days but typically crust over within the first 48 hours. Immunocompromised persons may present with friable, bleeding lips and ulcerations that have penetrated deep cutaneous layers, thus causing debilitating wounds.
Genital HSV HSV-1 and HSV-2 cause identical genital lesions; however, HSV-2 causes the majority of genital lesions. The disease usually presents with painful genital papules that progress to vesicles and then shallow ulcerations. Often, a prodrome of myalgias, fatigue, fever, and tender inguinal lymphadenopathy is present at the time of the first outbreak. Dysuria, pruritus, and vaginal and urethral discharge are also common findings. In some cases, urethritis in the absence of lesions may be the only presenting symptom of HSV infection. When lesions do occur, they typically crust over and reepithelialize within 7–10 days.
Ocular HSV HSV infection of the eye may lead to blindness. Classically, a prodromal phase consists of fatigue, low-grade fever, and malaise may last as long as 1 week. Soon after, the patient will present with acute onset of eye pain, chemosis, conjunctivitis, and blurry vision. An ulcerative keratitis is the most common manifestation. Along with the classic dendritic pattern on the eye, herpetic vesicles may be seen on the conjunctiva or on the lid margin. Furthermore, patients may develop blepharitis and edema of the eye associated with the inflammation. Recurrent ocular infections may include chronic ocular inflammation, loss of vision, and excruciating pain.
Encephalitis There may be a preceding viral-like illness before encephalitis occurs, or the onset may be sudden. Often headache, fever, and altered mental status indicated by focal seizures or speech disturbances may exist. Commonly, there is no cutaneous manifestation of HSV encephalitis.
Bell’s Palsy The clinical features of Bell’s palsy include facial hemiplegia or hemiparesis, taste disturbance, decreased blinking, dry eyes or increased tearing, jaw or face pain, and numbness of the face and or neck. Typically, the
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forehead is not spared in Bell’s palsy, though it is spared in the case of more central lesions. Attempting to close the eye on the affected side will commonly result in an upward gaze by the patient (i.e., Bell’s phenomenon). Paralysis of the stapedius muscle on the affected side will lead to hyperacusis.
Herpetic Whitlow The disease is usually limited to a single digit. It is marked by abrupt onset of digit pain, edema, erythema, tingling, burning, and vesicles on an erythematous base. Often, axillary adenopathy accompanies the rash. The prototypical vesicle of herpetic whitlow appears to contain pus when, in actuality, the vesicles are filled with necrotic epithelial cells. Herpetic whitlow is often misdiagnosed as a paronychia and incised, which leads to a delay in healing and allows a secondary infection to occur. When incised, no pus is expressed from the wound.
Immunocompromise Immunocompromised patients afflicted with herpes virus are at increased risk of disseminated infection, which can cause devastating infections of the esophagus, colon, lungs, and brain.
Herpes Zoster: Chickenpox In children, a prodrome of fever and malaise precedes the classic lesions on the face and trunk by approximately 48 hours. The lesions initially appear maculopapular and then turn to clear fluid-filled vesicles. As the lesions age, they begin to scab over. The rash starts centrally and then spreads to the extremities. The hallmark of chickenpox is lesions in different stages of healing. Systemic symptoms accompanying the lesions are fever, malaise, pruritus, and anorexia. Varicella encephalitis is characterized by chickenpox accompanied by altered level of consciousness, fever, vomiting, seizures, and headaches.
Herpes Zoster: Shingles The lesions of zoster are identical to those of chickenpox but are limited to a single dermatome in distribution. The most common dermatomes are those of the thoracic and lumbar region, specifically in the T3–L3 region. The cranial nerves may be affected as well, with the complications of Ramsay Hunt syndrome and herpes zoster ophthalmicus often seen. The Hutchinson sign, which is a lesion on the tip of the nose, may be noticed before ocular involvement is seen but is not necessary to make the diagnosis of herpes zoster ophthalmicus. The disease begins with a
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prodrome of pain in the affected area lasting 1–3 days before the outbreak of a maculopapular rash that quickly progresses to a vesicular rash. Ocular involvement can be seen in the presence of only a slight rash on the forehead. Often, there is facial pain, regional adenopathy, and occasionally a red eye preceding the appearance of the rash. A dendritiform corneal ulcer can often be identified with fluorescein staining. The skin rash helps differentiate herpes zoster ophthalmicus from ocular HSV. If the seventh cranial nerve is affected, intraoral lesions may occur or Ramsay Hunt syndrome, which is clinically similar to Bell’s palsy, may ensue. Findings associated with Ramsay Hunt syndrome include a unilateral facial motor weakness, loss of taste on the anterior two thirds of the tongue, and vesicles in the ear canal or on the tympanic membrane. The most common complication of shingles is postherpetic neuralgia, which increases in frequency with age. Immunocompromised patients afflicted with zoster may present with disseminated disease. They may have the classic rash involving multiple dermatomes or a rash that crosses the midline. They may also have diffuse organ involvement.
Epstein-Barr Virus A prodrome of fever, malaise, and myalgia may last for up to 2 weeks before the classic presentation of exudative pharyngitis, posterior anterior cervical lymphadenopathy, and splenomegaly begins. Infants and young children may be asymptomatic. Hepatomegaly and jaundice may be clinical manifestations in older adults. The most common presenting symptom is a severe sore throat with the presence of bilateral exudative tonsillitis/pharyngitis along with bilateral tender cervical lymphadenopathy, classically affecting the posterior chain. Approximately half of afflicted patients will have a palpable spleen during the course of their illness (most prominent during the second week of illness). If ampicillin is given to these patients, there is a 95% chance of a rash developing. Although neurological complications of EBV infection are rare, they may include encephalitis, meningitis, cranial nerve palsies, and Guillain-Barré syndrome. In immunocompromised patients, EBV infection may lead to B-cell lymphomas and other lymphoproliferative syndromes. Patients infected with HIV may develop hairy leukoplakia.
Cytomegalovirus CMV is capable of causing intrauterine infections. If a neonate is affected, he or she will show involvement of multiple organs, including jaundice, hepatosplenomegaly, microcephaly, petechiae, and inner ear problems, as well as CNS defects. The triad of petechiae, hepatosplenomegaly, and jaundice are seen in approximately 60%–80% of cases. Newborns may acquire CMV at the time of delivery by traveling through an infected
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birth canal or within the first month of life by drinking infected maternal milk. In the majority of cases, the child remains asymptomatic; however, CMV pneumonitis is a deadly complication that may occur. In healthy immunocompetent children and adults, CMV infection is usually asymptomatic. When CMV does cause disease in these persons, it typically resembles EBV mononucleosis. Presentations include fever, chills, myalgia, headache, lymphadenopathy, and splenomegaly. In CMV mononucleosis, unlike EBV mononucleosis, exudative pharyngitis and cervical adenopathy are rare. In HIV-positive patients, CMV infections can be deadly. CMV usually has its worst effects on those with low CD4 counts or in advanced stages of acquired immunodeficiency syndrome (AIDS). The most common illness is CMV retinitis. Patients may report only floaters or decreased vision. In immunocompromised patients, CMV may affect the liver, lungs, adrenal glands, colon, and CNS.
EXAMINATION Herpes Simplex Viruses 1 and 2 If HSV infection is suspected, the patient would be given a complete examination to include oral cavities, genitalia, and rectum with the aim to locate any painful, shallow ulcerations. Special attention should be paid to regional lymph nodes for enlargement and sensitivity. The posterior oropharynx should be inspected, looking for pharyngitis or tonsillitis. A full ophthalmological examination should be performed on patients suspected of ocular HSV, looking for herpetic vesicles on the conjunctiva or lid margins. Fluorescein staining should be initiated to examine for classic dendritic ulcerations of the cornea. In any patient presenting with altered mental status, fever, headache, focal seizures, or speech disturbances, a complete neurological examination should be performed. Special attention should be paid to any deficit of the seventh cranial nerve, which could be a harbinger of Bell’s palsy. Specifically, one should note facial hemiplegia or hemiparesis, taste disturbances, dry eyes, decreased blinking, or hyperacusis. The examiner should note whether forehead sparing is present which, when present, is more indicative of a central lesion rather than the peripheral lesion of Bell’s palsy. The rest of the cranial nerves along with the ears, tympanic membranes, mastoids, and parotid glands should be unaffected to make the diagnosis of Bell’s palsy. For herpetic whitlow, each digit should be inspected individually. Furthermore, careful attention should be paid to the axillary lymph nodes, looking for axillary adenopathy.
Herpes Zoster: Chickenpox A patient suspected of having chickenpox should be undressed so that a full skin examination can be accomplished. The examiner should look
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for lesions in different stages of healing. The classic lesion of chickenpox starts as a maculopapular rash and becomes a fluid-filled vesicle described by some as “dew drops on a rose petal.” In any patient suspected of varicella encephalitis, a full neurological examination should be performed, with special attention paid to the cerebellum to determine the presence or absence of cerebellar ataxia.
Herpes Zoster: Shingles Any patient suspected of having shingles should be undressed for a full skin examination; the practitioner should look specifically for rashes in dermatomal distributions. If there is a rash of the face, a careful ophthalmological examination should be done to look for herpes zoster ophthalmicus. A complete examination of the regional lymph nodes should also be performed. A thorough check of both ear canals should be accomplished, with the practitioner looking for lesions consistent with Ramsay Hunt syndrome.
Epstein-Barr Virus A complete physical examination should be performed for any patient suspected of having EBV infection, with special attention paid to the posterior oropharynx and tonsils in a search for exudates. The lymph nodes of the cervical chain should be palpated for enlargement and tenderness. A complete abdominal examination with palpation of the liver and spleen should be performed, looking for enlargement.
Cytomegalovirus If there is concern over a neonate with intrauterine exposure to CMV, an examination including head circumference measurements checking for microcephaly, abdominal examination palpating for hepatosplenomegaly, and skin examination looking for jaundice should be performed, at minimum. Furthermore, a neurological examination checking appropriate reflexes should also be done. In immunocompromised persons or patients with AIDS, a complete physical examination with emphasis on a funduscopic examination to look for retinal hemorrhages and exudates should be accomplished. Careful auscultation of the lungs to listen for signs of pneumonia should also be performed.
LABORATORY FINDINGS For oral, genital, and ocular herpes, the diagnosis is clinical. It can take weeks to get results from viral cultures, which in effect makes them useless
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for emergency department (ED) treatment and management. If confirmation is needed, staining of scrapings at the base of lesions with Wright’s, Giemsa, or Papanicolaou’s stain will show giant intranuclear inclusion bodies. Besides the lesions themselves, the virus may be obtained from samples of the cerebrospinal fluid (CSF), stool, urine, throat, nasopharynx, conjunctivae, cervix, or cornea. For HSV encephalitis, CT, magnetic resonance imaging, and electroencephalographic findings may include temporal abnormalities; however, these findings are not always present. CSF findings are nonspecific and usually show an elevated white blood cell count with mononuclear predominance. Conclusive diagnosis is made by biopsy with either culture or direct antibody testing with polymerase chain reaction of the CSF being the most sensitive way to isolate the virus. Again, these results can take weeks to obtain. The diagnosis of Bell’s palsy is largely clinical. If there are any atypical features, imaging should be considered to rule out stroke or tumor. Herpetic whitlow is a clinical diagnosis. For herpes zoster (chickenpox and shingles), the diagnosis is clinical. If confirmation is necessary for the diagnosis of herpes zoster, a variety of serological tools may be used, including the fluorescent antibody to membrane antigen test and the enzyme-linked immunosorbent assay. In the case of EBV, the diagnosis is largely clinical. EBV-specific antibody tests do exist, although they generally do not offer same-day results. A complete blood cell count should be drawn looking for elevations in lymphocytes and monocytes. A peripheral smear will commonly show a large percentage of atypical lymphocytes. Liver function tests may be a helpful adjunct. Tests for heterophile antibodies can be performed to help confirm the diagnosis. Most young children (younger than 4 years) will not produce heterophile antibodies, and false negatives in all patients are common in the first week of illness. In patients with a clinical picture compatible with EBV infection but a negative heterophile antibody test result, CMV infection should be considered. To make a diagnosis of CMV, a conversion from seronegative to seropositive must occur or an acute rise in antibody titer should be seen. Viral cultures can be drawn as well, although results are not readily available. In immunocompromised patients, a biopsy of the affected organ should be done. Emergently, the diagnosis is based on clinical grounds alone because definitive diagnosis is not available in a timely manner.
DIAGNOSIS In the case of oral, genital, and ocular herpes, the diagnosis is made based on clinical presentation. For HSV encephalitis, clinical presentation is the mainstay of diagnosis, with brain imaging and lumbar puncture being useful adjuncts. The diagnosis is clinical in the case of Bell’s palsy, herpetic
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whitlow, and herpes zoster. For EBV infection, clinical presentation is the key to diagnosis, and CBC, peripheral smear, liver function tests, and heterophile antibody tests serve as confirmatory adjuncts. CMV infection is a difficult diagnosis to be made on the basis of clinical examination alone. However, in the ED, appropriate confirmatory tests are not readily available, and results take too long to dictate treatment.
RADIOGRAPHS No specific radiographs are required of herpes viruses. Radiographs should be directed as needed. A patient with a fever and cough should receive a chest radiograph.
TREATMENT Oral and Genital HSV The treatment of recurrent oral and genital herpes is oral acyclovir, valacyclovir, or famciclovir. These medications shorten the course of illness but do not cure herpes. Taken daily, oral acyclovir has been shown to reduce outbreaks by 50%–75%. Furthermore, many recent studies suggest that acyclovir is safe to take during pregnancy. Topical penciclovir taken every 2 hours for 4 days has been proved to reduce the symptoms of oral herpes. Counseling is an important part of treatment of any herpes outbreak to reduce the spread of the disease. Patients should be warned that transmission of the virus is possible during asymptomatic shedding and that having sex while an outbreak is present is dangerous. In fact, up to 70% of HSV transmission occurs during viral shedding in the absence of clinical disease. Due to the high transmission rates of HSV, the use of condoms should be encouraged. Areas of the skin that remain uncovered by condoms are still at risk of infection.
Ocular HSV In the case of ocular HSV infection, immediate consultation with an ophthalmologist is mandated because there is a high risk of vision loss. The administration of intravenous acyclovir should be started immediately. As with oral and genital HSV infections, oral acyclovir can be taken to reduce recurrences.
HSV Encephalitis Due to the high mortality associated with untreated HSV encephalitis, intravenous acyclovir should be started immediately. Due to the poor
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penetration of intravenous acyclovir in to the CNS (30%–50% of plasma levels), the dose should be double that used to treat visceral or cutaneous infections.
Bell’s Palsy The treatment of Bell’s palsy is aimed at reducing the inflammation associated with the illness. Oral prednisone and acyclovir should be started. Follow-up should be set up with either a neurologist or an ear, nose, and throat specialist. Because of the inability to blink associated with the disease, eye care is very important. Artificial tears should be used liberally, and nighttime eye ointment with or without a patch should be applied. Special instructions should be given to the patient regarding eye safety because the eyelid will not provide its normal defense until the symptoms have subsided.
Herpetic Whitlow There is no specific treatment for herpetic whitlow. Patients should be advised to keep the area covered until symptoms resolve so as not to auto-inoculate or spread the disease to others. Local pain control and analgesics are appropriate.
Herpes Zoster: Chickenpox For children under the age of 12 years, treatment is symptomatic and may include skin care, bathing, and the administration of antipruritic agents. Oral acyclovir is indicated for children older than 12 years of age, persons with chronic illnesses, or persons receiving chronic aspirin therapy. The medication should be started within 24 hours of the outbreak of the rash for maximal effect. Any patient presenting with varicella encephalitis or pneumonia should immediately start receiving intravenous acyclovir to reduce mortality and should be admitted to the hospital. Pregnant or peripartum women with chickenpox should discuss treatment plans with a primary care physician or obstetrician and may need to start receiving intravenous acyclovir. Neonates who develop chickenpox or who have postpartum mothers with chickenpox should be admitted for the administration of intravenous acyclovir. Immunocompromised patients with chickenpox should also be admitted for intravenous acyclovir. Varicella zoster immune globulin should be given to any neonate with chickenpox or any neonate born to a mother who developed chickenpox within 5 days before delivery or 48 hours after delivery, regardless of symptoms.
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Herpes Zoster: Shingles The primary goal of the treatment of shingles is to reduce the incidence of postherpetic neuralgia. Studies have shown that antiviral agents such as acyclovir, famciclovir, and valacyclovir shorten the duration of postherpetic neuralgia but do not prevent it. For maximal benefit, the administration of antiviral drugs should be started within 72 hours of symptom onset. A long corticosteroid taper should be initiated in patients older than 50 years to reduce the inflammation associated with shingles. Systemic analgesics are the mainstay of therapy for shingles. If first-line analgesics and narcotics fail to ameliorate symptoms, carbamazepine or amitriptyline should be considered. Furthermore, amitriptyline given nightly in small doses may also reduce the incidence of postherpetic neuralgia by 50%. Immunocompromised patients with disseminated shingles should start receiving intravenous acyclovir and should be admitted to the hospital. Patients with herpes zoster ophthalmicus should have emergent ophthalmological consultation due to the threat of vision loss.
Epstein-Barr Virus In the absence of complications, the treatment of EBV infection is primarily supportive and includes rest and analgesia. The patient should be instructed to limit physical activity for the first month after infection to reduce the risk of splenic rupture. In the event of any airway compromise from tonsillar hypertrophy, prednisone should be given.
Cytomegalovirus There is no cure for CMV infection, but there are medications available for the suppression of the acute disease process. Ganciclovir should be used for AIDS-related CMV retinitis and for the prevention of CMV infection in transplant patients. In patients with CMV retinitis, ganciclovir is given in high doses for 2–3 weeks and then as lifetime suppressive therapy. In other cases, ganciclovir is given for 2–3 weeks and then stopped. Foscarnet is given to patients with resistant CMV infections or in the case of an inability to tolerate ganciclovir.
Bibliography Barker LR, Burton JR, Zieve PD (eds): Principles of Ambulatory Medicine, ed 6. Lippincott, Williams & Wilkins: Philadelphia, 2003, pp 478–480. Braunwald E, Fauci AS, Kasper DL, et al (eds): Harrison’s Principles of Internal Medicine, ed 15. McGraw-Hill: New York, 2001, pp 1100–1114. Jung BF, Johnson RW, Griffin DRJ, Dworkin RH: Risk factors for postherpetic neuralgia in patients with herpes zoster, Neurology 2004;62:1545–1551.
288 ESSENTIAL EMERGENCY MEDICINE FOR THE HEALTHCARE PRACTITIONER Lautenschlager S, Eichmann A: Urethritis: An underestimated clinical variant of genital herpes in men? J Am Acad Dermatol 2002;46:307–308. Nagasako EM, Johnson RW, Griffin DRJ, Dworkin RH: Rash severity in herpes zoster: Correlates and relationship to postherpetic neuralgia, J Am Acad Dermatol 2002;46:834–839. Rimsza ME: Sexually transmitted infections: New guidelines for an old problem on the college campus, Pediatr Clin North Am 2005;52:217–228. Shaikh S, Ta CN: Evaluation and management of herpes zoster ophthalmicus, Am Fam Phys 2002;66:1723–1730. Thomas SL, Hall AJ: What does epidemiology tell us about risk factors for herpes zoster? Lancet Infect Dis 2004;4:26–33. Tintinalli JE, Kelen GD, Stapczynski JS (eds): Emergency Medicine: A Comprehensive Study Guide, ed 5. McGraw-Hill: New York, 2000, pp 1050–1055. Yeung-Yue KA, Brentjens MH, Lee PC, Tyring SK: Herpes simplex viruses 1 and 2, Dermatol Clin 2002;20:249–266.
HIV Infections MARTIN A. DOCHERTY
ICD Code: HIV 079.53
Key Points In the ED evaluation of HIV-positive patients, the most important information to obtain is the CD4 count or viral load. Patients with CD4 counts between 200 and 500 cells/mm3 are at increased risk for opportunistic infections. ! Emergency Actions ! In patients for whom the CD4 count is unknown, careful examination for signs of cachexia, oral thrush or hairy leukoplakia, the purple lesions associated with Kaposi sarcoma, diffuse dermatitis, or signs of HSV infection can be a guide to the level of immunosuppression. Patients with altered mental status should be assumed to have toxoplasmosis, Cryptococcus infection, or both; these are the most common causative agents in CNS infection.
DEFINITIONS Human immunodeficiency virus is the retrovirus responsible for infection. Acquired immunodeficiency syndrome refers to the complex of opportunistic infections that occurs in patients who have developed immunosuppression as a result of infection with HIV.
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EPIDEMIOLOGY The first recognized cases of HIV infection in the United States date back to 1981. As of 2005, about 1 million persons in the United States were infected with HIV, and 40,000 new cases are reported each year. In some inner-city hospitals, about 10% of the population is HIV positive. Risk factors for infection include homosexual sex, intravenous drug use, sexual contact with at-risk persons, exposure to bodily fluids from at-risk persons, prostitution, blood transfusions received before 1985, and maternal-toneonatal transmission.
PATHOPHYSIOLOGY After infection, the virus binds to the CD4 receptor site of T-helper lymphocytes. The viral load increases exponentially during the first 6 weeks and becomes widely disseminated. During this time, many patients experience acute viral symptoms and lymphadenopathy. Eventually, an immune response develops, and the virus enters a period of latency that may last up to 10 years, although this is variable. Eventually, as CD4 cell counts decline, most patients develop AIDS. In the ED evaluation of HIV-positive patients, the most important information to obtain is the CD4 cell count or viral load. Patients with CD4 counts between 200 and 500 cells/mm3 are at increased risk for the following:
Oral thrush and oral hairy leukoplakia Mycobacterium tuberculosis Kaposi sarcoma Idiopathic thrombocytopenic purpura
With CD4 counts below 200 cells/mm3, there is increasing risk of infection with the following:
Pneumocystis carinii pneumonia (PCP) Toxoplasmosis and histoplasmosis Cryptococcus organisms Cryptosporidium organisms
In those patients with severe immunocompromise and CD4 counts less than 50 cells/mm3, Mycobacterium avium complex and CMV infection become more prevalent.
CLINICAL PRESENTATION Patients with HIV infection may visit the ED with fever or with symptoms specific to particular organ systems. As previously mentioned, the most important first step is to determine a patient’s CD4 cell count. Patients with CD4 counts greater than 500 cells/mm3 rarely arrive at the ED with symptoms of opportunistic infections. In patients whose counts are
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unknown, careful examination for signs of cachexia, oral thrush or hairy leukoplakia, the purple lesions associated with Kaposi sarcoma, diffuse dermatitis, or signs of HSV infection can be a guide as to the level of immunosuppression.
SPECIFIC SYMPTOMS Pulmonary System Respiratory symptoms are common in patients with AIDS. Such persons are at high risk for “typical” bacterial pneumonia due to Pneumococcus species or Haemophilus influenzae. In addition, tuberculosis and P. carinii infections need to be strongly considered. In patients with PCP, dyspnea on exertion is a hallmark finding. With tuberculosis, night sweats and bloody sputum may be present. Physical examination findings may be subtle, so, in addition to routine laboratory testing and pulse oximetry, chest radiography must be performed. Findings typical for PCP include a diffuse interstitial infiltrate. Tuberculosis infections may show up as hilar lymphadenopathy or, rarely, as cavitary lesions. Communityacquired pneumonia is most often associated with lobar infiltrates. It must be stressed, however, that there is significant overlap and the chest x-ray findings are by no means definitive regarding the causative agent. Intravenous trimethoprim (TMP)–sulfamethoxazole (SMX) is the recommended treatment for PCP. TMP/SMX is given at a dose of 20 mg/kg/day in three or four divided doses (dose is based on TMP). Because of the high prevalence of community-acquired pneumonia, most practitioners also add coverage of this condition with ceftriaxone plus a macrolide, or a newer fluoroquinolone. Treatment for tuberculosis need not be started in the ED, but respiratory isolation should be strongly considered pending definitive diagnosis. In patients with hypoxia and a PaO2 of less than 70 mmHg, prednisone at a dose of 40 mg twice daily should be added.
Gastrointestinal System Dysphagia is commonly due to candidal or herpes esophagitis. It is reasonable to treat for presumed candida with fluconazole or nystatin and reserve endoscopic examination for nonresponders. In patients presenting with abdominal pain, typical causes such as appendicitis, pelvic inflammatory disease, or bowel obstruction should always be considered. AIDS-specific causes may be related to lymphoma, CMV colitis, AIDS cholangiopathy, or medication-related pancreatitis (especially in patients taking the antiretroviral medication ddI). Evaluation and treatment depend on the cause. It is reasonable to order routine CBC and chemistry panels, including liver
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function tests and lipase. CT scanning and ultrasound may be needed in selected cases. Diarrhea is a common sign in patients with AIDS. Chronic diarrhea is usually due to parasitic infections such as Giardia and Cryptosporidium. Bacterial infection due to Shigella, Salmonella, and Campylobacter organisms should be considered in patients with new, acute diarrhea, or in persons with significant worsening of their chronic diarrhea. Clostridium difficile infection should always be considered if chronic antibiotic use is noted.
Central Nervous System CNS infections and neoplasms may have very subtle presentations. The neurological examination results are often normal, and the only relevant symptom may be of headache, with or without accompanying fever. A CT scan of the brain, followed by a lumbar puncture, should be performed in all patients with HIV/AIDS who present with a headache or any CNS symptoms. Toxoplasma and Cryptococcus organisms are the most common causative agents in CNS infections. Multiple brain lesions, found on CT scan, are typical with toxoplasmosis. Diagnosing cryptococcal meningitis requires a lumbar puncture. Opening pressures are often high in cryptococcal meningitis. CSF samples should be sent for routine studies, WBC and RBC counts, protein, and glucose. In HIV/AIDS patients an India ink fungal stain cryptococcal antigen, fungal cultures, and acid-fast bacillus stains should also be performed. The appropriate treatment for toxoplasmosis is with pyrimethamine 100 mg/day and sulfadiazine 100 mg/kg/day for 3–6 weeks. Cryptococcal infection is treated with intravenous amphotericin.
Ophthalmological System Gradual vision loss in patients with AIDS may be due to CMV retinitis. Although it may be possible to see the fluffy, whitish retinal lesions on funduscopic examination, early presentations may be missed. All new ocular symptoms in patients with HIV should mandate very early ophthalmological follow-up. Treatment is usually accomplished with ganciclovir.
Cutaneous System Chronic candidal infections can be treated with topical antifungal drugs such as clotrimazole or oral fluconazole. Diffuse scabies infections respond to treatment with lindane or permethrin. Hospitalization should be considered for patients with overwhelming HSV or varicella zoster infections. Treatment is with acyclovir, 10 mg/kg, given intravenously every
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8 hours. Be alert for the possibility of varicella pneumonia or herpes zoster ophthalmicus affecting the eyes.
POSTEXPOSURE PROPHYLAXIS Postexposure prophylaxis is an evolving field with treatment updates being proposed by the CDC, most recently with recommendations to provide HIV prophylaxis to victims of sexual assault. Most facilities have a protocol governing prophylaxis from inadvertent needle sticks or bodily fluid exposure. In general, a person experiencing a low-risk exposure is prescribed a three- to four-drug regimen of zidovudine and 3TC (lamivudine). Persons experiencing more significant exposures are treated with a three-drug regimen of zidovudine, 3TC, and indinavir. Follow-up for further testing and treatment should be part of the protocol.
Bibliography Hirschtick RE, Glassroth J, Jordan MC, et al: Bacterial pneumonia in persons affected with the human immunodeficiency virus, N Engl J Med 1995;333(13):845. Parente F, Cernushi M, Antinori S, et al: Severe abdominal pain in patients with AIDS: Frequency, clinical aspects, causes and outcome, Scand J Gastroenterol 1994;29:511. Quinn TC: The epidemiology of the acquired immunodeficiency syndrome in the 1990s, Emerg Med Clin North Am 1995;13:1. Simpson DM, Berger JR: Neurologic manifestations of HIV infection, Med Clin North Am 1996;80(6):1363. Weller IV, Williams IG: ABC of AIDS: Treatment of infections, BMJ 2001;322:1350.
Influenza AMY K. DITZEL
ICD Codes: Influenza 487, Influenza with other respiratory manifestations 487.1, Influenza with other manifestations 487.8
Key Points Influenza is a common seasonal viral illness. Complications are common with secondary infections.
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! Emergency Actions ! Any patient who presents to the emergency center with the diagnosis of influenza and shortness of breath should be administered oxygen. Dehydrated patients should be treated with vigorous fluid resuscitation. If the patient is in the extremes of age, very young, very old, or immunocompromised, admission to the hospital should be considered. Any patient with the diagnosis of influenza, who is experiencing any respiratory problems, and is not on oxygen should be admitted to the hospital.
DEFINITION Influenza involves acute, self-limited viral disease often accompanied by pulmonary complications. It occurs seasonally (late fall to winter) in epidemics.
EPIDEMIOLOGY Influenza viruses belong to the class Orthomyxoviridae. Although types A, B, and C exist, type A is the one responsible for the yearly outbreaks of influenza. The entire population is affected by influenza, with the very young most susceptible to infection and the very old most prone to death from complications associated with influenza. Additionally, certain conditions put patients at risk for developing complications, including cardiovascular disease, pulmonary disease (including asthma), hepatic or renal failure, hemoglobinopathies, asplenia, immunodeficiency, and diabetes. A local epidemic will last 5–6 weeks, peaking mid way through and generally affecting young children first. It is expected that 10%–20% of the local population will be affected at that time.
CLINICAL PRESENTATION Sudden onset of fever, chills, headache, and myalgia signals the onset of an influenza infection. These symptoms, along with malaise, anorexia, and ocular tearing and burning will predominate for about 3 days. As the fever decreases, respiratory symptoms (specifically, a dry cough, nasal drainage, and pharyngitis) will begin to appear. The severity and extent of symptoms can vary widely, with elderly persons possibly only displaying fever, confusion, and malaise. It is not uncommon for the convalescent period to extend to 2 weeks before full recovery. Although uncomplicated influenza is self-limited, it easily becomes complicated with the presence of bronchiolitis, croup, pneumonia, or acute exacerbation of chronic bronchitis. The clinician should investigate for the presence of secondary infection in all patients with influenza. Nonpulmonary complications rarely occur but include myositis, Guillain-Barré syndrome, toxic shock syndrome, pericarditis, and Reye’s syndrome.
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EXAMINATION A patient with uncomplicated influenza will often present febrile and tachycardic with watery, red eyes. He or she may be coughing but will generally not be dyspneic. The cervical lymph nodes will be enlarged and tender, and the pharynx will appear hyperemic. Lung sounds will generally be clear, but an occasional rhonchus may be heard.
LABORATORY FINDINGS Rapid, point-of-care testing should yield positive result for influenza A. Viral cultures of nasal secretions will yield positive results but are not appropriate for ED management.
DIAGNOSIS The diagnosis of influenza is generally made on the basis of history and examination within the context of a localized epidemic. Point-of-care testing can provide confirmation of diagnosis. If the patient is acutely ill, a CBC and chemistry panel should be performed.
RADIOGRAPHS Chest radiography may be useful to rule out pneumonia, if it is suspected.
TREATMENT Antiviral therapy is the treatment of choice for limiting the duration and severity of the course of the infection. If treatment is started within 48 hours of symptom onset, oseltamivir (75 mg twice daily, or 75 mg daily if creatine clearance 40 kg: 250/ 100 mg daily One tablet weekly 2–11 months: 1/ 8 tablet weekly; 1–3 yr: ¼ tablet weekly; 4–8 yr: ½ tablet weekly; 9–14 yr: 3/4 tablet weekly; >14 yr: 1 tablet weekly One tablet daily >8 years old: 2.2 mg/kg daily
BEGIN TREATMENT FINISH TREATMENT
COMMON SIDE EFFECTS
2 days before travel
7 days after return from travel
Nausea, vomiting, headache
1 week before travel
4–6 weeks after return Nausea, vomiting, from travel gastritis, headache, photosensitivity
2 days before travel
4 weeks after return from travel
Sun sensitivity, nausea, vaginal candidiasis
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Table 7-2 Malaria Prevention
Lariam (mefloquine) 250 mg
One tablet weekly >3 months 5–20 kg: ¼ tablet weekly; 21–30 kg: ½ tablet weekly; 31–45 kg: 3 /4 tablet weekly; >45 kg: 1 tablet weekly
1 week before travel
4 weeks after return from travel
Primaquine 15 mg
Two tablets daily
2 days before travel
7 days after return from travel
Aralen (chloroquine phosphate) 500 mg
One tablet weekly 5-mg base/kg weekly; 500 mg phosphate ¼ 300-mg base
1 week before travel
4 weeks after return from travel
Plaquenil (hydroxychloroquine sulfate) 400 mg
One tablet weekly 5 mg/kg weekly
1 week before travel
4 weeks after return from travel
0.6 mg/kg daily
Avoid use in patients with abnormality of cardiac conduction. Headache, nausea, insomnia, anxiety/depression, seizures Avoid use in G6PDdeficient patients due to potentially fatal effect. Nausea, vomiting Nausea, vomiting, headache, dizziness, blurred vision, increases psoriasis Nausea, vomiting, headache, dizziness, blurred vision, increases psoriasis
G6PD, Glucose-6-phosphate dehydrogenase.
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MEDICATION
ADULT DOSAGE
Malarone (atovaquone 4 tablets daily for 3 days 250 mg/proguanil 100 mg) Fansidar (pyrimethamine 25/ 2–3 tablets once sulfadoxine 500) Doxycycline 100 mg Lariam (mefloquine) 250 mg Primaquine 15 mg Aralen (chloroquine phosphate) 500 mg Plaquenil (hydroxychloroquine sulfate) 400 mg
1 5 2 2
tablet twice daily tablets once tablets daily tablets once, then 1 tablet in 6 hr, then 1 tablet daily for 2 days 2 tablets once, then 1 tablet in 8 hr, then 1 tablet daily for 2 days
PEDIATRIC DOSAGE 5–8 kg: 125/50 mg daily; 9–10 kg: 187.5/75 mg daily; 11–20 kg: 250/100 mg daily; 21–30 kg: 500/200 mg daily; 31–40 kg: 750/300 mg daily; >40 kg: 1000/400 daily 2–11 month: ¼ tablet once: 1–3 yr: ½ tablet once: 4–8 yr: 1 tablet once: 9–14 yr: 2 tablets once: >14 yr: 2–3 tablets once Must be >8 r 20–25 mg/kg once 0.6 mg/kg daily 10-mg base/kg once, then 5 mg/kg in 6 hr, then 5 mg/kg daily for 2 days 10 mg/kg once, then 5 mg/kg in 8 hr, then 5 mg/kg daily for 2 days
DURATION OF TREATMENT 3 days
One dose 2 weeks One dose 2 weeks 2 days 2 days
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Table 7-3 Treatment of Malaria
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Rabies CLAUDIO F. ZEBALLOS
ICD Code: Rabies 071
Key Points Rabies is a viral disease of the CNS usually transmitted by saliva of an animal bite. If left untreated, this disease is usually fatal. ! Emergency Actions ! Immediate thorough wound cleansing, rabies vaccine (RabAvert or Imovax), and human rabies immunoglobulin (HRIG) should be administered postexposure for any routine contact with animals at risk.
DEFINITIONS Exposure is defined as a scratch or bite from an animal that may have the risk of carrying rabies virus. Human rabies immunoglobulin consists of human antibodies and provides passive immunization that neutralize the rabies virus. Rabies vaccines can be either Imovax (human diploid cell vaccine) or RabAvert (purified chick embryo cell vaccine), both of which provide active immunization with inactivated virus. Pre-exposure prophylaxis is rabies vaccine given to persons who work in close contact with potentially infected animals and is given prior to any known exposure. Postexposure prophylaxis includes HRIG and vaccine (Imovax or RabAvert) and is given after a known exposure with a high risk of rabies transmission.
EPIDEMIOLOGY Rabies is a global disease that poses its greatest threat to public health in developing countries. The WHO estimates 30,000–70,000 deaths per year worldwide, mostly in developing countries as a result of inadequate control of the disease in domesticated animals. In the United States rabies is extremely rare, largely due to efforts in 1940s to vaccinate domestic animals. There has been an average of three U.S. cases per year since 1980. In developing nations, dogs are the most commonly infected animal causing transmission to humans. In the United States, however, wild
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animals account for the majority of transmissions. The particular wild animal varies with geography, but the four major animal reservoirs identified are raccoons, skunks, foxes, and bats. Raccoons are the most frequently infected wild animal in the United States. Silver-haired bats account for more than half of U.S. human transmissions since 1980. The majority of bat-to-human transmissions occurred without a known bite; in these cases, the method of transmission is unclear but unrecognized scratches, bites, or aerosolization of viral particles have all been postulated. Therefore, postexposure prophylaxis should be administered. Infected animals become sick and die usually within 3–9 days from when they begin secreting the virus in their saliva and are therefore at their most infectious stage—thus the rationale for a quarantine period for a domestic animal suspected of having rabies. Behavior that suggests an infected rabid animal includes staggering gait, overaggressive behavior, salivation, anorexia, or irritability in an animal that may display convulsions, paralysis, or a change in its usual behavior. In wild animals, a change in instinctual behavior can include a nocturnal or reclusive animal found ambulating in a densely populated neighborhood in broad daylight exhibiting an unwarranted or unprovoked attack.
PATHOLOGY Rabies virus belongs to family Rhabdoviridae and is a bullet-shaped ribonucleic acid virus that is usually transmitted via bite wound from a rabid animal or when the virus is introduced into open skin cuts or mucous membranes, with one documented case of transmission via scratch to mucous membrane. A rare method of rabies virus transmission through human tissue transplantation from an unrecognized infected donor has been documented. Once the virus infects the nervous system, it ascends peripheral nerves at a rate of 8–20 mm/day to reach the spinal cord and the brain, where massive replication and dissemination occurs; at this point, immunization is no longer effective. The incubation period from bite to disease in humans ranges from 30 to 90 days. The risk of developing rabies after a bite ranges from 5% to 80% without treatment and varies with the incidence in endemic species, skin penetration, the amount of salivary contamination, host immunity, degree of innervation at the site of exposure, and proximity to the CNS. Once active rabies develops, it is almost universally fatal; therefore, postexposure prophylaxis is key in the emergent setting.
CLINICAL PRESENTATION Patients will often visit a healthcare provider after an animal attack or animal exposure exhibiting no other medical symptoms. Healthcare
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providers should asses the exposure risk and make a decision either to treat or withhold treatment. Once human infection has occurred, rabies progresses over a period of 7–14 days. The mean time between initial presentation and death is 16.2 days. In the prodromal stage, fevers, pharyngitis, myalgia, and headache or accompanying nausea and vomiting are often earliest findings. This nonspecific prodromal period may last from 2 to 10 days. Paresthesia or pain at the site of the bite or scratch is one of earliest neurological manifestation and should raise suspicion. Back pain and spasms are also common symptoms. The neurological stage of the course of rabies can be either encephalitic (i.e., furious) or, less commonly, paralytic (i.e., dumb) rabies and can last 2–7 days. Encephalitic rabies is the most common form of rabies, manifesting as agitation, irritability, hyperactivity and esophageal and accessory respiratory muscle spasms when exposed to water (i.e., hydrophobia) or air (i.e., aerophobia). Approximately 80% of patients with classic rabies have the encephalitic form. Paralytic rabies can present with quadriparesis; sphincter involvement often mimics Guillain-Barré syndrome. Consciousness is often spared until late in the disease. Late in the course of the disease, hypotension, cardiac arrhythmias, coma, cardiac arrest, and disseminated intravascular coagulation may be seen.
EXAMINATION Most patients with rabies present to the ED after an animal exposure or bite. The healthcare provider should examine the wound and assess and clarify the exposure, including an assessment of risk of transmission and decision to treat. Once human rabies infection has occurred, the disease course begins. Persons with early rabies infection will present with high fevers, myoclonus, anxiety, agitation, hypersalivation or increased lacrimation, and rapidly progressing encephalitis or altered mental status.
LABORATORY FINDINGS For a patient seeking care for animal exposure, no laboratory studies are required. For a patient with suspected active rabies infection, a lumbar puncture and CT scan of the head are warranted. CSF studies may yield normal results but will usually have an elevated protein level and a modest elevated WBC (range, 5–30 cells/ml). A lumbar puncture will often not differentiate between rabies and other encephalitides. The virus can usually be isolated from CSF, saliva, or CNS tissue.
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DIAGNOSIS For a patient seeking care for an animal exposure, no diagnostic tests are required. A patient with suspected rabies should have a collection of samples for diagnosis drawn only in consultation with the state health department or with CDC. Saliva should be collected along with CSF and serum samples for antibody tests. A 5-mm neck biopsy specimen can be taken from the region of the hairline to obtain nerves surrounding hair follicles; this can be sent for direct fluorescent antibody for assistance in diagnosis. A brain biopsy performed postmortem may show Negri bodies along with perivascular inflammation of gray matter.
RADIOGRAPHS No imaging studies are required for asymptomatic patients seeking care for exposure. For a patient with suspected active rabies, a CT scan of the brain is usually performed during the workup for neurological symptoms.
TREATMENT AND OUTCOMES Pre-exposure immunization can be given to persons whose careers place them at risk for exposure such as veterinarians, animal handlers, taxidermists, or wildlife biologists. Imovax or RabAvert vaccine can be given intramuscularly in the deltoid on days 0, 7, and 21 Postexposure treatment consists of immediate thorough wound cleaning and prompt immunization with HRIG and vaccination with Imovax or RabAvert. There is no treatment for symptomatic disease. For treatment with antiserum HRIG 20 IU/kg, it is now recommended that the full dose or as much as possible be infiltrated at or around the wound site. The remainder can be given intramuscularly at a distant site. Treatment with active Imovax or RabAvert vaccine should be given intramuscularly in the deltoid at baseline and on days 3, 7, 14, and 28. It takes 7–12 days to induce immunity that lasts 2 years. Immunization is safe during pregnancy. If a person has been previously immunized, a booster can be given at baseline and on day 3. The risk of exposure is affected by the amount of skin penetration and the amount of saliva or CSF secreted. Open wounds or mucous membranes with deeper wounds and larger inoculums have the greatest risk of infection.
QUARANTINE The local health department should always be notified and guidance sought for individual cases of rabies. Domestic animals that may have been infected should be quarantined for 10 days and observed for any
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neurological symptoms or death. During that time, treatment can be started and discontinued if no symptoms occur. If a domestic animal has been vaccinated during the appropriate timeframe the likelihood of rabies is reduced, but the physician should inquire about any recent bites or fights with wild animals. Wild animals with rabies should be killed immediately to send the brain for diagnostic studies because the period of infectivity in wild animals is not always known. If the wild animal is not available for slaughter (as is usually the case) treatment should be based on the exposure. Small rodents, including mice, rats, gerbils, hamsters, guinea pigs, squirrels, and rabbits, rarely contract rabies and are considered to be at low risk, although exceptional cases have been documented. Treatment for these animals can usually be withheld. The local health department can be contacted for information regarding epidemiology in a particular region. Exposure to woodchucks, beavers, skunks, foxes, jackals, wolves, mongooses, and especially raccoons and bats should be considered a high risk and treated immediately. Dog bites near United States–Mexico border or nondomestic dog bites should be treated as high risk. Significant transmission has been found with bat exposure, and treatment is recommended even in the absence of bites in the setting of a person finding himself or herself in an enclosed space with a bat.
Bibliography Anderson LJ, Nicholson KG, Tauxe RV, Winkler WG: Human rabies in the United States, 1960 to 1979: Epidemiology, diagnosis, and prevention, Ann Intern Med 1984;100 (5):728–735. Auerbach PS: Wilderness Medicine, ed 4. Mosby: St Louis, 2001. Centers for Disease Control and Prevention: First human death associated with raccoon rabies—Virginia, 2003, MMWR Morb Mortal Wkly Rep 2003;52(45):1102. Centers for Disease Control and Prevention: Human death associated with bat rabies— California, 2003, MMWR Morb Mortal Wkly Rep 2004;53(2):33–35. Centers for Disease Control and Prevention: Human rabies—California, 1987, MMWR Morb Mortal Wkly Rep 1988;37:305. Centers for Disease Control and Prevention: Current recommendations for diagnosis of rabies, MMWR Morb Mortal Wkly Rep 1996;46:27–28. Centers for Disease Control and Prevention: Human rabies—California, 1995, MMWR Morb Mortal Wkly Rep 1996;45(17):353–356. Centers for Disease Control and Prevention: Human rabies—California, 2002, MMWR Morb Mortal Wkly Rep 2002;51(31):686–688. Centers for Disease Control and Prevention: Human rabies—Iowa, 2002, MMWR Morb Mortal Wkly Rep 2003;52(3):47–48. Centers for Disease Control and Prevention: Human rabies—Tennessee, 2002, MMWR Morb Mortal Wkly Rep 2002;51(37):828–829. Centers for Disease Control and Prevention: Human rabies—Texas and New Jersey, 1997, MMWR Morb Mortal Wkly Rep 1998;46:1. Centers for Disease Control and Prevention: Human rabies—Washington, MMWR Morb Mortal Wkly Rep 1995;44:625.
306 ESSENTIAL EMERGENCY MEDICINE FOR THE HEALTHCARE PRACTITIONER Centers for Disease Control and Prevention: Human rabies—West Virginia, 1994, MMWR Morb Mortal Wkly Rep 1995;44:86. Centers for Disease Control and Prevention: Investigation of rabies infections in organ donor and transplant recipients—Alabama, Arkansas, Oklahoma, and Texas, 2004, MMWR Morb Mortal Wkly Rep 2004;53(26):586–589. Centers for Disease Control and Prevention: Rabies. Available at: http://www.cdc.gov/ncidod/ dvrd/rabies. Centers for Disease Control and Prevention: Update: Investigation of rabies infections in organ donor and transplant recipients—Alabama, Arkansas, Oklahoma, and Texas, 2004, MMWR Morb Mortal Wkly Rep 2004;53(27):615–616. Fishbein D, Robinson L: Rabies, N Engl J Med 1993;329:1632. Fisher DJ: Resurgence of rabies: A historical perspective on rabies in children, Arch Pediatr Adolesc Med 1995;149:306. Human rabies prevention—United States, 1999. Recommendations of the Advisory Committee Immunization Practices (ACIP), MMWR Morb Mortal Wkly Rep 1999;48:1. Krebs JW, Wheeling JT, Childs JE: Rabies surveillance in the United States during 2002, J Am Vet Med Assoc 2003;223(12):1736–1748. Krebs J, Rupprecht CE, Childs JE: Rabies surveillance in the United States during 1999, J Am Vet Med Assoc 2000;217:1799. Lentz TL, Burrage TG, Smith AL, et al: Is the acetylcholine receptor a rabies virus receptor? Science 1982;215(4529):182–184. Messenger SL, Smith JS, Rupprecht CE: Emerging epidemiology of bat-associated cryptic cases of rabies in humans in the United States, Clin Infect Dis 2002;35(6):738–747. Noah DL, Drenzek CL, Smith JS, et al: Epidemiology of human rabies in the United States, 1980 to 1996, Ann Intern Med 1998;128:922. Smith JS, Fishbein DB, Rupprecht CD, Clark K: Unexplained rabies in three immigrants in the United States: A virologic investigation, N Engl J Med 1991;324:205. Udwadia Z, Udwadia F, Katrak S: Human rabies: Clinical features, diagnosis, complications, and management, Crit Care Med 1989;17:834. Warrell D, Warrell M: Human rabies and its prevention: an overview, Rev Infect Dis 1988;10:S726.
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Tetanus ROGER MATTHEW BAUTISTA
ICD Code: Tetanus 037
Key Points Elderly persons are at highest risk for the development of tetanus, with a recent study finding that only 30% of tested persons older than 70 years had adequate antibody levels. Increased central muscle tone with superimposed generalized spasms and relative sparing of the hands and feet strongly suggests tetanus. ! Emergency Actions ! Acute treatment includes aggressive supportive care, administration of antitoxin, elimination of toxin production, and active immunization. Respiratory and cardiac status must be monitored closely in an intensive care unit.
DEFINITION Tetanus is a toxin-mediated (tetanospasmin from Clostridium tetani) disease causing severe, uncontrolled skeletal muscle spasms. It can occur in four forms: generalized, cephalic, localized, and neonatal. Spasms of the respiratory muscles can lead to hypoxia and death.
EPIDEMIOLOGY Although tetanus is uncommon in the United States, the worldwide incidence is approximately 500,000 to 1 million cases per year, with a mortality rate ranging from 20% to 50%. It is more common in developing countries. The majority of cases in the United States, fewer than 100 per year, occurs in temperate areas such as California, Florida, and Texas and has a mortality rate of about 11%. Most patients have an inadequate immunization history. The disease is predominant in neonates and young children in countries with inadequate immunization standards and poor hygiene. Elderly populations are at highest risk for the development of tetanus, with a recent study finding that only 30% of tested persons older than 70 years had adequate antibody levels.
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ETIOLOGY C. tetani is an anaerobic, motile, spore-forming, gram-positive, rodshaped organism. The organism is found in soil, dust, and the feces of animals and humans. Neurotoxins are produced by the vegetative forms, which are highly susceptible to adverse environmental conditions. The spores, however, can survive in soil for years and are resistant to heating and chemical disinfectants.
PATHOPHYSIOLOGY Because C. tetani is a noninvasive organism, most cases occur after an acute break in the skin, such as a laceration, puncture wound, or abrasion. The injury could range from major to so minor that medical attention is not sought. Tetanus is also associated with burns, surgery, abortion, childbirth, frostbite, body piercing, and drug abuse. In some cases, no injury could be identified. The presence of damaged or devitalized tissue, foreign bodies, or other bacteria reduces the oxidation-reduction potential of the tissue and allows spores to convert to the vegetative form of the bacteria. In the vegetative form, three exotoxins are produced: tetanospasmin, tetanolysin, and nonconvulsive neurotoxin. Tetanospasmin is responsible for the clinical manifestations of tetanus. When tetanospasmin is released in the wound, it binds to peripheral motor neuron terminals, enters the axon, and is transported to the nerve-cell body in the brainstem and spinal cord by retrograde intraneuronal transport. In generalized tetanus, it enters the lymphatics and bloodstream, spreading widely to distant nerve terminals. In localized tetanus, only the nerves supplying the affected muscles are involved. It interferes with the release of inhibitory neurotransmitters, causes disinhibition of motor groups, and results in excessive, uncontrolled muscle activity. It may also cause autonomic nervous system dysfunction by its effects on the brainstem and autonomic interneurons.
CLINICAL PRESENTATION The incubation period of tetanus is usually between 3 and 14 days but can range from 1 day to several months. A shorter incubation period usually means a worse prognosis. The four clinical types are generalized, cephalic, localized, and neonatal. Generalized tetanus is the most common and severe form. It is the fully developed state of skeletal muscle hypertonicity. Trismus or lockjaw, caused by increased masseter muscle tone, is usually the presenting symptom. When other facial muscles become affected, the characteristic sardonic smile (i.e., risus sardonicus) develops. Other symptoms include myalgia, muscle cramps, dysphagia, hydrophobia, drooling, weakness, and irritability. At its most severe form, muscle rigidity becomes generalized and reflex muscle spasms
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may be precipitated by external stimuli (e.g., noise, light, touch) or spontaneously. Because the posterior trunk and extremities are stronger than the anterior muscle groups, opisthotonos develops. Laryngeal and respiratory muscle spasms can cause respiratory failure and death. Autonomic dysfunction is exhibited by tachycardia, hypertension, hyperthermia, cardiac dysrhythmias, peripheral vasoconstriction, and diaphoresis. Mentation is unimpaired. The illness usually progresses with an increase in clinical manifestations for the first 3 days, persistence for 5–7 more days, and reduction of spasms after 10 days. Recovery is complete in at least 4 weeks, if the patient survives. Mortality ranges from 0% to 50%. Cephalic tetanus is rare, exhibited by trismus with cranial nerve palsies. It usually occurs after facial or head trauma or otitis media and has associated ipsilateral cranial nerve palsies, with the facial nerve being the most common. It has a short incubation period. Two thirds of the cases progress to generalized tetanus, and the remaining one third completely resolve. The mortality rate of this form of tetanus is high. Localized tetanus is exhibited by persistent muscle spasms, mild or severe, in the area of inoculation. It may progress to the generalized form, but the majority of cases, after weeks to months, completely resolve. Neonatal tetanus is a generalized form primarily affecting persons in underdeveloped countries as a result of inadequate maternal immunization and contamination of umbilical cords. There is a short incubation period with symptoms of weakness, irritability, and poor sucking and swallowing appearing during the first 2 weeks of life. The prognosis is poor if the condition is left untreated. The main complication is acute respiratory failure; others include cardiovascular complications, fractures and dislocations, rhabdomyolysis, renal failure, infection, pulmonary embolism, and GI complications.
LABORATORY FINDINGS A CBC and chemistry panel to include calcium should be performed. No laboratory test exists to diagnose tetanus, but serum antitoxin titers greater than 0.01–0.015 IU/ml are considered protective. Wound cultures for C. tetani should be performed even though only about one third yield positive results. A CT scan of the brain can exclude intracranial pathology. A lumbar puncture can exclude meningitis. An electromyogram may assist in the diagnosis of cephalic or localized tetanus.
DIAGNOSIS Tetanus is clinically diagnosed. Increased central muscle tone with superimposed generalized spasms and relative sparing of the hands and feet strongly suggests tetanus. If a reliable history demonstrates the completion
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of a primary vaccination series with appropriate booster immunizations, tetanus is unlikely. The differential diagnosis includes alveolar abscess, dystonic reaction, hypocalcemia, strychnine poisoning, meningitis/ encephalitis, rabies, and an acute abdomen.
TREATMENT Acute treatment of tetanus includes aggressive supportive care, administration of antitoxin, elimination of toxin production, and active immunization. The patient’s respiratory and cardiac status must be monitored closely in an intensive care setting. The patient must be intubated for any signs of airway compromise. Gentle handling of patients and minimization of environmental stimuli must be ensured to minimize reflex muscle spasm. Benzodiazepines can help to reduce muscle spasms and anxiety and to assist in sedating patients for comfort. Nondepolarizing neuromuscularblocking agents, propofol, and dantrolene can also be used. Sympathetic overactivity from autonomic instability can be treated with labetalol. Bradydysrhythmias should be treated with temporary pacing. Hypertension can be treated with nitroprusside. Magnesium sulfate, narcotics, and spinal anesthesia can be used for autonomic instability. Human tetanus immunoglobulin (TIG) and tetanus toxoid should be given to all patients. TIG neutralizes any circulating toxin or toxin at the wound site and reduces mortality. TIG, 3000–8000 U, should be given intramuscularly at separate sites from the toxoid. Repeated doses are not needed because the half-life of TIG is 25 days. Only after TIG and toxoid are given should antibiotics and wound care be started to counteract the possible transient release of tetanospasmin. Penicillin G (10–24 million U/day given intravenously in divided doses for adults, or 100,000 U/kg/day in divided doses for children), metronidazole (500 mg taken orally every 6 hours), and doxycycline (100 mg given intravenously every 12 hours) have been described to be effective against C. tetani. Clindamycin and erythromycin are alternatives for patients who are allergic to penicillin. The wound should be debrided, foreign bodies removed, and the wound cleansed.
Bibliography Abrutyn E: Tetanus. In Kasper DL, Facuci AS, Longo DL (eds): Harrison’s Principles of Internal Medicine, ed 16. McGraw-Hill: New York, 2005. Carden DL: Tetanus. In Tintinalli. JE, Kelen GD, Stapczynski JS (eds): Emergency Medicine: a Comprehensive Study Guide, ed 6. McGraw-Hill: New York, 2004. Cook TM, Protheroe RT, Handel JM: Tetanus: A review of the literature, Br J Anaesth 2001;87:477–487. Farrar JJ, Yen LM, Cook T, et al: Tetanus, J Neurol Neurosurg Psych 2000;69:292–301. Fernandez-Frackelton M, Turbiak TW: Bacteria. In Marx JA (ed): Rosen’s Emergency Medicine, Concepts and Clinical Practice, ed 5. Mosby: St Louis, 2002.
Chapter 8
Medical Emergencies Acid–Base Problems BARBARA M. FISHMAN
ICD Codes: Metabolic acidosis 276.2, Metabolic alkalosis 276.3, Respiratory acidosis 276.2, Respiratory alkalosis 276.3
Key Points 1. Acid^base homeostasis is achieved as follows: (1) chemical buffering by intracellular and extracellular buffers, (2) changes in renal Hþ excretion, and (3) changes in the rate of alveolar ventilation for the excretion of carbon dioxide (CO2). 2. The bicarbonate (HCO3)/CO2 buffering system is key to the body’s maintenance of acid^base balance because CO2 and HCO3 can both be regulated independently. CO2 is regulated by alveolar ventilation via the lungs and HCO3 concentration is regulated by Hþ excretion via the kidney. 3. In any acid^base disturbance, there will be compensatory mechanisms that return the pH toward but not completely to normal (i.e., there is no overcompensation). 4. Metabolic acidosis results from endogenous production of acid, decreasedrenal excretion of acid,or HCO3 loss.The conditionis divided into two categories: high anion gap and normal anion gap (hyperchloremic acidosis). If a patient’s primary disorder is metabolic acidosis, the pH and HCO3 must be decreased. HCO3 therapy in metabolic acidosis is caused by the generation of endogenous organic acids (i.e., diabetic ketoacidosis [DKA] and lactic acidosis due to sepsis). 5. If a patient’s primary disorder is metabolic alkalosis, pH and HCO3 must be increased.To maintain the metabolic alkalosis there must also be impairment in renal HCO3 excretion. This usually occurs because of volume depletion or potassium (K) depletion. Metabolic alkalosis is divided into saline-responsive alkalosis and saline-resistant alkalosis. Treatment is aimed at increasing the renal excretion of HCO3. For this to occur,volume,Cland Kþ depletion must be corrected.
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312 ESSENTIAL EMERGENCY MEDICINE FOR THE HEALTHCARE PRACTITIONER 6. The presence of an acid pH and elevated PCO2 (>45 mmHg) establish the diagnosis of primary respiratory acidosis. Anxiety in these patients may be a sign of elevated PCO2; sedatives should be avoided because they will worsen the respiratory depression. Metabolic compensation for respiratory acidosis takes 3^5 days to develop. 7. Primary respiratory alkalosis is characterized by low PCO2 and elevated pH. Once the diagnosis of primary respiratory alkalosis has been established, the etiology should be sought. 8. The healthcare provider must determine whether the disturbance is simple or mixed. He or she must check the pH, arterial blood gas (ABG), and electrolyte levels to calculate the anion gap and check for appropriate compensation. Compensation returns the pH toward normal but not to normal. The degree of compensation is predictable; lack of appropriate compensation is a sign of a mixed disorder. In a simple acid^base disturbance that produces an elevated anion gap, the increase in anion gap from baseline should equal the decrease in serum HCO3. If the change in anion gap is greater or less than the change in HCO3, a mixed picture is present (i.e., metabolic alkalosis plus acidosis or anion gap acidosis plus non^anion gap acidosis).
DEFINITION Many diseases become evident through acid–base disorders. The acidity of a solution is based on its hydrogen ion activity. The level of activity of hydrogen ions in a solution is equal to the ratio of activity of the acid to its corresponding base, multiplied by its dissociation constant. Like other components of extracellular fluid (ECF), Hþ concentration [Hþ] must be maintained within narrow limits. The pH of any solution is the concentration of hydrogen ions expressed as a negative logarithm. The pH is computed by the HendersonHasselbalch equation: pH ¼ pKa þ log
protein acceptor ðbaseÞ protein donor ðacidÞ
In humans and animals, the pH (and [Hþ]) must remain fairly constant. This is achieved as follows: (1) chemical buffering by intracellular and extracellular buffers, (2) changes in renal Hþ excretion, and (3) changes in the rate of alveolar ventilation for the excretion of CO2, a volatile acid. Chemical buffers in the body are weak acids and can take up or release Hþ. The main extracellular buffer is HCO 3 ; plasma proteins are also buffers. Intracellular buffers are phosphate and protein, and in the red blood cell (RBC), hemoglobin. Bone is also an important buffer. Anemia, decreased muscle mass, and low protein levels all affect the
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body’s ability to buffer hydrogen ions. Patients with anemia, low protein levels, or decreased muscle mass are at a higher risk of severe acidosis.
Renal H+ Excretion and HCO3– Absorption The kidneys contribute to acid–base balance by absorbing filtered HCO 3 and excreting acid. Ammonia represents the majority of renal acid excretion. It is produced in the distal tubule from glutamine and other precursors. Acid is excreted with urine buffers by the phosphate þ (HPO2 4 /H2PO4 ) buffering system. Finally, H can be excreted directly, though a very small amount of acid is excreted in this manner. All of the filtered HCO 3 must be absorbed for the kidney to be able to excrete a daily acid load. The clinician should remember that loss of HCO 3 in the urine is the equivalent to a gain in Hþ to the body. Net renal acid excretion ¼ Acid buffered þ NHþ 4 urine HCO3
Numerous factors affect renal acid excretion. Extracellular pH is the primary regulator of renal acid excretion, but it is also affected by volume status, aldosterone, and plasma Kþ. These other factors will affect renal acid excretion in pathologic states independent of the pH. Ninety percent of filtered HCO 3 is absorbed in the proximal tubule. The sodium (Naþ)-hydrogen (Hþ) exchange in the proximal tubule results in Naþ resorption and Hþ excretion into the lumen. Distal urine acidification involves Hþ-Kþ exchange, Cl secretion, and (Cl)-(HCO 3) exchange. Dehydration or volume depletion will cause increased sodium and HCO 3 absorption in the proximal tubule. This becomes clinically important in dehydrated patients, in whom volume is maintained at the expense of an inability to excrete HCO 3 and resultant metabolic alkalosis. In volume overload, less sodium and HCO 3 will be absorbed. In states of hyperaldosteronism, there is an increase in sodium and chloride absorption in the distal nephron and excretion of K. Hþ is also excreted in response to aldosterone.
Respiratory Excretion of Volatile Acid CO2 is a by-product of the body’s metabolism of proteins, fats, and carbohydrates. It is excreted mainly by the lungs. CO2 is transported from tissues to lungs by plasma HCO 3 and hemoglobin. CO2 is present as carbonic acid in the arterial blood at a PCO2 of 40 mmHg.
Clinical Evaluation of Acid–Base Balance Acid–base balance is usually clinically evaluated in terms of the HCO 3/ CO2 buffer system.
314 ESSENTIAL EMERGENCY MEDICINE FOR THE HEALTHCARE PRACTITIONER Dissolved CO2 þ H2 O > H2 CO3 > Hþ þ HCO 3
The concentration of carbonic acid is usually so low that it can be ignored. The HCO 3 /CO2 buffering system is key to the body’s maintenance of acid–base balance because CO2 and HCO 3 can both be regulated independently. CO2 is regulated by alveolar ventilation via the lungs, and þ HCO 3 concentration is regulated by H excretion via the kidney. The Henderson-Hasselbalch equation for the HCO 3 /CO2 buffer system becomes: pH ¼ pKa þ log
ðHCO 3Þ ðH2 CO3 Þ
This shows the interrelationship between pH, HCO 3 (the base) and carbonic acid (H2CO3). This can be further derived to the more simplified Kassirer-Bleich equation, which is more clinically useful: ½Hþ ¼ 24
ðPCO2 Þ ðHCO 3Þ
This shows the interrelationship between Hþ concentration (and therefore pH), HCO 3 , and PCO2.
Liver The liver also has a role in acid–base homeostasis. Hepatic conversion of ammonia to urea consumes HCO 3 , though the role of this in acid–base regulation in humans is not fully understood. Nitrogen metabolism by the liver and by the kidney are connected by glutamine, which links renal ammonia production and hepatic urea synthesis to systemic acid–base regulation.
Base Deficit and Base Excess Base deficit or base excess is the measure of change of buffer base from normal. Base deficit (i.e., negative base excess) equals the amount of HCO 3 in mEq/L that is required to restore the total buffer base of ECF to a pH of 7.40. At a pH of 7.15 and HCO 3 of 24 mEq/L, the base deficit will be 6. At a pH of 7.47 with the same HCO 3 of 24, the base deficit will be 1 (i.e., negative base deficit ¼ metabolic alkalosis). Potassium has an inverse relationship with the pH due to intracellular fluid (ICF) shifts. Normal arterial values are as follows:
pH ¼ 7.40 0.03 PCO2 ¼ 40 mmHg Venous HCO 3 ¼ 25 mEq/L 2
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Anion Gap The unmeasured anion concentration is known as the anion gap. The anion gap is based on the principle that plasma is electrically neutral. Measured cations þ unmeasured cations ¼ measured anions þ unmeasured anions
Therefore, Measured cations Measured anions ¼ Unmeasured anions Unmeasured cations ¼ Anion gap
The predominant measured cation is sodium. Measured anions in plasma are chloride and HCO 3 . Unmeasured anions are serum proteins, phosphate, sulfate, and organic anions. Unmeasured cations include calcium (Caþ) and magnesium (Mgþ). The formula becomes: Anion gap ¼ Naþ ðCl þ HCO 3Þ
A normal anion gap is 12 4 but may be lower due to high chloride concentrations measured with newer autoanalyzers. Knowing the normal range for a specific laboratory value is necessary to interpret the anion gap correctly. The most common cause of an elevated anion gap is metabolic acidosis (i.e., increase in organic acids), but it can also be seen in hypocalcemia or hypomagnesemia where there is a fall in unmeasured cations. Decreased or negative anion gap can be seen when there is an increase in unmeasured cations, as in lithium toxicity, bromide, or the positively charged proteins of multiple myeloma. Hypoalbuminemic states like nephrotic syndrome or cirrhosis can cause a false decrease in the anion gap, so increased anion gap in these patients may be missed. In a simple acid–base disturbance that produces an elevated anion gap, the increase in anion gap from baseline should equal the decrease in serum HCO 3 . If the serum HCO3 change is greater or less than the change in anion gap, a coexistent non–anion gap metabolic acidosis or mixed acid–base disorder should be suspected.
METABOLIC ACIDOSIS Definition Metabolic acidosis is defined as a decrease in pH, elevated Hþ concentration, and decreased HCO 3 concentration. The respiratory compensation is hyperventilation, causing a decrease in PCO2.
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Epidemiology Metabolic acidosis results from endogenous production of acid, decreased renal excretion of acid, or HCO 3 loss. It is divided into high anion gap and normal anion gap (i.e., hyperchloremic acidosis). In high anion gap metabolic acidosis, there is increased production of organic acids. The most common causes are ketoacidosis (e.g., diabetic, starvation, and alcoholic), lactic acidosis (seen in persons who have experienced trauma and in critically ill patients), renal failure, and ingestions. The mnemonic MUDPILES can be used to help remember the causes of anion gap metabolic acidosis:
Methanol Uremia DKA Paraldehyde Ingestions, iron, INH Lactate Ethylene glycol Salicylates
It should be noted that many ingestions (i.e., cyanide, biguanides, iron) cause their toxicity by the generation of a lactic acidosis and that ethanol does not cause a significant metabolic acidosis. In non–anion gap metabolic acidosis, HCO 3 is replaced on an equimolar basis by chloride. The anion gap is normal, but there is a rise in the serum chloride concentration. Non–anion gap metabolic acidosis is caused by renal or gastrointestinal (GI) loss of HCO 3, inability of the kidney to excrete Hþ, or Hþ administration. This can be seen with severe diarrhea, ureterosigmoidostomy, intestinal fistulas, renal tubular acidosis (RTA) type 1, 2, or 4, hypoaldosteronism, and infusion or ingestion of HCl-containing compounds (e.g., NH4Cl, lysine-HCl).
Clinical Presentation and Examination In severe acidosis, decreases are evident in cardiac contractility, systemic blood pressure, and hepatic and renal perfusion. Fatal ventricular arrhythmias can occur. Neurological effects from lethargy to coma have been reported. Patients with severe metabolic acidosis may have an increased respiratory rate and may report dyspnea yet have a normal PO2 and lung examination results. This is due to the respiratory compensation for the metabolic acidosis. History is helpful in determining the etiology of the acidosis; possible causes include renal disease, diabetes mellitus, diarrhea, ingestions, and alcohol abuse.
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Laboratory Findings and Diagnosis pH and HCO 3 must be decreased if the primary disorder is metabolic acidosis. Electrolyte measurements and ABG analysis should be performed. Decreased pH with decreased HCO 3 (7.45, HCO 3 >25 mEq/L. Hypokalemia and hypochloremia are usually present. Magnesium and Caþ are also decreased. The etiology is often obtained from the history. If there is no pertinent history, surreptitious vomiting, diuretic use, or a mineralocorticoid excess state should be suspected. Electrolyte measurements and ABG analysis should be performed. A check of the urine chloride level may be helpful in differentiating the etiology and determining treatment. In metabolic alkalosis, the urine chloride may be a better indication of volume status than urine sodium. The urine chloride level is typically less than 20 mEq/L in the presence of vomiting, nasogastric suction, chronic diuretic use, chloride-wasting diarrheas (i.e., laxative abuse) and cystic fibrosis and after hypercapnia. The urine chloride level is greater than 20 mEq/L in primary mineralocorticoid excess states and in the presence of alkali loads and severe hypokalemia (Kþ45 mmHg) establish the diagnosis of respiratory acidosis. Diagnosis can often be made on the basis of the history. The metabolic compensation for respiratory acidosis differs for acute versus chronic respiratory acidosis. The renal response of renal Hþ excretion takes time to develop. Initial buffers are the intracellular buffers hemoglobin and proteins. In acute respiratory acidosis, for every 10-mmHg rise in PCO2, there is a 1.0-mEq/L increase in plasma HCO 3 . In chronic hypercapnia, there is a compensatory renal response of Hþ secretion, with a resultant addition of HCO 3 to the ECF. This takes 3–5 days to develop. In chronic
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respiratory acidosis, for every 10-mmHg increase in PCO2, there is a 3.5-mEq/L increase in plasma HCO 3.
Treatment and Outcome The goal of treatment of respiratory acidosis is to improve alveolar ventilation and increase minute ventilation. If minute ventilation is doubled, PCO2 will be decreased by 50%. Treatment of the underlying lung disease, oxygen, bronchodilators, steroids, reversal of sedation, and intubation/mechanical ventilation may be needed. Sedatives should be avoided because they can contribute further to respiratory depression. Diuretics and chronic low-flow oxygen may benefit patients with cor pulmonale. Chronic respiratory acidosis should not be corrected too quickly if mechanical ventilation is needed. A rapid lowering of PCO2 to “normal” levels can cause overshoot alkalemia (there is already renal compensation with increased plasma HCO 3 in these patients) and arrhythmias. The sudden increase of central nervous system (CNS) pH can result in seizures and coma.
RESPIRATORY ALKALOSIS Definition Primary respiratory alkalosis is characterized by low PCO2 and elevated pH. Respiratory alkalosis is due to increased effective alveolar ventilation beyond that needed to eliminate the daily load of metabolically produced CO2, with resultant increased pulmonary excretion of CO2 and a fall in PCO2. It is the most common acid–base abnormality in critically ill patients.
Etiology Respiratory alkalosis can be caused by hypoxia, pulmonary disease, direct stimulation of the respiratory center in the brainstem, and mechanical ventilation. Common causes of hypoxia include pneumonia, CHF, pulmonary embolism, parenchymal lung diseases, and severe anemia. Central respiratory stimulation can be due to pain, hyperventilation/anxiety, CNS lesions or strokes, liver failure, sepsis, salicylate toxicity, and pregnancy.
Clinical Presentation and Examination Many patients experiencing respiratory alkalosis will have tachypnea and will be hyperventilating. Tachycardia is frequent. Cyanosis may be present if the patient is hypoxic. Tinnitus may be present in the case
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of salicylate toxicity. Physical examination may yield a clue to underlying pulmonary or neurological disease. An acute decrease in PCO2 causes a decrease in Hþ concentration, resulting in protein binding of Caþ with a decrease in ionized Caþ. Symptomatic hypocalcemia can occur, including light-headedness, circumoral and extremity paresthesias, carpopedal spasm, and syncope. A variety of cardiac arrhythmias may also occur. In addition, respiratory alkalosis causes cerebral vasoconstriction and a leftward shift in the oxygen-hemoglobin dissociation curve, resulting in decreased tissue oxygen delivery.
Laboratory Findings In a simple respiratory alkalosis, pH will be greater than 7.40 and PCO2 will be less than 35 mmHg. An ABG analysis and Chem 7 test should be performed to help establish whether the respiratory alkalosis is primary or compensatory to a metabolic acidosis, and to look for hypoxia. A chest radiograph should be obtained if pulmonary disease is suspected. A head CT scan may be indicated if a central cause is suspected.
Diagnosis Alkaline pH and hypocapnia are diagnostic of respiratory alkalosis. Tachypnea may be an important clue to the presence of decreased PCO2. Once the diagnosis of primary respiratory alkalosis has been established, the etiology should be sought. Respiratory alkalosis may be the first sign of gram-negative sepsis or salicylate toxicity. Critically ill patients can present with hyperventilation; it should not be assumed that all hyperventilation is secondary to hysteria. As in respiratory acidosis, the metabolic responses to acute and chronic respiratory alkalosis that attempt to return the pH toward normal are different. The initial response in acute respiratory alkalosis is from intracellular buffers. The decrease in renal Hþ secretion that is seen with chronic respiratory alkalosis takes 2–3 days to be complete. In acute respiratory alkalosis, for each 10-mmHg decrease in the PCO2, the HCO 3 decreases by 2.0 mEq/L. In chronic respiratory alkalosis, for each 10-mmHg decrease in the PCO2, the HCO 3 decreases by 4 mEq/L.
Treatment and Outcome The treatment of alkalosis per se is not indicated but is directed at the identification and therapy of the underlying cause.
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APPROACH TO PATIENTS WITH AN ACID–BASE DISORDER The patient may have a single acid–base disturbance or a combination of abnormalities. For example, a patient with DKA and severe nausea and vomiting may have both a metabolic acidosis and a metabolic alkalosis. A patient with COPD and sepsis may have respiratory acidosis and metabolic acidosis. The only disturbance that cannot coexist is respiratory acidosis/alkalosis. A patient can hypoventilate or hyperventilate, but he or she cannot do both simultaneously. Compensation returns the pH toward normal but not to normal. The degree of compensation is predictable; the lack of appropriate compensation is a sign of a mixed disorder. Patient evaluation begins with a history and physical examination, including information regarding medications and ingestions, with attention to sources of acid or alkali gain or loss and renal and pulmonary disease. ABG analysis and electrolyte measurements should be performed. Once this is accomplished, the healthcare provider should take the following actions: 1. Look at the pH. If it is decreased, the primary disturbance is acidosis. If it is increased, the primary disturbance is alkalosis. 2. If the pH indicates acidosis, check the HCO 3 level. If the patient has a low pH and the HCO is low, a primary metabolic acidosis is present. 3 Calculate the anion gap. If the HCO 3 is increased, the metabolic acidosis is an anion gap type. If the anion gap is not elevated, the primary metabolic acidosis is of the non–anion gap (hyperchloremic) type. 3. If there is an anion gap acidosis, establish how the change in anion gap is related to the change in HCO 3: If the increase in anion gap is equal to the decrease in HCO3 , pure anion gap acidosis is present. If the increase in anion gap is greater than the decrease in HCO3 , concomitant metabolic alkalosis is present. If the increase in anion gap is less than the decrease in HCO3 , non–anion gap acidosis is present. 4. Check for the appropriate degree of respiratory compensation for the metabolic acidosis using the formula given on page 314. If the decrease in PCO2 is more than expected, a respiratory alkalosis is also present. If the decrease in PCO2 is less than expected, a concomitant respiratory acidosis exists. 5. If the pH indicates acidosis but the HCO 3 is not decreased and the PCO2 is elevated, a primary respiratory acidosis is present. Now check to see whether the metabolic compensation is appropriate. Apply the formula for metabolic compensation with acute or chronic respiratory acidosis. If the increase in HCO 3 is more than expected, a concurrent metabolic alkalosis is present. If the increase in HCO 3 is less than expected, a metabolic acidosis is present.
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6. If the pH indicates alkalosis, check the HCO 3 . If the HCO3 is elevated, there is a primary metabolic alkalosis. Check for the appropriate degree of respiratory compensation using the formula for expected PCO2 increase in primary metabolic alkalosis. If the PCO2 is lower than expected, a concurrent respiratory alkalosis is also present. If the PCO2 is higher than expected, a respiratory acidosis is also present. 7. If the HCO 3 level is normal and the PCO2 is decreased, primary respiratory alkalosis is present. Use the formula for expected change in HCO 3 to determine whether the compensation is appropriate.
Bibliography Nicolaou DD, Kelen GD: Acid–base disorders. In Tintinalli JE, Kelen GD, Stapczynski JS (eds): Emergency Medicine: A Comprehensive Study Guide, ed 6. McGraw-Hill: New York, 2004. Post TW, Rose BD: Approach to the adult with metabolic acidosis. In Rose BD (ed): UpToDate. Wellesley, MA, 2005. Rose BD: Simple and mixed acid–base disorders. In Rose BD (ed): UpToDate, Wellesley, MA, 2005. Rose BD, Post TW: Clinical Physiology of Acid–Base and Electrolyte Disorders, ed 5. McGraw-Hill: New York, 2001. Whittier FC, Rutecki GW: Fluids and Electrolytes: A Guide to Everyday Practice. The Little Yellow Book. Anadem: Columbus, OH, 2000.
Acute Ethanol Withdrawal ROBERT D. GRAYDON
ICD Code: Alcohol withdrawal 291.81
Key Points Hypoglycemia is common in the setting of ethanol use, especially in children, and may be a delayed effect. Chronic drinkers are often in a poorly fed, glycogen-depleted state and have multiple other nutritional deficiencies that can worsen this effect.
