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CLINICAL VETERINARY ADVISOR Dogs and Cats SECOND EDITION Editor-in-Chief
Etienne Côté Associate Professor Department of Companion Animals Atlantic Veterinary College University of Prince Edward Island Charlottetown, Prince Edward Island, Canada
With 551 illustrations
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Copyright
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3251 Riverport Lane St. Louis, Missouri 63043
CLINICAL VETERINARY ADVISOR: DOGS AND CATS
ISBN: 978-0-323-06864-2
Copyright © 2011, 2007 by Mosby, Inc., an affi liate of Elsevier Inc. No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopying, recording, or any information storage and retrieval system, without permission in writing from the publisher. Details on how to seek permission, further information about the Publisher's permissions policies and our arrangements with organizations such as the Copyright Clearance Center and the Copyright Licensing Agency, can be found at our website: www.elsevier.com/permissions. This book and the individual contributions contained in it are protected under copyright by the Publisher (other than as may be noted herein). Notices Knowledge and best practice in this fi eld are constantly changing. As new research and experience broaden our understanding, changes in research methods, professional practices, or medical treatment may become necessary. Practitioners and researchers must always rely on their own experience and knowledge in evaluating and using any information, methods, compounds, or experiments described herein. In using such information or methods they should be mindful of their own safety and the safety of others, including parties for whom they have a professional responsibility. With respect to any drug or pharmaceutical products identifi ed, 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 practitioners, relying on their own experience and knowledge of their patients, 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 authors, contributors, or editors, assume any liability for any injury and/or damage to persons or property as a matter of products liability, negligence or otherwise, or from any use or operation of any methods, products, instructions, or ideas contained in the material herein.
Library of Congress Cataloging-in-Publication Data or Control Number Clinical veterinary advisor. Dogs and cats / editor-in-chief, Etienne Cote.—2nd ed. p. ; cm. Other title: Dogs and cats Includes bibliographical references and index. ISBN 978-0-323-06864-2 (hardcover : alk. paper) 1. Dogs—Diseases. 2. Cats—Diseases. 3. Pet medicine. I. Côté, Etienne. II. Title: Dogs and cats. [DNLM: 1. Cat Diseases. 2. Dog Diseases. 3. Animals, Domestic. 4. Veterinary Medicine—methods. SF 981] SF991.C658 2011 636.7'089—dc22 2010037649
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Editors Editor in chief
Etienne Côté, DVM, DACVIM (Cardiology, Small Animal Internal Medicine) Cardiology, Chief Complaints, Other Topics, Procedures and Techniques, Differential Diagnosis, Drug Formulary Associate Professor, Department of Companion Animals, Atlantic Veterinary College, University of Prince Edward Island, Charlottetown, Prince Edward Island, Canada
Editors
Leah A. Cohn DVM, PhD, DACVIM (Small Animal Internal Medicine) Urology Professor, Veterinary Medicine and Surgery, Department of Veterinary Medicine and Surgery, College of Veterinary Medicine, University of Missouri, Columbia, Missouri
Susan M. Cotter, DVM, DACVIM (Small Animal Internal Medicine and Oncology) Hematologic/Immunologic Diseases Distinguished Professor of Clinical Sciences Emerita Department of Clinical Sciences, Tufts Cummings School of Veterinary Medicine, Tufts University, North Grafton, Massachusetts
Cheryl L. Cullen, DVM, MVetSc, DACVO Ophthalmology Associate Professor, Comparative Ophthalmology Department of Veterinary Clinical and Diagnostic Sciences, Faculty of Veterinary Medicine, University of Calgary, Calgary, Alberta, Canada CullenWebb Animal Neurology & Ophthalmology Centre, Riverview, New Brunswick, Canada
Curtis W. Dewey, DVM, MS, DACVIM (Neurology), DACVS Neurology Associate Professor, Neurology/Neurosurgery, Chief, Section of Neurology, Department of Clinical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, New York
Joseph Harari, MS, DVM, DACVS Orthopedics Co-Owner, Veterinary Surgical Specialists, Spokane, Washington
Sherri Ihle, DVM, MS, DACVIM (Small Animal Internal Medicine) Endocrinology Associate Professor, Department of Companion Animals, Atlantic Veterinary College, University of Prince Edward Island, Charlottetown, Prince Edward Island, Canada
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Safdar Khan, DVM, MS, PHD, DABVT Toxicology Senior Director of Toxicology Research ASPCA Animal Poison Control Center Urbana, Illinois
Michelle Kutzler, DVM, PhD, DACT Theriogenology Associate Professor, Department of Animal Sciences, College of Agricultural Sciences, Oregon State University, Corvallis, Oregon
Douglass K. Macintire, DVM, MS, DACVIM (Small Animal Internal Medicine), DACVECC Infectious Diseases Professor of Acute Medicine and Critical Care, Department of Clinical Sciences, College of Veterinary Medicine, Auburn University, Auburn, Alabama
Kathryn E. Michel, DVM, MS, DACVN Nutrition Associate Professor of Nutrition, Department of Clinical Sciences, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, Pennsylvania
Karen L. Overall, MA, VMD, PhD, DACVB, CAAB Behavior Research Associate, Center for Neurobiology and Behavior, Department of Psychiatry, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, Pennsylvania
Manon Paradis, DMV, MVSc, DACVD Dermatology Professor of Dermatology, Department of Clinical Sciences, Faculté de Médecine Vétérinaire, University of Montreal, Saint-Hyacinthe, Québec, Canada
Kenneth M. Rassnick, DVM, DACVIM (Oncology) Oncology Assistant Professor of Oncology, Department of Clinical Sciences, College of Veterinary Medicine, Cornell University Ithaca, New York
Alexander M. Reiter, Dipl Tzt, Dr Med Vet, DAVDC, DEVDC Dentistry/Oral Surgery Associate Professor of Dentistry and Oral Surgery, Department of Clinical Studies, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, Pennsylvania
Keith Richter, DVM, DACVIM (Small Animal Internal Medicine) Hepatobiliary/Pancreatic Diseases Hospital Director and Staff Internist, Veterinary Specialty Hospital of San Diego, San Diego, California,
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Lois Roth-Johnson, DVM, PhD, DACVP Laboratory Tests President, Dual Boarded, Inc., Eastham, Massachusetts
Elizabeth Rozanski, DVM, DACVECC, DACVIM (Small Animal Internal Medicine) Emergency and Critical Care Assistant Professor, Department of Clinical Sciences, Cummings School of Veterinary Medicine, Tufts University, North Grafton, Massachusetts
Rance K. Sellon, DVM, PhD, DACVIM (Small Animal Internal Medicine, Oncology) Respiratory Diseases Associate Professor, Department of Veterinary Clinical Sciences, College of Veterinary Medicine, Washington State University, Pullman, Washington
Richard Walshaw, BVMS, DACVS Soft-Tissue Surgery Surgical Oncologist, Animal Cancer & Imaging Center, Canton, Michigan
Debra Zoran, DVM, MS, PhD, DACVIM (Small Animal Internal Medicine) Gastroenterology Associate Professor and Chief of Medicine, Department of Small Animal Clinical Sciences, College of Veterinary Medicine Texas A&M University College Station, Texas
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Contributors Jonathan A. Abbott, DVM, DACVIM (Cardiology) Associate Professor, Department of Small Animal Clinical Sciences, Virginia-Maryland Regional College of Veterinary Medicine, Virginia Polytechnic Institute and State University Blacksburg, Virginia
Lisa M. Abbott, DVM, MRCVS Pet Emergency Treatment Services Limited, Maidstone, Kent, United Kingdom
Sarah K. Abood, DVM, PhD Assistant Dean, Associate Professor, Department of Small Animal Clinical Sciences, Assistant Dean, College of Veterinary Medicine, Michigan State University, East Lansing, Michigan
Christopher A. Adin, DVM, DACVS Assistant Professor of Small Animal Surgery, Department of Veterinary Clinical Sciences, College of Veterinary Medicine, The Ohio State University Columbus, Ohio
Darcy B. Adin, DVM, DACVIM (Cardiology) Associate Veterinary Cardiologist, Cardiology, Medvet, Worthington, Ohio
Sarah Allen, DVM, DACVECE Veterinarian Emergency/Critical Care, Massachusetts Veterinary Referral Hospital, In Town Veterinary Group Woburn, Massachusetts
Robin W. Allison, DVM, PhD, DACVP (Clinical Pathology) Associate Professor, Department of Veterinary Pathobiology, Center for Veterinary Health Sciences, Oklahoma State University Stillwater, Oklahoma
Jamie G. Anderson, RDH, DVM, MS, DAVDC, DACVIM (Small Animal Internal Medicine) Co-Owner, San Francisco Veterinary Specialists, San Francisco, California
Elizabeth Armitage-Chan, MA VetMB, FHEA, DACVA, MRCVS Anaesthetist, Davies Veterinary Specialists, Higham Gobion, Hertfordshire, United Kingdom
Clarke E. Atkins, DVM, DACVIM (Small Animal Internal Medicine, Cardiology) Jane Lewis Seaks Distinguished Professor, Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University Raleigh, North Carolina
Todd W. Axlund, DVM, MS, DACVIM (Neurology) Neurologist Ohio Veterinary Surgery and Neurology, LLC Akron, Ohio
Lenore M. Bacek, DVM Resident, Emergency/Critical Care, Department of Clinical Sciences, College of Veterinary Medicine, Auburn University, Auburn, Alabama
Jonathan Bach, DVM, DACVIM (Small Animal Internal Medicine), DACVECC Clinical Assistant Professor, Department of Medical Sciences, School of Veterinary Medicine University of Wisconsin—Madison, Madison, Wisconsin
Dennis Bailey, DVM, DACVIM (Oncology) Staff Oncologist Oradell Animal Hospital Paramus, New Jersey
Kerry Smith Bailey, DVM, DACVIM (Neurology)
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Staff Neurologist Neurology, Oradell Animal Hospital Paramus, New Jersey
Raviv J. Balfour, DVM, DACVS Associate Surgeon Animal Surgical and Emergency Center Los Angeles, California
Cheryl E. Balkman, DVM, DACVIM (Small Animal Internal Medicine) Lecturer, Department of Clinical Sciences, College of Veterinary Medicine Cornell University Ithaca, New York
Carsten Bandt, DVM, DACVECC Assistant Professor for Emergency Critical Care, Department of Small Animal Clinical Science, College of Veterinary Medicine, University of Florida, Gainesville, Florida
Gad Baneth, DVM, PhD, DECVCP Professor, Veterinary Internal Medicine The Hebrew University, Veterinary Teaching Hospital, School of Veterinary Medicine, Hebrew University, Rehovot, Israel
Lisa G. Barber, DVM, DACVIM (Oncology) Assistant Professor, Department of Clinical Sciences, Cummings School of Veterinary Medicine, Tufts University North Grafton, Massachusetts
Georgina Barone, DVM, DACVIM (Neurology) Staff Neurologist, Long Island Veterinary Specialists Plainview, New York
Kirstie A. Barrett, DVM, DACVIM (Cardiology) California Animal Hospital Veterinary Specialty Group Los Angeles, California
Cary L.M. Bassett, DVM, PhD, DACVIM (Small Animal Internal Medicine) Carolina Veterinary Specialists Greensboro, North Carolina
Jeff D. Bay, DVM, DACVIM (Small Animal Internal Medicine) Staff Internist Upstate Veterinary Specialties Latham, New York
Matthew W. Beal, DVM, DACVECC Assistant Professor, Emergency and Critical Care Medicine; Director, Emergency Services, Veterinary Medical Center, College of Veterinary Medicine, Michigan State University East Lansing, Michigan
Iveta Becvarova, DVM, MS, DACVN Clinical Assistant Professor Department of Large Animal Clinical Sciences, Virginia-Maryland Regional College of Veterinary Medicine, Virginia Polytechnic Institute and State University Blacksburg, Virginia
Marie-Claude Bélanger, DVM, MS, DACVIM (Small Animal Internal Medicine) Associate Professor of Internal Medicine and Cardiology, Department of Clinical Sciences, Faculty of Veterinary Medicine University of Montreal, SaintHyacinthe, Québec, Canada
Ellison Bentley, DVM, DACVO Clinical Associate Professor, Comparative Ophthalmology, Department of Surgical Sciences, School of Veterinary Medicine University of Wisconsin— Madison Madison, Wisconsin
Michael Bernstein, DVM, DACVIM (Small Animal Internal Medicine) Medical Director VCA South Shore Animal Hospital, South Weymouth, Massachusetts
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Adam Birkenheuer, DVM, PhD, DACVIM (Small Animal Internal Medicine) Assistant Professor, Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University Raleigh, North Carolina
Marie-Claude Blais, DVM, DACVIM (Small Animal Internal Medicine) Faculty, Clinical Sciences, Faculté de médecine vétérinaire, University of Montreal Saint-Hyacinthe, Quebec, Canada
Bernard D. Boisvert, BSc (Hons), DVM Owner, Mission Ridge Animal Hospital St. Albert, Alberta, Canada
Elise Mittleman Boller, DVM, DACVECC Staff Criticalist, Intensive Care Unit, Department of Clinical Studies, Section of Emergency and Critical Care, Matthew J. Ryan Veterinary Hospital, University of Pennsylvania, Philadelphia, Pennsylvania
John D. Bonagura, DVM, MS, DACVIM (Cardiology, Small Animal Internal Medicine) Professor Department of Veterinary Clinical Sciences; Cardiology Service Head, The Ohio State University Veterinary Hospital, Member, Davis Heart & Lung Research Institute, College of Veterinary Medicine, The Ohio State University Columbus, Ohio
Betsy R. Bond, DVM, DACVIM (Cardiology) Staff Cardiologist, The Animal Medical Center New York, New York
Dwight D. Bowman, PhD Professor of Parasitology, Department of Microbiology and Immunology, College of Veterinary Medicine, Cornell University Ithaca, New York
Søren R. Boysen, DVM, DACVECC Associate Professor, Faculty of Veterinary Medicine, Emergency and Critical Care, Veterinary Clinical and Diagnostic Sciences, University of Calgary Calgary, Alberta, Canada
David M. Brewer, DVM Neurology/Neurosurgery Resident, Department of Clinical Sciences, College of Veterinary Medicine, Cornell University Ithaca, New York
Catharina Brömel, DMV PhD, DACVIM (Small Animal Internal Medicine) Department of Population Health and Reproduction, School of Veterinary Medicine, University of California—Davis, Davis, California
Marjory B. Brooks, DVM, DACVIM (Small Animal Internal Medicine) Director, Comparative Coagulation Section, Animal Health Diagnostic Center, College of Veterinary Medicine, Cornell University Ithaca, New York
Michael R. Broome, DVM, MS, DABVP Owner, Advanced Veterinary Medical Imaging, Tustin, California
Andrew J. Brown, MA, VetMB, MRCVS, DACVECC Assistant Professor, Department of Small Animal Clinical Sciences, College of Veterinary Medicine, Michigan State University East Lansing, Michigan
M. Raquel Brown, DVM, DACVIM (Oncology, Small Animal Internal Medicine) Adjunct Professor, Department of Veterinary Clinical Sciences, College of Veterinary Medicine and Biomedical Sciences, Texas A&M University College Station, Texas; Staff Oncologist/Internist, Veterinary Oncology and Internal Medicine Austin, Texas
Lisa Brownlee, DVM, MS, DACVIM (Small Animal Internal Medicine) Assistant Professor Department of Veterinary Clinical Sciences, College of Veterinary Medicine, Oregon State University Corvallis, Oregon
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Stephanie R. Bruner, DVM, DACVD Staff Dermatologist, Greater Cincinnati Veterinary Specialists, Independent Consultant, Antech Diagnostics Cincinnati, Ohio
Jeffrey N. Bryan, DVM, MS, PhD, DACVIM (Oncology) Assistant Professor, Department of Veterinary Clinical Sciences, College of Veterinary Medicine, Washington State University Pullman, Washington
James W. Buchanan, DVM, M Med Sci, DACVIM (Cardiology) Emeritus Professor of Cardiology, Department of Clinical Studies, School of Veterinary Medicine, University of Pennsylvania Philadelphia, Pennsylvania
Gareth Buckley, MA, VetMB, MRCVS Resident Department of Clinical Sciences, Foster Hospital for Small Animals, Cummings School of Veterinary Medicine, Tufts University North Grafton, Massachusetts
Barret J. Bulmer, DVM, MS, DACVIM (Cardiology) Associate Professor Cardiology, Foster Hospital for Small Animals, Cummings School of Veterinary Medicine, Tufts University North Grafton, Massachusetts
Lyndsay N. Bunting, DVM Radiation Oncology Resident Department of Surgical Sciences, School of Veterinary Medicine University of Wisconsin—Madison Madison, Wisconsin
William J. Burkholder, DVM, PhD, DACVN Veterinary Medical Officer, United States Food and Drug Administration, Center for Veterinary Medicine, Division of Animal Feeds Rockville, Maryland
Derek P. Burney, DVM, PhD, DACVIM (Small Animal Internal Medicine) Chief Operating Officer, Internal Medicine and Critical Care, Gulf Coast Veterinary Specialists, Houston, Texas
Lisa Carioto, DVM, DVSc, DACVIM (Small Animal Internal Medicine) Clinician Small Animal Internal Medicine, Clinicienne en médecine interne des petits animaux, Centre hospitalier universitaire vétérinaire, Faculté de médecine vétérinaire, Université de Montréal Saint-Hyacinthe, Québec, Canada
Khristen J. Carlson, DVM Resident Small Animal Internal Medicine, Department of Clinical Sciences, College of Veterinary Medicine Auburn University, Auburn, Alabama
Maureen C. Carroll, DVM, DACVIM (Small Animal Internal Medicine) Department of Internal Medicine, Angell Animal Medical Center Boston, Massachusetts
Michaela Cautela, DVM Resident in Neurology/Neurosurgery, Department of Clinical Sciences—Neurology, Hospital for Animals College of Veterinary Medicine Cornell University Ithaca, New York
Tara Chapman, DVM, DACVIM (Small Animal Internal Medicine) Internal Medicine Alta Vista Animal Hospital Ottawa, Ontario, Canada
Michel Chénier, DMV Hôpital Vétérinaire Chénier Sainte-Adèle, Québec, Canada
Dennis J. Chew, DVM, DACVIM (Small Animal Internal Medicine) Professor; Attending Clinician, Department of Veterinary Clinical Sciences, Veterinary Medical Teaching Hospital, College of Veterinary Medicine, The Ohio State University Columbus, Ohio
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Jane O. Cho, DVM, DACVO Veterinary Ophthalmologist, Veterinary Eye Specialists, PLLCArdsley, New York
Ruthanne Chun, DVM, DACVIM (Oncology) Clinical Associate Professor Department of Medical Sciences, School of Veterinary Medicine University of Wisconsin Madison, Wisconsin
Cecile Clercx, DVM, PhD, DECVIM-CA (Internal Medicine) Professor Department of Veterinary Clinical Sciences of Companion Animals and Equine, Faculty of Veterinary Medicine University of Liege Liege, Belgium
Joan R. Coates, DVM, MS, DACVIM (Neurology) Associate Professor Department of Veterinary Medicine and Surgery; Neurology/Neurosurgery Service Section Leader, Department of Veterinary Neurology and Neurosurgery, Veterinary Medical Teaching Hospital, University of Missouri Columbia, Missouri
Leah A. Cohn, DVM, PhD, DACVIM (Small Animal Internal Medicine) Professor, Veterinary Medicine and Surgury, Department of Veterinary Medicine and Surgery College of Veterinary Medicine University of Missouri Columbia, Missouri
Gary Conboy, DVM, PhD Associate Professor, Veterinary Parasitology, Department of Pathology and Microbiology, Atlantic Veterinary College, University of Prince Edward Island, Charlottetown, Prince Edward Island, Canada
Audrey K. Cook, BVM&S, MRCVS, DACVIM (Small Animal Internal Medicine), DECVIM-CA Clinical Associate Professor, Department of Small Animal Clinical Sciences, College of Veterinary Medicine and Biomedical Sciences, Texas A&M University, College Station, Texas
Cynthia S. Cook, DVM, PhD, DACVO Ophthalmologist Veterinary Vision, Inc., San Carlos, California, San Francisco, California
Lilian Cornejo, DVM, DACVIM (Small Animal Internal Medicine) Clinical Assistant Professor, Department of Clinical Sciences, Cummings School of Veterinary Medicine, Tufts University North Grafton, Massachusetts
Yonaira E. Cortés, DVM, DACVECC Veterinarian Emergency Medicine/Critical Care Oradell Animal Hospital Paramus, New Jersey
Etienne Côté, DVM, DACVIM (Cardiology, Small Animal Internal Medicine) Associate Professor Department of Companion Animals, Atlantic Veterinary College, University of Prince Edward Island, Charlottetown, Prince Edward Island, Canada
Susan M. Cotter, DVM, DACVIM (Small Animal Internal Medicine, Oncology) Distinguished Professor of Clinical Sciences Emerita, Department of Clinical Sciences, Cummings School of Veterinary Medicine, Tufts University North Grafton, Massachusetts
Nancy B. Cottrill, DVM, MS, DACVO Staff Ophthalmologist Massachusetts Veterinary Referral Hospital Woburn, Massachusetts
Laura Ridge Cousins, DVM, MS, DACVIM (Small Animal Internal Medicine) Upstate Veterinary Specialists, Greenville, South Carolina
Bronwyn Crane, DVM, MS, DACT Assistant Professor of Theriogenology, Department of Health Management, Atlantic Veterinary College University of Prince Edward Island, Charlottetown,
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Prince Edward Island, Canada
Kate E. Creevy, DVM, MS, DACVIM (Small Animal Internal Medicine) Assistant Professor, Small Animal Internal Medicine, Department of Small Animal Medicine and Surgery, College of Veterinary Medicine, University of Georgia Athens, Georgia
Andrew Cruikshank, DVM, DACVECC Animal Emergency and Treatment Center, Chicago, Illinois
Ashley Cruse, DVM, DACVIM Internal Medicine Department, Animal Emergency Referral Center, Torrance, California
Cheryl L. Cullen, DVM, MVetSc, DACVO Associate Professor, Comparative Ophthalmology, Department of Veterinary, Clinical and Diagnostic Sciences, Faculty of Veterinary Medicine, University of Calgary, Calgary, Alberta, Canada; CullenWebb Animal Neurology and Ophthalmology Centre, Riverview, New Brunswick, Canada
Anne M. Dalby, DVM, DACVIM (Small Animal Internal Medicine) Animal Emergency and Specialty Center, Parker, Colorado
Sylvie Daminet, DVM, PhD, DACVIM (Small Animal Internal Medicine), DECVIM-CA (Internal Medicine) Associate Professor, Department of Medicine and Clinical Biology of Small Animals, Faculty of Veterinary Medicine, Ghent University, Ghent, Belgium
Autumn Davidson, DVM, MS, DACVIM (Small Animal Internal Medicine) Clinical Professor, Department of Medicine and Epidemiology, College of Veterinary Medicine, University of California—Davis, Davis, California
Deborah Groppe Davis, DVM, DACVP Clinical Pathologist, IDEXX Laboratories North Grafton, Massachusetts
Douglas J. DeBoer, DVM, DACVD Professor of Dermatology, Department of Medical Sciences, School of Veterinary Medicine University of Wisconsin—Madison, Madison, Wisconsin
Camille DeClementi, VMD, DABVT, DABT Senior Director, Animal Health Services, American Society for the Prevention of Cruelty to Animals; Adjunct Instructor, Department of Veterinary Biosciences, College of Veterinary Medicine, University of Illinois Urbana, Illinois
Amy E. DeClue, DVM, MS, DACVIM (Small Animal Internal Medicine) Assistant Professor, Department of Veterinary Medicine and Surgery, College of Veterinary Medicine, University of Missouri Columbia, Missouri
Vincent E. Defalque, DMV, DACVD Dermatologist, Canada West Veterinary Specialists & Critical Care Hospital, Vancouver, British Columbia, Canada
Alice Defarges, DVM, MSc, DES, DACVIM (Small Animal Internal Medicine) Faculty, Internal Medicine Department of Clinical Studies Ontario Veterinary College, University of Guelph Guelph, Ontario, Canada
Teresa DeFrancesco, DVM, DACVIM (Cardiology), DACVECC Associate Professor in Cardiology and Critical Care, Department of Clinical Sciences, College of Veterinary Medicine North Carolina State University Raleigh, North Carolina
Caroline de Jaham, DMV, MSc, DACVD Director of Professional ServicesDMV Veterinary Center, Montreal, Québec; Associate Professor Faculty of Veterinary Medicine, University of Montreal
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Saint-Hyacinthe, Québec, Canada
Alexander de Lahunta, DVM, PhD, DACVIM, DACVP James Law Professor of Anatomy, Emeritus, Department of Biomedical Sciences, College of Veterinary Medicine Cornell University Ithaca, New York
Eric de Madron, DVM, DACVIM (Cardiology), DECVIM-CA (Internal Medicine) Head of Internal Medicine, Director of Referral Services, Alta Vista Animal Hospital Ottawa, Ontario, Canada
Helio Autran de Morais, DVM, MS, PhD, DACVIM (Small Animal Internal Medicine) Associate Professor, Medicine, Department of Clinical Sciences, College of Veterinary Medicine, Oregon State University, Corvallis, Oregon
Erika D. de Papp, DVM, DACVIM (Small Animal Internal Medicine) Service Director, Department of Internal Medicine, Angell Animal Medical Center Boston, Massachusetts
Curtis W. Dewey, DVM, DACVIM (Neurology), DACVS Chief, Section of Neurology Department of Clinical Sciences College of Veterinary Medicine Cornell University Ithaca, New York
Ravinder S. Dhaliwal, DVM, MS, DACVIM (Oncology), DABVP Oncologist Pet Care Veterinary Hospital Santa Rosa, California All Care Animal Referral Center Fountain Valley, California
Ursula M. Dietrich, DMV, MRCVS, DACVO, DECVO Associate Professor, Department of Small Animal Medicine and Surgery, College of Veterinary Medicine University of Georgia, Athens, Georgia
Pedro Paulo Vissotto de Paiva Diniz, DVM, PhD Assistant Professor of Small Animal Internal Medicine, College of Veterinary Medicine Western University of Health Sciences, Pomona, California
Caroline W. Donaldson, DVM, DABT Toxicologist, Animal Poison Control Center American Society for the Prevention of Cruelty to Animals, Urbana, Illinois
Kenneth J. Drobatz, DVM, MSCE, DACVIM (Small Animal Internal Medicine), DACVECC Associate Chair, Professor and Chief, Section of Critical Care, Director, Emergency Service, Department of Clinical Studies School of Veterinary Medicine University of Pennsylvania Philadelphia, Pennsylvania
Yvan Dumais, DVM Veterinary Dentist Centre Vétérinaire DMV Montreal, Québec, Canada
Eric K. Dunayer, MS, VMD, DABT, DABVT Senior Toxicologist, Animal Poison Control Center American Society for the Prevention of Cruelty to Animals, Urbana, Illinois
Marilyn Dunn, DVM, MVSc, DACVIM (Small Animal Internal Medicine) Associate Professor in Internal Medicine, Clinical Studies, Centre Hospitalier, Universitaire Vétérinaire Saint-Hyacinthe, Québec, Canada
Samuel D. Durkan, DVM, DACVECC Medical Director, Head of Emergency and Critical Care, Veterinary Referral and Emergency Center, Norwalk, Connecticut
N. Joel Edwards, DVM, DACVIM (Cardiology) Cardiology Upstate Veterinary Specialties Latham, New York
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Millicent Eidson, DVM, MA, DACVPM Research Scientist, New York State Department of Health Albany, New York
Bruce E. Eilts, DVM, MS, DACT Professor of Theriogenology Department of Veterinary Clinical Sciences, Veterinary Teaching Hospital and Clinic, Louisiana State University, Baton Rouge, Louisiana
Amara H. Estrada, DVM, DACVIM (Cardiology) Associate Professor and Associate Chair for Instruction, Department of Small Animal Clinical Sciences, College of Veterinary Medicine, University of Florida Gainesville, Florida
Michael R.D. Ethier, DVM, DVSc, DACVECC Director of Emergency and Critical Care Medicine, Intensive Care Toronto Veterinary Emergency and Referral Hospital, Toronto, Ontario, Canada
Stephen J. Ettinger, DVM, DACVIM (Small Animal Internal Medicine and Cardiology) California Animal Hospital Veterinary Specialty Group Los Angeles, California
Susan Ettinger, DVM, DACVIM (Oncology) Staff Oncologist Department of Oncology Animal Specialty Center Yonkers, New York
James F. Evermann, MS, PhD Professor Department of Veterinary Clinical Sciences, Washington Animal Disease Diagnostic Lab, College of Veterinary Medicine Washington State University Pullman, Washington
Patty J. Ewing, DVM, MS, DACVP Clinical Pathologist Department of Pathology, Angell Animal Medical Center Boston, Massachusetts
John Farrelly, DVM, MS, DACVIM (Oncology), DACVR (Radiation Oncology) Director of Radiation Oncology, The Animal Medical Center New York, New York
Wenche K. Farstad, DVM, Dr.scient., PhD, DECAR Professor, Department of Production Animal Clinical Sciences, Norwegian School of Veterinary Science Oslo, Norway
Karen K. Faunt, DVM, MS, DACVIM (Small Animal Internal Medicine) Vice President, Medical Quality Advancement, Banfield The Pet Hospital Portland, Oregon
Edward C. Feldman, DVM, DACVIM (Small Animal Internal Medicine) Professor of Small Animal, Internal Medicine and Department Chair, Department of Medicine and Epidemiology, School of Veterinary Medicine University of California—Davis, Davis, California
Nathaniel K. Fenollosa, DVM, DACVIM (Cardiology) Staff Cardiologist, VCA Shoreline Veterinary Referral and Emergency Center, Shelton, Connecticut
Alberto Fernandez, DVM Emergency and Critical Care Cape Cod Veterinary Specialists, Buzzards Bay, Massachusetts
Fidelia R. Fernandez, DVM, MS, DACVP (Clinical Pathology) Veterinary Clinical Pathologist Antech Diagnostics Cary, North Carolina
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Janean Fidel, MS, DVM, DACVR (Radiation Oncology), DACVIM (Oncology) Associate Professor, Department of Veterinary Clinical Sciences, College of Veterinary Medicine, Washington State University Pullman, Washington
Wendy D. Fife, DVM, MS, DACVR Veterinary Radiologist Diagnostic Imaging, P.C. Boulder, Colorado
Deborah M. Fine, DVM, MS, DACVIM (Cardiology) Assistant Professor, Department of Veterinary Medicine and Surgery College of Veterinary Medicine, University of Missouri, Columbia, Missouri
Linda S. Fineman, DVM, DACVIM (Oncology) Veterinary Oncologist Veterinary Medical Specialists Campbell, California
James M. Fingeroth, DVM, DACVS Senior Staff Surgeon Orchard Park Veterinary Medical Center, Orchard Park, New York; Veterinary Information Network Consultant, Surgery, Neurology, and Oncology Davis, California
James A Flanders, DVM, DACVS Associate Professor of Small Animal Surgery, Department of Clinical Sciences, College of Veterinary Medicine, Cornell University Ithaca, New York
Polly A. Fleckenstein, DVM, MS, CVA Veterinary Medical Center of Central New York Veterinary Medical Officer, National Veterinary Response Team—1; NDMS, DHHS, Veterinary Medical Officer, Veterinary Medical, Assistance Team—1; AVMA East Syracuse, New York
Andrea B. Flory, DVM, DACVIM (Oncology) Co-Chief Department of Medical Oncology, The Animal Medical Center New York, New York
Peter Michael Foley, MSc, DVM, DACVIM (Small Animal Internal Medicine) Assistant Professor of Companion Animal Internal Medicine, Department of Companion Animals, Atlantic Veterinary College University of Prince Edward Island, Charlottetown, Prince Edward Island, Canada
Thierry Francey, Dr.med. vet., DACVIM (Small Animal Internal Medicine) Vetsuisse Faculty, Department of Clinical Veterinary Medicine, Small Animal Clinic—Internal Medicine, University of Berne Laenggass-Strasse, Bern, Switzerland
Boel A. Fransson, DVM, PhD, DACVS Assistant Professor, Small Animal Surgery, Department of Veterinary Clinical Sciences, College of Veterinary Medicine, Washington State University Pullman, Washington
Lisa M. Freeman, DVM, PhD, DACVN Professor, Department of Clinical Sciences, Cummings School of Veterinary Medicine, Tufts University North Grafton, Massachusetts
Laura D Garrett, DVM, DACVIM (Oncology) Clinical Associate Professor, Oncology Veterinary Clinical Medicine College of Veterinary Medicine University of Illinois Urbana, Illinois
Frédéric P. Gaschen, Dr. med.vet., Dr.med.vet habil., DACVIM (Small Animal Internal Medicine), DECVIM-CA (Internal Medicine) Professor of Companion Animal Medicine, Department of Veterinary Clinical Sciences, School of Veterinary Medicine Louisiana State University Baton Rouge, Louisiana
Cynthia Gaskill, DVM, PhD Associate Professor Department of Veterinary Science, College of Agriculture University of Kentucky Lexington, Kentucky
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Stephen D. Gaunt, DVM, PhD, DACVP Professor of Veterinary Clinical Pathology, Department of Pathobiological Sciences, School of Veterinary Medicine Louisiana State University, Baton Rouge, Louisiana
Hans Gelens, DVM, MSc, DACVIM (Small Animal Internal Medicine) Associate Professor of Internal Medicine, Department of Companion Animals, Atlantic Veterinary College University of Prince Edward Island, Charlottetown, Prince Edward Island, Canada
Anna R.M. Gelzer, DMV, DACVIM (Cardiology), DECVIM-CA (Cardiology) Assistant Professor, Department of Clinical Sciences, College of Veterinary Medicine Cornell University Ithaca, New York
Anne J. Gemensky-Metzler, DVM, DACVO Associate Professor Department of Veterinary Clinical Sciences, College of Veterinary Medicine, The Ohio State University Columbus, Ohio
Tracy Gieger, DVM, DACVIM (Small Animal Internal Medicine), DACVR Assistant Professor Department of Veterinary Clinical Sciences, School of Veterinary Medicine Louisiana State University Baton Rouge, Louisiana
Mathieu M. Glassman, VMD Small Animal Surgery Resident, Department of Small Animal Medicine and Surgery College of Veterinary Medicine, University of Georgia Athens, Georgia
Tony Glaus, PD, DMV, DACVIM (Small Animal Internal Medicine), DECVIM-CA (Internal Medicine and Cardiology) Head Division of Cardiology, Clinic for Small Animal Internal Medicine, Vetsuisse Faculty, University of Zurich Zurich, Switzerland
Joseph C. Glennon, VMD, DACVS Staff Surgeon, Veterinary Specialties Referral Center, Pattersonville, New York, Adjunct Associate Professor of Surgery, Albany Medical College Albany, New York
Cristina Gobello, MV, DVM, Sm Anim Special, DECAR Senior Lecturer, Laboratory of Reproductive Physiology, Department of Basic Sciences Faculty of Veterinary Medicine, National University of La Plata La Plata, Argentina, Researcher, National Research Council, Argentina
Richard E. Goldstein, DVM, DACVIM (Small Animal Internal Medicine), DECVIM-CA Associate Professor Department of Clinical Sciences, College of Veterinary Medicine Cornell University Ithaca, New York
Kristine L Gonzales, DVM, DACT Staff Veterinarian Guide Dogs for the Blind, Inc. San Rafael, California
Lillian Good, DVM, DACVECC Criticalist Pacific Veterinary Specialists Capitola, California
Sonya G. Gordon, DVM, DVSc, DACVIM (Cardiology) Associate Professor Department of Small Animal Clinical Sciences, College of Veterinary Medicine and Biomedical Sciences, Texas A&M University College Station, Texas
Cecilia Gorrel, BSc, DDS, MA, Vet MB, DEVDC, Hon FAVD, MRCVS Director Petdent Ltd. Verwood, Dorset and Swindon, Wilthshire, Veterinary Dentistry, Oral and Maxillofacial Surgery Referrals, Veterinary Oral Health Consultancy, Pilley, Hampshire, United Kingdom
Kinga Gortel, DVM, MS, DACVD Staff Dermatologist, C.A.R.E. Centre Animal Hospital, Calgary, Alberta, Canada
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Ruanna E. Gossett, DVM, PhD, DACVP (Clinical Pathology) Clinical PathologistIDEXX, Inc. West Sacramento, California
Margherita Gracis, DMV, DAVDC, DEVDC Clinica Veterinaria San Siro Milano, Italy, Clinica Veterinaria Città di Codogno, Codogno (Lodi), Italy
Carlos M. Gradil, DVM, MS, PhD, DACT Associate Professor Department of Veterinary and Animal Sciences, College of Natural Sciences University of Massachusetts Amherst, Massachusetts
Kristi L. Graham, DVM, MS, DACVIM (Small Animal Internal Medicine) Staff Internist, VCA-Veterinary Specialty Center, Indianapolis, Indiana
Bradley A. Green, DVM Internal Medicine Service Puget Sound Veterinary Referral Center, Tacoma, Washington
Pascale Christine Griessmayr, DVM, DACVIM (Oncology) Oncology Lecturer Department of Clinical Studies School of Veterinary Medicine Matthew J. Ryan Veterinary Hospital, Philadelphia, Pennsylvania
Sophie Alexandra Grundy, BVSc (Hons), MACVSc, DACVIM (Small Animal Internal Medicine) Internist, Northern California Veterinary Specialists, Sacramento, California
Norma C. Guy, DVM, MSc Assistant Professor, Companion Animals Department of Companion Animals, Atlantic Veterinary College University of Prince Edward Island, Charlottetown, Prince Edward Island, Canada
Sharon Gwaltney-Brant, DVM, PhD, DABVT, DABT Vice President and Medical Director, ASPCA Animal Poison Control Center, Adjunct Instructor Department of Veterinary Biosciences, College of Veterinary Medicine, University of Illinois Urbana, Illinois
John J. Haburjak, DVM, DACVS Head, Department of Surgery Veterinary Surgical Centers—Berkeley, Dublin, San Francisco East Bay, California
Jens Häggström, DVM, PhD, DECVIM-CA (Cardiology) Professor Department of Clinical Sciences, Faculty of Veterinary Medicine and Animal Sciences, University Teaching Hospital Swedish University of Agricultural Sciences Uppsala, Sweden
Edward J. Hall, MA, VetMB, PhD, DECVIM-CA (Internal Medicine) Professor of Small Animal Internal Medicine, Clinical Veterinary Science University of Bristol, Langford, Bristol, United Kingdom
Michael Hannigan, BVMS, CertSAD, MRCVS Island Consulting Services Victoria, British Columbia, Canada
Joseph Harari, MS, DVM, DACVS Co-Owner Veterinary Surgical Specialists Spokane, Washington
Kenneth R. Harkin, DVM, DACVIM (Small Animal Internal Medicine) Associate Professor Department of Clinical Sciences, College of Veterinary Medicine, Kansas State University Manhattan, Kansas
John R. Hart, DVM, DACVIM (Small Animal Internal Medicine)
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Staff Internist, Veterinary Specialty Hospital of San Diego San Diego, California
Katrin Hartmann, Dr Vet Med, Dr Vet Med Habil, DECVIM-CA (Internal Medicine) Department Head Professor of Small Animal Internal Medicine, Clinic of Small Animal Medicine, Center of Clinical Veterinary Sciences, LMU University of Munich Munich, Germany
Colin Harvey, BVSc, FRCVS, DACVS, DAVDC, FAVD Professor of Surgery and Dentistry, Department of Clinical Studies School of Veterinary Medicine University of Pennsylvania Philadelphia, Pennsylvania
Timothy V. Hatt, DVM, CCRP Department Head, Associate Veterinarian, Physical Rehabilitation Oradell Animal Hospital Paramus, New Jersey
Joseph G. Hauptman, DVM, MS, DACVS Professor of Surgery, Department of Small Animal Clinical Sciences, College of Veterinary Medicine Michigan State University East Lansing, Michigan
Cristine L. Hayes, DVM Consulting Veterinarian in Clinical Toxicology, Animal Poison Control Center American Society for the Prevention of Cruelty to Animals, Urbana, Illinois
Timothy M. Hazzard, PhD, DVM Assistant Professor, Senior Research, Department of Animal Sciences College of Veterinary Medicine Oregon State University Corvallis, Oregon
Geoff Heffner, DVM, DACVECC Criticalist, Intern Director, Director of Emergency and Critical Care Services, Animal Hospital Specialty Center, Highlands Ranch, Colorado
Alicia K. Henderson, DVM, DACVIM (Small Animal Internal Medicine) Staff Internist, Garden State Veterinary Specialists Tinton Falls, New Jersey
Charles Hendrix, DVM, PhD Professor Department of Pathobiology College of Veterinary Medicine Auburn University Auburn, Alabama
Kate E. Hill, BVSc (Hons), DACVIM (Small Animal Internal Medicine) Senior Lecturer Small Animal Medicine, Institute of Veterinary, Animal and Biomedical Sciences, Massey University, New Zealand
Steve Hill, DVM, MS, DACVIM (Small Animal Internal Medicine) Staff Internist Department of Internal Medicine, Veterinary Specialty Hospital of San Diego, San Diego, California
Mark E. Hitt, DVM, MS, DACVIM (Small Animal Internal Medicine) Chief of Medicine Atlantic Veterinary Internal Medicine, LLC, Annapolis, Maryland
Daniel F. Hogan, DVM, DACVIM (Cardiology) Associate Professor, Cardiology, Department of Veterinary Clinical Sciences, School of Veterinary Medicine Purdue University West Lafayette, Indiana
R. Bruce, Hollett DVM, MS, DACT Associate Professor, Director of Continuing Education, Large Animal Medicine College of Veterinary Medicine University of Georgia Athens, Georgia
Steven R. Hollingsworth, DVM, DACVO Associate Professor of Clinical Ophthalmology, Department of Surgical and Radiological Sciences, School of Veterinary Medicine University of California—Davis, Davis, California
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Cheryl A. Holloway, RVT Animal Health Technician College of Veterinary Medicine The Ohio State University Columbus, Ohio
Jennifer L. Holm, DVM, DACVECC Service Director Emergency and Critical Care Angell Animal Medical Center Boston, Massachusetts
Ian Gordon Holsworth, BVSc (Hons), MACVSc (Surgery), DACVS Surgeon Veterinary Medical and Surgical Group Ventura, California
David Holt, BVSc, DACVS Professor of Surgery Department of Clinical Studies School of Veterinary Medicine University of Pennsylvania Philadelphia, Pennsylvania
Katherine Albro Houpt, VMD, PhD, DACVB Professor Emeritus College of Veterinary Medicine Cornell University Ithaca, New York
Bryan Hux, DVM Resident, Emergency and Critical Care, Department of Clinical Sciences, Small Animal Teaching Hospital, College of Veterinary Medicine Auburn University Auburn, Alabama
Shern Ihle, DVM, MS, DACVIM (Small Animal Internal Medicine) Associate Professor Department of Companion Animals, Atlantic Veterinary College University of Prince Edward Island, Charlottetown, Prince Edward Island, Canada
Edward Jazic, DVM, DACVD Dermatology for Animals Campbell, California
Albert E. Jergens, DVM, MS, DACVIM (Small Animal Internal Medicine) Professor, Staff Internist Department of Veterinary Clinical Sciences College of Veterinary Medicine Iowa State University Ames, Iowa
Cheri Johnson, DVM, MS, DACVIM (Small Animal Internal Medicine) Professor, Chief of Staff Department of Small Animal Clinical Sciences, College of Veterinary Medicine Michigan State University East Lansing, Michigan
Susan E. Johnson, DVM, MS, DACVIM (Small Animal Internal Medicine) Associate Professor, Service Head, Small Animal Internal Medicine, Department of Veterinary Clinical Sciences, College of Veterinary Medicine The Ohio State University Columbus, Ohio
Spencer A. Johnston, VMD, DACVS Edward H. Gunst Professor of Small Animal Surgery, Department of Small Animal Medicine and Surgery, College of Veterinary Medicine, University of Georgia Athens, Georgia
Soraya V. Juarbe-Díaz, DVM, DACVB Veterinary Behaviorist Tampa, Florida
Brett Kantrowitz, DVM, DACVR Veterinary Medical and Surgical Group Ventura, California
Bruce W. Keene, DVM, MSc, DACVIM (Cardiology) Professor, Attending Cardiologist Department of Clinical Sciences, Veterinary Teaching Hospital North Carolina State University Raleigh, North Carolina
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Ninette Keller, BVSc (Hons), MMedVet (Med) Senior Lecturer, Faculty of Medicine, Health and Molecular Sciences, School of Veterinary and Biomedical Sciences, James Cook University Townsville, Queensland, Australia
Marc Kent, DVM, DACVIM (Neurology, Small Animal Internal Medicine) Neurologist Department of Small Animal Medicine and Surgery College of Veterinary Medicine University of Georgia Athens, Georgia
Marie E. Kerl, DVM, DACVIM (Small Animal Internal Medicine), DACVECC Associate Teaching Professor Department of Small Animal Medicine and Surgery, College of Veterinary Medicine University of Missouri Columbia, Missouri
Frank Kettner, BSc (Hons), BVSc (Hons), MMedVet (Med) Internist, Medicine Clinic Tygerberg Animal Hospital—Bellville Cape Town, South Africa
Safdar A. Khan, DVM, MS, PhD, DABVT Director of Toxicology Research, ASPCA Animal Poison Control Center, Urbana, Illinois
Greg Kilburn, DVM, DACVIM (Neurology) Staff Neurologist/Neurosurgeon, Veterinary Emergency Clinic and Referral Center Toronto, Ontario, Canada
Michael A. Kiselow, DVM, DACVIM (Oncology) Associate Oncologist Department of Oncology Veterinary Medical Specialists Campbell, California
Barbara E. Kitchell, DVM, PhD, DACVIM (Small Animal Internal Medicine, Oncology) Professor and Director Center for Comparative Oncology, Department of Small Animal Clinical Sciences, College of Veterinary Medicine, Michigan State University East Lansing, Michigan
Karen L. Kline, DVM, MS, DACVIM (Neurology) Staff Neurologist Neurology and Neurosurgery, VCA Veterinary Specialty Center of Seattle Lynnwood, Washington
Michael W. Knight, DVM, DABVT, DABT Senior Toxicologist, Animal Poison Control Center American Society for the Prevention of Cruelty to Animals Urbana, Illinois
Marc S. Kraus, DVM, DACVIM (Small Animal Internal Medicine, Cardiology) Senior Lecturer Department of Clinical Sciences, College of Veterinary Medicine Cornell University Ithaca, New York
Donald R. Krawiec, DVM, MS, PhD, DACVIM (Small Animal Internal Medicine) President, Internist, Internal Medicine California Veterinary Specialists San Marcos, California
Michelle Kutzler, DVM, PhD, DACT Companion Animal Industries Department of Animal Sciences, College of Agricultural Sciences, Oregon State University Corvallis, Oregon
Tracy A. LaDue, DVM, DACVIM (Oncology), DACVR (Radiation Oncology) Oncologist Southeast Veterinary Oncology Orange Park, Florida
Elizabeth J. Laing, DVM, DVSc, DACVS Surgical Referral Service Fort Atkinson, Wisconsin
Leigh A. Lamont, DVM, MS, DACVA
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Associate Professor of Anesthesiology, Department of Companion Animals, Atlantic Veterinary College University of Prince Edward Island, Charlottetown, Prince Edward Island, Canada
Cathy E. Langston, DVM, DACVIM (Small Animal Internal Medicine) Staff Internist Nephrology, Urology, and Hemodialysis, Animal Medical Center New York, New York
Andrea C. Lantis, DVM, DACVIM (Cardiology) Assistant Professor Department of Small Animal Clinical Sciences, Virginia-Maryland Regional College of Veterinary, Medicine Virginia Polytechnic Institute and State University Blacksburg, Virginia
Nancy J. Laste, DVM, DACVIM (Cardiology) Department Head, Cardiology Angell Animal Medical Center Boston, Massachusetts
Susanne K. Lauer, DVM, DACVS, DECVS Assistant Professor Department of Veterinary Clinical Sciences, School of Veterinary Medicine Louisiana State University Baton Rouge, Louisiana
Richard A. LeCouteur, BVSc, PhD, DACVIM (Neurology), DECVN Professor Department of Surgical and Radiological Sciences, School of Veterinary Medicine University of California—Davis Davis, California
Alfred M. Legendre, DVM, MS, DACVIM (Small Animal Internal Medicine) Professor of Medicine and Oncology, Department of Small Animal Clinical Sciences, College of Veterinary Medicine University of Tennessee Knoxville, Tennessee
Bruce E. LeRoy, DVM, PhD, DACVP (Clinical Pathology) Assistant Professor Department of Pathology College of Veterinary Medicine University of Georgia Athens, Georgia
John R. Lewis, VMD, FAVD, DAVDC Assistant Professor of Dentistry and Oral Surgery, Department of Clinical Studies School of Veterinary Medicine University of Pennsylvania Philadelphia, Pennsylvania
James D. Lincoln, DVM, MS Associate Professor of Small Animal Surgery, Department of Veterinary Clinical Sciences, College of Veterinary Medicine Washington State University Pullman, Washington
David S. Lindsay, PhD Professor of Parasitology, Department of Biomedical Sciences and Pathobiology, Virginia-Maryland Regional College of Veterinary Medicine, Virginia Polytechnic Institute and State University Blacksburg, Virginia
Kathleen Linn, DVM, MS, DACVS Associate Professor of Small Animal Surgery, Small Animal Clinical Sciences Western College of Veterinary Medicine, University of Saskatchewan Saskatoon, Saskatchewan, Canada
Meryl P. Littman, VMD, DACVIM (Small Animal Internal Medicine) Associate Professor of Medicine, Department of Clinical Studies School of Veterinary Medicine University of Pennsylvania Philadelphia, Pennsylvania
Remo Lobetti, BVSc, MMedVet (Med), PhD, DECVIM-CA (Internal Medicine) Internist Bryanston Veterinary Hospital Bryanston, South Africa
Andrea Looney, DVM, DACVA Senior Lecturer Cornell University Veterinary Specialists, Stamford, Connecticut Senior Lecturer, Department of Clinical Sciences, Cornell University Hospital for Animals, College of Veterinary Medicine Cornell University Ithaca, New York
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Cheryl Lopate, MS, DVM, DACT President Reproductive Revolutions, Inc. Newberg, Oregon
Andrew Lowe, DVM, MSc, DACVD Dermatologist, Dermatology Fox Valley Animal Referral Center, Appleton, Wisconsin
Lori L. Ludwig, VMD, MS, DACVS Associate Veterinary Surgical Care Mount Pleasant, South Carolina
Virginia Luis-Fuentes, MA, VetMB, PhD, MRCVS, DACVIM (Cardiology), DECVIM-CA (Cardiology) Senior Lecturer Department of Veterinary Clinical Sciences, Royal Veterinary College North Mymms, Hatfield, United Kingdom
Jody P. Lulich, DVM, PhD, DACVIM (Small Animal Internal Medicine) Professor Minnesota Urolith Center, Department of Veterinary Clinical Sciences, College of Veterinary Medicine University of Minnesota St. Paul, Minnesota
Bertrand Lussier, DMV, MSc, DACVS Associate Professor Department of Clinical Sciences, Faculty of Veterinary Medicine University of Montreal Saint-Hyacinthe, Québec, Canada
Kristin MacDonald, DVM, PhD, DACVIM (Cardiology) Clinical Cardiologist VCA—The Animal Care Center of Sonoma Rohnert Park, California
Douglass K. Macintire, DVM, MS, DACVIM (Small Animal Internal Medicine), DACVECC Professor, Acute Medicine and Critical Care Department of Clinical Sciences, College of Veterinary Medicine Auburn University Auburn, Alabama
David J. Maggs, BVSc (hons), DACVO Associate Professor Department of Surgical and Radiological Sciences, School of Veterinary Medicine University of California—Davis Davis, California
Orla Mahony, MVB, DACVIM (Small Animal Internal Medicine), DECVIM-CA (Internal Medicine) Clinical Assistant Professor Department of Clinical Sciences, Cummings School of Veterinary Medicine, Tufts University North Grafton, Massachusetts
Herbert W. Maisenbacher, VMD, DACVIM (Cardiology) Clinical Lecturer Department of Small Animal Clinical Sciences, College of Veterinary Medicine University of Florida Gainesville, Florida
Rebecca L. Malakoff, DVM, DACVIM (Cardiology) Staff Cardiologist Cardiology Department Angell Animal Medical Center Boston, Massachusetts
Ann Marie Manning, DVM, DACVECC Chief of Staff Angell Animal Medical Center Boston, Massachusetts
Steven L. Marks, BVSc, MS, MRCVS, DACVIM (Small Animal Internal Medicine) Clinical Associate Professor of Critical Care and Internal Medicine, Department of Clinical Sciences, College of Veterinary Medicine North Carolina State University Raleigh, North Carolina
Melissa Marshall, DVM, DACVECC Emergency and Critical Care Red Bank Veterinary Hospital Tinton Falls, New Jersey
Charles Lloyd Martin, BS, DVM, MS, DACVO Professor Emeritus Department of Small Animal Medicine, College of Veterinary Medicine University of Georgia Athens, Georgia
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Kyle G. Mathews, DVM, MS, DACVS Professor, Small Animal Surgery, Department of Clinical Sciences, College of Veterinary Medicine North Carolina State University Raleigh, North Carolina
Glenna E. Mauldin, DVM, MS, DACVIM (Oncology), DACVN Western Veterinary Cancer Centre, Western Veterinary Specialist and Emergency Centre Calgary, Alberta, Canada
Janet Kovak McClaran, DVM, DACVS Staff Surgeon, Co-Director of Post-Graduate Education, The Animal Medical Center New York, New York
Carol McClure, DVM, MS, PhD, DACT Research Scientist Department of Health Management, Atlantic Veterinary College University of Prince Edward Island, Charlottetown, Prince Edward Island, Canada
Brendan C. McKiernan, DVM, DACVIM (Small Animal Internal Medicine) Staff Internist Southern Oregon Veterinary Specialty Center Medford, Oregon
Maureen A. McMichael, DVM, DACVECC Associate Professor, Service Chief—Emergency and Critical Care, Department of Veterinary Clinical Medicine, College of Veterinary Medicine University of Illinois Urbana, Illinois
Elizabeth A McNiel, DVM, PhD, DACVIM (Oncology) DACVR (Radiation Oncology) Assistant Professor Department of Small Animal Clinical Sciences, College of Veterinary Medicine Michigan State University East Lansing, Michigan
Irina Meadows, DVM, DABT Consulting Veterinarian in Clinical Toxicology, Animal Poison Control Center American Society for the Prevention of Cruelty to Animals Urbana, Illinois
Katrina L. Mealey, DVM, PhD, DACVIM (Small Animal Internal Medicine), DACVCP Professor Department of Veterinary Clinical Sciences, College of Veterinary Medicine Washington State University Pullman, Washington
Charlotte Means, DVM, MLIS, DABVT, DABT Senior Toxicologist, Animal Poison Control Center, American Society for the Prevention of Cruelty to Animals Urbana, Illinois
Michele Menard, DVM, MSc, PhD, DACVP VDIC, Inc. Clackamas, Oregon
Donna Alice Mensching, DVM, MS, DABVT, DABT Senior Toxicologist, Animal Poison Control Center, American Society for the Prevention of Cruelty to Animals, Urbana, Illinois
Kathryn M. Meurs, DVM, DACVIM (Cardiology), PhD Professor Veterinary Clinical Sciences College of Veterinary Medicine Washington State University Pullman, Washington
Kathryn E. Michel, DVM, MS, DACVN Associate Professor of Nutrition, Department of Clinical Studies School of Veterinary Medicine University of Pennsylvania Philadelphia, Pennsylvania
David Benno Miller, BVSc (Hons), MMedVet (Med) Head Physician Johannesburg Specialist, Veterinary Centre Johannesburg, South Africa
James B. Miller, DVM, MS, DACVIM (Small Animal Internal Medicine) Professor of Medicine Department of Companion Animals, Atlantic Veterinary College University of Prince Edward Island, Charlottetown, Prince Edward
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Island, Canada
Sarah J. Miller, DVM, DACVIM (Cardiology) Staff Cardiologist Southern California Veterinary Specialty Hospital Irvine, California
Michael B. Mison, DVM, DACVS Affiliate Assistant Professor Department of Comparative Medicine, University of Washington School of Medicine, Seattle, Washington; Staff Surgeon, Department of Surgery Seattle Veterinary Specialists Kirkland, Washington
Peter Moak, DVM Assistant Professor Department of Companion Animals, Atlantic Veterinary College University of Prince Edward Island, Charlottetown, Prince Edward Island, Canada
Lenore A. Mohammadian, DVM, MSpVM, DACVR Staff Radiologist, California Veterinary Specialist Carlsbad, California
Lisa E. Moore, DVM, DACVIM (Small Animal Internal Medicine) Affiliated Veterinary, Specialists Maitland, Florida
Phillip A. Moore, DVM, DACVO Associate Professor Department of Small Animal Medicine and Surgery, College of Veterinary Medicine University of Georgia Athens, Georgia
Adam Mordecai, DVM, MS, DACVIM (Small Animal Internal Medicine) Veterinary Specialty Center, Buffalo Grove, Illinois
Sherry J. Morgan, DVM, PhD, DACVP, DABT, DABVT Senior Project Director Preclinical Safety Abbott Laboratories Alto, New Mexico
Helen M.C. Munro, BVMS MRCVS Honorary Fellow Veterinary Pathology and Veterinary Clinical Studies, Royal (Dick) School of Veterinary Studies University of Edinburgh Edinburgh, Scotland, United Kingdom
Laura A. Nafe, DVM Resident Small Animal Internal Medicine, Department of Veterinary Medicine and Surgery College of Veterinary Medicine, University of Missouri Columbia, Missouri
Sarah L. Naidoo, DVM, MS, DACVIM (Small Animal Internal Medicine) Staff Internist The Emergency Animal Hospital Springfield, Oregon
Jill Narak, DVM, MS Assistant Professor, Neurology & Neurosurgery, Department of Small Animal Clinical Sciences College of Veterinary Medicine, University of Tennessee Knoxville, Tennessee
O. Lynne Nelson, DVM, MS, DACVIM (Small Animal Internal Medicine, Cardiology) Associate Professor of Cardiology Department of Veterinary Clinical Sciences, College of Veterinary Medicine Washington State University Pullman, Washington
Nicole Northrup, DVM, DACVIM (Oncology) Associate Professor Department of Small Animal Medicine and Surgery College of Veterinary Medicine, University of Georgia Athens, Georgia
Dennis P. O'Brien, DVM, PhD, DACVIM (Small Animal Internal Medicine)
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Professor of Neurology Department of Small Animal Medicine and Surgery College of Veterinary Medicine, University of Missouri Columbia, Missouri
Mauria A. O'Brien, DVM, DACVECC Clinical Assistant Professor Department of Veterinary Clinical Medicine, College of Veterinary Medicine, University of Illinois Urbana, Illinois
Karine M. Verstegen-Onclin, DVM, PhD, DECAR Clinical Assistant Professor Large Animal Clinical Sciences Companion Animal Theriogenology, College of Veterinary Medicine University of Florida Gainesville, Florida
Arthur I. Ortenburger, DVM, MS Associate Professor of Surgery Department of Health Management, Atlantic Veterinary College University of Prince Edward Island, Charlottetown, Prince Edward Island, Canada
João S. Orvalho, DVM, DACVIM (Cardiology) Cardiology Veterinary Medical Teaching Hospital, University of California San Diego, California
Carl Osborne, DVM, PhD, DACVIM (Small Animal Internal Medicine) Professor, Department of Veterinary Clinical Sciences, College of Veterinary Medicine, University of Minnesota St. Paul, Minnesota
M. Lynne O'Sullivan, DVM, DVSc, DACVIM (Cardiology) Associate Professor Department of Clinical Studies, Ontario Veterinary College University of Guelph Guelph, Ontario, Canada
Elizabeth O'Toole, BSc, DVM, DVSc, DACVECC Consultant Advanced Veterinary Care Toronto, Ontario, Canada
Therese E. O'Toole, DACVIM (Small Animal Internal Medicine) Assistant Clinical Professor Department of Clinical Sciences, Cummings School of Veterinary Medicine, Tufts University North Grafton, Massachusetts
Karen L. Overall, MA, VMD, PhD, DACVB, CAAB Research Associate Center for Neurobiology and Behavior, Department of Psychiatry School of Veterinary Medicine, University of Pennsylvania Philadelphia, Pennsylvania
LeeAnn Pack, DVM, DACVR Assistant Professor Department of Companion Animals, Atlantic Veterinary College University of Prince Edward Island, Charlottetown, Prince Edward Island, Canada
Phillip Padrid, DVM Regional Medical Director, VCA, New Mexico, Arizona, Nevada, Utab, Nebraska Associate Professor of Molecular Medicine, Pritzker School of Medicine University of Chicago Chicago, Illinois; Associate Professor, Small Animal Medicine School of Veterinary Medicine The Ohio State University Columbus, Ohio
Nadia Pagé, DMV MSc, DACVD Veterinary Dermatologist Centre Vétérinaire DMV Montreal (Lachine), Québec, Canada
Marc Papageorges, DVM, MS, PhD, DACVR Radiologist VDIC, Inc. Clackamas, Oregon
Manon Paradis, DMV, MVSc, DACVD Dermatology Professor Department of Clinical Sciences, Faculté de Médecine Vétérinaire, University of Montreal Saint-Hyacinthe, Québec, Canada
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Rosa Maria Páramo-Ramírez, MVZ, PhD Professor, Reproduction Department, Faculty of Veterinary, Medicine and Animal Husbandry, Universidad Nacional Autónomade Mexico—UNAM Ciudad de México, México
Adam P. Patterson, DVM, DACVD Clinical Assistant Professor of Dermatology, Department of Small Animal Clinical Sciences, College of Veterinary Medicine & Biomedical Sciences, Texas A&M University College Station, Texas
April L. Paul, DVM, DACVECC Director, Emergency and Critical Care Department, Tufts VETS Walpole, Massachusetts
Michael M. Pavletic, DVM, DACVS Director of Surgical Services Department of Surgery, Angell Animal Medical Center Boston, Massachusetts
Michael E. Peterson, DVM, MS Instructor, Toxicology Oregon State University Corvallis, Oregon; Associate Veterinarian Reid Veterinary Hospital Albany, Oregon
Polly B. Peterson, DVM, DACVIM (Small Animal Internal Medicine) Associate Veterinarian; Intern Director Internal Medicine, VCA Veterinary Specialty Center of Seattle Lynnwood, Washington
Fred S. Pike, DVM, DACVS Surgeon Veterinary Specialty Hospital San Diego, California
Chantale L. Pinard, DVM, MSc, DACVO Assistant Professor Department of Clinical Studies Ontario Veterinary College University of Guelph Guelph, Ontario, Canada
Carlos R.F. Pinto, MedVet, PhD, DACT Associate Professor Service Head, Theriogenology and Reproductive Medicine, Department of Veterinary Clinical Sciences, College of Veterinary Medicine The Ohio State University Columbus, Ohio
Caryn E. Plummer, DVM, DACVO Assistant Professor of Comparative Ophthalmology, Departments of Small and Large Animal Clinical Sciences, Veterinary Medical Center College of Veterinary Medicine University of Florida Gainesville, Florida
Dan Polidoro, DVM Staff Surgeon Animal Surgical & Emergency Center Los Angeles, California
Brandy Porterpan, DVM, DACVIM (Small Animal Internal Medicine) Internist Animal Diagnostic Clinic Dallas, Texas
Thomas Mitchell Potter, DVM Resident, Small Animal Emergency and Critical Care Department of Clinical Sciences, College of Veterinary Medicine, Auburn University Auburn, Alabama
Barrak M. Pressler, DVM, PhD, DACVIM (Small Animal Internal Medicine) Assistant Professor of Internal Medicine, Department of Veterinary Clinical Sciences, School of Veterinary Medicine Purdue University West Lafayette, Indiana
Robert Prošek, DVM, MS, DACVIM (Cardiology), DECVIM-CA (Cardiology) Adjunct Professor of Cardiology, Department of Small Animal Medicine, University of Florida Gainesville, Florida Veterinary Specialists Inc.—Animal Heart Centers, Homestead, Florida Director Veterinary Institute for Interventional Therapy Ft. Lauderdale, Florida
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David R. Proulx, BS, MSpVM, DACVIM (Oncology), DACVR (Radiation Oncology) Head of Radiation Oncology California Veterinary Specialists San Marcos, California
David A. Puerto, DVM, DACVS Chief of Surgery Department of Surgery Center for Animal Referral and Emergency Services Langhorne, Pennsylvania
Gary Puglia, DVM Emergency and Critical Care Resident, Department of Clinical Sciences, Cummings School of Veterinary Medicine, Tufts University North Grafton, Massachusetts
Beverly J. Purswell, DVM, PhD, DACT Professor Department of Large Animal Clinical Sciences, Virginia-Maryland Regional College of Veterinary Medicine, Virginia Polytechnic Institute and State University Blacksburg, Virginia
Richard F. Quinn, DVM, DVSc, DACVO Veterinary Eye Specialists Denfield, Ontario, Canada
MaryAnn Radlinsky, DVM, MS, DACVS Associate Professor Department of Small Animal Medicine and Surgery, College of Veterinary Medicine University of Georgia Athens, Georgia
Louisa J. Rahilly, DVM, DACVECC Emergency and Critical Care Department Supervisor, Department of Emergency and Critical Care, Cape Cod Veterinary Specialist Buzzards Bay, Massachusetts
Gregg Rapoport, DVM, DACVIM (Cardiology) Assistant Professor, Department of Small Animal Medicine and Surgery, College of Veterinary Medicine University of Georgia Athens, Georgia
Kenneth M. Rassnick, DVM, DACVIM (Oncology) Assistant Professor of Oncology, Department of Clinical Sciences, College of Veterinary Medicine Cornell University Ithaca, New York
Jennifer E. Rawlinson, DVM, DAVDC Chief, Section of Dentistry and Oral Surgery, Department of Clinical Sciences, College of Veterinary Medicine Cornell University Ithaca, New York
Carol R. Reinero, DVM, DACVIM (Small Animal Internal Medicine), PhD Assistant Professor of Small Animal Internal Medicine, Department of Veterinary Medicine and Surgery, College of Veterinary Medicine University of Missouri Columbia, Missouri
Adam J. Reiss, DVM, DACVECC Veterinarian Department of Emergency/Critical Care, Southern Oregon Veterinary Specialty Center Medford, Oregon
Alexander M. Reiter, Dipl TZt, Dr Med Vet, DAVDC, DEVDC Associate Professor of Dentistry and Oral Surgery, Department of Clinical Sciences, School of Veterinary Medicine University of Pennsylvania Philadelphia, Pennsylvania
Elaine Reveler, ACT Veterinary Technologist Small Animal Hospital, Atlantic Veterinary College University of Prince Edward Island, Charlottetown, Prince Edward Island, Canada
Keith Richter, DVM, DACVIM (Small Animal Internal Medicine) Hospital Director, Staff Internist, Veterinary Specialty Hospital of San Diego San Diego, California
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Valeria Rickard, DVM Veterinarian/Chief of Staff North Oatlands Animal Hospital Leesburg, Virginia
Marcella D. Ridgway, VMD, MS, DACVIM (Small Animal Internal Medicine) Clinical Assistant Professor of Small Animal Medicine, Department of Veterinary Clinical Medicine, Veterinary Teaching Hospital University of Illinois Urbana, Illinois
Wesley J. Roach, DVM Small Animal Surgery Resident, Department of Small Animal Medicine and Surgery College of Veterinary Medicine, University of Georgia Athens, Georgia
Carlos O. Rodriguez, DVM, PhD, DACVIM (Oncology) Lecturer Department of Surgical and Radiological Sciences, School of Veterinary Medicine University of California—Davis, Davis, California;Staff Oncologist, San Francisco Veterinary Specialists San Francisco, California
Catherine L. Rogers, DVM, DACVECC Staff Veterinarian Emergency & Critical Care Medicine, Angell Animal Medical Center Boston, Massachusetts
Elisa Petrollini Rogers, CVT, VTS (ECC) Assistant Nursing Supervisor Emergency Service, Matthew J. Ryan Veterinary Hospital, College of Veterinary Medicine, University of Pennsylvania Philadelphia, Pennsylvania
Patricia L. Rose, DVM, MS, DACVS, DACVR Radiologist Veterinary Radiology Ltd. Beachwood, Ohio
Tracey A. Rossi, DVM, DACVIM (Small Animal Internal Medicine) Southern California Veterinary Specialty Hospital Irvine, California
Lois Roth-Johnson, DVM, PhD, DACVP President Dual Boarded, Inc. Eastham, Massachusetts
Philip Roudebush, DVM, DACVIM (Small Animal Internal Medicine) Director of Scientific Affairs and Technical Information Services, Hill's Pet Nutrition, Inc. Topeka, Kansas;Adjunct Professor Department of Clinical Sciences, College of Veterinary Medicine Kansas State University Manhattan, Kansas
Elizabeth A. Rozanski, DVM, DACVECC, DACVIM (Small Animal Internal Medicine) Assistant Professor Department of Clinical Sciences, Cummings School of Veterinary Medicine, Tufts University North Grafton, Massachusetts
Katrin Saile, DVM, MS Resident, Small Animal Surgery, Department of Clinical Sciences, College of Veterinary Medicine, Auburn University Auburn, Alabama
Véronique Sammut, DVM, MS, DACVIM (Neurology) Neurologist Vet Surg and Neurology Woodland Hills, California
Sherry Lynn Sanderson, BS, DVM, PhD, DACVIM (Small Animal Internal Medicine), DACVN Associate Professor Department of Physiology and Pharmacology, College of Veterinary Medicine University of Georgia Athens, Georgia
Lynne S. Sandmeyer, DVM, DVSc, DACVO Associate Professor, Ophthalmology Department of Small Animal Clinical Sciences Western College of Veterinary Medicine University of Saskatchewan Saskatoon, Saskatchewan, Canada
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John S. Sapienza, DVM, DACVO Staff Ophthalmologist, Department Chair Ophthalmology, Long Island Veterinary Specialists Plainview, New York
Frédéric Sauvé, DVM, MSc, DES, DACVD Clinical Instructor Centre Hospitalier Universitaire Vétérinaire, Faculté de médecine vétérinaire, University of Montreal Saint-Hyacinthe, Québec, Canada
Michael Schaer, DVM, DACVIM (Small Animal Internal Medicine), DACVECC Professor and Special Assistant to the Dean Department of Small Animal Clinical Sciences, College of Veterinary Medicine University of Florida Gainesville, Florida
Mary M. Schell, DVM, DABT, DABVT Senior ToxicologistASPCA/Animal Poison Control Center Urbana, Illinois
Patricia A. Schenck, DVM, PhD Section Chief, Endocrine Diagnostic Section, Diagnostic Center for Population and Animal Health; Assistant Professor Department of Pathobiology and Diagnostic Investigation, College of Veterinary Medicine Michigan State University Lansing, Michigan
Mandi Schmidt, DVM Resident, Cardiology Department of Small Animal Clinical Sciences, College of Veterinary Medicine University of Florida Gainesville, Florida
Johan P. Schoeman, BVSc, DSAM, MMedVet(Med), PhD, DECVIM-CA (Internal Medicine) Professor of Small Animal Internal Medicine, Head of Department of Companion Animal Clinical Studies, University of Pretoria;Specialist Physician, Onderstepoort Veterinary Academic Hospital Pretoria, South Africa
Diana M. Schropp, DVM, DACVECC Staff Veterinarian Southern Oregon Veterinary Specialty Center, Medford, Oregon
Danny W. Scott, DVM, DACVD Professor of Medicine Department of Clinical Sciences, College of Veterinary Medicine, Cornell University Ithaca, New York
Kersti Seksel, BVSc (Hons), MRCVS, MA (Hons), FACVSc (Animal Behavior), DACVB, DECVBM-CA Adjunct Senior Lecturer Charles Sturt University Wagga Wagga, New South Wales; Director Behavioural Service Sydney Animal Behaviour Service, Sydney, New South Wales;Director Behavioural Service, Melbourne Veterinary Specialist Centre Melbourne, Victoria, Australia
Rance K. Sellon, DVM, PhD, DACVIM (Small Animal Internal Medicine, Oncology) Associate Professor Department of Veterinary Clinical Sciences, College of Veterinary Medicine, Washington State University Pullman, Washington
Kim A. Selting, DVM, MS, DACVIM (Oncology) Assistant Teaching Professor Department of Veterinary Medicine and Surgery, College of Veterinary Medicine University of Missouri Columbia, Missouri
Jonathan Shani, BSc, DVM, DECVS Director of Surgery Department of Surgery Knowledge Farm Beit Berl, Kfar Saba, Israel
Claire R. Sharp, BSc, BVMS (Hons), MS Assistant Professor Department of Veterinary Clinical Sciences Cummings School of Veterinary Medicine, Tufts University North Grafton, Massachusetts
Darcy H. Shaw, DVM, MVSc, MBA, DACVIM (Small Animal Internal Medicine) Associate Dean, Professional Services, Department of Companion Animals, Atlantic Veterinary College University of Prince Edward Island, Charlottetown, Prince Edward Island, Canada
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Scott P. Shaw, DVM, DACVECC Assistant Professor Department of Clinical Sciences, Cummings School of Veterinary Medicine, Tufts University North Grafton, Massachusetts
G. Diane Shelton, DVM, PhD, DACVIM (Small Animal Internal Medicine) Professor Department of Pathology;Director, Comparative Neuromuscular Laboratory, School of Medicine University of California—San Diego La Jolla, California
Sharon L. Shields, DVM, DACVS Surgeon Veterinary Specialty Center Tucson, Arizona
Andy Shores, DVM, MS, PhD, DACVIM (Neurology) Clinical Professor Neurosurgery and Neurology Department of Clinical Sciences, College of Veterinary Medicine Auburn University Auburn, Alabama
David Sisson, DVM, DACVIM (Cardiology) Professor of Cardiovascular Medicine, Department of Clinical Sciences, College of Veterinary Medicine, Oregon State University Corvallis, Oregon
Meg Sleeper, VMD, DACVIM (Cardiology) Associate Professor of Cardiology, Department of Clinical Studies, School of Veterinary Medicine University of Pennsylvania Philadelphia, Pennsylvania
Frances O. Smith, DVM, PhD, DACT Adjunct Clinical Professor Department of Small Animal Clinical Sciences, College of Veterinary Medicine, University of Minnesota St. Paul, Minnesota; Owner, Smith Veterinary Hospital, Inc., Burnsville, Minnesota; President, Orthopedic Foundation for Animals, Inc. Columbia, Missouri
Mark M. Smith, VMD, DACVS, DAVDC Center for Veterinary Dentistry and Oral Surgery Gaithersburg, Maryland
Saralyn Smith-Carr, DVM, PhD, DACVIM (Small Animal Internal Medicine) Associate Professor Department of Clinical Sciences College of Veterinary Medicine Auburn University Auburn, Alabama
Elisabeth L.R. Snead, BSc, DVM, MSc, DACVIM (Small Animal Internal Medicine) Associate Professor Department of Small Animal Clinical Sciences, Western College of Veterinary Medicine, University of Saskatchewan Saskatoon, Saskatchewan, Canada
Katherine D. Snyder, DVM, DACVIM (Small Animal Internal Medicine) Lecturer, Internal Medicine and Emergency/Critical Care Department of Small Animal Clinical Sciences, College of Veterinary Medicine and Biomedical Sciences, Texas A&M University College Station, Texas
Mary E. Somerville, DVM, DACVS Staff Surgeon Animal Surgical Emergency Center, Los Angeles, California
Dennis Spann, DVM, DACVIM (Small Animal Internal Medicine) Staff Internist, Loomis Basin Veterinary Clinic Loomis, California
Jonathan Spears, DVM, MVSc Assistant Professor Department of Biomedical Sciences, Atlantic Veterinary College University of Prince Edward Island Charlottetown, Prince Edward Island, Canada
Erick S. Spencer, DVM, MS, DACVIM (Small Animal Internal Medicine) Clinical Assistant Professor Department of Veterinary Clinical Sciences, College of Veterinary Medicine Washington State University Pullman, Washington
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Alan W. Spier, DVM, PhD, DACVIM (Cardiology) Staff Cardiologist Florida Veterinary Specialists Tampa, Florida
Jörg M. Steiner, Dr Med Vet, PhD, DACVIM (Small Animal Internal Medicine), DECVIM-CA (Internal Medicine) Associate Professor and Director, Gastrointestinal Laboratory Department of Small Animal Clinical Sciences, College of Veterinary Medicine and Biomedical Sciences, Texas A&M University College Station, Texas
Rebecca L. Stepien, DVM, MS, DACVIM (Cardiology) Clinical Professor Department of Medical Sciences, School of Veterinary Medicine University of Wisconsin;Clinical Cardiologist Section Head, Cardiopulmonary ServiceU.W. Veterinary Care Madison, Wisconsin
Vladimir Stojanovic, DVM Resident, Small Animal Internal Medicine, Department of Companion Animals, Atlantic Veterinary Collage University of Prince Edward Island, Charlottetown, Prince Edward Island, Canada
Michael Stone, DVM, DACVIM (Small Animal Internal Medicine) Clinical Assistant Professor Department of Clinical Studies, Cummings School of Veterinary Medicine, Tufts University North Grafton, Massachusetts;Associate Veterinarian, Veterinary Internal Medicine Mobile Specialists North Woodstock, Connecticut
Elizabeth Streeter, DVM, DACVECC Emergency and Critical Care Medicine Eastern Iowa Veterinary Specialty Center, Cedar Rapids, Iowa
Keith N. Strickland, DVM, DACVIM (Cardiology) President Veterinary Cardiac Consultations, LLC, Baton Rouge, Louisiana
Shannon Stroup, DVM, MS, DACVIM (Small Animal Internal Medicine) Associate Department of Internal Medicine, Louisiana Veterinary Referral Center, Mandeville, Louisiana
Jan S. Suchodolski, MedVet, DrMedVet, PhD Clinical Assistant Professor and Associate Director Gastrointestinal Laboratory, Department of Small Animal Clinical Sciences, College of Veterinary Medicine and Biomedical Sciences, Texas A&M University College Station, Texas
Catherine M. Sumner, DVM Emergency Medicine/Critical Care Resident, Department of Emergency and Critical Care, Cummings School of Veterinary Medicine, Tufts University North Grafton, Massachusetts; Tufts Veterinary Emergency Treatment Services Walpole, Massachusetts
Graham Swinney, BVSc, FACVSc Canine Medicine Specialist Veterinary Teaching Hospital University of Sydney; Internal Medicine ConsultantIDEXX Laboratories, Sydney, New South Wales, Australia
Jane Sykes, BVSc (Hons), PhD, DACVIM (Small Animal Internal Medicine) Professor of Small Animal Medicine, Department of Medicine and Epidemiology, School of Veterinary Medicine University of California—Davis Davis, California
Joseph Taboada, DVM, DACVIM (Small Animal Internal Medicine) Associate Dean Office of Student and Academic Affairs; Professor of Small Animal Internal Medicine Department of Veterinary Clinical Sciences, School of Veterinary Medicine Louisiana State University Baton Rouge, Louisiana
Lauren R. Talarico, DVM Neurology/Neurosurgery Resident Department of Clinical Sciences, Hospital for Animals College of Veterinary Medicine, Cornell University Ithaca, New York
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Jaime Tarigo, DVM, DACVP Resident, Clinical Pathology Department of Comparative Biomedical Sciences, College of Veterinary Medicine, North Carolina State University Raleigh, North Carolina
Karen M. Tefft, DVM, DACVIM (Small Animal Internal Medicine) Assistant Professor of Internal Medicine, Department of Companion Animals, Atlantic Veterinary College University of Prince Edward Island, Charlottetown, Prince Edward Island, Canada
William B. Thomas, DVM, MS, DACVIM (Neurology) Professor, Neurology and Neurosurgery, Department of Small Animal Clinical Sciences, College of Veterinary Medicine, University of Tennessee Knoxville, Tennessee
Michael Thrusfield, MSc, BVMS, DTVM, CBiol, FSB, DECVPH, MRCVS Veterinary Clinical Studies Royal (Dick) School of Veterinary Studies, University of Edinburgh Roslin, Midlothian, United Kingdom
D. Michael Tillson, DVM, MS, DACVS Professor, Small Animal Surgery Department of Clinical Sciences, College of Veterinary Medicine Auburn University Auburn, Alabama
Karen M. Tobias, DVM, MS, DACVS Professor Department of Small Animal Clinical Sciences, College of Veterinary Medicine University of Tennessee Knoxville, Tennessee
Danna M. Torre, DVM, DACVECC Veterinary SpecialistVCA Shoreline Veterinary Referral and Emergency Center, Shelton, Connecticut
Nicholas J. Trout, MA, VetMB, MRCVS, DACVS, DECVS Staff Surgeon Angell Animal Medical Center Boston, Massachusetts
Mark T. Troxel, DVM, DACVIM (Neurology) Staff Neurologist, Neurosurgeon, Neurology & Neurosurgery Department, Massachusetts Veterinary Referral Hospital Woburn, Massachusetts
David C. Twedt, DVM, DACVIM (Small Animal Internal Medicine) Professor Department of Clinical Sciences, College of Veterinary Medicine and Biomedical Sciences, Colorado State University Fort Collins, Colorado
Shelly Vaden, DVM, PhD, DACVIM (Small Animal Internal Medicine) Professor, Internal Medicine Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University Raleigh, North Carolina
Beth A. Valentine, DVM, PhD, DACVP Professor Department of Biomedical Sciences, College of Veterinary Medicine, Oregon State University Corvallis, Oregon
Liesel van der Merwe, BVSc (Hons) MRCVS Faculty of Veterinary Science, Department of Companion Animal Clinical Studies Faculty of Veterinary Medicine, University of Pretoria Onderstepoort, South Africa
Mirinda (Nel) van Schoor, BVSc (Hons), MMedVet (Med) Senior Lecturer, Small Animal Internal Medicine, Department of Companion Animal Clinical Studies, Faculty of Veterinary Science University of Pretoria Onderstepoort, South Africa
Leen Verhaert, DVM, DEVDC Practice Assistant Department of Medicine and Clinical Biology of Small Animals, Faculty of Veterinary Medicine, Ghent University Merelbeke, Belgium;Associate, Trivet Veterinary Practice Hove, Belgium
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John P. Verstegen, DVM, MSc, PhD, DECAR Associate Professor Companion Animal Theriogenology, Department of Large Animal Clinical Sciences College of Veterinary Medicine, University of Florida Gainesville, Florida
Dietrich Volkmann, BVSc, MMedVet, DACT Professor in Theriogenology Department of Veterinary Medicine and Surgery, College of Veterinary Medicine, University of Missouri Columbia, Missouri
Lori S. Waddell, DVM, DACVECC Adjunct Assistant Professor of Critical Care Department of Clinical Studies, Matthew J. Ryan Veterinary Hospital, School of Veterinary Medicine University of Pennsylvania Philadelphia, Pennsylvania
Stephen Waisglass, BSc, DVM, CertSAD, DACVD Adjunct Professor Veterinary Dermatologist Dermatology Referral Service Veterinary Emergency Clinic and Referral Centre, Ontario Veterinary College University of Guelph Toronto, Ontario, Canada
Thomas Walker, DVM, DACVECC Assistant Professor of Pharmacology, Toxicology and Emergency Medicine, Department of Pathobiology School of Veterinary Medicine Ross University St Kitts, West Indies
Richard Walshaw, BVMS, DACVS Surgical Oncologist Animal Cancer and Imaging Center Canton, Michigan
Aubrey Webb, DVM, PhD Assistant Professor Department of Clinical Neurosciences, Faculty of Medicine, University of Calgary, Calgary, Alberta, Canada;Cullen Webb Animal Neurology and Ophthalmology Centre, Riverview, New Brunswick, Canada
Craig B. Webb, PhD, DVM, DACVIM (Small Animal Internal Medicine) Associate Professor Department of Clinical Sciences, College of Veterinary Medicine, Colorado State University Fort Collins, Colorado
Cynthia R.L. Webster, DVM, DACVIM (Small Animal Internal Medicine) Professor Department of Clinical Science, Cummings School of Veterinary Medicine Tufts University North Grafton, Massachusetts
Lisa P. Weeth, DVM, DACVN Clinical Nutritionist Red Bank Veterinary Hospital Tinton Falls, New Jersey
Claire M. Weigand, DVM, DACVIM (Small Animal Internal Medicine) Department of Internal Medicine, Veterinary Emergency and Specialty Hospital, South Deerfield, Massachusetts
Kristin M. Welch, DVM Resident, Emergency and Critical Care, Foster Hospital for Small Animals, Cummings School of Veterinary Medicine, Tufts University North Grafton, Massachusetts
Sharon L. Welch, DVM, DABVT, DABT Senior Toxicologist, Animal Poison Control Center American Society for the Prevention of Cruelty to Animals Urbana, Illinois
Elizabeth G. Welles, DVM, PhD, DACVP Professor Department of Pathobiology College of Veterinary Medicine, Auburn University Auburn, Alabama
Jocelyn Wellington, DVM, DACVD Dermatologist Animal Dermatology Services London, Ontario, Canada
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Aaron C. Wey, DVM, DACVIM (Cardiology) Cardiology Upstate Veterinary Specialties, PLLCLatham, New York
Richard Wheeler, DVM, DACT Faculty Department of Clinical Sciences, College of Veterinary Medicine, Colorado State University; Owner, Poudre River Veterinary Clinic, LLCFort Collins, Colorado
Megan Whelan, DVM, DACVECC Intern Director Department of Emergency and Critical Care, Angell Animal Medical Center Boston, Massachusetts
Christine L. Wilford, DVM Associate Veterinarian Cats Exclusive Veterinary Center Shoreline, Washington
David A. Wilkie, DVM, MS, DACVO Professor Department of Veterinary Clinical Sciences, College of Veterinary Medicine, The Ohio State University Columbus, Ohio
Michael Willard, DVM, MS, DACVIM (Small Animal Internal Medicine) Professor Department of Small Animal Clinical Sciences, College of Veterinary Medicine and Biomedical Sciences, Texas A&M University College Station, Texas
Laurel E. Williams, DVM, DACVIM (Oncology) Associate Professor Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University Raleigh, North Carolina
Jennifer E. Winter, DVM, DACVIM (Oncology) Medical Oncologist Southeast Veterinary Oncology Orange Park, Florida
Kimberly B. Winters, DVM, DACVIM (Small Animal Internal Medicine) Staff Internist Department of Internal Medicine, Animal Specialty Group Los Angeles, California
Tina Wismer, DVM, DABVT, DABT Senior Director of Veterinary Outreach and Education, Animal Poison Control Center American Society for the Prevention of Cruelty to Animals Urbana, Illinois
Christina Marie Wolf, DVM, DACVIM (Small Animal Internal Medicine) Louisville Veterinary Specialty & Emergency Services Louisville, Kentucky
Michael W. Wood, DVM, DACVIM (Small Animal Internal Medicine), PhD Clinical Assistant Professor Department of Population Health and Pathobiology, College of Veterinary Medicine North Carolina State University Raleigh, North Carolina
Kathy Wright, DVM, DACVIM (Cardiology, Small Animal Internal Medicine) Director of Cardiology Department of Medicine The CARE Center Cincinnati, Ohio
Hany M. Youssef, DVM, MS, BVSc Consulting Veterinary in Clinical Toxicology, Animal Poison Control Center American Society for the Prevention of Cruelty to Animals, Urbana, Illinois
Anthony A. Yu, DVM, MS, DACVD Associate Professor Department of Dermatology Ontario Veterinary College University of Guelph Guelph, Ontario, Canada
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Debra L. Zoran, DVM, PhD, DACVIM (Small Animal Internal Medicine) Associate Professor and Chief of Medicine, Department of Small Animal Clinical Sciences, College of Veterinary Medicine and Biomedical Sciences, Texas A&M University College Station, Texas
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Preface “Not what we have, but what we enjoy, constitutes our abundance.” -J Petit-Senn A second edition is both an opportunity and an enigma. It is an opportunity to improve on the original, to make it bigger, more insightful, clearer—simply better. Coming on the heels of a first edition that was very well received, it is a pleasure for us to aim higher. But if the original was a success, the revision is also an enigma, or even a hazard: how do we make a book that keeps the best of the old while adding the most of the new? The Clinical Veterinary Advisor: Dogs and Cats, second edition, has aimed from the very beginning to find the best possible balance in this regard. The basic structure and content of the book should be recognizable to all readers of the first edition. Nevertheless, there are many innovations to be found here. There are all-encompassing changes within the repeating template structure of chapters, and there are also dozens of individual new chapters. Individual overview statements in 800 of the chapters now help guide the readerpractitioner toward implementing recommendations in a practical fashion. A great deal of new information for clients and for technicians is now available. Every chapter that was included in the first edition appears again in the second edition fully revised and updated; some have changed names to remain current (hemobartonellosis now appears as hemotropic mycoplasmosis, hepatocutaneous syndrome is now superficial necrolytic dermatitis, and so on), but users of the first edition can be assured that they will find up-to-date versions of all chapters in this edition. This has indeed been the greatest challenge: keeping the very best, trimming or condensing obsolete or duplicated facts, and introducing worthwhile new material. Doing so has required a herculean effort from authors and editors. George Bernard Shaw faced the same issue when he finished a letter of recommendation for a friend. In a note pinned to the letter, Shaw wrote, “Sorry the letter is so long. I didn't have time to write you a short one.” Similarly, the Advisor's authors and section editors had ample material at their disposal, but unlike Shaw, they seem to have spared no effort in distilling the most valuable essentials out of it. Their efforts translate into chapters that are focused, user-friendly, and up to date. Like the unreachable horizon, the permanent goal for which the Advisor will continue to strive is for its users to read each paragraph on every page and think “This is exactly what I wanted to know.” A new edition is justified when there has been substantial change, and updates need to be introduced. These improvements should be evident to all readers through both changes in existing chapters, and the introduction of new chapters. Over 60 new topics have been created and added to this new edition. They are summaries of a wide range of disorders such as the MDR-1 (ABCB1) mutation, Xylitol toxicosis, Adulterated diets, Fear due to veterinary visits, Canine influenza, and dozens of others. The novelty of these topics is matched by their clinical relevance, and the appearance of these new chapters is a testament to their importance in veterinary practice. They are presented in the same chronological template format that reflects the way the patient is received and treated: Background information, then chief complaint and history, then physical exam, then analysis (etiology, pathophysiology, differential diagnosis), diagnosis, treatment, and outcome. Every topic has one or more current Suggested Reading sources for additional information, and these have, as much as possible, been drawn from easily accessible journals and textbooks. There are many, many new photographs and illustrations, to convey information graphically for those of us who are visual learners. The photographs in the printed version of the book are also available in color in the online edition of the book. Over a dozen new Procedures and Techniques have been added, bringing the number of procedure descriptions to over 100. These additions range from the immediately practical (Porcupine quill removal, Breeding soundness exam, Nebulization/coupage/respiratory therapeutics) to the referral-level (Tracheal stent placement, Ethanol ablation of parathyroid nodules, Brain biopsy [stereotactic]). As before, these procedures are described in a step-wise, template-based format, and their inclusion is as much for clinicians involved in actually performing them as for attending veterinarians who plan to refer the patient and simply want to understand what is involved in the procedure. An important set of specific improvements applied en masse to all Section I (Diseases & Disorders) chapters is the addition of clinical guidance statements. Chapters now have two new subsections within their Diagnosis and Treatment sections, called Diagnostic Overview and Treatment Overview, respectively. Briefly, the format of chapters in the first edition allowed for diagnostic tests to be presented in an orderly and clear manner. However, there was a risk of the “laundry list effect”: just because all relevant tests were stated
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did not mean that the reader would know how to apply them, or which tests to use when. The information might be encyclopedic, but veterinary practice runs more along the lines of a narrative. In this new edition, authors covering every disease and disorder were tasked with adding a Diagnostic Overview statement to provide basic clinical guidance for achieving a reasonable diagnosis of the disorder in question. The result is a positive and deeply rewarding one. These overview statements now provide the insight of authors not only on what can be done but realistically what should be done to achieve a basic working diagnosis. A typical Diagnostic Overview statement for parvoviral enteritis of dogs, for example, states: “The diagnosis is suspected based on the presence of anorexia, vomiting, diarrhea, lethargy, or a combination of these, typically in a young and usually unvaccinated dog; confirmation requires fecal assay such as a parvovirus ELISA snap test.” It need not be complicated, and is not meant to address every conceivable variation of the disease. Rather, these overviews are a starting point for outlining a reasonable course of action. They offer a summary of expertise, “from the trenches,” of what should be considered when working up a typical patient suspected of having a particular disorder. Similarly, Treatment Overviews aim to address the unspoken questions that come up when looking at a list of possible medications or interventions: which treatments should be applied? In which cases? Overall, these changes are meant to improve what the book has to offer: not just facts, but insights into application of the information provided. The “health care team” approach is far from an abstract concept. For many of us, our animal health technician colleagues spend as much time with our patients, if not more. To that end, the Advisor now contains hundreds of Technician Tips that were not available previously. The breadth of this information ranges from nursing care to client counseling, from technical skills required when caring for patients with a certain disorder, to common pitfalls to avoid. The overlap between what a veterinarian needs to know and what a technician needs to know is substantial, and this new chapter section recognizes this important interaction. Perhaps one of the most innovative changes for this edition relates to client education sheets. These templatebased, layperson's vocabulary-based summaries have been highly successful, with many, many positive comments and widespread use. While it was tempting to expand the collection by summarizing more diseases for clients to understand, it was apparent that there was an even greater need in client education: the importance of clients’ grasping not just disease processes, but the actual instructions we give them when they go home. These are the monitoring and treatment activities that we instruct owners to carry out as a followthrough on our care. Sources for information of this type are very few. Client education sheets from most veterinary textbooks are dedicated to informing, but not necessarily empowering, the client; they discuss the entire disease, from mechanism to outcome, rather than concentrating on what we expect the client to be actively doing. Public sources of information, such as dog care manuals or healthy cat books, are useful, but the extent of home medical care they describe is often very limited: how to trim the nails or how to give a tablet may be covered, but how to provide elevated feedings for a patient with esophageal disease usually is not. Niche sources such as websites or specialty books offer an individual approach for specific disorders but not a whole series of “How to” summaries for home care. This is what is missing: information that helps clients carry out the ancillary medical tasks we ask them to do at home after we discharge the patient. To address this information gap, the Advisor now contains a compilation of 50 original medical “Howto” client education sheets. These new information documents cover a wide range of common home management situations, including how to perform range-of-motion exercises on a patient with orthopedic or neurologic disease, how to adapt the home environment for a pet that has become blind or deaf, how to deal with incessant coughing, how to manage a dog or cat that is having a seizure, and how to feed a dog or cat that has an indwelling (PEG or other) feeding tube. The range of topics reaches from the simple (how to remove the scent from a dog or cat that has been sprayed by a skunk) through the mid-range (how to check a bandage or cast for tightness) to the more complex (how to assist appropriately during caesarian section). In many cases, one How-to client education sheet can apply to several diseases and disorders; How to monitor respirations and How to construct and use an Elizabethan collar are such examples. The goal of all of these sheets is to provide a reference that owners can consult when we have asked them to do something specific to help their companion. Variations and modifications to suit individual patients are inevitable, and these information sheets are written to provide a general summary that practitioners can use as a base for this type of information. Finally, one of the dominant features of the Advisor is the solid link between the print and electronic editions of the book. Since it is only possible to obtain both together (neither website access nor the print book is sold individually), the universal access of the web book and the hands-on gratification of opening the print book are literally bound together. This interchange has allowed for some of the less widely used material, or some chapters that overlap substantially with other chapters, to be updated and published only in the web
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version of the book for this edition. As a result, the paper book remains portable, and the web book is comprehensive. Over time, the growth of information together with the limitations of a single volume book meant to be portable, means that we may rely on the web book as the vault of information and the paper book as the wallet. It is my hope that this approach will bring about the best of both worlds: new information is introduced without expanding the physical size of the paper book, and all the information can be found, whether one has the paper book handy or not, anywhere at any time online. Even those of us who consider ourselves bookworms will recognize the value of having online availability if we have worked relief shifts at other hospitals where the textbook selection is poor, or have found ourselves in an emergency setting searching for information on an uncommon topic in the middle of the night. Ultimately, this balanced approach is meant to be the answer to the riddle “How do we grow without getting bigger?” As I noted in the first edition, it would be a pleasure to say that this edition of the Advisor will answer every question that comes up in small animal practice. We all know that an honest assessment of any book says otherwise. With the changes we have made, my hope is that past readers will be pleased to find that their early interest in the Advisor remains well founded, and that new readers will discover a source of information that speaks to their interests.
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Clinical Veterinary Advisor: 2nd Edition
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Acknowledgments It has been the selection of information and the careful consideration of what to include that has required the most energy when creating this second edition. To you, the Advisor's incredibly dedicated section editors and authors, I offer my heartfelt thanks. From this vantage point I can see perhaps better than anyone the time you took and the effort you expended to create this book. You painstakingly identified relevant new information from the literature and then carefully crafted the material, both old and new, into these compact synopses. For an enthusiastic and learned author, it can be much harder to write less than to write more. All of us know that with writing comes sacrifice: we are busy with many obligations, and much of the work of good writing and editing simply comes when time is available, at night, on weekends, or instead of doing something else. We are willing to do it when there is a positive result: something that shows we made a difference for the better. Ultimately, this collective effort has produced a result of which we deserve to be proud, as I hope you will be. I expect your efforts will be noticed by a great many readers, as they were for the first edition. Many, many readers have commented so favorably on it and this positive feedback is as good a validation as any for showing the effect of your work. Students and veterinarians have told me repeatedly that the Advisor is their first “go-to” resource when they want to learn about something they are unfamiliar with; in many hospitals, the book is used so heavily that it has been reduced to tatters (see below) and has had to be re-bound; several board-certified specialists have told me they use the book routinely for information within and outside their specialty; and I have received many, many emails and letters praising your work, simply summarized as: “I think this book is terrific.” These testimonials, as much as anything I can say, indicate the far reach of your work and the positive impact of your authorship.
Validation of our work: this is how a book ends up looking when it is used often.
Penny, you and your team deserve perhaps more credit and recognition than have ever been given to a publisher. Under your leadership, the group (Lauren Harms [Developmental Editor], Rachel McMullen [Senior Project Manager], Catherine Jackson [Publication Services Manager], Bruce Siebert [Senior Producer], and Lynn Hoops [Marketing Manager]) has exceeded my every expectation from the earliest planning stages onward. No one could hope for a kinder, more gratifying, and more effective approach for bringing the book together. It has been a pleasure, and my wish for other authors is that they be as fortunate as I have been to work with such a determined, proactive, and fun group. With or without realizing it, many individuals made this book possible by helping me personally during its creation. My mentor, Steve Ettinger, was unfailing in his constructive criticisms and support. Unbeknownst to him, his candid observations led to many improvements in this edition, both large and small. His positive feedback and kindness during the creation of this book are irreplaceable. Thank you as always, Steve. Elizabeth Charuvastra RN, CEO of Targeted Medical Pharma LLC, stepped in and offered me an editor's dream (office space and support) while I was in California during the final stages of completion of the book. I could not have imagined a better-timed or more welcome gift, Liz. Many, many thanks. Similarly, my good friend and colleague Kirstie Barrett made it possible for me to have an immediately-usable work space during my West coast visit, and for this I am truly grateful. My friend David Edward gets a testimony of gratitude for providing an industrial quantity of PG Tips tea. Many thanks to Richard, Deirdre, and Evan Denis for hospitality during multiple layovers in Toronto. I also wish to thank all readers who sent me feedback aimed at making the second edition better. These messages from the front lines of practice helped reshape some of the content of this edition for the better, as readers will see for themselves. I thank all members of the Atlantic Veterinary College who contributed directly or indirectly, especially my colleagues who provided feedback, the technical staff (notably Elaine Reveler) who made it possible to generate good images and graphics, and the administration and faculty association who provided the framework and support for my academic work and sabbatical leave to dedicate time to the Advisor specifically. Last and most personally, I thank my family for their support and understanding. An endeavor such as this book is built on sacrifices, and their acceptance of my well-worn refrain, “I can't—I have a deadline,” was the epitome of support. François, Diane, Antoine, and above all Jennifer: thank you.
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5-Fluorouracil Toxicosis
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5-Fluorouracil Toxicosis BASIC INFORMATION DEFINITION Adverse effects caused by exposure to 5-fluorouracil (5-FU), a pyrimidine analog-type antineoplastic antimetabolite drug used for palliative management of certain carcinomas in humans and occasionally in dogs.
SYNONYMS Common brand names: Efudex, Fluoroplex, and Carac. Generic: 2,4-dioxo-5-fluoropyrimidine; 5-fluoro-2,4(1H,3H); pyrimidinedione; 5-FU; NSC 19893; Ro2-9757; CAS 51-21-8.
EPIDEMIOLOGY SPECIES, AGE, SEX Dogs and cats of any age, breed, and either sex. Dog cases are more common. Dogs are more likely to develop neurologic effects (seizures) compared to humans. Cats are more sensitive to toxic effects of 5-FU than dogs. RISK FACTORS
Preexisting liver or kidney dysfunction can increase risk of toxicity Presence of 5-FU in a pet's environment
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT
History of exposure to product containing 5-FU Clinical signs begin within 30 minutes to 5 hours of exposure. Vomiting, hypersalivation, lethargy, vocalization, diarrhea, tremors, ataxia, seizures
Some animals show vomiting progressing quickly to seizures; others may show tremors and seizures and no vomiting.
PHYSICAL EXAM FINDINGS
Seizures (often status epilepticus) Vomiting (with or without blood) Diarrhea (with or without blood) Tremors Lethargy Ataxia Cardiac arrhythmias (all kinds) Respiratory depression
ETIOLOGY AND PATHOPHYSIOLOGY Source 5-FU or similar agents are available for use as injection, topical creams (0.5%-5%) or lotions (1%-5%), and capecitabine (prodrug of fluorouracil) as tablets. Flucytosine is an antifungal agent that must be converted to 5-FU. Toxicosis occurs after ingestion of products containing 5-FU and occasionally secondary to repeated use in dogs or cats. Mechanism of Toxicosis 5-FU inhibits RNA processing and function and DNA synthesis and repair, inhibiting cell division. Actively dividing cell lines (bone marrow stem cells, intestinal crypt cells) are most affected. The mechanism of neurotoxicity may be production of fluorocitrate, which limits cellular energy production by interfering with the Krebs cycle.
DIAGNOSIS DIAGNOSTIC OVERVIEW
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5-Fluorouracil Toxicosis
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History of exposure and presence of clinical signs consistent with exposure to 5-FU within 30 minutes to 5 hours after exposure
DIFFERENTIAL DIAGNOSIS Diseases or intoxications that could cause vomiting (see p. 1173) and/or seizures (see pp. 1009 and 1425)
INITIAL DATABASE
Serum biochemistry profile (elevated liver enzymes, azotemia possible in 24 hours) Electrolytes (hypokalemia possible due to severe vomiting, diarrhea) CBC with differential (baseline, monitor q 24-72 hours for 20 days); initial leukocytosis followed by evidence of myelosuppression, leukopenia, pancytopenia in 5-20 days. Hematocrit increased due to dehydration then decreased due to gastrointestinal (GI) bleeding. Blood gas analysis Urinalysis
ADVANCED OR CONFIRMATORY TESTING
Analysis of 5-FU and its metabolites in plasma is possible but often difficult to obtain in timely fashion for acute toxicoses. Necropsy lesions: hemorrhagic colitis, GI mucosal ulceration (throughout), stomatitis, myocardial ischemia, pulmonary edema, hepatic and renal congestion
TREATMENT TREATMENT OVERVIEW Stabilize the patient first; control vomiting and seizures. Provide supportive care once the animal has been stabilized.
ACUTE GENERAL TREATMENT
Decontamination of asymptomatic patient Emesis using activated charcoal with a cathartic if patient is showing no clinical signs and the ingestion is recent (20 mm Hg). This syndrome is likely underrecognized in veterinary medicine and has a high prevalence in human ICU patients.
SYNONYMS ACS, increased IAP, intraabdominal hypertension (IAH)
EPIDEMIOLOGY SPECIES, AGE, SEX No species, age, sex, genetic, or breed predisposition RISK FACTORS
Any patient with abdominal disease or accumulations of fluid, gas, or tissue in the abdominal cavity can develop elevated IAP. Specific risk factors include underlying diseases that lead to gas or fluid accumulation in the abdominal compartment (within organs, viscera or as free fluid) or interfere with the abdominal wall's ability to expand and compensate for increased abdominal contents. Abdominal effusion Abdominal neoplasia Abdominal surgery or trauma (most common causes) Abdominal wraps/bandages Decreased abdominal wall compliance (edema, hematoma, muscle activity) Hepatic abscess
High-volume fluid resuscitation Ileus Pancreatitis Peritonitis Sepsis
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES
Primary ACS: intraabdominal cause, most commonly postoperative or trauma patients Secondary ACS: extraabdominal cause, most commonly sepsis or burn patients that require aggressive fluid resuscitation Recurrent ACS: redevelopment of ACS after surgical or medical treatment for primary or secondary ACS
HISTORY, CHIEF COMPLAINT
Frequent history of abdominal trauma or surgery Indications to check IAP are (usually in combination): New or progressive organ failure Particularly azotemia, reduced urine output Elevated central venous, mean arterial, right and left atrial pressures
Rising intracranial pressure, altered mentation New vomiting and diarrhea Acidosis, rising blood lactate levels
PHYSICAL EXAM FINDINGS
Physical examination and abdominal perimeter (girth) measurements are insensitive for detecting elevated IAP. Progressive abdominal distension or tympany, jugular vein distension, tachypnea, tachycardia are possible
ETIOLOGY AND PATHOPHYSIOLOGY
IAP in healthy adults is subatmospheric − 0 mm Hg; IAP in critically ill adults is 5-7 mm Hg. IAH is defined as a sustained elevation in IAP = 12 mm Hg. ACS (sustained IAP > 20 mm Hg with new organ dysfunction/failure) develops if IAH is not recognized and treated.
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Abdominal Compartment Syndrome
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ACS is not a disease, but a distinct syndrome of clinical signs and abnormalities that can have multiple causes. At low intraabdominal volumes, the abdominal wall is very compliant. Large increases in abdominal volume result in minor increases in IAP. At higher abdominal volumes, abdominal wall compliance decreases, and even small increases in volume can cause major increases in IAP. Increased pressure in the abdomen leads to hypoperfusion and ischemia of abdominal organs and, when severe, direct compression of blood vessels. This leads to alterations in renal (most recognized), hepatic, and gastrointestinal functions. Anuria can occur with IAP > 30 mm Hg. Liver function, including cytochrome P450 function, is impaired. Intestinal edema can develop, as well as bacterial translocation through gastrointestinal walls. Reduced ability for the diaphragm to contract against the tense abdomen impairs tidal volume and compromises ventilation, resulting in hypoxia and hypercapnia. Mechanical/positive pressure ventilation is similarly affected. Increase in central venous pressure (CVP) and drop in cardiac output (increased systemic vascular resistance, decreased venous return to the heart, compression of vascular structures from increased intrathoracic pressure) result in altered cardiovascular function. Intracranial pressure elevations can occur because of elevated CVP. Hormonal changes occur in response to the altered cardiovascular state, including elevations in renin-angiotensin activity, antidiuretic hormone, and catecholamine levels. Ischemia-reperfusion injury occurs after shock resuscitation and can affect distant organ function. Abdominal wall complications can occur secondary to hypoperfusion, including delayed or impaired wound healing, dehiscence, and surgical site infection. Recognition of increasing IAP and prevention of ACS are crucial to reducing morbidity and mortality. There is no single threshold IAP that will result in organ dysfunction or failure in all patients and can be used for decision making. The critical IAP in most patients is between 10 and 15 mm Hg; at this pressure, initial organ dysfunction develops.
DIAGNOSIS DIAGNOSTIC OVERVIEW IAP must be measured to confirm the diagnosis of abdominal compartment syndrome.
INITIAL DATABASE Most common method of measuring IAP is the intravesicular or “bladder” technique, which is an indirect measurement.
A water manometer is attached to a stopcock in the evacuation line from a standard urinary (urethral) catheter. The urinary bladder is emptied, and a few milliliters of isotonic sterile saline are placed in the bladder (3-10 mL, depending on patient size). After 30-60 seconds (to allow the saline to warm and the detrusor muscle to relax, avoiding a falsely elevated reading), the zero mark on the manometer is held at the level of the cardiac atria (level of the umbilicus in lateral recumbency). The manometer is filled with saline. The stopcock is then opened to the bladder. The reading (in mm Hg) is taken when the column of saline reaches a stable level. The measurement should be taken at end expiration. Abdominal muscle contractions can increase IAP readings. Obese patients may have a higher baseline IAP. Alternative measurement techniques include nasogastric balloon catheter (good for continuous measurement), direct intraabdominal catheter/abdominal drain, and venous catheter in the caudal vena cava. These techniques give similar information but can be more cumbersome to place and maintain. Trends in pressure parameters may be more important than any single number. It is important to use the same positioning each time a measurement is taken. The IAP measured at one point in the abdominal cavity can be assumed to be the pressure throughout the abdominal cavity. Imaging can be helpful for looking for underlying causes of IAH but is insensitive at detecting increased IAP.
ADVANCED OR CONFIRMATORY TESTING
Repeated IAP measurements are essential for monitoring. Lactate levels, liver enzyme changes, urine output, blood urea nitrogen, and creatinine levels to identify abdominal organ dysfunction associated with ACS Measurements of cardiac output and other cardiovascular parameters and monitoring mentation and intracranial pressure give a more extensive assessment of cardiovascular function and perfusion. Abdominal perfusion pressure (APP; mean arterial pressure minus IAP) has been proposed as a more accurate predictor of visceral perfusion. It assesses the severity of IAP, as well as the adequacy of abdominal blood flow, and should be maintained at 50-60 mm Hg in patients with IAH/ACS.
TREATMENT TREATMENT OVERVIEW Medical management is crucial to prevention and treatment of IAH. Surgical decompression is the definitive treatment if medical management fails to prevent further increases in IAP and organ dysfunction and failure.
ACUTE, GENERAL TREATMENT
IAP of 10-20 mm Hg is a mild elevation and should be monitored. IAP of 20-35 mm Hg is a moderate to severe elevation. Consider active (centesis or surgical) decompression if pressure continues to rise or if other parameters continue to deteriorate. IAP > 35 mm Hg is a severe elevation.
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Abdominal Compartment Syndrome
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ACS is extremely likely. Abdominal decompression is required. If a correctible source is not identified, surgical exploratory laparotomy is indicated. Medical Management Sedation, analgesia, and/or neuromuscular blockade to reduce muscle tone secondary to pain, agitation, and ventilator dyssynchrony, which result in increased IAP Not effective at treating severe IAH/ACS Nasogastric or colonic decompression can reduce IAP and treat mild/moderate IAH. Prokinetic motility agents useful in decreasing visceral volume Aim for euvolemia. Hypervolemia can lead to ACS development. Hypertonic crystalloid and colloid resuscitation shown to reduce IAP and decrease risk of ACS Diuretics to mobilize third space fluid accumulation Percutaneous decompression to remove free abdominal fluid or air
If this fails to resolve IAH, patient must undergo surgical decompression. Surgical Management (VERY rare in companion animals, barring arterial hemorrhage) Direct removal of the fluid or tissue causing the problem Performed when organ dysfunction/failure and IAH are refractory to medical management Open abdomen or temporary abdominal closure techniques often employed in human medicine
CHRONIC TREATMENT
Placement of abdominal drains or repeated drainages/centeses in chronic conditions to maintain reduced pressure may be necessary. Treatment of the underlying disease is essential.
DRUG INTERACTIONS Hepatic and renal elimination of drugs may be altered by ACS, requiring dosage adjustment or alternative drug choices.
RECOMMENDED MONITORING IAP, CVP, blood pressure, blood chemistry, lactate, urine output, diagnostic imaging as indicated by underlying cause and progression of IAP over time
PROGNOSIS AND OUTCOME Prognosis depends on underlying cause and associated abnormalities, organ dysfunction, and disease. In human medicine, ACS is a significant cause of morbidity and mortality (approaching 70%). Disregard for elevated IAP and delay of surgery are associated with further increases in patient mortality.
PEARLS & CONSIDERATIONS COMMENTS
Most critically ill patients should have urethral catheters in place to monitor urine output, which allows for IAP monitoring and early detection of ACS. IAH may falsely elevate indirect intracardiac pressure readings due to abdominothoracic transmission of pressure. Monitoring and management of patients this ill requires 24-hour care.
TECHNICIAN TIP IAP is most easily measured in recumbent patients. If the patient is conscious and mobile, care must be taken to prevent the patient from chewing the catheter and retaining the proximal portion in the abdomen or bladder (Elizabethan collar essential).
PREVENTION Avoid excessive fluid volume resuscitation. Careful monitoring essential, with early preventive action taken if IAP rises.
SUGGESTED READING Cheatham ML: Abdominal compartment syndrome. Curr Opin Crit Care 15:154–162, 2009. Drellich S: Intraabdominal pressure and abdominal compartment syndrome. Compend Contin Educ Prac Vet 22:764–769, 2000. AUTHOR: CATHERINE SUMNER EDITOR: ELIZABETH ROZANSKI 1ST EDITION AUTHOR: SHARON DRELLICH
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Abdominal Distention
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Abdominal Distention BASIC INFORMATION DEFINITION Enlargement of the abdominal cavity
EPIDEMIOLOGY SPECIES, AGE, SEX: Dependent on underlying cause
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT
Abdominal enlargement (rate of distention is extremely variable, varies from acute to chronic and insidious)
Perceived weight gain Decreased activity Anorexia Tachypnea Abdominal discomfort/pain When ascites is present and the fluid accumulation is rapid, clinical signs of weakness and dyspnea are more likely to be apparent. History may include clinical signs associated with the primary disease (e.g., repeated, unproductive attempts at vomiting if gastric dilatation and volvulus; dyspnea, cough if cardiac disease; icterus if liver disease).
PHYSICAL EXAM FINDINGS
Visible abdominal enlargement Abdominal palpation: Fluid wave may be present (ballottement) with ascites. An abdominal mass or organomegaly (liver, spleen, kidney, etc.) may be palpable. Physical abnormalities associated with primary disease may be present: Cardiovascular abnormalities (heart murmur, arrhythmia, gallop sound, jugular distention) should warrant further investigation into the possibility of right heart failure. Marked generalized lymphadenopathy may suggest lymphoma. Muffled heart sounds are consistent with pericardial effusion and tamponade if ascites is present.
ETIOLOGY AND PATHOPHYSIOLOGY
Ascites: all causes Hyperadrenocorticism/Cushing's disease Cyst (renal, hepatic) Gastrointestinal dilation (food, air, water, foreign material) Lipoma Lymphadenopathy Mass, non-neoplastic (hematoma, granuloma, abscess) Neoplasia
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Abdominal Distention
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Abdominal Distention
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ABDOMINAL DISTENTION Dorsal view of a young English bulldog with marked ascites caused by right-sided congestive heart failure due to severe pulmonic stenosis. The abdominal distention hides the dog's weight loss and may be mistaken by the owner as an increase in lean body mass. This degree of abdominal distention was associated with poor appetite, lethargy, and dyspnea in this dog.
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Abdominal Distention
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Abdominal Distention
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ABDOMINAL DISTENTION Same dog 2 hours later when large-volume abdominal drainage was complete. The dog was breathing normally, was more active, and appeared markedly more comfortable. The extent of cardiac cachexia is revealed.
Pancreatitis
Parasitic (Mesocestoides) Peritonitis Pneumoperitoneum (peritonitis or postsurgical) Pyometra/hydrometra Obstipation Organomegaly (hepatomegaly, splenomegaly, renomegaly) Torsion (splenic, gastric dilation/volvulus, etc.) Urinary obstruction/bladder distention
DIAGNOSIS DIAGNOSTIC OVERVIEW Apparent on physical examination alone. Careful abdominal palpation and diagnostic imaging help to elucidate the cause.
DIFFERENTIAL DIAGNOSIS
Normal variation Obesity
Pregnancy
INITIAL DATABASE
Abdominal radiographs Loss of serosal detail (focal or generalized) is common if ascites is present. May have “ground-glass” appearance (carcinomatosis, peritonitis) Mass lesions, fat, or organomegaly may be apparent or suggested by displacement of gas-filled organs. Free air may be present with peritonitis (ruptured viscus). Thoracic radiographs Enlarged cardiac silhouette and/or caudal vena cava if congestive heart failure or pericardial effusion (rule out as cause of ascites) Metastatic pulmonary disease Pleural effusion CBC, biochemistry panel, and urinalysis are indicated for any animal with ascites or abnormal abdominal distention. Abnormalities depend on underlying cause and extent of organ damage. Abdominal ultrasonography Confirms presence of fluid if present and differentiates fluid from soft tissue or fat Identification of mass lesions, organomegaly, cyst, etc. Echocardiography Confirms diagnosis of right heart enlargement or pericardial effusion (rule out as cause of ascites) Abdominal paracentesis (see p. 1194 ) if ascites; obtain fluid for cytology and biochemical evaluation. Characterize fluid based on protein concentration, specific gravity, and total cell count. Transudate (pure) Clear and colorless
Protein 1.018Cells 5000-100,000/mm : neutrophils, mesothelial cells, macrophages, erythrocytes, lymphocytes, and bacteria
Hemorrhage
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Abdominal Distention
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Red Protein >5.5 g/dL Specific gravity 1.007-1.027 Cells consistent with peripheral blood; usually does not clot
Chyle
Pink, straw, or white Protein 2.5-7.0 g/dL Specific gravity 1.007-1.040
ADVANCED OR CONFIRMATORY TESTING
Fine-needle aspirate or needle biopsy (mass, enlarged organs, etc.). Biopsy not recommended if area is infected (abscess, pyometra) or likely to hemorrhage (e.g., suspected hemangiosarcoma). Prothrombin time if anticoagulant intoxication is suspected as cause of ascites (paracentesis contraindicated if coagulopathy is suspected) CT, MRI Abdominal exploratory may be indicated.
TREATMENT TREATMENT OVERVIEW Treatment of underlying disease and therapeutic abdominal drainage if large-volume ascites is causing the abdominal compartment syndrome (see p. 4)
ACUTE GENERAL TREATMENT
Treatment of underlying disease: Chemotherapy if lymphoma Pericardiocentesis if pericardial effusion is present Drug therapy for congestive heart failure Removal of fluid if discomfort or respiratory difficulty is present (see p. 1192 ). Surgery may be indicated for neoplasia, pyometra, peritonitis, and some causes of hemorrhage (e.g., ruptured splenic or hepatic hemangiosarcoma).
PROGNOSIS AND OUTCOME Dependent on underlying cause
PEARLS & CONSIDERATIONS COMMENTS
Approach to patient with abdominal distention is to determine the nature of the primary problem. Thoracic radiographs should be part of the routine evaluation for a patient with ascites so as not to overlook the possibility of cardiac, pericardial, or metastatic disease–or pleural effusion. The cause of abdominal distention may be benign (obesity, intraabdominal lipoma, cyst).
SUGGESTED READING Chambers G: Abdominal distension, ascites, and peritonitis. Textbook of veterinary internal medicine, ed 7, St Louis, 2010, Saunders Elsevier, pp 144–148. AUTHOR: KIRSTIE A. BARRETT EDITOR: ETIENNE CÔTÉ
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Aberrant Adrenocortical Disease (Increased Adrenal Sex Hormone Production)
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Aberrant Adrenocortical Disease (Increased Adrenal Sex Hormone Production) BASIC INFORMATION DEFINITION Clinical signs of hyperadrenocorticism are present, but cortisol test results are normal, and one or more of the adrenal sex hormones is/are increased.
SYNONYMS Atypical hyperadrenocorticism, sex hormone abnormality
EPIDEMIOLOGY SPECIES, AGE, SEX Middle-aged/old dogs and cats ASSOCIATED CONDITIONS AND DISORDERS Hyperadrenocorticism
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES
Pituitary dependent Adrenal dependent: adrenal carcinoma has mainly been reported (two cats and six dogs with hyperprogesteronism)
HISTORY, CHIEF COMPLAINT Identical to hyperadrenocorticism (see p. 548) PHYSICAL EXAM FINDINGS Identical to hyperadrenocorticism (see p. 548)
ETIOLOGY AND PATHOPHYSIOLOGY
The adrenal gland(s) secretes an excessive amount of one or more adrenal sex hormones. Adrenal tumors (particularly adenocarcinomas) may secrete adrenal sex hormones owing to disruption of adrenal tissue. Progestagens can act as glucocorticoid agonists. Cortisol concentrations may be normal to subnormal with sex hormone-secreting adrenal tumors, as high progestagen concentrations can suppress cortisol secretion.
DIAGNOSIS DIAGNOSTIC OVERVIEW The disorder is suspected when typical signs of hyperadrenocorticism are identified, but specific diagnostic tests (e.g., ACTH stimulation) are inconsistent with hyperadrenocorticism. Confirmation is obtained with identification of elevated serum levels of adrenal sex hormones.
DIFFERENTIAL DIAGNOSIS
Polyuria/Polydipsia (see p. 902) Polyphagia (see p. 899) Alopecia (see pp. 54 and 56)
INITIAL DATABASE Hyperadrenocorticism (see p. 548)
ADVANCED OR CONFIRMATORY TESTING
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Adrenocorticotropic hormone (ACTH) stimulation test with sex hormone panel (progesterone, 17-hydroxyprogesterone, estradiol, androstenedione, testosterone): Dogs with nonadrenal illness may have mildly increased adrenal sex hormones. Substantial overlap in sex hormone serum concentrations between healthy, nonadrenally ill, and hyperadrenocorticism patients make sex hormone assays ineffective screening tests for hypercortisolism. Approximately 71% sensitivity and specificity for 17-hydroxyprogesterone concentrations if a cutoff greater than 8.5 ng/mL is used for diagnosing atypical hyperadrenocorticism Low-dose dexamethasone suppression test to rule out typical hyperadrenocorticism ± endogenous ACTH concentrations, CT, MRI (see p. 548)
TREATMENT TREATMENT OVERVIEW Resolution of clinical signs is the goal of treatment; medications are typically used for controlling pituitary-based disease, and surgical excision is the treatment of choice for primary adrenal tumors.
ACUTE GENERAL TREATMENT
See Adrenal Neoplasia (Adenoma/Carcinoma), p. 43 Pituitary-dependent (see p. 548)
CHRONIC TREATMENT
As for hyperadrenocorticism, p. 548 The following recommended by some, with anecdotally supported results (see http://www.vet.utk.edu/diagnostic/endocrinology/pdf/TreatmentInfoAtypicalCushingsRevised201001.pdf): Melatonin (3-6 mg/dog PO q 12 h, based on body weight); inhibits aromatase and 21-hydroxylase enzymes Melatonin implants (www.melatek.net) 8, 12, 18 mg for dogs weighing 50 lb, respectively Lignan (from flaxseed hulls or HMR lignan) ≈ 2 mg/kg PO q 24 h; phytoestrogenic activity inhibits aromatase Elimination of exogenous (e.g., hormone cream) or endogenous (ovarian remnant, cryptorchid testicle) sources of androgens
DRUG INTERACTIONS See Hyperadrenocorticism, p. 548; Adrenal Neoplasia (Adenoma/Carcinoma), p. 43
POSSIBLE COMPLICATIONS See Hyperadrenocorticism, p. 548; Adrenal Neoplasia (Adenoma/Carcinoma), p. 43
RECOMMENDED MONITORING Medical therapy: ACTH stimulation testing every 3 months
Mitotane (o,p ‘-DDD) therapy: sex hormone concentrations (and cortisol if also increased) should decrease to normal. Trilostane therapy: progesterone and 17-hydroxyprogesterone concentrations may increase concurrent with resolution of clinical signs and a decrease in cortisol concentrations.
PROGNOSIS AND OUTCOME
Survival data unknown but subjectively similar to dogs with typical hyperadrenocorticism Adrenal tumor: good if surgically resectable Pituitary-dependent: good with treatment
PEARLS & CONSIDERATIONS COMMENTS
Limited information is available regarding this disease and the sensitivity and specificity of adrenal sex hormones in nonadrenal illness. Adrenal sex hormones are also increased in dogs with typical hyperadrenocorticism (i.e., hypercortisolemia).
TECHNICIAN TIP On both the pre- and post-ACTH stimulated serum, 2 mL of serum are required. Centrifuge, separate, and freeze the serum as soon as possible. Avoid submission of hemolyzed samples.
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SUGGESTED READING Benitah N, Feldman EC, Kass PH, Nelson RW: Evaluation of serum 17-hydroxyprogesterone concentration after administration of ACTH in dogs with hyperadrenocorticism. J Am Vet Med Assoc 227:1095–1101, 2005. Hill KE, Scott-Moncrieff JCR, Koshko MA: Secretion of sex hormones in dogs with adrenal dysfunction. J Am Vet Med Assoc 226:556–561, 2005. Sieber-Ruckstuhl NS, Boretti FS, Wenger M: Evaluation of cortisol precursors for the diagnosis of pituitary-dependent hypercortisolism in dogs. Vet Rec 162:673– 678, 2008. AUTHOR: KATE HILL EDITOR: SHERRI IHLE
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Abortion, Dog
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Abortion, Dog BASIC INFORMATION DEFINITION
The expulsion of one or more fetuses before full term pregnancy. Uncommon; in the dog, resorption is more common. Occurs more often during the fetal period. Induction of abortion (pregnancy termination): see p. 912.
SYNONYMS Fetal loss, pregnancy wastage
EPIDEMIOLOGY SPECIES, AGE, SEX Female dog; no specific age GENETICS & BREED PREDISPOSITION Inbreeding (inbreeding coefficient >0.25): early embryonic death, conceptus resorption RISK FACTORS
History of previous pregnancy loss
Malnutrition (pregnancy ketosis) Endocrinopathies (hypothyroidism, hypoluteoidism, diabetes mellitus) Infection (Brucella canis, Listeria monocytogenes, Streptococcus canis, Escherichia coli, Campylobacter sp., Leptospira sp. Salmonella sp., Mycoplasma sp., canine herpesvirus 1, canine parvovirus 1 [minute virus of canines], bluetongue virus, canine distemper virus, canine adenovirus [infectious hepatitis], Toxoplasma gondii, Leishmania infantum) Unsolicited treatment with endocrine disruptors, embryotoxic or teratogenic compounds (e.g., antifungal agents such as itraconazole or polyester textiles in contact with skin). Inadequate vaccination or deworming programs
CONTAGION & ZOONOSIS
Brucella canis is zoonotic. Salmonella sp. and Leptospira sp. have zoonotic potential. Canine herpesvirus 1 and minute virus of canines: transmission through direct contact via aerosol or contact with aborted fetuses and/or placentas. Maleto-female venereal contact is not a significant means of viral transmission.
GEOGRAPHY AND SEASONALITY
Canine brucellosis: endemic in parts of North and South America; eradicated in Europe since 1996. Canine herpesvirus: worldwide incidence; serologic prevalence of 60%-80%.
ASSOCIATED CONDITIONS & DISORDERS Abortion may be secondary to fetal death.
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT
Pregnant bitch whelps prematurely with live or dead pups, or no pups are born at term. Abnormal vulvar discharge during pregnancy (bloody or purulent discharge), fever, or signs of abdominal pain may be noted by owner. Usually abortion in the bitch goes unnoticed by the owner because the dam may consume the pups and the aborted tissues. Death may occur in one or more fetuses, whereas the remainder may continue to develop normally. Late-term abortions (between days 45 and 59) are typical of B. canis.
PHYSICAL EXAM FINDINGS
Often unremarkable Vulvar discharge occurs normally in pregnant bitches and is clear to mucoid or pink-tinged and odorless; purulent, hemorrhagic, greenish, blackish, or malodorous vulvar discharge may indicate pregnancy complications that could lead to abortion.
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ETIOLOGY AND PATHOPHYSIOLOGY
Canine pregnancy requires normal luteal function throughout its duration. Any toxic or hormonal substance that induces endogenous release of prostaglandin F-2 alpha (PGF2a) and subsequent luteolysis may cause abortion (e.g., bacterial toxins [coliforms, Staphylococcus sp.], adrenergic agonists [e.g., phenylephrine]). Fetal survival requires normal placental function and placental relaxin production. Relaxin concentration declines rapidly after the death of all fetuses but may remain elevated for some days after the loss of pregnancy. Pathogens that influence placental function (e.g., herpesvirus placentitis) may cause abortion.
DIAGNOSIS DIAGNOSTIC OVERVIEW The diagnosis is suspected when the pregnancy is previously confirmed on ultrasound or by radiography, and the bitch then presents nonpregnant or expelled fetuses have been observed.
DIFFERENTIAL DIAGNOSIS
Pseudocyesis (false pregnancy). Ultrasound evaluation on days 23-25 following breeding to confirm pregnancy and fetal heart beat. Vulvar discharge due to vaginitis or metritis (pyometra). Ultrasound evaluation of uterine disorders may be useful on days 23-25 of anticipated gestation.
INITIAL DATABASE
Serologic testing of affected dam. B. canis: Rapid slide agglutination test (RSAT) is an excellent screening test, but false-positive results occur. To reduce cross-reactivity and false positive results, 2-mercaptoethanol can be added to the RSAT. Dogs in a positive kennel or household that are negative on first test should be retested once a month for 3 consecutive months to confirm negative status. Vaginal secretions or semen can be tested by PCR to determine a positive B. canis status before seroconversion occurs. CHV-1: A serum neutralization test or ELISA test with a positive result greater than 1:16 is indicative of prior infection (exposure). Virus or bacterial isolation from microbial cultures from fetuses, placenta, milk, or vaginal secretions. B. canis: Repeated samples may be necessary. Antibiotics are usually ineffective because of the intracellular location of the infectious organism. In acute CHV-1 infections, viral isolation from infected tissues is possible for 2-3 weeks. Nasal or vaginal swabs may also be tested by PCR. Typically titers show 1:64-1:640. Two blood samples (acute and convalescent) at 1-month intervals are suggested to confirm a decline or rise in titer. Fetal gross necropsy (e.g., subcapsular hemorrhages in the kidneys indicative of CHV1) and visual inspection of associated fetal membranes Histologic assessment of fetal organs, liver, spleen, thymus, kidneys, adrenals, intestines and stomach, heart, lung, thymus, and brain Bacteriologic cultures from fetal organs and reproductive tract of the bitch Serum progesterone level of dam must be >2-3 ng/mL (6-9 nmol/L) to sustain pregnancy. Concentrations below this threshold for more than 48 hours may lead to pregnancy loss. Lower level at any time of pregnancy until day 55 indicates hypoluteoidism (luteal dysfunction/failure). When reported, hypoluteoidism generally occurs on days 25-35 past breeding (i.e., at the initiation of the fetal period). Since low progesterone level may occur secondary to fetal death, the diagnosis of hypoluteoidism is based on a low serum progesterone level, positive effect of progesterone supplementation in a bitch that once aborted, and absence of other risk factors, such as a possible genetic etiology. Thyroid hormone analyses: May reveal subclinical hypothyroidism aggravated to a clinically significant disease during periods of stress, such as pregnancy (see p. 588). Routine laboratory testing: CBC and serum biochemistry profile Normal hematocrit values: 45%-55% (nonpregnant) compared to 30%-35% (pregnant; due to an increase in plasma volume). Nonspecific Mild mature neutrophilia and hemoconcentration is normal in pregnant bitches, but an elevated presence of nonsegmented neutrophils or monocytosis is abnormal.
ADVANCED OR CONFIRMATORY TESTING
Ultrasonography may reveal fetal death before onset of abortion. Contact diagnostic laboratories for further recommendations for specific pathogens. For B. canis, blood culture with bacteriologic isolation provides a definitive diagnosis and may be attempted after 5 weeks. If the RSAT is positive, an agarose gel immunodiffusion (AGID) test on cytoplasmic protein antigens can be performed 12 weeks post infection and is the most accurate serologic test available. Toxicology of organs and/or blood when a specific toxin or drug is suspected
TREATMENT TREATMENT OVERVIEW
Acute supportive treatment of the bitch (e.g., intensive treatment of infection) is the main aim of treatment, since the prognosis for saving the ongoing pregnancy is poor. B. canis-infected dams should be euthanized or at least surgically sterilized, owing to the location of the organism in reproductive tissue. Premises should be cleaned, kennelmates should be quarantined, and humans should avoid direct contact with excretions or aborted material from potentially infected animals because of the zoonotic nature of Brucella sp. In cases of hypoluteoidism (see serum progesterone above), progesterone supplementation may be attempted to try to prevent abortion of remaining fetuses.
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ACUTE GENERAL TREATMENT
Supportive: intravenous fluids (e.g., lactated Ringer's solution) and antibiotics if fever. Antibiotics: empirical pending culture and sensitivity results (if clinically feasible). Typical choices include amoxicillin (22 mg/kg PO q 8 h), cephalexin or cefadroxil (20 mg PO q 8-12 h) or pivampicillin (30 mg/kg PO q 12 h). Enrofloxacin (5 mg/kg SQ, IM, or PO q 24 h) or trimethoprim/sulfadiazine (15 mg/kg PO q 12 h) are broad spectrum but potentially teratogenic. See p. 909
CHRONIC TREATMENT With confirmed hypoluteoidism, options include:
Progesterone in oil 2 mg/kg IM q 48 h until 10 days before term Altrenogest 0.09 mg/kg PO q 24 h is an alternative. Micronized progesterone (Prometrium [Solvay Medical Pharmaceuticals, Marietta, GA, USA]) has been recommended; 10 mg/kg PO q 24 h. Supplementation should be stopped at least 2 days prior to expected term (i.e., 60-61 days after the LH peak, to allow parturition).
If antibiotics are used in B. canis-infected dogs, antibiotic treatment should be continued for at least 4 weeks, based on culture and sensitivity results and clinical state.
NUTRITION/DIET See p. 909. A good-quality maintenance diet is indicated.
BEHAVIOR/EXERCISE Controlled physical activity during pregnancy
DRUG INTERACTIONS Glucocorticoids are unpredictable abortifacient drugs in dogs.
POSSIBLE COMPLICATIONS Supplementation with progesterone analogs (i.e., altrenogest) before sexual differentiation of the fetus is not recommended because of potential masculinization of female fetuses; nor is it recommended if the whelping date is unknown. Failure to discontinue supplementation at the appropriate time can cause prolonged gestation, fetal death, and lactation failure.
RECOMMENDED MONITORING
If suspicious of possible abortion, weekly monitoring of progesterone concentrations and fetal viability with abdominal ultrasound examinations can be valuable. If abnormal vaginal discharge is observed during gestation, the pregnancy should be monitored by ultrasound to assess the viability of the fetuses, and supportive therapy should be initiated.
PROGNOSIS AND OUTCOME
Poor for saving most ongoing pregnancies. Usually there is no problem in subsequent pregnancies, except in cases of B. canis infections and occasionally in herpesvirus-infected bitches with recrudescent infection. Bitches with hypoluteoidism may experience recurrent abortion, but the ongoing pregnancy is saved in most cases with supplementary progesterone.
PEARLS & CONSIDERATIONS COMMENTS
Abortion is uncommon in the bitch; embryonic death with fetal resorption or mummification is more common. Usually abortion in the bitch goes unnoticed by the owner, as the bitch may consume the aborted tissues. Infectious agents are the most common causes of canine abortion. The diagnosis of abortion should prompt a search for an underlying cause.
PREVENTION
A canine herpesvirus 1 vaccine is available in Europe (Eurican herpes 205 [Merial, Lyon, France]). Vaccination should be given 1 month prior to estrus, followed by vaccination within 8 days after mating. If titers are below 1:128 at midpregnancy, a third vaccination may be given 10 days prior to parturition. Limit contact with external dogs at breeding and during pregnancy. Isolate pregnant bitches from showing or performing dogs during pregnancy, especially if herpesvirus is endemic in the area. Maintain an adequate vaccination and deworming program.
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TECHNICIAN TIP Educate clients on normal pregnancy (see p. 909) and preventive measures for breeding animals.
CLIENT EDUCATION
Accurate pregnancy diagnosis should be done in bitches on days 25-30 post breeding (ultrasonography or relaxin test). See p. 909.
Regular medical evaluation of breeding dogs Genetic counseling to avoid inbreeding
SUGGESTED READING Schlafer DH: Canine and feline abortion diagnostics. Theriogenology 70:327–331, 2008. Verstegen J, Dhaliwal G, Verstegen-Onclin K: Canine and feline pregnancy loss due to viral and non infectious causes: A review. Theriogenology 70:304–319, 2008. AUTHOR: WENCHE K. FARSTAD EDITOR: MICHELLE KUTZLER
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Burns
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Burns BASIC INFORMATION DEFINITIONS Burns are the injuries that result from exposure to flame, extreme heat, scalding, inhalation, and chemical or electrical trauma. Burns produce clinical syndromes ranging from self-limiting injury to devastating long-term incapacitation and potentially death. Eschar: a thick, coagulated crust or slough that develops as a result of a burn Compartmentalization: a condition associated with third- and fourth-degree burns in which swelling within tissue compartments creates strictures that can decrease thoracic wall motion and ventilation or cause ischemic injury to limbs Transition zone: region between completely devitalized tissue and normal tissue
EPIDEMIOLOGY SPECIES, AGE, SEX Animals of any signalment are susceptible to burn injury. Debilitating conditions such as chronic renal disease or immunoincompetence carry increased risks for fatal complications. RISK FACTORS Both temperature and duration of exposure contribute to the degree of thermal injury. Common sources of companion animal burns include heating pads, hot water bottles, fire, exhaust systems, and hot pipes. ASSOCIATED CONDITIONS & DISORDERS Early gram-positive and later gram-negative infections are common in burn wounds.
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES First-degree (superficial) burns: Epidermis Typically thickened, erythematous, and desquamated Typically painful Second-degree (deep partial thickness) burns: Superficial layers of dermis Typically edematous and erythematous Typically wet and very painful Third- and fourth-degree burns: Superficial layers of dermis (third-degree) and subcutaneous layers, tendon, and bone (fourth-degree) Typically waxy and leathery in appearance Typically less painful than first- or second-degree Third- and fourth-degree burns carry a greater risk of wound sepsis, coagulation disorders, limb ischemia, or compression severe enough to cause ventilatory compromise or abdominal problems. Electrical burns (see p. 342 ): High-voltage: associated with compartmental syndromes and ischemia Low-voltage: seldom associated with complication Chemical or tar burns usually involve the superficial dermis layers. HISTORY, CHIEF COMPLAINT History and chief complaint reflect acute trauma. Recent anesthetic procedures should prompt suspicion of heating blanket or heating lamp burn. With acts of malicious intent, history may be unknown.
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PHYSICAL EXAM FINDINGS Physical examination findings depend on the location and extent of the burn. Burns from contact may not initially be apparent until rapid skin and hair loss occur 2-3 days later. Thermal burn resulting from a heating blanket or lamp will present as a defined injury reflective of the size of the blanket and the positioning of the animal during recumbency. Animals with extensive burns may present in hypotensive shock or with hypothermia. The presence of singed whiskers or burn debris in the mouth is strongly suggestive of inhalation (see p. 1027). Respiratory distress can occur rapidly from pharyngeal and laryngeal edema, progressive upper airway obstruction, pulmonary edema, inhalation of burn debris, or carbon monoxide toxicity. Corneal trauma may be present.
ETIOLOGY AND PATHOPHYSIOLOGY Localized wound inflammation results in release of inflammatory mediators and capillary leakage, causing extravasation of fluid. If systemic inflammation or vasculitis occurs, fluid losses may be severe and result in hypotension or cardiac collapse necessitating intensive IV fluid resuscitation. Burns are colonized initially by normal flora. Due to large volume of dead tissue and impaired blood supply and antimicrobial delivery, large burn areas are at high risk of infection. Initial organisms are gram-positive cocci, but in 3-5 days, gram-negative bacteria colonize the wound. Débridement and topical antibiotics are essential to treatment. Sepsis may result from wound infection, nosocomial infection due to the presence of multiple invasive catheters, or the development of pneumonia. Systemic inflammation may result in coagulopathy, including disseminated intravascular coagulopathy Inhalation injury: see Smoke Inhalation, p. 1027
DIAGNOSIS DIAGNOSTIC OVERVIEW Thorough history including initial time and duration of exposure typically will be suggestive or conclusive of thermal injury; however, the full extent of burns may not be apparent immediately after the injury. Determination of the severity of the burn and appropriate treatment course requires examination of the lesion, including underlying and surrounding normal tissue. Diagnostic testing for related disorders (e.g., smoke inhalation) is applied as indicated in each case.
DIFFERENTIAL DIAGNOSIS Severe bacterial pyoderma Immune-mediated disease Fungal infection Abscess Aspiration pneumonia Sepsis
INITIAL DATABASE CBC, including manual platelet count Serum biochemistry profile Urinalysis Coagulation panel, including prothrombin and partial thromboplastin times Survey radiographs Bacterial cultures if evidence of pneumonia
ADVANCED OR CONFIRMATORY TESTING Wound culture if infected Brain CT or MRI if unexplained alteration in mentation
TREATMENT
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TREATMENT OVERVIEW Wound management is vital to preventing septic complications and minimizing tissue loss. Intravenous fluids, broad-spectrum antimicrobials, and in some cases supplemental oxygen are cornerstones of treatment. Overall goals of treatment are to maintain a patent airway, adequate mean arterial blood pressure and plasma oncotic pressure, and adequate urine production.
ACUTE GENERAL TREATMENT Intensive IV fluid resuscitation with crystalloid fluids (e.g., 0.9% NaCl) during the initial 8-12 hours of injury to maintain adequate mean arterial blood pressure and urine production at 1-2 mL/kg/h Maintenance of airway patency in presence of pharyngeal or laryngeal edema, with early elective intubation if necessary First- and second-degree burns may be self-limiting. Greasy or oil-based dressings (e.g., Vaseline-impregnated gauze) should be avoided. Third- and fourth-degree burns may require early escharotomy (débridement/burn excision) or fasciotomy to limit wound sepsis, stricture, or limb ischemia. In cases with concurrent smoke inhalation, supplemental oxygen provided within the first 12 hours of injury will help treat carboxyhemoglobinemia. Mechanical ventilation may be required to maintain oxygen saturation. Broad-spectrum antimicrobial coverage if evidence of pneumonia until culture results are available (e.g., ampicillin, 22 mg/kg IV q 8 h, plus enrofloxacin, 3 to 5 mg/kg IM or off-label use [diluted 1 : 1 in 0.9% sterile saline and given slowly IV] q 12-24 h; maximum 5 mg/kg q 24 h in cats).
CHRONIC TREATMENT First- and second-degree burn wounds may require little débridement. Application of antimicrobial topical creams such as silver sulfadiazine or 0.5% silver nitrate is recommended. Small eschars should be débrided for primary closure early in the course of wound care. Large eschars not amenable to primary closure should be débrided, allowed to form granulation tissue, and grafted. Open wound management presents a high potential for wound sepsis and is thus not advised if avoidable. See Shearing/Degloving Wounds (p. 1016) for details of wound treatment. Serious burns involving the limbs should be débrided to avoid limb ischemia, and treated with variations of splinting to avoid contracture. Intravenous fluid therapy should be titrated to replace losses/correct dehydration, maintain arterial blood pressure, and sustain appropriate urine production. Systemic inflammation and leaky vessels may result in protein loss and severe hypoalbuminemia. Judicious use of synthetic colloids (Hetastarch 20 mL/kg/24 h or Voluven 40 mL/kg/24 h) may be required to maintain colloid oncotic pressure and mean arterial blood pressure. Transfusion with fresh frozen plasma is recommended in cases of coagulopathy (see Transfusion Reactions, p. 1111). Serum electrolytes should be monitored. In cases of severe inhalation injury, maintenance of long-term intubation or tracheostomy may be required until resolution of burn trauma and associated pharyngeal, laryngeal, and airway edema. Mechanical ventilation may be required for management of direct lung injury from inhalation of carbon debris, aspiration pneumonia, or pulmonary edema.
NUTRITION/DIET Parenteral or enteral nutrition should be instituted early in patients with large burns, as increased metabolic demand and protein losses can be significant (see p. 1267 and p. 1322).
BEHAVIOR/EXERCISE For third- and fourth-degree burns, especially when involving tissues affected by motion (limbs, axilla, inguinal region, flank, etc.) strict rest for 3-4 weeks may be necessary. Physical therapy or hydrotherapy may be beneficial to patients with large body surface regions affected.
POSSIBLE COMPLICATIONS Wound infection Aspiration pneumonia Nosocomial infection Sepsis Limb ischemia from wound contracture Coagulopathy
RECOMMENDED MONITORING
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Mean arterial blood pressure Central venous pressure Quantification of urine production Oxygen saturation CBC, serum biochemistry profile, coagulation tests
PROGNOSIS AND OUTCOME Outcome is generally good with first-and second-degree burns and more guarded with third- and fourth-degree burns. Prognosis is guarded to poor with inhalation injury. Prognosis relies on response to fluid resuscitation in severe burn injury. Prognosis improves with appropriate and successful wound management and worsens with development of complications like nosocomial infection and sepsis.
PEARLS & CONSIDERATIONS COMMENTS Third- and fourth-degree burns, and/or inhalation, are best treated in a tertiary care facility with 24-hour intensive care management and surgeons skilled in surgical burn management, including skin grafting. Severe eschars causing constriction of ventilatory muscles or limb ischemia require early débridement and primary would closure or grafting to limit wound infection and reduce the risk of compartmentalization. Large burns resulting in marked protein loss may be best treated with fresh frozen plasma transfusion to replenish proteins for tissue repair, oncotic support, coagulation factors, and acute phase proteins. Respiratory distress in a patient with evidence of inhalation (e.g., burned whiskers) may be due to pharyngeal or laryngeal edema and warrants intubation to obtain and maintain airway patency. Iatrogenic thermal burns as a complication from heating pads or lamps during anesthetic procedures may be the most common type of burn injury not resulting in death. Burn injury resulting in death occurs most commonly from house fires or malicious acts.
PREVENTION Use of circulating warm water or warm air blankets should be used for surgical or hospitalized patients rather than electric heating blankets. Patients should not be placed in direct contact with hot water bottles for warming. Duration of time in contact with the warming device influences the extent of injury; therefore, the patient or the warming device should be repositioned frequently.
TECHNICIAN TIPS Always place a towel or blanket between a patient and a warming device.
SUGGESTED READING Fossum TW, et al: Surgery of the integumentary system. In Small animal surgery, ed 3, St Louis, 2007, Mosby, p 228. Sheridan RL: Burns. Crit Care Med 30[Suppl]: S500–S514, 2002. Garzotto C: Thermal burn injury. In Hopper and Silverstein, editors: Small animal critical care, St Louis, 2008, Saunders, p 683. AUTHOR: KRISTIN WELCH EDITOR: ELIZABETH ROZANSKI 1ST EDITION AUTHOR: THERESE O’TOOLE
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Budd-Chiari-Like Syndrome and Cor Triatriatum Dexter
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Budd-Chiari-Like Syndrome and Cor Triatriatum Dexter BASIC INFORMATION DEFINITION Uncommon cardiovascular defects that partially obstruct the flow of blood into or through the right atrium Cor triatriatum dexter (CTD): Congenital cardiac defect resulting from persistence of the embryologic right sinus venosus valve The result is a membranous division of the right atrium, which obstructs hepatic venous return to the heart. Cranial vena caval flow is unaffected. Budd-Chiari syndrome (BCLS): Originally described as hepatic postsinusoidal hypertension secondary to inflammation and thrombosis of small hepatic veins. Result: obstruction of venous return to the heart, resulting in ascites, hepatomegaly, and abdominal pain. Currently, it is often used loosely to describe obstruction of venous return to the right heart caused by such diverse entities as cor triatriatum dexter, right atrial neoplasia, and caudal vena cava obstruction secondary to masses or traumatic kinking/fibrosis. These disorders are more appropriately referred to as Budd-Chiari-like syndromes.
EPIDEMIOLOGY SPECIES, AGE, SEX Canine: most often in patients 2.5 g/dL), relatively low nucleated cell count (usually 400 genetic diseases have been identified in dogs. Bitches requiring elective caesarean section (e.g., brachycephalics) require intense monitoring to establish the time of their luteinizing hormone (LH) surge during estrus. RISK FACTORS Advanced age of dam and/or sire Use of cooled or frozen semen Dam's or sire's history of unsatisfactory fertility Degenerative and/or infectious conditions within the reproductive tract CONTAGION & ZOONOSIS Brucella canis (see p. 162) GEOGRAPHY AND SEASONALITY Bitches cycle at any time of the year (except basenji—late summer/early fall). ASSOCIATED CONDITIONS & DISORDERS Estrus induction, artificial insemination, pregnancy diagnosis.
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT Owner desires litter from dam and wants to maximize fertility and fecundity. PHYSICAL EXAM FINDINGS Physical exam should be unremarkable. Overt signs of estrus should be evident: Swollen, edematous vulva Serosanguineous vaginal discharge Perineal stimulation results in lateral deviation of the tail (“flagging”), elevation of the vulva, and lordosis
ETIOLOGY AND PATHOPHYSIOLOGY
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Breeding Management
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Developing follicles secrete estradiol initially (proestrus), followed by progesterone after the LH surge has occurred (estrus). Follicles ovulate 2 days after the LH surge, and oocytes are fertile another 2 days later. Oocytes remain fertile for 4 days. Breeding should occur between 3 and 8 days after the LH surge.
DIAGNOSIS DIAGNOSTIC OVERVIEW For optimal timing of breeding, determine the day of the preovulatory LH surge by detecting the first day on which serum progesterone concentration exceeds 2 ng/mL or by measuring serum LH concentrations directly. Additional value may be found in vaginal cytology and vaginoscopy (see p. 1361 ), both of which are inexpensive, provide immediate results, and may be performed on site but are less accurate than hormone assays. Therefore, a typical protocol for a bitch whose signs of estrus are subtle involves daily vaginoscopy or vaginal cytology until characteristic changes of early estrus are noted at which time serum progesterone is measured q 24-48 h.
DIFFERENTIAL DIAGNOSIS Persistence of estrous behavior: granulosa cell tumor, endocrine-secreting anovulatory follicle(s) Discharge from an open pyometra Vaginal or uterine trauma resulting in bleeding
INITIAL DATABASE Vaginal cytologic evaluation: Start 0 to 5 days after the onset of vaginal bleeding and continue q 48 h to monitor estrogenization of the vaginal mucosa. Use a cotton swab moistened with saline, and extended with hemostat or artificial insemination pipette to reach through a vaginal speculum for collection of cells from cranial vagina. The vaginal cytology will contain 100% superficial cells (cornified; large, angular, often with folded edges) during estrus, many of which still have nuclear remnants or pyknotic nuclei. Presence of 50% or more cornified cells can be used as the threshold for beginning measurement of serum progesterone levels. Serum progesterone concentration Start determining serum progesterone concentration once there is maximal development of the squamous epithelium and/or the vaginal cytology contains 100% superficial cells. Refrigeration of whole blood during the first 2 hours after sample collection significantly decreases measured serum progesterone concentrations in dogs. When whole clotted blood is not centrifuged immediately after collection, it must not be refrigerated for at least 2 hours, because this will affect serum progesterone concentrations. The day of LH surge (d0) is the day preceding the first day on which serum progesterone concentration exceeds 2 ng/mL. Progesterone can be measured by laboratory assays (RIA or chemiluminescence) or by patient-side semiquantitative ELISA assay. Brucella canis testing is essential (see p. 162).
ADVANCED OR CONFIRMATORY TESTING Vaginoscopy (see p. 1361 ) Start 0 to 5 days after onset of vaginal bleeding; continue q 48 h to monitor estrogenization of the vaginal mucosa. Tubular Plexiglas speculum, 10-20 mm inner diameter, 15-25 cm length. Maximal development of the squamous epithelium (evident as paleness) and edema (evident as swollen, rounded folds) of the vaginal mucosa coincides with peak estradiol concentrations, just before LH surge. Serum LH concentration Commercial kits are available for semiquantitative assessment of serum LH concentrations. Once- or twice-daily testing is required; LH concentrations will only remain elevated for 18-24 h.
TREATMENT TREATMENT OVERVIEW
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Breeding Management
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Breeding management is preventive. Therefore, under most circumstances, treatment as such is not indicated. Proactive strategies help to optimize efficacy of breeding.
ACUTE GENERAL TREATMENT Breeding strategies Natural service, fresh or shipped (cooled) semen artificial insemination: Breed on days 4 and 6 after LH surge. Inseminate vaginally, using a 5-mm-thick plastic pipette that is advanced to the caudal end of the cervix (confirm placement by abdominal palpation). Once the pipette is placed, the semen is injected slowly through a syringe attached to the pipette, the pipette is withdrawn, and a finger is placed into the vestibulum and used to massage the floor of the cranial vestibulum (“feathering”) for 1-10 minutes (vaginal contractions result and facilitate movement of semen through the cervix). Elevation of the bitch's hindquarters (theoretical benefit of gravity) is often practiced but does not improve fertility. Artificial insemination with frozen or poor-quality fresh/cooled semen: Breed between days 5 to 7 after LH surge. Perform laparotomy and inject semen through uterine wall into the uterine lumen, or perform transcervical catheterization and inject semen directly into uterine lumen (see p. 1346). Transcervical catheterization can be performed either via an endoscopically guided transcervical catheter (dedicated equipment) or with a Norwegian catheter that can be guided through the cervix using abdominal palpation (advanced skill and experience needed). Transcervical catheterization allows for repeat inseminations on multiple days. With frozen semen, more than one insemination at daily intervals and a lower sperm dose produces better results than a single, well-timed insemination with a high sperm dose. Two to four daily vaginal inseminations with frozen-thawed semen extended with prostatic fluid have yielded excellent results as well. Natural copulation can be simulated by the use of a dedicated insemination catheter that allows for the insufflation of a large cuff that seals the vagina to prevent backflow of semen after insemination (MAVIC, Minitube of America).
BEHAVIOR/EXERCISE Unrestricted exercise To prevent unintentional matings, estrous bitches must not have contact with intact male dogs.
POSSIBLE COMPLICATIONS For surgical artificial insemination, clients must be warned that no anesthetic protocol is totally safe, and about 8% of all elective soft-tissue surgeries result in postoperative complications (e.g., infection, wound dehiscence, delayed healing) despite the use of modern techniques and procedures aimed at preventing such complications. Inappropriate timing of artificial insemination or use of poor-quality semen can result in a reduction of expected litter size.
PROGNOSIS AND OUTCOME Average pregnancy rates after artificial insemination with fresh, chilled, or frozen-thawed semen vary greatly between 45% and 90%.
PEARLS & CONSIDERATIONS COMMENTS Animals should be tested for brucellosis and heritable disorders before breeding. Semen quality should be assessed in advance of insemination. In-house test kits for semiquantitative determination of serum progesterone and luteinizing hormone concentrations of bitches are available for use when veterinary diagnostic laboratory services are not available. The day of LH surge (d0) is the day preceding the first day on which serum progesterone concentration exceeds 2 ng/mL.
TECHNICIAN TIP
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Follow instructions very carefully when performing in-house or patient-side serum progesterone or LH tests, as results are a cornerstone of success.
CLIENT EDUCATION Days 3-8, or days 4 and 6, after the LH surge are the most fertile days for breeding bitches, but pregnancies can result from breeding up to 3 days earlier or 2 days later using fresh semen. Estrus monitoring is also used to predict the most likely whelping date: 65 (±1) days after the LH surge or 57 (±1) days after cytologic diestrus (D1).
SUGGESTED READING Goodman M: Ovulation timing. Vet Clin North Am Sm Anim Pract 31:219, 2001. Lindsay FEF, Concannon PW: Normal canine vaginoscopy. In Burke T, editor: Small animal reproduction and infertility. Philadelphia, 1986, Lea & Febiger, pp 112–120. Nothling JO, Gerstenberg C, Volkmann DH: Success with intravaginal insemination of frozen-thawed dog semen: a retrospective study. J So Afr Vet Assoc 66:49, 1995. Volkmann DH: The effects of storage time and temperature and anticoagulant on laboratory measurements of canine blood progesterone concentrations. Theriogenology 66(6-7):1583, 2006. Wilson MS: Transcervical insemination techniques in the bitch. Vet Clin North Am Small Anim Pract 31:291, 2001. AUTHOR: DIETRICH VOLKMANN EDITOR: MICHELLE A. KUTZLER
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Brain Neoplasia
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Brain Neoplasia BASIC INFORMATION DEFINITION Primary brain tumors include meningioma (discussed separately; see p. 715), glioma (astrocytoma, oligodendroglioma), choroid plexus tumor, ependymoma, medulloblastoma, olfactory neuroblastoma, and primitive neuroectodermal tumor. Secondary brain tumors include pituitary tumors, tumors that invade by direct extension into the brain (e.g., nasal tumors), and metastatic tumors to the brain (e.g., hemangiosarcoma, lymphoma [latter is discussed separately]; see p. 671 ).
EPIDEMIOLOGY SPECIES, AGE, SEX Occurs in both dogs and cats of both sexes Incidence reported as high as 2.6% in dogs and 2.8% in cats Brain tumors typically occur in older dogs (most > 5 years old) and cats. Median age: 9 years (dogs), 11 years (cats). GENETICS & BREED PREDISPOSITION Canine: Dolichocephalic breeds (e.g., golden retriever, German shepherd dogs) tend to develop meningiomas. Brachycephalic breeds (e.g., boxer, Boston terrier) appear prone to developing gliomas. Feline: no breed predisposition. Meningioma is the most common brain tumor in cats.
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES Meningioma: tumor of the arachnoid membrane Glioma: tumor of the cells that form the interstitial tissue of the central nervous system (CNS) Choroid plexus papilloma: tumor of the cells of the choroid plexus, the intracranial vascular structure responsible for the formation of cerebrospinal fluid Ependymoma: tumor of the ependymal cells that line the ventricular system HISTORY, CHIEF COMPLAINT A brain tumor should be suspected in any older patient with an insidious onset of slowly progressive neurologic signs, and in any patient older than 5 years with a recent onset of seizures. Historic findings depend on lesion location. Clinical signs are often insidious and progressive; however, recent onset of clinical signs is possible. The most common chief complaints include seizures, circling, behavior change (aggression), altered consciousness, and nonspecific signs such as inappetence and lethargy. PHYSICAL EXAM FINDINGS Neurologic exam findings vary depending on lesion location (see p. 1311). Findings generally reflect a focal lesion with asymmetric clinical signs. However, a large case series found that half of canine brain tumors occupy more than one anatomic region of the brain (e.g., forebrain and brainstem). Cerebral brain tumors: seizures, contralateral menace and postural reaction deficits, behavior change, contralateral hemiparesis, altered mental status Brainstem brain tumors: ipsilateral cranial nerve deficits, hemiparesis or tetraparesis or tetraplegia, altered mental status, central vestibular dysfunction Cerebellar brain tumors: hypermetria, intention tremors, truncal sway, broad-based stance, paradoxical vestibular dysfunction
ETIOLOGY AND PATHOPHYSIOLOGY Etiology is unknown. Usually occur as solitary masses. Multiple tumors may be seen with metastatic disease.
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Most commonly reported in the supratentorial compartment (rostral to the tentorium cerebelli, including the cerebrum and diencephalon) Biological behavior (benign versus malignant) is generally irrelevant because neoplasia of the brain is detrimental via spaceoccupying effects.
DIAGNOSIS DIAGNOSTIC OVERVIEW Neoplasia of the brain is suspected based on signalment, history, and neurologic examination results. Confirmation requires intracranial imaging (CT or MRI).
DIFFERENTIAL DIAGNOSIS Infectious diseases (bacterial, viral, fungal, protozoal) Inflammatory diseases (e.g., granulomatous meningoencephalomyelitis) Cerebrovascular infarction if clinical signs are acute, nonprogressive, and asymmetric Toxin and metabolic diseases if clinical signs are acute, nonprogressive, and symmetric
INITIAL DATABASE CBC, serum biochemistry profile, urinalysis: usually normal Thoracic and abdominal radiographs: usually normal but performed to rule out extracranial neoplasia
ADVANCED OR CONFIRMATORY TESTING CT or MRI: MRI is markedly superior for soft-tissue detail (brain, spinal cord) and has higher resolution than CT. As a result, this is the current gold standard for brain imaging. CT is an adequate imaging modality, is superior for bone lesions (e.g., skull tumors), much faster, and may be cheaper than MRI. Focal mass identified for most brain tumors; however, multiple tumors may be identified with metastatic neoplasia. CT and MRI features are variable between tumor types. Cerebrospinal fluid (CSF) analysis: Used as an adjunct to advanced imaging, primarily to assess encephalitis With brain neoplasia, results are generally nonspecific and reveal normal to mildly elevated protein. Albuminocytologic dissociation (elevated CSF protein with normal white blood cell count) can occur but is not pathognomonic. Neoplastic cells are rarely identified within the CSF; however, the presence of lymphoblasts within the CSF supports a diagnosis of CNS lymphoma. Histopathologic analysis of tissue is required for definitive diagnosis. Tissue samples can be obtained via surgical excision or stereotactic brain biopsy.
TREATMENT TREATMENT OVERVIEW Definitive treatment involving surgical excision and/or radiation therapy and/or chemotherapy
ACUTE GENERAL TREATMENT Surgical excision: used for removing or debulking the tumor, if accessible, and for providing a definitive histologic diagnosis Radiation therapy: used as an adjunctive treatment to surgery or as a primary treatment Chemotherapy: most agents are not effective because the blood-brain barrier (BBB) prevents chemotherapeutic agents from entering the brain and spinal cord. The exception to this is nitrosourea drugs. Nitrosourea agents such as lomustine (CCNU; 60-90 mg/m2 PO q 6 wk) or carmustine (BCNU 50 mg/m2 IV q 6 wk), which can cross the BBB, appear to have some effect in canine gliomas and canine CNS lymphoma. The most serious potential adverse effects are bone marrow suppression (anemia, thrombocytopenia, leukopenia) and hepatotoxicity. The use of hydroxyurea (20 mg/kg PO q 24 h) has been shown to significantly increase survival times in dogs with
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meningiomas, compared with use of prednisone alone. Side effects at this dose are typically mild to nonexistent. Cluster seizures or status epilepticus: diazepam, 0.5 mg/kg IV (can be repeated at 5-minute intervals for a maximum of three doses). If diazepam is initially effective, but seizures recur, consider diazepam IV constant rate infusion (0.25-0.5 mg/kg/h) or loading dose of phenobarbital IV (to effect, up to 16-20 mg/kg total dose). A seemingly effective newer alternative therapy is intravenous levetiracetam. Cerebral edema/brain herniation: mannitol, 0.5 g/kg IV slowly over 10-15 minutes; furosemide (2 mg/kg IV) has synergistic effects with mannitol and can be given if needed.
CHRONIC TREATMENT Seizures: anticonvulsants should be used if there is more than one seizure every 6-8 weeks. Phenobarbital: 2-4 mg/kg PO or IV q 12 h Potassium bromide: 20-50 mg/kg PO q 24 h; dose can be divided q 12 h to reduce nausea and vomiting. (See p. 1009 and p. 353 .) Use with caution in cats; frequently causes reversible clinical signs consistent with bronchial asthma, but in rare cases has been fatal. Cerebral edema: prednisone, 0.5 mg/kg PO q 12 h initially, then taper to lowest dose that will control clinical signs.
DRUG INTERACTIONS Drug interactions or altered metabolism of medications have been reported between corticosteroids and amphotericin B, furosemide, thiazide diuretics, digitalis glycosides, cyclosporine, phenytoin, phenobarbital, and mitotane. Corticosteroids should not be given concurrently with nonsteroidal antiinflammatory drugs or other potentially gastric ulcerogenic medications. Phenobarbital may cause excessive sedation in dogs with intracranial mass lesions, even at low doses.
POSSIBLE COMPLICATIONS Progression of clinical signs, including status epilepticus, brain herniation, and sudden death
RECOMMENDED MONITORING Serial neurologic exam every 4-6 weeks Serum phenobarbital blood level 2 weeks after starting medication, or any change in dosage, or immediately after loading dose Serum bromide blood level 3-4 months after starting medication, or any change in dosage in dogs and 2 months in cats, or immediately after loading dose
PROGNOSIS AND OUTCOME In general, the prognosis is fair to guarded in both dogs and cats. In dogs, several small-scale reports have shown a median survival time of approximately 2-4 months with supportive care and nonspecific treatment only, 6-12 months with surgery alone, 7-24 months with radiation therapy alone, 6 months to 3 years with surgery and radiation, and 7-11 months with chemotherapy alone. There are no large-scale reports of survival times in cats, with the exception of meningiomas (see p. 715). However, the long-term prognosis for cats with other brain tumors is likely similar to that for dogs.
PEARLS & CONSIDERATIONS COMMENTS With neoplasia of the brain, asymmetric neurologic deficits are much more common than symmetric deficits. Symmetric neurologic deficits make other diagnoses more likely.
TECHNICIAN TIPS Postoperative craniotomy patients are very vulnerable to brain trauma, and comprehensive care (e.g., padding of cage walls, prevention of self-trauma through gentle restraint and padding over the surgical site) can make the difference between a excellent outcome and a life-threatening complication.
PREVENTION
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No known method to prevent disease
CLIENT EDUCATION Warn owner of corticosteroid side effects (e.g., polyuria, polydipsia, polyphagia, weight gain, gastrointestinal ulceration, iatrogenic hyperadrenocorticism). Phenobarbital and KBr: Short-term side effects include sedation/lethargy and pelvic limb weakness and ataxia. Long-term side effects include polyuria, polydipsia, polyphagia, weight gain. Less common adverse effects include hepatotoxicity and blood dyscrasias for phenobarbital and pancreatitis for KBr. See other sources for additional information.
SUGGESTED READING Dewey CW: Encephalopathies: disorders of the brain. In Dewey CW, editor: A practical guide to canine and feline neurology, ed 2, Ames, IA, 2008, Wiley Blackwell Publishing, pp 115–220. Snyder JM, et al: Canine intracranial primary neoplasia: 173 cases (1986-2003). J Vet Intern Med 20:669, 2006. AUTHOR: MARK T. TROXEL EDITOR: CURTIS W. DEWEY
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Brachycephalic Airway Syndrome
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Brachycephalic Airway Syndrome BASIC INFORMATION DEFINITION A syndrome of anatomic and functional abnormalities of the upper airway found in brachycephalic (short-nosed) dogs; results in variable degrees of upper airway distress
SYNONYMS Brachycephalic syndrome; brachycephalic upper airway syndrome; upper airway syndrome
EPIDEMIOLOGY SPECIES, AGE, SEX Brachycephalic airway syndrome occurs almost only in dogs. Mean age at presentation: 3 to 4 years. Age at presentation variable: Young dogs (3-12 months old); clinical signs often associated with stenotic nares Middle-aged dogs with increasingly severe respiratory problems over several years GENETICS & BREED PREDISPOSITION Breeds predisposed: English and French bulldogs, Boston terrier, pug, boxer, Pekinese, shih tzu (shih tzu: rarely elongated soft palate, frequently stenotic nares). RISK FACTORS Deterioration/decompensation producing severe dyspnea: Hot, humid weather Hot ambient temperature (e.g., in car with inadequate ventilation) Exertion GEOGRAPHY AND SEASONALITY More likely to trigger owner concern during summer, when increased ambient temperatures and activity can lead to episodes of severe dyspnea. ASSOCIATED CONDITIONS & DISORDERS Three primary anatomic components of the brachycephalic airway syndrome: Stenotic nares Elongated soft palate Hypoplastic trachea Any or all may be present in any given brachycephalic dog Secondary airway changes that can develop due to increased airway resistance include: Laryngeal saccule eversion Laryngeal collapse Seen in older dogs with chronic, severe, untreated brachycephalic syndrome Obesity: aggravating factor Noncardiogenic pulmonary edema (see p. 933), acute respiratory distress syndrome (see p. 34): Occurs if patient inspires forcefully and excessively against severe upper airway obstruction Can cause persistence of cyanosis/hypoxemia despite relief of upper airway obstruction
CLINICAL PRESENTATION
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HISTORY, CHIEF COMPLAINT History of exercise intolerance, cyanosis, or collapse Gagging or coughing Stertor (heavy snoring) most common, stridor (high pitched) less common PHYSICAL EXAM FINDINGS Stenotic or narrowed nares Stertor or stridor; increased inspiratory sounds Increased expiratory sounds on auscultation if concurrent pneumonia, bronchitis, or noncardiogenic pulmonary edema If in severe respiratory distress: cyanosis, stridor or apnea, hyperthermia
ETIOLOGY AND PATHOPHYSIOLOGY Breeding selection has led to dorsoventral flattening and rostrocaudal shortening of the skull and nasal passages of these dogs. The result is increased negative pressure in the nasal passages and pharynx during inspiration. These anatomic characteristics coupled with redundant and edematous nasopharyngeal and oropharyngeal soft tissues contribute to increased airway resistance and obstruction. If untreated, stenotic nares and an elongated soft palate increasingly interfere with breathing. Excessive negative nasopharyngeal pressure results in laryngeal saccule eversion and laryngeal collapse (inward folding of the epiglottis and arytenoid cartilages). As the nasopharyngeal mucosa becomes edematous and inflamed, it contributes to upper airway obstruction.
DIAGNOSIS DIAGNOSTIC OVERVIEW The characteristic inspiratory stertor in brachycephalic breeds is suggestive of the diagnosis on physical examination alone. Confirmation requires a sedated oropharyngeal examination and cervical and thoracic radiographs.
DIFFERENTIAL DIAGNOSIS Upper airway mass: neoplasia, polyp, granuloma, foreign body, abscess Laryngeal paralysis Cervical or laryngeal trauma Coagulopathy resulting in laryngeal hematoma Collapsing trachea
INITIAL DATABASE CBC, serum biochemistry profile, urinalysis: generally unremarkable Lateral cervical radiographs: length of soft palate, hypoplastic trachea Inspiratory and expiratory thoracic radiographs (to assess for complications and rule out differential diagnosis): Tracheal collapse Chronic small airway disease Pneumonia Noncardiogenic pulmonary edema
ADVANCED OR CONFIRMATORY TESTING Rapid-acting anesthetic induction and oropharyngeal/laryngeal examination (e.g., propofol, 4-6 mg/kg given slow IV to effect): be prepared to intubate and ventilate if necessary, given propofol's apnea-inducing qualities: Determine if soft palate excessively long Presence of laryngeal saccule eversion Presence of laryngeal collapse
TREATMENT
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TREATMENT OVERVIEW Immediately, if severe dyspnea: Relieve upper airway obstruction via sedation with or without endotracheal intubation or tracheostomy. Minimize patient's anxiety, and thus reduce the risk of noncardiogenic pulmonary edema, hyperthermia, and worsening dyspnea. Long-term: Relieve upper airway obstruction via surgical correction.
ACUTE GENERAL TREATMENT Stenotic nares: Remove excessive cartilaginous tissue of alae (wings) of nostrils by excision. Elongated soft palate: Shorten soft palate by removing excessive or redundant palatal tissue to improve glottal airflow, eliminate excessive negative pressure, and improve functional glottal size. Soft palate resection using sharp transection and suture, or CO2 laser Everted laryngeal saccules: excise everted mucosal tissue. Traction and amputation of everted mucosa with scissors, scalpel, or CO2 laser Laryngeal collapse: Cannot be surgically corrected Permanent tracheostomy may be necessary Hypoplastic trachea: no surgical treatment Complications: treatment as required should they occur
BRACHYCEPHALIC AIRWAY SYNDROME Preoperative open-mouth view of the elongated soft palate (asterisk) of a French bulldog with brachycephalic airway syndrome. A stay suture (arrow) is placed through the caudal tip of the soft palate in preparation for resection. (Courtesy Dr. Richard Walshaw.)
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BRACHYCEPHALIC AIRWAY SYNDROME Postoperative view of the same dog. Resection of the elongated soft palate is complete, creating a pharynx with a more normal conformation. Consequently, the larynx (arrows) is more easily seen, illustrating the improvement brought by the soft palate resection. (Courtesy Dr. Richard Walshaw.)
CHRONIC TREATMENT Avoid exposure to high ambient temperatures and humidity and other sources of stress. Maintain optimal body weight.
POSSIBLE COMPLICATIONS Hyperthermia (see p. 480 ) Noncardiogenic pulmonary edema (see p. 933). Sedate early to reduce the risk of this complication. Aspiration pneumonia (see p. 885 ) Excessive shortening of soft palate may result in nasal reflux of food or water or, more rarely, aspiration pneumonia. Laryngeal saccule eversion and collapse may develop if upper airway obstruction persists.
RECOMMENDED MONITORING Owner should be aware of any recurrent signs of upper airway obstruction (exercise intolerance, coughing, gagging, stridor, or stertor), which might indicate progressive degenerative changes in upper airway (laryngeal collapse).
PROGNOSIS AND OUTCOME Guarded prognosis if acute, severe dyspnea: a life-threatening state may exist, but with a good response to treatment, full resolution of signs is possible. Good to excellent long-term prognosis after correction of stenotic nares and resection of elongated soft palate, provided secondary changes have not developed Variable (poor to good) prognosis if laryngeal collapse has developed or if dog has a hypoplastic trachea, depending on degree of airway obstruction
PEARLS & CONSIDERATIONS COMMENTS
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Early detection and surgical treatment are recommended for best outcome and avoidance of secondary changes/complications. Lifestyle modifications are often necessary to minimize episodes of airway distress: Maintain ideal body weight. Avoid stressful situations. Hypoplastic trachea is often a subclinical problem, but if severe it may affect long-term prognosis and outcome after surgery.
PREVENTION Because brachycephalic syndrome is breed-associated and heritable, it is not preventable in a given patient. Episodes of respiratory distress may be minimized by avoiding stress, moderating exercise, preventing obesity, avoiding exposure to high ambient temperatures, and early surgical treatment for elongated soft palate and stenotic nares. Correction of stenotic nares in the puppy may reduce the severity of brachycephalic syndrome later in life.
TECHNICIAN TIPS Hospitalized patients with brachycephalic syndrome require preoperative and postoperative intensive care and constant monitoring. Respiratory obstruction is a potential problem at any time. Technicians caring for these patients perioperatively should be familiar with and comfortable performing: Orotracheal intubation in a brachycephalic dog Oxygen administration Administration of prescribed sedative and analgesic drugs Tracheostomy care Cardiopulmonary resuscitation
CLIENT EDUCATION Discuss breed association and heritability in brachycephalic dogs. Syndrome is progressive and exacerbated by stress, obesity, and exposure to high ambient temperatures. Early surgical intervention is important for most successful outcome.
SUGGESTED READING Davidson EB, et al: Evaluation of carbon dioxide laser and conventional incisional techniques for resection of soft palates in brachycephalic dogs. J Am Vet Med Assoc 219:776–781, 2001. Monnet E: Brachycephalic airway syndrome. In Slatter D, editor: Textbook of small animal surgery, ed 3, Philadelphia, 2002, WB Saunders, pp 808–813. AUTHOR: JOSEPH G. HAUPTMAN EDITOR: RICHARD WALSHAW 1ST EDITION AUTHOR: ELLEN DAVIDSON DOMNICK
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Brachial Plexus Abnormalities
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Brachial Plexus Abnormalities BASIC INFORMATION DEFINITION Dysfunction of the peripheral nerves or nerve roots of the brachial plexus (C6-T2 spinal segments)
EPIDEMIOLOGY RISK FACTORS Dependent on disease subtype: Trauma Antigenic stimulation/allergy ASSOCIATED CONDITIONS & DISORDERS With concurrent traumatic injuries: Shock, hypotension, head trauma, pneumothorax With neoplasia, intervertebral disk disease: +/− signs of unilateral C6-T2 myelopathy
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES Traumatic brachial plexus injury: Neurotmesis: complete avulsion of brachial plexus nerves Unilateral or bilateral; can involve some or all nerves in the brachial plexus Axonotmesis: partial brachial plexus avulsion (endoneurium remains intact) Neurapraxia: stretching/transient damage to nerve(s), without avulsion Brachial plexus neuritis: Idiopathic inflammatory neuropathy of the brachial plexus Nerve sheath tumors (see p. 763) Lymphoma (rare) HISTORY, CHIEF COMPLAINT Thoracic limb lameness, paresis, or paralysis (acute or chronic onset) History of trauma or antigenic stimulation (e.g., vaccination, allergic hypersensitivity [see p. 64 and p. 402 ]) PHYSICAL EXAM FINDINGS Variable, depending on nerve root(s) affected Abnormalities may include: Focal muscle atrophy Evident 5-10 days post injury Neurologic deficits in thoracic limb(s): normal pelvic limbs Thoracic limb monoparesis/monoplegia, or bilateral thoracic limb paresis/plegia Proprioceptive deficit of affected limb(s) Hyporeflexia/areflexia Loss of nociception (superficial or deep pain sensation) to various autonomous zones of thoracic limb(s): evaluate all autonomous zones and all digits for sensory loss (see p. 1412 ) Ipsilateral loss of cutaneous trunci reflex May occur with lateral thoracic nerve injury (C8-T1 spinal nerve roots) Ipsilateral Horner's syndrome May occur with injury of the sympathetic pathway (T1-T3 spinal nerve roots)
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ETIOLOGY AND PATHOPHYSIOLOGY Brachial plexus injury/avulsion: trauma to the thoracic limb(s) that results in abduction, caudal displacement, or extreme flexion/extension of the shoulder joint; results in traction injury to the nerve roots of the brachial plexus as they attach to the spinal cord Complete avulsion more common than partial, caudal nerve root avulsion more common than cranial Brachial plexus neuritis: idiopathic inflammatory response; theories include antigenic stimulation by vaccination, allergic reactions, or diet hypersensitivities (particularly diets containing horse meat). Neoplasia
DIAGNOSIS DIAGNOSTIC OVERVIEW The diagnosis is suspected based on evidence of thoracic limb hypotonic and hyporeflexive monoparesis/monoplegia with normal pelvic limbs. History may include trauma or recent vaccination. Electrodiagnostic testing and advanced imaging (CT/MRI) may confirm etiology and provide prognostic information.
DIFFERENTIAL DIAGNOSIS Neoplasia Musculoskeletal injury: Fractures Dislocations Muscle avulsions Central cord syndrome: Injury or dysfunction of the central spinal cord parenchyma (grey matter) Very rare; reported sporadically with spinal trauma, disk herniation, intramedullary neoplasia, syringomyelia Other focal neuropathies (e.g., early stages of rabies encephalomyelitis or acute canine polyradiculoneuritis/Coonhound paralysis)
INITIAL DATABASE Neurologic examination (see p. 1311 ) Cutaneous sensory evaluation (autonomous zones) and deep pain assessment (see p. 1412 )
ADVANCED OR CONFIRMATORY TESTING Electrodiagnostic testing (see online chapter: Electromyography and Nerve Conduction Velocity): may confirm loss of function but generally not essential for diagnosis Abnormal spontaneous muscle activity seen with electromyography Decreased motor or sensory nerve conduction velocities Myelography, CT, and MRI: often not effective in diagnosing brachial plexus injury; however, may rule out other compressive myelopathies or neuropathies Brachial plexus ultrasonography: not effective for diagnosing brachial plexus injury; may be useful to localize neoplasia located within the brachial plexus
TREATMENT TREATMENT OVERVIEW Treatment mainly consists of maintaining joint mobility and preventing muscle contracture and self-mutilation of affected limb(s) while awaiting return of neurologic function and ability to ambulate.
ACUTE GENERAL TREATMENT Supportive care/trauma resuscitation Prevent self-mutilation and external trauma to affected limb(s): Booties to protect paw from abrasions and scuffing E-collar to prevent licking, chewing, or other self-mutilation
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Neuropathic analgesia (i.e., gabapentin 10 mg/kg PO q 8 h) may help prevent paresthesia and self-mutilation. Corticosteroids may be beneficial in brachial plexus neuritis; however, insufficient information exists to confirm their efficacy.
CHRONIC TREATMENT Prevent self-mutilation. Physical therapy (see p. 1329 ): prevent muscle contracture and maintain range of motion/extensor ability should neurologic function return: Target-all joints, including carpus and digits. Perform range of motion (ROM) exercises for 10-15 minutes 3-5 times daily. Limb amputation: treatment of choice for permanent unilateral brachial plexus avulsion or if documented or highly suspected nerve sheath tumor Euthanasia is warranted in permanent bilateral avulsions. Limb-sparing treatments for brachial plexus avulsion have been attempted, including nerve root transplantation, transposition, neurotization, and muscle transposition. Treatment results are generally unsatisfactory. Transposition and neurotization of the intact contralateral C8 ventral root in dogs shows some promise, but at this time, recovery of neurologic function remains limited.
NUTRITION/DIET Avoid diets containing horse meat.
POSSIBLE COMPLICATIONS Paresthesias/sensory nerve injuries promote self-mutilation. Abrasions may occur on the dorsum of the paw from scuffing/dragging the affected limb during ambulation, creating a potential portal for infection. Peripheral nerve sheath tumor that goes on to invade the vertebral canal
RECOMMENDED MONITORING Serial assessment of cutaneous sensation and motor function every 2-4 weeks
PROGNOSIS AND OUTCOME Loss of deep pain sensation suggests avulsion and warrants a grave prognosis for return of function. Preservation of deep pain sensation warrants a guarded to good prognosis for return of function over weeks to months. Lack of any neurologic improvement over a 4-week period suggests permanent deficit. Brachial plexus neuritis has a guarded prognosis; recovery is possible.
PEARLS & CONSIDERATIONS COMMENTS Physical therapy is imperative in cases with potential for recovery. Splints or bandages are generally not recommended because they impair mobility. Evaluate all digits for deep pain sensation; peripheral nerve deficits may be localized and identified in only one digit. Neoplasia may present as an acute onset/trauma event.
PREVENTION Minimize risk of motor vehicle trauma (e.g., riding in open truck beds where pets could jump or be thrown from the vehicle).
CLIENT EDUCATION If recovery is possible/attempted, train clients to perform effective physical therapy or encourage referral for formal rehabilitation. If amputation is necessary, discuss benefits of amputation and how well pets adapt. Discuss importance of maintaining pet at a lean body weight and the negative impact of concurrent osteoarthritis or hip dysplasia on their pet's ability to ambulate.
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SUGGESTED READING da Costa RC, Parent JM, Dobson H, et al: Ultrasound-guided fine needle aspiration in the diagnosis of peripheral nerve sheath tumors in 4 dogs. Can Vet J 49(1):77–81, 2008. Dewey CW: Disorders of the peripheral nervous system. In CW Dewey, editor: A practical guide to canine and feline neurology, ed 2, Ames, IA, 2008, Wiley-Blackwell Publishing, pp 427–467. Rose S, Long C, Knipe M, et al: Ultrasonographic evaluation of brachial plexus tumors in five dogs. Vet Radiol Ultrasound 46(6):514–517, 2005. Rudich SR, Feeney DA, Anderson KL, et al: Computed tomography of masses of the brachial plexus and contributing nerve roots in dogs. Vet Radiol Ultrasound 45(1):46–50, 2004. AUTHOR: MICHAELA A. CAUTELA EDITOR: CURTIS W. DEWEY 1ST EDITION AUTHOR: REBECCA PACKER
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Botulism
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Botulism BASIC INFORMATION DEFINITION An acute, rapidly progressive generalized lower motor neuron (LMN) paralytic disorder caused by ingestion of an exotoxin produced by the bacterium Clostridium botulinum
EPIDEMIOLOGY SPECIES, AGE, SEX Any breed, either sex. Cats appear highly resistant to botulism (no natural cases reported). RISK FACTORS Ingestion of contaminated food or carrion. CONTAGION & ZOONOSIS There are seven antigenically identified types of botulinum neurotoxins (A-G). Dogs: type C. Large animals: type B. Humans: types A, B, F. ASSOCIATED CONDITIONS & DISORDERS Aspiration pneumonia, ventilatory failure (respiratory arrest)
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT Lower motor neuron paresis/paralysis that is often ascending Begins as weakness in the pelvic limbs and can progress to quadriplegia History of ingestion of carrion or other source of anaerobic bacterial contamination The incubation period after ingestion ranges from hours to 6 days. Botulism is especially likely if multiple animals are affected. PHYSICAL EXAM FINDINGS Decreased LMN reflexes (patellar, others) and muscle tone in all limbs Cranial nerve abnormalities (decreased/absent palpebral and menace, decreased jaw tone and gag, mydriasis, voice change) Level of consciousness maintained, pain perception preserved In severely affected animals, decreased abdominal and intercostal muscle tone is observed, which can require ventilation or lead to death from ventilatory failure. Tail wag is maintained. Parasympathetic dysfunction can also be observed (heart rate changes, regurgitation due to megaesophagus).
ETIOLOGY AND PATHOPHYSIOLOGY C. botulinum is a gram-positive, saprophytic, spore-forming bacterial rod in soil. Clinical signs develop after ingestion of the preformed toxin; it is absorbed from the stomach and small intestine and enters the lymphatics, where it is transported by an unknown mechanism to the neuromuscular junction of cholinergic nerves. A metalloprotease (botulinal toxin) prevents the presynaptic release of acetylcholine at the neuromuscular junction. Toxin binding is quick, irreversible, and independent of temperature and neural activity. Cell membrane receptors have a high affinity for the toxin (species and individual variation in sensitivity to toxin). The severity of the signs varies with the amount of toxin ingested and individual susceptibility. The blockage of release of acetylcholine from the presynaptic membrane results in progressive, symmetric, ascending lower
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motor neuron paresis/paralysis. Duration of illness in the dog: 14-24 days
DIAGNOSIS DIAGNOSTIC OVERVIEW The diagnosis is based on a history suggestive of toxin ingestion and the resultant clinical signs. Toxin identification may be undertaken to confirm the diagnosis, but treatment, which is supportive and may be urgently required, is initiated based on neurologic deficits and history.
DIFFERENTIAL DIAGNOSIS Early tick paralysis Early polyradiculoneuritis
INITIAL DATABASE CBC, serum biochemical analysis, and urinalysis: usually normal Neurologic examination consistent with diffuse lower motor neuron dysfunction Thoracic and abdominal radiographs may occasionally reveal megaesophagus (with or without signs of aspiration pneumonia) and carrion skeletal remains in the gastrointestinal tract, respectively, but radiographic abnormalities are not required to make the diagnosis of botulism.
ADVANCED OR CONFIRMATORY TESTING Confirmatory diagnosis is based on finding the toxin in serum, feces, vomitus, or food samples. Preferred method of toxin identification is the mouse neutralization test. Other in vitro tests (radioimmunoassay, passive hemagglutination, enzyme-linked immunosorbent assay and polymerase chain reaction) exist but have not replaced the mouse test to date. Electrophysiologic testing (see p. 1255 ): Marked reduction in muscle action potential amplitude evoked by electrical stimulation of the motor nerve Normal or only mildly reduced nerve conduction velocities Normal electromyography
TREATMENT TREATMENT OVERVIEW Treatment consists principally of supportive care during spontaneous recovery.
ACUTE GENERAL TREATMENT Antitoxin (type specific) must be administered before the botulinal toxin binds to receptors at the myoneural junction. Type C polyvalent antitoxin (dog): 10,000-15,000 IU/dog IV or IM, 2 doses given 4 hours apart Anaphylaxis (see p. 64) is a potential risk; intradermal skin testing is recommended prior to administration. Antitoxin may be effective to prevent further toxin binding if ongoing intestinal absorption/circulation. Antibiotic use is debated; penicillin and metronidazole have been given to dogs and humans to reduce potential intestinal growth of C. botulinum, but use is controversial (disease occurs due to ingestion of preformed toxin; these drugs could alter gastrointestinal flora). Antibiotics if secondary infection (i.e., aspiration pneumonia; based on culture and sensitivity testing).
CHRONIC TREATMENT Long-term physical rehabilitation (see p. 1329 ), frequent turning, and soft bedding are essential.
DRUG INTERACTIONS Avoid aminoglycosides (associated with neuromuscular blockade)
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POSSIBLE COMPLICATIONS Aspiration pneumonia Decubital ulcers Muscle atrophy and fibrosis Ventilatory failure
RECOMMENDED MONITORING Respiratory rate and character; temperature and pulse Chest radiographs Serial neurologic examinations
PROGNOSIS AND OUTCOME Good to guarded. Recovery usually occurs 2-3 weeks after regrowth of terminal motor branches; dependent on severity of signs and complications. Complete recovery can occur spontaneously in moderately affected animals.
PEARLS & CONSIDERATIONS COMMENTS The index of suspicion for botulism increases markedly if more than one animal is affected simultaneously. Referral may be necessary if long-term supportive care and ventilatory support are needed.
PREVENTION Prevention of access to carrion and spoiled food Thorough cooking of any foods fed to dogs and cats Botulinal toxin is destroyed by heating to 80°C for 30 minutes or 100°C for 10 minutes.
CLIENT EDUCATION See Prevention above.
SUGGESTED READING Barsanti JA: Botulism. In Greene CE, editor: Infectious diseases of the dog and cat, ed 3, St Louis, 2006, Elsevier, pp 388–394. AUTHOR: KAREN L. KLINE EDITOR: CURTIS W. DEWEY
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Borreliosis
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Borreliosis BASIC INFORMATION DEFINITION Borreliosis is a bacterial disease that infects humans, mammals, and birds. It is caused by a unicellular, spiral-shaped, gram-negative spirochete, transmitted primarily by Ixodes ticks.
SYNONYMS Lyme disease, Lyme borreliosis
EPIDEMIOLOGY SPECIES, AGE, SEX Susceptibility: humans, dogs, cats Younger dogs more commonly affected. GENETICS & BREED PREDISPOSITION Breeds associated with outdoor activities Labradors, golden retrievers, and Shetland sheepdogs appear predisposed to Lyme nephropathy. RISK FACTORS Tick exposure in endemic areas CONTAGION & ZOONOSIS Direct transmission does not occur from pets to humans. Seropositive dogs/cats are sentinel carriers. GEOGRAPHY AND SEASONALITY In 2005, 89% of human cases reported in the US were from 10 northeastern and mid-Atlantic states (PA, NY, NJ, MA, CT, RI, MD, DE, VA, NH); 6% were from upper Midwest states (WI, MN). Most cases are reported between May and November. ASSOCIATED CONDITIONS & DISORDERS Lyme nephropathy can develop in predisposed animals. Tickborne co-infections are common, especially anaplasmosis (p.66).
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT History of tick exposure in a Lyme-endemic area Most seropositive dogs (95%) show no clinical signs. In highly endemic areas, 70%-90% of healthy dogs are seropositive. Illness in seropositive cats is rare. Less than 5% of seropositive dogs show the syndrome “Lyme arthritis” (anorexia/fever/arthritis). This occurred 2-5 months after tick exposure in experimental beagle puppies (self-limiting), whereas adults showed no clinical signs. No experimental model exists for the less common syndrome “Lyme nephropathy” (protein-losing nephropathy [PLN] with glomerulotubular damage). Patients with this syndrome may present with signs of nephrotic syndrome, hypertension, thromboembolic events, and/or renal failure signs (vomiting/anorexia). PHYSICAL EXAM FINDINGS
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No abnormalities is most common. Lyme arthritis: warm, swollen, painful joint(s), fever (103-106°F, [40-41°C]), lymphadenopathy. Lyme nephropathy: dehydration (renal failure), ascites/edema (nephrotic), aortic thromboembolism/dyspnea (thromboembolic events), retinal hemorrhage/detachment (hypertension).
ETIOLOGY AND PATHOPHYSIOLOGY Borrelia burgdorferi is a small micro-aerophilic spirochete. The agent in North America is B. burgdorferi sensu stricto. The organism multiplies in the tick, entering the host at the end of the tick's bloodmeal (when it regurgitates) after 48-72 hours of attachment. Replication in the skin at the tick bite site is followed by interstitial tissue migration. Clinical signs appear to be due to an immune-mediated pathogenesis (e.g., Lyme-specific antigen-antibody complexes are in glomeruli of dogs with Lyme nephropathy). A persistent carrier state is likely both in healthy-appearing carriers and clinically ill patients. Vectors are I. scapularis (deer tick) in the eastern United States and I. pacificus in the western United States. The whitefooted deer mouse is the main reservoir and preferred host of larval and nymphal ticks. There is no transovarial transmission. Migratory birds are also carriers and disseminate infective ticks.
DIAGNOSIS DIAGNOSTIC OVERVIEW A presumptive diagnosis of borreliosis includes (1) evidence of natural exposure antibodies, (2) clinical signs consistent with borreliosis, (3) consideration of other differentials, and (4) response to treatment, although Lyme nephropathy may not respond well. Overdiagnosis should be avoided; in endemic areas, many dogs with no clinical signs are seropositive. Response to treatment does not confirm diagnosis and may occur by inadvertent treatment of causative co-infections (e.g., Rocky Mountain spotted fever [RMSF], anaplasmosis, ehrlichiosis, bartonellosis, leptospirosis), or the antiinflammatory/antiarthritic properties of doxycycline. All seropositive (clinical and nonclinical) dogs should be monitored for proteinuria. Treatment is not recommended for nonclinical, nonproteinuric seropositive carrier dogs. The dog's sentinel status is an opportunity to educate the owner about tick control and public health aspects of Lyme disease.
DIFFERENTIAL DIAGNOSIS Lyme arthritis versus other causes for lameness Septic arthritis, tickborne arthritides (anaplasmosis, ehrlichiosis, RMSF, bartonellosis), immune-mediated polyarthritis, systemic lupus erythematosus, rheumatoid arthritis Degenerative joint disease, intervertebral disk disease, trauma Panosteitis, osteomyelitis, polymyositis, neoplasia Cardiopulmonary, metabolic, neurologic disease Lyme nephropathy Proteinuria: urinary tract infection, neoplasia, calculi PLN: genetic, infectious, immune-mediated, amyloidosis, neoplasia Other causes for hypertension, hypercoagulable state, edema/effusions, and/or renal failure
INITIAL DATABASE To confirm exposure and rule out other causes of lameness/fever or PLN: CBC and serum biochemistry profile: no specific findings expected unless Lyme nephropathy: hypoalbuminemia, hypercholesterolemia, ± azotemia, hyperphosphatemia, anemia, thrombocytopenia possible. SNAP-4Dx (IDEXX Laboratories) for heartworm antigen and antibodies to C6 peptide (specific for natural exposure to B. burgdorferi), E. canis/chaffeensis, and A. phagocytophilum/A. platys. This test replaces previous two-tier testing with Western blot for differentiating natural exposure from vaccine-induced antibodies, because the C6 peptide of the VlsE antigen is not found in any Lyme vaccines. IgM/IgG titers are not warranted. Experimentally infected dogs did not show signs of Lyme disease until 2-5 months, well after seroconversion (there is no acute stage when they are seronegative), so paired acute/convalescent titers are unnecessary. All Lyme-positive dogs should be screened for proteinuria by urinalysis, microalbuminuria testing, or urine protein/creatinine ratio. Lyme nephropathy cases may also have glycosuria and/or active sediment due to tubular damage. Radiographs of leg(s) involved (nonerosive arthritis)
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Arthrocentesis: nonseptic suppurative inflammation Abdominal ultrasound and chest radiographs to rule out neoplasia
ADVANCED OR CONFIRMATORY TESTING Serology: C6 Quant (IDEXX Laboratories). C6 antibody is detected 3-5 weeks post exposure, before clinical signs appear; paired titers are not necessary. C6 > 30 proves natural exposure (not cause) and is not an indication for treatment in nonclinical, nonproteinuric dogs. Magnitude of titer is not predictive of or correlated with illness. PCR or paired serology for other infectious diseases: RMSF (if acute presentation), anaplasmosis/ehrlichiosis, bartonellosis, babesiosis, leptospirosis. Renal biopsy: glomerulonephritis, tubular necrosis/regeneration, interstitial lymphoplasmacytic inflammation.
TREATMENT TREATMENT OVERVIEW Goals of treatment are: Avoidance of treating patients that have positive titers alone (exposure) in the absence of compatible clinical abnormalities Resolution of lameness and fever if present Palliative/supportive care for complications of PLN
ACUTE GENERAL TREATMENT Doxycycline (10 mg/kg PO q 12-24 h)or amoxicillin (11 mg/kg PO q 8-12 h). Treatment for clinical cases is continued for 4 weeks to try to eliminate the carrier state. Treatment is not recommended for nonclinical, nonproteinuric carriers.
CHRONIC TREATMENT The length of time antibiotics are needed to clear the carrier state is unknown. Treatment for Lyme nephropathy often includes long-term combination doxycycline, angiotensin-converting enzyme inhibitor (e.g., enalapril, 0.5 mg/kg PO q 12-24 h), low-dose aspirin (0.5 mg/kg PO q 12 h), and omega-3 fatty acids. Immunosuppressive therapy protocols are being studied. Supportive care of renal disease may include antiemetics, phosphate binders, intravenous fluids/colloids, antihypertensives, and other agents Some dogs with Lyme arthritis do not improve with antibiotics alone. Corticosteroids are added for suspected immunemediated polyarthritis (e.g., prednisone, 1 mg/kg PO q 12 h, tapering to 0.5 mg/kg PO q 48 h).
RECOMMENDED MONITORING Lyme nephropathy is uncommon even in seropositive retrievers, but it is recommended to continue screening (duration/frequency unknown) all Lyme-positive dogs for proteinuria whether treated or not. If treated, C6 Quant is recommended at 0 and 6 months; the new baseline is for comparison if signs recur. High pretreatment titers usually drop > 50%; lower titers may not. Qualitative C6 (SNAP-4Dx) often remains positive post treatment. For Lyme nephropathy: Monthly monitoring of hematocrit, serum creatinine, serum albumin, urine protein/creatinine ratio, and blood pressure measurement are decreased to every 3-6 months if clinically stable.
PROGNOSIS AND OUTCOME Prognosis is good for Lyme arthritis. Most dogs respond immediately without recurrence. Prognosis is guarded to poor for Lyme nephropathy, especially in hypoalbuminemic/dehydrated/azotemic cases; life expectancy may be days to weeks.
PEARLS & CONSIDERATIONS COMMENTS In humans, the Borrelia vaccine was removed from the market because of poor sales over concern about possible immune-mediated
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sequelae in genetically predisposed individuals.
PREVENTION Tick prevention and control are paramount. Lyme disease vaccines are controversial because the most serious forms of Lyme disease in dogs have an immune-mediated pathogenesis.
CLIENT EDUCATION Proper tick removal and tick control.
SUGGESTED READING Littman MP, Goldstein RE, Labato MA, et al: ACVIM small animal consensus statement on lyme disease in dogs: diagnosis, treatment, and prevention. J Vet Intern Med 20:422–434, 2006. Littman MP: Canine borreliosis. Vet Clin North Am Small Anim Pract 33:827–862, 2003. Goldstein RE, Cordner AP, Sandler JL, et al: Microalbuminuria and comparison of serologic testing for exposure to Borrelia burgdorferi in nonclinical Labrador and golden retrievers. J Vet Diagn Invest 19:294–297, 2007. AUTHOR: MERYL P. LITTMAN EDITOR: DOUGLASS K. MACINTIRE 1ST EDITION AUTHOR: KHRISTEN J. CARLSON
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Boric Acid Toxicosis
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Boric Acid Toxicosis BASIC INFORMATION DEFINITION Toxicosis resulting from ingestion of inorganic compounds of boron used in ant or roach baits, flea products for dogs and cats, cleaning compounds, buffering agents, eye washes, and as an anticaking agent. While ingestions are common, toxicosis is uncommon because of the relatively large amount of product that needs to be ingested. However, clinically significant ingestions are characterized by vomiting, diarrhea, anorexia, lethargy, and (rarely) renal damage.
SYNONYMS Borax, boric acid, orthoboric acid, sodium biborate, sodium borate, sodium perborate, sodium pyroborate, sodium tetraborate
EPIDEMIOLOGY SPECIES, AGE, SEX All breeds of cats and dogs are susceptible. Cats may be exposed after walking through the agent when it is placed on small pieces of cardboard or in small cups in cupboards or closets, or when flea powders containing boric acid are used topically. RISK FACTORS Preexisting kidney disease may increase the risk of nephrotoxicosis from large ingestions.
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT History of using a boric acid–containing product on the animal or in the house (for fleas or control of other insects) Vomiting Hypersalivation Anorexia Lethargy PHYSICAL EXAM FINDINGS Findings tend to be nonspecific Common: Hypersalivation Lethargy Vomiting, diarrhea Possible: Oliguria/anuria Anorexia Ataxia (rare) Seizures (rare)
ETIOLOGY AND PATHOPHYSIOLOGY Source: Some ant baits may contain less than 1% boric acid, whereas some roach products can contain 100% boric acid. Boric acid–containing formulations are available as powders, liquids, or gels. Borates have been used in pharmaceutical preparations (mouthwash, toothpastes, cosmetics), as toiletries, in cleaning compounds, and as insecticides.
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Boric Acid Toxicosis
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Mechanism of Toxicosis: The exact mechanism is unknown. Boric acid is considered cytotoxic to all cells. Rapidly absorbed after oral ingestion through mucous membranes, as well as through abraded skin. Concentrated in the kidneys before excretion, excreted unchanged in the urine. Half-life in dogs is 12 hours, but total elimination may take up to 7 days. No death or serious systemic toxicosis reported in dogs when given 1.54-6.51 g/kg of borax or 1-3 g/kg of boric acid. Examples: 20 ounces (570 g) of a 5.4% boric acid ant bait would have to be ingested by a 20-kg dog to reach a dose of 1.5 g/kg. Similarly, 1.1 ounces (31 g) of a 99% boric acid agent would need to be ingested by a 20-kg dog to reach a dose of 1.5 g/kg. In either case, systemic signs are not likely, except for possibly vomiting and diarrhea.
DIAGNOSIS DIAGNOSTIC OVERVIEW Diagnosis rests on history and physical exam: suspected or witnessed exposure and presence of gastrointestinal disturbance signs (vomiting, diarrhea) that are typically self-limiting.
DIFFERENTIAL DIAGNOSIS Toxicologic: Garbage toxicosis Dietary indiscretion Nephrotoxic agents (ethylene glycol, pharmaceuticals, lilies [cats], grapes and raisins [dogs]) Spontaneous Nontoxicologic: Infectious enteritis (parvoviral, coronaviral, bacterial, etc.) Foreign body
INITIAL DATABASE CBC: microcytic hypochromic anemia Serum biochemistry panel: azotemia, hyperchloremia, hypernatremia, hyperkalemia, and metabolic acidosis may be noted in severe cases; rarely, elevated liver enzymes. Urinalysis: in severe cases causing oliguria or anuria with tubular necrosis, albuminuria, hematuria, proteinuria, and epithelial casts (acute renal failure), or isosthenuria concurrently with azotemia (chronic kidney disease) may be noted
ADVANCED OR CONFIRMATORY TESTING Boric acid may be detected in the urine, cerebrospinal fluid, blood, and plasma.
TREATMENT TREATMENT OVERVIEW Treatment is aimed at inducing emesis in large exposures and providing supportive care as needed, notably in uncommon instances of systemic effects. Most cases are self-limiting (signs resolve within a few hours).
ACUTE GENERAL TREATMENT Decontamination of patient: Emesis (see p. 1364 ): induce vomiting in cases involving large ingestions. Activated charcoal not useful in binding boric acid. Bathe the animal for dermal exposures, using diluted liquid dishwashing detergent. Supportive care: Control excessive vomiting with metoclopramide at 0.022-0.044 mg/kg PO, SQ, or IM, barring gastrointestinal
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obstruction Gastrointestinal protectants: sucralfate, 0.5-1 g q 8 h PO, and famotidine, 0.5 mg/kg PO, SQ, or IM q 12-24 h for 5-7 days IV fluid diuresis for 24-48 hours in cases involving large ingestions Treat renal failure as needed (see p. 31). Control seizures with diazepam, 0.5-2 mg/kg IV unless underlying cause is metabolic (e.g., hypoglycemia, hypocalcemia, hepatic encephalopathy)
CHRONIC TREATMENT Chronic problems not expected Renal injury is uncommon and when it occurs, generally responds to fluid therapy and supportive care.
POSSIBLE COMPLICATIONS May exacerbate preexisting kidney disease
RECOMMENDED MONITORING Recheck renal parameters (blood urea nitrogen, creatinine, urinalysis) at 24 and 48 hours postexposure. If renal parameters are within normal limits at that time, further problems not expected.
PROGNOSIS AND OUTCOME Excellent in animals with signs limited to vomiting/diarrhea after a low-dose exposure
PEARLS & CONSIDERATIONS COMMENTS Activated charcoal adsorbs boric acid poorly (boron compounds do not adhere well to charcoal). A 30:1 ratio of activated charcoal to boric acid was needed to absorb 38% of boric acid in an in vitro study; 5 to 10 times the normal activated charcoal dose would be required to be effective (risk of severe hypernatremia), so activated charcoal is not recommended as a routine part of treatment of boric acid toxicosis. In general, boron compounds have a wide margin of safety, and in most cases of toxicity, only vomiting and diarrhea are noted. Ant baits containing 1%-5% boric acid are not expected to cause a serious problem in dogs or cats. Concentrated boric acid product greater than 50% should be avoided, but products containing less than 5.4% concentration are considered relatively safe.
PREVENTION Avoid using highly concentrated boric acid products directly on animals or in the house (on the carpet especially if cats are around) where direct exposure to pets is likely.
SUGGESTED READING Kiesch-Nesselrodt A, Hooser SB: Boric acid. In Beasley VR, editor: Toxicology of selected pesticides, drugs, and chemicals. Vet Clin North Am Small Anim Pract 369–373, 1990. Welch S: Boric acid. In Plumlee KH, editor: Clinical veterinary toxicology. St Louis, 2004, Mosby, pp 143–145. AUTHOR: ERIC DUNAYER EDITOR: SAFDAR A. KHAN 1ST EDITION AUTHOR: CAROLINE W. DONALDSON
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Bordetellosis
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Bordetellosis BASIC INFORMATION DEFINITION An inclusive term for diseases caused by Bordetella bronchiseptica, a highly contagious aerobic gram-negative cocco-bacillus that is a primary respiratory pathogen for dogs and cats and can cause acute or chronic respiratory disease
SYNONYMS Infectious tracheobronchitis, kennel cough, canine respiratory disease complex. B. bronchiseptica is considered a contributing agent in the acute canine respiratory disease syndrome known by these names.
EPIDEMIOLOGY SPECIES, AGE, SEX Dogs, cats, rabbits, pigs Young animals more susceptible to disease, especially severe disease, than adults RISK FACTORS Increased incidence in dogs and cats exposed to other animals with respiratory infection or housed with large numbers of other animals (shelters, boarding kennels, breeding facilities) CONTAGION & ZOONOSIS B. bronchiseptica is highly contagious: animal-to-animal contact, aerosol, or fomites. Infected animals shed the organism in nasal and oropharyngeal secretions for 3 months or longer post infection. Infection can be transmitted between species. B. bronchiseptica is a rare cause of zoonotic disease: human infection can occur opportunistically (respiratory disease, pleuritis, meningitis, peritonitis) in infants or immunocompromised people. B. bronchiseptica can be isolated from the upper respiratory tract of healthy dogs and cats: up to 10% of healthy household dogs and 5%-11% of healthy household cats are Bordetella positive. GEOGRAPHY AND SEASONALITY Probable worldwide distribution, occurs year-round ASSOCIATED CONDITIONS & DISORDERS Bordetellosis is often part of a disease complex that can include co-infections with canine parainfluenza, canine adenovirus-2, canine distemper, Mycoplasma spp., and/or Streptococcus spp. in dogs and feline rhinotracheitis (feline herpesvirus), feline calicivirus, and other pathogens in cats. Bordetellosis is generally limited to the upper respiratory tract; in some cases, pneumonia can occur.
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT Typically includes exposure to multiple non-housemate animals (kennel/animal shelter, dog show) several days before onset of coughing Chief complaint in dogs is usually acute-onset nonproductive hacking cough, including fits of coughing that result in terminal retch. Chief complaint in cats is sneezing and oculonasal discharge + cough. Severe or complicated cases may be dyspneic, anorectic. PHYSICAL EXAM FINDINGS
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Bordetellosis
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Spontaneous or inducible cough ± Conjunctivitis ± Nasal or ocular discharge ± Submandibular lymphadenomegaly ± Mild to moderate fever, increased lung sounds (pneumonia) in severe cases
ETIOLOGY AND PATHOPHYSIOLOGY The organism colonizes respiratory epithelium of the nasal cavity and trachea and can establish persistent (often subclinical) infections. Infection occurs via contact of the organism with the upper airway and attachment/adherence to the respiratory epithelium by direct binding to cilia, inducing stasis of the cilia and reducing mucociliary escalator clearance of bacteria and other particulate matter from the airways. Airway colonization induces an inflammatory response and increased mucus production. Bordetella spp. produce multiple factors, allowing Bordetella to persist chronically and predispose the host to secondary infections.
DIAGNOSIS DIAGNOSTIC OVERVIEW Bordetellosis often is a suspected diagnosis that goes unconfirmed. Since many infections are mild and self-resolving, the urgency of establishing a diagnosis of bordetellosis specifically is low, and treatment is often initiated based only on clinical signs of upper respiratory infection.
DIFFERENTIAL DIAGNOSIS Dogs: Other agents of infectious tracheobronchitis: canine parainfluenza, canine influenza, canine adenovirus, canine herpesvirus, canine distemper, Mycoplasma spp. infection, Streptococcus spp. infection Chronic bronchitis Collapsing trachea Traumatic tracheitis Airway foreign body Mechanical or chemical airway irritant Other causes of pneumonia: fungal infection, aspiration Cats: Other upper respiratory infections/agents: feline rhinotracheitis (feline herpesvirus 1), feline calicivirus infection, Chlamydophila felis infection, other pathogenic causes of pneumonia
INITIAL DATABASE CBC: often unremarkable; neutrophilia with left shift or toxic neutrophil changes may be seen with pneumonia. Thoracic radiographs: usually unremarkable; pneumonia in severe/complicated cases
ADVANCED OR CONFIRMATORY TESTING Bacterial culture and sensitivity: many healthy animals are culture positive. Nasal or oropharyngeal swabs for bacterial culture: should be plated on selective medium to decrease overgrowth by other respiratory flora. Transtracheal wash or bronchoalveolar lavage if pneumonia or lower airway disease suspected Serologic testing not helpful; many healthy animals have positive titers PCR assays available that differentiate Bordetella spp. including B. bronchiseptica; no routine clinical application
TREATMENT TREATMENT OVERVIEW
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Treatment goals are initiation of appropriate antibiotic therapy and supportive care. Cough suppressants are often indicated to break the cough cycle but are contraindicated in cases with pneumonia or productive cough.
ACUTE GENERAL TREATMENT Antimicrobials: Should be based on culture/sensitivity, especially since Bordetella spp. show high level of antimicrobial resistance Options for empirical treatment pending culture results: Doxycycline (5 mg/kg PO q 12 h) is the antimicrobial of choice (most Bordetella isolates are susceptible). Treat adults for 14-21 days, young (growing) animals for 7-9 days (reduces risk of discoloration of teeth); or Amoxicillin-clavulanate (12.5-25 mg/kg PO q 12 h); or Trimethoprim-sulfonamide (15-30 mg/kg PO q 12 h); or In severe cases, other options include gentamicin, enrofloxacin, and cefazolin. Antimicrobial therapy helps alleviate clinical signs but does not alter shedding in recovered carriers. Antitussives: For suppression of dry, nonproductive cough in milder cases (animal is otherwise well); titrate dose to reduce cough without causing sedation Butorphanol 0.05-1 mg/kg PO q 8-12 h; or Hydrocodone 0.22 mg/kg PO q 8-12 h Contraindicated with pneumonia Bronchodilators: May be indicated in patients with pneumonia Nebulization therapy: Nebulization with sterile saline may help hydrate airway secretions and facilitate clearance, but patient must have adequate systemic hydration as a prerequisite. Nebulization with antibiotic solutions (gentamicin, kanamycin, or polymyxin B) has been suggested for refractory cases to reduce Bordetella populations in the trachea and bronchi, but unpredictable dose delivery to airways. Glucocorticoids: Antiinflammatory doses administered short term may reduce cough. E.g., prednisolone 0.25-0.5 mg/kg PO q 12-24 h for 3-5 days Does not shorten course of disease May exacerbate disease in immunocompromised animals Do not use in cases with severe/complicated disease Adequate systemic hydration very important to facilitate clearance of respiratory secretions
DRUG INTERACTIONS Reduce dose of trimethoprim-sulfa and avoid gentamicin in patients with renal disease. Tetracyclines may cause discoloration of dental enamel in young animals.
POSSIBLE COMPLICATIONS Pneumonia may develop secondary to Bordetella-induced impairment of respiratory defenses. Sulfonamides (trimethoprimsulfonamide) may induce keratoconjunctivitis sicca, hypersensitivity reactions, crystalluria, renal tubule obstruction, polyarthritis, and GI signs.
RECOMMENDED MONITORING Serial thoracic radiographs, CBC, and arterial blood gas to monitor patients with pneumonia Monitor tear production before and during treatment in patients receiving sulfonamides. Monitor BUN, creatinine, and urinalysis in patients receiving gentamicin.
PROGNOSIS AND OUTCOME Disease is usually self-limiting; uncomplicated cases resolve within approximately 2 weeks. Severe (potentially fatal) pneumonia may occur in young or debilitated animals.
PEARLS & CONSIDERATIONS
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COMMENTS Shedding of organisms may continue for 3 months or more after resolution of clinical signs. Transmission of infection to other animals and immunocompromised people may continue during that time; suitable precautions (avoidance of direct or indirect contact) should be taken. B. bronchiseptica is the evolutionary progenitor of B. pertussis, a human-specific pathogen that is the causative agent of whooping cough.
TECHNICIAN TIP Caution is warranted when preparing a vaccine: erroneous SQ injection of intranasal vaccine in dogs has caused severe acute hepatic injury.
PREVENTION Limit transmission by quarantine of new animals and isolation of infected animals. Decrease stress, provide adequate hygiene and care. Disinfect cages and other surfaces (1:32 dilute bleach solution). Vaccination: Parenteral and intranasal (IN) vaccinations are available for dogs, intranasal for cats. Effective in reducing infection rate and severity of clinical signs IN: rapid onset of immunity within 72 hours post vaccination; duration 1 year Vaccinate at least 5 days prior to anticipated exposure (boarding) if possible. Some IN vaccines may be used as early as 2 weeks of age. Intranasal vaccines may induce cough and/or nasal discharge. Animals receiving live vaccines will shed bacteria that may cause infection ± disease in susceptible animals and humans. Natural immunity lasts at least 6 months post infection.
SUGGESTED READING Edinboro CH, et al: A placebo-controlled trial of two intranasal vaccines to prevent kennel cough in dogs entering a humane shelter. Prev Vet Med 62:89–99, 2004. Egberink H, et al: Bordetella bronchiseptica in cats—ABCD guidelines on prevention and management. J Feline Med Surg 11:610, 2009. Ford RB: Canine infectious tracheobronchitis. In Greene CE, editor: Infectious diseases of the dog and cat, ed 3, Philadelphia, 2006, Saunders Elsevier, p 54. AUTHOR: MARCELLA D. RIDGWAY EDITOR: DOUGLASS K. MACINTIRE 1ST EDITION AUTHOR: JEFFREY SIMMONS
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Blue-Green Algae Toxicosis
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Blue-Green Algae Toxicosis BASIC INFORMATION DEFINITION Syndrome of sudden-onset neurologic signs or acute liver failure in dogs caused by ingestion of blue-green algae (BGA) toxins
SYNONYM Cyanobacteria toxicosis
EPIDEMIOLOGY SPECIES, AGE, SEX Dogs: all breeds, ages, and both sexes susceptible Cats: none reported RISK FACTORS BGA blooms are favored by stagnant water, warm water temperatures, ample sunlight, and high nutrients from fertilizer, animal waste, and sewage runoff. GEOGRAPHY AND SEASONALITY Blooms occur mostly in summer or fall.
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES Acute neurotoxic syndrome Subacute hepatotoxic syndrome HISTORY, CHIEF COMPLAINT History of swimming in or drinking water from a pond, lake, or river Vomiting, diarrhea, weakness, and collapse (>6 hr after exposure): hepatotoxic syndrome Salivation, vomiting, diarrhea, dyspnea, tremors, muscle fasciculations, ataxia, weakness, seizures, and death (>15 min after exposure): neurotoxic syndrome PHYSICAL EXAM FINDINGS Presence of algae on the muzzle or on the fur elsewhere on the body is common. Bluish-green and slimy, or may be dried if later presentation. Hepatotoxic syndrome: see History, Chief Complaint above; plus pale mucous membranes, poor capillary refill time, tachycardia or bradycardia, signs of abdominal pain, rapid weak pulse, hypothermia, and shock Neurotoxic syndrome: see History, Chief Complaint above
ETIOLOGY AND PATHOPHYSIOLOGY BGA are microscopic organisms that form colonies visible to the naked eye, rely on photosynthesis for energy, and have a cell wall similar to gram-negative bacteria. Accumulations of large amounts of BGA in lakes, ponds, or rivers are known as waterblooms. BGA blooms exist worldwide and are light to dark green or sometimes reddish-brown. Wind propels toxic algae to the shoreline, where animals are exposed to the organism by ingestion when they drink BGA-contaminated water. Common toxin-producing genera of fresh and brackish water BGA include Microcystis, Anabaena, Oscillatoria, Aphanizomenon, Nodularia, and Nostoc spp.
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Acute hepatotoxic syndrome: Most commonly described poisoning by BGA; caused by low-molecular-weight cyclic heptapeptides and pentapeptides known as microcystins and nodularins. Microcystin-LR (MCLR) is the most toxic and the most frequently encountered of approximately 50 similar peptides. After ingestion, BGA toxins are released from the cells and preferentially absorbed from the ileum. Once inside hepatocytes, toxins inhibit protein phosphatases (PP) types 1 and 2A (PP1 and 2A), causing hyperphosphorylation of cytosolic and cytoskeletal proteins, leading to cytoskeletal disruption, damage, and necrosis. Death is possibly due to massive intrahepatic hemorrhage, hypovolemia, and liver failure. Peracute neurotoxic syndrome; responsible toxins are: Anatoxin-a: an alkaloid and potent postsynaptic depolarizing neuromuscular blocking agent that affects nicotinic and muscarinic acetylcholine receptors Anatoxin-a(s): inhibits peripheral (but not central) cholinesterase irreversibly and is the only known naturally occurring organophosphorus cholinesterase inhibitor (similar to organophosphate pesticides)
DIAGNOSIS DIAGNOSTIC OVERVIEW A tentative diagnosis is based on history of exposure (drinking or swimming in a pond) and rapid onset of clinical signs (vomiting, shock, liver failure, or neurologic signs). Given the potential speed and intensity of progression, treatment may be initiated on this basis. Toxicosis can be confirmed by purification and identification of toxins, but turnaround time means these methods are not clinically useful to an affected patient (e.g., rather for preventative purposes or medicolegal reasons).
DIFFERENTIAL DIAGNOSIS Differentiate from other hepatotoxic agents: amanita mushroom, sago palm, acetaminophen Primary hepatic diseases (see p. 503)
INITIAL DATABASE Hepatotoxic syndrome: CBC: leukocytosis and thrombocytopenia Serum biochemistry panel: increased levels of all liver enzymes, glucose, and possibly creatine phosphokinase. Hypoglycemia is possible after hyperglycemia. Serum bile acids: increase commonly occurs early. Coagulation profile: whole blood clotting time may be normal; prothrombin time and activated thromboplastin times increase twofold to fourfold. Neurotoxic syndrome: Owing to rapid effect of the toxins, no significant serum biochemical changes are expected.
ADVANCED OR CONFIRMATORY TESTING Postmortem (hepatotoxicosis): rounding of hepatocytes, disruption of hepatic cords, loss of sinusoidal integrity, intrahepatic hemorrhage, and centrilobular necrosis Microscopic identification of toxigenic algae. Obtain large specimen (1-2 L) of the algae by straining the cells out of the water with cheesecloth. Specimens can be sent for identification, purification, and quantification of algal toxins, for mouse bioassay, or for ELISA to Dr. Wayne Carmichael's laboratories. Call before shipping specimens. Information available at: http://www.wright.edu/biology/faculty/carmichael/labhome/labhome.htm.
TREATMENT TREATMENT OVERVIEW Early decontamination (induce emesis and give charcoal) of patients not showing clinical signs. For overtly ill patients, treatment of muscarinic and central nervous system (CNS) signs, prevention/treatment of liver damage, and supportive care are cornerstones of therapy.
ACUTE GENERAL TREATMENT Decontamination of patient:
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Emesis: only in animals not showing any clinical signs (see p. 1364 ) Activated charcoal 2-4 g/kg PO Cholestyramine (200-300 mg/kg PO) may be more effective than charcoal (more expensive and must be obtained from a pharmacy). The noncompetitive bile-acid transport inhibitors, rifampicin, and bile salts such as cholate and deoxycholate can inhibit uptake of microcystins. Their utility, however, in clinical algal toxicoses has yet to be determined. Control muscarinic and neurologic signs: Atropine sulfate for muscarinic signs (0.04-0.1 mg/kg IV PRN) Diazepam for seizures 0.5-2 mg/kg IV PRN; other antiseizure medications (e.g., barbiturates) if diazepam is ineffective Supportive care: Control severe vomiting with metoclopramide (0.1-0.4 mg/kg PO, SQ, or IM q 6 h), only if intestinal obstruction has been ruled out (if present, usually unrelated to BGA) or use maropitant 1 mg/kg SQ q 24 h or 2 mg/kg PO q 24 h for 5 days. Treat signs of acute hepatic failure (see p. 503, and p. 501 ). Typical therapeutics may include: Lactulose S–adenosyl methionine (SAMe) Dietary management Vitamin K1 Plasma and/or whole blood transfusions as needed IV fluids (possibly including 5% dextrose) Broad-spectrum antibiotics for secondary infection
POSSIBLE COMPLICATIONS Permanent hepatic insufficiency
RECOMMENDED MONITORING Serum chemistry profile, especially liver-specific enzymes (ALT, AST, GGT, alkaline phosphatase) Serum bile acids CBC Hematocrit Body temperature Blood glucose
PROGNOSIS AND OUTCOME Poor prognosis with systemic signs of acute hepatic damage or severe neurologic dysfunction
PEARLS & CONSIDERATIONS COMMENTS In dogs, BGA poisoning is a sporadic but recurrent cause of acute illness and death. Lethal doses of purified MCLR: rat, 160 mg/kg IP; mouse, 100 mg/kg IP; LD50 of purified anatoxin-a in mouse = 200 mg/kg IP and anatoxin-a(s) = 30 mg/kg IP.
SUGGESTED READING Beasley VR, et al: Diagnostic and clinically important aspects of cyanobacterial (blue-green algae) toxicoses. J Vet Diag Invest, 1:359–365, 1989. Khan SA, et al: Comparative pathology of microcystin-LR in cultured hepatocytes, fibroblasts, and renal epithelial cells. Nat Toxins 3:119–128, 1995. Puschner B, Hoff B, Tor E: Diagnosis of ana-toxin-a poisoning in dogs from North America. J Vet Diagn Invest 20:89–92, 2008. AUTHOR: MARY SCHELL EDITOR: SAFDAR A. KHAN
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1ST EDITION AUTHOR: SAFDAR A. KHAN
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Blindness
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Blindness BASIC INFORMATION DEFINITION Loss of vision
SYNONYMS Amaurosis, central blindness: loss of vision due to a lesion in the central nervous system
EPIDEMIOLOGY SPECIES, AGE, SEX Dogs and cats; any age and sex may be affected, depending on etiology. GENETICS & BREED PREDISPOSITION Several, depending on causative disorder (see p. 448, p. 644, p. 985) RISK FACTORS Age: older animals may be predisposed to diseases associated with blindness, including neoplasia (intracranial, intraocular, optic chiasmal), cataracts, and retinal detachment (see p. 985 ) Outdoor access may predispose to infectious diseases associated with blindness (see p. 141)
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES Unilateral or bilateral Sudden or progressive “Red eye” blindness: associated with visible conjunctival redness on physical examination: Glaucoma (see p. 448), severe uveitis (see p. 1151 ), cataracts (see p. 181), lens luxation (see p. 644), complex corneal ulceration (see p. 250), orbital disease (see p. 790 ) Non-red, noninflamed eye (“quiet eye”) blindness: no conjunctival or scleral redness is observed in the blind eye(s): Prechiasmal/chiasmal blindness Lesion affecting retina, optic nerve, optic chiasm Associated with dilated pupils and pupillary light reflex (PLR) abnormalities Postchiasmal/cortical blindness Lesion affecting optic tracts, lateral geniculate nucleus (LGN), optic radiations, or visual cortex of the cerebrum Pupil size and PLRs usually normal unless optic tracts affected along portions common to PLR and vision pathways (see figure) and/or unrelated, concurrent iris condition (see p. 944) The PLR fibers split from the vision pathway just before the LGN. HISTORY, CHIEF COMPLAINT Variable depending on the underlying cause, whether the blindness is unilateral or bilateral, and sudden or progressive in onset In cases of sudden blindness, all or some of the following may be reported: Disorientation (see p. 314) Suddenly starts bumping into objects within familiar or unfamiliar environments Inability to find food bowl, toys, and the like Lethargy Anxiety In cases of progressive blindness, all or some of the following may be reported: Occasionally bumping into objects in own environment
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Frequently bumping into objects in unfamiliar or suddenly altered environment Vision deficits in dim light and/or darkness (loss of night vision/nyctalopia) (e.g., progressive retinal degeneration/atrophy; see p. 983 ) Patients may be lethargic and/or anxious but generally adjust and compensate better with progressive vision loss, especially if slowly progressive.
BLINDNESS Anatomy of visual pathway from the eye to the visual cortex of the cerebrum. Circles adjacent to “Visual Pathway” title indicate visual fields. M, Medial; L, lateral. PHYSICAL EXAM FINDINGS See also: Ophthalmic Examination p. 1313, ; Neurologic Examination,p. 1311 “Red eye” blindness (see p. 448 ,p. 1151 , and p. 790 ) Non-red, quiet eye blindness Prechiasmal/chiasmal blindness: Menace response (blink in response to hand motion toward the eye) absent Dazzle reflex (blink in response to a bright light) absent Pupil(s) dilated or fixed and dilated PLR(s) decreased (i.e., sluggish and incomplete) or absent ± Anisocoria (asymmetry between the size of the pupils), especially seen in unilateral lesions where only the affected pupil is more dilated) Postchiasmal/cortical blindness: Menace response variable depending on localization and severity of lesion Menace response absent or decreased in contralateral eye if a unilateral lesion present Small percentage of contralateral nasal/medial visual field may be preserved, owing to undecussated (those not crossed over) lateral optic nerve fibers. Menace response absent in both eyes in bilateral/diffuse optic tract, lateral geniculate nucleus, optic radiation, or visual cortical lesions Pupil size and PLRs normal unless certain portions of optic tract(s) affected that are common to both the PLR and visual pathways and/or unrelated, concurrent iris condition (see p. 944 ) Dazzle reflex(es) normal (like the PLR, the dazzle reflex does not involve the visual cortex.)
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ETIOLOGY AND PATHOPHYSIOLOGY “Red eye” blindness: the lesion is ocular or intraocular: Opacity of the ocular media (e.g., cornea, aqueous humor, lens, vitreous) in cases of corneal edema/ulceration /pigmentation, uveitis, cataract and vitreal debris or hemorrhage Retinal degeneration with or without detachment and optic nerve atrophy in glaucoma (see p. 448) Retinal detachment in cases of chorioretinitis (see p. 985 ) Non-red, quiet eye blindness: Prechiasmal/chiasmal: the lesion lies along the retinaoptic nerveoptic chiasm pathway Retinal diseases (see p. 983 and p. 985 ) Optic nerve lesions (e.g., congenital optic nerve hypoplasia, inflammation [see p. 784]), neoplasia (e.g., meningioma), or atrophy (e.g., glaucoma, trauma) Optic chiasmal lesions (e.g., neoplasia, abscess) Postchiasmal/cortical: the lesion affects the optic tract and/or radiations to and including the visual (occipital) cerebral cortex Encephalitis (extension to bilateral optic tracts via cerebrospinal fluid) Cerebral edema Cerebral infectious, inflammatory, neoplastic or traumatic disease
DIAGNOSIS DIAGNOSTIC OVERVIEW Lesion localization is the cornerstone of accurate diagnosis and treatment of causes of blindness. A complete cranial nerve and general neurologic examination () are an essential first diagnostic step. If the cause of blindness is not readily apparent, prompt referral of affected patients to a veterinary ophthalmologist is advised. Early diagnosis is key to determining whether or not return of vision with therapy is possible.
DIFFERENTIAL DIAGNOSIS “Red eye” blindness: May be confused with disorientation due to causes other than blindness (see p. 314 ) and concurrent non–visionthreatening cause(s) of “red eye,” including: conjunctivitis (see p. 237 and p. 239 ), episcleritis (see p. 356 ), and corneal disease (see p. 250 ) Non-red, noninflamed eye (“quiet eye”) blindness: May be confused with disorientation due to causes other than blindness Blindness may also be characterized as unilateral or bilateral. Note: unilateral processes listed more commonly affect only one eye but can affect both eyes in some cases; disorders that affect one or both eyes with equal frequency are listed in both categories. Unilateral: corneal trauma, complex corneal ulceration, lens luxation, cataract, severe uveitis, retinal detachment, subretinal hemorrhage, glaucoma, cerebral lesions (optic radiation/visual occipital cortex) Bilateral: cataracts, retinal detachment, subretinal hemorrhage, severe uveitis, glaucoma, optic neuritis, optic chiasm lesions, sudden ac quired retinal degeneration, progressive retinal degeneration/atrophy, diffuse cerebral/visual cortex disease
INITIAL DATABASE In order to accurately diagnose and treat causes of blindness, it is imperative to first localize the lesion causing the blindness. A thorough cranial nerve and general neurologic examination must be performed. Additional diagnostic tests may be indicated based on the site of the lesion. Cranial nerve (CN) examination: Menace response (CN II & VII), assessment of pupil symmetry and size and direct and consensual PLRs (CN II & sympathetic and parasympathetic innervation), dazzle reflex (blinking in response to bright light; CN II & VII), palpebral (CN V & VII) and corneal (CN V & VII) reflexes, assessment of physiologic nystagmus (i.e., vestibuloocular reflex or “Doll's eye;” CN III, IV, VI & VIII), evaluation of facial sensation (CN V) and motor function (CN VII) Normal PLRs: lesion usually postchiasmal/cortical (with a “non-red, noninflamed eye” [“quiet eye”] blindness) or due to opacity of ocular media Sluggish, incomplete/absent PLR and dilated pupil: lesion involves retina, optic nerve, optic chiasm (causes bilateral blindness), or optic tract; or a separate, primary lesion of the pupil is present General neurologic examination (see p. 1311) Complete ophthalmic examination including: Intraocular pressure assessment
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Examination of anterior segment Evaluate for opacity of the cornea, aqueous humor, lens, or vitreous Posterior segment/fundic examination after pharmacologic pupil dilation (1% tropicamide) Pharmacologic pupil dilation is contraindicated with glaucoma Evaluate optic nerve (size, shape, color; see p. 448and p. 784) Evaluate tapetum (dorsal reflective structure) for brightness and/or color changes Appears hyperreflective/bright with retinal degeneration and/or certain forms of retinal detachment Appears hyporeflective/dull grey to pigmented with subretinal inflammation and/or certain forms of retinal detachment Evaluate nontapetal fundus (located ventrally and typically pigmented) for whitish or grey discoloration (e.g., edema, inflammatory exudate or depigmentation from active or past inflammation or retinal detachment) or hemorrhages Evaluate vasculature of retina (should see small arteries and larger veins coming from the optic disk and coursing peripherally), and look for changes in vessel direction to indicate detachment or attenuation (thinning) to indicate degeneration. CBC, serum chemistry profile, urinalysis to assess systemic status +/− Blood pressure (see p. 985 , p. 1068, and p. 1209 ) if retinal hemorrhage and/or detachment is/are noted
ADVANCED OR CONFIRMATORY TESTING Thoracic radiographs (screen for neoplasia or systemic infectious disease if intraocular mass or uveitis, chorioretinitis are noted and/or if optic neuritis is suspected) Serologic titers for infectious diseases unique to geographic area: Rickettsial diseases (particularly if intraocular hemorrhage is noted) Blastomycosis, cryptococcosis, histoplasmosis, coccidioidomycosis (particularly if chorioretinal lesions with uveitis and/or optic neuritis are detected) Lyme disease (if history of tick exposure + uveitis) Bartonellosis (if history of flea exposure + uveitis) Toxoplasmosis (if history of rodent exposure + chorioretinal lesions) Aspiration of enlarged lymph nodes for cytologic evaluation Ocular ultrasonography if opacity of ocular media precludes fundic examination Histopathologic study in cases when eye is blind and painful and enucleation is advised Referral is advisable for all cases of blindness of undetermined cause for additional workup, including one or more of the following: Electroretinography to assess retinal function Visual-evoked potentials Cerebrospinal fluid tap MRI or CT Vitreous centesis with cytologic study, culture, titers
TREATMENT TREATMENT OVERVIEW Treatment is directed at addressing any underlying cause of blindness such as hypertensive retinopathy, uveitis, cataracts, and so forth In general, administration of empirical therapy is not recommended until a tentative or final diagnosis has been reached. Administration of systemic corticosteroids prematurely may preclude diagnosis of neoplasia and some inflammatory disorders and may exacerbate systemic infectious diseases.
ACUTE GENERAL TREATMENT Depends on underlying etiology
CHRONIC TREATMENT Manage any underlying conditions such as chronic renal failure, systemic hypertension, systemic infectious disease. Systemic mycoses and immune-mediated disorders typically require long-term therapy. Treat primary cause of blindness when possible (e.g., refer for surgery of mature cataracts).
RECOMMENDED MONITORING
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Monitor for return of vision, PLR, dazzle reflex after commencing therapy. Serial fundic examinations
PROGNOSIS AND OUTCOME Variable depending on underlying cause Restoration of vision after acute vision loss may be possible after rapid diagnosis of underlying condition and intensive appropriate therapy. In many cases, however, blindness is irreversible, and long-term management aims to provide comfort if pain is likely (e.g., glaucoma).
PEARLS & CONSIDERATIONS Assessment of the direct and consensual PLRs and dazzle reflexes is imperative in evaluation of blindness. Absence of the PLR and/or dazzle reflex is a poor prognostic indicator, because minimal retinal function is required to retain these reflexes. The PLR and dazzle reflexes are subcortical pathways (do not involve the cerebral cortex) and therefore are normal with blindness caused by optic radiation and cortical lesions. A PLR is dependent only on quantity of light; vision is dependent on quality of light; therefore, the PLR should remain intact despite opacity of the ocular media (such as nuclear sclerosis) if there is no concurrent retinal or optic nerve damage.
SUGGESTED READING Martin CL: Evaluation of patients with decreased vision or blindness. Clin Tech Small Anim Pract 16(1):62–70, 2001. Shamir MH, Ofri R: Comparative neuro-ophthalmology. In Gelatt KN, editor: Essentials of veterinary ophthalmology, ed 2, Blackwell Publishing, 2008, Oxford, p 445. AUTHOR: ANNE J. GEMENSKY-METZLER EDITOR: CHERYL L. CULLEN
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Blastomycosis
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Blastomycosis BASIC INFORMATION DEFINITION Systemic mycotic infection affecting many mammalian species. Animals usually have lung, skin, eye, and bone lesions.
EPIDEMIOLOGY SPECIES, AGE, SEX Occurs most often in people and dogs. Has been reported in domestic cats, lions, tigers, sea lions, wolves, ferrets, and a polar bear. Usually seen in 1- to 5-year-old large-breed male dogs GENETICS & BREED PREDISPOSITION Doberman pinschers may be at increased risk. RISK FACTORS Outdoor, roaming dogs in endemic areas living near a waterway are at increased risk. Exposure to sandy, acidic soil disrupted by construction involving earthmoving or excavation CONTAGION & ZOONOSIS Bites, needlesticks while doing aspirates, and cuts during necropsies of infected dogs have caused infection in people. Organisms can be transmitted when cultured (aerosol) if plates are opened outside a hood. Direct airborne animal-human or human-animal transmission does not occur, because the yeast phase in the infected patient is too large to be transmitted by aerosol. Dogs and people may become infected from the same environmental source, but illness usually occurs first in the dog. The dog can serve as a sentinel for human disease. GEOGRAPHY AND SEASONALITY Blastomyces dermatitidis is present in North America, Africa, and Central America. Endemic areas include the Mississippi, Missouri, and Ohio River valleys; mid-Atlantic states; and the Canadian provinces of Alberta, Manitoba, Ontario, and Quebec. No seasonal distribution in the southeastern United States May be seasonally distributed in the U.S. Midwest, with more cases seen during late spring through late fall in Wisconsin The specific location of the fungus in soil is unknown; the fungal colonies are not grossly visible and are difficult to isolate from the environment. A “microfocus” model for the ecology of B. dermatitidis suggests that environmental pockets of fungal growth occur when a suitable combination of soil type and moisture is present. Rain, physical disruption of soil, or both, may promote release of spores. Proximity of the face to soil increases likelihood of inhalation/infection.
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BLASTOMYCOSIS Geographic area in which blastomycosis is endemic. Areas of highest prevalence are cross-hatched. (From Rippon JW: Medical mycology, ed 3. Philadelphia, 1988, Saunders, pp 474–505. Reprinted with permission.)
BLASTOMYCOSIS Cytologic evaluation of a fine-needle aspiration from a patient with blastomycosis. The cytologic diagnosis is
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made based on the thick-walled, basophilic, spherical B. dermatitidis (arrows). The intense inflammatory infiltrate surrounding the yeasts is typical.
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES Cutaneous, pulmonary, ocular, and osseous forms. HISTORY, CHIEF COMPLAINT Any combination of anorexia, weight loss, cough, dyspnea, exercise intolerance, ocular changes, lameness, skin lesions, and neurologic signs is possible. PHYSICAL EXAM FINDINGS Fever, lethargy, emaciation, lymphadenomegaly Pulmonary involvement: Harsh, dry lung sounds; cough; dyspnea at rest Ocular changes: signs of uveitis (see p. 1151), endophthalmitis, corneal edema, glaucoma Skin lesions (nasal planum, face, nail beds): subcutaneous abscesses, ulcerated draining lesions, or granulomatous proliferative lesions Bone involvement: lameness due to fungal osteomyelitis, toe involvement
ETIOLOGY AND PATHOPHYSIOLOGY Blastomyces dermatitidis is a dimorphic fungus that exists in the mycelial form in the soil and as a yeast in the tissues. The mycelial form grows in soil, especially in manure-enriched soil, and produces infective spores which are released into the air. Soil disruption exposes organisms from deep within the soil. The yeast phase grows at body temperature and is too large for aerosol transmission/contagion The route of infection is by inhalation of mycelial spores that enter the terminal airways from the environment. At body temperature, the spores become yeasts and establish an infection in the lungs which disseminates throughout the body via blood and lymphatics. Organisms cause a pyogranulomatous inflammation with a predilection for the skin, eyes, bones, lymph nodes, subcutaneous tissues, mouth, nares, brain, mammary tissues, prostate and testes. Cats are less commonly infected but develop a similar spectrum of lesions as dogs, and may also have pharyngeal lesions. Direct inoculation into a wound from soil is uncommon.
DIAGNOSIS DIAGNOSTIC OVERVIEW Characteristic lesions on chest films of a patient having been in an endemic area alert the clinician to the possibility of fungal infection. Identification of organisms by cytology, culture, or histopathology is best. A urine antigen test for blastomycosis is more sensitive than serologic testing.
DIFFERENTIAL DIAGNOSIS Pulmonary form: metastatic tumors, especially hemangiosarcomas; bacterial or viral pneumonia. Bone form: bacterial osteomyelitis, primary or metastatic bone tumors Cutaneous form: bacterial, fungal, parasitic, autoimmune dermatitis Other systemic mycoses
INITIAL DATABASE CBC: Mild normocytic normochromic anemia Moderate leukocytosis (17,000 to 30,000 white blood cell/µL), left shift, lymphopenia Serum biochemistry panel: Hyperglobulinemia Hypoalbuminemia Hypercalcemia (occasionally)
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Thoracic radiographs: Diffuse, nodular interstitial and bronchointerstitial lung patterns common Solitary to multiple nodules may be seen Tracheobronchial lymphadenomegaly Less commonly: pleural effusion, pneumomediastinum Radiographs of bones: osteolytic or periosteal proliferation with soft-tissues welling
ADVANCED OR CONFIRMATORY TESTING Identification of the organism in more than half the cases by cytologic examination of lymph node aspirates, draining exudates, skin impression smears, or vitreous aspirates A thick-walled, broad-based budding yeast is characteristic of Blastomyces (see figure). Lung aspirates (see p. 1275 ) often identify the organism but pneumothorax may occur. Tracheal wash (see p. 1350 ) is less sensitive than a lung aspirate. Urine Blastomyces antigen test has >90% sensitivity and is the preferred approach when organisms are not found. The Blastomyces urine antigen test is done by Mira Vista Labs in Indianapolis, IN (http://www.miravistalabs.com /services.aspx?o=veterinary). Agar-gel immunodiffusion test: a positive test result is very specific, but the test is not sensitive early in the disease process.
TREATMENT TREATMENT OVERVIEW Itraconazole is the treatment of choice because of efficacy, low toxicity, and ease of treatment. Dogs with neurologic disease need to be treated with amphotericin B. Corticosteroids may be indicated in dogs with dyspnea.
ACUTE AND CHRONIC TREATMENT General supportive care to include supplemental oxygen to dyspneic patients. Dogs with dyspnea at rest or dogs that become dyspneic after starting antifungal treatment require corticosteroid therapy (prednisone/prednisolone 0.5 mg/kg q 12 h × 5-7 days) to reduce pulmonary inflammation. Corticosteroids should not be used before antifungal therapy is started. Antifungal drugs: Itraconazole is considered the drug of choice in most cases. Amphotericin B may be superior in severe disease and in dogs with neurologic involvement. Itraconazole: Dogs: 5 mg/kg q 12 h PO for 3 days, then 5 mg/kg PO q 24 h for at least 60 days and for 30 days after all signs of disease have resolved. The capsules should be given with canned food for maximal absorption. Brand-name itraconazole is preferred; poor absorption can occur with compounded itraconazole. Itraconazole is expensive in large dogs. Cats: 5 mg/kg PO q 12 h The pellets from the capsules can be mixed with palatable food for ease of administration. Oral liquid formulation available (10 mg/mL) Amphotericin B (IV): Dogs: 0.5 mg/kg IV in 5% dextrose 3 times a week at evenly spaced intervals. A cumulative dose of amphotericin B of 9 mg/kg is usually required. Amphotericin B should be temporarily discontinued when the blood urea nitrogen concentration (BUN) reaches 40 mg/dL (metric: 14 mmol/L). Therapy is continued until signs have resolved. When acute signs of blastomycosis have resolved, the treatment can be changed to itraconazole. Cats: 0.25 mg/kg IV 3 times weekly. Monitor closely for nephrotoxicosis. Animals must be adequately hydrated before receiving amphotericin B. The amphotericin B is usually given over a 30-minute period if there are no problems with nephrotoxicosis. Administration times of 3 hours will reduce the likelihood of nephrotoxicosis. Amphotericin B is light sensitive; therefore, the fluid bag containing the drug should be covered. Lipid-soluble amphotericin B: Dogs, cats: 1 mg/kg IV 3 times weekly at evenly spaced intervals. The lipid formulations are costly and usually not required for blastomycosis unless there is preexisting renal disease.
DRUG INTERACTIONS Itraconazole and ketoconazole should not be administered with drugs that inhibit cytochrome P450, such as some anticoagulants.
POSSIBLE COMPLICATIONS
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Itraconazole may cause hepatotoxicity and anorexia in dogs and cats but has fewer adverse effects than amphotericin B. Itraconazole at doses of 10 mg/kg/d may produce vasculitis, with ulcerative skin lesions that may resemble lesions of blastomycosis. BUN concentrations need to be monitored before every dose of amphotericin B, because the degree of nephrotoxicity varies greatly from dog to dog. Lung disease often worsens initially with treatment, owing to inflammation secondary to dying organisms. Corticosteroid therapy can be life saving in dyspneic dogs but should be given only after starting antifungal drugs.
RECOMMENDED MONITORING Liver enzymes should be monitored every 2-4 weeks during treatment in animals treated with itraconazole and measured if the patient develops anorexia. Assess BUN before each amphotericin B treatment. When BUN concentrations reach 40 mg/dL (metric: 14 mmol/L), treatment needs to be discontinued until BUN returns to normal. Thoracic radiographs should be done monthly to assess response to treatment in dogs with respiratory involvement.
PROGNOSIS AND OUTCOME Animals with severe lung involvement (dyspnea) or CNS involvement have a guarded prognosis. Most deaths occur in the first week of treatment. About 60% of dogs can be cured with the initial course of treatment. The mortality rate is about 20%. Recurrence of blastomycosis occurs in 20%-25% of treated dogs within a few months to a year after completion of treatment. Most dogs with recurrence are cured when given another course of treatment. Eyes that have anterior uveitis usually become glaucomatous and blind. Retinal lesions are more likely to be cured. Blind eyes should be enucleated because they can harbor organisms. The value of repeated urinary antigen testing in monitoring response to treatment and assessing duration of treatment is unclear but appears to be helpful.
PEARLS & CONSIDERATIONS COMMENTS Early recognition is critical for successful treatment. Comprehensive diagnostic testing should be done initially in suspect cases. Obtaining a travel history when dogs have signs suspicious of blastomycosis is an important step for raising or lowering the disease on the differential diagnosis.
PREVENTION No vaccine exists Restrict activity in endemic areas, particularly lakes, creeks, and heavily shaded areas with moist soil in endemic areas.
TECHNICIAN TIP Although the disease is infectious (acquired by inhalation in the wild), it is not transmitted by inhalation from an infected patient to other animals or humans. Never culture a lesion or exudate in-house if it could harbor Blastomyces; the spores aerosolize from culture medium and are highly infectious in this context. Bandages contaminated with exudates should be disposed of as infectious waste, but the likelihood of aerosolization is low, owing to the specific conditions Blastomyces organisms require to grow.
CLIENT EDUCATION Long-term treatment is necessary. Can be fatal despite treatment Yeast form found in animal tissues is not directly transmissible. Can be transmitted via penetrating wounds
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Blastomycosis
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SUGGESTED READING Spector D, Legendre AM, Wheat J, et al: Antigen and antibody testing for the diagnosis of blastomycosis in dogs. J Vet Intern Med 22:839–843, 2008. AUTHOR: ALFRED M. LEGENDRE EDITOR: DOUGLASS K. MACINTIRE 1ST EDITION AUTHOR: LISA TIEBER NIELSON
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Bilious Vomiting Syndrome
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Bilious Vomiting Syndrome BASIC INFORMATION DEFINITION A disorder resulting in vomiting of a bile-stained fluid, most likely due to gastric hypomotility or gastroduodenal reflux
SYNONYMS Gastroduodenal reflux, idiopathic gastric hypomotility
EPIDEMIOLOGY SPECIES, AGE, SEX Only reported in dogs, but likely occurs in cats RISK FACTORS Concurrent gastric, pancreatic, or intestinal disease (i.e., outflow obstruction) possible, but usually affects otherwise normal dogs.
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES Gastric hypomotility causing vomiting when stomach is empty, otherwise healthy Gastric hypomotility causing chronic-vomiting and weight loss HISTORY, CHIEF COMPLAINT Vomiting, typically in the morning (especially in animals fed once daily) Abdominal discomfort or increased “stomach noises” (borborygmi) Nausea Anorexia Weight loss Some or all of these may be present PHYSICAL EXAM FINDINGS Typically normal; abdominal palpation is unremarkable Dehydration and lethargy (chronic vomiting)
ETIOLOGY AND PATHOPHYSIOLOGY Presumed to be caused by gastroduodenal reflux that occurs when the dog's stomach is empty for long periods or due to abnormal gastroduodenal motility Classically, the pet vomits bile-stained fluid, usually late at night or in the morning just before eating, but otherwise feels well. Anatomic abnormalities or pyloric obstruction are not present, and there are no inflammatory changes in the gastrointestinal mucosa.
DIAGNOSIS DIAGNOSTIC OVERVIEW A working diagnosis is made based on presenting signs (vomiting when the stomach is likely empty in an otherwise well dog) and response to treatment. Diagnostic testing is warranted if features of the case suggest other disorders.
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Bilious Vomiting Syndrome
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DIFFERENTIAL DIAGNOSIS Outflow obstruction (e.g., pyloric stenosis, foreign bodies, polyps, neoplasia) Dietary intolerance or hypersensitivity Defective propulsion Gastric disorders (gastritis, gastroenteritis) Metabolic (hypokalemia, hypocalcemia, hypoadrenocorticism) Nervous inhibition (trauma, stress) Drugs (anticholinergics, others)
INITIAL DATABASE CBC, serum biochemistry profile, urinalysis usually unremarkable. Hypokalemia, hypochloremia, and metabolic alkalosis possible with voluminous or chronic vomiting. Abdominal radiographs: Normal Retention of food or fluid in the stomach longer than 8 hours, and often 12-16 hours after a meal, is suggestive of outflow obstruction or a motility disturbance.
ADVANCED OR CONFIRMATORY TESTING Motility studies are frequently difficult to perform, are not routinely available outside referral centers, and the repeatability and sensitivity of these studies are often questioned. Positive contrast radiography: Typically normal Incomplete gastric emptying following 4 hours (wide variability) Fluoroscopy: Often normal Decreased frequency of gastric contractions and incoordination of antropyloric movement (objective criteria are lacking) Abdominal ultrasound: Normal Abnormal contractile activity (subjective) Scintigraphy: Handling of radioisotopes limits the availability of scintigraphy to referral institutions. Gastroduodenoscopy is suggested to help rule out inflammatory, infectious, or structural causes of vomiting. The presence of an open pylorus with large amounts of bile reflux present in the stomach can be suggestive, but it is important to remember that certain anesthetic drugs can alter GI motility, creating the impression of reflux.
TREATMENT TREATMENT OVERVIEW Treatment goals consist of increasing gastric peristalsis and promoting gastric emptying. Nutrition and medical management using prokinetic therapy are important components of therapy.
ACUTE GENERAL TREATMENT Management/resolution of systemic disorder if present, including fluid and electrolyte disturbances or acid-base abnormalities
CHRONIC TREATMENT Medical management: structural disease first must be ruled out. Metoclopramide (0.2-0.4 mg/kg PO or SQ q 8 h); increases gastric peristalsis in some but not all affected dogs, or Cisapride (0.5-1 mg/kg PO q 24 h); accelerates gastric emptying in dogs by stimulating pyloric motor activity Erythromycin (1 mg/kg PO q 8-12 h); accelerates gastric emptying by inducing antral contractions, or Ranitidine (1-2 mg/kg PO or SQ q 12 h) or nizatidine (2-5 mg/kg PO q 12 h); stimulate gastric antral contractions
NUTRITION/DIET Feeding small, frequent meals (especially late at night) to prevent the stomach from being empty for long periods and to encourage normal gastric motility Diets low in fat and fiber promote gastric emptying and may be helpful to reduce gastric retention.
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Bilious Vomiting Syndrome
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Canned or liquefied diets (solids are retained in the stomach longer) are also beneficial in animals with abnormal gastric retention of foods.
POSSIBLE COMPLICATIONS Acid-base or electrolyte disorders may occur secondary to chronic vomiting. Weight loss
PROGNOSIS AND OUTCOME Prognosis is typically excellent; most dogs respond well to dietary and/or prokinetic therapy.
PEARLS & CONSIDERATIONS COMMENTS Differential diagnoses for bilious vomiting syndrome include primary and secondary disorders of gastric emptying. Primary disorders of gastric emptying may arise from mechanical obstruction or defective propulsion. Secondary disorders of gastric emptying include metabolic and electrolyte disturbances. Weight loss should prompt a complete diagnostic evaluation, because it is not a common feature of uncomplicated bilious vomiting syndrome.
SUGGESTED READING Hall JA, et al: Diagnosis and treatment of gastric motility disorders. Vet Clin North Am Small Anim Pract 29:377–395, 1999. Washabau RJ, et al: Diagnosis and management of gastrointestinal motility disorders in dogs and cats. Compend Contin Educ Pract Vet 19(6):721–737, 1997. AUTHOR: BRANDY PORTERPAN EDITOR: DEBRA L. ZORAN
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Bile Duct Obstruction, Extrahepatic
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Bile Duct Obstruction, Extrahepatic BASIC INFORMATION DEFINITION Pathologic obstruction of the extrahepatic bile duct system
EPIDEMIOLOGY SPECIES, AGE, SEX Dependent on the underlying cause. Dogs (middle-aged to older adults): pancreatitis; less commonly, neoplasia. Cats (middle-aged to older adults): neoplasia RISK FACTORS: Dogs: Pancreatitis Cats: Pancreatitis Cholangitis/cholangiohepatitis Inflammatory bowel disease Neoplasia ASSOCIATED CONDITIONS & DISORDERS Dogs: Cholecystitis Gallbladder mucocele Dogs and cats: Coagulopathy possible due to lack of absorption of fat-soluble vitamin K Cholelithiasis Bile peritonitis Neoplasia
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT Dogs: anorexia, lethargy, vomiting, diarrhea. Cats: anorexia, lethargy, weight loss, vomiting
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Bile Duct Obstruction, Extrahepatic
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BILE DUCT OBSTRUCTION Comparative anatomy of the canine and feline biliary systems. (Courtesy Glenda Clements-Smith.) PHYSICAL EXAM FINDINGS Dogs: icterus, fever, tachycardia. Cats: icterus, dehydration, fever or hypothermia
ETIOLOGY AND PATHOPHYSIOLOGY Dogs: See Pancreatitis, Dog, p. 820 Cholelithiasis: etiology poorly understood Cats: Extrahepatic biliary obstruction often associated with a “triad” of diseases: cholangitis, pancreatitis, and inflammatory bowel disease Common opening of the pancreatic and common bile ducts into the duodenum and the increased duodenal bacterial content may predispose cats to ascending cholangitis and pancreatitis after vomiting associated with inflammatory bowel disease. Dogs and Cats: Lack of bile entering intestinal tract: Decreases absorption of fat and fat soluble vitamins, notably vitamin K: potential coagulopathy. May also result in increased absorption of endotoxin from the gut. Other possible etiologies include neoplasia, stricture in biliary system, duodenal obstruction by a foreign body, diaphragmatic hernia, and parasitic infection.
DIAGNOSIS DIAGNOSTIC OVERVIEW
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Bile Duct Obstruction, Extrahepatic
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The diagnosis is suspected based on presenting history and physical examination findings. Confirmation requires demonstration that the icterus is caused by an obstructed common bile duct rather than inherent liver disease, typically involving abdominal ultrasound exam.
DIFFERENTIAL DIAGNOSIS Hyperbilirubinemia: Rule out hemolysis: Immune-mediated hemolytic anemia, toxicity (zinc, onions, etc.) and other diseases causing hemolytic anemia Rule out hepatic disease: Hepatitis: acute, chronic Cirrhotic/fibrosing liver disease Neoplasia Copper and other toxins in dogs, acetaminophen toxicosis in cats
INITIAL DATABASE CBC: Possible anemia; generally very mild if any (unless concurrent gastrointestinal ulceration). By contrast, hyperbilirubinemia/icterus caused by hemolysis generally produces moderate to marked anemia Inflammatory leukogram Serum biochemistry profile: Elevated bilirubin concentration Elevated liver enzyme concentrations Possible elevated amylase and lipase concentrations Hypokalemia Urinalysis: bilirubinuria is common in both species (but mild bilirubinuria is also normal in healthy dogs) Survey abdominal radiographs: Cranial abdominal detail may be decreased in cases with biliary leakage and peritonitis. May delineate radiopaque choleliths Survey thoracic radiographs: Rule out metastatic disease if neoplasia is suspected.
ADVANCED OR CONFIRMATORY TESTING Abdominal ultrasound examination: Common bile duct dilation >5 mm diameter: diagnostic of bile duct obstruction in the cat Visible contraction of the gallbladder is not expected in either healthy or diseased states. Peritoneal fluid analysis (obtained during abdominal ultrasound examination): Elevated bilirubin concentration: bile peritonitis Cytologic analysis and microbiologic (aerobic and anaerobic) culture and sensitivity testing: septic peritonitis Coagulation profile
TREATMENT TREATMENT OVERVIEW Patients require surgical correction of the problem along with appropriate intensive and supportive care. A major exception is transient biliary obstruction caused by acute pancreatitis, provided the patient's clinical course is mild and improves rapidly (few days) with medical therapy alone.
ACUTE GENERAL TREATMENT Rehydration by intravenous administration of balanced electrolyte solution Parenteral antibiotics effective against gram-negative bacteria and anaerobes: Empirical therapy: Cefoxitin, 30 mg/kg IV q 2 h perioperatively, then q 6 h, or Metronidazole, 7.5-15 mg/kg IV q 12 h with Enrofloxacin, 2.5-5 mg/kg IV q 12 h (5 mg/kg q 24 h maximum in cats, owing to risk of retinal toxicity) Specific long-term therapy based on culture and sensitivity test results Possible administration of fresh frozen plasma:
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Bile Duct Obstruction, Extrahepatic
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Hypoproteinemia Possible coagulopathy Vitamin K administration: 2.5 mg/kg SQ q 12 h × 3-5 days, then once weekly Relief of extrahepatic biliary obstruction—surgical intervention: Duodenotomy and retrograde and antegrade flushing of biliary system: all cases Common bile duct stenting: if temporary or dynamic obstruction likely (i.e., pancreatitis) and severe persistent hyperbilirubinemia Cholecystoduodenostomy/jejunostomy: if advanced or permanent obstruction Tube cholecystostomy Cholecystectomy: if gallbladder wall is devitalized Gastrointestinal biopsies: association of biliary disease with inflammatory bowel disease in cats Relief of intragallbladder luminal hypertension has been achieved via ultrasound-guided centesis of the gallbladder in dogs with pancreatitis-associated biliary obstruction
CHRONIC TREATMENT Maintenance of bile flow: Ursodeoxycholic acid, 10-15 mg/kg PO q 24 h. Contraindicated if biliary obstruction is still present.
NUTRITION/DIET Provide enteral feeding (e.g., gastrostomy tube; see p. 1270 and p.1267) if patient is anorexic
POSSIBLE COMPLICATIONS Ongoing pancreatitis, bile leakage, peritonitis, endotoxemia, sepsis, death
RECOMMENDED MONITORING Clinical and laboratory parameters assessing perfusion, including capillary refill time, pulse rate and quality, blood pressure, urine output, arterial pH, and lactate concentrations Respiratory function Serum liver enzyme and bilirubin concentrations Coagulation profile
PROGNOSIS AND OUTCOME Poor if biliary obstruction associated with neoplasia: 100% mortality in cats Guarded if biliary obstruction associated with nonneoplastic causes in cats Guarded to fair if biliary obstruction associated with nonneoplastic causes in dogs
PEARLS & CONSIDERATIONS COMMENTS Given the association of biliary obstructive disease in cats with cholangitis/cholangiohepatitis and inflammatory bowel disease, a liver biopsy and culture, bile culture, and small-intestinal biopsies must be obtained at the time of surgery in this species. A convenient site for duodenal biopsy is the edge of the duodenotomy performed to cannulate the duodenal papilla(e) or to perform a cholecystoduodenostomy. In assessing hyperbilirubinemia, total bilirubin concentration is important. Conjugated versus unconjugated bilirubin is not linked to the source of hyperbilirubinemia in dogs and cats as it is in humans.
SUGGESTED READING Mayhew PD, et al: Pathogenesis and outcome of extrahepatic biliary obstruction in cats. J Small Anim Pract 43:247, 2002. Aguirre AL, Center SA, Randolph JF, et al: Gallbladder disease in Shetland sheepdogs: 38 cases (1995-2005). J Am Vet Med Assoc 231:79–88, 2007. Herman BA, Brawer RS, Murtaugh RJ, Hackner SG: Therapeutic percutaneous ultrasoundguided cholecystocentesis in three dogs with extrahepatic biliary obstruction and pancreatitis. J Am Vet Med Assoc 227(11): 1753, 1782–1786, 2005.
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Bile Duct Obstruction, Extrahepatic
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AUTHOR: DAVID HOLT EDITOR: RICHARD WALSHAW
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Bicipital Tenosynovitis
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Bicipital Tenosynovitis BASIC INFORMATION DEFINITION Inflammation of the biceps brachii tendon and surrounding synovial sheath
SYNONYM Bicipital bursitis (inaccurate)
EPIDEMIOLOGY SPECIES, AGE, SEX Dogs Medium and large breeds Middle-aged to older RISK FACTORS Trauma, overuse of muscle, shoulder joint osteoarthritis ASSOCIATED CONDITIONS & DISORDERS Osteoarthritis or osteochondrosis of shoulder joint, supraspinatus tendonitis
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT Forelimb lameness exacerbated by exercise and unresponsive to nonsteroidal antiinflammatory drugs (NSAIDs); caused by trauma to shoulder or insidious in onset PHYSICAL EXAM FINDINGS Shortened forelimb stride, with head lifted as affected forelimb is advanced Pain on palpation of the bicipital tendon in the intertubercular groove Pain on flexion of shoulder and extension of the elbow while placing tendon and muscle under tension
ETIOLOGY AND PATHOPHYSIOLOGY Can be caused by blow to cranial aspect of shoulder during flexion Tendon may be strained or stretched with disruption of fibers In chronic conditions, dystrophic mineralization occurs in tendon Secondary to shoulder joint osteoarthritis or osteochondrosis if cartilage fragments collect within the communicating tendon sheath and cause inflammation Adhesions between tendon sheath and tendon can occur secondary to trauma. Tendon can also be avulsed from supraglenoid tubercle
DIAGNOSIS DIAGNOSTIC OVERVIEW Forelimb lameness raises the possibility of this diagnosis; pain on deep palpation of the bicipital tendon is characteristic.
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Bicipital Tenosynovitis
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DIFFERENTIAL DIAGNOSIS Supraspinatus tendonitis Supraglenoid tubercle fracture Biceps muscle tearing at the distal musculotendinous junction Shoulder joint collateral ligament injury Shoulder joint osteoarthritis Cervical nerve root compression
INITIAL DATABASE Patient database as indicated by stability and American Society of Anesthesiologists classification (p.1372) Medial to lateral radiograph of the scapulohumeral joint Skyline radiographic view of the intertubercular groove
ADVANCED OR CONFIRMATORY TESTING Contrast arthrography may reveal irregularity of tendon surface or sheath. Arthrocentesis may be consistent with osteoarthritis (increase nucleated cell counts 1500-4800 cells/mcL, primarily mononuclear; aseptic). Ultrasonography of the biceps tendon will identify irregular fiber arrangement and increased synovial sheath fluid content. MRI may be considered to identify tendon and sheath lesions. Arthroscopy for direct visualization of tendon and sheath
TREATMENT TREATMENT OVERVIEW Relieve pain due to tenosynovitis.
ACUTE GENERAL TREATMENT Local injection with methylprednisolone acetate (10-40 mg) followed by 2 weeks of rest. Repeat at 2-week intervals for 3 treatments; if no improvement, surgery is considered. Surgical treatment: Preserve tendon and release transverse humeral ligament if it is restricting biceps tendon excursion. Tenotomy via arthrotomy or arthroscopy Tenodesis to the proximal humerus by screw/washer or passing tendon through a bone tunnel and suturing to the periosteum
CHRONIC TREATMENT Exercise restriction for 6-8 weeks
POSSIBLE COMPLICATIONS Poor response to steroid treatment Chondromalacia in shoulder joint or biceps tendon rupture secondary to steroid injection Persistent lameness due to inadequate tenodesis
RECOMMENDED MONITORING Short-term postoperatively for seroma Long-term for restoration of limb function
PROGNOSIS AND OUTCOME Fair to good after steroid injection and rest Good after tenodesis or tenotomy (arthroscopic)
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Bicipital Tenosynovitis
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PEARLS & CONSIDERATIONS COMMENTS Establishing a diagnosis of bicipital tenosynovitis can be difficult. Disease of the supraspinatus tendon can be a conflicting cause of shoulder joint pain. This condition is best evaluated by MRI or arthroscopy to identify tendon impingement into the groove; splitting this tendon resolves pain and lameness. The synovial sheath of the biceps tendon is continuous with the shoulder joint capsule. Transverse humeral ligament thickening may constrict the tendon and cause pain.
SUGGESTED READING Lafuente MP, Fransson BA, Lincoln JD, et al: Surgical treatment of mineralized and nonmineralized supraspinatus tendi nopathy in twenty-four dogs. Vet Surg 38:380–387, 2009 AUTHOR: JAMES D. LINCOLN EDITOR: JOSEPH HARARI
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Behavior Problems, Miscellaneous
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Behavior Problems, Miscellaneous BASIC INFORMATION DEFINITION Species-typical and normal behaviors that may inconvenience clients Dogs: Coprophagy (see p. 244) Digging Mounting/humping Roaming Fence running/scratching Cats: Scratching of furnishings Late night activity, climbing on counters
EPIDEMIOLOGY SPECIES, AGE, SEX Younger animals more likely to exhibit exploratory and play behaviors that may irritate clients. Intact males may roam more frequently and greater distances. GENETICS & BREED PREDISPOSITION Hounds and northern dog breeds (e.g., husky, malamute, Samoyed) are anecdotally reported to look more readily for opportunities to roam. Highly active breeds or individuals with inadequate stimulation and exercise to satisfy their behavioral and cognitive needs may look for alternatives for behavioral expression, which may be intolerable to owners. RISK FACTORS Management practices that decrease enrichment (both mental and physical) or fail to establish a humane rule structure that meet a pet's physical, social, developmental, behavioral, and cognitive needs. Examples are lengthy confinement within a day for dogs (e.g., 8 of 24 hours), lack of interactive toys, lack of basic training, inadequate aerobic exercise, and inadequate social exposure. CONTAGION & ZOONOSIS Multiple-dog and multiple-cat households may experience social facilitation that fosters many of these behaviors. In social facilitation, the behaviors of one individual in a group stimulate others to do the same or similar behaviors. GEOGRAPHY AND SEASONALITY Access (e.g., digging in soil) and the level of provocative stimuli (e.g., other cats outside) may vary seasonally. ASSOCIATED CONDITIONS & DISORDERS Obsessive-compulsive disorders (see p. 775).
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES: Bouts of behaviors that can be interrupted and that seem only to occur opportunistically may be normal but annoying behaviors or management-related behavior problems. If the behaviors cannot be easily interrupted, or if the animal is constantly seeking ways to get access to do them, a more serious disorder should be suspected (e.g., obsessive-
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Behavior Problems, Miscellaneous
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compulsive disorder, see p. 775) HISTORY, CHIEF COMPLAINT Behavior that is annoying (e.g., cat walking on counters) or disgusting (e.g., dog rolling in feces) to the client, but not threatening or dangerous. The first step in eliciting relevant information is to get a good and complete description of the behaviors and the context in which they occur. Context is critical for assessment of whether the behaviors are “normal” or species-typical ones that can be redirected or managed while still meeting the animal's needs. For example, a cat's scratching at an inanimate object (e.g., furniture) is part of normal behavior and can be redirected, but scratching at humans or other cats may represent aggression. PHYSICAL EXAM FINDINGS Usually unremarkable, although history or evidence of minor self-trauma acquired during exploratory or escape behaviors may be present.
ETIOLOGY AND PATHOPHYSIOLOGY Clients must understand that animals do not undertake these behaviors to “spite” them or out of “jealousy;” attention-seeking is commonly involved, but the key to managing these disorders is having clients understand the significance of the behaviors in terms of normal dog and cat behavior. Most of these behaviors are normal behaviors in context, intensity, and frequency, at least at first. With time, if behaviors become increasingly abnormal, the context, intensity, and frequency with which they are exhibited will change, as will the animal's focus, interactions with humans and other animals, and daily time budget. Effective behavior modification: positive behaviors are encouraged and repeated if they result in a pleasurable outcome. This repetition leads to learning at the neurochemical level where new proteins at synapses are made. These more efficient neuronal connections make it more likely that the dog or cat will continue with the behavior. This sequence explains the importance of early identification and intervention.
DIAGNOSIS DIAGNOSTIC OVERVIEW Many “nuisance” behaviors are actually within the species repertoire of normal behaviors. A problem exists when their expression is undesirable to owners, but even then, they may not be a sign of abnormal behavior. Therefore, the history is diagnostic; the context in which the specific behavior occurs will determine whether the behavior is normal but inconvenient, or indicative of a true disorder.
DIFFERENTIAL DIAGNOSIS If any of the signs are excessive, repetitive, and performed to the exclusion of other comfort, social, and maintenance behaviors, an anxiety disorder such as obsessive-compulsive disorder (see p. 775) must be considered. Late-night activity in middle-aged to older cats that is new and uncharacteristic based on the pattern of previous nocturnal behavior could be a sign of feline cognitive dysfunction (see p. 225). Hyperthyroidism also should be ruled out whenever an adult cat's activity level increases uncharacteristically.
INITIAL DATABASE CBC, serum biochemistry profile, urinalysis: generally unremarkable Ingestion of feces or other nonnutritive items: fecal flotation, trypsin-like immunoreactivity (see p. 372 )
TREATMENT TREATMENT OVERVIEW Provide an acceptable outlet for the unmet behavioral, cognitive, and species-typical needs that lead the pet to engage in the behavior the client finds objectionable.
ACUTE GENERAL TREATMENT Increase aerobic activity through exercise and interactive play with humans or fellow dogs/cats. Play with compatible conspecifics, particularly for dogs, usually provides more effective exercise with greater aerobic scope than does play with
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Behavior Problems, Miscellaneous
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humans. Environmental modification should be used for preventing access to or limiting the repetition of the undesirable behavior, and to foster alternative, acceptable behaviors.
CHRONIC TREATMENT Behavior modification can provide outlets or encourage substitute behaviors that allow acceptable expression of the individual's mental and social needs. Depending on the problem, this may consist of continued aerobic exercise, goal-oriented activities (obedience, agility, tracking, coursing training in dogs; interactive predatory play in cats). Rewards—verbal, physical (e.g., petting or stroking), food—should be given for all spontaneous and calm behaviors (e.g., chewing on chew-toys, clawing on provided surfaces, digging in a sandbox provided for this purpose, pouncing on cat toys). Attention-seeking behaviors such as jumping or “playful” whining or biting need to be ignored completely. Elimination of the reward (of attention) will extinguish the behavior if, and only if, the client is consistent in not responding. In mild cases, devices that interrupt the behavior with an aversive stimulus can be useful early in the course of the problem, only if the animal is not afraid of the stimulus, and only if appropriate outlets to which the behavior can be redirected are also provided. Examples of aversive but not harmful or fear-inducing disruptive stimuli include inverted plastic carpet runners (spike side up), static electricity mats for surfaces the client wants to be off-limits to the pet, and pressurized air blasts triggered by motiondetector sensors. Note that some animals will be afraid of these stimuli. If this is the case, the devices should not be used. The purpose of a disruptive stimulus is to stop the behavior in a way that encourages the animal to seek information and engage in an alternative behavior that can be rewarded. If the animal is afraid, it cannot do this.
POSSIBLE COMPLICATIONS Poor client compliance can lead conversely to continued self-reinforcement and worsening of the problem, and deterioration of the pet-client relationship. Therefore a cornerstone of treatment is owner understanding of the basis for the behavior and the intention of the proposed treatment.
RECOMMENDED MONITORING Frequent follow-up will help many clients comply more reliably. Demonstrations that show clients new ways to interact with their pet are essential. By dedicating these tasks to one staff member, continuity and consistency in advice and follow-up are maintained. Clients also feel that their veterinarians care more about them under these conditions.
PROGNOSIS AND OUTCOME Excellent if the clients understand the pets' needs and are willing and able to meet them Poor if clients have unrealistic expectations, consider pets recyclable, feel guilty about discussing the issue with their vet, or are unwilling or unable to meet their pets' needs
PEARLS & CONSIDERATIONS COMMENTS In extreme forms that interfere with normal physical and social functioning, most of these “annoyance” behaviors are also characteristic of obsessive-compulsive disorder and other anxiety-related conditions. This does not mean that exhibition of these miscellaneous concerns will lead to obsessive-compulsive disorders. It does mean that the nonspecific signs and complaints can be similar, and clients should be aware of this and not dismiss unusual behaviors out of hand as just “bratty” behaviors without having them evaluated first. Referral to a veterinary behaviorist may be very helpful in such situations. Relinquishment and euthanasia are frequent sequelae to behaviors clients find undesirable, whether or not the behaviors were the pet's “fault.” The effect of this pattern on veterinary economics and veterinary staff morale is huge and often preventable. This is a quality of life (QoL) issue for pets.
PREVENTION Puppy and kitten classes, basic obedience and agility training, and understanding of basic behavioral, physical, and social needs of dogs and cats will help clients to intervene before behaviors become problems.
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CLIENT EDUCATION Veterinarians are encouraged to keep a loaning library of books, newsletters, videos covering basic behaviors of dog and cats, and a list of trainers and facilities that a staff member has verified use humane training techniques. This will provide the atmosphere of caring that will make it easier for clients to seek and get the help they need. A useful source of video and other training and behavioral material is http://abrionline.org/.
SUGGESTED READING Donaldson J: The culture clash. Berkeley, Calif., 1996, James and Kenneth Publishers. Miller P: The power of positive dog training. Dog Wise, 2003. Seksel K: Training your cat. Melbourne, Australia, 2001, Hyland House. AUTHOR: SORAYA V. JUARBE-DIAZ EDITOR: KAREN L. OVERALL
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Behavior Problem Prevention, Puppies
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Behavior Problem Prevention, Puppies BASIC INFORMATION DEFINITION The first few puppy visits set the stage for future veterinary visits. They educate the new puppy owner about normal canine behavior and social systems and help prevent problems with toilet training, digging, jumping up, barking, mouthing and chewing.
SYNONYMS Puppy socialization; puppy training; Puppy Preschool
EPIDEMIOLOGY SPECIES, AGE, SEX Dogs 3 months) and multiple activity appropriate groups. Problematic behavior often becomes more pronounced at social maturity (“18-24 months of age). RISK FACTORS Dogs not adequately exposed to varied stimuli, especially during the sensitive socialization period (3-12 weeks old; later for ongoing novel experiences), are at increased risk of neophobia (fear of humans, other dogs). CONTAGION & ZOONOSIS Dog bites are a public health risk. ASSOCIATED CONDITIONS & DISORDERS Increased risk of abandonment and euthanasia if owners do not understand normal canine behaviors and social structure and use this understanding to meet the dog's needs. Risk factors for surrender/abandonment include absence of castration, lack of housetraining, no veterinary attention, and no obedience/manners training. The average client with a problem dog keeps the dog 3 months before relinquishment. Dogs with inherited neurologic disorders (e.g., lissencephaly) often present with abnormal puppy behavior as the nonspecific complaint.
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT The owner may not report any difficulties with the puppy or may report some problems with toilet training, digging, jumping up, barking, mouthing, or chewing. PHYSICAL EXAM FINDINGS If there are no medical problems, it should be unremarkable.
ETIOLOGY AND PATHOPHYSIOLOGY Certain behaviors are normal for the individual/species and misunderstood by, or out of context for, an uninformed owner. Other behaviors are truly abnormal and warrant intervention.
DIAGNOSIS
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Behavior Problem Prevention, Puppies
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DIAGNOSTIC OVERVIEW Detailed history, discussion of expectations, and observation of interaction between owner and puppy are usually sufficient to identify potential misunderstandings and anticipate problems, allowing early intervention.
DIFFERENTIAL DIAGNOSIS Normal behavior that may not be acceptable to the owner versus behavioral disorder
INITIAL DATABASE History and physical exam are usually sufficient.
TREATMENT TREATMENT OVERVIEW Cornerstones of treatment are to identify the exact features of behaviors the owner considers abnormal, annoying, or troublesome and determine whether these are normal or pathologic; to counsel owners on behaviors that are normal for dogs; and to increase positive interaction between owner and puppy. The goal is to maximize positive interaction between puppy and owner, and with perceived or real behavioral disorders, to reduce the risk of surrender.
ACUTE AND CHRONIC TREATMENT Preventive health care for dogs should always include information about canine behavior. Many issues that lead to abandonment may be preventable with client education. Every veterinary visit should include an assessment of a puppy's behavior, thus educating the client about age-specific normal behavior and allowing early intervention. Sample questions could include: Does your puppy urinate in the house? Does your puppy avoid other dogs or strangers and/or appear concerned about them? Does your puppy vocalize when left alone? Does your puppy have any behaviors that concern you or that you do not like? Rewards (e.g., treats, pats, verbal praise) should be given for appropriate behaviors, including during veterinary visits. Inappropriate behaviors should be redirected and more appropriate behaviors substituted consistently and long term (e.g., the dog grabs a toy at the door, not the human's hand) Dogs should not be verbally or physically punished for inappropriate behaviors. Dogs should be taught to sit and settle/relax on cue. Head collars can help owners manage their puppy better with less need for “corrections.” Choke chains, prong collars, and electronic collars have no place in modifying or preventing unacceptable behaviors. Many behaviors such as jumping up, digging, or mouthing are normal behaviors that owners dislike or do not understand. They are best resolved by ignoring the behavior and teaching the dog an alternative response instead (response substitution), such as sitting for petting rather than jumping up and being pushed down. Many of these problem behaviors may be addressed by referral to a good positive-reinforcement trainer.
NUTRITION/DIET Dogs eat during the day and would naturally eat three meals. Using foraging devices/food toys can be used as way of enriching the dog's environment. Advice on prevention of obesity is important; use of only small treats and accurate exercise requirements must be explained.
BEHAVIOR/EXERCISE Age-appropriate physical and mental stimulation is necessary. These can include walking, swimming, games, interactive toys, agility, and tracking. Jumping up (see p. 133): May start inadvertently as the puppy seeks attention Puppy should be taught to sit on cue and quietly praised. The owner should not pay attention to the dog when he/she jumps up. Instead, the owner should stand still or turn his/her back on the dog and wait until all of the dog's four feet are firmly placed on the ground and the dog is quiet and attending to the owner. The dog should then be given quiet, calm praise immediately. Interactions only occur when the dog is calm. Making eye contact, pushing the dog down, kneeing, pinching the toes, or saying “no” will encourage jumping as the dog gains attention. Chewing objects (see also p. 654 ).
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Dogs use the mouth to investigate their environment, so it is important owners recognize this is a normal behavior. Dogs may also chew when they are anxious or distressed, and chewing may be a sign of such problems as separation anxiety (see and p. 654 ). Puppies need to be given suitable, safe toys to chew. Rotating toys or odors associated with toys may increase interest for some dogs. Foraging devices such as Kongs, Treat Balls, the Busy Buddy line of toys, and Buster Cubes are useful for puppies to chew. The toys should be as indestructible as possible and must be checked and cleaned regularly. The puppy should not have access to potentially valuable or unacceptable items. Puppies should not be given old shoes or other belongings of the owner to chew, as dogs cannot always tell the difference between what is a new shoe and what is an old shoe. Digging Many dogs dig, and this is a normal behavior. The dog may be given a digging pit (the size of a child's size sandpit) filled with loose sand or soil to encourage digging in this area. Burying bones, toys, and other treats in this area “rewards” the dog for digging there. Mouthing (see also p. 654 ) Puppies mouth to investigate their environment. They may also mouth in play. It is important for owners not to use hands to play with puppies, as that may encourage mouthing. Appropriate toys should be available for the puppy to chew and can be offered to the puppy if it mouths or bites. If a puppy uses its mouth excessively in play or bites, play should stop immediately and the person should walk away. Once the puppy is calm, play can resume. If the puppy persists in play biting, the owner needs to entirely discontinue any interaction or play for that session. Owners should not to use hands to hit the puppy or push him/her away, as this may encourage mouthing or biting. Puppies may perceive this as a game and will persist in biting. Barking: see p. 127
RECOMMENDED MONITORING Weekly phone call to monitor progress and help with troubleshooting for the first months of intervention.
PROGNOSIS AND OUTCOME New puppy owners often are very open to learning about their puppy's development. Encourage this by asking about behavior and viewing photos/videos with clients.
PEARLS & CONSIDERATIONS COMMENTS Educate owners often that rewarding appropriate behaviors while ignoring or redirecting inappropriate behaviors is the best way to manage potential problem behaviors. If behavior problems persist, refer to a veterinary behaviorist early in their development. Most dogs do not “grow out of it,” but instead learn to become more distressed and problematic with time.
PREVENTION Offer pre-pet selection advice, especially pertaining to size and grooming and exercise needs. Attendance at puppy socialization and training classes (Puppy Preschool) or puppy manners classes helps puppies to behave politely in society. The classes also help owners understand their dog's behavior and to have realistic expectations of their dog.
TECHNICIAN TIPS Regular contact with owners to educate them and assist them with any behavior modification advice will increase client compliance. Participation in Puppy Preschool and routine manners classes are great ways of building client trust and confidence.
CLIENT EDUCATION Exposing puppies to many stimuli in a manner where they are not distressed, or can easily overcome their distress, maximizes their chances to grow into well-behaved and accepted members of their households and society.
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SUGGESTED READING Brammeier S, et al: Good trainers: how to identify one and why this is important to your practice of veterinary medicine. J Vet Behav: Clin Appl Res 1:47–52, 2006. Seksel K: Preventative behavioral medicine for cats. In Horwitz D, Mills D, editors: BSAVA manual of canine and feline behavioral medicine, Gloucester, UK, 2002, British Small Animal Veterinary Association, pp 75–82. Landsberg G, Hunthausen W, Ackerman L: Handbook of behavior problems of the dog and cat. Oxford, 2003, Butterworth-Heineman. Overall KL: Clinical behavioral medicine for small animals. St Louis, Missouri, 1997, Mosby. AUTHOR: KERSTI SEKSEL EDITOR: KAREN OVERALL
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Behavior Problem Prevention, Kittens
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Behavior Problem Prevention, Kittens BASIC INFORMATION DEFINITION The first few kitten visits set the stage for future veterinary visits. They help the new kitten owner understand normal feline behavior and social systems and help prevent problems with litter box usage, scratching furniture, biting, and chewing.
SYNONYMS Kitten kindergarten, Kitten Kindy, kitten socialization, kitten training
EPIDEMIOLOGY SPECIES, AGE, SEX Cats 1:64) should be treated only after first considering the Bartonella species identified and the antibody prevalence
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Bartonellosis
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within the population before instituting therapy.
ACUTE GENERAL TREATMENT By extrapolation from human medicine: prolonged use of tetracyclines, erythromycin, rifampin, azithromycin, doxycycline, or a combination of these antibiotics could be effective (but efficacy and safety unproven in dogs and cats). Dogs: Azithromycin has been used: small dogs, 10 mg/kg; medium dogs, 7 mg/kg; large dogs, 5 mg/kg. Give PO q 24 h × 7 days, then q 48 h × 5 weeks. Doxycycline (10 mg/kg PO q 24 h) or enrofloxacin could possibly be beneficial; unproven in clinical veterinary medicine. In principle, prolonged treatment for 4-6 weeks is recommended, but the high rate of incidentally discovered infections in otherwise normal animals indicates that treatment should be considered only if compatible clinical signs are present and other possible causes have been ruled out. In dogs suffering from a life threatening Bartonella infection such as endocarditis, the use of aminoglycosides in the initial phase of treatment may be warranted. This class of antibiotics should only be considered if renal function is stable and kidney perfusion is going to be supported with intravenous fluid therapy. Cats: Azithromycin has been used: 10 mg/kg PO q 24 h × 7 days, then q 48 h × 5 weeks. However, there is no antibiotic protocol that has been shown to clear cats of infection. At the present time, there are no definitive recommendations for treatment of cats.
CHRONIC TREATMENT There are no clear recommendations for chronic relapsing disease in dogs and cats. Alternative diagnoses should be strongly considered in patients that “fail” treatment. Dogs that remain bacteremic after an initial treatment course of azithromycin may respond to combination therapy of continued azithromycin with the addition of rifampin (5 mg/kg PO q 24 h) for an additional 6 weeks. Development of antibiotic resistance is a risk and should be considered before deciding to institute therapy.
POSSIBLE COMPLICATIONS Recurrent/persistent infection
RECOMMENDED MONITORING Resolution of clinical signs after therapy Antibody titers can be followed during treatment (at 1 month) and post treatment (at 6 months) to follow antibody trends. A resolution of detectable antibodies is generally considered a positive outcome. Since persistently infected dogs may fail to have an increased antibody titer, serology in combination with BAPGM culture and PCR is recommended to ensure bacterial clearance. The significance of persistent antibody titers after treatment is unknown.
PROGNOSIS AND OUTCOME Depending on the clinical presentation, the prognosis can vary widely.
PEARLS & CONSIDERATIONS COMMENTS Coinfection with multiple Bartonella spp. and subtypes, as well as with other vector transmitted infections, is possible and should be considered. Defining bartonellosis as a clinical entity is still in its infancy. It remains unknown in many circumstances whether Bartonella is a primary pathogen, opportunistic invader, or incidental finding. It is well established that B. vinsonii subspecies berkhoffi is an important infective agent in dogs, but the clinical implications of B. henselae bacteremia in both dogs and cats remains to be elucidated.
PREVENTION Consistent use of flea and tick preventatives is recommended.
CLIENT EDUCATION
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Monitor for recurrence of presenting signs. Since the current understanding of the pathology and treatment of bartonellosis is far from complete, clients should be cautioned that treatment may not eliminate clinical disease. Zoonosis is possible, and immunocompromised individuals should be particularly cautious when adopting new pets.
SUGGESTED READING Breitschewerdt E: Feline bartonellosis and cat scratch disease. Vet Immunol Immunopathol 123:167–171, 2008. Breitschwerdt E, et al: Clinicopathological abnormalities and treatment response in 24 dogs seroreactive to Bartonella vinsonii (berkhoffi) antigens. J Am Anim Hosp Assoc 40:92–101, 2004. Brunt J, Guptill L, Kordick DL, Kudrak S, Lappin MR: American Association of Feline Practitioners, Academy of Feline Medicine Advisory Panel. American Association of Feline Practitioners 2006 Panel report on diagnosis, treatment, and prevention of Bartonella spp. infections. J Feline Med Surg 8(4):213–226, 2006. AUTHORS: MICHAEL W. WOOD, ADAM BIRKENHEUER EDITOR: DOUGLASS K. MACINTIRE
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Barking, Excessive
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Barking, Excessive BASIC INFORMATION DEFINITION Either a normal amount of barking that is deemed unacceptable to humans or a pathologic amount of barking as part of an anxiety or other behavioral disorder
EPIDEMIOLOGY SPECIES, AGE, SEX Dogs of any age and either sex. Puppy vocalizations: more often associated with care-seeking behaviors. Adult vocalizations: more often associated with care-giving behaviors, social interaction, cohesion. GENETICS & BREED PREDISPOSITION None; body size may affect the pitch. RISK FACTORS In breeds that have been selected for specific vocalization behaviors, such vocalizations may become more annoying to the clients and/or their neighbors and still be normal. CONTAGION & ZOONOSIS Naïve/newly added puppies or adults may learn barking by observation. GEOGRAPHY AND SEASONALITY Dogs kept outdoors, especially if confined and not walked, are more likely to use barking to communicate with other dogs in the vicinity. ASSOCIATED CONDITIONS & DISORDERS Barking may be a nonspecific sign in any anxiety-based disorder, including separation anxiety, aggression, obsessive-compulsive disorder, and noise, storm, and social phobias.
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT Excessive barking is noted by client at home. In some cases, however, clients may not know about the barking unless neighbors complain. Barking can appear indiscriminate or as a response to external stimuli. For example, barking associated with an anxiety disorder may also be characterized by hypervigilant behavior (continuous monitoring of the social and physical environments). In these cases, dogs may scan at windows, along fences, and at doors. Clients may also describe the patient as unable to rest or settle down for any considerable amount of time. Important elements of the history that should be elicited include whether it occurs in the owner's real or virtual absence (e.g., associated with separation anxiety) and whether it ends with the owner's inadvertently rewarding the behavior, as with a treat to “silence” the dog (i.e., learned behavior).
PHYSICAL EXAM FINDINGS Generally unremarkable If barking represents a change in behavior, vocal cords and surrounding tissue may become edematous; A change in quality of bark may be associated with oropharyngeal lesions (laryngeal paralysis, mass, and so on). Rarely, a source of pain or other physical abnormality can be identified as a trigger for barking or whining.
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ETIOLOGY AND PATHOPHYSIOLOGY Barking may be used for making contact with other individuals (including when reuniting after being apart), to signal alarm, to signal concern or distress, and to solicit information from other dogs (depending on pitch, tone, frequency, and pattern). Spectrographic analysis of canine barks has shown that their structure varies predictably according to context; barks can likely be divided into contextual subtypes and are thought to convey complex information to both canine and human listeners. Recent studies support the observation that people can distinguish between barks and can correctly identify the context in which a bark was given, even when the dogs are unfamiliar to the human listeners and the humans have never owned dogs. Barking can also be a sign of an anxiety disorder, including obsessive-compulsive disorder (see p. 1012 and 775).
DIAGNOSIS DIAGNOSTIC OVERVIEW The diagnosis is made based on history. The context in which the barking occurs will determine whether the behavior is normal but inconvenient, or indicative of a mood disorder.
DIFFERENTIAL DIAGNOSIS Normal barking, especially alarm barking by watch and guard dogs selected to alert by barking, reactive barking in terrier and hound breeds, and working barking in some herding breeds. These barking behaviors can be modified with humane training and are typically context-appropriate, although inconvenient or undesirable for some clients. Learned behavior: barking that elicits a response/reward from the client (e.g., the client lets the dog out when it barks, or pets it to “calm it down”) Separation anxiety Thunderstorm phobia Noise phobia Obsessive-compulsive disorder Change in vocalization: Laryngeal paralysis, laryngeal masses, and thyroid neoplasia can result in changes in bark quality (see p. 1172 ), which must be differentiated from barking-induced hoarseness and from owner-induced trauma to the cervical region through leash, choke chain, or pinch collar “corrections.”
INITIAL DATABASE Minimum database: complete blood count, serum chemistry profile, and urinalysis to rule out any underlying contraindications for psychotropic medication, if their use is warranted. Other laboratory or imaging procedures should address any other concurrent physical exam findings.
ADVANCED OR CONFIRMATORY TESTING Learned behaviors are ruled out if they are extinguished by complete removal of the reward. Extinction is a gradual waning in occurrence of a behavior in the absence of a reward. The longer the behavior has been ongoing, reinforced, or rewarded, the longer eradication of the learned behavior will usually take.
TREATMENT TREATMENT OVERVIEW The goal is to treat the disorder or modify the behavior (if normal) based on accurate identification of cause.
ACUTE GENERAL TREATMENT If barking is within the normal behavioral repertoire, given triggers and context, the dog can be taught when and when not to bark by rewarding “good barking” and not “bad barking” and coupling both to words used only in those situations. When the dog barks in a context that is unacceptable to the owner, redirecting the dog to an incompatible behavior (such as catching a toy with the mouth or playing tug) stops barking and rewards an alternative behavior. The offered alternative behavior must be of higher value to the dog.
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If barking is pathologic, the anxiety state that leads to the abnormal vocalization must be treated. Identify triggers and limit exposure to them whenever possible. When barking occurs, redirect the dog's attention and activity to alternative behaviors (play, relaxation) and reward for compliance; use a leash or head collar if necessary; reward all decreases in barking in response to triggers. A neutral stimulus (noise, citronella spray burst) may be used for interrupting the behavior, followed by positive engagement in a different, non barking-related behavior that can be rewarded. Treatment with psychotropic medication (amitriptyline, fluoxetine, or clomipramine) is only appropriate if barking is a manifestation of a behavioral disorder (e.g., anxiety); consider referral to a behaviorist. Punishment, yelling, and use of shock collars should be avoided. Aversive responses serve only to increase, rather than decrease, arousal and may exacerbate the barking behavior.
CHRONIC TREATMENT Dogs should be taught to relax while making eye contact with the clients as a preferred default/substitute behavior when the dog encounters a situation about which it is anxious or unsure. Systematic desensitization can be used if the triggers can be identified and manipulated (e.g., Manners Minder [www.premier.com]). Alternate ways of alerting (sitting in a designated spot or in front of the clients) should be taught so the dog is still allowed to signal information.
DRUG INTERACTIONS Amitriptyline, fluoxetine, and clomipramine should not be used with mono-amine oxidase inhibitors (e.g., some tick collars and flea, tick, and mite dips, and some medications used for treating cognitive dysfunction). Combinations of different classes of psychotropic medications at lowered doses are usually safe other than for the potential for sedation, in which case dosages can be adjusted downward. Fluoxetine, paroxetine, and possibly sertraline, if given with tramadol, which has a weak but similar effect, may increase the risk of serotonin syndrome. If coadministration is necessary, start both at reduced dosages, titrate each to effect, and monitor for serotonin syndrome.
POSSIBLE COMPLICATIONS Clients who try to work with behavior modification too quickly (e.g., rewarding sitting even if the dog is distressed, instead of working to teach the dog to relax), with force, or inconsistently (in a multiperson household) may experience slow or no progress. Leash, choke chain, or pinch collar “corrections” can damage the esophagus, trachea, larynx, thyroid, and recurrent laryngeal nerves, altering quality of vocalization +/− swallowing and respiratory functions.
RECOMMENDED MONITORING Frequent follow-up with the clients—at least weekly—is helpful. Medications should be monitored for cardiac, renal, or hepatic side effects (uncommon) or sedation (more common).
PROGNOSIS AND OUTCOME For species-appropriate but inconvenient barking, prognosis is very good to excellent when owners understand the diagnosis. For pathologic barking, prognosis ranges from fair to very good depending on severity and chronicity of disorder. Both are influenced by client compliance, environmental circumstances, and response to psychotropic medication in the case of pathologic barking.
PEARLS & CONSIDERATIONS COMMENTS Shock collars have no place in the treatment of any behavioral condition. They will always exacerbate anxiety, even if they may suppress some aspects of behavioral signs; the behavior of dogs trained with a shock collar changes even outside the context of the training environment (display of signs of anxiety). Assessment for the potential risk of physical abuse of pets, spouses, and children should be made in any case in which such techniques have been used or the clients wish to use them (see online chapter: Abuse).
TECHNICIAN TIP
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Verbal reprimands serve no useful purpose. If a dog is barking excessively in the hospital, changing stimuli (e.g., moving the dog to an area with less/more activity or different animals in surroundings) is far better.
PREVENTION Early intervention. When dogs are added to the home, education of the dog as to what level of barking is acceptable to the client should be instituted on the first episode of unwanted barking.
CLIENT EDUCATION Yelling at a dog to be quiet will increase arousal and is therefore counterproductive. Clients can teach their dog the level of alarm barking they will tolerate by calmly taking the barking dog away from the trigger (using a leash if necessary), asking for an alternative behavior (sitting while looking at the client in a relaxed fashion), and then rewarding the quiet response. Clients can also thank their dog for barking when the barking is appropriate (e.g., someone is in the driveway), and then reward them for stopping, which the dog will do when he or she looks at the client in response to the client's praise.
SUGGESTED READING Ascione FR, Arkow P, editors: Child abuse, domestic violence, and animal abuse: linking the circles of compassion for prevention and intervention. West Lafayette, IN, 1999, Purdue University Press. Pongrácz P, Molnár C, Miklósi A: Barking in family dogs: an ethological approach. Vet J 183(2):141–147, 2010. AUTHOR: SORAYA V. JUARBE-DIAZ EDITOR: KAREN L. OVERALL
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Barbiturates Toxicosis
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Barbiturates Toxicosis BASIC INFORMATION DEFINITION Barbiturates are hypnotic, sedative, anticonvulsant drugs derived from barbituric acid (2,4,6-trioxohexahydropyrimidine). Barbiturate toxicosis refers to the onset of clinical signs caused by an acute, excessive exposure by ingestion or injection to this class of substances. The chronic effects of therapeutic phenobarbital use are discussed in greater detail elsewhere (see p. 871).
EPIDEMIOLOGY SPECIES, AGE, SEX All species, breeds, and both sexes of companion animals are susceptible; dogs are more likely to be involved. GENETICS & BREED PREDISPOSITION Greyhounds and other sight hounds: prolonged duration of action RISK FACTORS Underlying liver disease (decreased metabolic capacity) Patients with kidney disease may accumulate parent drug (may require dose adjustment) or decompensate with barbiturateinduced hypotension. Cardiorespiratory disease (regarding arrhythmogenicity, potential hypoxemia) Puppies, kittens, starved animals (decreased metabolic capacity)
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT History/evidence of exposure Rapid onset of central nervous system (CNS), respiratory, and cardiovascular (CV) depression, ataxia, hyporeflexia PHYSICAL EXAM FINDINGS Decreased response to stimuli, obtunded mentation/coma Slow, shallow respirations Hypotension: poor pulse quality, prolonged capillary refill time Bradycardia Hypothermia
ETIOLOGY AND PATHOPHYSIOLOGY Source Based on their half-lives, barbiturates are divided into ultra-short-acting, short-acting, and long-acting drugs: Ultra-short-acting: methohexital (Brevital), thiamylal (Surital), thiopental (Pentothal) Short-acting: amobarbital, butabarbital (Buticaps, Butisol, Barbased, Butolan), butalbital (marketed in combinations with aspirin, acetaminophen, caffeine, codeine, and anticholinergic alkaloids), hexobarbital (Evipal), pentobarbital (Nembutal), secobarbital (Seconal) Long-acting: phenobarbital (Donnatal, in combination with anticholinergic alkaloids), primidone (metabolized to phenobarbital), metharbital (not available in United States) Mechanism of Toxicosis Toxicosis occurs when animals accidentally eat large amounts of prescription medication (phenobarbital), from an overdose or accidental administration of injectable solution (pentobarbital, euthanasia solution), or from eating flesh of an animal that
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had been euthanized with a barbiturate. Barbiturates cause nonselective depression of both presynaptic and postsynaptic excitability via several mechanisms (GABA and glutamate receptors, sodium channels). Toxicosis is characterized by hyporeflexia, ataxia, hypothermia, hypotension, coma, slow shallow respirations, and death.