326 ESSENTIAL EMERGENCY MEDICINE FOR THE HEALTHCARE PRACTITIONER ! Emergency Actions ! All patients with withdrawal should receive intravenous thiamine (100 mg), folate (1 mg), and multivitamins in the first liter of normal saline. Hypoglycemia should be treated with an intravenous push consisting of 25 mg of dextrose, followed by frequent blood sugar determinations.
DEFINITION Ethanol is a small, weakly polar, aliphatic hydrocarbon molecule that is both water and lipid soluble. It is a CNS depressant and is a widely used social stimulant.
EPIDEMIOLOGY Surveys of the U.S. general population show that approximately 65% of adults use alcoholic beverages, and many will experience problems due to their drinking. The prevalence of alcohol abuse and dependence is estimated to be between 7% and 10%. The cost to society is more than $200 billion per year in treatment costs and alcohol-related economic losses. The prevalence of alcohol use disorders in medical settings is estimated to be between 15% and 40%.
PATHOPHYSIOLOGY AND PHARMACOLOGY Ethanol is rapidly absorbed in the GI tract, with approximately 20% of the dose absorbed in the stomach and the remainder in the small intestine. Absorption is delayed by coingestion of foods/drugs and medical conditions that delay gastric emptying. Ethanol has a volume of distribution of 0.56–0.72 L/kg. Ethanol distributes throughout body fluids and tissues, easily crossing the blood–brain barrier and placenta. The metabolism of ethanol begins in the GI cells. Alcohol dehydrogenase is formed in the gastric mucosa. This enzymatic activity is decreased if the person is female, has atrophic gastritis, or has taken drugs such as aspirin and H2 blockers. This process results in increased ethanol levels. Most metabolism occurs through two hepatic enzymes systems: 1. Alcohol dehydrogenase is generally the predominant system. The alcohol dehydrogenase system uses alcohol dehydrogenase to oxidize ethanol to acetaldehyde and then acetaldehyde dehydrogenase to oxidize acetaldehyde to acetate, which ultimately becomes acetyl coenzyme A and either enters the Krebs cycle or undergoes ketone body formation or fatty acid synthesis. Acetate is also converted to acetone. During this process, nicotinamide adenine dinucleotide
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(NAD) is reduced, changing the reduced alcohol dehydrogenase– NADþ ratio. Changes in this ratio impair cellular oxidative processes, such as conversion of lactate to pyruvate and gluconeogenesis. Because gluconeogenesis is critical to maintaining serum glucose homeostasis, profound metabolic abnormalities such as hypoglycemia, acidosis, and other electrolyte disturbances may occur. Dehydrogenase enzymes have variable activity in different persons depending on genetic makeup, gender, and other factors. 2. The microsomal ethanol oxidizing system (MEOS), a cytochrome P450-dependent system, is usually a minor metabolic pathway. This enzyme system is inducible and allows chronic drinkers to degrade ethanol at high rates. Induction of this system can be responsible for multiple drug interactions for other drugs normally metabolized by this system, including increased production of the toxic metabolites of acetaminophen. Ethanol approximates Michaelis-Menten kinetics. At high ethanol levels, saturation of the alcohol dehydrogenase and MEOS enzyme systems occur, and the elimination half-life prolongs as metabolism shifts from concentration-dependent first-order kinetics to time-dependent zero-order kinetics. Ethanol is metabolized at rates of 100–200 mg/kg/ hr or more. Chronic exposure and high levels cause induction of the MEOS system, which accounts for the significant increase in metabolism and clearance seen in chronic drinkers. Other factors that influence the rate of ethanol clearance include continued absorption, liver disease, drug inhibition of the MEOS system, and genetic variation. Approximately 10% is excreted unchanged through the lungs and kidneys. Ethanol is a CNS depressant but may have variable effects on individuals. Early in intoxication, a paradoxical stimulatory effect with euphoria, giddiness, and loss of inhibitions may predominate. As intoxication worsens (levels of approximately 150/dl in the casual drinker), CNS depression becomes generalized, leading to ataxia, slurred speech, and sedation. At serum levels greater than 200 mg/dl, progression to coma, loss of protective reflexes, and autonomic dysfunction occur. Death often occurs at levels of 400 mg/dl. Blood ethanol levels do not always correlate precisely with the degree of intoxication. Persons with a history of chronic ethanol abuse and dependence can exhibit little clinical evidence of intoxication, even with levels approaching 400 mg/dl. Ethanol intoxication is poorly understood and is probably multifactorial. Hypoglycemia is common in the setting of ethanol use, especially in children, and may be a delayed effect. Chronic drinkers are often in a poorly fed, glycogen-depleted state and have multiple other nutritional deficiencies that can worsen this effect. Ethanol-induced hypoglycemia should always be suspected in these patients. Profound hypomagnesemia is a subtle but common and life-threatening complication of chronic
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ethanol ingestion. Low Mg states occur due to poor dietary intake, decreased GI absorption, and ethanol-induced increase in urinary excretion. Because the majority of Mg is stored in bone, serum levels may not reveal the extent of the loss. Many chronic drinkers have profound intracellular Mg losses despite normal serum levels. Thiamine deficiency can produce Wernicke’s encephalopathy. In addition, chronic ethanol abuse affects most of the hypothalamic-pituitary axis, leading to decreased testosterone production in men and amenorrhea in women. Elevated glucocorticoid levels may be seen, and many drinkers have physical manifestations resembling Cushing’s syndrome. Neurological manifestations include seizures (both during intoxication and withdrawal states), auditory hallucinations, and peripheral neuropathy. Dilated cardiomyopathy, atrial fibrillation, and other non–Mg-deficiency arrhythmias may occur. High-output congestive failure may be seen with thiamine deficiency. Other disorders seen in chronic ethanol abusers include skeletal muscle myopathy, thrombocytopenia, and coagulopathies. Because ethanol is a multisystem toxin, chronic use is associated with a host of medical illnesses, leading to acute complications such as esophageal variceal hemorrhage, hemorrhagic gastritis, pancreatitis, Mallory-Weiss tears, and Boerhaave’s syndrome. Hepatic disease can range from mild steatosis to cirrhosis with hepatic encephalopathy. Chronic alcohol consumption affects central a-adrenergic receptors, central b-adrenergic receptors, the inhibitory neurotransmitter g-aminobutyric acid (GABA), and dopamine turnover. Alcohol withdrawal occurs when an ethanol-dependent person reduces or ceases ethanol use. The classic study by Isbell in 1955 showed the relationship between alcohol and the withdrawal syndrome. This study also demonstrated that the severity of withdrawal was dependent on both the dose and duration of ethanol consumption. Withdrawal is triggered by a reduction in blood alcohol level. It is characterized by autonomic hyperactivity. Alcohol withdrawal is multifactorial and incompletely understood.
CLINICAL PRESENTATION Alcohol withdrawal develops 6–24 hours after cessation or reduction of alcohol use and lasts from 2 to 7 days. The severity of alcohol withdrawal ranges from mild irritability and insomnia to fever, hallucinations, diaphoresis, and disorientation. Minor alcohol withdrawal begins as early as 6 hours and peaks at 24–36 hours after cessation or reduction in alcohol intake. Minor withdrawal is characterized by mild autonomic hyperactivity manifested by nausea, anorexia, coarse tremor, tachycardia, hypertension, hyperreflexia, anxiety, and sleep disturbances.
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Major alcohol withdrawal occurs after more than 24 hours and usually peaks at 50 hours, but occasionally takes up to 120 hours after cessation. Manifestations of major withdrawal include worsening anxiety, insomnia, irritability, tremor, anorexia, tachycardia, hyperreflexia, hypertension, fever, decreased seizure threshold, auditory and visual hallucinations, and finally delirium. Delirium tremens is manifested by gross tremor, profound confusion, fever, incontinence, visual hallucinations, and mydriasis. It is seldom seen before the third day of abstinence. One of the most common causes of adult-onset seizures is alcohol withdrawal, with seizures occurring 6–48 hours after cessation of ethanol intake.
EXAMINATION Patients can present in any stage of withdrawal, experiencing symptoms from mild tremors to full-blown delirium. Patient history is often unreliable, and more reliable data can sometimes be obtained from paramedics, police officers, and family members. Accurate recording of vital signs is mandatory, as is frequent monitoring of vital signs. Hypothermia, hyperthermia, tachypnea, tachycardia may be indicators of serious underlying diseases such as sepsis, drug ingestion, intracranial hemorrhage, hypoglycemia, or diabetes. A rapid but thorough physical examination should be performed with attention paid to the level of consciousness, signs of hepatic failure, coagulopathy, occult trauma, and the cardiovascular, respiratory, digestive, and neurological systems. Vital signs and level of consciousness evaluation should be repeated at frequent intervals.
LABORATORY FINDINGS The healthcare provider should perform a complete blood count (CBC), coagulation studies, serum chemistries, urinalysis, urine drug screen, liver function studies, and measurements of blood urea nitrogen (BUN), creatine, Mg, phosphorus, and blood alcohol level. A rapid bedside glucose determination should also be performed, as should fecal occult blood testing.
RADIOLOGY A chest x-ray is mandatory for patients with fever or tachypnea. Blood and urine cultures should be considered in all febrile patients. CT scans of the head and lumbar puncture should also be considered, especially in patients with new-onset seizures or an unclear history. In cases of moderate-to-severe withdrawal, an electrocardiograph (ECG) should be obtained.
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TREATMENT The patient should be completely undressed and placed on a monitor with frequent reassessment of vital signs. Intravenous access should be obtained. A full physical examination should be performed and key components repeated at frequent intervals. The previously noted laboratory and radiological studies should be performed, as guided by history and physical examination. All patients experiencing withdrawal should receive intravenous thiamine (100 mg), folate (1 mg), and multivitamins in the first liter of normal saline. Hypoglycemia should be treated with an intravenous push of dextrose (25 g), followed by frequent blood sugar determinations. Benzodiazepines are the mainstay of treatment for alcohol withdrawal. By interacting with the GABA receptors, benzodiazepines substitute for the GABA-potentiating effect of ethanol and reduce signs and symptoms of withdrawal; they also have excellent anticonvulsant properties. Lorazepam is the preferred drug due to its relatively short half-life, good intramuscular absorption, and the absence of active metabolites. All benzodiazepines involve the complications of excessive sedation, confusion, and hypotension at high doses. The dosage of benzodiazepines required to treat alcohol withdrawal is highly individual and variable. A starting dose of 1–4 mg of lorazepam should be given intravenously, and then repeated at 15- to 30-minute intervals for patients in severe withdrawal. The dosage should be titrated to control the patient’s agitation. Patients with severe delirium tremens may require massive doses of benzodiazepines. Restraints may be required to prevent self-injury or injury to staff. Alcohol-related seizures should be treated with benzodiazepines. Volume depletion should be corrected with normal saline. Underlying electrolyte and metabolic disorders should be corrected. A careful search for underlying medical conditions and other causes of delirium should be sought.
DISPOSITION Patients with signs of major withdrawal—extreme agitation, fever, confusion, or hallucinations—always require admission. Patients with mild withdrawal should be observed in the emergency department (ED) for 6–8 hours and treated appropriately. If, after a period of observation and treatment, an alert, oriented patient with normal vital signs, physical examination, and normal laboratory study results may be released with an oral tapering dose of lorazepam (initially 6 mg/day in divided doses, tapering 1–2 mg/day over 4–6 days). This should be reserved for patients who are motivated to stop drinking and are reliable, or who can be
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supervised by a responsible, sober adult. All patients experiencing ethanol withdrawal should be offered treatment and referral for alcohol dependence.
Bibliography Goldfrank L: Goldfrank’s Toxicologic Emergencies, ed 7. McGraw-Hill: New York, 2002. Goldman L, Ausiello D: Cecil’s Textbook of Medicine, ed 22. WB Saunders: Philadelphia, 2004. Harris C: Emergency Management of Selected Drugs of Abuse. American College of Emergency Physicians: Dallas, 2003. Howell J (ed): Emergency Medicine. WB Saunders: Philadelphia, 1998. Isbell H, Fraser HF, Wikler A, et al: An experimental study of the etiology of rum fits and delirium tremens, Q J Study Alcohol 1955;16:1–33. Marx J, Hockberger R, Walls R: Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 5. Mosby: St Louis, 2002. Tintinalli JE, Kelen GD, Stapczynski JS (eds): Emergency Medicine: A Comprehensive Study Guide, ed 5. McGraw-Hill: New York, 2000. Watson W, Litovitz TL, Rodgers GC Jr, et al: 2003 Annual Report of the American Association of Poison Control Centers Toxic Exposure Surveillance System, Am J Emerg Med 2004;22(5):335–404.
Adrenal Insufficiency BENJAMIN P. HARRISON
ICD Codes: Addison’s disease 255.4, Adrenal crisis 255.4, Adrenal insufficiency 255.4, Sheehan’s syndrome 253.2
Key Points Classically, chronic adrenal insufficiency is associated with Addison’s disease,which develops over months to years and has primary symptoms of weakness, fatigue, anorexia,weight loss, and hyperpigmentation. ! Emergency Actions ! A rapid withdrawal of exogenous steroid may precipitate adrenal crisis, or sudden stress may induce cortisol requirements in excess of the adrenal glands’ ability to respond immediately.
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DEFINITION Adrenal insufficiency is an acute or chronic decreased or absent level of circulating aldosterone and cortisol. Classically, chronic adrenal insufficiency is associated with Addison’s disease, which develops over months to years and features primary symptoms including weakness, fatigue, anorexia, weight loss, and hyperpigmentation. Persons with chronic adrenal insufficiency can develop adrenal crisis. However, by definition, an acute adrenal crisis involves subphysiological levels of adrenal hormones that result in patients presenting with vomiting, abdominal pain, and hypovolemic shock.
EPIDEMIOLOGY The epidemiology of adrenal insufficiency is as follows:
Approximately 6 million people in the United States are considered to have undiagnosed adrenal insufficiency, which is clinically significant only during times of physiological stress. Critically ill patients with septic shock demonstrate a de novo (i.e., a matter anew, as though it was being tried for the first time) incidence ranging from 19% to 54%. Secondary adrenal insufficiency has been demonstrated in 31% of patients admitted to a critical care unit.
PATHOPHYSIOLOGY The adrenal gland consists of two parts: the cortex and the medulla. The cortex produces three steroid hormones: glucocorticoids (cortisol), mineralocorticoids (11-deoxycorticosterone and aldosterone), and androgens. Their secretion occurs under the control of the hypothalamicpituitary axis through the release of corticotropin-releasing factor and subsequently the activation of adrenocorticotropic hormone (ACTH). In contrast to aldosterone, 11-deoxycorticosterone is a weak mineralocorticoid. The hormones of importance in acute adrenal crisis are cortisol and aldosterone. The medulla secretes catecholamines (e.g., epinephrine and norepinephrine). Their secretion is under neural control. Cortisol has the following basic effects in the body:
Stimulates gluconeogenesis (i.e., glucose production) and decreases cellular glucose use Mobilizes amino acids and fatty acids Inhibits the effects of insulin Gives rise to ketone bodies in metabolism (i.e., ketogenesis) Elevates RBC and platelet levels
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Exhibits anti-inflammatory effects Diminishes cell-mediated immunity (destroying intracellular bacteria, eliminating viral infections, and destroying tumor cells) Enhances the pressor effects of catecholamines on the heart muscles and arterioles Facilitates free water clearance, enhances appetite, and suppresses ACTH synthesis (i.e., feedback inhibition to the hypothalamicpituitary axis)
Aldosterone is released in response to angiotensin II stimulation, hyperkalemia, hyponatremia, and dopamine antagonists. Its effect is on the kidney (the target organ) to promote reabsorption of sodium and secretion of K and hydrogen. Its release is regulated via negative feedback by the renin-angiotensin system and serum K concentration. Increased K stimulates aldosterone production, and decreased K inhibits production. The net effect is to increase intravascular volume. Primary adrenocortical insufficiency is the failure of the adrenal glands to release adequate amounts of these hormones to meet physiological needs, despite release of ACTH from the pituitary gland. The most common causes are infiltrative or autoimmune disorders (80% in the United States), but adrenal exhaustion from severe chronic illness can also occur. Secondary adrenal insufficiency can be caused by hypopituitarism due to the following:
Hypothalamic-pituitary disease (e.g., Sheehan’s syndrome, pituitary apoplexy) Suppression of the hypothalamic-pituitary axis by exogenous steroids (overall, the most common etiology of adrenal insufficiency) or endogenous steroids (e.g., tumor)
A rapid withdrawal of exogenous steroid may precipitate adrenal crisis, or sudden stress may induce cortisol requirements in excess of the adrenal glands’ ability to respond immediately. Bilateral massive adrenal hemorrhage (BMAH) occurs under severe physiological stress (e.g., septic shock, complicated pregnancy, myocardial infarction) or with concomitant coagulopathy or thromboembolic disorders. Surgery, burns, trauma, convulsions, and adrenal vein thrombosis can all precipitate adrenal hemorrhage. In a child or infant, BMAH can be precipitated by septicemia usually as a result of Pneumococcus, Meningococcus, Staphylococcus, Haemophilus, and gram-negative organisms. This classically occurs in WaterhouseFriderichsen syndrome, which is an overwhelming septicemia resulting from meningococcemia.
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CLINICAL PRESENTATION The clinical presentation of adrenal insufficiency consists of the following:
Prior steroid use Severe physiological stress (e.g., sepsis, trauma, burns, surgery), organisms associated with adrenal crisis (e.g., Haemophilus influenzae, Staphylococcus aureus, Streptococcus pneumoniae, fungi), meningococcemia Azotemia (i.e., presence of BUN in the blood) Anticoagulants, hemorrhagic diathesis Neonate; complicated pregnancy Adrenocorticotropin therapy, known primary or secondary adrenocortical insufficiency Acquired immunodeficiency syndrome (AIDS); fatigue is most common presenting symptom Invasive or infiltrative disorders (e.g., sarcoidosis, amyloidosis, neoplastic) Tuberculosis In bilateral adrenal hemorrhage and infarction, signs and symptoms in descending order are as follows: hypotension/shock (>90%); abdominal, flank, back, or lower chest pain (86%); fever (66%); anorexia, nausea, or vomiting (47%); neuropsychiatric symptoms such as confusion or disorientation (42%); abdominal rigidity or rebound tenderness (22%).
EXAMINATION The examination of a patient with adrenal insufficiency will reveal the following:
Unexplained shock, usually refractory to fluid and pressor resuscitation Nausea, vomiting, and abdominal or flank pain Hyperthermia or hypothermia Calcification of auricular cartilage (chronic insufficiency) Hyperpigmentation (most conspicuous in the face, neck, and backs of hands)
ETIOLOGY Possible causes of adrenal insufficiency include the following:
Drug use or abuse Rapid withdrawal of long-term steroid therapy Ketoconazole Phenytoin Rifampin Anesthesia (e.g., etomidate)
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Anticoagulant therapy (between 3rd and 18th day) Mitotane (chemotherapeutic agent used in the treatment in Cushing’s syndrome) Metastatic breast or prostate cancer Sarcoidosis, amyloidosis, neoplastic disease In BMAH: surgery, burns, pregnancy, trauma, convulsions, adrenal vein thrombosis Head trauma
DIFFERENTIAL DIAGNOSIS The differential diagnosis of adrenal insufficiency includes the following:
Shock from any source Septic shock Acute abdomen Anorexia nervosa Hypopituitarism Hypothyroidism and myxedema coma
LABORATORY FINDINGS Common laboratory tests to be performed in a patient with adrenal insufficiency include the following:
Serum chemistry panel results are as follows: Abnormalities are present in as many as 56% of patients. Hyponatremia is common (though not diagnostic). Hypoglycemia (67% occurrence) Hyponatremia (88%) Hyperkalemia (64%) Hypercalcemia (6%–33%) Serum cortisol: Less than 20 mg/dl in severe stress is indicative of adrenal insufficiency. ACTH test (diagnostic) The practitioner should determine the baseline serum cortisol level, then administer ACTH (250 mg intravenous push), and then draw serum cortisol 30 and 60 minutes after ACTH administration. An increase of less than 7 mg/dl is considered diagnostic of adrenal insufficiency. CBC: Anemia (mild and nonspecific), lymphocytosis, and eosinophilia (highly suggestive) may be present. Serum thyroid function tests: These should assess for autoimmune, infiltrative, or multiple endocrine disorders. Cultures: Blood, urine, and other cultures should be performed, as clinically indicated. Infection is a common precipitant of acute adrenal crisis. ABG analysis: Acidemia and hypoxia (neither sensitive nor specific) may be present.
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RADIOGRAPHS A chest radiograph should assess for tuberculosis, histoplasmosis, malignant disease, sarcoid, and lymphoma. It may also show a narrow cardiac silhouette resulting from decreased vascular volume. An abdominal CT scan should visualize adrenal glands for hemorrhage, atrophy, infiltrative disorders, and metastatic disease. Adrenal hemorrhage appears as hyperdense, bilaterally enlarged adrenal glands.
OTHER TESTS Other tests to be undertaken include ECG. Prolongation of the QT interval can induce ventricular arrhythmias. Elevated peaked T waves may indicate hyperkalemia, and deep negative T waves have been described in acute adrenal crisis.
TREATMENT Treatment for chronic adrenal insufficiency should include the following:
Cortisol, 15–20 mg every morning and 10 mg in the evening Fludrocortisone (Florinef), 0.05–0.1 mg every morning Halotestin or depot-testosterone Patent education and administration of an identification card or bracelet Stress dose cortisol (to prevent adrenal crisis) The usual oral dose should be doubled for stressful illnesses or injuries. Hydrocortisone 100 mg should be given intravenously every 8 hours, for at least the first 24 hours after major surgery, trauma, or infection. Treatment for adrenal crisis should proceed as follows:
Administer supplemental oxygen. Engage in coma protocol (i.e., glucose, thiamine, naloxone); administer glucagon if the patient is hypoglycemic and intravenous access cannot be obtained. Administer glucocorticoids in supraphysiological or stress doses (the only definitive therapy). The drug of choice is dexamethasone or a soluble form of cortisol (such as 100 mg hydrocortisone sodium succinate). Dexamethasone sodium phosphate 4 mg should be given intravenously. Dexamethasone is preferred for two reasons: it is long acting (12–24 hours) and it does not interfere with serum cortisol assay.
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However, because dexamethasone has little mineralocorticoid activity, fluid and electrolyte replacement is necessary. A short ACTH stimulation test may be performed during resuscitation. Once completed, hydrocortisone (100 mg intravenous every 6 hours) is the preferred treatment to provide mineralocorticoid support. Delaying glucocorticoid replacement therapy while awaiting the results of the ACTH stimulation test is inappropriate and dangerous. Aggressively replace fluids (2–3 L) with 5% or 10% intravenous dextrose and saline solutions. Administer empirical antibiotics, if indicated; seek and resolve precipitating stressors to include infections. Correct electrolyte abnormalities, especially hyperkalemia. Perform reverse coagulopathy with fresh frozen plasma. Correct hyperthermia or hypothermia by initiating cooling/warming measures. Administer pressors (e.g., dopamine, norepinephrine) to combat hypotension if it is present and unresponsive to intravenous crystalloid boluses. Mineralocorticoid therapy is not needed in the ED for initial treatment.
Admission Criteria All patients with acute adrenal crisis should be admitted to the hospital. ICU admission should be considered for unstable or potentially unstable patients.
Consultations Care for patients with adrenal insufficiency should include consultations with the following specialists:
Endocrinologist Infectious disease specialist Critical care physician for ICU admission Cardiologist, if acute coronary syndrome is suspected Surgeon for BMAH or acute abdomen
Bibliography Aono J, Mamiya K, Ueda W: Abrupt onset of adrenal crisis during routine preoperative examination in a patient with unknown Addison’s disease, Anesthesiology 1999;90 (1):313–314. Chin R: Adrenal crisis, Crit Care Clin 1991;7(1):23–42. Iga K, Hori K, Gen H: Deep negative T waves associated with reversible left ventricular dysfunction in acute adrenal crisis, Heart Vessels 1992;7(2):107–111.
338 ESSENTIAL EMERGENCY MEDICINE FOR THE HEALTHCARE PRACTITIONER Klauer K: Adrenal insufficiency and adrenal crisis, eMedicine. Last updated April 18, 2005. http://www.emedicine.com/emerg/topic16.htm. Kirkland L Adrenal crisis, eMedicine. Updated May 8, 2003. Available at: http://www. emedicine.com/med/topic65.htm. Koo DJ, Jackman D, Chaudry IH: Adrenal insufficiency during the late stage of polymicrobial sepsis, Crit Care Med 2001;29(3):618–622. Obenour RA, Ross S: Hospital Formulary of the University of Tennessee Medical Center. Knoxville, Tennessee, 1999. Passmore JM: Adrenal cortex. In Geehoed GW, Chernow B (eds): Endocrine Aspects of Acute Illness. Churchill-Livingstone: New York, 1985, pp 97–134. Rao RH: Bilateral massive adrenal hemorrhage, Med Clin North Am 1995;79(1):107–129. Salyer SW: The Physician Assistant Emergency Medicine Handbook. WB Saunders: Philadelphia, 1997. Schroeder S, Wichers M, Klingmuller D: The hypothalamic-pituitary-adrenal axis of patients with severe sepsis: Altered response to corticotropin-releasing hormone, Crit Care Med 2001;29(2):310–361. Vella A, Nippoldt TB, Morris JC 3rd: Adrenal hemorrhage: A 25-year experience at the Mayo Clinic, Mayo Clin Proc 2001;76(2):161–168. Williams GH, Dluhy RG: Disease of the adrenal cortex. In Braunwald E, Fauci AS, Kasper DL (eds): Harrison’s Principles of Internal Medicine, ed 13. McGraw-Hill: New York, 1994, pp 1953–1976. Xarli VP, Steele AA, Davis PJ: Adrenal hemorrhage in the adult, Medicine (Baltimore) 1978;57(3):211–221. Zaloga GP, Zaloga G, MacGregor D (eds): The Critical Care Drug Handbook. Mosby– Year Book: St Louis, 1991.
Alcoholic Ketoacidosis RICHARD J. SPITZ
ICD Codes: Ketoacidosis 276.2, Alcoholic withdrawal 291.81, Alcoholism 303.9
Key Points For any alcoholic patient who presents with altered mental status, an acute intracerebral hemorrhage should be included in the differential diagnosis. ! Emergency Actions ! Any patient suspected to be experiencing alcohol withdrawal or alcoholic ketoacidosis (AKA) should have his or her withdrawal symptoms treated aggressively. Alcoholics are particularly disposed to intracerebral hemorrhage due to several physiological and anatomical factors present in alcoholism.
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DEFINITION Alcoholic ketoacidosis is defined as an anion gap acidosis associated with abrupt cessation or relative decrease in alcohol consumption.
EPIDEMIOLOGY AKA tends to occur in chronic alcoholics.
PATHOLOGY The pathology of AKA is multifactorial and complex. The patient’s chronic alcohol use and poor nutritional status deplete glycogen reserves and the ability of the liver to perform gluconeogenesis (Fig. 8-1). The patients are volume depleted as a result of poor oral intake and vomiting. As a stress response, catecholamines are released, which leads to the burning of fat and the release of free fatty acids. The increased generation of free fatty acids ultimately leads to increased ketone formation, predominately b-hydroxybutyrate, which the body in its volume-depleted and stressed state is unable to adequately clear. This is further worsened by the continued burning of fat and ketone body formation (Fig. 8-2).
CLINICAL PRESENTATION The typical presentation of AKA includes abrupt cessation of heavy alcohol consumption and decreased food intake with associated nausea, vomiting, and abdominal pain in a chronic heavy drinker. The patients appear to be ill—showing signs of dehydration, tachycardia, and tachypnea—and feel generalized abdominal pain. The patient may manifest other signs and symptoms of the precipitating illness that initially led them to stop drinking, such as acute GI tract Dietary intake 1 Decreased Glycogen
2 Consumed
Glucose 3 Blocked Pyruvate
Increased
Lactate
Figure 8-1. Ethanol causes hypoglycemia through (1) decreased intake of glucose, (2) depletion of glycogen, and (3) blockade of gluconeogenesis. (From Ford M, Delaney KA, Ling L, Erickson T: Clinical Toxicology. WB Saunders: Philadelphia, 2001.)
340 ESSENTIAL EMERGENCY MEDICINE FOR THE HEALTHCARE PRACTITIONER Decreased insulin Increased: Catecholamines Glucagon Glucocorticoids
Lipolysis
Decreased KB metabolism by peripheral tissues
Volume depletion
Free fatty acid release
Ethanol
Acetate
Vomiting and ethanol blockage of ADH secretion
Acetyl CoA
Serum ketones
Tricarboxylic acid cycle
Decreased food intake
Decreased ketone elimination
Figure 8-2. Factors causing ketonemia in alcoholic ketoacidosis. KB, Ketone body; ADH, antidiuretic hormone; CoA, coenzyme. The tricarboxylic acid cycle is significantly slowed owing to intermediates being used for gluconeogenesis. (From Kleinschmidt KC, Delaney KA: Ethanol. In Haddad LM, Shannon MW, Winchester JF [eds]: Clinical Management of Poisoning and Drug Overdose, ed 3. WB Saunders: Philadelphia, 1998.)
bleeding, pancreatitis, hepatic encephalopathy, acute myocardial infarction, or infection.
EXAMINATION The examination of a patient who is suspected to be experiencing AKA should begin with the ABCs (i.e., airway, breathing, and circulation). Stabilization should occur contemporaneously during the initial assessment of the ABCs, with the practitioner keeping in mind that the patient may have a grave medical condition that led to his or her decrease or cessation of alcohol consumption.
Airway and Breathing Airway and breathing may be affected by factors that lead to a decreased mentation: hepatic encephalopathy and infections such as meningitis or encephalitis. Likewise, the patient’s ability to ventilate effectively may be encumbered by physical barriers to efficient respiration, such as lung infections or large pleural effusions.
Circulation Patients are usually volume depleted due to vomiting and poor Intake. They may be intravascularly depleted secondarily to the third spacing
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of fluid seen in patients with liver disease who, with their poor nutrition status, are unable to synthesize serum proteins and have a resulting low intravascular oncotic pressure. This is further worsened by concomitant portal hypertension. A patient with AKA can present in a state of shock and may be unable to provide sufficient tissue perfusion. These patients are at high risk for blood loss from GI tract bleeding (which can lead to hypovolemic shock), a myocardial infarction (which can progress to cardiogenic shock), or septic shock from an overwhelming infection.
Disability A patient with AKA may be obtunded secondarily to infections, head injury, metabolic derangement such as hypoglycemia, or hepatic encephalopathy. Patients with alcoholism are prone to falling down and may sustain an intracerebral hemorrhage. These patients are particularly disposed to intracerebral hemorrhage for several physiological and anatomical factors, as well. Patients with alcoholism may have insufficient clotting factors, ineffective or low platelet counts, and brain atrophy, which creates a greater potential space for bleeding and allows for a greater sheering affect of vessels in the subdural space. Therefore, a high index of suspicion for head trauma and a low threshold to perform C-spine protection should be used during the primary survey.
Exposure The patient should have all clothes removed to facilitate a full examination, otherwise signs of things such as underlying coagulopathy or concomitant trauma may be missed.
Secondary Survey A thorough head-to-toe examination should be performed.
LABORATORY FINDINGS A full panel of laboratory tests should be performed, including CBC, electrolyte panel, BUN and glucose measurements, liver profile, alcohol level test, lipase analysis, serum osmolarity test, urinalysis, blood gas analysis, and an ECG. On a case-by-case basis, blood cultures and an ammonia level test should be performed. Patients will have anion gap metabolic acidosis. The anion gap is usually in the 30- to 35-mEq/L range. Patients may have only small serum
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ketones because the sodium nitroprusside laboratory test used to detect ketones also tests for acetoacetate. A higher percentage of the ketones of a patient with AKA are in the form of b-hydroxybutyrate, not acetoacetate (6:10), compared with a patient with DKA (3:1). Anytime that a patient with AKA has an osmolar gap, the healthcare provider should consider the possibility of a toxic ingestant (e.g., methanol, ethylene glycol, isopropyl alcohol); these have a higher prevalence in this population. Serum osmolality is calculated as follows: ð½Naþ 2Þ þ ð½glucose 18Þ þ ð½BUN 2:8Þ þ ð½ethanol 4:6Þ
DIAGNOSIS Soffer and Hamburger’s criteria for the diagnosis of AKA include a serum glucose level less than 300, a recent history of alcohol intake or a relative or absolute decline in alcohol consumption in the past 24–72 hours before the visit, vomiting, and an otherwise unexplained metabolic acidosis.
TREATMENT The treatment strategy for a patient with AKA is rehydration with intravenous fluids, correction of electrolyte abnormalities (most commonly, low Mg, K, and phosphate), repletion of vitamins (i.e., multivitamins, thiamine, and folate), intravenous glucose administration, and admission to the hospital. Underlying precipitating illnesses should be evaluated and appropriately treated. There is no place for the administration of insulin or sodium bicarbonate in the treatment of AKA, unless the Ph is severely low. An elevated glucose level warrants consideration and treatment as DKA. The practitioner should remain vigilant for the development of alcohol withdrawal and delirium tremens. The patient’s condition typically normalizes within 12–24 hours.
Bibliography Brenner BM: Brenner & Rector’s The Kidney, ed 7. Elsevier: Philadelphia, 2004. Ford M, Delaney KA, Ling L, Erickson T: Clinical Toxicology. WB Saunders: Philadelphia, 2001. Goldman L, Ausiello D: Cecil Textbook of Medicine, ed 22. WB Saunders: Philadelphia, 2004. Halperin ML, Hammeke M, Josse RG, Jungas RL: Metabolic acidosis in the alcoholic: A pathophysiologic approach, Metabolism 1983;32:308. Hojer J: Severe metabolic acidosis in the alcoholic: Differential diagnosis and management, Hum Exp Toxicol 1996;15:482. Larsen PR, Kronenberg HM, Melmed S, Polonsky KS: Williams Textbook of Endocrinology, ed 10. Elsevier: Philadelphia, 2003.
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Levy LJ, Duga J, Girgis M, Gordon EE: Ketoacidosis associated with alcoholism in nondiabetic subjects, Ann Intern Med 1973;78:213. Machiels JP, Dive A, Donckier J, Installe E: Reversible myocardial dysfunction in a patient with alcoholic ketoacidosis: A role for hypophosphatemia, Am J Emerg Med 1998;16(4):371–373. Marx J, Hockberger R, Walls R: Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 5. St Louis: Mosby, 2002. Mason RJ, Broaddus VC, Murray JF, Nadel JA: Murray & Nadel’s Textbook of Respiratory Medicine, ed 4. WB Saunders: Philadelphia, 2005. Narins RG, Jones ER, Stom MC, et al: Diagnostic strategies in disorders of fluid, electrolyte and acid–base homeostasis, Am J Med 1982;72:496. Reichard GA Jr, Owen OE, Haff AC, et al: Ketone-body production and oxidation in fasting obese humans, J Clin Invest 1974;53:508. Rose BD, Post TW: Clinical Physiology of Acid–Base and Electrolyte Disorders, ed 5. McGraw-Hill: New York, 2001, pp 801–803. Schelling JR, Howard RL, Winter SD, Linas SL: Increased osmolal gap in alcoholic ketoacidosis and lactic acidosis, Ann Intern Med 1990;113:580. Wrenn KD, Slovis CM, Minion GE, Rutkowski R: The syndrome of alcoholic ketoacidosis, Am J Med 1991;91:119.
Diabetic Ketoacidosis JONATHON ALLEN
ICD Code: Diabetic ketoacidosis 250.1
Key Points Approximately 25% of episodes of DKA occur in patients with undiagnosed diabetes. ! Emergency Actions ! Aggressive intravenous fluid rehydration is the mainstay of treatment.
DEFINITION Diabetic ketoacidosis is a disease state in which insulin deficiency and glucagon excess combine to cause hyperglycemia, dehydration, ketoacidosis, and significant electrolyte imbalance.
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EPIDEMIOLOGY DKA most often occurs in persons with type 1 diabetes and is associated with inadequate insulin administration, infection and/or sepsis, or myocardial infarction. DKA can also occur in persons with type 2 diabetes and can be induced by any type of physical or emotional stress. Approximately 25% of episodes of DKA occur in patients with undiagnosed diabetes.
PATHOPHYSIOLOGY DKA is a result of a constellation of effects directly related to insulin deficiency and glucagon excess. The inadequate insulin level decreases glucose uptake by the cells, producing hyperglycemia. This hyperglycemia is further potentiated by increased levels of free fatty acids and amino acids in plasma, which stimulate gluconeogenesis. As plasma glucose levels continue to rise, the renal threshold for glucose reuptake is met, resulting in glycosuria. This produces a resulting osmotic diuresis and ion loss. Coupled with poor oral intake and frequent vomiting, the net result is a profound dehydration and electrolyte imbalance. DKA slows the uptake of lipids from circulation by adipose cells. The insulin deficiency results in the activation of an inducible lipase. The resulting lipolysis increases the levels of free fatty acids. These long-chain free fatty acids are partially oxidized and converted in the liver to acetoacetate and b-hydroxybutyrate. However, as cells are unable to extract glucose from the plasma, they begin to act as though the body is in a state of starvation. Amino acid uptake is decreased, as is the use of ketones as fuel by peripheral tissue. This decreased ketone use, combined with increased production, leads to ketoacidosis. The normal cellular response to starvation is to release the counterregulatory (with regard to insulin use) hormones epinephrine, glucagons, cortisol, and somatostatin. The degree of ketosis is directly related to the magnitude of release of these hormones. They are all catabolic, directly increasing rates of gluconeogenesis and glycogenolysis. Glucagon is frequently elevated four- to five-fold in DKA and is the most influential ketogenic hormone. Other hormones have been shown to indirectly affect ketogenesis through stimulation of lipolysis. As shown, all derangements of DKA are interrelated and are further induced by one another.
CLINICAL PRESENTATION Most patients in DKA will present with a recent history of polydipsia, polyuria, polyphagia, general body weakness, and nausea/vomiting. Up to one half of patients may report abdominal pain. In children, this pain typically decreases as the metabolic derangements are corrected.
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In adults, however, the presence of abdominal pain often signifies true abdominal pathology.
EXAMINATION Vital signs are of the utmost importance in assessing DKA. Peripheral vasodilation and vascular collapse can rapidly develop as the acidosis worsens. Patients can initially present with normal or altered mental status. Their neurological status should be monitored closely because this can deteriorate quickly. Typical other physical examination findings include tachypnea with Kussmaul’s respiratory pattern of deep and rapid breathing, tachycardia, frank hypotension or orthostatic hypotension, and the odor of acetone on the breath. An elevated temperature is rarely associated with DKA but should prompt a close look for a source of infection.
LABORATORY FINDINGS Initial laboratory studies should be directed at confirming the diagnosis of DKA and initiating emergent therapies. These should include a capillary blood glucose level, dipstick urinalysis including urinary ketones, electrolyte measurements, and arterial or venous blood gas (ABG/VBG) analysis. Recent studies have indicated that venous pH is not significantly different from arterial pH in patients with DKA and is much easier to obtain than repeated arterial samples. If an immediate K level is not available, a 12-lead ECG should be obtained to rule out significant hyperkalemia or myocardial infarction. Despite initially normal or high K levels, the total body K deficit may be several hundred milliequivalents. Acidosis and dehydration artificially increase the level due to acid-induced shifts and hypovolemic concentration. True serum K can be approximated by subtracting 0.6 mEq/L from the laboratory value for each 0.1-unit decrease in pH. The reported sodium level can also be misleading in DKA. Hyperglycemia can artificially decrease the reported value. True serum sodium levels can be approximated by adding 1.5 mEq/L to the reported level for each 100 mg/dl above the normal glucose level. Anion gap metabolic acidosis is primarily due to the increased plasma levels of ketones, although lactate, free fatty acids, and volume depletion could contribute to the gap as well. Subsequent tests should be aimed at determining the degree of dehydration, acidosis, and electrolyte imbalance and finding the precipitating factor of DKA. These include CBC with differential, complete urinalysis, chest x-ray, serum osmolarity, and measurements of BUN, creatinine, phosphorus, Caþ, Mg, lactate, and serum lipase levels. Leukocytosis may be present on CBC, but it may more closely indicate ketosis than presence of infection. Only bandemia can reliably demonstrate infection in a patient with DKA. Elevated urine-specific gravity,
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BUN, and hematocrit suggest volume contraction. Microscopic urinalysis and a chest x-ray can help eliminate urinary tract infection and pneumonia as precipitating sources. Serum lipase indicates the presence or absence of pancreatitis.
TREATMENT The care for a critically ill patient with DKA is identical as that for any other patient. The airway must be assessed and protected as the patient’s mental status dictates, especially if the patient is vomiting. Every patient should be placed on a cardiac monitor, and two large-bore intravenous lines should be established. Aggressive intravenous fluid rehydration is the mainstay of treatment. Although hypovolemic shock is the most common, other types of shock, including septic, should be ruled out. In patients with a history of cardiac or renal failure who may not tolerate such aggressive fluid therapy, a central venous pressure line can help to assess their intravascular volume. The severely dehydrated patient with DKA often has a fluid deficit of between 3 and 5 L with a sodium deficit of 450–500 mEq. With hypovolemic shock, 0.9% (normal) saline should be given as rapidly as possible in adults and in 20-ml/kg boluses in children until systolic blood pressure improves. Electrolyte levels should be periodically rechecked. As the serum sodium level approaches 155, adults should begin receiving hypotonic fluids, such as 0.45% (half-normal) saline. In the absence of shock, adults should generally receive 2 L of normal saline over the first 2 hours, followed by a slower continuous infusion. Children should receive constant normal saline infusion adjusted to achieve urine output of approximately 1–2 ml/kg/hr. Normal saline is preferred in children because hypotonic fluids may too rapidly decrease the serum hyperosmolarity of DKA, potentially precipitating cerebral edema. Fluid resuscitation alone may help to lower elevated blood sugar levels by as much as 18%. Acidosis also improves after rehydration, as increased tissue perfusion lowers lactate production and renal perfusion enhances hydrogen ion loss. DKA cannot be reversed without exogenous administration of insulin. Current recommendations suggest a 10-unit bolus of regular insulin followed by a continuous infusion of regular insulin at 0.1 U/kg/hr. This rate can be titrated as capillary blood glucose levels require. Because the half-life of regular insulin is 3–10 minutes, a continuous infusion produces more predictable results than repeated boluses. Should intravenous access be difficult or unobtainable, an intramuscular dose of 10–20 U/hr of regular insulin may also be given. Once blood glucose reaches 250– 300 mg/dl, the administration of dextrose-containing fluids should be started to avoid iatrogenic hypoglycemia and cerebral edema. As glucose levels continue to drop and ketones clear, the administration of
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subcutaneous insulin may be started. There should be an overlap between starting subcutaneous insulin and discontinuing the intravenous infusion. Potassium replacement is always necessary in DKA. Although initial levels are often normal or elevated, levels often sharply drop with correction of acidosis and dehydration and with administration of insulin. Initially, low levels indicate a potentially life-threatening hypokalemia, leading to respiratory paralysis, cardiac arrhythmias, or paralytic ileus. Potassium should be administered with fluids while the level is in the upper half of the normal range. Renal function should be monitored and the dosing adjusted accordingly. Patients experiencing DKA can require 100–200 mEq of K in the first 12–24 hours of treatment. Administration of K should be guided by serial chemistries drawn every 2 hours until the patient is out of DKA. Phosphate replacement is controversial in DKA. Phosphate levels can drop nearly four-fold in the first 12 hours of therapy. This may result in decreased production of 2,3-diphosphoglycerate (2,3-DPG), leading to poor oxygen transfer to erythrocytes (i.e., RBCs). Hypophosphatemia can also cause decreased myocardial and respiratory muscle performance, hemolysis, platelet dysfunction, and altered mental status. Despite its theoretical benefits, studies have shown no significant clinical benefit from the administration of phosphate in DKA. Bicarbonate therapy is indicated only for critically ill patients with a serum pH less than 7.0. In patients with less acidic pH, HCO 3 can antagonize other therapeutic measures. Alkalinizing serum results in decreased release of oxygen from already 2,3-DPG–depleted RBCs. Bicarbonate also increases the K requirement by driving K back into the intracellular space. The overaggressive use of HCO 3 may actually cause alkalosis, inducing cardiac dysrhythmias through the redistribution of various electrolytes. When HCO 3 therapy is clinically indicated, pH should not be corrected above 7.1.
DISPOSITION Nearly all patients experiencing DKA will require admission to the hospital. Most patients will be best suited for care in an ICU. Some patients with mild DKA, a pH greater than 7.35, and HCO 3 greater than 20 who show resolution of symptoms within 3–4 hours may be discharged home provided (1) the patient or caregiver is reliable, (2) the precipitating cause of DKA does not warrant admission, and (3) close follow-up is available.
Bibliography Brandenburg MA, Dire DJ: Comparison of arterial and venous blood gas values in the initial emergency department evaluation of patients with diabetic ketoacidosis, Ann Emerg Med 1998;31(4):459–465.
348 ESSENTIAL EMERGENCY MEDICINE FOR THE HEALTHCARE PRACTITIONER Chansky ME, Lubkin CL: Diabetic ketoacidosis. In Tintinalli JE, Kelen GD, Stapczynski JS (eds): Emergency Medicine: A Comprehensive Study Guide, ed 6. McGraw-Hill: New York, 2004. Ipp E, Westhoff TL: Diabetes mellitus and the critically ill patient. In Bongard F, Sue D (eds): Current Critical Care Diagnosis and Treatment, ed 2. McGraw-Hill: Montreal, 2002.
Disseminated Intravascular Coagulation MICHAEL K. SHAFE
ICD Code: 286.6
Key Points For a patient to survive disseminated intravascular coagulation (DIC) the underlying cause of DIC must be corrected. Otherwise, DIC will progress, causing death. ! Emergency Actions ! Initial therapy should address the underlying cause of the DIC. Good ventilator support is imperative.
DEFINITION Disseminated intravascular coagulation is a systemic deregulation of the coagulation and fibrinolytic systems that eventually depletes clotting factors and results in uncontrolled hemorrhage. DIC is usually triggered by disease states (e.g., trauma, septic shock or malignancies) that release large amounts of tissue factor (factor III) sufficient to consume the clotting and fibrinolytic intravascular protein stores.
PATHOLOGY Understanding DIC requires a basic understanding of coagulation and fibrinolytic systems. When tissue injury occurs, platelets attach to the exposed injured endothelium, forming a primary hemostatic plug. The platelets and injured endothelial cells release tissue factor, which stimulates the clotting cascades to deposit thrombin over the platelets catalyzing fibrin to cross-link into insoluble clot, forming a secondary hemostatic plug. The fibrinolytic system normally keeps the clotting
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system under control. Plasminogen is part of the fibrinolytic system that lyses the preformed clot, releasing fibrin fragments (D and E dimers) into the bloodstream. DIC occurs under a number of clinical circumstances where there is either a large amount of endothelial injury, a large release of tissue factor into the bloodstream, or both. When the clotting system is overstimulated by either of these events, microclots and microemboli begin to form and lodge in organ capillary beds, forming fibrin plugs and mesh-like screens. RBC membranes are damaged as they pass through these screens and become fragmented RBCs, or schistocytes, seen on peripheral blood smears. Eventually, blood will not be able to pass through the organ capillary beds, creating an ischemic environment and organ dysfunction. Eventually, the platelet, coagulation, and fibrinolytic systems are depleted, resulting in diffuse hemorrhaging into the organs and skin.
CLINICAL PRESENTATION Patients with DIC are invariably toxically ill and present with new petechiae or purpura, which may progress into ecchymosis. Patients may also begin to bleed from wounds that were once hemostatic. It is not uncommon for new hemorrhaging to occur around intravenous lines and in mucous membranes. The proximate cause of the DIC is usually clinically evident at the time of presentation. These include trauma (especially traumatic brain injury), massive hemorrhage, sepsis and septic shock, placental abruption, amniotic fluid embolism, and malignancies.
EXAMINATION A detailed skin examination looking for petechiae, purpura, or ecchymosis should be performed on any patient who is toxically ill, unstable, or has an unusual bleeding presentation. Retinal examination may demonstrate evidence of hemorrhage before formation of skin petechiae. Intravenous lines and oral mucosa should be examined for evidence of hemorrhage. Most importantly, serial examinations should be performed on patients at risk for DIC.
DIAGNOSIS The diagnosis is suspected on the basis of physical exam findings and a history of illness involving a high risk to develop DIC. The diagnosis is suspected clinically and confirmed by laboratory testing. The following laboratory tests should be performed for any patient in whom DIC is suspected: CBC, electrolyte measurements including Caþ and BUN/ creatine, prothrombin time (PT), partial thromboplastin time (PTT),
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international normalized ratio, measurements of fibrinogen level and fibrin split products, and D-dimer test. Request a manual differential on the CBC, and ask the laboratory personnel to specifically look for schistocytes and fragmented RBCs. Fluid cultures, radiographic studies, and chemistry testing should be directed by the patient’s clinical presentation.
LABORATORY FINDINGS The laboratory findings for DIC occur progressively. Initially the platelet count will decrease, followed by the fibrinogen level. The PT will rise before the PTT. The formation of thrombus will initiate the fibrinolytic system and release fibrin split products (e.g., D and E dimers). A rising or elevated D-dimer level in the face of low platelet counts, along with low or decreasing fibrinogen levels in a toxically ill patient with petechiae or purpura, confirms the diagnosis of DIC. As DIC progresses, there will be evidence of organ damage due to microemboli and tissue infarction. Note that the fibrinogen level in pregnant patients is 1.5–2 times that of nonpregnant patients. So, a “normal” fibrinogen level in a pregnant patient should be concerning in the clinical setting of possible DIC.
TREATMENT Initial therapy should focus on the underlying cause of the DIC. If the problem is placental abruption, an emergency cesarean section should be performed. If the patient is a septic, antibiotics and pressor agents should be administered and ventilation and oxygenation should be maximized. If DIC is present, platelets and clotting factors should be replaced simultaneously with multiple lines. Fresh frozen plasma contains all of the clotting proteins needed. Cryoprecipitate has high concentrations of fibrinogen and should be considered if the fibrinogen level is low. If anemia or active hemorrhaging is present, the administration of packed red cells should be initiated as well.
Bibliography Hoffman R, Benz EJ, Shattil SJ, et al: Hematology: Basic Principles and Practice, ed 4. Elsevier: New York, 200, pp 2169–2182. Marx J, Hockberger R, Walls R: Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 5. Mosby: St Louis, 2002, pp 1697–1698.
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Fluid and Electrolyte Emergencies BARBARA M. FISHMAN AND C. GORDON KING
ICD Codes: Hyponatremia 276.1, Hypernatremia 276.0, Hypokalemia 276.8, Hyperkalemia 276.7, Hypercalciuria 275.42, Hypocalciuria 275.41, Hypomagnesemia 275.2, Hypophosphatemia 275.3, Hypochloremia 276.9, Hyperchloremia 276.9
Key Points In general, fluid and electrolyte emergencies are diagnosed on the basis of laboratory test results. The history, physical examination, and radiographic studies, although useful, are not a substitute for accurate laboratory results. History, physical examination, and further laboratory tests will be useful in determining the cause and appropriate treatment. ! Emergency Actions ! Electrolyte disorders are usually not mutually exclusive. If one electrolyte is out of normal range, a reciprocal abnormal electrolyte is usually also out of range. The practitioner should always look for other electrolyte disorders if one is out of range. Often, one electrolyte cannot be corrected without addressing other electrolyte levels. In general, all electrolyte levels should not be corrected rapidly but, instead, over hours.
SODIUM Sodium is the main extracellular cation (positively charged ion). Ninetyeight percent of total body Naþ is in the ECF. The normal serum sodium level is between 135 and 145 mmol/L.
Key Points Hyponatremia is a serum Naþ level less than 135 mmol/L. Patients with hyponatremia may be hypovolemic, hypervolemic, or euvolemic, corresponding to varying degrees of total body Naþ. The treatment of hyponatremia depends on the time course, severity, and underlying cause of the disorder. Emergency treatment is warranted only for those
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with acute (duration 115 mmol/L), symptomatic hyponatremia. The change in serum sodium can be calculated and the sodium “deficit” can be replaced slowly. In a patient with symptomatic chronic hyponatremia, the serum sodium level should not be corrected to greater than 125 mmol/L. Severe neurological complications can occur if the serum sodium level is corrected too rapidly.
Hyponatremia The definitions of hyponatremia are as follows:
Hyponatremia: serum Naþ less than 135 mmol/L Severe hyponatremia: less than 115 mmol/L Acute hyponatremia: less than 36–48 hours’ duration
EPIDEMIOLOGY Hyponatremia can be classified into the following categories: 1. Pseudohyponatremia is associated with normal or elevated plasma tonicity, caused by hyperglycemia, mannitol, glycerol, radiographic contrast media, or any hyperoncotic substance that is confined to the ECF. The resultant movement of water from the intracellular to the intravascular compartment dilutes the serum Naþ. Marked hyperlipidemia was a cause of pseudohyponatremia with older flame photometers but is not a problem with newer analyzers that use ion-selective electrodes. 2. Hypovolemic hyponatremia is associated with low total body Naþ, low total body volume, low intravascular volume, and decreased ability of the kidney to excrete the excess water because of decreased volume status. Causes include protracted vomiting, bulimia nervosa, diarrhea, laxative abuse, blood loss, loop diuretic treatment, osmotic diuresis from hyperglycemia, excessive sweating, renal disease with defective concentrating ability, and fluid sequestration in a “third space” (e.g., severe pancreatitis). These patients get thirsty, drink water, cannot excrete the water load, retain the water, and become hyponatremic. 3. Hypervolemic hyponatremia is associated with high total body Naþ, high total body volume, high intravascular volume, and decreased ability of the kidney to excrete the excess water because of any of a variety of factors. These include decreased filtration capacity of the kidneys and therefore decreased capacity to excrete a water load; decreased cardiac output relative to body needs; inappropriate peripheral vasodilation, including a secondary excess of antidiuretic hormone (ADH); or a combination of these factors. Causes include CHF, cirrhosis, and nephrotic syndrome.
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4. Euvolemic hyponatremia is associated with essentially normal volumes of sodium in the ECF. Causes include syndrome of inappropriate antidiuretic hormone (SIADH), thiazide diuretic therapy, psychogenic polydipsia, pure glucocorticoid deficiency, thyroid hormone deficiency, “tea and toast diet,” and “beer drinkers’ potomania.” SIADH can be caused by cancers, especially oat cell carcinoma of the lung; CNS disorders, including mass lesions, hemorrhage, stroke, and trauma; pulmonary disorders, including pneumonias, respiratory failure, and positive-pressure ventilation; pain; nausea; the postoperative state; infection with the human immunodeficiency virus; and various drugs, including oxytocin, nicotine, selective serotonin reuptake inhibitors, nonsteroidal anti-inflammatory drugs (NSAIDs), opiates, phenothiazines, carbamazepine, cyclophosphamide, vincristine, and 3,4-methylenedioxymethamphetamine (MDMA). “Tea and toast diet” and “beer drinkers’ potomania” hyponatremia occur when patients do not eat food and drink dilute fluid in large amounts, and this overwhelms the kidneys’ ability to excrete a water load. Persons with healthy kidneys can decrease their urine osmolality to perhaps 50 mOsm/kg, but not to zero. The body’s ability to excrete a water load is therefore related to solute excretion. PRESENTATION Symptoms are dependent more on the rate of decrease than on the absolute serum sodium concentration, though levels less than 115 mmol/L are more likely to be associated with CNS symptoms. Not infrequently, patients with chronic hyponatremia can be asymptomatic with a serum sodium level as low as 105–110 mmol/L (!). Symptoms of hyponatremia include anorexia, nausea, vomiting, weakness, muscle cramps, headache, and difficulty concentrating. Severe symptoms include confusion, hallucinations, urinary and fecal incontinence, respiratory insufficiency, coma, seizures, and respiratory arrest. EXAMINATION Findings on examination will vary depending on the underlying condition. Most importantly, the patient’s volume status should be evaluated using standard criteria and classified as low, normal, or high volume based on the results of the bedside examination. A patient with hyponatremia can be hypovolemic, hypervolemic, or euvolemic. LABORATORY STUDIES In addition to routine ED studies, plasma osmolality, spot urine osmolality, spot urine Naþ, and spot urine creatinine tests should be performed. Urine sodium and osmolality tests will help classify the hyponatremia as renal or extrarenal losses. Other studies should be considered as well,
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including serum cortisol and thyroid-stimulating hormone (TSH) measurements, chest radiography, and CT/magnetic resonance scanning (to look for cancer associated with SIADH). Laboratory samples should be collected before treatment is begun. DIAGNOSIS The serum sodium level does not yield information about the patient’s volume status or about the etiology of the hyponatremia (Table 8-1). The history, examination, and screening laboratory studies mentioned previously will be sufficient to classify more than 90% of the patients and therefore guide therapy. In true hyponatremia, the osmolality is decreased (100 mOsm/kg), and normal cardiac, renal, adrenal, hepatic, and thyroid function. Of note, patients with SIADH can generally conserve and excrete sodium normally, and the spot urine Naþ or fractional excretion of Naþ (FENa) should not be part of the diagnostic criteria for SIADH. A low spot urine Naþ level may be helpful to confirm a hypovolemic state, but patients with volume overload (e.g., CHF) also commonly have a low spot Table 8-1 Hyponatremia Etiologies Factitious hyponatremia—normal or elevated serum osmolality Redistributive hyponatremia—elevated serum osmolality hyperglycemia, mannitol, glycerol infusions (for each 100-mg/dl increase in glucose, sodium falls 1.6 mEq/L) Hyponatremia with low serum osmolality Hypovolemic hyponatremia—loss of both sodium and water, more replacement of free water, low total body Naþ level Renal Losses Diuretics, salt-wasting nephropathy, osmotic diuresis, aldosterone deficiency Extrarenal Losses Gastrointestinal (e.g., diarrhea, vomiting) Sweating, cystic fibrosis Third-space losses (e.g., pancreatitis, peritonitis) Euvolemic hyponatremia—normal to slightly increased ECF, no edema, normal total body Naþ level SIADH Glucocorticoid deficiency Pain Drugs Chronic renal failure Primary polydipsia Hypervolemic hyponatremia—increase in ECF and total body sodium, water retention in excess of sodium retention Cirrhosis, CHF, nephrotic syndrome, acute or chronic renal failure SIADH, Syndrome of inappropriate antidiuretic hormone; CHF, congestive heart failure.
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urine Na and generally this test is not helpful in the confirm of a diagnosis. Patients with SIADH commonly have a low serum uric acid level. TREATMENT The treatment of hyponatremia depends on the time course, severity, and underlying cause of the disorder. Hypovolemia Hypovolemic patients with impaired peripheral perfusion (e.g., hypotension, metabolic acidosis, decreased renal function) can be treated with normal saline to restore adequate volume status, then given free water restriction. Hypervolemia Patients with hypervolemic hyponatremia are treated with free water restriction and treatment of the underlying cause (e.g., CHF). Diuretics or dialysis may also be required. Euvolemia Euvolemic hyponatremia is treated with free water restriction and correction of the underlying cause. Emergency treatment is warranted only for those with acute, severe, symptomatic hyponatremia. These patients are at risk of cerebral edema with resultant neurological damage. The most severe consequences of acute hyponatremia are seen in children and in premenopausal women. These patients should be corrected “rapidly,” but the change in serum sodium should not exceed 25 mmol/ L in the first 24 hours. The change in serum sodium can be calculated and the sodium “deficit” can be replaced slowly with 3%–5% saline with furosemide. Furosemide is given to prevent volume overload and to help increase free water loss by the kidney. Consultation with a renal specialist should be obtained if hypertonic saline is considered. In hypovolemic hyponatremia, Estimation of the Naþ deficit in mEq=L ¼ TBWðdesired Naþ current Naþ Þ
where TBW is total body water. Use the following formula to help estimate the initial change in serum Naþ per each liter of Naþ- or Kþ-containing fluids infused: Change in serum sodium ¼
ðinfusate Naþ þ infusate Kþ Þ serum Naþ ðTBW þ 1Þ
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Naþ and Kþ contents of some intravenous solutions are as follows:
Normal saline (0.9% NaCl) ¼ 154 mmol/L of Naþ ½ normal saline ¼ 77 mmol/L of Naþ Ringer’s lactated solution ¼ 130 mmol Naþ/L and 4 mmol Kþ/L 3% NaCl ¼ 513 mmol Naþ/L 5% saline ¼ 855 mmol Naþ/L
TBW is equal to approximately 60% of ideal body weight in males and to approximately 50% of ideal body weight in females and older males. Normal saline will only raise the Na concentration by 1–2 mEq/L for each liter of normal saline administered. By replenishing volume, however, the hypovolemic stimulus to ADH is removed and free water eventually will be excreted. Serial Na measurements are necessary during treatment to assess the adequacy of treatment and to ensure that the Naþ is not being corrected too rapidly. It remains unclear whether patients with chronic asymptomatic hyponatremia should be treated at all. Most of them will be refractory to treatment, perhaps because they have a “reset osmostat” and will therefore defend their low serum sodium concentration by appropriately concentrating or diluting their urine in response to water restriction or water load. In a patient with symptomatic chronic hyponatremia, the serum sodium concentration should not be corrected any faster than 0.5–1.0 mmol/L/hr. The total correction should not exceed 8–12 mmol/L/day. The serum sodium level should not be corrected to greater than 125 mmol/L. Severe neurological complications can occur if the serum sodium deficit is corrected too rapidly. Hyponatremia causes water to move into neurons. The swollen neurons compensate by losing electrolytes and other substances so that within a few days, the brain returns to its normal size. It is these adaptive changes that make the brain susceptible to damage during too-rapid correction of the hyponatremia. Rapid correction of hyponatremia can cause neuronal injury, possibly leading to osmotic demyelination syndrome or central pontine myelinolysis, a potentially devastating and usually avoidable neurological complication that may involve paralysis or other severe sequelae.
Hypernatremia KEY POINTS Hypernatremia represents a deficit of water in relation to the body’s Naþ stores and can result from a net water loss or a hypertonic Naþ gain. Hypernatremia is unusual in adults if thirst is intact and if the patient has access to water.
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Volume status and total body Naþ vary with the cause of the hypernatremia. Signs and symptoms of hypernatremia are caused by dehydration of brain cells and are most prominent when the serum Naþ increase is large or occurs rapidly. If the patient is significantly volume depleted—that is, volume depletion is sufficient to cause hemodynamic compromise, decreased tissue perfusion, and impairment of metabolism—then volume expansion with normal saline sufficient to restore tissue perfusion to normal is appropriate. For all other patients, treatment of hypernatremia is best accomplished with hypotonic fluid. Too-rapid rehydration and lowering of serum Naþ can cause brain cell swelling, cerebral edema, permanent neurological sequelae, and death. DEFINITION Hypernatremia is defined as a serum Naþ concentration greater than 150 mmol/L. EPIDEMIOLOGY Hypernatremia represents a deficit of water in relation to the body’s Naþ stores and can result from a net water loss or a hypertonic Naþ gain. Normal defenses against hypernatremia are thirst and the secretion of ADH. ADH causes the urine to become concentrated, that is, the kidney retains water. Hypernatremia is unusual in adults if thirst is intact and the patient has access to water. An altered level of consciousness with an inability to drink usually precedes the hypernatremia. Infants may easily become dehydrated through gastroenteritis or insensible water losses. REDUCED WATER INTAKE The reduced intake of water is seen in those patients with change in thirst, altered mental status, or immobility and in patients with unreplaced insensible losses, both dermal and respiratory. INCREASED WATER LOSS Renal or extrarenal losses of Naþ and water may occur, with loss of more water than Naþ, such as in the case of loop diuretic use, osmotic diuresis (e.g., hyperglycemia), recovery phase of acute renal failure, intrinsic renal disease with a concentrating defect, vomiting, nasogastric suction, diarrhea, and use of cathartic laxatives. Diabetes insipidus results in a lack of concentrating ability in the distal nephron. Diabetes insipidus can be central (ADH is inappropriately low) or nephrogenic (the kidney does not respond to ADH) and should be suspected when the urine volume is greater than 3 L/day. Most
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patients with diabetes insipidus have intact thirst and do not present with hypernatremia. SODIUM GAIN Patient with hypernatremia may have experienced a net gain of Naþ in an excess of water by Naþ intake or renal Naþ absorption. Common etiologies include iatrogenic administration of sodium bicarbonate (e.g., during a code), improper preparation of infant formula or tube feedings, ingestion of salt tablets, sea water ingestion, use of a hypernatremic dialysis bath, primary hyperaldosteronism, and Cushing’s syndrome. PRESENTATION The signs and symptoms of hypernatremia are caused by dehydration of brain cells and are most prominent when the serum Naþ increase is large or occurs rapidly. Thrombosis and multiple small or even massive brain hemorrhages can occur from brain shrinkage and the tearing of cerebral blood vessels. The level of consciousness is correlated with the severity of marked hypernatremia. Common symptoms in infants include hyperpnea, restlessness, muscle weakness, a characteristic high-pitched cry, insomnia, lethargy, and even coma. Sixteen percent of infants and children with serum sodium levels between 160 and 165 mmol/L will develop chronic neurological deficits. Adults are not usually symptomatic, aside from thirst, until the serum Naþ concentration exceeds 160 mmol/L. Intense thirst can be present initially but decreases as the serum Naþ level exceeds 160 mmol/L and is absent in patients with hypodipsia. Adults can be irritable and restless, and symptoms can progress to tremulousness and ataxia. Seizures and death can occur at serum osmolality greater than 430 mOsm/kg. EXAMINATION Findings on examination will vary, depending on the underlying condition. Most importantly, the patient’s volume status should be evaluated, using standard criteria, and should be classified as low, normal, or high volume based on the results of the bedside examination, not on the serum sodium concentration. LABORATORY FINDINGS Serum osmolarity and spot urine tests for Naþ, creatinine, calculated FENaþ, and osmolarity may prove helpful in confirming a diagnosis,
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but these are not usually necessary. They may, however, be useful in determining the cause and appropriate treatment. DIAGNOSIS Diabetes insipidus can present with hypernatremia, but the patients’ main signs will be polydipsia and polyuria (Table 8-2). There is loss of dilute urine, usually greater than 3 L/day, with urine osm typically 200–300 mOsm/L. Diabetes insipidus can be central (caused by a failure of ADH secretion) or nephrogenic (caused by renal unresponsiveness to ADH). Approximately 70% of central diabetes insipidus is secondary to surgery, trauma, or neoplasms, which destroy or replace the posterior pituitary and decrease ADH release. Approximately 30% is idiopathic.
Table 8-2 Hypernatremia Etiologies Reduced Water Intake Disorders of thirst perception Inability to obtain water—altered mentation, immobile Increased Water Loss/Increased Sodium Retention/Concentration Gastrointestinal Vomiting, diarrhea Nasogastric suction Third spacing Renal Tubular concentrating defects Osmotic diuresis—hyperglycemia, mannitol Diabetes insipidus—central or nephrogenic Post–urinary obstruction Skin Sweating Burns Hyperventilation (in intubated patient) Drugs Lactulose, charcoal/sorbitol Lithium, foscarnet, amphotericin B, cidofovir (nephrogenic diabetes insipidus) Sodium Gain Sodium Intake Na+ bicarbonate Hypertonic saline, enteral or parenteral nutritional fluids Salt tablets Improper infant formula preparation Salt water drowning Peritoneal dialysis Increased Sodium Resorption—mineralocorticoid or glucocorticoid excess Hyperaldosteronism, congenital adrenal hyperplasia Cushing’s disease, ectopic ACTH Exogenous corticosteroids ACTH, Adrenocorticotropic hormone.
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Nephrogenic and central diabetes insipidus can be differentiated by noting serum and urine osmolality after water deprivation and after administration of nasal, subcutaneous, or intravenous desmopressin (dDAVP). Failure of serum osmolality to rise to more than 295 mOsm/ L during water deprivation is diagnostic of diabetes insipidus but does not differentiate a central from a nephrogenic origin. In central diabetes insipidus the urine osmolality will be greater than 400–600 mOsm/L after the administration of dDAVP. Nephrogenic diabetes insipidus will not respond to dDAVP. Diabetes insipidus can result from many medications. TREATMENT If a patient is significantly volume depleted—that is, volume depletion is sufficient to cause hemodynamic compromise, decreased tissue perfusion, and impairment of metabolism—then volume expansion with normal saline sufficient to restore tissue perfusion to normal is appropriate. For all other patients, treatment of hypernatremia is best accomplished with hypotonic fluid, preferably administered orally. If the oral route is not feasible, then hypotonic fluid, preferably 5% dextrose in water (D5W), should be given intravenously. The total body free water deficit should be calculated. One half of the deficit should be replaced over 24 hours, then the remainder over the next 1–2 days. The serum Naþ concentration should not be reduced by more than 10–15 mEq/day. Estimation of the free water deficit in liters ¼ CBW
ðCurrent Na 1Þ 140
where CBW is current body water, which is about 10% less than TBW in patients who are water depleted. For women and elderly men, the CBW is the “ideal” body weight multiplied by 0.4, and for men the CBW is 0.5 times the ideal body weight. The Naþ and Kþ contents of some intravenous solutions are as follows:
Normal saline (0.9% NaCl): 154 mmol/L Naþ D5W: 0 Naþ/L 0.2% saline in D5W: 34 mmol Naþ/L ½ saline: 77 mmol/L Naþ Lactated Ringer’s solution: 130 mmol Naþ/L and 4 mmol Kþ/L 3% NaCl: 513 mmol Naþ/L 5% saline: 855 mmol Naþ/L
The following formula can be used to help estimate the change in serum Naþ per each liter of Naþ or Kþ containing fluids infused.
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ðinfusate Naþ þ infusate Kþ Þ serum Naþ ðTBW þ 1Þ
where TBW for men is 0.6 total ideal body mass, and TBW for women and for elderly men is 0.5 total ideal body mass. This formula estimates the amount of water deficit necessary to return the serum Naþ concentration to 140 mEq/L and does not include any additional iso-osmotic fluid deficit or ongoing insensible losses, which should be included in replacement fluids. In general, each liter of water deficit will result in a rise in the serum sodium of 3–5 mEq/L. In patients with CHF, rehydration should be undertaken more slowly with central monitoring. Dialysis should be considered in the case of severe hypernatremia (180–200 mEq/L). Central diabetes insipidus is treated with vasopressin or DDAVP. The Na level should be monitored closely during treatment. If the hypernatremia has persisted for more than several days, the brain cells have accumulated idiogenic osmoles, a protective mechanism to restore cell volume. Too-rapid rehydration and lowering of serum Naþ concentration can cause brain cell swelling, cerebral edema, permanent neurological sequelae, and death.
POTASSIUM Potassium is the primary intracellular cation. The normal daily Kþ intake is 50–150 mEq/day. Total body Kþ is approximately 50–55 mEq/L or about 3500 mEq in the normal 70-kg man. More than 95% of total body Kþ is located intracellularly, with 75% located in muscle. The serum Kþ concentration is normally 3.5–5 mEq/L, whereas the intracellular Kþ concentration is 110–150 mEq/L. Importantly, the relationship between total body Kþ and serum Kþ is not linear but instead follows an exponential curve. When the serum Kþ is mildly decreased at 3.0 mEq/L, the total body Kþ deficit is approximately 150–175 mEq. When the serum Kþ has dropped to 2.0 mEq/L, the total body Kþ deficit has increased to greater than 350–400 mEq. More than 90% of the daily K þload is excreted renally, with some losses in stool and sweat.
Hypokalemia KEY POINTS Potassium is the primary intracellular cation. Hypokalemia is defined as a serum Kþ concentration less than 3.5 mEq/L. Hypokalemia is usually caused by a shift of Kþ from the extracellular to the intracellular compartment or by increased Kþ losses from the kidney.
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In the case of excess vomiting and nasogastric suction, most of the Kþ is actually lost in the urine. In general, spot urinary Kþ values of greater than 20 mEq/L and/or transtubular Kþ gradient (TTKG) values of more than 2 in the presence of significant serum hypokalemia imply “inappropriate” renal Kþ wasting. The etiology of hypokalemia can often be obtained from the history. Hypokalemia causes arrhythmias and potentiates digoxin toxicity. Treatment is directed toward Kþ repletion and prevention of further Kþ loss with correction of the underlying disorder. Intravenous potassium chloride (KCl) should be given, not faster than 10–20 mEq/hr. No more than 40 mEq of Kþ should ever be put into a single bag of intravenous fluid. DEFINITION Hypokalemia is defined as a serum Kþ concentration less than 3.5 mEq/L. EPIDEMIOLOGY Hypokalemia is usually caused by a shift of Kþ from the extracellular to the intracellular compartment or by increased Kþ losses from the kidney. INTRACELLULAR SHIFTS Hypokalemia is frequently seen in the presence of metabolic alkalosis or correction of acidosis. For every rise in pH of 0.10, the serum Kþ concentration will fall by 0.5 as Kþ shifts into cells in exchange for hydrogen ions. ED patients who are NPO and receive dextrose in their intravenous line commonly become mildly hypokalemic. The decrease in Kþ does not usually exceed 1 mEq/L and is usually of no clinical significance. b2-adrenergic agonist therapy of asthma, if it results in marked hypokalemia, can cause muscle weakness and worsen CO2 retention. Hyperthyroid patients, usually those who have Graves’ disease, can become hypokalemic for the same reason: adrenergic-mediated cellular Kþ uptake. Patients with DKA are commonly Kþ depleted because of urinary losses. Insulin therapy causes Kþ to shift into cells. Severe hypokalemia can result. It is customary to replace Kþ early in these patients. Other conditions to be considered are hypokalemic periodic paralysis, acute increases in cell production causing Kþ uptake by bone marrow cells (e.g., vitamin B12 or folate therapy of megaloblastic anemias and granulocyte-macrophage colony-stimulating factor therapy), and barium salt intoxication (causes an “exit block” from cells).
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ETIOLOGY Gastrointestinal Losses GI tract losses of Kþ can occur through diarrhea, vomiting, nasogastric suction, intestinal fistulas, villous adenomas, or laxative abuse. In excess vomiting and nasogastric suction, most of the Kþ is actually lost in the urine. The loss of Hþ and the resultant metabolic alkalosis causes volume depletion, elevated renin, elevated aldosterone, and increased renal Kþ loss from Naþ/Kþ exchange in the distal nephron. Renal Losses Hyperaldosteronism causes the kidney to excrete Kþ and Hþ ions and retain sodium. Hyperaldosteronism can be primary (e.g., adrenal adenoma, carcinoma, or bilateral adrenal hyperplasia) or secondary (e.g., renovascular hypertension from renal artery stenosis). Other causes of excess renal loss of Kþare tobacco chewing, licorice ingestion, Bartter or Liddle syndromes, diuretic therapy, type I or II renal tubular acidosis, osmotic and postobstructive diuresis, and polyuric states. Drugs and Toxins Diuretics (especially loop diuretics in the presence of increased Naþ intake), amphotericin B, lithium, platinum-based chemotherapy, and aminoglycoside antibiotics can all cause renal Kþ wasting. Other Causes Other etiologies of hypokalemia can include inadequate intake (usually elderly or alcoholic patients), alcohol (causes renal Kþ and Mgþ wasting), hypomagnesemia (if severe, will interfere with the full correction of hypokalemia and hypocalcemia), hypercalcemia (increases renal Kþ and Mgþ wasting), excess sweat loss, and acute leukemia (certain types can cause renal Kþ wasting). CLINICAL PRESENTATION Patients with hypokalemia present with symptoms related to their serum K levels. At levels below 2–2.5 mEq/L, muscle weakness, ileus, and polyuria occur. At levels of 1.5–2 mEq/L, respiratory paralysis and arrhythmia are likely. EXAMINATION Volume status and blood pressure should be determined for these patients. Patients with mineralocorticoid excess may be hypertensive but are not usually edematous. Patients with renal or GI losses may be hypotensive and volume depleted. The muscle weakness associated with hypokalemia will be more proximal. Reflexes and sensation are usually intact. A variety of arrhythmias can be seen, from
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sinus bradycardia to ventricular fibrillation. ECG findings with a serum Kþ concentration of less than 3.0 mEq/L include depressed ST segments, flattened T waves, presence of U waves, and prolonged QT intervals. With more severe Kþ depletion, P wave prominence, PR prolongation, and widening of the QRS complex can occur. Patients with significant hypokalemia and ECG changes should be placed on a cardiac monitor. LABORATORY FINDINGS A serum Kþ concentration of less than 3.5 mEq/L is diagnostic of hypokalemia. In addition to routine chemistries, a check of the acid– base status with ABG (if HCO 3 is abnormal) should be performed, and serum Mgþ, serum Caþ, spot urine Kþ, spot urine Naþ, and spot urine osmolarity should be analyzed. The TTKG can be calculated as follows. (The normal range is 2–6.) TTKG ¼
ðspot urine Kþ serum osmolalityÞ ðspot urine osm serum Kþ Þ
In general, spot urinary Kþ values greater than 20 mEq/L and/or TTKG values of more than 2 in the presence of significant serum hypokalemia imply “inappropriate” renal Kþ wasting. The TTKG formula is not useful if the urine is hypo-osmolar with respect to plasma. Patients who are in a “maintenance” phase of contraction alkalosis and hypokalemia from vomiting or nasogastric suction will generally have a spot urine Cl concentration of less than 20 mEq/L. Conversely, patients with excess mineralocorticoid syndromes will generally have a spot urine Cl of greater than 20 mEq/L. DIAGNOSIS The etiology of hypokalemia can often be obtained from the history— for example, vomiting, diarrhea, or diuretic use may have occurred. If none of those are present in the history, a mineralocorticoid excess state may be present. The various forms of primary hyperaldosteronism present with hypertension, hypokalemia, and metabolic alkalosis. On the other hand, Bartter syndrome presents with hypokalemia and metabolic alkalosis but no hypertension. Patients with Bartter syndrome have elevated renin, aldosterone, and urine Cl levels. In children presenting with metabolic alkalosis, hypokalemia, and sodium and HCO 3 retention without hypertension or edema, Bartter syndrome should be considered. Of all adult patients suspected of having Bartter syndrome, most will turn out to have surreptitious loop-diuretic abuse. Gitelman’s syndrome presents in a similar manner to Bartter syndrome but is associated with hypocalciuria. Liddle syndrome is a rare familial
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form of pseudohyperaldosteronism, with hypertension, salt sensitivity, a tendency for hypokalemia to develop, decreased aldosterone levels, and decreased renin levels. TREATMENT The treatment of hypokalemia is directed toward Kþ repletion and prevention of further Kþ loss with correction of the underlying disorder. Kþ can be given orally to stable patients who can tolerate oral intake, or it can be given intravenously to patients with more severe hypokalemia. The usual oral dose is 20 mEq Kþ every 1–2 hours until the Kþ concentration is improved. Intravenous KCl should be given, though not faster than 10–20 mEq/hr. When receiving intravenous Kþ, the patient should ideally be on a cardiac monitor. No more than 40 mEq of Kþ should ever be put into a single bag of intravenous fluid. The rapid administration of intravenous Kþ is potentially life threatening. The usual dose of intravenous KCl is 10 mEq/hr or 40 mEq/L intravenous fluid over 4 hours. Depending on the patient’s acid–base status and ongoing losses, it may take 100–200 mEq of supplemental Kþ to raise the serum Kþ by 1 mEq. In patients who are being treated for metabolic acidosis or hyperglycemia, the practitioner should anticipate that the Kþ concentration will fall as the acidosis is corrected or as insulin is given and Kþ is driven into the cells. To determine the correct total body K deficit, one should look at the corrected pH level for the serum Kþ level (a rise in pH of 0.10 will lower Kþ by 0.5 mEq/L) and correlate these two values to determine the correct K loss.
Hyperkalemia KEY POINTS Hyperkalemia is defined by a serum Kþ concentration greater than 5.5 mEq/L. The most common cause is hemolysis during blood draw, or pseudohyperkalemia. ECG findings include tall and peaked precordial T waves. The initial evaluation of a patient with hyperkalemia should include a history of renal disease and any use of Kþ-sparing diuretics, angiotensin-converting enzyme (ACE) inhibitors, NSAIDs, Kþ supplements, and salt substitutes. Emergent treatment of hyperkalemia has three parts: membrane stabilization, shifting Kþ into the cells, and removing excess Kþ from the body. Cardiac monitoring should be performed during treatment. Immediate treatment should be initiated for severe hyperkalemia (Kþ >7–7.5 mEq/L), ECG changes resulting from hyperkalemia, or severe muscle weakness.
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The practitioner must not forget to correct the underlying cause, if possible. Remedies might include decreasing the dietary Kþ intake; stopping administration of the Kþ-sparing diuretic, ACE inhibitor, NSAID, or other offending medication; and arranging for hemodialysis if the patient has renal failure. DEFINITION Hyperkalemia is defined by a serum Kþ concentration greater than 5.5 mEq/L. EPIDEMIOLOGY Hyperkalemia can be divided into the following categories: “factitious” (i.e., pseudohyperkalemia), extracellular Kþ shifts, increased Kþ ingestion or endogenous load, and decreased renal excretion. FACTITIOUS The most common cause of hyperkalemia is hemolysis during blood draw, or pseudohyperkalemia. Other causes of pseudohyperkalemia are prolonged tourniquet use, leukocytosis, and thrombocytosis. If the blood specimen is not analyzed within 30 minutes of being drawn, this can cause a factitious increase in Kþ. EXTRACELLULAR SHIFTS Shifts of Kþ from the ICF to ECF are seen in acidosis, insulin deficiency, use of beta blockers, succinylcholine, and hyperkalemic periodic paralysis. INCREASED POTASSIUM LOAD Increased Kþ load can occur with ingestion of Kþ supplements (usually in the setting of renal insufficiency or taken with drugs that impair Kþ excretion, especially Kþ-sparing diuretics), blood transfusions, intravenous KCl or K3PO4, various Kþ-containing medications, rhabdomyolysis, tissue necrosis, crush injury, and post-chemotherapy tumor lysis syndrome. DECREASED RENAL EXCRETION Decreased renal excretion can occur with acute and chronic renal failure, Kþ-sparing diuretics, ACE inhibitors, NSAIDs, mineralocorticoid deficiency (e.g., Addison’s disease, hypoaldosteronism), and selective defects in renal Kþ excretion (e.g., diabetics with type IV RTA).
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CLINICAL PRESENTATION Hyperkalemia can cause skeletal and smooth muscle weakness, decreased myocardial performance, delays in cardiac conduction, and arrhythmias. In severe hyperkalemia, respiratory failure with CO2 retention can occur as a result of respiratory muscle weakness. Hyperkalemia should always be investigated as a possible cause of the above complications, especially in patients with tissue breakdown, decreased renal function, severe hemolysis, and in those taking Kþ-sparing diuretics, ACE inhibitors, or NSAIDs. EXAMINATION The first thing to do when examining a patient with reported or suspected hyperkalemia is to go to the bedside and perform a brief history and physical examination. Is the patient weak? Does the patient have an ileus? Does the patient have an obvious arrhythmia? If the diagnosis of hyperkalemia is suspected, an ECG should be obtained. The report of significant hyperkalemia in a patient with a normal ECG usually reflects laboratory error or factitious hyperkalemia. With true hyperkalemia, precordial T waves become tall and peaked as the Kþ reaches 5.6–6 mEq/L. At levels of 6–6.5 mEq/L, impulse conduction decreases, the QT interval is shortened, and the PR interval is prolonged. At 6.5–7.0 mEq/L, the P wave diminishes and the ST segment becomes depressed. At levels above 7 mEq/L, atrioventricular conduction is delayed and idioventricular rhythms occur. At levels above 7.5–8 mEq/L, the P wave disappears, the QRS complex widens, ST and T waves merge, and the ventricular rhythm becomes irregular. At levels greater than 10–12 mEq/L, the classic sine wave is seen. At this point, patients die of ventricular fibrillation or diastolic arrest. LABORATORY FINDINGS If pseudohyperkalemia is suspected, the Kþ measurement should be repeated. Cardiac monitoring should be initiated and an ECG should be obtained. Draw Chem 7 to assess renal function and Caþ concentration. The serum Kþ should be correlated with the pH. Acidosis is almost always present with hyperkalemia. Hypocalcemia and hypermagnesemia potentiate hyperkalemic cardiac toxicity. DIAGNOSIS The initial evaluation of a patient with hyperkalemia should include checking the history for any renal disease or use of Kþ sparing diuretics, ACE inhibitors, NSAIDs, Kþ supplements, or salt substitutes, which often contain KCl. In a patient with chronic hyperkalemia, normal renal function, and no other apparent etiology for the elevated Kþ, workup for one of the causes of hypoaldosteronism should be started.
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TREATMENT Emergent treatment of hyperkalemia has three parts: membrane stabilization, shifting Kþ into the cells, and removing excess Kþ from the body. Cardiac monitoring should be undertaken during treatment. Immediate treatment should be initiated for severe hyperkalemia (Kþ >7–7.5 mEq/L), ECG changes resulting from hyperkalemia, or severe muscle weakness. The practitioner should not forget to correct the underlying cause, if possible. Remedies might include decreasing the dietary Kþ intake; stopping administration of the Kþ-sparing diuretic, ACE inhibitor, NSAID, or other offending medication; and arranging for hemodialysis if the patient has renal failure. For mild hyperkalemia (serum Kþ, 5.5–6.5 mEq/L), a common treatment is to start the administration of normal saline at 125–200 ml/hr plus furosemide (40–80 mg given intravenously every 4–6 hours) to increase renal loss of Kþ, along with Kayexalate (sodium polystyrene; 25–50 g) with 50 ml of a 20% sorbitol solution every 4–6 hours orally to increase GI loss of Kþ. Along with Kþ, the previously described therapy will also increase urinary losses of Caþ and Mgþ. Patients with advanced age, renal insufficiency, CHF, cirrhosis, nephrotic syndrome, or other volume overload states will probably not be able to handle the extra volume or will require more than the usual amount of furosemide to establish an effective diuresis, and these factors should be taken into consideration when the initial orders are determined. Kayexalate can also be given rectally, as a 20-g dose with 20% sorbitol every 4 hours. Each gram of Kayexalate will eliminate 1 mEq of Kþ. Caution should be used in patients with impaired cardiac function, because the sodium in Kayexalate can cause acute water retention and CHF. Intestinal necrosis is another potential complication of this medication. For moderately severe hyperkalemia (serum Kþ, >6.5 mEq/L), albuterol should be given at 2.5 mg in 4 ml of normal saline nebulized over 20 minutes, 1 amp of D50W should be given as a slow intravenous push, 10 units of regular insulin should be given in by intravenous push, and D10W should be administered at a rate of 50–100 ml/hr. Albuterol, dextrose, and insulin will cause cellular Kþ uptake, but the effect is minimal and the effect is delayed for several minutes. D50W should not be administered rapidly; the slight increase in plasma osmolarity from the dextrose will cause cellular Kþ release and actually increase the serum Kþ slightly. A D10W drip is necessary to prevent hypoglycemia from insulin, a complication that occurs in approximately 40% of nondiabetic patients. If the ECG shows pronounced peaking of the T waves or widening of the QRS complex, 10 ml (one ampule) of a calcium gluconate 10% solution should be given intravenously, slowly over 2–3 minutes.
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Immediate treatment should be initiated for severe hyperkalemia (serum Kþ, >7–7.5 mEq/L), ECG changes occurring as a result of hyperkalemia, or severe muscle weakness. For severe hyperkalemia, the emphasis is on antagonizing the membrane effects of hyperkalemia by giving Ca, and on arranging for hemodialysis to remove the excess K from the body. Calcium gluconate 10% solution 10 ml (one ampule), slowly over 2–3 minutes, or calcium chloride 10% 5–10 ml can be given intravenously every 5–10 minutes until the most marked cardiac effects of hyperkalemia have subsided. The practitioner should use caution when giving Ca to patients who are taking digoxin. Hypercalcemia can potentiate the toxic effects of digoxin on the heart. If Ca is to be given to a hyperkalemic patient who is taking digoxin, it should be infused very slowly over 20–30 minutes. 1 ampule of NaHCO3 given by slow intravenous push can be considered to correct acidosis and thereby increase intracellular Kþ uptake, but NaHCO3 has been shown to be effective only in patients with azotemia and metabolic acidosis, and rapid administration of NaHCO3 can actually transiently increase the serum Kþ. The measures listed previously, including normal saline, furosemide, dextrose, insulin, and albuterol, can also be implemented. DIALYSIS Hemodialysis using a low Kþ bath is usually indicated for patients with severe hyperkalemia, for those who do not respond to the previously described measures, for those with ongoing tissue destruction and release of Kþ from intracellular stores, and for patients with significant azotemia. If the patient presents with severe hyperkalemia and is in renal failure, a renal consultation should be obtained for the initiation of hemodialysis.
CALCIUM More than 98% of calcium is stored in bone as hydroxyapatite. Calcium is found in three forms in the blood: 40% protein bound, 15% complexed, and 45% ionized, or free. Total plasma Ca ranges from 8.5 to 10.5 mg/dl. The ionized form is physiologically active form. Ionized Ca can be measured directly using a Ca-sensitive electrode. The common practice of “correcting” the serum Ca using the serum albumin, while generally producing linear results when compared with direct determination of ionized Ca, is in error when the serum pH or serum albumin are markedly abnormal. Calcium homeostasis is under the direct control of the parathyroid gland, parathyroid hormone (PTH), calcitonin, and calcitriol, which is a vitamin D metabolite. The parathyroid gland secretes PTH when ionized Ca levels are low. Calcium levels are increased by PTH, which increases bone resorption and renal Caþ
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uptake and stimulates synthesis of active vitamin D. Activated vitamin D increases intestinal and renal Caþ uptake and acts on bone to increase Caþ release. Vitamin D is absorbed directly from the GI tract or can be produced nonenzymatically by ultraviolet light acting on vitamin D precursors. Calcitonin, on the other hand, decreases the release of Ca from bone by inhibiting the activity of the osteoclasts (Caþ moves into bone) and stimulating renal Caþ excretion, lowering the serum Ca levels. Calcium is essential for muscle depolarization, neurotransmitter release in the CNS and peripheral nervous system, and for the function of the clotting cascade. It is also necessary for platelet aggregation and granule release. It acts as a membrane stabilizer and is needed for neutrophil chemotaxis and lymphocyte activation.
Hypocalcemia KEY POINTS The ionized form of hypocalcemia is the physiologically active form. Calcium homeostasis is under the direct control of the parathyroid gland, PTH, calcitonin, and calcitriol, which is a vitamin D metabolite. Hypocalcemia is defined as an ionized Caþ concentration less than 2.0 mg/dl or a serum Caþ concentration less than 8.5 mg/dl. Hypocalcemia can be the cause or the result of critical illness. Hypomagnesemia can cause or potentiate hypocalcemia. Tetany, seizures, hypotension, neuromuscular irritability, or ECG changes warrant emergent treatment. Hypomagnesemia should be treated concurrently, or it will be difficult to correct the Ca. DEFINITION Hypocalcemia is defined as an ionized Caþ concentration less than 2.0 mg/dl or a serum Caþ concentration less than 8.5 mg/dl. EPIDEMIOLOGY Hypocalcemia can be the cause or the result of critical illness. Common causes are renal failure, pancreatitis, shock, sepsis, hepatic failure, malabsorption, hypomagnesemia, drug use, and hypoparathyroidism. Hypocalcemia is seen in renal failure as a result of hyperphosphatemia (ionized Ca binds phosphate) and decreased production of vitamin D in the kidney, which decreases the intestinal absorption of Ca. Acute trauma, hyperpyrexia, and rhabdomyolysis can all cause acute hyperphosphatemia, which can lead to acute hypocalcemia. HYPOMAGNESEMIA Hypomagnesemia lowers secretion of PTH and impairs peripheral action of PTH, which decreases serum Ca. This is usually seen in the presence of alcoholism, malnutrition, and diuretic use.
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HYPOPARATHYROIDISM The most common cause of idiopathic hypoparathyroidism is polyglandular autoimmune syndrome type I, a familial disorder that manifests in childhood and is associated with mucocutaneous candidiasis, hypoparathyroidism, and adrenal insufficiency. The most common cause of acquired hypoparathyroidism is surgical, usually iatrogenic parathyroidectomy during thyroidectomy. Hungry bone syndrome can be seen after parathyroidectomy, with hypocalcemia and hypophosphatemia resulting from rapid remineralization of the skeleton after the parathyroid adenoma has been removed. These patients typically require very large amounts of Caþ, phosphate, Mgþ, and vitamin D postoperatively and will usually require supplemental Ca and vitamin D supplementation for life. PSEUDOHYPOPARATHYROIDISM Familial x-linked dominant disorder manifests by decreased end-organ responsiveness to PTH. Patients with this condition have hyperphosphatemia, hypocalcemia, and increased PTH. RICKETS OR VITAMIN D DEFICIENCY Vitamin D deficiency (i.e., rickets) is rare in the United States. Breastfeeding without adequate sun exposure can cause infantile rickets because breast milk is low in vitamin D. CLINICAL PRESENTATION Hypocalcemia can cause neuromuscular, respiratory, and cardiac complications. Patients may present with fatigue, weakness, paresthesia, tetany, mental status changes, or seizures. The most characteristic initial symptom after parathyroidectomy in patients who become hypocalcemic is paresthesia around the mouth and fingertips. Patients are often irritable with hyperactive reflexes; seizures may occur years after surgery. EXAMINATION Trousseau’s sign is carpal spasm when a blood pressure cuff is applied to the upper arm and maintained above systolic pressure for 3 minutes. If the test result is positive, the fingers will extend at the interphalangeal joints, the fingers will flex at the metacarpophalangeal joints, the wrist will be flexed, and the forearm will be pronated. Chvostek’s sign is a twitch at the corner of the mouth when the examiner taps over the facial nerve in front of the ear. This sign can be present in 10%–30% of healthy patients. Patients with pseudohypoparathyroidism typically have short round facies, brachycephaly, pudgy fingers and toes, growth failure of the fourth and fifth metacarpals, seizures, and mental retardation.
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LABORATORY FINDINGS Laboratory tests should include tests of Chem 7, albumin, Mgþ, phosphorus, and Caþ. Alkalosis lowers the ionized Caþ, though the total serum Caþ concentration will be normal. Each rise of 0.1 in the arterial pH will lower ionized Caþ by 3%–8%. Hypomagnesemia can cause or potentiate hypocalcemia. ECG findings when serum Caþ concentration is less than 6.0 mg/dl include prolonged QT interval, T wave of normal width, and a prolonged ST segment. Radiographs of skull and long bones may show characteristic changes of rickets. DIAGNOSIS When a patient’s Caþ concentration is less than 8.9 mg/dl, the presence of Chvostek’s and/or Trousseau’s signs supports the diagnosis of hypocalcemia. TREATMENT The treatment of hypocalcemia is based on replacing Ca and treating the underlying cause of the deficit. Oral Oral Ca with or without vitamin D can be used to treat an asymptomatic patient. Calcium is available in many oral preparations. Milk is a poor source of Ca in these patients because of its high phosphate content. Patients with hypocalcemia in the setting of chronic renal failure are treated with phosphate binders, oral Ca, and vitamin D (usually as calcitriol or another similar derivative). Emergent Treatment Parenteral treatment is needed in the case of severe acute hypocalcemia (ionized Caþ 20) or where the initial CT scan shows an acute hypodensity or edema with mass effect. However, the potential benefit of fibrinolytic therapy in these devastating strokes may outweigh the potential risk of hemorrhage. A bleeding diathesis workup must be initiated and hemorrhagic symptoms treated by infusion of packed red blood cells, cryoprecipitate, or fresh frozen plasma. Emergency consultations with hematology and neurosurgery are indicated. Continuous transcranial Doppler ultrasonography has been shown to augment the degree of rt-PA–induced arterial recanalization, with a trend toward better stroke outcome. Other fibrinolytic drugs, including streptokinase and ANCROD (a fibrinogen-depleting agent derived from snake venom) have been studied but are not presently approved for use. Intraarterial fibrinolytic therapy with tPA or prourokinase in middle cerebral
494 ESSENTIAL EMERGENCY MEDICINE FOR THE HEALTHCARE PRACTITIONER Table 9-13 Criteria for Tissue Plasminogen Activator (tPA) Therapy in Acute Ischemic Stroke Inclusion criteria for tPA therapy: Acute ischemic stroke within 3 hours of symptom onset Measurable deficit on NIH Stroke Scale examination No hemorrhage or nonstroke cause of neurological deficit on noncontrast brain CT scan Age >18 years Exclusion criteria for tPA therapy: Minor or rapidly improving symptoms Seizure at onset of stroke Stroke or serious head trauma within the previous 3 months Major surgery within the past 14 days Known history of ICH Sustained systolic BP >185 mmHg Sustained diastolic BP >110 mmHg Aggressive treatment is necessary to lower the BP Clinical symptoms are suggestive of SAH GI or GU hemorrhage within the past 21 days Arterial puncture at a noncompressible site within the past 7 days Heparin administration within the past 48 hrs with PTT elevation Elevated prothrombin time >15 seconds Platelet count 22 Large MCA infarction with CT signs of sulcal effacement or loss of gray-white junction in > one third of the MCA cerebral watershed area NIH, National Institutes of Health; CT, computed tomography; ICH, intracerebral hemorrhage; BP, blood pressure; SAH, subarachnoid hemorrhage; GI, gastrointestinal; GU, genitourinary; PTT, partial thromboplastin time; MCA, middle cerebral artery.
artery (MCA) or basilar artery occlusions after the 3-hour intravenous window has expired remains investigational in selected centers. There have been positive reports of intra-arterial thrombolytic infusions in posterior circulation strokes up to 12 hours after symptom onset. The majority of patients with stroke will not be eligible for fibrinolytic therapy due to the strict criteria and short time window for use. Consequently, antiplatelet therapies with aspirin, dipyridamole, clopidogrel, or ticlopidine are indicated for secondary stroke prevention. There is a risk reduction in mortality and stroke recurrence up to 20%–25% with the use of these drugs. Angiotensin-converting enzyme inhibitors may have vascular benefit beyond blood pressure control and may also be beneficial in reducing the risk and recurrence of stroke. The use of anticoagulation with unfractionated heparin, low-molecularweight heparin, or heparinoids has not been proved to be beneficial in treating acute ischemic stroke, any specific stroke subtype, or TIA. Heparin may increase the risk of ICH. Use of unfractionated heparin infusion, however, is discretionary and may be useful in preventing recurrent embolism
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or preventing thrombus propagation in TIA under the following circumstances: stroke in evolution, known high-grade stenosis in a vessel compatible with the clinical symptoms (especially internal carotid artery), cardioembolism from causes other than infective endocarditis, crescendo TIAs, posterior circulation TIA, and TIA refractory to antiplatelet therapy. Urgent carotid endarterectomy is indicated for TIAs resolving within the first 6 hours associated with carotid stenosis greater than 70%. Selective cerebral angioplasty or stenting of other cerebral vessels are currently investigational. Investigational neuroprotective agents targeted at preventing the neuronal physiological cascade initiated by cerebral ischemia include various antioxidants, calcium-channel blockers, N-methyl-D-aspartate (NMDA) inhibitors, glycine, and glutamate receptor antagonists. There is no benefit from the routine use of corticosteroids or anticonvulsants in acute ischemic stroke. The treatment of ICH, especially when consciousness is altered, is focused on stabilization of the ABCs, identification of other causes for mental status changes, and management of elevated ICP. Hypertension should be restored gradually to pretreatment levels when the initial blood pressure exceeds 220/120 mmHg. Patients with known hypertension should not have their blood pressure reduced beyond an estimate of their usual hypertensive level. The head of bed should be elevated 30 degrees above the horizontal. Elevated ICP should be treated with a loop diuretic (furosemide) or osmotic diuretic (mannitol). Intubation and mechanical hyperventilation to a target PCO2 of 30–35 mmHg should be performed when the Glasgow Coma Scale score is less than 9, when there is progressive neurological deterioration, or in situations where the CT scan shows mass effect, midline shift, or impending herniation. Seizure prophylaxis with diphenylhydantoin or fosphenytoin is indicated. An emergency neurosurgical consultation for placement of an ICP monitor and/or surgical intervention is warranted. Surgical decompression and evacuation of the hematoma is indicated in cerebellar hemorrhages greater than 3 cm size or in those involving the brainstem. Steroids are harmful and should not be used. Investigational treatments include barbiturate coma and hypothermia. The treatment of SAH is focused on avoiding rebleeding, which is greatest within the first 24 hours, and preventing vasospasm, which occurs from 2 days to 3 weeks after aneurysm rupture. Lowering systolic blood pressure to less than 160 mmHg or to prehemorrhage levels is associated with a reduced mortality rates and risk of rebleeding. Nimodipine (a calcium-channel blocker), 60 mg given orally every 4–6 hours, should be started within the first 72 hours in patients who can swallow to reduce the incidence and severity of vasospasm. Pain, nausea, vomiting, and seizures should all be treated appropriately to avoid sudden rises in systemic and intracranial pressure. Neurosurgical
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consultation for angiography and possible surgical intervention is indicated, especially when the Hunt and Hess Clinical Grading Scale score for cerebral aneurysms and SAH is less than 3. Other treatment modalities for aneurysmal SAH include coil or microsphere balloon embolization. All patients with an acute ischemic stroke, regardless of eligibility for fibrinolytic therapy, should be admitted to the hospital telemetry or intermediate care unit for monitoring and observation. A neurology specialist should be consulted. Patients with large hemispheric strokes, cerebellar stroke, or significant posterior circulation symptoms and those treated with fibrinolysis should be admitted to the intensive care unit. Patients with new-onset TIA should be admitted to the hospital for a workup to rule out a possible cardioembolic etiology or high-grade carotid stenosis. Some sources suggest discharge of these patients can be considered when carotid and cardiac imaging can be performed on a timely outpatient basis. This is a potentially dangerous disposition since the risk of stroke is nearly 5% within the subsequent 48 hours after discharge. Patients with TIA who have already undergone an extensive prior workup and do not have highgrade carotid stenosis may be discharged on antiplatelet therapy if the ED evaluation results are negative. Patients with repeated stroke who have been previously and extensively evaluated and present with another TIA or a mild completed stroke days to weeks old may be discharged home if the ED evaluation results are negative and aftercare is closely coordinated with the patient’s physicians and family.
Bibliography American College of Emergency Physicians, Emergency Medicine: A Comprehensive Study Guide, ed 6. McGraw-Hill: New York, 2004. American College of Emergency Physicians: Emergency Medicine Manual, ed 6. McGraw-Hill: New York, 2004. American College of Emergency Physicians Use of intravenous tPA for the management of acute stroke in the emergency department. Available at: http://www.acep.org. Cort MA, Kuo D: Ischemic stroke syndromes: The challenges of assessment, prevention, and treatment, Emerg Med Rep 25(5):23–31, 2004. Cort MA, Kuo D: Ischemic stroke syndromes: The challenges of assessment, prevention, and treatment, Emerg Med Rep 25(6):19–28, 2004. Gavin L, Wright D: Transient ischemic attacks: Transient trouble or action-warranted attacks, Emerg Med Pract 5:10, 2003. Ischemic stroke syndromes: The challenges of assessment, prevention, and treatment, Emerg Med Rep February 23, 2004;25(5):. Ischemic stroke syndromes: The challenges of assessment, prevention, and treatment, Emerg Med Rep March 8, 2004;25(6):. Personal Correspondence, Ms. Anne D. Leonard, RN, Nursing Coordinator, University Hospital Stroke Program, San Antonio, TX. September, 2005. The Internet Stroke Center at Washington University in St. Louis, Mo. 1997–2005. Available at: http://www.strokecenter.org. Transient ischemic attacks: Transient trouble or action-warranted attacks, Emerg Med Pract Volume 5, Number 10, October 2003. University of Texas Health Science Center Stroke Program: Internal Stroke Physician Education Services.
Chapter 10
Gynecological and Obstetric Emergencies Abruptio Placentae KHIM K. LAM
ICD Code: 641.2
Key Points The severity of fetal distress associated with abruptio placentae correlates with the degree of placental separation. ! Emergency Actions ! Two large-bore intravenous lines should be placed to draw blood for laboratory studies and for aggressive fluid resuscitation. The patient’s vital signs and urinary output should be monitored. Hypotension should be treated. The patient should be monitored for signs of hemorrhagic shock/disseminated intravascular coagulation (DIC) and treated as needed. Fetal heart tracing should be obtained to evaluate for possible fetal distress.
DEFINITION The term abruptio placentae refers to premature separation of the normally implanted placenta from the uterus before delivery of the fetus.
EPIDEMIOLOGY The reported incidence of placental abruption varies from 1 in 86 to 1 in 206 births. Abruption severe enough to kill the fetus is less common (1 in 420 to 1 in 830 births). Approximately 10% of cases of abruptio placentae are considered concealed (i.e., no vaginal bleeding). Perinatal mortality ranges from 15% to 25%, and in infants who survived, up to 14% of them could have serious neurological deficits.
ETIOLOGY The primary etiology of abruptio placentae is unknown, but multiple risk factors have been associated with abruptio placentae. Risk factors include the following:
Maternal hypertension: most common cause of abruption (40%–50% are associated with hypertensive disease of pregnancy) 497
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Maternal trauma (e.g., motor vehicle accidents, assaults, falls) Cocaine use Sudden decompression of the uterus (e.g., premature rupture of membranes, delivery of first twin) Multiple gestations/maternal age/grand multiparity Previous abruption: risk of recurrence ranges from 5.5% to 16% Inherited thrombophilia Retroplacental myoma Idiopathic factors: probable abnormalities of uterine blood vessels and decidua Cigarette smoking
PATHOPHYSIOLOGY Abruptio placentae is caused by bleeding from small arterial blood vessels into the decidua basalis. The resultant hematoma causes separation of the decidua from the uterine wall leading to obliteration of the intervillous space. This compromises the gas and nutrient exchange to the fetus, leading to fetal distress. The severity of fetal distress correlates with the degree of placental separation. Bleeding into the myometrium and extending to the uterine serosa can also occur; this is known as a Couvelaire uterus.
CLINICAL PRESENTATION Patients usually present in the third trimester with vaginal bleeding, abdominal or back pain, uterine tenderness, fetal distress or death, and hypertonic or high-frequency uterine contraction.
LABORATORY TESTS Laboratory tests that should be performed include a complete blood count (CBC) and measurements of partial thromboplastin time (PTT), international normalized ratio (INR), fibrinogen, and electrolyte levels. The patient should be type and cross-matched for 4–6 units of blood.
RADIOGRAPHS Ultrasound should be used to evaluate the placenta, to exclude the presence of placenta previa and to look for the presence of retroplacental clots. Negative findings do not exclude placental abruption.
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DIAGNOSIS The diagnosis of abruptio placentae is made on the basis of history, clinic examination, and ultrasound examination.
TREATMENT An obstetrician/gynecologist (OB/GYN) should be consulted, and the patient should be transferred to the Labor and Delivery department as soon as possible. Two large-bore intravenous lines should be placed to draw blood for laboratory studies and for aggressive fluid resuscitation. The patient’s vital signs and urinary output should be monitored. Hypertension should be treated. The patient should be monitored for signs of hemorrhagic shock/DIC and treated as needed. Fetal heart tracing should be obtained to evaluate for possible fetal distress.
Bibliography Ananth CV, Savitz DA, Williams MA: Placental abruption and its association with hypertension and prolonged rupture of membranes: A methodologic review and meta-analysis, Obstet Gynecol 1996;88:309. Benedetti TM: Obstetric hemorrhage. In Gabbe SG, Niebyl JR, Simpson JL (eds): Obstetrics: Normal and Problem Pregnancies, ed 4. Churchill Livingstone: New York, 2002, pp 510–516. Clark SL: Placenta previa and abruptio placentae. In Creasy RK, Resnik R (eds): Maternal-Fetal Medicine, ed 4. WB Saunders: Philadelphia, 1999, pp 621–629. Cunningham GF, Gant NF, Leveno KJ, et al: Williams Obstetrics, ed 21. McGraw-Hill: New York, 2001, pp 621–630. Toivonen S, Heinonen S, Anttila M, et al: Obstetric prognosis after placental abruption, Fetal Diagn Ther 2004;19:336.
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Amniotic Fluid Embolism KHIM K. LAM
ICD Code: 673.1
Key Points Amniotic fluid enters the circulation as a result of a breach in the physiological barrier that normally exists between the maternal and fetal compartment. This may trigger a massive anaphylactic reaction, activation of the complement cascade, or both. ! Emergency Actions ! Treatment should focus on cardiopulmonary resuscitation, providing oxygenation (i.e., 100% oxygenation with ventilator support) and support for the failing heart. Circulatory support and blood component replacement are crucial; aggressive fluid resuscitation should be undertaken.
DEFINITION Amniotic fluid embolism is a rare obstetrical emergency in which amniotic fluid/fetal cells enter the maternal circulation, causing cardiopulmonary collapse.
EPIDEMIOLOGY The reported incidence is between 1 in 8000 to 1 in 80,000 deliveries worldwide; the incidence is about 1 in 20,000 to 1 in 30,000 deliveries in the United States. Despite all these aggressive interventions, maternal prognoses have not been shown to improve with amniotic fluid embolism. Maternal mortality rates can reach as high as 86%. One study found a maternal mortality rate of 61% with only 15% neurologically intact, and with fetuses in utero, only 39% survived.
ETIOLOGY/PATHOGENESIS Amniotic fluid enters the circulation as a result of a breach in the physiological barrier that normally exists between the maternal and fetal compartment. This may trigger a massive anaphylactic reaction, activation
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of the complement cascade, or both. Progression usually occurs in two phases. In phase I, pulmonary artery vasospasm with pulmonary hypertension and elevated right ventricular pressure cause hypoxia. Hypoxia causes myocardial capillary damage and pulmonary capillary damage, left heart failure, and acute respiratory distress syndrome. Women who survive these events may enter phase II. This is a hemorrhagic phase characterized by massive hemorrhage with uterine atony and DIC; however, fatal consumptive coagulopathy may be the initial presentation.
CLINICAL PRESENTATION The major clinical findings are abrupt onset of hypotension (cardiogenic shock), hypoxia and respiratory failure, and consumptive coagulopathy. The onset of symptoms most commonly occurs during labor and delivery, in the immediate postpartum period, or during termination. The clinical presentation of amniotic fluid embolism is similar to that of septic or anaphylactic shock. The patient may report the acute onset of shortness of breath followed by severe hypotension. Other signs and symptoms are dyspnea, seizure, cyanosis, fetal bradycardia, pulmonary edema, cardiac arrest, and uterine atony resulting in postpartum bleeding.
LABORATORY TESTS Appropriate laboratory tests should include CBC; measurements of electrolytes, PTT, INR, and fibrinogen; and type and cross-match for 4–6 units of blood.
RADIOGRAPHS Chest radiography, electrocardiography, and arterial blood gas analysis are other diagnostic tests that should be performed.
TREATMENT Management should be multidisciplinary. An OB/GYN and critical care team should be consulted. Treatment should focus on cardiopulmonary resuscitation, providing oxygenation (i.e., 100% oxygenation with ventilator support) and support for the failing heart. Circulatory support and blood component replacement are crucial; aggressive fluid resuscitation should be undertaken. A Foley catheter should be placed for monitoring of urinary output. The patient should be transferred to the intensive care unit. Consideration of emergency perimortem cesarean delivery should be given in undelivered women with cardiac arrest—especially after 5 minutes of cardiopulmonary resuscitation.
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Bibliography Clark SL, Hankins GD, Dudley DA, et al: Amniotic fluid embolism: Analysis of the national registry, Am J Obstet Gynecol 1995;172:1158. Cunningham GF, Gant NF, Leveno KJ, et al: Williams Obstetrics, ed 21. McGraw-Hill: New York, 2001, pp 621–630. Dashow EE, Cotterill R, Benedetti TJ, et al: Amniotic fluid embolism, J Reprod Med 1989;34:660. Killam A: Amniotic fluid embolism, Clin Obstet Gynecol 1985;28:32. Sperry K: Amniotic fluid embolism, JAMA 1986;255:2183.
Breast Abscesses and Mastitis JACQUELYN L. SIMONDS
ICD Codes: Abscess of breast 675.1, Nonpurulent mastitis 675.2
Key Points Breast abscesses and mastitis are infections that must be differentiated. Common skin organisms are the usual cause of both infections. ! Emergency Actions ! Any patient who presents with an elevated white blood cell count, fever, and chills must be considered to have bacteremia. Most patients with breast abscess are not septic, but those patents who present with fever, chills, and hot, red swollen breast and have diabetes, should have blood cultures preformed.
DEFINITION Staphylococcus aureus and streptococcal species are the most common organisms isolated in puerperal breast abscesses. Nonpuerperal abscesses typically contain S. aureus, various Streptococcus species, and anaerobes. In mastitis, S. aureus is the most common cause. Streptococci, enterococci, Staphylococcus epidermidis, and Escherichia coli are less common. In light of the increasing incidence of methicillin-resistant S. aureus (MRSA) nosocomial infection, nursing mothers who develop breast abscesses or mastitis within the first 4 postpartum weeks should be considered to have antibiotic-resistant staphylococcal infections until it is proven otherwise.
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EPIDEMIOLOGY Breast abscesses are more common in nonlactating women and are typically found in the third to eighth decades of life. Postpartum mastitis occurs in 1%–5% of lactating women.
CLINICAL PRESENTATION The patient with a breast abscess typically presents with an edematous, painful, erythematous, and indurated area of the breast. Increased warmth is usual and associated symptoms of fever, chills, vomiting, and drainage from the nipple are common. A mass is commonly found in the subareolar or periareolar regions of the breast. Nipple inversion of recent onset may also be reported. The patient may or may not be actively breast-feeding at the time of onset. Patients with mastitis will report pain and are found on examination to have a warm, erythematous, indurated breast without localized mass. They may have fever.
EXAMINATION The provider should also check for axillary lymphadenopathy, which can be associated with a breast abscess or mastitis.
LABORATORY FINDINGS A CBC with differential may be helpful in assessing a patient with breast abscess. Aerobic and anaerobic cultures, although usually obtained in the operating room for breast abscess, may be helpful in the case of recurrent or nonimproving mastitis. If the patient has diabetes, a chemistry panel should be obtained, and if a fever is present blood cultures should be performed.
RADIOGRAPHS Ultrasound scanning should be performed to differentiate a solid mass from a cystic structure. A direct needle aspiration should be performed if prompt surgical consultation is not an available option. Noncystic structures should be followed up with a mammogram as an outpatient study with surgical follow-up.
TREATMENT Breast Abscess Treatment of breast abscess includes pain control, antibiotic therapy, and prompt surgical consultation. Patients are normally admitted for treatment
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with intravenous antibiotics, pain management, and surgical consultation. Although needle aspiration may be an effective first-line treatment, recurrent aspiration is usually necessary. Definite treatment frequently requires incision and drainage and fistulectomy, and it often necessitates general anesthesia. Aerobic and anaerobic cultures should be obtained to identify organism and to determine sensitivities. Medications in the postpartum female patient may include dicloxacillin, cephalexin, or clindamycin. If it is appropriate to suspect MRSA infection, treatment can include intravenous vancomycin; trimethoprim-sulfamethoxazole (TMP-SMX) given orally or parenterally in a range of 10 mg/kg/day (TMP) and 50 mg/kg/ day (SMX) to 15 mg/kg/day (TMP) and 75 mg/kg/day (SMX) in divided doses at 8- or 12-hour intervals for 2–4 weeks (for adults); rifampin (600 mg/day) given orally or parenterally; or either imipenem-cilastatin (500 mg every 6 hours) or meropenem (0.5–1 g every 8 hours) given parenterally. Nonpuerperal abscesses may be treated with amoxicillin/clavulanate, clindamycin, or a combination of metronidazole and cefadroxil, cefazolin, cephalexin, or dicloxacillin. Depending on the level of discomfort, pain medications may range from nonsteroidal anti-inflammatory drugs to Tylenol (acetaminophen) with oxycodone. All antibiotic regimens should be continued for 14 days. As with any breast mass, mammography and follow-up must be arranged.
Mastitis Mastitis should be treated with antistaphylococcal antibiotics, warm packs, and uninterrupted emptying of the breast by breast-feeding or pumping to reduce chance of breast abscess development. Medication choices include nafcillin, cefazolin, dicloxacillin, cephalexin, or clindamycin, and drug therapy should be continued for 14 days. Pain medication may be necessary, with care taken to ensure that the choice reflects one that is safe with lactation.
Bibliography August DA, Sondak VK: Breast. In Greenfield LJ, Mulholland MW, Oldham KT (eds): Surgery Scientific Principles and Practice, ed 2. Lippincott-Raven: Philadelphia, 1997, pp 1357–1415. Dixon JM: Outpatient treatment of non-lactational breast abscesses, Br J Surg 1992;79 (1):56–57. Maier WP, Au FC, Tang CK: Nonlactational breast infection, Am Surg 1994;60 (4):247–250. Ohara RJ, Dexter SP, Fox JN: Conservative management of infective mastitis and breast abscess after ultrasonographic assessment, Br J Surg 1996;83(10):1412–1414. Walker AP, Edmiston CE, Krepel CJ, et al: A prospective study of the microflora of nonpuerperal breast abscess, Arch Surg 1988;123:908–911.
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Ectopic Pregnancy CULLEN ARCHER
ICD Codes: Ectopic pregnancy ruptured 633.90, Ectopic pregnancy with intrauterine pregnancy 633.1, Tubal pregnancy 633.10
Key Points The most common symptoms of ectopic pregnancy are abdominal pain with a history of amenorrhea and vaginal bleeding. The most common finding in a woman with a symptomatic ectopic pregnancy is abdominal tenderness. ! Emergency Actions ! Intravenous access should be attained quickly with volume resuscitation if the patient is pregnant and hemodynamically unstable. In addition, the patient should be cross-matched for at least 4 units of packed red blood cells. Measurement of urine output can also assist in the assessment of volume status. Emergency consultation with a OB/GYN service is necessitated.
DEFINITION An ectopic pregnancy develops after implantation of the blastocyst anywhere other than the endometrium lining the uterine cavity. An abdominal pregnancy (1.37%) is a pregnancy that develops in any portion of the peritoneal cavity. It usually occurs after secondary implantation of the trophoblast after tubal abortion (i.e., secondary abdominal pregnancy). A primary abdominal pregnancy is one that implants directly into the peritoneal cavity. In a cervical pregnancy (0.15%), ectopic gestational tissue is located in the cervical canal below the level of the internal os. Pregnancy developing in one horn of a bicornuate uterus is called a cornual pregnancy (0.61%). A heterotopic pregnancy (1/6579) occurs when a combined intrauterine and extrauterine pregnancy is present, and an interstitial pregnancy (1.2%) is a pregnancy developing in the interstitial portion of the oviduct. Ovarian pregnancy (0.15%) occurs when pregnancy develops in the ovary. For the diagnosis to be made, the tube on the affected side should be intact, the gestational site must occupy the normal position of the ovary, the gestational site must be connected to the uterus by the
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ovarian ligament, and histologically identified ovarian tissue must be present in the sac wall. A tubal pregnancy (97%) is a pregnancy occurring in the oviduct in either the ampulla (75%–80%), fimbria (5%), or isthmus (10%–15%).
EPIDEMIOLOGY In 1992, ectopic pregnancies accounted for approximately 2% of reported pregnancies, and ectopic pregnancy–related deaths accounted for 9% of all pregnancy-related deaths. The incidence of ectopic pregnancy has been increasing since 1970, when the Centers for Disease Control and Prevention (CDC) first began collecting data, from 4.5 per 1000 reported pregnancies to 19.7 per 1000 pregnancies in 1992. The increased incidence is thought to be due to two factors: (1) the increased incidence of acute salpingitis, due to increased infection with Chlamydia trachomatis, and (2) improved diagnostic techniques, which enable diagnosis of unruptured ectopic pregnancy to be made earlier and with more precision. Other factors that appear to be associated with an increased risk of ectopic pregnancy include prior ectopic pregnancy, cigarette smoking, prior tubal surgery (especially for distal tubal disease), diethylstilbestrol exposure, increasing age, multiparity, and current use of an intrauterine device. The 10-year cumulative probability of ectopic pregnancy for all methods of tubal sterilization combined was shown to be 7.3 per 1000 procedures. Of all pregnancies found in that study after tubal sterilization, 32.9% were ectopic. An operative procedure on the oviducts themselves is a cause of ectopic pregnancy. The incidence of ectopic pregnancy after salpingoplasty or salpingostomy procedures to treat distal tubal disease ranges from 15% to 25%. The rate of ectopic pregnancy after reversal of sterilization procedures is about 4% because the tubes have not been damaged by infection. Women who have had a prior ectopic pregnancy, even if treated by unilateral salpingectomy, are at increased risk for a subsequent ectopic. Of women who conceive after having one ectopic pregnancy, about 25% of subsequent pregnancies are ectopic.
CLINICAL PRESENTATION The most common symptoms of ectopic pregnancy are abdominal pain (90%–100%), a history of amenorrhea (75%–95%), and vaginal bleeding (50%–80%). The most common findings in a woman with a symptomatic ectopic pregnancy is abdominal tenderness (80%–95%), which together with adnexal tenderness (75%–90%) is present in nearly all women with an advanced or ruptured ectopic pregnancy. An adnexal mass is palpable in 50% of the women.
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Many of these classical signs and symptoms are associated with an advanced or ruptured ectopic pregnancy and frequently require surgical intervention. In such cases, intravenous access should be attained quickly with volume resuscitation if the patient is hemodynamically unstable. In addition, the patient should be cross-matched for at least 4 units of packed red blood cells. Measurement of urine output can also assist in the assessment of volume status.
TREATMENT In cases in which the pregnant patient is hemodynamically stable and presents with abdominal or pelvic pain, a transvaginal ultrasound scan is warranted. The identification of an ectopic gestational sac is obviously diagnostic. The sensitivity and specificity of transvaginal ultrasound to detect an ectopic pregnancy are 90.9% and 99.9%, respectively, and positive and negative predictive values of 93.5% and 99.8%, respectively, were noted in the adnexal region when women were diagnosed with an ectopic pregnancy using transvaginal ultrasound if any of the following were present: (1) an inhomogeneous mass or blob sign adjacent to the ovary and moving separately from the ovary; (2) a mass with a hyperechoic ring around the gestational sac or bagel sign; or (3) a gestational sac with a fetal pole with or without cardiac activity. When any adnexal mass other than a simple cyst is used as diagnostic criterion for ectopic pregnancy, the specificity is 98.9%, sensitivity is 84.4%, positive predictive value is 96.3%, and negative predictive value is 94.8%. If an intrauterine pregnancy cannot be identified, a quantitative measurement of b human chorionic gonadotropin (hCG) should be performed (according to the First or Second International Reference Preparation). Transvaginal ultrasound can often detect an intrauterine pregnancy within 5 weeks of the last menstrual period. An intrauterine gestational sac in a healthy uterus can usually be seen with a hCG level between 1000 and 2000 mIU/ml. If the patient’s condition is stable, she may return in 48 hours for another quantitative hCG determination. The mean doubling time for hCG in a normal intrauterine pregnancy is 1.4–2.1 days. However, in patients with an ectopic pregnancy, the hCG will rise at a much slower rate. Based on studies of doubling time, hCG levels should rise by 66% in 48 hours in 85% of normal pregnancies. That is, 15% of normal intrauterine pregnancies will not have a normal doubling time. However, a rise of less than 50% is associated with an abnormal pregnancy 99.9% of the time.
Single-Dose Methotrexate Protocol Classically, uterine dilation and curettage has played an important role in the diagnosis of ectopic pregnancy. The absence of chorionic villi
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on curettage in the presence of an elevated b-hCG level is evidence of a presumptive diagnosis of ectopic pregnancy. Stovall’s protocol used dilation and curettage on day 0 followed by methotrexate 50 mg/m2 given intramuscularly on day 1 after liver and kidney function was verified to be normal. A repeated hCG level determination is performed on days 4 and 7. If the hCG level falls less than 15% between days 4 and 7, a repeat dose of methotrexate was given. If the hCG levels fell more than 15%, then hCG titers were followed weekly until undetectable.
Criteria for Receiving Methotrexate ABSOLUTE INDICATIONS Absolute indications for methotrexate are as follows:
Hemodynamic stability without active bleeding or signs of hemoperitoneum Patient desires future fertility General endotracheal anesthesia (GETA) poses a significant risk Patient is reliable and able to return for follow-up care Patient has no contraindications to methotrexate
RELATIVE INDICATIONS Relative indications for methotrexate are as follows:
Unruptured mass 3.5 cm in greatest dimension No fetal cardiac motion b-hCG level does not exceed a predetermined level (among women with initial hCG concentrations below 15,000 mIU/ml, 93% were successfully treated)
Contraindications to Medical Therapy ABSOLUTE CONTRAINDICATIONS Absolute contraindications for medical therapy include the following:
Breast-feeding Evidence of immunodeficiency Alcoholism or liver disease Preexisting blood dyscrasias Hypersensitivity to methotrexate Active pulmonary disease Peptic ulcer disease Hepatic, renal, or hematological dysfunction
Emergent Pelvic and Abdominal Pain
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RELATIVE CONTRAINDICATIONS Relative contraindications for medical therapy are as follows:
Gestational sac 3.5 cm Fetal cardiac motion
The presence of blood in the pelvis is not considered a contraindication to medical therapy. Approximately 50%–60% of unruptured ectopic pregnancies will have blood in the pelvis on pelvic ultrasound.
Bibliography ACOG Committee on Practice Bulletins: Medical management of tubal pregnancy, ACOG Practice Bulletin. No. 3, December 1998. Goldstein SR, Snyder JR, Watson C, Danon M: Very early detection of pregnancy with transvaginal ultrasound, Obstet Gynecol 1988;72:200–204. Kadar N, Freedman M, Zacher M: Further observation on the doubling time of human chorionic gonadotropin in early asymptomatic pregnancy, Fertil Steril 1980;54:783. Stovall TS, Ling FW: Single dose methotrexate: An expanded clinical trial, Am J Obstet Gynecol 1993;168:1759.
Emergent Pelvic and Abdominal Pain AMY DITZEL
ICD Codes: Pelvic inflammatory disease, female, acute 614.3, Pelvic pain, female 625.9, Ectopic pregnancy, ovarian 633.20, Ectopic pregnancy, tubal 633.10, Tubo-ovarian abscess 614.2
Key Points All female patients of childbearing age with pelvis or abdominal pain are considered pregnant until proven otherwise. Ultrasound and gynecological consult should be obtained. ! Emergency Actions ! Two large-bore intravenous lines with normal saline or lactated Ringer’s solution should be introduced. The patient should be administered oxygen. Laboratory tests, including CBC; measurements of electrolytes, prothrombin time (PT), PTT, and serum quantitative and qualitative hCG; and type and cross-match for 6 units of blood.
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DEFINITION A wide spectrum of conditions involving pelvic and abdominal pain can be categorized as those that pose an immediate threat to the life of the patient (“true emergencies”) and those that do not. These conditions are generally gynecological, obstetrical, or infectious in nature. True emergent causes of pelvic pain include the following: 1. 2. 3. 4. 5. 6. 7. 8. 9. 10.
Ruptured tubo-ovarian abscess Ruptured ectopic pregnancy Ruptured hemorrhagic ovarian cyst Premature rupture of membranes Preeclampsia and eclampsia Preterm labor Uterine perforation or rupture Abruptio placentae Placenta previa Molar pregnancy
Other causes of pelvic pain in women, which are gynecological in nature, include the following: 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12.
Pelvic inflammatory disease (PID) Mittelschmerz Dysmenorrhea Endometriosis Adnexal torsion Nonruptured ovarian cysts Ruptured corpus luteum cyst Vaginitis Pelvic neoplasm Foreign bodies Uterine leiomyoma Abortion (threatened, inevitable, or incomplete)
Additional causes of pelvic pain in females, not gynecological in nature, are as follows: 1. 2. 3. 4. 5. 6. 7. 8. 9. 10.
Appendicitis Lower-lobe pneumonia Colitis Diverticulitis Gastroenteritis Sickle cell crisis Myocardial ischemia Aseptic necrosis of the femoral head Gastric or duodenal ulcer Cholecystitis
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Pancreatitis Pyelonephritis Nephrolithiasis Musculoskeletal pain Pulmonary embolism
EPIDEMIOLOGY The epidemiology varies according to the cause of the pain.
CLINICAL PRESENTATION The nature of the pain varies according to the source of the pain. A thorough description of the pain should be obtained, including location, radiation, intensity, quality (throbbing, etc.), aggravating or alleviating symptoms, and length of time the pain has been present. Additionally, a thorough gastrointestinal, gynecological, and sexual history must be obtained. The following are guidelines regarding determining the source of pelvic pain from the patient’s description:
Sudden pain is usually caused by a vascular or ischemic insult or by an acute irritation of the peritoneum by a large amount of blood. Gradual onset of pain is generally caused by a slow vascular leak or an infection. Colicky pain suggests pain from a hollow organ such as the gallbladder or uterus. Dull throbbing pain suggests chronic inflammation. Pain from the pelvic organs can radiate to the upper and lower abdomen, back, shoulder, thighs, buttocks, and perineum.
EXAMINATION A complete physical examination, including pelvic and rectal examination, must be obtained. This will allow for the detection of a gravid or nongravid uterus, adnexal masses or tenderness, possible localization of the pain, and identification of vaginal bleeding or gastrointestinal tract bleeding. Depending on the severity of the illness, the patient may be tachypneic, tachycardiac, hypotensive, and diaphoretic or may be completely stable with only moderate adnexal tenderness.
LABORATORY FINDINGS Laboratory findings vary according to the underlying process. Elevated white blood cell counts should be expected with infectious processes,
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and lowered hemoglobin and hematocrits may be present with hemorrhagic processes. Hemoglobin and hematocrit levels are generally slightly depressed in a gravid patient. Additionally, the hemoglobin and hematocrit are late indicators of internal bleeding.
DIAGNOSIS A diagnosis is made on the basis of history, physical examination results, clinical presentation, laboratory values, and abdominal/pelvic ultrasound. Occasionally, the diagnosis cannot be made until a computed tomography (CT) scan is obtained or until the patient is taken to surgery. While the laboratory values and ultrasound scan are being obtained, a consultation with a gynecology specialist should be sought.
RADIOGRAPHS A pelvic ultrasound scan will provide valuable information and rule out or diagnose many conditions. This procedure is generally safe for gravid patients.
TREATMENT AND OUTCOME Treatment and outcome vary widely depending on the nature of the pain.
Bibliography Marx JA (ed): Rosen’s Emergency Medicine, ed 5. Mosby: St Louis, 2002.
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Genital Herpes AMY K. DITZEL
ICD Codes: Genital herpes, NOS 054.10, Vulval ulceration 054.12, Vulvovaginitis 054.11
Key Points Genital herpes is a viral infection that is usually sexually transmitted. The lesions are painful, and often vesicles are present, with itching and burning. Genital herpes is a lifelong disease, with variable presentation, but antiviral therapy can decrease recurrences. ! Emergency Actions ! The patient should always be asked about underlying immunocompromising disease like human immunodeficiency virus (HIV)/acquired immunodeficiency syndrome (AIDS). Any immunocompromised patient should undergo a detailed evaluation for other immunocompromise-associated disease.
DEFINITION Genital herpes is a common, viral, sexually transmitted disease (STD) for which effective treatment has been developed, but there is no cure.
EPIDEMIOLOGY Genital herpes is a common viral infection, with over half a million new cases diagnosed each year. Genital herpes is caused by the herpes simplex viruses type 1 (HSV-1) and type 2 (HSV-2). HSV-2 is more commonly associated with genital lesions, whereas HSV-1 is more commonly associated with oral lesions. However, oral-genital contact can result in either type accounting for genital lesions.
CLINICAL PRESENTATION Women with genital herpes present with a chief symptom of genital pain and rash or sores. Often, these women experience dysuria and may even
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have secondary urinary retention. Patients may have systemic, flu-like symptoms, including fever, headache, myalgias, and malaise. Often patients have had a new sexual contact recently. Approximately 48 hours to 1 week after exposure to an infected person, a patient will develop the initial episode of genital herpes. This is typically the patient’s worst outbreak, lasting up to 3 weeks if untreated. During this time, crops of lesions will appear, each taking an average of 8 days to resolve. Complications can occur with this seemingly localized disease, including aseptic meningitis, hepatitis, and autonomic nervous system dysfunction. Because there is no cure for genital herpes, it can recur, although generally with milder symptoms and a shorter duration of symptoms. Half of all patients will experience a prodrome before the appearance of lesions, including any of the following: localized burning or itching, tingling or paresthesias, or myalgias. Over time, many patients will begin to recognize their own personal prodromal symptoms.
EXAMINATION The findings on examination may vary depending on when in the course of the genital herpes outbreak the patient presents. Initially erythematous maculae appear, which then develop into vesicles on the erythematous base. Eventually, pustules form and often open, creating ulcers that will crust over. Throughout the majority of the course of the disease the lesions will be painful, often exquisitely so. The lesions can be found on the external genitalia as well as on the perineum, along the vaginal walls, and on the cervix. The extent of the speculum examination may be limited due to the severity of the pain. The initial or primary outbreak generally results in a larger number of lesions, which are present bilaterally, whereas recurrent disease will have more limited, often unilateral lesions. Deep inguinal lymphadenopathy is often present with primary disease.
LABORATORY FINDINGS Viral culture and typing will provide diagnosis confirmation. Additionally, these will identify the causative agent as HSV-1 or HSV-2 and will thereby help to predict recurrence patterns. Culture samples can be taken from the vesicular fluid or ulcers, cervix, or vaginal fluid. The earlier in the course of the outbreak, the more likely the culture will have a positive result. A Tzanck smear can be obtained to confirm the diagnosis more quickly than a culture, but the characteristic multinucleated giant cells are present only 50% of the time. The Tzanck smear is prepared by placing some of the vesicular fluid onto a slide and examining it with a Wright or methylene blue stain.
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DIAGNOSIS The diagnosis of genital herpes is made on the basis of physical examination results, with confirmation by Tzanck smear and culture.
TREATMENT The goals of treatment are to shorten the severity and duration of the outbreak with antiviral preparation and comfort measures. Acyclovir 500 mg PO five times a day for 7–10 days is the standard treatment. If complications are present or if the disease is severe, hospitalization with intravenous acyclovir (5 mg/kg every 8 hours) may be necessary. Treatment ideally should be started within 2 days of symptom onset for the most benefit. Suppressive treatment (acyclovir 400 mg given twice daily or 200 mg given five times a day) is also available for patients with greater than six recurrences in a year. Patients can take acetaminophen, ibuprofen, or aspirin in over-the-counter doses to help control the pain. In addition, sitz baths with lukewarm water, wearing loose clothing, and keeping the genitals clean and dry should help patients to be more comfortable. Patients should be advised to adhere to a strict handwashing protocol to decrease the risk of spreading the lesions and to avoid secondary infection to the lesions.
Bibliography Cohen J, Powderly WG (eds): Cohen and Powderly: Infectious Disease, ed 2. Mosby: London, 2004. Marx JA (ed): Rosen’s Emergency Medicine, ed 5. Mosby: St Louis, 2002.
Hyperemesis Gravidarum SHAWNA WALL
ICD Code: 536.2
Key Points Nausea and vomiting is a complication in up to 70% of all pregnancies. Hyperemesis gravidarum occurs in 0.5%^2% of these pregnancies.
516 ESSENTIAL EMERGENCY MEDICINE FOR THE HEALTHCARE PRACTITIONER ! Emergency Actions ! A bolus of normal saline can be given to increase intravascular volume, followed by 5% dextrose in normal saline or 5% dextrose in ½ normal saline to correct ketosis. Correction of vitamin deficiencies, especially thiamine, should also be considered.
DEFINITION Hyperemesis gravidarum is severe, persistent nausea and vomiting that causes dehydration, weight loss, ketonuria, and electrolyte imbalances in a pregnant patient.
EPIDEMIOLOGY Nausea and vomiting is a complication in up to 70% of all pregnancies. Hyperemesis gravidarum occurs in 0.5%–2% of these pregnancies. Onset can occur at 4–8 weeks of gestation, and nausea and vomiting usually resolve by 14–16 weeks of gestation. Those at higher risk are obese persons, nulliparous women, women with history of prior hyperemesis gravidarum, and women with prior molar pregnancy. Pregnant patients with a history of hyperemesis gravidarum should be encouraged to take a daily multivitamin at the time of conception. Multivitamins will lower the risk of similar symptoms occurring with this pregnancy. There is a loose association of hyperemesis gravidarum with a female fetus, history of motion sickness, or a history of migraine headaches.
ETIOLOGY The cause of hyperemesis gravidarum is unknown. Several hypotheses exist. Psychological predisposition has been cited as either a conversion disorder or a somatization disorder. The conversion and somatization disorders are thought to be caused by the inability to cope with life stressors during pregnancy. The second theory is that of an evolutionary adaptation to protect the fetus from potentially harmful foods. The third theory suggests that the hCG peaks during early pregnancy are associated with the timing of the nausea and vomiting. Estrogen has been noted as a possible contributor. When estradiol levels are increased, vomiting occurs. Smokers are less likely to be affected. Estradiol and hCG levels are lower in smokers.
CLINICAL PRESENTATION The patient with hyperemesis gravidarum will present with severe nausea, vomiting, and dehydration. Patients will be afebrile and will have neither abdominal pain nor central nervous system symptoms.
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EXAMINATION The examination should include a pelvic examination for evaluation of uterine size, adnexal tenderness, or mass and rectal examination.
RADIOGRAPHS Confirmation of intrauterine pregnancy should be performed by transvaginal ultrasound or abdominal ultrasound scan.
DIAGNOSIS Hyperemesis gravidarum is a diagnosis of exclusion. All other causes of nausea and vomiting must be ruled out before the diagnosis of hyperemesis gravidarum is made. Hyperemesis gravidarum is a diagnosis of the first trimester of the pregnancy. After the first trimester of pregnancy, a different diagnosis should be entertained for any pregnant patient with severe, persistent vomiting and dehydration. Pancreatitis, cholecystitis, hepatitis, thyroid disease, gastroenteritis, peptic ulcer disease, fatty liver of pregnancy, appendicitis, diabetic autonomic dysfunction, pyelonephritis, and gestational trophoblastic disease (i.e., complete/partial molar pregnancy) can also mimic hyperemesis gravidarum.
LABORATORY FINDINGS A CBC, Chem-10, urine analysis with culture and sensitivity, liver function tests, and measurements of amylase, lipase, thyroid-stimulating (TSH), triiodothyronine (T3), thyroxine (T4) should be performed, with special attention paid to the electrolytes. Thyroid and liver function study results are commonly elevated in patients with hyperemesis gravidarum. Patients who experience elevated TSH, T3, and T4 levels during pregnancy, as a result of hyperemesis gravidarum and without a history of hyperthyroidism or goiter, can expect to have their TSH, T3 and T4 elevation resolve within 20 weeks of gestation without medical intervention. TSH is consistently suppressed, whereas the T4 level is elevated up to 4–6 times normal and T3 is elevated up to 40% of normal. The ratio of T3/T4 should be less than 20 (greater than 20 is suggestive of Graves’ disease). Liver enzyme levels should not be elevated above 300 and bilirubin above 4 mg/dl. Pancreatic enzymes should not be elevated over five times that of normal. Urine analysis will show elevation in specific gravity and ketonuria
TREATMENT The initial treatment of hyperemesis gravidarum should include intravenous fluids when the patient cannot tolerate oral fluids. A bolus of normal saline can be given to increase intravascular volume, followed by 5%
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dextrose in normal saline or 5% dextrose in ½ normal saline to correct ketosis. Correction of vitamin deficiencies should also be considered, especially thiamine. Patients with severe vomiting should not be given anything by mouth for 24–48 hours to rest the bowel. Intravenous antiemetic therapy with promethazine, prochlorperazine, chlorpromazine, or metoclopramide should be considered. It is not recommended to use both phenothiazine and metoclopramide for risk of extrapyramidal reaction. Electrolytes should be replaced as necessary. When vomiting has resolved, a trial of oral fluids can be attempted. The patient should start with small meals, avoiding spicy or fatty foods and including high-protein snacks and meals. Meals high in protein decrease the occurrence of the nausea and vomiting symptoms. If the patient is taking an iron supplement, its use should be discontinued. Vitamin B6 (25 mg PO three times a day) and foods with ginger have been shown to decrease the episodes of nausea and vomiting. Other therapies noted to have some effect on the vomiting are as follows:
Pressure or electrical stimulation of the P6 point on the wrist has been shown to reduce the episodes of vomiting. Ten mg of vitamin B6 combined with 10 mg of doxylamine has been shown to elicit a 70% reduction in nausea and vomiting. This combination is safe for the fetus. Droperidol has been used for hyperemesis gravidarum. Droperidol in doses over 25 mg increases the risk of prolonged Q-T interval, leading to torsades de pointes. It is not recommended. Methylprednisolone, 16 mg three times a day for 3 days, has been used also. This medication improves symptoms and should be tapered over 2 weeks. Avoid use of steroids before the 10th week of gestation. There is an association with oral clefts with steroids used prior to the 10th week. If persistent weight loss continues along with the inability to tolerate oral intake, parenteral caloric replacement should be considered. Mallory-Weiss tears, esophageal rupture, and a number of cases of Wernicke encephalopathy have resulted from thiamine deficiency.
Bibliography ACOG compendium of selected publications 2005, nausea and vomiting of pregnancy, ACOG Practice Bulletin, April 2004, pp 52:601–612. Cunningham FG, Gant NF, Leveno KJ, et al: Gastrointestinal disorders. In Williams Obstetrics, ed 21. McGraw-Hill: New York, 2001, pp 1275–1276. Cunningham FG, Gant NF, Leveno KJ, et al: Prenatal care. In Williams Obstetrics, ed 21. McGraw-Hill: New York, 2001, p 242. Gabbe SG, Niebyl JR, Simpson JL: Endocrine diseases in pregnancy. In Obstetrics: Normal and Problem Pregnancies, ed 4. Churchill Livingstone: Philadelphia, pp 1126, 1145–1146. Gabbe SG, Niebyl JR, Simpson JL: Maternal physiology in pregnancy. In Obstetrics: Normal and Problem Pregnancies, ed 4. Churchill Livingstone: Philadelphia, p 80.
Hypertensive Disorders of Pregnancy (Preeclampsia and Eclampsia)
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Hypertensive Disorders of Pregnancy (Preeclampsia and Eclampsia) CULLEN ARCHER
ICD Code: 642.7
Key Points The cause of preeclampsia is not known.Chronic hypertension is defined as hypertension that is present and observable before pregnancy or that is diagnosed before the 20th week of gestation. The pregnancy-specific syndrome usually occurs after 20 weeks’ gestation, although it may occur earlier with gestational trophoblastic or collagen vascular disease. It is defined by an increase in blood pressure associated with proteinuria. ! Emergency Actions ! Any therapy for preeclampsia other than delivery must have as its successful end point the reduction of perinatal morbidity and mortality. The cornerstone of obstetrical management of preeclampsia is based on whether the fetus is more likely to survive without significant neonatal complications in utero or in the nursery.
DEFINITION Hypertension is defined as a blood pressure equal to or greater than 140 mmHg systolic or 90 mmHg diastolic.
EPIDEMIOLOGY Hypertensive disorders of pregnancy are the third-leading cause, after embolism and hemorrhage, of maternal mortality in the United States, accounting for up to 16% of deaths. Hypertensive disorders of pregnancy occur in 12%–22% of pregnancies.
PATHOPHYSIOLOGY The cause of preeclampsia is not known. The syndrome is characterized by both maternal and fetal manifestations. The maternal disease is
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characterized by vasospasm, activation of the coagulation system, and perturbations in many humoral and autocoid systems related to volume and blood pressure control. The pathologic features in this disorder are primarily ischemic in nature and affect the placenta, kidney, liver, and brain. Many consider the placenta to be the pathologic focus for all the manifestations of preeclampsia because delivery is the only definitive cure. Early in gestation, the spiral arteries (i.e., terminal branches of the uterine artery) are transformed from thick-walled, muscular vessels to sac-like flaccid vessels, which eventually accommodate a 10-fold rise in uterine blood flow. There is evidence in women destined to become preeclamptic that trophoblastic invasion of the uterine spiral arteries is incomplete, and the vessels remain thick-walled and muscular.
CLASSIFICATION AND DEFINITIONS Chronic Hypertension Chronic hypertension is hypertension that is present and observable before pregnancy or that is diagnosed before the 20th week of gestation. Hypertension is defined as a blood pressure equal to or greater than 140 mmHg systolic or 90 mmHg diastolic. Hypertension that is diagnosed for the first time in pregnancy that does not resolve during the postpartum period is also defined as chronic hypertension.
Preeclampsia The pregnancy-specific syndrome of preeclampsia usually occurs after 20 weeks’ gestation, although it may occur earlier with gestational trophoblastic or collagen vascular disease. It is defined by an increase in blood pressure associated with proteinuria. Blood pressure elevation is defined as a blood pressure equal to or greater than 140 mmHg systolic or 90 mmHg diastolic in a woman who was normotensive prior to 20 weeks’ gestation. In the past, a rise in blood pressure of 30 mmHg systolic or 15 mmHg diastolic was used as a diagnostic criterion even when the absolute values were below 140/90 mmHg. This definition is no longer included because the only available evidence shows that women in this group are not likely to experience increased adverse outcomes. According to the National Heart, Lung, and Blood Institute Working Group, however, women who demonstrate an elevation of more than 30 mmHg systolic or more than 15 mmHg diastolic above baseline “warrant close observation.” Proteinuria is defined as a urinary excretion of 0.3 g of total protein in a 24-hour collection. This quantity usually correlates with a concentration of 30 mg/dl (1þ on dipstick) or greater in a random urine determination and no evidence of urinary tract infection.
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The following findings increase the certainty of the diagnosis of preeclampsia:
Blood pressure of 160 mmHg or greater systolic or 100 mmHg of greater diastolic pressure on two occasions at least 6 hours apart while patient is on bed rest Proteinuria of 2.0 g or more within 24 hours (2þ or 3þ on qualitative urinalysis) Serum creatinine >1.2 mg/dl, unless previously elevated Platelet count 4.5 Fishy odor of vaginal discharge before or after addition of 10% potassium hydroxide (i.e., the whiff test)
Table 10-1 Treatment of Vaginitis DIAGNOSIS Candidiasis Trichomonas vaginalis Bacterial Vaginosis
RECOMMENDED Butoconazole 2% cream, 5 g intravaginally for 3 days
ALTERNATIVE
PARTNER
Fluconazole, 150-mg oral None recommended tablet for uncomplicated VVC Metronidazole, 2 g orally in a Metronidazole, 500 mg Metronidazole, 2 g single dose twice a day for 7 days orally in a single dose Metronidazole, 500 mg orally, Metronidazole, 2 g orally No treatment twice a day for 7 days or in a single dose or metronidazole gel 0.75%, one clindamycin, 300 mg full applicator (5 g) orally, twice a day for 7 intravaginally, once a day for 5 days days
IN PREGNANCY Topical azole therapy only Metronidazole, 2 g orally in a single dose Metronidazole, 500 mg orally twice a day for 7 days or metronidazole gel 0.75%, one full applicator (5 g) intravaginally, once a day for 5 days
Centers for Disease Control and Prevention: Sexually transmitted diseases treatment guidelines 2002, MMWR Morb Mortal Wkly Rep May 10, 2002;51(RR-6):1–80. VVC, Vulvovaginal candidiasis.
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TREATMENT All patients at risk for STDs should be referred for HIV screening and should be counseled regarding safe sex practices. Treatment as recommended by the CDC is listed in Table 10-1.
Bibliography Brook I: Microbiology and management of polymicrobial female genital tract infections in adolescents, J Pediatr Adolesc Gynecol 2002;15(4):217–226. Burtin P, Taddio A, Ariburnu O, et al: Safety of metronidazole in pregnancy: A metaanalysis, Am J Obstet Gynecol 1995;172:525–529. Centers for Disease Control and Prevention: Sexually transmitted diseases treatment guidelines 2006, MMWR Morb Mortal Wkly Rep Aug 4 2006;55(RR-11):49–55. Marx JA (ed): Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 5. Mosby: St Louis, 2002. Stevens DL: Invasive group A streptococcus infections, Clin Infect Dis 1992;14:2–13. Stevens DL: The toxic shock syndromes, Infect Dis Clin North Am 1996;10:4. Vaginitis. In Harwood-Nuss DL, et al: The Clinical Practice of Emergency Medicine, ed 3. Lippincott, Williams & Wilkins: Philadelphia, 2001, pp 394–396. The Working Group on Severe Streptococcal Infections: Defining the group A streptococcal toxic shock syndrome: Rationale and consensus definition, JAMA 1993;269 (3):390–391.
Chapter 11
Hematologic Emergencies Acute Bleeding Diathesis MICHAEL K. SHAFE ICD Codes: Congenital factor VIII 286, Congenital factor IX 286.1, Congenital factor XI 286.2, Congenital deficiency of other clotting factors 286.3, Von Willebrand’s disease 286.4, Hemorrhagic disorders due to intrinsic circulation anticoagulants 286.5
Key Points Bleeding is caused by failure of either the ‘‘intrinsic’’ or ‘‘extrinsic’’ pathways. The intrinsic pathway is associated with the partial thromboplastin time (PTT) and the extrinsic pathway is associated with the prothrombin time (PT). An understanding of these two pathways leads to the different treatments of bleeding diathesis. ! Emergency Actions ! Rapid assessment of the patient’s vital signs is imperative. A quick history can usually direct the practitioner to the cause of the bleeding.
DEFINITION Excessive hemorrhage can result from the following: (1) platelet disorders, (2) coagulation factor disorders, (3) fibrinolytic disorders, (4) vascular abnormalities, and (5) drug ingestion.
PATHOLOGY Injured tissue releases tissue factor, also termed tissue thromboplastin or factor III. The release of tissue factor stimulates the clotting cascade and exposes collagen for platelet adherence. The formation of a clot is a two-step process. The first step is platelet adherence to the site of vascular injury and formation of a primary hemostatic plug. The second is activation of the clotting cascade with deposition of fibrin and subsequent crosslinking of the fibrin to form an insoluble fibrin clot. Excessive bleeding may be caused by a defect of either process. Platelets are an enucleated discoid-shaped cellular blood component responsible for the initiation of clot formation. Their surfaces contain 555
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several binding proteins that allow platelets to attach to damaged tissue (assisted by von Willebrand’s factor [vWF]). Platelets will also link to each other via GIIb IIIa receptors. Once a platelet attaches to injured tissue, it releases vasoactive substances that recruit other platelets and stimulate the clotting cascade. Platelets contain many clotting and vasoactive substances, including fibrinogen, fibronectin, factors V and VIII, thromboxane A2, serotonin, and fibrinolytic inhibitors. Platelets have a serum half-life of about 9–11 days and are rendered dysfunctional by aspirin, clopidogrel bisulfate (Plavix), and GIIb-IIIa inhibitors. Platelet-induced bleeding abnormalities can be caused by medications, thrombocytopenia, and inherited or acquired platelet disorders. A prolonged bleeding time, with a normal PT and PTT, usually indicates a problem with platelets. Most platelet disorders will present with increased bruising, petechiae, epistaxis, or oral cavity hemorrhage. Coagulation factor disorders will typically present with hemarthrosis, intracranial, or deep muscle hemorrhage. Coagulation factors are proteins formed in the liver and endothelial tissues that, when activated, lead to the deposition and formation of insoluble fibrin. These proteins are called “factors” and are enumerated I, II, III, and so on for the order in which they were discovered (except for vWF). The clotting cascade is initiated by one of two pathways: “intrinsic” and “extrinsic.” Both of these pathways’ final proteins are the same, named the “common pathway.” The intrinsic pathway can be initiated by exposed collagen, platelets, or both. The intrinsic pathway is XII, XI, IX, which initiates the common pathway of X, II, XII, and I. Any defect or deficiency of the intrinsic pathway will cause the PTT to be elevated. Almost all cases of hemophilia will involve an elevated PTT. Heparin therapy is measured by the PTT. It binds antithrombin (i.e., antithrombin III) and inhibits many of the intrinsic and common pathway factors. The extrinsic pathway is initiated by factor III (i.e., tissue thromboplastin) released from damaged tissue, which activates factor VII and subsequently the common pathway. Defective or low levels of factor VII will elevate the PT. Factor VII has the shortest half-life (approximately 4.5 hours) of all the coagulation proteins. Thus, significant tissue damage will deplete factor VII levels and elevate the PT. Sodium warfarin therapy is measured by the elevations of the PT and international normalized ratio (INR). The activation of several factors in both the intrinsic and extrinsic pathways requires calcium as a cofactor. Calcium is a required electrolyte for normal coagulation. In fact, it is so important that it was named factor IV. Abnormal bleeding resulting from fibrinolytic disorders are rare and are caused by overactivation of plasmin, antithrombin (antithrombin III), or thrombomodulin. These proteins make up most of the anticoagulation system and maintain homeostasis with the coagulation proteins.
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Disorders of the fibrinolytic system usually cause a hypercoagulable state as a result of deficiencies of protein c, s, antithrombin, or a genetic mutation of factor V (i.e., Leiden mutation). The Leiden mutation is the most common hypercoagulable disorder, affecting 1 in 20 people. It renders factor V resistant to inactivation by activated protein C and increases the risk of deep venous thrombosis formation. Vascular bleeding is caused by defects in the supportive or connective tissue. There are several inherited disorders leading to defects in vascular wall formation and subsequent hemorrhagic diathesis. Most are induced by systemic inflammatory disorders such as Henoch-Schönlein purpura, Wegener’s granulomatosis, systemic lupus erythematosus, rheumatoid arthritis, and polymyositis. These can present with petechiae, purpura, and ecchymosis. The PT, PTT, platelet count, and bleeding times are all normal. Inflammatory disorders will have an elevated sedimentation rate. Vascular bleeding may also be acquired. Acquired vascular abnormalities include senile tissue, steroid induced atrophy, and scurvy.
CLINICAL PRESENTATION Patients can and will present with varied presentations. Gum bleeding, increased bruising with trivial injury, petechiae, joint edema, and effusions. Patients with central nervous system bleeding can present with altered mental status.
EXAMINATION Patients should have a complete physical examination, including examination of the retina, oral mucosa, and joint function and pain throughout the body.
LABORATORY FINDINGS Laboratory workup should include measurements of PT, PTT, INR, complete blood count (CBC), and bleeding time. If disseminated intravascular coagulopathy is suspected, fibrinogen levels, fibrin split products, and D-dimer should also be analyzed. Chemistry tests to be performed should include calcium. Direct drug-induced bleeding diathesis is most commonly caused by heparin, low-molecular-weight heparin, warfarin, clopidogrel (Plavix), and aspirin therapy. Indirect drug-induced bleeding may result from liver failure or thrombocytopenia resulting from bone marrow suppression.
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DIAGNOSIS Any patient presenting with abnormal bleeding or difficult hemostasis should be evaluated with a detailed history and physical examination. Particular attention should be paid to the location and frequency of the hemorrhage as well as family history.