DIAGNOSIS DIAGNOSTIC OVERVIEW Barbiturate toxicosis is suspected from a history of possible or confirmed exposure, and suspicion is heightened by the presence of one of more overt signs (ataxia, depression, coma, hypothermia, hyporeflexia, and CV and respiratory depression). In most instances, this is sufficient to proceed to treatment and monitoring. The diagnosis can be definitively confirmed by identification of drug in bodily fluids or tissues.
DIFFERENTIAL DIAGNOSIS Toxicologic: alpha-2 agonists (amitraz, detomidine, medetomidine, xylazine, etc.), benzodiazepines, cardiac drugs causing hypotension (calcium channel blockers, high doses of ACE inhibitors, and beta blockers), ethanol or other alcohols, essential oils, ethylene glycol, isoxazole mushrooms, ivermectin and other avermectins, marijuana, muscle relaxants (baclofen, methocarbamol, guaifenesin), opioids, phenothiazines, trazodone (tetracyclic antidepressant) Nontoxicologic disorders: hepatic encephalopathy, hypoglycemia, primary intracranial disorder (encephalitis, neoplasia, etc.), shock (septic, hypovolemic), trauma
INITIAL DATABASE CBC Serum chemistry profile Blood pressure Heart rate and rhythm Acid-base status: monitor for acidosis
ADVANCED OR CONFIRMATORY TESTING Barbiturates can be analyzed antemortem in stomach contents/vomitus, urine, serum, or plasma. Postmortem, barbiturates can be detected in liver, heart, or kidney.
TREATMENT TREATMENT OVERVIEW Treatment is aimed at decontamination of the patient (emesis, activated charcoal) if no clinical signs are seen. Supportive care—intravenous fluids to maintain blood pressure, thermoregulation, oxygen supplementation/assisted ventilation, and enhanced elimination of barbiturates—is implemented according to anticipated (ingested dosage known to be large) or visible (marked clinical signs) severity of toxicosis.
ACUTE GENERAL TREATMENT Decontamination of patient: Emesis (see p. 1364): Useful within 2 to 4 hours only in animals not showing clinical signs (3% hydrogen peroxide 2 mL/kg PO up to maximum of 45 mL/dose, may be repeated once if no results within 15 minutes) Activated charcoal (1-2 g/kg PO once, with sorbitol or other cathartic); repeating charcoal (half of the original dose; omitting the cathartic) q 6 to 8 hours until improvement of depression will help decrease severity and duration of signs. May be ingested by patient if conscious and stable or given by stomach tube in a recumbent animal if the airway is protected (see p. 1281 ). Gastric lavage: consider if large toxic doses have been ingested (see p. 1281) and the animal is not already comatose. Enema (5 mL/lb, lukewarm water) may help promote gastrointestinal evacuation; administer 1-2 hours after administration of activated charcoal. Peritoneal or hemodialysis may be considered if hemodynamic compromise occurs, but likely not any more helpful than fluids and repeated doses of activated charcoal. Lipid emulsion therapy: Intravenous administration of lipid emulsion is a potential new method of enhanced elimination
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of lipophilic barbiturates; efficacy/safety of this has not been established. Use when other measures fail. Risk of hyperlipidemia from therapy (see p. 127). Supportive care: Intravenous administration of isotonic crystalloid fluids (warmed if animal is hypothermic), rate titrated to support blood pressure If hypothermia: external warmth (see p. 587 ) If hypoventilation or apnea: Supplemental oxygen Cuffed endotracheal tube to protect airway (always with mouth gag/speculum in place to avoid tube chewing). Monitoring of tube and airway care are essential (tube cleaning, deflating, and repositioning PRN; avoid pressure injury from overinflated cuff). Positive-pressure ventilation (see p. 1362 )
CHRONIC TREATMENT (See p. 871)
DRUG INTERACTIONS Drugs that can increase barbiturate action: any CNS depressant, valproic acid, chloramphenicol Decreased efficacy of oral anticoagulants, chloramphenicol, corticosteroids, doxycycline, beta blockers, quinidine, theophylline, and metronidazole Rifampin may induce P450 enzymes and reduce the half-life of phenobarbital Increased risk of hypotension with concurrent furosemide
POSSIBLE COMPLICATIONS Aspiration pneumonia Renal impairment secondary to hypotension Cardiorespiratory arrest
RECOMMENDED MONITORING Oxygenation Blood pressure Body temperature Mentation
PROGNOSIS AND OUTCOME With coma, prognosis is guarded to poor if intensive supportive care is not pursued.
PEARLS & CONSIDERATIONS COMMENTS Induction of emesis at home should be considered only if no clinical signs are present, if an observed ingestion took place, or if the pet was found with the container. Boiling or freezing of meat does not destroy barbiturates. Barbiturate-contaminated meat is a high risk source of relay (secondary) toxicity for scavengers. Acute signs of toxicosis (depending on the dose and the type of agent involved) can last several days. Repeated doses of activated charcoal are useful even when overdose occurs from barbiturate injection, since plasma barbiturates diffuse into the acidic stomach environment. Be aware of possible hypernatremia from multiple doses of activated charcoal.
PREVENTION Keep medications out of animal's reach. Prevent unsupervised roaming of animals. To prevent secondary acute poisoning, animals euthanized with barbiturates should not be used for animal (or human)
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consumption. Proper disposal of euthanized carcasses
CLIENT EDUCATION Control and monitor pet's environment. Do not feed barbiturate-contaminated meat/euthanized animal to pets.
SUGGESTED READING Plumb DC: Pentobarbital sodium, p 613; Phenobarbital, In Plumb’s veterinary drug handbook, ed 5, Ames, IA, 2005, Blackwell, p 620. Rader JD: Anticonvulsants, In Plumlee K, editor: Clinical veterinary toxicology. St Louis, 2003, Mosby, p 284. Volmer PA: “Recreational” Drugs. In Peterson ME, Talcott PA, editors: Small animal toxicology, St Louis, 2006, Saunders/Elsevier, p 273. AUTHOR: DONNA MENSCHING EDITOR: SAFDAR A. KHAN 1ST EDITION AUTHOR: MARY SCHELL
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Baclofen and Other Centrally Acting Muscle Relaxants Toxicosis
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Baclofen and Other Centrally Acting Muscle Relaxants Toxicosis BASIC INFORMATION DEFINITION Syndrome developing following the ingestion of one of several centrally-acting skeletal muscle relaxants (SMR) and characterized mainly by central nervous system (CNS) depression.
SYNONYMS Generic Name
Trade Name(s)
Baclofen
Lioresal, Kemstro
Carisoprodol
Soma
Chlorphenesin carbamate Maolate Chlorzoxazone
Parafon Forte
Cyclobenzaprine
Flexeril
Guaifenesin
Gecolate
Metaxalone
Skelaxin
Methocarbamol
Robaxin, Robaxin-V
Orphenadrine
Norflex
Tizanidine
Zanaflex
EPIDEMIOLOGY SPECIES, AGE, SEX All species susceptible; dogs more likely because of indiscriminate eating habits. RISK FACTORS Availability of muscle relaxants in the animal's environment Many people taking skeletal muscle relaxants for diseases of spasticity (e.g., multiple sclerosis) take other medication as well, increasing the risk for accidental exposures to multiple drugs by pets (polypharmacy).
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT History of exposure to muscle relaxants or presence of drugs in environment (see Table).
Drug
Chief Complaint
Baclofen PHYSICAL EXAM FINDINGS Baclofen: As above Hypothermia (if recumbent), hyperthermia (if seizing) Hypertension or hypotension Tachycardia or bradycardia
Onset of signs within 15 minutes to 7 hours following ingestion Dogs: vomiting, ataxia, hypersalivation, depression, vocalization, disorientation/agitation, recumbency, coma, seizure Cats: vomiting, depression, ataxia, weakness, hypothermia, recumbency, coma, mydriasis, diarrhea
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Hypoventilation Miosis (dogs) or mydriasis (cats) Muscular hypotonia, weakness Cyclobenzaprine and orphenadrine Depression or agitation, hyperesthesia (cats), vocalization Miosis (dogs) or mydriasis (cats), nystagmus (occasional, dog and cat) Muscle weakness, tremors, fasciculation Panting Tachycardia or bradycardia Hyperthermia Tizanidine Depression, weakness, ataxia Hypotension, bradycardia Pale mucous membranes, prolonged capillary refill time Hypothermia Other SMR Depression, somnolence, weakness Hypoventilation, cyanosis Tachycardia, hypotension Hypothermia (if recumbent), hyperthermia (if seizuring)
ETIOLOGY AND PATHOPHYSIOLOGY Source Most centrally acting SMRs are used for controlling spasticity in humans with neuromuscular disorders. May also be prescribed for relief of musculoskeletal pain.
Mechanism of Toxicosis Baclofen: Mimics gamma-aminobutyric acid (GABA) within the spinal cord, blocking excitatory responses to sensory input and causing flaccid paralysis. Baclofen-induced seizures may be due to interference with GABA release from presynaptic neurons, resulting in excessive postsynaptic nerve firing. Cyclobenzaprine: Structurally and functionally related to tricyclic antidepressants. Skeletal muscle relaxation may be related to sedative effects as well as inhibition of brainstem and spinal cord gamma and alpha motor neurons. In overdose situations, anticholinergic and antihistaminic effects become exaggerated. Tizanidine has a mechanism of action similar to that of xylazine and clonidine, in that it stimulates alpha-adrenoreceptors in the brainstem, causing decreased vascular resistance, heart rate, and blood pressure. At therapeutic levels, skeletal muscle effects predominate, but in overdose situations, pronounced cardiovascular effects occur. Orphenadrine has pronounced anticholinergic and antihistaminic effects. Chlorphenesin carbamate, guaifenesin, and methocarbamol may act by blocking nerve impulse transmission within the brainstem, spinal cord, and subcortical levels of the brain. Some of the skeletal muscle relaxant effect is due to sedation. Carisoprodol causes skeletal muscle relaxation via depression of postsynaptic spinal reflexes. Some of the skeletal muscle relaxant effect is due to sedation. Chlorzoxazone and metaxalone have no direct effect on skeletal muscles; muscle relaxant properties are likely due to sedative effects.
DIAGNOSIS DIAGNOSTIC OVERVIEW Diagnosis is based on history of exposure or presence of drugs in animal's environment along with appropriate clinical signs (ataxia, depression, coma, vocalization).
DIFFERENTIAL DIAGNOSIS Toxicologic: Other CNS depressants: barbiturates, benzodiazepines, opioids, ivermectin, ethylene glycol, tick paralysis, botulinum toxin, ionophore ingestion (dogs). Other causes of seizures: amphetamines, ethylene glycol, metaldehyde, strychnine, methylxanthines, zinc phosphide, tricyclic
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antidepressants, serotonergic drugs. Nontoxicologic, Spontaneous: Spinal trauma Polyradiculoneuritis, tick paralysis Organic brain disease (neoplasia, inflammation, etc.)
INITIAL DATABASE CBC, serum biochemistry profile: minimal alterations expected from SMR (identify preexisting liver or kidney dysfunction that may interfere with drug elimination) Orphenadrine overdose in humans has been associated with hypokalemia, hypoglycemia, liver enzyme elevations, and bleeding disorder.
ADVANCED OR CONFIRMATORY TESTING Baclofen, carisoprodol, chlorzoxazone, cyclobenzaprine, guaifenesin, and methocarbamol levels can be determined in urine and/or serum; presence will confirm exposure. Turnaround time may limit usefulness in dealing with an acute intoxication. Cyclobenzaprine will result in a positive serum or urine assay for amitriptyline.
TREATMENT TREATMENT OVERVIEW Treatment is aimed at early decontamination of the patient (emesis induction then administration of activated charcoal) when clinical signs are absent, and supportive care to address overt signs when they are present.
ACUTE GENERAL TREATMENT Stabilize patient Maintain respiration: endotracheal intubation and positive-pressure mechanical ventilatory support may be required. Control seizures: diazepam (0.5-1 mg/kg slow IV, to effect); propofol or isoflurane may be considered in cases refractory to diazepam (induce, keep anesthetized 5-10 minutes, then recover). Barbiturates should be considered a last resort, as their use may result in severe exacerbation of CNS depression; diazepam also generally useful for managing agitation. Manage cardiovascular abnormalities: most arrhythmias and blood pressure irregularities resolve during supportive care. Nitroprusside constant-rate IV infusion (1-2 mcg/kg/min [dogs] or 0.5 mcg/kg/min [cats], increased incrementally q 3-5 min until target BP is obtained) has been successfully used to manage baclofen-induced hypertension in dogs. Use of atropine to manage bradycardia is contraindicated in orphenadrine or cyclobenzaprine toxicosis, because it exacerbates anticholinergic effects. Supportive care: Intravenous fluid therapy: as needed for hypotension/hypovolemia and to promote urine formation; may enhance excretion of baclofen Atipamezole (50 mcg/kg, give ¼ to ⅓ of dose IV, remainder IM) or yohimbine (0.025 mg/kg slow IV) can be helpful to reverse hypotension from tizanidine. Cyproheptadine (1.1 mg/kg PO or per rectum q 6 h) has been helpful in reducing vocalization in dogs. Thermoregulation is essential, especially in comatose or recumbent animals. Decontamination of patient (no clinical signs): Emesis (see p. 1364 ): Because of the potential for rapid onset of clinical signs, induction of emesis is best done under veterinary supervision (hydrogen peroxide 3%: 0.25-0.5 mL/kg PO once [dogs] or xylazine hydrochloride 0.44 mg/kg IM [cats]). Emesis is contraindicated in animals showing overt clinical signs. Gastric lavage (see p. 1281 ): Consider for large ingestions (many tablets); protect airway with cuffed endotracheal tube. Activated charcoal (see p. 1322 ): dose according to packaging label of product (e.g., 10 mL/kg of activated charcoal suspension PO made from 2 g activated charcoal suspended in 10 mL kg tap-water). Repeated doses of activated charcoal q 8 h × 24 h and a cathartic, given every 3rd charcoal dose, are recommended for cyclobenzaprine and orphenadrine; single doses are recommended for all other SMRs.
CHRONIC TREATMENT
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Ventilatory support may be required for several days (particularly with baclofen)
NUTRITION/DIET For animals requiring long-term ventilatory support, parenteral nutrition may be considered (see p. 1322 ).
DRUG INTERACTIONS Use caution when administering drugs to sedated agitated animals.
RECOMMENDED MONITORING Respiratory rate and rhythm, heart rate, blood pressure, body temperature, blood gases, electrolyte status, hydration status, fluid ins/outs
PROGNOSIS AND OUTCOME Signs can persist for hours to several days, depending on the SMR involved and the dose ingested. Most animals with mild to moderate signs and receiving prompt and appropriate veterinary attention have an excellent prognosis. Animals exhibiting respiratory depression requiring ventilatory support have a more guarded prognosis, depending on the availability of mechanical ventilators. Seizuring or comatose animals have a more guarded prognosis.
PEARLS & CONSIDERATIONS COMMENTS Because the primary effect of these drugs is CNS depression, when treating animals showing paradoxical excitation, it is important to use the lowest sedative dose necessary to relieve the stimulation in order to avoid oversedation once the agitation has resolved. Baclofen, cyclobenzaprine, and tizanidine have narrow margins of safety, and significant (potentially life-threatening) signs can be seen at low doses. Baclofen: doses >1 mg/kg can cause signs; doses 8-16 mg/kg can be fatal to dogs. Cyclobenzaprine: doses as low as 0.07 mg/kg have resulted in clinical signs in dogs. Tizanidine: doses as low as 0.05 mg/kg have been associated with clinical signs in dogs, with hypotension occurring at doses as low as 0.08 mg/kg. Methocarbamol, guaifenesin, and chlorphenesin carbamate have fairly wide margins of safety, and overdoses rarely cause life-threatening problems. Anecdotally, intravenous lipid solutions have hastened recovery of dogs with baclofen toxicosis. This treatment modality is new and considered experimental. Use 20% intravenous lipid solution (normally used for parenteral nutrition, readily available from pharmacies, human hospitals) Bolus 1.5 mL/kg, then constant rate infusion of 0.25 mL/kg/min for 30-60 minutes. Can repeat in 6-8 h if serum is not lipemic and animal is still showing clinical signs. More information on this treatment method may be found at www.lipidrescue.org.
TECHNICIAN TIP Be prepared for paradoxical excitement when a sedative is given to patients with this type of intoxication: be sure doors are closed to prevent escape, have the patient on a surface clear of sharp or breakable objects, and take precautions to avoid being injured.
PREVENTION Keep medications out of reach of pets.
CLIENT EDUCATION When taking medication, do so in a room away from pets with the door closed to prevent pets from ingesting an accidentally dropped tablet. Never administer human medications to pets without first consulting a veterinarian.
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SUGGESTED READING Gwaltney-Brant SM: Skeletal muscle relaxants. In Plumlee KH, editor: Clinical veterinary toxicology. St Louis, 2004, Mosby, p 324. AUTHOR: SHARON GWALTNEY-BRANT EDITOR: SAFDAR A. KHAN
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Back Pain
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Back Pain BASIC INFORMATION DEFINITION Pain localized to the thoracolumbar spinal column
SYNONYMS Spinal hyperesthesia, spinal hyperpathia
EPIDEMIOLOGY SPECIES, AGE, SEX Dependent on the underlying cause Dogs: middle-aged (type I intervertebral disk disease), older adults (type II intervertebral disk disease, neoplasia) Cats: older adults (neoplasia), males more commonly represented (aortic thromboembolism) GENETICS & BREED PREDISPOSITION Dogs: chondrodystrophic breeds (type I intervertebral disk disease) RISK FACTORS Cats: thromboembolism associated with cardiomyopathy
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT: Vocalization, reluctance to movement or activity, pain elicited if patient touched or moved PHYSICAL EXAM FINDINGS Hunched posture (kyphosis), pain elicited on epaxial palpation; ataxia, paresis, or paralysis; heat or swelling in epaxial region; splinting and pain on abdominal palpation Fever, if back pain is associated with infection (e.g., diskospondylitis) Heart murmur, diminished femoral pulses, cyanosis of toenails if back pain is associated with aortic thromboembolism
ETIOLOGY AND PATHOPHYSIOLOGY Neurogenic: compression, inflammation, or traumatic disruption of spinal cord, spinal roots, spinal nerves, dorsal root ganglia, or meninges Vertebral column: trauma, inflammation, or lysis of vertebral bone, intervertebral disks, or articular facets Epaxial muscle: inflammation, abscessation, ischemia, or trauma
DIAGNOSIS DIAGNOSTIC OVERVIEW Back pain often presents nonspecific physical signs (or absence of any observable deficits) and gentle, thorough physical manipulations during the physical examination are used for eliciting signs of back pain. Diagnostic imaging and specific techniques then help to elucidate the source of the pain.
DIFFERENTIAL DIAGNOSIS Intervertebral disk disease (IVDD)
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Vertebral fracture or luxation Meningitis or meningomyelitis (granulomatous) Polyarthritis (immune-mediated or infectious) Diskospondylitis Vertebral osteomyelitis Spondylosis deformans/degenerative joint disease of articular facets Neoplasia (primary or metastatic) Polymyopathy (traumatic or inflammatory myositis) Fibrocartilaginous embolism (FCE; acute but transient pain, resolving within hours) Pain not localized to the spinal column: aortic thromboembolism, abdominal pain
INITIAL DATABASE Neurologic examination (see p. 1311) CBC, serum biochemistry, urinalysis: often unremarkable unless systemic disease or infection present Radiographs: bone lysis or proliferation (neoplasia, osteomyelitis), vertebral fracture or luxation (trauma), intervertebral disk mineralization, disk space narrowing, wedging or displacement (IVDD), vertebral endplate lysis or proliferation (diskospondylitis), articular facet sclerosis and malformation, spondylosis
ADVANCED OR CONFIRMATORY TESTING Selection based on history, clinical signs, and results of initial database: Cerebrospinal fluid tap: cytologic evaluation, culture, serologic testing for immunoglobulin A (IgA) or infectious agents Myelogram: identify and discern between extradural compression (IVDD), intradural/extramedullary lesion (meningioma), or intramedullary lesion (other neoplasia or cord swelling [e.g., due to FCE]) Urine culture (diskospondylitis) Blood culture and sensitivity (discospondylitis, osteomyelitis, bacterial meningitis) Needle aspirate of intervertebral disk (diskospondylitis) Serology: Brucella canis (discospondylitis), rickettsial diseases (polyarthritis, meningitis) Arthrocentesis: cytology (polyarthritis), culture (septic polyarthritis or meningitis) Advanced imaging: CT or MRI if lesion is suspected but not identified on myelogram Biopsy of vertebral bone (neoplasia, osteomyelitis)
TREATMENT TREATMENT OVERVIEW Elimination of infectious or noninfectious paraspinal inflammatory causes Elimination of any compressive lesion on spinal cord or nerve roots Stabilization of vertebral column
ACUTE GENERAL TREATMENT Address the underlying cause.
CHRONIC TREATMENT Degenerative joint disease may require persistent or recurrent nonsteroidal antiinflammatory drug (NSAID) administration. Chronic intervertebral disk disease or immune-mediated disease may require intermittent or persistent corticosteroid treatment. Antibiotic therapy for diskospondylitis (see p. 312) or vertebral osteomyelitis continued for 6 weeks beyond resolution of clinical signs.
DRUG INTERACTIONS Corticosteroids and NSAIDs must not be administered concurrently, owing to the risk of severe gastrointestinal ulceration.
POSSIBLE COMPLICATIONS Worsening or recurrence of signs Progression of spinal cord lesions
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Myelomalacia Valvular endocarditis, for infectious conditions
RECOMMENDED MONITORING Repeat physical and neurologic examination within 12 to 24 hours of treatment Follow-up examination and radiographs as needed
PROGNOSIS AND OUTCOME Variable, depending on underlying cause
PEARLS & CONSIDERATIONS COMMENTS Localization of pain requires thorough physical and neurologic examination. Acute back pain with neurologic deficits may represent a surgical emergency and should be evaluated immediately.
CLIENT EDUCATION Owner should monitor for recurrence of signs. Acute worsening of signs warrants emergency evaluation and treatment.
SUGGESTED READING Lorenz MD, Kornegay JN: Handbook of veterinary neurology. St Louis, 2004, WB Saunders, pp 345–353. AUTHOR: PETER MOAK EDITOR: ETIENNE CÔTÉ
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Babesiosis
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Babesiosis BASIC INFORMATION DEFINITION Canine babesiosis is a tickborne disease caused by a hemoprotozoan parasite that infects red blood cells of dogs causing hemolytic anemia and thrombocytopenia. Two primary species have been identified: Babesia canis (large Babesia) and Babesia gibsoni (small Babesia).
SYNONYMS Babesiosis: piroplasmosis Babesia annae: B. microti-like parasite Babesia gibsoni: B. gibsoni (Asian genotype) Babesia conradae: Referred to in some literature as B. gibsoni (USA genotype)
EPIDEMIOLOGY GENETICS & BREED PREDISPOSITION American pit bull terriers (APBT) and Tosa Inus at risk for B. gibsoni Greyhounds at risk for B. canis vogeli RISK FACTORS Dog fights (particularly bites by an APBT) Tick infestation Blood transfusion Shared needles or surgical instruments Vertical transmission in affected breeds CONTAGION & ZOONOSIS Transmission is through blood contamination or arthropod infestation (Rhipicephalus, Haemaphysalis, or Dermacentor spp.). Canine babesiosis is not a documented zoonotic disease; B. microti is a small Babesia infecting human red blood cells. Canine species of Babesia causing infections in humans have not been well documented. GEOGRAPHY AND SEASONALITY Since babesiosis can be either acute or chronic, it can be diagnosed at any time of year. Small babesias: B. gibsoni was once limited to Asia but now has a worldwide distribution. B. annae: Spain B. conradae: southern California Large babesias: B. canis vogeli: worldwide B. canis canis: Europe B. canis rossi: southern Africa One of the novel large Babesia sp. has been diagnosed in the United States and the other in the United Kingdom. ASSOCIATED CONDITIONS & DISORDERS: Some patients with babesiosis have been concurrently diagnosed with other tickborne diseases. The novel large Babesia sp. identified in United States has been primarily diagnosed in dogs that have previously undergone splenectomy or are undergoing chemotherapy.
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Babesiosis
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CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES Babesiosis can cause severe, life-threatening disease in some dogs; others show few or no outward clinical signs. B. annae is commonly associated with azotemia and proteinuria. HISTORY, CHIEF COMPLAINT Owners may observe weakness, lethargy, anorexia, pallor, icterus, or discolored urine (bilirubinuria or hemoglobinuria). Other historic findings may include tick exposure, recent blood transfusion, or recent dog fight (especially with an APBT). PHYSICAL EXAM FINDINGS Pallor and splenomegaly, +/− lymphadenopathy, fever or icterus.
ETIOLOGY AND PATHOPHYSIOLOGY Sporozoites in tick salivary glands transmitted to dog during feeding (requires 2-3 days) Sporozoites enter red blood cells (RBCs), where they become merozoites and undergo asexual reproduction. Intravascular and extravascular hemolysis occur. Secondary immune-mediated destruction of RBCs and platelets may occur. Azotemia and proteinuria are presumed to be secondary to glomerulonephritis and are most commonly seen with B. annae infections.
DIAGNOSIS DIAGNOSTIC OVERVIEW Most dogs with babesiosis have one or more of the following abnormalities: thrombocytopenia, anemia, hyperglobu linemia or splenomegaly. PCR assays have become the primary means of accurately diagnosing Babesia infections.
DIFFERENTIAL DIAGNOSIS Immune-mediated hemolytic anemia Immune-mediated thrombocytopenia Zinc toxicity Splenic torsion Ehrlichiosis Leptospirosis Dirofilariasis with caval syndrome Neoplasia: lymphoma or hemangiosarcoma
INITIAL DATABASE One or more of the following may be identified in dogs with babesiosis: Regenerative anemia: It is important to note that not all dogs with Babesia infections have anemia. Thrombocytopenia: This is the most common hematologic abnormality in dogs with babesiosis; platelet counts can be as low as 10 kg, 500 mg (10 days’ duration, and any patient whose owner is concerned and wishes more than an exam-room evaluation Fecal analysis (Baermann) if lung-worms are locally endemic Heartworm antigen test in endemic areas Routine medical evaluation, including CBC, serum biochemistry profile, and urinalysis if patient shows systemic signs Prothrombin time, partial thromboplastin time, platelet count if the patient roams outdoors or could otherwise have been exposed to anticoagulant rodenticide
ADVANCED OR CONFIRMATORY TESTING Based on specifics of case as assessed with history, presenting signs, physical exam findings, and initial database results
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Cough
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TREATMENT TREATMENT OVERVIEW Correction/cure of inciting disorder when possible Palliation of cough if underlying cause cannot be eliminated
ACUTE AND CHRONIC TREATMENT Dependent on underlying cause: Purposeful cough: primary respiratory lesion requires correction (e.g., pneumonia treatment, foreign body removal, lung lobectomy) and treatments that increase the efficacy of the cough (e.g., nebulization and coupage). Cough suppression is contraindicated. Warning cough: systemic disorder must be identified and addressed promptly. (Cardiogenic pulmonary edema: diuretics. Pulmonary hemorrhage from anticoagulant toxicity: plasma transfusion, vitamin K1 replacement.) Treatments to increase the efficacy of the cough, such as nebulization and coupage, or treatments aimed at decreasing the cough (cough suppressants) are contraindicated. Nuisance cough: avoidance of triggers (e.g., allergens, dusts) and cough suppression. Treatment of complicating factors if they occur (e.g., infection). Cough suppressants (e.g., butorphanol, 0.25-1 mg/kg PO q 8-24 has needed; or hydrocodone, 0.25 mg/kg PO q 6-24 h as needed; or codeine 0.5-2 mg/kg PO q 6-12 h as needed): Only used when a sterile, uncomplicated process is responsible for the cough and the patient is systemically well. Examples: collapsing trachea, chronic sterile bronchitis, uncomplicated allergic airway disease. Empirical antibiotics or corticosteroids are not recommended in the absence of a diagnosis for the cause of the cough (minimum: completion of the initial database).
RECOMMENDED MONITORING Respiratory effort Resolution of cough is expected in 7-10 days, with no worsening or new clinical signs of illness, in cases of benign, self-contained processes such as infectious tracheobronchitis. Failure to self-resolve may indicate a more complex cause and warrants further evaluation.
PROGNOSIS AND OUTCOME Based on cause: Purposeful cough: prognosis fair to good if underlying cause can be controlled (eradication of pneumonia, removal of foreign body) Warning cough: short-term prognosis guarded. Long-term prognosis variable, based on response to acute treatment and underlying cause. Nuisance cough: short-term prognosis generally good, long-term prognosis fair (e.g., with collapsing trachea patients responding well to treatment) to good (e.g., patients with infectious tracheobronchitis)
PEARLS & CONSIDERATIONS COMMENTS Cough is a clinical sign, not a disease. Optimal management must involve an accurate diagnosis of the underlying cause. Cigarette smoke inhalation and obesity are common but reversible complicating factors in patients with chronic cough.
SUGGESTED READING Anderson-Wessberg K: Coughing. In Ettinger SJ, Feldman EC, editors: Textbook of veterinary internal medicine, ed 7, St Louis, 2010, Saunders Elsevier, pp 250–253. AUTHOR & EDITOR: ETIENNE CÔTÉ
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Coronaviral Enteritis
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Coronaviral Enteritis BASIC INFORMATION DEFINITION Infectious intestinal disease that causes a generally mild diarrhea in dogs and cats. Coronaviral infections causing feline infectious peritonitis are discussed in greater detail on .
SYNONYMS CCV (canine coronavirus), FECV (feline enteric coronavirus)
EPIDEMIOLOGY SPECIES, AGE, SEX Dogs: neonatal puppies are more severely affected. Cats: virus virtually ubiquitous in the cat population; however, clinical disease is more common in young kittens in catteries and shelters. RISK FACTORS Dogs: infection is prevalent in animal shelters and breeding farms (dense populations and concurrent infections). Cats: multicat households (more than five cats) or catteries. CONTAGION & ZOONOSIS Dogs: CCV is highly contagious and spreads rapidly through groups of susceptible dogs (dog to dog). Cats: FECV is highly contagious and spreads rapidly through multicat households (cat to cat). Transmission is by the fecal-oral route. CCV and FECV are not known to infect people.
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES Dogs: Subclinical in adult dogs Diarrhea and vomiting (neonatal puppies) Cats: Subclinical in adult cats Mild to moderately severe diarrhea in kittens Mutation to feline infectious peritonitis virus resulting in multisystemic disease (see p. 383) HISTORY, CHIEF COMPLAINT Some or all may be present: Mild to moderately severe diarrhea Blood in feces (infrequent) Vomiting is more common in dogs. Lethargy and inappetence Weight loss PHYSICAL EXAM FINDINGS Dehydration; degree depends on severity of the diarrhea
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Coronaviral Enteritis
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Occasionally concurrent ocular and nasal discharge, or weight loss in chronically infected kittens
ETIOLOGY AND PATHOPHYSIOLOGY Member of the virus family Coronaviridae; single-stranded RNA virus Dogs and cats: virus infects epithelial cells in the tips of small-intestine villi, causing a malabsorptive diarrhea. The virus remains infective for 2-3 days at room temperature (several days longer at temperatures just above freezing) and may be transmitted to other animals via infected litterboxes or fomites. Cats only: RNA mutations of FECV result in the formation of a new virus (feline infectious peritonitis [FIP] variant) that is able to enter and replicate within feline macrophages (see p. 383).
DIAGNOSIS DIAGNOSTIC OVERVIEW The diagnosis is suspected in dogs or cats with generally mild, self-limiting diarrhea. Most cases require little if any treatment, so diagnostic testing is not necessary for confirming the diagnosis. Rather, tests are indicated to rule out other more serious disorders that initially mimic (or coexist with) coronavirus infection.
DIFFERENTIAL DIAGNOSIS Intestinal disease caused by enteric bacteria (Campylobacter, salmonellosis), protozoa (coccidiosis), or other viruses (i.e., canine parvoviral enteritis, feline panleukopenia-associated enteritis) Dietary indiscretion (dogs) Parasites (both dogs and cats) Dietary intolerance (cats)
INITIAL DATABASE CBC, biochemistry panel, urinalysis: nonspecific changes Severe diarrhea can result in marked dehydration and electrolyte abnormalities. Fecal testing for parasites and protozoa
ADVANCED OR CONFIRMATORY TESTING Generally not performed, since corona-viral enteritis is usually self-limiting (exception: FIP) and even in severe cases, responsive to supportive care. Dogs: Detection of CCV in fresh feces by electron microscopy (false-negative findings possible) Virus isolation (however, CCV does not grow well). Reverse transcriptase PCR has been developed to detect CCV in fecal specimens (not commercially available). Serologic evaluation: positive titers only confirm exposure to CCV, not necessarily active infection. Cats: Serologic evaluation (indirect immunofluorescent antibody, ELISA) Does not differentiate FECV that causes isolated enteritis from FECV that causes FIP Does not correlate with severity of disease Positive titers only confirm exposure to FECV, not necessarily active infection. In multicat (more than six cats) households, virtually all cats are seropositive. Reverse transcriptase PCR has been developed to detect FECV in fecal specimens. Does not reliably differentiate FECV that causes isolated enteritis from FECV that causes FIP
TREATMENT TREATMENT OVERVIEW Treatment, if any is required, is primarily supportive during the time needed for the disease to run its natural course.
ACUTE GENERAL TREATMENT
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Coronaviral Enteritis
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Parenteral fluids to maintain fluid and electrolyte balance Broad-spectrum antimicrobial agents to treat secondary bacterial infections are rarely indicated. Good nursing care and hygiene
POSSIBLE COMPLICATIONS Dogs: Clinical course (typically 7-10 days) may be longer and more severe in dogs that develop secondary complications or infection. Dehydration, acidosis, shock Concurrent canine parvovirus or parasitic infections Cats: In immunocompromised kittens or cats, the virus may persist, resulting in chronic diarrhea or vomiting (months). Enteric coronavirus can mutate into feline infectious peritonitis virus. Monitor the affected cat and others in contact with it for signs of FIP (e.g., abdominal distension, fever, weight loss, neurologic signs, and icterus). However, the occurrence of coronaviral enteritis in an individual cat is not predictive of FIP.
RECOMMENDED MONITORING Response to therapy
PROGNOSIS AND OUTCOME Dogs: good; neonatal puppies with concurrent parvovirus and coronavirus infections have a more guarded prognosis. Cats: generally good; guarded to poor in cats in whom FECV mutates and causes FIP
PEARLS & CONSIDERATIONS COMMENTS Clinical disease is considered infrequent compared with other viral enteropathies. Dogs: CCV vaccines are not considered core vaccines but should be reserved for animals in which the risk of exposure may be higher (dense, stressful environments). Cats: Inapparent infection is common in normal cats. FECV-associated enteritis does not predispose a cat to development of FIP.
CLIENT EDUCATION Reducing the number of cats per household (especially kittens less than 12 months old) and keeping potentially FECV-contaminated surfaces clean (e.g., litterboxes) can reduce population loads of FECV and thus also reduce the risk of FIP.
RECOMMENDED READING Pederson NC, et al: Common virus infection in cats, before and after being placed in shelters, with emphasis on feline enteric coro-navirus. J Feline Med Surg 6(2):83–88, 2004. Sanchez-Morgado JM, et al: Molecular characterization of a virulent canine coronavirus BG strain. Virus Res 104(1):27–31, 2004. AUTHOR: BRANDY PORTERPAN EDITOR: DEBRA L. ZORAN
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Cornification Disorders
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Cornification Disorders BASIC INFORMATION DEFINITION A well-recognized class of scaling or greasy skin disorders resulting from primary (usually hereditary) or secondary (acquired) defects in epidermal maturation, desquamation, or sebum production. Many disorders were formerly grouped under the heading seborrhea, but this term was nonspecific and inaccurate and is now obsolete.
SYNONYMS Keratinization defects/disorders Keratoseborrheic disorders
EPIDEMIOLOGY SPECIES, AGE, SEX Primary (hereditary) causes: early in life for many conditions Secondary (acquired): any age; usually adult animals GENETICS & BREED PREDISPOSITION Primary idiopathic seborrhea: cocker spaniel, West Highland white terrier, basset hound, shar-pei, dachshund, Doberman pinscher, English springer spaniel, German shepherd, Irish setter, Labrador retriever Primary hereditary seborrhea oleosa: Persian, Himalayan, and exotic short hair cats Vitamin A–responsive dermatosis: cocker spaniel, Labrador retriever, miniature schnauzer Zinc-responsive dermatosis: Alaskan malamute, Siberian husky, Samoyed Lethal acrodermatitis: bull terrier Epidermal dysplasia: West Highland white terrier Sebaceous adenitis (see p. 1007): Akita, Samoyed, standard poodle, and many other breeds have been reported to have this condition. Ichthyosis: golden retriever, Norfolk terrier CONTAGION & ZOONOSIS Most are not contagious, but parasitic and fungal etiologies have contagious and zoonotic potential. GEOGRAPHY AND SEASONALITY Scaling (formerly called seborrhea sicca) is more common in the winter (low environmental humidity). ASSOCIATED CONDITIONS & DISORDERS Primary cornification disorders may be associated with ceruminous otitis externa.
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES Primary cornification disorders (usually hereditary and incurable) or secondary (acquired, usually curable) Generalized or localized HISTORY, CHIEF COMPLAINT Owners generally present pets for evaluation of an unpleasant-appearing hair coat or coat with a foul odor. Specific complaints may include a generalized waxy or scaly coat condition, often associated with a rancid odor. Pruritus is of variable intensity, depending on presence of parasites, dry skin, or secondary bacterial or yeast infection; however, scaling may be an incidental finding in some
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animals. PHYSICAL EXAM FINDINGS Primary cornification disorders: varying degrees of alopecia and dry scale that may be focal, multifocal, or generalized over the trunk. Animals may present with large hyperkeratotic patches of adherent scale. Follicular casts (waxy debris surrounding hair shafts), fronds (clumps of hairs stuck together like a paint brush), or severe “dandruff” with large flakes may be noted. Localized cornification disorders: Nasal hyperkeratosis of the Labrador retriever: restricted to the nasal planum Nasodigital hyperkeratosis: restricted to nasal planum and digital pads Ear margin dermatosis: alopecia and scaling of distal pinnal margins, possibly associated with fissures Feline acne: comedones on the chin +/− lips; papules, pustules, erosion, crust and pruritus if secondarily infected Secondary cornification disorders: general physical findings depend on underlying etiology or vary with underlying etiology. Cutaneous findings include a dull (or waxy) coat with various combinations of alopecia, scaling, crusting, collarettes, and excoriations secondary to self-trauma and pyoderma.
ETIOLOGY AND PATHOPHYSIOLOGY Cornification encompasses all the processes that lead to the formation of the stratum corneum. This includes keratinization and formation of the lipid-rich intercellular domain that binds corneocytes to maintain a relatively impermeable barrier. Disorders of cornification are due to a defective cornification process or excessive proliferation and/or defective desquamation (retention hyperkeratosis). Therefore, any alteration in epidermal turnover times, maturation processes, and/or desquamation or trans epidermal water loss lead to scaling. Other considerations include abnormal apocrine or sebaceous glandular secretions (either in volume or quality).
DIAGNOSIS DIAGNOSTIC OVERVIEW Scale formation is a common response of the skin to any insult. It is critical to evaluate the patient for underlying causes—in particular, the roles parasite and microbial dermatitis may be playing if any—before pursuing other etiologies.
DIFFERENTIAL DIAGNOSIS Secondary cornification disorders; underlying causes include: Microbial: pyoderma, Malassezia, dermatophytosis, leishmaniasis Parasitic: flea infestation, cheyletiellosis, sarcoptic mange, pediculosis, and demodicosis (including Demodex injai, the long-bodied Demodex mite that has been associated with a greasy seborrheic dermatosis, especially in adult terriers) Endocrinopathy: hypothyroidism, hyperadrenocorticism, sex hormone imbalance (e.g., Sertoli cell tumor) Allergic: dermatologic adverse food reaction (food allergy), atopic dermatitis Management deficiencies: low environmental humidity, inappropriate topical therapy or frequency, nutritionally inadequate diet (especially if high in phytates and fiber, low in fatty acids) Metabolic disease (especially liver disease) Immune-mediated disease: pemphigus foliaceus, systemic lupus erythematosus, adverse drug reaction Neoplasia: Cutaneous epitheliotropic lymphoma, exfoliative dermatitis associated with thymoma in cats Primary cornification disorders: usually genetically determined; may be multi-focal and generalized or localized: Multifocal and generalized: Idiopathic primary seborrhea (dogs) Hereditary seborrhea oleosa (cats) Vitamin A–responsive dermatosis Zinc-responsive dermatosis Sebaceous adenitis Epidermal dysplasia Schnauzer comedo syndrome Canine ichthyosis Localized: Nasal parakeratosis of the Labrador retriever (autosomal recessive) Footpad hyperkeratosis in dogues de Bordeaux and Irish terrier Feline acne Stud tail Ear margin dermatosis
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INITIAL DATABASE Comprehensive evaluation for ectoparasites (skin scrapings, flea combing, acetate tape preparations, fecal evaluation, ectoparasiticide response trial) Skin cytologic examination (to rule out bacterial and yeast involvement) Fungal culture (dermatophytosis) CBC, serum biochemical profile, urinalysis (as appropriate, to look for evidence of underlying disease)
ADVANCED OR CONFIRMATORY TESTING Skin biopsy: useful for many disorders once infectious and parasitic causes have been ruled out Elimination diet trial to rule out food allergy (if pruritic) Intradermal and serum allergy testing for atopic dermatitis (if pruritic) Response to dietary management (if poor-quality diet) Thyroid function testing Adrenal function testing
TREATMENT TREATMENT OVERVIEW The goal of treatment is to address the underlying etiology specifically if possible. In primary conditions, it is important to control secondary microbial dermatitis while controlling the amount of scale produced.
ACUTE GENERAL TREATMENT Systemic antibiotics, such as cephalexin, 22-30 mg/kg PO q 12 h for at least 2 weeks past resolution of clinical signs or until improvement plateaus (minimum of 4 weeks), if a bacterial component is suspected. Some animals require chronic treatment. Essential fatty acid (EFA) oral supplementation (omega-3 and omega-6); rarely provides complete control of scaling but may be beneficial as adjunctive therapy Systemic and topical antifungal treatment as needed (see Malassezia dermatitis, p. 682; Dermatophytosis, ) Topical therapy: clipping of hair coat may benefit topical therapy: Antiseborrheic shampoos contain keratolytic and/or keratoplastic compounds and are used initially twice weekly. Good choices of ingredients for dry, scaly coats include sulfur and salicylic acid; decrease frequency as needed. Topical antiseborrheic products containing phytosphingosine may be of benefit. Greasy, scaly skin in dogs can be degreased using products containing benzoyl peroxide, or selenium sulfide. These products should always be followed with a conditioner. Note: Shampoos containing benzoyl peroxide are drying and will bleach fabric. Mild dry scaling may respond to moisturizing or hypoallergenic shampoos. Conditioners containing lipids or humectants (agents that help the skin to retain moisture) are beneficial.
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CORNIFICATION DISORDERS Extensive erythroderma and scaling (exfoliative erythroderma) in a dog with epitheliotropic lymphoma. (Copyright Dr. Manon Paradis.)
CORNIFICATION DISORDERS Primary seborrhea oleosa in a Himalayan cat. Note the greasy haircoat especially apparent across the ventrum. (Copyright Dr. Manon Paradis.)
CHRONIC TREATMENT Generalized disease Primary idiopathic seborrhea: topical therapy as already described; EFA supplementation; antibiotics administered as already described. Consider retinoids; acitretin (Soriatane), 0.5-1 mg/kg PO q 24 h; or cyclosporine, 5-10 mg/kg PO q 12-24 h. Vitamin A–responsive dermatosis: topical therapy and antibiotics as already described; vitamin A 625-800 IU/kg PO q 24 h; usually 10,000 IU PO daily, lifelong, for the average cocker spaniel. Improvement is noted by 3 weeks, with remission in 8-10 weeks. Zinc-responsive dermatosis: zinc supplementation is recommended at 1-3 mg/kg elemental zinc PO q 24 h (see p. 1189). Epidermal dysplasia: address any bacterial, yeast, parasitic, atopic, and hypersensitivity disorders. Bathe the animal frequently with keratolytic and keratoplastic shampoos.
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Schnauzer comedo syndrome: benzoyl peroxide shampoos help the condition via follicular flushing. Systemic antibiotics (as already described) to control bacterial folliculitis. In some cases, retinoids such as isotretinoin (Accutane), 1-2 mg/kg PO q 24 h, may be helpful but can be costly. Wean to alternate day therapy after 4 weeks if a favorable response is noted. Canine ichthyosis: Antiseborrheic shampoos and a topical spray conditioner containing propylene glycol and humectants can be useful. Try isotretinoin (Accutane), 1-2 mg/kg PO q 24 h for 8-12 weeks, decreasing to alternate-day therapy if effective) in more severe cases Sebaceous adenitis (see p. 1007): Localized disease Feline acne (see p. 20) Ear margin dermatosis: local use of an antiseborrheic shampoo. If inflammation is severe, topical glucocorticoid such as 0.5%-1% hydrocortisone may reduce inflammation. Nasal and digital hyperkeratosis: moisturize affected area with water or wet dressings, and then apply petrolatum jelly. More severely affected animals may benefit from topical application of an ointment containing salicylic acid and urea, or 50%-75% propylene glycol, or 0.025 or 0.01% tretinoin gel (Retin-A).
DRUG INTERACTIONS Cyclosporine: Concurrent use of cyclosporine with other P-glycoprotein inhibitors or substrates can increase blood cyclosporine levels. This may be beneficial (e.g., lowers the dose of cyclosporine required by half when administered with standard doses of ketoconazole) but can also increase the potential toxicity.
POSSIBLE COMPLICATIONS High fatty acid treatment may increase the potential for gastrointestinal (GI) disturbance or pancreatitis. Retinoids: keratoconjunctivitis sicca, conjunctivitis, pruritus, hyperactivity, stiffness, mucocutaneous junction erythema, vomiting, diarrhea, teratogenicity, elevated liver enzymes Cyclosporine: diarrhea, vomiting, anorexia, gingival hyperplasia, gingivitis, renal effects, hypertension; monitor animals for tumors.
RECOMMENDED MONITORING Vitamin A, retinoids: monitor liver enzymes and tear production. Cyclosporine: physical examination (tumor, infection, gingival hyperplasia), urea, creatinine, urinalysis, and liver enzymes; blood pressure. Check trough serum cyclosporine levels if adverse reactions are noted or if there is a poor clinical response (see p. 1471).
PROGNOSIS AND OUTCOME Primary causes often require lifelong therapy; secondary syndromes usually recover with correction or control of underlying etiology.
PEARLS & CONSIDERATIONS COMMENTS Control secondary microbial dermatitis, and evaluate thoroughly for other underlying secondary etiologies before diagnosing a primary seborrheic syndrome. The term seborrhea as a diagnosis should be limited to the breed-specific diseases (e.g., idiopathic primary seborrhea of cocker spaniel, primary hereditary seborrhea oleosa of Persian cats). Use other descriptive terms such as scaling, exfoliation, crusting, greasiness, malodor to characterize skin changes, rather than the nonspecific term, seborrhea.
PREVENTION Animals affected with primary (genetically determined) cornification disorders should not be used for breeding.
CLIENT EDUCATION Concept of control versus cure
SUGGESTED READING
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Paradis M: Primary hereditary seborrhea oleosa. In August JR, editor: Consultation in feline medicine, ed 4, Philadelphia, 2001, Churchill-Livingstone, pp 202–207. AUTHOR: STEPHEN WAISGLASS EDITOR: MANON PARADIS
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Corneal/Scleral Trauma
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Corneal/Scleral Trauma BASIC INFORMATION DEFINITION Ocular injury secondary to blunt or sharp trauma. Penetrating infers partial-thickness injury; perforating infers full-thickness injury. Simple wounds involve only cornea or sclera; complicated wounds involve multiple ocular structures.
EPIDEMIOLOGY SPECIES, AGE, SEX Any species, age, or sex RISK FACTORS Young, active animals Hunting animals Interanimal fighting Dog's head out the window while car is in motion Existing visual impairment may predispose
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT Running through dense or dry vegetation just before onset of clinical signs Owner may or may not observe trauma or causal event. Acute onset of any or all of the following: Blepharospasm Ocular discharge Blood or fluid coming from eye Swelling around the eye (e.g., eyelids; conjunctiva) Cloudy eye PHYSICAL EXAM FINDINGS Signs of pain on ophthalmic examination (see p. 1313) manifested by blepharospasm and resistance to ophthalmic examination. Linear, V-shaped, or stellate corneal lesion of acute onset accompanied by any or all of the following: Hyphema (see p. 571) and/or sub-conjunctival hemorrhage Corneal edema with or without cellular infiltrate Uveal prolapse: appears as pigmented structure in damaged cornea or sclera; associated with: Dyscoric/misshapen pupil Hyphema (see p. 571) Foreign body embedded in cornea or perforating cornea Signs of uveitis, particularly with perforating trauma (see p. 1151) Fibrin in cornea may fill perforation; light brown in color, may be associated with blood. Yellowish/whitish lens material in anterior chamber and cataract (see p. 181) if lens involved Shallow anterior chamber if wound actively leaking Thorough examination of the entire conjunctival sac is necessary to identify any retained foreign material. Sedation, general anesthesia, or referral may be required in difficult cases or if this procedure is unfamiliar to the practitioner. Subconjunctival hemorrhage and hyphema should alert clinician to possibility of posterior scleral rupture if no anterior segment lesions are present, particularly if accompanied by very low intraocular pressure (i.e., 50% of the thickness of the corneal stroma or perforate the cornea or sclera. Eliminate infection. Control intraocular inflammation.
ACUTE GENERAL TREATMENT Do not put pressure on the globe until the possibility of rupture is eliminated. Elizabethan collar placement to prevent self-trauma Small, nonperforating or very small sealed perforating wounds without uveal prolapse, consider conservative therapy: Topical antibiotic solution (e.g., neomycin/polymyxin/gramicidin, gentamicin, or ciprofloxacin) q 6 h Add broad-spectrum systemic antibiotics if perforating (e.g., amoxicillinclavulanate, 13.75 mg/kg PO q 12 h; base long-term choice on culture and sensitivity). Systemic antiinflammatory therapy with either nonsteroidal antiinflammatories (e.g., meloxicam, 0.1 mg/kg PO q 24 h; or carprofen, 2 mg/kg PO q 12 h) or antiinflammatory doses of prednisone (e.g., 0.5-1 mg/kg PO q 24 h) Topical atropine 1% solution q 6-24 h if significant uveitis present (see p. 1151). Perforating or deep, large, or gaping penetrating wounds and wounds with uveal prolapse require primary surgical repair (referable procedure) involving: Replacement of viable uveal tissue or resection of nonviable uveal tissue Irrigation and reinflation of anterior chamber Repair of cornea with appropriate-size suture material (8-0 to 10-0) Careful inspection of lens; if lens rupture noted, lens should be removed by phacoemulsification.
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CHRONIC TREATMENT Monitor and treat for uveitis and wound dehiscence. Consider changing antibiotics if indicated by culture and sensitivity results.
DRUG INTERACTIONS Do not use topical ophthalmic ointments if globe rupture is suspected.
POSSIBLE COMPLICATIONS Retinal Detachment, p. 985 Cataracts, p. 181 Chronic Uveitis, p. 1151 Glaucoma, p. 448 Endophthalmitis (inflammation of the uveal tract and anterior and posterior compartments of the eye) Loss of vision and eye Cats may develop posttraumatic ocular sarcomas years after original injury, particularly if lens involved (see p. 620).
RECOMMENDED MONITORING Reevaluate in 24-48 hours to ensure wounds are sealed, inflammation is improving, and there are no signs of infection. Frequency of examination then depends on response to therapy.
PROGNOSIS AND OUTCOME Intuitively, small, shallow penetrating wounds of the cornea or lacerations involving only the cornea have a good prognosis, whereas complicated, perforating wounds with uveal and/or lens involvement have a poorer prognosis for vision. Posterior wounds involving sclera or sclera and uvea have a grave prognosis for vision. Blunt trauma usually has a grave prognosis for vision, particularly if extensive hyphema is present. Negative menace response and negative dazzle and pupillary light reflexes at initial examination of a patient with corneal or scleral trauma indicate grave prognosis for vision.
PEARLS & CONSIDERATIONS COMMENTS Consider sedation to keep patient calm and prevent self-trauma. Elizabethan collar to prevent self-trauma
PREVENTION Animals should be monitored when introduced to new environment with other animals.
CLIENT EDUCATION Discuss the possibility of long-term complications that could lead to loss of vision and loss of an eye.
SUGGESTED READING Miller PE: Ocular emergencies. In Maggs DJ, Miller PE, Ofri R, editors: Slatter’ s fundamentals of veterinary ophthalmology, ed 4, Philadelphia, 2008, WB Saunders, p 419. AUTHOR: ELLISON BENTLEY EDITOR: CHERYL L. CULLEN
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Corneal Vascularization
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Corneal Vascularization BASIC INFORMATION DEFINITION The presence of blood vessels in or on the cornea
SYNONYMS Corneal neovascularization, vascularized keratitis
EPIDEMIOLOGY SPECIES, AGE, SEX Varies depending on underlying cause ASSOCIATED CONDITIONS & DISORDERS Corneal ulceration, irritation, desiccation, uveitis, episcleritis, or scleritis
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT Some or all may be present: History: Ocular trauma Chronic ophthalmic disorder (e.g., keratoconjunctivitis sicca, indolent corneal ulcer, others) Chief complaint: Red discoloration of the eye Ocular discharge Signs of ocular pain, manifesting as behavior change, blepharospasm PHYSICAL EXAM FINDINGS Focal to diffuse red discoloration of the corneal surface or stroma New corneal vessels enter stroma at the limbus and may be small: May give the affected cornea a reddish haze Are leaky and cause surrounding corneal edema (bluish haze) May be missed altogether owing to a cursory exam Other findings will vary depending on the cause.
ETIOLOGY AND PATHOPHYSIOLOGY Blood vessel ingrowth occurs: As a response to injury of the corneal epithelium or stroma as a normal component of healing Neutrophils, which enter the cornea from the tear film and the limbus, are important sources for angioblast and fibroblast growth factors. There is a 3- to 4-day delay before the ingrowth of corneal blood vessels. Ingrowth then occurs at a rate of approximately 1 mm/d. As part of an immune-mediated inflammatory response Secondary to disease of adjacent ocular tissues, including uveitis, episcleritis, scleritis, glaucoma, and orbital disease
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DIAGNOSIS DIAGNOSTIC OVERVIEW The diagnosis is made on careful visual inspection of the corneal surface. Important features for pinpointing the underlying cause and treatment approach include the location and pattern of vascularization, and evaluation for other concurrent ocular disease.
DIFFERENTIAL DIAGNOSIS Corneal injury or inflammation: Corneal ulceration Chemical irritation Mechanical irritation: Distichiasis/ectopic cilia/trichiasis Entropion Exposure: Large palpebral fissure Lagophthalmos (incomplete closure of the eyelids) Ectropion Buphthalmos (chronic glaucoma) Exophthalmos Neuroparalytic keratitis (cranial nerve VII lesion) Neurotrophic keratitis (cranial nerve V lesion) Keratoconjunctivitis sicca Qualitative tear film abnormalities Chronic superficial keratitis (CSK/pannus) (dogs) Proliferative keratoconjunctivitis (cats) Corneal degeneration Adjacent ocular disease: Uveitis Episcleritis/scleritis Orbital disease Glaucoma
INITIAL DATABASE Neuroophthalmic examination, : evaluate palpebral reflexes (cranial nerves V and VII) and completeness of eyelid closure. Schirmer tear test: values 6 months from onset of signs of obstipation. Perform subtotal colectomy instead. Do not perform enema immediately before surgery for megacolon. It is more difficult to control contamination of the abdomen with liquid feces during surgery.
PREVENTION Early repair of pelvic fractures that cause obstruction of pelvic canal
CLIENT EDUCATION Warn owners that diarrhea can be severe after subtotal colectomy but that it usually resolves within 8 weeks. If the cecum is removed during surgery, consider treatment for bacterial overgrowth if diarrhea persists >8 weeks.
SUGGESTED READING Byers CG, Leasure CS, Sanders NA: Feline idiopathic megacolon. Compend Contin Educ Pract Vet 28:658, 2006. Washabau RJ, Holt DE: Diseases of the large intestine. In Ettinger SJ, Feldman EC, editors: Textbook of veterinary internal medicine, ed 6, St Louis, 2005, Elsevier, pp 1378–1408. AUTHOR: LORI LUDWIG EDITOR: RICHARD WALSHAW
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Conjunctivitis, Dogs
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Conjunctivitis, Dogs BASIC INFORMATION DEFINITION Inflammation of the conjunctiva, a thin mucous membrane lining the inner surface of the upper and lower eyelids (palpebral conjunctiva) and both sides of the third eyelid. In the conjunctival fornix (“cul-de-sac”), the conjunctiva reflects onto the globe (bulbar conjunctiva) and becomes continuous with the corneal epithelium. The conjunctiva is an immunologically active structure with an abundance of immune cells, blood vessels, and lymphatics. Conjunctivitis is one of the most commonly diagnosed ocular disorders in dogs.
SYNONYMS Canine adenovirus 1: infectious canine hepatitis
EPIDEMIOLOGY SPECIES, AGE, SEX Typically no age predisposition, although allergic conjunctivitis and follicular conjunctivitis typically occur in younger dogs No sex predisposition GENETICS & BREED PREDISPOSITION Breeds predisposed to: Pannus (Chronic Superficial Keratitis), see p. 825 Plasmacellular conjunctivitis: German shepherd, collie Keratoconjunctivitis sicca, see p. 628 Abnormal eyelid conformation (e.g., Entropion/Ectropion, p. 348) Deep orbits, narrow skull conformation, and inadequate tear drainage (i.e., medial canthal pocket syndrome): dolichocephalic breeds including Afghan hound, Doberman pinscher, standard poodle Ligneous conjunctivitis (rare): Doberman pinscher RISK FACTORS Outdoor activities (e.g., hunting: allergic conjunctivitis, follicular conjunctivitis) Unvaccinated animals, dog shelters, dog shows (see Distemper, Canine, p. 317; canine adenovirus [CAV-1, CAV-2] conjunctivitis) CONTAGION & ZOONOSIS Canine distemper virus and CAV-1, CAV-2: contagious dog-to-dog ASSOCIATED CONDITIONS & DISORDERS Allergic dermatitis/skin lesions, otitis externa (allergic conjunctivitis)
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES Unilateral or bilateral: Primary: allergic, follicular, immune-mediated, bacterial, parasitic Secondary: underlying ocular and/or systemic (infectious or noninfectious) disease, environmental, neoplasia, idiopathic (e.g., ligneous conjunctivitis)
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Conjunctivitis, Dogs
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HISTORY, CHIEF COMPLAINT Painful, red eye (unilateral or bilateral) Ocular discharge PHYSICAL EXAM FINDINGS Conjunctival hyperemia Conjunctival edema (chemosis) Lymphoid follicles on conjunctiva Thick, opaque palpebral conjunctival membrane formation (ligneous conjunctivitis) Ocular discharge (see p. 777 ) Blepharospasm (squinting) Protrusion of the third eyelid
ETIOLOGY AND PATHOPHYSIOLOGY Primary: Allergic conjunctivitis Follicular conjunctivitis (chronic antigenic stimulation) Immune-mediated conjunctivitis (clinical signs together with plasmacellular infiltration on cytologic/histologic evaluation suggestive of immune-mediated condition) Bacterial conjunctivitis (Staphylococcus spp. and other gram-positive organisms uncommon; more often secondary to keratoconjunctivitis sicca or eyelid abnormalities) Parasitic conjunctivitis (Thelazia spp.) Secondary: Other ocular causes of red eye (see p. 967) including: Keratoconjunctivitis sicca (see p. 628) Mechanical ocular irritation (e.g., entropion, ectropion, trichiasis, distichiasis, ectopic cilia, eyelid mass, exophthalmos [cranial displacement of the globe], lagophthalmos [incomplete closure of the eyelids], foreign body) Corneal ulceration (see p. 250) Anterior uveitis (see p. 1151 ) Ocular trauma Glaucoma (see p. 448) Blepharitis Dacryocystitis (see p. 280) Scrolled cartilage of the third eyelid and/or prolapsed gland of the third eyelid (see p. 1089) Environmental: Irritation from dust, smoke, or chemicals Actinic-related/solar conjunctivitis in dogs lacking pigment along margin of third eyelid Systemic infectious diseases: Viral (canine distemper, CAV-1, CAV-2) Systemic mycoses (see Blastomycosis, p. 138; Coccidioidomycosis, p. 222; Cryptococcosis, p. 266; Histoplasmosis, p. 538) Leishmaniasis (see p. 643) Systemic noninfectious diseases (e.g., systemic histiocytosis, polycythemia vera) Neoplasia (e.g., lymphosarcoma, multiple myeloma, mast cell tumor, squamous cell carcinoma, melanoma) Idiopathic: Ligneous conjunctivitis Conjunctival injury and exaggerated, inflammatory immune response implicated in human form of disease May be associated with membrane formation involving the oral mucosa, upper respiratory tract, or urinary tract
DIAGNOSIS DIAGNOSTIC OVERVIEW Conjunctivitis in dogs arises most commonly as a result of other causes of red eye (i.e., secondary), including KCS, mechanical ocular irritation, and systemic disease. Determining whether the conjunctivitis is primary versus secondary in nature requires physical examination and ophthalmic examination (), and is crucial to direct the appropriate treatment.
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DIFFERENTIAL DIAGNOSIS Primary conjunctivitis must be differentiated from secondary conjunctivitis (i.e., other causes of red eye; see Etiology and Pathophysiology).
INITIAL DATABASE Complete ophthalmic examination, including: Examination of all conjunctival surfaces, including lacrimal puncta, with diffuse light and magnification Conjunctival swabs for bacterial ± fungal culture(s) and sensitivity (done before other diagnostic tests) Conjunctival scrapings for cytologic evaluation: diagnosis of bacterial or fungal infection, intracytoplasmic inclusions in conjunctival epithelial cells in distemper infection Schirmer tear test (normal is >15 mm/min) Fluorescein dye application (monitor nares for exit of dye to determine if nasolacrimal system patent) Tear film break-up time (TFBUT; mean TFBUT = 19.7 seconds; 15 mm/min but can be variable in cats) Tear film break-up time (TFBUT): 16.7 (±4.5) seconds is normal in cats; decreased in cats with conjunctivitis. Fluorescein dye application (monitor nares for exit of dye to determine if nasolacrimal system patent). Intraocular pressures (normal is 15-25 mm Hg)
ADVANCED OR CONFIRMATORY TESTING
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Conjunctivitis, Cats
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Conjunctival samples may be submitted for PCR testing for infectious diseases (FHV-1, C. felis, Mycoplasma spp., FeLV). Conjunctival samples for indirect fluorescent antibody staining (FHV-1) Flush nasolacrimal system if suspect occlusion (see online chapter: Dacryocystitis). Conjunctival biopsy and histopathology (neoplasia)
TREATMENT TREATMENT OVERVIEW The treatment of feline conjunctivitis should be directed at the underlying etiology(ies). Depending on the underlying cause(s), conjunctivitis in cats may become chronic (e.g., C. felis) and/or recurrent (e.g., FHV-1) and require prolonged therapy. Lysine may help limit recurrences in some FHV-1-infected cats (see p. 524). Therapeutic goals are to treat the underlying cause, eliminate infection if possible, and eliminate ocular pain.
ACUTE GENERAL TREATMENT Primary: FHV-1 or bacterial: Topical broad-spectrum antibiotics (e.g., tobramycin) q 6-8 h for 7-10 days (to prevent secondary bacterial conjunctivitis if FHV-1-induced) Consider oral administration of lysine (500 mg PO q 12 h: lifelong treatment) to reduce herpesviral replication in cats with frequent recurrences and/or associated herpesviral keratitis (see p.524). C. felis and/or Mycoplasma spp.: Topical tetracycline ointment, q 6-8 h; continued for 10-14 days after clinical signs have resolved Eosinophilic: Topical corticosteroids (e.g., prednisolone acetate 1% suspension or 0.1% dexamethasone solution or ointment) q 6-8 h, tapered to indefinite maintenance dose Topical cyclosporine A (CsA; 0.2%-2%) q 8-12 h as indefinite treatment Secondary—treat underlying cause: Lipogranulomatous: Surgical excision typically curative
CHRONIC TREATMENT FHV-1: see p. 524 C. felis and/or Mycoplasma spp.: Prolonged topical tetracycline if concurrent infection with FIV is confirmed Oral antibiotics (e.g., doxycycline, 5 mg/kg PO q 12 h for 3-4 weeks for difficult cases)
POSSIBLE COMPLICATIONS FHV-1 may cause: Corneal Sequestration, Cats, p. 248 Symblepharon Keratoconjunctivitis sicca,
PROGNOSIS AND OUTCOME Variable depending on cause Usually good Conjunctivitis caused by C. felis may become chronic. Recurrent conjunctivitis is observed with FHV-1 infection.
PEARLS & CONSIDERATIONS COMMENTS
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Conjunctivitis, Cats
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FHV-1 infection may not only cause conjunctivitis but may also cause keratitis in cats. Topical corticosteroids should be avoided in cats with conjunctivitis, unless eosinophilic or lipogranulomatous conjunctivitis is confirmed cytologically and/or histologically.
TECHNICIAN TIP Some ophthalmic drugs have virtually identical names for their formulations with and without corticosteroids. This similarity presents a risk of using the wrong drug. It is extremely useful for technicians to carefully read the label of the tube/vial and identify whether it contains corticosteroids prior to topical application (read label of tube/bottle), and to check the medical record for consistency. Substitution error (especially administering corticosteroids when they are contraindicated) can be devastating and has been made by veterinarians, technicians, and clients.
PREVENTION Reduction of known stresses is useful (FHV-1).
CLIENT EDUCATION Monitor for recurrent signs of conjunctivitis (FHV-1). Stress factors (e.g., concurrent systemic disease [FeLV, FIV], systemic or topical corticosteroids, general anesthesia, multicat household, moving) can trigger flare-up of FHV-1-induced conjunctivitis.
SUGGESTED READING Read RA, Lucas J: Lipogranulomatous conjunctivitis: clinical findings from 21 eyes in 13 cats. Vet Ophthalmol 4:93–98, 2001. Spiess AK, Sapienza JS, Mayordomo A: Treatment of proliferative feline eosino-philic keratitis with topical 1.5% cyclospo-rine: 35 cases. Vet Ophthalmol 12:132–137, 2009. AUTHOR: URSULA M. DIETRICH EDITOR: CHERYL L. CULLEN
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Coma
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Coma BASIC INFORMATION DEFINITION A state of unconsciousness unresponsive to all stimuli; a well-recognized neurologic emergency
EPIDEMIOLOGY RISK FACTORS Any condition that increases intracranial pressure (ICP) Older animals: neoplasia Younger animals: trauma and toxins CONTAGION & ZOONOSIS Consider rabies.
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES Obtunded: conscious state with mild to moderate reduction in alertness Stupor: unconscious state that requires strong stimuli (usually noxious; toe pinch) to evoke a response (often reduced) HISTORY, CHIEF COMPLAINT Acute onset or rapid deterioration: consider toxin, trauma, rapidly bleeding tumor, or embolism/infarction Chronic slow progression: consider tumor, metabolic disease, or encephalitis PHYSICAL EXAM FINDINGS Recumbent with no response Patient may present in shock Neurologic exam: focus on level of consciousness (response to toe pinch and loud noise), pupillary size and light reflexes, ability to elicit physiologic nystagmus, limb rigidity, and respiratory patterns to determine prognosis
ETIOLOGY AND PATHOPHYSIOLOGY There are two general causes of unconsciousness: Diffuse cerebral cortical injury Interruption of the ascending reticular activating system located in the brainstem Diffuse cortical injury generally carries a better prognosis than brainstem injury. Brainstem (midbrain, medulla) injury may be suspected based on: Deficits in pupillary light response or pupil size: midbrain (assuming exam reveals no evidence of ocular or optic nerve lesion) Inability to elicit normal physiologic nystagmus: medulla (assuming no evidence of middle/inner ear abnormality on exam) Limb rigidity: medulla (assuming no spinal cord or neuromuscular signs) Respiration abnormalities: medulla or midbrain (barring primary airway/lung lesion) Kussmaul (rapid, deep, labored breathing, associated with diabetic coma) Cheyne-Stokes (abnormal breathing pattern with alternating periods of apnea and deep, rapid breathing; the cycle begins with slow, shallow breaths that gradually increase in depth and rate and is then followed by a period of apnea).
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Coma
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DIAGNOSIS DIAGNOSTIC OVERVIEW The diagnosis should be suspected in any recumbent animal that does not show a response to initial physical examination and stimulation, and then established following a neurologic examination that confirms the patient is recumbent and unresponsive to all stimuli (including noxious stimuli).
DIFFERENTIAL DIAGNOSIS Intracranial: Trauma, tumor, hemorrhage, status epilepticus, embolism/ischemic encephalopathy, granuloma, abscess, developmental disorders (hydrocephalus, storage diseases), and infections (rabies, feline infectious peritonitis, canine distemper, fungal, parasitic) Systemic: Toxins: lead, barbiturates, antidepressants, tranquilizers, alcohol, ethylene glycol Metabolic: hypoglycemia, diabetic ketoacidosis, hepatic encephalopathy, uremic encephalopathy, hypoadrenocorticism, myxedema coma Hyperosmolar syndromes: hyperosmolar nonketotic diabetes mellitus, ethylene glycol, hypernatremia Hyperviscosity: polycythemia, hyperglobulinemia Miscellaneous: severe hypovolemia/shock, post arrest, heat stroke, hyponatremia
INITIAL DATABASE Laboratory tests: CBC (infection or thrombocytopenia) Serum biochemistry panel (metabolic disorders) Urinalysis: Glucose, ketones (diabetes mellitus/ketoacidosis) Calcium oxalate monohydrate crystals (ethylene glycol intoxication) Ammonium biurate crystals (portosystemic shunt) Low urine specific gravity (USG)/ casts (renal disease [consider other causes of low USG]) Prothrombin time/partial thromboplastin time or activated clotting time (coagulopathies) Serum bile acids (liver failure) Imaging: Thoracic radiographs (metastatic lesions, trauma, or infections) Skull radiographs (trauma/skull fractures)
ADVANCED OR CONFIRMATORY TESTING MRI or CT followed by cerebrospinal fluid analysis after systemic disease is eliminated
TREATMENT TREATMENT OVERVIEW Coma can result from a number of underlying conditions; therefore, the initial therapy should focus on stabilization of the cardiovascular (perfusion), respiratory (oxygenation and ventilation), and neurologic (cerebral oxygen delivery and ICP) systems, followed by specific therapy tailored to the underlying cause.
ACUTE GENERAL TREATMENT Airway and breathing: Endotracheal intubation assists ventilation and protects the airways (comatose patients cannot swallow; salivary secretions, regurgitation, and vomiting may cause airway obstruction and aspiration pneumonia). Avoid cough reflexes, which increase ICP. Provide supplemental oxygen (maintain Pao2 > 60 mm Hg, SaO2 > 90%). Caution: nasal oxygen lines can induce sneezing, which increases ICP. Ensure ventilation (maintain Pco2 between 35-45 mm Hg).
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Coma
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Circulation: Place intravenous catheter (avoid jugular veins if ICP elevated). Correct hypovolemia. Fluid choice is controversial. Crystalloids usually sufficient. Administer ¼ shock dose (15 mL/kg, dogs; 10 mL/kg, cats) repeatedly in rapid IV increments until cardiovascularly stable. Avoid overhydration. Provide maintenance fluids, and replace ongoing fluid losses. With cardiac disease or hyperosmolar syndromes, administer fluids cautiously. Decrease ICP: In comatose patient, assume ICP elevated until proven otherwise. Elevate head 20-30 degrees. Avoid pressure on jugular veins. Give mannitol (0.5-2 mg/kg IV over 20-30 minutes) if diagnosis is unconfirmed or patient shows neurologic deterioration. Avoid mannitol in dehydrated, hypovolemic patients and when underlying cardiac disease or hyperosmolar states are present. Supportive care: Control seizures: Diazepam (0.5-1 mg/kg IV; can repeat twice in 15 minutes. If ineffective, then use constant rate infusion or different drug); or Phenobarbital (2-15 mg/kg slow IV bolus [monitor respiration]); or Propofol (if severe hepatopathy/hepatic coma) (1-6 mg/kg IV bolus; can repeat or switch to constant rate infusion [monitor respiration]). Treat hypoglycemia with IV dextrose: Dose: 0.5 g/kg slow IV. Dilute 50% dextrose, 1 mL/kg, into 0.9% NaCl, 3 mL/kg, and administer IV slowly. Avoid hyperglycemia. Glucocorticoids (e.g., methylprednisolone sodium succinate, 30 mg/kg IV initial dose, then according to standard protocols, or dexamethasone, 0.1 mg/kg IV) may be beneficial (neoplasia) or harmful (trauma). Try to confirm diagnosis before giving glucocorticoids. If life-threatening deterioration occurs before the diagnosis is confirmed, rapid-acting intravenous glucocorticoids can be administered for suspected neoplasia or encephalitis. Specific therapy : See specific diseases.
POSSIBLE COMPLICATIONS Hypotension Hypothermia Brain herniation Cardiac arrhythmias Hypoventilation Aspiration pneumonia Seizures
RECOMMENDED MONITORING Rapid deterioration possible: monitor until stable and deterioration unlikely. Neurologic examination every 30-60 minutes Continuous electrocardiogram Blood pressure every 30-60 minutes (systolic: > 90 mm Hg but < 180 mm Hg; mean: > 60 mm Hg but < 140 mm Hg) Blood gases (PaCO2 and Pao2) every 60 minutes or capnography and pulse oximetry continuously Blood glucose and electrolytes as needed
PROGNOSIS AND OUTCOME Varies with underlying disease
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Coma
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Generally guarded until diagnosis confirmed Declines as level of consciousness decreases Worse with systemic complications Unresponsive pupils, decerebrate rigidity, abnormal respiratory patterns, and loss of physiologic nystagmus carry a grave prognosis. Miotic responsive pupils suggest cortical lesions and a better prognosis. Can use modified Glasgow Coma Scale for prognosis in dogs with head trauma (see p. 464). Failure to improve over 5-7 days warrants poor prognosis.
PEARLS & CONSIDERATIONS COMMENTS Animals that display decerebrate rigidity are also comatose. Cranial nerve reflexes (depending on location of the lesion) and spinal reflexes are often present. Bradycardia with concurrent hypertension suggests elevated ICP. Can use caloric test to evaluate nystagmus (infusion of warm or cold water into the ear canal normally results in nystagmus). Administration of lidocaine during intubation (0.75 mg/kg IV) may suppress gag and cough reflexes, which would otherwise increase ICP.
TECHNICIAN TIPS Physical therapy, turning to change recumbencies, lubrication of the eyes, and moistening the mouth every 4 hours are important elements of support for comatose patients. A urinary catheter assists with monitoring urine output and preventing urine scald.
CLIENT EDUCATION Full neurologic recovery can take weeks to months. Long-term neurologic deficits and seizures can occur.
SUGGESTED READING Kline KL: Altered states of consciousness: coma and stupor. In Ettinger SJ, Feldman EC, editors: Textbook of veterinary internal medicine, ed 7, St Louis, 2010, Saunders Elsevier, pp 225–228. AUTHOR: SΦREN R. BOYSEN EDITOR: ETIENNE CÔTÉ
24-09-2011 18:22
Color Disorders of the Skin and Haircoat
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Color Disorders of the Skin and Haircoat BASIC INFORMATION DEFINITION Very common spectrum of innate or acquired pigmentary abnormalities of the skin or hair
SYNONYMS Hyperpigmentation: melanoderma, melanotrichia Hypopigmentation: depigmentation, leukoderma, leukotrichia, poliosis
EPIDEMIOLOGY SPECIES, AGE, SEX Some conditions present at birth (e.g., albinism). Most are acquired at any age in dogs and cats. GENETICS & BREED PREDISPOSITION Hyperpigmentation: Acanthosis nigricans: dachshund Recurrent flank alopecia: boxer, English bulldog, Airedale terrier Papillomavirus-associated plaques: pug, miniature schnauzer, shar-pei Hypopigmentation: Vitiligo: rottweiler, Belgian sheepdog, Siamese cat, others Waardenburg-Klein syndrome: dalmatian, bull terrier, others Premature graying: golden retriever, Labrador retriever, Irish setter Dermatomyositis: Shetland sheepdog, collie Color dilution alopecia: blue or fawn Doberman pinschers and other dogs Canine cyclic hematopoiesis: collie (rare) Chédiak-Higashi syndrome: Persian cat (rare) RISK FACTORS Depends on underlying cause CONTAGION & ZOONOSIS Dermatophytosis and Sarcoptes scabiei (may exhibit hyperpigmentation) GEOGRAPHY AND SEASONALITY “Snow nose”: decreased nasal pigmentation during winter months Recurrent flank alopecia: often seasonal ASSOCIATED CONDITIONS& DISORDERS Postinflammatory hyperpigmentation or hypopigmentation: see Differential Diagnosis Waardenburg-Klein syndrome: blue eyes, deafness Uveodermatologic syndrome: uveitis, blindness Dermatomyositis: may exhibit myositis Chédiak-Higashi syndrome: immunologic deficiency Canine cyclic hematopoiesis: usually lethal before age 6 months
CLINICAL PRESENTATION
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Color Disorders of the Skin and Haircoat
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HISTORY, CHIEF COMPLAINT Acquired change in skin or coat color tends to be gradual. Question owners about sun exposure, changes in overall health, any evidence of inflammation (e.g., pruritus). PHYSICAL EXAM FINDINGS Note distribution of color change, and examine skin for lesions, particularly for evidence of inflammation (e.g., erythema, lichenification). Certain physical abnormalities are associated with specific pigmentation disorders (e.g., uveitis, myositis, deafness, enlarged lymph nodes).
ETIOLOGY AND PATHOPHYSIOLOGY Normal pigmentation of the skin and hair is a highly complex process under the influence of numerous genetic and acquired factors. Both depigmentation and hyperpigmentation can be seen as a result of inflammatory dermatoses.
DIAGNOSIS DIAGNOSTIC OVERVIEW Causes of color disorders of dogs and cats are myriad but often visually distinctive.
DIFFERENTIAL DIAGNOSIS Acquired hyperpigmentation: Postinflammatory: common in dogs; can occur with any chronic inflammatory process, but particularly common with hypersensitivity disorders, Malassezia, demodicosis, pyoderma. In cats, it is almost exclusively seen with dermatophytosis. Inflammation also sometimes affects hair color (melanotrichia) in dogs and in Siamese and Himalayan cats. Endocrinopathy: hyperadrenocorticism, hypothyroidism, alopecia X, sex hormone dermatoses Neoplasia: feline Bowen's disease, other pigmented tumors Acanthosis nigricans in dachshunds: localized to axillae. A reaction pattern with multiple causes (friction, infection, hypersensitivity) is more likely than a primary genetic form. Lentigenes: macular melanosis (orange cats) Other: recurrent flank alopecia, sun exposure, drug therapy–induced, papillomavirus-associated plaques Acquired hypopigmentation: Postinflammatory: common. On the nasal planum, consider discoid lupus erythematosus, as well as pemphigus erythematosus or foliaceus, uveodermatologic syndrome, other immune-mediated diseases. Pyoderma, dermatomyositis, and other inflammatory conditions also may cause depigmentation in affected areas. Neoplasia: particularly epitheliotropic lymphoma, which may cause striking leukotrichia Vitiligo: multifactorial genetic cause likely. Symmetric patchy loss of pigment from hair, skin, and mucosa, most often on the face (including nose and lips). Nasal hypopigmentation: noninflammatory conditions include “snow nose,” in which partial depigmentation of the nasal planum occurs in winter. Nutrition (e.g., reddish-brown coat in black cats due to tyrosine deficiency) Lightening of the coat can occur with excessive exposure to chlorinated water, sunlight, or in hair cycle arrest (e.g., endocrine disease). Others: drug-induced, periocular leukotrichia/depigmentation in Siamese cats Congenital hyperpigmentation or hypopigmentation: Color dilution alopecia, albinism, Waardenburg-Klein syndrome, canine cyclic hematopoiesis, Chédiak-Higashi syndrome, Dudley nose
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COLOR DISORDERS OF THE SKIN AND HAIRCOAT Depigmentation of the nasal planum and leukotrichia in a golden retriever with cutaneous lymphoma.
INITIAL DATABASE May include: Skin scrapings Skin cytologic examination Skin biopsies Trichograms (microscopic examination of plucked hairs, useful for assessing color dilution alopecia) CBC, serum biochemistry profile, urinalysis
ADVANCED OR CONFIRMATORY TESTING For specific diseases, additional testing may include: Screening tests for endocrinopathy (hyperadrenocorticism, hypothyroidism) Ocular examination (uveodermatologic syndrome) Fungal examination: Wood's light, fungal culture Muscle evaluation (dermatomyositis) Auditory evaluation (Waardenburg-Klein syndrome) Serologic testing for deep fungal infections, leishmaniasis
TREATMENT TREATMENT OVERVIEW The goal is to restore normal pigmentation to skin and hair.
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CHRONIC TREATMENT Depends on underlying cause: Many conditions do not require or respond to treatment. Inflammation, endocrinopathy, or neoplasia may be treatable. Uveodermatologic syndrome requires aggressive therapy to save vision. Reduce sun exposure in alopecic dogs.
PROGNOSIS AND OUTCOME Good prognosis for acquired hyperpigmentation, providing the underlying condition can be controlled; variable for other conditions. Improvement may be very slow for all conditions.
PEARLS & CONSIDERATIONS COMMENTS When examining a nasal planum exhibiting hypopigmentation or depigmentation, inflammatory or infiltrative processes (e.g., discoid lupus erythematosus) typically cause loss of the normal cobblestone architecture. Skin biopsies are usually indicated. Conversely, processes with little or no inflammation (e.g., vitiligo, “snow nose”) spare the normal surface pattern. The best sites to biopsy the nasal planum (or other mucocutaneous junction) exhibiting depigmentation are gray, rather than completely depigmented. These areas are most likely to show active inflammation or pigment loss. Abundant melanosomes can be seen on surface cytologic examination from hyperpigmented skin. Although these small oval structures are easy to mistake for bacteria, they are distinctly brown rather than blue/purple on a Diff-Quik preparation.
SUGGESTED READING Paradis M: Pigmentary disorders of the skin. In Morgan RV, editor: Handbook of small animal practice, ed 5, St Louis, 2006, Saunders Elsevier, pp 901–905. Schmutz S, Berryere TG: Genes affecting coat colour and pattern in domestic dogs: a review. Anim Genet 38:539–549, 2007. AUTHOR: KINGA GORTEL EDITOR: MANON PARADIS
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Collapsing Trachea
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Collapsing Trachea BASIC INFORMATION DEFINITION A common condition in small- and toy-breed dogs, characterized by a weakening of tracheal cartilage support for large airways, resulting in cough and impaired conduction of air
SYNONYMS Collapsed trachea, tracheal collapse
EPIDEMIOLOGY SPECIES, AGE, SEX Primarily a disease of middle-aged, small-breed dogs; rarely reported in large-breed dogs No known sex predilection GENETICS & BREED PREDISPOSITION Breeds commonly affected include the Yorkshire terrier, toy and miniature poodle, and Pomeranian. RISK FACTORS Obesity may exacerbate frequency and severity of signs. ASSOCIATED CONDITIONS & DISORDERS Small-breed dogs with collapsing trachea often have concurrent noninfectious chronic tracheitis and bronchitis.
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES Grades of tracheal collapse: I: minor protrusion of dorsal membrane into airway lumen, 90% reduction in airway lumen, severely flattened tracheal rings, possibly with dorsal deviation of ventral tracheal surface; generally associated with frequent, constant, or severe clinical signs HISTORY, CHIEF COMPLAINT Owners often complain of a recurrent loud, honking cough, with gagging or retching commonly observed at the end of a series of coughs. Signs may worsen with excitement, heat, eating or drinking, or exercise. Milder clinical signs may have been present since early in life. Severely affected animals may exhibit cyanosis or syncope in addition to frequent coughing. PHYSICAL EXAM FINDINGS Dry cough elicited with tracheal palpation This finding is nonspecific, however, since many other respiratory disorders, including pulmonary parenchymal disorders (e.g., pulmonary edema), may cause a cough to be elicited easily with tracheal palpation. With cervical collapsing trachea, wheezes may be ausculted over the cervical tracheal region.
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Collapsing Trachea
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With thoracic collapsing trachea, loud snapping noises may be ausculted due to the dynamic opening and collapse of large airways (sound is due to airway opening during inspiration). Increased expiratory effort may be seen.
ETIOLOGY AND PATHOPHYSIOLOGY Decreased rigidity of tracheal cartilage rings results in dynamic collapse during inspiration with cervical involvement, and during expiration with thoracic involvement. The etiology is unknown, but suggested mechanisms include: Failure of chondrogenesis Acquired secondary to chronic small airway disease Cartilage degeneration Trauma Loss of innervation of the trachealis dorsalis muscle
DIAGNOSIS DIAGNOSTIC OVERVIEW The diagnosis is suspected in at-risk breeds based on the presence of a recurrent cough and/or wheezing; confirmation requires advanced diagnostics such as radiographs, fluoroscopy, or bronchoscopy.
DIFFERENTIAL DIAGNOSIS Sterile chronic bronchitis Congestive heart failure Infectious tracheobronchitis Bronchial compression due to left atrial enlargement or lymphadenopathy Pneumonia Tracheal or laryngeal obstruction Other causes of syncope (see p. 1065)
INITIAL DATABASE Routine laboratory testing is usually unremarkable. Thoracic and lateral cervical radiographs may reveal collapse. Ideally, obtain images during inspiration for cervical collapse and expiration for thoracic collapse. Can underestimate the degree of collapse
ADVANCED OR CONFIRMATORY TESTING Fluoroscopy is usually helpful in identifying dynamic collapse, with an elicited cough. Bronchoscopy can identify severity, characterize the collapse location, and facilitate collection of airway wash samples to rule out concurrent infectious and inflammatory conditions.
TREATMENT TREATMENT OVERVIEW Treatment consists of cough suppressants, anti-inflammatory medication, bronchodilators, and in severe cases, surgically or fluoroscopically/endoscopically placed stents to help decrease the severity and frequency of cough and associated clinical signs.
ACUTE GENERAL TREATMENT Oxygen and judicious use of sedatives and cough suppressants may be necessary in an acute crisis. Butorphanol (0.02-0.1 mg/kg SQ q 4-6 h) can lessen acute severe cough and respiratory distress. Low-dose acepromazine (0.05-0.1 mg/kg IM) can provide sedation that breaks the cycle of airway irritation and coughing when a bout of extremely severe, collapsing trachea-related coughing occurs.
CHRONIC TREATMENT
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Collapsing Trachea
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Obesity leads to decreased lung expansion and increased breathing effort. Therefore, weight loss is important in any obese dog diagnosed with collapsing trachea. Antitussives help reduce irritation or damage to the tracheal epithelium from chronic cough: Hydrocodone, 0.22 mg/kg PO q 6-12 h; or Butorphanol, 0.55-1.1 mg/kg PO q 8-12 h; or Diphenoxylate hydrochloride and atropine, 0.2-0.5 mg/kg PO q 12 h Antiinflammatory therapy may be needed to decrease laryngeal or tracheal inflammation: Prednisone 0.5-1 mg/kg PO q 12-24 h tapered and discontinued after 5-7 days of use Only short-term use is recommended. Bronchodilators may benefit dogs with intrathoracic collapse or expiratory effort that do not improve with initial therapy: β2 Agonists Terbutaline (total amount per dose): small dogs, 0.625-1.25 mg PO q 12 h; medium dogs, 1.25-2.5 mg PO q 12 h; large dogs, 2.5-5 mg PO q 12 h; or Albuterol: 0.05 mg/kg PO q 8 h Methylxanthines Not all long-acting theophylline products are equivalent in bioavailability in dogs. Implications are that failure to respond to a certain product should prompt the consideration of switching bronchodilators (to a different brand 2
of theophylline or a different class of bronchodilator altogether [e.g., a agonist]), and that certain animals may develop signs of toxicosis when receiving doses that are well tolerated by others. Extended-release theophylline is recommended at 10 mg/kg PO q 12 h; or Aminophylline or theophylline, 10 mg/kg PO q 8 h Surgical implantation of external prosthetic rings can be considered inpatients with grade II-IV collapse that fail medical management. Rings are more practical for cervical collapse but can be attempted for thoracic collapse through cranial retraction of the trachea. Several potential drawbacks exist, including implant failure and extension of the collapsing process beyond the length of the implant over time. Intraluminal stents placed under fluoroscopic guidance can be considered in patients that fail medical management. Such stents can be used for cervical or thoracic collapse. Stents are typically placed with endoscopic or fluoroscopic guidance (see p. 1342 ).
POSSIBLE COMPLICATIONS Cough suppressants: somnolence, sluggishness at higher doses Stents: stent migration, stent fracture, exuberant granulation tissue, tracheitis
RECOMMENDED MONITORING Clinical signs
PROGNOSIS AND OUTCOME The prognosis for survival is good. With appropriate treatment, most dogs show improvement but varying degrees of persistent clinical signs. The prognosis for cure is poor because collapsing trachea is irreversible and progressive. Dogs with severe clinical signs (cyanosis, syncope) have a guarded prognosis for comfortable survival if not effectively treated with medical therapy. Prognosis for these dogs is often improved with stents.
PEARLS & CONSIDERATIONS COMMENTS Hydrocodone cough suppressants may be more difficult to obtain. Of those available, many are combined with other medications (acetaminophen, guaifenesin, and various antihistamines) that may not be safe or routinely recommended. By reducing bronchial smooth-muscle contraction during cough (lessens dynamic component of cough) and slowing the velocity of air flow during coughing (by increasing bronchial diameter), bronchodilators may help patients with collapsing trachea even though the drugs do not act directly at the site of the lesion.
PREVENTION Affected dogs should probably not be bred.
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Collapsing Trachea
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TECHNICIAN TIPS When performing radiographs to evaluate for collapsing trachea, taking inspiratory films of the neck and expiratory films of the chest may help better demonstrate a dynamic collapse.
CLIENT EDUCATION For most dogs, the tracheal collapse is managed with weight control, antitussives, and periodic administration of anti-inflammatory drugs.
SUGGESTED READING Herrtage M: Medical management of tracheal collapse. In Bonagura JD, Twedt DC, editors: Kirk’s current veterinary therapy XIV. St Louis, 2009, Saunders, p 630. Johnson L: Tracheal collapse. Vet Clin North Am Small Anim Pract 30:1253–1266, 2000. Sura PA, Krahwinkel DJ: Self-expanding niti-nol stents for the treatment of tracheal collapse in dogs: 12 cases (2001-2004). J Am Vet Med Assoc 232:2, 2008. AUTHOR: LAURA RIDGE COUSINS EDITOR: RANCE K. SELLON
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Collapse
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Collapse BASIC INFORMATION DEFINITION Loss of the ability to support weight and ambulate without assistance; may include the loss of consciousness
EPIDEMIOLOGY SPECIES, AGE, SEX Dogs, cats Age and sex depend on underlying disease. GENETICS & BREED PREDISPOSITION Exercise-induced collapse in Labrador retrievers; intervertebral disk extrusion in chondrodystrophic breeds RISK FACTORS Increased ambient temperature, obesity CONTAGION & ZOONOSIS Common-source infections: Agents causing polyarthritis, such as Borrelia burgdorferi Agents affecting the neuromuscular junction, such as Clostridium botulinum GEOGRAPHY AND SEASONALITY Areas with a high incidence of infectious agents that can cause collapse RISK FACTORS Diabetes mellitus, cardiomyopathies, hypoadrenocorticism, immune-mediated hemolytic anemia, hemangiosarcoma, cervical vertebral instability (wobbler's syndrome)
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES Neuromuscular: paresis/paralysis but mentation normal Neurologic: alterations in intracranial (mentation, cranial nerves) and/or spinal (reflexes, reactions) function, without an underlying systemic cause Orthopedic: signs of joint or bone pain, reduced range of motion, or fracture Metabolic/endocrine: characteristic systemic signs Cardiovascular: characteristic signs of heart disease and/or vascular disturbances Respiratory: overt respiratory signs (usually dyspnea) in the absence of systemic, neuromuscular, or cardiovascular causes HISTORY, CHIEF COMPLAINT Dependent on underlying cause. Often includes one or more of the following: weakness, inability to rise, incontinence (urine or feces), anxiety/distress, abdominal distension, vomiting, diarrhea, respiratory distress, unconsciousness. PHYSICAL EXAM FINDINGS Dependent on underlying cause:
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Collapse
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Nonspecific signs commonly include recumbency, alterations in mentation (disorientation, unconsciousness), vomiting, variable heart rate (normal, bradycardic or tachycardic), variable pulse quality (absent, weak to hyperdynamic), and pale to hyperemic mucous membranes. Some underlying causes may be more likely in the presence of certain physical findings: Asynchronous pulse quality (cardiac arrhythmias), muffled heart sounds (pericardial effusion/cardiac tamponade, pleural effusion if muffled lung sounds also), stertorous upper airway noises (upper airway obstruction), abdominal fluid wave (hemoabdomen, right-sided congestive heart failure, or pyoabdomen/sepsis), moist lung sounds (respiratory, cardiovascular, or pulmonary hemorrhage), flaccid to fasciculating muscles (neuromuscular), decreased to increased spinal reflexes (neuromuscular or neurologic), neck or back pain (orthopedic, neurologic), joint effusion (orthopedic).
ETIOLOGY AND PATHOPHYSIOLOGY Collapse is caused by loss of normal, coordinated function of muscles that support the body. Neuromuscular: reduced nerve conduction, disturbance of neuromuscular junction, or primary myopathy (rare) Neurologic: intracranial or spinal failure to generate or communicate impulses for normal mentation and/or limb function Orthopedic: failure of the skeleton and/or joints to support weight Metabolic/endocrine: limitation of metabolic fuel for muscles, nerves, or central nervous system (e.g., hypoglycemia, hypocalcemia, hypokalemia) Cardiovascular: inadequate perfusion of muscles and/or central nervous system Respiratory: inadequate oxygenation of blood and therefore of tissues
DIAGNOSIS DIAGNOSTIC OVERVIEW The majority of conditions causing collapse can be identified with a good history, physical examination (including checking stool for toxins), and complete but basic diagnostic tests such as blood work and thoracic and abdominal radiographs.
DIFFERENTIAL DIAGNOSIS Neuromuscular/Musculoskeletal: myasthenia gravis, polyradiculoneuritis, tick paralysis, botulism, polyarthritis, toxins (metaldehyde, strychnine, marijuana) Neurologic: intervertebral disk extrusion, fibrocartilaginous emboli, spinal fracture, spinal tumor, meningitis, intracranial neoplasia, narcolepsy (rare) Metabolic/endocrine: anemia, shock (hemorrhagic, anaphylactic), sepsis, insulin overdose, insulinoma, eclampsia, hypoparathyroidism, renal disease, hepatic dysfunction, hypoadrenocorticism, heat stroke, toxins that affect oxygen binding to hemoglobin such as carbon monoxide and acetaminophen toxicity, additional toxins such as xylitol, paintball ingestion Cardiovascular: arrhythmias, arterial thromboembolism, cardiac tamponade Respiratory: pneumonia, laryngeal paralysis, brachycephalic upper airway syndrome, laryngeal masses, pharyngeal swelling/foreign body, tracheal collapse, tracheal foreign body, nasopharyngeal polyp
INITIAL DATABASE CBC, biochemical profile, electrolytes Electrocardiogram, blood pressure (multiple limbs if thromboembolism suspected) Thoracic and abdominal radiographs Remove any ectoparasites (ticks) Results variable depending on underlying cause
ADVANCED OR CONFIRMATORY TESTING As dictated by history, physical findings, and initial test results: Arterial blood gas, saline agglutination testing, tickborne disease titers, arthrocentesis, adrenocorticotropic hormone stimulation, abdominal ultrasound, echocardiography, MRI or myelogram, cerebrospinal fluid analysis, pharyngeal examination, laryngeal function assessment, abdomino/thoraco/pericardiocentesis, acetylcholine receptor antibody titers, Holter monitor/event recorder, insulin/glucose ratio, parathormone and ionized calcium, edrophonium (Tensilon) response test.
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TREATMENT TREATMENT OVERVIEW Correct acute/life-threatening disturbances (severe biochemical or electrolyte abnormalities, severe anemia, hypotension, body temperature abnormalities). Address underlying problem.
ACUTE GENERAL TREATMENT Intravenous fluids, oxygen supplementation, and/or intubation if needed, blood transfusion, dextrose supplementation (hypoglycemia), electrolyte supplementation, insulin (combined with dextrose) for hyperkalemia, analgesia/sedation if indicated Antibiotics, antiinflammatories, diuretics, and antiarrhythmic medications may be indicated depending on underlying problem. Dexamethasone (0.2-1 mg/kg IV) may be given if a hypoadrenocortical crisis is suspected; it will not interfere with diagnostic testing.
CHRONIC TREATMENT Dependent on underlying disease process
NUTRITION/DIET Hypoglycemic patients benefit from nutritional support in the form of frequent meals, hand feeding, or feeding tube placement (see p. 1270 )
POSSIBLE COMPLICATIONS Edrophonium can cause acute cholinergic crisis.
RECOMMENDED MONITORING Blood glucose, electrolytes, ECG, blood pressure
PROGNOSIS AND OUTCOME In general, prognosis is guarded but varies from good to poor depending on underlying disease process.
PEARLS & CONSIDERATIONS COMMENTS Many of the pathologic processes that cause collapse are not common, and establishing the diagnosis can be difficult. Common diseases, such as hemoabdomen secondary to mass rupture and intervertebral disk disease, should be considered first, and the diagnostic evaluation can proceed to less common etiologies afterwards. Two diseases leading to collapse that are commonly overlooked in general practice are pericardial effusion and hypoadrenocorticism.
TECHNICIAN TIP A good history is essential for identifying (or ruling out) important possible causes of collapse. Useful points to discuss with owners include travel history, exposure to medications/sugar free products/other potential toxins, inquiring whether the individual animal is curious by nature and prone to chewing or ingesting foreign material, and encouraging owners to investigate the animal's home environment looking for toxins.
SUGGESTED READING Rudloff E, Kirby R: Fluid resuscitation and the trauma patient. Vet Clin North Am Small Anim Pract 38(3):645–652, 2008. Platt SR, Garosi LS: Neuromuscular weakness and collapse. Vet Clin North Am Small Anim Pract 34(6):1281–1230, 2004.
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AUTHOR: ADAM J. REISS EDITOR: ETIENNE CÔTÉ
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Colitis, Chronic
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Colitis, Chronic BASIC INFORMATION DEFINITION A common cause for persistent (>3 weeks’ duration) signs of colonic inflammation, characterized by large-bowel diarrhea with tenesmus/dyschezia, urgency, and increased frequency of defecation. Feces often contain mucus and/or fresh blood. Systemic signs attributable to nutrient malabsorption (e.g., anorexia, weight loss) are uncommon.
EPIDEMIOLOGY SPECIES, AGE, SEX More common in middle-aged and older dogs and cats as a consequence of infiltrative mucosal disorders (e.g., inflammatory bowel disease [IBD] and neoplasia). Infectious disorders (e.g., Trichuris vulpis, gastrointestinal [GI] histoplasmosis, Tritrichomonas foetus) may be seen in younger dogs and cats (less common). GENETICS & BREED PREDISPOSITION Boxers are predisposed to histiocytic ulcerative colitis (HUC). German shepherds and purebred cats are at increased risk for lymphocytic-plasmacytic IBD. CONTAGION & ZOONOSIS Some bacterial enteropathogens (e.g., Clostridium perfringens, potentially contagious) may cause chronic colitis if not detected early. Also, some helminth parasites (Trichuris spp., potentially contagious) and protozoa (Giardia spp., potentially zoonotic; Tritrichomonas spp., potentially contagious and zoonotic) may cause persistent signs of colitis in pets. GEOGRAPHY AND SEASONALITY Midwestern United States for GI histoplasmosis ASSOCIATED CONDITIONS & DISORDERS Colonic motility disorders (e.g., irritable bowel syndrome in dogs and colonic constipation/obstipation in cats) may mimic mucosal inflammation and cause signs of large-bowel diarrhea with tenesmus. Note that these diseases are due to functional defects in colonic motility and have no mucosal/structural disease.
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES Dietary responsive disorders: includes both food intolerance (nonimmunologically mediated) and dietary sensitivity (immunologically-mediated; see p. 402 ). Food-responsive causes for GI signs, including large-bowel diarrhea, are common in both dogs and cats. Infectious disorders: includes select nematode/protozoal parasites, bacteria, and fungal organisms (especially GI histoplasmosis). Tritrichomonas foetus is being recognized with increased frequency as a cause for chronic intermittent colitis in young cats. Infiltrative mucosal diseases: includes fungal, benign (e.g., IBD), and malignant (e.g., mucosal neoplasia) diseases HISTORY, CHIEF COMPLAINT Persistent large-bowel diarrhea, which is characterized by tenesmus (straining to defecate), increased frequency of defecation, mucoid feces, and fresh (red) blood. Note that some disorders (e.g., IBD, GI histoplasmosis, GI lymphoma) may affect the small intestines as well, causing mixed large/small-bowel signs. PHYSICAL EXAM FINDINGS
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The animal is often well fleshed without systemic signs (e.g., unthriftiness, weight loss) of illness. Fungal disease, severe IBD, and neoplasia may selectively cause fever, alterations in appetite, and peripheral/mesenteric lymphadenopathy. Rectal examination: evaluate the character of the feces, obtain fecal samples for parasitic examination, procure exfoliative cytologic specimens, and evaluate the rectum for possible mass lesions.
ETIOLOGY AND PATHOPHYSIOLOGY Large-bowel diarrhea is characterized by increased amounts of mucus, owing to the large numbers of mucus-secreting goblet cells in the colon. Hematochezia indicates severe mucosal disruption of the distal colon and rectum. Parasites, both helminth and protozoa: Trichuris vulpis (dogs), Tritrichomonas foetus (cats), Giardia lamblia (dogs, cats) Dietary causes: incriminating antigens or dietary ingredients (nonimmunologic) Specific bacterial pathogens: cause colonic inflammation via invasion or enterotoxin production. Adherent/invasive E. coli is a newly recognized bacterial enteropathogen associated with HUC in boxers. Infiltrative mucosal disorders: benign, malignant, or infectious (e.g., fungal)
DIAGNOSIS DIAGNOSTIC OVERVIEW Diagnosis of many causes for chronic colitis will require histologic evaluation of mucosal biopsy specimens.
DIFFERENTIAL DIAGNOSIS Specific causes: see Etiology and Pathophysiology above. Occasionally patients with rectal diseases (e.g., perineal hernia, perineal fistula, diverticula, or rectal polyps or masses) will present with signs of large-bowel disease. These are generally distinguished by digital examination and careful inspection; normal pelvic and rectal structure on examination more strongly suggests large-bowel disease in such cases.
INITIAL DATABASE Physical examination: perform abdominal palpation and digital examination, with collection of feces. Fecal examination for nematode and protozoal parasites. Both fecal flotations and fecal smears should be performed. Note that multiple (three) zinc sulfate flotation tests using fresh feces may be required for identification of Giardia spp. trophozoites. Commercial ELISA kits are also sensitive for the detection of Giardia antigen. Rectal cytology may indicate evidence of bacterial pathogens (e.g., vegetative spores of Clostridia or increased numbers of fecal leukocytes indicative of acute mucosal inflammation). Exfoliative cytology (e.g., rectal scrape using a uterine curette or a curette of the same type used for bone graft harvesting) is also a useful tool for confirming the presence of Histoplasma organisms contained within colonic macrophages. PCR for detection of Tritrichomonas foetus infection Abdominal imaging (survey radiographs, pneumocolonography, and/or ultrasonography) may identify fecal impaction, mass lesions, or evidence of significant mesenteric lymphadenopathy. Generally, ultrasonography is a poor screening tool for colonic disease, owing to the obstructive effect of air in the colonic lumen on the ultrasound beam, and because intestinal wall thickness is difficult to standardize.
ADVANCED OR CONFIRMATORY TESTING Colonoscopy with procurement of multiple mucosal biopsy specimens is required to diagnose most infiltrative diseases. Exfoliative cytology at the time of GI endoscopy is a useful adjunct to mucosal biopsy. Proctoscopy can also be used to examine and obtain biopsy specimens of the distal colon and rectum when the disease is confined to distal aspects or when colonoscopy is unavailable. Colonic biopsies should not be obtained routinely by laparotomy, since the bacterial content of the colon and attendant risk of bacterial peritonitis after biopsy of a diseased colon is markedly greater than in the small intestine.
TREATMENT TREATMENT OVERVIEW Treatment of chronic colitis is based on the specific definitive diagnosis, because empirical therapies are often inadequate or deleterious (e.g., use of corticosteroids in animals with GI histoplasmosis).
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CHRONIC TREATMENT Treat for suspect nematode and protozoan parasites (even if fecal exams are negative for parasites) using appropriate broadspectrum anthelmintics or antiprotozoal (fenbendazole, 50 mg/kg PO q 24 h for 3-5 days) medications. Confirm efficacy of therapy with repeat follow-up fecal examinations. Feed a hypoallergenic diet to animals with dietary-responsive disorders and IBD. Reduction in the quantity of dietary antigens will assist in reducing mucosal inflammation with these disorders. Other animals with colitis but not requiring a specific antigen-restricted diet will benefit from being fed a low-fat, fiber-enriched, and highly digestible commercial ration. Choose diets (or supplement the diet) with increased n-3: n-6 fatty acids to reduce mucosal inflammation. Avoid all treats and supplements containing protein or flavors during the dietary trial period. Use diets with added soluble or mixed fiber or add small to moderate amounts of soluble fiber to the diet to reduce tenesmus and facilitate colonic epithelial repair. Only use antibiotics in animals with confirmed bacterial causes (e.g., colonization with enteropathogenic bacteria) for their signs. Antimicrobials used in this fashion are best chosen based on susceptibility testing to the incriminating pathogen. Exceptions to this caveat are animals with HUC (which may respond to oral fluoroquinolone therapy, enrofloxacin 10 mg/kg PO q 24 h) and lymphocytic-plasmacytic colitis (IBD), which may respond to metronidazole (10 mg/kg PO q 12 h, used as an immunomodulator) alone or in combination with other immunosuppressive drugs. Sulfasalazine (20-30 mg/kg PO q 8 h, typically for 3-6 weeks in dogs) or newer mesalamine drugs, and glucocorticoids (e.g., prednisone or prednisolone, 1 mg/kg PO q 12 h for dogs; 1-2 mg/kg PO q 12 h for cats) are first-choice immunosuppressive drugs for therapy of colonic IBD. Drugs effective against GI histoplasmosis: see p. 538 Treatment for colonic neoplasia: see p. 37
NUTRITION/DIET Appropriate dietary management may include elimination, fiber-supplemented, or low-residue diets. The remission of signs due to food-responsive causes for chronic colitis will require feeding an elimination (intact protein or hydrolysate) diet. Fiber supplementation is an important component of therapy because these dietary additives bind colonic irritants, normalize dysmotility, and promote colonic epithelial repair and renewal.
POSSIBLE COMPLICATIONS Cure is not possible with colonic IBD, but the prognosis for control of signs is good with effective therapy. Animals treated with amphotericin B for GI histoplasmosis are at risk for drug-induced renal disease. Myelosuppression may occur with use of multidrug chemotherapy for malignant colonic neoplasia.
RECOMMENDED MONITORING Ideally, animals responsive to elimination diets (e.g., those having dietary responsive causes for chronic colitis) should be returned to their normal (incriminating) diet to see if large-bowel signs recrudesce. This is impractical in most instances.
PROGNOSIS AND OUTCOME The prognosis varies according to the underlying cause, from good (dietary-responsive disorders when the inciting dietary constituent is removed) to poor (metastatic colonic neoplasia).
PEARLS & CONSIDERATIONS COMMENTS Major causes of chronic colitis include dietary, infectious, and infiltrative disorders. Most animals with chronic signs of large intestinal disease will require a thorough diagnostic evaluation to rule out the varied causes for colonic inflammation. Prophylactic deworming and dietary trials with an elimination diet and/or soluble fiber supplementation are easy and cost-effective empirical therapies to offer clients prior to more extensive diagnostic testing. Colonoscopy with mucosal biopsy is imperative for diagnosis of most forms of chronic colitis that fail rational empirical therapies.
PREVENTION Prophylactic deworming
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Avoid dietary indiscretion. Perform dietary trials.
CLIENT EDUCATION Dietary modification to a diet suitable for colonic disease may be required for the life of the pet.
SUGGESTED READING Washabau RJ, et al: Diseases of the large intestines. In Ettinger SJ, Feldman EC, editors: Textbook of veterinary internal medicine, ed 6, Philadelphia, 2005, WB Saunders, pp 1378–1408. AUTHOR: ALBERT E. JERGENS EDITOR: DEBRA L. ZORAN
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Colitis, Acute
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Colitis, Acute BASIC INFORMATION DEFINITION A common disorder characterized by sudden onset (7 years) with chronic liver disease. Middle-aged cats with chronic cholangiohepatitis may suffer from biliary cirrhosis. Copper storage hepatopathy (∼1-5 years) and idiopathic fibrosis are seen in younger dogs (160-180 mm Hg, diastolic BP >95 mm Hg) present in 20% of cats with CKD; may cause end-organ damage (especially heart, eyes, central nervous system, kidneys) Abdominal imaging: abdominal radiography or ultrasonography may further elucidate cause of CKD (i.e., obstructing or partially obstructing nephroliths or ureteroliths, renal neoplasia, cystic disease, perinephric pseudocysts). Alterations of shape, size, and echogenicity of kidneys are common.
ADVANCED OR CONFIRMATORY TESTING Urine protein/creatinine ratio. In dogs and cats with CKD, pathologic proteinuria (urine protein/creatinine [UPC] ratio >0.5 in dogs, >0.4 in cats; urinary sediment is inactive, and culture is negative) may indicate potential benefit from angiotensinconverting enzyme inhibition. Glomerular filtration rate (GFR) measurement: rarely measured when azotemia is present. Renal biopsy: indicated primarily with renomegaly (rule out lymphoma, feline infectious peritonitis, amyloidosis)
TREATMENT TREATMENT OVERVIEW The goals of treatment are to alleviate uremic signs and delay progression of kidney disease.
ACUTE GENERAL TREATMENT Compensated state: see Chronic Treatment below. Decompensated state (e.g., dehydrated, anorexic, vomiting): Hospitalization is ideal, since oral therapies often are poorly tolerated Rehydration over 24-36 hours usually appropriate Intravenous crystalloid fluid therapy (e.g., lactated Ringer's solution, Plasmalyte, 0.9% saline). Fluid rate: maintenance (66 mL/kg/d) plus replacement of dehydration (percent dehydration [as a decimal, e.g., 10% = 0.1] × kg body weight = liters deficit) plus ongoing losses (estimated volume of polyuria, vomiting). Maintenance: Maintenance rate plus 5%-6% body weight per 24 hours to promote diuresis Practically, twice the calculated maintenance rate is sufficient for most after rehydration. Potassium supplementation of fluids based on electrolyte measurement (not to exceed 0.5 mEq/kg/h; see p. 577 ). Other treatments described for chronic therapy may be applicable (e.g., H2 blockers, antiemetics; see Chronic Treatment below), but injectable forms are used until oral medications are tolerated.
CHRONIC TREATMENT Delay of progression: see p. 205 Additional therapies may be used, depending on presence of particular uremic signs. Anorexia or vomiting: decrease gastric acidity. Histamine blockers (famotidine, 0.5 mg/kg IV, SQ, PO q 24 h; ranitidine, 0.5-2.5 mg/kg SQ, PO q 24 h [avoid rapid IV administration, which may cause nausea] q 12-24 h); or proton pump inhibitors (e.g., omeprazole, 0.7 mg/kg PO q 24 h). Persistent vomiting: antiemetics (maropitant, 2 mg/kg PO q 24 h for 5 days approved for dogs only [often used off label for cats]; or metoclopramide, 0.2-0.4 mg/kg SQ q 6 h or 0.01-0.02 mg/kg/h as constant rate infusion; phenothiazines). 5HT serotonin antagonists for intractable vomiting (ondansetron, 0.22 mg/kg IV q 8-12 h, or dolasetron). GI ulceration (e.g., hematemesis, melena, anemia, elevated blood urea nitrogen/creatinine ratio): sucralfate, 0.25-1 g PO q 8 h until signs resolve. Hyperphosphatemia: diet ± medications.
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Phosphate binders to prevent absorption of phosphorus from ingested food Aluminum hydroxide or aluminum carbonate, 30-90 mg/kg/d, divided and administered with meals; dose titrated based on serum phosphorus concentration). Calcium acetate, 60-90 mg/kg/d; hypercalcemia possible side effect Chitosan (Epakitin) 1 gram/5 kg twice daily with food Lanthanum carbonate is a newer phosphate binder that is occasionally used in veterinary medicine (100 mg/kg/d PO). Hypokalemia (more likely in cats than dogs): potassium gluconate (2 mEq per 4.5 kg per day) or potassium citrate (75 mg/kg PO q 12 h). Acidosis (more likely in cats than dogs): consider treatment if total CO2 < 16 mEq/L or pH < 7.2. Potassium citrate, 75 mg/kg PO q 12 h (also addresses hypokalemia), sodium bicarbonate, 10 mg/kg PO q 12 h. Anemia: transfusion based on clinical need. Darbepoetin (Aranesp 0.45-1 mcg/kg SQ q 7 days until hematocrit rises; then q 14-21 days to maintain low-normal hematocrit) plus iron supplementation can be used for stimulating red blood cell production. Risk of pure red cell aplasia from cross-reactive antibodies appears lower with darbepoetin, compared to human recombinant erythropoietin (Epogen, Procrit). Hypertension: calcium channel blockers recommended. If proteinuria is present or calcium channel blocker is insufficient, add ACE inhibitor (see p. 1068 ). Chronic dehydration or persistent signs of uremia: subcutaneous fluid administration. Dose is empirical, based on subjective assessment of the patient's well-being, hydration status, and presence of other disorders (e.g., heart disease). Typically for cats without heart problems, 100 to 150 mL daily to every other day. Renal secondary hyperparathyroidism (see p. 976) Renal transplantation may be appropriate for some animals/owners. Maybe preceded by hemodialysis (see p.1286). Greatest chance of success in mildly to moderately azotemic cats without concurrent illness or infection.
NUTRITION/DIET Appropriate high-quality restricted protein and restricted phosphorus diets (“renal diet”) slow progression and decrease clinical uremia. Acceptance of diet changes can be problematic, particularly in severely affected patients. Maintaining adequate caloric intake to avoid weight loss takes precedence over nutrient composition of the diet (see p. 1377 ). Renal diets should be introduced when uremia (illness) is minimized. Nutritional support occasionally requires appetite stimulation (cats: cyproheptadine, 1 to 2 mg PO q 12 h; mirtazapine, 3.75 mg PO q 72-96 h) or tube feeding.
DRUG INTERACTIONS Phosphate binders can interfere with absorption of orally administered medications, especially antibiotics. Sucralfate works best in an acid environment and should be given at least 30 minutes before antacid therapy. Nephrotoxic drugs (e.g., aminoglycosides) or drug combinations (e.g., NSAIDs plus ACE inhibitors) should be avoided whenever possible. Drugs which undergo renal elimination may need adjustment in dose strength or frequency in animals with CKD.
POSSIBLE COMPLICATIONS Anorexia, vomiting, GI ulceration, hyperphosphatemia, hypokalemia, acidosis, anemia, and hypertension are common sequelae of CKD. Volume overload (pleural effusion, pulmonary edema, dyspnea, or peripheral fluid accumulation) is a concern at high rates of fluid administration, particularly in anemic animals or those with concurrent heart disease. Platelet dysfunction in CKD increases risks of bleeding (gingival, GI, bruising, bleeding after invasive procedures).
RECOMMENDED MONITORING Routine recheck, including physical exam, weight, chemistry panel, CBC, or packed cell volume. Frequency depends on disease severity. Stage I-II: recheck every 6 months. Stage III: recheck every 2-3 months. Stage IV: recheck monthly. Urinalysis and urine culture should be performed at least twice a year. Blood pressure measurement should be performed at least every 3 months, or 1-week after antihypertensive drug dose adjustments. Changes in clinical signs warrant recheck as well.
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PROGNOSIS AND OUTCOME Longevity is difficult to predict in an individual patient, with a range of days to years. Median survival times are 2 years in cats with stage III CKD and 1 month in cats with stage IV CKD.
PEARLS & CONSIDERATIONS COMMENTS At an early stage of decompensation, renal transplant can be considered for otherwise healthy cats. Renal biopsy is rarely informative in cats with chronic kidney disease and small kidneys (the inciting cause is rarely identified). Urine culture and sensitivity in patients with CKD is essential at the time of diagnosis and periodically thereafter. UTIs commonly occur without an active urine sediment on urinalysis in CKD patients. Correction of the UTI may improve renal function if subclinical pyelonephritis is present; few other complicating factors can be treated so easily and effectively.
TECHNICIAN TIPS Technicians can be invaluable in teaching owners how to administer subcutaneous fluids. They can also help emphasize the importance of allowing the animal a constant source of fresh water.
CLIENT EDUCATION CKD is in incurable condition in which treatments are aimed primarily at improving the quality of life. Renal transplantation is expensive and limited in availability. With successful renal transplant, intensive lifelong medication and frequent rechecks are required, but quality of life can be excellent.
SUGGESTED READING Boyd LM, et al: Survival in cats with naturally occurring chronic kidney disease (2000-2002). J Vet Intern Med 22:1111, 2008. Brown SA: Evaluation of chronic renal disease: a staged approach. Compend Contin Educ Pract Vet 21:752, 1999. Elliott J, Barber PJ: Feline chronic renal failure: clinical findings in 80 cases diagnosed between 1992 and 1995. J Small Anim Pract 39:78, 1998. King JN, et al: Prognostic factors in cats with chronic kidney disease. J Vet Intern Med 21:906, 2007. Lulich JP, Osborne CA, O’Brien TD, Polzin DJ: Feline renal failure: questions, answers, questions. Compend Contin Educ Pract Vet 14:127, 1992. Roudebush P, et al: Therapies for feline chronic kidney disease. What is the evidence? J Feline Med Surg 11:195, 2009. Wehner A, et al: Associations between protein-uria, systemic hypertension and glomerular filtration rate in dogs with renal and non-renal diseases. Vet Rec 162:141, 2008. AUTHOR: CATHY LANGSTON EDITOR: LEAH A. COHN
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Chronic Kidney Disease, Occult (“Asymptomatic”) BASIC INFORMATION DEFINITION Chronic kidney disease (CKD): kidney damage present for over 3 months. Azotemia and/or inadequately concentrated urine (specific gravity < 1.035 in cats; < 1.030 in dogs) is not necessary for CKD to be present. IRIS Staging System for CKD: classification scheme for CKD in dogs and cats is based on serum creatinine, with substages for proteinuria and blood pressure. Developed by International Renal Interest Society: Stage I: creatinine < 1.4 mg/dL, dogs; < 1.6 mg/dL, cats. Nonazotemic. Some other renal abnormality present (e.g., inadequate concentrating ability without identifiable nonrenal cause; abnormal renal palpation and/or abnormal renal imaging findings; proteinuria of renal origin; abnormal renal biopsy results). Stage II: creatinine 1.4-2 mg/dL, dogs; 1.6-2.8 mg/dL, cats. Mild renal azotemia (lower end of the range lies within the reference range for many labs, but the insensitivity of creatinine as a screening test means that animals with creatinine values close to the upper end of the reference range often have excretory failure). Clinical signs usually absent. Stage III: creatinine 2.1-5 mg/dL, dogs; 2.9-5 mg/dL, cats. Moderate renal azotemia. Systemic clinical signs usually present. Stage IV: creatinine > 5 mg/dL dogs and cats. Severe renal azotemia. Many extrarenal clinical signs present. Occult CKD: CKD in which no clinical signs are present. This generally corresponds to IRIS stage I or II. CKD is one of the most common diseases of older cats and is very common in dogs For information on CKD causing overt clinical signs, see p. 207.
SYNONYMS Latent CKD, preclinical CKD, asymptomatic CKD, compensated CKD, incidentally discovered CKD, stage I or II CKD, chronic renal failure (CRF; this term is no longer preferred for use)
EPIDEMIOLOGY SPECIES, AGE, SEX More common in cats than dogs Any age, but more common in older animals GENETICS & BREED PREDISPOSITION Familial nephropathies are reported in a number of dog and cat breeds (see p. 207). These nephropathies may lead to an early onset of renal failure. RISK FACTORS Advanced age, prior episode of acute renal failure, prior nephrotoxic exposure, pyelonephritis, nephrolith/ureterolith.
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT Incidental CKD is usually detected via routine geriatric or preanesthetic screening, or during investigation of unrelated illness. PHYSICAL EXAM FINDINGS Frequently no abnormal physical exam findings. The patient may have small or irregular kidneys.
ETIOLOGY AND PATHOPHYSIOLOGY CKD can be the end result of a variety of insults to the kidney, which may start as tubular, glomerular, or interstitial, because each nephron works as a unit. If the glomerulus is irreversibly damaged, the associated tubule will degenerate, and vice
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versa. As nephrons are lost, the remaining nephrons hypertrophy. Although initially adaptive, glomerular hypertension damages the nephron, leading to further nephron loss. After a certain amount of damage has been sustained (generally when creatinine > 3.5 mg/dL), kidney disease may be progressive despite resolution of initiating cause. The specific etiology of CKD is frequently undetermined: Tubulointerstitial nephritis most common cause (70% of cats, 60% of dogs) Glomerulonephritis also a common cause (30% of dogs, 15% of cats) Other demonstrable causes: amyloidosis, renal dysplasia, polycystic kidney disease, tubulonephrosis, lymphoma, chronic pyelonephritis, nephroliths or ureteroliths resulting in partial obstruction, vasculitis, infarction, and sequelae to acute renal failure with incomplete resolution Obstructive nephropathy from previous or current ureterolithiasis is increasingly recognized in cats.
DIAGNOSIS DIAGNOSTIC OVERVIEW CKD may be diagnosed based on structural (e.g., renal size/shape changes, polycystic disease) or functional (e.g., proteinuria, azotemia, inadequately concentrated urine) abnormalities.
DIFFERENTIAL DIAGNOSIS Azotemia: Prerenal azotemia (e.g., dehydration, high-protein diet, gastrointestinal bleeding), typically characterized by concentrated urine specific gravity Azotemia with inadequately concentrated urine may be due either to kidney disease or to dehydration (i.e., prerenal azotemia) combined with extrarenal impairment of urine concentration: Drug therapy (e.g., diuretics, glucocorticoids) Osmotic diuresis (e.g., diabetes mellitus) Impaired medullary concentration gradient (e.g., hypoadrenocorticism, portosystemic shunting) Central diabetes insipidus Nephrogenic diabetes insipidus (e.g., hypercalcemia, pyometra, pyelonephritis) Postrenal azotemia (urinary obstruction, rupture) is generally easily differentiated from kidney disease by dysuria.
INITIAL DATABASE CBC: usually unremarkable; occasionally mild anemia Serum biochemistry profile: azotemia may or may not be present; sometimes hyperphosphatemia, hypokalemia. Urinalysis: frequently isosthenuric or minimally concentrated specific gravity (dogs 1 year are still possible.
SUGGESTED READING Liptak JM, Kamstock DA, Dernell WS, et al: Oncologic outcome after curative-intent treatment in 39 dogs with primary chest wall tumors (1992-2005). Vet Surg 37:488, 2008. Waltman SS, Seguin B, Cooper BJ, Kent M: Clinical outcome of nonnasal chondrosar-coma in dogs: thirty-one cases (1986-2003). Vet Surg 36:266, 2007. ThÉon AP, Madewell BR, Harb MF, Dungworth DL: Megavoltage irradiation of neoplasms of the nasal and paranasal cavities in 77 dogs. J Am Vet Med Assoc 202:1469, 1993. AUTHOR: DENNIS B. BAILEY
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EDITOR: KENNETH M. RASSNICK
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Cholecystitis
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Cholecystitis BASIC INFORMATION DEFINITION Inflammation of the gallbladder wall; can be acute, chronic, necrotizing and/or emphysematous
EPIDEMIOLOGY SPECIES, AGE, SEX Necrotizing and emphysematous cholecystitis occur infrequently in dogs and are extremely rare in cats. Acute cholecystitis may occur in cats secondary to bacterial cholangitis/cholangiohepatitis. Mean age: 9.5 years Male dogs are at increased risk. GENETICS & BREED PREDISPOSITION Older, female, small-breed dogs appear to be at increased risk for cholelithiasis. Shetland sheepdogs appear to be predisposed. RISK FACTORS: Age (increased risk with age), history of previous cholecystitis, and concurrent systemic disease are associated with increased risk of cholecystitis. ASSOCIATED CONDITIONS & DISORDERS Cholangitis (inflammation of the bile ducts), choledochitis (inflammation of the common bile duct), and cholangiohepatitis (inflammation of the biliary tree and periportal hepatic parenchyma) Cholelithiasis, gallbladder rupture/perforation, and subsequent bile peritonitis (septic or sterile) can be sequelae to cholecystitis. Can occur as the result of gallbladder mucocele Diabetes mellitus and cystic duct obstruction: emphysematous cholecystitis (weak association)
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES Chronic and emphysematous forms may be incidental findings noted on abdominal ultrasound or abdominal radiographs (emphysematous—gas within gallbladder). Acute and necrotizing forms generally result in systemic illness. HISTORY, CHIEF COMPLAINT Presenting complaints are generally vague. May include vomiting, diarrhea, depression, lethargy, weight loss, abdominal pain. Profound weakness or collapse can occur with gallbladder perforation and peritonitis. PHYSICAL EXAM FINDINGS Nonspecific findings may include tachycardia, tachypnea, fever, dehydration, and cranial abdominal pain. Icterus often is present when there is concurrent extrahepatic biliary obstruction.
ETIOLOGY AND PATHOPHYSIOLOGY Necrotizing cholecystitis (type I): Secondary to infection with subsequent loss of viability of the gallbladder wall Gallbladder perforation does not occur despite wall necrosis. Acute (type II) and chronic (type III) cholecystitis: Etiology is poorly defined.
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Cholecystitis
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Bacterial infection (ascending from the common bile duct or via hematogenous spread) suspected Type II cholecystitis results in gallbladder perforation and peritonitis. Type III cholecystitis results in cholecystic adhesions (omental and hepatic adhesions) and/or fistulation. Emphysematous cholecystitis: Invasion of the wall with gas-forming bacteria Tympanic cholecystitis is the result of gas distension of the lumen of the gallbladder by gas-forming bacteria. Severe tympanic cholecystitis can be associated with emphysematous cholecystitis (gas dissection into the gallbladder wall).
DIAGNOSIS DIAGNOSTIC OVERVIEW Cholecystitis should be a differential for any patient with cranial abdominal pain and elevated serum hepatic enzyme activities or total bilirubin concentration. Cholecystitis should be the primary differential in a patient with bile peritonitis without a history of trauma. A definitive diagnosis is based on surgical findings and histopathologic analysis.
DIFFERENTIAL DIAGNOSIS Other hepatobiliary disease Pancreatitis Proximal small bowel disease
INITIAL DATABASE CBC results are variable depending upon severity and suddenness in onset of cholecystitis. Increased serum liver enzyme activities and bilirubin concentration are possible. Hypoglycemia possible in cases involving septic peritonitis Hyperglycemia may be seen in cases with concurrent diabetes mellitus and emphysematous cholecystitis. Abdominal radiographs may show air or calculi in gallbladder. Loss of cranial abdominal detail may be apparent (peritonitis). Abdominal ultrasound is highly reliable for the identification of gallbladder rupture (86% sensitivity). Loss of gallbladder wall continuity, hyperechoic fat in the cranial portion of the abdomen, and free abdominal fluid are possible findings. Choleliths may be seen.
ADVANCED OR CONFIRMATORY TESTING Definitive diagnosis requires surgical biopsy and histopathologic evaluation of a specimen of the gallbladder wall. Cultures of bile and/or gallbladder mucosa should be performed (Escherichia coli and Klebsiella spp. most common, but aerobic and anaerobic culture and sensitivity are warranted). Laparoscopic evaluation and liver biopsy may prove useful. Conversion to an open procedure and cholecystectomy should be anticipated. Ultrasonographic-guided, percutaneous cholecystocentesis: bile cytology and bacterial culture and sensitivity. Cholangiography: radiographic imaging of the biliary system; rarely performed. Abdominal paracentesis (p. 1192) or diagnostic peritoneal lavage (see online chapter: Diagnostic Peritoneal Lavage) should be performed if ultrasound is not available. Scintigraphy is an accurate indicator of canine extrahepatic biliary obstruction (EHBO).
TREATMENT TREATMENT OVERVIEW Surgical removal of a severely compromised or perforated GB and relief of EHBO are essential. Nonsurgical management may be appropriate in select cases without compromise of the GB wall's integrity.
ACUTE GENERAL TREATMENT Immediate surgical intervention in cases with gallbladder wall rupture and/or concurrent bile peritonitis Patients that are systemically ill must be aggressively supported before surgical management (fluids, antibiotics, colloids).
CHRONIC TREATMENT
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Select cases of cholecystitis can be managed without surgical intervention, provided (1) there are no signs of systemic illness such as severe lethargy, vomiting, or anorexia; (2) there is no evidence of EHBO or compromise of the gallbladder's integrity; and (3) serum biochemical values (liver enzymes and bilirubin) are decreasing over time or have normalized. Treatments that may be used in conservative (nonsurgical) management of these select cases include long-term antibiotic therapy (e.g., ampicillin, 10-20 mg/kg IV q 8 h; or amoxicillin-clavulanic acid, 10-20 mg/kg PO q 12 h until culture and sensitivity results are available), choleretics (ursodiol, 15 mg/kg PO q 24 h), and treatment of any underlying disease (e.g., pancreatitis, diabetes mellitus).
POSSIBLE COMPLICATIONS Gallbladder rupture and bile peritonitis (septic versus nonseptic) Recurrence of cholecystitis with inappropriate treatment EHBO
RECOMMENDED MONITORING Intensive monitoring in a critical care setting is indicated in markedly compromised patients (e.g., necrotizing cholecystitis, bile peritonitis). Serial serum biochemistry profiles and serial abdominal ultrasounds as indicated Monitoring coagulation profiles and vitamin K supplementation (0.5 mg/kg IM q 12 h until relief of obstruction) is indicated in patients with complete EHBO.
PROGNOSIS AND OUTCOME Mortality rates of 25%-39% with canine necrotizing cholecystitis Overall mortality rates of 50% with canine bile peritonitis (0% with nonseptic effusions and 73% with septic effusions) Septic peritonitis, preoperative elevated creatinine concentration, and immediate postoperative hypotension are associated with a poor clinical outcome.
PEARLS & CONSIDERATIONS COMMENTS Select cases can be managed medically. Surgical management is indicated in all cases involving gallbladder compromise, bile peritonitis, or EHBO (excluding select cases of pancreatitis).
TECHNICIAN TIP Early enteral nutrition is very important to a positive outcome. In severely debilitated patients, esophagostomy and nasogastric feeding should be implemented postoperatively.
CLIENT EDUCATION Recurrence is possible if cholecystectomy is not performed. Early intervention likely improves outcome.
SUGGESTED READING Aguirre AL, Center SA, Randolph JF, et al: Gallbladder disease in Shetland sheepdogs: 38 cases (1995-2005). J Am Vet Med Assoc 231(1):79–88, 2007. Mehler, SJ, Mayhew PD: Variables associated with outcome in dogs undergoing extrahe-patic biliary surgery: 60 cases (1988-2002). Vet Surg 33:644, 2004. AUTHOR: FRED S. PIKE EDITOR: KEITH P. RICHTER
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Cholecalciferol Toxicosis
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Cholecalciferol Toxicosis BASIC INFORMATION DEFINITION Cholecalciferol (vitamin D3) is used as both a dietary supplement and a rodenticide. Toxicity is characterized by clinical manifestations of hypercalcemia and hyperphosphatemia: anorexia and lethargy due to renal failure, cardiac arrhythmias, and seizures.
SYNONYM Vitamin D3
EPIDEMIOLOGY SPECIES, AGE, SEX All species susceptible; dogs more likely to be involved Young animals may be more sensitive RISK FACTORS Preexisting disease such as chronic kidney disease can increase severity of adverse effects. CONTAGION & ZOONOSIS Relay toxicosis (intoxication via consumption of prey that has itself consumed cholecalciferol) has not been reported. GEOGRAPHY AND SEASONALITY More cases in the fall and the winter months when more rodenticides are used
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT History or evidence of consuming bait Lethargy, anorexia, vomiting, diarrhea, polyuria, and polydipsia 12-72 hours post ingestion Renal failure 24-72 hours post ingestion PHYSICAL EXAM FINDINGS Anorexia, lethargy Dehydration Signs of abdominal pain Hematemesis, melena Dyspnea, cardiac arrhythmias (especially bradycardia) Seizures (uncommon)
ETIOLOGY AND PATHOPHYSIOLOGY Source: Cholecalciferol rodenticides Dietary supplements (over-the-counter and prescription) Common trade names are: Mouse-B-Gon, Rat-B-Gon, Quintox, Rampage, and True Grit. Most baits contain 0.075% cholecalciferol (0.75 mg cholecalciferol/gram bait). One IU of cholecalciferol (e.g., in dietary supplements) is equivalent to 0.025 mg of cholecalciferol.
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Cholecalciferol Toxicosis
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Mechanism of Toxicosis: Cholecalciferol is metabolized to calcitriol (1,25 dihydroxyvitamin D). Calcitriol increases intestinal absorption of calcium, stimulates resorption of calcium from bone, and increases renal tubular resorption of calcium. Toxic effects are due to hypercalcemia and hyperphosphatemia, resulting in metastatic mineralization of soft tissues, particularly kidney, myocardium, intima of large vessels, and gastrointestinal tract. Parathyroid hormone synthesis is suppressed.
DIAGNOSIS DIAGNOSTIC OVERVIEW Diagnosis is based on history of exposure to bait and evidence of hypercalcemia and hyperphosphatemia. Other causes of hypercalcemia need to be ruled out in cases where exposure history is not available; many possible causes (e.g., neoplasia, primary hyperparathyroidism) can be identified as unlikely on the basis of serum phosphorus level.
DIFFERENTIAL DIAGNOSIS Hypercalcemia: Toxicologic: Synthetic vitamin D3 ointment ingestion containing calcipotriene (Dovonex) or tacalcitol (Curatoderm) used for treating psoriasis in humans Chronic overdose of vitamin D3 supplements Spontaneous, nontoxicologic: Hypercalcemia of malignancy(lymphoma, perianal adenocarcinoma, multiple myeloma, others) Primary renal failure Primary hyperparathyroidism Feline idiopathic hypercalcemia Addison's disease (hypoadrenocorticism) Granulomatous diseases (e.g., blastomycosis, schistosomiasis)
INITIAL DATABASE CBC, serum biochemistry profile: Baseline if possible (60, an increased risk of soft-tissue mineralization exists Note that immature animals that are actively remodeling bone may normally have Ca P that exceeds 60 but it is not associated with soft tissue mineralization. Urinalysis: Isosthenuria (specific gravity 1.008-1.012) or hyposthenuria (specific gravity of 1.002-1.007) are common; isosthenuria indicates renal failure if concurrent azotemia Radiographs for soft-tissue calcification Ultrasound may suggest soft-tissue mineralization
ADVANCED OR CONFIRMATORY TESTING Serum 25-hydroxycholecalciferol level is elevated with cholecalciferol toxicosis. This assay will not detect calcipotriene found in psoriasis ointments (see p. 169). Serum parathyroid hormone levels are low with cholecalciferol toxicosis and hypercalcemia of malignancy but are normal with primary hyperparathyroidism, feline idiopathic hypercalcemia, and chronic kidney disease. Plasma parathyroid hormone–related protein may be detectable with hypercalcemia of malignancy but will be absent with other causes of hypercalcemia. Necropsy: fresh or frozen kidney. Total wet weight kidney calcium is typically elevated (300-1000 ppm [normal ranges, 100-150 ppm]). Histopathologic evaluation of lungs, kidney, aorta, myocardium, and gastric mucosa can reveal soft-tissue mineralization and necrosis.
TREATMENT
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Cholecalciferol Toxicosis
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TREATMENT OVERVIEW For recent exposures prior to elevations in serum calcium and phosphorus, treatment consists of decontamination (induction of emesis and administration of activated charcoal) and measures to minimize effects of the toxicant. For animals with elevated serum calcium and phosphorus levels, treatment is aimed at lowering serum calcium and phosphorus promptly and preventing or managing acute renal failure. Complicated cases may involve days of intravenous fluid therapy and associated care. Referral to a specialty clinic that can provide 24-hour care should be considered.
ACUTE GENERAL TREATMENT Confirmed cholecalciferol ingestions >0.1 mg/kg require decontamination of the patient and monitoring. Decontamination of patient: induction of vomiting within 4 hours of ingestion (hydrogen peroxide 3%, 0.25-0.5 mL/kg PO once [dogs], or xylazine hydro-chloride, 0.44 mg/kg IM [cats]) Repeated doses of activated charcoal (dose according to packaging label of product; e.g., 10 mL/kg of activated charcoal suspension PO made from 2 g activated charcoal suspended in 10 mL tap-water) and a cathartic, given q 8 h 24 hours Monitor serum electrolytes for development of hypernatremia 2-4 hours following repeated activated charcoal dosing. Treat hypercalcemia in animals showing overt clinical signs: Saline diuresis 0.9% saline at 90 (cats) to 130 (dogs) mL/kg/d Avoid calcium-containing fluids. Adjust dose if cardiac disease or other vascular volume-limiting condition. Furosemide 2.5-4.5 mg/kg PO, SQ, IM, or IV q 6-8 h Do not use thiazide diuretics (calcium-retaining). Example: hydrochlorothiazide. Prednisolone 1-3 mg/kg PO q 8-12 h High doses of dexamethasone at 1-2 mg/kg IV or SQ q 24 h have been recommended. Because dexamethasone has 10 times the glucocorticoid potency of prednisone, these high doses can cause substantial gastrointestinal ulceration and hemorrhage and should only be used as a last resort. Specific antagonists (must choose one or the other; do not combine): Pamidronate (preferred): 1.3-2 mg/kg as a slow IV infusion. Repeat in 5-7 days if needed. May cause a transient increase in BUN or creatinine. Calcitonin (use if supportive treatments are not effective): 4-6 IU/kg-SQ q 8-12 h. Some animals become refractory to salmon calcitonin.
CHRONIC TREATMENT Continue treatment until serum calcium stabilizes or Ca × P < than 60 (days to weeks of treatment). Treat other signs (renal failure, seizures, arrhythmias). Gradually wean off prednisolone/dexamethasone and furosemide when calcium levels reach normal range. Avoid sunlight.
NUTRITION Phosphate binders: aluminium hydroxide 10-30 mg/kg PO q 8 h. Discontinue phosphate binders when serum phosphorus level stabilizes. Low-calcium diet
POSSIBLE COMPLICATIONS Soft-tissue mineralization (irreversible) Pulmonary edema (mineralization and leakage of pulmonary vessels), hemorrhage, or aspiration pneumonia Sudden death associated with myocardial or aortic mineralization Gastric ulceration, hematemesis, shock, and collapse Hypocalcemia if animals are not weaned from treatment after calcium levels are normalized
RECOMMENDED MONITORING Monitor serum calcium and phosphorus for 5 to 7 days after values are normalized, then 2-3 times a week for 2 weeks, and then once at 1 month post exposure.
PROGNOSIS AND OUTCOME Prognosis good if animal receives prompt treatment, and if soft-tissue mineralization has not occurred
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Prognosis poor to guarded with prolonged elevations in calcium and phosphorus, causing soft-tissue mineralization
PEARLS & CONSIDERATIONS COMMENTS Dietary supplements generally list cholecalciferol, or vitamin D, in IU. One IU of cholecalciferol is equivalent to 0.025 mcg of cholecalciferol. Practitioners should be aware that products with the same brand name may contain various active ingredients. For example, Rampage may contain bromethalin or cholecalciferol. It is imperative that active ingredients be verified on the package. In nonsurvivors, total wet kidney calcium concentrations can be used for differentiating between ethylene glycol toxicosis (3000-12,000 ppm) and cholecalciferol toxicosis (300-1000 ppm).
TECHNICIAN TIPS In dogs, hypercalcemia frequently causes anorexia, so monitoring a dog's appetite may provide an early indication of increasing serum calcium levels.
CLIENT EDUCATION Provide information about pet proofing homes. Remind clients that rodenticides may be appealing to pets.
SUGGESTED READING Rumbeiha WK: Cholecalciferol. In Peterson ME, Talcott PA, editors: Small animal toxicology, ed 2, St Louis, 2006, Elsevier, pp 629–642. AUTHOR: SHARON GWALTNEY-BRANT EDITOR: SAFDAR A. KHAN 1ST EDITION AUTHOR: CHARLOTTE MEANS
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Chole(cysto)lithiasis
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Chole(cysto)lithiasis BASIC INFORMATION DEFINITION Formation of stones in the extrahepatic bile duct system (choleliths) and/or specifically in the gallbladder (cholecystoliths)
SYNONYM Gallstones
EPIDEMIOLOGY SPECIES, AGE, SEX Dogs: older, small-breed, spayed females appear to be predisposed. Cats: middle-aged to older adults ASSOCIATED CONDITIONS & DISORDERS Cats: In some cats, possible association with cholangitis, pancreatitis, inflammatory bowel disease Dogs: Cholecystitis Gallbladder perforation Bile peritonitis due to gallbladder rupture Rarely biliary adenocarcinoma
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES Cholelithiasis without specific clinical signs: Incidental finding on abdominal radiographs or ultrasound performed for another reason Cholelithiasis associated with clinical signs of: Gastrointestinal disease Biliary obstruction Peritonitis when cholelithiasis is associated with biliary disruption/rupture HISTORY, CHIEF COMPLAINT Generally nonspecific: malaise and gastrointestinal signs predominate. Dogs: vomiting, anorexia, lethargy, weakness, polydipsia, polyuria, weight loss Cats: vomiting, dehydration, anorexia, lethargy Note: choleliths may be an incidental finding in both dogs and cats and may not be associated with any clinical signs. PHYSICAL EXAM FINDINGS Icterus is commonly apparent when cholelithiasis is associated with cholangitis, cholecystitis, and/or gallbladder obstruction. Fever may be noted in dogs, in association with infection and/or bile peritonitis. Signs of abdominal pain are not consistently noted, even when biliary obstruction is present.
ETIOLOGY AND PATHOPHYSIOLOGY
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Chole(cysto)lithiasis
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Etiology unknown In dogs and cats, most choleliths contain mainly calcium rather than cholesterol, as seen in humans. Choleliths may obstruct the extrahepatic biliary system (see p. 135 ). Decreased absorption of fat and fat-soluble vitamins, notably vitamin K, and subsequent coagulopathy Decreased bile secretion into the intestine may result in decreased binding of endotoxin, predisposing to endotoxemia. Cholelithiasis has been associated with concurrent cholecystitis and gallbladder rupture, resulting in bile peritonitis.
DIAGNOSIS DIAGNOSTIC OVERVIEW Inasmuch as presenting history and physical examination findings are frequently nonspecific, the diagnosis of this problem generally requires diagnostic imaging. Abdominal ultrasonography is the modality of choice.
DIFFERENTIAL DIAGNOSIS Cholelithiasis with extrahepatic biliary obstruction and jaundice: Hyperbilirubinemia due to hemolysis: Immune-mediated hemolytic anemia or other diseases causing severe intravascular hemolysis Hepatic disease: cholangiohepatitis (cats), idiopathic chronic hepatitis (dogs), cirrhotic/fibrosing liver disease, neoplasia, copper/other toxins (dogs), acetaminophen toxicosis (cats) Extrahepatic biliary obstruction: pancreatitis, cholangitis, neoplasia, stricture, foreign body obstruction, diaphragmatic hernia Cholelithiasis without biliary obstruction: Other causes of vomiting and anorexia, because choleliths are an incidental finding: Viral enteritis Pancreatitis Foreign body obstruction Gastric, intestinal, or pancreatic neoplasia Inflammatory bowel disease Ingested toxins Hepatic and renal diseases
INITIAL DATABASE CBC: Possible anemia, though usually mild Inflammatory leukogram Serum biochemistry profile: Elevated bilirubin concentration Elevated liver enzyme concentration Possible elevations of amylase and lipase concentrations Hypokalemia Survey abdominal radiographs: May delineate radiopaque choleliths Survey thoracic radiographs: Rule out metastatic disease if neoplasia is suspected
ADVANCED OR CONFIRMATORY TESTING Abdominal ultrasound examination: Common bile duct dilation: Further delineate choleliths >5 mm diameter is diagnostic of bile duct obstruction in the cat Evaluate gallbladder in dogs with concurrent cholecystitis: Wall thickness Contents: choleliths, mucocele Presence of attached omentum Surrounding fluid Evaluate intestine for increased wall thickness and loss of layering associated with neoplasia or inflammatory bowel disease
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Peritoneal fluid analysis (obtained during abdominal ultrasound examination): Bilirubin concentration (elevated: bile peritonitis) Cytologic examination and microbiologic culture and sensitivity testing: septic peritonitis Coagulation profile
TREATMENT TREATMENT OVERVIEW If the choleliths are an incidental finding, no treatment is required. The patient should be monitored for development of clinical signs associated with cholelithiasis. If signs of biliary stasis, disruption, or obstruction are noted, then patient stabilization and surgical intervention will be necessary.
ACUTE GENERAL TREATMENT Rehydration by intravenous administration of balanced electrolyte solution Normalization of serum electrolyte concentrations Parenteral antibiotics effective against gram-negative bacteria and anaerobes: Empirical therapy: Cefoxitin, 30 mg/kg IV q 4-6 h perioperatively, then q 6 h; or Metronidazole, 7.5-15 mg/kg IV q 12 h with Enrofloxacin, 5-15 mg/kg q 24 h for dogs, 5 mg/kg q 24 h for cats Specific long-term therapy based on culture and sensitivity test results Possible administration of fresh frozen plasma (if hypoproteinemia, coagulopathy) Vitamin K administration Removal of choleliths/relief of extrahepatic biliary obstruction Duodenotomy and retrograde flushing of the biliary system Choledochotomy for removal of one or two large choleliths Cholecystectomy: Results in the best long-term prognosis if all stones are removed and biliary system is patent Common bile duct stenting Cholecystoduodenostomy/jejunostomy Tube cholecystostomy Treatment of bile peritonitis if biliary disruption has occurred (see p. 865 )
CHRONIC TREATMENT Maintenance of bile flow: ursodeoxycholic acid 10-15 mg/kg PO q 24 h; contraindicated while gallbladder obstruction is present.
NUTRITION/DIET Provide access for enteral feeding if patient is anorexic (see p. 1267 ,p. 1270, and p. 1322 ).
POSSIBLE COMPLICATIONS Recurrence of cholelithiasis, bile leakage, pancreatitis, peritonitis, endotoxemia, sepsis, death
RECOMMENDED MONITORING If clinical signs were/are present: Clinical and laboratory parameters assessing perfusion, including capillary refill time, pulse rate and quality, blood pressure, urine output, arterial pH, and lactate concentrations Respiratory function Serum liver enzymes and bilirubin concentrations Coagulation profile If incidental finding: Physical exam and serum biochemistry profile every 6 months
PROGNOSIS AND OUTCOME
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Chole(cysto)lithiasis
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Fair in clinically ill animals if all choleliths removed and a cholecystectomy is performed Guarded if cholelithiasis is associated with biliary leakage and aseptic bile peritonitis Poor in patients with septic bile peritonitis Open prognosis in patients without clinical signs (incidental finding)
PEARLS & CONSIDERATIONS COMMENTS Given the association of biliary obstructive disease (cholelithiasis) in cats with cholangitis/cholangiohepatitis and inflammatory bowel disease, a liver biopsy and culture, bile culture, and small intestinal biopsies should be obtained at the time of surgery in this species.
SUGGESTED READING Center SA: Diseases of the gallbladder and biliary tree. Vet Clin North Am Small Anim Pract 39(3):543–598, 2009. Eich CS, et al: The surgical treatment of cholelithiasis in cats: a study of nine cases. J Am Anim Hosp Assoc 38:290, 2002. Kirpensteijn J, et al: Cholelithiasis in dogs: 29 cases (1980-1990). J Am Vet Med Assoc 202:1137, 1993. AUTHOR: DAVID HOLT EDITOR: RICHARD WALSHAW
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Cholangitis/Cholangiohepatitis Complex of Cats
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Cholangitis/Cholangiohepatitis Complex of Cats BASIC INFORMATION DEFINITION Inflammation of the biliary tree and surrounding hepatocellular parenchyma. May occur as a primary process, a coexisting condition, or secondary to a variety of other feline diseases. Cholangitis: inflammation is centered around the bile ducts. Cholangiohepatitis: extension of cholangitis into the surrounding hepatic parenchyma Cholangitis/cholangiohepatitis (CCH) has been referred to as both a “complex” (CCHC) and a “syndrome” (CCHS). In either case, this designation emphasizes the fact that a variety of distinct forms of disease is included within a single umbrella term (see disease forms/subtype, below). The CCHC of cats is one of the most common feline hepatobiliary disorders.
SYNONYMS Acute neutrophilic CCH: suppurative CCH Chronic, lymphoplasmacytic CCH: nonsuppurative, lymphoplasmacytic, or lymphoproliferative CCH
EPIDEMIOLOGY SPECIES, AGE, SEX Himalayan, Persian, and Siamese cats may be predisposed. Patients with this disease range in age from 16 years old, but most are middle-aged. Cats presenting with acute (suppurative) disease tend to be several years younger than those with chronic (nonsuppurative) disease. Male cats appear to be overrepresented. RISK FACTORS Extrahepatic biliary obstruction, inflammatory bowel disease (IBD), pancreatitis, cholestatic disease, cholelithiasis, bacterial infection or splenic abscess, feline infectious peritonitis (FIP), toxoplasmosis, immunodeficiencies, choledochal stent placement, drugs (diazepam, tetracyclines, others). CONTAGION & ZOONOSIS Not considered either a contagious or zoonotic disease. There is a single report of H. pylori isolation from samples of feline bile. ASSOCIATED CONDITIONS & DISORDERS Triaditis is the term used for describing the combination of CCH with IBD and pancreatitis. IBD or pancreatitis is seen in 50%–85% of the cases of CCHC, with both present in up to 40% of CCHC patients. Cholangitis/cholangiohepatitis can also be associated with hepatic lipidosis, or secondary to a variety of other diseases/conditions (see Risk Factors above).
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES On the basis of histopathologic findings, three distinct entities exist within the CCHC, as defined by the World Small Animal Veterinary Association Liver Diseases and Pathology Standardization Research Group: Acute neutrophilic (suppurative) Chronic (lymphoplasmacytic or mixed) Lymphocytic (nonsuppurative) The forms can be quite different clinically (history, initial presentation, chief complaint, etiology, progression, and outcome). Chronic lymphocytic cholangitis is a form seen predominantly in Europe and is progressive. Some pathologists classify this as low-grade (well-differentiated) lymphoma. Lymphocytic portal hepatitis is a separate entity confined to portal triads and is often an incidental finding in older cats.
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Cholangitis/Cholangiohepatitis Complex of Cats
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HISTORY, CHIEF COMPLAINT Patients with the suppurative form of CCH usually present for an acute onset of illness: anorexia, fever, and vomiting in an icteric cat with abdominal discomfort. Patients with the nonsuppurative form of CCH usually present for a more chronic condition with subtle nonspecific signs, and less commonly present with acute signs. Patients with concurrent IBD and pancreatitis (“triaditis”) may present with a wide variety of signs and varying degrees of severity, depending on the severity of inflammation in these other organs. Patients with either form are usually icteric, and a few may have ascites. Patients with the chronic condition may rarely be polyphagic, although usually they will be presented for lethargy, anorexia, vomiting, and weight loss. PHYSICAL EXAM FINDINGS Suppurative CCH: The patient is usually febrile, dehydrated, and icteric and may have abdominal discomfort with palpation. Patients with the nonsuppurative form of CCH may have minimal physical exam abnormalities or may present icteric. Hepatomegaly may be appreciated with abdominal palpation.
ETIOLOGY AND PATHOPHYSIOLOGY Bacterial infection (Escherichia coli, Streptococcus, Clostridium, Salmonella [serovar typhimurium], Enterococcus faecium, other enteric organisms, anaerobes); ascending infection of the biliary tract (acute suppurative/neutrophilic cholangitis) In association with other infectious agents (i.e., toxoplasmosis, FIP) Immune-mediated disorder (chronic nonsuppurative/lymphocytic cholangitis) Extrahepatic biliary obstruction Secondary or concurrent pancreatitis, especially with suppurative form; pancreatic and bile ducts enter duodenum through a common opening in the cat (see p. 135 ) IBD
DIAGNOSIS DIAGNOSTIC OVERVIEW Lethargy and anorexia in a cat with elevated liver enzymes is consistent with CCH but also several other hepatobiliary disorders. The diagnosis is confirmed histologically from a liver biopsy.
DIFFERENTIAL DIAGNOSIS Hepatic lipidosis Hepatic neoplasia (especially lymphoma) Extrahepatic biliary duct obstruction Pancreatitis Inflammatory bowel disease FIP Sepsis
INITIAL DATABASE CBC: Leukocytosis; neutrophilia with a left shift and/or toxic neutrophils Lymphocytosis (nonsuppurative CCH) Mild nonregenerative anemia with poikilocytes and/or Heinz bodies Serum biochemistry panel: Elevated liver enzyme activities (alanine aminotransferase, ALP, aspartate aminotransferase, γ-glutamyltransferase) Possibly elevated total bilirubin concentration Increased bile acids concentration (fasting and postprandial) Hyperglobulinemia (nonsuppurative CCH) Other: High feline pancreatic lipase immunoreactivity (fPLI) possible with pancreatitis Low serum cobalamin concentration with severe IBD Possible clotting time abnormalities (prothrombin time, activated partial thromboplastin time, activated clotting time [ACT], proteins induced by vitamin K absence [PIVKA]), or portal vein thrombus (PVT).
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Cholangitis/Cholangiohepatitis Complex of Cats
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Hepatomegaly (radiographs or laparoscopy)
ADVANCED OR CONFIRMATORY TESTING Abdominal ultrasound: Hepatic parenchyma: mixed echogenicity, multifocal hyperechogenicity, diffuse hypoechogenicity, or a coarse or nodular appearance (nonspecific) Prominent portal vasculature Gallbladder distension, cholelithiasis, biliary sludge, thickened gallbladder wall Abdominal lymphadenopathy Evidence of pancreatic or intestinal inflammation Ascites (nonsuppurative CCH; high protein, low cellularity) Fine-needle aspiration (FNA) of the liver: Hepatocellular vacuolation (concurrent lipidosis is possible). Cellular infiltration: neutrophils, lymphocytes, or mixed, +/− intraluminal biliary inflammation Bacterial culture and sensitivity. In general, FNAs result in a greater number of false-negative and false-positive diagnoses compared to core or wedge biopsies. Percutaneous ultrasound-guided cholecystocentesis Minimally invasive; identification, culture and sensitivity for bacterial isolates Liver biopsy (wedge [laparotomy, laparoscopy] or ultrasound-guided core):as above for FNA, plus: Periportal hepatocellular necrosis, bile duct dilation and proliferation (suppurative) Periductal fibrosis, diminished bile duct number, and sclerosing cholangitis (nonsuppurative) Laparoscopy: Abdominal lymphadenopathy Ability to obtain wedge biopsy sample Laparotomy, as above for laparoscopy: Assess biliary system for extrahepatic biliary obstruction. Feeding tube placement possible
TREATMENT TREATMENT OVERVIEW In addition to supportive care and specific treatment, the treatment plan must address concurrent conditions (frequent) for optimal patient outcomes.
ACUTE GENERAL TREATMENT Treatment should be tailored to the individual patient. Fluids (Normosol, lactated Ringer's solution) with potassium supplementation Antibiotics (based on culture and sensitivity when possible): Amoxicillin-clavulanate, 62.5-125 mg/cat PO q 12 h, 1-2 weeks beyond normalizing liver enzymes, or Amoxicillin, 10-20 mg/kg PO q 12 h, or Cephalexin or cefadroxil, 22 mg/kg PO q 8 h, or Enrofloxacin, 5 mg/kg PO q 24 h, combined with metronidazole, 7.5 mg/kg PO q 12 h Vancomycin has been reported for one case of multidrug-resistant Enterococcus faecium Ursodeoxycholic acid (10-15 mg/kg PO q 24 h) for choleresis, unless physical obstruction to gallbladder outflow exists Vitamin K1 (5 mg/cat PO q 24 h) in cases of coagulation abnormalities Cannulation for removal of inspissated bile, surgery for extrahepatic biliary obstruction, and necessary treatments for associated conditions (especially pancreatitis, IBD, hepatic lipidosis).
CHRONIC TREATMENT Long-term management is highly dependent on an accurate diagnosis and requires histopathologic analysis of a liver biopsy. Continued antibiotics and ursodeoxycholic acid (see Acute General Treatment above) 3-6 months if suppurative CCH Prednisolone (for chronic or nonsuppurative CCH; 4 mg/kg/d initially, gradual taper over 2-4 months) combined with metronidazole (see Acute General Treatment above) Refractory cases of nonsuppurative CCH may require chemotherapeutics (e.g., methotrexate [0.13 mg PO q 8 h for 3 doses 2
at 7-day intervals, if tolerated], cyclosporine [3-5 mg/kg PO q 12 h], or chlorambucil [4 mg/m PO q 48 h]). Given the potential for severely detrimental side effects with these drugs and the need for close monitoring, their use is recommended only in consultation with an internist.
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Cholangitis/Cholangiohepatitis Complex of Cats
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Vitamin E (a-tocopherol acetate, 10-30 IU/kg) for all forms of CCHS S -adenosylmethionine (20 mg/kg PO q 24 h [enteric-coated tablet]) for all forms of CCHS Ursodeoxycholic acid, carnitine (see Acute General Treatment above) Continued treatment of concurrent conditions such as pancreatitis and/or IBD Treatment for ascites if present (furosemide [1-3 mg/kg PO q 12 h, ACE inhibitors [enalapril, 0.5 mg/kg PO q 12-24 h], salt restriction) For biliary cirrhosis (sclerosing CCHC), consider the addition of pulsatile therapy with methotrexate (0.13 mg PO q 8 h for 3 doses at 7-day intervals if tolerated), being cognizant of potentially adverse side-effects (GI, hepatic toxicity, renal toxicity, bone marrow suppression).
NUTRITION/DIET Route determined by clinical condition Protein restriction in cats is problematic because they are strict carnivores; protein restriction should be avoided unless there is clear evidence of hepatic encephalopathy (rare). Consider supplementation with L-carnitine (250 mg/cat PO q 24 h), taurine(250-500 mg/cat PO q 24 h), thiamine(B1) 50-100 mg PO q 24 h for 3 days, and vitamin B12 (1 mg SQ repeated weekly).
POSSIBLE COMPLICATIONS Hepatic lipidosis with prolonged anorexia or inadequate nutritional support Diabetes mellitus with corticosteroid treatment of nonsuppurative disease or IBD Hepatic sclerosis Progression of acute to chronic disease Necrotizing cholecystitis, choleliths Portal vein thrombosis
RECOMMENDED MONITORING Hepatic enzyme activity and total bilirubin concentration (at 2-week intervals until stable, then monthly) PIVKA and/or clotting times if abnormalities are present or to monitor vitamin K1 therapy Consider repeat bile acids measurement to monitor liver function.
PROGNOSIS AND OUTCOME Acute suppurative cholangiohepatitis may be a single curable event, or it may recur (especially if antibiotic therapy is curtailed prematurely), but the prognosis is generally good with timely diagnosis and appropriate treatment. Nonsuppurative cholangiohepatitis is a chronic condition but carries a fair to good prognosis with lifelong therapy. Concurrent pancreatitis and/or IBD may also affect the prognosis negatively.
PEARLS & CONSIDERATIONS COMMENTS The cholangitis/cholangiohepatitis complex of cats is a complex or constellation of distinct clinical signs, biochemical abnormalities, and structural derangements. The underlying etiology may be distinct as well, and determining whether an infectious process is a contributing factor has a critical bearing on treatment decisions. Following the appropriate and sufficient diagnostic steps in the workup of a cat with inflammatory liver disease is critical for therapeutic success. Acute (suppurative) CCH is often infectious in nature (and therefore treated initially with antibiotics), whereas chronic (nonsuppurative) CCH may have an immune-mediated basis (and is therefore treated with immunosuppressive drugs).
PREVENTION Avoid and/or treat contributing or concurrent conditions such as chronic pancreatitis or IBD.
CLIENT EDUCATION Vigilant monitoring is important for early detection of anorexia, lethargy, vomiting, or abdominal discomfort, because suppurative cholangiohepatitis may recur. Compliance with medication administration may be a lifelong commitment.
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Cholangitis/Cholangiohepatitis Complex of Cats
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Proper nutritional support (optimal high-protein diet) is important.
SUGGESTED READING Brian PH, et al: Feline cholecystitis and acute neutrophilic cholangitis: clinical findings, bacterial isolates and response to treatment in six cases. J Feline Med Surg 8:91–103, 2006. Gagne JM, et al: Clinical features of inflammatory liver disease in cats: 41 cases (1983-1993). J Am Vet Med Assoc 214:513–516, 1999. Twedt DC, Armstrong PJ: Feline inflammatory liver disease. In Bonagura JD, Twedt DC, editors: current veterinary therapy XIV. St Louis, 2009, Saunders Elsevier, pp 576–581. AUTHOR: CRAIG B. WEBB EDITOR: KEITH P. RICHTER
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Chocolate Toxicosis
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Chocolate Toxicosis BASIC INFORMATION DEFINITION Clinical signs caused by ingestion of chocolate products and byproducts
SYNONYM Methylxanthine toxicosis
EPIDEMIOLOGY SPECIES, AGE, SEX Dogs are most commonly affected; all breeds, ages, both sexes susceptible. RISK FACTORS Animals with cardiac or seizure disorders may be at increased risk for signs. GEOGRAPHY AND SEASONALITY Toxicosis can occur year-round; most prevalent (greater opportunity for exposure) during holiday seasons such as Easter, Christmas, and Valentine's Day.
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES Severity and onset of signs depend on amount and type of chocolate ingested. Chocolate and its by products contain methylxanthines—theobromine (primary) and caffeine (secondary)—plus sugars and fat. See table for methylxanthine content of products. Variable individual sensitivity to methylxanthines Methylxanthine dosages: 20-40 mg/kg: mild to moderate clinical signs 40-50 mg/kg: cardiac arrhythmias; potentially life-threatening >60 mg/kg: seizures HISTORY, CHIEF COMPLAINT Known ingestion of chocolate most common Onset of signs up to 6-12 hours post ingestion possible Initially: polydipsia, bloating, vomiting, diarrhea; restlessness Can progress to polyuria, agitation, tremors, rigidity, ataxia, seizures, collapse, coma PHYSICAL EXAM FINDINGS Agitation, nervousness Tachycardia Tachypnea Hypertension Hyperthermia Cardiac arrhythmias (premature ventricular contractions, sinus tachycardia, sinus bradycardia, others) Ataxia, tremors, seizures
ETIOLOGY AND PATHOPHYSIOLOGY
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Chocolate Toxicosis
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Behavior changes, central nervous system stimulation, and cardiovascular abnormalities: competitive inhibition of cellular adenosine receptors Enhanced cardiac and skeletal muscle contractility: increase in free intracellular calcium concentrations from inhibition of sarcoplasmic calcium reuptake and increased calcium entry into cells Death likely due to cardiac arrhythmias, respiratory failure, or hyperthermia-induced disseminated intravascular coagulation (DIC) High sugar and fat contents in chocolate: gastrointestinal signs, possibly pancreatitis *Exact methylxanthine content varies with growing conditions for cocoa beans as well as individual commercial formulations of products. Approximate methylxanthine dose ingested (in mg/kg) is: 1. Add product's theobromine concentration, in mg/oz (above) + product's caffeine concentration, in mg/oz (above). 2. Multiply this number by number of ounces of chocolate product ingested. 3. Divide by dog's body weight in kg. Metric conversion 1 oz = 28.5 g.
Approximate Methylxanthine Content of Various Products
*
Product
Theobromine
Caffeine
Cocoa powder
737 mg/oz
42 mg/oz
Baker's chocolate
393 mg/oz
118 mg/oz
Semisweet chocolate
138 mg/oz
22 mg/oz
Instant cocoa mix powder
136 mg/oz
15 mg/oz
Milk chocolate
56 mg/oz
6 mg/oz
White chocolate
0.25 mg/oz
0.85 mg/oz
Unprocessed cocoa bean shell mulch 285-1140 mg/oz (54-849 mg/oz in processed mulch) 20-103 mg/oz
DIAGNOSIS DIAGNOSTIC OVERVIEW Diagnosis based on any combination of history, presence of chocolate in the vomitus, and clinical signs consistent with chocolate toxicosis
DIFFERENTIAL DIAGNOSIS Other toxicoses that can cause central nervous system (CNS) excitation: amphetamines, pseudoephedrine, phenylpropanolamine, metaldehyde, cocaine, antidepressants, antihistamines Causes of cardiac arrhythmias (see p. 1165 , p. 1027, and p. 1025 ) Causes of dyspnea/tachypnea (see p. 327) Causes of hyperthermia (see p. 480) Causes of systemic hypertension (see p. 1068)
INITIAL DATABASE ECG (see p. 1253 ) Blood pressure (see p. 1209 ) Serum biochemistry panel: Renal values in animals with severe clinical signs Serum electrolyte levels in animals with overt clinical signs Evaluation of pancreas (serum assays, ultrasound) in animals with severe or persistent gastrointestinal clinical signs
TREATMENT TREATMENT OVERVIEW Intensity of treatment is guided by dose of intoxication (type and amount of chocolate ingested), time since ingestion (expected efficacy of emesis induction and charcoal administration; onset of clinical signs), and presence or absence of preexisting cardiac or renal disorders. Mild intoxications may be treated as benign gastroenteritis cases (after patient decontamination).
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Chocolate Toxicosis
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ACUTE GENERAL TREATMENT Manage clinical signs: CNS signs/neuromuscular Diazepam (0.5-2 mg/kg IV) for seizures Barbiturates, gas anesthetics if diazepam ineffective Methocarbamol (50-200 mg/kg slow IV; do not exceed 330 mg/kg/24 h) for tremors, rigidity Cardiac arrhythmias: Beta-blockers for severe, sustained supraventricular tachyarrhythmias, especially if preexisting heart disease Propranolol (0.04-0.06 mg/kg slow IV over 2-3 minutes; max 0.2 mg/kg), or Esmolol (0.2-0.5 mg/kg IV or 25-200 mcg/kg/min IV CRI), or Metoprolol (0.2-0.4 mg/kg PO q 8 h) Lidocaine for rapid sustained ventricular arrhythmias Dogs: 1-4 mg/kg IV, then 30 to 50 mcg/kg/min if necessary (if beta-blockers ineffective). Cats (use with caution): 0.5-2 mg/kg IV. Atropine (0.01-0.02 mg/kg IV) for bradyarrhythmias Control hyperthermia: Fluids, fans (see p. 480 ) Control vomiting (if needed) Maropitant 1 mg/kg SQ q 24 h or 2 mg/kg PO q 24 h up to 5 days; or Metoclopramide 0.2-0.5 mg/kg PO or SQ q 6-12 h Decontaminate patient after life-threatening issues addressed: Subclinical (or stabilized clinical) patient only Emesis: effective up to 8-12 h post ingestion (see p. 1364 ) Gastric intubation, gavage, lavage (see p. 1281 ) Consider when emesis is contraindicated (comatose, anesthetized) Activated charcoal: 1-4 g/kg (or labeled dosage) after emesis/lavage; repeat q 8 h during clinical signs of toxicosis Animals without clinical signs/pre-clinical cases: monitor 8-12 hours for development of signs: Maintain urine output (IV fluid diuresis) potassium supplementation Urinary catheter placement: Caffeine is reabsorbed from the urine; urinary catheter helps increase caffeine excretion.
NUTRITION/DIET Bland diet may be indicated for 3-5 days for diarrhea.
DRUG INTERACTIONS Erythromycin, cimetidine, corticosteroids may delay methylxanthine clearance and should be avoided.
POSSIBLE COMPLICATIONS DIC from hyperthermia Myoglobinuria from seizure-induced rhabdomyolysis; renal failure Pancreatitis
RECOMMENDED MONITORING ECG, blood pressure, body temperature Serum electrolytes Fluid ins/outs Urinalysis Pancreatic ultrasound enzymes
PROGNOSIS AND OUTCOME Prognosis is generally good with prompt and thorough care. If severe clinical signs are not controlled, prognosis is guarded to poor. Signs generally resolve in 12-72 hours, depending on methylxanthine dose, severity of signs, and aggressiveness of treatment.
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Chocolate Toxicosis
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PEARLS & CONSIDERATIONS COMMENTS The darker the chocolate, the more dangerous it is. To estimate amount of methylxanthine ingested, add amount of caffeine and theobromine together (see table), multiply by number of ounces ingested, and divide by body weight in kilograms. Half-life in dogs: theobromine = 17.5 hours; caffeine = 4.5 hours Chocolate may form a clump in the stomach, delaying absorption and onset of clinical signs for up to 12 hours.
PREVENTION Keep chocolate-containing products away from pets. Avoid leaving chocolate-containing gifts unsupervised (e.g., under the Christmas tree).
TECHNICIAN TIPS Induction of emesis even several hours after exposure can prevent signs or substantially reduce the severity of signs.
CLIENT EDUCATION Pets fed small amounts of chocolate may develop a taste for it and actively seek out chocolate, leading to intoxication.
SUGGESTED READING Albretsen JC: Methylxanthines. In Plumlee KH, editor: Clinical veterinary toxicology. St. Louis, 2004, Mosby, pp 322–325. Gwaltney-Brant SM: Chocolate intoxication. Vet Med 96:108–110, 2001. Available in PDF form online at: http://www.aspca.org/site/ DocServer/toxbrief_0201.pdf?docID-111. AUTHOR: CAROLINE W. DONALDSON EDITOR: SAFDAR A. KHAN 1ST EDITION AUTHOR: SHARON M. GWALTNEY-BRANT
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Chlamydiosis, Cat
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Chlamydiosis, Cat BASIC INFORMATION DEFINITION A bacterial infection associated mainly with acute and chronic conjunctivitis in cats
SYNONYMS Chlamydia psittaci infection (outdated; current name is Chlamydophila felis) Chlamydophila felis infection Feline pneumonitis (outdated term; the organism is primarily a conjunctival pathogen)
EPIDEMIOLOGY SPECIES, AGE, SEX The prevalence of C. felis in cats with upper respiratory tract disease has ranged from 10%-31%. Cats < 5 years old, and especially < 1 year old, are predisposed. There is no strong sex predilection. RISK FACTORS Young age is the most significant risk factor. CONTAGION & ZOONOSIS Highly contagious between cats (aerosol, direct contact, fomites). C. felis-associated conjunctivitis has been described in a single immunocompromised human. Other reports associating C felis infection with keratoconjunctivitis in people did not provide definitive evidence of infection. The DNA of C. felis has also been detected uncommonly in respiratory samples from humans. Maintenance of hygienic conditions and prompt treatment of cats should help prevent human disease. GEOGRAPHY AND SEASONALITY Worldwide distribution; may be more common in summer. ASSOCIATED CONDITIONS & DISORDERS May be associated with concurrent feline respiratory viral infections such as feline herpesvirus 1 or feline calicivirus infection.
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT Ocular discharge and redness Occasionally decreased appetite Nasal discharge Sneezing PHYSICAL EXAM FINDINGS Ocular signs: blepharospasm, chemo-sis, conjunctivitis, serous to mucopurulent ocular discharge Serous to mucopurulent nasal discharge (always accompanied by conjunctivitis) Possible fever Possible vaginal discharge
ETIOLOGY AND PATHOPHYSIOLOGY
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Chlamydiosis, Cat
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C. felis is an obligately intracellular bacterium related to gram-negative bacteria. The life cycle alternates between an extracellular, infectious elementary body, and an intracellular reticulate body. Reticulate bodies divide within a cytoplasmic vacuole called an inclusion, and are released from the host cell as elementary bodies. Natural transmission probably occurs by close contact with other cats and their aerosols, and via fomites. The incubation period is 3-5 days, and infection may persist for months. Feline chlamydiosis is a systemic disease, and organisms are shed from the conjunctiva, vagina, and rectum. Recently, another chlamydial species has been identified in cats, Neochlamydia hartmannellae; the clinical significance of this organism is yet to be determined.
DIAGNOSIS DIAGNOSTIC OVERVIEW Diagnosis may be suspected based on clinical signs (i.e., marked persistent conjunctivitis) and response to appropriate antimicrobials.
DIFFERENTIAL DIAGNOSIS Infectious causes: Feline herpesvirus 1 Feline calicivirus Bordetella bronchiseptica Mycoplasma spp. Cryptococcus neoformans Aspergillus spp. Noninfectious causes: Eyelid and nasal neoplasia (including nasopharyngeal polyps) Dental disease Congenital eyelid malformations Palate defects Chemical irritants Foreign bodies Trauma Immune-mediated/inflammatory (e.g., eosinophilic keratoconjunctivitis)
INITIAL DATABASE Conjunctival scrapings: may reveal inclusion bodies within epithelial cells when stained with Giemsa. Low sensitivity and specificity.
ADVANCED OR CONFIRMATORY TESTING Human ELISA antigen kits for Chlamydia trachomatis: performed on conjunctival swabs, variable sensitivity and specificity Cell culture: available in specialized laboratories, requires special transport media, and sensitivity varies depending on equipment and technical expertise PCR: performed on conjunctival swabs; sensitivity and specificity varies with the laboratory; quality control may be problematic in some laboratories; ensure positive and negative extraction controls are included with each run Positive serologic titers: correlate well with infection in unvaccinated cats, but reliable assays not yet readily available
TREATMENT TREATMENT OVERVIEW The cornerstone of treatment is antibiotics (doxycycline), with supportive care as needed.
ACUTE GENERAL TREATMENT Doxycycline, 10 mg/kg PO q 24 h for at least 4 weeks Treat all cats in the household simultaneously. Because infection is systemic, use of topical ocular treatment alone is not likely to be effective.
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Chlamydiosis, Cat
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Doxycycline is superior to azithromycin. A 4-week course of amoxicillin-clavulanic acid (2.5 mg/kg PO q 12 h) may also eliminate C. felis.
POSSIBLE COMPLICATIONS Risk of teeth discoloration in kittens if tetracyclines are used in the last 2-3 weeks of pregnancy or for kittens in the first few months of life. Little evidence that this occurs with doxycycline; amoxicillin-clavulanic acid is an acceptable alternative in this situation. Administration of doxycycline liquid oral suspension minimizes the risk of doxycycline-induced esophagitis associated with tablets (or follow tablet administration with a water bolus by syringe).
RECOMMENDED MONITORING Consider retesting with PCR or cell culture in problem cattery situations after treatment to ensure infection has been eliminated.
PROGNOSIS AND OUTCOME Excellent in households with low numbers of cats Fair in cattery situations; recurrent cases involve large numbers of cats and poor compliance. All cats in the household must be treated with the full course of antimicrobials and proper hygiene and quarantine maintained. Concurrent infections with feline calicivirus and feline herpesvirus 1 are a common problem.
PEARLS & CONSIDERATIONS COMMENTS There is some evidence that C. felis may infect the reproductive tract and cause vaginal discharge. Abortion and infertility have been documented in some cats infected with C. felis, but in general it appears that C. felis does not cause feline reproductive disease. There is experimental evidence that C. felis may be associated with lameness in cats.
PREVENTION Maintenance of environmental hygiene in catteries and disinfection of fomites with a 1:32 solution of bleach in tap water, to which detergent may be added Modified live and inactivated cell culture vaccines are available, which do not prevent infection or clinical signs, although the latter are reduced in severity. Associated with atypical reactions in a small percentage of cats, including fever, anorexia, and lameness 7-21 days after vaccination May be useful as part of a control program in catteries with endemic chlamydiosis
SUGGESTED READING Dean R, et al: Use of quantitative real-time PCR to monitor the response of Chlamydophila felis infection to doxycy-cline treatment. J Clin Microbiol 43(4):1858– 1864, 2005. McDonald M, et al: A comparison of DNA amplification, isolation and serology for the detection of Chlamydia psittaci infection in cats. Vet Rec 143:97–101, 1998. Sykes JE: Feline chlamydiosis. Clin Tech Small Anim Pract 20:129–134, 2005. AUTHOR: JANE SYKES EDITOR: DOUGLASS K. MACINTIRE
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Cheyletiellosis
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Cheyletiellosis BASIC INFORMATION DEFINITION Cheyletiellosis is a highly contagious, zoonotic skin disease of dogs, cats, and rabbits caused by the surface-living mite, Cheyletiella spp.
SYNONYM Walking dandruff
EPIDEMIOLOGY SPECIES, AGE, SEX Young animals are more frequently affected. GENETICS & BREED PREDISPOSITION Long-haired cats appear to be more commonly affected. RISK FACTORS More common in dogs and cats from shelter and breeding establishments or that have been in boarding and grooming facilities. CONTAGION & ZOONOSIS Cheyletiella spp. mites are very contagious and not host specific; they may transfer readily between dogs, cats, and rabbits. Cheyletiellosis is a zoonotic disease; humans are at risk if exposed to an infested pet (whether or not overt clinical signs are present in the pet).
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT Reason for presentation can be any combination of scaling, pruritus, or zoonosis. PHYSICAL EXAM FINDINGS Scaling (“dandruff”) noted primarily over the dorsum and neck and/or Mild to moderate pruritus or over-grooming in cats and/or Dorsal erythema, papules and crusting can be noted occasionally, particularly in cats (miliary dermatitis) Among the exfoliated epidermal cells, Cheyletiella mites can be seen moving. hence the name “walking dandruff.” The term should not be overinterpreted; the mites are much smaller than skin scales, and a pet has to be very still to enable the clinician to see the subtle movement of mites carrying scales and/or the mites themselves. Some pets not noted by the owner to have clinical signs are presented for evaluation because of suspected zoonotic lesions in a human in contact with the animal.
ETIOLOGY AND PATHOPHYSIOLOGY Cheyletiella is a relatively large mite (0.05 mm, barely visible to the naked eye) with prominent hooklike mouth parts; it lives on the skin surface and feeds on surface debris and exudates. These mites form pseudotunnels in the surface keratin. The mite eggs, smaller than lice eggs, are loosely attached to hair shafts. The entire life cycle is completed on the host within approximately 3 weeks. Although adult mites may survive in the environment for 10 days off the host, eggs are shed into the environment with the pet's hair and may be an important source of reinfestation beyond those 10 days.
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Cheyletiellosis
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DIAGNOSIS DIAGNOSTIC OVERVIEW The diagnosis is suspected from the history and clinical signs, which include any combination of scaling, pruritus, and/or zoonosis (possibly in presence of an animal without cutaneous lesions).
DIFFERENTIAL DIAGNOSIS In dogs, differential diagnosis depends on the clinical presentation. If only scaling is present, differential diagnoses include: Ectoparasites (fleas, lice) Ill thrift or nutritional imbalance (e.g., intestinal parasitism, poor nutrition) Cornification disorders (ichthyosis, primary seborrhea) If pruritus is present, differentials include: Ectoparasites (lice, sarcoptic mange) Hypersensitivities (flea bites, atopic dermatitis, food) Pyoderma Fungal infections (Malassezia, dermatophytosis) In cats, miliary dermatitis due to other causes such as hypersensitivity (flea bites, food, environmental) and dermatophytosis should be considered, as well as other causes of generalized scaling and pruritus. In humans, the pruritic papular eruption (papular urticaria) induced by a hypersensitivity reaction to Cheyletiella mites is often undistinguishable from other zoonotic (fleas, Sarcoptes spp., Dermanyssus spp.) or nonzoonotic arthropod (harvest mites, straw itch mites, bedbugs) bite reactions.
INITIAL DATABASE Confirmation relies on the collection and identification of the mites. Mites and eggs can be harvested using adhesive acetate tape (transparent “Scotch tape”) preparations, superficial skin scrapings, flea combing, fecal flotation, or simply by collecting dislodged scales from the skin surface following rubbing/petting the animal's back. The epidermal debris is examined with a magnifying lens or put on a glass slide, mixed with mineral oil, covered with a cover slip and examined under microscope at low power. The mites and eggs can be found in fairly large numbers, but occasionally they may be difficult to recover, especially in adult cats, owing to their grooming habits.
ADVANCED OR CONFIRMATORY TESTING Cheyletiella eggs and mites can sometimes be identified in a fecal flotation. Therapeutic trials with reliable acaricides are essential to confirm or rule out cheyletiellosis in pruritic or scaling animals with negative samplings, as well as when a human in contact has a pruritic papular eruption evocative of skin lesions caused by zoonotic arthropod bite reactions.
TREATMENT TREATMENT OVERVIEW The goal of treatment is to thoroughly eradicate the mites. All affected and in-contact animals should be treated with an appropriate acaricide regardless of presence or absence of clinical signs. All suspected cheyletiellosis cases should be treated even if the parasite has not been isolated. Environmental treatment may be required in severe cases.
ACUTE GENERAL TREATMENT Selamectin (Revolution/Stronghold [Pfizer]) and moxidectin/imidacloprid (Advantage Multi/Advocate [Bayer]) are not approved for the treatment of cheyletiellosis but appear effective when applied topically every 2-4 weeks for a treatment course of 2 months.
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Cheyletiellosis
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Off-labeled ivermectin remains a popular treatment option in cats and can still be a therapeutic alternative in dogs but should never be used in collies or related breeds carrying the ABCB1 (MDR1) mutation (see p. 706). The injectable product (Ivomec 1% injection for cattle and swine [Merial]) is usually given at a dosage of 0.3 mg/kg q 7 days PO or q 14 days SQ for a 6- to 8-week course of treatment. The 0.5% alcohol based pour-on ivermectin formulation (Ivomec Pour-On for cattle [Merial]) is also effective and practical when applied to the interscapular skin q 14 days at 0.5 mg/kg for 3-4 treatments. Milbemycin oxime (Interceptor [Novartis]) was shown to be effective in dogs but may require up to 9 weekly oral doses (at 2 mg/kg) for eradication of the mites.
POSSIBLE COMPLICATIONS In collies and other herding breeds, the MDR1 (ABCB1) mutation can cause intoxication with commonly recommended dosages of ivermectin or other off-label macrocyclic lactones (see pp. 625 and p. 706).
PROGNOSIS AND OUTCOME Prognosis is excellent. In humans, the zoonotic infestation is transient, with resolution of the pruritic papular eruption when the mites are eradicated from the dog.
PEARLS & CONSIDERATIONS COMMENTS Infested animals may show no clinical signs. Cheyletiellosis is possible even if there is only one animal with clinical signs among a household full of dogs and cats without any clinical signs whatsoever. Due to cross sensitization, a positive intradermal skin test result for the house dust mite antigen is seen in 50% of dogs with cheyletiellosis. All clinical signs resolve and intradermal reaction to house dust mites are generally negative within a few months following acaricidal therapy. This illustrates the importance of ruling out cheyletiellosis prior to testing for atopic dermatitis.
CLIENT EDUCATION Humans transiently infected with Cheyletiella spp. mites may develop an uncomfortable, pruritic papular eruption, especially on the arms, trunk, and buttocks. This should spontaneously resolve within 3 weeks when the mites are eradicated from the animals and the environment. Symptoms should prompt the person to consult with a physician.
SUGGESTED READING Chailleux N, Paradis M: Efficacy of selamectin in the treatment of naturally acquired cheyletiellosis in cats. Can Vet J 43:767–770, 2002. Loft KE, Willesen JL: Efficacy of imidacloprid 10 per cent/moxidectin 2.5 per cent spot-on in the treatment of cheyletiellosis in dogs. Vet Rec 160:528–529, 2007. AUTHOR EDITOR: MANON PARADIS
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Chemotherapy: Adverse Reactions
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Chemotherapy: Adverse Reactions BASIC INFORMATION DEFINITION Chemotherapy targets rapidly dividing cells. However, normal proliferating cells (gastrointestinal [GI] epithelial, bone marrow, others) may be affected, resulting in adverse reactions. In addition, some chemotherapy agents cause unique toxicities.
EPIDEMIOLOGY SPECIES, AGE, SEX Drugs that should not be administered to cats: Cisplatin: fatal pulmonary edema 5-Fluorouracil: fatal neurologic signs Toxicities not generally observed clinically in cats: Cyclophosphamide: hemorrhagic cystitis Doxorubicin: despite documented histologic changes, cardiotoxicity not seen clinically GENETICS & BREED PREDISPOSITION Several herding breeds (collie, Australian shepherd, Shetland shepherd, German shepherd, border collie, Old English sheepdog, and others), sight hounds (longhaired whippet and silken wind-hound), and mixed breed dogs have been reported to have mutations in the ABCB1 gene, which may result in decreased expression of P-glycoprotein (P-gp) and increased risk of toxicity with drugs that are substrates for this protein (see p. 706). RISK FACTORS ABCB1 mutation (see Genetics & Breed Predisposition above): increased toxicity with P-gp substrates including vincristine, vinblastine, doxorubicin, and others Significant infiltration of bone marrow by neoplastic cells: myelosuppression Neoplastic GI involvement: GI toxicity Clinically ill patients may be more likely to develop adverse effects and should receive concurrent supportive care. Preexisting cardiomyopathy: increased risk of doxorubicin cardiotoxicity Preexisting renal dysfunction: increased risk of toxicity with renally excreted drugs; increased risk of cisplatin nephrotoxicity Preexisting hepatic dysfunction: increased risk of toxicity with drugs eliminated by the liver and possible increased risk of hepatotoxicity
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT Administration of associated chemotherapeutic agent PHYSICAL EXAM FINDINGS Adverse reactions occurring during administration: Allergic reactions (L-asparaginase, doxorubicin, taxanes [rarely used]) Facial swelling, erythema, urticaria, panting, agitation, vomiting, diarrhea, dyspnea, tachypnea, collapse, hypotension Extravasation injury (vincristine/vinblastine, doxorubicin, actinomycin D, dacarbazine, mechlorethamine, cisplatin) No immediate signs Erythema, inflammation, licking site 7-14 days post treatment Can progress to slough of skin and subcutis Acute vomiting—Common: cisplatin, dacarbazine, streptozotocin. Less common: doxorubicin, cyclophosphamide, mechlorethamine, procarbazine Vomiting during/within 24 hours of chemotherapy Delayed adverse reactions:
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GI toxicity—Common: doxorubicin, MOPP (mechlorethamine, vincristine, procarbazine, prednisone) protocol, cisplatin, dacarbazine. Less common: vincristine, vinblastine, cyclophosphamide, CCNU (lomustine, rare), mitoxantrone, carboplatin, actinomycin Vomiting, diarrhea, lethargy, anorexia 2-5 days after chemotherapy Vincristine: may cause paralytic ileus and associated GI signs Doxorubicin: may cause life-threatening hemorrhagic colitis Myelosuppression/sepsis—Most common: CCNU, carboplatin. Possible: doxorubicin, mitoxantrone, cyclophosphamide (especially when combined with vincristine). Usually no overt manifestations Possible: lethargy, loss of appetite, fever with febrile neutropenia/sepsis, generally 1 week post administration Neutrophil count nadir (lowest) typically occurs 7 days after ad ministration. Neutrophil nadir and onset of signs with cisplatin, carboplatin, and CCNU (in cats) is more variable; can occur 1, 2, or 3 weeks post chemotherapy (rarely later) and may be prolonged Unique adverse reactions: Cardiac toxicity (doxorubicin) Arrhythmias, exercise intolerance, weakness, collapse, tachypnea, tachycardia Hemorrhagic cystitis (cyclophosphamide, ifosfamide) Stranguria, pollakiuria, hematuria, incontinence, pain Nephrotoxicity (cisplatin, streptozotocin; uncommon: doxorubicin [cats], CCNU; extremely rare: carboplatin) Often no clinical signs With progression, polyuria, polydipsia, lethargy, decreased appetite Hepatotoxicity (CCNU, streptozotocin) Often no clinical signs If progresses, icterus, lethargy, loss of appetite, GI signs, and abdominal effusion
ETIOLOGY AND PATHOPHYSIOLOGY Allergic reactions—L-asparaginase: type I hypersensitivity reaction. Doxorubicin: directly stimulates mast cell degranulation. Extravasation injury: vesicant injury to local tissue; multiple mechanisms Acute vomiting: irritation of chemoreceptor trigger zone Gastrointestinal toxicity: injury to GI crypt epithelium Myelosuppression/sepsis: injury to proliferating bone marrow cells causes neutropenia and possibly thrombocytopenia. Severe neutropenia allows opportunistic infection, usually by GI bacteria (usually gram-negative, but gram-positive and anaerobic infections possible). Cardiac toxicity: doxorubicin induces acute arrhythmias by increasing circulating catecholamines. Free radical formation by doxorubicin causes cumulative injury to myocardium and fibrosis (doses = 180-240 mg/m2) because of low levels of cardiac catalase and because doxorubicin decreases glutathione peroxidase activity. In addition, changes in transcriptional activity alter cardiac protein expression. Consequences include arrhythmias and decreased contractility, progressing to dilated cardiomyopathy weeks to months after treatment. Hemorrhagic cystitis: metabolite of cyclophosphamide (acrolein) directly toxic to the bladder urothelium Nephrotoxicity: cisplatin, streptozotocin: tubular injury and decreased glomerular filtration (cisplatin) Hepatotoxicity: CCNU causes hepatocellular and ductal epithelial injury with inflammation and cholestasis, eventually progressing to cirrhosis.
DIAGNOSIS INITIAL DATABASE CBC, serum biochemistry profile, urinalysis: Neutropenia, possibly thrombocytopenia (myelosuppression) Azotemia, low urine specific gravity (nephrotoxicity) Hematuria (hemorrhagic cystitis) Elevated liver enzymes (hepatotoxicity) Additional tests (e.g., diagnostic imaging) as determined by history, exam, and lab test results
TREATMENT TREATMENT OVERVIEW Control of toxic effects and prevention of secondary complications are the therapeutic goals.
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ACUTE GENERAL TREATMENT Adverse reactions occurring during administration: Allergic reactions Depends on severity. Dexamethasone, SP 0.2-0.5 mg/kg IV Diphenhydramine, 1-2 mg/kg IM Intravenous fluids, 90 mL/kg/h (dog) or 50 mL/kg/h (cat) Epinephrine if severe (Dilute 1 mL of 1:1000 solution in 9 mL of 0.9% NaCl. Give 0.1 mL/kg of 1:10,000 solution IV.) Extravasation injury Aspirate drug back before removing catheter. Apply compresses (cold for doxorubicin; warm for vincristine/vinblastine) for 10 minutes q 6 h for 72 hours after extravasation. Vincristine/vinblastine: infuse 1 mL 1% hyaluronidase for each mL extravasated. 2
Doxorubicin: administer dexrazoxane (anecdotal dose used by author: 400-600 mg/m IV in a different vein within 3 hours of administration; repeat at 24 and 48 hours). Topical DMSO (dimethyl sulfoxide) gel q 8 h for 14 days (wear gloves when applying) may also be helpful. Wound management: E collar, clip/clean, topical or systemic antibiotic, topical or systemic antiinflammatory Surgical débridement/grafting if severe Acute vomiting Stop administration Nothing by mouth Antiemetic therapy (See section on delayed vomiting for drugs and dosages below.) IV fluid support if indicated Delayed adverse reactions: Gastrointestinal toxicity Nothing by mouth Patient acting normally, self-limiting vomiting: antiemetics (maropitant citrate [dogs] 2 mg/kg PO q 24 h for up to 5 days (in cats has been used at 1 mg/kg PO q 24 h); metoclopramide [dogs or cats] 0.2-0.5 mg/kg PO q 8 h); water trial then bland diet trial. Decreased appetite: tempting bland foods, appetite stimulant (mirtazapine [dogs] 0.6 mg/kg, not to exceed 30 mg/d, PO q 24 h, [cats] 3-4 mg/cat PO q 72 h; or cyproheptadine [cats]: 1-2 mg PO q 12-24 h). Patient acting normally, diarrhea not bloody or watery: bland diet, consider metronidazole, 15 mg/kg PO q 12 h for colitis. Patient lethargic, vomiting/diarrhea continuing, or watery or bloody diarrhea: admit to hospital for supportive care. Intravenous fluids Antiemetics Maropitant citrate (dogs and cats): 1 mg/kg SQ q 24 h, up to 5 days, or Metoclopramide (dogs/cats): 0.2-0.5 mg/kg SQ q 8 h or IV as a CRI at 1.1-2.2 mg/kg/d (if maropitant does not control nausea; also for vincristine-induced ileus). If refractory: Dolasetron: (dogs/cats) 0.6-1 mg/kg IV slowly q 12-24 h Ondansetron: (dogs) 0.1-1 mg/kg IV slowly q 12-24 h; (cats) 0.1-0.15 mg/kg IV slowly q 6-12 h H2 receptor antagonist Famotidine, 0.5-1 mg/kg IV slowly q 12-24 h Antibiotic therapy if bloody vomiting/diarrhea, neutropenic, or febrile Parenteral feeding if prolonged vomiting, enteral feeding tube if prolonged anorexia (rare) Usually resolves in 2-3 days Myelosuppression/sepsis Usually no treatment required. Counts generally normalize within 2-3 days (except carboplatin-prolonged nadirs and CCNU in cats). If neutrophil count < 1000 cells/mcL, consider prophylactic antibiotics for dogs. A common choice is amoxicillin/clavulanic acid, 20 mg/kg PO q 12 h for 4-7 days. For breeds other than Doberman pinschers and if dogs have normal tear production, sulfadiazine-trimethoprim, 15 mg/kg PO q 12 h for 5-7 days is an option. Cats do not usually need prophylactic antibiotics. If febrile or ill, admit to hospital for intravenous fluids and intravenous antibiotics: Base on culture and sensitivity if available (urine, blood, infected site) Empirical treatment option while culture results pending: ampicillin, 22 mg/kg IV q 8 h, with enrofloxacin, 5 mg/kg (cats) or 10 mg/kg (dogs); dilute and give slowly IV q 24 h. Unique adverse reactions: Cardiac toxicity (doxorubicin)
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No treatment beyond management of cardiac disease Avoid additional doxorubicin. Hemorrhagic cystitis (HC) Treat bacterial cystitis if present. Generally self-limiting, but may take weeks to months to resolve. Some dogs show lifelong signs of cystitis. Antiinflammatory: nonsteroidal antiinflammatory drug or prednisone Analgesic: tramadol, 2-4 mg/kg q 8 h PO or another opioid agent Oxybutynin hydrochloride (0.2 mg/kg PO q 8-12 h) has been recommended for straining, pollakiuria Instillation of diluted dimethyl sulfoxide into the bladder may be helpful if refractory. Consultation with an oncologist is recommended for refractory HC. After HC, cyclophosphamide should not be administered again. Often chlorambucil is substituted. Nephrotoxicity Discontinue drug. Treatment usually not necessary, but if clinical or acute renal failure, hospitalize for therapy. Hepatotoxicity Discontinue drug. S -adenosyl-L-methionine (SAMe): anecdotally may be helpful; 18 mg/kg PO q 24 h or divided dose q 12 h. Administer on empty stomach. Treat hepatic dysfunction if indicated.
CHRONIC TREATMENT Cardiac toxicity, chronic bone marrow toxicity, nephrotoxicity, and hepatotoxicity may require ongoing therapy.
DRUG INTERACTIONS Many possible interactions of chemotherapy agents with each other and other drugs. It is the responsibility of veterinarians treating patients with chemotherapy to review possible interactions associated with each agent before administration.
RECOMMENDED MONITORING For all patients undergoing chemotherapy: CBC at the expected time of the neutrophil nadir the first time they receive each drug. CBC rechecked as indicated, especially before administration of potentially myelosuppressive chemotherapy. Serum chemistry profile should be performed every 2-3 months or more frequently if indicated (see p. 503 , p. 501). Urinalysis should be performed every 6 months or more often if indicated.
PROGNOSIS AND OUTCOME With appropriate treatment and supportive care, most patients will recover from delayed adverse reactions and those that occur during administration. Cardiac toxicity, chronic bone marrow toxicity, nephrotoxicity, and hepatoxicity generally do not resolve but may improve or stabilize.
PEARLS & CONSIDERATIONS COMMENTS Clinicians treating veterinary cancer patients must know the complications associated with chemotherapeutic agents and be able to take appropriate preventive measures and manage adverse effects. It is essential to understand the metabolism and excretion of chemotherapy agents when treating patients with organ dysfunction, because dose reductions or avoidance of certain drugs may be necessary. It is also essential to understand drug interactions that might exacerbate toxicity with chemotherapeutic agents.
TECHNICIAN TIPS Multiple toxicities are possible during chemotherapy administration. It is critical that technicians administering these drugs know these toxicities and how to prevent them, recognize them, and manage them. Signs of serious chemotherapy toxicity may be as subtle as lethargy and loss of appetite. It is important to educate clients to communicate with the veterinarian and veterinary technicians if their pet is not normal to them. The majority of adverse effects associated with chemotherapy occur on a predictable timetable. Veterinarians and technicians
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treating patients with these drugs should know when relevant toxicities would be expected and be able to recognize signs of these toxicities. It is important to remember that veterinary cancer patients receiving chemotherapy can develop illnesses unrelated to their cancer or chemotherapy.
PREVENTION Double-check all dose calculations, route of administration, and patient's history, exam, and lab test results prior to administration. Consider testing breeds at risk for MDR-1 mutation. Allergic reactions L-Asparaginase: premedicate (20 minutes pretreatment): diphenhydramine, 2 mg/kg IM, then monitor patient 30-60 minutes post treatment. If allergic reaction, patient should not receive this drug again. Doxorubicin: administer slowly (1 mg/min, not faster than 10 minutes for doses 104○F (>40○C) Joint swelling Pain Myalgia Oral ulcers possible Kitten/cat may eat well but be reluctant to walk Virulent systemic form: Fever Facial and limb edema that may progress to necrosis Upper respiratory signs Icterus with pancreatitis Dyspnea Epistaxis and/or hematochezia Ulcerations in mouth, face, muzzle, pinna, and extremities Pneumonia Pericarditis Death
ETIOLOGY AND PATHOPHYSIOLOGY Infection with FCV, an RNA virus with multiple subtypes of varying degrees of virulence and cross-reactivity, is acquired predominantly via ingestion. Spread by aerosol route less likely Replication occurs in oropharyngeal tissues, with spread primarily to epithelium of conjunctiva, nose, and oral cavity, including the tongue and palate. Rapid cytolysis of infected cells ensues. In the virulent systemic form, signs result from vasculitis and development of disseminated intravascular coagulation/systemic inflammatory response syndrome.
DIAGNOSIS DIAGNOSTIC OVERVIEW Presumptive diagnosis is primarily based on history, physical examination, and clinical signs. Virus identification must be interpreted carefully; it rarely affects treatment and is mainly of academic interest.
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Calicivirus, Cat
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DIFFERENTIAL DIAGNOSIS Feline herpesvirus 1: Cough and keratitis more likely with feline herpesvirus infection Oral ulceration less likely with feline herpesvirus infection Chlamydiosis Mycoplasmosis Bordetellosis Corneal injury/trauma Oral/lingual ulceration accompanied by fever may be caused by licking of surgical and/or hospital disinfectants from feet or fur.
INITIAL DATABASE Fluorescein staining of corneas to rule out corneal ulcers/injury Feline leukemia/feline immunodeficiency virus tests to rule out underlying immune compromise No characteristic findings on CBC, biochemical profile, or urinalysis
ADVANCED OR CONFIRMATORY TESTING Viral culture Viral identification usually not warranted except in cases of virulent systemic calicivirus infection
TREATMENT TREATMENT OVERVIEW Treatment is aimed at controlling pain, maintaining supportive care, treating secondary bacterial infection, and preventing spread to unaffected cats. Therapeutic goals are to maintain hydration and nutrition; provide pain relief for ulcers, joint/muscle pain; and control secondary bacterial infection.
ACUTE GENERAL TREATMENT Fluids to maintain hydration Syringe feeding if anorexic Erythromycin ophthalmic ointment to combat potential secondary Chlamydia or Mycoplasma infections Buprenorphine (0.01-0.03 mg/kg q 8-12 h IM, IV, PO) may be considered for analgesia. Sucralfate slurry dribbled on lingual ulcers may be beneficial. α-Interferon may inhibit viral replication.
CHRONIC TREATMENT Recrudescence of clinical disease is uncommon. Cats may be susceptible to infection with new subtypes.
NUTRITION/DIET Feeding tubes may be required for nutritional support in cases with severe or protracted oral ulceration (see p. 1270 ).
DRUG INTERACTIONS Nonsteroidal antiinflammatory drugs and steroids are discouraged, owing to risks and interference with therapeutic benefits of fever and cytokine release.
POSSIBLE COMPLICATIONS Interstitial viral pneumonia and/or secondary bacterial pneumonia can be life-threatening complications. Oral ulcers and arthritis usually resolve without complication. Sudden dyspnea may occur if pneumonia develops.
RECOMMENDED MONITORING
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Clinical signs
PROGNOSIS AND OUTCOME Prognosis is good for recovery from typical calicivirus infection with supportive care. By contrast, a mortality rate of 40% is reported for the virulent systemic form.
PEARLS & CONSIDERATIONS COMMENTS Constant viral mutation within individuals and endemically infected populations may account for extreme variation in virulence between subtypes. Recovered cats remain lifelong carriers. Virus is shed continuously from oral cavity, regardless of health status or stress. Properly vaccinated cats may become infected with different subtypes.
PREVENTION Proper husbandry to prevent cat-to-cat contact and cross-contamination during cleaning and feeding procedures. FCV is stable and resistant to many disinfectants, except bleach (sodium hypochlorite) diluted 1 part bleach to 32 parts tap water. Proper vaccination at 8-10 weeks, after 12 weeks of age, 1 year later, and every 3 years afterward.
TECHNICIAN TIPS All cats, especially kittens, seen with signs of upper respiratory tract infection should be considered FCV-infected so that appropriate precautions can be taken to limit spread within the hospital.
CLIENT EDUCATION Emphasize proper vaccination In catteries, consider immunizing kittens from carrier queen as early as 6 weeks of age.
SUGGESTED READING Hurley KF: Feline Calicivirus: What's virulent, what's not, and how worried should you be? Proceedings of the Feline Medicine Symposium 2009, University of California, Davis, January 25, 2009, last date of access is July 1, 2009, http://www.vin.com/Members /Proceedings/Proceedings.plx?CID–UCDFMC2009&PID–26536&O–VIN Hurley KF, et al: An outbreak of virulent systemic calicivirus disease. J Am Vet Med Assoc 224:241, 2004. Pesavento PA, et al: Pathologic, immunohisto-chemical, and electron microscopic findings in naturally occurring virulent systemic feline calicivirus infection in cats. Vet Pathol 41:257, 2004. AUTHOR: CHRISTINE L. WILFORD EDITOR: RANCE K. SELLON
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Calcium Channel Blocker Drug Toxicosis
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Calcium Channel Blocker Drug Toxicosis BASIC INFORMATION DEFINITION Calcium channel blocker (CCB) drugs are commonly used for the treatment of hypertension and tachyarrhythmias in human and veterinary medicine. Adverse effects at therapeutic dose or with overdose result in hypotension and bradycardia or tachycardia, causing weakness, ataxia, and inappetence within 30 minutes to 12 hours after ingestion.
EPIDEMIOLOGY SPECIES, AGE, SEX Animals of all breeds, ages, and both sexes are susceptible. Exposure is more common in dogs. RISK FACTORS Preexisting renal or cardiovascular disease may predispose to signs. Hepatic disease may reduce metabolism and elimination of CCBs.
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES Sustained/controlled/extended/delayed-release preparations may delay onset of signs (6-12 hours), whereas immediate-release preparations can cause signs within 30 minutes. HISTORY, CHIEF COMPLAINT History of suspected or observed exposure Weakness, depression, ataxia, vomiting possible PHYSICAL EXAM FINDINGS Hypotension and bradycardia are common; reflex tachycardia is possible if hypotension predominates (dihydropyridine CCBs). Pale mucous membranes Hypothermia possible (due to hypotension) Depression, ataxia, seizures, or coma possible Dyspnea possible (pulmonary edema)
ETIOLOGY AND PATHOPHYSIOLOGY Source: Prescription medication (human or veterinary) Dihydropyridine-type CCBs (e.g., amlodipine [Norvasc]) have effects that are confined to vascular smooth muscle. Thus they are used for treating hypertension. Nondihydropyridine-type CCBs (benzothiazepines such as diltiazem [Dilacor, Cardizem] or phenylalkylamines such as verapamil [Isoptin, Calan]) have greater potency in cardiac muscle and cardiac nodal tissues than in the vasculature. Thus they are used for treating arrhythmias and cardiomyopathy. Mechanism of Toxicosis: CCBs close L-type calcium channels by binding to their α-subunit. Decreased calcium influx results in vasodilation (dihydropyridine-type) or a decrease in cardiac contractility and electrical impulse conduction at the SA and AV nodes (nondihydropyridine-type). CCBs decrease pancreatic insulin secretion, resulting in hyperglycemia.
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CCBs may cause noncardiogenic pulmonary edema (mechanism unknown)
DIAGNOSIS DIAGNOSTIC OVERVIEW The diagnosis is suspected based on observation or evidence of ingestion (chewed container) along with physical exam findings of hypotension and/or bradycardia. Confirmation with plasma drug levels is uncommonly performed, and treatment generally should be initiated without such results.
DIFFERENTIAL DIAGNOSIS Toxicologic: β-Adrenergic receptor antagonists overdose (propranolol, metoprolol), α2-adrenergic receptor agonists (imidazoline-type decongestants), cardiac glycosides (example: digoxin, some cardiac glycoside containing plants; bufo toad toxicosis), antidepressant toxicosis, organophosphate and carbamate insecticides Spontaneous, nontoxicologic: Primary cardiac disease, systemic illness causing hypotension
INITIAL DATABASE Blood pressure (see ): hypotension Electrocardiogram (ECG; see ): Sinus bradycardia, AV block with verapamil or diltiazem Sinus tachycardia with dihydropyridines Serum chemistry profile: hyperglycemia, hypokalemia, hypophosphatemia, hypomagnesemia possible Acid-base status: lactic acidosis possible
ADVANCED OR CONFIRMATORY TESTING Plasma CCB levels may be measured at a human hospital for confirmation. Therapeutic monitoring to assess response to treatment is not useful, as reference ranges have not been established for animal.
TREATMENT TREATMENT OVERVIEW Treatment consists of decontamination (emesis and charcoal administration), stabilizing the cardiovascular system, and maintaining tissue perfusion by maintaining adequate blood pressure during the course of toxicosis. If no clinical signs are present, continuous monitoring in a veterinary facility for 12-24 hours or longer following ingestion is recommended; signs can be delayed, especially with extended release formulations.
ACUTE GENERAL TREATMENT Decontamination Emesis with a recent ingestion or in an animal showing no overt signs of toxicosis (see ) Activated charcoal: 1-2 g/kg (or labeled dosage) with a cathartic PO following emesis (if performed); repeat half the original dose q 6 h for large ingestions or extended-release preparations. Gastric lavage: if large number of tablets, which can form concretions Enema (see p. 1258): consider if the medication is an extended-release preparation, as significant absorption can occur in colon; 2.5-5 mL/kg of warm tap water or isotonic saline Fluid therapy Fluid rate should be guided by blood pressure monitoring; avoid volume overload (iatrogenic pulmonary edema). Treatment of hypotension IV crystalloid fluids Hetastarch for persistent hypotension Dogs: 20 mL/kg/d IV; initial 5 mL/kg bolus over 15-30 minutes, followed by CRI of 15 mL/kg/day Cats: 10 mL/kg/d IV Calcium chloride or calcium gluconate for refractory hypotension; monitor continuous ECG, and discontinue if bradycardia worsens. Calcium chloride provides 3 times more calcium per mL than calcium gluconate.
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Calcium Channel Blocker Drug Toxicosis
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Calcium chloride and calcium gluconate are very irritating and can cause tissue necrosis if extravascular; use indwelling catheter. Calcium chloride (10% solution; 27.2 mg Ca/mL): 0.1-0.5 mL/kg slow IV bolus or CRI of 0.01 mL/kg/h (5 mg/kg/h), or Calcium gluconate (10% solution; 9.3 mg Ca/mL): 50-150 mg/kg (0.5-1.5 mL/kg) slow IV over 5 minutes to effect or CRI of 5 mg/kg/h (0.05 mL/kg/h). If hypotension persists after crystalloids, hetastarch, and calcium supplementation, dopamine (1-20 mcg/kg/min IV CRI) may be used, provided the patient is volume-expanded/well hydrated. Severe bradycardia/AV block: Atropine: 0.02-0.04 mg/kg IV, SQ, or IM; repeat as needed; or Isoproterenol: 0.4 mg in 250 mL of D5W, drip slowly IV to effect; or Temporary cardiac pacing (see ) Control seizures (see p. 1009) with diazepam (0.5-1 mg/kg IV) or pentobarbital (3-15 mg/kg IV slowly to effect). Supplement potassium in hypokalemic patients when the potassium is below 2.5 mEq/L. Oxygen therapy if pulmonary edema occurs
CHRONIC TREATMENT Some animals may need continued treatment for renal insufficiency.
DRUG INTERACTIONS CCBs will increase blood levels of propranolol and digoxin. Propranolol, ketoconazole, and itraconazole increase CCB levels by reducing clearance of CCBs. Cimetidine will increase bioavailability of CCBs. Phenobarbital will increase clearance of CCBs.
POSSIBLE COMPLICATIONS Pulmonary edema Renal insufficiency due to decreased renal perfusion
RECOMMENDED MONITORING Blood pressure ECG Electrolytes Serum chemistry panel, especially renal parameters Respiration (rate, lung sounds, pulse oximetry) CNS signs
PROGNOSIS AND OUTCOME Prognosis is generally good with prompt treatment. Refractory hypotension, severe hyperglycemia, and pulmonary edema may convey a guarded prognosis. After recovery, long-term effects are uncommon. Organ dysfunction secondary to sustained hypotension is possible, such as myocardial ischemia or renal failure.
PEARLS & CONSIDERATIONS COMMENTS Many preparations of CCBs are sustained-, controlled-, extended-, or delayed-release medications, which may substantially lengthen the onset and duration of signs. Bezoar formation is possible with ingestion of large quantities of sustained/controlled/extended/delayed-release preparations, especially nifedipine. Signs of toxicosis can occur at veterinary therapeutic doses of CCBs. These medications have a narrow margin of safety. Noncardiogenic pulmonary edema is possible as a toxic effect; fluid overload should be avoided.
PREVENTION
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Owners should keep all medications out of reach of pets.
TECHNICIAN TIPS It is important to know whether CCB involved in the intoxication is regular or extended-release medication.
CLIENT EDUCATION Owners should be made aware of possible adverse effects when veterinary patients are prescribed CCBs.
SUGGESTED READING Costello M, Syring RS: Calcium channel blocker toxicity. J Vet Emerg Crit Care 18:54, 2008. AUTHOR: CRISTINE HAYES EDITOR: SAFDAR KHAN
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Calcipotriene/Vitamin D3 Analog Toxicosis
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Calcipotriene/Vitamin D3 Analog Toxicosis BASIC INFORMATION DEFINITION Synthetic vitamin D3 analogs are used topically for treating psoriasis in human and occasionally for treating some skin conditions in dogs and cats. Toxicosis manifests acutely with nonspecific signs of illness and within days may cause kidney disease/renal failure.
SYNONYMS Calcipotriene, calcipotriol = 1,25 dihydrocholecalciferol (= calcitriol) analog; Tacalcitol = 1,24 dihydrocholecalciferol analog; vitamin D2 = ergocalciferol; vitamin D3 = cholecalciferol. Popular brands (calcipotriene): Dovonex; Taclonex, Dovobet (calcipotriene 0.005% or 50 mcg/g)
EPIDEMIOLOGY SPECIES, AGE, SEX Dogs appear to be very sensitive to toxicosis RISK FACTORS Dogs, especially young dogs, with indiscriminate eating habits Patients with chronic kidney disease may be at higher risk for adverse renal effects Presence of vitamin D3 analog in pet's environment
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT History of ingestion of vitamin D3 analog (chewed up tube/capsules) possible Anorexia, vomiting, lethargy, diarrhea within 12-24 hours of ingestion PU/PD (due to renal failure) within24-72 hours PHYSICAL EXAM FINDINGS Depression, lethargy, and weakness Vomiting (hematemesis), diarrhea (melena) Signs of dehydration Cardiac arrhythmias Seizures (usually seen within 1-3 days of ingestion, if at all)
ETIOLOGY AND PATHOPHYSIOLOGY Source: Vitamin D3 analogs are available by prescription as creams, lotions, ointment, and capsules. Toxicosis occurs secondary to acute accidental ingestions by the patient. Mechanism of Toxicosis: Through calcium-binding proteins, vitamin D3 analogs increase the amount of calcium absorbed from the intestines, as well as increasing bone resorption of calcium and renal tubular resorption of calcium. The result is hypercalcemia and hyperphosphatemia. Unregulated increases in calcium and phosphorus result in soft-tissue mineralization, especially kidneys, myocardium, large blood vessels, and GI tract.
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Calcipotriene/Vitamin D3 Analog Toxicosis
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DIAGNOSIS DIAGNOSTIC OVERVIEW Diagnosis is based on suspected or confirmed history of exposure to calcipotriene or other vitamin D3 analogs and development of clinical signs including vomiting, anorexia, weakness, and lethargy initially; polydipsia, polyuria, and renal failure >24-72 hours after exposure. Hypercalcemia and hyperphosphatemia are noted in virtually all clinically important cases at first and may normalize while renal values rise (renal damage is due to precipitation of calcium in kidneys, and in certain cases, serum calcium and phosphorus levels may have normalized while azotemia persists), indicating renal failure. A patient with normal serum Ca, P, and renal values 3 or more days after exposure either was not exposed or received a minor exposure.
DIFFERENTIAL DIAGNOSIS Rodenticide cholecalciferol ingestion Other causes for hypercalcemia (see pp. 553 and 1397) plus hyperphosphatemia include chronic kidney disease, hypoadrenocorticism, lymphoma, perianal adenocarcinoma, multiple myeloma, osteolytic tumors.
INITIAL DATABASE CBC and serum biochemical profile (hyperphosphatemia and/or hypercalcemia usually in 12 hours; increased BUN, creatinine within 1-3 days if at all; monitor at least every 24 hours for 3-4 days or longer if abnormalities noted. Calcium (mg/dL) phosphorus (mg/dL) product (historically, >70 has suggested greater risk for dystrophic mineralization) Urinalysis including specific gravity Abdominal and thoracic radiographs +/− ultrasound (dystrophic mineralization)
ADVANCED OR CONFIRMATORY TESTING Rarely practical during active management of toxicosis Increased serum 25-hydroxycholecal-ciferol; no assays available to detect calcipotriene in clinical cases Total wet weight calcium may be elevated in kidneys. Histopathologic evidence of tissue mineralization (kidneys, aorta, GI mucosa, lungs, heart)
TREATMENT TREATMENT OVERVIEW Immediate treatment of renal failure, cardiac arrhythmias, and seizures as needed Prevention of absorption by inducing emesis and administering activated charcoal in promptly presented patient (no clinical signs) Promote calciuresis and limit calcium and phosphorus absorption from intestine. Inhibit release of calcium and phosphorus from bone. Judicious supportive care, notably with intravenous fluids
ACUTE GENERAL TREATMENT Prevent absorption: emesis if 180 bpm. Sustained fetal heart rates 15 mm after 1 minute in dogs, variable in cats) Fluorescein dye application Intraocular pressure (normal: 10-25 mm Hg) Examination of the eyelid margin and palpebral conjunctiva with magnification and a good light source Examination of the cornea
ADVANCED OR CONFIRMATORY TESTING Magnification 5 to 10× is often needed to visualize ectopic cilia.
TREATMENT TREATMENT OVERVIEW Treatment goals are to eliminate ocular irritation; to determine if distichiasis, trichiasis, or ectopic cilia are responsible for clinical signs of ocular disease; and to remove the offending cilia or direct the cilia away from the globe. The presence of distichiasis and/or trichiasis without signs of ocular irritation does not require treatment.
ACUTE GENERAL TREATMENT Distichiasis: Usually does not produce clinical signs; no treatment required Hairs regrow within 4-5 weeks with mechanical epilation/plucking. If clinical signs are present, consider surgical treatment: Before removal, expression of the meibomian glands pushes hidden hairs from the glands. Cryotherapy along the palpebral surface of the meibomian glands using a double freeze/thaw cycle is effective treatment for a large number of distichia in a patient. Electrolysis is useful for single or a low number of cilia; procedure is tedious, and excessive current may cause tissue damage. Carbon dioxide laser removal is tedious and can predispose to excessive tissue damage. Resection from the conjunctival surface effective for single or multiple cilia Eyelid-splitting techniques are not recommended because of the potential for postoperative eyelid deformities and regrowth of hairs. Ectopic cilia: Typically produce clinical signs; therefore treated surgically En-bloc resection of aberrant cilia, including associated conjunctiva and underlying meibomian gland Surgical removal usually successful, but regrowth can occur. Trichiasis: If minor ocular irritation, conservative management may be effective: Clipping hairs short to prevent ocular contact Variable surgical therapies depending on location of trichiasis:
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Distichiasis/Ectopic Cilia/Trichiasis
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Many procedures complex; consider referral to veterinary ophthalmologist. Medial canthal trichiasis may be corrected by permanent medial canthoplasty (pocket technique or Wyman technique) or cryotherapy. Nasal fold trichiasis may require resection of prominent nasal skin folds. Trichiasis associated with ptosis (drooping of the upper eyelid) may be corrected by a Stades procedure. Trichiasis associated with redundant dorsal skin folds may be corrected by extensive removal of tissue or by the use of anchoring sutures to the periosteum. Trichiasis associated with eyelid agenesis in cats may be corrected by cryotherapy until kitten is old enough for permanent surgery (e.g., rotational flap).
CHRONIC TREATMENT If recurrence, repeat treatment may be required
POSSIBLE COMPLICATIONS The most common complication to correction of distichiasis, ectopic cilia, and trichiasis is recurrence. Postoperative eyelid scarring ± entropion
RECOMMENDED MONITORING Have owner monitor animal for signs of recurrent ocular irritation postoperatively; may indicate regrowth of offending hair(s).
PROGNOSIS AND OUTCOME Generally good prognosis, but recurrence is possible regardless of treatment.
PEARLS & CONSIDERATIONS COMMENTS Distichiasis and trichiasis are among the most common eyelid abnormalities. Goal is not simply to diagnose distichiasis or trichiasis, but to determine if the abnormal hair(s) is/are causing ocular irritation, as this determination will help decide whether treatment is necessary. Keratitis that presents in a vertical pattern that follows the path of eyelid movement should raise the suspicion of an ectopic cilium in the upper eyelid. Magnification commonly is needed to identify ectopic cilia, and without a magnifying glass or loupe, the diagnosis should not be ruled out based on absence of visualization. Ectopic cilia and hairs causing distichiasis will regrow within 4-5 weeks with mechanical epilation/plucking. No single treatment guarantees permanent resolution of distichia, ectopic cilia, or trichiasis.
PREVENTION Avoid breeding affected or closely related dogs.
CLIENT EDUCATION Presence of distichiasis or trichiasis does not indicate disease. Animals with distichiasis, ectopic cilia, or trichiasis are monitored for signs of ocular irritation. Recurrence is possible regardless of treatment.
SUGGESTED READING Stades FC, Gelatt KN: Diseases and surgery of the canine eyelid. In Gelatt KN, editor: Veterinary ophthalmology, ed 4, Ames, 2007, Blackwell Publishing, p 563. AUTHOR: PHILLIP A. MOORE EDITOR: CHERYL L. CULLEN
24-09-2011 19:09
Distemper, Canine
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Distemper, Canine BASIC INFORMATION DEFINITION Viral disease principally of young dogs and caused by a morbillivirus of the family Paramyxoviridae. Clinical disease includes mild to severe systemic illness with high morbidity and variable mortality (mortality often related to central nervous system [CNS] infection).
SYNONYMS Distemper, hardpad disease
EPIDEMIOLOGY SPECIES, AGE, SEX Dogs, especially urban or suburban dogs between 3 and 6 months of age Other susceptible species include additional members of the order Canidae (coyote, dingo, wolf, fox), ferrets, mink, skunk, raccoon, panda, and select members of the order Felidae (lion, cheetah, jaguar, margay, ocelot). GENETICS & BREED PREDISPOSITION More common, with higher mortality rates, in dolichocephalic breeds versus brachycephalic breeds RISK FACTORS Inadequate vaccination, exposure to animals with clinical or subclinical disease, transplacental transmission, and exposure of vaccinated but immunocompromised animals to an infected animal CONTAGION & ZOONOSIS Highly contagious (aerosol route most common) between infected, shedding individuals and susceptible individuals. Not considered zoonotic. ASSOCIATED CONDITIONS & DISORDERS Hyperkeratosis of the footpads (hardpad disease) Ocular signs (anterior uveitis, optic neuritis, retinal degeneration, keratoconjunctivitis) can develop with systemic disease or as a sequela. Postencephalitic epilepsy Myoclonus Persistent anosmia (loss of sense of smell) possible in recovered patients
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES Subclinical to mild disease is probably most common, but systemic/generalized form is the most recognized. Generalized distemper: manifests initially as a respiratory infection followed by gastrointestinal (GI) signs and often CNS signs; CNS signs may manifest concomitant with or after resolution of respiratory and GI signs. Old-dog encephalitis (ODE) likely results from an inflammatory reaction associated with persistent canine distemper virus infection of the CNS gray matter. Clinical signs can include ataxia, compulsive movements such as head pressing or continual pacing, and uncoordinated hypermetric gait. Systemic signs are not associated with this form. Inclusion-body polioencephalitis is a variant of the disease, can occur after vaccination, and only manifests as a CNS disease. The pathogenesis is similar to ODE. HISTORY, CHIEF COMPLAINT
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Distemper, Canine
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With the generalized form of the disease, initial presentation typically includes one or more of the following: lethargy, ocular and nasal discharge (serous or mucopurulent), cough, inappetence, vomiting, diarrhea. A patient with a more advanced form of the disease often has a history of neurologic signs (seizures, ataxia, etc.). PHYSICAL EXAM FINDINGS Systemic disease: as above; fever, ocular signs (keratitis, conjunctivitis, uveitis), loud breath sounds on auscultation, dehydration, cachexia, poor haircoat. Dental abnormalities in dogs that survive neonatal infections (dental enamel hypoplasia, tooth impaction, oligodontia). Neurologic disease: signs indicative of encephalitis or encephalomyelitis (seizures, vestibular signs, cerebellar signs/hypermetria, paresis). Seizures are commonly manifested as “chewing-gum” seizures (vigorous repetitive opening and closing of the mouth) but can also be generalized. Hyperesthesia attributable to viral meningitis is uncommon. Myoclonus (rhythmic twitching of the head, neck, or one or more limbs) occurs as the disease progresses and is very suggestive of canine distemper. Optic neuritis and chorioretinitis can be observed. Systemic and neurologic signs are not always present at the same time. More often, neurologic disease occurs 1-3 weeks after recovery from systemic signs, but the two forms can coincide. Rarely, the neurologic signs will occur weeks to months later.
ETIOLOGY AND PATHOPHYSIOLOGY Certain strains of canine distemper virus (CDV) are more virulent and neurotropic; Snyder Hill strain is associated with polioencephalomyelitis; A75/17 and R252 strains are associated with CNS demyelination. Shedding of the virus begins by the seventh day after infection and may continue for up to 90 days. Shedding is primarily aerosol, but virus can also be recovered from urine, feces, nasal and ocular secretions, and skin. After initial exposure, CDV replicates in the upper-respiratory epithelium tissue macrophages. These cells are carried by the local lymphatics to the tonsils and retropharyngeal and bronchial lymph nodes. Here, the virus multiplies and disseminates systemically in mononuclear cells, creating an initial fever and leukopenia 3-6 days after exposure. Lymphopenia is associated with viral damage to both T and B lymphocytes. Viremia occurs by the ninth day post infection as the virus spreads hema-togenously to epithelial tissues and the CNS. Occurrence of viremia depends on host humoral and cell-mediated immunity. Infection of epithelial tissue correlates with shedding of the virus and occurs through all epithelial secretions, even in animals with subclinical infections. Dogs with adequate humoral and cell-mediated immunity clear the virus by day 14. Dogs with an intermediate level of immunity have infection of the epithelial tissues by day 14. Clinical signs that develop eventually resolve if the antibody titer increases and the virus is cleared from most tissues. Some virus may persist in footpads and CNS. In dogs with poor immunity, virus spreads to many tissues by day 14, including skin, endocrine glands, exocrine glands, and epithelial cells of the intestinal tract, the respiratory system, and the genitourinary tract. Clinical signs are usually severe; secondary bacterial infections are common (although this advances morbidity, studies indicate it does not increase mortality). CNS infection occurs hematogenously. CDV enters the CNS through meningeal perivascular spaces, the choroid plexus, and the ventricular ependymal cells. Acute CDV encephalomyelitis occurs early in the course of the disease of young and immune-deficient dogs, causing a polioencephalomyelitis. Full recovery from CDV infection in young animals is uncommon, but likely produces lifelong immunity. Transplacental infections can result in abortions or stillbirths. Puppies that survive transplacental infections can develop neurologic signs by 6 weeks of age and often have lifelong immunodeficiency. Some dogs will continue to shed the virus for up to 2 months after infection.
DIAGNOSIS DIAGNOSTIC OVERVIEW A presumptive diagnosis in a young, unvaccinated dog is made based on presentation of clinical signs that include oculonasal discharge, vomiting, and/or diarrhea with or without a recent onset of neurologic signs. Older dogs can initially present with signs consistent with infectious tracheobronchitis. Clinical confirmation typically comes from a blood sample submitted for immunofluorescent antibody testing of white blood cells, or anti-CDV antibody titers in cerebrospinal fluid (CSF).
DIFFERENTIAL DIAGNOSIS Canine infectious tracheobronchitis Canine parvoviral enteritis Other CNS diseases of young dogs
24-09-2011 19:08
Distemper, Canine
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INITIAL DATABASE CBC can reveal an absolute lymphopenia; rarely, CDV inclusions are identified in lymphocytes, monocytes, neutrophils, or erythrocytes. Serum biochemistry profile and urinalysis are variable and not definitive for CDV. Thoracic radiographs: interstitial pattern in early phases; evidence of bronchopneumonia in later stages with secondary bacterial infection
ADVANCED OR CONFIRMATORY TESTING Serum antibody testing: elevated serum IgM titers in unvaccinated dogs confirm recent exposure or current infection. CSF Elevated CSF protein and lymphocytic pleocytosis are typical. Presence of CSF antibody titers to CDV are confirmatory when there is no blood contamination of the sample. With potential blood contamination of the CSF sample, paired samples of CSF and serum are tested for CDV and canine parvovirus (CPV) antibody titers; since CPV does not cross the blood-brain barrier, a CDV/CPV ratio that is higher in CSF than in blood suggests CDV infection. Severely immunosuppressed patients or those with the noninflammatory demyelinating form of CDV may have normal CSF, often with low CSF protein (10 years of age. Purebred dogs may be predisposed, especially Great Danes. Has also been seen in small-breed dogs as well as in cats. GENETICS & BREED PREDISPOSITION German shepherds are overrepresented for fungal diskospondylitis. CONTAGION & ZOONOSIS Diskospondylitis caused by Brucella canis carries the possibility of zoonosis.
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT Variable clinical presentation Most dogs show progressive clinical signs over several weeks, but some dogs develop clinical signs acutely. Clinical signs are often nonspecific (fever, anorexia, weight loss, lethargy, depression) but usually include spinal hyperpathia. PHYSICAL EXAM FINDINGS General physical and neurologic examination findings (see p. 1311 ) vary depending on the location, severity, and secondary effects of the infection. Patients examined early in the course of the disease often show only signs of spinal hyperpathia without paraparesis. Later, patients may have more severe spinal hyperpathia with varying degrees of paraparesis. Occasionally, patients present with an acute onset of back pain with associated ambulatory or nonambulatory paraparesis/paraplegia.
ETIOLOGY AND PATHOPHYSIOLOGY Some dogs that develop diskospondylitis may have underlying immune compromise. Infectious organisms may gain access to the disk space and vertebrae via several mechanisms. Hematogenous spread of bacteria or fungi: the most common mechanism, although the primary source of infection is not always found. The urinary tract is the most likely source of infection. Other sources, although rare, are bacterial endocarditis and dental disease. Foreign-body migration: most commonly a grass awn. Plant materials have barbed ends that allow them to migrate through tissues (via inhalation and migration through the lungs or diaphragm, ingestion and subsequent penetration through the bowel wall, or transcutaneous penetration), carrying bacteria to the disk space. Iatrogenic: infection may develop after spinal surgery or paravertebral injection. Bacterial organisms that are involved are usually coagulase-positive Staphylococcus organisms (S. pseudintermedius, S. aureus.) Other bacterial pathogens include Streptococcus species, Brucella canis, and Escherichia coli. Less frequently isolated bacteria are Pasteurella, Proteus, Corynebacterium, Actinomyces, Nocardia,
24-09-2011 19:04
Diskospondylitis
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Bacteroides, and Mycobacterium species. Fungal organisms include Aspergillus and Paecilomyces species.
DIAGNOSIS DIAGNOSTIC OVERVIEW Radiographs are the most useful diagnostic tool. Changes first appear 2-4 weeks after the onset of clinical signs.
DIFFERENTIAL DIAGNOSIS Radiographically, diskospondylitis must be distinguished from spondylosis deformans and spinal neoplasia: Spondylosis and sclerosis are common both in spondylosis deformans and diskospondylitis, but vertebral endplate lysis is seen only in diskospondylitis. Typically, in spinal neoplasia the lytic lesion is confined to a single vertebra, whereas in diskospondylitis, the lysis is associated with adjacent vertebrae.
INITIAL DATABASE CBC, serum biochemistry panel: typically unremarkable Leukocytosis may be seen if there are concurrent systemic abnormalities (e.g., pyometra, prostatic abscess, endocarditis). Urinalysis reveals bacterial cystitis in up to 40% of cases. The same organism is occasionally identified in both urine and blood cultures. Blood cultures should be obtained whenever possible. Cerebrospinal fluid is typically normal. Brucella titers may be positive. Because of the zoonotic potential, this titer should be performed in all sexually intact patients suspected of having diskospondylitis. Radiographs are the most useful diagnostic tool. Changes first appear 2-4 weeks after the onset of clinical signs. Collapse of the disk space Proliferative bony changes adjacent to the intervertebral disk space Sclerosis at the bony margins The first radiographic signs are usually a collapsed intervertebral disk space, with or without subtle vertebral endplate erosion. With more chronic infections, the bone becomes more sclerotic, and ventral spur formation occurs. This is often accompanied by marked osteolysis and inflammatory new bone formation. Multiple sites of involvement are found in approximately 40% of cases. The most common site for diskospondylitis is L7/S1.
ADVANCED OR CONFIRMATORY TESTING The most sensitive procedure for identifying infectious organisms associated with diskospondylitis is culture of surgically obtained tissue. Samples can be taken at the time of surgery (if indicated for decompression), but otherwise it is an invasive diagnostic tool. Fluoroscopically guided percutaneous disk aspiration has been shown to be useful in obtaining a positive culture in approximately 75% of cases. Myelography and MRI are useful tools to identify spinal cord compression. The vertebral endplates often demonstrate strong contrast enhancement with MRI.
TREATMENT TREATMENT OVERVIEW Successful treatment of diskospondylitis depends on long-term antibiotic therapy.
ACUTE AND CHRONIC TREATMENT When a specific causative agent is not identified, empirical treatment with antibiotics is warranted. The most common causative bacteria are coagulase-positive Staphylococcus spp., which are generally sensitive to first-generation
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Diskospondylitis
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cephalosporins or β-lactamase-resistant penicillins. Antibiotic treatment usually results in improvement of spinal hyperesthesia within 4-5 days. If there is no improvement within 7-10 days of starting antibiotics, the case should be reevaluated (if not already done, consider blood or urine culture, fungal titers, aspiration of the lesion, etc.). Antibiotic therapy should be continued for at least 6 weeks after clinical and radiographic improvement is seen. Specifically, antibiotic therapy should be continued until there is no additional or persistent bony lysis, which is considered a radiographic sign of progression of the disease. In most cases, antibiotic therapy is prolonged and may easily be required for a year from onset of therapy. With positive Brucella test results, options include antibiotic treatment, with strict control of exposure to other dogs, or euthanasia (see Brucellosis, Dog, p. 162). Limited success is seen using itraconazole in fungal diskospondylitis. Surgical treatment: based on imaging studies and clinical signs (e.g., vertebral instability or spinal cord compression associated with neurologic deficits); spinal cord decompression via a dorsal or hemilaminectomy may be indicated.
Organisms That Cause Diskospondylitis and Recommended Antibiotics (Pending Culture and Sensitivity) Organism
Antibiotic
Staphylococcus species Cephalexin
Dosage 22 mg/kg PO q 8 h
Amoxicillin-clavulanate 13.75 mg/kg PO q 12 h Streptococcus species
Amoxicillin
22 mg/kg PO q 12 h
Brucella canis
Enrofloxacin
5 mg/kg PO q 12 h
Doxycycline
25 mg/kg PO q 12 h
Enrofloxacin
5 mg/kg PO q 12 h (dog)
Cephalexin
22 mg/kg PO q 12 h
Escherichia coli
Amoxicillin-clavulanate 13.75 mg/kg PO q 12 h Actinomyces species
Penicillin G
100,000 U/kg IM, SC q 6 h
Aspergillus species
Itraconazole
5 mg/kg PO q 12 h
BEHAVIOR/EXERCISE Exercise restriction is recommended for these patients to keep them comfortable and lessen the risk of trauma to the spine.
RECOMMENDED MONITORING In addition to clinical signs, radiographs should be monitored during the healing phase. The radiographic signs of healing diskospondylitis lesions are disappearance of the lytic focus and its replacement by bridging or fusion of involved vertebrae. In young dogs (2.5 mcg/kg/min not recommended and should be used with extreme caution
CHRONIC TREATMENT Thoracocentesis and abdominocentesis as needed Diuretics (as needed to control edema): Furosemide: Dogs—1-4 mg/kg PO q 8-24 h. Cats—1-2 mg/kg PO q 8-24 h. For chronic treatment of CHF where fluid retention is refractory to furosemide alone, add: Spironolactone (dogs, cats), 1-2 mg/kg q 12-24 h PO; and/or Hydrochlorothiazide (dogs, cats), 2-4 mg/kg q 12 h PO (alternative use: BID q 48 h [q 12 h alternating one day on, one day off] to start, and monitor renal values more closely once adding this diuretic to furosemide) ACE inhibitors: Enalapril: dogs, 0.5 mg/kg q 12-24 h PO; cats, 0.5 mg/kg q 24 h PO; or Benazepril: dogs, 0.5 mg/kg q 12-24 h PO; cats, 0.25-0.5 mg/kg q 24 h PO; or Lisinopril: dogs, 0.5 mg/kg q 24 h PO Digoxin: Dogs—0.003 mg/kg q 12 h PO (a dose preferred by author [other publications usually have a higher dose] that usually doesn't yield digoxin toxicosis and results in 70%-75% of dogs reaching therapeutic levels). Cats—0.01 mg/kg or ¼ of a 0.125 mg tablet PO q 48 h.
24-09-2011 18:59
Dilated Cardiomyopathy
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Pimobendan: dogs, 0.2-0.3 mg/kg q 12 h PO for heart failure Novel therapy (use after careful consideration of benefits and risks). Beta-blockers blunt cardiotoxic effects of sympathetic nervous system; however, heart failure must be well controlled first, and dose begun low and up-titrated slowly (days to weeks) with careful monitoring. Options include: Carvedilol: dogs, up to 0.5 mg/kg q 12 h PO (start with ¼ dose initially) Metoprolol: dogs and cats, up to 1 mg/kg q 8 h PO (start with ¼ dose initially) Atenolol: dogs and cats, up to 1 mg/kg q 12 h PO (start with ¼ to ½ dose initially) Arrhythmias In atrial fibrillation, slowing of ventricular response rate in DCM is achieved with digoxin and/or diltiazem (1-1.5 mg/kg PO q 8 h). If necessary, atenolol or carvedilol can be used instead of diltiazem. Use of atenolol or carvedilol in this situation should be done carefully, owing to their pronounced effect on contractility; consultation with a cardiologist might be warranted. Serious ventricular arrhythmias are managed with identification and treatment of underlying causes (e.g., hypoxemia from pulmonary edema); if rapid or causing clinical signs, these must be controlled (see p. 1165).
NUTRITION/DIET Diet: if CHF has occurred and is now controlled: Keep patient eating with adequate level of protein intake. Eliminate high-salt snacks. Sodium-restricted commercial diets such as Purina CV or Hills H/D (not at the expense of good appetite) or balanced home-cooked low-sodium diets Taurine: recommended in all cats (250 mg/cat PO q 12 h) with DCM until demonstrated that patient is unresponsive to taurine; dose in dogs is 500 mg/dog PO q 12 h. Omega-3 fatty acids may improve appetite and reduce cachexia (EPA, 30-40 mg/kg q 24 h; DHA, 20-25 mg/kg PO q 24 h). Consider L-carnitine (110 mg/kg PO q 12 h) in boxers and American cocker spaniels not responding to taurine.
BEHAVIOR/EXERCISE Absolute rest during treatment of CHF or life-threatening arrhythmias Once congestive heart failure is resolved, slowly increase activity back to normal; quality of life is important. Ask owner to use common sense (e.g., if patient is tired, take break from activity; if normally fetches the ball 100 times, consider 10 times now).
DRUG INTERACTIONS Quinidine, verapamil: will increase serum digoxin level (risk of toxicosis) Hypokalemia, hypercalcemia, renal dysfunction, and hypothyroidism predispose to digitalis intoxication (therefore, decrease dose of digoxin).
POSSIBLE COMPLICATIONS Sudden death due to arrhythmias (especially uncontrolled ventricular tachycardia) Renal insufficiency due to low cardiac output, medical treatment; however, mild to moderate azotemia (without associated clinical signs) is expected with diuretic treatment. Iatrogenic complications due to medical treatment (hypokalemia, azotemia, other electrolyte abnormalities)
RECOMMENDED MONITORING Monitor 7-10 days after discharge, then as needed (e.g., q 1-4 mon, barring decompensation): physical examination, thoracic radiographs, ECG, serum renal and electrolyte profile. Holter/event monitors, echocardiography, other: if significant or unexpected change in patient's condition Serum digoxin levels 1 week (dogs) or 2 weeks (cats) after start of therapy (therapeutic range = 0.8-1.8 ng/mL) taken 6-8 hours post pill. Renal/electrolyte panel 5-7 days after starting angiotensin-converting enzyme inhibitors Repeat echocardiogram in 3-6 months after initiating taurine supplementation to determine response to therapy.
PROGNOSIS AND OUTCOME Overall, death usually occurs 3-24 months after diagnosis. Paroxysmal ventricular tachycardia and atrial fibrillation are probable markers of shorter survival. Plasma cardiac Tn-I > 0.20 ng/mL is suggestive of shorter survival time.
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Dilated Cardiomyopathy
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Prognosis is influenced by treatment, time of diagnosis, and client compliance. Prognosis generally worse in Portuguese water dogs and Doberman pinschers than in other breeds, but some Dobermans live months to years after diagnosis. Prognosis in Irish wolfhounds with DCM is fair; lifespan virtually unaffected. In cats with DCM not due to taurine deficiency, the prognosis is usually grave.
PEARLS & CONSIDERATIONS COMMENTS Most dogs have left atrial enlargement, pulmonary venous enlargement, and perihilar/caudodorsal pulmonary edema if pulmonary infiltrates are cardiogenic, whereas cats usually have atrial enlargement with variable edema location and pulmonary vein enlargement. Low echocardiographic LV FS% is not pathognomonic for DCM; many normal hearts contract more in apical-to-basilar direction, and this motion is not accounted for by the FS%. Most small-breed dogs more likely to have chronic mitral valve endocardiosis > collapsing trachea > primary respiratory disease > DCM causing similar clinical presentation. DCM in cats is rare, hypertrophic cardiomyopathy is common; the opposite is true in dogs.
CLIENT EDUCATION Monitor for signs associated with progression of disease (coughing [dogs], open-mouth breathing [cats], respiratory changes, lethargy, collapse) and adverse side effects of medications (vomiting, diarrhea, anorexia).
TECHNICIAN TIPS Unlike most hospitalized cases, heart failure patients do not need fluids because they are hypervolemic (“drowning in their own fluids”); an exception is low-dose fluids used for delivery of IV heart medications. Heart patients generally need to be stress free as possible (e.g., avoid cats mixing with dogs, avoid having inexperienced technician draw blood). One of the best and simplest ways to monitor the heart patient is to monitor respiratory rate per minute instead of physically handling these patients.
SUGGESTED READING Meurs KM: Primary myocardial disease in the dog. In Ettinger SJ, Feldman EC, editors: Textbook of veterinary internal medicine, ed 6, Philadelphia, 2005, Elsevier Saunders, pp 1077–1082. Sisson DD, Thomas WP, Keene BW: Primary myocardial disease in the dog. In Ettinger SJ, Feldman EC, editors: Textbook of veterinary internal medicine, ed 5, Philadelphia, 2000, WB Saunders, pp 874–895. AUTHOR: ROBERT PROŠEK EDITOR: ETIENNE CÔTÉ
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Digoxin Toxicosis
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Digoxin Toxicosis BASIC INFORMATION DEFINITION Clinical signs caused by excessive administration of, or individual intolerance to, normal doses of digoxin
SYNONYMS Digitalis poisoning, digoxin intoxication. Digoxin and digitalis are used interchangeably; other digitalis derivatives, such as digitoxin, are no longer used clinically.
EPIDEMIOLOGY SPECIES, AGE, SEX Dogs and cats of any age, either sex GENETICS & BREED PREDISPOSITION Doberman pinschers appear predisposed. RISK FACTORS Renal failure Hypovolemia, dehydration Hypokalemia Concurrent administration of drugs that increase serum digoxin levels: diazepam, erythromycin, quinidine, tetracycline, verapamil Obesity (if digoxin is dosed on total body weight rather than lean body weight) Intravenous digoxin MDR-1 gene mutant ASSOCIATED CONDITIONS & DISORDERS Underlying heart disease prompting digoxin treatment
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES Systemic signs Cardiac arrhythmias HISTORY, CHIEF COMPLAINT Hallmarks of digoxin toxicosis: lethargy, anorexia, vomiting, and diarrhea, together or individually May be intermittent in mild cases Severe toxicosis: refractory vomiting, tenesmus, collapse, death Except for massive overdoses, digoxin treatment needs to have been underway for >24 hours (and usually weeks) to produce signs of toxicosis. Most commonly, patients are receiving digoxin as part of long-term cardiac treatment. Much less commonly, digoxin toxicosis occurs from a pet's consuming plants or human medication. PHYSICAL EXAM FINDINGS Lethargy, dehydration Physical findings attributable to underlying heart disease
24-09-2011 18:49
Digoxin Toxicosis
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Digoxin toxicosis can also produce virtually any cardiac arrhythmia. Bradycardia or tachycardia on examination
ETIOLOGY AND PATHOPHYSIOLOGY Digoxin is a cardiac glycoside drug derived from the foxglove plant. It is absorbed slowly (6-8 hours to peak serum concentration with oral tablets in dogs; faster with elixir) and is mainly excreted renally (>60%). The half-life is long: 14-56 hours (dogs), 30-173 hours (cats). Therefore, when intoxication occurs, it more often is a cumulative process (chronic treatment). Acute overdoses are amenable to activated charcoal administration for several hours after ingestion. All cardiac glycosides (therapeutic, e.g., digoxin, digitoxin [historic]; or botanical, e.g., foxglove, oleander) act on the +
2+
sodium/potassium/adenosine triphosphate pump of mammalian cells to increase intracellular Na and Ca Cardiovascular, neurologic, and gastrointestinal effects are responsible for clinical signs. With digoxin toxicosis, systemic clinical signs precede or occur concurrently with cardiac arrhythmias.
concentrations.
DIAGNOSIS DIAGNOSTIC OVERVIEW The diagnosis is strongly suspected on the basis of medication history and clinical signs. Initial testing offers supportive evidence, but the diagnosis is often established based on resolution of clinical signs when the drug is stopped.
DIFFERENTIAL DIAGNOSIS Primary gastrointestinal disease Uremia/renal failure Cardiac arrhythmias of primary cardiac or systemic origin
INITIAL DATABASE Serum biochemistry profile, urinalysis: Evidence of chronic kidney disease or hypokalemia increases likelihood of intoxication. Concurrent treatment with diuretics may cause azotemia and isosthenuria. Generally if azotemia is severe (blood urea nitrogen > 80 mg/dL and creatinine > 3 mg/dL), some degree of reduced renal function is expected, and digoxin elimination is likely reduced, predisposing to toxicosis. Electrocardiogram (ECG): First-degree atrioventricular (AV) block (see p. 120 ): early ECG manifestation of digoxin toxicosis Higher degrees of AV block, premature atrial or ventricular complexes common
ADVANCED OR CONFIRMATORY TESTING Serum digoxin concentration: confirmation (retrospective) Therapeutic level: 0.8-2.0 ng/mL >2-3 ng/mL with clinical signs: digoxin toxicosis Turnaround time of test limits immediate usefulness, but some local human hospitals may provide stat service. Evaluations of renal/central nervous/gastrointestinal systems: as dictated by clinical signs
TREATMENT TREATMENT OVERVIEW Acute overdoses: prevent digoxin assimilation. All cases: reduce serum digoxin concentration.
ACUTE GENERAL TREATMENT Acute overdoses (uncommon): activated charcoal and supportive care (see Etiology and Pathophysiology above) Toxicosis in dogs receiving normal digoxin doses chronically: the cornerstone of treatment is discontinuation of the drug. Treatment may be restarted 48 hours later at half the dose after signs of toxicosis have resolved.
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Intravenous fluid therapy: judicious if patient has cardiac disease Potassium supplementation in hypokalemic patients: essential, since hypokalemia may potentiate arrhythmias Ventricular antiarrhythmics if rapid ventricular arrhythmias (see p. 1165) Treatment for supraventricular arrhythmias if very rapid (see p. 111 ). Soluble antidigoxin antibodies may be administered in severely ill patients. Number of vials (38 mg each) given slowly IV = serum digoxin level [ng/mL] × body weight (kg)/100 For example, 2 vials slow IV, single dose for a 35-lb (16-kg) dog with serum digoxin level 12 ng/mL Very costly ($500 per vial)
RECOMMENDED MONITORING Monitoring serum concentrations is secondary to monitoring of clinical signs alone.
PROGNOSIS AND OUTCOME Dependent on dose, elimination (renal function, hydration), extent of signs, and response to treatment Severe digoxin intoxication can be fatal.
PEARLS & CONSIDERATIONS COMMENTS Differentiation between digoxin toxicosis and an unrelated problem (e.g., primary GI disturbance, renal failure, other) may be challenging. It is virtually always preferable to assume that digoxin toxicosis exists and discontinue the drug and use other cardiac drugs (e.g., beta-blockers, inotropes) as replacements if necessary while evaluation of the other differential diagnoses takes place; response to discontinuation helps confirm toxicosis retrospectively.
PREVENTION Early detection of clinical signs of toxicosis by owners, and if signs occur, discontinuation of the drug, monitoring, and supportive care
SUGGESTED READING Knight DH: Efficacy of inotropic support of the failing heart. Vet Clin North Am 21:879-904, 1991. Ward DM, Forrester SD, DeFrancesco TC, Troy GC: Treatment of severe chronic digoxin toxicosis in a dog with cardiac disease, using ovine digoxin-specific immuno-globulin G Fab fragments. J Am Vet Med Assoc 215:1808–1812, 1999. AUTHOR & EDITOR: ETIENNE CÔTÉ
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Dietary Intolerance
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Dietary Intolerance BASIC INFORMATION DEFINITION Adverse reactions to an ingested food or food additive due to nonimmunologic mechanisms (common)
SYNONYMS Adverse reaction to food, food intolerance, lactose intolerance
EPIDEMIOLOGY SPECIES, AGE, SEX Dogs and cats: no age or gender predilection RISK FACTORS Food contaminated with microorganisms or their toxic metabolites Specific foods (onions, chocolate) Toxic food preservatives (e.g., propylene glycol in cats) Preformed vasoactive amines (e.g., histamine) in food such as fish Dairy products Dietary indiscretion (gluttony, pica, ingestion of indigestible materials) ASSOCIATED CONDITIONS & DISORDERS Dietary hypersensitivity Inflammatory bowel disease
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT Vomiting, diarrhea, intermittent abdominal pain, abdominal distension, soft feces, excessive flatulence, increased frequency of defecation PHYSICAL EXAM FINDINGS Diarrhea (small or large bowel), vomiting, abdominal distension, urticaria, angioedema
ETIOLOGY AND PATHOPHYSIOLOGY Food poisoning: Eating foods (e.g., through scavenging, improperly cooked homemade foods, raw diets, contaminated moist or dry commercial foods [e.g., aflatoxin]) that are contaminated with bacteria, fungal toxins, or other toxins that cause an immediate gastrointestinal (GI) response (see p. 434) Idiosyncratic adverse reactions to food additives: Examples include food colorings (azo or non-azo dyes), certain preservatives and emulsifying agents, thickeners or stabilizers (e.g., seaweed extracts, seed gums) Occur infrequently and unpredictably in individuals, and are not apparently dose related Histaminergic reactions mediated by type 1 (mast cell mediated) or 2 (receptors for gastric acid release in the stomach) histamine receptors Pharmacologic reactions to vasoactive amines (e.g., histamine) found in food Carbohydrate intolerance (lactase deficiency): Mediated by lack of carbohydrate digestion (lactose intolerance) due to mucosal disease or lack of enzyme activity —either congenital or acquired
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A true allergic reaction to proteins in milk (e.g., bovine IgG) can mimic carbohydrate intolerance. Which of these types of reactions are causing the problem is rarely defined and not clinically relevant. Dietary indiscretion: Typically defined as the consumption of unusual or spoiled foods (as can occur with scavenging or raiding the garbage can), the consumption of too much food (gluttony), or pica (eating nonfood substances such as hair, rocks, bones, etc.) The insult occurring in the GI tract varies with the type of indiscretion observed, and thus no consistent clinical presentation is recognized.
DIAGNOSIS DIAGNOSTIC OVERVIEW Food intolerance is suspected on the basis of acute vomiting and/or diarrhea, often but not always occurring as a result of acute dietary alterations; confirmatory diagnosis is often retrospective, with resolution of clinical signs as a result of proper diet. In contrast to dietary hypersensitivity (food allergy), the response to the change in food is more rapid (few days to 2 weeks) with dietary intolerance. Therefore, if no response occurs during this time frame, the diagnosis of intolerance should be questioned.
DIFFERENTIAL DIAGNOSIS Any chronic disorder affecting the GI tract (e.g., hypoadrenocorticism, protein-losing enteropathy, infiltrative disease) Inflammatory bowel disease GI neoplasia Chronic parasitism Food hypersensitivity
INITIAL DATABASE CBC: nonspecific and usually normal Serum biochemistry profile: nonspecific and usually normal Urinalysis: nonspecific Fecal flotations to rule out parasitic causes of vomiting/diarrhea
ADVANCED OR CONFIRMATORY TESTING Proper nutrition/elimination food trial Further testing generally unnecessary for the primary diagnosis; used for identifying other disorders with similar signs or for identifying inciting causes (differential diagnosis) Abdominal radiography and ultrasonography: used for ruling out the other causes of vomiting and diarrhea for which imaging modalities are diagnostic (e.g., intestinal obstruction, intestinal mass) Endoscopy with biopsy and histopathologic evaluation of GI mucosa: mucosa may be normal or show increases in lamina propria lymphocytes or plasma cells, but inflammatory changes seen in dogs or cats with food intolerance are generally less profound than found in those with IBD or other diseases of the mucosa.
TREATMENT TREATMENT OVERVIEW Avoid exposure to food toxins, dairy products, certain carbohydrates, and dietary sources of vasoactive amines (e.g., certain types of fish). Control episodes of dietary indiscretion.
ACUTE GENERAL TREATMENT Nonspecific supportive care based on clinical signs (e.g., parenteral fluid administration for dehydration) Perform an elimination food trial (in general, a shorter trial of 7-10 days is all that is required to result in the resolution of the signs of dietary intolerance). Clinical signs of GI disease usually resolve within a few days on the new diet that does not contain the offending substance.
NUTRITION/DIET
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Maintain strict avoidance of offending foods or ingredients (e.g., dairy products). Find an acceptable commercial or homemade food for long-term maintenance. Control episodes of gluttony, pica, or ingestion of indigestible materials.
POSSIBLE COMPLICATIONS Certain types of food poisoning can cause serious and life-threatening disease.
PROGNOSIS AND OUTCOME Good prognosis if offending foods or ingredients are eliminated from the diet
PEARLS & CONSIDERATIONS COMMENTS In instances of recurrent food intolerance (versus one-time events), use of a food diary by the animal owner is important to monitor clinical response and compliance.
TECHNICIAN TIPS Gradual transition to a new food is critical for a pet with health problems and may be the single most important thing you can do to help a pet accept a new food. Mix more of the new food with less of the old food over a period of at least 7 days. An alternative method for transitioning, especially for cats, is to offer the new food side by side with the old food in identical dishes, instead of mixing them both in the same dish.
CLIENT EDUCATION Human food sources, snacks, treats, and food for other animals in the household (e.g., dog having access to cat food) can be a problem.
SUGGESTED READING Roudebush P, Guilford WG, Jackson HA: Adverse reactions to food. In Hand MS, Thatcher CD, Remillard RL, Roudebush P, Novotny BJ, editors: Small animal clinical nutrition, ed 5, Topeka, 2010, Mark Morris Institute, pp 609–635. AUTHOR: PHILIP ROUDEBUSH EDITOR: DEBRA L. ZORAN
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Diarrhea, Chronic
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Diarrhea, Chronic BASIC INFORMATION DEFINITION An increase in frequency of defecation, stool fluidity, and/or fecal volume (increased water content or fecal solids) that is persistent (more than 2-3 weeks) or episodic.
EPIDEMIOLOGY CONTAGION & ZOONOSIS Potentially zoonotic organisms; see Diarrhea, Acute, p. 303. GEOGRAPHY AND SEASONALITY See Diarrhea, Acute, p. 303.
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES Small-intestinal (SI) diarrhea versus large-intestinal (LI) diarrhea or both Further segregated into diseases caused by maldigestion or malabsorption Malabsorption further segregated into nonprotein-losing versus protein-losing disease
Clinical Signs of Small-Intestinal Versus Large-Intestinal Diarrhea Characteristic
Small Intestine
Large Intestine
Mucus
Uncommon
Common
Hematochezia (fresh blood in/on feces)
Absent
Often present
Melena (digested blood in feces)
± Present
Absent
Volume
Often increased
Normal to decreased (due to increased frequency)
Quality
Nearly formed to watery (“cowpile”); ± undigested food/fat; possibly malodorous
Loose to semisolid
Shape
Variable (dependent upon amount of water present)
Normal or narrowed
Steatorrhea (undigested fat in feces)
Present with maldigestive or malabsorptive disorders
Absent
Frequency
Normal to mildly increased (2-4 times/d)
Greatly increased (4-10 times/d)
Dyschezia (inability to defecate without straining or signs of pain)
Absent
Dogs: frequent. Cats: less common.
Feces
Defecation
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Characteristic
Small Intestine
Large Intestine
Tenesmus (straining)
Absent
Dogs: common. Cats: less common; rule out stranguria.
Urgency
Less common, unless severe acute enteritis
Frequent
Weight loss
Common
Uncommon. Possible with severe chronic colitis, diffuse neoplasia, histoplasmosis, pythiosis.
Vomiting
Possible
May be seen, especially with acute colitis (30%). Possible before onset of abnormal stools.
Appetite
Usually normal; may be ↑ or ↓ in bowel infiltration/inflammation depending on severity of lesion
Normal to decreased if severe disease (neoplasia, histoplasmosis)
Halitosis
± Present (maldigestion/malabsorption)
Absent
Borborygmus
Possible
Absent
Flatulence
Possible
Common
Fecal incontinence
Rare
Possible
“Scooting” or chewing of perianal area
Absent
Possible with proctitis
Associated Signs
HISTORY, CHIEF COMPLAINT Typical: persistent indoor fecal incontinence and/or loose stool Age, when/where the pet was acquired, vaccination and dietary history, environment, recent medications, and presence or absence of recent stressful episode (recent move, changes in family routine, etc.) help identify trigger factors. Differentiate SI diarrhea from LI (see table). PHYSICAL EXAM FINDINGS Hydration status Depression/weakness/lethargy Emaciation: malnutrition, chronic malabsorption, protein-losing enteropathy Dull hair coat: malabsorption (fatty acids, protein, vitamins) Fever: inflammation, infection, neoplasia Edema, ascites, decreased lung/heart sounds (pleural effusion): protein-losing enteropathy Pale mucous membranes: chronic GI blood loss, anemia of chronic illness/inflammation Abdominal palpation may reveal a mass (foreign body, neoplasm, granuloma, abscess, mesenteric lymph-adenopathy), thickened bowel loops (inflammation, neoplastic infiltration), “aggregated” bowel loops (mass, peritoneal adhesions), “sausage-shaped” intestinal loop (chronic, intermittent intussusception), evidence of pain (inflammation, obstruction, ischemia, gas distension), gas/fluid distension (diarrhea, obstruction [mass], ileus) Rectal palpation (mandatory unless intractably painful): mass (polyp, neoplasm, granuloma), circumferential narrowing (stricture, spasm, neoplasm), irregular mucosal texture (colitis, neoplasm, perineal fistula)
ETIOLOGY AND PATHOPHYSIOLOGY Small intestine Decreased fluid and electrolyte absorption Incomplete nutrient absorption (fats, carbohydrates) Increased fluid and electrolyte secretion Large intestine Decreased fluid and electrolyte absorption Secretion of fluid and electrolytes Failure of reservoir function
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Diarrhea, Chronic
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CAUSES OF CHRONIC SMALL- AND LARGE-INTESTINAL DIARRHEA Parasites causing SI: Isospora, hookworms, roundworms Parasites causing LI: Whipworms (Trichuris vulpis), amoebiasis, Balantidium coli. Giardia may be SI and/or LI. Dietary intolerance and dietary allergies may be SI and/or LI. Inflammatory bowel disease (IBD): lymphocytic-plasmacytic, eosinophilic, granulomatous enteritis may be SI and/or LI. Hypereosinophilic syndrome (cats primarily), neutrophilic (suppurative/purulent) enteritis and breed-specific (shar-pei, basenji, soft-coated Wheaten terrier) tend to cause SI. Chronic ulcerative colitis and histiocytic ulcerative colitis (primarily boxers) are most often LI. Neoplasia (lymphoma, adenocarcinoma, leiomyoma/leiomyosarcoma, mast cell tumour): SI and/or LI Infectious organisms causing: SI signs: Cryptosporidia parvum LI signs: salmonellosis, yersiniosis, Bacillus piliformis, pythiosis, protothecosis and Tritrichomonas foetus in cats Both SI and LI: campylobacteriosis, Clostridia spp., histoplasmosis, feline leukemia virus (FeLV), feline immunodeficiency virus (FIV) and feline infectious peritonitis (FIP) Chronic small intestinal bacterial overgrowth (SIBO) in dogs may occur secondary to idiopathic antibiotic responsive enteritis or tylosin-responsive diarrhea. It may be idiopathic or occur secondary to diseases such as an immunoglobulin A deficiency, exocrine pancreatic insufficiency (EPI), a partial obstruction (chronic intussusception) or blind loops of bowel, or disease causing abnormal motility and thereby clearance of organisms, as well as a gastric acid deficiency. Villous atrophy (idiopathic, gastrinoma, gluten-sensitive enteropathy) causes SI diarrhea. Endocrine causes such as hyperthyroidism (cats) and hypoadrenocorticism may cause SI and/or LI diarrhea. Protein-losing enteropathy such as intestinal lymphangiectasia is primarily SI in nature. Any of the preceding disorders can cause protein-losing enteropathy, depending upon disease progression and severity. Maldigestive diseases (EPI, lactase deficiency [especially cats]) cause SI signs. Functional disorder (irritable bowel syndrome [IBS]) is a diagnosis by exclusion and causes LI diarrhea. Other: chronic active pancreatitis (cats and dogs) causes SI signs (lethargy, agitation/abdominal discomfort, vomiting, +/− diarrhea).
DIAGNOSIS DIAGNOSTIC OVERVIEW The list of causes of chronic diarrhea is exhaustive, hence the extreme importance of obtaining a thorough history from the client and considering the pet's environment prior to embarking on a battery of tests that may be unwarranted. Every animal with chronic large-bowel or mixed diarrhea should have a rectal exam and a direct smear performed. Fecal examinations should always be performed on fresh samples.
DIFFERENTIAL DIAGNOSIS See Etiology and Pathophysiology above.
INITIAL DATABASE Fecal examinations Cytology (fresh saline smears): ova, larvae, certain bacteria, protozoa (Giardia, T. foetus, Entamoeba, Balantidium coli). Campylobacter fecal cytology alone not sufficient in making a diagnosis, as many are nonpathogenic. Flotation Gram stain Zinc sulfate centrifugal flotation (Giardia cysts) ELISA: Giardia-specific antigen Iodine stain: enhances visualization of Giardia trophozoites, stops motion of organism and cysts (stain light brown). CBC: to assess hydration status (PCV/TS), presence of leukocytosis (inflammation, infection, stress), eosinophilia (eosinophilic IBD, endoparasitism), lymphopenia (lymphangiectasia), anemia (chronic GI blood loss, anemia of chronic illness/inflammation, nutrient malabsorption), thrombocytosis with microcytic, hypochromic anemia (iron deficiency) Absence of a stress leukogram: hypoadrenocorticism Serum biochemical profile: hypoproteinemia (hypoalbuminemia, +/− hypoglobulinemia), elevated BUN (prerenal azotemia, GI bleeding, high-protein diet), elevated liver enzyme activities (primary hepatic disease, reactive hepatopathy, pancreatitis, or primary GI tract disease with portal bacterial translocation), hypocholesterolemia (lymphangiectasia, hepatopathy) Urinalysis to assess specific gravity (renal function [renal versus prerenal azotemia]), proteinuria Cats: serum thyroxine concentration (>6 years old), FeLV/FIV
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ADVANCED OR CONFIRMATORY TESTING Abdominal radiographs: survey and/or contrast radiography Abdominal ultrasonography: mass lesion, thickened bowel loops, loss of detail of the layers of GI wall, evaluation of other abdominal organs Adrenocorticotropic hormone stimulation test (hypoadrenocorticism) Fecal cultures (E. coli, Salmonella spp., C. jejuni, Clostridium spp., Y. enterocolitica). Efficacy in determining true infection is controversial; many of these bacteria are commensal organisms, and their presence in feces does not necessarily correlate with disease. T. foetus: culture of feces using the InPouch TF (BioMed Diagnostics, White City, OR)—young cats from cattery or shelter C. perfringens fecal endospore enumeration (unreliable and not recommended) C. perfringens enterotoxin: caution, discordant results amongst detection methods Recommendations for C. perfringens: ELISA for enterotoxin combined with PCR for the enterotoxin gene C. difficile: test for the enzyme glutamate dehydrogenase (GDH; constitutively produced), available as a commercial kit. If positive on fecal culture or positive detection of GDH enzyme, further testing for enterotoxin A and B recommended. PCR of toxin genes should be interpreted with caution (no difference in toxigenic C. difficile shedding by diarrheic dogs versus nondiarrheic dogs). Campylobacter: PCR; positive PCR result requires further testing techniques such as sequencing of the 16S rDNA gene, etc. Cryptosporidium: fecal ELISA test Salmonella: positive PCR samples should be cultured followed by sero-typing of suspected colonies. Occult blood: chronic blood loss; meat-based diet may cause false positives with some kits. Trypsin-like immunoreactivity (TLI) test: EPI (species-specific test) Serum cobalamin (vitamin B12), folate Folate: depends on jejunum's absorptive function (proximal SI) Cobalamin: depends on pancreatic intrinsic factor secretion and absorption in ileum (distal SI) ↓Folate and ↓cobalamin: diffuse malabsorptive disease ↓Cobalamin, ↑folate: antibiotic-responsive enteritis/SIBO TLI, cobalamin, and folate often run together. Species-specific pancreatic lipase immunoreactivity (PLI) test (spec CPL/cPLI, fPLI) for the diagnosis of chronic active pancreatitis If presence of hypoproteinemia and hypoalbuminemia, further diagnostics required to identify origin of loss; kidneys (urine protein/creatinine ratio if proteinuria noted on dipstick), liver (serum bile acids), or GI (fecal alpha-protease inhibitor) Serologic titers (histoplasmosis) Endoscopy: gastroduodenoscopy and colonoscopy indicated to determine extent of disease Exploratory laparotomy: full-thickness biopsies (biopsy even if no gross lesions) Molecular techniques (PCR, RT-PCR): increasing commercial availability (results highly dependent on laboratory's quality control) Empirical therapy may be elected because of client's financial constraints: probiotics, anthelmintics, antimicrobials (metronidazole, tylosin, enrofloxacin), dietary trials, antiinflammatories/immunomodulators.
TREATMENT TREATMENT OVERVIEW The goal of therapy is to treat the underlying cause of the diarrhea.
ACUTE GENERAL TREATMENT Low-fat, highly digestible low-fiber diets (low-fat cottage cheese, tofu, rice, potatoes) Small, frequent meals (3-6/d) High-fiber diets (colitis) Empirical treatment: anthelmintics (fenbendazole) or metronidazole, even with negative tests
CHRONIC TREATMENT Dependent on underlying cause; see specific disorders for details. Deworming medications Antimicrobials (see p. 303 and specific organism) Immunosuppressive agents such as prednisone/prednisolone/budesonide (use minimum effective dose), cyclosporine, azathioprine (not in cats), chlorambucil Possible immunomodulating/antiinflammatory activities, such as metronidazole and tylosin Antiinflammatories (sulfasalazine/olsalazine/mesalamine)
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Adjunctive therapy: cobalamin supplementation and probiotics Antifungal agents (histoplasmosis)
NUTRITION/DIET Dietary modifications such as feeding a novel protein source or a hydrolyzed protein for a trial period (minimum 3 to 4 weeks). All other foods and antigen sources (treats, flavored medications) must be eliminated during this time.
POSSIBLE COMPLICATIONS Immunosuppressive therapy (azathioprine, chlorambucil): myelosuppression 5-aminosalicylates: keratoconjunctivitis sicca Iatrogenic hyperadrenocorticism with chronic glucocorticoid use, therefore use minimum effective dose Excessive protein loss: edema/cavity effusions Buccal mucosal irritation: pancreatic enzyme supplementation (EPI)
PROGNOSIS AND OUTCOME Dependent on underlying cause, response to treatment, owner compliance, and interindividual variation Guarded: histoplasmosis, protothecosis, pythiosis, yersiniosis, regional granulomatous enterocolitis, FIP Poor to guarded: basenji, shar-pei, soft-coated Wheaten terrier–associated IBD, villous atrophy (clinical signs often persist despite treatment), feline hypereosinophilic syndrome Fair: histiocytic ulcerative colitis (lifetime therapy needed, difficult to control) Fair to good: antibiotic-responsive enteritis/SIBO, depending on underlying cause. Some require frequent or continuous treatment; others have prolonged remission with one course of antibiotics. FeLV/FIV (when secondary infections controlled). Fair to excellent: IBD (realistic expectation: maintenance of remission/control of relapses, rather than cure) Good: dietary intolerance/food allergy, giardiasis, salmonellosis (although mortality rate can be high [hospitalized, young, immune-compromised]), campylobacteriosis, Clostridium spp. (although fatalities reported) Good to excellent: hyperthyroidism, EPI (continual treatment), hypoadrenocorticism (lifelong treatment), hook-worms/roundworms/whipworms Lymphangiectasia: unpredictable. Remission in some (months to years), cachexia, cavity effusions, intractable diarrhea in others with inability to control protein loss. Neoplasia: dependent on tumor type
RECOMMENDED MONITORING Body weight, serum protein and albumin concentrations, frequent CBCs if using immunosuppressive agents Schirmer tear test (sulfasalazine, TMS)
PEARLS & CONSIDERATIONS COMMENTS During diagnostic procedures (laparotomy, laparoscopy or endoscopy), it is vital to always obtain biopsies, even if tissues appear grossly normal.
TECHNICIAN TIPS Proper hygiene is of paramount importance to avoid promoting contagion and to prevent zoonoses (handwashing between pets, gloves when cleaning a patient with diarrhea, never placing food in laboratory area where fecal analyses are performed).
CLIENT EDUCATION Some of the preceding diseases can be frustrating to treat (waxing and waning nature). Inform owner at time of diagnosis: avoids unrealistic expectations/disappointment.
SUGGESTED READING Hall, EJ, German, AJ: Diseases of the small intestine. In Ettinger SJ, Feldman EC, editors: Textbook of veterinary internal medicine vol. II, ed 6, Philadelphia, 2005, WB Saunders, pp 1332–1378.
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AUTHOR: LISA CARIOTO EDITOR: ETIENNE CÔTÉ
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Diarrhea, Acute
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Diarrhea, Acute BASIC INFORMATION DEFINITION An increase in frequency of defecation, stool fluidity, and/or fecal volume (increased water content or fecal solids) that is sudden in onset and of short duration (360 mg/dL (>20 mmol/L). Close monitoring of blood glucose is required; dose reduction is expected in the first 7 days. If close monitoring is not possible, it is safer to start with 1 U/cat SQ q12 h. Alternatively, recombinant human or pork-source Lente or beef/porksource PZI insulin can be used at an initial dose of 1 unit per cat SQ q 12 h. Keep daily exercise fairly consistent for dogs. Identify and treat concurrent disorders that interfere with insulin effectiveness. Treatment with the oral sulfonylurea, glipizide, may be considered in diabetic cats when the owner refuses to administer insulin, if ketonuria and peripheral neuropathy are not identified, and if the cat is relatively healthy. Treatment of DKA: see p. 299
NUTRITION/DIET Adjust dietary caloric intake to correct or prevent obesity. Divide total daily caloric intake in half, and offer at the time of each insulin injection. Consumption may be immediate or intermittent throughout the 12-hour period, depending on eating habits of the dog or cat. Some cats may prefer to “graze” throughout the day. For maintenance in dogs, increase fiber content of the diet unless concurrent disease or adverse effects dictate otherwise. Amount of fiber depends on fiber type: insoluble fiber should be >10%, soluble fiber should be 4%-8%, and mixtures of soluble and insoluble fiber should be >8% of diet on dry-matter basis. In cats, restrict carbohydrate content of diet, ideally to 15% or less of metabolizable energy. Fiber content of the diet can also be increased as described for dogs.
POSSIBLE COMPLICATIONS Insulin-induced hypoglycemia, diabetic ketoacidosis
RECOMMENDED MONITORING Initially, monitor clinical response and blood glucose concentrations weekly until diabetic control is attained, defined as resolution of clinical signs and blood glucose concentrations ranging between 100 and 300 mg/dL (5.5 and 16.7 mmol/L) during the 12 hours after insulin administration. With instruction, some clients may be able to obtain blood glucose curve results for their pet via home monitoring. However, any adjustments in insulin dose should only be done in consultation with the veterinarian. Monitor history, physical examination, body weight, and serum fructosamine concentration every 3-6 months once diabetes is controlled. Evaluate multiple blood glucose concentrations during the 12 hours after insulin administration if diabetic control is lost (i.e., return of clinical signs, abnormalities identified on physical examination, or progressive loss of body weight). Adjust insulin therapy accordingly.
TECHNICIAN TIPS Minimize stress to the patient. Perform blood sampling for glucose measurements in a quiet room, and have all equipment ready before taking the patient out of a cage for venipuncture.
PROGNOSIS AND OUTCOME Prognosis depends on owner commitment to treating the disorder, ease of glycemic regulation, presence and reversibility of concurrent disorders, and avoidance of chronic complications associated with the diabetic state. Mean survival time for diabetic dogs and cats is approximately 3 years from time of diagnosis, although diabetic dogs and cats that survive the first 6 months can easily maintain a good quality of life for longer than 5 years with proper care.
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Diabetes Mellitus
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SUGGESTED READING Feldman EC, Nelson RW: Canine diabetes mellitus. In Canine and feline endocrinology and reproduction, ed 3, St Louis, 2004, Saunders, pp 486–579. Monroe EW: Canine diabetes mellitus. In Bonagura JD, Twedt CD, editors: Kirk’ s current veterinary therapy XIV, St Louis, 2009, Saunders, pp 196–199. Rand JS: Feline diabetes mellitus. In Bonagura JD, Twedt CD, editors: Kirk’ s current veterinary therapy XIV, St Louis 2009, Saunders, pp 199–204. AUTHOR: VLADIMIR STOJANOVIC EDITOR: SHERRI IHLE 1ST EDITION AUTHOR: RICHARD NELSON
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Diabetes Insipidus
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Diabetes Insipidus BASIC INFORMATION DEFINITION Well-recognized disorder of insufficient antidiuretic hormone (ADH) secretion (central diabetes insipidus) or action (nephrogenic diabetes insipidus) resulting in inadequate urine-concentrating ability.
EPIDEMIOLOGY SPECIES, AGE, SEX Affects both dogs and cats No breed, gender, or age predilection
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES Central diabetes insipidus (CDI): hypothalamus/pituitary gland disorder Nephrogenic diabetes insipidus (NDI): renal disorder HISTORY, CHIEF COMPLAINT Polyuria, polydipsia, loss of house training, perceived urinary incontinence Stupor, disorientation, ataxia, and seizures may be reported if an underlying neurologic disorder is present. PHYSICAL EXAM FINDINGS Usually normal Dehydration may be noted if the animal has not had free access to water. Neurologic abnormalities (e.g., stupor, disorientation, ataxia) may be seen in CDI cases with underlying hypothalamic/pituitary lesions, or as a consequence of severe hypernatremia from hypertonic dehydration.
ETIOLOGY AND PATHOPHYSIOLOGY Normal daily water consumption: 10 kg), 60 mL/kg/24 hours for cats and small dogs (0.5 mEq/kg/h. Do not raise or lower serum sodium at a rate of >1 mEq/L/h.
NUTRITION/DIET If vomiting has resolved, gradual access to water for oral intake is recommended.
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Dehydration
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CHRONIC TREATMENT Depends on underlying disease process
DRUG INTERACTIONS Do not add sodium bicarbonate to calcium-containing fluids (precipitation reaction).
POSSIBLE COMPLICATIONS Overhydration: pulmonary edema, pleural or peritoneal effusion, hemodilution, cerebral edema, peripheral edema. Monitor more closely if heart or renal disease; consider colloidal therapy (plasma, albumin, hetastarch) if hypoalbuminemia is present.
RECOMMENDED MONITORING Body weight, urine output, heart rate, pulse quality, capillary refill time, skin turgor, blood pressure, packed cell volume/total solids, blood urea nitrogen, creatinine
PROGNOSIS AND OUTCOME Prognosis is good if the underlying disease process is identified and can be corrected.
PEARLS & CONSIDERATIONS COMMENTS Recheck electrolyte (sodium, potassium, chloride, and phosphorus) imbalances and acid-base status frequently (every 4-8 hours) during the first 24 hours of therapy to ensure treatment goals are being achieved. Body weight and urine output are among the easiest and most accurate ways to gauge the level of hydration.
PREVENTION See specific disease information.
TECHNICIAN TIP Assessing hydration status by skin turgor alone can be misleading, especially in cachectic patients, as the decreased fat content in their subcutaneous tissues will make them appear dehydrated no matter what their hydration status is. The conjunctival mucous membranes are often most reliable (barring ocular disease) because oral mucous membranes are prone to drying (open-mouth breathing/panting in dogs) or coating with mucus (vomiting).
CLIENT EDUCATION Anorexic animals or those vomiting and having diarrhea (especially very young or very old) can become dehydrated quickly and should be examined by a veterinarian as soon as possible.
SUGGESTED READING Rudloff E, Kirby R: Fluid resuscitation and the trauma patient. Vet Clin North Am Small Anim Pract May;38(3):645–652, 2008. DiBartola SB: Fluid therapy in small animal practice, ed 3, St Louis, 2006, Saunders Elsevier. AUTHOR: ADAM J. REISS EDITOR: ETIENNE CÔTÉ
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Degenerative Myelopathy
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Degenerative Myelopathy BASIC INFORMATION DEFINITION Canine degenerative myelopathy is an inherited degenerative disease, most severely affecting the thoracolumbar spinal cord.
SYNONYMS Canine degenerative radiculomyelopathy, German shepherd dog myelopathy
EPIDEMIOLOGY SPECIES, AGE, SEX Canine; age usually 8 years or older; mean age 9 years GENETICS & BREED PREDISPOSITION Presumed autosomal recessive with a mutation discovered in the canine superoxide dismutase 1 (SOD1) gene The genetic mutation is similar to some forms of human amyotrophic lateral sclerosis (Lou Gehrig's disease) Breed predisposition: purebred dogs—German shepherd, Pembroke and Cardigan Welsh corgi, standard poodle, Rhodesian ridgeback, collie, boxer, Chesapeake Bay retriever, Irish setter, Bernese Mountain dog, mixed breed, wire fox terrier, Kerry blue terrier
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT Progressive weakness of pelvic limbs Initially, affected dogs will drag nails and show pelvic limb ataxia. Difficulty jumping The disease results in a progressive paraparesis to paraplegia over 6-12 months from time of suspected diagnosis. If signs are allowed to progress, the thoracic limbs will eventually become affected. PHYSICAL EXAM FINDINGS Pelvic limb tremors Asymmetric truncal general proprioceptive (GP) ataxia to severe paraparesis and paraplegia Upper motor neuron spastic paraparesis (long stride length) Postural reaction deficits (e.g., toe dragging, absent conscious proprioception) Spinal reflexes present or exaggerated Patellar reflex may be decreased to absent Variable presence of crossed extensor reflex in pelvic limbs Disuse muscle atrophy of pelvic limbs which progresses to neurogenic muscle atrophy Absence of paraspinal hyperesthesia Urinary and fecal incontinence in later disease stage If euthanasia is delayed, the clinical signs will ascend, causing flaccid tetra-paresis and other lower motor neuron signs. Dogs at end stage may also have swallowing and respiratory dysfunction.
ETIOLOGY AND PATHOPHYSIOLOGY The etiology of degenerative myelopathy is a genetic mutation in the superoxide dismutase 1 (SOD1) gene, resulting in a toxic gain of function (the mutation results in misfolding of SOD1, causing abnormal accumulations of aggregates in the neuron). Dogs homozygous for the mutation are at risk for development of degenerative myelopathy. Neuropathologic lesion distribution in the CNS involves axons and myelin in all funiculi of the spinal cord; most severe in the dorsal funiculus and dorsal portion of the lateral funiculus of the thoracolumbar spinal cord.
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Neurons in degenerative myelopathy–affected dogs contain cytoplasmic aggregates that stain with anti-SOD1 antibodies. Some studies have shown degenerative changes in some neurons of the brainstem. Peripheral nerves show nerve fiber loss reflective of axonal degeneration and secondary demyelination. Muscle specimens show excessive variability in myofiber size, with large and small groups of atrophic fibers.
DIAGNOSIS DIAGNOSTIC OVERVIEW Diagnosis of degenerative myelopathy is based on exclusion of other disorders that mimic it. The genetic test may assist with interpretation of clinical signs and diagnostic testing toward a presumptive diagnosis of degenerative myelopathy.
DIFFERENTIAL DIAGNOSIS Other spinal cord disorders mimic signs of degenerative myelopathy: Intervertebral disk disease: Hansen type II Inflammatory disease of the spinal cord: myelitis Spinal cord neoplasia Degenerative lumbosacral stenosis Hip dysplasia Other coexisting orthopedic diseases
INITIAL DATABASE Neurologic examination (see p. 1311 ). See Physical Exam Findings above for clinical findings. Nonpainful progressive myelopathy Neuroanatomic localization: initial disease stage—upper motor neuron signs (T3 to L3 spinal cord segments); later disease stage involves lower motor neuron signs to the pelvic limbs; end stage—generalized lower motor neuron signs. Clinical pathologic tests: generally unremarkable Thoracic radiography Screening for metastatic neoplasia (central nervous system neoplasia differential diagnosis) Genetic testing Dogs that test homozygous for the mutation are AT RISK for developing degenerative myelopathy. Not all dogs that test AT RISK will develop degenerative myelopathy A direct mutation test for a susceptibility gene is offered. For recessive diseases, the results are expressed as follows: Normal—homozygous for the normal gene Carrier—heterozygous with one copy of the normal and mutated gene AT RISK—homozygous for the mutated gene
ADVANCED OR CONFIRMATORY TESTING Clinical working diagnosis is based on ruling out other diseases that cause progressive myelopathy. Cerebrospinal fluid analysis: may show increased protein concentration. Electrophysiologic testing Electromyography and nerve conduction studies (see p. 1253) Used for ruling out other neuropathic disorders In later disease stage, dogs with degenerative myelopathy will show evidence of axonopathy. Survey spinal radiography Myelography: no evidence of a compressive myelopathy Advanced imaging: no evidence of a compressive myelopathy CT combined with myelography MRI Definitive diagnosis is only ever determined postmortem by histopathologic examination of the spinal cord.
TREATMENT TREATMENT OVERVIEW
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There are no proven effective therapies for degenerative myelopathy. Supportive and palliative care are provided to maintain quality of life.
ACUTE AND CHRONIC TREATMENT Exercise, vitamin supplementation (B12, E, and C), and protease inhibitors (aminocaproic acid) have been advocated as potential therapies. Disclaimer: Although the following drugs have been recommended as supplements in dogs with degenerative myelopathy, efficacy still remains to be proven. Aminocaproic acid (500 mg/dog; 15 mg/kg PO q 8 h) Vitamin E (1000-2000 IU/dog PO q 24 h) Vitamin B12 (100-200 mcg/dog PO q 24 h) Encourage exercise and physical rehabilitation to slow onset of disuse muscle atrophy Assistive walking devices enable ambulation support and may improve quality of life. Monitor for urinary and fecal incontinence: Basic nursing care and hygiene if incontinence occurs, to prevent the onset of urine scald, infected decubital ulcers, or similar skin lesions When patient becomes nonambulatory, keep on a well-padded surface.
POSSIBLE COMPLICATIONS Urinary tract infections Decubital ulcer formation (see p. 174)
RECOMMENDED MONITORING Monitor for secondary urinary tract infection Monitor for proper nursing care
PROGNOSIS AND OUTCOME Long-term prognosis is considered poor. Dogs often lose their ability to ambulate in the pelvic within 6-12 months from time of diagnosis. The disease eventually will progress to affect the thoracic limbs. Owners of large-breed dogs often will elect for euthanasia when their dog needs ambulatory assistance.
PEARLS & CONSIDERATIONS COMMENTS Lack of paraspinal hyperesthesia is a key clinical feature of degenerative myelopathy. A suspected diagnosis is based on exclusion of other spinal cord disorders.
TECHNICIAN TIPS Physical rehabilitation (see p. 1329) using light exercise may improve the patient's quality of life. The patient will need to be closely monitored for urine scald and decubitus ulceration when the disease progresses to lower motor neuron involvement.
CLIENT EDUCATION Meticulous nursing care is essential in the recumbent patient. Keep patient clean and dry to prevent urine scald. Keep patient on a protective surface (optimize padding, traction, and ease of cleaning). A sling with wheels or a cart may assist with patient mobility. Physical therapy using range-of-motion and isometric exercises will help maintain joint flexibility and muscle strength (see p. 1329).
SUGGESTED READING
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Awano T, Johnson GS, Wade C, et al: Genome-wide association analysis reveals a SOD1 missense mutation canine degenerative myelopathy that resembles amyotrophic lateral sclerosis. Proc Natl Acad Sci U S A 106 (8):2794, 2009. March PA, Coates JR, Abyad R, et al: Degenerative myelopathy in 18 Pembroke Welsh Corgi dogs. Veterinary Pathology 46:241, 2009. AUTHOR: JOAN R. COATES EDITOR: CURTIS W. DEWEY
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Decongestant Toxicosis
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Decongestant Toxicosis BASIC INFORMATION DEFINITION Common decongestants are pseudoephedrine, ephedrine, phenylephrine, and imidazoline derivatives (oxymetazoline, naphazoline, tetrahydrozoline, xylometazoline). They are active ingredients in over-the-counter (OTC) human medications used for the treatment of cold, flu, sinusitis, and allergies. Toxicosis from other active ingredients is discussed separately ().
EPIDEMIOLOGY SPECIES, AGE, SEX All species, breeds, and both sexes are susceptible; dogs are more likely to be involved, based on their predilection for dietary indiscretion. RISK FACTORS Preexisting cardiac disease, systemic hypertension, and seizure disorders may exacerbate signs of toxicosis.
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT Direct observation or indirect evidence of exposure Pseudoephedrine: rapid onset (within 15-30 minutes with immediate release products; 3-6 hours with extended-release medications) of agitation, hyperactivity, restlessness, panting, mydriasis, shaking, circling or head bobbing Phenylephrine: less likely to result in clinical effects, owing to enterohepatic degradation by monoamine oxidases and resultant poor bioavailability (38%) and lack of norepinephrine release (hyperactivity, pacing, shaking) Imidazoline decongestants: rapid onset (within 60 minutes; not expected after 3-4 hours) of vomiting, weakness, collapse PHYSICAL EXAM FINDINGS Pseudoephedrine/phenylephrine: as above, plus injected mucous membranes, hyperthermia, tachycardia or reflex bradycardia; less commonly lethargy and staring Phenylephrine: as above, plus tachycardia, mydriasis Imidazoline: weakness, lethargy, bradycardia, hypotension, prolonged capillary refill time; less commonly hypertension, panting, nervousness, hyperactivity, and shaking
ETIOLOGY AND PATHOPHYSIOLOGY Source: Toxicosis can occur either when animals accidentally ingest OTC medications or are mistakenly given the medication. Decongestants stimulate alpha-adrenergic receptors, resulting in vasoconstriction of arterioles in the nasal passages, thus improving air flow. Pseudoephedrine, ephedrine (stereoisomer), ma huang (a herbal form of ephedra). Pseudoephedrine is available as a hydrochloride or sulfate salt. It is found as a single ingredient (30-mg or 60-mg regular pill), or extended-release (120 mg as 12-hour pill or 240 mg as 24-hour pill) or as a liquid (varying concentration). It is more commonly available in combination with other ingredients (cough suppressants, antihistamines, acetaminophen, ibuprofen). Common brand names of products that contain pseudoephedrine include Sudafed, Afrin, Tylenol, Vicks, Alka-Seltzer, and Contac. Phenylephrine is available for oral use (mostly 5- to 15-mg tablets), nasal sprays (0.25%-1%), or eye drops (0.1%). It is available in combination with other medications (antihistamines, cough suppressants, pain killers). Imidazoline decongestant examples are oxymetazoline, tetrahydrozoline, naphazoline, and xylometazoline. These are available as nasal and ophthalmic solutions of varying concentrations (0.01%-0.1%). Mechanism of Toxicosis:
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Adverse effects are dose-dependent and reflect excessive stimulation of the adrenergic nervous system. With pseudoephedrine, the release of norepinephrine increases the potential for central nervous system stimulation. Ingestion of >3 mg/kg in an otherwise healthy dog typically warrants decontamination of the patient and close monitoring. With imidazoline decongestants, overdoses cause excess stimulation of central alpha-2 receptors, which results in hypotension. The margin of safety is very narrow with these agents, with ingestion of even a small amount potentially resulting in toxicosis.
DIAGNOSIS DIAGNOSTIC OVERVIEW Diagnosis is suspected based on a combination of evidence of exposure along with presence of consistent signs. OTC urine drug-test kits can detect pseudoephedrine, or it can be detected in plasma at a diagnostic laboratory (can help determine exposure).
DIFFERENTIAL DIAGNOSIS Toxicologic: Pseudoephedrine/ephedrine/phenylephrine: amphetamines, antihistamines, cocaine, metaldehyde, methylxanthines, phenylpropanolamine, strychnine Imidazoline: alcohols, amitraz, barbiturates, benzodiazepines, calcium channel blockers, clonidine, essential oils, medetomidine, xylazine Spontaneous, nontoxicologic: Pseudoephedrine/phenylephrine: pheochromocytoma, renal disease, intracranial disease Imidazoline: hypoadrenocorticism, advanced cardiovascular disease/cardiogenic shock, sepsis, hypovolemic shock, trauma
INITIAL DATABASE CBC Serum biochemistry profile Arterial blood pressure ECG (heart rate and rhythm) Body temperature
ADVANCED OR CONFIRMATORY TESTING Urine drug screening with OTC test kit (optional)
TREATMENT TREATMENT OVERVIEW Treatment is indicated based on clinical suspicion (history and physical examination), without urine test confirmation. Treatment may consist of patient decontamination alone (emesis and administration of activated charcoal) if clinical signs are absent, or decontamination and management of cardiovascular and CNS aberrations and thermoregulation if clinical signs are present.
ACUTE GENERAL TREATMENT Decontamination of patient: Pseudoephedrine/ephedrine/phenylephrine: Induction of emesis (see p. 1364 ) with 3% hydrogen peroxide, 2 mL/kg PO 1-2 times to effect, maximum of 45 mL; useful only in asymptomatic animals within 1 hour of ingestion of immediate-release products and within a couple of hours of extended-release products. Activated charcoal (1-2 g/kg granules or 6.6-11 mL/kg of 10% solution with sorbitol or other cathartic PO). Repeat (3.3-5.5 mL/kg without cathartic PO) once 6-8 hours after initial administration if extended-release decongestant. Acidification of urine (use only if facility to run blood gases available): ammonium chloride, 50 mg/kg PO q 6 h; or ascorbic acid, 30 mg/kg PO q 8 h to promote excretion (ion trapping).
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Control CNS excitation (note: phenothiazines are drugs of choice for controlling CNS excitation: acepromazine, 0.02-0.05 mg/kg IV, IM, repeat as needed; useful for mild hypertension and CNS stimulatory signs; or chlorpromazine, 0.5-1 mg/kg IV. Control tachycardia: propranolol, 0.02-0.04 mg/kg IV, repeat in 4-8 hours; or use esmolol, 0.2-0.5 mg/kg IV or 25-200 mcg/kg/min IV as constant rate infusion. Imidazoline decongestants: Due to the rapid onset of signs after imidazoline decongestant ingestion, emesis and charcoal are generally not recommended. Specific treatment: Imidazoline decongestants: Atipamezole (50 mcg/kg IM to effect for hypotension); may be repeated as needed for life-threatening hypotension and bradycardia. A quarter to a third of the dose may be given IV for rapid effect, and the remainder IM. Yohimbine: 0.1 mg/kg IV; repeat in 2-3 hours if needed. Use if atipamezole is not available. Supportive care for all decongestant exposures: Intravenous fluid therapy Thermoregulation: cool fluids, external cooling measures as needed Keep the patient calm and reduce external stimuli (quiet surroundings).
DRUG INTERACTIONS Diazepam: paradoxical response (when given at high doses or when given too fast) may add to stimulatory signs from pseudoephedrine/ephedrine/phenylephrine. Propranolol: contraindicated if systemic hypertension is present (beta-2 blockade in vessels may cause vasoconstriction and worsen the hypertension). Atropine: contraindicated for reflex bradycardia due to hypertension.
POSSIBLE COMPLICATIONS Disseminated intravascular coagulation (DIC) due to hyperthermia Permanent brain damage from prolonged stimulation Renal failure from systemic hypo- or hypertension and/or rhabdomyolysis
RECOMMENDED MONITORING Heart rate/rhythm Blood pressure Body temperature Mentation Serum biochemistry profile, including electrolytes Acid-base status if acidifying urine
PROGNOSIS AND OUTCOME Generally favorable with prompt presentation and appropriate care. Presence of head bobbing, circling, or DIC carries a poor prognosis. Pseudoephedrine exposures exceeding 10 mg/kg are potentially lethal without treatment.
PEARLS & CONSIDERATIONS COMMENTS The use and availability of pseudoephedrine in several U.S. states has been restricted because of alleged use of this medication in illegal amphetamine synthesis. Pseudoephedrine is being replaced by phenylephrine. Other agents (nonsteroidal antiinflammatory drugs [p. 768], antihistamines [p. 87], cough suppressants) may also cause toxicosis if a combination product was ingested; be sure to monitor for signs and treat accordingly. The signs of pseudoephedrine toxicosis are very similar to amphetamine toxicosis in dogs. Several weight-loss OTC products contain varying levels of ma huang, a natural source of ephedrine.
TECHNICIAN TIPS
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The over-the-counter availability of these medications may give owners the wrong impression that they are harmless. Any casual mention by an owner of this type of medication is worth discussing with the veterinarian, especially if physical signs compatible with toxicosis are present.
PREVENTION Keep medications out of animal's reach. Awareness of where pets roam when unsupervised Never administer OTC medications to pets without consulting a veterinarian.
CLIENT EDUCATION Need to control or monitor pet's environment Location of nearest veterinary hospital at any time of day or night
SUGGESTED READING Daggy A, Kaplan R, Roberge R, Akhtar J: Pediatric Visine (tetrahydrozoline) inges-tion: case report and review of imidazoline toxicity. Vet Human Toxicol 45(4):210–212, Aug 2003. Kahn CM, editor: Toxicities from over the counter drugs. In: Merck veterinary manual, ed 9, Whitehouse Station, NJ, 2005, Merck & Co, Inc, pp 2525–2527. Means C: Decongestants. In Plumlee KH, editor: Clinical veterinary toxicology, St Louis, 2004, Mosby/Elsevier, pp 309–311. Welch SL: Oral toxicity of topical preparations. Vet Clin North Am Small Anim Pract. 32(2):443–453, vii, March 2002. AUTHOR: DONNA A. MENSCHING EDITOR: SAFDAR A. KHAN
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Deciduous Teeth, Persistent (“Retained”)
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Deciduous Teeth, Persistent (“Retained”) BASIC INFORMATION DEFINITION Deciduous teeth that failed to exfoliate
SYNONYM Retained deciduous teeth: retained refers to failure to erupt (emerge through the gingival surface); persistent is more accurate because it refers to failure to exfoliate (cause shedding of the deciduous tooth).
EPIDEMIOLOGY Dogs and cats. Permanent dentition eruption schedules dictate when a deciduous tooth is considered persistent (use table cautiously; breed and individual variation can be significant [±1 to 2 months]): GENETICS & BREED PREDISPOSITION High prevalence in toy dog breeds (Yorkshire terriers, miniature poodles, Pomeranians) suggests inheritance. Recent advances in the understanding of eruption and exfoliation suggest familial and/or genetic influence.
Permanent Dentition Eruption Times in the Dog and Cat Dog
Cat
Incisors
3-5 months 3-4 months
Canines
4-6 months 4-5 months
Premolars 4-6 months 4-6 months Molars
5-7 months 4-5 months
ASSOCIATED CONDITIONS & DISORDERS As a result of persistence of deciduous teeth: Periodontal disease Malocclusion Malposition, retarded eruption, impaction of permanent teeth Palatal/labial trauma
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT Teeth appear too numerous or are angled abnormally. A large percentage of persistent deciduous teeth are found on physical examination of adolescent dogs and cats presented for neutering. PHYSICAL EXAM FINDINGS A narrower deciduous tooth is observed alongside an erupting or fully erupted permanent tooth. The deciduous canine and incisor teeth are most commonly affected, though persistent deciduous premolars do occur (there are no deciduous molars or first premolars).
ETIOLOGY AND PATHOPHYSIOLOGY
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Commonly reported causes: Lack of permanent successors Dentoalveolar ankylosis of deciduous teeth Failure of the erupting permanent crown to apply pressure to the deciduous tooth root Hormonal abnormalities affecting growth or metabolism Pathophysiologically important information includes: Persistent deciduous teeth may result in malpositioned permanent teeth. Permanent mandibular incisors, canines, and premolars erupt lingual (i.e., toward the tongue) to persistent deciduous teeth; lingually deviated permanent mandibular canine teeth may cause palatal trauma. Permanent maxillary incisors and premolars erupt palatal (i.e., toward the palate) to persistent deciduous teeth. Permanent maxillary fourth premolars erupt buccal/labial (i.e., toward the cheek/lip) and distal (i.e., away from the midline of the dental arch) to persistent deciduous teeth. Permanent maxillary canine teeth erupt mesial (i.e., toward the midline of the dental arch) to persistent deciduous teeth. Food, debris, plaque, and calculus accumulating on and between deciduous and permanent teeth may cause periodontal disease even in young animals.
DIAGNOSIS DIAGNOSTIC OVERVIEW Physical exam is highly suggestive; presence of a deciduous tooth in a dog or cat with otherwise permanent dentition. Dental radiography is indicated prior to intervention.
DECIDUOUS TEETH, PERSISTENT (“RETAINED”) Bilateral persistent deciduous mandibular canine teeth in a dog (arrows), causing permanent canines (asterisks) to be displaced lingually. (Copyright Dr. Alexander M. Reiter.)