TREATMENT Treatment should be directed at the underlying proximate cause of the bleeding diathesis. Factor defects or deficiencies will respond to specific factor replacement. In the face of idiopathic bleeding, an elevated PT and PTT should be treated with fresh frozen plasma (FFP). If the PT and PTT are normal and the patient has an elevated bleeding time, platelet transfusion should be considered. If the patient is bleeding and has thrombocytopenia, platelet transfusion will also be necessary. Heparin toxicity should be treated with protamine sulfate, and warfarin toxicity will require vitamin K replacement and possibly FFP. Patients bleeding as a result of antiplatelet toxicity will respond to platelet transfusion and cessation of the medication.
Bibliography Hoffman R, Benz EJ, Shattil SJ, et al: Hematology: Basic Principles and Practice, ed 4. Elsevier: New York, 2005. Marx J: Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 5. Mosby: St Louis, 2002.
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Blood Transfusions JOHN ROBERT SCOTT
ICD Code: V59.01
Key Points Whole blood is almost never used for transfusions anymore. The threshold for transfusing red blood cells (RBCs) is now 8 g/dl. Each unit of platelets (random donor platelets; RDP) will raise the platelet count by 5000 to 10,000. In a nonbleeding patient, the threshold for transfusing platelets is 10,000. Transfusion-related acute lung injury can occur with FFP transfusions. Between 4 and 6 units of FFP will increase a patient’s clotting factors by 10% ^20%. Transfuse cryoprecipitate for fibrinogen less than 100 mg/dl. Each unit of cryoprecipitate will raise the fibrinogen level by 5^10 mg/dl. Leukoreduced blood products decrease the risk of human leukocyte antigen (HLA) alloimmunization, cytomegalovirus (CMV) infection, and transfusion-associated graft-versus-host disease (TA-GVHD). Irradiated blood products inactivate T lymphocytes and prevent TA-GVHD. Saline-washed blood products help to prevent allergic transfusion reactions.The universal donor is Oþ in all patients except women of childbearing age (for whom it is O). A massive blood transfusion is 50% ^100% of a patient’s blood volume in a 24-hour period. A hemolytic transfusion reaction is due to the transfusion of ABO-incompatible blood. A delayed hemolytic transfusion reaction is seen days to months later due to an anamnestic antibody response to minor RBC antigens. Febrile transfusion reactions are usually due to antibodies against donor leukocytes, but rarely can be due to bacterial contamination of donor blood products. Urticaria occurs in 3% of transfusions due to antibodies against plasma protein antigens. Anaphylactic transfusion reactions occur most often in immunoglobulin (Ig) A^deficient patients with anti-IgA antibodies (IgE). Hepatitis B infection occurs in approximately 1 in 50,000 units, hepatitis C infection in approximately 1 in 10,000 units, and human immunodeficiency virus (HIV) infection in approximately 1 in 150,000 units.
BLOOD COMPONENTS Blood is made up of noncellular and cellular components. FFP, albumin, and cryoprecipitate are all noncellular components of blood. RBCs, platelets, and white blood cells (WBCs) are cellular components of blood.
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Whole Blood A unit of whole blood contains approximately 450–500 ml of venous blood in 70 ml of a citrate-based anticoagulant solution at an average hematocrit of 40% (range, 36%–44%). A unit of stored whole blood lasts 21–35 days, depending on the citrate-based anticoagulant used. Whole blood is almost never used anymore. It has been replaced by component-specific blood products.
Packed Red Blood Cells Packed RBCs are made by removing 200–250 ml of plasma from whole blood. The typical volume is 250–300 ml per bag. Each bag will raise the patient’s hemoglobin approximately 1 g/dl (hematocrit 3%). Additive solutions are anticoagulant-preservative solutions that contain varying concentrations of adenine, which allow increased storage of RBCs to a maximum of 42 days. Packed RBCs may undergo further processing for specific indications, including leukocyte reduction, irradiation, or saline washing. The generally accepted threshold for transfusion of packed RBCs has recently been changed from a hemoglobin concentration goal of approximately 10 g/dl to a goal of 7 g/dl because of a recent randomized, prospective study. This hemoglobin concentration goal does not apply to trauma patients. RBCs may be frozen to significantly increase storage time. Glycerol penetrates the RBCs and allows them to freeze without causing damage to the cells. This technique is useful for rare blood types, autologous transfusions, and stockpiling reserves.
Platelets Platelet concentrates (RDP) are prepared by the centrifugation of 1 unit of whole blood. The RDP pool size is established by the individual hospital transfusion service. Single donor platelets (SDP) are prepared with an apheresis technique. One RDP unit contains platelets concentrated in 40–70 ml of plasma, and one SDP unit contains platelets concentrated in 200–300 ml of plasma. Between 5 and 6 units of RDP are equivalent to 1 unit of SDP. A provider will often order a “six-pack” of platelets, which means 6 units of RDP. Each unit of RDP will raise the patient’s platelet count 5000–10,000/ml. The standard six-pack of RDP will therefore raise the platelet count 30,000–60,000/ml. A single unit of SDP will raise the patient’s platelet count by the same amount (30,000–60,000/ml). SDP units are primarily used in patients who require long-term transfusions to prevent alloimmunization to HLA (anti-HLA antibodies) or platelet-specific antibodies. This practice, while common, is not supported by the Trial to Reduce Alloimmunization to Platelets (TRAP) Study Group. Because platelets cannot be frozen and must be stored with gentle
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agitation to maintain their activity, the storage time until expiration is only 5 days. Generally, platelet transfusion is indicated for platelet counts below 10,000/ml in the absence of bleeding. The range is 20,000– 50,000/ml, depending on local practice. Transfusion should be performed for counts less than 50,000 per microliter in actively bleeding patients or patients with a planned surgical procedure (100,000/ml for neurosurgery or ophthalmological surgery). Rh-negative patients should receive Rhnegative platelets; this is because of the approximately 0.1 ml of RBC contamination per unit of RDP. Platelets do not have Rh antigens. Alternatively, a standard injection of RhoGam can be given to Rh-negative patients who receive Rh-positive platelets. Be aware that platelets are stored at room temperature and they are therefore more susceptible to bacterial contamination. Pay particular attention to fevers, chills, rigors, and hypotension in patients receiving platelet transfusions because these signs and symptoms could represent a septic transfusion reaction. Beginning March 1, 2004, bacterial testing of platelets was mandated by voluntary standard-setting organizations to help mitigate this risk.
Fresh Frozen Plasma One unit of FFP is prepared by the centrifugation of 1 unit of whole blood. It contains 200–250 ml and has a storage time to expiration of 1 year. FFP contains all the coagulation factors, anti-thrombin III, protein C, protein S, fibrinogen, and albumin. The clinician should be aware of patients who experience shortness of breath or decreasing oxygen saturations while receiving FFP. Transfusion-related acute lung injury (TRALI) occurs during transfusions with plasma. A noncardiogenic pulmonary edema occurs due to alveolar membrane damage and capillary leak. Transfusions of preformed antibodies against the recipient’s leukocytes cross-react with the recipient’s alveolar membrane and cause transfusion-related acute lung injury. This should not be confused with febrile nonhemolytic transfusion reactions, which are caused by recipient antibodies to donor leukocytes. The typical dose of FFP transfused is 4–6 units or 10–20 ml/kg. This dose will increase all of a patient’s coagulation factors by 20%.
Cryoprecipitated Antihemophilic Factor (Cryoprecipitate) Cryoprecipitate is derived from the centrifugation of 1 unit of FFP after it is slowly thawed. The unit of cryoprecipitate is then refrozen with only 10–15 ml of plasma and has a storage time of 1 year. Each unit of cryoprecipitate contains 80–120 units of factor VIII (both factor VIII:C and factor VIII:vWF) and 150–250 mg of fibrinogen and fibronectin. Cryoprecipitate was used to treat patients with hemophilia in the past, but this is no longer necessary due to the development of factor-specific products.
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Cryoprecipitate is now primarily used to replace fibrinogen (below 100 mg/dl). Cryoprecipitate does not need to be type-specific because it has such little plasma. However, hemolysis can occur after large volumes of cryoprecipitate have been given. Each unit of cryoprecipitate will raise the fibrinogen level 5–10 mg/dl. A typical dose is 10 units.
Leukoreduced Blood Products Leukoreduction techniques can be used for RBC and platelet units. The units are filtered before storage or at the bedside. Current third-generation leukocyte filters are capable of removing more than 99.99% (4-log reduction) of leukocytes with less than 10% RBC loss. WBCs have HLA antigens (RBCs and platelets do not). Recipients of blood products form antibodies against these antigens. The antibodies cause transfusion reactions, and it becomes harder and harder to give these patients blood products. CMV is transmitted through the WBCs of a CMV-positive donor to an immunosuppressed CMV-negative recipient. Most persons are CMV-positive and are therefore immune to an acute CMV infection. Active donor WBCs can attack an immunosuppressed recipient, causing TA-GVHD. Leukoreduced blood products decrease the risk of HLA alloimmunization, CMV infection, and TA-GVHD.
Irradiated Blood Products RBC, platelet, and nonfrozen plasma units contain active T lymphocytes that are capable of causing TA-GVHD. These units are exposed to 15– 20 gray of gamma radiation to inactivate T lymphocytes and prevent TA-GVHD.
Saline-Washed Blood Products “Washed” RBC and platelet units are used to remove plasma proteins, antibodies, and electrolytes. The units are washed with normal saline in a standardized fashion. The technique removes 99% of the plasma proteins but also removes 20% of RBCs and 30% of platelets. The washing process also removes 90%–99% of leukocytes (but not enough to prevent HLA alloimmunization). Washed RBCs must be used within 24 hours, and washed platelets must be used within 4 hours. Saline-washed blood products help prevent anaphylactic transfusion reactions in IgA-deficient patients.
TRANSFUSIONS Blood transfusions should be administered through large-gauge intravenous tubing with a Y device so that warmed normal saline can be infused
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at the same time as the blood. Glucose- or calcium-containing solutions should not be used at the same time that the transfusion is being performed. Blood should always be warmed before administration. Cold blood can precipitate hypothermia. Pressure in infusion devices can be used, but they should not be inflated to greater than 300 mmHg. All transfused blood should be type specific and should be crossmatched when possible. In an emergency when blood is required immediately, type O blood can be used. Rh-positive O blood should be given to male patients, and Rh-negative O blood should be given to women of childbearing age. Type-specific, cross-matched RBCs should be given as soon as it is possible. Most military studies have been based on O-positive blood, and most civilian studies have been based on the use of O-negative blood. Autotransfusion is the reinfusion of the patient’s blood by collecting the blood from the thorax or peritoneal cavity after washing and antibiotic administration. A massive blood transfusion is when 50% of the patient’s blood volume is transfused in a 24-hour period or when 50% is transfused at one time. Massive blood transfusions have many complications, including acute respiratory distress syndrome, hypothermia, hypocalcemia, citrate toxicity, and coagulopathies.
TRANSFUSION REACTIONS There are four types of transfusion reactions: hemolytic, delayed hemolytic, febrile, and allergic.
Hemolytic Reactions A hemolytic blood transfusion reaction is due to transfusion of ABOincompatible blood. Most often this is due to a mislabeled blood sample or mislabeled blood products. Rapid destruction of transfused RBCs take place as a result of an antibody-mediated reaction. When RBCs are destroyed there is a release of free hemoglobin, which causes hemoglobinuria, hemoglobinemia, elevation of bilirubin, and depletion of haptoglobin. Anesthetized patients will develop hypotension. Patients who are awake will report low back pain, shortness of breath, fever, chills, and a burning sensation at the site of the blood transfusion. Patients with a hemolytic reaction develop hemoglobin in the urine, free hemoglobin in the blood serum, a direct and indirect Coombs’ test result, and coagulation problems. A red-topped tube and a lavendertopped tube should be sent to the blood bank for testing. A rapid, bedside screening sample for hemolytic reaction is taken to centrifuge in a CBC tube. If the color of the centrifuged blood is pink, it suggests free
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hemoglobin at levels of 50–100 mg/dl. If the centrifuged blood is pale brown, hemoglobin concentration is at a level below 20 mg/dl. The appropriate treatment of a hemolytic reaction is immediate discontinuation of the transfusion. Aggressive supportive care should be initiated, including endotracheal intubation, central venous access, arterial blood pressure monitoring, and vasopressor medications, where indicated. Very large amounts of normal saline should be used to maintain blood pressure and to increase urinary outflow. End points of fluid resuscitation include urine output of 0.5–1 ml/kg/hr or central venous pressure of 8–12 mmHg. Central venous pressure monitoring should be used in the event of anuric renal failure. Furosemide may be helpful in preventing renal failure but will render urine output invalid as an end point of fluid resuscitation.
Delayed Hemolytic Reactions Delayed hemolytic transfusion reactions can be seen several days to months after the transfusion. A decrease in hemoglobin level helps the clinician to make the diagnosis. The patient may report vague symptoms such as chills, myalgia, and low back pain. This reaction occurs as a result of the transfused RBCs becoming coated with antibodies and being removed by the tissue-bound macrophages in the spleen. Patients may have previously been sensitized to minor blood group antigens, but their antibody levels fall below detectable levels during the cross-match process. After transfusion, an anamnestic antibody response occurs, usually within 2 weeks. Only the transfused RBCs are destroyed, but occasionally this is enough to cause renal failure. If a delayed hemolytic reaction is suspected, blood should be sent to the blood bank for testing. Often the antibodies to these minor antigens will subside again, putting the patient at risk for recurrent problems. Treatment is supportive.
Febrile Reactions Febrile transfusion reactions are the most common reactions. Patients develop chills, malaise, and fever. Febrile reactions are frequently seen in multiparous patients and patients with a history of multiple transfusions due to their heavy exposure to foreign leukocytes. Fever usually occurs because of antibodies against donor leukocytes. A rarer cause of febrile reactions is transfusion of blood products contaminated with bacteria. Gram-negative bacteria such as Yersinia species and Pseudomonas species can multiply in refrigerated blood products. The fever seen in these patients is due to infusion of preformed endotoxin. Both donor and patient blood should be sent to the laboratory for culture and Gram stain. Treatment should include antibiotics and aggressive support. Anytime a febrile
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reaction occurs, the transfusion should be stopped and a blood sample from both donor and patient should be sent to the laboratory for analysis. Very rarely, leukocyte antibodies can produce lung injury and noncardiogenic pulmonary edema.
Allergic Reactions (Urticarial and Anaphylactic) Allergic transfusion reactions are of two types: urticarial and anaphylactic. Urticaria is seen in 3% of all transfusions. It is usually due to antibodies against minor donor plasma proteins. The transfusion should be stopped and blood work sent to the laboratory for analysis. The patient should respond to antihistamine therapy such as intravenous diphenhydramine. Anaphylactic transfusion reactions are seen in rapid un–cross-matched blood transfusions. They are usually seen in IgA-deficient recipients with anti-IgA antibodies who have a history of numerous allergies. The antibodies against IgA are IgE-type antibodies. When standard blood products (which contain IgA plasma proteins) are transfused, anaphylaxis occurs. A similar phenomenon occurs in patients deficient in haptoglobin. If an anaphylactic reaction occurs, the transfusion should be stopped immediately. Treatment with intravenous fluids, antihistamines, and epinephrine should be given along with good supportive care.
Hepatitis B and C Hepatitis B and C screening has significantly reduced the risk of transfusion-related infection. The risk of hepatitis B infection is approximately 1 in 50,000 units. The risk of hepatitis C is approximately 1 in 10,000 units.
Human Immunodeficiency Virus The use of voluntary blood donations that are screened by questionnaire and blood testing has dramatically reduced the risk of transfusion-related HIV infection. The risk of HIV infection is approximately 1 in 150,000 units.
Transfusion-Related Hemosiderosis Remember to consider hemosiderosis in patients who receive chronic transfusions. Conditions like thalassemia and sickle cell disease cause destruction of red blood cells, but iron is recycled. Every 1 ml of packed RBCs contains 1 mg of iron. This diagnosis requires a high index of suspicion. Signs and symptoms of liver and heart failure may be seen. Treatment should include deferoxamine.
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Bibliography Fakhry SM, Sheldon GF: Blood administration, risks, and substitutes, Adv Surg 1995;28: 71–92. Gelman M: Transfusion complications. In Schaider J, Hayden SR, Wolfe R, et al: Rosen and Barkin’s 5-Minute Emergency Medicine Consult, ed 2. Lippincott, Williams & Wilkins: Philadelphia, 2003. Herbert PC, Blajchman MA: A multicenter, randomized, controlled clinical trail of transfusion requirements in critical care. Transfusion Requirements in Critical Care Investigators, Canadian Critical Care Trials Group, N Engl J Med 1999;340:409. Hoffman R, Benz EJ, Shattil SJ, et al: Hematology: Basic Principles and Practice, ed 4. Elsevier: New York, 2005, pp 2410–2411. Marx J: Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 5. Mosby: St Louis, 2002, p 51. Rakel RE: Conn’s Current Therapy 2005, ed 57. Elsevier: Philadelphia, 2005, pp 539–543.
Hemophilia MICHAEL K. SHAFE ICD Codes: Congenital factor VIII disorder 286.0, Congenital factor IX disorder 286.1, Congenital factor XI deficiency 286, von Willebrand’s disease 286.4
Key Points Hemophilia A and B are clinically indistinguishable except for activity of factor VIII and IX, respectively. The PT is normal and the PTT is elevated in both A and B.vWF activity is normal in both. ! Emergency Actions ! Many patients have specific dosing regimens recommended by their hematologists. One unit of factor concentrate per kilogram of body weight will raise the plasma activity level by 2%–2.5%. Dosing should be approximately 10–15 units/kg, which will increase the factor VIII by 20%–30%. Severe bleeding will require a correction to 50%–100% for several days. In a 70-kg person, this will require an initial bolus of 3500 units.
DEFINITION Hemophilia is a disorder involving factor deficiencies in the intrinsic pathways. The three most common types of hemophilia are (1) factor
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VIII deficiency, hemophilia A; (2) factor IX deficiency, hemophilia B; and (3) von Willebrand’s disease, a decrease in vWF activity, a distinctly separate disease process that may present clinically similar to hemophilia A and B.
EPIDEMIOLOGY Hemophilias are x-linked inherited disorders of variable penetrance. Hemophilia A occurs in approximately 1 per 5000 male births and is four to six times as common as hemophilia B, estimated at 1 per 30,000 male births. Hemophilia in females is extremely rare; both parents would have to have hemophilia. Von Willebrand’s disease is an autosomal-dominant disease with variable degrees of severity and presentation, occurring in approximately 1 per 800 persons. There appears to be no racial or ethnic propensity for hemophilia or von Willebrand’s disease.
PATHOPHYSIOLOGY Clotting factors are proteins (except factor IV) within the clotting cascade necessary to form cross-linked fibrin. They were numbered in the order they were discovered. Calcium is factor IV, which is a critical cofactor in the activation of many of the proteins. Hemophilia A and B are sexlinked recessive disorders caused by a deficiency in factor VIII and IX, respectively. The disease is further classified based on the level of factor activity:
Severe: < 2% activity Moderate: 2%–5% activity Mild: 5%–30% activity
Hemophilia A and B are clinically indistinguishable except for activity of factor VIII and IX, respectively. The PT is normal and the PTT is elevated in both A and B. vWF activity is normal in both. vWF assists platelet binding to collagen and serves as a plasma carrier for factor VIII. Low levels of vWF will also be reflected by lower than normal factor VIII levels. Like hemophilia, von Willebrand’s disease has three general categories of mild, moderate, and severe.
CLINICAL PRESENTATION Patients with hemophilia will have a variable presentation of symptoms. Most cases with less than 1% factor activity will be diagnosed within the first year of life. Approximately 50% will sustain excessive bleeding during circumcision. Many will typically present with intra-articular or intramuscular bleeding. Inadequately treated incidents of recurrent joint
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bleeding can result in chronic synovial and intra-articular hemosiderin deposits, which lead to cartilage damage and subchondral bone cyst formation. Moderate hemophilia may not be diagnosed until the age of 2–5 years, with increased incidence of falls and trauma. Mild cases may not be diagnosed until the second or third decades of life; these cases involve easy bruising, heavy menses, recurrent bleeding with mild trauma, increased hemorrhage with minor surgical procedures, or hematuria after exercise. Some patients may present with groin pain after retroperitoneal hemorrhage into the psoas facial planes.
EXAMINATION If a bleeding disorder is suspected, a thorough physical examination must be performed, including rectal, funduscopic examination (looking for retinal hemorrhages), and joint and skin examination for petechiae, purpura, and contusions. Most patients with hemarthrosis will report swelling and pain in the affected joint. Hemarthrosis may not always present with an appreciable effusion.
LABORATORY FINDINGS Any patient with a suspected bleeding disorder should have a CBC, liver function tests, and measurements of electrolytes, calcium, blood urea nitrogen, creatinine, PT, INR, PTT, and bleeding time. Hemophilia A and B will present with an elevated PTT and a normal PT and bleeding time. Bleeding time is the time necessary for two standardized cuts on the forearm of a patient to stop bleeding. The laboratory profile found with von Willebrand’s disease includes a decreased VIII-C, vWF:Ag, and vWF activity. Since vWF affects both circulating factor VIII and platelet adherence, the PTT and bleeding times can be elevated in von Willebrand’s disease. Additionally, the results of analyses of vWF:Ag, vWF activity, factor VII-C, and factor IX will usually confirm the diagnosis. If these last test results are normal, one needs to consider other factor deficiencies.
DIAGNOSIS Family history, combined with a clinical presentation of abnormal bleeding, should alert the clinician to consider confirmatory laboratory testing. Intramuscular and hemarthrosis are more common in hemophilia or severe type III von Willebrand’s disease.
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TREATMENT Most patients with hemophilia have recombinant factor at home and often will bring it with them to the hospital. Many have specific dosing regimens recommended by their hematologists. One unit of factor concentrate per kilogram of body weight will raise the plasma activity level by 2%–2.5%. Dosing should be approximately 10–15 units/kg, which will increase the factor VIII by 20%–30%. Severe bleeding will require a correction to 50%–100% for several days. In a 70-kg person, this will require an initial bolus of 3500 units. If recombinant factor replacement is not available, then cryoprecipitate is a good source of concentrations of fibrinogen, factor VIII, vWF, and fibronectin. Each unit of cryoprecipitate contains 80–100 units of factor VIII. FFP contains only 1 unit of each factor per milliliter. Four units of FFP will increase most factors by approximately 10%. Most surgical procedures may be performed once the INR is reduced to less than 1.5. Desmopressin (DDAVP) is a synthetic agent that can raise factor VIII and vWF up to 300%–400% in 30–90 minutes. It stimulates release from endothelial stores. It is only indicated for raising factor VIII levels and for type I (minor) cases of von Willebrand’s disease. The appropriate dosage is 0.3–0.4 mg/kg. DDAVP is a vasoactive substance that should be used cautiously in elderly persons or patients with a history of coronary artery disease because it may precipitate hypertension. Factor IX deficiency should be treated with recombinant factor IX. The recommended dosing is 25 units/kg for minor bleeding, 35 units/ kg for moderate bleeding, and 45 units/kg for severe bleeding. All patients with hemophilia or von Willebrand’s disease who present with a bleeding problem should have consultation performed with a hematologist, and close follow-up should be undertaken within a few days.
Bibliography Hoffman R, Benz EJ, Shattil SJ, et al: Hematology: Basic Principles and Practice, ed 4. Elsevier: New York, 2005, Chapters 114, 115, and 116. Marx J: Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 5. Mosby: St Louis, 2002.
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Sickle Cell Anemia MICHAEL K. SHAFE ICD Code: Sickle cell anemia 282.60
Key Points Sickle cell anemia is a disease of painful recurrent vaso-occlusive episodes. The condition can be life threatening when infection is present, since sickle cell patients are functionally asplenic. ! Emergency Actions ! Any patient presenting with sickle cell crisis should be treated aggressively with the administration of fluids and analgesic medications. If fever is present, a search for the source of fever must be undertaken, and appropriate antibiotics should be administered.
DEFINITION Sickle cell anemia is a chronic hemolytic anemia with the cardinal feature of recurrent painful vaso-occlusive episodes resulting from RBC deformation and occlusion of the microvasculature.
EPIDEMIOLOGY Sickle cell trait is an autosomal-dominant gene carried by 8% of the African American population in the United States; 1 in 500 of carriers has the disease state. Persons from the Caribbean and Central and South America carry the trait gene in 4% of the population, and the disease prevalence is 1 in 2000 for this group. Sickle cell disease is also prevalent in persons of Arab, East Indian, Greek, or Italian descent. It is usually diagnosed between the age of 6 months and 15 years. Up to 15% of children born with the disease will die by the age of 20 years. The median life expectancy is 42 years for men and 48 years for women.
PATHOLOGY A single DNA nucleotide mutation causes valine to be substituted for glutamic acid on the sixth position of the hemoglobin beta subunit. This hemoglobin (HbS) has a lower solubility than normal hemoglobin
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(HbA), and when exposed to low-oxygen environments HbS molecules will polymerize into long rods that deform the RBC into a sickle shape. These abnormally shaped cells cannot pass through most capillary beds and cause local occlusion of the microvasculature. This occlusion leads to local ischemia, further hypoxia, tissue infarction, and hemolysis of the RBC. This process can affect every organ, and, when severe, can lead to multisystem organ failure. Recurrent occlusive events render patients functionally asplenic and susceptible to encapsulated bacterial organisms like Streptococcus pneumoniae, salmonella, Haemophilus influenzae, and Neisseria meningitides. Sickle SC (HbSC) is a variant that is detected later in life. Patients with HbSC have fewer but just as severe crisis episodes as patients with HbSS. The former will experience similar organ system dysfunction as HbSS patients, including vaso-occlusive crisis and fat emboli syndrome from infarcted bone marrow. There are other rare variants of sickle cell disease. These include HbSB thalassemia, HbSD, and HbSF fetal persistence. The clinical presentation of these varies from asymptomatic to severe. Sickle cell trait contains one normal and one sickle gene, HbSA. This is a benign condition, which is nothing more than a carrier state. Patients neither develop sickled cells nor any clinical manifestations of sickle disease. The peripheral smear of patients with sickle cell trait is essentially normal. Any patient with sickle cell trait who demonstrates clinical or hematological symptoms should be referred to a hematologist for confirmation of HbSA or presentation of an atypical variant of the carrier state.
CLINICAL PRESENTATION Patients with HbSS will not begin to demonstrate signs and symptoms of the disease process until 6 months of age when their fetal hemoglobin dissipates. African-American children who present with hemolytic anemia symptoms, unexplained bone pain, jaundice, or recurrent right upper quadrant pain should have sickle cell anemia included in their differential diagnosis. Acute pain is the first symptom in 25% of patients with sickle cell disease. Pain is also the most frequent symptom after the age of 2 years and the most frequent reason for seeking medical attention. There are several typical “crisis” in which a patient with sickle cell anemia may present. The first and most common is acute pain crisis (some authors have replaced this term with acute painful episode). Another term for this is vaso-occlusive crisis. Bone marrow infarction and subsequent release of inflammatory mediators is suspected to be the proximate cause of acute pain or vaso-occlusive crisis.
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Splenic sequestration crisis presents similar to an acute pain crisis, except that there is splenic enlargement. Since most adults are functionally asplenic, this crisis usually occurs in children. A patient experiencing an aplastic crisis presents with a decreasing hemoglobin level, low reticulocyte count, and decrease of RBC precursors in the bone marrow. Aplastic crisis is usually precipitated by an infectious event. In children, parvovirus B19 accounts for 68% of aplastic crises in children with sickle cell disease. In adults, S. pneumoniae, salmonellae, and Epstein-Barr virus have been demonstrated to account for transient marrow aplasia. Acute chest syndrome involves chest pain, dyspnea, fever, tachypnea, leukocytosis, and pulmonary infiltrates exhibited on chest x-ray. Infections or pulmonary emboli of a thrombus or fat from the bone marrow may account for this syndrome. This crisis carries a 10% mortality rate. Male patients with sickle cell disease may present with priapism. Some literature reports the incidence as high as 42%. Immediate urological consult is necessitated for these patients.
EXAMINATION The patient should be asked whether this is a typical or severe crisis episode. A thorough history and complete review of systems inquiring about stressful precipitating events, fever, or infectious symptoms should be pursued. A detailed physical examination, including neurological and funduscopic examinations, should be performed. Pediatric patients may present with hepatomegaly and splenomegaly.
LABORATORY FINDINGS A typical crisis in most patients with sickle cell anemia may be worked up with a CBC and reticulocyte count. More severe or “worst crisis” should elicit a more aggressive evaluation, including urine analysis, liver function testing, and measurements of electrolytes, blood urea nitrogen, creatinine, PT, PTT, and INR. If infection is suspected, blood and urine cultures should be performed. If chest pain is a presenting symptom, electrocardiography, cardiac enzyme analysis, and chest radiography should be performed. Sickle cell disease is a hemolytic process. Leukocytosis, thrombocytosis, worsening anemia, and reticulocytosis should be expected. Patients experiencing aplastic crisis will present with a low WBC count, low platelet count, and a normal or low reticulocyte count. The peripheral smear may demonstrate sickled cells. The presence of sickled cells does not
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correlate with the severity of vaso-occlusive crisis or level of pain. An elevated bilirubin level will also be present.
DIAGNOSIS The diagnosis is confirmed by family history and serum electrophoresis. Finding sickled cells on a peripheral blood smear may support the initial diagnosis in the office or emergency department.
TREATMENT Supplemental oxygen should be administered if the patient is hypoxic. If the patient is dehydrated, oral hydration will usually be adequate. If the crisis is severe or if the patient is vomiting, intravenous access should be established and hydration with normal saline initiated. The goal of fluid therapy should be a euvolemic state. Care should be taken not to overload these patients with fluid because they are subject to develop pulmonary edema and heart failure. Analgesic therapy should be pursued aggressively. Nonsteroidal antiinflammatory medications and narcotics should be administered. Most patients will have a tolerance to narcotics and will require much higher doses than the average patient. It is possible for patients to experience pain and still be somnolent. The single best measure of pain control is what the patient reports to the clinician. Transfusion therapy may be indicated if the patient has an acute drop of more than 2 g/dl of hemoglobin or a hemoglobin level of 5–6 g/dl. Liberal use of transfusions is discouraged in light of patients developing resistant antibodies and becoming more difficult to find matching blood in the future. Patients experiencing stroke, acute chest syndrome, or aplastic crisis may require exchange transfusions. Priapism that does not respond to ice compress within 1 hour should prompt urology consultation. If infection is present, broad-spectrum antibiotics should be administrated. The usual organisms causing sepsis in asplenic patients are H. influenzae and S. pneumoniae. Mycoplasma pneumoniae, Salmonella typhimurium, Staphylococcus aureus, and Escherichia coli should also be considered. Patients who have received multiple transfusions and have been treated with the chelating agent deferoxamine for iron overload, secondary to those multiple transfusions, are at risk for infection with Yersinia enterocolitica infection. Hematological consultation and admission are warranted if patients with sickle cell anemia do not achieve adequate pain control after several doses of narcotics or if they require prolonged or more aggressive treatment in the office or emergency department.
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Bibliography Hoffman R, Benz EJ, Shattil SJ, et al: Hematology: Basic Principles and Practice, ed 4. Elsevier: New York, 2005, pp 591–601, 605–634. Marx J: Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 5. Mosby: St Louis, 2002.
Chapter 12
Orthopedic Emergencies Basic Principles of Orthopedic Injuries STEVEN W. SALYER
ICD Codes: See ICD codes by fractured bone
Key Points Fractures in children differ from those in adults.Children’s bones are softer and more resilient than those of adults, and their bones can sustain greater forces and more incomplete fractures. In children, greenstick fractures, or incomplete fractures of long bones, are very common. The long bone bows with incomplete angulation. A torus fracture is an incomplete fracture, or a buckling or wrinkling of a bone cortex. ! Emergency Actions ! With any fracture, a good vascular and neurological examination must be performed and documented. Soft tissue must be examined along with range of motion and strength. A good rule to live by in providing orthopedic care is that pain over a bone implies a fracture until proven otherwise. Early referral to an orthopedic surgeon for every trivial bony deformity should be the norm. When in doubt, consult orthopedics early and often.
DEFINITION Patients can experience bone fractures from falls, direct trauma, and motor vehicle accidents. The age of the patient, the underlying medical problems, and whether the injury is open or closed all determine the therapy. Fractures are described by their location, whether they are open or closed, simple or comminuted, and their position, displacement, and angulation. Valgus denotes a deformity in which the described part is angled away from the midline of the body. Varus denotes a deformity in which the angulation of the body part is toward the midline. Fractures are described as either transverse, oblique, spiral, or comminuted. Fractures in children differ from those in adults. Children’s bones are softer and more resilient than those of adults, and their bones can sustain greater forces and more incomplete fractures. In children, greenstick fractures, or incomplete fractures of long bones, are very common. 575
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The long bone bows with incomplete angulation. A torus fracture is an incomplete fracture, or a buckling or wrinkling of a bone cortex. Of most concern in children with fractures are those involving the epiphyses or cartilaginous centers at or near the end of children’s growing bones. The cartilaginous portion of the epiphysis is not seen on radiographic examination. Injuries to the epiphysis can result from either compressive or shearing forces. In children, epiphyseal injuries are quite common, whereas sprains are rare. It is common for an inexperienced practitioner to label an epiphyseal injury as a sprain. Epiphyseal injuries are commonly classified by the Salter-Harris classification system. In a Salter-Harris type I fracture, there is a slip in the provisional calcification. Often this injury is very subtle and will require comparison views. There are no germinal layer disturbances in type I fractures. Any child with pain, edema, and a negative x-ray result should be treated as having a Salter-Harris type I injury, and the area should be x-rayed in 10 days. Salter-Harris type II fractures involve the metaphysis, and often the epiphyseal plate has also slipped. There is no germinal layer involved, thus there are no growth plate disturbances in type II injuries. Type II fractures involve a slip of the growth plate plus a fracture through the epiphysis involving the articular surface. Type III fractures involve the germinal layer and thus have a potential for growth disturbances. Type IV fractures involve the metaphysis and the growth plate, and these fractures have a high rate of growth disturbances. Type V fractures involve a crush injury to the epiphyseal plate. These injuries are often difficult to diagnose on a plain radiograph. There is usually a growth disturbance involved with type V injuries. All Salter-Harris fractures require a referral to an orthopedic surgeon for treatment and follow-up.
EXAMINATION For any fracture, a good vascular and neurological examination must be performed and documented. Soft tissue must be examined along with range of motion and strength. A good rule to live by in providing orthopedic care is that pain over a bone implies a fracture until proven otherwise. Another rule is to splint the patient where he or she lies. Do not perform a reduction until you have obtained a radiograph, unless there is neurological or vascular compromise. Probably no circular casts should be applied to any sprained or fractures extremity in the ED. If a patient presents to the ED wearing a cast and experiencing pain and neurovascular compromise, the cast should be bivalved or removed entirely.
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Early referral to an orthopedic surgeon, for every trivial bony deformity should be the norm. When in doubt, call early for a consultation to the ED.
Bibliography Kasper DL, Braunwald E, Fauci AS, Hauser SL: Harrison’s Principles of Internal Medicine, ed 16. McGraw-Hill: New York, 2005. Salyer SW: The Physician Assistant Emergency Medicine Handbook. WB Saunders: Philadelphia, 1997. Tintinalli JE, Kelen GD, Stapczynski JS: Emergency Medicine: A Comprehensive Study Guide, ed 6. McGraw-Hill: New York, 2004.
Acute Back Pain STEVEN W. SALYER
ICD Codes: Back pain 724.5, Lower back pain 724.2, Intervertebral disk 722.2, Myelopathy 722.71 (see specific disk)
Key Points Any patient with lower lumbar pain should undergo an abdominal examination. If the lower lumbar pain is not easily determined or if pelvic pathology is considered in a female patient, a pelvic examination should be performed. ! Emergency Actions ! Any patient with a history of trauma, especially to the cervical spine, should have a radiograph taken of the spine. If a compression fracture is suspected, radiographs should be taken.
DEFINITION The spine is made up of 7 cervical vertebrae, 12 lumbar vertebrae, and 5 lumbar vertebrae. There are five sacral nerves that exit from the sacrum.
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There are eight paired cervical spinal roots in the cervical spine that exit from intervertebral foramina. The atlas of C1 supports the occipital condyles and the axis of C2. There are seven fascial planes of muscles in the neck. The dorsal nerve is the sensory part of the spinal cord, and the ventral root is the motor root of the spinal cord. Thus, if the ventral root is compressed, then painless weakness will occur. If only the dorsal root is compressed, only pain, without weakness, will occur. The ligament structures of the spine consist of the anterior longitudinal ligament, posterior longitudinal ligament, ligamentum flavum, intraspinal ligament, supraspinal ligaments, intratransverse ligaments, and costotransverse ligaments. Acute back pain can be caused from trauma to the vertebrae, prolapse of the disks, osteoporosis, spurs, nerve entrapments, and numerous other pathologies leading to weakness, pain, and bowel or bladder problems.
CLINICAL PRESENTATION AND EXAMINATION The patient should undress completely for the back examination. It is often very helpful to watch the patient get undressed to evaluate the patient’s range of motion. If possible, the practitioner should watch the patient walk from the waiting room to the examination room; this will give some idea of the patient’s true gait and disability. The patient should always be asked whether there is pain, weakness, numbness, and in what distribution. Are there associated bowel or bladder problems? What was the patient doing when the pain occurred? Is there radicular pain? Has the patient ever had back pain before, and is the distribution the same as before? Are there any associated symptoms (e.g., visual, auditory, pharyngeal-laryngeal symptoms)? Was the onset of pain slow or sudden? Does the pain wake the patient during the night? The healthcare provider should check for flexibility of the neck and the thoracic and lumbar spine. The neck should be checked for pain and range of motion. When there is ipsilateral neck pain that radiates into the shoulder or arm, a radicular component is present (i.e., Spurling’s sign). When the head is moved to one side and there is ipsilateral neck pain on the side of movement, there is zygapophyseal joint irritability. If there is contralateral neck pain with neck movement, then there is probably a ligamentous or muscular source of pain. The thyroid gland should be palpated for enlargement or tenderness, and the carotid and subclavian arteries should be auscultated for bruits. The neck should be examined for lymphadenopathy. The posterior neck should be palpated. The pain of occipital neuralgia can be reproduced by palpating the occipital notch. If occipital neuralgia is present, this will produce scalp numbness and a burning dysesthesia in the occipital nerve distribution.
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The first cervical rib is located directly behind the angle of the mandible, and the transverse process of the atlas is between the angle of the mandible and the mastoid process. The hyoid bone is at the level of C3. The thyroid cartilage is anterior to C4. The patient should always be asked whether he or she has dysphagia or vocal hoarseness. Dysphagia can result from pharyngeal edema or retropharyngeal hematomas. Vocal hoarseness can occur because of the stretching of the larynx, with associated edema of the sternocleidomastoid muscles and carotid sheaths. If the patient reports vertigo, tinnitus, ear and eye pain, visual aberrations, and headache, this is termed Liéou-Barré syndrome. The temporomandibular joint should always be checked when a neck examination is performed. Crepitus over the joint with weakness of the temporalis muscle is indicative of joint dysfunction. The radial and ulnar pulses should always be evaluated with a back examination, especially when upper arm weakness or paresthesia is a presenting symptom. If the radial pulse is reduced with passive shoulder abduction in association with a bruit over the subclavian artery, it suggests thoracic outlet syndrome. A complete neurological examination is necessary for every patient. No back examination is complete without a rectal examination to check for tone or masses. Any patient with lower lumbar pain should have an abdominal examination performed. If the lower lumbar pain is not easily determined or if pelvic pathology is considered in a female patient, a pelvic examination should be performed. Straight leg raises should always be performed. Pelvic tilts should be done, and an examination for a positive Patrick’s sign (i.e., loss of hip internal rotation with medial groin pain) should be performed. The patient should be asked to walk on his or her heels and toes. If the patient cannot walk on his or her heels, this suggests an L5 radiculopathy; the inability to walk on the toes suggests an S1 root involvement. Problems with squatting or rising are indicative of quadriceps weakness and thus L4 compromise. Weak hip flexion suggests L3 involvement. The inability to extend the great toe suggests L5 involvement, and calf pain suggests S1 involvement. A positive straight leg raise test result involves the reproduction of sciatic pain when the hip is flexed and the leg is straightened at the knee (placed in extension). The “strum” sign is performed when the hip and knee are in flexion and the sciatic nerve is plucked behind the knee. If this procedure reproduces pain in the back, this sign is pathognomonic for a herniated disk. The crossed straight leg raise test has a positive result when the contralateral leg is elevated, which produces sciatic pain in the symptomatic leg. A positive crossed straight leg raise test result is suggestive of a herniated disk with an impacted nerve root.
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DIAGNOSIS AND SPECIFIC BACK PAIN ETIOLOGIES Pain bilaterally in the upper extremities usually results from C6 spinal radiculopathies. Biceps tenderness is usually caused by an acute subdeltoid bursitis. A patient with a cervical soft tissue injury often presents with a history of an automobile accident, sports injury, or an accidental fall. The patient often reports “whiplash” with very few objective findings. The new, more correct term for this injury is acceleration flexion-extension neck injury. Head-on injuries with extension of the neck produce ventral tears and hemorrhages in the sternocleidomastoid muscles and ruptures of the anterior longitudinal ligament and ventral parts of the annulus fibrosis. When the patient is rear-ended, this produces injury to the dorsal area of the spine, particularly injury to the annulus fibrosis and hemorrhage to the paraspinal muscles. A patient with an acute cervical disk herniation presents with acute radiculopathy, myelopathy, or both. Neck stiffness, occipital neuralgia, and pain are present. Posterior ruptures of the cervical disk present with cervical radiculopathy. The most common cervical herniation is of C5– C6, C6 nerve root on the right side, and C6–C7, C7 nerve root on the left side. The patient presents with the appropriate dermatome pattern into the correct finger and myotome pain pattern. If long-lasting, the patient will present with the appropriate atrophy and weakness in the innervations muscles (Table 12-1). The patient often presents to the ED for pain management of the chronic degenerative disk disease resulting from cervical spondylosis or osteoarthrosis. Pain is secondary to trauma. The most commonly fractured area of the thoracic spine is the T10–T12 vertebrae. These fractures are usually the result of trauma. The most commonly fractured area of the thoracic spine is the T10–T12 vertebrae. These fractures are usually seen in female patients older than 65 years as a result of osteoporosis. These patients present with severe pain without myelopathy. A metastatic malignancy should always be considered in elderly persons with pathologic fractures without trauma. Thoracic herniated nucleus pulposus (HNP) accounts for fewer than 1% of all HNPs. A patient who presents with acute thoracic pain in a unilateral dermatome radicular pattern should have herpes zoster or diabetic thoracic radiculopathy considered in the differential diagnosis. The most common back-related symptom is lower lumbar pain. Lumbosacral pain can be caused by diverticulitis, a kidney or bladder infection, a disorder of the pancreas, a gallbladder disorder, endometriosis, pregnancy, ectopic pregnancy, gastrointestinal tract bleeding, appendicitis, or chronic pelvic pain other than musculoskeletal pathologies.
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Table 12-1 Nerve Root Motor and Sensory Function NERVE ROOT
DISK SPACE
C1–C2 C5
C1–C2 C4–C5
C6
C5–C6
Biceps and brachioradialis
C7
C6–C7
Triceps
C8
C7–T1
Triceps
L1
L1–L2
Cremasteric
L2
L2–L3
Cremasteric and abductor
L3
L3–L4
Patellar
L4
L4–L5
Patellar, gluteal
L5
L5–S1
Tibial posterior
S1
Sacral foramina
Ankle and hamstring
S2
Sacral foramina
None
S3
Sacral foramina Sacral foramina Sacral foramina Tip of coccyx
Bulbocavernosus
Scalp Thumb and shoulder Biceps, deltoid, pronator Index finger, thumb, Biceps, deltoid, and lateral pronator teres, forearm and wrist extensors Forearm and middle Pronator teres and finger triceps Little finger and Flexor carpi ulnaris, half-ring finger triceps, and hand intrinsic muscles Back to trochanter Hip flexion and the groin Hip flexion and Back and anterior abduction thigh to the level of the knee Back, upper Hip flexion, hip buttocks to abduction, and anterior thigh, knee extension medial lower leg Inner calf to medial Knee extension foot and the first two toes Lateral lower leg, Toe extension and dorsum of the ankle foot, first two dorsiflexion toes Sole, heel, and the Ankle plantar lateral edge of the flexion and knee foot flexion Posterior and medial Ankle plantar upper thigh flexion and toe extension None None
Bulbocavernosus
None
None
Anal
None
None
Anal
None
None
S4 S5 C1
REFLEX TESTED Biceps
SENSORY DISTRIBUTION
MOTOR DISTRIBUTION
Lower lumbar pain that is made worse by ambulation can result from peripheral vascular disease. Parasagittal brain tumors and thoracic root lesions can also cause back pain. Neurofibromata can cause lover lumbar pain because of the compression of a nerve root. Thoracic nerve root lesions are usually worse at night while the patient is reclining and are
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improved when the patient is in the standing position. A patient can also present with an S1, tibial nerve entrapment in the tarsal tunnel, behind the medial ankle malleolus, which can present as lumbosacral pain.
LABORATORY FINDING Laboratory examinations are usually of little help in the diagnosis of back pain. An erythrocyte sedimentation rate (ESR) or C-reactive protein (CRP) test and a complete blood count (CBC) may be helpful, along with a rheumatoid factor analysis, in differentiating the cause of back pain. Any female patient with lower lumbar pain should have a urinalysis and a pregnancy test performed if she is in her childbearing years.
RADIOGRAPHS Any patient with a history of trauma, especially to the cervical spine, should undergo radiographs of the spine. If a compression fracture is suspected, radiography should be performed. Without a history of trauma, in most cases, radiographs of the spine are of little help in the diagnosis of acute back pain. Magnetic resonance imaging (MRI), computed tomography (CT), and myelography can be used to determine whether a fracture or HNP is present. Electromyography and nerve conduction velocity are used to evaluate degrees of progressive motor impairment or to determine the level of neural compromise. Cervical spinal evoked potential can be used to determine cervical spinal myelopathies and thoracic outlet syndromes.
TREATMENT The majority of cervical, thoracic, and lumbar pain can be treated with nonsteroidal, anti-inflammatory drugs and pain medications (e.g., indomethacin, naproxen, ibuprofen) on an outpatient basis. Early bed rest with ice and heat applied to the affected area for 24–72 hours is the key to early recovery. Physical therapy is essential for recovery from injuries sustained at work. All patients should receive follow-up in 72 hours to evaluate whether the pain is decreasing and to determine whether further testing is required.
Bibliography Kasper DL, Braunwald E, Fauci AS, Hauser SL: Harrison’s Principles of Internal Medicine, ed 16. McGraw-Hill: New York, 2005. Salyer SW: The Physician Assistant Emergency Medicine Handbook. WB Saunders: Philadelphia, 1997. Tintinalli JE, Kelen GD, Stapczynski JS: Emergency Medicine: A Comprehensive Study Guide, ed 6. McGraw-Hill: New York, 2004.
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Acute Knee Pain HOWELL J. SMITH III
ICD Codes: Osteoarthritis 715.9, Meniscal tear 836.2, Anterior horn meniscus 836.1, Posterior horn meniscus 836.1, Knee collateral lateral 717.81, Knee collateral medical 717.82, Knee cruciate anterior 717.83, Knee cruciate posterior 717.84, Gout 274.9, Rheumatoid arthritis 710.0, Tibia fracture (closed) 823.80, Tibia fracture (open) 823.92, Fibular fracture (closed) 823.81, Fibular fracture (open) 823.92, Femur fracture (closed) 821.0, Femur fracture (open) 820.11
Key Points The most common diagnoses for adult acute knee pain are osteoarthritis (34%), meniscal injury (9%), ligamentous injury (collateral [7%] and cruciate [4%]), gout (2%), fracture (1.2%), rheumatoid arthritis (0.5%), infectious arthritis (0.3%), and pseudogout (0.2%). ! Emergency Actions ! The neurovascular status should be evaluated first for patients with any extremity traumatic injury. Any neurovascular deficiency is a true medical/surgical emergency.
DEFINITION The knee is the largest articulating joint in the body. It involves three bones: the distal femur, the proximal tibia, and the patella. There are four ligaments involved: the anterior and posterior cruciate ligaments and the medial and lateral collateral ligaments. Additionally, the knee has the medial and lateral menisci.
EPIDEMIOLOGY Knee pain is one of the most common musculoskeletal reasons patients seek medical care. In 2000, more than 12.5 million persons presented for care of knee pain, making knee pain the fifth overall reason for doctor
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visits. The differential causes for knee pain are numerous, including referred pain from the hip or ankle, chronic causes with acute exacerbations, trauma, and inflammatory processes. The most common diagnoses for adult acute knee pain are osteoarthritis (34%), meniscal injury (9%), ligamentous injury (collateral [7%] and cruciate [4%]), gout (2%), fracture (1.2%), rheumatoid arthritis (0.5%), infectious arthritis (0.3%), and pseudogout (0.2%). The remaining causes include sprains and strains. Most acute injuries to the knee occur during sporting, motor vehicle, or occupational accidents. More than 3 million Americans sustain knee injuries annually, and knee trauma is the second leading cause of occupational accidents. The causes for knee pain in children differ from those of adults. Growth plate injuries (Salter-Harris fractures) of the femur, tibia, and fibula are more common than ligamentous fractures in skeletally immature children.
PHYSICAL EXAMINATION The examination of the knee is composed of several components. A detailed medical history and, in the case of trauma, a careful detailed description of the mechanism of injury followed by a meticulous physical examination to include specific knee tests are helpful in formulating a diagnosis and effective treatment plan for the patient. Additionally, as indicated, serum laboratory and imaging studies and arthrocentesis can be performed to give the clinician additional insight that will lead to a presumptive diagnosis. The acutely injured knee should be examined as soon as possible after injury because edema, point tenderness, and discoloration are initially localized over the injured structures. For ambulatory patients, the examination begins by assessing gait. The patient should be dressed to allow full exposure of both lower extremities from the feet to the upper thighs. Both lower extremities should be inspected for symmetry (e.g., quadriceps atrophy or knee effusion), skin should be examined for irregularity (e.g., erythema, ecchymosis, abrasions, wounds), and range of motion should be assessed. The examiner should carefully palpate the bony structures, joint lines, muscles, ligaments, tendons, bursae, and popliteal area, noting areas of tenderness or edema. Generally, range of motion and other specialized tests are performed on the uninjured knee first. Since many of the knee’s contours disappear when the knee is fully extended, more accurate diagnosis can be obtained when the knee is palpated in a flexed position. The patient should sit on the examination with the examiner sitting on a stool, facing the patient. The extensor mechanism should be palpated, proceeding from proximal to distal and including the quadriceps tendon, patella, patellar tendon, and tibia tubercle. The examiner should then proceed to the femoral
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condyles and should palpate the prepatellar and pes anserine bursae. The medial and lateral joint lines should be palpated for defects and tenderness, and the medial and lateral collateral ligaments and the tibial plateaus should also be palpated. The posterior area of the knee should be palpated for the pulse of the popliteal artery. Since it is well protected, injury is rare; however, suspicion of injury to popliteal artery is an emergency that requires immediate orthopedic and/or vascular consultation because damage must be repaired within hours to avoid potential amputation. A thorough neurovascular examination is essential. The popliteal nerve and vessels can be injured with posterior knee dislocation or with a femoral supracondylar fracture. Peroneal nerve injury can occur with lateral knee traumatic injuries. The bulge and patella ballottement tests are commonly used to detect for the presence of an effusion. Both tests are performed with the patient in the supine position with the knee extended and relaxed. The bulge test is performed by the clinician massaging or “milking” the suprapatellar pouch distally, with the examiner looking for a bulge at the medial sulcus. The examiner performs the patella ballottement test by applying downward pressure to the patella, compressing it against the femoral condyle. If an effusion is present, the examiner will appreciate a click. Range of motion is measured with the patient lying supine. The patient should be instructed to raise the entire lower extremity, with the knee fully extended, off the table. The patient is then instructed to flex the knee as far as possible (trying to touch the posterior thigh with the heel of the foot). The patient is then instructed to fully extend the knee. Normal knee range of motion is 0 degrees of extension to 135 degrees of flexion. A multitude of different manual specialized tests have been described to assess for cartilaginous tears and ligamentous injury to the knee. Due to the wide variation of ligamentous laxity among individuals, the uninjured knee should be examined first to establish a baseline. The McMurray test is used to detect tears in either the medial or lateral meniscus. The patient is placed in the supine position, and the knee is passively flexed. To test the medial meniscus, the leg is internally rotated by grasping the ankle with one hand and applying a slight valgus stress to the knee with the other, then slowly bringing the knee to full extension. To test the lateral meniscus, the leg is externally rotated and varus stress is applied. If the clinician appreciates a palpable or audible click at the joint line when the knee approaches full extension, suspicion for meniscus tear is raised. The valgus stress test is performed to assess the integrity of the medial collateral ligament. The patient is examined in the supine or sitting position with the examiner supporting the lower extremity to facilitate complete relaxation of the quadriceps and hamstring muscles. The examiner places one hand on the lateral aspect of the knee and the other hand on the medial ankle. Valgus stress is applied as the examiner pushes medially
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against the knee and pulls laterally at the ankle. The test is then repeated with the knee flexed at 30 degrees. Laxity or significant subjective pain along the medial joint line indicates injury to the medial collateral ligament. Medial collateral ligament injury is more common. The varus stress test is performed in either the supine or sitting position described previously for the valgus stress test. The examiner places a hand on the medical aspect of the patient’s knee and the other hand on the patient’s lateral ankle. Varus stress is applied as the examiner pushes laterally on the knee and medially at the ankle. Tests are performed with the knee at 0 and 30 degrees of flexion. Laxity or significant subjective pain along the lateral joint line indicates lateral collateral injury. The integrity of the anterior cruciate ligament is best assessed by Lachman’s test. The patient is placed in the supine position and the examiner stands next to the injured knee. The examiner then stabilizes the distal femur just above the knee with one hand (which prevents movement and hamstring relaxation) and passively flexes the knee to 15 degrees with slight external rotation. The tibia is then grasped with the other hand just below the knee, and a downward motion is applied to the femur while an upward motion is applied to the tibia. If the anterior cruciate ligament is intact, the degree of tibial translation in relationship to the femur should be equal to that of the uninjured knee. A positive result is when the tibia translates anteriorly (more than 5 mm) on the femur, without a discrete end point. Anterior cruciate ligament injury is relatively common and can occur from a variety of mechanisms. The integrity of the posterior cruciate ligament is assessed by pushing the tibia posteriorly. Posterior movement of the tibia is suggestive of a posterior cruciate ligament tear. Injury to the posterior cruciate ligament is indicative of major injury. Acute atraumatic knee pain can be the result of several etiologies, including septic arthritis, gout, pseudogout, or acute exacerbation of chronic conditions, including degenerative joint disease and rheumatoid arthritis. The knee is the most common site for benign and malignant tumors than any other joint.
RADIOGRAPHS Plain radiographic anteroposterior and lateral views are commonly used to assess for fractures, avulsions, and dislocation of the patella, femoral condyles, tibial tuberosity, and tibial plateau. The Ottawa rules criteria have been suggested to determine when radiography should be performed for patients with acute knee pain after trauma. The criteria dictate that radiographs should be obtained for patients older than 55 years who have clinical tenderness at the head of the fibula or isolated tenderness of the patella; patients unable to flex the knee to 90 degrees; and patients who are unable to bear weight on the extremity for at least four steps.
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An MRI evaluation is not commonly part of the ED workup. MRI is helpful to evaluate the menisci, ligamentous structures, and chondral surfaces; however, many orthopedic surgeons forgo MRI and proceed with knee arthroscopy to further assess internal knee integrity. Arteriography should be performed rapidly if there is a suspicion of injury to the popliteal artery, which may, for example, occur with posterior knee dislocation.
LABORATORY FINDINGS Synovial Fluid Analysis and Serum Laboratory Tests When an effusion is present, knee arthrocentesis is often performed to aid in diagnosis of joint aspirate for blood, crystals, or bacteria. The presence of blood indicates ligamentous or meniscal injury. Fat globules are pathognomonic for fracture. Cloudy or purulent synovial fluid samples should be sent for Gram stain, culture and sensitivity, and analysis of fungi, crystals, glucose, and protein. A silver stain can be performed to assess for Lyme arthritis. Knee sepsis accounts for 50% of all reported cases of septic arthritis. More than 20,000 cases of suppurative arthritis are reported in the United States annually. In young, sexually active adults, Neisseria gonorrhoeae is the most frequent pathogen; otherwise, Staphylococcus aureus is the cause of the vast majority of cases. Serum blood analysis for CBC, ESR, CRP, rheumatoid factor, and uric acid can also aid in diagnosis. An elevated white blood cell count and ESR in a patient with fever, warmth, swelling, and erythema over the knee joint also suggest an infectious process.
TREATMENT The key to successful ED or acute care evaluation of the knee is identification and immediate referral to a facility appropriate for the treatment of injuries with suspected or known neurovascular compromise (including posterior knee dislocation and compartment syndrome), open fractures or penetrating injury into the knee joint, and septic arthritis where urgent surgical intervention is generally indicated. Early referral to an orthopedic specialist for fractures, quadriceps and patellar tendon ruptures, first-time patellar dislocation, and obvious ligamentous injuries (i.e., unstable knee) is essential to reduce morbidity. In addition to prescribing analgesic medication (generally acetaminophen or one of the nonsteroidal anti-inflammatory agents), all knee injuries should be afforded the benefit of the RICE therapy while the patient
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awaits orthopedic evaluation or as treatment for simple strains or sprains. RICE therapy is defined as follows:
R: Rest crutch ambulation (with or without weight bearing) I: Ice (ice application 20 min/hr during the first 72 hours) C: Compression (if indicated with knee immobilizer, brace, or splint) E: Elevation of the knee above the level of the heart.
Bibliography Brusch J: Septic arthritis. eMedicine Available at: http://www.emedicine.com/med/ topic3394.htm. Accessed on November 25, 2005. Fletcher K: Ten most common health complaints. Available at: http://www.forbes.com/ execpicks/2003/07/15/cx_kf_0715health.html. Accessed on August 9, 2005. Jackson J, O’Malley G, Kroenke K: Evaluation of acute knee pain in primary care, Ann Intern Med 2003;139:575–583. Johnson M: Acute knee evaluation: A systemic approach to diagnosis, Available at: http:// www.aafp.org/afp/20000415/2391.html. Accessed on July 29, 2005. Levy D: Knee injury, soft tissue. eMedicine Available at: http://www.emedicine.com/ EMERG/topic288.htm. Accessed on November 25, 2005. Mosier R: Primary Care for Physician Assistants. McGraw-Hill: New York, 1998, pp 391–395.
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Acute Ankle Injuries BARBARA A.CARR
ICD Codes: Ankle fracture malleolus closed 824.8, Bimalleolar 824.4, Open ankle fracture 825.21 and 825.31, Trimalleolar fracture 824.6, Achilles tendon sprain, Ankle sprain deltoid 845.01, Talofibular ankle sprain 845.09
Key Points Every patient with an acute ankle injury should undergo assessment for deformity, swelling and pain, and a check of neurovascular status. Treatment of uncomplicated sprains and strains involves ‘‘RICE’’ therapy (i.e., rest, ice, compression, elevation), crutches, and pain control. Outpatient orthopedic referral for moderate sprains, strains, and simple nondisplaced fractures is appropriate. An orthopedic consultation in the ED is necessary in the treatment of dislocations and displaced or complicated fractures.When in doubt, get an x-ray! ! Emergency Actions ! Immediate evaluation of neurovascular status should be performed in any ankle dislocation or open fracture, and immediate reduction should be undertaken for any neurovascular compromise.
DEFINITION Ankle injuries comprise sprains, strains, dislocations, and fractures and usually occur from inversion or eversion injuries, external forces, or direct trauma. Sports-related injuries occur most frequently, but ankle injuries are also seen in falls, industrial accidents, and automobile accidents.
ANATOMY The ankle joint is a hinge joint that consists of three bones: the talus, the tibia, and the fibula. The talus forms the supporting body for the tibia and fibula, with the talus being wider anteriorly than posteriorly. The stability of the ankle depends on the bony and ligamentous integrity of these articulations. The calcaneus is also important to the motion and stability of the ankle.
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There are three groups of ligaments that connect the bony structures of the ankle. The medial side of the ankle is supported by the deltoid ligament, also known as the medial collateral ligament. This ligament has both deep and superficial fibers that originate from the broad, short, and strong medial malleolus, with the superficial fibers running in a sagittal plane and inserting on the navicular and talus. The deep fibers run horizontally and insert on the medial surface of the talus. The ankle is supported laterally by the anterior talofibular, calcaneofibular, and posterior ligaments. They insert as they are named. The tibia and fibula are held together by the syndesmotic ligaments, which consist of the interosseous ligament, the anterior and posterior tibiofibular ligaments, and the inferior transverse ligament. The muscles of the ankle make up four separate compartments. The anterior compartment is involved in dorsiflexion and consists of the tibialis anterior, extensor digitorum longus, and extensor hallucis longus. The medial compartment consists of the flexor digitorum longus, tibialis posterior, and flexor hallucis longus and contributes to inversion. The posterior compartment, which is involved in plantar flexion, is composed of the soleus and gastrocnemius. The lateral compartment contains the peroneus longus and brevis muscles and contributes to eversion and plantar flexion. Blood is supplied to the ankle and foot by the iliac, femoral, and popliteal arteries. The entire foot is innervated by branches of the sciatic nerve.
CLINICAL PRESENTATION A patient with an acute ankle injury will usually present after a fall or inversion/eversion injury. The patient will often report swelling, painful ambulation (or lack of ambulation), ecchymosis, or gross deformity. A complete history should include a timeline and mechanism of injury and whether or not the patient was able to bear weight immediately.
EXAMINATION The entire leg should be uncovered before the examination so that the joints above and below the injury (i.e., knee and foot) can be visualized and examined. The ankle should be examined for gross deformity, edema, and ecchymosis. The proximal fibular head and entire shaft of the fibula should be palpated for tenderness. The bony landmarks of the ankle and fifth metatarsal head should also be palpated. The ankle should be guided through gentle passive and active range of motion to assess for ligamentous stability and to determine which positions cause and alleviate discomfort. Anterior and posterior drawer testing should also be done.
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A neurological and vascular examination should always be documented during the examination of any extremity. The dorsalis pedis and posterior tibialis pulses should be evaluated, along with two-point discrimination. Weight-bearing ability should also be documented.
LABORATORY FINDINGS There are no specific laboratory tests required in the diagnosis of ankle injuries. However, patients receiving anticoagulant therapy should have their prothrombin time and international normalized ratio (INR) checked if excessive bleeding into the joint or injury site is suspected.
DIAGNOSIS Ankle Sprains The most common type of ankle sprain is a result of laxity of the anterior talofibular ligament. Laxity is assessed using the anterior drawer test, which is performed with the patient seated comfortably and with the knee in 90 degrees of flexion and the ankle in neutral position (i.e., 10 degrees of plantar flexion). The examiner then pulls on the heel with one hand and pushes the leg posteriorly with the other. The test result is positive when the talus displaces anteriorly, a “clunk” is heard, or an anteromedial sulcus over the joint is induced. Stress testing should always be done on the uninjured side for comparison. The talar tilt test evaluates both the anterior talofibular and calcaneofibular (medial collateral) ligaments. It is performed by inverting the heel with the knee in 90 degrees of flexion and the ankle in neutral position. Increased laxity compared with the uninjured side suggests partial or complete ligamentous tear. Distal tibiofibular syndesmotic ligamentous injury is assessed with the external rotation stress test. With the knee held in 90 degrees of flexion and the ankle in neutral position, the foot is rotated externally. Pain at the syndesmosis or the sensation of lateral talar motion suggests a partial or complete tear. This injury usually occurs as a result of hyperdorsiflexion and eversion, and patients may prefer to ambulate on their toes. There is often tenderness over the anterior and posterior ligaments, with some tenderness over the medial malleolus resulting from an associated medial collateral ligament injury. Ankle sprains are classified as grade I, II, or III. A grade I injury involves stretching or microscopic tearing of a ligament, causing local tenderness and minimal swelling. Weight bearing is usually possible, and x-ray findings are normal. A grade II sprain involves a partial tear of the ligament with moderate joint instability, often accompanied by significant localized swelling and pain. In a grade III injury, the ligament
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is completely ruptured. The patient will not be able to bear weight, and there is often an obvious deformity. Plain radiographs may show an abnormal relationship of the talus to the mortise. Grade I and II sprains are treated with RICE therapy and the optional use of crutches for a few days. Analgesics are often needed for shortterm use. Rarely, in severe grade II or III injuries, plaster splinting or casting for up to 3 weeks may be necessary, along with RICE. Follow-up with the patient’s primary care physician is necessary within the first 2 weeks after a minor sprain, whereas a severe sprain may require referral to an outpatient orthopedic specialist.
Tendon Injuries The most common ankle tendon injuries are Achilles tendon rupture and peroneal tendon dissociation or tear. An Achilles tendon rupture usually occurs in middle-aged patients during sporadic or weekend involvement in recreational sports (i.e., “weekend warriors”). This injury is frequently misdiagnosed. Rupture occurs from direct trauma or indirectly transmitted forces, including sudden unexpected dorsiflexion, forced dorsiflexion of a plantar flexed foot, or push-off of the foot with simultaneous knee extension and calf contraction. Factors that predispose patients to Achilles tendon injury include rheumatoid arthritis, gout, hyperparathyroidism, and fluoroquinolone antibiotic therapy. Patients often describe a sudden onset of pain with a loud “pop.” With complete ruptures the pain often subsides immediately after the injury, but weakness in plantar flexion persists. On examination, a visible and palpable tendon defect is usually present. Rupture can also be assessed using the Thompson test, which is performed with the patient prone and the knee flexed to 90 degrees. Squeezing the calf muscles should produce passive plantar flexion of the foot. Absence or weakened response compared with the uninjured side is suggestive of rupture of the tendon. Radiographic evaluation of Achilles tendon injuries can include plain radiographs, which may show evidence of opacification of the fatty space anterior to the tendon, known as Kager’s triangle. MRI or ultrasonography can also be used for evaluation. Treatment of Achilles tendon rupture is controversial. Emergency orthopedic referral is recommended, and the ankle should be splinted. The peroneal tendons are the primary everters and pronators of the foot and are also involved in plantar flexion. Both tendons travel posterior and inferior to the lateral malleolus; the peroneus brevis tendon inserts on the head of the fifth metatarsal, whereas the peroneus longus tendon inserts on the medial cuneiform and base of the first metatarsal. Peroneal tendon rupture can occur with forced dorsiflexion and reflex contraction of the peroneal muscles.
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The patient with a peroneal tendon dislocation reports sudden lateral ankle or foot pain with a snapping sensation. As with Achilles tendon ruptures, the pain often subsides while weakness on eversion persists. Tenderness and swelling will be present posterior to the lateral malleolus, and the dislocated tendons may be palpable in this area. Diagnosis is confirmed if the patient is unable to evert the foot while it is held in dorsiflexion. Plain radiographs may reveal an avulsion fracture of the distal fibula or head of the fifth metatarsal. CT scans or MRI may be helpful if the diagnosis is uncertain. Untreated cases of peroneal tendon rupture rarely resolve spontaneously. Orthopedic referral is necessary, and treatment involves either surgical or nonoperative repair with immobilization.
Ankle Fractures Fractures are caused by forces sufficient to overcome the structural strength of a bone. Ligament rupture can cause chip avulsion fractures where the ligament was attached to bone. Most malleolar fractures are transverse fractures or small avulsion fractures just below the joint line. If the talus shifts during injury, it can strike the opposite malleolus and can cause an oblique fracture, often on the side of the bone that was subjected to the compression force. The management of any acute ankle fracture involves identification, assessment of stability, and reduction with immobilization. The injured ankle should be elevated and iced promptly to minimize swelling and tissue damage. Appropriate analgesia and sedation should be used during fracture reduction, with close monitoring of vital signs if conscious sedation is used. Malleolar fractures account for 30% of all ankle fractures. Medial malleolar fractures typically occur from eversion or external rotation. Tension is exerted on the deltoid ligament, causing an avulsion of the tip of the malleolus or a rupture of the ligament. Medial malleolar fractures are often seen in association with lateral or posterior malleolar disruption. When a medial malleolar fracture is identified on a radiograph, careful evaluation and examination of the fibula (including the fibular head) should be performed to exclude fracture of the proximal fibula. Nondisplaced, isolated medial malleolar fractures can be treated with casting, avoidance of weight bearing, and referral to an orthopedic specialist. Lateral malleolar fractures are the most common ankle fracture. They are classified using the Danis-Weber system, which relates the fracture’s location to the tibiotalar joint. Fractures below this joint rarely disrupt other bony or ligamentous structures, are generally more stable, and can be immobilized and referred to orthopedics for outpatient management. The management of uncomplicated, isolated lateral malleolar fractures
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involves casting and avoidance of weight bearing. Associated fractures of the medial or posterior malleolus and fractures proximal to the tibiotalar joint line require orthopedic consultation in the ED. Posterior malleolar fractures are rarely isolated and are often associated with proximal fibular fractures and medial/lateral collateral ligament sprains. These fractures warrant orthopedic consultation in the ED. Significant fractures often require surgical repair. Bimalleolar and trimalleolar fractures are often caused by adduction or abduction injuries. They are considered to be unstable and require immediate orthopedic consultation. Bimalleolar fractures may be managed with external reduction and immobilization, whereas trimalleolar fractures are often managed with internal reduction. Open ankle fractures can occur with multiple trauma and require immediate surgical consultation. Neurovascular status of the affected extremity must be documented and an attempt must be made to reduce any gross deformity before immobilization. Tetanus status should be updated, and the patient should receive intravenous antibiotics for presumed contamination of the wound. Open fractures require early surgical debridement and irrigation.
Ankle Dislocations The ankle joint can bear five times the body’s weight during ambulation. In active dorsiflexion, the foot and the fibula rotate externally on the oblique outer articular surface of the talus. During weight bearing, the fibula descends and provides stability to the ankle mortise. Dislocation of the talus involves displacement of the talus from the mortise and often occurs in association with a fracture of a component of the mortise. Dislocations are often the result of significant trauma, including falls, motor vehicle accidents, or high-contact sports. Ankle dislocations are described according to the direction of displacement of the talus and foot in relation to the tibia. Medial dislocation is the most common. All ankle dislocations should be immediately reduced after radiographs are taken, unless there is vascular or neurological compromise. Reduction of a dislocation involves flexion of the knee to 90 degrees and downward traction on the foot while force is applied in the direction opposite the injury. After reduction, the neurovascular status is again examined and the ankle is splinted.
RADIOGRAPHS The minimum radiographs for any ankle injury are an anteroposterior view with the ankle in 5–15 degrees of adduction, a true lateral view that
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includes the base of the fifth metatarsal and an internal oblique view at a 45-degree angle. The radiograph taken from an anteroposterior view identifies fractures of the malleoli, distal tibia or fibula, talar dome body and lateral process of the talus, and calcaneus. The lateral view identifies fractures of the anterior and posterior tibial margins, talar neck, posterior talar process, and calcaneus, as well as any anterior or posterior displacement of the talus. The lateral view is also helpful in identifying an ankle effusion, which appears as a teardrop-shaped density displacing the normal fat adjacent to the anterior or posterior margin of the joint capsule. The presence of an effusion suggests the possibility of subtle intra-articular injuries. The mortise view, or internal oblique view, is taken with the ankle in 15–20 degrees of internal rotation. It is necessary for viewing the congruity of the articular surface between the dome of the talus and the mortise (which is formed by the medial and lateral malleolus and the distal, horizontal surface of the tibia). The lines formed between the articular surfaces should be parallel throughout the tibiotalar and talofibular components of the joint. Recently, the Ottawa ankle rules (OAR) were developed to assist healthcare practitioners in deciding whether an ankle injury necessitates ankle or foot radiographs. The OAR state that an ankle radiographic series is required if there is pain in the malleolar region and any of the following findings: 1. Bony tenderness occurs over the posterior edge or tip of the medial or lateral malleolus. 2. The patient is unable to bear weight for at least four steps both immediately after the injury and at the time of initial evaluation. Subtle ankle fractures, syndesmotic injuries, or osteochondral fractures can be missed in an evaluation of plain radiographs. When a patient has plain radiographs that appear to be negative for obvious injury, yet he or she continues to have unexplainable symptoms, other radiographic studies should be considered such as radionuclide bone scanning, CT scan, or MRI. Orthopedic consultation can also be considered for possible arthroscopy of the ankle.
TREATMENT Treatments for specific injuries are discussed previously. Ankle injuries may take weeks to months to completely resolve. Severe swelling or prolonged deformity may contribute to neurological sequelae or compartment syndrome, and failure to perform necessary rehabilitative exercises after an acute injury may result in chronic pain and stiffness.
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Bibliography Arnheim DD, Prentice WE: Arnheim’s Principles of Athletic Training, ed 11. McGrawHill: New York, 2002. Marx JA, Hockberger RS, Walls RM (eds): Rosen’s Emergency Medicine: Concepts and Clinical Practice, ed 5. Mosby: St Louis, 2002. Rivers CS, Dorfman T: Preparing for the Written Board Exam in Emergency Medicine, ed 4. Emergency Medicine Educational Enterprises: Milford, OH, 2003. Skinner HB: Current Diagnosis and Treatment in Orthopedics, ed 3. McGraw-Hill: New York, 2003. Tintinalli JE, Kelen GD, Stapczynski JS (eds): Emergency Medicine: A Comprehensive Study Guide, ed 6. McGraw-Hill: New York, 2003.
Acute Compartment Syndrome DAVID ZINSMEISTER
ICD Codes: Compartment syndrome 958.8
Key Points The majority of cases of acute compartment syndrome are caused by fractures. Acute compartment syndrome results in increased pressure that prevents perfusion within a fascial compartment. Pain, paresthesias, and paralysis are the signs of compartment syndrome. Delay in diagnosis and treatment results in tissue necrosis and Volkmann’s ischemic contracture.Treatment is immediate fasciotomy. ! Emergency Actions ! Immediate surgical consultation is appropriate when a compartment syndrome is suspected.
DEFINITION Acute compartment syndrome is a potentially devastating complication of injury to the extremities. Raised pressure within a closed fascial space reduces capillary perfusion below the level needed for tissue viability. The intracompartmental tissue pressure becomes elevated and produces a secondary elevation in venous pressure that obstructs venous outflow,
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thus resulting in an escalating cycle of continued pressure within the fascial compartment. If left untreated, necrosis of muscle and nerves can occur within a short period of time. Early diagnosis is paramount if severe, permanent disability is to be prevented.
EPIDEMIOLOGY Acute compartment syndrome can result from internal expanding forces or external compressive forces. Common causes due to internal expanding force are fractures, crush injuries, snake bites, extravasation of intravenous fluids, rhabdomyolysis, and hemorrhage within a compartment. External compressive force can result from tightly applied cast and splints, burn eschars, military antishock trousers, and sequential compression devices. The anterior compartment of the leg and flexor compartments of the forearm are most commonly affected. The compartments of the hand, foot, arm, thigh, shoulder, buttocks, and back can also be involved. Any muscle enclosed in fascia is subject to acute compartment syndrome. The initial injury results in swelling in the compartment that leads to local hydrostatic and osmotic pressure increases. Once the hydrostatic pressure exceeds a specific level, compression of the thin-walled venules occurs, resulting in hypertension at the venous end of the capillary beds that eventually causes arteriole compression. The cell wall membranes are then disrupted, leading to cytolysis and release of osmotically active cellular components that draw additional fluid into the compartment. The net effect is a vicious cycle of increasing pressure that compromises circulation. Ischemia of the muscles and nerve tissue then ensues, resulting in muscle infarction and permanent nerve damage. If the area of muscle infarction is significant, loss of the limb, myoglobinuria, renal failure, and death can occur.
CLINICAL PRESENTATION Patients will typically present with a fracture (approximately 45% of all cases of compartment syndrome involve fracture of the tibia). The symptoms are usually rapid in onset. Extremity pain is often the chief symptom, and the degree of pain experienced may appear to be out of proportion to the injury sustained. Paresthesias are commonly present in the extremity and in the distribution of the affected nerve distal to the involved compartment. The patient will be unable to actively move the muscles within the compartment involved. The problem arises in unconscious, traumatized patients who are unable to relate the classic symptoms of pain, paresthesias, and paralysis. The clinician must have a high index of suspicion in patients who are unable to communicate about their extremity fractures and crush injuries.
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EXAMINATION The most important clinical finding is severe pain on stretching of muscles in the involved compartment. Full, passive extension of the fingers and plantar flexion of the toes will stretch the muscles of the flexor compartment of the forearm and anterior compartment of the leg (most commonly involved in compartment syndrome) and elicit extreme pain. An inability to actively move the muscles indicates that paralysis is present and is often a late finding. Even though active contraction and passive stretching of muscles around a fracture is painful, it is usually tolerable. If not, the patient may have compartment syndrome. Sensory changes are a sensitive, reliable sign that compartment syndrome is present, and loss of two-point discrimination is often an early finding. The distribution of the sensory changes is also helpful in identifying the compartment(s) involved. The skin overlying the involved compartment may be erythematous and shiny with excessive sweating in the affected area. Upon palpation, the compartment is tender, tense, and swollen, a condition that is often described as having a “woody” feeling. Pulselessness and pallor indicates arterial trauma—not compartment syndrome—although the two may coexist. Pulses are typically normal in compartment syndrome because the intracompartmental pressure required to halt capillary perfusion rarely exceeds systolic blood pressure. Capillary refill time is also normal.
LABORATORY FINDINGS There is no specific laboratory test of use in diagnosing compartment syndrome. The following tests, however, are useful to determine the presence of muscle damage and its sequela: 1. Serum myoglobin and creatine kinase analysis: These assess muscle necrosis and possible rhabdomyolysis. 2. Potassium measurement: Level is elevated in rhabdomyolysis; severe hyperkalemia may result in arrhythmia. 3. Blood urea nitrogen and creatinine analysis: Elevation occurs in renal failure due to myoglobinuria. 4. CBC and coagulation studies: Anemia worsens muscle ischemia; the clinician should evaluate for disseminated intravascular coagulopathy. 5. Urinalysis: The presence or absence of myoglobin and creatine kinase in the urine should be determined. A urine dip positive for blood without the presence of erythrocytes on microscopic examination indicates myoglobin in the urine.
RADIOGRAPHS Radiographs are obtained to establish the presence of a fracture. There are no specific imaging studies to confirm or exclude compartment syndrome.
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DIAGNOSIS Acute compartment syndrome is a clinical diagnosis based on the signs and symptoms previously described. Compartment pressure measurements are adjunctive, and the only situations in which the diagnosis is established based solely on compartment pressure measurements are a patient with a head injury or an unconscious patient. The two most commonly used devices used to measure compartment pressure are the Whitesides apparatus and the STIC device. The Whitesides apparatus is made of items readily available in most EDs, and the STIC pressure monitor is manufactured by Stryker. The ideal zone for measuring compartment pressure is at the level of the fracture (if present) and within the area 5 cm proximal and distal to the fracture. Compartment pressure significantly decreases beyond this zone, even in the presence of compartment syndrome. Two methods are used to determine compartment pressure. The first involves the absolute pressure, which is established simply by measuring the pressure within the compartment(s). Second, is the delta P method, in which the highest compartment pressure is then subtracted from the mean arterial pressure to establish the differential pressure. It is well established that normal resting compartment pressure is 10 mmHg or less. There is, however, no agreed upon minimum pressure to absolutely confirm or exclude acute compartment syndrome. When using the absolute pressure method, 30 mmHg or above is commonly used to indicate decompression. If the delta P method is used, a differential pressure (i.e., the mean arterial pressure minus the highest compartment pressure) of 40 mmHg or less is commonly cited as the reference to determine that compartment syndrome is present.
TREATMENT Immediate fasciotomy is the appropriate treatment. Elevated compartment pressure for as little as 4–8 hours can result in muscle death, scarring, and shortening, which leaves the patient with clawing of the fingers and toes and little or no residual motion. The wrist and ankle develop contractures, and sensation is permanently impaired. There is no conservative treatment for acute compartment syndrome. Application of ice and elevation may seem like a good idea but actually further decreases perfusion. Considering the consequences, there is little negative risk to fasciotomy except an unsightly scar. However, failure to perform a fasciotomy can result in a lifetime disability for which late reconstructive surgery has little chance of restoring normal function.
Bibliography Blick SS, Brumback RJ, Poka A, et al: Compartment syndrome in open tibial fractures, J Bone Joint Surg Am 1986;68A:1348–1353.
600 ESSENTIAL EMERGENCY MEDICINE FOR THE HEALTHCARE PRACTITIONER Hamlin C: Compartment syndrome in the upper extremity, Emerg Clin North Am 1985; 3(2):283–291. Heppenstall RB, McCombs PR, DeLaurentis DA: Vascular injuries and acute compartment syndrome. In Bucholtz RW, Heckman JD (eds): Rockwood and Green’s Fractures in Adults, ed 5. Lippincott Williams & Wilkins: Philadelphia, 2001, pp 319–352. Hoover TJ, Siefert JA: Soft tissue complications of orthopedic emergencies, Emerg Med Clin North Am 2000;18(1):115–139. Perron AD, Brady WJ, Keats TE: Orthopedic pitfalls in the ED: Acute compartment syndrome, Am J Emerg Med 2001;19:413–416. Snider RK (ed): Essentials of Musculoskeletal Care. American Academy of Orthopaedic Surgeons: Rosemont, IL, 1997, pp 9–11. Tiwari A, Haq AL, Myint F, Hamilton G: Acute compartment syndrome, Br J Surg 2002;89:397–412.
Elbow Injuries GERALD DEPOLD AND CARRY DEPOLD
CPT Codes: Olecranon 813.01, Supracondylar injury 812.41, Humerus lower end 812.49, Radius 813.81, Radius upper end 813.07, Dislocation elbow anterior (closed) 832.01, Dislocation elbow (open) 832.11, Dislocation posterior (closed) 832.02, Dislocation posterior (open) 832.12
Key Points When elbow injury is present, rapid neurovascular assessment of the elbow and extremity must occur. Immediate corrective action must be taken if neurological or vascular function is compromised. The treatment goal in the case of a dislocated or fractured elbow is the concentrically reduced elbow determined by postreduction stability with reestablishment of neurovascular status. If the ED physician cannot reduce the elbow after two attempts, an orthopedic specialist must be consulted immediately. Severe elbow injuries require substantial force; a complete examination should be performed, based on the patient’s history, to rule out any other injuries. ! Emergency Actions ! Advanced trauma life support guidelines should be followed for the initial evaluation. Distal neurovascular status of the affected limb must be assessed. Distal neurovascular compromise should be treated with rapid reduction of dislocation or fracture, as appropriate. If neurovascular status is not restored after two attempts, an immediate referral to an orthopedic specialist and an arteriogram are required.
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DEFINITION The elbow is a very stable joint. As such, severe injuries to the elbow require a significant amount of force and commonly include dislocations and fractures. Dislocations are classified as simple or complex (with associated fracture or neurovascular injury) and by the direction of the dislocation (i.e., anterior, posterior, lateral, medial, and divergent). Fractures are distal humeral, proximal radial, and proximal ulnar. Radial head fractures are the most common, classified as type I, minimal to no displacement; type II, moderate displacement; type III, complete displacement; and type IV, with associated dislocation.
EPIDEMIOLOGY The radial head is the bone most commonly fractured in the adult elbow. The elbow is the second most common joint to be dislocated, with an incidence of 13 dislocations per 100,000 persons. Posterior dislocations are the most common. Dislocations in young persons are usually a result of a fall on an outstretched hand (FOOSH).
CLINICAL PRESENTATION The clinical presentation of dislocations and fractures varies. Patients with dislocations usually present with obvious deformity and the arm splinted at 45 degrees. Fractures may or may not present with deformity or edema and must be ruled out radiographically. An appropriate history will determine mechanism of injury, hand dominance, and any distal neuropathy.
EXAMINATION First, the patient’s distal neurovascular status must be assessed and documented. The elbow should be examined for deformity and evidence of open injury. Dislocation can be confirmed by inspecting the palpable anatomy and comparing it with the uninjured side. Bony landmarks should be palpated for crepitus and grimace, and range of motion should be measured. The physician should examine the carry angle of the injured elbow (formed by the arm and forearm) and compare it with the uninjured side, checking for malalignment. The examiner should also check for compartment syndrome, which is characterized by (1) pain on passive extension of the fingers and wrist, (2) a tense, swollen, painful extremity, and (3) pain out of proportion to the injury. Lacerations must be evaluated to determine whether the joint capsule is involved. The ipsilateral wrist, forearm, and shoulder should be examined for injuries.
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The elbow extension test can be used as a sensitive clinical screening test for patients with acute injury to the elbow. Patients who can fully extend the affected elbow can be safely treated without radiography.
LABORATORY FINDINGS No specific laboratory tests are helpful in the diagnosis of fractures. If the joint is open or if the patient will undergo surgery, a CBC and measurements of partial thromboplastin time (PTT) and INR should be performed.
DIAGNOSIS All extremities and suspected fractures or dislocations should be x-rayed. Diagnosis is made clinically and radiographically.
RADIOGRAPHS Plain anteroposterior and lateral views are required initially and are sufficient for simple dislocations; three-view radiographs should be obtained as soon as possible. The clinician should pay attention to the radiocapitellar line (i.e., Monteggia’s fracture), anterior humeral line, and any anterior fat pad displacement or posterior fat pad (i.e., occult fracture) that may be present. Radial head fracture is commonly missed. A radial head–capitellar view may be required. Osteochondral injuries are likely despite the absence of radiographic findings, and, if visible, they are usually larger than they appear. CT is used before operative stabilization of complex fractures and to locate osteochondral fragments. MRI is of limited use in the acute setting.
TREATMENT Dislocations Simple dislocations can be treated with reduction in the ED. First, neurovascular status should be assessed (the median and ulnar nerves and brachial artery at a minimum). Adequate analgesia should be established, and the patient should be placed in a supine position. The clinician should avoid hyperextension or use of excessive force. The bones of the elbow should be disengaged with traction to the forearm and counter-traction to upper arm. Any lateral or medial displacement should be corrected. The elbow should be flexed with pressure on the tip of the olecranon. Successful reduction is associated with a palpable “clunk.” The practitioner should check stability through the full range of motion. Reduction that
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cannot be maintained with less than 60% of flexion is an indication for surgical consultation. Neurovascular status should be reassessed, and postreduction radiography should be performed. The arm should be splinted at 90 degrees of flexion with the forearm in pronation, and follow-up should be performed in 24 hours for a neurovascular check. Complex dislocations and dislocation that cannot be reduced require an immediate orthopedic consultation. Dislocations reduced in the ED require routine orthopedic follow-up.
Fractures Fracture treatment depends on the type. The following require orthopedic referral: transcondylar or intracondylar fractures and displaced supracondylar, condylar, capitellar, radial, and olecranon fractures. Nondisplaced supracondylar, condylar, capitellar, radial, and olecranon fractures are immobilized with plaster, with follow-up carried out by an orthopedic specialist. Patients with elbow injuries must be continually reassessed for neurovascular compromise and compartment syndrome. Any significant edema requires regular distal neurovascular monitoring. All elbow injures should be referred to an orthopedic surgeon as soon as possible.
Bibliography Brady WJ: Upper extremity fractures and dislocations, Emerg Med Rep Thomson American Health Consultants. Accessed on May 10, 2005. Available at:http://www.emronline. com/textbooks_index.html. Docherty MA: Can elbow extension be used as a test of clinically significant injury? Ann Emerg Med 2003;41(5):760. Hildebrand KA, Patterson SD, King GJ: Acute elbow dislocations: Simple and complex, Orthop Clin North Am 1999;30(1):63–79. O’Driscoll SW: Difficult elbow fractures: Pearls and pitfalls, Instr Course Lect 2003;52:113–134. Saati AZ, McKee MD: Fracture-dislocation of the elbow: Diagnosis, treatment and prognosis, Hand Clin 2004;20(4):405–414. Sheps DM, Hildebrand KA, Boorman RS: Simple dislocations of the elbow: Evaluation and treatment, Hand Clin 2004;20(4):389–404. Work Loss Data Institute. In Disorders of the Elbow, Work Loss Data Institute: Corpus Christi, TX, 2004, p 110.
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Foot Injuries JENNY E. DUNLAVY
ICD Codes: Calcaneus fracture closed 825.0, Calcaneus fracture open 825.1, Metatarsal bone fracture (closed) 825.25, Metatarsal bone fracture (open) 825.35, Toe fracture (closed) 826.00, Toe fracture (open) 827.1, Puncture wound 892.00
Key Points The foot is divided into three regions. The Chopart’s joint separates the midfoot and hindfoot, and Lisfranc’s joint separates the midfoot and forefoot. ! Emergency Actions ! Any foot trauma presenting to the ED should be evaluated for bony fractures, foreign bodies, compartment syndrome, and infection.
DEFINITION Most injuries to the foot are due to direct or twisting forces resulting in acute soft tissue injury, fracture, or dislocation. As with many musculoskeletal injuries, an adequate patient history often aids in the diagnosis. Twisting forces are usually associated with less severe avulsion-type injuries. A history consistent with an increasing inability to ambulate and worsening pain may suggest a minor sprain or an impending vascular catastrophe. History of a puncture wound also requires special attention.
ANATOMY The foot contains 28 bones and 56 articular surfaces, divided into three regions. Chopart’s joint separates the midfoot and hindfoot, and Lisfranc’s joint separates the midfoot and forefoot. The hindfoot is composed of the talus and the calcaneum. The midfoot contains the cuboid bone, three cuneiform bones, and the navicular bone. The metatarsals and phalanges make up the forefoot. Many ligaments and muscles provide support for the foot.
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PHYSICAL EXAMINATION Essential elements of the physical examination include inspection, palpation, neurovascular assessment, and active and passive range of motion. The Ottawa ankle rules (OAR), as their name implies, are used for assessment of the ankle. The OAR also include criteria for assessing whether a foot radiograph is required for a midfoot injury. The OAR state that a foot radiograph series is required if there is pain in the midfoot region and any of the following: bone tenderness present at the navicular bone, bone tenderness present at the base of the fifth metatarsal, or the inability to bear weight for at least four steps, both immediately after the injury and at the time of evaluation. The OAR have a sensitivity approaching 100% in detecting acute midfoot zone fracture but cannot be applied to the hindfoot or forefoot. Normal findings on the physical examination and the ability to complete several weight transfers essentially rule out a significant injury, and a radiograph is not necessary. As always, clinical judgment should prevail. Any abnormal findings on physical examination or trial of ambulation mandate a three-view foot series. If there is tenderness along the heel, an axial view of the calcaneus should be included. A CT scan of the foot is occasionally performed to exclude a subtle diastasis at Lisfranc’s joint from the differential diagnosis.
HINDFOOT INJURIES Rare dislocations and significant fractures of the talus merit immediate surgical consultation for surgical reduction. Fractures of the calcaneus can be caused by any axial load to the heel, such as a fall from a height. Consequently, such fractures are often associated with spinal injuries, and a complete physical examination is mandatory. Calcaneus fractures may be subtle. Thus, when a calcaneus fracture is suspected despite an unremarkable radiograph, Boehler’s angle should be measured on the lateral view of the foot. Boehler’s angle is formed by the intersection of a straight line extending along the superior cortex of the body of the os calcis with a line extending from the dome to the anterior tubercle. If the angle is less than 20 degrees, a fracture is likely. All calcaneus fractures mandate a consultation with an orthopedic specialist.
MIDFOOT INJURIES Isolated fractures of the tarsal bones are rare and usually treated conservatively. An injury to Lisfranc’s joint should be suspected, with identification of a cuboid or cuneiform fracture. Injuries to the joint are rare and often missed in the ED. A fracture of the base of the second metatarsal is often considered pathognomonic for a disruption of the ligamentous complex. This injury should be suspected when there is point tenderness
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over the midfoot or when there is laxity between the first and second metatarsals. Injuries to Lisfranc’s joint may require open reduction or percutaneous pinning. Long-term morbidity may be significant.
FOREFOOT INJURIES Injuries to the metatarsals are often crush injuries. Most nondisplaced metatarsal shaft fractures can be treated conservatively. A notable exception is a fracture of the first metatarsal shaft, which must be treated with a period of avoidance of weight bearing. Displaced fractures of any of the metatarsal shafts are problematic, requiring avoidance of weight bearing and possibly surgical fixation. Fractures of the fifth metatarsal are the most common metatarsal fractures. Nondisplaced shaft fractures can be treated conservatively, as can avulsions from the proximal pole, often referred to as “pseudo-Jones” fractures. However, a true Jones fracture, a transverse fracture through the base of the fifth metatarsal, is prone to malunion and nonunion complications. Thus, the Jones fracture is treated with a non–weight-bearing cast and close orthopedic follow-up.
Phalangeal Injuries Nondisplaced phalangeal fractures are typically treated conservatively, with “buddy taping” or a cast shoe. Dislocations and displaced fractures may be reduced in the ED by the application of manual traction followed by buddy taping.
EXAMINATION When examining any foot for injury, the healthcare provider should remember that the examination includes the leg from the knee down. The skin, pulses, and neurovascular status of each foot should be examined and any differences noted. The skin temperature and tactile sensation of each foot should be compared. Hair growth, skin changes, and difference in toenail growth between the two feet should all be noted. Often this will lead to a nontraumatic diagnosis. The practitioner should always inquire about past medical history, including a history of diabetes and smoking. Reflexes and strength of each extremity should be noted.
LABORATORY FINDINGS There are no specific laboratory examinations for foot trauma. If the patient has diabetes or a cellulitis overlays the fracture, or if an open fracture is present, a CBC, Chem 7, and ESR and CRP measurements should
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be performed. If gout is suspected, a uric acid level measurement should be obtained.
RADIOGRAPHS Radiographs should be performed for all acute foot traumas. If a bone is fractured, the radiograph should include the bones above and below the fracture because of the relationship of associated fractures secondary to twisting forces of an injury.
DIAGNOSIS Diagnosis is based on clinical examination and radiographic examination. All patients with foot fractures should be referred to a podiatrist or orthopedic surgeon within 72 hours.
TREATMENT Open Fractures An open fracture should be protected from further contamination by the application of a wet, sterile dressing. Tetanus toxoid and tetanus immunoglobulin should be administered as indicated. Initially, the antibiotic of choice is a first-generation cephalosporin, or clindamycin if the patient is allergic to penicillin. If the injury appears to be grossly contaminated, an aminoglycoside can also be added.
Puncture Wounds Puncture wounds of the foot carry the risk of retained foreign body, deep tissue infection, or osteomyelitis. Deep penetration increases the risk of damage to bone and tendons, and penetration through a rubber sole may increase the chance of infection with Pseudomonas species. A normal radiograph does not rule out the possibility of bony injury or retained foreign body. The use of prophylactic antibiotics after a puncture wound is as yet controversial and may be reserved for immunocompromised patients or those who have bone or tendon involvement. Any patient presenting with a delayed puncture wound complicated by infection warrants aggressive treatment with antibiotics, wound opening, and irrigation. The first-generation cephalosporins are generally the first line of treatment. A fluoroquinolone can be added for additional coverage of Pseudomonas. An orthopedic consultation for operative debridement is required for complicated foot infections, gunshot wounds to the foot, and many lawnmower injuries.
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Bibliography Michael J, Stiell I: Foot injuries. In Tintinalli JE, Kelen GD, Stapczynski JS (eds): Emergency Medicine: A Comprehensive Study Guide ed 6. McGraw-Hill: New York, 2004. Stiell IG, McKnight RD, Greenberg GH, et al: Implementation of the Ottawa ankle rules, JAMA 1994;271:827–832. Stiell I, Wells G, Laupacis A, et al: Multicentre trial to introduce the Ottawa ankle rules for use of radiography in acute ankle injuries, BMJ 1995;311:594–597.
Injuries to the Forearm and Wrist BRENDA OSWALD AND CARL MENCKHOFF
ICD Codes: Monteggia’s fracture 813.03, Galeazzi’s fracture 813.42, Colles’ fracture 813.41, Smith’s fracture 813.41, Barton’s fracture 813.42, Hutchinson’s fracture 813.44, Torus fracture 813.45, Scaphoid fracture 814.01, Lunate fracture 814.02, Triquetrum fracture 814.03, Pisiform fracture 814.04, Hamate fracture 814.08, Capitate fracture 814.07, Trapezoid fracture 814.06, Carpal tunnel syndrome 354.0, de Quervain’s fracture 727.04
Key Points Any patient who presents to the ED with a wrist or forearm injury should have the entire arm examined from the shoulder down. All extremity examinations should have the neurovascular status evaluated and documented. ! Emergency Actions ! Any patient with an extremity injury that involves any neurovascular deficit should be immediately referred to an orthopedic surgeon.
DEFINITION Injuries to the wrist and forearm can result from traumas due to falls, lacerations, burns, contusions, crush injuries, or overuse that leads to tendonitis or
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carpal tunnel syndrome. If function is compromised, these injuries can be devastating; therefore, treatment is geared toward restoring as much of the previous function as possible. Most fractures occur as a result of a FOOSH, and osteoporosis causes postmenopausal women to have a higher rate of forearm fractures than other adults. Infants and toddlers have no sex predilection for fractures, but after the age of 2 years, fractures are more common in boys than in girls.
ANATOMY The forearm is composed of the radius and ulna bones, which are connected by a fibrous interosseous membrane. The ulna maintains a relatively fixed position during supination and pronation, while the radius rotates around it. Because of this close association, an injury to one bone generally has a direct impact on the other. The carpal bones are aligned in proximal and distal rows. The proximal carpal row from the radial side consists of the scaphoid, lunate, triquetrum, and pisiform bones. The distal carpal row from the radial side is made up of the trapezium, trapezoid, capitate, and hamate bones. The carpal bones are held together by the interosseous, volar, and dorsal ligaments and a triangular fibrocartilage complex. The dorsal ligaments are weaker than the volar ligaments, making dorsal dislocation more common. The wrist flexor-pronator muscle group is made up of the pronator teres, flexor carpi radialis, palmaris longus, and flexor carpi ulnaris. These four muscles originate from the medial epicondyle as a common tendon, and then split as they travel down the forearm. The pronator quadratus pronates the forearm at the superior and inferior radioulnar joints. The primary forearm supinators are the biceps brachii and the supinator. The wrist extensors, which originate from the lateral epicondyle and its supracondylar line, are the brachioradialis, the extensor carpi radialis longus, and the extensor carpi radialis brevis. The forearm and wrist are innervated by the radial, median, and ulnar nerves and receive their blood supply from the radial and ulnar arteries. The radial nerve provides sensory innervation to the posterior aspect of the hand from the thumb to the radial half of the ring finger and also branches to form the posterior interosseous nerve that controls the muscles that extend the fingers and thumb. The median nerve controls finger flexion, wrist movement, and sensation on the volar aspect of the hand from the thumb to the radial half of the ring finger. The ulnar nerve provides innervation to forearm muscles and controls the intrinsic muscles of the hand. It also provides sensation to the fifth finger and the ulnar half of the ring finger.
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EXAMINATION A thorough history and physical examination helps to elicit information regarding how the injury occurred, which will guide the clinician to the appropriate examination and treatment. It is important to note any previous physical injuries or limitations, to assess whether the patient is rightor left-handed, and to evaluate the joint above and below the area of pain. The physical examination includes palpation of the bones, muscles, ligaments, and radial and ulnar pulses. The forearm should be tested for range of motion with supination and pronation. The wrist should be examined for strength and the ability to flex, extend, and deviate in the radial and ulnar directions. Motor function maneuvers include having the patient make an “OK” sign to test the median nerve, extending the fingers or wrist against resistance to test the radial nerve, and separating the fingers against resistance to test the ulnar nerve. Two-point discrimination is the gold standard for sensory integrity. Tenderness of the anatomical “snuff box” may indicate a scaphoid fracture. Phalen’s maneuver or Tinel’s sign may indicate carpal tunnel syndrome.
CLINICAL PRESENTATION A detailed history, including the position of the limb during the injury, can aid in the diagnosis and appropriate treatment. Traumatic injuries from axial loading with the forearm in supination produces both radial and ulnar fractures, loading in a neutral position results in isolated radial head fractures, and loading in pronation causes radial head fractures with severe tearing of the interosseous membrane. The severity of the radial head injury is related to the percentage of contact within the radiocapitellar joint. The most commonly injured carpal bones are the scaphoid, triquetrum, and lunate. Falls with direct impact on the thenar eminence are more likely to cause injury to the scaphoid, and those on the hypothenar eminence are more likely to cause injury to the triquetrum and pisiform. Anteroposterior and lateral radiographic views of the wrist, forearm, and elbow are required to assess fractures. Immediate reduction of a fracture is necessary when there is vascular compromise, or tenting of the skin. Several anesthesia options exist to reduce fractures in the ED. Axillary blocks provide complete anesthesia and muscle relaxation, but they carry a risk of arterial or nerve damage. Hematoma blocks provide anesthesia and muscle relaxation but carry a risk of osteomyelitis. Intravenous regional anesthesia (Bier block) provides anesthesia and muscle relaxation but may cause lidocaine toxicity. Conscious sedation provides effective anesthesia, muscle relaxation, and amnesia, but it should only be
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performed on patients who are otherwise healthy or have only mild or moderate systemic disease that does not interfere with daily routines. Treatment for minor fractures is generally splinting, rest, elevation, and analgesia. An orthopedic specialist should be consulted for open fractures, operative fractures, and some dislocations.
Forearm Fractures The treatment of most fractures to the forearm requires an orthopedist. The exceptions are a nondisplaced ulnar shaft fracture with less than 10 degrees of angulation (i.e., nightstick fracture), which can be treated with a posterior long-arm splint, and a nondisplaced radial head fracture, which can be treated with a sling and early mobilization. Monteggia’s fracture is defined as a fracture of the proximal one third of the ulna with dislocation of the radial head. It frequently results from a fall on an outstretched hand in forced pronation. The radial head may be palpable in the anterolateral or posterolateral location, and the forearm may appear shortened and angulated. The radiocapitellar line is a line drawn down the center of the radius that should intersect the middle of the capitellum regardless of elbow flexion or extension. Malalignment of this line on an anteroposterior or lateral elbow radiograph indicates radial head displacement. Treatment is immobilization with a long-arm splint, with the elbow flexed at 90 degrees and the forearm in neutral position for children. Adults may require orthopedic consultation and open reduction internal fixation (ORIF). Complications include nonunion, redislocation, infection, compartment syndrome, and injury of the posterior interosseous nerve, which causes weakness or paralysis with extension of the fingers or thumb. Galeazzi’s fracture is defined as a fracture of the distal one third of the radius with dislocation of the distal radioulnar joint. It is a reverse Monteggia’s fracture and is three times more common. The radial fracture is generally obvious on radiograph, but the associated ulnar dislocation is best seen on lateral view. Studies have shown that 90% of patients treated with just immobilization in a long-arm splint had poor outcomes; therefore, the best treatment is referral to an orthopedic specialist and ORIF. If the fracture dislocation is missed initially, the patient may experience progressive subluxation of the distal radioulnar joint, limitation of supination and pronation, chronic pain, and weakness. Colles’ fracture is the most common wrist fracture in adults. It often results from a FOOSH injury causing the distal radius to displace and dorsally angulate. It may be described as a “dinner fork” or “silver fork” deformity. Patients may report palmar paresthesias due to tension or pressure on the median nerve. Stable fractures, those with less than 20 degrees
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of angulation and less than 1 cm of shortening, can be placed in a sugartong splint and have orthopedic follow-up. Unstable fractures require closed reduction and immobilization with orthopedic evaluation and possible ORIF. Complications include malunion, median nerve injuries, triangular fibrocartilage complex injuries, secondary radioulnar and radiocarpal instability patterns, and arthritis. Smith’s fracture is a reverse Colles’ fracture and is sometimes referred to as a “garden spade” deformity. It is a distal metaphyseal fracture with volar displacement and angulation. This injury results from a direct blow on the dorsum of the hand or wrist or from a hyperflexion injury. Treatment is the same as for Colles’ fractures. Barton’s fracture is a dorsal rim fracture of the distal radius. It results from a dorsiflexion and pronation force and may be associated with dislocation of the radiocarpal joint. Treatment is similar to that recommended for a Colles’ fracture. Hutchinson’s (chauffeur’s) fracture is an avulsion fracture of the distal radial styloid that occurs from a force transmitted from the scaphoid to the styloid. This injury is considered unstable because of the associated ligamentous injury, such as scapholunate dissociation and perilunate and lunate dislocation. Treatment is immobilization in a posterior splint and urgent orthopedic referral for percutaneous fixation. Torus fractures (i.e., buckling of the cortex) and greenstick fractures (i.e., cortex is broken on one side only) occur in children with only a moderate degree of trauma and can be managed with a long-arm cast when angulation is less than 10 degrees. However, referral to an orthopedic specialist is required for those with more than 10 degrees of angulation.
Carpal Fractures and Injuries The scaphoid is the most frequently fractured carpal bone. A fracture usually occurs from a fall on an outstretched dorsiflexed hand or by an axial load directed along the thumb’s metacarpal. There is generally pain along the radial side of the wrist and localized tenderness in the anatomical snuffbox. Although standard and scaphoid view radiographs are helpful to identify a fracture, 10% of initial fractures are undetected. High clinical suspicion of a fracture and nondisplaced fractures are treated with a thumb spica splint and orthopedic referral in 7–10 days for reexamination and repeat radiographs. Displaced or unstable fractures should be immediately treated by an orthopedic specialist or a hand surgeon. The more proximal, oblique, or displaced the fracture, the greater the risk of developing avascular necrosis (AVN). Other complications include delayed union, malunion, and early degenerative arthritis. The scapholunate ligament is the most commonly injured ligament of the wrist. It frequently results from a FOOSH injury with impact on the
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thenar eminence. Patients present with pain and swelling of the radial side of the wrist and may have a clicking sensation with wrist movement. Scapholunate dislocation is diagnosed radiographically when the scapholunate distance exceeds 3 mm on the anteroposterior radiograph. This may be increased on the clinched-fist view with the wrist in ulnar deviation and is often referred to as the “Terry Thomas” or “David Letterman” sign in reference to the gap between their front teeth. Scapholunate dissociation may be associated with a rotary subluxation of the scaphoid that will appear as a ring shadow superimposed over the scaphoid bone on anteroposterior radiograph; this is known as the “signet ring sign.” Treatment is a volar splint in neutral position with orthopedic referral for closed reduction or for open reduction with surgical repair of the ligament. Isolated lunate fractures are rare, usually occurring in association with other carpal injuries after a fall on an outstretched hand. Because the other carpal bones overlap the lunate bone, a fracture may be difficult to identify on plain radiographs and may require CT or MRI to confirm. Treatment is thumb spica splint and orthopedic follow-up. Complications include median nerve damage and AVN of the lunate (Kienböck’s disease), which may lead to lunate bone collapse, osteoarthritis, chronic pain, and decreased grip strength. Lunate and perilunate injuries usually occur from a fall on an outstretched upper extremity. The patient presents with a swollen wrist, decreased mobility, and severe pain. A median nerve injury may also be present. The lunate may be displaced either dorsally or volarly. Radiographs will show a triangular shape, often called a “piece-of-pie sign” on anteroposterior view and a “spilled teacup sign” seen on the lateral view. In perilunate injuries, the capitate is displaced. An orthopedic specialist should be consulted for immediate reduction and further care. Easily reducible dislocations may only require closed reduction and long-arm splint immobilization, but open, unstable, or irreducible dislocations may require ORIF. Both perilunate and lunate dislocations usually involve a scaphoid fracture or rotary subluxation of the scaphoid. Complications of perilunate and lunate dislocations include early degenerative arthritis, delayed union, malunion, AVN, and median nerve compression. Triquetrum fractures may be either dorsal avulsion (i.e., chip) fractures or fractures through the body of the bone. They often occur from hyperextension injuries. Perilunate and lunate dislocations may be associated with fractures through the body of the triquetrum and are best seen on the anteroposterior view. These fractures require casting for 6 weeks and orthopedic follow-up. Avulsion fractures are best viewed on the lateral radiograph and may be treated with a wrist splint for 6 weeks. Trapezium injuries are the result of a direct blow to the thumb or from a dorsiflexion and radial deviation force of the hand. A vertical fracture of the bone is rare and may be associated with a Bennett’s fracture, which
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is an intra-articular proximal thumb metacarpal fracture. Presentation is pain with movement of the thumb and tenderness of the apex of the anatomical snuffbox and at the base of the thenar eminence. Treatment for nondisplaced fractures is a thumb spica splint. Displaced fractures require ORIF. The pisiform may be fractured during a fall on the hypothenar eminence. Increased pain will be elicited with palpation of the pisiform bone. Damage may occur to the ulnar nerve and artery, which lie in Guyon’s canal, whose bony walls are formed by the pisiform and the hook of the hamate. Treatment is a compression dressing or a splint in 30 degrees of flexion and ulnar deviation to relax the tension on the flexor carpi ulnaris tendon, which houses the pisiform bone. Hamate fractures may involve the hook of the hamate, the body of the bone, or any of its articular surfaces. Most fractures involve the hook of the hamate and occur from mechanisms such as an interrupted swing with a golf club, bat, or racquet. Hamate body fractures are rare and are usually associated with a fracture or dislocation of the fourth or fifth metacarpal. Treatment is a compression dressing or splint. Complications include nonunion of the fracture and injuries to Guyon’s canal and the ulnar nerve or artery. Capitate fractures usually occur in association with scaphoid fractures during a forceful dorsiflexion of the hand with impact on the radial side. If the neck of the capitate bone is fractured, AVN may develop in the proximal fracture segment because it receives its blood supply from the distal end. Capitate neck fractures are best viewed on lateral view radiographs. Dislocated or displaced bones require orthopedic evaluation for closed or open reduction. Trapezoid fractures account for less than 1% of all carpal bone fractures. They usually occur from an axial load shifting onto the index metacarpal. Because these fractures are difficult to identify on plain radiographs, MRI or CT may be necessary to visualize the fracture. Treatment is placement in a thumb spica splint and orthopedic referral.
Wrist Nerve Entrapment and Overuse Syndromes The wrist is a common site for overuse injuries. Approximately 15% of workers are at risk of experiencing carpal tunnel syndrome. Overuse is defined as the level of repetitive microtrauma sufficient to overwhelm the tissue’s ability to adapt. Microtrauma results from repetitive loading episodes at a force or elongation level well within the physiological range. Fibrosis forms after continued or repeated release of inflammatory products that lead to thick, unyielding, restrictive tendon sheaths or retinacular tunnels.
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Occupational risk factors for developing an overuse injury include repetitive movements, high force, awkward joint posture, direct pressure, vibration, and prolonged constrained posture. Treatment is aimed at preventing fibrosis. The affected area should be rested for 2 weeks, the aggravating causes decreased, and postures or work tools shifted to avoid further injuries. Carpal tunnel syndrome is commonly seen in patients who perform repetitive hand movements, such as typists, cashiers, assembly line workers, and carpenters, but may also result from rheumatoid arthritis, pregnancy, diabetes, or thyroid disease. The transverse carpal ligament is subjected to a repeated mechanical stress that causes subsequent edema and fibrosis that compresses the median nerve. Presenting symptoms are pain and paresthesias over the distribution of the median nerve. In advanced stages, patients may develop impaired dexterity, altered sensation, and thenar weakness causing them to frequently drop items. The pain may radiate up the arm but will spare the fifth finger. Symptoms are generally worse at night and may awaken the patient from sleep because of the increased fluid accumulation in the supine position and the wrist flexion that occurs during sleep. Diagnosis is based on clinical findings. Plain radiographs will only indicate bony abnormalities. MRI and CT are only helpful to visualize any anatomical factors that may cause compression, but are not useful for specifically diagnosing entrapment neuropathy unless a mass or other lesion is found. Conservative treatment is to splint the wrist in neutral position and administer oral anti-inflammatory drugs to treat pain. Corticosteroid injections are occasionally used for transient relief of persistent symptoms. Patients should be cautioned that more than two or three injections may cause local tendon damage, and only 22% of those with minor symptoms are still pain-free 12 months after the injection. Surgical decompression is indicated when conservative treatments have failed, distal median neuropathy is severe, or thenar atrophy develops. The operation releases the transverse carpal ligament via a longitudinal incision from the wrist to the palm. Patients who undergo surgical correction have a good prognosis if the procedure is done before severe axonal loss develops. Ulnar tunnel syndrome occurs when the ulnar nerve is compressed as it passes through Guyon’s canal. Patients present with numbness of the fifth finger and the ulnar half of the fourth finger, with or without weakness of grip. Treatment is similar to that of carpal tunnel syndrome, with initial splinting, reduction of inciting activities, and surgical repair if refractory to conservative treatment. Tendonitis is usually the result of a repetitive motion that causes inflammation of the tendon with associated pain, edema, and tenderness over the affected area. De Quervain’s stenosing tenosynovitis involves the abductor pollicis longus and extensor pollicis brevis muscles. Patients report pain and mild
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edema, with increased pain when the Finkelstein’s test is performed. This test involves holding the thumb in the palm and making a fist, then deviating the wrist in an ulnar direction. Women are affected at a ratio of 10 to 1 compared with men. The tendon may be injected with corticosteroids, but this may cause weakness of the tendon or damage to surrounding tissues. A thumb spica splint may be applied to keep the thumb in neutral position for 3 weeks. A consultation with an orthopedic specialist is indicated if the patient’s pain is refractory to conservative treatment.
Bibliography Halimi KM, Jones TR: Wrist dislocation. Available at: http://www.emedicine.com. Accessed on April 8, 2005. Hoppenfeld S: Physical Examination of the Spine and Extremities Appleton & Lange: New York, 1995. Huang E, Grimes P: Fractures, forearm, Available at: http://www.emedicine.com. Accessed on February 2005. Knoop KJ, Stack LB, Storrow AB: Atlas of Emergency Medicine, ed 2. McGraw-Hill: New York, 2002. McGinley JC, Hopgood BC, Gaughan JP, et al: Forearm and elbow injury: The influence of rotational position, J Bone Joint Surg Am 2003;85A(12):2403–2409. Netter FH: Atlas of Human Anatomy, ed 3. ICON Learning Systems: Teterboro, NJ, 2002. Perron AD, Brady WJ: Evaluation and management of the high-risk orthopedic emergency, Emerg Med Clin North Am 2003;21:159–204. Simon R, Koenigsknecht S: Emergency Orthopedics: The Extremities, ed 3. McGraw-Hill: New York, 2000. Simon RR, Koenignsknecht SJ: Emergency Orthopedics: The Extremities, ed 4. McGrawHill: New York, 2001. Stone CK, Humphries RL: Current Emergency Diagnosis and Treatment, ed 5. Lange Medical Books/McGraw-Hill: New York, 2004. Tintinalli JE, Kelen GD, Stapczynski JS (eds): Emergency Medicine: A Comprehensive Study Guide, ed 5. McGraw-Hill: New York, 1999. Wellik GM: Nerve entrapments of the wrist, J Am Assoc Phys Assist 2005;18(4):18–23.
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Hand Injuries MARK S. SHORT AND BENJAMIN P. HARRISON
ICD Codes: Finger fracture 816.00, Metacarpal bone fracture 817.00, Tendosynovitis finger 727.05, Tendon laceration 848.9, Finger infection 681.00, Nail infection 681.02
Key Points All hand injuries should be evaluated as surgical emergencies. Loss of function of a digit or hand is devastating to a person’s recreational and professional life. Saving and maintaining function is of the utmost importance in treatment of any hand injury. ! Emergency Actions ! During the assessment of hand injuries, the entire upper extremity should be exposed for examination, and dressings applied in the field or in the triage area of the ED should be removed. Hemostasis should be achieved with direct pressure and elevation of bleeding sites. The patient’s neurovascular status should be assessed and treated, if compromised.
ANATOMY The anterior surface of the hand is referred to as palmar or volar, whereas the posterior surface is referred to as dorsal. The proximal and distal palmar creases can easily be identified in their generally horizontal orientation and can be important landmarks when describing injuries to a consultant. The sides of each finger or the sides of the hand itself are referred to as ulnar or radial, depending on which bone of the forearm they face. The joints of the hand are capable of various motions termed flexion, extension, hyperextension, and radial and ulnar deviation.
The Bones The hand skeleton consists of 19 bones: 14 phalanges of the digits and five metacarpals. Numbers 1 through 5, representing the thumb, index finger, middle or long finger, ring finger, and little finger, respectively, refer to each digit. Each finger has three phalanges—distal, middle, and
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proximal—and articulate with one another at the distal interphalangeal (DIP) and proximal interphalangeal (PIP) joints. The thumb has two phalanges, distal and proximal, that articulate at the interphalangeal joint (IP). The distal carpals of the wrist articulate with the metacarpals and will not be discussed in this section, except to note the importance of the fixed, much less mobile articulations of the second and third digits, also referred to as the first and second rays of the hand.
Blood Supply The vascular supply to the hand is provided by the radial and ulnar arteries, which form anastomoses named the superficial and deep palmar arches. The superficial arch extends more distally in the hand, and branches from it form the common digital arteries. These arteries bifurcate into the proper digital arteries, which have numerous arcades that nourish the fingers. This redundant blood supply makes it unlikely for a traumatic injury to cause distal hypoperfusion. Accordingly, if such an injury is suspected to have disrupted a major feeding vessel, the lack of distal hypoperfusion should not curtail an appropriate investigation to uncovering it.
Flexor Tendons The flexor digitorum profundus (FDP) and superficialis (FDS) are common to each finger, inserting on the proximal aspect of the distal and middle phalanges, respectively, whereas the thumb has only the flexor pollicus longus inserting on the distal phalanx. Each finger FDS bifurcates just distal to the metacarpophalangeal (MCP) joint into branches known as slips, allowing the FDS to emerge anteriorly between them. Synovial-lined flexor sheaths enclose the flexor tendons just distal to the distal palmar crease and regions of thickening provide a pulley effect, disallowing bowstringing of these tendons as they cross joints. Ulnar and radial collateral ligaments stabilize each of the IP joints of all digits.
Extensor Tendons The extensor system of the hand is composed of six dorsal compartments on the wrist through which the extensor tendons pass. The first compartment is located radially and houses the extensor pollicus brevis and the abductor pollicus longus. The compartments pass under the extensor retinaculum, which roofs the tendons to prevent them bowstringing in hyperextension. Both intrinsic and extrinsic muscle groups mobilize the extensor tendons.
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Sensory and Motor Function The ulnar, median, and radial nerves supply both motor and sensory functions of the hand. The intrinsic muscles of the hand are the thenar, hypothenar, lumbrical, and interosseus groups.
INJURY HISTORY As with most injuries, the patient’s, bystanders’, or paramedics’ history of hand injuries can provide valuable clues regarding particular injuries, and a detailed account of the mechanism of injury should always be obtained. All parties should be asked about any prehospital manipulations or reductions of deformities. The patient’s medical history should be taken, with the practitioner specifically noting prior hand surgeries, medications, and chronic illnesses such as diabetes that may predispose him or her to an immunocompromised state. Prior tetanus immunizations, smoking status, and drug allergies should be documented, as should the patient’s occupation, since these historical aspects may influence management. The time interval between the injurious event and the ED presentation is also important because this may affect wound management.
PHYSICAL EXAMINATION During the assessment of hand injuries, the entire upper extremity should be exposed and dressings applied in the field or in the triage area of the ED should be removed. Hemostasis should be achieved with direct pressure and elevation of bleeding sites. If this fails, a blood pressure cuff can be placed on the forearm and inflated until bleeding stops; however, it should not be left inflated for more than 20-minute intervals. All hand injuries should be assessed for point tenderness, vascular supply, and motor and sensory function. Two-point discrimination should be checked at the fingertips, and the integrity of the extensor and flexor tendons should be assessed. When evaluating the FDP, the practitioner should immobilize the PIP in extension since a disruption of the FDP can easily be missed if this maneuver is not performed. The range of motion of all joints of the hand should be evaluated, noting the presence of rotational deformities that suggest a phalanx or metacarpal fracture. The patient should be asked to make a fist, with the hand in supination, while the practitioner notes any overlapping of digits with this active flexion. It is helpful to also assess the uninjured hand for comparison.
Fractures Fractures of the phalanges and metacarpals are quite common and are classified as either open or closed and either transverse, intra-articular, comminuted, spiral, or oblique. Distal tuft fractures are common and
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involve the fingertips. Of note, subungual hematomas (i.e., blood collection beneath the nail plate) may occur with or without an underlying fracture and can be quite painful. Trephination of the nail plate should be undertaken using a disposable cautery device, or the practitioner can drill with an 18-gauge needle, to drain the hematoma. This can usually be done without analgesia, but occasionally a patient may require a digital block before the procedure. Finger fractures that are intra-articular, displaced, or angulated may require surgical fixation or it will cause significant deformity and dysfunction. Patients with these injuries should be referred to a hand surgeon after a finger splint is placed and/or the affected finger is taped to an adjacent finger (dynamic splint). Metacarpal fractures are also commonly seen by emergency care providers. The following summarizes the management of the four types of metacarpal fractures:
Transverse fractures without rotational deformity are splinted and an orthopedic referral is made, usually for evaluation within 72 hours. Oblique fractures usually have some degree of rotational deformity and require reduction and stabilization by an orthopedic surgeon. As little as 10 degrees of malrotation can result in significant disability. Metacarpal fractures of the second through fifth rays are classified into four anatomical areas: the metacarpal head, neck, base, and shaft. Fracture of the fifth metacarpal neck is the most common metacarpal fracture. It often occurs a result of a punch injury and is thus commonly referred to as a “boxer’s fracture.” These fractures are relatively easy to reduce, and a certain amount of angulation is permissible before splinting. However, referral to an orthopedist within 72 hours is still advised to ensure optimal management and follow-up. Conversely, fractures to the second and third metacarpal necks require near anatomical reduction of angulation before splinting or casting, and if this is unobtainable in the ED, an urgent referral is indicated. Fractures at the base of the fifth metacarpal are often associated with disruption of the metacarpal-hamate articulation and may require surgical reduction. Intra-articular thumb metacarpal base fractures are important to recognize. Bennet’s fractures are through the base of the thumb metacarpal and disrupt the joint at the volar base, with dislocation or subluxation of the carpometacarpal joint. They require ORIF by a surgeon and, despite optimal management, may cause prolonged disability. Likewise, Rolando’s fracture is a comminuted fracture at the thumb metacarpal base that requires thumb spica splinting and orthopedic referral; these fractures have the potential to cause long-term disability.
Dislocations Hand joint dislocations are commonly reported in the ED, and their associated ligamentous injuries range from simple mild sprains to complete
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disruptions with joint instability. Dislocations are frequently sports related and often have been reduced before arrival at the ED by the patient, other players, or trainers. Even a normal-looking hand must undergo meticulous evaluation to uncover such occult and potentially disabling injuries. Significant pain may hamper the patient’s ability to withstand such an examination, and digital block anesthesia can facilitate a thorough evaluation. DIP joint dislocations are almost always dorsally angulated and can usually be reduced easily. Longitudinal traction should be applied to the distal finger with simultaneously applied dorsal pressure to successfully reduce. Postreduction radiographs should be taken to ensure no avulsion fracture exists at the extensor tendon insertion site, then the DIP should be immobilized in a splint in neutral position. Importantly, the PIP should be left free of immobilization with this type of splint to avoid unnecessary stiffness of this joint. The patient should be advised to exercise early active range of motion as tolerance to pain allows. Occasionally, DIP dislocations will be irreducible as a result of intra-articular avulsed bone entrapment and will require operative reduction. Likewise, patients with unstable joints should receive early referral to a hand surgeon. The PIP is the most commonly dislocated finger joint. Due to its complex structures, complications such as persistent pain, flexion deformity, and joint instability are frequent sequelae. Of particular note, the examiner should always evaluate for a boutonniere deformity, which is a complete rupture of the central slip causing extension of the metaphalangeal and DIP joints and flexion of the PIP joint secondary to the unopposed flexors. To evaluate for this injury, the practitioner should have the patient try to extend the PIP against light resistance while held in 90 degrees of flexion. An inability to do so suggests central extensor disruption; however, these injuries are difficult to uncover in the acute setting and are often only discovered after the boutonniere deformity has already developed. MCP joint dislocations and ligamentous injuries are most common at the thumb MCP joint. Dorsal dislocations should be reduced with the wrist and thumb IP in flexion while volarly directed pressure is applied to the dorsum of the base of the proximal phalanx. These reductions may require prereduction ulnar and median nerve regional anesthesia. Postreduction splinting with a thumb spica is required. Irreducible thumb MCP dislocations may indicate dorsal or volar plate entrapment and require urgent referral. The integrity of the thumb ulnar (UCL) and radial collateral ligaments (RCL) should always be assessed. This is best accomplished with radial and ulnar stress applied to a slightly flexed thumb MCP. The degree of laxity, if present, should be compared with the contralateral thumb. UCL laxity, diminished pinch strength, and edematous tenderness at the dorsoulnar aspect of the thumb MCP may represent gamekeeper’s/skier’s thumb. This injury can be acute, chronic, or acute
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on chronic. Stener’s lesion represents trapping of the completely torn UCL proximal to the adductor pollicus aponeurosis, which can lead to significant long-term disability if not operatively repaired. RCL injuries are less common but can also lead to prolonged impairment. UCL/RCL injuries should be secured in a thumb spica splint, and referral should be arranged for further evaluation by an orthopedist.
Tendon Injuries While not uncommon, tendon injuries to the hand can be subtle and difficult to diagnose, whether they present as open or closed wounds after hand trauma. Again, a detailed history of the type of injury, the position of the hand during the injury, time elapsed since the injury, and subjective changes in functional status of the digits are important data to ascertain to lessen the incidence of missed diagnoses. Extensor tendon disruptions usually occur as a result of trauma to the dorsum of the hand, which affords little protection to these structures within the thin skin overlying their superficial position. In most cases, the extensors will be lacerated secondary to open injuries. Most extensor tendon injuries should be repaired by an orthopedist. Extensor tendon injuries over the dorsum of the metacarpals can be repaired by emergency care providers with the knowledge and experience of proper suturing techniques. The tendons here are more superficial and not associated with joint structures. To evaluate for flexor tendon injuries, each flexor tendon should be tested separately (see Dislocation section). Potentially devastating complications include concomitant injuries to the delicate pulley systems of the digits, and all flexor tendon disruptions require evaluation by an orthopedist. ED management includes adequate analgesia, wound irrigation, and splinting with consultation of a hand surgeon in the ED. Operative repair may be delayed for days, and the orthopedist may appropriately request that the skin over the wound be loosely closed before the patient is sent out for follow-up. Although not supported by evidence for uncontaminated wounds, many orthopedists also request oral antibiotics for patients with open flexor tendon lacerations.
Hand Infections Most patients with established hand infections require admission to the hospital and parenteral antibiotics. Exceptions include superficial or localized abscess collections such as paronychia. Simple lacerations should be copiously irrigated with high-pressure normal saline and should be fully
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explored in a well-lighted environment under a bloodless field/tourniquet. Bite wounds require prophylactic antibiotics (e.g., amoxicillin/clavulanate), but simple hand lacerations do not. Dorsal injuries to the metaphalangeal joints should be considered bite wounds until proven otherwise. Usually a result of the patient’s closed fist hitting the teeth of another person, these so-called fight bites require meticulous irrigation, examination through the entire range of motion, and antibiotic therapy. Pain with axial loading suggests septic arthritis, which requires intraoperative joint irrigation by an orthopedist. Often, these infections involve periarticular structures and are associated with open extensor tendon lacerations as well. Radiographs are required to assess for fractures and possible foreign bodies (e.g., teeth). Antibiotics should be administered (ampicillin/sulbactam is a good choice for all bite wound infections), and a hand surgeon should be consulted for further evaluation. A paronychia is an abscess of the medial or lateral nail fold that usually presents as a painfully erythematous and fluctuant swelling. There may or may not be a history of trauma. This type of infection is exquisitely tender on physical examination and, as with most abscesses, the treatment is incision and drainage. A No. 11 scalpel blade should be directed along the transverse diameter of the nail plate and into the point of maximal fluctuation after anesthesia with a digital block (very small, superficial paronychias may not require anesthesia). The practitioner should express the residual pus through the incision and irrigate the wound. Frequent warm tap water soaks for 3 days will allow continued drainage and prevent reaccumulation of purulence. Antistaphylococcal antibiotics should be administered for associated cellulitis or in the case of immunocompromised patients. A felon is an infection of the pulp space of the finger pad. This type of infection is most common on the thumb and index finger of the dominant hand. The pad is classically tender and enlarged, and there may be minimal fluctuation on physical examination. As with acute paronychia, purulence within a felon must be drained before healing can begin. Treatment is undertaken with a unilateral longitudinal incision sparing the midline of the volar aspect of the digit to preserve the sensory capability after digital block anesthesia. If the area of greatest fluctuation is over the midline, the clinician should make a longitudinal incision over this area just large enough to permit drainage. He or she should bluntly dissect the septae through the incision, but ensure the incision does not approach the distal flexor crease or extend to the fingertip. Wound culture samples should be sent for analysis, and the wound should be irrigated. A gauze or surgical wick should be placed to facilitate continued drainage before warm soaks are started in 1–2 days. Complications such as osteomyelitis are possible, and good follow-up is essential.
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Flexor tenosynovitis is a potentially devastating infection that can course within the flexor tendon sheath and requires surgical drainage. It usually results from penetrating trauma to the hand, and mismanagement can lead to loss of function of a digit or the entire hand. Flexed posture of the affected digit at rest, symmetrical edema of the involved digit, tenderness over the flexor tendon sheath, and exquisite pain on passive extension are the four components of the classic physical examination findings (i.e., Kanavel’s signs). Intravenous antibiotic therapy should be initiated in the ED, and a culture of the wound should be performed, if possible. Most cases require immediate drainage in the operating room, although orthopedists may request that patients for whom equivocal findings are available early be admitted to receive parenteral antibiotics and close observation. The emergency care provider should immobilize the hand and consult a hand surgeon immediately for definitive management.
High-Pressure Injection Injuries It is estimated that 100 lb per square inch (psi) is required to breach the skin with pressurized liquid. Industrial equipment can generate thousands of pounds of pressure, and these injection injuries can be limb threatening. The pressure, the amount, the location, and the type of material injected determine injury severity. The affected digit may present similar to a compartment syndrome with pain, pallor, and edema. The use of antibiotics in this situation is controversial but may be recommended by the consultant. Warm water soaks and digital blocks are contraindicated. Administer systemic analgesia and consult an orthopedist for immediate surgical debridement. Amputations are common, and many times patients with these injuries must undergo surgery within several hours of presentation to avoid this. The use of parenteral steroids is controversial; these should be administered only at the request of the hand surgeon.
LABORATORY FINDING There are no specific laboratory tests for hand injuries. Laboratory tests are directed to the specific kind of injury or the patient’s underlying illnesses.
RADIOGRAPHS Radiography is directed to the kind of injury that is suspected. Radiographs should be taken of all hand injuries to examine for fracture or foreign bodies.
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Bibliography Bowman SH, Simon RR: Metacarpal and phalangeal fractures, Emerg Med Clin North Am 1993;11(3):671–702. Harrison BH, Hilliard MW: Emergency department evaluation and treatment of hand injuries, Emerg Med Clin North Am 1999;17(4):793–822. Hart RG, Uehara DT, Kutz JE: Extensor tendon injuries of the hand, Emerg Med Clin North Am 1993;11(3):637–649. Henry M: Fractures and dislocations of the hand. In Rockwood CA, Green DP, Heckman JD, Bucholz RW (eds): Rockwood and Green’s Fractures in Adults, ed 5. Vol 1. Lippincott, Williams & Wilkins: Philadelphia, 2001, pp 656–748. Seaberg DC, Angelos WJ, Paris PM: Treatment of subungual hematomas with nail trephination: A prospective study, Am J Emerg Med 1991;9(3):209–210.
Hip Trauma KATHLEEN M. SAMSEY
ICD Codes: Femoral fracture (closed) 821.00, Femur condyle fracture 821.21, Fracture capital 820.01, Femur head 820.01, Femur trochanteric 820.01, Hip dislocations (closed) 835.00, Hip dislocation (anterior) 835.03, Congenital hip dislocations 754.30, Legg-Calve´-Perthes disease 732.1, Slipped capital femoral epiphysis 737.2, Septic hip or septic arthritis 711.0
Key Points Patients with suspected hip injuries should be undressed from the waist down to check for obvious deformities, leg shortening, internal/external rotation, and skin color. The patient should not have range-of-motion examination performed until radiographs have demonstrated no fracture. ! Emergency Actions ! All patients with suspected hip fracture or dislocation should have a “safety net” established. Two large-gauge intravenous lines delivering normal saline should be established, the patient should be administered oxygen, and full cardiac monitoring should be undertaken. The ABCs (i.e., airway, breathing, circulation) take precedence over all other evaluation and treatment.
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DEFINITION The hip is a ball-and-socket joint consisting of the acetabulum, made up of the three bones of the pelvis 5 inches below the iliac crest, and the proximal 4 inches of the femur, including the femoral head and neck. In a growing child, the femoral head may be referred to as the capital epiphysis, the presence of which can cause specific types of injuries. Dislocations can be classified as anterior, posterior, central, and inferior. Hip dislocations and fracture-dislocations are two of the few true orthopedic emergencies.
EPIDEMIOLOGY Approximately 250,000 hip fractures occur annually in the United States, and mortality from a hip fracture approaches 25% at 1 year. Age and sex predispose patients to certain types of hip and femur injuries. Fractures and dislocations in younger adults are often the result of direct trauma such as motor vehicle accidents and assault. In older adults and postmenopausal women (often with preexisting bone disease), falls are often the culprit. Pathologic fractures are often the result of cancer, radiation, and chemotherapy. Femoral neck fractures occur more in men, whereas intertrochanteric fractures occur more in women. Hip injuries in children are often the result of congenital or traumatic causes, and they are more common in boys.
ANATOMY The femur is the strongest and longest bone in the body. The two femurs extend obliquely from the pelvis medial to the knee, where they can best support the body. The hip joint itself is reinforced by a well-developed fibrous capsule, ligaments, and the proximal musculature of the lower extremity. The proximal femur consists of the femoral head, neck, and intertrochanteric region, with the greater trochanter located superolateral and the lesser trochanter located inferomedial. The greater trochanter is typically at the level of the palm of the hands when the arms are resting by the sides. The intertrochanteric line is an oblique line that connects the greater and lesser trochanter, marking the junction of the femoral neck and its shaft. The powerful musculature of the hip and thigh are located in three separate compartments, each containing associated nerves and blood vessels. The muscles are also grouped according to their primary action at the hip. The arterial supply for the hip includes the obturator, medial/lateral femoral circumflex, and the superior/inferior gluteal arteries. Of note, the circumflex arteries that branch off of the deep femoral artery provide
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the tenuous blood supply to the femoral head. The major nerves of the hip are the femoral and sciatic nerves.
EXAMINATION Patients with suspected hip injuries should be undressed from the waist down to check for obvious deformities, leg shortening, internal/external rotation, and color. The patient should not have range-of-motion examinations until radiographs have demonstrated no fracture. The joint itself should be palpated and a thorough neurological and vascular examination performed. Serious hip injuries will demonstrate pain with even mild axial loading (pressing up on the bottom of the foot). According to the old adage to check “one joint above and below” the site of suspected injury, the knee should also be examined and radiographs possibly obtained.
CLINICAL PRESENTATION All patients with suspected hip fracture or dislocation should have a safety net established. Two large-gauge intravenous lines of normal saline should be established, the patient should be administered oxygen, and full cardiac monitoring should be undertaken. The ABCs of resuscitation take precedence over all other evaluation and treatment, and the examiner must always remember that significant blood loss can accompany any femoral fracture. Proximal femoral fractures are generally categorized according to location (e.g., neck, trochanteric, intertrochanteric, and subtrochanteric). There are rare femoral head fractures, associated with dislocations, and an orthopedic surgeon should be consulted to manage these. There are also avulsion fractures, common in young adults and athletes, which often present as thigh pain. These generally occur at the anterior superior iliac spine, the anterior inferior iliac spine, and the ischial tuberosity. They present as a “snapping” or “popping” sensation. The appropriate treatment is rest and consultation with an orthopedic specialist. Femoral neck fractures are generally considered pathologic, due to underlying bone loss. They are classified as displaced or nondisplaced. Patients with nondisplaced fractures present with a history of minor trauma and a painful limp. The appropriate treatment is early ambulation or internal fixation, depending on the stability. Ninety-six percent of cases will heal without complication. If a fracture is suspected, but not evident on radiograph, the hip should be imaged again in 10–14 days. A CT may also be helpful. AVN of the femoral head is the most common complication. Patients with displaced fractures will present with pain and inability to ambulate. The limb will lie externally rotated, abducted, and slightly
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shortened. It will be evident on plain radiographs. Treatment is usually accomplished with closed reduction and internal fixation. Complications included AVN, infection (because the fracture line extends into the joint), and pulmonary embolism. Trochanteric fractures are rare. Greater trochanteric fractures are usually a result of a direct fall or avulsion at the insertion of the gluteus medius. In the young adult population, it is due to a true epiphyseal separation. The patient presents with hip pain when walking and pain upon palpation of the greater trochanter. Treatment is controversial: conservative versus internal fixation. Lesser trochanteric fractures are a result of an avulsion at the insertion of the iliopsoas muscle. Patients with this type of injury usually report pain with hip flexion and internal rotation. Treatment consists of pain control, early mobilization, and a return to weight bearing as tolerated. Intertrochanteric fractures, like most hip fractures, usually occur as a result of high-speed trauma in younger patients and falls in older patients. They will present with swelling and pain with any movement or weight bearing. The extremity may be shortened and externally rotated. These fractures are classified as stable or unstable and also according to the number of separate bone fragments. Caution should be exercised with these patients because the majority of them are often under-resuscitated; they are frequently dehydrated, and up to 3 units of blood may be lost into the fracture site. Most will require urgent, not emergent, internal fixation by an orthopedic specialist. If this is delayed greater than 48 hours, however, there is a 10-fold increase in mortality. It is also imperative to evaluate the patient for other associated fractures of the upper extremities, ribs, and spine. The femoral fracture can distract both the patient and the examiner. Subtrochanteric fractures occur between the lesser trochanter and the proximal 5 cm of the femoral shaft, often associated with an intertrochanteric fracture. The risk for hypovolemic shock from blood loss at the site is significant in these patients, and the injury should be immobilized with splint and the patient resuscitated with fluids. Hip dislocations and fracture-dislocations are two of the few orthopedic emergencies. Often the result of significant trauma, they require considerable forces to be produced. These patients should be evaluated as persons who have experienced major trauma because of the high rate of multisystem injury. Dislocations with associated fractures should not be reduced by an emergency care provider. Isolated dislocations can be reduced, but multiple attempts should be avoided. If reduction proves difficult, it should be performed with the patient under general anesthesia. Anterior dislocations (10%–15% of patients) occur as a result of forceful extension, abduction, and external rotation. As a result, patients with this type of injury present with the hip abducted, slightly flexed, and externally rotated. On radiograph, the femoral head will be inferior and medial
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to the acetabulum, best viewed laterally. Reduction can be achieved by placing the patient supine, applying traction along the long axis with the hip slightly flexed, and gently adducting/internally rotating the leg. This can be attempted in the ED with proper procedural sedation or with the patient under general anesthesia. Posterior dislocations (80%–90% of patients) are almost always due to motor vehicle crashes in which the patient strikes his or her knee on the dashboard. On presentation, the limb is shortened, adducted, and internally rotated. The hip is often mildly flexed. This type of injury will usually be obvious on anteroposterior and lateral radiographs, but another clue is the loss of the lesser trochanter on anteroposterior view, due to internal rotation. Posterior dislocations are particularly at risk of developing AVN, and this condition should be considered a true emergency. Reduction should be attempted quickly in the ED, with the patient under proper sedation. Commonly, the Allis technique is used, in which strong traction is applied along the axis of the femur with the hip and knee each flexed at 60–90 degrees. Assistants hold the pelvis to the bed as the operator applies traction. Gentle internal and external rotation can also be used while traction is applied. Postreduction radiographs should be obtained and the limb stabilized. A thorough prereduction and postreduction neurovascular examination should be performed, focusing on the sciatic nerve and femoral vessels. Sciatic injury occurs in approximately 10% of patients with posterior hip dislocations. Pediatric hip injuries are unique to that age group, and any hip injury has the potential for premature growth arrest. Congenital hip dislocations are more common in girls and in firstborn children. The diagnosis is made based on the results of the Ortolani test where pressure is applied along the axis of the femur with the hips and knees flexed, and the femurs are rotated outward. If the femoral head subluxes or an audible click is heard, orthopedic consultation is required. Traumatic dislocations are evaluated and managed similarly to those in adults. Traumatic pediatric fractures are rare. If one is suspected, however, the classic Salter-Harris system is not used. Rather, the Delbert classification is used, which separates fractures through the physis, transcervical, cervicotrochanteric, and intertrochanteric regions. Legg-Calvé-Perthes disease is idiopathic AVN of the pediatric femoral head. It occurs between ages of 2 and 10 years, with a peak incidence at 6 years of age. It is five times more common in boys. It presents insidiously with a painful limp. On radiograph, there will be necrosis, reabsorption, and regeneration of bone in different stages. Consultation with a pediatric orthopedic surgeon is needed. Slipped capital femoral epiphysis occurs between the ages of 10 and 17 years, with a peak incidence at 13 years for boys and 11 years for girls. It occurs twice as frequently in boys as in girls, and 25% of cases are
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bilateral. It is thought to occur due to structural weakness in the physeal cartilage at the onset of puberty. Risk factors include obesity, previous radiation or chemotherapy, renal osteodystrophy, hypothyroidism, and neglected septic arthritis. Patients present with insidious onset of groin, thigh, or knee discomfort, which develops into hip stiffness and limp. Examination will reveal hip tenderness and decreased range of motion. Initially, anteroposterior, lateral, and frog-leg radiographs should be obtained, and findings may be normal. Comparative bilateral views should be obtained if slipped capital femoral epiphysis is suspected but not obvious on radiograph. One should look for the “scoop slipping off the ice cream cone” as the epiphysis slides off the femoral head. If occult fracture is suspected, CT or MRI should be used. A consultation with an orthopedic surgeon is warranted for traction and fixation. Septic hip or septic arthritis, though not traumatic injuries, should be included in the differential for a pediatric patient with painful hip. Septic arthritis is the most common finding in an infant with a painful hip. Infants will be fussy and febrile, will cry when held, and will likely be feeding poorly. The most common causes are group B Streptococcus, Staphylococcus epidermidis, and Haemophilus influenzae. Older children present with limp or painful weight bearing. On examination, there is decreased or painful range of motion. Blood cultures and ESR test should be performed. If septic hip is suspected, immediate orthopedic consultation is warranted.
RADIOGRAPHS All suspected hip dislocations and fractures should be evaluated with at least a low anteroposterior pelvis view. Lateral films are also helpful if the injury is not obvious from this angle. Trauma patients should not be put in a frog-leg position. If injury is suspected but not obvious, the integrity of Shenton’s line should be evaluated. This line (on anteroposterior view) is a smooth, curved line drawn along the superior border of the obturator foramen and the medial aspect of the femoral metaphysis. If the line is disrupted, femoral neck fracture or hip dislocation is more likely.
LABORATORY EVALUATION All patients with suspected hip fractures should be type and crossmatched for at least 2–4 units of blood. They should undergo a CBC, coagulation panel, serum chemistry test, and a urinalysis.
Bibliography Bedi A, Le T: Subtrochanteric femur fractures, orthopedic, Clin North Am 2004; 35(4):473–483.
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Canale ST: Campbell’s Operative Orthopedics, ed 10. Mosby: St Louis, 2003. Mirza A, Ellis T: Initial management of pelvic and femoral fractures in the multiply injured patient, Crit Care Clin 2004;20(1):159–170. Roberts J, Hedges J: Clinical Procedures in Emergency Medicine, ed 4. WB Saunders: Philadelphia, 2004. Rosen P, Marx R: Emergency Medicine: Concepts and Clinical Practice, ed 5. Mosby: St Louis, 2002. Salyer S: The Physician Assistant Emergency Medicine Handbook. WB Saunders: Philadelphia, 1997. Vlauvelt C, Nelson F: Manual of Orthopaedic Terminology, ed 6. Mosby: St Louis, 1998.
Infections of the Bones and Joints BENJAMIN H.TAYLOR
ICD Codes: Osteoarthrosis 715.9, Osteomyelitis periostitis 730.0, Pyogenic arthritis 711.0
Key Points Osteomyelitis can be either acute or chronic. Septic arthritis usually occurs from hematogenous spread. ! Emergency Actions ! Septic arthritis in children whose growth plates are not closed is a medical emergency and requires evaluation by an orthopedic surgeon.
DEFINITIONS Osteomyelitis Osteomyelitis, inflammation of bone and bone marrow, is the name given to infections of the bone. This condition may present in an acute or chronic stage. The affecting organisms are bacteria, mycobacteria, or fungi.
Septic Arthritis Infectious or septic arthritis is an inflammatory reaction resulting from hematogenous spread, direct inoculation, or direct extension from an adjacent focus of the joint space by pathogenic microorganisms, resulting in
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pain, swelling, redness, limitation of joint motion, and eventually joint destruction and permanent disability, if the condition is left untreated.
EPIDEMIOLOGY Osteomyelitis The overall prevalence of acute hematogenous osteomyelitis is cited as affecting 1% of hospitalized patients and occurring in 1 case per 5000 children. Male children have a modestly greater susceptibility to this disease than do female children, with a male-to-female ratio of 2–3:1. The majority of children diagnosed with osteomyelitis have no previous medical history or risk factors, with the exception of patients with sickle cell disease. Although most children in whom osteomyelitis is diagnosed have no identifiable risk factors, the opposite is true for adults, among whom the majority of cases occur in the chronically ill patients, patients with altered immune states, persons with diabetes, and patients with peripheral vascular occlusive disease. Osteomyelitis after open fracture or orthopedic surgery is the most common form of the disease in adults. Patients of lower socioeconomic status are more prone to present with osteomyelitis. The prevalence of chronic osteomyelitis is 2 cases per 10,000 persons.
Septic Arthritis Septic arthritis occurs in all age groups but is more common in children than adults. Half of all cases of septic arthritis occur in children younger than 3 years of age. Males are usually affected more commonly than females, although in patients with underlying rheumatoid arthritis, females are affected more often. Other groups at high risk include intravenous drug users, patients receiving dialysis, and patients with sickle cell disease, diabetes, and acquired immunodeficiency syndrome. Disseminated gonococcal infection with associated gonococcal infective arthritis is the leading cause of hospital admission in these patients.
PATHOLOGY Osteomyelitis Osteomyelitis causing microorganisms involved in the development of osteomyelitis (e.g., pyogenic bacteria, mycobacteria, fungi) can spread to bone by one of three routes: hematogenous spread, direct extension from a contiguous site of infection or direct introduction, and vascular
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disease. More than 90% of acute osteomyelitis cases are caused by S. aureus, but Streptococcus pyogenes and H. influenzae may also cause acute infection of the bone. Pyogenic bacteria cause almost 90% of bone and joint infections in injection drug users, with S. aureus and Pseudomonas species reported as the most frequent etiology. Gram-negative osteomyelitis may follow gastrointestinal or genitourinary infections. Bacteroides fragilis or pneumococcal osteomyelitis is often preceded by a severe respiratory infection. S. aureus, S. epidermidis, Pseudomonas aeruginosa, Serratia marcescens, and Escherichia coli are typically responsible for persistent osteomyelitis. Acute osteomyelitis can be caused by blood-borne pathogens or infection resulting from injury. Chronic osteomyelitis refers to an untreated exogenous or hematogenous infection or one that has failed treatment. There have been several classification systems proposed for osteomyelitis, yet none have achieved universal acceptance. The most common system continues to be the Waldvogel classification system. Hematogenous osteomyelitis occurs predominately in children before the age of epiphysial closure (60 mmHg, SaO2 >90%
879
POTENTIAL ABG RESULTS
Low pH (20% Nitrofurantoin 100 mg bid for 7 days Use only in patients with good renal function; pregnancy risk category B—avoid at 36 weeks’ gestation Ciprofloxacin 250 mg bid for 3 days Avoid use in pregnant patients; not advised in patients aged 18 years and younger; interacts with other medications; other quinolones may be considered but have an increased cost *Adapted from Guidelines from the Infectious Disease Society of America. Warren et al: Guidelines for Antimicrobial Treatment of Uncomplicated Acute Bacterial Cystitis and Acute Pyelonephritis in Women, Clin Infect Dis 1999;745-758. TMP-SMX, Trimethoprim-sulfamethoxazole; bid, twice a day.
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In ED settings serving indigent populations, the incidence of subclinical pyelonephritis may approach 70%. It is necessary to assess each patient’s ability to follow-up. If follow-up compliance is not expected, or if there is a risk of subclinical pyelonephritis, the patient should be prescribed a 10- to 14-day regimen. Women who present with signs and symptoms of pyelonephritis must be treated with vigorous oral or IV fluid and a dose of parenteral antibiotics. A popular regimen, includes 2 L of fluid (IVor orally) and 2 g of ceftriaxone IV. The patient may then be discharged home if she is able to tolerate oral fluid and oral antibiotics. Women with repeated UTIs (two or more over 6 months or three or more over 12 months) may require prophylaxis. She should be advised to follow up with her primary care provider and should receive consideration for referral to a urologist. In the case of a UTI in a male patient, the possibility that infection has ascended to the kidney must be assumed. Outpatient treatment includes TMP-SMX or one of the quinolones such as ciprofloxacin to be taken for a minimum of 10 days. If the patient appears toxic, is unable to tolerate fluid orally, or is unable to care for himself at home, hospital admission should be considered. Appropriate inpatient antimicrobial therapy includes a third-generation cephalosporin, such as ceftriaxone, or an aminoglycoside. Adequate hydration, antipyretics, and pain medicine should also be considered. Consultation with a urologist is necessary; however, this can be done on an outpatient basis.
Bibliography Bent S, Nallamothu B, Simel D, et al: Does this woman have an acute uncomplicated urinary tract infection? JAMA 2002;287:2701–2710. Chambers S: Cystitis and urethral syndromes. In Cohen J, Powderly WG: Infectious Diseases, ed 2. Elsevier: St Louis, 2004, pp 737–743. Fihn S: Acute uncomplicated urinary tract infection in women, N Engl J Med 2003;349:259–266. Fitzgerald M: Urinary tract infection: Providing the best care. Available at: http://www. medscape.com/viewprogram/1920_pnt. Accessed on February 16, 2005. Hooton T, Scholes D, Stapleton A, et al: A prospective study of asymptomatic bacteriuria in sexually active young women, N Engl J Med 2000;343:992–997. Howes D: Urinary tract infection, female. Available at: http://www.emedicine.com/emerg/ topic626.htm. Accessed on February 16, 2005. Howes D: Urinary tract infection, male. Available at: http://www.emedicine.com/emerg/ topic626.htm. Accessed on February 16, 2005. Howes D, Bogner M: Urinary tract infections. In Tintinalli JE, Kelen GD, Stapczynski JS (eds): Emergency Medicine: A Comprehensive Study Guide, ed 6. McGraw-Hill: New York, 2004, pp 606–612. Warren J, Abrutyn E, Hebel J, et al: Guidelines for antimicrobial treatment of uncomplicated acute bacterial cystitis and acute pyelonephritis in women, Clin Infect Dis 1999;29:745–758.
Chapter 20
Transplantation Emergencies Cardiac and Lung Transplantation SCOTT B. JOHNSON, JOHN T. DEEL, SANDEEP J. KHANDHAR, ERIC R. PRESSER, AND JOHN H.CALHOON
ICD Codes: Cardiomyopathy (includes the various kinds) 425, Left heart failure 428.1, Chronic obstructive pulmonary disease 496, Idiopathic pulmonary fibrosis 516.3, Interstitial lung disease 515, Sarcoidosis 135, Pulmonary hypertension 416, Cystic fibrosis 277.02, Emphysema 492.8, Scleroderma 710.1, Complication of transplanted organ, rejection, heart 996.83, Complication of transplanted organ, rejection, lung 996.84, Carditis 429.89, Lung infection 518.89, Pneumonia 486 CPT Codes: Lung transplant, single, without cardiopulmonary bypass 32851, Lung transplant, single, with cardiopulmonary bypass 32852, Lung transplant, double, without cardiopulmonary bypass 32853, Lung transplant, double, with cardiopulmonary bypass 32854, Donor pneumonectomy 32850, Heart transplantation, with or without recipient cardiectomy 33945, Bronchoscopy, rigid or flexible 31622 ! Emergency Actions ! Patients who have had a heart transplant or a lung transplant, or are on the waiting list for the same, usually have one or more of the following problems when presenting to an emergency department: heart failure, pulmonary failure, rejection, or infection. For any of these acute problems, one must remember the simple ABCs: airway, breathing, and circulation. Caregivers who are not familiar with prethoracic or postthoracic transplant recipients may find themselves overwhelmed at times with the complexity of a patient’s illness and the medicines they may be taking to treat their underlying disease or to prevent allograft rejection. If one just keeps in mind that most transplantrelated life-threatening problems are treated with usual supportive care, the caregiver can confidently initiate lifesaving therapy in a more timely fashion. Patients either pretreatment or posttransplant may require emergent intubation and mechanical ventilation. Oxygen saturation monitoring as well as close blood pressure monitoring should be undertaken. Oxygen
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1148 ESSENTIAL EMERGENCY MEDICINE FOR THE HEALTHCARE PRACTITIONER should not be withheld if it is needed. Patients on the transplant waiting list may be receiving a continuous infusion of inotropes (e.g., dopamine, milrinone, dobutamine) if experiencing heart failure and waiting for a heart, or they may be receiving pulmonary vasodilators if diagnosed with primary pulmonary hypertension if waiting for a lung—if so, a quick check to make sure that the portable pump is working should be done. Patients experiencing profound heart failure may require inotropes (e.g., milrinone, which decreases afterload, increases inotropy, and may actually decrease the blood pressure; dobutamine, which has similar affect, also decreases afterload and increases inotropy, but probably increases chronotropy more than milrinone) if they are not already taking them, or new ones or higher doses of the same if they already are receiving these medications. If volume is overloaded, a patient may benefit from intravenous furosemide or another diuretic agent. Patients with severe cardiac rejection can present experiencing profound heart failure; likewise, patients with severe pulmonary rejection can present in profound pulmonary failure. Supportive care, rather than definitive care (e.g., high-dose immunosuppressive therapy) should be the mainstay of treatment, at least initially.
DEFINITION Patients who are on the transplant list waiting for an appropriate donor are usually quite ill from their underlying diagnosis. Most of these patients have undergone an intense pretransplant evaluation and hence are quite familiar and knowledgeable about their disease state. Likewise, patients who have already undergone a heart or lung transplant are usually knowledgeable concerning the nuances of their graft and the medicines they are taking to sustain it. Similarly, they are usually quite aware of problems that may be recurring. Therefore, a quick history is often sufficient to determine current problems and to better define the problem. Usually, a patient who is awaiting or has just received a heart or lung transplantation will present with either one or a combination of the following problems: heart failure, pulmonary failure, rejection, or infection. It is important to remember that heart transplantation and lung transplantation trade one problem (heart failure and pulmonary failure, respectively) for another, creating an immunocompromised host who is susceptible to usual as well as to opportunistic infections (e.g., fungal, viral) not commonly seen in otherwise healthy persons.