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DECIDUOUS TEETH, PERSISTENT (“RETAINED”) Radiograph of lower jaw of same dog. Persistent deciduous canine teeth (arrows) block normal eruption pathway of permanent successors (asterisks). Radiograph arranged in labial mounting; rostral is toward top of image, patient's left is on right of image. (Copyright Dr. Alexander M. Reiter.)
DIFFERENTIAL DIAGNOSIS Missing, malformed, malpositioned or unerupted permanent tooth Supernumerary permanent tooth Malocclusion
INITIAL DATABASE CBC, serum chemistry panel, urinalysis: preoperative, generally unremarkable Full-mouth dental radiographs: evaluate root structures, confirm and document presence of healthy permanent teeth.
ADVANCED OR CONFIRMATORY TESTING Hormone levels if metabolic/endocrine disease is suspected
TREATMENT TREATMENT OVERVIEW Extraction is indicated in virtually all cases (exception: no equivalent permanent tooth) to alleviate dental crowding, soft-tissue trauma, and/or dental interlock; prevent periodontal disease; prevent malpositioning of permanent teeth and malocclusion; and
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correct existing malocclusion.
ACUTE GENERAL TREATMENT No treatment is needed for uncrowded, healthy persistent deciduous teeth that have no permanent counterpart. Extraction of all other persistent deciduous teeth is advised. Closed and open extraction techniques are acceptable, depending on tooth to be extracted and degree of root resorption. Closed extraction for mobile teeth Open extraction via creation of a mucoperiosteal flap and alveolar bone removal for solid teeth with complete root structures Slow, steady pressure with a dental elevator is key for inducing periodontal ligament fatigue and successful extraction. Be sure to keep all instrumentation away from the erupting permanent tooth. Extraction sites should be closed using rapidly absorbable synthetic suture material while avoiding placing sutures directly over an erupting tooth. Postoperative dental radiographs are recommended to ensure complete extraction, evaluate surrounding structures for damage, and provide documentation. Antibiotics are not usually necessary post extraction. Pain management: intraoperative nerve block (0.5% bupivacaine hydrochloride, 0.2 to 0.3 mL near middle mental, inferior alveolar, infraorbital or maxillary nerve) followed by oral nonsteroidal antiinflammatory medication (e.g., carprofen, 2 mg/kg PO q 12 h) for 2-3 days postoperatively.
POSSIBLE COMPLICATIONS Root fracture and retained root tips, leading to infection of the permanent tooth Retarded eruption, malpositioning, and/or mechanical damage to the permanent tooth Accidental extraction of permanent tooth
RECOMMENDED MONITORING Examination in 1-2 weeks to evaluate extraction sites Examination in 4-6 weeks to evaluate occlusion if necessary; if abnormalities persist, therapeutic recommendations are offered.
PROGNOSIS AND OUTCOME Excellent for regional healing and reduction of risk of periodontal disease
PEARLS & CONSIDERATIONS COMMENTS Early extraction (5-7 months of age) of persistent deciduous teeth is key to success. Deciduous teeth have a thin dentinal layer and long, spindly roots. They are difficult to extract and break easily. The first rule is to go slow!
PREVENTION Selective breeding
TECHNICIAN TIPS One tooth in one place at one time is the general rule of thumb. If deciduous and permanent teeth of the same type are occupying the same space, the deciduous tooth is persistent.
CLIENT EDUCATION Genetic counseling
SUGGESTED READING
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Hobson P: Extraction of retained primary canine teeth in the dog. J Vet Dent 22:132, 2005. AUTHOR: JENNIFER E. RAWLINSON EDITOR: ALEXANDER M. REITER
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Deafness
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Deafness BASIC INFORMATION DEFINITION Deafness is the inability to hear. Sensorineural deafness results from an abnormality in the inner ear and/or vestibulocochlear nerve and/or the auditory pathways in the brain. Conduction deafness results from a lesion in the outer ear and/or tympanum and/or middle ear.
SYNONYM Hearing loss
EPIDEMIOLOGY SPECIES, AGE, SEX Dogs and cats; any age, either gender GENETICS & BREED PREDISPOSITION Congenital, inherited, sensorineural deafness is associated with coat and iris color. Cats with white haircoats and blue irides are commonly affected by congenital deafness. Dog breeds with white, spotted, merle, or dapple haircoats are predisposed to congenital deafness. Inherited sensorineural deafness is also seen in breeds not related to white, spotted, merle, or dapple coat colors (e.g., Doberman pinscher). Breeds with presumed inherited conditions involving the conduction portion of the ear (external and middle ears) are predisposed to developing hearing loss (e.g., Cavalier King Charles spaniels with secretory otitis media (see p. 807 ). RISK FACTORS Genotype: white, piebald, extreme piebald, or merle genes Old age Repeated exposure to loud noises Breeds of cats or dogs susceptible to otitis externa and/or otitis media Exposure to high dosages of systemic ototoxic drugs, such as aminoglycosides, erythromycin, loop diuretics, cisplatin, nitrogen mustard, or topical chlorhexidine antiseptic. Topical drugs are potentially more ototoxic if the tympanum is not intact. ASSOCIATED CONDITIONS & DISORDERS Otitis externa and/or media External or middle ear canal neoplasia Nasopharyngeal polyps (cats)
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES: Described as: Congenital or adult-onset Inherited or noninherited Sensorineural or conduction deafness HISTORY, CHIEF COMPLAINT Animals with bilateral congenital or adult-onset deafness: Overly aggressive with other puppies in a litter (congenital deafness) Nonresponsive to auditory stimuli (particular frequencies and/or magnitudes)
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Difficult to obedience train, or the adult animal becomes unresponsive to auditory commands to which it was previously responsive Tendency to startle when approached from a position out of visual field Increased tendency to sleep Not aroused from sleep with auditory stimuli Diagnosis of unilateral deafness is not possible with behavioral markers alone; electrodiagnostic evaluation is required to establish a diagnosis of unilateral deafness. PHYSICAL EXAM FINDINGS Animals with normal hearing may not respond to loud sounds in the clinical setting; behavioral response to auditory stimuli is unreliable for evaluating deafness. Animals with peripheral sensorineural deafness typically have no abnormal physical examination findings. Animals with acquired conduction deafness may have one or all of the following clinical signs: Abnormal aural examination Head tilt Facial droop Horner's syndrome Head shaking Signs of pain upon manipulation of the ears Animals with deafness resulting from diseases affecting the vestibulocochlear nerve or central components of the auditory pathways will typically demonstrate other concurrent abnormal neurologic signs.
ETIOLOGY AND PATHOPHYSIOLOGY Acquired conduction deafness resulting from otitis externa/media Impaired conduction of sound waves to the tympanic membrane from hyperplasia and exuberant cerumen production or the presence of pus in the external ear canal Impaired transduction of sound waves to the otic ossicles due to stiffened, fibrotic, or ruptured tympanic membrane Impaired mechanoelectrical transduction due to sclerosis of otic ossicles Acquired conduction deafness from external or middle ear masses Obstruction of sound waves to the tympanic membrane Destruction of middle ear structures Presbycusis (senile deafness) Degeneration of the neural components of the inner ear ± Stiffening of the tympanic membrane ± Ankylosis of the otic ossicles Loud noise exposure Damage to inner ear hair cells and/or ossicles and/or tympanic membrane Congenital hereditary deafness associated with coat color Associated with coat-color genes Abnormal migration of neural crest cells (precursor to melanocytes) to the inner ear (thought to provide nourishment to inner ear); associated with sacculocochlear-type degeneration
DIAGNOSIS DIAGNOSTIC OVERVIEW Bilateral complete deafness is apparent from lack of response to loud noises; diagnostic evaluation should consider history, neurologic exam findings, and otoscopic exam findings. Unilateral or partial bilateral deafness may only be apparent on auditory testing and is generally of interest in preventive medicine (breeders).
DIFFERENTIAL DIAGNOSIS Primary behavioral/psychological disorder Canine cognitive dysfunction syndrome (geriatric dogs)
INITIAL DATABASE Distant and proximal physical examinations Neurologic examination (see p. 1311 ) Thorough aural examination (see p. 1316 )
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Deafness
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ADVANCED OR CONFIRMATORY TESTING Brainstem auditory evoked response/potential (BAER or BAEP) testing using air or bone-conducting stimuli (see p. 1216)
TREATMENT TREATMENT OVERVIEW Prevent hearing loss from developing or progressing. Improve hearing ability.
ACUTE GENERAL TREATMENT No treatment for congenital inherited sensorineural deafness; careful selection of breeding animals by only using non-deaf animals for breeding (perform BAER tests on untested adults and all puppies). No practical treatments for animals with sensorineural deafness. Custom-fit hearing aids are offered by some specialty practices (consult with neurologist or audiologist). For acquired conduction deafness, treat the underlying cause of the disease. Use ototoxic drugs with caution or not at all (topically) if the tympanum is not known to be intact.
RECOMMENDED MONITORING Repeated BAER testing to monitor response to therapy in animals with incomplete deafness
PROGNOSIS AND OUTCOME Inherited sensorineural deafness and deafness resulting from degeneration of inner ear is permanent. Variable prognosis for animals with conduction deafness (depends on chronicity and/or severity of the disease)
PEARLS & CONSIDERATIONS COMMENTS Unilaterally deaf animals are as likely as bilaterally deaf animals to produce deaf offspring. Animals with bilateral deafness require special care, including: Keeping animals on leash, especially when near traffic Obedience training using hand signals To minimize the risk of bite injury, prevent children from startling the animal. Animals with presbycusis may have concurrent cognitive decline, accounting for behavioral changes.
PREVENTION Use non-deaf animals for breeding. For breeds predisposed to congenital deafness, use animals with non-blue irides for breeding.
CLIENT EDUCATION For dog breeders: Inherited sensorineural deafness is a multifactorial genetic condition and is not easily eliminated from particular breeds. Breeding unilaterally or bilaterally deaf animals together increases the incidence of deafness in the offspring; conversely, the incidence of deafness decreases when two hearing dogs are bred together. Breeding two hearing dogs together can still result in producing unilaterally or bilaterally deaf puppies (for inherited deafness). Avoid producing animals homozygous for the merle gene. For owners: Inform owners that the dog has special training needs. Recommend Susan Cope Becker's book, Living with a Deaf Dog: A Book of Advice, Facts and Experiences about
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Deafness
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Canine Deafness (Cincinnati, 1997, Susan Cope Becker).
SUGGESTED READING Deafness in dogs and cats: Information on deafness prevalence, causes and management for owners, breeders and researchers © George M. Strain: http://www.lsu.edu/deafness/deaf.htm Listing of worldwide BAER test sites © George M. Strain: http://www.lsu.edu/deafness/baersite.htm AUTHOR: AUBREY A. WEBB EDITOR: ETIENNE CÔTÉ
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Dacryocystitis
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Dacryocystitis BASIC INFORMATION DEFINITION Although dacryocystitis is technically inflammation of the lacrimal sac, the term is commonly used for describing inflammation anywhere along the tear drainage (i.e., nasolacrimal) system, including the lacrimal puncta, canaliculi, lacrimal sac, and nasolacrimal duct. Dacryocystitis is an acquired condition resulting in ocular discharge (see p. 777).
EPIDEMIOLOGY SPECIES, AGE, SEX Dogs and cats; no age or sex predisposition GENETICS & BREED PREDISPOSITION Brachycephalic breeds (lacrimal stasis): most common conformation associated with dacryocystitis Some extremely dolichocephalic breeds (Doberman pinschers, collies, etc.) also have poor tear drainage and stasis due to a small, deeply set eye and loss of eye-to-lid contact in the medial canthal area. RISK FACTORS The most common causes of dacryocystitis in dogs and cats are foreign bodies (e.g., plant awns that become lodged in the nasolacrimal system) and descending infections due to poor conformation and subsequent lacrimal stasis. Animals that spend time outdoors are at increased risk. GEOGRAPHY AND SEASONALITY Areas with an abundance of plants Increased incidence in spring and summer
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT Ocular discharge (serous, mucoid, purulent, or a combination) Owner may report swelling and/or draining tract in skin ventral to medial canthus. PHYSICAL EXAM FINDINGS Ocular discharge in the form of tears, mucus, or pus, with any or all of the following: Conjunctivitis Lacrimal punctal foreign body Swelling and signs of pain in the medial canthal area If sufficiently chronic, fistulous tracts may be present in the medial canthal area.
ETIOLOGY AND PATHOPHYSIOLOGY Most common cause of dacryocystitis is migration of foreign bodies, most frequently plant material, into the nasolacrimal system. Descending infections from ocular surface flora, often associated with poor tear drainage and lacrimal stasis, also incriminated with initiating inflammation.
DIAGNOSIS
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Dacryocystitis
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DIAGNOSTIC OVERVIEW Suspicion for the diagnosis arises based on chief complaint and physical exam findings indicative of ocular abnormalities including ocular discharge. Determination of whether dacryocystitis involves an obstruction or is secondary to inflammation is the key to diagnosis and prompt treatment. This is accomplished by checking for nasolacrimal passage of fluorescein dye and nasolacrimal flushing.
DIFFERENTIAL DIAGNOSIS Other causes of blockage of the nasolacrimal system: Congenital disorders, including micropunctum or imperforate lacrimal punctum Acquired disorders, including traumatic lacerations or neoplastic invasion or compression of the nasolacrimal drainage apparatus Other causes of ocular discharge (see p. 777)
INITIAL DATABASE Complete ophthalmic examination (see p. 1313) including: Schirmer tear test (rule out keratoconjunctivitis sicca [KCS; see p. 1406 ] as cause for ocular discharge). Normal >15 mm after 1 minute in dogs, variable in cats. Fluorescein dye application Rule out corneal ulceration as cause for ocular discharge. Fluorescein dye application also tests for nasolacrimal system patency. Dye normally traverses the nasolacrimal apparatus to exit the nares within 5 minutes (dogs and cats). Visualization of the dye in the nares can be assisted with a Wood's lamp (dye fluoresces). False-negative results may occur if animal licks dye from nares before dye is visualized, or dye may drain caudally into nasopharynx (mainly brachycephalic breeds). Nasolacrimal flushing if suspect complete or partial nasolacrimal duct blockage: May be done under firm restraint with topical ocular anesthesia (e.g., proparacaine 0.5% [dogs]). Resistant animals or signs of discomfort warrant routine preanesthetic evaluation and subsequent sedation or general anesthesia (cats have small lacrimal puncta). Lacrimal puncta can be cannulated but not distal nasal puncta (dogs and cats), which are difficult to identify in many or most individuals irrespective of dacryocystitis. Identify dorsal and ventral lacrimal puncta (oval in dog and round in cat, with or without circumferential pigment), 1 to 2 mm from eyelid margin in palpebral conjunctiva near medial canthus. Gently insert cannula or intravenous catheter (stylet removed; 22 to 24 gauge, dogs; 24 to 26 gauge, cats), with 3-mL syringe filled with sterile saline or eyewash attached, approximately 3 mm into the dorsal lacrimal punctum. Slowly inject the saline/eyewash until it flows from the ventral lacrimal punctum (confirms puncta, canaliculi, and lacrimal sac are patent). Next, occlude ventral lacrimal punctum with digital pressure and flush 3-12 mL saline/eyewash through the nasolacrimal duct. Collect fluid/discharge at naris in sterile basin. Culture and sensitivity testing of purulent discharge if present Consider referral to a veterinary ophthalmologist if unable to establish patency of nasolacrimal system.
ADVANCED OR CONFIRMATORY TESTING Dacryocystorhinography (contrast study of nasolacrimal system) with standard radiography can identify an obstruction site. Recently, CT-dacryocystorhinography has been demonstrated to allow highly accurate characterization of lesions obstructing the nasolacrimal duct.
TREATMENT TREATMENT OVERVIEW Determine character (i.e., plant material, inflammatory debris, etc.) and location of obstruction and relieve it.
ACUTE GENERAL TREATMENT If foreign body is lodged in canaliculi or lacrimal sac, it may be manually removed by flushing lacrimal punctum. If a foreign body is present in nasolacrimal duct, removal may be accomplished by dacryocystotomy (surgical incision of nasolacrimal duct; referable procedure).
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Dacryocystitis
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CHRONIC TREATMENT Care after any of the preceding surgeries would include topical antibiotic/steroid combination medication (neomycin/polymyxin /dexamethasone suspension or ointment q 4-6 h) for the first 2-4 postoperative weeks. Dacryocystotomy requires placement and maintenance of a Silastic cannula and oral antibiotics for 3-4 weeks after surgery.
POSSIBLE COMPLICATIONS If foreign bodies are left in the nasolacrimal drainage system, scarring, permanent occlusion, and chronic epiphora may result.
PROGNOSIS AND OUTCOME Depends on underlying cause Good prognosis with successful removal of foreign body
PEARLS & CONSIDERATIONS COMMENTS Prompt retrieval of foreign bodies from the proximal portions of the nasolacrimal system is essential; surgical removal from the nasolacrimal duct is technically difficult and has many potential complications. False-negative results can occur when attempting nasolacrimal fluorescein dye passage in brachycephalic breeds, because fluorescein may drain into the back of the oral cavity, owing to the characteristic shape of a brachycephalic dog or cat's maxilla.
PREVENTION Keep pets away from areas with tall grass, especially in the late summer.
SUGGESTED READING Grahn BH: Diseases and surgery of the canine nasolacrimal system. In Gelatt KN, editor: Veterinary ophthalmology, ed 3, Philadelphia, 1999, Lippincott Williams & Wilkins, pp 569–581. Miller PE: Lacrimal System. In: Slatter’s fundamentals of veterinary ophthalmology, ed 4, St Louis, 2008, Saunders Elsevier, pp 157–174. Nykamp SG, et al: Computed tomography dacryocystography evaluation of the naso-lacrimal apparatus. Vet Radiol Ultrasound 45:23, 2004. AUTHOR: STEVEN R. HOLLINGSWORTH EDITOR: CHERYL L. CULLEN
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Eyelid Defects: Trauma, Masses
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Eyelid Defects: Trauma, Masses BASIC INFORMATION DEFINITION Eyelid trauma is associated with any external injury to the eyelid predisposing to inflammation or laceration. Eyelid masses are very common and are associated with neoplastic or inflammatory conditions.
SYNONYMS Chalazion: hordeolum, meibomian gland cyst Meibomian glands: tarsal glands, palpebral glands
EPIDEMIOLOGY SPECIES, AGE, SEX Dogs and cats Eyelid trauma may occur at any age. Eyelid mass: average age 9-10 years (eyelid neoplasia, dogs) but depends on type of mass GENETICS & BREED PREDISPOSITION Eyelid trauma: more common in young animals, outdoor animals, and sporting breeds of dogs Eyelid mass (dogs): more common in American cocker spaniel, boxer, poodle, golden retriever, Labrador retriever, English springer spaniel, beagle, collie, Siberian husky, and English setter RISK FACTORS: Excessive sunlight and white hair in the periocular region both predispose to squamous cell carcinoma (SCC), the most common eyelid neoplasm in cats. ASSOCIATED CONDITIONS & DISORDERS EYELID TRAUMA Corneal/scleral trauma (see p. 249) Uveitis (see p. 1151) Eyelid mass: Blepharitis (eyelid inflammation) Conjunctivitis (see pp. 239 and 237) Corneal ulceration (see p. 250)
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT Eyelid trauma: Witnessed traumatic event Swollen eyelid(s) (blepharoedema) ± Eyelid laceration Eyelid mass: Growth on eyelid and/or eyelid margin Persistent or intermittent bleeding of eyelid Signs of ocular pain if mass large and causing conjunctival and/or corneal irritation Ocular discharge
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EYELID DEFECTS Eyelid mass. (Courtesy Dr. Phillip A. Moore.) PHYSICAL EXAM FINDINGS Eyelid trauma (some or all of the following): Blepharoedema Eyelid laceration (partial- or full-thickness) Blepharospasm Ocular discharge Conjunctival hyperemia/edema (chemosis) Keratitis (ulcerative or nonulcerative) Eyelid mass (some or all of the following): Mass located along eyelid margin or adjacent to margin of eyelid Size, location, and appearance vary with type of mass: Neoplasm associated with the meibomian gland appears as an irregular, raised, variably sized mass ± pigment. SCC appears as an erosive, ulcerated mass along the eyelid, often near the medial canthus. Chalazion (meibomian gland cyst) presents as smooth, raised, yellow to white mass associated with the meibomian gland. Ocular discharge, blepharospasm, conjunctivitis, keratitis if mass irritating the eye Eyelid hemorrhage Lagophthalmos (incomplete closure of the eyelids)
ETIOLOGY AND PATHOPHYSIOLOGY Eyelid trauma is generally associated with blunt trauma, penetration by sharp objects, or self-mutilation (pawing at eye). Eyelid mass (neoplastic) Common in dogs; most are benign. Rare in cats; most are SCC (malignant). Similar to those of the skin; arise from epithelial, mesenchymal, and melanogenic cells. In dogs, 82% of eyelid neoplasms are sebaceous adenomas, papillomas, or melanomas. Sebaceous gland tumors (sebaceous adenoma, sebaceous epithelioma, and sebaceous adenocarcinoma) arise from the meibomian glands. Focal eyelid inflammation: a chalazion is a pyogranuloma associated with retained meibomian gland secretions.
DIAGNOSIS DIAGNOSTIC OVERVIEW
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Eyelid Defects: Trauma, Masses
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The diagnosis of eyelid trauma is suspected based on the presence of blepharoedema and/or blepharitis with or without ocular discharge. The diagnosis of an eyelid mass is suspected based on the presentation of a “mass”-type lesion or swelling adjacent to or along the lid margin; confirmation of the nature of the mass requires cytologic and/or histopathologic assessment.
DIFFERENTIAL DIAGNOSIS Eyelid swelling: Anaphylaxis Conjunctival/subpalpebral foreign body
INITIAL DATABASE Complete ophthalmic examination (see p. 1313 ) including: Schirmer tear test Fluorescein dye application Intraocular pressures Examination of periocular (e.g., conjunctiva) and intraocular structures, especially if trauma suspected Examination of eyelid margin for extent of laceration or extent and point of origin of mass
ADVANCED OR CONFIRMATORY TESTING Fine-needle aspiration and cytologic evaluation of eyelid masses Histopathologic evaluation of all surgically removed eyelid masses
TREATMENT TREATMENT OVERVIEW Treatment goals are to restore normal eyelid conformation, eliminate ocular irritation, and prevent recurrence of eyelid mass. Treatment for an eyelid mass should be initiated early in the course of the disease to ensure normal eyelid conformation.
ACUTE GENERAL TREATMENT Eyelid trauma: Laceration requires primary/surgical closure of wound. If full-thickness laceration, close in two layers (conjunctiva followed by skin) starting at eyelid margin to ensure accurate apposition of eyelid margin. Eyelid mass: Neoplasia: Surgical removal: If involves eyelid margin and ≤⅓ length of eyelid, remove by a full-thickness V-shaped or “house”-shaped excision. Close in two layers (see Eyelid Trauma under Acute General Treatment above). Eyelid margin mass > ⅓ eyelid length requires a plasty procedure to ensure proper eyelid length (e.g., H-plasty). Consider referral to ophthalmologist or surgeon. Cryosurgery: Useful in treating benign eyelid mass in older animals May be performed under sedation Recurrence rate higher with cryotherapy than with full-thickness excision. Chalazion: Surgical treatment: Scalpel incision of overlying palpebral conjunctiva with curettage; heals by second intention Topical antibiotic/corticosteroid (e.g., neomycin-polymyxin-dexamethasone suspension) q 8 h for 7 days after surgery; corticosteroid contraindicated if cornea is not intact.
POSSIBLE COMPLICATIONS Poor apposition of eyelid margin results in cicatrix (scar) formation, predisposing to entropion or ectropion, or “step” to eyelid margin, resulting in corneal irritation and ulceration.
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Improperly placed sutures at the eyelid margin can predispose to corneal ulceration. Local regrowth of eyelid mass, if mass not completely removed
RECOMMENDED MONITORING Reevaluate apposition of eyelid margin, and remove skin sutures 10 days after surgery.
PROGNOSIS AND OUTCOME Eyelid laceration: prognosis good if apposition of eyelid margin is achieved. Removal of eyelid neoplasm: dogs, prognosis good, majority are benign; cats, prognosis guarded, majority are malignant. Local recurrence is possible if an eyelid mass is not completely excised.
PEARLS & CONSIDERATIONS COMMENTS Eyelid lacerations are treated surgically, not as open wounds, to prevent eyelid scarring, contraction, and distortion of the eyelid margin. Eyelid masses should be removed early to prevent the need for plasty procedures.
PREVENTION Limit actinic radiation (sunlight) exposure in white cats to decrease the potential for SCC.
CLIENT EDUCATION Recurrence is possible after the removal of any eyelid mass.
SUGGESTED READING Stades FC, Gelatt KN: Diseases and surgery of the canine eyelid. In Gelatt KN, editor: Veterinary ophthalmology, ed 4, Ames, 2007, Blackwell Publishing, p 563. AUTHOR: PHILLIP A. MOORE EDITOR: CHERYL L. CULLEN
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Exocrine Pancreatic Insufficiency
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Exocrine Pancreatic Insufficiency BASIC INFORMATION DEFINITION A syndrome caused by insufficient secretion of pancreatic digestive enzymes by the exocrine pancreas
SYNONYM EPI
EPIDEMIOLOGY SPECIES, AGE, SEX: Occurs more commonly in dogs than in cats; any age. In dog breeds that are affected by pancreatic acinar atrophy (PAA), exocrine pancreatic insufficiency (EPI) is most commonly diagnosed in young adults. In other dog breeds and cats, EPI can occur at any age. GENETICS & BREED PREDISPOSITION: In dogs, EPI most commonly occurs in the German shepherd, for which an autosomal recessive inheritance has been proposed. A breed predilection has also been reported for rough coated collies and Eurasians. There is no known breed predilection in cats. See Etiology, below, regarding PAA. RISK FACTORS Chronic pancreatitis can lead to destruction of exocrine pancreatic tissue and EPI. Pancreatic adenocarcinoma or surgery could lead to obstruction of the pancreatic duct, leading to lack of pancreatic enzyme secretion into the small intestine. ASSOCIATED CONDITIONS & DISORDERS: Many canine and feline patients with EPI have other gastrointestinal disorders. Dogs with EPI due to PAA commonly have secondary small-intestinal bacterial overgrowth (also termed antibiotic-responsive diarrhea [see p. 81]); other dogs and cats often have concurrent inflammatory bowel disease (see p. 605).
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT Weight loss is the most common clinical sign in both dogs and cats. Loose stools and less commonly diarrhea Ravenous appetite PHYSICAL EXAM FINDINGS Poor body condition (Note: nowadays patients often are diagnosed much earlier in the disease process, and emaciated patients with EPI are rare.) Poor hair coat and sometimes in cats, greasy soiling of the hair coat
ETIOLOGY AND PATHOPHYSIOLOGY The most common cause of EPI in the dog is pancreatic acinar atrophy. This condition is mostly seen in German shepherds, rough coated collies, and Eurasians. The most common cause of EPI in the cat and the second most common cause of EPI in dogs is chronic pancreatitis. Other potential causes of EPI include obstruction of the pancreatic duct by a pancreatic adenocarcinoma and pancreatic aplasia or hypoplasia, but these have not yet been reported in dogs or cats. Surgical obstruction of the pancreatic duct, leading to EPI, has recently been described. Decreased secretion of exocrine pancreatic digestive enzymes leads to lack of digestive enzymes in the small intestine, which will lead to maldigestion and associated clinical signs. Secondary cobalamin deficiency is very common in dogs and occurs in almost all cats with EPI. In patients with EPI due to chronic pancreatitis, pancreatic inflammation may also lead to destruction of islets of Langerhans and cause concurrent diabetes mellitus.
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Exocrine Pancreatic Insufficiency
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DIAGNOSIS DIAGNOSTIC OVERVIEW The most reliable diagnostic test for EPI for both dogs and cats is serum trypsin-like immunoreactivity concentration (TLI), which is measured by a species-specific assay.
DIFFERENTIAL DIAGNOSIS Primary small intestinal disease (e.g., inflammatory or infiltrative bowel disease) Other secondary causes of chronic diarrhea and weight loss (i.e., hepatic failure, renal failure, hypoadrenocorticism, hyperthyroidism [cats])
INITIAL DATABASE CBC, serum chemistry profile, and urinalysis are usually within normal limits (including serum total protein concentration). Imaging studies are usually within normal limits.
ADVANCED OR CONFIRMATORY TESTING Serum TLI is the diagnostic test of choice for the diagnosis of EPI. A severely decreased serum TLI concentration is diagnostic of EPI. In dogs: ≤2.5 µg/L (canine TLI; reference range 5.7–45.2 µg/L) In cats: ≤8.0 µg/L (feline TLI; reference range 12–82 µg/L) Some patients with EPI may have a serum TLI concentration in the questionable range (>2.5 but 8.0 but 5 years old; dogs with acanthomatous ameloblastoma usually >7 years old (but can affect dogs as young as 1 year of age) Sex: conflicting results; female dogs more often affected than males with acanthomatous ameloblastoma, male dogs more often affected than females with peripheral odontogenic fibroma and giant cell epulis
EPULIDES A, Clinical photograph of rostral upper jaw in a dog with peripheral odontogenic fibroma. Note smooth-surfaced and minimally ulcerated/inflamed gingival mass associated with palatally displaced right maxillary second incisor (asterisk). B, Dental radiograph of rostral upper jaw in same patient (radiograph arranged in labial mounting; rostral toward bottom of image, and patient's right side is on left of image). Note displaced right maxillary second incisor (asterisk) and presence of hard tissue (arrow) within tumor's soft-tissue shadow. (Copyright Dr. Alexander M. Reiter; used with permission.)
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Epulides
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EPULIDES A, Clinical photograph of rostral lower jaw in a Shetland sheepdog with acanthomatous ameloblastoma. Note red, cauliflower-like and easily bleeding mass located between left mandibular third incisor and canine tooth. B, Dental radiograph of rostral lower jaw in same patient (radiograph arranged in labial mounting; rostral toward the top of image, and patient's left side is on right of image). Note displacement of involved teeth, lysis of alveolar bone (asterisks), and sunburst pattern at left lateral mandibular border (arrows). (Copyright Dr. Alexander M. Reiter; used with permission.) Cats: Prevalence: uncommon Distribution: Peripheral odontogenic fibroma ∼63%, giant cell epulis ∼29%, and acanthomatous ameloblastoma ∼8% Breed: no predilection reported Age: cats with single peripheral odontogenic fibroma and giant cell epulis usually >7 years old; acanthomatous ameloblastoma and multiple feline epulides particularly in young-adult cats Sex: no predilection reported ASSOCIATED CONDITIONS & DISORDERS: oral tumors, benign (see p. 786). Hypercalcemia of malignancy has been reported in some dogs with acanthomatous ameloblastomas (increased serum concentrations of ionized calcium, total calcium, and parathyroid hormone-related peptide).
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES Peripheral odontogenic fibroma: Slow growth; gingiva-like Fibroblast is main component in mass. Slow recurrence after incomplete excision Multiple feline epulides may not originate from the periodontal ligament but may represent reactive lesions arising from the periosteum. Giant cell epulis: Rapid growth; inflammatory and ulcerative changes ○ Multinucleated giant cell is main component in mass; osteoid and woven bone formation. Rapid recurrence after incomplete excision Acanthomatous ameloblastoma: Rapid growth; cauliflower-like Basal cell is main component in mass. HISTORY, CHIEF COMPLAINT Gingival mass noticed by owner or at routine oral examination Clinical complaints mostly absent with peripheral odontogenic fibromas; dysphagia, increased salivation, bloody oral
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Epulides
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discharge, and halitosis occasionally reported with giant cell epulides and acanthomatous ameloblastomas. PHYSICAL EXAM FINDINGS Peripheral odontogenic fibroma: Firm, rarely ulcerated gingival mass that measures 0.5 to 3 cm in diameter Located near canine, premolar, and molar teeth (less commonly in the incisor tooth area) and variably fixed to the gum line Covered by oral epithelium; ulceration infrequent Giant cell epulis: Soft, reddish purple Ulcerated and inflamed Acanthomatous ameloblastoma: Cauliflower-like, red, ulcerated, easily bleeding gingival mass that measures 0.5 to 10 cm in diameter Most commonly located in the rostral lower jaw near incisor and canine teeth; less often in the rostral upper jaw (incisor and canine tooth area), caudal lower jaw (near first molar), and caudal upper jaw (near fourth premolar)
ETIOLOGY AND PATHOPHYSIOLOGY Peripheral odontogenic fibroma: Mixed or mesenchymal (dependant on literature studied) odontogenic tumor Arising from cells in the periodontal ligament Giant cell epulis: considered to be a variant of the peripheral odontogenic fibroma in which extensive ulceration and inflammation results in strongly increased osteoclastic activity, but the real origin remains unknown. Acanthomatous ameloblastoma: Epithelial odontogenic tumor Debatable whether arising from epithelial rests of Malassez in periodontal ligament (intraosseous/central ameloblastoma) or epithelial rests of Serres in gingival connective tissue (extraosseous/peripheral ameloblastoma)
DIAGNOSIS DIAGNOSTIC OVERVIEW Diagnosis requires staging, including oral examination under anesthesia, thoracic radiographs, regional diagnostic imaging (dental radiographs, computed tomography), lymph node palpation and aspiration, and biopsy of the gingival mass.
DIFFERENTIAL DIAGNOSIS Dogs: Gingival hyperplasia (often generalized) Pyogenic granuloma (uncommon) Dentigerous cyst (around crown of an unerupted tooth) Odontoma (not a real tumor, but a hamartoma, i.e., accumulation of normal cells in an abnormal manner) Viral papillomatosis (usually in puppies or immunocompromised adults) Plasmacytoma (usually solitary, pink-red, well circumscribed) Osteoma (slow-growing) Malignant melanoma (most common malignant oral tumor) Squamous cell carcinoma (second most common oral malignant tumor) Fibrosarcoma (third most common malignant tumor) Peripheral nerve sheath tumor (along major nerves) Osteosarcoma (usually osteolytic type; variant: multilobular tumor of bone) Lymphosarcoma (also look for lesions on skin around mouth and nasal plane, bilateral enlargement of tonsils and regional lymph nodes) Amyloid-producing odontogenic tumor (rare) Erythema multiforme (also look for lesions on skin) Autoimmune diseases (bullous pemphigoid, lupus erythematosus) Eosinophilic granuloma (usually on soft palate and lateral edges of the tongue) Cats: Gingival hyperplasia, osteoma, plasmacytoma
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Epulides
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Squamous cell carcinoma (most common malignant oral tumor) Fibrosarcoma (second most common oral malignant tumor) Inductive fibroameloblastoma (rare) Amyloid-producing odontogenic tumor (rare) Eosinophilic granuloma (usually on upper lip, tongue, sublingual tissues, and palate)
INITIAL DATABASE Physical examination, chemistry screen, CBC Dental and skull radiographs: Peripheral odontogenic fibromas are not invasive, and radiographic changes to alveolar bone are unlikely. Acanthomatous ameloblastomas are invasive, and changes to alveolar bone are often visible on dental radiographs. CT: considered to be superior to radiography, particularly for maxillary and caudally located mandibular lesions Biopsy Cytologic techniques are less diagnostic. Biopsy for histopathologic examination is the only definitive test to establish an accurate diagnosis. For small lesions, excisional biopsy can be performed during the initial oral examination, which may be curative. For larger lesions, an incisional biopsy should be performed. Confirmation of the tumor type will allow the clinician to properly plan for future definitive surgery.
ADVANCED OR CONFIRMATORY TESTING CT is valuable to determine local disease extension and bony invasion in dogs with maxillary or caudal mandibular acanthomatous ameloblastoma. This facilitates achieving wide surgical margins and allows for radiation therapy planning.
TREATMENT TREATMENT OVERVIEW The primary goal of treatment is complete tumor removal with minimal functional and cosmetic compromise.
ACUTE GENERAL TREATMENT Surgery: conservative and radical Peripheral odontogenic fibroma: gingival excision with conservative margins, extraction of the associated tooth (or teeth in case pinpointing the lesion to one tooth is difficult), and curettage of the alveolar socket(s) to remove the periodontal ligament; local excision without tooth extraction and socket curettage is rarely curative (recurrence is likely, as these tumors arise from cells in the periodontal ligament). Acanthomatous ameloblastoma: mandibulectomy and maxillectomy with at least 1 cm margins (depending on location of the tumor) Radiation therapy: considered for nonresectable masses, incomplete resections, and recurrent tumors Peripheral odontogenic fibroma: effective but rarely required, as surgical resection typically results in complete cure. Acanthomatous ameloblastoma: effective, with tumor control achieved in about 90% of dogs, especially for smaller tumors; larger tumors (>4 cm) are more likely to recur (only about 30% tumor control); higher radiation doses may be required to improve control rates. Acute and late side effects can occur, most notably radiation-induced tumors (many years after radiation therapy in about 3.5%–12.5% of dogs with acanthomatous ameloblastoma) and bone necrosis. Cryosurgery: causes cellular death after controlled freezing and thawing of the tumor. Best for low-grade tumors 15 mm in 1 minute in dogs) Fluorescein dye application Intraocular pressures (normal >15 mm Hg and 10 kg; clinical response may take 1-2 months; occasional gastrointestinal side effects from niacinamide.
POSSIBLE COMPLICATIONS Chronic ocular pain Uveitis Secondary glaucoma Blindness Azathioprine may cause severe life-threatening myelosuppression; potentially hepatotoxic.
RECOMMENDED MONITORING Monitor for regression of disease every 2–3 weeks until clinical signs resolve, then as needed depending on response to therapy. In animals receiving azathioprine therapy, CBC and liver enzymes should be assessed every 1–2 weeks for the first 2 months then regularly (e.g., monthly) once clinically stable.
PROGNOSIS AND OUTCOME Variable depending on underlying condition and cause Episcleritis: prognosis usually good Recurrence possible
PEARLS & CONSIDERATIONS
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Episcleritis/Scleritis
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COMMENTS Lifelong treatment is typically required.
TECHNICIAN TIP Some ophthalmic drugs have virtually identical names for their formulations with and without corticosteroids. This similarity presents a risk of using the wrong drug. Prior to topical application, it is extremely useful for technicians to carefully read the label of the tube/vial and identify whether it contains corticosteroids and to check the medical record for consistency. Substitution error (especially administering corticosteroids when they are contraindicated) can be devastating and has been made by veterinarians, technicians, and clients.
SUGGESTED READING Grahn BH, Sandmeyer LS: Canine episcleritis, nodular episclerokeratitis, scleritis and necrotic scleritis. Vet Clin North Am Small Anim Pract 38:291–308, 2008. AUTHOR: URSULA M. DIETRICH EDITOR: CHERYL L. CULLEN
24-09-2011 19:56
Epilepsy, Idiopathic
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Epilepsy, Idiopathic BASIC INFORMATION DEFINITION A syndrome characterized by chronic recurrent seizures for which there is no identifiable cause. Other terms: Status epilepticus: a seizure lasting more than 5 minutes, or two or more seizures in which there is incomplete recovery of consciousness. Cluster seizures (also called serial or acute repetitive seizures): three or more isolated seizures occurring within a short period of time.
EPIDEMIOLOGY SPECIES, AGE, SEX Dogs: commonly affected, 1-5 years old, slightly more common in males Cats: uncommonly affected compared with dogs, but not rare in this species GENETICS & BREED PREDISPOSITION More common in large-breed dogs, but any breed can be affected. Inherited in beagle, Belgian Tervuren, keeshond, dachshund, British Alsatian, Labrador retriever, golden retriever, Shetland sheepdog, Irish wolfhound, Viszla, Bernese mountain dog, English springer spaniel, and probably others ASSOCIATED CONDITIONS & DISORDERS: During status epilepticus, hyperthermia can occur secondary to muscle activity.
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT One or more seizures Most common are generalized tonic-clonic seizures characterized by loss of consciousness and sustained contraction of all muscles, followed by paddling motions of the limbs or rhythmic muscle contractions, especially of the limbs and masticatory muscles. Also possible are milder generalized tonic-clonic seizures in which consciousness is maintained, and focal seizures in which only part of the body is involved (e.g., fly-biting movements). With idiopathic epilepsy, the interictal period (period between seizures, after recovery) is normal, and owners do not report evidence of ongoing neurologic deficits. An effort should be made to clarify any possible sources of intoxication (e.g., lead, ethylene glycol, organophosphate, carbamate, metaldehyde). PHYSICAL EXAM FINDINGS Normal unless examined immediately after a seizure when temporary postictal deficits are possible, including generalized ataxia, abnormal behavior, and blindness that proceed to resolve over minutes to hours. Persistent neurologic deficits such as hemiparesis, abnormal behavior, or visual deficits are inconsistent with idiopathic epilepsy and suggest an underlying structural neurologic lesion. Persistent fontanelle may or may not be associated with hydrocephalus; however, it offers an acoustic window for ultrasonography to pursue this diagnosis. A fundic examination is essential. Uveal, retinal, or optic disk diseases that may correlate with causes of seizures and are inconsistent with idiopathic epilepsy include optic neuritis, feline infectious peritonitis, toxoplasmosis/neosporosis, systemic mycoses, rickettsial diseases, systemic hypertension, lymphoma, and metastatic neoplasia.
ETIOLOGY AND PATHOPHYSIOLOGY Theories include inborn abnormalities in neuronal excitability, neurotransmitter, or receptor function.
24-09-2011 19:54
Epilepsy, Idiopathic
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DIAGNOSIS DIAGNOSTIC OVERVIEW Idiopathic epilepsy is a clinical diagnosis based on the typical age of onset, lack of persistent neurologic deficits, and exclusion of other potential causes based on laboratory testing. A presumptive diagnosis of idiopathic epilepsy may be made without comprehensive diagnostic testing when the patient's signalment and history are consistent with epilepsy, and physical and neurologic examination findings and initial database results are normal. In such cases, further testing may be pursued if deterioration or failure to respond to medication is noted. By declining a comprehensive evaluation, the patient's owner must assume the responsibility that an underlying progressive lesion, rather than epilepsy, may be present.
DIFFERENTIAL DIAGNOSIS Metabolic disorders: hepatic encephalopathy including portosystemic shunt, hypoglycemia, polycythemia, hypocalcemia Toxins: lead, ethylene glycol, organophosphate, carbamate, metaldehyde Brain malformations: hydrocephalus, lissencephaly Inherited degenerative diseases such as lysosomal storage diseases Encephalitis: granulomatous meningoencephalitis, necrotizing encephalitis, distemper, tickborne infections, fungal encephalitis, Neospora caninum, Toxoplasma gondii, feline infectious peritonitis Neoplasia: primary and metastatic brain tumor Vascular lesions: infarct, hemorrhage Head injury Also consider nonepileptic episodes such as syncope, narcolepsy, exercise-induced weakness, vestibular dysfunction, and episodes of pain.
INITIAL DATABASE CBC: generally unremarkable. Nucleated red blood cells and/or basophilic stippling suggest lead toxicosis rather than epilepsy; acanthocytes nonspecifically suggest hepatic disease. Serum chemistry profile, urinalysis: help identify hypoglycemia, hepatic encephalopathy, and renal failure (uremic encephalopathy) as possible causes of seizures instead of idiopathic epilepsy. Fasting hypercholesterolemia may suggest hypothyroidism and attendant central nervous system effects if hyperlipidemia is severe. Hypocalcemia can produce intense muscle tremors that may be misinterpreted as seizures. Hyperglobulinemia in cats raises the possibility of feline infectious peritonitis–based encephalitis as the cause of seizures rather than epilepsy. Serum bile acids (preprandial and postprandial): Elevation of either or both suggests hepatic encephalopathy (portosystemic shunt, cirrhotic/fibrosing liver disease, other) rather than idiopathic epilepsy. However, moderate elevations in bile acids routinely may occur soon after a seizure of any cause. In these cases, it is warranted to recheck bile acids 2-4 weeks later to see if the abnormality persists. Blood lead concentration if potential exposure
ADVANCED OR CONFIRMATORY TESTING Brain CT/MRI and cerebrospinal fluid (CSF) analysis are indicated in the following patients presenting with seizures and no identifiable systemic cause: dogs female, large breeds > small breeds. In the dog, the left-sided heart valves (aortic and mitral) are by far the most frequently affected. RISK FACTORS Congenital aortic valve disease (e.g., subaortic stenosis) and other congenital heart diseases that cause disturbances of blood flow and subsequent changes in the endocardium Glucocorticoid use predisposes to endocarditis, and many cases appear to have a nosocomial origin. Infected intravenous catheters, prosthetic heart valves, heart surgery, and interventional cardiac catheterization all enhance the risk. Infection with potentially immunosuppressive organisms (e.g., Bartonella spp., Ehrlichia spp.) enhances the risk of endocarditis. Predisposing factors for endocarditis in dogs include sources of chronic bacteremia (e.g., urinary tract infection, discospondylitis) and systemic illnesses that facilitate bacterial infection (e.g., diabetes mellitus, hyperadrenocorticism/Cushing's disease). GEOGRAPHY AND SEASONALITY: Infective endocarditis is recognized more in warmer climates (e.g., southern and western United States).
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES: Endocarditis is classified as acute or subacute-chronic based on the duration, rate of progression, and severity of clinical signs. HISTORY, CHIEF COMPLAINT Extracardiac manifestations of systemic infection and inflammation are the source of most of the historic complaints. Manifestations of fever (e.g., lethargy, anorexia) are the most common sign, although they may be intermittent, minimal, or even absent in patients with less virulent organisms (e.g., Bartonella spp., some gram-positive organisms) or severe debilitation. Weight loss Reluctance to move (back pain, polyarthritis) Intermittent lameness (muscle embolization, polyarthritis) PHYSICAL EXAM FINDINGS: Most patients diagnosed with endocarditis have a heart murmur: The murmur may be newly recognized or may have changed in intensity, quality, timing, or duration. Many animals with endocarditis have a preexisting heart murmur (e.g., from subaortic stenosis). The presence of a diastolic murmur in a systemically ill animal dramatically raises the index of suspicion for infective endocarditis. Aortic insufficiency often causes a soft, blowing murmur with a distant quality that is difficult to hear.
24-09-2011 19:33
Endocarditis, Infective
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ETIOLOGY AND PATHOPHYSIOLOGY Staphylococcus spp., Streptococcus spp., Erysipelothrix spp., Corynebacterium spp., and Escherichia coli have been the most common bacterial isolates in canine infective endocarditis. Bartonella spp. is being isolated with increasing frequency and appears to have a tropism for the aortic valve. A wide variety of other organisms has been cultured from individual cases, with many nosocomial cases involving Pseudomonas spp., Proteus spp., or other antibiotic-resistant isolates. Anaerobic bacteria (e.g., Bacteroides spp.) are occasionally found.
DIAGNOSIS DIAGNOSTIC OVERVIEW Endocarditis is suspected based on clinical signs and the presence of a heart murmur on physical exam. The index of suspicion may increase substantially based on echocardiographic findings, but a positive bacterial blood culture is required to establish the clinical diagnosis.
DIFFERENTIAL DIAGNOSIS Presenting complaints of animals with infective endocarditis tend to be vague and associated with some aspect of systemic illness (e.g., fever, lameness). Endocarditis should be included in the differential diagnosis of any persistent fever of unknown origin, especially in the presence of a heart murmur.
INITIAL DATABASE Definitive diagnosis requires the synthesis of clinical, laboratory (microbiologic), and echocardiographic data. CBC or serum biochemical changes are not specific. Echocardiography reveals an oscillating mass at a site of endocardial injury (i.e., a mass near but separate from the valve, whose movements are distinct from those of the valve; it is important to note that this excludes valves that are merely thickened, as in myxomatous valve disease/endocardiosis). Two separate blood cultures must be positive for a typical organism and obtained by separate venipunctures an hour apart (three cultures are recommended if time, money, and patient size permit; at least two must be positive). In acutely ill patients with apparent sepsis syndrome, three blood cultures 5-10 minutes apart should be obtained if the patient's size permits, followed by empirical antibiotic therapy.
ADVANCED OR CONFIRMATORY TESTING Patients with suspected or definite endocarditis should have electrocardiograms recorded (and repeated regularly during their clinical course), because the onset of AV or bundle-branch block suggests perivalvular extension of the infection. When blood cultures from suspected infective endocarditis patients remain sterile after 72 hours of incubation, the laboratory should intensify efforts to grow fastidious organisms such as Bartonella spp., and the clinician should initiate alternative (e.g., serologic, PCR) assessment. Panbacterial PCR amplification of the 16s ribosomal bacterial DNA from patients with suspected or definite endocarditis is available. Currently, the sensitivity of this technique is equivalent to standard blood culture techniques.
TREATMENT TREATMENT OVERVIEW Provide effective antiinfective therapy to minimize valve damage. Manage complications (e.g., heart failure).
ACUTE GENERAL TREATMENT Treatment is usually begun with parenteral antibiotic combinations in hospitalized dogs, but once the fever has resolved and clinical improvement (e.g., return of appetite) is evident (generally not more than 3-5 days), treatment is completed on an outpatient basis with oral antibiotics. Treatment is based on blood culture and sensitivity results; these results are not available for the first critical hours or days of therapy.
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Endocarditis, Infective
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Empirical antibiotic therapy for dogs with a clinical history and echocardiographic findings compatible with endocarditis is started with a combination of fluoroquinolone and penicillin-based antibiotics. Parenteral enrofloxacin (5 mg/kg IV q 12 h) and amoxicillin (20 mg/kg IV q 8 h) are most often chosen. Although discussed by some veterinary authors, anticoagulation does not appear to diminish the risk of bacterial embolization in humans and is not generally recommended.
CHRONIC TREATMENT Therapy is generally continued for 12 weeks, and blood cultures are ideally obtained after 10-14 days (on antibiotics) and then again 1 week after stopping antibiotics. If Bartonella spp. is identified by culture or serology, azithromycin, 5–10 mg/kg PO q 24 h is recommended for the first 7 days, then every other day for 6–12 weeks.
POSSIBLE COMPLICATIONS Congestive heart failure, renal failure, or neurologic events are the complications that appear to have the greatest influence on prognosis.
PROGNOSIS AND OUTCOME Prognosis at the time of diagnosis is guarded, owing to the future possibilities of embolic complications and/or congestive heart failure. Factors negatively associated with short-term survival include thrombocytopenia, renal complications, and thromboembolism. Long-term prognosis depends primarily on the valve damage that has been done at the time of diagnosis, as well as the response to antibiotic therapy. Recurrence or treatment failure is likely with inadequate duration of therapy, inappropriate antibiotic selection, or owner noncompliance. Despite optimal therapy and therapeutic monitoring, cure rates for endocarditis do not appear to be especially promising in dogs, and heart failure or deteriorations due to recurrent embolic events is often the long-term result.
PEARLS & CONSIDERATIONS COMMENTS Although both can cause valve thickening and heart murmurs, taking a broader perspective of the case can more clearly demonstrate the differences between acute bacterial endocarditis (typically medium- to large-breed dogs of any age, overt clinical signs of recurrent infection/sepsis, new-onset heart murmur; overall, occurs uncommonly) and endocardiosis (medium- to small-breed dog, generally older adult, no link to overt signs of infection, murmur may be new in onset or long standing; common). The murmur of aortic insufficiency is often heard best by placing the diaphragm of the stethoscope in the animal's left armpit, with the animal lying on its left side (on top of the stethoscope). A high index of suspicion for endocarditis is warranted in cases of disco-spondylitis and in any animal with fever and a diastolic murmur. With appropriate therapy, prognosis appears to be better for animals with less aggressive organisms such as Bartonella spp. if valve damage is not too severe at time of diagnosis.
PREVENTION Animals with subaortic stenosis, animals with cardiac implants (e.g., transvenous pacemakers), and animals that have undergone balloon valvuloplasty should receive routine antibiotic prophylaxis for all procedures that are likely to induce transient bacteremia.
CLIENT EDUCATION Owner compliance is perhaps an even bigger issue in the treatment of endocarditis than it is with other heart diseases, and effective explanation of the rationale for extended (often expensive) antibiotic treatment and a guarded prognosis is therefore critical.
SUGGESTED READING Wall M, Calvert CA: Cardiovascular infections. In Greene CE, editor: Infectious diseases of the dog and cat, ed 3, St Louis, 2006, Elsevier Saunders, pp 841–865.
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Endocarditis, Infective
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AUTHORS: ANDREA C. LANTIS, BRUCE W. KEENE EDITOR: ETIENNE CÔTÉ
24-09-2011 19:33
Encephalopathy, Vascular
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Encephalopathy, Vascular BASIC INFORMATION DEFINITION Brain dysfunction caused by ischemia, or lack of oxygen delivery. These are most commonly focal events (i.e., infarcts or strokes) but occasionally manifest as widespread brain ischemia (i.e., global ischemia).
SYNONYMS Infarct, ischemic encephalopathy, stroke, cerebrovascular accident
EPIDEMIOLOGY SPECIES, AGE, SEX: Dogs and cats of any age and either sex GENETICS & BREED PREDISPOSITION: Cavalier King Charles spaniels may be predisposed to cerebellar infarcts; this may be related to local pressure abnormalities due to caudal occipital malformation syndrome in this breed. Greyhounds may also be predisposed to brain infarction, possibly related to their relatively high resting blood pressure. Brachycephalic breeds may be predisposed to developing global brain ischemia. RISK FACTORS: Focal ischemic events (strokes): hypertension, hypercoagulability, and hyperviscosity. The most prevalent diseases that cause these disturbances in patients with vascular encephalopathy are chronic kidney disease and hyperadrenocorticism. Other conditions include diabetes mellitus, hypothyroidism, hyperthyroidism, hepatic failure, pheochromocytoma, and infectious diseases. Feline ischemic encephalopathy has been linked to intracranial migration of Cuterebra larvae. Risk factors for global brain ischemia include inadequate anesthetic monitoring, cardiac arrest, severe hypoxemia, and the use of ketamine in anesthetic protocols (especially in brachycephalic breeds).
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES: Focal brain ischemic events (strokes, infarcts) can be small (lacunar) or large (territorial) and either hemorrhagic or nonhemorrhagic (the latter are more common). Global brain ischemia usually involves some degree of diffuse oxygen deprivation in the brain and is much less common than focal brain ischemia. HISTORY, CHIEF COMPLAINT The characteristic historic feature of both focal and global ischemic encephalopathy is acute to peracute onset of brain dysfunction, which is nonprogressive after the first 24 hours. Typical chief complaints include sudden-onset, mentation change, vocalizing/crying, or seizures. PHYSICAL EXAM FINDINGS Physical and neurologic examination findings depend primarily on the underlying disorder leading to the ischemic event (physical examination findings) and the region of the brain affected by the ischemic event. Strokes affecting the cerebrum (e.g., propulsive pacing, disorientation, seizures), diencephalon/midbrain (e.g., depression, obtundation/coma), or cerebellum (hypermetria, intention tremor) are seen with some frequency in affected dogs.
ETIOLOGY AND PATHOPHYSIOLOGY Interruption of oxygen delivery to brain tissue Disruption of cellular energy metabolism (i.e., ATP production) Brain necrosis and edema Generation of cytotoxic mediators of secondary brain injury
DIAGNOSIS
24-09-2011 19:32
Encephalopathy, Vascular
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DIAGNOSTIC OVERVIEW The diagnosis is suspected based on a history of sudden-onset neurologic deficits that are typically nonprogressive and asymmetric. Suspicion is heightened when a procoagulable state or other possible inciting factor is identified. Confirmation requires intracranial imaging (e.g., MRI).
DIFFERENTIAL DIAGNOSIS Brain neoplasm Inflammatory brain disease: sterile or infectious encephalitides Trauma (suggested at outset if history unknown, or supportive of trauma)
INITIAL DATABASE CBC, serum biochemistry profile: abnormalities depend on underlying cause (e.g., polycythemia or hyperglobulinemia with hyperviscosity syndrome); changes consistent with kidney disease if hypertension; hypoalbuminemia with hypercoagulability due to loss of antithrombin III (protein-losing nephropathy or enteropathy). Neurologic examination (see p. 1311): deficits according to site of ischemia; symmetric deficits with global ischemia, asymmetric with focal ischemia Serial blood pressure measurement (see p. 1209): rule out systemic hypertension. Urinalysis: pathologic proteinuria in cases of hypercoagulability due to protein-losing nephropathy
ADVANCED OR CONFIRMATORY TESTING MRI of brain (see p. 1302): diagnostic test of choice Helps differentiate focal from global ischemia, but this distinction should be apparent from the history and neurologic exam alone. Cerebrospinal fluid examination (see p. 1228): may be unremarkable or show nonspecific changes.
TREATMENT TREATMENT OVERVIEW Therapeutic goals include: Minimize secondary brain swelling and tissue damage Treat underlying cause of brain ischemia Physical rehabilitation (see p. 1329)
ACUTE GENERAL TREATMENT Mannitol, 0.5–1 g/kg body weight slowly IV over 10-15 minutes Oxygen supplementation
CHRONIC TREATMENT Treat underlying condition (e.g., antihypertensive drugs if hypertension is documented). Physical rehabilitation
POSSIBLE COMPLICATIONS Recumbency-associated pneumonia Pressure sores (see p. 174) Recurrent stroke Exacerbation of underlying condition leading to ischemic event
RECOMMENDED MONITORING Serial neurologic examinations Blood pressure (if hypertension documented) Progression or regression of underlying condition (e.g., diabetes control, control of hyperadrenocorticism)
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Encephalopathy, Vascular
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PROGNOSIS AND OUTCOME Most patients recover fully from focal ischemic events. Prognosis for stroke is more closely associated with the underlying cause than the stroke event itself Global brain ischemia is associated with a more guarded prognosis than focal brain ischemia.
PEARLS & CONSIDERATIONS COMMENTS Recovery from vascular encephalopathy may take several weeks to several months. Aggressive physical therapy and nursing care are essential to a positive outcome. History and symmetry versus asymmetry of neurologic deficits are the main elements that allow the differentiation of global versus focal ischemia, respectively. Although dogs and cats can develop vascular encephalopathy (a true stroke) as described previously, overall this disorder occurs much less commonly than acute vestibular syndrome, which is an acute disorder that does not involve the brain (peripheral vestibular disease), does not involve infarction, and yet is often referred to inaccurately as a “stroke.”
SUGGESTED READING Garosi LS, et al: Results of diagnostic investigations and long-term outcome of 33 dogs with brain infarction (2000-2004). J Vet Intern Med 19:725, 2005. Garosi LS, et al: Treatment of cerebrovascular disease. In Bonagura JD, Twedt DC, editors: Kirk’s current veterinary therapy XIV: 2009, p 1074. Hillock, et al: Vascular encephalopathies in dogs: diagnosis, treatment, and prognosis. Compend Contin Educ Pract Vet 28:208, 2006. AUTHOR & EDITOR: CURTIS W. DEWEY
24-09-2011 19:32
Emphysema and Pulmonary Bullae
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Emphysema and Pulmonary Bullae BASIC INFORMATION DEFINITION Emphysema: pathologic accumulation of air within an organ or tissue Bulla: an air-filled space within the pulmonary parenchyma that arises from alveolar distention or destruction of alveolar walls Bleb: an accumulation of air within the mesothelial covering and layers of elastic fibers and connective tissue cells that comprise the visceral pleura
SYNONYM Bullous emphysema
EPIDEMIOLOGY SPECIES, AGE, SEX Reported most commonly in dogs of middle age, although dogs of any age can be affected. Cats are rarely affected. GENETICS & BREED PREDISPOSITION A familial or genetic predisposition has not been demonstrated. Large, deep-chested dog breeds are considered at greater risk of pulmonary blebs and bullae. RISK FACTORS Congenital bronchial hypoplasia (uncommon) reported in both dogs and cats. Chronic obstructive pulmonary diseases are a recognized risk factor in people and could be so in dogs (e.g., chronic sterile bronchitis). ASSOCIATED CONDITIONS & DISORDERS Congenital bronchial hypoplasia Congenital bronchial cartilage hypoplasia/dysplasia Spontaneous pneumothorax Pneumomediastinum (uncommon) Subcutaneous emphysema (uncommon) Pneumopericardium (uncommon)
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES Congenital forms of bullous lung disease have been described, usually secondary to bronchial hypoplasia or bronchial cartilage defects. HISTORY, CHIEF COMPLAINT Animals may be clinically normal: A pulmonary bleb or bulla may be found incidentally during thoracotomy or thoracoscopy. Clinical signs, when present, can be acute, intermittent, or slowly progressive: Anorexia Lethargy Respiratory distress The rupture of a bleb or bulla, causing spontaneous pneumothorax, is typically associated with acute dyspnea. Cough
24-09-2011 19:31
Emphysema and Pulmonary Bullae
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Exercise intolerance PHYSICAL EXAM FINDINGS Respiratory distress Increased inspiratory effort (pneumothorax from ruptured bleb or bulla) Increased expiratory effort (pulmonary emphysema without pneumothorax) Tachypnea Tachycardia Diminished heart and lung sounds on one or both sides if pneumothorax Subcutaneous emphysema in occasional patients
ETIOLOGY AND PATHOPHYSIOLOGY Histopathologic assessment of resected tissues classifies lesions as blebs or bullae. Exact mechanisms leading to bulla or bleb formation are not defined: Suspected to reflect the effects of distensile or traction forces on the lung surface, or the effects of inflammation or degradative enzymes in the alveoli to break down alveolar walls. Increased alveolar pressure relative to transpleural pressure may also contribute.
DIAGNOSIS DIAGNOSTIC OVERVIEW Definitive diagnosis usually depends on exclusion of other causes of pneumothorax after evaluation of patient history, physical examination, and radiographic imaging, and then surgical observation of typical lesions.
DIFFERENTIAL DIAGNOSIS Other causes of pneumothorax: Trauma, either blunt or penetrating, to the thoracic wall, trachea, esophagus, or pulmonary parenchyma Inflammatory lung disease Neoplastic lung disease Parasitic lung disease, especially Paragonimus kellicotti and Dirofilaria immitis Obstructive airway disease Migrating foreign bodies
INITIAL DATABASE Thoracic radiographs: May demonstrate the features of pneumothorax (see p. 889) Often unremarkable; observation of a bleb or bulla is uncommon. Animals with paragonimiasis may have thick-walled bullae evident, even with pneumothorax. Thoracic radiographs may in some cases show air-filled dilations within the parenchyma. Occasional animals may have pneumomediastinum, pneumopericardium, or subcutaneous emphysema evident. Results of a CBC, biochemical profile, and urinalysis are typically unaffected by the disease. Hypoxemia will be the most consistently present abnormality on arterial blood gas analysis. Fecal examinations (flotation and sedimentation techniques) to rule out respiratory parasites
ADVANCED OR CONFIRMATORY TESTING Definitive diagnosis is usually made by detection of bullae, blebs, or air leaking from the lung surface during thoracotomy or thoracoscopy and confirmed with histopathologic examination of resected tissue. Median sternotomy is the preferred approach in patients with spontaneous pneumothorax. Cranial lung lobes are most commonly affected, although other lung lobes can also have lesions. Tracheoscopy, bronchoscopy, and esophagoscopy are usually normal in patients with bullous lung disease unless airway hypoplasia is present. In a small number of reported cases, CT scans of the thorax have proved more sensitive than plain thoracic radiographs for the detection of bullous lung lesions in dogs with spontaneous pneumothorax.
24-09-2011 19:31
Emphysema and Pulmonary Bullae
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TREATMENT TREATMENT OVERVIEW Improve respiratory function and oxygenation in patients with respiratory distress, typically by thoracocentesis, as most such patients will have pneumothorax. Remove bullae or blebs. Treat underlying obstructive disease, if present
ACUTE GENERAL TREATMENT Thoracocentesis if pneumothorax is present (see p. 1338): Thoracostomy tubes with continuous suction may be needed in some patients for management of persistent air accumulation. Oxygen provided by mask, nasal catheter, oxygen cage Cage rest
CHRONIC TREATMENT Long-term resolution of spontaneous pneumothorax from rupture of blebs or bullous lung lesions, if not from parasitic diseases, is most reliably achieved with surgical resection of the affected lung tissue by either partial or complete lung lobectomy. Persistence or recurrence of clinical signs is more likely if the patient is managed nonsurgically. Partial or complete lung lobectomy may be accomplished via thoracotomy or thoracoscopy. Treat underlying obstructive disease, if present
POSSIBLE COMPLICATIONS Pneumothorax from leakage at suture or staple site of a lobectomy Postoperative complications of infection, wound dehiscence
RECOMMENDED MONITORING Clinical signs Thoracic radiographs
PROGNOSIS AND OUTCOME Prognosis is good with surgical resection of bullous lung lesions.
PEARLS & CONSIDERATIONS COMMENTS Often in patients with spontaneous pneumothorax of uncertain origin and no history of trauma, bleb or bulla rupture ultimately is found to be the underlying cause. Some animals can be successfully managed with nonsurgical methods (thoracocentesis, thoracostomy tubes), but the literature supports early lung lobectomy for the best long-term outcomes. Affected animals can have multiple lesions scattered over different lung lobes, and lung lobes on both sides of the thoracic cavity can be affected. It is thus imperative to examine the entirety of both lungs during thoracotomy or thoracoscopy.
PREVENTION There is no means of preventing the disease. Animals with congenital bronchial hypoplasia should probably not be bred.
TECHNICIAN TIPS Thoracocentesis is most often done at around the 7th or 8th intercostal space, so these areas should be clipped in
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Emphysema and Pulmonary Bullae
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preparation for the procedure. When the goal of thoracocentesis is to remove air, preferred recumbency is that in which the patient is most comfortable.
CLIENT EDUCATION Nonsurgical treatment approaches are more likely to be associated with persistence or recurrence of clinical signs. Postsurgical outcomes are usually excellent.
SUGGESTED READING Au JJ, et al: Use of computed tomography for evaluation of lung lesions associated with spontaneous pneumothorax in dogs: 12 cases (1999-2002). J Am Vet Med Assoc 228:733, 2006. Brissot HN, et al: Thoracoscopic treatment of bullous emphysema in 3 dogs. Vet Surg 32:524, 2003. Lipscomb VJ, et al: Spontaneous pneumotho-rax caused by pulmonary blebs and bullae in 12 dogs. J Am Anim Hosp Assoc 39:435, 2003. Puerto DA, et al: Surgical and nonsurgical management of and selected risk factors for spontaneous pneumothorax in dogs: 64 cases (1986-1999). J Am Vet Med Assoc 220:1670, 2002. AUTHOR & EDITOR: RANCE K. SELLON
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Electrocution
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Electrocution BASIC INFORMATION DEFINITION The passage of electricity through tissue, resulting in electrophysiologic disruption of the tissue
EPIDEMIOLOGY SPECIES, AGE, SEX Most common in young cats and dogs (5 weeks to 1.5 years of age), with no sex predilection RISK FACTORS Young age and environmental access GEOGRAPHY AND SEASONALITY Seasonal associations: Christmas holidays (decorative holiday lights) or perhaps most often from late spring to early autumn, when owners are likely to operate electrical devices (e.g., fans), and there may be an increase in acquisition of puppies and kittens. ASSOCIATED CONDITIONS & DISORDERS Noncardiogenic pulmonary edema, cardiac arrhythmias, oral burns, and seizures
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES High-voltage injury versus low-voltage injury, based on the nature and intensity of the current. The most severe injuries result from a high-current and high-voltage situation and thus produce a worse clinical outcome. Electrical sources can produce energy levels that range from relatively low (e.g., 9-volt battery) to intermediate (e.g., household outlets) to very high (e.g., electrical metal utility cover). Household current is the most common. HISTORY, CHIEF COMPLAINT Sometimes witnessed; other times the owner reports sudden onset of dyspnea, collapse, or dysphagia. PHYSICAL EXAM FINDINGS Oral burns: to the tongue, palate, and commissures of the lips Respiratory problems: dyspnea (harsh lung sounds, upper airway edema), cyanosis, coughing Cardiac problems: arrhythmias (ventricular fibrillation), asystole Neurologic abnormalities: loss of consciousness, focal muscle tremors, seizures
ETIOLOGY AND PATHOPHYSIOLOGY Electricity (usually 60 Hz of alternating current and 120 volts is found in most households in North and much of South America; in most of the rest of the world, it is usually 50-60 Hz of alternating current and 220 volts) disrupts the electrophysiologic activity of tissue, causing muscle spasms, ventricular arrhythmias, and vasomotor changes in the central nervous system, resulting in acute pulmonary edema. The electric energy is also transformed into heat, which can cause coagulation of tissue proteins. Sudden death may result from these processes. Electrocution is almost always accidental, typically with a young pet chewing on an electric cord.
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Electrocution
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ELECTROCUTION A, Dorsoventral thoracic radiograph of a 4-month-old male English bulldog that chewed on an electrical cord and was presented for evaluation of severe dyspnea. Heavy interstitial infiltrate is distributed caudally and symmetrically (left-right). B, Same dog 2 weeks later after making a complete recovery. Infiltrate has resolved. (Courtesy Dr. Julio Lopez, California Animal Hospital.)
DIAGNOSIS DIAGNOSTIC OVERVIEW If unwitnessed, the diagnosis is suspected if it is a young pet with the presence of oral burns and dyspnea. Thoracic radiographs classically show noncardiogenic edema (interstitial/alveolar pattern with a caudodorsal distribution).
DIFFERENTIAL DIAGNOSIS Chemical or thermal burns, exposure to fire, and smoke inhalation
INITIAL DATABASE Initial database is dependent on the severity of injury. In some cases, if the animal has no physical exam abnormalities, no testing is required. In other cases, if the pet is dyspneic or pulmonary crackles are auscultated, chest radiographs are warranted. In severely affected animals, CBC, serum biochemistry profile, coagulation profile, and urinalysis are warranted.
ADVANCED OR CONFIRMATORY TESTING Pulse oximetry or arterial blood gas analysis may be useful to document hypoxemia. However, in young or small animals, the stress of arterial sample collection should be weighed against the potential benefits.
TREATMENT TREATMENT OVERVIEW Treatment mainly consists of supportive care, but the degree of intervention depends on the severity of the case. Burns should be cleaned; if severe, surgical débridement is indicated when the patient is stable. Noncardiogenic pulmonary edema is treated with supplemental oxygen administration. If severe or if pharyngeal edema is present, intubation and ventilation may be necessary.
ACUTE GENERAL TREATMENT Noncardiogenic pulmonary edema is treated with rest and supplemental oxygen (see pp. 1318 and p. 1362).
CHRONIC TREATMENT Treat burns with antibiotics, wound cleaning, soft food/feeding tube if burns are in the mouth, surgical débridement, and closure. Puppies in particular will commonly eat despite severe oral injury.
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Electrocution
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NUTRITION/DIET If oral burns are severe and the patient will not eat, enteral nutrition may be instituted via placement of a nasoesophageal (see p. 1267) or esophagostomy (see p. 1269) tube.
POSSIBLE COMPLICATIONS Infection of nonhealing burns, acute lung injury, acute respiratory distress syndrome. A rare but possible long-term complication is cataract formation.
RECOMMENDED MONITORING Respiratory rate and effort, as well as the healing of any burns, should be monitored.
PROGNOSIS AND OUTCOME Depends on the degree of noncardiogenic pulmonary edema. Cats appear to do better than dogs in overall survival. Critical period is the first 24-48 hours after electrical shock; if the animal survives this period, he/she will likely survive to discharge with minimal/no permanent aftereffects.
PEARLS & CONSIDERATIONS COMMENTS Noncardiogenic pulmonary edema can be difficult to treat. There are no known specific treatment recommendations.
PREVENTION When left unobserved, puppies and kittens should be crated or otherwise confined so access to electrical cords in use can be avoided. Remove access to wires that are plugged into outlets.
TECHNICIAN TIPS When administering treatments to these pets, stress should be minimized, and treatments should be conducted in a stepwise manner.
CLIENT EDUCATION Education about reexposure, removal of damaged or faulty electrical cords
SUGGESTED READING Drobatz KJ, et al: Noncardiogenic pulmonary edema in dogs and cats: 26 cases (1987-1993). J Am Vet Med Assoc 206:1732–1736, 1995. AUTHOR: MEGAN WHELAN EDITOR: ELIZABETH ROZANSKI
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Elbow Luxation
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Elbow Luxation BASIC INFORMATION DEFINITION Dislocation between brachium (humerus) and antebrachium (radius and ulna)
SYNONYM Elbow dislocation
EPIDEMIOLOGY SPECIES/AGE/SEX Uncommon in dogs; rare in cats Any breed, age, or sex for traumatic luxations Juvenile dogs for congenital luxations GENETIC & BREED PREDISPOSITION Congenital luxations generally more common in small breeds of dogs, but radial head luxation specifically occurs more frequently in larger breeds. Suspected hereditary predisposition Chondrodystrophic breeds are prone to asynchronous growth between radius and ulna, thereby resulting in subluxation. RISK FACTORS Forelimb trauma ASSOCIATED CONDITIONS & DISORDERS Some forms of congenital luxation may be associated with more generalized joint laxity syndromes.
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES Traumatic Congenital, complete Congenital, partial (radial head luxation only) HISTORY, CHIEF COMPLAINT Forelimb trauma secondary to motor vehicle accident, fall, or rough play/fighting Spontaneous lameness/deformity in young dog PHYSICAL EXAM FINDINGS Traumatic: non-weight-bearing lameness with antebrachium and paw abducted, elbow flexed, and severe elbow swelling and pain Congenital: partial weight-bearing lameness and joint thickening; discomfort during range-of-motion maneuvers
ETIOLOGY AND PATHOPHYSIOLOGY Majority of traumatic luxations are lateral (proximal radius/ulna are lateral to distal humerus). Medial luxations are associated with severe soft-tissue derangements. Traumatic injuries may cause avulsion fracture(s) of collateral ligament(s).
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Elbow Luxation
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Congenital/developmental luxations and subluxations may be associated with asynchronous growth of the radius and ulna.
DIAGNOSIS DIAGNOSTIC OVERVIEW Diagnosis is based on history, physical exam, and radiographs (sedated patient) of the affected limb, to include carpus, elbow, and shoulder joints.
DIFFERENTIAL DIAGNOSIS Distal humeral fracture Monteggia fracture (cranial displacement of radial head and proximal ulna fracture) Elbow neoplasia
INITIAL DATABASE Craniocaudal and mediolateral radiographs of the elbow Survey radiographs for other traumatic injuries, especially thoracic cavity Radiographs of the contralateral elbow in patients with congenital or developmental luxations Assess for neurologic injury: check for limb withdrawal and pain sensation.
TREATMENT TREATMENT OVERVIEW Goal of therapy is to achieve anatomic reduction of joint surfaces so normal joint mobility is restored, with eventual return to full weight bearing and elimination of discomfort.
ACUTE GENERAL TREATMENT Traumatic elbow luxations are best managed via early closed reduction before muscle contraction makes manipulations difficult (see Pearls, below, and for closed reduction procedure). Patient must be anesthetized for reduction. Concurrent injuries may result in postponement of anesthesia and early reduction. If closed reduction is not achieved, open reduction and reconstruction of the collateral ligaments are indicated. If open reduction is needed, the limb should be bandaged to reduce patient discomfort and tissue swelling before surgery. Appropriate analgesics should be administered. Congenital/developmental luxations do not require “acute” treatment, but intervention is preferred to help slow progression of secondary osteoarthritis. Congenital luxations are less amenable to closed reduction. Congenital luxations may require osteotomies or ostectomies for treatment.
CHRONIC TREATMENT Immobilization with elbow bandaged in extension for 1–2 weeks Initially, a heavy padded bandage (or more rigid splint for open reductions and those with severe collateral ligament damage), with gradual reduction in bandage thickness/stiffness as swelling subsides and stability increases Gentle, passive range-of-motion (flexion/extension) physiotherapy instituted after bandage removal Continued use of analgesic/antiinflammatory agents as needed for patient comfort
POSSIBLE COMPLICATIONS Recurrent luxation/instability Articular cartilage damage and secondary osteoarthritis Ligament damage Reduced range of motion from pericapsular fibrosis Chronic lameness
RECOMMENDED MONITORING
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Elbow Luxation
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Postreduction radiographs to confirm restoration of joint congruency Weekly bandage check/change until removal Lameness evaluations 2, 4, and 8 weeks after surgery; radiographs at 2 weeks, also at 6-8 weeks if open reduction/implants
PROGNOSIS AND OUTCOME Good if mild articular cartilage or ligamentous lesions Chronic fibrosis will result in a permanently thickened elbow. Most dogs with properly treated traumatic luxations will return to normal or near-normal function. More guarded prognosis for congenital/developmental luxations Severe complications/failures might necessitate salvage surgery (arthrodesis, total joint arthroplasty, or amputation).
PEARLS & CONSIDERATIONS COMMENTS Early diagnosis is critical for promoting successful closed reduction. Closed reduction achieved by flexing elbow (moves anconeal process caudally), followed by abduction of the antebrachium, with the paw flexed (moves anconeal process medially, attempting to “hook” anconeal process medial to lateral epicondylar crest of the humerus), followed by adduction and pronation of the antebrachium (attempting to “snap” the radial head medially to its proper location under the capitulum of the humerus as the anconeal process acts as a fulcrum). Can consider paralyzing the patient pharmacologically (requires ventilation of patient for gas exchange) to achieve greater muscle relaxation to facilitate reduction maneuvers.
CLIENT EDUCATION Bandage/splint care Controlled activity (kennel/leash) Passive range-of-motion physiotherapy after removal Neuter dogs with congenital luxations, owing to potential heritability.
SUGGESTED READING Dassler C, Vasseur PB: Elbow luxation. In Slatter DH, editor: Textbook of small animal surgery, ed 3, Philadelphia, 2003, WB Saun-ders, pp 1919–1927. AUTHOR: MARY SOMERVILLE EDITOR: JOSEPH HARARI
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Elbow Hygroma
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Elbow Hygroma BASIC INFORMATION DEFINITION Fluid-filled (serum) cavity between skin and bony prominence (olecranon)
SYNONYMS Elbow seroma, olecranon bursitis (incorrect term, as tendon bursa is not involved)
EPIDEMIOLOGY SPECIES, AGE, SEX Dogs: any age, either sex GENETICS & BREED PREDISPOSITION Large-breed, heavy dogs RISK FACTORS Insufficient callus over elbow Thin skin Small amount of subcutaneous fat Chronic pressure trauma to elbow Lying on hard surfaces ASSOCIATED CONDITIONS & DISORDERS Orthopedic problems (hip dysplasia) that increase trauma to skin and other soft tissues overlying the elbows as dog rises or lies down
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT Gradually enlarging, fluid-filled swelling over point of elbow Initially soft, then more turgid as fluid accumulates Ulceration of overlying skin may develop if continued trauma PHYSICAL EXAM FINDINGS Fluid-filled, fluctuant to turgid swelling over the point of the elbow. Unilateral or bilateral.
ETIOLOGY AND PATHOPHYSIOLOGY Caused by chronic repetitive pressure and trauma to the elbow Serum accumulates in subcutaneous space superficial to triceps fascia over the olecranon. Over time, fibrous proliferation occurs, causing nonpitting, nonpainful thickening of skin and subcutis.
DIAGNOSIS DIAGNOSTIC OVERVIEW
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Elbow Hygroma
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The diagnosis is suspected based on patient signalment, presenting history, and physical examination findings. Confirmation requires fine-needle aspiration cytology of the fluid-filled swelling.
DIFFERENTIAL DIAGNOSIS Abscess Neoplasia
INITIAL DATABASE If indicated, presurgical CBC, serum chemistry profile, urinalysis Fine-needle aspiration cytologic evaluation with or without bacterial culture and sensitivity: rule out abscess, neoplasia. Radiographs of elbow: rule out underlying orthopedic problems (degenerative joint disease, olecranon fracture).
TREATMENT TREATMENT OVERVIEW Successful treatment of this problem requires: Complete drainage of fluid from the cavity and prevention of its reaccumulation Apposition and subsequent healing of fibrous tissue surfaces of the cavity together to obliterate the cavity and prevent reformation Prevention of continued trauma to the elbows and therefore recurrence of the problem
ACUTE GENERAL TREATMENT Three suggested methods of treatment: Aseptic aspiration of fluid and pressure coaptation bandage Rarely successful for larger or chronic hygromas Penrose drainage and padded bandage Suture obliteration and padded bandage
CHRONIC TREATMENT Padded bandage must remain in place for at least 4 weeks to allow the fibrous tissue surfaces to heal together and thereby obliterate the subcutaneous space in which fluid could accumulate. Dog should be restricted from lying on hard surfaces. Suitable padded bedding should be provided. Elbow(s) should be padded until healing and adequate protective callus have developed.
POSSIBLE COMPLICATIONS Recurrence Penrose drain removed too soon Inadequate period of bandaging to allow fibrous healing to occur Suitable padded bedding not provided after bandages have been removed Infection Repeated needle drainage Inadequate sterile surgical technique Inadequate protective bandage over Penrose drains Development of a chronic nonhealing ulcer over olecranon Infected hygroma Dehiscence of suture line after surgery Continued trauma to hygroma
RECOMMENDED MONITORING See Chronic Treatment above Observe elbow area for evidence of: Recurrence of the hygroma
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Elbow Hygroma
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Infection of the overlying skin Development of necrosis/ulceration of the overlying skin Be aware that problem may develop on other elbow if preventive measures are not taken.
PROGNOSIS AND OUTCOME Good with appropriate treatment Poor if: Hygroma becomes infected Dehiscence of suture line occurs Nonhealing ulcer develops May require extensive reconstructive surgery to correct these problems
PEARLS & CONSIDERATIONS COMMENTS Do not attempt surgical excision of the hygroma. Successful primary closure is difficult to achieve with excision, owing to tension and motion at surgical site; high risk of complications.
PREVENTION Dog should be restricted from lying on hard surfaces: Especially if other orthopedic problems are present that restrict the dog's ability to rise and lie down Suitable padded bedding should be provided. Elbow(s) should be padded until adequate protective callus has developed.
TECHNICIAN TIPS In-hospital care: Ensure adequate bedding is provided to reduce pressure trauma to elbow(s). Ensure that bandage(s) remain securely in place and are clean and dry. Assist patient in getting up and down and ambulating as needed, to prevent additional elbow trauma. Client education before and at time of patient discharge: correct bandage care including being aware of potential problems/complications. Advise clients on home management/prevention: Assisting dog getting up and down and ambulating while leg(s) bandaged Appropriate bedding, avoiding hard surfaces Purchase of custom-made elbow pads
CLIENT EDUCATION Seek veterinary care and advise as soon as hygroma develops: easier to treat and less risk of complications if treated early (e.g., before infection).
SUGGESTED READING Johnston DE: Hygroma of the elbow in dogs. J Am Vet Med Assoc 167:213, 1975. Swaim SF, Henderson RA: Wounds on the limbs. In Small animal wound management. Philadelphia, 1990, Lea & Febiger, pp 181–188. AUTHOR & EDITOR: RICHARD WALSHAW
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Elbow Dysplasia
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Elbow Dysplasia BASIC INFORMATION DEFINITION A common group of developmental disorders including fragmented medial coronoid process (FCP), ununited anconeal process (UAP), osteochondritis dissecans (OCD), and elbow incongruity (uneven radial head and medial coronoid surfaces) that cause degenerative joint disease in the elbow FCP is a separation of the medial aspect of the coronoid process from the ulna. UAP is a failure of the anconeal process to fuse to the ulna. Osteochondrosis is an abnormality of endochondral ossification, whereas OCD implies separation of the diseased cartilage from the subchondral bone.
EPIDEMIOLOGY SPECIES, AGE, SEX Primarily in dogs between 6 and 9 months old FCP may be present in older dogs with degenerative joint disease. GENETICS & BREED PREDISPOSITION Elbow dysplasia is hereditary but also is associated with rapid growth and high-energy diet. UAP is found primarily in German shepherds, basset hounds, and Saint Bernards. FCP and OCD affect primarily retriever breeds, Bernese mountain dogs, and rottweilers. Other large breed dogs may be affected by elbow dysplasia, including the Newfoundland, mastiff, and Australian shepherd; however, elbow displasia is also becoming more prevalent in smaller breeds.
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT History of lameness on one or both forelimbs, often worse after exercise Reluctance to play or take long walks PHYSICAL EXAM FINDINGS Lameness on one or both forelimbs Pain on manipulation of the elbow, especially on extension If osteoarthrosis is advanced, crepitation or effusion may be palpable along with a decreased amount of flexion to the joint (reduced range of motion).
ETIOLOGY AND PATHOPHYSIOLOGY OCD occurs when there is osteochondrosis (a failure of endochondral ossification), which leads to cartilage thickening and fissure formation. Factors such as diet, rapid growth, hormonal imbalance, trauma, and genetics may lead to the development of OCD as well as FCP and UAP. Joint incongruity, leading to increased pressure on the anconeus, has been implicated as a cause for UAP. UAP may also be a form of osteochondrosis with abnormal thickened cartilage, leading to failure of unification. The underlying pathophysiology of FCP is unknown but is believed to be secondary to elbow incongruity or a form of osteochondrosis. Incongruity of the joint, especially an increase in length of the ulna in relation to the radius, can lead to increased weight-bearing load on the medial aspect of the coronoid process, leading to fissuring and fragmentation. Osteochondrosis may lead to a delay in ossification of the coronoid region and subject the joint to fragmentation when weight bearing.
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Elbow Dysplasia
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DIAGNOSIS DIAGNOSTIC OVERVIEW Radiography is the standard means of diagnosing elbow dysplasia. However, canine elbow dysplasia can be present without radiographic signs, and advanced imaging (nuclear scintigraphy, ultrasonography, CT, and MRI) or arthroscopy may help diagnose subtle lesions.
DIFFERENTIAL DIAGNOSIS Panosteitis OCD of the shoulder Elbow luxation
INITIAL DATABASE CBC and serum chemistry panel based on signalment: Consider before treatment or sedation/anesthesia Generally unremarkable for elbow dysplasia alone Mediolateral, craniocaudal, and flexed lateral radiographs of both elbows: ○
○
An oblique craniocaudal view with the elbow flexed 30 and rotated medially 15 may help to assess the medial coronoid process. The flexed lateral is the best radiographic view to identify a UAP. OCD is seen on the medial condyle of the humerus, primarily on the craniocaudal view. Elbow congruity is best assessed on the mediolateral view, and the beam should be centered on the elbow joint.
ELBOW DYSPLASIA Mediolateral (left panel) and craniocaudal (right panel) projections of a canine elbow with fragmented medial coronoid process (arrows). (Courtesy Dr. J. Harari; reproduced with permission.)
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Elbow Dysplasia
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ELBOW DYSPLASIA Mediolateral projection of a flexed canine elbow joint with an ununited anconeal process (arrowheads). (Courtesy Dr. J. Harari; reproduced with permission.)
ADVANCED OR CONFIRMATORY TESTING A bone scan can be used for localizing the lameness if a complete orthopedic examination and radiographs are inconclusive. CT or MRI can be used for characterizing and delineating the elbow lesion. Arthroscopy can be used to confirm abnormalities in the elbow joint found with imaging modalities. Arthrocentesis may be performed to rule out other causes of joint effusion.
TREATMENT TREATMENT OVERVIEW In persistently lame dogs with elbow dysplasia, treatment involves removal of the FCP, OCD, or UAP fragment, which will result in an improvement in limb function. In dogs with elbow incongruity, surgery to improve congruity will minimize ongoing degenerative changes to the joint. However, degenerative joint disease is still expected to progress in most cases of elbow dysplasia.
ACUTE GENERAL TREATMENT Elbow arthroscopy via a medial portal is used for treatment of FCP and OCD and to assess elbow incongruity. The FCP is identified and removed with grasping forceps or a motorized shaver. Curettage or removal of the medial coronoid process via a subtotal coronoid ostectomy can be used when fissuring or chondromalacia of the coronoid is present without gross fragmentation. OCD lesion is identified and the cartilage flap removed. A motorized shaver is used for removing fragments and to treat the underlying subchondral bone. Osteochondral autograft transfer is being researched as a treatment option for OCD lesions. A sliding humeral osteotomy has been proposed to redistribute forces within the medial compartment of the elbow, thereby decreasing pain associated with medial coronoid disease. In skeletally mature dogs, a UAP is often surgically removed via a lateral approach. Various other surgical procedures have been described, such as lag screw fixation. However, these approaches result in no better success and have a higher complication rate related to the implants. In skeletally immature dogs, a dynamic ulnar osteotomy may be used for removing the pressure on the anconeal process and allowing bone or fibrous union of the fragment. This may be used simultaneously with lag screw fixation of the anconeal process. Lag screw fixation causes compression of the anconeal process to the ulna and leads to bone fusion. If elbow incongruity exists, a dynamic ulnar osteotomy is performed to allow proximal movement (triceps muscles pull) of the
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Elbow Dysplasia
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ulna to improve joint congruency. An intramedullary pin is placed in the ulna by some surgeons to provide stabilization and reduce callus formation. Total elbow replacement or elbow arthrodesis may be performed in dogs with moderate to severe elbow osteoarthritis secondary to elbow dysplasia.
CHRONIC TREATMENT If an ulnar osteotomy is performed, postoperative placement of a soft padded bandage for 2-4 weeks is used for support. Exercise should be restricted to short leash walks for 4-6 weeks after surgery. Physical therapy may be useful to maintain range of motion within the elbow joint after surgery. Medical therapy may be necessary after surgery if a significant amount of degenerative joint disease is present. Nonsteroidal antiinflammatory drugs (NSAIDs): Aspirin, 10–25 mg/kg PO q 8-24 h; or Carprofen, 2 mg/kg PO q 12 h; or Etodolac, 10–15 mg/kg PO q 24 h or Deracoxib, 1–2 mg/kg PO q 24 h (may use 3-4 mg/kg PO q 24 h for first 7 days only); or Meloxicam, 0.1 mg/kg PO q 24 h; or Meclofenamic acid, 1.1 mg/kg PO q 24 h after eating, 5 days maximum; or Tepoxalin, 10 mg/kg PO q 24 h (new product, objective data pending); or Others Chondroprotective agents: Polysulfated glycosaminoglycan, 5 mg/kg IM once weekly × 4–6 weeks; or Pentosan polysulfate (from beech-wood hemicellulose) 3 mg/kg SQ once weekly; or Oral formulations (glucosamine, chondroitin sulfate, hyaluronan): according to formulation/labeled instructions
POSSIBLE COMPLICATIONS Infection Implant failure if performing lag screw fixation
RECOMMENDED MONITORING Suture removal and recheck 2 postoperative weeks Repeat radiographs 6 postoperative weeks if an ulnar osteotomy, lag screw fixation of the anconeal process, sliding humeral osteotomy, or total elbow replacement was performed.
PROGNOSIS AND OUTCOME Surgery will help alleviate lameness for OCD, FCP, and UAP, but most affected dogs will continue to have progressive DJD and need medical therapy. Prognosis for return to full function depends on the degree of preexisting DJD. Medical treatment consisting of weight control, exercise restriction, NSAIDs, and polysulfated glycosaminoglycan therapy is reported to have a similar outcome to surgical treatment of OCD and FCP.
PEARLS & CONSIDERATIONS COMMENTS Clinical signs of FCP may not correlate with radiographic evidence of disease. Initial radiographic change will be mild osteophytosis on the anconeal process. Some dogs may show mild or no radiographic changes, yet be profoundly lame; such a patient needs MRI, CT, or arthroscopy. Conversely, some dogs are not lame, yet have radiographic evidence of DJD. Hence, treatment is directed toward the patient and not the radiograph. Unilateral forelimb lameness may not be detectable if bilateral forelimb disease is present. Because of the prevalence of bilateral disease, both elbows may undergo arthroscopy with one anesthetic episode if clinically indicated. The anconeal process does not fuse until 4-5 months of age and cannot be diagnosed radiographically as ununited before that time. When manipulating the elbow to check for pain, avoid movement of the shoulder, which may obscure localization of the
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Elbow Dysplasia
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discomfort.
CLIENT EDUCATION Because of the hereditary component of elbow dysplasia, affected dogs should not be used for breeding.
SUGGESTED READING Cook C, Cook J: Diagnostic imaging of canine elbow dysplasia: a review. Vet Surg 38:144– 153, 2009. Fitzpatrick N, Yeadon R: Working algorithm for treatment decision making for developmental disease of the medial compartment of the elbow in dogs. Vet Surg 38:285–300, 2009. Schulz KS: Canine elbow dysplasia. In Fossum TW, editor: Small animal surgery, ed 3, St Louis, 2007, Mosby, Inc., pp 1197–1212. Schulz KS, Krotscheck U: Canine elbow dys-plasia. In Slatter D, editor: Textbook of small animal surgery, ed 3, Philadelphia, 2002, WB Saunders, pp 1927–1952. AUTHOR: RAVIV J. BALFOUR EDITOR: JOSEPH HARARI
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Eisenmenger's Syndrome
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Eisenmenger's Syndrome BASIC INFORMATION DEFINITION Uncommon syndrome involving any large communication between the left and right sides of the heart, in association with severe pulmonary hypertension, which results in right-to-left shunting of blood.
SYNONYMS Eisenmenger's physiology or reaction Eisenmenger's complex (large, nonrestrictive ventricular septal defect [VSD] plus pulmonary hypertension causing right-to-left shunting with or without dextroposition of the aorta) The term cyanotic congenital heart disease includes Eisenmenger's syndrome as well as right-to-left cardiac shunts without pulmonary hypertension (i.e., VSD with concurrent pulmonic stenosis).
EPIDEMIOLOGY SPECIES, AGE, SEX Dogs and cats Young animals Female dogs more predisposed to patent ductus arteriosus (PDA); 15% of dogs with PDA may develop severe pulmonary hypertension. GENETICS & BREED PREDISPOSITION Dependent on the underlying cause: PDA: quasi-continuous or threshold trait with high degree of heritability. Miniature and toy poodles, collie, Pomeranian, Shetland sheepdog, American cocker spaniel, German shepherd, Maltese, keeshond, Yorkshire terrier. VSD: autosomal-dominant trait with incomplete penetrance or a polygenic trait. English springer spaniel, English bulldog. RISK FACTORS Living at high altitude ASSOCIATED CONDITIONS & DISORDERS Eisenmenger's syndrome can originate from an isolated cardiac defect (i.e., PDA) or from a combination of VSD or ASD and PDA.
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT Dyspnea (most common sign in cats) Exercise intolerance Syncope Lethargy Cough Cyanosis Hind limb collapse PHYSICAL EXAM FINDINGS Heart murmur (timing and location determined by defect[s] present) Right or left apical systolic murmurs (inconsistent) Tachycardia
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Eisenmenger's Syndrome
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Tachypnea Generalized or regional cyanosis, depending on underlying cause Loud second heart sound Split second heart sound
ETIOLOGY AND PATHOPHYSIOLOGY Size of the defect and severity of pulmonary hypertension determine the degree of shunting and thus the occurrence and extent of clinical signs. Hypoxemia from shunting of venous blood into the arterial circulation leads to erythropoietin production and polycythemia. Polycythemia, if severe, can produce hyperviscosity and pulmonary embolism, central neurologic signs, and/or coagulopathies. Congenital: High pulmonary vascular resistance is maintained after birth. Abnormal maturation of the pulmonary vasculature Acquired: Large systemic-pulmonary communication (left-to-right shunt) offers minimal resistance to systolic flow. Relative flows are determined by systemic and pulmonary vascular resistance. Prolonged pulmonary hypertension leads to pulmonary vascular disease, an abnormal maturation of the pulmonary vasculature, and right ventricular hypertrophy. Pulmonary arterial histologic features: medial muscular hypertrophy, laminar intimal fibrosis, necrotizing arteritis, plexiform lesions. With progression, pulmonary vascular resistance may increase to a value greater than the systemic vascular resistance, causing right-to-left or bidirectional shunting (mixing of venous and arterial blood).
DIAGNOSIS DIAGNOSTIC OVERVIEW The diagnosis is suspected in a young patient presenting with dyspnea, cyanosis, and collapsing episodes. Polycythemia and right heart enlargement are usually present. An echocardiogram with contrast is required for confirmation.
DIFFERENTIAL DIAGNOSIS Radiographic/electrocardiographic: Right heart enlargement: other types of cardiac disease (pulmonic stenosis, tetralogy of Fallot, heartworm disease, tricuspid valve dysplasia, atrial septal defect), cor pulmonale Echocardiographic: Pulmonic stenosis Tetralogy of Fallot Heartworm disease
INITIAL DATABASE CBC: polycythemia (usually progressive with age) Heartworm test: antigen, antibody (cats), and microfilaria tests Thoracic radiographs: right heart enlargement, enlarged main pulmonary artery, normal to mildly enlarged pulmonary vasculature Systemic arterial blood pressure measurement: hypotension contraindicates performing phlebotomy without fluid replacement Electrocardiogram: tall P waves in lead II, deep S waves in lead II, right axis deviation; arrhythmias are uncommon Echocardiogram: 2D: right ventricular hypertrophy, enlarged main pulmonary artery, identification of structural defects M mode: right ventricular free wall and septal hypertrophy, septal flattening, paradoxical septal motion Color flow Doppler: aliased or laminar flow across the congeni-tal defect, tricuspid regurgitation (uncommon) Spectral Doppler: tricuspid regurgitant velocity > 3.5 m/s, pulmonic insufficiency velocity > 3 m/s, reversed E/A ratio of mitral valve inflow profile, midsystolic notching of the pulmonary flow profile (severe cases) Contrast echo: contrast appears in the left heart (intracardiac shunt) or in the abdominal aorta (extracardiac shunt).
ADVANCED OR CONFIRMATORY TESTING Cardiac catheterization: used for confirming diagnosis and to assess degree of shunting
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Eisenmenger's Syndrome
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Angiogram: outlines the congenital defect(s) (PDA, VSD, ASD or aorticopulmonary communication) Pressure measurements: increased pulmonary artery pressures. With large defects, right and left ventricular pressures have a tendency to equalize. Oximetry: decreased aortic Po2 Transesophageal echocardiography: better identification of the congenital defect
TREATMENT TREATMENT OVERVIEW Initial control of polycythemia and signs of hyperviscosity can be achieved with periodic phlebotomies. Hydroxyurea and a phosphodiesterase-V inhibitor (to reduce severity of pulmonary hypertension) may be started if clinical signs persist. Consider referral to cardiologist for diagnosis and advice on treatment plan.
ACUTE GENERAL TREATMENT Phlebotomy: if PCV > 60%. Withdrawal of 10%-20% of circulating blood volume (= 1-2 mL/kg) with or without intravenous fluid replacement. Repeated as needed (typically every several weeks) based on recurrence of clinical signs. Calcium channel blocker (e.g., amlodipine), phosphodiesterase V inhibitors (e.g., sildenafil): reduce pulmonary hypertension (see 935)
CHRONIC TREATMENT Medical therapy: Hydroxyurea, 20-25 mg/kg PO q 12-24 h until hematocrit is lower; then 25-50 mg/kg PO q 48 h as needed to maintain stable hematocrit. Recommended when patient requires frequent phlebotomies. Diuretics, ACE inhibitors, and antiarrhythmics following the treatment guidelines. See Heart Failure, Acute/ Decompensated, 468; Heart Failure, Chronic, 470; Ventricular Arrhythmias (Premature Ventricular Complexes, Ventricular Tachycardia), .
BEHAVIOR/EXERCISE Restrict exercise and excitement in patients with collapsing or syncopal episodes.
DRUG INTERACTIONS Hydroxyurea: reversible bone marrow suppression (pancytopenia), anorexia, vomiting and diarrhea, sloughing of nails are possible.
RECOMMENDED MONITORING Recheck examinations should include: CBC, serum renal profile, and systolic blood pressure measurement.
PROGNOSIS AND OUTCOME Long-term prognosis is guarded to poor, depending on severity of pulmonary hypertension.
PEARLS & CONSIDERATIONS COMMENTS Large systemic-pulmonary communications are uncommon in dogs and cats. Surgery is contraindicated, owing to severe pulmonary hypertension.
PREVENTION Do not breed affected animals.
TECHNICIAN TIPS
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Check mucous membranes for cyanosis. The jugular vein is usually the best phlebotomy site; when administering fluids, use a different vein (e.g., cephalic vein)
CLIENT EDUCATION Monitor respiratory rate at rest, exercise tolerance, and appetite. Advise client not to breed affected animals.
SUGGESTED READING Côté E, Ettinger SJ: Long-term clinical management of right-to-left (“reversed”) patent ductus arteriosus in 3 dogs. J Vet Intern Med 15:39–42, 2001. Moore KW, Stepien RL: Hydroxyurea for treatment of polycythemia secondary to right-to-left shunting patent ductus arteriosus in 4 dogs. J Vet Intern Med 15(4):418–421, 2001. AUTHOR: JOAO S. ORVALHO EDITOR: ETIENNE CÔTÉ
24-09-2011 19:25
Ehrlichiosis, Canine Monocytic
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Ehrlichiosis, Canine Monocytic BASIC INFORMATION DEFINITION Tick-transmitted disease caused by Ehrlichia canis or Ehrlichia chaffeensis infection. These organisms predominantly infect circulating monocytes, macrophages, and lymphocytes, causing nonspecific signs (fever, anorexia, lethargy, inappetence), bleeding, anemia, and cytopenias. Chronically, E. canis infection can cause bone marrow suppression, pancytopenia, glomerulonephritis, and death.
SYNONYMS Canine monocytotropic ehrlichiosis (E. canis), human monocytic ehrlichiosis (E. chaffeensis), tropical pancytopenia
EPIDEMIOLOGY SPECIES, AGE, SEX Ehrlichiosis is most commonly seen in dogs; rarely in cats. GENETICS & BREED PREDISPOSITION German shepherd dogs have a more fulminant illness, owing to reduced cellular immune response. RISK FACTORS E. canis is transmitted by Rhipicephalus sanguineus (brown dog tick), whereas E. chaffeensis is transmitted by Amblyomma americanum (lone star tick) or Dermacentor variabilis (American dog tick). R. sanguineus is an urban tick capable of completing its entire life cycle indoors (exposure risk when boarding, pet stores, etc.) Therefore, access to wooded areas, outdoor activities, and tick season are risk factors for E. chaffeensis infection but not for E. canis infection. CONTAGION & ZOONOSIS Most Ehrlichia spp. may be infectious to humans, but there is no direct dog-to-dog or dog-to-human transmission. Personal protective equipment (gloves and safety glasses) should be used when handling biological samples (inoculation risk). GEOGRAPHY AND SEASONALITY E. canis infection has been found in most tropical and subtropical regions in the world, based on distribution of the vector. Because of different disease forms (acute, subacute, and chronic), there is no true seasonality. E. chaffeensis has been described predominantly in the United States, with emergence in South Korea, southern China, and Cameroon. ASSOCIATED CONDITIONS & DISORDERS Other tickborne diseases (Rocky Mountain spotted fever, cyclic thrombocytopenia, babesiosis, bartonellosis, hepatozoonosis) may occur concurrently.
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES Acute phase: onset 8-20 days post infection; signs last 2-4 weeks and may resolve spontaneously. Subclinical phase: onset 6-9 weeks post infection; clinically inapparent cytopenias The infection may be cleared spontaneously at this time (uncommon) but if not, the chronic phase ensues. Chronic phase: onset is weeks to months after infection; signs are variable in severity, ranging from mild illness to a life-threatening syndrome. HISTORY, CHIEF COMPLAINT
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Ehrlichiosis, Canine Monocytic
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History may include tick exposure weeks/months earlier; not always recalled by pet owners. Overt signs: depression, anorexia, weight loss, ocular or nasal discharge, bleeding tendencies, lameness. Clinical signs of the chronic phase may include overt bleeding, cachexia, lameness, ocular, and neurologic abnormalities. PHYSICAL EXAM FINDINGS Fever may be present but is not always detected. Joint pain and shifting leg lameness Hepatomegaly, splenomegaly, peripheral lymphadenopathy, increased vesicular breath sounds Bleeding disorders: cutaneous and/or mucosal petechiae, ecchymoses, unilateral or bilateral epistaxis, melena, retinal hemorrhage, hyphema Signs of uveitis: blepharospasm, photophobia, excessive lacrimation, hyperemia of scleral vessels, and decreased intraocular pressure. Blindness due to retinal detachment can occur. Neurologic signs: ataxia, seizures, vestibular signs, anisocoria, and hyperesthesia (severe cases) Subcutaneous edema due to chronic protein-losing nephropathy (chronic cases) or vasculitis Arrhythmias due to vasculitis and myocardial injury may occur in severe cases. Mild cases may have unremarkable clinical findings.
ETIOLOGY AND PATHOPHYSIOLOGY Ticks acquire the organism by feeding as either larvae or nymphs on infected animals. No transovarial transmission occurs in the tick (i.e., life cycle requires the mammal). When an infected tick ingests a blood meal, the organism is transmitted via saliva to the vertebrate host. Infection leads to multiplication in mononuclear cells and tissues (spleen, liver, and lymph nodes). Infected cells attach to vascular endothelium in lungs, kidneys, joints, myocardium, and meninges, leading to vasculitis and subendothelial tissue infection and the acute phase of disease initially. Thrombocytopenia occurs secondary to increased platelet consumption and decreased platelet half-life, as a result of antiplatelet antibodies production, platelet migration-inhibition factor production, and splenic sequestration. Dysfunction of remaining platelets (thrombocytopathy) may occur secondary to antiplatelet antibodies binding to platelet receptors. Systemic inflammation may occur, with varying degrees of thrombosis, hyperviscosity, and red cell destruction. Subclinical phase is a result of ongoing bone marrow effects. Those unable to clear the infection in the subclinical phase develop chronic disease with hyperglobulinemia and immune complex formation, as well as bone marrow suppression, possibly leading to pancytopenia.
DIAGNOSIS DIAGNOSTIC OVERVIEW The diagnosis is suspected based on the presence of anorexia, fever, lethargy, and/or bleeding tendencies in a dog with tick exposure, hematologic and clinical chemistry abnormalities, and response to therapy. Presumptive diagnosis is often based on specific antibody detection. Definitive diagnosis depends upon visualization of the organisms, microbial DNA amplification and genetic sequencing, or a fourfold change in antibody titers between acute and convalescent samples, but treatment often is indicated in patients showing overt clinical signs of ehrlichiosis before such results are available.
DIFFERENTIAL DIAGNOSIS Acute phase is similar to Rocky Mountain spotted fever (see p. 994). Chronic disease differentials include immune-mediated diseases, myeloma, lymphoma, hepatozoonosis, malignant histiocytosis, leukemia, myelodysplasia, leptospirosis, bartonellosis, and babesiosis.
INITIAL DATABASE CBC, serum biochemistry profile, urinalysis Thrombocytopenia (mild to severe) is the typical finding in all stages of illness, but absence does not rule out ehrlichiosis. Neutropenia, nonregenerative anemia, lymphocytosis (sometimes marked), monocytosis, and eosinophilia may be observed. Hyperglobulinemia is common; polyclonal gammopathy is typical, but in rare cases a monoclonal gammopathy is present. Increase in alanine aminotransferase (ALT) and alkaline phosphatase (ALP) activities. Pathologic proteinuria (e.g., elevated urine protein/creatinine ratio in the absence of urinary tract infection) occurs
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Ehrlichiosis, Canine Monocytic
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secondary to glomerulonephritis. Fundic examination: retinal hemorrhages/detachment may be seen. Abdominal imaging if splenomegaly/signs of abdominal pain Lymph node aspirates if lymphadenopathy Arthrocentesis and limb radiography if signs of polyarthritis. Sterile, nonerosive polyarthritis with predominance of nondegenerate neutrophils may occur. Bone marrow aspirate if pancytopenia is present Cerebrospinal fluid tap if neurologic signs are present Antinuclear antibody and Coombs' tests: to help identify primary or secondary immune-mediated disease. Coombs' test may be positive in Ehrlichia infection.
ADVANCED OR CONFIRMATORY TESTING Buffy coat, blood smear evaluation: rarely identify morulae in mononuclear cells (many false-negative results) Serologic titers: IFA or ELISA (antibody tests): Negative results may occur in acute cases. Confirmation with a convalescent titer (2–4 weeks later; ≥fourfold increase) is necessary for definitive diagnosis. Positive results suggest exposure, not infection. Antibody titers can persist from months to more than a year. Antibodies from dogs infected with E. canis cross-react with E. chaffeensis antigens and occasionally with E. ewingii (IFA only) but do not cross-react with Anaplasma phagocytophilum antigens. PCR amplification: may be applied to tissue or whole blood. It provides definitive diagnosis, since it can differentiate between A. phagocytophilum, A. platys, E. canis, E. chaffeensis, E. ewingii, and other bacteria from the Anaplasmataceae family. False-negative PCR tests can occur if low numbers of circulating organisms.
TREATMENT TREATMENT OVERVIEW The treatment of choice for both E.canis and E. chaffeensis infection is doxycycline or tetracycline, with rapid clinical improvement (beginning within 24-48 hours) in the majority of cases. Dogs with slow or partial recovery might be coinfected with other tickborne organisms. There is no consensus whether or not the antibiotic therapy clears these organisms from infected dogs, and chronic subclinical infections may be possible. Some manifestations such as glomerulonephritis may persist after treatment, but progression should be halted.
ACUTE GENERAL TREATMENT Clear organism: Doxycycline, 5–10 mg/kg PO or IV q 12 h for 28 days (treatment of choice); or Tetracycline, 22 mg/kg PO q 8 h for 21 days (alternative treatment) For puppies under 1 year of age: chloramphenicol, 15-25 mg/kg PO (or IV, SQ) q 8 h for 14-21 days (to avoid discoloration of the teeth) Supportive care depends on clinical manifestation (i.e., transfusions for anemia, analgesics for polyarthritis pain). The authors do not routinely use corticosteroids for the treatment of ehrlichiosis. Reduction of ehrlichial antigens through appropriate antibiotic therapy should reduce secondary immune-mediated pathology. Despite being controversial, some clinicians have used corticosteroids at immunosuppressive doses (e.g., prednisone, 2–4 mg/kg PO q 24 h during first 2–7 days of acute stage).
CHRONIC TREATMENT Chronic infections can occur with E. canis; however, response to doxycycline after 28 days of treatment is expected.
DRUG INTERACTIONS Imidocarb dipropionate or enrofloxacin are not effective against Ehrlichia canis. Tetracycline derivatives should not be used in the last half of pregnancy. Oral doxycycline should be given with food to avoid GI effects (nausea and vomiting). Tetracycline derivatives should not be given concomitant with oral antacids, cathartics, or other GI products containing cations (aluminum, calcium, magnesium, zinc, or bismuth).
POSSIBLE COMPLICATIONS Hemorrhage from severe thrombocytopenia or disseminated intravascular coagulation (DIC)
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Ehrlichiosis, Canine Monocytic
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Protein-losing glomerular disease Blindness associated with retinal hemorrhages and detachment Immune-mediated diseases Medullary aplasia and persistent pancytopenia Sudden death due to organ failure may occur in chronic cases. Dogs receiving incomplete or inadequate treatment may enter the subclinical phase.
RECOMMENDED MONITORING Resolution of clinical, hematologic, and biochemical abnormalities should be used to assess the response to therapy. Antibody titers may persist for months to years despite the absence of infection, so serologic testing is unreliable as a monitoring tool. PCR may aid in monitoring the response to treatment: a positive PCR test post treatment would be consistent with a treatment failure or reinfection.
PROGNOSIS AND OUTCOME Good prognosis with quick improvement in acute and mild chronic cases. Expect dramatic positive response to doxycycline or tetracycline beginning within 24-48 hours. Severely pancytopenic patients with hemorrhagic complications or concurrent infections have a guarded to poor prognosis.
PEARLS & CONSIDERATIONS COMMENTS E. canis infection occurs in some cats, with clinical signs resembling acute canine monocytic ehrlichiosis. E. canis has been detected in at least six sick humans in Venezuela. Human E. canis cases have not been described from other countries. E. chaffeensis is the most frequent Anaplasma/Ehrlichia infection in humans in the United States, with 1137 cases reported in 2008. E. chaffeensis may produce similar but less severe signs in dogs than E. canis, although as a result of cross-reactivity, the true incidence of E. chaffeensis in dogs is poorly defined.
PREVENTION Adequate tick control is the best prevention.
TECHNICIAN TIPS Low platelet numbers might increase bleeding time after blood sample collection. Despite a relatively low risk of infection, handling biological samples from animals suspected of Ehrlichia spp. or Anaplasma spp. infection should always be performed with precautions and with adequate personal protective equipment.
CLIENT EDUCATION Infected dogs pose little to no hazard to humans, so long as ticks are well controlled. Dogs are sentinels of human exposure to the pathogen in the shared environment; therefore owners should take proper actions to prevent tick bites.
SUGGESTED READING Cohn LA: Ehrlichiosis and related infections. Vet Clin Small Anim 33:863-884, 2003. Neer TM, et al: Consensus statement on ehrlichial disease of small animals from the Infectious Disease Study Group of the ACVIM. J Vet Intern Med 16:309-315, 2002. AUTHORS: PEDRO PAULO DINIZ AND ADAM BIRKENHEUER EDITOR: DOUGLASS K. MACINTIRE
24-09-2011 19:24
Edema, Subcutaneous
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Edema, Subcutaneous BASIC INFORMATION DEFINITION Subcutaneous edema is the local or generalized observable swelling from excessive fluid accumulation within the interstitial tissue spaces under the skin. Under normal circumstances, only a small amount of fluid leaks from vessels to form interstitial fluid, which is then removed by lymphatic vessels.
SYNONYMS Peripheral edema (edema of the paws and legs), anasarca (generalized, massive subcutaneous edema)
EPIDEMIOLOGY SPECIES, AGE, SEX Dogs and cats: any age, either sex RISK FACTORS Severe hypoproteinemia (from kidney, liver, or gastrointestinal disease), right-sided heart failure, systemic inflammation/vasculitis, extensive trauma or heat, hereditary or congenital malformation of the lymphatic system
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES Pitting edema versus nonpitting edema HISTORY, CHIEF COMPLAINT Limb swelling or a swollen appearance may be historical findings suggestive of subcutaneous edema. PHYSICAL EXAM FINDINGS The subcutaneous tissues appear locally or diffusely swollen. The hock with its lateral saphenous vein, the Achilles tendons, and the bony prominence of the mandible are useful to evaluate for subcutaneous edema; these areas are well defined even in obese animals. With edema, these areas are less defined and have a “jelly-like” appearance of the skin. Edema is by definition nonpainful and neither very warm nor very cool to the touch unless secondary infection is present. Edema tends to accumulate where gravity draws it, where lymphatic obstruction or insufficiency is greatest, or a combination of both. Therefore, the pattern of edema distribution can be variable. It may be possible to “pit” edema: digital pressure exerted on edematous skin may leave a depression, or pit, for several seconds after the pressure is released. Pitting edema represents interstitial fluid accumulation, whereas nonpitting edema is formed by intra-cellular swelling (e.g., a wheal). In dogs and cats, pitting edema is more common than nonpitting edema. Hyperemia, or the reddening of the subcutaneous tissue due to engorgement of oxygenated blood, indicates an active process causing arteriolar dilation. Congestion, or the cyanotic (“blue-red”) appearance of the subcutaneous tissue, is a passive process that occurs as worsening congestion leads to accumulation of deoxygenated hemoglobin. Capillary bleeding can occur uncommonly as a result of chronic congestion and may appear as petechiae, purpura, ecchymosis, or hematoma.
ETIOLOGY AND PATHOPHYSIOLOGY More fluid leaves the capillaries than enters: Increased hydrostatic pressure in vessels Right-sided congestive heart failure Impaired venous flow Iatrogenic fluid overload
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Edema, Subcutaneous
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Decreased plasma oncotic pressure Hypoalbuminemia due to increased loss (protein-losing nephropathy/enteropathy, nephrotic syndrome) or decreased production (cirrhosis, malnutrition) Increased vascular permeability Allergic response causing increased histamine Acute inflammation Burn injury Normal volume of interstitial fluid not reabsorbed by the lymphatic system: Lymphatic obstruction (usually localized) Neoplasia Inflammation Trauma
EDEMA, SUBCUTANEOUS Subcutaneous edema in the hindlimb of a dog. In this image, the clinician just removed her index finger after applying digital pressure for several seconds, revealing the depression or pit (arrows) that characterizes pitting edema.
DIAGNOSIS DIAGNOSTIC OVERVIEW Subcutaneous edema can be identified on physical exam (readily if it is very pronounced but less easily if it is mild in degree). The presence of subcutaneous edema warrants assessing the serum albumin concentration and also ruling out heart disease (thoracic radiographs, echocardiogram).
DIFFERENTIAL DIAGNOSIS When edema affects only one leg, local factors such as neoplasia, trauma, or phlebitis should be considered. Swollen extremities and ventral edema are uncommonly seen with congestive heart failure. In the rare instance (in small animals) where subcutaneous edema is present secondary to congestive heart failure, the edema is usually symmetric in distribution.
INITIAL DATABASE CBC: evaluate for hypoalbuminemia, anemia, or inflammation. Serum biochemistry profile: evaluate for electrolyte abnormalities.
ADVANCED OR CONFIRMATORY TESTING Thoracic radiographs, echocardiography, and electrocardiography: evaluate for right-sided congestive heart failure.
TREATMENT
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Edema, Subcutaneous
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TREATMENT OVERVIEW The therapeutic goal is to identify the cause and reverse it if possible.
ACUTE AND CHRONIC TREATMENT Management of subcutaneous edema is typically nonemergent and is primarily achieved by treatment of the underlying condition while considering specific therapies to restore water balance within the body. Patients with decreased oncotic pressure (hypoproteinemia), decreased osmotic balance (anemia), or increased endothelial permeability (inflammation) may benefit from plasma products, hetastarch, or dextran 70 to increase intravascular volume and favor water retention within the vasculature. Patients with increased hydrostatic pressure secondary to severe right-sided heart failure can benefit from potent loop diuretics such as furosemide. Furosemide causes increased sodium excretion by the kidneys, with resultant water loss and edema mobilization from the interstitial tissues. Trauma, inflammation, or neoplasia causing subcutaneous edema should be addressed primarily.
PROGNOSIS AND OUTCOME The prognosis for patients with subcutaneous edema depends on the underlying condition and the ability to treat and resolve this primary disease. Edema due to inflammation or infection, congestive heart failure, or hypoproteinemia can often be successfully managed or resolved. Treatment response for lymphatic obstruction is variable; lymph-edema (see p. 667) can be challenging to manage long term, and there is no curative therapy.
SUGGESTED READING Mathews KA: Monitoring fluid therapy and complications of fluid therapy. In Dibartola SP, editor: Fluid, electrolyte, and acid-base disorders in small animal practice, ed 3, St Louis, 2006, Elsevier Saunders, p 385. Raffe MR, Roberts J: Edema. In Ettinger SJ, Feldman EC, editors: Veterinary internal medicine, ed 6, St Louis, 2005, Elsevier Saunders, p 70. AUTHOR: MANDI SCHMIDT EDITOR: ETIENNE CÔTÉ
24-09-2011 19:23
Eclampsia
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Eclampsia BASIC INFORMATION DEFINITION Moderate to severe hypocalcemia of the lactating female, most often occurring in the first four weeks postpartum.
SYNONYMS Lactation tetany, periparturient hypocalcemia, puerperal tetany
EPIDEMIOLOGY SPECIES, AGE, SEX Dogs: younger, postparturient bitches Cats: rare in queens GENETICS & BREED PREDISPOSITION More likely to occur in small-breed dogs, although any lactating bitch may be affected RISK FACTORS Primiparous bitches may be at greater risk. Decreased nutrition in the periparturient period as a result of stress or underlying illness. Excess dietary calcium during gestation Large litter size is thought to be a risk factor. ASSOCIATED CONDITIONS & DISORDERS Hypoglycemia can arise secondarily due to energy demands of tetany.
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES Prepartum eclampsia Intrapartum eclampsia Postpartum eclampsia (most common) HISTORY, CHIEF COMPLAINT Lactating bitch with signs of aberrant behavior, ataxia, muscle tremors, seizures, and/or tetany PHYSICAL EXAM FINDINGS In approximate order of disease progression/severity: Anxiety, restlessness, pacing, whining, disinterest in pups Pruritus and biting at feet Ataxia, staggering, and muscle stiffness Panting; respiration eventually becomes labored as the condition progresses. Mydriasis and diminished pupillary light reflexes Tachycardia or bradycardia Muscle tremors, collapse, clonic spasms (tetany), and seizures (musculoskeletal signs are often exaggerated with tactile stimulus). Hyperthermia secondary to tetanic muscle contractions
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Eclampsia
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Arrhythmias: premature ventricular complexes
ETIOLOGY AND PATHOPHYSIOLOGY Circulating ionized calcium is depleted due to lactation and fetal development, possibly in conjunction with underlying nutritional imbalance. Decreased circulating ionized calcium alters cellular membrane potentials and allows for spontaneous discharge of nerve fibers to induce contraction of skeletal muscles and alteration of central nervous system function.
DIAGNOSIS DIAGNOSTIC OVERVIEW A presumptive diagnosis (based on history, clinical signs, and physical exam) warrants immediate treatment. Response to therapy is the most reliable diagnostic aid.
DIFFERENTIAL DIAGNOSIS Hypocalcemia of alternate origin Hypoglycemia (may be concurrent) Cerebral edema (possibly secondary in eclampsia ± hypoglycemia) Toxin ingestion
INITIAL DATABASE Total serum calcium < 6–7 mg/dL (102.5°F [>39.1°C]) due to altered thermoregulatory mechanisms in the hypothalamus. Fever of unknown origin (FUO) is a fever that is documented repeatedly, lasts for 3 weeks or longer, and for which a cause is not identified initially (human medical definition). The normal range of body temperatures in calm, normal individuals in a cool environment is 100.2°F-102.5°F (37.8°C-39.1°C) in the dog and 100.5°F-102.5°F (38.0°C-39.1°C) in the cat.
SYNONYM Pyrexia Note: Fever is a subset of hyperthermia, not a synonym. Nonfebrile hyperthermia (e.g., physical exertion, heat stroke, muscle fasciculations) does not involve alterations in the hypothalamic thermoregulatory mechanisms and is not treated with antipyretic drugs.
EPIDEMIOLOGY SPECIES, AGE, SEX Any age, breed, or sex Young dogs may be more likely to have infectious causes. Older dogs may be more likely to have neoplastic causes. GENETICS & BREED PREDISPOSITION Shar-pei: idiopathic, possible cytokine abnormality Weimaraner: neutrophil function deficiency Irish setter: leukocyte adhesion deficiency RISK FACTORS Immunosuppression Exposure to infectious agents or vectors Travel to endemic areas of disease CONTAGION & ZOONOSIS: Risk varies, dependent on causative agent. GEOGRAPHY AND SEASONALITY: Some regions are endemic for particular infectious diseases. See individual specific topics.
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT: Will vary with organ systems involved and causative agent but usually associated with nonspecific clinical signs such as lethargy, depression, and anorexia PHYSICAL EXAM FINDINGS A complete physical exam in all patients with FUO must include rectal exam (dog), fundic exam (dog, cat), oral exam (dog, cat), meticulous examination of the skin (dog, cat), orthopedic, and neurologic exam (dog, cat) Fever: Individual (haircoat, anxiety) and environmental (ambient temperature) influences may raise the body temperature of normal, healthy dogs and cats and must be considered when interpreting a patient's temperature. Depression Lethargy Tachycardia
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Fever of Unknown Origin
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Hyperpnea Dehydration Lymphadenopathy with infectious or neoplastic disease Neck or back pain or central signs with meningitis, meningoencephalitis, diskospondylitis Joint pain or swelling with monoarthritis or polyarthritis Heart murmur may indicate bacterial endocarditis Chorioretinitis or hemorrhage suggestive of infectious cause Localized swelling and/or pain with wounds or abscesses
ETIOLOGY AND PATHOPHYSIOLOGY Etiology: Infectious: Localized or systemic bacterial infections (dog, cat): diskospondylitis, osteomyelitis, bacterial endocarditis, septic arthritis, prostatitis, pyelonephritis, septic meningitis, cholangiohepatitis, abscesses, pyothorax, peritonitis, pneumonia, pyometra, catheter site infections Specific bacterial infections: leptospirosis (dog), borreliosis (dog), brucellosis (dog), mycobacterial infections (dog, cat), bartonellosis (dog, cat), hemotropic Mycoplasma (Haemobartonella) (dog, cat), tularemia (dog, cat), salmonellosis (dog, cat) Viral: canine influenza (dog), canine distemper virus (dog), parvovirus/panleukopenia (dog/ cat), feline leukemia (FeLV) (cat), feline immunodeficiency virus (FIV) (cat), feline infectious peritonitis (cat), systemic calicivirus (cat) Rickettsial: ehrlichiosis/anaplasmosis (dog, cat), Rocky Mountain spotted fever (Rickettsia rickettsii) (dog) Fungal (dog, cat): histoplasmosis, blastomycosis, coccidioidomycosis cryptococcosis, systemic aspergillosis Protozoal: babesiosis (dog), leishmaniasis (dog), trypanosomiasis (dog), hepatozoonosis (dog), toxoplasmosis (dog, cat), cytauxzoonosis (cat) Immune mediated: immune-mediated polyarthritis (dog, cat), systemic lupus erythematosus (SLE) (dog, cat), rheumatoid arthritis (dog), vasculitis (dog, cat), meningitis (dog), pemphigus (dog, cat), immune-mediated hemolytic anemia (IMHA) (dog, cat), immune-mediated thrombocytopenia (ITP; dog, cat), transfusion reaction (dog, cat) Neoplastic (dog, cat): histiocytic sarcoma, lymphoma, leukemia, multiple myeloma, necrotic solid tumors Other (dog, cat): Pancreatitis Drug induced (tetracyclines, penicillins, sulfas), toxins, metabolic bone disorders, hyperthyroidism, tissue necrosis Pathophysiology: The hypothalamus is responsible for thermoregulation. Fever occurs when the hypothalamic setpoint is reset to higher than normal. Inflammation and bacterial endotoxins increase the hypothalamic set point by causing the release of endogenous pyrogens such as interleukin (IL)-1, IL-6, and tumor necrosis factor a.
DIAGNOSIS DIAGNOSTIC OVERVIEW The diagnosis of FUO is justified when an elevated body temperature has been documented on several occasions (typically over a period of several days) in the absence of confounding factors, which are common: anxiety in the hospital setting and warm ambient temperatures. Confirmation justifies testing to differentiate infectious from noninfectious causes.
DIFFERENTIAL DIAGNOSIS Rule out nonpyrogenic causes of an elevated body temperature (heat stroke, overexertion, muscle fasciculations, etc.)
INITIAL DATABASE CBC, chemistry profile, urinalysis: results will vary with organ system involvement. Urine bacterial culture and sensitivity should be performed in all cases of FUO even if urine sediment is inactive. Helpful with detection of pyelonephritis or prostatitis. FeLV antigen and FIV antibody tests in all cats
ADVANCED OR CONFIRMATORY TESTING
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Fever of Unknown Origin
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Further laboratory testing depends on history, physical exam findings, and minimum database results. Laboratory tests: Serial blood cultures: to detect bacteremia associated with diskospondylitis, endocarditis, or other foci of infection. A negative culture does not rule out bacteremia (intermittent bacterial showering). Specific serologic tests: antibody titers or antigen tests are obtained for evidence of infectious disease. If infectious disease is suspected and initial titers are negative, repeat in 2-4 weeks. PCR testing for specific infectious agents Fungal cultures and/or serologic titers Fungal antigen tests: blastomycosis (urine, blood), cryptococcosis (blood) Cytology and cultures of cerebrospinal fluid (CSF) or synovial fluid Immune tests: antinuclear antibody test if suspected SLE; Coombs' test if suspicion of IMHA or immune-mediated thrombocytopenia (ITP); serum protein electrophoresis Imaging: Thoracic radiographs: to evaluate for evidence of neoplasia, effusions, or pulmonary infiltrates Abdominal radiographs: evaluate for abdominal masses, effusions, free gas. Spinal and long bone radiographs: examine for evidence of diskospondylitis, osteomyelitis, periosteal proliferation. Abdominal ultrasound: rule out pyelonephritis, prostatitis, or pyometra; identify ± aspirate any enlarged abdominal organs or masses (unless highly vascular or bleeding disorder). Echocardiogram: identify vegetative valvular lesions associated with bacterial endocarditis. CT/MRI often indicated before CSF tap to rule out an intracranial mass and decrease risk of herniation Diagnostic procedures: Arthrocentesis: polyarthritis Cytologic study of enlarged lymph nodes or affected organs: neoplasia or identification of infectious agents Bone marrow aspirates and/or biopsy: if CBC changes are reflective of bone marrow involvement or neoplasia is suspected CSF tap if neurologic signs (± fundic exam) suggest meningoencephalitis or meningitis Muscle biopsy: hepatozoonosis Abdominocentesis: peritonitis and pancreatitis Transtracheal wash or bronchoalveolar lavage if respiratory involvement
TREATMENT TREATMENT OVERVIEW The goal in all cases of FUO is to obtain a specific diagnosis and treat accordingly. A therapeutic trial should be initiated only when a specific diagnosis cannot be ascertained.
ACUTE GENERAL TREATMENT Intravenous crystalloid fluid therapy at 1.5-2 times maintenance for fevers where temperature >103.5°F (>39.7°C) Mechanical cooling methods such as cool water baths or fans when patient's temperature >106°F (>41.1°C) Antipyretic agents (e.g., nonsteroidal antiinflammatories [NSAIDs], to be given only when animal is fully hydrated) may be considered if temperature exceeds 106°F (41.1°C) and does not respond to fluids and cooling. Antipyretic drugs should be reserved only for patients with fevers >105°F (40.6°C) and have failed to respond to fluids and mechanical cooling, as such drugs can mask the effects of other therapies and can be associated with adverse effects such as gastrointestinal ulceration and hepatic and/or renal toxicity. Patients with persistent fevers 1.035), proteinuria +/− crystalluria. Urine culture and susceptibility: infection is rare in the United States, seemingly more common in European studies. For cats with a typical initial presentations, no additional diagnostic tests may be required.
ADVANCED OR CONFIRMATORY TESTING For cats with complicated initial presentations or recurrent episodes, diagnostic testing is aimed at ruling out the most common alternative diagnosis. With idiopathic LUTS, no abnormalities are expected. Radiography of the entire lower urinary tract (including the distal urethra) CBC, biochemical analysis and FIV/FeLV testing Other lower urinary tract imaging (e.g., ultrasonography, double contrast cystography) or cystoscopy are rarely indicated.
TREATMENT TREATMENT OVERVIEW Treatment focuses on stress reduction through owner education and environmental enrichment (EE). Lower urinary tract obstruction is a life-threatening condition requiring prompt attention to manage the associated metabolic derangements and reestablish urine flow.
ACUTE GENERAL TREATMENT If the cat is obstructed, relieve the obstruction (see p. 1355), reestablish urine flow, and correct fluid, electrolyte, and acid-base imbalances.
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Drugs Commonly Used for Cats With LUTS Drug
Dose
Potential Side Effects
0.2-0.4 mg/kg IV, IM, SQ q 8 h (IV: use lower end of dose range)
Sedation
Acute Analgesic Butorphanol (Torbugesic)
Buprenorphine (Buprenex) 0.01-0.02 mg/kg IM, IV, or SQ q 8-12 h; 0.015 mg/kg PO or sublingual q 8-12 h (anecdotal) Fentanyl (Duragesic) patch
25 mcg/h
Respiratory depression, bradycardia
Bladder/Urethral Contractility Acepromazine (PromAce) 0.05 mg/kg SQ q 8 h
Sedation, hypotension
Prazosin (Minipress)
0.5 mg per cat PO q 12 h
Phenoxybenzamine (Dibenzyline)
2.5 mg per cat PO q 12 h
Hypotension
Bethanechol (Urecholine)
2.5-5 mg per cat PO q 12 h
Salivation, vomiting, diarrhea
Chronic Analgesic/Anxiolytic Clomipramine (Anafranil)
0.5 mg/kg PO q 24 h
Sedation, anticholinergic effects
Amitriptyline (Elavil)
5-12.5 mg per cat PO q 12-24 h
Sedation, weight gain, urine retention; urolith formation
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Drug
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Potential Side Effects
Establish IV access and provide appropriate analgesia. Submit samples for serum biochemical profile, CBC, and urinalysis. It is not necessary to evaluate the results before treating obstructed cats that present with urethral obstruction and severe systemic signs, with the exception of the potassium concentration. Resuscitate moribund cats with intravenous (IV) fluids, and correct serious electrolyte and acid-base disturbances before anesthesia for placement of a urinary catheter. Obtain an electrocardiogram (ECG) of all systemically ill cats with urethral obstruction, as rescue from the cardiotoxic effects of severe hyper-kalemia may be necessary even before laboratory values for serum potassium (K+) return if arrhythmias are present: Slow IV administration of 2-10 mL of 10% calcium gluconate to effect will protect the myocardium from the deleterious effects of hyperkalemia, without lowering serum potassium concentration (monitor ECG for slowing of heart rate of 10% or more, warranting termination of calcium administration). Usually 0.2-0.5 mL/kg over 15 minutes is adequate (i.e., 1-2.5 mL/5 kg cat); can be repeated in 5 minutes if no improvement. Administration of sodium bicarbonate (1-2 mEq/kg IV) or insulin (0.2-0.4 U regular insulin IV, while supplementing IV fluids to 2.5% dextrose and closely monitoring blood glucose concentration, owing to risk of hypoglycemia) may be used to drive potassium intracellularly and lower serum potassium concentrations prior to reestablishment of urine flow. Consider decompressing the bladder by cystocentesis before attempting to pass a urinary (urethral) catheter. Insert a 22- or 23-gauge butterfly needle into the bladder wall midway between the apex and urethral outflow and directed caudoventrally. If a longer needle is necessary, it can be attached to an extension set and urine removed using a syringe. Palpate the bladder during drainage to empty it as completely as possible. Rare complications include extravasation of urine into the peritoneal cavity and damage to the bladder wall. This procedure may be sufficient to restore normal urine flow but remains controversial because of potential complications. Pass a urinary catheter only if necessary. General anesthesia is needed to allow proper manipulation of the penis to pass the catheter. If the combination of IV ketamine and diazepam does not provide adequate relaxation, isoflurane gas in oxygen, or propofol infusion may provide both adequate sedation and urethral relaxation. If a plug or urethrolith is retrieved, it should be submitted for quantitative analysis. An indwelling urinary catheter (e.g., 3.5-Fr red rubber feeding tube–type) is placed in cats with pronounced azotemia or poor urinary stream after catheter placement. An indwelling urinary catheter also is used for cats with very large bladders at presentation, as they are more likely to develop detrusor atony. Manage cats medically unless future recurrent obstructions occur. For most, analgesics (see table) and appropriate fluid therapy are indicated. Some α-blocking drugs (e.g., phenoxybenzamine) have not been shown to be effective. They act on the proximal feline urethra, whereas most obstructions in cats involve the distal urethra. Monitor urine output frequently in severely ill cats. Those that recover from severe postrenal uremia generally undergo a substantial post-obstructive diuresis >2 mL/kg/h shortly after relief of obstruction and rehydration). During this period, it is essential to give sufficient IV fluids to replace the volume lost as urine. The diuresis declines to normal during 2-5 days. The role of glucocorticoids (e.g., prednisone), and nonsteroidal antiinflammatory drugs (e.g., aspirin, meloxicam) remains poorly defined, and none of these drugs has been shown to be an effective treatment for acute LUTS.
CHRONIC TREATMENT Step 1: Environmental enrichment (EE)/multimodal environmental modification (MEMO). Provide at least one food bowl, one water bowl, and one litter box per cat, plus one. Locate these resources in quiet places where the cat is not startled during use. Provide opportunities for the cat to hide safely and explore its environment. Placing “perches” at windows so the cat can look outside and structures the cat can climb on seem to be important parts of EE. Provide a regularly scheduled time for petting, play, and/or trick-teaching, working toward at least 10 minutes a day. Identify and resolve intercat conflict to the extent possible. If ineffective, proceed to step 2. Step 2: step 1 plus consider use of pheromones (Feliway). If ineffective, proceed to step 3. Step 3: steps 1 and 2 plus consider use of a tricyclic agent such as clomipramine or amitriptyline at the lowest effective dose possible (see table). These drugs should be used only after steps 1 and 2 have been implemented and the cat is so severely affected he/she continues to have recurrences. Conclusive results regarding the efficacy of behavior-modifying drugs are lacking. A perineal urethrostomy may be needed in severe recurrent obstructive cases. This surgery increases the risks of bacterial urinary tract infections, however, and postoperative strictures are a potential complication. Clients should be made aware that this surgery does not correct the underlying problem, and recurrent episodes of
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urolithiasis and LUTS still can occur.
NUTRITION/DIET Dietary therapy may be indicated if uroliths or crystals are identified and will depend on the type of urolith. Glycosaminoglycan (GAG) supplementation has been suggested, but its efficacy remains unproven in cats.
BEHAVIOR/EXERCISE See recommendations for environmental enrichment under Chronic Treatment.
POSSIBLE COMPLICATIONS When introducing EE, offer changes to the cat (e.g., new food in a separate bowl rather than in place of the familiar diet) to avoid precipitating a threat response. Make changes the client wants to make, if possible, to secure support and adherence to the EE effort. Make changes sequentially. When tricyclic drugs are used, they should be tapered slowly over at least 2 weeks to avoid adverse reactions.
RECOMMENDED MONITORING Liver and kidney function should be assessed before use of tricyclic drugs and at least annually in young animals if therapy is extended.
PROGNOSIS AND OUTCOME Most cases of idiopathic, nonobstructive, feline LUTS are self-limiting, usually resolving in 5-10 days. However, recurrent episodes of clinical signs, including urinary tract obstruction, occur with variable frequency. Overall prognosis depends on the cat, client, and environment: Cat: Genetic predisposition Duration of the problem Frequency of occurrences Number of areas and different types of surfaces soiled Client: Ability to identify modifiable causes Strength of bond to affected cat Willingness to pay for treatment Amount of time to devote to solution Willingness to accept and use medications Environment: Number of cats in the household Number of affected cats Practicality of allowing limited outdoor access Ability to rearrange the environment
PEARLS & CONSIDERATIONS COMMENTS EE often is sufficient to suppress clinical signs and should be offered to all owners of cats exclusively housed indoors.
PREVENTION EE recommendations should be provided to all owners of indoor cats, not just those with a clinical problem.
CLIENT EDUCATION Client-oriented information is available at www.indoorcat.org.
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SUGGESTED READING Buffington CAT, Westropp JL, Chew DJ, Bolus RR: Clinical evaluation of multimodal environmental modification (MEMO) in the management of cats with idiopathic cystitis. J Feline Med Surg 8:261–268, 2006. Westropp JL, Buffington CAT: Feline idio-pathic cystitis: current understanding of pathophysiology and management. Vet Clin North Am Small Anim Pract 34:1043, 2004. AUTHOR: CLAIRE SHARP EDITOR: LEAH COHN 1ST EDITION AUTHOR: C.A. TONY BUFFINGTON
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Feline Leukemia Virus Infection
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Feline Leukemia Virus Infection BASIC INFORMATION DEFINITION Virus infection of cats that can result in immunosuppression, myelosuppression, and neoplasia
SYNONYM FeLV
EPIDEMIOLOGY SPECIES, AGE, SEX Mainly domestic cats (rare examples in wild felids) are infected Young cats ( males. At least 60% of all veterinary patients may be affected. GENETICS & BREED PREDISPOSITION: Onset/worsening: possibly worse in breeds with apparent familial behavioral concerns associated with social anxieties (e.g., Bernese mountain dogs: generalized anxiety disorder), fear (e.g., German shepherd dogs), phobias (e.g., German shepherd dogs, Australian shepherds, Border collies for noise phobia) and/or panic (many herding and coursing breeds) RISK FACTORS +/− Social maturity (occurring during age 12-18 [up to 36] months in dogs, 24-48 months in cats) Dogs/cats who appear developmentally delayed and/or overly fearful within their first few months of life may be more susceptible to this form of learned fear. CONTAGION & ZOONOSIS: This condition is the result of learning about environments viewed as threatening or uncertain from behavioral cues given by other animals and people. Affected animals often bite veterinary professionals. ASSOCIATED CONDITIONS & DISORDERS Generalized anxiety disorder Noise phobia Fear (generalized or specific) Fear aggression
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT: Clients recognize that their pets “do not like to go to the vet.” Physical and behavioral signs of stress, distress, and anxiety are generally recognized by most people present but ignored because they are considered “normal” for veterinary patients. PHYSICAL EXAM FINDINGS: Physical exam findings are those associated with the physical and behavioral signs of stress, distress, and anxiety. These may include but are not restricted to: Social withdrawal with or without complete freezing (no interaction with anyone) Physical freezing and rigidity Salivation and/or clear nasal discharge Panting Shaking/trembling Increased shedding of hair/exfoliation of dry skin Avoidance of stimulus or stimulus modality that triggers response (e.g., metal table, smell of alcohol, all flooring that is not nonslip) Vocalization including whining, barking, growling, hissing, whimpering Mydriasis Escape behaviors Grabbing with mouth or paws
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Fear Due to Veterinary Visits/Treatments
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Yawning/licking lips Scratching Chewing through restraints (e.g., leads) Hiding Crouching Tucking tail Tachypnea Tachycardia Hyperthermia Increased or decreased sensitivity to pain Increased or decreased reactivity to touch or approach Hyperemic mucous membranes Dehydration Exacerbation of any cardiac, respiratory, or skeletal condition that may be comorbid
ETIOLOGY AND PATHOPHYSIOLOGY The etiology is exposure to stimuli and environments animals feel are worrisome, threatening, or uncertain and from which they cannot escape in time or space, despite signaling their need to do so. Regardless of whether the humans feel the environment is not threatening, what matters is the animal's perception and response. The pathophysiology is as for any condition involving behavioral stress, distress, and/or anxiety and appears to be rooted in neurochemical encoding of information in the amygdala. Rodent studies show that fear is most easily erased in very young animals whose brains are still developing. After this period (which is undefined for cats and dogs), perineuronal nets protect memories of fear from modification. This is why it is so important not to learn to fear.
DIAGNOSIS DIAGNOSTIC OVERVIEW The diagnosis is made based on visual observation of signs of stress, distress, and/or anxiety in association with veterinary premises or activities. Since this problem is highly prevalent, such signs are at risk of being downplayed or ignored, and the diagnosis missed.
DIFFERENTIAL DIAGNOSIS All signs of this iatrogenic condition are shared by other behavioral conditions and by many physical conditions including various neuropathies and toxicoses. The key to assigning a cause to the signs is to ask whether the signs are manifest only under physical and behavioral environmental conditions involving veterinary care.
INITIAL DATABASE No diagnostic testing is required to make the diagnosis. Many laboratory databases can be skewed by the condition. Examples include but are not restricted to: Altered lymphocyte/neutrophil ratios and leukocytosis, often with a left shift (stress leukogram) Increased cortisol Hyperglycemia (especially cats) Increased creatine phosphokinase Increased hematocrit due to splenic pooling and/or margination associated with mild dehydration
TREATMENT TREATMENT OVERVIEW Treatment should be focused on ameliorating any signs of stress, distress, or anxiety as they appear, and at preventing them from worsening by learning in the future. This means specific triggers must be identified and addressed for the patient population as a whole and for each animal as an individual. A list of potential triggers of stress, distress, or anxiety should be compiled at each visit and long-term and short-term plans made for how to address the triggers (e.g., replace slippery tile flooring with nonslip flooring; vaccinate outside while dog is watching other dogs).
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ACUTE AND CHRONIC TREATMENT Cease exposure to or engagement in whatever environments or behaviors are provoking the animal (e.g., if animals are resistant to getting on the table, let them sit on the floor; if they slip on the table, give them a nonslip mat). If the animal continues to manifest distress, consider panicolytic medication to abort the distress while the animal is with the veterinarian. The first drug of choice is alprazolam (dogs, 0.01-0.1 mg/kg [likely most effective range: 0.02-0.04 mg/kg] PO q 4-6 h PRN; cats, 0.0125-0.025 mg/kg PO q 12-24 h PRN; some published sources mistakenly recommend a tenfold higher dose). May also be used as a preventive: 0.5-1 dose given 2 hours before the expected provocative event and repeated 30 minutes beforehand. Alternatively, clonidine (dogs: 0.01 mg/kg PO q 12-24 h increased stepwise up to 0.05 mg/kg PO q 12-24 h (maximum dose 0.9 mg/day) or gabapentin (dogs: 10-20 mg/kg PO q 8-12 h) may be useful. Have all staff work to reward the dog for calm and comfortable behaviors. Integrate Certified Pet Dog Trainers (CPDTs) with extensive experience in behavior modification into the practice (www.ccpdt.org). Treatment of phobias (see p. 875 ) and separation anxiety (see p. 1012 ) as needed.
BEHAVIOR/EXERCISE Prophylactic veterinary visits should be fun. Interventional veterinary visits should be nonthreatening, calming, reassuring, and as stress free as possible. Animals learn fear as they age, so early appointments should involve treats, play, massage, and lots of fun activities before anything threatening (e.g., a vaccination) should be attempted. Therefore, puppy and kitten visits should be longer, and the animals should be allowed to interact with the staff and explore the hospital. On-site puppy/kitten and young dogs manners classes are an excellent vehicle for these exposures. Environments should be friendly to animals. This means that practices should attempt to do the following: Modulate the noise environment by using acoustic tiles, plexiglass cage doors/walls when possible. Consider Muttmuffs (www.muttmuffs.com) for hospitalized/anesthetized animals. Modulate the visual environment by the use of movable barriers and flexible and non-harsh lighting conditions. Consider calming caps (www.premier.com), Doggles (www.doggles.com), or eye shades as needed, especially when recovering from anesthesia. Modulate the olfactory environment by allowing animals to have T-shirts or gloves worn by their humans with them in cages and during manipulations or anesthetic inductions. Rinse common areas with plain water. Spraying hands with pheromonal analog products (e.g., Feliway) has been anecdotally reported to decrease locomotor behavior/increase calm behaviors in cats. Provide hiding and perching boxes/containers for caged cats. Change tactile environments through nonskid flooring, yoga mats, and covering tables and scales with nonslip surfaces. Use treats to reward good behaviors, and teach animals to participate in the exam process by offering body parts.
POSSIBLE COMPLICATIONS Left untreated, these animals are more at risk for relinquishment, euthanasia, or absence of any preventative veterinary care.
RECOMMENDED MONITORING Screen each animal at every visit for behavioral concerns manifest at home or during examinations/interventions.
PEARLS & CONSIDERATIONS COMMENTS Iatrogenic fear conditioned by veterinary visits and care may trigger otherwise latent pathologic behavioral conditions. Because manifestations of fear are commonly cited as reasons for relinquishment, euthanasia, or avoidance of veterinary visits, the single most important welfare concern for pet animals may be how they react to veterinary care and visits. Everyone can recognize the signs associated with this condition. Only if we begin to find it unacceptable to scare animals will we stop doing it.
PREVENTION This condition is completely preventable. Cats should be exposed to humane interactions with people between 2-9 weeks of age, and dogs should be exposed to nonterrifying interactions with people and other animals and to new environmental experiences between 3 weeks and 16 weeks of age. Any profoundly fearful or distressed reactions during this period should trigger a behavioral consult and inform
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the quality and quantity of future interactions/exposure.
TECHNICIAN TIPS This is one condition where technicians, particularly those with an interest in behavior modification, can make a huge change for the better in an animal's life. Technicians should be comfortable with how to examine cats in carriers using towels, how to use head collars and no-pull harnesses, how to trim toenails and draw blood without restraints, how to teach dogs and cats to offer body parts for examination, and how to modify the environment according to the pet's needs. Many practices have one or a few technicians who are very adept at deciphering and acting favorably and appropriately on cues of stress (the “pet whisperers”), and much can be learned by example from these individuals.
CLIENT EDUCATION Clients should be taught that this condition need never develop and that it need not be normal for pets to fear veterinary visits or care. Working with a good CPDT, they can teach their pets to willingly participate in the physical exam.
SUGGESTED READING Brennan J, et al: Attending to patient behavior: where, when, and how. North Am Vet Conf Clin Brief 3(4):19–20, 2005. D öring D, et al: Fear-related behaviour of dogs in veterinary practice. Vet J 182:38–43, 2009. Pizzorusso T: Erasing fear memories. Science 325:1214–1215, 2009. AUTHOR & EDITOR: KAREN OVERALL
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Fanconi Syndrome
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Fanconi Syndrome BASIC INFORMATION DEFINITION Uncommon constellation of renal tubular resorptive defects (including amino acids, phosphates, glucose, bicarbonate, calcium, and potassium) with renal tubular acidosis and antidiuretic hormone (ADH)-resistant polyuria
EPIDEMIOLOGY SPECIES, AGE, SEX Primarily affects dogs; has been seen in cats No sex predilection Onset of phosphaturia and renal sodium loss around 3 years of age, with glucosuria and aminoaciduria at 4 years of age in inherited forms GENETICS & BREED PREDISPOSITION Inherited form in basenji; mode of inheritance unknown; affects 10%-30% of basenji dogs in United States Documented disease in other breeds (not necessarily inherited): border terriers, Norwegian elkhounds, single reports in a Yorkshire terrier, Labrador retriever, cocker spaniel, dachshund, whippet, Shetland sheepdog, and mixed breed Bedlington terrier, West Highland white terrier, Skye terrier, Dobermanpinscher, Labrador retriever, and dalmatian dogs are predisposed to copper storage diseases; West Highland white terriers and other breeds with copper storage disease have been noted to have a reversible Fanconi syndrome. RISK FACTORS Copper storage hepatopathy has been associated with transient Fanconi syndrome, similar to Wilson's disease in humans. Newly recognized form of acquired Fanconi syndrome is suspected but not proven to be caused by ingestion of contaminated jerky treats (pathophysiology unknown). ASSOCIATED DISEASES & CONDITIONS: Metabolic acidosis, electrolyte disorders, urinary tract infection; bone abnormalities are uncommon in adult dogs (rickets common in children with Fanconi syndrome).
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES: Not all dogs have all components of tubular resorptive defects, and the degree of each defect varies from dog to dog. HISTORY, CHIEF COMPLAINT Polyuria Polydipsia Weight loss Poor haircoat None (routine screening/incidental finding) Severe GI signs (vomiting, diarrhea, anorexia) if associated with jerky treat ingestion PHYSICAL EXAM FINDINGS Dehydration Muscle weakness Exam may be unremarkable
ETIOLOGY AND PATHOPHYSIOLOGY Can be acquired or inherited. Acquired disease can be due to heavy metal intoxication (lead, copper, mercury, organomercurials),
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maleic acid, Lysol, drugs (outdated tetracycline, gentamicin, cephalosporins, cisplatin, salicylate), contaminated jerky treats (presumptive), copper storage hepatopathy, nephrotic syndrome, amyloidosis, neoplasia (multiple myeloma), hyperglobulinemia, hyperparathyroidism, vitamin D deficiency, hypokalemia, or interstitial nephritis associated with antibodies to the glomerular basement membrane or transplantation. Defects are primarily proximal tubular resorptive defects. Filtered glucose is normally completely reabsorbed in the proximal tubule, so long as tubular concentration (similar to plasma concentration) does not exceed the transport maximum (about 180 mg/dL). A defect in the transport mechanism can lead to renal glucosuria despite normoglycemia. Aminoaciduria may be generalized or involve only certain groups of amino acids, because different carrier molecules are involved in transport of acidic, basic, and neutral amino acids. Some dogs have cystinuria with minor defects in resorption of methionine, glycine, and dibasic amino acids. Phosphate is reabsorbed primarily in the proximal tubule, with very little reabsorbed in the distal tubule. Excessive phosphaturia due to tubular defects may lead to hypophosphatemia. Hyperchloremic metabolic acidosis may develop secondary to severe bicarbonaturia. Hypokalemia may result from excess renal potassium loss associated with bicarbonaturia. In addition to proximal tubular defects, dogs with Fanconi syndrome are resistant to ADH, creating a form of nephrogenic diabetes insipidus. This results in urinary concentrating defects. Before the onset of renal failure, urine specific gravity is frequently less than 1.008.
DIAGNOSIS DIAGNOSTIC OVERVIEW The presence of glucosuria and ketonuria in the absence of hyperglycemia is a hallmark of Fanconi syndrome, but other tubular defects will be present in addition.
DIFFERENTIAL DIAGNOSIS Diabetes mellitus Central diabetes insipidus Any cause of nephrogenic diabetes insipidus Renal failure Primary renal glucosuria (glucosuria only without aminoaciduria, etc.)
INITIAL DATABASE Urinalysis: isosthenuria or minimally concentrated urine, glucosuria and proteinuria common, +/− ketonuria Urine culture: glucosuria leads to increased risk of UTI. CBC: anemia occurs late in disease secondary to kidney failure. Serum biochemistry panel: normoglycemia; hyperchloremic metabolic acidosis, and azotemia occur late in disease process. Venous blood gas (preferred to total CO2 from serum biochemistry panel because of artifactual changes associated with storage and handling): metabolic acidosis
ADVANCED OR CONFIRMATORY TESTING In a basenji with glucosuria and normoglycemia, no further confirmation necessary For other breeds: Amino acids Cyanide nitroprusside-based array for cystinuria Urine amino acid excretion: either 24-hour excretion or fractional excretion compared to creatinine excretion; normally 98%-100% resorption (available from http://research.vet.upenn.edu/penngen) Fractional excretion of electrolytes: (Ux/Sx)× (Scr/Ucr) × 100, where Ux is urine concentration of electrolyte, Sxis serum concentration of electrolyte, Scr is serum creatinine, and Ucris urine creatinine Expect elevated fractional excretion values (normal values in parentheses): Na+ (0.31 ± 0.2), Cl− (0.31 ± +
++
0.25), K (9.3 ± 5.9), Phos (21 ± 9), Ca (0.15 ± 0.13) Parathyroid hormone level if suspicion of hypoparathyroidism (hypocalcemia) Heavy metal testing if indicated
TREATMENT
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Fanconi Syndrome
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TREATMENT OVERVIEW One treatment protocol (www.basenji.org/fanconi.pdf) replaces nutrients excreted in urine to maintain plasma concentrations. This protocol has not been compared to other (potentially simpler) protocols to determine whether it improves survival or quality of life, but it is used by many owners of basenji dogs with Fanconi syndrome.
ACUTE GENERAL TREATMENT If acute uremic crisis, hospitalize for intravenous fluid therapy and other management appropriate for decompensated chronic renal failure (see p. 207) Electrolyte and acid base disorders treated as appropriate If severe GI signs associated with jerky treats, hospitalization for IV fluid therapy and potentially feeding tube placement may be appropriate.
CHRONIC TREATMENT Acidosis: sodium bicarbonate titrated to keep venous pH normal. Doses may exceed 11 mEq/kg per day (650 mg = 10 grain = 7.8 mEq). Starting dose can be based on pH and Pco2 using a chart in the basenji club website protocol, or if immediate blood gas monitoring not available, 30 grains q 12 h. +
Hypokalemia: supplement 5-15 mEq per day, depending on severity of hypokalemia. Potassium gluconate has 8 mEq K per +
tsp. Potassium citrate provides 5 mEq K per 540 mg tablet; the citrate is metabolized to 5 mEq bicarbonate, which may help control acidosis. Chelation therapy if copper storage hepatopathy
NUTRITION/DIET Vitamin and mineral replacement: 1-2 canine multivitamins per day (e.g., Pet-Tab Plus), 1-2 Pet-Cal (calcium, phosphorus, and vitamin d supplement) per day, and 1 human multivitamin with trace minerals (i.e., Centrum) per week in dogs with polyuria and polydipsia. Do not give Pet-Cal if dog is in renal failure. Amino acid replacement: 1 AminoFuel tablet per week
POSSIBLE COMPLICATIONS Neurologic signs (seizures, ataxia, dementia, or central blindness) of unknown cause are seen in up to 20% of dogs. Manipulation of electrolyte and acid-base balance can lead to overcorrection of deficiencies.
RECOMMENDED MONITORING Recheck chemistry panel and venous blood gas 8-10 weeks after starting therapy, then in 6 months. Recheck annually if animal remains stable and requires no dose adjustments. Recheck potassium 1 week after any dose adjustment. Culture urine at least every 6 months.
PROGNOSIS AND OUTCOME Lifespan is not substantially reduced from normal (median survival time 5.25 years from diagnosis). Renal failure is the most common cause of death (40%).
PEARLS & CONSIDERATIONS COMMENTS Overall, this is a rarely encountered disease.
PREVENTION Inherited disease in basenji dogs. Dogs with this disease should not be bred, although late onset of disease (3-8 years) complicates reproductive planning.
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SUGGESTED READING The Basenji Club of America: www.basenji.org/fanconi.pdf. Yearley JH, et al: Survival time, lifespan, and quality of life in dogs with idiopathic Fanconi syndrome. J Am Vet Med Assoc 225:377–383, 2004. AUTHOR: CATHY LANGSTON EDITOR: LEAH A. COHN
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Facial Paralysis, Idiopathic
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Facial Paralysis, Idiopathic BASIC INFORMATION DEFINITION An acute neuropathy of unknown etiology affecting one or both facial nerves
EPIDEMIOLOGY SPECIES, AGE, SEX: Mature (>5 years) dogs and cats may be affected. GENETICS & BREED PREDISPOSITION: Cocker spaniels, golden retrievers, beagles, and domestic long-haired cats are overrepresented.
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT Rapid onset of drooling from one side of the mouth Inability to blink: This deficit may be somewhat inapparent to owners, since dogs and cats with facial paralysis retain the ability to periodically retract the globe, which may give the appearance of a blink, owing to passive motion of the third eyelid. Dogs usually have an apparent ear droop and occasionally will have deviation of the nose away from the affected side. Food may collect in the affected commissure of the lips, and there may be associated halitosis. Occasionally clinical signs are bilateral, but they may begin on one side and take several days or weeks to affect the contralateral side. PHYSICAL EXAM FINDINGS The menace response and palpebral reflex on the affected side are absent. Facial drooping, ptyalism, and ptosis may be evident. When a noxious stimulus is applied to the upper lip, the muscles of facial expression will fail to contract (trigeminofacial reflex); sensation of the face remains unaffected. In chronic cases, there may be permanent lip contracture. Corneal ulceration may be evident as a result of damage to the parasympathetic fibers responsible for tear production and/or exposure keratitis from the inability to blink.
ETIOLOGY AND PATHOPHYSIOLOGY The pathogenesis in domestic animals is unknown, but in humans, a similar condition (Bell's palsy) is associated with herpes simplex virus infection. Histopathologic studies reveal active degeneration of large- and small-caliber myelinated fibers. Inflammation is absent.
DIAGNOSIS DIAGNOSTIC OVERVIEW The diagnosis of idiopathic facial paralysis requires a complete neurologic exam and eliminating structural or metabolic causes of facial nerve dysfunction.
DIFFERENTIAL DIAGNOSIS Idiopathic facial paralysis must be differentiated from other conditions involving the peripheral aspect of the facial nerve (e.g., otitis media interna, hypothyroidism, ear polyps, and polyneuropathies). When they cause facial paralysis, disorders of the central nervous system such as neoplasia, encephalitis, congenital malformations, and trauma are usually accompanied by additional neurologic deficits.
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Facial Paralysis, Idiopathic
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INITIAL DATABASE Complete neurologic and otoscopic examination (see p. 1311 and p. 1316, respectively) Serum chemistry panel and CBC: un remarkable with idiopathic facial paralysis Thyroid panel Schirmer tear test
ADVANCED OR CONFIRMATORY TESTING Advanced imaging (e.g., CT, MRI) may be indicated for evaluation of the tympanic bullae and brainstem. Enhancement patterns in the intratemporal segment of the facial nerve as seen on MRI may be used for predicting recovery times.
TREATMENT TREATMENT OVERVIEW The main goal is prevention of corneal ulceration. No specific therapy is indicated for the remaining manifestations of facial paralysis.
ACUTE GENERAL TREATMENT Treatment is primarily supportive. Sterile lubricant ophthalmic ointment should be applied to the affected eye(s) at least q 6-8 h to prevent exposure keratitis and corneal ulceration. The use of corticosteroids is controversial and unlikely to be of benefit, given the paucity of inflammation. However, in people with Bell's palsy, such drugs may be efficacious in hastening recovery.
CHRONIC TREATMENT Some animals require lifelong eye lubrication. Others will eventually begin to reflexively use the third eyelid to moisten the cornea and will no longer need topical medication.
PROGNOSIS AND OUTCOME Prognosis for complete recovery is guarded. Some animals will regain variable levels of function to the facial nerve, but many have some degree of residual deficit.
PEARLS & CONSIDERATIONS COMMENTS Facial paralysis was reported to be idiopathic in 75% of dogs and 25% of cats in one study. Therefore it is imperative that practitioners do a complete neurologic evaluation to rule out other common causes of facial nerve dysfunction (see Differential Diagnosis above).
SUGGESTED READING Dewey CW: Encephalopathies: Disorders of the brain. In Dewey CW editor: A practical guide to canine and feline neurology, ed 2, Ames, IA, 2008, Wiley-Blackwell Publishing, pp 160–162. Varejao AS, et al: Magnetic resonance imaging of the intratemporal facial nerve in idio-pathic facial paralysis in the dog. Vet Radiol Ultrasound 47:328, 2006. AUTHOR: GEORGINA BARONE EDITOR: CURTIS W. DEWEY
25-09-2011 21:18
Facial Muscle Wasting
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Facial Muscle Wasting BASIC INFORMATION DEFINITION Atrophy of the muscles of mastication, mainly the temporal and masseter muscles
SYNONYM Masticatory muscle atrophy
EPIDEMIOLOGY SPECIES, AGE, SEX: Dogs (most commonly) and cats (rarely), any age, any sex; with muscular dystrophy (MD), only males affected; with hereditary Labrador retriever myopathy (HLRM), males and females affected. GENETICS & BREED PREDISPOSITION German shepherd, retrievers, Doberman pinscher, spaniels: masticatory myositis (MM) Shetland sheepdogs, rough- and smooth-coated collies: dermatomyositis German shepherds, other large breeds: idiopathic polymyositis (IP) Large-breed dogs: glucocorticoid-induced muscle atrophy Young male golden retriever: muscular dystrophy Labrador retriever: HLRM Bassett hounds: temporomandibular joint (TMJ) dysplasia ASSOCIATED CONDITIONS & DISORDERS Submandibular and prescapular lymphadenopathy (see p. 662) Generalized muscle atrophy
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT Detailed history to include inquiries regarding previous bouts of painful mastication or chronic corticosteroid use History may reflect abnormalities isolated to facial musculature or reflective of generalized myopathy. Facial: Prominence of external occipital protuberance noticed by owner Difficulty or inability to prehend food (less common) Reflects either weakness (decreased jaw tone) or masticatory muscle fibrosis (increased jaw tone or trismus [inability to open the mouth]) Prior episode(s) of painful mastication and crying while chewing: MM Generalized: Concomitant mild to severe weakness, exacerbated by exercise; generalized muscle atrophy: IP Bunny hopping gait, progressing to a more stilted gait with a plantigrade stance: MD PHYSICAL EXAM FINDINGS Full physical examination, paying particular attention to the head, the condition of other muscle groups, and the skin Bilateral atrophy of the temporal and masseter muscles; skull-like appearance of the head Dogs with MM can show salivation, dysphagia, and difficulty in opening their mouths, progressing to trismus. Dogs with dermatomyositis can show generalized muscle atrophy, decreased jaw tone, facial nerve paralysis, stiff gait, dysphagia, regurgitation, and skin lesions. Enophthalmos, with third eyelid protrusion and small palpebral fissure due to dramatic loss of retrobulbar muscular support Unilateral temporal muscle atrophy: ipsilateral denervation of the mandibular branch of the trigeminal nerve
ETIOLOGY AND PATHOPHYSIOLOGY
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Facial Muscle Wasting
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Developmental MD HLRM Dermatomyositis Idiopathic Trigeminal neuropathy Infectious Toxoplasmosis (rare) Neosporosis (rare) Immune-mediated Systemic lupus erythematosus Idiopathic polymyositis MMM Iatrogenic Glucocorticoid administration Metabolic Hyperadrenocorticism Cardiac cachexia Neoplastic Cachexia and protein energy malnutrition resulting in muscle atrophy are features of many chronic neoplastic and inflammatory conditions. Disuse atrophy TMJ dysplasia Traumatic luxation of the TMJ (cats) TMJ ankylosis (cats)
DIAGNOSIS DIAGNOSTIC OVERVIEW The specific diagnosis is often made histopathologically, with the exception of serologic titers for infectious causes or for the detection of antibodies against type 2M muscle fibers.
DIFFERENTIAL DIAGNOSIS As for Etiology, above
INITIAL DATABASE CBC usually normal by the time the muscles are atrophied Serum biochemistry profile Elevated muscle enzyme levels (creatine kinase and aspartate aminotransferase): IP, MM, DM, MD, HLRM Hyperglobulinemia: IP
ADVANCED OR CONFIRMATORY TESTING Muscle biopsies and histopathology (see p. 1305 ): Immunohistochemistry shows lack of dystrophin (MD). Paucity of type 2 myofibers (HLRM) Antibodies against type 2 myofibers on frozen sections of muscle (MM) Myofiber necrosis with mononuclear cell infiltrates, atrophy, and fibrosis (dermatomyositis) Multifocal necrosis and phagocytosis of type 1 and type 2 myofibers (IP) Circulating serum antibodies against type 2 myofiber muscle fibers: MM Serology for Toxoplasma and Neospora: protozoal myositis Electromyography is more useful in determining neurologic rather than muscular etiology of the atrophy.
TREATMENT TREATMENT OVERVIEW Immunosuppressive drugs are the mainstay of treatment and have to be instituted early to halt the process of muscle inflammation
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and atrophy. Antibiotics should be used for protozoal myositis.
CHRONIC TREATMENT Glucocorticoid therapy Masticatory myositis (see p. 704) Idiopathic polymyositis (prednisone, 1-2 mg/kg q 12 h for 14 days, then tapering over at least 4 weeks to 12 months or longer) Dermatomyositis (variable response) Upright feeding of dogs with concomitant megaesophagus Clindamycin (12-25 mg/kg PO q 12 h): protozoal myositis
POSSIBLE COMPLICATIONS Corticosteroid side effects
RECOMMENDED MONITORING Monitor for corticosteroid side effects, and taper the dose depending on muscle condition and function.
PROGNOSIS AND OUTCOME Variable, depending on the underlying etiology. Process is reversible provided the muscles have not yet undergone extensive fibrosis.
PEARLS & CONSIDERATIONS COMMENTS Facial muscle atrophy is a common feature of many emaciating conditions in which there is also accompanying generalized loss of lean body mass. Generalized muscle atrophy is often first noticed in the facial muscles, especially in long-haired breeds. Of all the differentials discussed in this section, only trigeminal nerve abnormalities, MM, and anomalies of the TMJs are strictly confined to facial muscle atrophy.
CLIENT EDUCATION Encourage clients to present patients early in the disease process
SUGGESTED READING Taylor SM: Disorders of muscle. In Nelson RW, Couto CG, editors: Small animal internal medicine, St Louis, 2003, Mosby, pp 1062–1070. AUTHOR: JOHAN P. SCHOEMAN EDITOR: ETIENNE CÔTÉ
25-09-2011 21:18
Gunshot Wounds
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Gunshot Wounds BASIC INFORMATION DEFINITION A type of projectile injury involving handguns, air-powered weapons, shotguns, or rifles
EPIDEMIOLOGY SPECIES, AGE, SEX Dogs and cats of any age Male dogs may be overrepresented RISK FACTORS Unsupervised roaming, notably intact male dogs Night and early morning hours Stray dogs in rural areas (e.g., deliberately shot if considered a nuisance or potential threat to livestock) During hunting season, dogs may be mistakenly shot as game or maliciously for sport. Guard dogs, police dogs, and hunting dogs are at risk of being shot during work. GEOGRAPHY AND SEASONALITY Higher-crime urban neighborhoods In rural areas, shotgun and rifle injuries are more common. Air-powered weapons: more likely discharged in residential or rural areas
CLINICAL PRESENTATION Subtypes: Pellet guns and BB guns (air-powered projectiles) Handguns Rifles Shotguns HISTORY, CHIEF COMPLAINT Pets may present with respiratory distress, internal hemorrhage, neurologic injury, or musculoskeletal injuries (fracture). Wound may escape notice, especially if event was not witnessed Dogs and cats with extensive blood loss will present in shock, with pale mucous membranes and tachycardia. Patient may present in pain; in minor cases, the patient may show little evidence of overt discomfort. PHYSICAL EXAM FINDINGS Open wounds: Circular, oval, or angular cutaneous entry wounds with solitary projectiles, often smaller than the projectile Cutaneous burns/lesions if firearm was at close range There may be no exit wound if the projectile is retained: low-velocity projectiles are more likely to be retained than high velocity projectiles. Exit wounds are frequently larger and irregular in shape; shards of bone form secondary projectiles, increasing exit wound size. At close range, shotgun injuries can cause extensive destruction of the skin and underlying tissues. Low-velocity BBs and pellets (air-powered) create small entry wounds. Because of their low mass and comparatively low velocity, many of these projectiles will be retained (no exit wound). Internal injuries: Clinical signs are commensurate with tissues impacted and the severity of trauma (orthopedic, spinal, ocular,
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Gunshot Wounds
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gastrointestinal, pulmonary involvement). Elastic tissues (lung, muscle) are capable of stretching, thereby partially dissipating the kinetic energy of the projectile. Inelastic organs, such as the liver (low collagen content), may show massive tissue destruction from the high-velocity rifle round compared to a low-velocity bullet. Abdominal gunshot wounds have a high probability for peritonitis (gastrointestinal tract penetration).
GUNSHOT WOUNDS Hunting rifle round, shattering the patient's femur. Note the bone and projectile fragments, creating secondary projectiles within the wound, enhancing soft tissue trauma.
ETIOLOGY AND PATHOPHYSIOLOGY The destructive potential of a projectile can be assessed in part by the formula:
Bullets may have an outer metallic jacket to control the shape or expansion of the bullet as it impacts a target. Hollow points are designed to mushroom on impact. Frangible bullets are designed to break apart on impact. Military-style full metal jacket bullets are designed to minimize deformation. Projectiles are capable of lodging and then migrating through the respiratory tract, urogenital tract, gastrointestinal tract, cardiovascular system, and fascial planes. Shotgun pellets expand in a conical pattern; they are very destructive in the first 20 yards or less.
DIAGNOSIS DIAGNOSTIC OVERVIEW Bullets, BBs, and pellets may be found as an incidental finding on radiographs. This may cause confusion when evaluating an acutely sick or injured patient. It is important to remember that acute gunshot wounds will have an entry wound. Gunshot wounds are most commonly mistaken for bite wounds and vehicular trauma. Because most animals are shot while wandering, radiographs are an important tool in looking for evidence of a retained projectile.
DIFFERENTIAL DIAGNOSIS Other penetrating objects can create a skin opening that may mimic a bullet wound, including sticks, pointed metallic objects, and the like.
INITIAL DATABASE CBC, serum chemistry profile, and urinalysis as indicated by likely organs injured Radiographs (two-view minimum) for the body region shot, based on bullet retention or entry/exit wound locations. In a gunshot wound with no evidence of exit, additional views may be needed to locate a retained projectile.
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Gunshot Wounds
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ADVANCED TESTING OR CONFIRMATORY TESTING Abdominocentesis (see p. 1194), fluid analysis, cytology, and gram stains may be used to confirm the possible presence of peritonitis. Thoracocentesis can be both life saving and diagnostic for patients with pneumothorax or hemothorax; aerobic and anaerobic cultures if infection is suspected.
TREATMENT TREATMENT OVERVIEW A team effort by doctors and technical support is necessary to efficiently stabilize critically injured patients. Control visible blood loss. Maintain an established airway, and assure patient is breathing satisfactorily. Placement of one or more intravenous lines for fluid support. Address life-threatening injuries and overlapping medical crises. Initiate pain therapy to reduce patient discomfort and stress. Initiate wound care and a plan for long-term management of the injuries.
ACUTE GENERAL TREATMENT Control external hemorrhage by external compression, tourniquets, ligatures, vascular clips. Attendants should wear gloves to prevent bacterial contamination and protect individuals from bloodborne disease. Intravenous fluid support (crystalloids, colloids, hypertonic saline, whole blood products) Establish and maintain respiratory system: intubation, emergency tracheotomy, thoracic tube insertion (hemo-thorax, pneumothorax, etc.) if indicated. Initiate pain medications that will not mask or compromise the patient's status. Consider a pure opioid agonist such as morphine, 0.1-1 mg/kg IV or IM q 2-6 h, for good analgesic activity and the ability for reversal as needed. Partial agonists (buprenorphine) and agonist/antagonists (butorphanol) acceptable for minor gunshot wounds. A muzzle or Elizabethan collar may be used to protect health care providers from being bitten by the anxious or painful patient. The external gunshot wound can be clipped, cleansed, and pressure lavaged (35-mL syringe and an 18-G needle); the wound may require enlargement to prevent entrapment of lavage fluids. A protective dressing may then be applied to the individual wounds. Broad-spectrum intravenous antibiotics (e.g., cefazolin, 22 mg/kg IV q 6 h) can be initiated in the seriously injured patient. Not all critical patients can be fully stabilized prior to surgery. For example, following initial attempts to support the hypovolemic patient, surgical intervention may be needed to control massive hemorrhage. Wound exploration is best performed under general anesthesia for detailed wound examination, débridement, and definitive wound repair. All acute abdominal gunshot wounds should be explored because of the high risk of peritonitis secondary to bowel penetration/perforation. All organs must be inspected closely for concomitant trauma.
CHRONIC TREATMENT Prolonged open wound management (serial débridement, multiple dressing applications, etc.) may be needed for contaminated or necrotic injuries. Peritonitis may require prolonged wound drainage (open abdomen, vacuum drain systems, sump drains), abdominal lavage, and possible reexploration (see p. 1250). Problematic soft-tissue wounds, including extensive skin loss, may require reconstructive surgery. With extensive orthopedic trauma (reparable), vacuum drains and lidocaine infusion catheters can be used for controlling dead space and reduce tissue pain. Lidocaine also may be temporarily infused using the tubing in a vacuum drain system (Jackson-Pratt drains).
POSSIBLE COMPLICATIONS The eyes are especially vulnerable to projectile wounds. Blindness and loss of the eye may result from extensive trauma. Paresis or paralysis may result from spinal cord trauma. Infection is a primary concern in gunshot wounds highlighted by extensive tissue destruction. Patients generally are at low risk for lead poisoning, except for lead in joints (should be removed). Delayed or nonhealing wounds
RECOMMENDED MONITORING
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Gunshot Wounds
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Vital signs in critical injuries
PROGNOSIS AND OUTCOME Determined by extent of injury and subsequent treatment Prompt stabilization of the patient and definitive medical/surgical intervention can improve the rate of survival and positive long-term outcome of the patient. Gunshot wounds to the brain, spinal cord, and abdomen normally carry a worse prognosis.
PEARLS & CONSIDERATIONS COMMENTS Due to potential legal ramifications of gunshot wounds, records must be detailed and accurate; all conversations should be detailed, complete, and noted in the medical record. Photographs of the injuries (entry, exit, tissue trauma inflicted) are useful evidence in court, along with supporting radiographs. A board-certified veterinary pathologist is best utilized to conduct detailed postmortem examination of deceased animals. It is critically important to transfer bullets and bullet fragments only to a qualified law enforcement officer, handling bullets gently (no metal forceps; wrap in tissue paper, and place in labeled, sealed container) should they be used as evidence in court.
SUGGESTED READINGS Pavletic MM: Atlas of small animal wound management and reconstructive surgery, Ames, Iowa, 2010, Wiley-Blackwell. AUTHOR: MICHAEL PAVLETIC EDITOR: RICHARD WALSHAW
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Grapes and Raisins Toxicosis
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Grapes and Raisins Toxicosis BASIC INFORMATION DEFINITION Acute renal failure (ARF) following ingestion of grapes (Vitis spp.) or raisins
EPIDEMIOLOGY SPECIES, AGE, SEX Documented in dogs only Anecdotally reported in cats, ferrets No known age or sex predisposition; all breeds susceptible Ingestion of grapes or raisins does not consistently cause acute renal failure in all dogs. RISK FACTORS Animals with preexisting kidney disease may be at increased risk of developing ARF. GEOGRAPHY AND SEASONALITY Intoxication can occur any time of the year.
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT Ingestion suspected or directly observed Evidence of grapes/raisins in vomitus or stool Most common signs are manifestations of acute renal failure: vomiting, lethargy, anorexia, diarrhea, decreased urine output, signs of abdominal pain, ataxia, and weakness Vomiting, lethargy, anorexia within 24 hours; vomiting is usually seen within 12 hours after ingestion. PHYSICAL EXAM FINDINGS Dehydration Signs of abdominal pain in some dogs Lethargy
ETIOLOGY AND PATHOPHYSIOLOGY Etiology unknown Renal tubular necrosis is a consistent histopathologic finding. Tubular basement membrane often remains intact, providing possibility for recovery. Evidence of tubular regeneration may be present in some dogs. Mineralization of kidneys, gastric mucosa, myocardium, lungs, and blood vessels
DIAGNOSIS DIAGNOSTIC OVERVIEW Diagnosis of grape or raisin toxicosis is suspected based on possibility or certainty of exposure, presence of grapes/raisins in the vomitus/stool, and if several hours have passed, possibly the onset of vomiting, anorexia, lethargy, diarrhea, decreased urine output, ataxia or weakness, or a combination of these. Azotemia and other serum chemistry changes consistent with ARF are seen in 1-3 days, but supportive treatment is warranted as soon as possible.
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Grapes and Raisins Toxicosis
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DIFFERENTIAL DIAGNOSIS Rule out other causes of ARF: Ethylene glycol toxicosis Leptospirosis Bacterial pyelonephritis Lily toxicosis in cats Iatrogenic/medication nephrotoxicosis (e.g., aminoglycoside antibiotics) Renal thromboembolism (usually accompanied by thromboembolism of other aortic branches)
INITIAL DATABASE Serum chemistry profile, CBC, calcium × phosphorus product (Ca × P): Azotemia, hyperphosphatemia, elevated Ca × P (>60 when both are measured in mg/dL) almost always present if enough time has passed and ingestion was substantial; hypercalcemia frequent Serum creatinine, phosphorus, and Ca × P can be elevated in less than 24 hours. Blood urea nitrogen and calcium may be slower to rise (1-3 days). Urinalysis before giving fluids: Urine specific gravity 10-12 grapes in an 8-kg dog) or raisins (>0.1 oz/kg [>3 g/kg]), treatment is justified to reduce the risk of permanent renal lesions. Treatment aims to decrease absorption (induction of vomiting and administration of activated charcoal) in early/mild ingestions when no clinical signs are apparent. When clinical signs are present, treatment consists of fluid diuresis, nutritional support, vomiting, seizure control, and management of acute renal failure (see p. 31) as needed.
ACUTE GENERAL TREATMENT Decontamination of patient: Emesis: useful 6-12 hours after exposure (see p. 1364) Activated charcoal (1-2 g/kg PO): useful up to 12-24 hours after exposure Fluid diuresis: Intravenous fluid diuresis for 48 hours in patients not yet showing clinical signs may prevent ARF. Treat signs of ARF as needed (see p. 31). Currently no unique treatment identified. If concurrent hypercalcemia, consider using 0.9% normal saline. Manage vomiting: Metoclopramide: 0.2-0.4 mg/kg q 6 h PO, SQ or IM or 1-2 mg/kg/d constant rate infusion (CRI); or Maropitant: 1 mg/kg SQ (or 2 mg/kg PO) q 24 h up to 5 consecutive days Treat anuria/oliguria: Correct dehydration first. Mannitol: 0.25-0.5 g/kg IV over 3-5 minutes or CRI of 2-5 mL/min of 5%-10% mannitol in lactated Ringer's solution Furosemide: 2-4 mg/kg IV up to 6 mg/kg if needed (if subnormal urine production persists) q 8 h; or combine 1 mg/kg/h furosemide (CRI or IV boluses) with dopamine CRI Dopamine: 2-5 mcg/kg/min IV CRI. Efficacy in ARF questioned, and may cause nausea Hemodialysis or peritoneal dialysis may be useful in some cases.
CHRONIC TREATMENT
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Grapes and Raisins Toxicosis
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Ongoing supportive care based on initial severity, response to treatments, individual's intrinsic ability to compensate, and extent of permanent renal injury
POSSIBLE COMPLICATIONS Uremia-related neurologic signs (seizures, ataxia) Metastatic mineralization (renal, cardiac, vascular, pulmonary) Pancreatitis
RECOMMENDED MONITORING Baseline blood urea nitrogen, creatinine, calcium, phosphorus, Ca × P, potassium, total protein, hematocrit, daily at first then as needed Urine output Signs of overhydration (respiratory character/effort, body weight) Acidosis
PROGNOSIS AND OUTCOME Of 43 dogs with grape/raisin toxicosis, 53% recovered with treatment, 12% died, and 35% were euthanized. Oliguria/anuria, ataxia, and weakness indicate poor prognosis. Higher serum [calcium] and Ca × P indicate poor prognosis.
PEARLS & CONSIDERATIONS COMMENTS Raisins at 0.1 oz/kg (3 g/kg) and grapes (10 to 12 grapes in an 8-kg dog) have led to ARF. Not all dogs that ingest raisins or grapes develop ARF. Raisins are 4.5 times more concentrated than grapes on an ounce-per-ounce basis. Treatment may be required for days to weeks.
PREVENTION Keep raisins and grapes out of dogs' reach.
TECHNICIAN TIPS Decontamination with induction of vomiting can be effective up to 6-12 hours after exposure, and administration of charcoal up to 24 hours after exposure. Oliguria is defined as 5000 mg/kg. NOEL (no observable effect level) for 1 year in dogs is 500/mg/kg/day. Clinical signs of toxicosis (hypersalivation, vomiting, and diarrhea) are more related to the surfactant in the formulation than the active-ingredient glyphosate.
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Glyphosate Herbicide Toxicosis
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Certain surfactants in the formulation are more toxic to fish and invertebrates; therefore, some formulations are not for aquatic applications. Structurally, glyphosate is classified as an organophosphate herbicide. However, this agent does not inhibit cholinesterase like organophosphate pesticides (see p. 792). Therefore, no cholinergic signs of toxicosis are seen in animals.
PREVENTION Keep pets out of the sprayed area until it has completely dried.
CLIENT EDUCATION Use products per label directions. Keep animals away from treated area until the product is dried on the plants. Store pesticides out of reach of pets.
SUGGESTED READING Farmer D: Inhibitors of aromatic acid biosynthesis. In Kreiger RI, editor: Handbook of pesticide toxicology agents, ed 2, San Diego, 2001, Academic Press, p 1667. Internet source: Integrated Risk Information System, US Environmental Protection Agency, retrieved March 30, 2009 from http://www.epa.gov/iris/subst/0057.htm http://www.epa.gov/EPA-PEST/1998/ October/Day-08/p26906.htm. AUTHOR: CAROLINE DONALDSON EDITOR: SAFDAR KHAN
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Gluten-Sensitive Enteropathy
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Gluten-Sensitive Enteropathy BASIC INFORMATION DEFINITION A chronic small-intestinal disease triggered in susceptible animals by the ingestion of gluten, a protein found in wheat
SYNONYMS Celiac disease (humans), gliadin enteropathy, gluten enteropathy, GSE, wheat-sensitive enteropathy
EPIDEMIOLOGY SPECIES, AGE, SEX Uncommon disorder in dogs Can potentially occur in cats but poorly documented Disease is first seen in young dogs (4-7 months old) after weaning. No gender predisposition described GENETICS & BREED PREDISPOSITION Irish setter, Samoyed, soft-coated Wheaten terrier (SCWT), but potentially any breed. In SCWT, gluten-sensitive enteropathy may be part of a spectrum of small-intestinal disease, as resolution of clinical signs does not occur with dietary restriction. RISK FACTORS Exposure to gluten-containing cereal grains after weaning Inflammatory small-bowel disease may lead to secondary gluten sensitivity. ASSOCIATED CONDITIONS & DISORDERS Humans with gluten-sensitive enteropathy may also suffer from gluten-sensitive skin disease (dermatitis herpetiformis) and are predisposed to alimentary lymphoma.
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES Chronic intermittent gastrointestinal signs (diarrhea is most common) Ill thrift but lack of overt gastrointestinal signs sometimes seen HISTORY, CHIEF COMPLAINT Chronic intermittent or persistent small-bowel diarrhea, with weight loss or failure to thrive. PHYSICAL EXAM FINDINGS Thin and/or stunted dog Poor body and coat condition
ETIOLOGY AND PATHOPHYSIOLOGY Gliadins are antigenic proteins that make up part of gluten, the main protein of wheat. Other proteins of flour from various grains have different degrees of crossreactivity: secalins (rye), hordeins (barley), and avenins (oats) are also implicated in gluten-sensitive enteropathy, whereas oryzenins (rice) and zeins (corn) do not exacerbate this disorder. These peptides cause intestinal damage, probably by an immune-mediated mechanism.
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Gluten-Sensitive Enteropathy
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An underlying defect in the intestinal mucosal barrier of Irish setters is reported and may predispose to this disease. This predisposition may be related to MHC gene expression. Serum antibody reactivity to gluten and serum immune complexes was not demonstrated in affected setters but has been seen in intestinal inflammation. The age of exposure to and dose of gluten may modulate expression of the disease.
DIAGNOSIS DIAGNOSTIC OVERVIEW Chronic gastrointestinal signs in dogs of susceptible breeds that fail to thrive are typical. Confirmation comes from resolution of clinical signs after withdrawal of gluten from the diet, followed by recurrence of signs with reintroduction of gluten.
DIFFERENTIAL DIAGNOSIS Other dietary sensitivities/hypersensitivities Idiopathic inflammatory bowel disease (IBD) Antibiotic-responsive diarrhea (small-intestinal bacterial overgrowth) Exocrine pancreatic insufficiency (EPI) Intestinal parasitism (e.g., giardiasis) Atypical hypoadrenocorticism Chronic intussusception Any cause of malabsorption (e.g., lymphangiectasia)
INITIAL DATABASE CBC, serum biochemistry profile, urinalysis: usually unremarkable Fecal parasite examination Normal trypsin-like immunoreactivity: rule out EPI Abdominal radiographs and ultrasound are typically unremarkable.
ADVANCED OR CONFIRMATORY TESTING Serum folate and cobalamin levels are variable; often normal, but decreased serum folate is the most common abnormality (see p. 220). Intestinal biopsy shows nonspecific changes of villous atrophy and intraepithelial lymphocyte infiltration, but similar changes are seen in other dietary sensitivities and idiopathic IBD. Serologic tests cannot reliably diagnose this condition, although reductions in fecal IgE excretion during a gluten-free diet trial have been reported in SCWT. Conclusive diagnosis: proof of gluten sensitivity depends on demonstration of resolution of signs and histologic changes on a gluten-free diet (typically 2-4 weeks) and relapse when challenged with gluten.
TREATMENT TREATMENT OVERVIEW All clinical signs should resolve when the patient is treated with a gluten-free diet. The therapeutic goal is complete resolution of clinical signs through elimination of gluten-containing grains (wheat, rye, barley, oats, buckwheat) from diet, treats, supplements, and chewable/flavored medications.
ACUTE GENERAL TREATMENT Feed a diet lacking wheat and other gluten-containing related cereals.
CHRONIC TREATMENT Evaluate for other causes of small-bowel diarrhea if response to dietary modification is suboptimal.
NUTRITION/DIET
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Gluten-Sensitive Enteropathy
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Feed a diet lacking wheat gluten and related cereals (cornerstone of diagnosis and treatment).
BEHAVIOR/EXERCISE No specific recommendations required
POSSIBLE COMPLICATIONS Potential for nutritional deficiencies with homemade diets (see p. 868)
RECOMMENDED MONITORING Centered on response to treatment (resolution of clinical signs) and physical exam (body weight, quality of coat, etc.)
PROGNOSIS AND OUTCOME Good to excellent in dogs that respond to strict gluten-free diet
PEARLS & CONSIDERATIONS COMMENTS This is predominantly a disease of young Irish setter dogs/puppies. Consider the development of gluten-sensitive enteropathy as a potential complication to underlying inflammatory small-bowel disease (IBD, protein-losing enteropathy). Gluten sensitivity has not been recorded in cats and is probably quite rare in dogs. Be aware that owner noncompliance may be a cause of treatment failure.
PREVENTION Selective breeding, as condition is probably familial Feeding a gluten-free diet will prevent disease.
CLIENT EDUCATION Awareness of gluten content of various foodstuffs Awareness of cross-reactivity to rye, barley, and possibly oats Monitor for recurrence of clinical signs Lifetime careful attention to diet may be required, although some affected dogs may develop tolerance over time.
SUGGESTED READING Hall EJ, German AJ: Diseases of the small intestine. In Ettinger SJ, Feldman EC, editors: Textbook of veterinary internal medicine, ed 7, St Louis, 2010, Elsevier, pp. 1526–1572. Vincenzetti, S, et al: Evidence of anti-gliadin and transglutaminase antibodies in sera of dogs affected by lymphoplasmacytic enteritis. Vet Res Commun 30:219, 2006. AUTHOR: EDWARD J. HALL EDITOR: DEBRA L. ZORAN
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Glomerulonephritis
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Glomerulonephritis BASIC INFORMATION DEFINITION Glomerulonephritis is a common disorder characterized by proteinuria due to immune complex deposition in the glomeruli and resultant inflammation. The condition is often idiopathic, but it can result from inflammatory, infectious, or neoplastic disease processes.
EPIDEMIOLOGY SPECIES, AGE, SEX Dogs affected more often than cats, with no gender predilection. While animals of any age may be affected, most are middle-aged or older at diagnosis. GENETICS & BREED PREDISPOSITION Membranoproliferative glomerulonephritis Bernese mountain dogs Labrador retrievers and golden retrievers with positive Borrelia titers RISK FACTORS Chronic bacterial infections (e.g., pyoderma, endocarditis, pyelonephritis, borreliosis, mycoplasmal polyarthritis) Fungal infection (e.g., coccidioidomycosis) Parasitic (e.g., heartworm disease) Rickettsial disease (e.g., ehrlichiosis) Protozoal infection (e.g., babesiosis, hepatozoonosis, leishmaniasis) Viral disease (e.g., feline immunodeficiency virus, feline leukemia virus, canine adenovirus) Neoplasia (e.g., mastocytosis, leukemia, lymphoma, systemic histiocytosis) Immune-mediated disease (e.g., polyarthritis, pemphigus, systemic lupus erythematosus) Chronic inflammatory disease (e.g., inflammatory bowel disease, pancreatitis, cholangiohepatitis, granulomatous meningoencephalitis, thyroiditis) Corticosteroid excess Trimethoprim-sulfa therapy Congenital C3 deficiency Genetic predisposition See p. 1391. CONTAGION & ZOONOSIS Some causes of secondary glomerulonephritis are zoonotic (e.g., leptospirosis, leishmaniasis). GEOGRAPHY AND SEASONALITY Several causes of secondary glomerulonephritis have specific geographic distributions (e.g., borreliosis in the northeastern and north central United States). ASSOCIATED CONDITIONS & DISORDERS Protein-losing nephropathy Nephrotic syndrome Chronic kidney disease Hypertension Hyperlipidemia
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Thromboembolic disease, including pulmonary thromboembolism Sideroblastic anemia
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES Morphologic classification: histopathologic (clinical correlates to therapy and prognosis not as well developed as in human nephrology) Membranoproliferative glomerulonephritis: most common Type I: mesangiocapillary glomerulonephritis associated with infectious disease; most common type Type II: dense deposit disease Proliferative glomerulonephritis: relatively rare HISTORY, CHIEF COMPLAINT Clinical signs may be absent. When signs are present, they may be due to uremia (see p. 207), nephrotic syndrome (see p. 762), or to the underlying disease responsible for glomerulonephritis: Vomiting (uremia or underlying disease) Lethargy (uremia or underlying disease) Anorexia (uremia or underlying disease) Weight loss (uremia, proteinuria, or underlying disease) Peripheral edema (hypoalbuminemia) Pendulous abdomen/ascites (hypoalbuminemia) Polyuria/polydipsia (chronic kidney disease) Halitosis (uremia) Dyspnea/panting (pulmonary thromboembolism events, ascites) Blindness (systemic hypertension) Signs associated with underlying infectious, inflammatory, or neoplastic disease PHYSICAL EXAM FINDINGS Clinical findings may be absent or may include: Poor body condition Dehydration Poor haircoat Signs associated with hypoalbuminemia: Peripheral edema Ascites (pure transudate) Pleural effusion (rare) Signs associated with uremia: Oral ulceration Halitosis (uremia) Pallor (either due to anemia [chronic disease, renal failure] or poor perfusion [severe illness]) Lipid corneal deposits Retinal hemorrhage/detachment (systemic hypertension) Kidneys may be normal sized or small. Other findings related to underlying disease
ETIOLOGY AND PATHOPHYSIOLOGY Immune complexes form or are trapped in the glomeruli. While it is often a primary process (idiopathic), there are many infectious, inflammatory, endocrine, or neoplastic conditions that can provide the antigen to which antibody is produced, resulting in secondary immune complex formation. Glomerular immune complexes initiate an inflammatory cascade. Inflammation directly damages the glomerulus, neutralizes glomerular endothelial electrical charge, and results in vasoconstriction and decreased glomerular filtration. The glomerulus responds to these insults with cellular proliferation. Albumin and similarly sized proteins are lost in the urine and may result in hypoalbuminemia and the nephrotic syndrome (see p. 762). Eventually, tubular function is lost as well, resulting in azotemia and uremia.
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Glomerulonephritis
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DIAGNOSIS DIAGNOSTIC OVERVIEW The diagnosis is suspected based on the identification of proteinuria, an elevated urine protein/creatinine ratio, and characteristic blood and imaging findings. Confirmation requires renal biopsy.
DIFFERENTIAL DIAGNOSIS Proteinuria: Preglomerular (e.g., Bence Jones proteinuria, exercise, hemolysis, fever, seizure) Glomerular Glomerulonephritis Amyloidosis Glomerulosclerosis, including chronic kidney disease Familial renal disease Postglomerular (e.g., urinary tract infection, neoplasia, urolithiasis)
INITIAL DATABASE Retinal exam: tortuous retinal vessels, retinal hemorrhages (acute or chronic), or retinal detachments are possible (a result of systemic hypertension). Blood pressure: systemic hypertension (repeatable systolic readings > 180 mm Hg in calm environment) is commonly noted. CBC: often unremarkable; nonregenerative anemia (due to chronic kidney disease), leukocytosis (if inflammatory disease is present) Serum biochemical profile: Hypoalbuminemia with normal globulin level Hypercholesterolemia Hypocalcemia (relative, owing to hypoalbuminemia) Azotemia, hyperphosphatemia, hyperamylasemia, metabolic acidosis (in advanced disease) Urinalysis: proteinuria, variable urine concentration, sometimes hematuria Proteinuria must be interpreted in light of urine concentration and urine sediment examination. Dipstick measure of proteinuria should be confirmed by sulfosalicylic acid test (SSA) method or quantitative measures (e.g., urine protein: creatinine ratio). Significant proteinuria may often precede loss of urine concentration or azotemia. Urine culture: indicated in all cases Thoracic radiographs: unremarkable. Evidence of underlying disease (neoplasia, chronic infectious or inflammatory disease) or pulmonary thromboembolism occasionally identified. Abdominal radiographs: often unremarkable. Kidneys may be small. May identify evidence of underlying disease (neoplasia, chronic infectious or inflammatory disease) or be unremarkable. Abdominal ultrasound: hyperechoic, small kidneys, decreased corticomedullary distinction, evidence of underlying disease (neoplasia, chronic infectious or inflammatory disease), or unremarkable.
ADVANCED OR CONFIRMATORY TESTING Urine protein/creatinine ratio: Concurrent culture and sensitivity must be negative to rule out bacterial infection as cause of elevated ratio. Normal for dogs, 30 mm Hg = glaucoma (dogs and cats).
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Glaucoma
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ADVANCED OR CONFIRMATORY TESTING Referral to veterinary ophthalmologist for: Additional or multiple tonometric measurements Gonioscopy (direct observation of the iridocorneal angle) Ophthalmoscopy of the ocular fundus (posterior segment of the eye including retina and optic nerve) Ocular ultrasound if ocular media are opaque and prevent evaluation of deeper ocular structures; helps rule out concurrent ocular abnormalities (i.e., lens luxation; lens capsule rupture; retinal detachment; intraocular masses)
TREATMENT TREATMENT OVERVIEW In acute cases, it is critical that the IOP be lowered as soon as possible to maintain or restore vision (topical and oral medications). If tonometry is unavailable, glaucoma suspects should be referred to a veterinary ophthalmologist (as an emergency) for IOP measurement. Early surgical intervention may permit better and longer control of IOP; the clinician is urged to consider early referral, especially when vision in one eye has already been lost. Long-term treatment of glaucoma can be a frustrating endeavor, since the disease tends to progress despite medical therapy, particularly with primary glaucoma. Diligent monitoring, regular reassessment of therapeutic success, and client education are critical. Therapeutic goals are to lower IOP of affected eye to maintain vision for as long as possible, eliminate ocular pain, and treat contralateral eye prophylactically with IOP-lowering drugs to delay onset of glaucoma from ~6 months (untreated) to 30 months (with prophylactic treatment) (primary glaucoma).
ACUTE GENERAL TREATMENT Medical: Regardless of the type of glaucoma, the following may be administered initially and then long term if indicated: Topical β-adrenergic antagonists or blockers (0.5% timolol or 0.5% betaxolol, usually q 8 h) and Topical or systemic carbonic anhydrase inhibitors (CAI; topical: 2% dorzolamide or 1% brinzolamide q 8 h; oral: methazolamide, 5 mg/kg q 12 h) Mannitol (1-2 g/kg IV over 20 minutes) to rapidly lower IOP (first effects in 1-2 hours; maximum effect in 4-6 hours; duration ∼8-10 hours) when there is a chance for return of vision (e.g., acute primary glaucoma) Topical (1% q 6 h) and/or systemic (1-2 mg/kg PO q 24 h) prednisolone is indicated when anterior uveitis is also present, unless an infectious cause for the uveitis is documented or strongly suspected (see p. 1151)
CHRONIC TREATMENT Medical: Topical prostaglandins (PGF analogs, 0.005% latanoprost, 0.03% bimatoprost, or 0.004% travoprost q 12-24 h): used for primary glaucoma in dogs; not effective in the feline glaucomas) ± Topical and/or systemic prednisolone (when anterior uveitis also present; taper to lowest effective dose) In all of the breed-related primary glaucomas, the disease continues to progress (even though IOP may be controlled), and often combinations of several topical and systemic IOP-lowering drugs or surgery (see below) are eventually necessary. Surgical: Anterior chamber shunts and laser cyclophotocoagulation are procedures offered by most veterinary ophthalmologists to prolong vision and prevent ocular pain. Laser cyclophotocoagulation may be performed with either a transscleral approach or with the assistance of a microendoscope. Removal of the lens (referable procedure; glaucoma secondary to lens luxation, see p. 644). This should be performed as soon as possible in cases of anterior lens displacement. End-stage blind and buphthalmic glaucomatous globes may be treated by: Enucleation Evisceration and intrascleral prosthesis Intravitreal gentamicin injection (dogs) Enucleation or evisceration and implant surgeries should be followed with histopathologic examination of the removed tissue to help determine cause of glaucoma (i.e., primary versus secondary) and prognosis for fellow eye.
DRUG INTERACTIONS Topical β-adrenergic blockers may lower heart rate and blood pressure and may cause bronchoconstriction in small-breed
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Glaucoma
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dogs and in cats. Systemic CAIs in dogs and cats may cause metabolic acidosis and electrolyte imbalances as evidenced by depression (perhaps related to hypokalemia), and in dogs, vomiting and diarrhea that require drug cessation. Topical CAI preparations are not associated with these side effects. Topical prostaglandins often cause conjunctival hyperemia within minutes after instillation that gradually declines over an hour or so, and miosis that persists with the IOP reduction. Mannitol, an osmotic diuretic, should be avoided in patients with heart disease (risk of fluid overload/iatrogenic pulmonary edema) or oliguric/anuric renal failure (rarely concurrent with acute glaucoma).
POSSIBLE COMPLICATIONS With poor or inadequate control of IOP, any or all of the following may occur: Buphthalmos (see Ocular Size Abnormalities, ) causing increased corneal exposure ± recurrent corneal ulceration/corneal vascularization/corneal pigmentation Lens luxation/subluxation Optic nerve and retinal degeneration Ocular, head pain Blindness
RECOMMENDED MONITORING Regular reexaminations with tonometry (e.g., monthly once IOP control initially achieved) are necessary to control IOP (should be maintained at 1.030; hemoconcentration/elevated packed cell volume) Electrolyte imbalances Hypochloremia occurs in 51% of cases and is the most common abnormality. Hypokalemia: 25% Hyponatremia: 20% (occurs more commonly with linear rather than discrete foreign bodies) Metabolic alkalosis with proximal obstruction; metabolic acidosis with hypoperfusion, sepsis secondary to peritonitis, or other systemic effects Abdominal radiographs: often the most informative test. Urgent consultation with a radiologist may be very helpful. Radiopaque foreign objects may be visualized. Fluid-or gas-distended intestinal loops Pathologic dilation of intestinal loops: bowel lumen should not exceed the diameter of twice the width of a rib or be greater than 1.6 times the height of the fifth lumbar vertebra. Radiographs that demonstrate a foreign body must be recent (minutes or hours before induction of general anesthesia, or better still, retaken just after induction) if surgery is planned. A gastric or duodenal foreign body can be displaced into the esophagus during anesthetic induction, while an intestinal foreign body may have been defecated since the original radiographs were taken.
ADVANCED OR CONFIRMATORY TESTING Contrast radiographs Barium sulfate suspension for upper GI study unless perforation suspected (see p. 1351) If perforation suspected, consider using nonionic iodinated contrast medium or other diagnostic techniques (centesis, lavage). Barium enema (see p. 1204) For assessing an obstructive pattern in the distal intestine For differentiating small bowel from large bowel if it is not clear whether a gas-filled viscus is a pathologically distended segment of small intestine or the normal colon Abdominocentesis (see p. 1194) and fluid analysis if perforation/peritonitis suspected Abdominal ultrasound Site of obstruction may be visualized. Identification of small amounts of free abdominal fluid Localization of free fluid for accurate centesis Diagnostic peritoneal lavage (see p.1250) If peritonitis is suspected but centesis is unrewarding Limited efficacy Thoracic radiographs in older animals with suspected neoplasia
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Gastrointestinal Obstruction: Foreign Body or Mass Lesion
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GASTROINTESTINAL OBSTRUCTION: FOREIGN BODY OR NEOPLASIA Radiographic appearance of the abdomen of a dog with small-intestinal obstruction, lateral view. A small-intestinal segment is markedly distended with gas (arrows), and another is markedly distended with fluid/soft tissue (arrowheads). (Courtesy Dr. Richard Walshaw.)
TREATMENT TREATMENT OVERVIEW Rehydration and rapid surgical intervention are recommended in any patient with intestinal obstruction. Correct dehydration and electrolyte abnormalities with intravenous fluid administration. Exploratory laparotomy is indicated to relieve the obstruction.
ACUTE GENERAL TREATMENT Exploratory laparotomy for foreign-body retrieval or mass resection An enterotomy may suffice for acute foreign body removal; if intestinal viability is questionable, resection and anastomosis are warranted. Wide margin (4-8 cm) resection and anastomosis should be performed if neoplastic disease is suspected based on the gross appearance of the lesion. In this case, also perform lymph node and liver biopsies. Omentum or serosal patch may be placed to reinforce suture line. Change gloves and surgical instruments before abdominal lavage and closure to minimize contamination. Administer prophylactic antibiotics. Cefazolin, 22 mg/kg IV q 2 h during the perioperative period Obtain gastric, small-intestinal, and liver biopsies, even if all appear grossly normal. Biopsy any abnormal-looking organ. Future course of illness may evolve in such a way as to make these specimens essential for diagnosis.
CHRONIC TREATMENT Postoperative considerations: Continue rehydration and daily electrolyte monitoring. Treat accordingly (especially hypokalemia arising from dilution [IV fluids] and anorexia). Nothing by mouth (NPO) 6-12 hours post enterotomy, 12 hours post resection and anastomosis Administer GI protectants as needed. Famotidine, 0.5-1 mg/kg IV, IM, SQ, or PO q 12-24 h; or Ranitidine, 0.5-2 mg/kg slow IV, IM, SQ, or PO q 8-12 h Ranitidine also has promotility properties similar to those of metoclopramide. Administer antiemetics as needed. Contraindicated before resolution of obstruction Metoclopramide, 0.2-0.4 mg/kg PO, SQ, or IM q 6 h; or Cisapride, 0.1-0.5 mg/kg PO q 8 h
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Gastrointestinal Obstruction: Foreign Body or Mass Lesion
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POSSIBLE COMPLICATIONS Dehiscence: animals should be monitored in hospital for 48-72 hours in the postoperative period for signs of peritonitis. Risk factors include presence of preoperative peritonitis, serum albumin concentration 16 weeks old). Metoclopramide (0.2-0.4 mg/kg SQ q 6-8 h) must be given frequently to manage vomiting or provided as a constant rate infusion. Gastric acid–reducing drugs may reduce the risk of esophagitis; are always appropriate if hematemesis is noted. Famotidine (0.5 mg/kg PO, IV, or SQ q 12-24 h) has a longer duration of effect than other drugs in this class. Protectants/adsorbents provide little clinical benefit and may be aspirated in vomiting animals. Products containing salicylate should be avoided in cats. Anticholinergics (e.g., aminopentamide) are not recommended; GI motility can be substantially compromised. Other side effects include dry mouth and tachycardia. Antibiotics are generally not indicated and may contribute to intestinal microbial disturbances and prolongation of diarrhea.
NUTRITION/DIET Food should be provided as soon as the patient is interested in eating. Easily digestible diets may be beneficial (e.g., boiled white rice with cottage cheese, boiled chicken, commercially available highly digestible enteric diets) because gastric emptying times are shorter, and fecal volume is minimized. Probiotics +/− prebiotics should be considered in patients with diarrhea, as disruption of the normal intestinal flora is both a likely cause and consequence of acute nonspecific gastroenteritis.
DRUG INTERACTIONS Maropitant is protein bound and may affect metabolism of other highly protein-bound drugs such as nonsteroidal antiinflammatories and anticonvulsants. Metoclopramide may increase absorption of drugs absorbed primarily in the small intestine; the adverse CNS effects of metoclopramide may be enhanced by concurrent use of sedatives (such as phenothiazines), tranquilizers, and narcotics.
RECOMMENDED MONITORING Hydration status Temperature, pulse, respiratory rate Volume of fluid losses
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Gastroenteritis: Acute, Nonspecific
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PROGNOSIS AND OUTCOME Prognosis is excellent; this disorder usually resolves within 48 hours of onset.
PEARLS & CONSIDERATIONS COMMENTS Animals with marked dehydration, hypovolemia, depression, or abdominal pain require a prompt and detailed diagnostic evaluation. Melena or substantial hematemesis are not consistent with a diagnosis of acute nonspecific gastroenteritis. Patients with these signs may require more investigation and aggressive management.
CLIENT EDUCATION This disorder should resolve within 48 hours. Further veterinary care should be sought if vomiting or diarrhea are persistent. Neonates, geriatric animals, and those with preexisting disorders are more prone to dehydration and may need more aggressive fluid support.
SUGGESTED READING Neiger R: Diseases of the stomach. In Steiner JM editor: Small animal gastroenterology. Hannover, 2008, Schlutersche, pp 155–161. AUTHOR: AUDREY K. COOK EDITOR: DEBRA L. ZORAN
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Gastrinoma
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Gastrinoma BASIC INFORMATION DEFINITION Uncommon malignant amine precursor uptake and decarboxylation (APUD) cell tumors that secrete excessive amount of gastrin, resulting in gastric acid hypersecretion
SYNONYM Zollinger-Ellison syndrome
EPIDEMIOLOGY SPECIES, AGE, SEX Dogs: average age 8.2 years (range 3.5-12 years). Cats: average age 10-12 years Female dogs and cats may be at a slightly higher risk than males. GENETICS & BREED PREDISPOSITION: No breed predisposition is known.
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT Associated with gastrointestinal ulceration: Chronic vomiting (most common) Anorexia or ravenous appetite Weight loss Depression Lethargy Diarrhea Polydipsia Obstipation Hematemesis Melena Pale mucous membranes Abdominal pain Associated with perforating ulcer and peritonitis: Collapse Acute abdomen (pain) Shock PHYSICAL EXAM FINDINGS Nonspecific findings: lethargy, depression, poor body condition Pale mucous membranes Melena on rectal exam or apparent on rectal thermometer Palpable abdominal mass reported in one cat May be unremarkable
ETIOLOGY AND PATHOPHYSIOLOGY APUD-cell tumors secrete excessive gastrin, resulting in hypersecretion of gastric acid by the stomach wall parietal cells. Gastric mucosal hypertrophy, gastrointestinal ulceration, esophagitis, and malassimilation secondary to enzyme inactivation and bile salt precipitation follow.
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Gastrinoma
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DIAGNOSIS DIAGNOSTIC OVERVIEW The diagnosis is suspected based on the presence of vomiting, anorexia, weight loss, and diarrhea or a combination of these, typically in a middle-aged to older dog/cat. Confirmation requires the presence of hypergastrinemia in fasted patients, in conjunction with histopathologic and immunohistochemical evaluation of excised pancreatic or duodenal neoplasms.
DIFFERENTIAL DIAGNOSIS Refractory gastritis/gastric ulcer disease Inflammatory bowel disease Gastrointestinal tract neoplasia Chronic pancreatitis Common bile duct obstruction
INITIAL DATABASE CBC: regenerative anemia due to gastrointestinal bleeding; neutrophilia associated with gastrointestinal ulceration. Serum chemistry panel and electrolytes: hypoalbuminemia and hypoproteinemia due to protein loss through gastroduodenal ulcerations. Chronic vomiting may result in hypokalemia, hyponatremia, and hypochloremia. Metabolic alkalosis, with or without aciduria, is consistent with a gastric outflow obstruction, which may be present in some cases. Metastasis to the liver may result in bilirubinemia and elevated liver enzymes. Abdominal radiographs: loss of abdominal detail if gastrointestinal perforation has occurred; otherwise, they are generally unremarkable. Contrast radiographs may reveal deep ulcers, prominent gastric rugae, or gastric outflow obstruction in some cases. Three-view thoracic radiographs: usually are within normal limits. Metastatic lesions usually occur late in the course of the disease. Abdominal ultrasound: thickened gastric wall or pylorus; evidence of metastatic disease to the liver or lymph nodes; diffuse increased echogenicity of the liver with severe gallbladder dilation and marked dilation of the cystic duct, common bile duct, and extrahepatic ducts.
ADVANCED OR CONFIRMATORY TESTING Endoscopy: esophagitis, gastric or duodenal ulceration, hypertrophy of gastric mucosa are evident on visual inspection. Histopathologic evaluation: rugae often appear normal, suggesting submucosal or muscular hypertrophy; duodenal villous blunting and ulceration is supportive of chronic hyperacidity but not diagnostic of gastrinoma. Basal gastric acid secretion: increased in more than 80% of human gastrinoma patients. Of the four reported dogs tested, all values were low. Basal serum gastrin concentration: best survey test in humans (increased in 98% of human gastrinoma patients). Correlates with dog and cat disease but can also be elevated in nonfasting sample, renal failure, gastric outflow obstruction, hypochlorhydria, pyloric stenosis, gastric dilatation and volvulus, atrophic gastritis, chronic gastritis, small intestine resection, hepatic disease, drug administration (H2 blockers, proton pump inhibitors, or glucocorticoids), immunoproliferative enteropathy of basenji dogs, and possibly Helicobacter spp. infection. Secretin stimulation test (2-4 U/kg IV, samples at 0.2, 5, 10, and 20 minutes postinjection): preferred provocative test for the diagnosis of gastrinoma in humans (gastrin levels greater than 200 pm/mL diagnostic in humans). Data regarding the procedure and its interpretation are limited in dogs and cats. Calcium stimulation test: data regarding the procedure and its interpretation are limited in dogs and cats (may be risky). 111
Iridium-octreotide or pentetreotide: somatostatin analogs bind to receptors expressed on gastrinomas and have facilitated localizing metastatic lesions in one dog. Histopathologic evaluation with immunohistochemistries or radioimmunoassay of extracts from the gastrinoma allow for a definitive diagnosis. Electron microscopy may also be used for detecting pancreatic Langerhans D cell intracytoplasmic secretory granules that are found in gastrinomas.
TREATMENT TREATMENT OVERVIEW Treatment mainly includes medical therapy to control clinical signs associated with gastric acid hypersecretion. Surgical reduction of
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Gastrinoma
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gastrinoma and metastatic lesions is palliative.
ACUTE GENERAL TREATMENT Intravenous fluids and electrolyte therapy to correct abnormalities associated with vomiting Control gastric hyperacidity: H2 receptor antagonists (cimetidine, 10 mg/kg IV, IM, SQ, or PO q 8 h; ranitidine, 0.5-2 mg/kg IM, SQ, PO [minimal efficacy in the dog; IV may cause vomiting] q 8-12 h; famotidine, 0.2-1 mg/kg IV, IM, SQ, or PO q 12-24 h; or nizatidine, 2.5-5 mg/kg PO q 24 h) H+ /K+ -ATPase (proton pump) inhibitors (omeprazole, 0.7-1 mg/kg PO q 12-24 h) Somatostatin analog (octreotide, 10-40 mg [per dog] q 8-12 h) Promote healing: Sucralfate, 0.25-1 g per dog PO q 6-12 h Misoprostol, 1-5 mcg/kg PO q 8 h Surgical and medical management for gastrointestinal ulceration/perforation
CHRONIC TREATMENT Acute treatment management, along with antiemetics Surgical debulking of the primary and metastatic lesions decreases clinical signs associated with gastrinomas. Chemotherapy, receptor-mediated radiotherapy, and long-acting somatostatin analogs (+/− alpha-interferon) yield mixed responses.
POSSIBLE COMPLICATIONS Gastrointestinal ulceration/perforation if hyperacidity is not controlled; common bile duct obstruction if due to a duodenal gastrinoma
RECOMMENDED MONITORING According to clinical signs
PROGNOSIS AND OUTCOME Poor due to high rate of metastasis Animals that are managed medically and surgically live 1 week to 18 months (mean, 4.8 months).
PEARLS & CONSIDERATIONS COMMENTS A palpable abdominal mass or one that is visualized either at ultrasound or at surgery is uncommon with gastrinoma.
CLIENT EDUCATION Monitor for recurrence of clinical signs. Rapid deterioration is possible if gastrointestinal perforation occurs.
SUGGESTED READING Hughes SM: Canine gastrinoma: a case study and literature review of therapeutic options. N Z Vet J 54(5):242, 2006. AUTHOR: M. RAQUEL BROWN EDITOR: DEBRA L. ZORAN
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Gastric Ulcer
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Gastric Ulcer BASIC INFORMATION DEFINITION Disruption of the gastric mucosa as a result of coagulative necrosis that breeches the muscularis layer and exposes the submucosa or deeper layers of the stomach wall
EPIDEMIOLOGY SPECIES, AGE, SEX: Dogs and cats; no age, sex, or breed predisposition RISK FACTORS Iatrogenic: administration of cyclooxygenase (COX) inhibitors, other nonsteroidal antiinflammatory drugs (NSAIDs), or corticosteroids Hypergastrinemia due to any number of causes Severe hypovolemia or ischemia (shock) leads to reduced gastrointestinal (GI) blood flow and increased risk of gastritis/ulcer.
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT Vomiting, hematemesis, melena are common complaints. Inappetence or anorexia and hyper-salivation are variably seen. Acute encephalopathic signs (e.g., stupor, seizures, or drooling in cats) may be observed in patients with concurrent severe liver disease. PHYSICAL EXAM FINDINGS Generally nonspecific Abdominal pain, either on palpation or manifested as a “praying” position, is possible. Pale mucous membranes and circulatory shock possible with severe bleeding or gastric perforation
ETIOLOGY AND PATHOPHYSIOLOGY Primary gastroduodenal diseases (e.g., toxins or foreign bodies, chronic gastritis, Helicobacter spp. infection, inflammatory bowel disease, neoplasia [mastocytosis, lymphoma, adenocarcinoma, or gastrinoma], pyloric outflow obstruction) Gastric hyperacidity disorders (e.g., gastrinomas, hypergastrinemia due to drugs) Drug-induced ulcers (e.g., COX inhibitors, other NSAIDs, corticosteroids) Other metabolic, endocrine, or systemic causes (e.g., pancreatitis, disseminated intravascular coagulation, hypoadrenocorticism, chronic kidney disease, liver failure, hypovolemic/septic shock, neurologic diseases, especially intervertebral disk disease or stress) The causes of ulceration are similar to those of gastritis and erosion, but for unknown reasons the reparative mechanisms of the mucosa are overwhelmed, resulting in deep indolent lesions. The process of ulcer healing starts as the necrotic mucosa sloughs and granulation tissue fills the ulcer. Mucus and bicarbonate are actively secreted by the neighboring mucosa to protect the ulcer. Granulation tissue eventually organizes, a connective-tissue bed develops, and epithelial tissues finally slide across the surface to reepithelialize it. Glandular structures are the last to repopulate the denuded area. Reduced gastric acid secretion facilitates this process, both by decreasing tissue damage from acid and by decreasing further damage from pepsin, which is less active at higher pH.
DIAGNOSIS DIAGNOSTIC OVERVIEW Gastric ulceration typically should be suspected in patients with any signs of GI disturbance that persist or worsen beyond the
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Gastric Ulcer
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degree expected for the primary diagnosis. A history of receiving ulcerogenic medications is suggestive but not essential. In many mild cases, clinical confirmation is only presumptive (response to antiulcer medications); a definitive clinical diagnosis requires endoscopy or laparotomy, particularly if severe/associated with gastric perforation and peritonitis.
DIFFERENTIAL DIAGNOSIS Acute vomiting: Dietary indiscretion Parasites Helicobacter gastritis Foreign bodies Pancreatitis Other acute metabolic conditions (renal failure, hypercalcemia, etc.) Hematemesis: Coagulopathies or lack of platelets (number or function) Ingested blood (nasopharyngeal, oral, esophageal, or pulmonary bleeding) Hemorrhagic gastroenteritis (all causes of severe gastrointestinal erosion) Melena: All causes of hematemesis ○ Intestinal neoplasia Intestinal parasites (hookworm) Intestinal ischemia Inflammatory bowel disease or other infiltrative enteropathies Abdominal pain: Hepatitis Splenomegaly/splenic rupture/torsion Intestinal obstruction Acute renal failure Intussusception/mesenteric torsion Peritonitis Pancreatitis
INITIAL DATABASE Rectal examination should be performed to assess presence of melena. CBC, serum biochemistry profile, urinalysis: important to identify underlying cause of gastric ulceration, and are especially needed if hematemesis or melena is present. CBC may show anemia (variably regenerative if acute, depending on the time between onset of bleeding and time of testing; nonregenerative in the presence of underlying chronic disease; and microcytic, hypochromic, and regenerative [dogs] if associated with iron deficiency from chronic blood loss), neutrophilia (± left shift if associated with perforation), hypoproteinemia, or mild thrombocytopenia (rarely less than 75,000/µL). Serum biochemistry profile may show an elevated blood urea nitrogen (BUN)/creatinine ratio or identify conditions associated with ulcers (renal failure, etc.). Not all cases will demonstrate an elevated BUN, however. Urinalysis: essential for differentiating BUN elevation due to kidney disease (urine specific gravity 1.008-1.020) from BUN elevation due to prerenal causes (urine specific gravity > 1.035) Fecal occult blood test has limited utility. O-tolidine-based tests are significantly more specific (0/108 false-positive results in healthy dogs) than guaiac-based tests (64/108 false-positive results in same dogs). Imaging studies: Plain radiographs cannot confirm gastric ulceration. However, if perforation has occurred, loss of detail (suggesting peritonitis or free abdominal fluid) or free peritoneal gas may be present. Contrast radiographs may identify a mucosal filling defect. Ultrasonography may show local gastric wall thickening, loss of normal layering, the presence of a wall defect or “crater,” fluid accumulation in the stomach, and diminished gastric motility. In animals with perforation due to the ulcer, there may be evidence of free fluid in the abdomen.
ADVANCED OR CONFIRMATORY TESTING Serum gastrin levels may help diagnose gastrinoma (see p. 442), but the animal must not have been on histamine-2 receptor blockers or proton pump inhibitors before testing. If a gastrointestinal perforation is suspected, abdominocentesis (see p. 1194) is indicated. If free fluid can be obtained during the ultrasound examination, that is often sufficient. However, a diagnostic peritoneal lavage may be needed to obtain samples if the perforation is relatively recent and the fluid accumulation is minimal. Gastroscopy: preferred for confirmation of gastric ulcer and tissue sampling; however, if a perforation is suspected, endoscopic examination is contraindicated, as it will increase abdominal contamination.
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Gastric Ulcer
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A solitary ulcer in an otherwise normal stomach should raise the suspicion of gastric neoplasia, especially if the edges and surrounding mucosa are thickened. NSAID-induced ulcers can be solitary, but the surrounding mucosa is usually not normal, owing to generalized mucosal disease (gastritis and other erosions are common). Multiple diffuse small ulcers can be seen with NSAIDs, uremia, liver disease, mastocytosis, gastrinoma, and possibly Helicobacter gastritis. Biopsies should be obtained from the ulcer periphery to avoid perforation. Repeated biopsies from the same site may improve the likelihood of identifying neoplasia. However, in some cases, endoscopic biopsies will be inadequate for diagnosis (neoplastic tissue is deeper than superficial mucosal tissues sampled with endoscopic biopsies), and laparotomy is required for full-thickness biopsies.
TREATMENT TREATMENT OVERVIEW Remove primary cause Promote healing Stabilization of patient with circulatory collapse from massive bleed or perforation
ACUTE GENERAL TREATMENT Supportive care: Intravenous fluids, antibiotics, antiemetics, and opioid analgesics may be required for the patient with severe vomiting that has resulted in dehydration and electrolyte disturbances. Blood transfusion for the patient with severe anemia as a result of massive bleeding Surgery: Surgical resection is indicated when the ulcer appears deeply penetrating (volcano crater appearance), is bleeding continuously, has perforated, or is very large and fails to heal. Surgical exploration may identify the etiology (neoplasia) and allow resection of the mass/ulcer. Medical: H2 blockers. Options include: Famotidine: 0.5-1 mg/kg PO, IV, or SQ q 12-24 h Ranitidine: 1-4 mg/kg PO, IV, or SQ q 8-12 h Cimetidine: 5-10 mg/kg PO, IV, or SQ q 6-8 h Proton pump inhibitor: reduces gastric acid by >90% (not for use in cats). Options include: Omeprazole: 0.7 mg/kg PO q 24 h (alternately 20 mg/dog) Esomeprazole (Nexium): 1 mg/kg PO q 24 h Lansoprazole (Prevacid): 1 mg/kg IV q 24 h Prostaglandin E2-inhibitor: drug of choice for prevention/treatment of NSAID-induced ulcers; not for use in cats or pregnant females: Misoprostol: 3-5 mcg/kg PO q 8 h Sucralfate: mucosal protectant. As oral suspension, or dissolved in 6-10 mL tap water if tablet; is most effective if administered in an acidic environment (give 1-2 hours before acid-blocking drugs): Dogs: 0.5-1 g PO q 8 h Cats: 0.25 g PO q 8 h Antiemetics: use as needed to control emesis: Metoclopramide: 0.2-0.4 mg/kg PO or SQ q 8 h Dolasetron: 0.3 mg/kg IV q 12-24 h
CHRONIC TREATMENT Misoprostol is indicated for preventing ulcers in dogs that need to be on NSAIDs (e.g., arthritis) but are prone to developing ulcers.
DRUG INTERACTIONS Cimetidine and ranitidine inhibit a subset of the cytochrome P450 enzyme systems and may delay metabolism of some drugs. The dose of ranitidine must be altered (reduced) in dogs with kidney disease.
POSSIBLE COMPLICATIONS The most important complications of gastric ulceration are blood-loss anemia (can be severe, requiring transfusions) and perforation, resulting in septic peritonitis and shock.
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RECOMMENDED MONITORING In dogs or cats with acute hematemesis, the packed cell volume/total protein must be monitored to determine if a blood transfusion or surgical intervention is needed.
PROGNOSIS AND OUTCOME The prognosis for most gastric ulcers is good unless the underlying etiology is not identified or cannot be corrected.
PEARLS & CONSIDERATIONS COMMENTS Careful endoscopic evaluation of the lesser curvature of the stomach is critical for identification of gastric adenocarcinoma. Patients with GI bleeding often have BUN elevations with normal creatinine, concentrated urine, and normal renal function. The combination of an H2 blocker with sucralfate is frequently used in the belief that healing is improved with the combination. A study in people comparing ranitidine to ranitidine-sucralfate showed no benefit from using the combination. Proton pump inhibitors (e.g., omeprazole) are the only effective means of completely reducing acid secretion. H2 blockers are much less potent, and of the group, only famotidine has been shown in dogs to adequately decrease gastric acid levels.
PREVENTION Careful administration of NSAIDs, or use of NSAIDs with COX-2 selective properties, to minimize the risk of ulceration
CLIENT EDUCATION Advise clients of the dangers of consistent NSAID use, and provide them with signs to watch for that may indicate gastritis or ulcer formation. Advise clients about the potential dangers of over-the-counter NSAIDs in dogs and cats, as some of the most potent ulcerogenic drugs in dogs are ibuprofen, regular aspirin, and naproxen. Advise clients about the risk of potentially life-threatening complications from any over-the-counter NSAID given to cats.
SUGGESTED READING Cariou M, Lipscomb VJ, Brockman DJ, et al: Spontaneous gastroduodenal perforations in dogs: a retrospective study of 15 cases. Vet Rec 165(15):436–441, 2009. Cariou MP, Halfacree ZJ, Lee KC, et al: Successful surgical management of spontaneous gastric perforations in three cats. J Feline Med Surg 12(1):36–41, 2010. AUTHOR: KENNETH R. HARKIN EDITOR: DEBRA L. ZORAN
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Gastric Parasites
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Gastric Parasites BASIC INFORMATION DEFINITION Nematode parasites of the stomach affecting dogs and cats
EPIDEMIOLOGY SPECIES, AGE, SEX:Physaloptera spp. infect dogs and cats. Ollulanus tricuspis is found exclusively in the cat. There is no age or sex predisposition. RISK FACTORS Dogs and cats that habitually ingest the intermediate host (crickets, beetles, cockroaches) or transport hosts (e.g., rodents and snakes) for Physaloptera spp. are at greater risk of infection. Multicat households are a risk factor for Ollulanus spp. infection. CONTAGION & ZOONOSIS: These are not zoonotic diseases. Ollulanus spp. is spread from cat to cat in the vomitus. GEOGRAPHY AND SEASONALITY: Worldwide
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT: Chronic vomiting is the chief complaint for both parasitic infections. A good appetite is usually retained, and weight loss is usually insignificant, particularly for Physaloptera spp. infections. Cats with Ollulanus spp. infection may have chronic weight loss. The duration of signs may be from a few days to many months. PHYSICAL EXAM FINDINGS: Typically there are no significant abnormal findings on physical examination. Emaciation may be present.
ETIOLOGY AND PATHOPHYSIOLOGY Physaloptera spp., most commonly P. rara. They range in length from 1 to 6 cm, although most are 1 to 2 cm. Subclinical infections are believed to occur in many animals, but chronic vomiting due to gastritis or penetration of parasite into the gastric wall is the typical pathophysiologic presentation. Intermediate hosts: beetles and crickets O. tricuspis. Size range is 0.7-1 mm long. Presence of Ollulanus may induce gastric irritation and inflammation or in severe cases, a chronic fibrosing gastritis; however, infections with the parasite can also be inapparent. Life cycle is direct: infection from eating vomitus containing larvae.
DIAGNOSIS DIAGNOSTIC OVERVIEW Affected individuals are identified by a chief complaint of vomiting that resolves with anthelmintic treatment (presumptive diagnosis based on response to treatment); alternatively, confirmation may come from demonstration of the parasites (endoscopic or microscopic).
DIFFERENTIAL DIAGNOSIS Dietary indiscretion Food intolerance or hypersensitivity/allergy Gastric foreign body Helicobacter gastritis Drugs or toxins (nonsteroidal antiinflammatory drugs, antibiotics, plants, lead)
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Idiopathic gastritis (lymphoplasmacytic, eosinophilic) Pyloric antral hypertrophy Pythiosis
INITIAL DATABASE CBC, serum biochemistry profile, and urinalysis are usually normal, although a rare dog or cat may have peripheral eosinophilia. Fecal flotation is usually negative. On rare occasions, the translucent eggs of Physaloptera spp. may be identified. Abdominal radiographs are normal. Abdominal ultrasound is normal. Microscopic examination of the vomitus may yield the presence of Ollulanus spp.
ADVANCED OR CONFIRMATORY TESTING In many cases of unconfirmed Physaloptera- or Ollulanus-associated gastritis, empirical anthelminthic treatment is highly effective, and advanced testing may be unnecessary. Gastroscopy is the only method to reliably identify the presence of Physaloptera spp. in the stomach. Ollulanus spp. can be identified from microscopic examination of vomitus, squash preps, or touch preps of gastric mucosal biopsies (endoscopy or surgery), or on histologic evaluation of the biopsies (less reliable).
TREATMENT TREATMENT OVERVIEW Removal of the parasite rapidly resolves vomiting.
ACUTE GENERAL TREATMENT Mechanical removal of Physaloptera spp. resolves clinical signs. Anthelminthics for Physaloptera spp.: Pyrantel: 5 mg/kg PO (dog), 20 mg/kg PO (cat). Using a higher dose in dogs (10-15 mg/kg) and repeating in 2-3 weeks may yield a higher response rate. Fenbendazole: 50 mg/kg/d PO for 3 days is reportedly effective (dog, cat). This author uses 75 mg/kg/d PO for 5 days in dogs. Ivermectin: may be effective at 0.2 mg/kg PO (dog, cat). Not for use in ivermectin-sensitive breeds. Anthelminthics for O. tricuspis: Fenbendazole: 50 mg/kg/d PO for 3 days Pyrantel: 20 mg/kg PO, repeat in 2-3 weeks
POSSIBLE COMPLICATIONS Fenbendazole is not labeled for use in cats and may be associated with idiosyncratic hepatotoxicosis with high doses or prolonged use.
PROGNOSIS AND OUTCOME The prognosis for complete resolution of chronic vomiting is excellent. Reinfection with Physaloptera spp. is likely in most cases, as repeated ingestion of intermediate and transport hosts occurs. Treatment of all cats in a household for O. tricuspis should eliminate the parasite.
PEARLS & CONSIDERATIONS COMMENTS At gastroscopy, the presence of small erosions or pinpoint hemorrhages on the gastric mucosa should prompt a careful inspection for Physaloptera spp. The elusive nature of the parasites, minimal severity of clinical signs, and expense of endoscopy all warrant a therapeutic trial
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Gastric Parasites
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with an anthelminthic before advanced diagnostic testing. Gastric parasites may still be found after a failed therapeutic trial.
PREVENTION Block access to intermediate hosts or transport hosts. Administration of a monthly heartworm preventive that contains pyrantel may be beneficial in management of dogs with continued access to intermediate or transport hosts.
SUGGESTED READING Guilford WG, Strombeck DR: Chronic gastric diseases: parasitic gastritis. In Guilford WG, et al, editors: Strombeck’s small animal gas-troenterology, ed 3, Philadelphia, 1996, WB Saunders, pp 285–286. Theisen SK, et al: Physaloptera infection in 18 dogs with intermittent vomiting. J Am Anim Hosp Assoc 34:74–78, 1998. AUTHOR: KENNETH R. HARKIN EDITOR: DEBRA L. ZORAN
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Gastric Neoplasia
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Gastric Neoplasia BASIC INFORMATION DEFINITION Benign or malignant tumors of epithelial, lymphoid, or mesenchymal origin. These tumors affect gastric function, are often painful, and may cause secondary systemic effects such as electrolyte disturbances, anemia, and weight loss.
SYNONYMS Gastric adenocarcinoma, gastric adenoma, gastric polyps (benign), gastric carcinoma, gastric extramedullary plasmacytoma, gastric lymphoma (see p. 678), gastrointestinal stromal tumor (GIST), leiomyoma, leiomyosarcoma, scirrhous carcinoma of the stomach.
EPIDEMIOLOGY SPECIES, AGE, SEX In dogs, gastric tumors account for 7 years old. GENETICS & BREED PREDISPOSITION Gastric adenocarcinomas: rough collies, Staffordshire terriers, Belgian shepherds, and chow chows (may be familial) Leiomyoma and GIST: German shepherds RISK FACTORS Gastric adenocarcinomas: Chronic nitrosamine exposure experimentally Association of gastric carcinoma and lymphoma with chronic inflammation from Helicobacter pylori infection in people; unproven in companion animals CONTAGION & ZOONOSIS Helicobacter spp. organisms may be frequently found in normal dogs and cats, but significance is undetermined. Zoonotic potential exists for H. pylori, but the prevalence of infection in animals is low. ASSOCIATED CONDITIONS & DISORDERS: Gastric lymphoma in cats is generally not associated with retroviral infection (feline leukemia virus, feline immunodeficiency virus).
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT Chronic vomiting Hematemesis/melena Anorexia, weight loss Depression and lethargy, pain or restlessness PHYSICAL EXAM FINDINGS May include some or all of the following: Physical exam may be normal Poor body condition score (e.g., body condition score 1/9-2/9)
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Gastric Neoplasia
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Pale mucous membranes, signs of anemia Abdominal mass Abdominal pain
ETIOLOGY AND PATHOPHYSIOLOGY Chronic vomiting may result in weight loss, electrolyte imbalance. Anemia secondary to chronic gastrointestinal (GI) bleeding may be hypochromic, microcytic due to iron depletion. Panhypoproteinemia due to GI blood loss Hypoglycemia may occur secondary to insulin-like growth factor II release from smooth muscle tumors. GISTs are associated with activating mutation of the c-kit receptor tyrosine kinase oncogene.
DIAGNOSIS DIAGNOSTIC OVERVIEW The diagnosis is typically reached when nonspecific signs of gastrointestinal disturbance fail to respond to conservative management and/or are accompanied by systemic disturbances (e.g., weight loss). Radiographs and ultrasound may help to localize the lesion; confirmation requires a biopsy.
DIFFERENTIAL DIAGNOSIS Any gastrointestinal or systemic cause of chronic vomiting may mimic gastric neoplasia: Gastric foreign body Gastric ulceration Granulomatous gastritis Chronic pancreatitis Systemic disease associated with chronic vomiting (renal, hepatic, diabetic ketoacidosis)
INITIAL DATABASE CBC, serum chemistry panel with electrolytes, urinalysis: frequently normal or changes are nonspecific and secondary to GI electrolyte or blood losses (nonregenerative anemia, increased blood urea nitrogen, normal creatinine, normal urine specific gravity). Three-view thoracic staging radiographs (metastasis) Abdominal ultrasound evaluation: to assess gastric wall changes often not seen on routine radiographs and to rule out other causes of vomiting (pancreatitis, liver disease, etc.) Positive contrast gastrogram: assessment for outflow obstruction; does not differentiate neoplasia from other infiltrative diseases such as pythiosis Ultrasound-guided fine-needle aspiration cytology: if a gastric wall abnormality or lymphadenopathy is present. Lymphoma exfoliates most readily; GIST or gastric muscle tumors do not. Endoscopic biopsy: histopathologic diagnosis is essential for treatment and prognosis. Endoscopy rapidly and effectively provides mucosal tissue specimens, but if the tumor is in the gastric muscular or serosal layers, results may be inadequate, requiring surgical biopsy. Surgical biopsy: exploratory surgery provides opportunity for both diagnosis and treatment (surgical removal of the affected region).
ADVANCED OR CONFIRMATORY TESTING Diagnosis is confirmed by biopsy with histopathology: Immunohistochemical stains for c-kit in GIST Cytokeratin, vimentin immunohistochemistry for undifferentiated tumors Immunophenotyping for lymphoma
TREATMENT TREATMENT OVERVIEW
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Benign gastric lesions may be cured surgically, as can early-diagnosed low-grade malignancy. Other surgical goals might be to relieve gastric obstruction or remove tumors that are painful or bleeding for palliation. Chemotherapy is potentially helpful in prolonging survival, although malignant gastric tumors are typically incurable.
ACUTE GENERAL TREATMENT Antiemetics (maropitant, 1 mg/kg PO, SQ; or dolasetron, 0.3 mg/kg q 12-24 h IV, SQ; or metoclopramide, 0.2-0.4 mg/kg q 8 h, PO, or IV if no obstruction present), gastroprotectants (famotidine, 0.5 mg/kg IV, PO q 12 h). Rehydration with intravenous fluids Antibiotics for Helicobacter infection if indicated Blood transfusion and hematinic therapy as indicated for nonregenerative iron-deficiency anemia Analgesic management as indicated by clinical signs Diet modification to easily digested, high-energy content food Parenteral alimentation as indicated (if the patient has not eaten for > 3 days or will not be able or willing to eat after surgery)
CHRONIC TREATMENT Gastric tumor resection often results in motility disorders. May require motility modifiers (metoclopramide, 0.2-0.4 mg/kg IV, PO q 8 h; or cisapride, 0.25 mg/kg q 24 h PO) Chronic antiemetic therapy may be required. Chemotherapy with doxorubicin, platinum agents, or antimetabolites may prove helpful. Systemic chemotherapy for gastric lymphoma provides remission and prolonged survival (see p. 678).
POSSIBLE COMPLICATIONS Surgical wound dehiscence with secondary peritonitis, pneumoperitoneum Chemotherapy-induced leukopenia might predispose to infection. Chemotherapy-induced thrombocytopenia might increase gastric hemorrhage. Chemotherapy might result in gastric perforation of transmural lesions.
RECOMMENDED MONITORING Postoperative follow-up with chest radiographs and abdominal ultrasound for signs of recurrence or metastasis on a 1-to 2-month basis for 1 year Monitor CBC for recovery from nonregenerative anemia. Monitor for signs of dissemination of alimentary lymphoma.
PROGNOSIS AND OUTCOME Favorable for benign lesions (adenomas, leiomyomas), although complete resection of mesenchymal tumors is unlikely Poor for adenocarcinoma, carcinoma, GIST, especially when metastatic: These dogs generally do not live beyond 6 months even with therapy. Guarded to fair for focal mass presentation of lymphoma Guarded for diffuse or multicentric alimentary lymphoma, as these lesions typically regress slowly and may have an indolent course but are ultimately incurable
PEARLS & CONSIDERATIONS COMMENTS Gastric carcinoma is associated with early lymphatic spread. Lymph nodes detected on ultrasound can be used for diagnosis and prognosis. Gastric carcinomas may overexpress cyclooxygenase-2; nonsteroidal antiinflammatory drugs (piroxicam, 0.3 mg/kg PO q 24 h) may be palliative. Scirrhous carcinoma is rapidly fatal.
SUGGESTED READING Frost D, Lasota J, Miettinen M: Gastrointestinal stromal tumors and leiomyomas in the dog: a histopathologic, immunohistochemical
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and molecular genetic study of 50 cases. Vet Pathol 40:42, 2003. AUTHOR: BARBARA E. KITCHELL EDITOR: DEBRA L. ZORAN
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Gastric Dilatation/Volvulus
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Gastric Dilatation/Volvulus BASIC INFORMATION DEFINITION Rotation of the stomach on its mesenteric axis associated with gastric distention, well recognized in large-and giant-breed dogs
SYNONYMS Bloat, gastric torsion, GDV
EPIDEMIOLOGY SPECIES, AGE, SEX: Older dogs (>7 years) are at greatest risk; rarely reported in cats. GENETICS & BREED PREDISPOSITION Large-and giant-breed dogs Purebred dogs at greater risk than mixed breeds Having a first-degree relative with gastric dilatation/volvulus (GDV) is associated with an increased risk. The most commonly affected breeds are the Great Dane, weimaraner, Saint Bernard, Gordon setter, Irish setter, Doberman pinscher, Old English sheepdog, and standard poodle. Bassett hound is at greatest risk among smaller breeds. RISK FACTORS Increased risk may be associated with: Narrow and deep thoracic cavity Long hepatogastric ligament Stress Fearful temperament Being underweight Nutritional risk factors including once-daily feeding, rapid ingestion of food, exercise after eating, consumption of large volumes of food or water, eating from a raised feeding bowl, and feeding dry dog food with oil or fat listed as one of the first four ingredients GEOGRAPHY AND SEASONALITY: Possible increased incidence in the months of November, December, and January (United States) ASSOCIATED CONDITIONS & DISORDERS Inflammatory bowel disease Previous splenectomy for splenic torsion or mass
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT Abdominal distension Abdominal pain Ptyalism Retching or vomiting (may be nonproductive) Acute collapse PHYSICAL EXAM FINDINGS Abdominal distension and tympany: Simultaneous auscultation and percussion of the abdomen may reveal a tympanic sound, indicating the presence of a
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taut, gas-filled viscus (stomach). Splenomegaly Clinical signs of hypovolemic shock: weak pulses, tachycardia, pale mucous membranes, prolonged capillary refill time, dyspnea
ETIOLOGY AND PATHOPHYSIOLOGY In most cases, the pylorus moves ventrally and from right to left; the rotation may be 90○-360○. Gastric dilation occurs secondary to failure of eructation and pyloric outflow obstruction. This occurs before or after gastric rotation. The distended stomach results in caudal vena cava and portal vein compression, causing decreased venous return to the heart. Decreased venous return results in decreased cardiac output, decreased arterial blood pressure, and myocardial ischemia. Myocardial ischemia causes cardiac arrhythmias. In the case of volvulus, increased intraluminal gastric pressure, portal hypertension, and avulsion of the short gastric vessels compromise blood flow to the gastric wall. Gastric necrosis and perforation can result. Portal vein compression/hypertension causes sequestration of splanchnic blood and decreased ability to clear gram-negative endotoxins. Endotoxemia further potentiates hypotension and decreased cardiac output. Pressure on the diaphragm, decreased lung perfusion, and decreased lung compliance cause respiratory dysfunction and exacerbate tissue hypoxia.
GASTRIC DILATATION/VOLVULUS Lateral abdominal radiograph of a dog with gastric dilatation/volvulus. Characteristic septation (arrows) of the gastric shadow is seen; displaced, gas-filled antrum is cranial to the arrows (to the left on this image), whereas gas-filled fundus is caudal (arrows are within it). A gas-filled esophagus and evidence of ileus in the form of distended, gas-filled small intestine are also present. (Courtesy Dr. Richard Walshaw.)
DIAGNOSIS DIAGNOSTIC OVERVIEW GDV should be suspected in large-or giant-breed dogs presenting with an acute history of a distended or painful abdomen, often with preceding or concurrent attempts at vomiting. Physical examination usually reveals a tympanic abdomen and often signs of shock. The diagnosis is confirmed with radiography, but treatment for shock is initiated beforehand based on clinical suspicion alone.
DIFFERENTIAL DIAGNOSIS
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Gastric Dilatation/Volvulus
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Gastric bloat associated with overeating Mesenteric volvulus Splenic torsion Diaphragmatic hernia with stomach herniation
INITIAL DATABASE Abdominal radiographs: Right lateral view is preferred. Shows gas-filled pylorus cranial and dorsal to the fundus (“popeye sign,” “C sign,” or “double bubble”) Free abdominal air suggests gastric perforation. Quick assessment tests: Packed cell volume/total solids (PCV/TS): often increased due to hypovolemia Serum electrolyte and glucose concentrations: hypokalemia and hypoglycemia may be seen. Acid-base analysis: metabolic acidosis due to lactic acidosis frequently seen Coagulation panel and platelet count: thrombocytopenia, increased prothrombin time/activated partial thromboplastin time/fibrinogen concentration and/or fibrin degradation product concentration associated with disseminated intravascular coagulation Electrocardiogram (ECG): ventricular arrhythmias are common
ADVANCED OR CONFIRMATORY TESTING Diagnosis confirmed at surgery Measurement of lactic acid concentration prior to surgery may assist in determining prognosis Lactic acid (lactate) concentration >6.0 mmol/L associated with gastric necrosis and increased mortality
TREATMENT TREATMENT OVERVIEW The initial therapeutic goal is to manage hypovolemia with intravenous (IV) fluids and to decompress the stomach to reestablish systemic and gastric mural perfusion. Definitive treatment involves surgery to correct the position of the stomach, remove devitalized tissue, and perform a gastropexy to prevent recurrence.
ACUTE GENERAL TREATMENT Place large-bore IV catheters in both cephalic veins and infuse isotonic crystalloids at a rate of 90 mL/kg/h. Colloids can be administered in combination with crystalloids at 5-20 mL/kg over 15-30 minutes. For severe shock, hypertonic saline can be administered at 4 mL/kg over 5 minutes followed by crystalloids. Prophylactic antibiotic therapy Decompress the stomach by orogastric intubation (see p. 1281). If orogastric intubation is not possible and patient has visible abdominal distension with a radiographically confirmed GDV, perform percutaneous trocarization of the stomach: Aseptically clip and prepare an area at least 4 × 4 in. (10 × 10 cm) on the left lateral or dorsolateral abdomen, just caudal to the last rib and over the region of most obvious distension. Identify a point that is within the prepared area and ventral to the hypaxial muscles and caudal to the last rib. Using a large-bore needle or needlestyleted catheter (e.g., 16 or 14 G) directed ventrally and slightly cranially, penetrate all layers of the body wall and stomach. When successful, the procedure should produce a hissing sound associated with a release of fetid-smelling gas through the needle. Immediate surgery to return stomach to a normal position: Placing traction on the pylorus and elevating it while putting downward pressure on the fundus will aid derotation in a counterclockwise direction (most but not all cases will have rotated clockwise). Evaluate stomach and spleen for irreversible vascular compromise and necrosis. Perform partial or complete splenectomy if splenic necrosis, infarction, or torsion. Perform resection or invagination of necrotic areas of stomach. Perform gastropexy of pyloric antrum to the right body wall. Medical treatment alone (repeated intubation, trocarization) has been uniformly disappointing.
CHRONIC TREATMENT Postoperative potassium supplementation if hypokalemic: Do not exceed 0.5 mEq/kg/h IV.
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If ventricular arrhythmias are noted on the ECG: Is hypokalemia present? If so, institute potassium replacement immediately. Ventricular arrhythmias are caused by hypokalemia. Ventricular arrhythmias are refractory to treatment with lidocaine, procainamide, and other antiarrhythmics when hypokalemia is present. Is there anemia, hypoxemia, or acidosis? Many ventricular arrhythmias will resolve spontaneously if these systemic disturbances are corrected. Is the rate rapid (>160 bpm), or is the pulse weak, despite addressing the systemic disturbances already mentioned? If so, consider treatment with lidocaine (see p. 1165). Treat peritonitis (see p. 865) if gastric perforation has occurred (fluids, antibiotics, abdominal lavage ± drainage). Treat gastric ulceration with H2 receptor antagonists: Famotidine, 0.5-1 mg/kg IV, IM, SQ, or PO q 12-24 h; or Ranitidine, 0.5-2 mg/kg IV, IM, SQ, or PO q 8-12 h Ranitidine also has promotility properties similar to those of metoclopramide. Use drugs that increase gastric motility (i.e., metoclopramide, 0.2-0.4 mg/kg PO, SQ, or IM q 6 h, or 1-2 mg/kg/d IV as a continuous infusion; or cisapride, 0.1-0.5 mg/kg PO q 8 h) if recurrent bloating occurs after gastropexy, without evidence of gastric outflow obstruction. Pain management
NUTRITION/DIET Enteral/oral feeding can begin the day after surgery if the patient is not vomiting. Several recommendations are made to prevent gastric bloat after discharge or to prevent GDV in dogs that have not had a gastropexy: Divide feedings into several small meals a day. Do not feed dry foods that contain an oil or fat ingredient listed as one of the first four ingredients. Avoid stress during feeding. Do not elevate feeding bowl during eating. Restrict exercise before and after meals.
POSSIBLE COMPLICATIONS Cardiac arrhythmias Reperfusion injury Gastric necrosis with peritonitis if devitalized tissue not removed Gastric ulceration Esophagitis and regurgitation Gastroparesis and ileus Disseminated intravascular coagulation Aspiration pneumonia Recurrence of dilation Recurrence of volvulus if inadequate gastropexy
RECOMMENDED MONITORING ECG: ventricular arrhythmias common within 36 hours of surgery Electrolyte concentrations: hypokalemia Blood glucose concentration: hypoglycemia PCV/TS: hemoconcentration indicates need for increased fluid therapy. Anemia can occur from bleeding of torn short gastric vessels. Physical parameters: mucous membrane color, capillary refill, pulse quality, temperature, respiratory effort, lung auscultation, abdominal distension, bruising
PROGNOSIS AND OUTCOME Approximately 15% mortality rate for patients with GDV treated surgically Gastric necrosis and need for gastric resection are associated with >30% mortality Increased risk of death if ≥5 hours time lag from onset of clinical signs to admission, hypothermic at admission, or if hypotension occurs at any time during hospitalization Serum lactate level in dogs with GDV: 99% survival if 6 mmol/L
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Gastric Dilatation/Volvulus
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PEARLS & CONSIDERATIONS COMMENTS Begin fluid resuscitation before abdominal radiography. Do not assume the stomach is not rotated just because a stomach tube can be passed. Assess suspect areas of stomach for viability 10-15 minutes after derotation by palpation, evaluating blood flow and stomach wall color. If stomach wall is green or gray, this area will need to be resected. Ventricular arrhythmias have not been shown to worsen prognosis. Rather, they may identify arrhythmogenic disturbances (commonly in GDV: hypokalemia, anemia, or acidosis) that must be corrected for the arrhythmia to resolve.
PREVENTION See Nutrition/Diet Do not breed dogs if history of GDV Prophylactic gastropexy in breeds at high risk for GDV Performed during ovariohysterectomy, during splenectomy, or as an elective procedure Commonly performed with the aid of laparoscopy
SUGGESTED READING Beck JJ, Staatz AJ, Pelsue DH, et al: Risk factors associated with short-term outcome and development of perioperative complications in dogs undergoing surgery because of gastric dilatation-volvulus: 166 cases (1992-2003). J Am Vet Med Assoc 229:1934, 2006. Brockman DJ, Washabau RJ, Drobatz KJ: Canine gastric dilatation volvulus syndrome in a veterinary critical care unit: 295 cases (1986-1992). J Am Vet Med Assoc 207:460, 1995. De Papp E, Drobatz KJ, Hughes D: Plasma lactate concentration as a predictor of gastric necrosis and survival among dogs with gastric dilatation-volvulus: 102 cases (1995-1998). J Am Vet Med Assoc 215:49, 1999. AUTHOR: LORI LUDWIG EDITOR: RICHARD WALSHAW
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Garbage Toxicosis
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Garbage Toxicosis BASIC INFORMATION DEFINITION Gastroenteritis or hemorrhagic gastroenteritis caused by ingestion of food or garbage contaminated with bacteria or preformed bacterial toxins. Tremors or seizures can occur secondary to presence of tremorgenic mycotoxins. Garbage toxicosis is a common occurrence in dogs but less commonly seen in cats, owing to their more discriminating dietary habits.
SYNONYMS Bacterial food poisoning, carrion toxicosis, garbage gut, songbird fever
EPIDEMIOLOGY SPECIES, AGE, SEX Potentially all animals; dogs are more likely to ingest spoiled foods. Cats that hunt and consume birds may develop this disorder. RISK FACTORS Roaming animals Dogs fed food considered unfit for human consumption Raw food diets CONTAGION & ZOONOSIS Disease is transmissible between animals because of habits of licking and sniffing. Dogs also might eat vomitus or feces containing bacteria or bacterial toxins. Zoonotic transmission possible, especially in young children or people with compromised immune systems. GEOGRAPHY AND SEASONALITY: Disease common during warmer months, or year round in tropical and subtropical regions. ASSOCIATED CONDITIONS & DISORDERS Botulism Tremorgenic mycotoxicosis
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT History of exposure to carrion or garbage or raw food diets Clinical signs within 15 minutes to 6 hours post ingestion; diarrhea can be delayed for 48 hours Severe vomiting, diarrhea, lethargy, anorexia PHYSICAL EXAM FINDINGS Signs of abdominal pain Abdominal distension from gas Foul smelling feces; watery or bloody diarrhea Fever Ataxia Weak pulse, muddy mucous membranes, increased capillary refill time, hypovolemic shock Hypothermia as the shock state progresses
ETIOLOGY AND PATHOPHYSIOLOGY
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Source: Streptococcus spp., Salmonella spp., Bacillus spp., Escherichia coli, and Clostridium perfringens are the most common bacteria involved. Endotoxemia and enterotoxemia are possible. Mechanism of Toxicosis Via different mechanisms; endotoxins produce hypovolemic shock, collapse, and death. Tremors, seizures, hyperthermia may occur from tremorgenic mycotoxins. Gastrointestinal (GI) epithelial cells irritated/eroded: Permeability disturbed, initiating vomiting, GI hemorrhage, fluid and electrolyte loss Normal absorptive capabilities of the GI tract may be disrupted. Stasis and GI dilation with gas accumulation follows. GI stasis encourages growth of gram-negative bacteria which liberate endotoxin.
DIAGNOSIS DIAGNOSTIC OVERVIEW Diagnosis is based on a history of ingesting garbage, spoiled food, carrion, songbirds (cats), and the like and typical clinical signs of gastroenteritis or tremors/seizures (with tremorgenic mycotoxins). The disorder is different from benign self-resolving gastroenteritis in the following ways: known ingestion of contaminated substances and/or presence of systemic signs (endotoxemia, neurologic dysfunction, other). In the absence of historical evidence of ingestion, other causes of gastroenteritis must be ruled out with appropriate testing.
DIFFERENTIAL DIAGNOSIS Toxicologic: Plants: castor beans, sago palm, ornamental bulbs, autumn crocus, etc. Metals: arsenic, antimony, iron, etc. Others: disulfoton (an organophosphate pesticide), gastrointestinal-irritant mushrooms Nontoxicologic, Spontaneous: Viral gastroenteritis Hemorrhagic gastroenteritis Acute pancreatitis Acute hepatopathies “Salmon poisoning”
INITIAL DATABASE CBC and serum biochemistry profile: nonspecific changes Abdominal radiographs: to identify abnormal ingesta or rule in/rule out other disorders Monitor blood glucose (hypoglycemia associated with endotoxemia)
ADVANCED OR CONFIRMATORY TESTING Bacterial fecal culture is of mixed value (healthy animals often have cultures that are positive for “pathogenic” bacteria). Blood culture if sepsis is suspected Serologic identification of staphylococcal or clostridial toxins Penitrem A or roquefortine (tremorgenic mycotoxins) can be analyzed in the contaminated food or stomach contents (through a diagnostic laboratory).
TREATMENT TREATMENT OVERVIEW
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Treatment is aimed at limiting absorption of bacterial toxins by inducing emesis and administering activated charcoal, controlling vomiting, correcting fluid and electrolyte disorders, and other supportive measures (preventing shock and preventing secondary infection). Initial approach is similar to any general intoxication, and specific treatments are indicated if systemic signs arise.
ACUTE GENERAL TREATMENT In animals with a known recent exposure but no clinical signs, induction of vomiting is indicated: hydrogen peroxide 3%: 1-2 mL/kg (maximum 45 mL total) PO once; or apomorphine, 0.04 mg/kg IV or instilled in conjunctival sac and rinsed out when vomiting begins (dogs); or xylazine, 0.44 mg/kg IM (cats). Activated charcoal, 1-3 g/kg PO (dose according to packaging label of product; e.g., 10 mL/kg of activated charcoal suspension PO made from 2 g/kg activated charcoal suspended in 10 mL/kg tap water) Appropriate fluid and electrolyte therapy Antibiotics Injectable aminoglycosides generally contraindicated because of synergistic action with endotoxins in depressing the myocardium and risk of nephrotoxicosis in hypovolemia. Oral aminoglycosides (streptomycin, 5-10 mg/kg PO q 12 h; or neomycin 10-20 mg/kg PO q 8-12 h) work well. Metronidazole, 25 mg/kg PO q 12 h (for a maximum of 5 days at this dosage) can also be used. If a cat has known songbird fever, routine antibiotics are not recommended, as this tends to alter normal GI flora, allowing colonization by Salmonella. Gastrointestinal protectants such as sucralfate ¼ to a whole 1-gram tablet PO q 8 h Treatment for shock as needed (see p. 585) Appropriate treatment if disseminated intravascular coagulation occurs (e.g., including heparin 75 IU SQ q 8 h (see p. 315) Control tremors and seizures with methocarbamol (55-220 mg/kg IV, repeat as needed; max dose 330 mg/kg/day) or diazepam (0.5-2 mg/kg IV, repeat as needed) in cases involving tremorgenic mycotoxins. Profuse, persistent vomiting after the toxin has been expelled may be controlled with maropitant, 1 mg/kg SQ q 24 h; dolasetron mesylate, 0.6 mg/kg IV q 24 h; or metoclopramide, 0.2-0.4 mg/kg IM or SQ q 8 h.
NUTRITION/DIET Bland diet Canned prescription gastrointestinal therapeutic diets Low-fat, low-spice homemade diet (e.g., boiled white rice with either boiled skinless/boneless chicken breast or 2% cottage cheese)
POSSIBLE COMPLICATIONS Chronic diarrhea with clostridial enteritis Pancreatitis, malabsorption syndromes with repeated episodes of garbage toxicosis
RECOMMENDED MONITORING Temperature Heart rate Blood pressure Glucose CBC
PROGNOSIS AND OUTCOME Prognosis good provided shock does not occur Poor or guarded if endotoxemic shock
PEARLS & CONSIDERATIONS COMMENTS Clinical signs generally resolve in 3-5 days. The term songbird fever arises from the source of intoxication, namely the decayed carcasses of songbirds that cats hunt. Consumption of decomposing organic material, moldy refrigerated foods, cottage cheese, cream cheese, or moldy walnuts can cause tremors and seizures due to contamination with tremorgenic mycotoxins such as penitrem A and roquefortine.
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PREVENTION Prevent roaming and scavenging. Feed fresh, high-quality food.
CLIENT EDUCATION Discuss nutrition. Discuss potentially zoonotic aspects of raw diets.
SUGGESTED READING Beasley VR, et al: Garbage toxicosis—carrion toxicoses—bacterial food poisoning. In Beasley VR, editor: A systems affected approach to veterinary toxicology. Urbana IL, 1999, University of Illinois, p 738. AUTHOR: SHARON GWALTNEY-BRANT EDITOR: SAFDAR A. KHAN 1ST EDITION AUTHOR: CHARLOTTE MEANS
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Gallops and Other Extra Heart Sounds
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Gallops and Other Extra Heart Sounds BASIC INFORMATION DEFINITION Extra heart sounds are classified as sounds or vibrations other than the normally ausculted first and second heart sounds. They alter the sound of a heartbeat but not the rhythm of the heartbeat. Gallops and extra heart sounds are different from premature cardiac beats and arrhythmias.
SYNONYMS Third heart sound, fourth heart sound, diastolic heart sound, protodiastolic heart sound, presystolic heart sound, summation diastolic heart sound
EPIDEMIOLOGY SPECIES, AGE, SEX Dogs and cats of any age and either sex, in the presence of heart disease/failure (gallop sounds) RISK FACTORS Gallop sounds: congestive heart failure, systolic and diastolic ventricular dysfunction Systolic clicks: early mitral valvular insufficiency or flail leaflet Split heart sounds: increased ventricular pressures (causing splitting sounds due to delayed aortic or pulmonic valve closure under specific circumstances) Pericardial friction rubs: pericarditis, inflammation of the external pericardial lining
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT: Clinical signs relating to heart failure of virtually any etiology (see p. 468) are associated with gallop sounds. Splitting sounds may be normal or an indication of delay in valvular closure due to increased pressures on one or both sides of the heart or due to high pressure delaying valvular opening. Systolic clicks are not associated with clinical signs. Pericardial rubs are associated with pericardial diseases and their associated clinical signs. PHYSICAL EXAM FINDINGS: A triple heart sound sequence with accentuated low-frequency sounds mimicking a cantering horse best describes a gallop sound. This sound is of low frequency, heard best with the bell of the stethoscope and usually over the mitral and or tricuspid valve area. The sound is likely to be associated with other signs of heart failure such as dyspnea, tachypnea, heart murmurs, and an increase in the heart rate.
ETIOLOGY AND PATHOPHYSIOLOGY Normally, only the S1 and S2 sounds are heard when auscultating the heart of the dog or cat. When the usually inaudible third or fourth sounds are so loud that they can be heard (gallops), they are an indication of the presence of ventricular systolic and/or diastolic dysfunction and are usually an indication of heart failure. By definition they occur during diastole and are generated by the vibration of ventricular walls during active ventricular filling (S3) or final ventricular filling by atrial contraction (S4) in a poorly compliant ventricle. Other additional sounds within the normal cardiac cycle can include: Splitting of the normal heart sounds: either split S1, due to the asynchronous closure of AV valves, or split S2, due to asynchronous closure of aortic and pulmonic (semilunar) valves; caused by alterations in pressures within the heart and great vessels causing early or delayed valve closure Extracardiac rubbing sounds Systolic clicks: etiology unidentified, possibly caused by the warping/snapping of a diseased, prolapsed mitral valve. They are usually heard best with the diaphragm of the stethoscope, in contrast to the gallop sound which is a lower frequency sound heard better with the bell. The systolic click may be single or multiple. It also may come and go between consecutive cardiac cycles. Opening snaps: heard in diastole and indicative of a calcified or hardened valve leaflet making a snapping sound when the valve opens during that phase of the cardiac cycle. These are unusually heard in dogs and cats, and they may be demonstrated by phonocardiography.
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Gallops and Other Extra Heart Sounds
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Friction rubs: due to rubbing of a diseased pericardium against portions of the thorax
DIAGNOSIS DIFFERENTIAL DIAGNOSIS Triple heart sounds occurring at a slow rate are not likely to be gallop rhythms and must be differentiated from extra beats, heart block, systolic clicks, split heart sounds, and opening snaps. Systolic clicks are higher-frequency sounds heard with the diaphragm of the stethoscope and usually are heard at the point of maximal intensity on the thorax. The sound may be consistent or variable and may be single or multiple. It can easily mimic a gallop sound except in the frequency of the ausculted sound. Split heart sounds are usually heard cranially and left over the aortic and pulmonic valve regions. They tend to be higher-frequency sounds heard best with the diaphragm of the stethoscope.
INITIAL DATABASE Cardiac evaluation in the form of auscultation, radiography of the thorax, laboratory analyses, and echocardiographic examination usually are sufficient to identify the specific abnormality present.
TREATMENT TREATMENT OVERVIEW Extra heart sounds in and of themselves are NOT treated. Attention is directed to identifying the underlying cause and determining whether treatment is required for the primary etiology.
PROGNOSIS AND OUTCOME Variable, depending on cause
PEARLS & CONSIDERATIONS COMMENTS The bell of the stethoscope is useful for differentiating low-frequency sounds such as gallop sounds (bell disproportionately enhances the third heart sound) from other heart sounds of higher frequency such as split heart sounds and systolic clicks (heard more clearly with the diaphram of the stethoscope).
SUGGESTED READING Prosek, R: Abnormal heart sounds and murmurs. In Ettinger SJ, Feldman EC, editors: Textbook of veterinary internal medicine, ed 7, St Louis, 2010, Elsevier, p 259. AUTHOR: STEPHEN J. ETTINGER EDITOR: ETIENNE CÔTÉ
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Gallbladder Rupture
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Gallbladder Rupture BASIC INFORMATION DEFINITION Loss of gallbladder wall integrity
EPIDEMIOLOGY SPECIES, AGE, SEX Dogs: Associated with trauma: younger dogs (mean 2.8 years) Associated with intrinsic gallbladder disease: middle-aged dogs (mean 8.1 years) GENETICS & BREED PREDISPOSITION Shetland sheepdogs and possibly cocker spaniels are overrepresented. ASSOCIATED CONDITIONS & DISORDERS Dogs: Cholelithiasis, cholecystitis, bile peritonitis, sepsis Associated with gallbladder mucocele Gallbladder infarction Hypothyroidism and hyperadrenocorticism may predispose a subset of dogs to gallbladder infarction/rupture.
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES Gallbladder infarction/necrotizing cholecystitis: Without rupture With hepatic and omental adhesions and possibly fistulae to other abdominal structures With gallbladder perforation and diffuse peritonitis Gallbladder perforation associated with penetrating trauma and subsequent bile peritonitis HISTORY, CHIEF COMPLAINT Nonspecific signs: vomiting, anorexia, weakness, polydipsia, polyuria, weight loss. Often chronic (duration from onset of signs to presentation: up to 1 month; mean = 12 days) Some owners may notice icterus, discolored urine (bilirubinuria). PHYSICAL EXAM FINDINGS Icterus: very common (77% of bile peritonitis cases) Abdominal distension: common (65% of bile peritonitis cases), may be subtle Signs of abdominal pain Pyrexia Shock
ETIOLOGY AND PATHOPHYSIOLOGY Causes of gallbladder rupture: Necrotizing cholecystitis
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Gallbladder Rupture
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Gallbladder infarction Penetrating trauma Inadequate choleresis due to excessively thick bile, defective gallbladder contractility, and/or altered outflow Gallbladder rupture may result in the development of septic or nonseptic peritonitis (see p. 865). Lack of bile secretion into the intestine results in: Lack of digestion and absorption of fat and fat-soluble vitamins, most importantly vitamin K (coagulopathy)
DIAGNOSIS DIAGNOSTIC OVERVIEW The diagnosis is suspected based on nonspecific history and physical examination finding of icterus +/− abdominal signs. Confirmation requires abdominal ultrasound examination and peritoneal fluid analysis.
DIFFERENTIAL DIAGNOSIS Icterus: Hyperbilirubinemia due to hemolysis: immune-mediated hemolytic anemia and other diseases causing severe intravascular hemolysis Hepatic diseases: cholangiohepatitis, cirrhotic/fibrosing liver disease, neoplasia, copper and other toxins Extrahepatic biliary obstruction: choleliths, pancreatitis, cholangitis, neoplasia, stricture Biliary leakage from other parts of the biliary system: Traumatic rupture of the common or hepatic ducts Abdominal distension (if icterus not apparent): Septic peritonitis: gastrointestinal perforation, penetrating trauma Uroabdomen Hemoabdomen: ruptured mass/viscus, bleeding disorder Abdominal organ dilation/enlargement: gastric dilation/volvulus, mesenteric volvulus, splenic torsion, overeating, hyperadrenocorticism Intraabdominal abscess: severe pancreatitis, hepatic abscess, ruptured prostatic abscess, ruptured pyometra Portal hypertension Congestive heart failure (right-sided)
INITIAL DATABASE CBC: Inflammatory leukogram Degenerative left shift with toxic changes: Septic bile peritonitis Serum biochemistry profile: Elevated bilirubin concentration (virtually all cases) Elevated liver enzymes concentration (virtually all cases) Hypokalemia Survey abdominal radiographs: Increased opacity/loss of detail in anterior abdomen Cholelithiasis (in dogs, 14%-48% are radiopaque) Generalized loss of abdominal detail/fluid: Bile peritonitis
ADVANCED OR CONFIRMATORY TESTING Abdominal ultrasound examination: Evaluate gallbladder wall thickness and integrity (cholecystitis); contents (choleliths, mucocele), presence of attached omentum, and surrounding fluid, suggesting either bile peritonitis or unrelated (e.g., other differential diagnoses) Peritoneal fluid analysis (obtained during abdominal ultrasound examination): Bilirubin concentration: > twice that of serum bilirubin is diagnostic of bile peritonitis Cytologic evaluation and bacterial culture and sensitivity testing (aerobic and anaerobic): septic peritonitis Coagulation profile (prothrombin time is first to be abnormal with vitamin K deficiency/malabsorption)
TREATMENT
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TREATMENT OVERVIEW Treatment consists of patient stabilization followed by surgical exploration of the abdomen, with removal of the ruptured gallbladder and treatment of associated bile peritonitis; adjunctive pain control is important.
ACUTE GENERAL TREATMENT Rehydration: intravenous administration of balanced electrolyte solution Normalization of serum electrolyte concentrations Parenteral antibiotics effective against gram-negative bacteria and anaerobes Empirical therapy: Cefoxitin, 22 mg/kg IV q 2 h peri-operatively, then q 6 h; or Metronidazole, 10-15 mg/kg IV q 12 h with: Enrofloxacin, 2.5-5 mg/kg IV q 12 h (maximum 5 mg/kg q 24 h in cats) Specific long-term therapy based on culture and sensitivity test results Possible administration of fresh frozen plasma: (see p. 1347) Hypoproteinemia Possible coagulopathy Vitamin K administration: 2.5 mg/kg SQ q 12 h × 3 days, then weekly Exploratory laparotomy once animal is stabilized: Cholecystectomy Ensure patency of biliary system Aerobic and anaerobic microbiologic culture of peritoneal fluid Treatment of bile peritonitis: consider open peritoneal drainage
CHRONIC TREATMENT Maintenance of bile flow: ursodeoxycholic acid 10-15 mg/kg/day PO—only after biliary obstruction is definitively ruled out/corrected, because stimulates gallbladder contraction
NUTRITION/DIET Nutritional support via placement of feeding tube if indicated (see pp. 1322 and p. 1267)
POSSIBLE COMPLICATIONS Ongoing/recurrent bile leakage Failure to resolve septic bile peritonitis: Endotoxemia Sepsis Biliary obstruction: Recurrence of cholelithiasis Pancreatitis
RECOMMENDED MONITORING Clinical and laboratory parameters assessing perfusion, including capillary refill time, pulse rate and quality, blood pressure, urine output, arterial pH, and lactate concentrations Respiratory function Serum liver enzymes and bilirubin concentrations Coagulation profile
PROGNOSIS AND OUTCOME Guarded to fair in animals with aseptic bile peritonitis Poor to guarded in animals with septic bile peritonitis
PEARLS & CONSIDERATIONS COMMENTS
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In dogs and cats with bile peritonitis: Peripheral white blood cell count is significantly lower in survivors (mean = 20,608/µL) compared with nonsurvivors (mean = 35,715/µL). The immature neutrophil count is significantly lower in survivors (mean = 686/µL) than in nonsurvivors (mean = 4852/µL).
SUGGESTED READING Aguirre AL, Center SA, Randolph JF, et al: Gallbladder disease in Shetland sheepdogs: 38 cases (1995-2005). J Am Vet Med Assoc 231(1):79–88, 2007. Holt DE, et al: Canine gallbladder infarction. Vet Pathol 41:416, 2004. Ludwig LL, et al: Surgical treatment of bile peritonitis in 24 dogs and 2 cats: a retrospective study (1987-1994). Vet Surg 26:90, 1997. AUTHOR: DAVID HOLT EDITOR: RICHARD WALSHAW
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Gallbladder Mucocele
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Gallbladder Mucocele BASIC INFORMATION DEFINITION An abnormal accumulation of bile-laden mucus within the gallbladder (GB) lumen; the mucosa of the GB wall is characterized histologically by glandular hyperplasia. Once a rare condition, GB mucocele has recently been reported as the most common cause of canine extrahepatic biliary obstruction (EHBO).
SYNONYMS Kiwi GB, cystic mucinous hyperplasia of the GB
EPIDEMIOLOGY SPECIES, AGE, SEX: Older small or medium-size dogs usually affected, with no sex predilection reported. GB mucocele formation in humans is the result of cystic duct obstruction and not cystic mucinous hyperplasia. GENETICS & BREED PREDISPOSITION: Cocker spaniels and Shetland sheepdogs are predisposed. In recent reports, miniature schnauzers are overrepresented. ASSOCIATED CONDITIONS & DISORDERS: A weak association exists between hyperadrenocorticism and GB mucocele.
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES GB mucocele can be an incidental finding or it can be responsible for the presenting complaint (approximately 75% of patients diagnosed with GB mucocele show overt signs of illness). Inflammation and necrosis of the GB wall can lead to rupture and peritonitis (focal or diffuse). HISTORY, CHIEF COMPLIANT: Vomiting, inappetence, and lethargy are the most common presenting complaints. Other complaints include weight loss, diarrhea, ptyalism, and polyuria/polydipsia. PHYSICAL EXAM FINDINGS: Abdominal pain, ascites, tachypnea, tachycardia, fever, hepatomegaly, and icterus
ETIOLOGY AND PATHOPHYSIOLOGY Abnormal accumulation of intraluminal mucus and inspissated bile Potential mechanisms for mucocele formation include progressive biliary sludging and alterations in water absorption across the GB mucosa. Histologic evidence of GB wall inflammation is not present in the majority of cases.
DIAGNOSIS DIAGNOSTIC OVERVIEW GB mucocele diagnosis requires abdominal ultrasound. The stellate intraluminal pattern and non–gravity-dependent GB contents are considered pathognomonic. Less organized mucoceles can be more challenging to confirm.
DIFFERENTIAL DIAGNOSIS Cholecystitis (acute, chronic or necrotizing) Cholelithiasis Biliary sludge
INITIAL DATABASE
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Gallbladder Mucocele
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CBC: most common abnormalities reported are leukocytosis characterized by a mature neutrophilia and monocytosis. In dogs, leukocytosis is significantly higher (21,200 cells/µL) with GB rupture than when the GB is intact (12,500 cells/µL). Serum biochemistry profile: common abnormalities include elevated serum alanine transaminase (ALT), alkaline phosphatase (ALP), aspartate transaminase (AST), and gammaglutamyl transpeptidase (GGT) activities. Increasing serum GGT activity may be associated with increased risk for mortality. Total bilirubin concentration is elevated in 63%-77% of cases. Hypercholesterolemia, hyperglobulinemia, and hypoalbuminemia are less common findings. Urinalysis: generally unremarkable; bilirubinuria may be noted. Abdominal radiography: generally unremarkable. In cases with GB rupture, decreased serosal detail may be noted if ascites is present. Abdominal ultrasonography: characteristic stellate/striated intraluminal GB contents. Increased GB volume/subjective distension can be noted. Other potential findings include common bile duct (BD) distension and ascites. The pancreas should be evaluated for ultrasonographic evidence of pancreatitis.
TREATMENT TREATMENT OVERVIEW Surgical intervention is indicated, with cholecystectomy generally considered the treatment of choice.
ACUTE GENERAL TREATMENT Emergency surgery is indicated for cases of suspected GB rupture. If present, ascitic fluid should be evaluated to determine whether the effusion is septic. GB rupture is suspected if (1) GB wall continuity can not be confirmed, (2) hyperechoic cranial abdominal fat is noted, (3) free abdominal fluid is present, and/or (4) stellate echogenic material is present within the peritoneal cavity. Patients with GB rupture are often hemodynamically unstable and require aggressive perioperative supportive care. Initial presurgical therapy generally includes fluid therapy, intravenous antibiotics (gram-negative anaerobes are the most common isolate), antiemetics, and analgesics. Cholecystectomy, cholecystoenterostomy, and cholecystotomy have been described for the treatment of GB mucoceles. Given that GB wall dysfunction appears to be associated with the etiopathogenesis of mucocele formation, the author believes that cholecystectomy is the treatment of choice. During surgery, confirmation of patency of the common BD is imperative. Gastrointestinal and hepatic biopsies should be considered. Samples of the GB wall and/or intraluminal contents should be collected for aerobic and anaerobic culture. Laparoscopic cholecystectomy has been reported for the treatment of uncomplicated cases of GB mucocele.
CHRONIC TREATMENT The nonsurgical resolution of GB mucocele has been reported in two dogs; however, the current literature is lacking adequate numbers to validate medical treatment. Patients with biliary sludge without mucocele formation generally do not require therapy unless clinical findings suggest GB disease. In these rare cases, medical management with antibiotic therapy, choleretics, and hepatoprotectants may prove helpful.
NUTRITION/DIET Esophagostomy, gastrostomy, or nasogastric tube placement should be encouraged, as postoperative inappetence is common in the author's experience (see pp. 1267, p. 1269, p. 1270).
POSSIBLE COMPLICATIONS The most commonly reported postoperative complications include pancreatitis and bile peritonitis. Aspiration pneumonia has also been reported. Postoperative common BD obstruction has been reported, emphasizing the need to confirm patency of the common BD at the time of cholecystectomy.
PROGNOSIS AND OUTCOME Perioperative mortality ranges from 21.7%-32%. The long-term prognosis for patients surviving to release from hospital is excellent.
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Gallbladder Mucocele
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Mortality rates do not differ significantly between ruptured or intact mucoceles. If GB rupture results in diffuse bile peritonitis, mortality rates are as high as 68%-100%.
PEARLS & CONSIDERATIONS COMMENTS Mucocele rupture does not preclude a successful outcome. Diffuse bile peritonitis with mucocele rupture is unlikely, owing to containment of bile salts within a solid mucinous matrix that limits exposure of bile salts to the peritoneal surface. To prevent reobstruction with mucocele material within the common BD and hepatic ducts, confirmation of patency of the common BD is imperative following cholecystectomy. Intestinal biopsies should be considered in patients with a history of chronic gastrointestinal disease.
SUGGESTED READING Aguirre AL, Center SA, Randolph JF, et al: Gallbladder disease in Shetland sheepdogs: 38 cases (1995-2005). J Am Vet Med Assoc 231(1):79–88, 2007. Pike FS, Berg RJ, King NW, et al: Gallbladder mucocele in dogs: 30 cases (2000-2002). J Am Vet Med Assoc 224(10):1615–1622, 2004. AUTHOR: FRED S. PIKE EDITOR: KEITH RICHTER
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Hypothyroidism
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Hypothyroidism BASIC INFORMATION DEFINITION The clinical syndrome that occurs as a result of decreased circulating levels of serum thyroid hormones (thyroxine [T4] and triiodothyronine [T3])
SYNONYM Congenital hypothyroidism: cretinism
EPIDEMIOLOGY SPECIES, AGE, SEX Dogs: Middle-aged at onset (2-9 years of age) No sex predilection Cats Spontaneous hypothyroidism is very rare. Iatrogenic disease: middle-aged or older GENETICS & BREED PREDISPOSITION Dogs: Can occur in any breed, including mixed breeds Reported to be more prevalent in boxers, dachshunds, Doberman pinschers, golden retrievers, Great Danes, Irish setters, miniature schnauzers, poodles, and a number of other breeds ASSOCIATED CONDITIONS & DISORDERS Can occur as part of an autoimmune polyglandular syndrome (rare) along with hypoadrenocorticism or diabetes mellitus
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES Congenital hypothyroidism (cretinism); rare Primary hypothyroidism (most common): disruption or atrophy of the thyroid glands Secondary hypothyroidism (rare): inadequate pituitary secretion of thyroid-stimulating hormone (TSH) HISTORY, CHIEF COMPLAINT Acquired disease: Signs are often nonspecific and gradual in onset. Metabolic: weight gain, lethargy, mental dullness, exercise intolerance/inactivity, and cold intolerance are common. Dermatologic: alopecia (bilaterally symmetric truncal) or thin hair, hyperkeratosis, seborrhea, hyper-pigmentation, otitis, “rat tail,” and pyoderma are often present, with alopecia or thin hair most common. Reproductive (uncommon): persistent anestrus, infertility, and decreased libido Neuromuscular: weakness/exercise intolerance are sometimes seen; other signs (ataxia, seizures, facial drooping/paralysis, head tilt/circling [vestibular signs], and stridor/change in bark [laryngeal paralysis]) are uncommon. Cretinism: disproportionate dwarfism, short limbs, persistent “puppy coat” or alopecia/thin dull hair, broad head, thick protruding tongue, mental dullness/retardation, delayed dental eruption, constipation
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Hypothyroidism
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PHYSICAL EXAM FINDINGS Exam findings are similar to signs described by the owners. Additional findings (uncommon) may include ocular changes (corneal lipid deposits most common), bradycardia or other arrhythmias, constipation, decreased spinal reflexes, and decreased conscious proprioception.
ETIOLOGY AND PATHOPHYSIOLOGY Primary hypothyroidism is the most common form and is usually due to lymphocytic thyroiditis or idiopathic thyroid gland atrophy. Less common causes include follicular cell hyperplasia and infiltrative neoplasia. Secondary hypothyroidism is rare. Decreased TSH secretion leads to atrophy of the follicular cells of the thyroid gland. Loss of normal TSH secretion can occur as a result of a congenital pituitary malformation, pituitary neoplasia, or suppression of pituitary thyrotropic cells (most commonly from excess glucocorticoids [exogenous or endogenous hyperadrenocorticism]). Reversibility is possible if glucocorticoid concentrations are returned to normal. Tertiary hypothyroidism (decreased secretion of thyrotropin-releasing hormone [TRH]) has not been reported in the dog. Iatrogenic hypothyroidism can occur as a result of antithyroid medications (e.g., methimazole), bilateral thyroidectomy, or 131 radioiodine therapy (see p. 562). Clinical signs reflect the widespread metabolic effects of thyroid hormones. Surgery or anesthesia, a wide range of concurrent illnesses, and various nonthyroidal medications (e.g., glucocorticoids, phenobarbital, sulfonamides, carprofen, clomipramine) also affect circulating thyroid hormone concentrations, but not to the extent of producing clinical hypothyroidism.
DIAGNOSIS DIAGNOSTIC OVERVIEW The diagnosis is suspected in a middle-aged dog presenting one or more of the common clinical signs. Confirmation is not always straightforward, but the presence of typical clinical signs in conjunction with a decreased serum FT4 ED value and an increased serum TSH value can be considered diagnostic.
DIFFERENTIAL DIAGNOSIS Alopecia (see p. 58) Seborrhea (see p. 255) Obesity/weight gain (see p. 773)
INITIAL DATABASE CBC, serum biochemical profile, urinalysis: hypercholesterolemia is most common and must be differentiated from normal postprandial hypercholesterolemia. A mild normocytic, normochromic, nonregenerative anemia; fasting hyperlipidemia/hypertriglyceridemia; mild increases in liver enzymes; and a mild increase in creatine kinase may also be seen. Basal serum total thyroxine concentration (T4): Includes both free (99%) T4 Low levels in hypothyroid dogs: sensitivity: 89%-100%; specificity: 75%-82%; accuracy: 85% If T4 is in the middle or upper end of the reference range, hypothyroidism is generally ruled out. An exception is the presence of antithyroid antibodies that interfere with the assay. If clinical signs strongly suggest hypothyroidism and T4 is normal, free thyroxine concentration by equilibrium dialysis (FT4ED), anti-T4 antibody, and thyroglobulin autoantibody concentrations should be measured. If T4 is low or is at the low end of the reference range, it may be due to hypothyroidism, concurrent illness, medications, or may be normal (euthyroid). Basal serum free thyroxine concentration by equilibrium dialysis (FT4ED): Measures just the free (i.e., metabolically available) T4 An assay based on equilibrium dialysis should be used; it is more time intensive and expensive than radioimmunoassay but much more accurate. Low levels in hypothyroid dogs: sensitivity: 80%-98%; specificity 93%-94%; accuracy: 95% Most accurate single hormone test for the diagnosis of hypothyroidism Basal serum TSH concentration: A validated canine TSH assay should be used. The test should not be evaluated alone but is best used in conjunction with T4 and/or FT4ED results. High TSH with low T4: sensitivity: 63%-67%; specificity: 98%-100%; accuracy: 82%-88% High TSH with low FT4ED: sensitivity: 74%; specificity: 98%; accuracy: 86% Increased TSH with decreased T4 or FT4ED is strongly supportive of hypothyroidism.
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A normal TSH in conjunction with decreased T4 or FT4ED does not rule out hypothyroidism. Also see the Hypothyroidism algorithm, .
ADVANCED OR CONFIRMATORY TESTING If basal thyroid hormone concentrations do not rule in/out hypothyroidism, a few options exist: TSH stimulation test. Protocol: Many protocols reported; consult the laboratory performing the thyroid assays for the desired protocol and reference ranges for resting and poststimulation T4 concentrations. 0.1 units/kg (maximum 5 units) medical-grade bovine TSH IV; evaluate serum T4 concentrations in preadministration and 6-hour postadministration samples. Dogs 20 kg: 50 or 100 mcg recombinant human TSH IV; evaluate serum T4 concentrations in preadministration and 6-hour postadministration samples. Interpretation: If both results are below the reference range, hypothyroidism is present. If post-TSH T4 concentration is >3 mcg/dL, the dog is not hypothyroid. Results in between these parameters are equivocal; consider retesting 1-2 months later. Medical-grade, bovine TSH is no longer available in most places. TRH stimulation test Originally designed to identify secondary hypothyroidism. When the availability of bovine TSH became very limited, this test was used as a replacement. However, it is less reliable and so is uncommonly used. Response to therapy Serum thyroglobulin antibodies: increased levels suggest lymphocytic thyroiditis. However, lymphocytic thyroiditis does not always lead to or correlate with the presence of hypothyroidism. Serum thyroid hormone antibodies: if present, can interfere with testing and lead to spuriously high or low T4 results, depending on the T4 assay used. Thyroid scintigraphy may be useful for differentiation between hypothyroidism and nonthyroidal illness but is limited by cost and availability. Histopathologic evaluation of skin biopsies: vacuolated or hypertrophied erector pili muscles, increased dermal mucin, and a thickened dermis are consistent with hypothyroidism. A variety of other nonspecific changes supportive of an endocrinopathy may also be present.
TREATMENT TREATMENT OVERVIEW The mainstay of treatment is oral thyroid hormone replacement. Therapy should be designed to raise serum TT4 values to the normal range and eliminate clinical signs. Therapy is lifelong.
ACUTE GENERAL TREATMENT Hypothyroidism is generally a chronic condition that does not require acute therapy. Myxedema coma (rare): levothyroxine for injection 5 mcg/kg IV q 12 h until oral administration possible.
CHRONIC TREATMENT Oral thyroid supplementation: Levothyroxine sodium (synthetic T4): Initial dose (tablets): 0.02 mg/kg PO q 12 h. Maximum dose: 0.8 mg/dog q 12 h. A novel liquid formulation of L-thyroxine available in Europe is often effective with once-daily dosing (0.02 mg/kg PO q 24 h). If concurrent heart failure, renal failure, liver disease, hypoadrenocorticism, or diabetes is present, the initial dose should be decreased by 25%-50%, then slowly increased over the following 2-4 months. Also, hypothyroidism is rarely life threatening, so the concurrent disease should be controlled first before treatment of the hypothyroidism is pursued. A brand-name preparation for animal use should be used, as bioavailability of generic forms can vary. Adjust dose based on clinical response and serum T4 concentrations (see Recommended Monitoring below). Absorption kinetics vary between brands, so serum concentrations should be reassessed if the levothyroxine brand is changed.
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Hypothyroidism
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Liothyronine sodium (synthetic T3): Very rarely indicated Consider only if a dog with confirmed hypothyroidism has failed to respond clinically, has normalized serum T4 concentrations, and at least two brands of levothyroxine have been tried. Initial dosage is 4-6 mcg/kg PO q 8 h. Combination products (levothyroxine and liothyronine) are not recommended.
POSSIBLE COMPLICATIONS Iatrogenic hyperthyroidism
RECOMMENDED MONITORING A physical examination and serum thyroxine concentration (4-6 hours post-pill) should be evaluated at 4 weeks, then q 6-8 weeks for 6-8 months, then q 6-12 months. Serum T4 concentrations (4-6 hours post-pill) should be in the upper half of the normal range. Monitoring clinical signs: expected evolution of response. An increase in alertness and activity commonly is seen within 1-2 weeks. Neurologic improvement may begin within the first month, but several months may be needed for full resolution. Dermatologic improvement often takes 1-4 months Resolution of reproductive manifestations may take several months. If major clinical improvement is not seen in 3 months despite normal serum T4 concentrations, a concurrent as yet unidentified disease should be considered.
PROGNOSIS AND OUTCOME Primary hypothyroidism: long-term prognosis is good to excellent for return to function. Secondary hypothyroidism: long-term prognosis is usually guarded, since pituitary neoplasia is the most common underlying cause.
PEARLS & CONSIDERATIONS COMMENTS The presence of nonthyroidal illness can make it difficult to obtain a definitive diagnosis of hypothyroidism. “Sick euthyroid syndrome” describes the condition that occurs when nonthyroidal illness results in a decrease in the basal T4 (and less commonly, FT4ED) concentrations. Subnormal T4 concentrations are not an immediate indication for supplementation with levothyroxine, which may at times be deleterious. The history and physical exam must be critically evaluated both for features supportive of hypothyroidism and for signs of other illness that could be causing the sick euthyroid syndrome. In the latter case, resolution/treatment of nonthyroidal illness returns T4 concentrations to normal. Obesity is much more prevalent (21%-40% of the North American pet dog population is or may become obese) than hypothyroidism (0.2% of dog population, possibly higher). Therefore, obese body condition can only be attributed to hypothyroidism in a small fraction of cases.
TECHNICIAN TIP Avoid lipemia and hemolysis when obtaining samples for diagnosis and therapeutic monitoring; fasted sample recommended. An artifactual increase in T4 and FT4ED occurs if the blood or serum sample is not kept cold.
SUGGESTED READING Feldman EC, Nelson RW: Hypothyroidism. In Canine and feline endocrinology and reproduction. Philadelphia, 2004, WB Saunders, pp 86–151. Scott-Moncrieff JC, Guptill-Yoran L: Hypothy-roidism. In Ettinger SJ, Feldman EC, editors: Textbook of veterinary internal medicine. St Louis, 2005, Elsevier Inc., pp 1535–1544. AUTHOR: KRISTI L. GRAHAM EDITOR: SHERRI IHLE
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Hypothermia
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Hypothermia BASIC INFORMATION DEFINITION Body temperature below 99.5°F (37.5°C) in the dog and 100°F (37.8°C) in the cat
EPIDEMIOLOGY SPECIES, AGE, SEX Any species, any age, and either sex can be affected. RISK FACTORS Very old, very young animals Short-haired animals General anesthesia Cold environment Cardiac disease
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES Mild hypothermia: 90°F-99.5°F (32.2°C-37.5°C) Moderate hypothermia: 82°F-90°F (27.8°C-32.2°C) Severe hypothermia: 20% plasma cells in multiple myeloma or plasma cell leukemia Echocardiogram (with microbubble contrast): to identify right ventricular hypertrophy and right-to-left cardiac shunt if present Ehrlichia canis titer, Leishmania direct agglutination test, others: as indicated by geographic exposure and other features of case
TREATMENT TREATMENT OVERVIEW As hyperviscosity syndrome is a secondary condition, it is imperative to recognize that patients may present with chief complaints that are actually sequelae (i.e., epistaxis, blindness, retinal hemorrhage) of the underlying condition. Identifying and treating the primary disease process is the cornerstone of long-term care. Acutely, the most important treatment interventions are to ensure the patient is adequately hydrated, oxygenated, and producing urine. Phlebotomy or other treatments to reduce circulating blood components may
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Hyperviscosity Syndrome
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be used immediately if clinical signs are severe and clinical improvement is needed prior to the onset of benefit of treating the underlying cause.
ACUTE GENERAL TREATMENT Plasmapheresis or phlebotomy to decrease Hct to 1.035. Treatment renders all hyperfunctional thyroid tissue, including ectopic tissue, nonfunctional. Disadvantages: special handling facilities and posttherapy isolation for several days to weeks are required. The length of isolation is dependent upon the facility. Prior to therapy, the cat must be eating and able to tolerate the required period of time in isolation. The necessity of discontinuing medical antithyroid drugs before treatment is controversial. Consult the facility administering the radiotherapy.
RECOMMENDED MONITORING Medical therapy: exam including body weight, CBC, serum biochemical profile, urine specific gravity, T4 at 2 weeks; if normal, reassess q 6 months or if adverse effect or recurrent signs of hyperthyroidism occur. Thyroidectomy: exam including body weight, postoperative monitoring of serum calcium if bilateral thyroidectomy; CBC, serum biochemical profile, urinalysis and T4 at 2 weeks, then monitor T4 q 3-6 months. Radioactive iodine therapy: exam including body weight, CBC, serum biochemical profile, urinalysis, and T4 2 weeks after treatment, then monitor T4 q 3-6 months.
PROGNOSIS AND OUTCOME With successful radioactive iodine therapy or thyroidectomy the short-term prognosis is excellent and long-term prognosis is good. Cure may be obtained in many cases. These patients are older at the time of diagnosis, and other conditions may be present or soon develop; length of survival has been documented to be approximately 2 years post diagnosis regardless of the type of therapy chosen. With the presence of renal dysfunction the short-term prognosis is good, but the long-term prognosis is guarded to poor, as both hyperthyroidism and renal dysfunction are progressive illnesses and treatments may be mutually antagonistic.
PEARLS & CONSIDERATIONS COMMENTS Concurrent hyperthyroidism and chronic kidney disease should be treated according to which disorder is predominantly responsible for clinical signs: Hyperthyroid cats with polyphagia, weight loss, and/or hyperactivity who are also incidentally found to be azotemic should be treated for hyperthyroidism. Chronic kidney disease (see p. 205) is monitored and managed secondarily. Cats with chronic kidney disease and overt anorexia, dehydration, uremic oral ulcers, and/or vomiting who are also incidentally found to be hyperthyroid should be treated for chronic kidney disease. In these cases, hyperthyroidism is monitored and generally not treated unless it is causing characteristic signs. Cats with no clinical signs attributable to either chronic kidney disease or hyperthyroidism but who are found to have both syndromes incidentally on routine laboratory testing should be monitored periodically (see Recommended Monitoring above) and not treated specifically for either disorder, other than preventive measures (e.g‥ nutrition). Cats with clinical signs of both chronic kidney disease and hyperthyroidism may require medical treatment for chronic kidney disease and “partial treatment” of hyperthyroidism (i.e‥ medical treatment to lower the T4 somewhat but still above the normal range).
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Hyperthyroidism
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TECHNICIAN TIPS Serum submitted for T4 should be free of hemolysis. Serum submitted for FT4 ED should be free of hemolysis and lipemia; a fasted sample is recommended.
SUGGESTED READING Feldman EC, Nelson RW: Feline hyperthyroid-ism (thyrotoxicosis). In Feldman EC, Nelson RW, editors: Canine and feline endocrinology and reproduction. Philadelphia, 2004, WB Saunders, pp 152–218. Mooney CT: Hyperthyroidism. In Ettinger SJ, Feldman EC, editors: Textbook of veterinary internal medicine. St Louis, 2005, Elsevier, pp 1544–1560. Trepanier LA: Pharmacologic management of feline hyperthyroidism. Vet Clin Small Anim Pract 37:775–788, 2007. AUTHOR: KRISTI L. GRAHAM EDITOR: SHERRI IHLE
25-09-2011 21:59
Hyperparathyroidism, Primary
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Hyperparathyroidism, Primary BASIC INFORMATION DEFINITION Primary hyperparathyroidism (PHPTH) is an uncommon disease of dogs caused by increased synthesis and secretion of parathyroid hormone (PTH). The source of increased PTH is autonomously functioning parathyroid cells due to parathyroid adenoma, hyperplasia, or carcinoma. For secondary causes of hyperparathyroidism, see pp. 976 and p. 770.
EPIDEMIOLOGY SPECIES, AGE, SEX Older dogs predominantly; no gender predilection Rare in cats. Typically older cats are affected. GENETICS & BREED PREDISPOSITION Any breed Keeshonden overrepresented. In Keeshonden, PHPTH is heritable (autosomal dominant). A genetic test is available to determine if a Keeshond patient has the affected form of the gene. Hereditary neonatal PHPTH has been reported in two German shepherd dogs.
CLINICAL PRESENTATION HISTORY/CHIEF COMPLAINT Polyuria/polydipsia (≈50% dogs; ≈10% cats) Lower urinary tract signs (caused by infection or cystic calculi) including pollakiuria, stranguria, and hematuria (≈50% of dogs) Weakness, lethargy (≈40-50% of dogs and cats) Inappetence (≈25-30% of dogs; ≈40% of cats), vomiting (≈10% of dogs; ≈40% of cats) Some (≈30%) affected dogs have no clinical signs; hypercalcemia is an incidental finding. PHYSICAL EXAM FINDINGS Physical examination is typically unremarkable. A parathyroid mass is not usually palpable in dogs. Parathyroid masses may be palpable in the ventral neck of cats.
ETIOLOGY AND PATHOPHYSIOLOGY PHPTH is most often due to a solitary parathyroid adenoma. Less common causes include hyperplasia of one or more glands or (rarely) parathyroid carcinoma. In normal animals, serum PTH concentration is controlled by ionized calcium via negative feedback. In PHPTH, the gland(s) function autonomously, and feedback inhibition is lost. Increased serum PTH concentrations cause hypercalcemia and hypophosphatemia. Clinical signs are due to hypercalcemia (see p. 553).
DIAGNOSIS DIAGNOSTIC OVERVIEW Concurrent hypercalcemia and low to low-normal serum phosphorus concentration suggest the possibility of PHPTH; however, these findings are also characteristic of humoral hypercalcemia of malignancy, a far more common disorder. The presence of cystic calculi and/or the absence of other historical or physical signs further increase suspicion for PHPTH. One or more parathyroid masses may be visible with ultrasonography; failure to visualize a parathyroid mass does not rule out the diagnosis.
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Hyperparathyroidism, Primary
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The diagnosis is established by measuring concurrent serum ionized calcium and PTH concentrations.
DIFFERENTIAL DIAGNOSIS Hypercalcemia (see p. 553)
INITIAL DATABASE CBC, serum biochemical profile, urinalysis, urine culture: hypercalcemia, low or low-normal phosphorus concentration, and isosthenuria are typical. Urinary tract infection is relatively common. Confirm hypercalcemia by repeating the test on a new sample and/or measure serum ionized calcium concentration. Abdominal radiographs: possible cystic calculi Other tests to rule out more common of causes of hypercalcemia, particularly hypercalcemia of malignancy, may include thoracic and abdominal radiographs, abdominal ultrasound, aspiration of lymph nodes and/or bone marrow, and/or serum parathyroid hormone-related protein (PTHrP) concentration.