EPIDEMIOLOGY In 2005, 2125 heart transplants and 1407 lung transplants were performed in the United States. Common diseases that lead to end-stage
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heart disease and the need for cardiac transplantation include cardiomyopathy from any cause (e.g., ischemic, viral, alcoholic, familial, and idiopathic), congenital abnormalities not amenable to surgical correction, and postsurgical pump failure from any cause. Common diseases that lead to end-stage pulmonary disease and the need for lung transplantation include chronic obstructive lung disease, pulmonary fibrosis from any cause, primary pulmonary hypertension, and septic lung disease such as cystic fibrosis. Single lung transplantation is often all that is needed; however, septic lung disease of both lungs necessitates the removal of both lungs and hence is one of the absolute indications for bilateral lung transplantation. Combined heart and lung transplantation is relatively rare but is usually reserved for end-stage disease of both the heart and lungs when surgical correction of either organ is not possible. Most patients awaiting transplant are usually in close proximity to the transplant center where they are receiving care, since they typically have to be able to get to the hospital within a set time period if called for a transplant when a donor becomes available. Patients who have had a transplant likewise are usually in relatively close proximity to the center where the transplant was performed (because of the close follow-up necessary with most of these patients) or at least in close proximity to a transplant center that serves as a surrogate. As a consequence, most of these patients can and should be transferred to the tertiary transplant center familiar with their care once stabilized for transport. Occasionally, however, these patients find themselves relatively far away from a tertiary transplant center. In these cases, the patient may require admission to the hospital to which they present themselves, even though the hospital itself is not specifically trained or equipped to handle services required to either accurately diagnose or definitively treat the presenting problem. In these cases, supportive care in the form of pulmonary and cardiac support should be the mainstay of treatment. Treating a presumed rejection episode with high-dose immunosuppressive agents without a relatively firm diagnosis should be discouraged, since treatment can be fatal if the problem turns out to be infection or sepsis. The ability to distinguish between these two diagnoses strictly on clinical grounds can often be very difficult, and a misdiagnosis and treatment can be potentially fatal (see later text).
CLINICAL PRESENTATION Heart Failure Symptoms of heart failure include shortness of breath, abdominal pain and nausea, weakness or lethargy, and poor mentation or obtundation. Left heart failure typically produces respiratory symptoms (e.g., cough, shortness of breath, frothy sputum), and right heart failure produces peripheral swelling and abdominal symptoms.
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Pulmonary Failure Symptoms of pulmonary failure include shortness of breath, tachypnea, an inability to talk in complete sentences, tachycardia, cough, weakness, and lethargy. This can occur both in patients awaiting lung transplant and in recipients, as well as awaiting or who have received cardiac transplantation.
Rejection Rejection of a transplanted organ can present as either heart failure or pulmonary failure, depending on whether it occurs in a lung or heart transplant recipient. Sometimes symptoms are subtle and can include weakness, malaise, cough, and low-grade subjective fevers.
Infection Infection can occur anywhere in the body, given that most lung and heart transplant recipients are taking immunosuppressive medication. Lung transplant recipients not uncommonly get community-acquired pneumonia that can cause fevers, chills, productive or nonproductive cough, shortness of breath, and pleuritic chest pains. Other common sites of infection include the urinary tract (e.g., dysuria, urgency, and frequency), soft tissue and skin (e.g., redness, pain, and purulence), sinuses (e.g., pain, drainage), biliary tract (e.g., right upper quadrant pain, jaundice), and gastrointestinal tract.
EXAMINATION Heart Failure Examination findings in the presence of heart failure include peripheral swelling, cold/clammy periphery with poorly palpable distal pulses, tachycardia (although bradycardia may be present as well), S3 heart sound audible on cardiac examination, jugular venous distention, pulmonary crackles, diminished breath sounds, pleural effusions, and/or a pulsatile liver. Hypotension is also a common finding, although patients can be experiencing heart failure with high blood pressure as well (though the latter usually implies another cause of heart failure besides primary pump failure).
Pulmonary Failure In the presence of pulmonary failure, examination findings will include a cold/clammy periphery, accessory muscle use, wheezing, cyanosis of the
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lips or fingers, and low oxygen saturations. Patients may present with pneumothoraces (i.e., diminished breath sounds on one side, possible mediastinal shift either toward [nontension] or away [tension] from the side of pneumothorax), pleural effusion (i.e., dullness to percussion, diminished breath sounds on the affected sided), and pulmonary consolidation (i.e., bronchial breath sounds, diminished breath sounds, crackles, and rhonchi in the larger airways).
Rejection Examination findings related to organ rejection can include those of both heart failure and pulmonary failure, depending on whether the patient is a heart or lung transplant recipient. Signs can include those mentioned above and can also mimic infection, especially if it occurs in a lung transplant recipient.
Infection If infection is present, examination findings can be very nonspecific and can include lethargy, weakness, and mental obtundation. More specific findings can include productive cough, fevers, and findings consistent with pulmonary consolidation or pleural effusion, as described previously. Depending on the location of the infection, symptoms can be variable (e.g., redness, purulent drainage if in the skin or soft tissue; abdominal tenderness in the biliary tree or gastrointestinal tract). Signs and symptoms may be very subtle, and what would normally be expected to be present in a nonimmunocompromised patient may be totally absent or only slightly present in an immunocompromised transplant recipient. Any foreign bodies such as pacemakers, automatic implantable defibrillators, central lines, and indwelling implantable venous reservoirs should be carefully examined for any signs of infection (e.g., tenderness, redness, drainage). Indwelling catheter infections are common and must be suspected in any immunocompromised host.
LABORATORY FINDINGS All patients awaiting transplant or transplant recipients with suspected pulmonary and/or heart failure should undergo arterial blood gas examination to determine hypoventilation (carbon dioxide), acid-base balance, and degree of hypoxemia (oxygen saturation), as well as a complete blood count. A basic chemistry panel, including blood urea nitrogen, serum creatinine, and basic electrolytes (including potassium and sodium) as well as blood glucose, should also be performed. A urinalysis should also be performed with microscopic analysis, since many urinary tract infections
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can be asymptomatic in immunocompromised persons. Blood levels of immunosuppressive medications (e.g., cyclosporine, Prograf) should also be performed if available because this can indicate compliance to medication instructions. In addition, certain disease states can radically alter the blood levels of certain immunosuppressive drugs, making the patient more susceptible to other problems such as renal failure, infection, or rejection when an acute change in the patient’s condition occurs. Sputum samples should be collected from patients suspected of having pneumonia, to be sent for immediate Gram stain as well as culture and sensitivity tests. Blood cultures should also be performed in any patient suspected of having bacteremia, and liver/pancreatic enzymes should be measured in anyone suspected of having biliary infections or obstruction.
DIAGNOSIS The diagnosis of heart failure is suspected on both clinical and radiographic grounds. Echocardiography and pulmonary arterial catheterization can help confirm the diagnosis. Pulmonary arterial catheterization will typically reveal a low cardiac output, high pulmonary arterial pressures relative to the systemic pressures, and high pulmonary wedge pressures reflecting high left atrial filling pressures. The diagnosis of pulmonary failure is made mainly on clinical grounds, with radiographic findings aiding in the diagnosis. It is important to remember that although radiographic findings may be subtle or even completely absent, the diagnosis and subsequent treatment of pulmonary failure should not be withheld if clinically apparent. Cardiac rejection in a heart transplant recipient may be difficult to diagnose and usually requires an endomyocardial biopsy to confirm. This is usually done in the heart catheterization laboratory with the patient under local anesthesia. A catheter is inserted into the right jugular vein and guided fluoroscopically into the right ventricle, where a myotome is used to obtain a small piece of endomyocardium for histological analysis. If rejection is suspected, biopsy should be performed as soon as possible by an experienced surgeon or cardiologist. The diagnosis of acute cardiac rejection may be problematic and as such may be made not uncommonly on clinical grounds alone. Rejection in a lung transplant recipient may also be difficult to ascertain and distinguish from infection (e.g., pneumonia), since it may appear quite similar radiographically, and, as a result, usually requires a bronchoscopic transbronchial biopsy to confirm. This is performed in the bronchoscopy suite by an experienced pulmonologist and usually requires a highly skilled pathologist to confirm. Consequently, such a procedure is usually best performed at a lung transplant center with staff skilled in performing such procedures.
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Infection is usually diagnosed clinically with radiographic help and cultures growing confirmatory organisms. Often a responsible organism cannot be isolated, a not uncommon event in cases of viral or fungal infections.
RADIOGRAPHS An upright and lateral chest radiograph should be performed in all patients awaiting heart or lung transplant and in transplant recipients presenting to the emergency department with any of the previously described signs or symptoms. In addition, computed tomography (CT) scanning should be considered in patients with chest findings seen on plain radiography that are considered to be potential sites for infection. In addition, CT scanning of the abdomen and pelvis should be done in immunocompromised patients presenting with abdominal findings. Plain radiographs of the extremities should be performed when soft tissue infections are suspected so that osteomyelitis can be ruled out. It is important to remember that both rejection and infection can often yield similar radiographic findings in lung transplant recipients.
TREATMENT The treatment priority of heart failure, pulmonary failure, rejection, and infection in a patient awaiting cardiac or lung transplant or in a recipient of one of these organs should first be supportive in nature. Addressing the usual ABCs of airway, breathing, and circulation is of paramount importance when dealing with acute decompensation of a thoracic transplant patient. Heart failure is treated with intravenous diuretics and inotropic support with the main goals being to increase cardiac output, decrease afterload, and decrease demand (i.e., rest and mechanical ventilation, if necessary). Common inotropes include milrinone (increases cardiac contraction and decreases afterload), dobutamine (same action as milrinone, although much shorter acting; may also cause more tachycardia than milrinone); dopamine (increases inotropy and increases renal blood flow at low levels), and epinephrine (increases inotropy, increases chronotropy, and at high doses actually increases afterload). Mechanical support may become necessary if the usual pharmacological support fails. Mechanical support may take the form of the insertion of an intra-aortic balloon pump that augments diastolic blood flow (both distally and into the coronary arteries) and diminishes afterload (thereby off-loading and increasing left ventricular ejection). It accomplishes this by means of a sausage-shaped balloon positioned in the proximal descending thoracic aorta that undergoes quick inflation-deflation cycles timed with the ejection cycles of
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the heart. It can be inserted through the femoral artery, usually using fluoroscopic guidance (although in emergency situations can be inserted at the bedside.) In most severe cases, cardiac assist devices may need to be placed emergently by a cardiac surgeon, with the hope being that the underlying acute event is reversible. If the underlying condition is not reversible, mechanical devices can be inserted surgically and occasionally remain in place for months until a new donor heart can be found. Pulmonary failure is first treated with supportive measures in the form of oxygen administration and then mechanical ventilation (if necessary) commensurate with the degree of clinical decompensation. Endotracheal intubation and positive-pressure mechanical ventilation should not be withheld even in the case of relatively recent lung transplant recipients in which the fear of disrupting new bronchial suture lines may be present, so long as peak pressures are kept within reason (i.e., preferably less than 34 cmH2O). Definitive treatment of pulmonary failure must be aimed at the underlying cause, which is usually rejection versus infection versus both in a lung transplant recipient. This can also be true for a heart transplant recipient who has developed pneumonia as a result of being immunocompromised, or who has developed pulmonary edema from left-sided heart failure from primary graft failure from any reason.
REJECTION Once the diagnosis is confirmed, treatment usually occurs in the form of a steroid pulse bolus, followed by a slow taper. More advanced cases of rejection or patients unresponsive to steroid bolus can be treated with cytolytic therapy, usually in the form of OKT3 monoclonal antibody. It is important to remember that treatment of rejection should be first confirmed with biopsy, since infection can actually be made worse, leading to sepsis and then death if misdiagnosed. However, maintenance immunosuppressive therapy should almost never be withheld from a heart or lung transplant recipient, even when he or she is being treated for a life-threatening infection.
INFECTION Treatment of infection can be local (e.g., drainage of an abscess, removal of a necrotic gallbladder or appendix, removal of an infected intravenous line or port) and/or systemic (e.g., administration of intravenous antibiotics). Specific treatment is aimed at the underlying organism. Usually this is bacterial, but the infection can be an opportunistic fungal or viral organism considering the immunocompromised state of the heart or lung transplant recipient. If life-threatening infection is suspected, appropriate therapy should not be withheld once culture samples have been taken,
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even if confirmatory cultures do not yield a specific organism. Often systemic infections are necessarily treated presumptively, once rejection has been ruled out. It is important to remember that infections can occur simultaneously with rejection episodes, and that even certain infections may predispose the transplant recipient to subsequent or concurrent rejection episodes. The overall prognosis in transplant recipients is variable, depending on the patient’s comorbidities, the severity and number of rejection episodes, the severity and underlying cause of infectious events, and the degree of chronic rejection present, which most certainly eventually occurs in all recipients to some degree. It is important to note that all transplant recipients trade one set of problems for another and that transplantation is by no means considered a “cure.”
Bibliography Bag R: Fungal pneumonias in transplant recipients, Curr Opin Pulm Med 2003;9(3):193–198. Collins J: Imaging of the chest after lung transplantation, J Thorac Imag 2002;17 (2):102–112. Emond JC: What’s new in transplantation, J Am Coll Surg 2002;194(5):636–641. Estenne M, Hertz MI: Bronchiolitis obliterans after human lung transplantation, Am J Respir Crit Care Med 2002;166(4):440–444. Faro A, Visner G: The use of multiple transbronchial biopsies as the standard approach to evaluate lung allograft rejection, Pediatr Transplant 2004;8(4):322–328. Grover FL, Barr ML, Edwards LB, et al: Thoracic transplantation, Am J Transplant 2003;3(Suppl 4):91–102. Kaufman DB, Shapiro R, Lucey MR, et al: Immunosuppression: Practice and trends, Am J Transplant 2004;4(Suppl 9):38–53. Knoop C, Haverich A, Fischer S: Immunosuppressive therapy after human lung transplantation, Eur Respir J 2004;23(1):159–171. Kotloff RM, Ahya VN: Medical complications of lung transplantation, Eur Respir J 2004; 23(2):334–342. Nathan SD: Lung transplantation: Disease-specific considerations for referral, Chest 2005;127(3):1006–1016. Pierson RN 3rd, Barr ML, McCullough KP, et al: Thoracic organ transplantation, Am J Transplant 2004;4(Suppl 9):93–105. Ratjen F, Doring G: Cystic fibrosis, Lancet 2003;361(9358):681–689. Stewart KC, Patterson GA: Current trends in lung transplantation, Am J Transplant 2001;1 (3):204–210. Vilchez RA, Dauber J, Kusne S: Infectious etiology of bronchiolitis obliterans: The respiratory viruses connection—myth or reality? Am J Transplant 2003;3(3):245–249. Vilchez RA, Dauber J, McCurry K, et al: Parainfluenza virus infection in adult lung transplant recipients: An emergent clinical syndrome with implications on allograft function, Am J Transplant 2003;3(2):116–120. Zamora MR: Cytomegalovirus and lung transplantation, Am J Transplant 2004;4 (8):1219–1226. Zuckermann A, Klepetko W: Use of cyclosporine in thoracic transplantation, Transplant Proc 2004;36(2 Suppl):331S–336S.
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Liver Transplantation ALFREDO ESPINOZA, K.VINCENT SPEEG, KENNETH WASHBURN, AND GLENN HALFF
ICD Code: Liver failure 572.8
Key Points Hepatitis C virus (HCV) cirrhosis is the most common reason for liver transplantation in the United States. The recurrence rate of HCV is virtually 100% in the transplanted liver and cirrhosis recurs in up to 30% of HCV-infected patients at 5 years. Liver transplant recipients with normal liver function are more likely to acquire unusual infections or tumors relative to the general population but often have common medical illnesses similar to the typical population. It is important to check which medicines interact metabolically with the immunosuppressive medications transplant recipients are taking before prescribing new medications. Renal function is frequently compromised in patients who have received liver transplantation due to a combination of many factors.
DEFINITION Liver transplantation has grown tremendously since Thomas Starzl performed the first orthotopic liver transplantation in 1963. Orthotopic liver transplants occur when a whole donor liver is transplanted into the same location as the recipient’s previous liver. From perfections in surgical technique to the ground-breaking discovery of cyclosporine in 1979, liver transplantation, which was approved as a nonexperimental treatment for end-stage liver disease in 1983, has continued to benefit the lives of thousands of patients and their families. The overall selection of patients for liver transplant is a lengthy and sometimes difficult process. It is dependent on a medical evaluation of other organ systems such as cardiac and pulmonary. A social evaluation is performed to assess whether adequate social support will be present before and after transplant and to determine whether the patient has a history of medical compliance. An evaluation is done to ensure that any substance abuse has stopped for a period of at least 6 months, in combination with counseling, if necessary. This section will primarily focus on the presentation, evaluation, and treatment of some of the complications that occur in patients after they have received a liver transplant.
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SURGICAL PROCEDURE The waiting list for liver transplantation is prioritized based on degree of illness, which is calculated from a formula incorporating laboratory values such as the international normalized ratio (INR), bilirubin, and creatinine. Therefore, most patients who are chosen to receive transplants are the most ill patients, and actual waiting time has little influence on the choice of recipient. The transplant procedure typically takes 3–5 hours with a 7-day hospitalization. Longer posttransplant hospitalizations are common with patients whose conditions are severely deteriorated. The operation involves removing the native cirrhotic liver and reconnecting the donor liver in the same position in which the native liver rested. The vena cava may be connected with an anastomosis below and above the liver (standard) or with only one anastomosis from the cava to the recipient cava (piggy back). The recipient vena cava remains intact with the piggyback technique and the donor cava is a dead end, with one end tied off and the other draining end to the side into the recipient cava. This technical differentiation is important when interpreting a posttransplant ultrasound scan. Living donor liver transplants and pediatric split liver transplants require a piggy back caval anastomosis. The hepatic artery is generally sewn end to end, recipient to donor, but in about 5% an iliac artery graft to the recipient infrarenal aorta is necessary. The portal vein is usually end to end but an iliac vein graft to the superior mesenteric vein may be necessary if the recipient has a thrombosed portal vein. The biliary anastomosis can be done in one of two ways: end to end, in which case a postoperative endoscopic retrograde cholangiopancreatography (ERCP) may be done, or connected to a Roux-en-Y loop of small bowel, in which case an ERCP cannot reach the anastomosis and a percutaneous transhepatic cholangiogram must be done if the biliary system needs to be studied. Magnetic resonance cholangiogram is sometimes helpful to study the biliary system as well. The patients are usually sent home with no drains in place unless a T tube has been inserted in the bile duct. Routine ultrasound scans are done postoperatively to check vessel patency (Tables 20-1 and 20-2).
EPIDEMIOLOGY End-stage liver disease causes 25,000 deaths per year in the United States. According to the United Network for Organ Sharing (UNOS), 17,455 patients were on the liver waiting list as of September 2005 but only 6169 patients were transplanted in 2004. This disparity is a consequence of a donor pool that is unable to keep up with a growing waiting list. Survival after transplant is different for various etiologies of liver disease. Cumulative survival (all etiologies) at 1, 3, and 5 years is 85%, 78%, and 72%, respectively, according to UNOS.
1158 ESSENTIAL EMERGENCY MEDICINE FOR THE HEALTHCARE PRACTITIONER Table 20-1 Indications for Liver Transplantation CHOLESTATIC DISORDERS Primary biliary cirrhosis Primary sclerosing cholangitis Biliary atresia
CHRONIC PARENCHYMAL DISEASES Hepatitis C
ACUTE FULMINANT LIVER FAILURE
OTHER
Hepatitis A, B, rarely C, Polycystic liver rarely E disease Toxin ingestion (e.g., Budd-Chiari acetaminophen) syndrome
Hepatitis B
Cryptogenic cirrhosis Wilson’s disease (NASH) Alcohol-related cirrhosis Unknown Autoimmune cirrhosis Hemochromatosis a1 antitrypsin deficiency Wilson’s disease
Primary liver neoplasm Amyloidosis
NASH, Nonalcoholic steatohepatitis.
Table 20-2 Common Immunosuppressive Medications MEDICATION
METABOLISM EXCRETION
Prednisone
Hepatic
Renal
Cyclosporine
Hepatic
Bile
Tacrolimus (Prograf)
Hepatic
Bile
Mycophenolate mofetil (Cellcept)
Hepatic
Renal
Azathioprine (Imuran)
Hepatic
Renal
Sirolimus (Rapamune)
Hepatic
Bile
MAJOR TOXICITIES Hypertension, neurotoxicity, hyperlipidemia, and hyperglycemia Nephrotoxicity, hypertension, hyperkalemia, hypomagnesemia, neurotoxicity (e.g., seizures, tremors), hyperlipidemia, hyperglycemia, and gingival hyperplasia Nephrotoxicity, hyperkalemia, hypomagnesemia, neurotoxicity (e.g., seizures, tremors), hyperlipidemia, and hyperglycemia Leukopenia, anemia, thrombocytopenia, pancreatitis, and gastrointestinal toxicity (e.g., diarrhea) Leukopenia, anemia, thrombocytopenia, and gastrointestinal toxicity (e.g., diarrhea, nausea and vomiting) Leukopenia, anemia, thrombocytopenia, hyperlipidemia, and poor wound healing
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CLINICAL PRESENTATION The posttransplant presentation of a liver transplant recipient can vary widely from that of a completely normal patient to a patient with recurrence of cirrhosis that presents with ascites, encephalopathy, gastrointestinal tract bleeding, or sepsis. It is important to recognize that liver transplant recipients are just as susceptible to common medical problems as they are to more complex ones that are associated with their immunocompromised state.
EXAMINATION Careful evaluation of the patient’s mentation should be one of the initial assessments. Asterixis or flapping tremor of the wrists, which is best seen when the arms are outstretched with the wrists in hyperextension, is a common finding of hepatic encephalopathy. Pretransplant encephalopathy is most commonly related to infection, gastrointestinal tract bleeding, or overdiuresis. Posttransplant encephalopathy may be related to infection or medication adverse effects. A change in mental status usually requires that a head CT or magnetic resonance imaging (MRI) scan be performed to evaluate for intracranial bleeding, tumor, or infection. A yellowish discoloration of the sclera (i.e., icterus) may represent an elevated bilirubin level. The lungs should be examined for the presence of fluid or consolidation. Pleural effusions in the first few months after the transplant are common, as is some degree of ascites. The abdomen should reveal a Mercedes-Benz (inverted Y) incision and should be examined for liver size, tenderness, ascites, or splenomegaly. If edematous, the lower extremities and sometimes upper extremities may give an indication of liver, heart, or kidney failure. The skin may become jaundiced (yellow) in the course of liver failure and spider angiomata (i.e., vascular dermatological aberrations commonly seen in patients with cirrhosis) may be present. If bleeding is suspected, a nasogastric lavage and a rectal examination should be done.
LABORATORY FINDINGS Laboratory data from a liver transplant recipient must be assessed carefully and must be made with reference to the patient’s transplant date and etiology of transplant. For example, most patients’ liver-associated enzyme levels will not have fully normalized at the time of discharge after their transplant. On the other hand, patients with HCV infection may never have fully normalized liver-associated test results. The interpretation of trends is extremely useful to the transplant clinician in compiling a proper diagnostic plan and treatment course. Initial laboratory data in
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the emergency care setting should include complete blood count; coagulation studies (e.g., INR, partial thromboplastin time); measurements of total bilirubin, direct bilirubin, alkaline phosphatase, aspartate aminotransferase, alanine aminotransferase, gamma-glutamyltransferase, chemistry, and ammonia level; and blood and urine cultures, if infection is suspected. If ascites is present and infection is suspected, a paracentesis should be performed with attention to cell count, Gram stain, and culture. Tacrolimus or cyclosporine trough levels are usually drawn 12 hours after the last dose. The interpretation of a tacrolimus measurement taken too soon after the last dose may produce a falsely high reading, which may in turn lead to an inappropriate lowering of the dose by the transplant clinician. Many liver transplant recipients taking tacrolimus can discontinue all other means of immunosuppression by 1 year posttransplant. Adrenal insufficiency may be present in these patients.
DIAGNOSIS A diagnosis of the complications after transplant can usually be initiated on the basis of laboratory test results. However, more complex problems may require more extensive workup such as Doppler sonography of the hepatic vessels (to evaluate for a thrombosed or stenotic hepatic artery or portal vein or hepatic vein outflow stenosis), liver biopsy (to evaluate for rejection, drug toxicity, or viral infections), CT scan (to evaluate for possible intraabdominal infection), MRI, and sometimes surgical exploration. Thrombosis of the hepatic artery, especially early in the posttransplant period, may cause ischemia of the biliary system and may result in diffuse biliary strictures, bile duct leak, or intrahepatic bilomas. Table 20-3 outlines potential complications.
RADIOGRAPHS Plain radiography such as a chest x-ray or an abdominal series should be tailored to the patient’s presentation. A chest radiograph is necessary Table 20-3 Complications of Liver Transplantation Medical
Diabetes mellitus, hyperlipidemia, hypertension, infections (especially CMV), malignancies, neurological complications (especially seizures), obesity, renal disease, lymphoproliferative disease Postoperative Biliary tract (strictures, leaks, etc.), hepatic artery stenosis, portal vein thrombosis Recurrence of primary Hepatitis C, hepatitis B, PSC, PBC, malignancy disease Rejection Acute, chronic (rare)
CMV, Cytomegalovirus; PSC, primary sclerosing cholangitis; PBC, primary biliary cirrhosis.
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for suspected infection, changes in mentation, or shortness of breath. These can provide a wealth of information and are often sufficient for the diagnosis of pneumonias, bowel obstruction, or ileus. An elevation in the trend of liver-associated enzymes may lead to the suspicion of a biliary or vascular problem. A Doppler ultrasound of the liver should be ordered at this point. If there is still doubt about the findings, an MRI/MR angiograph and MR cholangiopancreatograph or a three-phase CT scan (avoid if renal function is impaired) of the liver may become necessary. If a bile duct problem is suspected, the biliary system should be studied with an ERCP if the patient has a duct-to-duct biliary anastomosis, or with a percutaneous transhepatic cholangiogram if the patient has a Roux-en-Y biliary connection.
TREATMENT As stated previously, most patients after a liver transplant present with common medical problems. These can be treated as they would in the general patient population. However, it is important to understand that commonly prescribed medications can and often do interfere with the immunosuppressant medications (Table 20-4). Biliary and vascular complications will usually involve the multidisciplinary care of a transplant surgeon, a hepatologist, a radiologist, and a biliary endoscopist. Rejection and recurrence of disease can be treated in the transplant clinic or in the acute setting by an experienced transplant clinician. Severe infection may require decreasing the immunosuppression in addition to standard treatment. Adrenal insufficiency may require stress steroids even in the face of infection. Table 20-4 Drug Interactions IF THESE ARE COADMINISTERED, INCREASE DOSES OF CYCLOSPORINE/TACROLIMUS Carbamazepine Phenobarbital Phenytoin Primidone Rifabutin
IF THESE ARE COADMINISTERED, DECREASE DOSES OF CYCLOSPORINE/TACROLIMUS Clarithromycin Daunorubicin Diltiazem Etoposide Erythromycin Fluconazole Grape fruit juice Itraconazole Posiconazole Quinupristin/dalfopristin Ritonavir Saquinavir Vinblastine Verapamil Voriconazole
1162 ESSENTIAL EMERGENCY MEDICINE FOR THE HEALTHCARE PRACTITIONER
If doubt exists about the appropriate treatment of a particular complication, the transplant center or team should always be consulted.
Bibliography Carithers R: AASLD guideline: Liver transplantation, Liver Transplant 2000;6:122. Dedmon M: Liver transplantation: Managing complications in primary care, JAAPA 2005;18(2):41–49. Gane EJ, Portmann BC, Naoumov NV, et al: Long-term outcome of hepatitis C infection after liver transplantation, N Engl J Med 1996;334:815. Killenberg P, Clavien P-A: Medical Care of the Liver Transplant Patient, ed 2. Blackwell Science: Malden, MA, 2001. Kok T, Slooff MJ, Thijn CJ, et al: Routine Doppler ultrasound for the detection of clinically unsuspected vascular complications in the early postoperative phase after orthotopic liver transplantation, Transplant Int 1998;11(4):272–276. Maceneaney PM, Malone DE, Skehan SJ, et al: The role of hepatic arterial Doppler ultrasound after liver transplantation: An “audit cycle” evaluation, Clin Radiol 2000;55 (7):517–524. Saab S, Wang V: Recurrent hepatitis C following liver transplant: Diagnosis, natural history, and therapeutic options, J Clin Gastroenterol 2003;37(2):155–163. Schafer D: Liver transplantation: Looking back looking forward, In Maddrey WC, Schiff ER, Sorrell MF (eds): Transplantation of the Liver, ed 3. Lippincott, Williams & Wilkins: Philadelphia, 2001. Stein JH, Klippel JH, Reynolds HY, et al (eds): Internal Medicine, ed 5. Mosby: St Louis, 1998, p 2160. United Network for Organ Sharing, Center Data. Available at: http://www.unos.org. Accessed September 17, 2005.
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Renal Transplantation GREG A. ABRAHAMIAN AND ROBERT M. ESTERL
CPT Code: Renal failure 586
Key Points Renal transplant recipients can experience complications that are related directly to the renal graft to immunosuppressive drug therapy to the underlying medical illness that led to their renal disease and to other comorbid medical and surgical problems. An increase in the serum creatinine level is nonspecific and can be due to a number of problems in addition to graft rejection. Transplant recipients are generally monitored closely by their transplant centers and early involvement with that team may yield important insight into the patient being evaluated in the emergency department. ! Emergency Actions ! Emergency action should be dictated by the clinical presentation of the patient, always addressing airway, breathing, and circulation first.
DEFINITION Renal transplantation has become the therapy of choice for patients with end-stage renal disease. More than 16,000 renal transplants are performed annually in the United States for patients with renal disease resulting most commonly from diabetes, hypertension, and glomerulonephritis. Approximately half of the recipients receive organs from living donors and the remainders are from deceased (cadaveric) donors. Many of these patients have associated comorbidities due to their primary disease processes such as coronary artery disease or peripheral vascular disease. Complications arising from chronic immunosuppressive therapy include infections, cancer, metabolic derangements, worsening hypertension and hyperglycemia, and progression or exacerbation of existing illnesses. In addition, a renal transplant recipient is always at risk of rejecting the organ, either acutely or in a chronic fashion.
EPIDEMIOLOGY Early surgical complications involving the renal graft include arterial or venous thrombosis or stenosis, lymphocele formation, ureteral leak with
1164 ESSENTIAL EMERGENCY MEDICINE FOR THE HEALTHCARE PRACTITIONER
“urinoma,” and hemorrhage. Early medical complications involving the grafted organ include rejection, drug toxicities, including tacrolimus or cyclosporine toxicities, infections such as pneumonia or urinary tract infection, and recurrence of the primary disease process. Most opportunistic infections (unusual organisms) do not develop until after the first postoperative month. Late complications affecting the graft and the recipient include rejection, opportunistic infections, arterial stenosis, ureteral stenosis or reflux, cancer, and progression of cardiovascular disease. It is important to note that cardiovascular disease is still the predominant cause of death in patients after renal transplantation.
CLINICAL PRESENTATION The majority of complications in renal transplant recipients are discovered during routine outpatient visits. The following symptoms may be associated with several complications that are unique to the renal transplant recipient. Arterial or venous thromboses are considered catastrophic events after transplantation. Patients may present with sudden graft pain, markedly decreased urine output, and swelling of the ipsilateral leg. Collections that develop around the renal graft include lymphoceles, urinomas, and hematomas. Patients may present with decreased urine output, pelvic pain or fullness, leg swelling, drainage from the incision, and in the case of a hematoma, symptoms related to anemia. Immunosuppressed patients are more susceptible to infections, and in most cases symptoms will be typical for the infected site. Although these persons are at increased risk for opportunistic infections similar to those seen in the patients with human immunodeficiency virus infection, community-acquired bacterial and viral infections still predominate. Cytomegalovirus is the most important viral infection affecting transplant recipients, and symptoms can include fever, diarrhea, dysphagia, fatigue, and evidence of bone marrow suppression on laboratory studies. Patients who develop symptomatic ureteral complications frequently present with recurrent urinary tract infections or graft pyelonephritis. Urinary tract infections are the most frequent cause of bacteremia in renal transplant recipients. Symptoms may include fever, graft tenderness, decreased urine output, and dysuria. The highest incidence of acute rejection occurs within the first 6 months after transplantation. However, it can occur at anytime during the life of the graft. Patients experiencing graft rejection can be asymptomatic or may present with symptoms consistent with acute renal failure. Lowgrade fever, worsening hypertension, weight gain, decreased urine output, graft tenderness, and ipsilateral leg swelling are common symptoms.
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Patients may give a history of having recently stopped or altered their immunosuppressive medications.
EXAMINATION As in most clinical situations, a complete physical examination is necessary. The vital signs noted should always include a temperature, blood pressure, and weight to compare with baseline levels. The general appearance of the patient is important to note because a patient in distress may signify shock or hypoxia due to septicemia or a cardiac or pulmonary event. It is important to palpate the graft to elicit tenderness or the presence of a mass and to auscultate the area to assess for a bruit, which may be associated with an arterial stenosis. Examination of the lower extremities should include notation of the presence or absence of edema. The rectal examination should always include stool guaiac testing. A thorough examination of the skin should be performed, noting any lesions that may be infectious or cancerous.
LABORATORY FINDINGS The serum creatinine measurement is the single most useful test to assess the function of a renal transplant. Most transplant recipients will know their baseline creatinine levels. Elevations in the serum creatinine level may be due to rejection, infection, dehydration, hyperglycemia, vascular or ureteral complications, perinephric fluid collections, recurrent renal disease, and drug toxicities, including tacrolimus or cyclosporine nephrotoxicity. A complete metabolic panel should also be included to assess for other electrolyte abnormalities that may be associated with renal dysfunction. A complete blood count should be performed. Pancytopenia may present in viral infections, most notably cytomegalovirus; however, the diagnosis of a cytomegalovirus infection is most commonly made on the basis of a quantitative polymerase chain reaction analysis. Although immunosuppressed, renal transplant recipients typically will respond to an infection with leukocytosis. A urinalysis with urine culture is necessary to assess for a urinary tract infection as well as for the presence of blood, protein, and glucose. A tacrolimus or cyclosporine serum trough level should be obtained, but to be clinically relevant, samples should only be drawn 10–12 hours after the last dose is administered. Any patient suspected of having bacteremia or sepsis should have blood culture samples drawn from two sites before the initiation of treatment with antibiotics. Drainage from the incision should be sent for Gram stain and culture.
1166 ESSENTIAL EMERGENCY MEDICINE FOR THE HEALTHCARE PRACTITIONER
RADIOGRAPHS A sonogram of the renal recipient is necessary to assess the vasculature and to note the presence or absence of fluid collections or hydronephrosis. A nuclear medicine renal scan may also be performed to further assess graft perfusion and excretion and possibly the presence of a urine leak. Additional radiographs should be ordered based on the patient’s presentation and physical findings.
DIAGNOSIS The diagnosis of a number of complications in renal transplant recipients can be made after a thorough history is taken and physical examination is performed in conjunction with the appropriate laboratory and radiographic data. The diagnosis of rejection, recurrent renal disease, and a small number of unique infections involving the graft can only be made by microscopic examination of the transplant renal biopsy sample. Refer to Tables 20-2 and 20-4 for common immunosuppressive medications and drug interactions, respectively.
TREATMENT Empirical antibiotic therapy should always be initiated early if an infection is suspected. Avoidance of nephrotoxic agents should always be considered, and dosing adjustments made with regard for renal function should be performed. Appropriate culture samples should be obtained before the initiation of therapy. Intravascular volume status should be assessed, and intravenous fluid should be devoid of potassium if renal dysfunction is present. It is important to note that macrolide antibiotics and azole antifungal agents may significantly increase serum levels of tacrolimus and cyclosporine, resulting in drug toxicities. Infections due to opportunistic organisms are often diagnostic dilemmas, frequently requiring multiple tests to achieve the diagnosis. Treatment is geared toward the particular organism identified, often in consultation with infectious disease specialists. If discovered early, most opportunistic infections can be eradicated. Overall, 50% of infections are viral, 30% are bacterial, 5% are fungal, and 15% are polymicrobial. Vascular and ureteral complications, as well as perinephric fluid collections, will frequently require radiological intervention as determined by the transplant team or nephrologists. Surgical intervention is performed after less invasive treatments have failed or are not possible. Treatment for rejection should only be initiated after other causes of renal dysfunction are ruled out and after biopsy confirmation. Often, bolus intravenous steroids are given with adjustments in the maintenance immunosuppression. More potent antibody agents are reserved for bolus steroid
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failures, and treatment is usually undertaken in an inpatient setting. Graft loss due to rejection is rare, with 1-year graft survival rates exceeding 90%.
Bibliography Morris PJ (ed): Kidney Transplantation, ed 5. WB Saunders: Philadelphia, 2001. United Network for Organ Sharing. Available at: http://www.unos.org.
Index AAA. See Abdominal aortic aneurysm ABC. See Airway-breathing-circulation Abdomen. See also Bowel; Gastrointestinal bleeding; Gastrointestinal emergencies anatomy of, 1058 pain in, 389, 509–512, 731–735 clinical presentation, 511 CT scan for, 512 definitions, 510–511 diagnosis, 512 emergency actions, 509–510 endometriosis, 510 examination, 511 geriatric, 389 geriatric emergencies, 389 key points, 509 laboratory findings, 512 pediatric emergencies, 731–735 ultrasound scanning, 512 pediatric emergencies, 731–735, 1078 clinical presentation, 733–734 definition, 732 emergency actions, 731 epidemiology, 732–733 key points, 731 laboratory tests and radiology, 734–735 physical examination, 734 trauma, 1078 treatment, 735 surgical emergencies aortic aneurysm, 1–4 appendicitis, 5–8, 510 cholelithiasis and cholecystitis, 9–14 hernias, 15–18 intestinal obstruction, 18–22 trauma to, 1057–1062, 1078 Abdominal aortic aneurysm (AAA), 1–4 clinical presentation, 2–3 asymptomatic, 2 CT scan/ultrasound for, 4 definition of, 1 diagnosis, 3 emergency actions, 1 epidemiology, 2 examination, 3 key points, 1 laboratory findings, 3
Abdominal aortic aneurysm (AAA), (Continued) pseudoaneurysm, 1 radiographs for, 3–4 treatment and outcome, 4 Abducens nerve examination, 457–458, 458f. See also Cranial nerve examination ABG analysis. See Arterial blood gas analysis Abortion (miscarriage), 510, 525–528. See also Pregnancy Abruptio placentae, 497–499, 510, 1108. See also Pregnancy clinical presentation, 498 definition, 497 emergency actions, 497 epidemiology, 497 etiology, 498 key points, 497 laboratory tests, 498 pathophysiology, 498 traumatic injury causing, 1108 treatment, 499 ultrasound scanning, 499 Abscess, anorectal clinical presentation, 117 definition, 114 examination, 118 pathology, 115 treatment and outcomes, 120 Abscess, brain Bell's palsy v., 426–427, 426t headaches from, 434 Abscess, breast, 502–504 clinical presentation, 503 definition, 502 emergency actions, 502 examination, 503 key points, 502 laboratory findings, 503 treatment, 503–504 mastitis, 504 ultrasound scanning, 503 Abscess, ovarian, 510 A/C ventilation. See Assist-control ventilation Accelerated idioventricular rhythm (AIVR), 51, 51f
1169
1170 INDEX ACE inhibitors. See Angiotensinconverting enzyme inhibitors ACEP. See American College of Emergency Physicians Acetaminophen acute otitis media treatment, 170 genital herpes treatment, 515 pediatric seizures and status epilepticus, 786 thyroid storm treatment, 397 toxicity, 931–936, 934f clinical presentation, 932–933 definition, 931–932 metabolism, 932 diagnosis, 933–935, 934f emergency actions, 931 examination, 933 key points, 931 laboratory findings, 933 overdose nomogram, 933–935, 934f treatment, 931, 935 activated charcoal, 931 Acetylcholine receptor site, myasthenia gravis, 447 Acetylcholinesterase inhibitors, myasthenia gravis requiring, 450 Acetylparaminophenolacetaminophen (APAP), 931. See also Acetaminophen Acid–base emergencies, 311–325 anion gap, 315–317, 324 approach to patients with, 324–325 base deficit/excess, 314 clinical evaluation, 313–314 definition, 312–313 hepatic role in acid-base homeostasis, 314 key points, 311–312 metabolic acidosis, 311, 315–317, 363, 1021, 1023 clinical presentation and examination, 316 definition, 315–316 epidemiology, 316 laboratory findings, 317 treatment and outcome, 317 metabolic alkalosis, 311, 317–320 alkali administration, 318 clinical presentation, 318 contraction alkalosis, 318 definition, 317 epidemiology, 317–318 examination, 319 gastrointestinal Hþ loss, 318 intracellular shifts, 318
Acid–base emergencies, (Continued) laboratory findings, 319 renal Hþ loss, 318 treatment, 319–320 renal excretion and absorption, 313 respiratory acidosis, 312, 320–322, 845 clinical presentation, 320–321 definition, 320 diagnosis, 321–322 epidemiology, 320 examination, 321 laboratory findings, 321 treatment and outcome, 321 respiratory alkalosis, 312, 321–323 clinical presentation and examination, 321–322 definition, 321 diagnosis, 323 etiology, 321 laboratory findings, 323 treatment and outcome, 323 respiratory excretion of volatile acid, 313 theophylline toxicity, 1046 Acidosis alcoholic keto-, 338–343, 339f, 340f, 1021 diabetic keto-, 311, 343–347, 1021. See also Diabetes hyperglycemic hyperosmolar nonketotic coma v., 390–393 pediatric emergencies, 770–774 treatment, 346–347 lactic, 410–413, 411t, 1020 metabolic, 311, 315–317, 363, 1021, 1023 respiratory, 312, 320–322, 845 ACLS. See Advanced cardiac life support Acoustic neuroma, Bell's palsy v., 426–427, 426t Acquired immunodeficiency syndrome (AIDS), 271t. See also Human immunodeficiency virus infection exfoliative dermatitis from, 100, 100b HIV v., 288–289 Activated charcoal. See Charcoal, activated Acute bleeding diathesis, 555–558 clinical presentation, 557 definition, 555 diagnosis, 558 emergency actions, 555 examination, 557 key points, 555 laboratory findings, 557–558
Index Acute bleeding diathesis, (Continued) pathology, 555–556 treatment, 558 Acute compartment syndrome, 596–599 clinical presentation, 597 definition, 596–597 diagnosis, 599 emergency actions, 596 epidemiology, 597 examination, 598 key points, 596 laboratory findings, 598 lower leg, 641 radiographs, 598 treatment, 599 Acute disseminated encephalomyelitis, multiple sclerosis v., 442 Acute mountain sickness (AMS), 184t, 185, 187t, 191 treatment, 188 Acute otitis media (AOM), 169–170, 798–802 barotrauma causing, 207 pediatric emergency, 798–802 Acute renal failure (ARF), 1113–1117. See also End-stage renal disease; Kidneys; Renal disease anti-inflammatory drugs causing, 1114 caustic ingestion causing, 963 clinical presentation, 1115 acute tubular necrosis, 1114 definition, 1113 diagnosis, 1116 emergency actions, 1113 glomerular filtration rate, 1113–1117 key points, 1113 laboratory findings, 1116 lithium poisoning causing, 1018–1019 pathology, 1113–1115 physical examination, 1115 radiography, 1115 treatment, 1116–1117 Acute respiratory distress syndrome (ARDS), 852–854 clinical presentation, 852–853 definition, 852 diagnosis, 853 emergency actions, 852 epidemiology, 852 examination, 853 key points, 852 laboratory findings, 853 PEEP influenced by, 859–861 treatment, 853–854
1171
Acute rheumatic fever (ARF), 774–778 clinical presentation, 775 definition, 775 diagnosis, 775 antecedent GAS infection evidence, 777 Jones criteria for, 775–777 epidemiology, 775 key points, 774 laboratory findings, 777 pathology, 775 treatment, 777 Acute tubular necrosis (ATN), 1114 intrarenal acute renal failure presenting as, 1114 ACV. See Assist-control ventilation Acyclovir, genital herpes treatment, 515 Adnexal torsion, 510 Adrenal insufficiency, 331–338 clinical presentation, 333 consultations with specialists for, 337 definition, 332 differential diagnosis, 334 emergency actions, 331 epidemiology, 332 etiology, 333–334 examination, 333 hospital admission for, 337 key points, 331 laboratory findings, 334 pathophysiology, 332–333 radiographs, 336 treatment, 336–337 Advanced cardiac life support (ACLS), 43, 44 AICD malfunction requiring, 43 lightning injuries requiring, 234 toxic epidermal necrolysis requiring, 103 AED. See Automatic external defibrillator AEDs. See Antiepileptic drugs Aerogastria barotrauma, 207 Aganglionic megacolon (Hirschsprung's disease), 745–748, 748f AICD. See Automatic implantable cardioverter-defibrillator AIDS. See Acquired immunodeficiency syndrome Airway management, 913–916, 914b, 915b. See also Airway-breathingcirculation; Bag-valve-mask device adult clinical presentation, 913 definition, 913
1172 INDEX Airway management, (Continued) equipment for, 673–674 rapid sequence induction COPD patient, 914b head injury patient, 915b treatment, 914–916, 914b, 915b pediatric anesthesia induction, 676 clinical presentation, 671–672 definition, 670 diagnosis, 672 epidemiology, 670 equipment for, 673–674 examination, 672 key points, 670 laboratory findings, 672 neuromuscular blockade, 676–677 pathology, 671 rapid sequence intubation, 672, 674–677 resuscitation formula, 1073–1075, 1074t surgical airway, 677 Airway-breathing-circulation (ABC). See also Airway management; Bag-valvemask device amphetamine overdose, 938 beta-blocker overdose, 954 burns, 196 cardiac arrhythmia emergency securing of, 44 cardiac emergency actions, 58 iron toxicity requiring, 1009–1010 lithium poisoning, 1019 mercury poisoning, 1026 pediatric cardiac arrest, 659, 660 phenytoin toxicity, 1036–1037 theophylline toxicity, 1047 AIVR. See Accelerated idioventricular rhythm Albuterol anaphylactic shock requiring, 921 asthma treatment, 860, 862 Alcoholic ketoacidosis (AKA), 338–343, 339f, 340f, 342, 1021. See also Acidosis; Ethyl alcohol airway and breathing/circulation, 340–341 clinical presentation, 339–340 definition, 339 diagnosis, 342 Soffer and Hamburger's criteria for, 342 disabilities accompanying, 341
Alcoholic ketoacidosis (AKA), (Continued) emergency actions, 338 epidemiology, 339 examination, 340 exposure and secondary survey, 341 key points, 338 laboratory findings, 341–342 pathology, 339, 339f, 340f treatment, 342 Alkalosis. See also Acid-base emergencies metabolic, 311, 317–320 respiratory, 312, 321–323 Allergic conjunctivitis, 164 Alpha–2-adrenergic receptor agonist, 965–968 Alprazolam, panic disorder treatment, 816 ALTE syndrome. See Apparent lifethreatening event syndrome Alternobaric vertigo barotrauma, 207 Altitude-related emergencies, 183–191, 184t, 187t acute mountain sickness, 184t, 185, 187t treatment, 188 cerebral edema, 184t, 185–186, 187t, 189 treatment, 189 definitions, 183 diagnosis, 187–188 epidemiology, 183–185, 184t examination and laboratory findings, 187 key points, 183 peripheral edema, 190 pharyngitis and bronchitis, 190 pulmonary edema, 184t, 186, 187t treatment, 189–190 radiographs, 188 retinopathy, 190 sleep disorders, 191 summary, 191 ultraviolet keratitis, 190–191 Aluminum acetate, toxicodendron dermatitis treatment, 108–109 American Academy of Family Physicians, otitis media treatment, 801 American Academy of Pediatrics, otitis media treatment, 801 American Association for Poison Control Centers, hydrocarbon poisoning, 1004–1005 American Burn Association, 197, 197b
Index American College of Emergency Physicians (ACEP), seizures and status epilepticus, 469, 472 American Psychiatric Association, 815 American Thoracic Society, 883–884 Amide class of anesthesia, 28 Amnesia, high-altitude global, 184t Amniotic fluid embolism, 500–502. See also Pregnancy clinical presentation, 501 definition, 500 emergency actions, 500 epidemiology, 500 etiology/pathogenesis, 500–501 key points, 500 laboratory tests for, 501 radiographs, 501 treatment, 501 Amoxicillin adult bacterial pneumonia, 867, 867t otitis media treatment, 170 pediatric, 801 Amphetamines “ecstasy,” “ice,” 353, 936–937 overdose causing seizures, 938 toxicity, 936–938 clinical presentation, 937 definition, 936 diagnosis, 937 emergency actions, 936 key points, 936 laboratory tests, 937 pathology, 937 treatment, 937–938 Amylase and lipase tests, diverticulitis requiring, 125 Anal fissures clinical presentation, 117 definition, 114 epidemiology, 115 examination, 118 treatment and outcome, 120 Analgesia. See also Morphine; specific type diving injuries treatment, 211 intubated patient, 906–908, 907t contraindicated medications, 908 fentanyl, 907t, 908 hydromorphone, 907t, 908 morphine sulfate, 906, 907t Society for Critical Care Medicine guidelines for, 906 opioid, pulmonary embolism treatment, 903 pediatric, 805–813, 808–809
1173
Analgesia, (Continued) local, 808–809 systemic, 811–812 topical, 808 Anaphylactic reaction, hymenoptera sting causing, 230–233 Anaphylaxis, asthma mimicked by, 857 Anatomy abdominal, 1058 ankle joint, 589–590 central nervous system, 452t foot, 604 forearm and wrist, 609–610 hand, 617–619 hip, 626–627 lower leg, 638–639 neurological examination, 452–453, 452t pelvic, 1081–1082 peripheral nervous system, 452–453 shoulder, 647–648 Anemia conjugated hyperbilirubinemia, 136 hypoalbuminemia state, 315 methemoglobinemia, 964 multiple sclerosis v. pernicious, 442 sickle cell, 570–574 Anesthesia amide and ester classes of, 28 local bupivacaine, 28, 29, 29t EMLA, 28–29 lidocaine, 28, 29, 29t, 914b, 929, 1080 wound management with, 28 pediatric anesthesia induction, 676 pediatric status epilepticus treatment, 787 Aneurysm abdominal aortic, 1–4 geriatric patient susceptibility to, 2 Hunt and Hess Clinical Grading Scale for, 496 pseudo-, 1 Angiotensin-converting enzyme (ACE) inhibitors, 74 Anion gap. See also Metabolic acidosis acid-base problems involving, 315–317, 324 diabetic ketoacidosis causing wide, 1021 isoniazid poisoning causing wide, 1021 lactic acidosis causing wide, 1021
1174 INDEX Anion gap, (Continued) methanol poisoning causing wide, 1021 paraldehyde poisoning causing wide, 1021 Ankle injuries, 589–596 clinical presentation, 590 definitions, 589 diagnosis dislocations, 594 fractures, 593–594 radiographs, 594–595 sprains, 591–592 tendon rupture/dissociation/tear, 592–593 emergency actions, 589 examination, 590–591 joint anatomy, 589–590 key points, 589 laboratory findings, 591 treatment, 595 Anorectal disorders abscess and fistula clinical presentation, 117 definition, 114 examination, 118 pathology, 115 treatment and outcomes, 120 anal fissures clinical presentation, 117 definition, 114 epidemiology, 115 examination, 118 treatment and outcome, 120 hemorrhoids clinical presentation, 116–117 definition, 114 emergency action, 114 examination, 117–118 laboratory findings, 119 pathology, 115 treatment and outcomes, 119–120 hidradenitis suppurativa, definition, 114 pilonidal disease clinical presentation, 117 cysts, 118 definition, 114 epidemiology, 115 pathology, 116 treatment and outcomes, 120 proctalgia fugax, 114–115 pruritus ani clinical presentation, 117 definition, 115
Anorectal disorders, (Continued) examination, 119 pathology, 116 treatment and outcomes, 120–121 rectal prolapse clinical presentation, 117 definition, 115 examination, 118 pathology, 116 treatment, 120 Antibiotics adrenal insufficiency treatment, 337 adult bacterial pneumonia, 867, 867t AICD infection requiring, 42–43 appendicitis requiring, 8 beta-lactam for toxic shock syndrome, 549 community-acquired pneumonia, 867, 867t diving injury treatment, 211 dosages for neonatal emergencies, 666t endocarditis from prosthetic valve infection, 91–92 epididymitis, 1126 heart transplant complications requiring, 96 hernia requiring, 18 intestinal obstruction requiring, 21 marine fauna envenomation requiring, 240–241 neonatal dosages, 666t otitis externa, 170 otitis media, 801 pediatric urinary tract infection, 757t renal transplant emergency requiring, 1166–1167 rheumatic fever treatment, 777 toxic shock syndrome, 549 urinary tract infection treatment, 1145t, 1146 vasogenic shock requiring, 922 wound management prophylactic, 35 Anticholinergics pediatric asthma treatment, 721–724 toxicity, 938–943 clinical presentation, 940 definition, 939 electrocardiograph, 941 emergency actions, 939 epidemiology, 939 examination, 940–941 history taking, 940 key points, 938 pathology, 939–940
Index Anticholinergics, (Continued) treatment for, 941–943 gastric decontamination, 942 ICU, 942 “safety net,” 941 temperature reduction, 941–942 Anticoagulant agents AICD-associated thrombosis requiring, 43 prosthetic heart valve dysfunction requiring, 91–92 pulmonary embolism requiring, 898, 901, 903–904 Anticonvulsants pediatric seizure treatment, 786 toxicology emergencies requiring, 929 Antidepressant toxicity, 980–984, 982f. See also Cyclic antidepressant toxicity Antiepileptic drugs (AEDs), 471–472, 471t Antihistamines, urticaria treatment requiring, 112 Anti-inflammatory drugs, non-steroidal, 437–438, 1114 Anti-lewisite, 946 Antimicrobial therapy. See also Antibiotics prostatitis requiring, 1133–1134 Antipyretics, thyroid storm treatment, 397. See also Acetaminophen Antisocial personality disorder, 828–829 definition, 828 treatment and outcome, 829 Antivenom, 253, 254 AOM. See Acute otitis media APAP. See Acetylparaminophenolacetaminophen Apparent life-threatening event (ALTE) syndrome, 765–769 Appendicitis, 5–8, 510 abdominal pain from, 510 clinical presentation, 6 definition of, 5 diagnosis, 7 emergency actions for, 5 epidemiology, 5–6 examination, 6–7 key points, 5 laboratory findings, 7 radiography, 7–8 treatment and outcome, 8 ARDS. See Acute respiratory distress syndrome ARF. See Acute renal failure; Acute rheumatic fever
1175
Arrhythmia. See Cardiac arrhythmia Arsenic poisoning, 943–947 clinical presentation, 944 definition, 944 diagnosis, 946 emergency actions, 943 epidemiology, 944 examination, 945 key points, 943 laboratory findings, 945–946 radiographs, 946 treatment, 946–947 Arterial blood gas (ABG) analysis acid-base problems requiring, 312, 324 ARDS diagnostic, 853 hyperglycemic hyperosmolar nonketotic coma, 392 monitoring of, during mechanical ventilation, 877 neonatal emergencies, 668–669 pneumothorax diagnosis, 893 pulmonary embolism diagnostic, 901 shock diagnostic, 919 submersion incident requiring, 245, 246t, 247 toxicology emergencies, 927 Arterial gas embolism (AGE), 205, 208 decompression sickness v., 208 diving injury, 205, 208 Liebermeister's sign, 208 Arteriography, knee pain emergency requiring, 587 Arthralgia, acute rheumatic fever causing, 776 Arthritis. See also Joint and bone infections poly-, acute rheumatic fever causing, 776 septic, 630, 632, 633 Aspergillus, heart transplant infection, 95 Aspirin, 73, 169 acute rheumatic fever treatment, 777 cardiac chest pain treatment, 74 genital herpes treatment, 515 pediatric Kawasaki disease treatment, 794 pediatric seizures and status epilepticus, 786 Assist-control ventilation (ACV), (A/C), 847, 849t, 850–851 Association of Poison Control Centers, iron toxicity, 1007 Asthma, adult, 854–862 clinical presentation, 857
1176 INDEX Asthma, adult, (Continued) definition, 855 diagnosis, 859 disposition, 861–862 emergency actions, 854 epidemiology, 855 examination, 857–858 key points, 854 laboratory findings, 858–859 mechanical ventilator exacerbation of, 876 pathophysiology, 855–857 radiographs, 859 treatment and outcome, 859–861 beta–2 agonists, 860, 861 magnesium sulfate, 223 theophylline, 722 Asthma, pediatric, 714–724, 717t–719t definition, 714 emergency actions, 714 epidemiology, 714–715 evaluation, 716–720 severity classifications, 717t–719t key points, 714 laboratory findings and radiographs, 720–721 pathophysiology, 715–716 presentation, 716 treatment, 721–724 epinephrine, 722 heliox, 223 intubation/mechanical ventilation, 223 magnesium sulfate, 223 methylxanthines, 722 oxygen/beta–2 agonists/ corticosteroids/anticholinergic agents, 721–724 terbutaline, 722 theophylline, 722 Ataxia, dizziness, vertigo, 418–423 cerebellar, 464 clinical presentation, 419–421 CT or MRI scan for, 418, 422 definitions, 418 diagnosis, 422 emergency actions, 418 examination, 421–422 key points, 418 laboratory findings, 422 pathology, 419 subarachnoid hemorrhage causing, 418 syncope, 418 treatment, 422–423
Ataxia, dizziness, vertigo, (Continued) underwater injury causing, 207 ATN. See Acute tubular necrosis Atrial arteries dysrhythmia, heart transplant rejection causing, 95 fibrillation, 49, 49f flutter, 49–50, 50f Atrioventricular bradycardia first-degree, 52, 52f second-degree type I, 52, 52f type II, 52–53, 53f third-degree, 53, 53f Atropine airway management pretreatment, 914b insecticides poisoning antidote, 1033 pediatric trauma medication, 1080 Aural barotrauma, 206. See also Barotrauma Automatic external defibrillator (AED), 658 Automatic implantable cardioverterdefibrillator (AICD), 40–43 Avascular necrosis (AVN), 612–614 AVN. See Avascular necrosis Avoidant personality disorder, 835–836 clinical presentation, 835 definition, 835 diagnosis, 836 epidemiology, 835 key points, 835 treatment and outcome, 836 Azithromycin, adult bacterial pneumonia, 867, 867t Bacillus cereus, infectious disease emergency, 266t Back pain emergency, 577–582, 581t clinical presentation and examination, 578–579 definition, 577–578 diagnosis and specific etiologies, 579–582, 581t emergency actions, 577 key points, 577 laboratory findings, 582 radiographs, 582 treatment, 582 Backward/forward/right pressure (BURP), 915
Index Bacteremia definition, 706–707 pediatric, 706–713, 708t, 710t, 711t Bacteria. See also Infections; Infectious disease emergencies conjunctivitis, 164 infection from, 706–713, 708t, 710t, 711t Bag-valve-mask (BVM) device, 914. See also Airway management pediatric cardiopulmonary resuscitation using, 662, 670 BAL. See British anti-lewisite Balanoposthitis, 1127–1128 Balloon pump, cardiac chest pain treatment, 74 Barbiturate overdose, 948–951 clinical presentation, 949–950 definition, 948 diagnosis, 950 emergency actions, 950 epidemiology, 948–949 key points, 948 laboratory findings, 950 variability of test sensitivity, 950 pathophysiology, 949 treatment, 951 Barium enema, intestinal obstruction diagnosis, 21 Barodontalgia barotrauma, 207 Barotitis media barotrauma, 207 Barotrauma aerogastria, 207 alternobaric vertigo, 207 aural, 206 barodontalgia “tooth squeeze,” 207 barotitis media, 207 inner ear, 207 pulmonary overpressurization syndrome, 206 Bell's palsy clinical presentation, 425 definition, 424 diagnosis, 426–427, 426t differential diagnosis, 426–427, 426t epidemiology, 424 examination, 425–426 herpes virus, 276, 279–280, 286, 423–428, 426t, 484t key points, 423 laboratory findings, 427 pathology, 424 risk factors for, 424–425
1177
Bell's palsy, (Continued) stroke syndromes v., 484t treatment, 427 Benadryl aqueous, 28, 29 urticaria treatment, 111–112 Benign intracranial hypertension (pseudotumor cerebri), headaches from, 434, 435 Benign rolandic epilepsy, treatment, 787 Benzathine penicillin, acute rheumatic fever treatment, 777 Benzodiazepines amphetamine overdose requiring, 938 anesthesia after wound examination, 28 cyclic antidepressant toxicity treatment, 983–984 ethanol withdrawal requiring, 326 panic disorder treatment, 816 Benzoin, wound closure option, 30 Beta–2 agonists, asthma treatment, 860, 861 pediatric, 721–724 Beta-blockers bradycardia as sign of overdose, 953 cardiac chest pain treatment, 74 hyperthyroidism and thyroid storm treatment, 394 norepinephrine as overdose treatment, 952 overdose, 952–955 clinical presentation, 953 definition, 952 diagnostic for, 954 emergency actions, 952 epidemiology, 952–953 examination, 953 key points, 952 laboratory findings, 953 treatment and outcome, 954–955 thyroid storm treatment, 398 Betadine, pre-surgery wound preparation, 29 Beta-lactam antibiotics, toxic shock syndrome, 549 Bicarbonate therapy pediatric diabetes treatment, 773–774 septic shock, 413 Bilevel positive airway pressure (BiPAP) ventilator, 848, 849t Bilirubin conjugated hyperbilirubinemia, 136 measurement, iron toxicity requiring, 1009
1178 INDEX Bilirubin, (Continued) metabolism, 136 BiPAP ventilator. See Bilevel positive airway pressure ventilator Black widow spider bite, 256–258, 259 Bladder injuries, 1064 Bleeding diathesis, 555–558 Blood. See also Blood transfusion; Blood urea nitrogen analysis; Gastrointestinal bleeding; Hemophilia; Hemorrhage; Oncologic and hematologic emergencies; White blood cell count cultures cardiac tamponade requiring, 62 diverticulitis requiring, 125 ethanol withdrawal requiring, 329 heart transplant complications requiring, 94 neonatal emergencies, 668–669 pediatric seizures and status epilepticus, 786 glucose hypoglycemia, 399–405 methanol poisoning treatment, 1022 pediatric diabetes, 773–774 pediatric seizures and status epilepticus, 786 toxicology emergencies, 927–928 nose bleed, 171–172 type and crossmatch abdominal aortic aneurysm requiring, 4 cardiac tamponade requiring, 62 diverticulitis requiring, 125 hip trauma requiring, 630 iron toxicity requiring, 1009 shock diagnostic, 919 Blood transfusion, 559–565, 565 arsine gas intoxication requiring, 943 blood components, 559–562 cryoprecipitated antihemophilic factor, 561–562 iron toxicity requiring, 1009–1010 key points, 559 multiple trauma requiring, 1055, 1055t reactions to delayed hemolytic, 563 febrile, 563–564 hemolytic, 562–563 hemosiderosis causing, 565 hepatitis B and C causing, 565 human immunodeficiency virus causing, 565
Blood transfusion, (Continued) urticarial v. anaphylactic, 565 Blood urea nitrogen (BUN) analysis abdominal aortic aneurysm requiring, 4 caustic ingestion requiring, 964 disseminated intravascular coagulation emergency, 350 diverticulitis requiring, 125 hymenoptera sting requiring, 232 hyperglycemic hyperosmolar nonketotic coma, 392 pediatric seizures and status epilepticus, 787 salicylates toxicity, 1041 toxicology emergencies, 927–928 Bone and joint infections, 631–637 clinical presentation, 634 emergency actions, 631 epidemiology, 632 imaging, 635–636 key points, 631 laboratory findings, 634–635 osteomyelitis definitions, 631 epidemiology, 632 pathology, 632–633 treatment, 636 septic arthritis definitions, 630, 632 epidemiology, 632 pathology, 633 treatment, 637 Bone marrow studies, exfoliative dermatitis requiring, 101 Borderline personality disorder, 830–831 definition, 830 diagnosis, 831 examination, 830 key points, 830 treatment and outcome, 831 Bordetella pertussis, COPD infection, 884 Botulism, 428–431 clinical presentation, 430 Clostridium botulinum diarrhea from, 744t, 745 infectious disease emergency, 266t definition, 428–429 diagnosis, 430 emergency actions, 428 epidemiology, 429 examination, 430 Guillain-Barré syndrome v., 430 key points, 428
Index Botulism, (Continued) myasthenia gravis v., 430 pathology, 429 risk factors for contracting, 429–430 treatment, 431 Bowel decompression, intestinal obstruction requiring, 21 irrigation of, clonidine overdose treatment, 967–968 irritable bowel syndrome, 126 Bradycardia, 52–53, 52f, 53f AICD causing, 40 atrioventricular first-degree, 52, 52f second-degree type I, 52, 52f type II, 52–53, 53f third-degree, 53, 53f beta-blocker overdose sign, 953 pediatric, 659 sinus, 52, 52f Brain. See also Central nervous system; Head abscess Bell's palsy v., 426–427, 426t headaches from, 434 gray-white matter loss, 487, 490f hyperdense cerebral artery sign, 487, 489f intracerebral hemorrhage, 487f stroke syndromes, 480f subarachnoid hemorrhage, 488f trauma to, 1055, 1067–1072 airway management for, 915b computed tomography scan for, 1055 tumor Bell's palsy v., 426–427, 426t headaches from, 434 stroke syndromes v., 484t Branhamella catarrhalis, COPD infection, 884 Breast abscesses and mastitis, 502–504 clinical presentation, 503 definition, 502 emergency actions, 502 examination, 503 key points, 502 laboratory findings, 503 treatment, 503–504 mastitis, 504 ultrasound scanning, 503
1179
Breast, (Continued) gynecomastia (male mammary gland development), exfoliative dermatitis causing, 101 British anti-lewisite (BAL), 946 British Pacing and Electrophysiology Group, pacemaker circuitry types, 84, 85t Bronchiolitis, 687–692, 725–728. See also Bronchitis asthma mimicked by, 857 clinical presentation, 689 definition, 688, 725 diagnosis, 690 emergency actions, 688, 725 epidemiology, 688–689 examination, 689 key points, 725 laboratory findings, 690 radiographs, 690 treatment, 690–692 Bronchitis. See also Bronchiolitis altitude-related emergencies, 190 asthma mimicked by, 857 bronchial injury, 1102 bronchodilators for COPD, 886 Bronchoscopy, prosthetic heart valve requiring, 92 Brown recluse spider bite, 256, 258, 259–260 Brudzinski sign, 464–465 BUN analysis. See Blood urea nitrogen Bundle branch blocks, cardiac arrhythmia from, 53, 54f Bupivacaine, 28, 29 toxicity of, 29, 29t Burns, 192–197, 194f, 196b, 197b. See also Chemical burns American Burn Association, 197, 197b burn department for toxic epidermal necrolysis, 103–106 carbolic acid, 203 child abuse, 763f clinical presentation, first/second/third degree types, 193 definition, 193 emergency actions, 192–193 epidemiology, 193 examination, 193–195, 194f Rule of Nines assessment, 194f hypernatremia etiology involving, 359t key points, 192 laboratory findings, 195 Parkland formula for, 196, 196b
1180 INDEX Burns, (Continued) radiographs, 195–196 sunburn, 100, 100b toxic epidermal necrolysis from, 103–106 treatment, 196–197, 196b “ABC” care, 196 BURP. See Backward/forward/right pressure Burrow's solution, toxicodendron dermatitis treatment, 108–109 Butorphanol tartrate, headache treatment, 437–438 BVM device. See Bag-valve-mask device C1 esterase inhibitor concentrate, urticaria treatment, 112 CAD. See Coronary artery disease Calamine, toxicodendron dermatitis treatment, 108–109 Calcium. See also Hypercalcemia; Hypocalcemia chloride, pediatric trauma medication, 1080 fluid and electrolyte emergencies, 369–377 measurement, toxicology emergencies requiring, 927 pediatric seizure treatment, 787 sign, thoracic aortic dissection diagnosis, 25 toxicology emergencies requiring, 929, 954 Calcium channel blockers (CCBs), overdose, 956–959 clinical examination, 957 congestive heart failure from, 958 definition, 956 diagnosis, 957–958 emergency actions, 956 epidemiology, 957 key points, 956 laboratory findings, 957 treatment, 958–959 Calculi cholelithiasis, 9–14 nephrolithiasis, 511, 1135–1138 sialolithiasis, 175–176 Campylobacter jejuni diarrhea from, 744t infectious disease emergency, 266t Cancer. See also Malignancy; Oncologic and hematologic emergencies; Tumor diverticulitis v., 126