ADVANCED OR CONFIRMATORY TESTING Concurrent serum ionized calcium and PTH concentrations: A serum PTH concentration within the reference range is inappropriate with concurrent increased ionized calcium concentration; thus in a patient with increased ionized calcium, a serum PTH concentration that is either high or within the reference limits supports a diagnosis of PHPTH. Elevated PTH: ≈one-fourth of cases PTH within reference range: ≈three-fourths of cases; of these, over half reported in the lower half of the reference range. Ultrasonography of the neck to evaluate the parathyroid glands requires an experienced ultrasonographer and sensitive ultrasound equipment. Visualization of an enlarged parathyroid gland(s) in conjunction with compatible serum ionized calcium and PTH concentrations strongly supports the diagnosis of PHPTH. Diagnosis is confirmed by exploratory surgery of the neck or by response to ablation therapy.
TREATMENT TREATMENT OVERVIEW Goals of treatment are to remove or ablate affected parathyroid gland(s) and monitor/treat for postoperative hypocalcemia. Refenal is indicated if the attending clinician is unfamiliar with thyroid/parathyroid evaluation and surgery, or if 24-hour care and in-house serum calcium monitoring cannot be provided during the immediate postprocedural period. Treat urinary tract infections and remove cystic calculi.
ACUTE GENERAL TREATMENT +/-Nonspecific treatment of hypercalcemia (see p. 553) while awaiting a definitive diagnosis or surgery (see p. 553). Contrary to patients with other causes of hypercalcemia, animals with PHPTH rarely require treatment for hypercalcemia. Surgical exploration of the neck, with removal of the affected parathyroid gland(s). Most often a solitary parathyroid mass is easily identified and removed. Occasionally evaluation/identification of affected glands can be difficult. In rare instances, removal of all four parathyroid glands and both thyroid glands is considered. Newer therapies (percutaneous ultrasound-guided ethanol ablation or radiofrequency heat ablation) are effective and less invasive than surgery but technically challenging and still require general anesthesia (see p. 1263).
CHRONIC TREATMENT Surgical or ablation therapy is curative in most patients, so chronic therapy is not required. If all four parathyroid glands are removed, lifelong vitamin D and thyroid hormone replacement are indicated (see pp. 580 and 588).
POSSIBLE COMPLICATIONS The most important complication is postprocedural hypocalcemia, which may occur with parathyroidectomy or ablation. Unaffected glands often atrophy with prolonged increased serum PTH concentrations. After removal of the affected gland(s), serum PTH and calcium may decline more rapidly than normal glands can recover. Hospitalization is recommended for at least 5 days after surgery to minimize physical activity, monitor for signs of hypocalcemia, and monitor serum calcium concentrations (q 12-24 h). Treatment for hypocalcemia (vitamin D +/-calcium) must be individualized. The goal of therapy is to keep the serum calcium
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Hyperparathyroidism, Primary
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concentration in the slightly low/low-normal range (8–9.5 mg/dL; 2-2.4 mmol/L) to prevent clinical signs of hypocalcemia while stimulating recovery of function in atrophied parathyroid glands (see p. 576 for vitamin D dosage). In general, if serum calcium concentration 25% in 1 day), or if clinical signs of hypocalcemia occur. If pretreatment serum calcium concentration >14 mg/dL (3.5 mmol/L), prophylactic treatment with vitamin D and calcium is begun the morning of surgery. If pretreatment serum calcium concentration >18 mg/dL (4.5 mmol/L), prophylactic treatment is begun 36 hours before surgery. If only 1-3 parathyroid glands were removed, vitamin D treatment can be tapered over 3-6 months based on serum calcium levels. Additional complications following ultrasound-guided heat or ethanol ablation occur uncommonly and include cough, voice change, and Horner's syndrome.
RECOMMENDED MONITORING Although rare, PHPTH recurrences may be observed even longer than 12 months after successful treatment; evaluation of serum calcium is recommended every 3-6 months.
PROGNOSIS AND OUTCOME Prognosis is excellent following successful surgery or ablation.
PEARLS & CONSIDERATIONS COMMENTS Renal failure and associated azotemia occur uncommonly with PHPTH. A normal serum PTH level is consistent with PHPTH when there is concurrent hypercalcemia, because it should be low in response to calcium elevations.
TECHNICIAN TIP Postoperative (parathyroid ablation/removal) patients should be monitored for the first signs of hypocalcemia (muscle fasciculations/twitching, stiff gait, eventually seizures) as immediate grounds for measuring serum calcium level.
SUGGESTED READING Feldman EC, Hoar BH, Pollard R, et al: Pre-treatment clinical and laboratory findings in dogs with primary hyperparathyroidism: 210 cases (1987-2004). J Am Vet Med Assoc 227:756–761, 2005. Rasor L, Pollard R, Feldman EC: Retrospective evaluation of three treatment methods for primary hyperparathyroidism in dogs. J Am Anim Hosp Assoc 43:70–77, 2007. Goldstein RE, Atwater DZ, Cazolli DM, et al: Inheritance, mode of inheritance, and candidate genes for primary hyperparathyroid-ism in Keeshonden. J Vet Intern Med 21:199–203, 2007. AUTHOR: CARY L. M. BASSETT EDITOR: SHERRI IHLE
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Hypernatremia
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Hypernatremia BASIC INFORMATION DEFINITION A serum sodium concentration >158 mEq/L in dogs or >165 mEq/L in cats, which represents a deficit of water in relation to the body's sodium stores. Hypernatremia can result from a net water loss or a hypertonic sodium gain.
EPIDEMIOLOGY SPECIES, AGE, SEX Dogs and cats of any age and either sex GENETICS & BREED PREDISPOSITION Primary hypodipsia in miniature schnauzers RISK FACTORS Inadequate access to water, fever, high ambient temperature, altered mental status
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES Pure water deficit: a net water loss in the absence of sodium deficit; majority of water loss is from the intracellular fluid compartment Hypotonic fluid loss: water loss along with sodium loss; most common form encountered in veterinary medicine Impermeant solute gain HISTORY, CHIEF COMPLAINT Often discovered incidentally When present, signs of hypernatremia largely reflect central nervous system dysfunction. Severity of signs correlates positively with the degree of hypernatremia and rapidity of onset. PHYSICAL EXAM FINDINGS Primarily neurologic signs: seen when plasma sodium is >170 mEq/L. Signs are due to movement of water out of brain cells. Tachypnea, muscular weakness, restlessness, ataxia, seizure, coma. Polydipsia may occur initially but dissipates as disease progresses. With hypotonic fluid loss, signs of volume depletion (hypotension, dehydration) may be present. With impermeant solute gain (rare), signs of volume overload (overhydration: serous nasal discharge, dyspnea from pulmonary edema) may be present. Other findings depend on underlying condition.
ETIOLOGY AND PATHOPHYSIOLOGY Pure water deficit: a net water loss from the body in the absence of sodium deficit; majority of water loss is from the intracellular fluid compartment. Causes include: Unreplaced insensible losses Hypodipsia: primary hypodipsia in miniature schnauzers Neurogenic (central) diabetes insipidus: posttraumatic, neoplastic, idiopathic, meningitis, encephalitis, hypoxic or ischemic encephalopathy Nephrogenic diabetes insipidus: renal disease, hypercalcemia, hypokalemia Hypotonic fluid loss: water loss along with some degree of sodium loss. Causes include: Renal: loop diuretics, osmotic diuretics, postobstructive diuresis
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Hypernatremia
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Polyuric phase of acute tubular necrosis, intrinsic renal disease Gastrointestinal: vomiting, diarrhea, osmotic cathartics Cutaneous: burns Impermeant solute gain. Causes include: Administration of hypertonic sodium bicarbonate, sodium chloride, or hypertonic fluid Ingestion of table salt or salt water Hyperaldosteronism or hyperadrenocorticism
DIAGNOSIS DIFFERENTIAL DIAGNOSIS See Etiology and Pathophysiology above.
INITIAL DATABASE CBC, serum biochemistry profile, urinalysis. By definition, identifies hypernatremia. Provides further information regarding possible underlying causes (e.g., renal parameters) Serum osmolality (calculated or measured) Elevated with hypernatremia of any cause; sodium is the main determinant of serum osmolality. Serial measurement possible for monitoring response to treatment Advantage of measured osmolality over calculated osmolality or serum sodium measurement alone: measurement of otherwise undetected high-osmolality molecules (e.g., ethylene glycol)
ADVANCED OR CONFIRMATORY TESTING As dictated by history, physical exam findings, and preliminary tests. May include adrenocorticotropic hormone stimulation test, thyroid profile, imaging studies of the brain.
TREATMENT TREATMENT OVERVIEW Replace water and electrolytes, restore effective circulating volume, and treat underlying cause. Rate of correction depends on whether hypernatremia was acute in onset (began within the previous 24 hours, as with recent administration of hypertonic saline) or chronic or unknown in time of onset (vast majority; hypernatremia is known or suspected to have begun >24 hours earlier, as with most naturally occurring hypernatremia). Acute: replace at a rate such that the decrease in serum sodium does not exceed 1 mEq/L/h and does not exceed 24 mEq/L/day Chronic or unknown: replace at a rate such that the decrease in serum sodium does not exceed 0.5 mEq/L/h and does not exceed 12 mEq/L/day The cornerstone of successful treatment is frequent monitoring of the patient's mentation and serum sodium concentration.
ACUTE GENERAL TREATMENT Pure water loss: calculate water deficit. Replace the deficit over 24-48 hours with 5% dextrose in water, not exceeding limit (see Pearls and Considerations below). Water deficit (Liters) = body weight (kg) × 0.6 × ([present serum Na/desired serum Na]-1). Administer calculated water deficit over the recommended time frame for acute or chronic hypernatremia. Total body water is normally 60% of body weight. This value (0.6 in the equation) can be increased in pediatric/neonates or can be decreased in cachectic animals. Hypotonic fluid loss: replace with a limited amount of isotonic crystalloids to improve hemodynamic parameters. Once improved/stabilized, switch to a hypotonic solution and administer/titrate based on monitoring, not exceeding limit. Gain of impermeant solute: 5% dextrose diuresis and administer/titrate based on monitoring, not exceeding limit (see Pearls and Considerations below). Persistent hypernatremia despite fluid therapy adjustments: Central diabetes insipidus: DDAVP, 1 mcg/kg SQ q 8-12 h; or aqueous vasopressin, 1-2 U/cat or 3-5 U/dog q 24-48 h (see p. 296) Nephrogenic diabetes insipidus: thiazide diuretics (see p. 296)
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CHRONIC TREATMENT Remove offending drugs. Treat underlying condition.
POSSIBLE COMPLICATIONS Rapid correction of hypernatremia can lead to cerebral edema as excess water moves into brain cells. The signs of cerebral edema may not be seen for 2-3 days post correction of hypernatremia. Edema is more likely to occur in patients with prolonged hyperosmolality and aggressive hypotonic fluid replacement.
RECOMMENDED MONITORING Check serum electrolytes q 4-8 h.
PROGNOSIS AND OUTCOME Mortality varies according to the severity of hypernatremia, rapidity of onset, and underlying condition
PEARLS & CONSIDERATIONS COMMENTS When correcting hypernatremia, the rate of decrease of blood/serum sodium concentration must not exceed 0.5 mEq/L/h. Decreasing sodium concentration at a rate >0.5 mEq/L/h risks complications such as cerebral edema. Exception: up to 1 mEq/L/h is possible if hypernatremia is known to have begun within 24 hours (e.g., hypertonic saline administration).
PREVENTION Ensure adequate drinking water access. prevent excessive drinking of salt water or consumption of pure salt. Do not administer table salt as an emetic in cases of toxin ingestion. Use hydrogen peroxide or syrup of ipecac instead.
SUGGESTED READING DiBartola SP: Disorders of sodium and water: hypernatremia and hyponatremia. In diBar-tola SP, de Morais HSA, eds: Fluid therapy in small animal practice, ed 3, St Louis, 2006, Saunders Elsevier, pp 47–79. Temo K, et al: Hypernatremia in critically ill cats: pathophysiology. Compend Contin Educ Pract Vet 26:422–433, 2004. Temo K, et al: Hypernatremia in critically ill cats: evaluation and treatment. Compend Contin Educ Pract Vet 26:434–445, 2004. AUTHORS: MELISSA MARSHALL, ANN MARIE MANNING EDITOR: ETIENNE CÔTÉ
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Hyperlipidemia
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Hyperlipidemia BASIC INFORMATION DEFINITION Increased fasting blood cholesterol and/or triglyceride (TG) concentrations; a well-recognized (dogs) to uncommon (cats) disorder in small animals.
SYNONYMS Hyperlipoproteinemia, lipemia
EPIDEMIOLOGY SPECIES, AGE, SEX Primary: middle-aged/older (dogs); variable age of onset (cats) Secondary: varies with primary cause GENETICS & BREED PREDISPOSITION Idiopathic hypertriglyceridemia: miniature schnauzers, Burmese cats Idiopathic hypercholesterolemia: Doberman pinschers, rottweilers, briards, rough collies Feline familial hyperlipidemia: autosomal recessive trait in domestic short-haired cats RISK FACTORS Obesity (dogs) Drugs: glucocorticoids, phenobarbital (dogs), megestrol acetate (cats) High-fat diets or parenteral nutrition Hypothyroidism Hyperadrenocorticism Pancreatitis Diabetes mellitus Protein-losing nephropathy Cholestasis ASSOCIATED CONDITIONS & DISORDERS Pancreatitis Vacuolar hepatopathy Gallbladder mucocele Seizures Xanthomas (intraocular or cutaneous nodules/plaques composed of lipid-containing histiocytes) Peripheral neuropathy Behavior changes
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES Primary hyperlipidemia: Dogs: Idiopathic hyperlipidemia/idiopathic hypertriglyceridemia Increased very low-density lipoproteins (VLDL) ± Increased chylomicra (CM) ± Mild hypercholesterolemia
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Idiopathic hyperchylomicronemia Increased TG and CM Idiopathic hypercholesterolemia Increased low-density lipoproteins (LDL) Cats: Familial hyperlipidemia/hyperchylomicronemia: Increased CM and VLDL Inactive lipoprotein lipase Secondary Hyperlipidemia: see Risk Factors above HISTORY, CHIEF COMPLAINT Clinical signs, when present, are the result of hypertriglyceridemia; hypercholesterolemia virtually never causes clinical signs. Dogs: vomiting, diarrhea, abdominal discomfort (pancreatitis), seizures, anorexia, lethargy Cats: cutaneous/subcutaneous masses (xanthomas), lameness (neuropathy) PHYSICAL EXAM FINDINGS Hypertriglyceridemia Dogs: signs of abdominal discomfort, hepatosplenomegaly, lipemia retinalis, lipemic aqueous humor, intraocular xanthogranuloma Cats: xanthomas, decreased reflexes (peripheral neuropathy), pale mucous membranes, lipemia retinalis, lipid keratopathy, lipemic aqueous humor Hypercholesterolemia Dogs: lipemia retinalis, lipid keratopathy, arcus lipoides corneae
ETIOLOGY AND PATHOPHYSIOLOGY Lipoproteins Lipids (TG and cholesterol) do not circulate free in circulation; rather, they are complexed in varying proportions as circulating particles called lipoproteins. Four major types (listed in decreasing order of TG concentration and increasing order of cholesterol concentration in the lipoprotein particle): CM VLDL Low-density lipoproteins High-density lipoproteins Hyperlipidemia From excessive dietary lipid, excessive endogenous lipid production/mobilization, and/or impaired lipid clearance from blood. Types: Postprandial hyperlipidemia: CM in circulation 2-10 hours after fatty meal Primary hyperlipidemia: Inborn error in lipoprotein metabolism Lack of lipoprotein lipase activity Absence of surface apolipo-proteins (CII) Secondary hyperlipidemia: Underlying disease (see Risk Factors above) causing altered lipid metabolism Secondary hyperlipidemias are more common than primary.
DIAGNOSIS DIAGNOSTIC OVERVIEW Lipemic serum suggests hypertriglyceridemia; hypercholesterolemia alone does not cause serum to appear lipemic. Persistent increases in triglycerides or cholesterol after a 12-hour fast indicate disease and should prompt investigation for secondary causes of hyperlipidemia.
DIFFERENTIAL DIAGNOSIS Postprandial hyperlipidemia
INITIAL DATABASE
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CBC, serum biochemical profile (including serum cholesterol and TG concentrations), urinalysis: Perform after > 12-hour fast Identify causes of secondary hyperlipidemia Subsequently, consider: Tests for hypothyroidism (see p. 588) Tests for hyperadrenocorticism (see p. 548) Urine protein/creatinine ratio Abdominal ultrasound Serum trypsinlike immunoreactivity Pre- and postprandial bile acids
ADVANCED OR CONFIRMATORY TESTING If a cause of secondary hyperlipidemia is not found, additional tests may help define the primary hyperlipidemia. Chylomicron (CM) test: lipemic serum is left undisturbed for 12 hours at 4°C. If CM are present they will form a surface “cream layer” over a clear infranatant of serum, suggesting a disorder of CM metabolism such as idiopathic hyperchylomicronemia. A nonfasting sample is an important differential. If the sample remains turbid, VLDL retention (and therefore a secondary hyperlipidemia such as that due to diabetes mellitus) is likely. Formation of a “cream layer” over turbid serum suggests a combined disorder. Lipoprotein electrophoresis, ultracentrifugation, and precipitation tests can be useful but are not routinely available. Lipoprotein lipase activity can be assessed by measuring TG (± lipoprotein) concentrations before and 15 minutes after heparin (dog: 90 IU/kg IV; cat: 40 IU/kg IV) administration. If no change, lipoprotein lipase inactivity is suspected.
TREATMENT TREATMENT OVERVIEW Treatment primarily consists of management of secondary causes and nutritional therapy. Medications are reserved for unresponsive severe cases of hyperlipidemia (TG > 500 mg/dL or cholesterol > 800 mg/dL). Goal of treatment is to reduce fasting TG or cholesterol concentrations to < 500 mg/dL. Treatment is lifelong.
ACUTE GENERAL TREATMENT Treat underlying diseases.
CHRONIC TREATMENT Hypertriglyceridemia Dietary management should be the mainstay of treatment (see Nutrition, below) Menhaden fish oils: 200-330 mg/kg/d PO (dogs); or Gemfibrozil: 200 mg/kg PO q 24 h (dogs); 7.5-10 mg/kg PO q 12 h (cats); or Niacin 100 mg PO q 24 h (dogs) Hypercholesterolemia A primary cause is often (almost always) present, and its control resolves the hypercholesterolemia. Otherwise, dietary management should be the mainstay of treatment (see Nutrition, below). Cholestyramine: 1-2 g PO q 12 h (dogs); or Lovastatin: 10-20 mg PO q 24 h (dogs)
NUTRITION/DIET Hypertriglyceridemia Dietary fat restriction (dog: 7.0 mEq/L) can have either normal ECG patterns or show minimal changes that would be expected only at lower serum levels. Some patients with serum potassium levels 1.4:1. In rare cases, injuries to gastrointestinal tract or biliary tract are undetectable for several days.
PREVENTION Keep cats housed indoors. Walk dogs on a leash at all times. Frequently check fences and other enclosure systems for damage. Do not allow dogs to sleep or lie in driveways.
SUGGESTED READING Rochlitz I: Clinical study of cats injured and killed in road traffic accidents in Cambridgeshire. J Small Anim Pract 45(8):390– 394, 2004. Day T: Shock syndromes in veterinary medicine. In DiBartola S, editor: Fluid therapy in small animal practice. Philadelphia, 2000, WB Saunders, pp 428–447. AUTHOR: JENNIFER L. HOLM EDITOR: ELIZABETH ROZANSKI
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Histoplasmosis
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Histoplasmosis BASIC INFORMATION DEFINITION A systemic fungal disease caused by the soil-dwelling dimorphic fungus, Histoplasma capsulatum; affects both companion animals and humans.
EPIDEMIOLOGY SPECIES, AGE, SEX Dogs and cats are equally likely to develop histoplasmosis once exposed. Young adult (2 years old. Only dogs receiving “excellent” or “good” evaluations should be bred. The PennHIP method is an objective measure of hip laxity performed as early as 16 weeks of age. Breeding just dogs that are in the top 50% (dogs with less joint laxity) of the breed will help to decrease laxity within the breed and decrease the incidence of hip dysplasia for that breed. Avoid high-energy diets in young, rapidly growing large-dog breeds. Based on equivalent human medical approaches, low-impact activities such as walking, swimming, and underwater treadmill therapy under the guidance of a trained canine rehabilitation specialist may provide benefit to affected individuals by increasing muscle mass and subsequently coxofemoral joint congruity (see p. 1329).
CLIENT EDUCATION Knowledge and careful screening of genetic history of the siblings and parents of potential pets Early sterilization of affected dogs and dogs treated with TPO or JPS Minimize the phenotypic expression of the disease in affected dogs through diet, low-impact exercise (see Prevention), and medical management.
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Hip Dysplasia
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SUGGESTED READING Schulz: Hip dysplasia. In Fossum TW, editor: Small animal surgery, ed 3, St Louis, 2007, Mosby, pp 1233–1246. AUTHORS: MATHIEU M. GLASSMAN, SPENCER A. JOHNSTON EDITOR: JOSEPH HARARI 1ST EDITION AUTHORS: JAMES BOULAY, BARBARA GORES
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High-Rise Syndrome
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High-Rise Syndrome BASIC INFORMATION DEFINITION A collection of traumatic injuries sustained by an animal that falls from a substantial height. The term was originally coined in reference to cats, associated with a triad of injuries (epistaxis, hard palate fracture and pneumothorax) sustained by falls from a height of two or more stories. The orofacial aspects of high-rise syndrome are discussed in detail separately (see online chapter: High-Rise Syndrome, Craniofacial).
SYNONYMS High-flyer syndrome, jumper's syndrome (both in humans)
EPIDEMIOLOGY SPECIES, AGE, SEX Predominantly young animals; cats less than 3 years old (reported age range 2.5 months to 20 years) and dogs less than 5 years old (range 2.5 months to 13 years 8 months). RISK FACTORS Urban areas Tall buildings, particularly high-rise apartment buildings Open windows and balcony doors; access to roof tops GEOGRAPHY AND SEASONALITY Falls occur more frequently in summer, followed by autumn, when windows and balcony doors are open, and outdoor play is a factor.
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT A witnessed (most commonly in dogs) or suspected (more common in cats) fall from a height such as a window sill, balcony, or roof PHYSICAL EXAM FINDINGS A substantial number of animals present in a life-threatening condition requiring emergency treatment (7.8%-57.6% of cats and 44% of dogs) Clinical signs consistent with shock/cardiovascular instability (seen in 10%-24% of cats; exact incidence not known in dogs) including: Tachycardia or bradycardia Poor pulse quality and/or low blood pressure Pale mucous membranes Prolonged capillary refill time Decreased core body temperature Respiratory distress (e.g. dyspnea, tachypnea, paradoxical respiration, cyanosis, and open-mouth breathing) due to pulmonary contusion, pneumothorax, rib fractures, diaphragmatic hernia and/or pain Facial injuries (see p. 531) Orthopedic injuries: Limb fractures (39%-61% of cats; 80% of dogs) Femoral and tibial fractures most common in cats Dogs that jump tend to land on their thoracic limbs, resulting in a higher percentage of forelimb injuries, whereas dogs that fall accidentally are reported to land predominantly on their pelvic limbs, resulting in a higher percentage of hindlimb injuries. Open fractures occur commonly. Pelvic fractures
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Luxations (e.g. coxofemoral, elbow and tibiotarsal) Ligamentous injuries: Rupture (e.g., cruciate ligament, Achilles tendon) Carpal hyperextension (more prevalent in dogs than cats) Evidence of visceral injury due to blunt abdominal trauma: Uroabdomen secondary to urinary tract rupture (most commonly bladder) Hematuria secondary to urinary bladder contusion Hemoabdomen (may be mild and self-limiting or require surgical intervention [e.g., secondary to splenic rupture]) Abdominal wall rupture/herniation Prepubic tendon rupture Spinal injuries (e.g., fracture, luxation or traumatic intervertebral disk herniation resulting in caudal paresis/plegia, tetraparesis or brachial palsy (due to brachial plexus avulsion) Penetrating abdominal or thoracic wounds secondary to impalement. May be accompanied by subcutaneous emphysema, abdominal wall herniation, or flail chest. Reported predominantly in cats falling onto spiked wrought iron fences. Evidence of head trauma/traumatic brain injury including: Cranial neurologic abnormalities (such as anisocoria, Horner's syndrome) Depressed level of consciousness Soft-tissue abrasions
ETIOLOGY AND PATHOPHYSIOLOGY Jumping during play or while chasing a squirrel, bird, insect, other animal (e.g., dogs chasing cats or other dogs), intruders, owners driving away in the street below or objects thrown while playing. Most common in dogs. Slipping while walking on the edge of a balcony railing or window, including icy ledges; suspected to be most common in cats. Thunderstorms or fireworks may incite a dog to jump if phobic. Range of documented heights fallen by cats (1-32 stories) and humans (1-20 stories) is high compared to that by dogs (1-6 stories) Injuries result from extreme vertical deceleration trauma. Impact surface is usually concrete; less commonly grass, rocks, snow, rubble, or dirt. Rarely impalement on metal railings. Objects encountered during the fall (e.g., potted plants on balcony railings, metal structures for hanging laundry, fire escapes, awnings, and trees) may result in additional injury or could help reduce injury by breaking the fall. Height of the fall is thought to have the greatest effect on injury pattern. In cats, severity of injury has been reported to increase up to seven stories (each story is 12-15 feet), after which further increases in height do not exacerbate injury severity; however, not all case series are consistent with this theory. Cats are better able to withstand free falls than dogs or humans due to their: Highly developed vestibular system and righting reflex resulting in a unique ability to fall in a feet-first position from heights up to −100 feet, thereby minimizing postural torque, tumbling and rotation Rapid achievement of terminal velocity (60 mph after −5 stories) such that their vestibular system is no longer stimulated by acceleration, reflex limb extension resolves, and the cat adopts a horizontal position, favoring a wider distribution of energy on impact Dogs experience a higher proportion of limb injuries, suggested to be associated with the greater size and strength of their limbs absorbing more of the impact before their trunk. Spinal injuries increase with increasing height of fall, as dogs have a tendency to tumble, landing on their back or in a vertical position.
DIAGNOSIS DIAGNOSTIC OVERVIEW High-rise syndrome is usually diagnosed via history and physical examination. Following stabilization, thorough orthopedic and neurologic examination is vital. Diagnostic imaging (radiography, ultrasonography and/or CT) is then used to further characterize injury.
DIFFERENTIAL DIAGNOSIS Hit-by-car trauma Hit by a blunt object Kicked by an ungulate animal Fights with other animals Foreign body penetration Gunshot trauma Malicious injury
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INITIAL DATABASE Orthopedic and neurologic examination (following stabilization if necessary) CBC, serum biochemistry panel, urinalysis Abdominal and thoracic ultrasound (abdominal and thoracic focused assessment sonography for trauma [AFAST and TFAST, respectively]; description of the procedures has been published for dogs but can be applied in cats if tolerated). Radiographs of thorax, abdomen, spine, and limbs Abdominocentesis and fluid analysis Full mouth (intraoral) dental radiographs Radiographs of the head, temporomandibular joints, and bullae
ADVANCED OR CONFIRMATORY TESTING CT of head and spine
TREATMENT TREATMENT OVERVIEW Stabilize animal; priorities are to resolve/improve dyspnea and shock and minimize stress (especially in cats). Orthopedic manipulations, radiography, or surgical procedures may initially need to be delayed, with adjunctive pain control, if the patient is systemically unstable at the time of presentation.
ACUTE GENERAL TREATMENT Management of respiratory distress: Oxygen supplementation Thoracocentesis if respiratory pattern suggestive of pneumothorax Fluid resuscitation from shock: Obtain IV access in an uninjured limb. Administer isotonic crystalloid ± colloid fluids to effect. Start with 20 mL/kg crystalloid bolus in dogs or 10 mL/kg in cats, and titrate to effect up to 80-90 mL/kg/h in dogs and 50-60 mL/kg/h in cats. Consider judicious fluid use, particularly in animals with evidence of pulmonary contusions. Consider addition of colloids if cardiovascular instability persists; start with a 5 mL/kg bolus in dogs and 1-2 mL/kg in cats, and titrate to effect up to 20 mL/kg in dogs and 10 mL/kg in cats. Consider hypertonic saline (3-5 mL/kg once) ± hetastarch if evidence of traumatic brain injury. Blood product transfusion (whole blood or packed red blood cells) may be necessary if severe hemorrhage has occurred. Provision of appropriate analgesia (opioid analgesia is recommended initially; nonsteroidal antiinflammatory drugs may be added following patient stabilization and assessment of suitability). Broad-spectrum antibiotic coverage in animals with penetrating body cavity wounds prior to exploratory surgery Further treatment, if sedation or general anesthesia is required, depends on the successful outcome of this initial stabilization. Surgical treatment of skeletal injuries Exploratory thoracotomy or celiotomy in patients with penetrating thoracic or abdominal wounds, respectively Oral/dental treatment (see p. 531)
CHRONIC TREATMENT If response to emergency treatment is poor, visceral injury (abdominal and thoracic) with possible hemorrhage should be considered and pursued diagnostically, even in the absence of penetrating body cavity wounds as blunt trauma can occur. Chronic oronasal communication: medially positioned double flaps with releasing incisions along dental arch or overlapping double flaps. Temporomandibular joint injury (chronic luxation or ankylosis): unilateral or bilateral condylectomy. Extraction or endodontic therapy of teeth with pulp exposure.
NUTRITION/DIET With dental injuries, soft food is usually adequate; esophagostomy tubes are rarely necessary.
POSSIBLE COMPLICATIONS Chronic oronasal communication
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Temporomandibular joint ankylosis in very young animals with difficulty or inability to open the mouth Chylothorax
RECOMMENDED MONITORING In-patient monitoring until discharge Reexamination and removal of skin sutures in 2 weeks Removal of cerclage wire around mandibles in 4-5 weeks Routine follow-up and radiography to ensure fracture healing following orthopedic surgery
PROGNOSIS AND OUTCOME Good prognosis for survival for ∼90% of cats and dogs Euthanasia due to client financial constraints is reported, given the high percentage of animals requiring surgery. Death, excluding euthanasia, is generally due to shock, stress, and respiratory distress due to thoracic trauma. Most deaths occur within 24-36 hours of admission or in the immediate postoperative period It is suspected that most dogs falling >6 stories do not survive and hence are not brought to the hospital and assessed in case series
PEARLS & CONSIDERATIONS COMMENTS Number and severity of injuries increase with increasing height of fall; it has been reported that the association between injuries and height of fall follows a curvilinear pattern.
CLIENT EDUCATION Close windows and balcony doors in the presence of animals
SUGGESTED READING Gordon LE, et al: High-rise syndrome in dogs: 81 cases (1985-1991). J Am Vet Med Assoc 202:118, 1993. Papazoglou LG, et al: High-rise syndrome in cats: 207 cases (1988-1998). Aust Vet Pract 31:98, 2001. AUTHOR: CLAIRE R. SHARP EDITOR: ELIZABETH ROZANSKI
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High-Rise Syndrome, Craniofacial
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High-Rise Syndrome, Craniofacial BASIC INFORMATION DEFINITION Triad of craniofacial, thoracic, and limb injuries sustained by an animal that falls from a height of one or more stories. The term was originally coined in reference to cats, associated primarily with falls from a height of two or more stories. For systemic effects of high-rise syndrome, see 529.
SYNONYMS High-flyer syndrome (in humans), jumper's syndrome, extreme deceleration trauma
EPIDEMIOLOGY SPECIES, AGE, SEX Predominantly affects cats 5 years but continue to be free of clinical signs while receiving decoquinate.
PROGNOSIS AND OUTCOME Without treatment, American hepatozoonosis is usually fatal within several months. With antiprotozoal combination therapy alone, relapses occur requiring repeated therapy. Relapses become more frequent and refractory to treatment. Death usually occurs within 1 year of the initial diagnosis. Long-term cure (>5 years) has been achieved with combination therapy followed by long-term decoquinate therapy.
PEARLS & CONSIDERATIONS PREVENTION Effective tick control with a topical acaricide and a repellent collar is recommended.
TECHNICIAN TIPS Making a buffy coat smear may enhance the possibility of finding gametocytes. Gametocytes appear as oblong intracellular single inclusions in leukocytes (rare). Spurious hypoglycemia can occur if the blood sample is not run immediately, because WBCs can metabolize glucose in the tube.
CLIENT EDUCATION Clean matted eyes with a warm, moist towel as needed. Provide soft bedding. Bring food and water to dogs that are nonambulatory. Continue all medications for recommended duration. Stopping decoquinate too early can result in reinfestation of the dog and
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exacerbation of the disease.
SUGGESTED READING Macintire DK, Vincent-Johnson NA: Canine hepatozoonosis. In Bonagura JD, editor: Kirk’ s current veterinary therapy XIII small animal practice, Philadelphia, 2000, WB Saunders, pp 310–313. Vincent-Johnson NA: American canine hepa-tozoonosis. Vet Clin North Am Small Anim Pract 33:905–920, 2003. Ewing SA, Panciera RJ: American canine hepa-tozoonosis. Clin Microbiol Rev 26:688–697, 2003. Li Y, Wang C, Allen K, et al: Diagnosis of canine Hepatozoon spp. infection by quantitative PCR. Vet Parasitol 157:50–58, 2008. Johnson EM, Allen KE, et al: Experimental transmission of Hepatozoon americanum to rodents. Vet Parasitol 151:164–169, 2007. Johnson EM, Allen KE, et al: Infectivity of Hepatozoon americanum cystozoites for a dog. Vet Parasitol 154:148–150, 2008. Allen KE, Li Y, et al: Diversity of i species in naturally infected dogs in the southern United States. Vet Parasitol 154:220–225, 2008. AUTHOR & EDITOR: DOUGLASS K. MACINTIRE
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Hepatopathy, Copper-Associated
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Hepatopathy, Copper-Associated BASIC INFORMATION DEFINITION Accumulation of copper within hepatocytes, leading to hepatotoxicosis
EPIDEMIOLOGY SPECIES, AGE, SEX Primarily in dogs; rare in cats. Copper accumulates slowly, so clinical signs are typically not present until middle age. GENETICS & BREED PREDISPOSITION Autosomal recessive in Bedlington terriers Predisposition in dalmatians, West Highland white terriers, and Skye terriers Possible association in Doberman pinschers and Labrador retrievers Reported in other canine breeds, but it is unknown if copper accumulation is the cause or effect of hepatopathy.
CLINICAL PRESENTATION DISEASE FORM/SUBTYPES Subclinical Chronic inflammatory liver disease/cirrhosis Acute hepatic failure with hemolytic anemia (rare) HISTORY, CHIEF COMPLAINT, AND PHYSICAL EXAM FINDINGS: Patients usually present with features of chronic hepatic disease such as lethargy, vomiting, abdominal distention, or encephalopathy (see p. 212) or less commonly with acute hepatic failure (see p. 503) and hemolytic anemia (see p. 71).
ETIOLOGY AND PATHOPHYSIOLOGY Copper homeostasis is maintained by biliary excretion of excess copper. Copper is absorbed from ingesta in the small intestine and extracted by hepatocytes. Chaperoned around the hepatocyte by a number of proteins before being either released into the serum or excreted in bile. A small amount is stored in lysosomes. Abnormal hepatic copper accumulation occurs because of primary inborn error of metabolism or secondary to acquired cholestatic liver disease. In Bedlingtons, copper accumulation in lysosomes is due to a genetic defect in the COMMD1 gene, leading to excessive copper binding by an abnormal metallothionein (a protein required for the final stages of copper excretion into the bile). When the storage capacity of the lysosomes is exceeded, copper breaks out into the cytoplasm, where it is toxic. Genetic basis for copper accumulation in other breeds is unknown. Excess copper damages hepatocytes by inducing the formation of free radicals. Secondary copper accumulation is due to a generalized impairment in biliary excretion (i.e., cholestasis).
DIAGNOSIS DIAGNOSTIC OVERVIEW The disorder may be suspected in two contexts: either as part of any cholestatic liver disease (detected as part of evaluation of liver biopsy specimens) or in cases where copper accumulation is the dominant feature of hepatopathy in a dog (e.g., Bedlington terrier) with or without overt clinical signs. Definitive quantification of hepatic copper content, which carries important treatment implications, requires a liver biopsy.
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Hepatopathy, Copper-Associated
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DIFFERENTIAL DIAGNOSIS Chronic: Infectious, immune, or toxic causes of inflammatory hepatic disease Hepatic neoplasia Congenital portosystemic shunts Acute: Infectious, immune, drug, or toxin-induced (zinc) hemolytic anemia Exposure to hepatotoxic drugs or environmental toxins Infectious canine hepatitis, leptospirosis
INITIAL DATABASE See pp. 503, 513, , and .
ADVANCED OR CONFIRMATORY TESTING Determination of hepatic copper concentration: Quantitative analysis on hepatic wedge or needle biopsies Qualitative analysis by rhodanine or rubeanic acid staining of histopathology specimen. Permits determination of copper distribution within the hepatic lobule. Normal hepatic copper levels from 200-400 mcg/g dry weight (DW) Secondary copper accumulation levels 2000 mcg/g dry weight suggests a primary copper abnormality. In Bedlingtons, copper levels gradually increase with age, with levels reported from 850-12,000 mcg/g DW. In West Highland white terriers, copper accumulation does not correlate as well with age (levels up to 3500 mcg/g DW reported). Lower copper levels (1000-2000 mcg/g dry weight) associated with toxicity in some Labradors and Dobermans. Histopathologic findings: In Bedlingtons, copper initially accumulates centrilobularly. Initial finding is centrilobular hepatocellular vacuolation followed by degeneration/necrosis and finally inflammation and fibrosis. Progresses to become more panlobular eventually with periportal orientation. Findings can mimic idiopathic chronic hepatitis. In secondary copper accumulation, copper staining located primarily in areas of inflammation or degeneration. Genetic test, microsatellite marker (C04107) available to screen Bedlingtons, but may miss disease in some pedigrees (5%-10% false negatives). No test for COMMD1 mutation available.
TREATMENT TREATMENT OVERVIEW Decrease hepatic copper concentration, decrease copper absorption.
ACUTE GENERAL TREATMENT Manage the complications of acute or chronic hepatic disease (see pp. 503, p. 212, and 501).
CHRONIC TREATMENT Copper chelators for initial decoppering of liver and maintenance therapy: Penicillamine (10-15 mg/kg PO q 12 h). Increases urinary copper excretion. Works slowly (removes ∼900 mcg/g per year), so copper levels take several months to years to decrease. Vomiting is a common side effect; begin at low end of dosage range and titrate upward. Trientine (10-15 mg/kg PO q 12 h). Increases urinary copper excretion and may also block intestinal uptake. Fewer side effects than penicillamine but more expensive. Give all medications on an empty stomach, and follow with a water bolus. Inhibit intestinal copper absorption, maintenance therapy. Zinc (100 mg elemental zinc PO q 12 h). Induces intestinal metallothionein, a protein that binds copper, keeping it sequestered within the enterocyte and thus preventing copper absorption. May be combined with chelators (separate administration by 2 hours). Side effects include gastritis, hemolytic anemia, and iron deficiency. Keep serum zinc levels 200 mcg/dL.
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Hepatopathy, Copper-Associated
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Reduce dietary intake of copper. Avoid shellfish, nuts, chocolate, mushrooms, and organ meats. Check water supply if not public. Copper restricted prescription diets are available. Antioxidants Induction of oxidant stress is central to copper-induced hepatic damage. Vitamin E supplementation (200-400 IU PO q 24 h) S-adenosylmethionine (20 mg/kg PO q 24 h).
RECOMMENDED MONITORING Serum liver enzymes every 4-6 months
PROGNOSIS AND OUTCOME Subclinical disease: excellent with therapy Chronic: depends on stage. Mild to moderate inflammatory disease: good. Severe inflammatory disease/cirrhosis: guarded. Acute: grave
PEARLS & CONSIDERATIONS COMMENTS All Bedlington terriers should be tested at 1 year of age by determination of hepatic copper concentration and/or genetic testing. Affected dogs should not be bred. All dogs with chronic inflammatory hepatitis, particularly West Highland white terriers, Doberman pinschers, Skye terriers, Labrador retrievers and dalmatians, should have hepatic copper analysis. If concentrations are > 1000-2000 mcg/g DW, they should be treated to decrease hepatic copper.
SUGGESTED READING Hoffmann G, Jones PG, Biourge V, et al: Dietary management of hepatic copper accumulation in Labrador Retrievers. J Vet Intern Med 23(5):957–963, 2009. Hoffmann G: Copper-associated liver diseases. Vet Clin North Am Small Anim Pract 39(3):489–511, 2009. AUTHOR: CYNTHIA R. L. WEBSTER EDITOR: KEITH P. RICHTER
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Hepatomegaly
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Hepatomegaly BASIC INFORMATION DEFINITION Liver enlargement
EPIDEMIOLOGY SPECIES, AGE, SEX Observed in both dogs and cats, more frequently in middle-aged to older animals owing to age-related prevalence of associated diseases. However, younger animals can also present with hepatomegaly (e.g., with feline infectious peritonitis [FIP], congenital veno-occlusive disease, infectious disease, lymphoma). GENETICS & BREED PREDISPOSITION Dogs: Doberman pinschers (inflammatory liver disease), cocker spaniels, Labrador retrievers, Skye terriers; Labrador retrievers (tricuspid dysplasia causing right-sided heart failure) Cats: Abyssinians (amyloidosis), Asian breeds (FIP)
CLINICAL PRESENTATION HISTORY/CHIEF COMPLAINT Depends on etiology: Can be an incidental finding Abdominal distention Polyuria, polydipsia Anorexia, lethargy/weight loss Exercise intolerance Vomiting/diarrhea Pale mucous membranes Hepatic encephalopathy Coagulopathy Cutaneous disease/hair loss/poor haircoat PHYSICAL EXAM FINDINGS Abdominal distention Palpable cranial organomegaly Ascites Icterus Concurrent hepatosplenomegaly suggests a multicentric neoplastic, passive congestive, systemic inflammatory/infectious, or anemia-inducing process, or unrelated disorders.
ETIOLOGY AND PATHOPHYSIOLOGY Hepatomegaly is caused by inflammation, infiltration, congestion/obstruction, infection, or hyperplasia of the liver.
DIAGNOSIS DIAGNOSTIC OVERVIEW The presence of an enlarged liver is noted on physical examination, radiographs, or abdominal ultrasound. The first diagnostic step
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Hepatomegaly
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consists of reviewing the history and physical examination for evidence of liver dysfunction. Benign causes of hepatomegaly are common, but hepatomegaly may be the first clue that nonspecific clinical signs are caused by liver disease. Routine blood and urine tests and abdominal ultrasonography, postprandial serum bile acid levels, and diagnostic sampling of the liver help identify cases that require treatment and follow-up.
DIFFERENTIAL DIAGNOSIS Inflammatory diseases of the liver: Cholangitis/cholangiohepatitis complex (cats) Cirrhosis (end stage usually produces microhepatica, not hepatomegaly) Abscess Neoplasia Chronic active hepatitis (idiopathic chronic hepatitis) (dogs) Canine breed-specific hepatopathies Neoplastic/cystic diseases: Lymphoma, biliary cystadenoma, bile duct carcinoma, hemangiosarcoma, metastatic neoplasia Hepatocellular carcinoma, hepatoma (enlargement of a single lobe) Malignant histiocytosis Diffuse mast cell tumor Parenchymal/biliary cysts Extrahepatic obstruction: Pancreatitis Cholelithiasis (rare in dogs and cats) Bile duct neoplasia Biliary mucocele Inspissated bile syndrome of cats Metabolic disease: Diabetes mellitus (lipid accumulation) Hepatic lipidosis (cats) Amyloidosis (Abyssinian/Chinese shar-pei) Storage disease (rare in cats and dogs) Hyperadrenocorticism (dogs/glycogen accumulation) Drugs: Glucocorticoids Phenobarbital Infectious disease (many cause hepatosplenomegaly due to systemic immune stimulation): Bacterial, rickettsial, protozoal, fungal Liver abscess (enlargement localized to a single lobe) FIP Erythrocyte parasitism (Mycoplasma baemofelts/hemobartonellosis, Babesia spp.) Immune-mediated disease (hepatosplenomegaly common secondary to systemic immune stimulation): Immune-mediated hemolytic anemia (IMHA) Immune-mediated thrombocytopenia (ITP) Systemic lupus erythematosus Vasculitis Any systemic immune-mediated disease Congestion (often associated with ascites): Right-sided heart failure Budd-Chiari syndrome/venoocclusive disease (rare) Liver lobe torsion (rare) Intoxications Benign conditions: Nodular hyperplasia (older dogs) Nodular regeneration (associated with severe liver disease) Extramedullary hematopoiesis Individual variation (pseudohepatomegaly) Radiographic differential diagnosis for hepatomegaly: Cranial abdominal mass, marked splenomegaly, ascites, dyspnea (caudal displacement of liver), youth (nonmineralized distal ribs gives false impression of liver protruding beyond costal arch)
INITIAL DATABASE CBC, chemistry profile, urinalysis, and urine culture Abdominal radiographs (most accurate assessment of liver size)
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Hepatomegaly
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Abdominal ultrasound Thoracic radiographs (cardiac structures, metastatic disease)
ADVANCED OR CONFIRMATORY TESTING Coagulation profile (prothrombin time/activated partial thromboplastin time/platelet count), buccal mucosal bleeding time Preprandial and postprandial serum bile acids Urine bile acids Serum ammonia (poor specificity/sensitivity) Liver aspirate or biopsy for histopathologic evaluation and culture (aerobic/anaerobic). See p. 1298. Copper quantification of biopsy specimen Amylase/lipase/pancreatic lipase immunoreactivity Adrenocorticotropic hormone (ACTH) stimulation, ACTH level, low-dose dexamethasone suppression test Antinuclear antibody test Infectious disease titers/PCR FIP serology Echocardiography/central venous pressure Abdominocentesis (if ascites) Abdominal CT Venography (Budd-Chiari, veno-occlusive disease) D-dimer (thromboembolic disease) Bone marrow aspirate (immune-mediated hemolytic anemia/immune-mediated thrombocytopenia, lymphoma staging)
TREATMENT TREATMENT OVERVIEW Treat specifically on the basis of an established diagnosis. Hepatomegaly is a sign, not an etiology. Suppress the disease process/manage the metabolic condition/treat any infectious or immune-mediated disease with appropriate medication or surgical intervention.
GENERAL TREATMENT Inflammatory diseases: Immunosuppressant therapy (i.e., glucocorticoids, azathioprine, cyclosporine) Antioxidant therapy (S-adenosylmethionine, silymarin, zinc, vitamin E) Immune-modulatory medications; ursodeoxycholate, metronidazole Antifibrotics: colchicine, D-penicillamine, methotrexate Antibiotics: metronidazole, amoxicillin, cephalexin, enrofloxacin Gastric protectants Vitamins: carnitine (lipidosis), vitamin C, vitamin E, zinc, vitamin K (if coagulopathy) Dietary therapy Treatment for hepatic encephalopathy: lactulose, neomycin, metronidazole Management for ascites (abdominocentesis/abdominal drainage; diuretics: spironolactone) Fluid therapy Neoplastic diseases: surgery/chemotherapy Extrahepatic obstruction: supportive care, surgery Metabolic diseases: Insulin therapy Colchicine/dimethylsulfoxide for amyloidosis Aggressive feeding (hepatic lipidosis) Lysodren/trilostane/ketoconazole for hyperadrenocorticism Infectious diseases: Treatment depends on the organism Immune-mediated diseases: Immunosuppressant therapy/depends on the disorder Congestion: Treatment depends on the cause
RECOMMENDED MONITORING Dictated by the disease process. Examples include liver enzyme profile 1-2 weeks post diagnosis, then monthly for 3 months, then
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Hepatomegaly
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every 3-4 months. Repeat serum or urine bile acids/liver aspirate or biopsy at 6- to 12-month intervals; ACTH-stimulation every 3-6 months; convalescent infectious disease titers/PCR at 4-week to 6-month intervals.
PROGNOSIS AND OUTCOME Varies with the cause of each disease
PEARLS & CONSIDERATIONS COMMENTS Bile acids are an unnecessary test in an icteric patient (rare exception: icteric patient suspected of having both hemolysis and hepatobiliary disease concurrently, where bile acids can help differentiate). Fine-needle aspiration and cytologic evaluation of the liver does not reliably assess hepatic structure or function, even with diffuse hepatopathies. Normal serum bile acid levels in a patient with progressively increasing liver enzymes does not preclude the need for liver biopsy. Cats with hepatic lipidosis tend to have greater bleeding after liver biopsy than those with other diseases. Abnormal urine bile acids test result should be confirmed with serum bile acids measurement before liver biopsy. In cats, most diseases of the liver (including cirrhosis) result in hepatomegaly, whereas in dogs this is not necessarily the case. Ursodeoxycholate (e.g., Actigall) therapy can interfere with the interpretation of the urine bile acids test.
SUGGESTED READING Poldervaart RP, et al: Primary hepatitis in dogs: a retrospective review (2002-2006). J Vet Intern Med 23:72–80, 2009 AUTHOR: MAUREEN CARROLL EDITOR: ETIENNE CÔTÉ
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Hepatitis, Canine Infectious
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Hepatitis, Canine Infectious BASIC INFORMATION DEFINITION A specific form of liver disease caused by canine adenovirus-1 (CAV-1) that can cause acute death or chronic hepatitis. Infectious canine hepatitis (ICH) is uncommon in well-vaccinated dog populations. Antigenically and genetically distinct from CAV-2 which causes infectious tracheobronchitis.
SYNONYMS CIH (canine infectious hepatitis); ICH; “blue eye”
EPIDEMIOLOGY SPECIES, AGE, SEX Dogs, coyotes, foxes, wolves, and bears can be infected. Usually the disease is seen in dogs 1000 mcg/g dry liver weight. d-penicillamine or trientine (10-15 mg/kg PO q 12 h) is administered to remove copper. Following chelation, chronic zinc supplementation is used for blocking GI absorption of copper. Zinc has antioxidant and antifibrotic effects. Hepatic zinc deficiency occurs in advanced liver disease, and supplementation is indicated with zinc gluconate at 2-3 mg/kg PO q 24 h with deficiency. Higher doses of zinc will block intestinal copper absorption (see p. 517). Ursodeoxycholic acid (10-15 mg PO q 24 h) is a hydrophilic bile acid that has immunomodulatory, antioxidant, hepatoprotective, and choleretic effects. Antifibrotic drug colchicine (0.03 mg/kg PO q 24 h) inhibits collagen formation. However, few studies report its use in dogs, and human studies fail to show prolonged survival. Side effects are often GI. The angiotensin receptor antagonist, losartan (0.5 mg/kg PO q 12-24 h), recently has shown promise in inhibiting fibrosis in humans. Antioxidant therapy is used as adjunct liver support. Selection of one or several antioxidants is suggested, including vitamin E (10 IU/kg PO q 24 h), S-adenosylmethionine (20 mg/kg PO q 24 h or q 48 h), milk thistle (silybin complexed with phosphatidylcholine 24-70 mg/day), or others could be used for oxidative damage shown to occur in many dogs having hepatic disease. Antibiotics are used to modify GI bacterial flora in HE (see p. 501), to treat or reduce the incidence of secondary infection, or to treat a primary pathogen (leptospirosis or other pathogen). Ascites: Medical treatment involves diuretics for long-term chronic management. Spironolactone (0.5-1 mg/kg PO q 12 h) is suggested as the initial diuretic. If failure of ascites control, furosemide (0.5-2 mg/kg PO q 12 h) or combination of both drugs should be considered. Centesis/drainage may be performed intermittently as needed for comfort when patients develop tense ascites (very large volumes of abdominal fluid). Caution is advised because abdominocentesis will result in protein loss to the patient.
NUTRITION/DIET Diet is important to supply adequate calories. Palatability is important in advanced cases. Dietary protein is restricted only with protein intolerance (HE). Dietary protein content should represent 18%-22% of digestible kcal/day. Feed a high-quality moderate-protein diet given in small multiple feedings. Milk and vegetable protein sources are more beneficial in HE than meat protein-based diets. Fermentable fiber may also be beneficial in controlling HE.
DRUG INTERACTIONS Avoid drugs that require hepatic metabolism or alter hepatic biotransformation (e.g., cimetidine). Glucocorticoids may cause sodium retention, promote GI ulceration, or precipitate hepatic failure with advanced disease. Glucocorticoids also result in a steroid hepatopathy, making laboratory evaluation of treatment response difficult. Penicillamine and zinc should not be given together; penicillamine may chelate zinc. Animals with hepatic failure are anesthetic risks. Barbiturates should be avoided, and benzodiazepines should be used with care. Isoflurane or sevoflurane are the gas anesthetics of choice. Propofol, although hepatically metabolized, may be administered to effect (usually requiring a small fraction of normal doses) for anesthetic induction or for controlling seizures due to HE. Lidocaine, theophylline, propranolol, captopril, and tetracyclines should be avoided if possible. Diuretics may worsen HE, promote dehydration or metabolic alkalosis, and should be used only in otherwise stable patients for the long-term delay of return of ascites or for concurrent conditions (e.g., congestive heart failure). NSAIDs may exacerbate GI ulceration.
POSSIBLE COMPLICATIONS Ascites, HE, GI ulceration, sepsis, disseminated intravascular coagulation, hepatic failure, and death
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Hepatitis (Chronic, Idiopathic) of Dogs
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RECOMMENDED MONITORING Monitor general condition, body weight, and behavior. Periodic evaluation of laboratory tests (CBC and serum biochemical profile) Follow-up liver biopsy provides the best means of evaluating treatment response.
PROGNOSIS AND OUTCOME Guarded to fair based on clinical signs at the time of diagnosis and extent of liver damage as determined grossly and histopathologically. Most dogs are diagnosed when clinical signs occur, which is usually associated with advanced hepatitis and a guarded prognosis. When severe signs of liver failure occur, such as ascites, HE, and hypoalbuminemia, the prognosis is grave. Early diagnosis and therapy will prolong survival, but limited studies are available on survival times (cirrhosis 1-2 months; chronic hepatitis I month to 5 years).
PEARLS & CONSIDERATIONS COMMENTS The first clue to chronic hepatitis is unexplained abnormal serum liver enzyme activities. Because of the great reserve capacity of the liver, signs of liver failure do not occur until the disease is advanced. Therapy in early stages of hepatitis may prolong survival.
CLIENT EDUCATION A complete cure is unlikely. Medication is generally lifelong but may prolong quality of life and survival times. There are few studies evaluating therapy for chronic hepatitis in the dog; repeat liver biopsies are recommended to monitor response to therapy.
SUGGESTED READING Watson PJ: Chronic hepatitis in dogs: a review of current understanding of the aetiology, progression and treatment. Vet J 167(3):228– 241, 2004. Favier RP: Idiopathic hepatitis and cirrhosis in dogs. Vet Clin North Am Small Anim Pract 39(3):481–488, 2009. AUTHOR: DAVID C. TWEDT EDITOR: KEITH P. RICHTER
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Hepatitis (Chronic) of Doberman Pinscher Dogs
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Hepatitis (Chronic) of Doberman Pinscher Dogs BASIC INFORMATION DEFINITION A progressive chronic inflammatory liver disease associated with hepatic copper accumulation distinct to Doberman pinschers
SYNONYMS Chronic active hepatitis in Doberman pinschers, copper-associated chronic hepatitis, Doberman hepatitis
EPIDEMIOLOGY SPECIES, AGE, SEX Doberman pinschers. Most are diagnosed between the ages of 2 and 7 years. Most are females. GENETICS & BREED PREDISPOSITION The high incidence in this breed suggests a genetic predisposition. Occurrence in this breed may have a prevalence of 2%-20% depending on clinical reports. Mode of genetic transmission is unknown.
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES Subclinical hepatitis Clinical hepatitis/cirrhosis HISTORY, CHIEF COMPLAINT Dogs with subclinical hepatitis show no clinical signs; the disease is usually discovered incidentally (e.g., diagnostic workup triggered by elevated serum liver enzyme activities on serum biochemistry panel or microhepatica on abdominal imaging). Historic signs of early clinical hepatitis are often vague and may be associated with intermittent gastrointestinal signs and weight loss. When clinical hepatitis progresses, some or all of the following historic signs may occur: Polydipsia, polyuria Weight loss Abdominal distension Altered mental status associated with hepatic encephalopathy In advanced disease liver failure ensues, and the patient may have a rapid deterioration. PHYSICAL EXAM FINDINGS With clinical hepatitis some or all of the following may be found: Weight loss Icterus Ascites Signs of hepatic encephalopathy (depression/drowsiness, propulsive pacing, seizures; see p. 501) Evidence of hemorrhage (gastrointestinal, overt)
ETIOLOGY AND PATHOPHYSIOLOGY The etiology and mode of genetic transmission are unknown. Two theories suggested include either primary copper hepatotoxicity autoimmune mechanisms: Primary copper hepatotoxicosis is supported by the fact that hepatic copper accumulation occurs in affected dogs
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Hepatitis (Chronic) of Doberman Pinscher Dogs
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prior to hepatitis, and studies demonstrating affected dogs have a defect in biliary copper excretion, and copper chelation therapy improves pathology. Oxidative damage was also shown to occur in the liver from copper accumulation. Inappropriate major histocompatibility complex (MHC) class II antigen expression in affected dogs suggests the disease could be an autoimmune disorder, but presence of MHC class II can also occur as a secondary phenomenon.
DIAGNOSIS DIAGNOSTIC OVERVIEW The combination of signalment (breed) and physical and/or biochemical signs of hepatobiliary disease are strongly suggestive of the diagnosis; confirmation is obtained with liver biopsy.
DIFFERENTIAL DIAGNOSIS Hepatic disease from other causes Nonhepatic conditions associated with abnormal liver enzymes
INITIAL DATABASE Subclinical disease: Elevation in serum alanine aminotransferase (ALT) activity first, followed by increases in other liver enzymes Clinical disease: Elevation in serum ALT, aspartate aminotransferase, g-glutamyl transferase (GGT), and alkaline phosphatase (ALP) activities Abnormal serum bile acid concentrations Advanced disease with loss of liver function: some or all of the following abnormalities may result: Elevation in serum total bilirubin concentration Low serum albumin, blood urea nitrogen, and glucose concentrations Abnormal clotting times
ADVANCED OR CONFIRMATORY TESTING Abdominal radiographs show a small liver ± evidence of ascites (loss of serosal detail, abdominal distention). Abdominal ultrasound may demonstrate: A small liver with altered parenchymal echogenicity. Findings vary from normal appearance (in early disease) to heterogeneous mottling, microhepatica with nodular changes, and an irregular surface. Ascites which, on centesis, may be a pure transudate or a modified transudate; the cellular composition is not usually helpful diagnostically. Vascular changes (e.g., multiple extrahepatic portosystemic shunts) associated with portal hypertension Surgery or laparoscopy: liver may appear normal in subclinical disease or may be small, micronodular, macronodular, and/or fibrotic in clinical disease. Liver biopsy and histopathology: Large biopsies (obtained via laparoscopy or laparotomy) are preferred over small-diameter needle core biopsies or fine-needle aspirates, owing to superior diagnostic accuracy and ability to adequately measure hepatic copper concentrations. Subclinical disease is associated with copper accumulation and infiltration of mononuclear inflammatory cells in centrilobular areas. Clinical disease can progress to a micronodular cirrhosis with bridging fibrosis, piecemeal necrosis, progressive inflammatory infiltrates in the portal triads, and eventually macronodular cirrhosis with regenerative nodules. Histochemical staining for copper is generally positive when copper concentrations are above 1000 mg/g dry weight liver. Hepatic metal quantitative analysis: Hepatic copper concentrations often range from 1000 to 2000 mg/g dry weight liver (normal 600 mg/g liver). D-penicillamine or trientine (15 mg/kg PO q 12 h) for 2-4 months or longer after measuring hepatic copper concentrations. Liver lesions improve as a result of lowering copper concentrations. Chelator therapy use should be based on identifying the characteristic histopathologic lesions and hepatic copper concentrations. Glucocorticoid therapy (prednisone or prednisolone, 2-4 mg/kg PO q 24-48 h; maximum dose 80 mg/d) may be beneficial in slowing inflammatory component of liver disease. Ensure adequate nutrient intake. Advanced clinical hepatitis (see 513): Treatment for hepatic encephalopathy (see 501): high-quality low-protein diet, lactulose (0.1-0.5 mL/kg PO q 12 h, adjusted to achieve loose fecal consistency) and/or intestinal antibiotics (e.g., neomycin, 20 mg/kg PO q 8 h; ampicillin, 22 mg/kg PO q 8 h; metronidazole, 7.5 mg/kg PO q 12 h; or amoxicillin-clavulanate, 15 mg/kg PO q 12 h). If encephalopathy is severe enough to warrant these efforts, the prognosis is poor. Treatment for ascites: see pp. 93, 501, and . Treatment for gastric ulceration: famotidine (0.5 mg/kg PO q 12 h) or omeprazole (0.5-1 mg/kg PO q 24 h)
CHRONIC TREATMENT Copper chelation to maintain hepatic concentrations near normal Affected dogs should be placed on a low copper-containing diet (most therapeutic liver diets are low in copper). After adequate chelation, zinc acetate or gluconate may be used for blocking enteric copper uptake. Adequate chelation is most accurately determined by rebiopsy; if rebiopsy is not possible, the change from chelation therapy to zinc therapy is generally warranted after 6-12 months of treatment if the dog is doing well clinically, with improving biochemical parameters. Zinc acetate: 100 mg elemental zinc PO q 12 h as loading dose for 2 months, then 50 mg PO q 12 h. Zinc gluconate: 2-3 mg/kg PO q 12 h. Zinc dose should be adjusted to keep serum zinc concentrations between 200 and 800 mcg/dL. NOTE: blood samples for zinc levels must be drawn into specific tubes (navy top), because standard rubber tops contain zinc. Antiinflammatory therapy using prednisolone or prednisone (2 mg/kg PO q 24 h; maximum dose 80 mg/d). Dosage is often tapered to an alternate-day therapy once there is clinical improvement. Glucocorticoids cause a secondary steroid hepatopathy, and monitoring liver enzymes is generally not helpful. However, there should be a decline in serum bilirubin concentration and an increase in serum albumin concentration as the patient improves. With ascites, dexamethasone (0.2 mg/kg PO q 24 h) should be used instead to avoid mineralocorticoid effect. For glucocorticoid-intolerant animals or when additional immunomodulation is desired, azathioprine or cyclosporine can be given alone or in combination with glucocorticoids (see 513). Ascites long-term management: In the hydrated patient, diuretics (see previous) also may be used long term, either alone or as an adjunct to abdominal drainage, to delay the recurrence of ascites. Repeated abdominocentesis or drainage (when ascites becomes large-volume/tense, and causes lethargy/inappetence) is also possible for long-term management of ascites (see ,pp. 1192 ). Diet is important to supply adequate calories. Palatability is important in advanced cases. Diets low in copper content should be fed. Dietary protein restriction is necessary only as protein intolerance occurs (i.e., hepatic encephalopathy). Feed a high-quality moderate-protein diet given in small multiple feedings. Milk and vegetable protein sources are better for avoiding hepatic encephalopathy than meat protein–based diets. Fermentable fiber may also be beneficial in controlling hepatic encephalopathy. General liver support may include ursodeoxycholic acid (15 mg/kg PO q 24 h), antioxidants (vitamin E, 10-15 IU/kg PO q 24 h); S-adenosylmethionine, 20 mg/kg PO q 24 h, or milk thistle [silybin complexed with phosphatidylcholine] 24-70 mg/d and antifibrotics (colchicine, 0.03 mg/kg PO q 24 h; or losartan, 0.5 mg/kg PO q 12-24 h).
DRUG INTERACTIONS Penicillamine and zinc should not be given together, as penicillamine may chelate zinc. Animals with hepatic failure are anesthetic risks. Barbiturates should be avoided, and benzodiazepines should be used with care, if at all. Isoflurane or sevoflurane are the gas anesthetics of choice. Propofol, although hepatically metabolized, may be administered to effect (usually requiring a small fraction of normal doses) for anesthetic induction and for controlling seizures due to hepatic encephalopathy. Lidocaine, theophylline, propranolol, captopril, and tetracyclines should be avoided. Diuretics may worsen hepatic encephalopathy, promote dehydration or metabolic alkalosis, and should be used only in otherwise stable patients for the long-term delay of return of ascites or for concurrent conditions (e.g., congestive heart
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Hepatitis (Chronic) of Doberman Pinscher Dogs
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failure). Nonsteroidal antiinflammatory drugs may exacerbate gastrointestinal ulceration. Avoid drugs that require hepatic metabolism or alter hepatic biotransformation (e.g., cimetidine). Glucocorticoids may cause sodium retention, promote gastrointestinal ulceration, or precipitate hepatic failure in advanced disease.
POSSIBLE COMPLICATIONS Glucocorticoids may precipitate ascites, hepatic encephalopathy, and early death in advanced cases. Therefore, if ascites develops shortly after starting prednisone, consider switching to dexamethasone. If gastrointestinal ulceration develops, it should be addressed as discussed previously. Penicillamine and zinc should be given on an empty stomach but may cause vomiting. The risk of vomiting may be reduced by beginning penicillamine at the low end of the dosage range and titrating up. Zinc overdose may cause hemolysis, although the doses required to reach toxic levels are extremely high (many times higher than the therapeutic dose). Because von Willebrand disease (see p. 1176) is common in the breed, von Willebrand factor, buccal mucosal bleeding time (see p. 1222), or both should be evaluated prior to biopsy procedures.
RECOMMENDED MONITORING CBC, serum biochemistry profile, and urinalysis for disease progression, remission, or complications Periodic liver biopsies are the best means of evaluating the stage and progression of the disease during therapy.
PROGNOSIS AND OUTCOME Diagnosis and appropriate therapy in subclinical cases may delay or lessen the disease for years. Overt clinical manifestations of hepatitis denote advanced disease, and the long-term prognosis is guarded.
PEARLS & CONSIDERATIONS COMMENTS The first abnormality observed in young, subclinically affected dogs is an increase in serum ALT activity, and therefore unexplained ALT activities should be investigated. Copper reduction appears to be helpful, but clinical studies evaluating therapy are limited to a small population of affected dogs. Diagnosis is confirmed with a liver biopsy; treatment and prognosis depend mainly on whether disease is subclinical (incidental finding, no clinical signs) or clinically overt (presence of advanced signs of liver disease, including encephalopathy and portal hypertension).
CLIENT EDUCATION The incidence and genetic mode of inheritance are unknown. Affected dogs or related dogs should not be used for breeding. Screening serum levels of liver enzymes in young dogs will lead to an early diagnosis and improved prognosis with therapy. Since the disease is common in the Doberman breed, all dogs should undergo yearly or biannual blood biochemical screening after 2 years of age.
SUGGESTED READING Mandigers PJJ, et al: Improvement in liver pathology after 4 months of d-penicillamine in 5 Doberman pinschers with subclinical hepatitis. J Vet Intern Med 19:40–43, 2004. Speeti M, et al: Subclinical versus clinical hepatitis in the Doberman: evaluation of changes in blood parameters. J Small Anim Pract 37:465–470, 1996. Mandigers PJJ, et al: Chronic hepatitis in Doberman pinschers. A review. Vet Quarterly 26(3):98–106, 2004. AUTHOR: DAVID C. TWEDT EDITOR: KEITH P. RICHTER
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Hepatitis (Chronic) of Cocker Spaniel Dogs
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Hepatitis (Chronic) of Cocker Spaniel Dogs BASIC INFORMATION DEFINITION A progressive chronic inflammatory liver disease distinct to cocker spaniels
SYNONYMS Cocker spaniel hepatitis, chronic hepatitis, chronic idiopathic hepatitis
EPIDEMIOLOGY SPECIES, AGE, SEX English and American cocker spaniels are affected. Most are diagnosed between the ages of 2 and 6 years. Both sexes appear to be affected; male predominance. GENETICS & BREED PREDISPOSITION The high incidence in this breed suggests a genetic predisposition, but the mode of genetic transmission is unknown. Certain lines of dogs seem to be more affected.
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES Subclinical hepatitis Clinical hepatitis HISTORY, CHIEF COMPLAINT Dogs with subclinical hepatitis show no overt signs. Historic signs of early clinical hepatitis are often vague and may be associated with intermittent gastrointestinal signs and weight loss. When clinical hepatitis progresses to liver failure, some or all of the following historic signs may occur: Polydipsia, polyuria Weight loss Abdominal distension Anorexia and vomiting Altered mental status associated with hepatic encephalopathy PHYSICAL EXAM FINDINGS With clinical hepatitis some or all of the following may be found: Weight loss Icterus Ascites Signs of hepatic encephalopathy Hemorrhage
ETIOLOGY AND PATHOPHYSIOLOGY Etiology is unknown, but α-1 antitrypsin (AAT) may be involved. Hepatitis is not associated with AAT (also called α-1 protease inhibitor) deficiency, but rather cocker spaniels were found to be prone to abnormal accumulation of AAT (type I) in hepatocytes compared to other breeds. Researchers speculate AAT accumulation may contribute to progression of chronic hepatitis but may not be the causative agent.
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Hepatitis (Chronic) of Cocker Spaniel Dogs
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Immune mechanisms have not yet been documented in cocker spaniel hepatitis. Hepatic copper accumulation is not a consistent feature.
DIAGNOSIS DIAGNOSTIC OVERVIEW The combination of signalment (breed) and physical and/or biochemical signs of hepatobiliary disease are strongly suggestive of the diagnosis; confirmation is obtained with a liver biopsy.
DIFFERENTIAL DIAGNOSIS Hepatic disease from other causes Nonhepatic conditions associated with abnormal liver enzyme activities
INITIAL DATABASE Subclinical disease: Elevation in serum alanine aminotransferase (ALT) activity Clinical disease: Elevation in serum ALT, aspartate aminotransferase (AST), g-glutamyl transferase, and alkaline phosphatase activities Elevated serum bile acid concentrations Advanced disease: Elevation in serum total bilirubin concentration Low serum albumin, blood urea nitrogen, and glucose concentrations Abnormal clotting times
ADVANCED OR CONFIRMATORY TESTING Abdominal radiographs: microhepatica ± signs of ascites (loss of serosal detail) Ultrasound: microhepatica with altered parenchymal echogenicity, ± ascites, ± vascular changes associated with portal hypertension Surgery or laparoscopy: small liver; micronodular or macronodular, and fibrotic in advanced clinical disease Liver histopathology: subclinical disease is associated with infiltration of mononuclear inflammatory cells into portal and parenchymal areas; clinical disease has evidence of active hepatitis with areas of piecemeal and bridging necrosis. Cirrhosis develops as the disease advances. Histochemical staining for AAT may show globoid accumulations within hepatocytes. Hepatic metal quantitative analysis: hepatic copper usually normal, but secondary increases in copper may occur. Hepatic iron is increased, thought to be secondary to chronic inflammation; zinc concentrations may be reduced.
TREATMENT TREATMENT OVERVIEW Goals of treatment are to slow progression of liver disease in subclinical cases, provide specific therapy for chronic hepatitis, and provide general supportive care, treating complications of liver disease such as hepatic encephalopathy, ascites, gastrointestinal ulceration, and nutritional imbalance.
ACUTE GENERAL TREATMENT Fluid support Treatment of hepatic encephalopathy (see 501) Coagulopathies or sepsis are treated as they occur (see 513)
CHRONIC TREATMENT Subclinical and early clinical hepatitis (see 513): Glucocorticoid therapy (prednisone or prednisolone, 2 mg/kg PO q 24-48 h; maximum of 80 mg/d) may be beneficial in slowing inflammatory component of the liver disease. Anecdotal reports suggest improved survival following therapy.
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Other immunosuppressive therapy such as azathioprine or cyclosporine may be used in addition to or in place of glucocorticoid therapy. Ensure adequate nutrient intake. Provide liver support with antioxidants (vitamin E, 10 IU/kg PO q 24 h; S-adenosylmethionine, 20 mg/ kg PO q 24 h; and/or milk thistle [silybin complexed with phosphatidylcholine], 24-70 mg PO q 24 h). Antifibrotics (see ) such as colchicine can be used (0.03 mg/kg PO q 24 h), but few studies report its use in dogs, and human studies fail to show prolonged survival. Gastrointestinal side effects are well-recognized. The angiotensin II receptor antagonist, losartan (0.5 mg/kg PO q 12-24 h), recently has shown promise in inhibiting fibrosis in humans. Ursodeoxycholic acid (15 mg/kg PO q 24 h) is given for hepatic support and choleresis. If secondary copper accumulation occurs, chelator or zinc therapy should be used (see 517). Advanced clinical hepatitis (see 517): Treatment for hepatic encephalopathy (see 501): high-quality, low-protein diet, lactulose (0.1-0.5 mL/kg PO q 12 h, titrated to achieve loose fecal consistency) and/or intestinal antibiotics (metronidazole, 7.5-10 mg/kg PO q 12 h; or amoxicillin-clavulanate, 15 mg/kg PO q 12 h) Ascites therapy: spironolactone (1 mg/kg PO q 12 h) or furosemide (0.5-2 mg/kg PO q 12 h) Gastric ulceration: famotidine (0.5 mg/kg PO q 12 h) or omeprazole (0.5-1 mg/kg PO q 24 h)
DRUG INTERACTIONS Avoid drugs that require hepatic metabolism.
POSSIBLE COMPLICATIONS Glucocorticoids may precipitate ascites, hepatic encephalopathy, and result in an early death in advanced cases.
RECOMMENDED MONITORING Young dogs should have periodic liver enzymes measured as screening test to help identify affected dogs. Routine CBC, serum biochemistry profile, and urinalysis to monitor disease progression, remission, or complications Periodic liver biopsies (yearly) are the best means of evaluating the stage and progression of the disease during therapy.
PROGNOSIS AND OUTCOME Diagnosis and appropriate therapy in subclinical cases may slow progression of disease. Clinical hepatitis denotes advanced disease and the long-term prognosis is guarded.
PEARLS & CONSIDERATIONS COMMENTS The first abnormality observed in young subclinical dogs is an increase in serum ALT activity. Unexplained elevated serum ALT activities in this breed should be investigated. The disease continues to be explored; there is little objective information on chronic hepatitis in cocker spaniels. Many dogs are presented when the disease is advanced. The prognosis is poor at this stage.
CLIENT EDUCATION The incidence and genetic mode of inheritance are unknown. Affected dogs or related dogs should not be used for breeding. Screening laboratory enzymes in young dogs will lead to an early diagnosis and may improve prognosis with therapy.
SUGGESTED READING Anderson M, et al: Breed, sex, and age distribution in dogs with chronic liver disease: a demographic study. J Small Anim Pract 32:1–5, 1991. Watson PJ: Chronic hepatitis in dogs: a review of current understanding, aetiology, progression and treatment. Vet J 167(3):228– 241, 2004. Hardy RM: Chronic hepatitis in dogs: a syndrome. Compend Contin Educ Pract Vet 8:904–913, 1986.
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AUTHOR: DAVID C. TWEDT EDITOR: KEITH P. RICHTER
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Hepatic Nodules, Benign
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Hepatic Nodules, Benign BASIC INFORMATION DEFINITION Hepatic adenoma: benign neoplasia of hepatocytes Nodular hyperplasia: discrete accumulation of hyperplastic hepatocytes surrounded by normal hepatocytes Nodular regeneration: discrete accumulation of hyperplastic hepatocytes surrounded by abnormal hepatocellular parenchyma, particularly fibrotic changes
SYNONYMS Nodular hyperplasia: hyperplastic nodules; nodular regeneration: regenerative nodules
EPIDEMIOLOGY SPECIES, AGE, SEX Hepatic adenomas: rare tumors in dogs and cats; patients usually >10 years old Nodular hyperplasia: common lesion in old dogs. Incidence in dogs >14 years old: 70%-100% Nodular regeneration: seen in dogs with acquired parenchymal hepatic disease. Middle-aged to older dogs GENETICS & BREED PREDISPOSITION Nodular regeneration: seen in breeds predisposed to chronic hepatitis (Doberman pinscher, cocker spaniel, Labrador retriever) and copper-storage hepatopathy (Bedlington terrier, West Highland white terrier, Skye terrier) RISK FACTORS Nodular regeneration: chronic hepatic disease, cirrhotic/fibrosing liver disease
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT Nodular hyperplasia: incidental finding, no clinical signs, rare hepatic failure Adenoma: incidental finding, no clinical signs; rarely, abdominal discomfort or rupture with hemoperitoneum or abscessation with signs of chronic infection Nodular regeneration: see sections on chronic hepatic diseases (, 512, and 513). PHYSICAL EXAM FINDINGS Hepatic adenoma: rarely abdominal pain, inappetence, ascites and pallor (if ruptured) Nodular hyperplasia: normal exam Nodular regeneration: see sections on chronic hepatic disease noted above.
ETIOLOGY AND PATHOPHYSIOLOGY Nodular hyperplasia: unknown; may be associated with nutritional factors or a result of focal areas of ischemia; not preneoplastic Adenoma: unknown; may be associated with chronic inflammation or hepatotoxicity Nodular regeneration: compensatory response of the liver to chronic injury
DIAGNOSIS DIAGNOSTIC OVERVIEW
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Their benign nature makes these lesions almost always incidentally encountered during abdominal ultrasound exams or abdominal surgery, or occasionally on abdominal palpation if very large.
DIFFERENTIAL DIAGNOSIS Nodular hyperplasia: Primary or metastatic hepatic neoplasia Cirrhosis with nodular regeneration Vacuolar hepatopathy Adenoma: Nodular hyperplasia Primary or metastatic hepatic neoplasia Hepatic abscess Nodular regeneration: Nodular hyperplasia Metastatic hepatic neoplasia Vacuolar hepatopathy
INITIAL DATABASE Nodular Hyperplasia: Commonly associated with mild to moderate increases in serum alkaline phosphatase (ALP) activity, less commonly with mild increases in serum alanine transaminase (ALT) and aspartate aminotransferase (AST) activities Serum bile acids concentration usually normal Abdominal ultrasonography reveals single to multiple lesions with highly variable appearance. Easily mistaken for primary or metastatic neoplasia or nodular regeneration. Hepatic Adenoma: Variable increases in ALP, ALT, and AST activities Serum bile acids concentration usually normal Leukocytosis ± monocytosis if necrotic regions within adenomas Anemia if adenoma ruptures and hemoperitoneum Radiographs may identify a mass in the cranial abdomen or rarely a gas pocket in a necrotic region. Abdominal ultrasonography demonstrates a solitary mass with variable echogenicity that may contain cystic cavities and/or blood-or gas-filled spaces. Ascites seen with rupture and hemoperitoneum. Nodular Regeneration: Serum bile acids concentration usually abnormal See sections on chronic hepatic disease ( pp. 212 and 513).
ADVANCED OR CONFIRMATORY TESTS General: Hepatic histopathology differentiates the three conditions but often requires wedge biopsy, as adjacent hepatic tissue is necessary to make a definitive diagnosis. Fine-needle aspiration or single needle biopsies of these focal lesions may result in misdiagnosis of hepatic vacuolar hepatopathy. MRI of focal hepatic masses may provide better discrimination of these lesions (future direction). Preliminary studies with contrast enhanced ultrasonography have shown some ability to discriminate benign nodules from malignant ones. Specific: Nodular hyperplasia: Well-circumscribed expansive nodule usually 1460 days, with high serum ALT and AST activity and right-sided tumors conveying a worse prognosis. The prognosis for nodular or diffuse hepatocellular carcinoma is poor. Biliary carcinoma, hepatic carcinoids, and hepatic sarcomas have a worse prognosis, as they are commonly nodular or diffuse, resistant to chemotherapy, and have high metastatic rates. Hepatic lymphoma has a variable prognosis depending on the grade and response to chemotherapy. The liver is a common site of metastasis for a variety of cancers, and metastatic liver disease has a poor prognosis.
PEARLS & CONSIDERATIONS COMMENTS The most common primary hepatobiliary tumor in dogs is a massive hepatocellular carcinoma. With liver lobectomy providing a complete excision of massive hepatocellular carcinoma, long-term survival or cure is common. The most common feline hepatobiliary tumors are bile duct carcinoma and biliary cystadenoma. Bile duct carcinoma has a high metastatic rate and a poor prognosis, whereas biliary cystadenoma is benign and generally has a good prognosis.
SUGGESTED READING Scherck MA, Center SA: Toxic, metabolic, infectious, and neoplastic liver diseases. In Ettinger SJ, Feldman EC, editors: Textbook of veterinary internal medicine, ed 7, St Louis, MO, 2010, Saunders Elsevier, pp 1672–1689. Mayhew PD, et al: Massive hepatocellular carcinoma in dogs: 48 cases (1992-2002). J Am Vet Med Assoc 225:1225–1230, 2004. Withrow SJ: Cancer of the gastrointestinal tract: hepatobiliary tumors. In Withrow SJ, MacEwen EG, editors: Small animal clinical oncology, ed 4, Philadelphia, 2007, WB Saunders, pp 483–491. AUTHOR: STEVE HILL EDITOR: KEITH P. RICHTER
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Hepatic Lipidosis
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Hepatic Lipidosis BASIC INFORMATION DEFINITION A well-recognized syndrome in cats, characterized by excessive accumulation of fat (triglyceride) in the liver; associated with severe intrahepatic cholestasis and hepatic dysfunction
SYNONYMS Fatty liver syndrome, feline hepatic lipidosis (FHL), idiopathic hepatic lipidosis
EPIDEMIOLOGY SPECIES, AGE, SEX Cats; middle-aged or older RISK FACTORS Obesity before onset of anorexia; prior stressful event (boarding, surgery, change in living arrangements, diet change) preceding anorexia; systemic diseases associated with anorexia and a catabolic state. May be associated with pancreatitis. ASSOCIATED CONDITIONS & DISORDERS Cholangitis, pancreatitis, inflammatory bowel disease, systemic neoplasia, diabetes mellitus, toxin-or drug-induced injury (stanozolol, tetracyclines), and many other systemic disorders associated with anorexia and weight loss
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES Idiopathic hepatic lipidosis: primary disorder of unknown cause Secondary hepatic lipidosis: associated with inciting cause (see Associated Conditions and Disorders above) HISTORY, CHIEF COMPLAINT Prolonged anorexia, often several weeks in duration; rapid weight loss (often >25% of body weight). History of stressful event (see Risk Factors above), or nonhepatic diseases associated with anorexia. Other signs: lethargy, depression, sporadic vomiting, constipation, or diarrhea. PHYSICAL EXAM FINDINGS Icterus, hepatomegaly, dehydration, muscle wasting, seborrhea, pale mucous membranes, weight loss. Overt findings of hepatic encephalopathy (ptyalism, severe depression, stupor) or bleeding are uncommon and indicate severe liver failure. Head or neck ventroflexion may occur with severe electrolyte imbalances (hypokalemia, hypophosphatemia) or thiamine deficiency.
ETIOLOGY AND PATHOPHYSIOLOGY Cats have higher nutritional requirements for protein, essential amino acids, and essential fatty acids than dogs. Systemically ill cats have a propensity for accumulating fat in their hepatocytes. Profound anorexia and stress may be associated with hormonal (catecholamines, other) alterations that influence fat metabolism and predispose to peripheral fat mobilization and hepatic fat uptake. Obese cats appear unable to adapt to metabolism of fat for energy during starvation. The exact metabolic or biochemical aberrations in cats with hepatic lipidosis are unknown, but there appears to be an imbalance between mobilization of peripheral fat, hepatic use of fatty acids for energy, and hepatic dispersal of triglycerides. Lipid accumulation is not directly toxic to liver but is a marker for an underlying metabolic disorder.
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DIAGNOSIS DIAGNOSTIC OVERVIEW The diagnosis is suspected based on the findings of icterus in an afebrile obese cat with a history of anorexia and weight loss and laboratory features of hyperbilirubinemia, increased serum alkaline phosphatase (ALP) activity with normal to mildly increased serum gamma-glutamyltransferase (GGT) activity and a non-inflammatory CBC. Definitive diagnosis requires liver biopsy, but cytology often suffices for a presumptive diagnosis (though cytology can yield false-positive results).
DIFFERENTIAL DIAGNOSIS Cholangitis/cholangiohepatitis Pancreatitis Hepatic manifestations of feline infectious peritonitis Hepatic neoplasia Drug-or toxin-induced hepatic injury Extrahepatic bile duct obstruction
INITIAL DATABASE CBC: Normocytic, normochromic anemia Poikilocytosis (acanthocytes and elliptocytes) Hemolysis (secondary to hypophosphatemia or Heinz bodies) Mature neutrophilia and lymphopenia (stress response) Serum biochemistry profile: ALP: moderate to marked increases. Earliest biochemical change; precedes hyperbilirubinemia. Alanine aminotransferase (ALT): mild to moderate increases GGT: normal to mild increase (as opposed to increased serum GGT activity seen with other feline cholestatic disorders). The finding of a greater magnitude of elevation of ALP compared with GGT is highly suggestive of feline hepatic lipidosis (seen in virtually 100% of cases). Hyperbilirubinemia Hyperammonemia, hypoalbuminemia, hypoglycemia (severe hepatic dysfunction) Urinalysis: may show bilirubinuria (always abnormal in the cat) Coagulation abnormalities (prothrombin time and proteins induced by vitamin K antagonism increased; hypofibrinogenemia) Abdominal radiographs: normal to increased liver size Abdominal ultrasound: normal to increased liver size; diffusely hyperechoic parenchyma (seen in virtually 100% of cases), far field beam attenuation, vessels difficult to recognize. Ascites rare. Evaluate for concurrent pancreatitis or other disorders causing secondary hepatic lipidosis. Bile acids: usually elevated (not necessary to measure if hyperbilirubinemia is present)
ADVANCED OR CONFIRMATORY TESTING Fine-needle aspiration and cytologic evaluation of the liver are preferred over liver biopsy (less invasive, allows presumptive diagnosis of hepatic lipidosis). However, cytologic evaluation is not accurate in diagnosing other hepatopathies, and therefore these may be missed. False-positive results also commonly occur. In hepatic lipidosis, cytologic evaluation reveals vacuolated hepatocytes without inflammation. Correction of any coagulopathy with vitamin K1 prior to performing liver aspirate or biopsy is warranted. However, coagulation studies do not necessarily predict bleeding tendency after liver aspirate or biopsy. Liver biopsy provides definitive diagnosis. Not routinely performed when supporting lab work (in particular the elevated serum ALP activity relative to serum GGT activity) and fine-needle aspirate and cytologic study suggest the diagnosis, unless there is failure to respond to therapy for hepatic lipidosis or a high level of suspicion of other primary hepatic disorder(s) exists. With hepatic lipidosis, the biopsy sample typically is a pale tan/yellow color and floats in formalin. Biopsy results show severe vacuolization of hepatocytes (>50% of acinar unit involved). Inflammation and necrosis absent. Vacuoles stain positive for fat with oil red O. Consider serum feline pancreatic lipase immunoreactivity to evaluate for concurrent feline pancreatitis (see p. 817). Consider serum cobalamin (vitamin B12) levels if underlying primary intestinal disorder suspected. Evaluate for underlying systemic disorder as necessary.
TREATMENT TREATMENT OVERVIEW
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Correct fluid and electrolyte abnormalities. Control complications of liver failure. Give nutritional support to provide adequate calorie and protein intake. Treat underlying systemic disorder if identified.
ACUTE GENERAL TREATMENT Initial fluid therapy: intravenous balanced electrolyte solution supplemented with KCl using conventional sliding scale (20-40 mEq/L). Monitor serum potassium twice daily initially and readjust as needed; avoid lactated Ringer's solution (impaired lactate metabolism in severe hepatic lipidosis); avoid dextrose supplementation unless hypoglycemic (promotes hepatic lipid deposition). Vitamin K1 (0.5-1.5 mg/kg SQ q 12 h for three injections) for coagulopathy Water-soluble vitamin supplementation: B-complex vitamins (added to fluids: 1-2 ml/L). Cobalamin (vitamin B12): 250 mcg SQ initially while awaiting serum cobalamin levels. If decreased serum cobalamin is documented (primary intestinal disease), continue with 250 mcg SQ once weekly. Thiamine supplementation (if severe ventroflexion of neck): 50-100 mg PO/cat/d for 1 week. Use with caution: potential anaphylactic reactions. Blood transfusion as needed for anemia (preferably fresh; stored blood can exacerbate encephalopathy due to high ammonia concentration).
NUTRITION/DIET Nasogastric tube feeding of CliniCare (Abbott Veterinary Diets) for initial 24-48 hours (see p. 1269). This will allow initial stabilization prior to general anesthesia for long-term feeding tube placement. Place gastrostomy or esophagostomy tube (by least invasive method possible; see pp. 1267 and p. 1273). Feed Maximum Calorie (The Iams Co.), Prescription Diet a/d (Hill's Pet Nutrition), or other complete and balanced feline diet. Do not restrict dietary protein unless overt signs of hepatic encephalopathy are present. Provide 40-60 kcal/kg/d. Start with ¼ to ½ of daily requirements given through tube and divided into 4-6 feedings. Gradually increase to daily requirements over 3-4 days. If vomiting occurs, consider metoclopramide (0.4 mg/kg q 8 h SQ or through the tube 30 minutes before feeding), cisapride (1 mg/kg q 8 h through the tube), prochlorperazine (0.1-0.3 mg/kg q 8-12 h SQ or IV) or maropitant (1 mg/kg IV, SQ, PO), or tube feedings by slow constant rate infusion. Be sure that any tablet-formulated medications are ground to a fine powder before being administered through the tube; otherwise, there is a risk of tube occlusion. Tube feeding usually required for 3-6 weeks (or longer in some cases) pending clinical and biochemical improvement. Do not remove tube until cat eating on its own for at least a week. Other dietary supplements used empirically: l-carnitine 250-500 mg PO q 24 h (essential cofactor for fatty acid oxidation; relative carnitine deficiency in hepatic lipidosis) Taurine 250-500 mg PO q 24 h for initial 7-10 days (plasma levels have been found to be decreased in many cats with hepatic lipidosis; required for bile acid conjugation) Vitamin E (water soluble form) 50-100 units/cat PO q 24 h (antioxidant) s-adenosylmethionine (SAMe; Denosyl SD4 [Nutramax Labs]) 20 mg/kg PO q 24 h (glutathione source). Do not give through the tube (would disrupt enteric coating).
POSSIBLE COMPLICATIONS Hepatic encephalopathy (see p. 501): Hypophosphatemia (see p. 969) Heinz body hemolysis: Cats with hepatic lipidosis have decreased hepatic glutathione and are at risk for red blood cell oxidant injury/Heinz body hemolysis. For critical Heinz body hemolytic anemia, provide glutathione source as N-acetylcysteine 140 mg/kg (20% solution diluted at least 1:2 with saline) IV over 20 to 30 minutes through 0.25-mm nonpyrogenic filter; then 70 mg/kg IV q 8-12 h depending on clinical signs. When enteral feeding is established, switch to SAMe 20 mg/kg PO q 24 h (do not give through the tube so the enteric coating is not disrupted) as a glutathione source. Propofol does not appear to be a risk factor for Heinz body hemolytic anemia in cats with hepatic lipidosis. Hypomagnesemia: Monitor serum magnesium. Supplement if mg < 1.2 mg/dL. Magnesium sulfate (8.13 mEq/g) and magnesium chloride (9.25 mEq/g) salts available in 50% solution; dilute to a concentration of 20% or less in 5% dextrose in water. Give 0.75-1 mEq/kg/d constant rate infusion.
RECOMMENDED MONITORING Biochemical improvement (decreases in bilirubin, ALP, ALT) usually seen within 1-2 weeks of initiating tube feeding. Normalization
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may take several weeks.
PROGNOSIS AND OUTCOME Early diagnosis is key to successful management. Recovery in approximately 60%-85% of cases. If the cat survives the initial few days, the prognosis for complete recovery is excellent. Poorer prognosis with concurrent pancreatitis
PEARLS & CONSIDERATIONS COMMENTS Oral appetite stimulants usually are inadequate for aggressive nutritional support required for feline hepatic lipidosis therapy. Oral diazepam is associated with idiosyncratic hepatic necrosis in cats. Correct fluid and electrolyte imbalances before anesthesia for tube placement. In critically ill cats with hepatic lipidosis, the stress of general anesthesia may be fatal. Therefore initial feeding through a nasogastric tube (placed in awake state) before anesthesia for long-term feeding tube placement is recommended. Once the patient is more stable, anesthesia for long-tereeding tube placement can be more safely accomplished. Establishing the diagnosis, identifying any underlying causes (which may require long-term treatment), and initial management (often requires several days of hospitalization, including anesthesia and feeding tube placement) can be costly, time consuming, but ultimately rewarding. Evaluate for underlying systemic disorder (feline hepatic lipidosis may be secondary). Strategies to control vomiting are important for a successful outcome.
PREVENTION Do not switch obese cats to unpalatable diet for weight loss. Consider smaller amounts of favorite food given in parallel (not mixed in) with a weight-loss diet to avoid reducing appetite while allowing the cat to become accustomed to the new food. l-carnitine (250 mg/cat PO q 24 h) may improve fatty acid oxidation in obese cats undergoing weight loss but won't prevent hepatic lipidosis.
CLIENT EDUCATION Tube feeding for 3-6 weeks (or longer) at home will be required for recovery. Recurrence is unlikely unless an underlying chronic cause is present; the owner should take care to not allow cat to become anorexic again.
SUGGESTED READING Center SA: Feline hepatic lipidosis. Vet Clin North Am Small Anim Pract 35:225, 2005. Holan KM: Hepatic lipidosis. In Bonagura JD, Twedt DC, editors: Kirk’s current veterinary therapy XIV small animal practice, St Louis, 2009, Saunders Elsevier, pp 570–575. AUTHOR: SUSAN E. JOHNSON EDITOR: KEITH P. RICHTER
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Hepatic Injury, Acute
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Hepatic Injury, Acute BASIC INFORMATION DEFINITION Sudden insult to the liver, which if severe enough to compromise at least 70%-80% of functional hepatic tissue, results in acute hepatic failure
SYNONYM Acute or fulminant hepatic failure
EPIDEMIOLOGY SPECIES, AGE, SEX Dogs and cats; no age or sex predilection RISK FACTORS Drug administration; free-roaming animals with access to potential hepatotoxins (chemicals and pesticides, pond water [blue-green algae], poisonous mushrooms, cycad palms) CONTAGION & ZOONOSIS Infectious diseases (see Etiology and Pathophysiology below) for dog-to-dog or cat-to-cat transmission; leptospirosis (dog-to-human) GEOGRAPHY AND SEASONALITY Cycad palm toxicosis (dogs): southern United States and Hawaii; fungal: Mississippi and Ohio River Valley (dogs: histoplasmosis), southwestern United States (dogs: coccidioidomycosis). Blue-green algae hepatotoxicity (dogs): late summer or early fall.
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES Unexpected finding of increased serum liver enzyme activities and bilirubin concentration detected on routine biochemistries (mild hepatic injury or reactive hepatopathy secondary to systemic disorder) in patient who is asymptomatic or has only minimal clinical signs Clinical and biochemical evidence of acute hepatic failure (liver dysfunction occurring in the absence of known preexisting liver disease, accompanied by hepatic encephalopathy and coagulopathy). Findings reflect general hepatic dysfunction rather than specific underlying cause HISTORY, CHIEF COMPLAINT History of recent drug administration (prescription, over-the-counter, herbals, or dietary supplements may be implicated) or exposure to other potential hepatotoxins (e.g., aflatoxin-contaminated pet food: feeding from a new bag of food, or multiple affected dogs in a household) Acute onset of anorexia, lethargy, vomiting, and diarrhea in previously healthy animal Other signs: polyuria/polydipsia, hepatic encephalopathy, signs of extrahepatic or multisystemic disease, dependent on underlying cause PHYSICAL EXAM FINDINGS Dehydration, icterus (+/−), excessive bleeding (hematemesis, melena, hemorrhages of skin or mucous membranes) and hepatic encephalopathy indicate severe hepatic failure. Other findings dependent on specific cause (e.g., fever: consider infectious causes or secondary to acute pancreatitis; signs of abdominal pain: acute pancreatitis, cholangitis, liver abscess, acute swelling and stretching of liver capsule [nonspecific])
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ETIOLOGY AND PATHOPHYSIOLOGY Drugs and anesthetics: Hepatic drug reactions may be classified as predictable (e.g., acetaminophen) or idiosyncratic (most drugs). Usually acute but may be chronic (phenobarbital, primidone, lomustine). Acetaminophen (dogs and cats), amiodarone (dogs), azathioprine (dogs), carprofen and other nonsteroidal antiinflammatory drugs (NSAIDs) (dogs), clonazepam (cats), danazol (dogs), diazepam (cats), doxycycline (dogs), glipizide (cats), griseofulvin (cats), halothane (dogs), itraconazole (dogs and cats), ketoconazole (dogs and cats), lomustine (dogs), methimazole (cats), methoxyflurane (dogs), mitotane (dogs), nitrofurantoin (dogs), oxibendazole (dogs), phenobarbital (dogs), primidone (dogs), potentiated sulfonamides (dogs), stanozolol (cats), tetracycline (dogs and cats), thiacetarsemide (dogs) Idiosyncratic reaction can occur with any drug. Diagnosis is presumptive; cannot be proven. Do not rechallenge with suspect drug. Withdrawal of hepatotoxic drug can result in improvement or resolution of hepatic injury (within days to weeks), depending on severity of lesion. Biological substances: Aflatoxin (contaminated dog food) Amanita mushrooms Blue-green algae Sago palms Hornet stings Herbal derivatives (pennyroyal oil, chaparral leaf, comfrey, jin bu huan, kava kava) Xylitol (5-carbon sugar alcohol used as a sugar substitute and is anticariogenic) Chemicals and toxins: Carbon tetrachloride Dimethylnitrosamine Metals (e.g., copper, lead, iron, zinc) Organochloride pesticides Many others Infectious agents: Viral: infectious canine hepatitis, canine herpesvirus, feline infectious peritonitis, virulent feline calicivirus Bacterial: leptospirosis, liver abscess, cholangitis/cholangiohepatitis, Bartonella spp. Fungal: histoplasmosis, coccidioidomycosis, others Protozoal: Toxoplasma gondii, Babesia spp., Cytauxzoon felis Rickettsial: Ehrlichia spp., Rickettsia rickettsiae Systemic or metabolic disorders: Acute pancreatitis Extrahepatic infection, septicemia, endotoxemia Hemolytic anemia and DIC Inflammatory bowel disease Feline hepatic lipidosis Copper storage hepatopathy Miscellaneous causes of liver injury: Trauma Heat stroke Liver lobe torsion Thromboembolic disease Shock Surgical hypotension and hypoxia
DIAGNOSIS DIAGNOSTIC OVERVIEW When acute hepatic injury or overt hepatic failure is detected, obtain a thorough history for potential hepatotoxin exposure, and evaluate for systemic disorders that could secondarily affect the liver. Evaluate for primary hepatobiliary disease with biochemical and imaging studies. If a cause of liver injury/failure is not apparent, consider liver biopsy to further characterize the type of injury and look for an underlying cause.
DIFFERENTIAL DIAGNOSIS For acute hepatic injury accompanied by icterus/hyperbilirubinemia: Prehepatic causes (hemolytic anemia)
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Posthepatic causes (biliary obstruction) Sepsis Chronic hepatic disease; recent decompensation of chronic hepatic disease may mimic acute hepatic injury: Determine if subtle signs of chronic illness (weight loss, poor body condition) are present. Findings of ascites, small liver, and hypoalbuminemia suggest chronic rather than acute disease. Chronic liver disease in the final phases of decompensation may not warrant the same aggressive therapeutic approach as acute hepatic failure, because the long-term prognosis is poor.
INITIAL DATABASE Routine hematologic and biochemical evaluation: Inflammatory CBC (infectious diseases, acute pancreatitis, extrahepatic infections with secondary reactive hepatopathy); also for ruling out hemolytic anemia as cause of icterus. Serum biochemistry profile: increased serum alanine aminotransferase activity, especially with hepatic necrosis; increased alkaline phosphatase activity; hyperbilirubinemia; hypoglycemia (like hyperammonemia and coagulopathy) suggests severe hepatic dysfunction; xylitol toxicosis also associated with hypoglycemia due to excess insulin release; hypoalbuminemia suggests chronic rather than acute disease; azotemia: consider dehydration or concurrent renal damage (leptospirosis, NSAIDs) Increased serum bile acids Coagulopathy: prolonged PT and APTT, low fibrinogen, low plasma protein C, thrombocytopenia Other findings depend on underlying systemic disorder. Urinalysis: hyperbilirubinuria (small degrees of bilirubinuria may be normal in dogs, because dogs can conjugate bilirubin renally). In cats, all bilirubinuria is considered pathologic. Imaging: Abdominal radiographs: liver normal or increased in size Abdominal ultrasound: liver normal or increased in size; variable changes in echogenicity; hypoechoic mass or fluid collection possible (abscess). Evaluate gallbladder and bile ducts to rule out disorders other than acute hepatic injury as a cause of jaundice/icterus, such as posthepatic disorders including extrahepatic biliary tract disease (gallbladder mucocele, cholecystitis, cholelithiasis) or obstruction (distended gallbladder and bile ducts). Evaluate pancreas for acute pancreatitis; other findings dependent on underlying multisystemic or extrahepatic disorder.
ADVANCED OR CONFIRMATORY TESTING Liver biopsy: Characterize hepatic lesion histologically; hepatic necrosis most common lesion associated with acute hepatic failure; differentiate acute from chronic (fibrosis, nodular regeneration). May provide specific diagnosis (infectious diseases). Fine-needle aspiration and cytologic evaluation of the liver: rapid screening for mycoses, neoplasia, feline hepatic lipidosis, abscess (ultrasound-guided); accuracy is poor for many hepatic diseases. Bacterial cultures: aerobic and anaerobic of liver and bile (cholangitis, abscess) Serum antibody titers for infectious diseases (leptospirosis, mycoses, toxoplasmosis, others) Tests to evaluate for systemic or extrahepatic disorders (pancreatic lipase immunoreactivity for acute pancreatitis; thoracic radiographs for systemic fungal infection, toxoplasmosis, metastatic neoplasia) If aflatoxin contamination of pet food is suspected, save a sample of suspect food in an airtight bag, with packaging information including product and date code. Submit food for aflatoxin level determination. Because of the rapid metabolism and excretion of aflatoxin, detection of aflatoxin in serum and liver tissue is less reliable.
TREATMENT TREATMENT OVERVIEW For patients with mild hepatic injury (not in acute hepatic failure) showing few or no clinical signs, treat underlying systemic disorder, discontinue any potentially hepatotoxic medications, provide supportive care including oral hepatoprotective agents such as S-adenosylmethionine (SAMe) and silybin, and monitor liver biochemistries to assess response. For patients with acute hepatic failure, intensive supportive therapy is warranted as described below. The goal of treatment is to allow adequate time for hepatic regeneration and repair, prevent or control complications of liver failure, and treat the underlying cause when possible.
ACUTE GENERAL TREATMENT IV fluid therapy with balanced electrolyte solution; supplement with KCI using conventional sliding scale(20-40 mEq/L to start); maintain normoglycemia by adding 2.5%-5% dextrose to fluids. Avoid alkalosis in hepatic encephalopathy (give 0.9% saline rather than lactated Ringer's solution). Treat underlying cause when possible; discontinue any suspect drug; start amoxicillin or penicillin for empirical treatment of
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suspected leptospirosis (dogs), or broad-spectrum systemic antibiotics for sepsis. Give N-acetylcysteine as a glutathione source/antioxidant for treatment of acetaminophen toxicity at 140 mg/kg (10% or 20% solution diluted at least 1:2 with saline) IV over 20-30 minutes through 0.25-m nonpyrogenic filter; then 70 mg/kg IV or PO q 6 h for 7 treatments. May also be beneficial for treatment of other drug-induced injuries (carprofen, potentiated sulfonamides, diazepam, methimazole, others), aflatoxin-induced hepatic injury, or organic solvents and heavy metal toxicity. Other hepatoprotective therapy (empirical therapy): SAMe, 20 mg/kg PO q 24 h, as a glutathione source (given as follow-up to IV N-acetylcysteine when oral therapy is tolerated) Silybin (milk thistle) protective against Amanita mushroom toxicity in an experimental study in dogs at 50 mg/kg IV. Oral dose for dogs and cats is 20-50 mg/kg q 24 h of 60%-80% silybin but poor absorption. Veterinary product, Marin (Nuramax Laboratories Inc.), 5-10 mg/kg q 24 h, contains silybin bound to phosphatidylcholine to improve gastrointestinal absorption. Vitamin E (15 IU/kg PO q 24 h) as an antioxidant For nonspecific control of vomiting use antiemetics such as maropitant (1 mg/kg SQ q 24 h or 2 mg/kg PO q 24 h), metoclopramide (0.2-0.4 mg/kg IV, IM, SQ, PO q 6-8 h or 1-2 mg/kg/24 h IV constant rate infusion), or ondansetron (0.1-0.2 mg/kg SQ or slow IV q 8 h). Treat or prevent gastric ulceration with famotidine (0.5-1 mg/kg IV or PO q 12-24 h), omeprazole (0.7-1 mg/kg PO q 12-24 h) or pantoprazole (0.7-1 mg/kg IV q 12-24 h). For treatment of coagulopathy, give fresh-frozen plasma and parenteral vitamin K1 (0.5-1 mg/kg q 12-24 h SQ for two or three doses or until PT normalizes). Treat for hepatic encephalopathy (if present; see p. 501) using a high-quality low-protein diet, lactulose (0.1-0.5 mL/kg PO q 12 h, adjusted to achieve soft fecal consistency), and/or intestinal antibiotics such as metronidazole (7.5-10 mg/kg PO q 12 h) or amoxicillin-clavulanate (15 mg/kg PO q 12 h).
CHRONIC TREATMENT Consider empirical oral hepatoprotective therapy (SAMe, silybin, or vitamin E) until evidence of hepatic injury resolves. Glucocorticoids are generally not warranted.
NUTRITION/DIET Provide adequate dietary protein and calories. Do not restrict dietary protein unless hepatic encephalopathy is present (see p. 501); choose nonmeat protein sources such as dairy (e.g., cottage cheese) and eggs.
DRUG INTERACTIONS Avoid drugs that require hepatic metabolism
POSSIBLE COMPLICATIONS Hepatic encephalopathy Hypoglycemia Coagulopathy and anemia Gastrointestinal ulceration Septicemia
RECOMMENDED MONITORING Serum biochemistry profiles Blood glucose Serum bile acids (anicteric patients) Packed cell volume/total protein (anemia/bleeding)
PROGNOSIS AND OUTCOME If patient presents with signs of advanced liver failure (e.g., hepatic encephalopathy, coagulopathy, hypoglycemia), the prognosis is guarded. For milder hepatic injury, complete recovery is possible, especially when underlying cause is detected and treated.
PEARLS & CONSIDERATIONS
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Hepatic Injury, Acute
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COMMENTS Clinical and laboratory features reflect general hepatic failure; they are not specific for underlying cause of hepatic injury. Always consider an adverse drug reaction as the cause of acute hepatic injury or failure, as discontinuing suspect drug can result in improved hepatic function.
PREVENTION Vaccinate for infectious diseases (e.g., infectious canine hepatitis, leptospirosis). Monitor liver enzymes when prescribing a drug with potential to cause hepatotoxicity; promptly discontinue if enzyme elevations arise. Avoid reexposure of patient to drug suspected to have caused hepatic reaction.
SUGGESTED READING Dereszynski DM, Center SA, Randolph JF, et al: Clinical and clinicopathologic features of dogs that consumed foodborne hepato-toxic aflatoxins: 72 cases (2005-2006). J Am Vet Med Assoc 232:1329, 2008. Dunayer EK, Gwaltney-Brant SM: Acute hepatic failure and coagulopathy associated with xylitol ingestion in eight dogs. J Am Vet Med Assoc 229:1113, 2006. AUTHOR: SUSAN E. JOHNSON EDITOR: KEITH P. RICHTER
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Hepatic Encephalopathy
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Hepatic Encephalopathy BASIC INFORMATION DEFINITION A reversible metabolic central nervous system (CNS) disturbance secondary to hepatic disease
EPIDEMIOLOGY SPECIES, AGE, SEX Dogs and cats Congenital hepatic vascular disease: young Acquired hepatic disease: middle-aged to older GENETICS & BREED PREDISPOSITION Hepatic vascular disease: several breed predispositions (see p. 905) Acquired liver disease: see pp. 1054, and 513. RISK FACTORS Acute hepatic disease Hepatotoxic drugs and toxins Congenital hepatic vascular disease: Single portosystemic vascular anomalies Primary hypoplasia of the portal veins (microvascular dysplasia) Hepatic arteriovenous fistula or malformation Multiple acquired portosystemic shunts secondary to portal hypertension from chronic hepatic disease
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT: Historic signs of chronic liver disease typically are episodic, involving three systems: Neurologic: diffuse cerebral disturbance: lethargy, poor appetite, aimless wandering, head pressing, disorientation, seizures, blindness, depression, stupor, coma, behavioral changes. Poor anesthesia tolerance/prolonged recovery. Gastrointestinal (GI): vomiting, diarrhea, poor weight gain, ptyalism (cats) Urinary: polyuria and polydipsia, stranguria, pollakiuria, dysuria, and/or hematuria associated with ammonia biurate uroliths PHYSICAL EXAMINATION Signs of diffuse cerebral disease but may be subclinical at the time of examination owing to the episodic nature of hepatic encephalopathy. Rarely, multifocal and lateralizing neurologic signs are present. Congenital patients: stunted growth possible Cats with congenital portosystemic shunts often have copper-colored irises. Acquired hepatic disease: ascites, icterus Acute hepatic failure: initial neuroexcitatory behavior (restlessness, agitation, seizure) progressing to more neuroinhibitory states (depression, coma) Hepatic arteriovenous fistula: a continuous murmur may be ausculted on the cranioventral abdomen.
ETIOLOGY AND PATHOPHYSIOLOGY Complex multifactorial etiology: Associated with the accumulation of neurologic toxins, most likely of gut origin, that escape hepatic detoxification as a result of shunting of blood away from the portal vasculature into the systemic vasculature. GI toxins derived primarily from bacterial metabolism of proteinaceous waste Ammonia generation in the colon
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Hepatic Encephalopathy
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Endogenous benzodiazepine-like substances Alterations in inhibitory (γ-aminobutyric acid) and excitatory (glutamate) neurotransmitter balance playing a secondary role Low-grade cerebral edema due to astrocyte detoxification of ammonia to glutamine may also play a role in the development of chronic hepatic encephalopathy associated with portosystemic shunting. Pathophysiology of encephalopathy associated with acute hepatic failure is distinct from chronic hepatic en cephalopathy and is complicated by development of overt intracranial hypertension with cerebral edema secondary to alterations in the blood-brain barrier, disturbances in cerebral blood flow, and release of neurotoxic substances by the necrotic liver; frequently is complicated by neuroglycopenia.
DIAGNOSIS DIAGNOSTIC OVERVIEW A tentative diagnosis is made when a patient with liver disease shows signs of neurologic dysfunction.
DIFFERENTIAL DIAGNOSIS Neurologic signs: hypoglycemia, lead toxicity, congenital CNS malformation such as hydrocephalus or storage disease, infectious encephalitis/meningitis (e.g., feline infectious peritonitis infection, toxoplasmosis, neosporosis, canine distemper encephalitis), granulomatous meningoencephalitis, CNS neoplasia, thiamine deficiency (cats). Chronic GI or urinary signs may mimic primary GI disease or suggest primary genitourinary or endocrine disorders.
INITIAL DATABASE CBC: microcytosis, poikilocytosis (cats) Serum biochemistry profile: Hepatic vascular disease: profile results may be normal or show mild hypoalbuminemia, low blood urea nitrogen, mild increases in serum alanine aminotransferase and serum alkaline phosphatase (ALP) activities (some elevation of ALP activity in young animals may be normal bone isoenzyme), hypocholesterolemia, hypoglycemia (especially in young toy breeds) Acquired hepatic disease: hypoalbuminemia, moderate to severe increases in all serum hepatic enzyme activities, ± hyperbilirubinemia, hypercholesterolemia or hypocholesterolemia, hypoglycemia (with acute hepatic failure) Urinalysis: isosthenuria common; ammonia biurate crystalluria, hematuria, pyuria, bacteruria possible
ADVANCED OR CONFIRMATORY TESTING Clinical Pathology: Total serum bile acids: sensitive for the detection of congenital or acquired portosystemic shunting (2-hour postprandial sample more sensitive) Blood ammonia: specific indicator of hepatic encephalopathy but can be normal even during overt hepatic encephalopathy. Ammonia tolerance test more sensitive to detect hepatic encephalopathy but may induce severe neurologic signs. Urinary bile acids: less sensitive than serum bile acids in the dog (but may be more convenient) Abdominal effusion: pure or modified transudate Imaging: Abdominal ultrasound: Portosystemic vascular anomaly: identification of a vascular communication between the intrahepatic or extrahepatic portal circulation and the systemic vasculature (see p. 905), microhepatica, renomegaly, urolithiasis Primary hypoplasia of the portal veins (see p. 723): ± microhepatica, ± abdominal effusion, may be unremarkable Hepatoarteriovenous fistula or malformation: identification of fistula, abdominal effusion Chronic hepatitis/hepatopathies, cirrhotic/fibrosing liver disease: microhepatica, possible nodular liver with cirrhosis, abdominal effusion; visualization of multiple portosystemic shunts may be difficult. Rectal or splenic technetium scans (see p. 1259): Abnormal with single or multiple portosystemic shunts and normal with primary hypoplasia of the portal veins without portal hypertension (microvascular dysplasia) Histopathology: Hepatic histopathology: Same pattern of changes (arteriolar proliferation, hepatic atrophy, attenuation of portal vasculature, lobular collapse)
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seen with all forms of hepatic vascular disease
TREATMENT TREATMENT OVERVIEW Goals of treatment are to lower levels of circulating neurotoxins by modulating GI protein metabolism, maintain optimum nutritional plane, and control precipitating factors.
ACUTE AND CHRONIC TREATMENT Nothing per os if stupor or coma is present Address fluid and electrolyte imbalances, avoid lactated solutions with acute hepatic failure, sodium restrict fluids with ascites, potassium and glucose supplementation as needed, B vitamins (especially thiamine and cobalamin in cats). Medications that increase GI protein tolerance Lactulose: drug of choice. Nonabsorbable disaccharide broken down by colonic bacteria into short-chain fatty acids. Traps soluble NH3 as NH4+ , which is nonabsorbable and thus excreted in the feces. Alters bacterial metabolism so that less ammonia is generated. Titrated from an initial dose of 0.5 to 1 mL/kg PO q 8-12 h to dose that produces 3-4 soft stools per day. If stupor or coma is present, may be given rectally in a retention enema (see p. 1258). Antibiotics: Alter bacterial metabolism, synergistic with lactulose Metronidazole (7.5 mg/kg PO q 8-12 h, low dose to avoid neurotoxicity secondary to decreased hepatic metabolism of the antibiotic); or Neomycin (10-22 mg/kg PO q 12 h) (may be difficult to obtain; can be given orally or as a retention enema) or ampicillin (22 mg/kg PO q 12 h) Seizures: control seizure activity: Barbiturates (e.g., phenobarbital 6-10 mg/kg slowly IV to effect); the patient should be monitored closely for respiratory depression. Propofol is useful for controlling hepatic encephalopathy–induced status epilepticus. Because it is metabolized by the liver, small doses may be used and may have a longer duration of action. Maintain an anesthetized state for several hours before tapering and observing for recurrence. Monitor for apnea during use. If patient is seizuring due to hepatic encephalopathy from acute liver injury: cerebral edema is likely, and the prognosis is grave (seizures often refractory to treatment). Mannitol (0.5 g/kg given IV over 10-15 minutes). Infusion of N-acetylcysteine (140 mg/kg IV initially followed by 70 mg/kg as needed) may correct disturbances in microcirculation. Corticosteroids of no benefit and may be detrimental. Monitor closely (q 4 h) for hypoglycemia; may require infusion of high concentrations of dextrose-containing solutions. Control precipitating factors: Oral protein loading: gastrointestinal hemorrhage, high protein meals Catabolic conditions such as infections, dehydration, azotemia Alkalosis with hypokalemia: increases renal ammonia production Synergistic neural inhibition with sedatives, tranquilizers, or anesthetic agents; use these with caution if at all (e.g., diazepam). Constipation Transfusion with stored blood products containing high ammonia concentrations Medications to increase GI protein tolerance are first-line therapy (see Acute General Treatment above).
NUTRITION/DIET Adequate calories to avoid catabolism of muscle, which is highly ammongenic and may make control of hepatic encephalopathy difficult. Modulation of protein content: high-quality protein derived preferably from plant and dairy products. Start with diet containing minimum daily protein requirements (cat: 6.5 g/100 kcal; dog: 5.1 g/100 kcal) in combination with medications to increase protein tolerance and decrease protein only if necessary. Increase fiber content (e.g., by adding bran or canned/cooked pumpkin). Vitamin supplementation: thiamine in cats (50-100 mg PO daily), vitamin K (if associated coagulopathy) initially parenterally (0.5 mg/kg SQ q 12 h) for 5-7 days then once weekly. Sodium restriction necessary only with ascites: 0.04-0.05 g/100 kcal.
DRUG INTERACTIONS
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Neuroinhibitory drugs (e.g., sedatives, anesthetics, and tranquilizers) should be used cautiously, as they may potentiate the neuroinhibition of hepatic encephalopathy. Avoid drugs that depend heavily on hepatic metabolism and/or excretion if possible.
RECOMMENDED MONITORING Blood ammonia concentration Mentation and appetite at home Body weight and body condition score Serum albumin
PROGNOSIS AND OUTCOME Depends on nature of underlying liver disease causing encephalopathy: Hepatic vascular disease (portosystemic shunt, microvascular dysplasia, arteriovenous fistula or malformation): in general, clinical signs of hepatic encephalopathy due to congenital hepatic vascular disease respond quickly and fully to appropriate drug and dietary intervention. Long-term prognosis depends on whether the congenital intrahepatic or extrahepatic shunt can be fully attenuated or the arteriovenous fistula can be resected (in which case signs of hepatic encephalopathy typically abate) and whether these conditions are complicated by primary hypoplasia of the portal veins (microvascular dysplasia), which causes continued shunting of blood from the portal circulation. Acquired chronic hepatic disease: clinical signs of hepatic encephalopathy generally abate with proper intervention, but long-term prognosis depends on severity of the underlying hepatic disorder. Generally, patients with signs of severe hepatic encephalopathy due to acquired hepatic diseases have a very poor prognosis unless the underlying disease can be reversed. Acute liver failure: encephalopathy generally is more refractory to therapy, probably reflecting a more complex underlying cerebral lesion or process. Encephalopathy progressing to coma or stupor (grade 3-4) is considered a grave prognostic sign and is one of the criteria used for determining the need for transplantation in human patients.
PEARLS & CONSIDERATIONS COMMENTS Normal blood ammonia concentration does not rule out the presence of hepatic encephalopathy. Initial treatment of hepatic encephalopathy involves steps to increase dietary protein tolerance (nonabsorbable disaccharides and antibiotics) in combination with dietary protein modulation, but not excessive restriction. Be aware of common comorbid conditions that can complicate control of hepatic encephalopathy, such as GI bleeding, dehydration, hypokalemia, azotemia, constipation, and alkalosis. Encephalopathy accompanying acute hepatic failure differs from that accompanying congenital vascular disorders or chronic hepatic failure in that it involves the development of overt cerebral edema and an initial neuro-excitatory state often refractory to therapeutic intervention. In addition, patients with signs of severe hepatic encephalopathy due to acquired hepatic diseases have a very poor prognosis.
CLIENT EDUCATION Hepatic encephalopathy is an episodic chronic condition that cannot be cured but can be controlled with strict adherence to dietary modulation and drug therapy.
SUGGESTED READING Häussinger D, Schliess F: Pathogenetic mechanisms of hepatic encephalopathy. Gut 57:1156–1165, 2008. Maddison JE: Hepatic encephalopathy: current concepts of pathogenesis. J Vet Intern Med 6:341–353, 1992. AUTHOR: CYNTHIA R.L. WEBSTER EDITOR: KEITH P. RICHTER
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Hemotropic Mycoplasmosis, Cat
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Hemotropic Mycoplasmosis, Cat BASIC INFORMATION DEFINITION An infection of feline red blood cells (RBCs) with the bacterial organisms Mycoplasma haemofelis, “Candidatus Mycoplasma turicensis” or “Candidatus Mycoplasma haemominutum.” Mycoplasma haemofelis is the most pathogenic species and it causes hemolytic anemia, which is usually extravascular.
SYNONYM Haemobartonella felis (outdated); feline hemotropic (or hemotrophic) mycoplasmosis; feline infectious anemia
EPIDEMIOLOGY SPECIES, AGE, SEX Domestic and wild felines of all ages. Young cats may be more likely to present with hemolytic anemia secondary to Mycoplasma haemofelis infection. Male cats are more likely to be infected than females, possibly due to roaming and fighting behavior. RISK FACTORS Access to outdoors Bloodsucking arthropods, including fleas, ticks, and mosquitoes, have been suggested to play a role in transmission. Underlying retrovirus infection, in particular with feline immunodeficiency virus A history of cat bite abscess often precedes hemoplasmosis by a few weeks, and hemoplasmas have been detected in saliva, suggesting a possible mode of transmission. CONTAGION AND ZOONOSIS Transplacental spread has been hypothesized. Transmission via blood transfusion is possible. The DNA of Mycoplasma haemofelis has been detected in a person coinfected with HIV and Bartonella henselae from Brazil, so these organisms may have zoonotic potential. GEOGRAPHY AND SEASONALITY Worldwide
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES Acute, chronic, or subclinical Clinical signs depend on anemia (severity and rate of development) HISTORY, CHIEF COMPLAINT Acute: sudden death, weakness, depression, collapse, pale mucous membranes, tachypnea, anorexia, ± vomiting, neurologic signs Chronic: lethargy, anorexia, weight loss Subclinical: no abnormalities reported; more likely with “Candidatus M. turicensis” and “Candidatus M. haemominutum” infections PHYSICAL EXAM FINDINGS Acute: pale mucous membranes, fever, tachypnea, tachycardia, mental depression, weakness, splenomegaly, systolic cardiac murmur due to amnesia, rarely icterus
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Hemotropic Mycoplasmosis, Cat
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Chronic: pale mucous membranes, poor body condition, weakness, splenomegaly
ETIOLOGY AND PATHOPHYSIOLOGY Three species of feline hemotropic mycoplasmas have been identified in cats: Mycoplasma haemofelis: this is the most pathogenic species, causing hemolytic anemia in immunocompetent cats. “Candidatus Mycoplasma haemominutum”: this is detected in as many as one in five cats visiting veterinary hospitals and is usually not associated with hemolytic anemia. “Candidatus Mycoplasma turicensis”: this is the most recently recognized species, and its pathogenicity may lie between that of M. haemofelis and “Candidatus M. haemominutum.” Coinfection may occur with two or more hemoplasma species. Organisms reside on the surface of—and possibly replicate within—RBCs, causing RBC destruction, which is predominantly extravascular, and ultimately a regenerative anemia, possibly via increased RBC fragility, erythrophagocytosis, and/or immune-mediated destruction. Appearance of large numbers of organisms on blood smears is associated with precipitous declines in the hematocrit, after which organisms may disappear for several days. Eventually cats recover from this phase of infection, after which the hematocrit increases, and organisms disappear from blood smears. A carrier state may develop in some cats, especially those infected with “Candidatus M. haemominutum.”
DIAGNOSIS DIAGNOSTIC OVERVIEW This diagnosis becomes suspected either when a cat is anemic or when a blood smear appears to be consistent with RBC infection by these organisms. Hemoplasmas are unculturable mycoplasmas, so diagnosis relies on organism identification on blood smears (which has low sensitivity and specificity) or molecular diagnosis using PCR. PCR assays are considered the gold standard for diagnosis, but results must be interpreted differently depending on the hemoplasma species detected.
DIFFERENTIAL DIAGNOSIS Primary immune-mediated hemolytic anemia Heinz body anemia (acetaminophen toxicity, zinc toxicity, diabetic ketoacidosis, ingestion of onions or baby food containing onion powder) Cytauxzoonosis Hereditary erythrocyte disorders such as those of Abyssinian and Somali cats External or internal blood loss Feline leukemia virus (FeLV) infection
HEMOTROPIC MYCOPLASMOSIS, CAT Hematologic differential diagnosis. The larger Howell-Jolly body (large arrow) or multiple punctate appearance of basophilic stippling (seen throughout the two red cells in the center of the image [small arrows]) should not be mistaken for M. haemofelis (many arrowheads).
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Hemotropic Mycoplasmosis, Cat
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(Courtesy of Department of Clinical Pathology, Atlantic Veterinary College; reproduced with permission.)
INITIAL DATABASE Blood smear: visual identification of organism: Nonrefractile basophilic cocci, rods, or ring-forms on the surface of RBCs Such cytologic detection of organisms is 3% should be viewed as having a hemorrhagic contribution.
DIFFERENTIAL DIAGNOSIS Other pleural space disease Hydrothorax (see p. 882), pyothorax, chylothorax, pneumothorax Diaphragmatic hernia Pulmonary parenchymal disease Intrathoracic neoplasia Pericardial effusion
INITIAL DATABASE
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Hemothorax
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CBC: Can be normal if hemorrhage is acute; may reveal mild anemia if hemorrhage is chronic and slow Increased numbers of nucleated red cells, thrombocytopenia, acanthocytes, and schistocytes are suggestive of hemangiosarcoma. Inflammatory and/or stress leukogram Serum biochemistry profile: Hypoalbuminemia (if enough time has passed for fluid shifts) Hypoalbuminemia, hypocholesterolemia, hypoglycemia, and low BUN in patients with coagulopathy secondary to hepatic failure. Thoracic radiographs: Radiographic appearance depends on fluid volume: Small volumes may result in only the presence of interlobar fissure lines. Larger volumes may reveal scalloping or retraction of lung lobes from the thoracic wall, blunting of the lung lobes, impaired visualization of the cardiac silhouette (especially on dorsoventral views), or the presence of a soft tissue opacity ventrally on lateral views. May help with visualization of primary or metastatic neoplasms The presence of pleural effusion can obscure parenchymal lesions, so if neoplasia is a concern, repeat thoracic radiographs after thoracocentesis. May reveal evidence of trauma (rib fractures and pulmonary contusions) Assess integrity of the diaphragm Thoracocentesis prior to radiography increases ability to visualize underlying cause such as neoplasia or diaphragmatic hernia, or concurrent disease such as pulmonary contusions. Thoracocentesis (see p. 1338): Fluid obtained should be collected in EDTA (purple-top) and plain (red-top) tubes for evaluation. PCV and TP will be similar to that of peripheral blood in acute cases. Prothrombin time (OSPT) and activated partial thromboplastin time (APTT) if anticoagulant rodenticide intoxication or congenital coagulopathy is suspected. Prolonged OSPT and APTT are expected in patients with vitamin K rodenticide intoxication. Abnormalities of coagulation times seen with congenital coagulopathy will reflect the specific defect; prolongation of only the OSPT, only the APTT, or both are possible. Can also be supportive of disseminated intravascular coagulation (DIC).
ADVANCED OR CONFIRMATORY TESTING Pleural effusion cytologic examination: Useful for neoplasia (lymphoma) and infectious cases, although an absence of either does not preclude them as causes of hemothorax. Erythrophagocytosis or hemosiderin in macrophages is indicative of chronicity. Thoracic ultrasonography: Should be performed prior to thoracocentesis to improve visualization of intrathoracic structures unless the patient is in respiratory distress Confirms pleural effusion Can guide thoracocentesis Investigation for tumors (pulmonary, mediastinal, heart base, or right auricular masses), lung lobe torsion, abdominal organs within the thoracic cavity, pulmonary thromboembolism Thoracic CT: Similar to thoracic ultrasonography, but thoracocentesis should be performed prior to imaging to improve visualization of parenchyma and vasculature. Proteins induced by vitamin K antagonism (PIVKA): Abnormality is suggestive of rodenticide ingestion. More sensitive than OSPT and APTT D-Dimers: Elevations are supportive of DIC and thromboembolism. Exploratory thoracotomy (usually median sternotomy): Diagnostic test of choice when the cause of hemothorax is not explained by history, physical examination, and results of other diagnostic tests.
TREATMENT TREATMENT OVERVIEW Stabilization of patient and treatment for shock if hemothorax is secondary to trauma Improve respiratory function with supplemental oxygen and/or removal of hemorrhage in patients that are in distress.
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Because autotransfusion occurs rapidly, resulting in resolution of hemothorax within days, complete removal of blood is typically unnecessary unless large volumes of hemorrhage are present. Consequently, thoracocentesis should be performed primarily to alleviate respiratory distress. Identification and treatment of underlying cause when possible
ACUTE GENERAL TREATMENT Improve oxygenation via an intranasal cannula, face mask, or oxygen cage (see p. 1318). Thoracocentesis if in respiratory distress Complete drainage is generally not necessary. Transfusion with whole blood, packed red blood cells, and/or plasma (coagulation disorders) if severe anemia. Vitamin K1 1-2.5 mg/kg PO q 12 h for 14-30 days depending on the anticoagulant rodenticide ingested Can administer subcutaneously initially at same dose Anaphylactic reactions have been reported following intravenous administration. Stabilization of respiratory and circulatory function if secondary to trauma or diaphragmatic hernia Mechanical ventilatory support may be necessary if pulmonary contusions are present.
CHRONIC TREATMENT Repeated thoracocentesis or thoracostomy tube placement Relieves respiratory distress Prevents atelectasis Can quantify hemorrhage Removal of blood can reduce the risk of development of pleuritis, empyema (pyothorax), and pleural fibrosis. Management of pneumonia or systemic disease if present Exploratory thoracoscopy or thoracotomy to surgically excise tumors or locate and ligate bleeding vessels if hemothorax is unexplained or persists despite conservative interventions For some patients, chemotherapy may be indicated following cytologic or histologic confirmation of tumor type.
BEHAVIOR/EXERCISE Activity should be limited until hemorrhage, anemia, or traumatic injuries have resolved.
POSSIBLE COMPLICATIONS Recurrent effusion Dyspnea from large-volume pleural effusion Related to thoracocentesis or thoracostomy tube placement Pneumothorax Parenchymal injury and further hemorrhage Pleuritis, empyema, or fibrosis Rapid reexpansion of lungs can result in reexpansion pulmonary edema. More common with chronic effusions Risk can be minimized by removing large-volume effusions gradually over several hours.
RECOMMENDED MONITORING Respiratory rate and effort Thoracic radiographs or ultrasound Assess need for repeated thoracocentesis.
PROGNOSIS AND OUTCOME Dependent on underlying cause Variable with trauma Good with appropriate treatment of anticoagulant rodenticide intoxication Poor to guarded with most neoplasms and congenital coagulation disorders
PEARLS & CONSIDERATIONS
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Hemothorax
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COMMENTS Hemorrhagic pleural effusion fluid should not clot after removal from the pleural space unless there is continuous bleeding. Trauma significant enough to cause hemothorax will likely result in pulmonary contusions. Cats may require thoracocentesis prior to other diagnostics, as they are easily stressed and can decompensate quickly. In patients with no history of trauma and no evidence of a coagulation defect, neoplasia is a common cause of hemothorax.
PREVENTION Minimize risk of blunt trauma (automobile accident) by using leashes or keeping in enclosed areas. Limit access to anticoagulant rodenticides.
TECHNICIAN TIPS When obtaining blood from patients with known or suspected hemothorax, ideally draw as much blood as needed to accomplish all laboratory diagnostics (CBC, biochemical profile, coagulation tests) at the first draw to minimize venipunctures in case other bleeding tendencies are present. Maintain pressure on venipuncture sites a bit longer than for normal dogs in case there is a more widespread bleeding disorder present. Avoid cystocentesis urine collection until cause of hemothorax has been identified. Collect effusion as aseptically as possible; in occasional cases, especially traumatic hemothorax, hemorrhagic effusion may be autotransfused.
CLIENT EDUCATION Most cases of hemothorax can be avoided by minimizing risk of trauma and access to anticoagulant rodenticides.
SUGGESTED READING Nakamura R, Rozanski E, Rush J: Non-coagu-lopathic spontaneous hemothorax in dogs. J Vet Emerg Crit Care 18(3):292–297, 2008. Prittie J, Barton L: Hemothorax and sanguineous effusions. In King LG, editor: Textbook of respiratory disease in dogs and cats, St Louis, 2004, Saunders, p 610. AUTHOR: ERICK SPENCER EDITOR: RANCE K. SELLON
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Hemorrhagic Gastroenteritis
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Hemorrhagic Gastroenteritis BASIC INFORMATION DEFINITION Acute and profuse hematemesis and hemorrhagic diarrhea accompanied by hypovolemia; may progress to circulatory collapse, multiple organ dysfunction and death
SYNONYMS Acute hemorrhagic enteritis, acute hemorrhagic enteropathy, HGE
EPIDEMIOLOGY SPECIES, AGE, SEX: Dogs, usually young (mean of 5 years) GENETICS & BREED PREDISPOSITION: Hemorrhagic gastroenteritis (HGE) can occur in any breed; toy and small breed dogs may be predisposed. RISK FACTORS: None known; most dogs are otherwise healthy. CONTAGION & ZOONOSIS: Does not appear to be contagious or zoonotic GEOGRAPHY AND SEASONALITY: More prevalent in urban dogs
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT Anorexia and lethargy may be noted initially. Acute onset of vomiting; this may be profuse and often contains fresh blood. Acute onset of diarrhea; this may be brown initially but soon becomes grossly bloody; consistency varies from watery to jamlike. PHYSICAL EXAM FINDINGS Depressed but afebrile Markers of perfusion: heart rate, pulse quality, gum color, capillary refill time (CRT) are all normal in the early stages of the disease. As fluid is lost into the gastrointestinal tract, signs of hypovolemia quickly develop, characterized by pallor, slow CRT, and tachycardia. Skin turgor may not reflect the full extent of fluid losses. Patients may be moribund at presentation if veterinary attention is delayed. Abdominal palpation reveals fluid-filled bowel loops with nonlocalized discomfort. Rectal examination: fresh dark blood or strawberry jam–like feces.
ETIOLOGY AND PATHOPHYSIOLOGY Cause unknown, but an anaphylactic reaction to unidentified bacterial antigens has been implicated. Clostridium perfringens enterotoxins and enteropathogenic/enterotoxigenic E. coli have been associated with HGE, but causal relationships have not been demonstrated. Peracute, massive increase in intestinal permeability results in extravasation of fluid, proteins, and red blood cells into the intestinal lumen. Loss of plasma water, electrolytes, and protein can be extreme. Packed cell volume will rise rapidly and often exceeds 65%. If untreated, disease can progress to hypovolemic shock and death.
DIAGNOSIS
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Hemorrhagic Gastroenteritis
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DIAGNOSTIC OVERVIEW A presumptive diagnosis (sufficient to start treatment) is made based on acute gastroenteritis associated with erythrocytosis (hematocrit often >65%). Dogs with HGE can die unless the disorder is recognized quickly and treated aggressively. It is important to rule out other possible causes of bloody vomiting and diarrhea, but treatment should not be delayed while diagnostic tests are performed.
DIFFERENTIAL DIAGNOSIS Infectious: viral (parvovirus) or bacterial (Salmonella, Campylobacter enteritidis) Dietary indiscretion, toxicity Hypoadrenocorticism Intestinal volvulus, partial obstruction or intussusception Other causes of hypovolemic or endotoxic shock, such as intestinal perforation, peritonitis Necrotizing pancreatitis Coagulopathy
INITIAL DATABASE Hematocrit is classically elevated, often >65%; total solids are low or borderline normal. CBC: expect to see hemoconcentration with a stress leukogram; immature neutrophils or mild toxicity may be noted; modest thrombocytopenia is common. Serum biochemistry profile: increased blood urea nitrogen and alanine aminotransferase activity are expected; hypokalemia and panhypoproteinemia are also common; metabolic acidosis may be severe. Urinalysis: unremarkable; high specific gravity expected in response to hypovolemia Coagulation profile: usually normal early on; may show abnormalities if condition progresses to disseminated intravascular coagulation (DIC) Fecal evaluation (centrifuged flotation and saline preparation): no pathogens noted Fecal stained microscopic exam: increased numbers of red cells, some white cells; organisms consistent with clostridial spores (“safety pins”) may be present. Fecal ELISA for parvovirus (if neonate or unvaccinated): negative Abdominal radiographs: fluid and gas-filled small-intestinal loops; colon may be empty. Colloid oncotic pressure (COP): usually normal at presentation but then declines +/− Cortisol (if breed type or other clinical findings suggest hypoadrenocorticism): baseline cortisol should be >2 µg/dL/55 nmol/L.
TREATMENT TREATMENT OVERVIEW Quickly restore and maintain an effective circulating volume. Recognize the need for colloid support along with crystalloid fluid replacement. Anticipate complications of hypovolemia and widespread gastrointestinal mucosal compromise.
ACUTE GENERAL TREATMENT Initiate fluid resuscitation with IV fluid therapy: Colloids (e.g., Hetastarch) should be started immediately. Administer a bolus of 5 mL/kg over 20 minutes if the patient is substantially hypovolemic; otherwise begin a continuous rate infusion of 1 mL/kg/h; total daily dose should not exceed 20 mL/kg. Crystalloid fluids should be administered concurrently. Replacement-type fluids should be used (e.g., Normosol-R, lactated Ringer's, Plasmalyte 148, 0.9% NaCl). If necessary, calculate a shock dose of crystalloids (90 mL/kg), and bolus one-third of this amount over 20-30 minutes. Do not administer Normosol-R rapidly, as this fluid contains acetate and may cause refractory hypotension. Aim to replace lost volume (estimated by % dehydration × body weight in kg) over 12 hours. Continue fluids at a rate necessary to replace ongoing losses and meet maintenance requirements. If available, use COP measurement to guide colloid administration. Electrolyte disturbances are common; hypokalemia should be addressed specifically, but changes in sodium and chloride should self-correct with standard fluid therapy. Antibiotics are recommended, given the potential for bacterial translocation across the intestinal epithelium. Ampicillin: 30 mg/kg IV q 8 h (adequate choice in most cases); or Ampicillin/sulbactam (Unasyn): 50 mg/kg IV q 8 h (effective against β-lactamase-producing bacteria); or
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Hemorrhagic Gastroenteritis
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Enrofloxacin: 10 mg/kg slow IV q 24 h (if sepsis is suspected) Antiemetics should be administered if vomiting is persistent Maropitant (1 mg/kg SQ q 24 h) is an effective first choice (patient must be >16 weeks old); or Metoclopramide (1.1-2.2 mg/kg/24 h given as constant rate infusion) Antacids and gastric protectants should be administered in patients with hematemesis Famotidine (0.5 mg/kg IV or SQ q 12-24 h); and/or Sucralfate (250-1000 mg/dog PO q 8 h); begin when vomiting has stopped
NUTRITION/DIET Withhold water until vomiting is adequately controlled, then offer small amounts every 1-2 hours. Food should be provided as soon as the patient is interested in eating and vomiting is reduced. Easily digestible diets may be beneficial (e.g., boiled white rice with cottage cheese or boiled chicken), as gastric emptying times are shorter, and fecal volume is minimized. Probiotics +/− prebiotics should be considered, as disruption of the normal intestinal flora is both a likely cause and consequence of HGE.
POSSIBLE COMPLICATIONS Condition may progress to hypovolemic shock, DIC, and death if not treated appropriately. Esophagitis may occur if vomiting is persistent. Obtunded patients are vulnerable to aspiration pneumonia. Translocation of bacterial across the compromised gastrointestinal mucosa may result in sepsis. Cardiac arrhythmias can occur secondary to poor perfusion.
DRUG INTERACTIONS Metoclopramide is incompatible with many antibiotics (including ampicillin); the infusion must be discontinued while other medications are administered.
RECOMMENDED MONITORING Monitor vital parameters (temperature, heart rate, mucous membranes, CRT, pulse quality, blood pressure) and ongoing fluid losses every 2 hours. Hematocrit and total solids every 4-6 hours. Glucose, BUN, and electrolytes should be checked every 6-8 hours initially. COP should be checked every 6-8 hours or as needed to guide decisions about colloid therapy.
PROGNOSIS AND OUTCOME Recovery is usually rapid and complete over 1-2 days; some severely affected dogs may require supportive therapy for several days before return of normal GI function. Condition can progress quickly to multiple organ dysfunction syndrome, DIC, and death without appropriate fluid therapy. A total of 10% of affected dogs may die despite therapy.
PEARLS & CONSIDERATIONS COMMENTS The diagnostic hallmark for HGE is a markedly elevated hematocrit with normal to slightly low total protein. Colloid support is often essential and should not be overlooked. Rule out hypoadrenocorticism, especially in a high-risk breed (e.g., Nova Scotia Duck Tolling Retriever Portuguese water dog, standard poodle, West Highland white terrier).
CLIENT EDUCATION A total of 10%-15% of dogs will have repeated episodes of HGE.
SUGGESTED READING
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Hemorrhagic Gastroenteritis
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Boag AK, Hughes D: Assessment and treatment of perfusion abnormalities in the emergency patient. Vet Clin North Am Small Anim Pract 35:319, 2005. AUTHOR: AUDREY K. COOK EDITOR: DEBRA L. ZORAN 1ST EDITION AUTHOR: AMIE KOENIG
25-09-2011 21:43
Hemorrhage
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Hemorrhage BASIC INFORMATION DEFINITION The loss of blood from the vascular space into surrounding tissues or from body surfaces Clinical signs of hemorrhage result from one of two general mechanisms: Blood loss from damaged or diseased blood vessels Bleeding diatheses: defects causing failure of normal hemostatic processes
EPIDEMIOLOGY SPECIES, AGE, SEX: Dogs and cats of all breeds and either sex may be affected, with specific predilections depending on underlying cause. Blood vessel defects are generally acquired disorders, whereas bleeding diatheses may be hereditary traits (e.g., von Willebrand disease) or acquired disorders (e.g., coagulopathy of rodenticide poisoning). GENETICS & BREED PREDISPOSITION See pp. 491, , and online chapter: Platelet Dysfunction. RISK FACTORS: See pp. 491, , and . ASSOCIATED CONDITIONS & DISORDERS Blood vessel defects typically arise from: Traumatic or surgical injuries Inflammatory or neoplastic conditions causing vessel erosion and infiltration Bleeding diatheses are classified as: Failure of platelet plug formation (primary hemostatic defects) Failure of fibrin clot formation (secondary hemostatic defects = coagulopathies) Disease conditions such as hypertension, anemia, and hyperviscosity alter the normal flow properties of blood (hemorrheology) and are associated with microvascular hemorrhage.
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES: Subtype classification based on: Duration: acute versus chronic hemorrhage Location: focal or regional versus multiple anatomic sites Tissue or vessel involvement: capillary bleeding versus hemorrhage into joint space, body cavities Primary hemostatic defects (failure of platelet plug formation [e.g., from thrombocytopenia or platelet dysfunction] cause signs of hemorrhage involving capillaries and small vessels [arterioles, venules], clinically evident as petechiae, ecchymoses, bleeding from mucosal surfaces, and nonspecific bleeding from surgical and traumatic wounds). Secondary hemostatic defects (coagulopathies; failure of fibrin clot formation [e.g., from coagulation factor deficiency]) generally cause spontaneous hemorrhage into body cavities or potential spaces (i.e., pleural space, intramuscular tissue planes), resulting in hemothorax, hemoabdomen, hemarthrosis, hematoma formation, and nonspecific bleeding from surgical and traumatic wounds. HISTORY, CHIEF COMPLAINT: Depends on underlying cause. Frank hemorrhage, hematoma formation, and petechiae are obvious signs that may prompt owners to seek veterinary care. Additional signs include pallor and collapse due to acute hemorrhagic shock, or gradual onset of weakness due to chronic blood-loss anemia. PHYSICAL EXAM FINDINGS Physical exam alone may differentiate vessel defects from systemic bleeding diatheses: Frank hemorrhage due to traumatic or surgical blood vessel injury, or vessel infiltration due to solid tumors or inflammatory mass lesions, may be obvious on physical exam or via ancillary diagnostics (endoscopy, radiography). Petechiae evident on cutaneous or mucosal surfaces or funduscopic exam indicate primary hemostatic defect.
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Hemorrhage
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Retinal hemorrhage and alterations of the normal retinal vasculature may result from abnormal blood flow (hemorrheologic defects such as systemic hypertension, hyperviscosity, anemia). Other signs are nonspecific (epistaxis, hematuria, melena, hematemesis, hemothorax, hemoabdomen). Hemorrhage from multiple anatomic sites and/or recurrent episodes are suggestive of a bleeding diathesis rather than blood vessel defects.
ETIOLOGY AND PATHOPHYSIOLOGY Blood vessel defects: physical disruption, as described above Bleeding diatheses: Acquired primary hemostatic defects: Thrombocytopenia is the most common bleeding diathesis. Platelet dysfunction Hereditary primary hemostatic defects: Platelet dysfunction/thrombopathia von Willebrand disease Acquired coagulopathies (secondary hemostatic defects): Vitamin K deficiencies (anticoagulant rodenticide intoxication, biliary obstruction, chronic oral antibiotic administration, warfarin overdose, neonatal) Hepatic synthetic failure (hepatic necrosis, atrophy, portosystemic shunts) Consumptive coagulopathy (disseminated intravascular coagulation [DIC]) Drug intoxications, envenomation, complication of heparin, hetastarch, dextran, fibrinolytic drug therapy Dilutional coagulopathy: platelet and/or factor deficiency secondary to massive transfusion with stored blood products or high-volume fluid administration Hereditary coagulopathies (secondary hemostatic defects): Hemophilia Autosomal factor deficiencies
DIAGNOSIS DIAGNOSTIC OVERVIEW Vascular injury is by far the most common cause of hemorrhage, and clinicians should begin with a thorough physical exam to identify a source of injury. If history and exam are inconsistent with injury, a prompt evaluation for hemostatic defects is warranted to avoid delays in treatment.
DIFFERENTIAL DIAGNOSIS Blood vessel defect versus bleeding diathesis: Initial physical exam and imaging studies may define the site and cause of vessel defects. If a vessel defect cannot be defined on physical exam, blood pressure measurement and screening tests to rule out bleeding diatheses must be performed before performing invasive procedures.
INITIAL DATABASE Thorough physical exam to define nature and location of hemorrhage Baseline hematocrit and plasma protein Platelet count Blood pressure measurement: Normal in calm setting, awake and resting patient, repeatable measures using Doppler: systolic 40°C (105.8°F). Note that emergency treatment by owner before arrival may lower the rectal temperature so that the actual peak temperature is not known. Altered mental status Hyperemic mucous membranes
25-09-2011 21:40
Heat Stroke/Hyperthermia
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Increased respiratory effort and loud upper airway sounds Petechiae
ETIOLOGY AND PATHOPHYSIOLOGY Elevation of core body temperature results in activation of inflammatory cytokines, alters mitochondrial function, breaks down lipids within cell walls, denatures proteins and enzymes, and leads to cell necrosis. Pulmonary: disruption of pneumocytes of the alveolar endothelium and pulmonary capillary beds leads to protein-rich fluid accumulating within the alveolar space, altering surfactant and inciting additional inflammation, which in turn reduces gas exchange, increases the shunt fraction, and reduces pulmonary compliance. This can lead to noncardiogenic pulmonary edema (), severe hypoxemia, and acute respiratory distress syndrome (). Cardiovascular: hyperthermia, hypoperfusion and acidosis cause ischemia and necrosis of cardiac myocytes and Purkinje fibers, leading to ventricular arrhythmias (), conduction disturbances, and myocardial dysfunction. Hematologic: endothelial cells are particularly prone to thermal injury. When damaged, these cells release procoagulant factors, activate and/or destroy platelets, activate complement and clotting cascades, which causes a systemic inflammatory response and coagulation. Disseminated intravascular coagulation (DIC; ) is a common cause of death in severely affected patients. Renal: acute kidney injury can occur as a result of direct thermal injury, microemboli, hypoxia, and hypoperfusion. Renal failure is common in severe heatstroke. Neurologic: excess inflammatory and endogenous cytokines and microemboli can result in cerebral edema and neuronal tissue death. Malignant hyperthermia is an extremely rare genetically based disorder involving rapid-onset hyperthermia, usually triggered by such specific agents as halothane or succinylcholine.
DIAGNOSIS DIAGNOSTIC OVERVIEW Diagnosis of hyperthermia is generally straightforward (markedly elevated body temperature), and diagnostic efforts are mainly aimed at identifying and monitoring secondary complications that occur in severe cases, and an inciting cause if one is not known from the history alone.
DIFFERENTIAL DIAGNOSIS Hyperthermia: heat stroke, fever
INITIAL DATABASE Complete physical exam including neurologic examination (see p. 1311) In heat stroke, mental status is important prognostically, as dogs that are obtunded are less likely to survive. CBC: hemoconcentration is common and can be severe. The presence of nucleated red blood cells occurs in up to 68% of cases. A neutrophilic leukocytosis is most common, but patients can also be leukopenic due to peripheral neutrophil chemotaxis and migration. Most animals (62%) are thrombocytopenic at admission, and 83% become thrombocytopenic during hospitalization. Serum biochemistry profile: elevation in creatinine kinase from muscle damage is the most common abnormality noted, occurring in nearly every case. Elevations in ALT, AST, and ALP are also very common but rarely affect patient outcome. Hypoglycemia and elevated creatinine values can occur in more than 50% of patients and are negative prognostic features. Prothrombin time (PT), activated partial thromboplastin time (APTT) are frequently prolonged in severely affected patients and these elevations are of negative prognostic value.
TREATMENT TREATMENT OVERVIEW Treatment goals: With obtunded/comatose patients, immediate intubation to secure a patent airway is paramount to improve gas exchange, provide additional oxygen supplementation, reduce the risk of aspiration. and allow for additional heat dissipation. Active cooling Determine etiology and treat underlying cause as needed. Manage complications such as DIC, acute renal failure, sepsis, or cerebral edema.
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Heat Stroke/Hyperthermia
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ACUTE GENERAL TREATMENT Lukewarm (room temperature) IV fluids and cool water baths to decrease temperature while avoiding excessive peripheral vasoconstriction. Additional cooling techniques can include infusing the bladder with sterile, lukewarm fluid or cold water gastric lavage. Peritoneal lavage invasive, time consuming, and not clearly superior. Active external cooling should be discontinued once the rectal temperature reaches 103-103.5°F (39.2-39.4°C) to reduce the risk of severe hypothermia. Treat hypoglycemia () if present. Mannitol (20% injectable solution [200 mg/mL]: 0.5-1 g/kg given IV slowly over 15-20 minutes) may be used if increased intracranial pressure is suspected. Seizure activity should be managed with diazepam, 0.2-0.5 mg/kg IV, repeated up to three times; if ineffective, either phenobarbital (4 mg/kg IV q 30 minutes up to 16 mg/kg) or propofol continuous rate infusion (CRI) (6 mg/kg IV bolus followed by 0.1-0.2 mg/kg/min). Ventricular arrhythmias (see p. 1165) should be triaged and treated if necessary. Fresh frozen plasma (10-15 mL/kg) should be administered if coagulation times are prolonged or there is clinical evidence of bleeding. Broad-spectrum antibiotics such as cefazolin (22 mg/kg IV q 8 h), enrofloxacin (5-20 mg/kg IV q 24 h), and metronidazole (10-15 mg/kg IV q 12 h) are indicated empirically owing to venous pooling within the splanchnic circulation and risk for bacterial translocation.
POSSIBLE COMPLICATIONS DIC Acute renal failure Gastrointestinal sloughing/bacterial translocation Hepatic failure Other components of multiple organ dysfunction syndrome (MODS) Cerebral edema Bone marrow dysfunction may result in leukopenia and circulating nucleated red blood cells.
RECOMMENDED MONITORING Continuous ECG monitoring for changes in heart rate or worsening arrhythmia Frequent respiratory monitoring and blood gas evaluation as clinically indicated Serial neurologic evaluation Blood pressure monitoring (try to maintain systolic at >100-120 mm Hg) and blood glucose assessment (aim for 80-140 mg/dL) q 2-4 h as clinically indicated) Urine output (goal of >1-2 mL/kg/h) Coagulation times if initially prolonged or evidence of bleeding Platelet count
PROGNOSIS AND OUTCOME The prognosis associated with heatstroke varies widely depending on clinical severity at hospital admission. Animals recovering from heatstroke do not generally have any long-term side effects but may be at increased risk of future heatstroke. Initial body temperature has NOT been correlated with outcome. The following have been associated with a poor prognosis: Coagulopathy (PT >18 sec, APTT >30 sec) at admission Nucleated red blood cells >18/100 WBC Hypoglycemia (1.5 mg/dL) after 24 hours Seizures Delayed admission Obesity
PEARLS & CONSIDERATIONS COMMENTS Aggressive early cooling warranted
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Heat Stroke/Hyperthermia
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Avoid overcorrection/hypothermia. Multiple organ failure including DIC is possible.
PREVENTION Avoid exposing the animal to high ambient temperature or prolonged physical activity.
TECHNICIAN TIPS Avoid jugular venipuncture until patient coagulation status can be ascertained. Avoid hypothermia by discontinuing active cooling when temperature reaches 103°F-103.5°F (39.2-39.4°C). Monitor for recurrent respiratory distress upon extubation, particularly in those animals with brachycephalic syndrome or laryngeal paralysis. Prolonged intubation, temporary tracheotomy (see p. 1344) or definitive airway correction may be required. Placement of a urinary catheter and closed collection system allows for frequent, accurate calculation of urine output and characterization.
CLIENT EDUCATION Educate clients about the dangers of leaving dogs in cars on hot days, or prolonged exercise on hot days, or if upper airway diseases exist. Clinical signs such as weakness and panting in hot weather may be an emergency; institute cooling measures and consult a veterinarian.
SUGGESTED READING Bruchim Y, Klement E, Saragusty J, et al: Heat stroke in dogs: a retrospective study of 54 cases (1999-2004) and analysis of risk factors for death. J Vet Intern Med 20(1):38– 46, 2006. AUTHOR: GEOFF HEFFNER EDITOR: ELIZABETH ROZANSKI 1ST EDITION AUTHOR: KRISTEN AARBO
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Heartworm Disease, Dog
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Heartworm Disease, Dog BASIC INFORMATION DEFINITION Heartworm disease is the clinicopathologic manifestation of infestation with Dirofilaria immitis, an intravascular parasite that resides in the pulmonary arteries, and less often the right side of the heart and venae cavae. It results in pneumonitis, pulmonary endarteritis, pulmonary hypertension (PH), pulmonary thromboembolism (PTE), and/or cor pulmonale. An occult heartworm (HW) infection is defined as an infection in which microfilariae are not detectable in blood.
SYNONYM Heartworm (HW) infection
EPIDEMIOLOGY SPECIES, AGE, SEX Wild and domestic canids most commonly; lower prevalence in cats Most dogs are 3-6 years old when diagnosed (uncommon in dogs 18°C) during a 30-day period. Prevalence: in shelter cats (up to 14%) and 9% in pet cats presented for cardiorespiratory signs (26% of these cats were HW antibody positive, indicating HW exposure). Nationwide in the United States, exposure rate likely exceeds 12%. Clinical signs associated with early infection occur in late fall and early winter. ASSOCIATED CONDITIONS & DISORDERS Aberrant migration of larvae more common in cats (neurologic, dermatologic, and ophthalmic complications) Heartworm-associated respiratory disease (HARD): clinical and histopathologic findings of cats when they abort infections before heartworm maturation (“pulmonary larval dirofilariasis”). Pulmonary thromboembolism (PTE) may be due to dead worms (natural or pharmacologic death) or intravascular thrombi formed in response to the infection, resulting in vascular occlusion, infarction, and sometimes acute respiratory death. Pulmonary edema, often fulminant, with pulmonary thromboembolism possibly representing acute respiratory distress syndrome (ARDS). This may result acutely after adult worm death. Eosinophilic pneumonitis with cough, wheezing, dyspnea Congestive heart failure (CHF) is uncommon; signs of right-sided heart failure occur, usually a pleural effusion (either hydrothorax or chylothorax) and/or ascites. Wolbachia sp. (see p. 477): vital for filariae reproduction and possible contributor to pulmonary lesions; elimination of this symbiotic bacterium may play a role in adulticide therapy.
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES
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Heartworm Disease, Cat
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Clinical classification: (1) no clinical signs, (2) acute or peracute, and (3) chronic (most common) Most feline HW infections are occult infections, defined as an infection in which microfilaria are not detectable; microfilaremia in cats is uncommon ( females), restrictive/unclassified cardiomyopathy GENETICS & BREED PREDISPOSITION DCM: Doberman pinschers, Great Danes, Irish wolfhounds, and other large-and giant-breed dogs Mitral and tricuspid regurgitation due to chronic myxomatous valve disease: geriatric small-breed dogs including Cavalier King Charles spaniels, dachshunds, and many others HCM: inherited in Maine coon cats and Ragdoll cats. It is possible that feline HCM generally is a genetic disease RISK FACTORS: Electrocardiographic and echocardiographic variables that predict the development of HF in Doberman pinschers have been described. In Irish wolfhounds and other giant-breed dogs, atrial fibrillation sometimes precedes the development of HF. In small-breed dogs, a murmur caused by myxomatous mitral degeneration is a risk factor for development of HF, but there is great interindividual variability in the rate at which valvular disease progresses. In cats, echocardiographically evident left atrial enlargement is associated with the development of HF.
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES Left-sided HF results in pulmonary edema. Right-sided HF causes ascites and sometimes concurrent pleural effusion. In cats, pleural effusion results from left-, right-, or biventricular HF; ascites is uncommon. HISTORY, CHIEF COMPLAINT: Clinical signs such as respiratory distress generally have improved or resolved with initial treatment, but signs such as progressive abdominal distension, syncope, lethargy, and weight loss may persist. Patients with chronic heart failure are subject to episodes of acute/decompensated heart failure. PHYSICAL EXAM FINDINGS Patients with HF due to mitral/tricuspid myxomatous valve disease have a cardiac murmur; usually the murmur is loud, and its intensity is generally not affected by treatment.
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Heart Failure, Chronic
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An audible third or fourth heart sound—a gallop—reflects high atrial pressures and reduced ventricular compliance. In dogs, it is a relatively specific marker of HF.
ETIOLOGY AND PATHOPHYSIOLOGY Congestive signs result when high venous pressures cause the development of edema or cavitary effusions. In dogs, HF that results primarily from systolic dysfunction—failure of the ventricle to completely empty—is most common. HF in cats usually results from diseases that impair ventricular filling; diastolic ventricular pressures are abnormally high when ventricular volume is normal or small. High filling pressures are reflected upstream to the venous circulation, resulting in edema or pleural effusion. HF is associated with neuroendocrine activation: specifically, impaired cardiac performance leads to increased activity of the renin-angiotensin-aldosterone system (RAAS) and the adrenergic nervous system (ANS). Angiotensin II (ATII) is the biologically active product of a biochemical cascade for which the final step is catalyzed by angiotensin-converting enzyme (ACE). ATII is a vasoconstrictor, but it also stimulates the release of aldosterone, augments activity of the ANS, and acts as a cardiomyotrophic factor. Activation of the RAAS and ANS serves to temporarily maintain perfusion pressure and cardiac output. Vasoconstriction increases vascular resistance so that blood pressure is maintained when cardiac output is subnormal. In patients with mitral/tricuspid myxomatous valve disease or DCM, vascular resistance is high, causing a detrimental increase in after-load; this partly explains the beneficial effect of vasodilators. It is now generally accepted that neuroendocrine activation associated with cardiac dysfunction is initially beneficial but ultimately detrimental and contributes importantly to the pathogenesis of progressive cardiac dysfunction. Current therapies for chronic HF reflect this conceptual framework.
DIAGNOSIS DIAGNOSTIC OVERVIEW Chronic heart failure is present when acute/decompensated heart failure is treated successfully, but the underlying cause cannot be cured. Therefore, clinical features of chronic heart failure include a history of acute/decompensated heart failure, with partial or complete resolution of signs with treatment but persistence of the underlying cardiac lesion.
DIFFERENTIAL DIAGNOSIS Other causes of respiratory distress, cough, abdominal distension, lethargy, inappetence, and weight loss (cardiac cachexia)
INITIAL DATABASE Thoracic radiography: Left atrial enlargement with pulmonary opacities is diagnostic of left-sided HF (see p. 468). With diuretic treatment of decompensated HF, clinical improvement is usually rapid (minutes to hours), but radiographic resolution of pulmonary infiltrates may take 12-24 hours. Cats commonly develop pleural effusion in association with left-sided cardiac disease. Electrocardiography (ECG) is indicated when arrhythmias complicate the presentation. Atrial fibrillation is commonly associated with heart failure in large-breed dogs, but tachyarrhythmia of virtually any type may complicate the presentation of heart failure (see p. 468). Noninvasive estimation of systemic blood pressure using the Doppler cuff or oscillometric method should be considered. The finding of systemic hypertension (SH) provides evidence of concurrent disease; that is, SH may complicate HF, but it is not a result of HF. However, documented SH should be treated, since untreated SH may accelerate the progression of the primary cardiac disorder. Serum biochemistry profiles: provide useful ancillary information and are important in monitoring the effects of therapy (especially renal and electrolyte effects).
ADVANCED OR CONFIRMATORY TESTING B-type natriuretic peptide (BNP) is released by cardiomyocytes in response to increases in ventricular filing pressures. Elevated circulating BNP is a marker of the heart failure state, but the diagnostic utility assay has yet to be fully clarified. Echocardiography generally provides the diagnosis of the underlying cardiac disorder. Echocardiography is complementary to physical examination and thoracic radiography but does not replace them.
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Heart Failure, Chronic
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TREATMENT TREATMENT OVERVIEW Correction/cure of the underlying cause when possible In all cases, increase in quality and duration of life Although individual patient characteristics must be taken into account, poly-therapy consisting of furosemide, an ACE inhibitor, and pimobendan with or without digoxin has become standard treatment for management of class C HF in the dog. There is uncertainty regarding optimal therapy for cats with HF resulting from diastolic dysfunction; furosemide and an ACE inhibitor, with or without beta-blockade, are widely used.
CHRONIC TREATMENT Diuretics. Furosemide is the most effective agent for management of congestive signs. In dogs, a dose of 1 mg/kg PO q 12 h is often initially adequate when given concurrently with ancillary agents such as ACE inhibitors and pimobendan. Cats with HF generally require lower initial doses (0.5-1 mg/kg PO q 12-24 h). Furosemide is used first, but the progressive nature of the HF state generally requires adjustment of doses. If clinical signs suggest diuretic resistance or if electrolyte derangements are documented, other diuretics such as hydrochlorothiazides (2-4 mg/kg PO q 12 h) or spironolactone (1-2 mg/kg PO q 12 h [dog]) can be added. Doing so allows for synergistic diuretic action: Different diuretics act in different parts of the nephron, which minimizes the negative effects of long-term (weeks or more) administration of high doses of a single diuretic (e.g., >3-4 mg/kg q 8-12 h furosemide). Diuretic dose should be determined by clinical response; the optimal dose is the lowest one that eliminates congestive signs. Excessive diuretic administration may decrease renal perfusion, creates electrolyte imbalances, and contributes to potentially harmful neuroendocrine activation. Most patients require lifelong diuretic administration; progression of the underlying disorder generally necessitates increases in furosemide dose and/or the use of additional diuretics. Furosemide administration sometimes can be tapered or temporarily discontinued in cats with hypertrophic cardiomyopathy. ACE inhibitors partially blunt the effects of RAAS activation and reduce afterload. ACE inhibition has proven benefits for patients with chronic HF caused by systolic dysfunction; preliminary evidence suggests a benefit for patients with chronic HF caused by diastolic dysfunction (e.g., cats with HF caused by hypertrophic or restrictive/unclassified cardiomyopathy). Of the ACE inhibitors, veterinary experience is greatest with enalapril (0.5 mg/kg PO q 12-24 h [dog]), benazepril (0.25-0.5 mg/kg PO q 24 h [dog], 0.5-1 mg/kg PO q 24 h [cat]), and ramipril (0.125 mg/kg PO q 24 h [dog]). Digoxin: 2
0.22 mg/m PO q 12 h [dog]; 0.03125 mg/cat PO q 48 h Weak positive inotrope that has potentially beneficial neuroendocrine effects; digoxin inhibits adrenergic activity and increases vagal tone. Important in management of patients with both systolic dysfunction (e.g., dilated cardiomyopathy) and atrial fibrillation; benefit to patients with sinus rhythm is uncertain. Digoxin is generally contraindicated in HCM. Pimobendan (0.1-0.3 mg/kg PO q12 h administered when stomach is empty) is a phosphodiesterase inhibitor that acts as an “inodilator.” It is indicated for the treatment of dogs that have developed Class C heart failure due to valvular disease or dilated cardiomyopathy. Pimobendan decreased mortality when compared to benazepril in patients with HF due to valvular disease. The evidence that pimobendan decreases mortality in Doberman pinschers with class C heart failure due to DCM is strong. Unfortunately, information that relates to the effect of pimobendan in dogs receiving standard therapy of an ACE inhibitor and furosemide is sparse. While it is accepted that these drugs can and probably should be used together, there are unanswered questions that relate to staging of therapy. The concurrent use of pimobendan, an ACE inhibitor, and furosemide as initial therapy can be justified, as can staged therapy in which an ACE inhibitor or pimobendan is used as rescue therapy in the event of clinical deterioration. Adverse effects associated with the administration of pimobendan are apparently uncommon, although there is some evidence that pimobendan might harm patients with mild subclinical valvular disease. Accordingly, the use of this drug should be reserved for patients with Class C or D HF due to valvular or myocardial disease. A proarrhythmic effect is possible but appears uncommon, if it even exists in dogs. β-Blockers (BB). There is experimental evidence that supports the use of BB in dogs with dilated cardiomyopathy or advanced mitral/tricuspid valve disease. BB are negative inotropes that can induce acute HF if given at an inappropriately high initial dose or if the dose is increased too quickly; dose must be gradually titrated over weeks from a low initial dose to a target dose, typically beginning at 0.1 mg/kg PO q 12 h (carvedilol) or 0.1-0.2 mg/kg PO q 12 h (metoprolol). BB are never started before a patient's pulmonary edema has resolved.
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Heart Failure, Chronic
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Spironolactone (1-2 mg/kg PO q 12 h [dog]) In chronic HF, excess aldosterone may contribute to the development of myocardial fibrosis. Spironolactone is an aldosterone antagonist, and as such it may limit the detrimental effects of hyperaldosteronemia; careful monitoring of electrolytes is advised. Minimal diuretic efficacy as monotherapy in the dog. Severe facial dermatitis in 30% of cats makes this drug relatively contraindicated in this species. Cautious addition of amlodipine (0.0625-0.25 mg/kg PO q 24 h [dog],0.125 mg/kg-0.25 mg/kg PO q 24 h [cat]) to conventional therapy can be considered for patients with refractory HF or for those in which SH complicates the clinical presentation. Blood pressure monitoring is essential. Moderate dietary sodium restriction generally is indicated. If palatable to the patient, low-sodium diets may reduce diuretic requirements.
NUTRITION/DIET Moderate sodium restriction, adequate protein and energy content, and palatability are important attributes of an optimal diet for HF patients (see p. 168).
POSSIBLE COMPLICATIONS “Cardiorenal syndrome”: azotemia associated with diuretic administration and diminished cardiac performance When azotemia is encountered in patients receiving furosemide and ACE inhibitors, furosemide is first decreased by 50%, provided the patient is free of congestive signs. If creatinine does not decrease, diuretic therapy is discontinued, provided congestive signs are not evident. Only if this is unsuccessful is the ACE inhibitor discontinued. There are unfortunately few alternatives for patients that develop clinical signs specifically due to azotemia when congestive signs are present concurrently; this may reflect medically intractable heart failure. However, caution must be exercised, as “overinterpretation” of radiographs or abnormal lung sounds (e.g., pulmonary rales/crackles due to interstitial lung fibrosis, not edema) can lead to inappropriately high diuretic doses, volume depletion, and azotemia.
RECOMMENDED MONITORING Serum urea, creatinine, and electrolytes Serum digoxin concentration
PROGNOSIS AND OUTCOME Despite favorable initial response, heart failure is generally associated with a poor long-term prognosis unless the causative disorder is curable.
PEARLS & CONSIDERATIONS COMMENTS Current therapy of heart failure reflects the understanding that activation of the ANS and RAAS is central to the pathogenesis of the syndrome. When the causative disorder is not curable, chronic HF is a progressive and terminal syndrome. Therefore attempts to identify a correctable cause are important; some patients with dilated cardiomyopathy respond to supplementation with nutraceuticals such as taurine and L-carnitine.
PREVENTION In patients with clinically silent dilated cardiomyopathy, the onset of heart failure may be delayed by the administration of ACE inhibitors and BB. ACE inhibition has a modest but probably positive effect on the time to development of class C HF in canine patients with left atrial enlargement due to mitral valve regurgitation. Evidence that medical therapy slows the progression HCM is currently lacking.
CLIENT EDUCATION Management of the veterinary patient with chronic HF requires careful monitoring and relatively frequent adjustment of medical therapy.
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Heart Failure, Chronic
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SUGGESTED READING Atkins C, Bonagura J, Ettinger S, et al: ACVIM consensus statement. Guidelines for the diagnosis and treatment of canine chronic valvular heart disease. J Vet Intern Med 23:1142–1150, 2009. Haggstrom J, Boswood A, O’Grady M, et al: Effect of pimobendan or benazepril hydrochloride on survival times in dogs with congestive heart failure caused by naturally occurring myxomatous mitral valve disease: the QUEST study. J Vet Intern Med 2008. Keene BW, Bonagura JD: Management of heart failure in dogs. In Bonagura JD, Twedt DC, editors: Kirk’s current veterinary therapy XIV. St Louis, 2009, Saunders Elsevier, pp 769–780. Luis Fuentes V: Management of feline myocar-dial disease. In Bonagura JD, Twedt DC, editors: Kirk’s current veterinary therapy XIV. St Louis, 2009, Saunders Elsevier, pp 809–815. AUTHOR: JONATHAN A. ABBOTT EDITOR: ETIENNE CÔTÉ
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Heart Failure, Acute/Decompensated
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Heart Failure, Acute/Decompensated BASIC INFORMATION DEFINITION Acute (or decompensated) congestive heart failure (HF) is characterized by the sudden onset of clinical signs associated with pulmonary edema or cavitary effusions that develop as a consequence of heart disease. Acute/decompensated HF is a common cause of respiratory distress that is most often associated with worsening cardiac performance in patients with chronic heart disease.
SYNONYMS Acute congestive heart failure, decompensated heart disease, overt heart failure
EPIDEMIOLOGY SPECIES, AGE, SEX: Signalment reflects predispositions for the causative heart disorder. Examples: Geriatric small-breed dogs: chronic mitral/tricuspid regurgitation (myxomatous valve disease) Cats: hypertrophic cardiomyopathy (HCM) GENETICS & BREED PREDISPOSITION Dilated cardiomyopathy (DCM): Doberman pinschers, Great Danes, Irish wolfhounds, and other large-and giant-breed dogs Mitral/tricuspid myxomatous valve disease: Cavalier King Charles spaniels, dachshunds, many others HCM: inherited in Maine coon cats and in Ragdoll cats; it is possible that feline HCM generally is a genetic disease. RISK FACTORS In patients with underlying heart disease: Dietary sodium excess Acute intravascular volume load (e.g., parenteral fluids) Possibly corticosteroids (HCM cats) Possibly ketamine/tiletamine (HCM cats) Electrocardiographic, echocardiographic variables: predictive of likelihood of future HF or sudden, unexpected death in Doberman pinschers with DCM
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES Left-sided HF results in pulmonary edema. Right-sided HF causes ascites and sometimes concurrent pleural effusion. In cats, pleural effusion may result from left-and/or right-sided heart disease. HISTORY, CHIEF COMPLAINT Respiratory signs predominate. Specifically, the characteristic manifestations include tachypnea, dyspnea, and, in the dog, cough. Heart failure seldom causes coughing in cats. Clients may report that the patient appears to be uncomfortable, restless, or unwilling to lie down. PHYSICAL EXAM FINDINGS Tachycardia is a relatively consistent, although nonspecific, finding in dogs with HF. Heart rate of cats with acute HF differs little from heart rate of healthy cats. Some cats with acute HF have bradycardia. The presence of respiratory sinus arrhythmia is generally inconsistent with acute HF; other explanations for the clinical signs should be considered. In patients with pulmonary edema, tachypnea and respiratory distress are usually apparent during the physical examination. Dogs with acute HF due to mitral or tricuspid regurgitation caused by myxomatous valve disease have a cardiac murmur;
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usually the murmur is loud (=III/VI). An audible, low-frequency third or fourth heart sound—a gallop—reflects high atrial pressures and reduced ventricular compliance. Relatively specific marker of acute HF in dogs.
ETIOLOGY AND PATHOPHYSIOLOGY Congestive signs result when high venous pressures cause the development of edema or cavitary effusions. In dogs, HF that results primarily from systolic dysfunction—failure of the ventricle to completely empty—is most common. HF in cats usually results from diseases that impair ventricular filling (diastolic dysfunction). HF is associated with neuroendocrine activation that temporarily maintains perfusion pressure and cardiac output through vasoconstriction and increases in heart rate and contractility. In patients with systolic dysfunction, systemic vascular resistance rises disproportionately, causing a detrimental increase in after load; this explains the beneficial effect of vasodilators.
DIAGNOSIS DIAGNOSTIC OVERVIEW Heart failure is a clinical or radiographic diagnosis: Left heart failure is defined by the presence of radiographic pulmonary opacities in association with left atrial enlargement. Right heart failure is defined by the finding of ascites in association with jugular venous distension and/or evidence of right atrial/right ventricular enlargement from imaging studies.
DIFFERENTIAL DIAGNOSIS Other causes of respiratory distress and/or cough: Chronic sterile bronchitis Collapsing trachea Allergic airway disease Noncardiogenic pleural effusion Intrathoracic mass Pneumonia Pneumothorax
INITIAL DATABASE Thoracic radiographs: radiographic findings of left atrial enlargement together with pulmonary opacities are diagnostic of left-sided HF. Electrocardiography (ECG) is indicated when arrhythmias complicate the presentation. Serum biochemistry profile and urinalysis: in all cases, preferably before initiating treatment
ADVANCED OR CONFIRMATORY TESTING Echocardiography defines the causative disorder. Elevated circulating NT-proBNP is a marker of HF; the diagnostic utility of the assay has yet to be fully clarified.
TREATMENT TREATMENT OVERVIEW The goal of treatment is to restore ventilatory function by eliminating lung edema or pleural effusion, and in some cases, improving cardiac performance.
ACUTE GENERAL TREATMENT Rest Judicious/minimal restraint and other measures for reducing anxiety are essential. Furosemide: diuretic of choice in acute HF. Dose and dosage interval are best determined by clinical response.
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Initially: relatively high dose (2-6 mg/kg IV, IM). If no overt (e.g., respiratory) evidence of effect, this dose can be repeated within 45-60 minutes. If respiratory rate and effort decrease: 1-2 mg/kg IV or IM q 1-6 h until respirations normalize. The effect of furosemide is rapid but short lived; low doses at short intervals may limit adverse effects. Constant rate infusion of furosemide is an alternative to frequent bolus administration, but advantages in veterinary patients are uncertain; dosage = total projected daily dosage of furosemide divided by 24 as the hourly rate of the infusion. In general, cats require lower doses than dogs. Supplementary oxygen Morphine (0.05-0.3 mg/kg SQ, IM, or IV) should be considered for dogs that are anxious from respiratory distress. Thoracocentesis (see p. 1338) if physical or radiographic findings indicate that pleural effusion is likely responsible for respiratory distress. Transdermal nitroglycerin (0.5-3 cm q 12 h) may reduce venous pressures. Efficacy undetermined. Patients with systolic dysfunction and evidence of diminished cardiac output at rest may benefit from intravenous administration of nitroprusside (0.5-15 mcg/kg/min) and/or dobutamine (2-15 mcg/kg/min) constant rate infusion. Careful monitoring required. Dogs with acute/decompensated HF due to valvular disease or dilated cardiomyopathy may benefit from administration of the inodilator pimobendan (0.25 mg/kg PO q 12 h), particularly if there are findings such as prerenal azotemia, hyponatremia, or hypothermia that suggest diminished cardiac output. The use of pimobendan in acute (or decompensated) HF has not been systematically evaluated. IV or SQ fluid administration is generally contraindicated unless used as a vehicle for the administration of drugs or electrolytes. Angiotensin-converting enzyme inhibitors, other diuretics: considered once patient is stable (see p. 470).
POSSIBLE COMPLICATIONS Hypovolemia/impaired renal perfusion due to excessive diuresis Hypotension
RECOMMENDED MONITORING Frequent monitoring of vital signs, mucous membranes, body weight ECG if arrhythmias Flow-directed (Swan-Ganz) pulmonary artery catheterization and/or arterial cannula can be considered for hemodynamic monitoring of severely affected dogs admitted to an intensive care unit; rarely performed.
PROGNOSIS AND OUTCOME Most patients presented for first treatment of acute HF respond promptly to conservative therapy consisting of rest, supplemental oxygen, furosemide, and in some cases nitroglycerin. Despite favorable initial response, HF is generally associated with a poor long-term prognosis unless the causative disorder is curable.
PEARLS & CONSIDERATIONS COMMENTS Although ancillary therapy including vasodilators and inotropes may speed recovery from acute HF, most patients that are destined to recover respond to conservative management. Response to empirical therapy is diagnostically useful. When treatment is based on a presumptive diagnosis, failure to respond to diuretic suggests the possibility that clinical signs are due to primary respiratory tract disease or that the patient has refractory HF.
CLIENT EDUCATION Chronic medical therapy is generally required even after apparent recovery.
SUGGESTED READING Atkins C, Bonagura J, Ettinger S, et al: ACVIM consensus statement. Guidelines for the diagnosis and treatment of canine chronic
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valvular heart disease. J Vet Intern Med 23:1142–1150, 2009. Keene BW, Bonagura JD: Management of heart failure in dogs. In Bonagura JD, Twedt DC, editors: Kirk’s current veterinary therapy XIV, St Louis, 2009, Saunders Elsevier, pp 769–780. Luis Fuentes V: Management of feline myocar-dial disease. In Bonagura JD, Twedt DC, editors: Kirk’s current veterinary therapy XIV, St Louis, 2009, Saunders Elsevier, pp 809–815. AUTHOR: JONATHAN A. ABBOTT EDITOR: ETIENNE CÔTÉ
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Heart Base Tumor
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Heart Base Tumor BASIC INFORMATION DEFINITION A general term describing a cardiac tumor of any type located at the base of the heart in association with the ascending aorta and/or pulmonary trunk, but without right atrial involvement
SYNONYMS Chemoreceptor cell tumor: chemodectoma, aortic body tumor, nonchromaffin paraganglioma
EPIDEMIOLOGY SPECIES, AGE, SEX Dogs: second most common cardiac tumor, mean age 10 years (range (5-15 years), males may be overrepresented in predisposed breeds. Cats: reported but rare GENETICS & BREED PREDISPOSITION: Brachycephalic breeds (English bulldogs, boxers, Boston terriers) appear to be predisposed. RISK FACTORS: Chronic hypoxemia may be a contributing factor. ASSOCIATED CONDITIONS & DISORDERS: Pericardial effusion, right-sided congestive heart failure
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES Most commonly causes clinical signs due to pericardial effusion and cardiac tamponade May be an incidental finding HISTORY, CHIEF COMPLAINT Acute collapse Lethargy/exercise intolerance Abdominal distension Anorexia/inappetence Cough or tachypnea/dyspnea PHYSICAL EXAM FINDINGS Findings associated with pericardial effusion (tachycardia, weak peripheral pulses, and muffled heart sounds) Findings consistent with right-sided congestive heart failure (ascites, hepatomegaly jugular distention/pulsation) ± Tachypnea/dyspnea
ETIOLOGY AND PATHOPHYSIOLOGY Chemodectoma: Tumor of specialized neuroepithelial cells within the adventitia of the aortic arch; majority of heart base tumors in dogs Typically benign and slow growing but may be very large at the time of diagnosis; occasionally locally invasive and rarely metastatic Ectopic thyroid carcinoma: 5%-10% of heart base tumors in dogs; usually nonfunctional Biological behavior not well characterized Mesothelioma may occasionally form a mass lesion at the heart base (dogs).
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Regardless of type, heart base tumors typically result in pericardial effusion, causing cardiac tamponade and right-sided congestive heart failure. Compression of cardiac structures and great vessels impeding inflow or outflow is possible with a large mass.
DIAGNOSIS DIAGNOSTIC OVERVIEW The diagnosis is most often made with echocardiographic identification of a mass at the heart base. While a presumptive diagnosis of chemodectoma is often based on echocardiographic appearance, Definitive diagnosis of the tumor type requires histopathologic evaluation of tissue.
DIFFERENTIAL DIAGNOSIS Other intrapericardial tumors (hemangiosarcoma, mesothelioma, lymphoma, rare primary cardiac tumors, metastatic tumors) Other causes of pericardial effusion (see p. 854)
INITIAL DATABASE Echocardiography: diagnostic test of choice. Heart base tumors typically originate from the ascending aorta, most commonly the left cranial aspect, and lie between the aorta and the main pulmonary artery. They are usually homogeneous with smooth margins. Presence and severity of pericardial effusion is also assessed. Thoracic radiographs: enlarged or globoid cardiac silhouette in most but not all cases of pericardial effusion (80%). A soft-tissue mass effect at the heart base; may cause dorsal and lateral deviation of the trachea. Electrocardiogram: normal sinus rhythm or sinus tachycardia with low amplitude QRS complexes. Electrical alternans is suggestive but insensitive for pericardial effusion (50%). CBC, serum biochemistry profile, and urinalysis: often unremarkable
ADVANCED OR CONFIRMATORY TESTING Cytology and pH of the pericardial effusion: not generally useful. Heart base tumors typically do not exfoliate cells, reactive mesothelial cells mimic malignant cells, and there is much overlap in pH between causes. Histopathology of the tumor: allows a Definitive diagnosis of tumor type. Requires surgical biopsy and often does not alter treatment plan.
TREATMENT TREATMENT OVERVIEW Treatment is generally aimed at removal of pericardial fluid when cardiac tamponade occurs and eliminating recurrent effusion. When a heart base tumor is an incidental finding, initially no treatment may be necessary.
ACUTE GENERAL TREATMENT Pericardiocentesis (see p. 1325) is essential when cardiac tamponade is present but may not be necessary if only mild effusion is present and not causing hemodynamic effects. Diuretics are contraindicated in acute treatment of cardiac tamponade.
CHRONIC TREATMENT Repeated pericardiocentesis as needed for recurrent pericardial effusion Diuretics to delay effusion recurrence are controversial. Pericardiectomy alone is an effective palliative treatment for recurrent pericardial effusion. Less-invasive alternatives to surgical pericardiectomy include thoracoscopic pericardiectomy (see p. 1340) and percutaneous balloon pericardiotomy. Complete surgical resection is rarely possible owing to high vascularity of the tumor and close association with great vessels.
POSSIBLE COMPLICATIONS Pericardiocentesis related (see p. 1325)
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Surgical complications related to pericardiectomy. Surgical resection carries substantial risks. As most heart base tumors are benign, metastasis is rare but has been reported.
RECOMMENDED MONITORING Follow-up exams and echocardiography to assess for recurrent pericardial effusion and tumor progression Thoracic radiographs and possibly abdominal ultrasound for tumor staging
PROGNOSIS AND OUTCOME Guarded to fair without pericardiectomy Pericardiectomy alone improves survival time considerably.
PEARLS & CONSIDERATIONS COMMENTS Characteristic echocardiographic findings lead to the presumptive diagnosis of a heart base tumor and the possibility of a better prognosis with pericardiectomy than with other cardiac tumors such as hemangiosarcoma. Cytologic and biochemical evaluation of pericardial fluid are unreliable.
CLIENT EDUCATION Pericardiocentesis and pericardiectomy are both palliative and not curative. Pericardiectomy will likely lead to longer survival time, with fewer clinical signs in the interim.
SUGGESTED READING Ehrhart N, Ehrhart EJ, Willis J, et al: Analysis of factors affecting survival in dogs with aortic body tumors. Vet Surg 31:44, 2002. Tobias AH: Pericardial disorders. In Ettinger SJ, Feldman EC, editors: Textbook of veterinary internal medicine, ed 6, St Louis, 2005, Elsevier Saunders, p 1104. AUTHOR: HERBERT W. MAISENBACHER, III EDITOR: ETIENNE CÔTÉ 1ST EDITION AUTHOR: ERIN VICARI
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Head Trauma
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Head Trauma BASIC INFORMATION DEFINITION Traumatic injury resulting in damage to soft tissues of the head, the skull, intracranial structures, or some combination of these
EPIDEMIOLOGY SPECIES, AGE, SEX: Animals of any age or breed. Young animals may be overrepresented (lifestyle, increased risk of traumatic injury). ASSOCIATED CONDITIONS & DISORDERS Traumatic injuries affecting other body systems Head trauma may increase the risk for future seizure disorders.
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT History of traumatic event Owners may report loss of consciousness, inappropriate behavior, or seizure activity. PHYSICAL EXAM FINDINGS Signs of hypotensive shock (e.g., tachycardia, hypotension, pale mucous membranes) may be present. Neurologic exam (see p. 1311): indicators of intracranial injury: Pupil asymmetry, abnormal pupil reactivity (excluding ocular trauma).Dilated unresponsive pupils (in the absence of ocular trauma or atropine) indicate severe neurologic injury and a poor outcome. Diminished or absent oculocephalic (doll's eye) reflex Postural reaction deficits (may be due to spinal injury [see p. 1039]; note remainder of neurologic findings). Diminished or altered consciousness (may be due to shock; note remainder of physical exam). Skull fractures may be palpable. Respiratory, musculoskeletal, and other body systems may show signs of traumatic injury.
ETIOLOGY AND PATHOPHYSIOLOGY Cerebral blood flow (CBF) is mainly determined by blood pressure. Auto-regulation maintains blood flow to brain over a variety of pressures but is lost when systolic arterial blood pressure 90 mm Hg): essential in management of head trauma, managed via titration of intravenous fluids. Options: Crystalloids (e.g., 0.9% NaCl or lactated Ringer's solution) at shock doses IV (60-90 mL/kg for dog, 45-60 mL/kg for cat), unless renal/cardiovascular/dilutional contraindication; exact dose is titrated to blood pressure. Concurrent use of colloids or hypertonic saline may limit cerebral edema that can occur with aggressive fluid administration. Avoid fluids with excessive free water (maintenance fluids, 5% dextrose in water, 0.45% saline). Colloids, e.g., hetastarch, pentastarch (10-20 mL/kg/d IV). Oncotic effect draws free water from the interstitium into the vasculature. May potentiate effects of lower molecular weight substances (i.e., mannitol). Useful for intravascular support with limited fluid volumes. Hypertonic saline (7.5%), 4 mL/kg IV slowly. Short-lived osmotic action draws fluid from cerebral interstitium; combination with crystalloids prolongs osmotic effect. May also limit other secondary effects of head injury. Only used if patient is adequately hydrated.
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Head Trauma
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Decrease intracranial pressure: Mannitol (0.5-1 g/kg IV q 6-8 h; limit to three bolus injections/24-h period). Osmotic diuretic with free-radical scavenging properties. Increases intravascular osmolarity and draws fluid in from cerebral tissue. Decreases blood viscosity, increases cerebral blood flow. Potential adverse effects: Diuresis may decrease blood volume and consequently blood pressure (ensure adequate blood pressure and volume status before administration). May result in “reverse osmotic shift.” In areas of hemorrhage, mannitol may leak into interstitium, worsening cerebral edema. The effects of mannitol on lowering ICP may outweigh these potential effects on damaged areas. Furosemide (2-5 mg/kg IV in coordination with mannitol). Decreases production of cerebrospinal fluid and causes diuresis; may potentiate effects of mannitol and decrease ICP. Caution: diuretic action may also worsen intravascular volume contraction and lead to hypovolemia. Maintain adequate oxygenation: Supplemental oxygen as needed (see p. 1318) Ensure adequate oxygen-carrying capacity (hematocrit/hemoglobin) and delivery (adequate blood pressure). Miscellaneous therapies: Surgery: Craniotomy may be indicated for removal of hematomas, control of hemorrhage in the case of depressed skull fractures, or for removal of penetrating objects. Results in a substantial decrease in ICP (15% with craniotomy and an additional 65% reduction with durotomy) and is superior in relief of elevated ICP compared to any medical therapy. CT is useful for evaluation of injuries and determining need for surgical intervention. Hyperventilation: Has been advocated in head injury, although its use is controversial Lowers CO2. Resultant vasoconstriction decreases cerebral perfusion pressure and decreases ICP. However, decreased perfusion to brain parenchyma may have deleterious consequences. Current recommendation: ventilate patient such that Paco2 = 30-35 mm Hg. Barbiturates: Can use pentobarbital to effect (4-16 mg/kg IV titrated for induction, then 0.2-1 mg/kg/h to maintain sedation Decreases cerebral metabolic rate and vasoconstricts, decreasing ICP Studies evaluating efficacy controversial May cause respiratory or cardiac depression, which is severely problematic in the head-injured patient If used, intensive nursing care is essential to monitor respiration (intubation and mechanical ventilation may be necessary) as well as blood pressure and temperature. Often discussed as “last resort” May be beneficial for seizure control or in an extremely agitated animal Hypothermia: Results in decreased cerebral metabolic rate, decreased cerebral perfusion via reflex vasoconstriction, and consequently decreases ICP May also limit secondary brain injury by limiting neuroexcitatory activities and suppression of local inflammatory response Can be associated with coagulation abnormalities, cardiac disturbances, and hypotension Moderate hypothermia (32-33°C) has been reported to be efficacious in human trials and animal models of brain injury. Clinical use in veterinary patients is uncertain Glucocorticoids: Methylprednisolone sodium succinate (30 mg/kg slow IV over 10 minutes) after initial resuscitation may be best choice Use of corticosteroids in head injury is highly controversial and generally not recommended. Human studies have failed to show benefit. Potential benefits due to antiinflammatory and free radical scavenging effects May be associated with several complications (hyperglycemia, gastric ulceration, decreased wound healing, and infection)
NUTRITION/DIET Supplemental nutrition may be needed in severely compromised patients. Enteral route preferred if possible/safe (see p. 1267) Parenteral nutrition (see p. 1322) may be needed in patients at risk for aspiration pneumonia.
BEHAVIOR/EXERCISE Animals with severe neurologic deficits may be recumbent with limited mobility. Range-of-motion exercises and physical rehabilitation (see p. 1329) may be beneficial for these patients.
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POSSIBLE COMPLICATIONS Infection (aspiration pneumonia, nosocomial infection) Seizures Renal failure Persistent neurologic deficits
RECOMMENDED MONITORING Assess neurologic status: Repeated examination may aid in the evaluation of efficacy of therapy. Imaging (CT scan) may be helpful in assessing injury. Therapy to decrease intracranial pressure if indicated Monitor oxygenation (arterial blood gas/pulse oximetry). Ensure adequate blood pressure.
PROGNOSIS AND OUTCOME Prognosis is dependent on severity and type of injury: Fair to good with minor, nonprogressive injury Severely injured animals have poorer short-term recovery rates and may have longer rehabilitation/recovery periods if they survive. Modified Glasgow Coma Score (MGCS; see box) has been used for scoring injury severity in head trauma and has been correlated to outcome.
PEARLS & CONSIDERATIONS COMMENTS Head trauma is a common and serious injury in dogs and cats. Clinicians must recognize the signs of progressive neurologic injury. The MGCS may be helpful as a monitoring tool. Modified Glasgow Coma Score
Motor Activity Normal gait, normal spinal reflexes
6
Hemiparesis, tetraparesis, or decerebrate activity
5
Recumbent, intermittent extensor rigidity
4
Recumbent, constant extensor rigidity
3
Recumbent, constant extensor rigidity with opisthotonos
2
Recumbent, hypotonia of muscles, depressed or absent spinal reflexes
1
Brainstem Reflexes Normal pupillary light reflexes and oculocephalic reflexes
6
Slow pupillary light reflexes and normal to reduced oculocephalic reflexes
5
Bilateral unresponsive miosis with normal to reduced oculocephalic reflexes
4
Pinpoint pupils with reduced to absent oculocephalic reflexes
3
Unilateral unresponsive mydriasis with reduced to absent oculocephalic reflexes
2
Bilateral unresponsive mydriasis with reduced to absent oculocephalic reflexes
1
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Level of Consciousness Occasional periods of alertness, responsive to environment
6
Depression or delirium, capable of responding to environment but response may be inappropriate 5 Stupor, responsive to visual stimuli
4
Stupor, responsive to auditory stimuli
3
Stupor, responsive only to repeated noxious stimuli
2
Coma, unresponsive to repeated noxious stimuli
1
Total: _____ Assessment Good prognosis 15-18 Guarded prognosis 9-14 Grave prognosis 3-8
TECHNICIAN TIPS Diligent monitoring and nursing care are important for an optimal outcome. Even subtle changes in neurologic assessment can be important and should be brought up with the attending veterinarian. Comprehensive nursing care is important to prevent complications such as nosocomial infection or aspiration pneumonia.
CLIENT EDUCATION Clients must be informed of the potential for long recovery periods with severely injured animals. Clients should also be made aware of the need for intensive treatment and monitoring of animals with head injury. The MGCS may be helpful in quantitating injury severity in order to provide the client with a prognosis.
SUGGESTED READING Dewey CW: Brain trauma. In Wingfield WE, Raffe MR, editors: The veterinary ICU book, Jackson Hole, 2002, Teton New Media, pp 910–920. Dewey CW: Emergency management of the head trauma patient. Principles and practice. Vet Clin North Am Small Anim Pract 30:207, 2000. Platt SR, Radaelli ST, McDonnell JJ: The prognostic value of the Modified Glasgow Coma Scale in head trauma in dogs. J Vet Intern Med 15:581, 2001. AUTHOR: ELIZABETH M. STREETER EDITOR: ELIZABETH ROZANSKI
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Head Tilt
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Head Tilt BASIC INFORMATION DEFINITION Tilting of the head in a clockwise or counterclockwise direction along the long axis of the body. The head may be tilted due to a disorder of balance (vestibular disease) or due to discomfort from a dermatologic problem (acute moist dermatitis of the lateral face, or otitis externa). Head tilt due to an orthopedic problem (torticollis) is rare in small animals.
EPIDEMIOLOGY SPECIES, AGE, SEX: Idiopathic vestibular disease dogs >8 years; any age in cats GENETICS & BREED PREDISPOSITION Otitis externa/dermatitis: usually “floppy eared” breeds of dogs with long pinnae (e.g., spaniels, retrievers) Congenital vestibular disease (uncommon): Doberman pinscher, cocker spaniel, German shepherd, others GEOGRAPHY AND SEASONALITY: Idiopathic vestibular disease in cats may predominate in late summer/early fall ASSOCIATED CONDITIONS & DISORDERS If head tilt is of vestibular origin, concurrent nystagmus, ataxia, circling, and/or vomiting may occur. If head tilt is associated with otitis externa/dermatitis, concurrent vigorous head shaking is common.
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES Vestibular disease (peripheral or central) Associated with discomfort (e.g., otitis externa or dermatitis ventral to the ear) HISTORY, CHIEF COMPLAINT Head tilt associated with idiopathic vestibular disease; usually acute onset: Vomiting followed by head tilt, ataxia, and circling/rolling for the next 1-2 hours is common Owners may not report nystagmus. Head tilt associated with otitis externa/dermatitis: Signs of pain of the affected ear/dermatitis lesion Scratching of ear/affected skin Rubbing of face on the floor PHYSICAL EXAM FINDINGS Head tilt associated with peripheral vestibular disease (one or more maybe present): Head tilt is always toward the side of the lesion. Nystagmus (horizontal or rotary) with fast phase away from the side of the head tilt (see p. 772). Circling Ataxia with falling to the side of the head tilt Head tilt associated with central vestibular disease (one or more may be present): Head tilt is toward the side of the lesion. Nystagmus (horizontal, rotary, or vertical) with fast phase away from the side of the head tilt (see p. 772) Circling Ataxia Proprioceptive deficits, motor weakness on the side of the lesion Rarely, central vestibular disease may cause paradoxical signs (head tilt away from the side of the lesion). Proprioceptive deficits indicate the true side of the lesion (ipsilateral). Other cranial nerve deficits (V, VI, VII)
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Head tilt associated with otitis externa/dermatitis: Otitis externa (frequently suppurative) Moist dermatitis (“hot spot”) just ventral to the ear but covered by the pinna
ETIOLOGY AND PATHOPHYSIOLOGY Peripheral vestibular disease: Idiopathic Infection (otitis media/interna) Neoplasia Hypothyroidism (rare) Post middle ear surgery Intoxication (e.g., aminoglycoside antibiotics; rare) Congenital/hereditary Central vestibular disease: Infection Inflammation Neoplasia Trauma Otitis externa/dermatitis: Dogs: secondary to atopy, food hypersensitivity/allergy, hypothyroidism Bacterial Yeast Mites (cats)
DIAGNOSIS DIAGNOSTIC OVERVIEW Head tilt is most commonly caused by vestibular dysfunction. Therefore, the diagnostic process should seek to identify whether the brain (central) or inner/middle ear (peripheral) is the site of the lesion, which can usually be determined with a clinical neurologic exam. Further testing is selected based on a differential diagnosis list elaborated from history, physical exam, and neurologic exam findings.
INITIAL DATABASE CBC, serum chemistry profile, and urinalysis: usually normal Otoscopic exam: Otitis externa, polyp, blood (head trauma) are possible. Careful examination may reveal fluid in the middle ear with infectious causes. Tympanic bulla radiographs In otitis externa, consider evaluation for atopy, food hypersensitivity/allergy, and hypothyroidism
ADVANCED OR CONFIRMATORY TESTING Serum thyroid assays if cutaneous, biochemical, or other signs suggesting hypothyroidism are present (dogs). MRI or CT if inner ear or intracranial lesion is suspected based on case information to date. Cerebrospinal fluid analysis if intracranial disease is considered.
TREATMENT TREATMENT OVERVIEW Improve the clinical condition by decreasing nausea, anorexia, skin and external ear irritation, and pain. Treat primary cause when possible.
ACUTE GENERAL TREATMENT Vestibular: No specific therapy is available for treatment of idiopathic vestibular syndrome in dogs or cats. Glucocorticoids do not
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Head Tilt
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appear to help. Other specific causes will require treatment based on etiology. It may be difficult for the animal to walk or stand, so good nursing care including ability for the animal to get to food and water as well as appropriate care to prevent urine or fecal scalding are very important. Dermatologic: In cases of moist dermatitis, clipping the hair of the affected area and gentle cleaning with an antiseptic are recommended (see p. 30).
PROGNOSIS AND OUTCOME Vestibular: The prognosis for idiopathic vestibular disease is excellent (dog and cat), but recurrence is possible. With idiopathic vestibular disease, a head tilt may remain after resolution of all other signs. The prognosis for neoplasia and all causes of central vestibular nystagmus is guarded to poor, depending on the exact cause, ability to treat, and response to therapy. Dermatologic: The prognosis for otitis externa is good, but chronic cases may require advanced treatment or occasionally surgery. Moist dermatitis ventral to the ear has an excellent prognosis.
PEARLS & CONSIDERATIONS COMMENTS In a majority of cases in dogs and cats, acute-onset head tilt is caused by idiopathic peripheral disease and will resolve spontaneously in 1-2 weeks. Idiopathic vestibular disease is a diagnosis of exclusion. Nearly all central vestibular disease cases will have other central nervous system signs (proprioceptive defects, weakness, other cranial nerve involvement).
CLIENT EDUCATION When idiopathic vestibular disease is the primary consideration, the owners need to know that the problem will usually resolve with time. Otitis externa may become a chronic problem; owners should be advised that rechecks are needed even if the animal appears normal.
SUGGESTED READING Lorenz M, Kornegay J: Ataxia of the head and the limbs. In Lorenz M, Kornegay J, editors: Handbook of veterinary neurology, Philadelphia, 2004, WB Saunders, pp 219–243. AUTHOR: JAMES B. MILLER EDITOR: ETIENNE CÔTÉ
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Halitosis
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Halitosis BASIC INFORMATION DEFINITION An offensive odor emanating from the oral cavity, which may arise from intraoral or extraoral causes
SYNONYMS Bad breath, oral malodor
EPIDEMIOLOGY SPECIES, AGE, SEX: Any species, age, and sex may be affected.
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT: Halitosis is a leading concern of pet owners, as it can negatively affect their relationship with the beloved pet. PHYSICAL EXAM FINDINGS A complete physical examination must always include a thorough oral examination. Most intraoral disorders that cause halitosis are apparent upon examination of the oral cavity and surrounding tissues. General physical findings can vary greatly depending on the underlying disease process. For example, oral manifestations of leptospirosis vary depending on the serovar and may include halitosis, petechiae, oral hemorrhages, ulceration, glossitis with necrosis, and sloughing of the tongue. Attention should also be paid to the prepuce/vulva via inspection and to the anal sacs via palpation, because licking of these structures or their secretions is a recognized cause of halitosis in dogs and cats.
ETIOLOGY AND PATHOPHYSIOLOGY Intraoral causes: Plaque and calculus accumulation, gingivitis, periodontitis, stomatitis Cheilitis, lip fold pyoderma Osteomyelitis, osteonecrosis Oral tumors (particularly those that outgrow their blood supply and become necrotic, e.g., malignant melanoma, osteosarcoma) Foreign bodies, oral implants Oronasal communications Extraoral causes: see Differential Diagnosis
DIAGNOSIS DIAGNOSTIC OVERVIEW Physical examination helps differentiate between intraoral and extraoral causes; further diagnostic tests are selected accordingly.
DIFFERENTIAL DIAGNOSIS The DAMNIT scheme can be utilized as a guide to differential diagnosis: Developmental, degenerative: congenital and acquired palate defects/oronasal communications Autoimmune, anatomic, allergic: pemphigus vulgaris, systemic lupus erythematosus, erythema multiforme, drug eruption; “mouth breathing” associated with brachycephalic head conformation Metabolic, mechanical: diabetic ketoacidosis, uremia/renal failure, hepatic dysfunction causing hyperammonemia; retention of food debris
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Nutritional, neoplastic: gastroesophageal reflux; oral, pharyngeal, esophageal, gastric neoplasia; dietary indiscretion/consumption of spoiled food Infectious, inflammatory or idiopathic: dental plaque/calculus (oral bacteria), periodontal disease (gingivitis and periodontitis), gingival hyperplasia, contact mucositis and contact mucosal ulceration, stomatitis; leptospirosis; local and systemic fungal diseases; cheilitis and lip fold pyoderma; bronchitis, pneumonia; infection with feline leukemia virus (FeLV), feline immunodeficiency virus (FIV), feline calicivirus (FCV) or feline herpesvirus (FHV) Toxic, traumatic: toxic epidermal necrolysis, trauma from malocclusion, tooth fracture, jaw fracture, nonhealing oral wounds, oral foreign body
INITIAL DATABASE Sensory evaluation and complete physical examination (including oral examination in the awake patient)
ADVANCED OR CONFIRMATORY TESTING CBC, chemistry panel, urinalysis: if history and physical examination suggest an extraoral cause Viral testing: FeLV and FIV in cats with stomatitis (feline coronavirus and feline herpesvirus testing uncommonly performed because of great number of clinically healthy carriers, and positive results likely would not change treatment plan). General anesthesia, oral examination, and biopsy of suspicious lesions Case-specific advanced diagnostics centered on the mouth and upper airway when an intraoral cause is suspected (e.g., dental radiography, CT, thoracic radiographs for metastasis check of suspected oral neoplasms) and systemic evaluations (e.g., leptospirosis testing) when an extraoral diagnosis is suspected. Identify and quantify volatile sulfur compounds or volatile organic compounds with gas chromatography, mass spectroscopy, and sulfide meters (in research settings).
TREATMENT TREATMENT OVERVIEW The goal of treatment is to control halitosis by addressing its underlying intraoral or extraoral causes. For intraoral causes, primary treatment is often followed by preventive care. For extraoral causes, treatment of the underlying disorder is the basis of therapy.
ACUTE GENERAL TREATMENT Improve oral hygiene via professional dental cleaning and periodontal therapy, with specific attention to treatment of oral disease associated with halitosis (e.g., extraction of teeth with severe periodontitis). Specific treatment for halitosis caused by extraoral disorders is directed towards the underlying disorder.
CHRONIC TREATMENT Maintain a healthy periodontium via routine home oral hygiene (daily tooth brushing, application of chlorhexidine products onto teeth and gums, use of diets, treats, and chew toys that help control plaque and calculus accumulation) and professional dental cleaning and periodontal therapy. Treat extraoral causes of halitosis.
NUTRITIONAL/DIETARY THERAPEUTICS Home oral hygiene products, diets, treats, and toys proven to control plaque and calculus accumulation (see the Veterinary Oral Health Council website: http://vohc.org/)
RECOMMENDED MONITORING Follow-up as indicated for routine management of underlying intraoral or extraoral cause
PROGNOSIS AND OUTCOME Generally depends on the ability to eliminate underlying cause Fair to good prognosis: periodontitis, gingival hyperplasia, anal sac disease when treatment and prophylaxis are implemented properly and maintained consistently (active disorders that usually require ongoing care)
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Guarded prognosis: oral neoplasia, leptospirosis, opportunistic infection secondary to retroviral disease; the severity of the causative problem may make halitosis difficult to control.
PEARLS & CONSIDERATIONS COMMENTS A nonmalodorous oral cavity improves the human-animal bond as well as the pet's health and well-being.
PREVENTION Plaque accumulation on teeth, a major cause of halitosis, can easily be prevented by daily home oral hygiene and yearly professional dental cleaning and periodontal therapy. Other intraoral causes of halitosis can be recognized early by means of home oral examination by the owner and professional oral examination by the veterinarian during wellness visits.
TECHNICIAN TIPS Technicians are on the frontline of identifying oral disorders pathologies including halitosis in at least two important ways: bringing oral abnormalities to the attention of the clinician and demonstrating proper home oral hygiene techniques to the owner.
CLIENT EDUCATION The oral cavity can be easily assessed by most owners. Halitosis is obvious, abnormal, and requires appropriate veterinary intervention. Home oral hygiene is important to general health.
SUGGESTED READING Tonzetich J: Production and origin of oral malodor: a review of mechanism and methods of analysis. J Periodontol 48:13, 1977. Veterinary Oral Health Council (VOHC): http://vohc.org/ AUTHOR: JAMIE G. ANDERSON EDITOR: ALEXANDER M. REITER
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Ivermectin Toxicosis
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Ivermectin Toxicosis BASIC INFORMATION DEFINITION Clinical syndrome associated with exposure to the macrocyclic lactone antiparasitic drug, ivermectin
EPIDEMIOLOGY SPECIES, AGE, SEX Very young animals may be at increased risk: immature blood-brain barrier. Dogs more likely to be involved; however, some sensitive cats may show clinical signs at the recommended doses. GENETICS & BREED PREDISPOSITION A defect in p-glycoprotein multidrug transporter in the blood-brain barrier has been identified as an autosomal recessive trait (MDR-1/ABCB1 gene mutation) in some individuals of several dog breeds including collies, Shetland sheepdogs, Australian shepherds, English shepherds, and Old English sheepdogs (see p. 706). Some German shepherds and greyhounds or other breeds may be relatively more sensitive to ivermectin and may show clinical signs at doses lower than previously reported. RISK FACTORS Use of large-animal formulations in small animals holds risks of dilution errors and accidental overdosage. Animals with preexisting central nervous system (CNS) disease or disruption of the blood-brain barrier (e.g., due to trauma) may be at increased risk of toxicosis.
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES Acute: onset of signs within 4-12 hours of exposure Subacute: onset of signs within 48-96 hours, especially with exposure by injection or after multiple daily doses HISTORY, CHIEF COMPLAINT History of exposure to ivermectin-containing product Depression, disorientation, vocalization, stupor, ataxia, tremors, vomiting, anorexia, recumbency, blindness, coma, seizure, death PHYSICAL EXAM FINDINGS Mydriasis (bilateral) ± blindness (clinical: pupillary light reflexes generally intact) CNS depression: mild to stupor or coma Ataxia (proprioceptive) Disorientation Hypersalivation Tremors ± Bradycardia ± Vomiting ± Seizures Hypothermia (recumbency) or hyperthermia (tremor/seizure)
ETIOLOGY AND PATHOPHYSIOLOGY Macrocyclic lactones enhance the release of γ-aminobutyric acid (GABA), an inhibitory neurotransmitter: In insects, GABA-mediated neurons are present throughout the peripheral nervous system, and enhanced GABA release
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results in paralysis. In mammals, GABA-mediated neurons are restricted to the CNS, and in normal mammals the blood-brain barrier excludes ivermectin at therapeutic dosages. In overdose situations or in mammals with blood-brain barrier defects, ivermectin enters the CNS and exerts an inhibitory effect, resulting in CNS depression.
DIAGNOSIS DIAGNOSTIC OVERVIEW The combination of suspected or known exposure (acute or repeated) and CNS signs (progressive ataxia, weakness, mydriasis, seizures, coma) 12-96 hours after exposure is sufficient to establish a working diagnosis and begin treatment. There is no specific confirmatory test.
DIFFERENTIAL DIAGNOSIS Other intoxications (marijuana, benzodiazepines, barbiturates, ethylene glycol, isoxazole mushrooms) Brain neoplasia Encephalitis Hepatic encephalopathy
INITIAL DATABASE Neurologic exam (see p. 1311 ): asymmetric neurologic deficits are inconsistent with intoxication. No specific clinical pathologic alterations expected Baseline CBC, serum chemistry profile, urinalysis, postprandial bile acids (± thoracic/abdominal diagnostic imaging) to rule out other possible etiologies
ADVANCED OR CONFIRMATORY TESTING A comatose animal may return to temporary consciousness after physostigmine administration (1 mg/40 lb or 0.06 mg/kg IV). This should not be considered confirmatory, as physostigmine can reverse depression from many CNS depressants. Physostigmine should be used with care; may trigger seizure activity. Ivermectin sensitivity testing (see p. 706) Ivermectin can be detected in liver, adipose tissue, brain, or serum. Serum levels may not correlate well with clinical signs, however. Presence of ivermectin in the serum can help confirm exposure (if uncertain/ unknown).
TREATMENT TREATMENT OVERVIEW First priority is given to managing critical CNS abnormalities (seizures, coma). If signs are less severe or absent, treatment consists of inducing vomiting (within 2 hours of ingestion) and giving activated charcoal (within 8–12 hours of ingestion). Experimental treatments exist for severe toxicoses.
ACUTE GENERAL TREATMENT Manage seizures (see p. 1009): Diazepam (0.25–2 mg/kg IV) PRN Gas anesthetics, propofol if diazepam ineffective Avoid barbiturates because of residual CNS depression. Minimize sensory stimuli. Manage comatose animals: Maintain airway, assist respiration as needed. Thermoregulation essential Atropine (0.01–0.02 mg/kg IV) for bradycardia Frequent turning to prevent decubital ulcers Urinary catheter and hygiene to avoid urine scald Physostigmine (as above)
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Duration of action 30-90 minutes (may allow time for feeding animal). Does not shorten recovery time. Decontamination of patients: Emesis (see p. 1364 ) Not recommended in animals already showing clinical signs (risk of aspiration). Gastric lavage (see p. 1281 ) For large ingestions Activated charcoal (majority of ingested ivermectin is excreted in feces): Initial dose: 1-4 g/kg PO or labeled dosage of commercial product when ingestion occurred 24 hours have reasonable prognosis, even though supportive care may be necessary for days or possibly weeks.
PEARLS & CONSIDERATIONS COMMENTS
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Other macrocyclic lactones with similar mechanisms of action and clinical effects include milbemycin, moxidectin, selamectin, doramectin, eprinomectin, and abamectin. In general, doses up to 10 times the recommended heartworm preventive doses of milbemycin and ivermectin are well tolerated, even by sensitive (e.g., MDR-1 mutant) dogs. Toxic dose of ivermectin in collies and other sensitive breeds ranges between 0.1 and 0.2 mg/kg (15–30 times the therapeutic heartworm preventative dose but equal to the doses sometimes recommended for dermatologic or heartworm microfilaricide treatment) and 2.5–40 mg/kg (>200 times) in beagles. Because ivermectin is eliminated primarily through the bile and undergoes enterohepatic recirculation, activated charcoal can be of benefit even if the exposure was parenteral. Animals receiving repeated high doses of ivermectin for dermatologic or other reasons should be closely monitored for mydriasis or ataxia that may develop after several doses. Very high risk of moxidectin overdose when some equine moxidectin products containing 1.87% moxidectin (18,700 mcg/mL) are used in dogs.
PREVENTION Avoid large-animal products (concentration: 10 mg/mL which equals 10,000 mcg/mL) in companion animals to avoid risk of dilution errors. To prevent accidental exposure of dogs to spilled product, keep dogs out of area while horses are being dewormed.
TECHNICIAN TIPS Ivermectin toxicosis is less common (and therefore, more easily overlooked), owing to the wide availability of other effective antiparasitics. Profoundly affected patients may be comatose, and in such cases, the patient's life can depend on good airway protection (when tube feeding or if vomiting), hygiene (to prevent urine scald and fecal contamination), and pressure sore prevention (turning, topical therapy PRN).
SUGGESTED READING Merola V, Khan SA, Gwaltney-Brant S: Iver-mectin toxicosis in dogs: a retrospective study. J Am Anim Hosp Assoc 45:106–111, 2009. AUTHOR: CAROLINE DONALDSON EDITOR: SAFDAR A. KHAN 1ST EDITION AUTHOR: SHARON M. GWALTNEY-BRANT
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Iris Abnormalities
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Iris Abnormalities BASIC INFORMATION DEFINITION Iris abnormalities include any change in the color, character, or appearance of the iris, including acquired changes secondary to anterior uveitis, neoplasia, ocular melanosis, or cyst formation, as well as developmental changes (e.g., persistent pupillary membranes [PPMs]). Other relevant definitions include those for rubeosis iridis (blood vessel formation on the surface of the iris) and synechia (adhesion of iris-to-cornea [anterior] or iris-to-lens [posterior]).
SYNONYMS Uveal disease, ocular melanosis (once termed pigmentary glaucoma)
EPIDEMIOLOGY SPECIES, AGE, SEX Dogs and cats Anterior uveal neoplasia usually is seen in middle-aged to older animals. Ocular melanosis is seen in Cairn terriers and does not demonstrate age or sex predisposition. Uveal cysts most frequently are found in middle-aged to older animals (rare in cats). PPMs are congenital; pupillary membranes usually atrophy by 6 weeks of age in most puppies, but if not PPMs may be detected in all age groups (rare in cats). GENETICS & BREED PREDISPOSITION Uveal melanoma has a suspected genetic predisposition in the Labrador retriever, golden retriever, and German shepherd. Ocular melanosis is an inherited, probably autosomal dominant condition in Cairn terriers. Uveal cysts: predisposed breeds include golden retrievers, Labrador retrievers, Boston terriers, Great Danes, rottweilers; see p. 1149). Heritable cause suspected for PPMs in basenjis, Pembroke Welsh corgis, chow chows, mastiffs, and others.
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES Uveitis (see p. 1151) Uveal neoplasia (see p. 620) Uveal cysts (see p. 1149) PPMs HISTORY, CHIEF COMPLAINT Anterior uveitis: see p. 1151 Uveal neoplasia: see p. 620 Ocular melanosis: any or all of the following: Change in color of the iris to dark brown Cloudy/hazy appearance to the eye in cases of secondary glaucoma Uveal cysts: see p. 1149 PPMs: any or all of the following: Usually incidental findings Cloudiness of eye Cloudiness/opacities in pupil PHYSICAL EXAM FINDINGS See History, Chief Complaint above.
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Ocular melanosis: any or all of the following: Dark pigment-colored thickening of the iris root/base Episcleral/scleral pigment plaques Release of pigment into aqueous humor, with pigment deposition in aqueous drainage pathways Pigmentation of the tapetal fundus +/− on the surface of the optic disk Secondary glaucoma in severe cases PPMs: any or all of the following: Single or multiple fine strands (rarely sheets) of iris tissue originating from the iris collarette and inserting on: Adjacent iris; typically benign, incidental finding Anterior lens; often associated with anterior capsular cataracts Corneal endothelium; associated with varying degrees of corneal scarring and/or edema Iris sheets; most severe form (sheet of tissue bridging pupil); associated with vision impairment
ETIOLOGY AND PATHOPHYSIOLOGY The uveal tract (or vascular layer) of the eye is composed of the iris, ciliary body, and choroid (see figure,p. 1151 ). The iris is the most anterior of these and is a thin diaphragm containing blood vessels, connective tissue, melanocytes, and two muscles—the iris sphincter and the iris dilator. In the center of the iridal diaphragm is a circular aperture, the pupil. Anterior uveitis (see p. 1151) Uveal neoplasia (see p. 620) Ocular melanosis: inherited thickening and pigmentation of the iris caused by increased melanocytes and (to a lesser extent) melanophages, with release of pigmented material into the aqueous humor and pigment deposition in the episclera/sclera ± posterior segment. Secondary glaucoma can result from extensive pigment deposition in the aqueous drainage pathways. Uveal cysts (see p. 1149) PPMs: nonvascular remnants of the tunica vasculosa lentis, which appear as iris strands or sheets originating in the iris collarette (midway point between iris base and pupillary margin). PPMs extend across the iris to insert on adjacent iris, lens, or cornea. When they insert on lens or cornea, opacification of these structures may occur. PPMs are a developmental defect that may have a heritable component in some breeds.
DIAGNOSIS DIAGNOSTIC OVERVIEW The diagnosis is generally suspected via the chief complaint or emerges as an incidental finding on physical exam. Characterization of an iris problem is based on a careful examination of the anterior chamber and iris surface with magnifying head loupes and diffuse and focal light sources.
DIFFERENTIAL DIAGNOSIS Discoloration of iris: Pigmentation: Uveal melanoma (variable appearance in the dog [focal] versus cat [mainly diffuse]; solid tissue; may cause dyscoria [misshapen/distorted pupil] and/or anisocoria [unequal or asymmetric pupils]) Ocular melanosis of Cairn terriers Uveal cyst (round to ovoid, single or multiple, often translucent; see p. 1151 ) Chronic anterior uveitis Depigmentation: Chronic anterior uveitis Uveal neoplasm Reddening: Rubeosis iridis Iridal hemorrhage Uveal neoplasm Iris mass: Uveal neoplasm Uveal cyst Iris strands: PPMs (arise from iris collarette; typically fine strands) Synechiae (anterior: typically arise from base of iris or pupillary margin; posterior: arise from pupillary margin or posterior aspect of iris; often result in dyscoria [abnormal pupil shape])
INITIAL DATABASE
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Complete ophthalmic examination Variable depending on underlying condition
ADVANCED OR CONFIRMATORY TESTING Variable depending on underlying condition: Ocular ultrasound (differentiate uveal neoplasm from cyst)
TREATMENT TREATMENT OVERVIEW Treatment of iris abnormalities varies widely, but fortunately diagnosis and subsequent treatment decisions are usually straightforward based on clinical signs.
ACUTE GENERAL TREATMENT Directed at underlying condition and, when possible, cause PPMs do not generally require treatment unless substantial corneal and/or lens opacification is/are present: Iris-to-cornea PPMs may cause significant corneal edema which may benefit from topical 5% hypertonic saline ophthalmic solution or ointment q 6–12 h; continued long-term if clinical improvement noted. Iris-to-lens PPMs can lead to cataract formation; if cataract is causing vision impairment, cataract surgery may be warranted (see p. 181).
POSSIBLE COMPLICATIONS Variable depending on underlying condition Cataracts and corneal edema associated with PPMs are rarely progressive.
PROGNOSIS AND OUTCOME Prognosis for anterior uveitis depends on severity at presentation, individual variation on severity and frequency of recurrences, underlying etiology, and client compliance. Primary intraocular neoplasia usually carries a poor prognosis for saving the eye but good prognosis for systemic health. Ocular melanosis has a variable rate of progression and usually carries a poor prognosis for saving the eye if secondary glaucoma develops. Uveal cysts and PPMs rarely cause problems with vision or ocular comfort.
PEARLS & CONSIDERATIONS COMMENTS Most iridal abnormalities can be readily diagnosed on basis of clinical signs. Anterior uveitis requires immediate therapeutic intervention.
PREVENTION Avoid breeding affected or closely related dogs predisposed to breed-related iris abnormalities.
SUGGESTED READING Miller PE: Uvea. In: Slatter’s fundamentals of veterinary ophthalmology, ed 4, St Louis, 2008, Saunders Elsevier, pp 203–229. Petersen-Jones SM, Forcier J, Mentzer AL: Ocular melanosis in the Cairn terrier: clinical description and investigation of the mode of inheritance. Vet Ophthalmol 10(1):63–69, 2007. AUTHOR: STEVEN R. HOLLINGSWORTH
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EDITOR: CHERYL L. CULLEN
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Ionophore Toxicosis
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Ionophore Toxicosis BASIC INFORMATION DEFINITION Ionophores are antiparasitic fermentation products of Streptomyces fungi. They are used primarily as feed additives to increase feed efficiency and weight gain, and as coccidiostats in ruminants and poultry. Toxicosis results from accidental ingestion of livestock or poultry feed containing ionophores and is character-ized by acute central nervous system (CNS) dysfunction within 12 hours of large ingestions. Signs relate mainly to muscle damage within 24-96 hours of smaller ingestions.
SYNONYMS Some of the commonly available ionophores are monensin (Rumensin, Coban), lasalocid (Bovatec, Avatec), salinomycin (Sacox, Bio-Cox), narasin (Monteban), semduramicin (Aviax), laidlomycin propionate (Cattlyst)
EPIDEMIOLOGY SPECIES, AGE, SEX All animals susceptible; dogs mainly involved compared to cats Dogs are attracted to livestock or poultry feed that may contain the ionophore. Cats rarely attracted to these products. GENETICS & BREED PREDISPOSITION Farm dogs have greater access to ionophore-containing poultry or cattle feed. RISK FACTORS Ionophore premix formulations (concentrated) are much more dangerous than ready-to-feed products. Patients with underlying cardiac or myopathic conditions could be at heightened risk of toxic effects.
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES Acute onset from high doses (34 mg/dL; creatinine is often disproportionately elevated), hyperkalemia, and hyperphosphatemia are common. Occasionally, hypercalcemia, elevated pancreatic enzymes. Urinalysis: isosthenuria, epithelial granular casts, and glucosuria in the absence of hyperglycemia are typical findings.
ADVANCED OR CONFIRMATORY TESTING There is no definitive confirmatory test for lily toxicosis. Histologically, the renal lesion generally includes acute necrosis of proximal convoluted tubules. Renal tubular mineralization may be present. Pancreatic acinar cells may show degeneration. Ultrasound can be used for measuring renal size and cortical thickness and to rule out other causes of acute renal failure. Renal biopsy may help determine extent of renal damage and prognosis (rarely done, since history and exclusion of other causes are usually sufficient).
TREATMENT TREATMENT OVERVIEW When cats are presented prior to the onset of clinical signs, the aim of treatment is early decontamination (induction of emesis, ideally within 2 hours, and administration of activated charcoal) and to prevent the development of acute renal failure. Such treatment, including therapy aimed at avoiding acute renal failure, is appropriate in all cases including exposures that are suspected but unconfirmed, because unchecked, toxicosis may have devastating and irreversible results
ACUTE GENERAL TREATMENT Decontamination of patient (no clinical signs): Emesis: in cats with recent ingestion (within a few hours) and not showing clinical signs, induce vomiting (see p. 1364), and give activated charcoal 1-4 g/kg PO. Protect airway with cuffed endotracheal tube if patient is unconscious. Prevent/slow development of renal failure (if cat is suspected or known to have ingested lilies in the preceding 2 days).
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Important: Treatment is implemented regardless of whether or not signs are present: Intravenous fluids: Intravenous fluid diuresis for a minimum of 48-72 hours at two to three times maintenance fluids plus volume deficit (adjust based on hydration, fluid volume tolerance, and response to treatment) Cats with normal renal values throughout diuresis may be weaned off fluids after 48 hours. In cats with elevations in renal values, IV fluids should be continued until azotemia resolves. In some cases, this may mean days to weeks of treatment. Monitor urine output in azotemic patients. If oliguria is present (urine production < 0.25 mL/kg/h), furosemide (2.2-4.4 mg/kg IV q 8-12 h) may increase urine output. Treat hyperkalemia if present (see p. 556). Supportive care: Persistent nausea: if gastrointestinal obstruction has been ruled out, consider maropitant, 1 mg/kg SQ q 24 h; dolasetron mesylate, 0.6 mg/ kg IV q 24 h; or metoclopramide, 0.1-0.5 mg/kg SQ q 6-12 h. Abdominal pain may be managed with opiates such as butorphanol, 0.1-0.2 mg/kg IV. Peritoneal dialysis (see online chapter: Peritoneal Dialysis) or hemodialysis (see p. 1286) possibly oriented toward renal transplantation if response is positive; can be considered if anuric renal failure develops. Control seizures with diazepam (0.5-2 mg/kg IV PRN).
RECOMMENDED MONITORING Serum biochemistry profile baseline, 24, 48, and 72 hours (especially electrolytes and renal values). Recheck BUN and creatinine daily during clinical syndrome or for 72 hours if no abnormalities are seen. Urinalysis (baseline, 24, 48, 72 hours): ensure isosthenuria/hyposthenuria as sign of adequate fluid diuresis. If azotemia develops, monitor urine output. Monitor for fluid overload: respiratory character, onset of gallop sound on cardiac auscultation, central venous pressure if possible.
PROGNOSIS AND OUTCOME If treatment is initiated within 18 hours of ingestion, before onset of renal failure, prognosis is good. Prognosis after renal failure has developed is guarded to poor.
PEARLS & CONSIDERATIONS COMMENTS Even when vomiting is mild and self-limiting, the presence of plant material in vomitus makes it critical to initiate treatment, including intravenous fluids, to avoid subsequent renal failure. Lily toxicosis is high on the differential list for any cat with acute renal failure and an extremely high serum creatinine level. Neither lily-of-the-valley (Convallaria majalis) nor peace lily (Spathiphyllum spp.) belong to the Lilium or Hemerocallis genera. They are not true lilies and do not cause acute renal damage in cats.
TECHNICIAN TIP Some florists believe that plucking the stamens out of lily flowers renders them nontoxic, which is wrong. Therefore, presence of any part of the lily plant in vomitus should be considered evidence of possible toxic exposure.
PREVENTION Do not keep any Lilium or Hemerocallis species in the cat's environment
CLIENT EDUCATION Clients should make sure plants are safe before bringing them into a cat's environment.
SUGGESTED READING Hall JO: Lilies. In Peterson ME, Talcott PA, editors: Small animal toxicology, ed 2, St Louis, 2006, Saunders, p 807. Milewski LM, Khan SA: An overview of po tentially life-threatening poisonous plants in dogs and cats. J Vet Emerg Crit Care
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16(1):25–33, 2006. Rumbeiha WK, Murphy MJ: Nephrotoxicants. In Bonagura JD, Twedt DC, editors: Kirk’s current veterinary therapy XIV, St Louis, MO, 2009, Saunders Elsevier, pp 159–164. AUTHOR: SHARON GWALTNEY-BRANT EDITOR: SAFDAR A. KHAN 1ST EDITION AUTHOR: CHARLOTTE MEANS
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Licking and Barbering Behavioral Disorders
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Licking and Barbering Behavioral Disorders BASIC INFORMATION DEFINITION Self-directed, repetitive, apparently purposeless behaviors that may derive from otherwise normal processes such as grooming or eating but are abnormal in that they are excessive in duration, frequency, or intensity in the context in which they are performed.
SYNONYMS Acral lick granuloma (ALG; see p. 22), feline hyperesthesia syndrome, obsessive-compulsive disorders (OCD; see p. 775 ).
EPIDEMIOLOGY SPECIES, AGE, SEX Age of onset may overlap with social maturity (dogs 12-36 months of age, cats 24-48 months of age). Excessive licking has been reported in all ages and sexes. GENETICS & BREED DISPOSITION Some lines of some larger canine breeds may be more predisposed to acral lick granuloma (e.g., Doberman, dalmatian, Labrador retriever, golden retriever). Asian breeds of cats such as the Siamese appear to be more predisposed to OCDs such as wool eating. RISK FACTORS: Pain, stress, or anxiety; injury to area that changes sensory function GEOGRAPHY AND SEASONALITY: Hot humid weather has been associated with acute moist dermatitis, which in turn has been speculated to be associated with acral lick granulomas. ASSOCIATED CONDITIONS & DISORDERS: Hypothyroidism in dogs, hyperthyroidism in cats, allergies, bacterial or fungal infections, nerve damage. Coexisting anxiety-related conditions are common.
CLINICAL PRESENTATION DISEASES FORMS/SUBTYPES Feline: hyperesthesia, overgrooming, self-mutilation, and psychogenic alopecia Canine: acral lick dermatitis/granuloma (ALD/G) HISTORY, CHIEF COMPLAINT: Persistent chewing, barbering, plucking, or licking of the skin and hair PHYSICAL EXAM FINDINGS Hair loss and discoloration occur only on the parts of the body that can be reached by the teeth and tongue. In cats, it is especially evident around the sides and rump, back legs, and inguinal region; other areas may have normal hair coat (e.g., head and back of neck). Alopecia is usually patchy and asymmetric. Skin may look normal. Feline overgrooming may become true self-mutilation with cutaneous ulceration. Secondary bacterial infections may then occur. In dogs, ALG lesions appear as thickened oval plaques, often with secondary bacterial and/or fungal infection.
ETIOLOGY AND PATHOPHYSIOLOGY Normal adult cats spend about 30%-50% of their time awake grooming. Grooming behaviors such as licking and chewing serve many purposes, including cleaning, removal of parasites, thermoregulation, and potentially, alleviation of stress (e.g., after punishment, intercat aggression). Hair can be removed by plucking, barbering, or just by licking and excoriation. The plucked hair has evidence of shearing.
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DIAGNOSIS DIAGNOSTIC OVERVIEW Diagnosis is based on a history of licking, chewing, or barbering excessively that has led to skin lesions that have no physical underlying cause. Trichography is an easy way to confirm that alopecia is due to hair plucking/removal, not hair spontaneously falling out.
DIFFERENTIAL DIAGNOSIS Pruritic skin disease: External parasites Bacterial and/or yeast dermatitis Food allergy dermatitis Endocrine dermatopathies (hair loss symmetric) Pain associated with any condition including trauma, infection, anal sac disorders, or feline lower urinary tract signs/disease Behavioral response to environmental changes, such as moving, a new baby or spouse, separation from owner, too many cats in the household or area, presence of new cats in the area, changes in the social and physical environment, punishment from the owner, and lack of stimulation
INITIAL DATABASE Behavioral history CBC, serum biochemistry profile, urinalysis; serum thyroxine level in adults (hyper-/hypothyroidism): to rule out systemic disorders and prior to medication initiation Dermatologic examination, including scraping and culture (see p. 1248), to assess causes such as atopy, external parasites, food allergy Microscopic examination of plucked hair (trichogram) for evidence of shearing (broken hair shafts). Hair that is lost due to endocrine conditions may have visible telogen bulbs.
TREATMENT TREATMENT OVERVIEW Goals of treatment are to minimize or resolve the licking, chewing, or barbering of the hair and skin by removing or minimizing the underlying cause of the anxiety, and to treat any lesions and pruritus.
ACUTE GENERAL TREATMENT Treatment of any concurrent or underlying medical problem, such as elimination of fleas, or resolution of food allergy (see pp. 397 , p. 400, p. 402) Remove or minimize the cause of the anxiety if possible. Provide a regular predictable routine, such as feed and play at a set time each day.
CHRONIC TREATMENT Treatment involves altering the neurochemical as well as the physical environment. Anxiolytic medication has also proved useful in some cases: Tricyclic antidepressants (TCAs): Cats: Amitriptyline (0.5-1 mg kg PO q 12-24 h; average of 5-10 mg/cat PO q 24 h; start at the lowest dose and increase after 10 days if no response): or Clomipramine (0.5 mg/kg PO q 24 h); or Doxepin (0.5-1 mg/kg PO q 12-24 h) Dogs: Amitriptyline (1-2 mg/kg PO q 12 h); or Clomipramine 1-2 mg/kg PO q 12 h for 2 weeks, then 3 mg/kg PO q 12 h; or Doxepin 3-5 mg/kg PO q 12-24 h
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Selective serotonin reuptake inhibitors (SSRIs): Cats: Fluoxetine (0.5 mg/ kg PO q 24 h); or Paroxetine (2.5 mg/cat PO q 24 h) Dogs: Fluoxetine (1 mg/kg PO q 12-24 h) Benzodiazepines such as diazepam (0.2-0.4 mg/kg PO q 12 h, average of 1-2 mg/cat PO q 12 h) or oxazepam (0.2-0.5 mg/kg PO q 12-24 h) are effective in some cats Medication may be necessary for a prolonged period (up to 6-12 months) and for some animals treatment may be lifelong. When long-term control of signs is successful, gradual withdrawal of medication may be attempted under veterinary supervision.
BEHAVIOR/EXERCISE Punishment is not effective in changing behavior. It serves to further increase the anxiety as well as impede learning of nonanxious behavior. Increasing physical and mental exercise may help decrease stress. Environmental enrichment may provide additional stimulation.
DRUG INTERACTIONS TCAs and SSRIs should not be used concurrently with monoamine oxidase (MAO) inhibitors such as those present in medications or some flea and tick collars.
POSSIBLE COMPLICATIONS May progress or coexist with other anxiety-related disorders such as panic disorders. Referral to a veterinary behaviorist should be considered.
RECOMMENDED MONITORING Serum biochemistry profile every 6-12 months or as needed based on clinical signs. Response to treatment should be monitored every 4-6 weeks. If long-term medication is needed, repeat blood work is recommended.
PROGNOSIS AND OUTCOME Prognosis is variable and depends on owner commitment, success in determining underlying cause, and management of the underlying problem. Early treatment leads to the best prognosis.
PEARLS & CONSIDERATIONS COMMENTS Avoid punishing the behavior; doing so may increase the anxiety and arousal and exacerbate the undesirable behavior.
PREVENTION Early intervention and redirection of concerning behaviors may be useful for cats and dogs without a genetic predisposition for the development of such conditions. Research has shown that even in cats with familial OCD, the specific behaviors involved do not substantially manifest until some social stressor (e.g., moving house) is involved. Clients who anticipate such stressors should be given guidance on prevention strategies.
TECHNICIAN TIPS Educating clients about normal versus abnormal grooming behaviors in animals as well as early intervention can be very useful.
CLIENT EDUCATION Clients should record the occurrence of these behaviors to assist in monitoring and managing triggers. Lifelong management and medication may be necessary.
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SUGGESTED READING Landsberg G, Hunthausen W, Ackerman L: Handbook of behavior problems of the dog and cat, Oxford, 2003, Butterworth-Heineman. Overall KL, Dunham EA: Clinical features and outcome in dogs and cats with obsessive compulsive disorder: 126 cases (1989-2000) J Am Vet Med Assoc 221:1445–1452, 2002. AUTHOR: KERSTI SEKSEL EDITOR: KAREN OVERALL
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Leukemias, Chronic
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Leukemias, Chronic BASIC INFORMATION DEFINITION Chronic leukemias are neoplastic diseases characterized by clonal proliferation of malignant mature hematopoietic cells in the bone marrow and blood. They are categorized as lymphoid or myeloid. Chronic lymphocytic leukemia (CLL) involves the proliferation of mature lymphocytes and is clinically indolent, similar to small lymphocytic lymphoma. Chronic myeloid (myelogenous) leukemias (CML) involve the proliferation of myeloid cells and include myeloid, monocytic, myelomonocytic, basophilic, mastocytic, megakaryocytic, and erythrocytic leukemias.
EPIDEMIOLOGY Chronic leukemias are rare in dogs and cats. CMLs are extremely rare. SPECIES, AGE, SEX: Typically older dogs and cats but can occur at any age GENETICS & BREED PREDISPOSITION: Mast cell leukemia (MCL): associated with derangement of KIT receptor or its ligand (stem cell factor) in dogs and humans RISK FACTORS: In contrast to acute lymphocytic leukemia, most cats with CLL are not infected with feline leukemia virus (FeLV) or feline immunodeficiency virus (FIV). ASSOCIATED CONDITIONS & DISORDERS CLL: monoclonal gammopathy, hyperviscosity syndrome CML: myelofibrosis Chronic basophilic leukemia (CBL) and MCL: hyperhistaminemia resulting in urticarial rashes and gastrointestinal (GI) signs/ulceration PV: hyperviscosity syndrome
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES Chronic lymphocytic leukemia: T-cell: 70%-90% canine CLL B-Cell: 12%-30% canine CLL Granular lymphocyte CLL (GL CLL; cytotoxic T cells or natural killer cells): 55%-80% of canine CLL; suspected to originate in the spleen CML: chronic myeloid leukemias CNL: chronic neutrophilic leukemia CMoL: chronic monocytic leukemia CMML (or CMMoL): chronic myelomonocytic leukemia CEL: chronic eosinophilic leukemia CBL: chronic basophilic leukemia MCL: mast cell leukemia PV: primary erythrocytosis (polycythemia vera) ET: megakaryocytic myelosis (essential thrombocythemia) HISTORY, CHIEF COMPLAINT Insidious onset of increased peripheral blood count of affected cell line noted as incidental finding. Initially no clinical signs Later, nonspecific signs (lethargy, loss of appetite, weight loss) and signs associated with cytopenias (weakness, hemorrhage, infection) PV (rarely CLL) can cause neurologic signs (seizures, behavior changes, blindness, ataxia) due to hyperviscosity. Polyuria/polydipsia also possible.
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CEL in cats usually results in gastrointestinal (GI) signs due to infiltration. Some forms of CML frequently cause clinical signs due to production of cytokines or other factors (e.g., CBL, MCL: GI signs due to histamine). PHYSICAL EXAM FINDINGS Initially, normal physical examination Hepatomegaly/splenomegaly common as disease progresses Lymphadenomegaly frequent in dogs with CLL Brick-red mucous membranes and neurologic signs possible with PV Palpable GI wall thickening possible with CEL and MCL Fundic examination: large, tortuous retinal vessels and retinal hemorrhages possible with PV
ETIOLOGY AND PATHOPHYSIOLOGY Chronic leukemias arise from neoplastic transformation of a pluripotent stem cell in the marrow or spleen. Progression is insidious, with gradual increases in marrow and peripheral blood cell counts of the leukemic cell type. Bone marrow infiltration may eventually result in myelophthisis (crowding of normal cells, changes in the marrow microenvironment, and secretion of suppressor factors) or myelofibrosis. These conditions result in anemia, neutropenia, and thrombocytopenia. Hepatic and splenic infiltration with leukemic cells is gradual, resulting in organomegaly, abdominal distension, and loss of appetite. Organ infiltration and dysfunction are possible in chronic stages or with transformation to acute leukemias. Transformation into a blast phase (acute leukemias) may occur in the terminal stages of chronic leukemias.
DIAGNOSIS DIAGNOSTIC OVERVIEW The diagnosis of chronic leukemias has traditionally been based on detection of a high count of a cell line on CBC and bone marrow cytologic findings. Recently, flow cytometric immunophenotyping of cells in blood or bone marrow has become readily available for diagnosing leukemias in veterinary patients. This technique is used in combination with cytologic exam and allows more accurate identification of cell type and count, primarily for CLL and acute leukemias.
DIFFERENTIAL DIAGNOSIS Based on the type of cell(s) with elevated counts on CBC and bone marrow cytology Lymphocytes: CLL Small cell or large granular cell lymphoma Ehrlichiosis Viral infection (feline leukemia virus, feline herpes virus type 1) Chronic antigenic stimulation (e.g., inflammatory bowel disease, cholangiohepatitis) Recent vaccination Stress/epinephrine in cats (redistribution of lymphocytes, typically 60,000/mcL. Treat 2
with prednisone (dogs: 30-40 mg/m PO once daily for 7 days and then every other day; cats: prednisolone, 5-10 mg 2
daily) and chlorambucil (6-8 mg/m PO every other day; cats 2 mg PO every 2nd or 3rd day depending on size). Some protocols add vincristine (0.7 mg/m2 IV for dogs) during the first 1-4 weeks. When these drugs fail, other drugs for lymphoma may be used. CML: Treatment depends on diagnosis. Because these are exceptionally rare diseases, referral to/consultation with a veterinary oncologist is recommended. PV, CML, and CEL: treated with hydroxyurea (dogs: 30 mg/kg PO once daily for 7-10 days, then 15 mg/kg PO once daily; cats: 125 mg PO q 3-4 days. Dosages are adjusted long term based on response and toxicity.). It is important to know the potential side effects of hydroxyurea before using this drug. PV may be able to be managed with phlebotomy and fluid replacement initially. Busulfan has also been used in the treatment of CML and ET, but a recommended dosage has not been established. Imatinib mesylate is a tyrosine kinase inhibitor used in people with chronic myelogenous leukemia. Use in veterinary patients has been limited by cost and hepatotoxicity in dogs. A receptor tyrosine kinase inhibitor (toceranib) is currently FDA approved for dogs, but at this time it is unknown whether CML in dogs has the same genetic abnormality as the disease in humans, so the role of this drug is not known. Consultation with a veterinary oncologist is recommended.
CHRONIC TREATMENT Patients responding to treatment typically receive chemotherapy for the rest of their lives or until they develop bone marrow toxicity.
POSSIBLE COMPLICATIONS Myelosuppression: neutropenia, thrombocytopenia Chronic bone marrow injury Hydroxyurea can cause methemoglobinemia in cats. It can also cause anemia and skin/hair/nail changes. Gastrointestinal toxicity Rare hepatic, renal, pulmonary, or neurologic toxicity
RECOMMENDED MONITORING Will depend on diagnosis and how severely patient is affected. Physical examinations: weekly or more frequently if needed in induction period. Monthly to every other month once on chronic maintenance therapy. CBC: to monitor myelosuppression and remission status. Performed weekly or more frequently if needed during the induction period. Monthly to every other month once on chronic maintenance therapy, must monitor for chronic bone marrow injury and
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relapse. Serum biochemistry profile, urinalysis (free catch if risk of hemorrhage): 1 month after starting therapy and then q 3-4 months to monitor overall health, paraneoplastic syndromes, and toxicity; more frequently if indicated.
PROGNOSIS AND OUTCOME In general, the prognosis for chronic leukemias is better than acute leukemias because of the indolent nature of chronic leukemias. Dogs and cats with CLL can enjoy long-term survival. There is less information for CML. CLL: progresses slowly; responsive to chemotherapy; survival times of 1-3 years expected for dogs and suspected to be similar for cats. If CLL transforms into lymphoma/acute leukemia (as indicated by recurrence of clinical signs and/or appearance of blast cells on a blood smear), the prognosis is poor. CML: depends on type. There is little or no information describing the prognosis for some of these conditions. CML/CBL: some dogs may live 1 year or more with treatment. PV: survival times of >1 to >6 years reported. CEL: in cats, not very responsive to treatment. Survival times of a few months. Unclear if dogs develop CEL, but if they do, it may respond to prednisone. ET: Early attempts at treatment did not yield responses. More recently a dog experienced long-term control (>500 days) with busulfan.
PEARLS & CONSIDERATIONS COMMENTS Chronic leukemias have a slow onset and often progress slowly. Patients are initially clinically normal and then show nonspecific signs. Diagnosis is based on identifying proliferating mature hematopoietic cells in blood and bone marrow. Use of flow cytometry for immunophenotyping is becoming more routine. Patients with chronic leukemias can enjoy long survival times.
TECHNICIAN TIPS Patients with chronic leukemias often undergo chronic chemotherapy. Monitoring of CBCs for chronic bone marrow injury and relapse is important. Owners should be educated on how to monitor their pet and precautions to protect themselves from chronic exposure to chemotherapy.
SUGGESTED READING McManus PM: Classification of myeloid neoplasms: a comparative review. Vet Clin Pathol 3:189–212, 2005. Moore AS, Ogilvie GK: Bone marrow disorders. In Ogilvie GK, Moore AS, editors: Feline oncology, a comprehensive guide to compassionate care, Trenton, NJ, 2001, Veterinary Learning Systems, pp 222–224. Tasca S, et al: Hematologic abnormalities and flow cytometric immunophenotyping results in dogs with hematopoietic neoplasia: 210 cases (2002-2006). Vet Clin pathol 38:2–12, 2009 Vail EM, MacEwen EG, Young KM: Canine lymphoma and lymphoid leukemias. In Withrow SJ, MacEwen EG, editors: Small animal clinical oncology, ed 3, Philadelphia, 2001, pp 558–590. Vernau W, Moore PF: An immunophenotypic study of canine leukemias and preliminary assessment of clonality by polymerase chain reaction. Vet Immunol Immunopathol 69:145–164, 1999. Williams MJ, Avery AC, Lana SE, et al: Canine lymphoproliferative disease characterized by lymphocytosis: immunophenotypic markers of prognosis. J Vet Intern Med 22:596–601, 2008. Workman HC, Vernau W: Chronic lymphocytic leukemia in dogs and cats: the veterinary perspective. Vet Clin North Am Small Anim Pract 33:1379–1399, 2003. Young KM, MacEwen EG: Canine myeloproliferative disorders. In Withrow SJ, MacEwen EG, editors: Small animal clinical oncology, ed 3, Philadelphia, 2001, pp 611–626.
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AUTHOR: NICOLE C. NORTHRUP EDITOR: KENNETH M. RASSNICK
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Leukemias, Acute
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Leukemias, Acute BASIC INFORMATION DEFINITION Acute leukemias are uncommon neoplastic diseases characterized by clonal proliferation of malignant immature progenitor cells in the bone marrow and blood and are broadly categorized as lymphoid or nonlymphoid (myeloid). The specific diagnosis depends on the cell of origin. Acute lymphoblastic leukemias (ALL) involve the proliferation of lymphoblasts and prolymphocytes. Acute myeloid leukemias (AML), involve the proliferation of myeloid cells and include myeloid, monocytic, megakaryocytic, and erythrocytic leukemias. Historically AML and myelodysplastic syndromes in veterinary patients have been classified according to the Animal Leukemia Study Group modified version of the French-American-British system used in humans.
EPIDEMIOLOGY SPECIES, AGE, SEX Young cats and dogs (median 4-5 years) are more commonly affected with acute leukemias. Recent studies indicate older median age at incidence (7-9 years) for dogs with ALL. ALL: uncommon. Because it is difficult to distinguish ALL from stage V lymphoma, the percentage of leukemic dogs with ALL is unclear but reported to be 25%-30%. When considering only acute leukemic dogs, 40%-60% have ALL. Golden retrievers are overrepresented in cases of T-cell lymphoproliferative disorders. Specifically considering ALL, purebred dogs, in particular large breeds, predominate; German shepherd dogs and retrievers. AML: rare. In studies of leukemic dogs, 15%-40% have AML. Considering acute leukemic dogs only, 40%-60% have AML. The reported frequencies of canine AML types vary; M1 has been cited as most common, but a new study of 33 dogs with AML described 10 cases of M0, 3 M1, 5 M2, 12 M4, 2 M5, and 1 M7 (no M3 or M6). In 99 cats, 21% had M1, M2 was most common at 32%, and M6 was seen in 29%. Less common AMLs were M4 in 5%, M5 in 7%, and AUL in 8%. There is a possible male predilection in dogs and cats but no known breed predispositions. RISK FACTORS: FeLV infection: 60%-80% of cats with ALL are FeLV positive and ≥90% of cats with AML are FeLV positive. Some patients with myelodysplastic syndromes will progress to AML. ASSOCIATED CONDITIONS & DISORDERS ALL in dogs: paraneoplastic hypercalcemia AML in cats: myelofibrosis, hypercalcemia, glomerulonephritis
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES Acute lymphoblastic leukemias: B-cell origin: most common type in dogs T-cell origin: most common type in cats Acute myeloid leukemias (classified based on bone marrow nucleated cell population): Acute undifferentiated leukemia (AUL): ≥30% of bone marrow nucleated cells are blasts of uncertain lineage. Myeloblastic leukemia without maturation (M1): ≥30% of marrow nucleated cells are myeloblasts; 10% of nonerythroid cells are maturing granulocytes. Promyelocytic leukemia (M3): ≥30% of marrow nucleated cells are myeloblasts; >10% of nonerythroid cells are maturing granulocytes, predominantly atypical promyelocytes. Has not been reported in animals. Acute myelomonocytic leukemia (M4): ≥30% of marrow nucleated cells are myeloblasts and monoblasts; differentiated granulocytes and monocytes each represent >20% of nonerythroid cells. Monoblastic/monocytic leukemia (M5): ≥30% of marrow nucleated cells are monoblasts or promonocytes. Erythroleukemia (M6): ≥50% of marrow nucleated cells are erythroid precursors, and ≥30% of nonerythroid cells are myeloblasts and monoblasts, or ≥30% of bone marrow nucleated cells are rubriblasts, myeloblasts, and monoblasts. Erythremic myelosis (M6-Er): ≥50% of marrow nucleated cells are erythroid precursors; ≥30% are erythroblasts.
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Megakaryoblastic leukemia (M7): ≥30% of marrow nucleated cells are megakaryoblasts. HISTORY, CHIEF COMPLAINT Acute onset of nonspecific signs such as lethargy, weakness, loss of appetite, and weight loss Hemorrhage (e.g., epistaxis or petechiae) may be noted. Lameness due to bone pain is possible. PHYSICAL EXAM FINDINGS Lethargy, weakness, pallor, weight loss, and dehydration are common. Fever due to secondary infection Tachypnea/dyspnea and tachycardia may be noted secondary to anemia. Hepatomegaly and splenomegaly are common. Lymphadenomegaly is often mild. Evidence of hemorrhage secondary to thrombocytopenia (petechiae, ecchymoses, epistaxis, intestinal bleeding) Ocular lesions (hyphema, uveitis, chorioretinitis, retinal detachment, chemosis, and conjunctivitis)
ETIOLOGY AND PATHOPHYSIOLOGY Acute leukemias are primary diseases of the bone marrow. As leukemic cells infiltrate the marrow, they crowd normal cells, change the marrow microenvironment, and secrete suppressor factors (myelophthisis). Consequently, normal hematopoiesis decreases, causing anemia, neutropenia, and thrombocytopenia. Cytopenias may result in weakness, secondary infections, and hemorrhage. Hepatic and splenic infiltration with leukemic cells is common, resulting in organomegaly, abdominal distention, and contributing to loss of appetite. Other sites may be involved, including lymph nodes, nervous system, kidneys, and gastrointestinal tract. Organ infiltration causes signs referable to failure of affected organs or nonspecific signs such as malaise and gastrointestinal disturbances.
DIAGNOSIS DIAGNOSTIC OVERVIEW Diagnosis is made by identification of abnormal numbers of blast cells on peripheral blood or bone marrow smears. Morphologic differentiation of acute leukemias and stage V lymphoma is limited. Recently, flow cytometric immunophenotyping (FCI) and PCR for antigen receptor rearrangements (PARR) have become routinely available for definitive diagnosis and classification of acute leukemias.
DIFFERENTIAL DIAGNOSIS Stage V lymphoma Ehrlichiosis
INITIAL DATABASE Laboratory tests: CBC and peripheral blood smear may reveal a leukocytosis with circulating blasts and cytopenias of other cells. Nonregenerative anemia and thrombocytopenia are common (nearly 100% and 90% of canine patients, respectively) and may be severe. Neutropenia occurs in 60%-80% of dogs and neutrophilia in 10%-20%. Aleukemic or subleukemic patients have normal or low white blood cell counts with no or some circulating blasts, respectively. Serum chemistry profile and urinalysis evaluate overall health and identify paraneoplastic syndromes. FeLV/feline immunodeficiency virus ELISA test for all cats. Consider PCR test for FeLV using bone marrow (submit marrow sample in EDTA). Rickettsial titers are indicated if in endemic area, history of tick exposure, or other compatible features. Bone marrow cytologic analysis (if unable to obtain a diagnostic sample, a core biopsy is indicated): If the blast cell count is ≥30% of all nucleated cells in the bone marrow, a diagnosis of acute leukemia can be made. Fine-needle aspiration and cytology of enlarged peripheral lymph nodes or organs frequently reveals infiltration with blasts. Imaging is performed to stage patients with leukemias and evaluate overall health: Thoracic radiography Abdominal ultrasonography
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ADVANCED OR CONFIRMATORY TESTING Flow cytometric immunophenotyping is now routine for determining the cell lineage of acute leukemias. Morphologic appearance is not as accurate in distinguishing ALL from AML. Fresh blood in EDTA should be submitted for flow cytometry if there is a high number of circulating blasts; blood or bone marrow smears should be submitted for PARR in cases with rare abnormal cells. Flow cytometry provides cell counts, identification, and classification of leukemias. PARR identifies and confirms clonality of abnormal cells. Information for submission of samples for flow cytometry or PARR to the Colorado State University Veterinary Diagnostic Laboratory can be found at http://www.cvmbs.colostate.edu/mip/people/Faculty/clinimmunosubmit-form.pdf and for the North Carolina State University College of Veterinary Medicine Clinical Immunology Lab can be found at http://www.cvm.ncsu.edu/dphp/labs/documents/ncsu_flow_cytometry_sub_form_052010.pdf Cytochemical, immunocytochemical, or immunohistochemical staining are used by some centers to distinguish lymphoid from nonlymphoid leukemias and allow classification of AMLs. Acute leukemias are currently being examined for molecular abnormalities that might be prognostic or serve as targets for novel therapies. Mutations in RAS, FLT3, and C-KIT have been identified.
TREATMENT TREATMENT OVERVIEW Goals are to eradicate leukemic cells with chemotherapy and support the patient with transfusions and other measures until normal hematopoiesis resumes. Patients with ALL can respond to chemotherapy for short periods of time. AML are less responsive.
ACUTE GENERAL TREATMENT Intensive supportive care is important in patients with acute leukemias: Broad-spectrum antibiotic therapy for treating/preventing secondary infections (see p. 188) Intravenous fluid therapy for patients with infection, fever, or decreased appetite Situations that might result in hemorrhage (e.g., jugular vein venipuncture or catheterization) should be avoided if severe thrombocytopenia is present. Transfusions as needed (see p. 1347) Nutritional support for patients with decreased appetite Chemotherapeutic agents are used for eradicating leukemia cells (induce remission). Clinically significant myelosuppression is expected because of myelophthisis. Hospitalization for supportive care during the induction period is indicated. Special handling requirements and potentially severe or life-threatening adverse patient effects exist with these chemotherapeutic drugs; these concerns and rapid evolution of protocols warrant consultation with/referral to an oncologist. ALL: treatment is generally with standard chemotherapy protocols for lymphoma (see p. 674). Agents include prednisone, vincristine, cyclophosphamide, doxorubicin, and L-asparaginase. AML: Chemotherapy protocols generally include cytosine arabinoside and doxorubicin. Agents such as 6-thioguanine, mitoxantrone, cyclophosphamide, busulfan, melphalan, vincristine, vinblastine, prednisone, and L-asparaginase have also been used. To date, results with chemotherapy have been disappointing. Future treatments may include targeted therapies and bone marrow transplant.
CHRONIC TREATMENT Patients responding to treatment will likely receive chemotherapy for the rest of their lives.
POSSIBLE COMPLICATIONS Myelosuppression: Neutropenia: sepsis Thrombocytopenia: hemorrhage Anemia requiring transfusion Gastrointestinal toxicity: vomiting, diarrhea, lethargy, loss of appetite
RECOMMENDED MONITORING Physical examinations and CBC: weekly to every other week, more frequently if needed during the induction period; to monitor remission status and myelosuppression due to therapy Serum chemistry profile: every 2 months to monitor renal and liver status, electrolytes, and critical parameters; more frequently if indicated
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Leukemias, Acute
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PROGNOSIS AND OUTCOME In general, the prognosis for acute leukemias is poor. Because many patients are euthanized at diagnosis and acute leukemias are relatively uncommon, there is limited information available regarding treatment outcomes. Most patients are clinically ill at presentation and if left untreated or given supportive care only, survival times are generally less than 2 to 4 weeks. CD34 expression: a stem cell marker; in dogs, expression of this antigen supports a diagnosis of acute leukemia and is associated with poor prognosis (median survival 16 days, range 3-128). ALL: for cats, a remission rate of 65% for a median of 7 months has been reported. Information about prognosis in dogs is confounded by the difficulty distinguishing ALL from stage V lymphoma; 30%-50% respond to chemotherapy for an average survival of 2-4 months. In dogs with CD8+ (cytotoxic T cell) lymphocytosis, higher cell counts are associated with poorer prognosis. The median survival for dogs with large cell CD21+ (B cell) lymphocytosis is 129 days. Note that this study of lymphocytosis included dogs with stage V lymphoma, CLL, and ALL. If chemotherapy is not an option, prednisone may be palliative. AML: A few cases surviving 3-4 months have been reported. Treatments attempted to date have done little to alter the course of AML, and prognosis is grave for cats and dogs.
PEARLS & CONSIDERATIONS COMMENTS Cytologic examination of a blood smear is imperative for all patients with leukocytosis or significant cytopenias. Patients with acute leukemias present with an acute onset of nonspecific signs. Cytologic evaluation of peripheral blood and bone marrow smears will generally provide a diagnosis, but special diagnostics are needed to differentiate ALL, AML, and stage V lymphomas. Flow cytometry is recommended. Because acute leukemias progress rapidly, consultation with an oncologist should be pursued quickly, and emergency referral should be considered for sick patients. Owners should be advised of the poor prognosis and the potential for complications with treatment of acute leukemias. Supportive care may help reduce complications with treatment. Better characterization of acute leukemias and development of novel treatments targeting the molecular abnormalities that cause them will improve the treatment and prognosis of dogs and cats with acute leukemias in the future.
TECHNICIAN TIPS Patients with acute leukemias are often sick and pancytopenic. Hospitalization for supportive care and monitoring will be required at treatment induction. Precautions should be taken to avoid exposure to infectious diseases and hemorrhage during phlebotomy or treatment. Owners should be educated on how to monitor their pet and precautions to protect themselves from exposure to chemotherapy.
SUGGESTED READING Jacobs RM, Messick JB, Valli VE: Tumors of the hemolymphatic system. In Meuten DJ, editor: Tumors in domestic animals, ed 4, Ames, IA, 2002, Iowa State Press, pp 119–198. McManus PM: Classification of myeloid neoplasms: a comparative review. Vet Clin Pathol 3:189–212, 2005. Moore AS, Ogilvie GK: Bone marrow disorders. In Ogilvie GK, Moore AS, editors: Feline oncology, a comprehensive guide to compassionate care. Trenton, NJ, 2001, Veterinary Learning Systems, pp 222–224. Tasca S, Carli E, Caldin M, et al: Hematologic abnormalities and flow cytometric immunophenotyping results in dogs with hematopoietic neoplasia: 210 cases (2002-2006). Vet Clin Path 38:2–12, 2009. Usher SG, Radford AD, Villiers EJ: RAS, FLT3, and C-KIT mutations in immunophenotyped canine leukemias. Experimental Hematology 37:65–77, 2009. Vail EM, MacEwen EG, Young KM: Canine lymphoma and lymphoid leukemias. In Withrow SJ, MacEwen EG, editors: Small animal clinical oncology, ed 3, Philadelphia, 2001, pp 558–590. Vernau W, Moore PF: An immunophenotypic study of canine leukemias and preliminary assessment of clonality by polymerase chain reaction. Vet Immunol Immunopathol 69:145–164, 1999.
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Weiss DJ: Flow cytometric and immunophenotypic evaluation of acute lymphocytic leukemia in dog bone marrow. J Vet Intern Med 15:589–594, 2001. Williams MJ, Avery AC, Lana SE, et al: Canine lymphoproliferative disease characterized by lymphocytosis: immunophenotypic markers of prognosis. J Vet Intern Med 22:596–601, 2008. AUTHOR: NICOLE C. NORTHRUP EDITOR: KENNETH M. RASSNICK
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Lethargy
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Lethargy BASIC INFORMATION DEFINITION Inert or apathetic state; lack of interest and/or energy; morbid drowsiness
SYNONYM Listlessness
EPIDEMIOLOGY SPECIES, AGE, SEX: Any patient ASSOCIATED CONDITIONS & DISORDERS: Any disease process affecting any organ system, if sufficiently severe (systemic and/or direct intracranial involvement), can cause lethargy.
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT The owner presents the pet because of a period of decreased activity, depressed mentation, and/or associated loss of appetite. A detailed history includes information as to the pet's water intake, presence or absence of vomiting/diarrhea, and whether the pet is eating. Additional useful information includes the pet's exercise level in the preceding days, whether other pets are affected, current medication history, and vaccination and de worming status. PHYSICAL EXAMINATION Temperature, pulse, and respiratory rate: comparison to normal to look for early signs of shock. Examination of the mouth for severe dental disease and mucous membrane color. Capillary refill time to assess peripheral perfusion. Palpation of all lymph nodes for enlargement, suggesting hyperplasia (e.g., inflammation) or infiltration (e.g., neoplastic). Chest auscultation must include listening to 3 to 5 breath sounds in each of a few quadrants of the chest as well as heart auscultation. Evaluate the pulse while auscultating the heart. Abdominal palpation must be methodical. It focuses on quadrants within the abdomen, involving specific palpation of individual organs. The examination includes palpating the small intestine a second time for a foreign body/mass or for fluid accumulation. Rectal examination: to check for perianal masses, to assess the prostate, and to collect feces for a fecal flotation. Manipulation of the neck for pain and palpation of the whole spine. Simultaneous palpation of the abdomen is important, as pressure on hyperpathic points in the spine always causes abdominal tensing. Manipulation of all joints
ETIOLOGY AND PATHOPHYSIOLOGY Direct central nervous system (CNS) insult (inflammatory, vascular, neoplastic, other) More commonly, lethargy is the result of systemic disturbances with CNS effects, such as: Inflammation: cytokine effects Vascular: decreased perfusion Metabolic: hypoglycemia, electrolyte disturbance, acid-base imbalance Environmental: hyperthermia/hypothermia Many others
DIAGNOSIS DIAGNOSTIC OVERVIEW
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Lethargy
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Lethargy is one of the most common yet least specific chief complaints in small-animal practice. A useful approach to diagnosis is to use the history to differentiate between medical and social/ behavioral causes; to also use the history to identify other concurrent clinical signs with an onset that coincides more or less with that of the lethargy (guiding testing towards a particular body system); and to identify abnormalities on the physical exam that can focus diagnostic efforts. In most cases, routine blood tests and urinalysis are justified as screening tools.
DIFFERENTIAL DIAGNOSIS Any disease process (metabolic, infectious, neoplastic, traumatic, vascular, degenerative)
INITIAL DATABASE Minimum database on each case: Return to/repeat the physical exam (most important diagnostic test in these cases) Urinalysis Blood smear: evidence of infection versus inflammation; platelet count Fecal flotation
ADVANCED OR CONFIRMATORY TESTING CBC, serum biochemistry profile, urinalysis The minimum database and physical exam orient the selection of additional tests. The more tests are performed, however, the greater the likelihood of a false-positive result. Thoracic radiographs (two views) Abdominal ultrasound and/or radiographs
TREATMENT TREATMENT OVERVIEW Treatment for confirmed disease processes Antibiotics are reserved for confirmed or highly suspected bacterial disease. Withholding of glucocorticoids unless their need has been proven. Glucocorticoids complicate many further diagnostics and can cause clinical deterioration if used inappropriately.
ACUTE AND CHRONIC TREATMENT If no trigger is found after the history, physical exam, and initial database, and the pet is not very ill, outpatient empirical treatment can be acceptable (e.g., in patients with gastrointestinal signs, using intestinal formula diet and asking owner to watch and return if pet is no better). Antibiotics are only considered if the blood smear/CBC shows signs of infection or if there is fever with a second sign of infection (e.g., blood in the feces). Specific aspects of treatment are guided by results of the minimum database and advanced testing: Fluids if dehydrated Analgesics if needed
POSSIBLE COMPLICATIONS Lack of communication. It is essential to explain to the owner that an underlying trigger exists and must be found to provide optimal treatment.
PROGNOSIS AND OUTCOME Highly variable, depending on the underlying cause of lethargy
PEARLS & CONSIDERATIONS COMMENTS
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First do no harm; treatment is centered on identified triggers and underlying causes. More than 35% of sick pets presented to veterinary clinics have acute gastrointestinal upsets. Confident presentation of information is essential. Otherwise, owners can mistakenly sense uncertainty rather than a logical stepwise approach to a biological system.
SUGGESTED READING Osborne CA: The problem orientated medical system. Improve knowledge, wisdom and understanding of patient care. Vet Clin North Am Small Anim Pract 13(4):745–753, 1983. AUTHOR: DAVID MILLER EDITOR: ETIENNE CÔTÉ
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Leptospirosis
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Leptospirosis BASIC INFORMATION DEFINITION A bacterial disease affecting humans and animals, caused by pathogenic subtypes (serovars) of the aerobic gram-negative filamentous spirochetes, Leptospira interrogans and L. kirschneri
SYNONYMS Weil's disease, Stuttgart disease, fall fever
EPIDEMIOLOGY SPECIES, AGE, SEX Dogs: 4-7-year-old males more commonly affected Younger dogs are more susceptible to severe disease Cats: not clinically affected nor renal carriers; do seroconvert with exposure GENETICS & BREED PREDISPOSITION: More common in hounds, working dogs, and herding breeds (likely greater exposure risk) RISK FACTORS Suburban or rural environment Outdoor exercise areas/activities Exposure to wildlife or livestock (maintenance hosts) Exposure to moist environments/ standing water or to raw sewage Flooding Human risk factors: direct contact with domestic animals, environmental exposure (e.g., fisheries, rice fields, water sports), exposure to wild rodents (urban areas of poor sanitation) CONTAGION & ZOONOSIS Readily contagious and zoonotic, typically via exposure to infected urine. When handling patients suspected of having leptospirosis, veterinary personnel and laypersons must use gloves and personal protective equipment to avoid exposure to urine and fomites. Leptospirosis is the most widespread zoonosis worldwide, accounting for up to 30% of human cases of acute renal failure in developing countries. Most human infections are asymptomatic or associated with mild, self-limiting flulike symptoms. GEOGRAPHY AND SEASONALITY Worldwide distribution but predominant serovar(s) responsible for disease vary by region. In North America, serovars grippotyphosa, pomona, and bratislava are most common (historically, serovars canicola and icterohaemorrhagiae prior to vaccines targeting them). Previously considered a rural disease, leptospirosis is now also urban (rodents) and suburban (wildlife). The organisms survive in warm, moist environments, especially water but also mud and soil. The incidence of disease is highest in warmer months.
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES There are at least 8 serovars (L. interrogans: autumnalis, bataviae, bratislava, canicola, hardjo, icterohaemorrhagiae, pomona; L. kirschneri: grippotyphosa) infectious to dogs and cats, causing variable degrees of renal and liver disease in dogs. Most infections are asymptomatic. Clinical disease: peracute (rare; sudden death from massive leptospiremia), acute, subacute (common), or chronic (common)
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Leptospirosis
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forms Some reported variation in tissue tropism and disease severity depending on the infecting serovar and the age and immune status of the host HISTORY, CHIEF COMPLAINT Acute form: younger animals; lethargy, anorexia, shivering, muscle tenderness, vomiting Subacute form: lethargy, anorexia, vomiting, polydipsia/polyuria, reluctance to move, lumbar pain, icterus, hemorrhage Chronic form: +/− polyuria/polydipsia, icterus, inappetence PHYSICAL EXAM FINDINGS General: Anorexia Lethargy Fever Dehydration +/− progression to hypovolemic shock Injected mucous membranes Conjunctivitis, uveitis Petechial and ecchymotic hemorrhages Nasal discharge Increased lung sounds +/− Abdominal pain, myalgia Additional findings vary based on tissue tropism and severity of injury: Most cases show hypovolemia. Manifestations of renal disease are very common. Liver involvement is common; overt signs of liver failure (icterus, hepatic encephalopathy) may be present. Vomiting is common. Diarrhea is very common in experimentally infected puppies, less common in naturally occurring infections (but more common than in other causes of renal failure). Pulmonary disease (labored breathing, cough) is much less common.
ETIOLOGY AND PATHOPHYSIOLOGY Leptospires enter the body by penetrating intact mucous membranes or bruised, abraded, or water-softened skin. Leptospiremia (7-10 days) causes dissemination to kidney, liver, spleen, central nervous system, eyes, and genital tract. Leptospires can express hemolysin and other factors which cause endothelial damage and vasculitis. Renal tubular epithelial-cell colonization occurs in most infected dogs, causing shedding for months to years post infection if not appropriately treated. Hepatic disease may result from toxin-induced injury and may be severe; some cases present with acute hepatic dysfunction as the predominant feature. Leptospirosis has been implicated as a cause of chronic hepatitis (serovar grippotyphosa).
DIAGNOSIS DIAGNOSTIC OVERVIEW Unexplained fever or signs of renal and/ or hepatic insufficiency should prompt consideration of leptospirosis. Diagnosis is multimodal: a serum titer alone is rarely sufficient, and a combination of history (exposure, clinical signs), physical examination, routine blood test results, serologic titers, and organism demonstration (via PCR) all contribute to confirming or refuting the clinical diagnosis.
DIFFERENTIAL DIAGNOSIS Other causes of acute renal failure (e.g., toxin, pyelonephritis, heat stroke, shock; see p. 31) Other causes of vasculitis (e.g., sepsis, rickettsial disease, pancreatitis) Other causes of hepatic injury (e.g., bacterial cholangiohepatitis, toxin, sepsis, idiopathic chronic hepatitis)
INITIAL DATABASE CBC: Often inflammatory leukogram, with or without a left shift +/− Variable degree of anemia
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Leptospirosis
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+/− Thrombocytopenia; a third of cases, mild to moderate (90,000-150,000/mm ), especially if vasculitis or disseminated intravascular coagulation (DIC) Serum biochemistry profile: Azotemia and hyperphosphatemia are common. Electrolyte disturbances: hyponatremia, hypochloremia, and hypokalemia Metabolic acidosis +/− Hypoalbuminemia in cases with vasculitis or severe liver dysfunction Liver parameters: increased alanine aminotransferase (ALT), alkaline phosphatase (ALP), and bilirubin usually peak at 6-8 days after the onset of disease. Urinalysis: Glucosuria, proteinuria, granular casts, pyuria, and hematuria may be present. Variable specific gravity Thoracic radiographs: interstitial, nodular, or patchy alveolar infiltrates with pulmonary involvement or vasculitis Abdominal radiography and ultrasonography: +/— enlargement of liver, spleen, kidneys; renal “medullary rim sign” (hyperechoic concentric ring); perinephric effusion
ADVANCED OR CONFIRMATORY TESTING Microscopic agglutination test (MAT): In animals with compatible clinical signs, the following results are considered diagnostic: Titer > 1:800 in unvaccinated animal Titer > 1:3200 in vaccinated (previous 3-4 months) animal Paired titers 2-4 weeks apart with fourfold increase from first to second titer. Cross-reactivity among serovars is common, and highest serovar's titer often is not the causative serovar. ELISA: used as field tests for human infections PCR assays: sensitive and specific; may be positive in early infection before rise in specific antibody detected by MAT or ELISA is present. Current techniques distinguish pathogenic organisms but not serovars. Darkfield microscopy: examination of fresh urine for leptospires; low sensitivity (intermittent shedding means frequent falsenegative results) and not routinely used Bacterial culture: leptospires are difficult to grow in culture; frequent false-negative results; does allow identification of infecting serovar (important epidemiologically) Fluorescent antibody techniques: fluid and tissue samples; not widely used Histopathologic assessment: lesions nonspecific (lymphoplasmacytic tubulointerstitial nephritis); organisms may be identified using special stains.
TREATMENT TREATMENT OVERVIEW Treatment goals are to treat bacteremia/leptospiremia, maintain renal perfusion and urine output to minimize renal injury, eliminate bacteria to prevent disease progression and shedding to environment, and treat associated conditions (renal failure, hepatic insufficiency, DIC, uveitis).
ACUTE GENERAL TREATMENT Penicillins: antimicrobial of choice for bacteremic phase (crystalline [transparent] formulations for IV use) Penicillin sodium, 20,000 IU/kg IV q 4 h; or Ampicillin, 22 mg/kg IV or PO q 8 h; or Amoxicillin, 22 mg/kg IV or PO q 8 h Intravenous fluid therapy to replace deficits (vomiting, polyuria, decreased intake) and initial management of renal injury: target is rapid rehydration without volume overload (see p. 31) Adjunctive management of organ dysfunction and other consequences of infection as indicated for individual case (see Acute Renal Failure, p. 31; Acute Liver Injury, ; Disseminated Intravascular Coagulation p. 315; Vasculitis ; Sepsis p. 1014)
CHRONIC TREATMENT Doxycycline, 5 mg/kg PO q 12 h for 2 weeks to eliminate leptospires from tissues, eliminate renal shedding
RECOMMENDED MONITORING Serum electrolyte levels, renal and hepatic parameters: to assess response to treatment or disease progression and to tailor therapy
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Leptospirosis
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Hypertension may occur, requiring modification of treatment (see p. 1068). Urine output monitoring is essential in patients with acute renal failure. Monitor for development of complications (DIC, respiratory failure).
PROGNOSIS AND OUTCOME Survival rates for patients with clinical leptospirosis: 70%-85% Patients with acute renal failure are frequently oliguric to anuric and may require dialysis. Survivors may have persisting/chronic kidney (common) or liver dysfunction.
PEARLS & CONSIDERATIONS COMMENTS Leptospirosis should be considered as a differential in any case of acute renal failure, fever of unknown origin, vasculitis, and/or acute or chronic liver disease in a dog. Due to the zoonotic potential of Leptospira pathogens, extreme caution should be used when handling suspected leptospirosis cases (dogs with acute febrile disease, especially with evidence of acute renal or liver disease). Human physicians are often unfamiliar with leptospirosis and its zoonotic potential. Intensive early therapy is important both for the patient's benefit and to reduce the risk of transmission to humans and other animals (empirical penicillin therapy in leptospirosis suspects while awaiting confirmatory test results). Serovars icterohaemorrhagiae and pomona: liver disease > renal disease. Serovars canicola and grippotyphosa: renal disease > liver disease. Leptospirosis is a reportable disease in many U.S. states; contact regional authorities.
PREVENTION Vaccination: whole-cell killed bacterin and subunit vaccines exist; vary in duration of immunity (6-13 months) and which serovars are included; prevent clinical disease and development of carrier state; most protect against icterohaemorrhagiae and canicola, newer vaccines include pomona and grippotyphosa. Vaccine protection is serovar specific: no cross-protection against nonvaccine serovars. Adverse reactions have been reported with disproportionate frequency with whole-cell leptospirosis vaccines; patients with a history of intolerance should either not receive the vaccine or be premedicated with antihistamines (e.g., diphenhydramine, 2 mg/ kg IM) and glucocorticoids (e.g., dexamethasone, 0.2 mg/kg IM) 15-30 minutes before vaccination Rodent control, avoidance of contact with reservoir hosts, and proper sanitation/drainage are also important.
TECHNICIAN TIPS Leptospirosis can be transmitted from infected animals to humans. To prevent exposure of people and other animals to the disease, strict protective measures should be used in handling animals, their bedding, and all laboratory samples. Use of hoses to clean cages of infected animals may result in generation of aerosols that can spread the organisms to people and other animals, and seed building surfaces with bacteria. Goggles, masks, and gloves should be worn to prevent exposure via mucous membranes (eyes, nose, mouth) and skin. Leptospirosis patients or suspects should be isolated from other patients and their movement restricted (patient remains in assigned cage unless absolutely necessary). If moved, patients should be transported by gurney or portable carrier that can be thoroughly disinfected.
CLIENT EDUCATION Leptospirosis can be transmitted to people, principally through direct or indirect contact with urine. Owners should be advised to contact their family physician for recommendations following exposure to an infected pet. The Centers for Disease Control and Prevention (CDC) maintains an informational page for lay persons, “Leptospirosis and Your Pet” at: www.cdc.gov/ncidod/dbmd/diseaseinfo/leptospirosis_g_pet.htm. Dogs should be supervised to prevent direct exposure to wildlife and should not be allowed to play in/drink from pools of stagnant water.
SUGGESTED READING Guerra M: Zoonosis update: leptospirosis. J Am Vet Med Assoc 234 (4):472–478, 2009.
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Leptospirosis
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Van de Maele I, Claus A, Haesebrouck F, et al: Leptospirosis in dogs: a review with emphasis on clinical aspects. Vet Rec 163:409–413, 2008. AUTHOR: MARCELLA D. RIDGWAY EDITOR: DOUGLASS K. MACINTIRE
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Lens Luxation
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Lens Luxation BASIC INFORMATION DEFINITION Complete dislocation of the lens anteriorly (into the anterior chamber) or posteriorly (into the posterior segment/ vitreous) from its normal position. Occurs as a result of abnormal development or degeneration (primary: usually bilateral inherited condition in dogs) or rupture or degeneration (secondary: acquired) of the lens zonules (fibers from the ciliary body that hold the lens in place).
SYNONYM Lens subluxation: partial dislocation of the lens
EPIDEMIOLOGY SPECIES, AGE, SEX Primary: occurs most commonly in middle-aged dogs, especially terrier breeds Secondary: dogs and cats; any age GENETICS & BREED PREDISPOSITION Primary: terrier breeds predisposed; typically between 3 and 7 years old German shepherd, border collie, and some spaniels may also be predisposed. RISK FACTORS: See Etiology and Pathophysiology below. ASSOCIATED CONDITIONS & DISORDERS Anterior uveitis Cataract Corneal endothelial-associated edema (anterior luxation) Glaucoma Vitreous degeneration Intraocular neoplasia Retinal detachment
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT Signs of ocular pain in cases of anterior lens luxation including tearing, redness, and squinting/blepharospasm. The cornea may be cloudy from edema. Vision change noted by the owner, depending on the visual status of the contralateral eye. PHYSICAL EXAM FINDINGS Systemic: generally unremarkable Ophthalmic: Anterior chamber depth abnormal: shallow with anterior luxation; deep with posterior luxation Iridodonesis (trembling of the iris) Phacodonesis (trembling of the lens) Aphakic crescent (portion of pupil no longer containing the lens) Vitreous presentation in the anterior chamber (appears as fine white cotton strands) Retina visualized without an ophthalmoscope (i.e., with penlight or transilluminator) Focal or diffuse corneal edema from mechanical damage to corneal endothelium with anterior luxation. Glaucoma (see p. 448) can result in secondary lens luxation by buphthalmos; conversely, primary lens luxation can also result in secondary glaucoma.
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Lens Luxation
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Cataract: with chronic lens luxation Blindness from cataract, glaucoma, retinal detachment
ETIOLOGY AND PATHOPHYSIOLOGY Primary lens luxation occurs as a result of an autosomal recessive inherited, progressive defect in the lens zonules. Secondary lens luxation occurs as a result of degeneration and/or stretching of the lens zonules; causes include: Chronic anterior uveitis (see p. 1151) Glaucoma with associated buphthalmos (see p. 448) Intraocular neoplasia (see p. 620) Hypermature cataract (see p. 181) Severe ocular trauma (results in other significant ocular damage; see p. 248) Age-related (older dogs/cats)
DIAGNOSIS DIAGNOSTIC OVERVIEW Suspected on physical examination subsequent to owner presentation for reduced vision or observed ocular abnormality. A complete ophthalmic examination is indicated to confirm and characterize the luxation and identify predisposing causes that can be treated.
DIFFERENTIAL DIAGNOSIS Glaucoma (see p. 448) Anterior uveitis (see p. 1151 )
INITIAL DATABASE Ophthalmic examination (see p. 1313 ): Menace response and pupillary light reflexes Intraocular pressure (IOP); normal = 10-18 mm Hg with TonoPen Penlight or slit-beam examination to determine if the lens luxation is primary or secondary, evaluate depth of anterior chamber, and assess cornea, lens, and vitreous for opacities Direct or indirect ophthalmoscopy to evaluate the posterior segment for retinal detachment (see p. 985), and optic nerve and retinal degeneration (see p. 983)
ADVANCED OR CONFIRMATORY TESTING Ocular ultrasound if opacities of the lens or transmitting media prevent complete examination
TREATMENT TREATMENT OVERVIEW Therapeutic goals are to remove anterior lens luxation or lens subluxation early to avoid secondary complications, and to remove posterior lens luxation or prevent lens from entering anterior chamber by constriction of the pupil.
ACUTE GENERAL TREATMENT Primary: Acute anterior lens luxation is considered an emergency. Determine IOP; treat if pressure elevated (see p. 448). Prompt referral of acute anterior lens luxation to a veterinary ophthalmologist for surgical lens removal (lensectomy): Intracapsular lens extraction (entire lens removed) ± intraocular lens sutured in place to restore emmetropia (normal vision, neither far- or near-sighted; without an intraocular lens implant, animals are 14 diopters hyperopic [far-sighted] with abnormal vision). If lens only subluxated, phacoemulsification (ultrasonic fragmentation of the lens) may be attempted. A capsular tension ring may be placed to stabilize the subluxation and a foldable acrylic intraocular lens (IOL) placed.
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Lens Luxation
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If referral is not possible and the lens is luxated anteriorly, consider pupil dilation and intravenous mannitol to shrink the vitreous and shift the lens into the vitreous (seep. 448). If lens luxation is posterior, consider use of a miotic (e.g., prostaglandin analog; see p. 448 ) to constrict the pupil and thus restrict lens movement; consider referral for surgery. Secondary: treat underlying cause.
CHRONIC TREATMENT See Cataracts, p. 181
POSSIBLE COMPLICATIONS See Cataracts, p. 181
RECOMMENDED MONITORING See Cataracts, p. 181 Contralateral eye should be monitored for lens position and anterior chamber vitreous presentation in predisposed breeds with unilateral lens luxation. If lens instability is noted, phacoemulsification should be considered prior to complete luxation.
PROGNOSIS AND OUTCOME Variable depending on underlying cause, duration and extent of the lens displacement, and location of the lens (anterior versus posterior). Most common complications are glaucoma and retinal detachment; in some reports, complication rate may be as high as 50%. Early surgical intervention while the lens is subluxated will increase success. The use of a capsular tension ring and foldable acrylic IOL may allow restoration of normal vision, with reduced complications and risk of luxation.
PEARLS & CONSIDERATIONS COMMENTS Terriers affected with lens luxation, regardless of severity, should not be used for breeding.
PREVENTION Dilated ophthalmic examination of all individuals of predisposed breeds, to detect early phacodonesis and anterior vitreous presentation (presence of vitreous rostral to the lens) Genetic testing of terriers to be used for breeding Complete dilated examination of the contralateral eye, especially in breeds with primary lens luxation Avoid head-shaking behaviors such as toys or rough playing in animals with phacodonesis or primary lens luxation in one eye.
CLIENT EDUCATION Breed predisposition and predilection for bilateral involvement in terriers With or without surgical intervention, affected eyes are at increased risk for retinal detachment and glaucoma. Genetic testing is available to distinguish affected, carrier and normal dogs. Homozygus affected dogs will luxate their lenses between 4-8 years of age. Animals that undergo surgical removal of the lens and do not receive an IOL implant have vision that, in human equivalence, is worse than 20/400 and corresponds to being “legally blind.”
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Lens Luxation
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LENS LUXATION Canine eye with anterior lens luxation. There is corneal edema, conjunctival hyperemia, deep corneal vascularization, an aphakic crescent (*), and the lens is cataractous.
SUGGESTED READING Davidson MG, Nelms SR: Diseases of the lens and cataract formation. In Gelatt KN, editor: Veterinary ophthalmology, ed 4, Iowa, 2007, Blackwell Publishing, pp 859–887. Farias FH, Johnson GS, Taylor JF, et al: An ADAMTS17 splice donor site mutation in dogs with primary lens luxation. Invest Ophthalmol Vis Sci 2010 Apr 7. (Epub ahead of print.) Wilkie DA, Colitz CMH: Surgery of the canine lens. In Gelatt KN, editor: Veterinary ophthalmology, ed 4, Iowa, 2007, Blackwell Publishing, pp 888–931. AUTHOR: DAVID A. WILKIE EDITOR: CHERYL L. CULLEN
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Leishmaniasis
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Leishmaniasis BASIC INFORMATION DEFINITION Leishmaniasis is a vector-borne zoonotic disease that is endemic in the Mediterranean region and South America (70 countries worldwide) and has recently been found in dogs in the United States.
EPIDEMIOLOGY SPECIES, AGE, SEX: Dogs, cats, foxes, jackals, humans in endemic areas GENETICS & BREED PREDISPOSITION: Boxers; most dogs with leishmaniasis in the United States have been foxhounds. RISK FACTORS: Dogs that have travelled to endemic areas (Middle East, southern Europe, Central and South America), foxhounds, outdoor dogs living in areas where sandflies are endemic CONTAGION & ZOONOSIS: Dogs are an important reservoir for human disease. In people, the disease occurs most commonly in infants, children, and immuno-suppressed or malnourished individuals. GEOGRAPHY AND SEASONALITY: Disease is limited to temperate, warm, humid areas where vector sandflies are present. The sandfly vectors in the Old World (Middle East, southern Europe) are Phlebotomus spp. and in the New World (Central and South America), Lutzomyia spp. ASSOCIATED CONDITIONS & DISORDERS Skin lesions: alopecia; exfoliative dermatitis, ulceration of face, pinnae, or limbs Glomerulonephritis Ocular lesions: keratoconjunctivitis, uveitis Lymphadenopathy Epistaxis Abnormal growth and elongation of nails (onychogryposis)
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT: One or more of the following: chronic weight loss, exercise intolerance, lymphadenopathy, skin lesions, eye lesions/vision loss, lameness, epistaxis PHYSICAL EXAM FINDINGS Lymphadenopathy Splenomegaly Ulcerative skin lesions of pinnae, face, and limbs Ocular discharge Miosis, photophobia secondary to uveitis
ETIOLOGY AND PATHOPHYSIOLOGY Leishmania infantum is the cause of human and canine visceral leishmaniasis in Europe, the Middle East, Africa, Asia, China, and the Americas. It is synonymous with L. chagasi found in Latin America. The parasite's life cycle is diphasic (vector and host phases). Promastigotes develop in the gut of the sandfly and migrate to the proboscis. They are transmitted to the mammal host during a blood meal and are phagocytized by macrophages. Inside the macrophage, they become amastigotes and multiply by binary fission until the macrophage ruptures, and the amastigotes are then disseminated to other macrophages and throughout the body.
DIAGNOSIS
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Leishmaniasis
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DIAGNOSTIC OVERVIEW Highly sensitive and specific diagnostic serologic and molecular techniques to detect Leishmania infection are now widely available in commercial laboratories. Quantitative serologic and molecular (PCR) techniques are the assays of choice. These should be used wisely and take into consideration that in endemic areas, a large part of the canine population may be infected subclinically and could present for veterinary care for unrelated reasons. Diagnostic testing is usually performed to confirm disease in dogs with suspected clinical signs, to monitor response to treatment, or to evaluate possible infection in apparently healthy blood donors, imported dogs, or dogs who have traveled to endemic areas.
DIFFERENTIAL DIAGNOSIS Tickborne diseases: borreliosis, ehrlichiosis Leptospirosis Dirofilariasis Pyoderma Immune-mediated skin diseases, vasculitis, glomerulonephritis Demodicosis Lymphoma Malnutrition, poor husbandry
INITIAL DATABASE CBC: may show leukopenia or leukocytosis, nonregenerative anemia, thrombocytopenia Serum chemistry profile: hyperglobulinemia, hypoalbuminemia ± azotemia Cytologic evaluation of lymph node, skin, splenic, and bone marrow aspirates may reveal amastigote forms of Leishmania. Urinalysis: may reveal isosthenuria and proteinuria secondary to immunoproliferative glomerulonephritis Urine protein/creatinine ratio may be elevated (>0.5).
ADVANCED OR CONFIRMATORY TESTING Histopathologic evaluation and immunohistochemical staining of skin biopsies may reveal organisms. Serologic tests: indirect immunofluorescent antibody test (IFAT) titers >1:32 indicate suspected exposure; titers >1:200 are consistent with active infection. Specific quantitative recombinant antigen rK39 ELISA or crude-antigen ELISA may also detect subclinical infection. PCR test: most sensitive test (confirmatory test of choice); will also detect subclinically infected dogs.
TREATMENT TREATMENT OVERVIEW Current drugs used for treating canine leishmaniasis, including newly developed therapies such as treatment with miltefosine or synergistic combinations of drugs, have limited efficacy and do not clear infection completely in most dogs. Treatment of dogs is usually followed by clinical improvement, but the parasite is rarely eliminated, and treated dogs remain latent carriers that may relapse and continue to harbor a zoonotic infection.
ACUTE GENERAL TREATMENT Sodium stibogluconate (Pentostam: available from the Centers for Disease Control and Prevention in Atlanta, GA) 30 mg/kg q 24 h IV or SQ for 3-4 weeks; or Meglumine antimonite (Glucantime): 100 mg/kg SQ or IV q 24 h for 3-4 weeks Allopurinol (20 mg/kg/d PO) for 6-12 months; can be administered in combination with meglumine antimonate at the same doses as above for both drugs Miltefosine (2 mg/kg/d PO) for 4 weeks with allopurinol (20 mg/kg/d PO) for 6-12 months
CHRONIC TREATMENT Dogs with renal insufficiency and protein-losing nephropathy do not respond well to therapy. Euthanasia should be considered in dogs with chronic poorly responsive disease or in households with immunosuppressed persons.
RECOMMENDED MONITORING
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Leishmaniasis
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Negative PCR or declining titers post treatment. Periodic monitoring of renal parameters every 3 months in dogs with no initial azotemia and more frequently in dogs with azotemia at admission.
PROGNOSIS AND OUTCOME Prognosis is guarded owing to inability to completely eradicate the organism.
PEARLS & CONSIDERATIONS PREVENTION There is no vaccine available in the United States. A vaccine is marketed in Brazil, and there are progressive experiments on new commercial canine vaccines. Insecticidal collars and topical insect repellent may prevent vector transmission. If possible, keep pet dogs inside during dawn and dusk, the feeding times of sandflies.
CLIENT EDUCATION Leishmaniasis is a zoonotic disease that can be fatal in humans. Leishmaniasis does not respond very well to treatment. Leishmaniasis is often a chronic infection in dogs that may not manifest for years after the initial exposure.
SUGGESTED READING Rosypal BS, Zajac AM, Lindsay DS: Canine visceral leishmaniasis and its emergence in the United States. Vet Clin Small Anim 33:921–937, 2003. Baneth G, Koutinas AF, Solano-Gallego L, et al: Canine leishmaniasis-new concepts and insights on an expanding zoonosis—part one. Trends Parasitol 24:324–330, 2008. Miró G, Cardoso L, Pennisi et al: Canine leish-maniosis-new concepts and insights on an expanding zoonosis—part two. Trends Par-asitol 24:371–377, 2008. AUTHOR: GAD BANETH EDITOR: DOUGLASS K. MACINTIRE
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Leiomyoma, Leiomyosarcoma
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Leiomyoma, Leiomyosarcoma BASIC INFORMATION DEFINITION Leiomyoma: uncommon benign tumor of smooth muscle origin Leiomyosarcoma: uncommon malignant tumor of smooth muscle origin Either can be found wherever smooth muscle is present. Most common sites: gastrointestinal (GI) tract, spleen, genital tract
SYNONYMS Smooth muscle tumors
EPIDEMIOLOGY SPECIES, AGE, SEX: Uncommon in dogs and rare in cats Leiomyoma: gastric: mean age 16 years (dogs) Leiomyoma: colonic: median age 12 years (dogs) Leiomyosarcoma: GI; median age 10.5-12 years (dogs) Leiomyo(sarco)ma: genital, urinary tract, or intestinal; female > male GENETICS & BREED PREDISPOSITION: Leiomyosarcoma more common in large-breed dogs, notably in German shepherds (intestinal). ASSOCIATED CONDITIONS & DISORDERS: Paraneoplastic syndromes: Hypoglycemia Nephrogenic diabetes insipidus (one dog with intestinal leiomyosarcoma) Polycythemia due to elevated plasma erythropoietin levels (one dog with cecal leiomyosarcoma)
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT GI leiomyoma: Incidental finding during endoscopy or necropsy. Occasionally, tenesmus or dyschezia if rectal; vomiting or regurgitation if gastroesophageal. GI leiomyosarcoma: Signs referable to the GI tract, including chronic vomiting, weight loss, melena, hematemesis, gastric dilation, or regurgitation Peripheral leiomyosarcoma: progressively enlarging mass noticed by the owner Rarely, animals with leiomyosarcoma first present with signs related to paraneoplastic hypoglycemia. PHYSICAL EXAM FINDINGS Abdominal mass possible with any visceral leiomyo(sarco)ma Signs of peritonitis possible as a result of intestinal rupture, especially with cecal leiomyosarcoma Abdominal pain, distended loops of bowel, and/or mass palpable per rectum in some cases Weakness or collapse due to gastric hemorrhage Subcutaneous mass with peripheral leiomyosarcoma Physical exam may be unremarkable, especially with leiomyoma.
ETIOLOGY AND PATHOPHYSIOLOGY Both leiomyomas and leiomyosarcomas have been associated with paraneoplastic hypoglycemia. Potential mechanisms: excessive glucose metabolism by the tumor, diminished hepatic gluconeogenic capacity due to hepatic damage by the tumor, associated peritonitis, or due to production of insulin-like growth factors by the tumor. Those tumors associated with
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Leiomyoma, Leiomyosarcoma
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production of insulin-like growth factors have been associated with long-term disease-free intervals or cure as a result of resection of the tumor. Although not confirmed, leiomyosarcomas in the female urogenital organs are thought to develop secondary to hormonal stimulation.
DIAGNOSIS DIAGNOSTIC OVERVIEW The diagnosis is suspected based on gastrointestinal signs in an older dog, typically with a mass visible on abdominal ultrasound; confirmation is obtained via histopathologic and immunohistochemical evaluation.
DIFFERENTIAL DIAGNOSIS GI: foreign body, enteritis causing ileus, other GI neoplasm, GI granuloma (fungal, other), GI inflammation/infiltration (inflammatory bowel disease), renal disease, hepatic disease Other sites: other neoplasms (benign or malignant), abscess, granuloma, hematoma
INITIAL DATABASE CBC: 63% of dogs are anemic. Serum biochemistry panel: 50% are hypoglycemic Three-view thoracic radiographs: usually within normal limits Abdominal radiographs: may reveal GI mass, evidence of lymphadenopathy, changes consistent with peritonitis, or no abnormalities Abdominal ultrasound: 66% have evidence of an abdominal mass. Lymphadenopathy may also be noted. Fine-needle aspirate cytologic evaluation, if possible, may help identify the tumor type before invasive diagnostic testing (biopsy).
ADVANCED OR CONFIRMATORY TESTING GI contrast radiography (e.g., barium series), endoscopy, or CT may confirm gastroesophageal or intestinal obstruction and/or mass. The gold standard for diagnosis is biopsy with histopathologic evaluation, preferably surgically (rather than endoscopically) to resect the entire neoplasm if possible. Histopathologic grade may be prognostic. Immunohistochemical staining is required to differentiate leiomyosarcomas from gastrointestinal stromal tumors.
TREATMENT TREATMENT OVERVIEW Treatment requires stabilizing the patient and attempting wide and complete surgical resection of the entire tumor (if possible).
ACUTE GENERAL TREATMENT Stabilization of systemic effects: hypoglycemia, anemia (e.g., due to GI hemorrhage), electrolyte and acid-base disturbances (e.g., due to chronic vomiting).
CHRONIC TREATMENT Complete surgical resection: Curative of leiomyoma, and leiomyosarcoma in the absence of metastases. If small intestinal, removal of 5 cm of normal bowel on either side of the tumor and resection of the corresponding mesentery are recommended. Even with gross metastatic disease, surgical resection of leiomyosarcomas can afford long-term survival. Mesenteric lymph nodes, liver, and suspected metastatic lesions should be biopsied for staging purposes. Dogs with metastasis or a high likelihood of metastasis (based on tumor location; see Prognosis and Outcome below) can be considered candidates for chemotherapy, although no studies have shown promising efficacy of chemotherapy against these tumors.
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POSSIBLE COMPLICATIONS Variable, depending on the types of treatments and the location of the primary tumor A 50% rate of localized peritonitis associated with tumor rupture has been reported.
RECOMMENDED MONITORING According to clinical signs Exam and three-view thoracic radiographs and abdominal ultrasound q 3 mon for postoperative GI leiomyosarcoma patients. Exact frequency based on clinical signs and tumor location (see Prognosis and Outcome below).
PROGNOSIS AND OUTCOME Prognosis depends on the location of the tumor: Dogs with hepatic leiomyosarcoma frequently develop metastases and have a grave prognosis. Dogs with gastric or intestinal leiomyosarcomas may have metastatic rates >54%, but many can have a good prognosis, even with confirmed metastasis (e.g., median survival 21.7 months for those surviving the perioperative period, including dogs with metastatic disease); 1-year survival rate 75%, 2-year survival rate 66%, and 3-year survival rate 60%. Dogs with cecal leiomyosarcomas may have a lower metastatic rate (10%) and better overall prognosis. Most dogs with successful resection of the cecal tumor eventually die of causes unrelated to the tumor. Colorectal leiomyomas: mean survival 31.6 months
PEARLS & CONSIDERATIONS COMMENTS Leiomyosarcomas most commonly occur in the cecum and jejunum. They are the second most common intestinal tumor in dogs. Even with metastatic disease, including gross hepatic and mesenteric involvement apparent at laparotomy, GI leiomyosarcoma is associated with a fair life expectancy (mean: 2 years) postoperatively. Some gastrointestinal leiomyosarcomas (GILMS) have been reclassified as gastrointestinal stromal tumors (GIST) via immunohistochemical techniques (they express c-kit, CD-117 positive; true GILMS do not). GIST are derived from interstitial cells of Cajal, which are the pacemaker cells of the gastrointestinal tract (regulate motility and peristalsis). One study indicated that in dogs, it may be that GILMS and GIST behave differently (GILMS more commonly located in the stomach and small intestine; GIST more commonly located in the cecum and large intestine). GIST were also thought to be more locally invasive and more likely to result in perioperative death as a result of gastrointestinal wall perforation and sepsis. Another study found no clinical importance of reclassification, but did note that future treatments may be dictated by this division.
CLIENT EDUCATION If leiomyosarcoma: monitor for signs indicating recurrence or abdominal metastasis (e.g., vomiting, diarrhea, abdominal distention, and abdominal pain).
SUGGESTED READING Cohn M, Post GS, Wright JC: Gastrointestinal leiomyosarcoma in 14 dogs. J Vet Intern Med 17:107, 2004. Mass CP, Haar GT, Van Der Gaag I, et al: Reclassification of small intestinal and cecal smooth muscle tumors in 72 dogs: clinical, histologic, and immunohistochemical evaluation. Vet Surg 36:302–313, 2007. Russell KN, Mehler SJ, Skorupski KA, et al: Clinical and immunohistochemical differentiation of gastrointestinal stromal tumors from leiomyosarcomas in dogs: 42 cases (1990-2003). J Am Vet Med Assoc 230:1329–1333, 2007. AUTHOR: M. RAQUEL BROWN EDITOR: DEBRA L. ZORAN
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Left Bundle Branch Block
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Left Bundle Branch Block BASIC INFORMATION DEFINITION An intracardiac conduction disturbance sometimes associated with left ventricular enlargement. There is failure of normal (rapid) conduction from the bundle of His through the left bundle branch to the Purkinje fibers in the left ventricle. Conduction to the left ventricle still occurs but is very slow because it must travel from muscle cell to muscle cell. This results in a marked delay in conduction to the left ventricle, and the QRS complex becomes wider on the electrocardiogram (ECG).
EPIDEMIOLOGY SPECIES, AGE, SEX: Dogs and cats of either sex and any age RISK FACTORS: Left ventricular enlargement, particularly left ventricular dilation
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES Intermittence: in some cases, left bundle branch block (LBBB) may occur only when the heart rate surpasses a certain individual threshold (heart rate dependent). Left anterior fascicular block: Historically, it was believed the left bundle branched into anterior and posterior fascicles as it does in humans, and that left anterior fascicular block was implicated in causing a marked left axis deviation on the surface ECG, with only slight prolongation of left ventricular depolarization. However, the left bundle does not branch into two distinct fascicles in dogs and cats, making this extrapolation inaccurate. Still, a marked left axis deviation in cats, which has been called left anterior fascicular block by some, has often been observed both in cats with hypertrophic cardiac disease and in normal cats. Thus, it is important to recognize this pattern of left axis deviation (tall R wave in leads I and aVL, S wave present in leads II, III, and aVF), although the name left anterior fascicular block is inappropriate. HISTORY, CHIEF COMPLAINT: Reflective of the underlying structural heart disease. Chief complaints range in severity from none (uncommon; LBBB is an infrequent incidental finding on ECG) to decompensated states of heart disease, such as congestive heart failure (dyspnea, lethargy, abdominal distension possible) or syncope. PHYSICAL EXAM FINDINGS Typically LBBB is clinically silent. However, in some individuals, split heart sounds may be present due to prolonged left ventricular ejection time and delayed closure of the mitral valve (causing a split first heart sound). LBBB does not alter the rhythm of the heartbeat or the pulse. Findings relating to underlying structural heart disease (heart murmur, arrhythmia, gallop sound, dyspnea) are common.
ETIOLOGY AND PATHOPHYSIOLOGY LBBB usually indicates significant underlying cardiac disease such as: Cardiomyopathy Congenital heart disease, in particular subaortic stenosis Cardiac ischemia Certain drug toxicoses (doxorubicin)
DIAGNOSIS DIAGNOSTIC OVERVIEW
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The diagnosis is made entirely on the electrocardiogram: LBBB is suspected when QRS duration is longer than normal (canine: >0.07 sec; feline: >0.06 sec), wide and positive R waves are present in leads I, II, III, aVF and the left precordial leads, and the rhythm appears to be supraventricular in origin.
DIFFERENTIAL DIAGNOSIS Wide QRS complex(es) on ECG: Left ventricular hypertrophy Ventricular ectopy (premature ventricular complexes, ventricular tachycardia) Ventricular escape rhythm ± Motion artifact
LEFT BUNDLE BRANCH BLOCK Lead II ECG from a dog showing normal sinus rhythm with left bundle branch block. The QRS duration is 0.1 sec (normal £0.07). The heart rate is 90 beats/min. 50 mm/sec, 1 cm =1 mV.
INITIAL DATABASE Electrocardiography is the definitive diagnostic test. Electrocardiographic characteristics of LBBB: Prolonged QRS complex duration (canine >0.07 sec, feline >0.06 sec) Wide and positive QRS complexes in leads I, II, III, aVF, and left precordial leads (CV6LL [V2] and CV6LU [V4]) Negative QRS complexes in leads aVR and CV5RL (rV2)
ADVANCED OR CONFIRMATORY TESTING Thoracic radiographs to evaluate for left ventricular enlargement Echocardiogram to assess heart structure and function
TREATMENT TREATMENT OVERVIEW No treatment is necessary for LBBB. LBBB does not result in any hemodynamic sequelae by itself and therefore does not require specific treatment. However, LBBB is often associated with underlying structural heart disease. Treatment of this underlying condition is indicated if present.
POSSIBLE COMPLICATIONS Complete block of both the right and left bundle branches produces complete (third-degree) atrioventricular block
PEARLS & CONSIDERATIONS COMMENTS The bizarre QRS morphology seen with bundle branch block can be confused with premature ventricular complexes or
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Left Bundle Branch Block
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ventricular tachycardia (ventricular ectopy). If P waves are present and the PR interval is consistent for every heartbeat, the complex is likely coming from a supraventricular site (and the bizarre QRS morphology is due to bundle branch block rather than ventricular ectopy). However sometimes P waves are buried and not visible, although the rhythm is supraventricular in origin (particularly with tachycardias). Because most dogs with heart rates 2-3 mg/dL (>176-264 mmol/L), rising serum creatinine >0.5 mg/dL (>44 mmol/L) in 48 hours, or nonphysiologic oliguria. The lungs are a common site of organ dysfunction in MODS, manifesting as acute lung injury (ALI) or acute respiratory 2
2
distress syndrome (ARDS; see p. 1369). ALI is characterized by a Pao :Fio ratio between 300 and 200. ARDS is characterized by the presence of acute respiratory distress, bilateral radiographic pulmonary alveolar infiltrates, decreased pulmonary compliance, the absence of left-sided heart failure (pulmonary capillary wedge pressure 0.8 is strongly indicative of the absence of a PSS. Transcolonic or transsplenic portal scintigraphy: distinguishes hepatic microvascular dysplasia from PSS. There is significant hepatic uptake of the radionuclide in the liver with micro vascular dysplasia (1 week Overlooking the “divided q 12 h” indication and prescribing the high enteric dose q 12 h Failing to reduce the dose in patients with liver disease Failing to accurately divide the 250-mg tablets in cats or very small dogs, where small differences in tablet fractions correspond to relatively large excesses in dose per kg body weight
DIAGNOSIS DIAGNOSTIC OVERVIEW The diagnosis is based entirely on medication history and physical signs.
DIFFERENTIAL DIAGNOSIS Encephalitis Neoplasia
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Metronidazole Toxicosis
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INITIAL DATABASE Routine laboratory tests are usually normal, but mild elevations in liver enzymes are possible.
ADVANCED OR CONFIRMATORY TESTING Diagnosis is based on clinical features, history of metronidazole administration, and recovery on stopping the drug.
TREATMENT TREATMENT OVERVIEW The goal of treatment is to stop metronidazole administration and provide supportive care until the signs resolve, usually within 3-5 days.
ACUTE GENERAL TREATMENT Discontinue the metronidazole. Parenteral hydration and nutrition if necessary Antiseizure medication such as diazepam as needed Oral diazepam administration (0.5 mg/kg q 8 h) may speed recovery from metronidazole toxicosis in dogs, including those that are not showing seizure activity.
RECOMMENDED MONITORING Clinical response to discontinuation of metronidazole. Deterioration or worsening of clinical signs should prompt evaluation for another diagnosis.
PROGNOSIS AND OUTCOME The prognosis is excellent with prompt withdrawal of the offending drug. Most patients show improvement within 48 hours, although it may take a week for complete resolution.
PEARLS & CONSIDERATIONS COMMENTS Clinicians should consider metronidazole toxicosis in any patient developing neurologic signs while taking this antibiotic. With prompt recognition and withdrawal of the offending drug, complete recovery is expected. In many instances of intestinal parasitosis, metronidazole may not be the best choice of treatment. Alternative medications (e.g., fenbendazole) have shown greater efficacy and far fewer adverse effects in canine Giardia infection, for example.
PREVENTION Avoid doses of metronidazole higher than 30 mg/kg/d. Some published doses are high enough to cause toxicity.
SUGGESTED READING Caylor KB, Cassimitis MK: Metronidazole neurotoxicosis in two cats. J Am Anim Hosp Assoc 37:258, 2001. Dow SW, et al: Central nervous system toxicoses associated with metronidazole treatment of dogs: five cases (1984-1987). J Am Vet Med Assoc 195:365, 1989. Evans J, et al: Diazepam as a treatment for metronidazole toxicosis in dogs: a retrospective study of 21 cases. J Vet Intern Med 17:304, 2003. AUTHOR: WILLIAM B. THOMAS EDITOR: CURTIS W. DEWEY
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Metaldehyde Toxicosis
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Metaldehyde Toxicosis BASIC INFORMATION DEFINITION An acute toxicosis manifested by rapid onset of clinical signs such as vomiting, anxiety/restlessness, panting, hypersalivation, increasingly vigorous muscle tremors, hyperesthesia, hyperthermia, and seizures. This toxicosis can be rapidly fatal (hours from onset of signs, which begin 30 minutes to 5 hours after ingestion).
SYNONYMS Slug or snail bait poisoning Ortho Bug-Geta, Corry's Slug and Snail Pellets, Deadline Force II, Dragon Snail and Slug Killer Pellets, Last-Bite Snail and Slug Killer Pellets, Lilly Miller Slug and Snail Bait, Corry's Liquid Slug and Snail Control, Corry's Slug Snail, and Insect Killer are some metaldehyde-containing commercial products.
EPIDEMIOLOGY SPECIES, AGE, SEX Toxic to all species Poisoning seen mostly in dogs. Bait is more attractive to dogs. All breeds, ages, and both sexes susceptible RISK FACTORS: Animals with preexisting liver or kidney problems may be more sensitive to the toxic effects of metaldehyde. GEOGRAPHY AND SEASONALITY: Toxicosis can occur anywhere; most common in areas with large populations of snails and slugs (e.g., the North American Pacific Northwest coast [especially California] and East Coast), Hawaii, Caribbean, Upper Midwest region. Less common in drier states.
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT Witnessed or suspected ingestion or recent use of bait in the pet's environment Rapid onset of vomiting, restlessness, muscle tremors and seizures PHYSICAL EXAM FINDINGS Rapid, progressively more frequent (or sustained) muscle fasciculations/tremors are characteristic of metaldehyde intoxication and may progress to extensor rigidity/tetany. Secondary hyperthermia, which may be severe (104○F-108○F [40○-42.2○C]), is common. Hyperthermia is not a true fever but rather the result of muscle fasciculations. Seizures Concurrent nonspecific signs are common: Tachycardia Tachypnea Hypersalivation Vomiting Diarrhea
ETIOLOGY AND PATHOPHYSIOLOGY Metaldehyde is a tetramer of acetaldehyde used as a molluscicide. Common sources include metaldehyde-containing baits formulated as liquid, granules, powder, or pellets. Most poisonings occur in dogs when they consume metaldehyde-containing baits. 50
Oral LD of metaldehyde in dogs in various sources = 100-1000 mg/kg, and in cats = 207 mg/kg. Clinical signs of toxicosis can be seen within 30 minutes to 5 hours after ingestion.
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Metaldehyde Toxicosis
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Metaldehyde is rapidly absorbed orally. Acetaldehyde is produced upon exposure to gastric (low) pH. Acetaldehyde is presumed to contribute to acidosis and other central nervous system signs such as seizures. Minimum toxic dose of metaldehyde in dogs is not known. Consumption of 1 tablespoon (15 g) of 2% powder or granular bait will provide approximately 300 mg of metaldehyde; possibly a significant hazard for a 10-kg dog (30 mg/kg of metaldehyde). Standard 2% bait = 20 mg metaldehyde/g bait. Clinical signs could be due to decreased level of cerebral γ-aminobutyric acid, norepinephrine, and serotonin, which can cause seizures; and increased monoamine oxidase activity, which further decreases serotonin and norepinephrine levels.
DIAGNOSIS DIAGNOSTIC OVERVIEW The diagnosis is based on some or all of the following elements: geographic location (presence of snails/slugs in region), history of observed or suspected ingestion, and characteristic physical examination findings. No definitive confirmatory clinical test exists. A presumptive diagnosis is generally sufficient to initiate treatment, given the severity of signs in most cases and negative consequences of leaving such signs untreated.
DIFFERENTIAL DIAGNOSIS Strychnine toxicosis (see p. 1055 ) Tremorgenic mycotoxins Caffeine, nicotine toxicosis Permethrin toxicosis in cats Organophosphate and carbamate insecticide toxicosis (see p. 792) Zinc phosphide intoxication (see p. 1186 ) Garbage toxicosis (see p. 434) Primary central nervous system disease (neoplasia, encephalitis, idiopathic epilepsy, tetanus, other)
INITIAL DATABASE Acid-base status (acidosis may be present) Baseline serum liver enzyme (levels usually normal) Creatine phosphokinase (may be elevated due to muscle tremors) Baseline body temperature (commonly 104○-108○F [40○-42.2○C]) Kidney function (myoglobinuria possible due to tremors)
ADVANCED OR CONFIRMATORY TESTING Metaldehyde may be detected in stomach contents, vomitus, serum, liver, and urine. Acetaldehyde smell (similar to formal dehyde) in the stomach or gastrointestinal tract may help in diagnosis.
TREATMENT TREATMENT OVERVIEW Immediate treatment of tremors and seizures when present is a primary goal, in order to curtail the development of severe hyperthermia. Active cooling is also indicated when body temperature >105○F (40.6○C), especially if seizures/muscle tremors are persistent. In patients without clinical signs (mild exposures and/or early presentation), induction of emesis is indicated. Activated charcoal administration is appropriate in essentially all cases, via stomach tube (with airway protection) if the patient is unconscious. Overall goals of treatment are to decontaminate the patient (remove remaining toxin), control tremors and seizures, correct acid-base abnormalities, control hyperthermia, and offer supportive care.
ACUTE GENERAL TREATMENT Decontamination of patient: Induction of vomiting (see p. 1364) in patients not showing any clinical signs; useful within 30 minutes of exposure: Hydrogen peroxide, 1 mL/kg PO, repeat once in 10-20 minutes if needed, maximum dose in largest dogs is 45 mL.
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Metaldehyde Toxicosis
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Apomorphine, 0.04 mg/kg IM or IV, or instill into conjunctival sac part of a crushed tablet dissolved in water. Give activated charcoal after inducing emesis at 1-3 g/kg PO mixed with a cathartic such as magnesium or sodium sulfate, 250 mg/kg; or sorbitol 1-3 mL/kg. Use label dose for commercial preparations; multiple doses may be helpful with large ingestion (Caution: aspiration risk in vomiting patient). Gastric lavage (see p. 1281) if large ingestion in animal showing clinical signs; follow with activated charcoal. Control tremors/seizures (see p. 1009): Methocarbamol, 55-220 mg/kg IV; repeat as needed (maximum dose 330 mg/kg/d). Diazepam, 1-2 mg/kg IV; repeat as needed (and/or consider diazepam constant rate infusion). General anesthesia if no response to above measures: Pentobarbital, 10-30 mg/kg IV to effect, repeat as needed; or Propofol, up to 5-6 mg/kg slow IV to effect, then constant rate infusion 0.1-0.6 mg/kg/min titrated to effect; and/or Isoflurane inhalant anesthesia Fluid diuresis for hydration, renal perfusion Control hyperthermia (cold bath, fans). Control acid-base balance with sodium bicarbonate.
POSSIBLE COMPLICATIONS Disseminated intravascular coagulation secondary to prolonged hyperthermia possible Acute hepatic failure (see p. 503 ) in some dogs 2-3 days after exposure can occur (uncommonly) when the patient seems to have recovered; monitor closely. Acute renal failure due to myoglobinuria (uncommon)
RECOMMENDED MONITORING Body temperature Liver enzymes for 3 days (baseline, 24, 48, 72 hours) Acid-base status
PROGNOSIS AND OUTCOME Good with prompt decontamination of patient and control of tremors and seizures Guarded with poorly controlled tremors or seizures or prolonged hyperthermia
PEARLS & CONSIDERATIONS COMMENTS Most commercial baits contain 2%-5% metaldehyde. Some formulations may also contain 5% carbaryl (a carbamate insecticide) along with metaldehyde (see p. 792). Toxicity of carbaryl is much less than metaldehyde. Read the label carefully. Several recently introduced Slug and Snail Baits contain ferric phosphate 1% as the active ingredient. Ingestion of 1% ferric phosphate-containing slug bait in dogs mostly results in mild to moderate signs of stomach upset (vomiting, diarrhea, anorexia, lethargy).
TECHNICIAN TIPS If a client calls with a suspected ingestion of any “bait,” metaldehyde is the most immediately urgent of the common bait poisonings, and the animal should be brought to be examined promptly. The client also should be told to bring the container or product sheet to make it easier to confirm the active component of the ingested bait.
PREVENTION Placement of bait in areas inaccessible to animals Use of relatively less toxic baits (e.g., iron-based baits) to control slugs and snails
SUGGESTED READING
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Puschner B: Metaldehyde. In Peterson ME, Talcott PA, editors: Small animal toxicology, ed 2, St Louis, 2006, Saunders Elsevier, pp. 830–839. AUTHOR: MICHAEL KNIGHT EDITOR: SAFDAR A. KHAN 1ST EDITION AUTHOR: ERIC DUNAYER
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Mesothelioma
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Mesothelioma BASIC INFORMATION DEFINITION A neoplasm of mesodermal origin that may arise from the pleural, pericardial, or peritoneal surfaces. Also reported from scrotum or tunica vaginalis.
EPIDEMIOLOGY SPECIES, AGE, SEX: Dogs > cats, males are overrepresented. Generally older. GENETICS & BREED PREDISPOSITION: German shepherd dogs (particularly male) are overrepresented. Large-breed dogs are more commonly affected. RISK FACTORS: Possibly asbestos exposure. The type of cancer caused by chronic asbestos exposure in human beings is mesothelioma, and the same histopathologic findings (ferruginous bodies) have been noted in both canine and human mesothelioma. ASSOCIATED CONDITIONS & DISORDERS: Pleural, pericardial, and peritoneal effusion with attendant dyspnea, acute cardiac tamponade and right-sided heart failure, or abdominal distension, respectively, are common.
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES Mesenchymal form: multiple focal nodules of solid or papillary neoplastic growth; historically, more common Sclerosing form: characterized by an intense fibroblastic reaction and thick fibrous adhesions involving all abdominal organs but most markedly centered around the stomach and prostate; uncommon in dogs HISTORY, CHIEF COMPLAINT: Patients most commonly are presented for dyspnea or cough; possibly abdominal distension. This disease should be suspected in any adult patient with a cough that does not respond to standard treatment for nonspecific respiratory problems, or evidence of chronic disease and effusion in any body cavity. Depending on the anatomic location of the malignancy and the subsequent effusion, the patient may present with dyspnea, cough, weight loss, acute cardiac tamponade and right-sided heart failure, or abdominal distension. PHYSICAL EXAM FINDINGS Dyspnea due to pleural effusion in dogs and cats is usually identified by forceful inspiration and prolonged expiration (“holding its breath”). In cats, a noncompressible cranial thorax suggests other diagnoses: thymoma, mediastinal lymphoma. Tachypnea, open-mouth breathing, cyanosis, muffled heart and lung sounds ventrally with increased bronchovesicular sounds dorsally, poor peripheral pulses, jugular distension, and abdominal distension are possible. In a standing patient, thoracic percussion may reveal a “fluid line” (zone of hyporesonance) ventrally.
ETIOLOGY AND PATHOPHYSIOLOGY Mesothelioma involves a malignant transformation of mesothelial cells that line body cavities. Pleural, pericardial, and peritoneal effusion from mesothelioma are most likely due to increased capillary permeability (parietal foci) secondary to vasculitis.
DIAGNOSIS DIAGNOSTIC OVERVIEW The diagnosis is suspected based on chronic recurrent body-cavity effusions with no identified infectious, inflammatory, or other neoplastic cause. This is often a diagnosis of exclusion. Definitive diagnosis requires a biopsy.
DIFFERENTIAL DIAGNOSIS Pleural effusion (see p. 882)
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Pericardial effusion (see p. 854) Ascites (see p. 93)
INITIAL DATABASE The effusion should be sampled and evaluated with fluid analysis and cytological assessment. CBC, serum biochemical analysis, and urinalysis: no specific changes These tests should be supplemented with fungal, viral, and parasitic (tick and heartworm) serologic evaluations and microbial (fungal and bacterial) culture as clinical suspicion and history warrant. Radiographs (especially after removal of as much fluid as possible) Ultrasonographic studies (abdomen, heart, and pleural space)
ADVANCED OR CONFIRMATORY TESTING Definitive diagnosis requires tissue for histopathology. A normal fibronectin level in the effusion could help rule out mesothelioma.
TREATMENT TREATMENT OVERVIEW The primary and immediate goal of treatment is the removal of body-cavity fluid that is causing clinical signs.
ACUTE GENERAL TREATMENT Stabilization of the patient by relieving the cardiovascular or respiratory embarrassment is paramount. This generally revolves around removal of large-volume effusions and doing so without delay if clinical signs are severe. Oxygen therapy is often indicated before centesis or obtaining blood or urine samples if patients are extremely dyspneic or volatile in their behavior, in order to prevent life-threatening cardiovascular or respiratory decompensation (especially cats).
CHRONIC TREATMENT For dogs with pericardial mesothelioma, surgical or thoracoscopic pericardectomy (see p. 1340 ) can palliate clinical signs and reduce tumor burden (disease cytoreduction). Periodic thoracocentesis (see p. 1338) or pericardiocentesis (see p. 1325) can be performed when fluid accumulation or symptoms are slow to return (weeks or more). The placement of a Pleuralport may aid in treatment. Some clients may be willing to learn proper care and use of such a device for home care. Administration of chemotherapy via intracavitary infusion on an every-3-week schedule can be attempted for long-term control. Cisplatin, 50-70 mg/m2 body surface area, along with saline fluid diuresis; or Carboplatin, 250-350 mg/m2 (has limited penetration); or 2
Mitoxantrone, 5-6 mg/m Potential benefits (unproven on a large scale) must be weighed against the real drawbacks of possible adverse reactions to these agents. At this time, only small numbers of patients have been evaluated, so efficacy remains unproven. Intravenous chemotherapy with cisplatin, carboplatin, or doxorubicin may have a role in some patients. Consultation with an oncologist for the most current treatment recommendations is indicated, but because of the rarity of this disease, multicenter clinical trials will be required to test and develop effective treatments.
POSSIBLE COMPLICATIONS Pneumothorax, cardiac puncture, hemopericardium, hemothorax, infection
RECOMMENDED MONITORING Hourly for critical (ICU) patients: respiratory rates, degree of dyspnea, blood gases Daily to weekly for outpatients: respiratory rates, quality of life assessments, repeat thoracic radiographs as warranted or required As required per protocol for chemotherapy patients (i.e., CBC), quality of life assessments, repeat thoracic radiographs as
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warranted or required
PROGNOSIS AND OUTCOME Poor to fair. Survival is dependent on rate of accumulation of the fluid and degree of compensation, which are both variable from patient to patient. Many patients are euthanized at the time of diagnosis. For those that are treated, the reported survival time varies considerably from weeks to years. Some animals may have a dramatic improvement after pericardiocentesis or thoracocentesis and a prolonged (weeks to months) period without clinical signs, whereas others have a reaccumulation of fluid and return of tamponade or dyspnea within hours or days. A good quality of life for months to 1-2 years with pericardial or pleural mesothelioma is realistically possible if a good response to the first centesis occurs, and owners are willing to follow up regularly with centesis on an as-needed basis. In this author's experience, owners rarely agree to continue with repeat pericardiocentesis after more than 2 or 3 episodes of acute decompensation.
PEARLS & CONSIDERATIONS COMMENTS Thoracocentesis should be considered before blood or urine sample acquisition or radiographic or ultrasonographic studies in patients that are unstable. The removal of even a small amount of fluid may dramatically relieve the respiratory embarrassment and stabilize the patient. Although it shares similarities with mesothelioma in terms of distribution (body cavity surfaces), carcinomatosis refers to seeding of pleural or peritoneal surfaces with malignant carcinoma cells. Management of dogs and cats with carcinomatosis may include treatment with intracavitary chemo-therapeutics as described for mesothelioma.
TECHNICIAN TIP The pericardial effusion caused by mesothelioma is usually thick and hemorrhagic (indistinguishable from blood). If blood clots form in the discarded effusion during the pericardiocentesis procedure, this important observation should be brought to the attention of the clinician performing the procedure (catheter may be in the heart).
CLIENT EDUCATION Teaching the client to monitor respiratory rate will give both the client and the clinician an objective measure of progression and acuity of decompensation in the patient. Pleuralport management for dedicated clients.
SUGGESTED READING Garrett LD: Mesothelioma. In Withrow SJ, Vail DM, editors: Withrow & MacEwen’s small animal clinical oncology, ed 4, St Louis, 2007, Elsevier Saunders, pp 804–808. Glickman LT, et al: Mesothelioma in pet dogs associated with exposure of their owners to asbestos. Environ Res 32:305, 1983. AUTHOR: CARLOS RODRIGUEZ EDITOR: KENNETH M. RASSNICK
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Mesocestoides Infection
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Mesocestoides Infection BASIC INFORMATION DEFINITION Infection with an adult cestode (tapeworm) in the small intestine of mammals (frequently dogs) and birds. The larval or metacestode form of this tapeworm, the tetrathyridium, may infect serous cavities of many animals, particularly canines, causing ascites and pleural effusion.
SYNONYMS Mesocestoides lineatus, Mesocestoides corti
EPIDEMIOLOGY SPECIES, AGE, SEX: There is a wide range of intermediate hosts (reptile, avian, amphibian, and mammals), especially carnivores. Domestic and wild canids may serve as definitive hosts and harbor the adult stages of the tapeworm. Cats may also be infected. RISK FACTORS: Hunting, scavenging carrion, and exposure to wildlife CONTAGION & ZOONOSIS: Unknown; infections with adult tapeworms have been reported in humans. GEOGRAPHY AND SEASONALITY: Many parts of the world, including Africa, Asia, and throughout the United States. There is no seasonal association for this cestode/metacestode.
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT: Anorexia, respiratory distress, abdominal distension PHYSICAL EXAM FINDINGS: Signs of abdominal or pleural effusion (see p. 93and p. 882)
ETIOLOGY AND PATHOPHYSIOLOGY Life cycle involves two intermediate hosts. First intermediate host unknown but may be a ground-dwelling coprophagous arthropod (oribatid mite, beetle) Second intermediate host (reptile, amphibian, bird, rodent, cat) becomes infected by ingestion of the larval forms (cysticercoids) within the first intermediate host. Within this second intermediate host, the cysticercoid develops into a tetrathyridium. The tetrathyridium is the second larval stage and often occurs in the peritoneal cavity and musculature of the second intermediate host. Dogs and cats (definitive hosts) are presumably infected by ingestion of the tetrathyridia within the second intermediate host (i.e., from capturing infected birds, snakes, and small mammals as prey). Dogs often serve as definitive hosts, harboring the adult tapeworms, but may also be infected by the larval stages of the parasite, the tetrathyridia. Tetrathyridia develop into adult tapeworms within the intestines and rarely produce clinical disease. Development into adults may take 16-20 days in dogs. In cats, development into adults may take longer. Some tetrathyridia migrate through the intestinal wall and continue as tetrathyridia within subcutaneous tissues, liver, lungs, retroperitoneal space, or abdominal and thoracic cavities. These tetrathyridia are capable of asexual multiplication by binary fission; one tetrathyridium splits into two tetrathyridia, two into four, and so on. The tetrathyridia multiply to the point that they completely fill and expand both the peritoneal and pleural cavities. Tetrathyridia may incite a nonpurulent granulomatous inflammatory response on serosal surfaces.
DIAGNOSIS DIAGNOSTIC OVERVIEW A patient with abdominal or pleural effusion whose centesed fluid is grossly milky white should be suspected of having Mesocestoides infection, especially if the patient appears less ill than would be expected if the fluid were chylous or septic.
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Confirmation is through cytologic examination of aspirated fluid.
DIFFERENTIAL DIAGNOSIS Abdominal and pleural effusions: congestive heart failure, portal hypertension, liver disease, hemorrhagic effusions, neoplastic effusions, hypoalbuminemia, septic effusions, chylous effusions. The latter two would be most likely to be confounded grossly with Mesocestoides-related effusions (color).
INITIAL DATABASE Abdominocentesis or thoracocentesis typically reveals a distinctive thick, opaque white fluid, which often contains hundreds to thousands of tetrathyridia. Cytologic evaluation of fluid may show a mixed inflammatory exudate ± hemorrhage and necrosis. Calcareous corpuscles (clear to yellow-gold round to oval structures that are remnant tissues of the cestodes) may be present. Tetrathyridia are often found on aspiration of cystic lesions.
ADVANCED OR CONFIRMATORY TESTING Recovery of organism from peritoneal cavity, with identification of cestode DNA via PCR
TREATMENT TREATMENT OVERVIEW The adult stage of this parasite within the canine small intestine can be easily treated. The larval tetrathyridium stage within serous cavities is almost impossible to eliminate, owing to its ability to undergo asexual multiplication, and the goal of ongoing treatment becomes palliation of the infection.
ACUTE AND CHRONIC TREATMENT Laparotomy and lavage of peritoneal cavity may be helpful to decrease larval tetrathyridia burdens. Anthelmintics: Praziquantel for adult organisms: 5 mg/kg PO q 24 h Fenbendazole for larvae: 100 mg/kg PO q 24 h for 28 days. Off-label use. Side effects (bone marrow, others) possible.
POSSIBLE COMPLICATIONS Gastrointestinal signs may be seen with antiparasitics.
RECOMMENDED MONITORING Regular fecal examinations
PROGNOSIS AND OUTCOME Guarded for infection with larval tetrathyridia, since infection generally persists
PEARLS & CONSIDERATIONS PREVENTION Prevent dogs and cats from roaming and ingesting second intermediate hosts such as birds, amphibians, reptiles, and rodents as live prey or carrion. Regular anthelminthic therapy
TECHNICIAN TIPS During microscopic examinations, look for the characteristic ovum on fecal flotation. Following administration of anthelminthics, look
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for the characteristic gravid proglottids expelled in the feces of infected dogs. Look for the unique tetrathyridia within serous cavities.
SUGGESTED READING Bowman DD, Hendrix CM, Lindsay DS, et al, editors: Feline clinical parasitology. Ames, IA, 2002, Iowa State University Press, pp 199–204. Caruso KJ, et al: Cytologic diagnosis of peritoneal cestodiasis in dogs caused by Mesocestoides sp., Vet Clin Pathol 32(2):50–60, 2003. Crosbie PR, et al: Diagnostic procedures and treatment of 11 dogs with peritoneal infections caused by Mesocestoides species. J Am Vet Med Assoc 213(11):1578–1583, 1999. Parker MD: An unusual cause of abdominal distension in a dog. Vet Med 189–195, 2002. Toplu N, Yildiz K, Tunay R: Massive cystic tetrathyridiosis in a dog. J Small Anim Pract 45(8):410–412, 2004. AUTHOR: CHARLES M. HENDRIX EDITOR: DOUGLASS K. MACINTIRE 1ST EDITION AUTHOR: LISA M. TIEBER
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Mesenteric Volvulus
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Mesenteric Volvulus BASIC INFORMATION DEFINITION An uncommon disorder characterized by a twisting of the intestine around the root of the mesentery, a process that potentially can be rapidly fatal
SYNONYMS Intestinal volvulus, mesenteric torsion
EPIDEMIOLOGY SPECIES, AGE, SEX: Young adult (>3 years old), male dogs predisposed. Also reported in cats. GENETICS & BREED PREDISPOSITION: Large-breed dogs, German shepherds, and English pointers ASSOCIATED CONDITIONS & DISORDERS: Conditions that have been associated with mesenteric volvulus include exocrine pancreatic insufficiency, recent gastrointestinal surgery, gastrointestinal foreign bodies, enteritis, intestinal neoplasia, blunt trauma, and gastric dilatation volvulus (GDV).
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT: Acute-onset abdominal distension, pain, vomiting, and hematochezia PHYSICAL EXAM FINDINGS Physical findings consistent with hypovolemic shock: tachycardia (or bradycardia in cats), weak pulses, pale mucous membranes, prolonged capillary refill time, weakness or collapse Abdominal distension, palpably gas-filled intestinal loops
ETIOLOGY AND PATHOPHYSIOLOGY Twisting of intestine occurs around mesenteric axis or root, causing vascular occlusion to the intestines. Thin-walled veins and lymphatics become obstructed, causing edema in the intestinal wall. Blood flow through cranial mesenteric artery and its branches is partially or completely occluded due to twisting. Ischemic necrosis of intestine occurs, and blood is lost into the intestinal lumen. Endotoxins and bacteria translocate into the abdomen through the damaged intestinal mucosa. Patients eventually die from circulatory shock and endotoxemia/sepsis.
DIAGNOSIS DIAGNOSTIC OVERVIEW The diagnosis is suspected based on physical exam and appearance of abdominal radiographs. Differential diagnoses must be ruled out to the extent possible (e.g., ileus due to parvoviral enteritis: testing as appropriate). Confirmation of the diagnosis is made at the time of surgery.
DIFFERENTIAL DIAGNOSIS Any condition associated with acute abdominal pain or hematochezia and vomiting: Gastric dilatation/volvulus (GDV) Cecocolic volvulus Intussusception Splenic torsion
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Gastrointestinal obstruction or rupture Peritonitis Pancreatitis Hemorrhagic gastroenteritis Parvoviral enteritis
INITIAL DATABASE Abdominal radiography: multiple severely distended gas-filled intestinal loops; poor abdominal detail associated with peritoneal fluid; concurrent GDV CBC: Packed cell volume usually normal Serum biochemistry profile: Hypoproteinemia, hypokalemia Preoperative laboratory evaluation is often limited to on-site tests because of the potentially rapid deterioration of the patient's condition with mesenteric volvulus. Abdominocentesis (see p. 1193) with fluid evaluation: modified transudate (early) or septic exudate (eventually, with bacterial translocation or peritonitis). With bowel necrosis, the fluid may be dark and fetid.
ADVANCED OR CONFIRMATORY TESTING Surgical confirmation of diagnosis
MESENTERIC VOLVULUS Lateral abdominal radiograph of dog with mesenteric volvulus; cranial is to the left. Marked gas distension of bowel present; a differential diagnosis would be severe enteritis. (Courtesy Dr. Richard Walshaw.)
MESENTERIC VOLVULUS Same dog, gross appearance of bowel during exploratory laparotomy. Severe discoloration of much of small intestine and volvulus of mesenteric root are diagnostic.
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(Courtesy Dr. Richard Walshaw.)
TREATMENT TREATMENT OVERVIEW Patients with mesenteric volvulus should be treated for circulatory shock as appropriate and have immediate surgical intervention to correct the volvulus and resect diseased bowel.
ACUTE GENERAL TREATMENT Crystalloids should be administered at shock doses (90 ml/kg/hr). Colloid boluses of 5 ml/kg can be administered simultaneously. Treat endotoxemia/sepsis with antibiotics: Third-generation cephalosporin. 22 mg/kg IV q 2 h during perioperative period, then q 6 h postoperatively; or Ampicillin, 22 mg/kg IV q 6 h combined with enrofloxacin, 5-10 mg/kg IV q 24 h (5 mg/kg maximum in cats) Correct hypokalemia and acid-base abnormalities with fluid therapy. If only parts of the intestine are devitalized, resect affected segment(s) before derotation, to reduce reperfusion effects. Perform derotation of intestines and monitor for perfusion. Perform thorough exploratory for associated conditions. Lavage abdomen, and consider postoperative drainage if peritonitis is present.
POSSIBLE COMPLICATIONS Septic peritonitis if diseased bowel not removed, contamination of abdomen not cleared, or resection and anastomosis site dehiscence Reperfusion injury Short bowel syndrome if >70% of small intestine resected
RECOMMENDED MONITORING Postoperative monitoring of hydration and electrolyte concentrations Blood pressure monitoring for hypotension Body temperature and blood glucose monitoring for sepsis
PROGNOSIS AND OUTCOME Grave prognosis unless volvulus recognized and treated immediately Most reports of mesenteric volvulus cite a 100% mortality rate unless the volvulus is found incidentally during exploratory celiotomy. One study reported a 58% mortality rate in patients with mesenteric volvulus presenting in shock and attributed increased survival to rapid initiation of treatment.
PEARLS & CONSIDERATIONS COMMENTS Surgery should not be delayed if an animal presents in shock with multiple gas-filled intestinal loops on radiographs, but parvoviral enteritis should be ruled out. Consideration should be given to the use of drugs that block the formation of, or scavenge, oxygen free radicals (i.e., corticosteroids).
SUGGESTED READING Junius G, Appeldoorn AM, Schrauwen E: Mesenteric volvulus in the dog: a retrospective study of 12 cases. J Sm Anim Pract 45:104, 2004. Nemzek JA, Walshaw R, Hauptman JG: Mesenteric volvulus in the dog: A retrospective study. J Am Anim Hosp Assoc 29:357, 1993.
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Shealy PM, Henderson RA: Canine intestinal volvulus: A report of nine new cases. Vet Surg 21:15, 1992. AUTHOR: LORI LUDWIG EDITOR: RICHARD WALSHAW
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Meningioma
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Meningioma BASIC INFORMATION DEFINITION A neoplasm of the meninges surrounding the brain or spinal cord
EPIDEMIOLOGY SPECIES, AGE, SEX Meningiomas occur in both dogs and cats and usually affect older patients. Dogs are usually older than 8 years, and females are affected slightly more than males. Cats are usually older than 10 years, and males are affected slightly more often than females. GENETICS & BREED PREDISPOSITION In dogs, dolichocephalic breeds are more likely to develop meningiomas than other breeds. There is no breed predisposition in cats. GEOGRAPHY AND SEASONALITY: Reported worldwide ASSOCIATED CONDITIONS & DISORDERS: Meningiomas have been reported to occur in young cats with mucopolysaccharidosis type I.
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT Historic findings in general reflect neurologic compromise, but specific signs depend on lesion location. Clinical signs are often insidious and progressive; less commonly, acute onset of clinical signs is possible. The most common chief complaints for intracranial meningiomas include seizures, circling, behavior change (aggression), altered consciousness, and nonspecific signs such as inappetence and lethargy. The most common chief complaints for spinal meningiomas include acute to chronic onset of paresis, ataxia, and neck or back pain. PHYSICAL EXAM FINDINGS Neurologic exam findings (see p. 1311) vary depending on lesion location. Cerebral meningioma: seizures, contralateral menace and postural reaction deficits, behavior change, contralateral hemiparesis Brainstem meningioma: ipsilateral cranial nerve deficits, hemiparesis or tetraparesis or hemiplegia or tetraplegia, or signs of central vestibular dysfunction Cerebellar meningioma: hypermetria, intention tremors, truncal sway, broad-based stance Spinal meningioma: paresis, ataxia, spinal pain
ETIOLOGY AND PATHOPHYSIOLOGY Etiology is unknown. Meningiomas usually occur as solitary masses, but multiple meningiomas are relatively common in cats. By definition, they originate on the periphery (neoplastic outgrowths of the meninges), adjacent to cranial or vertebral bone. Biological behavior and histopathologic characteristics are benign; clinical effects are due to space-occupying nature within confines of skull or vertebral canal. Most commonly reported in the supratentorial compartment (rostral to the tentorium cerebelli, including the cerebrum and diencephalon) in the brain Tumor tends to invade into the brain parenchyma in dogs but not in cats. Cervical portion of spinal cord is the most commonly affected segment in cases of spinal meningioma, but any location is possible.
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DIAGNOSIS DIAGNOSTIC OVERVIEW The diagnosis is suspected in a middle-aged to older dog or cat with neurologic deficits suggesting a slowly growing intracranial or spinal lesion. Advanced imaging (preferably MRI) is the clinical confirmatory test of choice; the final diagnosis is obtained histologically.
DIFFERENTIAL DIAGNOSIS Other brain tumors (e.g., glioma, lymphoma, metastatic tumors) Infectious diseases (bacterial, viral, fungal, protozoal) Inflammatory diseases (e.g., granulomatous meningoencephalomyelitis) Intervertebral disk disease Diskospondylitis
INITIAL DATABASE CBC/serum biochemical profile/urinalysis: usually normal Survey thoracic and abdominal radiographs should be performed in older patients to rule out extracranial and/or concurrent diseases.
ADVANCED OR CONFIRMATORY TESTING CT (see p. 1233 ) or MRI (see p. 1302): intracranial mass located outside the brain or spinal cord parenchyma, with marked, often homogeneous, contrast enhancement. Compression of underlying brain or spinal cord is common. Cerebrospinal fluid analysis: used as an adjunct to advanced imaging, primarily to rule out encephalitis or myelitis. Results are generally nonspecific with meningioma and reveal normal to mildly elevated protein. Sterile neutrophilic pleocytosis is relatively common with meningioma but is not pathognomonic. Histopathologic evaluation is required for definitive diagnosis. Tissue samples can be obtained via surgical excision or stereotactic brain biopsy (see p. 1214 ).
TREATMENT TREATMENT OVERVIEW Definitive treatment involving surgical excision and/or radiation therapy
ACUTE GENERAL TREATMENT Cluster seizures or status epilepticus: see p. 1425 Cerebral edema/brain herniation: mannitol, 0.5 g/kg IV slowly over 15 to 20 minutes; furosemide (2 mg/kg IV) has synergistic effects with mannitol and can be given if needed.
CHRONIC TREATMENT Surgical excision for histologic diagnosis and definitive treatment if tumor is accessible In general, tumors located in superficial (dorsal or lateral) regions of the skull/vertebrae overlying cerebrum, cerebellum, and spinal cord are the best candidates for surgical excision. Radiation therapy: used as an adjunctive treatment to surgery or as a primary treatment Chemotherapy: generally less effective because the blood-brain barrier (BBB) prevents most chemotherapeutic agents from entering the brain and spinal cord. There are special handling requirements and potentially life-threatening adverse patient effects associated with these drugs; consultation with an oncologist for appropriate usage and the most current treatment recommendations is indicated. Hydroxyurea (20 mg/kg PO q 24 h) crosses the BBB and appears to be effective in dogs as it is in humans with intracranial meningioma. Possible adverse effects include bone marrow suppression (anemia, thrombocytopenia, leukopenia), pulmonary fibrosis, gastrointestinal upset, stomatitis, sloughing of nails, alopecia, and dysuria. Methemoglobinemia has been reported in cats at high dosages (>500 mg). 2
Anecdotally, nitrosourea agents such as lomustine (CCNU; 60-90 mg/m PO q 6 weeks) or carmustine (BCNU 50
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2
mg/m IV q 6 weeks), which can cross the BBB, appear to have some effect; these agents are more specifically used for treating patients with gliomas. The most serious potential adverse effects are bone marrow suppression (anemia, thrombocytopenia, leukopenia) and hepatotoxicosis. Seizures: anticonvulsants should be used if more than one seizure occurs every 6 to 8 weeks (see p. 1009 ). Cerebral edema: prednisone, 0.5 mg/kg PO q 12 h initially, then taper to lowest dose that will control clinical signs.
DRUG INTERACTIONS Drug interactions or altered metabolism of medications have been reported between corticosteroids and amphotericin B, furosemide, thiazide diuretics, digitalis glycosides, cyclosporine, phenytoin, phenobarbital, and mitotane. Corticosteroids should not be given concurrently with nonsteroidal antiinflammatory drugs or other potentially gastrointestinally ulcerogenic medications. Phenobarbital: may cause excessive sedation in patients with intracranial tumors, even at low doses
POSSIBLE COMPLICATIONS Progression of clinical signs, including status epilepticus, brain herniation, and sudden death
RECOMMENDED MONITORING Serial neurologic exam every 4-6 weeks. Therapeutic drug monitoring of serum levels of anticonvulsants if relevant.
PROGNOSIS AND OUTCOME Dogs: prognosis is fair. Median survival time for cerebral meningioma is 5-9 months with surgery alone and 16-30 months with surgery and radiation therapy. Radiation therapy alone yields a survival time of approximately 6-12 months. Cats: prognosis is good after surgical excision, with a median survival time of approximately 2 years with surgical excision alone. Surgical excision can be curative in cats. Prognosis for meningiomas in other anatomic locations is fair to guarded. Many patients treated with supportive nonspecific treatments (e.g., anticonvulsants, corticosteroids) are euthanized within 3 months because of progression of clinical signs. Dogs with intracranial meningiomas treated with oral hydroxyurea have a mean survival time of approximately 7 months.
PEARLS & CONSIDERATIONS COMMENTS Meningiomas are the most common primary brain tumor in dogs and cats. Surgical excision followed by radiation therapy provides the longest survival times for dogs. Surgical excision alone provides prolonged survival times for cats and may be curative in some cases. In canine intracranial meningioma cases with seizure activity, relatively nonsedative anticonvulsant drugs (e.g., felbamate, zonisamide, levetiracetam) should be considered, especially if surgical removal of the tumor is planned (see p. 1009and p. 353 ).
CLIENT EDUCATION With patients receiving corticosteroids, warn owner of expected side effects (e.g., polyuria, polydipsia, polyphagia, weight gain) and of effects warranting notification (obesity, signs of gastrointestinal ulceration, signs of iatrogenic hyperadrenocorticism). Phenobarbital (see p. 871): short-term side effects include sedation/lethargy and pelvic limb weakness and ataxia. Long-term side effects include polyuria, polydipsia, polyphagia, weight gain. Less common adverse effects warranting intervention include hepatotoxicity, blood dyscrasias.
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MENINGIOMA A, Brain MRI of a patient with meningioma (left panel).B, Normal patient for comparison (right panel), T2-weighted image. Patient's right is on the left of each image. Patient with meningioma has a large, sessile mass originating from the right dorsal calvarium; severe compression and displacement of right cerebral hemisphere and midline shift are seen. Bar = 1 cm.
SUGGESTED READING Sessums K, Mariani C: A comparative review of intracranial meningioma in dogs and cats. Compend Contin Educ Vet Pract 31(4):E1–E10, 2009. Sturges BK, et al: Magnetic resonance imaging and histological classification of intracranial meningiomas in 112 dogs. J Vet Intern Med 22:586–595, 2008. Troxel MT, et al: Feline intracranial neoplasia: Retrospective review of 160 cases (1985-2001). J Vet Intern Med 17:850, 2003. AUTHOR: MARK T. TROXEL EDITOR: CURTIS W. DEWEY
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Melena
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Melena BASIC INFORMATION DEFINITION Dark, tarlike, often foul-smelling stools, as a result of digested blood (specifically oxidized hemoglobin)
EPIDEMIOLOGY SPECIES, AGE, SEX: Any age, breed, sex RISK FACTORS: Anything that will cause hemorrhage into the proximal or mid-gastrointestinal (GI) tract (esophagus, stomach, small intestine) or the mouth, pharynx, nose, or lungs
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT The patient will normally present for signs associated with blood loss (i.e., weakness, pale mucous membranes, bleeding from other sites or due to the melena [foul-smelling flatulence or black tarry feces]). Medication history includes those known to have gastrointestinal ulcerogenic potential (e.g., glucocorticoids, nonsteroidal antiinflammatory drugs [NSAIDs]). Intoxication history: known exposure or accessibility of vitamin K antagonists (rodenticides, pharmaceutical) in the environment Specific questions related to potential specific sources of bleeding: coughing, sneezing, vomiting, diarrhea Some patients have a history of recent surgical skin lump removal (possibility of mast cell tumor). Overdiagnosis due to leading questions (e.g., “Are the stools dark and tarry?”) should be avoided; open-ended questions are preferred (e.g., “Have the color and consistency of the stools changed? How so?”) to avoid this error. Rule out false-positive results: Animals eating meat-based diets Diets high in iron Drugs such as charcoal and bismuth Normal variation PHYSICAL EXAM FINDINGS Rectal exam to confirm the diagnosis Evaluation for petechial hemorrhages on the mucous membranes and for signs of bleeding on the skin Auscultation of the chest for signs of lung hemorrhage (bronchovesicular sounds that are either louder [interstitial or airway hemorrhage] or softer [pleural effusion]) Thorough abdominal palpation: abnormal GI loops or masses Careful examination of the skin for suspect mast cell tumors Additionally, specific aspects of the physical exam will vary depending on the source of bleeding. The blood can originate from the mouth, nose, lungs, pharynx, esophagus, stomach, or small intestine.
ETIOLOGY AND PATHOPHYSIOLOGY Blood presented to proximal or mid-GI tract (via any route already mentioned). Slow GI transit time of longer than 8 hours (in humans) allows greater degree of oxidation of hemoglobin. Melena occurs based on the duration of the presence of blood in the GI tract, rather than the anatomic site of blood loss.
DIAGNOSIS DIAGNOSTIC OVERVIEW Gross inspection of feces should allow confirmation of melena. If uncertainty persists, a fecal occult blood test is indicated. Diagnosis of the source of melena begins with history and physical exam in an attempt to differentiate generalized bleeding disorders from primary gastrointestinal bleeding.
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Melena
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DIFFERENTIAL DIAGNOSIS GI bleeding (stomach, small intestine; or large intestine in anorexic animals with slow GI transit time). Examples: hemorrhagic gastroenteritis, foreign body, intussusception, volvulus, inflammatory bowel disease, helminthiasis, or neoplasia. Liver or renal failure (coagulopathy or gastric ulceration) Pulmonary or upper respiratory tract bleed with swallowing of blood Shock (shock gut) Pancreatitis Hypoadrenocorticism Mast cell tumor or (rarely) gastrinoma High meat-based diet or diet high in iron Drugs such as charcoal and bismuth darken the color of feces but do not signify digested blood.
INITIAL DATABASE Recheck history and repeat abdominal palpation CBC, serum biochemistry profile (including preprandial and postprandial bile acids if liver disease suspected), urinalysis. Thrombocytopenia may explain or be a result of hemorrhage. Microcytosis and hypochromia suggest chronic blood loss. Fecal flotation Imaging: survey radiographs of chest and abdomen; abdominal ultrasound Coagulation profile
ADVANCED OR CONFIRMATORY TESTING If still no diagnosis: Repeat abdominal ultrasound exam Thorough nasal and pharyngeal exam [with radiographs]; systemic blood pressure measurement if epistaxis is present Endoscopy (see p. 1284) Exploratory laparotomy: Biopsy, aspiration, and/or resection of any lesions seen Biopsies of liver, stomach, duodenum, ileum, and jejunum if no macroscopic lesion seen If still no diagnosis: Scintigraphy (radiolabeled albumin) Arteriography Small-bowel radiographic contrast study
TREATMENT TREATMENT OVERVIEW Control hemorrhage and any secondary complications of hemorrhage Cure the trigger
ACUTE GENERAL TREATMENT Largely depends on underlying cause Identify shock early, and treat aggressively with IV fluids. Blood transfusion: if anemia with resultant clinical signs or for coagulopathy Plasma transfusion: for coagulopathy Antiemetics and antiulcer therapy as needed Stop the inciting medications
DRUG INTERACTIONS Sucralfate inhibits the absorption of fluoroquinolone antibiotics for up to 8 hours, so patients receiving sucralfate and requiring quinolone antibiotics should receive the quinolones parenterally if feasible.
PROGNOSIS AND OUTCOME Dependent on the trigger
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Melena
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PEARLS & CONSIDERATIONS COMMENTS These cases generally are far more difficult to diagnose than hematochezia cases. A thorough and methodical approach is essential.
CLIENT EDUCATION Advise all owners on the potential dangers of NSAIDs.
SUGGESTED READING Kelly K: Melena and hematochezia. In Ettinger S, Feldman E, editors: Textbook of veterinary internal medicine, ed 6, St Louis, 2005, Elsevier Saunders, pp 141–143. AUTHOR: DAVID MILLER EDITOR: ETIENNE CÔTÉ
25-09-2011 22:37
Melanoma
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Melanoma BASIC INFORMATION DEFINITION Melanoma is a common neoplasm in the dog and is rare in the cat. Classification of melanomas by location generally has more clinical utility than by histologic subtype. Oral melanomas are uniformly malignant, locally invasive, and highly metastatic (>60%) tumors (see p. 708) Subungual (nail bed) melanomas are locally invasive tumors with a lower rate of metastasis (30%-60%) Cutaneous melanomas are generally (but not always) benign. Ocular melanomas are discussed elsewhere in this text (see p. 620 ).
SYNONYMS Malignant melanoma, melanocytic tumor, melanocytoma
EPIDEMIOLOGY SPECIES, AGE, SEX: Melanoma generally occurs in older patients (9-12 years). GENETICS & BREED PREDISPOSITION Predisposed dog breeds include chow chow, Doberman pinscher, golden retriever, Gordon setter, Irish setter, giant schnauzer, miniature schnauzer, Scottish terrier. Breed predisposition suggests an underlying genetic mechanism for melanoma in veterinary patients. Black dogs may be predisposed, but any color dog may be affected.
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT Oral melanoma: Detection of an oral mass by a veterinarian during routine examination or dental prophylaxis (common) Identification of an oral mass by the owner Recent onset of halitosis and ptyalism Cutaneous or subungual (nail bed) melanomas: Identification of a mass by the owner PHYSICAL EXAM FINDINGS Examination typically reveals a mass lesion. Oral examination should be thorough; some tumors are located at the base of the tongue or in the tonsils. Cutaneous and subungual tumors may become ulcerated. Melanomas may be pigmented or amelanotic. Thorough examination of draining lymph nodes is always indicated, but cytologic evaluation should be performed regardless of physical exam findings.
ETIOLOGY AND PATHOPHYSIOLOGY Underlying genetic mutations and ultraviolet light exposure are known etiologic agents in humans. Melanomas do not have to arise from pigmented skin.
DIAGNOSIS DIAGNOSTIC OVERVIEW
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Melanoma
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Biopsy of an identified mass is the test of choice to establish a diagnosis of melanoma.
DIFFERENTIAL DIAGNOSIS Oral: squamous cell carcinoma, soft tissue sarcoma, epulides Cutaneous: any mass lesion of skin (neoplastic or non-neoplastic) Subungual: squamous cell carcinoma, nail bed infection
INITIAL DATABASE CBC, serum biochemistry profile, urinalysis, lymph node aspiration, thoracic radiographs, abdominal ultrasound (in patients with hind limb or caudally located masses)
ADVANCED OR CONFIRMATORY TESTING Biopsy and histopathologic examination of tissue Immunohistochemical staining with S-100 or Melan-A may confirm the diagnosis of melanoma in undifferentiated and amelanotic tumors. Determination of mitotic index may be used for distinguishing benign and malignant canine cutaneous melanomas. Determination of mitotic index requires histopathologic evaluation of tissue and cannot be reliably assessed on fine-needle aspiration/cytology. Tumors with a mitotic index of 120 mm Hg in clinical setting) CBC, serum biochemistry panel, urinalysis (to assess for preexisting conditions): no significant changes expected
ADVANCED OR CONFIRMATORY TESTING Over-the-counter illicit drug test kits (urine) may help confirm exposure during the early course of exposure. Caution: such kits have not been validated in dogs, and some do not appear to be accurate; a negative result does not preclude exposure. Rapid analysis at human hospital labs is also an option for confirmation.
TREATMENT TREATMENT OVERVIEW Treatment goals are early decontamination (induction of emesis and administration of activated charcoal) of the patient, correcting hypothermia, and providing supportive care. In a patient showing no clinical signs and presenting more than 1 hour after possible
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Marijuana Toxicosis
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ingestion, treating with activated charcoal only and monitoring for onset of signs, without further treatment if no signs emerge, is acceptable.
ACUTE GENERAL TREATMENT Decontamination of the patient: Emesis: can be induced within 15-30 minutes of exposure as long as no overt clinical signs of toxicosis are present. Use hydrogen peroxide at 2.2 mL/kg PO; max 45 mL. Repeat once if emesis does not occur first time. Apomorphine: not likely to work as an emetic because of the strong central antiemetic effect of marijuana Activated charcoal: very beneficial. Indicated when emesis is absent in patients with or without clinical signs. In patients with clinical signs or large ingestions, multiple doses can be used every 8 hours to reduce enterohepatic recirculation; 1-3 g/kg or labeled dosage of commercial products. Caution: risk of hypernatremia when using repeated doses of charcoal products containing a purgative (e.g., Toxiban) Supportive care: IV fluids as needed for dehydration, hypovolemia Thermoregulation (heating pads for hypothermia) Monitor cardiovascular function. Atropine, 0.022-0.044 mg/kg IM or SQ can be given for bradycardia in normotensive patients. Control tremors with diazepam at a low dose of 0.25 mg/kg IV. Monitor for signs of aspiration pneumonia in recumbent animals. Pass cuffed endotracheal tube if needed, ensuring a mouth gag/speculum is also used in order to avoid the patient biting and transecting the tube when recovering. Control severe vomiting with metoclopramide, 0.2-0.4 mg/kg q 6 h PO, SQ, or IM; or maropitant, 1 mg/kg SQ or 2 mg/kg PO q 24 h, once ingested material has been expelled.
DRUG INTERACTIONS Other CNS depressants (barbiturates, benzodiazepines) may exacerbate signs.
RECOMMENDED MONITORING Heart rate Blood pressure Body temperature
PROGNOSIS AND OUTCOME Excellent with treatment Fatalities are extremely rare.
PEARLS & CONSIDERATIONS COMMENTS Until proven otherwise, a dog presenting with acute-onset ataxia, CNS depression, and urinary incontinence that improves with stimulation and then gets worse again with decreased stimulation should be considered suspect of marijuana ingestion. Marijuana may be mixed with other substances for smoking (e.g., phencyclidine [PCP]) which may alter the patient's signs.
TECHNICIAN TIP Some owners may mention the possibility of this type of drug exposure in the veterinarian's absence (due to embarrassment, oversight, or fear of consequences). If the client raises the possibility with any member of the technical staff, this valuable piece of information could determine the course of treatment and the patient's outcome and therefore should be mentioned to the attending veterinarian.
SUGGESTED READING Pawel J, Donaldson CW, Gwaltney S: Marijuana toxicosis in dogs 213 cases (1998-2001). Vet Hum Toxicol 46:1, 2004. Volmer PA: "Recreational" drugs. In Peterson ME, Talcott PA, editors: Small animal toxicology, ed 2, St Louis, 2006, Saunders Elsevier, pp 273–311.
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Marijuana Toxicosis
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AUTHOR: ERIC DUNAYER EDITOR: SAFDAR A. KHAN 1ST EDITION AUTHOR: CAROLINE DONALDSON
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Mammary Gland Neoplasia, Dog
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Mammary Gland Neoplasia, Dog BASIC INFORMATION DEFINITION Mammary gland tumors are benign or malignant neoplasms arising from mammary tissue.
SYNONYMS Mammary cancer, breast cancer Benign mammary tumors: Adenoma/cystadenoma (very common) Benign mixed mammary tumor (very common) Fibroadenoma (uncommon) Malignant mammary tumors: Adenocarcinoma/cystadenocarcinoma (common) Carcinoma (common) Inflammatory carcinoma (uncommon) Malignant mixed mammary tumor (uncommon) Carcinosarcoma (rare) Sarcoma (uncommon) Note: Different pathologic classification schemes exist.
EPIDEMIOLOGY SPECIES, AGE, SEX Mammary gland tumors are the most common tumor in female dogs, according to some surveys. Incidence ∼ 2:1000. Due to the common practice of early-age ovariohysterectomy (OHE), the incidence has decreased in the United States. In European countries, mammary tumors represent 40%-50% of all tumors in female dogs. Greater prevalence with older age; median age 10-11 years Mammary gland tumors in male dogs are uncommon (approximately 1% of mammary tumors occur in males). GENETICS & BREED PREDISPOSITION Breeds at increased risk include: Spaniel breeds Pointer breeds Poodles Dachshunds German shepherds Yorkshire terriers A genetic factor in the development of mammary tumors seems to be present; however, a specific, common mutation has not been identified. The following genes have been found to be mutated in select canine mammary gland tumors: p53 c-erb-2 (Her-2/neu) BCRA 1, 2 RISK FACTORS Timing of OHE: the relative risk for developing mammary gland tumors: 0.5% if OHE is performed before the first estrus 8% if OHE is performed between the first and second estrus 26% if OHE performed between the second and third estrus
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Mammary Gland Neoplasia, Dog
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Intact females and females neutered after 2 years of age have a sevenfold greater risk of mammary neoplasia compared to those neutered before age 6 months. Body condition/diet: reduced risk in dogs with lean body condition at age 9-12 months Progesterone treatment: increases the risk for the development of benign and malignant mammary tumors. Pregnancy, lactation, pseudopregnancy: Unlike people, pregnancy does not afford a protective effect against the development of mammary tumors in dogs. Lactation and pseudopregnancy also do not seem to have an influence. ASSOCIATED CONDITIONS & DISORDERS: Ovarian cysts, cystic endometrial hyperplasia
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES Clinical staging: Tumor: T1, 5 cm Regional lymph node: N0, no metastasis; N1, metastasis detected Distant metastasis: M0, no metastasis; M1, metastasis detected Histologic staging: 0 Without stromal invasion I With stromal invasion II With neoplastic emboli in vessels
Stage Grouping T
N
M
I
T1
N0
M0
II
T2
N0
M0
III
T3
N0
M0
IV
T1-3 N1
M0
V
T1-3 N0, N1 M1
HISTORY, CHIEF COMPLAINT Owners may note a swelling, “lump,” or ulceration in their dog's mammary chain, or these may be incidental findings on routine physical examination. Duration of clinical signs is highly variable, ranging from days to months. In cases of metastasis or inflammatory carcinoma, dogs may be presented due to general signs of illness or specific complaints attributable to a certain site of metastasis (e.g., lameness in cases of bone metastasis). PHYSICAL EXAM FINDINGS Variable depending on extent and stage of the disease Single or multiple nodules may be present. Multiple tumors are common in dogs, and both mammary chains may be affected. Multiple tumor types are common. Signs of malignancy include fixation to skin or underlying structures, rapid increase in size, ill-defined borders, ulceration, pain, inflammation or edema. Absence of these signs does not exclude malignancy. Inflammatory carcinomas present with diffuse, firm, and painful swelling of the affected gland or chain. The adjacent extremity may be affected. Cutaneous involvement in form of small beadlike nodules may also be found. Regional lymph nodes (inguinal and axillary) may be enlarged (due to metastasis or reactive hyperplasia) or normal on palpation. The internal iliac, popliteal, and prescapular nodes may also be affected.
ETIOLOGY AND PATHOPHYSIOLOGY Estimates of malignancy rates range from 30%-50%. Metastasis most common to the regional lymph nodes and lungs Tumors are classified according to their tissue of origin into epithelial, mesenchymal, and mixed tumors. Inflammatory carcinoma is not a specific histologic subtype but an aggressive high-grade carcinoma with invasion into the dermis and dermal lymphatics. The inflammatory cell infiltrate is moderate in most cases and consists of lymphocytes, plasma cells, and macro-phages.
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Mammary Gland Neoplasia, Dog
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Primary mesenchymal mammary tumors (e.g., fibrosarcoma, osteosarcoma) are infrequent. Malignant mesenchymal mammary tumors often behave aggressively, with frequent metastasis and a short survival. Mixed mammary tumors consist of epithelial, myoepithelial, and mesenchymal tissue. Most mixed mammary tumors are benign. Malignant mixed mammary tumors and carcinosarcomas are rare exceptions.
DIAGNOSIS DIAGNOSTIC OVERVIEW The diagnosis is suspected based on the presence of a mass in the mammary chain. Histologic evaluation is required for definitive diagnosis which is usually obtained from an excisional biopsy.
DIFFERENTIAL DIAGNOSIS Mastitis Other cutaneous and subcutaneous tumors Inguinal/axillary lymphadenopathy (reactive, neoplastic) Inguinal hernia
INITIAL DATABASE Physical examination: Measure primary tumor (T) Describe possible signs of invasiveness (ulceration, fixation) Evaluation of regional lymph nodes (N): palpation and cytologic study Thoracic radiographs (three views) Abdominal ultrasound in case of suspected metastasis to abdominal organs or lymph nodes CBC, serum biochemistry profile, urinalysis Coagulation profile in cases of suspected inflammatory carcinoma (risk of disseminated intravascular coagulation)
ADVANCED OR CONFIRMATORY TESTING Excisional biopsy of the tumor and thorough histologic examination are necessary to obtain a definitive diagnosis. Fine-needle aspiration cytology is not recommended: Poor differentiation between malignant and benign mammary tumors, owing to their heterogeneous composition Incisional biopsy also may not represent the whole tumor and is not recommended. Lymph node metastasis: fine-needle aspiration and cytologic evaluation of lymph nodes has been shown to increase diagnostic accuracy of mammary tumor metastasis. Metastases may be present in palpably normal nodes. Advanced imaging (CT, MRI) may be more sensitive to detect metastatic lesions in the thoracic and abdominal cavities and should be considered in cases in which metastasis is strongly suspected but cannot be detected on radiographs or ultrasound.
TREATMENT TREATMENT OVERVIEW Treatment consists of complete surgical removal of the mammary tumor(s). The role of chemotherapeutics to delay the onset of metastatic disease has not been well defined in dogs. For dogs with inoperable tumors or inflammatory carcinomas, palliation with piroxicam or other antiinflarnmatory medications may improve quality of life.
ACUTE GENERAL TREATMENT Mainstay of treatment is surgical excision of the mammary tumor(s) with wide margins (at least 2 cm in all planes if possible). Type of surgery (nodulectomy, regional or radical mastectomy) depends on the size, location, and number of tumors present. Type of surgery does not influence survival so long as the entire tumor is removed with histologically clean margins. Lumpectomy possible for freely move-able tumors 50% of affected dogs; multiple tumor types occurring concunently or sequentially are common. Highest-risk patients that will benefit most from postoperative adjuvant chemotherapy still need to be identified. These may include patients with advanced clinical stages (II-V), histologic evidence of vascular/lymphatic invasion, and/or high degree of anaplasia on histopathologic evaluation. The benefit of OHE at the time of mammary tumor surgery remains controversial, but a subset of dogs with differentiated estrogen receptor-positive tumors may indeed benefit from concurrent OHE.
PREVENTION OHE at age 2 years: no benefit Treatment with progesterone and estrogen/progesterone combinations is associated with a threefold increased risk of development of benign and malignant mammary tumors in cats (progesterone treatment: 36% of male cats with mammary carcinoma).
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES: Clinical staging: Tumor: T1: 3 cm Regional lymph node: N0, no metastasis; N1, metastasis detected Distant metastasis: M0, no metastasis; M1, metastasis detected
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Mammary Gland Neoplasia, Cat
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Stage Grouping T
N
M
I
T1
N0
M0
II
T2
N0
M0
III
T1, T2 N1
M0
IV
T3
N0, N1 M0
T1-3
N0, N1 M1
HISTORY, CHIEF COMPLAINT A swelling, “lump,” or often ulcerated tissue may be noted in a cat's mammary chain. In cases of metastasis or inflammatory carcinoma, cats may be presented for general signs of illness or specific complaints attributable to a certain site of metastasis (e.g., dyspnea due to pulmonary metastases or pleural effusion). Duration of clinical signs is variable, ranging from a few days to several months. PHYSICAL EXAM FINDINGS Clinical signs vary depending on extent and stage of disease. More than 50% of cats will have more than one mammary tumor present, and both mammary chains may be affected simultaneously. Tumors may be firm on palpation and occasionally fixed to underlying structures. Discrete to infiltrative, soft to firm swelling within mammary gland or overlying skin is most common. Ulceration is frequently present. Can have associated discharge from nipple. Regional lymph nodes (inguinal and axillary) may be enlarged or normal on palpation. Lymph node enlargement can indicate metastasis or reactive change secondary to inflammation. Inflammatory carcinomas occur rarely in cats after mastectomy for mammary carcinoma. These cats present with local erythema, edema, pain, and involvement of the extremities.
ETIOLOGY AND PATHOPHYSIOLOGY The vast majority (85%-93%) of feline mammary tumors are malignant, with more than 80% of feline mammary tumors classified as adenocarcinoma. Metastasis is common (61%). Preferred sites of metastasis include the lungs (76%), pleura (40%), and lymph nodes (27% or more). Inflammatory carcinomas occur rarely in cats after mastectomy for mammary carcinoma. These are aggressive anaplastic carcinomas with considerable inflammatory cell infiltrate, intradermal and dermal lymphatic invasion that leads to edema, pain, and rapid metastasis. Benign tumors including adenomas, fibroadenomas, and duct papillomas occur uncommonly in cats.
DIAGNOSIS DIAGNOSTIC OVERVIEW The diagnosis is suspected based on the presence of a mass in the mammary chain. Histologic evaluation is required for definitive diagnosis which is usually obtained from an excisional biopsy.
DIFFERENTIAL DIAGNOSIS Fibroepithelial hyperplasia: involves multiple glands, most often in young intact females and spayed females given progesterone compounds Mastitis Other cutaneous and subcutaneous tumors Inguinal/axillary lymphadenopathy (reactive, neoplastic) Inguinal hernia Enlarged inguinal fat pad
INITIAL DATABASE
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Mammary Gland Neoplasia, Cat
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Physical examination: Measure primary tumor (T) Describe possible signs of invasiveness (ulceration, fixation) Evaluate regional lymph nodes (N): palpation and cytologic analysis Thoracic radiographs (three views) for pulmonary metastasis Abdominal ultrasound in case of suspected metastasis to abdominal organs or lymph nodes Fine-needle aspiration and cytologic evaluation are of limited utility and generally not recommended. Although seemingly more accurate than in dogs, feline mammary mass aspirates often are not representative of the entire mass, and cytologic criteria of malignancy are not correlated to histologic findings nor clearly defined. CBC, serum biochemistry profile, urinalysis, coagulation profile in cases of suspected inflammatory carcinoma
ADVANCED OR CONFIRMATORY TESTING Definitive diagnosis is via biopsy and histopathologic evaluation of mammary masses Histologic grading scheme is based primarily on mitotic activity, areas of necrosis, and degree of infiltration into soft tissue and vasculature. Because >85% of feline mammary tumors are malignant, histopathologic examination most often is performed on tumor tissue obtained from a radical mastectomy. When fibroepithelial hyperplasia (see Differential Diagnosis above) or other nonmammary tumors are suspected, incisional (wedge) biopsies may be done. Lymph node evaluation: In general, the ipsilateral inguinal lymph node should be removed during radical mastectomy and assessed histopathologically. Axillary lymph nodes may be difficult to isolate, but fine-needle aspiration or biopsies can be done if they are enlarged. Distant metastasis: Cytologic evaluation of pleural effusion can aid in the diagnosis of thoracic metastatic disease. Advanced imaging (CT, MRI) may increase diagnostic accuracy of metastatic lesions in the thoracic and abdominal cavities.
TREATMENT TREATMENT OVERVIEW Treatment consists of complete surgical removal of the mammary tumor(s). The recommended surgical approach for cats is radical mastectomy. Adjuvant chemotherapy is advised for cats with poor prognostic factors, although the true survival benefit is not known.
ACUTE GENERAL TREATMENT Surgery: Radical mastectomy of the affected mammary chain(s) is recommended. In contrast to individual mastectomies or lumpectomies, radical mastectomy significantly reduces the risk for local tumor recurrence. Affected lymph node(s) should be removed along with mammary chain. Fixation of the tumor to underlying muscle or fascia necessitates en bloc removal of these structures. In cats with advanced metastatic disease, local mastectomy to remove ulcerated or infected mammary tumors may be palliative. Inflammatory carcinoma is nonresectable.
CHRONIC TREATMENT Chemotherapy: Single-agent doxorubicin, doxorubicin in combination with cyclophosphamide or single-agent carboplatin may lead to complete and partial responses in cats with metastatic disease or nonresectable mammary gland tumors. Adjuvant chemotherapy using the previously mentioned drugs as single agents or in combination is recommended in cats after radical mastectomy. However, a true survival benefit has yet to be proven. Consultation with an oncologist for the most current treatment recommendations is indicated. Radiation therapy: Radiation to palliate nonresectable disease may be an option in some cats. Immunotherapy: Treatment with levamisole, bacterial vaccines, and other immunomodulators has not led to any improvement in local tumor control or survival. Analgesics:
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Mammary Gland Neoplasia, Cat
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Analgesics should be used in cats that present with advanced disease.
POSSIBLE COMPLICATIONS Inflammatory carcinoma after mastectomy for mammary carcinoma: rare
RECOMMENDED MONITORING Regular examination of surgical site, local lymph nodes, lung fields
PROGNOSIS AND OUTCOME Local recurrence rate: 51%-66% (female), 45% (male) Prognostic factors for cats with mammary gland carcinomas: Tumor size: >3 cm: median survival of 4-6 months (female), 1.6 months (male) 2-3 cm: median survival of 1-2 years (female), 5.2 months (male) 3 years after mastectomy (female), 14 months (male) Type of surgery: Radical mastectomy significantly reduces the risk for local tumor recurrence compared with conservative surgery but does not appear to improve survival time. o Degree of histologic differentiation: high grade is associated with a shorter survival time. Other unfavorable prognostic factors include old age of the cat and incomplete surgical excision. Benign tumors and low-grade malignant tumors may be cured by wide excision.
PEARLS & CONSIDERATIONS COMMENTS Mammary carcinoma in the cat is a highly malignant neoplastic disease that warrants early diagnosis and an aggressive treatment approach. Adjuvant chemotherapy should be considered in cats with resectable mammary carcinoma after radical mastectomy. In cats with advanced disease, palliative measures including surgery, chemotherapy, radiation, and analgesics may be considered.
PREVENTION Ovariohysterectomy before age 6 months reduces the risk but will not prevent mammary carcinoma in female cats. Castration does not prevent mammary carcinoma in male cats.
CLIENT EDUCATION Early ovariohysterectomy of queens not intended for breeding Regular examination of the mammary chain Prompt presentation for veterinary examination when abnormalities are found
SUGGESTED READING MacEwen EG, et al: Prognostic factors for feline mammary tumors. J Am Vet Med Assoc 185(2):201–204, 1984. Novosad CA, Bergman PJ, O’Brien MG, et al: Retrospective evaluation of adjunctive doxorubicin for the treatment of feline mammary gland adenocarcinoma: 67 cases. J Am Anim Hosp 42:110–120, 2006. Overly B, Shofer, FS, Goldschmidt MH, et al: Association between ovariohysterectomy and feline mammary carcinoma. J Vet Intern Med 19:560–563, 2005. AUTHOR: CHERYL BALKMAN EDITOR: KENNETH M. RASSNICK 1ST EDITION AUTHORS: DANIELA SIMON, BETH A. VALENTINE
25-09-2011 22:31
Mammary Disorders, Non-Neoplastic
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Mammary Disorders, Non-Neoplastic BASIC INFORMATION DEFINITION Mastitis: inflammation of the mammary gland, usually septic; blood-milk barrier not intact Mammary hyperplasia: aseptic noninflammatory enlargement of mammary glands
SYNONYMS Mammary hyperplasia, fibroadenomatous mammary hyperplasia, benign feline mammary hyperplasia
EPIDEMIOLOGY SPECIES, AGE, SEX Mastitis: more common in the postpartum bitch than the bitch with overt false pregnancy or the postpartum queen. Occasionally occurs in spayed bitches. Older bitches may be at greater risk (unverified). Mammary hyperplasia: usually young intact cats or pregnant queens GENETICS & BREED PREDISPOSITION: Mastitis: short-legged breeds and dogs with pendulous mammary glands have greater risk of trauma. RISK FACTORS Mastitis: poor hygiene, trauma (environmental or secondarily to puppies nursing), infections from other sites in the body Mammary hyperplasia: young intact cats, pregnant queens or cats with false pregnancy. Cats of either sex with recent gonadectomy. Cats of either sex receiving exogenous progestogen treatment. GEOGRAPHY AND SEASONALITY: Mammary hyperplasia: spring when queens cycle; incidence is 40%-50% post ovulation in cats with false pregnancy. ASSOCIATED CONDITIONS & DISORDERS Mastitis: Bitches and queens with secondary septicemia from other infections may have hematogenous spread to mammary tissue. Galactostasis following weaning or overt pseudopregnancy Benign mammary hyperplasia in queens May be associated with mammary neoplasia Mammary hyperplasia: Secondary mastitis and/or necrosis Conditions which may result in treatment with exogenous progestogens
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES Mastitis: acute, fulminate or chronic, near subclinical Mammary hyperplasia: acute
HISTORY, CHIEF COMPLAINT Mastitis: Lactating bitch or queen Uncomfortable dam may or may not want to nurse puppies; neonates do not nurse (crying puppies or kittens) Rarely, pseudopregnant bitch Mammary hyperplasia: acute enlargement of mammary glands
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PHYSICAL EXAM FINDINGS Mastitis: Firm, warm, swollen, often painful mammary gland (one or more) Lethargy Dehydration May be possible to express purulent or discolored milk from gland Gland may abscess, become gangrenous, and rupture. +/− Fever May progress to septic shock Mammary hyperplasia Enlarged mammary glands All glands usually involved Can be painful Can develop necrosis
ETIOLOGY AND PATHOPHYSIOLOGY Mastitis Possible ascending infection from poor environmental hygiene or traumatic injury from nursing offspring Incidence highest in stimulated mammary glands; may be due to presence of abundant substrate (milk), open ducts, trauma from nursing, and increased trauma because glands are enlarged Mammary hyperplasia Hormonally induced condition Hormones include progesterone, growth hormone, and prolactin. Key: high progestogen concentrations, either endogenous or exogenous
DIAGNOSIS DIAGNOSTIC OVERVIEW History and physical examination are generally sufficient to formulate a diagnosis: enlarged, painful mammary glands (usually during lactation) in mastitis patients, or rapidly enlarged nonseptic mammary glands in cats with mammary hyperplasia.
DIFFERENTIAL DIAGNOSIS Mammary adenocarcinoma (inflamed or septic) usually in older females with no concurrent lactation (see pp. 690 and 692) Galactostasis: dam not ill, nonseptic
INITIAL DATABASE CBC in mastitis unremarkable or leukocytosis with left shift; if acute sepsis, leukopenia is possible. CBC in mammary hyperplasia normal. Cytologic examination of mammary secretions: in mastitis, many toxic neutrophils; in mammary hyperplasia, normal Mastitis: pH of mammary secretions will help determine which antibiotic to use.
ADVANCED OR CONFIRMATORY TESTING Bacterial culture and sensitivity of mammary secretions Biopsy of mammary tissue (to rule out neoplasia and benign mammary hyperplasia)
TREATMENT TREATMENT OVERVIEW Goals of treatment are returning the patient to normal mammary function and preventing septicemia. For mammary hyperplasia: prevention of mastitis.
ACUTE GENERAL TREATMENT
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Mastitis: If mammary necrosis is present or milk is too contaminated for puppies and kittens, offspring should be removed and the necrotic tissue surgically drained and débrided. Signs include milk that is grossly purulent, malodorous, or markedly discolored, or hungry neonates that are not nursing on their own or are developing diarrhea, vomiting, or losing weight. Antiprolactin therapy may be administered to stop lactation (cabergoline, 5 mcg/kg PO q 24 h; response usually seen within 3-4 days; over 80% response by day 7). Systemic antibiotic treatment of the dam is required. General guidelines are initially based on Gram stain and on whether neonates are still nursing; subsequently use culture and sensitivity results for definitive treatment. The therapeutic goal is to achieve significant antibiotic concentrations in the milk. While awaiting culture results, the choice of antibiotic for initial empirical treatment is limited (e.g., cefadroxil, 22 mg/kg PO q 8 h or amoxicillin-clavulanic acid 12.75 mg/ kg PO q 12 h) if the dam's offspring continue to nurse. Nursing puppies and kittens can be negatively affected by antibiotic concentrations in the dam's milk. Recommendations for nursing dam: Aerobic bacteria: Gram-negative: cefoxitin, 30 mg/kg IV q 6 h; or chloramphenicol, 40 mg/kg PO q 8h Gram-positive: first-generation cephalosporins (e.g., cefadroxil, 22 mg/kg PO q 8 h; or erythromycin, 10-20 mg/ kg PO q 8 h) Anaerobic bacteria: erythromycin, cefoxitin, chloramphenicol Mycoplasma: erythromycin, chloramphenicol Recommendations for dam not nursing neonates: Aerobic bacteria: Gram-negative: quinolones (e.g., enrofloxacin, 5 mg/kg PO q 12 h [5 mg/kg PO q 24 h in cats]), or second- or third-generation cephalosporins (e.g., cefoxitin) Gram-positive: first-generation cephalosporins, amoxicillin/clavulanic acid, or erythromycin Anaerobic bacteria: Penicillin (e.g., procaine penicillin G, 20,000 IU/kg IM or SQ q 12-24 h); metronidazole (15 mg/kg PO q 12 h); clindamycin (5-11 mg/kg PO q 12 h); erythromycin or cefoxitin Mycoplasma: tetracyclines (e.g., doxycycline, 5 mg/kg PO q 12 h), erythromycin, or quinolones. Warm packing and ongoing nursing. Unless the gland is necrotic, continued nursing by the offspring and warm packing the affected glands will prevent galactostasis and promote drainage. Mammary hyperplasia: Progesterone withdrawal Usually self-limiting in 2-3 weeks If sexually intact, ovariectomy or ovariohysterectomy recommended Pain control Medical therapy Progesterone receptor blocker: aglepristone (15 mg/kg SQ q 24 h × 2 days or 20 mg/kg SQ once). Note: not approved for use in cats in the United States; will abort pregnant cats. Prolactin inhibitor: bromocriptine mesylate (0.25 mg per cat PO q 24 h × 5-7 days. Note: not approved for use in cats in the United States; will abort pregnant cats. Androgens: testosterone enanthate or testosterone cypionate (2 mg/ kg IM once). Note: not approved for use in cats in the United States.
CHRONIC TREATMENT Mastectomy
BEHAVIOR/EXERCISE Limit activity which might induce mammary trauma. This may include weaning puppies and kittens.
DRUG INTERACTIONS Antiprolactinics will stop lactation. Some antibiotics are contraindicated in lactating bitches. Aglepristone is abortifacient in the cat.
POSSIBLE COMPLICATIONS Systemic antibiotic therapy in lactating dams may interfere with normal bacterial colonization of gastrointestinal flora in nursing neonates, resulting in diarrhea.
RECOMMENDED MONITORING Temperature, respiration and heart rate
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Physical signs of septicemia Offspring that are nursing: weigh daily to determine adequate milk intake.
PROGNOSIS AND OUTCOME Prognosis is generally good unless sepsis occurs.
PEARLS & CONSIDERATIONS COMMENTS Neonates 4½ to 5 weeks old should be allowed access to dam's food, and the bitch or queen should have an area where she can remove herself from the neonates (e.g., top of crate, raised platform). Neonates will then start eating solid food for a portion of their caloric intake, decreasing the amount of time they are nursing on the mother. Additionally benefits the dam by greatly reducing her metabolic requirements. Older neonates with teeth nurse more aggressively and can induce both bite and nail trauma to the mammary gland, greatly increasing the risk of inflammation and infection. Frequently, chronic mastitis has been suspected when neonates fail to thrive. However, subclinical mastitis has not been demonstrated in dogs and cats.
PREVENTION Adequate husbandry, particularly clean bedding for mother and offspring Keep mammary glands clean, monitor glands for trauma from neonate's claws or teeth. Clipping neonates’ toenails Mammary hyperplasia: limit the clinical use of exogenous progestogens.
CLIENT EDUCATION Primarily husbandry issues of proper hygiene and weaning instructions.
SUGGESTED READING Feldman E, Nelson R: Canine and feline endocrinology and reproduction, Philadelphia, 2003, Saunders. Johnston SD, Root-Kustritz MV, Olsen PNS: Canine and feline theriogenology, Philadelphia, 2001, Saunders. AUTHOR: MICHAEL PETERSON EDITOR: MICHELLE KUTZLER
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Malocclusion
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Malocclusion BASIC INFORMATION DEFINITION An abnormal position of the teeth. In dental malocclusion, one or several teeth is/are in an abnormal position, whereas in skeletal malocclusion there is an upper/lower jaw discrepancy.
SYNONYM Malalignment of teeth
EPIDEMIOLOGY SPECIES, AGE, SEX: Malocclusion can be seen in all species, all age groups, and is usually present from the time of eruption of the deciduous or permanent dentition. GENETICS & BREED PREDISPOSITION: Occlusal development is determined by genetic and environmental factors. Most brachycephalic cats and dogs show malocclusion due to a shortened upper jaw. RISK FACTORS Persistent deciduous teeth Facial trauma during tooth and jaw development Selective breeding for exaggerated head types ASSOCIATED CONDITIONS & DISORDERS Discomfort and pain can result from maloccluding teeth. Linguoverted mandibular canines may lead to oronasal fistula formation. Crowded teeth are at risk for early periodontitis from plaque retention.
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES Dental malocclusion: Neutroclusion (class 1 malocclusion; a normal rostrocaudal relationship of the maxillary and mandibular dental arches, with malposition of one or more individual teeth) Distoversion/mesioversion/lin-guoversion/labioversion/bucco-version: tooth in its anatomically correct position in the dental arch is abnormally angled in a distal/mesial/lingual/labial/buccal direction, respectively. Crossbite: malocclusion in which a mandibular tooth or teeth have a more buccal or labial position than the antagonist maxillary tooth Rostral crossbite: one or more of the mandibular incisor teeth is labial to the opposing maxillary incisor teeth when the mouth is closed Caudal crossbite: one or more of the mandibular cheek teeth is buccal to the opposing maxillary cheek teeth when the mouth is closed Symmetric skeletal malocclusion: Mandibular distoclusion (class 2 malocclusion; an abnormal rostrocaudal relationship between the dental arches in which the mandibular arch occludes caudal to its normal position relative to the maxillary arch) Mandibular mesioclusion (class 3 malocclusion; an abnormal rostrocaudal relationship between the dental arches in which the mandibular arch occludes rostral to its normal position relative to the maxillary arch) Asymmetric skeletal malocclusion: Maxillary-mandibular asymmetry describes skeletal malocclusions that can occur in a rostrocaudal, side-to-side, or dorsoventral direction. Rostrocaudal: mandibular mesioclusion or distoclusion is present on one side of the face, but the contralateral side retains normal dental alignment. Side-to-side: there is loss of the midline alignment of the maxilla and mandible. Dorsoventral: results in an open bite, defined as an abnormal vertical space between opposing dental arches
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when the mouth is closed HISTORY, CHIEF COMPLAINT Abnormal incisor occlusion (show and breeding dogs) Abnormal tooth position Obvious length difference between upper and lower jaws or between left and right
MALOCCLUSION Clinical photograph of a cat with mesioversion of the right maxillary canine tooth (asterisk). There is no diastema between the right maxillary canine and third incisor, which the right mandibular canine tooth could occlude into when the mouth is closed (compare with normal left side). Mesioversion of the right maxillary canine tooth resulted in mild labioversion of the right mandibular canine tooth and an open bite (incomplete closure of the mouth). (Copyright Dr. Alexander M. Reiter.) PHYSICAL EXAM FINDINGS Normal occlusion (in the dog): Maxillary incisor teeth are positioned rostral to mandibular incisor teeth. Crown cusps of mandibular incisor teeth contact the cingulum of maxillary incisor teeth. Mandibular canine tooth inclined labially and bisecting the interdental space between the maxillary third incisor tooth and canine tooth Maxillary premolar teeth do not contact mandibular premolar teeth. Crown cusps of mandibular premolar teeth positioned lingual to the arch of maxillary premolar teeth. Crown cusps of mandibular premolar teeth bisect the interdental spaces rostral to corresponding maxillary premolar teeth. Mesial crown cusp of the maxillary fourth premolar tooth positioned lateral to the space between the mandibular fourth premolar and first molar teeth Dental malocclusion: Abnormal positioning of one or more teeth No jaw discrepancy Trauma to soft tissue or other teeth Skeletal malocclusion: Abnormal maxillary-mandibular incisor relationship Loss of premolar interdigitation Incorrect mandibular canine occlusion Jaw length discrepancy (symmetric or asymmetric) Trauma to soft tissue or other teeth
ETIOLOGY AND PATHOPHYSIOLOGY Jaw length, tooth bud position, and tooth size are independently inherited. Unharmonious development of upper and lower jaw and teeth results in malocclusion. Persistent deciduous teeth are associated with malpositioned permanent teeth. Significant facial trauma at a young age may lead to abnormal development and malocclusion.
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Significant facial trauma at any age may cause changes in jaw relationship.
DIAGNOSIS DIAGNOSTIC OVERVIEW The diagnosis is based entirely on physical examination to identify malpositioned teeth.
DIFFERENTIAL DIAGNOSIS Skeletal malocclusion versus dental malocclusion Functional (mal)occlusion versus clinically relevant malocclusion (causing discomfort or pain)
INITIAL DATABASE Physical examination: Look for persistent deciduous teeth. Differentiate between dental and skeletal malocclusion.
TREATMENT TREATMENT OVERVIEW The goal of treatment is to have a pain-free, comfortable patient with a functional bite. Cosmetic considerations should not play a role.
ACUTE AND CHRONIC TREATMENT Extract maloccluding deciduous teeth as early as possible (6-10 weeks of age) if they appear to cause discomfort or interfere with jaw growth. Treatment options for maloccluding permanent teeth causing trauma to soft tissue or other teeth: Extraction Surgical crown reduction and vital pulp therapy Orthodontic movement (passive or active) Linguoversion of mandibular canines: “Verhaert's rubber ball technique” is useful for young dogs (below 7 months of age) with normal jaw relationships and sufficiently wide diastema between maxillary third incisor and canine teeth. The dog is stimulated to actively play with a smooth-surfaced hard rubber ball for at least 15 minutes 3 times daily.
POSSIBLE COMPLICATIONS Inappropriate extraction technique of deciduous teeth may cause trauma to developing permanent teeth. Surgical crown reduction may lead to pulpitis and pulp necrosis. Orthodontic treatment usually requires several corrective procedures under general anesthesia and may cause soft-tissue trauma from the appliance, tooth ankylosis and root resorption, displacement of anchor tooth, overcorrection of target tooth, avulsion of anchor or target tooth, discomfort, and pain.
RECOMMENDED MONITORING Teeth treated by surgical crown reduction should be monitored radiographically after 4-6 months and then on a yearly basis. During orthodontic treatment, regular monitoring is necessary to assess tooth movement and to recognize possible complications at an early stage.
PROGNOSIS AND OUTCOME Prognosis is good once a functional bite has been accomplished.
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PEARLS & CONSIDERATIONS COMMENTS Dental malocclusions are not considered inherited unless a familial predisposition exists. Skeletal malocclusion is considered inherited unless a developmental cause (e.g., significant facial trauma) can be identified. Inherited malocclusion should only be corrected by orthodontic movement if the animal is neutered.
PREVENTION Selective breeding Remove persistent deciduous teeth
CLIENT EDUCATION Neuter animals with skeletal malocclusion (if not “normal” for the breed).
SUGGESTED READING Gorrel C: Veterinary dentistry for the general practitioner. Edinburgh, 2004, WB Saunders, pp 35–46. Hennet P: Orthodontics. In Slatter D, editor: Textbook of small animal surgery, ed 3, Philadelphia, 2003, WB Saunders, pp 2686–2695. AUTHOR: LEEN VERHAERT EDITOR: ALEXANDER M. REITER
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Malnutrition
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Malnutrition BASIC INFORMATION DEFINITION Malnutrition is the inappropriate intake of nutrients, resulting in nutritional deficiencies or excesses.
EPIDEMIOLOGY SPECIES, AGE, SEX: Malnutrition can affect animals of any species, age, life stage, or lifestyle. GENETICS & BREED PREDISPOSITION: No specific genetic link or breed disposition is known for malnutrition associated with nutritional deficiencies. An increased prevalence of obesity resulting from excessive caloric intake has been associated with basset hounds, beagles, Cairn terriers, Cavalier King Charles spaniels, cocker spaniels, long-haired dachshunds, Labrador retrievers, and Shetland sheepdogs. RISK FACTORS Animals fed vegetarian, homemade, or single-food diets may be at risk for nutrient deficiencies (see p. 686). Animals with a history of chronic vomiting or diarrhea could have altered digestion or absorption, resulting in decreased nutrient assimilation. Drugs such as corticosteroids, cancer chemotherapeutic agents, antibiotics, or diuretics may adversely affect nutritional homeostasis. Neutering, decreased physical activity, age or calorie-dense foods may predispose dogs or cats to obesity. GEOGRAPHY AND SEASONALITY: Inadequate food or water intake during severe weather conditions may result in nutrient deprivation. ASSOCIATED CONDITIONS & DISORDERS Decreased protein/calorie intake negatively effects immune function. Increased risk of orthopedic problems or diabetes mellitus (cats) with prolonged excessive food intake
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES Weight loss, emaciation, low body condition score (1 or 2 on a scale of 1-5 or 1-9). Weight gain, obesity, high body condition score (4 or 5 on a scale of 1-5 or 8 or 9 on a 1-9 scale) HISTORY, CHIEF COMPLAINT Nutrient-deprived animals present with a history of failure to thrive and inappetence or anorexia. Overnourished or obese animals often present with clinical signs associated with lameness or endocrinopathy. PHYSICAL EXAM FINDINGS: Nutrient-deprived animals are often in poor physical appearance: thin body condition; dry, coarse haircoat; flaky skin; hyperkeratosis; muscle wasting; broken or missing teeth; skeletal abnormalities; pressure sores; poor wound healing. Obese animals are also in poor physical condition with fat deposition over the ribs, hips, tail head, and throughout the abdomen. Some are unable to adequately groom themselves, which can result in an unkempt hair coat, dry skin, skinfold dermatitis, and the inability to walk, run, or jump.
ETIOLOGY AND PATHOPHYSIOLOGY Inadequate or excessive nutrient intake results in malnutrition. Decreased nutrient intake diminishes immune cell response and production, as well as protein turnover, tissue synthesis, and wound healing. Altered drug metabolism results from protein/calorie malnutrition and may increase or decrease both drug efficacy and drug toxicity.
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Although not well documented in hospitalized veterinary patients, malnutrition is thought to increase morbidity and mortality.
DIAGNOSIS DIAGNOSTIC OVERVIEW The diagnosis of malnutrition is made on the basis of a thorough diet history and the physical examination findings.
DIFFERENTIAL DIAGNOSIS Gastrointestinal disease: protein-losing enteropathy, lymphocytic-plasmacytic enteritis, inflammatory bowel disease
INITIAL DATABASE A thorough diet history should include sufficient information to purchase all food items necessary to feed the patient exactly as the owner does at home. The physical examination should include a body weight, body condition score (1-5 or 1-9 scale), and muscle mass score (1-3 scale). Laboratory evaluation plays a limited role in diagnosing nutrition-related problems.
TREATMENT TREATMENT OVERVIEW The goals of treatment are to correct nutrient deficiencies or excesses and return patient to a normal plane of nutrition and a more appropriate body weight and body condition.
ACUTE GENERAL TREATMENT Stabilize patient: rehydrate, correct electrolyte imbalances, hemodynamic abnormalities, and hypothermia before initiating nutritional support. Determine whether the gastrointestinal tract is functional and how nutrition support is to be delivered (enteral or parenteral). For patients unable or unwilling to prehend, choose the type of feeding tube for enteral delivery that fits your patient (e.g., gastrotomy tube for patients with persistent regurgitation or vomiting, esophagostomy tube for facial trauma). See p. 1267 and p. 1273 . Estimate an initial daily caloric goal for resting energy needs based upon animal's current weight (rather than an ideal 0.75
weight), using the equation: 70 × BWkg For patients weighing between 15 and 30 kilograms, use the equation: 30 × BWkg + 70. This provides a reasonably accurate assessment of resting energy needs. Select a diet or food type that meets the nutritional needs of the patient. Determine a feeding regimen (continuous or intermittent feedings) that will deliver the estimated caloric goals over a 24-hour period. Administer nutrition to patients by assisted feeding until patient is eating at least 50% resting energy needs. Plan to get the animal eating its own food in its own environment as soon as possible.
CHRONIC TREATMENT Identify dietary, animal-related, owner-related or environmental issue(s) that caused or contributed to the nutritional deficiency or excess. Educate owner(s) about nutritional needs of their animal, given the species, age, life stage, and lifestyle. Provide information about, or resources for, complete and balanced homemade diets (website formulation services, laboratory analyses, and continuous monitoring). Provide information and support for owners considering a weight management program for their animal.
DRUG INTERACTIONS Medical therapies instituted for primary conditions will be altered without adequate nutrition support.
RECOMMENDED MONITORING
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Client education and repeated follow-up is critical for animals enrolled in weight management programs, or those who are fed homemade or raw meat diets.
PROGNOSIS AND OUTCOME Prognosis is good to excellent with immediate identification and correction of nutrient deficiencies or excesses. Prognosis is poor to good with prolonged identification and correction of nutrient deficiencies or excesses.
PEARLS & CONSIDERATIONS COMMENTS Obesity prevention is much easier than obesity management. Client education campaigns should focus on prevention at every well-pet visit. Obesity management programs should be directed by veterinarians and delivered by trained, licensed veterinary technicians who are excellent communicators. Pet owners interested in feeding homemade or raw meat diets should consult with a veterinarian, identify a balanced recipe to use, and plan on regular monitoring of both their pet and the diet (see online chapter: Malnutrition: Home-Prepared Diets).
PREVENTION Complete nutritional assessments should be performed daily on hospitalized patients to identify patients at risk of malnutrition before it occurs. Clients should be educated on the basic nutrient needs of animals, considering species, age, life stage, and environmental conditions.
TECHNICIAN TIPS Technicians can be instrumental in providing client education about the proper diet and feeding management of dogs and cats and in overseeing patients enrolled in weight management programs. In the outpatient setting, technicians should ensure that every patient is weighed, body condition scored, and has a diet history taken. In the inpatient setting, technicians can aid in identifying patients at risk of malnutrition.
CLIENT EDUCATION Consultation for customized homemade diet formulations is available through the American College of Veterinary Nutrition (ACVN.org), or diets can be purchased at www.balanceit.com or www.petdiets.com. Homemade diet recipes can be analyzed through the Nutrition Laboratory in the Diagnostic Center for Population and Animal Health at Michigan State University: 517-353-9312.
SUGGESTED READING Abood S, McLoughlin M, Buffington T: Enteral nutrition. In DiBartola SP, editor: Fluid, electrolyte, and acid–base disorders small animal practice, ed 3, St Louis, 2006, Saunders Elsevier, pp 601–620. Buffington T, Holloway C, Abood S: Manual of veterinary dietetics. St Louis, 2004, Elsevier. Chan DL: Nutritional requirements of the critically ill patient, Clin Tech Small Animal Pract 19:1–5, 2004. Eirmann L, Michel, K: Enteral Nutrition. In Silverstein D, Hopper K, editors: Small animal critical care medicine, St Louis, 2009, Saunders. Freeman L, Chan D: Total parenteral nutrition. In DiBartola SP, editor: Fluid, electrolyte, and acid–base disorders small animal practice, ed 3, St Louis, 2006, Saunders Elsevier, pp 548–600. Remillard RL, Armstrong PJ, Davenport DJ: Assisted feeding in hospitalized patients: enteral and parenteral nutrition. In Hand MS, Thatcher CD, Remillard RL, Roudebush PR, editors: Small animal clinical nutrition, ed 4, Topeka, 2000, Mark Morris Institute. AUTHOR: SARAH K. ABOOD
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Malnutrition
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EDITOR: KATHRYN E. MICHEL
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Malnutrition, Home-Prepared Diets
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Malnutrition, Home-Prepared Diets DEFINITION Feeding of an unbalanced diet of uncooked and cooked foods as a sole source of nutrition; this practice is becoming more common among pet owners.
SYNONYMS Home-cooked diet, homemade diet
EPIDEMIOLOGY SPECIES, AGE, SEX: Dogs more likely to be fed home-prepared diets than cats. Young and reproductive animals at increased risk for deficiencies and excess. All animals at risk of illness from foodborne pathogens. GENETICS & BREED PREDISPOSITION: Dogs and cats: all breeds affected. Dogs: large and giant breeds at increased risk of developmental orthopedic disease. Cats: taurine-deficient cardiomyopathy and/or central retinal degeneration. CONTAGION & ZOONOSIS: Dogs and cats: Salmonella, Escherichia coli, Campylobacter, Toxoplasma, Cryptosporidium ASSOCIATED CONDITIONS & DISORDERS: Poor skin and coat, obesity, vomiting, diarrhea, pathologic fractures, seizures, pancreatitis (high-fat diet), oral trauma, intestinal obstruction/perforation
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES Incidental: no clinical signs Overt illness: varies with dietary imbalance/excess or ingredients HISTORY, CHIEF COMPLAINT: Vomiting, diarrhea, lethargy, decreased activity, poor skin and coat, reproductive failure, fetal resorption, dystocia, failure to gain weight (young), weight loss (adult). May be an incidental finding during routine history-taking. PHYSICAL EXAMINATION: Varied: dull coarse coat, coat color change, dental fractures, skeletal abnormalities, fractures, heart murmur, loss of vision (cats), abdominal pain, dehydration, poor body condition (obese or cachectic)
ETIOLOGY AND PATHOPHYSIOLOGY Essential nutrient deficiency Lethargy, anorexia, reproductive failure: any Poor skin and coat: zinc, iron, iodine, phenylalanine-tyrosine, niacin, biotin, linoleic acid, linolenic acid and/or total protein Osteopenia/osteomalacia: calcium and/or vitamin D Anemia: iron, copper, folate and/or total protein Hypoalbuminemia: individual amino acids, total protein and/or total calories Heart murmur (cats, large-breed dogs, cocker spaniels): taurine Central retinal degeneration (cats): taurine Essential nutrient excess Anorexia: vitamin A, vitamin D, iron, calcium, iodine Hypercalcemia: vitamin D Vomiting and/or diarrhea: sodium and/or selenium; total fat (pancreatitis or fat malabsorption) Dietary contamination Vomiting and/or diarrhea: foodborne pathogen, bone ingestion Seizures: Neospora, Toxoplasma
DIAGNOSIS DIAGNOSTIC OVERVIEW The diagnosis is suspected when an unusual dietary history is revealed, suggestive physical abnormalities are noted, or both.
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DIFFERENTIAL DIAGNOSIS Allergic dermatitis, underlying end-organ disease (hepatic, renal, intestinal, central nervous system)
INITIAL DATABASE Diet history: consider adequate energy content, type and amount of protein, source of essential fatty acids, source of calcium, and source of trace minerals and vitamins. Serum biochemistry, CBC, urinalysis, may be unremarkable or show nonspecific changes (e.g., hypoalbuminemia, hypocalcemia, hypokalemia, hypomagnesemia, increased alkaline phosphatase, and anemia).
TREATMENT TREATMENT OVERVIEW Manage sequelae of imbalance and correct underlying deficiency.
ACUTE GENERAL TREATMENT Varies with imbalance Vomiting and/or diarrhea: correct dehydration with intravenous (IV) fluids Supplemental calcium gluconate, magnesium sulfate, or balanced B-vitamin solution (IV if needed) Foodborne pathogens respond to supportive and antimicrobial therapy unless sustained end-organ damage If no clinical signs of disease: dietary deficiencies and/or excesses are corrected with feeding a complete and balanced diet.
POSSIBLE COMPLICATIONS None known if home-prepared diet complete and balanced
RECOMMENDED MONITORING Diet recipes evaluated and balanced by trained veterinary nutritionist Physical examination, biochemistry, CBC and urinalysis every 6-12 months Diet and supplement review at each visit Diet reformulation may be necessary if health status changes.
PROGNOSIS AND OUTCOME Good if dietary imbalance corrected
PEARLS & CONSIDERATIONS COMMENTS Home-prepared diets are becoming more common among dog and cat owners as all or part of the daily diet. Normal test results do not rule out deficiency or suboptimal nutrient intake.
PREVENTION Client education important to help prevent foodborne illness and dietary imbalances Review diet history at each visit; owner substitution of ingredients and omissions of essential nutrients is common.
CLIENT EDUCATION Important to understand motivations for feeding home-prepared diets to help direct client education and prevent diet-induced disease. Feeding raw meat increases risk of pathogenic bacteria exposure for people and other animals in household; especially at risk are young, old, and immune-compromised adults. Proper food sanitation and hygiene are essential if home-prepared diet
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is fed.
SUGGESTED READING Michel KE: Unconventional diets for dogs and cats. Vet Clin North Am Small Anim Pract 36:1269–1281, 2006. Remillard R: Homemade diets: attributes, pitfalls, and a call for action. Top Companion Anim Med 23:137–142, 2008. Laflamme DP, Abood SK Fascetti AJ, et al: Pet feeding practices of dogs and cat owners in the United States and Australia. J Am Vet Med Assoc 232:687–694, 2008. AUTHOR: LISA P. WEETH EDITOR: KATHRYN E. MICHEL
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Malignant Fibrous Histiocytoma
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Malignant Fibrous Histiocytoma BASIC INFORMATION DEFINITION An uncommon primary tumor made up of fibrous and inflammatory cells thought to arise from a primitive mesenchymal cell. It is not to be confused with malignant histiocytosis (histiocytic sarcoma), a disease of localized or multisystemic histiocytic infiltration (see p. 535).
SYNONYMS Epithelioid sarcoma, giant cell fascial sarcoma, giant cell tumor, reticulum cell sarcoma
EPIDEMIOLOGY SPECIES, AGE, SEX: Malignant fibrous histiocytoma is an uncommon tumor of the skin and subcutaneous tissue of dogs and cats, and can also occur in the spleen in dogs. This tumor type has been reported at injection sites in cats (see p. 610 ). GENETICS & BREED PREDISPOSITION: Golden retrievers and rottweilers may be overrepresented.
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES Different pathologic types include storiform-pleomorphic, inflammatory, and a giant cell variant. The giant cell variant, which occurs in dogs but is very rare in cats, is associated with metastasis and a poor prognosis. Malignant fibrous histiocytoma has been reported at injection sites in cats (see p. 610). HISTORY, CHIEF COMPLAINT Pets with malignant fibrous histiocytomas in the skin and subcutaneous tissue usually present for a progressively enlarging mass noticed by the owner. Dogs with malignant fibrous histiocytomas of the spleen usually present for signs related to an abdominal mass or abdominal hemorrhage. PHYSICAL EXAM FINDINGS Malignant fibrous histiocytomas in the skin and subcutaneous tissue often present as firm, palpable masses. Occasionally they are hairless or ulcerated. Regional lymphadenomegaly may be present secondary to inflammation or (rarely) lymph node metastasis. Dogs with splenic tumors may present with abdominal mass, pain, or abdominal enlargement.
ETIOLOGY AND PATHOPHYSIOLOGY Malignant fibrous histiocytomas are typically firm, slow-growing tumors that commonly infiltrate into surrounding soft tissues and along fascial planes. Overall they have a moderate metastatic potential, but some variants or grades may be more likely to metastasize (see prognosis). Lesions caused by malignant fibrous histiocytoma depend on the location of the primary tumor. These tumors are considered a separate entity from the other histiocytic diseases. Peripheral tumors can metastasize, but usually to the lungs.
DIAGNOSIS DIAGNOSTIC OVERVIEW Definitive diagnosis can only be confirmed via histopathologic analysis, although additional testing such as diagnostic imaging is often helpful in defining the extent of the tumor.
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DIFFERENTIAL DIAGNOSIS Other skin and subcutaneous tumors: Soft-tissue sarcoma Mast cell tumor Others Other splenic tumors: Hemangiosarcoma Lymphoma Others
INITIAL DATABASE Fine-needle aspirate cytologic analysis may help identify the tumor type before other diagnostics. Three-view thoracic radiographs to rule out pulmonary metastases Radiographs of the affected area may reveal involvement of underlying bone. Abdominal ultrasound to identify splenic tumors and rule out metastasis. However, abdominal ultrasound cannot be relied on to differentiate malignant fibrous histiocytoma from other splenic tumors. Fine needle aspirate of draining lymph nodes to help rule out metastasis
ADVANCED OR CONFIRMATORY TESTING CT or MRI may be necessary to delineate the local extent of the tumor and plan for surgery or radiation therapy. Biopsy: diagnosis of malignant fibrous histiocytoma is based on histopathologic evaluation of tissue. Special stains may be necessary to differentiate malignant fibrous histiocytoma from other soft-tissue sarcomas, especially poorly differentiated tumors. Care should be taken to differentiate these tumors from other histiocytic tumors, including histiocytic sarcoma and malignant histiocytosis (see p. 535). These other tumors usually have a different prognosis and recommended course of treatment. Histopathologic grade of the tumor is necessary for determining the prognosis and treatment of most soft tissue sarcomas (see p. 610). Histopathologic grading typically involves using the general grading system for soft-tissue sarcomas based on mitotic rate, percent necrosis, and degree of differentiation. Tumors are graded as low, intermediate, or high grade. In most cases, high-grade tumors are larger and more invasive, but gross size and invasiveness cannot be used as a substitute for histopathologic grading.
TREATMENT TREATMENT OVERVIEW Definitive treatment is based on complete eradication of the primary tumor whenever possible. However, additional treatment such as chemotherapy may be indicated to prevent or delay metastases or in dogs with high-grade tumors, the giant-cell variant of this tumor or tumors that have already metastasized. Palliative treatment options, such as palliative radiation, may help control pain or discomfort in patients with advanced tumors or in patients where definitive treatment cannot be tolerated.
ACUTE AND CHRONIC TREATMENT Aggressive surgical resection, radiation therapy, and/or chemotherapy may be used for treatment (see p. 610). Chemotherapy may be indicated to delay or prevent metastasis for malignant fibrous histiocytoma affecting the spleen, high-grade tumors, or giant-cell variants of malignant fibrous histiocytoma.
POSSIBLE COMPLICATIONS Complications of treatment depend on types of treatments and location of the primary tumor.
RECOMMENDED MONITORING After appropriate local treatment, follow-up examination should be done routinely to monitor for recurrence (every 2-3 months) and metastasis (thoracic radiographs at 6 months and 1 year). High-grade tumors may require more frequent monitoring (at least every 2-3 months) for metastases during and after chemotherapy administration.
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PROGNOSIS AND OUTCOME Prognosis is excellent for histologically low- to intermediate-grade tumors with appropriate treatment. This includes either surgical resection with clean histopathologic margins or incomplete resection combined with radiation therapy. Dogs with the giant-cell variant of this tumor often have metastases at the time of diagnosis or soon afterward, and prognosis is usually poor despite treatment. Few cats with this variant develop metastases. Dogs with splenic tumors are more likely to develop metastases and therefore have a poor prognosis. High-grade malignant fibrous histiocytoma: like other soft-tissue sarcomas, prognosis is considered guarded based on the increased likelihood for metastases.
PEARLS & CONSIDERATIONS COMMENTS Aside from the giant-cell variant, malignant fibrous histiocytoma should be considered like other soft tissue sarcomas (see p. 1034) in treatment and prognosis. Tumors at injection sites in cats should be treated like injection-site sarcomas (see p. 610).
CLIENT EDUCATION Pet owners can be educated to monitor their pets for palpable or visible masses and have them evaluated in a timely fashion. Early detection may allow for easier treatment via surgery and may help avoid the need for radiation therapy.
SUGGESTED READING Liptak JM, Forrest LJ: Soft tissue sarcomas. In Withrow SJ, Vail DM, editors: Small animal clinical oncology, Philadelphia, 2007, WB Saunders, pp 425–454. Waters CB, et al: Giant cell variant of malignant fibrous histiocytoma in dogs: 10 cases (1986-1993). J Am Vet Med Assoc 205:1420–1424, 1994. AUTHOR: JOHN FARRELLY EDITOR: KENNETH M. RASSNICK
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Malassezia Dermatitis
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Malassezia Dermatitis BASIC INFORMATION DEFINITION An extremely common pruritic dermatosis caused by the overgrowth of Malassezia spp. yeast. Most infections are caused by the lipophilic unicellular organism Malassezia pachydermatis.
SYNONYMS Malasseziasis, yeast dermatitis
EPIDEMIOLOGY SPECIES, AGE, SEX: Very common in dogs of all ages; uncommon in cats of any age; either sex GENETICS & BREED PREDISPOSITION: May occur in any breed of dog or cat. Terriers, shih tzus, dachshunds, shar-peis, spaniels, hounds, and German shepherd dogs seem predisposed, likely to underlying conditions favorable to yeast overgrowth. Devon Rex cats are more susceptible. RISK FACTORS Excessive sebum production, poor sebum quality, cutaneous moisture accumulation (particularly in skin folds), a disrupted epidermal surface, and altered host immune defenses. These alterations are often the result of primary underlying diseases (e.g., allergy, endocrinopathy). Specific disorders that predispose to cutaneous yeast overgrowth include allergic skin disease (e.g., atopic dermatitis, food allergy, flea allergy, contact allergy), endocrinopathies (e.g., iatrogenic or spontaneous hyper-adrenocorticism, hypothyroidism, hyperthyroidism, diabetes mellitus), primary or secondary cornification disorders, folliculitis (e.g., pyoderma, demodicosis, dermatophytosis), ectoparasitism (e.g., demodicosis, sarcoptic mange, notoedric mange), metabolic diseases (e.g., superficial necrolytic dermatitis, zinc-responsive dermatosis), nutritional deficiencies, cutaneous or internal neoplasia, and in cats, retroviral infections. CONTAGION & ZOONOSIS:Malassezia yeasts have been transmitted from the contaminated hands of dog-owning health care workers to infants in an intensive care nursery, causing mycotic sepsis. Therefore Malassezia yeast should be considered a potential zoonotic agent, especially in immunoincompetent individuals. GEOGRAPHY AND SEASONALITY:Malassezia dermatitis may occur more frequently in humid geographic regions, and/or with underlying causes that worsen seasonally (e.g., atopic dermatitis).
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES Localized dermatitis: involving the face (perioral, muzzle, ears), ventral aspect of the trunk (neck, axillae, inguinal area), perineal region (ventral tail, perianal area), and paw (interdigital web and nail fold) Generalized dermatitis: involving several regions as noted above HISTORY, CHIEF COMPLAINT: Intense pruritus: most common chief complaint. Rancid offensive odor; an oily coat; hair loss (alopecia); redness (erythroderma); thickened, elephant-like skin (lichenification); scaling (dander); and/or relapsing and remitting dermatitis unresponsive to antibiotics or glucocorticoids are also frequently noted. PHYSICAL EXAM FINDINGS Skin lesions reflect existing pruritus and seborrhea and are not specific to Malassezia dermatitis. Lesional skin may be erythematous, hyperpigmented, hyperkeratotic, lichenified, scaly, greasy or dry, alopecic, saliva-stained, and excoriated. Hyperpigmented lichenification implies chronicity. Intertriginous areas (skin folds) are typically affected. Occasionally, yellow/orange to slate gray seborrheic plaques are present in body folds. A brown waxy discharge may be evident in the nail folds, signifying paronychia.
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A brown discoloration around the base of white nails may be seen in dogs with Malassezia pododermatitis. Follicular casts (keratosebaceous material adhered to the proximal hair shaft) might be suggestive of an underlying keratinization disorder. Cats, particularly Devon Rex, may present with alopecia, erythema, and greasy exudation of the axillae, groin, and paws.
MALASSEZIA DERMATITISMalassezia dermatitis in a miniature poodle. Alopecia, erythema, and lichenification on the ventral neck. (Copyright Dr. Manon Paradis.)
ETIOLOGY AND PATHOPHYSIOLOGY Malassezia spp. yeasts are part of the normal skin microflora. They become opportunistic invaders when changes occur in the cutaneous microclimate (e.g., lipid composition, relative humidity) or defense mechanisms (e.g., epidermal barrier dysfunction, immunosuppression). Once colonization takes place, yeasts may release proteases and lipases that alter cutaneous homeostasis, allowing for continued yeast overgrowth. In some atopic dogs with cytologic demonstration of yeasts, Malassezia may elicit a type-1 cutaneous hypersensitivity reaction.
DIAGNOSIS DIAGNOSTIC OVERVIEW Malassezia dermatitis should be considered in any pruritic dog or cat. Confirmation requires typical clinical signs, cytological demonstration of yeast, and most importantly, response to antifungal therapy. Underlying primary conditions must be identified and corrected. Importantly, Devon Rex cats may not have an identifiable predisposing disease.
DIFFERENTIAL DIAGNOSIS Since Malassezia dermatitis is a secondary complication of underlying disorders in most cases, the chief differential diagnosis consists of identifying whether the underlying disorder (see Risk Factors, above) exists in an uncomplicated state or if secondary Malassezia dermatitis is present.
INITIAL DATABASE Skin cytologic analysis is performed on every case with compatible historical/physical findings. Cytologic examination specimens can be obtained by direct impressions, acetate tape preparations, or dry or wet swabs.
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Malassezia are ovoid, monopolar budding yeasts that resemble the shape of footprints or peanuts. They are 3-8 mcm in diameter (the same size as, or slightly smaller than, a red blood cell). Yeasts are best visualized using high power (40x) or oil immersion (100x). Multiple skin scrapings to exclude superficial and deep ectoparasites Especially with cats: dermatophyte culture to exclude ringworm
ADVANCED OR CONFIRMATORY TESTING Biopsy and histopathologic analysis: rarely necessary Suggestive but nonspecific findings include parakeratotic hyperkeratosis, epidermal hyperplasia, superficial perivascular dermatitis, and possibly eosinophilic microabscesses. Occasionally, yeast may be found in the superficial keratin layer and/or in hair follicles. Other histopathologic findings may represent changes associated with the underlying dermatosis. Loss of surface scale during processing may decrease the chance of finding yeast organisms. Elimination diet trial to exclude food allergy Intradermal and/or immunoglobulin (Ig)E serologic testing if history and clinical findings are supportive of atopic dermatitis CBC, serum chemistry panel, and urinalysis to screen for internal diseases Hormonal testing (e.g., screening tests for hyperadrenocorticism, hypothyroidism, and diabetes mellitus) Feline retroviral testing
TREATMENT TREATMENT OVERVIEW The main goal your job is to reduce pruritus and remove seborrhea. This is accomplished by killing yeast and controlling for underlying primary diseases and risk factors.
ACUTE GENERAL TREATMENT Keratomodulating (antiseborrheic) and antiyeast topical therapies (e.g., sulfur/salicylic acid, phytosphingosine, benzoyl peroxide, selenium sulfide, boric/acetic acid, miconazole, clotrimazole, ketoconazole, terbinafine, enilconazole, lime sulfur, or chlorhexidine) can be applied daily to weekly depending on the formulation used (e.g., shampoo, solution, lotion, spray, wipe, powder). Systemic antifungal therapy may be warranted for severe infections or those not responding to sole topical therapy. Duration of systemic therapy should persist beyond (e.g., 1-2 weeks) clinical and cytologic improvement (usually a minimum of 3-4 weeks). Griseofulvin has no effect against Malassezia species. Ketoconazole, 5-10 mg/kg PO q 24 h with food; other azoles better suited for cats, or Itraconazole, 5-10 mg/kg PO q 24 h with (capsules) or without (suspension) food, or Fluconazole, 2.5-5 mg/kg PO q 24 h (generic available in some countries), or Terbinafine, 30 mg/kg PO q 24 h with food Because dogs with Malassezia dermatitis frequently have concurrent staphylococcal pyoderma, treating any secondary bacterial infection with oral antibiotics at an appropriate dose and duration (minimum 21 days) will help improve cutaneous signs.
CHRONIC TREATMENT Therapy for underlying predisposing diseases Topical keratomodulating and/or antiyeast therapy at reduced frequencies of application if possible Azole pulse therapy can be used for remitting and relapsing episodes of Malassezia dermatitis, as these drugs concentrate in the skin. Typically, the same initial dose is prescribed for 2 consecutive days per week or given daily for 1-week-on/1-to4-weeks-off cycles after the initial induction dose described in Acute Treatment above.
DRUG INTERACTIONS Azole therapy may alter the metabolism or distribution of other prescribed medication by inhibiting cytochrome P450 metabolizing enzymes and P-glycoprotein transporting pumps. Terbinafine does not inhibit these enzymes. Specifically, azoles cannot be given with macrocyclic lactones (e.g., avermectins); if so, dosage reduction and close monitoring is required (see p. 706).
POSSIBLE COMPLICATIONS Idiosyncratic cutaneous adverse reactions to topical therapies (e.g., pruritus, erythroderma, papular rash, pustulation, vesiculation, necrosis, ulceration) may occur on the patient or person applying therapy and must be considered along with
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reassessment of possible underlying causes in “refractory” cases of Malassezia dermatitis. The patient may have adverse reactions to systemic azoles (e.g., vomiting, diarrhea, hepatotoxicity, vasculitis, lightening of haircoat, pruritus). Ketoconazole may inhibit cortisol synthesis at doses greater than 10 mg/kg/d.
RECOMMENDED MONITORING Clinical signs and skin cytology every 2-4 weeks during therapy Other monitoring recommendations are at the discretion of the clinician, based on underlying predisposing diseases.
PROGNOSIS AND OUTCOME Failure to detect and treat underlying problems will result in partial treatment success, treatment failure, or relapse. For incurable diseases (e.g., primary cornification disorders), therapy for Malassezia dermatitis may need to be lifelong.
PEARLS & CONSIDERATIONS COMMENTS Malassezia dermatitis is one of the most overlooked causes of pruritus in the dog. Malassezia dermatitis tends to occur in body areas rich in sebaceous glands and high in relative humidity, and is commonly associated with allergic dermatitis. How many yeast are cytologically significant? Finding any yeast from typical clinical lesions is significant. Dogs with atopic dermatitis may be hypersensitive to Malassezia, resulting in yeast numbers disproportionate to the level of pruritus experienced by the animal. Skin culture for Malassezia yeast is not recommended in clinical practice, as these organisms are residents on the skin. Biopsy with histopathologic evaluation is not considered superior to cytologic evaluation for the diagnosis of Malassezia dermatitis (most of the surface scale is lost during biopsy processing) but may be useful in the diagnosis of primary skin disorders in addition to which Malassezia dermatitis is a secondary phenomenon. Do not use selenium sulfide on cats; it is too irritating to their skin. Enilconazole is not approved for small-animal use in some countries. Griseofulvin has no effect against Malassezia species. Cats tend to have gastrointestinal upset with oral ketoconazole, so other systemic antifungals are preferred. When given in tablet or capsule form, the azole drugs, ketoconazole and itraconazole, are best absorbed systemically if administered with food; failure to do so may reduce bioavailability of these drugs by up to 40%.
PREVENTION Correctly identifying and treating for all underlying predisposing factors favorable to yeast overgrowth
TECHNICIAN TIPS Technicians managing patients with Malassezia dermatitis should be proficient in collection and examination of cytologic skin samples, and capable of instructing owners on appropriate use of topical therapy.
SUGGESTED READING Åhman S, Perrins N, Bond R: Treatment of Malassezia pachydermatis-associated seborrheic dermatitis in Devon Rex cats with itraconazole—a pilot study. Vet Dermatol 18:171–174, 2007. Chen TA, Hill PB: The biology of Malassezia organisms and their ability to induce immune responses and skin disease. Vet Dermatol 16:4–26, 2005. Negre A, Bensignor E, Guillot J: Evidencebased veterinary dermatology: a systematic review of interventions for Malassezia dermatitis in dogs. Vet Dermatol 20:1–12, 2008. AUTHOR: ADAM P. PATTERSON EDITOR: MANON PARADIS
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Macadamia Nut Toxicosis
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Macadamia Nut Toxicosis BASIC INFORMATION DEFINITION Acute and often self-limiting toxicosis of dogs resulting from ingestion of macadamia nuts. It is characterized by paresis, depression, vomiting, ataxia, tremors, hyperthermia, abdominal pain, lameness, and/or stiffness. Toxicosis can occur after ingestion of commercially available macadamia nuts or macadamia nut-containing cookies or candies.
EPIDEMIOLOGY SPECIES, AGE, SEX Currently, the syndrome has been described in dogs only. All breeds, ages, and both sexes are susceptible. RISK FACTORS Dogs develop signs of toxicity after ingesting 2.2-62.4 g/kg macadamia nuts. Dogs will readily eat large amounts of chocolate-coated macadamia nuts. GEOGRAPHY AND SEASONALITY Macadamia nuts are obtained from Macadamia integrifolia and Macadamia tetraphylla trees, mostly cultivated in Hawaii in the United States. Toxicosis can occur year round, although it is more likely to occur during holiday seasons.
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES Severity and onset of signs will depend on amount of macadamia nuts ingested. Majority of dogs show clinical signs within 12 hours after ingestion. Clinical signs usually resolve within 24-48 hours. HISTORY, CHIEF COMPLAINT History of exposure to macadamia nuts Evidence of macadamia nuts in the vomitus or in the stool Hind limb weakness, depression, vomiting PHYSICAL EXAM FINDINGS Hind limb weakness with no evidence of central nervous system involvement, musculoskeletal pain, or trauma Rarely, generalized weakness is possible. Forelimb weakness without hind limb weakness is inconsistent with macadamia nut toxicosis. Respiratory muscle paralysis likewise has not been a feature of macadamia nut toxicosis in dogs. Mild tremor of hind limbs Depression Vomiting Ataxia Hyperthermia (due to tremor; not true fever)
ETIOLOGY AND PATHOPHYSIOLOGY Exact cause and mechanism of macadamia nut toxicosis are not clear. Evidence suggests that the syndrome is dog specific. Toxic principle in macadamia nuts is not known at this time.
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DIAGNOSIS DIAGNOSTIC OVERVIEW Diagnosis is based entirely on history and physical signs: observed or suspected ingestion of macadamia nuts, especially if concurrent signs (paresis, ataxia, stiffness, hyperthermia, and/or vomiting within 12 hours of exposure) are present, is sufficient to warrant treatment.
DIFFERENTIAL DIAGNOSIS Rule out other toxicoses that can cause hind limb weakness, ataxia, and vomiting: Ethylene glycol Cholinesterase inhibitor pesticides: organophosphates and carbamates Marijuana (dogs) Phenoxy herbicide (2,4 D) Coral snake bite Bromethalin (dogs) Rule out nontoxic causes for hindlimb weakness and ataxia (see p. 837): Systemic disturbances (e.g., anemia, acid-base or electrolyte abnormalities, cardiac arrhythmias) Neuromuscular disorders (polyradiculoneuritis, myasthenia gravis, tick paralysis, botulism) Orthopedic disorders Trauma Right-to-left shunting patent ductus arteriosus (weakness confined to hind limbs)
INITIAL DATABASE Abdominal radiographs (may show a large amount of ingesta in the gastrointestinal tract) Examination of stomach contents for presence of macadamia nuts (if vomiting occurs) Rectal palpation may show presence of macadamia nuts in feces. Body temperature A complete medical examination is needed if concurrent ingestion of other harmful compound is suspected and to rule out any preexisting condition.
ADVANCED OR CONFIRMATORY TESTING Serum biochemistry profile: mild elevation in serum triglycerides and serum alkaline phosphatase may be noted but is nonspecific.
TREATMENT TREATMENT OVERVIEW Treatment is general and supportive: induction of emesis and administration of activated charcoal if ingestion is suspected or confirmed and patient is stable. Management of complications of severe intoxications (e.g., nursing care if recumbent; treatment of hyperthermia) is applied as needed. Most clinical signs resolve within 24-48 hours with or without treatment.
ACUTE GENERAL TREATMENT Decontamination of patient: Emesis (within 2-4 hours after ingestion in dogs not showing overt clinical signs; see p. 1364 ); or Apomorphine (0.03-0.04 mg/kg IV or IM, or crush tablet portion with water and instill into conjunctival sac, rinse after emesis); or Hydrogen peroxide 3% (2 mL/kg, max 45 mL PO, repeat in 10-15 minutes if no vomiting) Activated charcoal: Give after inducing emesis or if a few hours have elapsed after exposure; administer activated charcoal (1-4 g/kg) with a cathartic such as 70% sorbitol (3 mL/kg) orally. Warm tap water enema (5-10 mL/ kg) with large ingestion may help move the macadamia nuts more quickly through the gastrointestinal tract. Supportive care: Administer IV fluids as needed. Thermoregulation (cold bath, cooling fans if needed)
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RECOMMENDED MONITORING Serum electrolytes, biochemistry profile, and triglycerides in severely affected dogs
PROGNOSIS AND OUTCOME Generally, excellent prognosis Dogs recover with or without treatment within 24-48 hours
PEARLS & CONSIDERATIONS COMMENTS Consider concurrent methylxanthine (chocolate) toxicosis if macadamia nuts were covered with chocolate and large amounts of macadamia have been ingested. Mild uncomplicated cases may resolve with home observation for 12 hours.
PREVENTION Keep macadamia nuts out of reach of dogs
SUGGESTED READING Gwaltney-Brant SM: Macadamia nuts. In Peterson ME, Talcott PA, editors: Small animal toxicology, ed 2, St Louis, 2006, Saunders Elsevier, pp 817–821. AUTHOR: SHARON WELCH EDITOR: SAFDAR A. KHAN 1ST EDITION AUTHOR: MOAZZAM KHAN
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Nystagmus
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Nystagmus BASIC INFORMATION DEFINITION Repetitive, rapid, and involuntary movement of the globe of the eye in a horizontal, rotary, or vertical manner
EPIDEMIOLOGY SPECIES, AGE, SEX Any age or breed, either sex Idiopathic vestibular disease is more common in older dogs (>8 years) but affects cats of all ages. GENETICS & BREED PREDISPOSITION Cats: pendular nystagmus occurs in otherwise normal Siamese cats. Vestibular nystagmus is a congenital abnormality in Siamese, Tonkinese, and Burmese breeds. Dogs: vestibular nystagmus is a congenital abnormality in the Doberman pinscher, cocker spaniel, German shepherd, and other breeds. GEOGRAPHY AND SEASONALITY: Idiopathic vestibular disease in cats may predominate in late summer/early fall. ASSOCIATED CONDITIONS & DISORDERS: Frequently associated with head tilt, ataxia, circling, vomiting, and anorexia
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES: Types of nystagmus: Vestibular nystagmus: eye movements are faster in one direction than in the other (fast phase and slow phase for each cycle of the nystagmus); also called jerk nystagmus. Pendular nystagmus: no fast or slow phase. Pendular nystagmus is uncommon, is a congenital anomaly, and is not associated with vestibular disease or progression of signs.
HISTORY, CHIEF COMPLAINT Vestibular nystagmus usually is acute in onset (e.g., idiopathic vestibular disease): The animal may initially exhibit vomiting, followed by vestibular ataxia, circling, or even whole-body rolling. The owners may not notice the nystagmus. Much less common are pendular nystagmus or congenital vestibular nystagmus that are present from birth and not associated with deteriorating vestibular function; chief complaint is limited to eye movements.
PHYSICAL EXAM FINDINGS Nystagmus due to peripheral vestibular disease (not all signs may be present): Jerk nystagmus (horizontal or rotary) with fast phase away from the side of the vestibular lesion and away from the side of the head tilt The nystagmus may be difficult to observe, especially in the cat, and may be observed only when the animal's head is changed in position (especially dorsal extension of the neck) or when the animal is placed on its back. Head tilt Circling Ataxia with falling to the side of the lesion and to the side of the head tilt Nystagmus due to central vestibular disease (not all signs may be present): Jerk nystagmus (horizontal, rotary, or vertical) with fast phase away from the side of the vestibular lesion and away from the side of the head tilt Head tilt toward the side of the lesion Circling Ataxia
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Nystagmus
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Proprioceptive deficits, motor weakness on the side of the lesion Central vestibular disease may (rarely) cause paradoxical signs (the nystagmus fast phase is away from the side of the lesion). Proprioceptive deficits indicate the true side of the lesion (ipsilateral). Other cranial nerve deficits (V, VI, VII)
ETIOLOGY AND PATHOPHYSIOLOGY The vestibular system allows the body to know its position in space (proprioception) relative to head position, gravity, and linear or rotary acceleration. Sensory fibers in the peripheral vestibular system send impulses to the nuclei of cranial nerves III, IV, and VI, coordinating eye movements and allowing the eyes to remain centered on an object until it is beyond the visual field; then, the eyes are able to jerk back to again center on an object (“watching railroad cars go by”). Damage to the vestibular system can stimulate these eye movements inappropriately, producing nystagmus.
DIAGNOSIS DIAGNOSTIC OVERVIEW Nystagmus is specific to vestibular dysfunction. Therefore, the diagnostic process identifies whether the brain (central) or inner/middle ear (peripheral) is the site of the lesion, which can usually be determined with a clinical neurologic exam. Further testing is selected based on a differential diagnosis list elaborated from history, physical exam, and neurologic exam findings.
DIFFERENTIAL DIAGNOSIS Nystagmus from peripheral vestibular disease: Idiopathic Bacterial infection (otitis media/interna) Neoplasia Hypothyroidism (rare) Post surgery on the middle ear (ear ablation in the dog, removal of polyps in the cat) Congenital or hereditary Central vestibular nystagmus: Infection Neoplasia Trauma Pendular nystagmus: congenital disease affecting the visual pathway
INITIAL DATABASE Neurologic examination (see p. 1311 ) CBC, serum biochemistry profile, urinalysis: usually unremarkable Otoscopic exam Otitis externa, polyp, blood (head trauma) possible Careful examination may reveal fluid in the middle ear for cases with infectious causes Radiographs of the tympanic bullae
ADVANCED OR CONFIRMATORY TESTING MRI or CT of the middle ear and posterior fossa of the brain (see p. 1302 and p. 1233 ) Cerebrospinal fluid (CSF) analysis if signs of central vestibular disease are present (see p. 1228 ) For cases in which there is no nystagmus but other clinical signs suggest vestibular disease, a postrotary nystagmus evaluation may be performed: The animal is rotated in a circle first in one direction for 10 rotations, and the duration of nystagmus is noted. The animal is then rotated in the opposite direction, and the duration of the postrotary nystagmus is again noted. Postrotary nystagmus is usually less or absent when the animal is spun away from the side of the lesion.
TREATMENT TREATMENT OVERVIEW
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Nystagmus
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Treatment goals are improvement in the clinical condition by decreasing nausea and anorexia, and treatment of the primary cause when possible.
ACUTE GENERAL TREATMENT Nystagmus is a clinical sign associated with various underlying causes. Therefore, treatment is aimed at the primary disorder. Since it may be difficult for the animal to walk or stand, good nursing care is very important: The animal should be able to get to food and water and should be cleaned after urinating or defecating so urine or fecal scalding is avoided.
POSSIBLE COMPLICATIONS Treatment of otitis with products that contain aminoglycoside antibiotics may be detrimental (ototoxic), particularly if the tympanum is not intact.
PROGNOSIS AND OUTCOME The prognosis for idiopathic vestibular disease and nystagmus caused by otitis media/interna are good to excellent for both dogs and cats, but recurrence is possible. A head tilt may remain after resolution of all other signs. The prognosis for neoplasia and virtually all causes of central vestibular nystagmus is guarded to poor.
PEARLS & CONSIDERATIONS COMMENTS Idiopathic peripheral vestibular disease causes nystagmus in the majority of cases (for cats and dogs); the condition should resolve spontaneously in 1-2 weeks. Idiopathic vestibular disease is a diagnosis of exclusion. Nearly all patients with nystagmus caused by central vestibular disease will have other central nervous system (CNS) signs (proprioceptive defects, weakness, other cranial nerve involvement).
CLIENT EDUCATION When idiopathic vestibular disease is the primary consideration, the owners need to know that the problem will usually resolve with time.
SUGGESTED READING Lorenz M, Kornegay J: Ataxia of the head and the limbs. In Lorenz M, Kornegay J, editors: Handbook of veterinary neurology. Philadelphia, 2004, WB Saunders, pp 219–243. AUTHOR: JAMES B. MILLER EDITOR: ETIENNE CÔTÉ
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Nutritional Secondary Hyperparathyroidism
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Nutritional Secondary Hyperparathyroidism BASIC INFORMATION DEFINITION Chronic elevation of circulating parathyroid hormone (PTH) resulting from low serum ionized calcium concentrations (iCa) due to deficiency of absorbed calcium or vitamin D or due to a calcium/phosphorus (Ca:P) imbalance
SYNONYMS NSHP, nutritional osteodystrophy. The term rickets describes bony changes consistent with a vitamin D deficiency.
EPIDEMIOLOGY SPECIES, AGE, SEX: Nutritional secondary hyperparathyroidism (NSHP) is seen in young, growing animals of any sex or species that have been fed an improperly formulated diet. The condition is occasionally seen in older animals, especially those with malabsorptive disorders. GENETICS & BREED PREDISPOSITION: Young, large-breed dogs may be at increased risk because of rapid growth rate. RISK FACTORS Animals fed improperly formulated homemade (especially all-meat) diets, particularly during growth. Such diets typically contain decreased calcium and/or increased phosphorus, with a Ca:P ratio of =1:16 (1:1-2:1 for dogs and 1:1-1.5:1 for cats is recommended) and inadequate vitamin D. Exotic pets, since dietary requirements for calcium, phosphorus, and vitamin D are not always known Animals with severe gastrointestinal disease that limits calcium or vitamin D absorption GEOGRAPHY AND SEASONALITY: Condition may be more common in winter months in some indoor-housed exotic pets, owing to decreased exposure to sunlight. ASSOCIATED CONDITIONS & DISORDERS: Animals may have decreased bone density or fractures related to increased circulating PTH.
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES Inadequate dietary calcium or vitamin D concentration or altered dietary Ca:P ratio Inadequate absorption of dietary calcium and vitamin D due to intestinal disease HISTORY, CHIEF COMPLAINT History of a poorly formulated homemade diet Excessive use of supplements such as meats, vitamins, and minerals History of malabsorption due to intestinal disease Reluctance to walk, stiff gait, bone pain, lameness, or limb deformities (pathologic bone fractures); tooth loss; ± neurologic signs if the axial skeleton is involved Signs of hypocalcemia: twitching, tremors, stiffness, or seizures (rare)
PHYSICAL EXAM FINDINGS Bone palpation may elicit pain; fractures may be noted. Swelling of costochondral junctions or metaphyses may be evident.
ETIOLOGY AND PATHOPHYSIOLOGY Inadequate calcium absorption decreases iCa, increasing PTH production.
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Nutritional Secondary Hyperparathyroidism
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Inadequate absorbed vitamin D decreases calcitriol production, decreasing iCa and increasing PTH production. PTH stimulates renal 1,25-dihydroxyvitamin D (calcitriol, the active metabolite of vitamin D) synthesis and bone resorption and increases renal calcium resorption and phosphorus excretion. Calcitriol also stimulates bone resorption to raise iCa into the normal range and decreases PTH production. Excessive PTH production reduces bone density, and pathologic fractures may occur. Excess circulating phosphorus also inhibits calcitriol synthesis and can lower iCa by the mass law effect.
DIAGNOSIS DIAGNOSTIC OVERVIEW The diagnosis is strongly suspected in young animals with a history of an inadequate diet, radiographic evidence of diffuse bone loss, and pathologic fractures.
DIFFERENTIAL DIAGNOSIS Other causes of lameness, bone pain, loss of bone density, or fractures, including congenital problems in young animals Renal secondary hyperparathyroidism (ruled out based on serum biochemistry profile and urinalysis) Hyperadrenocorticism associated secondary hyperparathyroidism in older dogs (ruled out based on adrenal function testing and clinical signs) Genetic defects in calcitriol production or utilization (rare). Clinical signs are the same in the absence of compatible diet history or malabsorptive disorder.
INITIAL DATABASE CBC and serum biochemical profile: serum total calcium concentration normal to low. NOTE: Serum phosphorus and alkaline phosphatase may be elevated in normal animals, especially in those who are young and growing. Radiography of the skull, axial skeleton, and limbs: diffusely decreased cortical bone density; fractures possible. Dietary history
ADVANCED OR CONFIRMATORY TESTING Measure PTH (increased), iCa (low to normal), and 25-hydroxyvitamin D (25-OH-D; typically low) concentrations to confirm the diagnosis. Serum calcitriol determination, although helpful, currently is not readily available. Vitamin/mineral analysis of homemade diets may be useful.
TREATMENT TREATMENT OVERVIEW Goals of treatment are to increase intestinal absorption of calcium and vitamin D and decrease PTH production.
ACUTE GENERAL TREATMENT Feed a properly formulated diet. Stop the feeding of all supplements. Supportive therapy for pain or fractures (cage rest or limited activity as indicated) Treatment of malabsorption when present Dietary supplementation with oral calcium (25-50 mg/kg elemental Ca [e.g., 62.5-125 mg/kg calcium carbonate] daily) if clinical signs of hypocalcemia are present, discontinuing when signs resolve (see p. 576)
CHRONIC TREATMENT Ensure that a properly formulated diet is fed. If a homemade diet is fed, a sample of the diet may be sent for vitamin D and mineral analysis. Supplemental oral calcium may be indicated in cases of chronic malabsorption.
RECOMMENDED MONITORING
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Clinicians should repeat tests of PTH, iCa, and 25-OH-D concentrations 3-4 weeks after initiating treatment. PTH should be decreased and 25-OH-D increased compared to pretreatment values. Clinicians should monitor the animals monthly until levels are normal. Clinicians can measure PTH, iCa, and 25-OH-D concentrations every 3-4 months, even if secondary hyperparathyroidism has resolved and if intestinal malabsorption is present. Clinicians should order repeat radiography tests to assess bone density and fracture healing.
PROGNOSIS AND OUTCOME Depends on presence of pathologic fractures, which worsen the prognosis because of pain and a potentially long convalescent period. Incidentally discovered NSHP that is due to inappropriate diet typically carries a good prognosis. For animals with malabsorption, the prognosis depends on the underlying cause and effectiveness of therapy.
PEARLS & CONSIDERATIONS PREVENTION Clinicians should inform owners to: Feed their pets nutritionally complete and balanced pet foods rather than improperly formulated homemade diets. Avoid supplementing balanced diets with meats, vitamins, or minerals.
CLIENT EDUCATION Clinicians should explain skeletal problems associated with deficiencies of calcium or vitamin D or with the excess of phosphorus to clients feeding homemade diets to their pets, especially to young, growing animals. Clinicians should have the adequacy of homemade diets verified by a veterinary nutritionist. Clinicians should suggest periodic nutrient analysis of homemade diets, especially for vitamin D and mineral content.
SUGGESTED READING Cook SD, et al: A quantitative histologic study of osteoporosis produced by nutritional secondary hyperparathyroidism in dogs. Clin Orthop 175:105–120, 1983. DeLay J, Laing J: Nutritional osteodystrophy in puppies fed a BARF diet. AHL Newsl 6(2): 23, 2002. Tomsa K, et al: Nutritional secondary hyperparathyroidism in six cats. J Small Anim Pract 40(11):533–539, 1999. AUTHOR: PATRICIA A. SCHENCK EDITOR: KATHRYN E. MICHEL
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Nonsteroidal Antiinflammatory Drug Toxicosis
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Nonsteroidal Antiinflammatory Drug Toxicosis BASIC INFORMATION DEFINITION A common toxicosis secondary to acute overdose or chronic administration of a nonsteroidal antiinflammatory drug (NSAID), most commonly affecting the gastrointestinal (GI) tract or kidneys. Hepatopathy is also possible.
EPIDEMIOLOGY SPECIES, AGE, SEX Cats generally more sensitive than dogs because of deficiency in enzymes which metabolize these drugs. Most cases are reported in dogs. All breeds and both sexes are susceptible. Elderly and very young animals are at higher risk. GENETICS & BREED PREDISPOSITION: Labrador retrievers are not considered at greater risk for developing hepatic adverse effects from carprofen administration, despite the fact that one third of the initially reported cases of hepatic syndrome were in Labradors. RISK FACTORS Preexisting renal, cardiovascular, or hepatic disease may increase severity of signs. Dehydration, hypotension, and concurrent use of other potentially nephrotoxic drugs can potentiate signs. Concurrent use of other NSAIDs or corticosteroids may lead to severe complications. Hypoproteinemia or concurrent use of other highly protein-bound drugs can result in higher active drug levels.
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES Acute toxicosis: after a single large ingestion (usually 5-10 times the recommended dose) Chronic toxicosis: in sensitive animals after NSAID use for days, weeks, or months at recommended doses HISTORY, CHIEF COMPLAINT History of exposure (acute or chronic) to an NSAID Clinical signs typically begin within hours after acute exposure (exception: days or weeks with chronic therapeutic use or when hepatopathy develops). Vomiting (±hematemesis), anorexia, lethargy, diarrhea (melena) Polyuria and polydipsia (PU/PD; due to kidney disease/renal failure)
PHYSICAL EXAM FINDINGS Variable, from minor GI upset to life-threatening effects of GI perforation Minor to moderate toxicosis: signs of abdominal pain, vomiting, diarrhea, lethargy, anorexia Severe toxicosis: dehydration, pallor, tachycardia, icterus, bruising (aspirin), hyperthermia (aspirin), ataxia, seizures, sudden death Hematemesis or melena is not reliably linked to GI perforation, and absence of hematemesis is not an indicator of absence of perforation.
ETIOLOGY AND PATHOPHYSIOLOGY Examples of commonly-implicated NSAIDs: *
Acetic acid derivatives: diclofenac, etodolac (EtoGesic) , indomethacin, nabumetone Cyclooxygenase (COX)-2 inhibitors: celecoxib, deracoxib (Deramaxx)* Fenamic acids: meclofenamic acid
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*
Oxicams: meloxicam (Metacam) , piroxicam Propionic acids: carprofen (Rimadyl)*, flurbiprofen, ibuprofen, ketoprofen, naproxen Pyrazolones: phenylbutazone Salicylic acid derivatives: aspirin, flunixin meglumine NSAIDs inhibit COX enzymes, blocking prostaglandin (PG) production. PGs formed by COX-1 are important for normal physiologic function (GI protection, renal medullary blood flow). PGs formed by COX-2 mediate inflammation. Therefore adverse effects are generally fewer when COX-2 is selectively inhibited. NSAID hepatopathy is due to the formation of antigenic proteins that trigger an immune-mediated attack against the liver. *Approved for use in dogs in the United States
DIAGNOSIS DIAGNOSTIC OVERVIEW In most cases, exposure is known (whether acute overdose or ongoing therapeutic administration). In acute overdoses, history and clinical signs may be sufficient to make the diagnosis. In chronic treatment-associated toxicosis, detailed diagnostic testing and/or drug discontinuation to monitor for regression of signs (if mild toxicosis) is often required to distinguish between NSAID toxicosis and naturally occurring disorders mimicking NSAID toxicosis.
DIFFERENTIAL DIAGNOSIS Any disease process that can cause GI, renal, or hepatic adverse effects.
INITIAL DATABASE CBC: anemia from GI hemorrhage (regenerative), leukocytosis (stress or peritonitis) possible Serum chemistry profile: azotemia (prerenal or primary renal insult [usually within 24-48 hours after exposure in acute toxicosis]) or elevated liver enzymes and bilirubin (hepatopathy) Urinalysis: hematuria, glycosuria, pyuria, proteinuria, casts, and isosthenuria possible with renal injury Abdominal radiographs: free air in peritoneal cavity strongly suggests GI tract perforation.
ADVANCED OR CONFIRMATORY TESTING Usually, serum/plasma drug levels are not useful clinically. Endoscopy (with persistent nonspecific GI signs, especially when NSAID therapy is not discontinued): GI ulceration/irritation /perforation Histopathologic evaluation: Stomach (endoscopic or surgical): irritation/duodenal ulceration/hemorrhage; peritonitis if gastric perforation Kidneys (postmortem): renal tubular or papillary necrosis or interstitial nephritis Liver (if persistent enzyme elevation; rarely performed): multifocal to bridging hepatocellular degeneration and necrosis (apoptosis), with mild to moderate periportal inflammation (neutrophils and lymphocytes)
TREATMENT TREATMENT OVERVIEW Goals of treatment are decontamination of the patient (induce vomiting and give repeated doses of activated charcoal), preventing/managing/monitoring GI, renal, and hepatic effects, and providing supportive care.
ACUTE GENERAL TREATMENT Decontamination of patient: Induction of vomiting (see p. 1364): indicated in any acute overdose patient not showing clinical signs Activated charcoal: 1-3 g/kg PO (or as labeled) with a cathartic, repeated (half dose) q 6-8 h to reduce enterohepatic recirculation of NSAID 2
Prevent and/or manage GI effects with combination therapy (sucralfate + H receptor antagonist or proton pump inhibitor + misoprostol): Misoprostol for dogs: 1-3 mcg/kg PO q 8 h. Prostaglandin analog, helps replace NSAID-induced PG depletion. 2
H receptor antagonist: famotidine: 0.5 mg/kg PO, SQ, IM, IV q 12-24 h (dogs, cats)
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Proton pump inhibitor: omeprazole 0.5-1 mg/kg PO q 24 h (dogs, cats) Sucralfate: 0.25-1 g PO q 8-12 h (dogs, cats) Prevent and/or manage renal effects: Fluid diuresis (2-3 times maintenance rate, barring cardiovascular disease) to enhance NSAID excretion and maintain renal perfusion. For at least 48 h if potential renal toxicity dose has been ingested. Prevent and/or manage hepatic effects: Discontinue use of NSAID. Begin IV fluids. Administer vitamin K1 (1-2 mg/kg PO) if evidence of coagulation disruption. S-adenosyl-L-methionine (SAMe), 18 mg/kg PO q 24 h for 1-3 months Supportive care: Control vomiting with metoclopramide (0.2-0.4 mg/kg q 6 h PO, SQ, or IM or 1-2 mg/kg/d IV as constant rate infusion) or maropitant, 1 mg/kg SQ q 24 h for up to 5 consecutive days. Correct fluid losses and electrolyte changes. Control seizures with diazepam 1-2 mg/kg IV. Administer a blood transfusion if needed. Treat GI tract perforation (laparotomy, antibiotics) if suspected.
CHRONIC TREATMENT Some animals may need long-term therapy for renal or hepatic insufficiency.
NUTRITION/DIET Use appropriate prescription diets in patients with kidney or liver dysfunction.
DRUG INTERACTIONS Concurrent use of corticosteroids or other NSAIDs may dramatically increase the risk for adverse effects. Increased serum drug levels: phenytoin, valproic acid, oral anticoagulants, sulfonamides, sulfonylurea hypoglycemic agents, ketoconazole, methotrexate, and fluconazole Increased risk of nephrotoxicity: aminoglycosides, angiotensin-converting enzyme (ACE) inhibitors, and diuretics
POSSIBLE COMPLICATIONS Chronic kidney disease Hepatopathy GI perforation and peritonitis
RECOMMENDED MONITORING Blood urea nitrogen, serum creatinine, electrolytes, urinalysis (baseline, 24, 48, 72 hours in acute cases) Serum liver enzymes and bilirubin (for hepatopathy)
PROGNOSIS AND OUTCOME Excellent from mild to moderate gastric irritation/ulceration with appropriate treatment Guarded to poor with GI tract perforation Renal effects of NSAIDs are reversible if discovered early and treated intensively. Recovery from idiosyncratic hepatic toxicity is good when NSAID is discontinued and with supportive care.
PEARLS & CONSIDERATIONS COMMENTS For most NSAIDs, the minimum toxic/lethal dose is unknown. Generally, a single acute ingestion of 5-10 times more than the recommended dose could cause potentially severe GI irritation/ulceration in dogs. Some NSAIDs (naproxen and meclofenamic acid) have a much longer half-life in the dog, owing to extensive enterohepatic recirculation (naproxen: 92 hours).
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Check baseline CBC and serum biochemistry profile in all patients before long-term use of NSAIDs.
PREVENTION Clinicians should inform owners to keep all NSAIDs, especially chewables, out of the reach of pets.
TECHNICIAN TIPS Clients may ask casually about using over-the-counter NSAIDs like ibuprofen in their dog or cat. Ibuprofen is not recommended in small animals; it is the most commonly reported NSAID toxicity.
CLIENT EDUCATION Discuss common adverse effects associated with NSAIDs. Owners should not give any medications to their pets without first consulting a veterinarian.
SUGGESTED READING Talcott PA: Nonsteroidal antiinflammatories. In Peterson ME, Talcott PA, editors: Small animal toxicology, ed 2, St Louis, 2006, Saunders Elsevier, pp 902–933. AUTHOR: CAMILLE DECLEMENTI EDITOR: SAFDAR KHAN 1ST EDITION AUTHOR: TINA WISMER
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Nodular Skin Disorders
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Nodular Skin Disorders BASIC INFORMATION DEFINITION A large group of diseases that manifest as solid elevated lesions of the skin of >1 cm in diameter, usually as a result of infiltration of inflammatory or neoplastic cells into the dermis or subcutis
EPIDEMIOLOGY SPECIES, AGE, SEX Seen in cats and dogs Neoplastic conditions are more common in mature individuals. GENETICS & BREED PREDISPOSITION Familial vasculopathy and nodular dermatofibrosis of German shepherd Histiocytic sarcoma complex in Bernese mountain dog, Rottweiler, golden retriever (see p. 535) Sterile nodular panniculitis in dachshunds (see p. 824) Mucinosis in the shar-pei RISK FACTORS Any disease or medication that causes immune compromise (e.g., feline leukemia virus [FeLV] infection, feline immunodeficiency virus [FIV] infection, hyperadrenocorticism, hypothyroidism, diabetes mellitus) predisposes animals to infections, which in turn may cause nodular dermatoses. Foreign-body penetration, bite wound: increased risk of infectious nodular dermatitis Mineralizing fat necrosis/panniculitis in dogs with pancreatitis or pancreatic carcinomas CONTAGION & ZOONOSIS Dermatophytic granuloma: Microsporum canis and Trichophyton mentagrophytes are potentially contagious to human and other animals. Sporotrichosis: Cat-to-human transmission is extremely high. Dog-to-human transmission has not yet been described. Blastomycosis, coccidioidomycosis, histoplasmosis: risk of zoonosis by aerosol from culture plates; in-house culture is always contraindicated. GEOGRAPHY AND SEASONALITY: Straelensiosis: France, Spain, Portugal; Sporotrichosis: outbreak in Brazil; See Blastomycosis, p. 138; Histoplasmosis, p. 538; Coccidioidomycosis, p. 222; Pythiosis and Lagenidiosis, p. 960; Protothecosis, p. 926. ASSOCIATED CONDITIONS & DISORDERS: Renal cystadenocarcinoma is typically a concurrent finding with nodular dermatofibrosis.
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT: Animals present with acute to chronic onset of single or multiple subcutaneous nodules, with or without draining tracts, and potentially accompanying systemic signs such as fever, cough, rhinitis, anorexia lethargy. PHYSICAL EXAM FINDINGS: Lesions are elevations above the epidermal surface of 1 cm or greater in diameter. They can be solitary to multiple, localized to generalized, firm to fluctuant, draining or intact, and pruritic to nonpruritic, all depending on the underlying etiology. Depending on etiology, systemic signs such as fever and/or coughing may be noted.
ETIOLOGY AND PATHOPHYSIOLOGY Nodules, which are larger than papules (1 hour after ingestion; spontaneous vomiting, salivation, and diarrhea. Initial central nervous system (CNS) excitation and tachypnea PHYSICAL EXAM FINDINGS Hypersalivation Nausea Tenesmus Bradycardia (sinus); may be followed by tachycardia. Shallow, slow respiration, eventually leading to cyanosis, respiratory paralysis Neuromuscular weakness, tremors, collapse
ETIOLOGY AND PATHOPHYSIOLOGY Source: Sources include cigarettes, cigars, chewing tobacco, Bidi cigarettes, nicotine gum, nicotine skin patches (Nicorette, Nicotrol), inhalers, nasal sprays, nicotinic insecticides (nicotine sulfate is available at a concentration of 0.05%-4% as insecticide dust or sprays and as a concentrated 40% solution [Black Leaf 40]; banned in the United States since 2001). Nicotine is a water-soluble alkaloid found primarily in cultivated tobacco (Nicotiana tabacum) but also in wild tobacco (N. attenuata and N. trigonophylla). Tree tobacco (N. glauca) contains mostly anabasine (a teratogen) but does contain some nicotine. Indian tobacco (Lobelia inflata) contains mostly lobeline (curare-like paralytic) and some nicotine. Mechanism of Toxicosis: Nicotine mimics acetylcholine at sympathetic and parasympathetic ganglia, neuromuscular junctions of skeletal muscle, and at some synapses in the CNS. Low doses cause depolarization and stimulation of receptors similar to acetylcholine. Higher doses cause stimulation followed by blockade of autonomic ganglia and neuromuscular junctions of skeletal muscle. Stimulation of sympathetic cardiovascular ganglia and adrenal medulla can lead to release of catecholamines. GI effects: parasympathetic stimulation can lead to increased tone and motility. Death can result from respiratory paralysis.
DIAGNOSIS
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Nicotine Toxicosis
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DIAGNOSTIC OVERVIEW A tentative diagnosis is made based on nicotine in the animal's environment and appropriate clinical signs. Confirmation with nicotine in-clinic tests is possible, especially if history of exposure is uncertain, but it is not essential.
DIFFERENTIAL DIAGNOSIS Other intoxications: strychnine, methylxanthines, tremorgenic mycotoxins/garbage toxicosis, organophosphates/carbamates The initial stages of nicotine poisoning produce physical signs that are similar to those of anticholinesterase insecticide poisoning. The latter stages produce signs that are similar to intoxication with depressants (ethanol, barbiturates, marijuana, etc.).
INITIAL DATABASE Serum chemistry profile: electrolyte abnormalities, azotemia (vomiting, dehydration) Blood gas analysis Electrocardiogram (ECG): sinus bradycardia or sinus tachycardia most common, ventricular arrhythmias possible
ADVANCED OR CONFIRMATORY TESTING Nicotine can be detected in urine, blood, GI contents, vomitus, or lavage washings. Clinicians can contact a veterinary diagnostic laboratory or a human hospital for analysis, but such confirmation should not delay initiation of treatment if nicotine toxicosis is known or suspected. Necropsy samples: nicotine in liver and kidney
TREATMENT TREATMENT OVERVIEW Treatment consists of management of severe signs first (e.g., seizures) if present, followed by decontamination of the patient (induce vomiting and give activated charcoal) in all cases not showing overt clinical signs, and enhancement of excretion of nicotine in all likely or confirmed cases.
ACUTE GENERAL TREATMENT Decontamination of patient: Decontamination of dermal exposure consists of bathing the patient with liquid dishwashing detergent solution (wear thick rubber gloves). Induction of emesis (see p. 1364) is indicated only if the patient is not showing any clinical signs (10 years of age. The most common feline malignant oral tumor is SCC (see p. 1045), representing 70% of oral tumors in cats. Average age of onset is 10 years, but cats as young as 5 months have been affected. GENETICS & BREED PREDISPOSITION: Breeds with pigmented oral mucosa may be predisposed to malignant melanoma. RISK FACTORS: Factors that increase the risk of feline SCC 3- to 5-fold: Exposure to flea collars High intake of canned cat food Regular ingestion of canned tuna
ORAL TUMORS, MALIGNANT A, Clinical photograph of a cat with squamous cell carcinoma affecting the left lower jaw (arrow).B, Radiograph obtained with dental film of same patient (extraoral lateral oblique technique), showing severe lysis of left mandible and sunburst pattern at ventral mandibular border (arrows). (Copyright Dr. Alexander M. Reiter.) CONTAGION & ZOONOSIS: Canine transmissible venereal tumor (seep. 1114 ) can manifest as a primary or metastatic tumor on the lips, buccal mucosa, and tonsils.
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES Dogs: malignant melanoma, SCC, fibrosarcoma, osteosarcoma, osteochondrosarcoma (multilobular tumor of bone), mast cell
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Oral Tumors, Malignant
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tumor, hemangiosarcoma, peripheral nerve sheath tumor, lymphosarcoma (epitheliotropic lymphoma) Cats: SCC, fibrosarcoma, osteosarcoma, hemangiosarcoma, malignant melanoma HISTORY, CHIEF COMPLAINT Swelling of mandible or maxilla Oral bleeding, halitosis Dysphagia if the mass is large enough to affect masticatory function Appetite and activity level are often unaffected PHYSICAL EXAM FINDINGS Specifics may vary with tumor type: Malignant melanoma is pigmented (melanotic) or nonpigmented (amelanotic) and often lobulated, ulcerative, and friable; necrosis may be present when the tumor outgrows its blood supply. Fibrosarcoma is often smooth and firm and may cause generalized disfigurement but rarely bleeds spontaneously. Peripheral nerve sheath tumor tends to grow along larger nerves (e.g., infraorbital nerve into infraorbital canal and inferior alveolar nerve into mandibular canal). SCC is pink, friable, often verrucous (cauliflower-like), and may be either proliferative or ulcerative. Desmoplasia (formation of fibrous tissue) secondary to SCC development may result in a firm tumor on palpation. Osteosarcoma can manifest as a diffuse swelling of the maxilla or mandible but often also exhibits a fleshy, pink or red proliferative component that bleeds easily. Osteochondrosarcoma is locally invasive but slow to metastasize and usually located at mandibular ramus, caudal maxilla, zygomatic arch, or calvarium. Halitosis, oral bleeding, facial/oral swelling Enlarged mandibular lymph nodes possible Maxillary, retroorbital and caudal pharyngeal masses: decreased ability to retropulse the eye globes and decreased range of jaw opening if rostral movement of the mandibular coronoid process is prevented by the tumor or if the tumor involves the temporomandibular joint.
ETIOLOGY AND PATHOPHYSIOLOGY Etiology is unknown, but genetic predisposition may play a role.
DIAGNOSIS DIAGNOSTIC OVERVIEW Diagnosis of malignant oral masses usually requires histopathologic analysis of a biopsy, since many oral masses do not exfoliate well on fine-needle aspirates. Incisional (rather than excisional) biopsy is the preferred initial step for suspected malignancies in order to provide the clinician and client with further information prior to deciding on radical surgery and/or radiation therapy.
DIFFERENTIAL DIAGNOSIS As for benign oral tumors (see p. 786)
INITIAL DATABASE CBC, serum biochemistry profile, urinalysis, and thoracic radiographs: to assess for metastases, concurrent illnesses
ADVANCED OR CONFIRMATORY TESTING Anesthetized oral examination Dental radiography CT: particularly helpful for maxillary and caudal mandibular masses Cytologic examination of oral masses (fine-needle aspiration, “woodpecker” technique, or scraping from tumor cut surface) Cytologic examination of aspirated material or histopathologic examination of resected lymph nodes Histopathologic evaluation of incisional or excisional biopsy
TREATMENT
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Oral Tumors, Malignant
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TREATMENT OVERVIEW Merely debulking aggressive tumors is rarely helpful. Once a diagnosis is obtained, the mass together with a margin of normal surrounding tissue should be removed comprehensively to prevent local recurrence. If complete removal is not an option, radiation or chemotherapy may decrease the rate of growth, depending on tumor type.
ACUTE GENERAL TREATMENT Removal of a circumscribed mass to the normal level of the surrounding gingiva will often serve as an adequate biopsy but may not prevent local recurrence. Incisional biopsies of large masses are warranted to provide information prior to performing a radical maxillectomy or mandibulectomy. Aspiration and/or removal of head and neck lymph nodes are warranted for staging of animals with malignant oral tumors.
CHRONIC TREATMENT Depending on biopsy results and tumor extent, radical surgery and/or radiation therapy may be treatment options. Even when surgery is an option, consult with a medical oncologist and/or radiation oncologist regarding the need for adjuvant or postoperative treatment. Chemotherapy may be used as an adjunctive therapy but is rarely effective by itself against most oral tumors. Immunotherapy of certain tumors shows great promise, and a commercially available melanoma vaccine is available through oncologists (seep. 711 ). Radiation therapy offers good long-term control for treatment of microscopic disease, but bulky tumors rarely respond well. Piroxicam, 0.3 mg/kg PO q 24 h in dogs may slow the progression of some carcinomas. Short-term (10 days) use of piroxicam in cats appears to be safe at 0.3 mg/kg PO q 24 h. Further studies are necessary to determine long-term gastrointestinal safety in cats. If prescribed long-term for cancer palliation, the author prescribes 0.3 mg/kg q 48 h.
NUTRITION/DIET Soft food/esophagostomy tube if necessary because of inability to prehend or chew food
DRUG INTERACTIONS Piroxicam and other NSAIDs may cause significant gastric ulceration; clinicians should avoid concurrent use of corticosteroids and consider gastric protectants such as misoprostol.
POSSIBLE COMPLICATIONS Recurrence of primary tumor. Surgeons should remove at least 1 cm of clinically and radiographically healthy tissue surrounding malignant tumors. Many locally aggressive tumors (fibrosarcoma, peripheral nerve sheath tumor, malignant melanoma) require even wider margins. Intraoperative or postoperative bleeding: having blood products available is important with mandibulectomy and maxillectomy procedures. Dehiscence of the surgical site: avoid using electrocautery on mucosal edges because it can obscure histologic examination of margins of excised tissue and increases the likelihood of wound dehiscence, which may result in the need for further surgical intervention (such as repair of an oronasal fistula). Sublingual or cervical mucoceles may occur if transection of salivary ducts is necessary; these ducts should be ligated if transected.
RECOMMENDED MONITORING Oral examination to monitor for local recurrence 1 month after surgery and at a maximum of 6-month intervals thereafter. Thoracic radiographs and lymph node palpation should be performed every 6 months.
PROGNOSIS AND OUTCOME Median survival time for most malignant oral tumors after surgical excision has been 7-12 months. However, when surgeons obtain clean surgical margins in the absence of microscopic metastasis, patients can be cured. Prognosis with SCC is good if found while still surgically resectable. Malignant melanomas >8 cm3 (2 × 2 × 2 cm) have a high incidence of microscopic metastasis at the time of diagnosis. Mandibular osteosarcoma has been reported to have a lower metastatic rate and better prognosis than appendicular osteosarcoma. Tonsillar SCC in dogs commonly metastisizes to regional lymph nodes, with 85% having regional metastasis at necropsy.
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Oral Tumors, Malignant
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PEARLS & CONSIDERATIONS COMMENTS Incisional biopsy should be performed for larger oral masses. Excisional biopsy may be curative but carries the risk of inadequate tumor removal. When submitting excisional biopsies, clinicians should request that the pathologist evaluate margins for the presence of neoplastic cells. Clean margins according to histologic examination do not rule out the possibility of recurrence, but animals with clean margins have a better long-term prognosis. Dental radiography (see p. 1246) is invaluable in providing diagnostic and treatment planning information for oral tumors. Benign tumors tend to displace teeth that often remain firmly seated, whereas more aggressive tumors will cause root and alveolar bone resorption, which may manifest as very mobile (floating) teeth. Benign tumors may have a smooth layer of reactive bone surrounding the neoplastic tissue, whereas a malignant tumor often exhibits destruction of cortical bone, with formation of a classic radiographic “sunburst” appearance (see figure). Right or left total mandibulectomy (previously referred to as hemimandibulectomy) and maxillectomy surgeries carry with them the potential for profuse bleeding. Blood type and cross matching may be warranted preoperatively. Sublingual edema seen within 48 hours after mandibulectomy should not be confused with a sublingual mucocele (ranula). Edema will usually resolve without treatment. Pigmentation is not a reliable indicator of tumor type. About 40% of oral malignant melanomas may be amelanotic (unpigmented). Malignant tumors other than melanoma may be partially pigmented if the patient's oral mucosa is normally pigmented. Removal of regional lymph nodes may be beneficial at the time of oral surgery. A single surgical approach to parotid, mandibular, and retropharyngeal lymph nodes has been described. If the biological behavior of a tumor does not match histopathologic results, clinicians should have the biopsy reread or retaken. A type of fibrosarcoma exists which appears histologically benign but is biologically (clinically) very aggressive. Nonhealing dental extraction sites, particularly in cats, may be a clinical manifestation of SCC; clinicians should biopsy any suspicious tissues at the time of extraction. Dehiscence and inappropriate healing often occur when oral surgery is performed on irradiated sites.
TECHNICIAN TIPS Technicians are on the front line of identifying oral tumors during professional dental cleanings. Do a complete oral examination on each anesthetized patient, including the sublingual area, palate, and tonsils. Bring all identified oral masses to the attention of the clinician for possible biopsy under the same episode of general anesthesia. Provide as much information as possible on histopathology forms. Include size (in three dimensions), surface characteristics (ulcerated, smooth, verrucous), complete history, and specific location of tumors. When an excisional biopsy is performed, ask the pathologist to evaluate the specimen for evidence of “clean” or “dirty” margins.
CLIENT EDUCATION Complete surgical removal of oral tumors provides the best long-term prognosis. Tumors that are detected early are likely to be operable. Clinicians should advise new pet owners to socialize puppies and kittens and allow them to feel comfortable with periodic examination of the oral cavity. Animals adapt remarkably well after radical resection of oral tumors (mandibulectomy or maxillectomy), though one study noted that 12% of cats did not regain the ability to eat on their own. Altered cosmesis is usually well accepted by owners if masticatory function can be restored. Clients should be shown before-and-after pictures of similar surgical cases to ensure their understanding of cosmetic changes (see online version of this chapter). Lymph node aspirates and thoracic radiographs are important for preoperative animal staging, but microscopic metastasis cannot be totally ruled out by these tests.
SUGGESTED READING Bertone ER, et al: Environmental and lifestyle risk factors for oral squamous cell carcinoma in domestic cats. J Vet Intern Med 17:557, 2003. Ciekot PA, et al: Histologically low-grade, yet biologically high-grade, fibrosarcomas of the mandible and maxilla in dogs: 25 cases (1982-1991). J Am Vet Med Assoc 204:610, 1994. Straw RC, et al: Canine mandibular osteosarcoma: 51 cases (1980-1992). J Am Anim Hosp Assoc 32:257, 1996. AUTHOR: JOHN R. LEWIS EDITOR: ALEXANDER M. REITER
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Oral Tumors, Benign
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Oral Tumors, Benign BASIC INFORMATION DEFINITION Tumor generally refers to a swollen or distended area. A second definition refers more specifically to a benign or malignant neoplastic disease. Benign and malignant oral tumors are common in dogs, whereas oral tumors in cats tend to be malignant. Benign tumors may be locally invasive but do not metastasize to distant sites.
SYNONYMS Benign oral neoplasia “Epulis” (plural = “epulides”) is a nonspecific clinical descriptive term referring to a local exophytic growth on the gingiva (e.g., focal fibrous hyperplasia, peripheral odontogenic fibroma [fibromatous epulis and ossifying epulis], acanthomatous ameloblastoma [acanthomatous epulis], nonodontogenic tumors). Seep. 359 .
EPIDEMIOLOGY SPECIES, AGE, SEX Dogs: usually gingival hyperplasia, peripheral odontogenic fibroma, acanthomatous ameloblastoma; occasionally pyogenic granuloma, dentigerous cyst, odontoma, papilloma, osteoma, plasmacytoma; rarely giant cell epulis, amyloid-producing odontogenic tumor Cats: usually gingival hyperplasia; occasionally giant cell epulis, osteoma, plasmacytoma; rarely peripheral odontogenic fibroma, acanthomatous ameloblastoma, inductive ameloblastoma (feline inductive odontogenic tumor), amyloid-producing odontogenic tumor, odontoma Benign oral tumors can occur at any age. Oral papillomas (seep. 830 ) usually occur in dogs 30 mm Hg with glaucoma; may be low at 3 g/dL 9
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Nucleated cell count >7 10 /L, often >30 × 10 /L Degenerate neutrophils predominate, with macrophages and activated mesothelial cells also present. Intraleukocytic bacteria are diagnostic (septic pyothorax). Gram stain: Guides initial empirical antimicrobial therapy: Oropharyngeal bacteria (e.g., Pasteurella spp., Bacteroides spp., Fusobacterium spp.) common in cats; Escherichia coli in dogs (both gramnegative rods) Actinomyces (anaerobe) and Nocardia (aerobe): both grampositive short rods and filaments; important potential pathogens in dogs from regions where grass awn endemic Anaerobic and aerobic bacterial culture and susceptibility (C&S): Test of choice for planning long-term antimicrobial therapy Survey thoracic radiographs: Initially to identify pleural effusion After therapeutic thoracocentesis, to evaluate pleural space, mediastinum, and pulmonary parenchyma for potential primary cause of pyothorax Thoracic ultrasound examination: Identify masses and evaluate their internal structure. Identify site of greatest pleural effusion for centesis (if overall small volume of effusion). Identify foreign material in the pleural space if possible (may be very challenging).
ADVANCED OR CONFIRMATORY TESTING CT scan: Potentially identify cause of pyothorax. Evaluate mass(es) in thoracic cavity and determine if resectable.
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Pyothorax
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TREATMENT TREATMENT OVERVIEW Patient stabilization, pleural drainage (thoracostomy tubes for pleural lavage), +/− surgical exploration and débridement of the thoracic cavity and long-term antimicrobial therapy are the standard of care. Long-term antimicrobial therapy is based on results of microbiologic C&S testing.
ACUTE GENERAL TREATMENT Stabilization of respiratory compromise: Therapeutic (and diagnostic) thoracocentesis (see p. 1338) Oxygen administration (seep. 1318 ) Intensive care monitoring Correction of fluid and electrolyte deficits Antimicrobial therapy: Empirical therapy active against both aerobic and anaerobic bacteria: Gram stain results (as previously described) Amoxicillin/ampicillin, 22 mg/kg IV or PO q 8 h, if Actinomyces suspected Trimethoprim-sulfa, 15 mg/kg PO q 12 h, if Nocardia, E. coli, or Pasteurella suspected Medical management: Bilateral thoracostomy tube placement Thoracic lavage every 6-8 hours with body-temperature warmed sterile saline Serial cytologic evaluation of pleural fluid to assess success of lavage therapy: Improvement includes change from degenerate neutrophils with intracellular or extracellular bacteria to nondegenerate neutrophils without bacteria. Surgical management: Indicated if: Definitive cause identified and retained in thoracic cavity (foreign body, lung lobe abscess) Fluid loculated within the pleural space (lavage cannot access portions of fluid accumulation) Patient fails to respond to intensive medical therapy (4-5 days of pleural lavage and antibiotics) Actinomyces present (in dogs, notoriously poor response to medical management alone) Consists of aggressive débridement of the pleural space, removal of underlying cause if identified, thorough intraoperative lavage, and postoperative intermittent pleural aspiration, lavage, and antimicrobial therapy.
CHRONIC TREATMENT Thoracostomy tube removal based on overt clinical and cytologic resolution of infection Long-term antibiotic therapy in all cases: Based on accurate identification of organism(s) involved Up to 3 months of therapy may be required.
POSSIBLE COMPLICATIONS Failure to resolve/recurrence of pyothorax: Cause not removed Failure of medical management: Ineffective pleural lavage Ineffective/inappropriate antibiotic therapy
RECOMMENDED MONITORING Survey thoracic radiographs: At completion of antibiotic therapy Periodically (every 3 months)
PROGNOSIS AND OUTCOME
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Pyothorax
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Surgical management is associated with a better prognosis than medical management in dogs with pyothorax: disease-free at 1 year: 78% (surgical) versus 25% (medical). Development of fibrosing pleuritis is associated with poor outcome. Lower heart rate and hypersalivation are both associated with poorer outcomes in cats. Overall, 66% of cats and 80% of dogs can survive if treated appropriately.
PEARLS & CONSIDERATIONS COMMENTS Intensive therapy should start immediately upon diagnosis. Undertreatment is thought to be a major contributor to morbidity/mortality. Surgical treatment has been associated with a better outcome than medical treatment alone. Bilateral thoracostomy tubes are helpful in aspiration and lavage of the pleural space. Antimicrobial therapy should be guided by culture and susceptibility, with attention paid to Actinomyces and Nocardia. Obligate anaerobes are common in pyothorax and are present in combination with aerobes; antimicrobial treatment should be aimed at both types of bacteria until culture results are available.
TECHNICIAN TIPS Knowledge of and experience in working with thoracostomy tubes is important in the management of patients with pyothorax: Used as the primary treatment modality for nonsurgical thoracic drainage and lavage Used in the postoperative period for continued thoracic drainage +/− lavage.
SUGGESTED READING Barrs VR, Allan GS, Beatty JA, et al: Feline pyothorax: a retrospective study of 27 cases in Australia. J Feline Med Surg 7:211, 2005. Johnson MS, Martin MWS: Successful medical treatment of 15 dogs with pyothorax. J Small Anim Pract 48:12, 2007. AUTHOR: MARYANN G. RADLINSKY EDITOR: RICHARD WALSHAW
26-09-2011 22:15
Pyometra
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Pyometra BASIC INFORMATION DEFINITION Very common uterine disease of middle-aged to older female dog or cat; characterized by an accumulation of purulent material in the uterine lumen or uterine stump
SYNONYMS Purulent endometritis, purulent metritis, pyo, pyometritis
EPIDEMIOLOGY SPECIES, AGE, SEX Female canine or feline (more common in bitches than queens) Any age after puberty (more common after 5-6 years of age) RISK FACTORS In dogs, age, hormonal (estrogen and/or progestin) treatments and estrous cycle irregularities are proposed risk factors. In cats, pseudopregnancy and ovarian diseases (e.g., granulosa cell tumor) are risk factors. ASSOCIATED CONDITIONS & DISORDERS Sepsis Septic shock Systemic inflammatory response syndrome (SIRS) Multiple organs dysfunction syndrome (MODS) Disseminated intravascular coagulation (DIC) Acute renal failure Acute hepatic injury Vaginitis and UTI Peritonitis
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES Open pyometra: mucoid, purulent, mucopurulent or hemorrhagic vulvar discharge Closed pyometra: no (or minimal) vulvar discharge HISTORY, CHIEF COMPLAINT Diestrus or anestrus (from a few weeks following the end of estrus up to a few months) Anorexia, vomiting Lethargy, depression Polyuria and polydipsia (PU/PD) Abdominal distension (less common) Vulvar discharge may be noted by owner. Intact female or history of incomplete ovariohysterectomy Previous treatment to induce abortion or parturition In the queen, the disease is generally more subacute or chronic and associated with few clinical signs but irregular cycles, vaginal discharge, and/or abdominal distension. PHYSICAL EXAM FINDINGS
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Pyometra
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Purulent vulvar discharge is common and should always prompt the consideration of pyometra: Absence of vulvar discharge does not rule out pyometra. Abdominal palpation: Signs of abdominal pain Enlarged uterus (may be difficult to palpate if only a moderate enlargement and/or the abdomen is tense) Abdominal distension Dehydration Fever (or hypothermia if severe, such as in septic shock) Red mucous membranes (hyperdynamic stage of sepsis) or pale mucous membranes (septic shock) Normal pulse and cardiac auscultation or tachycardia, weak pulse, and cool extremities possible with septic shock Normal respiration or hyperpnea
ETIOLOGY AND PATHOPHYSIOLOGY Two proposed pathways: Chronic degenerative uterine process associated with progesterone and bacterial contamination and proliferation; in older animals, often associated with cystic endometrial hyperplasia (CEH): Excessive diestrous endometrial hyperplasia (progesterone-induced), causing cyst formation, decrease myometrial activity, local immune suppression. Pyometra results when bacteria colonize the uterus via ascension through the cervix, or hematogenously. The bacterium most commonly isolated from pyometra is Escherichia coli, but Staphylococcus spp., Streptococcus spp., Pseudomonas spp., and Proteus spp. also reported. In the queen, the pathogenesis is most likely associated with prolonged progesterone impregnation during pseudopregnancy. Pyometra not associated with CEH; trophoblastic reaction: Subclinical bacterial infection in early to mid-diestrus induces uterine endometrial hypertrophy followed by a trophoblastic like hyperplasia of the endometrium and endometrial glands. Increase in glandular secretions exacerbates the infection. This mechanism may explain the occurrence of pyometra in younger bitches.
DIAGNOSIS DIAGNOSTIC OVERVIEW Pyometra may be strongly (open pyometra) or weakly (closed pyometra) suspected on physical exam; noting that the patient is an intact female is a critical element of the initial suspicion. Leukocytosis on CBC further supports the diagnosis but is not always present. Clinical confirmation justifying treatment (most commonly ovariohysterectomy) comes from abdominal ultrasound.
DIFFERENTIAL DIAGNOSIS Mucometra (uterine lumen filled with mucoid endometrial gland secretions without infection; no systemic signs or leukocytosis expected) CEH Pregnancy Vaginitis and purulent UTI Reproductive tract tumors Uterine torsion Postpartum metritis Other systemic diseases resulting in an acute abdomen
INITIAL DATABASE CBC: Mild to moderate normocytic, normochromic anemia (packed cell volume 30%-35%) Leukocytosis with left shift and/or toxic changes Approximately 25% of leukograms are within normal range in pyometra cases. Serum biochemistry profile: elevated hepatic and renal values possible A vaginal swab, particularly if it is collected near the external cervical os, may allow detection of a purulent exudate in closed pyometra. Vaginal cytologic exam: presence of numerous degenerate neutrophils Urinalysis:
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Pyometra
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Cystocentesis is contraindicated in suspected or confirmed pyometra cases. Catheterized or free-catch samples may show evidence of infection, either as a real finding (bacterial cystitis is often concurrent with pyometra) or as an artifact of collection. Abdominal radiographs: Distended viscus consistent with enlarged, fluid-filled uterus: Note: Abdominal radiographs will not differentiate between pyometra and pregnancy of less than 45 days of gestation or mucometra. Abdominal radiographs may not detect slightly enlarged uterus. Ultrasonographic examination: Enlarged fluid-filled uterus: Note: easily differentiates from pregnancy; abdominal ultrasound is the method of choice for establishing a diagnosis of pyometra.
ADVANCED OR CONFIRMATORY TESTING Open pyometra: cranial vaginal (near external cervical os) culture and sensitivity (C&S) Closed pyometra: transcervical endoscopy with uterine sample for C&S Gross and histopathologic examination of the surgically removed uterus
TREATMENT TREATMENT OVERVIEW Supportive care followed by ovariohysterectomy (majority of cases) or medical management (bitches with reproductive value) Queens: same approach; more resistant to luteolytic treatments and require higher doses
ACUTE GENERAL TREATMENT General systemic treatment: Stabilization and treatment of acute renal failure if identified (seep. 1591 ) IV fluid therapy: typically to correct dehydration, using replacement fluids such as lactated Ringer's solution or 0.9% NaCl, with or without colloids. Rate is calculated based on dehydration and ongoing fluid losses. Treatment/prophylaxis for disseminated intravascular coagulation (DIC; see p. 315) Broad-spectrum antibiotic therapy: oral route is indicated for stable patients; individuals showing systemic signs of illness should receive antibiotics parenterally: Amoxicillin with clavulanic acid, 20 mg/kg PO q 8-12 h; or Enrofloxacin, 5 mg/kg PO or diluted 1:1 with saline and given slowly (over 5 minutes) IV q 6-12 h as needed (maximum 5 mg/kg q 24 h in cats); or Cephalexin, 22-30 mg/kg PO q 8 h Pain management (e.g., buprenorphine, 0.01-0.03 mg/kg SQ, IM, or IV q 6-12 h as needed based on pain parameters) Surgical pyometra treatment: ovariohysterectomy Medical pyometra treatment: Prostaglandin F-2alpha (PGF2α, dino-prost [Lutalyse]) When used alone, high doses are required (>0.1 mg/kg SQ), which can be associated with significant, sometimes life-threatening, side effects (hypersalivation, emesis, diarrhea, tremor, ataxia, tachypnea, tachycardia, hypovolemic shock). PGF2α alone cannot be used for treating a closed pyometra because of the potential of uterine rupture. Synthetic PGF2α (e.g., cloprostenol [Estrumate] 0.001-0.005 mg/kg SQ from once a day to every 3 days) will produce similar results but more side effects. 2α
Low, increasing doses of PGF (0.01-0.05 mg/kg SQ q 5-8 h for 7-10 days or until uterine evacuation is complete as assessed by ultrasonography) are not associated with clinical side effects but must be combined with either a dopamine agonist or a progesterone receptor antagonist. Dopamine agonists are used for hastening luteolysis via prolactin inhibition: Cabergoline (Dostinex), 0.005 mg/kg PO q 24 h for 8-10 days; or Bromocriptine (Parlodel), 0.03 mg/kg PO q 8-12 h for 10 days; given orally, adverse effects are uncommon at this dose. Progesterone receptor antagonists are used for mimicking luteolysis through progesterone antagonism: Mifepristone (Mifeprex), 2.5 mg/kg PO q 24 h for 5 days; or Aglepristone (Alizine), 10 mg/kg SQ twice at 24 hours apart Closed pyometra can safely be treated with PGF2α, starting at 0.01 mg/kg SQ q 5-8 h on day 1, then 0.025 mg/kg SQ q 5-8 h on day 2, then 0.05 mg/kg q 5-8 h the following days in association with dopamine agonists or progesterone antagonists. This treatment will first induce cervical opening before uterine contractions.
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Pyometra
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Queens should receive higher natural prostaglandin (dinoprostum [Dynolytic; Upjohn]) doses (generally ranging from 0.05-0.1 mg/kg SQ q 5-8 h for 7-10 days or until uterine evacuation is complete) associated with dopamine agonists. Medical management of dogs with transcervical endoscopic catheterization technique (TECT) hastens uterine emptying time. Treatment efficacy is evaluated using transabdominal ultrasonography. At least 50% reduction of the uterine luminal diameter should be observed in less than 5-7 days after treatment initiation; complete by 5-10 days. Antimicrobial treatment should be continued for at least 2 weeks after the cessation of PGF2α and other specific treatments.
CHRONIC TREATMENT If necessary, for chronic kidney disease (antigen/antibody complex-induced glomerulonephritis). Seepp. 205 and 450.
DRUG INTERACTIONS Antiemetic drugs should not be used, as they stimulate prolactin release which would delay luteolysis and prolong medical pyometra treatment.
POSSIBLE COMPLICATIONS Peritonitis (resulting from uterine rupture) Stump pyometra (resulting from incomplete ovariohysterectomy) Bacterial cystitis (often concurrent with pyometra) Abdominal abscesses (resulting from bacteremia) DIC, SIRS, MODS Septic shock
RECOMMENDED MONITORING Intensive/critical care Cardiovascular support with IV fluid therapy Pain management Monitor for DIC (CBC, platelet count, coagulation profile, D-dimer test) Monitor for liver and kidney failure with a chemistry profile Ultrasonographic examination of the uterus every other day during treatment to monitor response
PROGNOSIS AND OUTCOME Always guarded depending on presence of sepsis and liver or renal failure; otherwise good In medically managed dogs, is generally advised to breed during the first subsequent cycle No difference in the incidence of recurrent pyometra in medically treated dogs compared to intact dogs of the same age that did not previously have pyometra
PEARLS & CONSIDERATIONS COMMENTS Clinical signs are not related to the size of the distended uterus. Pyometra should always be included as a differential diagnosis in a female dog with clinical signs of an acute abdomen or with nonspecific clinical signs. A closed pyometra can be a life-threatening condition. Treatment, particularly general, should not be delayed even if the animal appears to be healthy.
PREVENTION Ovariohysterectomy in females that are not going to be bred and in females that have retired from breeding Avoid prophylactic antibiotic treatment, as this is often associated with progressive development of bacterial resistance and virulence.
CLIENT EDUCATION
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Pyometra
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If the animal is not to be used for reproduction, a complete ovariohysterectomy will prevent the development of pyometra. Contact the veterinarian immediately if any of the above clinical signs is observed in a post estrus, intact aging female.
SUGGESTED READING England GC, Freeman SL, Russo M: Treatment of spontaneous pyometra in 22 bitches with a combination of cabergoline and cloprostenol. Vet Rec 160:293–296, 2007. Gobello C, et al: A study of two protocols combining aglepristone and cloprostenol to treat open cervix pyometra in the bitch. Theriogenology 60:901, 2003. Johnston S, et al: Disorders of the canine uterus and uterine tubes. In Johnston SD, Root-Kustritz MV, Olson PNS, editors: Canine and feline theriogenology. Philadelphia, 2000, WB Saunders, pp 206–224. AUTHOR: KARINE ONCLIN EDITOR: MICHELLE KUTZLER
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Pyoderma
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Pyoderma BASIC INFORMATION DEFINITION Pyoderma is a bacterial infection of the skin. It is one of the most common diseases of dogs.
SYNONYM Bacterial dermatitis
EPIDEMIOLOGY SPECIES, AGE, SEX Common in dogs, rare in cats. Impetigo (superficial form of pyoderma, typically in juvenile patients): noted in puppies sometimes in conjunction with immunosuppression, poor nutrition, endoparasitism, or poor hygiene. Acne is a type of pyoderma that occurs more commonly in young dogs. Feline: deep bacterial infections (cellulitis, abscess) are more common in outdoor animals. GENETICS & BREED PREDISPOSITION Intertrigo (skin fold pyoderma): English bulldogs Mucocutaneous pyoderma: German shepherd, Bichon frise, poodle Familial idiopathic deep pyoderma: German shepherd Acne: short-coated breeds such as boxers, Doberman pinschers, bulldogs, Great Danes, mastiffs, rottweilers, and German short-haired pointers RISK FACTORS Some forms of pyoderma, particularly superficial bacterial folliculitis (SBF) and bacterial overgrowth syndrome (BOGS) are often secondary to underlying etiologies such as hypersensitiv-ity skin disease (atopic dermatitis, food allergy, flea bite hypersensitivity), endocrinopathies (hypothyroidism, hyperadrenocorticism), parasitic skin disease (Sarcoptes, Demodex spp.), immune-mediated diseases, or cornification disorders. Deep pyoderma may be associated with underlying immunoincompe-tence. CONTAGION & ZOONOSIS Staphylococcus pseudintermedius, the cause of 90% of canine pyoderma cases, is considered nonpathogenic to humans. GEOGRAPHY AND SEASONALITY Warm and humid environments predispose animals to pyoderma.
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES Surface pyoderma: infection restricted to the surface layer of the epidermis: Dog: intertrigo (skin fold pyoderma), acute moist dermatitis (pyotraumatic dermatitis, hot spots), BOGS Superficial pyoderma: infection involving the epidermis and the infundibular portion of the hair follicle: Dog: impetigo, SBF, superficial spreading pyoderma, mucocutaneous pyoderma Deep pyoderma: bacterial infection extending beyond the hair follicle to involve the dermis and subcutis, which may lead to cellulitis: Dog: acne, pyotraumatic furunculosis, nasal folliculitis (inflammation of the hair follicle) and furunculosis (simultaneous occurrence of many furuncles, which are inflamed hair follicles that have ruptured, triggering pyogranulomatous dermal inflammation), interdigital furunculosis/pododermatitis, infected aerai lick dermatitis (lick granuloma), callus pyoderma, and postgrooming furunculosis; German shepherd pyoderma Cat: bite wounds, cellulitis, abscess, feline acne
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Pyoderma
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HISTORY, CHIEF COMPLAINT Animals typically are presented for evaluation of skin changes: pustules, crusts, epidermal collarettes, hair loss and/or pruritus. Animals with deep pyoderma may show signs of pain. PHYSICAL EXAM FINDINGS Impetigo: small nonfollicular pustules and crusts on the ventral abdomen BOGS: pruritus, greasy coat, offensive odor, erythema, lichenification, hyper-pigmentation, excoriations and alopecia SBF: papules, pustules, and epidermal collarettes with patchy alopecia, producing a “moth-eaten” appearance of the haircoat over the trunk. Resolving lesions may show central hyperpig-mentation (“bull's-eye” lesion). Superficial spreading pyoderma: large epidermal collarettes with an erythematous leading edge noted over the trunk; associated exúdate may form crusts. Canine acne: deep furunculosis and folliculitis, with crusting and possible scarring on the lips and chin of young dogs Mucocutaneous pyoderma: crusts and erosions affecting the lip margin, nasal planum, eyelid margin, vulva, prepuce, and perianal area Pyotraumatic folliculitis and furunculosis: may occur anywhere on the body depending on underlying cause; atypical acute moist dermatitis with superficial ulceration but also a component of deep folliculitis and occasional furunculosis. Clinically, this lesion may be thickened and plaque-like and have satellite papules and pustules. Nasal folliculitis and furunculosis: initially a papular/pustular eruption on the bridge of the nose that progresses to ulceration, crusting, and hemorrhage Interdigital folliculitis/pododermatitis: lesions of the feet; interdigital papulonodules, pustules, and ulceration with draining tracts and fibrosis; alopecia secondary to licking Callus pyoderma: develops over pressure points. Skin is thickened, fibrotic, and hyperpigmented with foci of papules, pustules, and ulceration. Postgrooming folliculitis/furunculosis: papular/pustular rash, crust formation, self-induced alopecia German shepherd pyoderma: lesions include ulcerations and draining tracts on the lateral thighs, trunk, and groin ± lips. Infected feline acne: comedones, papules, pustules, and alopecia confined to the mandibular and perilabial areas Feline bite wounds/abscess/cellulitis: swelling, pain, and alopecia in the affected area; possible dermal and cutaneous necrosis with ulceration, purulent exudate, and hemorrhage
PYODERMA Epidermal collarettes on ventral abdomen of a dog with pyoderma. (Copyright Dr. Manon Paradis.)
ETIOLOGY AND PATHOPHYSIOLOGY Canine skin is characterized by a relatively thin stratum corneum, a paucity of intercellular lipids, lack of a follicular plug, and a higher pH than that of humans and other domestic species. This predisposes the dog to overgrowth of commensal flora and colonization by potentially pathogenic bacteria. Superficial infection may occur if the integrity of the skin is weakened by trauma or there are changes in surface immunity. Deep bacterial infections are generally an extension of a superficial pyoderma. As infection progresses deeper into the hair follicle, rupture of the follicle (furuncles) occurs. This leads to a pyogranulomatous endogenous foreign-body reaction on the part of the host. This reaction occurs initially in the dermis and is an inflammatory response to keratin, bacterial organisms, and cellular debris.
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Pyoderma
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Approximately 90% of cases in dogs are caused by coagulase-positive S. pseudintermedius, a normal component of canine skin flora. A small number of cases are caused by Staphylococcus aureus, the most common human pathogen. Staphylococcus intermedius was reclassified as S. pseudintermedius in 2007. The gram-negative organisms, Proteus spp., Escherichia coli, and Pseudomonas spp. may act as secondary invaders. Deep pyoderma is occasionally associated with Actinomyces, Nocardia, mycobacteria, and Actinobacillus spp. In cats, Pasteurella multocida and beta-hemolytic Streptococcus are routinely involved.
DIAGNOSIS DIAGNOSTIC OVERVIEW The dermatological exam alone may provide a strong suspicion of pyoderma (see signs listed above). With clinical signs of deep pyoderma, systemic signs, or recurrence despite therapy, additional tests beyond basic dermatologic testing are often indicated to rule out predisposing causes.
DIFFERENTIAL DIAGNOSIS Demodicosis Dermatophytosis Pemphigus foliaceus Cutaneous epitheliotropic lymphoma Subcutaneous mycoses (deep pyoderma) Atypical mycobacterial infections (deep pyoderma) Hookworm (deep pedal pyoderma) Foreign-body granulomas (deep pyoderma)
INITIAL DATABASE Skin scrapings to confirm or rule out Demodex and Sarcoptes Skin cytologic examination: direct smear from pustule reveals bacteria, neutrophils in varying stages of degeneration, and active bacterial phagocytosis. Fungal culture (for dermatophytes and possibly for deep mycosis if draining tracts are present)
ADVANCED OR CONFIRMATORY TESTING Culture and sensitivity (C&S): not normally employed in superficial pyoderma cases unless there has been a failure to respond to rational antibiotic therapy or bacilli are noted on skin cytologic examination. Skin biopsy and histopathologic exam: normally not performed unless cases are not responding to appropriate antibiotic therapy. Findings include intraepidermal neutrophilic pustules, folliculitis, or furunculosis ± underlying cause (e.g., Demodex, pemphigus foliaceus, epitheliotrophic lymphoma). Endocrine status: thyroid function and adrenal function tests Allergy testing: intradermal or serum allergy testing for environmental allergies, and elimination diet trial for food allergy
TREATMENT TREATMENT OVERVIEW The main goals are to treat the infection and determine the underlying cause(s).
ACUTE GENERAL TREATMENT Topical Therapy: Most commonly used: mupirocin (Bactroderm) and fusidic acid (Fucidin). Silver sulfadiazine and benzoyl peroxide 5% gels are also available. Shampoo therapy very effectively decreases bacterial skin colonization (adjunctive therapy). Shampoo therapy (10-15 minutes contact time) with products containing benzoyl peroxide, chlorhexidine, ethyl lactate, and povidone-iodine may improve the condition. Clip the fur off affected areas. Deep pyoderma: bathe animal or soak lesion with Epsom salts solution (magnesium sulfate, 2 tablespoons/liter of lukewarm
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Pyoderma
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water) or Burow's solution (magnesium sulfate-aluminum acetate solution) daily. Systemic Antibiotic Therapy: Bactericidal antibiotics are generally recommended for skin infections; however, bacteriostatic drugs may be effective in an immunocompetent animal. The chosen drug should have a narrow spectrum to limit the effects on the normal flora of both the skin and gastrointestinal (GI) tract. Cases should be treated for a minimum duration of 3-4 weeks, or 7-14 days beyond clinical cure. Deep pyoderma may take as long as 12 weeks to resolve. The most commonly used antibiotics include (generally monotherapy): Cephalexin, 22-30 mg/kg PO q 12 h (most common choice in dogs) Clavulanic acid-potentiated amoxicillin, 12.5-25 mg/kg PO q 12 h Clindamycin, 5.5-11 mg/kg PO q 12 h Cefovecin injectable, 8 mg/kg SQ q 14 days Other suggested drugs/dosages include (generally monotherapy; all PO): cefpodoxime, 5-10 mg/kg q 24 h; cefadroxil, 22 mg/kg q 12 h; oxacillin, 22 mg/kg q 8 h; erythromycin, 10-20/ kg q 8 h (vomiting and diarrhea common); lincomycin, 15-25 mg/kg q 12 h; azithromycin, 5 mg/kg q 24 h; tylosin, 10-20 mg/kg q 12 h; trimeth-oprim-sulfa, 15-30 mg/kg q 12 h; difloxacin, 5-10 mg/kg q 12 h (not in immature animals); enrofloxacin, 5-20 mg/kg q 24 h (not in immature animals); marbofloxacin, 2.75-5.5 mg/kg q 24 h (not in immature animals); orbifloxacin, 2.5 mg/kg q 24 h (not in immature animals); doxycycline, 5 mg/kg (day 1), then 2.5 mg/kg q 12 h Appropriate pain management
CHRONIC TREATMENT In face of an idiopathic recurrent pyoderma (generally SBF) that recurs less than three or four times a year, it is often more economical and reasonable to treat each event with an appropriate course of antibiotics. Moreover, when an antibiotic (e.g., cephalexin) is effective in treating an episode of pyoderma, there is no need to change for another antibiotic when the pyoderma recurs later on. In cases of idiopathic recurrent pyoderma where several episodes occur annually and/or when total annual antibiotic administration is more than 12 weeks, adjunctive immunomodulatory therapy or extended antibiotic regimens (both controversial in veterinary dermatology) may be needed to maintain clinical remission. Immunomodulatory therapy: Staphage Lysate (SPL [Delmont Laboratories]) may help decrease recurrences of pyoderma in up to 35% of dogs. The dog should initially receive a 4- to 6-week course of oral antibiotic in conjunction with a 20- to 30-week course of SPL (0.5 mL twice weekly SQ). If the pyoderma does not recur during that period of time, the frequency of injections is gradually reduced to once weekly, then every other week. Extended regimens of antibiotic therapy (or pulse therapy). Pyoderma has to be eliminated by standard appropriate, safe, bactericidal antibiotic therapy (e.g., cephalexin) before extended regimen is used. Many different treatment regimens have been recommended. Pulse therapy implies using full therapeutic doses on an intermittent basis. One proposed regimen involves 1 week at full recommended daily dose, followed by 1 week off medication, and so on. If recurrence is prevented, the duration of the time off the antibiotic can be extended to up to 3 weeks. Two days per week dosing (at full daily dose) is another popular regimen. A third recommended regimen involves once-daily to once-every-other-day dosing. Antimicrobial shampoo or lotions used on a regular basis may assist in the prevention of relapses by limiting the bacterial surface flora.
POSSIBLE COMPLICATIONS Many antibiotics occasionally cause vomiting and diarrhea. Fluoroquinolones: cartilage damage in growing puppies Potentiated sulfonamides: keratoconjunctivitis sicca, arthritis, uveitis, immune-mediated dermatitis, hepatobiliary disease, drug interaction, decreased thyroid function (possible hypothyroidism at high dose) Benzoyl peroxide gel has to be used with care because it may be irritating with repeated use and causes fabric and hair discoloration. Drug-induced pemphigus foliaceus (cephalosporins)
RECOMMENDED MONITORING It is important to assess response to therapy before the antibiotic course is completed in order to determine the appropriate duration of antibiotic administration and also to determine if there is residual pruritus, which would suggest underlying allergy or ectoparasite or concurrent Malassezia dermatitis.
PROGNOSIS AND OUTCOME
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Superficial pyoderma: good prognosis as long as underlying factors are addressed adequately Deep pyoderma: some cases of deep pyoderma will result in scarring. Affected animals are often immuno-suppressed or have other intercurrent diseases.
PEARLS & CONSIDERATIONS COMMENTS Epidermal collarettes are extremely useful secondary skin lesions to look for (clip some hair if needed); they are strongly suggestive of a superficial pyoderma. Any therapeutic plan for controlling pyoderma without considering underlying predisposing factors is destined to fail. Most dermatologists use cephalexin as their first drug choice because it has been shown to be a very effective drug against S. pseudintermedius, with minimal change in resistance pattern over the years. Both pemphigus foliaceus and epitheliotrophic lymphoma may present as pyodermas that fail to respond to appropriate antibiotic therapy. Skin biopsy is indicated. The use of immunomodulating therapy and extended antibiotic regimen should be limited to veterinary dermatologists.
TECHNICIAN TIPS Whenever medicated shampoos are used, it is important to respect the contact time, typically 10-15 minutes. Using a timer will aid in providing sufficient contact time. Clipping the hair coat may facilitate topical treatment and accelerate healing. However, one needs the client's permission first.
CLIENT EDUCATION Counsel clients concerning the potential chronicity of the disease, owing to underlying predisposing factors. The need of long antibiotic therapy regimens, the importance of treating for 1-2 weeks beyond cure, and the need for recheck must be explained thoroughly.
SUGGESTED READING Scott DW, Miller WH, Griffin CE: Muller and Kirk’s small animal dermatology, ed 6, Philadelphia, 2001, WB Saunders, pp 274–335. AUTHOR: MICHAEL HANNIGAN EDITOR: MANON PARADIS
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Pyloric Hypertrophy Syndrome
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Pyloric Hypertrophy Syndrome BASIC INFORMATION DEFINITION Stenosis of the gastric outflow tract secondary to one of the following: hypertrophy of the circular muscle of the pylorus, hyperplasia of the mucosa of the pyloric antrum, or combination of muscular and mucosal thickening
SYNONYMS Acquired antral pyloric hypertrophy, chronic hypertrophic pyloric gastropathy, gastric antral mucosal hypertrophy, hypertrophy of the muscular layer of the pylorus, pyloric stenosis
EPIDEMIOLOGY SPECIES, AGE, SEX Congenital: dogs and cats, identified sometime after animal starts eating solid food, usually at 4-12 months of age Acquired: canine, middle-aged (4-7 years) and older GENETICS & BREED PREDISPOSITION Congenital: brachycephalic breeds including Boston terriers, English bulldogs, boxers, and Siamese cats Acquired: small, often Asian-breed dogs including Lhasa apso, shih tzu, Pekingese, and Maltese
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES Congenital: selective hypertrophy of the circular pyloric muscle Acquired: mucosal hypertrophy or combination of mucosal and muscular hypertrophy; mucosal hypertrophy may be focal (polyp) or more generalized involving entire pyloric antrum HISTORY, CHIEF COMPLAINT Chronic vomiting, usually of food several hours after eating; may be projectile In congenital form, vomiting begins after animal starts eating solid foods Anorexia Mild weight loss Regurgitation PHYSICAL EXAM FINDINGS Generally unremarkable Thin body condition is possible
ETIOLOGY AND PATHOPHYSIOLOGY Cause is unknown, and genetics of congenital form are not described. Excessive secretion of gastrin may stimulate growth of gastric smooth muscle and mucosa of gastric body. Some cases of “acquired” form may be slow progression of congenital form. Regurgitation can develop secondary to reflux esophagitis or persistent vomiting. Metabolic alkalosis (hypochloremic, hypokalemic) may develop, although only with severe luminal obstruction as fluid typically passes to the duodenum in most cases. In those cases with hypochloremic, hypokalemia, metabolic alkalosis, paradoxic aciduria is possible, although this is not clinically significant.
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DIAGNOSIS DIAGNOSTIC OVERVIEW Chronic vomiting is the main historical clue to this disorder, particularly if it is projectile in nature and/or in a brachycephalic dog. Suspicion may be increased with characteristic contrast radiographic findings, but confirmation requires direct visualization (endoscopic or via laparotomy).
DIFFERENTIAL DIAGNOSIS For clinical presentation: other causes of chronic vomiting such as parasitism or viral, bacterial, fungal, or protozoal infection, inflammatory bowel disease, food allergy or intolerance, neoplasia, obstruction, systemic disease (liver disease, kidney disease), central nervous system disease, and drugs must be ruled out by a systematic evaluation. For imaging findings: infiltrative diseases such as neoplasia, pythiosis, or other fungal diseases
INITIAL DATABASE CBC, serum biochemistry profile, and urinalysis: often unremarkable but hyponatremic, hypochloremic metabolic alkalosis and paradoxic aciduria may be present due to vomiting of gastric contents only. May have prerenal azotemia without concentrated urine secondary to inability to concentrate urine because of hypokalemia. Radiographs: usually unremarkable. Stomach may be distended with fluid, uncommonly with air. Severe pyloric hypertrophy may occasionally be noted on plain films. Ultrasound: mucosal or muscular thickening of pylorus
ADVANCED OR CONFIRMATORY TESTING Contrast radiographs using barium sulfate: delayed gastric emptying, thickening of the pylorus, abrupt narrowing of the pyloric canal filled with contrast (beaklike appearance), or a narrow band of contrast filling the pylorus. Endoscopy (seep. 1284 ): the mucosa appears normal in color, but abundant antral folds or polyps with or without erosive lesions may be seen. Muscular hypertrophy can be more difficult to appreciate, but the pylorus will not distend with air. Either lesion may create a narrowed pyloric lumen through which it is difficult to pass an endoscope. Celiotomy: thickened pylorus and abundant mucosal folds in the antrum and pylorus Histopathologic evaluation of tissue: mucosa normal or thickened with erosions, edema, and hyperplasia or cystic changes in gastric glands; increased numbers and prominent branching pattern of surface gastric pits; erosions may have lymphocyte and plasma cell infiltration; Campylobacter-like organisms have been reported.
TREATMENT TREATMENT OVERVIEW The treatment goal is elimination of pyloric canal obstruction caused by the exuberant tissue, which is achieved surgically.
ACUTE GENERAL TREATMENT Surgery is indicated for all forms of pyloric hypertrophy syndrome. Y-U pyloroplasty is the most common procedure, allows for resection of hypertrophied mucosa, and is recommended in most cases. Gastroduodenal anastomosis (Billroth I) for cases with extensive mucosal involvement, particularly when thickening results in loss of normal pliability Pyloromyotomy is often ineffective and is not recommended for any type of pyloric hypertrophy. Short-term postoperative compromise of gastrointestinal motility may be treated with metoclopramide (0.2-0.4 mg/kg q 8-12 h PO, SQ; or constant rate infusion IV 1-2 mg/kg/d).
POSSIBLE COMPLICATIONS Potential complications of surgery include infection, leakage, and dehiscence. The risk of dehiscence is greater with the Billroth I procedure. Gastrointestinal motility may be temporarily compromised after surgery.
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PROGNOSIS AND OUTCOME Prognosis is excellent if no postoperative complications occur.
PEARLS & CONSIDERATIONS COMMENTS Should be suspected in brachycephalic breeds with chronic vomiting Some cases of “pyloric stenosis” may be functional defects rather than anatomic defects. Surgery may not improve measured gastric transit time. Hypertrophic gastritis is distinct from this syndrome in that it typically spares the pylorus despite remarkable mucosal hypertrophy of the body and fundus. Seen primarily as a familial disorder as part of immunoproliferative enteropathy of Basenji dogs and familial stomatocytosis-hypertrophic gastritis of Drentse Patrijshond dogs. Reported in a single Old English sheepdog. The author has seen pyloric hypertrophy syndrome present as acute gastric dilatation without volvulus in older (8-10 years old) Labrador retrievers.
SUGGESTED READING Bellenger CR, et al: Chronic hypertrophic pyloric gastropathy in 14 dogs. Aust Vet J 67:317–320, 1990. Hedlund CS, Fossum TW: Benign gastric outflow obstructions. In Fossum TW, Hedlund CS, et al, editors: Small animal surgery, ed 3, St Louis, 2007, Mosby Elsevier, pp 433–436. AUTHOR: KENNETH HARKIN EDITOR: DEBRA L. ZORAN 1ST EDITION AUTHOR: AMIE KOENIG
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Pyelonephritis
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Pyelonephritis BASIC INFORMATION DEFINITION Pyelonephritis describes inflammation of the renal pelvis and interstitium typically associated with or originating from ascending bacterial infection. Acute pyelonephritis is uncommon; chronic pyelonephritis is more common but often clinically inapparent.
SYNONYM Pyelitis
EPIDEMIOLOGY SPECIES, AGE, SEX Dogs and cats are susceptible, with females predisposed; most common in older animals or in younger animals with predisposing cause (e.g., congenital urinary malformations, uroliths). RISK FACTORS Dogs and cats: Anatomic abnormalities: Ectopic ureter(s) Urethral/ureteral obstruction Hydroureter/hydronephrosis Perineal urethrostomy Urolithiasis Vulvar conformational abnormalities Functional abnormalities: Urine retention (>0.25 mL/kg following complete voiding) Urine reflux due to increased intra-vesicular pressure Isosthenuria or hyposthenuria from any cause Immunocompromise Indwelling urinary catheter or repeated catheterization Lower genitourinary tract infection: Dogs and cats: various bacteria; Escherichia coli most common isolate in urinary infections o Fungal and yeast pyelonephritis possible, especially in immunocompromised animals Bacterial prostatitis: intact male dogs CONTAGION & ZOONOSIS Rarely, shared clones of bacteria involved in urinary tract infections (UTI) have been found in people and their dogs. ASSOCIATED CONDITIONS & DISORDERS Acute renal failure Chronic kidney disease Hypokalemia (cats) Bacterial cystitis Urolithiasis
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES Ascending pyelonephritis Hematogenous pyelonephritis: rare; may be associated with septicemia HISTORY, CHIEF COMPLAINT
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Clinical signs may be absent; chronic pyelonephritis is a common complicating factor in chronic kidney disease. When present, clinical signs may include: Polyuria and polydipsia (PU/PD; acute or chronic pyelonephritis) Malaise (uncommon) Hematuria Pollakiuria, stranguria (if concurrent lower urinary tract disorder) Abdominal, lumbar, or general discomfort (usually associated with acute pyelonephritis) Recurrent lower urinary infections (chronic pyelonephritis) History of predisposing cause may be present (e.g., urinary catheterization, uroliths) PHYSICAL EXAM FINDINGS Exam may be normal, especially in the more common chronic form of infection. Abnormalities, when present, may include: Fever (more often associated with acute pyelonephritis) Dehydration Renomegaly (acute pyelonephritis) Renal asymmetry (chronic pyelonephritis) Abdominal/renal/lumbar pain Oral ulcerations/halitosis (uremia) Debris or secretions in the oral cavity (vomitus, saliva) Bladder discomfort (if concurrent lower urinary infection)
ETIOLOGY AND PATHOPHYSIOLOGY Infectious agent (bacteria, fungus, yeast) usually ascends to renal pelvis from lower urinary tract. The agent rarely infects the kidneys hematogenously. Onset may be acute (less common) or insidious (more common). Renal response to injury causes clinical signs: Acute infection results in nephritis (renal inflammation), causing renomegaly and renal pain. Acute or chronic infection causes nephrogenic diabetes insipidus via bacterial toxin actions on antidiuretic hormone receptors. Chronic infection results in renal scarring, resulting in smaller than normal kidneys. Infection may result in acute renal failure, overt chronic kidney disease, or exacerbation of preexisting chronic kidney disease.
DIAGNOSIS DIAGNOSTIC OVERVIEW The diagnosis of pyelonephritis should be considered in any animal with pyuria and/or bacteriuria (especially in absence of lower urinary tract signs), polyuria/polydipsia, kidney disease, chronic lower urinary tract infection, or immunocom-promise. Although acute pyelonephritis may cause dramatic illness, chronic pyelonephritis with obscure clinical signs occurs more commonly.
DIFFERENTIAL DIAGNOSIS PU/PD (see p. 902) PD from psychogenic causes, hyperosmolarity, or alteration of the thirst center (e.g., central nervous system [CNS] neoplasia) Osmotic diuresis (e.g., diabetes mellitus, renal glucosuria, drug or toxin) Nephrogenic diabetes insipidus (e.g., congenital, electrolyte abnormalities, hormonal abnormalities, renal failure) Deficient interstitial concentrating gradient (e.g., medullary washout, hyponatremia, portosystemic shunt) Lack of antidiuretic hormone (i.e., central diabetes insipidus) Bacteria (see pp. 276 and ) Pyelectasia (seep. 547 )
INITIAL DATABASE CBC: may be normal (chronic pyelonephritis) or may show leukocytosis with left shift (acute pyelonephritis); normocytic, normochromic nonregenerative anemia is possible with concurrent chronic kidney disease. Serum biochemical profile: often normal, but when acute or chronic renal disease is present, azotemia (elevated blood urea nitrogen [BUN], creatinine), hyperphosphatemia, hypokalemia, or hyperkalemia, and/or metabolic acidosis are often identified.
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Urinalysis: isosthenuria is common; bacteria is inconsistent and often absent; occasionally leukocyte casts (acute pyelonephritis), pyuria, hematuria, and/or crystalluria. Abdominal radiographs: variable renal shadow (normal, large, or small and irregular). Radiopaque urinary (upper or lower) calculi (suspect struvite) are sometimes present. Abdominal ultrasound: renal pelvic dilation is common; renomegaly or small and irregular kidneys, alterations in renal parenchymal echogenicity also can be present. Urine culture prior to treatment whenever suspicion of pyelonephritis exists (even if urine sediment inactive): In occult pyelonephritis, urine culture can be negative.
ADVANCED OR CONFIRMATORY TESTING Pyelocentesis (ultrasound guided) to obtain urine directly from the renal pelvis for culture; this procedure is uncommonly used. Begin with routine cystocentesis instead and choose pyelocentesis if trying to pinpoint source of infection to one kidney (rarely clinically necessary). Excretory urogram and/or cystourethrogram to rule out anatomic abnormalities. Abdominal ultrasound is the preferred first choice instead. If clinical signs are compatible, rule out hyperadrenocorticism as a predisposing cause. Renal cortex biopsy: typically not helpful to diagnose pyelonephritis, owing to localization of disease (renal pelvis and interstitium).
TREATMENT TREATMENT OVERVIEW The mainstay of treatment is long-term therapy with appropriate type and dose of antimicrobial drugs. It is often a challenge to obtain a positive urine culture, despite renal infection. Since pyelonephritis often occurs secondary to another disease process, recurrence is common unless the predisposing condition can be addressed. Renal failure is addressed as needed (see pp. 31, , and ).
ACUTE GENERAL TREATMENT Antimicrobial therapy: Antibiotic selection is based on culture and antimicrobial susceptibility (C&S) results whenever possible. Pending results, or if culture is negative despite clinical suspicion of pyelonephritis, therapy is indicated using an antibiotic with gram-negative spectrum that is renally excreted (fluoroquinolone, augmented penicillin, trimethoprimsulfa) to reach adequate tissue concentrations. Examples: Fluoroquinolone, such as enrofloxacin, 5-20 mg/kg q 12-24 h (dogs), or 5 mg/kg q 24 h (cats) PO, IM, or diluted 1:1 with sterile saline and given slowly IV (oral therapy instituted when practical) Amoxicillin with clavulanic acid, 22 mg/kg PO q 8-12 h For intact male dogs, it is preferable to select an antimicrobial that will penetrate the blood-prostate barrier (e.g., fluoroquinolone, trimethoprim-sulfa). Due to the sluggish rate of renal medullary blood flow, duration of antibiotic therapy should be greater than that for a simple lower urinary tract infection. Therapy typically lasts 3-6 weeks depending on clinical improvement, underlying disease, and follow-up test results. If initial urine sediment was active, a repeat urinalysis about 1 week after starting antibiotic therapy is recommended to ensure resolution of bacteruria and pyuria. If predisposing cause cannot be resolved, urine cultures should be repeated regularly to address future infections. Fungal pyelonephritis may be more difficult to eradicate than bacterial pyelonephritis (see online chapter: Cystitis, Fungal/Algal). Treatment of uremic renal failure starts with isotonic crystalloid fluid therapy (see pp. 31 and ). Medical therapy for hypokalemia: Occurs commonly in cats with chronic PU/PD Potassium chloride (KCl) supplementation of IV fluids used for diuresis, based on sliding scale (see table): Do not exceed a rate of 0.5 mEq KCl/kg per hour for potassium replacement. Recheck potassium levels are indicated at least daily during fluid therapy. When the patient is eating, oral potassium gluconate replacement can be initiated at a starting dose of 2 mEq per cat q 12 h, adjusted as needed based on serial serum potassium measurements. Uremic signs are managed as for acute renal failure and chronic kidney disease (see pp. 31 and 207). Maintain fluid balance: Hospitalization is not indicated if the patient is drinking and eating enough to maintain hydration. If the patient is hospitalized for IV fluid therapy, fluids should be tapered slowly over 2-3 days and discontinued once hydration is maintained by oral intake. Administer as constant rate infusion via infusion pump to minimize risk of overly rapid delivery, and adjust supplementation as needed
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based on repeated assessments of serum potassium concentrations. Not for oliguric/anuric patients.
Potassium Supplementation in Intravenous Fluid Therapy Serum Potassium Concentration Potassium Supplementation to IV Fluids Potassium 3.5–5.5 mEq/L
Add 20 mEq KCl/L crystalloid
Potassium 3–3.4 mEq/L
Add 30 mEq KCl/L crystalloid
Potassium 2.5–2.9 mEq/L
Add 40 mEq KCl/L crystalloid
Potassium 2–2.4 mEq/L
Add 60 mEq KCl/L crystalloid
Potassium < 2 mEq/L
Add 80 mEq KCl/L crystalloid
In cats and small dogs, the ability to maintain hydration might require a period of adaptation. Following hospital discharge, SQ crystalloid fluid therapy might be indicated q 12-48 h (seepp. 31 and ).
CHRONIC TREATMENT Identification, treatment, or cure of predisposing cause if possible (e.g., hyperadrenocorticism, ectopic ureter, urolithiasis) Other treatments for chronic kidney disease as necessary (see pp. 205 and 207)
NUTRITION/DIET Recommend diets appropriate for management of renal failure if it exists. A diet restricted/optimized in protein and phosphorus is ideal. Regardless, ensure the availability of fresh drinking water at all times.
DRUG INTERACTIONS Cats should be treated cautiously with enrofloxacin, since acute retinal degeneration can occur. Avoid trimethoprim-sulfa antibiotics in Doberman pinschers or dogs with keratoconjunctivitis sicca.
POSSIBLE COMPLICATIONS Failure to resolve infection. Bacterial resistance is common if there is infection secondary to an underlying process or a structural lesion. Urolithiasis (nephrolithiasis), ureteral obstruction due to urolithiasis
RECOMMENDED MONITORING A repeat urine culture 1-2 weeks after completion of antibiotics and approximately 1 and 2 months later are indicated to ensure negative culture. If predisposing cause cannot be resolved (e.g., chronic kidney disease), monitoring should include urinalysis and urine culture every 3-6 months to identify recurrence. When initial urine culture is negative despite clinical suspicion of pyelonephritis, monitoring should include water consumption daily before and after initiation of antibiotics to assess efficacy of therapy. If water consumption decreases within 2 weeks of antimicrobial therapy, treatment should be continued for a total of 3-6 weeks.
PROGNOSIS AND OUTCOME Guarded to good depending on ability to correct predisposing cause and antimicrobial susceptibility of pathogen Prognosis for recurrent pyelonephritis is guarded, since infections can cause chronic or acute renal failure, and recurrent infections tend to develop multiple antimicrobial resistance over time.
PEARLS & CONSIDERATIONS COMMENTS Pyelonephritis is often difficult to confirm, especially after antimicrobial therapy has been initiated.
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Evidence of renal pelvic dilation (pyelectasia) on ultrasound, without other supportive clinical findings, might indicate a past infection with permanent renal injury instead of active infection. Vigorous IV fluid therapy can also cause pyelectasia and should be considered an ultrasonographic differential diagnosis for pyelonephritis. Chronic pyelonephritis can occur without producing any overt clinical signs and without changes on CBC, serum biochemical profile, or urine sediment exam. A urine C&S is warranted in the management of any chronic renal disorder, because pyelonephritis may be clinically silent and difficult to detect (e.g., diluted urine may give the mistaken appearance of an inactive sediment); however, the condition is treatable, potentially resulting in a reversal of renal tubular damage.
PREVENTION Address anatomic or functional abnormalities directly. Treatment of infections with the appropriate antimicrobial therapy at the correct dose for at least 3-6 weeks Regular follow-up visits to identify recurrent infections as early as possible
TECHNICIAN TIPS Urinary catheterization can introduce bacteria; therefore, strict aseptic technique should be used. Animals that are hospitalized should be allowed to empty their bladder on a regular basis. Dogs that are particularly well housetrained can retain urine when kenneled, which can predispose to ascending pyelonephritis. Cats may have preferences for the type of cat litter used. Monitoring frequency and volume of urine output in hospitalized animals is vitally important.
CLIENT EDUCATION Owner education regarding signs of lower and upper urinary tract infection before pyelonephritis develops Treatment of resistant strains of bacteria causing pyelonephritis may be costly and require prolonged therapy. Chronic kidney disease may predispose animals (especially cats) to recurrent renal infections.
SUGGESTED READING Bartges JW: Diagnosis of urinary tract infections. Vet Clin North Am Small Anim Pract 34:923, 2004. Bartges JW, Barsanti JA: Bacterial urinary tract infections in cats. In Bonagura JD, editor: Kirk’s current veterinary therapy XIII. Philadelphia, 2000, WB Saunders, pp 880–882. Cowgill LD, Francey T: Acute uremia. In Ettinger SJ, Feldman EC, editors: Textbook of veterinary internal medicine, vol 2, ed 6, St Louis, 2005, Elsevier, pp 1731–1751. Newman SJ, et al: Cryptococcal pyelonephritis in a dog. J Am Vet Med Assoc 222:180, 2003. AUTHOR: MARIE E. KERL EDITOR: LEAH A. COHN
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Pustular and Crusting Skin Disorders
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Pustular and Crusting Skin Disorders BASIC INFORMATION DEFINITION Pustules and crusts are common skin lesions. Pustules are small, circumscribed elevations of the skin filled with pus. Healing or ruptured pustules may form crusts, the dried accumulation of exúdate (blood, pus, serum) over a lost or damaged epidermis.
EPIDEMIOLOGY SPECIES, AGE, SEX Dogs and cats In dogs, impetigo, demodicosis, juvenile cellulitis and dermatophytosis are typically seen in young animals. Pemphigus is more common in middle-age adults. Hereditary mechanobullous disease: epidermolysis bullosa develops shortly after birth. Drug eruptions may occur at any age. GENETICS & BREED PREDISPOSITION Juvenile cellulitis (seep. 627 ): dachshund, golden and Labrador retrievers, Gordon setters, pointers. More than one puppy can be affected in a litter. Subcorneal pustular dermatosis and superficial suppurative necrolytic dermatitis: miniature schnauzer Pemphigus foliaceus: Akita, chow chow, dachshund Drug eruption (especially sulfon-amides): Doberman pinscher Canine linear immunoglobulin A (IgA) pustular dermatosis: dachshund RISK FACTORS Pyoderma, the most common cause of pustular and crusting dermatitis in dogs, is often secondary to a predisposing skin disease (atopic dermatitis, food allergy, demodicosis, end ocrinopathies). With the exception of abscesses, pyoderma is uncommon in cats. Cats affected with feline immunodeficiency virus (FIV) are more susceptible to dermatophytosis. CONTAGION & ZOONOSIS Dermatophytosis is contagious to other animals and is zoonotic. GEOGRAPHY AND SEASONALITY Pemphigus foliaceus and pemphigus erythematosus (see p. 850) can be aggravated by exposure to sunlight. Pyodermas associated with underlying atopic dermatitis may have a seasonal occunence. ASSOCIATED CONDITIONS & DISORDERS Bullous impetigo in adult dogs is often associated with immunosuppression (e.g., hyperadrenocorticism, diabetes mellitus, hypothyroidism).
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT Pustules are usually short-lived and may go unnoticed. Scaling and crusting are often the dominant presentation. Pruritus varies with the skin disorder. It can be a major presenting complaint in pyodermas, with or without underlying allergies or ectoparasitism. A variable degree of hair loss may accompany follicular damage. Systemic signs of lethargy and anorexia can be part of the presenting picture with pemphigus foliaceus, cutaneous drug eruptions, or superficial suppurative necrolytic dermatitis of the miniature schnauzer.
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PHYSICAL EXAM FINDINGS Pustules are most commonly yellow. Green pustules may indicate the presence of gram-negative bacteria or marked toxic change. Larger flaccid pustules are more common in the pemphigus complex and bullous impetigo. Scales, epidermal collarettes, crusts of various color (brown, honey-colored) and texture (adherent, flaky), alopecia, erythema, and focal areas of hyperpig-mentation or hyperkeratosis may be noted. Depending on the condition and severity, the extent and location of lesions may be variable.
ETIOLOGY AND PATHOPHYSIOLOGY Pustules result from a loss of epidermal intercellular cohesion (edema, degeneration, inflammation, autoantibody formation, etc.), causing epidermal or subepidermal cavities that eventually fill with inflammatory cells.
DIAGNOSIS DIAGNOSTIC OVERVIEW The combined presence of crusts and pustules restricts the differential diagnosis, but pustules can be short lived, and the clinician should perform a careful examination before confirming their absence. Cytologic examination of the content of an intact pustule or from the exudates under a crust is an important step to orient the diagnosis. When pustules or crusts are present in dogs, skin scrapings should always be performed to rule out demodicosis. Skin biopsies are recommended in most cases presenting with pustules and crusts once pyoderma, demodicosis, and dermatophytosis have been ruled out.
DIFFERENTIAL DIAGNOSIS Infectious: pustules most often have a follicular orientation. Bacterial: pyoderma (bacterial folliculitis*, impetigo*, furunculosis), dermatophilosis Fungal: dermatophytosis *
Parasitic: demodicosis , Pelodera dermatitis Protozoal: leishmaniasis *
*
Immune mediated: juvenile cellulitis, pemphigus complex (especially pemphigus foliaceus ), canine eosinophilic folliculitis and *
*
furunculosis, canine sterile eosinophilic pustulosis , subcorneal pustular dermatosis , and canine linear IgA pustular *
dermatosis Drug eruption: superficial suppurative necrolytic dermatitis of schnauzers (associated with shampoo therapy), drug-induced pemphigus foliaceus, and eosinophilic pustulosis (subcorneal to follicular neutrophilic pustulosis) *Intact pustules are often present
INITIAL DATABASE The medical history of the animal is important in determining etiology: age of onset, breed, presence or absence of pruritus, previous medications, other animals affected, progression, chronicity, and seasonality. Lesion distribution is important to orient the diagnosis: Face (lips, muzzle, eyelids, ear pinnae): juvenile cellulitis, pemphigus erythematosus, demodicosis, eosinophilic folliculitis and furunculosis, nasal pyoderma, mucocutaneous pyoderma, drug eruption Feet: pyoderma, dermatophytosis, demodicosis, pemphigus foliaceus Trunk: superficial pyoderma, demodicosis, subcorneal pustular dermatosis, pemphigus foliaceus, drug eruption, impetigo (abdomen) Cytologic examination of pustular contents: Bacteria: phagocytized bacteria (often cocci, because staphylococcal organisms are the primary isolates from dogs and cats with pyoderma). Neutrophils: pyoderma, pemphigus complex, subcorneal pustular dermatosis, and canine linear IgA pustular dermatosis Eosinophils: abundant eosinophils with eosinophilic folliculitis/furunculosis and sterile eosinophilic pustulosis; eosinophils are also associated with superficial pyodermas with parasitic or allergic disorders, deep pyodermas (furunculosis), drug eruptions, and pemphigus foliaceus. Acantholytic keratinocytes: seen in pemphigus complex in conjunction with numerous intact neutrophils and/or eosinophils Skin scrapings: Demodex spp. Fungal culture: dermatophytosis CBC, serum biochemistry profile, and urinalysis if systemic disease is suspected; results often unremarkable besides
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mild/moderate neutrophilic or eosinophilic leukocytosis.
ADVANCED OR CONFIRMATORY TESTING Skin biopsies for histopathologic evaluation Bacterial culture and sensitivity (C&S) indicated if bacilliform bacteria are noted on cytologic examination or if poor response to previous appropriate antibiotic therapy. Endocrine tests if history and physical exam suggest underlying endocrinopathy. Serologie testing for FIV, feline leukemia virus (FeLV), leishmaniasis, based on history and environment
TREATMENT TREATMENT OVERVIEW Pyoderma is the most common cause of pustules and crust formation in dogs. Most pyodermas are successfully addressed with antibiotic therapy. Because etiologies of crusting and pustular skin diseases are often infectious or parasitic, glucocorticoids should not be used until a final diagnosis has been reached.
ACUTE AND CHRONIC TREATMENT Depends on etiology of the disorder: Antibiotic therapy: common empirical choices include cephalexin, 22-30 mg/kg PO q 12 h; or amoxicillin-clavulanate, 15-20 mg/kg PO q 12 h, usually for 1-2 weeks beyond resolution of lesions. A more specific selection can be made based on results of C&S. Antifungal therapy: itraconazole, 5 mg/kg PO q 24 h for 3-6 weeks (pulse or continuous) is a good first-choice therapy in cats with dermatophytosis. Antiparasitics: choice depends on the parasite identified. Glucocorticoids for immune-mediated disorders such as juvenile cellulitis, pemphigus complex, eosinophilic folliculitis/furunculosis, eosinophilic pustulosis Prednisone/prednisolone is a common first choice in dogs, usually for 10-14 days at high induction dosage (2-4 mg/kg PO q 24 h) then gradually tapered according to clinical response. Prednisolone (specifically) is preferred in cats.
PROGNOSIS AND OUTCOME Varies according to the disease Excellent for most parasitic and infectious skin diseases Excellent for some immune-mediated skin diseases such as juvenile cellulitis, sterile eosinophilic folliculitis, and furunculosis
PEARLS & CONSIDERATIONS COMMENTS Crusts alone are noted in certain diseases, such as in cornification disorders or zinc-responsive dermatosis. Crusts secondary to excoriations are frequently seen in atopic dermatitis, food intolerance, and flea bite dermatitis. Treat and rule out the presence of pyoderma before taking biopsies.
CLIENT EDUCATION In lay terms, pustules are “pimples” and crusts are “scabs.”
SUGGESTED READING Bensignor E: Diagnostic approach to crusting dermatoses. In Gaguère E, Prélaud P, editors: A practical guide to feline dermatology, Lyon, France, 1999, Merial, pp 20.1–20.4. Medleau L, Hnilica KA: Small animal dermatology, a color atlas and therapeutic guide, ed 2, St Louis, 2006, Saunders Elsevier.
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Scott DW, Miller WH, Griffin CE: Diagnostic methods. In Scott DW, Miller WH, Griffin CE, editors: Muller and Kirk’s small animal dermatology, ed 6, Philadelphia, 2001, WB Saunders, pp 71–206. AUTHOR: CAROLINE DE JAHAM EDITOR: MANON PARADIS
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Pupil Abnormalities
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Pupil Abnormalities BASIC INFORMATION DEFINITION Abnormalities include pupils that are inappropriately dilated or constricted as well as pupils with distorted shape.
SYNONYMS Anisocoria: unequal or asymmetric pupils Dyscoria: misshapen/distorted pupil Miosis: constricted pupil Mydriasis: dilated pupil
EPIDEMIOLOGY SPECIES, AGE, SEX Dogs and cats Iris atrophy is a normal aging change and is therefore seen in older animals. Iris coloboma (absence of or defect in iris) is a developmental/heritable condition that is usually noticed initially in young animals, most frequently dogs. GENETICS & BREED PREDISPOSITION Distorted pupil: A distorted pupil, such as iris coloboma, may be breed-related in dogs. Australian shepherds and dal-matians are overrepresented. Dilated pupil: Glaucoma, primary (predisposed breeds) Toy and miniature poodles are predisposed to optic nerve hypoplasia. Heritable retinal degeneration in many breeds of dogs (see p. 983)
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES Conditions that lead to pupil abnormalities can be divided into those that cause: Pupillary dilation (mydriasis) Pupillary constriction (miosis) Abnormal pupil shape (dyscoria) HISTORY, CHIEF COMPLAINT The pet's owner may notice abnormalities in pupil size and shape. More likely, veterinarians notice the pupil abnormalities in animals presenting for painful, red, or blind eyes. PHYSICAL EXAM FINDINGS Dilated pupil and the following: Scalloping at pupillary margin: Iris coloboma: focal; young animal Iris atrophy: typically multifocal and/or “moth-eaten” effect in iris stroma; typically age-related change (i.e., older animals) Blindness (negative menace response): See Retinal Degeneration, p. 983; Retinal Detachment, p. 985.
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Optic nerve lesion (e.g., optic nerve hypoplasia, congenital, glaucoma [seep. 1559 ], optic neuritis (seep. 784) Optic chiasmal lesion (see p. 784) “Quiet” (i.e., nonred) sighted (visual) eye: Internal ophthalmoplegia (paralysis of the iris and ciliary muscles) caused by: Pharmacologic pupillary dilation (e.g., parasympatholytics such as atropine and topical tropicamide) Iris atrophy Lesions involving the parasympathetic fibers of the oculomotor nerve (cranial nerve [CN] III); relatively rare Fearful animal (i.e., sympathetic stimulation): transient mydriasis; resolves once animal becomes calm Constricted pupil and the following: Red eye with or without vision impairment: See Uveitis, . Corneal ulceration (seep. 250 ) and “axon reflex” miosis through trigeminal and oculomotor nerves (CNs V and III) Pharmacologic pupillary constriction (e.g., parasympathomimetic, such as topical pilocarpine, dem-ecarium, or synthetic prostaglan-dins; such analogs include latanoprost, bimatoprost, and tra-voprost; may cause conjunctival hyperemia). Quiet eye with or without vision impairment: Horner's syndrome (see p. 543): other signs include ptosis (drooping of upper eyelid), enophthal-mos (caudal displacement of the eye), and third eyelid protrusion. Distorted pupil and the following: Scalloping at pupillary margin: Iris coloboma: focal; young animal Iris atrophy: typically multifocal and/or “moth-eaten” effect in iris stroma; typically age-related change (i.e., older animals) Red eye with or without vision impairment: Adhesions of iris to lens and/or iris to cornea (posterior and anterior synechiae, respectively) from current or past anterior uveitis (see p. 1151) Iris prolapse through full-thickness corneal lesion (see p. 249) Iridodonesis (tremulousness of the iris on movement of the eye) noted, with loss of iris support subsequent to lens subluxation/luxation (see pp. 644 and ) Anisocoria: Primary iridal disease (age-related atrophy); heritable or developmental coloboma, active inflammatory process causing miosis; chronic inflammation leading to degeneration and/or posterior synechia Primary neurologic cause (CN III abnormality, Horner's syndrome, fright response) Pharmacologic agents (miotics such as pilocarpine, mydriatics such as atropine and tropicamide) Unresponsive pupil(s): Retinal disease (seep. 141 ) Optic nerve disease Iridal disease (see p. 141) Pharmacologic agents Posterior synechia secondary to anterior uveitis
DIAGNOSIS DIAGNOSTIC OVERVIEW Diagnosis of pupil abnormalities requires consideration of the entire eye as well as the orbit and the brain. Pupil abnormalities are frequently indicative of serious but nonocular problems.
INITIAL DATABASE Complete ophthalmic examination (seep. 1313 ), including: Neuro-ophthalmic examination (seep. 1311 ) (i.e., menace response; dazzle, palpebral, pupillary light, and vestibulo-ocular reflexes) Fluorescein stain application (miosis commonly occurs in animals with corneal ulceration) Intraocular pressures (>30 mm Hg with glaucoma; often low [< 10-15 mm Hg] with uveitis)
ADVANCED OR CONFIRMATORY TESTING Variable depending on underlying condition:
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Pharmacologic testing (e.g., 10% phen-ylephrine) for Horner's syndrome CT scans, MRIs, and other imaging procedures; cerebrospinal fluid tap for diseases of the neurologic system (e.g., optic neuritis; optic chiasmal lesions) or orbital disorders Electroretinogram (see p. 1255) to assess retinal function (also see p. 983)
TREATMENT TREATMENT OVERVIEW If a specific systemic cause of oculomotor neuropathy, optic neuropathy, anterior uveitis, or Horner's syndrome can be identified, treatment should address the specific cause. Treatment is either not indicated or not available for iris atrophy, iris coloboma, optic nerve hypoplasia, retinal degeneration, and optic nerve atrophy/degeneration.
ACUTE AND CHRONIC TREATMENT Directed at underlying cause
PROGNOSIS AND OUTCOME Prognosis varies widely depending on underlying condition and cause. Many causes of pupil abnormalities are completely innocuous, while others may be life threatening.
PEARLS & CONSIDERATIONS COMMENTS Many pupil abnormalities can be diagnosed with careful consideration of the signalment and the presence or absence of other ophthalmic signs.
CLIENT EDUCATION Pupil abnormalities can be an early sign of serious disease. Early detection may improve prognosis
SUGGESTED READING Grahn BH, Cullen CL, Peiffer RL: Neuro-ophthalmology. In: Veterinary ophthalmology essentials. Philadelphia, 2004, Butterworth Heinemann, pp 200–224. Ofri R: Neuro-ophthalmology. In Maggs DJ, Miller PE, Ofri R, editors: Slatter’s fundamentals of veterinary ophthalmology, ed 4, St Louis, 2008, Saunders Elsevier, pp 318–351. AUTHOR: STEVEN R. HOLLINGSWORTH EDITOR: CHERYL L. CULLEN
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Pulse Abnormalities
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Pulse Abnormalities BASIC INFORMATION DEFINITION The arterial pulse is produced by the fluctuation between diastolic and systolic arterial pressure and can be palpated as an impulse in superficial arteries, such as the femoral artery. Pulse deficit refers to a heartbeat that is heard on auscultation or felt on the chest wall but does not generate a palpable arterial pulse.
SYNONYMS Hyperkinetic pulse: strong, bounding, or “water-hammer” pulse Hypokinetic pulse: weak or “thready” pulse
EPIDEMIOLOGY SPECIES, AGE, SEX Dogs and cats of either sex and any age ASSOCIATED CONDITIONS & DISORDERS Reduced pulse amplitude (hypokinetic pulse): Decreased cardiac output (hypovo-lemia, systolic dysfunction) Left ventricular outflow tract obstruction (aortic stenosis, systolic anterior motion of the mitral valve). The pulse is not transmitted normally to the peripheral arteries; with aortic stenosis, it may be decreased and delayed (pulsus parvus et tardus). Increased pulse amplitude (hyperkinetic pulse): Increased stroke volume (anemia, pregnancy, increased sympathetic tone, hyperthyroidism, bradyarrhythmias) Decreased diastolic arterial pressure (patent ductus arteriosus, aortic insufficiency). Diastolic runoff through the ductus arteriosus or aortic valve, respectively, causes a greater difference between systolic and diastolic pressures (greater pulse pressure) and a correspondingly stronger pulse. Variation in pulse amplitude: Exaggerated effect of respiration: pulsus paradoxus (pericardial effusion with cardiac tamponade). The pulse is stronger during expiration and weaker during inspiration. Tachyarrhythmias (atrial fibrillation, ventricular and atrial premature complexes, ventricular tachycardia). Generally, in a given animal with one of these arrhythmias, the pulse becomes weaker with higher heart rates or beats that are more premature. Severe myocardial failure (pulsus alternans). The pulse amplitude alternates between a strong pulse and a weak (or absent) pulse. Regional variation in pulse amplitude: Arterial thromboembolism (feline myocardial disease, infective endocarditis, hypercoagulable states) Variation in pulse rhythm: Tachyarrhythmias (atrial fibrillation, premature atrial and ventricular complexes) Bradyarrhythmias (second-degree atrioventricular block)
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT Highly variable and dependent on underlying cause PHYSICAL EXAM FINDINGS Systemic or primary cardiac problems may alter the pulse; therefore, a complete physical exam is necessary. Femoral pulses are easiest to palpate in cats and dogs. The dorsal metatarsal pulse can also be palpated. Auscultate heart sounds simultaneously (by definition, a pulse deficit exists when a heart sound does not have a
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corresponding palpable peripheral pulse). Pulse quality relates mainly to pulse amplitude (also affected by rate of rise of arterial pressure in systole and affected by pulse duration).
ETIOLOGY AND PATHOPHYSIOLOGY Pulse pressure: difference between systolic and diastolic blood pressure (BP) Variations in left ventricular stroke volume are detected as variation in arterial pulse pressure. With premature beats, the weak ventricular contraction may not generate sufficient systolic pressure to open the aortic valve, 2
and no S or pulse is produced (S! is still normally heard). Variations in stroke volume will also occur with the phase of respiration with cardiac tamponade, where increased filling of the right heart during inspiration leads to decreased filling of the left heart and a reduced pulse pressure. Pulsus alternans is an uncommon finding characterized by alternate pulses that are very weak or even absent despite consistent electrical activation (due to abnormal intracellular calcium cycling in myocardial failure).
DIAGNOSIS DIAGNOSTIC OVERVIEW A pulse abnormality is inherently a physical exam finding, and its significance may vary from harmless (e.g., seemingly weak pulse in an obese patient) to indicative of systemic or primary cardiac disturbances. An intermittent pulse deficit should be investigated initially with an electrocardiogram; a weak pulse should be assessed with evaluation of the patient's intravascular volume status (hydration) and cardiac function (auscultation, thoracic radiographs, echocardiogram).
DIFFERENTIAL DIAGNOSIS Hypokinetic pulse: obesity, arterial disease/disorder. The combination of hypokinetic pulse and a palpably strong or hyperdynamic heartbeat (apex beat) is strongly suggestive of outflow obstruction (e.g., moderate to marked aortic stenosis or, less commonly, pulmonic stenosis). Hyperkinetic pulse: thin body condition Variation in pulse amplitude: normal variation as occurs with respiratory sinus arrhythmia (pulse is stronger after pause)
INITIAL DATABASE The presence of pulse deficit should prompt recording of an electrocardiogram. The presence of alternate pulse deficits with normal sinus rhythm (pulsus alternans) should prompt a thoracic radiographic exam and an echocardiographic exam.
TREATMENT TREATMENT OVERVIEW Management of underlying cause
PROGNOSIS AND OUTCOME Highly variable and dependent on underlying cause
PEARLS & CONSIDERATIONS COMMENTS Palpation of the peripheral arterial pulse can give useful information about stroke volume and cardiac output. Palpation of the arterial pulse is not a useful way of detecting systemic hypertension. Presence of a hyperkinetic pulse may be more obvious than a diastolic murmur with severe aortic insufficiency (as with infective endocarditis of the aortic valve). Pulsus paradoxus is a very helpful finding when cardiac tamponade is suspected, but it may be difficult to detect if the dog is
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panting.
SUGGESTED READING Perloff JK: The arterial pulse. In Perloff JK, editor: Physical examination of the heart and circulation, ed 3, Philadelphia, 2000, WB Saunders Company, pp 65–111. AUTHOR: VIRGINIA LUIS FUENTES EDITOR: ETIENNE CÔTÉ
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Pulmonic Stenosis
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Pulmonic Stenosis BASIC INFORMATION DEFINITION A fixed or dynamic impediment to the ejection of blood from the right ventricle (RV) due to abnormal narrowing of the right ventricular outflow tract, pulmonic valve orifice, or main pulmonary artery
SYNONYM Pulmonic valve dysplasia
EPIDEMIOLOGY SPECIES, AGE, SEX Pulmonic stenosis (PS) is the third most common congenital heart defect in dogs. It is an uncommon congenital defect in cats, which are more likely to develop acquired, benign dynamic infundibular RV outflow tract obstructions as adults, most often in association with other systemic or cardiac diseases. GENETICS & BREED PREDISPOSITION Inherited as a polygenic trait or single gene defect with variable penetrance. English bulldogs, miniature Schnauzers, Chihuahuas, Samoyeds, miniature pinschers, boxers, Labrador retrievers, mastiffs, beagles, fox terriers, Scottish terriers, West Highland white terriers, other terrier breeds are overrepresented. ASSOCIATED CONDITIONS & DISORDERS Pulmonic stenosis occurs most often as an isolated defect but may be combined with other defects of the conotruncal septum (e.g., tetralogy of Fallot). The tricuspid valve apparatus is concurrently malformed in about one-third of dogs with pulmonic stenosis.
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES Four anatomic types of obstruction can occur: supravalvular, valvular, subvalvular, and infundibular. While the functional consequences of these different types of obstruction are similar, their distinction is important if repair is contemplated. HISTORY, CHIEF COMPLAINT Affected animals may show no overt clinical manifestations or may exhibit exercise intolerance or syncope. Signs of right heart failure (venous engorgement, hepatomegaly, ascites) or sudden death occur in severely affected animals. PHYSICAL EXAM FINDINGS A systolic ejection murmur is typically best heard at the left heart base, specifically over the pulmonic area. It may also radiate loudly cranially along the sternal border. Arterial pulses are unremarkable unless severe heart failure is present. Jugular distension, jugular pulses, hepatosplenomegaly, and ascites develop with the onset of right heart failure. Cyanosis may be observed when PS is complicated by right-to-left shunting across a patent foramen ovale or coexisting atrial or ventricular septal defect.
ETIOLOGY AND PATHOPHYSIOLOGY Increased resistance to ejection results in concentric RV hypertrophy (RVH), which develops in proportion to the severity of obstruction. The resulting decline in right ventricular diastolic compliance impairs ventricular filling, resulting in elevated right atrial pressure. Tricuspid regurgitation from progressive ventricular dilation or concurrent valvular dysplasia further increases right atrial pressure.
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Hypertrophy of the infundibular region of the right ventricular outflow tract may also contribute to outflow tract obstruction, particularly during exercise. This additional mechanism of obstruction can be particularly problematic following surgical valvotomy or balloon valvuloplasty.
DIAGNOSIS DIAGNOSTIC OVERVIEW The diagnosis is suspected in a patient with a systolic heart murmur with point of maximal intensity over the left cardiac base. Signalment, pattern of murmur radiation on the chest and neck, and thoracic radiographic findings can help raise or lower suspicion of pulmonic stenosis (versus subvalvular aortic stenosis or other lesions); confirmation requires echocardiography.
DIFFERENTIAL DIAGNOSIS Other congenital heart defects causing a systolic murmur, such as subvalvular aortic stenosis, ventricular septal defect, and tetralogy of Fallot
INITIAL DATABASE Electrocardiography: RVH is usually evident; right axis deviation, S1; S2, S3 deep S waves in CV6LU (or V4), CV6LL (or V2). Thoracic radiography: characteristic findings include right ventricular enlargement and dilation of the main pulmonary artery segment. These changes are usually most evident on the dorsoventral view. Pulmonary vasculature is usually normal, but in severe cases, the lungs may appear hypoperfused. Echocardiography: site of obstruction, severity of RVH, and poststenotic dilation of the main pulmonary artery are best demonstrated by a two-dimensional echocardiogram. The pulmonic valve area is best visualized from right parasternal short-axis views, from the left cranial parasternal position, or by transesophageal echocardiography. Color flow and spectral Doppler studies are useful to confirm the diagnosis and determine the severity of obstruction. Estimation of peak blood flow velocity through the stenotic area by Doppler interrogation permits calculation of the pressure gradient using the modified Bernoulli equation, pressure gradient = 4 × V2.
ADVANCED OR CONFIRMATORY TESTING Angiocardiography is performed as a prelude to balloon valvuloplasty or surgical repair. Such studies are useful for clarifying the anatomic location of the obstruction, identifying leaflet fusion and thickening, identifying the severity of RV hypertrophy, and verifying the presence of other abnormalities such as hypoplasia of the pulmonic annulus, tricuspid regurgitation, or a patent foramen ovale. Left ventricular angiography or coronary arteriography should be performed when abnormalities of the left heart are suspected or when concurrent developmental abnormalities of the coronary arteries are suspected in boxer dogs and English bulldogs. The hemodynamic severity of outflow tract obstructions is determined by measuring the systolic pressure gradient across the lesion and estimating the effective valve orifice area.
TREATMENT TREATMENT OVERVIEW Definitive treatment eliminates severe obstructing lesions prior to the development of heart failure
ACUTE GENERAL TREATMENT Dogs with mild pulmonic stenosis that is not causing overt manifestations do not require treatment. Dogs with such overt manifestations as exercise intolerance, syncope, or signs of right heart failure and dogs with severe fixed anatomic obstructions should be referred for surgical repair or balloon valvuloplasty, depending on the precise anatomy of the defect and/or presence of concurrent defects. Balloon valvuloplasty is the preferred method of treatment when the main abnormality is fusion of the pulmonic leaflets. Surgery is often required to effectively remedy complex lesions with annular hypoplasia and fixed or persistent subvalvular obstruction. Dynamic obstructions during stress or exercise can often be effectively palliated by beta-receptor blockade (e.g., atenolol 0.25-0.5 mg/kg PO q 12 h). Such therapy is sometimes required following balloon valvuloplasty or surgical repair. When balloon valvuloplasty or surgical correction are not possible, treatment with beta-receptor blocking drugs and exercise restriction are thought to minimize the chance of sudden death.
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POSSIBLE COMPLICATIONS Dogs with severe untreated disease frequently develop progressive right heart enlargement, tricuspid regurgitation, right heart failure, and atrial fibrillation. Recurrent syncope is common and sudden death has been reported.
RECOMMENDED MONITORING Color-flow Doppler echocardiography is the most useful tool for assessing dogs with pulmonic stenosis over time. Some lesions that are modest in severity in juvenile animals can become progressively more severe over time. The short-and long-term success of surgery or balloon valvuloplasty is best determined by periodic echocardiographic evaluation. Chest radiographs and electrocardiography are useful for evaluating overall heart size and cardiac arrhythmias, respectively.
PROGNOSIS AND OUTCOME Dogs with mild obstructions have a very good prognosis and often reach old age. Dogs with severe obstructions (systolic pressure gradient >100 mm Hg) have a guarded prognosis, as they often develop heart failure or die suddenly. Balloon valvuloplasty improves outcome, particularly when the pressure gradients are substantially reduced. Restenosis occurs in about 10% of dogs treated by balloon valvuloplasty.
PEARLS & CONSIDERATIONS PREVENTION Conscientiously performed physical examinations with careful cardiac auscultation are key to early recognition. Dogs with confirmed pulmonic stenosis should not be bred.
CLIENT EDUCATION Owners should be advised of the high likelihood of heart failure or sudden death in animals with severe untreated pulmonic stenosis. Balloon valvuloplasty and surgical repair are recommended for patients with severe obstructions.
SUGGESTED READING Estrada A, et al: Prospective evaluation of the balloon-to-annulus ratio for valvuloplasty in the treatment of pulmonic stenosis in the dog. J Vet Intern Med 20:862, 2006. Johnson MS, et al: Pulmonic stenosis in dogs: balloon dilation improves clinical outcome. J Vet Intern Med 18:656, 2004. Oyama M, Sisson DD, Thomas WP, et al: Congenital heart disease. In Ettinger SJ, Feldman E, editors: Textbook of veterinary internal medicine, ed 6, Philadelphia, 2005, WB Saunders, pp 972–1021. AUTHOR: D. DAVID SISSON EDITOR: ETIENNE CÔTÉ
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Pulmonary Thromboembolism
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Pulmonary Thromboembolism BASIC INFORMATION DEFINITION The occlusion of a pulmonary artery or arteriole by a thrombus that forms in the systemic venous system/right heart (i.e., embolism) or in the pulmonary arterial system (i.e., in-situ thrombus). Pulmonary thromboembolism (PTE) is infrequently confirmed by direct visualization; therefore diagnosis can be difficult and incidence may be underestimated.
EPIDEMIOLOGY SPECIES, SEX, AGE Dogs: 10 months to 18 years, median age 11 years Cats: 2-14 years, median age 7 years RISK FACTORS Numerous predisposing conditions are identified as risk factors for PTE, and treatment of these underlying causes is a cornerstone of case management. Neoplasia Heartworm disease Sepsis Hyperadrenocorticism Disseminated intravascular coagulation Immune-mediated hemolytic anemia Protein-losing nephropathy/enteropathy Central catheters Vasculitis Pancreatitis Cardiac disease Surgical procedures especially total hip replacement Trauma ASSOCIATED CONDITIONS & DISORDERS Hypoxemia, right-sided congestive heart failure, pulmonary hypertension
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT Acute onset dyspnea/tachypnea; may be mild or progressive when PTE is small or gradual Signs of the underlying disorder may predominate. Occasionally signs of right-sided heart failure (abdominal distension, exercise intolerance) Uncommonly, cough or hemoptysis Nonspecific signs (lethargy, anorexia/inappetence, weight loss, collapse) PHYSICAL EXAM FINDINGS Dyspnea/tachypnea Cyanosis Pulmonary crackles/increased bronchovesicular sounds; however, pulmonary auscultation often is normal. Tachycardia and weak pulses Findings reflecting the predisposing condition Occasionally, findings consistent with right-sided congestive heart failure are present (jugular venous distension/pulsation, ascites)
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Right apical murmur or split second heart sound possible with pulmonary hypertension
ETIOLOGY AND PATHOPHYSIOLOGY Generally, PTE should be thought of as secondary to an underlying condition which causes venous stasis, endothelial damage, and/or hyperco-agulability (Virchow's triad). PTE leads to mechanical obstruction of a pulmonary artery or arteriole and reactive pulmonary vasoconstriction. This results in reduced blood flow to the affected region of lung. Other forms of emboli including parasites, neoplastic cells, fat, or gas may also cause pulmonary vascular obstruction. While small PTE are often clinically silent and rapidly lysed endogenously, large or numerous PTE cause ventilation/perfusion mismatch and hypoxemia. Since the lung has a dual blood supply with bronchial arteries from the aorta perfusing the lung parenchyma with oxygenated blood, even massive PTE generally does not cause lung infarction. Increased pulmonary vascular resistance due to pulmonary vascular obstruction and pulmonary vasoconstriction may cause pulmonary hypertension. This leads to a pressure overload of the right ventricle and if severe, right-sided heart failure.
DIAGNOSIS DIAGNOSTIC OVERVIEW Clinical diagnosis is challenging, and definitive diagnosis may require advanced imaging. Often a presumptive diagnosis is made based on high clinical suspicion from identifying a predisposing disorder, plus thoracic diagnostic imaging results.
DIFFERENTIAL DIAGNOSIS Pulmonary parenchymal disease (bron-chopneumonia, pulmonary edema, neoplasia, parasitism, contusion, hemorrhage) Upper or lower airway disease (bronchitis/asthma, acquired or congenital structural abnormalities, neoplasia, obstruction) Pleural space disease (pleural effusion, restrictive pleuritis, neoplasia) Other causes of pulmonary hypertension (see p. 1422)
INITIAL DATABASE Thoracic radiographs; initial test of choice, though minimally specific and sensitive: central pulmonary artery dilation, abrupt distal pulmonary artery attenuation, regional oligemia, interstitial or alveolar pulmonary parenchymal pattern (often with lobar distribution), right heart enlargement, pleural effusion. Radiographs may be normal. Coagulation profile: not useful because rapid (abnormally low) coagulation values do not indicate a hypercoagulable state. CBC, serum biochemistry panel, and urinalysis: not useful in the diagnosis of PTE but important for diagnosis of predisposing diseases Echocardiography: evidence of pulmonary hypertension, right atrial and ventricular enlargement, occasionally visible thrombus
ADVANCED OR CONFIRMATORY TESTING Blood gas analysis: hypoxemia/hypocapnia (hypercapnia if severe); metabolic acidosis; elevated alveolar-arterial (A-a) gradient A-a gradient = Fio2 (Pb-Ph2o) -(Paco2/R) − Pao2, where Fio2 is the fraction of inhaled oxygen (e.g., 0.21 for room air; 0.4 for 40% oxygen; etc.), Pb = barometric pressure (627-643 mm Hg; www.weather.com), Ph2o = 47 mm Hg, R = 0.8, and Pao2 and Pco2 are obtained from the arterial blood gas result. Normal: 2000 ng/mL) consistent with thromboembolic disease in the dog. Normal D-dimer levels should reduce the suspicion of PTE. Nuclear ventilation/perfusion scanning: safe and noninvasive but very limited availability Pulmonary angiography: gold standard for definitive diagnosis. Invasive and unstable patient condition may preclude sedation/anesthesia. CT and magnetic resonance angiography: noninvasive, but require anesthesia
TREATMENT TREATMENT OVERVIEW
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PTE is often a life-threatening emergency, and initial treatment is focused on respiratory support. If clinical suspicion is high or a definitive diagnosis can be made, specific therapy should be provided.
ACUTE GENERAL TREATMENT Oxygen therapy (see p. 1318) Ventilation with positive end expiratory pressure if severe (see p. 1362) Judicious parenteral fluid therapy to maintain tissue perfusion without exacerbating right heart failure Anticoagulant therapy to prevent additional thrombus formation: Unfractionated heparin: 100-300 U/kg IV or SQ q 6-8 h to prolong PTT to 1.5-2 times baseline; or Low-molecular-weight heparin (LMWH): dalteparin, 100-150 U/kg SQ q 8-12 h; or enoxaparin, 1 mg/kg SQ q 12 h. Doses not well defined. Antiplatelet therapy may be considered: Aspirin, 0.5 mg/kg PO q 12-24 h (dogs); 5-20 mg PO q 3 d (cats); or Clopidogrel, 1-2 mg/kg PO q 24 h (dogs); 18.75 mg PO q 24 h (cats) Thrombolytic therapy (streptokinase, tissue plasminogen activator) may be useful in acute stage, but experience is limited in veterinary medicine, and proposed dosing regimens vary widely. Surgical embolectomy is feasible with central thrombi but associated with significant morbidity/mortality. Percutaneous catheter thrombectomy/thrombolysis may be possible with reduced mortality/morbidity but requires specialized equipment.
CHRONIC TREATMENT Treatment of underlying condition Anticoagulant therapy: LMWH: dalteparin or enoxaparin as above; or Warfarin, 0.05-0.2 mg/kg PO q 24 h, to attain an international normalization ratio of 2-3. Must be overlapped with heparin therapy for 3-5 days owing to initial hypercoagulable phase. Antiplatelet therapy: Aspirin or clopidogrel as above
POSSIBLE COMPLICATIONS Pulmonary hypertension and right-sided heart failure Potentially severe hemorrhage is possible with any anticoagulant or thrombolytic therapy. This limits the use of warfarin and thrombolytics but risk appears low with LMWH.
RECOMMENDED MONITORING Respiratory rate, arterial blood gas analysis, and thoracic radiography provide relative indications of response to therapy or deterioration of patient condition. Careful monitoring of coagulation times with unfractionated heparin or warfarin therapy. This may not be necessary with LMWH.
PROGNOSIS AND OUTCOME Variable depending upon size of thrombus and degree of pulmonary vascular occlusion. Large thrombi resulting in occlusion of large portions of the pulmonary vascular bed are associated with a poor prognosis.
PEARLS & CONSIDERATIONS COMMENTS PTE should be suspected in any patient with severe dyspnea and/or hypoxemia and normal thoracic radiographs. Even with management of an underlying disease, recurrence is possible, and long-term anticoagulant therapy may be necessary.
PREVENTION Elimination of predisposing conditions is imperative. Prophylactic anticoagulant therapy may be considered when this is not possible.
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SUGGESTED READING Hackner SG: Pulmonary thromboembolism. In Bonagura JD, Twedt DC, editors: Kirk’s current veterinary therapy XIV. St Louis, 2009, Saunders, p 689. AUTHOR: HERBERT W. MAISENBACHER, III EDITOR: ETIENNE CÔTÉ 1ST EDITION AUTHOR: BRUCE KORNREICH
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Pulmonary Nodules
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Pulmonary Nodules BASIC INFORMATION DEFINITION Single or multiple masses of varying sizes occurring in the lung parenchyma; usually detected radiographically
SYNONYM Lung nodules
EPIDEMIOLOGY SPECIES, AGE, SEX Dogs: 9-11 years Cats: 11-12 years Females may be at increased risk. The prevalence of pulmonary nodules in dogs and cats is not known. Pulmonary neoplasms have an average reported incidence rate of 5.6/100,000 in dogs and 2.2/100,000 in cats. RISK FACTORS Exposure to secondhand smoke may be a risk factor. ASSOCIATED CONDITIONS & DISORDERS Paraneoplastic syndromes reported to occur secondary to primary or metastatic lung neoplasms: Hypertrophic osteopathy Hypercalcemia Fever Elevated ACTH with associated signs of hyperadrenocorticism
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES Most primary lung neoplasms are adenocarcinomas (75%) or carcinomas (20%). HISTORY, CHIEF COMPLAINT Pulmonary nodules or masses may be found incidentally in patients undergoing radiography for other reasons. When lung neoplasms cause clinical signs, the most frequent complaints from the owner are cough and dyspnea. Sputum with or without blood or hemoptysis is possible. Other possible signs: fever, weight loss, dysphagia, vomiting, regurgitation, wheezing Cats often manifest signs related to metastatic disease to their digits as opposed to respiratory signs. PHYSICAL EXAM FINDINGS Physical exam: usually normal Pulmonary nodules due to metastatic disease: physical abnormalities from the primary tumor may be found in other parts of the body. In patients with pulmonary nodules, careful evaluation of the more common sites of origin of tumors that metastasize to the lungs is indicated, including the oral cavity, the area of the thyroid, mammary glands, and toenails (especially in cats). A rectal exam is essential in every dog with pulmonary nodules (assess prostate, anal sacs, bladder/urethra, sub-lumbar lymph nodes). A fundic exam (seep. 1313 ) and careful dermatologic evaluation (see ) may be helpful in identifying disseminated fungal
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disease.
ETIOLOGY AND PATHOPHYSIOLOGY The main concern with pulmonary nodules is malignancy; neoplasms from virtually any part of the body, including primary lung tumors, may metastasize to the lungs. Metastatic neoplasia may reach the lungs via lymphatics or via the bloodstream; both can produce a nodular pulmonary pattern. The development of metastasis is a complex, multistep process, and failure to complete any of the steps will prevent the development of a metastatic focus. It is estimated that less than 1 in 100 neoplastic cells that leaves the primary tumor survives the metastatic cascade. This multistep process includes the induction of neovascularization detachment of the tumor cell from the primary tumor, dissolution of the basement membrane and invasion into the bloodstream, evasion of the host immunity and survival in the bloodstream, margination in a new capillary and attachment to the endothelium, dissolution of the basement membrane and extravasation into the extracellular matrix, survival in the new tissue by evading the host immunity, and finally the induction of neovascularization to support continued growth of the new metastatic focus. This neovascularization begins the process again.
DIAGNOSIS DIAGNOSTIC OVERVIEW The diagnosis of pulmonary nodules is usually made with a radiographic evaluation. A systematic approach to rule out infectious or granulomatous causes (as warranted by geography) or other foci of neoplasia (i.e., primary lesions elsewhere that have resulted in the identified pulmonary nodules) is paramount.
DIFFERENTIAL DIAGNOSIS Solitary lung mass: primary neoplasia, metastatic neoplasia, granuloma, cyst, infarct, localized hemorrhage, focal pneumonia, abscess Multiple pulmonary masses: primary or metastatic neoplasia, fungal disease (blastomycosis, histoplasmosis), pulmonary osteomas (rarely more than 3-4 mm in diameter and more radiopaque than soft-tissue nodules because of mineral composition). Bacterial abscesses and granulomas uncommonly cause multiple pulmonary masses. One or more cutaneous or subcutaneous nodules, one or more nipples, and intrahepatic mineralizations can be mistaken for focal pulmonary lesions, especially if only one radiographic projection is made.
INITIAL DATABASE Thoracic radiographs: the source of initial identification of pulmonary nodules in most cases (less commonly at surgery or necropsy) CBC, serum biochemistry profile, urinalysis: typically unremarkable in patients with incidentally discovered pulmonary nodules. Hypercalcemia may occur with neoplasia, fungal, and other granulomatous diseases. Pleural effusion, if present, should be sampled and evaluated with fluid and cytologic analysis, and if evidence of infection exists, bacterial culture (aerobic and anaerobic). Repeated meticulous physical exam (with particular attention paid to the mammary chains, anal sacs, oral cavity, skin, and digits)
ADVANCED OR CONFIRMATORY TESTING Thoracic radiographs: three views if the lesion was found incidentally Ultrasonographic studies (of the abdomen and of the heart to screen for primary sites of disease; of the lesion with aspiration for diagnosis if possible) CT to assess for lesions too small to be identified with plain-film radiography and/or to be used for CT-guided aspirates or biopsies. See p. 1233. The minimum database should be supplemented with fungal serologic examination and microbial (fungal and bacterial) culture based on clinical suspicion and history. Thoracotomy with histopathologic evaluation of biopsy specimens. The hilar lymph nodes and lung lobes should be carefully evaluated and sampled as necessary at the time of thoracotomy.
TREATMENT
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TREATMENT OVERVIEW Resolution of clinical signs (for instance, cough or dyspnea) if present Control or elimination of primary disease process (exception: clinically unimportant pulmonary nodules, i.e., pulmonary osteomas) Single pulmonary masses are more commonly addressed surgically (focal process). Multiple pulmonary masses are usually not addressed surgically, because they typically are part of a generalized process (e.g., neoplastic, fungal). Rather, identifying the underlying cause and systemic (medical) treatment are usually most important.
ACUTE GENERAL TREATMENT Once a lesion has been identified, surgical excision should be considered. Treatment of choice for primary pulmonary neoplasia (single pulmonary nodule in which the diagnosis was established with ultrasound- or CT-guided aspiration or biopsy). Surgical excision may be considered for solitary pulmonary nodules/masses of unknown tissue type. The slow-growing nature of some single pulmonary nodules means that other concerns (concurrent illnesses, patient age, etc.) may supersede the need for thoracotomy. In specific cases, metastasectomy (excision of metastases) can be performed. Consultation with an oncologist is recommended beforehand.
CHRONIC TREATMENT Chemotherapy may be attempted for primary pulmonary neoplasia deemed unresectable or with evidence of lymphatic metastasis at the time of diagnosis. Options may include doxorubicin, platinum compounds (cisplatin, carbo-platin), gemcitabine, or vinorelbine. Chemotherapy is largely unproven in the management of pulmonary tumors in veterinary medicine.
POSSIBLE COMPLICATIONS Hypertrophic osteopathy; typically resolves with removal of pulmonary disease Digital or ocular metastasis (cats), particularly with angioinvasive neoplasms
RECOMMENDED MONITORING Monthly to quarterly radiographs to assess for recurrence, progression, or changes (cavitation is not uncommon but is often misinterpreted as abscess/infection) As required per protocol for chemotherapy patients (i.e., CBC), quality-of-life assessments
PROGNOSIS AND OUTCOME Guarded and extremely variable (median survivals in parentheses) Dogs with primary lung tumors: 50% of dogs without clinical signs and having peripheral, solitary, small (1 year (12-20 months). In contrast, median survival is shorter (8 months) for patients with clinical signs referable to the pulmonary nodule/mass, or with a large solitary (>5 cm or 100 cm3) neoplasm, one that involves an entire lobe, squamous cell carcinoma histologically, or nodal metastasis (1-2 months) Cats with primary lung tumors: median survival 4 months after lobectomy. Cats with poorly differentiated tumors or enlarged tracheobronchial lymph nodes: median 2 months.
PEARLS & CONSIDERATIONS COMMENTS Metastatic neoplasia is much more common than primary pulmonary neoplasia. Half of patients with newly diagnosed pulmonary neoplasia are deemed inoperable because regional or systemic extension is identified at presentation. Pulmonary osteomas are benign mineralizations often identified incidentally on the radiographs of older dogs. The diagnosis
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of osteoma versus metastasis can be made empirically based on size and relative opacity. The limit of detection for soft-tissue lesions in the pulmonary parenchyma is considered to range from 5-10 mm. Because osteomas are of mineral or bone density, they can be identified in the 2-5 mm range. In this author's experience, cats with pulmonary metastases tend to show overt signs, have more advanced disease at the time of presentation, and have markedly shorter survival times than dogs.
SUGGESTED READING Withrow SJ: Tumors of the respiratory system c. lung cancer. In Withrow SJ, Vail DM, editors: Withrow and MacEwen’s small animal clinical oncology, ed 4, St Louis, 2007, Saunders Elsevier, pp 517–524. AUTHOR: CARLOS O. RODRIGUEZ, JR. EDITOR: KENNETH M. RASSNICK
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Pulmonary Lymphoid Granulomatosis
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Pulmonary Lymphoid Granulomatosis BASIC INFORMATION DEFINITION Rare lymphoproliferative neoplasm in which infiltrates of atypical lymphoid cells develop around and destroy pulmonary blood vessels
SYNONYMS PLG, lymphomatoid granulomatosis
EPIDEMIOLOGY SPECIES, AGE, SEX: Rare in dogs and reported in a single cat. Young to middle-aged adults of either gender are typically affected. ASSOCIATED CONDITIONS & DISORDERS: Lymphomatoid granulomatosis may be observed in sites other than the lungs, including lymph nodes, liver, heart, spleen, kidneys, pancreas, adrenal gland, or skin.
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT Nonproductive cough that is unresponsive to treatment with antimicrobials Increased respiratory effort Lethargy Anorexia and weight loss Rarely: fever, lameness, peripheral lymphadenopathy, ascites, or vomiting PHYSICAL EXAM FINDINGS Nonproductive cough Tachypnea Areas of decreased bronchovesicular lung sounds Areas of increased bronchovesicular lung sounds Peripheral lymphadenomegaly (occasionally) Other sites of infiltration may be identified, including the skin
ETIOLOGY AND PATHOPHYSIOLOGY In humans, pulmonary lymphoid granulomatosis (PLG) is considered a precursor to low-grade T-cell lymphoma. The disease also seems to be T-cell mediated in the few animals studied to date, although T-and B-cell infiltrates have been documented in a single dog. Infiltrates of atypical lymphocytes are centered on the vasculature. While pulmonary vasculature is most commonly targeted, other lymphatic tissues or solid organs may be affected as well.
DIAGNOSIS DIFFERENTIAL DIAGNOSIS Metastatic pulmonary neoplasia Pulmonary lymphoma Other primary lung tumors Granulomatous fungal pneumonia Eosinophilic bronchopneumopathy/pulmonary infiltrates with eosinophils/eosinophilic granulomatosis Severe bacterial pneumonia
INITIAL DATABASE
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CBC: leukocytosis, eosinophilia, and basophilia are common. Serum biochemistry profile and urinalysis: usually unremarkable Heartworm serology: negative Thoracic radiographs: Large pulmonary masses or lobar consolidation are typical. An interstitial lung pattern is commonly observed. Tracheobronchial and/or sternal lymph nodes are often enlarged. Pleural effusion is sometimes present.
ADVANCED OR CONFIRMATORY TESTING Pulmonary biopsy is the only means of definitive diagnosis. Samples may be obtained via sternal or intercostal thoracotomy, keyhole biopsy, or thoracoscopy. Tracheal wash, bronchoalveolar lavage, and fine-needle aspirates may reveal cells suggestive of either inflammation or lymphoma, but cytologic examination cannot confirm a diagnosis of PLG. These tests are, however, useful in ruling out other potential causes of lung disease.
TREATMENT TREATMENT OVERVIEW Goals of treatment are to achieve remission via chemotherapy, and provide short-term support for hypoxemia if required.
ACUTE GENERAL TREATMENT If required, oxygen supplementation for hypoxemic animals (seep. 1318 ) Chemotherapy protocols (see pp. 675 and 674) similar to those used for treatment of lymphoma, including the use of cytotoxic agents Glucocorticosteroids alone will seldom produce remission.
CHRONIC TREATMENT Chemotherapy should proceed as for lymphoma (see pp. 671 and 675).
POSSIBLE COMPLICATIONS Extensive and serious adverse reactions, including leukopenia and immune suppression, are possible in response to many chemotherapeutic agents; drug-specific reactions are also possible (e.g., cyclophosphamide-induced sterile hemorrhagic cystitis).
RECOMMENDED MONITORING Repeat thoracic radiographs 2-3 weeks after initial chemotherapy and periodically thereafter. The interval between radiographs can be prolonged as the duration of remission endures. Periodically assess CBC for dogs receiving chemotherapy for lymphoma; other specific tests may be needed, depending on the chemotherapeutic agent employed (e.g., cardiac ultrasound for dogs receiving doxorubicin).
PROGNOSIS AND OUTCOME Guarded Many dogs attain durable remission. Lymphoma may follow PLG by months to years.
PEARLS & CONSIDERATIONS COMMENTS In humans, PLG is regarded as a slowly progressive precursor to lymphoma.
PREVENTION
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There is no means to prevent development of PLG.
TECHNICIAN TIPS Needle aspiration of lung lesions is commonly performed with 23-G needles and a 6- or 12-mL syringe (seep. 1277 ).
CLIENT EDUCATION Owners should understand that even if durable remission is achieved, the disease may progress to lymphoma years later.
SUGGESTED READING Berry CR, et al: Pulmonary lymphomatoid granulomatosis in seven dogs (1976-1987). J Vet Intern Med 4:157, 1990. Fitzgerald SD, et al: Eight cases of canine lymphomatoid granulomatosis. Vet Pathol 28:241, 1991. Park HM, et al: Pulmonary lymphomatoid granulomatosis in a dog: evidence of immunophenotypic diversity and relationship to human pulmonary lymphomatoid granulomatosis and pulmonary Hodgkin’s disease. Vet Pathol 44:921, 2007. Smith KC, et al: Canine lymphomatoid granulomatosis: an immunophenotypic analysis of three cases. J Comp Pathol 115:129, 1996. Valentine BA, et al: Pulmonary lymphomatoid granulomatosis in a cat. J Vet Diagn Invest 12:465, 2000. AUTHOR: LEAH A. COHN EDITOR: RANCE K. SELLON
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Pulmonary Hypertension (Arterial)
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Pulmonary Hypertension (Arterial) BASIC INFORMATION DEFINITIONS Pulmonary hypertension (PH) is defined as elevated pulmonary arterial pressure (PAP) secondary to various disease mechanisms causing cor pulmonale (right ventricular hypertrophy secondary to PH) and eventually right sided heart failure. The World Health Organization (WHO) classification of PH is based on similarities in pathophysiologic mechanisms (see box). Pulmonary arterial hypertension (PAH) is a progressive vasoproliferative condition characterized by increased PAP. Patients with PAH by definition do not have significant left heart disease, lung disease, or chronic thromboembolic disease. Idiopathic PAH (formerly primary PH or PPH) is diagnosed when no underlying cause for PH is found, and characteristic histologic abnormalities in small pulmonary arteries can be identified. Histologic abnormalities include intimal, medial, and adventitial proliferation, plexogenic changes consisting of proliferating epithelial cells mixed with myofibroblasts, and necrotizing arteritis. Specific hemodynamic criteria include systolic PAP > 30 mm Hg, diastolic PAP > 20 mm Hg, mean PAP > 25 mm Hg, pulmonary capillary wedge pressure < 15 mm Hg.
EPIDEMIOLOGY SPECIES, AGE, SEX Dogs: dependent on underlying cause Cats: data on any cause of PH are scant, but PAH associated with congenital cardiovascular shunt is probably underrecognized. GENETICS & BREED PREDISPOSITION Depending on underlying cause: Myxomatous mitral valve disease in poodles, dachshunds, terriers, and other small breeds Chronic obstructive upper airway disease in brachycephalic breeds Pulmonary fibrosis in West Highland white terriers
Classification of Pulmonary Hypertension From WHO classification in Chin KM, Rubin U: Pulmonary arterial hypertension, J Am Coll Cardiol 51:1527-1538, 2008, modified and adapted for the dog
WHOGroup 1:Pulmonary Arterial Hypertension (PAH) Idiopathic (formerly primary PH, PPH) Associated with congenital systemic-to-pulmonic shunts Persistent pulmonary hypertension of the newborn Associated with drugs, toxins, inflammatory conditions
Group 2:Pulmonary Hypertension Associated With Left Heart Disease Left ventricular or atrial disease Left-sided valvular disease
Group 3:Pulmonary Hypertension Associated With Respiratory Disease and/or Hypoxemia Interstitial lung disease (e.g., pulmonary fibrosis) Chronic upper airway obstruction Chronic exposure to high altitude
Group 4:Pulmonary Hypertension Due to Thromboembolic Disease Primary pulmonary arterial lesion (e.g., Dirofilaria immitis, Angiostrongylus vasorum)
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Medical conditions predisposing to pulmonary thromboembolism
Group 5:Miscellaneous
RISK FACTORS Protein-losing nephropathies and enteropathies, hyperadrenocorticism, immune-mediated hemolytic anemia, pancreatitis, neoplasia, heartworm disease are risk factors for pulmonary thromboembolism (PTE). Ingestion of snails for infection with Angiostrongylus vasorum (French heartworm) in Europe and Newfoundland, Canada Septic shock, pancreatitis, other systemic inflammatory states for adult respiratory distress syndrome (ARDS) GEOGRAPHY AND SEASONALITY Dirofilaria immitis in endemic areas A. vasorum in endemic areas, Europe, and Newfoundland, Canada High altitude (hypobaric hypoxia) causes or contributes to pulmonary hypertension. Dogs living at 2300 m and 3500 m altitude (7500 ft and 11,500 ft) have a mean arterial Po2 of around 62 mm Hg and 52 mm Hg, respectively, and a mean systolic pulmonary artery pressure of around 30 mm Hg and 40 mm Hg, respectively, as determined by Doppler evaluation of tricuspid regurgitation.
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES From an intensive care and therapeutic point of view, PH may be further subdivided into acute and chronic categories. Acute PH may reflect a sudden worsening of a chronic condition causing PH (e.g., left-sided congestive heart failure), or it may be precipitated by an acute condition (e.g., acute respiratory distress syndrome, massive PTE). HISTORY, CHIEF COMPLAINT Depends on underlying cause Signs of PH itself or of the underlying cause may predominate. Signs associated with PH include: Exercise intolerance Collapse, syncope (reflex bradycardia caused by high resistance to forward flow from the right ventricle) Dyspnea, coughing Abdominal distension Rear limb weakness in reverse patent ductus arteriosus (PDA) Right ventricular hypertrophy as incidental finding during echocardiography or electrocardiography PHYSICAL EXAM FINDINGS PAH: exam may be unremarkable. Possible findings include: Pale mucous membranes Respiratory distress May be precipitated or exacerbated by exercise Tachycardia Weak pulse Signs of right-sided congestive heart failure (distended jugular veins or jugular venous pulse, abdominal distension) o Split second heart sound (pulmonic valve closing after aortic valve) Murmur of tricuspid regurgitation (systolic, right-sided) Murmur of pulmonic regurgitation (rare; diastolic and loudest over left heart base) Cyanosis Red oral and conjunctival mucous membranes due to polycythemia in reverse PDA Differential cyanosis in reverse PDA PH with left-sided heart disease: depends on underlying disease; possible findings include: Same as PAH (except polycythemia signs and differential cyanosis) Loud murmur of mitral regurgitation Arrhythmia associated with dilated cardiomyopathy Increased lung sounds
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Crackles PH with respiratory disease/hypoxia: Same as PAH (except differential cyanosis) Stertorous breathing in brachycephalic syndrome Cough Increased lung sounds, wheezes, crackles PH due to PTE: Same as PAH (except polycythemia signs and differential cyanosis) Cough Hemoptysis Increased lung sounds
ETIOLOGY AND PATHOPHYSIOLOGY In PAH, the underlying vascular injury is thought to be a final common response to various inciting factors coupled with genetic susceptibility. Eliciting factors may be mechanical (overperfusion), drugs (experimentally inducible with appetite suppressants), toxins, infections, and genetically determined susceptibility to such injuries. Thrombosis elicited by diseased vessel walls may complicate PAH. PH is a common complication of different cardiac and extracardiac diseases and results from two main mechanisms: increased left atrial pressure and increased pulmonary vascular resistance. Important causes are: Cardiac: Pulmonary venous hypertension due to increased left atrial pressure in left myocardial failure, most common in advanced chronic mitral regurgitation, also in dilated cardiomyopathy; cor triatriatum sinister, mitral stenosis Hypoxic vasoconstriction: Chronic obstructive lower airway disease (bronchitis, emphysema) Chronic obstructive upper airway disease High-altitude hypoxia Occlusion of the pulmonary vascular bed: PTE Parasites (D. immitis, A. vasorum) Pulmonary parenchymal disease: Pulmonary fibrosis (seep. 615 ) ARDS Combination of mechanisms (e.g., heartworm infection; D. immitis, A. vasorum): obstruction by intravascular parasites, vasculitis, thrombosis, and hypoxic vasoconstriction.
DIAGNOSIS DIAGNOSTIC OVERVIEW A practical clinical diagnosis of PH is made when high-velocity valvular regurgitation (tricuspid, pulmonic, or both) is documented by Doppler echocardiography in the absence of pulmonic stenosis.
DIFFERENTIAL DIAGNOSIS For right-sided heart failure: Congenital cardiac disease: pulmonic stenosis, tricuspid dysplasia, tetralogy of Fallot, tricuspid stenosis, cor triatriatum dexter Acquired cardiovascular disease: severe tricuspid myxomatous valve disease/endocardiosis, right ventricular dilated cardiomyopathy, peri-cardial effusion For right ventricular hypertrophy: Pulmonic stenosis, tetralogy of Fallot
INITIAL DATABASE Thoracic radiographs; dorsoventral view is particularly important. Document right ventricular and main pulmonary artery enlargement; somewhat nonspecific, as findings of “reversed D” and “increased sternal contact” on the lateral view are often overinterpreted in normal dogs and cats (expiratory films, rotation of patient, thoracic conformation). Peripheral pulmonary vasculature may be tortuous and enlarged. Peripheral pulmonary arterial markings may abruptly stop with PTE. Left atrium is enlarged and pulmonary veins are congested with underlying left atrial, ventricular, or mitral valve
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disease. Signs of underlying bronchial, interstitial, or alveolar pulmonary disease may be evident. Echocardiogram, dual role: Rule in or out causes of PH, including acquired left ventricular heart disease (myxomatous mitral valve disease, dilated cardiomyopathy) and congenital cardiovascular shunt. Confirmation of PH qualitatively and quantitatively: Qualitatively: characteristic two-dimensional and M-mode findings in moderate to severe PH are dilation of right ventricle and atrium, thickening of right ventricular wall and papillary muscles, paradoxical septal motion, and decreased left ventricular chamber size. Quantitatively: Doppler examination is the most useful noninvasive clinical tool to confirm and quantitate severity of PH. Systolic: velocity of tricuspid regurgitation (TR) correlates to right ventricular systolic pressure, and therefore, barring pulmonic stenosis, to pulmonary arterial systolic pressure. The modified Bernoulli equation allows Doppler-derived blood flow velocities to be used for estimating intracardiac pressures: PG = 4 × (Vmax)2, where PG is the peak pressure gradient between right ventricle and right atrium, in mm Hg, and Vmax is the peak velocity of tricuspid regurgitation (TR), in m/sec. It is assumed that right atrial pressure approximates 0 mm Hg during ventricular systole, such that the right atrial/right ventricular systolic PG equals systolic right ventricular pressure. A TR-PG > 30mmHg (Vmax > 2.8 m/s) suggests/indicates systolic PH. Diastolic pulmonary artery pressure is calculated with Doppler quantification of pulmonary valve insufficiency (PI) instead of tricuspid regurgitation; by this method, PH is considered to be present when PI-PG is >20 mm Hg (Vmax > 2.2 m/s). ECG: document right ventricular hypertrophy (RVH; deep S waves in leads I, II, III, aVF), right axis deviation, and possible arrhythmias; in acute PH, ECG abnormalities may not be present; in chronic PH, marked PH must be present to cause ECG abnormalities. Less sensitive and specific than echocardiography. Serology for D. immitis and Baermann fecal examination for A. vasorum Platelet count, coagulation profile, and parameters associated with hypercoagulability (e.g., antithrombin levels, D-dimer levels) may be abnormal with vasculitis and thrombosis. Arterial blood gas analysis: may show hypoxemia in primary respiratory disease or right-to-left cardiovascular shunt. CBC, biochemistry panel, urinalysis: may show abnormalities suggestive of parasitic disease (eosinophilia, baso-philia), chronic inflammation (throm-bocytosis, hyperglobulinemia), and systemic disease predisposing to PTE (e.g., proteinuria, hypoproteinemia, hypoalbuminemia, increased liver enzyme activities consistent with steroid hepatopathy, increased amylase and lipase activity, and increased pancreatic lipase activity consistent with pancreatitis).
ADVANCED OR CONFIRMATORY TESTING Contrast ultrasound (microbubbles) of the heart and descending aorta to rule out cardiovascular right-to-left shunt. Shunt is also possible due to pulmonary arteriovenous fistula secondary to pulmonary hypertension; in this case, bubbles will take at least three cardiac cycles from their appearance in the right atrium until their appearance in the left atrium. Right-sided cardiac catheterization for invasive measurement of pulmonary wedge pressure as an estimate of left atrial pressure, systolic and diastolic pulmonary artery pressure; evaluation of therapeutic intervention Pulmonary angiography; tortuous pulmonary arteries indicate PH; perfusion deficits are present in PTE. Pulmonary CT to identify/rule out parenchymal disease and CT-angiography for PTE Pulmonary ventilation/perfusion scintigraphy to rule out PTE Pulmonary histopathologic evaluation to confirm PAH
TREATMENT TREATMENT OVERVIEW PH of any genesis with signs referable to right ventricular forward or backward failure: lower pulmonary artery pressure. PH of any genesis with signs referable to hypoxia: improve oxygenation. PH with known pathogenesis and treatable cause: focus should be to correct/improve underlying disease.
ACUTE GENERAL TREATMENT Oxygen therapy (cage or nasal). See p. 615.
CHRONIC TREATMENT There is no randomized trial documenting efficacy of medical treatment in naturally occurring PH in dogs; thus the following are merely treatment considerations:
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Therapeutic trial with amlodipine (Norvasc) in moderate PH, starting at 0.05 mg/kg PO q 24 h and titrating dose based on response and systemic blood pressure (avoid hypotension) Anticoagulant therapy with low-dose aspirin, 0.5 mg/kg PO q 12 h (dog) Sildenafil (Viagra) in severe PH, 2-3 mg/kg PO q 8-12 h. Improves clinical condition in the absence of significant effects on PAP as estimated by TR-PG. Oral L-arginine, a precursor of nitric oxide, may be a simple and useful oral medical treatment; however, there are no studies documenting a positive effect. Dedicated owner may consider intermittent oxygen therapy at home. Pimobendan may lower PAP. Furosemide, ACE inhibitor, spironolactone in cases of overt right-sided congestive heart failure (seep. 470 ) Specific treatment of underlying mechanism or disease in secondary PH (see Heart Failure, Chronic, p. 470; Pulmonary Thromboembolism, p. 940; Heartworm Disease, Dog, p. 477; Heartworm Disease, Cat, p. 474; Acute Respiratory Distress Syndrome, p. 34)
POSSIBLE COMPLICATIONS PH: right ventricular failure Treatment: systemic arterial hypotension with syncope, prerenal azotemia
RECOMMENDED MONITORING Most important are simple clinical parameters: general attitude, exercise tolerance, respiration, severity of ascites Systemic blood pressure Vmax of TR and PR
PROGNOSIS AND OUTCOME Depends on underlying disease and stage of disease: Good in parasitic pulmonary vasculature disease with acute PH Fair in right-to-left cardiovascular shunts, myxomatous mitral valve disease, PH secondary to chronic parasitic pulmonary vasculature disease Poor in advanced PAH, advanced pulmonary fibrosis, ARDS, nonparasitic PTE, presence of right-sided heart failure
PEARLS & CONSIDERATIONS COMMENTS Most causes of secondary PH are readily detectable. Pulmonary thromboembolism and right-to-left PDA in particular may be missed if not considered. Idiopathic PAH is a clinical diagnosis of exclusion and definitive confirmation is available only histologically. Newer human drugs to decrease pulmonary artery pressure are very expensive: iloprost = prostaglandin analog for inhalation, and bosentan = endo-thelin antagonist for oral administration.
TECHNICIAN TIPS Oxygen can be administered to patients with respiratory distress secondary to PH by nasal oxygen catheters, flow-by techniques, or by placing the animal in an oxygen cage. Changes in Pao2 following a change in inspired oxygen concentration require time to be appreciated by an arterial blood gas measurement.
CLIENT EDUCATION In dogs with cardiac disease, travel to higher altitude (above 7000 feet) may aggravate PH to a clinically relevant degree, owing to hypobaric hypoxia.
SUGGESTED READING Chin KM, Rubin LJ: Pulmonary arterial hypertension. J Am Coll Cardiol 51:1527–1538, 2008. Glaus TM, et al: Pulmonary hypertension induced by hypoxia at different high altitude levels in dogs. Vet Res Commun 27:661–770,
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Pulmonary Hypertension (Arterial)
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2003. Glaus TM, et al: Clinical and pathological characterisation of primary pulmonary hypertension in a dog. Vet Rec 154:786–789, 2004. Johnson L, et al: Clinical characteristics of 53 dogs with Doppler-derived evidence of pulmonary hypertension: 1992-1996. J Vet Intern Med 13:440–447, 1999. Kellum HB, Stepien RL: Sildenafil citrate therapy in 22 dogs with pulmonary hypertension. J Vet Intern Med 21:1258–1264, 2007. Pyle RL, et al: Pulmonary hypertension and cardiovascular sequelae in 54 dogs. Intern J Appl Res Vet Med 2:99–109, 2004. AUTHOR: TONY M. GLAUS EDITOR: ETIENNE CÔTÉ
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Pulmonary Edema, Noncardiogenic
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Pulmonary Edema, Noncardiogenic BASIC INFORMATION DEFINITION The well-recognized phenomenon of pulmonary interstitial/alveolar fluid accumulation caused by a disorder other than cardiac congestion
SYNONYMS Acute respiratory distress syndrome (ARDS), neurogenic pulmonary edema
EPIDEMIOLOGY SPECIES, AGE, SEX Dogs and cats of any age or sex may be affected. RISK FACTORS Acute upper airway obstruction (laryngeal paralysis, brachycephalic upper airway syndrome, critical tracheal collapse, foreign body, mass or infiltration, strangulation, others) Electrocution Protracted seizures or head trauma Major trauma or surgery Sepsis or nonseptic systemic inflammatory disease (e.g., pancreatitis, hepatitis) Any cause of vasculitis Acid aspiration or pneumonia Smoke inhalation or other inhaled irritants Near-drowning experience Drug reaction or overdose
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT Cough, tachypnea, and respiratory distress are the most common: Severe edema may cause coughing with expectoration of blood-tinged fluid. Other complaints could reflect primary diseases, as already mentioned. PHYSICAL EXAM FINDINGS Acute severe respiratory distress and tachypnea Increased effort noted during inspiration and expiration from increased lung stiffness Cyanosis may be present if there is severe alveolar involvement. Fine crackles, often at end inspiration and early expiration, in the dorsocau-dal lung fields: Coarse crackles throughout inspiration more often indicate airway disease or progression of an interstitial disease into airways. Crackles may be absent in early or mild edema. Lung sounds may be exceptionally quiet in very severe edema, particularly in cats. Cardiac murmurs and arrhythmias do not always indicate that edema is of cardiogenic origin. Other clinical signs associated with the primary underlying disease process may be present.
ETIOLOGY AND PATHOPHYSIOLOGY Pulmonary edema results in arterial hypoxemia and respiratory distress: Hypoxemia is caused by ventilation/perfusión mismatches and, to a lesser extent, diffusion barriers to oxygenation of pulmonary capillary blood.
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Pulmonary Edema, Noncardiogenic
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Noncardiogenic pulmonary edema arises from three mechanisms: Increased vascular permeability is the most common and is seen with a wide variety of pulmonary and systemic disorders as akeady described. Decreased plasma oncotic pressure, most often from hypoalbuminemia. Pleural effusions (transudative) are more common than pulmonary edema in animals with reduced oncotic pressure as a single driving mechanism. Impaired lymphatic drainage is an uncommon etiology that is usually secondary to neoplasia or lymphangitis. Regardless of the mechanism, the edema fluid that infiltrates the interstitial and alveolar spaces is rich in protein (same concentration as plasma), in contrast to cardiogenic pulmonary edema that is characterized by protein-poor fluid. Cardiogenic pulmonary edema arises most commonly from increased pulmonary venous hydrostatic pressure secondary to left-sided congestive heart failure (seepp. 468 and 470).
DIAGNOSIS DIAGNOSTIC OVERVIEW Noncardiogenic edema is typically a secondary phenomenon; recognizing its existence is not analogous to diagnosing the patient's underlying condition. Early differentiation from cardiogenic edema is helpful to discern prognosis and delineate the next diagnostic steps.
DIFFERENTIAL DIAGNOSIS Any cause of tachypnea, cough, or pulmonary parenchymal infiltration, such as: Pneumonia Neoplasia Fungal disease Protozoal infection (e.g., toxoplasmosis in cats) Thromboembolic disease Complicated bronchial disease Inflammatory respiratory disease (i.e., pulmonary infiltrates with eosinophils/eosinophilic bronchopneumopathy) Pulmonary contusions Cardiogenic pulmonary edema
INITIAL DATABASE Thoracic radiographs: “fluffy” interstitial opacities that may progress to an alveolar pattern. Opacities are most often in the caudodorsal lung fields with edema caused by increased vascular permeability (similar to cardiogenic edema). Absence of cardiac and pulmonary venous abnormalities can help distinguish cardiogenic from noncardiogenic edema. CBC, biochemical profile, urinalysis, and other tests deemed clinically appropriate may be helpful in determining underlying causes (e.g., pancreatitis, sepsis). Historic information may help confirm underlying causes, such as electrocution, major trauma, or near-drowning experience.
ADVANCED OR CONFIRMATORY TESTING Respiratory washes or lung aspiration do not often yield abnormalities; occasionally, a primary pulmonary disorder is detected. Arterial blood gas (ABG) analysis: Hypoxemia Hypocapnia Widened alveolar-arterial (A-a) gradient The ratio of protein content of expectorated edema fluid (E) to circulating plasma protein content (P) in noncardiogenic edema is 79%-90%, whereas E:P ratio in cardiogenic edema is typically 20 mm Hg are indicative of cardiogenic pulmonary edema). Rarely performed clinically. Measurement of plasma BNP and ANP levels: may help distinguish between cardiac and noncardiogenic causes of congestive heart failure. Response to treatment: administration of appropriate doses of diuretics should be followed by improvement/resolution of radiographic markings in 24-48 hours.
TREATMENT TREATMENT OVERVIEW Three main goals: (1) reduction of excessive pulmonary venous return (preload); (2) reduction of systemic vascular resistance (afterload); and (3) inotropic support in a subset of patients (see pp. 468 and 470)
ACUTE GENERAL TREATMENT Avoid/reduce stress. Oxygenation Intravenous furosemide (2-5 mg/kg in dogs, 2-4 mg/kg in cats) q 1-2 h until labored respirations and respiratory rate decrease to normal, then decrease the dose of furosemide and frequency of administration based on clinical response.
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Pulmonary Edema, Cardiogenic
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Furosemide constant rate infusion IV CRI for refractory cases (0.7-1 mg/kg/h, cats and dogs). The authors have used up to 2 mg/kg/h. If starting a CRI, initially give a 2 mg/kg IV bolus, then start the CRI. Judicious monitoring of blood pressure and renal function is necessary. ± Nitroprusside (seep. 468 ) ± Dobutamine (seep. 468 )
CHRONIC TREATMENT See Heart Failure, Chronic (p. 470)
POSSIBLE COMPLICATIONS Pulmonary edema eventually returns despite medical therapy (lesion progression).
RECOMMENDED MONITORING Thoracic radiographs to assess response to therapy. A 12- to 24-hour lag period between clinical improvement and radiographic improvement is common, however. Serum electrolytes and renal status Respiratory status
PROGNOSIS AND OUTCOME Long-term prognosis is guarded because underlying disease is rarely cured. Exceptions can include correctable congenital defects (patent ductus arteriosus, pulmonic stenosis, others) and taurine-responsive dilated cardiomyopathy.
PEARLS & CONSIDERATIONS COMMENTS Owners should monitor resting respiratory rate at home. If it increases by more than 25% for 2 days in a row, a call to the veterinarian is warranted.
CLIENT EDUCATION Monitor for recurrence of presenting signs (see History, Chief Complaint above). Rapid deterioration is possible; rechecks necessary.