Cancer, (Continued) exfoliative dermatitis from, 100, 100b Candidiasis, treatment, 553–554, 553t CAP. See Community-acquired pneumonia Captopril, hypertensive emergency treatment, 79–80 Carbamate and organophosphorus insecticides poisoning, 1130–1132 Carbamazepine benign rolandic epilepsy, treatment, 787 seizures and status epilepticus, 471t Carbolic acid, chemical burn from, 203 Carbon monoxide poisoning, 959–962 clinical presentation, 960 definition, 960 emergency actions, 960 epidemiology, 960 key points, 959 laboratory findings, 960 metabolic acidosis from, 1021 pathophysiology, 960 treatment, 960–961 Carcinoma, asthma mimicked by, 857 Cardiac arrhythmia, 44–57, 46f, 47f, 48f, 49f, 50f, 51f, 52f, 53f, 54f, 55f, 56f. See also Cardiac chest pain evaluation; Dysrhythmia bradycardia, 52–53, 52f, 53f AICD causing, 40 atrioventricular first-degree, 52, 52f third-degree, 53, 53f beta-blocker overdose sign, 953 pediatric, 659 sinus, 52, 52f bundle branch blocks, 53, 54f clinical presentation, 45 clonidine overdose monitoring for, 967–968 definition, 44–45 emergency actions, 44 advanced cardiac life support protocols, 43, 44 examination/stable or unstable condition, 45 hypercalcemia, 54, 55f hyperkalemia, 54, 55f hypocalcemia, 54, 55f hypokalemia, 54, 55f key points, 44 laboratory findings, 45 organ rejection causing, 93–96
Index Cardiac arrhythmia, (Continued) pathophysiology of submersion incident, 244 pulmonary embolism causing, 56, 56f radiographs, 45 respiratory acidosis causing, 320 tachycardia, 46–49, 46f, 47f, 48f Wolff-Parkinson-White syndrome, 56–57, 56f Cardiac chest pain evaluation, 68–75, 71f, 72f. See also Cardiac arrhythmia; Cardiac examination; Cardiology clinical presentation, 69–70 definition, 68–69 diagnosis, 73 electrocardiogram findings, 71–72, 71f, 72f emergency actions, 68 epidemiology, 69 examination, 70–71 key points, 68 laboratory findings, 72–73 radiographs, 73 special considerations, 75 treatment and outcome, 73–74 Cardiac enzyme measurements lightning injuries requiring, 236 shock diagnostic, 919 Cardiac examination, 58–60. See also Cardiac chest pain evaluation; Cardiology airway-breathing-circulation emergency actions, 58 clinical presentation, 58 definition, 58 examination, 58–59 key points, 58 radiographs, 59 treatment/outcome, 60 Cardiac life support. See also Advanced cardiac life support Cardiac monitoring calcium channel blockers overdose requiring, 958–959 hyperglycemic hyperosmolar nonketotic coma treatment, 392–393 Cardiac output, exfoliative dermatitis causing increased, 101 Cardiac tamponade, 60–63, 62f, 63f cardiopulmonary arrest from, 664 clinical presentation, 61 definition, 60–61 diagnosis, 62, 62f, 63f epidemiology, 61
1181
Cardiac tamponade, (Continued) etiology, 61 examination, 61–62 key points, 60 laboratory findings, 62 trauma causing, 1099–1100 treatment, 62–63 Cardiac transplantation emergencies, 93–96, 1150, 1151, 1154 Cardiology. See also Cardiac chest pain evaluation; Cardiac examination; Cardiac transplantation emergencies; Toxicology emergencies acute pericarditis, 37–40 advanced cardiac life support, 43, 44 arrhythmias, 44–57, 46f, 47f, 48f, 49f, 50f, 51f, 52f, 53f, 54f, 55f, 56f atrial dysrhythmia, 95 congestive heart failure, 64–67 defibrillator implantation follow-up, 40–43 examination, 58–60 hypertensive emergencies, 76–80 mitral valve prolapse, 80–82 pacemaker complications, 83–88, 85t pain evaluation, 68–75, 71f, 72f pediatric cardiopulmonary arrest, 655–660 automatic external defibrillator for, 657 laryngeal mask airway for, 657 prosthetic heart valve dysfunction, 89–92, 91b rheumatic carditis, 776 tamponade, 60–63, 62f, 63f thoracic aortic dissection, 22–26 transplantation emergencies, 93–96, 1150, 1151, 1154 Cardiopulmonary arrest, pediatric, 655–660 clinical presentation and physical examination, 656 CPR for, 656, 657–659, 660, 661–664 definition, 655 epidemiology, 655–656 key point, 655 laboratory findings, 656 pathophysiology, 656 summary, 660 treatment, 656–660 asystole/pulseless electrical activity, 659 bradycardia with pulse, 659
1182 INDEX Cardiopulmonary arrest, pediatric, (Continued) unstable tachycardia with pulse, 659–660 ventricular fibrillation/tachycardia without pulse, 658–659 Cardiopulmonary resuscitation (CPR). See also Resuscitation emergencies pediatric emergency, 656, 657–659, 660, 661–664 submersion incidents requiring, 243 Carpal tunnel syndrome, 615. See also Forearm and wrist injuries Cat scratch disease, multiple sclerosis v., 442 Catheter Angiocath, wound preparation requiring irrigation, 30 aspiration for pneumothorax, 895–896 Foley, rhabdomyolysis treatment, 416–417 percutaneous cardiac intervention, 74 Caustic ingestion emergency, 962–965 clinical presentation, 963 definition, 962–963 diagnosis, 964 emergency actions, 962 epidemiology, 963 examination, 963 key points, 962 laboratory findings, 964 radiographs, 964 treatment, 964 CBC. See Complete blood count CDCP. See Centers for Disease Control and Prevention Cefdinir, adult bacterial pneumonia, 867, 867t Cefuroxime, adult bacterial pneumonia, 867, 867t Centers for Disease Control and Prevention (CDC), 271t botulism treatment, 431 Centor criteria for pharyngitis diagnosis, 173 Central nervous system (CNS). See also Brain; Cranial nerve examination; Head; Spinal cord injuries anatomy and function, 452t gliosis, 440 heart transplant infection involving, 95 respiratory acidosis treatment influencing, 322 trauma to, 1067–1072
Central retinal vein occlusion, 165 Cephalexin, marine fauna envenomation requiring, 240–241 Cephalosporins adult bacterial pneumonia, 867, 867t marine fauna envenomation requiring, 240–241 Cerebellar ataxia, 464 Cerebral edema, 184t, 185–186, 187t, 189 Cerebrospinal fluid (CSF) analysis, 271t pediatric infection requiring, 710–712 Cesarean section, postmortem, 1111 Chalazion, 163 Charcoal, activated acetaminophen toxicity treatment, 931 barbiturate overdose treatment, 951 beta-blocker overdose treatment, 954 calcium channel blockers treatment, 958–959 clonidine overdose treatment, 967–968 lithium poisoning treatment, 1019 phenytoin toxicity treatment, 1037 salicylates toxicity treatment, 1042 theophylline toxicity treatment, 1048 Chelation therapy arsenic intoxication requiring, 943 lead poisoning requiring, 1016 Chemical burns, 198–204, 199b. See also Burns airway and breathing, 198 circulation assessment, 199 clinical presentation, 200 definition, 199 types of, 199b diagnosis, 201 emergency actions, 198 epidemiology, 199–200 examination, 200–201 key points, 198 laboratory findings, 201 special situations, 203–204 hydrofluoric acid, 203–204 phenol (carbolic acid), 203 treatment, 202–203 Chemical warfare, cyanide poisoning, 976 Chest evaluation, pediatric trauma requiring, 1078 Chickenpox, 276, 280, 282–283 treatment, 286 Child. See also Pediatric analgesia and sedation; Pediatric bacteremia, sepsis, and meningitis; Pediatric emergencies abuse, 758–765 clinical presentation, 759–761
Index Child, (Continued) definitions, 758–759 emergency actions, 758 epidemiology, 759 examination, 761–763, 762f, 763f marks from burns, 763f marks from instruments, 762f key points, 758 laboratory findings, 764 radiographs, 764 treatment, 764–765 definition of, 657 Chlamydia species, chronic obstructive pulmonary disease from, 884 Chloride, fluid and electrolyte emergencies, 383–385. See also Hyperchloremia Cholelithiasis and cholecystitis, 9–14 clinical presentation, 11 definition of, 9–10 diagnosis, 12 disposition, 14 emergency actions, 9 epidemiology, 10 examination, 12 key points, 9 laboratory findings, 12 Murphy's sign, 12 pathophysiology, 10–11 radiographs, 13 treatments and outcomes, 13–14 Cholesteatoma, Bell's palsy v., 426–427, 426t Chorea, acute rheumatic fever causing, 776 Chronic fatigue syndrome, multiple sclerosis v., 442 Chronic obstructive pulmonary disease (COPD), 46, 49, 883–887, 914b, 915b. See also Respiratory distress syndrome acid-base disorder with, 324 American Thoracic Society definition of, 883–884 asthma mimicked by, 857 clinical presentation, 884–885 definition, 883–884 electrocardiogram, 886 emergency actions, 883 examination, 885 key points, 883 laboratory findings, 885–886 mechanical ventilation required for, 848, 850
1183
Chronic obstructive pulmonary disease (COPD), (Continued) mechanical ventilator exacerbation of, 875–876 pathology, 884 radiographs, 885 stages of, 884 treatment, 886–887 bronchodilators, 886 emergency department, 887 fluid administration, 886 rapid sequence induction, 914b, 915b Cigarette smoking COPD from, 884 pulmonary embolism risk factor, 899 Ciguatera fish poisoning, infectious disease emergency, 270t Cimetidine anaphylactic shock requiring, 921 urticaria treatment, 112 Ciprofloxacin, urinary tract infection treatment, 1145t Clarithromycin, adult bacterial pneumonia, 867, 867t Classic migraine, 433 Clonazepam panic disorder treatment, 816 pediatric status epilepticus treatment, 787 Clonidine hypertensive emergency treatment, 79–80 overdose, 965–968 clinical presentation and examination, 966–967 definition, 965–966 diagnosis, 967 emergency actions, 965 epidemiology, 966 key points, 966 laboratory findings, 967 pathophysiology, 966 pharmacokinetics, 966 treatment, 967–968 Clopidogrel bisulfate, international normalized ratio for, 169 Clostridium botulinum diarrhea from, 744t, 745 infectious disease emergency, 266t Clostridium difficile, diarrhea from, 744t Cluster headache, 434. See also Headache CMV. See Controlled mandatory ventilation; Controlled mechanical ventilation
1184 INDEX CNS. See Central nervous system Coagulation panel analysis heart transplant complications requiring, 94 hip trauma requiring, 630 hymenoptera sting requiring, 232 neonatal emergencies, 668–669 Cocaine toxicity, 969–973 clinical presentation and examination, 970–972 definition, 969 diagnosis, 972 emergency actions, 969 epidemiology, 969–970 key points, 969 laboratory findings, 972 pathology, 970 treatment, 971–973 Colitis, 510 diverticulitis v., 126 Collagen vascular disease, erythema multiforme v., 98 Colonoscopy, diverticulosis requiring, 127 Coma adrenal insufficiency causing, 336 Glasgow Coma Scale, 453, 454t global assessment, 453, 454t head injury examination and disposition, 1071 modified for infants and children, 1076t multiple trauma diagnostic, 1054, 1054t hyperglycemic hyperosmolar nonketotic, 390–393 myxedema, 406–409 submersion incident causing, 246t Community-acquired pneumonia (CAP), 863, 864 antibiotics for, 867, 867t Compartment syndrome, 596–599, 641 Complete blood count (CBC) abdominal aortic aneurysm requiring, 4 cardiac tamponade requiring, 62 caustic ingestion requiring, 964 diabetic patient with otolaryngological emergency, 169 disseminated intravascular coagulation emergency, 350 diverticulitis requiring, 125 exfoliative dermatitis requiring, 101 heart transplant complications requiring, 94 hernias requiring, 17
Complete blood count (CBC), (Continued) hip trauma requiring, 630 hymenoptera sting requiring, 232 hyperglycemic hyperosmolar nonketotic coma, 392 iron toxicity requiring, 1009 knee pain emergency, 587 lightning injuries requiring, 236 neonatal emergencies, 668–669 ovarian torsion, 534 pediatric seizures and status epilepticus, 786 pneumothorax diagnosis, 893 salicylates toxicity, 1041 shock diagnostic, 919 toxic epidermal necrolysis requiring, 105 toxicology emergencies, 927–928 Working Group on Severe Streptococcal Infection, toxic shock syndrome requiring, 548 Computed tomography (CT) scan abdominal aortic aneurysm requiring, 4 adrenal insufficiency requiring, 336 angiographic, thoracic aortic dissection requiring, 25 appendicitis requiring, 7–8 ataxia, dizziness, vertigo, 418, 422 cholelithiasis and cholecystitis requiring, 13 with contrast, abdominal trauma, 1060 diverticulitis requiring, 125, 127 diverticulosis requiring, 127 emergent pelvic and abdominal pain, 512 ethanol withdrawal requiring, 329 head -ache, 432 trauma to, 1055 hernia diagnosis, 17 intestinal obstruction diagnosis, 21 methanol poisoning requiring, 1022 multiple trauma, 1052 neonatal emergencies, 668–669 ovarian torsion, 535 pediatric neurological evaluation, 1077 seizures and status epilepticus, 786 pneumothorax diagnosis, 893, 894f pulmonary embolism, 902, 905t Reye's syndrome, 797 seizures and status epilepticus, 469, 789 spinal cord injury, 1055 basilar life-threatening skull fractures, 1068–1069
Index Concussion, 1069. See also Central nervous system; Coma; Head Congenital aganglionic megacolon (Hirschsprung's disease), 745–748, 748f Congestive heart failure (CHF), 64–67 asthma mimicked by, 857 beta-blocker overdose diagnostic, 954 calcium channel blockers causing, 958 clinical presentation and historical findings, 65 definition of, 64 epidemiology, 64 examination, 65 heart transplant rejection causing, 95 key points, 64 laboratory findings, 66 pathophysiology, 64–65 primary prosthetic valve failure causing, 91 radiographs, 66 treatment, 66–67 diuretics, 66–67, 74 Conjugated hyperbilirubinemia, 136 Conjunctivitis, 164 Constipation, pediatric, 736–740 clinical presentation, 738 definition, 736–737 diagnosis, 738–739 emergency actions, 736 epidemiology, 737 examination, 738 key points, 736 laboratory findings, 738 pathology, 737 treatment, 739–740 Contact dermatitis, toxicodendron, 106–109 Continuous positive airway pressure (CPAP), 848 Controlled mandatory ventilation (CMV), 847 Controlled mechanical ventilation (CMV), 849t, 850 Conversion disorder, 819–821 clinical presentation, 820 definition, 820 diagnosis, 821 epidemiology, 820 examination, 820 key points, 819 laboratory findings, 820 treatment, 821 Co-oximetry measurement, toxicology emergencies diagnostic, 927
1185
COPD. See Chronic obstructive pulmonary disease Coral snake bite, 253, 254 Cornea abrasions of, 166–167 foreign bodies on, 167 ulcers of, 164 Coronary artery disease (CAD), 49 graft, after heart transplant, 94 Coronary bypass graft, cardiac chest pain treatment, 74 Cortisol, adrenal insufficiency treatment, 336 Corynebacterium diphtheriae, 261 Coumadin, 169 CPAP. See Continuous positive airway pressure CPR. See Cardiopulmonary resuscitation Cramps, heat, 221, 224 Cranial nerve examination, 456–462, 458f, 459f. See also Abducens nerve examination; Central nervous system CN I (olfactory), 456 CN II (optic), 456 CN III, IV, VI (oculomotor, trochlear, abducens), 457–458, 458f functional layout of extraocular movements and innervations, 458f CN IX, X (glossopharyngeal and vagus), 461 CN V (trigeminal), 459–460, 459f sensory nerve branch divisions, 459f CN VII (facial), 460–461 CN VIII (vestibulocochlear), 461 CN XI (spinous accessory), 461–462 CN XII (hypoglossal), 462 Creatinine study caustic ingestion requiring, 964 diverticulitis requiring, 125 hymenoptera sting requiring, 232 hyperglycemic hyperosmolar nonketotic coma, 392 pediatric seizures and status epilepticus, 787 toxicology emergencies requiring, 927–928 Crohn's disease, diverticulitis v., 126 Cryoprecipitated antihemophilic factor, as blood transfusion component, 561–562 Cryptosporidium diarrhea from, 745 infectious disease emergency, 268t
1186 INDEX Crystalloid infusion, pulmonary embolism treatment, 903 CSF. See Cerebrospinal fluid analysis CT scan. See Computed tomography scan Cyanide poisoning, 974–980 chemical warfare, 976 clinical presentation, 976–977 definition, 975 diagnosis, 977–978 emergency actions, 975 epidemiology, 975–976 examination, 977 key points, 974 laboratory findings, 977 metabolic acidosis from, 1021 pathology, 976 treatment, 978–980 Cyanosis, ARDS causing, 859–861 Cyclic antidepressant toxicity, 980–984, 982f clinical presentation, 982 definition, 980–982 antagonism of GABA receptors, 982 physiological effects, 981 sodium and potassium-channel blockade, 981 tricyclic antidepressants, 981 diagnosis, 982–983, 982f ECG abnormalities, 981f emergency actions, 980 examination, 982 key points, 980 treatment and outcome, 983–984 Cyclospora diarrhea from, 745 infectious disease emergency, 269t Cysts anorectal disorder, 118 cholecystitis, 9–14 ovarian, 510, 529–532 Pneumocystis carinii pneumonia, 95 Cytomegalovirus (CMV) clinical presentation, 281–282 definition, 277 epidemiology, 278 examination, 283 heart transplant infection, 95 treatment, 287 “Dawn phenomenon,” hypoglycemia from, 402 DCS. See Decompression sickness D-Dimer testing, pulmonary embolism diagnostic, 901
De Quervain's stenosing tenosynovitis, 615–616 DeBakey classification, thoracic aortic dissection, 23 Debridement, wound preparation requiring, 30 Decompression sickness (DCS), 205, 207–208 arterial gas embolism v., 208 Deep tendon reflexes, 462–464, 463t scale for grading of, 463t Defibrillator implantation follow-up automatic implantable cardioverterdefibrillator, 40–43 infection in, 42–43 clinical presentation, 41 diagnosis, 42 emergency defibrillation/cardiac passing, 40 epidemiology, 41 examination, 41–42 key points, 40 laboratory findings, 42 radiographs, 42 treatment, 42–43 pediatric automatic external, 657 Dehydration hyperglycemic hyperosmolar nonketotic coma, 390–393 pediatric emergency, 694–699 clinical presentation/examination, 696 definitions, 694–695 emergency actions, 694 epidemiology, 695 intravenous therapy for severe cases, 698–699 key points, 694 laboratory findings, 696–697 treatment, 697–699 oral rehydration therapy for, 694, 695, 697–699 Delirium haloperidol for intubated patient with, 910–911 respiratory acidosis causing, 320 sedation for intubated patient with, 910–911 Dementia, stroke syndromes v., 484t Demerol, headache treatment, 437–438 Dental emergencies, 154–158 definition, 154–155 diagnosis and treatment, 155–157
Index Dental emergencies, (Continued) emergency actions, 154 epidemiology, 155 examination, 155 key points, 154 “tooth squeeze” barotrauma, 207 Dental trauma, 179–182 definitions, 179–180 emergency actions, 179 epidemiology, 180 examination, 180 key points, 179 radiographs, 181 treatment, 181–182 Dependent personality disorder, 836–838 clinical presentation, 837 definition, 836 diagnosis, 837 epidemiology, 837 examination, 837 key points, 836 treatment and outcome, 837 Depot-testosterone, adrenal insufficiency treatment, 336 Dermatologic emergencies erythema multiforme, 97–99 exfoliative dermatitis, 99–102, 100b lymphadenitis, 101 toxic epidermal necrolysis, 103–106 toxicodendron dermatitis, 106–108, 106–109 urticaria, 109–113 Dermatopathic lymphadenitis, exfoliative dermatitis causing, 101 Detached retina, ophthalmologic emergencies, 166 Dexamethasone adrenal insufficiency treatment, 336–337 pediatric trauma medication, 1080 Diabetes. See also Diabetic ketoacidosis early, with hypoglycemia, 401 hyperglycemic hyperosmolar nonketotic coma, 390–393 insipidus, hypernatremia etiology involving, 359t otolaryngological emergencies with, 169 pediatric, 770–774 clinical presentation, 771 emergency actions, 770 epidemiology, 771 examination, 772 key points, 770 laboratory findings, 772
1187
Diabetes, (Continued) radiographs, 772–773 treatment, 773–774 Type I diabetes mellitus (juvenile diabetes), 770 Type II diabetes mellitus (insulin resistance), 770–771 Diabetic ketoacidosis (DKA), 311, 343–347, 390–393 pediatric, 770–774 Diagnostic and Statistical Manual of Mental Disorders (DSM-IV), 815–816 Diagnostic peritoneal lavage (DPL), 1060–1061 Dialysis disequilibrium syndrome, 1119 peritoneal, salicylates toxicity treatment, 1043 Diaphragmatic injury, 1103–1104 Diarrhea definition, 272 pediatric, 740–745, 744t clinical presentation, 742 definition, 741 emergency actions, 741 epidemiology, 741–742 examination, 742 key points, 740 laboratory findings and diagnosis, 742–743 treatment, 743–744, 744t common enteropathogens and therapies, 744t Diathesis, acute bleeding, 555–558 Diazepam intubated patient sedation, 911 pediatric status epilepticus treatment, 787 pediatric trauma medication, 1080 DIC. See Disseminated intravascular coagulation Diet fiber-rich, diverticulosis requiring, 127 Third National Health and Nutrition Examination Survey, 1014 vitamin D deficiency (rickets), 371 Diethylenetriamine penta-acetic acid (DTPA), gadolinium complex with chelating agent, 442 Digitalis glycoside toxicity, 984–988 definition, 985–986 diagnosis, 987 emergency actions, 984–985
1188 INDEX Digitalis glycoside toxicity, (Continued) examination, 987 key points, 984 laboratory findings, 987 presentation, 986 treatment and outcome, 987–988 Dihydroergotamine, headache treatment, 437–438 Dilantin, contraindicated for hyperglycemic hyperosmolar nonketotic coma, 393 Diltiazem, thyroid storm treatment, 398 Dimercaprol lead poisoning treatment, 1016 mercury poisoning treatment, 1026 Dimercaptopropanesulfonic acid (DMPS), arsenic intoxication treatment, 946–947 Dimercaptosuccinic acid (DMSA) arsenic poisoning treatment, 946 mercury poisoning treatment, 1026 Dimethyl sulfoxide (DMSO), 204 Diphenhydramine, anaphylactic shock requiring, 922 Diphtheria, 261–264 clinical presentation, 261 definition, 261 diagnosis, 263 emergency actions, 261 epidemiology, 261 examination, 263 key points, 261 pathology, 261 treatment, 263–264 Diplococcus pneumoniae, chronic obstructive pulmonary disease from, 884 Disinfection hair, wound preparation requiring, 29 skin, wound preparation requiring, 29 Dislocation ankle injuries, 594 elbow injuries, 602–603 ED reduced, 603 hand injuries, 620–622 hip injuries, 628 anterior, 628–629 posterior, 629 shoulder injuries, 650–651 Disseminated encephalomyelitis, multiple sclerosis v., 442 Disseminated intravascular coagulation (DIC), 232, 348–350
Disseminated intravascular coagulation (DIC), (Continued) clinical presentation, 349 diagnosis, 349–350 emergency actions, 348 examination, 349 key points, 348 laboratory findings, 350 mechanical ventilation for, 348 pathology, 348–349 treatment, 350 Diuretics congestive heart failure treatment, 66–67, 74 syndrome of inappropriate antidiuretic hormone, 353 Divers Alert Network, hyperbaric chamber referrals, 211 Diverticular hemorrhage, 124, 128 Diverticulitis, 510 acute/uncomplicated, treatment and outcomes, 128–129 clinical presentation, 124 complicated, 125, 129 definition of, 122 differential diagnosis, 125–126 epidemiology of, 122–123 examination, 124 complicated diverticulitis, 125 heart transplant infection, 95 laboratory findings, 125 pathophysiology of, 123 radiographs for, 127 in special situations, 127 treatment and outcome, 128–129 complicated diverticulitis, 129 Diverticulosis clinical presentation, 123–124 differential diagnosis, 125–126 emergency actions, 122 epidemiology, 122–123 examination, 124 key points, 122 laboratory findings, 125 pathology, 123 treatment and outcome, 127 Diving injuries, 205–211, 210b arterial gas embolism, 205, 208 barotrauma aerogastria, 207 alternobaric vertigo, 207 aural, 206 barodontalgia “tooth squeeze,” 207
Index Diving injuries, (Continued) barotitis media, 207 inner ear, 207 pulmonary overpressurization syndrome, 206 clinical presentation, 206 contaminated gases, 209 decompression sickness, 205, 207–208 definitions arterial gas embolism, 205 decompression sickness, 205 diagnosis, 210 focused diving history, 210b Divers Alert Network, hyperbaric chamber referrals, 211 emergency actions, 205 epidemiology, 206 examination, barotrauma, 209 key points, 205 laboratory findings, 210 nitrogen narcosis, 209 treatment, 210–211 analgesics/antibiotics, 211 hyperbaric, 211 rapid recompression, 211 supplemental oxygen, 211 Diving reflex, protective role of, 247–248 Dizziness. See Ataxia, dizziness, vertigo DKA. See Diabetic ketoacidosis DMPS. See Dimercaptopropanesulfonic acid DMSA. See Dimercaptosuccinic acid DMSO. See Dimethyl sulfoxide Dobutamine congestive heart failure treatment, 66–67 pediatric trauma medication, 1080 Domeboro, toxicodendron dermatitis treatment, 108–109 Dopamine congestive heart failure treatment, 66–67 pediatric trauma medication, 1080 Doxepin, urticaria treatment requiring, 112 Doxycycline, adult bacterial pneumonia, 867, 867t DPL. See Diagnostic peritoneal lavage Drowning. See Submersion incidents Drugs. See also Toxicity, drug barbiturate dependence, 949 exfoliative dermatitis from, 100, 100b, 101 hypercalcemia from, 374 hypernatremia etiology involving, 359t
1189
DSM-IV. See Diagnostic and Statistical Manual of Mental Disorders DTPA. See Diethylenetriamine pentaacetic acid Duke criteria for prosthetic heart valve dysfunction, 91b Dysmenorrhea, 510 Dysmetria, 464 cerebellar examination indicating, 464 Dyspnea exfoliative dermatitis causing, 101 pulmonary embolism causing, 898, 903 Dysrhythmia. See also Cardiac arrhythmia beta-blocker overdose sign, 953 cyclic antidepressant toxicity causing, 983–984 heart transplant rejection causing atrial, 95 Reye's syndrome causing, 797 shock causing, 920 theophylline toxicity causing, 1048 E. coli, diarrhea from, 744t, 745 ECF volume. See Extracellular fluid volume ECG. See Electrocardiography Echocardiography neonatal emergencies, 668–669 pulmonary embolism, 902, 905t tetralogy of Fallot, 782 transesophageal, thoracic aortic dissection diagnosis, 25 Eclampsia, 401, 510, 519–525. See also Preeclampsia and eclampsia definition of, 524 “Ecstasy.” See Methylenedioxymethamphetamine Ectopic pregnancy, 505–509 clinical presentation, 506–507 definitions, 505–506 emergency actions, 505 epidemiology, 506 key points, 505 treatment, 507 methotrexate, 507–508 Eczema, exfoliative dermatitis from, 100, 100b ED. See Emergency department Edema cerebral, high-altitude-related, 184t, 185, 187t, 191 treatment, 189 heat, 221, 224
1190 INDEX Edema, (Continued) peripheral, high-altitude-related, 184t, 190 pulmonary, high-altitude-related, 184t, 186, 187t, 191 treatment, 189–190 EEG. See Electroencephalogram Elbow injuries, 600–603 clinical presentation, 601 emergency actions, 601 epidemiology, 601 examination, 601–602 key points, 600 laboratory findings, 602 treatment dislocations, 602–603 ED reduced, 603 fractures, 603 x-ray for diagnosis, 602 Electrical injuries, 212–215. See also Injury clinical observation, 213–214 definitions, 212–213 emergency actions, 212 epidemiology, 213 key points, 212 laboratory findings, 214 treatment, 214–215 Electrocardiography (ECG) anticholinergic toxicity, 941 arrhythmias, 46f, 47f, 48f, 49f, 50f, 51f, 52f, 53f, 54f, 55f, 56f beta-blocker overdose diagnostic, 953 calcium channel blockers overdose treatment, 958–959 cardiac tamponade, 62, 63f cyclic antidepressant toxicity, 982f hypercalcemia, 375 hypomagnesemia, 378 moderate to severe ethanol withdrawal, 329 pacemaker complications, 86–87 pericarditis, acute, 38–39 permanent pacemakers, 86–87 Electroencephalogram (EEG), status epilepticus diagnostic, 470 Electrolyte and fluid management caustic ingestion requiring, 964 diverticulitis requiring, 125 hernias requiring, 17 hymenoptera sting requiring, 232 hyperglycemic hyperosmolar nonketotic coma, 392 ovarian torsion, 534
Electrolyte and fluid management, (Continued) pediatric emergencies, 700–705, 701 clinical presentation, 701–703 calculation of deficit fluids, 702–703, 704t calculation of maintenance fluids, 701–702 definition, 701 diagnosis, 703–704 emergency actions, 700 examination, 703 key points, 700 laboratory findings, 703 seizures and status epilepticus, 787 treatment, 704–705 salicylates toxicity, 1041 shock, 920 theophylline toxicity treatment, 1048 thyroid storm treatment, 397 ELISA. See Enzyme-linked immunosorbent assay EM. See Erythema multiforme Embolism. See also Prothrombin time measurement amniotic fluid, 500–502 arterial gas, 205, 208 decompression sickness v., 208 diving injury, 205, 208 Liebermeister's sign, 208 pulmonary, 897–905, 904f, 905t anticoagulant agents for, 898, 901, 903–904 cardiac arrhythmia from, 56, 56f cigarette smoking as risk factor for, 899 crystalloid infusion for, 903 CT scan for, 902, 905t enzyme-linked immunosorbent assay for, 902 Geneva (Wicki) assessment model, 900–901, 900t immuno-turbidimetric D-Dimer assay for, 901, 905t thrombocardiopulmonary arrest from, 664 extracranial sources of, 478f Emergency department (ED) abdominal aortic aneurysm, 4 asthma, 854–862 cholelithiasis and cholecystitis requiring, 12–13 ethanol withdrawal requiring, 330 headache treatment, 437–438
Index Emergency department (ED), (Continued) hymenoptera sting requiring, 232 hyperthyroidism and thyroid storm treatment, 394 pediatric seizures and status epilepticus, 786 snakebite requiring, 253 submersion incident requiring, 246t, 247 urticaria treatment requiring, 112–113 Emergency medical services (EMS) personnel, 236 Emesis arsenic poisoning treatment, 946 hyperemesis gravidarum, 516–518 ovarian torsion causing, 534 theophylline overdose causing, 1048 EMLA local anesthetic, 28–29 EMS personnel. See Emergency medical services personnel Encephalitis, herpes virus causing, 279 treatment, 285–286 Endocarditis erythema multiforme v. bacterial, 98 heart transplant recipient at risk for, 96 prosthetic valve infection, 91–92 Endocrinopathy hypercalcemia from, 374 hypoglycemia from, 402 Endometriosis, 510 Endoscopic retrograde cholangiopancreatography, prosthetic heart valve requiring, 92 Endotracheal tube pediatric emergency use of, 674 pediatric trauma requiring, 1079, 1079t, 1080t countershocks, 1079t medications, 1080t size v. patient age, 1074t End-stage renal disease (ESRD), 1117–1123. See also Renal disease cardiovascular complications with, 1119–1123 dialysis disequilibrium syndrome, 1119 hyperkalemia, 1119, 1123 hypertension, 1119–1121 hypotension, 1121 peritoneal dialysis and peritonitis, 1123 skeletal emergencies, 1121–1122 transplant rejection, 1122–1123, 1158t, 1161t, 1163–1167 chest x-ray, 1123
1191
End-stage renal disease (ESRD), (Continued) definition, 1118 emergency actions, 1117 key points, 1117 laboratory findings, 1123 pathophysiology, 1118–1119 coagulopathy, 1119 treatment, 1123 Enema, barium, intestinal obstruction diagnosis, 21 Enoxaparin sodium, hyperglycemic hyperosmolar nonketotic coma, 393 Entamoeba histolytica diarrhea from, 744t infectious disease emergency, 269t Environmental emergencies altitude-related conditions, 183–191, 184t, 187t burns, 192–197, 194f, 196b, 197b chemical, 198–204, 199b diving injuries, 205–211, 210b electrical injuries, 212–215 frostbite, 215–219 heat injuries, 220–225 hymenoptera sting, 230–233 hypothermia, 225–229 lightning injuries, 234–237 marine fauna envenomations, 238–242 snakebite, 249–254 spider bite and scorpion sting, 255–260 submersion incidents, 242–248, 246t Enzyme-linked immunosorbent assay (ELISA), pulmonary embolism diagnostic, 902 EPAP. See Expiratory positive airway pressure Epididymitis, 1124–1126 clinical presentation, 1125 definitions, 1124 diagnosis, 1126 Doppler ultrasound for differential diagnosis, 1126 emergency actions, 1124 epidemiology, 1125 examination, 1125 key points, 1124 laboratory findings, 1125 pathology, 1125 treatment, 1126 Epilepsy, 465–472, 466t, 468t, 471t. See also Seizures and status epilepticus benign rolandic, treatment for, 787
1192 INDEX Epilepsy, (Continued) juvenile myoclonic, 787 Epinephrine, 28 anaphylactic shock requiring, 921 asthma treatment, 722 pediatric trauma medication, 1080 urticaria treatment with aqueous, 111 vasoconstriction treatment, 28 Epi-Pen autoinjector, urticaria treatment requiring, 112–113 Epistaxis, 171–172 Epstein-Barr virus (EBV) infection, 276–277, 278, 281, 283 multiple sclerosis v., 440 treatment, 287 Erythema marginatum, acute rheumatic fever causing, 776 Erythema multiforme (EM), 97–99 clinical presentation, 97, 98 definition, 97 examination, 98 key point, 97 pathology, 97 treatment, 98 Erythromycin epididymitis, 1126 marine fauna envenomation requiring, 240–241 Escherichia coli diarrhea from, 744t infectious disease emergency, 266t Esophagus transesophageal echocardiography, 25 traumatic injury to, 1104 ESRD. See End-stage renal disease Ester class of anesthesia, 28 Esterase acetylcholinesterase inhibitor, 450 anticholinesterase inhibitor, 942 C1 esterase inhibitor concentrate, 112 Ethanol. See Ethyl alcohol Ethyl alcohol (ETOH), 271t. See also Alcoholic ketoacidosis clinical presentation, 328–329 definition, 326 dispensation, 330–331 emergency actions, 326 epidemiology, 326 examination, 329 intoxication, 989–994 clinical presentation, 991–992 definition, 989 disposition, 993 epidemiology, 989
Ethyl alcohol (ETOH), (Continued) examination, 992 hypoglycemia from, 326 laboratory findings, 992 pathophysiology and pharmacology, 989–991 treatment, 993 key points, 325 laboratory findings, 329 as methanol poisoning treatment, 1022–1023 pathophysiology and pharmacology, 326–328 radiology, 329 treatment, 330 withdrawal, 325–331 Ethylene glycol toxicity, 994–998 clinical presentation, 995–996 definition, 994 disposition, 998 emergency actions, 994 epidemiology, 995 key points, 994 laboratory findings, 996–997 pathophysiology, 995 sequela, 998 treatment, 997–998 ETOH. See Ethyl alcohol Etomidate, airway management treatment, 915b Euvolemia, hyponatremia with, 353, 355–356 Exfoliative dermatitis, 99–102, 100b clinical presentation, 100–101 definition, 99–100 emergency actions, 99 epidemiology, 100 examination, 101 intensive care unit for, 99 key points, 99 laboratory findings and diagnosis, 101–102 pathology, 100, 100b treatment, 102 Exhaustion, pathophysiology of submersion incident, 244 Expiratory positive airway pressure (EPAP), 848 External hordeolum, 163 Extracellular fluid (ECF) volume, 694 Extracellular shifts, hyperkalemia, 366 Eye. See also Ophthalmologic emergencies acute narrow-angle closure glaucoma, 164–165
Index Eye, (Continued) blowout fracture, 168 blunt trauma to, 167–168 chemical injury to, 167 cornea abrasions of, 166–167 foreign bodies on, 167 ulcers of, 164 ultraviolet keratitis, 190–191 vitreous hemorrhage, 165–166 detached retina, 166 emergency examination, 63 glaucoma, acute narrow-angle closure, 164–165 infection Haemophilus influenzae, 164 HIV with ophthalmologic symptoms, 291 ocular herpes simplex virus, 275–276, 279, 285 Staphylococcus aureus, 163 Streptococcus pneumoniae, 164 oculomotor nerve examination, 457–458, 458f red, 164 ruptured globe, 168 Facial nerve examination, 460–461 Fall on outstretched hand (FOOSH), 601 Fasciotomy, acute compartment syndrome treatment, 599 FAST. See Focused abdominal sonography for trauma Female sex organs. See also Obstetrics and gynecology; Pregnancy dysmenorrhea, 510 endometriosis, 510 ovaries, 510, 529–535 sexual assault, 543–545 toxic shock syndrome, 545–549 uterine leiomyoma, 510 uterine perforation, 510 vaginitis, 510 vulvovaginitis, 550–554 Femur herniated, 20 neck, fractured, 627–628 necrosis of, 511 slipped capital femoral epiphysis, 629–630 Fentanyl airway management treatment, 915b intubated patient analgesia, 907t, 908 Fetal distress, 498. See also Pregnancy
1193
Fever acute rheumatic, 774–778 antipyretics, 170, 397, 515, 786, 931–936, 934f blood transfusion causing, 563–564 high, exfoliative dermatitis causing, 101 pediatric, with seizures, 785, 789–792 definition, 789 emergency actions, 789 epidemiology, 789 key points, 789 laboratory findings, 790 pathology, 790 treatment, 790–792 Rocky Mountain spotted, 98 Fibrinolysis, cardiac chest pain treatment, 74 Finkelstein's test, De Quervain's stenosing tenosynovitis diagnostic, 615–616 Fissures, anorectal clinical presentation, 117 definition, 115 examination, 118 treatment and outcomes, 120 Fistula, anorectal clinical presentation, 117 definition, 114 examination, 118 pathology, 115 treatment and outcomes, 120 Flow-cycle mode mechanical ventilation, 847 Fludrocortisone, adrenal insufficiency treatment, 336 Fluid and electrolyte emergencies, 351–393, 354t, 359t, 369, 382t anaphylactic shock, 921 calcium, 369–377 hypercalcemia clinical presentation, 374–375 definition, 373 diagnosis, 375 drugs causing, 374 ECG findings, 375 endocrinopathies causing, 374 etiology, 373 examination, 375 granulomatous diseases causing, 374 key points, 373 laboratory findings, 375 malignancies causing, 373 medications for, 376–377 redistribution causing, 374 surgery or radiation for, 377
1194 INDEX Fluid and electrolyte emergencies, (Continued) treatment, 376 volume repletion with normal saline, 376 hypocalcemia clinical presentation, 371 definitions, 370 diagnosis, 372 emergency treatment, 372–373 epidemiology, 370 examination, 371 hypomagnesemia, 370 hypoparathyroidism, 371 key points, 370 laboratory findings, 372 pseudohypoparathyroidism, 371 treatment, 372 vitamin D deficiency (rickets), 371 chloride, 383–385 hyperchloremia, 385 hypochloremia, 384 emergency actions, 351 key points, 351 magnesium, 377–380 hypermagnesemia, 379–380 treatment, 380 hypomagnesemia clinical presentation, 378 definition, 377 diagnosis, 379 electrocardiography, 378 epidemiology, 377–378 examination, 378 laboratory findings, 378 treatment, 379 pediatric diabetes treatment, 773–774 phosphorus hyperphosphatemia, 382–383 hypophosphatemia, 380–382 potassium, 361–369 hyperkalemia clinical presentation, 367 definition, 366 diagnosis, 367 epidemiology, 366 examination, 367 extracellular shifts, 366 key points, 365–366 laboratory findings, 367 pseudo-, 366 treatment, 268–369 hypokalemia, 361–365 clinical presentation, 363
Fluid and electrolyte emergencies, (Continued) definition, 362 epidemiology, 362 etiology, 363 examination, 363–364 intracellular shifts, 362 key points, 361–362 laboratory findings, 364–365 sodium, 351–361, 354t, 359t hypernatremia, 357–361, 359t definition, 357 diagnosis, 359–360 epidemiology, 357 etiologies, 359t examination, 358 increased water intake, 357 increased water loss, 357–358 key points, 356–357 laboratory findings, 358–359 presentation, 358 reduced water intake, 357 sodium gain, 358 treatment, 360–361 hyponatremia, 353–356 definition, 352 diagnosis, 354–355 epidemiology, 352–353 etiology, 354t euvolemia with, 353, 355–356 examination, 353 hypervolemia with, 355 hypovolemia with, 355 laboratory studies, 353–354 presentation, 353 treatment, 355 Fluid boluses, intestinal obstruction requiring, 21 Fluid replacement pediatric trauma requiring, 1074t rhabdomyolysis treatment, 416–417 thyroid storm treatment, 397 Flumazenil, pediatric analgesia and sedation reversal, 812–813 Fluoroquinolone, bacterial pneumonia treatment, 867, 867t Fluoxetine, panic disorder treatment, 816 Focused abdominal sonography for trauma (FAST) abdominal trauma, 1060 multiple trauma diagnostic, 1052 thoracic life-threatening injury requiring, 1100 Fomepizole, methanol poisoning treatment, 1022
Index Food and Drug Administration (FDA), haloperidol for intubated patient sedation, 910–911 Foodborne and waterborne illnesses, 264–275, 266t–271t clinical presentation, 265–272, 266t–271t definition, 264–265 diagnosis, 272 emergency actions, 264 epidemiology, 265 examination, 272 FoodNet surveillance for, 274 key points, 264 laboratory findings, 272 radiographs, 273 treatment, 273–274 FoodNet, 274 FOOSH. See Fall on outstretched hand Foot injuries, 604–608 anatomy, 604 definition, 604 emergency actions, 604 examination, 606 forefoot, 606 fractures and punctures, 643–646 hindfoot, 605 key points, 604 laboratory findings, 606–607 midfoot, 605–606 phalangeal, 606 physical examination, 605 radiographs, 607 treatment, puncture wounds, 607 Forced vital capacity (FVC) test, 884 Forearm and wrist injuries, 608–616. See also Tendons anatomy, 609–610 carpal fractures and injuries, 612 clinical presentation, 610–611 definition, 609 emergency actions, 608 examination, 610 forearm, 611–612 key points, 608 wrist nerve entrapment and overuse syndromes, 614–616 carpal tunnel syndrome, 615 De Quervain's stenosing tenosynovitis, 615–616 tendonitis, 615 ulnar tunnel syndrome, 615 Fosphenytoin, toxicity, 1034–1137
1195
Fractures ankle, 593–594 blowout eye, 168 carpal, 612 clavicle, 648 elbow, 603 femoral, 627–628 foot, 607 hand, 619–620 hip dislocations and fracturedislocations, 628 humerus, 649 humoral shaft, 649 intertrochanteric, 628 lower leg, 640–642 multiple long bone, 1056 multiple trauma causing, 1056 open, 643–646 classifications, 644–645 clinical presentation, 643 definition, 643 diagnosis, 644 emergency actions, 643 epidemiology, 643 examination, 644 key points, 643 laboratory findings, 644 radiographs, 645 treatment, 645–646 pelvic type I, 1083–1085 type II, 1085 type III, 1085–1086 type IV, 1086 penile, 1128 scapular, 649 skull, 1068–1069 basilar life-threatening, 1068 tibial tuberosity, 642 trochanteric, 628 Fresh frozen plasma (FFP) acute bleeding diathesis treatment, 558 adrenal insufficiency treatment, 337 as blood transfusion component, 561 urticaria treatment requiring, 112 Frostbite, 215–219 clinical presentation and examination, 217 definition, 216 diagnosis, 217–218 emergency actions, 216 epidemiology, 216 key points, 215
1196 INDEX Frostbite, (Continued) laboratory findings, 218 pathophysiology, 216–217 summary, 219 treatment, 218–219 Furosemide congestive heart failure treatment, 66–67 pediatric trauma medication, 1080 rhabdomyolysis treatment, 416–417 FVC test. See Forced vital capacity test GABA receptors. See Gamma aminobutyric acid receptors GABHS. See Group A beta-hemolytic streptococci GAD. See Generalized anxiety disorder Gadolinium contrast, 442 Gamma aminobutyric acid (GABA) receptors, 330 barbiturate overdose influencing, 949, 950, 951 cyclic antidepressant toxicity influencing, 982 Gamma globulin, pediatric Kawasaki disease treatment, 794–795 GAS infection. See Group A streptococcal infection Gastric lavage arsenic poisoning treatment, 946 iron toxicity requiring, 1009–1010 salicylates toxicity treatment, 1042 Gastric tube, abdominal trauma requiring, 1062 Gastrointestinal bleeding, 130–134 clinical presentation, 131 definition, 130 diagnosis, 133 emergency actions, 130 epidemiology, 131 examination, 131–132 key points, 130 laboratory findings, 132 radiographs, 133 treatment, 133–134 Gastrointestinal emergencies anorectal disorders, 114–121 bleeding, 130–134 diverticulosis and diverticulitis, 122–129 gastroenteritis, 510 jaundice and hepatitis, 135–143, 137f, 138f, 139f metabolic acidosis, 316 pancreatitis, 144–148
Gastrointestinal emergencies, (Continued) peptic ulcer disease, 149–152 Gastrointestinal (GI) system, 271t GCS. See Glasgow Coma Scale Generalized anxiety disorder (GAD), 817–819. See also Panic disorder clinical presentation, 817 definition, 817 diagnosis, 818 epidemiology, 817 examination, 818 key points, 817 laboratory findings, 818 treatment, 818–819 Geneva (Wicki) assessment model, pulmonary embolism risk, 900–901, 900t Genital herpes, 279, 285, 513–515. See also Genitourinary tract; Herpes virus clinical presentation, 513–514 definition, 513 diagnosis, 515 emergency actions, 513 epidemiology, 513 examination, 514 key points, 513 laboratory findings, 514 treatment, 515 Genitourinary tract. See also Genital herpes trauma, 1063–1066 clinical presentation, 1063–1065 genital injuries, 1065 renal contusions/lacerations/ ruptures, 1064 ureter/bladder injuries, 1064 urethral injuries, 1065 definition, 1063 diagnosis, 1066 emergency actions, 1063 examination, 1065–1066 key points, 1063 laboratory findings, 1066 treatment, 1066 Gentamycin, endocarditis from prosthetic valve infection, 91–92 Geriatric patient aneurysm susceptibility, 2 emergencies, 386–393 abdominal pain, 389 clinical presentations, 387 definition, 387 emergency actions, 386 epidemiology, 387 examination and history, 388
Index Geriatric patient, (Continued) myocardial infarction, 388 pneumonia, 388 psychiatric illness, 389 trauma, 389 urinary tract infection, 388–389 glaucoma, acute narrow-angle closure, 164–165 hyperglycemic hyperosmolar nonketotic coma, 390–393 reduced toxicodendron dermatitis sensitivity, 107 retinal artery occlusion in, 165 Gestational hypertension. See also Preeclampsia and eclampsia definition of, 521 GFR. See Glomerular filtration rate GI system. See Gastrointestinal system Giant cell arteritis, ophthalmologic emergencies, 166 Giardia lamblia diarrhea from, 744t infectious disease emergency, 269t Glasgow Coma Scale (GCS), 453, 454t global assessment, 453, 454t head injury examination and disposition, 1071 modified for infants and children, 1076t multiple trauma examination, 1054, 1054t Glaucoma, acute narrow-angle closure, 164–165 Gliosis, 440 Glomerular filtration rate (GFR), 1113–1117 Glossopharyngeal nerve examination, 461 Glucocorticoid replacement therapy, adrenal insufficiency treatment, 337 Glucose level determination hypoglycemia, 399–405 pediatric diabetes, 773–774 pediatric seizures and status epilepticus, 786 toxicology emergencies, 927–928 pediatric trauma medication, 1081 Goodpasture's syndrome, 889–890 Granulomatous diseases hypercalcemia from, 374 Wegener's granulomatosis, 889–890 Group A beta-hemolytic streptococci (GABHS), 173, 174, 802–805
1197
Group A streptococcal (GAS) infection, 774–778 Guillain-Barré syndrome arsenic poisoning v., 946 botulism v., 430 Gynecology. See Female sex organs; Obstetrics and gynecology Gynecomastia (male mammary gland development), exfoliative dermatitis causing, 101 H2 antagonists, urticaria treatment, 112 Haemophilus influenzae type b (HIB) chronic obstructive pulmonary disease from, 884 eye infection, 164 pediatric infection, 708, 708t, 712–713 Hallucinogen toxicity, 999–1003 clinical presentation, 1001–1002 definition, 999 diagnosis, 1002–1003 emergency actions, 999 key points, 999 laboratory findings, 1002 pathophysiology, 999–1001 Haloperidol, delirium requiring, 910–911 Halotestin, adrenal insufficiency treatment, 336 Hand injuries, 617–624 anatomy, 617–619 emergency actions, 617 history (from patient/bystander/ paramedic), 619 key points, 617 physical examination, 619–625 dislocations, 620–622 fractures, 619–620 high-pressure injection injuries, 624 infections, 622–624 radiographs, 624 tendon injuries, 622 HAP. See Hospital-acquired pneumonia HAV. See Hepatitis A virus HBV. See Hepatitis B virus HCV. See Hepatitis C virus Head. See also Brain; Central nervous system trauma to, 1055, 1067–1072 airway management for, 915b computed tomography scan for, 1055 definition, 1067–1068 disposition, 1071–1072 Glasgow Coma Scale, 1071 emergency actions, 1067
1198 INDEX Head, (Continued) hematomas, 1069–1071 epidural, 1069–1070 herniation from, 1070 ICP monitoring for, 1070 subdural, 1070 key points, 1067 minor injuries, 1069 concussion, 1069 outcome, 1072 pathophysiology, 1068 physical examination, 1071 skull fractures, 1068–1069 systemic v. neurologic complications, 1072 Headache, 432–438 clinical presentation, 435–436 CT or MRI scan for, 432 definition, 432 emergency actions, 432 epidemiology, 433 examination, 436 heart transplant infection causing, 95 key points, 432 laboratory findings, 437 migraine, 431–432 classic, 433 common, 433 hemiplegic, 433 ophthalmoplegic, 433 stroke syndromes v., 484t treatment, 437–438 pathology, 433–435 acute narrow-angle glaucoma, 435 brain tumor, 434 classic migraine, 433 cluster headache, 434 common migraine, 433 dural bleeding, 434 hemiplegic migraine, 433 hypertension induced, 434 ophthalmoplegic migraine, 433 post-lumbar puncture, 435 pseudotumor cerebri, 434, 435 subarachnoid hemorrhage, 434–435 temporal arteritis, 435 toxic metabolic, 434 traction induced, 434 trigeminal neuralgia, 435 radiology for, 437 treatment, 437–438 Hearing loss (sudden), 170–171 Heart transplant, 93–96, 1150, 1151, 1154
Heart transplant, (Continued) antibiotic prophylaxis for, 96 definition, 93–94 diagnosis, 94–95 drug toxicity causing, 95 emergency actions for recipient of, 93 endocarditis risk for, 96 epidemiology, 94 examination, 94 infection causing, 94, 95 typical infections, 95 key points, 93 laboratory findings, 94 rejection causing, 93–96, 1150, 1151, 1154 treatment, 95–96 Heat injuries, 220–224 clinical presentation, 221 cramps, 221, 224 definition, 220 diagnosis, 223 edema, 221, 224 emergency actions, 220 epidemiology, 220–221 examination, 222–223 exhaustion, 222, 224 key points, 220 laboratory findings, 223 prickly heat, 222, 224 radiographs, 223 stroke, 222, 225 syncope, 221, 224 treatment, 223–224 Heliox, asthma treatment, 223 HELLP syndrome hemolysis-elevated liver enzyme levels-low platelet count, 401 preeclampsia and eclampsia with, 523 Hematocrit, shock diagnostic, 919 Hematomas Bell's palsy v., 426–427, 426t cranial herniation from, 1069–1071 epidural, 1069–1070 herniation from, 1070 ICP monitoring for, 1070–1071 subdural, 1070 evacuation of, 161 Hemodialysis arsenic intoxication, 943 hyperkalemia requiring, 369 lithium poisoning treatment, 1019 mercury poisoning treatment, 1026
Index Hemodialysis, (Continued) methanol poisoning treatment, 1022–1023 salicylates toxicity treatment, 1043 Hemoglobin analysis, shock diagnostic, 919 Hemoglobinuria, arsine poisoning v., 946 Hemolytic uremic syndrome, infectious disease emergency, 266t Hemophilia, 566–569 clinical presentation, 567–568 cryoprecipitated antihemophilic factor, as blood transfusion component, 561–562 definition, 566–567 diagnosis, 568 emergency actions, 566 epidemiology, 567 examination, 568 key points, 566 laboratory findings, 568 pathophysiology, 567 treatment, 569 Hemoptysis, 888–891 clinical presentation, 889 definition, 888 diagnosis, 890 emergency actions, 888 epidemiology, 888–889 examination, 889 key points, 888 laboratory findings, 889–890 Goodpasture's syndrome, 889–890 systemic lupus erythematosus, 889–890 Wegener's granulomatosis, 889–890 pulmonary embolism causing, 898 treatment, 890–891 surgical intervention, 891 Hemorrhage. See also Blood; Oncologic and hematologic emergencies; Subarachnoid hemorrhage diverticular, 124, 128 maternal-fetal, 1109–1110 MRI of intracerebral, 487f ophthalmologic emergency, 165–166 subconjunctival, 167 ruptured ovarian cyst, 510 salicylates toxicity complication, 1043 shock from, 920 stroke syndromes, 484t, 486–489, 487f, 488f, 489f, 490f, 491f, 492f
1199
Hemorrhoids, 114–120 clinical presentation, 116–117 definition, 114 emergency action, 114 examination, 117–118 laboratory findings, 119 pathology, 115 treatment and outcomes, 119–120 Hemostasis, wound preparation requiring, 29 Heparin cardiac chest pain treatment, 74 contraindications for, 74–75 hyperglycemic hyperosmolar nonketotic coma, 393 low-molecular weight v. unfractionated, 74 pulmonary embolism treatment, 903–904 Hepatic impairment. See also Hepatitis caustic ingestion causing, 964 exfoliative dermatitis causing, 101 hepatitis causing enlargement, 136 hepatomegaly, exfoliative dermatitis causing, 101 hepatotoxicity acetaminophen overdose causing, 931–936, 934f hypoglycemia causing, 401 liver transplantation emergencies, 1156–1162, 1158t, 1160t, 1161t theophylline toxicity, 1046 Hepatitis, 135–143, 137f, 138f, 139f. See also specific type cirrhosis from, 1156 definition of, 136 opioid injection risk of, 1028 Reye's syndrome causing, 797 Hepatitis A virus (HAV), 136, 137, 137f, 139 infectious disease emergency, 268t Hepatitis B virus (HBV), 136, 137–138, 138f, 139 Hepatitis C virus (HCV), 136, 138–139, 139f. See also Liver transplantation emergencies cirrhosis from, requiring liver transplantation, 1156 Hepatobiliary iminodiacetic acid (HIDA), 12–13 cholelithiasis and cholecystitis diagnostic, 12–13 Herniation, 15–20, 797, 1069–1071 abdominal, 15–18
1200 INDEX Herniation, (Continued) cerebral, Reye's syndrome causing, 797 clinical presentation, 16 definition, 15–16 diagnosis, 17 emergency actions for, 15 epidemiology, 16 examination, 16–17 femoral, 20 hematoma causing, 1069–1071 incarcerated, 16, 17, 20 incisional, 16, 20 inguinal, 15, 17, 20 key points, 15 laboratory findings, 17 radiographs for, 17 strangulated, 16, 17 treatment and outcome, 17–18 umbilical, 15 Herpes keratitis, 164 Herpes simplex viruses (HSV), 275–276, 277, 279, 282, 285 Herpes virus, 275–288. See also Genital herpes Bell's palsy clinical presentation, 279–280 definition, 276 differential diagnosis, 426–427, 426t, 484t risk factors for, 424–425 treatment, 286 clinical presentation encephalitis, 279 genital lesions, 279 immunocompromise, 280 oral lesions, 278–279 cytomegalovirus clinical presentation, 281–282 definition, 277 epidemiology, 278 examination, 283 treatment, 287 definition, 275 diagnosis, 284–285 emergency actions, 275 epidemiology, 277 Epstein-Barr virus clinical presentation, 281 definition, 276–277 epidemiology, 278 examination, 283 treatment, 287 heart transplant recipient susceptibility, 95
Herpes virus, (Continued) herpes zoster shingles clinical presentation, 280–281 definition, 276 epidemiology, 277–278 examination, 283 treatment, 287 herpetic whitlow clinical presentation, 280 definition, 276 treatment, 286 key points, 275 laboratory findings, 283–284 ocular HSV clinical presentation, 279 definition, 275–276 treatment, 285 radiographs, 285 simplex viruses 1 and 2 definition, 275 epidemiology, 277 examination, 282 ocular, 275–276, 279, 285 treatment, 285 encephalitis, 285–286 oral and genital lesions, 285 varicella-zoster clinical presentation, 280 definition, 276 epidemiology, 277 examination, 282–283 immune globulin, 96 treatment, 286 Herpes zoster shingles, 276, 277–278, 280–281, 283, 287 Herpetic whitlow, 275, 276, 280 treatment, 286 HIB. See Haemophilus influenzae type b HIDA. See Hepatobiliary iminodiacetic acid Hidradenitis suppurativa, definition, 114 High altitude-related emergencies, 183–191, 184t, 187t global amnesia, 184t headache, 434 High-altitude cerebral edema (HACE), 184t, 185, 187t, 189, 191 High-altitude pulmonary edema (HAPE), 184t, 186, 187t, 189–190, 191 Hip trauma, 625–630 anatomy, 626–627 clinical presentation, 627–630 anterior dislocations, 628–629 femoral neck fractures, 627–628
Index Hip trauma, (Continued) hip dislocations and fracturedislocations, 628 intertrochanteric fractures, 628 Legg-Calvé-Perthes disease, 629 pediatric hip dislocations, 629 posterior dislocations, 629 septic hip or septic arthritis, 630, 632, 633, 637 slipped capital femoral epiphysis, 629–630 trochanteric fractures, 628 definition, 626 emergency actions, 625 epidemiology, 626 examination, 627 key points, 625 laboratory evaluation, 630 radiographs, 630 Hirschsprung's disease (congenital aganglionic megacolon), 745–748, 748f clinical presentation, 746 definition, 746 diagnosis, 747 emergency actions, 746 epidemiology, 746 examination, 746–747 key points, 745 laboratory findings, 747 radiographs, 747, 748f treatment, 747–748 Histrionic personality disorder, 832–833 clinical presentation and examination, 832 diagnosis, 833 epidemiology, 832 key points, 832 treatment and outcome, 833 Hordeolum, 163 Hormone replacement, hypothyroidism and myxedema coma treatment, 408–409 Hospital admission adrenal insufficiency, 337 bacterial pneumonia from, 863 diabetic ketoacidosis, 347 heart transplant complications, 95–96 hyperglycemic hyperosmolar nonketotic coma, 393 hypothyroidism and myxedema coma, 408–409 pediatric emergency dehydration, 699 pediatric Kawasaki disease, 794–795
1201
Hospital admission, (Continued) phenytoin toxicity, 1037 pulmonary embolism risk factor, 899 renal stones, 1138 salicylates toxicity, 1043 theophylline toxicity, 1048 urticaria treatment, 112 Hospital-acquired pneumonia (HAP), 863 HSV. See Herpes simplex viruses Human immunodeficiency virus (HIV) infection, 288–292, 1028 acquired immunodeficiency syndrome, 271t exfoliative dermatitis from, 100, 100b Bell's palsy v., 426–427, 426t clinical presentation, 289–290 definitions, 288 HIV v. AIDS, 288–289 emergency actions, 288 epidemiology, 289 key points, 288 multiple sclerosis v., 442 opioid injection risk of, 1028 pathophysiology, 289 postexposure prophylaxis, 292 renal stones treatment for patients with, 1135, 1137 symptoms central nervous system, 291 cutaneous system, 291–292 gastrointestinal system, 290–291 ophthalmologic system, 291 pulmonary, 290 Human T-lymphotropic virus (HTLV), multiple sclerosis v., 442 Hunt and Hess Clinical Grading Scale, 496 Hydralazine, pediatric trauma medication, 1080 Hydrocarbon poisoning, 1003–1007 clinical presentation, 1005 definition, 1004 diagnosis, 1005–1006 emergency actions, 1004 epidemiology, 1004–1005 examination, 1005 key points, 1003 laboratory findings, 1005 radiographs, 1006 treatment, 1006–1007 Hydrocortisone adrenal insufficiency treatment, 336 hypothyroidism and myxedema coma treatment, 408–409 pediatric trauma medication, 1080
1202 INDEX Hydrocortisone, (Continued) thyroid storm treatment, 397 Hydrofluoric acid, chemical burn from, 203–204 Hydromorphone, intubated patient analgesia, 907t, 908 Hymenoptera sting, 230–233 clinical presentation, 231–232 definition, 230–231 diagnosis, 232 emergency actions, 230 epidemiology, 231 key points, 230 pathophysiology, 231 treatment, 232–233 Hyperbaric chamber referrals, Divers Alert Network for, 211 Hyperbilirubinemia, 136 Hypercalcemia. See also Calcium; Hypocalcemia cardiac arrhythmia from, 54, 55f clinical presentation, 374–375 definition, 373 diagnosis, 375 drugs causing, 374 ECG findings, 375 endocrinopathies causing, 374 etiology, 373 examination, 375 granulomatous diseases causing, 374 key points, 373 laboratory findings, 375 malignancies causing, 373 medications for, 376–377 redistribution causing, 374 surgery or radiation for, 377 treatment, 376 volume repletion with normal saline, 376 Hypercapnia definition of, 845 headaches from, 434 respiratory acidosis causing, 320 Hyperchloremia, 385. See also Chloride, fluid and electrolyte emergencies; Hypochloremia fluid and electrolyte emergencies, 385 Hyperemesis gravidarum, 516–518 clinical presentation, 516 definition, 516 diagnosis, 517 emergency actions, 516 epidemiology, 516 etiology, 516
Hyperemesis gravidarum, (Continued) examination, 517 key points, 515 laboratory findings, 517 treatment, 517–518 Hyperglycemia. See also Hyperglycemic hyperosmolar nonketotic coma theophylline overdose causing, 1046 Hyperglycemic hyperosmolar nonketotic coma (HHNC), 390–393. See also Hyperglycemia clinical presentation, 391–392 definition, 390–391 diabetic ketoacidosis v., 390–393 diagnosis, 392 disposition, 393 emergency actions, 390 epidemiology, 391 key points, 390 laboratory findings, 392 pathophysiology, 391 treatment, 392–393 Hyperkalemia. See also Hypokalemia cardiac arrhythmia from, 54, 55f cardiopulmonary arrest from, 664 clinical presentation, 367 definition, 366 diagnosis, 367 end-stage renal disease causing, 1119, 1123 epidemiology, 366 examination, 367 extracellular shifts, 366 hemodialysis for, 369 key points, 365–366 kidney disease causing, 1119, 1123 laboratory findings, 367 pseudo-, 366 treatment, 268–369 Hypermagnesemia, 379–380. See also Hypomagnesemia; Magnesium treatment, 380 Hypernatremia, 357–361, 359t. Hyponatremia definition, 357 diagnosis, 359–360 epidemiology, 357 etiologies, 359t examination, 358 increased water intake, 357 increased water loss, 357–358 key points, 356–357 laboratory findings, 358–359 presentation, 358
Index Hypernatremia, (Continued) reduced water intake, 357 sodium gain, 358 treatment, 360–361 Hyperosmolarity, hyperglycemic hyperosmolar nonketotic coma, 390–393 Hyperphosphatemia, 382–383. See also Hypophosphatemia Hypertension. See also Hypertensive emergencies; Hypotension acute, 524–525 benign intracranial, 434, 435 chronic, definition of, 520 end-stage renal disease causing, 1119–1121 gestational, 521 headaches associated with, 434 Hypertensive emergencies, 76–80. See also Hypertension; Hypotension asymptomatic, 79–80 definitions, 76 epidemiology, 76–77 examination and history taking, 77 physical, 77 key points, 76 laboratory findings, 77 preeclampsia and eclampsia, 401, 510, 519–525 radiographs, 78 treatment, 78–79 Hyperthermia, 664. See also Hypothermia Hyperthyroidism and thyroid storm, 394–398. See also Hypothyroidism and myxedema coma clinical presentation, 395–396 definitions, 394 diagnosis, 396 emergency actions, 394 epidemiology, 394–395 examination, 396 key points, 394 laboratory findings, 396–397 pathology, 395 treatment, 397–398 Hyperventilation. See also Hypoventilation asthma mimicked by, 857 hypernatremia etiology involving, 359t Hypervolemia, 355. See also Hypovolemia Hyphema, as ophthalmologic emergency, 168 Hypoalbuminemia state, 315 Hypocalcemia. See also Calcium; Hypercalcemia
1203
Hypocalcemia, (Continued) cardiac arrhythmia from, 54, 55f caustic ingestion causing, 964 clinical presentation, 371 definitions, 370 diagnosis, 372 emergency treatment, 372–373 epidemiology, 370 examination, 371 hypomagnesemia, 370 hypoparathyroidism, 371 key points, 370 laboratory findings, 372 pseudohypoparathyroidism, 371 treatment, 372 vitamin D deficiency (rickets), 371 Hypochloremia, 384. See also Hyperchloremia Hypoglossal nerve examination, 462 Hypoglycemia, 326, 399–405, 399f, 434, 484t alcoholic ketoacidosis, 339, 339f causes of “dawn phenomenon,” 402 early diabetes, 401 endocrine disorders, 402 ethanol intoxication, 326, 402 HELLP syndrome, 401 hepatic impairment, 401 hypothyroidism, 408–409 insulinoma, 401 kwashiorkor, 401 medications, 403 meningitis, 401 mesenchymal tumors, 401 renal disease, 402 salicylate intoxication, 403 sepsis, 401 Somogyi syndrome, 402 clinical presentation, 400–403 definition, 399–400 diagnosis, 404 emergency actions, 399 epidemiology, 400 examination, 403 glucose level determination, 399–405 headaches from, 434 hyperosmolar nonketotic, 390–393 insulin-dependent patient, 402 key points, 399 laboratory findings, 403–404 medical emergency, 399–405 mental status alteration from, 404–405
1204 INDEX Hypoglycemia, (Continued) stroke syndromes v., 484t treatment and outcome, 404–405 Hypokalemia, 361–365. See also Hyperkalemia cardiac arrhythmia from, 54, 55f clinical presentation, 363 definition, 362 epidemiology, 362 etiology, 363 examination, 363–364 intracellular shifts, 362 key points, 361–362 laboratory findings, 364–365 metabolic alkalosis causing, 319 theophylline overdose causing, 1046, 1048 Hypomagnesemia, 370, 377–379. See also Hypermagnesemia; Magnesium caustic ingestion causing, 964 clinical presentation, 378 definition, 377 diagnosis, 379 electrocardiography, 378 epidemiology, 377–378 examination, 378 laboratory findings, 378 treatment, 379 Hyponatremia, 353–356. See also Hypernatremia definition, 352 diagnosis, 354–355 epidemiology, 352–353 etiology, 354t euvolemia with, 355–356 examination, 353 hypervolemia with, 355 hypothyroidism and myxedema coma causing, 408–409 hypovolemia with, 355 laboratory studies, 353–354 presentation, 353 treatment, 355 Hypoparathyroidism, 371 pseudo-, 371 Hypophosphatemia, 380–382. See also Hyperphosphatemia Hypopyon, corneal ulcer with, 164 Hypotension. See also Hypertension; Hypertensive emergencies arsenic poisoning causing, 946 beta-blocker overdose sign, 953 clonidine overdose causing, 965, 967–968
Hypotension, (Continued) cyclic antidepressant toxicity causing, 983–984 end-stage renal disease causing, 1121 morphine and nitroglycerin causing, 75 primary valve failure causing, 91 pulmonary embolism causing, 898 respiratory acidosis causing, 321 theophylline toxicity causing, 1048 Hypothermia, 225–229. See also Hyperthermia clinical presentation, 227 definition, 226 diagnosis, 227–228 emergency actions, 226 epidemiology, 226 exfoliative dermatitis causing, 101 hypothyroidism and myxedema coma causing, 409 key points, 225 laboratory findings, 228 pathophysiology, 226–227 pathophysiology of submersion incident, 244 physical examination, 227 submersion incident causing, 246t, 247, 248 summary, 229 treatment, 228–229 Hypothyroidism and myxedema coma, 406–409. See also Hyperthyroidism and thyroid storm clinical presentation and examination, 407–408 definition, 406 diagnosis, 408 emergency actions, 406 epidemiology, 406–407 key points, 406 laboratory findings, 408 pathology, 407 treatment, 408–409 Hypoventilation, metabolic alkalosis causing, 319. See also Hyperventilation Hypovolemia. See also Hypervolemia cardiopulmonary arrest from, 664 hyponatremia with, 355 Hypoxemia cardiopulmonary arrest from, 664 definition of, 845 Hypoxia headaches from, 434 pulmonary embolism causing, 903
Index Hypoxia, (Continued) sudden infant death syndrome, 765–769 “Ice.” See Methylenedioxymethamphetamine ICP. See Intracranial pressure IgM. See Immunoglobulin M Immobilization, pulmonary embolism risk with prolonged, 899 Immunoglobulin G (IgG), toxic shock syndrome requiring, 549 Immunoglobulin M (IgM), 271t Immuno-turbidimetric D-dimer assay, pulmonary embolism, 901, 905t Imuran, myasthenia gravis requiring, 450 IMV. See Intermittent mandatory ventilation Incarcerated hernias, 16, 17, 20 Incisional hernias, 16, 20 Indomethacin, headaches from, 434 INF. See Interferon Infant. See also Child; Pediatric emergencies; Pregnancy definition of, 657 Infections. See also Bacteremia; Bacteria; Infectious disease emergencies; Sepsis; specific pathogen automatic implantable cardioverterdefibrillator, 42–43 bone, 631–637 Epstein-Barr viral, 276–277, 278, 281, 283, 287, 440 hand, 622–624 hand injuries with, 622–624 heart transplant complications, 94, 95 infection risk after marine fauna envenomation, 240–241 joint, 631–637 Listeria, 95 lithium poisoning with, 1018 pharyngitis viral, 172–173 prosthetic valve, 91–92 Staphylococcus aureus, 42, 163, 267t, 502, 1127–1128 Staphylococcus epidermidis, 42 streptococcal group A acute pediatric rheumatic fever from, 774–778 beta-hemolytic, 173, 174, 802–805 pneumoniae, 164, 707–708, 708t toxoplasma, 95 urinary tract, 1142–1146, 1145t pediatric, 388–389
1205
Infections, (Continued) Working Group on Severe Streptococcal Infection, toxic shock syndrome requiring, 548 Infectious disease emergencies. See also Infections diphtheria, 261–264 foodborne and waterborne illnesses, 264–275, 266t–271t herpes virus, 275–288 human immunodeficiency virus, 288–292 Bell's palsy v., 426–427, 426t multiple sclerosis v., 442 influenza, 292–295 Haemophilus, 164, 708, 708t, 712–713 Isospora belli, 269t knee pain as, 587 malaria, 295–300, 298t–299t, 300t rabies, 301–306 tetanus, 307–310 Inflammatory skin disorders. See also Dermatologic emergencies exfoliative dermatitis from, 100, 100b Influenza, 292–295 carbon monoxide poisoning mimicking, 960 clinical presentation, 293–294 definition, 293 diagnosis, 294 emergency actions, 293 epidemiology, 293 examination, 294 Haemophilus eye infection from, 164 pediatric infection, 708, 708t, 712–713 key points, 293 laboratory findings, 294 radiographs, 294 treatment, 294 Inguinal hernias, 15, 17, 20 Injection drug use Epi-Pen autoinjector, 112–113 high-pressure injection injuries, 624 opioid intoxication, 1027–1030 Injury. See also Caustic ingestion emergency; Trauma; Wound management ankle, 589–596 aortic (traumatic), 1102–1103 diving, 205–211, 210b arterial gas embolism, 205, 208
1206 INDEX Injury, (Continued) inner ear barotrauma, 207 elbow, 600–603 electrical, 212–215 foot, 604–608 forearm and wrist, 608–616 hand, 617–624 head or spinal cord, 1050–1056, 1054t, 1055t, 1067–1072, 1077, 1090–1095 adult v. child spinal cord, 1077 heat, 220–224 lightning, 234–237 lower leg, 638–642 pediatric, 642 maxillofacial and dental, 158–161 ophthalmologic, 161–168 blunt trauma to eye, 167–168 chemical injury to eye, 167 shoulder, 647–652 INR. See International normalized ratio Insecticides poisoning, 1130–1132 antidotal therapy, 1033 clinical presentation, 1131 SLUDGe mnemonic for, 1131 definition, 1130 emergency actions, 1130 epidemiology, 1131 key points, 1130 laboratory findings, 1033 pathology, 1131 treatment, 1033 Inspiratory positive airway pressure (IPAP), 848 Insulin /glucose, calcium channel blockers overdose treatment, 958–959 infusion diabetic ketoacidosis requiring, 347 hyperglycemic hyperosmolar nonketotic coma, 392–393 pediatric diabetes treatment, 773–774 pediatric trauma medication, 1080 Insulinoma, hypoglycemia from, 401 Intensive care unit (ICU), 271t adrenal insufficiency treatment, 337 beta-blocker overdose treatment, 954 calcium channel blockers overdose treatment, 959 diabetic ketoacidosis requiring, 347 exfoliative dermatitis requiring, 99 hyperglycemic hyperosmolar nonketotic coma, 393 shock, 917–920
Intensive care unit (ICU), (Continued) thoracic aortic dissection requiring, 26 Interferon (INF), 440 Intermittent mandatory ventilation (IMV), 847, 850 Internal hordeolum, 163 International normalized ratio (INR), 169 Intestinal obstruction, 18–22 clinical presentation, 20 CT scan for diagnosis of, 21 definition, 19 diagnosis based on examination and history, 21 emergency actions, 18 epidemiology, 19 examination, 20 key points, 18 laboratory findings, 20 treatment and outcome, 21 Intra-aortic balloon pump, cardiac chest pain treatment, 74 Intracellular shifts, hypokalemia, 362 Intracranial pressure (ICP) headache indicative of, 432 hematomas influencing, 1070–1071 Intubation asthma treatment requiring, 223 hymenoptera sting requiring, 233 patient with delirium requiring, 910–911 primary prosthetic valve failure requiring, 91 Invasive positive-pressure ventilation mechanical ventilation, 849–851 IPAP. See Inspiratory positive airway pressure Iron toxicity, 1007–1010 clinical presentation, 1008 definition, 1008 diagnosis, 1009 emergency actions, 1008 epidemiology, 1008 examination, 1008–1009 key points, 1007 laboratory findings, 1009 metabolic acidosis from, 1021 radiographs, 1009 treatment, 1009–1010 Irradiated blood products, as blood transfusion component, 562 Irrigation whole-bowel clonidine overdose treatment, 967–968 iron toxicity requiring, 1009–1010
Index Irrigation, (Continued) lead poisoning requiring, 1016 lithium poisoning treatment, 1019 theophylline toxicity, 1048 wound preparation requiring, 29–30 Irritable bowel syndrome, diverticulitis v., 126 Ischemia. See also Myocardial infarction diverticulitis v. colitis, 126 MRI of, 491f myocardial, 511 stroke syndromes, 476f, 488, 491f transient ischemic attacks, 469 zones of, 475f Isoniazid poisoning, anion gap from, 1021 Isopropanol toxicity, 1010–1013 clinical presentation, 1011–1012 definition, 1011 diagnosis, 1012 emergency actions, 1011 epidemiology, 1011 examination, 1012 key points, 1010 laboratory findings, 1012 radiographs, 1013 treatment, 1013 Isoproterenol, pediatric trauma medication, 1080 Isospora belli, infectious disease emergency, 269t Jaundice and hepatitis, 135–143, 137f, 138f, 139f clinical presentation and examination, 139–140 definitions of, 136 diagnosis, 142 epidemiology, 136–139, 137f, 138f, 139f key points, 135 laboratory findings, 140–141 radiographs, 141–142 treatment, 142–143 JCAHO. See Joint Commission on Accreditation of Healthcare Organizations Joint and bone infections, 631–637. See also Arthritis clinical presentation, 634 definitions osteomyelitis, 631 septic arthritis, 630, 632 emergency actions, 631 epidemiology, 632
1207
Joint and bone infections, (Continued) osteomyelitis, 632 septic arthritis, 632 imaging, 635–636 key points, 631 laboratory findings, 634–635 pathology osteomyelitis, 632–633 septic arthritis, 633 treatment osteomyelitis, 636 septic arthritis, 637 Joint Commission on Accreditation of Healthcare Organizations (JCAHO), pediatric analgesia and sedation, 806 Jones criteria for acute rheumatic fever, 775–777 Juvenile myoclonic epilepsy, treatment, 787 Kawasaki disease erythema multiforme v., 98 pediatric, 792–795 clinical presentation, 793–794 definition, 792–793 diagnosis, 794 epidemiology, 793 etiology, 793 key points, 792 laboratory findings, 794 treatment, 794–795 Kernig sign, neurological examination, 464–465 Ketamine airway management pretreatment, 914b anesthesia after wound examination, 28 intubated patient sedation, 911 pediatric analgesia and sedation, 812 Ketorolac tromethamine, headache treatment, 437–438 Ketosis, hyperglycemic hyperosmolar nonketotic coma v., 390–393 Kidneys. See also Acute renal failure; Endstage renal disease; Renal disease; Renal transplantation emergency acid-base problems involving, 314, 318 contusions/lacerations/ruptures, 1064 excretion and absorption function, 313 hypernatremia etiology involving, 359t nephrolithiasis, 1135–1138 transplant rejection, 1122–1123, 1158t, 1161t, 1163–1167 urinary tract infection influencing, 1146
1208 INDEX Knee pain emergencies, 583–588 definition, 583 emergency actions, 583 epidemiology, 583–584 key points, 583 laboratory findings, 587 physical examination, 584–586 radiographs, 586–587 RICE therapy for, 587–588 Kwashiorkor, hypoglycemia from, 401 Labetalol, hypertensive emergency treatment, 79–80 Lactate measurements, neonatal emergencies requiring, 668–669 Lactic acidosis, 410–413, 411t, 1020 definition, 410–412, 411t emergency actions, 410 epidemiology, 410 hypoxia causing, 410 key points, 410 summary, 413 treatment bicarbonate therapy in cardiopulmonary resuscitation, 412 bicarbonate therapy in septic shock, 413 wide anion gap from, 1021 Lactulose, hypernatremia etiology involving, 359t Lamotrigine, seizures and status epilepticus, 471t Laryngeal mask airway (LMA), 657 pediatric emergency use of, 674 Laryngoscope blades, airway equipment, 673–674, 915b Lavage diagnostic peritoneal, 1060–1061 gastric arsenic poisoning treatment, 946 iron toxicity requiring, 1009–1010 salicylates toxicity treatment, 1042 Lead poisoning, 1014–1016 clinical presentation, 1015 definition, 1014 diagnosis, 1015 emergency actions, 1014 epidemiology, 1014 key points, 1014 laboratory findings, 1015 pathophysiology, 1014–1015 radiographs, 1015–1016 treatment, 1016
Legg-Calvé-Perthes disease, 629 Leptospirosis, toxic shock syndrome v., 548 Lesions herpes, 278–279 treatment, 285 mass, headaches from, 434 LET local anesthetic, 28, 29 Lethargy, lithium poisoning causing, 1018–1019 Leukocytosis ARDS causing, 859–861 iron toxicity causing, 1009 Leukoreduced blood products, as blood transfusion component, 562 Levetiracetam, seizures and status epilepticus, 471t Levofloxacin, adult bacterial pneumonia, 867, 867t Levothyroxine, hypothyroidism and myxedema coma treatment, 408–409 Lewisite, anti-, 946 Lidocaine, 28, 29 airway management pretreatment, 914b pediatric trauma medication, 1080 toxicity of, 29, 29t toxicology emergencies requiring, 929 Liebermeister's sign, arterial gas embolism diagnostic, 208 Lightning injuries, 234–237 clinical presentation, 235 definition, 234–235 diagnosis, 236 emergency actions, 234 epidemiology, 235 examination, 235–236 key points, 234 laboratory findings, 236 radiographs, 237 treatment and outcome, 237 Listeria monocytogenes heart transplant infection, 95 pediatric infection, 707–708, 708t Lithiasis cholelithiasis, 9–14 nephrolithiasis, 511, 1135–1138 sialolithiasis, 175–176 Lithium battery, 83 Lithium poisoning, 1017–1019 clinical presentation, chronic intoxication, 1018 definition, 1017 diagnosis, 1018 emergency actions, 1017