SUGGESTED READING Adin DB, Taylor AW, Hill RC, Scott KC, Martin FG: Intermittent bolus injection versus continuous infusion of furosemide in normal adult greyhound dogs, J Vet Intern Med 17(5):632–636, 2003. Atkins C, Bonagura J, Ettinger S, et al: ACVIM consensus statement. Guidelines for the diagnosis and treatment of canine chronic valvular heart disease. J Vet Intern Med 23:1142–1150, 2009. Fuentes VL: Use of pimobendan in the management of heart failure, Vet Clin North Am Small Anim Practice 34:1145–1155, 2004. Sisson D: Neuroendocrine evaluation of cardiac disease, Vet Clin North Am Small Anim Pract 34:1105–1126, 2004. Thomason JD, Fallaw TL, Carmichael KP, et al: Gingival hyperplasia associated with the administration of amlodipine to dogs with degenerative valvular disease (2004-2008). J Vet Intern Med 23(1):39–42, 2009. Ware W, Bonagura JD: Pulmonary edema. In Fox PR, Sisson D, Moise NS, editors: Textbook of canine and feline cardiology. Philadelphia, 1999, WB Saunders, pp 251–264. AUTHORS: MARC S. KRAUS, ANNA R. M. GELZER EDITOR: ETIENNE CÔTÉ
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Pulmonary Contusions
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Pulmonary Contusions BASIC INFORMATION DEFINITION A pulmonary contusion is a lesion consisting of intrapulmonary hemorrhage and inflammation secondary to blunt trauma.
SYNONYM Traumatic lung injury
EPIDEMIOLOGY SPECIES, AGE, SEX Young male dogs are at increased risk of trauma. GENETICS & BREED PREDISPOSITION None; larger dogs are more likely to roam unsupervised. RISK FACTORS Free-roaming behavior GEOGRAPHY AND SEASONALITY More common in warmer months ASSOCIATED CONDITIONS & DISORDERS Pneumothorax Diaphragmatic hernia Flail chest Hit by car (HBC) injury Fracture
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT Traumatic event; increased respiratory rate and effort PHYSICAL EXAM FINDINGS External evidence of trauma: cutaneous abrasions or lacerations, fractures Increased respiratory rate and effort Increased bronchovesicular sounds Pale mucous membranes Tachycardia
ETIOLOGY AND PATHOPHYSIOLOGY Trauma results in intraparenchymal pulmonary hemorrhage. Extracapillary hemorrhage results in the recruitment of inflammatory cells and protein into the alveolar and interstitial spaces. Pulmonary hemorrhage results in ventilation/perfusion mismatch and subsequent hypoxemia. Sequelae of pulmonary contusion may vary from very mild to rapidly fatal.
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Pulmonary Contusions
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DIAGNOSIS DIAGNOSTIC OVERVIEW Suspected clinically because of association with blunt trauma; clinical confirmation is generally radiographic.
DIFFERENTIAL DIAGNOSIS Nontraumatic pulmonary hemorrhage (anticoagulant rodenticide, neoplasia) Congestive heart failure (pulmonary edema) Pneumonia Pain (tachypnea)
INITIAL DATABASE Thoracic radiographs: document a patchy to diffuse interstitial alveolar pattern. Radiographic changes may lag behind clinical signs. May be indistinguishable from other patchy interstitial infiltrates, especially pulmonary edema in cats CBC, serum biochemistry profile: generally unremarkable
ADVANCED OR CONFIRMATORY TESTING Arterial blood gas (ABG) analysis (seep. 1196 ) or pulse oximetry may be useful to characterize the degree of hypoxemia. These are especially useful for determining whether tachypnea is due to pain (results are normal) or pulmonary lesions (hypoxemia commonly observed). Central venous pressure monitoring (seep. 1227 ), pulmonary wedge pressure measurement: Assess right- and left-sided vascular pressures, respectively (helps rule out cardiogenic causes). Pulmonary wedge pressure specifically assesses the propensity for pulmonary edema but is a somewhat cumbersome procedure and is especially challenging in cats and small dogs.
TREATMENT TREATMENT OVERVIEW Treatment goals are to maintain adequate intravascular volume but avoid overhy-dration, which may worsen pulmonary contusions, and to provide supplemental oxygen and rest.
ACUTE GENERAL TREATMENT Judicious administration of IV fluids as needed to maintain perfusion Administration of boluses of 5-10 mL/kg of crystalloid fluids (e.g., lactated Ringer's solution) until adequate blood pressure (BP) and pulse quality are obtained Administration of supplemental oxygen Evaluation for other associated injuries Note that glucocorticoids, antibiotics, and diuretics are not indicated for treatment of pulmonary contusions.
POSSIBLE COMPLICATIONS Infection (rare) Respiratory failure Severe pulmonary contusion may require intermittent positive-pressure ventilation (see p. 1362) with positive end-expiratory pressure (PEEP) and/or may progress to acute respiratory distress syndrome (ARDS).
RECOMMENDED MONITORING Hourly respiratory rate and effort Pulse oximetry
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PROGNOSIS AND OUTCOME Guarded to good prognosis. Most animals surviving a trip to the hospital will also survive pulmonary contusions with appropriate supportive care. Concurrent injuries (e.g., vertebral body fractures) are more likely to compromise the prognosis; other than very severe cases, pulmonary contusions are generally incidental findings that resolve with supportive care.
PEARLS & CONSIDERATIONS COMMENTS Avoid excessive volume resuscitation; administer IV fluids judiciously, and adjust the rate frequently based on the animal's response and evolution of the case.
PREVENTION Prevent roaming.
CLIENT EDUCATION Pulmonary contusions are “lung bruises;” the injured animal will often get worse over the first 24 hours, and then the lesions regress in the following 48 hours.
SUGGESTED READING Powell LL, et al: A retrospective analysis of pulmonary contusion secondary to motor vehicle accidents in 143 dogs: 1994-1997. J Vet Emerg Crit Care 9:127–136, 1999. AUTHOR & EDITOR: ELIZABETH ROZANSKI
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Ptyalism
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Ptyalism BASIC INFORMATION DEFINITION Production of excessive amounts of saliva, commonly manifested as drooling
SYNONYMS Hypersalivation, polysialia, sialonhea
EPIDEMIOLOGY SPECIES, AGE, SEX No species, age, or sex predilection except as dependent on underlying etiology Young animals: portosysternie shunts, seizure disorders Older animals: oral neoplasia, such as malignant melanomas (dogs), and squamous cell carcinoma (cats) GENETICS & BREED PREDISPOSITION Predisposition dependent on underlying cause RISK FACTORS Trauma of oral/pharyngeal region or nerves Exposure to toxins Esophageal disorders (esophagitis, esophageal obstruction) Oral foreign bodies Severe dental disease and/or dental abscesses Metabolic or physical disorders causing nausea or abdominal pain Primary or secondary neurologic disorders affecting saliva production Nausea Unvaccinated pets exposed to contagious diseases that may cause oral lesions or metabolic disorders CONTAGION & ZOONOSIS Zoonotic: rabies Contagion: viral infections causing oral lesions, such as calicivirus in cats
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT All or some may be present: Dysphagia Pawing at mouth Halitosis Oral discomfort with oral or pharyn-geal causes Anorexia or weight loss Coughing and/or dyspnea (from aspiration pneumonia) Gagging or retching with esophageal or gastric causes Seizures, facial twitching, behavioral changes possible with intoxications or portosystemic shunts PHYSICAL EXAM FINDINGS Saliva around mouth, salivary staining of fur
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Ptyalism
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Oral lesions, including masses, foreign bodies, abscesses, stomatitis, gingivitis, or other dental diseases Swelling of salivary glands, facial paralysis, atrophy of temporal or facial muscles Loss of gag reflex, inability to use tongue, dysphagia Mentation changes, seizures, tremors, or anxiety Painful abdomen Nausea
ETIOLOGY AND PATHOPHYSIOLOGY Etiology: Oral lesions: stomatitis, gingivitis, dental disease, neoplasia, foreign bodies Neurologic: peripheral nerve injury affecting swallowing, movement of tongue, pharynx; central nervous system (CNS) lesions, including neoplasia and infectious disorders such as rabies and feline infectious peritonitis (cats) Neuromuscular disorders (myasthenia gravis causing megaesophagus; masticatory myositis, muscular dystrophies) Metabolic: hepatic disease (portosystemic shunts), renal disease, nausea Toxins: caustic or noxious substances, pesticides (organophosphates), drugs (marijuana) Immune disease: polymyositis, pemphigus Pain, anxiety, excitement, fear Pathophysiology: Oral secretions are produced by sub-mandibular, parotid, and sublingual salivary glands. Innervation to salivary glands is controlled by the autonomic nervous system, with primary control by the parasympathetic nervous system. Many environmental, physical, or metabolic events may stimulate increased saliva production.
DIAGNOSIS DIAGNOSTIC OVERVIEW A complete medical history and thorough oral examination, possibly under sedation, will often lead the clinician in the right direction for diagnosis. For instance, an outdoor cat with acute onset of drooling may have oral ulcers, evidence of intoxication, or a foreign body.
DIFFERENTIAL DIAGNOSIS Ptyalism must be differentiated from drooling caused by certain conformations of the lips (but in which the amount of saliva produced by the salivary glands is normal). History (ptyalism is usually recent in onset, whereas conformation-associated drooling is chronic) and physical examination of the lips are generally sufficient for correct identification.
INITIAL DATABASE CBC to evaluate for anemia and evidence of infectious/inflammatory disease Serum biochemistry profile and urinalysis to evaluate for metabolic disorders Neurologic exam (seep. 1311 ) Thoracic, abdominal, and neck/head radiographs
ADVANCED OR CONFIRMATORY TESTING Oral examination with sedation or anesthesia Serum bile acids if history, exam, and minimum database consistent with liver disorder Abdominal ultrasound Electroencephalogram/CT scan, and MRI to evaluate CNS lesions Endoscopy to evaluate esophageal or gastric lesions Toxin screens Specific tests, such as acetylcholine (ACh) receptor antibody testing for myasthenia gravis
TREATMENT TREATMENT OVERVIEW
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Ptyalism
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Ptyalism is a sign of a predisposing disorder; therefore treatment is aimed at resolution of underlying cause
ACUTE GENERAL TREATMENT Supportive and nonspecific; possible use of anticholinergics and antinausea or antianxiety medications; identification of underlying etiology and prevention of aspiration
CHRONIC TREATMENT Treatment as appropriate for underlying etiology. Although surgical ligation or transposition of salivary ducts is sometimes performed in people with ptyalism, this surgery is usually not indicated in animals.
BEHAVIOR/EXERCISE Behavioral modification and anti-anxiety medication for stress-related hypersalivation
POSSIBLE COMPLICATIONS Anticholinergics often cause tachycardia, constipation, and behavioral changes; these require frequent dosing. Antiemetics such as chlorpromazine may cause sedation. Antisialagogues may reduce salivary output but do not correct the underlying problem. Antianxiety medications may cause sedation, anorexia, gastrointestinal upset.
RECOMMENDED MONITORING Monitor signs, including coughing, breathing difficulty, and fever, which may suggest aspiration of excessive saliva.
PROGNOSIS AND OUTCOME Fair to guarded prognosis depending on response to treatment of underlying etiology of disorder. Removal of foreign bodies, resolution of dental disease, repair of traumatic injury, and response to decontamination may have very favorable outcomes. Prognosis may be guarded with more serious disease processes such as immune diseases and neoplasia.
PEARLS & CONSIDERATIONS COMMENTS Ptyalism is usually a sign of a more serious disorder and deserves attention aimed at identifying the underlying cause. In addition, many owners find that their pets’ hypersalivation is unacceptable even if caused by minor problems and may cause them to choose euthanasia for the animals.
SUGGESTED READING Sherding B: Diagnosis and management of feline esophageal disease. World Small Animal Veterinary Association World Congress Proceedings, Vancouver, 2001. Sherman BL, Mills DS: Canine anxieties and phobias: an update on separation anxiety and noise aversions. Vet Clin North Am Small Anim Pract 38:1081–1106, 2008. AUTHORS: DIANA M. SCHROPP, ADAM J. REISS EDITOR: ETIENNE CÔTÉ
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Pseudorabies
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Pseudorabies BASIC INFORMATION DEFINITION Disease caused by infection with pseudorabies virus (PRV), an alphaherpesvirus in the family Herpesviridae. An economically important disease of swine, pseudorabies is capable of causing subclinical, neurologic, or respiratory disease in pigs and causing a rare but severe and almost inevitably fatal central nervous system (CNS) disease in dogs and cats.
SYNONYMS Aujeszky's disease, mad itch, bulbar paralysis
EPIDEMIOLOGY SPECIES, AGE, SEX: Dogs and cats are sporadically affected with pseudorabies (uncommon). Pigs are the primary reservoir of the virus because they have become well adapted to the virus and are often only subclinically affected. RISK FACTORS Pets living in areas where pseudorabies virus is enzootic in the swine population Feeding raw pork from endemic areas to dogs and cats CONTAGION & ZOONOSIS Pseudorabies virus may be found in porcine respiratory secretions, saliva, blood, and in the CNS and tonsillar tissues. Dogs and cats are commonly infected via the oral route after ingesting contaminated porcine tissue. Pseudorabies has also reportedly been transmitted to a dog by either biting or being bitten by an infected pig. Pseudorabies is not considered a zoonotic disease. GEOGRAPHY AND SEASONALITY: Pseudorabies can be found in most countries of the world except Australia.
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT Acute onset and rapid progression of neurologic signs until death occurs (usually within 48 hours of disease onset). Initial signs may include lethargy, depression, restlessness, or aggression and occasionally vomiting and diarrhea. Hypersalivation is commonly noted. Intense pruritus, usually of the head region, is probably the most clinically striking and consistent sign of pseudorabies. Animals will frequently excoriate the skin of the face and ears secondary to violent scratching. PHYSICAL EXAM FINDINGS Pruritus with swelling, erythema, excoriation, or ulceration of the skin secondary to self-mutilation, especially of the face and head. Intense scratching may include rubbing the head against floors or walls. Altered mentation Ptyalism Cranial nerve deficits indicative of a brainstem lesion(s) Dyspnea secondary to severe pulmonary edema Seizures Anisocoria and a hoarse voice (seep. 1172 ) are highly consistent signs in cats.
ETIOLOGY AND PATHOPHYSIOLOGY Once infection with pseudorabies virus has occurred, the virus travels retrograde along peripheral nerves from the site of inoculation to the CNS. Damage to brain parenchyma results from inflammation and interference of normal neuronal function by the virus. Microscopic lesions are located almost exclusively in the brainstem. The incubation period for pseudorabies in dogs and cats
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is 3-6 days.
DIAGNOSIS DIAGNOSTIC OVERVIEW Diagnosis is suspected in dogs with a history of exposure to pigs or raw pork products. Dogs present with severe, acute pruritus of the head and neck. Confirmation requires histopathologic evaluation of the brainstem.
DIFFERENTIAL DIAGNOSIS Rabies Canine distemper Neurotoxicoses
INITIAL DATABASE A provisional diagnosis of pseudorabies is usually made on clinical suspicion of the disease. Confirmatory testing is required for definitive diagnosis. There are no characteristic hematologic or biochemical abnormalities associated with pseudorabies.
ADVANCED OR CONFIRMATORY TESTING Cerebrospinal fluid analysis may show increased protein and mononuclear pleocytosis. Definitive diagnosis of pseudorabies has classically been made postmortem. Histopathologic abnormalities are generally limited to the brainstem and include perivascular cuffing, multifocal gliosis, neuronal degeneration, and weak eosinophilic inclusions within the nuclei of glial cells and neurons. Immunohistochemical techniques can be used for identifying viral antigen in fixed tissue sections (brain, tonsils). Alternatively, inoculation of cell cultures with brain homogenate for virus isolation can be performed. Cultures are observed for cytologic changes characteristic of herpesvirus infection, and immunofluorescent techniques can be applied to the cultures to identify pseudorabies virus.
TREATMENT TREATMENT OVERVIEW With very few exceptions, the treatment of pseudorabies in dogs and cats is futile, owing to a generally unavoidable fatal outcome. If treatment is initiated, it is aimed at controlling the major clinical signs and providing supportive care until the animal recovers (rare) or dies.
ACUTE GENERAL TREATMENT Heavy sedation or anesthesia as required for control of self-mutilation and/or seizures IV fluids if needed and patient not showing dyspnea Furosemide (1-3 mg/kg IV, IM, or PO q 6-12 h) for pulmonary edema if causing dyspnea
PROGNOSIS AND OUTCOME Grave prognosis; despite treatment, death usually occurs within 2-3 days of the onset of clinical signs.
PEARLS & CONSIDERATIONS COMMENTS Vaccination of dogs and cats against pseudorabies virus (usually in endemic areas) is possible but of questionable efficacy in the prevention of disease.
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Pseudorabies
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PREVENTION Preventing contact with infected pigs or contaminated pork products is paramount to the prevention of pseudorabies in dogs and cats.
SUGGESTED READING Buergelt CD, et al: Pseudorabies in two dogs. Vet Med 95:439–442, 2000. Vandevelde M: Pseudorabies. In Greene CE, editor: Infectious diseases of the dog and cat, ed 3, St Louis, 2006, Saunders Elsevier, pp 183–187. AUTHOR: MAUREEN A. MCMICHAEL EDITOR: DOUGLASS K. MACINTIRE 1ST EDITION AUTHOR: JODI SMITH
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Pseudocyesis
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Pseudocyesis BASIC INFORMATION DEFINITION A common syndrome observed in nonpregnant diestrous or early anestrous bitches. It is characterized by different degrees of maternal behavior, mammary gland enlargement, and lactation.
SYNONYMS Nervous anorexia, pseudopregnancy, overt false pregnancy
EPIDEMIOLOGY SPECIES, AGE, SEX Postpubertal female dogs of any age; has not been described in cats GENETICS & BREED PREDISPOSITION Any breed; incidence is higher in dalmatian, basset hound, and pointer-breed dogs. German shepherds are rarely affected. RISK FACTORS Exogenous administration of progestins, diestrous ovariectomy, and hypothyroidism may trigger its occurrence.
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES Depending on intensity of clinical signs: Covert (physiologic although recognizable from the rest of the estrous cycle) Overt, where manifestations can become a clinical problem (clinical pseudocyesis) HISTORY, CHIEF COMPLAINT Estrus 6-12 weeks earlier without an ensuing pregnancy Chief complaints: mammary problems (engorgement, lactation, licking of the glands) and abnormalities associated with aberrant maternal behavior (nesting, digging, adoption of animals or objects) Depression or anxiety, anorexia, and excessive vocalization (whining) are possible. PHYSICAL EXAM FINDINGS Mammary enlargement, ranging from turgid nipples to painful engorgement and galactostasis: Most evident in the caudal pair of glands Intramammary dermatitis is occasionally present if excessive licking occurs. Mastitis may also be present.
ETIOLOGY AND PATHOPHYSIOLOGY The high plasma concentration of prolactin at the end of the luteal phase, when progesterone concentrations decrease abruptly, is associated with the development and maintenance of pseudocyesis. Individual and breed sensitivity to these hormonal changes and environmental factors have been hypothesized to influence its occurrence.
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Pseudocyesis
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DIAGNOSIS DIAGNOSTIC OVERVIEW The diagnosis is suspected in any diestrous, nonpregnant bitch with mammary enlargement (and milk secretion) in which other mammary disease has been ruled out. Diagnostic imaging confirms absence of pregnancy if necessary.
DIFFERENTIAL DIAGNOSIS Pregnancy Pyometra Mastitis Mammary tumors Any other cause of anorexia, depression, or anxiety should be ruled out. Pseudocyesis can coexist with pyometra, mastitis, and mammary tumors.
INITIAL DATABASE CBC results are unremarkable.
ADVANCED OR CONFIRMATORY TESTING Ultrasonographic or radiographic confirmation of the absence of pregnancy or pyometra
TREATMENT TREATMENT OVERVIEW Treatment mainly consists of the administration of prolactin-decreasing drugs (dopamine agonists or antiserotonergic compounds).
ACUTE GENERAL TREATMENT Administer dopamine agonists with food to reduce digestive side effects: Cabergoline, 5 mcg/kg PO q 24 h for 5-7 days, is a safer choice compared to other prolactin-decreasing compounds. Avoid steroid hormones (progestins/androgens); they usually postpone the problem. Treat mastitis (seep. 688 ), acute moist dermatitis (seep. 30 ).
CHRONIC TREATMENT Clinical chronic, unresponsive, or recurring pseudocyesis cases should be treated surgically (ovariectomy) after the acute phase of the syndrome has been controlled or during anestrus.
NUTRITION/DIET No benefit from short-term partial food restriction
BEHAVIOR/EXERCISE Discourage maternal behavior, using aversion methods. Avoid stimulation of the mammary glands (e.g., padding [either hot or cold], touching, or milking). If necessary, Elizabethan collars can be used for preventing licking and self-milking.
DRUG INTERACTIONS Avoid administering phenothiazine drugs during pseudocyesis; they increase plasma prolactin concentrations. Do not administer antiserotonergic drugs (e.g., metergoline) for anxious and restless bitches because this could potentiate pseudocyesis behavior.
POSSIBLE COMPLICATIONS
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Mammary dermatitis and mastitis (seep. 688) are the most frequent complications and may have an influence in perpetuating the problem. Repeated episodes of pseudocyesis have been hypothetically associated with the future development of mammary tumors.
RECOMMENDED MONITORING Follow up cases until complete resolution. If pseudocyesis does not resolve spontaneously, look for predisposing
PROGNOSIS AND OUTCOME Pseudocyesis typically resolves spontaneously within a few weeks (2 or 3 weeks) from its onset but can occasionally persist until the next estrous cycle.
PEARLS & CONSIDERATIONS COMMENTS Pseudocyesis is a good indicator of ovulatory estrous cycles. Predisposed bitches usually suffer the syndrome after each estrous cycle, with the disorder becoming more severe throughout life.
PREVENTION Ovariectomy in predisposed bitches Pregnancy does not prevent future episodes.
CLIENT EDUCATION Teach clients to recognize pseudocyesis and to ask for treatment if it becomes clinically relevant.
SUGGESTED READING Gobello C, et al: Canine pseudopregnancy: A review. In Concannon PW, et al, editors: Recent advances in small animal reproduction. Ithaca, NY, 2001, International Veterinary Information Service, A1215.0801. AUTHOR: CRISTINA GOBELLO EDITOR: MICHELLE KUTZLER
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Pruritus
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Pruritus BASIC INFORMATION DEFINITION The unpleasant sensation that triggers the desire to scratch, chew, rub, lick, or bite at the skin
SYNONYM Itch
EPIDEMIOLOGY SPECIES, AGE, SEX Common in dogs and cats Sex and age of onset depend on the underlying etiology. Contagious acarioses (mite infestations) are more common in young animals. Canine atopic dermatitis is first seen in young adults (6 months to 3 years of age). Food allergy, although seen most commonly in young adults, may develop at any age.
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT Animals scratch, chew, rub, lick, or bite at the skin. In addition, cats can be secretive lickers and present only for extensive self-induced alopecia. PHYSICAL EXAM FINDINGS Skin lesions vary according to etiology. Self-induced alopecia, excoriation, and erythema are common findings. Typically, no primary skin lesions are noted in canine atopic dermatitis. Papules and/or pustules are noted in infectious or parasitic conditions. In cats: miliary dermatitis, eosinophilic granuloma complex, self-induced symmetric alopecia, or self-induced ulcerative facial dermatitis.
ETIOLOGY AND PATHOPHYSIOLOGY Etiologies of pruritus are numerous. For most parasitic infestations, a hyper-sensitivity reaction develops and is responsible for most if not all of the pruritus (often disproportionate to the number of parasites found). Pyoderma and yeast dermatitis are frequent causes of pruritus in dogs but are uncommon in cats.
DIAGNOSIS DIAGNOSTIC OVERVIEW Causes of pruritus are numerous, and the history (notably environment) and physical exam (e.g., lesion distribution) help focus the differential diagnosis. Diagnostic procedures aimed at identifying infections or infestations should be selected first, as these disorders are common, and treatment is generally straightforward. A precise diagnosis is necessary to administer a specific treatment.
DIFFERENTIAL DIAGNOSIS Parasitic: fleas, contagious acarioses (Sarcoptes, Notoedres, Cheyletiella, Otodectes spp.), lice, Trombicula (chiggers), and Pelodera spp.
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Pruritus
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Bacterial: staphylococcal pyoderma Fungal: Malassezia sp. dermatitis and otitis Allergic: flea bite hypersensitivity, atopic dermatitis, food hypersensitivity, contact hypersensitivity, drug reaction Miscellaneous: calcinosis cutis, cutaneous lymphoma
INITIAL DATABASE Complete history and dermatologic examination (see p. 1248) Skin scrapings Skin cytologic examination Wood's lamp and dermatophyte culture (in cats)
ADVANCED OR CONFIRMATORY TESTING Therapeutic trial with broad-spectrum antiparasitic agents (this is an integral part of the case work-up) is always indicated whenever there is a possibility of a parasitic problem, even if it is low, and in spite of negative skin scrapings. Clinicians occasionally use therapeutic trials with antibiotics or antifungal agents in dogs to document the contribution of bacteria and yeast in the degree of pruritus seen. Elimination diet: a hypoallergenic dietary trial ideally using home-cooked novel protein and carbohydrate sources; should be initiated after infections and infestations have been excluded/controlled. Intradermal skin test: preferred test for identifying atopic dermatitis. Serologic testing is also available, but false-positive reactions are more common. Skin biopsies are useful in unusual cases (e.g., calcinosis cutis, cutaneous lymphoma) and may be considered if the diagnosis remains elusive despite approaches described above, or if the clinician suspects these unusual disorders from other aspects of the case. A biopsy may corroborate the diagnosis of allergic skin disease but rarely confirms the specific cause.
TREATMENT TREATMENT OVERVIEW The goal is to find the cause to find as specific a treatment as possible. When possible, treatment is limited to one medication at a time to facilitate interpretation of response. When doing therapeutic trials, the most effective treatment regimen that is available and safe should be used to eradicate parasites or infections so interpretation of response is clear.
ACUTE GENERAL TREATMENT An acute intense pruritic episode can be treated with IM or IV short-acting glucocorticoids (dexamethasone sodium phosphate, 0.1-0.2 mg/kg) followed by a few days of prednisone or prednisolone (1 mg/kg PO q 24 h). Short-term use of glucocorticoids seldom causes serious problems.
CHRONIC TREATMENT In long-term management of pruritus, such as in cases of canine atopic dermatitis (seep. 106 ), clinicians rely on immunotherapy (hyposensitization), glucocorticoids, oral cyclosporine, anti-histamines and/or essential fatty acid supplementation. Long-term administration of glucocorticoids should be avoided if possible, unless the maintenance dose is low and/or if the treatment is intermittent. For example, a maintenance dose of 0.2-0.3 mg/kg q 48 h of prednisone and/or a total annual dose of 30-50 mg/ kg or less are rarely responsible for significant side effects. Induction and maintenance doses of prednisolone are typically 30% lower than prednisone doses, at least when administered concomitantly with trime-prazine (Temaril-P, Vanectyl-P). Along term treatment goal with these combination products is also to try to administer the minimal effective dose q 48 h. In food hypersensitivity, clinicians must find a commercial hypoallergenic diet that maintains the animal free of clinical signs. In flea bite hypersensitivity, maintain an effective flea elimination treatment.
RECOMMENDED MONITORING Animals receiving chronic glucocorticoid therapy should be monitored every 6 months for signs of iatrogenic hyperadrenocorticism or other complications (e.g., urinary tract infection, pyoderma).
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Pruritus
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PROGNOSIS AND OUTCOME Varies according to the etiology Excellent for most parasitic and infectious skin problems and food hypersensitivity Atopic dermatitis is an incurable disease that requires long-term management of pruritus.
PEARLS & CONSIDERATIONS COMMENTS Treatment of pruritic dermatoses does not always imply use of antipruritic drugs specifically. In fact, antiparasitic drugs, antibiotics, and antifungal drugs (for yeast dermatitis), which are not inherently antipruritic, are among the most useful “antipruritic” drugs. They have a key role in pruritus management because they control or eliminate the underlying cause. Superficial pyoderma is a frequent cause of pruritus in dogs. Always rule out parasitic and infectious causes of pruritus before administering long-term steroidal or nonsteroidal antipruritic drugs or before initiating an elimination diet (food trial). If pruritus is refractory to a usual maintenance dose of glucocorticoid (i.e., >0.5 mg/kg q 48 h of prednisone in dogs), consider the following diagnoses: sarcoptic mange/scabies, Malassezia dermatitis, pyoderma, food hypersensitivity, calcinosis cutis, contact allergic dermatitis, epitheliotropic lymphoma. More than one disease may be contributing to pruritus; for example, dogs with atopic dermatitis often have secondary bacterial and/or yeast infections. In cats, prednisone is generally not as effective as other glucocorticoids at equivalent doses. Instead, use oral prednisolone, methylprednisolone, dexamethasone, or triamcinolone.
CLIENT EDUCATION Owners of dogs with canine atopic dermatitis must be well informed of the chronic and multifaceted aspect of the disease. In order to evaluate response to treatment or disease progression, a pruritus score (e.g., on a scale of 0 to 10, 0 = normal and 10 = worst level of pruritus observed so far) can be very useful. It is worth explaining it to the animal's owner. Doing so can add a measure of objectivity and may reduce the owner's perception that treatment is ineffective, or conversely, may support the severity of pruritus perceived by the owner.
SUGGESTED READING Scott DW, Miller WH, Griffin CE, eds: Muller and Kirk’s small animal dermatology, ed 6, Philadelphia, 2001, WB Saunders. AUTHOR & EDITOR: MANON PARADIS
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Protozoal Enteritides
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Protozoal Enteritides BASIC INFORMATION DEFINITION Infection of the small or large intestine with protozoal organisms
EPIDEMIOLOGY SPECIES, AGE, SEX Giardiasis, trichomoniasis, and amebiasis occur in dogs, cats, humans, and many other domestic species. Balantidiasis is common in pigs but can also occur in dogs and humans. Tritrichomonas foetus infection principally causes reproductive problems in cattle but may also cause enteric signs in cats. Cystoisospora enteritis may affect dogs, cats, pigs, fowl, and other domestic animals. Young animals are at higher risk of developing overt, and potentially more severe, clinical signs. RISK FACTORS: Overcrowding, kennel boarding, unsanitary conditions, and immunosuppression increase the risk of protozoal enteritis. CONTAGION & ZOONOSIS Cystoisospora: each species of the organism is host specific and cannot be transmitted between other domestic animal species. Giardia lamblia, Balantidium coli, and Pentatrichomonas hominis enteritides pose a known or suspected zoonotic risk. Entamoeba histolytica can be transmitted from humans to dogs or cats but generally not from dogs or cats to humans. Dogs and cats do not shed the infective cyst form of E. histolytica. GEOGRAPHY AND SEASONALITY: Protozoal enteritides are distributed worldwide, with increased infection rates in areas of poverty, overcrowding, and poor sanitation-characteristics often associated with puppy mills, animal shelters, and pounds. ASSOCIATED CONDITIONS & DISORDERS Many protozoal enteritides are detected as secondary infections due to underlying primary gastrointestinal (GI) diseases.
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES B. coli (balantidiasis), Cystoisospora or related organisms (coccidiosis; protozoan parasites formerly known as Isospora), E. histolytica (amebiasis), G. duodenalis (giardiasis; see p. 447), P. hominis or T. foetus (trichomoniasis; see ), Cryptosporidium parvum (see ) HISTORY, CHIEF COMPLAINT Most infections with protozoa are subclinical. However, severe infections or infections in young or immunosuppressed animals may be serious, with overt, potentially debilitating clinical signs. The most common clinical sign is acute to chronic diarrhea. Some animals may be depressed or occasionally vomit. G. duodenalis and Cystoisospora spp. may cause small- or large-bowel diarrhea, while other protozoa generally cause only large-bowel diarrhea. PHYSICAL EXAM FINDINGS Physical examination findings may be nonspecific and include depression, mild to severe dehydration, and discomfort on abdominal palpation, with gas or fluid-filled intestinal loops. In milder cases, no physical abnormalities may be present.
ETIOLOGY AND PATHOPHYSIOLOGY
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Protozoal Enteritides
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Transmission of protozoal enteritides is fecal-oral. Infective cysts are ingested from the environment and commonly from water contaminated with feces. Upon exposure to intestinal enzymes, cysts open and release motile trophozoites that mature and attach to the intestinal epithelium. G. duodenalis and Cystoisospora spp. remain on the surface of the epithelium, causing damage to the microvilli. Entamoeba and Balantidium spp. may invade the colonic wall, causing ulceration. P. hominis is considered rarely pathogenic.
DIAGNOSIS DIAGNOSTIC OVERVIEW Standard fecal examinations are simple and provide a definitive diagnosis for these disorders; they are indicated in all cases of acute or chronic diarrhea.
DIFFERENTIAL DIAGNOSIS Young dogs: parvoviral, distemper viral, and bacterial enteritides; enteritis caused by helminths (Toxocara, Ancylostoma, Trichuris spp.) Young cats: feline panleukopenia, feline leukemia virus (FeLV) Sarcocystis oocysts may be observed on fecal examination; however, this coccidian is not pathogenic in dogs or cats. Herbivores are the intermediate host and develop parasitic cysts in muscle and nervous tissues after consuming the infected feces of dogs. Hammondia and Besnoitia oocysts may be seen on fecal examination; these coccidians are also nonpathogenic. Older animals with acute to chronic diarrhea may have a primary underlying intestinal disorder such as inflammatory bowel disease or neoplasia (dogs and cats), ulcerative colitis (dogs), or feline immunodeficiency virus-associated enteritis (cats). Cryptosporidium parvum (see p. 269) may also produce a primary gastroenterocolitis in both dogs and cats.
INITIAL DATABASE Direct fecal smear may reveal motile trophozoites. Zinc sulfate fecal flotation may reveal protozoal cysts. CBC and chemistry panel are nonspecific but may help rule out other diseases.
ADVANCED OR CONFIRMATORY TESTING Multiple fecal examinations may be necessary to find trophozoites or cysts, which may be shed intermittently. Three fecal examinations performed over a period of 3-5 days are recommended in challenging cases. A therapeutic trial with fenbendazole and metronidazole may be helpful in animals with chronic diarrhea but multiple negative fecal samples.
TREATMENT TREATMENT OVERVIEW Treatment consists of antiprotozoal medication in most cases. Supportive care may be indicated in severe cases.
ACUTE GENERAL TREATMENT Initial treatment consists of parenteral fluid therapy to correct hypovolemia and electrolyte and acid base disturbances. Fenbendazole, 50 mg/kg PO q 24 h for 3-5 days is the current treatment of choice for giardiasis. Metronidazole, 10-20 mg/kg PO q 12-24 h for 5-7 days is an effective treatment for enteritis caused by Pentatrichomonas, Entamoeba, and Balantidium spp. Cystoisospora enteritis may be treated with amprolium, 110-200 mg/kg PO q 24 h (dogs), or 50-60 mg/kg PO q 24 h (cats); or sulfadimethoxine for 14 days. Combination therapy may be more effective and allow use of lower doses with fewer side effects. There are no effective treatments known at this time for eradication of T. foetus in cats. Paromomycin, 125-160 mg/kg PO q 12 h for 5 days may be effective, but some cases of renal toxicity have been reported with the use of this drug in cats.
NUTRITION/DIET
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Protozoal Enteritides
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High-quality, easily digestible diets. High-fiber diets may help formation of a firm stool.
PROGNOSIS AND OUTCOME Prognosis for most protozoal enteritides is good. Recurrent infection is possible, and complete elimination of the organism may be challenging because some protozoa are commensalistic organisms and/or opportunistic pathogens. The prognosis for elimination of T. foetus from cats is guarded, although treatment may reduce clinical signs.
PEARLS & CONSIDERATIONS COMMENTS Protozoal enteritides are often secondary infections in adult animals. If appropriate antiprotozoal therapy is not effective, further testing is warranted to seek an underlying disease. Protozoal enteritis should not be eliminated as a possible cause of diarrhea in a young animal based on a single negative fecal result.
PREVENTION Prevention of overcrowding and maintaining a clean environment for young animals will help prevent protozoal infections. Prompt removal of feces should be encouraged.
TECHNICIAN TIPS Technicians should be able to recognize all forms (both cysts and trophozoites) of the organisms producing protozoal enteritides.
CLIENT EDUCATION Clients should be advised to seek medical attention if their pet has been diagnosed with protozoal enteritis; G. duodenalis, B. coli, and P. hominis enteritides carry a zoonotic risk.
SUGGESTED READING Barr SC, Greene CE, Gookin JL: Enteric protozoal infections. In Greene CE, editor: Infectious diseases of the dog and cat, ed 3, St Louis, 2006, Saunders Elsevier, pp 736–749. Dubey JP, Greene CE: Enteric coccidiosis. In Greene CE, editor: Infectious diseases of the dog and cat, ed 3, St Louis, 2006, Saunders Elsevier, pp 775–784. Washabau RJ: Gastrointestinal infectious diseases of dogs and cats. Western Veterinary Conference, Las Vegas, NV, Feb. 15-19, 2004. Available from: www.vin.com/ Members/Proceedings/Proceedings.plx?CID =WVC2004&O=VIN. Accessed July 31, 2006. AUTHOR: CHARLES M. HENDRIX EDITOR: DOUGLASS K. MACINTIRE 1ST EDITION AUTHOR: KATHRYN TAYLOR
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Protothecosis
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Protothecosis BASIC INFORMATION DEFINITION A multisystemic disease caused by infection with Prototheca algal species
EPIDEMIOLOGY SPECIES, AGE, SEX Cats: cutaneous infection Dogs: disseminated infections are more common. Female dogs are overrepresented. GENETICS & BREED PREDISPOSITION Collies and German shepherds appear to be predisposed to infection. RISK FACTORS Successful infection requires some degree of immunodeficiency in the host. CONTAGION & ZOONOSIS Prototheca is an opportunistic pathogen found in soil, sewage, and tree slime flux. Clinical disease has been reported in multiple animal species including humans. Zoonotic transmission is not recorded, but immunocompromised persons should observe hygienic precautions around affected animals (and the environmental source). GEOGRAPHY AND SEASONALITY In North America, most cases are reported in the southeastern United States.
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT Colitis-type diarrhea: mucoid, bloody, and foul-smelling; intermittent or protracted. Weight loss possible in chronic cases. Many dogs with diarrhea have ocular lesions (owners may note red or cloudy eyes). Central nervous system (CNS) signs include depression, stumbling, falling, or head tilt. PHYSICAL EXAM FINDINGS Palpable fluid-filled bowel loops and blood on thermometer can be noted. Rectal palpation may reveal thickened rectal tissues in some dogs. Cachexia with muscle atrophy possible Ocular manifestations include signs of conjunctivitis, uveitis, vitreous clouding, and acute blindness due to retinal detachment. Neurologic examination findings are consistent with disseminated CNS disease; asymmetric signs of ataxia, head tilt, circling, and paresis are reported in fewer cases. Mucocutaneous ulceration, ulcerative, and/or nodular cutaneous lesions: less common
ETIOLOGY AND PATHOPHYSIOLOGY Prototheca zopfii and Prototheca wick-erhamii are the two algae species responsible for clinical disease. Immu-nosuppression due to concurrent disease, administration of immunosup pressive agents, or genetic predisposition at time of exposure are considered key to development and persistence of infection. Prototheca organisms can be found in the kidney (where they may cause renal failure), liver, heart, intestine, brain, and eyes of infected animals.
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Protothecosis
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DIAGNOSIS DIAGNOSTIC OVERVIEW The diagnosis is suspected in a patient with signs of chronic colitis, with or without ocular or neurologic signs, who lives in a geographic area where Prototheca spp. are endemic. Clinical confirmation requires demonstration of the organism cytologically (usually via rectal scrape) or histologically (intestinal biopsy).
DIFFERENTIAL DIAGNOSIS Bloody diarrhea: parvovirus infection, clostridial infection, salmon poisoning, giardiasis, Salmonella enteritis, inflammatory bowel disease/ulcerative colitis, rectal adenocarcinoma, pythiosis, whipworm infection, coagulopathies caused by tickborne diseases or rodenticide poisoning, and gastrointestinal (GI) lymphoma In dogs with protothecal colitis, ocular lesions, and/or neurologic signs, systemic infectious diseases (e.g., mycoses) and lymphoma are important differential diagnoses.
INITIAL DATABASE CBC is usually unremarkable. Serum chemistry analysis usually shows mild increases in liver enzymes (alkaline phosphatase [ALP] and alanine amino-transferase [ALT]). Urinalysis usually is unremarkable, but inflammatory urine sediment may be seen, indicating possible renal involvement. Prototheca organisms have been isolated from the urine of dogs with renal failure secondary to renal invasion. Fecal analysis consisting of Sheather's flotation and ZnSO4 flotation is indicated in all suspected cases; Prototheca is occasionally found this way (many false-negative results).
ADVANCED OR CONFIRMATORY TESTING Organisms can be demonstrated in the cytologic examination of a rectal scrape (see p. 1334) stained with Diff-Quik or Wright's stain. Many falsenegative results. Intestinal biopsy (surgical or endoscopic) may yield a diagnosis when lesser invasive means are unsuccessful. A complete ophthalmic examination (seep. 1313 ) is indicated in suspected or confirmed cases, since ocular lesions may be missed initially. Organisms can be recovered from vitreous centesis. Neurologic examination (seep. 1311 ) should be performed on dogs showing CNS signs. Spinal radiographs or CT may be needed in dogs showing paresis. Organisms can be recovered from cerebrospinal fluid, which indicates severe clinical disease and dissemination. Culture can be performed on rectal scrape or any biopsy samples. Fluorescent antibody testing can differentiate P. zopfii from P. wicker-hamii
TREATMENT TREATMENT OVERVIEW Abort infection. Reduce or prevent further dissemination of infection, particularly to CNS. Decrease frequency and volume of diarrhea.
ACUTE GENERAL TREATMENT Initial treatment consists of parenteral fluid therapy. Antifungal treatment (amphotericin B with/without one of the following: itraconazole, ketoconazole, tetracycline, doxycycline) is beneficial to prevent immediate dissemination. Amphotericin B (patient must be hydrated): 0.25-0.5 mg/kg diluted in 5% dextrose and given IV q 48 h to total cumulative dose of 8-10 mg/kg or first signs of nephrotoxicity (monitor BUN, creatinine daily). Liposomal amphotericin B: as above, but SQ and for a shorter time period. Less nephrotoxic but still requires monitoring.
CHRONIC TREATMENT Tetracycline, 25 mg/kg PO q 8 h for 30 days; or doxycycline, 5-10 mg/kg PO q 24 h for 30 days; or ketoconazole or itraconazole, 5-10 mg/kg PO q 24 h with food for 30 days. Limited or no success in most cases.
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Protothecosis
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DRUG INTERACTIONS Ketoconazole, itraconazole: vomiting, inappetence, and elevated liver enzymes possible. If such signs occur, the drug therapy should be stopped and liver enzymes evaluated.
POSSIBLE COMPLICATIONS Treatment of concurrent infections and secondary Escherichia coli and Clostridium infections can reduce frequency and volume of diarrhea. Metronidazole, 7.5-15 mg/kg PO q 12 h can be used for Clostridium overgrowth.
RECOMMENDED MONITORING Monthly monitoring of the success of therapy is recommended. Rectal scrapes with cytologic analysis and culture, ophthalmologic examinations, CBC, serum chemistry, and urinalysis are recommended.
PROGNOSIS AND OUTCOME Prognosis is poor, especially with CNS signs, multiple organ involvement, and/or renal failure. Survival for >1 year has been reported in some animals with only GI and ocular lesions.
PEARLS & CONSIDERATIONS COMMENTS Prototheca is a ubiquitous organism and only an opportunistic pathogen in the irnmunocompromised dog. Further immunosuppressive therapy with glucocorticoids or other agents is contraindicated and counterproductive.
PREVENTION If a potential area of patient exposure can be identified, the patient and possibly humans should be prevented from further contact with this environment.
CLIENT EDUCATION The disease is not transmissible. However, owners who are irnmunocompromised should be cautious in handling the feces of infected animals.
SUGGESTED READING Greene CE, Rakich PM, Latimer KS: Protothecosis. In Greene CE, editor: Infectious diseases of the dog and cat, ed 3, St Louis, MO, 2006, Elsevier Saunders, pp 659–665. Hollingsworth SR: Canine protothecosis. Vet Clin North Am Small Anim Pract 30(5):1091– 1101, 2000. AUTHOR: SARALYN SMITH-CARR EDITOR: DEBRA L. ZORAN
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Protein-Losing Nephropathy
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Protein-Losing Nephropathy BASIC INFORMATION DEFINITION A common cause of kidney disease and kidney failure in dogs but less common in cats. Protein-losing nephropathy (PLN) is any condition in which glomerular damage leads to biologically significant loss of plasma proteins. Subsequent nephron loss may lead to chronic or acute kidney failure.
SYNONYMS PLN, proteinuric renal failure
EPIDEMIOLOGY SPECIES, AGE, SEX Familial nephropathy: Dogs > cats Age at onset of illness varies with breed. Sex predilection present for some (see Genetics & Breed Predisposition) Glomerulosclerosis: Either sex Incidence increases with age; average 8 years Membranous nephropathy: Either sex Most common PLN in the cat Mean age: cats 3-4 years; dogs 7 years Minimal change nephropathy: Uncommonly described in dogs and cats See Glomerulonephritis, p. 450 See Amyloidosis, p. 61 GENETICS & BREED PREDISPOSITION Familial nephropathy: inheritance not always defined; typical age of onset of signs is in parentheses. Glomerular disease: Bernese mountain dog (2-5 years), suspected autosomal recessive inheritance Brittany spaniel (4-9 years), autosomal recessive inheritance Rottweiler (90% cornification of epithelial cells Abdominal ultrasonography to look for endogenous sources of estradiol: Identification of abnormal ovarian structures: anechoic spherical regions in the ovary (follicles) or mixed echogenicity of a tumor Identification of ovarian remnant in an ovariohysterectomized animal
ADVANCED OR CONFIRMATORY TESTING Vaginoscopy to rule out foreign body and vaginitis Exclusion of abnormal karyotype Coagulation panel to rule out coagulopathy LH testing (using an in-house kit) is 99% reliable at diagnosing ORS in both cats and dogs.
TREATMENT TREATMENT OVERVIEW Treatment of abnormal estrus consists of removing the source of estradiol. For persistent estrus, induction of follicular luteinization, with subsequent monitoring of progesterone concentrations and vaginal cytology for signs of diestrus, or alternatively performing an ovariohysterectomy. For ORS, surgically remove any remaining ovarian tissue.
ACUTE GENERAL TREATMENT Medical: Follicular cysts in dogs and cats may be treated with gonadotropin-releasing hormone (GnRH, 25 mcg IM; use 2.2 mcg/kg if >11 kg) or human chorionic gonadotropin (hCG, 500-1000 IU IM), which results in luteinization of the follicles. Monitor serum progesterone, and perform a vaginal cytologic examination weekly following GnRH or hCG administration; monitor for signs of diestrus or anestrus. Canine GnRH vaccine can be used in the treatment of ORS where surgical removal of the remnant is not an option. Surgical: When genetic qualities of the dam are not superior, ovariohysterectomy is the treatment of choice following reduction of current hyperestrogenic state. Removal of remaining ovarian tissue is the recommended treatment for ORS.
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Prolonged Estrus
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CHRONIC TREATMENT If acute medical treatment is not effective, surgical treatment is required.
POSSIBLE COMPLICATIONS Pyometra sequelae: Progesterone promotes endometrial growth and glandular secretion while decreasing myometrial activity. Cystic endometrial hyperplasia and accumulation of uterine secretions ultimately develop and provide an excellent environment for bacterial growth. Chronic estradiol production by the cystic follicles upregulates progesterone receptors in the uterus. This enhances the effect of the progestins produced following treatment to luteinize the cystic follicles. Complication rate for surgical removal of an ovarian remnant in dogs is unknown.
RECOMMENDED MONITORING Monitor signs of estrus that should subside within 5-7 days of treatment.
PROGNOSIS AND OUTCOME Recurrence is possible, but prognosis is good if signs of diestrus follow treatment. If estrus persists, increased suspicion of neoplasia or abnormal karyotype yields a poorer prognosis for subsequent fertility, and an ovariohysterectomy is indicated. Surgical removal of ovarian remnants results in a good prognosis if signs of cycling cease.
PEARLS & CONSIDERATIONS COMMENTS Although ovarian cancer is rare in the bitch or queen, failure of medical treatment to end signs of behavioral estrus or decrease circulating estradiol concentrations greatly increases the possibility of this diagnosis. Timing of exploratory surgery to remove ovarian remnants is important: surgery should be performed when the animal is under an estrogenic influence so ovarian tissue is enlarged and easier to identify.
PREVENTION In animals of nonbreeding stock, complete ovariohysterectomy will prevent reproductive abnormalities and their sequelae.
CLIENT EDUCATION Train owners to recognize signs of estrus, or discuss outward signs of behavioral estrus for the bitch and queen. Clinicians and owners should discuss multiple benefits of spaying nonbreeding stock while young. Recurrence is more likely in animals with previous follicular cysts.
SUGGESTED READING England GCW: Infertility in the bitch and queen. In Noakes DE, Parkinson TJ, England GCW, editors: Arthur’s veterinary reproduction and obstetrics. Philadelphia, 2001, WB Saunders, pp 639–670. Little S: Feline reproduction and breeding management. Cat Fanciers’ Association website. Available from: http://cfa.org/ articles.reproduction.pdf. Accessed July 31, 2006. AUTHOR: TIMOTHY HAZZARD EDITOR: MICHELLE KUTZLER
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Prolonged Anestrus
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Prolonged Anestrus BASIC INFORMATION DEFINITION Duration of interestrous interval >40 weeks. Overall, a rare disorder.
SYNONYMS Primary or secondary anestrus; prolonged interestrous interval
EPIDEMIOLOGY SPECIES, AGE, SEX Female dogs and cats Bitches > 12 months old (more common in older bitches) Queens > 6 months old GENETICS & BREED PREDISPOSITION: Longhaired queens have a tendency to experience delayed puberty. RISK FACTORS: Previous ovariectomy, exogenous hormonal treatment (including glucocorticoids), hyperthyroidism, ovarian disease (cysts or neoplasia), or abnormal karyotype GEOGRAPHY AND SEASONALITY Bitches are nonseasonally monoestrous (exception: basenji dog that only comes into estrus in the fall). The normal interestrous interval in dogs is 26-36 weeks. The queen is a seasonally polyestrous long-day breeder (see p. 909). The normal interestrous interval in queens is 12-22 days. ASSOCIATED CONDITIONS & DISORDERS Ambiguous or infantile external genitalia may be associated with an intersex condition or abnormal karyotype.
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES Primary anestrus: delayed puberty Secondary anestrus: increased interestrous interval HISTORY, CHIEF COMPLAINT Failure to show external signs of proestrus or estrus (failure to cycle) PHYSICAL EXAM FINDINGS Abnormal physical findings may include poor or excessive general body condition, overall immature appearance, and ambiguous or infantile external genitalia. The physical examination may be unremarkable.
ETIOLOGY AND PATHOPHYSIOLOGY Variable, depending on the cause Disruption in the normal cyclical hormonal milieu
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Prolonged Anestrus
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DIAGNOSIS DIAGNOSTIC OVERVIEW The diagnosis is suspected based on the absence of estrous behaviors in an intact animal, followed by excluding anatomic abnormalities and endocrine-related illnesses. Confirmation requires histopathologic identification of oophoritis or diagnostic imaging (CT scan) demonstrating pituitary abnormalities.
DIFFERENTIAL DIAGNOSIS Dogs: Silent heat Abnormalities in sexual differentiation Hyperadrenocorticism Hypothyroidism Pituitary insufficiency Lymphocytic oophoritis Luteal ovarian cyst Ovarian aplasia Ovariohysterectomy Cats: Seasonal or lighting changes Pseudopregnancy Diabetes mellitus Silent heat (social stress in cattery) Ovariohysterectomy
INITIAL DATABASE CBC and serum biochemistry profile for systemic health status Assessment of endocrine-related illnesses via thyroid hormone analysis and dexamethasone suppression tests Exclusion of silent heats, using exfoliative vaginal cytologic examination and serum progesterone determination Exclusion of abnormal reproductive tract, using abdominal ultrasonography Exclusion of abnormal karyotype
ADVANCED OR CONFIRMATORY TESTING Confirmation of oophoritis with ovarian histologic examination CT scan of pituitary to identify cystic dilation or absence of the gland
TREATMENT TREATMENT OVERVIEW Treatment mainly consists of correcting insufficiencies or excesses in endocrine hormones (e.g., hyperadrenocorticism), as well as observation and monitoring for reproductive cyclicity.
ACUTE GENERAL TREATMENT Observe bitch or queen closely while housing her near an intact male dog or tom. Monitor serum progesterone concentrations monthly to assess cyclicity (serum progesterone >2 ng/mL for 2 months after each estrus in the normal bitch). Cohouse anestrous bitch with cycling bitches to stimulate a “dormitory” effect. Increase lighting in cattery to 14 hours of light per day.
CHRONIC TREATMENT
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Prolonged Anestrus
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Estrus induction: no approved methods of estrus induction in the dog or cat, but many protocols have been described. Possible methods: Dogs: after confirming a progesterone concentration 60-80 mL/kg/d) Polyuria (PU): production of excessive volumes of urine (>30-40 mL/kg/d)
EPIDEMIOLOGY SPECIES, AGE, SEX Cats and dogs, any age, either sex ASSOCIATED CONDITIONS & DISORDERS Diet (e.g., formulation [dry kibble versus moist/canned], salt content) will affect water consumption in both normal and ill dogs and cats.
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES PU with secondary PD PD with secondary PU HISTORY, CHIEF COMPLAINT Common chief complaints: Increased frequency and amount of drinking “Water-starved” behavior (pets actively seeking to drink water from abnormal or typically inaccessible locations) is possible in extreme cases or if owner is restricting water intake. Urination in inappropriate indoor locations Prolonged duration of individual urinations Need to change litter with increased frequency (cats) Clinicians should initially ask owners what the water consumption is like as compared with 6-12 months earlier. The clinician can also ask whether there has been any change in water consumption, not whether water consumption has increased (to avoid leading the owner's answer). It is usually not possible to determine whether PU is primary, with secondary PD, or vice versa from the history alone. History should aim to differentiate PU from pollakiuria, stranguria, inappropriate elimination/urinary incontinence, and urinary marking/spraying. Basic environmental questions include duration of time indoors between walks (most normal dogs need to urinate at least every 8-12 hours), introduction of new pets or family members (suggesting behavioral changes/marking), new environment (behavior/marking or exposure to toxins), and change in litter type, location, or hygiene (cats). Some owners may not be aware of water consumption or urination because the pet mainly lives outdoors. Clinicians should view PD in dogs in a hospital setting with initial skepticism because occasionally, dogs drink voluminous amounts of water because of anxiety or excitement. More commonly, dogs with a history of PD drink less in the hospital as a result of excitement or anxiety. Medication history: glucocorticoids, phenobarbital, diuretics, thyroid supplementation can cause PU/PD Intoxication history should cover recent and distant potential exposures (ethylene glycol, grapes, raisins, lilies [cats]) and nephrotoxic medications (see p. 1411). PHYSICAL EXAM FINDINGS Dehydration: consistent with any cause of PU/PD other than psychogenic PD Thin body condition Some dogs with diabetes insipidus drink excessively and choose water over food, leading to weight loss. With a poor haircoat: consistent with chronic kidney disease, chronic liver disease, diabetes mellitus, hyperthyroidism,
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Polyuria/Polydipsia
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chronic gastrointestinal (GI) disease Dyspnea, tachypnea: may occur concurrently with metabolic acidosis, severe hypovolemia/shock (many possible causes) Panting (excessive): may be noted in dogs whose PU/PD is due to: Hyperadrenocorticism Hyperthyroidism Also common in anxious or obese animals (i.e., nonspecific finding) Bilaterally symmetric truncal alopecia: endocrine disease (e.g., hyperadrenocorticism) Rectal examination: assess for primary disorders (e.g., adenocarcinoma of the anal sac causing PU/PD via hypercalcemia) and for causes of urinary incontinence other than PU (urethral or trigone thickening, suggesting inflammation or infiltration; prostatitis). Vaginal exam (seep. 1360 ): Always attempt to identify a neoplastic process (mass) that might cause PU/PD via hypercalcemia of malignancy. Purulent exudative discharge suggests pyometra. Abdominal palpation: Kidneys: small (e.g., chronic kidney disease) or large (e.g., polycystic kidney disease, renal lymphoma, other renal neoplasia, pyelonephritis) Hepatomegaly (e.g., primary hepatopathies, hyperadrenocorticism, diabetes mellitus, iatrogenic [glucocorticoids, barbiturates], lymphoma causing malignancy-associated hypercalcemia) Splenomegaly (e.g., lymphoma causing malignancy-associated hypercalcemia) Duodenal/jejunal thickening may be palpable with diffuse intestinal infiltrative diseases. Uterine enlargement may be palpable (abdominal palpation must be performed gently because the uterus is potentially friable) with pyometra. Cardiac auscultation: tachycardia, heart murmur, third heart sound/gallop, and/or arrhythmia possible with hyperthyroidism
ETIOLOGY AND PATHOPHYSIOLOGY Normal daily water consumption: Dogs: up to 60-80 mL/kg/d (higher in dogs 1.012 but 1.025) without glucosuria is inconsistent with PU/PD; other causes to explain clinical signs, such as lower urinary tract disorders, should be sought. Diabetes mellitus causes PU but relatively concentrated urine (USG 1.025-1.045), at least in part due to glucosuria. Isosthenuria (USG = 1.008-1.012) can be caused by kidney disease (tubules fail to concentrate urine) or by normal free water excretion (e.g., after a normal animal has drunk a large volume of water). Calcium oxalate dihydrate crystals suggest postacute ethylene glycol ingestion. Ammonium biurate crystals suggest liver failure (shunt, cirrhosis, etc). Urine culture and sensitivity (C&S): routinely performed in all animals with PU/PD. Urinary tract infection may complicate virtually any cause of PU/PD, may not produce additional overt clinical signs, often escapes diagnosis on urinalysis alone due to dilute urine, and is treatable and curable. Serum thyroid hormone levels: rule out hyperthyroidism (cats >6 years old).
ADVANCED OR CONFIRMATORY TESTING Abdominal ultrasound: evaluate kidneys (chronic kidney disease, pyelonephritis, neoplasia); urinary bladder (signs of cystitis, urolithiasis, or mass [e.g., neoplasm] producing pollakiuria or stranguria rather than PU); GI tract (evidence of infiltration); liver (chronic hepatopathies, portosystemic shunt, nonspecific enlargement, and hyperechogenicity [diabetes mellitus, hyperadrenocorticism, others]); adrenal glands (mass; subtle changes related to pituitary-dependent hyperadrenocorticism, although 50% of dogs with pituitary-dependent hyperadrenocorticism have structurally normal adrenal glands on ultrasound exam); and uterus (pyometra) Radiographs (thoracic, abdominal) Others as dictated by specific etiologies suspected
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Polyuria/Polydipsia
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TREATMENT TREATMENT OVERVIEW Successful treatment requires identification of cause. PU and PD are not diseases but clinical manifestations of primary underlying disorders. Therefore, nonspecific treatment such as withholding water is unlikely to succeed and may be dangerous.
GENERAL TREATMENT Withholding water can be dangerous or life threatening in all cases of PU/PD for which the underlying disease produces primary PU with secondary PD (see Etiology and Pathophysiology above).
POSSIBLE COMPLICATIONS Dehydration Progression of the primary problem if not identified and addressed
RECOMMENDED MONITORING Physical examination, including body weight; diagnostic testing as indicated by underlying disease process, results obtained to date, and evolution of case.
PROGNOSIS AND OUTCOME Highly variable from excellent to poor, depending on underlying cause and response to treatment.
PEARLS & CONSIDERATIONS COMMENTS Any time an owner is concerned about their pet exhibiting “inappropriate urination” (any problem with urine), they should be instructed to collect about a teaspoon (5 mL) of urine to bring in at the time of examination. This allows easy separation of a pet with lower urinary tract disease (bladder stones) from one with diabetes mellitus (glycosuria) from one with nondiabetic PU/PD. Urine specific gravity p. 1070): Antibodies to nuclear material, immune complex formation, and subsequent deposition in tissues cause multisystemic disease that commonly manifests with nonerosive polyarthritis, dermatitis, and/or glomerulonephritis (GN). Erosive IMP As include rheumatoid arthritis (rare in the cat) and periosteal proliferative polyarthritis (common in the cat). Rheumatoid arthritis (see','','');return false;">p. 989) is usually associated with autoantibodies to immunoglobulin G (rheumatoid factor). Periosteal proliferative polyarthritis is characterized by periosteal new bone formation and bony erosions. It affects young adult cats, often castrated males, and is usually acute in onset. Chronic progressive polyarthritis is a milder form, is insidious in onset, and affects older cats.
DIAGNOSIS DIAGNOSTIC OVERVIEW Polyarthritis can be suspected and occasionally diagnosed with history and physical examination alone. Fever, lethargy, lameness, and the presence of painful or swollen joints, especially distal joints, should arouse the clinician's suspicion. Confirmation rests on arthrocentesis with fluid analysis of multiple joints. Radiography may be done to evaluate for erosive changes. Further testing —including tick titers, cultures, screening for cancer—is required to determine an underlying cause and guide management. Successful management of polyarthritis requires that any underlying cause be identified and treated.
DIFFERENTIAL DIAGNOSIS Many conditions should be ruled out for a patient that is unable to rise and ambulate normally: Neurologic disease (e.g., spinal cord or brain disorders, neuromuscular diseases)
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Polyarthritis
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Muscular disease (e.g., polymyositis) Orthopedic disease (e.g., bilateral cranial cruciate ligament rupture, degenerative joint disease) Cardiac disease (e.g., pericardial effusion) Metabolic disease (e.g., hypoglycemia, hypocalcemia) Hematologic disease (e.g., acute blood loss)
INITIAL DATABASE Orthopedic and neurologic examinations to help rule out other disorders CBC, serum biochemistry profile, urinalysis: Anemia and leukocytosis are common in idiopathic polyarthritis but are nonspecific. Serum chemistry profile to assess dysfunction in other organs Proteinuria may be indicative of GN (immune-mediated) or amyloidosis Radiographs to distinguish erosive from nonerosive polyarthritis: Erosive polyarthritis is characterized by subchondral bone destruction, which is seen as an irregular joint surface or “punched-out” erosion of bone at the joint space. In advanced cases of joint deformity, loss of mineralization of the epiphysis and calcification of soft tissues of the joint may be seen. Nonerosive polyarthritis presents no bony radiographic abnormalities; signs of joint effusion and soft-tissue swelling may be apparent.
ADVANCED OR CONFIRMATORY TESTING Arthrocentesis (see ','','cesec49');return false;">p. 1199); two or more joints should be sampled. The tarsi and carpi are especially useful because of frequency of involvement and ease of access to the synovial space. Gross appearance: normal synovial fluid is viscous (tenacious), scant in volume, and clear, whereas synovial fluid of animals with polyarthritis is generally thin/watery and may be copious (several milliliters) and potentially turbid (more so with infectious/septic polyarthritis). Synovial fluid analysis; neutrophils are the predominant cell in inflammatory polyarthritis (distinguishing them from the more common degenerative arthropathies), and total cell counts are always >3000/µL and often 40,000/µL or higher. Cytologic examination is seldom helpful in distinguishing septic from nonseptic arthritis (only occasionally are intracellular, phagocytized organisms seen), although the presence of degenerate or toxic neutrophils is suggestive of septic arthritis. Culture: synovial fluid cultures are usually negative. When clinicians suspect septic arthritis, they should consider a culture of synovial membrane, blood, and/or urine. Special media are needed to culture L-form bacteria and Mycoplasma. Titers: Lyme disease (Borrelia burgdorferi), Ehrlichia (especially canis, ewingii), and Anaplasma phagocytophila (formerly Ehrlichia equi). Echocardiogram if suspicious of bacterial endocarditis (e.g., heart murmur, especially if new in onset, and/or diastolic; see ','','para693');return false;">p. 346) Serum antinuclear antibody and rheumatoid factor if the clinician suspects SLE or rheumatoid arthritis, respectively; the tests are of limited accuracy Cerebrospinal fluid tap if the clinician suspects meningitis Thoracic radiographs and abdominal ultrasound examination to evaluate for remote infection, GI disease, or neoplasia if suspected
TREATMENT TREATMENT OVERVIEW Treatment depends on the etiology. Sometimes despite treating the underlying cause, however, a course of prednisone is required to resolve the polyarthritis. For cases of IMPA, immunosuppressive doses of prednisone/prednisolone are the treatment of choice and following resolution of clinical signs, usually within 2 weeks, corticosteroids should be slowly tapered over 4-6 months. Insufficient dosages and/or administration for insufficient periods of time are important causes of treatment failure.
ACUTE GENERAL TREATMENT Doxycycline, 10 mg/kg PO q 24 h for 28 days for tickborne infections, Mycoplasma, and L-form bacteria Prednisone/prednisolone, 1.1 mg/kg PO q 12 h initially for nonerosive and erosive noninfectious IMPA Broad-spectrum antibiotics (e.g., amoxicillin-clavulanate, 22 mg/kg PO q 12 h) or cephalosporins (e.g., cephalexin, 22 mg/kg PO q 8 h) pending cultures in suspected or confirmed cases of septic arthritis Surgical joint lavage and drainage sometimes are required for septic arthritis.
CHRONIC TREATMENT
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Polyarthritis
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For IMPA: prednisone/prednisolone, 1.1 mg/kg PO q 12 h (20 mg/m PO q 12 h for dogs >25 kg; seep. 675 ) until resolution of signs (usually 2-4 weeks), then slowly reduce the dose and administer q 48 h. Average of 3-6 months and rarely lifelong treatment is required. If glucocorticoid side effects are marked or high doses are necessary, to suppress signs, consider other immunosuppressive drugs such as azathioprine, cyclophosphamide, gold salts, methotrexate, or leflunomide to keep clinical signs suppressed while using lower doses of glucocorticoids. Septic arthritis: antibiotics required until 2 weeks after infection has resolved; often a minimum of 6 weeks.
NUTRITION/DIET Caloric control is necessary to avoid weight gain in patients on corticosteroids. Treatment of obesity when present is an important adjunctive therapy for chronic polyarthritis cases.
DRUG INTERACTIONS Many drugs can potentially interact negatively with the drug in question; clinicians should consult a formulary for possible interactions.
POSSIBLE COMPLICATIONS Secondary infections from immuno-suppressive drugs Prednisone has many potential adverse effects including polyuria and polydipsia (PU/PD), polyphagia, panting, weight gain, muscle wasting, and elevated liver enzymes. Azathioprine: myelosuppression, hepatotoxicity, acute pancreatitis; avoid in cats Cyclophosphamide: myelosuppression, hemorrhagic cystitis
RECOMMENDED MONITORING Primarily resolution of clinical signs; if uncertainty exists, repeat arthrocentesis to see if cell counts have returned to normal. Monthly CBCs are required for animals receiving cyclophosphamide or azathioprine. Monitor liver enzymes in animals receiving glucocorticoids.
PROGNOSIS AND OUTCOME Nonerosive IMPA: good to guarded. About 30% of cases relapse and may be difficult to control or may require lifelong treatment. Juvenile hereditary arthritis of Akitas: very poor. Does not respond to immunosuppressive therapy. Calicivirus infection of cats: excellent. Generally resolves in 3 days with supportive care. Noninfectious erosive arthritis: guarded. Arthrodesis may improve quality of life. Infectious arthritis: provided the condition is nonerosive and the infection can be treated, the prognosis is good.
PEARLS & CONSIDERATIONS COMMENTS Polyarthritis should be suspected in any animal that is reluctant to walk or in any case of fever of unknown origin. Even in the absence of joint pain or swelling, arthrocentesis of multiple joints is indicated in such animals to confirm or refute a diagnosis of IMPA. Cats with polyarthritis may be described only as lethargic by owners; polyarthritis might be missed unless cats are observed walking in the exam room. Empirical treatment with doxycycline may be considered while completing a workup. The majority of cases of polyarthritis are idiopathic, immune mediated, and nonerosive.
TECHNICIAN TIPS Dogs receiving immunosuppressive doses of prednisone/prednisolone should be monitored closely for adverse effects (see above). The goal is to start at a high dose, resolve clinical signs, then taper gradually to lowest possible dose so as to minimize unacceptable side effects including polyuria and muscle wasting. Pain associated with polyarthritis should not be mistaken for reluctance or other behavioral traits; these patients may be too painful to walk, may be more prone to aggression if handled, or both.
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Polyarthritis
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PREVENTION Tick prevention if relevant (dogs in endemic regions)
CLIENT EDUCATION Close monitoring is required while patients are receiving immunosuppressive therapy. Relapses are possible. Genetic counseling for hereditary forms
SUGGESTED READING Clements DN, et al: Type 1 immune-mediated polyarthritis in dogs: 39 cases (1997-2002). J Am Vet Med Assoc 224:1323–1327, 2004. Stull JW, et al: Canine immune-mediated polyarthritis: clinical and laboratory findings in 83 cases in western Canada (1991-2001). Can Vet J 49:1195–1203, 2008 AUTHOR: ORLA MAHONY EDITOR: SUSAN M. COTTER
26-09-2011 21:53
Pollakiuria, Stranguria
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Pollakiuria, Stranguria BASIC INFORMATION DEFINITION Pollakiuria: increased frequency of attempts to urinate Stranguria: straining to urinate Both are clinical signs of lower urinary tract inflammation, infection, and/or obstruction.
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT Owners may confuse these clinical signs with inappropriate elimination, polyuria, or tenesmus. Other clinical signs can include dysuria and malodorous urine. Often pollakiuria/stranguria is the only presenting clinical sign. PHYSICAL EXAM FINDINGS Important to determine if urethral obstruction is the cause: Obstruction: bladder enlarged/firm, nonexpressible, often painful Nonobstruction: bladder small/soft, expressible; bladder wall may be thickened, often painful as well. Bladder should be palpated before and after the patient voids: Uroliths, masses, and bladder wall thickness/irregularities may be assessed more easily in the flaccid bladder. Rectal exam may reveal urethral, prostatic, or bladder trigone abnormalities.
ETIOLOGY AND PATHOPHYSIOLOGY Any disease that causes lower urinary tract infection (LUTI), inflammation, or obstruction can cause pollakiuria or stranguria. Localizes the lesion to the lower urinary tract (bladder, urethra)
DIAGNOSIS DIAGNOSTIC OVERVIEW Beyond a complete history and physical exam, a sterile urine sample for urinalysis (and bacterial culture and sensitivity [C&S] in the canine patient) should be the first diagnostic test in the pollakiuric or stranguric patient. Diagnostic imaging should be considered in a patient with a negative culture in the face of pollakiuria/stranguria.
DIFFERENTIAL DIAGNOSIS Feline: Most common cause is idiopathic feline lower urinary tract signs (FLUTS; see p. 387): Also called feline idiopathic cystitis (FIC), feline lower urinary tract disorder (FLUTD), and feline urologic syndrome (FUS) Primary bacterial infection in cats is rare; infection is present in 200 mL/kg), no end point, or recurrent pneumothorax, then place thoracostomy tubes (see ). Apply the “three-strike rule,” meaning if three or more thoracocenteses are required within 24 hours following a trauma, a thoracostomy tube should be placed. Spontaneous pneumothorax (no trauma): If the clinician suspects a bulla or bleb (no masses on radiographs), a thoracotomy is warranted. If the clinician suspects a necrotic neoplasm, a thoracic CT scan followed by thoracotomy is warranted. If the clinician suspects an underlying feline asthma or chronic bronchitis, conservative therapy may be adequate. Iatrogenic: If there are no clinical signs (radiographic diagnosis only), monitoring of the patient is adequate. If the patient is showing clinical signs, repeating the thoracocentesis and monitoring the animal closely are recommended. The animal may require a thoracostomy tube or exploratory thoracotomy if not responsive. Underlying disease may require specific treatment.
CHRONIC TREATMENT Correction of the underlying cause if applicable
POSSIBLE COMPLICATIONS Ongoing pleural effusion or pneumothorax
RECOMMENDED MONITORING Respiratory rate and effort Pulse oximetry
PROGNOSIS AND OUTCOME Fair to good; often with trauma, the associated injuries are more likely to predict outcome. Dyspnea and duration of intensive care are negative prognostic factors in dogs and cats with pneumothorax.
PEARLS & CONSIDERATIONS COMMENTS Traumatic pneumothorax rarely requires surgical correction; most cases rapidly resolve (within 72 hours). Spontaneous pneumothorax commonly requires surgical treatment because most cases will not resolve without surgery.
TECHNICIAN TIP Technicians involved in caring for patients with pneumothorax should be familiar with management of chest tubes.
PREVENTION Owners should prevent free roaming of pets. Clinicians should use caution when performing a thoracocentesis.
SUGGESTED READING Kern DA, et al: Radiographic evaluation of induced pneumothorax in the dog. Vet Radiol Ultrasound 35:411–417, 1996. Puerto DA: Surgical and nonsurgical management of and selected risk factors for spontaneous pneumothorax in dogs: 64 cases (1986-1999). J Am Vet Med Assoc 220(11):1670–1674, 2002. White HL, et al: Spontaneous pneumothorax in two cats with small airway disease. J Am Vet Med Assoc 222(11):1573–1575, 1547, 2003. AUTHOR & EDITOR: ELIZABETH ROZANSKI
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Pneumonia, Bacterial
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Pneumonia, Bacterial BASIC INFORMATION DEFINITION Inflammation of the lower respiratory tract or interstitium from bacterial infection
EPIDEMIOLOGY SPECIES, AGE, SEX: Puppies acquired from community situations (shelters, pet stores) are more likely to have pneumonia from Bordetella bronchiseptica than other pathogens. No other species, age, or gender predilections noted except in cases of bacterial pneumonia secondary to congenital defects (e.g., primary ciliary dyskinesia). GENETICS & BREED PREDISPOSITION: No breed or genetic predispositions other than for those associated with underlying primary diseases or associated conditions RISK FACTORS: Any disease that compromises respiratory defenses or increases the potential for aspiration: Laryngeal disease: Laryngeal paralysis post tieback surgery Laryngeal neoplasia Esophageal disease Esophagitis Megaesophagus Esophageal diverticula Altered consciousness Chronic vomiting Bronchial masses or foreign bodies Bronchiectasis Viral respiratory infection (e.g., distemper) Congenital immune deficiencies Ciliary dyskinesia Risk factors for B. bronchiseptica pneumonia include dense housing (dogs and cats) and the presence of a dog with clinical signs of upper respiratory tract disease (cats). ASSOCIATED CONDITIONS & DISORDERS Sepsis Systemic inflammatory response syndrome Multiple organ dysfunction syndrome Respiratory foreign body Bronchial obstruction (foreign body, mass) Hemothorax (uncommon)
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES: Bronchopneumonia involves inflammation of both airways and alveolar/interstitial compartments. HISTORY, CHIEF COMPLAINT: Chief complaint may be related to pneumonia or to the predisposing disease: Pneumonia: Cough Nasal discharge Sneezing Exercise intolerance Anorexia, lethargy Hemoptysis (uncommon) Acute death (uncommon but reported) Predisposing disease:
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Pneumonia, Bacterial
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Regurgitation Recurrent/persistent infections (usually respiratory, but occasionally other) Some animals may exhibit no clinical signs. Mild, vague signs (e.g., delayed postoperative recovery, failure to thrive) may be the earliest manifestations of the onset of bacterial pneumonia as a complication of another disorder (e.g., sepsis, systemic inflammatory response syndrome, multiple organ dysfunction syndrome). The lack of signs referable to the respiratory system does not exclude the diagnosis. PHYSICAL EXAM FINDINGS: Physical examination may be unremarkable or reflect only signs relating to the underlying predisposing disorder in the presence of mild or moderate bacterial pneumonia. Lack of signs referable to the respiratory system cannot exclude the diagnosis. Findings are variable: Cough Hemoptysis possible Nasal discharge Crackles or wheezes, sometimes focally; focal absence of breath sounds also possible Fever Tachypnea Increased respiratory effort or overt respiratory distress
ETIOLOGY AND PATHOPHYSIOLOGY Bacterial pneumonia is most often a complication of another disease that disrupts mechanical or immunologic pulmonary clearance and defense mechanisms: Impaired mucociliary clearance Impaired reflex closure of the glottis Absent or impaired cough reflex Abnormal immune function: Innate Acquired B. bronchiseptica is capable of causing disease as a primary pathogen in dogs or cats without other apparent underlying risk factors or concurrent disease. Bacteria most often enter lungs via airways but can enter hematogenously. With impaired clearance and defense mechanisms, bacteria can proliferate and initiate local inflammatory responses: Common isolates in dogs and cats include gram-negative aerobes such as Escherichia coli, Klebsiella, Bordetella, Pasteurella, and Staphylococcus spp. Acutely fatal pneumonia associated with hemothorax and bleeding into airways, caused by Streptococcus equi subsp. zooepidemicus, has been described in dogs from dense housing situations. Regionally endemic diseases, such as plague and tularemia, can be causes of primary pneumonia. Local inflammatory responses cause pulmonary lesions, impair lung function, and can contribute to respiratory and systemic disease manifestations.
DIAGNOSIS DIAGNOSTIC OVERVIEW Definitive diagnosis of bacterial pneumonia hinges on demonstration of bacteria either by culture and sensitivity testing (most sensitive) or by cytologic examination of respiratory wash samples. A second key for many patients is pursuit of underlying or concurrent disease that increases risk for bacterial pneumonia.
DIFFERENTIAL DIAGNOSIS Many diseases share clinical and diagnostic similarities, including: Noninfectious inflammatory respiratory diseases Pulmonary neoplasia Respiratory parasites Pulmonary edema Fungal pneumonia, particularly blastomycosis and coccidioidomycosis in dogs
INITIAL DATABASE
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Pneumonia, Bacterial
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CBC: inflammatory leukogram (with or without left shift) expected although not seen in all cases Neutropenia is also possible, especially with severe sepsis. Conversely, bacterial pneumonia can develop secondary to primary neutropenic disorders (e.g., myelosuppression from chemotherapy). Serum biochemical profile/urinalysis: often normal Thoracic radiographs: Two or more views (at least one lateral and either a ventrodorsal [VD] or dorsoventral [DV]) are recommended in all cases. Obtaining both right and left lateral recumbent views can be useful, since pneumonia infiltrates may only be apparent in nondependent lung. Alveolar pattern in dependent regions of lung lobes expected in most cases. Right middle lung lobe is commonly affected and may require careful examination on the lateral projection because it overlies the heart. Interstitial patterns, with or without alveolar patterns, are also possible. In some cases, lobar consolidation will be the prominent radiographic abnormality. Other abnormalities that reflect underlying primary disease (as examples): Megaesophagus Bronchiectasis Neoplasia
PNEUMONIA, BACTERIAL A, Left lateral thoracic radiograph in a 14-year-old mixed-breed dog with pneumonia. Alveolar infiltrates are visible over the cardiac silhouette (especially the apex) but are not striking. Microcardia is also present, suggesting hypovolemia. B, Dorsoventral thoracic radiograph of same dog. Left-sided alveolar infiltrates are more clearly apparent than in A, where they were obscured by being on the dependent side and overlying the cardiac silhouette.
ADVANCED OR CONFIRMATORY TESTING Confirmatory tests help rule out predisposing diseases/risk factors: Respiratory washes (see p. 1350) and bronchoalveolar lavage (see p. 1220 ): Primarily septic, suppurative inflammation: Bacteria are not always evident in cytologic exams, so clinicians should submit wash specimens for culture and sensitivity testing irrespective of cytologic findings. Fine-needle aspiration for cytologic analysis: may help exclude fungal pneumonia or neoplasms: Limited sensitivity: absence of neoplastic cells or fungal organisms does not definitely exclude their presence Theoretical risk of needle-tract seeding if aspiration of a solitary pulmonary tumor Bronchoscopy (see p. 1220): Endobronchial masses or foreign bodies may be evident in some cases. Mucopurulent exudate in airways of affected regions may be seen. Dilated/sacculated airways (bronchiectasis) CT scan: superior delineation of the extent of pneumonia but often not needed when good-quality thoracic radiographs are consistent with the diagnosis. Barium esophagram: if clinician suspects megaesophagus or esophageal motility dysfunction, and this condition is not clearly apparent on survey thoracic radiographs. Arterial blood gas (ABG) analysis: Hypoxemia and hypocapnia are the most common abnormalities; when present, generally indicate severe pneumonia or presence of a complicating factor (e.g., acute respiratory distress syndrome [ARDS]) and therefore a more guarded prognosis.
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Pneumonia, Bacterial
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Other tests specific for underlying diseases (e.g., serum acetylcholine receptor antibody titers for myasthenia gravis-induced megaesophagus).
TREATMENT TREATMENT OVERVIEW Administration of antimicrobials is the cornerstone of treatment, but clinicians also need to treat/resolve predisposing factors to the extent possible.
ACUTE GENERAL TREATMENT Broad-spectrum antibiotics: Clinically unstable animals should be treated with broad-spectrum IV antibiotics: Ampicillin (22 mg/kg IV q 8 h) or cefazolin (22 mg/kg IV q 8 h) and either enrofloxacin (3-5 mg/kg IV q 24 h [dogs]) or an aminoglycoside such as amikacin (20 mg/kg SQ or IV q 24 h); aminoglycosides, however, should not be used in animals that are dehydrated or that have renal compromise. The clinical condition of the animal, if severe, may warrant therapy before obtaining respiratory samples for culture. Clinically stable animals may be treated with oral antibiotics, ideally selected based on culture and sensitivity (C&S) testing. Empirical choices while awaiting results include: Ampicillin or amoxicillin/clavulanate 22 mg/kg q 8 h; or Trimethoprim-sulfa 15 mg/kg q 12 h Because of concerns about the pathogenic potential of Mycoplasma species in pneumonia, doxycycline (3-5 mg/kg PO q 12 h) may be considered, particularly for animals that show no response to therapy with other antibiotic choices. Saline nebulization several times daily Oxygen (nasal cannula, oxygen cage, face mask) for hypoxemic animals or those in respiratory distress (seep. 1318 ) IV fluids as needed Bronchodilators as needed Theophylline: dosage varies with formulation. Terbutaline: 1.25-5 mg/dog PO q 8 h; 0.625 mg/cat PO q 12 h, or 0.1-0.2 mg/kg PO q 12 h (cat)
CHRONIC TREATMENT Thoracic coupage and position changes in recumbent animals Identification and management of underlying causes when identified Antibiotic therapy continued at least 1 week beyond radiographic resolution of infection Lung lobectomy is occasionally needed to resolve infection when extensive single-lobe involvement has failed medical therapy or is associated with recurrent infection. Prognosis associated with lobectomy is considered best if done for foreign-body pneumonia.
POSSIBLE COMPLICATIONS Lung lobe abscess Bronchiectasis Recurrence if underlying cause not identified and treated
RECOMMENDED MONITORING Clinical signs (respiratory rate, effort, etc.): Carefully reevaluate animals that are not clinically better within 48-72 hours of starting empirical therapy or deteriorate substantially at any time; consider pursuing more diagnostic tests and/or changing therapy. Thoracic radiographs: Radiographic changes can lag as much as 48 hours behind clinical changes. Repeating thoracic radiographs approximately 1 week after cessation of antibiotics may demonstrate focal primary diseases (e.g., neoplasia) not evident on initial radiographs. ABG analysis CBC
PROGNOSIS AND OUTCOME
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Pneumonia, Bacterial
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Varies with severity of disease and nature of predisposing factors: Prognosis for uncomplicated pneumonia is generally good. Prognosis for animals with risk factors depends on ability to treat/resolve the risk factor. Recurrent infections are common in animals with unresolved primary diseases.
PEARLS & CONSIDERATIONS COMMENTS Bacterial pneumonia should be viewed as a complication of another underlying disease; B. bronchiseptica infections are an exception. Therefore, patients should be rigorously evaluated for risk factors if such factors are not immediately apparent.
TECHNICIAN TIPS Puppies with bacterial pneumonia, particularly those that came from pet stores or shelters, should ideally be isolated from other animals in the hospital, including cats, because B. bronchiseptica is common in those animals. For respiratory washes, make sure the wash solution does not contain bacteriostatic agents.
CLIENT EDUCATION Following recommended diagnostic and monitoring suggestions is important for most effective long-term resolution. Home treatment may include: Respiratory humidification by inhalation of “cold steam” is best accomplished by having a pet in a closed, unventilated bathroom (but not in the bath/shower) for 10-15 minutes once to three times a day while a warm shower runs. This is often followed by coupage, which is a series of brusque pats to both sides of the chest, performed for 10-30 seconds after each humidification session, with the intention of loosening pulmonary secretions and pus to facilitate expectoration. Pet owners should only perform these treatments on the recommendation of a veterinarian; they can make a condition worse if used inappropriately.
SUGGESTED READING Egberink H, Addie D, Belák S, et al: Bordetella bronchiseptica infection in cats: ABCD guidelines on prevention and management. J Feline Med Surg 11:610, 2009. Pesavento PA, Hurley KF, Bannasch MJ, et al: A clonal outbreak of acute fatal hemorrhagic pneumonia in intensively housed (shelter) dogs caused by Streptococcus equi subsp. zooepidemicus. Vet Pathol 45:51, 2008. Radhakrishnan A, Drobatz KJ, Culp WTN, et al: Community-acquired infectious pneumonia in puppies: 65 cases (1993-2002). J Am Vet Med Assoc 230:1493, 2007. AUTHOR & EDITOR: RANCE K. SELLON
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Pneumonia, Aspiration
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Pneumonia, Aspiration BASIC INFORMATION DEFINITION Infection associated with inhalation of oropharyngeal secretions. In veterinary medicine, the term is often used in reference to aspiration pneumonitis, which is chemical injury caused by inhalation of gastric contents (most commonly) or other materials (e.g., barium, mineral oil).
SYNONYMS Aspiration pneumonitis, Mendelson syndrome
EPIDEMIOLOGY SPECIES, AGE, SEX: Dogs and cats of either sex and any age RISK FACTORS Diseases of: Pharynx or larynx (e.g., laryngeal paralysis) Esophagus (e.g., megaesophagus) Stomach or intestine (e.g., pyloric obstruction) Forced enteral administration of drugs or foods Impaired protective reflexes (e.g., coma, anesthesia, seizure) ASSOCIATED CONDITIONS & DISORDERS Acute respiratory distress syndrome Bacterial pneumonia Hypoxemia Lung lobe abscessation Pneumothorax Shock Airway obstruction
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES Acute or chronic Fulminant or insidious HISTORY, CHIEF COMPLAINT: Clinical signs may be absent or severe; when present, they may include: Anorexia Collapse Cough Lethargy Respiratory distress Others that reflect predisposing cause (e.g., regurgitation, anesthetic episode) PHYSICAL EXAM FINDINGS: Findings may be absent or severe; when present, they may include: Tachypnea Inspiratory and expiratory distress Auscultatory abnormalities (may be localized if present): Crackles
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Pneumonia, Aspiration
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Wheezes Increased or decreased bronchovesicular sounds Cyanosis Fever (fewer than half of affected animals are febrile) Shock Others that reflect predisposing cause (e.g., exercise intolerance with myasthenia gravis)
ETIOLOGY AND PATHOPHYSIOLOGY Inhalation of particulates or fluid into the larynx and lower respiratory tract triggers injury. Gastric contents are typically sterile, but acid and particulate matter can cause potentially severe damage: Acid causes direct, caustic epithelial damage that is followed by inflammation. Particulate material may obstruct airways. Infection may follow aspiration of colonized oropharyngeal secretions or is a secondary (opportunistic) complication of respiratory damage. Severity of injury depends on volume, toxicity, pH, and particulate and pathogen content of aspirated material. Sequelae may include: Airway obstruction Bronchoconstriction Pulmonary hemorrhage Epithelial necrosis Pulmonary inflammation
DIAGNOSIS DIAGNOSTIC OVERVIEW Differentiation of aspiration pneumonia from bacterial pneumonia or pulmonary edema is often dependant on circumstantial evidence such as witnessed episodes of aspiration, history of vomiting or regurgitation, or involvement of the typical lung lobes.
DIFFERENTIAL DIAGNOSIS Infectious pneumonia Cardiogenic or noncardiogenic pulmonary edema Neoplastic infiltrates
INITIAL DATABASE Neurologic examination reflects underlying neurologic disease if present. CBC: neutrophilic leukocytosis common but not essential (absence does not exclude aspiration pneumonia) Serum biochemical profile and urinalysis: no specific changes Thoracic radiographs: abnormalities may lag aspiration by up to 24 hours: Both right and left lateral views should be acquired. Alveolar or interstitial pattern or consolidation in affected lung lobes: Common in the lobes that were dependent at the time of aspiration If the patient was conscious during aspiration, abnormalities usually occur in the right middle, right cranial, or caudal portion of the left cranial lung lobe.
ADVANCED OR CONFIRMATORY TESTING Pulse oximetry and/or arterial blood gas (ABG) analyses to assess oxygenation Tracheal lavage (submit samples for aerobic culture and sensitivity [C&S]): Neutrophilic inflammation Bacteria possible Hemorrhage Particulates/debris Lipid-laden macrophage Bronchoscopy indicated only if clinician suspects large-airway obstruction Search for predisposing cause of aspiration (e.g., acetylcholine receptor antibody titer for myasthenia gravis-related megaesophagus)
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Pneumonia, Aspiration
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TREATMENT TREATMENT OVERVIEW Severity of aspiration pneumonia varies, and therefore intensity of therapeutic intervention varies as well. Adequate oxygenation must be assured and further aspiration prevented when possible. Most animals are treated with antimicrobial drugs because of concerns related to secondary bacterial infection.
ACUTE GENERAL TREATMENT If aspiration is witnessed, immediately suction material from pharynx/airways and ensure airway patency. If respiratory distress or evidence of hypoxemia exists, administer supplemental oxygen using the lowest effective oxygen concentration (typically, Fio2 around 40%). See p. 1318. If Pao2 < 50 mm Hg or if Pco2 > 50 mm Hg, intubate for positive-pressure ventilation. Bronchodilators may relieve bronchospasm (cats especially): aminophylline (dose varies with preparation of the medication) or terbutaline (0.01 mg/kg SQ). IV crystalloid fluids may be warranted: Maintenance rate of 60 mL/kg per day after correction of dehydration; more if there are ongoing losses Rarely, shock occurs, requiring aggressive fluid therapy. Caution: excessive parenteral fluids may precipitate edema in the damaged lung. Antimicrobials are often suggested for these animals, since secondary infection is common. Choice ideally based on C&S (tracheal or bronchial lavage) Initial choice often parenteral broad-spectrum antibiotics (e.g., combination of ampicillin, 22 mg/kg IV q 8 h; and enrofloxacin, 5 mg/kg 12 h [dogs] or 5 mg/kg q 24 h [cats]) Physiotherapy: coupage, movement (see p. 1310) Saline nebulization If aspiration is suspected but respiratory distress is absent, only careful observation may be warranted.
CHRONIC TREATMENT Prevent further aspiration or reduce severity of injury from aspiration (see Prevention below) Discontinue oxygen when Pao2 remains above 65 mm Hg and the animal can breathe comfortably without it. Continue antibiotics 1 week past radiographic resolution (typically 3-4 weeks).
NUTRITION/DIET Animals with severe ongoing vomiting/regurgitation should not be fed by mouth.
BEHAVIOR/EXERCISE Recumbent animals with severe pneumonia should not be allowed to lie with the most functional lobes on the down side. Movement may facilitate beneficial cough and airway clearance.
POSSIBLE COMPLICATIONS Administration of high concentrations of oxygen for prolonged periods can contribute to respiratory epithelial injury. Parenteral fluids may worsen noncardiogenic pulmonary edema.
RECOMMENDED MONITORING Oxygenation (ABG or pulse oximetry): depending on severity of disease, q 4-24 h until normalized Thoracic radiographs: until abnormalities are resolved with frequency determined by severity of signs and baseline abnormalities; ideally repeated 1-2 weeks after discontinuation of antibiotics CBC: rechecked at least weekly until leukocytosis resolved
PROGNOSIS AND OUTCOME Depends on volume and character of aspirated material. Prognosis cannot be predicted by severity of radiographic change.
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Pneumonia, Aspiration
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PEARLS & CONSIDERATIONS COMMENTS Because aspiration pneumonia rarely occurs in the absence of an underlying cause, animals should be evaluated for risk factors.
TECHNICIAN TIPS Sudden respiratory signs in hospitalized animals should be brought to the attending veterinarian's attention immediately. For animals with regurgitation, maintaining an upright position with the head and chest elevated above the stomach for at least 30 minutes after oral feeding may minimize the risk of aspiration.
PREVENTION Address underlying diseases that predispose the animal to aspiration. Fast animals at least 6 hours before general anesthesia, and use properly inflated, cuffed endotracheal tubes during anesthesia. For animals at high risk, consider administration of antacids (H2 antagonists, proton pump inhibitors) to increase gastric pH, and administration of prokinetic agents (e.g., metoclopramide) to enhance gastric emptying and increase lower-esophageal sphincter tone. Unfortunately, these measures have not been shown to improve outcomes in humans at high risk for aspiration. Use caution in forced administration of drugs or foodstuffs. Feeding tubes should not cross the lower-esophageal sphincter.
CLIENT EDUCATION When a predisposing cause is not reversible (e.g., idiopathic megaesophagus), repeated aspiration events are common.
SUGGESTED READING Kogan DA, et al: Clinical, clinicopathologic, and radiographic findings in dogs with aspiration pneumonia: 88 cases (2004-2006). J Am Vet Med Assoc 233:1742, 2008. Kogan DA, et al: Etiology and clinical outcome in dogs with aspiration pneumonia: 88 cases (2004-2006). J Am Vet Med Assoc 233:1748, 2008. Marik PE: Aspiration pneumonitis and pneumonia: a clinical review. N Engl J Med 344:665, 2001. AUTHOR: LEAH A. COHN EDITOR: RANCE K. SELLON
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Pneumocystosis
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Pneumocystosis BASIC INFORMATION DEFINITION Infectious opportunistic disease of the lungs; associated with immune incompetence
SYNONYM Pneumocystis carinii pneumonia
EPIDEMIOLOGY SPECIES, AGE, SEX: Young animals, primarily dogs of either sex GENETICS & BREED PREDISPOSITION: Miniature dachshunds, Shetland sheepdogs, and Cavalier King Charles spaniels RISK FACTORS Congenital or acquired immune-suppressive diseases Syndrome of common variable immunodeficiency in the miniature dachshund CONTAGION & ZOONOSIS: Transmission to an HIV-infected person is possible.
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT: Some or all of the following may prompt an owner to seek veterinary consultation: Tachypnea/respiratory distress Exercise intolerance Weight loss PHYSICAL EXAM FINDINGS Tachypnea Respiratory distress Poor body condition Marked increase in respiratory sounds on thoracic auscultation Cyanosis with severe infections
ETIOLOGY AND PATHOPHYSIOLOGY Pneumocystosis is caused by P. carinii, a saprophyte of the mammalian respiratory tract whose life cycle is completed within the alveolar spaces. Only a single species name has been assigned to the genus Pneumocystis, but antigenic differences suggest that several strains may exist. Based on nucleic acid analysis, the organism is classified as an atypical fungal organism. P. carinii can be present in low numbers in the pulmonary alveoli of healthy animals and is only associated with pneumonia and respiratory distress when there is immune compromise. With immune compromise, P. carinii proliferates within the alveoli, resulting in alveolar capillary blockage and ventilation/perfusion mismatch. Thickening of alveolar septa occurs, but there is rarely extension of the infection into the pulmonary interstitium.
DIAGNOSIS
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Pneumocystosis
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DIFFERENTIAL DIAGNOSIS Other infectious pneumonias: Bacterial Viral Protozoal Mycotic Pulmonary fibrosis Congestive heart failure
INITIAL DATABASE CBC: Erythrocytosis Thrombocytosis Mild neutrophilic leukocytosis Eosinophilia and monocytosis in some cases Serum biochemistry profile: Normal serum protein levels or a low to low-normal globulin level Urinalysis: usually normal Serum protein electrophoresis: hypogammaglobulinemia Thoracic radiographs: Mixed alveolar and interstitial pattern Bronchial pattern Cor pulmonale (right-sided cardiomegaly)
ADVANCED OR CONFIRMATORY TESTING Other laboratory tests: Arterial blood gas (ABG) analysis: Hypoxemia Normocapnia to hypocapnia Increased alveolar-arterial (A-a) oxygen gradient Serologic tests: available for humans but of uncertain value for dogs Other diagnostic procedures: Definitive antemortem diagnosis of P. carinii is established by direct visualization of either the trophozoite or cyst in respiratory washes collected by transtracheal aspiration or bronchoalveolar lavage, lung needle aspirates, or lung biopsies obtained by thoracotomy or thoracoscopy. Histochemical stains and diagnostic immunohistochemistry tests may facilitate observation of organisms. PCR test on respiratory samples can also document presence of the organisms.
TREATMENT TREATMENT OVERVIEW Eradicate infection.
ACUTE GENERAL TREATMENT Oxygen administration (see p. 1318) Mucolytics: Acetylcysteine (10% or 20% solution) 50 mL/hr for 30-60 minutes q 12 h by nebulization Bromhexine, 1 mg/kg PO q 12 h Administration of bronchodilators beforehand is recommended. Bronchodilators: aminophylline, 10 mg/kg PO q 8 h; or terbutaline, 0.625-2.5 mg PO total dose q 8 h Saline nebulization to liquefy hyperviscous mucus and thus promote the removal of secretions from the respiratory tree
CHRONIC TREATMENT Drug of choice: trimethoprim-sulfonamide, 15 mg/kg PO q 8 h for 3 weeks Pentamidine isethionate: 4 mg/kg IM q 24 h for 2 weeks Atovaquone: 15 mg/kg PO q 24 h for 3 weeks
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Pneumocystosis
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Clindamycin and primaquine: 3-13 mg/kg PO q 8 h for 3 weeks Carbutamide: 50 mg/kg IM q 12 h for 3 weeks Drug combinations: dapsone (1 mg/kg PO q 8 h) and pyrimethamine (1 mg/kg PO q 24 h)
POSSIBLE COMPLICATIONS Respiratory failure, respiratory arrest
RECOMMENDED MONITORING Thoracic radiographs ABG analysis
PROGNOSIS AND OUTCOME Dependent on severity of infection
PEARLS & CONSIDERATIONS COMMENTS Infection with P. carinii is associated with immunologic defects.
PREVENTION Because of the probable genetic basis to immune compromise in most animals, owners should not breed affected animals.
TECHNICIAN TIPS When preparing for respiratory washes, be sure to use solutions that do not contain bacteriostatic additives. If available, prewarm solutions for respiratory lavage in a 37°C incubator (or suitable alternative). Needle aspiration of the lung is commonly performed with 23-G needles and a 6- or 12-mL syringe in the dorsal lung fields, defined by rib spaces 6-8. Educate the owners to the importance of ensuring good nutrition and warmth, short leash-controlled walks, and avoiding close contact with animal's face.
CLIENT EDUCATION Affected animals have an underlying immunologic defect. May be a zoonosis in persons who are immunocompromised.
SUGGESTED READING Greene CE, Chandler F, Lobetti RG: Pneumocystosis. In Greene CE, editor: Infectious diseases of the dog and cat, ed 3, St Louis, 2005, Saunders, Elsevier, p 651. Lobetti RG: Common variable immunodeficiency in miniature dachshunds affected with Pneumocystis carinii pneumonia. J Vet Diagn Invest 12:39, 2000. Lobetti RG: Review of Pneumocystis carinii infection in miniature dachshunds. Compend Contin Educ Pract Vet 23:320, 2001. AUTHOR: REMO LOBETTI EDITOR: RANCE K. SELLON
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Pleural Effusion
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Pleural Effusion BASIC INFORMATION DEFINITION Accumulation of fluid within the pleural space
SYNONYMS Pleural fluid, thoracic effusion, hydrothorax (pure transudate or modified transudate), hemothorax (hemorrhage; see p. 493), chylothorax (chyle; see ), pyothorax (exudate; see p. 956)
EPIDEMIOLOGY SPECIES, AGE, SEX Dogs and cats Pyothorax may be more common in younger cats. Pleural effusion secondary to congenital cardiac disease is more common in young animals, and pleural effusion secondary to acquired heart disease (including thyrotoxicosis) is more common in middle-aged to older animals. GENETICS & BREED PREDISPOSITION Pyothorax secondary to aspiration of grass awns is most common in hunting/sporting dogs. As a component of congestive heart failure, pleural effusion may occur more commonly in specific breeds predisposed to certain cardiovascular diseases. RISK FACTORS Hydrothorax: heart disease (cats > dogs), hypoalbuminemia, neoplasia, lung lobe torsion Hemothorax: trauma, intrathoracic neoplasia, anticoagulant toxicity Chylothorax: heart disease (cats > dogs), neoplasia, trauma, intestinal lymphangiectasia Pyothorax: penetrating injury, inhalation of foreign body, pneumonia, mediastinitis, esophageal perforation (septic); feline infectious peritonitis (FIP) (nonseptic). Higher incidence of FIP in multicat households. CONTAGION & ZOONOSIS: Based on certain specific causes (e.g., FIP)
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES Hydrothorax Hemothorax Chylothorax Pyothorax HISTORY, CHIEF COMPLAINT Severity of clinical signs varies with underlying cause, volume of effusion, and rate of fluid accumulation If rate of accumulation is slow, large volumes may be present before clinical signs are apparent (especially cats). Restrictive breathing pattern, tachypnea, orthopnea/general discomfort, dyspnea (e.g., abdominal component of respirations) noted by owners Lethargy, exercise intolerance Cough Signs related to underlying disease: Chronic cough Weight loss Inappetence
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Pleural Effusion
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Abdominal effusion Diarrhea Other signs of trauma Exercise intolerance PHYSICAL EXAM FINDINGS: In general for pleural effusion: Dyspnea, including wide chest excursions, possibly abducted elbows when standing, extension of the neck, reluctance to lie in lateral recumbency, anxious facial expression, and abdominal lift (cats). These animals typically have a prolonged inspiratory phase and very short expiratory phase. Muffled heart and lung sounds ventrally Normal to increased bronchovesicular lung sounds (breath sounds) dorsally Ventral hyporesonance with thoracic percussion; a fluid line may be detected. Other signs associated with specific underlying cause
ETIOLOGY AND PATHOPHYSIOLOGY Etiology and fluid classification reflect basic pathophysiologic mechanisms of effusion formation: Reduced plasma colloid oncotic pressure (hydrothorax: pure transudate) Hypoalbuminemia: protein loss (renal: glomerulonephritis [GN], amyloidosis; gastrointestinal [GI]: inflammatory bowel disease, lymphangiectasia, neoplasia, others; vasculitis: infectious or noninfectious) or synthetic failure (chronic hepatopathy, portal vascular anomalies) Increased capillary hydrostatic pressure (hydrothorax: usually modified transudate) Congestive heart failure, Budd-Chiari-like syndromes Thoracic or mediastinal neoplasia Reduced lymphatic drainage/lymphatic obstruction (hydrothorax, chylothorax, or pyothorax: modified transudate to exudate): Thoracic or pulmonary neoplasia Chylothorax Increased vascular permeability (pyothorax: exudate): Pyothorax FIP Disruption of vascular integrity or hemostatic abnormalities (hemothorax): Rupture of neoplastic mass Coagulopathy Trauma Respiratory dysfunction can reflect hypoventilation and ventilation/perfusion mismatch
DIAGNOSIS DIAGNOSTIC OVERVIEW Physical examination can provide a suggestion of pleural effusion. Presence of the effusion can be confirmed via imaging (thoracic radiographs, thoracic ultrasound) or thoracocentesis. Thoracocentesis and fluid analysis can provide more precise information on the nature of the fluid and perhaps the etiology.
DIFFERENTIAL DIAGNOSIS Other pleural space disease: Masses Pneumothorax Constrictive/fibrosing pleuritis (can occur concurrently with pleural effusion—often chylothorax or pyothorax—and typically causes very rounded lung lobe contours that may be difficult to distinguish radiographically from those caused by pleural effusion). Pulmonary parenchymal or airway disease Thoracic wall disease Diaphragmatic hernia Neuromuscular disease
INITIAL DATABASE In animals with pleural effusion causing severe dyspnea, some clinicians prefer to perform thoracocentesis first and then take thoracic radiographs.
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Pleural Effusion
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Advantages of centesis first: therapeutic value (removal of effusion), diagnostic value (fluid analysis, improved radiographic visualization of parenchymal structures) Advantage of radiographs first: safety (confirms pleural effusion; can identify displacement of cardiac silhouette, to be avoided during centesis) Thoracic radiographs; radiographic signs of pleural effusion vary with fluid volume and can include: Interlobar fissures: Approximately 100 mL of fluid is present in a medium-sized dog if fissure lines are evident. Small volumes may be better appreciated on ventrodorsal views. Impaired heart visualization, especially on dorsoventral view Retraction (“scalloping”) of lungs from thoracic wall with interposed fluid opacity On lateral radiographs, increased opacity dorsal to the sternum and ventral scalloping of lung margins. The lateral view is prone to misinterpretation, and standard two-view thoracic radiography is recommended in all cases. Blunting of lung margins at costophrenic angles (ventrodorsal view) Obscured diaphragm Widened mediastinum Fractured ribs, diaphragmatic hernia, and other orthopedic injuries may be present if traumatic etiology. Pyothorax and chylothorax may cause constrictive pleuritis, preventing full expansion of lungs after thoracocentesis. The lung lobes appear rounded in contour. Evaluation of radiographs post thoracocentesis for underlying pulmonary disease as visualization of intrathoracic structures improves Clinicopathologic abnormalities depend on etiology; possibilities include: CBC: Inflammatory leukogram Thrombocytopenia Anemia Biochemical panel: Hypoalbuminemia Hypoglobulinemia or hyperglobulinemia Hypoglycemia Hypocholesterolemia Azotemia Electrolyte abnormalities Increased liver enzyme activities Hypercalcemia possible with mediastinal lymphoma Urinalysis: Proteinuria Thoracocentesis (see p. 1338): Fluid in EDTA (lavender top) and plain (red top) tubes for analysis; prepare fresh smears. If pyothorax is suspected, a culture and sensitivity (C&S) is indicated (aerobic and anaerobic in all cases): Most common canine isolates are Peptostreptococcus, Bacteroides spp., Escherichia coli, Klebsiella pneumoniae, Enterobacter, Fuso-bacterium, Pasteurella spp., Actinomyces spp., and Nocardia spp. Most common in cats are Bacteroides spp., Pasteurella spp., Peptostreptococcus, Fusobacterium spp., and Actinomyces spp. Measurement of effusion triglyceride and cholesterol concentration if chylothorax suspected An effusion albumin/globulin ratio of >0.8 makes FIP unlikely (exception: if protein clot forms in vitro; false negative). Thoracic ultrasonography: Often performed before thoracocentesis to improve the acoustic window, unless the animal is uncomfortable/dyspneic during restraint for the examination Can identify mediastinal masses, consolidated lung lobes, pulmonary masses, and abdominal organs in the thoracic cavity with hernias Can help identify localized fluid for sampling
ADVANCED OR CONFIRMATORY TESTING Based on nature of effusion and diagnostic test results to date. Hydrothorax: pure transudate (effusion [total protein] canine) Canine leproid granuloma syndrome: nodules on convex pinna caused by an unidentified species of mycobacteria with a distinct geographic distribution Leishmaniasis (dogs > cats): pinnal scaling and alopecia; infected animals are systemically ill. Pigmented viral plaques: deeply pigmented, scaly plaques Hypersensitivity disorders: Atopic dermatitis and food allergy: commonly cause pinnal erythema and pruritus Contact hypersensitivity: most often due to topically applied ear medications (e.g., neomycin, propylene glycol) Mosquito bite hypersensitivity (cats): seasonal; convex pinna is a common site Immune-mediated disorders: Pemphigus foliaceus: may resemble pyoderma, which is rare on the pinna. Very common site of lesions in cats. Vasculitis and ischemic dermatopathy: fairly common cause of pinnal lesions in dogs, this diverse group of diseases may be idiopathic, hereditary (e.g., Jack Russell terriers), or iatrogenic (e.g., rabies vaccine-induced). Ulcerative and crusted lesion, often on the distal concave pinna. Less common, also affecting other sites: pemphigus erythematosus, discoid lupus erythematosus, bullous pemphigoid, cold agglutinin disease, alopecia areata Less common, limited to the pinna: proliferative thrombovascular necrosis auricular chondrosis (swollen, misshapen, painful pinnae) Hereditary causes: Acquired pattern alopecia: affects dogs (most commonly dachshunds) before 1 year and progresses to complete pinnal alopecia due to diminution of still-active hair follicles Canine familial dermatomyositis: lesions usually present by 6 months of age; immune-mediated cause suspected. Color dilution alopecia: progressive hair loss in blue or fawn dogs Other: primary seborrhea, psoriasiform-lichenoid dermatosis of English springer spaniels, hereditary lupoid dermatosis of German shorthaired pointers, congenital hypotrichosis, black hair follicular dysplasia Neoplastic diseases: Squamous cell carcinoma: most common in light-colored cats; often preceded by premalignant actinic keratoses (small areas of crusting and hyperkeratosis). Pinnal lesions on light-colored cats warrant investigation. Histiocytoma and sebaceous gland tumor: the pinna is a common location in dogs. Basal cell tumor: the pinna is a common location in cats. Miscellaneous conditions: Aural hematoma (see p. 120): usually straightforward diagnosis. Subcutaneous accumulation of hemorrhagic fluid forming a flocculent pocket within the pinna. Assess for causes of head shaking (e.g., otitis externa). Ear margin seborrhea: pendulouseared dogs, particularly dachshunds. Keratinous deposits on concave and convex pinnal margins; fissures may form in chronic cases. Similar changes can be seen in hypothyroid dogs. Sebaceous adenitis: scaling and follicular casts predominantly in the haired pinna Acquired folding of ear pinnae: associated with iatrogenic hyperadrenocorticism in cats due to topical or systemic steroid use. Proliferative and necrotizing otitis externa of cats: highly characteristic presentation of adherent, dark, keratinous debris on the concave aspect of the pinna, usually in young cats Canine sterile eosinophilic pinnal furunculosis Melanoderma and alopecia of Yorkshire terriers (probably a variant of pattern alopecia)
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Pinnal Diseases
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PINNAL DISEASES Pinnal crusting in a cat with pemphigus foliaceus.
INITIAL DATABASE Varies depending on differential diagnoses but may include: None; diagnosis may be presumptive (e.g., aural hematoma, acquired pattern alopecia) Skin scrapings (see p. 1248) Pinnal-pedal reflex: 82% sensitivity and 94% specificity for canine sarcoptic mange (seep. 1006 ) Cutaneous cytology Wood's light examination, fungal culture Trichography (demodicosis, color dilution alopecia, pediculosis) Fine-needle aspirates from nodular lesions Acid-fast stain of aspirates if mycobacteria suspected Skin biopsies Prior to the procedure, advise clients that pinnal biopsies might result in permanent cosmetic changes. Skin biopsies from the pinna can be difficult and may require general anesthesia, so sample other areas of the skin if they are similarly affected. The pinna may be clipped to identify the major blood vessels (to be avoided). Do not clip hair from the biopsy site, however. For a good cosmetic outcome, sample lesions on the edge of the pinna with a thin shave biopsy of the pinnal margin. Larger wedges can be removed, leaving skin distal to the cartilage for closure. With extensive pinnal necrosis, affected tissue may be excised to create a more proximal margin. Use a biopsy punch to sample skin from nonmarginal lesions. Take care not to cut through underlying cartilage; otherwise a permanent hole will result. Allow skin to heal by second intention. Always include crusts in the biopsy. CBC, serum chemistry profile, thyroid hormone levels, urinalysis, antinuclear antibody titers, and so forth as appropriate. Response to empirical therapy (e.g., Sarcoptes)
TREATMENT TREATMENT OVERVIEW Varies depending on cause. For aural hematomas, various surgical and medical techniques are described (see p. 120).
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Pinnal Diseases
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PROGNOSIS AND OUTCOME Varies depending on cause
PEARLS & CONSIDERATIONS COMMENTS Due to the difficulty of collecting diagnostic skin biopsies from the pinna, seek out and sample other affected areas of skin to sample. While both diseases are most common in dachshunds, ear margin seborrhea is characterized by scaling and skin lesions, whereas pattern alopecia is not. Consider empirical treatment for Sarcoptes in dogs with pinnal pruritus, even with negative skin scrapings and no pinnal-pedal reflex.
TECHNICIAN TIPS The ear margins in dogs bleed easily with trauma, biopsies, and certain diseases. Head shaking greatly exacerbates hemorrhage. A gentle and effective technique to protect the pinnae from this self-trauma uses a surgical stockinette “tube” placed over the head and secured to the forehead by surgical tape. The stockinette may be used in a single layer or doubled over with loose holes cut out for the ears in the bottom layer. The stockinette is placed over the head such that the ears rest in an anatomically normal position; the stockinette must not be tight. The aim is to keep the ears from “flapping” when the head is shaken.
SUGGESTED READING Matousek JL: Diseases of the ear pinna. Vet Clin North Am Small Anim Pract 34:511, 2004. AUTHOR: KINGA GORTEL EDITOR: MANON PARADIS
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Pilonidal Cyst
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Pilonidal Cyst BASIC INFORMATION DEFINITION Tubular skin lesion that extends ventrally from dorsal midline, usually as a blind sac but may connect to dura mater; congenital defect
SYNONYMS Pilonidal sinus, dermoid cyst, dermoid sinus
EPIDEMIOLOGY SPECIES, AGE, SEX: Young dogs, either sex GENETICS & BREED PREDISPOSITION: Primarily Rhodesian ridgeback; believed to be hereditary (simple recessive gene)
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES Single or multiple dermal draining tracts Subcutaneous cystic mass(es) along dorsal midline HISTORY, CHIEF COMPLAINT Opening in the skin on dorsal midline, with hair protruding from opening Mass in hair on dorsal midline (mass is a concretion of accumulated hair, sebum, and debris overlying the lesion) PHYSICAL EXAM FINDINGS Single or multiple openings in the skin along dorsal midline: Occurs precisely on the dorsal midline Hair protruding from opening Cord of tissue palpably extending down through subcutaneous tissue toward the spine: May be confined to subcutaneous tissue Can extend to the spine: Cervical sinus often attached to dorsal spinous process of C2 Lumen filled with inspissated sebum, exfoliated keratin, hair: May be infected Subcutaneous cystic mass and swelling on dorsal midline If cyst is infected and connects with the spine: Clinical signs associated with myelitis, meningomyelitis, or encephalitis may be seen: Pain, weakness Neurologic deficits in limbs Seizures
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Pilonidal Cyst
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PILONIDAL CYST Dorsal lumbosacral region of a Rhodesian ridgeback dog; cranial is to the left. Appearance of a porelike opening and/or subcutaneous nodule on the dorsal midline skin is the main physical characteristic of a pilonidal cyst. (Courtesy Dr. Richard Walshaw.)
PILONIDAL CYST Excised pilonidal cyst from same dog. This longitudinal section of the cyst shows its length as well as the haired nature of the cystic tissue. Exterior (skin surface) is at bottom right; other extremity of the cyst (upper left of image) was its deepest point, near the spinal cord. (Courtesy Dr. Richard Walshaw.)
ETIOLOGY AND PATHOPHYSIOLOGY Congenital neural tube defect: Incomplete separation of the skin and neural tube during embryonic development Sinus can extend to and connect with dura mater.
DIAGNOSIS DIAGNOSTIC OVERVIEW The diagnosis is established entirely with signalment (breed) and physical examination findings.
DIFFERENTIAL DIAGNOSIS
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Pilonidal Cyst
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Epidermal inclusion cyst Follicular retention cyst Sebaceous cyst Foreign body Abscess Hair follicle tumor Myiasis
INITIAL DATABASE Presurgical CBC and serum chemistry profile
ADVANCED OR CONFIRMATORY TESTING Rarely necessary; physical findings are usually sufficient: Fistulography and myelography: If there is concern about connection to the spine and neurologic signs are present Histopathologic examination of excised tissue to confirm diagnosis Cytologic examination and microbiologic culture and sensitivity (C&S) testing: If infected If connects to spine
TREATMENT TREATMENT OVERVIEW Complete excision of sinus tract, and cyst if present, is required.
ACUTE AND CHRONIC TREATMENT Complete surgical resection: strict aseptic technique is essential if sinus extends to dura mater.
POSSIBLE COMPLICATIONS Recurrence due to incomplete excision: Potential problem if extends to and involves dura mater Development of a chronic draining tract Postoperative meningitis: If dura mater involved and surgical wound infection occurs
RECOMMENDED MONITORING Monitor the incision site for evidence of recurrent draining tract. Look for appearance of new lesions: Examine animals for subcutaneous cystic structures.
PROGNOSIS AND OUTCOME Excellent with complete excision and no involvement of spinal structures Guarded if: Neurologic signs are present prior to surgery Surgical wound infection develops and dura mater is involved
PEARLS & CONSIDERATIONS COMMENTS Avoid clipping, shaving, or cutting a mat of hair located on the dorsal midline without first cleaning and carefully examining the area.
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Pilonidal Cyst
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Trauma to a pilonidal cyst may lead to subsequent infection and potentially myelitis.
CLIENT EDUCATION Common problem in the Rhodesian ridgeback breed Clients should be aware of this problem if considering purchasing a Rhodesian ridgeback Believed to be a heritable defect Does occur rarely in other purebred dogs; infundibular keratinizing acanthomas or benign sebaceous adenomas (which can occur anywhere on the body) are much more common, especially in aged dogs. Seepp. 275 , .
SUGGESTED READING Angarano DW, Swaim SF: Congenital skin diseases. In Bojrab MJ, editor: Disease mechanisms in small animal surgery, ed 2, Philadelphia, 1993, Lea & Febiger. Hedlund CS: Surgery of the integumentary system. In Fossum TW, editor: Small animal surgery, ed 2, St Louis, 2002, Mosby, pp 194–195. AUTHOR & EDITOR: RICHARD WALSHAW
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Phosphate Enema Toxicosis
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Phosphate Enema Toxicosis BASIC INFORMATION DEFINITION Toxicosis due to administration of sodium phosphate enemas in cats and small-breed dogs, resulting in severe hyperphosphatemia, hypernatremia, and hypocalcemia
SYNONYM Fleet enema toxicosis
EPIDEMIOLOGY SPECIES, AGE, SEX: Younger animals; cats and small-breed dogs. Small body size produces a disproportionate ratio of enema fluid to body weight. RISK FACTORS: Constipation, obstipation, colonic disease, and renal disease may increase the risk for problems from administration of sodium phosphate enemas by decreasing sodium and phosphate excretion (renal disease) or enhancing sodium and phosphate absorption (others). ASSOCIATED CONDITIONS & DISORDERS: Hyperphosphatemia, hypernatremia, hypocalcemia (potentially severe/critical)
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT: Within 30 minutes to 4 hours of administration of enema, signs that may be apparent include: Depression Ataxia Vomiting Diarrhea with or without blood PHYSICAL EXAM FINDINGS Common: Tachycardia Pallor Prolonged capillary refill time Weakness Possible: Hyperthermia or hypothermia Tachypnea Tetany Seizure
ETIOLOGY AND PATHOPHYSIOLOGY Source: Phosphate enemas are available over-the-counter (without a prescription) at pharmacies and in the drug aisles of supermarkets and convenience stores. Mechanism of Toxicosis: Hypernatremia and hyperphosphatemia can occur after administration of sodium phosphate enemas via massive absorption of sodium and phosphate from the colon. Prolonged retention, overdose, colonic disease (dilation or ulceration), or
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Phosphate Enema Toxicosis
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preexisting electrolyte disturbances as seen with chronic kidney disease increase the risk of toxicosis. Hypocalcemia occurs if calcium-phosphorus solubility product is exceeded; phosphorus binds and precipitates calcium, leading to hypocalcemia. Hyperosmolality: Hypernatremia Hyperglycemia is only a minor contributor to increased osmolality and is believed to be due to stress release of catecholamines and hypertonicity that alter cellular glucose uptake and metabolism; it can also result from pancreatic insulin release. Metabolic acidosis with increased anion gap
DIAGNOSIS DIAGNOSTIC OVERVIEW History of administration of an enema to a patient weighing 2 mmol/L may be predictive of septic peritonitis in the dog Hyperbilirubinemia: Bile leakage: bile peritonitis Urinalysis: Avoid cystocentesis in animals with peritonitis; catheter preferable (indwelling may be desired for monitoring critical cases; contrast cystography for uroperitoneum, etc.) Whole-abdomen clipping of hair: if possibility of penetrating wound with (e.g., stick, projectile) or without (e.g., tooth, claw) retention of penetrating object Survey abdominal radiographs: Findings suggestive of peritonitis: Fluid, causing loss of serosal detail Free gas: Mottling throughout viscera or “gas cap effect” (clearest with horizontal beam radiograph) Ileus Mass(es) Ultrasound examination: Integrity of organs Evaluate mass(es) Confirm presence of fluid and obtain sample for analysis (see below) Abdominal fluid analysis: Obtain by ultrasound guidance: Preferable to blind abdominocentesis or diagnostic peritoneal lavage Analysis: Glucose, lactate concentrations (see previous) Urea nitrogen, creatinine concentrations: Fluid/blood creatinine concentration ratio = 2:1 highly predictive of uroabdomen in the dog Bilirubin concentration: Compare to serum: fluid bilirubin concentration > serum concentration highly suggestive of bile peritonitis Electrolytes: Fluid/blood potassium concentration ratio = 1.4:1 highly predictive of uroabdomen in the dog Cytologic examination: Neutrophils: Inflammation: increased count, nondegenerative, no intracellular bacteria Septic peritonitis: increased count, toxic changes, intracellular bacteria Plant material: GI leakage Bacteria: Gram stain to aid choice of antibiotic therapy pending culture results Microbiologic culture and sensitivity (C&S) testing: Aerobic and anaerobic
ADVANCED OR CONFIRMATORY TESTING Contrast radiographic studies: Uroabdomen: cystography (lower urinary tract) or excretory urography (upper urinary tract; less commonly indicated) to confirm site of disruption prior to surgery Coagulation profile: DIC
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Peritonitis (General)
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TREATMENT TREATMENT OVERVIEW Patients with primary peritonitis (e.g., FIP) require supportive care and specific medical treatment of the underlying cause. Patients with secondary peritonitis require surgical exploration of the abdomen with: Surgical correction of the cause Peritoneal lavage and possible drainage Intensive postoperative care Some cases (e.g., severe pancreatitis) may have elements both favoring and disfavoring surgical exploration, and consultation with an internist and a surgeon should be considered for optimal planning.
ACUTE AND CHRONIC TREATMENT Correction of fluid and electrolyte abnormalities: Hypovolemia Hypokalemia or hyperkalemia: Uroabdomen, hyperkalemia: Potassium-free fluids: 0.9% NaCl (seep. 55 ) Blood products if necessary (see p. 1111): Whole blood (if anemia or bleeding disorder) Packed red cells (if anemia) Fresh frozen plasma (if hypoproteinemia or coagulopathy) Appropriate antimicrobial therapy if septic: Empirical therapy (aerobic and anaerobic coverage): Second-generation cephalosporin: Cefoxitin, 22 mg/kg IV q 2 h during the perioperative period, then q 6 h Combination therapy: Metronidazole, 10-15 mg/kg IV q 12 h; enrofloxacin, 2.5-5 mg/kg (diluted 1:1 in sterile saline and given via slow IV q 12 h); and ampicillin, 22 mg/kg IV q 6 h Ultimately based on culture results Surgical exploration of abdomen to identify and correct underlying cause of peritonitis if appropriate (e.g., evidence of septic peritonitis; hemorrhage in the absence of systemic bleeding disorder) Thorough lavage of the abdominal cavity Consideration of need for postoperative drainage of the abdominal cavity: Specific sites within the abdomen; drain placement: Pancreatic abscess Prostatic abscess Necrotizing cholecystitis Entire abdominal cavity: Open abdominal drainage Closed suction drainage Postoperative intensive care with continuous monitoring of animal until peritonitis has resolved
NUTRITION/DIET Feeding tue placement if anorexia (seepp. 1267 , ) Coax-feeding (see p. 1377)
POSSIBLE COMPLICATIONS See Peritonitis, Septic, ; Feline Infectious Peritonitis, p. 383; other relevant topics
RECOMMENDED MONITORING Dependent on cause of peritonitis; see Peritonitis, Septic, ; Sepsis and Septic Shock,p. 1014; Systemic Inflammatory Response Syndrome, ; Multiple Organ Dysfunction Syndrome,p. 732.
PROGNOSIS AND OUTCOME Variable; dependent on underlying cause
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Peritonitis (General)
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PEARLS & CONSIDERATIONS TECHNICIAN TIPS Peritonitis patients (septic) are often in a critical state and require intensive care. Technicians treating and caring for these patients should be familiar with and competent in a number of intensive patient care techniques: Fluid and blood component therapy Intensive patient monitoring including blood pressure, CBC and serum biochemistry profile, blood gases, urine output Nutritional support Analgesia
SUGGESTED READING Bonczynski JJ, Ludwig LL, Barton LJ, et al: Comparison of peritoneal fluid and peripheral blood pH, bicarbonate, glucose, and lactate concentration as a diagnostic tool for septic peritonitis in dogs and cats. Vet Surg 32:161–166, 2003. King LG: Postoperative complications and prognostic indicators in dogs and cats with septic peritonitis: 23 cases (1989-1992). J Am Vet Med Assoc 204:407–414, 1994. Kirby BM: Peritonitis. In Slatter, editor: Textbook of small animal surgery, ed 3, Philadelphia, 2003, WB Saunders, pp 421–429. Schmiedt C, Tobias KM, Otto CM: Evaluation of abdominal fluid: peripheral blood creatinine and potassium ratios for diagnosis of uroperitoneum in dogs. J Vet Emerg Crit Care 11(4):275–280, 2001. AUTHOR: JOSEPH G. HAUPTMAN EDITOR: RICHARD WALSHAW 1ST EDITION AUTHOR: ELLEN DAVIDSON DOMNICK
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Peritoneopericardial Diaphragmatic Hernia
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Peritoneopericardial Diaphragmatic Hernia BASIC INFORMATION DEFINITION Embryologic malformation of the diaphragm, resulting in communication between peritoneal and pericardial cavities and allowing herniation of cranial abdominal organs and omentum into the pericardial space (from most to least common: liver, gallbladder, small intestine, spleen, stomach) Can result in vascular compromise or obstruction of herniated organs and (rarely) cardiac tamponade
SYNONYMS Pericardioperitoneal diaphragmatic hernia, pericardial diaphragmatic hernia, PPDH
EPIDEMIOLOGY SPECIES, AGE, SEX Dogs and cats Age at diagnosis highly variable (30% diagnosed at >4 years of age) No sex predilection GENETICS & BREED PREDISPOSITION Not known if hereditary but reported in littermates Predisposed breeds: weimaraners, cocker spaniels; Persians, Himalayans, domestic longhair cats RISK FACTORS: Prenatal injury, possibly systemic illness or toxin exposure affecting pregnant dam ASSOCIATED CONDITIONS & DISORDERS Cranioventral abdominal hernias Caudal sternal abnormalities (pectus excavatum, malformed or absent sternebrae) Ventricular or atrial septal defects, pulmonic stenosis, pericardial cysts Polycystic kidney disease in cats
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT Often incidental finding with no clinical signs Nonspecific signs (lethargy, anorexia, pyrexia, weight loss) Respiratory signs (dyspnea, tachypnea, coughing) Gastrointestinal (GI) signs (vomiting, diarrhea) Rarely, signs of cardiac tamponade and right heart failure (weakness, collapse, ascites) PHYSICAL EXAM FINDINGS May be normal Displaced or absent apical cardiac impulse on thorax Muffled or displaced heart sounds Cardiac murmur if congenital cardiac defect is also present Palpable sternal or cranial abdominal defects Inability to palpate cranial abdominal organs if herniated into pericardial space Borborygmi (GI sounds) over heart
ETIOLOGY AND PATHOPHYSIOLOGY
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Peritoneopericardial Diaphragmatic Hernia
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Abnormal development of septum transversum (forms ventral portion of the diaphragm) ± pleuroperitoneal folds (form dorsolateral diaphragm), resulting in an hourglass-like shape of the joined peritoneal and pericardial cavities (that should instead be separate body cavities) PPDH is always a congenital abnormality, not an acquired one.
DIAGNOSIS DIAGNOSTIC OVERVIEW Definitive diagnosis can be made on the basis of history, physical exam, and thoracic radiographs alone if characteristic radiographic findings are seen, including heterogeneous radiopacities (gas and/or fat) within an enlarged cardiac silhouette and concurrent loss of distinct diaphragmatic border.
DIFFERENTIAL DIAGNOSIS Other causes of generalized cardiomegaly: Pericardial effusion Congenital or acquired cardiac diseases True diaphragmatic hernias do not involve the presence of abdominal viscera in the pericardial space.
INITIAL DATABASE CBC and serum biochemistry panel: no characteristic abnormalities Thoracic radiographs: o Cardiomegaly Silhouetting of the caudal cardiac border with the diaphragm Discontinuity of the diaphragm Presence of irregular and heterogeneous radiopacities (soft tissue, fat, gas) within cardiac silhouette Dorsal mesothelial remnant on lateral view in cats: curvilinear soft-tissue opacity ventral to caudal vena cava, representing dorsal aspect of hernia Sternal deformities Abdominal radiographs: Small or absent liver Cranial displacement or absence of stomach or spleen GI gas pattern extending from abdomen into pericardial space
ADVANCED OR CONFIRMATORY TESTING Ultrasound: fat or abdominal organs within the pericardial sac, ± small amount of pericardial effusion and discontinuity of diaphragm Consolidation of the accessory lung lobe can be an extremely misleading impostor for PPDH ultrasonographically; fluid-filled bronchi appear identical to portal veins, and atelectatic lung mimics liver parenchyma. If any uncertainty exists (e.g., clinical features inconsistent with PPDH, such as previously normal thoracic radiographs), a radiologist's evaluation of the thoracic radiographs is strongly recommended. Upper GI barium series: may confirm presence of GI segments in pericardial space; often not required for diagnosis Positive contrast peritoneography: 2 mL/kg of water-soluble, iodinated radiopaque contrast agent such as iohexol injected aseptically into peritoneal cavity, followed by elevation of the animal's caudal end and thoracic radiography (contrast may flow into pericardial cavity). Often not required for diagnosis; many false negatives (omental/visceral plugging of the hernia).
PERITONEOPERICARDIAL DIAPHRAGMATIC HERNIA A, Lateral radiograph of thorax and cranial abdomen of a cat with
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Peritoneopericardial Diaphragmatic Hernia
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peritoneopericardial diaphragmatic hernia (PPDH). Note cardiomegaly, irregular soft-tissue and fat opacities over the heart, indistinct ventral diaphragm, and small liver. B, Magnified view of A, showing dorsal mesothelial remnant (between the arrows), which is characteristic of PPDH. CdVC, Caudal vena cava. (Courtesy Dr. Stephanie Nykamp.)
TREATMENT TREATMENT OVERVIEW Surgical correction is generally indicated to eliminate clinical signs and prevent vascular compromise or obstruction of organs.
ACUTE GENERAL TREATMENT Oxygen supplementation if the patient is dyspneic Surgical correction via laparotomy: return of all abdominal organs to correct location and closure of the diaphragmatic defect Assessment of liver function prior to general anesthesia in order to choose anesthetic protocol accordingly It may be appropriate not to pursue surgical repair in some cases (e.g., geriatric animal without clinical signs, small incidentally discovered PPDH).
POSSIBLE COMPLICATIONS If the PPDH is left uncorrected, the risk of hepatic or splenic incarceration, bowel obstruction, or (rarely) cardiac tamponade, and right heart failure persists. Surgical complications: difficulty ventilating, hypotension, reexpansion pulmonary edema
PROGNOSIS AND OUTCOME Excellent prognosis with surgical correction Left with an uncorrected PPDH, the patient may remain free of clinical signs, but there is always a risk of complications as listed above.
PEARLS & CONSIDERATIONS COMMENTS PPDH is the most common congenital pericardial disorder in dogs and cats. PPDH is a congenital defect (failure of complete separation of the pericardial and abdominal cavities) in contrast to a true diaphragmatic hernia, which is almost always acquired as a result of trauma. PPDH is an important rule-out for cardiomegaly and in young animals with cranial abdominal or sternal defects.
SUGGESTED READING Fossum TW: Surgery of the lower respiratory system: pleural cavity and diaphragm. In Fossum TW, editor: Small animal surgery, ed 3, St Louis, 2007, Mosby Elsevier, pp 896–929. Reimer SB, Kyles AE, Filipowicz DE, et al: Long-term outcome of cats treated conservatively or surgically for peritoneopericardial diaphragmatic hernia: 66 cases (1987-2002). J Am Vet Med Assoc 224:728, 2004. AUTHOR: M. LYNNE O’SULLIVAN EDITOR: ETIENNE CÔTÉ
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Perirenal Pseudocysts
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Perirenal Pseudocysts BASIC INFORMATION DEFINITION Collection of fluid (usually transudate, but sometimes urine) between the renal capsule and kidney that is rare in cats and extremely rare in dogs. Pseudocysts may be unilateral or bilateral.
SYNONYMS Perinephric pseudocyst, capsulogenic renal cyst, capsular cyst, pararenal pseudocyst, capsular hydronephrosis, pseudohydronephrosis
EPIDEMIOLOGY SPECIES, AGE, SEX Rare in cats, extremely rare in dogs Older cats; some reports have shown male cats to be overrepresented. RISK FACTORS Chronic kidney disease (transudative pseudocysts) Trauma, obstruction, neoplasia of renal pelvis or ureter, causing urine leakage (uriniferous pseudocysts) ASSOCIATED CONDITIONS & DISORDERS Chronic kidney disease Urinary tract infection
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT Usually abdominal enlargement/abdominal mass (noted by owner or incidental finding during exam) Less frequently: weight loss, vomiting, anorexia, polyuria, and polydipsia PHYSICAL EXAM FINDINGS: Palpable abdominal mass (renomegaly; common but depends on size of cyst) ± thin body condition
ETIOLOGY AND PATHOPHYSIOLOGY Incompletely understood pathophysiology Lack of epithelial lining in fibrous sacs means that these are not true cysts. Renal interstitial fibrosis may impair venous and lymphatic drainage, causing transudate to escape the renal parenchyma and accumulate under the capsule, forming a transudative pseudocyst. Uriniferous pseudocysts may form when damage to the renal parenchyma, pelvis, or ureter allows urine to leak between the renal capsule and renal parenchyma. The distinction between transudative and uriniferous pseudocysts may be useful with respect to initial management. Transudative pseudocysts suggest chronic kidney disease (International Renal Interest Society [IRIS] stage 2-4, consider appropriate treatment), whereas uriniferous pseudocysts suggest physical disruption of the integrity of the kidney or proximal ureter (identify and correct source of leakage).
DIAGNOSIS DIAGNOSTIC OVERVEIW
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Perirenal Pseudocysts
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Ultrasonographic identification of hypoechoic fluid between the renal capsule and parenchyma strongly supports the diagnosis but does not usually identify a cause.
DIFFERENTIAL DIAGNOSIS For enlarged kidneys: perinephric abscess, renal lymphoma or other neoplasia, ureteral obstruction with hydronephrosis, feline infectious peritonitis, hematoma, polycystic kidney disease, and compensatory hypertrophy (Note: abscess, other neoplasia, ureteral obstruction, hematoma, and compensatory hypertrophy: more commonly unilateral than bilateral)
INITIAL DATABASE CBC: possibly nonregenerative anemia of chronic kidney disease Serum biochemistry profile: usually evidence of mild to moderate renal failure (e.g., azotemia, hyperphosphatemia) Urinalysis: isosthenuric or minimally concentrated urine specific gravity Urine culture: often positive even in the absence of pyuria Abdominal radiographs: unilateral or bilateral renomegaly
ADVANCED OR CONFIRMATORY TESTING Abdominal ultrasound: method of choice to confirm diagnosis. Transudative and uriniferous pseudocysts are characterized by an accumulation of completely anechoic fluid between renal parenchyma and capsule. Septations, particulate matter in the perirenal fluid, and other variations suggest a diagnosis other than perirenal pseudocysts. Excretory urography if ultrasound unavailable. Decreased renal function may result in poor contrast study. Small risk of contrast-induced renal failure. If the diagnosis remains in question after ultrasound, aspiration of anechoic/hypoechoic region for cytologic analysis can differentiate pseudocyst from perinephric abscess, hematoma, or lymphoma. Concentration of creatinine will be higher in fluid from uriniferous pseudocysts than concurrent serum creatinine concentration.
TREATMENT TREATMENT OVERVIEW Transudative pseudocysts may be managed conservatively, with the goal of preventing renal and ureteral compression. Uriniferous pseudocysts may require surgical intervention.
ACUTE GENERAL TREATMENT If transudative pseudocyst, percutaneous drainage or surgical intervention If uriniferous, identify (i.e., via excretory urography) and correct source of urine leakage.
CHRONIC TREATMENT Repeated percutaneous drainage of transudative pseudocysts Surgical resection of pseudocyst ± omentopexy Treat existing bacterial cystitis, if present (see p. 276). With transudative pseudocysts: treat appropriately for chronic kidney disease (see pp. 205 and 2.5 mg/dL; often >3.5 mg/dL Neutrophils and erythrocytes are predominant cell types. Others: macrophages, reactive mesothelial cells, degenerative neutrophils, etiologic agent Microbial culture of the effusion: Always do both aerobic and anaerobic cultures. Secondary invaders are common with aerobic cultures. Histopathologic examination: Lesions dependent on etiology
TREATMENT TREATMENT OVERVIEW Treatment consists of pericardiocentesis if pericardial effusion is causing cardiac tamponade, with the goal of delaying or eliminating recurrent effusion. Antibiotic therapy is ideally based on culture and susceptibility results. Aggressive therapy such as continuous chest drainage may be indicated in chronic cases where pericardiectomy +/− epicardial stripping has been performed.
ACUTE GENERAL TREATMENT Pericardiocentesis (see p. 1325) if cardiac tamponade is present Thoracocentesis (see p. 1338) if respiratory compromise Abdominocentesis (see p. 1193): Usually unnecessary Can be performed if ascites is causing discomfort and/or respiratory compromise
CHRONIC TREATMENT Subtotal pericardiectomy: Pericardial window not recommended May require epicardial stripping if pericardium is severely thickened Continuous chest drainage after the pericardiectomy Aggressive antibiotic therapy based on culture and susceptibility
BEHAVIOR/EXERCISE Animals will naturally limit their own activity if pericardial effusion with cardiac tamponade is present. Weakness and/or collapse may be observed.
DRUG INTERACTIONS Diuretics contraindicated if cardiac tamponade is present: Contract intravascular volume Reduce venous filling pressure and stroke volume
POSSIBLE COMPLICATIONS Infectious effusion can lead to constrictive pericarditis. Dyspnea due to pleural effusion or ascites
RECOMMENDED MONITORING Follow-up exam and echocardiography 24 hours after the pericardiocentesis or sooner if poor perfusion Periodic reassessment for recurrent effusion
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Pericarditis, Infectious
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PROGNOSIS AND OUTCOME If treated aggressively with pericardiectomy, continuous chest drainage, and appropriate antibiotics, prognosis is good in acute phase. If the animal is systemically ill and treatment is not aggressive, prognosis is poor.
PEARLS & CONSIDERATIONS COMMENTS Infectious pericarditis is a rare cause of pericardial effusion in dogs and cats. A normal cardiac silhouette on radiographs, a negative culture, and the absence of fever may exist in patients with infectious pericarditis. Some antibiotics achieve high concentrations well in pericardial fluid.
PREVENTION Minimize foreign body exposure. Treat local infections, wounds, and bacteremia aggressively. Minimize viral exposure.
TECHNICIAN TIPS If heart sounds are difficult to auscultate, pulses are weak and/or variable, and/or mucous membrane color is pale during status checks, alert the attending veterinarian; pericardial disease could be the cause.
CLIENT EDUCATION If this disorder is treated aggressively with pericardiectomy, continuous chest drainage, and appropriate antibiotics, prognosis is good in early stages. Prognosis worsens with time and degree of fibrosis (pericardial and epicardial scarring).
SUGGESTED READING Aronson LR, et al: Infectious pericardial effusion in five dogs. Vet Surg 24:402–407, 1995. Berg RJ, et al: Pericardial effusion in the dog: a review of 42 cases. J Am Anim Hosp Assoc 20:721–730, 1984. Calvert CA: Cardiovascular infections. In Greene CE, editor: Infectious diseases of the dog and cat, Philadelphia, 1998, WB Saunders, pp 580–581. AUTHOR: SARAH J. MILLER EDITOR: ETIENNE CÔTÉ
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Pericarditis, Idiopathic Sterile
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Pericarditis, Idiopathic Sterile BASIC INFORMATION DEFINITION Non-neoplastic inflammatory pericardial effusion of undetermined etiology; frequently accompanied by thickening of the pericardium, epicardial fibrin formation, and adhesions between the serosal layer of the pericardial sac and the epicardium
SYNONYMS Benign pericardial effusion, idiopathic sterile pericarditis
EPIDEMIOLOGY SPECIES, AGE, SEX: Canine, more common in males, middle aged and older GENETICS & BREED DISPOSITION: Dogs: golden retrievers, German shepherd, St. Bernard, Great Pyrenees, mastiff, Lhasa apso, shih tzu. RISK FACTORS: Associated with immune complex diseases, chronic inflammatory diseases; idiopathic second most common cause of pericardial effusion in the dog
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES: Chronic loss of stamina, acute cardiac tamponade HISTORY, CHIEF COMPLAINT Exercise intolerance, episodic weakness, dyspnea, acute collapse, ascites Associated with gradual accumulation of pericardial fluid leading to tamponade PHYSICAL EXAM FINDINGS: Tachycardia, muffled heart sounds, thready pulses, jugular distension, pulsus paradoxus, positive hepatojugular reflux, abdominal distension
ETIOLOGY AND PATHOPHYSIOLOGY Unknown etiology, may be several causes Generally associated with increasing amounts of sanguineous, inflammatory fluid by damaged blood vessels, lymphatics, mesothelial cells, and microvilli of the serosal layer of the pericardial sac Gradually the pericardial sac becomes distended; when intrapericardial pressures exceed right atrial (RA) and RA filling pressures, tamponade develops.
DIAGNOSIS DIAGNOSTIC OVERVIEW The diagnosis is suspected based on presenting physical signs and confirmation of pericardial effusion with echocardiography. The definitive confirmation of benign disease can be extremely challenging, as cytologic analysis of fluid is often misleading (both false positives and false negatives for malignancy). Some malignancies, particularly mesothelioma and small hemangiosarcoma masses that bleed vigorously, mimic idiopathic benign pericarditis on echocardiographs: hemorrhagic pericardial effusion with no visible mass. In many cases, idiopathic benign pericarditis is either a histologic diagnosis when recurrent effusion prompts subtotal pericardiectomy, or a presumptive diagnosis (albeit imperfect) based on self-resolution of pericardial effusion after one or two centesis procedures.
DIFFERENTIAL DIAGNOSIS Major differential is cardiac hemangiosarcoma
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Pericarditis, Idiopathic Sterile
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Other forms of pericardial disease Often a diagnosis by exclusion where no specific cause of the effusion can be identified.
INITIAL DATABASE CBC: may be mild anemia, monocytosis, lymphocytosis, mild neutrophilia Serum chemistry: usually unremarkable Should screen for immune-mediated disease (ANA, RF, Coombs, thyroid profile, serum protein electrophoresis) Electrocardiography (ECG): electrical alternans (25% of cases), diminished amplitudes (50% of cases) Thoracic/abdominal radiographs: enlarged globoid cardiac silhouette, vena caval distension, hepatomegaly, ascites, pleural effusion Echocardiography: anechoic fluid surrounding heart; may see fibrin tags in fluid, thickened pericardial sac (occasionally), no tumor mass seen
ADVANCED OR CONFIRMATORY TESTING Pericardiocentesis: for cytologic analysis and pH (see and ; difficult differentiation from malignancy) Lack of evidence of neoplasia of liver, spleen on abdominal ultrasound Lack of evidence of thoracic neoplasia on thoracic ultrasound and radiography
TREATMENT TREATMENT OVERVIEW Therapeutic goal is relief of effusion/tamponade.
ACUTE GENERAL TREATMENT Pericardiocentesis (see p. 1325): fluid is sanguineous, nonclotting, and may contain small fragments of fibrin. Verify complete drainage and resolution of tamponade by echocardiography. Corticosteroids, initially at immunosuppressive doses (e.g., prednisone, 2-4 mg/kg PO q 24 h), taper to antiinflammatory dose (1-2 mg/kg PO q 24 h) in 2 weeks.
CHRONIC TREATMENT Repeat pericardiocentesis Partial pericardial fenestration using balloon technique to allow drainage into pleural space Subtotal pericardectomy with histopathologic confirmation of inflammation; preferred procedure if more than two repeat pericardiocentesis procedures required
POSSIBLE COMPLICATIONS May progress to constrictive pericarditis
RECOMMENDED MONITORING Follow-up echocardiography 24 hours after initial pericardiocentesis and monthly thereafter
PROGNOSIS AND OUTCOME Often favorable with initial pericardiocentesis and corticosteroid therapy Usually favorable following subtotal pericardectomy
PEARLS & CONSIDERATIONS COMMENTS Subtotal pericardectomy may lead to development of pleural effusion, pleural thickening, and compartmentalization of lung
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lobes Initial postsurgical management may require chest drainage. Following initial pericardiocentesis, monthly follow-up echocardiograms advised to evaluate resolution of effusion or subsequent visualization of tumor mass not seen on initial evaluation If effusion/tamponade returns following initial pericardiocentesis, consider subtotal pericardectomy rather than repeated attempts at pericardiocentesis where surgery is an appropriate option, either by thoracotomy or thoracoscopy. Differentiation from mesothelioma maybe extremely difficult until late in the course or without pericardial tissue histopathology, as reactive mesothelial cells are a common cytological finding on fluid analysis.
CLIENT EDUCATION May spontaneously recur after apparent cure Some patients require long-term steroid therapy, leading to development of iatrogenic hyperadrenocorticism
SUGGESTED READING Kienle RD: Pericardial disease and cardiac neoplasia. In Kittleson MD, Kienle RD, editors: Small animal cardiovascular medicine, St Louis, 1998, Mosby, pp 413–432. Sisson D, Thomas WP: Pericardial disease and cardiac tumors. In Fox PR, Sisson D, Moise NS, editors: Textbook of canine and feline cardiology, Philadelphia, 1999, WB Saunders, pp 679–701. AUTHOR: N. JOEL EDWARDS EDITOR: ETIENNE CÔTÉ
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Pericardial Effusion
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Pericardial Effusion BASIC INFORMATION DEFINITION Pathologic accumulation of fluid (blood, plasma, neoplastic cells, pus, chyle, or combinations) in the pericardial space
SYNONYM Pericardial fluid accumulation
EPIDEMIOLOGY SPECIES, AGE, SEX: Dependent on underlying cause; dogs: older adults (neoplastic, idiopathic) GENETICS & BREED PREDISPOSITION Dogs: golden retrievers, Labrador retrievers, German shepherds, other large breeds (hemangiosarcoma, mesothelioma); boxers, bulldogs (and other brachycephalics), terriers (chemodectoma) Cats: rare predispositions. Asian breeds, feline infectious peritonitis (FIP) RISK FACTORS Dogs: mesothelioma associated with asbestosis; speculative link between lymphoma and exposure to volatile chemicals Cats: multicat household, FIP CONTAGION & ZOONOSIS: Cats: FIP (cat-to-cat only)
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES Incidental/unexpected finding; no clinical signs caused by pericardial effusion: During echocardiography Cardiomegaly on radiographs Electrocardiogram (ECG) changes: electrical alternans or small QRS complexes Cardiac tamponade: pericardial effusion is causing overt signs. HISTORY, CHIEF COMPLAINT Acute collapse, usually without loss of consciousness Exercise intolerance/episodic weakness Abdominal distension General discomfort, with or without dyspnea Pale mucous membranes PHYSICAL EXAM FINDINGS Tachycardia Soft or muffled heart sounds Weak pulse Abdominal distension possible Dyspnea/attenuated lung sounds possible if pleural effusion
ETIOLOGY AND PATHOPHYSIOLOGY Etiology:
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Primary: Neoplasia (hemangiosarcoma [dogs], heart base tumors [chemodectoma, ectopic thyroid carcinoma], mesothelioma, lymphoma) Idiopathic pericardial effusion (dogs) Left atrial rupture Systemic: Congestive heart failure (effusion volume usually very small) Infectious (FIP [cats], bacterial [very uncommon]) Anticoagulant intoxication Uremia Mechanism: Rate and volume of fluid accumulation and pericardial distensibility determine onset of clinical signs. When overt signs are present as a result of pericardial effusion, cardiac tamponade exists. In general, pericardial effusions caused by systemic processes rarely produce cardiac tamponade (exception: anticoagulant intoxication), whereas pericardial effusions caused by primary lesions within the pericardial space commonly produce cardiac tamponade.
DIAGNOSIS DIAGNOSTIC OVERVIEW Pericardial effusion is suspected in one of two very different contexts: either as an incidental finding during diagnostic testing (typically small volume, no overt clinical signs of right-sided congestive heart failure) or as the cause of clinical signs of cardiac tamponade. Confirmation requires echocardiography; thoracic radiographs, abdominal sonography, and routine complete blood and urine testing are typically necessary to investigate the underlying cause.
DIFFERENTIAL DIAGNOSIS Physical: Hypovolemia Hypotension Causes of ascites (seep. 93 ) Causes of pleural effusion (see p. 882) Radiographic: Cardiac enlargement from heart disease Expiratory radiograph Normal variation Echocardiographic: Pleural effusion Oblique views Specific causes can be determined by etiology (previously described)
INITIAL DATABASE Echocardiogram: confirmation of the diagnosis and investigation for right atrial/ventricular (hemangiosarcoma) or periaortic (heart base) masses. Right ventricular diastolic collapse is highly indicative of severe cardiac tamponade; right atrial collapse is less specific. Thoracic radiographs: large cardiac silhouette (80% of cases), globoid cardiac silhouette (60% of cases), caudal vena cava enlargement; metastatic lesions, pleural effusion CBC, serum biochemistry panel, and urinalysis are usually unremarkable except with systemic disorders. ECG: Electrical alternans is unreliable and only found in 50% of dogs with pericardial effusion. Prothrombin time if anticoagulant intoxication is suspected
ADVANCED OR CONFIRMATORY TESTING Pericardial effusion cytologic examination: useful for lymphoma, infectious causes; otherwise, malignant versus benign is totally unreliable with Cytologie examination. Pericardial effusion pH: generally unreliable, much overlap between benign and malignant Transesophageal echocardiography Serum cardiac troponin-I level: elevation is suggestive of hemangiosarcoma.
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Effusion vascular endothelial growth factor (VEGF) concentration: nondiagnostic
TREATMENT TREATMENT OVERVIEW Removal of pericardial effusion if causing cardiac tamponade Delaying or eliminating recurrent effusion is a long-term goal, including correction of the underlying cause of the effusion if possible.
ACUTE GENERAL TREATMENT Pericardiocentesis (see p. 1325): if cardiac tamponade is present; contraindicated if coagulopathy is a cause of effusion, unless there are critical circulatory effects (severe/periterminal tamponade). Abdominal drainage is usually unnecessary if ascites is secondary to congestion (resorbs in 24-48 hours). Treatment of underlying cause if systemic disorder Diuretics contract intravascular volume and therefore are contraindicated in treating cardiac tamponade acutely.
CHRONIC TREATMENT Management/resolution of systemic disorder if present Recurrent pericardiocentesis if needed Pericardiectomy if recurrent effusion occurs secondary to idiopathic pericarditis or heart base mass Diuretics are indicated if the animal has congestive heart failure (and secondary pericardial effusion) due to myocardial or valvular heart disease; otherwise, chronic diuretic treatment for delaying recurrence of primary pericardial effusion is controversial.
POSSIBLE COMPLICATIONS Recurrent effusion; follow-up echocardiography to assess need for recentesis ± pericardiectomy Dyspnea from severe pleural effusion or ascites Pericardiocentesis-related (seep. 1325 )
RECOMMENDED MONITORING Follow-up exam and echocardiography 24 hours after the pericardiocentesis (sooner if poor perfusión): assessment for recurrent effusion Follow-up exam and echocardiography 2-4 weeks after the pericardiocentesis Serial echocardiography and thoracic radiographs as dictated by recurrence
PROGNOSIS AND OUTCOME Guarded (average: days to months) with hemangiosarcoma; worse if a mass is seen on the right atrium or if pulmonary metastases exist, but better if nonhemorrhagic ascites is present Guarded to fair with heart base tumors, better if pericardiectomy Guarded to fair with mesothelioma (months to a year or more) Guarded to fair with idiopathic (risk of constrictive pericarditis or of mesothelioma) Hemorrhagic effusion that recurs in hours to 1 to 2 days after the pericardiocentesis is rarely benign; prognosis is worse.
PEARLS & CONSIDERATIONS COMMENTS Grossly malignant pericardial effusions and benign pericardial effusions can both appear equally hemorrhagic. Normal-looking heart on radiographs does not rule out pericardial effusion. If a weak pulse, tachycardia, and muffled heart sounds are all present, pericardial effusion is possible, and an echocardiogram is warranted.
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CLIENT EDUCATION Clients need to monitor for recurrence of presenting signs as described previously. Rapid deterioration is possible; re-checks are necessary.
SUGGESTED READING Dunning D, et al: Analysis of prognostic indicators for dogs with pericardial effusion: 46 cases (1985-1996). J Am Vet Med Assoc 212:1276–1280, 1998. Rush JE, et al: Pericardial disease in the cat: a retrospective evaluation of 66 cases. J Am Anim Hosp Assoc 26:39–46, 1990. AUTHOR & EDITOR: ETIENNE CÔTÉ
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Perianal Fistula
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Perianal Fistula BASIC INFORMATION DEFINITION A chronic inflammatory disease of the tissues surrounding the anus in the dog. The lesions are painful, ulcerative, with sometimes deep, draining tracts adjacent to the anus. The anus itself is not usually involved.
SYNONYM Anal furunculosis
EPIDEMIOLOGY SPECIES, AGE, SEX: Dogs, usually >5 years old; males may be overrepresented. GENETICS & BREED PREDISPOSITION: German shepherds are by far the most common breed affected. Irish setters may be predisposed. Any breed may be affected. RISK FACTORS: Possibly broad-based tail, low tail carriage, and increased density of apocrine sweat glands in the perianal region ASSOCIATED CONDITIONS & DISORDERS: Food allergy has been theorized to be a causative or associated condition resulting in inflammation of the colon or pruritus of the perineum.
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT: Initially the owners may notice a foul odor or observe the dog licking the perianal region excessively. As the lesions progress, the dog may have dyschezia, hematochezia, tenesmus, and fecal incontinence; the dog may engage in self-mutilation. In the severe cases, inappetence, lethargy, and weight loss are also possible. PHYSICAL EXAM FINDINGS In mild to moderate cases, physical examination abnormalities are confined to the perianal region. In more severe cases, the dog may also be in poor body condition. Examination of the perianal region may be very difficult in some patients due to pain, and sedation is often necessary. Visual and digital rectal exams are indicated. Visually, the lesions appear as multiple ulcerated, draining tracts that may be superficial or extend deeply into the perianal tissues. The lesions may extend 360° around the anus and involve the ventrum of the tail base. Upon rectal palpation, rectal strictures, loss of anal tone, anal sac rupture or abscessation, and/or roughened rectal mucosa may also be found.
ETIOLOGY AND PATHOPHYSIOLOGY An immunologic basis is suspected based on clinical improvement with immunosuppressive medications, as well as a few pathologic studies identifying sterile chronic inflammatory changes. Secondary bacterial infection is common, often due to fecal microflora or skin contaminants.
DIAGNOSIS DIAGNOSTIC OVERVIEW In general, a diagnosis can be made with history and physical examination, including visual examination of the perianal region.
DIFFERENTIAL DIAGNOSIS Perianal neoplasia (anal sac adenocarcinoma) Anal sac abscessation/rupture Trauma, bite wounds
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Perianal hernia (early phase of fistula, prior to ulcerated lesions)
INITIAL DATABASE CBC, serum chemistry panel, and urinalysis are often unremarkable; may occasionally have a mature neutrophilia. Abdominal radiographs may show evidence of constipation.
ADVANCED OR CONFIRMATORY TESTING Colonoscopy may reveal inflammatory colitis (usually lymphoplasmacytic), rectal strictures. Occasionally, rectal balloon dilation or surgery may be needed if the stricture is severe.
TREATMENT TREATMENT OVERVIEW Goals of treatment include reducing the size and number of strictures (often to the point of no visible lesions), control of infection, and treatment of colitis if present or rectal stricture if present.
ACUTE GENERAL TREATMENT Under sedation or general anesthesia, the hair in the area should be clipped, feces and debris removed, and surrounding tissues cleansed. Enemas may be needed if constipation is present. Antibiotics (cephalexin, 22 mg/kg PO q 8-12 h for at least 2 weeks) can be helpful to treat secondary infections.
CHRONIC TREATMENT Immunosuppression is the initial therapy of choice. Cyclosporine results in a reported 90% success rate. This can be expensive in larger dogs. Starting dose using the emulsion form (Atopica, Neoral, cyclosporine modified generic) is 3-5 mg/kg PO q 12 h for 16 weeks. Ideally, whole-blood trough cyclosporine levels should be run and maintained at 400-600 ng/mL. Adding ketoconazole at 10 mg/kg PO q 24 h allows a reduction in cyclosporine dose to 1 mg/kg PO q 12 h, while achieving similar cyclosporine levels. Azathioprine 2 mg/kg PO q 24 h for 2-4 weeks, then tapered, may be an effective alternative in some dogs. Prednisone alone may be effective in about 33% of dogs. A starting dose of 2 mg/kg PO q 24 h for 2-4 weeks followed by a taper is recommended. The dose should be tapered to 0.5 mg/kg q 48 h. Tacrolimus 0.1% topical applied q 12-24 h resulted in resolution of lesions in 50% of dogs with mild to moderate lesions. Stool softeners such as lactulose at 0.25-0.5 mL/kg PO q 12 h are indicated to prevent constipation, assist defecation if strictures are present, and keep stool soft when defecation is painful. If appropriate medical management does not resolve the lesions to an acceptable degree, surgery can be considered. Nd: YAG laser and cryotherapy as well as en bloc resection have been reported with variable success rates. Surgical procedures that may be needed include anal sacculectomy, removal of skin overlying the tracts, débridement of diseased tissue, and rectal pull-through for rectal strictures. Balloon dilation is recommended as first line of therapy for rectal strictures, because surgical removal of strictures may result in fecal incontinence.
NUTRITION/DIET Dietary therapy has been used in conjunction with immunosuppression. Novel antigen diets have been recommended because there is a suspected association with food hypersensitivity. Most important, animals should avoid high-fiber (bulking) foods/diets, and owners should feed highly digestible diets that will result in a softer, smaller stool (low-residue diets).
DRUG INTERACTIONS Ketoconazole decreases metabolism of cyclosporine and can be given for this purpose.
POSSIBLE COMPLICATIONS Recurrence of fistulae with discontinuation of immunosuppressive drugs Rectal strictures secondary to chronic inflammation Constipation secondary to pain or rectal strictures Fecal incontinence secondary to chronicity or surgery
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RECOMMENDED MONITORING Follow-up examinations of the perianal region every 2 weeks until healed, then periodically thereafter to check for recurrence Whole-blood trough cyclosporine levels at 2 weeks, then monthly CBC when azathioprine is being used
PROGNOSIS AND OUTCOME Fair to good prognosis with early treatment Long-term prognosis may be guarded with more severe lesions and the need for indefinite medical therapy.
PEARLS & CONSIDERATIONS COMMENTS Improvement on cyclosporine will usually be seen within 4 weeks. If the signs recur once the drug is discontinued, long-term therapy may be needed, with the lowest effective dose determined with a taper. Most dogs will respond to medical management but may also require long-term therapy to maintain remission.
PREVENTION Recurrent cases may need long-term medications or novel protein diet to prevent recurrences. Keeping lesions under control with immunosuppressive medications and diet can help prevent infections, rectal strictures, and constipation.
TECHNICIAN TIPS These lesions may be painful, and a gentle approach to any manipulation of the anal region (e.g., rectal temperature) is important.
CLIENT EDUCATION Advise clients on the clinical signs and lesions that warrant early intervention if lesions recur.
SUGGESTED READING House AK, Guitian J, Gregory SP, et al: Evaluation of the effect of two dose rates of cyclosporine on the severity of perianal fistulae lesions and associated clinical signs in dogs. Vet Surg 35:543–549, 2006. Lombardi RL, Marino DJ: Long-term evaluation of canine perianal fistula disease treated with exclusion fish and potato diet and surgical excision. J Am Anim Hosp Assoc 44:302–307, 2008. Paricelli AJ, Hardie RJ, McAnulty JF: Cyclosporine and ketoconazole for the treatment of perianal fistulas in dogs. J Am Vet Med Assoc. 220:1009–1016, 2002. AUTHOR: LISA MOORE EDITOR: DEBRA L. ZORAN
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Pemphigus Complex
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Pemphigus Complex BASIC INFORMATION DEFINITION A group of autoimmune blistering diseases of the skin and/or mucous membranes characterized by keratinocyte acantholysis (separation from cell-cell detachment), producing varying degrees and depth of cutaneous ulceration, pustules, vesicles, and crusting. Subsets of pemphigus are classified based on the level of blistering in the epidermis. Spontaneous, drug-induced, and paraneoplastic forms are reported. The most common type in dogs and cats is pemphigus foliaceus.
EPIDEMIOLOGY SPECIES, AGE, SEX: Seen in dogs and cats; more common in middle-aged animals (average age of onset is 5 to 6 years, with a range of 0.5-16 years). GENETICS & BREED PREDISPOSITION Pemphigus foliaceus (PF): Akita, Australian shepherd, chow chow, cocker spaniel, dachshund, Doberman pinscher, Finnish spitz, schipperke (drug-induced PF in Doberman pinscher and Labrador retriever) Pemphigus erythematosus (PE): collie and German shepherd Canine benign familial chronic pemphigus has been reported in English setters and their crosses and appears inherited (autosomal dominant) RISK FACTORS: PF and PE may be aggravated by sunlight. Some cases of pemphigus are triggered by drug reactions. Paraneoplastic pemphigus (PNP) in dogs has been associated with underlying lymphoma, thymoma, and (in one case) Sertoli-cell tumor. GEOGRAPHY AND SEASONALITY: A lower incidence of canine PF exists in the northeastern United States, and a higher prevalence exists in warmer regions. Seasonal exacerbation of lesions may occur during months of increased sunlight exposure.
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES: Subsets of pemphigus are described and listed in decreasing order of frequency: Superficial pemphigus complex: PF, PE (a possible local and milder variant of PF), panepidermal pustular pemphigus (PPP; possibly a more extensive subtype of PF). Deep variants: pemphigus vulgaris (PV), pemphigus vegetans (PVg), and PNP. A few cases of benign familial pemphigus have also been reported in dogs. HISTORY, CHIEF COMPLAINT PF: progressive multifocal or generalized skin disease, often with facial and footpad involvement. Degree of pain appears to be variable. Pruritus is noted in 30%-50% of the cases. The initial complaint can be lameness due to footpad disease. With PV and PNP, disease of the oral cavity is common, and presenting signs include hypersalivation, halitosis, anorexia, and weight loss. Fever, anorexia, lethargy, and limb edema are reported in severe cases of pemphigus. PHYSICAL EXAM FINDINGS PF: a pustular and crusting dermatitis, with crusts on the trunk and/or the facial area being the most common lesion. Inner pinnae and dorsal muzzle are often the first areas affected, and the disease can stay restricted to the head and face. Other commonly involved areas are the feet, footpads, and nail beds (nail beds are affected more often in cats; it is sometimes the only physical exam abnormality). The disease progresses and becomes generalized or multifocal in most cases. Range of lesions noted includes erythema, pustules, dry honey-colored crusts, scales, alopecia, and erosions bordered by collarettes. Secondary bacterial pyoderma (a third of PF cases) and peripheral lymphadenopathy are common. PE: a milder form of PF with crusts, erosions, alopecia, and scales restricted to the face PV: a deep and severe form of pemphigus, presenting with transient flaccid vesicles rapidly replaced by large erosions and ulcers of the mucosal surfaces and mucocutaneous junctions. Affected areas include oral cavity (>70% of cases), inner pinnae, nasal planum, lip margins, genitalia, and anus. Erosions of the nail beds are reported in 14% of cases. A milder form
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of PV is reported where lesions are restricted to one body area (nail beds, nasal planum, oral cavity). PVg and PPP: Severe erosions and ulcerations of the oral cavity, nose, vulva, and haired skin
PEMPHIGUS COMPLEX A 5-year-old male castrated Siamese cat with pemphigus foliaceus affecting the face and pinnae. (Courtesy Dr. Caroline de Jaham.)
ETIOLOGY AND PATHOPHYSIOLOGY Intraepithelial acantholysis (loss of intercellular cohesion between keratinocytes) leading to vesicles/pustules formation due to antikeratinocyte autoantibodies (IgG) binding to components of desmosome complex.
DIAGNOSIS DIAGNOSTIC OVERVIEW The diagnosis of PF, the most common form of pemphigus, is suspected in a middle-aged dog or cat presented for evaluation of a progressive crusting and pustular dermatitis that does not typically respond to appropriate systemic antibiotic therapy. The definitive diagnosis requires skin biopsies showing histopathologic changes of acantholysis.
DIFFERENTIAL DIAGNOSIS PF, PE, and PNP: bacterial folliculitis, demodicosis, dermatophytosis, eosinophilic folliculitis and furunculosis, cornification disorders, cutaneous (discoid) and systemic lupus erythematosus, drug eruptions PV and PPP: bullous pemphigoid, epidermolysis bullosa acquisita, erythema multiforme, toxic epidermal necrolysis, StevensJohnson syndrome, epitheliotropic lymphoma, ulcerative stomatitis, vesicular cutaneous lupus erythematosus, systemic lupus erythematosus.
INITIAL DATABASE Cytologic examination of content of intact pustules or of exudate under a crust may strongly suggest pemphigus: intact neutrophils, varying number of eosinophils, and clusters of acantholytic keratinocytes can be seen in most cases, but biopsies are still required because other disorders may present similar findings. CBC, serum biochemistry profile: nonspecific changes, mild to moderate leukocytosis with neutrophilia, mild nonregenerative anemia, and hypoalbuminemia
ADVANCED OR CONFIRMATORY TESTING Skin biopsies: confirmatory test. Histopathologic findings of acantholysis with pustule formation are diagnostic. Lesional epidermal location is related to depth of autoantibody deposition: subcorneal and intragranular layers in PF and PE; suprabasilar level in PV and PPP; panepithelial in PNP. Immunohistochemical and immuno-fluorescent analysis of skin biopsies or serum may be helpful but depends on the
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sensitivity of the methods being used; not routinely performed.
TREATMENT TREATMENT OVERVIEW The treatment goal is to implement immunosuppressive therapy that will induce and maintain remission of skin lesions without significant or life quality-altering side effects. The therapeutic modalities and response to treatment will vary with the type of pemphigus and the species treated. Cases refractory to initial systemic glucocorticoids should be referred to a dermatologist.
ACUTE TREATMENT Systemic glucocorticoids alone induce remission in most cases of PE and in a third to half of cases of PF in dogs and in most cats. Other forms of pemphigus are more refractory. Response should be seen within 10-14 days. Dogs (initially): Prednisone/prednisolone: 2-4 mg/kg PO q 24 h; or Dexamethasone: 0.2-0.4 mg/kg PO q 24 h for more refractory cases Cats (initially): Prednisone/prednisolone: 4-8 mg/kg PO q 24 h (prednisolone is preferred in cats); or Dexamethasone: 0.2-0.4 mg/kg PO q 24 h; or Triamcinolone: 1-2 mg/kg PO q 24 h High (shock) dosages of glucocorticoid used in the acute phase in severe cases of PF or PV. Prednisolone sodium succinate, 10 mg/kg IV over 4 hours; or prednisone, 10 mg/kg PO given 1-3 days consecutively. Potential side effects such as gastrointestinal ulceration are increased.
CHRONIC TREATMENT The dose of glucocorticoid is slowly reduced on a daily basis over 30-40 days once remission of active skin lesions is attained (2-4 weeks). Lowering to an alternate-day regimen with an ideal maintenance dose of 1 mg/kg q 48 h of prednisone/prednisolone or less is the ultimate goal. Concurrent immunosuppressive drugs are used initially in conjunction or added later to glucocorticoids to enhance or maintain adequate immune suppression to induce or maintain remission with fewest/no glucocorticoid adverse effects. Azathioprine: 2.2 mg/kg PO q 24-48 h in conjunction with prednisone/prednisolone; first choice in dogs, contraindicated in cats; or Chlorambucil: 0.1-0.2 mg/kg PO q 24-48 h in conjunction with prednisone/prednisolone; first choice in cats; or Cyclosporine: 5-10 mg/kg PO q 24 h has shown good effectiveness with prednisone/prednisolone for PF in dogs and cats. Alternative immunosuppressive drugs: Tetracycline and niacinamide: milder or localized cases of PF and PE (250 mg of each PO q 8 h for dogs 10 kg) for 2-3 months to achieve remission then gradually decrease to q 12-24 h or alternate days if remission is maintained. Topical therapy is indicated as a sole treatment in some localized forms of PF and PE and in conjunction with systemic therapy on persistent focal lesions that remain active despite satisfactory control of the overall disease. Person applying treatment must wear gloves. Potent topical glucocorticoid initially: fluocinolone acetonide, triamcinolone, betamethasone valerate; when adequate response, treatment is changed to l%-2% hydrocortisone for maintenance. Tacrolimus 0.1%: has shown efficacy for treating both PE and PF.
POSSIBLE COMPLICATIONS Recurrence of skin lesions with discontinuation of immunosuppressive drugs Side effects are common with long-term oral glucocorticoid therapy (signs of iatrogenic hyperadrenocorticism, urinary tract infections, pyoderma). Persistent use (daily for >14 days) of potent topical glucocorticoids can create skin atrophy, alopecia, and comedone formation.
DRUG INTERACTIONS Ketoconazole potentiates cyclosporine activity; adjust dosage accordingly and monitor serum cyclosporine levels. Azathioprine is contraindicated in cats because of a profound myelosuppressive effect in this species.
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RECOMMENDED MONITORING Semiannual CBC, serum biochemistry profiles, urinalysis, and urine cultures for all patients receiving long-term oral glucocorticoids Azathioprine, chlorambucil: CBC monitoring for cytopenias every 2-3 weeks for the first 3 months then q 3-6 months. For azathioprine, also monitor liver and pancreatic enzyme activity.
PROGNOSIS AND OUTCOME PF: fair to good prognosis with the majority achieving partial or complete remission with oral glucocorticoid +/− other immunosuppressive drugs. Time to improvement with therapy is 2-6 weeks; time to complete remission is 3-9 months. Mortality (euthanasia) rate in dogs with PF averages 20%-30% within the first year owing to lack of response or adverse effects of treatment, notably glucocorticoids (implying a need to use combination therapy prior to triggering adverse effects that are unacceptable to the owner, deleterious to the patient, or both). Mortality rate in cats with PF: 12 weeks old); or ○ Ivermectin 0.2 mg/kg SQ once
NUTRITION/DIET High-protein, high-calorie foods (e.g., Eukanuba Max Calorie, Hill's Science Diet A/D) diluted with as little water as possible It is the author's opinion that a small volume of food is far more important than a low-fat content.
DRUG INTERACTIONS Flunixin meglumine is nephrotoxic and gastric ulcerogenic and should be avoided in animals that are hypovolemic. Fluoroquinolones (5 mg/kg q 24 h) used for 5-8 days should be safe and not cause cartilage problems. Ivermectin deworming is not advised in debilitated patients.
POSSIBLE COMPLICATIONS Intussusception or rectal prolapse Septic arthritis or endocarditis Acute respiratory distress syndrome Pneumonia (embolic, aspiration, or opportunistic [e.g., canine distemper])
RECOMMENDED MONITORING Clinicians should monitor the following at admission, after 2 hours of fluid therapy, and then at least on a daily basis in patients that are still ill: Body weight Blood glucose Hematocrit and total solids Serum potassium Pediatric sampling tubes and very small quantities of blood should be used. Once the puppy is eating, monitoring should be curtailed or stopped to avoid overinterpretation of results in an animal that is improving.
PROGNOSIS AND OUTCOME Good with correct therapy. Following the treatment protocol, a 93%-95% success rate is expected with severely ill, confirmed cases of parvoviral enteritis.
PEARLS & CONSIDERATIONS COMMENTS Essential aspects of management include: Normalize hydration, potassium, and glucose. Control vomiting. Control pain. Feed early.
TECHNICIAN TIPS Become familiar with estimating the volume of fluid on a surface such as the cage floor. This helps in calculating daily fluid requirements. Wear gloves and use strict hygiene when handling these patients, not only for contagion prevention but because of their immunocompromised state (often leukopenic); this applies to doctors and anyone else in contact as well.
PREVENTION Ensure adequate vaccination status. Owners should limit environmental access for puppies until they are fully vaccinated. Dogs that survive parvoviral enteritis generally have immunity to reinfection (lifelong).
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Parvoviral Enteritis
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CLIENT EDUCATION Parvovirus remains in the environment for up to 7 months or more. Indoor surfaces should be cleaned and then disinfected with diluted bleach, and only vaccinated adult dogs should be allowed in the dog's immediate environment. Serial vaccination of all puppies until at least 12 weeks of age is essential; typical protocols involve vaccination at age 6, 9, 12, and possibly 16 weeks, the latter being for breeds at risk. Annual re vaccination of adult, and especially geriatric, dogs with a complete history of vaccinations is controversial, since titers remain high for more than 1 year. The debate over the appropriate interval of vaccination interval in adult dogs remains unresolved, with a recent advisory board recommending vaccination every 3 years.
SUGGESTED READING Mantione NL, Otto CM: Characterization of the use of antiemetic agents in dogs with parvoviral enteritis treated at a veterinary teaching hospital: 77 cases (1997-2000). J Am Vet Med Assoc 227(11):1787–1793, 2005. Mohr AJ, et al: Effect of early enteral nutrition on intestinal permeability, intestinal protein loss, and outcome in dogs with severe parvoviral enteritis. J Vet Intern Med 17:791– 798, 2003. Prittie J: Canine parvoviral enteritis: a review of diagnosis, management, and prevention. J Vet Emerg Crit Care 14(3):167–176, 2004. AUTHOR: DAVID MILLER EDITOR: ELIZABETH ROZANSKI
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Parturition, Normal
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Parturition, Normal BASIC INFORMATION DEFINITION The act or process of giving birth to puppies or kittens
SYNONYMS Queening: parturition in the queen (female cat) Whelping: parturition in the bitch
EPIDEMIOLOGY SPECIES, AGE, SEX: Dogs and cats: adult, female CONTAGION & ZOONOSIS:Brucella canis (see p. 162) and canine herpesvirus 1 (see p. 525) can be shed in lochia (parturient uterine fluids) during term parturition, preterm parturition, and/or abortion. GEOGRAPHY AND SEASONALITY With the exception of the basenji, bitches are nonseasonal, meaning that parturition occurs year round. However, in the basenji, ovulation only occurs in October, and parturition associated with a resulting pregnancy only occurs in December. By contrast, queens are seasonal, long-day breeders; estrous cycles cease during October-December (Northern Hemisphere) unless they are exposed to 14 hours of light (natural and artificial). Parturition associated with any resulting pregnancy could be expected about 65 days from breeding (February-December). ASSOCIATED CONDITIONS & DISORDERS Dystocia Premature parturition Abortion
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT: Bitch or queen uncomfortable about 60 days after breeding, may have a vaginal discharge PHYSICAL EXAM FINDINGS In the bitch, rectal temperature is normal to low normal (98°F-100°F; 36°C-37°C) in the hours before parturition and increases to normal or slightly higher than normal during parturition. In the queen, rectal temperature is normal to low normal (100.5°F102.5°F; 37.8°C-39.3°C), with additional variation based on environment, body condition, and other factors. Respiration and heart rates are slightly increased to normal. Uterine contractions may be visible through the abdominal wall. Examiner may be able to palpate fetuses transabdominally.
ETIOLOGY AND PATHOPHYSIOLOGY Three stages of labor: Stage 1: cervical dilation, 3-6 hours Stage 2: fetal expulsion, 3-6 hours (depends upon litter size) Stage 3: placental expulsion, occurs at the same time or within minutes of each fetal expulsion (however, two fetuses and then two placentas may be delivered). Dystocia may occur for a variety of reasons (see p. 329).
DIAGNOSIS
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DIAGNOSTIC OVERVIEW Parturition is identified when a gravid dam is at term gestation and is showing clinical signs of labor or has began delivering fetuses.
DIFFERENTIAL DIAGNOSIS Abortion Dystocia Pseudopregnancy Premature birth Pyometra
INITIAL DATABASE Pups or kittens are present on abdominal palpation Confirmation of fetal skeletons in the normal position and not too large for dam's bony pelvis: abdominal radiography after 42 days’ gestation Evaluation of fetal distress: see p. 162
ADVANCED OR CONFIRMATORY TESTING Tocodynamometry can be used for monitoring uterine contractility (see p. 162) PARTURITION, NORMAL A tocodynamometer used for monitoring uterine contractility in bitches.
TREATMENT TREATMENT OVERVIEW Goal: delivery of healthy puppies or kittens without compromising mother's health Bitches and queens with normal parturition do not require any treatment.
ACUTE GENERAL TREATMENT In normal parturition, treatment is not needed. If parturition is not normal, see p. 329.
NUTRITION/DIET Administration of a calcium carbonate tablet (e.g., Tums) at the onset of parturition may increase the strength of uterine contractions and prevent dystocia secondary to uterine inertia. However, administration of any calcium supplementation prior to parturition is contraindicated.
BEHAVIOR/EXERCISE Dams can have unrestricted exercise before and during parturition.
POSSIBLE COMPLICATIONS If the bitch or queen has prolonged abdominal contractions without delivery of a fetus, or appears to be in constant intense pain, she should be evaluated by a clinician (see p. 162).
RECOMMENDED MONITORING Clinicians can monitor the puppy or kitten delivery and be available to assist if needed (e.g., if dystocia occurs, if puppies experience distress). Clinicians should make sure a placenta is delivered following each fetus.
PROGNOSIS AND OUTCOME
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Good if parturition is normal Fair to guarded in cases of dystocia
PEARLS & CONSIDERATIONS COMMENTS As parturition is a normal process, many animal owners and breeders prefer that the female deliver pups or kittens at home in familiar surroundings. Oxytocin treatment should be used only if the cervix is open (see p. 162). Dark-green colored lochia or postpartum vaginal discharge before the delivery of any pups in the bitch is an indication of premature placental separation. The bitch should be evaluated for fetal viability by abdominal ultrasonography and may require a caesarean section to remove the fetuses.
PREVENTION Ovariohysterectomy
TECHNICIAN TIP Technicians involved in whelping/queening should be familiar with Basic asepsis and hygiene of neonates Normal neonatal responses that indicate viability (versus signs of distress) Normal maternal behavior Neonatal resuscitation
CLIENT EDUCATION For prepartum bitches, the client should monitor the rectal temperature two to three times daily beginning at 56 days postbreeding. Rectal temperature decreases by 1°F-2°F (0.5-1°C) about 8-12 hours before whelping.
SUGGESTED READING Johnston S, Root Kustritz M, Olson P: Canine and feline theriogenology, Philadelphia, 2001, WB Saunders. AUTHORS: MUSHTAQ A. MEMON, MICHELLE A. KUTZLER EDITOR: MICHELLE A. KUTZLER
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Paresis, Hind Limb
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Paresis, Hind Limb BASIC INFORMATION DEFINITION Paraparesis is defined as partial loss of motor function to the pelvic limbs. Para-paralysis or paraplegia is a complete loss of voluntary motor function to the pelvic limbs.
EPIDEMIOLOGY SPECIES, AGE, SEX: Any species, age, or sex can be affected. GENETICS & BREED PREDISPOSITION Young to middle-aged chondrodystrophoid dogs (e.g., basset hounds, dachshunds, beagles) are predisposed to intervertebral disk disease (IVDD), especially Hansen type I. Middle-aged to older nonchondrodystrophoid dogs (e.g., German shepherds) are predisposed to IVDD, especially Hansen type II. German shepherds (geriatric) are over-represented in degenerative myelopathy. CONTAGION & ZOONOSIS: In some cases where underlying etiology is infectious (e.g., rabies)
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES: Hind limb paresis or paralysis can present as difficulty or inability to use the hind limbs due to weakness, ataxia (incoordination), or spasticity (limb stiffness caused by a neurologic lesion). Weakness suggests a lower motor neuron or neuromuscular lesion, whereas spasticity and ataxia suggest an upper motor neuron lesion. HISTORY, CHIEF COMPLAINT: Inability to walk on the hind leg(s) PHYSICAL EXAM FINDINGS Assessment of the femoral pulse; if absent, consider aortic thromboembolism as a diagnosis. Palpation of the bones of limbs, pelvis (including rectal exam in dogs), and vertebral column for fractures/luxations Fundic exam: for evidence of multifocal/diffuse central nervous system (CNS) inflammation Neurologic injuries: physical findings depend on severity of lesion. Gait varies from mild hind limb ataxia to a nonambulatory status without deep pain perception. Spinal reflexes (e.g., patellar): Hyporeflexia: lesion in L4-S2 spinal cord segments Hyperreflexia: lesion in T3-L3 spinal cord segments Spinal hyperpathia (back pain on palpation): Presence: may indicate IVDD, neoplasia, or trauma Absence: may indicate embolism or degenerative cord process Muscle tone: Increased (spasticity): lesion in T3-L3 spinal cord segments Decreased: lesion in L4-S2 spinal cord segments
ETIOLOGY AND PATHOPHYSIOLOGY IVDD (see p. 1571): Degenerative disk changes lead to herniation of the nucleus pulposus into the spinal canal. Hansen type I disk rupture: focal, acute myelopathy Hansen type II disk rupture: chronic, progressive disk (annulus) bulging into the spinal canal; chronic, slowly progressive myelopathy Concussive type III disk rupture: high velocity rupture that leaves little residual compression Fibrocartilaginous embolization (seep. 392 ): Herniation of disk material into vertebral body and entrance into the venous plexus Degenerative myelopathies (see p. 286: Progressive, diffuse degeneration of spinal cord myelin and axons
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DIAGNOSIS DIAGNOSTIC OVERVIEW Patients with weakness or motor dysfunction confined to the pelvic limbs most likely have neurologic or orthopedic disease. Definitive diagnosis begins with neurologic and orthopedic exams and usually requires advanced spinal cord imaging (myelogram, CT, MRI)
DIFFERENTIAL DIAGNOSIS Acute, nonprogressive: orthopedic intervertebral disk rupture, fracture/luxation, fibrocartilaginous embolism, aortic thromboembolism Acute progressive: intervertebral disk rupture (type I), hemorrhagic myelomalacia, neoplasia, infectious/inflammatory (distemper myelitis; bacterial, protozoal, or fungal myelitis; granulomatous meningoencephalitis; feline infectious peritonitis; diskospondylitis) Chronic progressive: IVDD (type II), degenerative myelopathies, neoplasia, infectious/inflammatory (as previously stated)
INITIAL DATABASE CBC, serum biochemistry panel, urinalysis: may reflect stress or underlying infectious cause (less common) Complete orthopedic (see p. 1315), neurologic (see p. 1311) and cardiovascular evaluation to rule out concurrent disease Spinal radiographs to evaluate animal for bony lesions such as fracture, neoplasm, or infection
ADVANCED OR CONFIRMATORY TESTING Myelogram, CT, or MRI (seepp. 1306 ,1233 , and 1302): spinal cord compression secondary to IVDD or neoplasia or changes consistent with infection Cerebrospinal fluid (CSF) analysis (): evidence of infection, inflammation, exfoliating neoplasia Serum or CSF titers: to assess for infectious etiologies, especially if initial CSF analysis suggests active inflammation CSF culture if indicated by cytologic examination report
TREATMENT TREATMENT OVERVIEW Treatment should address the underlying cause: surgical decompression if a compressive lesion is found (IVDD, neoplasia, granuloma, etc.) or medical management as indicated (antibiotics, antiinflammatory medication, antifungal medication). The main goal of treatment is pain relief and resolution of neurologic dysfunction.
ACUTE GENERAL TREATMENT Acute traumatic spinal cord injuries (no spinal cord compression): consider initial methylprednisolone (30 mg/kg IV, then 15 mg/kg IV 2 and 4 hours later; if no improvement, consider surgical intervention). Must be given within the first 8 hours to be effective Further evaluation to determine need for surgery Dexamethasone is contraindicated, as there is no evidence of efficacy, and gastrointestinal side effects can be severe. Pain secondary to intervertebral disk rupture with no neurologic deficits: consider nonsteroidal antiinflammatory drug (NSAID) at appropriate dose OR tapering course of prednisone (start at 0.5 mg/kg PO q 12 h and decrease by 50% every 5 days) and methocarbamol (20 mg/kg PO q 8 h) for 2 weeks and strict cage confinement for 4 weeks. Animals that have neurologic deficits should be evaluated with advanced imaging (myelogram, CT, MRI), followed by surgical decompression if indicated; referral to veterinary surgeon or neurosurgeon is recommended.
CHRONIC TREATMENT Nursing care: Preventing pressure sores, urinary tract infections, muscle atrophy Hygiene: providing clean, dry, well-padded bedding Performing manual urinary bladder expression or catheterization if not voiding normally Performing physical rehabilitation exercises as indicated (seep. 1329 )
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POSSIBLE COMPLICATIONS Methylprednisolone may cause gastrointestinal (GI) ulceration. Ascending myelomalacia from severe cord injury is somewhat unpredictable and has a grave prognosis.
RECOMMENDED MONITORING Reevaluation of animal's neurologic function at 4-week intervals; duration of reevaluation is based on the animal's progress. If the dog remains nonambulatory after weeks or months, without signs of improvement in limb function, a canine cart is an option.
PROGNOSIS AND OUTCOME Based on preoperative neurologic exam and underlying disease Acute spinal lesion in an animal with good deep pain perception: fair to excellent for return to near-normal neurologic function with surgery If deep pain perception is not present: prognosis is guarded to poor if surgical lesion is addressed in the first 8 hours and poor to grave if after 8 hours. Chronic spinal cord compression in an animal with good deep pain perception: guarded to good prognosis, depending on number of lesions and duration of clinical signs, with a prospect of a longer recovery with surgical decompression. Nonsurgical spinal cord disease has a variable prognosis depending on underlying etiology.
PEARLS & CONSIDERATIONS COMMENTS Immediate referral to a surgeon or neurosurgeon is warranted for an animal that is decompensating neurologically.
TECHNICIAN TIPS Care should be taken when moving these patients, especially if clinical signs are acute and history of trauma is unknown. Two technicians per patient and/or rigid support are recommended.
CLIENT EDUCATION Prognosis often guarded, depending on preoperative neurologic examination; potential for prolonged postoperative nursing care. It is essential to respect a recommendation of a period of cage rest/confinement.
SUGGESTED READING Hart RC, Jerram RM, Schulz KS: Postoperative management of the canine spinal patient. Compend Contin Educ Pract Vet 19(10): 1133–1149, 1997. Levine JM, Levine GJ, Boozer L, et al: Adverse effects and outcome associated with dexa-methasone administration in dogs with acute thoracolumbar intervertebral disk herniation: 161 cases (2000-2006). J Am Vet Med Assoc 232(3):411–417, 2008. AUTHOR: SHARON L. SHIELDS EDITOR: ETIENNE CÔTÉ
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Paresis, Forelimb
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Paresis, Forelimb BASIC INFORMATION DEFINITION Monoparesis: partial loss of motor function to one limb; voluntary movement but will not initiate gait and unable to support weight Monoplegia/paralysis: complete loss of motor function to one limb Mononeuropathy: disease or injury of a peripheral nerve or its nerve roots
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT: Weakness, lameness, or inability to use a forelimb ASSOCIATED DISEASES & DISORDERS Horner's syndrome Loss of ipsilateral cutaneous trunci (panniculus) reflex Self-mutilation/trauma to affected limb PHYSICAL EXAM FINDINGS Lower motor neuron (LMN) signs to the affected limb: weakness and decreased muscle tone Variable degree: mild forelimb lameness to complete loss of sensory and motor function Denervation atrophy of forelimb musculature, usually within 7-10 days of nerve injury. Differentiate from disuse atrophy, which is slower to develop and generally less severe. Nerve root signature: lameness and pain of affected forelimb caused by entrapment of a nerve root within the brachial plexus (see pp. 149 and ) Suspicion of neoplasia if chronic progressive monoparesis, nerve root signature, and denervation atrophy Variable exam findings also may include: Horner's syndrome (ipsilateral); common with traumatic injuries to the brachial plexus Loss of cutaneous trunci (panniculus) reflex (ipsilateral); may be seen with brachial plexus injuries Palpable mass in axilla; uncommon Dysesthesia/paresthesia of limb and secondary self-trauma Traumatic injury/fracture
ETIOLOGY AND PATHOPHYSIOLOGY Central nervous system (CNS): Lesions affecting spinal cord segments C6-T2 can cause LMN forelimb signs. Flaccid forelimb monoparesis Basis: injury to LMN cell bodies that innervate forelimb musculature Usually associated with upper motor neuron signs to ipsilateral pelvic limb Peripheral nervous system: Spinal/peripheral nerve disorders cause sensory and motor dysfunction distal to the lesion (permanent nerve damage or temporary, self-resolving trauma called neurapraxia). Trauma: brachial plexus avulsion and radial nerve injury as examples Neoplasia: commonly affected are brachial plexus and dorsal nerve roots Cervicothoracic spinal cord, nerve roots, sympathetic trunk: Horner's syndrome (ipsilateral) Lateral thoracic nerve (C8, T1) disruption causes ipsilateral loss of the panniculus reflex.
DIAGNOSIS DIAGNOSTIC OVERVIEW A complete orthopedic and neurologic exam (including distribution of sensory loss) is the best means of differentiating musculoskeletal disease from neural involvement. Electromyography and nerve conduction can also aid in confirming the diagnosis
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of a nerve injury, determining the distribution, estimating the prognosis and monitoring recovery, though these procedures are uncommonly performed. Advanced imaging (MRI, CT) and/or surgical exploration and biopsy may be necessary to achieve a definitive diagnosis.
DIFFERENTIAL DIAGNOSIS CNS Trauma Vascular Neoplasia Infectious Inflammatory Peripheral nervous system Trauma Vascular Neoplasia Inflammatory
INITIAL DATABASE CBC, serum biochemistry panel, urinalysis: generally unremarkable Orthopedic (see p. 1315) and cardiovascular evaluation: rule out concurrent diseases Neurologic exam (gait, posture, spinal reflexes; seep. 1311 ) Distribution and severity of sensory loss aids in localizing the injury to a particular nerve or within 2-3 spinal cord segments: most important test for establishing prognosis for peripheral nerve injuries. Forelimb, spinal radiographs (bone fractures, luxations, neoplasia, or infection)
ADVANCED OR CONFIRMATORY TESTING Myelogram (see p. 1306) or MRI (see p. 1302) to localize unilateral spinal cord compression (intervertebral disk disease [IVDD] or neoplasia) MRI or CT scan to evaluate for nerve/nerve sheath tumors Electrodiagnostics (electromyography [EMG], motor nerve conduction [see online chapter: Electromyography and Nerve Conduction Velocity]) to localize the dysfunctional spinal cord segment, nerve root, or peripheral nerve EMG used for determining if LMN, myelin, or muscle fibers are the site of the lesion. Fibrillation potentials, positive sharp waves, and fasciculations can be seen beginning 5 days after denervation. Nerve conduction will be polyphasic and prolonged with LMN disease (with severe loss of myelin sheath) and absent with avulsion injury (or injury resulting in wallerian degeneration). Surgical exploration (based on imaging results): Biopsy, histopathologic examination for suspected neoplasia o Evaluation of type, extent, and severity of nerve injury
TREATMENT TREATMENT OVERVIEW Short-term treatment is dictated by the etiology, anatomic localization, and severity of the lesion/injury. Long-term treatment may involve appropriate medications, physical rehabilitation, protection of affected limb from trauma, and an adequate duration of supportive care to allow for recovery/reinnervation.
ACUTE GENERAL TREATMENT CNS Trauma; intervertebral disk herniation (see pp. 1039 and ) Vascular (see p. 392) Neoplasia; treatment based on tumor type, location, and invasiveness Infectious (e.g., diskospondylitis []) Peripheral nervous system Trauma (see pp. 149 and 1016) Surgical management: referral to neurosurgeon for primary nerve repair (lacerated/entrapped nerve). Carpal arthrodesis or transposition of a flexor tendon may be helpful in radial nerve injury. Vascular: ischemic thromboembolic neuromyopathy involving the subclavian or brachial artery Pain management, anticoagulation therapy, treatment of underlying heart disease
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Neoplasia: surgical recommendations depend on the type, location, and invasiveness of the tumor. Inflammatory: brachial plexus neuritis (hypertrophic, chronic or idiopathic). Medical management may include prednisolone, chlorambucil versus supportive care only.
CHRONIC TREATMENT Physical rehabilitation (see p. 1329); the animal should continue treatment for 3-6 months or until it shows signs of reinnervation. Adequate protection of an affected limb to prevent secondary trauma and self-mutilation
POSSIBLE COMPLICATIONS Failure to regain adequate function of affected limb Local recurrence of nerve root tumors Persistent trauma, self-mutilation, or contracture of paretic limb, necessitating amputation
RECOMMENDED MONITORING Monitoring of limb daily for signs of trauma or self-mutilation Serial neurologic examinations for up to 6 months to evaluate limb for reinnervation Serial electrodiagnostics to monitor recovery Monitoring for evidence of recurrence of nerve root tumor by physical exam and MRI or CT scan if indicated
PROGNOSIS AND OUTCOME Largely depends on the neurologic exam at presentation and response to treatment Central Intervertebral disk herniation: Fair to excellent if good deep pain perception Guarded to poor with poor deep pain sensation if addressed within 8 hours Poor to grave if poor deep pain sensation and addressed after 8 hours FCE: Approximately 50% chance for return to function of limb Neoplasia: Guarded to poor based on surgical accessibility and follow-up care Peripheral Brachial plexus avulsion: Generally poor; often requires amputation Guarded to fair if deep pain sensation is present Brachial plexus neuritis: Guarded but recovery is possible Peripheral nerve injuries: Fair to good for mild neurologic deficits, sharp lacerations with prompt surgical repair and short distance from site of injury to end organ Guarded to poor for severe neurologic deficits; stretching, crushing, and avulsion injuries; contaminated wounds with delayed surgical repair; and large distance from site of injury to end organ (>12 inches/>30 cm) Ischemic thromboembolic neuromyopathy Prognosis more favorable for forelimb emboli Nerve sheath tumors: Guarded to poor because local recurrence is common
PEARLS & CONSIDERATIONS COMMENTS Brachial plexus avulsions with severe traction on the nerve roots may cause damage to the spinal pathways, resulting in pelvic limb deficits that are generally ipsilateral but can be bilateral.
TECHNICIAN TIPS
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Fractures or luxations can cause damage to peripheral or spinal nerves. Use caution when manipulating a patient that has suspected fractures or luxations so as to avoid secondary nerve injuries.
CLIENT EDUCATION Clinicians should inform clients of prognosis, expected duration of forelimb paresis, and potential for failure to regain adequate function of limb, which necessitates amputation. Clinicians should perform or recommend physical rehabilitation techniques.
SUGGESTED READING de Lahunta A, Glass E: Lower motor neuron: spinal nerve, general somatic efferent system. Veterinary neuroanatomy and clinical neurology, ed 3, St Louis, 2009, Saunders Elsevier, p 77. AUTHOR: DAN POLIDORO EDITOR: ETIENNE CÔTÉ
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Paraquat and Diquat Toxicoses
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Paraquat and Diquat Toxicoses BASIC INFORMATION DEFINITION Paraquat and diquat are herbicides with corrosive properties, causing acute gastrointestinal (GI) signs, abdominal pain, and oral mucosal ulcerations when ingested. Delayed pulmonary toxicity (pulmonary fibrosis) occurs with paraquat toxicosis, and central nervous system (CNS) effects can occur with diquat.
SYNONYMS Paraquat: 1,1′-dimethyl-4,4′-bipyridinium or N,N′-dimethyldipyridyl dichloride Diquat: 9,10-dihydro-8a,10a-diazoniaphenanthrene dibromide or ethylene dipyridylium dibromide
EPIDEMIOLOGY SPECIES, AGE, SEX: Dogs are more commonly involved than cats. GEOGRAPHY AND SEASONALITY: Accidental poisonings are more common during growing seasons; paraquat has been used year round for malicious poisonings in dogs. CONTAGION/ZOONOSIS: Paraquat penetrates transcutaneously in animals and humans; users and veterinary personnel should wear gloves and protective clothing.
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT Known/suspected exposure to paraquat or diquat herbicide Clinical signs within hours to days after exposure; with acute ingestions, neurologic signs may occur within 2-6 hours, whereas the respiratory effects are seen in 3-5 days Paraquat: vomiting (all cases), lethargy, anorexia, diarrhea, ataxia; eventually, tachypnea and respiratory distress are apparent. Diquat: vomiting, lethargy, anorexia, diarrhea, ataxia PHYSICAL EXAM FINDINGS Paraquat: initially, patient may experience oral, esophageal, and gastric irritation leading to ulceration; abdominal pain; dermatitis if topical contact. Patient may then experience hypotension, arrhythmias, weakness, and disorientation/depression due to cerebral edema. Onset of cough, dyspnea, and hemoptysis may occur 3-14 days after ingestion. Diquat: oral/pharyngeal mucosal ulceration, oliguria/anuria, dermal irritation/burns, weakness, coma; rarely, arrhythmias, seizures, and dyspnea due to noncardiogenic pulmonary edema.
ETIOLOGY AND PATHOPHYSIOLOGY Paraquat concentrates in lung tissue (type I and II pneumocytes). Free radicals are produced, causing cellular injury (especially pulmonary, GI, renal, and erythrocytic). Cell wall injury leads to mononuclear macrophage activation and, notably, pulmonary fibrosis, which can be fatal 3-14 days after ingestion. Paraquat is a restricted-use pesticide (RUP) owing to its toxicity; only certified applicators can purchase and use the product. The mechanism of diquat toxicity is similar, but diquat does not accumulate in the lungs (no pulmonary fibrosis); instead, diquat may cause cerebral hemorrhage, coma, and renal failure.
DIAGNOSIS DIAGNOSTIC OVERVIEW
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The clinical diagnosis is made from history and physical exam: observed or suspected exposure, typically in a patient with fresh oral ulcers. Delayed pulmonary effects (3-5 days from paraquat) and CNS signs (hours after exposure to diquat) help support the diagnosis during/after treatment. Definitive diagnosis is possible through toxicologic analysis of vomitus, bait, blood, plasma, or other tissues (liver) within 48 hours of exposure.
DIFFERENTIAL DIAGNOSIS Toxicosis involving any caustic or corrosive agent (acids, alkali, cationic detergents, potpourri) Kidney disease/renal failure (uremic ulcers)
INITIAL DATABASE Paraquat: CBC: neutrophilia, monocytosis, lymphopenia Serum biochemistry panel: moderate increases in blood urea nitrogen (BUN), aspartate aminotransferase, and alanine aminotransferase in 24-96 hours and slight increases in total protein, creatinine, cholesterol, and bilirubin Urinalysis: myoglobinuria (from rhabdomyolysis); proteinuria, hematuria (acute renal injury) Thoracic radiographs: initially normal, progressing to noncardiogenic pulmonary edema (marked interstitial lung pattern); pneumomediastinum is a common, early finding. Diquat: serum biochemistry panel shows BUN, creatinine elevations (within 24-96 hours) and liver enzyme elevations
ADVANCED OR CONFIRMATORY TESTING Analysis of vomitus, bait, plasma, blood, tissues, urine: samples must be obtained within 48 hours of exposure, because initial excretion is rapid; contact the laboratory first. Histopathologic lesions: Paraquat: marked pulmonary edema, hemorrhage, congestion, eventually fibrosis; mild hepatic congestion, degeneration; mild renal tubular degeneration, glomerulonephritis Diquat: myocardial necrosis, cerebral hemorrhages, renal tubular damage
TREATMENT TREATMENT OVERVIEW Since no antidote exists for either substance, treatment is general and supportive.
ACUTE AND CHRONIC TREATMENT Decontamination of the animal: Paraquat: Emesis: induction of vomiting (see p. 1364) as soon as possible after ingestion, even though paraquat can be irritating or corrosive to the esophagus; the possible benefits of early removal outweigh the potential risks. Fuller's earth or bentonite (either is a preferred choice over activated charcoal, because they bind paraquat/diquat more effectively, but most clinics do not carry them) or activated charcoal (1-4 g/kg q 4-8 h) can be used as an adsorbent and are most useful if given PO within 4 hours of exposure. Multiple doses are recommended. Clinicians should bathe the entire patient if there is any dermal exposure. Paraquat is absorbed well through abraded or injured skin (wear protective clothing). With ocular exposures, irrigate eyes with copious amounts of tepid water for at least 15 to 30 minutes (see p. 250). Diquat Induction of vomiting is usually not recommended unless the patient has been exposed to a very large dose of the toxin. Activated charcoal, bentonite clay, or Fuller's earth: same dosage as for paraquat With dermal exposure, the animal's skin should be immediately washed with soap and water. Diquat can be absorbed through damaged or injured skin, resulting in systemic poisoning. Absorption through intact skin is minimal. Ocular exposures: same treatment as for paraquat Supportive care: IV fluids as indicated to correct hypovolemia, electrolyte changes associated with vomiting Control pain as needed (e.g., for dogs/cats: buprenorphine, 0.005-0.03 mg/kg IV, IM, or SQ q 6-12 h; or fentanyl patch).
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Ascorbic acid (antioxidant), 20-30 mg/kg IM, IV, or PO q 8 h, may be useful. Avoid supplemental oxygen therapy because it increases the formation of superoxide free radicals. Control vomiting as needed with maropitant, 1 mg/kg SQ q 24 h; or metoclopramide, 0.1-0.4 mg/kg SQ or IM q 6 h. Treatment of ventricular arrhythmias (see p. 1165), seizures (see p. 1009), secondary infections, oral ulcers (see ), gastric ulcers (see ), and renal complications (see p. 31) as needed. Positive-pressure ventilation (see p. 1362) may be used, but lung lesion may become (or may already be) irreversible.
POSSIBLE COMPLICATIONS Paraquat: pneumothorax, pneumopericardium, and subcutaneous emphysema Diquat: pneumonia, renal failure
RECOMMENDED MONITORING Paraquat: baseline thoracic radiographs and blood gases and serial monitoring for several days (CBC and renal and liver panels) Diquat: renal values (monitor for 3-4 days with large ingestions) and monitor CBC, liver enzymes, and electrolytes.
PROGNOSIS AND OUTCOME Paraquat: outcome appears to be related to dose and early intervention (decontamination of animal); poor prognosis for affected animals showing any clinical signs; those that survive the acute toxicosis often succumb to chronic pulmonary fibrosis. Diquat: good prognosis with early and aggressive treatment
PEARLS & CONSIDERATIONS COMMENTS Paraquat LD50 (dogs, oral) 25-50 mg/kg Diquat LD50 (dogs, oral) 100 mg/kg Concentration of diquat in most ready-to-use weed and grass killer products is castrated male dogs; rare in cats 4 months to 13 years of age (average: 2.9 years) GENETICS & BREED PREDISPOSITION Boxer, Chihuahua, cocker spaniel, Doberman, German shepherd, German short-haired pointer, Great Pyrenees, Labrador retriever, poodle, and mixed-breed dogs Boxers (n = 4), poodles (n = 2), and mixed-breed dogs (n = 12) have had more than one case reported. RISK FACTORS Developmental preputial anomalies (e.g., small preputial opening, aplastic or hypoplastic prepuce, hypospadias [urethra opening is on the ventral penis or perineum], male pseudohermaphroditism) Infectious (e.g., transmissible venereal tumor, balanoposthitis) Neurologic deficits associated with posterior paresis (e.g., intervertebral disk disease [IVDD], spinal tumors) Trauma (e.g., os penis fracture) CONTAGION & ZOONOSIS Transmissible venereal tumor preventing penile retraction ASSOCIATED CONDITIONS & DISORDERS Balanoposthitis: inflammation of the glans penis (balanitis) and preputial mucosa (posthitis) Phimosis: inability to extrude the penis from the prepuce (paraphimosis occurs 14 times more frequently than phimosis in the dog) Priapism: prolonged penile erection with or without sexual arousal
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES: Acute paraphimosis usually resolves within 12 hours; chronic paraphimosis may be intermittent or continuous. HISTORY, CHIEF COMPLAINT: History may include recent mating, penile or preputial trauma, masturbation, balanoposthitis, neurologic disease, and/or promazine tranquilizer administration. PHYSICAL EXAM FINDINGS Protrusion of the penis from the prepuce: extent of penile protrusion can vary from only the apex to the entire length of the penis. Penile mucosa may be erythematous, dry, inflamed, edematous, ischemic, and painful, which may lead to self-mutilation. Chronic protrusion of the penis may lead to excoriation and subsequent cornification of the mucosa.
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ETIOLOGY AND PATHOPHYSIOLOGY Most commonly associated with a relatively stenotic preputial orifice or with ineffective preputial musculature that cannot effectively retract the penis into the prepuce; hair ring or scar tissue also possible. Following sexual excitement or copulation, the engorged penis may become entrapped outside the prepuce, causing penile strangulation, congestion, and paraphimosis. Cranial preputial muscles (paired muscles originating from the cutaneous trunci) draw the prepuce cranially, normally about 1 cm beyond the tip of the penis.
DIAGNOSIS DIAGNOSTIC OVERVIEW Paraphimosis is diagnosed conclusively on physical exam alone. Additional testing may help elucidate the cause, although in dogs roughly 30% of cases are idiopathic.
DIFFERENTIAL DIAGNOSIS Balanoposthitis Phimosis Priapism
INITIAL DATABASE Neurologic exam (see p. 1311) with specific attention to posterior peripheral motor and sensory function.
ADVANCED OR CONFIRMATORY TESTING Electromyographic testing and/or histopathologic evaluation of cranial preputial muscles: to identify abnormal function or cellular architecture; rarely necessary Radiographs: to identify concomitant os penis fracture
TREATMENT TREATMENT OVERVIEW Paraphimosis is an emergency condition. Immediate treatment should protect the penile mucosa, prevent additional swelling (edema, inflammation) and trauma, and return the penis within the prepuce as quickly as possible. The underlying cause is then addressed to reduce the risk of recurrence.
ACUTE GENERAL TREATMENT Conservative: reduction of penis size via topical cold compresses, topical hyperosmotic solutions (e.g., sugar, honey), and systemic antiinflammatory therapy (e.g., prednisolone sodium succinate [SoluDeltaCortef] 10 mg/kg slow IV bolus) Passage of urinary catheter: to ensure patency of urethra If paraphimosis occurred secondarily to promazine-induced priapism, benztropine mesylate (0.015 mg/kg IV) should be administered as soon as possible (i.e., within 6 hours of onset of clinical signs). Removal of hair from around the preputial orifice Manual replacement of the penis in the preputial sheath using lubrication and gentle digital pressure. If unsuccessful, emergency surgical intervention is required.
CHRONIC TREATMENT Surgical intervention: Attempt manual reduction under general anesthesia. If unsuccessful, incisional enlargement of preputial orifice and retraction of penis within prepuce Options for preserving reduction: purse-string suture at the preputial orifice, preputial orifice narrowing, preputial lengthening (preputioplasty), preputial advancement, preputial muscle myorrhaphy, and phallopexy. None entirely eliminates the possibility of recurrence.
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Chronic paraphimosis can be eliminated with amputation of the penis and concurrent scrotal urethrostomy. Castration is often performed in conjunction with surgical correction of paraphimosis, but castration alone is not successful in correcting paraphimosis.
BEHAVIOR/EXERCISE Affected intact males should be separated from estrous females for at least 4 weeks afterward. Efforts should be made to prevent excessive licking of the penile and prepuce that may result in self-mutilation.
POSSIBLE COMPLICATIONS Erection and ejaculation may be impaired following longstanding paraphimosis. Balanoposthitis secondary to phimosis may occur following surgical retention of the penis within the preputial cavity. Urethral stricture formation and recurrent urinary tract infections may result following penile amputation.
PROGNOSIS AND OUTCOME The prognosis is good to guarded for the resolution of paraphimosis, depending on the severity and duration of clinical signs.
PEARLS & CONSIDERATIONS COMMENTS Dogs with developmental preputial conditions associated with paraphimosis should not be used for breeding.
PREVENTION Hairs around the preputial orifice should be kept short in long-haired dogs. Following mating or semen collection, application of a topical lubricant to penile mucosa around the preputial opening will prevent inversion of the prepuce during detumescence (natural resolution of erection and penile retraction). PARAPHIMOSIS Ventral caudal abdomen of a longhaired male dog; cranial is to the top of the image. Following semen collection for an infertility evaluation, this dog developed paraphimosis secondary to inversion of the prepuce during detumescence. This was resolved quickly with application of a topical lubricant to penile mucosa near the preputial opening and gently sliding the prepuce over the swollen glans penis.
CLIENT EDUCATION Paraphimosis may occur as a learned behavior secondary to penile licking (masturbation). Owners should be cautioned not to promote paraphimosis by positive behavioral reinforcement.
SUGGESTED READING Chaffee VW, Knecht CD: Canine paraphimosis: sequel to inefficient preputial muscles. Vet Med Small Anim Clin 70(12):1418–1420, 1975. Kustritz MV, Olson PN: Theriogenology question of the month. Priapism or paraphimosis. J Am Vet Med Assoc 214(10):1483–1484, 1999. Ndiritu CG: Lesions of the canine penis and prepuce. Mod Vet Pract 60(9):712–715, 1979. Olsen D, Salwei R: Surgical correction of a congenital preputial and penile deformity in a dog. J Am Anim Hosp Assoc 37(2):187– 192, 2001. Papazoglou LG: Idiopathic chronic penile protrusion in the dog: a report of six cases. J Small Anim Pract 42(10):510–513, 2001. Pavletic MM, O’Bell SA: Subtotal penile amputation and preputial urethrostomy in a dog. J Am Vet Med Assoc 2007(230):375–377. Root Kustritz MV: Disorders of the canine penis. Vet Clin North Am Small Anim Pract 31(2):247–258, 2001. Somerville ME, Anderson SM: Phallopexy for treatment of paraphimosis in the dog. J Am Anim Hosp Assoc 37(4):397–400, 2001.
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AUTHOR & EDITOR: MICHELLE KUTZLER
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Paraneoplastic Syndromes
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Paraneoplastic Syndromes BASIC INFORMATION DEFINITION Pathologic change in structure or function which develops secondary to and distant from a primary neoplasm. Certain paraneoplastic syndromes (PNS) occur very frequently, whereas others are rare. PNS mostly commonly arise secondary to hormonal or other cytokine factors produced by the tumor. In some instances, the PNS can be more harmful than the physical tumor.
EPIDEMIOLOGY SPECIES, AGE, SEX: Both canine and feline patients may experience PNS. In most cases, there is no sex predilection, with few exceptions (e.g., feline acromegaly in association with pituitary adenomas occurs more commonly in males). GENETICS & BREED PREDISPOSITION PNS are rarely directly induced by genetic factors, with occasional exceptions (e.g., nodular dermatofibrosis associated with autosomal dominant heritable mutation of Birt-Hogg-Dube gene in German Shepherds). Affected dogs commonly develop bilateral renal cysts or cystadenocarcinomas. Female dogs may also develop uterine leiomyoma. Certain purebreds are predisposed to individual cancers, so incidence of PNS will be relatively higher (e.g., boxer has higher incidence of T-cell lymphoma; boxer, pug, Labrador retriever have higher incidence of mast cell tumors). RISK FACTORS: Individual PNS associated with specific tumors: Hypercalcemia: T-cell lymphoma, anal sac apocrine gland adenocarcinoma, and parathyroid adenoma most common. Also reported sporadically with malignant melanoma, squamous cell carcinoma, mammary adenocarcinoma, thyroid carcinoma, bronchoalveolar carcinoma, multiple myeloma, and others. Cachexia: multiple tumor types Hypoglycemia: beta-cell tumor (insulinoma), gastrointestinal leiomyosarcoma, hepatocellular carcinoma most common; others sporadically Gastroduodenal ulceration: mast cell tumor (MCT), pancreatic gastrinoma (Zollinger-Ellison syndrome) Erythrocytosis: renal tumors, nasal fibrosarcoma Disseminated intravascular coagulopathy: hemangiosarcoma, acute leukemia, lymphoma Hyperviscosity syndrome: multiple myeloma, lymphoma, leukemia, primary polycythemia Hyperadrenocorticism: pituitary adenoma, primary adrenocortical adenoma/carcinoma Cardiac arrhythmias/altered blood pressure: pheochromocytoma, hemangiosarcoma Anemia: hemangiosarcoma, lymphoma, leukemia, multiple myeloma, estrogen-producing tumors (Sertoli cell), other chronic neoplasia Thrombocytopenia: lymphoma, leukemia, multiple myeloma, hemangiosarcoma Leukocytosis: lung tumor, renal transitional cell carcinoma (TCC) Peripheral neuropathy: many tumors Alopecia: pancreatic carcinoma Hypertrophic osteopathy: lung tumor (primary or metastatic), Sertoli cell tumor, renal TCC, nephroblastoma, adrenocortical carcinoma Myasthenia gravis: thymoma Acromegaly: pituitary adenoma (cats), mammary adenocarcinoma (dogs) Superficial necrolytic dermatitis (hepatocutaneous syndrome): glucagonoma ASSOCIATED CONDITIONS & DISORDERS Chronic hypercalcemia can result in renal failure via tubular mineralization and ischemic damage. Hyperglobulinemia/hyperviscosity syndrome can lead to coagulopathy and hypertension, resulting in retinal detachment, seizures, renal infarction, cerebral/pulmonary thromboembolism, congestive heart failure. Hypoglycemia usually causes depression, ataxia, and seizures. Gastroduodenal ulceration from excessive histamine-induced gastric hydrochloric acid (HCl) production results in melena, hematemesis, and anemia. Pancytopenia predisposes patients to opportunistic infections and spontaneous hemorrhage. Myasthenia gravis-induced megaesophagus predisposes to aspiration pneumonia. Hypertrophic osteopathy causes fever and lameness.
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Hyperadrenocorticism may predispose to thromboembolism. Acromegaly commonly causes insulin resistance, hypertrophic cardiomyopathy, and renal failure. Hepatocutaneous syndrome results in superficial necrolytic dermatitis of skin, paw pads.
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT Hypercalcemia: most common clinical signs include polyuria and polydipsia (PU/PD). Patients may also be lethargic with inappetence, vomiting from renal failure. Cachexia: patient has profound loss of lean body mass, often despite normal appetite. Hyperviscosity syndrome: presenting clinical signs depend on organ system(s) affected: seizures, blindness, syncope, dyspnea. Hypoglycemia: depression, ataxia, and seizures Gastroduodenal ulceration: anorexia, melena, hematemesis Myasthenia gravis: regurgitation, dyspnea, weakness/collapse Hypertrophic osteopathy: lameness, lethargy Hyperadrenocorticism: PU/PD, polyphagia, bilaterally symmetric hair loss, muscle wasting, pot-bellied appearance, comedones Acromegaly: PU/PD, weight gain, enlarged head and limbs Peripheral neuropathy: cranial nerve deficits, altered proprioception, urinary/fecal incontinence Superficial necrolytic dermatitis: ulcerated cutaneous lesions, cracked/painful paw pads PHYSICAL EXAM FINDINGS: Dependent on tumor type; see History, Chief Complaint
ETIOLOGY AND PATHOPHYSIOLOGY Hypercalcemia: due to excessive parathyroid hormone (PTH) production by parathyroid adenomas or humoral production of PTH-related peptide (PTHrp) and other cytokines (interleukin [IL]-1, transforming growth factor [TGF]-β), prostaglandins, and receptor activator of nuclear factor κB ligand (RANKL) Cachexia: complex metabolic derangement due to altered cytokine milieu (especially increased IL-1β, IL-6, tumor necrosis factor [TNF]-a), increased anaerobic glycolysis, and misappropriation of nutrients Hypoglycemia: due to excessive insulin or insulin-like growth factor 1 (IGF-1) production Gastroduodenal ulceration: most commonly result of hyperhistaminemia leading to excessive gastric acid in mast cell tumors and rarely hypergastrinemia in pancreatic gastrinoma Erythrocytosis: due to excessive production of erythropoietin (Epo) Bleeding disorder: due to antibody coating of platelets, platelet loss/sequestration/consumption, or inappropriate activation of the secondary coagulation cascade Hyperviscosity syndrome: due to excessive immunoglobulin production and subsequent antibody coating of red blood cells, leading to aggregation Hyperadrenocorticism: due to excessive cortisol production in adrenal glands; most commonly due to excessive ACTH release from pituitary tumors but may also be primarily produced by adrenal tumors, or rarely ectopically Cardiac arrhythmias/altered blood pressure: due to excessive catecholamine production, hypoxia, sepsis Cytopenias: due to hemorrhage, chronic inflammation, immune-mediated hemolysis, hormone-induced suppression, myelophthisis Leukocytosis: due to excessive production of granulocyte-macrophage colony stimulating factor (GM-CSF) or G-CSF Myasthenia gravis: due to antibody production targeted against acetylcholine receptors at neuromuscular junctions Acromegaly: due to excessive growth hormone (GH) production
DIAGNOSIS DIAGNOSTIC OVERVIEW Definitive diagnosis of PNS requires observation of associated clinical signs, documentation of syndrome with laboratory testing when applicable, and confirmation of underlying cancer.
DIFFERENTIAL DIAGNOSIS Hypercalcemia: granulomatous disease, hypoadrenocorticism, renal secondary hyperparathyroidism, hypervitaminosis D, young/growing, spurious, osteogenic disease Cachexia: intestinal parasites, poor-quality diet, inadequate feeding, malabsorptive/maldigestive disorder Hypoglycemia: sepsis, iatrogenic (insulin overdose), spurious/old sample
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Gastroduodenal ulceration: nonsteroidal antiinflammatory medications (NSAIDs), corticosteroids, foreign body, toxin ingestion Erythrocytosis: hemoconcentration, breed-related variation (greyhounds, sled dogs) Bleeding disorder: anticoagulant rodenticide ingestion, sepsis, idiopathic immune-mediated thrombocytopenia Hyperadrenocorticism: iatrogenic (corticosteroid administration) Cardiac arrhythmias/altered blood pressure: primary cardiac disease, renal failure Cytopenias: infectious disease (especially Rickettsiae) Myasthenia gravis: hypothyroidism, hypoadrenocorticism, lead intoxication, esophagitis, idiopathic
INITIAL DATABASE CBC, serum chemistry panel, urinalysis, coagulation profile, thoracic radiographs, abdominal ultrasound, tumor aspiration/biopsy to confirm neoplasia
ADVANCED OR CONFIRMATORY TESTING Hypercalcemia: measure PTH/PTHrp and ionized calcium to identify inappropriate function of hormone axis; parathyroid gland ultrasound to identify tumor; bone marrow aspiration to identify sequestered neoplasia. Hypoglycemia: measure serum insulin. Concentration should be below reference range; if level is high or within reference range with concurrent hypoglycemia, this suggests inappropriate function of the hormonal feedback axis. Pancytopenia: bone marrow aspiration to evaluate for infiltrative disease versus maturation arrest of cell lines Hyperviscosity syndrome: serum/urine protein electrophoresis to document monoclonal gammopathy Hyperadrenocorticism: urine cortisol/creatinine ratio, ACTH stimulation test, dexamethasone suppression test, endogenous ACTH to identify inappropriate function of pituitary-adrenal hormone axis. Myasthenia gravis: measure serum acetylcholine receptor antibody titer to prove autoimmunity. Acromegaly: measure serum GH, IGF-1 to confirm inappropriate hormone secretion.
TREATMENT TREATMENT OVERVIEW The severity of a PNS tends to parallel the status of the neoplasm. Direct treatment of the primary tumor (surgical excision, chemotherapy, or radiation therapy) should be the ultimate goal and usually causes resolution of the PNS. However, in some cases, the patient may be debilitated by the PNS and initially unable to undergo definitive therapy. Other supportive measures include the following: Hypercalcemia: saline diuresis, loop diuretics, corticosteroids, bisphosphonates, calcitonin to reduce serum calcium to normal range and/or to alleviate clinical signs Hyperviscosity syndrome: phlebotomy, plasmapheresis to reduce serum globulins to normal range Gastroduodenal ulceration: gastroprotectants (histamine receptor antagonists, proton pump inhibitors, coating agents, prostaglandin analogues) to reduce gastric HCl production; antiemetics, antidiarrheals as needed Myasthenia gravis: cholinesterase inhibitors and/or immunosuppressive therapy to improve esophageal muscular tone; upright feedings versus permanent gastrostomy tube to reduce risk of aspiration Cytopenias: blood product transfusion as needed; prophylactic antibiotics to prevent opportunistic infection in neutropenic patients Hypoglycemia: dextrose, corticosteroids, and diazoxide to increase serum glucose concentration; small frequent meals with complex carbohydrates to prevent spikes in serum glucose Seizures: anticonvulsant medications, corticosteroids, and mannitol as needed for increased intracranial pressure Hypertrophic osteopathy: analgesic medications such as NSAIDs, opioids, bisphosphonates as needed
PROGNOSIS AND OUTCOME Usually dependent on individual tumor type, although some PNS influence long-term prognosis: Hypercalcemia shortens survival in lymphoma +/− anal sac apocrine gland adenocarcinoma. Myasthenia gravis: megaesophagus shortens survival in thymoma. Gastroduodenal ulceration: patients with MCT and clinical signs have shorter survival.
PEARLS & CONSIDERATIONS
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COMMENTS Recrudescence of a PNS can indicate cancer relapse. If cause for hypercalcemia cannot be determined based on history and baseline diagnostic testing, consider bone marrow aspiration to investigate occult neoplasia.
TECHNICIAN TIPS PNS can cause clinical signs not typically associated with individual cancer types. Understanding the dynamic behavior of PNS can be helpful in distinguishing recurrence of cancer from treatment-related complications.
SUGGESTED READING Withrow SJ, Vail DM: Paraneoplastic syndromes. In Withrow & MacEwen’s small animal clinical oncology, ed 4, St Louis, 2007, Saunders, pp 77–94. Ogilvie GK, Moore AS: Nutritional support. In Managing the canine cancer patient. A practical guide to compassionate care, Yardley, 2006, Veterinary Learning Systems, p 230. AUTHOR: MICHAEL KISELOW EDITOR: KENNETH M. RASSNICK
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Paraneoplastic Syndromes, Cutaneous
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Paraneoplastic Syndromes, Cutaneous BASIC INFORMATION DEFINITION Uncommon non-neoplastic skin lesions that serve as markers for internal neoplasia
SYNONYMS Exfoliative dermatitis, nodular dermatofibrosis, paraneoplastic alopecia, paraneoplastic pemphigus
EPIDEMIOLOGY SPECIES, AGE, SEX Paraneoplastic alopecia: older cats (7-16 years) Exfoliative dermatitis: middle-aged to old cats Nodular dermatofibrosis: middle-aged dogs (3-9 years) Paraneoplastic pemphigus: dogs GENETICS & BREED PREDISPOSITION: Nodular dermatofibrosis: German shepherds, autosomal dominant inheritance ASSOCIATED CONDITIONS & DISORDERS Paraneoplastic alopecia (cats): pancreatic carcinoma, bile duct carcinoma, hepatocellular carcinoma Exfoliative dermatitis (cats): thymoma Nodular dermatofibrosis (dogs): renal cystadenocarcinomas/cystadenomas, polycystic kidneys, concurrent uterine leiomyoma Paraneoplastic pemphigus (dogs): lymphoma, Sertoli cell tumor, mammary carcinoma
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT Paraneoplastic alopecia: progressive alopecia, weight loss, lethargy, excessive grooming. The alopecia may be noted as the first manifestation (harbinger) of internal neoplasia. Internal disease is often advanced at the time of presentation, but the chief complaint commonly relates to alopecia. Exfoliative dermatitis: scaling dermatitis; alopecia; brown, waxy deposits noted on the skin Nodular dermatofibrosis: cutaneous nodules on the limbs, head Paraneoplastic pemphigus: anorexia, ptyalism, erosive/ulcerative skin and mucosal lesions PHYSICAL EXAM FINDINGS Paraneoplastic alopecia: nonpruritic symmetric alopecia on ventrum, legs, face, and neck; glistening skin; fur epilates easily; dry, fissured footpads; erythema; scale; + dehydration, emaciation Exfoliative dermatitis: nonpruritic scaling dermatitis on pinnae, head, generalized; variable alopecia; brown, waxy deposits around mucocutaneous areas, nail beds; variable erythema Nodular dermatofibrosis: nonpainful, firm cutaneous nodules on extremities; also present on the head, neck, ventral trunk Paraneoplastic pemphigus: depressed attitude; ulcers and erosions of the oral mucosa, mucocutaneous junctions
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PARANEOPLASTIC SYNDROMES, CUTANEOUS Paraneoplastic alopecia in a 14-year-old cat with pancreatic adenocarcinoma. (Copyright Dr. Manon Paradis.)
ETIOLOGY AND PATHOPHYSIOLOGY Paraneoplastic alopecia: pathogenesis may involve cytokine production, leading to atrophy of hair follicles. Exfoliative dermatosis: a tumor-induced immune-mediated process has been suggested. Nodular dermatofibrosis: collagen production within the skin may be stimulated by growth factors produced by the renal tumors; lesions develop separately through a common genetic abnormality, or simultaneous fibrosis of the skin and kidneys results in collagenous nevi and renal outflow obstruction. Paraneoplastic pemphigus: cross-reactivity between tumor antigen and self-antigen or secretion of excessive immunostimulatory cytokines may be involved.
DIAGNOSIS DIAGNOSTIC OVERVIEW The association between cutaneous lesions and internal neoplasia should be remembered (but not overinterpreted) to avoid under-and overdiagnosis of these syndromes. Diagnosis of the different cutaneous paraneoplastic syndromes is confirmed with skin biopsy and dermatohistopathologic evaluation. The histologic diagnosis of the skin lesions then suggests which underlying metabolic derangement or internal neoplasm to pursue as the cause of the paraneoplastic disorder.
DIFFERENTIAL DIAGNOSIS Paraneoplastic alopecia: demodicosis, dermatophytosis, endocrine (hyperadrenocorticism, hyperthyroidism, hypothyroidism), immune-mediated (alopecia areata), neoplasia, telogen effluvium Exfoliative dermatosis: demodicosis, infectious agents (dermatophytosis, bacterial infections, feline leukemia virus [FeLV] infection), hypersensitivities, cutaneous drug reactions, autoimmune disorders, neoplasia (cutaneous lymphoma) Nodular dermatofibrosis: primary cutaneous neoplasms Paraneoplastic pemphigus: pemphigus vulgaris, bullous pemphigoid, systemic lupus erythematosus, erythema multiforme, toxic epidermal necrolysis, cutaneous lymphoma
INITIAL DATABASE CBC, serum biochemical panel, and urinalysis. Nonspecific changes may be noted. FeLV and feline immunodeficiency virus (FIV) serologic examination is indicated in all cats, but these neoplasms are not expected to be associated with seropositive status. Paraneoplastic alopecia: Dermatohistopathologic examination: hair follicle atrophy, telogenization, hyperkeratosis, or hypokeratosis Abdominal ultrasonography: liver or pancreatic lesions due to neoplasia Exfoliative dermatosis: Dermatohistopathologic examination: cell-poor interface dermatitis with apoptotic keratinocytes in the stratum basal and stratum spinosum layers Thoracic radiographs/ultrasound: mediastinal mass
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Nodular dermatofibrosis: Dermatohistopathologic examination: nodular areas of collagenous hyperplasia Abdominal imaging: renal cysts, renal masses (neoplasms), or uterine masses (neoplasms) Paraneoplastic pemphigus: Dermatohistopathologic examination: intraepithelial acantholysis, apoptotic keratinocytes, vacuolar interface dermatitis Abdominal and thoracic imaging: masses (primary neoplasm, metastases)
ADVANCED OR CONFIRMATORY TESTING Paraneoplastic alopecia: Exploratory laparotomy with pancreatic, liver or biliary tract biopsies Exfoliative dermatosis: Fine-needle aspiration of the mediastinal mass and cytologic examination Core biopsies of the mediastinal mass Nodular dermatofibrosis: Biopsy of renal masses Paraneoplastic pemphigus: Biopsy of tumor Indirect immunofluorescence testing: Positive on stratified and nonstratified squamous epithelia Western blot analysis; target antigen proteins include envoplakin (210 kD), periplakin (190 kD), desmoglein III (130 kD), and an unidentified antigen (170 kD)
TREATMENT TREATMENT OVERVIEW The goal of treatment is to resolve the primary neoplasm if possible, since control or resolution of the cutaneous lesions is ultimately dependent on control or resolution of the underlying internal neoplasm. Palliative care for dermatologic lesions should be provided.
ACUTE GENERAL TREATMENT Paraneoplastic alopecia: surgical excision of neoplasm, if possible Exfoliative dermatosis: surgical excision of thymoma Nodular dermatofibrosis: unilateral nephrectomy is rarely curative but is indicated if renal cysts are severe; bilateral renal disease is common. Paraneoplastic pemphigus: none reported
CHRONIC TREATMENT Nodular dermatofibrosis: surgical excision of collagenous nevi until end-stage renal failure develops
PROGNOSIS AND OUTCOME Paraneoplastic alopecia: grave; euthanasia due to advanced disease Exfoliative dermatosis: guarded; outcome depends on complete thymoma removal Nodular dermatofibrosis: poor for long-term survival; slowly progressive renal disease; average lifespan: 9 years of age Paraneoplastic pemphigus: grave unless neoplasm can be removed; euthanasia for failure to respond to immunosuppression
PEARLS & CONSIDERATIONS COMMENTS Cutaneous clinical signs represent the “tip of the iceberg.” Internal disease is often advanced at the time of presentation. Earlier recognition may improve outcome in some cases (at least in thymoma). Nodular dermatofibrosis may precede clinical signs of renal disease by 3-5 years and does not warrant immediate consideration of euthanasia.
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SUGGESTED READING Lemmens P, et al: Paraneoplastic pemphigus in a dog. Vet Dermatol 9:127–134, 1998. Matousek JL: Paraneoplastic skin diseases. In Campbell KL, editor: Small animal dermatology secrets, Philadelphia, 2004, Hanley & Belfus, pp 300–304. Scott DW, et al: Paraneoplastic acquired alopecias. In Scott DW, Miller WH, Griffin CE, eds: Muller and Kirk’s small animal dermatology, ed 6, Philadelphia, 2001, WB Saunders, pp 902–905. Turek ME: Cutaneous paraneoplastic syndromes in dogs and cats: a review of the literature. Vet Dermatol 14:279–296, 2003. AUTHOR: STEPHANIE R. BRUNER EDITOR: MANON PARADIS
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Papillomas, Oral and Cutaneous
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Papillomas, Oral and Cutaneous BASIC INFORMATION DEFINITION Benign tumors of the skin and oral cavity caused by site-specific papilloma viruses (see p. 786)
SYNONYMS Lentiginosis profuse, papillomas, pigmented epidermal nevi, verrucae, warts
EPIDEMIOLOGY SPECIES, AGE, SEX Young dogs (6 months to 4 years) or immunocompromised adults Cutaneous papillomas are more often seen in males, likely due to their aggressive interactive behavior. GENETICS & BREED PREDISPOSITION Cutaneous papillomas: cocker spaniels, Kerry blue terriers Pigmented sessile papillomas: miniature Schnauzers and pugs RISK FACTORS Young and immunologically naive individuals with damaged skin or mucous membranes Immunosuppressed individuals (chronic use of glucocorticoids and/or oral cyclosporine) CONTAGION & ZOONOSIS: Contagious to other dogs via direct and indirect (fomite) contact but not to humans or cats ASSOCIATED CONDITIONS & DISORDERS Hyperadrenocorticism Squamous cell carcinoma (SCC) Bowen's disease (SCC in situ, cats)
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT Oral: owner-observed intraoral nodule(s); oral discomfort, dysphagia, halitosis, and ptyalism Cutaneous: owner-observed cutaneous growth that often involves a distal extremity and may bleed if scratched or chewed upon; occasional lameness (footpad) PHYSICAL EXAM FINDINGS Canine oral papilloma virus (COPV) presents with multiple growths in the oral cavity (a few millimeters to 1 cm in diameter). Initially develop as smooth white nodules before progressing to gray pedunculated masses with fronds. In contrast, cutaneous lesions are normally solitary and can either present as: Pedunculated growth with multiple fronds; found anywhere on the body (head, eyelids, and feet most commonly affected); rarely >1 cm diameter Inverted papilloma with a small pore opening (ventral trunk and abdomen most common); typically 1-2 cm diameter Pigmented sessile plaques/nevi/lentigines dispersed in numbers from 3 or 4 up to 80, involving the ventral neck, trunk, and medial surfaces of limbs of pugs and miniature schnauzers (autosomal dominant inheritance) Multiple papillomas affecting the footpads of dogs (digital keratomas). Firm, hyperkeratotic, hornlike growths that occur on multiple footpads, sometimes resulting in lameness as the primary presenting complaint.
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PAPILLOMAS, ORAL AND CUTANEOUS Multiple papilloma on the lips and oral cavity in a weimaraner. (Copyright Dr. Manon Paradis.)
ETIOLOGY AND PATHOPHYSIOLOGY Papilloma viruses (PV) are host specific and fairly site specific, nonenveloped, double-stranded DNA viruses that induce proliferative cutaneous and mucosal tumors in dogs. Infection requires inoculation via breaks in the epidermal or mucosal barrier by means of direct contact with other infected dogs or iatrogenic transmission through use of contaminated instruments. Replication: PV attaches to cell receptors and undergoes endocytosis. Viral DNA (vDNA) makes its way to the nucleus and establishes a pool of vDNA in basal cells. Amplification of vDNA in differentiated cells and virion maturation in nucleus and infected cells are immortalized by PV infection. Reactivation of the latent PV occurs if the patient is immunocompromised naturally or iatrogenically. Early genes stimulate cell hyperplasia followed by benign tumor formation showing as warts. Incubation period is 1-8 weeks; regression typically occurs in 1-5 months, and lesions may persist for 24 months or more.
DIAGNOSIS DIAGNOSTIC OVERVIEW The diagnosis is primarily visual, at least for the oral papillomas. Biopsy and histopathologic examination may be necessary for diagnostic confirmation of cutaneous papillomas.
DIFFERENTIAL DIAGNOSIS Oral papilloma: Fibromatous epulis Transmissible venereal tumor SCC, especially if ulcerated Cutaneous papilloma: Pedunculated with fronds: sebaceous adenoma/hyperplasia Pigmented: melanomas Inverted: intracutaneous cornifying epitheliomas
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Papillomas, Oral and Cutaneous
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INITIAL DATABASE Oral papillomatosis: clinical appearance is characteristic, followed by biopsy for dermatohistopathologic examination if a definitive diagnosis is desired (uncommon). Cutaneous papillomatosis is not as clinically evident and thus requires dermatohistopathologic examination to diagnose the lesion. Cytologic evaluation of smears may identify koilocytes, a type of dysplastic squamous cell found in potentially precancerous lesions with the following characteristics: nuclear enlargement (two to three times normal size), irregularity in the nuclear contour (occasionally), hyperchromasia, perinuclear clearing. Dermatohistopathologic evaluation of biopsies reveals fingerlike projections into the dermis and parakeratotic hyperkeratosis, inclusion bodies in keratinocytes.
ADVANCED OR CONFIRMATORY TESTING Virtually never needed in the clinical setting Immunohistochemistry: avidinbiotin complex method to detect papilloma virus group-specific antigen in tissue PCR to identify cutaneous papillomas Electron microscopy is the gold standard for diagnosis but is primarily used for research or publication purposes.
TREATMENT TREATMENT OVERVIEW Because of frequent spontaneous regression, benign neglect can be an option in mild and early cases. In face of persistent or numerous lesions, various treatment options are available. Clinicians should also identify and correct any underlying cause of immunosuppression.
ACUTE GENERAL TREATMENT Lesions may regress spontaneously within 1-2 months. Some reports claim that crushing of 5 to 15 tumors may induce spontaneous regression. Azithromycin (suspension, tablet, and injectable), 10 mg/kg, q 24 h for 10 days, has been recently reported to result in clinical remission within 10-15 days, possibly as a result of an antiviral essential factor binding and/or immunomodulatory components. Surgical removal: especially if compromising normal body function (e.g., airway obstruction, dysphagia) using CO2 laser ablation, excision, cryosurgery, or electrosurgery. Discontinue use of systemic glucocorticoids or cyclosporine, particularly if oral or cutaneous disease recurs or persists.
CHRONIC TREATMENT Interferon (IFN), either at immunostimulatory low doses of 30,000 IU/mL-0.1 mL (3000 IU) PO q 24 h OR high doses given at 1-1.5 million IU/m2 SQ q 48-72 h for 4-8 weeks pending response Imiquimod 5% (Aldara) is a topically applied, human-approved immunomodulator that activates toll-like receptors and upregulates interleukin (IL)-6, IL-12, tumor necrosis factor (TNF)-α, IFN-α and IFN-γ. Also activates Langerhans cells and provides antiproliferative and antiviral effects at an application rate of two to three times weekly to affected areas; irritation is anticipated as part of the immune response against the virus and can sometimes be difficult to differentiate from resolving lesions. Vaccines (autologous, fractional) are currently experimental. Contact your local veterinary dermatologist for updates regarding this option.
RECOMMENDED MONITORING If benign neglect is chosen, clinicians should monitor lesions for ulceration, purulent exudation, and proliferation of growths, any of which might mandate intervention. Clinicians should monitor for abnormal persistence (e.g., development into large, ulcerated mass), which could warrant biopsy because of the potential for malignant transformation of affected cells to SCC.
PROGNOSIS AND OUTCOME Prognosis usually good
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Spontaneous regression is likely, with subsequent lifelong immunity.
PEARLS & CONSIDERATIONS COMMENTS Once thought to be more of a nuisance often treated by benign neglect with spontaneous regression, persistent lesions should be addressed sooner to minimize the potential metaplasia to SCC.
PREVENTION Owners should separate dogs with oral papillomatosis from other susceptible individuals.
CLIENT EDUCATION Contagious to other dogs but not to humans and cats
SUGGESTED READING Yağci BB, Ural K, Ocal N, Haydardedeoğlu AE: Azithromycin therapy of papillomatosis in dogs: a prospective, randomized, doubleblinded, placebo-controlled clinical trial, Vet Dermatol 19:194–198, 2008. AUTHOR: ANTHONY YU EDITOR: MANON PARADIS
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Panting
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Panting BASIC INFORMATION DEFINITION Rapid, shallow breathing with a small tidal volume, usually with the mouth open It is a normal and very common thermoregulatory mechanism in dogs, and rare in cats. Excessive panting occurs with elevated ambient temperature, exercise, or anxiety (e.g., a visit to the veterinarian's office) in dogs or in the absence of severe ambient temperature elevations in cats.
SYNONYMS Hyperpnea, hyperventilation, polypnea, tachypnea
EPIDEMIOLOGY SPECIES, AGE, SEX Dependent on underlying cause Common in normal dogs (thermoregulation, anxiety) but rare in normal cats, except in stressful situations (e.g., car ride) Older cats (hyperthyroidism) Middle-aged to older dogs, with mild female predominance (hyperadrenocorticism) RISK FACTORS: Common and physiologic condition with emotional stress in both dogs and cats GEOGRAPHY AND SEASONALITY: Summer (normal thermoregulation in dogs)
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES: Normal panting due to elevated ambient temperature or anxiety versus inappropriate panting due to underlying disease HISTORY, CHIEF COMPLAINT Increased amount of panting or panting at inappropriate times Increased with elevated environmental temperatures and/or humidity Perceived evidence of pain Glucocorticosteroid or narcotic drug administration Polyuria, polydipsia, polyphagia, weight gain (canine hyperadrenocorticism) Polyphagia, weight loss, hyperactivity (feline hyperthyroidism) Seizures, abnormal mentation (brain disease) Exercise intolerance, lethargy, coughing, dyspnea (cardiac or respiratory disease) PHYSICAL EXAM FINDINGS Rapid (200-400 breaths/min), shallow breathing without evidence of respiratory distress Elevated body temperature if fever or hyperthermia Signs of pain Truncal hair loss, pot-bellied appearance, hepatomegaly (canine hyperadrenocorticism) Enlarged thyroid, tachycardia, heart murmur, or gallop heart sound (feline hyperthyroidism) Neurologic deficits (brain disease) Heart murmur, tachyarrhythmia (cardiac disease) Harsh lung sounds, wheezing (bronchial disease) Obesity
ETIOLOGY AND PATHOPHYSIOLOGY Primary means of thermoregulation in dogs via evaporative cooling within the mouth and nasal passages; passage of air,
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Panting
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blood flow, and secretions are increased in these areas during panting. Muscular work of breathing is minimally increased during panting. Causes respiratory alkalosis only if prolonged or severe. Hyperthyroidism rarely causes panting at rest but commonly with any stress. Possible reasons include respiratory muscle weakness, increased carbon dioxide production, and chemical thermogenesis. Hyperadrenocorticism and glucocorticosteroid administration may cause panting because of respiratory muscle weakness, muscle wasting, hepatomegaly, and abdominal fat deposition. Pure agonist narcotics commonly cause dose-dependent panting that is independent of route of administration. Cardiac disease and tachyarrhythmias may lead to panting due to anxiety or angina. Animals with pheochromocytoma may pant because of epinephrine induced chemical thermogenesis. A similar mechanism may be inferred for anxiety-associated panting. Hypocalcemia may lead to panting, most likely because of anxiety and pain caused by tetany. Obese animals fail to lose as much heat through evaporation and radiation, which increases the need for heat loss through panting. Furthermore, the tidal volume may be reduced due to fat deposition in the thorax, further increasing the respiratory rate.
DIAGNOSIS DIAGNOSTIC OVERVIEW Complete history and physical examination findings can help determine whether panting is normal (thermoregulation or anxiety) or a sign of disease, and aid in ranking the importance of additional tests, which can be varied and extensive.
DIFFERENTIAL DIAGNOSIS Elevated ambient temperature, hyperthermia Fever Anxiety, nervousness Pain Narcotic administration Glucocorticosteroid therapy Hyperadrenocorticism Hyperthyroidism Hypocalcemia Pheochromocytoma Cardiac disease, tachyarrhythmia Feline bronchial disease Brain disease Obesity
INITIAL DATABASE Blood pressure: moderate-severe hypertension possible with hyperthyroidism or pheochromocytoma; mild hypertension possible with severe anxiety CBC: possible erythrocytosis, thrombocytosis, leukocytosis, lymphopenia, and eosinopenia in dogs with hyperadrenocorticism Serum biochemical profile: elevated alkaline phosphatase (ALP) and cholesterol in dogs with hyperadrenocorticism; elevated liver enzymes in cats with hyperthyroidism; hypocalcemia Urinalysis: low specific gravity and/or proteinuria in dogs with hyperadrenocorticism Serum T 4: elevated in cats with hyperthyroidism Thoracic radiographs: heart enlargement + pulmonary edema, pleural effusion with cardiac disease; bronchiolar lung pattern, lung hyperinflation in feline asthma
ADVANCED OR CONFIRMATORY TESTING Arterial blood gas may show respiratory alkalosis (diminished carbon dioxide, elevated pH) in animals with severe panting. Hyperadrenocorticism screening via urine protein/creatinine ratio, adrenocorticotropic hormone (ACTH) stimulation, or low-dose dexamethasone suppression tests if history and initial database are suggestive Abdominal ultrasound to locate adrenal mass(es) Electrocardiogram and echocardiogram to confirm cardiac disease Bronchial wash cytologic evaluation to confirm feline asthma Brain CT scan or MRI
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Panting
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TREATMENT TREATMENT OVERVIEW Clinicians should treat the underlying condition to eliminate excessive panting.
ACUTE GENERAL TREATMENT Clinicians should: Reduce anxiety. Control pain if present. Decrease ambient temperature if elevated. Ensure adequate hydration in animals with elevated body temperature and provide external cooling (e.g., cool water bath, fan, cool water enema, or gastric lavage) in animals with a body temperature above 106○F (41.1○C). Discontinue or decrease dose of narcotic or glucocorticosteroid therapy if possible. Manage underlying cause (± antiarrhythmic therapy) for tachyarrhythmias. Administer calcium supplementation for hypocalcemic animals. Manage underlying cause (± antihypertensive medication) for hypertensive animals with hyperthyroidism or pheochromocytoma. Eliminate or control underlying trigger (± glucocorticosteroid and bronchodilator therapy) for feline bronchial disease.
CHRONIC TREATMENT Clinicians should: Start cats with hyperthyroidism on oral or topical methimazole and/or schedule them for radioactive iodine therapy. Treat hyperadrenocorticism with mitotane, trilostane, or adrenalectomy. Perform an adrenalectomy for animals with pheochromocytoma.
NUTRITION/DIET Initiate program for weight loss if the animal is obese.
POSSIBLE COMPLICATIONS Bronchodilator therapy may worsen primary cardiac disease.
PROGNOSIS AND OUTCOME Highly variable, owing to range of severity of underlying causes
PEARLS & CONSIDERATIONS COMMENTS Any panting cat should be evaluated for underlying disease. An exception is cats that only pant under predictable conditions of stress (e.g., car ride), the panting has not progressed in severity to resting dyspnea, and an initial physical exam has revealed no abnormalities.
TECHNICIAN TIPS Obtaining complete historical and physical examination information can assist in determining whether a patient is panting because of normal reasons (thermoregulation, anxiety) or because of underlying illness.
SUGGESTED READING Hackner SG: Panting. In King LG, editor: Textbook of respiratory disease in dogs and cats, St Louis, 2004, Saunders, p 46.
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Panting
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Vaisanen MA, Valros AE, Hakaoja E, et al: Pre-operative stress in dogs—a preliminary investigation of behavior and heart rate variability in healthy hospitalized dogs. Vet Anaesth Analg 32:158, 2005. AUTHOR: JEFF D. BAY EDITOR: ETIENNE CÔTÉ
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Panosteitis
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Panosteitis BASIC INFORMATION DEFINITION A spontaneous, self-limiting painful condition of diaphyseal and metaphyseal portions of long bones commonly diagnosed in young, large breed dogs
SYNONYMS Enostosis, juvenile osteodystrophy, eosinophilic osteomyelitis, eosinophilic panosteitis, juvenile osteomyelitis, osteomyelitis of young German shepherd dogs
EPIDEMIOLOGY SPECIES, AGE, SEX Young (5 months to 2 years), medium-and large-breed dogs Occasionally seen in younger or older dogs and in small breeds More common in males than females GENETICS & BREED PREDISPOSITION German shepherds have been reported to be at highest risk. Basset hounds may be overrepresented.
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT The hallmark chief complaint is acute, shifting limb lameness of variable severity that typically lasts 1-3 weeks (each leg). Systemic signs (e.g., anorexia, lethargy) occasionally can be severe and may require nutritional and physical support. PHYSICAL EXAM FINDINGS Orthopedic examination demonstrates pain on deep palpation/firm digital pressure of the diaphyseal and metaphyseal (midshaft and distal, respectively) portions of affected bones. Frequency: ulna (42%), radius (25%), humerus (14%), femur (11%), and tibia (8%) Fever, depression, and anorexia can be seen in more severe (unusual) cases.
ETIOLOGY AND PATHOPHYSIOLOGY Panosteitis has an unknown etiology. Infectious agents (bacteria, canine distemper virus, modified live viral vaccines) have been suspected but never proven to cause panosteitis. Other suggested inciting causes include localized vascular congestion, metabolic diseases, genetic diseases, parasitism, hyperestrinism, and hemophilia. Panosteitis is associated with excessive bone remodeling after the death of intramedullary adipocytes and hematopoietic cells. Cell death is attributed to vascular congestion, but the true cause remains unknown. The necrotic marrow cells are replaced with fibrous tissue. Woven bone is formed within the fibrous tissue. Endosteal bone formation is a prominent histologic finding with panosteitis. Periosteal bone formation is occasionally noted. Eventually, endosteal bone resorption occurs, and normal vascularity and marrow adipose tissue are reestablished.
DIAGNOSIS
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Panosteitis
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DIAGNOSTIC OVERVIEW Panosteitis is typically a mild, self-limiting condition and should be a primary consideration in any lame dog < 2 years of age. Panosteitis may occur in a single bone or limb or as a recurrent “shifting leg” lameness. It is suspected from signalment, history, and physical exam, and is confirmed radiographically.
DIFFERENTIAL DIAGNOSIS Infectious diseases (septic arthritis, osteomyelitis), immune-mediated arthropathies, and other developmental bone diseases (hypertrophic osteodystrophy, ununited anconeal process, osteochondrosis, hip dysplasia, etc.)
INITIAL DATABASE Anamnesis and physical examination: Pain during deep palpation of the affected bone (diaphysis or metaphysis) Radiography: Diagnostic test of choice Characteristic radiographic lesions: Patchy areas of increased intramedullary opacity Increased radiographic lucency near the nutrient foramen of the bone Increased periosteal bone formation Characteristic lesions may not be present during acute phase of the disease. Radiographs of other nonpainful limbs may also have characteristic lesions. CBC, serum biochemical panel, and urinalysis, as indicated by presence of systemic signs
ADVANCED OR CONFIRMATORY TESTING Nuclear scintigraphy may be used if radiographs are inconclusive.
TREATMENT TREATMENT OVERVIEW Generally, no specific therapy is required, but clinicians should provide analgesia during acute phase of panosteitis to permit the dog to have normal activity with minimal discomfort and maintain appetite.
ACUTE GENERAL TREATMENT Supportive care as required; hospitalization is rarely needed. Nonsteroidal antiinflammatory drugs (NSAIDs) generally provide adequate analgesic relief for dogs with panosteitis. Carprofen: 2 mg/kg PO q 12 h, or Etodolac: 10-15 mg/kg PO q 24 h, or Deracoxib: 1-2 mg/kg PO q 24 h, or Meloxicam 0.1 mg/kg PO q 24 h, or Firocoxib 5 mg/kg PO q 24 h Misoprostol (synthetic prostaglandin E 1 analog; 2-5 mcg/kg PO q 8-12 h) can be given to decrease the risk of gastrointestinal ulceration. There is no indication for the use of glucocorticoids in panosteitis. Use of opioid analgesics for discomfort is rarely required but can be considered in patients that have a contraindication to the use of NSAIDs. Butorphanol: 1-4 mg/kg PO q 4-6 h. or Tramadol: 1-4 mg/kg PO q 6-8 h
CHRONIC TREATMENT Seldom required, since this is a self-limiting condition An occasional severe case will require use of stronger analgesics (opioids), nutritional support (i.e., feeding tube placement), or short-term hospitalization.
NUTRITION/DIET A well-balanced maintenance diet should be recommended if the patient is not already receiving this.
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Panosteitis
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Use of additional supplements have not been shown to alter the course of panosteitis and could further complicate the development of other orthopedic conditions.
BEHAVIOR/EXERCISE Limited activity in patients that are painful
DRUG INTERACTIONS AND CONTRAINDICATIONS Gastric ulceration and other side effects may rarely occur with use of NSAIDs; clinicians should be familiar with specific product information and inform owners of possible side effects and actions to be taken if side effects are encountered (i.e., discontinue medication, veterinary evaluation, etc.). Corticosteroids should not be used in patients receiving NSAIDS; increases risk of gastric ulceration.
POSSIBLE COMPLICATIONS Most complications arise from treatment rather than disease. Gastrointestinal (GI) hemorrhage, ulceration, and perforation (NSAIDs). Liver toxicity or failure and renal dysfunction are possible with NSAIDs. Coagulation abnormalities are rare with most NSAIDs.
RECOMMENDED MONITORING Radiographic examination when other legs become affected Repeated evaluation in dogs with protracted lameness to rule out other developmental bone diseases CBC (blood loss anemia), biochemical profile (changes in liver or renal parameters), and urinalysis (urine specific gravity, sediment for evidence of real casts) are recommended with long-term NSAID usage.
PROGNOSIS AND OUTCOME Disease may last several weeks to months. The condition may shift among limbs. Long-term prognosis is very good; seldom causes permanent disability.
PEARLS & CONSIDERATIONS COMMENTS Panosteitis should be a primary differential diagnosis in any young dog with acute onset of lameness. Panosteitis is “self-limiting” in most cases. Panosteitis may repeatedly flare up over several months. Panosteitis is most common in dogs prone to other developmental orthopedic conditions. If the patient does not improve with supportive care, other underlying conditions should be ruled out. Nutraceuticals and vitamin supplementation have not been shown to decrease clinical signs, duration, or severity of panosteitis.
CLIENT EDUCATION Clients should be reminded that panosteitis is a self-limiting condition and will resolve with minimal treatment in the majority of dogs. There are potential side effects of NSAID use in dogs: Long-term use of NSAIDs may require concurrent administration of gastroprotectants. Panosteitis can mask other developmental orthopedic conditions.
SUGGESTED READING Sculz K: Other diseases of bones and joints. In Fossum TW, editor: Small animal surgery, ed 3, St Louis, 2007, Elsevier Mosby, pp 1334–1335. AUTHOR: D. MICHAEL TILLSON
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Panosteitis
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EDITOR: JOSEPH HARARI
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Pannus (Chronic Superficial Keratitis)
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Pannus (Chronic Superficial Keratitis) BASIC INFORMATION DEFINITION A typically bilateral, progressive, immune-mediated, inflammatory disease of the cornea characterized by infiltration of vessels and granulation tissue and/or pigmentation
SYNONYMS CSK, degenerative pannus, German shepherd pannus, Uberreiter's syndrome
EPIDEMIOLOGY SPECIES, AGE, SEX Dogs only Age of onset: 2-5 years of age; depends on breed and altitude GENETICS & BREED PREDISPOSITION Primarily affects large-breed dogs; may occur in any breed Breed predisposition: German shepherd, greyhound, Belgian Tervuren, Belgian sheepdog, dachshund, border collie, Shetland sheepdog, Siberian husky, Scotch collie, Australian shepherd, miniature pinscher, pointer, dalmatian, English springer spaniel, Airedale terrier RISK FACTORS Ultraviolet radiation exposure GEOGRAPHY AND SEASONALITY: Increased incidence and severity of disease in geographic regions with high altitude (i.e., elevation of 4500 feet [1500 m] or higher) and intense sunlight. Dogs that live at lower altitudes respond better to therapy (e.g., dogs living in the southeastern part of the United States are less severely affected and respond better to therapy than dogs living in the Rocky Mountains). ASSOCIATED CONDITIONS & DISORDERS: Lymphocytic/plasmacytic conjunctivitis
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES Early chronic superficial keratitis (CSK): lesions occur in the lateral to latero ventral cornea. Chronic CSK: entire cornea may be affected CSK may present as a: Vascular form Pigmentary form Combination of vascular and pigmentary forms in same eye or between eyes HISTORY, CHIEF COMPLAINT Corneal discoloration: rapidly or slowly progressive; reddish and/or brown film covering surface of the eyes Progressive loss of vision PHYSICAL EXAM FINDINGS Typically bilateral; often symmetrical Generally nonulcerative, pinkish-red, vascularized, and/or pigmentary superficial corneal lesions commencing in the lateral to ventrolateral cornea; progressively involving the medial, ventral, and dorsal aspects of the cornea, including the central
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Pannus (Chronic Superficial Keratitis)
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cornea Conjunctivitis present in most cases Multifocal white, crystalline lipid deposits often present at the leading edge of the corneal lesions (see p. 245) ± Third eyelid involvement as evidenced by pink proliferative lesions and depigmentation along leading edge of third eyelid Early CSK: Vascularization and/or pigmentation at lateral to ventrolateral cornea adjacent to limbus Progresses centrally Chronic CSK: Fleshy lesion (i.e., granulation tissue) with corneal vascularization and/or pigmentation Entire cornea may be affected, predisposing the animal to blindness
ETIOLOGY AND PATHOPHYSIOLOGY Immune-mediated disease Ultraviolet radiation exposure at high altitude potentiates the disorder. Tissue-specific antigens in the cornea are altered with ultraviolet radiation exposure. Dogs with CSK develop a hypersensitivity response to corneal proteins, predisposing them to chronic inflammation. CSK is a more rapidly progressive and severe disease in young dogs ( 10 kg, or 250 mg of each for dogs < 10 kg, PO q 8 h until improvement (about 2-3 months), then tapering gradually Pentoxifylline, 10-30 mg/kg PO q 8 h until resolved, then tapering gradually Prednisone, 2.2 mg/kg PO q 24 h, or methylprednisolone for dogs, 1.6 mg/kg PO q 24 h; or prednisolone for cats, 4.4 mg/kg PO q 24 h until resolution (about 2-6 weeks), then gradually tapering Azathioprine, 2 mg/kg PO q 24 h (dogs); or chlorambucil, 0.1-0.2 mg/kg PO q 24 h (cats and small dogs): corticosteroid-sparing alternatives for long-term treatment. After a 4-to 8-week lag phase associated with both of these medications, dosage may be q 48 h (or less frequent) on alternate days of glucocorticoid use (if still required). Dietary elimination trial: adverse food reaction may be a trigger in immune-mediated panniculitis (rare).
DRUG INTERACTIONS Clinicians should adjust dosage or minimize combination therapy with drugs that alter cytochrome P450 and/or p-glycoprotein activity (e.g., ketoconazole).
POSSIBLE COMPLICATIONS Glucocorticoid side effects (iatrogenic hyperadrenocorticism)
RECOMMENDED MONITORING Schirmer tear test if long-term use of sulfa-based drugs CBC, platelet count, serum chemistry profile, and urinalysis typically after 2-4 weeks (initially) to q 3-6 months (when stable) if using immunosuppressive agents
PROGNOSIS AND OUTCOME Variable, from guarded to good; healed lesions may leave scars. Most cases of panniculitis involve lengthy treatment (months). Amputation may be a serious consideration to prevent further spread of the disease should traditional therapies provide minimal improvement in a lesion localized to one limb.
PEARLS & CONSIDERATIONS COMMENTS A complete diagnostic workup to identify the underlying etiology leads to the most appropriate and successful treatment plan and outcome. More commonly a medically treated condition rather than a surgically managed disorder Clinicians should review the complexity of the differential diagnoses with clients, and ensure they are willing to pursue prolonged treatment before starting extensive diagnostic testing beyond histologic confirmation. Clinicians should obtain and freeze extra serum for future diagnostic tests based on histologic findings.
TECHNICIAN TIP In some cases, a biopsy punch may not reach the hypodermis (subcutaneous fat), impeding proper diagnosis. Therefore, wedge biopsy may be preferred if panniculitis is suspected.
PREVENTION Weight loss for obese animals. Reduces amount of fat to which the body can react; may allow medication discontinuation. Owners should minimize pets' access to high-risk areas (swamps, riverbeds) and should rinse/bathe the pet after high-risk area exposure. Owners can give their pets routine vitamin E antioxidant.
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Panniculitis
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CLIENT EDUCATION Extensive diagnostic testing can be involved; need to determine infectious versus immune-mediated cause. Treatment is generally lengthy, especially when addressing atypical mycobacteria, Actinomyces, Nocardia, and intermediate/systemic fungal infections; but with appropriate therapy, the prognosis in most cases is positive. Healed lesions may leave scars, however.
SUGGESTED READING Medleau L, Hnilica KA: Small animal dermatology—a color atlas and therapeutic guide, ed 2, Philadelphia, 2006, WB Saunders, pp 212–213. Scott DW, Miller WH, Griffin CE, eds: Muller and Kirk’s small animal dermatology, ed 6, Philadelphia, 2001, WB Saunders, pp 1156–1162. Yager JA, Wilcock BP: Color atlas and text of surgical pathology of the dog and cat. Volume 1. Dermatopathology and skin tumors, London, 1994, Mosby-Wolfe, pp 199–215. AUTHOR: ANTHONY YU EDITOR: MANON PARADIS
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Panleukopenia, Cat
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Panleukopenia, Cat BASIC INFORMATION DEFINITION Highly contagious parvoviral infection of cats that typically causes severe, sometimes fatal, acute gastroenteritis and leukopenia. No longer common, owing to effective vaccination protocols.
SYNONYMS Feline infectious enteritis, feline parvovirus (FPV)
EPIDEMIOLOGY SPECIES, AGE, SEX All Felidae: domestic housecats, tigers, lions, cheetahs Also affects raccoons, ferrets, mink, civet cats Can affect all susceptible cats, primarily kittens 75%) are subclinical. RISK FACTORS Unvaccinated cats > 6 weeks old Vaccinated kittens 8-20 weeks old, when maternal antibodies wane but may still neutralize vaccine-induced antibodies Pregnant queens receiving modified live-virus vaccines: risk of kittens with cerebellar hypoplasia Diagnosed most frequently in dense feral or shelter populations (frequent new animals, lower vaccination rates) CONTAGION & ZOONOSIS Highly contagious to other cats; quarantine/isolation required Virus is shed in all body secretions, primarily feces. Virus extremely stable in the environment (up to 1 year). Susceptible cats infected by exposure to infected feces, secretions, or fomites. Can also be transmitted in utero. Does not infect dogs or humans, but cats are susceptible to canine parvovirus 2 (CPV-2) antigenic subtypes, which cause the same clinical course as FPV. GEOGRAPHY AND SEASONALITY: Worldwide
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES Classical feline enteritis: kittens and susceptible adults Silent abortion/fetal death: queens (first trimester) Central nervous system (CNS) form: kittens infected in utero in second or third trimester or up to 9 days postpartum Virus infects replicating neurons. Neurologic signs are nonprogressive, and affected kittens can still make good pets. HISTORY, CHIEF COMPLAINT Classic enteritis, acute onset: Sudden death, “fading kitten syndrome” Vomiting, anorexia, and/or diarrhea Extreme lethargy or depression, hiding In utero infection: Queening of mummified fetuses Ataxia and intention tremors noted once kittens start to walk (10-14 days old) Altered mentation and dullness (usually not noted until several weeks old) Seizures
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Panleukopenia, Cat
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PHYSICAL EXAM FINDINGS Classic enteritis; kitten is infected with FPV: Fever or hypothermia in severe cases Marked dehydration or hypovolemic shock Vomiting, diarrhea Thickened bowel loops, abdominal discomfort CNS form; mother was infected with panleukopenia virus when pregnant: Cerebellar ataxia, hypermetria, intention tremors Optic nerve hypoplasia, dark foci/folding/streaking of retina Mental dullness, behavior abnormalities
ETIOLOGY AND PATHOPHYSIOLOGY Single-stranded nonenveloped DNA virus Replicates in rapidly dividing cells; clinical signs reflect destruction of these cells: Lymphoid tissue: lymphopenia, lymph node necrosis Bone marrow: panleukopenia, occasionally other short-lived cell lines (thrombocytes) Intestinal mucosal crypt cells: damage results in malabsorptive diarrhea, increased permeability, increased risk for bacterial translocation. Nervous system: cerebellar hypoplasia, hydrocephalus, hydranencephaly, retinal dysplasia from destruction of developing neural tissue
DIAGNOSIS DIAGNOSTIC OVERVIEW Confirmatory FPV laboratory testing is not readily available; diagnosis is typically based on history, signalment, clinical signs, and initial laboratory findings. Severe gastroenteritis with neutropenia in a 3-to 5-month-old kitten is sufficiently suggestive of FPV infection to proceed with treatment, contagion precautions, and prognostication.
DIFFERENTIAL DIAGNOSIS Gastroenteritis: Foreign body Other bacterial or viral infections (coronavirus, Salmonella spp., Clostridium spp.) Inflammatory bowel disease Neoplasia Toxin ingestion Leukopenia: Feline leukemia virus (FeLV) Salmonellosis
INITIAL DATABASE CBC: mild anemia unless severe gastrointestinal (GI) bleeding; leukopenia, especially neutropenia, is typical, but normal leukogram does not rule out FPV; thrombocytopenia due to bone marrow suppression or disseminated intravascular coagulation (DIC). Serum biochemistry profile: often unremarkable; prerenal azotemia, increases in alanine aminotransferase/aspartate aminotransferase/bilirubin possible Coagulation panel: may see evidence of DIC Radiographs: typically unremarkable
ADVANCED OR CONFIRMATORY TESTING Confirmatory diagnostic tests for enteric FPV exist (e.g., serologic titers, immunofluorescent antibody testing, PCR assay, and virus isolation), but are often labor-or time-intensive, expensive, and not readily available. Canine parvoviral fecal ELISA test kits can reliably detect FPV antigen. As with vaccination in puppies, false-positive results can occur within 2 weeks of vaccination with modified live feline panleukopenia vaccine. Since definitive antemortern diagnosis of the CNS form is not realistically possible, the practitioner should rely on history, signalment, and neurologic exam to point to in utero or perinatal FPV infection. Histologic findings are also similar to those of canine parvovirus.
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TREATMENT TREATMENT OVERVIEW There is no specific antiviral drug for FPV infection, so comprehensive supportive care is required to carry the patient through the acute episode of enteritis. There is no treatment that will change the course of the neurologic form.
ACUTE GENERAL TREATMENT Supportive care: IV crystalloids/colloids to correct shock, dehydration, and electrolyte abnormalities Broad-spectrum antibiotics (e.g., ampicillin, 22 mg/kg IV q 8 h; and gentamicin, 4 mg/kg IV q 24 h, only when hydration is normal) to combat secondary bacterial infections Withholding of food/water during acute episode to decrease crypt cell division and subsequent viral replication Antiemetics (e.g., metoclopramide 0.2-0.4 mg/kg SQ q 8 h or 1-2 mg/kg/d as an IV contrast rate infusion)
CHRONIC TREATMENT Cats that recover are immune for life.
NUTRITION/DIET Appetite stimulants (cyproheptadine, 2 mg per cat PO q 12 h; or mirtazapine, 3.75 mg PO q 72 h); or enteral tube feeding during recovery period if anorexia persists. Trickle feeding of a liquid diet through a nasogastric tube after acute enterocyte destruction has stopped may improve gut healing and hasten return of appetite. 12
Vitamin B , 0.25 mg IM or SQ per cat once
RECOMMENDED MONITORING Repeat CBC: rebound leukocytosis (24-48 h). If leukopenia persists, clinicians should rule out other causes (e.g., FeLV).
PROGNOSIS AND OUTCOME Guarded (short-term) for acute gastroenteritis Guarded to good for kittens with cerebellar hypoplasia, depending on ability to compensate for deficits; neurologic signs are not treatable but are also nonprogressive. Grave to poor for kittens with fore-brain signs
PEARLS & CONSIDERATIONS COMMENTS Kittens cannot have both neurologic signs and signs of enteritis simultaneously from panleukopenia, because neurologic signs occur from in utero infection of the dam. Routine vaccination has profoundly decreased the incidence of disease. Disease is maintained due to persistence of FPV in the environment and birth of susceptible animals in unvaccinated populations.
PREVENTION Modified live vaccines (MLV) are preferred because they are rapid and provide more effective immunity. Clinicians should administer the vaccine after the kitten is 8 weeks old to avoid inactivation by maternal antibodies, then 2 and 4 weeks after first vaccination, and again 1 year later. Initial vaccinations probably provide lifelong immunity, but clinicians should revaccinate triennially per American Association of Feline Practitioners. MLV is contraindicated in pregnant queens or kittens < 4 weeks old.
TECHNICIAN TIPS Because the virus is easily spread via fomites (towels, bowls, shoes) and persists up to 1 year, a strict isolation protocol is essential
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in these cases (e.g., disposable gowns, booties, and gloves; monitoring equipment such as stethoscopes and thermometers cannot leave the isolation area). Disinfection of the environment or fomites requires 1:32 diluted sodium hypochlorite (bleach), formaldehyde, or glutaraldehyde.
CLIENT EDUCATION Breeders should vaccinate new, susceptible cats 1 week prior to introduction to cattery.
SUGGESTED READING Greene CE, Addie DD: Feline parvovirus infections. In Greene CE, editor: Infectious diseases of the dog and cat, ed 3, St Louis, MO, 2006, Saunders Elsevier, pp 78–88. AUTHOR: SHANNON T. STROUP EDITOR: DOUGLASS K. MACINTIRE
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Pancreatitis, Dog
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Pancreatitis, Dog BASIC INFORMATION DEFINITION Pancreatitis is an inflammatory condition of the pancreas. It can be acute or chronic, which can only be differentiated histopathologically.
EPIDEMIOLOGY SPECIES, AGE, SEX: There are no known age or sex predilections. GENETICS & BREED PREDISPOSITION: Miniature schnauzers appear to be more commonly affected. As in some humans with hereditary pancreatitis, a mutation of the SPINK gene may be responsible. RISK FACTORS Dietary indiscretion Blunt abdominal trauma Hypercalcemia Pancreatic hypoperfusion Pharmaceuticals: potassium bromide, phenobarbital, L-asparaginase, azathioprine, trimethoprim-sulfa, and others There is little evidence that corticosteroids cause pancreatitis in dogs, and pancreatitis or a history of pancreatitis are not considered contraindications for corticosteroid use. Severe hypertriglyceridemia and disorders of lipid metabolism ASSOCIATED CONDITIONS & DISORDERS: Peritonitis (in severe cases)
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT History of dietary indiscretion (often high-fat foods) Anorexia and vomiting are most common (reported in 91% and 90% of patients in one study, respectively). Weakness Abdominal pain is reported in more than 50% of dogs with pancreatitis. Diarrhea is reported in about 33% of dogs with pancreatitis. PHYSICAL EXAM FINDINGS Abdominal pain Dehydration Fever Possible icterus
ETIOLOGY AND PATHOPHYSIOLOGY The cause of pancreatitis is unknown in many dogs. There is a common pathogenetic pathway, regardless of the initiating cause. Any number of insults can lead to premature activation of trypsinogen to trypsin. Trypsin, in turn, activates more trypsinogen and other pancreatic zymogens. Prematurely activated pancreatic digestive enzymes lead to local and systemic damage. This process also leads to recruitment of inflammatory cells and cytokine release, causing further systemic changes. In general, premature activation of pancreatic digestive enzymes leads to initiation of pancreatitis, while the inflammatory response leads to progression of the disease and systemic complications.
DIAGNOSIS
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DIAGNOSTIC OVERVIEW Measurement of serum pancreatic lipase immunoreactivity (now measured by Spec cPL) is the most sensitive and specific laboratory test currently available for pancreatitis, but the diagnosis rests on a combination of clinical signs, diagnostic imaging results, and pancreas-specific serologic tests.
DIFFERENTIAL DIAGNOSIS Primary acute or chronic gastrointestinal disorders: infectious, inflammatory, neoplastic, toxic, mechanical, or other Acute or chronic metabolic or systemic disorders: hepatic, renal, adrenal, thyroid (less likely), reproductive, or central nervous system (CNS) disease
INITIAL DATABASE CBC findings are variable and nonspecific: most commonly observed changes are thrombocytopenia, neutrophilia with a left shift, and anemia. Findings on a serum chemistry profile are variable and nonspecific: hypochloremia, hypophosphatemia, elevated hepatic enzyme activities, azotemia, hyperbilirubinemia, hypoalbuminemia, hypoglycemia, or hyperglycemia. Results from a serum chemistry profile are most useful in assessing the patient for systemic complications and ruling out other disorders with overlapping clinical signs. Abdominal radiographs are not useful in diagnosing pancreatitis but are useful in ruling out other differential diagnoses of pancreatitis.
ADVANCED OR CONFIRMATORY TESTING Abdominal ultrasound is useful for the diagnosis of canine pancreatitis: Diagnostic criteria: enlargement of the pancreas, fluid accumulation around the pancreas, pancreatic mass effect, hypoechoic pancreas (necrosis), hyperechoic peripancreatic fat, or dilated pancreatic duct. Resolution of equipment and operator expertise have increased significantly over the last 2 decades. Clinicians must exercise caution not to overdiagnose pancreatitis. Serum amylase and lipase activities have been used for the diagnosis of pancreatitis for several decades. Measurements of serum amylase or serum lipase activities are neither sensitive (approximately 50% sensitivity) nor specific (approximately 50% specificity) for pancreatitis and are thus clinically not very useful. SNAP cPL is a patient-side test for immediate rule out of canine pancreatitis. A negative SNAP cPL test should prompt the clinician to evaluate the patient for other differential diagnoses. A positive SNAP cPL should be confirmed by measurement of a Spec cPL test. Serum canine pancreatic lipase immunoreactivity (cPLI) concentration (now measured by the Spec cPL assay):0 Measures the concentration of pancreatic lipase in serum (many other lipases contribute to serum lipase activity measurement). Reference range: 12 hours to be effective. Buprenorphine: 0.01-0.02 mg/kg IM or IV Antiemetic therapy can be important. Metoclopramide antagonizes dopamine at the receptor site, which may have a negative impact on pancreatic perfusion and therefore is not the drug of first choice. Dolasetron and ondansetron are 5-HT 3 serotonergic receptor antagonists that have much stronger antiemetic properties than metoclopramide. Dolasetron and ondansetron can be safely used in the dog. Dolasetron can be used at dosages of 0.3-0.6 mg/kg IV, 1
SQ, or PO q 12-24 h. Maropitant is an NK receptor antagonist which has both peripheral and central antiemetic properties (1 mg/kg SQ q 24 h or 2 mg/kg PO q 24 h). Patients can be treated with a 5 HT 3 and an NK1 inhibitor simultaneously. Dogs with severe pancreatitis (associated with dehydration, electrolyte and acid-base abnormalities, disseminated intravascular coagulation [DIC], and/or other systemic complications) should receive plasma transfusions on a daily basis (10 mL/kg given IV for 1-2 hours). While there is little scientific evidence that plasma administration is clinically useful in human patients with pancreatitis, many veterinary gastroenterologists feel that there appears to be a clinical benefit. One recent retrospective study of dogs with acute pancreatitis showed no benefit from plasma administration. Antibiotics have failed to show any benefit in human patients with pancreatitis. In addition, dogs with pancreatitis rarely have the infectious complications of pancreatitis commonly seen in humans with the condition. Thus, antibiotic therapy should only be implemented when there is a specific suspicion for a concurrent infectious disease or an infectious complication of pancreatitis. There is no evidence that any other therapeutic strategy is clinically efficacious in dogs with pancreatitis.
CHRONIC TREATMENT Dogs with chronic pancreatitis should be evaluated for potential risk factors for pancreatitis. An 18-hour fasting serum triglyceride concentration should be measured, and treatment measures should be employed in hyperlipidemic animals to keep the serum triglyceride concentration below 500 mg/dL (see p. 1398). Also, a serum calcium concentration should be measured and a detailed drug history taken. Dietary measures are important in the successful treatment of dogs with chronic pancreatitis (see below). Antioxidants may also be of benefit. Measurement of serum Spec cPL concentration can be used to objectively monitor animals with pancreatitis.
NUTRITION/DIET Recommending nothing per os (NPO) for the animal was once standard therapy for dogs with acute pancreatitis. However, nutritional support, preferably enteral nutritional support, can have beneficial effects in animals with pancreatitis. NPO should only be chosen in animals for which vomiting cannot be controlled. If the patient vomits and has to be kept NPO for several days, total or partial parenteral nutrition (TPN or PPN; see p. 1322) should be considered for nutritional support. Alternatively, jejunostomy tube placement surgically or via endoscopy (see ) can be used for nutritional support. Dogs with pancreatitis should be fed an ultra low-fat diet. Care should also be taken to avoid any treats that may be high in fat.
DRUG INTERACTIONS Any drugs implicated in causing pancreatitis should be avoided. However, corticosteroids, formerly implicated in causing pancreatitis, probably pose little risk of leading to worsening of pancreatitis in the dog.
POSSIBLE COMPLICATIONS A pancreatic pseudocyst (an encapsulated fluid collection in the region of the pancreas) rarely develops in dogs with pancreatitis. Little is known about appropriate management in dogs. In humans, pancreatic pseudocysts are carefully monitored and are only drained if they increase in size. Pancreatic abscesses have only been reported in approximately 40 dogs. Most of these were not infected. Surgical removal may be the best option. Aggressive antibiotic therapy should be instituted after draining the abscess, at least until culture results show absence of any infectious organisms. Pancreatitis can lead to extrahepatic biliary obstruction. In most cases, the obstruction will resolve with supportive care.
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However, some patients will need surgery to reroute the bile duct. Systemic complications may include DIC, thrombocytopenia, acute renal failure, pleural effusion, pulmonary emboli, myocarditis, peritonitis, and aspiration pneumonia.
RECOMMENDED MONITORING Short-term monitoring: CBC, chemistry profile, coagulation panel, Spec cPL Ultrasound is of little value in monitoring short-term progress. Long-term monitoring: Spec cPL
PROGNOSIS AND OUTCOME The prognosis for dogs with pancreatitis is directly related to the severity of disease. Mild disease without pancreatic and systemic complications carries a good prognosis. Severe disease with pancreatic (e.g., pancreatic necrosis, pancreatic pseudocyst, pancreatic abscess, or other) or systemic (e.g., renal failure, pulmonary failure, DIC, or other) complications carries a poor to grave prognosis. There is no commonly accepted scoring system that would allow prediction of the outcome of the disease in a specific animal. Such scoring systems are routinely utilized in human patients with pancreatitis.
PEARLS & CONSIDERATIONS COMMENTS Pancreatitis is being diagnosed with increasing frequency in dogs. A recent study has shown histopathologic changes of the exocrine pancreas in most dogs that died for any reason, suggesting that subclinical exocrine pancreatic disease and, more specifically, inflammation are common in dogs. However, at this point, the clinical importance of subclinical pancreatic inflammation in dogs is unknown.
PREVENTION Avoiding high-fat foods and treats may prevent pancreatitis, especially in animals that have had previous episodes of pancreatitis. Eliminating risk factors will aid in the prevention of pancreatitis.
SUGGESTED READING Steiner JM: Exocrine pancreas. In Steiner JM, editor: Small animal gastroenterology, Hannover, 2008, SchlüterscheVerlagsgesellschaft mbH, pp 283–306. Xenoulis PG, Suchodolski JS, Steiner JM: Chronic pancreatitis in dogs and cats. Compend Contin Educ Vet 30(3):166–180, 2008. AUTHOR: JÖRG M. STEINER EDITOR: KEITH P. RICHTER
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Pancreatitis, Cat
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Pancreatitis, Cat BASIC INFORMATION DEFINITION Pancreatitis is an inflammatory condition of the pancreas. It can be acute or chronic, which can only be differentiated histopathologically. In contrast to acute pancreatitis, chronic pancreatitis is associated with permanent changes such as pancreatic fibrosis and/or atrophy.
EPIDEMIOLOGY SPECIES, AGE, SEX: There are no known age or sex predilections for feline pancreatitis. RISK FACTORS Blunt abdominal trauma Hypercalcemia Pancreatic hypoperfusion Pharmaceuticals: organophosphates and others Corticosteroids are no longer implicated in causing pancreatitis in humans, and there is no evidence that they cause pancreatitis in cats. Infections: Toxoplasma gondii, hepatic fluke infestation (Amphimerus pseudofelineus), possibly feline infectious peritonitis (FIP), and others ASSOCIATED CONDITIONS & DISORDERS Feline pancreatitis often concurrently occurs with cholangitis and inflammatory bowel disease (termed “triaditis” when inflammation is present in all three sites), but a cause-and-effect relationship between these conditions has not been demonstrated.
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES Acute or chronic Mild (not associated with systemic or pancreatic complications) or severe (associated with systemic or pancreatic complications) HISTORY, CHIEF COMPLAINT: Vague complaints are typical: Lethargy Anorexia Vomiting occurs only in approximately 33% of cases. PHYSICAL EXAM FINDINGS: Vague findings: Lethargy Dehydration Hypothermia Abdominal pain is only reported in approximately 25% of cases. Possible icterus
ETIOLOGY AND PATHOPHYSIOLOGY The causes for feline pancreatitis are not well defined. Several risk factors (see previous paragraphs) have been identified. There is a common pathogenetic pathway regardless of the initiating cause. Any number of insults can lead to premature activation of trypsinogen to trypsin. Trypsin, in turn, activates more trypsinogen and other pancreatic zymogens. Prematurely activated pancreatic digestive enzymes lead to local and systemic damage, which in turn leads to recruitment of inflammatory
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cells and cytokine release, leading to further systemic complications. In general, premature activation of pancreatic digestive enzymes leads to initiation of pancreatitis, while the inflammatory response leads to progression of the disease and systemic complications.
DIAGNOSIS DIAGNOSTIC OVERVIEW Serum feline pancreatic lipase immunoreactivity concentration (fPLI), now measured by a commercially available assay, Spec fPL, is the most sensitive and specific laboratory test currently available for feline pancreatitis. However, it should be noted that integration of all clinical data available will afford the most accurate diagnosis.
DIFFERENTIAL DIAGNOSIS Primary acute or chronic gastrointestinal (GI) disorders: infectious, inflammatory, neoplastic, toxic, mechanical, or other conditions Acute or chronic metabolic or systemic disorders: hepatic, renal, adrenal, thyroid, systemic, or (less likely) central nervous system (CNS) or heart-worm disease
INITIAL DATABASE CBC findings are variable and nonspecific: most commonly observed changes are anemia and leukocytosis. Findings on a serum chemistry profile are also variable and nonspecific: increased serum hepatic enzyme activities, hyperbilirubinemia, hypercholesterolemia, hyperglycemia, azotemia, hypokalemia, hypocalcemia, and hypoalbuminemia. Results from a serum chemistry profile are very useful in assessing the patient for systemic complications of pancreatitis and ruling out other disorders with overlapping clinical signs. Abdominal radiographs are not useful for diagnosing pancreatitis but are useful for ruling out other differential diagnoses of pancreatitis.
ADVANCED OR CONFIRMATORY TESTING Abdominal ultrasound is useful for the diagnosis of feline pancreatitis: Diagnostic criteria: enlargement of the pancreas, fluid accumulation around the pancreas, pancreatic mass effect, hypoechoic (necrosis) or, less common, hyperechoic (fibrosis) pancreas, hyperechoic peripancreatic fat, or dilated pancreatic duct Resolution of equipment and operator expertise have increased significantly over the last 2 decades. Clinicians should exercise caution and avoid overdiagnosing pancreatitis. Serum amylase and lipase activities are not useful for the diagnosis of feline pancreatitis. Serum feline trypsinlike immunoreactivity (fTLI) is highly specific (abnormally high value indicates pancreatitis with a high degree of accuracy) but not very sensitive (only 30%-60% of feline pancreatitis cases have an abnormal fTLI result). Serum feline pancreatic lipase immunoreactivity (Spec fPL [Idexx Laboratories, Portland, Maine]) concentration. Measures concentration of pancreatic lipase in serum (many other lipases contribute to total serum lipase activity). Reference range: 0.1-3.5 µg/L Cutoff value for pancreatitis: 5.4 µg/L Highly specific for exocrine pancreatic function Highly sensitive for both acute and chronic pancreatitis One-time measurement does not allow assessment of disease severity, but serial measurements do allow for monitoring of disease progression in a specific animal.
TREATMENT TREATMENT OVERVIEW Treatment of the underlying cause if identified Treatment of clinical signs that cause morbidity (e.g., abdominal pain, vomiting) Identification and treatment of systemic and pancreatic complications Nutritional support
ACUTE GENERAL TREATMENT
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If an underlying cause can be identified, it should be treated accordingly. Examples: The drug history of the animal should be carefully assessed; if the animal has been treated with any medication that has been implicated in causing pancreatitis, the medication should be discontinued. In addition, medications the patient requires for a concurrent condition should be switched to a different class of drug with the same or similar effect. The mainstay of pancreatitis therapy is supportive care. This includes intensive but judicious fluid therapy and careful monitoring for any signs of ensuing complications. Once a complication has established itself in a patient, treatment of such a complication becomes increasingly difficult. Supportive therapy for signs that cause morbidity is also important. Foremost, analgesia is very important. Abdominal pain is a key clinical sign in people with pancreatitis and should be assumed to be present in any cat with pancreatitis, whether the sign is clinically apparent or not. Analgesia can be achieved with intermittent dosing or continuous rate infusion. Acceptable options include one of the following: Meperidine: 2-4 mg/kg IM, as needed; short half-life or adverse effects can be limiting. Butorphanol: 0.1-0.4 mg/kg SQ, IM, or IV Morphine: 0.05-0.2 mg/kg q 2-6 h SQ or IM; may cause dysphoria or nausea Fentanyl: 0.002-0.003 mg/kg IV once, then if needed, as a constant rate infusion: 0.001-0.004 mg/kg/h IV Buprenorphine: 0.005-0.01 mg/kg IM or IV Antiemetic therapy can be important. Metoclopramide antagonizes dopamine at the receptor site, which may have a negative 3
impact on pancreatic perfusion and therefore is not the first drug of choice. Dolasetron and ondansetron are 5-HT serotonergic receptor antagonists that have much stronger antiemetic properties than metoclopramide. Dolasetron and ondansetron can be safely used in the cat. Dolasetron can be used at dosages of 0.3-0.6 mg/kg IV, SQ, or PO q 12-24 h. 1
Maropitant is an NK receptor antagonist, which has both peripheral and central antiemetic properties and can be used at 1 mg/kg SQ or PO q 24 h. Patients can be concurrently treated with a 5 HT 3 and an NK1 inhibitor. Recommending nothing per os (NPO), nothing taken orally, was once standard therapy for cats with pancreatitis. However, nutritional support, preferably enteral nutritional support, can have beneficial effects in animals with pancreatitis. Thus, NPO should only be ordered for cats in which vomiting cannot be controlled. In animals that are eating and not vomiting, a low-fat diet should be offered in small amounts and given multiple times a day. If the animal vomits and has to be kept NPO, total or partial parenteral nutrition (TPN or PPN; see p. 1322) should be considered for nutritional support. If the animal is not vomiting but has prolonged anorexia, tube feeding (nasogastric, esophagostomy, or percutaneous endoscopic gastrostomy tube; see , , , ) is warranted. Nutritional support is especially important in cats. Many cats with pancreatitis have been partially or fully anorectic for some time before presentation and are thus at increased risk for secondary hepatic lipidosis. Antibiotics have failed to show a reproducible benefit in human patients with pancreatitis. In addition, infectious complications, which are a common cause for morbidity and mortality in human patients with severe pancreatitis, are extremely rare in cats with pancreatitis. Thus, antibiotic therapy should only be implemented when there is a specific suspicion for a concurrent infectious disease or an infectious complication of pancreatitis. Glucocorticoid therapy may be helpful, especially if there is concurrent histologically confirmed inflammatory bowel disease and/or cholangiohepatitis. There is no evidence that any other therapeutic strategy is clinically efficacious in cats with pancreatitis.
CHRONIC TREATMENT Cats with chronic pancreatitis often have concurrent inflammatory conditions such as inflammatory bowel disease (IBD) and/or cholangitis (known as “triaditis” when inflammation is present in all three sites). While there is little scientific evidence to suggest that these concurrent conditions cause pancreatitis, oftentimes the overall health of the cat will improve as these conditions are being appropriately diagnosed and managed. Serum calcium and fasting triglyceride concentrations should be measured in cats with pancreatitis, and conditions causing abnormalities in these parameters should be managed if present. While there is little evidence that high-fat diets are a cause of pancreatitis in cats, it still seems prudent to place cats with pancreatitis on a low-fat diet. Measurement of serum fPLI concentrations can be used for objectively monitoring animals with pancreatitis. Many cats with chronic pancreatitis have a lymphocytic infiltration of the pancreas. This is similar to humans with autoimmune pancreatitis. Thus, if no risk factors are identified and the patient does not improve spontaneously, a therapeutic trial with corticosteroids can be undertaken. A baseline serum fPLI concentration is measured, and prednisolone, 2 mg/kg PO q 12 h, is then given for 10 days. A second serum fPLI concentration measured at this point indicates whether to stop treatment (fPLI the same or higher) or continue on a tapering schedule based on positive response (fPLI lower).
DRUG INTERACTIONS Any drugs implicated in causing pancreatitis should be avoided. However, corticosteroids, formerly implicated in causing pancreatitis, probably pose little risk of leading to worsening of pancreatitis in cats.
POSSIBLE COMPLICATIONS Pancreatic abscessation has only been reported in a single cat.
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Pancreatitis can lead to extrahepatic biliary obstruction. Most of these obstructions will resolve with supportive care. A small number of these cats need surgery to reroute the bile duct. Systemic complications may include disseminated intravascular coagulation (DIC), thrombocytopenia, acute renal failure, pleural effusion, and peritonitis. These are rare in cats.
RECOMMENDED MONITORING Short-term monitoring: CBC, chemistry profile, coagulation panel, fPLI Ultrasound is of little value in monitoring short-term progress. Long-term monitoring: fPLI
PROGNOSIS AND OUTCOME The prognosis for cats with pancreatitis is directly related to the severity of disease. Mild disease without pancreatic and systemic complications carries a good prognosis. Severe disease with pancreatic (such as pancreatic necrosis, pancreatic pseudocyst, pancreatic abscess, or other) or systemic (such as renal failure, pulmonary failure, DIC, or other) complications carries a poor to grave prognosis.
PEARLS & CONSIDERATIONS COMMENTS Pancreatitis is diagnosed with increasing frequency in cats. In addition, autoimmune pancreatitis has been described with increasing frequency in humans. It is intriguing to speculate that at least some cats with chronic pancreatitis have a similar condition and, like humans with autoimmune pancreatitis, may benefit from corticosteroid administration (see above).
PREVENTION There is no known prevention for pancreatitis in cats.
SUGGESTED READING Xenoulis PG, Suchodolski JS, Steiner JM: Chronic pancreatitis in dogs and cats. Compend Contin Educ Vet 30(3):166–180, 2008 Mar. Steiner JM: Exocrine pancreas. In: Steiner JM, editor: Small animal gastroenterology, Hannover, 2008, SchlüterscheVerlagsgesellschaft GmbH, pp 283–306. AUTHOR: JÖRG M. STEINER EDITOR: KEITH P. RICHTER
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Pancreatic Adenocarcinoma
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Pancreatic Adenocarcinoma BASIC INFORMATION DEFINITION Most commonly a malignant, highly metastatic epithelial tumor of the pancreas, of ductular or acinar origin
EPIDEMIOLOGY SPECIES, AGE, SEX Uncommon tumor of dogs and cats ( T. leonina),but alternatives with a wider safety margin are preferred. Many products used for heartworm prevention are also effective against roundworms.
CHRONIC TREATMENT Environmental decontamination should be considered in all animals, especially those with repeated infections or adult animals with infection.
DRUG INTERACTIONS The parasiticidal dose of ivermectin (200 mcg/kg) should not be used in collies or other susceptible breeds/individuals (see pp. 625 and ).
PROGNOSIS AND OUTCOME Prognosis is excellent for appropriately treated animals.
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Roundworm Infection
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PEARLS & CONSIDERATIONS COMMENTS All puppies and kittens should be strategically dewormed to prevent environmental contamination and human exposure. The zoonotic risk associated with Toxocara spp. parasites outweighs their impact on dogs and cats.
PREVENTION Treatment of pregnant dogs and cats can decrease the level of transplacental and transmammary infection of puppies and kittens. Common treatment regimes described for dogs include fenbendazole, 50 mg/kg PO q 24 h, from day 40 of gestation to day 14 of lactation; or ivermectin, 200 mcg/kg, once a week from 3 weeks prior to whelping to 3 weeks after whelping. Pregnant cats may be treated with topical selamectin, 6 mg/kg, 6 weeks and 2 weeks before parturition and 2 weeks and 6 weeks after parturition.
TECHNICIAN TIPS Warn all clients of the risks of exposure to Toxocara, especially those clients with young children or those who are immunosuppressed.
CLIENT EDUCATION Clients should be encouraged to commit to regular deworming of puppies and older dogs. Good hygiene is important in kennels and catteries; all feces should be properly removed from the area.
SUGGESTED READING Kazacos KR: Larval migrans from pets and wildlife. In 2002 Tufts Animal Expo Proceedings Online. North Grafton, MA. www.vin.com/Members/Proceedings.plx?CID=TUFTS2002&O=VIN Reinemeyer CR: Canine gastrointestinal parasites. Kirk's current veterinary therapy XII, Philadelphia, 1995, WB Saunders, pp –. 711716 AUTHOR: CHARLESHENDRIX EDITOR: DOUGLASS K.MACINTIRE 1ST EDITION AUTHOR: KATHRYNTAYLOR
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Round Cell Tumors
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Round Cell Tumors BASIC INFORMATION DEFINITION Round cell tumors are composed of a homogenous population of cells that have well-defined cytoplasmic margins, are round in shape, and have a round nucleus. Distinct cytologic characteristics of each type of round cell aid in definitive diagnosis. Tumor types include lymphoma, mast cell tumor (MCT), transmissible venereal tumor (TVT), histiocytoma, and plasma cell tumor/multiple myeloma. Malignant melanoma is highly variable in appearance and is often classified as a round cell tumor. Each of these is discussed in greater detail in individual chapters. Round cell tumors can be either malignant (e.g., lymphoma, grade II or III mast cell tumors) or benign (histiocytoma, grade I mast cell tumor). Most primarily affect the skin (mast cell tumor, histiocytoma, plasma cell tumor, transmissible venereal tumor) and may metastasize internally. Lymphoma primarily affects lymphoid organs and less commonly affects the skin and other organ systems.
SYNONYM Discrete cell tumors
EPIDEMIOLOGY SPECIES, AGE, SEX: Dependent on tumor type
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES Lymphoma (malignant lymphoma, lymphosarcoma) is seen in dogs and cats of all ages and can affect any organ system. In dogs, the most common form involves generalized lymph node infiltration; in cats, the gastrointestinal form prevails. Mast cell tumors (mastocytomas, mast cell sarcomas) are seen in dogs and cats; most common form is skin/subcutaneous mass. In cats, a splenic or visceral form can occur. Transmissible venereal tumors (TVT) are transplanted from dog to dog by direct contact. TVT is most commonly seen in intact dogs in the genital regions and oral and nasal cavities. Histiocytomas are most commonly seen in young dogs (1 week) +/− Ipsilateral Horner's syndrome (T1-T3) +/− Ipsilateral cutaneous trunci deficit (C8, T1) Paraspinal pain, resistance to cervical manipulation Axillary or inguinal pain Palpable axillary mass (uncommon) Paraparesis, hemiparesis, or tetraparesis if involvement of the spinal cord Evidence of external trauma
ETIOLOGY AND PATHOPHYSIOLOGY Lateralized or foraminal intervertebral disk extrusion Neoplasia (peripheral nerve sheath tumors, lymphoma, primary neural tumors, metastatic) Trauma Degenerative lumbosacral stenosis Discospondylitis
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Root Signature (Nerve)
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Summary: clinical signs result from a sensory disturbance within the dorsal root or spinal nerve, typically by compression. The spinal cord may be affected in all cases, causing long tract signs (e.g., gait deficit distal to the lesion). The dorsal longitudinal ligament of the vertebral column is thicker in the cervical region, predisposing animals to lateral disk extrusions at this site.
DIAGNOSIS DIAGNOSTIC OVERVIEW Nerve root signature is a clinical diagnosis made by distinguishing lameness due to neurogenic pain from orthopedic lameness. Paravertebral pain, muscle atrophy, and neurologic deficits and a normal orthopedic exam are all helpful in identifying nerve root signature.
DIFFERENTIAL DIAGNOSIS Orthopedic disorders Soft-tissue injury
INITIAL DATABASE Complete neurologic (see p. 1311) and orthopedic (see p. 1315) examinations Vertebral radiographs: rule out orthopedic causes, bony neoplasia, chronic diskospondylitis; may support a diagnosis of IVDD, degenerative lumbosacral stenosis, or nerve sheath neoplasm (enlarged intervertebral foramen). Many animals have orthopedic disease unrelated to the clinical signs.
ADVANCED OR CONFIRMATORY TESTING MRI is far superior to all other imaging modalities for ruling out nerve sheath neoplasia and neuritis. Myelography and epidurography: useful for IVDD, degenerative lumbosacral stenosis, nerve sheath neoplasm CT (see p. 1233) and MRI (see p. 1302): permit evaluation of the nerve roots, location of extruded disk material. Electromyography (EMG see online chapter: Electromyography and Nerve Conduction Velocity): changes are present 1 week following denervation of muscle. Cerebrospinal fluid (CSF) analysis (see p. 1228) Biopsy: allows definitive diagnosis of confirmed mass lesions; benefit must be weighed against risk of procedure. Surgical exploration
TREATMENT TREATMENT OVERVIEW Removal of the source of nerve root or spinal nerve impingement Provision of the optimal environment for nerve recovery
ACUTE GENERAL TREATMENT Dependent on underlying cause: Surgical decompression for IVDD, degenerative lumbosacral stenosis Tumor resection with or without limb amputation and laminectomy for peripheral nerve sheath neoplasm; surgical intervention should be considered early in these cases (reduce extension of tumor/spinal cord involvement). Conservative therapy: generally ineffective in relieving pain of cervical IVDD
CHRONIC TREATMENT Attempt conservative therapy (protection of the distal limb with a boot, physiotherapy) for traumatic injuries. Amputation should be delayed for 6 months if possible to allow for reinnervation. Radiation therapy: nerve sheath tumors Lifelong exercise modification: IVDD Physiotherapy: if trauma has compromised limb use
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Root Signature (Nerve)
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POSSIBLE COMPLICATIONS Persistent or progressive clinical signs Recurrence or acute progression of clinical signs (IVDD) Self-mutilation associated with dysesthesia Distal limb trauma associated with decreased sensation and normal activity Surgical complications
RECOMMENDED MONITORING Follow-up exam and serial diagnostic studies as directed by the animal's clinical progression
PROGNOSIS AND OUTCOME Dependent on underlying cause: Good to excellent (according to clinical signs) with IVDD treated with decompression Fair to good (according to clinical signs) with degenerative lumbosacral stenosis Guarded to fair with traumatic injury Poor with nerve sheath neoplasia
PEARLS & CONSIDERATIONS COMMENTS It can be difficult to distinguish orthopedic from neurologic causes for clinical signs, and both may be present with traumatic injury. Careful examination with particular attention to muscle tone and sensory deficits is important. A ruptured cranial cruciate ligament is often mistaken for a lumbar nerve root signature and vice versa. Nerve sheath neoplasms are most common in the cervical intumescence (80%).
CLIENT EDUCATION Monitor for recurrence of clinical signs
SUGGESTED READING McDonnell J: Neurologic conditions causing lameness in companion animals. Vet Clin North Am Small Anim Pract31120011738 AUTHOR: GREGKILBURN EDITOR: ETIENNECÔTÉ
26-09-2011 23:01
Rocky Mountain Spotted Fever
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Rocky Mountain Spotted Fever BASIC INFORMATION DEFINITION An acute, potentially life-threatening tickborne rickettsial disease affecting dogs and people
EPIDEMIOLOGY SPECIES, AGE, SEX Species: dogs and people are primarily affected. Seropositive cats are not clinically ill. Age: young dogs (6 mg/dL in dogs; 5.5 mg/dL in cats): increased total serum Ca occurs in 10%-20% of dogs and cats with CKD before treatment; Cai may be increased, normal, or low. Hypercalcemia is dangerous only when Cai is increased. When Ca is increased: Change calcitriol supplementation from once daily administration to giving twice the dose every other day, or decrease the daily dose by 50% to decrease Ca absorption from the intestine. If serum phosphorus is too low with phosphate restricted diets, increase the animal's dietary phosphorus intake. Change to a class of non-calcium containing intestinal phosphate binder if hypercalcemia develops while the animal is receiving calcium salt phosphate binders, or decrease the daily dose by 50%.
RECOMMENDED MONITORING Measure PTH and Cai (from the same sample) after 1, 3, and 6 months of therapy to determine initial and subsequent adequacy of RSHP control and twice yearly thereafter for stable animals. Modify extent of dietary phosphorus restriction, dosage, and types of intestinal phosphorus binders and changes in calcitriol dose on PTH and Cai results. Measure serum phosphorus to ensure control of hyperphosphatemia. Refer animals with persistently increased Cai for evaluation of primary or tertiary hyperparathyroidism. Monitor the animal's CKD as needed.
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Renal Secondary Hyperparathyroidism
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PROGNOSIS AND OUTCOME Days to weeks of survival if CKD is severe and renal secondary hyperparathyroidism cannot be controlled Months to years of survival is possible but guarded to poor for animals with CKD and uncontrolled RSHP. Long-term survival in cats with treatment of CKD is far more common than in dogs. Worse for animals with uncontrollable hyperphosphatemia Survival increases with appropriate PTH-lowering therapy.
PEARLS & CONSIDERATIONS COMMENTS Nearly impossible to lower PTH if serum P > 6 mg/dL Reference ranges for serum phosphorus levels often include results from growing animals, which are much higher than for adult animals. The goal for serum phosphorus during CKD is 4 mg/dL (midrange to lower half of reference range) versus the upper limit of many reference ranges for adults ( dogs) and accelerates gastric emptying. This drug can be difficult to obtain.
POSSIBLE COMPLICATIONS Aspiration pneumonia Esophageal rupture due to foreign bodies Esophageal stricture formation Esophageal reflux
RECOMMENDED MONITORING Check for resolution of clinical signs for animals whose causes were systemic. Regularly check thoracic radiographs for signs of aspiration pneumonia.
PROGNOSIS AND OUTCOME Depend greatly on the cause of the regurgitation and presence or absence of complications
PEARLS & CONSIDERATIONS COMMENTS Clinicians should make sure the animal is regurgitating and not vomiting. Aspiration pneumonia often does not increase the white blood cell (WBC) count, even if extensive.
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Regurgitation
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CLIENT EDUCATION The owner should be aware of the clinical signs of aspiration pneumonia and seek immediate veterinary attention if they occur.
SUGGESTED READING Woolley CS: Dysphagia and regurgitation. In Ettinger SJ, editor: Textbook of veterinary internal medicine, Philadelphia, 2010, WB Saunders, pp 191–195. AUTHOR: NINETTE KELLER EDITOR: ETIENNE CÔTÉ
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Reflex Dyssynergia
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Reflex Dyssynergia BASIC INFORMATION DEFINITION Upper motor neuron (UMN) dysfunction preventing coordinated urinary bladder contraction and urethral sphincter relaxation during micturition. Sacral spinal cord lesions, diseases associated with the urethra, and an idiopathic condition can each mimic reflex dyssynergia.
SYNONYMS Detrusor-sphincter dyssynergia, detrusor-sphincter incoordination, functional urethral obstruction, UMN bladder
EPIDEMIOLOGY SPECIES, AGE, SEX: Affects dogs and cats of any age, depending on causation. More often observed in male dogs; an idiopathic dyssynergia-like condition affects predominantly large-breed male dogs. RISK FACTORS Thoracolumbar spinal cord injury/disease Dyssynergia-like condition: Following relief of urethral obstruction Sacral spinal cord injury/disease ASSOCIATED CONDITIONS & DISORDERS Bladder atony/hypotonia Urinary tract infection
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES True reflex dyssynergia: neurogenic suprasacral lesions Dyssynergia-like conditions: neurogenic and non-neurogenic disorders HISTORY, CHIEF COMPLAINT Frequent attempts at voiding with inability to empty bladder completely are characteristic. Normal initiation of voiding with interruption of urine stream; short spurts of urine followed by cessation of urine flow. Animal may strain with no urine produced. PHYSICAL EXAM FINDINGS Manual bladder expression difficult Clinicians should palpate the bladder before and after voiding: turgid, incomplete emptying of bladder, increased residual urine volume are expected. Perineal reflex is present or exaggerated. Neurologic dysfunction unrelated to urination may be present. Rectal and vaginal examinations are indicated to assess structural causes (e.g., sacral vertebral lesion) versus other causes of dysuria (e.g., urethral lith or mass). Anal tone is normal/good. Observation of urination: thin, interrupted urine stream
ETIOLOGY AND PATHOPHYSIOLOGY Disordered urinary retention resulting from central nervous system (CNS) lesion located between the pontine micturition center and the sacral spinal cord (suprasacral spinal cord: L7 to brainstem)
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Reflex Dyssynergia
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UMN lesion causes a loss of inhibitory pathways: To sympathetic innervation of the internal urethral sphincter (smooth muscle) To somatic innervation (pudendal nerve) of the external urethral sphincter (striated muscle) Additional factors include increased sensory input (sacral nerves), increased sympathetic output, and bladder neck hypertrophy. Neurogenic dyssynergia-like conditions occur when pelvic nerve damage results in weakened detrusor contraction that cannot override urethral sphincter tone. In animals with non-neurogenic dyssynergia-like conditions, there is a similar failure of simultaneous relaxation of the internal or external urethral sphincter with detrusor contraction. This may be idiopathic or may follow irritation/disease of the urethra.
REFLEX DYSSYNERGIA Neurologic pathways to and from the urinary bladder.
DIAGNOSIS DIAGNOSTIC OVERVIEW A diagnosis of primary reflex dyssynergia is made by exclusion of other conditions that mimic signs. The diagnostic plan should include eliminating conditions that cause mechanical (anatomic) obstruction of the urethra. The physical and neurologic examinations can define an anatomic or neurologic differential.
DIFFERENTIAL DIAGNOSIS Anatomic urethral obstruction: Intraluminal (e.g., urethral plug/lith, transitional cell carcinoma, urethritis) Extraluminal (e.g., prostatomegaly, pelvic granuloma) Functional urethral obstruction (dyssynergia-like conditions): Neurogenic: Sacral spinal cord disease Pelvic plexus injury Cauda equina disease Non-neurogenic: Idiopathic Following relief of urethral obstruction Secondary urinary tract infection Bladder neck obstruction a-Adrenergic agonist administration (e.g., phenylpropanolamine, pseudoephedrine) Myopathic disease Bladder wall atony (see p. 104)
INITIAL DATABASE
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Reflex Dyssynergia
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Urethral catheterization: unobstructed. Residual urine volume increased (normal, 0.2-0.4 mL/kg in dogs; or 125 mEq/L, water intake may be restricted to a volume less than urine output to promote free water loss and restore normal body fluid volume.
CHRONIC TREATMENT Chronic management of SIADH is directed at treating the underlying cause. A selective ADH receptor antagonist, OPC-31260 (Otsuka Pharmaceutical, Tokyo), has been reported to palliate signs in a dog with SIADH over a 3-year treatment period (3 mg/kg PO q 12 h). Other antidiuretic hormone receptor antagonists (e.g., tolvaptan, conivaptan) are available for human patients, but their use in dogs with clinical hyponatremia remains poorly described (novel treatment).
POSSIBLE COMPLICATIONS Rapid correction of chronic hyponatremia can result in osmotic demyelination syndrome due to brain dehydration as free water moves out of the brain and into the relatively hypertonic serum (see 1402). Clinical signs of osmotic demyelination syndrome occur 3-4 days after rapid correction of hyponatremia, are neurologic in nature (lethargy, ataxia, hypermetria, paresis), and may be fatal.
RECOMMENDED MONITORING Serial (q 4 h) monitoring of serum sodium concentration during acute correction phase and periodic monitoring during chronic management
PROGNOSIS AND OUTCOME Prognosis is dependent on the underlying cause of SIADH.
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Syndrome of Inappropriate Antidiuretic Hormone Secretion
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PEARLS & CONSIDERATIONS COMMENTS ADH release may be stimulated by various drugs used during anesthesia (barbiturates, narcotics) and can result in impaired free water excretion and hyponatremia in the postoperative period, similar to what is seen in animals with SIADH. Restriction of water intake is generally sufficient to restore normal water balance in these animals. During treatment, never increase serum sodium concentration by more than 0.5 mEq/L/h (risk of osmotic demyelination syndrome and life-threatening cerebral complications).
SUGGESTED READING DiBartola SP: Disorders of sodium and water. In DiBartola SP, editor: Fluid therapy in small animal practice, ed 2, Philadelphia, 2000, WB Saunders, pp 64–65. Feldman EC, Nelson RW: Water metabolism and diabetes insipidus. In Feldman EC, Nelson RW, editors: Canine and feline endocrinology and reproduction, ed 3, St Louis, 2004, WB Saunders, pp 41–42. AUTHOR: SARAH L. NAIDOO EDITOR: SHERRI IHLE
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Syncope
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Syncope BASIC INFORMATION DEFINITION A sudden and transient loss of consciousness resulting in collapse, followed by spontaneous recovery. The cause is a transient cerebral deficiency of oxygen.
SYNONYMS Faint, collapse Neurocardiogenic syncope: vasovagal syncope Tussive syncope: “cough-drop” phenomenon
EPIDEMIOLOGY SPECIES, AGE, SEX: Dependent on underlying cause: cardiac versus noncardiac causes. Acquired heart disease: middle-aged to older animals; congenital heart disease: young animals. GENETICS & BREED PREDISPOSITION Tussive syncope (older small-breed dogs with pulmonary disease) Neurocardiogenic syncope (boxer, golden retrievers, brachycephalic breeds?) According to underlying heart disease (many breed predilections) RISK FACTORS Autonomic dysfunction (neurocardiogenic syncope) Drugs: -blockers, diuretics, vasodilators (hypotensive syncope)
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT Acute collapse, with altered or loss of consciousness Either no clinical signs or staggering or ataxia prior to the event Exercise, excitement, or coughing may precipitate the event. ± Clonic movements ± Involuntary urination or defecation No postictal phase Duration: seconds (and virtually always < 1 minute; otherwise, likely to be fatal) Recovery: complete and rapid PHYSICAL EXAM FINDINGS: Dependent on underlying disorder(s): Cardiac: ± Murmur ± Arrhythmia ± Altered arterial pulse quality ± Pulse deficits ± Cyanotic mucous membranes ± Pulmonary rales or crackles Neurologic exam (see p. 1311): ± Cranial nerve abnormalities ± Altered reflexes ± Proprioceptive deficits ± Altered mentation Upper airway exam:
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Syncope
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± Brachycephalic syndrome (i.e., stenotic nares, hypoplastic trachea, everted laryngeal saccules, elongated soft palate)
ETIOLOGY AND PATHOPHYSIOLOGY Cardiac: Bradyarrhythmias: syncope can result when there is a >6-8 second pause in electrical activity (i.e., failure of subsidiary pacemaker in third-degree atrioventricular [AV] block, sinus arrest associated with sick sinus syndrome [SSS]). Tachyarrhythmias: rates > 300 bpm for >6 seconds (i.e., supraventricular tachycardia [SVT] or ventricular tachycardia) in dogs; cats uncommonly experience syncope with tachyanhythmias but more so with bradycardias. Heart rate and time necessary for syncope may vary depending on underlying cardiac structure (i.e., a slower heart rate for a shorter duration may cause syncope in an animal with underlying myocardial or valvular heart disease). Various outcomes: nonsustained tachyarrhythmia results in a return to sinus rhythm; overdrive suppression leads to sinus arrest or possibly ventricular fibrillation. Outflow obstruction (i.e., pulmonic stenosis, subaortic stenosis, cor pulmonale due to heartworm disease with secondary pulmonary hypertension): Classic theory: exercise results in vasodilation of systemic arterioles. Fixed obstruction to flow results in inadequate increase in cardiac output, leading to hypotension and syncope. Alternate theory: contractility, cardiac output, and flow increase through stenosis during exercise. Increased left ventricular systolic pressure causes overstimulation of left ventricular mechanoreceptors. Reflex activation of cardiac afferent vagal fibers results in increased parasympathetic tone to heart and systemic blood vessels, resulting in bradycardia, vasodilation, and subsequent syncope. Cyanotic heart disease: (i.e., right-to-left patent ductus arteriosus, tetralogy of Fallot): syncope is due to hypoxemia and/or hyperviscosity of blood from polycythemia, or else is from arrhythmias. Masses obstructing inflow or outflow of blood (rare): intracardiac mass lesions reduce cardiac output by restricting blood flow through atrioventricular valves or obstructing a ventricular outflow tract. Pericardial disease compromises cardiac output by interfering with systemic venous return (i.e., cardiac tamponade). Congestive heart failure: syncope mechanism presumed to be similar to autonomic dysfunction (see below). Noncardiac: Neurologic syncope: increased intracranial pressure with resultant decrease in cerebral perfusion (i.e., cerebral edema, brain tumors, meningitis, encephalitis, cerebral vascular obstructions, acute bleed). Syncope occurs very rarely, in contrast to seizures, with these diseases. Metabolic syncope: abrupt decrease in oxygen or nutrient delivery (i.e., glucose) to the brain (oxygen concentration is affected by blood flow, hemoglobin concentration, and oxygen tension). Seizures > syncope. Tussive syncope: proposed mechanisms: Increased intrathoracic pressure transiently increases intracranial pressure and diminishes cardiac venous return and resultant cardiac output; cerebral blood flow is decreased during paroxysms of coughing. Coughing stimulates vagal afferent transmission to the vasomotor center in the medulla, with subsequent stimulation of vagal efferente to the heart and blood vessels (bradycardia, hypotension). Autonomic dysfunction: excessive baroreflex resulting in cardiac inhibition and/or peripheral vasodilation (i.e., neurocardiogenic syncope, carotid sinus sensitivity, carotid body tumor). Peripheral vasomotor dysfunction: abnormality of peripheral vasoconstriction, muscle tone, heart rate, and/or respiration, resulting in syncope (postural hypotension). Undetermined: ~40% of human syncope cases despite extensive testing; likely similar percentage in veterinary medicine
DIAGNOSIS DIAGNOSTIC OVERVIEW Diagnosis is largely based on patient signalment; historical events prior to, during, and after the episode; and complete cardiovascular and neurologic exams. Since the episode often is not witnessed directly by the veterinarian (to confirm or refute syncope), a simple test is video recording by the owner when an event occurs at home. Confirmatory testing may involve ambulatory electrocardiogram (ECG) monitoring and/or central nervous system (CNS) imaging depending on the suspected cause. Consider consultation with and/or referral to a veterinary cardiologist +/− veterinary neurologist.
DIFFERENTIAL DIAGNOSIS Primary cardiac disease (see above) Hypotension (inadequate cardiac output, poor vascular tone) Hypoxemia (pulmonary thromboembolism, pulmonary disease, right-to-left shunt)
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Syncope
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Abnormal blood or metabolic constituents (hypoglycemia, hypokalemia, anemia) Neoplasia (splenic hemangiosarcoma) Neurologic and neuromuscular disorders (epilepsy, structural central nervous system disorders, narcolepsy, myasthenia gravis)
INITIAL DATABASE CBC: ± anemia, thrombocytopenia Serum biochemistry panel: ± electrolyte abnormalities, ± metabolic derangements Urinalysis: ± proteinuria with AT III loss and subsequent hypercoagulable state (thromboembolism) Blood pressure: normal result does not rule out transient hypotension ± Heartworm antigen test ± Heartworm microfilaria test Thoracic radiographs: ± evidence of structural heart disease, ± pulmonary parenchymal abnormalities (i.e., pulmonary artery abnormalities with heartworm disease, cardiogenic pulmonary edema) Echocardiogram: ± congenital or acquired heart disease Resting ECG: ± rhythm abnormalities Neurologic exam (see p. 1311): ± neurologic deficits
ADVANCED OR CONFIRMATORY TESTING Videotaping: episodes that are not convincingly syncopal based on history alone (a common problem) and do not occur in the veterinary facility may be evaluated objectively by having the owner videotape them at home. Holter monitor (see p. 1287): 24-hour ECG; helpful in establishing a diagnosis 42% of the time Cardiac event recorder: digital loop recorder that is patient or owner activated, programmed to capture the heart rate and rhythm prior to and after the syncopal episode(s); diagnostic yield 85% Abdominal ultrasound: may be helpful in identification of mass(es) CT/MRI/cerebrospinal fluid tap: neurologic disease. see pp. 1233, 1302, and 1228.
TREATMENT TREATMENT OVERVIEW Treatment involves addressing the primary etiology in order to alleviate syncopal episodes and prevent sudden death.
ACUTE GENERAL TREATMENT Acute treatment is aimed at the underlying cause or at stabilization procedures: Blood loss: fluids, blood products, etc. Pericardial effusion with cardiac tamponade: pericardiocentesis Continuous ECG Bradyarrhythmias SSS, third-degree AV block: medical management may be effective if arrhythmia is due to excessive vagal tone and atropine responsive (i.e., anticholinergics [propantheline] and -agonists [terbutaline]; see individual diseases for specific treatment recommendations). Temporary pacemaker if bradyarrhythmia is refractory to medical management and animal is showing persistent clinical signs. Tachyarrhythmias: Ventricular tachycardia: oral or intravenous medical management depending on malignancy of the arrhythmia (i.e., oral options: mexiletine, sotalol, amiodarone, atenolol; intravenous options: lidocaine, procainamide, esmolol); see p. 1165. Cautious use of or avoid -blockers in cases with systolic dysfunction/dilated cardiomyopathy.
CHRONIC TREATMENT Treatment of underlying cause if systemic disorder Bradyarrhythmias: Medically refractory SSS, high-grade second-degree AV block, third-degree AV block: permanent pacemaker Tachyarrhythmias: see p. 1165 Severe outflow obstructions: Limit exertion in all cases. Subaortic stenosis (SAS; see p. 1057): -blockers if severe Pulmonic stenosis (see p. 941): -blockers if severe
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Syncope
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Hypertrophic obstructive cardiomyopathy (see p. 565): β-blocker, calcium channel blocker Heartworm disease with secondary pulmonary hypertension (see pp. 474 and ) Cyanotic heart disease-induced polycythemia: phlebotomy, or hydroxyurea 50 mg/kg PO q 48-72 h, adjusted based on response Congestive heart failure (see p. 470) Neurologic syncope: treatment of underlying cause Metabolic syncope: treatment of underlying cause Tussive syncope: cough suppressant (e.g., butorphanol, 0.1-0.5 mg/kg PO q 8-12 h), bronchodilator (aminophylline, 10 mg/kg PO q 8 h), treatment with diuretics (e.g., furosemide, 2 mg/ kg IV, SQ) if pulmonary edema is present Autonomic dysfunction: anticholinergics (e.g., propantheline bromide, 0.5-1 mg/kg PO q 8 h if bradycardia related), -blocker (e.g., atenolol, 0.25-1 mg/kg PO q 12 h if tachycardia related). Treatment modalities are aimed at maintaining heart rate and/or preventing sympathetic surge. Medical management fails to address hypotensive component of reflex arc, and animals may continue to faint, potentially requiring a pacemaker.
BEHAVIOR/EXERCISE Limit exertion/excitement in severe outflow obstructions, cyanotic heart disease, impending/decompensated left congestive heart failure, ventricular arrhythmias, and neurocardiogenic syncope.
DRUG INTERACTIONS β-Blockers, diuretics, and vasodilators can exacerbate hypotension.
POSSIBLE COMPLICATIONS Sudden death
RECOMMENDED MONITORING Serial evaluations as needed to acquire initial database and confirmatory testing
PROGNOSIS AND OUTCOME Highly dependent on underlying etiology Excellent for bradyarrhythmias treated with pacemaker implantation Fair to good with supraventricular tachycardia responsive to medical therapy Guarded with ventricular tachycardia treated medically; poor if systolic dysfunction/dilated cardiomyopathy present Variable prognosis with outflow obstructions (i.e., severe SAS has a poor long-term prognosis). Good with tussive syncope treated medically if cough responds well to therapy Good prognosis with autonomic dysfunction. Treatment is usually unrewarding. Fortunately, sudden death is not common. Poor prognosis: neoplasia
PEARLS & CONSIDERATIONS COMMENTS Syncopal episodes may be difficult to differentiate from seizures. Video-recording and ECG event monitoring (see p. 1287) are simple, noninvasive tests that greatly help differentiate between the two. Syncope, while uncommon in cats, occasionally occurs with hypertrophic obstructive cardiomyopathy and with bradyarrhythmias (e.g., third-degree AV block). In SSS, bradyarrhythmias (e.g., sinus arrest) typically cause syncopal episodes warranting pacemaker therapy prior to addressing tachyarrhythmias (e.g., SVT; see p. 111). In 40% of human cases, an etiology is never identified; similar percentages are suspected in veterinary medicine.
PREVENTION Tussive syncope: cough suppressant, bronchodilator, treatment with diuretics if pulmonary edema is present Autonomic dysfunction: anticholinergics, β-blocker
TECHNICIAN TIPS
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Syncope
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In-house ECG telemetry is useful for identifying bradyarrhythmias and tachyarrhythmias. “Seizure bells” can be placed on hospitalized patients presenting for syncope to help alert the staff when an animal has an episode.
CLIENT EDUCATION Treatment and prognosis are dependent on the underlying etiology. Sudden death is possible but is dependent on the underlying etiology.
SUGGESTED READING Davidow EB, et al: Syncope: pathophysiology and differential diagnosis. Compend Contin Educ Pract Vet 23(7):609–618, 2001. AUTHOR: SARAH J. MILLER EDITOR: ETIENNE CÔTÉ
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Supraspinatus/Infraspinatus Tendon Disorders
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Supraspinatus/Infraspinatus Tendon Disorders BASIC INFORMATION DEFINITION Disorders of the extraarticular tendons in the shoulder area of dogs, often representing degenerative changes bilaterally
SYNONYMS Supraspinatus mineralization: calcification of supraspinatus tendon Supraspinatus tendinosis: nonmineralized tendinopathy, chronic tendinopathy, chronic tendon injury, chronic tendinitis, biceps tendon impingement, tendon enlargement
EPIDEMIOLOGY SPECIES, AGE, SEX: Medium to large-breed adult dogs of both genders GENETICS & BREED PREDISPOSITION: Supraspinatus tendon disorders have been associated with Labrador retrievers and rottweilers. Infraspinatus contracture is classically seen in hunting or working dogs. Ossification of infraspinatus tendon-bursa has only been described in Labrador retrievers.
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES Supraspinatus mineralization and tendinosis represent degenerative disorders and are likely related. Infraspinatus muscle contracture may be of traumatic origin. Ossification of the infraspinatus tendon-bursa is a recently described disorder of unknown origin. HISTORY, CHIEF COMPLAINT: Supraspinatus mineralization and tendinosis, and infraspinatus tendon-bursa ossification lead to intermittent or waxing-waning weight-bearing unilateral front limb lameness with gradual onset. Infraspinatus contracture is associated with acute onset of lameness, resolving initially but leading to a subsequent chronic lameness, with characteristic stance and gait abnormalities. PHYSICAL EXAM FINDINGS All disorders may be associated with disuse atrophy of spinatus muscles. Dogs with supraspinatus mineralization or tendinosis tend to show signs of pain on shoulder flexion. They may or may not show signs of pain on digital palpation of the supraspinatus tendon. Signs of pain are elicited by palpation of the bicipital tendon in some cases. Dogs with infraspinatus contracture, in the acute stage, may show tenderness/pain during muscle palpation. In the chronic stage, this disorder leads to a stance with the elbow adducted and the foot abducted. During the stride, the distal limb circumducts in a lateral arc. There is atrophy of the infraspinatus muscle, and the limb is permanently supinated. In lateral recumbency with the affected side up, the dog may be unable to rest the distal limb on the floor/table. Pain is usually not evident in the chronic stage. Infraspinatus tendon-bursa ossification is associated with pain on direct digital pressure over the tendon insertion in half of affected individuals.
ETIOLOGY AND PATHOPHYSIOLOGY Supraspinatus mineralization and tendinosis are probably overuse syndromes and are localized in the avascular zone of the tendon, an area predisposed to poor healing. These two conditions have very similar histopathologic features and may both represent chronic tendon injury. Supraspinatus disorders lead to swelling and increased mass of the tendon insertion, which may cause pressure and impingement/displacement of the underlying bicipital tendon. Infraspinatus contracture may be a result of traumatic incomplete rupture of the muscle, which becomes replaced with fibrotic tissue. Ossification of the infraspinatus tendon of insertion may coincide with ossification (osteochondromatosis) of the bursa, or each condition can occur alone. A degenerative cause is suspected.
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Supraspinatus/Infraspinatus Tendon Disorders
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DIAGNOSIS DIAGNOSTIC OVERVIEW Infraspinatus contracture in the chronic stage may be diagnosed with physical examination. Supraspinatus mineralization and ossification of infraspinatus tendon-bursa require radiographic examination. Supraspinatus tendinosis is not evident on radiographic examination and requires advanced imaging. Supraspinatus mineralization and ossification of the infraspinatus tendon-bursa may be coincidental, and other reasons for lameness must be ruled out before pursuing treatment.
DIFFERENTIAL DIAGNOSIS Bicipital tenosynovitis, with or without tendon mineralization Osteoarthritis of the glenohumeral joint Shoulder instability/luxation Elbow dysplasia Osteosarcoma of the proximal humerus Nerve sheath tumor (especially prior to onset of neurologic dysfunction)
INITIAL DATABASE Orthopedic and neurologic evaluations Radiography of the scapulohumeral joint; lateral, craniocaudal, and cranioproximal-craniodistal views—the latter for supraspinatus/biceps tendon imaging. Supraspinatus mineralization is located craniomedial to the greater tubercle but not centered within the intertubercular groove. CBC, serum biochemistry panel, urinalysis: in older dogs
SUPRASPINATUS/INFRASPINATUS TENDON DISORDERS Radiographic skyline view. Supraspinatus mineralization is evident medial to the greater tubercle (arrow). GT, Greater tubercle; LT, lesser tubercle.
ADVANCED OR CONFIRMATORY TESTING Localization of pain involves applying digital pressure to the insertion of the supraspinatus tendon (craniomedial greater tubercle of humerus), the bicipital tendon (intertubercular groove), and infraspinatus tendon of insertion (lateral and distal to greater tubercle). Note that these disorders inconsistently result in pain on direct palpation of the structures. MRI of the shoulder joint is an excellent imaging modality in these disorders and many of their differential diagnoses. Ultrasonographic examination of the cranial shoulder area may identify the increased tendon mass of supraspinatus, tendinosis, mineralization/ossification of supra- or infraspinatus tendons, and may identify differential or coinciding diagnoses such as bicipital tenosynovitis. Arthroscopic examination of the shoulder joint further identifies differential or coinciding disorders.
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Supraspinatus/Infraspinatus Tendon Disorders
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TREATMENT TREATMENT OVERVIEW Surgical treatment is usually indicated if lameness is refractory to rest and antiinflammatory medication. With infraspinatus contracture, the goal is return to full function of the affected limb.
ACUTE GENERAL TREATMENT Supraspinatus tendinopathies usually do not respond to nonsteroidal antiinflammatory drug (NSAID) treatment, and corticosteroid injections are likely contraindicated. Extracorporeal shockwave therapy has led to improvement in a few dogs with supraspinatus mineralization. If acute infraspinatus trauma is suspected, early fasciotomy may be indicated to decompress the muscle and avoid compartment syndrome. However, the acute phase is often not identified, owing to the spontaneous recovery of the initial lameness. Seven of 13 dogs with ossification of the infraspinatus tendon-bursa improved after injection of long-acting corticosteroid (methylprednisolone acetate, 20 mg/mL, 1-2 mL IA once or twice, 3 weeks apart) into the glenohumeral joint, or NSAID treatment. One case improved after 4 months of restricted activity only. Medical management should be attempted prior to considering surgery.
CHRONIC TREATMENT Surgery for supraspinatus mineralization entails longitudinal tendon incisions to evacuate the mineralized deposits. Surgery for supraspinatus tendinosis has only been reported in a few cases, but good to excellent results have been achieved by resection of the mass in the tendon insertion and thus decompression of the bicipital tendon. Arthroscopic examination of the shoulder joint in the same session is usually indicated to rule out other intraarticular coinciding or differential disorders. Degenerative tendon disorders in people may be treated with rest alone for 6 months or more, and some human studies show similar outcomes of long-term rest as in surgically treated cases. Infraspinatus contracture treatment consists of tenotomy and excision of the tendon insertion. Immediate ability to pronate the limb is achieved. Leash walks are performed immediately postoperatively, and normal activity is resumed 10-14 days after infraspinatus tenotomy. Ossification of infraspinatus tendon-bursa in cases refractory to medical management have been treated by excision of ossified masses, leading to improvement in 4/6 cases.
SUPRASPINATUS/INFRASPINATUS TENDON DISORDERS Transverse magnetic resonance mage (MRI) through proximal humerus in a dog with supraspinatus tendinosis. An increased mass of high signal intensity is located within the insertion of the supraspinatus tendon, craniomedially on the greater tubercle (arrowheads). Biceps tendon is visible medially in intertubercular groove (arrow).
NUTRITION/DIET
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Dietary management to prevent or treat obesity is likely beneficial for long-term management.
BEHAVIOR/EXERCISE Exercise is restricted for 2-4 weeks after supraspinatus surgery. Physical therapy with passive range-of-motion exercises and walking are recommended as soon as possible after surgery. However, swimming may not be indicated, as it has been suggested to put increased strain on the supraspinatus tendon. Swimming or other vigorous exercise should be avoided until 8-12 weeks after supraspinatus surgery. Supraspinatus disorders may be caused by overuse. Excessive high-impact activities may have to be discontinued. Jumping and digging have been proposed to result in increased supraspinatus strain. After supraspinatus healing is complete, consistent daily low-impact physical activity (walking, swimming, running on soft surfaces) is recommended. Surgical treatment for infraspinatus contracture usually returns the dog to full function.
POSSIBLE COMPLICATIONS Seroma Infection Unresolving lameness, reflecting a degenerative process such as mineralization, may be an incidental finding.
PROGNOSIS AND OUTCOME Dogs with supraspinatus mineralization have shown good to excellent outcome (mild intermittent lameness to normal function) in 80%–90% of operated cases and in all of 3 cases treated conservatively (rest and NSAIDs). Extracorporeal Shockwave therapy resolved lameness in 2 dogs reexamined at 20 and 49 days, respectively. Surgical treatment of supraspinatus tendinosis has shown good to excellent outcome in 7/8 cases. Surgical treatment of infraspinatus contracture usually leads to en excellent outcome. Though 12/13 dogs with ossification of infraspinatus tendon-bursa improved with medical and/or surgical treatment, the majority continued to show a mild lameness.
PEARLS & CONSIDERATIONS COMMENTS Supraspinatus mineralization and tendinosis may lead to increased pressure on the bicipital tendon and have been associated with bicipital tenosynovitis. Deeply positioned supraspinatus mineralizations may be more prone to cause clinical signs than superficial ones because of increased interference with the biceps tendon. None of the tendon disorders have an inflammatory background, and antiinflammatory treatment with corticosteroids is dubious and potentially harmful. However, clinical response has been noted with glenohumeral joint injection of corticosteroids in ossification of infraspinatus tendon-bursa. Never inject corticosteroids into a joint if the synovial fluid is discolored, cloudy, or has decreased viscosity. Do not inject corticosteroids into a tendon, because it severely impairs tendon healing. Long-term rest alone (>6 months) and other physical therapy modalities such as eccentric loading may be effective treatments for degenerative tendinopathy but have not been evaluated in veterinary medicine.
SUGGESTED READING Fransson BA: Treatment of supraspinatus tendon disorders in dogs. In Bonagura JD, Twedt DC, editors: Kirk’s current veterinary therapy, ed 14, St Louis, 2009, Saunders Elsevier, pp 1117–1120. AUTHOR: BOEL A. FRANSSON EDITOR: JOSEPH HARARI
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Superficial Necrolytic Dermatitis
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Superficial Necrolytic Dermatitis BASIC INFORMATION DEFINITION A progressively debilitating skin disease associated with a severe internal disease process
SYNONYMS Hepatocutaneous syndrome, glucagonoma syndrome, metabolic epidermal necrosis, necrolytic migratory erythema, diabetic dermatopathy
EPIDEMIOLOGY SPECIES, AGE, SEX Uncommon in dogs, rare in cats Middle-aged to geriatric patients; no sex predilection GENETICS & BREED PREDISPOSITION: Cocker spaniel, Shetland sheepdog, West Highland white terrier, and Scottish temer RISK FACTORS: Administration of phenobarbital. Ingestion of mycotoxin. ASSOCIATED CONDITIONS & DISORDERS: Most cases have been associated with hepatopathy, which explains the former name, hepatocutaneous syndrome. A few cases have been associated with a functional pancreatic α-cell glucagon secreting tumor (also known as glucagonoma syndrome). Other associated conditions in dogs include cirrhosing or fibrosing hepatopathy (see p. 212), idiopathic vacuolar hepatopathy (see p. 1153), diabetes mellitus (see p. 1547), extrapancreatic glucagonoma (liver, spleen, adrenal glands and mesenteric lymph nodes), copper storage disease, hyperglucagonemia. Associated diseases in cats include pancreatic carcinoma, hepatopathies, and thymic amyloidosis. CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT: Owners usually observe footpad lesions first, as dermatologie changes may precede onset of clinical signs of internal disease. Lethargy, anorexia, weight loss, lameness, reluctance to walk/signs of pedal pain, and pruritus are frequently reported. Other chief complaints may include polyuria and polydipsia. Dermatitis may wax and wane. PHYSICAL EXAM FINDINGS: Dermatologie lesions are characterized by thickening, Assuring, and crusting of footpads, and interdigital erythema. Crusts, erosions, and ulcers can affect pinnae, mucocutaneous junctions (oral cavity, eyes, anus and genitalia), elbows and other pressure points, ventral abdominal and inguinal regions. Regional lymphadenopathy and hyperthermia are possible.
ETIOLOGY AND PATHOPHYSIOLOGY A proposed mechanism: glucagonemia-induced glycogenesis from amino acids or increased hepatic catabolism of amino acids results in low plasma amino acid concentration and epidermal cellular starvation (i.e., keratinocyte degeneration, necrosis, and epidermal edema). Deficiencies of essential fatty acids, zinc, and biotin and hypoalbuminemia may also be involved.
DIAGNOSIS DIAGNOSTIC OVERVIEW The diagnosis of SND is initially suspected on physical exam of the skin (especially footpads), hepatic ultrasonographic findings, or a combination of both. No single test result is pathognomonic for SND; a conclusive clinical diagnosis is reached with histopathologic analysis of skin biopsies and hepatic ultrasonographic findings, and is further solidified if a commonly associated disorder (see above) is present. If serum levels of liver enzymes/bile acids are normal, and the liver does not show the typical ultrasonographic pattern but typical dermatohistopathologic findings are present, consider glucagonoma as the primary cause.
DIFFERENTIAL DIAGNOSIS
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Autoimmune/immune mediated causes: pemphigus foliaceus, drug-induced pemphigus, systemic lupus erythematosus, paraneoplastic pemphigus, cutaneous vasculitis, erythema multiforme, toxic epidermal necrolysis Infectious causes: bacterial (pyoderma), fungal (dermatophytosis, Malassezia dermatitis), protozoal (leishmaniasis) Parasitic causes: demodicosis Nutritional causes: zinc-responsive dermatosis Neoplastic causes: epitheliotropic lymphoma Idiopathic: nasodigital hyperkeratosis
INITIAL DATABASE The minimal dermatologic database includes deep skin scrapings (typically negative, although secondary demodicosis may occur), cytologic evaluation of the skin (patients often have a bacterial or Malassezia overgrowth) +/− dermatophyte culture (typically negative). The minimal clinicopathologic database includes a CBC (nonregenerative anemia, leukocytosis are possible), serum biochemistry profile (elevated alkaline phosphatase, alanine aminotransferase, serum glucose and fructosamine levels; hypoalbuminemia; decreased blood urea nitrogen) and urinalysis (glucosuria).
ADVANCED OR CONFIRMATORY TESTING Abdominal ultrasonography: Ultrasonographic hepatic findings are characterized by hypoechoic nodules with a hyperechoic trabecular network throughout the liver, resulting in a “honeycomb” or “Swiss cheese” pattern of the hepatic parenchyma. Occasionally hepatic metastases are detected. Ultrasonographic detection of pancreatic and extrapancreatic glucagonomas can be difficult. Histopathology and immunohistochemistry: Skin biopsy: epidermis has a “French or Dutch flag” (i.e., red-white-blue layers) appearance: Upper layer (stratum corneum): parakeratotic hyperkeratosis staining red (eosinophilic); crusts Middle layer (stratum spinosum): intracellular edema, vacuolation, and necrosis of the keratinocytes staining white (pallor) Deep layer (stratum basale): hyperplasia staining blue (basophilic) Ultrasound-guided hepatic biopsy (first perform platelet count, arterial blood pressure, and coagulation panel to assess bleeding risk). Hepatic neoplasia or idiopathic vacuolar hepatopathy (characterized by nodular hyperplasia and hepatocyte vacuolar degeneration adjacent to areas of parenchymal collapse). Immunohistochemistry can demonstrate antiglucagon antibody-positive neoplastic cells on samples obtained from pancreas, liver, spleen, adrenal glands, and mesenteric lymph nodes by ultrasound-guided biopsy, exploratory laparotomy, or postmortem. Other assays: Fasting and postprandial bile acid values are frequently elevated (nonspecific). Complete plasma amino acids (hypoaminoacidemia supportive of diagnosis of SND) testing is available at Amino Acid Analysis Laboratory Service (University of California, Davis). Contact laboratory for sample handling and cost (www.vetmed.ucdavis.edu/vmb/aal/aal.html). Because of their lack of specificity, usefulness of plasma glucagon (hyperglucagonemia) and serum insulin (hyperinsulinemia) testing is limited.
TREATMENT TREATMENT OVERVIEW Treatment consists of a threefold approach: supportive therapy for the dermatologic manifestations, management of internal disease process (which may require hospitalization), and surgical removal of neoplasm whenever possible.
ACUTE GENERAL TREATMENT Pain management Treat secondary bacterial and fungal infections with appropriate therapy (avoid systemic azole antifungal therapy because of potential hepatotoxicosis). Gentle shampoo therapy
CHRONIC TREATMENT Slow intravenous amino acid infusions: 25 mL/kg over 6-8 hours. Repeat every 7-14 days based on response. Some dermatologists recommend 3 treatments the first week, followed by once or twice weekly thereafter. Most patients will demonstrate clinical improvement within 5-10 days.
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10% crystalline amino acid crystalline solution (Aminosyn [Abbott Laboratories]) is product of choice. Because of the high osmolality of this solution, a central (jugular) venous catheter is recommended to reduce risk of thrombophlebitis. 3% amino-acid and electrolyte solution (ProcalAmine [B. Braun]) is an alternative product. Lower cost and lesser hypertonicity (can therefore be injected in peripheral veins). Insulin therapy if indicated Somatostatin analog, octreotide (inhibits glucagon release), 2 mcg/kg SQ q 12 h, can improve skin lesions and systemic signs in patients with nonresectable or relapsing glucagonoma-associated disease. Anorexia is a likely side effect.
NUTRITION/DIET High-quality, high-protein diet. Adding 3-6 entire hard-boiled eggs or egg whites per day to the diet may be beneficial. Vitamin E supplementation, 400 IU q 12 h PO Oral essential fatty acid and zinc methionine supplementation (Zinpro), 1.5 mg/kg q 24 h PO Oral nutraceutical S-adenosylmethionine, 18-22 mg/kg PO q 24 h (SAMe, Denosyl SD-4, Zentonil, S-Adenosyl) can attenuate liver damage.
DRUG INTERACTIONS Using antiinflammatory doses of oral glucocorticosteroids is controversial. It may give temporary relief, but diabetes and deterioration of the liver are possible complications.
POSSIBLE COMPLICATIONS Discomfort experienced while walking may become sufficiently severe to constitute a reason for euthanasia. Monitor for signs of encephalopathy (slow down infusion rate if indicated) when using intravenous amino acid infusions. Postsurgical pancreatitis and biliary obstruction may occur.
PROGNOSIS AND OUTCOME SND in dogs: guarded to poor, even in dogs with a history of phenobarbital administration, and despite drug discontinuation. Glucagonoma syndrome in dogs: good. Surgical excision of pancreatic tumor may result in remission. SND in cats: poor
PEARLS & CONSIDERATIONS TECHNICIAN TIP The pododermatitis associated with SND may be extremely painful. Use care and a gentle approach when walking dogs suspected or confirmed of having SND (may be reluctant to walk owing to intense foot pain; do not misinterpret this as “stubbornness”).
SUGGESTED READING Byrne KP: Metabolic epidermal necrosis: hepatocutaneous syndrome. Vet Clin North Am Small Anim Pract 29:1337, 1999. March PA, et al: Superficial necrolytic dermatitis in 11 dogs with a history of phenobarbital administration (1995-2002). J Vet Intern Med 18:65, 2004. AUTHOR: VINCENT DEFALQUE EDITOR: MANON PARADIS
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Subinvolution of Placental Sites
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Subinvolution of Placental Sites BASIC INFORMATION DEFINITION Delay of the normal uterine involution process in the bitch beyond 12 weeks after whelping, manifesting as persistent bloody vaginal/vulvar discharge in a dog that is otherwise well
SYNONYMS SIPS, metrorrhagia (uterine bleeding) postpartum, placentitis postpartum
EPIDEMIOLOGY SPECIES, AGE, SEX Not often observed clinically; however, histopathologic prevalence is 8%–21%. Young bitches < 3 years old; no effect of litter size RISK FACTORS: Low parity (especially in first pregnancy/litter) ASSOCIATED CONDITIONS & DISORDERS: Anemia, postpartum metritis, and uterine rupture could occur as a result of subinvolution of placental sites but are very rare sequelae.
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT History of recent whelping Likely primiparous bitch (first litter) Hemorrhagic vaginal/vulvar discharge persistent even after pups are weaned Persistent postparturient serosanguineous vaginal/vulvar discharge Bitch is otherwise in good health. PHYSICAL EXAM FINDINGS Discharge is red rather than normal brown lochia. Slight pallor of mucous membranes if discharge is copious Abdominal palpation: discrete uterine swellings of various sizes often felt on palpation Physical exam generally reveals an otherwise healthy animal.
ETIOLOGY AND PATHOPHYSIOLOGY Normally, expulsion of the fetal membranes and lochia takes place in the immediate postpartum period, and a mild serosanguineous discharge may last 3-5 weeks after parturition. With SIPS, the endometrium and myometrium are invaded by placental cells (trophoblasts). Failure of these cells to regress prevents normal involution, which then results in chronic hemorrhagic vaginal/vulvar discharge in a bitch that usually has no other clinical signs. Severe metrorrhagia is rare in absence of coagulopathy or uterine laceration.
DIAGNOSIS DIAGNOSTIC OVERVIEW The diagnosis is often presumptive (history and physical exam). Typically primiparous younger bitches with a range of hemorrhagic vaginal discharge: from a few drops of blood passing from the vulva for several weeks postpartum that usually subside without therapy, to acute life-threatening metrorrhagia requiring transfusion.
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DIFFERENTIAL DIAGNOSIS Proestrus Metritis Cystic endometrial hyperplasia/pyometra Vaginitis Vulvar, vaginal, or uterine tumor Urinary tract hemorrhage (e.g., bacterial cystitis, calculi) Coagulopathy Brucellosis Trauma
INITIAL DATABASE CBC: unremarkable. Note: mild normocytic, normochromic anemia is normal in postpartum bitches. Serum biochemistry profile: unremarkable Vaginal cytologic examination showing trophoblasts
ADVANCED OR CONFIRMATORY TESTING Definitive diagnosis: histologic examination based on biopsy specimen of placental sites (rarely done) Vaginoscopy (see p. 1361): to distinguish vaginal bleeding from blood derived from the uterus Abdominal ultrasound: focal thickenings of the uterine wall and a fluid-distended lumen; color Doppler velocity measurements of blood flow differentiates SIPS from normally involuting uteruses. Abdominal radiographs: focal areas of uterine irregularity
SUBINVOLUTION OF PLACENTAL SITES Vaginoscopic view of the cranial vagina from a bitch with subinvolution of placental sites (SIPS), showing bloody discharge originating from the uterus. (Courtesy Auke C. Schaefers-Okkens.)
TREATMENT TREATMENT OVERVIEW Often, spontaneous remission occurs without the need for medical or surgical intervention. Ovariohysterectomy (OHE) is required in
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acute cases with severe metrorrhagia.
ACUTE GENERAL TREATMENT Observation (benign neglect): Erosion through the uterine wall resulting in peritonitis is possible but rare. In most cases, SIPS resolves spontaneously. OHE indicated if: Bitch is not intended for future breeding. Hemorrhage is severe. Acute life-threatening uterine bleeding may require blood transfusion (see p. 1347) Systemic and intrauterine antibiotics may be indicated when metritis or peritonitis is present. Megestrol acetate (not earlier than 6 weeks after parturition): first week of treatment, 0.1 mg/kg once daily PO; second week of treatment, 0.05 mg/kg once daily PO
POSSIBLE COMPLICATIONS Infection: bloody vaginal discharge in bitches > 6 weeks after parturition with no signs of endometritis (this is a period in which endometritis is normally not seen): By not treating the discharge, can continue until next proestrus/estrus Endocrine adverse effects of megestrol acetate
RECOMMENDED MONITORING Recheck animals showing any signs of systemic illness.
PROGNOSIS AND OUTCOME With spontaneous remission, future reproductive success is not compromised. Affected bitches are not predisposed to SIPS in subsequent pregnancies.
PEARLS & CONSIDERATIONS COMMENTS SIPS is the most common cause for persistent postparturient serosanguineous vaginal/vulvar discharge in an otherwise healthy bitch.
PREVENTION Ovariohysterectomy or not breeding an intact female dog will prevent this problem from occurring.
CLIENT EDUCATION Careful monitoring for complications such as vaginitis (foul smelling) that may lead to metritis and systemic illness.
SUGGESTED READING Dickie MB, et al: Diagnosis and therapy of the subinvolution of placental sites in the bitch. J Reprod Fertil Suppl 47:471, 1993. AUTHOR: CARLOS GRADIL EDITOR: MICHELLE KUTZLER
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Subcutaneous Emphysema
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Subcutaneous Emphysema BASIC INFORMATION DEFINITION Accumulation of air in subcutaneous tissues
EPIDEMIOLOGY SPECIES, AGE, SEX: More often seen in cats than in dogs (cats have a thin dorsal tracheal membrane compared to dogs). RISK FACTORS Endotracheal intubation, especially in cats Jugular venipuncture Trauma to airways Bite wounds (anaerobic infection of subcutis; disruption of the pulmonary system by penetrating wounds) Surgery of the airways, especially upper airway surgery ASSOCIATED CONDITIONS & DISORDERS Pneumomediastinum Pneumoretroperitoneum Pneumopericardium Pneumothorax
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT History of recent anesthesia with intubation, trauma, or surgery History of recent jugular venipuncture, transtracheal aspiration, or other penetrating medical procedure of the neck Dyspnea, discomfort Rapid onset of swelling of the body, initially around the neck but may progress to total body PHYSICAL EXAM FINDINGS: Animal may manifest respiratory discomfort. Characteristic crackling sensation (crepitus) on palpation of the skin overlying the trapped air is pathognomonic. Initially focal (especially around the neck) and progressing rapidly to affect the whole body: suggests airway perforation/rupture as source; dyspnea, discomfort may or may not be present. Focal in an animal showing signs of severe illness; may suggest infection-related subcutaneous emphysema. A meticulous search for penetrating wounds is indicated.
ETIOLOGY AND PATHOPHYSIOLOGY A break in the integrity of the airway at any point between the pharynx and terminal bronchioles An independent source of gas formation (bacteria) in the subcutis With any of the following three mechanisms, air may remain trapped in the subcutaneous tissues by unidirectional valve action of the airway trauma: Rupture of dorsal tracheal membrane (cats > dogs) Rupture of dorsolateral or ventrolateral tracheal annular ligament Penetrating wound in cervical area Specific etiologies: Related to anesthetic administration of intubation: Overinflation of endotracheal cuff Use of a stiff stylet to guide the endotracheal tube through the larynx causes punctures in trachea
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Subcutaneous Emphysema
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Manipulation of the head without disconnecting the endotracheal tube Surgical Traumatic: Bite wounds Lacerations or penetrating foreign objects, including jugular venipuncture and transtracheal aspirates Infectious: Inoculation of gas-forming bacteria (e.g., anaerobes) during penetrating injuries such as bite wounds anywhere on the body can produce infection of the subcutis. Idiopathic
SUBCUTANEOUS EMPHYSEMA External appearance of a domestic long-haired cat with marked subcutaneous emphysema. Note severe distention of the subcutaneous space, manifesting as a diffusely bloated appearance over the torso but not the head.
DIAGNOSIS DIAGNOSTIC OVERVIEW A history of recent intubation or tracheal trauma with or without acute onset of increased body size is suggestive. The characteristic “bubble wrap”–like feeling on palpation and/or the presence of subcutaneous air on radiographs confirms the diagnosis.
DIFFERENTIAL DIAGNOSIS Tracheal avulsion/rupture; radiographs reveal physical separation of the trachea; surgery is required.
INITIAL DATABASE CBC and serum biochemical profile: generally unremarkable for cases of airway trauma; may show evidence of infection (neutrophilia, left shift, toxic changes) if subcutaneous emphysema is due to anaerobic infection of the subcutis. Radiographs of neck and thorax show presence of air trapped under the skin.
ADVANCED OR CONFIRMATORY TESTING Tracheoscopy: Lesions may be difficult to visualize. Negative finding does not rule out tracheal trauma as cause for subcutaneous emphysema. CT scan of trachea may be required to detect presence and/or extent of tracheal rupture. Surgical exploration if severe
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TREATMENT TREATMENT OVERVIEW Most patients will heal spontaneously in 1-2 weeks. More severe trauma requires surgical repair.
SUBCUTANEOUS EMPHYSEMA Radiograph showing severe subcutaneous emphysema, apparent as gas lucencies throughout the subcutis.
ACUTE GENERAL TREATMENT In animals without respiratory discomfort: Supportive care while awaiting spontaneous absorption of the air Cage rest In animals with mild discomfort: Consider light sedation Removal of air via an 18-G or 16-G needle. Air may be gently massaged toward the needle for evacuation. Needle suction alone may not able to remove the trapped air. Air removal via skin stab incisions is not advised. Repeat this procedure to keep the animal comfortable as needed. Penrose drains can be placed into the subcutis (similar to treating a subcutaneous abscess) to allow for continuous drainage of air. Generally less labor intensive and more effective than repeated centesis. Analgesia (e.g., with butorphanol, 0.1-0.3 mg/kg IV q 4-6 h) In animals with recurrent/refractory subcutaneous emphysema and progressive respiratory distress: If dyspnea is due to compression of the airways by trapped air in the subcutis or mediastinum, trapped air should be allowed to drain, leading to improved respiratory effort. Surgical repair of the trachea if conservative measures are inadequate or if radiography suggests tracheal avulsion/rupture Analgesia (e.g., with butorphanol, 0.1-0.3 mg/kg IV q 6-8 h)
DRUG INTERACTIONS Avoid subcutaneous drug administration until normalized.
POSSIBLE COMPLICATIONS Depending on the etiology of the subcutaneous emphysema: tracheal rupture, pneumothorax, and pneumoretroperitoneum are possible, as is sepsis (if bacterial infection of the subcutis).
RECOMMENDED MONITORING Evaluate rate and depth of respiration as an indicator for the level of comfort in the animal and consider the need for surgical
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treatment.
PROGNOSIS AND OUTCOME In animals that do not develop respiratory distress, the prognosis is good, and spontaneous recovery will occur between 3 and 15 days.
PEARLS & CONSIDERATIONS COMMENTS Most animals will recover with supportive care and will not require surgery. Sloughing of the skin is not a recognized complication of subcutaneous emphysema. Some animals show discomfort and pain during the presence of subcutaneous emphysema. Analgesic treatment should be initiated. Avoid subcutaneous drug administration in patients with subcutaneous emphysema (variable absorption).
TECHNICIAN TIPS Prevent overinflation of endotracheal cuffs. Perform cautious, appropriate jugular venipuncture, especially in cats. Disconnect endotracheal tubes prior to repositioning of the animal's head.
SUGGESTED READING Bhandal J, Kuzma A: Tracheal rupture in a cat: diagnosis by computed tomography, Can Vet J 49:595–597, 2008. Hardie EM, et al: Tracheal rupture in cats: 16 cases (1983-1998), J Am Vet Med Assoc 214(4):508–512, 1999. AUTHOR: HANS GELENS EDITOR: ELIZABETH ROZANSKI
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Subaortic Stenosis
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Subaortic Stenosis BASIC INFORMATION DEFINITION Common congenital malformation of the canine heart; uncommon in kittens. Hallmark: a narrowing of the outflow tract of the left ventricle (LVOT) May be fixed (fibrous nodule, band, annulus, fibromuscular tunnel) or dynamic (systolic anterior motion of the mitral valve or SAM, asymmetric septal hypertrophy)
SYNONYMS Subvalvular aortic stenosis, SAS
EPIDEMIOLOGY SPECIES, AGE, SEX First noted in puppies < 12 months old (usually after 6 to 8 weeks of age) The lesion has never been documented during fetal life in any species. The severity of narrowing often is progressive during a puppy's growth, and the true severity of narrowing cannot be determined until the dog is fully grown (at least 1 year old). Depending on the study, subaortic stenosis (SAS) is either the most common congenital heart defect of dogs or is second to patent ductus arteriosus. In cats, hypertrophic cardiomyopathy (see p. 565) affecting the interventricular septum or associated with SAM may produce the same effect of left ventricular outflow obstruction as SAS. GENETICS & BREED PREDISPOSITION Large-breed dogs (Newfoundland, golden retriever, rottweiler, boxer, German shepherd, Bouvier des Flandres, Bernese mountain dogs and Dogues de Bordeaux) Hereditary transmission (autosomal dominant with a polygenic pattern) has been demonstrated in the Newfoundland dog and is suspected in the golden retriever (autosomal recessive) Cannot be attributed specifically to sire or dam in any breed (no apparent sex linkage) Recognized risk of mildly affected dogs to produce more severely affected offspring ASSOCIATED CONDITIONS & DISORDERS Mild/moderate aortic valvular regurgitation/insufficiency: very commonly observed echocardiographically in dogs with SAS; often inaudible on auscultation. Mitral dysplasia, patent ductus arteriosus, and a variety of aortic arch abnormalities have also been associated with some SAS cases. Dogs with SAS are predisposed to bacterial endocarditis of the aortic valve. A decreased aortoseptal angle is often seen with SAS and possibly represents a predisposing anatomic factor.
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES: Many distinct malformations are grouped under the heading of SAS. Fixed obstruction: Grade 1: small raised nodules of thickened endocardium Grade 2: narrow ridge of thickened endocardium that partially encircles the left ventricular outflow tract Grade 3: fibrous band, ridge, or collar completely encircles the left ventricular outflow tract. This grading system is only for gross pathologic findings. It is unrelated to murmur intensity or clinical signs. Dynamic obstruction: Systolic anterior motion of the mitral valve: Narrowing of the left ventricular outflow tract and papillary muscle distortion caused by left ventricular hypertrophy slightly distort the mitral valve such that a small amount of mitral regurgitation occurs.
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Subaortic Stenosis
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Septal hypertrophy or malalignment: The left ventricular hypertrophy induced by SAS may itself further contribute to left ventricular outflow obstruction because of hypertrophy of the interventricular septum. The aortic arch may be congenitally malaligned in its attachment to the left ventricular outflow tract, resulting in SAS due to protrusion of the interventricular septum into the subvalvular area. HISTORY, CHIEF COMPLAINT: In most cases, the condition causes a heart murmur in a dog not showing any overt clinical signs. However, severe cases may show: Exertional fatigue or syncope Congestive heart failure (CHF) (rare) Sudden death Some moderate cases show exaggerated or long-lasting panting after exercise as their only clinical sign PHYSICAL EXAM FINDINGS: Often unremarkable except for a systolic, ejection-type (crescendo-decrescendo) heart murmur, heard loudest in the left cranial thorax (between the third and fifth intercostal spaces) or at the thoracic inlet (immediately lateral to the trachea). Intensity of the heart murmur grossly correlates with severity of disease: Grades 1 to 3/6 = mildly to moderately affected dogs Grades 4 to 6/6 = severely affected dogs Murmur may radiate cranially through the carotid arteries to the neck and head or to the right hemithorax Weak and slow rising femoral pulse (pulsus parvus et tardus) in severe cases A diastolic heart murmur is sometimes heard with aortic valve insufficiency Premature beats and pulse deficits (due to ventricular arrhythmias) may be detected, in severe cases
ETIOLOGY AND PATHOPHYSIOLOGY The etiology is multifactorial and may be caused by the combination of persistence of embryonal endocardial tissue that retains potential capacity for chondrocytes proliferation and predisposing anatomic characteristics of the LVOT such as increased mitral-aortic separation, decreased aortoseptal angle and a small aortic annulus which increase the shear stress and stimulate cellular proliferation The consequence of SAS, regardless of its subtype is an elevated left ventricular pressure overload that results in: An increase in left ventricular systolic pressure and a pressure gradient across the subaortic lesion. An increased blood flow velocity through the left ventricular outflow tract. Compensatory left ventricular concentric hypertrophy (diffuse, symmetrical thickening of the left ventricle). This process may lead to left-sided CHF in some cases. With worsening SAS over time, left ventricular thickening may exceed intra-myocardial (coronary) blood supply, which does not grow along with the hypertrophied myocardial cells: The result is relative underperfusion of left ventricular tissue and ventricular arrhythmias or, less commonly, myocardial infarction. Either process may be responsible for sudden death (common in severe SAS).
DIAGNOSIS DIAGNOSTIC OVERVIEW The diagnosis is first suspected on auscultation of a systolic heart murmur loudest at the left or right heart base or cranial sternal region. Electrocardiography, thoracic radiographs, and blood tests may help raise or lower the likelihood of SAS, but a definitive diagnosis requires Doppler echocardiography.
DIFFERENTIAL DIAGNOSIS Other systolic heart murmur heard between the left second and fourth intercostal spaces: Pulmonic stenosis Tetralogy of Fallot Atrial septal defect Incompletely ausculted patent ductus arteriosus High output states: Hyperthyroidism Anemia Fever
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Exercise (rare); note that physical activity increases the heart rate, which may make apparent a murmur of SAS that was not audible at rest. The distinction between this phenomenon and a benign, exercise-induced heart murmur requires echocardiography. Juvenile “innocent” heart murmur: Puppies and kittens < 6 months old Soft heart murmur, grades 1 to 3/6, short (early to midsystolic) Often disappears with a change in body position or exercise/increase in heart rate Electrocardiogram (ECG), thoracic radiographs, and echocardiogram are normal
INITIAL DATABASE ECG: May be normal in mild to moderate cases Left ventricular hypertrophy pattern often present (R wave > 3 mV in lead II) but not striking even in some moderate to severe cases; unreliable as a screening tool ST segment may be slurred, depressed, or elevated in severe cases (myocardial hypoxia) Ventricular arrhythmias in severe or long-standing cases Thoracic radiographs: Often normal; unreliable as a screening tool for SAS Helpful mostly to rule out congestive heart failure Variable left-sided cardiomegaly (left ventricular and atrial enlargement), usually only with moderate to severe cases Poststenotic dilatation of the aortic root may be visible in severe cases Echocardiogram: (definitive diagnosis): Two-dimensional (2-D): Often normal in mildly affected dogs Subvalvular obstruction lesion or narrowed left ventricular outflow tract Left ventricular concentric hypertrophy (diffuse, symmetrical left ventricular thickening) Variable dilatation of the left atrium Dilated ascending aorta M-Mode: Normal to increased left ventricular fractional shortening (poorly sensitive) SAM sometimes observed Doppler study: Turbulent, high-velocity systolic signal in the left ventricular outflow tract and aortic root. Normal range (controversial) = up to 2 m/s; “gray zone” = 2-2.3 m/s; >2.3 m/s = highly suggestive of SAS when corresponding murmur and breed are also present; exception in the boxer breed and possibly others, where such elevated velocities may be normal (requiring two-dimensional aortic measurements for further evaluation) Determination of the peak pressure gradient in combination with the indexed effective orifice area (IEOA) estimates the severity of disease; peak pressure gradient = 4 × (Doppler-derived LVOT velocity in m/s)2 16-40 mmHg = mild SAS 40-100 mmHg = moderate SAS >100 mmHg = severe SAS 2
2
IEOA < 0.6 cm /m = severe SAS Diastolic signal of aortic regurgitation is present in most cases of SAS
ADVANCED OR CONFIRMATORY TESTING Cardiac catheterization and angiography: virtually never used for diagnosis. The procedure is invasive, requires general anesthesia, and provides little additional information over echocardiography.
TREATMENT TREATMENT OVERVIEW No definitive treatment exists for curing SAS Only severe cases need therapy. True moderate and mild cases are asymptomatic and do not need therapy. Rarely, some moderate cases will have ventricular arrhythmias which will be addressed through medical treatment. Excision of the stenotic tissue via open-heart surgery or dilatation of the stenosis via non-invasive balloon valvuloplasty have not yet been shown to provide an outcome that is superior to conservative, medical management. Recurrence of the stenotic lesion is often observed after balloon dilation or surgery possibly as a result of anatomic characteristics of the LVOT that were left unaltered after surgery (e.g., abnormal aortoseptal angle).
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ACUTE GENERAL TREATMENT see Ventricular Arrhythmias, p. 1165; Heart Failure, Acute/Decompensated, p. 468.
CHRONIC TREATMENT Mild SAS: no treatment Moderate SAS: mild exercise restriction (only avoid vigorous activity) and ß-adrenergic blocking agent to prevent or control ventricular arrhythmias when present: Atenolol, 0.25-1 mg/kg PO q 12-24 h; begin at low dose and increase titration over 2-4 weeks until upper end of dose range or signs of intolerance (lethargy, inappetence) warranting dosage reduction; or Sotalol, 0.5-2 mg/kg PO q 12 h, up titration as per atenolol. Sotalol might be more effective in certain breeds (e.g., boxers). Severe SAS: Open resection of the obstructing lesion is possible. Balloon dilation of the stenosis; survival not longer than with medical management β-Adrenergic blocking agent to prevent or control ventricular arrhythmias: Atenolol or sotalol (see above); exercise restriction SAS with CHF: see p. 468
DRUG INTERACTIONS Concurrent use of antacids can alter the bioavailability of atenolol. Calcium channel blockers may cause hypotension and bradycardia when administered together with atenolol. Effects of theophylline can be blocked by β-adrenergic blocking agents like propranolol.
POSSIBLE COMPLICATIONS Ventricular arrhythmias/ventricular tachycardia Exertional syncope or sudden death Left-sided heart failure Aortic valve endocarditis
RECOMMENDED MONITORING Control ventricular arrhythmias when present (ambulatory ECG recordings [see ] recommended if syncope is noted and for monitoring efficacy of antiarrhythmic treatment if possible). SAS is a progressive disease when a dog is growing; therefore, the final cardiac evaluation should be done at 12 months of age or older to stage the severity of disease.
PROGNOSIS AND OUTCOME Favorable: mild to moderate SAS Normal quality of life and longevity, especially when follow-up visit shows no progression of SAS Poor: severe SAS Median survival time is 19 months when untreated. Most dogs die suddenly, usually within the first 3 years of life. Medical management might increase median survival to 4.5 years.
PEARLS & CONSIDERATIONS COMMENTS The combination of a =grade 4/6 ejection heart murmur that radiates cranially to the thoracic inlet and over the carotid arteries along with a weak femoral pulse in a puppy is highly suggestive of severe SAS. The severity of ventricular arrhythmias detected by extended (24-hour) ambulatory ECG recordings correlates with the severity of disease. Dogs with peak pressure gradients > 125 mm Hg are very likely to develop serious complications or sudden death. Because of the progressive nature of SAS during growth, the lesion/heart murmur may be clinically silent in very young puppies but becomes increasingly prominent at >2-3 months of age.
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Overtly healthy boxer dogs may have systolic murmurs without obvious SAS. This phenomenon is potentially caused by a relatively smaller outflow tract in that breed, predisposing them to increased ejection velocity and development of murmurs. Grades I-III/VI murmur No SAS lesion on echocardiography Differentiation between SAS and the normal state in these dogs is challenging and requires echocardiography (left ventricular thickening, left atrial enlargement, and aortic insufficiency suggest SAS), ECG (ventricular arrhythmia of left ventricular origin suggests SAS), and follow-up exams (progression of these abnormalities and of Doppler-derived pressure gradient suggest SAS). Identification of the most mildly affected animals (clinically silent “carrier”) such as dogs with a soft systolic murmur only apparent at higher heart rates, and a structurally normal heart on two-dimensional echocardiography, remains extremely challenging. Diagnosis in these cases involves a combination of physical examination, Doppler echocardiography, and tightly controlled follow-up exams (both the animal in question and its siblings and/or offspring).
PREVENTION Vigilance regarding the possible need for antibiotics is important in all SAS cases during periods of anticipated bacteremia (dental procedures, surgery, severe skin disease, other concurrent bacterial disease); avoiding overuse of antibacterials is also important. Use breeding dogs that have been screened for SAS.
CLIENT EDUCATION In cases of severe SAS, avoid prolonged, vigorous exercise. Contact breeders to notify them of SAS cases.
SUGGESTED READING Pyle RL, Abbott JA: Subaortic stenosis. In Bonagura JD, Twedt DC, editors: Kirk’s current veterinary therapy XIV. St Louis, 2008, Saunders Elsevier, pp 757–761. AUTHOR: MARIE C. BÉLANGER EDITOR: ETIENNE CÔTÉ
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Stunted Growth
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Stunted Growth BASIC INFORMATION DEFINITION Slowed or retarded growth rate; failure to attain expected body size/stature; uncommon disorder
SYNONYMS Cretinism (congenital hypothyroidism [rare]); delayed growth, dwarf, runt, poor-doer, unthrifty; pituitary dwarfism (growth hormone deficiency, hyposomatotropism [rare])
EPIDEMIOLOGY SPECIES, AGE, SEX Dogs and cats, age and sex vary with cause Failure to grow is usually recognized by 1 year of age (most noted prior to 2 years). First 3 months: growth hormone deficiency, congenital hypothyroidism, cleft palate, congenital megaesophagus, persistent right aortic arch (PRAA), other vascular ring anomaly, parasitism, juvenile hyperparathyroidism Under 1 year: juvenile diabetes, portosystemic shunt, exocrine pancreatic insufficiency, cardiac abnormalities, renal disease, osteochondrodystrophies, ciliary dyskinesia Under 2 years: most noted prior to 2 years. Nutritional deficiencies in giant breed dogs might manifest later. Renal diseases, hepatopathies. GENETICS & BREED PREDISPOSITION Pituitary dwarfism: German shepherd, Karelian bear dog, spitz, toy pinscher Congenital hypothyroidism: fox terrier, boxer, giant schnauzer, Abyssinian cat Osteochondrodysplasia: various, including Labrador retriever, Irish setter Cleft palate: shih tzu, English bulldogs, pointers, Swiss sheepdog, Brittany spaniel Congenital megaesophagus: Irish setter, German shepherd, Labrador retriever, miniature schnauzer Vascular ring anomaly: German shepherd, Irish setter Pancreatic acinar atrophy: German shepherd Portosystemic shunt: Havanese, Yorkshire terrier, Maltese, Dandy Dinmont terrier, pug, miniature schnauzer Polycystic kidney disease: Cairn terrier, West Highland white terrier, Persian, Himalayan Hereditary nephritis: English cocker spaniel, Samoyed Renal dysplasia: Malamute, chow chow RISK FACTORS Varies with disease Most risk factors are not identified except genetic diseases. Malnutrition: poor-quality feed 131
Hypothyroidism: maternal exposure to iodine-131 (
I)
CONTAGION & ZOONOSIS: Some intestinal parasites present risks of visceral larval migrans to humans. ASSOCIATED CONDITIONS & DISORDERS Juvenile diabetes mellitus: pancreatic acinar atrophy and exocrine pancreatic insufficiency Pituitary dwarfism: hypoadrenocorticism Portosystemic shunt: urate urolithiasis, microvascular dysplasia Megaesophagus: myasthenia gravis, vascular ring anomaly Cleft palate: middle ear abnormalities
CLINICAL PRESENTATION
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DISEASE FORMS/SUBTYPES Nutritional: Poor feed or insufficient supply Mechanical problems: cleft palate, megaesophagus, PRAA Maldigestion/malabsorption: parasites, intestinal infections (salmonella, histoplasmosis), pancreatic acinar atrophy Endocrine: Congenital hyposomatotropism, congenital hypothyroidism, juvenile hyperparathyroidism, diabetes mellitus Cardiac diseases: Patent ductus arteriosus, others Metabolic: Portosystemic shunt, microvascular dysplasia Renal dysplasia, other nephritis Chondrodysplastic HISTORY, CHIEF COMPLAINT May be unnoticed by owner Pet lags behind littermates in growth. Diet history, deworming history, onset and progression of signs are important. Medication exposure Signs of mental dullness Polyuria/polydipsia PHYSICAL EXAM FINDINGS Varies with disease. Important distinctions are good versus poor body condition and proportionate versus disproportionate dwarfism: Hyposomatotropism and chondrodysplastic animals are in good body condition, whereas other disorders lead to poor body condition. Congenitally hypothyroid patients and chondrodysplastic patients are disproportionate dwarfs (limbs are exceptionally short). This is in contrast to proportional dwarfism (e.g., toy poodle) in which the limbs, trunk, and head are of appropriate relative sizes. Examine patient for: Mental dullness or disorientation Dwarfism Cleft palate Cough, respiratory distress Heart murmur Bloated abdomen Signs of diarrhea staining coat
ETIOLOGY AND PATHOPHYSIOLOGY Specific pathophysiologic mechanism varies with disease: Inability to ingest, absorb, or utilize nutrients Inability to properly execute growth
DIAGNOSIS DIAGNOSTIC OVERVIEW Stunted growth may be obvious on the physical exam or subtle. Evaluation for inciting factors begins with history (errors in management or basic care) and physical examination (signs of concurrent or contributory disorders) and proceeds to basic laboratory tests and diagnostic imaging as needed. Unusual endocrinopathies may be considered diagnoses of exclusion.
DIFFERENTIAL DIAGNOSIS see Disease Forms/Subtypes, above.
INITIAL DATABASE
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Fecal flotation CBC: Microcytic anemia: portosystemic shunt, polycythemia Eosinophilia: hypoadrenocorticism, parasitism Lymphocytosis/neutropenia: hypoadrenocorticism Serum biochemistry panel: Low albumin: exocrine pancreatic insufficiency, portosystemic shunt, infiltrative bowel disease Hyperglycemia: diabetes mellitus Hypoglycemia: hypoadrenocorticism High calcium with normal or low phosphorus: hypoparathyroidism High blood urea nitrogen: renal disease versus prerenal azotemia Urinalysis: Urine specific gravity < 1.035: kidney disease, hypothyroidism; may be normal in nonazotemic patient (elimination of free water) Glucose: diabetes mellitus Protein: nephritis, glomerulopathies Casts, infection: nephritis Urate uroliths: portosystemic shunt, microvascular dysplasia T4: congenital hypothyroidism
ADVANCED OR CONFIRMATORY TESTING Trypsinlike immunoreactivity: pancreatic acinar atrophy/exocrine pancreatic insufficiency Urine bacterial culture and sensitivity ACTH stimulation test: hypoadrenocorticism Abdominal ultrasound: kidney disease, portosystemic shunt Scintigraphy: portosystemic shunt, ciliary dyskinesia Xylazine stimulation, serum level of insulin-like growth factor: hyposomatotropism
TREATMENT TREATMENT OVERVIEW Correct diseases that are reversible.
ACUTE GENERAL TREATMENT Generally not acute presentations
CHRONIC TREATMENT Varies with disease Examples, depending on disorder: close portosystemic shunt, treat parasitism, improve diet, provide thyroxine, insulin, pancreatic enzyme replacement.
POSSIBLE COMPLICATIONS Death: patent ductus arteriosus, portosystemic shunt, extreme malnutrition Diabetic ketoacidosis: congenital diabetes mellitus Aspiration pneumonia: megaesophagus, PRAA
RECOMMENDED MONITORING Frequent physical exams
PROGNOSIS AND OUTCOME Guarded; most of the diseases are serious and irreversible. With surgical reversal, improved longevity of portosystemic shunt patients and patent ductus arteriosus patients may be achieved as long as underlying microvascular dysplasia and irreversible cardiac changes, respectively, are not present.
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Osteochondrodysplastic dogs can fare well, but the disorder is irreversible.
PEARLS & CONSIDERATIONS COMMENTS Key to diagnosis is distinction between good and poor thrift and proportionate and disproportionate dwarfism. Adequate nutrition and effective deworming should be assured prior to more expensive diagnostics.
PREVENTION Careful attention to genetic lines in purebred dogs
CLIENT EDUCATION The prognosis varies with the disease.
SUGGESTED READING Ihle SL: Failure to grow. In Ettinger SJ, Feldman EC, editors: Textbook of veterinary internal medicine, ed 6, Philadelphia, 2005, WB Saunders, pp 80–83. AUTHOR: DENNIS SPANN EDITOR: ETIENNE CÔTÉ
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Strychnine Toxicosis
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Strychnine Toxicosis BASIC INFORMATION DEFINITION A rapid-onset (30 minutes to 2 hours after ingestion), potentially fatal toxicosis characterized by neurologic dysfunction. Now rare, mainly of historical interest.
SYNONYM Strychnine: Nux vomica
EPIDEMIOLOGY SPECIES, AGE, SEX All animals are susceptible; dogs are more commonly involved than cats. Male dogs are more commonly involved. GENETICS & BREED PREDISPOSITION: Younger dogs and large-breed dogs, such as German shepherds, are overrepresented. GEOGRAPHY AND SEASONALITY Year-round Rural and urban dogs equally affected Most cases are reported in the western part of the United States and in the Midwest.
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT Availability or presence of strychnine-containing bait in pet's environment; evidence of exposure Rapid onset of apprehension (30 minutes to 2 hours), nervousness, chewing movements, muscular rigidity, tonic-clonic convulsions PHYSICAL EXAM FINDINGS Hyperesthesia, apprehension, nervousness initially Severe muscle stiffness, rigidity Hyperthermia (>104°F[>40°C]), caused by muscle activity and not febrile in origin Sawhorse stance Eventually, tetanic seizures (marked by violent, stiff limb movements): Occur spontaneously or may be initiated by external stimuli (touch, sound, sudden bright light) Opisthotonos, mydriasis, exophthalmos, and cyanosis may be present before death. Vomiting and hypersalivation (uncommon)
ETIOLOGY AND PATHOPHYSIOLOGY Source: Strychnine is a bitter indole alkaloid from the seeds of the vinelike Southeast Asian or Australian trees, Strychnos nux-vomica and Strychnos ignatii. Since 1978 in the United States, strychnine has been a restricted-use pesticide and rodenticide (licensed exterminators only) or has been forbidden in certain U.S. states. Over-the-counter preparations contain 20 per 10 HPF); and (3) percent necrosis (0%, 50%). High-grade (grade 3) tumors are more likely to lead to metastasis. Typical metastatic rates are considered to be 40% for grade 3 tumors, up to 20% for grade 2 tumors, and 10% or less for grade 1 tumors. It is unclear whether this grading scheme is applicable in feline soft-tissue sarcomas.
PEARLS & CONSIDERATIONS COMMENTS Many patients with soft-tissue sarcomas can be successfully treated with wide surgical excision alone. Patients with soft-tissue sarcomas that may be more difficult to treat (oral sarcomas, grade 3 sarcomas, nonresectable tumors, etc.) should be referred for consultation with specialists, including a surgeon, oncologist, or radiation oncologist, to develop a multimodality treatment approach.
PREVENTION In most cases, prevention of soft-tissue sarcomas is not possible. Early detection and treatment may result in easier treatment and better prognosis.
CLIENT EDUCATION Owners should be educated to monitor their pets for the emergence of cutaneous or other masses and have them evaluated in a timely fashion. Early detection may allow for easier treatment via surgery and may help avoid the need for radiation therapy.
SUGGESTED READING Liptak JM, Forrest LJ: Soft tissue sarcomas. In Withrow SJ, Vail DM, editors: Small animal clinical oncology, Philadelphia, 2007, WB Saunders, pp 425–454. AUTHOR: JOHN FARRELLY
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EDITOR: KENNETH M. RASSNICK
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Sneezing
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Sneezing BASIC INFORMATION DEFINITION An explosive expiration of air from the nose for the purpose of clearing the nasopharynx. Sneezing is mediated by a central reflex as a result of stimulation of the nasal mucosa. Occasional sneezing is normal. Reverse sneezing is characterized by paroxysmal, forceful, and loud inspiratory efforts that are triggered by nasopharyngeal irritation. The syndrome, most commonly seen in small- and toy-breed dogs, is self-limiting and rarely progressive. Reverse sneezing serves to move irritating debris from the nasopharynx into the oropharynx where it can be swallowed (see p. 987). All causes of nasal discharge and/or irritation are potential causes of sneezing. The type and duration of the discharge varies with the underlying cause (see Etiology and Pathophysiology below).
EPIDEMIOLOGY SPECIES, AGE, SEX Young cats may have viral upper respiratory infections or nasopharyngeal polyps. Young unvaccinated dogs are more likely to have canine viral respiratory infections. Younger animals may have congenital deformities. Older animals are more likely to have neoplastic or dental-related causes of nasal discharge and sneezing. Hunting and working dogs are more likely to have nasal foreign bodies. GENETICS & BREED PREDISPOSITION: Brachycephalic breeds have upper airway problems that may lead to sneezing and/or nasal discharge. Certain breeds can be affected by primary ciliary dyskinesia or by cleft palate/cleft lip complex. RISK FACTORS Lack of adequate immunization against viral respiratory infections Exposure to unvaccinated animals and high-density husbandry situations Geographic locations where grass awns are ubiquitous Dental disease and poor dental care Immunosuppression (fungal disease) Compromise of nasal mucosa (secondary bacterial infections) CONTAGION & ZOONOSIS: Viral upper and lower respiratory tract infections GEOGRAPHY AND SEASONALITY: Geographic locations where grass awns are ubiquitous ASSOCIATED CONDITIONS & DISORDERS: Sneezing itself can be a cause of acute nasal trauma (nose hits floor).
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES: Sneezing versus reverse sneezing HISTORY, CHIEF COMPLAINT: Acute onset of paroxysmal sneezing may suggest nasal foreign bodies or early viral disease. Husbandry and management predispose to certain disorders: for example, recent boarding, exposure to new animals, and/or history of inadequate vaccination (viral infections); hunting and geographic location (nasal foreign bodies); pertinent medical history (dental disease, history of neoplasia, immunosuppression); exposure to irritating aerosols (hairspray, paints, etc.) or anticoagulants (rodenticides, pharmaceuticals). PHYSICAL EXAM FINDINGS Serous, mucopurulent, or hemorrhagic discharge that may be unilateral or bilateral Facial deformity Exophthalmos Maxillary swelling dorsal to carnassial tooth (apical dental [“tooth root”] abscess) Oronasal fistula Ocular discharge
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Petechiation, ecchymoses Pawing at face
ETIOLOGY AND PATHOPHYSIOLOGY All causes of nasal discharge and/or irritation are potential causes of sneezing. Types of nasal discharge: Serous: clear and watery (acellular); due to local irritation, early viral infection, allergic rhinitis, or excessive lacrimation Mucoid: clear and thicker (acellular with higher protein content); due to chronic noninfectious irritation and overproduction of mucus by nasal epithelial cells Purulent: yellow-tan, thick discharge (neutrophilic with bacteria) usually due to secondary bacterial infection Sanguineous: red-tinged (blood mixed with another type of discharge) due to compromise of the nasal mucosa Hemorrhagic (epistaxis): frank red blood due to local or systemic causes of bleeding
DIAGNOSIS DIAGNOSTIC OVERVIEW Important diagnostic elements include whether nasal discharge is present and if so, of what type; whether air flow is normal or reduced in one or both nostrils (glass slide fog test); and whether there are systemic signs of illness. These features allow the clinician to choose tests that evaluate the nasal passages specifically (e.g., rhinoscopy) or to opt for conservative treatment and monitor evolution.
DIFFERENTIAL DIAGNOSIS Feline viral upper respiratory tract infections (feline rhinotracheitis, feline calicivirus, Chlamydophila felis) Neoplasia (adenocarcinoma, lymphoma, undifferentiated carcinoma, osteosarcoma, chondrosarcoma, fibrosarcoma, transmissible venereal tumor) Foreign bodies Apical dental (“tooth root”) abscess Oronasal fistula Nasopharyngeal polyps Canine viral infections (canine distemper virus, canine parainfluenza virus, canine herpesvirus, canine adenovirus types 1 and 2) Mycotic infection (Aspergillus spp. in dogs; Cryptococcus neoformans in cats) Parasitic rhinitis (Cuterebra spp., Pneumonyssoides caninum, Linguatula serrata) Bacterial infections (usually secondary) Rhinitis (allergic/eosinophilic type I hypersensitivity, lymphoplasmacytic, chronic hyperplastic) Congenital defects (cleft palate-cleft lip complex, primary ciliary dyskinesis) Trauma Inhaled irritants (cat litter dust, aerosols, smoke) Epistaxis: Local causes: mycotic infections, neoplasia, foreign body, trauma Systemic causes: inherited or acquired coagulopathies, thrombocytopenia, thrombocytopathia, hypertension, vasculitides Nasopharyngeal stenosis
INITIAL DATABASE Assessment for unilateral versus bilateral nasal disease by holding a glass microscope slide close to the external nares while the patient breathes on it through its nose (mouth held closed). Presence or absence of steam on the slide suggests unilateral obstruction, bilateral obstruction, or normal air flow. Neoplasia, foreign bodies, and dental disease are often causes of unilateral nasal disease, whereas other local and systemic causes often result in bilateral disease. Examination of the oral cavity to look for hard-palate masses; fundic examination to look for evidence of neoplasia, fungal disease, or hypertension and associated retinal hemorrhage Eye globe retropulsion ± ocular ultrasound to assess for retrobulbar masses Blood pressure measurement to assess for hypertension CBC including platelet count to look for evidence of infection, inflammation, or thrombocytopenia Serum biochemistry profile, urinalysis Feline leukemia and feline immunodeficiency viral testing
ADVANCED OR CONFIRMATORY TESTING
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Rocky Mountain spotted fever, Ehrlichia, and Bartonella testing, prothrombin time, partial thromboplastin time, thoracic radiographs, nasal swabs, fungal titer determinations, nasal radiography, CT (see p. 1233), rhinoscopy (see p. 1335), biopsy, deep tissue cultures, exploratory rhinotomy—as dictated by history, physical exam, and preliminary findings
TREATMENT TREATMENT OVERVIEW Eliminate underlying etiology of sneezing. Restore normal nasal function. Reduce pain and discomfort. Provide supportive care. Relieve dyspnea, especially in cats who oftentimes will not readily open-mouth breathe.
ACUTE GENERAL TREATMENT If nasal discharge or nasal mucosal edema is causing dyspnea, oxygen therapy may be needed. Treatment for underlying coagulopathy (e.g., vitamin K1, 0.25-2.5 mg/kg for first-generation rodenticide intoxication or 2.5-5 mg/kg for second generation, SQ or PO divided q 12 h for 7-21 days, and fresh frozen plasma). Correct dehydration and electrolyte abnormalities as necessary. Broad-spectrum antibiotics if secondary nasal or dental infection (bacteria are rarely the primary cause of nasal disease, but secondary infection with normal nasal flora is common) or pneumonia (culture and sensitivity from the lower airways is essential if pneumonia is present). Bartonella has been implicated as a cause of chronic rhinitis and epistaxis; azithromycin may be used (5-10 mg/kg PO q 24 h. Start at 5 mg/kg and if tolerated, increase by 2.5 mg/kg each day to 10 mg/kg limit. After 1 week, reduce to q 48 h). Analgesics if painful (opiates and/or nonsteroidal antiinflammatory drugs [NSAIDs]) Removal of animal from environmental agents (e.g., smoke, dust, allergens) Surgery should be considered for dental disease, neoplasia, nasopharyngeal polyps, cleft palate, foreign bodies, or traumatic causes. Radiation and/or chemotherapy for neoplasia Chemoembolization (an interventional radiology technique) of nasal tumors can be considered in cases where surgery, radiation, or chemotherapy are associated with excessive morbidity, cost, or a poor outcome. Rhinoscopy may be useful for removing a foreign body. Fungal: local or systemic treatment Parasitic rhinitis: ivermectin, 0.2 mg/kg SQ or PO twice 3 weeks apart, is reported to be successful; avoid in breeds susceptible to toxicosis (collies, Shetland sheepdogs, Old English sheepdogs, and others; see p. 706). Decongestants and cleaning of the nares (pediatric Neo-Synephrine, 1 drop in alternating nares q 24 h) Nasopharyngeal stenting for nasopharyngeal stenosis Embolization for epistaxis
CHRONIC TREATMENT Nutrition: cats especially may not eat if unable to smell food; consider coax-feeding (see p. 1377) or placement of a tube (e.g., esophagostomy; see p. 1267) for nutritional support. Analgesics Antibiotics for secondary infections In animals with chronic rhinitis, anti-histamines, inhaled corticosteroids, and systemic NSAIDs may provide some relief.
POSSIBLE COMPLICATIONS Anorexia (especially in cats with severe nasal congestion) Keratitis (feline viral upper respiratory infections) Upper airway obstruction following extubation after general anesthesia Hemorrhage following surgery or rhinoscopy Dehiscence of surgical site (e.g., cleft palate) Progression of underlying disease Acute nasal trauma due to paroxysmal sneezing in small, short-legged dogs whose noses may hit the floor while sneezing (e.g., dachshunds)
RECOMMENDED MONITORING Respiratory rate and effort; ventilation and oxygenation
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Appetite Ongoing hemorrhage Volume and nature of discharge Monitoring as normal for antimicrobials and NSAIDs Appropriate laboratory testing or diagnostic imaging, dependent on underlying disease
PROGNOSIS AND OUTCOME Dependent on etiology Good if the underlying problem is canine viral upper respiratory tract infection, foreign body, successful surgery, teeth extractions Guarded for feline chronic viral upper respiratory tract infections Guarded to good for fungal rhinitis, depending on response to therapy Poor if neoplasia is not amenable to surgery and radiation therapy. Interventional techniques such as chemoembolization of nasal tumors may be considered in cases where surgery or radiation are not options, or if a less invasive approach is desired.
PEARLS & CONSIDERATIONS PREVENTION Isolation of cats with viral infections Appropriate vaccination regime and retroviral testing Good dental care Limit exposure to irritating aerosols or materials
SUGGESTED READING Doust R, Sullivan M: Nasal discharge, sneezing and reverse sneezing. In King LG, editor: Textbook of respiratory disease in dogs and cats, St Louis, 2004, Saunders, pp 17–29. AUTHORS: ELISE MITTLEMAN BOLLER, ANDREW J. BROWN EDITOR: ETIENNE CÔTÉ
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Snakebite
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Snakebite BASIC INFORMATION DEFINITION Injury resulting from a snake biting an animal
SYNONYM Snake envenomation
EPIDEMIOLOGY SPECIES, AGE, SEX: Any age or species; either sex GENETICS & BREED PREDISPOSITION: Large-breed, outdoor dogs appear to have an increased risk. RISK FACTORS Environment: exposure to outdoors in warm climates Behavior: curiosity CONTAGION & ZOONOSIS The same snakes that are venomous to dogs and cats are venomous to humans. No zoonosis associated with snakebites GEOGRAPHY AND SEASONALITY There are two main families of venomous snakes: Elapidae and Viperidae. Elapids: coral snakes, cobras, mambas, kraits, and the tiger snake; in North America, these are found predominantly in the southeastern areas of the United States. Vipers: rattlesnakes (Crotalus and Sistrus spp.) and cottonmouths and copperheads (Agkistrodon spp.); found throughout the United States Increased incidence of bites in summer months (in North America, 90% of bites occur between April and October). Toxicity increased in young or very large snakes during springtime. ASSOCIATED CONDITIONS & DISORDERS Neurologic dysfunction: elapids Local tissue damage and possibly systemic bleeding/coagulation: vipers
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES Vipers (e.g., rattlesnakes) inflict 99% of the estimated 150,000 annual snake bites of dogs and cats in North America. “Dry” bites possible: contain little or no toxic venom (22% of rattlesnake bites are dry; higher proportion in elapids) HISTORY, CHIEF COMPLAINT Observed bite: Dogs, head and neck; cats, abdomen, thorax. Common scenario: the dog cries out after sniffing in the bushes or behind a rock where snake is hidden. Unobserved bite: facial or neck swelling and pain after being outdoors without supervision PHYSICAL EXAM FINDINGS
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Snakebite
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Fang marks with swelling and bruising around the area may exist. The animal may show signs of mild discomfort to profound hemorrhagic and neurologic alterations. Fang marks are often difficult to find, especially in longhaired or thick-coated dogs and cats. Coral snakes: Leave tiny fang or tooth marks with little or no local swelling Signs may be delayed 1-7.5 hours. Salivation Vomiting Convulsions Quadriplegia Death Rattlesnakes: Usually leave two fang marks Swelling Pain Erythema Petechiae or ecchymoses Cyanosis and tissue sloughing
SNAKEBITE Viper (rattlesnake) bite to a dog's muzzle. Note marked diffuse swelling of face and lips.
ETIOLOGY AND PATHOPHYSIOLOGY Elapid venom is neurotoxic and hemolytic: Signs appear 1-7.5 hours after the bite was inflicted and progress rapidly. Signs start with salivation, vomiting, and apprehensive behavior. Signs progress to convulsions, quadriplegia, and eventually may lead to death from respiratory paralysis. Crotalid venom is vasculotoxic and necrogenic. Bites lead to immediate regional swelling. Area around the bite may have swelling, pain, erythema, ecchymosis, cyanosis, and tissue sloughing. Bites are most often inflicted on the face and head and occasionally on the paws. In severe cases, the tissue around the fang marks turns black within 30 minutes, and the blood oozing from the site is dark and watery. Swelling typically worsens over the first 24 hours after the bite was inflicted, and the swollen tissue may be similar to a hematoma (occasionally requiring transfusion).
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Snakebite
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SNAKEBITE Viper (rattlesnake) bite to a cat's distal forelimb. Note marked swelling, moist exudation, and dark discoloration of skin, which suggests necrosis.
DIAGNOSIS DIAGNOSTIC OVERVIEW The diagnosis is suspected when a patient develops acute swelling with bruising, often around the face (vipers), or acute neurologic dysfunction (elapids) in a geographic region known to harbor venomous snakes. Identification of puncture marks in the skin from the bite is confirmatory; in many cases the diagnosis remains presumptive.
DIFFERENTIAL DIAGNOSIS Other animal attacks Scorpion bite Insect bite Wound of unknown origin Intoxication with neurotoxic substance (versus elapid envenomation)
INITIAL DATABASE CBC with platelet count: may reveal hemoconcentration, leukocytosis, echinocytosis, or thrombocytopenia Serum biochemistry profile: may reveal hypokalemia, high creatine kinase Urinalysis: may reveal hematuria or myoglobinuria Coagulation profile: prolonged activated clotting time (ACT), prothrombin time (PT), partial thromboplastin time (PTT), and increased fibrin/fibrinogen degradation products (FDPs) possible Aerobic and anaerobic bacterial culture and sensitivity (C&S) of the wound
ADVANCED OR CONFIRMATORY TESTING No test exists that is diagnostic for a snake bite, but echinocytes found on a blood smear are a common finding in animals with envenomation. Echinocytes are “burred” red blood cells (RBCs) that appear soon after envenomation and last 24-48 hours. These cells often precede the massive tissue swelling and necrosis that occur with serious bites.
TREATMENT TREATMENT OVERVIEW Management/prevention of hypotension Neutralization of venom (minimizing local and systemic effects) Prevention of secondary bacterial infection Pain management Avoidance of iatrogenic complications, particularly during first-aid efforts in the field
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Snakebite
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ACUTE GENERAL TREATMENT All animals that are bitten by a snake, regardless of their apparent hemodynamic stability, should be hospitalized for a minimum of 8 hours to assess for clinical signs that may first manifest during this period. IV fluid therapy: First line of therapy to treat hypotension or hypovolemic shock (see p. 1592) and decreased cardiac output Crystalloids (e.g., lactated Ringer's solution or 0.9% NaCl) at maintenance rates (e.g., 30 mL/lb/d [65 mL/kg/d] plus deficit for extravasated fluid; estimate amount of tissue swelling) if animal is stable; or at shock rates (90 mL/lb/h [200 mL/kg/h]) if animal is in hypovolemic shock. Colloids indicated for animals with hypoalbuminemia; plasma preferred because both albumin and acute phaseproteins are administered (see p. 1347). Antivenom (antivenin; polyvalent Crotalidae): Administered immediately for viper bites; increased survival when given closer to time of bite, but beneficial effects noted for at least 60 hours after envenomization A dose of up to 10 to 25 vials is routinely recommended in human cases, but very high cost (up to $400 per vial hospital cost), reduced availability, smaller animal size, and mild extent of some bites generally limit the number of vials used to 1-3. Protocol: Reconstitute antivenin (10 mL diluent into lyophilized antivenin). Warm to body temperature (e.g., armpit method) and not warmer. Gently swirl to dissolve over 10 to 15 minutes; avoid shaking solution. Pretreat the patient (diphenhydramine, 2 mg/kg IM). Dilute antivenin into 50-200 mL IV fluids, and administer test dose IV(10-20 mL over several minutes) while monitoring for anaphylaxis (see pp. 64 and 1111). If no anaphylaxis, administer remainder over 1 hour while continuing to monitor. CroFab (polyvalent immune Fabovine) is less antigenic; dissolves more rapidly and is more potent but twice as expensive. Antivipmyn: similar to antivenin; obtained from Mexico Antibiotics (controversial): chosen empirically at first while culture results are pending; first- or second-generation cephalosporins (e.g., cefazolin, 22 mg/kg IV q 8 h) Analgesics: opiates for sedation and analgesia while ensuring that the animal does not develop respiratory depression; buprenorphine (0.01 mg/kg IV q 6 h) or fentanyl at a constant rate infusion (3 mg/kg IV, then 3-6 mg/kg/h) Corticosteroids: antiinflammatory doses (e.g., prednisone, 0.5 mg/kg/d PO, maximum 5 days) may be of benefit. Antihistamines: not recommended (have been shown to potentiate the toxicity of venom) except in pretreatment doses prior to antivenin administration Urgent airway management (critical from time of presentation to 72 hours later): prepare endotracheal tubes and tracheostomy kits when facial, neck, or tongue bites have occurred, even if swelling is initially unimpressive. see p. 1344.
CHRONIC TREATMENT Surgical débridement of necrotic tissue is necessary in some cases.
NUTRITION/DIET Most patients can continue to prehend and swallow despite facial bites; if not, placement of a feeding tube should be considered (see p. 1270).
DRUG INTERACTIONS Antivenin may cause an anaphylactic reaction (see p. 64). Monitor vital signs during infusion; if signs of anaphylaxis develop, temporarily stop the infusion, and then restart the infusion at a slower rate when signs have subsided.
POSSIBLE COMPLICATIONS Renal failure may result from myoglobinuria, hemoglobinuria, toxic nephropathy, and hypovolemic shock.
RECOMMENDED MONITORING Monitor respiratory rate and effort as well as blood pressure (BP), electrocardiogram (ECG), coagulation status and urine output.
PROGNOSIS AND OUTCOME The prognosis is worse in animals with high-venom burdens, shock, severe cardiac arrhythmias, hematologic complications, and infection. Nevertheless, the spectrum of severity is wide, and the majority of dog or cat snakebite victims survive without permanent
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Snakebite
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sequelae if treated early and thoroughly. Although death may occur in spite of the timely use of crotalid-specific antivenin, a higher survival rate has been found in dogs that received antivenin than in dogs that did not.
PEARLS & CONSIDERATIONS COMMENTS With viper bites, marked worsening of tissue swelling in the 24-48 hours following the bite is common, even with excellent treatment: Warn owners in advance, in order to preempt their perception that treatment is unsuccessful. Prepare airway mobilization material (endotracheal tube or tracheostomy kit) if the snake bit the animal on the head or neck. Ineffective first-aid techniques include tourniquet application, incision and suction of the bite, electroshock of the bite, and hot or cold pack application. These maneuvers can harm the animal by fostering infection. Effective first aid involves minimizing exertion immediately after the bite (reducing cutaneous blood flow/venom absorption) and immediate transport to a veterinary hospital for diagnosis and treatment as outlined previously. Snakebites on digits or in very small animals may require 50% more antivenin on a body weight basis than bites excluding digits or in larger animals: Relatively small volume of body fluid in smaller animals (higher absolute venom concentrations) Difficulty attaining high antivenin concentrations in digits Rattlesnakes may bite for up to 30 minutes after they are killed, including death by decapitation. Therefore, the body or head of a snake that has bitten and is then killed and transported for identification should be kept in a rigid, closed container, and the head should not be handled directly.
PREVENTION The best way to prevent snakebites is to avoid snakes. Vipers bite in self-defense or when they are surprised (as occurs in veterinary and human medicine), or to immobilize and consume prey, such as small rodents. Vipers may strike with unavoidable speed (8 ft [2.5 m]/sec) but typically for a distance corresponding only to half the snake's length (e.g., half of 3-5 ft [1-1.6 m]). Keeping dogs in enclosed areas with cement walls or keeping dogs on leashes while outside may help prevent contact with snakes. Keeping cats indoors will help to prevent their contact with snakes. In regions where rattlesnakes are common, courses are offered to try to teach dogs to avoid snakes. Bitten dogs and cats cannot be counted on to avoid snakes in the future; repeat victims occur.
CLIENT EDUCATION Most North American snakes bite when surprised or threatened; vigilance and avoidance of snakes during warm months are the best approach to preventing bite incidents.
SUGGESTED READING Najman L, Sashadri R: Rattlesnake envenomation. Compend Contin Educ Pract Vet 29(3):166–177, 2007. AUTHOR: APRIL PAUL EDITOR: ELIZABETH ROZANSKI
26-09-2011 23:19
Smoke Inhalation
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Smoke Inhalation BASIC INFORMATION DEFINITION Injury to the respiratory system due to breathing of harmful gases, vapors, and particulate matter contained in smoke. Neurologic dysfunction and burns may occur concurrently.
SYNONYMS Smoke exposure, smoke intoxication
EPIDEMIOLOGY RISK FACTORS: Exposure to closed-space fires GEOGRAPHY AND SEASONALITY: More residential fires in winter ASSOCIATED CONDITIONS & DISORDERS: Carbon monoxide intoxication, acute respiratory distress syndrome (ARDS), burns, secondary bacterial pneumonia, systemic inflammatory response syndrome (SIRS)
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES Inhalation injury generally manifests in three clinical stages: Hypoxie injury Neurologic compromise Secondary lung injury Occasionally, smoke inhalation injury may be confined to the nasal passages and pharynx. HISTORY, CHIEF COMPLAINT Complaint of respiratory difficulties following smoke inhalation Weakness, stupor, or coma following rescue PHYSICAL EXAM FINDINGS Dyspnea, coughing, tachypnea, short or shallow respirations, harsh or moist airway sounds, crackles, wheezes, loud laryngeal or tracheal sounds. In milder cases, signs may be limited to the nasal cavity (inflammation-induced nasal congestion, obstruction to nasal airflow). Postural adaptations to respiratory distress may be seen. Mentation and motor dysfunction may include ataxia, weakness, depression, stupor, or coma. Mucous membranes may be hyperemic (due to carboxyhemoglobin [COHb], cyanide [CN], or vasodilation), pale, or cyanotic. Dermatologic findings include smoky smell, singed or burnt hair and skin, soot, or skin lacerations.
ETIOLOGY AND PATHOPHYSIOLOGY Causes of respiratory injury: Thermal damage is usually limited to the upper-airway mucosa, owing to rapid heat dissipation. Steam, soot (particles 90 mm Hg) and central venous pressure (CVP > 5 cm H2O). Restoration of volume can include the following fluid types: Crystalloids: requires a replacement fluid (e.g., lactated Ringers, 0.9% NaCl): 40-90 mL/kg IV to reach desired effect Synthetic colloids (e.g., Voluven, Hetastarch): 5-20 mL/kg IV to reach desired effect, up to 50 mL/kg/24 h for Voluven Blood (see p. 1347) Plasma may be required if massive quantities of crystalloids, synthetic colloids, or blood have been given to an animal, and the animal has developed a dilutional coagulopathy. Locate and control any source of hemorrhage.
CHRONIC TREATMENT Unless cause of fluid loss is located and controlled, fluid replacement must continue past initial stabilization to meet ongoing loss and maintenance fluid needs.
POSSIBLE COMPLICATIONS Complication of prolonged shock include: Renal failure Loss of gastrointestinal integrity, with bacteria and toxin translocation Myocardial dysfunction Brain ischemia Loss of vascular tone Systemic inflammatory response syndrome (see p. 1070) Disseminated intravascular coagulation Acute lung injury Sepsis
RECOMMENDED MONITORING Serial BP monitoring, either indirectly or directly, until goal-directed end-point is reached (systolic > 90 mm Hg). Monitor heart rate: persistent tachycardia may indicate inadequate fluid loading. Recognize that persistent hypotension or tachycardia often implies ongoing hemorrhage, systemic vasodilation, or capillary leakage and the need for continued volume resuscitation and end-point monitoring. Monitor PCV/TS for evidence of adequate fluid therapy. Utilize trends in central venous pressure as an indicator of volume status (a central multilumen catheter is also recommended for rapid fluid administration and frequent blood sampling). see p. 1227. If the CVP is 105○F, the patient may need hospitalization and intensive antipyretic management (see pp. 389 and 480). Presentation in early stage, temperature £105○F (40.6○C): NSAIDs for fever (e.g., carprofen, 2.2 mg/kg PO q 12 h) Presentation in late stage, immediate supportive care: Judicious use of IV fluids for volume resuscitation/rehydration and diuresis if renal failure. If nephrotic syndrome is present, fluids may worsen edema and be contraindicated. Antacids if vomiting, anorexia, or other evidence consistent with uremic gastropathy (e.g., famotidine, 0.5 mg/kg PO or IV q 12-24 h) Antihypertensives if systemic hypertension (e.g., enalapril 0.5 mg/kg PO q 24 h and/or amlodipine, 0.125-0.25 mg/kg PO q 24 h)
CHRONIC TREATMENT Colchicine, 0.03 mg/kg PO q 24 h for 2 weeks; if no gastrointestinal (GI) signs, may increase to 0.03 mg/kg PO q 12 h Used in people with familial Mediterranean fever; no controlled trials in shar-pei dogs Recommend early in the course of the disease to prevent or delay the development of amyloidosis; no effect on fibrosis once established Renal disease: see pp. 450, 205, and 207. Liver disease: dogs can respond to supportive care and colchicine therapy.
26-09-2011 23:08
Shar-Pei Fever
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DRUG INTERACTIONS Colchicine given with NSAIDs may increase myelosuppressive effects.
POSSIBLE COMPLICATIONS Colchicine in humans can cause anorexia, vomiting, diarrhea, renal failure, hepatotoxicity, pancytopenia, and paralysis. Vomiting and diarrhea have been reported in dogs taking colchicine and may resolve with dose reduction.
RECOMMENDED MONITORING Periodic CBC, serum biochemistry profile, and urinalysis with urine protein/creatinine ratio
PROGNOSIS AND OUTCOME Early stage: guarded to fair long-term prognosis; colchicine may improve survival. Late stage: very poor; most dogs die of renal failure, and thromboembolism and hepatic rupture have also been reported.
PEARLS & CONSIDERATIONS COMMENTS Shar-pei dogs with episodic fever are at high risk of developing amyloidosis. The most common cause of renal failure in shar-pei dogs is renal amyloidosis.
PREVENTION Removal of affected dogs from the breeding pool Colchicine treatment may help prevent or delay amyloidosis once early stage of disease is confirmed with biopsy.
CLIENT EDUCATION Closely monitor temperature of an animal during a fever episode. Monitor the patient's lab work if treating with colchicine. Inform the owner of the guarded long-term prognosis.
SUGGESTED READING DiBartola SP, et al: Familial renal amyloidosis in Chinese shar-pei dogs. J Am Vet Med Assoc 197:483–487, 1990. Loeven KO: Hepatic amyloidosis in two Chinese shar-pei dogs. J Am Vet Med Assoc 204:1212–1216, 1994. Rivas AL, Tintle L, et al: A canine febrile disorder associated with elevated interleukin-6. Clin Immunol Immunopathol 64:36–45, 1992. Tintle LJ: Familial shar-pei fever and familial amyloidosis of Chinese shar-pei dogs: www.royalsharpei.com/FSF.htm. AUTHOR: ORLA MAHONY EDITOR: SUSAN M. COTTER
26-09-2011 23:08
Sepsis and Septic Shock
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Sepsis and Septic Shock BASIC INFORMATION DEFINITION Sepsis is the occurrence of systemic inflammation in response to infection (see p. 1070). It generally implies systemic circulation of infectious agents (e.g., bacteremia). Septic shock is defined as sepsis with concurrent hypotension that is refractory to fluid therapy and requires vasopressor therapy.
EPIDEMIOLOGY SPECIES, AGE, SEX: Dogs and cats of any age and either sex may develop sepsis or septic shock. RISK FACTORS Animals with established infections Animals with diseases resulting in immunosuppression (such as hyperadrenocorticism or diabetes mellitus) Noninfectious diseases that may predispose an animal to bacteremia include neoplasia, glucocorticoid therapy, trauma, surgery, cytotoxic therapy, IV and urinary tract catheters, burns, and hematologic abnormalities (e.g., leukocyte function defects).
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES: Sepsis and early septic shock initially present a hyperdynamic phase characterized by increased metabolic processes: tachycardia, fever, warm extremities, injected mucous membranes, and a bounding pulse. If unchecked, the hyperdynamic phase progresses to a more critical and potentially terminal hypodynamic phase of septic shock characterized by normothermia or hypothermia, pallor, cool extremities, a weak or absent pulse, and decreased mentation. HISTORY, CHIEF COMPLAINT: Complaints vary depending on the source of sepsis. Animals with abdominal sources of sepsis may present with vomiting, anorexia, or abdominal pain, while those with thoracic sepsis often present with a history of coughing, labored breathing/dyspnea, or respiratory distress. Sepsis from an occult source (anywhere in the body) may not produce localizing signs, and some animals with sepsis present with only vague signs of general malaise, such as anorexia and lethargy. PHYSICAL EXAM FINDINGS General: Hyperthermia (>104°F [>40°C]): fever in response to infection (hyperdynamic phase) Hypothermia (70%). Kidney failure: at advanced stages, evident on physical exam (anuria) and/or blood work and urinalysis (concurrent azotemia and isosthenuria) Narcolepsy/cataplexy: animal “falls asleep” but can be awakened; usually associated with excitement or food. Sleep disorder: excessive “jerky” movements occurring exclusively during sleep. The animal can be awakened and exhibits normal wakening behavior (i.e., no postictal signs). Obsessive/compulsive behavior (e.g., “fly biting”): complex behavior that is usually goal directed and/or can be interrupted; more common in dogs. Affected dogs often have other behavioral problems (e.g., separation anxiety). Movement disorders: Focal motor signs are not associated with loss of consciousness or postictal signs. One of these signs is the “head bob,” which is occasionally seen in Doberman pinschers, boxers, bulldogs and occasionally in other breeds (movement of the head from side to side or up and down); another sign is dyskinesia in the bichon frise.
INITIAL DATABASE Fundic examination (see p. 1313): clues include papilledema (as can be seen with optic neuritis/encephalitis); retinal hemorrhage or detachment (which would suggest hypertension, polycythemia, or coagulopathy); lesions of chorioretinitis suggestive of a systemic infection (e.g., ehrlichiosis, toxoplasmosis, neosporosis, fungal disease). CBC, serum biochemistry panel, and urinalysis: evaluate for hypoglycemia, electrolyte imbalance (e.g., hypocalcemia), signs of liver or kidney disease, anemia, polycythemia, and calcium oxalate monohydrate crystals in antifreeze toxicity. Usually normal in cases of primary brain disease After severe seizures or status epilepticus, hyperglycemia (or rarely, hypoglycemia if prolonged seizures last for more than 20 minutes), increased liver enzymes (reduced perfusion or congestion), increased creatine kinase (CK; muscular damage or necrosis), and metabolic acidosis are typical.
26-09-2011 23:07
Seizures
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Electrocardiogram (ECG): evaluate for arrhythmias. Thoracic and abdominal radiographs: usually unremarkable Serum bile acids assay: indicated if hepatic encephalopathy is suspected and/or if a young animal presents with seizures. More than 90% of dogs and cats with portosystemic shunts have abnormal 2-hour postprandial serum bile acid levels.
ADVANCED OR CONFIRMATORY TESTING Portable electrocardiogram (ECG; cardiac event monitor or Holter monitor) if distinction between syncope and seizure is unclear on history and physical exam. Helps rule in (severe tachycardia or severe bradycardia occurs during episode) or rule out (cardiac rhythm is normal during episode) a cardiac arrhythmia as the cause of episodic clinical signs. Important prior to proceeding to general anesthesia, as for advanced imaging or CSF tap. Advanced imaging of the brain (MRI or CT scan (see p. 1302 and p. 1233)): brain tumor, multifocal lesions suggestive of inflammation, vascular lesion. MRI is slightly more sensitive. Radiographs of the skull are unrewarding except in cases of head trauma or palpable skull abnormalities. CSF analysis: often nonspecific but can be helpful in confirming brain disease or inflammation Serologic testing (e.g., fungal diseases, Toxoplasma, Neospora, and others; selection based on physical findings and initial database) Tests for toxins if exposure (e.g., plasma lead concentration, serum cholinesterase level) Electroencephalogram (EEG): limited availability; usefulness has yet to be proven.
TREATMENT TREATMENT OVERVIEW Control or elimination of the underlying cause is the overarching long-term goal but is not possible in all cases. Reduction in seizure frequency and severity is a principal goal; acceptable seizure control for the owner (e.g., could be 100 species of wild and domestic mammals, amphibians, arthropods, birds, and humans Seroprevalence indicates latent infection is common in dogs and cats in endemic areas. Clinical disease occurs occasionally in cats and rarely in dogs. Cats often severely affected; dogs more resistant and milder signs; puppies and kittens more susceptible than adults RISK FACTORS: Exposure to ticks or wild rabbits or rodents; humans at greater risk include veterinarians, farmers, hunters, landscapers, meat handlers, cooks, and laboratory personnel. CONTAGION & ZOONOSIS: Highly infectious zoonotic disease; the infectious dose for humans is 68%, perform a phlebotomy, replacing the removed volume with a balanced crystalloid (100%-150% of volume removed).
CHRONIC TREATMENT Assuming definitive repair is not possible, long-term benefits can be achieved by referral for extracardiac thoracic surgery. A palliative left-to-right shunt between a systemic artery and the pulmonary artery (e.g., modified Blalock-Taussig shunt) increases pulmonary blood flow and usually raises arterial oxygen saturation to >90%. Alternatively, “partial” balloon valvuloplasty of the stenotic right ventricular outlet can be considered, provided a residual pulmonary obstruction is maintained to prevent severe left-to-right shunting across the unrestrictive VSD. Theoretically, catheterization of the aorta (through the VSD) may permit identification of excessive collateral vessels that may be occluded by coil embolization. Periodic phlebotomy, maintaining PCV < 68% (target 62%-65%, although lower values may be well tolerated). The nonspecific beta-blocker, propranolol (0.5-1 mg/kg PO q 8 h; begin low and titrate upward), can mitigate dynamic right ventricular outflow tract obstruction from hypertrophy while preventing drug-induced vasodilation. Consider a trial course of hydroxyurea (30-50 mg/kg PO q 24-48 h; titrate based on PCV) to suppress the bone marrow when frequent phlebotomies are needed. Prescribe low-dose aspirin to animals with surgically created palliative shunts (to impede thrombosis). Limit exercise, and avoid high heat/ humidity conditions; prevent dehydration.
26-09-2011 23:42
Tetralogy of Fallot
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Consider pentoxifylline to improve red blood cell (RBC) flexibility in the micro-circulation (however, use in animals with TF is completely empirical).
POSSIBLE COMPLICATIONS Adverse effects of the aforementioned drugs Gradual spontaneous closure or thrombosis of a surgically created palliative shunt Acute pulmonary edema from creation of a large palliative shunt or overzealous balloon valvuloplasty for relief of PS Paradoxical (right-to-left) thromboembolic episode following venipuncture, causing stroke or coronary embolus. In cats with TF, atrial thrombi may result in arterial thromboembolism.
RECOMMENDED MONITORING Clinical signs: exercise capacity and respiratory effort at home Mucous membrane color and arterial oxygen saturation (oximetry) Hematocrit or full CBC with platelet count if the patient is taking hydroxyurea Resting heart rate, as bradycardia (2 cm diameter. Leydig cell tumor: excellent following testicular removal; metastasis is not expected. Mixed sex cord/stromal tumor: excellent following testicular removal; metastasis is not expected.
PEARLS & CONSIDERATIONS COMMENTS Histopathologic examination is needed for determination of tumor type. Unilateral castration may result in up to 50% hypertrophy of the remaining testis. Return to fertility following unilateral castration depends on the severity of testicular atrophy secondary to hormonal downregulation and presence of underlying disease (testicular degeneration with loss of spermatogo-nia).
PREVENTION Testicular removal, especially of cryptorchid testes
CLIENT EDUCATION Regular examination of testes and evaluation of the semen in breeding animals Prompt presentation for veterinary examination if an abnormality is detected
SUGGESTED READING MacLachlan NJ, Kennedy PC: Tumors of the genital systems. In Meuten DJ, editor: Tumors in domestic animals, ed 4, Ames, IA, 2002, Iowa State Press, pp 561–567. AUTHOR: BETH A. VALENTINE EDITOR: MICHELLE A. KUTZLER
26-09-2011 23:40
Tenesmus
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Tenesmus BASIC INFORMATION DEFINITION Ineffectual or painful straining to defecate due to obstruction or inflammatory lesions of distal colon, rectum, or anus
SYNONYM Straining to defecate
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT Frequent posturing to defecate/urinate without producing feces/urine Turning around/looking at hind end while attempting to defecate Excessive licking/chewing of perineal region Flattened, ribbon-like stools Vocalizing (cats most often) Inappropriate defecation in the house/ outside litter box or refusal to defecate owing to severe pain and secondary constipation Common error in cats: overdiagnosis of constipation by owner or veterinarian; careful history/observation reveals lower urinary tract signs PHYSICAL EXAM FINDINGS Observe the animal defecate/urinate; assess if the animal's tail between the legs, low carriage of the tail, resentment of tail elevation (discomfort), presence of an arched back (abdominal or back pain). Examine anus/perianal area: erythema of anal/perineal region, perineal fistulas, perineal masses, pseudocoprostasis (anal obstruction due to severe matting of fur with feces). Abdominal palpation: mass, signs of discomfort despite gentle palpation Rectal palpation may require sedation/ general anesthesia if patients have very painful perineal conditions. Assess for presence of perineal hernia, mass, prostatomegaly, pelvic fractures, fecal consistency (constipation, foreign material), stricture, foreign bodies (e.g., bones, rocks, grass, fur, food wrappers) Cytologic analysis (infection, inflammation) If origin of clinical signs are unclear, catheterize urethra/urinary bladder Palpation of anal sacs (mass, impaction, infection, abscess, or rupture)
ETIOLOGY AND PATHOPHYSIOLOGY Perianal (specifically adjacent to anus) and perineal (whole region between tail and pubis) disorders may be due to anal sac impaction, anal sacculitis, anal sac abscess, perianal gland tumors, perineal hernia, perianal fistula, neoplasia (anal sac adenocarcinoma), pseudocoprostasis. Large bowel: acute diarrhea (see p. 303) Genitourinary (GU) tract: in general, GU abnormalities produce disorders of urination rather than tenesmus (careful history and examination for accurate diagnosis). Prostatomegaly (benign prostatic hyperplasia/hypertrophy [BPH], prostatitis, abscess, neoplasia), paraprostatic cyst, GU neoplasia Caudal abdominal cavity disorders include mass (organ compression), pelvic fractures (misaligned healing of old pelvic fractures), pelvic osteosarcoma
DIAGNOSIS DIAGNOSTIC OVERVIEW Tenesmus is a clinical sign, not a disease; successful management requires identifying the underlying cause. Diagnostic test selection is highly dependent upon obtaining a clear history, observing the animal urinate and defecate, and
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performing a thorough examination of the rectum, perineal, and perianal areas.
DIFFERENTIAL DIAGNOSIS see Etiology and Pathophysiology, above.
INITIAL DATABASE Observe the animal defecating/ urinating. Proper examination of the perineal, perianal area, anus, and rectum (may require sedation if very painful) Urogenital system: vaginal examination to exclude impostors for tenesmus (see p. 1360) Neurologic exam (see p. 1311): perineal reflex, and tone, presence of lumbosacral/back pain CBC, serum biochemical profile, urinalysis: elucidate possible urinary tract or systemic abnormalities Radiographs (abdominal/pelvic): constipation, megacolon, prostatomegaly, pelvic fractures, malunion of pelvic fractures, foreign bodies, masses, or sublumbar lymphadenopathy
ADVANCED OR CONFIRMATORY TESTING Abdominal ultrasonography: gastrointestinal (GI)/pelvic mass, ± lymphadenopathy, urogenital tract, GI motility, distension/wall thickening Intrarectal ultrasonography: specific probes required Colonoscopy: rigid and/or flexible to biopsy polyp/mass(es), strictures or infiltrative lesions Urogenital system (to exclude impostors for tenesmus): vaginal examination, ultrasonography and/or urinary tract contrast radiography, urethroscopy/cystoscopy, culture and sensitivity of urine/prostatic fluid, cytologic examination, and/or biopsies of urinary tract/prostate.
TREATMENT TREATMENT OVERVIEW Treatment should address the underlying cause and relieve any discomfort the animal is experiencing.
ACUTE GENERAL TREATMENT Clip fur and gently wash perineal area if needed. Hydrotherapy to affected area multiple times per day if indicated Enemas: soften impacted feces if constipation Topical cutaneous glucocorticoids/ anesthetics (creams, ointments, suppositories): reduce inflammation/pain Corticosteroid enemas if severe, non-infectious colitis: budesonide (Entocort) 2 mg dissolvable tablet. Give 0.5-1 mg (¼-½ tablet dissolved in enema diluent) per rectum (dose is for most small animals). Budesonide does not tend to reach high concentrations outside the GI-hepatoportal system (high first-pass metabolism), which minimizes systemic glucocorticoid effects. Drain/flush anal gland abscesses. Cyclosporine (3-5 mg/kg PO q 12 h) or topical tacrolimus ointment (0.03%-0.1%) for perianal fistula; cyclosporine more effective Surgery: perineal hernias (repair), colonic or rectal polyps (excision), colonic/rectal/anal sac tumors (resection), rectal strictures (rectal “pull-through”) Adjunctive chemotherapy and/or palliative therapy with piroxicam (0.3 mg/ kg PO q 24-48 h) for anal sac adenocarcinomas
CHRONIC TREATMENT Dependent on the underlying cause
DRUG INTERACTIONS/SIDE EFFECTS Immunosuppressive therapy (azathioprine, chlorambucil): myelosuppression 5-aminosalicylates: keratoconjunctivitis sicca Iatrogenic hyperadrenocorticism with chronic glucocorticoid use Nonsteroidal antiinflammatories (e.g., piroxicam) can cause GI ulceration, renal failure. Blood work prior to initiation recommended to assess liver and renal function. Do not use glucocorticoids and nonsteroidal antiinflammatories concurrently: increased risk of GI ulceration.
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POSSIBLE COMPLICATIONS Recurrent tenesmus, a colonic/rectal obstruction causing obstipation, or a rectal prolapse (uncommon; usually young patients 10 years of age and queens between 5 and 10 years of age Accounts for 1%-19% of all reproductive tumors in dogs and l%-2% of all reproductive tumors in cats GENETICS & BREED PREDISPOSITION: Boxers may be overrepresented. RISK FACTORS: Older age, intact reproductive tract CONTAGION & ZOONOSIS: Transmissible venereal tumor (TVT) uterine metastases can result in TVT dysgerminoma. ASSOCIATED CONDITIONS & DISORDERS: Uterine torsion and/or rupture may occur as a result of uterine neoplasia.
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES: May involve the endometrium (polyp); myometrium (leiomyoma, fibroma, fibroleiomyoma, fibroadenoma, adenoma, leiomyosarcoma, adenocarcinoma, fibrocarcinoma); lipoma; or metastatic disease (lymphoma; transmissible venereal tumor dysgerminoma).
HISTORY, CHIEF COMPLAINT Bloody, mucoid, mucopurulent or mucohemorrhagic vulvar discharge Abdominal distension Ascites Depression or lethargy Vomiting Anorexia Dysuria Constipation Chronic low-grade fever: uncommon PHYSICAL EXAM FINDINGS Bloody vulvar discharge Abdominal distension with palpable midcaudal abdominal mass Weight loss Depression Lymph node enlargement (especially inguinal): uncommon
ETIOLOGY AND PATHOPHYSIOLOGY Uterine tumors may be of endometrial, myometrial, serosal origin; may be primary or metastatic. Leiomyoma is the most common tumor and may be found incidentally or concurrent with pregnancy.
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Uterine Neoplasia
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DIAGNOSIS DIAGNOSTIC OVERVIEW Diagnosis is typically suspected with a history of bloody vulvar discharge with supportive cytologic findings and/or ultrasound evidence of a uterine mass. Histopathologic examination of a specimen from the mass is the confirmatory test of choice.
DIFFERENTIAL DIAGNOSIS Pyometra Segmental endometrial hyperplasia Uterine lithiasis Pregnancy Mummified fetus Subinvolution of placental sites (SIPS) Adenomyosis Granuloma Mural abscess Decidual reaction Remnant of the mesonephric duct Serosal inclusion cysts
INITIAL DATABASE CBC, serum biochemistry profile, urinalysis (avoid unguided cystocentesis): results may be normal with benign tumors to abnormal with metastatic disease, depending on metastatic location. Cytologic examination of vulvar discharge may demonstrate neoplastic cells. Radiographs may reveal an enlarged caudal abdominal viscus. Abdominal ultrasound examination reveals a mass in the uterine, cervical, or vaginal lumen: If mass appears solid (homogeneous, minimally vascularized), fineneedle aspiration for cytologic examination is appropriate. Thoracic radiographs for evidence of metastasis
ADVANCED OR CONFIRMATORY TESTING Hysteroscopy may reveal a luminal or mural mass. Biopsy may be taken via transcervical endoscopic collection technique (TECT). MRI may better delineate the mass and provide further evidence of metastasis (rarely necessary).
TREATMENT TREATMENT OVERVIEW Ovariohysterectomy (OHE): either partial or complete
ACUTE GENERAL TREATMENT Typically, complete OHE is recommended to ensure that any small masses not palpable or visible are removed at the time of initial surgery. Abdominal inguinal lymph nodes may be submitted for assessment of metastasis. If the tumor is long-standing, necrosis of the uterine wall is possible, or adhesions to other abdominal tissues may require resection.
CHRONIC TREATMENT Depending on tumor type and presence of metastasis, chemotherapy, immune modulators, or radiation therapy may be appropriate. Consultation with an oncologist is recommended.
POSSIBLE COMPLICATIONS
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If malignancy is present, complications associated with tumor metastasis in other locations may occur.
RECOMMENDED MONITORING If malignant, monitoring of other organ systems for metastasis may be required.
PROGNOSIS AND OUTCOME Good for benign tumors; guarded to poor for metastatic or malignant tumors
PEARLS & CONSIDERATIONS PREVENTION Ovariohysterectomy will prevent uterine disorders from developing.
CLIENT EDUCATION Brood bitches, regardless of their age, should be spayed after the last litter to prevent tumors from developing.
SUGGESTED READING Johnston SD, Root Kustritz MV, Olson PN: Disorders of the canine uterus and uterine tubes. In Canine and feline theriogenology. Philadelphia, 2001, WB Saunders, p 206. AUTHOR: CHERYL LOPATE EDITOR: MICHELLE KUTZLER
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Uterine Disorders, Non-Neoplastic
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Uterine Disorders, Non-Neoplastic BASIC INFORMATION DEFINITION Uterine torsion: an uncommon condition involving twisting of one or both uterine horns or the uterine body on its own axis Uterine prolapse: a rare condition where the uterus everts through the cervix and vagina (one or both horns may be involved)
EPIDEMIOLOGY SPECIES, AGE, SEX: Either condition may occur at any age or parity. Uterine torsion may occur unrelated to pregnancy. RISK FACTORS Large litter size may predispose to torsion. Any condition causing excessive straining may predispose to prolapse (dystocia, necrotic vaginitis, severe cystitis, diarrhea, constipation). ASSOCIATED CONDITIONS & DISORDERS: Both uterine torsion and uterine prolapse may be associated with shock, sepsis, disseminated intravascular coagulation (DIC), multiple organ dysfunction syndrome (MODS), and systemic inflammatory response syndrome (SIRS).
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES Torsion may involve one or both horns or the uterine body and may be from 90○ to 2160○ (6 complete turns described in one case). Prolapse occurs in the puerperal period and may involve one or both horns, be partial or complete, and occurs rarely prior to delivery of all fetuses. HISTORY, CHIEF COMPLAINT Torsion: History of no progression from stage 1 to stage 2 of labor, or cessation of ongoing stage 2 labor Acute abdominal pain Shock Prolapse: History of prolonged straining (labor, other) Tissue protrudes from the vulvar lips. Queens may present up to 48 hours after delivery of last kitten. PHYSICAL EXAM FINDINGS Acute abdominal pain and splinting Crying Hemorrhagic vulvar discharge Excessively vulvar licking Abdominal distension Tachycardia and tachypnea Pale mucous membranes with increased capillary refill time +/− Collapse +/− Devitalized prolapsed tissue
ETIOLOGY AND PATHOPHYSIOLOGY
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Torsion: unknown etiology; may be due to fetal or bitch activity or abnormal uterine motility (inertia) with continued fetal activity Prolapse: eversion of the tip of a uterine horn followed by excessive straining (due to any cause) during uterine involution or eversion of the tip of a horn due to uterine inertia followed by normal uterine contraction patterns
DIAGNOSIS DIAGNOSTIC OVERVIEW Torsion: diagnosis is based on cessation of labor or acute abdominal pain. Ultrasound may be supportive, but the diagnosis is conclusively made on exploratory laparotomy. Prolapse: diagnosis is based on physical exam findings of prolapsed tissue from the vulvar lips following parturition. Inability to locate the uterus on ultrasound of the abdomen is confirmatory.
DIFFERENTIAL DIAGNOSIS Uterine torsion: Pyometra Uterine rupture Uterine inertia (primary or secondary) Acute gastrointestinal disorders (bloat, gastric or mesenteric torsion), other causes of the acute abdomen Uterine prolapse: Bladder or vaginal prolapse Vaginal, cervical, or uterine neoplasia
INITIAL DATABASE CBC: +/− leukocytosis +/− toxic neutrophils, evidence of dehydration Serum biochemistry profile: normal to increased renal and hepatic values and electrolyte disturbance depending on duration. Abdominal ultrasonography: Hemorrhage into the uterine lumen and edema (hypoechogenicity) of the uterine wall adjacent to the torsion Fetuses may be viable or dead. Intraluminal gas may be present.
ADVANCED OR CONFIRMATORY TESTING
TREATMENT TREATMENT OVERVIEW Treatment goals are: Patient stabilization (IV fluid resuscitation, pain control) Exploratory laparotomy for correction of torsion, Caesarian section to deliver remaining fetuses if still viable, or ovariohysterectomy (OHE) if tissue is devitalized. Prolapsed tissue is cleaned and replaced with combination of manual manipulation externally +/− abdominal approach. OHE may be necessary if tissue devitalized.
ACUTE GENERAL TREATMENT Torsion: Broad-spectrum antibiotics (ampicillin, 10-20 mg/kg IV q 6-8 h + enrofloxacin, 2.5-5 mg/kg IM q 12 h; maximum 5 mg/kg q 24 h in cats) as soon as the diagnosis is confirmed and when devitalized tissue is present. Do not detorse the affected horn(s), as this may result in reperfusion injury and allow systemic circulation of bacteria and
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toxin. If only one horn is affected, a partial OHE may be performed, oversewing the uterine body at the level of the bifurcation. Prolapse: Initially, digital pressure and inversion of the horn into itself starting distally and working towards the tip Care should be taken to invert the entire horn to its tip (ultrasound may be used to confimi this). Oxytocin may be administered after complete inversion. If manual reduction is impossible, uterine amputation is indicated.
CHRONIC TREATMENT Long-term antibiotics (2 weeks) should be administered.
BEHAVIOR/EXERCISE If the dam is stable, she may be allowed to nurse the neonates.
RECOMMENDED MONITORING CBC, serum biochemistry profile
PROGNOSIS AND OUTCOME With early diagnosis, the prognosis is good for survival. With systemic illness, the prognosis for survival may be guarded to poor. Recurrence is unlikely.
PEARLS & CONSIDERATIONS COMMENTS Caution should be taken when handling either condition, as the uterine wall may be friable. Do not administer calcium or oxytocin to patients suspected of torsion or prolapse.
PREVENTION Ovariohysterectomy will prevent uterine disorders from developing.
CLIENT EDUCATION Failure of an animal to continue to progress through labor should instigate a veterinary examination. Bloody discharge or abdominal pain during or after delivery is abnormal.
SUGGESTED READING Shull, RM, Johnston SD, Johnston GR, et al: Bilateral torsion of uterine horns in a non-gravid bitch. J Am Vet Med Assoc 172:601–603, 1978. Johnston SD, Root Kustritz MV, Olson PN: Disorders of the canine uterus and uterine tubes, and disorders of the feline uterus and uterine tubes. In Canine and feline theriogenology, Philadelphia, 2001, WB Saunders, pp 206, 463. http://www.vetmed.lsu.edu/eiltslotus/theriogenology-5361/canine_surgery.htm AUTHOR: CHERYL LOPATE EDITOR: MICHELLE KUTZLER
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Urolithiasis, Urate/Biurate
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Urolithiasis, Urate/Biurate BASIC INFORMATION DEFINITION Organized concretions within the urinary tract, composed of uric acid and its salts; these comprise approximately 5%-10% of uroliths in dogs (except dalmatians, which form mostly urate uroliths) and cats.
SYNONYMS Biurate urolithiasis, purine urolithiasis, ammonium urate urolithiasis, uric acid urolithiasis, urate calculi/stones
EPIDEMIOLOGY SPECIES, AGE, SEX Urate uroliths account for ∼6% of canine uroliths and 5% of feline uroliths. Urate uroliths are the most common urolith of dalmatian dogs (prevalence ∼35%) and occur predominantly in middle-aged males. Most often seen in young to middle-aged adult dogs and young adult cats GENETICS & BREED PREDISPOSITION All dalmatians are unique in their excretion of uric acid instead of allantoin as an end product of purine metabolism, but only a subset develop urate urolithiasis. The tendency to form uroliths is heritable, although genetics are incompletely understood. Predisposed non-dalmatian breeds include English bulldog and Russian black terrier. Miniature schnauzer, shih tzu, and Yorkshire terriers are over-represented (likely due to congenital portosystemic shunts). RISK FACTORS Portosystemic shunt (PSS; see p. 905) Hepatic microvascular dysplasia Hepatic cirrhosis Acidic urine and/or urinary infection with urease producing bacteria ASSOCIATED CONDITIONS & DISORDERS Urinary tract infection Ureteral or urethral obstruction
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT: Clinical signs often absent. When apparent, signs may include: Hematuria Pollakiuria Inappropriate elimination (penuria) Dysuria Stranguria If congenital hepatic disease is present, growth retardation If hepatic dysfunction is present, encephalopathy and/or hypoglycemia (e.g., altered mentation, seizures) Rarely, systemic illness due to urinary obstruction PHYSICAL EXAM FINDINGS: Physical exam is usually unremarkable. Abnormalities may include: Hematuria (stains on prepuce, vulva, hocks) Palpable cystic calculi Palpable urethral calculi (via digital rectal exam in dogs)
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Urolithiasis, Urate/Biurate
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Enlarged, turgid bladder if urethral obstruction present Renomegaly related to PSS or hydronephrosis Small body size if PSS present Neurologic deficits related to encephalopathy and/or hypoglycemia if due to congenital hepatic disease
ETIOLOGY AND PATHOPHYSIOLOGY Dalmatians: During protein catabolism in non-dalmatian dogs, purine metabolism leads to uric acid oxidation by hepatic uricase, with resultant allantoin production. Despite normal uricase activity, dalmatians convert uric acid to allantoin inadequately, resulting in increased urinary excretion of poorly soluble uric acid. Contributing mechanisms may include decreased tubular resorption of uric acid and less activity of urinary crystalinhibiting proteins. Dogs with hepatic dysfunction: reduced uricase production and increased renal excretion of uric acid and ammonia, resulting from reduced hepatic conversion/urea synthesis Non-dalmatian dogs and cats without hepatic dysfunction: unknown
DIAGNOSIS DIAGNOSTIC OVERVIEW Diagnosis is suspected in dogs with radiolucent uroliths and either a breed predisposition (dalmatian, English bulldog) or hepatic dysfunction. Diagnosis in cats and healthy dogs of other breeds is usually based on quantitative stone analysis.
DIFFERENTIAL DIAGNOSIS Urinary tract infection Other types of uroliths Urinary tract neoplasia
INITIAL DATABASE CBC: often unremarkable, but PSS is associated with microcytosis. Serum biochemical profile: often unremarkable, but may suggest hepatic dysfunction (low blood urea nitrogen [BUN], hypoglycemia, hypocholesterolemia, hypoalbuminemia; hyperbilirubinemia if cirrhosis present). Urinary obstruction leads to azotemia, hyperkalemia, and metabolic acidosis. Urinalysis: frequently aciduria; urate crystals sometime identified; physical irritation and/or secondary infection sometimes leads to hematuria, pyuria, or bacteruria Urine culture and sensitivity to rule out secondary infection Abdominal radiographs: urate uroliths are often radiolucent (radiopacity: struvite = oxalate = CaPO4 = silica > cystine > urate). If visible, often few smooth round uroliths identified Microhepatica is suggestive of PSS, cirrhosis Abdominal ultrasound: confirm urolithiasis, which may be missed on abdominal radiographs. Confirms location of uroliths within the urinary tract; may identify PSS, hepatic abnormalities.
ADVANCED OR CONFIRMATORY TESTING In non-dalmatian dogs or when appropriate: serum bile acids or other tests to rule out hepatic disease Contrast cystography/urethrography: alternative to ultrasound for confirmation/localization of radiolucent stones (see pp. 1237 and 1357) Urolith analysis: retrieved stones submitted for quantitative analysis (crystallography, x-ray diffraction, infrared spectroscopy) to determine urolith type Cystoscopy may facilitate urolith removal for analysis and therapy (see p. 1239).
TREATMENT TREATMENT OVERVIEW
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Urolithiasis, Urate/Biurate
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Although uncommon, urinary tract obstruction requires immediate removal of uroliths. In the absence of urinary obstruction, treatment consists of either medical stone dissolution or manual removal of stones, as well as treatment of underlying disorders (e.g., PSS) or preventive therapy.
ACUTE GENERAL TREATMENT Relieve urinary tract obstruction (see pp. 1353 and 1355). If present, treat hepatic encephalopathy (see p. 501). If present, treat urinary infection (see p. 276). Choose between medical dissolution (see Chronic Treatment, below) and mechanical removal: Urinary tract obstruction should be relieved mechanically. Mechanical removal allows for urolith analysis, culture. Cats are poorly amenable to medical dissolution of urate uroliths. Mechanical removal of calculi: Urohydropropulsion (voiding, retrograde; see pp. 1353 and 1355) Avoid performing voiding urohydropropulsion in male cats. Catheter-assisted retrieval Cystoscopic-assisted retrieval (see p. 1239) Cystotomy/urethrotomy/urethrostomy/pyelotomy/nephrotomy Lithotripsy (see p. 1297; intracorporeal or extracorporeal shock wave lithotripsy)
CHRONIC TREATMENT Animals with hepatic disease: Surgical correction of PSS prevents recurrence; cystotomy may be used to remove uroliths during surgical correction of hepatic shunt. If hepatic disease cannot be corrected, institute medical management (including restricted protein diet), and monitor for recurrence. Promote water consumption to avoid concentrated urine (e.g., canned food, wetting dry food, use of cat water fountains). Feed low-purine calculolytic diet (see Nutrition/Diet, below). If urine remains acidic after diet change, consider adding sodium bicarbonate (25-50 mg/kg PO q 12 h) or potassium citrate (50-150 mg/kg PO q 12 h), with dose adjustment to maintain urine pH of 7.0 to 7.5. Allopurinol 10-15 mg/kg q 12 h PO, with dose reduction for azotemic dogs
NUTRITION/DIET Reduced protein (therefore reduced purine) diet: Dogs: for example, Hills u/d, Royal Canin Urinary UC Low Purine, Royal Canin Vegetarian Formula. For English bulldogs, a renal diet may be preferred, as ultra low-protein diets have been associated with cardiomyopathy. Cats: for example, Hills l/d or k/d
POSSIBLE COMPLICATIONS Chronic use of low purine diets may result in cardiomyopathy, perhaps related to carnitine or taurine deficiency (esp. English bulldogs). Severely protein-restricted diets are inappropriate for growing, pregnant, or lactating animals. Xanthine urolith formation with allopurinol administration
RECOMMENDED MONITORING Serum biochemical profile and urinalysis 2 weeks after diet change. Goal is urine pH 7.0 to 7.5, specific gravity < 1.020, and absent crystals. Assuming adequate renal function and diet adherence, BUN should be < 10 mg/dL. Monitor urinalysis q 2-4 weeks until uroliths resolved and q 3-6 months thereafter. Monitor dissolution of uroliths q 2-4 weeks via lower urinary tract contrast studies or ultrasound. Monitor for recurrence in like manner q 3-6 months for a year, then q 6-12 months.
PROGNOSIS AND OUTCOME Prognosis for dissolution is good in dogs. Recurrence is common unless cause resolved (e.g., PSS corrected).
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PEARLS & CONSIDERATIONS COMMENTS Non-dalmatian dogs with urate uroliths should be evaluated for hepatic disease, even when showing no overt clinical signs of hepatopathy. Cats with urate urolithiasis have underlying hepatic disease less commonly than non-dalmatian dogs.
PREVENTION Avoid high-protein diets in at-risk dogs (e.g., dalmatian), but severely protein-restricted diets or allopurinol prior to a first episode of urate urolithiasis is not recommended. Heritability of tendency to form urate uroliths suggests breeding affected dalmatians should be avoided. Long-term dietary +/− allopurinol therapy is indicated for dalmatians after first episode of urolithiasis.
CLIENT EDUCATION Urethral obstruction is life threatening. Stranguria should prompt immediate veterinary attention. Adherence to dietary therapy must be strict. Implications for heritability in dalmatians should be addressed. Once dalmatians have formed urate uroliths, preventive therapy should continue lifelong.
SUGGESTED READING Albasan H, et al: Evaluation of the association between sex and risk of forming urate uroliths in dalmatians. J Am Vet Med Assoc 227:565, 2005. Bannasch DL, et al: Inheritance of urinary calculi in the dalmatian. J Vet Intern Med 18:483, 2004. Bartges JW, et al: Canine urate urolithiasis. Etiopathogenesis, diagnosis, and management. Vet Clin North Am Small Anim Pract 29:161, 1999. AUTHORS: KAREN K. FAUNT, LEAH A. COHN EDITOR: LEAH A. COHN
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Urolithiasis, Struvite
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Urolithiasis, Struvite BASIC INFORMATION DEFINITION Organized concretions within the urinary tract composed of magnesium ammonium phosphate; struvite uroliths occur commonly in both dogs and cats.
SYNONYMS Magnesium ammonium phosphate stones, struvite calculi/struvite stones, triple phosphate calculi/stones, urease calculi/stones
EPIDEMIOLOGY SPECIES, AGE, SEX Dogs: The most common urolith of dogs, canine struvite uroliths are usually associated with urinary tract infections (UTI) involving urease-producing bacteria. Sterile struvite urolithiasis is rare in dogs. Found at any age, they occur nearly twice as often in females as in males, as females are more likely to have UTIs. Cats: The second most common urolith of cats, struvite uroliths are typically found in sterile, alkaline urine. Male cats may be at increased risk. Compared to calcium oxalate uroliths (most common in cats), cats with struvite uroliths are generally younger (4-7 years of age) and are more likely to be neutered. GENETICS & BREED PREDISPOSITION Dogs: any breed can be affected, but miniature Schnauzers, shih tzus, bichon frises, miniature poodles, cocker spaniels, and Lhasa apsos are overrepresented. Cocker spaniels may form sterile struvite uroliths. Cats: commonly affected breeds include the domestic shorthair, foreign shorthair, ragdoll, Chartreux, Oriental shorthair, and Himalayan. RISK FACTORS Dogs: UTI Highly concentrated urine Infrequent urination Cats: Highly concentrated urine Alkaline urine Diets high in magnesium ASSOCIATED CONDITIONS & DISORDERS Dogs: UTI Cats: feline lower urinary tract signs/disease (FLUTS/D), urethral obstruction
CLINICAL PRESENTATION
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Urolithiasis, Struvite
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HISTORY, CHIEF COMPLAINT: Clinical signs often absent. When signs are apparent, they may include: Hematuria Pollakiuria Dysuria Stranguria Inappropriate elimination (penuria) Rarely, systemic illness due to urinary obstruction or to ascending infection causing pyelonephritis PHYSICAL EXAM FINDINGS: Physical exam is usually unremarkable. Abnormalities may include: Hematuria (stains on prepuce, vulva, or hocks) Painful urinary bladder Palpable cystic calculi Palpable urethral calculi (via digital rectal exam in dogs) Enlarged turgid bladder, if urethral obstruction Renomegaly, if secondary hydronephrosis
ETIOLOGY AND PATHOPHYSIOLOGY Infection-associated struvite urolithiasis (mainly dogs): Bacterial urease converts urea to ammonia and bicarbonate The most common urease-producing pathogens are Staphylococcus and Proteus spp. Other urease-producing pathogens include Pseudomonas. Klebsiella, and Ureaplasma (urease-producing Mycoplasmd) spp. Ammonium binds to phosphorus and magnesium, forming struvite crystals. Bicarbonate increases urine pH. Alkalinity decreases solubility of magnesium ammonium phosphate crystals. Crystals aggregate with organic material (including viable bacteria) and combine to form uroliths. Decreased presence of glycosaminoglycans suggested as a cause in some cases of FLUTS/D. Sterile struvite urolithiasis (mainly cats): there appears to be a complex relationship between diet, water intake, individual predisposition and subsequent urine pH and relative supersaturation. Diets high in magnesium, phosphorus, calcium, chloride, and fiber, with moderate protein content may predispose to struvite crystal formation.
DIAGNOSIS DIAGNOSTIC OVERVIEW Diagnosis is suspected in dogs with radiopaque bladder stones, alkaline urine, and/or urinary infection. The diagnosis is suspected in cats with radiopaque bladder stones, alkaline urine, and/or struvite crystalluria. Quantitative stone analysis is necessary to confirm the diagnosis and provide an optimal treatment/prevention plan.
DIFFERENTIAL DIAGNOSIS Urinary tract infection Other types of uroliths Urinary neoplasia
INITIAL DATABASE CBC: unremarkable Serum biochemistry profile (including electrolytes): unremarkable unless urinary tract obstruction present (see p. 1131) Complete urinalysis: neutral or alkaline (common) urine pH, bacteria (especially likely in dogs), pyuria (especially likely in dogs), hematuria (inconsistent), and crystalluria (inconsistent) are possible. Storage of urine may lead to precipitation of struvite crystals; therefore, urine sediment should be examined within 1 hour of collection. Urine culture (identify uropathogen) and susceptibility (influence antimicrobial therapy) Abdominal radiographs: Struvite calculi are generally radiopaque (radiopacity: struvite = oxalate = CaPO4 = silica > cystine > urate). o Often smooth or round in shape Most commonly located in bladder, sometimes urethra, ureter, or kidney.
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ADVANCED OR CONFIRMATORY TESTING Abdominal ultrasound: little benefit beyond abdominal radiography but will confirm location of stones, assess kidneys for evidence of pyelonephritis or hydronephrosis Urolith analysis: retrieved stones should be submitted for quantitative analysis (crystallography, x-ray diffraction, infrared spectroscopy) to determine urolith type. Urolith culture: retrieved stones can be cultured if urine culture obtained by cystocentesis is negative.
TREATMENT TREATMENT OVERVIEW Although uncommon, urinary tract obstruction requires immediate removal of uroliths. In the absence of urinary obstruction, treatment consists of either a stone-dissolution diet or manual removal of stones as well as treatment of UTI.
ACUTE GENERAL TREATMENT Relieve urinary tract obstruction if present (see pp. 1353 and 1355). Antibiotics for urinary tract infection, based on culture and susceptibility results (dogs > cats; see see p. 276). Generally, antimicrobial therapy is continued until struvite urolith has dissolved or been removed. Choose between medial dissolution and mechanical calculi removal: Urethral obstruction should be relieved mechanically. Mechanical removal allows for urolith analysis, culture. Even large struvite uroliths can be amenable to medical dissolution. Provided urethral obstruction is absent, trial of medical dissolution prior to mechanical removal is reasonable; potential drawbacks include risk of obstruction prior to complete dissolution and ineffective dissolution. For medical dissolution, calculolytic diets (see Nutrition/Diet, below) and appropriate antimicrobials are required: Mean time to dissolution is 3 months (less for sterile uroliths, longer time for nephroliths than for cystoliths). Urinalysis and urine culture should be repeated 5-7 days after initiating medical therapy. Goals are urine pH < 7.0, urine specific gravity 1.010-1.020, and negative culture. Medical therapy is continued 1 month beyond radiographic disappearance of uroliths. Small urolith may become lodged in the urethra (especially males) during urolith dissolution. Mechanical removal of uroliths: Urohydropropulsion (voiding, retrograde; see pp. 1353 and 1355) Avoid performing voiding urohydropropulsion in male cats. Catheter-assisted retrieval Cystoscopic-assisted retrieval (see p. 1239) Cystotomy/urethrotomy/urethrostomy/pyelotomy/nephrotomy Lithotripsy (intracorporeal or extracorporeal shock wave lithotripsy)
CHRONIC TREATMENT Predisposing causes of UTI should be addressed (e.g., control glucosuria in diabetic animals, treat hyperadrenocorticism). For animals in which UTI is a recurrent problem, chronic prophylactic therapy may be considered after appropriate therapy of recognized infection (see p. 276). Promote water consumption to avoid concentrated urine (e.g., canned food, wetting dry food, use of cat water fountains; see p. 387). Dietary therapy is crucial; see Nutrition/Diet, below. Urinary acidifiers are seldom required if the pet is eating an appropriate diet and urinary tract infection is eliminated.
NUTRITION/DIET Many commercially diets designed to aid in struvite urolith dissolution (e.g., Hill's prescription diet s/d, Innovative Veterinary Diets dissolution formula, Royal Canin SO). Monitor urolith size periodically via radiographs (see monitoring). Some dissolution diets provide inadequate nutrition for long-term feeding. Calculolytic diet is continued 1 month past radiographic disappearance of uroliths. Other diets aid in the prevention of recurrent struvite urolithiasis and can be fed long-term (e.g., Hills Pet nutrition c/d and w/d, Royal Canin SO, Eukanuba Low pH/S/Feline)
POSSIBLE COMPLICATIONS
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Risk of urethral obstruction either from small stones or during medical dissolution as the stones become small enough to pass into the urethra (males): Urinary tract obstruction Hydronephrosis Hydroureter Urinary tract infection Urinary polyp formation Uroliths inadvertently may be left behind during surgery (up to 20% of stones are not removed). Some diets appropriate for treatment/prevention of struvite urolithiasis may predispose to calcium oxalate urolithiasis. Malnutrition due to long-term feeding of certain dissolution diets
RECOMMENDED MONITORING Repeat radiographs every 2-4 weeks during medical dissolution to evaluate the size and number of uroliths. If no improvement is seen on radiographs after 4-8 weeks, mechanical removal is indicated. Repeat urinalysis 5-7 days after initiating medical dissolution therapy to ensure pH between 6.5 and 7, specific gravity between 1.010 and 1.020, absent struvite crystals, and absent bacteruria. Ideally, urine culture is repeated 5-7 days after initiating medical dissolution therapy to ensure sterile urine. Repeat urine culture 5-7 days after stopping antibiotics to evaluate for recurrence of infection, then again 3-4 weeks later. If predisposing causes of bacterial cystitis cannot be corrected, or in animals with sterile struvite urolithiasis, repeat urinalysis every 4-6 months. If predisposing causes of bacterial cystitis cannot be corrected, or in animals with sterile struvite urolithiasis, repeat abdominal radiographs initially every 3-6 months for 1 year, then every 6 months thereafter.
PROGNOSIS AND OUTCOME Prognosis for dissolution of uroliths is good. Recurrence of struvite urolithiasis is common.
PEARLS & CONSIDERATIONS COMMENTS Struvite urolithiasis in dogs is routinely associated with a UTI. Elimination of infection is crucial for dissolution of stones with a calculolytic diet. Struvite urolithiasis in cats is rarely associated with UTI; long-term diet modification is often necessary to prevent recurrence. If uroliths fail to resolve with medical therapy, consider: Inadequate infection control Failure to comply with diet restrictions Mixed or alternative urolith composition Struvite crystalluria can be found in normal urine and does not reliably predict struvite urolithiasis.
PREVENTION Dogs: if urinary infection can be eliminated, long-term diet change is usually not necessary. Cats: long-term use of canned struvite-management diets (e.g., Waltham SO or Hills Pet Nutrition c/d or w/d) is best if recurrence noted. The merit of supplementing with glycosaminoglycans is unknown.
TECHNICIAN TIPS Any voided urinary stone should be saved for analysis.
CLIENT EDUCATION Adherence to dietary therapy must be strict. Urinary tract obstruction is life threatening. Stranguria should prompt immediate veterinary attention.
SUGGESTED READING
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Koehler LA, et al: Canine uroliths: frequently asked questions and their answers. Vet Clin North Am Small Anim Pract 39:161, 2009. Lekcharoensuk C, et al: Association between dietary factors and calcium oxalate and magnesium ammonium phosphate urolithiasis in cats. J Am Vet Med Assoc 219:1228, 2001. Lulich JP, et al: Efficacy and safety of laser lithotripsy in fragmentation of urocystoliths and urethroliths for removal in dogs. J Am Vet Med Assoc. 234:1279, 2009. Osborne CA, et al: Analysis of 451,891 canine uroliths, feline uroliths, and feline urethral plugs from 1981 to 2007: perspectives from the Minnesota urolith center. Vet Clin North Am Small Anim Pract 39:183, 2009. AUTHORS: KAREN K. FAUNT, LEAH A. COHN EDITOR: LEAH A. COHN
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Urolithiasis, Oxalate
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Urolithiasis, Oxalate BASIC INFORMATION DEFINITION Organized concretions within the urinary tract composed of calcium oxalate; oxalate uroliths occur commonly in both dogs and cats.
SYNONYMS Jackstones. Calcium oxalate dihydrate crystals: weddellite.
EPIDEMIOLOGY SPECIES, AGE, SEX: Dogs: The relative frequency of calcium oxalate urolithiasis has increased over the last 20 years. Since 2004, they have become the most common canine urolith analyzed at the Minnesota Urolith Center. Incidence is greatest in middle-aged to older castrated male dogs. Calcium oxalate uroliths tend to occur at a younger age in bichon frise dogs. Cats: In recent years, calcium oxalate uroliths have become the second most common feline urolith analyzed at the Minnesota Urolith Center. Incidence is greatest between 7 and 10 years of age, with males accounting for ∼60% of affected cats. GENETICS & BREED PREDISPOSITION Dog breeds at increased risk for developing calcium oxalate stones include the miniature schnauzer, Lhasa apso, Yorkshire terrier, bichon frise, Pomeranian, shih tzu, and miniature poodle. Cat breeds at increased risk for forming calcium oxalate stones include the ragdoll, British shorthair, foreign short-hair, Himalayan, Havana brown, Scottish fold, Persian, and exotic shorthair. RISK FACTORS Hypercalcemia Acidic urine Highly concentrated urine Infrequent urination Primary hyperparathyroidism Hyperadrenocorticism Chronic metabolic acidosis Obesity Diets designed to minimize struvite formation in cats ASSOCIATED CONDITIONS & DISORDERS: Feline lower urinary tract signs/disease (FLUTS/D), urethral obstruction, chronic kidney disease, urinary tract infection
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT: Clinical signs are often absent. When clinical signs are apparent, they may include: Hematuria Pollakiuria Dysuria Stranguria Inappropriate elimination (penuria) Rarely, systemic illness due to urinary obstruction
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Polyuria/polydipsia if concurrent hypercalcemia or renal failure PHYSICAL EXAM FINDINGS: Physical exam is usually unremarkable. Abnormalities may include: Hematuria (stains on prepuce, vulva, or hocks) Painful urinary bladder Palpable cystic calculi Palpable urethral calculi (via digital rectal exam in dogs) Enlarged, turgid bladder if urethral obstruction Renomegaly if secondary hydronephrosis Findings associated with predisposing factors (e.g., hyperadrenocorticism: pot-bellied appearance, alopecia, hepatomegaly)
ETIOLOGY AND PATHOPHYSIOLOGY Hypercalciuria and/or hyperoxaluria promote formation of calcium oxalate urolithiasis. Hypercalciuria may result from increased intestinal absorption of calcium, increased renal excretion of calcium, or increased resorption of calcium from bone with or without hypercalcemia. Hypercalcemia is identified in ∼35% of cats and ∼4% of dogs with calcium oxalate urolithiasis. Hyperoxaluria in cats may be related to dietary sources, inadequate vitamin B6, and hepatic enzyme deficiencies. Urolith formation is potentiated by diminished concentrations of urinary crystallization inhibitors (e.g., citrate, pyrophosphate, glycosaminoglycans, Tamm-Horsfall mucoprotein). Diets with moderate fat and carbohydrate levels are associated with an increased risk of calcium oxalate stone formation, while diets high in moisture with a moderate magnesium, phosphorus, and calcium content result in a diminished risk.
DIAGNOSIS DIAGNOSTIC OVERVIEW Diagnosis is suspected in animals with radiopaque bladder stones and acidic urine, or in animals with radiopaque nephroliths. Quantitative stone analysis is necessary to confirm the diagnosis and identify an optimal treatment/prevention plan.
DIFFERENTIAL DIAGNOSIS Urinary tract infection Other types of uroliths Urinary neoplasia
INITIAL DATABASE CBC: unremarkable Serum biochemistry profile (including electrolytes) typically unremarkable: Hypercalcemia or evidence of endocrinopathy detected uncommonly Urinary tract obstruction leads to azotemia, hyperkalemia, and metabolic acidosis. Urinalysis: acidic to neutral pH unless secondary bacterial infection present; crystalluria (inconsistent); hematuria and/or pyuria (occasional): Storage of urine may lead to precipitation of oxalate crystals (artifact); urine sediment should be examined within 1 hour of collection. Urine culture and sensitivity to rule out secondary infection Abdominal/pelvic radiographs: radiopaque calculi most commonly located in bladder, sometimes urethra, ureter, or renal pelvis: Relative radiopacity of uroliths: struvite = oxalate = CaPO4 = silica > cystine > urate Shape varies from spiculated (dihydrate) to smooth (monohydrate), sometimes jackstone. The perineum must be included in the radiographic field in order to see uroliths located in the urethra.
ADVANCED OR CONFIRMATORY TESTING Abdominal ultrasound: little benefit beyond abdominal radiography but will confirm location of stones, assess kidneys for evidence of pyelonephritis or hydronephrosis. Urolith (stone) analysis: retrieved stones should be submitted for quantitative analysis (crystallography, x-ray diffraction, infrared spectroscopy) to determine urolith type. Urolith culture: retrieved stones can be cultured if urine culture obtained by cystocentesis is negative. Cystoscopy may facilitate stone removal for analysis and therapy (see p. 1239).
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Specific diagnostic tests may be indicated to identify predisposing conditions (e.g., parathyroid hormone assay).
TREATMENT TREATMENT OVERVIEW Although uncommon, urinary obstruction requires immediate removal of uroliths. Oxalate stones cannot be dissolved through medical therapy, so uroliths in the bladder or urethra should be removed mechanically if they are causing clinical signs. Recurrence is common (up to 50% in 3 years in dogs).
ACUTE GENERAL TREATMENT Relieve urinary tract obstruction (see pp. 1353 and 1355). Antibiotics (choice based on culture and susceptibility) if secondary urinary tract infection is identified If uroliths are found incidentally in the absence of clinical signs, it is reasonable to institute preventive measures to minimize growth of uroliths and adopt a program of regular follow-up, including periodic urinalysis, urine culture, and radiography. Mechanical removal of bladder/urethral calculi producing clinical signs. Radiographs should be repeated afterwards to ensure complete removal: Urohydropropulsion (voiding, retrograde; see pp. 1353 and 1355) Avoid performing voiding urohydropropulsion in male cats. Catheter-assisted retrieval Cystoscopic-assisted retrieval (see p. 1239) Cystotomy/urethrotomy/urethrostomy/pyelotomy/nephrotomy Lithotripsy (see p. 1297; intracorporeal or extracorporeal shock wave lithotripsy) Calcium oxalate is the most common type of nephrolith/ureterolith. Because surgical removal of nephroliths may be associated with loss of renal function (see p. 760), it is not uniformly indicated.
CHRONIC TREATMENT Determine whether underlying disorder (e.g., hyperadrenocorticism, hyperparathyroidism) is present, and treat appropriately. For cats with idiopathic hypercalcemia, a diet high in fiber may be beneficial. To simultaneously alkalinize the urine, add potassium citrate (75 mg/kg PO q 12 h, adjusted to increase urine pH to 6.5-7.0). Initiate measures to prevent recurrence, as described (see Prevention, below).
NUTRITION/DIET Avoid calcium supplements. Avoid foods high in oxalate. Feed reduced protein diets which promote diuresis and formation of alkaline urine. For example, Hill's Pet Nutrition u/d or w/d, Royal Canine Urinary SO, CNM NF-Formula (dogs) or Hill's Pet Nutrition Feline c/d Multicare, Royal Canine Urinary SO, CNM NF-Formula (cats) Feed canned food when possible.
POSSIBLE COMPLICATIONS Urinary tract obstruction Hydronephrosis Hydroureter Chronic kidney disease (nephrolithiasis) Urinary tract infection Some diets appropriate for prevention of calcium oxalate urolithiasis may predispose to struvite urolithiasis.
RECOMMENDED MONITORING Repeat urinalysis q 2 weeks, starting 2 weeks after removal of stones and initiation of dietary changes until pH is between 6.5 and 7.0, specific gravity is between 1.010 and 1.020, and no calcium oxalate crystals are found. If goals are not met, consider adding supplementary therapies (see Prevention, below). Repeat abdominal radiographs and a urinalysis every 3-6 months for the first year, then every 6-12 months thereafter to evaluate for recurrence of uroliths. Monitor and treat any concurrent conditions such as hypercalcemia.
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PROGNOSIS AND OUTCOME Recurrence is common; therefore, long-term monitoring and care are required. Nephrolithiasis may be associated with diminished renal function.
PEARLS & CONSIDERATIONS COMMENTS Calcium oxalate urolithiasis frequently recurs. Therefore, long-term management and observation are necessary. Calcium oxalate crystalluria does not necessarily correlate with the presence of calcium oxalate uroliths. Calcium oxalate dihydrate crystals (square envelope or Maltese cross shape) are more commonly associated with nutritional or artifactual causes, whereas calcium oxalate monohydrate crystals (picket fence board or flattened hexagon shape) are sometimes associated with ethylene glycol intoxication. Calcium oxalate dihydrate crystalluria can be found in normal urine and does not reliably predict oxalate urolithiasis. Large quantities of calcium oxalate dihydrate crystals or large crystal aggregates should prompt evaluation of hyperoxaluric or hypercalciuric conditions. The appearance of calcium oxalate monohydrate crystals in a dog presenting with acute renal failure is strongly suggestive of ethylene glycol intoxication (see p. 369). Because it is an acute intoxication, ethylene glycol does not lead to oxalate urolithiasis.
PREVENTION Treat any identified cause of hypercalcemia/hypercalciuria. Initiate measures to prevent recurrence in a stepwise manner, adding the next measure when the first one is found to be insufficient to produce urine with a pH between 6.5 and 7.0, a urine specific gravity between 1.010 and 1.020, or prevent calcium oxalate crystal formation: Promote water consumption (e.g., canned diet, wetted food, water fountains for cats). Provide diet with restricted oxalate, sodium, and protein and which does not acidify the urine (see Nutrition/Diet, above). Potassium citrate can be added if the urinary pH remains acidic. Initial dose of 50-75 mg/kg PO q 12 h is adjusted to maintain urine pH 6.5-7.0. If calcium oxalate crystalluria persists despite prior measures, hydrochlorothiazide (2-4 mg/kg PO q 12 h) or vitamin B6 (2 mg/kg PO q 12 h) can be added. Avoid supplementation of vitamins C and D. For male cats with recurrent history of urethral obstruction, consider perineal urethrostomy.
CLIENT EDUCATION Adherence to dietary therapy must be strict. Urinary tract obstruction is life threatening. Stranguria should prompt immediate veterinary attention.
SUGGESTED READING Bartges JW, et al: Update: management of calcium oxalate uroliths in dogs and cats. Vet Clin North Am Small Anim Pract 34:969, 2004. Lekcharoensuk C, et al: Patient and environmental factors associated with calcium oxalate urolithiasis in dogs. J Am Vet Med Assoc 217:55, 2000. Lekcharoensuk C, et al: Association between dietary factors and calcium oxalate and magnesium ammonium phosphate urolithiasis in cats. J Am Vet Med Assoc 219:1228, 2001. Lulich JP, Osborne CA: Changing paradigms in the diagnosis of urolithiasis. Vet Clin North Am Small Anim Pract 39:79–91, 2009. AUTHORS: KAREN K. FAUNT, LEAH A. COHN EDITOR: LEAH A. COHN
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Urolithiasis, Other
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Urolithiasis, Other BASIC INFORMATION DEFINITION Organized concretions within the urinary tract composed of cystine, calcium phosphate (CaPO4), or silica; these are uncommon to rare in dogs and cats.
SYNONYMS CaPO4: apatite uroliths. Cystine: cysteine
EPIDEMIOLOGY SPECIES, AGE, SEX Cystine: uncommon in dogs, rare in cats. Onset in middle age; occurs predominantly in males. CaPO4: uncommon in dogs, rare in cats. Middle-aged to older. Gender prevalence varies: brushite—mostly males; hydroxyapatite—either sex; carbonate apatite—female. Silica: very rare in dogs. Onset in middle age; males predominate. GENETICS & BREED PREDISPOSITION: Several breeds are overrepresented for each urolith type: Cystine: many dog breeds, including Newfoundland and Labrador (autosomal recessive trait), English bulldog, Siamese cats. Prevalence greater in Europe than in the United States. CaPO4: Yorkshire terrier, miniature schnauzer, bichon frise, shih tzu, pug, springer spaniel, Pomeranian, miniature poodle, and cocker spaniel Silica: German shepherds, Labrador, boxer, Old English sheepdogs, rottweiler, miniature schnauzer, shih tzu, Lhasa apso, bichon frise, and Yorkshire terrier RISK FACTORS Cystine: renal tubular transport defect CaPO4: primary hyperparathyroidism, distal renal tubular acidosis, hypercalcemia ASSOCIATED CONDITIONS & DISORDERS Urethral obstruction Urinary tract infection Renal dystrophic mineralization A link between cystinuria and taurine-deficient dilated cardiomyopathy has been proposed in the Newfoundland dog but remains unproven (cystine is a precursor for taurine synthesis).
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT: Clinical signs may be absent. If present, they may include: Hematuria Pollakiuria Dysuria Stranguria Inappropriate elimination (periuria) Rarely, systemic illness due to urinary obstruction PHYSICAL EXAM FINDINGS: Examination is often unremarkable. Abnormalities, if present, may include: Hematuria (stains on prepuce, vulva, if present, or hocks) Painful urinary bladder Palpable cystic calculi
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Palpable urethral calculi (via digital rectal exam) Enlarged turgid bladder, if urethral obstruction Renomegaly, if secondary hydronephrosis
ETIOLOGY AND PATHOPHYSIOLOGY Cystine: Inborn error of metabolism leads to defective renal tubular transport of cystine (± other amino acids) resulting in cystinuria, but not all animals with cystinuria form uroliths. Cystine becomes insoluble in acidic urine. CaPO4: Hypercalcemia is contributory but not necessary. Hypercalciuria may occur without hypercalcemia. Factors decreasing the solubility of calcium salts (e.g., urine pH) or promoting crystallization (e.g., deficient inhibitor substances, epitaxy [concentric layered formation of a stone of mixed composition]) also contribute. Silica: Poorly understood. May be associated with ingestion of silica-rich feedstuffs such as rice or soybean hulls.
DIAGNOSIS DIAGNOSTIC OVERVIEW Radiolucent uroliths can be missed by routine abdominal radiography but are often identified via ultrasonography. Confirmation of the specific urolith type, which dictates optimal treatment and prevention, ultimately depends upon analysis of uroliths after removal.
DIFFERENTIAL DIAGNOSIS Other types of uroliths (struvite, calcium oxalate uroliths most common) Urinary neoplasia Urinary tract infection (UTI)
INITIAL DATABASE CBC: unremarkable Serum biochemical profile: hypercalcemia in some animals with CaPO4 uroliths. If urinary obstruction present, azotemia and electrolyte abnormalities (see p. 1131) Complete urinalysis: hematuria, bacteruria, pyuria are found inconsistently. Cystine: aciduria to neutral urine pH; sometimes flat, hexagonal crystals CaPO4: alkaluria (apatite/hydroxyapatite) to neutral to aciduria (brushite); sometimes amorphous or long, thin prism-like crystals Silica: pH variable (solubility not linked to pH) Urine culture and susceptibility to rule out UTI Abdominal radiographs: Cystine uroliths: radiolucent to slightly radiopaque, round to oval, typically smooth CaPO4 uroliths: radiopaque, round or faceted, smooth Silica uroliths: radiopaque, jackstone (radial spokes from round center) Relative radiopacity: struvite ≥ oxalate = CaPO4 = silica > cystine > urate Abdominal ultrasound: confirm/identify radiopaque/radiolucent uroliths, assess kidneys for pyelonephritis, hydronephrosis. If urethral obstruction is suspected, catheterization to identify or rule out obstruction.
ADVANCED OR CONFIRMATORY TESTING Contrast cystography/urethrography for radiolucent uroliths Urolith analysis: retrieved stones should be submitted for quantitative analysis (crystallography, x-ray diffraction, infrared spectroscopy) to determine urolith type Cystoscopy may facilitate stone removal for analysis and therapy. Screening tests for cystinuria (Metabolic Screening Laboratory, Veterinary Hospital, University of Pennsylvania: www.vet.upenn.edu/penngen) Assay of urine calcium excretion rarely used to document hypercalciuria Specific tests to identify cause of hypercalcemia, if present (see p. 553)
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TREATMENT TREATMENT OVERVIEW Although uncommon, urinary obstruction requires immediate removal of uroliths. Appropriate treatment depends upon identification; mechanical removal facilitates identification of these uncommon uroliths. Silica and CaPO4 uroliths are not amenable to medical dissolution.
ACUTE GENERAL TREATMENT Relieve urinary tract obstruction if present (see pp. 1353 and 1355) Antibiotics for documented urinary tract infection; selection based on culture and susceptibility Choose between medical dissolution and mechanical calculi removal: Urinary obstruction should be relieved mechanically. Mechanical removal allows for urolith analysis, culture. Cystine uroliths are amenable to medial dissolution; CaPO4 and silica uroliths are not. Medical dissolution: see Chronic Treatment, below. Mechanical removal of calculi: Urohydropropulsion (voiding, retrograde; see and ) Avoid performing voiding urohydropropulsion in male cats. Catheter-assisted retrieval Cystoscopic-assisted retrieval (see p. 1239) Cystotomy/urethrotomy/urethrostomy/pyelotomy/nephrotomy Lithotripsy (see p. 1297; intracorporeal or extracorporeal shock wave lithotripsy)
CHRONIC TREATMENT Promote water consumption to avoid concentrated urine (e.g., canned food, wetting dry food, use of cat water fountains). Precipitation/concretion of minerals less likely in dilute urine. Cystine uroliths: dissolution may require 1-6 months Limit dietary cystine with a restricted protein diet low in methionine (e.g., Hill's u/d). See Nutrition/Diet, below. If urine remains acidic, add potassium citrate (50-150 mg/kg PO q 12 h; dose adjusted to maintain urine pH of 7.0-7.5). Avoid sodium bicarbonate. Solubility of cystine in dogs is increased by administration of N-(2-mercaptopropionyl)-glycine (2-MPG) A higher dose (15-20 mg/kg PO q 12 h) promotes urolith dissolution. A lower dose (10-15 mg/kg PO q 12 h) is used to prevent recurrence. CaPO4: medical dissolution not possible. After mechanical removal, address conditions causing hypercalcemia when present. Silica: medical dissolution not possible. After mechanical removal, decrease consumption of vegetable materials and soil (see Nutrition/Diet, below).
NUTRITION/DIET Cystine: Calculolytic diet with restricted protein and low in methionine (e.g., Hills Prescription Diet u/d) fed at least 1 month past dissolution. If an ultra low-protein diet is not appropriate, consider a renal diet (e.g., Hill's k/d) with the addition of potassium citrate to keep the urine pH > 7.2. Low purine diets (e.g., Royal Canine Urinary UC Low Purine, Hill's k/d) can be fed to reduce cystine recurrence. Silica: although dissolution not possible, feeding a diet low in vegetable materials and soil may reduce recurrence (e.g., avoid rice, soybean hulls).
POSSIBLE COMPLICATIONS Risk of urethral obstruction (small stones or during medical dissolution of cystine uroliths) Urinary tract obstruction Hydronephrosis Hydroureter Urinary tract infection Urinary polyp formation Uroliths may be left behind during surgery (up to 20% of stones are not removed). Cystinuric dogs (especially English bulldogs) fed ultra low-protein diets may be at risk of dilated cardiomyopathy. Although uncommon, 2-MPG can lead to aggression, dermatopathy, myopathy, proteinuria, spherocytic anemia,
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thrombocytopenia, or increased hepatic enzymes.
RECOMMENDED MONITORING Repeat urinalysis 2 weeks after initiation of medical therapy or diet changes, and again every 2-4 weeks thereafter to assess for pH, crystals, specific gravity, or evidence of infection. When pH and specific gravity have met goals (specific gravity < 1.020, pH as appropriate for urolith type), monitoring frequency can be extended to q 3-6 months for a year, then q 6-12 months. Imaging (radiographs for CaPO4 and silica; contrast or ultrasound for cystine) should be repeated after mechanical removal or q 2-4 weeks during dissolution (cystine). Thereafter, imaging should be repeated q 6-12 months. Urine should be cultured if signs/uroliths recur or an active urine sediment is identified on urinalysis.
PROGNOSIS AND OUTCOME Because cystinuria is due to a persistent renal tubular defect, recurrence of cysteine urolithiasis is likely without dietary modification ± 2-MPG
PEARLS & CONSIDERATIONS COMMENTS All of these uroliths are rare, and only the cystine urolith can be medically dissolved.
PREVENTION Promote water consumption (e.g., canned food, wetted food, water fountains). Cystine: restricted protein diet, urine alkalinization as necessary, ± long-term use of 2-MPG. Avoid breeding carrier dogs. CaPO4: address hypercalcemic disorders directly (e.g., surgical correction of hyperparathyroidism). Avoid low-calcium diets (paradoxic hypercalciuria). Other therapies (e.g., thiazide diuretics, dietary modifications, acidification of urine) may be warranted in cases with multiple recurrences. Silica: avoid feedstuffs high in silica (e.g., rice, soybean hulls).
CLIENT EDUCATION Adherence to dietary therapy must be strict for urolith dissolution. Animals with metabolic defects should not be bred. Genetic tests are available for cystinuria in Newfoundlands and Labradors (University of Pennsylvania). Urinary tract obstruction is life threatening. Stranguria should prompt immediate veterinary attention.
SUGGESTED READING Kruger JM, et al: Canine calcium phosphate uroliths. Etiopathogenesis, diagnosis, and management. Vet Clin North Am Small Anim Pract 29:141, 1999. Osborne CA, et al: Canine cystine urolithiasis. Cause, detection, treatment, and prevention. Vet Clin North Am Small Anim Pract 29:193, 1999. Osborne CA, et al: Canine silica urolithiasis. Risk factors, detection, treatment, and prevention. Vet Clin North Am Small Anim Pract 29:213, 1999. Osborne CA, et al: Analysis of 451,891 canine uroliths, feline uroliths, and feline urethral plugs from 1981 to 2007: perspectives from the Minnesota urolith center. Vet Clin North Am Small Anim Pract 39:183, 2009. Sanderson SL, et al: Evaluation of urinary carnitine and taurine excretion in 5 cystinuric dogs with carnitine and taurine deficiency. J Vet Intern Med 15:94, 2001. AUTHORS: KAREN K. FAUNT, LEAH A. COHN EDITOR: LEAH A. COHN
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Uroabdomen
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Uroabdomen BASIC INFORMATION DEFINITION A condition characterized by accumulation of urine within the peritoneal and/or retroperitoneal spaces; caused by leakage of urine from the kidneys, ureters, bladder, or proximal urethra
SYNONYMS Urinary tract rupture, uroperitoneum
EPIDEMIOLOGY SPECIES, AGE, SEX: May affect all species and ages and both sexes; males may be slightly more predisposed due to anatomic characteristics. RISK FACTORS: Preexisting compromise of the urinary tract owing to urinary obstruction (urolith[s], neoplasia, other), iatrogenic causes (urethral catheterization, aggressive bladder palpation, surgical complication [laceration or ligation of urinary tract]), or abdominal or pelvic trauma (hit by car, pelvic fractures of any cause, penetrating abdominal wounds) ASSOCIATED CONDITIONS & DISORDERS Hyperkalemia Metabolic acidosis Septic abdomen (if urine was infected) Postrenal azotemia
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT Nonspecific lethargy, anorexia, discomfort, vomiting Signs identifying or suggesting the underlying cause (e.g., witnessed being hit by a car; worsening pollakiuria due to obstruction) Urination: ability to pass urine does not rule out urinary tract rupture or uroabdomen; patient may or may not be hematuric. PHYSICAL EXAM FINDINGS Dehydration Abdominal pain: Lack of signs of abdominal pain does not rule out uroabdomen, but because of chemical peritonitis, most are painful. Lack of a palpable bladder: Palpable bladder does not rule out urinary tract rupture/uroabdomen (small rupture, but still potentially life threatening). Bruising (perineum, ventral abdomen, and inguinal region) Depression Inappropriate bradycardia (from hyperkalemia): Unlike dogs, cats may have severe hyperkalemia and maintain a normal or elevated heart rate.
ETIOLOGY AND PATHOPHYSIOLOGY Accumulation of urine in the abdominal cavity results in the following consequences: Translocation of solutes that are normally higher in urine concentration (urea, creatinine, potassium, hydrogen) across the peritoneal lining into the extracellular fluid spaces and systemic circulation Postrenal azotemia Metabolic acidosis Hyperkalemia
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Uroabdomen
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Chemical peritonitis
DIAGNOSIS DIAGNOSTIC OVERVIEW Definitive diagnosis is based on demonstration of urine in the abdomen. Plasma-to-abdominal fluid gradients of creatinine and potassium are helpful to differentiate uroabdomen from other causes of azotemia and ascites.
DIFFERENTIAL DIAGNOSIS Acute abdomen Ascites of other causes (e.g., hypoalbuminemic, cardiogenic, hemorrhagic) Acute (oliguric/anuric) renal failure
INITIAL DATABASE CBC: generally unremarkable Serum biochemistry profile: moderate or marked blood urea nitrogen (BUN), creatinine, and potassium elevations as well as low Hco3− are common. Urinalysis: cystocentesis not feasible if bladder has collapsed; catheter acceptable if no urethral resistance. Hematuria is most common finding. Abdominal radiographs: loss of serosal detail Abdominal ultrasound: free abdominal fluid (anechoic); ultrasound contrast cystography may confirm bladder rupture (e.g., bladder bubble study). Abdominocentesis, with increased creatinine and potassium of fluid compared with serum
ADVANCED OR CONFIRMATORY TESTING Positive contrast radiography (cystourethrography [bladder, urethra; see and ] or IV excretory urography [kidneys, ureters; see ]). The most sensitive method to confirm urine leakage and localize the site of leakage.
TREATMENT TREATMENT OVERVIEW The mainstay of treatment is normalization of perfusion and correction of hyperkalemia if present. Once the animal is stable, surgical exploration is usually required for definitive repair. Urethral and ureteral surgery is technically demanding, and transfer of the patient to a center with advanced surgical facilities should be considered.
ACUTE GENERAL TREATMENT Intensive fluid therapy to treat shock if present and correct severe dehydration: Fluid without potassium is recommended as an initial choice (e.g., 0.9% NaCl) High fluid rates are often necessary for dehydration correction or for management of postobstructive diuresis. Fluid type and rate are continually reassessed based on physical monitoring and serial electrolyte levels. If the patient's potassium > 7-8 mEq/L and/or there are clinical (e.g., bradycardia) or electrocardiographic (ECG) (e.g., no P waves in all ECG leads) changes due to hyperkalemia, immediate medical therapy and stabilization is required (see p. 556). For animals with lower urinary tract injury and urine accumulation in the peritoneal space: Placement of peritoneal drainage catheter (see p. 1192; simple and life-saving!). Placement of urethral catheter (bladder decompression and prevention of further urine leakage) Placement of prepubic tube cystostomy in animals with severe urethral trauma Analgesia and sedation as indicated, nonsteroidal antiinflammatory drugs should be avoided until azotemia has resolved and renal function has normalized. If urinary tract infection is suspected, broad spectrum antimicrobial drugs are indicated. Every effort should be made to collect urine for culture, and ongoing antimicrobial usage should be guided by culture and sensitivity.
CHRONIC TREATMENT Fluid therapy to replace ongoing losses, including the presence of postobstructive diuresis
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Surgical correction of the site of leakage
NUTRITION/DIET All animals with uroabdomen, but especially cats, can have a long recovery from surgery. Consideration should be given to the placement of a feeding tube (nasoesophageal or esophageal; see and ) at the time of surgery.
DRUG INTERACTIONS Do not add potassium chloride (KC1) to IV fluids until serum potassium level is known to be normal or low.
POSSIBLE COMPLICATIONS Obstruction of the peritoneal drainage catheter with omentum Injury to other intraabdominal structures during placement of peritoneal drainage catheter Urethral stricture formation and urinary incontinence Persistent renal insufficiency
RECOMMENDED MONITORING Frequent monitoring of vital signs, including blood pressure (BP) ECG monitoring if hyperkalemia Fluid input and urine output from both peritoneal drainage and urethral catheters q 2-4 h Serum chemistry, venous blood gas (VBG), packed cell volume (PCV) q 8-12 h during initial stabilization Patient's weight q 12 h
PROGNOSIS AND OUTCOME Prognosis is good with early diagnosis, aggressive emergency management, and definitive repair. The mortality rate is increased in animals with concurrent injuries or underlying neoplasia.
PEARLS & CONSIDERATIONS COMMENTS Consider uroabdomen in animals with a history of abdominal or pelvic trauma, urinary obstruction, or urethral catheterization. A palpable bladder and the ability to void urine do not rule out uroabdomen, because animals with urinary tract disruption may continue to urinate. The abdominal fluid obtained is serosanguineous and may not look like urine; creatinine and potassium concentrations of the fluid are diagnostic when compared to serum levels. Asepsis (urethral and peritoneal drainage catheters, sterile collection system) is essential for preventing complications secondary to infection. In dogs and cats, lower urinary tract injuries are more common than renal/ureteral injuries. Therefore, contrast cystography and retrograde urethrography take precedence over intravenous excretory urography. Surgical repair should not be attempted until the animal has been stabilized with fluid therapy and abdominal drainage.
TECHNICIAN TIPS Fluid therapy is a challenge in these patients, and accurate recording of fluid administration and fluid output are crucial. Patients with uroabdomen often have concurrent disease or injuries and may have a long recovery period; adequate attention to analgesia and nutrition can be of huge benefit to their recovery.
SUGGESTED READING Gannon KM, Moses LM: Uroabdomen in dogs and cats. Compend Contin Educ Pract Vet 24(8):604–612, 2002. AUTHOR: GARETH BUCKLEY EDITOR: ELIZABETH ROZANSKI
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1ST EDITION AUTHOR: KRISTI GANNON
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Urinary Bladder and Urethral Rupture
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Urinary Bladder and Urethral Rupture BASIC INFORMATION DEFINITION Traumatic rupture of the urinary bladder and/or urethra.
EPIDEMIOLOGY SPECIES, AGE, SEX: Urethral trauma more common in males RISK FACTORS Ability to roam freely Blunt trauma (e.g., vehicular accident, kicks, falls) Penetrating injury (e.g., gunshot wound, cystocentesis) Pelvic fracture Fracture of the os penis Urolithiasis Lower urinary tract obstruction Urethral catheterization Urogenital surgery ASSOCIATED CONDITIONS & DISORDERS Azotemia/uremia Hyperkalemia
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT Precipitating event (e.g., trauma, penetrating injury) Dysuria or anuria (common); ability to produce urine stream does not rule out urinary bladder rupture. Hematuria (common) Vomiting (common) Depression (common) Anorexia (common) Abdominal pain (may not be noticed by owners) Urethrocutaneous fistula (uncommon; chronic) PHYSICAL EXAM FINDINGS Abdominal effusion (especially with bladder rupture) Caudal abdominal pain (especially common with bladder rupture) Dehydration (common) Depression (common) Dysuria (especially common with urethral rupture) Halitosis (with uremia) Hematuria (especially common with urethral rupture) Hypovolemia secondary to urine peritonitis/uroabdomen Inability to palpate bladder (especially common with bladder rupture) Pelvic fracture (sometimes present when trauma causes urinary tract rupture) Stranguria (especially common with urethral rupture) Uremic oral ulcers +/− Ventral abdominal wall or perineal bruising +/−
ETIOLOGY AND PATHOPHYSIOLOGY
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Blunt external trauma, penetrating projectiles, perforation by fracture fragments Iatrogenic: secondary to catheterization, cystocentesis, or other diagnostic procedure errors; forceful bladder expression Intraperitoneal accumulation of urine results in chemical peritonitis, azotemia, hyperkalemia, and acidemia; death may occur in 3-5 days if animal is left untreated. Extraperitoneal accumulation of urine results in cellulitis and tissue death acutely and may result in formation of urethrocutaneous fistulas if the rupture is not treated. See Uroabdomen, .
DIAGNOSIS DIAGNOSTIC OVERVIEW Urinary tract rupture should be suspected in animals with uremia and dysuria/oliguria, especially after either abdominal trauma or suspected urethral obstruction. Whereas animals with simple urethral obstruction often have large bladders, the bladder may be small or nonpalpable in animals with urinary bladder rupture.
DIFFERENTIAL DIAGNOSIS Bladder rupture: Urinary tract infection Urine leakage from upper urinary tract Other causes of peritonitis Urethral rupture: Urinary tract obstruction due to urolithiasis, neoplasia, granulomatous urethritis, or prostatic disease Periurethral hematoma or abscess
INITIAL DATABASE CBC: Initially unremarkable, progressing to neutrophilic leukocytosis, often with left shift as urinary peritonitis develops Serum biochemical profile: Azotemia common Hyperkalemia worsens with time (may be life threatening; i.e., >8 mEq/L) Metabolic acidemia common Abdominal/pelvic radiographs: Loss of serosal detail as urine accumulates in peritoneal space Pelvic or os penis fracture occasionally identified Abdominocentesis (see p. 1193) or peritoneal lavage (see online chapter: Diagnostic Peritoneal Lavage) with fluid analysis: Compare fluid and serum creatinine; fluid creatinine 2× greater than serum creatine is strongly supportive of urinary tract rupture. Abdominal fluid potassium 4× greater than serum potassium also strongly supportive. Urethral catheterization should normally encounter no friction/resistance.
ADVANCED OR CONFIRMATORY TESTING Positive-contrast urethrocystogram (see pp. 1357 and 1237) Ultrasonography
TREATMENT TREATMENT OVERVIEW Rupture of the bladder or urethra represents an urgent problem. Immediate therapy is aimed at stabilization of fluid, electrolyte and acid-base disturbances, with a goal of restoring urinary tract integrity via surgical intervention or temporary urinary diversion while smaller tears in the urinary tract heal on their own.
ACUTE GENERAL TREATMENT Temporary urinary diversion by transurethral catheter or cystostomy tube Correct electrolyte and acid-base disturbances:
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If potassium >7 mEq/L, consider one or more of the following (see p. 556): Regular crystalline insulin (¼ unit/kg IV bolus) with IV dextrose (2 g dextrose/unit insulin over 6 hours IV; 50% dextrose is 0.5 g/mL, 5% dextrose is 0.05 g/mL. Generally administered as 5% dextrose infusion; dextrose concentrations >10% can cause phlebitis). Sodium bicarbonate: 1 mEq/kg IV bolus Calcium gluconate (10% solution): 1 mL/kg slow IV bolus (cardio-protective) Monitor electrocardiogram (ECG) and stop infusion if new arrhythmia occurs. If pH < 7.1, institute sodium bicarbonate therapy: Calculate bicarbonate deficit: [(0.3) × (BW in kilograms) × (base deficit)]. Base deficit is (24 -patient's Hco3−) in milliequivalents per liter. Administer half of deficit in IV fluids over 6 hours. Provide crystalloid fluids at an adequate rate: Rehydration: % dehydration* × body weight (kilograms) = deficit (liters); the asterisk sign* for this equation refers to dehydration entered as a decimal, so 10% is 0.1, 7% is 0.07, and so on. Maintenance: 60 mL/kg per day Ongoing loss: estimate loss from vomiting, third-space loss, and other such losses. Abdominocentesis (see p. 1193) or peritoneal lavage to decrease the effects of uroabdomen Primary repair of rupture or conservative management by urine diversion until adequate healing occurs: Primary repair: Bladder ruptures due to blunt trauma; complete abdominal exploration Complete urethral transections Conservative management by urine diversion: Small bladder perforations (e.g., from catheter trauma) Incomplete urethral lacerations Bladder rupture: urethral catheter ± peritoneal lavage catheter Urethral rupture: urethral catheter or cystostomy tube
CHRONIC TREATMENT Antimicrobial therapy for bacterial cystitis may be necessary after urinary diversion catheter is removed. Stricture formation or urethral dehiscence postoperatively may necessitate antepubic urethrostomy.
POSSIBLE COMPLICATIONS Cardiac bradyarrhythmia due to hyperkalemia Urinary tract infection as a result of urinary catheterization Continued leakage after surgical correction
URETHRAL STRICTURE RECOMMENDED MONITORING Positive-contrast urethrocystography after conservative management to assess adequacy of healing and identify formation of any strictures Observation of animal for dysuria or stranguria Urinalysis and/or urine culture after removing urinary diversion catheter
PROGNOSIS AND OUTCOME Good to excellent for bladder rupture and incomplete urethral transection Guarded to good with complete urethral transection, especially if complicated by urethrocutaneous fistula formation
PEARLS & CONSIDERATIONS COMMENTS Emergency surgery to repair bladder or urethral rupture is rarely necessary if urinary diversion can be established. Address life-threatening shock and metabolic disorders prior to surgery.
PREVENTION Avoid excessive force during bladder expression or catheterization.
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TECHNICIAN TIPS Urinary bladder rupture is possible with aggressive manipulation, especially when urinary obstruction is present. Do not attempt manual bladder expression against firm resistance.
CLIENT EDUCATION Do not allow pets to roam. Dysuria/stranguria can indicate a life-threatening problem and warrant rapid veterinary evaluation. Dysuria and/or stranguria after treatment of urinary tract rupture could indicate stricture formation.
SUGGESTED READING Anderson, RB, et al: Prognostic factors for successful outcome following urethral rupture in dogs and cats. J Am Anim Hosp Assoc 42:136–146, 2006. Meige F, et al: Management of traumatic urethral rupture in 11 cats using primary alignment with a urethral catheter. Vet Comp Orthop Traumatol 21:76–84, 2008. Schmiedt C, et al: Evaluation of abdominal fluid: peripheral blood creatinine and potassium ratios for diagnosis of uroperitoneum in dogs. J Vet Emerg Crit Care 11:275–280, 2001. Waldron DR: Urinary bladder. In Slatter D, editor: Textbook of small animal surgery. Philadelphia, 2003, WB Saunders, pp 1629–1637. EDITOR: LEAH A. COHN 1ST EDITION AUTHOR: ERIC POPE
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Urethral Sphincter Mechanism Incompetence
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Urethral Sphincter Mechanism Incompetence BASIC INFORMATION DEFINITION Urethral sphincter mechanism incompetence is a common cause of involuntary voiding of urine (urinary incontinence). It is most frequently identified in ovariohysterectomized bitches.
SYNONYMS Estrogen-responsive or hormone-responsive incontinence, hormone-responsive urethral incompetence
EPIDEMIOLOGY SPECIES, AGE, SEX: Middle-aged female dogs predominantly affected, although hormone-responsive incontinence can occur in bitches of any age and occurs rarely in neutered males. Onset of incontinence may be months to years after ovariohysterectomy (OHE). GENETICS & BREED PREDISPOSITION: Usually medium- to large-breed dogs. A positive association between tail docking and hormone-responsive incontinence has been demonstrated. Over-represented breeds include boxer, Doberman pinscher, German shepherd, Old English sheepdog, rottweiler, springer spaniel, weimaraner RISK FACTORS: Intrapelvic bladder, short urethra, and obesity. Often occurs in association with ectopic ureter. Any cause of polyuria may initiate or exacerbate clinical signs.
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT Urinary incontinence, often most evident during rest (i.e., patients leave “puddles” after sleeping) Excessive licking of perineum Dogs retain ability to produce normal voluntary urine stream. PHYSICAL EXAM FINDINGS Usually unremarkable. Complete neurologic examination should be conducted, including evaluation of tail and anal tone. Observed episode of urination is normal; bladder will empty nearly completely after voluntary voiding. Perineal urine staining or perivulvar dermatitis sometimes observed.
ETIOLOGY AND PATHOPHYSIOLOGY The vast majority of neutered dogs remain continent. It is unclear why only a minority of neutered bitches develop urethral sphincter mechanism incompetence. Sex hormones apparently sensitize the internal urethral sphincter to the effects of α-adrenergic stimulation. The bladder may be positioned in a relatively caudal position in neutered bitches, lessening the intraabdominal pressures on the urethra that help maintain urethral closure. Urethral sphincter mechanism incompetence is commonly found in intact dogs with ectopic ureter, and may account for continued incontinence after surgical correction of ectopia.
DIAGNOSIS DIAGNOSTIC OVERVEIW The diagnosis is suspected when an otherwise healthy neutered bitch develops urinary leakage, especially during sleep. Ruling out other causes of incontinence and response to therapy are usually used to confirm the diagnosis.
DIFFERENTIAL DIAGNOSIS
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For inappropriate urination, distinguish between urinary incontinence and pollakiuria, polyuria, or behavioral disorders. Differentials for urinary incontinence: lower motor neuron disease/peripheral neuropathy; upper motor neuron disease; dysautonomia; urge incontinence; partial urethral obstruction; and congenital and acquired urinary tract structural defects (ectopic ureter[s], vaginal stricture/stenosis, urethrovaginal fistula).
INITIAL DATABASE Complete neurologic examination (see p. 1311): normal CBC and serum biochemistry profile: unremarkable Complete urinalysis: occasionally reveals evidence of secondary urinary tract infection Urine culture: to rule out urinary tract infection Abdominal radiographs or ultrasound of urinary structures: unremarkable, or bladder may display intrapelvic positioning.
ADVANCED OR CONFIRMATORY TESTING Contrast studies (see p. 1357) and/or cystoscopy (see p. 1239): not routinely required, but can rule out structural causes of urinary incontinence. Urethral pressure profile (UPP) and/or leak point pressure (requires specialized equipment/expertise): not routinely employed for clinical diagnosis but can objectively identify urethral sphincter incompetence. May have prognostic utility in animals with ectopic ureter to predict resolution of incontinence after surgical correction. Positive response to therapy is often used for supporting the diagnosis, but interpretation of result should be cautious because optimal response may require dosage adjustment over weeks.
TREATMENT TREATMENT OVERVIEW Medical treatment with either phenylpropanolamine or hormone therapy usually results in control of incontinence. Endoscopic and surgical therapies are also options.
ACUTE GENERAL TREATMENT If polyuria is identified, the cause should be sought and treatment instituted (underlying cause is likely not hormoneresponsive incontinence alone or at all). Medical therapy with phenylpropanolamine or estrogen compounds Treatment of secondary urinary tract infection with appropriate antimicrobials
CHRONIC TREATMENT Phenylpropanolamine is an α-agonist sympathomimetic used for increasing internal urethral sphincter tone. Available as chewable tablets or oral solution (1-1.5 mg/kg PO q 8-12 h) or as time-released 75-mg capsules (100 lb: 1.5 capsules daily). Discontinue if anxiety, hyperactivity, or tachycardia. Diethylstilbestrol (DES) is a synthetic estrogen that increases sensitivity of internal urethral sphincter to catecholamines. Dosage is empirical, with reduction in frequency and dose to least possible that controls clinical signs. Starting dose: 0.1 mg (small dog), 0.3 mg (medium dog), or 0.7 mg (large dog) total daily dose PO q 24 h for 3-5 days. Then the same dose is given q 5-8 days as needed to control incontinence. Conjugated estrogens (e.g., Premarin, 20 mcg/kg PO q 4 days) have been used in place of DES. Testosterone cypionate (2.2 mg/kg IM q 30 days) can be used in castrated males (but phenylpropanolamine is preferred). Gonadotropin releasing hormone (GnRH) analog can be used in place of DES but is less effective than phenylpropanolamine. Hormones may be administered concurrently with phenylpropanolamine when incontinence persists despite therapy (synergistic actions). Surgical therapies are usually reserved for refractory patients: Cystoscopically administered periurethral injections of collagen or Teflon; may need to be repeated Adjustable hydraulic urethral sphincter placed at surgery Colposuspension, cystourethropexy, urethroplasty, or urethral intussusception
DRUG INTERACTIONS/CONTRAINDICATIONS Hormone therapy may cause adverse reactions: estrogen compounds (e.g., bone marrow suppression), testosterone (e.g., prostatomegaly, behavioral changes) AVOID estradiol cypionate because of increased risk of marrow suppression.
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Phenylpropanolamine may cause adverse reactions (e.g., lethargy, decreased appetite, GI upset, hyperactivity, hypertension). Use with caution or avoid if there is systemic hypertension, heart disease, cardiac arrhythmias, central nervous system disease, or if monoamine oxidase inhibitors or other sympathomimetic agents are used.
POSSIBLE COMPLICATIONS Secondary urinary tract infection
RECOMMENDED MONITORING Periodic urinalysis with Gram stain of sediment and/or bacterial culture and sensitivity if incontinence persists Periodic monitoring of blood pressure in dogs treated with phenylpropanolamine Periodic monitoring of CBC in dogs treated with estrogen drugs
PROGNOSIS AND OUTCOME Most dogs respond to medical therapy with improvement or resolution of clinical signs. Some dogs require more than a single type of medication, and ancillary surgical procedures may be required in some cases.
PEARLS & CONSIDERATIONS COMMENTS Hormone-responsive urinary incontinence is a common cause of urinary incontinence. Diagnosis usually based on clinical presentation, ruling out other common causes of incontinence, and response to therapy. Minimal evaluation includes neurologic examination, observation of urination and palpation of bladder afterwards, urinalysis and urine culture, and imaging of the urinary tract with radiographs or ultrasound.
PREVENTION Hormone-responsive incontinence occurs in only a small percentage of ovariohysterectomized bitches. There is little evidence that early neutering increases likelihood of developing incontinence.
SUGGESTED READING Barth A, et al: Evaluation of long-term effects of endoscopic injection of collagen into the urethral submucosa for treatment of urethral sphincter incompetence in female dogs: 40 cases (1993-2000). J Am Vet Med Assoc 226:73–76, 2005. Byron JK: Effect of phenylpropanolamine and pseudoephedrine on the urethral pressure profile and continence scores of incontinent female dogs. J Vet Intern Med 21:47–53, 2007. Rose SA, et al: Long-term efficacy of a percutaneously adjustable hydraulic urethral sphincter for treatment of urinary incontinence in four dogs. Vet Surg 38:747–753, 2009. AUTHOR & EDITOR: LEAH A. COHN
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Urethral Prolapse
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Urethral Prolapse BASIC INFORMATION DEFINITION Prolapse of urethral mucosa from urethral orifice
EPIDEMIOLOGY SPECIES, AGE, SEX: Young, intact male dogs GENETICS & BREED PREDISPOSITION: English bulldog RISK FACTORS Intact male dog Brachycephalic breed ASSOCIATED CONDITIONS & DISORDERS: Brachycephalic airway syndrome
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT Excessive licking of prepuce or penis Blood from preputial opening Stranguria PHYSICAL EXAM FINDINGS Hemorrhagic discharge from prepuce Red or purple mass protruding from urethral orifice A prolapsed urethra typically appears as a small red bulb of smooth, congested (red) mucosa at the tip of the penis surrounding the urethral opening.
ETIOLOGY AND PATHOPHYSIOLOGY Possible causes include: Excessive sexual excitement Masturbation Genitourinary infection Urolithiasis Secondary swelling of the prolapsed segment prevents spontaneous reduction.
DIAGNOSIS DIAGNOSTIC OVERVIEW Diagnosis is based on patient signalment, presenting history, and physical examination findings.
DIFFERENTIAL DIAGNOSIS Penile trauma Urethritis Neoplasia (transmissible venereal tumor [TVT])
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INITIAL DATABASE Presurgical CBC, serum chemistry profile: generally unremarkable Urinalysis (cystocentesis) ± microbiologic culture: Rule out associated urinary tract infection (UTI), prostatic disease.
ADVANCED OR CONFIRMATORY TESTING Impression smear of prolapsed tissue for cytologic examination: Rule out TVT Abdominal ultrasound examination: Rule out prostatic disease
TREATMENT TREATMENT OVERVIEW The prolapsed urethral mucosa requires surgical correction. Postoperatively appropriate measures should be taken to prevent recurrence of the problem.
ACUTE GENERAL TREATMENT Surgical correction of prolapsed urethra: Urethropexy technique: inversion of urethral mucosa using several mattress sutures
CHRONIC TREATMENT Prevent masturbation in the immediate postoperative period. Treat UTI, prostatic disease, and urolithiasis if present. Consider castration to reduce sexual arousal: Dog should not be used for breeding purposes because of genetic predisposition.
POSSIBLE COMPLICATIONS Recurrence of prolapse after surgical correction
RECOMMENDED MONITORING Observe animals for recurrence of bleeding from prepuce; the signs may indicate recurrence of prolapse.
PROGNOSIS AND OUTCOME Excellent prognosis with appropriate surgical technique
PEARLS & CONSIDERATIONS COMMENTS The hallmark of diagnosis is the physical finding of a red bulb-like mass at the tip of the penis in a patient with stranguria or penile self-trauma.
PREVENTION Recognize genetic predisposition for the problem: English bulldog. Early castration to reduce sexual activity or excitement Prevention of masturbation Prevention of obesity
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TECHNICIAN TIPS Perioperative in-hospital care consists of: Preoperative prevention of additional trauma to prolapsed urethra Sedation, Elizabethan collar Postoperative prevention of trauma to surgical site (see above) Ensuring that adequate analgesia is provided in the postoperative period
CLIENT EDUCATION Early castration in predisposed breeds to reduce sexual activity or excitement Prevention of masturbation and self-trauma to penis Avoid circumstances that would exacerbate respiratory problems in brachycephalic dogs: Obesity Stress Heat, humidity
SUGGESTED READING Kirsch JA, Hauptman JG, Walshaw R: A urethropexy technique for surgical treatment of urethral prolapse in the male dog. J Am Anim Hosp Assoc 38:381–384, 2002. AUTHOR & EDITOR: RICHARD WALSHAW
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Urethral Obstruction
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Urethral Obstruction BASIC INFORMATION DEFINITION A common condition that involves obstruction of the lower urinary tract, usually due to urolith or matrix formation. Other causes (e.g., neoplasia, stricture, infections) are less common.
EPIDEMIOLOGY SPECIES, AGE, SEX Cats and less commonly dogs of any age Males are anatomically predisposed to obstruction. GENETICS & BREED PREDISPOSITION Certain breeds predisposed to specific urolith formation (e.g., Dalmatians: urate uroliths) Other breed predisposed to urethral neoplasia (e.g., Scottish terrier) RISK FACTORS Feline lower urinary tract signs/disease (FLUTS/D) Neoplasia Urinary tract infection Risk factors associated with urolithiasis (see pp. 1138, 1141, 1143, and 1145) ASSOCIATED CONDITIONS & DISORDERS Hydronephrosis Azotemia/uremia Hyperkalemic cardiac dysrhythmia Urinary bladder rupture Bladder atonia/hypotonia Urinary tract infection Post obstructive diuresis
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT Stranguria Anuria/oliguria Hematuria Lethargy Anorexia Vocalization Restlessness Dribbling urine Licking prepuce/vulva (urethral discharge) Dyschezia History of urinary infection or urolithiasis PHYSICAL EXAM FINDINGS Enlarged, turgid urinary bladder (characteristic) Abdominal discomfort (common) Dribbling urine (occasionally)
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Bloody preputial/vulvar discharge (occasionally) Palpable urethral urolith or tumor (digital rectal exam in dogs) (occasionally) Bradycardia if severe hyperkalemia (in very advanced cases)
ETIOLOGY AND PATHOPHYSIOLOGY Urine supersaturation, urinary tract infection, certain disease states, and breed predisposition contribute to urolithiasis. In cats especially, urethral plugs may be composed of matrix (cellular debris, virus-like particles, +/− bacteria, urinary crystals). Uroliths or plugs can obstruct the urethra; urethral anatomy favors obstruction in males.
DIAGNOSIS DIAGNOSTIC OVERVIEW The diagnosis of urethral obstruction is suspected in any patient that is straining to urinate and has an enlarged, firm urinary bladder present on abdominal palpation.
DIFFERENTIAL DIAGNOSIS Detrusor atony FLUTS/D Fungal granulomas Reflex dyssynergia Trauma (pelvic fracture) with urethral damage, bladder entrapment hernia, penile fracture Urethral neoplasia Urethral stricture Urethral tissue valve/flap Urethritis Urolithiasis
INITIAL DATABASE CBC: unremarkable Serum biochemical profile: possible azotemia, hyperkalemia, findings consistent with predisposing conditions Urethral catheterization: distinguish functional from structural urethral obstruction, localize structural obstruction, may relieve obstruction and provide urine for analysis Urinalysis: possible hematuria, crystalluria, pyuria, epithelial cells, dilute urine, bacteruria. Rarely, fungal hyphae or neoplastic cells 3
Urine culture: if sample is obtained by catheterization, quantitative culture to distinguish contamination (7 mEq/L, consider calcium gluconate, sodium bicarbonate, or insulin/dextrose therapy (see pp. 31 and 556). Small plug/urolith at the tip of the penis: remove via gentle massage (cats) Urethral catheterization can be attempted without sedation in male dogs; in cats, bitches, or dogs resistant to catheterization, sedation/anesthesia is usually required (see pp. 1266, 1353, and 1355). Insert a sterile red rubber catheter or open-ended polypropylene catheter into the urethra to the point of obstruction. Once encountered, retropulse the urolith/debris into the urinary bladder using sterile saline or a 75% sterile saline and 25% sterile water-based lubricant mixture. In male cats, a sterile 22-G, 1-inch intravenous catheter (without stylet) may be used to dislodge urethral plug. The urinary bladder is emptied; if debris is identified, lavage with sterile saline. An indwelling urinary catheter attached to a sterile, closed urine collection system is often indicated (e.g., pending correction of anatomic or functional obstruction, in cats with FLUTS/D, or to prevent urolith movement back into urethra following retropulsion and pending cystotomy). For indwelling purposes, polypropylene catheters should be replaced with red rubber or Foley catheters. Ideally, radiographs are obtained to identify remaining radiopaque urethral/bladder uroliths and to evaluate appropriate catheter placement. The catheter should just enter the trigone. If a urinary catheter cannot be passed, periodic cystocentesis can be performed to temporarily empty the urinary bladder pending definitive treatment. See Urethral Obstruction (Canine): Medical Management, ; Urethral Obstruction (Feline): Medical Management, .
CHRONIC TREATMENT Maintain indwelling urinary catheter appropriately (sterile, closed collection system): Typically for 24-72 hours in cats with crystalluria or FLUTS/D Phenoxybenzamine (dog: 0.25 mg/kg PO q 12 h; cat: 2.5 mg/cat PO q 12-24 h) may decrease urethral spasm. Antibiotic therapy based on urine culture/sensitivity; obtain culture when removing catheter. Address urolithiasis: Diet/medical dissolution possible for some types, but risk of repeated obstruction Consider cystotomy, urohydropulsion (voiding, retrograde), cystoscopic-assisted retrieval. Perineal urethrostomy considered for male cats (or dogs) with recurrent obstruction Tube cystostomy for urethral neoplasia while waiting for chemotherapy to work
POSSIBLE COMPLICATIONS Urethral tear Urinary bladder rupture Urethritis Iatrogenic urinary tract infection Urethral stricture Recurrent urinary tract infections with perineal urethrostomy and tube cystostomy
RECOMMENDED MONITORING Daily bladder palpation during hospitalization after removing urinary catheter Repeat urinalysis and urine culture when urinary catheter is removed and again 1 week later. Monitor as appropriate for urolith type or FLUTS/D (see p. 1555).
PROGNOSIS AND OUTCOME Urethral obstruction is rapidly life threatening. If obstruction is alleviated and electrolyte disorders are addressed, prognosis is good (exception: neoplasia). Risk for recurrence is present regardless of cause.
PEARLS & CONSIDERATIONS
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PREVENTION Dietary/medical therapy are indicated when uroliths are identified. Predisposing factors for urolith formation should be addressed directly whenever possible.
TECHNICIAN TIPS Overly aggressive attempts at manual expression of the bladder must be avoided because bladder rupture can result. Straining to urinate without producing a urine stream is highly suggestive of urethral obstruction.
CLIENT EDUCATION Urinary tract obstruction is life threatening. Stranguria or dysuria should prompt immediate veterinary attention. Adherence to dietary therapy for urolith dissolution must be strict.
SUGGESTED READING Bartges JW, et al: Pathophysiology of urethral obstruction. Vet Clin North Am Small Anim Pract 26:255, 1996. Lekcharoensuk C, et al: Evaluation of trends in frequency of urethrostomy for treatment of urethral obstruction in cats. J Am Vet Med Assoc 221:502, 2002. Osborne CA, et al: Medical management of feline urethral obstruction. Vet Clin North Am Small Anim Pract 26:483, 1996. AUTHOR: ANNE M. DALBY EDITOR: LEAH A. COHN
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Ureteral Obstruction
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Ureteral Obstruction BASIC INFORMATION DEFINITION Obstruction of urine flow through one or both ureters. Ureteral obstruction is recognized with increasing frequency, especially in cats.
EPIDEMIOLOGY SPECIES, AGE, SEX: Dogs or cats of any age or sex RISK FACTORS Intraluminal obstruction (e.g., urolith, trauma, inflammation, fibrosis/stricture, congenital stenosis, blood clots) Intramural obstruction (e.g., fibrosis/stenosis, ureterocele, fibroepithelial polyps, proliferative ureteritis, neoplasia) Extramural obstruction (e.g., retroperitoneal or pelvic masses, prostatic/bladder neoplasia, inadvertent ligation or fibrotic entrapment of ureter)
ASSOCIATED CONDITIONS & DISORDERS Renal failure +/− uremia Hydronephrosis/hydroureter Pyelonephritis Uroabdomen (associated with ruptured ureter)
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES Partial or complete Unilateral or bilateral HISTORY, CHIEF COMPLAINT: Clinical signs are often absent, especially with unilateral obstruction. When signs are present, they may be related to acute renal failure or to overt chronic kidney disease. Any of these may be seen: Lethargy/depression (due to uremia or renal pain) Anorexia/vomiting (due to uremia or renal pain) Polyuria and polydipsia (with chronic kidney disease) Dysuria, stranguria, pollakiuria, or hematuria Oliguria or anuria (bilateral obstruction) PHYSICAL EXAM FINDINGS: Physical examination is often normal; abnormalities can include: Dehydration Poor body condition Enlarged kidney(s) (due to hydronephrosis) Abdominal mass Abdominal discomfort (severity related to rate of onset of obstruction rather than degree of obstruction) Halitosis and/or oral ulceration (due to uremia) Abdominal fluid wave (if rupture and uroabdomen)
ETIOLOGY AND PATHOPHYSIOLOGY Urolithiasis is an especially common cause of ureteral obstruction. However, there are many other potential causes (see above).
DIAGNOSIS
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DIAGNOSTIC OVERVIEW Ureteral obstruction may be discovered incidentally during imaging studies or (less often) may be identified as the cause of acute renal failure due to bilateral obstruction. Animals with subclinical or overt chronic kidney disease may be identified as having ureteral obstruction during imaging examinations.
DIFFERENTIAL DIAGNOSIS Other causes of renomegaly (see p. 979), other causes of acute renal failure (see p. 31)
INITIAL DATABASE CBC generally unremarkable: Normocytic, normochromic, nonregenerative anemia (if chronic kidney disease or chronic inflammation) Leukocytosis with left shift possible if concurrent pyelonephritis Serum biochemical profile; abnormalities depend on degree of obstruction and/or nephron loss: Azotemia Hyperphosphatemia Hyperkalemia Metabolic acidosis Urinalysis may be normal or may reveal: Isosthenuria Hematuria Pyuria Urine culture and sensitivity (C&S) indicated even if sediment is inactive (occult infection) Blood pressure (BP) to rule out hypertension (see p. 1209) Abdominal radiographs; renomegaly common; may identify: Urolithiasis Prostatomegaly Abdominal mass Loss of retroperitoneal/abdominal contrast Distended ureter Mass associated with ureter or bladder
ADVANCED OR CONFIRMATORY TESTING Abdominal ultrasound (sensitive and specific): Pyelectasia (dilation of renal pelvis) common Hydronephrosis common Hydroureter common Often allows identification of a cause of ureteral obstruction (e.g., urolithiasis, mass) Excretory urography (intravenous pyelography [IVP]; see ), percutaneous nephropyelography: Pyelectasia Ureteral dilatation or lack of filling (IVP only) Renal scintigraphy or CT: Affected kidney contributes little to overall glomerular filtration rate (GFR). Quantitative analysis and culture of uroliths
TREATMENT TREATMENT OVERVIEW When unilateral obstruction is believed to be long-standing, specific therapy may not be necessary. Acute bilateral ureteral obstruction requires intervention both to relieve obstruction and address consequences such as uremia, electrolyte, and acid-base disorders. Whenever possible, attempts should be made to prevent further obstruction (e.g., prophylaxis of urolithiasis, correction of anatomic defects, removal of obstructive masses).
ACUTE GENERAL TREATMENT Correct hydration, acid-base, and electrolyte disorders if present: Crystalloid fluid therapy for azotemia, dehydration (see p. 31): Initial rate of 120 mL/kg per day unless diuresis contraindicated
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Postobstructive diuresis may require the “ins-and-outs” method of adjustment (rate based on measured urine output). Diuresis may flush out ureterolith. Address electrolyte disorders and acidosis (see pp. 1131 and ). Consider hemodialysis or peritoneal dialysis for stabilization. Percutaneous nephrostomy tubes may be used for preventing further renal damage while assessing renal function prior to surgical intervention: Only possible if renal pelvis dilated Placed with ultrasound guidance or via laparotomy Analgesia for abdominal pain (e.g., buprenorphine, 0.01 mg/kg IM, IV, or SQ q 6-8 h) Address uremic signs (see pp. 31 and 207).
CHRONIC TREATMENT Intervention is not always required if obstruction is partial, there is adequate renal function, and infection is absent. Ureteral surgery or stenting is indicated for bilateral obstruction or when function of contralateral kidney is impaired; major complication is postoperative ureteral stricture formation. Nuclear scintigraphy or CT provides quantitative assessment of each kidney's contribution to glomerular filtration rate: Ureterotomy: for intraluminal or intramural obstruction in the proximal third of the ureter Ureteroneocystostomy: for resection of distal ureter Ureteroureterostomy: to repair ureter after resection or transection (anastomosis of proximal ureter to distal portion of ureter on ipsilateral side), usually when proximal third cannot be implanted directly into bladder neck Highest incidence of postoperative obstruction Ureteral stent placed via interventional endoscopy or surgery should be considered, but has limited availability. Surgery is more widely available, especially if the patient is unstable to transfer to referral centers equipped to perform this noninterventional method. Nephrectomy: reserved for animals with unilateral obstruction, adequate function in contralateral kidney, and infection or loss of function in the affected kidney. Antibiotics if appropriate (e.g., pyelonephritis, bacterial cystitis) based on C&S. Therapeutic or prophylactic measures for urolithiasis if present (see pp. 1141, 1143, and 1138) Therapeutic measures for other identified causes of obstruction (e.g., removal of tumors obstructing urine flow)
POSSIBLE COMPLICATIONS Renal failure Postoperative ureteral stenosis Urinary rupture and uroabdomen
RECOMMENDED MONITORING Repeat ultrasound 10-12 weeks after initial evaluation. Remaining renal parenchymal changes are likely permanent. Animals with permanent hydroureter/hydronephrosis are monitored as for chronic kidney disease (see pp. 205 and 207). Azotemic animals are monitored more intensively than nonazotemic animals.
PROGNOSIS AND OUTCOME Dependent on underlying cause, duration of obstruction, extent of renal parenchymal damage, presence of concurrent infection, and ability to resolve underlying cause. Structural renal changes persisting 14-45 days or more after relief of ureteral obstruction are generally permanent. Complete bilateral obstruction of more than 3 days is fatal without appropriate treatment.
PEARLS & CONSIDERATIONS COMMENTS Ureteral obstruction should be considered in the differential diagnosis for renal failure, especially in patients with evidence of nephrolithiasis or pyelonephritis. Bilateral ureteral obstruction is rare compared to unilateral obstruction but is life threatening. Ureteral obstruction can recur, especially in the presence of existing nephroliths.
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PREVENTION Strategies that limit the formation of urolithiasis (see pp. 1141, 1143, and 1138)
TECHNICIAN TIPS Animals in acute renal failure should have urine output carefully quantified. One possible correctible cause of oliguria/anuria is bilateral ureteral obstruction.
CLIENT EDUCATION Strict adherence to dietary recommendations can minimize the risk of ureteral or urethral obstruction due to urolithiasis.
SUGGESTED READING Hardie EM, et al: Management of ureteral obstruction. Vet Clin North Am Small Anim Pract 34:989, 2004. Kyles AE, et al: Clinical, clinicopathologic, radiographic, and ultrasonographic abnormalities in cats with ureteral calculi: 163 cases. J Am Vet Med Assoc 226:932–936, 2005. Kyles AE, et al: Management and outcome of cats with ureteral calculi: 153 cases (1984-2002). J Am Vet Med Assoc 226:937–944, 2005. AUTHORS: ADAM MORDECAI, RANCE K. SELLON EDITOR: LEAH A. COHN
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Urachal Diverticulum
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Urachal Diverticulum BASIC INFORMATION DEFINITION Embryonic remnant at the apex of the urinary bladder; although diverticula occur commonly, they seldom result in clinical problems.
SYNONYM Vesicourachal diverticulum
EPIDEMIOLOGY SPECIES, AGE, SEX: Dogs and cats RISK FACTORS: Microscopic diverticula in cats may create risk for developing macroscopic diverticula following urinary tract obstruction from any cause. ASSOCIATED CONDITIONS & DISORDERS Urinary tract infection (UTI)/bacterial cystitis Urolithiasis (especially struvite) Feline lower urinary tract signs/disease (FLUTS/D)
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES Macroscopic: intramural and extramural Microscopic Acquired macroscopic HISTORY, CHIEF COMPLAINT: Clinical signs are often absent. When clinical signs are apparent, they may include any of the following: Hematuria Pollakiuria Dysuria Stranguria Inappropriate elimination Systemic illness due to urinary tract obstruction (rare) PHYSICAL EXAM FINDINGS: Physical exam is usually unremarkable. When present, abnormalities are nonspecific and may include: Hematuria (stains on prepuce, vulva, or hocks) Painful urinary bladder Enlarged, turgid bladder with urethral obstruction
ETIOLOGY AND PATHOPHYSIOLOGY The urachus is a canal connecting the fetal bladder with the allantois. The urachal lumen normally becomes obliterated during development, but on occasion the lumen remains patent (patent urachus) or the obliteration is incomplete, leaving a remnant diverticulum. Cause of incomplete urachal atrophy is unknown. Macroscopic: Most common form in dogs May not be associated with clinical signs
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May be associated with or predispose the animal to chronic/recurrent UTI and urolithiasis Microscopic: Most common form in cats Remnants of urachus at bladder apex that can extend from the level of the submucosa to the subserosa Not associated with clinical signs Acquired macroscopic: Microscopic diverticula may become macroscopic secondary to sustained increase in bladder intraluminal pressure. May spontaneously regress if the cause of increased bladder pressure is removed
DIAGNOSIS DIAGNOSTIC OVERVIEW Diagnosis of urachal diverticulum is based on imaging of the urinary tract through ultrasonography, contrast radiography, or visual inspection at surgery. Often, diverticula are incidental findings.
DIFFERENTIAL DIAGNOSIS Neoplasia Polyps Urolithiasis Blood clots
INITIAL DATABASE CBC: unremarkable Serum chemistry profile: unremarkable unless urinary obstruction exists; in these rare instances, azotemia, hyperkalemia, or acidemia are identified. Urinalysis: often unremarkable; sometimes shows pyuria, hematuria, bacteruria, or struvite crystalluria Urine culture and sensitivity (C&S) is used for identifying urinary tract infection. Abdominal radiographs to rule out radiopaque uroliths
ADVANCED OR CONFIRMATORY TESTING Contrast cystography: Positive-contrast cystography Double-contrast cystography Ultrasonography Cystoscopy Exploratory celiotomy and cystotomy
TREATMENT TREATMENT OVERVIEW Incidentally discovered urachal diverticula may not require therapy. Those associated with recurrent urinary tract infection or urolithiasis are surgically addressed.
ACUTE GENERAL TREATMENT Relieve urethral obstruction if present (see 1353) Fluid therapy and correction of electrolyte disturbances if present (see pp. 1353 and 1555) Antimicrobial therapy for bacterial cystitis if present (see 276)
CHRONIC TREATMENT Animals with clinical signs or a urinary tract infection related to either congenital macroscopic diverticula or nonresolving acquired macroscopic diverticula should undergo surgical resection of the diverticulum: Exploratory celiotomy Ventral midline cystotomy
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Identification of diverticulum at apex of bladder Excision of diverticulum with elliptical incision Routine closure Address chronic feline lower urinary tract signs/disease (see 387). Address urolithiasis (see 1143).
URACHAL DIVERTICULUM Lateral radiographic projection of a double-contrast cystogram performed on a 4-year-old male domestic shorthaired cat with a history of chronic urinary tract infections. A small “out-pouching” of the bladder wall is present at the apex (white arrow). Diagnosis: bladder diverticulum predisposing the animal to chronic cystitis. (Courtesy Dr. Stephanie Essman, University of Missouri.)
NUTRITION/DIET Animals with urinary tract infection may develop struvite urolithiasis. Diets low in ash designed to acidify the urine may be used in conjunction with appropriate antimicrobial therapy to aid in dissolution of struvite calculi (see 1143).
POSSIBLE COMPLICATIONS Obstruction of the urinary tract as a result of struvite urolithiasis is a possible complication of urinary tract infection associated with urachal diverticula. Suture-line leakage with peritonitis is a possible complication following surgical excision of diverticula.
RECOMMENDED MONITORING Monitor cats with acquired macroscopic diverticula for regression of diverticulum by contrast cystography 2-3 weeks after treatment of obstruction and resolution of clinical signs. Monitor for recurrence of signs of FLUTS/D (see 387).
PROGNOSIS AND OUTCOME Surgical excision for congenital macroscopic diverticula is curative. Acquired macroscopic lesions that spontaneously resolve may recur with repeated episodes of lower urinary tract obstruction.
PEARLS & CONSIDERATIONS COMMENTS
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Patent urachus causes umbilical urine dribbling in neonates and should be corrected surgically.
PREVENTION Prevention of lower urinary tract obstruction will prevent acquired diverticula formation.
CLIENT EDUCATION Recurrent UTI may be a sequela to uncorrected congenital macroscopic diverticula. Recurrent or persistent UTI may lead to struvite urolithiasis.
SUGGESTED READING Waldron DR: Urinary bladder. In Slatter D, editor: Textbook of small animal surgery. Philadelphia, 2003, WB Saunders, pp 1629–1637. Groesslinger K, et al: Prevalence and radiologic and histologic appearance of vesicourachal diverticula in dogs without clinical signs of urinary tract disease. J Am Vet Med Assoc 226:383–386, 2005. EDITOR: LEAH A. COHN 1ST EDITION AUTHOR: ERIC POPE
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Upper Respiratory Infection, Cat
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Upper Respiratory Infection, Cat BASIC INFORMATION DEFINITION A complex of viral and bacterial agents can cause upper respiratory tract signs such as sneezing, nasal congestion, and nasal discharge in cats. Etiologies include feline herpesvirus (FHV), feline calicivirus (FCV), Bordetella bronchiseptica. Chlamydophila felts, and (less commonly) feline reovirus, cowpox virus, and mycoplasmas.
SYNONYMS Feline infectious respiratory disease, feline respiratory disease complex C. felts previously known as Chlamydia psittaci Feline herpesvirus: feline rhinotracheitis
EPIDEMIOLOGY SPECIES, AGE, SEX: The main causative infectious agents (herpesvirus and calicivirus) are confined to the family of Felidae and are typically found in young animals. Mycoplasmas are often found as normal flora in the upper respiratory tract of many species. RISK FACTORS Poor husbandry and overcrowding in catteries or rescue shelters Exposure to free-roaming cats in high-density feral populations CONTAGION & ZOONOSIS FHV and FCV are shed in ocular, nasal, and oral secretions and are passed via direct cat-to-cat contact. Both viruses spread easily through susceptible populations and are perpetuated by carrier animals not showing overt signs. Disease can be spread via fomites such as contaminated cages, bowls, and clothing. FCV can persist in the environment for up to 1 month. Direct aerosol transmission is actually an unlikely cause of respiratory disease spread, owing to the small feline tidal lung volume and lower numbers of pathogenic organisms in the respiratory volume. Sneezing of nasal/oral secretions, however, may disseminate a virus more readily over a radius of several feet (>1 m). GEOGRAPHY AND SEASONALITY: Worldwide and no true seasonally; more cases may be noted in late spring and summer when many susceptible kittens are added to the population.
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES Herpesvirus: in young animals, usually acute, severe upper respiratory signs; in chronic adult cases, often manifests as a chronic conjunctivitis/keratitis without respiratory signs. Calicivirus: typical upper respiratory signs; isolated highly virulent strains that cause severe systemic disease and death have been noted. HISTORY, CHIEF COMPLAINT General signs of respiratory disease complex include anorexia, lethargy, ocular and nasal discharges, sneezing, epiphora, blepharospasm. Specific to calicivirus (see p. 172), herpesvirus (see p. 524), and C. felts (see p. 193) PHYSICAL EXAM FINDINGS: Respiratory disease complex: Serous to mucopurulent nasal and ocular discharge Epiphora, blepharospasm, chemosis, conjunctival hyperemia
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Fever Dyspnea, increased airway sounds, wheezes, cough In addition: Herpesvirus: conjunctivitis, ± dendritic corneal ulcers Calicivirus: oral, nasal, lip ulcers, or generalized stomatitis and gingivitis Rare severe cases of very virulent calicivirus strains: facial/limb edema, dermal necrosis, vomiting, diarrhea, icterus, petechiae and ecchymoses from disseminated intravascular coagulation, or sudden death B. bronchiseptica: fever, submandibular lymphadenopathy, and cyanosis/dyspnea in cases of severe bronchopneumonia
ETIOLOGY AND PATHOPHYSIOLOGY Feline herpesvirus: A double-stranded DNA alpha-herpes-virus specific to Felidae. It attacks mucosal epithelial cells of the soft palate, tonsils, turbinates, cornea, and conjunctiva, leading to multifocal epithelial necrosis and secondary clinical signs. Pulmonary involvement is rare. Incubation period is 2-6 days; disease usually runs its course in 10-20 days. Turbinate destruction due to herpesvirus infection may be permanent and can predispose the cat to chronic rhinitis, even in the absence of active infection. Chronic conjunctivitis/keratitis can lead to symblepharon (adhesion of bulbar conjunctiva to palpebral conjunctiva), corneal scarring, or keratoconjunctivitis sicca (KCS). Essentially all cats infected with FHV become chronic carriers; the virus remains latent in the trigeminal ganglia. However, a smaller proportion of cats are truly susceptible to recrudescence, and these animals act as the FHV reservoir for the feline population. Recrudescence and viral shedding often occur 1-3 weeks after a stressful event. Not all recrudescence is accompanied by obvious clinical signs. Feline calicivirus: see p. 172 B. bronchiseptica: see C. felis: see
DIAGNOSIS DIAGNOSTIC OVERVIEW Usually the diagnosis is based on clinical presentation: a cat with signs of conjunctivitis, anterior uveitis, ocular or nasal discharge, gingivitis, faucitis, stomatitis, glossitis, fever, and lymphadenomegaly has an upper respiratory infection. Specific identification of a causative agent is not always necessary, but ruling out non-viral causes is important for treatment considerations.
DIFFERENTIAL DIAGNOSIS Nasal signs: nasal neoplasia, nasopharyngeal polyps, periodontal disease, foreign body, fungal infection, structural malformation of nasal passages/sinuses, esophageal motility dysfunction Ocular signs: corneal and/or conjunctival trauma, corneal foreign body, eosinophilic keratoconjunctivitis, neoplasia, KCS, uveitis, glaucoma Cough or dyspnea: feline asthma, intrathoracic neoplasia (pulmonary, lymphoid, mediastinal, or pleural), congestive heart failure (CHF), pleural effusion of other causes, feline heartworm disease
INITIAL DATABASE CBC: neutrophilia with left shift if secondary bacterial infection is severe. Stress leukogram is possible. Results are often normal. Serum biochemistry profile and urinalysis: may reflect dehydration but typically unremarkable. With virulent calicivirus infections, increases in alanine aminotransferase (ALT), creatine kinase (CK), and bilirubin levels; and decreased albumin level possible. Thoracic radiographs: assessing for signs of pneumonia in cats with lower respiratory tract signs CT scan of the skull, with rhinoscopy and nasal biopsy/culture can help rule out neoplasia, fungal infection, dental disease, nasopharyngeal polyps, and structural deformities as causes of chronic respiratory signs.
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ADVANCED OR CONFIRMATORY TESTING Serologic testing for herpesvirus and calicivirus is unrewarding because of widespread vaccination. Virus isolation from nasal, conjunctival, or oropharyngeal swabs is the best diagnostic assay for FHV and FCV. Requires special swabs or media for transport; however, FCV is commonly isolated from the oral/respiratory mucosa of healthy cats, so positive viral culture should be supported by appropriate clinical presentation. Feline upper respiratory disease panel: www.idexx.com or www.antechonline.net; requires swab samples depending on location of predominant clinical signs. Conjunctival scrapes may demonstrate basophilic intracytoplasmic inclusions indicative of C. felis infection. Culture or PCR on conjunctival swabs can also be used to rule out C. felis. Special transport medium is required for culture. Serologic testing may also be helpful in the unvaccinated cat, because affected animals typically have high titers. Transtracheal or bronchoalveolar washes with cytologic examination and culture and sensitivity (C&S) are helpful in isolating B. bronchiseptica, C. felis, or secondary bacteria as causative agents of pneumonia. Cryptococcal antigen titer to rule out cryptococcosis.
TREATMENT TREATMENT OVERVIEW Treatment is typically supportive, with the goal of controlling secondary bacterial infections and maintaining comfort and appetite.
ACUTE GENERAL TREATMENT Most cats with upper respiratory infections can and should be managed at home by the owner to decrease pathogen dissemination in the hospital setting. Animals that are febrile, dehydrated, severely depressed, or compromised should be treated in the hospital until they are stable and can be sent home; they should be isolated from other cats. Acute treatment includes: IV crystalloids and colloids if patients are febrile and/or dehydrated or have evidence of hypovolemia Broad-spectrum antibiotics (one of the following): Amoxicillin-clavulanate, 13.75 mg/kg PO q 12 h Cefadroxil, 10-30 mg/kg PO q 8-12 h Cephalexin, 22-30 mg/kg PO q 8-12 h Enrofloxacin, 5 mg/kg PO q 24 h Antibiotics most effective against specific bacteria (see pp. 144 and 193): Doxycycline, 5 mg/kg PO q 12 h; or tetracycline, 20 mg/kg PO q 8 h Topical ophthalmic preparations: Artificial tears q 2-6 h Tetracycline ophthalmic preparations are the treatment of choice for C. felis and Mycoplasma spp. conjunctivitis and in FHV cats to prevent secondary bacterial infections. Topical tetracyclines can be irritating. Chloramphenicol, erythromycin, or fluoroquinolone topicals are alternative options. Topical or systemic corticosteroids should not be used in suspected FHV keratitis. Most “triple-antibiotic” ophthalmic preparations (neomycin, polymyxin, and bacitracin/gramicidin) are typically ineffective against C. felis, Mycoplasma spp., and FHV-1. Topical and systemic antiviral drugs for FHV keratitis/conjunctivitis (see p. 524) Treatment duration with antibiotics and antivirals should be determined on an individual case basis, but typically 1-2 weeks is required while the viral disease runs its course.
CHRONIC TREATMENT Home nebulization (putting the cat on a dry surface in a steamy bathroom) may help ease nasal or airway congestion. Owners should be instructed to cleanse the face, mouth, and nares regularly to minimize accumulation of discharges or saliva. Herpesvirus carriers that have bouts of recrudescence can be treated on as-needed basis with L-lysine (250-500 mg PO q 12 h for life) to decrease severity of outbreaks.
NUTRITION/DIET Appetite stimulants may be necessary: Cyproheptadine, 2 mg/cat PO q 12-24 h; or Diazepam, 0.05-0.15 mg/kg IV q 24 h; may cause extreme sedation soon after administration. Paradoxically in some cats, may lead to hyperexcitability and fractiousness. Feed animals very pungent, highly palatable foods to overcome a decreased sense of smell from nasal infection (see p.
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1377). Tube feeding may be necessary in chronic cases with prolonged anorexia.
POSSIBLE COMPLICATIONS FHV keratoconjunctivitis can predispose the animal to KCS.
PROGNOSIS AND OUTCOME Except in very young or compromised animals or in cases of virulent calicivirus, prognosis is usually good for recovery from acute bouts of respiratory disease. Some animals develop chronic rhinitis and/or keratoconjunctivitis and will have recurrent bouts of disease that may require lifelong management.
PEARLS & CONSIDERATIONS PREVENTION Several modified live or killed vaccines are available for protection against herpesvirus and calicivirus. They offer good to moderate protection against clinical disease but are not guaranteed to prevent infection or development of a carrier state. Modified live vaccines (MLV) may induce a mild form of respiratory disease. Vaccines are available for B. bronchiseptica and C. felis, but because these diseases are relatively benign and easy to treat, the benefit of immunization in most pet cats is questionable. Vaccination may be warranted in cattery or shelter situations. Dilute bleach (1 part bleach to 32 parts water) is the best disinfectant for preventing FHV and FCV spread in the hospital environment. FCV has shown resistance to common disinfectants such as quaternary ammonium compounds and chlorhexidine.
SUGGESTED READING Gaskell R, Dawson S: Feline respiratory disease. In Greene CE, editor: Infectious diseases of the dog and cat. St Louis, 2006, Elsevier Saunders, pp 145–154. Gaskell RM, Radford AD, Dawson S: Feline infectious respiratory disease. In Chandler EA, Gaskell CJ, Gaskell RM, editors: Feline medicine and therapeutics. Denmark, 2004, Blackwell Publishing, pp 577–595. Hurley KF, Sykes JE: Update on feline calicivirus: new trends. Vet Clin North Am Small Anim Pract 33:4, 2003. AUTHOR: LENORE M. BACEK EDITOR: DOUGLASS K. MACINTIRE 1ST EDITION AUTHOR: SHANNON STROUP
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Upper Airway Obstruction
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Upper Airway Obstruction BASIC INFORMATION DEFINITION Inability to move air effectively through trachea, larynx, pharynx, or nose and mouth
SYNONYMS Choking, occlusion of the upper airway
EPIDEMIOLOGY SPECIES, AGE, SEX Airway foreign body more likely in young dogs; neoplasia, laryngeal paralysis more likely in adult older dogs Young cats may have nasopharyngeal polyps. GENETICS & BREED PREDISPOSITION: Short-nosed (brachycephalic) animals are predisposed to airway obstruction (see p. 151). RISK FACTORS: Environmental factors: excitement, heat, and exercise, especially in animals with physical predisposition (e.g., elongated soft palate, laryngeal paresis) GEOGRAPHY AND SEASONALITY: More common in warmer climates (heat stress) ASSOCIATED CONDITIONS & DISORDERS: Brachycephalic upper airway syndrome, laryngeal paralysis, neoplasia
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES Supraglottic structures: brachycephalic upper airway syndrome (see p. 151), laryngeal paralysis (unilateral/bilateral), foreign bodies (pharyngeal), laryngeal collapse, laryngeal edema, and nasopharyngeal polyps (cats) Subglottic structures: tracheal neoplasia, tracheal hypoplasia, tracheal collapse, foreign body aspiration, trauma HISTORY, CHIEF COMPLAINT Owners often report that their pet appears anxious or agitated, that he or she is having difficulty breathing, and that they can hear loud respiratory noises or a honking cough. Clinical signs can occur more commonly after exercise, excitement, or on a warm day. Animals may have been witnessed aspirating a foreign object (e.g., ball/marble/acorn), although the mistaken belief that a foreign body has been aspirated is a common error that some clients believe passionately (“something stuck in the throat”) even when the problem is clearly different (e.g., pulmonary edema, pleural effusion). PHYSICAL EXAM FINDINGS Noisy and/or stridorous breathing Hyperthermia possible (excessive muscle activity from inspiratory effort) Conformation changes (e.g., short nose) raise the suspicion of associated malformations as the underlying cause. Loud sounds may be ausculted over the trachea and may be referred to the lower airways.
ETIOLOGY AND PATHOPHYSIOLOGY Most of the resistance to airflow occurs in the upper airways. Any fixed or dynamic obstruction in the upper airways will increase the resistance to breathing and, subsequently, the work of breathing. Inspiration against a partially or completely closed upper airway may cause flooding of pulmonary alveoli with plasma (i.e., noncardiogenic pulmonary edema due to negative pressure generated in the air space).
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Upper Airway Obstruction
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DIAGNOSIS DIAGNOSTIC OVERVIEW Diagnosis is based on physical exam findings, including difficulty breathing and/or stridorous breathing. Specifically, inspiratory dyspnea, often with the point of stridor audibly in the upper airway (making the site of obstruction manifestly clear on distant physical exam alone) helps localize the anatomic lesion. Oral examination, diagnostic imaging, and endoscopy are cornerstones for confirming the site (and sometimes nature) of the obstruction, and are selected based on suspected location of the obstruction, available means, and patient stability.
DIFFERENTIAL DIAGNOSIS Occasionally, pleural effusion in cats will mimic upper respiratory obstruction.
INITIAL DATABASE Oral examination under sedation is the most important diagnostic test (see p. 1295). The clinician should be prepared for an emergent tracheostomy (and possibly positive-pressure ventilation, if noncardiogenic pulmonary edema is present; see and ) if needed. Doxapram may be used for stimulating ventilation during oral examination in sedated dogs and cats. Other ancillary testing includes radiographs (thoracic and neck), ultrasound, CBC/serum biochemistry profile, and evaluation of oxygenation (pulse oximetry or arterial blood gas [ABG] analysis).
ADVANCED OR CONFIRMATORY TESTING Bronchoscopy, fluoroscopy, or CT scan may be useful for evaluating focal lesions or obtaining biopsies or cytologic specimens.
TREATMENT TREATMENT OVERVIEW Minimize stress and address the clinical signs until a definitive diagnosis is made; sometimes the diagnosis and treatment occur simultaneously (e.g., foreign body is identified and removed).
ACUTE GENERAL TREATMENT Tranquilizers or analgesics, corticosteroids at antiinflammatory doses, and oxygen supplementation. Secure airway if necessary (see pp. 1292 and 1318). If hyperthermia is due to exertion or anxiety (i.e., muscle activity, not true fever), it can respond to physical cooling measures but not to antiinflammatory drugs (see p. 1564).
CHRONIC TREATMENT Either medical or surgical management of the underlying problem: Medical: anxiolytics, antitussives, and environmental control Surgical: stenotic nares repair; soft palate resection; everted laryngeal saccule resection; abscess drainage; tracheal ring implants/stent placement; removal of foreign body, tumor, or polyp; permanent tracheostomy; or temporary tracheotomy
BEHAVIOR/EXERCISE Ideally, pets that are at risk should be kept calm and in an air-conditioned area. At the least, exercise or exertion should be avoided in those animals that are predisposed.
POSSIBLE COMPLICATIONS Postsurgical complications include the recurrence of clinical signs, aspiration pneumonia, noncardiogenic pulmonary edema, and/or respiratory arrest.
RECOMMENDED MONITORING
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Upper Airway Obstruction
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Monitor respiratory rate/effort and mucous membrane color.
PROGNOSIS AND OUTCOME Depend on the actual underlying problem and the severity of clinical signs. For example, presence of noncardiogenic pulmonary edema substantially worsens prognosis.
PEARLS & CONSIDERATIONS COMMENTS Up to half the diameter of the airway can be compromised without obvious clinical signs. Major errors in the initial treatment include underestimation of the patient's distress, overzealous examination, and performance of diagnostics that are detrimental to the condition of the patient at that time. A common radiographic misdiagnosis is the interpretation of a prominent or mineralized (but normal) larynx as a foreign body, especially if the neck is radiographed obliquely. Thoracic radiography and positive-pressure ventilation should be planned in case dyspnea and/or hypoxemia persist after relief of upper airway obstruction, as can occur when noncardiogenic pulmonary edema is also present.
PREVENTION Avoid overexertion, prevent heat stress, and know the medical options that are available to help break the cycle of distress and resultant respiratory difficulty.
TECHNICIAN TIPS When administering treatments to these pets, stress should be minimized (minimal restraint) and treatments should be conducted in a stepwise manner.
CLIENT EDUCATION Explain to owners that a brachycephalic animal is predisposed to developing upper airway problems
SUGGESTED READING Costello MF: Upper airway disease. In Silverstein DC, Hopper K, editors: Small animal critical care medicine, ed 1, St Louis, 2009, Saunders Elsevier, p 67. AUTHOR: MEGAN WHELAN EDITOR: ELIZABETH ROZANSKI
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Unerupted Teeth
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Unerupted Teeth BASIC INFORMATION DEFINITION Teeth that have not emerged into the mouth are unerupted. Clinically, the tooth appears to be missing. Radiographic diagnosis is required.
SYNONYMS Embedded teeth (teeth exhibiting a lack of eruptive force without physical obstruction) Impacted teeth (teeth not erupting owing to a physical barrier)
EPIDEMIOLOGY SPECIES, AGE, SEX: Unerupted teeth occur more commonly in the younger dog and less commonly in cats. They may not be recognized until animals have reached adulthood. GENETICS & BREED PREDISPOSITION: Familial delayed eruption does occur in Tibetan and Wheaten terriers, and toy breeds can have overall slower eruption times. Because erupting teeth can be influenced by internal and external causes, a genetic link is suspected but difficult to prove. Symmetrically unerupted or missing teeth are usually genetic in origin. Brachycephalic and toy dog breeds appear to be predisposed to unerupted and missing premolar and molar teeth. RISK FACTORS Persistent deciduous teeth (see 282) Regional trauma Certain endocrine disorders Malnutrition Canine distemper ASSOCIATED CONDITIONS & DISORDERS: Dentigerous (tooth-containing) cyst (also called follicular cyst)
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT: Animals are sometimes presented for evaluation of missing teeth, but the majority of unerupted teeth are found incidentally on routine physical examination. PHYSICAL EXAM FINDINGS: Most animals are in good health. Oral examination reveals an edentulous (toothless) region. Permanent premolars are the most common unerupted teeth, but any tooth can be affected. If a dentigerous cyst is present, a fluctuant soft-tissue swelling may be located in the edentulous region.
ETIOLOGY AND PATHOPHYSIOLOGY Complications leading to abnormal tooth eruption are many and varied: primary defects in the eruptive process, genetic/traumatic displacement of the tooth bud or surrounding bone, mechanical obstruction from adjacent structures, regional odontogenic and nonodontogenic neoplasia. The most commonly unerupted teeth in the dog are the mandibular first premolar and third molar teeth. Endocrine abnormalities (hypothyroidism, cretinism, hypogonadism, mongolism, hypopituitarism, hyperparathyroidism) can prevent or slow the eruption of teeth. Unerupted teeth can incite dentigerous cyst formation: an epithelial-lined soft tissue is attached to the cementoenamel junction of an unerupted tooth, with the crown protruding into the fluid-filled cyst, causing pressure resorption of alveolar bone, displacement of adjacent teeth, abscess, and fistulation.
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Unerupted Teeth
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UNERUPTED TEETH A, Clinical photograph of rostral lower jaw of an adult dog. Note swelling in the area of a missing left mandibular first premolar tooth (asterisk) and distally displaced left mandibular second premolar tooth. B, Radiograph of left rostral mandible of same patient arranged in labial mounting (rostral toward the left, caudal toward the right of image). Note that left mandibular first premolar tooth (asterisk) is unerupted, and a dentigerous cyst (dotted oval) has developed around the unerupted tooth, causing pressure resorption of the roots of the caudally displaced left mandibular second premolar tooth (arrow). (Copyright 2010 Dr. Alexander M. Reiter.)
DIAGNOSIS DIAGNOSTIC OVERVIEW Dental radiography is necessary to differentiate unerupted teeth from missing teeth.
DIFFERENTIAL DIAGNOSIS Edentulous region: Partially erupted, ankylosed, embedded, and impacted teeth Presence of an operculum (tough gingival covering preventing tooth eruption) Anodontia and hypodontia resulting from a large variety of causes Fractured tooth ± retained tooth roots Previously extracted tooth Edentulous region associated with soft-tissue swelling: Odontogenic tumor (e.g., compound or complex odontoma) Cyst (e.g., radicular, dentigerous) Abscess Neoplasia
INITIAL DATABASE CBC, serum biochemistry panel, urinalysis (preanesthetic): generally unremarkable Full-mouth (intraoral) dental radiography
ADVANCED OR CONFIRMATORY TESTING CT scan (see ): if associated cystic structure is large and to define surgical margins and/or regions for débridement
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Unerupted Teeth
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TREATMENT TREATMENT OVERVIEW Treatment goals are to preserve normal anatomic arrangement and structure, encourage complete tooth eruption or extract tooth if eruption impossible or impractical, and prevent cyst/abscess formation.
ACUTE AND CHRONIC TREATMENT No treatment if entire tooth is missing on radiographs Some unerupted teeth can be orthodontically coaxed into position if tooth, patient, and owner are willing. If an operculum is present, dissect gingiva to allow for tooth eruption (operculectomy). To prevent dentigerous cyst development, surgically extract unerupted teeth without eruption potential. Curettage of the extraction site is recommended to remove remnant odontogenic tissue. Postoperative radiographs ensure complete removal of all tooth structures. If a dentigerous cyst is present, the tooth and cyst are removed en bloc. If this is not possible, extensive curettage to remove all epithelial cyst lining is mandatory because small islands of remaining epithelium can lead to cyst reoccurrence or malignant transformation. The débrided cyst cavity need not be filled with osteopromotive materials; natural bone remodeling will likely be clinically adequate. Flaps should be closed with synthetic absorbable suture material. Administration of antibiotics is not usually necessary after the extraction procedure unless another medical condition or extensive tissue trauma at the extraction site is present. Pain management: regional nerve block (0.5% bupivacaine) intraoperatively, followed by nonsteroidal antiinflammatory drugs (e.g., carprofen, 2 mg/kg PO q 12 h in dogs) ± opioid medications (butorphanol, 0.2-0.4 mg/kg PO q 4-6 h) given postoperatively for 2-3 days.
POSSIBLE COMPLICATIONS Inability to locate the unerupted tooth Extraction of a healthy erupting permanent tooth Cyst recurrence Regional trauma due to improper extraction technique Infection
RECOMMENDED MONITORING Examination 1-2 weeks postoperatively to evaluate extraction sites Cyst: examination with radiographs in 6 months
PROGNOSIS AND OUTCOME Unerupted teeth with operculectomy: fair for tooth eruption (depends on tooth eruption potential) Extracted unerupted teeth: excellent for extraction site healing Dentigerous cyst: excellent if all cystic lining is removed
PEARLS & CONSIDERATIONS COMMENTS No tooth should be considered “missing” without radiographic diagnosis. Extraction of unerupted teeth may be unnecessary in older pets (>8-9 years) if there is no radiographic evidence of associated lesions. The odds a dentigerous cyst will form at this age are low.
PREVENTION Removal of persistent deciduous teeth Early recognition of “missing” teeth in young animals Selective breeding
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Unerupted Teeth
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TECHNICIAN TIPS Technicians are at the frontline for identifying unerupted teeth during professional dental cleanings and pointing them out to the veterinarian if they were not noted previously.
SUGGESTED READING Gioso MA, Carvalho VG: Maxillary dentigerous cyst in a cat. J Vet Dent 20:28, 2003. Mulligan TW, Aller MS, Williams CA: Atlas of canine and feline dental radiography. Trenton, NJ, 1998, Veterinary Learning Systems, pp 91–103, 188–189. Harvey CE, Emily PP: Small animal dentistry. St Louis, 1993, Mosby, pp 276–281. AUTHOR: JENNIFER E. RAWLINSON EDITOR: ALEXANDER M. REITER
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Umbilical Hernia
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Umbilical Hernia BASIC INFORMATION DEFINITION Full-thickness congenital abdominal wall defect at the umbilicus
EPIDEMIOLOGY SPECIES, AGE, SEX Dogs and cats Greater incidence in females of predisposed breeds GENETICS & BREED PREDISPOSITION Breed predisposition in dogs: Airedale terrier, basenji, Pekingese, pointer, and weimaraner Could be an inherited defect: Polygenic inheritance possible ASSOCIATED CONDITIONS & DISORDERS Fucosidosis, an inherited lysosomal storage disease reported in English springer spaniels Cryptorchidism Incomplete caudal sternal fusion Peritoneopericardial diaphragmatic hernia Exstrophy of the bladder Hypospadias Imperforate anus
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES Uncomplicated: Single umbilical hernia without incarceration or strangulation of abdominal contents, concurrent anatomic abnormalities, or multiple hernias Complicated: Presence of multiple hernias; other associated anatomic abnormalities, defects, or diseases; or strangulation or contamination of abdominal contents Omphalocele: Large midline umbilical hernia and skin defect that allow abdominal organs to protrude externally. The umbilical sac is merely a thin transparent membrane (amniotic sac). The membrane is attached to the hernia edges and may rupture easily. Most affected puppies die or are euthanized before treatment is sought. Gastroschisis: Grossly similar to omphalocele, but the defect is paramedian. HISTORY, CHIEF COMPLAINT None; incidental finding (most common) Soft swelling at umbilicus may be noticed by some owners. Systemic signs of illness (anorexia, vomiting, lethargy) are possible if abdominal contents are strangulated (least common). PHYSICAL EXAM FINDINGS Protruding mass at the umbilicus: Soft, fluctuant, and reducible, especially if animal is placed in dorsal recumbency
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Umbilical Hernia
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Large, firm, and irreducible if contents are incarcerated Acute intestinal incarceration or strangulation: Firm, painful mass; vomiting, abdominal pain, signs of sepsis are possible.
ETIOLOGY AND PATHOPHYSIOLOGY Abdominal wall of the embryo normally is formed by migration of cephalic, caudal, and lateral folds. Umbilical aperture remains after normal migration and fusion of the folds. Umbilical hernia results when the lateral folds, principally the rectus abdominis muscle and fascia, fail to fuse or have delayed fusion after the midgut relocates in the sixth week of gestation.
DIAGNOSIS DIAGNOSTIC OVERVIEW The diagnosis is made entirely on physical examination. In complex cases with entrapped viscera, the identity of herniated organs is confirmed at surgery.
DIFFERENTIAL DIAGNOSIS Traumatic umbilical hernia: peripartum insult caused by traction on umbilical cord or cutting cord too close to abdominal wall
INITIAL DATABASE Survey abdominal and thoracic radiographs: only needed if hernia is very large and if other anomalies (diaphragmatic hernia, incomplete sternal fusion, strangulation/incarceration) are present.
ADVANCED OR CONFIRMATORY TESTING Ultrasound examination (uncommonly used): only considered with large and/or incarcerated hernia contents to determine contents of hernia.
TREATMENT TREATMENT OVERVIEW Resolve any existing visceral entrapment. Reduce or eliminate risk of herniation of abdominal viscera.
ACUTE GENERAL TREATMENT Conservative treatment: Small hernia (less than the size of the intestine; i.e., the size of a fingertip) Spontaneous closure may occur as late as 6 months of age. Surgical correction: Large hernia but no associated clinical problems (incarceration of abdominal contents): Elective surgical correction; also repaired when another elective surgical procedure (ovariohysterectomy, orchiectomy) is performed Large hernia with evidence of incarcerated or strangulated viscera: Immediate surgical correction Omphalocele: Immediate surgical correction to prevent further organ damage or contamination
POSSIBLE COMPLICATIONS Dehiscence of repair: Large defect Excess tension on repair Friability of abdominal wall Gastroschisis and omphalocele may be associated with early neonatal death:
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Umbilical Hernia
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Contamination of abdominal contents Inability to correct defect
RECOMMENDED MONITORING Counsel owners to watch for enlargement of hernia or acute gastrointestinal (GI) signs in animals that are managed conservatively; onset warrants immediate evaluation and consideration of surgical correction.
PROGNOSIS AND OUTCOME Excellent with uncomplicated umbilical hernia and successful closure Guarded to poor with complicated or open hernia Status of animal at presentation and health of herniated contents determine prognosis
PEARLS & CONSIDERATIONS COMMENTS There are usually no clinical signs associated with umbilical hernias. Correction is usually an elective procedure. Entrapment of abdominal contents can occur with larger hernias. Always examine animals with umbilical hernias for additional congenital abnormalities.
PREVENTION Consideration should be given to avoiding breeding affected dogs or cats, because this condition is usually an inherited defect. At the time of the animal's birth, carefully ligate and transect the umbilical cord—without excessive traction—at least 1-2 cm from the neonate's body wall.
CLIENT EDUCATION Treatment may be conservative, or a herniorrhaphy may be required to prevent complications. Veterinarians should train breeders in proper neonatal care.
SUGGESTED READING Robinson R: Genetic aspects of umbilical hernia incidence in cats and dogs. Vet Rec 100:9–10, 1977. Smeak DD: In Slatter D, editor: Textbook of small animal surgery, ed 3, Philadelphia, 2003, WB Saunders, pp 449–450. AUTHOR: JOSEPH G. HAUPTMAN EDITOR: RICHARD WALSHAW 1ST EDITION AUTHOR: ELLEN B. DAVIDSON DOMNICK
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Ulcers, Oral Mucosal
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Ulcers, Oral Mucosal BASIC INFORMATION DEFINITION Focal or multifocal loss of superficial epithelial integrity affecting the oral mucosa
EPIDEMIOLOGY SPECIES, AGE, SEX: Dogs and cats of either gender and all ages can be affected. GENETICS & BREED PREDISPOSITION: Maltese, Cavalier King Charles spaniel, cocker spaniel, and Bouvier des Flandres dogs are predisposed to chronic ulcerative periodontal stomatitis (CUPS). Abyssinian and Somali cats are predisposed to lymphocytic/plasmacytic stomatitis (LPS). CONTAGION & ZOONOSIS: Feline leukemia virus (FeLV), feline immunodeficiency virus (FIV), feline herpesvirus (FHV), and feline calicivirus (FCV) in cats are transmissible to other cats. Leptospirosis is transmissible to other animals and human beings.
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT Lethargy Anorexia Behavior change due to oral pain Halitosis Hypersalivation PHYSICAL EXAM FINDINGS Gingivitis Faucitis (inflammation of the archway between the pharyngeal and oral cavities [formed by the tongue, anterior and posterior tonsillar pillars, and soft palate]) Pharyngitis Dental plaque accumulation Oral mass Buccitis/buccal mucosal ulceration Lingual ulceration Kissing ulcers: mucosal ulceration (common in CUPS) Scar tissue formation on lateral margins of tongue (CUPS) ETIOLOGY AND PATHOPHYSIOLOGY Metabolic causes: renal failure (uremia; common), diabetes mellitus, hypothyroidism, hypoparathyroidism Immune-mediated disease: oral ulcers occur with pemphigus vulgaris (90% of cases), bullous pemphigoid (80% of cases), systemic lupus erythematosus (SLE) (50% of cases), and discoid lupus erythematosus and can also be drug-induced (toxic epidermal necrolysis) Infectious: FeLV, FIV, FCV, FHV, leptospirosis (dogs), periodontal disease (dogs and cats) Neoplastic: melanoma, squamous cell carcinoma (SCC), fibrosarcoma Traumatic: foreign body, electric cord shock, malocclusion, “gum chewer's disease“ (chronic chewing of cheek) Idiopathic: eosinophilic granuloma (cats, Siberian huskies, Samoyeds), LPS, CUPS Miscellaneous: caustic burns (acids), thallium toxicity, protein-calorie malnutrition, riboflavin deficiency
DIAGNOSIS DIAGNOSTIC OVERVIEW
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Ulcers, Oral Mucosal
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Oral mucosal ulcers may be easily noted on physical exam or may be subtle. A heightened index of suspicion is warranted with hypersalivating or anorexic patients. Features of the history and physical exam should guide the selection of diagnostic tests once ulcers have been observed. DIFFERENTIAL DIAGNOSIS History, physical, and oral exam can differentiate foreign bodies, malocclusions, toxin/chemical exposure, and electrical burns. Breed predispositions and response to therapy can help identify idiopathic disorders. INITIAL DATABASE Thorough oral examination (may require sedation or general anesthesia) CBC: inflammatory leukogram may be present with infectious or immunemediated diseases. Serum biochemical profile: evidence for metabolic disease (e.g., renal failure) Urinalysis: urine specific gravity may support a diagnosis of renal failure. Proteinuria may be present if immune-mediated, neoplastic, or infectious disorders cause secondary glomerular damage. ADVANCED OR CONFIRMATORY TESTING Serologic titers or other tests (e.g., PCR for infectious agents such as FeLV, herpesvirus) or systemic immune-mediated disease (e.g., antinuclear antibody titer for SLE) Thyroid hormone assays Thoracic radiographs: evaluation for metastatic disease Oral radiographs: evaluation for concurrent osteomyelitis secondary to severe periodontal disease or bony involvement from malignant neoplasia Mucosal or gingival biopsy: support for diagnosis of idiopathic, immune-mediated, chronic inflammatory, and neoplastic diseases
TREATMENT TREATMENT OVERVIEW Correct underlying cause if possible. ACUTE GENERAL TREATMENT Supportive therapy: Soft diets Fluid support (SQ or IV) if the patient is dehydrated Nutrition: esophagostomy or gastrostomy feeding tubes (see pp. 1269 and 1270) may be required if oral disease or pain is resulting in steadfast and prolonged anorexia. CHRONIC TREATMENT For idiopathic conditions (i.e., CUPS, LPS), meticulous dental care to prevent plaque accumulation is necessary. In addition, dental extractions (partial, caudal, or full mouth) may be necessary to remove the source of inflammation. Treat metabolic conditions if present. Immunosuppressive drug therapy (e.g., corticosteroids, azathioprine) may be required for immune-mediated diseases. Antimicrobial therapy may be required to treat secondary periodontal or oral infections. Topical solutions (e.g., chlorhexidine solution) to inhibit bacterial growth or promote improved dental health may be beneficial. POSSIBLE COMPLICATIONS Side effects from corticosteroid (e.g., polyuria and polydipsia [PU/PD]) or immunosuppressive medications (e.g., myelosuppression) RECOMMENDED MONITORING Dependent on cause and therapies employed
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Ulcers, Oral Mucosal
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PROGNOSIS AND OUTCOME Dependent on underlying cause The idiopathic conditions (CUPS, LPS) can be difficult to treat and require considerable client commitment and compliance.
PEARLS & CONSIDERATIONS CLIENT EDUCATION For idiopathic conditions, clients should be encouraged to keep their pets' teeth as free from plaque as possible using both at-home (brushing, cleansing solutions; see ) and veterinary (dental cleaning) therapies.
SUGGESTED READING Mason IS: Erosions and ulcerations. In Ettinger SJ, Feldman EC, editors: Textbook of veterinary internal medicine, ed 6, St Louis, 2005, Elsevier Saunders, pp 46–50. Smith MM: Oral and salivary gland disorders. In Ettinger SJ, Feldman EC, editors: Textbook of veterinary internal medicine, ed 6, St Louis, 2005, Elsevier Saunders, pp 1290–1297. AUTHOR: DARCY H. SHAW EDITOR: ETIENNE CÔTÉ
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Ulcerative and Erosive Skin Disorders
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Ulcerative and Erosive Skin Disorders BASIC INFORMATION DEFINITION A cutaneous erosion is a shallow epidermal defect that does not penetrate the basal membrane. Erosions are usually associated with self-trauma or mild epidermal affections. A cutaneous ulcer is produced by a break in the continuity of the epidermis, with exposure of the underlying dermis. Ulcers are usually a consequence of a deep and serious pathologic process. Healing ulcers typically result in scarring.
EPIDEMIOLOGY SPECIES, AGE, SEX: Vary according to the underlying pathologic process: Some dermatoses are seen more frequently or strictly in one species rather than another (e.g., eosinophilic granuloma in cats). Young animals are predisposed to genetic defects or infectious diseases, whereas older animals are predisposed to immunemediated diseases or neoplasia. GENETICS & BREED PREDISPOSITION: Some diseases tend to have a genetic basis or are related to anatomic defects (e.g., intertrigo in such breeds as the Chinese shar-pei).
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT: A thorough history of the animal is important, considering the extensive list of differential diagnoses. Some essential clues help define the condition: Travel history (e.g., leishmaniasis in dogs traveling to Europe), grooming and boarding (contagion risk; e.g., herpesvirus infection in cats), and similar environmental information may affect a patient's risk of developing a certain condition. Dietary history (e.g., food allergy) Presence of signs of systemic illness (e.g., lethargy, anorexia, lameness, etc.) may narrow the differential diagnosis, and diagnostic methods will be oriented differently (e.g., toward systemic lupus erythematosus [SLE], leishmaniasis, systemic mycoses). Prior treatments: response to prior therapy or therapy administered prior to onset of clinical signs allows the inclusion or exclusion of some dermatoses (e.g., drug eruption).
PHYSICAL EXAM FINDINGS Dermatologic examination for identifying erosive and ulcerative lesions, and general physical examination to detect signs of underlying systemic diseases. The clinician should take note of primary lesions such as vesicles, bullae, and pustules and the distribution of the lesions (e.g., involvement of the mucosa). This information can suggest a specific group of diseases. Secondary lesions such as crusts are common. Exact description of the lesions varies according to the underlying disease.
ETIOLOGY AND PATHOPHYSIOLOGY Variable, depending on underlying cause. Congenital, hereditary, and conformational defects: for example, ulcerations can result from skin friction (e.g., intertrigo) or can be secondary to abnormal fragility of the dermoepidermal junction (e.g., epidermolysis bullosa). Infectious diseases (bacterial, viral, parasitic, fungal, rickettsial): some organisms infect and lyse keratinocytes (e.g., herpesvirus) or can cause epidermal necrosis secondary to either vasculitis (e.g., canine Rocky Mountain spotted fever) or a substantial inflammatory reaction, leading to ulcerative dermatitis. Immune-mediated disorders: ulcers may follow the rupture of vesicles and bullae caused by the action of antibodies. Drug-induced conditions Self-induced lesions Environmental injuries (e.g., coagulation necrosis of the epidermis/dermis associated with thermal or chemical burns results in ulcerations)
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Ulcerative and Erosive Skin Disorders
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Secondary to systemic diseases (e.g., uremia resulting from renal failure may cause oral ulceration). Ischemic disorders: any dermatopathy that interferes with vascular supply of the skin can potentially cause ulcers secondary to skin necrosis. Neoplasia: ulcerations noticed in skin tumors, such as cutaneous epitheliotropic lymphoma or squamous cell carcinoma (SCC), are usually secondary to the infiltration of the skin by neoplastic cells and often correlate with the aggressiveness of the tumor. Idiopathic condition
DIAGNOSIS DIAGNOSTIC OVERVIEW A definitive diagnosis is required in order to institute the appropriate treatment regimen.
DIFFERENTIAL DIAGNOSIS Congenital and hereditary: idiopathic facial dermatitis of Persian and Himalayan cats, aplasia cutis, epidermolysis bullosa (EB), familial canine dermatomyositis Infectious diseases: demodicosis, flea bite hypersensitivity, feline mosquito bite hypersensitivity, fly dermatitis; systemic mycoses, sporotrichosis, phaeohyphomycosis, zygomycosis, candidiasis, dermatophyte granuloma, pseudomycetoma, protothecosis, pythiosis, aspergillosis; deep pyoderma, mucocutaneous pyoderma, pyotraumatic dermatitis; feline leukemia virus (FeLV), feline cowpox, feline calicivirus (FCV), feline herpesvirus (FHV); canine Rocky Mountain spotted fever, leishmaniasis Immune-mediated disorders: pemphigus, bullous pemphigoid, erythema multiforme, toxic epidermal necrolysis, vasculitis, lupus erythematosus, EB acquisita, cold-agglutinin disease, cutaneous drug eruption Self-induced lesions: pruritic dermatoses, psychogenic dermatoses, neuropathies Environmental injuries: burns, frostbites Systemic diseases: superficial necrolytic dermatitis (hepatocutaneous syndrome), calcinosis cutis, uremia Neoplasia: SCC, cutaneous epitheliotropic lymphoma, mast cell tumor, paraneoplastic alopecia Conformational dermatoses: intertrigo, pressure sores Iatrogenic: radiation therapy, thermal or tissue injury Miscellaneous: feline indolent ulcer, feline eosinophilic plaque, feline plasma cell pododermatitis, feline ulcerative dermatitis with linear sub-epidermal fibrosis, snakebite
INITIAL DATABASE Patient history and physical examination are very important in the diagnostic process. Cytologic examination of any exudate contents: bacteria, inflammatory cells, acantholytic keratinocytes (pemphigus), fungal organisms CBC, serum biochemistry panel, and urinalysis if systemic signs are observed
ADVANCED OR CONFIRMATORY TESTING Skin biopsies for histopathologic examination are indicated in most cases of ulcerative dermatoses. Endocrine tests and serologic examination depend on suspected disease. Coombs' test: cold-agglutinin disease Antinuclear antibody (ANA) test: positive in virtually all animals with SLE Imaging, if relevant, to confirm systemic disease or stage tumors
TREATMENT TREATMENT OVERVIEW Varies considerably according to the disease. It must address the primary cause of the erosions or ulcers.
ACUTE AND CHRONIC TREATMENT Immunosuppressive treatments are required in immune-mediated diseases, whereas infectious diseases require proper antimicrobial treatment. Antiparasitic treatments as required
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Neoplastic diseases should be addressed according to the type of tumor. Some patients with conformational dermatoses may need surgery to correct the skin defect. Supportive care may be required, especially in animals with severe lesions or systemic illness.
PROGNOSIS AND OUTCOME Ranges widely from good to poor, depending of the primary cause
PEARLS & CONSIDERATIONS COMMENTS Considering the wide range of treatments, make a definitive diagnosis to correctly address the disease and prevent adverse effects of an improper treatment trial. Primary lesions (e.g., vesicles, bullae, and pustules) or skin surrounding erosion/ulcer should be sampled when skin biopsy is performed. Some of these diseases are life threatening. Be aware of the zoonotic potential of some of these diseases (e.g., sporotrichosis).
SUGGESTED READING Mason IS: Erosions and ulcerations. In Ettinger SJ, Feldman EC, editors: Textbook of veterinary internal medicine, ed 6, St Louis, 2005, Elsevier Saunders, pp 46–50. Scott DW, Miller WH, Griffin CE, eds: Muller and Kirk’ s small animal dermatology, ed 6, Philadelphia, 2001, WB Saunders. AUTHOR: FRÉDÉRIC SAUVÉ EDITOR: MANON PARADIS
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Vulvar Discharge
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Vulvar Discharge BASIC INFORMATION DEFINITION Discharge of substance from the urogenital tract (most likely vagina or uterus). May be abnormal or physiologically appropriate. Very common in the bitch during the normal estrous cycle and periparturient period
EPIDEMIOLOGY SPECIES, AGE, SEX: More common in dogs (spayed or intact) RISK FACTORS Sexually intact bitch Post partum bitch or queen Vaginal stricture or septum, vaginal foreign body, vaginal neoplasia Ovarian remnant syndrome Urethral neoplasia, ectopic ureters, redundant lateral/dorsal vulvar fold Mibolerone treatment CONTAGION & ZOONOSIS Bruceila canis Transmissible venereal tumor (TVT) ASSOCIATED CONDITIONS & DISORDERS Frequently associated with pyometra Not uncommon in association with abortion/premature labor, metritis, or endometritis Rarely noted secondary to subinvolution of placental sites (SIPS) in the bitch Others: vulvar fold pyoderma, urinary tract infection (UTI), urinary incontinence, urethritis, pseudohermaphroditism, hermaphroditism
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT Visible vulvar discharge Malodor Increased genital grooming Staining of carpet/bedding “Scooting” (rubbing perineum on floor) Pollakiuria Attracting males Hair staining in perineal area
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Vulvar Discharge
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VULVAR DISCHARGE Ulcerative perivulvar pyoderma typically seen in association with chronic vulvar discharge in dogs. Lethargy, inappetence in cases of sepsis or hypovolemic shock (e.g., pyometra) Polyuria and polydipsia with pyometra PHYSICAL EXAM FINDINGS Generally, physical abnormalities are restricted to genital tract; exceptions: pyometra with sepsis, or coagulopathy Inflamed, moist, red perivulvar skin ± moist or ulcerative pyoderma Red ± ulcerated vulvar mucosa; clitoral enlargement Classification of discharge type assists diagnostic approach: Color (colorless, brown, green, red, purulent) Smell (malodorous or not) Volume (mild, moderate, copious) Discharge associated with bacterial infection is typically purulent/mucosanguineous and malodorous with moderate to copious volume. Discharge due to inflammation is typically mucoid, white or clear, mild to moderate volume, and not malodorous. Rectal palpation may reveal foreign body or mass in the posterior vaginal vault and/or pelvic urethra. Digital vaginal examination (see p. 1360) may reveal discharge; small mucosal nodules (reactive lymphoid tissue) may be palpable with any inflammation and are not pathognomonic for any one cause. Most vaginal strictures are palpable at the level of the urethral papilla because of embryologic fusion of müllerian ducts and urogenital sinus. Fever, signs of septic shock, distended uterine horns, and/or abdominal discomfort: possible if pyometra Petechiae and bleeding of other mucous membranes (nose, gums) may be present when coagulopathy is the cause of vaginal discharge; may also be noted in association with sepsis.
ETIOLOGY AND PATHOPHYSIOLOGY Purulent vaginal discharge in adult intact animal (diestrous): commonly due to pyometra (see p. 954) Vaginal discharge in adult animals: commonly from secondary bacterial vaginitis due to anatomic abnormalities (lateral/dorsal vulvar fold dermatitis, vaginal stricture, septum), foreign body, urinary tract infection with urethritis/vestibulitis, or neoplasia Lymphoplasmacytic vaginitis and juvenile-onset “puppy” vaginitis: unknown etiology Strictures are associated with adult-onset vaginitis due to a change in vaginal mucus drainage.
DIAGNOSIS DIAGNOSTIC OVERVIEW Purulent vaginal discharge requires immediate evaluation for pyometra (or metritis/endometritis in the periparturient period). Hemorrhagic vaginal discharge warrants evaluation for systemic bleeding disorders (see p. 493). More chronic discharges should be initially evaluated with a thorough physical examination, including rectal and vaginal palpations, cytologic exam of the discharge, and routine database for detection of urinary tract infection, vulvar abnormalities, vaginal strictures, foreign body, and palpable neoplastic change. Additional imaging, culture, and biopsy sample acquisition for detection of uterine stump abnormalities, ovarian remnants,
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urinary tract abnormalities, and vaginitis should be guided by preliminary findings and may require referral.
DIFFERENTIAL DIAGNOSIS Normal vaginal discharge; none should be malodorous: Estrus: hemorrhagic, low volume Parturition: moderate to large volume, hemorrhagic, green or brown Postpartum: low to moderate volume for up to 4-6 weeks, green initially then brown Endometritis/metritis: purulent, mucosanguineous, malodorous, moderate volume in association with a febrile post partum bitch Subinvolution of placental sites (see p. 1060): hemorrhagic, moderate volume in association with periparturient period Juvenile-onset vaginitis: white, mucoid, moderate in volume Secondary bacterial vaginitis due to stricture, foreign body: mucoid, blood-tinged discharge; may be malodorous; scant to moderate in volume Herpesvirus, Brucella canis infection (abortion): abortion-associated discharge is typically brown, moderate in volume. Urogenital neoplasia: variable; may be hemorrhagic, serous, or mucoid; scant to moderate in volume Bleeding disorder: hemorrhagic; volume depends on degree of coagulation impairment Lymphoplasmacytic vaginitis: typically low volume, scant, and serous initially; may become mucoid with secondary bacterial infection; occasionally serosanguineous Primary bacterial vaginitis (uncommon) Urinary tract infection/urethritis Vulvar fold pyoderma: malodor is typically noted from the vulvar area; discharge may be mild to moderate in volume; mucoid and occasionally blood tinged TVT: vulvar mass typically noted; associated discharge is typically serosanguineous (see p. 1114).
INITIAL DATABASE Physical examination, including evaluation of vulvar lip conformation, mucosa, and digital rectal and vaginal examination Vaginal cytologic examination CBC: leukocytosis with left shift, toxic changes: common with pyometra; leukopenia possible with endometritis; anemia may be noted postpartum or in association with SIPS. Serum biochemical analysis: generally unremarkable unless systemic involvement Urinalysis, sediment examination, and culture: assess for concurrent UTI. Avoid cystocentesis if there is a possibility of pyometra or coagulopathy. Ultrasonographic evaluation of genitourinary tract: diagnostic test of choice for pyometra
ADVANCED OR CONFIRMATORY TESTING Guarded cranial vaginal aerobic/mycoplasma bacterial culture to evaluate bacterial population Retrograde double-contrast vaginocystourethrogram Cystoscopy and vaginoscopy, including examination of cervix if present: foreign body, congenital malformation, mass Vaginal biopsy ± mass biopsy Coagulation profile Urethral pressure profile
TREATMENT TREATMENT OVERVIEW Treatment goals are to restore patient's comfort, correct underlying cause, and prevent recurrence.
ACUTE AND CHRONIC TREATMENT The nature and extent of treatment is determined by the underlying cause; vaginal discharge is simply a clue of underlying disease.
BEHAVIOR/EXERCISE If discharge is associated with an infectious disease (e.g., Brucella canis, TVT), then bitch should be quarantined from other dogs to prevent transmission.
POSSIBLE COMPLICATIONS
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Chronic estrogen supplementation may cause myelotoxicity.
RECOMMENDED MONITORING When diethylstilbestrol (DES) is used in high doses or for chronic therapy, regular evaluation of patient's CBC is advised (myelotoxicity). Patients with diminished renal function receiving cephalosporins may require more frequent renal monitoring. Baseline CBC, complete serum biochemistry, and urinalysis should be obtained prior to commencement of carprofen and rechecked on an ongoing basis during therapy. Nonsteroidal antiinflammatory drug (NSAID) use may be associated with hepatotoxicity, renal toxicity, and gastrointestinal disturbance. Clinical response for uncomplicated bacterial vaginitis Reexamination and reevaluation if complete resolution is not achieved after 14 days of therapy
PROGNOSIS AND OUTCOME Good prognosis for secondary bacterial vaginitis if underlying cause is identified and corrected. Idiopathic lymphoplasmacytic vaginitis is often recurrent but responsive to steroid therapy.
PEARLS & CONSIDERATIONS COMMENTS Always rule out pyometra in an intact animal with vaginal discharge. Always perform digital vaginal and rectal palpation when initially evaluating a patient with vaginal discharge. Normal vaginal flora is mixed (Escherichia coli, Pasteurella multocida, β-hemolytic Streptococcus group G most common). Abnormal flora is typically a single isolate and/or heavy growth. Vaginal cytologic examination is always helpful to detect discharge due to estrus in the bitch and the presence of estrogen influence. Surgical correction of strictures is not advised; clitorectomy is advised in cases of clitoral hypertrophy.
PREVENTION Pyometra may be avoided by ovariectomy/ovariohysterectomy.
TECHNICIAN TIPS When taking a medical history, always ask owners when their bitch's last estrous cycle occurred or confirm previous ovariohysterectomy.
CLIENT EDUCATION Positive bacterial culture does not indicate disease is present. Prebreeding antibiotics do not prevent vaginitis or pyometra. Puppy vaginitis is usually self-limiting and does not require antimicrobial treatment; antimicrobial treatment of puppy vaginitis may prolong resolution of the problem.
SUGGESTED READING Johnston SD, et al: Disorders of the canine vagina, vestibule, and vulva. In Canine and feline theriogenology. Philadelphia, 2001, WB Saunders, pp 225–242. AUTHOR: SOPHIE GRUNDY EDITOR: MICHELLE A. KUTZLER
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von Willebrand Disease
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von Willebrand Disease BASIC INFORMATION DEFINITION Hereditary primary hemostatic defect caused by a quantitative or functional deficiency of von Willebrand factor (VWF). VWF is an adhesive protein required for normal platelet-collagen binding at sites of small vessel injury. Clinical expression varies in severity from a mild bleeding tendency manifesting primarily after injury to more severe forms characterized by recurrent mucosal hemorrhage and prolonged bleeding from normal processes, such as deciduous tooth loss.
SYNONYMS Factor-VIII related antigen (old terminology; protein is now referred to as VWF), VWD
EPIDEMIOLOGY SPECIES, AGE, SEX von Willebrand disease (VWD) is the most common hereditary bleeding disorder of dogs. It is a rare hemostatic defect of cats. Severe forms typically manifest by 1 year of age, and milder forms may be inapparent unless the patient undergoes surgery or trauma. GENETICS & BREED PREDISPOSITION Autosomal trait with three type classifications: Type 1 VWD: mild to moderate; recessive or incomplete dominant inheritance Types 2 and 3 VWD: severe; recessive inheritance Males and females express and transmit VWD with equal frequency. In recessive forms, affected pups inherit a VWF mutation from both dam and sire. Affected breeds: Type 1 VWD: Airedale, Akita, Bernese mountain dog, dachshund, Doberman pinscher, German shepherd, golden retriever, greyhound, Irish wolfhound, Kerry blue terrier, Manchester terrier, miniature pinscher, Papillon, Pembroke Welsh corgi, poodle, schnauzer, and sporadic cases in any breed Type 2 VWD: German short-haired pointer, German wirehaired pointer Type 3 VWD: Chesapeake Bay retriever, Dutch kooiker, Scottish terrier, Shetland sheepdog, and sporadic cases (recent cases in Australian shepherd, border collie, cocker spaniel, Labrador retriever, Maltese)
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES Type 1 VWD: quantitative protein deficiency. Low plasma concentration of VWF (von Willebrand factor antigen [VWF:Ag]) with proportionate reduction in VWF function; the VWF protein has a full distribution of multimeric forms. Type 2 VWD: both quantitative and functional protein deficiency; low plasma VWF:Ag has a disproportionate decrease in VWF function measured by collagen binding or support of platelet agglutination. VWF protein lacks the high molecular weight multimers. Type 3 VWD: severe VWF deficiency, no detectable plasma VWF HISTORY, CHIEF COMPLAINT Severe forms: recurrent mucosal bleeds, prolonged bleeding from loss of deciduous teeth or minor wounds, blood loss anemia after surgery or trauma Mild forms: few spontaneous or severe bleeds; abnormal bleeding typically observed after surgical or traumatic injury PHYSICAL EXAM FINDINGS Abnormal hemorrhage: Mucosal bleeding
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Abnormal bleeding from traumatic/surgical wounds Pallor due to blood loss anemia
ETIOLOGY AND PATHOPHYSIOLOGY Distinct VWF mutations causative for type 3 VWD have been described in Scottish terriers and Dutch kooiker dogs. Homozygosity for a mutation located at a splice site of the VWF gene has been associated with low VWF protein in type 1 VWD. Types 2 and 3 VWD cause a moderate to severe bleeding tendency. The clinical severity of type 1 VWD generally correlates with decrease in VWF concentration. VWF is an adhesive protein required for normal platelet-collagen binding at sites of small vessel injury under high shear. A lack of VWF impairs platelet plug formation and causes bleeding despite normal in vitro platelet numbers, normal platelet aggregation, and normal coagulation cascade parameters (normal coagulation profile).
DIAGNOSIS DIAGNOSTIC OVERVIEW Von Willebrand disease typically causes signs of mucosal hemorrhage and prolonged postsurgical/traumatic hemorrhage. Platelet count and coagulation screening tests are normal in dogs (or cats) with VWD.
DIFFERENTIAL DIAGNOSIS Primary hemostatic defects: Thrombocytopenia Acquired or hereditary platelet dysfunction (thrombocytopathias; e.g., patient taking aspirin) Coagulation factor deficiency Vasculopathy or erosive/infiltrative vessel defect causing mucosal hemorrhage
INITIAL DATABASE Thorough physical exam to define single versus multiple sites of hemorrhage Baseline hematocrit and plasma protein: normal or decreased if bleeding is severe and chronic Platelet count or platelet estimate from blood smear: usually normal Point-of-care coagulation screening tests: usually normal: Activated clotting time (ACT) Activated partial thromboplastin time (APTT) Prothrombin time (PT) Bleeding time (buccal mucosal bleeding time): increased (see p. 1222)
ADVANCED OR CONFIRMATORY TESTING Clinical diagnosis is based on specific measurement of plasma VWF concentration: VWF concentration (VWF:Ag): VWF:Ag < 50% is evidence of VWF deficiency, but clinical bleeding tendency is usually seen in animals having more severe deficiency ( 3145 mcg/L is considered toxic (normal: 200-1600). Toxic levels in feline liver (postmortem): 8590-39,570 mcg/g In dogs, serum/plasma retinol > 20,000 mcg/L is considered toxic (normal: 300-1000 mcg/L)
TREATMENT TREATMENT OVERVIEW With acute intoxication, general decontamination procedures (induction of vomiting and administrations of activated charcoal) are indicated, whereas with chronic toxicosis, treatment simply consists of removing the source of excess vitamin A and providing supportive care. There is no antidote.
ACUTE GENERAL TREATMENT Decontamination of patient: Induction of vomiting (see 1364) Activated charcoal: 1-2 g/kg PO if recent large ingestion (within few hours) Remove source (excess vitamin A). Supportive care: IV fluids Vomiting may be controlled with metoclopramide at 0.1-0.4 mg/kg body weight PO, SQ, or IM q 8 h; or maropitant, 1 mg/kg SQ q 24 h. Management of liver damage (rare) as needed (see 503)
DRUG INTERACTIONS Hypervitaminosis A can interfere with the action of other fat-soluble vitamins.
RECOMMENDED MONITORING Serum biochemistry profile Body weight
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Vitamin A Toxicosis
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PROGNOSIS AND OUTCOME Excellent in acute cases Chronic: guarded prognosis; bony changes are permanent, and some cats that were fed only liver may refuse to eat anything else.
PEARLS & CONSIDERATIONS COMMENTS Vitamin A deficiency far more common than intoxication Dogs can convert beta-carotene into vitamin A, but cats cannot. The amount of vitamin A needed to cause toxic effects is usually 10-1000 times the dietary requirements for most species. The vitamin A requirement for cats is 10,000 IU/kg of diet fed, with levels up to 100,000 IU/kg of diet tolerated. For dogs, the requirement is 3333 IU/kg of diet fed, with up to 33,330 IU/kg of diet tolerated. Vitamin A is fat soluble; 90% is stored in the liver and 10% in adipose tissue.
TECHNICIAN TIP An owner may mention that a cat eats a diet composed mainly of raw liver, and this information is worth relaying to the attending veterinarian because of the possibility of vitamin A toxicosis.
PREVENTION Do not overfeed raw beef liver to cats.
CLIENT EDUCATION Teach owners the value of a balanced diet.
SUGGESTED READING Doireau V, et al: Vitamin A poisoning revealed by hypercalcemia in a child with kidney failure. Arch Pediatr 3(9):888–890, 1996. Puls R: Vitamin A in dogs, vitamin A in cats. In Vitamin levels in animal health. Clearbrook, British Columbia, 1994, Sherpa International, pp 14, 20. Rader JD: Vitamin A. In Plumlee K, editor: Clinical veterinary toxicology. St Louis, 2003, Mosby, p 330. National Library of Medicine: http://www.nlm. nih.gov/medlineplus/ency/article/000350. htm AUTHOR AND EDITOR: SAFDAR A. KHAN 1ST EDITION AUTHOR: MARY SCHELL
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Vestibular Disease
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Vestibular Disease BASIC INFORMATION DEFINITION Category of disorders affecting the central or peripheral vestibular system of dogs and cats; usually cause clinical signs of head tilt, nystagmus, and/or loss of balance
EPIDEMIOLOGY SPECIES, AGE, SEX Occurs in both dogs and cats Idiopathic vestibular disease occurs in older dogs (usually >8 years) but in cats of any age. ASSOCIATED CONDITIONS & DISORDERS: Nausea, vomiting
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES Peripheral vestibular disease (PVD): vestibular nerve lesion in inner ear Central vestibular disease (CVD): brainstem lesion (medulla) HISTORY, CHIEF COMPLAINT Regardless of the underlying cause, most animals present with a peracute to subacute onset of clinical signs. The most common chief complaints are head tilt, nystagmus, and ataxia. Acute-onset vestibular disorders may produce such profound dysequilibrium and ataxia that owners are concerned about the animal's having “had a stroke.” PHYSICAL EXAM FINDINGS Head tilt, nystagmus, and vestibular ataxia (possibly to the extent of causing recumbency and whole-body rolling) are the hallmarks of both peripheral and central vestibular disorders. The most important aspect in localization of a lesion to the central vestibular system is identification of neurologic signs that cannot be attributed to PVD. Mental status: Central: often altered (depression, stupor, or coma) Peripheral: animal should be alert and responsive and can often appear disoriented. Gait: vestibular ataxia (falling, veering, leaning, rolling, circling), usually toward the side of the lesion; seen with both CVD and PVD. Hypermetria, intention tremors, and truncal sway may be observed if the cerebellum is affected (central). Head tilt: usually toward the side of the lesion; seen with both CVD and PVD. Spontaneous nystagmus: occurs with both CVD and PVD. Vertical nystagmus occurs only in animals with CVD, while horizontal or rotary nystagmus can be seen with either PVD or CVD. The fast phase of the nystagmus is usually away from the side of the lesion. Change in direction of the fast phase with altered head positions suggests CVD. Cranial nerve deficits: cranial nerve VII (facial nerve) paresis is sometimes seen in animals with PVD, owing to its proximity to peripheral vestibular structures. Cranial nerves V, VI, IX, and XII ipsilateral to lesion may be affected in animals with CVD but not PVD. Horner's syndrome: possible with PVD but rare with CVD ipsilateral to lesion Postural reaction deficits are commonly seen with CVD but should not be observed with PVD. Paradoxical CVD: lesion location as suggested by clinical signs related to the head (head tilt, nystagmus, etc.) does not match the lesion location suggested by the postural reaction deficits; the latter indicate the true side of the lesion (same side as hopping/proprioceptive deficit). Bilateral PVD: head tilt and nystagmus may not be present; animals may walk with a crouched gait. Clinical signs related to disease in other central nervous system (CNS) locations, such as seizures, behavioral changes, hypermetria, intention tremors, and truncal sway, suggest multifocal central neurologic disease.
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Vestibular Disease
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ETIOLOGY AND PATHOPHYSIOLOGY Basic neuroanatomy of the vestibular system: Peripheral: vestibular receptors (semicircular canals, saccule, utricle) located within the petrous temporal bone and cranial nerve VIII (vestibulocochlear nerve) Central: vestibular nuclei in the dorsal portion of the medulla oblongata, vestibular pathways of the brainstem and spinal cord (medial longitudinal fasciculus, vestibulospinal tracts), vestibular components in the cerebellum, and vestibular pathways through the caudal cerebellar peduncle Etiology for idiopathic vestibular disease in dogs and cats is unknown; an immune-mediated mechanism is suspected, but immunosuppressive drugs such as glucocorticoids have not been shown to help.
DIAGNOSIS DIAGNOSTIC OVERVIEW Clinical signs of vestibular disease are usually distinctive (see above). The diagnostic challenge consists of identifying peripheral versus central disease, which can be done on physical exam in most cases. The underlying cause is found using specific diagnostic tests ranging from hormonal assays (hypothyroidism) to advanced imaging (structural brain lesion).
DIFFERENTIAL DIAGNOSIS Peripheral vestibular diseases: Otitis media/interna Idiopathic vestibular disease Nasopharyngeal polyps: cats >> dogs Hypothyroidism: dogs Neoplasia: squamous cell carcinoma (SCC), ceruminous gland adenocarcinoma, and other related conditions Ototoxicity: topical chlorhexidine or iodine; systemic aminoglycosides and other drugs Central vestibular diseases: Canine distemper virus (CDV) encephalomyelitis Feline infectious peritonitis (FIP) Rickettsial encephalitis: Rocky Mountain spotted fever (RMSF), ehrlichiosis Fungal encephalitis: Cryptococcus neoformans most common; blastomycosis or coccidioidomycosis in certain regions of North America Granulomatous meningoencephalomyelitis (GME) Protozoal encephalitis: Toxoplasma gondii, Neospora caninum Neoplasia: meningioma, choroid plexus tumor, lymphoma, metastatic neoplasia Metronidazole toxicosis Cerebrovascular accident (infarct)
INITIAL DATABASE CBC, serum biochemical analysis, urinalysis: results often normal Thyroid hormone analysis: low total T 4 and free T 4 and elevated thyroid-stimulating hormone (TSH) in dogs with hypothyroidism Otoscopic examination: evaluate tympanic membranes for integrity.
ADVANCED OR CONFIRMATORY TESTING Bulla radiographs: dorsoventral, oblique lateral, and rostroventral-caudodorsal open-mouthed views. Abnormalities include soft-tissue or fluid opacity within the bulla and sclerosis of the tympanic bulla. Oropharyngeal and otoscopic examination under general anesthesia to identify nasopharyngeal polyps and otitis media. Abnormalities include soft-tissue or fluid opacity within and sclerosis of the affected tympanic bulla (see p. 1316). Brainstem auditory evoked response (BAER) test may be useful for distinguishing PVD from CVD (see p. 1216). CT scan (see p. 1233): useful for examination of the middle ear in patients with PVD. CT scans can also be used for CVD; however, beam-hardening artifacts in the caudal brain may preclude evaluation of the brainstem, and small lesions may not be visualized (MRI preferable for this location). MRI (see p. 1302): useful for examination of both the peripheral and central vestibular structures. It provides superior resolution of brain parenchyma.
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Vestibular Disease
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Cerebrospinal fluid (CSF) analysis (see p. 1228): used as an adjunct to advanced imaging, primarily to rule out encephalitis. Infectious disease titers may be required in certain cases to rule out infectious encephalitis. CSF is the preferred sample for CDV, FIP, and cryptococcosis. Serum titers are performed for Toxoplasma and Neospora spp. CSF culture and sensitivity (C&S) may be required for ruling out bacterial encephalitis. Histopathologic examination is required for definitive diagnosis in many diseases causing structural lesions (e.g., masses). Tissue samples can be obtained via surgical excision or stereo-tactic brain biopsy (see p. 1214).
TREATMENT TREATMENT OVERVIEW Definitive treatment for vestibular disease is based on diagnosis of the underlying cause.
ACUTE GENERAL TREATMENT Meclizine (25 mg PO q 24 h in dogs; 12.5 mg PO q 24 h in cats) or diazepam (0.1-0.5 mg/kg PO q 8 h in dogs) may help alleviate clinical signs of nausea and vomiting. Meclizine causes less sedation than diazepam and can be purchased as an over-the-counter drug. Oral diazepam should be used with caution in cats because of the reported incidence of idiosyncratic hepatic necrosis. Idiopathic vestibular disease: clinical signs improve spontaneously over 1-2 weeks; no treatment has been shown to accelerate natural resolution of the disorder. Otitis media/interna: systemic antibiotics ± antifungals for 4-6 weeks, ideally based on bacterial C&S. Surgical treatment (bulla osteotomy and total ear canal ablation) may be required to remove infected tissues. Nasopharyngeal polyps: bulla osteotomy Hypothyroidism: thyroid supplementation (see p. 588) Neoplasia: surgical excision may be possible for meningioma and choroid plexus tumors depending on lesion location. Surgical excision of tumors in the middle and inner ear may be possible but is difficult. Radiation therapy may provide some relief of clinical signs, and consultation with an oncologist is recommended in these cases. CDV and FIP encephalomyelitis: no specific therapy is available. Nonspecific supportive therapy with antibiotics and corticosteroids may alleviate signs temporarily (see pp. 317 and 383). Rickettsial encephalitis: doxycycline (5 mg/kg PO q 12 h) or chloramphenicol (50 mg/kg PO q 8 h) for 3-4 weeks. Fungal encephalitis: fluconazole (5 mg/kg PO q 12 h) penetrates the CNS to a greater degree than other antifungal medications. Itraconazole and amphotericin B can be used with blastomycosis. Oral treatment should be continued for at least 6 months, barring adverse reactions, and may be required long term to control clinical signs. GME: immunosuppressive dose of prednisone, initially at 2 mg/kg PO q 12 h for 1-2 days, then 1 mg/kg PO q 12 h for at least 2 weeks. Then slowly taper the drug over 4-8 months to reach the minimal effective dose (see p. 457). Protozoal encephalitis: clindamycin (10 mg/kg PO q 12 h to q 8 h) for 4 weeks; or combination of trimethoprim/sulfadiazine (TMS; 15 mg/kg PO q 12 h) and pyrimethamine (1 mg/kg PO q 24 h) Metronidazole toxicosis: discontinue metronidazole. In dogs, diazepam administration (0.5 mg/kg IV once, followed by 0.5 mg/kg PO q 8 h until resolution of signs) appears to shorten the duration of clinical signs. Oral diazepam should be used with extreme caution in cats, owing to the reported incidence of idiosyncratic hepatic necrosis.
POSSIBLE COMPLICATIONS A permanent mild head tilt may persist after resolution of other clinical signs.
RECOMMENDED MONITORING Serial neurologic exam every 4 weeks Serial infectious disease titers if indicated
PROGNOSIS AND OUTCOME Prognosis for most PVDs is good with specific treatment, with the exception of neoplasia, which carries a guarded to poor prognosis. CDV and FIP encephalomyelitis: poor even with treatment Rickettsial and protozoal encephalitis: good with early and specific treatment Fungal encephalitis: fair to guarded. Long-term treatment may be required to control clinical signs. GME: fair to guarded. Many dogs respond initially to treatment; however, relapse is common. In some dogs, corticosteroids eventually can be discontinued. Neoplasia: generally poor long-term prognosis
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Metronidazole toxicosis: excellent
PEARLS & CONSIDERATIONS COMMENTS Compensation for vestibular diseases will occur in many animals regardless of lesion location, and clinical signs may improve slightly if the lesion is slow growing. In general, animals with PVD carry a good prognosis for recovery following specific therapy. The long-term prognosis for animals with CVD is variable depending upon the specific cause; however, treatment should be attempted to alleviate clinical signs.
PREVENTION Thyroid supplementation in dogs with hypothyroidism Avoidance of high doses and/or prolonged courses of metronidazole treatment. A common error is to prescribe a high dose of the drug (e.g., 30-65 mg/kg PO q 12 h). The recommendation is to limit the maximum daily dose to 30 mg/kg/day, divided into two daily doses.
CLIENT EDUCATION Head tilt may be persistent.
SUGGESTED READING Sanders SG, Bagley RS: Disorders of hearing and balance: the vestibulocochlear nerve (CN VIII) and associated structures. In Dewey CW, editor: A practical guide to canine and feline neurology, ed 2, Ames, IA, 2008, Wiley-Blackwell, pp 261–285. AUTHOR: MARK T. TROXEL EDITOR: CURTIS W. DEWEY
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Ventricular Septal Defect BASIC INFORMATION DEFINITION Well-recognized, anomalous communication between the right ventricle (RV) and left ventricle (LV), resulting in interventricular shunting of blood
SYNONYMS Interventricular septal defect, VSD
EPIDEMIOLOGY SPECIES, AGE, SEX Dogs and cats First or second most common congenital heart defect in cats Typically diagnosed at a young age No sex predilection GENETICS & BREED PREDISPOSITION Hereditary in a family of English springer spaniels and keeshonden Predisposed breeds: Akita, basset hound, bloodhound, English bulldog, English springer spaniel, keeshonden, Lakeland temer, Old English sheepdog, West Highland white terrier ASSOCIATED CONDITIONS & DISORDERS Aortic valvular insufficiency (AI) due to decreased support of aortic valve Pulmonic stenosis, overriding aorta, atrial septal defects
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES In small animals, ventricular septal defect (VSD) most commonly involves the high membranous septum below the aortic valve on left side and below the tricuspid valve on the right side (perimembranous VSD). Left to right (L→R) shunting across the VSD is most common. A very large VSD or VSD accompanied by other defects that increase RV pressure (e.g., severe pulmonic stenosis or pulmonary hypertension) may result in shunting of blood from right to left (R→L, “reverse shunting”). HISTORY, CHIEF COMPLAINT Usually there are no overt clinical signs reported by the owner (incidental finding of heart murmur during routine exam). In the case of a large L→R VSD or in R→L VSD, the following may be observed: Exercise intolerance Dyspnea, tachypnea Cough (L→R) Cyanosis (R—>L) Syncope PHYSICAL EXAM FINDINGS Systolic murmur, loudest around the fourth intercostal space (ICS) on the ventral thorax to the right of the sternum (most common) or left base If substantial AI is present, a diastolic murmur may be heard on the left cranial thorax (heart base, third ICS). Tachycardia, dyspnea, tachypnea, crackles may be apparent if left-sided congestive heart failure (CHF) is present
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R→L shunt: cyanosis, generally no murmur unless another malformation is present (e.g., pulmonic stenosis)
ETIOLOGY AND PATHOPHYSIOLOGY Magnitude and direction of shunting and thus clinical consequences depend on size of defect, relative pulmonary and systemic vascular resistances, and presence of other cardiopulmonary defects. L→R shunting VSD causes volume overload of pulmonary circulation and left side of the heart; ultimately the result may be left-sided CHF and/or pulmonary hypertension. R→L shunting VSD (much less common) causes systemic arterial hypoxemia, which can lead to polycythemia and hyperviscosity syndrome.
DIAGNOSIS DIAGNOSTIC OVERVIEW While very strong clinical suspicion of VSD may be based on physical examination alone (typically, systolic murmur with a point of maximal intensity on the right hemithorax), definitive diagnosis requires echocardiography.