Index Lithium poisoning, (Continued) hypernatremia etiology involving, 359t key points, 1017 laboratory findings, CNS symptoms v. serum levels, 1018 pathology, 1017–1018 treatment, 1019 Liver function test (LFT), 271t. See also Hepatic impairment; Hepatitis cardiac tamponade requiring, 62 caustic ingestion requiring, 963 diverticulitis requiring, 125 heart transplant complications requiring, 94 lightning injuries requiring, 236 neonatal emergencies requiring, 668–669 Reye's syndrome requiring, 797 toxicology emergencies requiring, 927–928 Liver transplantation emergencies, 1156–1162, 1158t, 1160t, 1161t. See also Hepatic impairment; Hepatitis clinical presentation, 1159 complications of, 1161t definition, 1156 diagnosis, 1160 epidemiology, 1157 examination, 1159 immunosuppressive medications for, 1158t indications for, 1158t key points, 1156 laboratory findings, 1159–1160 organ rejection, 1156–1162, 1158t, 1160t, 1161t radiographs, 1160–1161 surgical procedure of, 1157 treatment, 1161–1162, 1161t drug interactions, 1161t LMA. See Laryngeal mask airway Local analgesics, 808–809 Lorazepam intubated patient sedation, 909t, 910 pediatric status epilepticus treatment, 787 Lower leg injuries, 638–642 anatomy, 638–639 clinical presentation and examination, 639 definition, 638 emergency actions, 638 key points, 638 laboratory findings, 639 pediatric, 642 radiographs, 639
1209
Lower leg injuries, (Continued) treatment Achilles tendon rupture, 641 compartment syndrome, 641 fibular fractures, 640 medial head of gastrocnemius muscle injury, 641 stress fractures, 640–641 tibial fractures, 640, 642 Lumbar puncture ataxia/dizziness/vertigo requiring, 418 headaches from, 434 heart transplant complications requiring, 94 pediatric seizures and status epilepticus, 786 Lung transplantation complications, 1150, 1151, 1154 organ rejection, 1150, 1151, 1154 Lyme disease, multiple sclerosis v., 442 Lymphadenopathy, exfoliative dermatitis causing, 101 Lymphoma, exfoliative dermatitis from, 100, 100b Macrolide, adult bacterial pneumonia, 867, 867t Magill forceps, for upper airway clearing, 662 Magnesium. See also Hypermagnesemia asthma treatment, 860 fluid and electrolyte emergencies, 377–380 measurement for toxicology emergencies, 927 Magnetic resonance imaging (MRI) ataxia, dizziness, vertigo, 418, 422 cholelithiasis and cholecystitis requiring, 13 gadolinium contrast, 442 headache, 432 hemorrhage, 487f hyperdense cerebral artery sign, 489f intracerebral hemorrhage, 487f ischemia, 491f ovarian torsion, 535 pulmonary embolism, 902, 905t subarachnoid hemorrhage, 488f Malaria, 295–300, 298t–299t, 300t, 1028 clinical presentation, 296 definition, 295 diagnosis, 297 emergency actions, 295 epidemiology, 295–296
1210 INDEX Malaria, (Continued) examination, 296 key points, 295 laboratory findings, 296–297 opioid injection risk of, 1028 prevention, 298t–299t treatment, 297, 300t–301t Male mammary gland development (gynecomastia), exfoliative dermatitis causing, 101 Male sex organs epididymitis, 1124–1126 penis disorders, 1127–1130 clinical presentation, 1128 definition, 1127–1128 emergency actions, 1127 epidemiology, 1128 examination, 1128 key points, 1127 laboratory findings and radiographic findings, 1129 penile fracture, 1128 treatment and outcomes, 1129–1130 prostate gland exfoliative dermatitis of, 101 prostatitis, 1131–1134 testicular torsion, 1139–1141 testosterone, 336 Malignancy. See also Cancer; Oncologic and hematologic emergencies; Tumor diverticulitis v., 126 exfoliative dermatitis from, 100, 100b hypercalcemia from, 373 insulinoma, 401 malignant external otitis, 170 mesenchymal tumors, 401 Mannitol arsine gas intoxication requiring, 943 pediatric diabetic emergency requiring, 774 pediatric trauma medication, 1080 rhabdomyolysis treatment, 416–417 Marine fauna envenomations, 238–242 clinical presentation and examination, 239–240 definition, 238 emergency actions, 238 epidemiology, 238–239 key points, 238 pathology, 239 treatment, 240–241 8 hours observation, 242 infection risk, 240–241
Marine fauna envenomations, (Continued) radiographs for sponge envenomation, 241 saltwater v. freshwater, 242 steroids contraindicated, 241 vinegar, 241 Mass lesion, headaches from, 434 Mastitis, 502–504 clinical presentation, 503 definition, 502 emergency actions, 502 examination, 503 key points, 502 laboratory findings, 503 treatment, 504 ultrasound scanning, 503 Maxillofacial and dental emergencies dental, 154–158 trauma, 179–182 injuries, 158–161 ophthalmologic, 161–168 otolaryngological, 169–172 pharyngitis, 172–174 sialolithiasis, 175–176 sinusitis, 177–179 MBP. See Myelin basic protein MDI. See Metered dose inhaler MDMA. See Methylenedioxymethamphetamine Measles, toxic shock syndrome v., 548 Mechanical ventilation. See also Pulmonary emergencies asthma treatment, 223 disseminated intravascular coagulation, 348 emergency department basics for, 844–851 indications for, 844–845 types of, 845–851, 849t assist-control ventilation, 850 bilevel positive airway pressure, 848 continuous positive airway pressure as adjunct, 848 controlled mechanical ventilation, 850 expiratory positive airway pressure, 848 flow-cycle mode, 847 inspiratory positive airway pressure, 848 invasive positive-pressure ventilation, 849–851
Index Mechanical ventilation, (Continued) negative-pressure ventilation, 845–846 noninvasive positive-pressure ventilation, 847–848 positive-pressure ventilation, 91, 846–851 pressure support ventilation, 849–850, 849t pressure-cycled v. volume-cycled modes, 846–847, 849t Mechanical ventilator alarms, 882 complications, 882 monitoring, 877–881, 881t acronyms, 881t arterial blood gas, 877 equipment, 877 oxygenation, 877–878 patient positioning, 877 peak and plateau pressures, 878–881, 879t–880t PEEP and auto-PEEP, 846, 849t, 859–861, 881 ventilation, 878 settings, 872–876, 875t initiating, 872–875, 875t fraction of inspired oxygen, 873–874 inhalation/exhalation ratio, 874–875 positive end-expiratory pressure, 874 respiratory rate, 872–873 tidal volume, 849t, 873 special considerations, 875–876, 876t acute respiratory distress syndrome, 876 asthma exacerbation, 876 COPD exacerbation, 875–876 pregnancy, 876 Medical emergencies acid-base imbalances, 311–325 adrenal insufficiency, 331–338 alcoholic ketoacidosis, 338–343, 339f, 340f diabetic ketoacidosis, 343–347 disseminated intravascular coagulation, 348–350 ethyl alcohol withdrawal, 325–331 fluid and electrolyte, 351–393, 354t, 359t, 382t geriatric, 386–393 hyperthyroidism and thyroid storm, 394–398
1211
Medical emergencies, (Continued) hypoglycemia, 399–405 hypothyroidism and myxedema coma, 406–409 lactic acidosis, 410–414, 411t rhabdomyolysis, 414–417 seizures and status epilepticus, 465–472, 466t, 468t, 471t stroke syndromes, 473–496, 475f, 476f, 477f, 478f, 480f, 484t, 485t, 487f, 488f, 489f, 490f, 491f, 492f, 494t Medications hypoglycemia from, 403 multiple sclerosis v. toxicity from, 442 Meningitis, 706–713, 708t, 710t, 711t Bell's palsy v., 426–427, 426t definition of, 706, 707 erythema multiforme v., 98 heart transplant infection, 95 hypoglycemia from, 401 Neisseria meningitidis, pediatric infection, 707–708, 708t, 710t, 711t, 712–713 pediatric, 706–713, 708t, 710t, 711t Meningoencephalitis, stroke syndromes v., 484t Mental status hyperglycemic hyperosmolar nonketotic coma, 392–393 hypoglycemia, 404–405 lithium poisoning impairing, 1018–1019 monitoring of, for hypothyroidism and myxedema coma, 408–409 salicylates toxicity influencing, 1043 Meperidine hydrochloride, headache treatment, 437–438 Mercury poisoning, 1024–1026 clinical presentation, 1025 definition, 1023 diagnosis, 1025 emergency actions, 1023 epidemiology, 1023 key points, 1023 laboratory findings, 1025–1026 pathophysiology, 1024–1025 radiographic findings, 1026 treatment, 1026 Mesenchymal tumors, hypoglycemia from, 401 Mestinon, myasthenia gravis requiring, 450
1212 INDEX Metabolic acidosis, 315–317, 363, 1021, 1023. See also Anion gap alcoholic ketoacidosis causing, 1021 carbon monoxide poisoning causing, 1021 caustic ingestion causing, 964 clinical presentation and examination, 316 cyanide poisoning causing, 1021 definition, 315–316 epidemiology, 316 iron poisoning causing, 1021 isoniazid poisoning causing, 1021 laboratory findings, 317 methanol poisoning causing, 1021, 1023 MUDPILES mnemonic for causes of, 315 toluene poisoning causing, 1021 treatment and outcome, 317 uremia causing, 1021 Metabolic alkalosis, 311, 317–320 alkali administration, 318 clinical presentation, 318 contraction alkalosis, 318 definition, 317 epidemiology, 317–318 examination, 319 gastrointestinal Hþ loss, 318 intracellular shifts, 318 laboratory findings, 319 renal Hþ loss, 318 treatment, 319–320 saline-resistant alkalosis, 320 saline-responsive alkalosis, 319–320 Metabolic panel, iron toxicity requiring, 1008 Metered dose inhaler (MDI), 854 asthma treatment, 860, 862 Methanol poisoning, 1020–1023 clinical presentation, 1021 CT scan of head, 1022 definition, 1020 diagnosis, 1021 emergency actions, 1020 epidemiology, 1021 examination, 1021 key points, 1020 laboratory findings, 1021 treatment and outcome, 1022 Methemoglobinemia, caustic ingestion causing, 964 Methicillin-resistant Staphylococcus aureus (MRSA), 502
Methimazole, thyroid storm treatment, 397 Methohexital, airway management treatment, 915b Methotrexate, ectopic pregnancy treatment, 507–508 Methylenedioxymethamphetamine (MDMA), 353, 935–936 Methylprednisolone anaphylactic shock requiring, 921 multiple sclerosis treatment, 439 pediatric trauma medication, 1080 urticaria treatment, 112 Metoprolol, cardiac chest pain treatment, 74 MFAT. See Multifocal atrial tachycardia MG. See Myasthenia gravis MI. See Myocardial infarction Michaelis-Menton elimination (toxicology diagnostic), 924 Midazolam, intubated patient sedation, 909t, 910 Migraine headache, 431–432 stroke syndromes v., 484t treatment, 437–438 Miscarriage (abortion), 525–528 definition, 526 emergency actions, 525 epidemiology, 526 etiology, 526–527 examination, 527 key points, 525 laboratory findings, 527 treatment, 527–528 ultrasound scan, 527 Mitral valve prolapse (MVP) clinical presentation, 81 definition of, 80 diagnosis, 81 epidemiology, 80–81 key points, 80 laboratory and ancillary findings, 82 pathology, 81 physical examination, 81 treatment, 82 Mittelschmerz, 510 Molar pregnancy, 510 MONA. See Morphine-oxygennitroglycerin-aspirin Morphine caution for, 75 congestive heart failure treatment, 66–67 hydromorphone, 907t, 908 intubated patient analgesia, 906, 907t morphine-oxygen-nitroglycerin-aspirin, 73
Index Morphine, (Continued) pediatric trauma medication, 1080 tetralogy of Fallot requiring, 779 Morphine-oxygen-nitroglycerin-aspirin (MONA), cardiac chest pain treatment, 73 Motor examination, 455–456, 456t Mountain sickness, 184t, 185, 187t, 191 MRI. See Magnetic resonance imaging MRSA. See Methicillin-resistant Staphylococcus aureus MS. See Multiple sclerosis MUDPILES mnemonic, for causes of metabolic acidosis, 315 Multifocal atrial tachycardia (MFAT), 48–49, 48f Multiple myeloma, multiple sclerosis v., 442 Multiple sclerosis (MS), 438–447 Bell's palsy v., 426–427, 426t clinical presentation, 441 definition, 439 diagnosis and laboratory findings, 442–443 disseminated encephalomyelitis v., 442 emergency actions, 439 epidemiology, 439 examination, 441 key points, 438 myelin basic protein, 440 pathology, 439–440 relapsing-remitting, 443–444 risk factors, 440–441 treatment, 443–446 methylprednisolone, 439 Multiple trauma. See also Injury; Trauma challenges to treatment of, 1056 coma, Glasgow Coma Scale for, 1054, 1054t computed tomography for, 1052 focused abdominal sonography for, 1052 fractures, 1056 pregnant patient with, 1056 Multiple trauma requiring, blood transfusion for, 1055, 1055t Murphy's sign, 12 Musculoskeletal disorder, 511 MVP. See Mitral valve prolapse Myasthenia gravis (MG), 447–450 acetylcholine receptor site blockage, 447 Bell's palsy v., 426, 426t botulism v., 430 clinical presentation, 448–449 definition, 447
1213
Myasthenia gravis (MG), (Continued) diagnosis, 449–450 Tensilon test for, 449 emergency action, 447 epidemiology, 447 examination, 449 key points, 447 pathology, 448 treatment, 450 Mycoplasma species, chronic obstructive pulmonary disease from, 884 Myelin basic protein (MBP), 440 Myocardial infarction (MI). See also Ischemia clonidine overdose causing, 967–968 geriatric emergency, 388 shock, 920 zones of cerebral infarction and ischemia, 475f Myxedema coma, 406–409 Naloxone clonidine poisoning treatment, 965 opioid intoxication, 1030 pediatric analgesia and sedation reversal, 812–813 pharmacological shock requiring, 921 phenytoin toxicity treatment, 1037 Narcissistic personality disorder, 833–835 clinical presentation, 834 definition, 834 diagnosis, 834 epidemiology, 834 key points, 833 treatment and outcome, 834–835 Narcotics anesthesia after wound examination, 28 pharmacological shock from, 921 Nasogastric tube, intestinal obstruction requiring, 21 Nasopharyngeal airway device, airway equipment, 673–674 National Heart, Lung, and Blood Institute, pulmonary embolism epidemiology, 898 National Institute of Child Health and Human Development (NICHD), SIDS prevention, 766–769 National Institutes of Health (NIH) stroke severity scale, 485t Necrosis. See also Caustic ingestion emergency acute tubular, 1114 avascular, 612–614
1214 INDEX Necrosis, (Continued) femoral, 511 toxic epidermal necrolysis from burns, 103–106 ACLS for, 103 Negative-pressure ventilation, 845–846 Neisseria gonorrhoeae, epididymitis from, 1124–1126 Neisseria meningitidis, pediatric infection, 707–708, 708t Neomycin, otitis externa treatment, 170 Neonatal emergencies. See also Pediatric emergencies antibiotic dosages for, 666t clinical presentation, 665–667 definition, 665 emergency actions, 664–665 examination, 667 key points, 664 laboratory findings, 668–669 patent ductus arteriosus, 666–667 treatment, 669 vital signs, 667–668 Neonate. See also Neonatal emergencies definition of, 657 Neoplasm, 510 Nephrolithiasis, 511, 1135–1138. See also Kidneys; Renal disease Nesiritide, congestive heart failure treatment, 66–67 Neurological emergencies ataxia, dizziness, vertigo, 418–423 Bell's palsy, 423–428 botulism, 428–431 examination, 451–465, 451t, 452t, 454t, 456t, 458f, 459f, 463t headaches, 432–438 multiple sclerosis, 438–447 myasthenia gravis, 447–450 Neurological examination anatomical considerations, 452–453, 452t central nervous system anatomy and function, 452t Brudzinski sign, 464–465 cerebellar examination, 464 cerebellar ataxia, 464 dysmetria, 464 point-to-point test, 464 Romberg test, 464 cranial nerve examination, 456–462, 458f, 459f CN I (olfactory), 456 CN II (optic), 456
Neurological examination, (Continued) CN III, IV, VI (oculomotor, trochlear, abducens), 457–458, 458f functional layout of extraocular movements and innervations, 458f CN IX, X (glossopharyngeal and vagus), 461 CN V (trigeminal), 459–460, 459f sensory nerve branch divisions, 459f CN VII (facial), 460–461 CN VIII (vestibulocochlear), 461 CN XI (spinous accessory), 461–462 CN XII (hypoglossal), 462 deep tendon reflexes, 462–464, 463t scale for grading of, 463t global assessment, 453 Glasgow Coma Scale, 453, 454t indications for, 451, 451t Kernig sign, 464–465 motor examination, 455–456, 456t pediatric trauma, 1075–1077, 1076t adult v. child spinal cord, 1077 CT scan, 1077 head injury, 1076–1077 modified Glasgow Coma Scale, 1076t sensory function examination, 454–455 pain sensation, 455 vibration sense, 454–455 Neurologist consultation, head or spinal cord injury requiring, 1055 NHANES III. See Third National Health and Nutrition Examination Survey NICHD. See National Institute of Child Health and Human Development Nifedipine, hypertensive emergency treatment, 79–80 Nitrates, congestive heart failure treatment, 66–67 Nitrofurantoin, urinary tract infection treatment, 1145t Nitrogen narcosis, diving injury, 205 Nitroglycerin caution for, 75 congestive heart failure treatment, 66–67 headaches from, 434 Nitroprusside, congestive heart failure treatment, 66–67 Nocardia, heart transplant infection, 95 Noninvasive positive-pressure ventilation mechanical ventilation, 847–848
Index Nonpharmacological anxiolysis, pediatric analgesia and sedation, 807 Nonsteroidal anti-inflammatory drugs (NSAIDS), headache treatment, 114, 437–438 Norepinephrine. See also Epinephrine beta-blocker overdose treatment, 954 North American Society of Pacing and Electrophysiology, pacemaker circuitry types, 84, 85t Norwalk/Norwalk-like viruses, infectious disease emergency, 268t Nose bleed, 171–172 NSAIDS. See Nonsteroidal antiinflammatory drugs Oatmeal baths, toxicodendron dermatitis treatment, 108–109 Obesity, pulmonary embolism risk factor, 899 OB/GYN. See Obstetrics and gynecology Obsessive-compulsive personality disorder, 838–839 clinical presentation, 838 definition, 838 diagnosis, 839 epidemiology, 838 examination, 838 key points, 838 treatment and outcome, 839 Obstetrics and gynecology (OB/GYN). See also Female sex organs; Pregnancy abruptio placentae, 497–499, 510, 1108 amniotic fluid embolism, 500–502 breast abscesses and mastitis, 502–504 ectopic pregnancy, 505–509 emergent pelvic and abdominal pain, 509–512 fetal distress, 498 genital herpes, 279, 285, 513–515 hyperemesis gravidarum, 515–518 miscarriage (abortion), 525–528 ovarian cysts, 529–532 pelvic inflammatory disease, 536–540 placenta previa, 540–542 Obstructive sleep apnea, high-altitudeexacerbated illness, 184t Occult bacteremia, 707. See also Bacteremia Ocular herpes simplex virus, 275–276, 279, 285 Oculomotor nerve examination, 457–458, 458f Ogilvie's syndrome, 19
1215
Olfactory sense, cranial nerve examination, 456 Oncologic and hematologic emergencies. See also Cancer; Malignancy; Tumor acute bleeding diathesis, 555–558 blood transfusions, 559–565 hemophilia, 566–569 sickle cell anemia, 570–574 Operating room (OR), open fractures, 646 Ophthalmologic emergencies, 161–168. See also Eye clinical presentation, 162 definition, 162 diagnosis based on eye examination, 63 epidemiology, 162 examination, 162–163 key points, 162 ocular herpes simplex virus, 275–276, 279, 285 radiographs, 63 treatment, 163–168 blowout fractures, 168 blunt trauma, 167–168 cellulitis, 164 chemical injury, 167 conjunctivitis, 164 corneal abrasions, 166–167 corneal foreign bodies, 167 corneal ulcers, 164 glaucoma, 164–165 herpes keratitis, 164 hyphema, 168 ruptured globe, 168 subconjunctival hemorrhage, 167 ultraviolet keratitis, 167 vision loss (painless), 165 central retinal artery or vein occlusion, 165 detached retina, 166 giant cell arteritis, 166 optic neuritis, 166 temporal arteritis, 166 vitreous hemorrhage, 165–166 Opioids as analgesic for pulmonary embolism, 903 intoxication, 1027–1030 clinical presentation, 1028–1029 clonidine overdose mimicking, 967–968 definition, 1027 diagnosis, 1030 emergency actions, 1027
1216 INDEX Opioids, (Continued) epidemiology, 1028 examination, 1029 history taking, 1029 HIV/malaria/tetanus infection risk with, 1028 injection drug use complications with, 1028 key points, 1027 laboratory findings, 1029 pathology, 1028 treatment and disposition, 1030 Optic nerve. See also Eye; Ophthalmologic emergencies examination of, 456 neuritis emergency, 166 OR. See Operating room Oral contraceptives. See also Pregnancy headaches from, 434 pulmonary embolism risk factor, 899 Oral rehydration therapy (ORT), pediatric dehydration requiring, 694, 695, 697–699 Orbital cellulitis, 164 Organ rejection. See also Transplantation emergencies cardiac, 93–96, 1150, 1151, 1154 liver, 1156–1162, 1158t, 1160t, 1161t lung, 1150, 1151, 1154 renal, 1122–1123, 1158t, 1161t, 1163–1167 Organophosphorus and carbamate insecticides poisoning, 1130–1132 Oropharyngeal airway device, 673–674 Orthopedic emergencies acute compartment syndrome, 596–599 ankle injuries, 589–596 back pain, 577–582, 581t elbow injuries, 600–603 foot injuries, 604–608 forearm and wrist injuries, 608–616 hand injuries, 617–624 hip trauma, 625–630 infections of bones and joints, 631–637 knee pain, 583–588 lower leg injuries, 638–642 principles of, 575–577 examination, 576–577 shoulder injuries, 647–652 Osgood-Schlatter disease, pediatric lower leg injury, 642 Osteomyelitis, 631, 632–633, 636 definitions, 631
Osteomyelitis, (Continued) epidemiology, 632 pathology, 632–633 treatment, 636 Otitis externa, 170 Otitis media, 169–170, 798–802 barotrauma causing, 207 pediatric emergency, 798–802 clinical presentation, 800 complications of, 802 definition, 169–170, 799 diagnosis, 800 emergency actions, 798 epidemiology, 799 etiology, 799–800 examination, 800 key points, 798 laboratory findings, 800 treatment, 800–802 American Academy of Pediatrics guidelines on, 801 Otolaryngological emergencies, 169–172 definitions epistaxis, 171–172 hearing loss (sudden), 170–171 malignant external otitis, 170 otitis externa, 170 otitis media, 169–170, 798–802 emergency actions, 169 key points, 169 for diabetic patients, 169 laboratory findings, 172 radiographs, 172 Ovaries. See also Female sex organs abscess, 510 cysts, 510, 529–532 clinical presentation and examination, 530–531 definition, 529 diagnosis, 531 emergency actions, 529 key points, 529 laboratory findings, 531 pathophysiology, 529–530 treatment, 531–532 torsion, 532–535 clinical presentation, 533 definition, 532 diagnosis, 534 epidemiology, 533 examination, 533–534 key points, 532 laboratory findings, 534
Index Ovaries, (Continued) magnetic resonance imagining and CT scanning, 535 radiographs, 534–535 treatment, 535 Overdose. See Caustic ingestion emergency; Toxicology emergencies Oxygen carbon monoxide poisoning treatment, 960 saturation monitoring for pediatric airway compromise, 672 supplemental adrenal insufficiency treatment, 336 hyperglycemic hyperosmolar nonketotic coma, 392 iron toxicity requiring, 1009 mercury poisoning treatment, 1026 methanol poisoning treatment, 1022 monitoring of, during mechanical ventilation, 877–878 pneumothorax treatment, 894 pulmonary embolism treatment, 903 seizures and status epilepticus, 786 tetralogy of Fallot requiring, 779 toxicity, diving injury causing, 205 Pacemakers complications, 83–84, 85t chest radiograph identification, 84, 85t, 87 circuitry, 84, 85t clinical observation, 84, 86 definition, 83–84, 85t electrocardiography for, 86–87 emergency actions, 83 epidemiology, 84 examination, 86 five-letter pacemaker code, 84, 85t key points, 83 magnet rate, 84 treatment, 87–88 acute intervention, 88 types of, 84, 86–87 North American Society of Pacing and Electrophysiology circuitry types, 84, 85t permanent, 86–87 Packed red blood cells, as blood transfusion component, 560 PACs tachycardia. See Premature atrial contractions tachycardia Pain abdominal, 389, 509–512, 731–735
1217
Pain, (Continued) CT scan for, 512 geriatric, 389 abortion (miscarriage), 510 abruptio placentae, 510 abscess, ovarian, 510 adnexal torsion, 510 appendicitis, 510 arteriography, knee pain emergency requiring, 587 aspirin for, 74 back, 577–582, 581t cardiac chest, 74 chest evaluation of, 68–75, 71f, 72f fibrinolysis for, 74 morphine-oxygen-nitroglycerinaspirin for, 73 colitis, 510 diverticulitis, 510 dysmenorrhea, 510 endometriosis, 510 knee emergencies, 583–588 RICE therapy for, 587–588 molar pregnancy, 510 musculoskeletal disorder, 511 neoplasm, 510 nephrolithiasis, 511 obstetric and gynecological, 509–512 orthopedic emergencies, 577–582, 581t ovarian cysts, 510 pancreatitis, 511 pediatric abdominal, 731–735 patient's underestimation of pain, 806 pelvic, 731–735, 806 pelvic, 509–512, 731–735, 806 pelvic inflammatory disease, 510 pulmonary embolism, 511 pyelonephritis, 511 sensory function examination, 455 sickle cell anemia, 510 Pancreatitis, 144–148, 511 clinical presentation, 145–146 definition, 144 diagnosis, 147 epidemiology, 144–145 examination, 146 infectious agents, 145 key points, 144 laboratory findings, 146 medical treatment, 145 radiographs, 147 Reye's syndrome causing, 797
1218 INDEX Pancreatitis, (Continued) treatment and outcome, 147–148 Pancuronium, intubated patient sedation, 912 Panic disorder, 814–816. See also Generalized anxiety disorder asthma mimicked by, 857 clinical presentation, 816 definition, 814, 815–816 diagnosis, 816 emergency actions, 814 epidemiology, 814 examination, 816 key points, 814 laboratory findings, 816 radiographs, 816 treatment, 816 Paraldehyde poisoning, anion gap from, 1020 Paralytic shellfish poisoning, infectious disease emergency, 271t Paranoid personality disorder, 823–824 diagnosis/treatment/outcome, 824 epidemiology, 824 key points, 823 Paraphimosis, 1127–1128 Parathyroidism, 371 Parkland formula for burn treatment, 196, 196b Parotid tumor, Bell's palsy v., 426–427, 426t Paroxetine, panic disorder treatment, 816 Partial thromboplastin time (PTT) diabetic patient with otolaryngological emergency, 169 disseminated intravascular coagulation emergency, 350 iron toxicity requiring, 1009 pneumothorax diagnosis, 893 Patent ductus arteriosus (PDA), 666–667 PCI. See Percutaneous coronary intervention PCR. See Polymerase chain reaction PDA. See Patent ductus arteriosus PE. See Pulmonary embolism Peak expiratory flow rate (PEFR), 858, 859, 861–862 Pediatric analgesia and sedation, 805–813 definition complications, 807 equipment, 806–807 fasting/aspiration risk, 806 Joint Commission on Accreditation of Healthcare Organizations, 806
Pediatric analgesia and sedation, (Continued) monitoring, 807 qualified personnel, 807 subjectivity and underestimation of pain, 806 local, 808–809 local analgesics, 808–809 nonpharmacological anxiolysis, 807 reversal agents, 812–813 systemic, 809–812 analgesics, 811–812 combined analgesia and sedation, 812 sedatives, 809–811 topical analgesics, 808 Pediatric bacteremia, sepsis, and meningitis, 706–713, 708t, 710t, 711t clinical presentation, 708–709 definitions, 706–707 emergency actions, 706 epidemiology, 707–708 examination, 709 Haemophilus influenzae type b, 708, 708t, 712–713 key points, 706 laboratory findings, 710, 710t treatment meningitis, 711t, 712–713 occult bacteremia, 710–712, 711t sepsis, 711t, 712 Pediatric emergencies. See also Neonatal emergencies abdominal pain, 731–735 airway management, 670–678, 1073–1075, 1074t analgesia and sedation for, 805–813 approach to, 652–654 asthma, 714–724, 717t–719t bacteremia, sepsis, and meningitis, 706–713, 708t, 710t, 711t bronchiolitis, 725–728 cardiopulmonary arrest, 655–660 cardiopulmonary resuscitation, 656–664 child abuse, 758–765, 762f, 763f constipation, 736–740 CPR, 656, 657–659, 660, 661–664 dehydration, 694–699 diabetes and diabetic ketoacidosis, 770–774 diarrhea, 740–745 electrolyte and fluid management, 700–705
Index Pediatric emergencies, (Continued) Hirschsprung's disease (congenital aganglionic megacolon), 745–748, 748f Kawasaki disease, 792–795 neonatal, 664–669 otitis media, 798–802 overview of child development, 652 pharyngotonsillitis, 802–805 pneumonia, 728–731 pyloric stenosis, 749–753, 751f, 752f questions to ask, 653 Reye's syndrome, 795–798 rheumatic fever, 774–778 seizures and status epilepticus, 783–788 sudden death syndrome and lifethreatening event syndrome, 765–769 tetralogy of Fallot, 778–782, 781f, 782f trauma, 629, 1073–1080, 1074t, 1076t, 1079t, 1080t abdomen evaluation, 1078 airway management for, 1073–1075, 1074t blood pressure, 1074t cardiovascular management, 1075 chest evaluation, 1078 endotracheal tube size v. age, 1074t evaluation and stabilization, 1078–1079, 1079t vital signs, 1079t fluid resuscitation, 1074t hip dislocation, 629 induction and intubation, 1079, 1079t, 1080t countershocks, 1079t medications, 1080t neurological evaluation, 1075–1077, 1076t adult v. child spinal cord, 1077 CT scan, 1077 head injury, 1076–1077 modified Glasgow Coma Scale, 1076t renal perfusion assessment, 1075 upper respiratory, 678–692 urinary tract infections, 753–757, 757t PEEP. See Positive end-expiratory pressure PEFR. See Peak expiratory flow rate Pelvic inflammatory disease (PID), 510, 536–540. See also Pelvis clinical presentation, 537–538 definition, 536
1219
Pelvic inflammatory disease (PID), (Continued) diagnosis, 538 emergency actions, 536 epidemiology, 536 key points, 536 laboratory findings, 538 pathology, 537 treatment, 538–539 inpatient therapy, 539 outpatient therapy, 539–540 Pelvis. See also Pelvic inflammatory disease anatomy of, 1081–1082 pain in, 509–512, 731–735, 806 clinical presentation, 511 definitions, 510–511 diagnosis, 512 emergency actions, 509–510 examination, 511 key points, 509 laboratory findings, 512 pediatric, 731–735, 806 ultrasound scanning, 512 pelvic inflammatory disease, 536–540 trauma to, 1081–1089 associated injuries, 1083 clinical diagnosis and presentation type I fractures, 1083–1085 type II fractures, 1085 type III fractures, 1085–1086 type IV fractures, 1086 definition and epidemiology, 1081 emergency actions, 1081 examination, 1087 key points, 1081 laboratory studies, 1088 mechanisms of injury, 1082–1083 radiographs, 1088 treatment, 1088–1189 Penicillin benzathine, as rheumatic fever treatment, 777 marine fauna envenomation requiring, 240–241 vasogenic shock requiring, 921 Penis disorders, 1127–1130. See also Male sex organs clinical presentation, 1128 definition, 1127–1128 emergency actions, 1127 epidemiology, 1128 examination, 1128 key points, 1127
1220 INDEX Penis disorders, (Continued) laboratory findings and radiographic findings, 1129 treatment and outcomes, 1129–1130 Peptic ulcer disease, 149–152 clinical presentation, 150 definition, 149 epidemiology, 150 examination, 150–151 key points, 149 laboratory findings, 151 radiographs, 152 treatment, 152 Percutaneous coronary intervention (PCI), cardiac chest pain treatment, 74 Pericarditis, acute, 37 clinical presentation, 38 diagnosis, 39 electrocardiographic findings, 38–39 emergency actions, 37 epidemiology, 37–38 examination, 38 key points, 37 laboratory findings, 39 radiographs, 39 treatment, 39 Peripheral nervous system anatomy and function, 452–453 edema of, as high-altitude-related illness, 184t Personality disorders, 822–839, 822t. See also Psychiatric emergencies classifications of, 822t definition, 822–823 treatment and outcome, 823 types of, 823–839 Peyronie's disease, 1127–1130 Pharyngitis, 172–174 acute pediatric rheumatic fever, 774–778 altitude-related emergencies, 190 definition, 172 diagnosis, 173 Centor criteria, 173 epidemiology, 172–173 group A beta-hemolytic streptococci causing, 173, 174 laboratory findings, 173 treatment, 174 Pharyngotonsillitis, 802–805 clinical presentation, 803–804 definition, 802 diagnosis, 804 emergency actions, 802
Pharyngotonsillitis, (Continued) epidemiology, 802 key points, 802 laboratory findings, 804 physical examination, 804 treatment, 804–805 Phenformin, wide anion gap from, 1021 Phenobarbital activated charcoal for overdose of, 951 pediatric status epilepticus treatment, 787 seizures and status epilepticus, 471t Phenylephrine, beta-blocker overdose treatment, 954 Phenytoin pediatric seizures and status epilepticus, 786 seizures and status epilepticus, 471t toxicity, 1034–1037 clinical presentation, 1035–1036 definition, 1034 diagnosis, 1036 emergency actions, 1034 epidemiology, 1034 key points, 1034 laboratory studies, 1036 pathophysiology, 1034–1035 pharmacokinetics, 1035 treatment, 1036–1037 Phimosis, 1127–1128 Phosphorus, fluid and electrolyte emergencies, 380–383. See also Hyperphosphatemia; Hypophosphatemia Physostigmine, anticholinesterase inhibitor, 942 PID. See Pelvic inflammatory disease Pilonidal disease clinical presentation, 117 cysts, 118 definition, 114 epidemiology, 115 pathology, 116 treatment and outcomes, 120 Placenta previa, 510, 540–542. See also Pregnancy definition, 541 diagnosis, 541–542 emergency actions, 540 epidemiology, 541 key points, 540 laboratory findings, 542 presentation, 541 radiographs, 542 treatment, 542
Index Platelets, as blood transfusion component, 560–561 Plavix, 169 international normalized ratio for, 169 Pneumocystis carinii pneumonia, heart transplant infection, 95 Pneumonia, 510; See also specific pathogens aspiration, 868–870 clinical presentation, 869 definition, 868 diagnosis, 870 epidemiology, 868 laboratory findings, 869 physical examination, 869 radiographs, 869 treatment, 870 bacterial, 863–867, 867t antibiotic therapy, 867, 867t asthma mimicked by, 857 clinical presentation, 865 community-acquired, 863, 864 definitions, 864 diagnosis, 865 disposition, 866–867 emergency actions, 863 epidemiology, 864 geriatric, 388 hospital-acquired, 863 key points, 863 laboratory findings, 866 pathophysiology, 864–865 Diplococcus pneumoniae, 884 pediatric, 728–731 clinical presentation, 729 definition, 729 diagnosis/treatment, 730–731 documentation by chest radiograph, 731 emergency actions, 728 epidemiology, 729 examination, 729–730 key points, 728 laboratory findings, 730 pneumocystis carinii, heart transplant infection, 95 respiratory acidosis from, 321 Streptococcus pneumoniae eye infection from, 164 pediatric infection, 707–708, 708t Pneumothorax, 891–896, 894f clinical presentation, 893 definition, 892 diagnosis, 893, 894f disposition, 896
1221
Pneumothorax, (Continued) emergency action, 892 iatrogenic, 892 key points, 891 laboratory findings, 893 radiograph, 893 spontaneous, 892 tension, 892 treatment goals, 894–896 catheter/needle aspiration, 895–896 tube thoracostomy, 895–896 Point-to-point test (cerebellar examination), 464 Poison ivy/poison oak, toxicodendron dermatitis, 106 Polymerase chain reaction (PCR), 271t Polymyxin B-hydrocortisone, otitis externa treatment, 170 POPS. See Pulmonary overpressurization syndrome Porphyria, arsenic poisoning v., 946 Positive end-expiratory pressure (PEEP), 846, 849t, 881 ARDS treatment, 859–861 ventilator setting, 874 Positive-pressure ventilation, 846–851 primary prosthetic valve failure requiring, 91 Postictal Todd's paralysis, stroke syndromes v., 484t Postmortem cesarean section, 1111 Potassium fluid and electrolyte emergencies, 361–369 hyperglycemic hyperosmolar nonketotic coma treatment, 392–393 intracellular shifts in, 362 pediatric diabetes treatment, 773–774 replacement of, diabetic ketoacidosis requiring, 347 Pralidoxime, insecticides poisoning antidote, 1033 Prednisone myasthenia gravis requiring, 450 toxicodendron dermatitis treatment, 108–109 Preeclampsia and eclampsia, 510, 519–525. See also Pregnancy HELLP syndrome, 523 hypoglycemic emergency with, 401 treatment, 522–523
1222 INDEX Pregnancy. See also Abortion (miscarriage); Obstetrics and gynecology; Oral contraceptives abruptio placentae, 497–499, 510, 1108 amniotic fluid embolism, 500–502 fetal distress, 498 hyperemesis gravidarum, 515–518 hypertension, 521 hypoglycemic emergency with, 401 mechanical ventilation during, 876 miscarriage, 525–528 multiple trauma during, 1056 physiology of, 1106–1108 placenta previa, 510, 540–542 preeclampsia and eclampsia, 401, 510, 519–525 preterm labor, 510 prevention of, post sexual assault, 545 traumatic injury during, 1105–1111 clinical presentation, 1109 definition, 1105 emergency actions, 1105 epidemiology, 1106 examination and treatment, 1109–1110 fetal distress, 1108 key points, 1105 laboratory findings, 1110 maternal-fetal hemorrhage, 1108–1109 placental abruption, 1108 postmortem cesarean section, 1111 radiographs, 1110–1111 urinary tract infection during, 1145–1146, 1145t Pregnancy test, diverticulitis requiring, 125 Premature atrial contractions (PACs) tachycardia, 46, 46f Premature ventricular contractions (PVCs) tachycardia, 46, 47f Pressure support ventilation (PSV), 849–851, 849t Preterm labor, 510 Priapism, 1127–1128 Primidone, seizures and status epilepticus, 471t Prochlorperazine, headache treatment, 437–438 Proctalgia fugax, 114–115 Propofol, intubated patient sedation, 909t, 910 Propranolol, thyroid storm treatment, 398
Prostate gland. See also Male sex organs exfoliative dermatitis causing enlargement of, 101 prostatitis, 1131–1134 clinical presentation, 1132 definition, 1131 diagnosis, 1132–1133 emergency actions, 1131 epidemiology, 1131 examination, 1132 key points, 1131 laboratory findings, 1132 pathology, 1132 radiographs, 1133 treatment, 1133–1134 Prosthetic heart valve dysfunction, 89–92, 91b clinical presentation, 90 definition, 89–90 diagnosis, 90–91, 91b epidemiology, 90 examination, 90 laboratory findings, 90 radiographs for, 91 treatment, 91–92 Prothrombin time (PT) measurement, 350. See also Embolism iron toxicity requiring, 1009 pulmonary embolism diagnostic, 901 salicylates toxicity, 1041 shock diagnostic, 919 Pruritus ani clinical presentation, 117 definition, 115 examination, 119 pathology, 116 treatment and outcomes, 120–121 Pseudoaneurysm, 1 Pseudohyperkalemia, 366 Pseudohypoparathyroidism, 371 Pseudotumor cerebri, headaches from, 434, 435 PSV. See Pressure support ventilation Psychiatric emergencies, 814–844. See also Suicide American Psychiatric Association, 815 conversion disorder, 819–821 generalized anxiety disorder, 817–819 geriatric, 389 panic disorder, 814–816 personality disorders, 822–839, 822t antisocial personality disorder, 828–829
Index Psychiatric emergencies, (Continued) avoidant personality disorder, 835–836 borderline personality disorder, 830–831 dependent personality disorder, 836–838 histrionic personality disorder, 832–833 narcissistic personality disorder, 833–835 obsessive-compulsive personality disorder, 838–839 paranoid personality disorder, 823–824 schizoid personality disorder, 825–826 schizotypal personality disorder, 826–828 suicide, 840–843 PT. See Prothrombin time PTT. See Partial thromboplastin time Pulmonary edema, 184t, 186, 187t beta-blocker overdose diagnostic, 954 treatment, 189–190 Pulmonary embolism (PE), 897–905, 904f, 905t cardiac arrhythmia from, 56, 56f clinical presentation, 898–899 definition, 898 diagnosis, 902–903 likelihood ratio, 905t stepwise approach to, 903, 904f emergency actions, 897–898 epidemiology, 898 key points, 897 laboratory findings, D-Dimer testing, 901, 905t National Heart, Lung, and Blood Institute on, 898 pelvic and abdominal pain from, 511 risk factors, 899–901 clinical gestalt, 899 Geneva criteria, 900–901, 900t laboratory findings, 901 arterial blood gas analysis, 901 ELISA and immuno-turbidimetric assays, 902 prothrombin time/activated PTT, 901 radiographs, 902 Wells criteria, 899–900, 900t tachycardia from, 899 treatment, 903, 905
1223
Pulmonary emergencies, 844–913. See also Mechanical ventilation acute respiratory distress syndrome, 852–854 asthma, 854–862 chronic obstructive pulmonary disease, 883–887 hemoptysis, 888–891 pneumothorax, 891–896, 894f pulmonary embolism, 897–905 905t, 904f pulmonary overpressurization syndrome, 206 sedation and analgesia for intubated patient, 906–913 ventilator management in ED, 844–851 Pulmonary overpressurization syndrome (POPS), 206 Pulmonary wedge pressure, ARDS influencing, 853 Pulse generator, 83 PVCs tachycardia. See Premature ventricular contractions Pyelonephritis, 511 urinary tract infection with, 1146 Pyloric stenosis, pediatric, 749–753, 751f, 752f clinical presentation, 750 definition, 749 diagnosis, 751 emergency actions, 749 epidemiology, 749–750 examination, 750 key points, 749 laboratory findings, 751 radiographs, 751–752, 751f, 752f “should sign” created by barium collection, 752f sonogram, 751f QRS voltage on electrocardiogram, heart transplant rejection causing, 95 Rabies viral infection, 301–306 clinical presentation, 302–303 definitions, 301 diagnosis, 304 emergency actions, 301 epidemiology, 301–302 examination, 303 key points, 301 laboratory findings, 303 pathology, 302
1224 INDEX Rabies viral infection, (Continued) quarantine, 304–305 radiographs, 304 treatment and outcomes, 304 Racemic epinephrine, pediatric trauma medication, 1080 Radiation, hypercalcemia requiring, 377 Radiopaque markers, permanent pacemaker, 84 Rapid sequence intubation (RSI), 672, 674–677. See also Airway management Rapid ventricular response (RVR), 49 Rectal prolapse clinical presentation, 117 definition, 115 examination, 118 pathology, 116 treatment, 120 Red blood cells bilirubin formation from, 136 as blood transfusion component, 560 Red eye, 164 RED MAN mnemonic, exfoliative dermatitis pathology identification, 100, 100b Rehydration adrenal insufficiency treatment, 337 appendicitis requiring, 8 hernia requiring, 18 salicylates toxicity treatment, 1042 Relapsing-remitting multiple sclerosis (RRMS), 443–444 Renal disease. See also Acute renal failure; Kidneys; Renal stones; Renal transplantation emergency end-stage renal disease, 1117–1123 hypoglycemia from, 402 rhabdomyolysis from, 414–417 Renal failure, 1113–1117. See also Endstage renal disease; Kidneys anti-inflammatory drugs causing, 1114 caustic ingestion causing, 964 clinical presentation, 1115 acute tubular necrosis, 1114 definition, 1113 diagnosis, 1116 emergency actions, 1113 glomerular filtration rate, 1113–1117 key points, 1113 laboratory findings, 1116 lithium poisoning causing, 1018–1019 pathology, 1113–1115 physical examination, 1115
Renal failure, (Continued) radiography, 1115 treatment, 1116–1117 Renal stones, 1135–1138. See also Renal disease clinical presentation, 1136 definition, 1135 diagnosis, 1137 emergency actions, 1135 epidemiology, 1135–1136 examination, 1136–1137 HIV-infected patients with, 1135, 1137 key points, 1135 laboratory findings, 1137 radiographs, 1137 Renal transplantation emergency, 1122–1123, 1158t, 1160t, 1161t, 1163–1167. See also End-stage renal disease; Kidneys clinical presentation, 1164–1165 definition, 1163 diagnosis, 1166 emergency actions, 1163 epidemiology, 1164 examination, 1165 immunosuppressive medications for, 1158t key points, 1163 laboratory findings, 1165–1166 radiographs, 1166 treatment, 1166–1167 drug interactions, 1161t Respiratory acidosis, 312, 320–322, 845 clinical presentation, 320–321 definition of, 320, 845 delirium from, 320 diagnosis, 321–322 epidemiology, 320 examination, 321 laboratory findings, 321 treatment and outcome, 321 Respiratory alkalosis, 321–323 clinical presentation and examination, 321–322 definition, 321 diagnosis, 323 etiology, 321 laboratory findings, 323 treatment and outcome, 323 Respiratory distress syndrome, 852–854. See also Chronic obstructive pulmonary disease clinical presentation, 852–853 definition, 852
Index Respiratory distress syndrome, (Continued) diagnosis, 853 emergency actions, 852 epidemiology, 852 examination, 853 key points, 852 laboratory findings, 853 treatment, 853–854 Respiratory failure, Reye's syndrome causing, 797 Respiratory system, theophylline overdose influencing, 1046 Rest, intestinal obstruction requiring, 21 Resuscitation emergencies. See also Cardiopulmonary resuscitation airway management, 913–916, 914b, 915b pediatric, 1073–1075, 1074t shock, 917–921 Retinal artery occlusion, 165 Reye's syndrome, 795–798 clinical presentation and examination, 796–797 diagnosis, 797 emergency actions, 796 epidemiology, 796 imaging findings, 797 key points, 798 laboratory findings, 797 pathology, 796 treatment, 797–798 intracranial pressure, 797–798 Rhabdomyolysis, 414–417 clinical presentation, 415 definition, 414 diagnosis, 416 emergency actions, 414 epidemiology, 414–415 examination, 415 key points, 414 laboratory findings, 415–416 treatment, 416–417 Rheumatic fever, 774–778 clinical presentation, 775 definition, 775 diagnosis, 775 antecedent GAS infection evidence, 777 Jones criteria for, 775–777 epidemiology, 775 key points, 774 laboratory findings, 777
1225
Rheumatic fever, (Continued) pathology, 775 treatment, 777 Rheumatoid factor analysis, knee pain emergency, 587 RICE therapy, knee pain treatment, 587–588 Rickets (vitamin D deficiency), hypocalcemia, 371 Rocky Mountain spotted fever erythema multiforme v., 98 toxic shock syndrome v., 548 Roentgenogram, tetralogy of Fallot, 782 Romberg test, 464 cerebellar examination including, 464 Rotavirus, infectious disease emergency, 268t RSI. See Rapid sequence intubation Rule of Nines assessment for burns, 194f Rumack-Matthew acetaminophen overdose nomogram, 933–935, 934f RVR. See Rapid ventricular response SADPERSONS scale, 842t Salicylate toxicity, 1038–1043 clinical presentation, 1040 definition, 1038 diagnosis, 1041 emergency actions, 1038 epidemiology, 1038–1039 hypoglycemia from, 403 key points, 1038 laboratory findings, 1040–1041 pathology, 1039–1040 radiography, 1041 treatment, 1042–1043 altered mental status, 1043 gastric lavage, 1042 hemodialysis, 1042 hemorrhagic complications with, 1043 hospital admission, 1043 peritoneal dialysis, 1043 rehydration, 1042 sodium bicarbonate, 1042 wide anion gap from, 1021 Saline solution hypercalcemia requiring, 376 hyperglycemic hyperosmolar nonketotic coma requiring, 390 rhabdomyolysis treatment, 416–417 -washed blood products, 562 wound irrigation with, 30
1226 INDEX Salmonella diarrhea from, 744t, 745 non-typhoid v. typhoid, 266t Sandimmune, myasthenia gravis requiring, 450 Sarcoidosis asthma mimicked by, 857 Bell's palsy v., 426–427, 426t multiple sclerosis v., 442 SBI. See Serious bacterial infection SCCM. See Society for Critical Care Medicine Schizoid personality disorder, 825–826 Schizotypal personality disorder, 826–828 clinical presentation, 827 definition, 826 diagnosis, 827 epidemiology, 827 key points, 826 treatment and outcome, 827–828 Scombroid poisoning, infectious disease emergency, 271t Scorpion sting, 256, 257, 259 Second-degree atrioventricular bradycardia type I, 52, 52f type II, 52–53, 53f Sedation intubated patient, 906, 908–913, 909t analgesics with, 906–908, 907t, 912–913 conclusion, 912 delirium, 910–911 dosages/durations/advantages, 909t last resort paralytics, 911–912 lorazepam, 909t, 910 midazolam, 909t, 910 propofol, 909t, 910 pediatric, 805–813 toxicology emergencies requiring, 929 Seizures and status epilepticus, 465–472, 466t, 468t, 471t amphetamine overdose causing, 938 antiepileptic drugs for, 466t, 471–472, 471t arsenic poisoning causing, 946 beta-blocker overdose sign, 953 clinical presentation, 467–469 clonidine overdose causing, 967–968 CT scan for, 469 cyclic antidepressant toxicity, 982 definitions, 466–467 EEG for, 470 emergency actions, 466 epidemiology, 467
Seizures and status epilepticus, (Continued) key points, 465 laboratory findings, 470 pathology, 467 pediatric, 783–788 clinical presentation, 785–786 definitions, 783–784 diagnosis, 786 emergency actions, 783 epidemiology, 784 examination, 786 febrile, 785, 789–792 definition, 789 emergency actions, 789 epidemiology, 789 key points, 789 laboratory findings, 790 pathology, 790 treatment, 790–792 key points, 783 laboratory findings, 786 pathology, 784–785 age-related, 784–785 metabolic-related, 785 treatment, 786–788 adverse effects of medications, 788 anticonvulsants, 786 oxygen, 786 post-trauma, 786–787 predisposing factors for, 468t theophylline overdose causing, 1046, 1047 treatment, 470–472, 471t antiepileptic drugs, 471t Selective serotonin reuptake inhibitors (SSRIs), panic disorder treatment, 816 Sensory function examination, 454–455 pain sensation, 455 vibration sense, 454–455 Sepsis, 706–712, 708t, 710t, 711t. See also Infections; Infectious disease emergencies definition, 706, 707 hypoglycemia from, 401 pediatric, 706–713, 708t, 710t, 711t Septic arthritis, 630, 632, 633, 637 definitions, 630, 632 epidemiology, 632 pathology, 633 treatment, 637
Index Septic shock, 413, 707 Serious bacterial infection (SBI), 706–713, 708t, 710t, 711t Sertraline, panic disorder treatment, 816 Serum acetaminophen, toxicity evaluation, 931 Serum electrolyte measurement, toxicology emergencies, 927–928 Serum glucose, hyperglycemic hyperosmolar nonketotic coma treatment, 392–393 Serum glutamate oxaloacetate transaminase (SGOT), 548 Serum glutamate pyruvate transaminase (SGPT), 548 Serum iron test, iron toxicity requiring, 1009 Serum ketones absence of, 390–393 hyperglycemic hyperosmolar nonketotic coma, 392 Sexual assault, 543–545 definition, 543 emergency actions, 543 epidemiology, 543 examination, 543–544 key points, 543 laboratory findings, 544 treatment, 544–545 pregnancy prevention, 545 Sexually transmitted disease (STD), 544. See also Human immunodeficiency virus infection genital herpes, 279, 285, 513–515 syphilis erythema multiforme v., 98 multiple sclerosis v., 442 treatment, 554 Sézary cells, exfoliative dermatitis associated with, 101 SGOT. See Serum glutamate oxaloacetate transaminase SGPT. See Serum glutamate pyruvate transaminase Shigella diarrhea from, 744t, 745 infectious disease emergency, 267t Shingles, 276, 277–278, 280–281, 283, 287 treatment, 287 Shock, 917–921 beta-blocker overdose causing, 953 clinical presentation anaphylactic, 919 treatment, 920
1227
Shock, (Continued) dysrhythmia, treatment, 920 hemorrhage, 920 hypovolemic (nontraumatic), 917–918 treatment, 920 myocardial infarction, treatment, 920 neurogenic, 919 treatment, 921 pharmacological, 919 treatment, 920 traumatic cardiogenic, 918 treatment dobutamine, 920 dopamine, 920 goals, 920 pericardiocentesis, 920 thoracotomy, 920 vasogenic, 919 treatment, 921 definition, 917 laboratory findings, 919 pathology, 917 treatment, 919–921 Shoulder injuries, 647–651 anatomy, 647–648 clinical presentation acromioclavicular joint injuries, 650 clavicle fractures, 648 humoral shaft fractures, 649 proximal humerus fractures, 649 rotator cuff tears, 651 scapular fractures, 649 shoulder dislocations, 650–651 sternoclavicular joint injuries, 649–650 definition, 647 emergency actions, 647 key points, 647 laboratory findings, 648 radiographs, 648 SIADH. See Syndrome of inappropriate antidiuretic hormone Sialolithiasis, 175–176 definition, 175 emergency actions, 175 examination, 176 key points, 175 treatment, 176 Sickle cell anemia, 570–574 clinical presentation, 571–572 definition, 570 diagnosis, 573 emergency actions, 570
1228 INDEX Sickle cell anemia, (Continued) examination, 572 high-altitude-exacerbated illness, 184t key points, 570 laboratory findings, 572–573 pain from, 510 pathology, 570–571 treatment, 573 SIDS. See Sudden death syndrome Sigmoidoscopy, diverticulosis requiring, 127 SIMV. See Synchronized intermittent mandatory ventilation Sinus bradycardia, 52, 52f Sinus tachycardia, 46 Sinusitis, 177–179 clinical presentation, 178 definition, 177 emergency actions, 177 epidemiology, 177 key points, 177 treatment, 178–179 Sitz bath, genital herpes treatment, 515 Skeletal emergency, end-stage renal disease causing, 1121–1122 Skin biopsy, exfoliative dermatitis requiring, 101 hypernatremia etiology involving, 359t tape, wound closure option, 30 Sleep disorders high altitude-related, 191 obstructive sleep apnea, 184t SLUDGe mnemonic, insecticide poisoning signs, 1131 Snakebite, 249–254 clinical presentation, 251 definition, 249–250 diagnosis, 252 emergency actions, 249 epidemiology, 250 examination, 251–252 key point, 249 laboratory findings, 252 pathology, 250–251 treatment, 252–254 antivenom, 253, 254 coral snake, 253, 254 limb elevation, 253 pertinent history taking for, 253 tetanus immunization, 253 Society for Critical Care Medicine (SCCM), analgesia and sedation for intubated patient (over 12 years old), 906
Sodium, 351–361, 354t, 359t fluid and electrolyte emergencies, 351–361, 354t, 359t intake, hypernatremia from, 359t Sodium bicarbonate cyclic antidepressant toxicity treatment, 983–984 pediatric trauma medication, 1080 rhabdomyolysis treatment, 416–417 salicylates toxicity treatment, 1042 tetralogy of Fallot requiring, 779 Soffer and Hamburger's criteria for alcoholic ketoacidosis, 342 Solu-Medrol, urticaria treatment, 112 Somogyi, hypoglycemia from, 401 Sorbitol, theophylline toxicity treatment, 1048 Spider bites and scorpion stings, 255–260 clinical presentation black widow spider, 257–258 brown recluse spider, 258 scorpion, 257 definitions, 255–256 diagnosis, 258 emergency actions, 255 epidemiology black widow spider, 256–257 brown recluse spider, 256 scorpion, 256 examination, 258 key points, 255 laboratory findings, 258 tarantula spiders, 260 treatment and outcome black widow spider, 259 brown recluse spider, 259–260 scorpion, 259 Spinal cord injuries, 1050–1056, 1054t, 1055t, 1067–1072, 1077, 1090–1095. See also Trauma clinical presentation, 1091–1093 definition, 1090 diagnosis, 1094 emergency actions, 1090 epidemiology, 1091 examination, 1093 key points, 1090 laboratory findings, 1093 multiple, 1055 radiographs, 1094 treatment, 1094–1095 Spinous accessory nerve examination, 461–462
Index Splenomegaly, exfoliative dermatitis causing, 101 SSRIs. See Selective serotonin reuptake inhibitors St. Vitus' dance, acute rheumatic fever causing, 776 Stanford classification of thoracic aortic dissection, 23 Staphylococcal TSS (STSS), toxic shock syndrome from, 545–549 Staphylococcus aureus, 267t AICD infection, 42 balanoposthitis from, 1127–1128 breast abscesses from, 502 eye infection, 163 infectious disease emergency, 267t methicillin-resistant, 502 Staphylococcus epidermidis, AICD infection, 42 Staples, wound closure option, 30 STD. See Sexually transmitted disease Steroids contraindicated for marine fauna envenomations, 241 cortico-, asthma treatment, 721–724 non-steroidal anti-inflammatory drugs, 437–438, 1114 toxicodendron dermatitis treatment, 108–109 STIC pressure monitor, acute compartment syndrome diagnosis, 599 Stool cultures foodborne and waterborne illness diagnosis, 272 heart transplant complications requiring, 94 softeners, anorectal disorders treatment, 120 Strangulated hernias, 16, 17 Streptococcal infection group A acute pediatric rheumatic fever from, 774–778 beta-hemolytic, 173, 174, 802–805 pneumoniae eye infection from, 164 pediatric infection, 707–708, 708t Working Group on Severe Streptococcal Infection, 548 Stroke syndromes. See also Embolism Bell's palsy v., 484t definition, 473
1229
Stroke syndromes, (Continued) diagnosis, 486–489, 487f, 488f, 489f, 490f, 491f, 492f gray-white matter loss, 488, 490f hemorrhagic v. nonhemorrhagic, 484t, 486–489, 487f, 488f, 489f, 490f, 491f, 492f hypoattenuation in middle cerebral artery, 488 hypodensity or ischemia, 488, 491f intracerebral hemorrhage, 487f subarachnoid hemorrhage, 486, 488f sulcal effacement in middle cerebral artery, 488, 492f differential diagnosis, 484t epidemiology, 473–494 laboratory findings, 485–486, 485t NIH stroke severity scale, 485t pathophysiology, 474–479, 475f, 476f, 477f, 478f arterial circle of Willis, 477, 477f brain control centers, 480f collateral blood flow to ischemic penumbra, 476f extracranial sources of thromboemboli, 478f homunculus distribution of innervation on parietal cortex, 480f zones of cerebral infarction and ischemia, 475f physical examination, 483–485, 484t risk factors for, 474 treatment, 490–496 tissue plasminogen activator, 494t STSS. See Staphylococcal TSS Subarachnoid hemorrhage (SAH). See also Hemorrhage headache indicative of, 432 headaches from, 434 Hunt and Hess Clinical Grading Scale for, 496 MRI of, 488f radiology for, 437 Submersion incidents, 207, 242–248, 246t ataxia, dizziness from, 207 clinical presentation, 245 definitions, 243 diagnosis, 246 emergency actions, 243 epidemiology, 243–244 key points, 242 laboratory findings, 245
1230 INDEX Submersion incidents, (Continued) pathophysiology, 244 physical examination, 245 radiographs, 246 treatment and outcome, 246–248, 246t Succinylcholine airway management pretreatment, 914b airway management treatment, 915b Sudden death syndrome (SIDS), 765–769 clinical presentation, 767 definitions, 766 diagnosis, 768 emergency actions, 765–766 epidemiology, 766–767 examination, 768 key points, 765 laboratory findings, 768 NICHD's recommendations, 769 pathology, 767 radiographs, 768 treatment, 768–769 Sudden hearing loss, 170–171 Suicide, 840–843. See also Psychiatric emergencies clinical presentation, 841 definition, 840 diagnosis, 841–842 SADPERSONS scale, 842t emergency actions, 840 epidemiology, 841 key points, 840 laboratory findings, 841 radiographs, 842 treatment, 842–843 Sulfonylureas, hypoglycemia from, 401 Sumac, toxicodendron dermatitis from, 106 Sunburn, exfoliative dermatitis from, 100, 100b Supraventricular tachycardia (SVT), 47–48, 47f, 48f AICD causing, 43 Surgery, hypercalcemia requiring, 377 Surgilope lubricating jelly, 204 Sutures removal of, 35, 36t wound closure, 30–34, 31t, 32t, 33f–34f SVR. See Systemic vascular resistance SVT. See Supraventricular tachycardia Sweating, hypernatremia etiology involving, 359t Sydenham's chorea, acute rheumatic fever causing, 776
Synchronized intermittent mandatory ventilation (SIMV), 847, 849t, 850–851 Syncope ataxia, dizziness, vertigo and, 418 heat, 221, 224 pulmonary embolism causing, 899 Syndrome of inappropriate antidiuretic hormone (SIADH), 353 Synovial fluid analysis knee pain emergency, 587 septic arthritis diagnostic, 637 Syphilis. See also Sexually transmitted disease erythema multiforme v., 98 tertiary, multiple sclerosis v., 442 Systemic analgesia and sedation, 809–812 Systemic lupus erythematosus (SLE), 889–890 multiple sclerosis v., 442 Systemic vascular resistance (SVR), clinical presentation, 779–780 Tachycardia, 46–49, 46f, 47f, 48f ARDS causing, 859–861 exfoliative dermatitis causing, 101 pediatric, 658–659, 659–660 pulmonary embolism causing, 899 supraventricular, 50, 50f AICD causing, 40, 43 Tachypnea ARDS causing, 859–861 pulmonary embolism causing, 899 TAI. See Traumatic aortic injury Tamponade. See Cardiac tamponade TEE. See Transesophageal echocardiography Teeth. See Dental emergencies; Dental trauma Telemetry unit observation, AICD malfunction requiring, 43 Temporal arteritis, ophthalmologic emergencies, 166 TEN. See Toxic epidermal necrolysis Tendons. See also Forearm and wrist injuries Achilles tendon rupture, 641 ankle tendon rupture/dissociation/tear, 592–593 deep tendon reflexes, 462–464, 463t scale for grading of, 463t hand injuries, 622 tendonitis, 615
Index Tensilon test, myasthenia gravis diagnostic, 449 Tension pneumothorax, cardiopulmonary arrest from, 664 Terbutaline, asthma treatment, 722 Testicles epididymitis, 1124–1126 torsion of, 1139–1141 clinical presentation, 1139 definition, 1139 diagnosis, 1140 emergency actions, 1139 epidemiology, 1139 examination, 1140 key points, 1139 laboratory findings, 1140 radiographs, 1140 treatment, 1141 Testosterone, depot-, 336 Tetanus, 307–310, 1028 clinical presentation, 308–309 definition, 307 diagnosis, 309–310 emergency actions, 307 epidemiology, 307 etiology, 308 immunization for snakebite, 253 wound management, 35 for wound management, 35 key points, 307 laboratory findings, 309 opioid injection risk of, 1028 pathophysiology, 308 treatment, 310 Tetracycline, adult bacterial pneumonia, 867, 867t Tetralogy of Fallot, 778–782, 781f, 782f clinical presentation, 779–780 definition, 779 diagnosis, 780 emergency actions, 779 epidemiology, 779 examination, 780 key points, 778 laboratory findings, 780 radiographs, 780, 781f, 782f treatment, 781–782 Tetrodotoxin fish poisoning, infectious disease emergency, 271t Thallium poisoning, arsenic poisoning v., 946 Theophylline overdose, 1044–1049 clinical presentation, 1045
1231
Theophylline overdose, (Continued) definition, 1044–1045 diagnosis, 1047 emergency actions, 1044 emesis from, 1048 epidemiology, 1045 examination cardiovascular, 1045–1046 gastrointestinal, 1046 respiratory system, 1046 seizures, 1046 hyperglycemia from, 1047 hypokalemia from, 1046, 1048 intentional, 1047 key points, 1044 laboratory findings, 1046 liver function impairment, 1047 pediatric seizures and status epilepticus, 786 radiographs, 1047 serum levels, 1047 treatment “ABC” care, 1047 cardiac and respiratory stabilization, 1047 electrolyte disturbances, 1048 seizures, 1047 Thiamin, ethanol withdrawal requiring, 330–331 Thiopental, airway management treatment, 915b Third National Health and Nutrition Examination Survey (NHANES III). See also Diet lead poisoning, 1014 Third-degree atrioventricular bradycardia type II, 53, 53f Thorax American Thoracic Society, 883–884 thoracic aortic dissection, 22–26 classification of, 23 clinical presentation, 24 definition of, 22–23 diagnosis, 22–26, 25 emergency actions, 22 epidemiology, 23 examination, 24 key points, 22 laboratory findings, 24 radiograph, 25 Stanford classification, 23 transesophageal echocardiography for, 25 treatment and outcome, 25–26
1232 INDEX Thorax, (Continued) thoracotomy, 920 trauma to, 1095–1104 al presentation, 1096 clinical presentation and examination, 1096–1097 definition, 1096 emergency actions, 1096 emergency department resuscitation thoracotomy, 1101 key points, 1095 life-threatening injuries, 1100 airway obstruction, 1097 cardiac tamponade, 1099–1100 FAST examination, 1100 flail chest and pulmonary contusion, 1098–1099 massive hemothorax, 1099 open pneumothorax, 1097 tension pneumothorax, 1097–1098 potentially life-threatening injuries aortic disruption and penetrating injury, 1102–1103 blunt cardiac injury, 1103 esophageal, 1104 hemothorax, 1102 simple pneumothorax, 1101–1102 tracheobronchial injury, 1102 traumatic diaphragmatic injury, 1103–1104 tube thoracostomy, 895–896 Thromboembolism. See also Embolism; Stroke syndromes cardiopulmonary arrest from, 664 extracranial sources of, 478f thrombolytic agents for, 904 Thrombolytic agents. See also Embolism prosthetic heart valve dysfunction requiring, 91–92 pulmonary embolism treatment, 904 Thyroid glands, exfoliative dermatitis causing enlargement of, 101 TIAs. See Transient ischemic attacks Tibial tuberosity fractures, 642 Tidal volume (Vt), 849t, 873 Tissue adhesives, wound closure option, 30 Tissue plasminogen activator (tPA), 494t TMP/SMX. See Trimethoprimsulfamethoxazole Toluene poisoning, metabolic acidosis from, 1021
“Tooth squeeze” barotrauma, 207 Topical analgesics, 808 Topiramate, seizures and status epilepticus, 471t Torsades de pointes, 51, 51f Toxic epidermal necrolysis (TEN), 103–106 clinical presentation, 104 definition, 103–104 emergency actions, 103 epidemiology, 104 examination, 104–105 key points, 103 laboratory findings, 105 treatment and outcome, 105–106 Toxic metabolic headaches, 434 Toxic shock syndrome (TSS), 545–549 clinical presentation and examination, 547 definition, 546 diagnosis, 547–549 emergency actions, 545 epidemiology, 546 erythema multiforme v., 98 examination, 549 key points, 545 laboratory findings, 549 pathology, 546–547 treatment, 549 Toxicity, drug. See also Toxicology emergencies cardiopulmonary arrest from, 664 heart transplant complications from, 95 toxic epidermal necrolysis from, 103–106 Toxicodendron dermatitis, 106–108 clinical presentation, 107–108 definition, 106 demographics and epidemiology, 107 key points, 106 nomenclature and plant identification, 107 pathophysiology, 107 treatment, 108–109 water irrigation for, 108–109 Toxicology emergencies, 923–930. See also Toxicity, drug acetaminophen, 931–936, 934f amphetamines, 936–938 anticholinergics, 938–943 antidotes, 929–930 arsenic, 943–947 barbiturates, 948–951
Index Toxicology emergencies, (Continued) beta-blockers, 952–955 calcium channel blockers for, 956–959 carbon monoxide, 959–962 caustic ingestion, 962–965 clonidine overdose, 965–968 cocaine toxicity, 969–973 cyanide poisoning, 974–980 cyclic antidepressant toxicity, 980–984, 982f decontamination, 928 definition, 923 digitalis glycoside, 984–988 disposition, 930 electrocardiogram, 927 enhanced elimination techniques, 930 epidemiology, 923 ethanol intoxication, 989–994 ethylene glycol, 994–998 examination, 926–927 hallucinogens, 999–1003 history-taking of event, 926 hydrocarbon poisoning, 1003–1007 iron toxicity, 1007–1010 isopropanol toxicity, 1010–1013 laboratory findings, 927–928 lead poisoning, 1014–1016 lithium poisoning, 1017–1019 mercury, 1024–1026 methanol poisoning, 1020–1023 opioid intoxication, 1027–1030 organophosphorus and carbamate insecticides poisoning, 1130–1132 phenytoin, 1034–1037 “safety net” and initial evaluation, 925 salicylates, 1038–1043 supportive care, 928–929 drug-associated agitation medications, 929 IV fluids, 929 lidocaine, 929 sedatives, 929 seizure medications, 929 serum calcium, 929 theophylline, 1044–1049 toxicokinetics and pharmacokinetics, 923–924 first-order (renal elimination), 924 Michaelis-Menton elimination, 924 questions to ask, 924 zero-order (enzyme kinetics), 924 treatment approach, 924–925
1233
Toxicology screening, neonatal emergencies requiring, 668–669 Toxoplasma, heart transplant infection, 95 TPA. See Tissue plasminogen activator Transdermal therapeutic system (TTS), 965–966 Transesophageal echocardiography (TEE), thoracic aortic dissection diagnosis, 25 Transient ischemic attacks (TIAs), 469 Transplantation emergencies, 1147–1167. See also Organ rejection cardiac and pulmonary, 93–96, 1150, 1151, 1154 clinical presentation heart failure, 1149–1150 infection, 1150 organ rejection, 1150 pulmonary failure, 1150 definition, 1148 diagnosis, 1152–1153 emergency actions, 1147–1148 epidemiology, 1149 examination heart failure, 1150 infection, 1151 organ rejection, 1151 pulmonary failure, 1151 laboratory findings, 1151–1152 radiographs, 1153 treatment, 1153–1154 infection, 1154–1155 organ rejection, 1154 liver transplantation, 1156–1162, 1158t, 1160t, 1161t renal, 1122–1123, 1158t, 1160t, 1161t, 1163–1167 Trauma. See also Injury; Wound management abdominal, 1057–1062 anatomy, 1058 clinical presentation and examination, 1059 CT scan with contrast, 1060 definition, 1058 diagnosis, 1059–1060 diagnostic peritoneal lavage, 1060–1061 emergency actions, 1057 FAST examination, 1060 key points, 1057 treatment, 1061–1062 gastric tube placement, 1062
1234 INDEX Trauma, (Continued) barotrauma, 206–207 brain, 915b, 1055, 1067–1072 genitourinary tract, 1063–1066 geriatric emergency, 389 head, 915b, 1055, 1067–1072 headaches from, 434 multiple injury, 1050–1056, 1054t, 1055t hip, 625–630 life-threatening injuries airway obstruction, 1097 cardiac tamponade, 1099–1100 FAST examination, 1100 flail chest and pulmonary contusion, 1098–1099 massive hemothorax, 1099 open pneumothorax, 1097 tension pneumothorax, 1097–1098 maxillofacial and dental emergencies, 179–182 multiple injury blood transfusion for, 1055, 1055t bone fracture from, 1056 clinical presentation, 1053 diagnosis, 1056 epidemiology, 1050–1051 examination, 1053–1056 Glasgow Coma Scale, 1054, 1054t head or spinal cord, 1050–1056, 1054t, 1055t, 1067–1072, 1077, 1090–1095 CT scans, 1052, 1055 FAST, 1052 neurologist consultation, 1055 ophthalmologic, 167–168 pediatric, 629, 1073–1080, 1074t, 1079t, 1080t abdomen evaluation, 1078 adult v. child spinal cord, 1077 airway management for, 1073–1075, 1074t blood pressure, 1074t cardiovascular management, 1075 chest evaluation, 1078 endotracheal tube size v. age, 1074t evaluation and stabilization, 1078–1079, 1079t fluid resuscitation, 1074t induction and intubation, 1079, 1079t, 1080t countershocks, 1079t medications, 1080t
Trauma, (Continued) neurological evaluation, 1075–1077, 1076–1077, 1076t CT scan, 1077 Glasgow Coma Scale (modified), 1076t renal perfusion assessment, 1075 seizures and status epilepticus, posttrauma, 786–787 vital signs, 1079t pelvic, 1081–1089 anatomy, 1081–1082 associated injuries, 1083 emergency actions, 1081 examination, 1087 key points, 1081 laboratory studies, 1088 mechanisms of injury, 1082–1083 treatment, 1088–1189 type I fractures, 1083–1085 type II fractures, 1085 type III fractures, 1085–1086 type IV fractures, 1086 potentially life-threatening injuries aortic disruption and penetrating injury, 1102–1103 blunt cardiac injury, 1103 diaphragmatic injury, 1103–1104 esophageal, 1104 hemothorax, 1102 simple pneumothorax, 1101–1102 tracheobronchial injury, 1102 pregnant patient with, 1105–1111 pulmonary embolism risk factor from, 899 spinal cord, 1050–1056, 1054t, 1055t, 1067–1072, 1077, 1090–1095 thoracic, 1095–1104 clinical presentation and examination, 1096–1097 definition, 1096 emergency actions, 1096 emergency department resuscitation thoracotomy, 1101 key points, 1095 life-threatening injuries, 1100 Traumatic aortic injury (TAI), 1102–1103 Tremors, respiratory acidosis causing, 320 Trendelenburg's position, hernia treatment requiring, 17 Trichomonas vaginalis, treatment, 553–554, 553t
Index Trigeminal nerve examination, 459–460, 459f Trimethoprim-sulfamethoxazole (TMP/ SMX), 271t urinary tract infection treatment, 1145t, 1146 Trochlear nerve examination, 457–458, 458f TSS. See Toxic shock syndrome TTS. See Transdermal therapeutic system Tubular necrosis, 1114 intrarenal acute renal failure presenting as, 1114 Tumor. See also Malignancy; Oncologic and hematologic emergencies acoustic neuroma, 426–427, 426t parotid, Bell's palsy v., 426–427, 426t Tzanck smear and culture, genital herpes diagnosis, 515 Ulcer colitis v diverticulitis, 126 gastric or duodenal, 511 Ulnar tunnel syndrome, 615. See also Forearm and wrist injuries Ultrasonography abdominal aortic aneurysm requiring, 4 abdominal pain, 512 abruptio placentae, 499 abscesses of breast requiring, 503 appendicitis, 7–8 cholelithiasis and cholecystitis, 13 Doppler epididymitis differential diagnosis, 1126 testicular torsion, 1140 focused abdominal sonography for trauma, 1052, 1060, 1100 hernia diagnosis, 17 hyperemesis gravidarum, 517 mastitis, 503 miscarriage (abortion), 527 pelvic pain, 512 pulmonary embolism, 905t Ultraviolet keratitis, as altitude-related emergency, 190–191 Ultraviolet keratitis, ophthalmologic emergency, 167 Umbilical hernias, 15 Unconjugated hyperbilirubinemia, 136 Upper respiratory pediatric emergencies, 678–692 bronchiolitis, 687–692 clinical presentation, 689
1235
Upper respiratory pediatric emergencies, (Continued) definition, 688 diagnosis, 690 emergency actions, 688 epidemiology, 688–689 examination, 689 laboratory findings, 690 radiographs, 690 treatment, 690–692 clinical presentation, 680–681 definitions, 678–679 diagnosis, 683–684 emergency actions, 678 epidemiology, 679–680 examination, 681–682 key points, 678 laboratory findings, 682–683 radiographs, 684–685 treatment, 685–687 Uremia, metabolic acidosis with, 1021 Ureter injuries, 1064 Urethra dilation of, prosthetic heart valve requiring, 92 injuries to, 1065 Urinalysis hip trauma requiring, 630 hymenoptera sting requiring, 232 lightning injuries requiring, 236 neonatal emergencies, 668–669 ovarian torsion, 534 toxicology emergencies, 927–928 Urinary tract infection (UTI), 1142–1146, 1145t. See also Urology emergencies clinical presentation and examination, 1143–1144 definition, 1142 diagnosis, 1144 epidemiology, 1143 geriatric emergency, 388–389 key points, 1142 laboratory findings, 1144 pediatric, 753–757, 757t clinical presentation, 754–755 definition, 753 diagnosis, 755 emergency actions, 753 epidemiology, 754 examination, 755 key points, 753 laboratory findings, 756 pathology, 754
1236 INDEX Urinary tract infection (UTI), (Continued) treatment, 756, 757t antibiotics, 757t radiographs, 1145 treatment, 1145–1146, 1145t oral medications, 1145t Urine culture pediatric urinary tract infection diagnostic, 755 shock diagnostic, 919 Urology emergencies. See also Urinary tract infection adults, urinary tract infections, 1142–1146, 1145t epididymitis, 1124–1126 penis disorders, 1127–1130 prostatitis, 1131–1134 renal failure, 1113–1117 testicular torsion, 1139–1141 Urticaria, 109–113 clinical presentation, 111 definition, 110 emergency actions, 109 epidemiology, 110 etiology, 110 examination, 111 hymenoptera sting causing, 232 key points, 109 laboratory findings, 111 pathophysiology, 110–111 treatment, 111–113 Uterine perforation/leiomyoma, 510 UTI. See Urinary tract infection Vaginitis, pelvic and abdominal pain from, 510 Vagus nerve examination, 461 Valproate, pediatric seizures and status epilepticus, 786 Valproic acid, seizures and status epilepticus, 471t Valsalva maneuver, hernia diagnosis, 17 Vancomycin AICD infection requiring, 42–43 endocarditis from prosthetic valve infection, 91–92 vasogenic shock requiring, 921 Varicella-zoster virus, 276, 280, 282–283 immune globulin, 96 treatment for, 286 Vasoconstriction, epinephrine for, 28 Vecuronium, airway management pretreatment and treatment, 915b, 916
Venous blood gas analysis, hyperglycemic hyperosmolar nonketotic coma, 392 Ventilation/perfusion (V/Q) scanning, pulmonary embolism, 902, 905t Ventricular fibrillation (VF), 50–51, 51f AICD causing, 40 Ventricular septal defect (VSD), 779–782, 782f Ventricular tachycardia (VT), 50, 50f AICD causing, 40, 43 Versed, airway management treatment, 916 Vertigo, 418–423. See also Ataxia, dizziness, vertigo alternobaric vertigo barotrauma, 207 Vestibulocochlear nerve examination, 461 VF. See Ventricular fibrillation Vibration sense, sensory function examination, 454–455 Vibrio cholerae diarrhea from, 744t, 745 infectious disease emergency, 267t Vinyl gloves, toxicodendron dermatitis treatment requiring, 108–109 Viral conjunctivitis, 164 Viral hepatitis, 135–143, 137f, 138f, 139f definition of, 136 Vital signs, pediatric trauma evaluation, 1079t Vitamin D deficiency (rickets), hypocalcemia, 371 Vocal cord dysfunction, asthma mimicked by, 857 Vomiting arsenic poisoning treatment, 946 hyperemesis gravidarum, 515–518 ovarian torsion causing, 534 theophylline overdose causing, 1048 VT. See Ventricular tachycardia Vt. See Tidal volume Vulvovaginitis, 550–554 clinical presentation and examination, 552 definition, 550–551 diagnosis and laboratory findings, 552–554 emergency actions, 550 epidemiology, 551 key points, 550 pathology, 551–552 treatment, 553–554, 553t Water -borne illnesses, 264–275, 266t–271t fluid and electrolyte emergencies, 351–393, 354t, 359t, 382t
Index Water (Continued) intake, 357–358 hypernatremia from reduced, 359t increased, 357 reduced, 357 irrigation with, toxicodendron dermatitis requiring, 108–109 marine fauna envenomations, 238–242 submersion incidents, 207, 242–248, 246t WBC count. See White blood cell count Wegener's granulomatosis, 889–890 Wells assessment model, pulmonary embolism risk, 899–900, 900t White blood cell (WBC) count appendicitis requiring, 7 as blood component, 559 Whitesides apparatus, acute compartment syndrome diagnosis, 599 Whole blood, as blood transfusion component, 560 Wicki (Geneva) assessment model, pulmonary embolism risk, 900–901, 900t Wolff-Parkinson-White syndrome, 56–57, 56f Working Group on Severe Streptococcal Infection, toxic shock syndrome requiring, 548 Wound management, 26–36, 29t, 31t, 32t, 33f, 34f, 36t. See also Injury anesthesia after examination, 28 antibiotic prophylaxis, 35 closure, 30–34, 31t, 32t, 33f, 34f disposition, 35–36, 36t dressings, 34–36
1237
Wound management, (Continued) epidemiology of traumatic wounds, 27 foot injuries, 607 key points, 26 medical history required for, 27–28 physical examination, 28 preparation, 29–30 radiographs, 36 stages of healing, 27 tetanus immunization, 35 Wrist and forearm injuries, 608–616 X-ray chest adrenal insufficiency requiring, 336 cardiac chest pain evaluation, 73 cardiac tamponade, 62 ethanol withdrawal requiring, 329 hypertensive emergencies, 78 isopropanol toxicity, 1012 respiratory acidosis requiring, 321 Reye's syndrome, 797 submersion incident requiring, 246 elbow injury diagnosis, 602 neonatal emergencies, 668–669 permanent pacemakers, 87 Yersinia, infectious disease emergency, 267t Zantac, urticaria treatment, 112 Zonegran, seizures and status epilepticus, 471t Zonisamide, seizures and status epilepticus, 471t Zyrtec, urticaria treatment requiring, 112