DIFFERENTIAL DIAGNOSIS Other congenital causes of systolic murmurs: aortic/subaortic or pulmonic stenosis, atrio ventricular (AV) valve dysplasia, tetralogy of Fallot (of which VSD is one component) Acquired heart diseases: acquired AV valve regurgitation (dogs), dilated cardiomyopathy (dogs or cats), hypertrophic cardiomyopathy (cats)
INITIAL DATABASE CBC/serum biochemistry panel: Typically normal Polycythemia if R→L shunting Thoracic radiographs: Normal with small VSD Larger L→R VSD: left-sided cardiomegaly, pulmonary overcirculation, ± pulmonary edema, ± right ventricular enlargement R→L VSD: right-sided cardiomegaly, variable pulmonary artery pattern (e.g., normal to enlarged if pulmonary arterial hypertension; normal or small if pulmonic stenosis) Electrocardiogram (ECG): Often normal Left atrial (LA) and/or LV enlargement if large L→R shunt or RV enlargement if R→L shunt ± Wide and/or notched Q wave, representing abnormal septal activation Echocardiography: A visible defect in the interventricular septum may be noted. Beware of artifactual defects (“septal drop-out”). L→R VSD: turbulent jet from LV to RV with color Doppler, ± LA enlargement, ± LV enlargement Peak velocity (V in m/s) of VSD jet with continuous wave Doppler reflects the pressure gradient (∆P [mm Hg]) between LV and RV according to modified Bernoulli equation (∆P = 4V2), which generally speaks to size of defect (small VSD: V > 4.5 m/s; moderate-size VSD: 3 < V < 4.5 m/s; large VSD: V < 3 m/s). Beware of underestimation of velocity due to erroneous/oblique alignment of Doppler sample. R→L VSD: right ventricular hypertrophy, flattening of the interventricular septum, main pulmonary artery dilation ± AI with color and spectral Doppler
ADVANCED OR CONFIRMATORY TESTING Contrast echocardiography (bubble study) to confirm R→L shunt Cardiac catheterization for angiography, shunt quantification, and measurement of cardiac pressures (virtually never used; mainly preoperative if open-heart surgery)
TREATMENT TREATMENT OVERVIEW
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Often no treatment is required, since the majority of VSDs are small and do not result in volume overload of the left ventricle or other significant clinical consequences. Treatment of large L→R VSDs is directed at decreasing the shunt volume and preventing or eliminating the signs of CHF. Treatment of R→L VSDs tends to be palliative only.
ACUTE GENERAL TREATMENT L→R VSD with significant left-sided volume overload (moderate to marked left ventricular enlargement): Surgical repair via thoracotomy uncommon (requires cardiopulmonary bypass, which is available at very few referral institutions) Percutaneous transcatheter repair using a variety of devices has been described and may be available at some referral institutions. Pulmonary artery banding is a palliative surgical technique to decrease L→R shunt. Arterial vasodilators used with caution to decrease L→R shunt; contraindicated if complex malformations or R→L shunt If CHF present, may use angiotensin-converting enzyme (ACE) inhibitors, diuretics, ± pimobendan, ± digoxin (see p. 468) R→L VSD: Surgical repair contraindicated Phlebotomy to palliate signs and maintain PCV at 55%-65%
CHRONIC TREATMENT Treatment of CHF as already described (see p. 470) Periodic phlebotomy ± hydroxyurea as needed if R→L shunt
POSSIBLE COMPLICATIONS Left-sided CHF Pulmonary hypertension Shunt reversal (R→L) over time (Eisenmenger's complex); rare in dogs and cats
RECOMMENDED MONITORING Following diagnosis in puppies/kittens with no clinical signs, examination at 6 months, 1 year, then yearly thereafter Frequent monitoring for animals with overt decompensation and requiring treatment
PROGNOSIS AND OUTCOME Excellent prognosis for small, uncomplicated VSD Guarded prognosis for larger VSD (risk CHF and/or pulmonary hypertension) Concurrent substantial AI carries poor prognosis. Guarded to poor prognosis for R→L shunts; severe exercise limitations
PEARLS & CONSIDERATIONS COMMENTS In L→R shunting VSDs, the RV and pulmonary arterial circulation essentially act as conduits for VSD flow. The LA and LV, however, receive increased venous return, resulting in increased diastolic pressures. In addition, effective forward flow into the systemic circulation is reduced as a result of the shunt flow. The latter two points account for the increased LV workload and predominant occurrence of left heart failure, not right heart failure, in L→R VSDs. VSD and tricuspid dysplasia are the two main differential diagnoses for a systolic murmur heard best on the right side of the chest in dogs or cats (murmurs due to subaortic stenosis may radiate prominently to the right side in some cases; hypertrophic cardiomyopathy is another common differential in cats). Most VSDs are relatively small, well tolerated, and do not require therapy.
PREVENTION Genetic basis possible but unproven in the breeds listed previously. Consider discouraging breeding of affected animals.
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SUGGESTED READING Oyama MA, Sisson DD, Thomas WP, et al: Congenital heart disease. In Ettinger SJ, Feldman EC, editors: Textbook of veterinary internal medicine, ed 7, St Louis, 2010, Elsevier Saunders, pp 1250–1298. AUTHOR: M. LYNNE O’SULLIVAN EDITOR: ETIENNE CÔTÉ
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Ventricular Arrhythmias
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Ventricular Arrhythmias BASIC INFORMATION DEFINITION Ventricular arrhythmias are excessive electrical discharges occurring spontaneously and prematurely in the ventricles. By definition, the term premature ventricular complex(es) (PVCs) applies to one, two, or three consecutive premature ventricular impulses, whereas four or more in a row are defined as ventricular tachycardia (VT). By definition, ventricular tachycardia involves a ventricular rate of 180 beats per minute (bpm) or more in dogs and 240 bpm or more in cats. Strictly speaking, these are ventricular tachyarrhythmias (to distinguish them from ventricular escape rhythms); for simplicity, the term ventricular arrhythmia will be used here for designating PVCs and VT.
SYNONYMS Ventricular ectopy, extrasystoles, or tachyarrhythmias PVCs are synonymous with ventricular premature complexes or contractions (VPCs), premature ventricular depolarizations (PVDs), and similar variations.
VENTRICULAR ARRHYTHMIAS Lead II ECG in a dog with ventricular tachycardia, 50 mm/sec, 10 mm/mV. The ventricular tachycardia is monomorphic (PVCs all of the same shape) and extremely rapid (375 bpm) in this critically septic dog.
VENTRICULAR ARRHYTHMIAS Single-lead ECG in a dog with immune-mediated hemolytic anemia and an ausculted arrhythmia, 50 mm/sec, 5 mm/mV. The 5th beat is a normal sinus beat; the remaining beats are of ventricular origin. Despite the ventricular arrhythmia, the rate is not rapid (115 bpm) and likely only slightly faster than the underlying sinus rate. This is accelerated idioventricular rhythm, a benign rhythm that does not require therapy beyond proactive treatment of its inciting cause (here, anemia).
EPIDEMIOLOGY SPECIES, AGE, SEX: Any can be affected. GENETICS & BREED PREDISPOSITION Boxers: arrhythmogenic cardiomyopathy (see p. 90) Doberman pinschers and other breeds: dilated cardiomyopathy German shepherds: inherited ventricular tachycardia of young adults Large-breed dogs: splenic masses Large-breed dogs (Great Danes, setters, retrievers, and many others): gastric dilatation/volvulus (GDV) Cats (male > female): hypertrophic cardiomyopathy RISK FACTORS: Outdoor, roaming dogs: traumatic myocarditis (hit by car). Primary heart disease or any systemic disturbance, if sufficiently severe, can cause ventricular arrhythmias. GEOGRAPHY AND SEASONALITY: Chagas' disease: myocarditis (southern parts of the United States and Latin America)
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ASSOCIATED CONDITIONS & DISORDERS: Syncope (rapid VT)
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES Incidental finding Clinically overt (e.g., causing syncope) Accelerated idioventricular rhythm HISTORY, CHIEF COMPLAINT Incidental finding (more common): Animal is presented for evaluation of a disorder other than syncope. Arrhythmia is noted during physical examination or subsequent monitoring. Clinically overt: Syncope/episodic collapse Episodic stumbling, disorientation, confusion Animal may be well (and even playful and active) before and after episodes or may be lethargic, weak, or anorexic. PHYSICAL EXAM FINDINGS Incidental finding: Physical exam findings reflect the underlying disorder; however, an arrhythmia is noted on physical exam. Common Causes of Ventricular Arrhy thmias *†
Hypokalemia ,
Hypoxemia (e.g., due to cardiogenic pulmonary edema, pleural effusion, primary lung disease)* Cardiomyopathy *
Gastric dilatation/volvulus
Traumatic myocarditis/hit by car *
Abdominal mass, especially splenic or hepatic Advanced valvular heart disease Hypomagnesemia*,† *
Acidos is
Intoxication (digitalis; oleander, foxglove, lily of the valley, azalea, and yew plants; many over-the-counter, prescription, or illicit drugs) * Potentially correctable/curable. † Presence makes ventricular antiarrhythmic drugs such as lidocaine, procainamide, and mexiletine ineffective. With ventricular tachycardia, the arrhythmia is rapid and may be irregular (usually polymorphic on electrocardiogram [ECG]) or regular (usually monomorphic on ECG). Pulse deficit: Premature heartbeat ausculted, without a corresponding palpable pulse for that beat Common with ventricular arrhythmias Depends on the degree of prematurity of PVCs (“How underfilled are the ventricles when the PVC causes them to contract again?”)
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Clinically overt: Wide range of presentations, from clinically normal and alert if arrhythmia is intermittent, to profoundly weak and hemodynamically collapsed with very rapid, sustained ventricular tachycardia Regularity or irregularity and pulse deficit, as for incidental finding (above)
ETIOLOGY AND PATHOPHYSIOLOGY Enhanced or abnormal automaticity, microreentry, and triggered activity (early or delayed after depolarizations) are mechanisms that underlie ventricular arrhythmias. These mechanisms can be activated or potentiated by systemic disturbances such as those previously listed (see Associated Conditions & Disorders, above). The result is one or more spontaneous electrical depolarizations originating prematurely in the ventricles. The prematurity is manifested on the electrocardiogram (ECG) as a shorter R-R interval. The ventricular origin results in a QRS complex that is of a different shape than a sinus QRS complex. A greater degree of prematurity of PVCs (or a higher rate of ventricular tachycardia) reduces the time the ventricles have for filling prior to contracting. Therefore, faster ventricular arrhythmias compromise diastolic filling time more severely and are more likely to produce clinical signs or hemodynamic deterioration (e.g., poor pulse, cerebral hypoperfusion) than slower or infrequent ventricular arrhythmias. Accelerated idioventricular rhythms are seen commonly in hospitalized patients in association with noncardiac diseases (e.g., GDV surgery, splenic disease, immune-mediated hemolytic anemia, post trauma, and neurologic disease). These are often benign, the rate is not rapid, and they often do not require therapy.
DIAGNOSIS DIAGNOSTIC OVERVIEW Ventricular arrhythmias can be suspected on history (syncope), physical exam (premature beats), and ECG (classically, wide and bizarre QRS complexes occurring prematurely). Careful inspection of the ECG allows differentiation from other similar-appearing but clinically very different ECG deflections.
DIFFERENTIAL DIAGNOSIS PVCs can occur in many situations and do not automatically equate to an underlying serious cardiac disorder. Additionally, they can be seen in normal animals in low numbers (220/min in smallbreed dogs, >260/min in cats) despite the three steps described so far, then antiarrhythmic treatment should be considered. The following are recognized treatments for ventricular arrhythmias: Lidocaine, 1-2 mg/kg (dog) or 0.25-1 mg/kg (cat) IV bolus (can repeat up to three times in 10-15 minutes); can be followed with IV constant rate infusion (CRI) at 40-80 mcg/kg/min (dog) or 10-20 mcg/kg/min (cat) To make lidocaine CRI: withdraw 25 mL from a 500-mL bag of crystalloid fluid (e.g., lactated Ringer's solution) and replace with 25 mL of 2% lidocaine. Concentration in bag is 1000 mg/mL. Administer IV at usual fluid maintenance rate (66 mL/kg per day) assuming congestive heart failure (CHF) is not present. Infusion at this rate will be 50 mcg/kg/min. Procainamide, 6-15 mg/kg (dog) or 1-2 mg/kg (cat) slow IV bolus; may follow with IV CRI at 25-50 (dog) or 10-20 (cat) mcg/kg/min. Usually administered instead of lidocaine if lidocaine was ineffective, but both may be given together. see treatment algorithm, .
CHRONIC TREATMENT Ongoing management of the underlying cause Oral antiarrhythmic drugs may be used for treating rapid and/or clinically overt (syncopal) ventricular arrhythmia. Options include one of the following: Sotalol, 0.5-2 mg/kg PO q 12 h (dogs); 10-20 mg per cat PO q 12 h Mexiletine, 4-8 mg/kg PO q 12 h to q 8 h; and atenolol, 0.2-0.75 mg/kg PO q 12 h (dogs) Amiodarone, 10 mg/kg PO q 12 h for 1 week (loading), then 5-8 mg/kg PO q 24 h (dogs) Atenolol (cats), 6.25-12.5 mg per cat PO q 24 h to q 12 h Procainamide sustained release (dogs) has been given at 10-20 mg/kg PO q 8 h to q 6 h, but variable dissolution of tablets makes pharmacokinetics unpredictable.
DRUG INTERACTIONS Digoxin can cause ventricular arrhythmias (see p. 309).
POSSIBLE COMPLICATIONS Uncontrolled ventricular arrhythmias may progress to ventricular flutter and ventricular fibrillation (cardiac arrest); however, normalization of the ECG to sinus rhythm using antiarrhythmic drugs alone has never been shown to improve the prognosis for
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survival. Therefore, complications can be minimized by treating/correcting inciting factors (see table), reserving ventricular antiarrhythmic drugs for cases in which overt signs such as syncope are present or in which a very high rate (e.g., >220 bpm in dogs, >260 bpm in cats) is present despite management or correction of the underlying cause.
RECOMMENDED MONITORING ECG as dictated by clinical evolution; ranges from continuous ECG with ventricular tachycardia in an unstable animal to periodic ECG or Holter monitoring during visits in stable animals Follow-up tests as listed for initial diagnosis to monitor underlying condition
PROGNOSIS AND OUTCOME Ventricular arrhythmias that occur at a faster rate are more likely to produce clinical signs and carry a more guarded prognosis than slower ventricular arrhythmias. Ventricular arrhythmias that fail to respond to correction of the underlying problem (or for which the underlying problem cannot be corrected) usually indicate cardiac manifestations of a serious problem that carries a guarded short-term prognosis. Long-term prognosis depends on the exact nature of the underlying problem.
PEARLS & CONSIDERATIONS COMMENTS Virtually any disease or disorder, if sufficiently severe to have systemic effects, can cause ventricular arrhythmias. Ventricular escape beats and PVCs often look identical. Ventricular escape beats occur at a rate of 40-100 bpm against a background of second- or third-degree AV block or asystole—they are saving the heart from arrest and should never be treated with ventricular antiarrhythmics. By contrast, PVCs are excessive, unwanted ventricular complexes that occur in addition to the heart's usual rhythm. The most common correctable underlying causes of ventricular arrhythmias are hypokalemia, hypoxia, GDV, abdominal masses, anemia, metabolic acidosis, and pain. The most common treatable but non-correctable causes of ventricular arrhythmias are cardiomyopathy, degenerative valvular heart disease, and traumatic myocarditis (hit by car). Ventricular arrhythmias most commonly are manifestations of an underlying disorder. Attempting to eliminate ventricular arrhythmias with antiarrhythmic drugs in a stable animal is analogous to “shooting the messenger.” Rather, the underlying cause needs to be found and addressed. Perhaps no antiarrhythmic drug is as beneficial to a patient with ventricular arrhythmias as correction of the underlying cause.
TECHNICIAN TIP Impostors for ventricular arrhythmias are common on in-hospital telemetry monitors, but ventricular arrhythmias are an important signal requiring attention. Unusual-appearing heartbeats on an ECG monitor should be printed and reviewed with the attending veterinarian.
PREVENTION Ventricular arrhythmias are clues to a primary cardiac or systemic disturbance; therefore, preventing them relies on identifying and managing the underlying disease whenever possible.
CLIENT EDUCATION Ventricular arrhythmias are serious disturbances of the cardiac rhythm. Their impact can range from minimal to life threatening, and sudden cardiac death is always possible when an animal has a disorder that causes ventricular arrhythmias.
SUGGESTED READING Côté E, Ettinger SJ: Electrocardiography and cardiac arrhythmias. In Ettinger SJ, Feldman EC, editors: Textbook of veterinary internal medicine, ed 6, St Louis, 2005, Elsevier, pp 1040–1076. Kittleson MD: Diagnosis and treatment of arrhythmias (dysrhythmias). In Kittleson MD, Kienle RD, editors: Small animal cardiovascular disease. St Louis, 1998, Mosby, pp 449–494. AUTHOR: AMARA ESTRADA
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EDITOR: ETIENNE CÔTÉ 1ST EDITION AUTHOR: ETIENNE CÔTÉ
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Vasculitis
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Vasculitis BASIC INFORMATION DEFINITION Vasculitis is an uncommon pathologic syndrome of inflammation and necrosis of the vessel wall, characterized by purpura, edema, necrosis and ulceration, often involving the extremities. Vasculitis may be limited to the skin (see online chapter: Vasculitis, Cutaneous) or may be an early sign of systemic disease.
SYNONYMS Inflammatory vasculopathy, angiitis
EPIDEMIOLOGY SPECIES, AGE, SEX: Vasculitis is rare in cats and when it occurs, is often associated with neoplasia such as lymphangiosarcoma. GENETICS & BREED PREDISPOSITION: Dogs: Jack Russell terriers, Scottish terriers, German shepherds, greyhounds (cutaneous and renal vasculopathy), dachshunds, rottweilers, beagles (rare: juvenile polyarteritis syndrome, [JPS], primary polyarteritis). Poodles, Maltese, bichon frise are reported to experience vaccine reactions more commonly. RISK FACTORS Dogs: infectious diseases (Rocky Mountain spotted fever [RMSF], ehrlichiosis, babesiosis, bacteremia, canine corona virus, canine parvovirus, leishmaniasis, dirofilariasis, sarcocystosis, staphylococcal hypersensitivity); drug exposure, vaccination (rabies vaccine), blood component transfusions (human albumin), flea bite or food hypersensitivity Cats: infectious diseases (feline infectious peritonitis [FIP], feline leukemia virus [FeLV], feline immunodeficiency virus [FIV]), drug exposure, vaccination (rabies, herpesvirus/calicivirus panleukopenia) CONTAGION & ZOONOSIS Dogs: canine corona virus (dog-to-dog only), canine parvovirus (dog-to-dog only) leishmaniasis (potential zoonosis) Cats: FIP, FeLV, FIV (cat-to-cat only) GEOGRAPHY AND SEASONALITY: Regional variation in etiology (i.e., RMSF) ASSOCIATED CONDITIONS & DISORDERS: Multisystemic clinical signs are uncommonly reported, including anemia, thrombocytopenia, polyarthropathy, myopathy, neuropathy, hepatopathy.
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES Cutaneous vasculitis is more common than systemic vasculitis. Vasculitis is more commonly secondary; a careful history including all medications/vaccinations received in the most recent 3 months is critical to identifying the etiology. Primary vasculitis is diagnosed by exclusion. HISTORY, CHIEF COMPLAINT Nonspecific signs: lethargy, inappetence, or anorexia +/− Medications/vaccination in past 3 months Erythema, plaques, papules/pustules, necrosis/ulcers Bruising Ventral or dependent edema (limbs, ventrum, prepuce) PHYSICAL EXAM FINDINGS Lesions in dependent/ventral regions, over pressure points, extremities (pinna, tail):
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Nonblanching erythema typically sharply demarcated from adjacent “normal” tissue; may be focal or generalized. Plaques, papules/pustules, necrosis/ulcers Petechia or ecchymotic hemorrhages Dependent edema +/− Fever +/− Peripheral lymphadenopathy
ETIOLOGY AND PATHOPHYSIOLOGY Toxic, immune-mediated, infectious, inflammatory and neoplastic disorders can all result in vasculitis. >50% of cases are idiopathic. Secondary vasculitis more common than primary vasculitis; search for underlying cause. Type III hypersensitivity is the predominant mechanism of cutaneous vasculitis. Vasculitis is characterized histologically by inflammatory cells in and around the vessel wall. Histologic classifications include neutrophilic, eosinophilic, lymphocytic, granulomatous, mixed and cell-poor forms. Neutrophilic vasculitis can be further classified into leukoclastic or nonleukoclastic (more common). Damage to vascular endothelium results in increased permeability, inflammation, and microvascular thrombosis.
DIAGNOSIS DIAGNOSTIC OVERVIEW The diagnosis is suspected based on the presence of nonblanching dermal erythema with or without edema; diagnosis is confirmed by skin biopsy. Vasculitis is a clinical problem with many etiologic possibilities, rather than a diagnosis, and efforts should be directed at identifying the underlying etiology.
DIFFERENTIAL DIAGNOSIS Coagulopathy, disseminated intravascular coagulation (DIC), systemic lupus erythematosus, cold agglutinin disease, discoid lupus, bullous pemphigoid, lymphoreticular neoplasia, hypersensitivity (primarily urticaria)
INITIAL DATABASE CBC: changes related to underlying disease +/− mild leukocytosis Serum biochemistry panel: changes related to underlying disease +/− hyperglobulinemia, mild hypoalbuminemia Urinalysis: +/− proteinuria if renal involvement Skin biopsy: confirmatory test of choice
ADVANCED OR CONFIRMATORY TESTING Rickettsial testing (dogs), viral serology (FeLV/FIV, cats) Coagulation testing (platelet count, prothrombin time (PT), activated partial thromboplastin time (APTT), fibrin degradation products (FDPs) Direct immunofluorescence, immunohistochemical testing: often not needed in diagnosis, short window for sampling (within 4-24 hours of lesion formation)
TREATMENT TREATMENT OVERVIEW Vasculitis may be acute and nonprogressive or chronic and recurrent. The therapeutic goal is to identify the underlying cause and minimize end organ damage if there is systemic involvement. Treatment of idiopathic cases is immunosuppressive or immunomodulatory. For treatment to be successful, the underlying cause must be treated or removed if possible.
ACUTE GENERAL TREATMENT Discontinue all unnecessary drugs until the inciting cause is identified. Glucocorticoids: prednisone or prednisolone (cats), 2-4 mg/kg PO q 24 h: Use caution with immunosuppressive doses if underlying infectious etiology Supportive care including IV fluids and analgesics, based on clinical judgment
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Sulfasalazine: 20-40 mg/kg q 8 h in dogs for cases refractory to glucocorticoids or if dermal involvement only: Monitor for side effects: anemia, thrombocytopenia, KCS, elevated ALT, and more serious side effects such as neuropathy, nephropathy May require addition of second immunosuppressive if not responding or prednisone intolerant: Azathioprine, chlorambucil, and cyclophosphamide have been reported.
CHRONIC TREATMENT Glucocorticoids: slowly taper to lowest effective dose. Pentoxifylline: 10 mg/kg q 8-12 h, tapered over 1-3 months to q 12-24 h: May take 1-3 months for response, synergistic action with glucocorticoids Therapy may be able to be tapered and discontinued over 4-6 months.
NUTRITION/DIET Vitamin E therapy has been reported, as has a combination of tetracycline and niacinamide.
DRUG INTERACTIONS Immunosuppressive doses of glucocorticoids may complicate treatment of underlying infectious etiology and should be used with extreme caution in these cases.
POSSIBLE COMPLICATIONS Necrosis: predisposes to infection or necessitates surgical débridement or amputation Consumptive coagulopathy (DIC) in severe cases Glomerulonephritis (GN) if immune complex deposition in the kidneys Hypoalbuminemia with severe or diffuse vasculitis or GN Glucocorticoids: immunosuppression, iatrogenic hyperadrenocorticism Sulfasalazine: side effects (above)
RECOMMENDED MONITORING Recheck in 3-5 days to assess response to initial therapy (extent and severity of lesions); reassess blood work if abnormalities present. CBC and serum biochemistry profile in 7 days if using sulfasalazine; every 4-6 weeks during initial treatment Reassess potentially infarcted dermal regions daily for evidence of necrosis; surgically address when patient stable.
PROGNOSIS AND OUTCOME Open depending on the underlying cause Drug-induced vasculitis tends to have a favorable prognosis once the inciting cause is eliminated, but chronic therapy may be required to limit the recurrence of clinical signs.
PEARLS & CONSIDERATIONS COMMENTS Most cases of vasculitis are secondary, so aggressive efforts to identify the etiology should be made; however, 50% of cases remain idiopathic. A skin biopsy including the junction between affected and normal skin is critical to diagnose vasculitis and may be helpful in identifying the possible underlying etiology.
PREVENTION Mark patient charts with medications/vaccinations associated with vasculitis to prevent potential administration in the future.
TECHNICIAN TIPS Obtain a detailed history from owners.
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CLIENT EDUCATION Medical therapy may involve combinations of medications and multiple dose adjustments until therapeutic goal is reached. Frequent reassessment is critical to treatment success.
SUGGESTED READING Fox PR, Petrie JP, Hohenhaus: Vasculitis in peripheral vascular disease. In Ettinger SJ, Feldman EC, editors: Textbook of veterinary internal medicine, ed 6, St Louis, 2005, Elsevier Saunders, p 1153. Nichols PA, et al: A retrospective study of canine and feline cutaneous vasculitis. Vet Dermatol 12:255–264, 2001. Scott DW, Miller WH, Griffen CE: Vasculitis in immune mediated disease. In Muller and Kirk’s small animal dermatology, ed 6, Philadelphia, 2001, Saunders, p 742. AUTHOR: KRISTIN WELCH EDITOR: ELIZABETH ROZANSKI
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Vasculitis, Cutaneous BASIC INFORMATION DEFINITION A well-recognized condition characterized by blood vessel damage that results in ischemia of the skin and resultant tissue necrosis
SYNONYM Cutaneous vasculopathy
EPIDEMIOLOGY GENETICS & BREED PREDISPOSITION: Any breed, but certain syndromes show breed predisposition: Familial cutaneous vasculopathy (autosomal recessive): Jack Russell terrier, Scottish terrier, German shepherd Alabama rot (see p. 491): greyhounds Thrombovascular pinnal vasculitis: dachshund, weimaraner Rabies vaccine injection-site vasculitis (see p. 610): rottweiler, miniature poodle, bichon frise, silky terrier, Yorkshire terrier, Pekingese, Maltese, and miniature pinscher Familial canine dermatomyositis (see p. 291): collie, Shetland sheepdog, and Beauceron shepherd RISK FACTORS Drug therapy (oral or injectable) Malignancy Infection (viral, bacterial, fungal, rickettsial) Immune-mediated diseases Insect bites Food allergy/hypersensitivity ASSOCIATED CONDITIONS & DISORDERS Systemic lupus erythematosus (SLE) Familial canine dermatomyositis
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES Clinically the lesions can be localized, regional, or multifocal to generalized. They are classified as small-vessel necrotizing vasculitis, hypersensitivity vasculitis, and large-vessel vasculitis. They are categorized histologically as neutrophilic (leukocytoclastic, nonleukocytoclastic), eosinophilic, lymphocytic, granulomatous, or cell-poor. HISTORY, CHIEF COMPLAINT: Patients may present with crusted or ulcerative macules or patches that may be a source of self-trauma. Patients with urticarial vasculitis may present with erythematous and often pruritic wheals. These patients are often anorexic and lethargic. PHYSICAL EXAM FINDINGS Description of the lesions varies according to the disease. Fever is often present. Thrombovascular pinnal vasculitis: notching of pinnal margins at tip and/or well-demarcated ulcers on the concave aspect of the pinna. Idiopathic vasculitis: well-demarcated necrosis and ulceration, particularly at the extremities and pressure points; may include edema, alopecia, or crateriform ulcers on the central aspect of the footpads. Some of these cases could be a rare manifestation of rabies vaccine-induced generalized ischemic dermatopathy. Urticarial vasculitis: generalized pruritus associated with papules, purpura, and wheals
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Vasculitis, Cutaneous
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Familial canine dermatomyositis: erythema, ulceration, and mild crusting in the young dog. Affected areas include face, pressure points, digits, and tail tip.
ETIOLOGY AND PATHOPHYSIOLOGY Suspected type III hypersensitivity, although multiple pathomechanisms likely play a role. Antigen-antibody complexes become trapped along the basement membrane of vessel walls and activate the complement cascade. Other mechanisms proposed include direct antibody binding to the vessel wall and the release of toxic mediators, leading to a bystander reaction. In many cases, the exact mechanism is not known.
DIAGNOSIS DIAGNOSTIC OVERVIEW Cutaneous vasculitis is first suspected based on the appearance of skin lesions. The definitive diagnosis is based on a detailed drug history and skin biopsy. Unremarkable hematologic and biochemical profiles help confirm that the problem is “skin deep.” It is often wise to consider the option of submitting tissue samples for fungal and bacterial culture at the time of biopsy.
DIFFERENTIAL DIAGNOSIS Cold-agglutinin disease Disseminated intravascular coagulation Frostbite Demodicosis (focal lesions) Dermatophytosis (focal lesions)
INITIAL DATABASE Thorough history to assess risk of drug-induced vasculitis Routine CBC, serum biochemical profile, urinalysis: results are typically within normal limits. Skin scrapings for focal (not ulcerated) lesions Diascopy (hemorrhagic lesions [e.g., vasculitis] do not blanch when a glass slide is pressed over the top, in contrast to vascular dilation/congestion). Biopsy: histopathologic evaluation reveals varying degrees of neutrophilic, eosinophilic, lymphocytic, granulomatous, or cell-poor vasculitis.
ADVANCED OR CONFIRMATORY TESTING Selected according to signalment and clinical features of case: Bacterial serologic titers (dogs: Rickettsia rickettsii, Ehrlichia canis, Borrelia burgdorferi) Viral serologic titers (cats: feline leukemia virus [FeLV], feline immunodeficiency virus [FIV]) Coagulation profile, Coombs' test, antinuclear antibody (ANA) test, and rheumatoid factor test may be indicated based on history, physical exam, and initial database supporting immune-mediated disease. Blood culture if sepsis is suspected Tissue culture of nodular or granulomatous lesions Hypoallergenic dietary trial (urticarial form of food hypersensitivity)
TREATMENT TREATMENT OVERVIEW The goal of treatment is to improve circulation to the affected area (e.g., using pentoxifylline, which increases RBC plasticity), control self-trauma, and suppress the immune reaction (e.g., using corticosteroids or other immunosuppressors) while evaluating for the inciting cause.
ACUTE GENERAL TREATMENT Discontinue current drug therapies.
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Bandage pressure points and keep wounds clean. Prevent self-trauma (Elizabethan collar).
CHRONIC TREATMENT One or more may be indicated: Pentoxifylline: 25-35 mg/kg PO q 12 h following a meal Tetracycline and macinarmele: >10 kg. 500 mg of each drug PO q 8 h (15 kg expected adult weight). Heritability is suspected in German shepherds and greyhounds. ASSOCIATED CONDITIONS & DISORDERS Persistent left cranial vena cava and patent ductus arteriosus (PDA) can be associated vascular anomalies. Megaesophagus and aspiration pneumonia are secondary problems associated with chronic partial esophageal obstruction.
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT: Most dogs and cats develop clinical signs once they start to ingest solid food, because the vascular ring obstructs passage of food down the esophagus. Postprandial regurgitation is the usual presenting complaint, and the majority of cases are diagnosed before 6 months of age. Occasionally, animals may have coughing or respiratory distress due to aspiration pneumonia or tracheal compression. PHYSICAL EXAM FINDINGS: Animals have a good appetite but may be thin as a result of chronic regurgitation. An enlarged esophagus may occasionally be palpated in the thoracic inlet, especially after eating. In dogs with a concurrent PDA (minority of cases), a continuous left basilar murmur is ausculted; however, in the absence of PDA, cardiac auscultation is normal. Animals with aspiration pneumonia may be febrile with harsh ventral lung sounds.
ETIOLOGY AND PATHOPHYSIOLOGY Normal embryogenesis: In the embryo, the great vessels are formed from six aortic arches that connect paired ventral and dorsal aortas. During development, these vessels undergo regression and reconnection that normally result in a left-sided aorta, left-sided ligamentum arteriosum, and normal branching of the brachiocephalic trunk and left subclavian arteries off the ascending aorta. Pathophysiology: Developmental anomalies of the great vessels appear to be relatively common; however, these anomalies are only clinically important when the vessels entrap the esophagus and trachea within a vascular ring. Passage of food down the esophagus is impeded by the vascular ring, causing esophageal dilation, food stasis, and regurgitation. Regurgitation with aspiration can cause pneumonia. PRAA (most common in dogs): The normal left aortic arch regresses, while the right aortic arch is retained. The left ligamentum arteriosum passes over the esophagus, connecting the right aortic arch to the left-sided pulmonary artery and compressing the esophagus at the base of the heart. PRAA can also occur with an aberrant left subclavian artery. This causes an incomplete ring that dorsally compresses
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Vascular Ring Anomaly
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the esophagus (the left subclavian arises from the right aorta and courses dorsally over the esophagus). Double aortic arch: Both left and right aortic arches persist, encircling the esophagus and trachea as the two vessels merge to form the descending aorta. Persistent right ligamentum arteriosum with normal left aorta is an uncommon cause of a vascular ring anomaly. It is important to note that correction by a left lateral thoracotomy is more difficult for this malformation than for the other vascular ring anomalies. An aberrant right subclavian artery with a normal left aorta can cause an incomplete ring because the aberrant vessel courses over and dorsally compresses the esophagus.
DIAGNOSIS DIAGNOSTIC OVERVIEW A history of regurgitation beginning immediately after weaning is highly suggestive; plain thoracic radiographs provide the basis for a diagnosis of vascular ring anomaly (e.g., ventral and leftward tracheal deviation, dilated cranial esophagus) and also screen for associated aspiration pneumonia.
DIFFERENTIAL DIAGNOSIS Differential diagnoses for regurgitation include congenital megaesophagus, stricture, foreign body, neoplasia, granuloma, hiatal disorder, and esophageal diverticulum. Esophageal stricture is the major differential diagnosis to consider for radiographic esophageal dilation that terminates at the base of the heart.
INITIAL DATABASE Thoracic radiographs: The esophagus may appear dilated up to the base of the heart on plain films. Its visualization may be enhanced by residual food. Lateral radiographs often show ventral deviation of the trachea cranial to the heart, and the tracheal lumen may be narrowed in this deviated segment. Leftward curvature of the trachea near the cranial border of the heart on the dorsoventral (DV) or ventrodorsal (VD) view reliably differentiates dogs with vascular ring anomalies from dogs with generalized megaesophagus. These radiographic findings may obviate the need for a barium esophagram. CBC is indicated if there is evidence of aspiration pneumonia.
ADVANCED OR CONFIRMATORY TESTING Often unnecessary when a working diagnosis is made from thoracic radiographs. Barium esophagram: barium given in food can be used to radiographically outline the focal dilation of the esophagus that narrows at the base of the heart. Although this finding is diagnostic for a vascular ring anomaly, it does not reveal the type of anomaly present. Nonselective CT angiography has been used for producing a 3-dimensional anatomic reconstruction of the anomalous vasculature for diagnosis and to assist in surgical approach.
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Vascular Ring Anomaly
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VASCULAR RING ANOMALY Lateral thoracic radiograph demonstrating marked ventral deviation of the trachea and severe esophageal filling with fluid/soft-tissue opacity material cranial to the carina. The cause was a vascular ring anomaly.
VASCULAR RING ANOMALY A, Ventrodorsal thoracic radiograph of a normal dog. B, Ventrodorsal thoracic radiograph of a dog with vascular ring anomaly. Leftward deviation of the trachea (arrow) is characteristic of vascular ring anomaly.
TREATMENT TREATMENT OVERVIEW Esophageal constriction caused by vascular ring anomalies is treated surgically by ligation and division of the aberrant vessel, with the ultimate goal being a reduction or elimination of regurgitation. Intensive pre- and postoperative care may be required for debilitated patients.
ACUTE GENERAL TREATMENT Young malnourished animals may benefit from fluid therapy with dextrose. Animals with aspiration pneumonia require antibiotic therapy prior to surgical intervention. Surgical division of the vascular ring:
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For the vast majority of vascular ring anomalies, the preferred surgical approach is a left fourth intercostal thoracotomy. Ventilation is required after entering the thorax (thoracostomy tube after surgery for 24 hours to evacuate air). When the vascular ring is caused by PRAA, the left ligamentum arteriosum is ligated and divided, releasing the constriction on the esophagus. When the vascular ring is caused by an aberrant subclavian artery coursing over the esophagus, this artery is ligated and divided. No adverse effects are noted from this ligation, as the vertebral artery supplies adequate collateral flow. When a double aortic arch is present, the smaller arch is ligated and divided. Thoracoscopic ligation of a left ligamentum arteriosum (with PRAA) has been reported as a less invasive surgical option.
NUTRITION/DIET Severely malnourished animals may require nutritional support prior to surgery, including elevated feedings of slurried food or, in some cases, placement of a gastrostomy tube (see p. 1270). Give slurried food to the patient from an elevated position for several weeks after surgery. After feeding, the patient should be kept in a vertical position for 10 minutes. Then introduce solid food from an elevated position. If no regurgitation occurs, most dogs can be returned to a normal feeding regimen 1-2 months after surgery.
POSSIBLE COMPLICATIONS Most common complication: aspiration pneumonia. Regurgitation may continue after surgical disruption of the vascular ring because of loss of neuromuscular esophageal function. Some animals may never be able to ingest solid food and may need to be fed a slurry diet indefinitely. Other possible complications are related to thoracic surgery and include lung lobe laceration, intraoperative hemorrhage, or thoracic duct injury leading to postoperative chylothorax.
RECOMMENDED MONITORING Thoracic radiographs should be used to monitor for postoperative aspiration pneumonia and document resolution of megaesophagus.
PROGNOSIS AND OUTCOME Prognosis is dependent on age at the time of surgical therapy, severity of malnourishment, presence of aspiration pneumonia, and degree of esophageal constriction. A study found that 6 months after surgery, the majority (92%) of dogs did not regurgitate, and the remainder regurgitated only occasionally.
PEARLS & CONSIDERATIONS COMMENTS Oral passage of a stomach tube into the esophagus by an assistant during surgery can help locate the stricture and facilitates dissection around the esophagus. Intraoperative balloon dilation of the esophagus is particularly helpful to remove constricting fibrous bands after the ring has been resected.
CLIENT EDUCATION Although the prognosis is good for most dogs following surgical therapy, counsel owners about the potential for continued esophageal dysfunction.
SUGGESTED READING Buchanan JW: Tracheal signs and associated vascular anomalies in dogs with persistent right aortic arch. J Vet Intern Med 18:510–514, 2004. Kyles AE: Esophagus. In Slatter DH, editor: Textbook of small animal surgery. Philadelphia, 2003, WB Saunders, p 577.
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Vascular Ring Anomaly
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AUTHORS: DARCY B. ADIN, CHRISTOPHER A. ADIN EDITOR: ETIENNE CÔTÉ
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Vaginitis
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Vaginitis BASIC INFORMATION DEFINITION Inflammation/irritation of the vagina
EPIDEMIOLOGY SPECIES, AGE, SEX Spayed or intact bitches Prevalence 1 year of age RISK FACTORS: Anatomic abnormalities (strictures or septa), perivulvar dermatitis with atrophic juvenile vulva and excessive skin folds, perivascular dermatitis in overweight dogs with urinary incontinence, systemic illness (e.g., diabetes mellitus, hyperadrenocorticism) CONTAGION & ZOONOSIS: Bruceila cants, canine herpesvirus GEOGRAPHY AND SEASONALITY: Hot and humid climates may trigger or exacerbate vaginitis.
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES Juvenile onset versus adult onset Acute versus chronic HISTORY, CHIEF COMPLAINT Vulvar discharge (chronic, if present for >1 month) In juvenile-onset vaginitis, bitches usually are not systemically ill. Pollakiuria, discomfort (e.g., excessive vulvar licking, pain when urinating) Clinical signs of concurrent disease (e.g., polyuria/polydipsia, urinary incontinence, pruritus, infertility) may be contributing causes of vaginitis. PHYSICAL EXAM FINDINGS Vulvar mucoid, purulent, occasionally blood-tinged discharge Vulvar hyperemia Digital vaginal examination (see p. 1360) may reveal vaginal stenoses or septa Atrophic or juvenile vulva with excessive skin folds, with concurrent perivulvar dermatitis Overweight dogs with urinary incontinence, with excessive perivulvar skin folds and persistent moisture and urine scalding
ETIOLOGY AND PATHOPHYSIOLOGY Physical abnormalities impede normal evacuation of secretions, compromise natural barrier. Systemic diseases may compromise immunity (e.g., diabetes mellitus, hyperadrenocorticism) or infect reproductive tract directly (e.g., brucellosis). Many dogs have idiopathic vaginitis.
DIAGNOSIS DIAGNOSTIC OVERVIEW The diagnosis is generally suspected as a result of vulvar discharge. Vaginoscopy +/− bacterial culture are used for confirming the
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diagnosis.
DIFFERENTIAL DIAGNOSIS Urinary tract infection Metritis Cystic endometrial hyperplasia/pyometra Uterine stump pyometra Vulvar, vaginal, or uterine tumor Brucellosis Canine herpesvirus infection
INITIAL DATABASE CBC, serum biochemistry profile: generally unremarkable Serologic titer for Brucella canis (see p. 162) Vaginoscopy assesses discharge present in the vagina; vesicular lesions (e.g., canine herpesvirus associated or lymphoid follicles) seen as nonspecific indicators of inflammation; urine pooling, masses, foreign bodies possible. Vaginal Cytologic examination shows WBCs with or without bacteria.
ADVANCED OR CONFIRMATORY TESTING Vaginal bacterial culture: moderate to heavy growth of 1 to 2 bacterial types (more might suggest normal flora). Urinalysis and bacterial culture: concurrent urinary tract infection (UTI) is common. Contrast radiography, biopsy: rarely if ever needed
VAGINITIS Contrast vaginogram showing vestibulovaginal stenosis with marked narrowing of vagina cranial to urethral papilla. Top, Preoperatively. Bottom, Five months after surgical resection of the stenosis and vestibulovaginal anastomosis. (From Kyles AE, Vaden S, Hardie EM, et al: Vestibulovaginal stenosis in dogs: 18 cases (1987-1995). J Am Vet Med Assoc 209:1889-1893, 1996.)
TREATMENT
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Vaginitis
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TREATMENT OVERVIEW Correction of the underlying cause is the cornerstone of effective long-term resolution. In adult-onset vaginitis, treatment of the underlying cause is usually curative. Most therapy for vaginitis is supportive and nonspecific because most cases are idiopathic. Many cases resolve spontaneously in both juvenile- and adult-onset vaginitis, particularly when there is no identifiable underlying cause.
ACUTE AND CHRONIC TREATMENT If the primary problem is UTI (up to 60% of cases with identifiable underlying cause): Antibiotics based on culture and sensitivity testing (empirical antibiotics acceptable for first 48-72 h pending culture results) Antibiotics, if used, should be administered for 4 weeks and based on a guarded sample collected from the cranial vagina and culture and sensitivity. Diethylstilbestrol (DES), 0.1-0.2 mg/kg PO, maximum dose = 1 mg, q 24 h for 5 days, tapering to 2× a week; or phenylpropanolamine, 1-1.5 mg/kg PO q 8-12 h. Note: Do not use DES in dogs that have not reached adult stature (may induce premature long-bone physeal closure). In overweight urinary-incontinent dogs with excessive perivulvar skin folds, vulvoplasty (episioplasty) is recommended. If the primary problem is vaginal anatomic anomalies (up to 36% of cases with identifiable underlying cause), surgical repair may be indicated. If the primary problem is systemic disease (up to 15% of cases with identifiable underlying cause): treat the underlying systemic disease. If the primary problem is idiopathic: DES to treat subclinical urinary incontinence Glucocorticoids may be beneficial in some bitches (do not use in cases of concurrent urinary incontinence). Treatment for atopic dermatitis if present concurrently (see p. 106) Vaginal douches with antiseptics or antibiotics have not been reported to be an effective treatment. Owners should be instructed to keep the perivulvar skin folds clean.
POSSIBLE COMPLICATIONS Ascending UTIs can result from chronic vaginitis. Self-mutilation can result from excessive licking of the perivulvar skin secondary to vaginitis.
RECOMMENDED MONITORING Recheck animals showing any signs of systemic illness, and look for complications such as metritis.
PROGNOSIS AND OUTCOME With spontaneous remission, future reproductive success is not compromised.
PEARLS & CONSIDERATIONS COMMENTS Urethral sphincter mechanism incompetence (see p. 1134) may be misdiagnosed as vaginitis, especially when there is positive response to treatment for suspected vaginitis with DES or phenylpropanolamine. Daily record of the frequency and severity of clinical signs (e.g., vulvar discharge, vulvar licking) will help the veterinarian to assess response to therapy. Limited understanding of the causes of vaginitis makes it difficult to predict when and if clinical signs will resolve.
CLIENT EDUCATION Owners should consider not breeding bitches with poor vulvar conformation or congenital vaginal defects to avoid perpetuating these problems in the female offspring.
SUGGESTED READING Root Kustritz MV: Vaginitis in dogs: a simple approach to a complex condition. Vet Med 103:562–567, 2008.
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Vaginitis
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AUTHOR: CARLOS GRADIL EDITOR: MICHELLE A. KUTZLER
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Vaginal Hyperplasia and Vaginal Prolapse
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Vaginal Hyperplasia and Vaginal Prolapse BASIC INFORMATION DEFINITION Edematous swelling of the vaginal mucosa cranial to the urethral orifice; an uncommon disorder that occurs during estrogen stimulation in the intact bitch. It may progress to vaginal protrusion through the vulvar lips.
SYNONYMS Vaginal edema, hypertrophy, hyperplasia, eversion, or protrusion
EPIDEMIOLOGY SPECIES, AGE, SEX: Intact bitch, any age (7 months to 16 years old) GENETICS & BREED PREDISPOSITION More common in large-breed dogs Breeds predisposed: bulldog, mastiff, boxer, dalmatian, German shepherd, Saint Bernard, Labrador and Chesapeake Bay retrievers, weimaraner, Walker hound, springer spaniel, Airedale terrier, and American pit bull terrier RISK FACTORS Young bitch under the influence of estrogen during proestrus or estrus; may occur or recur during diestras, pregnancy, or parturition Can be observed as side effect of estrus induction with estrogen ASSOCIATED CONDITIONS & DISORDERS: Markedly prolapsed vaginal tissue is subject to self-mutilation and may be dry, ulcerated, necrotic, and devascularized; possible dysuria or pollakiuria.
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES Vaginal hyperplasia: Type I: slight to moderate eversion of the vaginal floor cranial to the urethral orifice; confined to the vestibulum, appearing as a bulge at the perineum. Type II: well-developed swelling of the vaginal floor, which may include the lateral vaginal walls, protruding through the vulvar lips. The swelling appears dome shaped.
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Vaginal Hyperplasia and Vaginal Prolapse
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VAGINAL HYPERPLASIA AND VAGINAL PROLAPSE A, Well-developed swelling of vaginal floor, which may include lateral vaginal walls, protruding through vulvar lips. Swelling appears dome-shaped (type II vaginal hyperplasia). B, Well-developed protrusion of entire circumference of vaginal wall through vulvar lips. Swelling appears doughnut shaped (vaginal prolapse). Type III: well-developed protrusion of the entire circumference of the vaginal wall through the vulvar lips. The swelling appears doughnut shaped and is a vaginal prolapse. HISTORY, CHIEF COMPLAINT Previous occurrence of vaginal hyperplasia Onset of proestrus or estrus Licking or irritation of the vulva Mass protruding from vulva or bulge at the perineum Dysuria or pollakiuria Failure to allow intromission during breeding Tenesmus PHYSICAL EXAM FINDINGS: Bulge at the perineum or protrusion of a pink dome-shaped or doughnut-shaped mass from vulva; surface of protrusion may be dry, necrotic, or ulcerated. Vaginal examination reveals: A urethral orifice located ventrally in all three types of vaginal hyperplasia A vaginal lumen located dorsally in types I and II but centrally located in type III By contrast, uterine prolapse is distinguished by the presence of tubular masses within the vagina or protruding from the vulva.
ETIOLOGY AND PATHOPHYSIOLOGY Vaginal hyperplasia: an exaggerated response of the vaginal mucosa to estrogen (hyperemia, edema, keratinization). The swelling begins as an eversion in the vaginal floor, cranial to the urethral orifice. With vaginal prolapse: histopathologic examination of affected vaginal tissue is consistent with submucosal edema rather than with hyperplasia or hypertrophy.
DIAGNOSIS
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Vaginal Hyperplasia and Vaginal Prolapse
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DIAGNOSTIC OVERVIEW The diagnosis is suspected based on the presence of a vulvar swelling or protrusion in a young intact bitch.
DIFFERENTIAL DIAGNOSIS Benign or malignant vaginal neoplasia Vaginal polyp True vaginal prolapse with concurrent entrapment of visceral organs (rare) Uterine prolapse Urethral neoplasia
INITIAL DATABASE Stage of hormonal cycle based on vaginal cytologic examination Vaginal examination to locate the urethral orifice, vaginal lumen, origin of the protruding mass, and the size of its base (see p. 1360) Ensure that the animal is able to urinate.
ADVANCED OR CONFIRMATORY TESTING Biopsy of vaginal mass confirms diagnosis in atypical bitches. In severe cases, survey radiographs can be used to evaluate for visceral organ involvement; contrast radiography can confirm the location of the urethral orifice and vaginal lumen.
TREATMENT TREATMENT OVERVIEW Treatment goals are to prevent drying, necrosis, and devitalization of exposed vaginal tissue, prevent future recurrence, and prevent urethral obstruction.
ACUTE GENERAL TREATMENT Insertion of a urethral catheter to relieve obstruction when present Ensuring that vaginal tissue is kept clean Topical application of sterile water-soluble lubrication or antibiotic ointment Application of an Elizabethan collar or protective pants Provision of a clean environment to minimize tissue trauma Scheduling an ovariohysterectomy, which prevents recurrence and may hasten resolution; regression of tissue is reported to occur within 21 days. Recognition that spontaneous regression at end of estrus is common
CHRONIC TREATMENT Ovariohysterectomy prevents recurrence in nonbreeding bitches. Surgical excision of prolapsed vaginal tissue in bitches intended for breeding or in those with severely inflamed or devitalized vaginal tissue: May prevent recurrence during subsequent estrous cycles or at parturition Various surgical techniques are described involving circumferential incision at the base of the prolapse. Episiotomy may be needed. Manual reduction of prolapsed tissue and placement of stay sutures in the vagina do not prevent recurrence and may cause the bitch discomfort. Artificial insemination can be performed in breeding bitches. Induction of ovulation during a nonbreeding cycle may hasten regression of vaginal tissue by decreasing estrogenic stimulation: gonadotropin-releasing hormone (2.2 mcg/kg IM) or human chorionic gonadotropin (1000 IU IM, irrespective of body weight as a single injection, or 500 IU IM, irrespective of body weight and repeated in 48 hours); a 1-week regression follows ovulation. Treatment is ineffective if given after ovulation.
DRUG INTERACTIONS Avoidance of progestational drugs that contribute to pyometra
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Vaginal Hyperplasia and Vaginal Prolapse
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POSSIBLE COMPLICATIONS Necrosis, infection, and devascularization of vaginal tissue Evisceration of abdominal organs Urination and defecation difficulties
RECOMMENDED MONITORING Monitor viability of prolapsed vaginal tissue. Evaluate ability to urinate.
PROGNOSIS AND OUTCOME Good prognosis with ovariohysterectomy Recurrence rate is 66% in untreated bitches
PEARLS & CONSIDERATIONS COMMENTS Vaginal hyperplasia may progress to vaginal prolapse (type III), but other disorders less commonly may also cause vaginal prolapse. If excision of vaginal tissue is performed in late estrus or early diestrus, bleeding is minimized. If ovariohysterectomy is performed in anestrus (serum progesterone concentrations ALP or if hypoalbuminemia, hyperbilirubinemia, or markedly increased serum bile acids concentration are present, a more serious primary hepatobiliary disorder may be present and should be identified and treated. In rare instances, severe vacuolar hepatopathy has been associated with overt hepatic dysfunction, which may be fatal. Presence of increased serum ALP activity and vacuolar hepatopathy does not preclude continued use of corticosteroids if their administration is necessary. Liver function is generally preserved; benign lesion. Whenever possible, make an attempt to minimize systemic effects of glucocorticoids with alternate-day therapy using lowest effective dose possible (prednisolone or prednisone), and/or use other immunosuppressive drugs (azathioprine, cyclosporine). Cats that are receiving glucocorticoids (or with hyperadrenocorticism) rarely develop vacuolar hepatopathy.
PREVENTION If long-term glucocorticoid therapy is necessary, give oral prednisolone or prednisone (rather than oral dexamethasone or injectable long-acting forms) at the lowest dose possible on alternate days to minimize the systemic (including hepatic) effects of glucocorticoids. Also consider administering other immunosuppressive drugs (e.g., azathioprine, cyclosporine) to allow dose reduction of glucocorticoids.
CLIENT EDUCATION Idiopathic vacuolar hepatopathy appears to be clinically benign.
SUGGESTED READING Gary AT, Webb CB, Twedt DC: Investigation of idiopathic vacuolar hepatopathy in Scottish terriers and the role of progesterone steroids in the etiology. Proceedings of the American College of Veterinary Internal Medicine forum, Louisville, KY, May 31-June 3, 2006. Sepesy LM, Center SA, Randolph JF, et al: Vacuolar hepatopathy in dogs: 336 cases (1993-2005). J Am Vet Med Assoc 229:246, 2006. AUTHOR: SUSAN E. JOHNSON EDITOR: KEITH P. RICHTER
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Wolff-Parkinson-White Syndrome
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Wolff-Parkinson-White Syndrome BASIC INFORMATION DEFINITION A cardiac disorder characterized by extremely rapid, inappropriate tachycardias. The underlying defect is an accessory pathway or additional conductive fiber connection between atria and ventricles, separate and parallel to the normal atrioventricular (AV) node-bundle of His connection. The accessory pathway can participate as one limb of a rapid re-entrant tachycardia.
SYNONYMS Premature activation of the ventricles by the atria: Accessory AV pathway (or bypass tract) Ventricular pre-excitation Macro re-entrant tachycardia: AV reciprocating tachycardia
EPIDEMIOLOGY SPECIES, AGE, SEX: Any; most commonly identified in dogs 5 years old) Fecal flotation
ADVANCED OR CONFIRMATORY TESTING Trypsinlike immunoreactivity (TLI), if there is small-bowel diarrhea, to rule out exocrine pancreatic insufficiency (EPI) Fecal α1-protease inhibitor activity if PLE is suspected but no diarrhea Abdominal ultrasound to identify GI tract thickening or layer loss, neoplasms, granulomas, pancreatitis Upper GI endoscopy to rule out esophageal or gastric foreign body, ulcerations, or luminal neoplasms GI biopsies via endoscopy or exploratory laparotomy Bile acids to rule out liver failure (portosystemic shunt) Urine protein/creatinine (UPC) ratio to rule out protein-losing nephropathy Adrenocorticotropic hormone (ACTH) stimulation test to rule out hypoadrenocorticism Infectious disease testing when indicated
TREATMENT
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Weight Loss
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TREATMENT OVERVIEW Treat underlying disease and provide nutritional support.
ACUTE GENERAL TREATMENT Improve appetite/symptomatic therapy: Diet change Antacids (H2 blockers [famotidine, ranitidine] or proton pump inhibitors [omeprazole]) Antinausea medications (metoclopramide, ondansetron, maropitant) unless contraindicated Appetite stimulants (mirtazapine [dogs], cyproheptadine [cats]) Increase caloric intake.
CHRONIC TREATMENT Treat underlying disease and maintain adequate caloric intake.
NUTRITION/DIET Enteral nutrition is preferred in animals that have a functioning GI tract. Assisted feeding through a nasoesophageal, esophagostomy, gastrostomy, or jejunostomy tube may be required (see p. 1267). Parenteral nutrition may be necessary in animals that cannot tolerate enteral feeding or if enteral feeding alone cannot meet caloric requirements. Caloric requirements are estimated by calculating resting energy requirements (RER) and illness energy requirements (IER): RER (in kilocalories) can be calculated as: 70 × (body weight [BW] in kilograms)0.75 IER is calculated by multiplying RER by an illness factor (1.2 to 1.4 for dogs; 1.1 to 1.2 for cats).
BEHAVIOR/EXERCISE Exercise should not be encouraged until weight is controlled.
POSSIBLE COMPLICATIONS Refeeding syndrome if anorexia is chronic and/or severe Aspiration pneumonia in patients that are regurgitating, vomiting, or being force-fed
RECOMMENDED MONITORING Body weight Other testing based on underlying cause
PROGNOSIS AND OUTCOME Weight stabilization occurs in the majority of surviving patients through treatment of the underlying disease and appropriate nutrition.
PEARLS & CONSIDERATIONS COMMENTS If the patient has other clinical signs (e.g., vomiting, diarrhea, fever, etc.), the diagnostic approach should not focus on the weight loss alone. In the initial stages of therapy, changes in body weight often reflect changes in fluid dynamics.
PREVENTION Dependent upon the underlying cause
CLIENT EDUCATION
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Weight loss is caused by a wide array of diseases; many are treatable. Obtaining a diagnosis often requires extensive testing.
SUGGESTED READING Remillard RL, Armstrong PJ, Davenport DJ: Assisted feeding in hospitalized animals. In Hand MS, Thatcher CD, Remillard RL, et al, editors: Small animal clinical nutrition, ed 4, Topeka, KS, 2000, Mark Morris Institute, pp 351–399. Sanderson S, Bartges JW: Management of anorexia. In Bonagura JD, editor: Current veterinary therapy XIII, Philadelphia, 2000, WB Saunders, pp 69–74. AUTHORS: BRADLEY GREEN, HELIO AUTRAN DE MORAIS EDITOR: ETIENNE CÔTÉ
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Zinc-Responsive Dermatosis
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Zinc-Responsive Dermatosis BASIC INFORMATION DEFINITION Uncommon but well-recognized zinc-responsive scaling disorder of the skin; can be hereditary or secondary to a dietary imbalance
EPIDEMIOLOGY SPECIES, AGE, SEX Syndrome I: age of onset is typically 1-3 years; range: 2 months to 11 years Syndrome II: most common in young, rapidly growing dogs GENETICS & BREED PREDISPOSITION Syndrome I: northern canine breeds, such as Alaskan malamute, Siberian husky, and Samoyed; also reported in Doberman pinschers and Great Danes Syndrome II: any breed; Great Dane, Doberman pinscher, beagle, German shepherd, German short-haired pointer, Labrador retriever, Rhodesian ridgeback, and standard poodle may be predisposed. RISK FACTORS: Rapidly growing puppies fed diets deficient in zinc or high in phytates (high plant/grain content) or calcium
CLINICAL PRESENTATION DISEASE FORMS/SUBTYPES Syndrome I: hereditary Syndrome II: dietary HISTORY, CHIEF COMPLAINT Owner may note scaling and crusting dermatosis. Pruritus may precede development of other clinical signs and is present in nearly half of cases. PHYSICAL EXAM FINDINGS Focal cutaneous erythema and alopecia progress to scaly and crusted lesions. Secondary microbial (bacterial and yeast) dermatitis Predilection sites: periocular, ears, bridge of the nose, perioral, footpads, pressure points on limbs. Scrotum, prepuce, perianal region, and vulva may also be affected. Dull, dry coat Some puppies with syndrome II present with depression, anorexia, delayed growth, fever, and lymphadenopathy.
ETIOLOGY AND PATHOPHYSIOLOGY Genetic defect involving zinc absorption reported in Alaskan malamutes. Diets high in calcium or phytates (plant/grain products) bind zinc, decreasing absorption. Zinc absorption is also negatively affected by essential fatty acid deficiency, high levels of iron in water, or prolonged diarrhea. It is suspected that low zinc levels cause poor lytic enzyme function (thus affecting epidermal maturation) or increased epidermal turnover rate (leading to hyperkeratosis).
DIAGNOSIS DIAGNOSTIC OVERVIEW
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The diagnosis is based on identification of lesions both clinically and histopathologically in an animal of a breed that is at risk, an animal that has a current history of nutritional inadequacy (high in phytates, high iron-content drinking water), or an animal with chronic diarrhea.
DIFFERENTIAL DIAGNOSIS Superficial necrolytic dermatitis (hepatocutaneous syndrome) Dermatophytosis Nutritionally deficient diets Demodicosis Pemphigus foliaceus
INITIAL DATABASE Skin scrapings: generally negative Fungal (dermatophyte) culture: expect negative result If diarrhea is noted, perform fecal flotation and any additional appropriate testing.
ADVANCED OR CONFIRMATORY TESTING Skin biopsy: epidermal parakeratotic hyperkeratosis is the most common finding, and follicular parakeratosis is highly suggestive. Zinc concentration in serum or hair: not used in small animal clinical dermatology. Overall, lower levels are present in zinc-responsive dermatosis patients, but substantial overlap exists with the normal range.
ZINC-RESPONSIVE DERMATOSIS Alopecia and crusting of the face in a Siberian husky with zinc-responsive dermatosis. (Courtesy Dr. Stephen Waisglass.)
TREATMENT TREATMENT OVERVIEW The goals of treatment are to resolve the scaling +/− alopecia and inflammation, control the secondary microbial dermatitis, and ensure the patient is eating a nutritionally balanced diet.
ACUTE GENERAL TREATMENT Assess and correct dietary deficiencies. Treat secondary bacterial or yeast dermatitis (see pp. 682 and 951). Keratomodulating shampoos (e.g., salicylic acid/sulfur shampoos) to remove scales and crusts Syndrome I: Supplementation is recommended at 1-3 mg/kg of elemental zinc daily. Start at the lower dose, but in some cases doses in the order of 2-3 mg/kg may be needed. Zinc gluconate (generic) 5 mg/kg PO q 24 h, or zinc sulfate 10 mg/kg PO q 24 h. Response to treatment is usually noted within 6 weeks. Lifelong treatment is required. Syndrome II: Correct diet. Lesions improve within 2-6 weeks in most cases. Some animals require zinc supplementation, as
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above. Essential fatty acid supplementation (omega-3 and omega-6) may aid zinc absorption.
CHRONIC TREATMENT Treatment for patients with syndrome I is usually lifelong. It has been suggested that low (0.15 mg/kg PO q 24 h) doses of prednisone or prednisolone can be added to the regimen to aid gastrointestinal (GI) absorption if response is inadequate. Improved response may also be due to an antiinflammatory effect on the skin. Different forms of zinc may be tried if there is poor response to therapy. It has been suggested that IV sterile zinc sulfate administration (10-15 mg/kg diluted 1:1 with saline and infused slowly) may help animals that do not respond to oral supplementation because of poor intestinal absorption. Treat weekly for at least 4 weeks (monitor with electrocardiogram [ECG] when administering), then every 1-6 months as maintenance.
DRUG INTERACTIONS Zinc salts may reduce the absorption of some fluoroquinolones and chelate oral tetracycline, reducing the absorption of zinc. Penicillamine and ursodiol may inhibit zinc absorption.
POSSIBLE COMPLICATIONS Emesis: zinc in the form of methionine or acetate may be less likely to cause stomach irritation. If vomiting occurs, lower the dose or give with food. Large doses of zinc can inhibit copper absorption in the intestine. Carefully consider the use of zinc in copper-deficient animals. IV zinc sulfate treatment may result in cardiac arrhythmias. Always monitor ECG during administration.
PROGNOSIS AND OUTCOME Syndrome I: fair to good prognosis in most animals Syndrome II: excellent prognosis if cause is of dietary origin
PEARLS & CONSIDERATIONS COMMENTS Zinc chelated as an amino acid such as methionine offers greater bioavailability than sulfate or gluconate, but response has been noted using all forms. If one form is not working, try another. Zinc plus linoleic acid (e.g., safflower oil) has been shown to improve skin and coat condition in normal dogs eating a properly balanced diet. Avoid confusion regarding zinc formulations: note whether dosed as mg/kg of the compound or mg/kg elemental zinc. Zinc sulfate contains 1 mg element zinc/4.4 mg zinc sulfate; zinc acetate contains 1 mg elemental zinc/3.33 mg zinc acetate; zinc gluconate contains 1 mg elemental zinc/7.14 mg zinc gluconate.
CLIENT EDUCATION Syndrome I: animals should not be used for breeding purposes. Syndrome II: nutritional counseling on benefits of feeding good-quality diets
SUGGESTED READING White SD, et al: Zinc-responsive dermatosis in dogs: 41 cases and literature review. Vet Dermatol 12:101–109, 2001. AUTHOR: STEPHEN WAISGLASS EDITOR: MANON PARADIS
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Zinc Toxicosis
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Zinc Toxicosis BASIC INFORMATION DEFINITION Syndrome that occurs after ingestion of zinc-containing objects such as pennies, scrap metal pieces, wires, and hardware. Clinical signs arise due to acute gastrointestinal (GI) irritation or hemolysis (zinc-mediated red blood cell [RBC] injury) and possible renal and hepatic damage.
SYNONYMS Elemental zinc; Zn
EPIDEMIOLOGY SPECIES, AGE, SEX: Toxicosis is reported mostly in dogs (all breeds and ages, both sexes) from ingesting zinc-containing objects; cats are less likely cases.
CLINICAL PRESENTATION HISTORY, CHIEF COMPLAINT Inappetence, lethargy, protracted vomiting, diarrhea Red-colored urine Animal occasionally may vomit pennies or other metallic objects or pass pennies in the feces Animal owners often are unaware of ingestion of any foreign metallic object by their pets In these cases, zinc toxicosis becomes suspected based on hemolytic anemia and/or presence of metallic object in the GI tract on radiographs or in vomitus/feces. PHYSICAL EXAM FINDINGS As already described Signs of abdominal discomfort or pain on palpation Pale mucous membranes Icterus Discolored urine (hemoglobinuria)
ETIOLOGY AND PATHOPHYSIOLOGY Source: Metallic zinc is used in galvanizing, welding, and soldering. Zinc salts are used as astringents, antiseptics, deodorants; in galvanized nuts and cage wires; and in smoke generators, wood preservatives, pigments, and insecticides. Zinc gluconate is about 14% elemental zinc and is frequently found in cough drops. Zinc oxide (10%-40%) is found in ointments and sunblocks (see p. 1180). U.S. pennies minted after 1982 weigh 2.5 g and are 97.6% zinc and 2.4% copper. Canadian pennies prior to 1997 were approximately 98% copper and 1.75% zinc. From 1997 to 2001, Canadian pennies were made with 96% zinc and 4% copper. Since 2001, Canadian pennies have been made of copper-plated steel (94% steel, 1.5% nickel, 4.5% copper). Mechanism of Toxicosis: Zinc has an antagonistic effect on copper and iron. It can interfere with iron absorption, making RBCs susceptible to hemolysis. Zinc also causes direct, severe GI mucosal irritation. Zinc leaches from metallic objects owing to an acidic gastric pH, providing continuous GI absorption. Toxicosis occurs when zinc-containing objects are retained or embedded in the GI tract.
DIAGNOSIS
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DIAGNOSTIC OVERVIEW Suspicion of zinc toxicosis arises in one of three contexts: observed ingestion or vomiting/defecation of metallic objects; incidental finding of metallic object on abdominal palpation or radiography; or investigation of hemolytic anemia. A patient in any of these categories should undergo a minimum database of a CBC (hemolytic anemia), serum biochemistry profile, urinalysis, and abdominal radiography. Protracted vomiting, lethargy, diarrhea, inappetence and hemoglobinuria lend further support to the diagnosis. Toxicosis should be confirmed (or ruled out) by measuring concentration of zinc in serum, whole blood or urine.
DIFFERENTIAL DIAGNOSIS Other toxicoses: onions/garlic, acetaminophen, mothballs (naphthalene), local anesthetics Immune-mediated hemolytic anemia Tickborne diseases
INITIAL DATABASE CBC: regenerative anemia, hemoglobinemia, reticulocytosis, spherocytosis; neutrophilic leukocytosis Serum biochemistry profile: azotemia; elevation in serum bilirubin, liver enzymes, amylase, lipase Urinalysis: hemoglobinuria, proteinuria
ADVANCED OR CONFIRMATORY TESTING Definitive diagnosis: blood or tissue zinc levels For blood collection, use special tubes (royal-blue top) and syringes that contain no rubber grommets. Do not use traditional syringes, rubber grommets, and Vacutainer tubes, because the rubberized surfaces contain some amount of zinc and may give erroneous results. Toxic levels in dogs: Serum: 10-54 ppm (adequate levels 0.7-2 ppm) Whole blood: 45 ppm has been fatal Liver: 130-436 ppm (adequate levels 30-70 ppm) Kidney: 175-295 ppm (adequate levels 16-30 ppm) Urine: 10-25 ppm (adequate levels 2-5 ppm)
TREATMENT TREATMENT OVERVIEW Life-threatening abnormalities, if present, must be identified and managed first: severe anemia may require transfusion, pigment nephropathy should be addressed with intravenous fluids, and GI tract perforation may require medical treatment with or without surgical correction. Then the source of zinc should be removed from the GI tract. Finally, general supportive care is indicated during recovery. Chelation with calcium EDTA or dimercaprol or D-penicillamine is rarely needed after the source of zinc has been removed.
ACUTE GENERAL TREATMENT Management of life-threatening abnormalities if present: Anemia: if severe (e.g., hematocrit 25 kg: 20-gauge White tape, 2 cm (1 inch) width Heparinized sterile saline flush Pressure transducer and monitor (if continuously monitoring direct arterial pressure) For arterial blood sample (one time): 1-mL heparinized syringe Needles (guidelines for size same as for arterial catheters, above)
ANTICIPATED TIME About 5 minutes (arterial blood sample) About 10-15 minutes (arterial catheter)
PREPARATION: IMPORTANT CHECKPOINTS Thoracic radiographs are indicated prior to or concurrently with ABG sampling when the purpose of arterial sampling is to assess arterial oxygen or CO2 levels. Samples for venous blood gas measurement generally are easier to obtain and may be useful for measuring certain parameters in arterial blood (e.g., pH, Pco2, Hco− 3). Confirmation of normal platelet count Confirmation of absence of overt signs of bleeding disorders or history of bleeding
POSSIBLE COMPLICATIONS AND COMMON ERRORS TO AVOID Pressing excessively firmly on the artery when palpating for the pulse to locate the proper site for puncture; excessive pressure abolishes the pulse and makes accurate puncture virtually impossible Inserting the needle or catheter without having convincingly identified the course of the artery (by repeated palpation of the arterial pulse) Crossing both artery and vein with the needle, resulting in venous contamination of arterial sample (artifactual low Po2 result) Mistakenly advancing the needle or catheter with the bevel up rather than down Inadequate manual pressure on the site after the procedure: Hematoma possible if inadequate direct pressure is applied after the procedure or if animal has a bleeding disorder or vasculitis. Artery may not be patent after arterial catheterization, but the effect of this loss of patency on the animal typically is minimal (limits the source of access for arterial blood samples in the immediate future but rarely causes ischemia distal to the site of puncture).
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PROCEDURE Clip hair over the area of interest (dorsal metatarsus: dorsal surface of distal hind limb, from hock to beginning of phalanges; inguinal area: femoral triangle, from inguinal crease [medial side of proximal hind limb where thigh meets caudal abdomen] toward stifle). Restrain animal in lateral recumbency (example here: left lateral): Dorsal metatarsal arterial approach: Right-handed clinician: fully extend animal's hock by drawing paw of upper hind limb (right paw if animal is in left lateral recumbency) toward self using the left hand. While keeping leg extended using traction on the right hind paw with the left hand, palpate the dorsal metatarsal pulse with the tips of the index and middle fingers of the right hand on the dorsal surface of the right metatarsus. The artery lies between the third and fourth metatarsal bones. Palpating the dorsal metatarsal pulse simultaneously with two fingers reveals the course of the dorsal metatarsal artery. Caution: The course of the metatarsal artery must be identified convincingly by repeated palpation of the dorsal metatarsal pulse before beginning to insert the needle or catheter. Then proceed as described further below (after “Femoral arterial”): “Both dorsal metatarsal and femoral approaches.” Femoral arterial approach: Right-handed clinician: Fully extend the animal's dependent hind limb (e.g., left hind leg, if in left lateral recumbency) to expose the medial inguinal area of that leg. In cooperative (or anesthetized) cats and dogs, the leg may be restrained minimally or not at all. In recalcitrant animals, a second restrainer is needed to hold the leg in an extended stable position. Palpate the femoral pulse at its dorsal-most location, near the inguinal crease. It should be palpated with the tips of the index and middle fingers of the right hand (for a right-handed clinician). The femoral artery lies midway between the cranial-most and caudal-most aspects of the thigh, at the usual location for palpation during physical examination. Palpating the pulse of a femoral artery simultaneously with two fingers 1-2 cm apart reveals the course of the femoral artery, namely a straight line between the two points on the artery where the pulse is palpated (i.e., between the two fingers). Caution: This line (the artery) must be identified convincingly by repeated palpation of the femoral pulse before beginning to insert the needle or catheter. Both dorsal metatarsal and femoral approach: Repeat brief aseptic scrubbing procedure once pulse has been palpated satisfactorily. There is no need for the assistant to “hold off” or “raise” the vessel, as is done for venous samples, because of the normal arterial pressure. Break the seal in the syringe by withdrawing and depressing the plunger once. The syringe (with needle) is held in the right hand like a pen. It enters the skin obliquely at 45°. If placing an arterial catheter, the 45° angle between skin and catheter is also necessary, but the catheter is held the same way an IV catheter is normally held. The bevel of the needle/catheter points down, not up (contrary to venous blood samples and IV catheters). The needle is introduced under the skin and into the artery, again advancing while maintaining a 45° angle between the syringe and the vessel. A flashback of blood indicates successful entry into the artery. Pulsatile flow is visible when an uncapped catheter is used. With a needle and syringe, arterial pressure will slowly but steadily “self-fill” the syringe, and negative pressure (as with a venous blood sample) is not necessary. Typically, a sample for ABG analysis requires approximately 0.5 mL of blood, which should be placed in an ice bath if analysis in the following 10 minutes is not possible. An arterial catheter should be fixed in place, capped, and flushed, or it should be connected to a pressure transducer for pressure measurement. It should be identified clearly with a label as being arterial.
ARTERIAL BLOOD SAMPLING AND ARTERIAL CATHETERIZATION Blood sampling from femoral artery, dog in left lateral recumbency. Cranial is to lower right. Assistant holds right hind limb elevated and prepuce retracted. Phlebotomist identifies course of left femoral artery between middle and index fingers by palpation of femoral pulse with both fingers and prepares to enter artery, needle bevel down.
POSTPROCEDURE Successful outcome: Successful arterial puncture for blood gas measurement improves animal care via treatment adjustments.
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Successful arterial catheter placement improves animal care via minute-by-minute adjustments of factors that influence arterial BP (e.g., IV fluids, pressor drugs, anesthetic agents) in anesthetized or critically ill animals.
ARTERIAL BLOOD SAMPLING AND ARTERIAL CATHETERIZATION Placement of arterial catheter in a dog's right metatarsal artery. A, Palpation of arterial pulse. B, Introduction of catheter, using right hand while simultaneously palpating arterial pulse for orientation using left hand (right-handed clinician). C, Flashback of blood confirms proper placement. D, Removal of stylet in preparation for placement of catheter cap. E, Capped catheter is flushed with heparinized saline, wrapped, and clearly marked as arterial.
ALTERNATIVES AND THEIR RELATIVE MERITS Repeat thoracic radiographs: Noninvasive; provides information on lesions of respiratory system only. Minimal usefulness for assessing subtle, moment-by-moment changes. Venous blood gas analysis: Sampling is easier.
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Few other advantages over arterial blood, unhelpful regarding Po2 Arterial cutdown for arterial blood sampling: Easier access to vessel More invasive AUTHOR: ETIENNE CÔTÉ
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Angiogram, Nonselective SYNONYMS Nonselective radiographic contrast study of the heart
OVERVIEW AND GOAL To perform an IV contrast study that highlights the venous return to the heart and the right-sided cardiac structures
INDICATIONS Suspected venous obstruction (see p. 263) Ill-defined abnormalities of the right side of the heart when echocardiography is equivocal or unavailable Pulmonary thromboembolism: rarely diagnostic as a nonselective procedure (often requires power-injected contrast through large-bore catheter in pulmonary artery)
CONTRAINDICATIONS Lesions that are equally or better defined without the administration of contrast (i.e., via echocardiography) Hypersensitivity to contrast material Acute renal failure (decreased ability to excrete contrast material and/or risk of contrast-induced renal failure) Arteriovenous (AV) fistulae are not an indication for this procedure. AV fistulae shunt from artery to vein and require selective arteriography.
EQUIPMENT, ANESTHESIA Can be done with or without anesthesia; sedation in most patients (see end pages inside text cover). Hair clippers Surgical scrub solution, rubbing alcohol, and gauze/sponge for prepping skin IV catheter (jugular or peripheral) A 19- or 20-gauge catheter for cats or small dogs; a 16- or 18-gauge catheter for medium or large dogs The catheter cap or T-port should be a screw tip to avoid detachment under high pressure of contrast injection. ± Sterile surgical gloves if using a nonsheathed jugular catheter ± Lidocaine for local anesthesia if large-bore jugular catheter (e.g., 18 gauge or larger) Routine tape and bandage material for catheter fixation to skin ± Suture material (e.g., 3-0 nylon), needle holders, and suture scissors if anchoring jugular catheter to skin of neck Syringe for IV contrast material. A syringe with a screw tip is recommended to avoid pressure-induced separation of the syringe from the T-port or catheter cap during high-pressure injection of contrast. Transparent, aqueous IV contrast material (iodinated, ionic; e.g., Renografin-76, Renovist 69%, Hypaque-M75, Conray 60%); maximal total cumulative dose given during procedure, assuming maintenance IV fluid administration to promote diuresis: 3 mL/kg Radiographic facility, including radiographic machine, films and cassette, and developer and/or fluoroscopic unit Adapted from Wise M: Nonselective angiocardiography in the normal dog and cat, Vet Radiol 23:144–151, 1982.
DOG
CAT
Site Enhanced by Contrast Time (sec) from Start of Injection Time (sec) from Start of Injection Cranial vena cava
1–2.5
0.5–1.5
Right ventricle
2–3
1.5–2.5
Pulmonary arteries
2–3
1.5–2.5
Left atrium
4–5.5
4.5–7
Left ventricle
4.5–6
5–7
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DOG
CAT
Site Enhanced by Contrast Time (sec) from Start of Injection Time (sec) from Start of Injection Aorta
4.5–6.5
5–7
ANGIOGRAM, NONSELECTIVE Lateral nonselective angiogram in a normal cat. Contrast was injected in a cephalic vein; right side of the heart and pulmonary circulation are opacified, and early opacification of left side of the heart and aorta is also seen. (Courtesy Dr. Brett Kantrowitz.)
ANGIOGRAM, NONSELECTIVE Lateral nonselective angiogram in a dog with valvular pulmonic stenosis. Contrast was injected in a jugular vein. Narrowing (stenosis) is seen at the level of the pulmonic valve (arrow). Marked poststenotic dilatation of the pulmonary trunk is apparent (arrowheads).
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(Courtesy Dr. Brett Kantrowitz.)
ANTICIPATED TIME About 15-30 minutes after catheter placement
PREPARATION: IMPORTANT CHECKPOINTS Thoracic radiographs: must precede contrast study, because a diagnosis may be apparent from these alone. Congestive heart failure must be controlled prior to procedure. Clipping of hair over vein to be catheterized (typically jugular or cephalic); jugular may be preferable in small animals ( 5% appear as red as blood. Odor; foul smell commonly associated with anaerobic infections. Note: Be aware of the possibility of airborne zoonoses if applicable (e.g., systemic fungal, other), and avoid assessing odor in such cases. Hematocrit: compare to peripheral blood to rule out hemorrhage. Total protein: compare to peripheral blood to rule out hemorrhage, exudative process. Creatinine, potassium: compare to peripheral blood to rule out uroabdomen. Cytologic evaluation The fluid should be fractionated into two tubes (EDTA [lavender-top tube], and sterile glass [red-top tube]), and a sample should also be saved on a sterile swab for bacterial culture. The two tubes are submitted for standard fluid analysis including cytologic evaluation. The bacterial swab can be submitted for culture immediately if bacterial infection is suspected clinically, or it can be saved for later submission in case cytologic results indicate the possibility of bacterial infection.
POSTPROCEDURE Subcutaneous pooling of ascitic fluid is common with partial drainage of large-volume ascites; may resolve spontaneously or require abdominal wrap (barring dyspnea).
ALTERNATIVES AND THEIR RELATIVE MERITS Repeat centesis under ultrasound guidance: Better ability to reach small pockets of ascites Diagnostic peritoneal lavage (see online chapter: Diagnostic Peritoneal Lavage): Increases ability to sample small volumes of ascites Often poorly diagnostic, somewhat cumbersome Generally replaced by ultrasound-guided centesis Laparoscopy (see p. 1298) or exploratory laparotomy for nonexfoliating, primary intraabdominal disorders causing ascites: Definitive diagnosis for abdominal masses, mesothelioma/carcinomatosis, and other similar conditions AUTHOR: ETIENNE CÔTÉ
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Abdominal Drainage SYNONYMS Large-volume abdominal paracentesis, peritoneal drainage
OVERVIEW AND GOAL To evacuate large-volume ascites via percutaneous placement of a sterile tube into the abdomen
INDICATIONS Tense ascites caused by chronic passive congestion (right heart failure, chronic hepatopathies) Abdominal compartment syndrome
CONTRAINDICATIONS Hemoabdomen: voids autotransfusion; delays control of cause of hemoabdomen Coagulopathy: risk of hemorrhage if laceration of abdominal organ occurs with needle tip
EQUIPMENT, ANESTHESIA Local anesthesia Manual restraint; sedation needed only rarely. Note: Animals often are restless during restraint owing to pressure of ascites on diaphragm; in such cases, the procedure may be preceded by large-volume needle centesis or may need to be performed with the animal in standing position. Hair clippers Surgical scrub solution, rubbing alcohol, and gauze/sponge for prepping skin Use 0.5-15 mL 2% lidocaine for local anesthesia. The volume is based on body weight, 1-70 kg. Discomfort from lidocaine infusion can be reduced by adding 0.05-0.2 mL sodium bicarbonate for injection (8.4% = 84 mg/mL = 1 mEq/L) and by warming solution to body temperature (armpit method). Alligator forceps (preferable) or mosquito hemostats, 1 pair Red rubber feeding tube: sterile 5-16 Fr tube, based on body size Sterile surgical gloves Suture material (e.g., nylon 2-0) and needle A #11 sterile scalpel blade Sterile needle holders Sterile suture scissors Elizabethan collar Sterile gauze squares (postprocedure) Tissue glue (postprocedure)
ANTICIPATED TIME 15-40 minutes, plus drainage time
PREPARATION: IMPORTANT CHECKPOINTS Weigh animal immediately before procedure (to quantify volume of fluid lost). Advise owner of possible drawbacks: Hair clipping required Procedure generally palliative; underlying problem not corrected Low risk of infection or other complications Have Elizabethan collar ready to place on the animal as soon as tube placement is complete.
POSSIBLE COMPLICATIONS AND COMMON ERRORS TO AVOID
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Overall, complications very uncommon; approximately 5%-10% incidence of irritation or dehiscence of incision, responding to topical treatment. Major complications are 5 mm, a skin suture or staple may be placed.
ABDOMINAL DRAINAGE Sterile red rubber feeding tube with additional holes in its distal part (arrowheads). Tube is grasped in jaws of alligator forceps and passed into abdominal cavity through a small incision on ventral abdominal midline.
POSTPROCEDURE Weigh the animal; record weight of lost fluid (for future reference and also to know accurate lean body weight for medication dosages). Dripping of ascitic fluid from incision is common despite tissue glue and generally resolves in minutes to hours. If it is persistent, a skin suture or staple may be necessary. Dripping and any subcutaneous pooling of ascitic fluid are minimized by allowing complete rather than partial drainage during procedure.
ALTERNATIVES AND THEIR RELATIVE MERITS Abdominocentesis with needle and syringe: Less invasive Very time-consuming for large volumes (e.g., 1 l or more) Generally ineffective at removing most or all of ascites Abdominocentesis with suction/vacuum: Faster May aspirate omentum or other abdominal structure Drainage less complete AUTHOR: ETIENNE CÔTÉ
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Buccal Mucosal Bleeding Time SYNONYMS Bleeding time, BMBT
OVERVIEW AND GOALS To quickly and easily assess primary hemostasis and evaluate formation of a platelet plug
INDICATIONS Presence of mucosal hemorrhage (petechiae/ecchymoses, gingival bleeding, epistaxis, melena, hematuria) in animals with a normal platelet count. May also be used for assessing primary hemostasis in preoperative animals.
CONTRAINDICATIONS Thrombocytopenia
EQUIPMENT, ANESTHESIA Anesthesia is generally not required in dogs. Sedation or general anesthesia necessary in cats Template bleeding device (device with a spring-loaded blade that creates a standard incision in the buccal mucosa) Filter paper or gauze for blotting blood Muzzle gauze (or equivalent) Stopwatch
BUCCAL MUCOSAL BLEEDING TIME Template bleeding device placed against buccal mucosa.
ANTICIPATED TIME A total of 5-10 minutes
PREPARATION: IMPORTANT CHECKPOINTS Evaluate platelet count prior to evaluating buccal mucosal bleeding time (BMBT).
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BUCCAL MUCOSAL BLEEDING TIME Blotting blood below the incision.
POSSIBLE COMPLICATIONS AND COMMON ERRORS TO AVOID Animal may become agitated; use sedation as needed to keep animal still for entire test. Do not manually disrupt clot while assessing clotting time.
PROCEDURE Place animal in lateral recumbency. Evert upper lip and secure in everted position with muzzle gauze. This allows exposure of the buccal mucosa and causes the vessels to become slightly engorged. Place template firmly on mucosa, and activate the blade. Begin timing when the incision is made. Hold filter paper beneath the incision to absorb blood. Continue timing until a clot has formed and bleeding has ceased. Normal BMBT is about 3 minutes in cats and about 4 minutes in dogs.
POSTPROCEDURE After the clot has formed and the test is completed, it may be necessary to apply pressure as needed if the clot becomes disrupted and bleeding resumes.
ALTERNATIVES AND THEIR RELATIVE MERITS Cuticle (“toenail”) bleeding time; less reliable as a measure of primary hemostasis and more painful to the animal. AUTHOR: ERIKA DE PAPP
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Bronchoscopy OVERVIEW AND GOALS To view and assess both the anatomy (mucosal, structural) and function (dynamic collapse) of the airways from larynx to distal bronchi and to obtain samples from the distal airways for analysis
INDICATIONS Diagnostic: evaluation of lower airway and parenchymal disease (culture/cytologic examination, biopsy) and documentation of airway caliber disorders (malacia, collapse, compression, bronchiectasis, bronchial stenosis) Therapeutic: foreign body/secretion removal
CONTRAINDICATIONS Major: severe hypoxemia, unstable cardiac arrhythmias, heart failure Minor: significant resting expiratory effort, bronchomalacia, inexperience
EQUIPMENT, ANESTHESIA Equipment: Flexible endoscope: 3-5 mm in diameter, 55-85 cm in length Mouth gag, sterile gauze, suction capabilities Sterile saline: Preloaded in 3 or 4 10- to 20-mL syringes for bronchoalveolar lavage (BAL) For rinsing and cleaning Sterile, water-soluble lubricant Forceps: if foreign body removal or mucosal biopsy is required Anesthesia: Pretreatment with a bronchodilator is recommended, especially in small dogs and all cats; use injectable terbutaline, 0.01 mg/kg SQ at least 15 minutes prior to the procedure. IV catheter for administration of a short-acting injectable anesthetic protocol: either atropine, 0.02-0.04 mg/kg IM; or glycopyrrolate, 0.01-0.02 mg/kg IM; in addition, butorphanol, 0.05-0.1 mg/kg IM and diazepam, 0.1 mg/kg IV followed by propofol, 3-6 mg/kg, slow IV titrated to effect, with repeated miniboluses of propofol (1 mg/kg) as needed over the duration of the procedure to maintain anesthetized state. Intubation is rarely used for the procedure; an anesthesia “T” piece is required if the scope will be passed through the tube; jet ventilation can be used if available. Provide oxygen before, during, and after the procedure; insufflate oxygen through the endoscope channel or via a 3-8 Fr urinary catheter passed alongside the scope during the procedure; use an endotracheal tube or a face mask for oxygen administration before and after. Topical 2% lidocaine if needed to decrease pharyngeal/laryngeal sensation, excessive coughing, and movement Doxapram HCl, 2.2 mg/kg IV once to assist with the evaluation of intrinsic laryngeal function Electrocardiogram (ECG), oximetry, blood pressure (BP) cuff, and other monitoring equipment
ANTICIPATED TIME A complete bronchoscopy and bronchoalveolar lavage can be completed within 10-20 minutes by an experienced endoscopist; animal recovery time is additional and varies with the type of anesthetic used.
PREPARATION: IMPORTANT CHECKPOINTS The bronchoscopist must have a good understanding of normal bronchial mucosa and lung anatomy to diagnose subtle airway abnormalities. The bronchoscope should be cleaned and ready for use. All supplies and equipment should be available before starting the procedure; anesthetic monitoring and image capture equipment should be turned on and ready to use. Antibiotics should be discontinued at least 72 hours prior to the procedure for accurate culture results. Chest radiographs are useful to help select specific lung regions for examination and for BAL.
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BRONCHOSCOPY Diagrammatic representation of the normal canine tracheobronchial tree. (Reprinted with permission from Amis T, McKiernan BC: Systematic identification of endobronchial anatomy during bronchoscopy in the dog, Am J Vet Res 47:2649–2657, 1986.)
POSSIBLE COMPLICATIONS AND COMMON ERRORS TO AVOID Contamination of the BAL sample is possible if care is not taken to avoid touching the upper airways during insertion of the scope. Guarded catheters may be used for decreasing the potential for BAL contamination, although catheter cost limits their use. Pulmonary barotrauma (tracheobronchial or lung rupture) is possible if the oxygen insufflation rate exceeds the ability of the gas to exit the lungs; this is of concern in smaller animals when the bronchoscope diameter is close to the tracheal size and pressure builds up in the lungs as active insufflation continues. Airway collapse during recovery can result in severe hypoxemia; anticipate when active expiratory effort is noted prior to anesthesia; slow recovery from anesthesia helps minimize this concern.
PROCEDURE Sternal recumbency is the recommended position in cats and dogs. Topical anesthesia (1%-2% lidocaine) may be applied to the pharyngeal/laryngeal mucosa to minimize laryngospasm or excessive coughing.
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Provide oxygen as already outlined. Evaluate the oropharyngeal/laryngeal region; use IV doxapram HCl (2.2 mg/kg once) to stimulate intrinsic laryngeal motion. Insert the bronchoscope into the airways, noting changes in shape (stenosis, stricture), dynamic caliber (malacia, collapse), and mucosa (secretions, erythema, edema, masses). In the normal animal, the dorsal tracheal membrane is taut so that there is little if any redundancy (no visible protrusion or collapse into the airway). The healthy tracheobronchial mucosa is a smooth, light-pink surface with a rich supply of submucosal capillaries; if these capillaries are not visible, mucosal edema or cellular infiltration is likely present. Healthy mucosa has a slightly glistening appearance; mucosal edema is readily apparent because it imparts a gelatinous appearance to the epithelial surface. The clinician should examine the carina for abnormalities (widening, compression, mucosal infiltration) before evaluating each lobar and as many segmental and/or subsegmental bronchi as possible (as both the animal and endoscope size will allow). Airway bifurcations beyond the carina are referred to simply as a spur. Like the carina, these should also form a sharp V, but they become widened and appear U shaped with chronic airway inflammation and/or mucosal edema. Small polypoid mucosal nodules are commonly encountered in the bronchi of dogs with chronic bronchitis. Small amounts of white or slightly opaque mucus may be noted in a healthy animal, but larger accumulations or secretions of unusual color are abnormal. The normal monopodial branching system results in a gentle, smooth tapering of the airways. Changes may be focal or generalized and include those of shape and size of the airway lumen, such as an intraluminal stricture/tumor, external compression (tumor or lymphadenopathy), bronchiectasis, or dynamic collapse (malacia). Whether or not abnormalities are noted, samples should be obtained for culture and cytologic examination. Following the initial airway evaluation, the endoscope is removed from the animal and cleaned by alternatively suctioning the channel with sterile saline and air immediately prior to reinsertion. The BAL site (lobe and bronchus) is chosen based on both radiographic and gross bronchoscopic findings. If no site is clearly abnormal, BALs from both “middle” lung lobes should be collected. To perform a BAL, the bronchoscope is first gently wedged into a segmental or smaller bronchus. Aliquots of 10-20 mL sterile saline (depending on the size of the animal) are instilled into the airway (via the suction channel or a washing pipette) and then immediately aspirated using slow, gentle hand suction. Ideally, at least two different sites (lung lobes) should be lavaged, with two aliquots per site. A 40%-90% return of the volume instilled is expected. Difficulty in fluid recovery results when a proportionately large endoscope is used (prevents wedging into a small bronchus) or if malacic airways collapse when suction is applied. If there is enough time and anesthetic depth is appropriate, the nasopharynx should also be examined.
POSTPROCEDURE Provide supplemental oxygen until fully recovered. Crackles are commonly noted on auscultation for a short time following a BAL procedure. Process samples immediately. Quantitated aerobic cultures should be made if possible. Mycoplasma and anaerobic cultures are processed using Amies transport media, or submit fluid in a sterile tube. Cytologic analysis: Total white blood cell (WBC) and differential cell counts should be done. The predominant cell in all species should be the alveolar macrophage (70+%), with usually less than 3%-8% of all other cell types (except the cat, which may have up to 20+% eosinophils and still be normal). Handling the scope: Immediately rinse/wipe the scope down when finished to prevent secretions from drying. Clean and sterilize the scope as outlined in the manufacturer's manual. Store the scope hanging up (to fully dry it) in a protected space/closet.
ALTERNATIVES AND THEIR RELATIVE MERITS Tracheal wash procedures are less expensive and easier to perform, but they lack the ability to direct sampling into specific sites, provide no information regarding anatomic, structural, or functional airway abnormalities, and have no therapeutic capability. Fine-needle lung aspiration biopsy has been used successfully to sample consolidated lung lobes and larger masses. AUTHOR: BRENDAN C. MCKIERNAN
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Breeding Soundness Exam: Male Dog OVERVIEW AND GOAL Evaluate the physical and physiologic parameters of the breeding male
INDICATIONS Prior to breeding, especially with a virgin male, a male with a history of systemic disease or when the male has not been used for breeding for several months Less than 50% whelping rate Prepurchase evaluation of a male intended for breeding
EQUIPMENT, ANESTHESIA Scrotal calipers A semen collection vessel such as: 15-mL centrifuge tube and plastic cone Sterile urine cup Whirl-Pak bag Microscope Morphology stain (eosin-nigrosin) and Diff-Quik stain for cytologic analysis Hemocytometer and WBC Unopette Ultrasound
ANTICIPATED TIME 30-90 minutes
PREPARATION: IMPORTANT CHECKPOINTS 1 week sexual rest recommended prior to a breeding soundness exam (BSE) It is recommended to fill out an evaluation form when performing a BSE, as this will help ensure all important points are covered and provide a valuable record. An evaluation form is available from the Society for Theriogenology.
POSSIBLE COMPLICATIONS AND COMMON ERRORS TO BE AVOIDED It is important to prevent thermal, mechanical, or chemical injury to the semen once collected. A poor-quality semen sample, especially one with low sperm numbers, should be interpreted with caution, as it may be an incomplete ejaculate. Seminal alkaline phosphatase (ALP; of epididymal origin) can be used to distinguish between an incomplete ejaculate and true azoospermia. Normal ALP of a complete ejaculate would be between 5000 and 40000 IU/L. An incomplete ejaculate usually would usually measure 10 kg. Hands should be placed over the heart for patients < 10 kg. Interruption of chest compressions should be minimized to 5 mm. Maintain a sterile dressing and bandage over the incision site for 12-24 hours. ANALYSIS: Evaluate color: clear fluid is not expected when peritonitis exists. Flocculent fluid indicates possible peritonitis. Red fluid indicates hemoabdomen. Green fluid likely contains bile. Perform packed cell volume (PCV) count: > 5% indicates significant hemoabdomen. Perform white blood cell (WBC) count: normal is approximately 1000 cells/mm3. Perform cytologic examination of fluid for degenerative neutrophils, toxic change, intracellular bacteria, bilirubin crystals, neoplastic cells, and other such abnormalities. Consider aerobic/anaerobic culture if septic peritonitis is suspected. Consider chemistry evaluation of lavage fluid, with comparison to peripheral blood: Elevated creatinine in lavage fluid indicates ruptured urinary tract. Elevated bilirubin indicates ruptured biliary tree. Elevated amylase indicates pancreatitis.
POSTPROCEDURE Monitor recovery from sedation/anesthesia. Supportive care as indicated for condition.
ALTERNATIVES AND THEIR RELATIVE MERITS Percutaneous needle abdominocentesis (see p. 1194): Technically easier to perform Requires less equipment Higher probability of a negative tap with small fluid volumes or pocketed areas of disease
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Abdominal ultrasonography: Noninvasive Allows visualization of the entire abdomen and detection of small or pocketed areas of fluid accumulation Ultrasound-guided aspiration allows fluid collection without risk of side effects secondary to instillation of lavage fluid. Diagnostic accuracy is operator dependent. Not available at all veterinary facilities Abdominal CT scan (see p. 1233) or MRI (see p. 1302): High diagnostic accuracy rate Typically requires anesthesia Limited to referral institutions Expensive Laparoscopy (see p. 1298): High diagnostic accuracy rate Requires anesthesia Expensive Not available at many veterinary facilities Exploratory laparotomy: High diagnostic accuracy rate Requires anesthesia Highly invasive AUTHOR: LILLIAN I. GOOD
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Dermatologic Diagnostic Procedures SYNONYMS Diagnostic techniques in dermatology, diagnostic testing in dermatology
OVERVIEW AND GOALS Tests that are performed to confirm a diagnosis and/or to rule out differential diagnoses for skin lesions The most common diagnostic procedures in dermatology are examination of the haircoat and skin with a good light source and magnifying lens, flea combing, acetate tape preparation, skin scrapings, skin cytologic examination, Wood's lamp examination, fungal culture for dermatophytes, and skin biopsies.
INDICATIONS Skin scrapings: used primarily to find mites and occasionally nematode infestation Skin cytologic examination: extremely useful diagnostic procedure indicated in almost every dermatology case. It can rapidly and inexpensively detect the presence of inflammation, infection (bacteria, fungi), autoimmune disease (acantholytic keratinocytes in pemphigus), or neoplasia. Wood's lamp examination: useful screening tool when dermatophytosis caused by Microsporum canis is suspected Dermatophyte culture: indicated when a dermatophytosis is suspected. In fact, it is indicated in virtually any cat with undiagnosed skin disease. Trichography is the microscopic examination of forcefully plucked hairs. This test is most useful for finding ectoparasites (particularly louse ova and Demodex), identifying hair shaft fracture, and finding large melanin clumps (macromelanosomes) causing hair shaft distortion in color dilution alopecia and black hair follicular dysplasia. It can be a useful tool in evaluating alopecic dogs, but normal anagen/telogen ratios have not been established for most breeds. Skin biopsies: performed to confirm a diagnosis or to provide direction (without always receiving a definitive diagnosis). Skin biopsies are recommended with any neoplastic or suspected neoplastic lesion, any persistent or unusual lesion, any vesicular dermatosis, and any undiagnosed alopecia.
CONTRAINDICATIONS Virtually none
EQUIPMENT, ANESTHESIA Simple equipment is required to perform veterinary dermatologic tests. Standard equipment and materials consist of: Biopsy kit, including biopsy punches One or two dull #10 scalpel blades Glass microscope slides and coverslips (20 × 40 or 22 × 50 mm) Mineral oil Cotton-tipped applicators Acetate tape (clear adhesive tape) Microscope Hemostat Handheld magnifying lens Flea combs Otoscope and several otoscopic cones Cytologic examination stain Wood's lamp Dermatophyte test media Sterile toothbrushes Syringes A few 22-, 23-, and 25-gauge needles Biopsy kit Local anesthetic (e.g., lidocaine 2%) Biopsy jars containing 10% neutral buffered formalin
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ANTICIPATED TIME The procedure takes a few minutes.
POSSIBLE COMPLICATIONS AND COMMON ERRORS TO AVOID Skin scrapings: to avoid false-negative results, it is important to clip hair before performing skin scrapings. However, it is preferable to use scissors when surface mites such as Cheyletiella are suspected, because they can be lost if electric clippers are used. Note: A positive scraping allows the clinician to find and identify a parasitic infestation, but its sensitivity in ruling out a diagnosis depends on the parasitic disease and the aggressiveness of sampling. Skin biopsies: do not scrub—or wipe or rub with alcohol or antiseptic—the surface of a biopsy site prior to performing punch biopsies; pathologic changes on the skin surface, which often are critical in making a diagnosis, may be altered or removed. For the same reason, do not shave the area of interest; gently clip the hair with scissors if necessary.
PROCEDURE Skin scrapings: Apply a few drops of mineral oil to the area of skin selected for scraping or coat the dull scalpel blade that is used for performing the scraping with mineral oil. Broad superficial scrapings that collect scales and crusts should be performed when looking for mites living on the surface (Cheyletiella) or in the superficial layers of the skin (Sarcoptes, Notoedres). Deeper skin scrapings must be performed when suspecting the presence of deep-dwelling mites (Demodex). In the latter case, the skin must be squeezed to help extrude the mites from the hair follicles first, and the scrapings should be deep enough to create capillary oozing. The skin scraping material that is collected on the scalpel blade is then smeared on a glass slide; additional mineral oil is added, and a cover slip is applied. The specimen is then examined with 40× (Cheyletiella, Sarcoptes, Notoedres) or 100× (Demodex) magnification. Demodex mites are part of the skin's normal flora, but it is extremely rare to find them on skin scrapings. If one or a few mites are found, more deep skin scrapings should be taken to confirm the diagnosis of demodicosis. Conversely, numerous negative skin scrapings from appropriate areas should reliably eliminate demodicosis and notoedric mange. In addition, in areas that are difficult to scrape, hair can be plucked and the proximal ends examined under a microscope for the presence of Demodex mites. Negative skin scrapings (even if several are performed) do not eliminate the possibility of sarcoptic mange or cheyletiellosis. Skin cytologic examination: Allows microscopic examination of fluid or material collected from nodules, tumors, cysts, plaques, draining tracts, ulcers, pustules, vesicles, papules, and surface of the skin or ears. Several techniques may be used for obtaining samples. Specimens may be collected by: Impression smears made from the surface of intact lesions or from cut surfaces of surgically
DERMATOLOGIC DIAGNOSTIC PROCEDURES Materials used for performing dermatologic diagnostic tests.
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A, Biopsy punches. B, #10 scalpel blades. C, Glass microscope slides. D, Mineral oil. E, Cotton-tipped applicators. F, Acetate tape (clear adhesive tape). excised lesions, such as nodules or tumors Impression smears made after lancing pustules or papules Fine-needle aspiration (FNA) of cells or material from lesions Smears made by rolling the cotton-tipped applicator across a glass slide (particularly useful for ear specimens) Scrapings of superficial epithelial cells with a dry, dull scalpel blade. This cellular material is then pressed firmly onto a glass slide. After the specimen has dried, the slide is stained with a modified Wright's stain (e.g., Diff-Quik) and examined microscopically. When a drop of mineral oil is put on the stained dried specimen and then covered with a large coverslip (22 × 40 or 22 × 50 mm), visualization of cells and most microorganisms at 400× is enhanced, so there is no need to perform an examination under oil immersion (1000×) in most cases. Wood's lamp examination: This ultraviolet light's wavelength of 253.7 nm is temperature dependent, and the lamp should be turned on for 5-10 minutes before use. Certain dermatophytes (mainly Microsporum canis in veterinary medicine) may cause infected hairs (not scales or crusts) to fluoresce an apple green color. This occurs in about 50% of cases with M. canis. It is a fast and inexpensive screening tool for dermatophytosis. False positives are unfortunately frequent. Glowing hair should be plucked and the proximal end further examined with the Wood's lamp or used for culture or direct examination for fungal elements under microscope. A negative examination does not rule out dermatophytosis. Dermatophyte culture (see p. 292): Generally performed in clinics on commercial dermatophyte test medium (DTM), available in either glass jars or flat plates. The culture medium consists of Sabouraud's dextrose agar, antibacterial and antifungal agents to inhibit growth of contaminants, and phenol red (pH indicator). Select hairs and scales for culture along the edge of newly developing lesions. Broken or frayed hairs and those that fluoresce with Wood's lamp are the best specimens. The plucked hairs should be firmly pressed onto the surface of the medium. Alternatively, vigorous brushing of the animal's haircoat with a sterile toothbrush or a small piece of sterile carpet can be used for collecting hairs and scales (more useful to identify carriers not showing obvious lesions). This material can be removed from the toothbrush with a sterile hemostat and placed into the culture medium. Alternately, if plates are used, the DTM is inoculated by gently embedding or repeatedly dabbing the toothbrush into the medium. Ideally, the culture medium should be incubated at 22○C-30○C (72○F-86○F) and at about 30% of relative humidity for 2-3 weeks, and it should be checked daily for fungal growth. Desiccation hinders growth. It is recommended to keep the culture medium for up to 3-4 weeks in animals with antifungal pretreatment or suboptimal culture environment fungal growth. A red color change with visible mycelial growth (typically cream color) is seen with dermatophytes on DTM. Contaminants (environmental molds) will eventually turn the media red; however, colony growth is usually well established before any color change appears in the medium. In addition, most saprophyte colonies are pigmented. Nonetheless, identification of the fungi is essential if a suspected dermatophyte is grown on culture. Macroconidia must be collected from the mycelial surface by gently applying the sticky side of clear acetate tape to the aerial surface. The tape with sample is then pressed onto a glass slide over a drop of methylene blue or lactophenol cotton blue stain and examined under microscope for characteristic macroconidia. Skin biopsies: The biopsy technique selected (punch biopsy, wedge biopsy, excisional biopsy) varies according to the type of lesions. Site selection is crucial. Choose several representative lesions that may represent various stages of the same pathologic process or multiple problems, with emphasis on primary lesions if possible (e.g., pustules, vesicles). Punch biopsy specimens (usually 6 mm) can be obtained under local anesthesia (1 mL of 2% lidocaine per site, injected subcutaneously beneath the specimen; do not exceed 1 mL per 5 kg of body weight). If a papule, pustule, vesicle, or any small lesion is selected, the lesion should be centered in the biopsy specimen. The biopsy punch should be rotated in only one direction to minimize shearing artifact. Handle the specimen carefully. The forceps should grasp either the hairs of the biopsy sample or its deepest surface (e.g., subcutis), never the core of the biopsy sample itself. The specimen must be put rapidly in 10% neutral buffered formalin. Skin biopsy punch sites can be sutured with one or two interrupted sutures. Skin biopsies, along with a detailed history and animal description, should be submitted to a veterinary dermatopathologist.
ALTERNATIVES AND THEIR RELATIVE MERITS Therapeutic trials (e.g., antiparasitic, antimicrobial) are frequently performed in veterinary dermatology and represent very useful diagnostic tools. For example, therapeutic trials with acaricidal agents such as macrocyclic lactones are often required when sarcoptic acariosis or cheyletiellosis is suspected but skin scrapings are negative. AUTHOR: MANON PARADIS
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Dental Radiography, Basic OVERVIEW AND GOAL To obtain diagnostic images of the teeth and surrounding structures using x-rays.
INDICATIONS Diagnosis, treatment planning, and postoperative assessment of treatment efficacy for various dental, oral, and maxillofacial conditions Dental radiographs should be obtained prior to tooth extraction to evaluate alveolar bone health and variations in root anatomy, and to determine the presence of dentoalveolar ankylosis or root replacement resorption that could potentially complicate the extraction procedure. They are essential when performing endodontic procedures. Specifically, to diagnose and monitor: Regressive changes of the dentition including: caries, attrition, abrasion, and tooth resorption Dental (change in number or shape of teeth) and jaw size anomalies, including malocclusion, supernumerary teeth, and developmentally missing teeth Infection and inflammation of teeth, alveolar bone, and maxillofacial bones, including periodontitis, endodontic disease (pulp necrosis), periapical disease (apical granuloma, cyst or abscess, condensing osteitis, osteosclerosis), and osteomyelitis Oral and maxillofacial cysts and tumors Oral and maxillofacial trauma Disorders of joints of the head: mandibular symphysis separation; temporomandibular joint osteoarthritis, luxation, fracture, and ankylosis; open-mouth jaw locking Diseases of bone with manifestation in the jaws: craniomandibular osteopathy, calvarial hyperostosis, secondary hyperparathyroidism, fibrous osteodystrophy Diseases of the nose, orbit, and ear Partial or full-body imaging studies in small mammals and exotics
CONTRAINDICATIONS Because dental radiography requires chemical restraint, it is contraindicated in patients that cannot undergo sedation or general anesthesia.
EQUIPMENT, ANESTHESIA Sedation or general anesthesia Radiolucent positioning and film-holding devices (e.g., bite blocks, foam rolls, syringe cases, gauze pads, paper towels, rubber bands) to keep the mouth open and the dental film packet in position without superimposition of maxillary and mandibular dental arches Dental x-ray machines: Either handheld, stand-supported, or (more commonly) wall-/ceiling-mounted Extension arm allowing vertical, horizontal, and rotational movement of the tube head without changing the patient's position Adjusting exposure time based on patient size and tissue thickness to be imaged (between 0.1-0.6 seconds for teeth and jaws when using non-screen dental films and 1/10 of that time when using digital sensors) Dental x-ray films: Nonscreen (providing greater detail than screened film used with standard x-ray machines) Sizes 0, 1, 2, 3 and 4 (0, 2 and 4 most commonly utilized). Most jaw lesions can be satisfactorily assessed with size 2 and 4 dental film and intraoral imaging techniques. Dot in corner of packet and also on the film: convex (raised) surface facing x-ray beam during exposure; after developing, dimple is used for distinguishing right side of mouth from left. Contents of moisture resistant dental film packet: Outer plastic wrap Black paper on either side of the film Layer of lead foil located at back of packet next to tab opening (protecting film from secondary radiation, which may cause fogging) X-ray film Types of film: Ultra-speed (group D): most commonly utilized Ekta-speed (group E): faster (reducing patient exposure and radiation), but image of slightly lesser quality than that obtained with ultra-speed film Dental x-ray films can also be used with standard x-ray machines, using a technique of 100 mA, a film focal distance of 12 to 16 inches, and an exposure time of 1/10 second, with the kVp varying from 60 to 70 dependent on patient size. Other equipment: Chairside darkroom (or automatic film processor) with small containers for the following solutions (from left to right): rapid developer, water, rapid fixer, and again water (or fixer, dependent on number of radiographs obtained) Film clips and hangers Dental view box Envelopes or other storage system Digital imaging: Most modern dental x-ray machines compatible with most digital hardware and software packages Sensor pads (sizes 0 and 2) or photostimulable phosphor plates (size 4 also available) transferring images to a computer Less radiation required to produce images Digital image improvable with software programs
ANTICIPATED TIME Obtaining a full-mouth dental series: Cats (8-10 films): 10-15 minutes
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Dogs (10-14 films): 15-20 minutes Processing a full-mouth dental series: Cats: 5-10 minutes Dogs: 10-15 minutes
PREPARATION: IMPORTANT CHECKPOINTS Observe radiation safety guidelines: Be protected against three sources of radiation: primary beam, secondary radiation emitted from the patient, and radiation leakage from the machine housing. Wear film badges that monitor occupational exposure to radiation. Keep amount of radiation exposure to a minimum. Have x-ray machine accurately collimated and equipped with an accurate exposure timer. Leave the room when radiographs are obtained. If leaving the room is not possible, wear protective lead-lined gear, use a protective barrier, or stand at least 6 feet from the x-ray source and at an angle of 90°-135° to the central ray of the x-ray beam when the exposure is made. Film-processing solutions (rapid developer and fixer) should be disposed of properly in accordance with regional/local law, and lead foil from film packets should be separated and stored for recycling. Patient positioning varies; lateral recumbency allows for easy rotation of the head if needed and is a good starting position for obtaining most dental radiographs in cats and dogs. A full-mouth dental series may contain the following views: Right maxillary premolars and molars Right maxillary canine (lateral or lateral oblique view) Right and left maxillary canines and incisors (occlusal view) Left maxillary canine (lateral or lateral oblique view) Left maxillary premolars and molars Left mandibular premolars and molars Left mandibular canine (lateral or lateral oblique view) Right and left mandibular canines and incisors (occlusal view) Right mandibular canine (lateral or lateral oblique view) Right mandibular premolars and molars
POSSIBLE COMPLICATIONS AND COMMON ERRORS TO BE AVOIDED POSITIONING ERRORS: Elongation: abnormally long teeth due to tube angle too perpendicular to apico-coronal axis of teeth when bisecting angle technique is used Foreshortening: abnormally short teeth due to tube angle too perpendicular to film when bisecting angle technique is used Superimposition: summation effect due to tube head aligned too far in rostral or caudal direction Clear circular perimeter: cone cut Blurred image: movement of patient, tube head, or film during exposure Image distortion: excessive bending of film during positioning White crescents or lines: sharp bend or pressure on film prior to exposing Dark crescents or lines: sharp bend or pressure on film after exposing but before processing Area of interest not on image: tube head misaligned Blurry, magnified image: film too far from subject to be imaged Stipple pattern on light film: film placed backward EXPOSING ERRORS: Dark film: overexposed Light film: underexposed Double image: double exposure PROCESSING ERRORS: Entire film clear: emulsion detached from film or unexposed film Clear area along one edge: processing solution level too low Incomplete variable processing: paper stuck to film during processing Dark film (not overexposed): overdeveloped Light film (not underexposed): underdeveloped Black spots: contamination of film with developer prior to processing Yellow or brown stains: inadequate fixation, inadequate rinsing (incomplete removal of fixer) White spots: contamination of film with fixer before processing Green discoloration: films in contact during processing Fingerprints: film touched with contaminated fingers Frosted film surface: inadequate rinsing (incomplete removal of fixer) Small white circles: bubbles in processing solutions Thick white lines: scratched emulsion during processing Streaks: inadequate processing, solution contamination, contaminated hanger clips Mottled areas (too light or too dark): poorly mixed processing solutions, with temperature variances (too low or too high) Fogged film: light contamination or overprocessing
PROCEDURE OBTAINING DENTAL RADIOGRAPHS:
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Parallel technique: Film placed parallel to apico-coronal axis of the teeth X-ray beam directed perpendicular (90○) to the film and the teeth Used for imaging the molars and caudal premolars of the mandible and the nasal cavity Bisecting angle technique: Film placed as close to the teeth as possible Angle formed by the apico-coronal axis of the teeth and the plane of the film bisected by an imaginary line, with the tube head (x-ray beam) positioned perpendicular to this imaginary line Used for imaging all maxillary teeth and the rostral premolars, canines, and incisors of the mandible Peculiarity in cats: radiographs of the maxillary premolars and molars utilizing the bisecting angle technique results in superimposition of the zygomatic arch over the root apices of the teeth. To eliminate this superimposition: An extraoral technique may be utilized; or Premolars and molars may be intentionally elongated slightly when using the intraoral technique to eliminate the superimposition of the zygomatic arch by decreasing the vertical angulation of the tube head. PROCESSING EXPOSED FILMS: Chairside darkroom: Close lid of the chairside darkroom. Hold film packet in one hand and a film clip in the other. Slide both hands through front sleeves into the chairside darkroom. Remove exposed x-ray film from packet, and place it in film clip. Place film first into developer for about 30 seconds. Briefly (few seconds) rinse in water. Then place film into fixer for at least 60 seconds before viewing. After a final water rinse, view film using a dental view box to make a diagnosis. After viewing, place film for another 15 minutes into fixer, followed by thorough rinsing in water for 20 minutes and air drying. Store completely dry films in a labeled envelope (or other storage system), and keep as part of the patient's medical record. Automatic processor: Automatic processors designed for dental films can deliver processed film in a fully fixed, dried condition within 5 minutes. Dental film can also be processed if taped to a larger film that serves as a leader by dragging the dental film through a large automatic processor.
POSTPROCEDURE INTERPRETING PROCESSED FILMS: Labial mounting: Place processed film on view box so that raised dot is projecting toward the viewer. Determine if image is of upper or lower jaw. Rotate film so that maxillary tooth crowns point downward and mandibular tooth crowns point upward. View image as if one is looking from outside at a closed mouth whose maxillary and mandibular teeth are made visible after raising upper and lower lips. Radiographic landmarks: All three-rooted teeth are located in the upper jaw. Palatine fissures are also located in the upper jaw. Upper jaw will often have white lines visible on lateral and lateral oblique views that are superimposed on teeth (indicating maxillary conchal crest and line of conjunction between body and palatine process of the maxilla). Lower jaw will often have ventral mandibular cortex, mandibular canal (radiolucent tubular structure in the mandible), and mental foramina (rostral, middle and caudal; sometimes mistaken for periapical pathology) visible on lateral and lateral oblique views.
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DENTAL RADIOGRAPHY, BASIC A, Full-mouth dental radiographic series in a 2-year-old dog with complete permanent dentition: radiographs are arranged in labial mounting (with raised dot facing the viewer). Maxillary tooth crowns point downward, and mandibular tooth crowns point upward. L, Left side; R, right side. B, Lateral radiographic view of right maxillary incisors, canine, and premolars in a dog (labial mounting). Note the palatine fissures (asterisks), the line of conjunction between the body and palatine process of the maxilla (large white arrows), and the conchal crest (large black arrow). LD, Lamina dura; PS, periodontal space. C, Lateral radiographic view of left mandibular incisors, canine, and premolars in a dog (labial mounting). Note the mandibular canal (asterisk). AM, Alveolar margin; Cr, crown; D, dentin; E, enamel; F, furcation; MMF, middle mental foramen; PC, pulp cavity; R, root; VMC, ventral mandibular cortex. (Copyright Dr. Alexander M. Reiter.) Components of the tooth and its supporting structures: Crown and root(s) Enamel (covering the crown) and dentin (core hard tissue of the tooth) Cementum (covering the root), periodontal space (containing the periodontal ligament), and lamina dura (cortical bone extending into the alveoli) Pulp cavity (pulp chamber in crown and root canal in root) Furcation (area where two roots meet at the crown) Alveolar margin (most coronal extension of the alveolar bone)
ALTERNATIVES AND THEIR RELATIVE MERITS The largest dental films (size 4) may also find use for radiographic evaluation of the nasal cavity, orbit, zygomatic arch, mandibular ramus, temporomandibular joint and tympanic bulla in cats and small dogs and for partial or full-body imaging studies in small mammals and exotics. AUTHOR: ALEXANDER M. REITER
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Dental Prophylactic Treatment SYNONYMS Dental cleaning and polishing, dental prophylaxis
OVERVIEW AND GOALS Complete oral examination Removal of calculus and plaque buildup on teeth to create a healthier dentogingival environment Polishing teeth surfaces to make them less prone to calculus accumulation
INDICATIONS Accumulation of bacterial plaque (soft) or dental calculus (hard) on the dental surface Treatment of gingivitis Prevention of periodontal disease Annual dental examination Part of the maintenance phase in the treatment of periodontitis
CONTRAINDICATIONS Established periodontitis: animal should receive more involved diagnostic and treatment procedures rather than prophylactic treatment. Diagnosis includes dental examination, periodontal probing and full-mouth intraoral radiographic examination. The first stage of treatment is aimed at controlling the infection; it includes dental cleaning and polishing, root planing, dental extractions and antimicrobials as needed. It is followed by a period of maintenance with home care and reevaluation. The second stage of treatment, periodontal surgery, is done a month later once the periodontium has healed, if the level of compliancy of the owner with home dental care is adequate and if the periodontium still needs to be restored to help prevent reinfection. When general anesthesia is contraindicated because of systemic illness Old age is not a contraindication. Note: Dogs with mitral valve endocardiosis have not been shown to have a greater risk of dental procedure–associated bacterial endocarditis than dogs with normal heart valves.
EQUIPMENT, ANESTHESIA General anesthesia and tracheal intubation Hand instruments: Scalers (H 6-7) Curettes (Gracey 3/4, Gracey 13/14, Mini-five 1/2) Dental explorer and periodontal probe (XP-17/0W) Dental mirror Instrument tray Ceramic sharpening stone Power instruments: Ultrasonic (magnetostrictive with metal stack, magnetostrictive with ferrite rods, or piezoelectric) or sonic scaler One tip for removal of gross and moderate calculus buildup One perio (or universal) tip for removal of subgingival calculus and debris. The energized water spray at the end of the tip also kills bacteria with what is referred to as the cavitation effect. Dental unit, either air or electric powered, with low-speed handpiece and contra-angle attachment. Since the speed of the prophy cup should be around 4000 rpm, a contra-angle-attachment with a 4:1 gear ratio is usually necessary with air-driven units. Prophy head, multi-use or single-use Rubber prophy cups; prophy paste (jars or unidose cups) or flour pumice medium grit Chlorhexidine solution 0.12% Good lighting conditions, magnifying glasses Dental chart
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ANTICIPATED TIME About 20 minutes for a cat and 45 minutes for a dog
PREPARATION: IMPORTANT CHECKPOINTS Operator protection: Surgical mask, gloves, eye protection, scrub top or gown Instill 0.12 % chlorhexidine solution in the animal's mouth before starting the procedure to reduce bacterial counts in the aerosols generated during power scaling. Animal protection: Keep the animal warm because of the cooling effect of the water spray during power scaling. Protect the eyes (lubrication, towel), and sterilize the instruments. Appropriately inflate the cuff of the endotracheal tube, and use lubricating gel. Administer antibiotics only if animal is immunosuppressed, has an internal prosthesis, or has a severe infection: 20 mg/kg ampicillin IV 1 hour prior to the procedure; or clindamycin, 5 mg/kg, or clavulanic acid-amoxicillin, 13.5 mg/kg, PO 12 hours prior to the procedure. Place cotton gauze in the oropharynx to catch pieces of calculus that could otherwise enter the trachea after extubation.
POSSIBLE COMPLICATIONS AND COMMON ERRORS TO AVOID Forgetting to remove the cotton gauze in the oropharynx before extubation Causing thermal damage to the dental pulp by staying too long over a tooth during power scaling or polishing or inadequate water spray during power scaling Damaging the tooth surface by being heavy-handed during scaling and polishing or by using burs (Rotosonics) to remove calculus Dental cusp (tip) fracture caused when using extraction forceps to chip away the calculus (not recommended) Power instrumentation: use the lowest effective intensity (power) setting; use a light touch; work with the last 3 mm at the end of the tip; keep the tip moving, with adequate water spray. Use a gauge to check tip wear, and replace when 2 mm has been lost (50% loss of efficacy).
PROCEDURE The anesthetized, intubated animal is placed in lateral recumbency, and all stages of the procedure described here are performed on the lingual side of the teeth on the recumbent side and the labial side of the teeth on the non-recumbent side. Then the animal is turned over, and the procedure can be repeated (avoids turning the animal multiple times). Remove very heavy calculus deposits with a dental scaler or hoe. Remove gross and moderate supragingival calculus using hand instrumentation (dental curette, scaler) or power instrumentation (sonic or ultrasonic with a heavier tip at moderate- to high-intensity setting). The working surface of the power scaler should be held parallel not perpendicular to the tooth surface. Remove light supragingival and subgingival calculus with hand instrumentation (dental curette) or power instrumentation (sonic or ultrasonic with slim perio or universal tip at low-to moderate-intensity setting). A disclosing solution can be used for checking for the presence of dental plaque, or an air spray from an air/water syringe for the presence of calculus. The teeth are polished with prophy paste or flour pumice. Dental examination with dental explorer; periodontal examination with periodontal probe. Chart all the findings. Flush the gingival sulcus with an atraumatic needle and saline to remove the prophy paste or flour pumice, calculus debris, and bacteria. Perform final rinse with 0.12% chlorhexidine.
POSTPROCEDURE Discuss home oral care with owners, and find appropriate regimen. Provide the owner with information about the postoperative treatment plan, including the date of the next dental appointment.
ALTERNATIVES AND THEIR RELATIVE MERITS The wrong alternative to preventing periodontal disease with dental prophylactic treatment and home dental care is to wait until periodontal disease has progressed, and periodontal treatment is necessary to help control disease progression. This is
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obviously not an option that benefits the animal or owner. Brushing the teeth will not remove existing calculus. Dental prophylactic treatment performed without general anesthesia provides some cosmetic improvement but no long-term benefit. AUTHOR: YVAN DUMAIS
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Dental Preventive (Home) Care OVERVIEW AND GOALS A regimen of home dental care is designed to help keep the periodontium healthy in between professional oral prophylactic or therapeutic treatments.
INDICATIONS Accumulation of bacterial plaque (soft) or dental calculus (hard) on the dental surface Prevention of gingivitis and periodontal disease Part of the maintenance phase in the treatment of periodontitis
CONTRAINDICATIONS When the animal needs professional dental prophylactic treatment (gingivitis, calculus, or plaque buildup) or periodontal treatment (periodontitis, loss of dentogingival attachment) Oral hygiene complements and does not replace professional dental care.
EQUIPMENT, MATERIAL Soft-bristle toothbrush; pet toothpaste Food that is specially designed to reduce dental plaque or calculus formation Oral rinses to help reduce dental plaque formation Chew toys
ANTICIPATED TIME The home dental care regimen is discussed during regular visits or as part of a comprehensive oral prophylactic treatment or periodontal treatment. Once the regimen is well accepted by the pet and the owner, it is a daily routine that takes only 1 or 2 minutes.
PREPARATION: IMPORTANT CHECKPOINTS The home dental care regimen should be selected after considering the animal's needs; the will, availability, and dexterity of the owner; and the compliance of the animal. The implementation may require some form of training or behavior positive reinforcement before the pet associates home dental care with something fun.
POSSIBLE COMPLICATIONS AND COMMON ERRORS TO AVOID The desire to achieve thorough oral hygiene right at the beginning is often a deterrent for the owner and the animal. Most pets will not tolerate more than 20 seconds of toothbrushing and will not allow brushing the aspect of the teeth facing the palate or the tongue. In pets that have minimal calculus buildup, an annual thorough dental examination/cleaning under anesthesia often is not recommended. As a result, these animals may end up having severe dental or periodontal problems for an extended period of time before the problem gets noticed. It is sad that after investing a lot of effort in home dental care for prevention, these owners are not getting the success they were expecting because the recommendation for professional dental care was never made until it was clinically obvious that a problem was present. Pets, just as humans, need both: home dental care and professional dental care. Many chew toys have a round cross-sectional shape and are so hard that the carnassial teeth are prone to break when the pet bites down on them. There are so many products on the market and so many claims, most unsupported by credible independent research, that it is difficult to choose what to recommend to clients. A credible and independent source of information on the efficacy of dental products is the Veterinary Oral Health Council website (www.vohc.org), and products bearing the council's seal are recommended.
PROCEDURE
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Training for toothbrushing; instructions for the owner: Start with a bare finger and apply pet toothpaste on the rostral (front) teeth. Massage the gingiva for a few seconds. Repeat many times a day. As the pet gets used to it, go farther caudally in the mouth until the pet tolerates the procedure being done up to and including the molars. Once the pet is comfortable with the procedure, start using a toothbrush with soft bristles, and apply the toothpaste again on the rostral teeth, brushing for a few seconds. Go farther caudally as the pet tolerates the procedure. Give praise and rewards immediately after. Brush daily. Movement: for the incisors, brush from the gingiva toward the tip of the teeth. For the other teeth, brush with a circulatory movement with the bristles slightly oriented toward the gingiva of the upper jaw, then lower jaw, so that the action is focused on the area next to the gingival margin. With the mouth closed, the last teeth of the lower jaw are hidden behind the teeth of the upper jaw; however, the area next to the gingiva can still be brushed. Other alternatives: Food specially designed to prevent calculus or plaque formation either mechanically (fibers) or chemically. Fibers help clean the caudal teeth. Rinses: chlorhexidine 0.12% for treatment and prevention of gingivitis (not for periodontitis, because it is ineffective on organic material, cannot reach bottom of periodontal pockets); zinc and ascorbic acid, mainly for their action on epithelium and connective tissue post treatment. Products containing enzymes that enhance the antimicrobial action of saliva and leukocytes Products that stimulate oral exercise, production of saliva, and removal of plaque and calculus
POSTPROCEDURE Professional dental care once a year to allow complete oral examination, removal of plaque and calculus in areas where they still build up despite home dental care, and tooth polishing
ALTERNATIVES AND THEIR RELATIVE MERITS In absence or ineffectiveness of home dental care, the frequency of professional dental care is adjusted to prevent or control periodontal disease. AUTHOR: YVAN DUMAIS
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Dental Extraction SYNONYM Exodontics
OVERVIEW AND GOALS Removal of a tooth in a way that ensures complete removal of the root(s) and rapid healing of the dental alveolus and oral soft tissue Simple extraction is indicated for simple rooted teeth, except canine teeth or any tooth that has already lost most of its attachment. Canines and multirooted teeth usually require surgical extraction.
INDICATIONS Nonvital (dead) teeth; teeth with exposure or contamination of the endodontic system Moderate to severe periodontal disease Nonrestorable dental lesions: dental resorptions, dental fractures Persistent primary teeth, retained roots or impacted teeth, some teeth involved in jaw fracture Dental malocclusions Oral surgery, removal of oral tumors, oral cysts
CONTRAINDICATIONS When general anesthesia is contraindicated because of severe uncontrolled metabolic disease Animals with a bleeding disorder Animals undergoing chemotherapy or radiotherapy
EQUIPMENT, ANESTHESIA General anesthesia, preemptive pain control, and regional or local anesthesia are utilized as needed. Simple extraction: Dental radiograph (see p. 1246) A #11 or #15 scalpel blade Dental elevator(s) Dental forceps Surgical extraction: as above, plus: Periosteal elevator Dental unit with high-speed handpiece and FG dental burs (No. 699-701, regular, long shank, and surgical lengths) Bone rongeurs or bone rasp Bone curette Sterile saline with syringe and atraumatic needle Soft-tissue scissors (LaGrange) Tissue forceps Needle holder, 4-0 resorbable suture material with swaged-on needle
ANTICIPATED TIME About 5 minutes for most simple extractions and 20 minutes for most surgical extractions
PREPARATION: IMPORTANT CHECKPOINTS Dental radiographs: check for the number of roots, their shape, and their structural integrity (root resorption); the condition of the surrounding bone; and the presence or absence of a periodontal ligament with possible root ankylosis.
POSSIBLE COMPLICATIONS AND COMMON ERRORS TO AVOID
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Oronasal fistula: if occurs, should be closed with a mucoperiosteal flap, either at the time the extraction is done or as a delayed surgery if the gingival tissue is so inflamed that its capacity to hold sutures is questionable. Root fracture: Most easily prevented by examination of the preoperative radiographs and proper treatment planning. If the root is in advanced stage of resorption, is ankylosed, and has no evidence of periodontal or endodontic infection, it could be left in place for continued resorption. Although the clinician should try to remove as much root material as possible in an animal with root fracture, the risk of damaging surrounding tissue should be weighed against the benefit of finding the last piece of root material. When a root fragment is left in situ, the owner should be informed of that aspect of the surgery, and follow-up radiographs should be included in the treatment plan. The risk of causing an abscess is higher when the root fragment has been mobilized and its blood supply severed during its attempted extraction. Jaw fracture: usually the result of a blind attempt at extracting a tooth on the mandible without preoperative dental radiographs and appropriate treatment planning. Small-breed dogs with severe periodontal disease of the first lower molars and cats during extraction of the mandibular canines are the most likely to be at risk for jaw fracture during dental extraction. Root fragments in the nasal cavity or the mandibular canal should be retrieved.
PROCEDURE Simple extraction: Incision of the gingival attachment around the tooth with a scalpel blade Mobilization of the tooth with dental elevators using first-class lever, wheel-and-axle, or wedge types of forces: The tip of the elevator is used circumferentially as a wedge between the root and the bone to stretch the periodontal ligament, or as a wheel and axle with the side of the blade engaged under the enamel bulge mesial or distal to the tooth, to elevate the tooth out of the alveolus. Use light forces over a longer period (at least 10 seconds each time) to break the attachment without fracturing the root. Extend the index finger (of the hand holding the elevator) along the shaft of the elevator to protect deeper structures in case of slippage. Extraction with dental forceps once the tooth is mobile. Light rotation force may help. Check that extraction is complete; perform a postoperative radiograph if needed. Brief digital pressure to help hemostasis, reduce expansion of the alveolar wall caused by the extraction, and approximate the gingival margins Suture if needed Surgical extraction: Incision of the gingival attachment around the tooth with a scalpel blade Elevation of a mucoperiosteal flap with a periosteal elevator With a dental bur, buccal cortical bone and alveolar bone is removed to expose the root surface up to half its length. On a multirooted tooth, the crown is sectioned between the roots. Each individual root with its attached piece of crown is elevated. Check that the extraction is complete. Smooth the edge of the alveolar bone with a bone rongeur or rasp; curette and flush debris out of the alveolus. Trim the border of the soft tissue if needed (LaGrange scissors). Suture with a simple suture pattern. After a surgical extraction, the gingiva is sutured back in place, even in the case of an abscess. It is important to cover the bone exposed during elevation of the soft tissue.
POSTPROCEDURE Surgical extractions: pain medication for 4 days, soft food for 10 days Antibiotics are used if the animal shows systemic clinical signs (fever, loss of appetite, etc.) or if the condition has progressed to osteomyelitis. Recheck in 10-14 days.
ALTERNATIVES AND THEIR RELATIVE MERITS Endodontics, periodontics, and orthodontics are other alternative treatments. They have the advantage of preserving the teeth and are often a better option when the owner is interested in doing the necessary aftercare and home dental care. AUTHOR: YVAN DUMAIS
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Defibrillation, Electrical OVERVIEW AND GOALS Electrical defibrillation is the treatment of choice for cardiac arrest characterized by ventricular fibrillation. It consists of application of an electric shock to the heart, causing massive depolarization; when defibrillation is successful, this massive depolarization is immediately followed by spontaneous resumption of sinus rhythm.
INDICATIONS Ventricular fibrillation
CONTRAINDICATIONS Conscious animal Normal cardiac rhythm but electrocardiographic (ECG) artifact mimics ventricular fibrillation Poor or inappropriate contact between defibrillation paddles and animal Inability to electrically isolate animal from surrounding animals or humans (e.g., in contact with same pool of water/urine/other conductive medium) Ventricular fibrillation > 10 minutes’ duration
EQUIPMENT, ANESTHESIA Clippers for hair Defibrillator; ideally, combined defibrillator-electrocardiograph to avoid risk of electrical damage to stand-alone ECG machine Defibrillation coupling gel
ANTICIPATED TIME About 1 to 10 minutes
PREPARATION: IMPORTANT CHECKPOINTS Is it ventricular fibrillation? ECG shows coarse or fine patternless electrical activity with no synchronized activity (no QRS complexes) when ventricular fibrillation is present. If the animal is conscious, the rhythm is not ventricular fibrillation. If a pulse is palpable, the rhythm is not ventricular fibrillation. Is the animal prepared correctly? Dorsal or lateral recumbency on a dry, insulated surface (e.g., foam mat or linoleum floor) Hair clipped from both hemithoraces over heart (fourth through sixth intercostal spaces [ICS], right and left) Note: The limbs of the animal will flail when the shock is administered, and any objects (e.g., monitoring instruments, drug bottles, etc.) in their trajectory must be removed prior to shock delivery.
POSSIBLE COMPLICATIONS AND COMMON ERRORS TO AVOID Electric shock can be transmitted to bystanders. Note: This complication can cause cardiac arrest in human or animal onlookers. This result is best avoided by ensuring that no one is in contact with the animal or anything the animal is touching before delivering a shock. It is also important to ensure that no indirect contact from urine, saline, or any other fluids that may be trickling from the animal is occurring between the animal and the shoes of surrounding individuals. Shouting “clear” is not enough, since most people do not know what to do in response. Defibrillation is too late. The success of defibrillation approaches 100% when it is performed within the first minute of ventricular fibrillation, then decreases by 10%-15% per minute. Defibrillation is the most important treatment when there is ventricular fibrillation, and some have suggested revising the “ABCs” of resuscitation to the “DABCs,” with D for defibrillation. Poor application of paddles on animal Paddles must be set widely apart (i.e., one on each side of the thorax); if too close, an electric arc between them can cause severe skin burns and operator injury.
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Defibrillator gel must be applied between the defibrillator paddles and the animal's skin. Note: Any facility that owns a defibrillator must also own a tube of defibrillator gel, because alternatives are inadequate: ultrasound gel is contraindicated (nonionic/nonconductive), alcohol is flammable, and bare skin without a coupling agent can be burned by electric arcs.
PROCEDURE The animal is placed in lateral or dorsal recumbency. Rapid clip of hair over the left and right precordia (area of chest overlying the heart): 20 seconds. The ECG diagnosis of ventricular fibrillation is confirmed: Animals with ventricular fibrillation are always unconscious (nonperfusing rhythm) and pulseless. Alcohol or gel must be present at all points of contact between the ECG wires/clips and the animal (to rule out poor connection artifact/“pseudofibrillation”). Click from leads I to II and then to III on the ECG monitor to check for organized electrical cardiac activity in any lead. If present, defibrillation is contraindicated. The defibrillator is charged: 5 J/kg. Defibrillator gel is smeared on the surface of both paddles. The paddles are applied to the thorax: paddle marked “Left” or “Apex” is on left hemithorax, and paddle marked “Right” or “Sternum” is on the right. All onlookers and assistants must stand back and be neither in direct nor indirect contact with the animal. The only contact point between the animal and the person administering the shock is the paddles. The shock is delivered. The ensuing ECG rhythm is assessed immediately.
DEFIBRILLATION, ELECTRICAL Typical defibrillator. Paddles are clipped to side of unit, and screen displays both electrocardiographic (ECG) information and defibrillation charge (at 200 J in image). Controls for energy selection, charging, and shock administration on front panel are also present as finger controls directly on the paddles (not shown).
DEFIBRILLATION, ELECTRICAL Tube of defibrillator gel.
POSTPROCEDURE If the rhythm still appears to be ventricular fibrillation, it should be quickly confirmed (check other ECG leads on the monitor, and
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ensure ECG connection between animal and machine is good); if confirmed, defibrillation is immediately warranted once again at 8 J/kg. Up to 12 J/kg may be administered. When the rhythm is any other than defibrillation, standard cardiopulmonary resuscitation procedures are followed (see p. 1223).
ALTERNATIVES AND THEIR RELATIVE MERITS Precordial thump (physical blow to the chest): theoretically delivers physical “equivalent” of electrical shock; unproven value, many potential drawbacks, and never preferred over electrical defibrillation. Pharmacologic defibrillation (bretylium, potassium chloride/calcium chloride, etc.): unproven and not known to be widely successful in the clinical setting. AUTHOR: ETIENNE CÔTÉ
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Excretory Urogram SYNONYMS IVP, intravenous (IV) pyelogram, IV urogram
OVERVIEW AND GOALS When the kidneys are difficult to assess by plain-film radiography or when qualitative renal functional information is needed, an excretory urogram could be performed. On survey abdominal radiographs, the renal silhouette may not be visualized in animals that have decreased abdominal detail (young, thin, peritoneal fluid).
INDICATIONS Identify kidneys (if poor abdominal detail) Mass lesions of kidneys (or mass in region of kidney) Qualitative assessment of renal function Patency, continuity of urinary tract Prior to nephrectomy Abnormal renal size, shape Persistent hematuria Suspected renal or ureteral calculi Suspected hydronephrosis Suspected ureteral ectopia, ureterocele Suspected ureteral rupture To evaluate the urinary bladder when it cannot be catheterized Postoperative assessment of urinary tract (patency, strictures, leakage)
CONTRAINDICATIONS Dehydration Previous reaction to iodinated contrast medium (a nonionic medium should be used) Caution should be used in animals with the following conditions: Diabetes mellitus Multiple myeloma Congestive heart failure Hypertension Concurrent drug administration (cardiac glycosides) Severe debilitation
EQUIPMENT, ANESTHESIA Many recommend the use of general anesthesia or heavy sedation; however, an excretory urogram can be performed in an unanesthetized animal. IV catheter Hair clippers Surgical scrub solution, rubbing alcohol, and gauze/sponges for prepping skin where catheter is placed Tape/releasing elastic (Vetrap-type) bandage Iodinated contrast medium (sodium iothalamate, sodium diatrizoate) Nonionic contrast medium (iohexol, iopamidol) if clinically warranted Syringe Heparin/saline for flush Enema set Antianaphylactic agents (e.g., diphenhydramine, 2-4 mg/kg for IM injection) Oxygen and a drug cart to address any possible complication during the procedure.
ANTICIPATED TIME Approximately 1 hour
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PREPARATION: IMPORTANT CHECKPOINTS The owner should be advised that hair will be removed from the site of IV catheter placement. Animal should have fasted 24 hours. Water given ad libitum Enema given at least 2 hours prior to study to remove a maximum of the fecal material from the colon to allow visualization of kidneys and ureters Assess hydration: proceed only if normal. Clip the hair where the IV catheter is to be placed. The site for the catheter placement should be prepped with surgical scrub solution, rubbing alcohol, and gauze sponges. Place an IV catheter in a cephalic or jugular vein; it is imperative that the catheter be properly placed. Secure the catheter in place with tape or releasing elastic (Vetrap-type) bandage. Add 900 mg iodine per kg body weight contrast material into syringe. Add an appropriate amount of heparin/saline flush into syringe.
POSSIBLE COMPLICATIONS AND COMMON ERRORS TO AVOID Vomiting: this often occurs immediately after injection of the contrast medium. If the animal is muzzled, the muzzle should be removed immediately to avoid aspiration. Systemic hypotension, bradycardia Anaphylaxis (airway edema, vascular collapse, bronchospasm) Perivascular injection may result in sloughing of surrounding tissue. Contrast media–induced renal failure The administration of iodinated contrast media may affect urine specific gravity, urine sediment, and urine culture results for 24 hours following administration. Blood values (blood urea nitrogen [BUN], creatinine, prothrombin time [PT], partial thromboplastin time [PTT], activated partial thromboplastin time [APTT], thromboplastin time [TT], and hematocrit) might also be affected for up to 24 hours after contrast administration.
PROCEDURE Preliminary abdominal radiographs are made to determine adequate animal preparation and to set radiographic technique.
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EXCRETORY UROGRAM Excretory urogram, ventrodorsal view. Normal study. Both kidneys and both ureters are clearly seen; contrast material is also seen in urinary bladder (right of midline). L, Left.
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EXCRETORY UROGRAM Excretory urogram, ventrodorsal view. Ectopic ureter (left side), normal ureter (right side). Ectopic ureter is diffusely enlarged (hydroureter), especially distally where it inserts in an ectopic location (arrow). L, Left.
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EXCRETORY UROGRAM Excretory urogram, ventrodorsal view. Pyelonephritis (right side). Right-sided hydronephrosis and severe hydroureter are apparent. L, Left. The kilovoltage peak (kVp) should be set between 65 and 75 to maximize contrast due to the photoelectric effect (K-edge of iodine). Flush the catheter to again ensure patency. Inject contrast material rapidly as a bolus. Flush the catheter of residual contrast material. A ventrodorsal view is obtained at 20 seconds. Ventrodorsal and right lateral views are obtained at 5 minutes, 20 minutes, and 40 minutes. Oblique views are obtained at 5 minutes to visualize ureteral termination at the urinary bladder.
POSTPROCEDURE If anesthesia is used: routine anesthetic recovery Maintain adequate hydration. The IV catheter should remain in place for at least 15-20 minutes after the study is completed. The port for venous access might be necessary should a contrast media adverse reaction occur. Remove the catheter > 20 minutes after the procedure.
ALTERNATIVES AND THEIR RELATIVE MERITS Plain abdominal radiographs: inexpensive means to survey the abdomen. Radiopaque renal or ureteral calculi can be visualized. Size and shape of the kidneys can be assessed if abdominal detail is adequate and fecal material is not obscuring their visualization. Abdominal ultrasound: excellent potential for visualization of kidneys, especially in animals that show poor radiographic abdominal detail. Renal size, shape, position, and echogenicity relative to the liver and spleen can be assessed. The size of the renal pelvis can also be evaluated. The internal architecture of the kidneys can be assessed. Ultrasound can determine if
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masses are solid or cystic in nature. Resistive index can be calculated. CT scan: provides excellent detail of the size, shape, and margination of the kidneys. IV contrast media can also be used to enhance findings in the kidneys and or ureters. This imaging modality can also be used for assessing renal vascular anatomy when screening feline renal transplant donors. CT scans, however, are more costly to perform than other studies already listed and require general anesthesia. Nuclear scintigraphy: Diethylenetriaminepentaacetate (DTPA): to determine global and individual kidney glomerular filtration rates; to evaluate the animal's response to treatment; to evaluate function of contralateral kidney prior to surgery and possible removal of diseased kidney; to identify and determine the severity of subclinical renal disease in an animal receiving nephrotoxic agents; and to examine renal perfusion by obtaining rapid serial images during first pass circulation Mercaptoacetyltriglycine (MAG3): to determine global and individual kidney effective renal plasma flow AUTHOR: LEEANN PACK
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Ethanol Ablation of Thyroid and Parathyroid Tumors
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Ethanol Ablation of Thyroid and Parathyroid Tumors SYNONYMS Percutaneous ethanol injection, PEI, chemical ablation
OVERVIEW AND GOALS Ethanol ablation, under ultrasound guidance, has been used most commonly in veterinary medicine for the minimally invasive treatment of parathyroid tumors. Additional reported uses of this procedure include benign thyroid tumors in cats, as well as other tumors, and renal, liver, and pancreatic cysts. The goal of this procedure is to eliminate the detrimental secretory function of a benign endocrine tumor in a minimally invasive fashion.
INDICATIONS For parathyroid ablation in cases of primary hyperparathyroidism (PHPT). For thyroid ablation, consider in cases of feline unilateral hyperthyroidism or feline thyroid cysts.
CONTRAINDICATIONS There are few contraindications to percutaneous ethanol injection (PEI) therapy in hyperparathyroid dogs. Successful therapy does require a large enough nodule (typically over 3-4 mm in diameter), a skilled ultrasonographer, and advanced ultrasound equipment. It should not be attempted if these criteria are not met. It should also not be attempted in multiple nodules at the same time, especially bilaterally, for fear of transient laryngeal swelling and dysfunction after the injection. PEI has not worked well in cats with bilateral thyroid disease and should also never be performed bilaterally in cats. It can be considered as an alternative to surgery, radioiodine therapy, or methimazole in cats with unilateral hyperthyroidism.
EQUIPMENT, ANESTHESIA Intravenous or inhalant general anesthesia High-quality ultrasound equipment with a high-frequency probe (at least 10 MHz) and an ultrasonographer experienced at evaluating cervical structures and aspirating small nodules in an accurate fashion 96% ethanol At least one 2.5- to 3-mL syringe Low-flow extension set 25- to 27-gauge 1½-inch needles
ANTICIPATED TIME The procedure itself lasts seconds once the needle has been properly inserted into the parathyroid nodule. Depending on the experience and expertise of the ultrasonographer, the size of the nodule, and the ultrasound equipment, 30 minutes to an hour are a reasonable time frame for completion of the procedure.
PREPARATION: IMPORTANT CHECKPOINTS The diagnosis of primary hyperparathyroidism should be confirmed utilizing ionized calcium and PTH testing and by ruling out other causes of hypocalcemia. The dog's neck should then be examined ultrasonographically, and the parathyroid nodule should be definitively located and measured. The dog should then be anesthetized and placed in dorsal recumbency for the procedure, with the ventral aspect of the neck clipped. 1 mL of 96% ethanol should be prepared with no air bubbles and attached to a 25- to 27-gauge 1½-inch syringe, and a low-flow extension set should be placed between the needle and syringe and primed with ethanol prior to injection. In the case of a hyperthyroid cat, unilateral hyperthyroidism should be confirmed based on hormonal testing and nuclear scintigraphy. Once confirmed, the preparation is identical to dogs with PHPT.
POSSIBLE COMPLICATIONS AND COMMON ERRORS TO BE AVOIDED Possible errors include: Not offering owners surgery as an alternative to injection. This is especially true if there is concurrent urolithiasis or another reason to have surgery.
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Ethanol Ablation of Thyroid and Parathyroid Tumors
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Attempting to inject a nodule that is too small, without the right equipment, experience, or expertise and without proper anesthesia or sedation Not properly identifying the parathyroid nodule and differentiating it from the carotid artery, which can look very similar in a crosssection ultrasonographic view of the cervical region. The nodule must be round or elliptical in the longitudinal plane as well and ideally should also be documented to have no laminar flow using color-flow Doppler. Assuming the tip of the needle is in the nodule and the injection will be successful without a proper test injection. Once the area has been infiltrated with a large amount of ethanol around the nodule, it becomes very hard to visualize the nodule or the needle, and the attempt often must be aborted.
PROCEDURE The parathyroid or thyroid nodule is definitively identified and differentiated from the carotid artery. A 25- or 27-gauge needle attached to an extension set and syringe and filled with 96% ethanol is carefully advanced into the nodule under ultrasound guidance. Once the tip of the needle is thought to be in the center of the nodule, a small test dose of alcohol (less than 0.1 mL) is given. This should produce a small, white, hyperechoic “cloud” within the nodule that should not be seen dispersing rapidly along tissue planes. If there is a doubt that the tip is not in the nodule, the needle should be removed from the nodule and repositioned and the test dose repeated. If the tip of the needle appears to be within the nodule, the ethanol should be injected until all parts of the nodule become hyperechoic. This may require slight repositioning of the needle in a large nodule. Within approximately 10 minutes, the injected area will become hypoechoic, so the decision whether the nodule has been completely filled with ethanol or not must be done within that time frame after starting the injection. When the filling is complete, the needle is removed, and the animal can be recovered.
POSTPROCEDURE No life-threatening or persistent complications have ever been observed following this procedure in dogs. Transient unilateral laryngeal swelling/paresis and Horner's syndrome can occur and tend to resolve within 1-4 days. Bilateral injections should not be attempted due to the risk of bilateral postprocedure laryngeal swelling. Dogs with PHPT should be monitored closely for 5-10 days after ablation for signs of hypocalcemia and should be supplemented as necessary with calcium and vitamin D. Clinical decision-making regarding calcium and vitamin D supplementation, as well as postinjection calcium monitoring, is the same as when surgical parathyroidecto mies are performed for the definitive treatment of PHPT.
ALTERNATIVES AND THEIR RELATIVE MERITS PEI is only one way to definitively treat PHPT. Alternatives are surgical removal of the parathyroid nodule or nodules and percutaneous heat ablation, which is performed in a similar fashion to PEI, but heat rather than ethanol is used to necrose the tissue via the inserted needle. Surgery is still the gold standard and should always be offered as such to the owner. Heat ablation may be superior to ethanol ablation in terms of fewer transient effects of the leakage of ethanol into the surrounding tissue but does require additional specialized equipment. The advantages of both heat ablation and PEI over surgery include shorter anesthetic time, a more rapid recovery, and less surgical healing or scar formation. Their disadvantage, in addition to the occasional transient local side effects of PEI, is the potential to fail, meaning the needle will not be properly inserted or the nodule will not be completely destroyed. Another disadvantage to the two less invasive options is that no tissue is obtained; hence the tumor cannot be classified histologically. Since almost all parathyroid tumors behave in a benign fashion regardless of their histopathologic features, this is not as severe a disadvantage as it would be in the case of other neoplasms.
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Ethanol Ablation of Thyroid and Parathyroid Tumors
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ETHANOL ABLATION OF THYROID AND PARATHYROID TUMORS Anesthetized dog properly positioned in dorsal recumbency and prepared for percutaneous ethanol injection.
ETHANOL ABLATION OF THYROID AND PARATHYROID TUMORS Ultrasound image of a parathyroid nodule, with the thyroid gland, in a dog with primary hyperparathyroidism.
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Ethanol Ablation of Thyroid and Parathyroid Tumors
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ETHANOL ABLATION OF THYROID AND PARATHYROID TUMORS Ultrasonographic images of percutaneous ethanol injection (PEI) therapy in a dog with primary hyperparathyroidism. A, Needle entering the parathyroid nodule, with tip clearly visible within the nodule. B, Test dose of ethanol being injected, and hyperechoic material remaining within the nodule. C, Parathyroid nodule has been completely infiltrated with ethanol immediately following successful PEI therapy.
SUGGESTED READING Goldstein RE, Long C, Swift NC, et al: Percutaneous ethanol injection for treatment of unilateral hyperplastic thyroid nodules in cats. J Am Vet Med Assoc 218(8):1298–1302, 2001. Long CD, Goldstein RE, Hornof WJ, et al: Percutaneous ultrasound-guided chemical parathyroid ablation for treatment of primary hyperparathyroidism in dogs. J Am Vet Med Assoc 215(2):217–221, 1999. Schaefer C, Goldstein RE: Canine primary hyperparathyroidism. Compend Contin Educ Pract Vet 31(8):382–390, 2009. AUTHOR: RICHARD E. GOLDSTEIN
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Epidural Analgesia/Anesthesia
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Epidural Analgesia/Anesthesia SYNONYM Extradural blockade
OVERVIEW AND GOALS Administration of drugs into the epidural space to provide decreased sensory and sympathetic pain transmission modulation (analgesia) and/or complete motor blockade (anesthesia). Drugs can be administered in one dose (single shot) repetitively or by continuous infusion: Epidural analgesia: injection of an opioid a phencyclidine an alpha-agonist or a nonsteroidal antiinflammatory drug (NSAID) Epidural anesthesia: injection of a local anesthetic
INDICATIONS Caesarean section thoracostomy pelvic or hind limb orthopedic manipulations amputations (forelimb and hind limb) abdominal procedures tail or perineal procedures diaphragmatic repair pancreatitis peritonitis intervertebral disk disease (IVDD) thoracic trauma Advantages: Lengthy quick-onset analgesia Few systemic side effects for acute/chronic medical or surgical pain Reduced requirements for parenteral and inhalant drugs Alternative to general anesthesia for animals at high risk (American Society of Anesthesiologists III IV V E categories; see p. 1372) Adjunct to balanced anesthesia regimes
CONTRAINDICATIONS Absolute contraindications: Coagulopathy/bleeding disorder Localized infection/inflammation over entry to epidural space Increased intracranial/intraspinal pressure (head trauma space-occupying mass) Risk of or present severe respiratory depression (phrenic nerve injury tentorial herniation) Relative contraindications (requires alteration of dose frequency drugs or placement site): Urinary retention Meningitis encephalitis diskospondylitis Severe anatomic/neurologic disturbance or obesity at landmarks Inexperienced administration Contraindications for use of local anesthetics in epidurals: Uncorrected hypovolemia Vasodilatory shock Severe clinical cardiac disease or liver impairment (third-spaced fluid disease ascites) Acute renal failure Sympathetic disturbance (e g autonomic disease dysautonomia) Use of potent systemic vasodilators
EQUIPMENT, ANESTHESIA Most animals that receive an epidural are heavily sedated or under general anesthesia at the time of administration. Premedication with both anxiolytic and analgesic drugs (opioid, alpha-agonist) is recommended even if continued progression into general anesthesia is not anticipated, owing to the pain of positioning, approach, and administration of epidural agents. Equipment: Hair clippers Surgical scrub solution, isopropyl alcohol or saline, gauze/sponge
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Epidural Analgesia/Anesthesia
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Epidural or spinal needle (Quincke, Husted, or Tuohy needles); 22- to 20-gauge, 1½- to 3½-inch small hypodermic needles (22 gauge, ½-1½ inch) can also be used for tiny animals. Sterile gloves Sterile saline “Test syringe” for saline and air mix Syringe for administration of combination of local and/or opioid A few 20-gauge needles (used for withdrawing drugs from vials) Local anesthetics for epidural injection: 0.5% bupivacaine, 2% lidocaine, or 0.75% ropivacaine (all must be preservative- and epinephrine-free) Opioids for epidural injection: morphine, preferably preservative free (Duramorph, Astramorph, preservative-free morph), but parenteral morphine has been used for single-dose injection without complications anecdotally; buprenorphine, oxymorphone, hydromorphone, dexmedetomidine, and ketamine may also be utilized. A second operator (assistant) to allow strict attention to aseptic technique For epidural catheterization, the following will also be required: Blunt-tipped, lateral-faced opening needle with curved bevel (Tuohy needle) Continuous or indwelling epidural catheter Injection port with screw or lock fitting to avoid inadvertent disconnection Sterile scissors to tailor-cut the catheter to proper length Microfilter Sterile covering for site and/or part/total catheter (Tegaderm) Suture material (3-0 nylon or other monofilament, nonabsorbable suture) Needle holders Suture scissors
ANTICIPATED TIME Experienced operator: 3-5 minutes Inexperienced operator, anatomic/animal positioning issues, dermatologic uncleanliness: 20 minutes
PREPARATION: IMPORTANT CHECKPOINTS Base doses on lean body weight. Review anatomy for placement of entrance needle: most epidurals are performed at the lumbosacral junction because the cord terminates cranial to this area in dogs and near this area in cats; however, epidurals can be administered at any intervertebral space if lumbosacral (LS) access is limited. Consider ratio of each component: opioid, local anesthetic, alpha agent, ketamine, and/or others. Positioning of animal: sternal with hind legs pulled fully cranially under body or else flexed and stable under pelvis (“froglegged”). Aged, debilitated, or traumatized animals may be uncomfortable in either position, so lateral positioning is also used. Obese animals are best placed in sternal, not only because of ease in identifying LS space but also because oxygenation and ventilation may be optimal. Premedication: Medetomidine, 0.005-0.01 mg/kg (5-10 mcg/kg) IM or IV Can also instead use a combination of anxiolytic plus analgesic: anxiolytic (acepromazine, 0.02-0.05 mg/kg IM or IV; or midazolam, 0.2-0.5 mg/kg IM or IV), plus analgesic (hydromorphone, 0.1 mg/kg IM or morphine 0.5-2 mg/kg IM)
POSSIBLE COMPLICATIONS AND COMMON ERRORS TO BE AVOIDED The following can be seen with technical difficulty in prepping or identifying (finding) the epidural space: infection, hemorrhage, spinal or nerve root trauma. The following can be seen with use of certain agents: respiratory depression, urinary retention, pruritus, nausea and vomiting (opioids), motor paralysis, systemic vasodilation (lidocaine or high doses of bupivacaine/ropivacaine). Subarachnoid injection frequently results in superb analgesia but can cause respiratory and cardiac arrest or seizures with cranial advancement of drugs.
PROCEDURE The lumbosacral space is identified by palpating the most cranial dorsal aspects of each ilial wing, drawing an imaginary line between wings, and palpating the spinous process of L7 caudal to this line. The spinous process of L7 is smaller and shorter than that of L6 and, as such, is often more difficult to find. Staying directly on midline, the site of entry (LS space) is identified by placing a fingertip on the spinous process of L7 and gently rocking the finger caudally into the depression behind the process. The needle entry site is within this depression. The animal is positioned appropriately, the approximate LS area clipped, then aseptically prepped three times using
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Epidural Analgesia/Anesthesia
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alternating chlorhexidine scrub and saline. Sterile gloves are unwrapped, and the paper sleeve is used as a sterile field; syringes, needles, and instruments are opened on the sleeve around the gloves. Epidural drugs are aseptically drawn into a syringe; dosages: some clinicians prefer combined local anesthetic bupivacaine, 0.1-0.3 mg/kg (motor sparing at 0.5%), with morphine, 0.02-0.1 mg/kg, for canine patients. This combination can be diluted to a total volume of 0.1-0.15 mL/kg with saline if advancement of the solution into the thoracic area is needed (thoracotomy, forelimb amputation, diaphragmatic repair, etc.). Total volume rarely exceeds 6 mL of saline, local, and opioid combined for canine patients for an injection made from the lumbosacral space. Injections made more cranially are reduced in volume by 25% per four to five vertebral bodies. Saline addition to the mixture is dictated by need for cranial spread of the agents. For cats, 0.02-0.1 mg/kg morphine is diluted with saline to a total volume of 0.1-0.2 mL/kg. Local anesthetic is rarely used because of the propensity to administer this into the subarachnoid space and the increased toxicity potential in this species. Both species: 0.5-2 mL saline with 0.5-2 mL of air are drawn into another syringe, which will act as an epidural space “tester” or identifier. TECHNIQUE OF EPIDURAL INJECTION: Clinician approaches the patient from behind (facing in the same direction as the patient) if sternal recumbency, or from either behind or dorsal (the side of the table/hip against the patient's back, facing caudally) when the patient is in lateral recumbency. Brace the hand holding the needle on the patient's back. Use the other hand to identify the LS space as outlined above. The needle is then advanced transcutaneously at a 90○ angle to the skin surface over the LS site. The primary source of resistance is the dorsal spinous ligament, the ligamentum flavum. This is the hardest layer to penetrate and millimeter depth pushes are required to realize first, entry into the ligament, and second, the classic “loss of resistance” or “pop” as the epidural space is entered ventral to the ligament. Many clinicians will remove the stylet from the needle once ligamentum resistance is palpated, and add a small amount of saline to the hub of the needle in order to ascertain entry below the ligamentum. Once the ligamentum is penetrated, the hub of the needle is inspected for presence of blood or cerebrospinal fluid (CSF): If blood is seen, the needle tip is partially redrawn and redirected. If CSF is encountered, the needle is probably within the subarachnoid space, and should be withdrawn slightly. If no blood or CSF is seen, assurance of epidural space is made by: Loss-of-resistance technique: the syringe containing the saline and air is attached to the hub of the needle. The syringe plunger is then depressed. If there is no increase in resistance to pushing the plunger, the needle is correctly positioned in the epidural space. If the air bubble in the syringe is compressed or pushed against the saline as the plunger is depressed, the needle tip lies in the paraligamentous tissue, and the placement is incorrect. Hanging drop technique: when the ligamentum flavum is encountered—the first sign of resistance—the stylet is withdrawn and the hub is filled with saline so the liquid forms a meniscus. As the space is entered, the normally negative pressure will cause aspiration down the needle shaft, and the fluid and meniscus will disappear. Once the correct positioning is confirmed, the injection proceeds over a 30-60 second time frame. Often, respiratory and cardiac rate increase during injection.
EPIDURAL ANALGESIA/ANESTHESIA Lumbosacral region of dog in left lateral recumbency. On the dorsal midline, the caudal-most dorsal spinous process, L7, is palpated (clinician's left hand). This process, shorter and smaller than that of L6 (clinician's right hand), is located caudal to an imaginary line that joins the most cranial dorsal aspects of both iliac crests. The point of epidural entry is the lumbosacral space, which is directly caudal to the dorsal spinous process of L7.
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Epidural Analgesia/Anesthesia
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TECHNIQUE OF EPIDURAL CATHETERIZATION: Once the needle enters the space, the bevel of the needle must face cranially. The catheter is then threaded down the needle. Catheter advancement should proceed without resistance. The catheter should never be withdrawn into the needle because of the possibility of shear/breakage. Once the catheter is advanced to the appropriate space, the needle is then withdrawn over the catheter. A section of skin adjacent to the site of entry is then penetrated with the needle. The needle is tunneled parallel to the surface of skin for 1.5-2 cm and then exits the skin. The catheter's free end is then fed retrograde up the needle. The needle is then withdrawn, and the catheter is effectively “tunneled” away from the epidural site. This provides for decreased chances of bacteremia/infection in the epidural space. Excess catheter length is cut from the catheter, using sterile scissors. The filter and injection port are secured. The epidural medications are then administered through the catheter, with the amount reduced to accommodate for placement of catheter tip. The catheter cap and filter are secured with suture. A protective sterile covering is placed over the catheter and LS space.
POSTPROCEDURE Onset of analgesia varies from immediate for lidocaine epidurals, to 30-60 minutes for bupivacaine epidurals, to 2-4 hours for morphine and oxymorphone epidurals. Duration of analgesia varies from 1 hour for lidocaine epidurals, to 3-6 hours for bupivacaine epidurals, to 12-15 hours for morphine epidurals. Pain of injection is severe with local anesthetics and ketamine. Some clinicians strongly suggest utilizing each as diluted solutions only and administering bupivacaine only if the animal is under the influence of heavy sedation/analgesia or is anesthetized. Vomition, nausea, and drooling are common when catheters are placed in the thoracic spinal canal, when heavy volumes or concentrated morphine is used, or when pain/sudden hypotension is sensed during an injection (“awake bupivacaine epidurals”). The injection cap, filter, and dressing should be replaced every 72-96 hours using aseptic technique in catheters that are routinely used (q 12 h to q 8 h treatments). Swelling or pain over the tunneled site or, more importantly, over the catheter entry site warrants removal of the catheter. Replacement should then be questioned; alternative analgesic methods are suggested instead.
ALTERNATIVES AND THEIR RELATIVE MERITS General inhalant anesthesia: cardiorespiratory depression; expense Systemic narcotic administration: side effects of gastrointestinal (GI) stasis, respiratory depression, and mild anxiety; expense Recent electrostimulation and ultrasound techniques have allowed placement of blockades very close to nerves, nerve roots, and plexi; these may afford safe, economical, and less technically challenging means to providing analgesia without sympathetic blockade, although they do frequently include motor blockade.
SUGGESTED READING Hansen BD: Epidural catheter analgesia in dogs and cats: technique and review of 182 cases (1991-1999). J Vet Emerg Crit Care 11(2), 2001. Valverde A: Epidural analgesia and anesthesia in dogs and cats. Vet Clin North Am Small Anim Pract 38(6), 2008. www.vasg.org (veterinary anesthesia analgesia support group) AUTHOR: ANDREA L. LOONEY
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Enema: Scintigraphic (Radionuclide)
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Enema: Scintigraphic (Radionuclide) SYNONYMS Nuclear portogram, per rectum portal scintigraphy, transcolonic portal scintigraphy
OVERVIEW AND GOAL Portosystemic shunts (PSS) are a relatively common congenital disorder in dogs and cats. Scintigraphy provides a rapid, noninvasive screening test for this disorder.
INDICATIONS Confirm the presence of a macroscopic PSS Evaluate the effectiveness of previous surgical shunt vessel attenuation Provide limited information regarding the number (single versus multiple) and location (intrahepatic versus extrahepatic) of the PSS vessel(s)
CONTRAINDICATIONS Critical animal condition precluding relative isolation necessary to comply with regulatory requirements
EQUIPMENT, ANESTHESIA Gamma camera and either an analog recorder (microdot) or preferably a nuclear medicine computer are necessary for calculation of shunt fraction.
ANTICIPATED TIME Procedure time of 5 minutes Isolation time (varies by local regulatory agency) of 6-60 hours
PREPARATION: IMPORTANT CHECKPOINTS Animal: No animal preparation is required. Ideally, animals are fed the morning of the procedure. Discontinuation of oral lactulose for 36 hours prior to procedure may improve rectal uptake. Evacuation enemas are encouraged as a form of preparation by some clinicians but may not be routinely used by other clinicians. Radionuclide setup: Prepare a dose of sodium 99m T-pertechnetate (37-74 MBq/kg) in a small volume ( 20 kg: 1 L; dogs > 40 kg: 2 L). Use a funnel and a large tube. Treatment of severe acute hepatic encephalopathy: First perform a cleansing enema to evacuate all remaining colonic content. Retention enema (total amount of 15 mL/kg): allows the delivery of fermentable substrates or colonic pH modification: Lactulose (1:2 dilution with water) Neomycin in water (10-20 mg/kg) An alternative is to use diluted povidone iodine (1:10, rinse thoroughly after 15 minutes). See also Hepatic Encephalopathy, p. 501.
ANTICIPATED TIME About 15-30 minutes
PREPARATION: IMPORTANT CHECKPOINTS Fluid therapy is an essential part of the management of colon impaction. Animals should be well hydrated.
POSSIBLE COMPLICATIONS AND COMMON ERRORS TO AVOID
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Some enemas, such as docusate, can promote GI water loss and should be used with caution if the animal is dehydrated. If enemas are administered too quickly, they can lead to discomfort and vomiting. Enemas should be administered after they are warmed to body temperature. Do not administer mineral oil with docusate. Do not administer sodium phosphate enemas to small dogs or cats, because such enemas can induce dehydration, neurologic signs, and severe hyperphosphatemia, hypernatremia, and hypocalcemia. If the animal has much anal or rectal pain, enemas should be replaced by an extra administration of an oral GI lavage solution. If the animal is not cooperative, sedation or general anesthesia can be necessary.
ENEMA (EVACUATION, RETENTION) Enema tube that is well lubricated before going into the anus. Distal end of tube must be smooth and rounded and not have sharp edges. It is generously lubricated, passed into the anus, and advanced to a maximum point that corresponds to the distance from the anus to the last rib.
ENEMA (EVACUATION, RETENTION) Large volumes of fluid instilled using gravity, a funnel, and tube. This procedure is performed either for preparation for colonoscopy or as a treatment for constipation.
PROCEDURE Slowly insert a very well-lubricated catheter or feeding tube through the anus (10-14 Fr). In cats, a 60-mL syringe and a urinary catheter can be used. Enema solution should be warmed and administered slowly. It may be administered by syringe, or larger volumes may be instilled more easily using a funnel and gravitational flow. When there is no resistance, the tube is inserted for a total length equal to that from the anus to the last rib (pre-measure the tube).
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POSTPROCEDURE Animals usually have diarrhea. If enema administration was unsuccessful, animals with colon impaction may require manual extraction of impacted feces (under anesthesia). After the administration of an oral GI lavage solution, the animal should be kept quiet in a cage to avoid the potential risk of developing gastric dilatation/volvulus. Dogs should be regularly walked on a leash to allow defecation.
ALTERNATIVES AND THEIR RELATIVE MERITS Pediatric suppositories (dosage is 1 to 3, according to body weight [cat/small dog to large dog]) such as glycerol, docusate (Colace), or bisacodyl (Dulcolax) can be used as an alternative to enemas. These are safer than the use of phosphate enemas, especially for cats or smaller dogs. AUTHOR: SYLVIE DAMINET
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Electroretinogram
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Electroretinogram SYNONYM ERG
OVERVIEW AND GOALS Evaluation of retinal function (quantitative or qualitative) through measurement of the electrical response generated after the photoreceptors receive a light stimulus An electroretinogram (ERG) by itself does not determine whether an animal can see; the retina is only one part of the visual system.
INDICATIONS Differentiation of causes of sudden blindness (i.e., sudden acquired retinal degeneration syndrome [SARDS] and optic neuritis) Evaluation of retinal function to determine cataract surgery suitability Identifying inherited retinal disease (i.e., progressive retinal atrophy [progressive rod-cone degeneration] or progressive rod-cone dysplasias) at an early age well before clinical signs and gross retinal changes occur Evaluation of damage incurred by glaucoma or toxic effects of drugs Evaluation of the effects of optic nerve hypoplasia on retinal function
ELECTRORETINOGRAM Normal ERG. The number 1 marks the nadir of the a-wave, and the number 2 marks the peak of the b-wave.
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Electroretinogram
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ELECTRORETINOGRAM ERG from dog with SARDS. No normal waves are detectable.
CONTRAINDICATIONS Panuveitis Corneal ulcer Any contraindication for general anesthesia or sedation
EQUIPMENT, ANESTHESIA Equipment: Gold-foil contact lens electrode or an atraumatic wire electrode (placed in conjunctival cul-de-sac). Contact lens electrodes are used most often. Reference and ground electrodes Standardized light source for light stimulus “Safe” light, red light, or small red penlight Timer for dark adaptation Conducting agent to facilitate electrical contact between the contact lens electrode and the eye; methylcellulose (Gonak) or GenTeal Tear Gel Table; if stainless steel, cover with nonconducting material (rubber padding). Optional: head rest for elevation and positioning of head; this may be made of foam, rolled-up blankets, or sandbags. Anesthesia or sedation: General anesthesia or sedation; some animals will tolerate the procedure with topical anesthesia only (and contact lens electrode), but the risk of artifact is increased. General anesthesia prevents animal movement (artifact source) and allows more precise direction of the light stimulus into the eye via fixation of the eye. Sedation; one of these three protocols can be considered: Acepromazine (0.03 mg/kg IV) and hydromorphone (0.05 mg/kg IV): Observe precautions/contraindications, especially with acepromazine. Diprivan (propofol) 4-6 mg/kg IV to effect (low doses will be sufficient in most cases). Medetomidine (0.005-0.01 mg/kg [dogs, cats] IM) combined with butorphanol (0.2 mg/kg [dogs, cats] IM) Other anesthetic or sedation protocols may be employed; be consistent to aid in correct interpretation of the recordings. General anesthesia and sedation depress the ERG response. Butorphanol is the sedative most likely to depress ERG response. Topical anesthetic (i.e., proparacaine)
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Electroretinogram
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Personnel (two people): One to monitor anesthesia or sedation, position the animal's head, ensure that light stimulus is directed into the eye during the flash, cover the fellow eye, and check to see that all electrodes are in position during test One to run the computer program during the test
ANTICIPATED TIME About 1-1½ hours, including time for pupillary dilation
PREPARATION: IMPORTANT CHECKPOINTS Knowledge of retinal physiology Familiarity with ERG equipment Control of inflammation; especially important in a precataract surgery evaluation. Lens-induced uveitis will decrease ERG amplitudes. Dilation of pupils Bleaching of retinal pigments in rods by exposure to bright light before dark adaptation Dark adaptation (4 minutes minimum, 20 minutes desirable) Lock room to avoid inadvertent exposure to light and necessity of starting procedure again. Use grounded outlet to decrease/eliminate 60-cycle interference. Take off wristwatch to decrease 60-cycle interference. Set up computer, supplies, equipment before dark adaptation.
POSSIBLE COMPLICATIONS AND COMMON ERRORS TO AVOID POSSIBLE COMPLICATIONS: Corneal ulcers, especially in diabetics with decreased corneal sensitivity and increased risk of corneal ulceration Hypoxemia or death due to failure to monitor animal during general anesthesia COMMON ERRORS: Preparation errors: Failure to dilate pupils fully Procedural errors: Failure to direct light stimulus directly into eye Failure to prevent “light spill” into fellow eye while recording “first” eye; this decreases amplitude of “second” eye by bleaching retinal pigments. Error in labeling which eye is which on recordings Lack of standardized protocol for specific model of equipment on premises Lack of standardized anesthesia/sedation, leading to difficulty in interpretation of results Excess noise due to failure to use signal averaging and filters Excess muscle fasciculations in eyelids due to inadequate sedation, leading to excess noise in the readings. The use of an eyelid speculum exacerbates muscle activity due to muscle stretching. Dull electrode needles Gap in gold-foil electrode ring on contact lens electrode, leading to inaccurate reading or artifact Expulsion of contact lens or reference electrodes during procedure, leading to artifact or inaccurate reading 60-cycle interference caused by lights, appliances in same room, using a non-insulated table “Stray” light stimulus from computer monitor during procedure, leading to lower amplitude readings Animal-derived errors: Eyes are closed, leading to very low amplitude readings. Blinking during light stimulation, leading to low amplitude readings Third eyelid is prolapsed, expelling the contact lens or leading to very low-amplitude readings due to the failure of light to reach retina. Interpretation errors: Misinterpretation of findings due to lack of knowledge of retinal physiology and basis of the test
PROCEDURE
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Dilate pupils with short-acting mydriatic (i.e. tropicamide) 30 minutes before sedation. Sedate or induce general anesthesia as necessary. Place reference electrode in skin over ipsilateral zygomatic arch, 5 cm distal to lateral canthus. Place ground electrode in skin over top of muzzle. If dog must be muzzled, place ground electrode in skin on forehead. If electrode needles do not go into skin easily, discard and use new electrodes to avoid discomfort to animal and increase accuracy of reading. Dark adapt patient for minimum of 4 minutes, optimum of 20 minutes. Place topical anesthetic in eye. Place conducting gel on concave surface of contact lens. Place contact lens in eye, ensuring that the lens is centered on the cornea and not on top of the nictitating membrane. Perform standardized protocol. Protocols are available in ERG units’ software. To determine rod function, important in progressive rod-cone degeneration, a blue filter under scotopic conditions must be used. Use signal averaging. This produces an averaged response after a predetermined number of flashes (5-10) and enhances the signal-to-noise ratio. Use band-pass filters to screen out unwanted frequencies. A normal ERG consists of a low-amplitude negative a-wave 10-12 msec after the light stimulus, followed by a large positive b-wave. In some tracings, the c-wave (a third wave) is seen as a positive deflection. The a-wave is produced by the photoreceptors and the b-wave by movement of potassium in and out of Müller cells and indirectly by bipolar cells.
POSTPROCEDURE Remove electrodes from eye and skin. Soak contact lens electrode in distilled water; do not rub the inside surface of the lens to clean it, because this action will remove the gold-foil circle, rendering it useless. Flush eye with sterile eye wash and stain for corneal ulcer. Partially reverse butorphanol sedation with naloxone, or recover from general anesthesia. Measure amplitude of recordings, the amplitude from the nadir (lowest point) of the negative a-wave to the peak of the positive b-wave. Record findings on a separate disc or CD for a backup copy, and print hard copy for animal's record.
ALTERNATIVES AND THEIR RELATIVE MERITS Genetic testing for inherited retinal disease: Many tests are available for specific dog breed–related inherited retinopathies but not for all breeds. Only requires blood test, so simpler than ERG Maze test under photopic and scotopic conditions: May be gross screening test for retinal atrophy Unable to determine anatomic source of defect in sudden blindness cases
SUGGESTED READING Komaromy AM, Brooks DE, Dawson WW, et al: Technical issues in electrodiagnostic recording. Vet Ophthalmol 5(2):85–91, 2002. Mentzer AE, Eifler DM, Montiani-Ferreira F, et al: Influence of recording electrode type and reference electrode position on the canine electroretinogram. Doc Ophthalmol 111(2):95–106, 2005. Sims MH: Electrodiagnostic evaluation of vision. In Gelatt KN, editor: Veterinary ophthalmology. Baltimore, 1999, Lippincott, Williams & Wilkins, pp 484–504. AUTHOR: NANCY B. COTTRILL
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Electromyography (EMG) and Motor Nerve Conduction Velocity (NCV)
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Electromyography (EMG) and Motor Nerve Conduction Velocity (NCV) SYNONYMS Electrodiagnostics; EMG, NCV
OVERVIEW AND GOALS Integral component of diagnostic evaluation of animals suspected of having neuromuscular disorders (neuropathy, myopathy, neuromuscular junctional disease). May confirm and characterize the presence of nerve, neuromuscular junction, or muscle disease in these animals. If the EMG is abnormal, a neuromuscular disease is present but a normal EMG does not rule out the possibility of a neuromuscular disease. Useful for differentiating denervation from disuse atrophy. Is very sensitive but not very specific. Generally part of a diagnostic workup that may also involve nerve and muscle biopsy, cerebrospinal fluid (CSF) analysis, laboratory testing (serology, endocrine testing, measurement of metabolites), radiographs and advanced imaging (MRI or CT).
INDICATIONS Animals with clinical signs and neurologic examination suggestive of neuromuscular disease (diffuse or focal). Animals with peripheral nerve injuries. May help confirm the presence of endocrine disease (hyperadrenocorticism-pseudomyotonia).
CONTRAINDICATIONS Electrodiagnostics require general anesthesia, so relative contraindications include megaesophagus or severe weakness (hypoventilation).
EQUIPMENT, ANESTHESIA General anesthesia and tracheal intubation are required. For sensory nerve conduction studies in which paralysis with atracurium is required, a ventilator is needed. Should ideally be performed in electrically shielded room to minimize background noise. Differential amplifier, computer with appropriate software for labeling and calculations, needle electrodes for stimulating and recording impulses (concentric needle electrode preferred for electromyography [EMG]), isopropyl alcohol, and measuring tape. Surgical pack: often, muscle and nerve biopsies (see p. 1305) are done following electrodiagnostics. In some cases, percutaneous endoscopic gastric (PEG) tube placement (see p. 1270) is beneficial while animal is anesthetized (providing nutritional support, administering medications, etc.).
ANTICIPATED TIME EMG: 10–20 minutes EMG + nerve conduction velocity (NCV): 40-60 minutes
PREPARATION: IMPORTANT CHECKPOINTS Monitor body temperature and prevent hypothermia, which prolong nerve conduction times (1.8 m/s drop for every 1°C drop in limb temperature). Draw blood for chemistries prior to procedure, as EMG will cause a transient increase in CK.
POSSIBLE COMPLICATIONS AND COMMON ERRORS TO AVOID Complications related to anesthesia Regurgitation and aspiration pneumonia in animals with megaesophagus/ esophageal dysfunction or dysphagia
PROCEDURE Animal is premedicated, anesthetized, intubated, and then maintained with inhalational anesthetic (isoflurane, sevoflurane). Placed in lateral recumbency EMG: Needle electrodes are used for recording electrical activity in major muscle groups in appendicular muscles and in epaxial and masticatory muscles; rarely esophageal, laryngeal muscles, and tongue. Evaluation is performed both by listening for characteristic sounds of electrical potentials and visually examining the waveforms produced by the potentials on the monitor. Sensitivity is greatly increased by increasing the number of “passes” through the muscle (by continually redirecting the needle within the muscle) and by increasing the number of muscles sampled, as denervation potentials may be present in only a few areas. A short burst of electrical activity occurs during needle placement is normal due to temporary disruption of muscle fibers (insertional activity). Other normal electrical potentials called miniature end plate potentials and endplate spikes may occur as a result of spontaneous depolarization of part or all of a myofiber. Normal healthy muscle is otherwise electrically silent at rest. Other spontaneous electrical discharges in resting muscle (i.e., anesthetized animal) are abnormal and indicate neuromuscular disease. Abnormal EMG activity includes fibrillation potentials, positive sharp waves, complex repetitive discharges, or myotonic discharges. In general, the type of waveform is not specific for neuroanatomic location (nerve versus muscle) or pathophysiologic mechanism of disease. Abnormal EMG activity confirms the presence of neuromuscular disease and helps localize which muscle groups are affected; however, abnormal EMG activity cannot differentiate between myopathic or neuropathic disease. EMG changes due to denervation may not be detected for 5 to 10 days after initial injury. Severity of clinical signs does not always correlate with severity of EMG changes. Motor NCV: Using stimulating needle electrodes, a nerve is stimulated at various accessible points along its anatomic pathway. Needle or surface electrodes within or over a muscle innervated by the nerve record a compound muscle action potential (CMAP), which results in a simple biphasic waveform. Measurements made include the nerve conduction velocity (NCV), as well as the CMAP, amplitude, duration and area Nerves commonly tested in domestic animals include the sciatic, peroneal, cranial tibial, radial, musculocutaneous, and median. The recurrent laryngeal, facial nerve, and trigeminal nerves are rarely tested. Nerve conduction velocity along various segments of axon may be determined by measuring the distance between points of stimulation (ideally at least 100 mm to decrease the effect of human measurement error) and difference in latency of waveforms (velocity [meters per second] = Ddistance/D time). The amplitude of the waveform is proportional to the number of available axons. Axonal disease results in a decreased number of axons and decreased CMAP amplitude and may also cause secondary EMG changes due to denervation. Nerve conduction velocity measures the speed at which action potentials travel down the axon. Decreases in NCV may be due to demyelination or due to loss of the large, fastest conducting axons. Demyelinating diseases, in addition to causing decreases in NCV, cause a widening and distortion of the CMAP waveform, and temporal dispersion or distortion of the waveform over the time axis. Many peripheral nerve diseases result in both axonal loss and demyelination, causing decreased amplitude, temporal dispersion, and decreased conduction velocity in addition to abnormal EMG activity due to denervation. Measuring nerve conduction velocity is helpful in determining whether disease is demyelinating, axonal, or both, as well as whether the nerves are more affected proximally or distally. It is also helpful in determining which nerves are affected. Pathophysiologic mechanism of disease cannot be determined using NCV. Nerve and muscle biopsies are often necessary to determine the etiology of disease, although EMG and nerve conduction velocity help determine the nature of disease (demyelinating versus axonal versus myopathy) and optimal biopsy sample site.
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Electromyography (EMG) and Motor Nerve Conduction Velocity (NCV)
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ELECTROMYOGRAPHY (EMG) AND MOTOR NERVE CONDUCTION VELOCITY (NCV) Types of electrical activity seen in normal muscle during electromyography evaluation. A, Insertional activity. Note abrupt onset and termination of activity associated with needle placement (100 mV/div; 200 msec/div). B, Miniature end-plate potentials with two end-plate spikes indicating close proximity of needle to an end plate (100 mV/div; 10 msec/div). C, Motor unit action potentials seen during voluntary muscle activity in an awake animal (100 mV/div; 10 msec/div). (Reprinted with permission from Cuddon PA: Electrophysiology in neuromuscular disease, Vet Clin North Am Small Anim Pract 32:31-62, 2002.)
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ELECTROMYOGRAPHY (EMG) AND MOTOR NERVE CONDUCTION VELOCITY (NCV) Electromyography: abnormal spontaneous electrical activity. A, Fibrillation potentials, moderate density (100 mV/div, 10 msec/div). Fibrillation potentials may be associated either with denervation secondary to axonopathy or with primary myopathy. Density and consistency of observed fibrillation potentials are accurate reflections of severity of muscle involvement. B, Spontaneous electrical activity in the form of positive sharp waves (100 mV/div; 10 msec/div). (Reprinted with permission from Cuddon PA: Electrophysiology in neuromuscular disease, Vet Clin North Am Small Anim Pract 32:31-62, 2002.)
ELECTROMYOGRAPHY (EMG) AND MOTOR NERVE CONDUCTION VELOCITY (NCV) Motor nerve conduction studies recorded from the plantar interosseous muscles following stimulation of the sciatic-tibial nerve at the hock, stifle, and hip in a normal dog (A) and in a dog with generalized muscle disease (B) (mitochondrial myopathy). Note marked generalized decrease in compound muscle action potential (CMAP) amplitudes (3.12, 3.37, and 4.51 mV) from all sites of stimulation in the myopathic dog when compared with the normal dog (23.02, 19.86, and 20.34 mV). Despite CMAP amplitude reduction, the dog with myopathy has normal MNCVs (101 and 85 m/sec). Generalized CMAP amplitude decrease can also be observed in prejunctional neuromuscular diseases such as botulism, as well as in primary axonopathies. (Recording parameters: A, 5 mV/div and 2 msec/div; B, 1 mV/div and
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Electromyography (EMG) and Motor Nerve Conduction Velocity (NCV)
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2 msec/div.) (Reprinted with permission from Cuddon PA: Electrophysiology in neuromuscular disease, Vet Clin North Am Small Anim Pract 32:31-62, 2002.)
POSTPROCEDURE Monitor recovery from anesthesia. Nerve and muscle biopsies are often indicated after electrodiagnostic testing to determine the pathophysiology of disease (e.g., inflammatory, infectious, neoplastic, degenerative, toxic, endocrine). See Muscle and Nerve Biopsy, . For additional details, consult recommended methods for submission of samples in Shelton and Engvall, 2002. In some cases, PEG tube placement is indicated while the animal is anesthetized.
ALTERNATIVES AND THEIR RELATIVE MERITS Muscle and nerve biopsies as already described
SUGGESTED READING Cuddon PA: Electrophysiology in neuromuscular disease. Vet Clin North Am Small Anim Pract 32(1):31–62, 2002. Sheldon GD, Engvall E: Muscular dystrophies and other inherited myopathies. Vet Clin North Am Small Anim Pract 32:103–124, 2002. AUTHOR: GREG KILBURN
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Electrocardiography SYNONYMS Electrocardiogram: ECG, EKG Electrocardiograph: ECG machine
OVERVIEW AND GOALS To obtain a tracing that represents the rhythm of the heartbeat Electrocardiography is the diagnostic test of choice for evaluating cardiac arrhythmias. Electrocardiography may also provide some limited information regarding cardiac structure (sizes and proportions of waves and complexes sometimes indicate chamber enlargement) and systemic disturbances (e.g., hyperkalemia, hypoxemia).
INDICATIONS Evaluation of a cardiac arrhythmia noted during physical examination Part of routine cardiovascular monitoring during general anesthesia or intensive care Monitoring of a cardiac arrhythmia noted during anesthesia or hospitalization Evaluation of an animal with clinical signs suggesting syncope Evaluation of an animal with suspected or confirmed hyperkalemia
CONTRAINDICATIONS Severe dyspnea contraindicates restraint in lateral recumbency for ECG.
EQUIPMENT, ANESTHESIA Electrocardiograph (ECG machine). Each ECG wire should end in an atraumatic clip that connects the machine to the animal's skin. A table with a waterproof foam-core pad on which the animal can lie comfortably (to reduce electrical interference emerging through the table) Isopropyl alcohol for improving contact between ECG clips and skin
ANTICIPATED TIME Basic tracing: 5 minutes Ongoing monitoring: any duration For prolonged monitoring, see Holter/Cardiac Event Monitoring, .
PREPARATION: IMPORTANT CHECKPOINTS Check that the electrocardiograph has sufficient paper supply and is functioning. There is no ink in most electrocardiographs (heat-sensitive paper and thermal stylus).
POSSIBLE COMPLICATIONS AND COMMON ERRORS TO AVOID Animals that are in respiratory distress should not be restrained for electrocardiography; these animals should be assessed while they are standing (or in any other position in which they are not distressed), or the ECG should be postponed until dyspnea has improved or resolved. Artifact can be minimized by: Using enough isopropyl alcohol at the point of contact between the skin clips and skin Avoiding metal-on-metal contact between clips; often, with smaller dogs and cats, the wires need to be held apart by the person performing the ECG to avoid wire-to-wire or clip-to-clip contact during the procedure. Choosing a quiet, comfortable environment to perform the tracing; a cold or stressful environment may trigger shivering (and motion artifact), whereas an excessively warm or stressful environment can induce panting in dogs (and motion artifact). Replacing the ECG wire set every 5 years under all circumstances or annually with heavy use (e.g., used multiple times weekly) because the wires tend to fracture internally with age Evaluating multiple ECG leads rather than just one lead; each lead provides a different perspective on the electrical activity of the heartbeat, and lead II is not necessarily the lead in which the clearest P waves, QRS complexes, T waves, and minimal artifact are seen. Overinterpretation of the dimensions of P waves and T waves as indicating cardiac chamber enlargement is a common pitfall; echocardiography is much more sensitive and specific than electrocardiography for assessing cardiac structure. Motion artifact may mimic abnormal cardiac activity and cause misdiagnosis. In-hospital monitoring that lasts for hours or more should involve the use of atraumatic or minimally traumatic skin clips: either (1) a small patch of skin can be shaved on each side of the thorax and stick-on, human ECG patches can be used or (2) loops of small-gauge steel suture may be passed through the skin in the usual locations on the four limbs, and the ECG wires are clamped to these loops instead of directly to the skin.
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ELECTROCARDIOGRAPHY Patient is comfortably restrained in right lateral recumbency, with proximal long bones of the limbs perpendicular to long axis of body. Insulating (waterproof, foam core) pad and fleece blankets are under patient to reduce the influence of electrical interference.
ELECTROCARDIOGRAPHY Placement and utility of precordial leads.
ECG Clip/Electrode Placement for Standard Limb Leads (I, II, III, aVR, aVL, aVF) RA, white Right forelimb; clip to skin just proximal to the olecranon (caudal triceps region). LA, black
Left forelimb; clip to skin just proximal to the olecranon (caudal triceps region).
RL, green Right hind limb; clip to skin just proximal to the stifle (cranial thigh); ground wire. LL, red
Left hind limb; clip to skin just proximal to the stifle (cranial thigh).
PROCEDURE The procedure is the same for cats and dogs. Performing an ECG requires two people (clinician and assistant), unless animal restraint is not necessary (anesthetized or unconscious
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animal). The assistant restrains the animal in right lateral recumbency. Sitting, sternal, and dorsal positions are equally acceptable; determination of the mean electrical axis from these other positions is inaccurate, but this has no effect on assessing the cardiac rhythm. The assistant stands or sits behind (dorsal to) the right-laterally recumbent animal and holds the animal's limbs perpendicular to the long axis of the animal's body. Note: For the humeri and femurs to be truly perpendicular to the long axis of the body, the assistant needs to extend the limbs sometimes quite substantially. Fore-limbs (at the level of the carpi) are held in the assistant's right hand and hind limbs (at the level of the tarsi) in the left. The clinician attaches the ECG clips (electrodes) to the appropriate points on the animal for the limb leads as well as the precordial leads. A standard ECG includes representative recordings from all six limb leads, usually 3-15 seconds each for I, II, III, aVR, aVL, and aVF, and will provide further information if precordial leads are also recorded. A standard ECG also includes a “rhythm strip,” which is a continuous tracing of the same lead for 12 seconds to 1 minute or more: The most commonly used lead for the rhythm strip is lead II, but the lead that is chosen should be the one that shows the clearest P waves, QRS complexes, and T waves. The duration of the rhythm strip depends on the reason for performing the ECG and can be as long as is needed (several minutes) when an intermittent arrhythmia is being sought. Generally, if an abnormality has not been detected over a period of 1-4 minutes of ECG recoding on paper, then the procedure is terminated. The tracing obtained thus far is reviewed meticulously, and if further ECG evaluation is needed, ongoing ECG monitoring either with an in-hospital display monitor (e.g., oscilloscope) or portable telemetry (see p.1287) can be used.
POSTPROCEDURE The clips are carefully detached from the skin prior to releasing the animal's restraint.
ALTERNATIVES AND THEIR RELATIVE MERITS Thoracic radiographs: provide some information on cardiac structure (e.g., chamber enlargement), but this information is limited by substantial overlap between normal and mild to moderate abnormalities. Also indicated when ST-segment elevation or depression is present (assess for pulmonary or airway lesions). Echocardiography: the clinical gold standard for assessing cardiac chamber size; indicated if cardiac enlargement is suspected based on ECG and/or radiographs Pulse oximetry/arterial blood gas measurement: if ST segment elevation or depression is noted in the absence of structural heart disease (e.g., cardiomyopathy, advanced valvular disease, congenital heart disease) Serum potassium measurement: if lack of P waves is noted, especially in an animal with a history and/or physical findings suggesting a reason for hyperkalemia (urgent) AUTHOR: ETIENNE CÔTÉ
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Echocardiography
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Echocardiography SYNONYMS Cardiac ultrasound; echo; transthoracic echocardiography
OVERVIEW AND GOALS A complete echocardiographic study should: Reveal the pertinent acquired or congenital cardiac lesions Evaluate valvular function Quantify ventricular systolic and diastolic function Estimate the hemodynamic burden through quantification of chamber size (dilation, hypertrophy)
INDICATIONS Congenital or acquired cardiac disease (valvular, myocardial, pericardial), cardiac neoplasia, pulmonary hypertension, systemic hypertension, and pleural effusion or respiratory distress of uncertain etiology Limited echo studies can be useful in selected emergency situations (e.g., pericardial effusion, estimation of atrial size, or ventricular ejection fraction during initial stabilization if other initial diagnostic modalities are hazardous or nondiagnostic).
CONTRAINDICATIONS Animal should be stable enough to handle restraint. Animals with life-threatening problems (e.g., pleural effusion, pulmonary edema, and other causes of respiratory distress) need to be stabilized (limited echo study might be warranted or postponed).
EQUIPMENT, ANESTHESIA Scanning table with holes cut out because examination from beneath the animal improves image quality Ultrasonic transmission gel Isopropyl alcohol Hair clippers might be needed. Ultrasound equipment; sector-scanning transducers preferred: For cats and small dogs (usually 7.0-8.0-MHz transducer), medium-sized dogs (5.0-MHz transducer), large dogs (2.5-3.5-MHz transducer) It may be necessary to use two different probes during one examination. The echocardiography machine should have M-mode, two-dimensional (2D), Doppler (pulsed-wave, continuous-wave, and color-coded), and electrocardiogram (ECG) capabilities. Sedation/anesthesia is neither required nor desired except in very uncooperative animals.
ANTICIPATED TIME Variable due to experience and case complexity (5-40 minutes).
PREPARATION: IMPORTANT CHECKPOINTS Dogs and cats usually require little preparation for echocardiographic examination. Fasting is not needed. Hair might be clipped over the right third to the sixth intercostal spaces (ICS) and left at the fourth to the seventh ICS (precordial transducer locations); however, in most dogs and cats, satisfactory images can be obtained by parting the haircoat, applying isopropyl alcohol liberally over area of interest, and finally applying transmission gel.
POSSIBLE COMPLICATIONS AND COMMON ERRORS TO AVOID Although the technique has no known physical hazard, there are risks associated with the improper interpretation or use of the results of the ultrasound. Use high-frequency transducers to obtain quality images of near-field structures. Use low-frequency transducers for quality Doppler (color, pulse wave, continuous wave) signals.
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Echocardiography
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Adjust depth of the real-time image to fill the field of view (reduce amount of lung field). Adjust gain to avoid producing a white, distorted image due to a high setting; too low a setting will produce a weak signal. Remember the concept of blue/away and red/toward (BART) for color-flow Doppler studies.
PROCEDURE Image quality is improved in lateral recumbency; however, dogs and cats may be examined in a standing, sitting, or sternal position. The ultrasound machine's ECG clips are attached to the legs as recommended by the manufacturer (ECG is used for measurements and timing within the cardiac cycle). Starting in right lateral recumbency (animal's legs toward the examiner), the right parasternal location (window) is between the right third and sixth ICS, between the sternum and costochondral junctions (landmark: palpate right precordial heartbeat and place transducer at this location to start). Attention is paid to having the assistant restrain the animal, with the forelegs drawn cranially to open the axilla/acoustic window. Long-axis views: The beam plane is oriented slightly clockwise from perpendicular to long axis of the body, parallel to the long axis of the heart, and with the transducer index mark pointing toward the heart base (craniodorsal, approximately toward the animal's shoulder). The following two views are obtained: first, a four-chamber view with the ventricles displayed to the left and the atria to the right; second, a view obtained by slight clockwise rotation of the transducer from the four-chamber view into a slightly more craniodorsal orientation revealing the left ventricular outflow tract, aortic valve, and aortic root. Short-axis views: Rotate the transducer about 90○ toward the sternum from the four-chamber view (keep probe in same position except for the rotation) such that the beam plane is oriented perpendicular to the long axis of the heart, with the transducer index mark now pointing cranially toward the animal's elbow (proper orientation identified by circular symmetry of the left ventricle or aortic root). There are five standard transverse images (left ventricle with papillary muscles, left ventricle at mitral chordae tendineae level, left ventricle at mitral valve level, heart base–aorta/left atrium level, and heart base–pulmonary artery) obtained from this position by pivoting the transducer from the apex to the base of the heart (caudal/ventral to cranial/dorsal). Turn animal over into left lateral recumbency, with the animal's legs still toward the sonographer. Left caudal (apical) parasternal location: The location is between the left fifth and seventh ICS, as close to the sternum as possible (landmark: palpable left apical heartbeat): Left apical two-chamber views: The transducer index mark is pointing toward the heart base (dorsal), and the beam plane parallel to the long axis of the heart—the left side of the heart—is visualized (left atrium, left ventricle, and mitral valve). Slight rotation of the transducer into a craniodorsal to caudoventral orientation reveals left ventricle, outflow tract, aortic valve, and aortic root in a long-axis view.
ECHOCARDIOGRAPHY Right parasternal four-chamber long-axis view in a normal dog (obtained without shaving). IVS, Interventricular septum; LA, left atrium; LV, left ventricle; LVW, left ventricular wall; PV, pulmonary vein; RA, right atrium; RV, right ventricle; RVW, right ventricular wall.
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Echocardiography
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ECHOCARDIOGRAPHY Right parasternal short-axis view at the left ventricular papillary muscle level in same dog. From this view, gentle pivoting motion (caudal/ventral to cranial/dorsal) of the transducer beam toward the base will reveal the other four standard views obtained from this location. APM, anterior papillary muscle; IVS, interventricular septum; LV, left ventricle; PPM, posterior papillary muscle; RV, right ventricle.
ECHOCARDIOGRAPHY Remaining in the same right parasternal window as the two previous views, gently pivoting toward the heart base, the right parasternal short-axis view at the left atrium/aorta level was obtained in the same dog. AS, atrial septum; LA, left atrium; LAu, left auricle; LC, left coronary cusp; NC, noncoronary cusp; PV, pulmonary vein; PVs, pulmonic valve; RC, right coronary cusp; RV, right ventricle.
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Echocardiography
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ECHOCARDIOGRAPHY Five-chamber view is obtained at left apical parasternal location. Left apical parasternal location is the only time during echocardiographic examination when index mark on head of transducer is directed caudally. Ao, aorta; LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle. Left apical four-chamber views: This is the only view in which the transducer index mark is pointing to the left and caudally, opposite of all other views. Note: The transducer should be as far back toward the apex of the heart as possible, often around the seventh ICS, and tilted to point cranially. The beam plane is in a left-caudal to right-cranial orientation and then directed dorsally toward the heart base, revealing the ventricles in the near field closest to the transducer and the atria in the far field (heart is oriented vertically; left ventricle, mitral valve, and left atrium should appear to the right). Modest cranial tilting of the beam from the above view will bring the left ventricular outflow region into view (five-chamber view). Left cranial parasternal location: The location is between the left third and fourth ICS, between the sternum and costochondral junctions. Long-axis views: With the transducer index mark pointing cranially and the beam plane oriented parallel to the long axis of the body and heart, a view of the left ventricular outflow tract, aortic valve, and ascending aorta is obtained (left ventricle will be displayed to the left and aorta to the right). From this position, angling of the beam ventral (toward the sternum) to the aorta brings out the right atrium/right auricle, tricuspid valve, and inflow region of the right ventricle (displayed to the right, while the left ventricle will be noted to the left). Finally, angling the transducer dorsally (transducer will almost be horizontal and parallel with the table) in relation to the ascending aorta produces a view of the main pulmonary artery, pulmonary valve, and right ventricular outflow tract.
ECHOCARDIOGRAPHY Two M-mode studies of left ventricle. Left, Normal dog shows vigorous excursions of the interventricular septum (above) and left ventricular free wall (below) from systole to diastole. The absolute diameter of the left ventricle is within normal limits. Right, Dog with dilated cardiomyopathy has visibly poor left ventricular systolic function (almost no difference between systole and diastole) and a very enlarged left ventricular diameter compared to normal. LVIDd, left ventricular internal diameter in diastole; LVIDs, left ventricular internal diameter in systole; FS%, fractional shortening. Short-axis views: Remain in the same location as for the cranial long axis, and rotate the transducer until the transducer's index mark is toward the thoracic spine (dorsally, about 90○ from the location of long-axis view; aorta should appear circular in the center of the image). The right ventricular inflow tract should be to the left, and outflow tract and pulmonary artery to the right.
POSTPROCEDURE Remove ECG clips. Wipe gel and alcohol from animal.
ALTERNATIVES AND THEIR RELATIVE MERITS Transesophageal echocardiography: Semi-invasive procedure Requires general anesthesia in animals Provides superb clarity and resolution
SUGGESTED READING
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Echocardiography
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Bonagura JD: Echocardiography. J Am Vet Med Assoc 204:516–522, 1994. Oyama MA: Advances in echocardiography. Vet Clin North Am Small Anim Pract 34(5):1083–1104, 2001. Thomas WP, Gaber CE, Jacobs GJ, et al: Recommendations for standards in transthoracic two-dimensional echocardiography in the dog and cat. J Vet Intern Med 7:247–252, 1993. AUTHOR: ROBERT PROŠEK
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Foreign-Body Removal, Esophageal (Endoscopic) SYNONYM Minimally invasive removal of esophageal foreign bodies
OVERVIEW AND GOALS Objects causing esophageal obstruction are most commonly found in one of three locations: at the thoracic inlet, at the level of the base of the heart, or immediately cranial to the gastroesophageal sphincter. About 90% of foreign bodies obstructing the esophagus can be removed without performing a thoracotomy. An attempt should be made to try to remove these foreign bodies via esophageal endoscopy in order to avoid surgery and its complications (e.g., difficult access, limited healing ability, and associated morbidity). Removal of these objects is achieved by making use of rigid or flexible endoscopes. If a foreign object cannot be removed via the oral route, an attempt can be made to pass the object through into the stomach using a large-bore stomach tube and copious lubrication, provided complications such as esophageal perforation (from a sharp-edged foreign body, esophageal wall devitalization, or overly aggressive forward pressure) are avoided. Objects passed from the esophagus into the stomach may then be removed via a gastrotomy or left to be digested (in the case of bones and other digestible objects).
INDICATIONS Presence of foreign objects lodged in the esophagus (e.g., bones, fishhooks, needles, toys, partially regurgitated hair balls)
CONTRAINDICATIONS Esophageal perforation is an absolute contraindication to minimally invasive approaches; thoracotomy is indicated in these cases.
EQUIPMENT, ANESTHESIA General anesthesia Cuffed endotracheal tube Mouth gag/speculum Rigid tube for esophageal dilation (optional); typical external diameters are 2 cm (cat, small dog), 3 cm (medium-size dog), and 4 cm (large dog). The end of the tube should have smooth edges (may heat with flame, then trim edges when cool before using). Rigid proctoscope or flexible fiberoptic endoscope Endoscopic basket or grasping forceps (recommended) or endoscopic biopsy forceps (second choice) Water-soluble lubricating jelly Polyethylene catheter or feeding tube (optional) Suctioning apparatus
ANTICIPATED TIME Approximately 20-90 minutes, depending on size of object and ease with which it can be grasped, atraumatically dislodged, and retrieved
PREPARATION: IMPORTANT CHECKPOINTS Assess for location of foreign body, presence of signs of aspiration pneumonia, and evidence of esophageal perforation by performing survey and contrast radiography using low osmolality, nonionic contrast medium. Radiographs should be performed or repeated immediately prior to induction of general anesthesia to avoid anesthetizing an animal in which a foreign body has spontaneously passed into the stomach. Endoscopic evaluation of location of foreign body and state of esophageal mucosa Ensure adequate hydration and perfusion. Antibiotic therapy if indicated by complications (described in following paragraphs); often empirically at first (e.g., ampicillin, 22 mg/kg IV q 8 h; and enrofloxacin, 5 mg/kg diluted 1:1 in 0.9% saline and given slowly IV q 24 h [cats] or q 12 h [dogs]) and then guided by results of culture and sensitivity (C&S).
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Advise the owner of possible complications. There may be a need for emergency thoracotomy if perforation occurs or if removal via the oral route is impossible; possible gastrotomy may result if the foreign body has to be pushed through into the stomach and is unlikely to be digested.
POSSIBLE COMPLICATIONS AND COMMON ERRORS TO AVOID Esophageal mucosal trauma (erosion, ulceration) Esophageal perforation, pyothorax, pleuritis, mediastinitis Aspiration of esophageal contents and aspiration pneumonia Tension pneumothorax (associated with esophageal insufflation when using flexible fiberoptic endoscope) Bradycardia due to vagal stimulation Sepsis (due to aspiration or to esophageal rupture) Esophageal stricture (first clinical manifestations usually >2 weeks postoperatively) Bronchoesophageal fistulation (rare) Failure to radiograph immediately prior to induction (foreign body may have passed spontaneously)
PROCEDURE General anesthesia Place endotracheal tube and inflate cuff to prevent aspiration of esophageal contents. Animal in sternal or left lateral recumbency (allows the esophagus to lie over the aorta) Examine the mouth (especially the sublingual region) for the presence of objects such as thread, needles, or fishhooks. Suction esophagus to remove any liquid contents and contrast medium. Insert mouth gag/speculum. Rigid proctoscope technique: Lubricate proctoscope. Pass the proctoscope orally and into the esophagus to the level of the foreign body, visualizing the foreign body and any evidence of perforation that would contraindicate further endoscopic manipulations. Lubricant can be placed at the site of the foreign body, using a polyethylene catheter with the tip placed at the level of the foreign body, between the foreign body and esophageal mucosa. Using grasping forceps, bring the foreign body close to the end of the proctoscope. If the foreign body is small enough, it can be partially or entirely pulled into the lumen of the proctoscope. The foreign body, proctoscope, and grasping forceps are pulled out together via the mouth by gentle manipulation and with adequate lubrication. Continuous visualization and gentleness of traction are essential through this process. This is to ensure that complications such as esophageal laceration or perforation are noticed immediately if they occur, that the retrieval can be stopped immediately, and that the foreign body be repositioned or the procedure be aborted in favor of thoracotomy if serious complications are noted. If retrieval is not possible, an attempt should be made to gently push the foreign body through to the stomach using a well-lubricated stomach tube, provided no evidence of esophageal devitalization (e.g., deep mucosal lacerations and discolorations or other signs of possibly imminent perforation) are seen. Careful examination of the esophageal wall after foreign body removal; any suspicion of possible esophageal perforation warrants close radiographic and clinical monitoring. Flexible fiberoptic endoscope technique: For medium-size or larger dogs, a rigid tube can first be placed to assist in dilating the esophagus. The endoscope can then be passed through this tube. Lubricate the endoscope. Pass the endoscope to the level of the foreign body, visualizing the foreign body and assessing the integrity of the adjacent esophagus.
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FOREIGN-BODY REMOVAL, ESOPHAGEAL (ENDOSCOPIC) A 1-m flexible fiberoptic endoscope. This endoscope is adequate for esophageal procedures in dogs and cats of all body sizes.
FOREIGN-BODY REMOVAL, ESOPHAGEAL (ENDOSCOPIC) Large (top) and two small (below) rigid proctoscopes, used for retrieving esophageal foreign bodies, and small proctoscopic stylet (bottom). Stylet is placed into proctoscope for advancing into esophagus. Once desired degree of insertion is achieved, stylet is withdrawn, and glass port (seen in the open position in the large proctoscope, top) may be closed for most effective visualization.
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FOREIGN-BODY REMOVAL, ESOPHAGEAL (ENDOSCOPIC) Operator (left) examines esophagus of an animal, using a flexible fiberoptic endoscope; assistant adjusts endoscope's insertion and rotation according to operator's instructions. Insufflation of air will allow dilation of the esophagus around the foreign body. This may also be useful in dislodging foreign bodies such as bones that are embedded in the esophageal wall. Lubrication can also be placed at the site of the foreign body, using a catheter or feeding tube as already described. Grasping forceps or biopsy forceps can be passed through the endoscope biopsy channel. The use of biopsy forceps is a last resort, because dulling and damage to the instrument are possible. Grasp the foreign body, and pull it close to the endoscope. The endoscope, forceps, and foreign body are gently pulled out together via the mouth while ensuring adequate esophageal dilation and lubrication. If the foreign body is lodged to the extent that it cannot be retrieved easily, an attempt could be made to either slightly push it aborally or to rotate it gently. If the maneuvers result in dislodging the object, another attempt can be made to retrieve it. If retrieval is not possible, an attempt should be made to push the foreign body through to the stomach. The esophageal mucosa is carefully examined endoscopically after removal of the foreign body.
POSTPROCEDURE If esophageal mucosa is damaged (e.g., suspected on endoscopic observation of darkened/discolored esophageal mucosa, deep mucosal lacerations, or after prolonged, difficult procedure; confirmation comes from intraprocedure or postprocedure radiographs): Clean lacerations that do not extend through the full thickness of the esophageal wall can be left to heal by epithelialization. Full-thickness tears and areas of esophageal necrosis require immediate surgical resection or repair. Withhold food and water for 24 hours. Maintain hydration and electrolyte balance. Pain management: antibiotics (as already described), prokinetic agents, corticosteroids, and/or gastric antacids may be indicated (see pp. 365 and p. 367). Gastrostomy feeding tube placed distal to the site of the foreign body if prolonged withholding of food is indicated (such as in cases of esophageal mucosal damage). Once the animal has recovered, first introduce liquids, followed by gruel if no adverse reactions are noted once liquids have been introduced.
ALTERNATIVES AND THEIR RELATIVE MERITS Advancement of foreign body into stomach followed by gastrotomy: If a foreign body is too large or awkward to grasp, an attempt could be made to gently push it through into the stomach. Digestible objects such as bones could be left in the stomach to digest, but sharp objects and objects such as toys should not be pushed into the stomach (risk of esophageal perforation). Follow-up radiography is advised to ensure that foreign bodies were either digested or passed through the digestive tract. For cases in which esophageal perforation and its complications have already developed (see p. 363), surgical removal of the foreign body via thoracotomy is the only alternative. AUTHOR: MIRINDA NEL (VAN SCHOOR)
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Fistulogram SYNONYM Positive-contrast fistulogram
OVERVIEW AND GOAL Fistulograms are radiographic contrast procedures that may be utilized in the evaluation of a cutaneous draining tract.
INDICATIONS Identify soft-tissue foreign bodies (e.g., splinters, plant awns, glass) Locate potential source of a draining tract (e.g., orthopedic implants, sutures) Identify communication of tract with body cavity or organ
CONTRAINDICATIONS Known sensitivity to contrast media
EQUIPMENT, ANESTHESIA Contrast media: Ionic or nonionic organic iodinated contrast agents Catheters: Variable length and size depending on extent of lesion Preferably semirigid without balloon tip, such as a tomcat catheter; no stylets Sedation/anesthesia may be required for fractious animals.
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FISTULOGRAM Lateral radiographic projection of torso of a dog prior to contrast injection. There is a suggestion of minor radiopacity in dorsal body wall dorsal to location of a draining tract. (Courtesy Dr. Phil Gill.)
ANTICIPATED TIME About 5–20 minutes
PREPARATION: IMPORTANT CHECKPOINTS Sedation/anesthesia if required Hair clipped and area scrubbed/disinfected Survey radiograph of region
POSSIBLE COMPLICATIONS AND COMMON ERRORS TO AVOID Systemic reaction to contrast agents (rare) Local irritation from hypertonic contrast agents (rare; can dilute with saline or sterile water for prevention) Leakage of contrast into fascial planes leading to nondiagnostic study (common) Inability to follow full extent of draining tract (common) Masking of small foreign bodies by opacity of contrast agent (common)
PROCEDURE Catheter is placed retrograde into draining tract as far as possible. Injection (usually 1-12 mL) while catheter in place or while drawing it back out Appropriate radiographic projections; two views at right angles are usually sufficient.
ALTERNATIVES AND THEIR RELATIVE MERITS
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Ultrasound: Easy to perform Variable information obtained; may detect foreign bodies Difficult to follow extent of tract CT scan and MRI: Expensive Variable information obtained
FISTULOGRAM Lateral radiographic projection of same dog after contrast injection into a cutaneous draining tract on lateral thorax. Study shows extent of draining tract, with pooling of contrast media in dorsal body wall. Filling defect in contrast-filled tract created by catheter. (Courtesy Dr. Phil Gill.) AUTHOR: BRETT KANTROWITZ
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Fine-Needle Sampling for Cytologic Analysis: Lung OVERVIEW AND GOALS Minimally invasive diagnostic tool with a good diagnostic yield for focal lesions. Good technique increases the diagnostic yield and reduces complications.
INDICATIONS Pulmonary masses and nodules Areas of pulmonary consolidation Lower diagnostic yield and greater risk to animal for diffuse (interstitial) pulmonary diseases
CONTRAINDICATIONS Bleeding disorders (coagulopathy, thrombocytopenia, thrombocytopathia)
EQUIPMENT, ANESTHESIA A few sterile 22-gauge needles (1-3½” [2.5-9 cm]) A 12-mL syringe A standard 33” (84-cm) flexible extension set for IV lines Glass slides Blow dryer Image guidance if possible (ultrasound, CT scan, fluoroscopy, radiology) General anesthesia is recommended to reduce risks of pulmonary lacerations and pneumothorax.
ANTICIPATED TIME About 30 minutes
PREPARATION: IMPORTANT CHECKPOINTS Warn owners that hemorrhage and pneumothorax are possible complications, warranting intensive care and sometimes presenting a life-threatening situation. Rule out bleeding disorders.
POSSIBLE COMPLICATIONS AND COMMON ERRORS TO AVOID Hemorrhage (pulmonary, pleural, airways) Pneumothorax Proceeding too slowly. While the procedure must be prepared for and carried out carefully, time is of the essence during fine-needle sampling. Tissue trauma activates coagulation, which can rapidly plug the needle or degrade the quality of the sample. Short and slow needle passes. A slow or timid back-and-forth motion does not detach a sufficient number of cells. The needle tip, however, must remain within the target tissue during this part of the procedure to avoid contamination by, or damage to, surrounding tissues. Changing directions while the needle is deep in the lesion causes shearing of tissue, lung lacerations, bleeding, and pain. The needle should always be withdrawn to the skin's surface (almost out but not quite) before being redirected. Aspiration. When aspiration is used in the lungs, air is aspirated as soon as the bevel enters an air-filled space, and the sample is lost in the syringe or extension set. A vigorous back-and-forth motion without aspiration is sufficient to detach cells, create mild bleeding, and fill the needle with a diagnostic sample. Multiple sites. An important point is to obtain three to five cellular biopsies of different areas of large lesions, because masses or large lesions may contain a mixture of necrotic, inflamed, hemorrhagic, neoplastic, and normal tissues. Nondiagnostic samples. With experience, a clinician can identify cellular smears with the naked eye. If the smear does not appear cellular, the procedure should be repeated. If there is any doubt, the sample can be evaluated immediately by in-house microscopic examination.
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PROCEDURE Induce general anesthesia, including endotracheal intubation. Clip the hair from the sampling site(s), and prepare the site with surgical scrub. Connect extension set between syringe and needle. Fill syringe with 5-10 mL of air. The clinician hangs the syringe and extension tubing around his or her neck (like a stethoscope) and holds the needle like a pen to allow precise manipulations. Localize lesion with diagnostic imaging. Fine-needle procedures guided only by radiographs can be performed on large masses or when large areas of the lungs are affected. Note: Sonographic guidance works only if the mass, nodule, or consolidated lobe is in contact with the thoracic wall. Rapidly position the needle tip within the lesion. Avoid keeping the needle tip close to pleural surfaces, to reduce lacerations during respiratory motion. Move the needle rapidly back and forth using long needle passes (away from major blood vessels), and try staying within the lesion. Do not use negative pressure. Rapidly withdraw the needle. Immediately expel the sample on glass slides using the air-filled syringe. Make smear using the standard blood smear technique or a gentle squash technique. Immediately air-dry the smear with a blow dryer. Repeat the procedure to obtain two to three cellular smears of the lesion(s).
POSTPROCEDURE Risks of pneumothorax are significantly reduced (5% versus 40%-50%) if the animal is kept in lateral recumbency (biopsy side down) for 30-60 minutes following the procedure. If the animal is stable, keep under anesthesia 15-20 minutes after the procedure. This simple precaution takes advantage of recumbency atelectasis to rapidly seal any lung perforations or lacerations.
ALTERNATIVES AND THEIR RELATIVE MERITS Tru-Cut or core biopsy: May be associated with more complications May be more accurate for diffuse pulmonary diseases Bronchoscopy/bronchoalveolar lavage: Minimally invasive: lowest risk of iatrogenic pneumothorax Requires disease process that is exfoliating cells into the alveoli or airways (e.g., useful for lung consolidation due to pneumonia), so false negatives are possible. Surgical biopsy: More costly More invasive Most definitive diagnostic sampling technique for diffuse (interstitial) pulmonary diseases AUTHORS: MARC PAPAGEORGES, MICHÈLE MENARD
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Fine-Needle Aspirate, Ultrasound-Guided
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Fine-Needle Aspirate, Ultrasound-Guided SYNONYM Needle biopsy
OVERVIEW AND GOAL Procedure to obtain small tissue or fluid samples using ultrasound guidance and real-time monitoring of needle placement
INDICATIONS Ultrasonographic evaluation of focal mass lesion or nodule Ultrasonographic evaluation of diffuse or focal parenchymal organ abnormalities Drainage of cysts, abscesses, or fluid
CONTRAINDICATIONS Cavitated mass: risk of hemorrhage Bleeding disorder: risk of hemorrhage Suspected transitional cell carcinoma: possibility of seeding tumor along needle tract
EQUIPMENT, ANESTHESIA A few 22- or 25-gauge standard sterile injection needles, 1½ inches (4 cm) in length: Longer needle (3½ inch [9 cm]) required if using biopsy guide A few 6-mL syringes Glass microscope slides Hair clippers Surgical scrub, rubbing alcohol, gauze Sector or linear-array ultrasound transducer Sector transducers allow sampling of deep structures Linear-array transducers provide better resolution of superficial structures. ± Biopsy guide: easiest method, but angle of needle insertion is fixed. Sedation often not needed for fine-needle aspirate (FNA) Occasionally, IV or gas anesthesia required (e.g., anxious animal, small structure in close proximity to large vessel)
ANTICIPATED TIME About 5-10 minutes
PREPARATION: IMPORTANT CHECKPOINTS Perform coagulation profile, platelet count, and arterial blood pressure (BP) measurement if animal is at an increased risk of bleeding. Determine if sedation is required; place IV catheter if needed. Ensure proper animal restraint.
POSSIBLE COMPLICATIONS AND COMMON ERRORS TO AVOID To decrease hemodilution, avoid the suction method in sampling vascular organs (e.g., spleen). Identify and avoid large vessels within the organ being sampled or those adjacent to the structure (e.g., aorta adjacent to lymph node). Hemorrhage is uncommon if 22- or 25-gauge needle is used and the movement of the needle through the entire procedure is one-dimensional (in and out only, with no side-to-side motion).
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FINE-NEEDLE ASPIRATE, ULTRASOUNDGUIDED Importance of correct alignment between needle and ultrasound probe. Left, Correct alignment is present, and full extent of needle is seen. Right, Needle is not aligned with ultrasound beam, and only proximal portion of needle is seen. Here, trauma to deeper tissues is possible because location of needle tip is unknown. (Reprinted from Fife WD: Abdominal ultrasound: aspirations and biopsies. In Ettinger SJ, Feldman EC, editors: Textbook of veterinary internal medicine, ed 6, St Louis, 2005, Saunders, pp 271-275.)
FINE-NEEDLE ASPIRATE, ULTRASOUND-GUIDED Views as seen on monitor of ultrasound machine, perpendicular to other figure. Left, Correct alignment produces complete visualization of needle. Right, Probe/needle malalignment underrepresents depth of needle. Do not move the needle side to side within an organ, because this will cause tissue trauma. If redirecting needle orientation, withdraw needle tip to subcutis and then reinsert. Redirecting with needle fully advanced is ineffective (position changes little or not at all) and dangerous (shearing of tissue with needle tip). Cells may dry and clot in the needle very quickly. Therefore, when the needle is withdrawn, the expulsion of needle contents onto a microscope slide and the slide smearing technique should all be completed within seconds. Avoid penetrating bowel lumen, especially with larger gauge needles, because of risk of peritonitis. Sample the left aspect of the liver when possible to avoid the gallbladder and hilar vessels on the right. If the liver is small or cranially located, consider an intercostal approach. With renal aspirates, sample the caudal cortex of the kidney to avoid the medulla and hilar vessels.
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In cases of bilateral renal abnormalities, the left kidney should be sampled owing to its more caudal location. Do not pass through an organ other than the one being aspirated. Avoid administering drugs that cause splenomegaly or panting (e.g., phenothiazines, some opiates). If aspirating an adrenal gland mass, be aware of possible BP alterations and severe hemorrhage in the case of pheochromocytoma.
PROCEDURE Restrain the animal in dorsal or lateral recumbency. A padded U-shaped trough can be used for the animal so that it is more comfortable when lying down (see p. 1236). Clip hair from the ventral abdomen. Thoroughly evaluate area of interest, characterize lesion, identify adjacent or internal vessels to be avoided, and determine least traumatic location and direction of needle placement. Prepare skin with surgical scrub. Obtain ultrasound image of area to be sampled. Ensure probe marker location on screen corresponds with desired needle course. Freehand technique: hold transducer in one hand, and insert needle with other. The suction technique is useful in aspirates of less vascular structures (e.g., lymph node) but often results in hemodilution when aspirating vascular organs like the spleen. Without syringe suction: Introduce a 22- or 25-gauge needle parallel to plane of ultrasound beam, visualizing needle as it is advanced. Slowly fan transducer side to side to identify entire needle length to tip. Advance and retract needle three to four times to fill needle shaft with tissue cells. If using a spinal needle, remove the stylet before beginning the advancing and retraction of the needle. Withdraw needle from animal, and quickly attach a 6-mL syringe prefilled with 5 mL room air. Expel contents onto microscopic slide(s) immediately, and lightly smear using standard blood smear technique. With syringe suction: Attach 6-mL syringe to 22- or 25-gauge needle. Introduce needle parallel to plane of ultrasound beam, as already described. Apply suction to syringe three to four times while gently advancing and retracting needle. Disconnect syringe and withdraw needle from animal. Retract plunger to fill syringe with air, and reconnect syringe to needle. Expel contents onto microscopic slide(s) immediately, and lightly smear using standard blood smear technique. Multiple samples of each organ or lesion should be obtained.
POSTPROCEDURE Scan to evaluate for hemorrhage (very uncommon with this procedure).
ALTERNATIVES AND THEIR RELATIVE MERITS Tissue-core and surgical biopsy are more invasive but of greater diagnostic quality because of the ability to collect larger tissue samples.
SUGGESTED READING Nyland TG, et al: Ultrasound-guided biopsy. In Nyland TG, Mattoon JS, editors: Small animal diagnostic ultrasound, ed 2, Philadelphia, 2002, WB Saunders, pp 30–48. Penninck DG, Finn-Bodner ST: Updates in interventional ultrasonography. Vet Clin North Am Small Anim Pract 28:1017–1040, 1998. AUTHOR: WENDY D. FIFE
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Feeding Tube Placement: Percutaneous Endoscopic Jejunostomy (PEJ) SYNONYMS Percutaneous endoscopic-assisted placement of jejunostomy feeding tube; percutaneous gastrojejunostomy feeding tube
OVERVIEW AND GOALS Placement of a jejunal feeding tube using endoscopic assistance, rather than laparotomy or laparoscopy, to provide postgastric enteral feeding to nutritionally deficient or debilitated animals. The jejunostomy tube is placed using a concurrent/existing percutaneous gastrostomy (PEG) tube. Use of percutaneous endoscopic jejunostomy (PEJ) is uncommon because of the relative cost and stocking of supplies, inexperience, and infrequency of needs that are not accommodated by surgical or laparoscopicassisted placement of jejunal feeding tubes. Enteral feeding provides the advantage of improved overall metabolism and health of the intestinal tract. Enteral feeding reduces intestinal bacterial translocation, maintains glutamine synthesis, and improves and maintains gut immunologic barrier functions.
INDICATIONS Postgastric feeding is advised for animals with uncontrolled vomiting from any cause. Following gastric or biliary surgery Pancreatitis Disorders causing persistent gastroparesis (e.g., following intestinal surgery) Animals at increased risk of active or passive gastroesophageal reflux and aspiration (e.g., prolonged recumbency, pharyngeal dysfunction, laryngeal paralysis, altered mentation)
CONTRAINDICATIONS Unresolved peritonitis Anesthetic risks Large-volume peritoneal effusion
EQUIPMENT, ANESTHESIA General anesthesia is required, with endotracheal intubation. Postprocedural analgesia Mouth gag Sterile water-soluble lubricant for endoscope passage Supplies as needed to place percutaneous endoscopic gastrostomy (PEG) tube (see p. 1270) 2-0 monofilament suture material Iohexol as water-soluble radiographic contrast agent Flexible video or fiberoptic endoscope and ancillary equipment appropriate to size of animal (generally 7-9 mm diameter with 100 cm length is acceptable for most cases). Endoscopic snare or grasping forceps Vacuum source for endoscopic suction PEG tube that is 18-24 Fr in diameter, as a kit with PEJ or as a separate item (e.g., Pezzer mushroom-tip catheter) PEJ tube that is 6-12 Fr in diameter (e.g., Wilson-Cook Medical, Global Veterinary Products, Compat brand by Novartis) and 35-150 cm in length; PEJ kits with gastrostomy tubes are also available (e.g., Mila International Inc. Medical Instrumentation for Animals); variable diameters and lengths based on supplier and animal size; internally coated catheters have an internal lubricant that activates when flushed with sterile water; 1 mm = 3 Fr. Weighted PEJ tubes are less commonly used; they have a tungsten bulb at the tip that adds weight to help prevent migration of the tube back to the stomach; these are preferred by some endoscopists and not by others. A 0.021- to 0.037-mm (50-150 cm) flexible guide wire matched to selected PEJ feeding tube Fluoroscopy is preferred to be available, especially while staff is learning the technique. Flash (then saved) images on the preview monitor of digital radiographic equipment can help in identifying the location of the distal tip of the PEJ if fluoroscopy is not available. Elizabethan collar or other restraint to prevent patient's removal of PEJ or PEG tubes Orthopedic stockinette appropriate to size of animal to create a “sweaterlike” effect
ANTICIPATED TIME
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About 40-80 minutes (including placement of PEG tube)
PREPARATION: IMPORTANT CHECKPOINTS Test or check integration of guide wire, PEG tube, and PEJ tube for compatibility of diameters and lengths. Plan for coordination of staff regarding anesthesia, endoscopy, and fluoroscopy/radiography. Discuss with client the potential that the PEJ tube may become occluded or may migrate back to stomach despite best efforts and cost of catheters. Check or estimate the fill volume of catheter prior to placement.
POSSIBLE COMPLICATIONS AND COMMON ERRORS TO AVOID Stoma site infection Premature removal by animal of tube (teeth, rubbing on objects in environment) Peritonitis if adhesion of body wall to stomach breaks down Diarrhea induced by feeding enteral formula Reflux of enteral feeding product aborally PEJ tube migration back to the stomach and possible vomition of the tube aborally Complications occur with about the same frequency as with use of PEG tubes.
PROCEDURE Clip and prep left side of animal from approximately the eighth intercostal space (ICS) to just cranial to the stifle and from dorsal spinous process to ventral midline. General anesthesia, with endotracheal intubation Animal is positioned in right lateral recumbency. A PEG tube is placed (see p. 1270). Endoscope is passed to stomach from oral cavity. A snare or retrieval basket is passed via the gastrostomy (PEG) tube to the stomach. Endoscope is then maneuvered through the snare or basket. Pylorus is then visualized, and the endoscope is passed through to the mid-duodenum. Guide wire is passed via the operating channel of endoscope and continued forward blindly along the lumen of the small intestine until it is estimated that the tip is located in the proximal third of the jejunum. Guide wire is fed through the endoscope while the endoscope is slowly withdrawn from the body; the position of the guidewire in the body remains the same. Guide wire should then be in the center of the snare or basket. This is tightened and withdrawn via the gastrostomy (PEG) tube to the exterior so as to pull guide wire through the gastrostomy (PEG) tube (proximal tip is in jejunum, and distal end extends out the gastrostomy tube). Location of proximal tip of guide wire is checked with fluoroscopy and may be adjusted in position.
FEEDING TUBE PLACEMENT: PERCUTANEOUS ENDOSCOPIC JEJUNOSTOMY (PEJ) Endoscopic image. Luminal view of stomach, showing gastrostomy/PEG tube with jejunostomy/PEJ tube inserted. (Courtesy Dr. Al Jergens.)
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FEEDING TUBE PLACEMENT: PERCUTANEOUS ENDOSCOPIC JEJUNOSTOMY (PEJ) Gastrojejunostomy combined kit from Wilson-Cook. (Courtesy Dr. Al Jergens.)
FEEDING TUBE PLACEMENT: PERCUTANEOUS ENDOSCOPIC JEJUNOSTOMY (PEJ) Endoscopic image. Luminal view of duodenum, showing jejunostomy/PEJ tube over the guide wire (guidewire not seen). (Courtesy Dr. Al Jergens.) PEJ tube is flushed with copious amounts of water to activate lubricant. PEJ tube is passed over the guide wire until it extends a length adequate for the proximal tip to be in the proximal third of the jejunum. PEJ tube location is assessed with fluoroscopy or radiography with test infusion of a few milliliters of water-soluble contrast agent (iohexol); the PEJ tube may be repositioned as needed.
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Guide wire is removed slowly while the PEJ is held stable. PEJ tube is secured to animal's body or to the PEG tube as it exits the left side of the abdomen.
POSTPROCEDURE Place Elizabethan collar on the animal to prevent removal of both PEG and PEJ tubes. To protect tubes, place and adjust orthopedic stockinette “sweater” over animal's body, including two holes cut for the forelegs; this should be “comfortable” to reduce stimulus for premature removal by animal. Monitor recovery from anesthesia. Instill the volume of sterile water needed to fill tube every 2 hours to keep tube patent. Begin enteral nutrition via the PEJ tube 12 hours following PEG tube placement. Monitor stoma site; expect mild inflammation and swelling; discharge from stoma may appear serous or mildly purulent, but cytologic analysis should reveal no bacteria; cleanse stoma gently with sterile saline and gauze squares as needed; surgical scrub can be used if needed but should be rinsed off completely. PEJ tube may be used as long as it remains functional and needed; often used for days to many weeks. Enteral feedings, either as boluses or constant drip infusion, are started with goal of one-third of daily caloric requirements being given the first day, two-thirds the second day, and full feedings by the third day. After removal of the PEJ tube, the remaining gastrostomy (PEG) tube may be used for nutrition if appropriate. The gastrostomy tube is left in place a minimum of 10 days to ensure adequate adhesion of stomach to the abdominal wall. The gastrostomy tube is removed by gentle progressive traction in a caudal direction that is also directed slightly away from the body; the remaining stoma will often close over within 4 to 8 hours after tube is removed.
ALTERNATIVES AND THEIR RELATIVE MERITS Nasojejunostomy tubes are placed with endoscopic or fluoroscopic assistance. These have the advantage of not requiring a gastrostomy tube. However, they have problems with nasal irritation, short duration of use (often a few days), difficulty in placing the tip distally enough in the jejunum, and problems with postprocedural retrograde migration back to the stomach or being vomited aborally. Laparoscopic-assisted jejunostomy tubes can be placed at the end of a diagnostic or therapeutic laparoscopy. This technique involves exteriorizing a loop of jejunum, which then is held with four stay sutures while a pursestring suture is placed in the antimesenteric side. The jejunostomy tube is placed through an incision in the center of the purse-string suture. This suture is tightened when the tube has been placed successfully (using fluoroscopy to confirm location and aboral direction). A box suture technique is used for creating an adhesion of the intestine to the body wall that secures the safe position of the jejunostomy tube. Problems can involve aboral migration or confusion in the direction for placement of the tube. Other complications include those that would be possible with surgically placed jejunostomy tubes. AUTHOR: MARK E. HITT
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Gastroscopy/Duodenoscopy SYNONYM Upper gastrointestinal (GI) endoscopy
OVERVIEW AND GOALS Minimally invasive endoscopic method of visualizing the mucosal surface of the stomach and proximal duodenum. This procedure offers the possibility of retrieving foreign bodies, performing mucosal biopsies, and placing a gastrostomy or jejunostomy tube.
INDICATIONS Chronic or acute vomiting Gastric foreign body Suspicion of gastric or duodenal ulcer Suspicion of gastric or duodenal neoplasia Suspicion of inflammatory bowel disease Placement of percutaneous endoscopic gastrostomy (PEG) tube for enteral feeding
CONTRAINDICATIONS Food in stomach Large and/or sharp foreign body
EQUIPMENT, ANESTHESIA General anesthesia required Endotracheal intubation required Mouth gag/speculum Flexible fiberoptic or video endoscope with monocular or video display: Diameter of 9-10 mm and length of 1000-1250 mm are sufficient for both gastroscopy and duodenoscopy of most medium- to large-sized dogs and for only gastroscopy of cats and small dogs. A diameter of 5.5 mm or less is usually necessary to enter the duodenum of cats or small dogs. A length of 900-1000 mm is usually sufficient for cats and small dogs. Vacuum source for endoscopic suction Endoscopic biopsy forceps Endoscopic foreign body retrieval forceps, snares, or baskets Biopsy jar with 10% buffered formalin
ANTICIPATED TIME Usually 60-90 minutes anesthesia time (30-60 minutes endoscopy time) Complex foreign body retrieval may take >60 minutes.
PREPARATION: IMPORTANT CHECKPOINTS Animal should have fasted for 12 hours prior to the procedure if possible. Simpler, less invasive diagnostic procedures are performed prior to endoscopy (e.g., CBC, serum biochemistry profile, urinalysis, abdominal radiographs in all cases, abdominal ultrasound, fecal flotation, adrenocorticotropic hormone stimulation test, and others as indicated by the specific features of each case).
POSSIBLE COMPLICATIONS AND COMMON ERRORS TO AVOID Narcotic analgesics (e.g., morphine, meperidine, and butorphanol) increase motility of the pyloric antrum and may make passage of the endoscope into the duodenum difficult. Gastric or duodenal rupture:
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Usually only occurs when the wall is compromised by a deep ulcer or neoplasia. Overinsufflation, usually of the stomach, may cause potentially severe bradycardia due to abdominal compartment syndrome (see p. 4) and creates the risk of gastric rupture. Prior administration of barium may make visualization difficult, and aspirating it with suction through the endoscope may be damaging to the suction channel of the endoscope. Failure to recognize the major duodenal papilla as a normal structure (major and minor duodenal papillae in cats) could lead to inadvertent biopsy, which in turn presents the potential for fibrosis and obstruction of the pancreatic and common bile ducts.
PROCEDURE Induce general anesthesia. Position the animal in left lateral recumbency. This is the position in which the pylorus is most easily entered. Place a mouth gag to keep the jaws open. Lubricate the endoscope with water-based lubricating jelly. Introduce the endoscope into the mouth, and feed it gently through the upper esophageal sphincter. Examine the esophageal mucosa as the scope is advanced down to the lower esophageal sphincter. Insufflate the esophagus with enough air to prevent the walls from collapsing on the scope and reducing visibility. An assistant may be required to gently occlude the upper esophagus by gently squeezing the cervical region externally, immediately cranial to the larynx, to prevent insufflated air from escaping out of the mouth. This will not be necessary once the tip of the endoscope is in the stomach. Whenever the scope is traveling down a tubular structure such as the esophagus or duodenum, it is important to keep repositioning the scope so the lumen of the tube is kept in the center of the screen. This maximizes visibility and minimizes trauma to the gut wall. Thread the scope through the lower esophageal sphincter by keeping the opening to the stomach in the center of the screen/view piece while gently advancing the scope. Once the distal end of the endoscope is in the stomach, insufflate the stomach with air to separate the walls and improve visibility. Insufflate until the rugal folds of the stomach are less prominent but still present. If the rugal folds are completely flattened, the stomach is so inflated that there is risk of compromising respiration or rupturing the stomach. If duodenoscopy is to be performed, it is best to proceed directly to the pylorus while it still may be relaxed. Prolonged insufflation or other activity in the stomach stimulates pyloric tone and motility, making threading the scope through the pylorus more difficult. Advancing the scope through the pylorus is usually the most difficult part of this procedure. The tone and degree of patency of the pylorus can be quite variable. If it is difficult to advance the scope to the opening of the pylorus (i.e., the scope is fed into the animal but advances no closer to the pylorus), suction some air out of the stomach—it may have been overinflated. This is common in large-breed dogs. If the pylorus is open, immediately advance the scope into the duodenum. If the pylorus is closed, maintain the opening to the pylorus in the middle of the screen while gently advancing the scope. If resistance is encountered, do not force the scope. Sometimes insufflating some air at the opening of the pylorus will stimulate it to open. If the pylorus is impossible to thread, try feeding a closed pair of endoscopic biopsy forceps through the pylorus. Use the threaded forceps as a stylet to feed the scope into the duodenum. If the scope still will not pass through the pylorus, consider using a smaller scope. Once the distal end of the endoscope is in the duodenum, advance the scope down to the limit of its length. Identify, if possible, the major duodenal papilla where the pancreatic duct and common bile duct empty into the duodenum. Do not biopsy this structure accidentally.
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GASTROSCOPY/DUODENOSCOPY Endoscopic view of the normal pylorus (P).
GASTROSCOPY/DUODENOSCOPY Endoscopic view of the normal duodenum.
GASTROSCOPY/DUODENOSCOPY Endoscopic view of the pylorus (P) and a large craterlike gastric ulcer (U).
GASTROSCOPY/DUODENOSCOPY Endoscopic view of a duodenal ulcer (U). Examine and identify any irregularities to the duodenal mucosa and any foreign bodies.
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Obtain multiple (6-12) mucosal biopsies using biopsy forceps. Store these biopsies in 10% formalin. Any brushings or fluid samples for cytologic analysis or culture may be obtained now as well. Slowly withdraw the endoscope from the duodenum while obtaining mucosal biopsies and deflating the duodenum. Once the tip of the endoscope is back in the stomach, examine the entire stomach, including obtaining a retroflexed view to visualize the gastric cardia. This maneuver requires maximal flexion of the endoscope tip such that the endoscope itself is seen emerging through the cardia. Identify any mucosal irregularities, masses, ulcers, or foreign bodies. Obtain multiple (6-12) biopsies of any irregular structures and normal mucosa. Be cautious about taking a biopsy of deep gastric ulcers, because this could cause perforation of the stomach wall. Deflate the stomach before withdrawing the endoscope into the esophagus. Deflate the esophagus while slowly continuing to withdraw the endoscope from the esophagus. Suction any fluid in the esophagus, because it may be refluxed gastric acid that may ulcerate the esophagus if left behind. Take the scope out of the animal, remove the mouth gag, and recover the animal from anesthesia.
POSTPROCEDURE This procedure is minimally invasive, and the animal rarely requires analgesics after the endoscopy. Anesthetic recovery is usually routine. Clean the endoscope (internal and external surfaces) immediately before secretions and fluid have dried and are difficult to remove.
ALTERNATIVES AND THEIR RELATIVE MERITS Exploratory laparotomy: Large, full-thickness biopsies may be taken from anywhere in the GI tract. All the abdominal organs may be visualized and biopsied if needed. Virtually any foreign body may be retrieved anywhere in the stomach or intestine. Serosal surfaces and wall thickness can be evaluated. Gastrostomy tube or jejunostomy tube may be placed. Tumors or abnormal tissue may be surgically excised. More invasive May be more costly May be more time consuming More painful for the animal/longer recovery time Greater risk of peritonitis and incisional dehiscence Unable to visualize the esophagus Unable to visualize the mucosal surface of stomach or intestines unless a gastrotomy or an enterotomy is performed AUTHOR: PETER FOLEY
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Gastric Intubation, Gavage, Lavage SYNONYMS Gastric decompression, orogastric feeding, orogastric intubation
OVERVIEW AND GOAL Passage of a hollow tube into the mouth and through the oropharynx into the stomach to facilitate decompression of gas, removal of stomach contents (lavage), or administration of large volumes of liquid, food, or medication (gavage)
INDICATIONS Gastric intubation: Preoperative stabilization of gastric dilatation/volvulus (GDV); allows evacuation of gas and fluid, resulting in an improved hemodynamic state Relief of discomfort associated with gaseous dilatation (without torsion) of the stomach Gavage: Administration of large volumes of liquid medication, including: Activated charcoal after toxin ingestion Barium for gastrointestinal (GI) contrast radiography Hyperosmotic laxative agent prior to colonoscopy Administration of formula to neonatal animals that are not nursing on their own Lavage: Preoperative stabilization of GDV. Removal of stomach contents may help decrease the speed of gas reaccumulation while the animal is being prepared for surgery, thus slowing or preventing cardiovascular deterioration. Removal of stomach contents with suspected intoxications Note: Gastric lavage may not be indicated in all cases of toxin ingestion. Substance ingested, consistency, time since ingestion, and animal status will influence whether gastric lavage is appropriate.
CONTRAINDICATIONS Esophageal disease that could lead to tube-induced trauma or perforation. Conditions of concern include esophageal stricture, neoplasia, ulceration, megaesophagus, and recent esophageal surgery. Gastric disease that could lead to tube-induced trauma or perforation. Conditions of concern include neoplasia, ulceration, and recent gastric surgery. Any swallowing disorder (megaesophagus, esophageal motility disorder, etc.), pharyngeal disorder, or laryngeal disorder (paralysis, previous tie-back surgery, etc.) that could predispose a nonendotracheally intubated animal to aspiration. If even one of these conditions is present, the risk of the procedure versus its benefits must be considered (and will vary from case to case) before deciding whether to perform the procedure.
EQUIPMENT, ANESTHESIA Gastric intubation: Two assistants (minimum) Flexible plastic tubing of various length and diameter. The distal end must be smooth and atraumatic; smoothing may be achieved by brief heating of the end of the tube over a flame, cooling, and trimming edges with a scalpel blade. One to three side holes may facilitate evacuation of stomach contents by minimizing obstruction of a single distal hole with gastric mucosa or ingesta. A roll of clinic-type white cloth tape Water-soluble lubrication jelly Mouth gag/speculum If gastric lavage, all of the above, plus: Funnel or stomach pump Container (e.g., bucket) to collect stomach contents and lavage fluid
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Lavage fluid: usually warm (body temperature) water
ANTICIPATED TIME Dependent on cooperation of animal; additional time may be needed for sedation or general anesthesia: Gastric intubation: 2-5 minutes Gavage: 3-10 minutes Lavage: 10-60 minutes
PREPARATION: IMPORTANT CHECKPOINTS Ensure that adequate manual or chemical restraint for the procedure is planned. Personal preference and animal stability may dictate the degree of sedation or anesthesia chosen. Note: Some clinicians prefer to ensure a patent and protected airway to minimize the potential for aspiration pneumonia through the use of general anesthesia and a cuffed endotracheal (ET) tube when gastric lavage is performed. Maximize cardiovascular stability prior to the procedure.
POSSIBLE COMPLICATIONS AND COMMON ERRORS TO AVOID Inadvertent passage of the orogastric tube into the trachea can result in mild to severe complications: Tracheal irritation leading to transient coughing or mucosal bleeding is possible. Tracheal or bronchial placement of the gastric tube can result in airway obstruction until the tube is repositioned. Tracheal or bronchial tearing can result in pneumomediastinum, pneumothorax, and death. Tracheal or bronchial administration of gavage or lavage fluids can result in severe aspiration pneumonia and death. See procedure (as explained in following paragraphs) for avoidance of this complication. Oral, pharyngeal, laryngeal, esophageal, or gastric trauma can result if excessive force is used for passing the gastric tube. Full-thickness tearing is possible, especially with a preexisting underlying disease. Inability to pass the tube into the stomach may be due to the choice of a tube with a diameter that is too large, esophageal obstruction (foreign body, stricture, neoplasia), torsion of the stomach, or excessive lower esophageal sphincter (LES) tone. Discontinuation of metoclopramide prior to elective gastric intubation is recommended to minimize LES tone. Inadequate sedation of an uncooperative animal will lead to longer procedure times and increased risk of injury to the animal and veterinary staff. Inability to effectively remove gastric contents through lavage may be related to excessive size or adhesive nature of gastric contents, gastric compartmentalization, or other factors. Regurgitation during lavage, gastric overfilling, or esophageal administration of large volumes of lavage fluid can result in aspiration if a cuffed ET tube is not in place. Excessive tube advancement can cause occlusion of the distal end of the tube against stomach mucosa. Palpation of the tube pressing against the stomach wall may indicate a need for partial retraction.
GASTRIC INTUBATION, GAVAGE, LAVAGE Materials and equipment used for gastric intubation and lavage. A, Orogastric tube. B, Metal speculum or roll of tape to be used as a mouth gag. C, Stomach pump for lavage.
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PROCEDURE Manual restraint, sedation, or general anesthesia as indicated Position animal in sternal recumbency. If animal is uncomfortable, alternate positions may be better tolerated (sitting, standing, lateral, etc.). Placement of the animal on an elevated surface will allow gravity-assisted efflux of stomach contents and lavage fluid once the tube is in place. Choose appropriate tube diameter for esophageal size and procedure planned. Example: A tube with an outer diameter of 1.5 inches (3.5 cm) is appropriate for most medium-sized dogs (45 lb [20 kg]). A larger tube size may be necessary for effective lavage versus gas decompression. Measure the length of tube necessary to pass from the nose to the xiphoid. Mark this distance on the tube with a piece of tape or nontoxic marker. Place a mouth gag (speculum) to prevent the animal from chewing on the tube. A roll of 2-inch (5 cm)-wide clinic-type white cloth tape works well in many animals. The tube will pass through the hole in the tape roll. Place tape roll on top of the tongue and behind all 4 canine teeth. Have an assistant hold the mouth closed around the mouth gag. Avoid using a gag that will damage the teeth. Generously lubricate the distal portion of the stomach tube. Pass the tube into the mouth through the mouth gag. Advance the tube through the oropharynx and into the esophagus. Steps to promote and confirm esophageal and subsequent gastric intubation include: Choice of a larger gastric tube size than appropriate ET tube size will lessen the possibility of tracheal intubation. A neutral or very slightly ventro-flexed position of the head (i.e., avoiding extension of the neck) will reduce the opportunity for the tube to pass into the trachea. In the awake animal, allow the swallowing reflex to facilitate tube passage through the pharynx. If substantial coughing occurs, reassess placement, because the orogastric tube may be in the trachea. Palpate the tube in the esophagus (separate from the tracheal rings). Direct visualization of tube passage through the esophagus along the left side of the neck (lean, short-haired patients). Small amounts of air infused into the stomach tube result in a gurgling sound when the stomach is ausculted. Mild suction applied to the tube should reveal negative pressure, stomach contents, or odorous gastric gas with proper gastric intubation, whereas air flow and absence of negative pressure suggest that the tube is in the airways. Pass the tube up to the marked point that indicates where the tube should have entered the stomach. Relief of gas pressure can be assessed through auditory, tactile, and olfactory observations. Certain conditions such as GDV may inhibit tube passage into the stomach. Choice of a smaller tube, gentle rotational pressure on the tube, repositioning of the animal, or percutaneous needle gastric decompression may facilitate passage. DECOMPRESSION: Place the external portion of the stomach tube lower than the animal's head and body to allow gravity-assisted evacuation of stomach contents. Gentle massage of the stomach through the body wall may help to increase efflux. GAVAGE: Using syringe, funnel, or stomach pump, instill the desired medication through the tube into the stomach. With administration of viscous materials, dilution with water may facilitate passage through the tube. Coughing, dyspnea, or cyanosis at any point suggests the tube may be in the respiratory tree. The procedure is terminated immediately, with kinking of the proximal tube (to avoid leakage of tube contents during withdrawal), tube removal, and animal care (physical examination, thoracic radiography as warranted, etc.). LAVAGE: Using a funnel or stomach pump, instill approximately 5-10 mL/kg of lukewarm (body temperature) water into the tube. Acute onset of coughing, dyspnea, or cyanosis warrants immediate termination, as already described. Hold the tube higher than the animal's head to prevent efflux of the lavage fluid until desired. Gently massage the stomach to facilitate mixing of the stomach contents with the lavage fluid. Lower the stomach tube below the level of the head to allow the lavage fluid to efflux. Gentle manipulation of the tube forward or backward 1-3 cm may improve efflux. If the tube obstructs with stomach contents, flushing or manual breakdown may relieve the obstruction. If this is unsuccessful, the tube should be removed and the entire process repeated. Repeat lavage administration and efflux until the efflux is clear and the stomach contents have been removed.
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REMOVAL: Kink the tube during removal to prevent laryngeal/pharyngeal contamination with liquid remaining in the tube lumen. Remove the mouth gag.
POSTPROCEDURE Monitor recovery from sedation/anesthesia. Supportive care as indicated for the condition.
ALTERNATIVES AND THEIR RELATIVE MERITS Nasoesophageal/nasogastric intubation: May be less stressful to the animal than orogastric intubation Tube can be left in place for repeated aspirations/instillations. Small tube diameter prevents administration of viscous substances and effective lavage. Withdrawal of large volumes of gastric contents is not possible. Percutaneous needle decompression/gastrocentesis: May be easier to perform in a fractious animal Allows gastric gas decompression when degree of torsion or another esophageal obstruction prevents tube passage Potential for splenic puncture/laceration, gastric vessel or wall laceration, or other abdominal trauma Ineffective for removing ingesta or large volumes of gastric contents Manual oral administration of medications or formula (pediatric animals): Decreased chance of complications associated with orogastric intubation and gavage Administration of large volumes to an uncooperative animal is labor intensive. Risk of aspiration with force feeding Induced emesis to clear gastric contents: Often more effective at removing stomach contents than lavage Risk of aspiration, especially with decreased mentation or laryngeal/pharyngeal dysfunction Not indicated with caustic ingestions Not effective in all animals AUTHOR: LILLIAN I. GOOD
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Holter/Cardiac Event Monitoring SYNONYMS Ambulatory electrocardiography, cardiac telemetry
OVERVIEW AND GOALS Goal: to assess the cardiac rhythm during an extended period of time. The monitor may record the cardiac rhythm continuously for 24-48 hours (Holter monitor) or only when triggered to record over a period of days to weeks (event monitor). With both devices, the pet is able to be in their home environment, and the owner is able to observe pet behavior.
INDICATIONS Syncope Episodic clinical signs of uncertain type but that might represent syncope Screening of breeding or at risk animals (boxers, Dobermans) for latent arrhythmia (arrhythmia not causing overt clinical signs) Monitoring of antiarrhythmic drug effects (Holter monitor only)
CONTRAINDICATIONS Animal thought to be likely to damage a portable monitor Animal that will be bathed or will be swimming Animal too small to carry monitor (monitoring may still take place, but animal stays mainly in pet carrier or cage for recording period)
EQUIPMENT, ANESTHESIA Clippers for hair Isopropyl alcohol Gauze squares or cotton balls Cardiac electrode adhesive patches (cutaneous) Ultrasound gel Bandage material: roll gauze, Esmarch-type bandage material (e.g., Vetrap), stretch adhesive-type cotton bandage (e.g., Elastikon, Elastoplast), 2-inch white medical tape, +/− cast padding Holter or event monitor, including wires to connect to animal, new batteries, and a blank digital card (Holter only), +/− Holter vest Interpretation system and printer or access to such a system Note: Monitors are expensive systems not routinely owned by general practices. They are available for rental from many sources, including www.labcorp.com, www.vetheart.com, www.idexx.com, and www.pdsheart.com. Additionally, many veterinary college cardiology services have mail-out Holter programs. Veterinary sources are preferred because knowledge of common veterinary diseases (boxer dogs with arrhythmogenic right ventricular cardiomyopathy [ARVC], miniature schnauzers with sick sinus syndrome [SSS]), normal veterinary findings (sinus arrhythmia, sinus tachycardia, sinus pauses during daytime rest), and common veterinary artifacts (purring, panting, shaking) are important parts of interpretation. The monitor itself is sent by courier to the hospital for placement on the animal. Instructions for placement and patient daily diaries are usually sent with the monitor. When the monitoring period is over, the monitor is mailed back or transmitted via transtelephonic signal (event monitor), and findings and interpretations are reported back. Some mail-out programs (mostly veterinary colleges) will also provide consultation on the case as part of the service, along with the written Holter/event monitor report.
ANTICIPATED TIME Installation: 10 minutes (event monitor) or 20 minutes (Holter) Monitoring period: 24 or 48 hours (Holter); 7-30 days (event monitor, longer if battery is replaced; weeks to many months for surgically implanted event monitors)
PREPARATION: IMPORTANT CHECKPOINTS
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If the reason for using cardiac monitoring is the occurrence of sporadic clinical signs, a complete medical evaluation is usually indicated first: CBC, serum biochemistry panel, urinalysis: all cases, hypoglycemia, hypocalcemia Serum preprandial and postprandial bile acids (if consistent with case): hepatic encephalopathy Electrocardiogram (ECG; standard, in-hospital): all cases; the diagnosis may be apparent without the need for Holter or cardiac event monitoring. Thoracic radiographs, echocardiogram: all cases; assessment of cardiac structure, presence or absence of signs of congestive heart failure. The monitor itself is checked for proper function before preparing to install it on the animal. These instructions are usually sent with the monitor. Discussion of care of the monitor with the owner: the monitor must stay dry, clean, intact, and undamaged. It is customary to have the owner leave a deposit in the sum of the replacement cost of the monitor before leaving the hospital with the machine.
POSSIBLE COMPLICATIONS AND COMMON ERRORS TO AVOID Wet monitor: no swimming or bathing during the recording period. In the rain, a plastic bag should be placed over the monitor by the owner. Damaged/chewed monitor or wires: if the owner observes the animal damaging the monitor, an immediate recheck is warranted. The equipment can be examined, and subsequently the monitor may simply be more heavily wrapped to prevent damage, or the monitoring period may be terminated and the monitor removed. Unstuck electrode patches: prevented by cleaning and preparing the skin with isopropyl alcohol prior to patch placement. Although not routine, in very active patients, a small amount of tissue glue can be used to prevent this. Poor electrode patch contact with skin: prevented by cleaning and preparing the skin with isopropyl alcohol prior to patch placement and adding a small amount of ultrasound gel to the center of the patch before applying it to the skin (see following paragraphs). Monitoring period is inexplicably shorter than expected: prevented by using new batteries every time. In addition, for audiotape Holter monitors, it is important to be sure that the audiotape is not put into the monitor backwards. Poor triggering of event button (Holter) or record button (event monitor): prevented by carefully showing the owners how to trigger the event and record buttons on the monitor at the time of installation. Letting batteries run out, causing the captured events to be deleted (event monitor): clients need to return 1 day prior to expected end of battery life to replace battery.
PROCEDURE HOLTER MONITOR: The animal's apex beat (heartbeat on the thorax) is palpated on both the right and left side of the chest. These will be the sites of electrode patch placement. The hair is clipped over these areas bilaterally, starting close to the sternum and working upwards ensuring a generous clip: There must be room for the electrode patches and a few centimeters of space separating them. The hairless skin is wiped clean with isopropyl alcohol–soaked gauze or cotton and allowed to dry before placing the electrodes. Technician Tip: The patient should be standing during the application of the Holter or event monitor to ensure proper positioning of the leads and for taping purposes. Some cardiologists prefer to attach the patches to the wires of the monitor prior to placing the patches on the animal, which is acceptable. The following method will describe the alternative approach. Patch preparation: a very small dollop of ultrasound gel is placed on the center of each electrode patch. For very active patients, a tiny amount of tissue glue ( 5%) Total/partial parenteral nutrition (T/PPN) administration In animals with severe vomiting and diarrhea that require IV access
CONTRAINDICATIONS Hypercoagulable states (e.g., protein-losing nephropathy) Increased intracranial pressure (holding off jugular vein may increase intracranial pressure) Hypocoagulable states (e.g., liver failure, rodenticide anticoagulant intoxication) Thrombocytopenia Thrombocytopathia Skin infection over site of jugular catheter placement
EQUIPMENT, ANESTHESIA Sedation generally not necessary in critically ill animals but may be needed in fractious animals Clippers Sterile surgical gloves Surgical scrub soap Gauze squares for surgical prep of site Heparinized saline flushes Suture material White cloth-type tape Bandaging material (e.g., roll gauze, cast padding, and Elastikon/Elastoplast-type adhesive roll bandage) Injection cap Triple-antibiotic ointment Guide-wire technique: the following four items are available in kits manufactured by Cook, Mila, and Arrow: Hypodermic needle Guide wire Dilator Polyurethane IV catheter Other materials: A #11 scalpel blade Suture material (e.g., 2-0 to 4-0 nylon)
ANTICIPATED TIME About 20 minutes
PREPARATION: IMPORTANT CHECKPOINTS
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Check coagulation profile (prothrombin time [PT], partial thromboplastin time [PTT], platelet count, platelet function)
POSSIBLE COMPLICATIONS AND COMMON ERRORS TO AVOID Do not use leashes that go around the neck (neck leads) when a jugular catheter is in place. Place needle guard when using through-the-needle catheters before removing the stylet. Otherwise, the needle can lacerate or transect the catheter. Avoid excessively tight neck bandaging.
PROCEDURE Catheter placement should always be done aseptically. Animal should be in lateral recumbency, with the nonrecumbent side being the side with the jugular to be catheterized. Clip hair from site. Centered over the jugular furrow, the clip and aseptic prep extend approximately as follows: From slightly beyond the ventral midline of the neck ventrally to halfway between the ventral and dorsal midlines dorsally From the thoracic inlet caudally to the angle of the mandible cranially Prepare site aseptically with complete surgical scrub. GUIDE-WIRE TECHNIQUE: Use sterile surgical gloves when placing the catheter. Drape site with sterile drape. Check that catheter or needle about to be used for venipuncture can accept guide wire (compatible diameters). Insert needle in vessel (jugular venipuncture): Catheter (generally needs to be larger than 20-gauge) may used in place of needle. In thick-skinned animals, a two-step approach may be better: Raise the jugular vein. Lift (tent) the skin overlying the jugular vein. Enter only the skin with the needle/catheter, or make a small stab incision in the skin with a sterile scalpel blade. Gently return the skin to a normal position (keeping the needle in place in the skin). Advance the needle into the raised jugular vein. Place guide wire into vessel through needle or catheter, J-tip (not straight tip) first. To do so, the guide wire is retracted into the J-tip straightening device (a small, tapered sleeve), and the device with the straightened J-tip is placed into the catheter. The guide wire may then be advanced easily through the catheter and into the jugular vein, with the J shape emerging from the peripheral catheter in the jugular vein to avoid trauma from a straight guide wire tip. After advancing the guide wire a few cm into the jugular vein (4-10 cm, depending on the patient's size), do not move the guide wire for the rest of the procedure until the catheter is in place. While holding the guide wire firmly with one hand (guide wires are Teflon-coated and slippery), remove needle or catheter from vessel and off the wire while ensuring the guide wire stays in the vessel. Maintain digital pressure over the catheter placement site to minimize hemorrhage. Measure length of guide wire protruding from skin; it should be a few cm greater than the length of the dilator (withdraw guide wire slightly as needed). Place dilator over the wire into the vessel (this dilates the vessel insertion site so the catheter can be placed more easily into the vessel). Expect some bleeding around the site, which should be controlled with direct pressure. Some jugular catheter kits have a combined catheter-dilator configuration, which allows the dilation step and the catheter placement step to occur simultaneously. While holding the guide wire firmly in place, remove the dilator back over the wire, making sure that wire stays in the vessel. Apply pressure over the site to minimize hemorrhage. Thread IV catheter over the wire, and advance catheter into the vessel. Remove wire, making sure the catheter stays in place. Remove air in the catheter line with the use of a 3-mL syringe that contains heparinized saline. Flush catheter with heparinized saline without administering air to animal. Suture catheter to skin. Cover site with nonadhesive bandage. Bandage catheter in a stable position (neck wrap).
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JUGULAR CATHETER PLACEMENT AND MANAGEMENT Guide wire–type jugular catheter kit. A, Triple-lumen jugular catheter. B, Flexible Teflon-coated stylet with J-tip straightening sleeve (arrowhead). C, Vessel dilator. D, Peripheral IV catheter (large-bore needle may be used instead, but guide wire must fit through it). E, Local anesthetic. F, Syringe for injecting anesthetic. G, Disposable scalpel for making skin incision. H, Suture material. THROUGH-THE-NEEDLE CATHETER TECHNIQUE: Insert needle into vessel. The two-step technique may help (as just described). Advance catheter through the needle into the vessel. Lock catheter into needle hub. Withdraw needle from vessel and skin (i.e., withdraw needle by 3-4 cm, ensuring catheter remains well in the jugular vein), and place the needle guard over needle. Remove stylet from catheter. Cap catheter and flush catheter with heparinized saline. Suture catheter to skin. Cover site with nonadhesive bandage. Bandage catheter in a stable position (neck wrap).
JUGULAR CATHETER PLACEMENT AND MANAGEMENT Through-the-needle jugular catheter. Inside the kit (left) are the catheter (center) and needle guard (right). Note plastic sheath of catheter, which allows catheter to be advanced through needle into
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the patient without wearing sterile gloves; also note large needle that remains with the patient and must be covered with needle guard.
POSTPROCEDURE Assess tightness of bandage around animal's neck after each layer is placed. A finger should easily pass between skin and bandage. For walks, leashes should be placed around shoulders, or use a harness. If using multiple-lumen catheters, be sure animal cannot chew lumen lines. When using multiple lumens, designate one for TPN (usually the most distal). Flush line(s) with heparinized saline every 6 hours to maintain patency.
ALTERNATIVES AND THEIR RELATIVE MERITS Peripheral catheter: technically simpler and cheaper but does not allow jugular catheter functions as already described. AUTHORS: ELISA A. PETROLLINI ROGERS, KENNETH DROBATZ
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Luxation Reduction (Closed): Shoulder, Elbow, or Hip SYNONYMS Coxofemoral luxation (hip); dislocated shoulder, elbow, hip; scapulohumeral luxation (shoulder)
OVERVIEW AND GOALS Severe joint trauma can cause ligament/joint capsule damage, resulting in displacement of the bones of a joint. Closed reduction aims to restore the normal alignment of the joint without surgical intervention, and to maintain stability until these soft tissues heal.
INDICATIONS Traumatic luxation of normal shoulder, elbow, hip joints Acute luxation (5 to 7 days) Dysplastic joint: Glenoid dysplasia Total hip replacement may be a better option in cases of severe hip dysplasia. Femoral head and neck ostectomy (FHO) may be an acceptable alternative to closed/open hip reduction in a small dog or cat.
EQUIPMENT, ANESTHESIA General anesthesia Rope or leash to provide counterpressure (hip luxation) Assistant Bandage material
ANTICIPATED TIME About 10-30 minutes
PREPARATION: IMPORTANT CHECKPOINTS Advise owner of aftercare and possible drawbacks: Recurrence Degenerative joint disease Decreased range of motion Possible need for open reduction Postreduction bandage care Postreduction exercise restriction After anesthetic induction: Minimum of two views of the joint to confirm luxation versus fracture Animal in lateral recumbency, affected limb up (affected limb on the nonrecumbent side) Hanging the affected limb can be useful (elbow luxation) for 5-10 minutes: secure the carpus, and hoist the limb vertically with traction. Be sure to secure the limb proximal to the metacarpi, and use a thick, soft rope (or roll gauze) in a double-loop technique, rather than single loop, to distribute pressure evenly on the distal limb. These measures reduce the risk of
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iatrogenic damage.
POSSIBLE COMPLICATIONS AND COMMON ERRORS TO AVOID If there is excessive instability following closed reduction, open reduction should be performed. Failure to critically evaluate plain radiographs to assess joint anatomy or damage, avulsion fragments, and intraarticular debris Trying to reduce a luxation with sedation alone Failure to appropriately bandage the luxation Removal of bandage too soon Inadequate patient exercise restriction When hanging the forelimb to help with elbow luxation reduction: be sure to secure the limb proximal to the metacarpi, and use a thick, soft rope (or roll gauze) in a double-loop technique to distribute pressure evenly on the distal limb. These measures reduce the risk of iatrogenic damage.
PROCEDURE All luxation reductions are performed with the animal under general anesthesia and in lateral recumbency, affected side up (nondependent). Shoulder: Forelimb held in extension (in a ventral direction perpendicular to the long axis of the body, as in the standing animal) For lateral luxation of the humeral head, apply medial pressure to the head at the same time as lateral pressure on the scapula. Check range of motion and stability. Place leg in a Spica splint. For medial luxation of the humeral head, apply lateral pressure to the head at the same time as medial pressure on the scapula. Check range of motion and stability. Place the leg in a Velpeau sling. Splint or sling can be removed after 2 weeks. Passive range-of-motion exercises can begin after bandage removal, but restricted exercise is essential for another 2-4 weeks. Elbow: Radius and ulna are usually luxated laterally relative to the distal humerus. With the elbow in flexion, inwardly rotate the antebrachium. Combined with elbow flexion, this movement enables the anconeal process of the ulna (caudal-most extent of the trochlear notch in the ulna) to hook into the olecranon fossa of the humerus. This maneuver is followed by careful extension of the elbow. Hook the anconeal process of the ulna between the humeral condyles, and carefully extend the elbow. With this part of the maneuver, the joint should now be reduced. Passive range-of-motion exercises can begin after bandage removal, but restricted exercise is essential for 4-6 weeks, followed by 2 weeks of leash exercise only. Hip: Assistant stands on opposite side of animal, holding the ends of a padded rope or leash placed in the animal's groin to provide counterpressure. Craniodorsal hip luxation (more common): The tarsus is grasped and externally rotated while the femur is pulled caudally. The head of the femur rides up (moves laterally and then caudally) and over the dorsal acetabular rim. Internal rotation while maintaining distal traction on the femur, together with direct pressure on the greater trochanter, will seat the head in the acetabulum. Place hip in an Ehmer or modified Ehmer sling for 2 weeks. Caudoventral luxation: The femur should be abducted and externally rotated to seat the femoral head in the acetabulum. Hobbles may be applied for 10-14 days. Medially-directed pressure can be applied to the reduced proximal femur as the hip is passively flexed and extended in an attempt to drive debris from the acetabulum.
POSTPROCEDURE Radiograph to evaluate the reduction. Toes should be accessible or visible to monitor for heat, cold, swelling, or pain. Bandage needs to be protected from moisture and kept clean and dry.
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ALTERNATIVES AND THEIR RELATIVE MERITS Open reduction: Requires surgical intervention Greater cost Carries a higher rate of success than closed reduction for the shoulder, elbow, and hip FHO may be worth considering for cats and small dogs, as the possibility of hip reluxation is eliminated. Arthrodesis can provide pain relief for a chronically unstable joint. Aside from cost, complications include nonunion, stress fractures, implant failure and infection. Excision glenoid arthroplasty for the shoulder joint. There are few reports of glenoid arthroplasty, but an abnormal gait is to be expected. Amputation AUTHOR: NICHOLAS J. TROUT
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Local and Regional Anesthesia SYNONYM Local blocks
OVERVIEW AND GOALS Local anesthesia and regional anesthesia refer to a broad range of techniques that utilize local anesthetic agents delivered to a discrete anatomic area (as opposed to systemic delivery). With these techniques, the local anesthetic agent inhibits pain by blocking transmission of noxious input (and other types of sensory input) before it ever reaches the brain. The animal's level of consciousness is not affected. This contrasts with general anesthesia, during which nociceptive processing continues to occur, but the animal is not able to perceive pain owing to the unconscious state.
INDICATION Infiltrative anesthesia: Incisional block: supplemental analgesia for a variety of surgical procedures (e.g., abdominal wall incisions, total ear canal ablation incisions) Peripheral nerve blocks: Dental nerve block: supplemental analgesia for tooth extractions, maxillary/mandibular surgeries Brachial plexus block: supplemental analgesia for surgical procedures involving the forelimb distal to shoulder Distal radial, ulnar, and median nerve blocks: supplemental analgesia for feline onychectomy or any surgical procedure involving the distal forepaw Intercostal nerve blocks: supplemental analgesia after lateral thoracotomy or desensitizing area around isolated rib fractures Epidural anesthesia/analgesia: Lumbosacral injection of local anesthetic: indicated for caudal procedures/injuries only (e.g., involving hind limb, tail, perineum, caudal abdomen) Lumbosacral injection of opioid: hydrophilic opioids (i.e., morphine) indicated to supplement analgesia for a variety of procedures (e.g., hind limb, tail, abdominal, forelimb, thoracic, cervical procedures) Other regional techniques: Intraarticular anesthesia/analgesia: supplemental analgesia for procedures involving the joint space (stifle most common) Interpleural anesthesia: supplemental analgesia for thoracic and cranial abdominal pain (especially pancreatitis) IV regional anesthesia: desensitization of a distal limb to facilitate surgery
CONTRAINDICATIONS Infiltrative anesthesia, peripheral nerve blocks, others: Injection into infected tissue Epidural anesthesia/analgesia (see p.1260): Injection into infected tissue (at lumbosacral junction) Coagulopathy Septicemia Uncorrected hypotension (especially with local anesthetics) Significant trauma/lesion at lumbosacral junction
EQUIPMENT, ANESTHESIA Infiltrative anesthesia: Incisional block: Hypodermic needle (22, 25 gauge), syringe, sterile gloves, local anesthetic Dosages (total per animal): lidocaine, ≤5 mg/kg (dog), ≤3 mg/kg (cat); bupivacaine, ≤2 mg/kg (dog), ≤1 mg/kg (cat) Animal is usually under general anesthesia, and block is done either before incision is made or at the end of the surgery prior to complete closure. Peripheral nerve blocks:
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Dental nerve block: Hypodermic needle (22, 25 gauge), syringe, local anesthetic Dosages (total per animal): lidocaine, ≤5 mg/kg (dog), ≤3 mg/kg (cat); bupivacaine, ≤2 mg/kg (dog); ≤1 mg/kg (cat) Animal is usually under general anesthesia. Brachial plexus block: Hypodermic needle (22 gauge) or spinal needle (22 gauge, 2-3 inches [5-8 cm]), syringe, local anesthetic Dosages (total per animal): lidocaine, ≤5 mg/kg (dog), ≤3 mg/kg (cat); bupivacaine, ≤2 mg/kg (dog), ≤1 mg/kg (cat) Specialized insulated needle (22 gauge, 3 inches) required if a nerve locator is to be used. Animal is usually sedated or under general anesthesia. Distal radial, ulnar, median nerve blocks: Hypodermic needle (22, 25 gauge), syringe, local anesthetic Dosages (total per animal): lidocaine, ≤5 mg/kg (dog), ≤3 mg/kg (cat); bupivacaine, ≤2 mg/kg (dog), ≤1 mg/kg (cat) Animal is usually under general anesthesia, and block is done prior to surgical procedure. Intercostal nerve block: Hypodermic needle (22, 25 gauge), syringe, local anesthetic. Dosages (total per animal): lidocaine, ≤5 mg/kg (dog), ≤3 mg/kg (cat); bupivacaine, ≤2 mg/kg (dog), ≤1 mg/kg (cat) Animal is usually sedated or under general anesthesia. Epidural anesthesia/analgesia (see p.1260): Spinal needle (18, 20, 22 gauge; Quincke or Huber point, 1½-3½ inches [4-9 cm]), syringe, sterile gloves, local anesthetic (preservative-free lidocaine, bupivacaine), ± opioid (preservative-free morphine) Other regional techniques: Intraarticular anesthesia/analgesia: Hypodermic needle (22 gauge), syringe, sterile gloves, local anesthetic (lidocaine, bupivacaine) ± opioid (morphine) Dosages (total per animal): lidocaine, ≤5 mg/kg (dog), ≤3 mg/kg (cat); bupivacaine, ≤2 mg/kg (dog), ≤1 mg/kg (cat) Animal is usually sedated or under general anesthesia. Interpleural anesthesia: Butterfly catheter (22 gauge) or through-the-needle catheter (20 gauge, 2 inches); preplaced chest tube or commercial interpleural anesthesia tray, syringe, sterile gloves, local anesthetic Dosages: lidocaine, ≤5 mg/kg (dog) q 2-4 h; ≤3 mg/kg (cat) q 4h. Bupivacaine, ≤2 mg/kg (dog) initially, then ≤1 mg/kg q 6 h; ≤1 mg/kg (cat) initially, then ≤0.5 mg/kg q 6 h Animals are usually sedated or under general anesthesia. IV regional anesthesia: Cling-and-release bandage material (e.g., Vetrap), IV catheter (22 gauge), tourniquet, hypodermic needle (22 gauge), syringe, local anesthetic (lidocaine) Dose: lidocaine, 2.5-5 mg/kg (dog only) Animal is usually sedated.
ANTICIPATED TIME This time period does not include clipping of hair and preparation of the site where indicated. Infiltrative anesthesia: Incisional block: 5 g/dL of unoxygenated hemoglobin in the peripheral capillaries (corresponds to SpO2 75%-80%); therefore, cyanosis indicates severe hypoxemia, and anemic animals may have critical hypoxemia without cyanosis.
CONTRAINDICATIONS Causing distress to an already compromised animal is a contraindication. Several methods of oxygen delivery are available. Selection of the optimal technique depends on the animal's respiratory status, desired inspired O2 content, anticipated duration of therapy, equipment available and its size, and conformation and temperament of the animal.
EQUIPMENT, ANESTHESIA See description for placement of devices.
ANTICIPATED TIME Less than 10 minutes for any of the procedures
PREPARATION: IMPORTANT CHECKPOINTS Pretreat animal with an anxiolytic that is not hypotensive and does not decrease respiratory effort. Most of these cases are in respiratory distress, so the less anxiety the better. Low-dose benzodiazepines or morphine, buprenorphine, or fentanyl are feasible choices.
POSSIBLE COMPLICATIONS AND COMMON ERRORS TO AVOID Excessive oxygen supplementation: Administration of 100% oxygen for 12 hours or 80%-90% for 18 hours can lead to alterations in pulmonary function and signs of oxygen toxicosis. Oxygen toxicosis is often difficult to recognize because the clinical signs can be similar to those seen with hypoxemia. However, oxygen toxicosis is relatively uncommon, takes at least 12 hours to occur, is preventable, and is reversible in the early stages if oxygen is discontinued. Supplementation with 50% oxygen appears safe in the dog.
PROCEDURE Emergency oxygen supply: holding an oxygen-delivery tube so a high flow occurs directly into the animal's mouth is an option that can be used in an emergency situation until more optimal oxygen-delivery methods are instituted.
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MASK: The mask is perhaps the easiest and least invasive technique for oxygen supplementation. Purpose-made veterinary masks are preferable (better fit). These masks come in an assortment of sizes that range from pediatric size to large dog size and are designed to fit over the muzzle. It is often awkward to administer oxygen via mask to brachycephalic dogs and some cats. The mask can be connected via tubing to a 100% oxygen source, and if used for long periods of time, the oxygen should be humidified. With a well-fitted mask, flow rates of 8-12 L/min achieve a fraction of inspired oxygen (Fio2) of 0.4 to 0.5 (room air 0.2). The advantages of a mask are related to ease and speed of administration, and no specialized equipment is required. In addition, during oxygen administration, the animal can be closely monitored. Disadvantages of this technique include lack of tolerance by some animals and the requirement of constant manual application of the mask unless the animal is moribund or otherwise immobile. INTRANASAL CANNULA: There are various types of tubes available for nasal catheterization, including feeding tubes and urinary catheters. Some clinics use flexible feeding tubes or Foley catheters with multiple fenestrations to avoid mucosal jet lesions. The largest tube size possible should be passed. These tubes are placed in the conscious animal, but local anesthesia is recommended. Topical 2% lidocaine is used. The toxic lidocaine dose is 4 mg/kg in the cat, and one-fourth to half this dose is usually sufficient therapeutically. The tube is premeasured to the medial canthus of the eye, and the level of the external nares is marked on the tube to indicate the maximal distance of insertion. The animal's head is tilted with the muzzle pointing upwards. A few drops of lidocaine are applied to the external nares to desensitize the nasal mucosa. The tube is advanced until the tip is at the level of the medial canthus of the eye (until mark on tube is at nares). Insertion is usually easier if the nostril is pushed dorsally and the tube is directed medially. Once placed, the tube can be secured as close to the nostril as possible with suture or methacrylate glue (superglue). The tube should also be attached on the muzzle, below the eye and on the neck. These animals should also be fitted with an Elizabethan collar to prevent self-directed removal of the tube. The advantages of this technique include ease of application, no special equipment required, versatility in animals that are different sizes, and lack of interference with animal monitoring. Disadvantages include lack of animal tolerance, variable flow rates required to provide oxygen, nasal mucosal irritation, and gastric distention at high flow rates (rare). Recommended flow rates to achieve a specific Fio2 are listed in the table. TRANSTRACHEAL: Oxygen may be administered transtracheally via a nasal catheter, which is advanced through the nasopharynx to the proximal trachea or through a catheter placed percutaneously through the cervical trachea. A long, flexible IV (jugular-type) catheter can be placed percutaneously into the trachea through the cricothyroid membrane or between tracheal rings. These catheters can be over-the-needle types or through-the-needle types. The entry area should be infiltrated with a local anesthetic prior to catheter introduction. In an emergency situation (e.g., cat with critical laryngeal spasm), a hypodermic needle or an over-theneedle catheter attached to a fluid extension set can be used for administering oxygen intratracheally. Oxygen lines used with this technique should be humidified. The disadvantages of this technique include difficulty with tube placement and poor animal tolerance when it awakens or is more alert. Reproduced with permission from Drobatz KJ, Hackner S, Powell S: Oxygen supplementation. In Bonagura JD, editor: Kirk's current veterinary therapy XII: small animal practice, Philadelphia, 1995, Saunders, pp 175–179. Intranasal flow rates of >3l per minute often are not tolerated by animals; these rates may cause the animal to close its oropharynx in response to rapid air/O2 flow. If a hissing sound is heard because oxygen is mostly or entirely refluxing from the nostrils, common sense dictates that the tube and apparatus be checked; if no defects are found, the clinician should try a lower flow rate.
Approximate Oxygen Flow Rates for Supplementation Administration Via Nasal Catheter OXYGEN FLOW RATES (L/MIN) REQUIRED TO DELIVER AN Fio2 OF: 30%-50% 30%-75% 75%-100% Weight (kg) 0-10
0.5-1
1-2
3-5
10-20
1-2
3-5
>5
20-40
3-5
>5
?
OXYGEN CAGE: Oxygen-cage equipment usually involves a chamber that can be flooded with oxygen to provide an oxygenenriched environment. The advantage of this equipment is a controlled environment. The disadvantages include poor access to animal, difficulty in monitoring the animal, and inadvertent uncontrolled environmental conditions (especially overheating). Alternative oxygen-enriched environments include oxygen tents or a cage with a “fitted door” into which O2 is pumped. These systems are inefficient and generally have no way to remove or scavenge CO2. This works well for cats that present in acute congestive heart failure or status asthmaticus, because the clinician can supplement oxygen for a period of time without the stress of nasal oxygen. Human neonatal incubators have also been used for supplementing oxygen in small animals, and kits to modify normal clinic cages into oxygen cages are available. Covering some of the carrier holes with cellophane and providing a humidified oxygen source can
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convert pet carriers into emergency oxygen cages. Elevated temperatures and carbon dioxide levels may be a problem with this technique, however.
OXYGEN SUPPLEMENTATION Animal receiving oxygen supplementation via an intranasal Foley catheter.
OXYGEN SUPPLEMENTATION Animal receiving oxygen supplementation via a tent.
OXYGEN SUPPLEMENTATION Animal receiving oxygen supplementation via an Elizabethan collar partly covered with cellophane, creating an oxygen canopy. Note the oxygen tube entering through the caudal edge of the collar. MISCELLANEOUS: With an Elizabethan collar, cellophane, and a humidified oxygen line, it is possible to easily create an oxygen
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canopy. The animal is fitted with an Elizabethan collar (E-collar), and the lower 50%-75% of the collar diameter is covered with cellophane. The oxygen line is run inside the E-collar and provides oxygen into the cellophane-covered area. In this way, the animal's head is essentially within an oxygen tent. In areas with high ambient temperatures, this device is poorly tolerated. The advantages of this technique include ease of application and no special equipment requirements. The major disadvantage is animal intolerance. Note: Oxygen can also be administered in acute situations via a transparent plastic bag placed over the animal's head.
POSTPROCEDURE Most animals requiring oxygen supplementation will be hospitalized in an intensive care unit and observed closely because of the nature of the underlying disease. In addition, it is important to closely monitor the typical vital parameters, including temperature, pulse, and respiratory rate. Specific evaluation for animals on oxygen supplementation includes thoracic auscultation, observation of respiratory effort, evaluation of mucous membrane color, capillary refill time, blood gas analysis, and/or pulse oximetry. Knowing when and how to discontinue oxygen therapy can present the clinician with a dilemma. Generally it is worthwhile to slowly wean animals off oxygen supplementation. The rate of tapering should be based on the animal's condition and response but is generally done over a 24-48 hour period. It is also important to remember that oxygen is often an adjunctive therapy, and treatment directed toward the underlying disease process is paramount. AUTHOR: DAVID MILLER
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Otoscopy (Video)
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Otoscopy (Video) OVERVIEW AND GOALS Minimally invasive examination technique for the external ear canal, tympanic membrane, and middle ear Allows excellent visualization, sampling, and documentation during ear flushing, myringotomy (deliberate perforation of the tympanum), removal of feline ear polyps, and biopsy procedures
INDICATIONS When clinical signs of ear disease are present: otic discomfort, pruritus, discharge, swelling or erythema, head-shaking, Horner's syndrome, vestibular signs, deafness Ear flushing using video otoscopy is indicated in unresponsive or recurrent otitis or if otitis media or a mass in the ear canal is suspected.
CONTRAINDICATIONS Very painful ears (in conscious animal) Severely stenotic ear canals
EQUIPMENT, ANESTHESIA The main piece of equipment for the procedure is a video otoscope. Ear examination: The examination can be performed in a conscious animal if the ear is not too painful. Manual restraint by an experienced handler is required. A small amount of isopropyl alcohol is needed for cleaning the otoscope tip; a commercial antifog solution improves visualization. Ear flushing: Ear flushing, myringotomy, and biopsy procedures require general anesthesia and endotracheal intubation to prevent lower respiratory tract contamination. Analgesia is essential and should be part of the anesthetic protocol. Ceruminolytic agent (dogs only) Bulb syringe Sterile physiologic saline solution, approximately 1 L in bowl (may be warmed to body temperature) A 5 Fr, 22-inch (56 cm) polypropylene urinary catheter, red rubber feeding tube or Tomcat catheter, tip dulled by heating briefly over a flame Two 30-mL syringes Three-way stopcock valve Culturette tubes Video otoscope: compatible biopsy and grasping instruments and ear curettes are available. Optional: suction unit and flushing and suction apparatus
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OTOSCOPY (VIDEO) Otoscopic view of a normal ear canal and tympanum. The asterisk indicates the optimal site for myringotomy. (Courtesy Dr. Louis N. Gotthelf.)
OTOSCOPY (VIDEO) Otoscopic view of an external ear canal partially obstructed by a large polyp in a dog. (Courtesy Dr. Michel Chenier.)
ANTICIPATED TIME Ear examination: 25 mm Hg, repeat with next additional weight. Record IOP in mm Hg (not as scale readings). Clean tonometer after use. Tono-Pen: Properly fit a clean tip cover, turn on, and calibrate if necessary. Gently touch the instrument tip to the cornea, keeping it perpendicular to the eye; it does not need to be horizontal. Repeat several times until a long beep is heard. A bar over the “5%” at the bottom indicates a statistically significant reading (mean given in mm Hg). TonoVet: Properly insert a new probe tip. Turn on and ensure that proper species calibration is on. Holding the instrument horizontal with the tip 4-8 mm from the cornea, repeatedly press the button to take readings until a long beep is heard. A nonblinking “d” before the reading indicates a statistically significant, dog/cat-calibrated reading. Normal IOP in dogs and cats is 15-25 mm Hg.
OPHTHALMIC EXAMINATION Equipment and materials that may be used during an ophthalmic examination. A, Finnoff transilluminator. B, STT strips. C, Fluorescein dye–impregnated strip. D, Lens. E, Sterile eye irrigating solution. F, 1% tropicamide solution. G, 0.5% proparacaine solution. H, Tonometer—Tono-Pen. I, Tonometer—Schiøtz. J, Direct ophthalmoscope.
POSTPROCEDURE Flush corneas of excess fluorescein if necessary. Protect eyes from light if mydriatics were used. AUTHOR: JANE CHO
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Prostatic Sampling Techniques SYNONYMS Prostatic fine-needle aspiration (FNA) “Tru-cut”: automated needle biopsy Prostatic massage Traumatic catheter biopsy
OVERVIEW AND GOAL Nonsurgical techniques for obtaining prostate tissue samples for culture and cytologic and histopathologic examination in practices with ultrasound capabilities
INDICATIONS Pyuria Hematuria Penile/urethral discharge Prostate enlargement Prostatic mineralization Asymmetric/irregular/nodular prostate
CONTRAINDICATIONS Inadequate restraint Bleeding disorder Prostate abscess (for automated needle biopsy and large-needle FNA) Acute prostatitis
EQUIPMENT, ANESTHESIA FNA: 18-gauge needle 12-mL syringe Usually does not require sedation Ultrasound machine Automated needle biopsy: Automated biopsy needle (14-20 gauge) General anesthesia Ultrasound machine Prostatic massage: Urinary catheter that is long enough to reach the urinary bladder Two 5-mL syringes Two 5-mL aliquots of sterile saline Two sterile sample containers capable of holding at least 5 mL of fluid Manual restraint to general anesthesia, depending on the demeanor of the patient Traumatic catheterization: Urinary catheter that is long enough to reach the prostatic urethra 12-mL syringe Sedation pending patient
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Ultrasound or x-ray machine are helpful.
ANTICIPATED TIME Abdominal ultrasound time will take between 10 and 40 minutes depending on operator expertise. FNA takes about 5 minutes. Automated needle biopsy with anesthesia, prostatic massage, or traumatic catheterization will take about 20-30 min.
PREPARATION: IMPORTANT CHECKPOINTS The patient can be in lateral or dorsal recumbency. These procedures usually require the attending veterinarian and one to two assistants. Needle aspiration can be performed on a fully awake animal, provided the animal is adequately restrained. Automated needle biopsies require heavy sedation with analgesia or general anesthesia. For prostatic massage and traumatic catheterization, both digital rectal palpation and urethral catheterization are necessary. If the patient resists these procedures, sedation is advised. A soft red rubber (Sovereign type) feeding tube is less traumatic than a polypropylene catheter.
POSSIBLE COMPLICATIONS AND COMMON ERRORS TO AVOID FNA and automated needle biopsy procedures require the placement of a needle or biopsy instrument directly into the prostate. Adjacent large vessels such as the distal abdominal aorta and caudal vena cava can be lacerated with patient movement or a biopsy miss. These procedures should not be performed on animals with inadequate coagulation systems. If acute bacterial prostatitis is present, the prostatic massage could result in release of bacteria into the bloodstream, and septicemia. Traumatic catheterization and automated needle biopsy may lacerate the urethra. If an abscess or cyst is present, rupture is possible secondary to all of these procedures.
PROCEDURE Fine-needle aspiration, guided: The animal should undergo a full abdominal ultrasound evaluation, and an appropriate area for aspiration should be identified. The skin is clipped of hair and aseptically prepared with surgical scrub. The needle with a syringe attached is then advanced through the skin into the prostate under ultrasound guidance. The prostate gland is aspirated, and the sample is handled for evaluation (as already described) Fine-needle aspiration, nonguided: If the prostate is sufficiently enlarged that it can be palpated externally (abdominally) and stabilized by caudal abdominal palpation, then the procedure can be performed nonguided (without the use of ultrasound). The external surface of the skin over the prostate is clipped of hair and aseptically prepared with surgical scrub. The needle is affixed to the syringe, the needle tip is placed through the prepared skin, and the tip is advanced into the prostate gland. Material is aspirated into the needle by drawing on the syringe plunger to create negative pressure in the syringe. Negative pressure is released before withdrawing the needle. The needle and syringe are then withdrawn quickly, the syringe is detached from the needle and filled with air, and then the syringe is reattached to the needle; the contents are vigorously expelled onto a microscope slide to make fresh smears for cytologic analysis. A portion of the material can be placed in appropriate media for culture and sensitivity (C&S) instead of being smeared, or else the procedure can be repeated to obtain more material for this purpose. Automated needle biopsy: Automated needle biopsies are attained either guided or nonguided as described above for needle aspiration. As this is a more invasive and painful procedure, general anesthesia is recommended. Care must be taken not to transect the urethra with this full-thickness biopsy procedure. With this in mind, the biopsy should be taken in an orientation parallel to the urethra, not perpendicular to the urethra. A portion of the biopsy is taken for culture. The biopsy is then rolled on a slide for cytologic analysis. The sample is then placed in formalin and processed for histopathologic examination.
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Prostatic massage: The tip of the penis is extended from the prepuce and cleaned with a mild disinfectant. A urinary catheter is placed into the bladder, and the urine is completely removed. Sterile saline (5 mL) is instilled into the bladder. This fluid is then aspirated back and placed in a sterile tube labeled tube #1. The veterinarian then places an index finger in the rectum and palpates both the prostate and the catheter. The catheter is retracted until the tip can be felt caudal to the prostate. The prostate is then massaged for 1 minute. The palpating finger is retracted until it is caudal to the holes in the catheter. Pressure is applied to the catheter rectally so that fluid injected into the catheter will not leak out of the penis but will move forward into the bladder. Another 5 mL of sterile saline is then injected into the catheter. The fluid flows across the prostatic urethra into the bladder. The catheter is then pushed into the bladder, and the fluid is aspirated into a syringe and placed into a sterile tube labeled tube #2. Both tubes are presented for fluid analysis and culture. Sample #1 will have only bladder material, whereas sample #2 will have both prostate and bladder material. Comparing the two samples allows the clinician to localize the disease process to the prostate and/or the urinary bladder. Traumatic catheterization: Prepare the penis and empty the bladder as above. The urinary catheter is placed into the prostatic urethra. Correct catheter placement can be verified by digital rectal examination, by radiograph, or by ultrasound. A 12-mL syringe is attached to the end of the catheter, and negative pressure is applied so that prostate tissue is aspirated into the holes of the catheter. While maintaining negative pressure on the syringe, remove the catheter from the urethra. This will tear tissue from the prostate that is aspirated into the catheter. This prostatic tissue can be evaluated by cytologic analysis, and sometimes a large enough piece is obtained for histopathologic evaluation.
POSTPROCEDURE These are outpatient procedures, and the client may be sent home the same day provided that its clinical condition allows. The patient should be sent home on an antibiotic for 5 days or longer if the culture comes back positive. The client should be counseled that there may be hematuria transiently postprocedure.
ALTERNATIVES AND THEIR RELATIVE MERITS A technique for performing a needle aspiration biopsy of the prostate per rectum using a guarded needle has been described. This technique has the problem of injecting bacteria directly into the prostate, as the colon cannot be sterilized. The advent or ultrasoundguided techniques has made this procedure obsolete. AUTHORS: DONALD KRAWIEC, LENORE MOHAMMADIAN
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Prostatic Massage SYNONYMS Expressed prostatic fluid sampling by urethral catheter, prostatic wash or washing, traumatic catheter biopsy
OVERVIEW AND GOALS Nonsurgical technique for obtaining prostate tissue samples for practices without ultrasound capabilities. This technique can also be performed when needle aspiration of the prostate has provided inconclusive or inadequate results.
INDICATIONS Pyuria Hematuria Penile/urethral discharge Prostate enlargement Asymmetric, irregular, or nodular prostate
CONTRAINDICATIONS Inadequate restraint Bleeding disorder Acute prostatitis Prostatic or rectal pain (contraindication to performing the procedure awake)
EQUIPMENT, ANESTHESIA Urinary catheter of sufficient length to reach the urinary bladder. A soft, red rubber (Sovereign-type) feeding tube is preferable because it is less traumatic than a polypropylene catheter. Two 5-mL syringes Two 5-mL aliquots of sterile saline solution Two sterile sample containers capable of holding at least 5 mL of fluid Routine surgical scrub soap and gauze squares for disinfecting the distal penis Manual restraint to general anesthesia, depending on the demeanor of the animal
ANTICIPATED TIME Approximately 20-30 minutes
PREPARATION: IMPORTANT CHECKPOINTS The patient can be standing or in lateral recumbency. The procedure usually requires three people: the veterinarian and two assistants. The procedure requires both digital rectal palpation and urethral catheterization. If the animal resists these procedures, sedation or anesthesia is advised.
POSSIBLE COMPLICATIONS AND COMMON ERRORS TO AVOID This procedure requires digital massage of the prostate. If acute bacterial prostatitis is present, the prostatic massage could result in release of bacteria into the bloodstream, and septicemia. If an abscess or cyst is present, rupture is possible secondary to this procedure. The urinary bladder must be completely empty before starting the procedure, or the prostate sample will be diluted by the excess urine. Premeasuring the catheter makes it possible to place the catheter into the urinary bladder without causing catheter-induced bladder trauma or allowing it to loop back on itself to form a knot. Bladder infections will make the prostate wash difficult to interpret. Animals with bacterial cystitis should be treated with an
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appropriate antibiotic before undergoing a prostatic wash.
PROCEDURE While one assistant restrains the animal, the other assistant retracts the prepuce to expose the penis and cleans the distal penis with a mild surgical disinfectant. The veterinarian passes a urinary catheter into the urethra until the tip is in the bladder and completely removes the urine. The veterinarian instills 5 mL of sterile saline via the catheter into the bladder. This fluid is then aspirated back with a syringe and placed in a sterile tube labeled tube #1. The veterinarian then places an index finger in the animal's rectum and palpates both the prostate and the catheter. The catheter is retracted until the tip can be felt to be distal (caudal) to the prostate. The prostate is then gently massaged for 1 minute. The palpating finger is retracted until it is distal/caudal to the holes in the catheter, and gentle pressure is applied to the catheter rectally so that fluid injected into the catheter will not leak out of the penis but will move cranially into the bladder. A total of 5 mL of sterile saline is then injected into the catheter so the fluid flows across the prostatic urethra into the bladder. The catheter is then advanced into the bladder, and the fluid is aspirated into a syringe and placed into a sterile tube labeled tube #2. Both tubes are presented for fluid analysis and culture. If the above procedure yields either inadequate sample size or equivocal results, a traumatic catheter biopsy can be performed. General anesthesia or sedation with systemic analgesia is indicated. The urinary catheter in placed into the urethra as already described. The tip of the catheter should be in the prostatic urethra. Correct catheter placement can be verified by digital rectal examination or by radiograph. A 12-mL syringe is attached to the catheter, and negative pressure is applied so that prostatic tissue is aspirated into the holes of the catheter. While maintaining negative pressure on the syringe, the catheter is withdrawn from the urethra. Doing so will tear tissue from the prostate that is then aspirated into the catheter. This prostatic tissue can be used for cytologic evaluation, and sometimes a sufficiently large piece is obtained to allow histopathologic examination.
POSTPROCEDURE The animal should be discharged with an antibiotic for 5 days to reduce the risk of inducing a bladder infection. Sample #1 will have only bladder material, whereas sample #2 will have both prostate and bladder material. Comparing the two samples allows the clinician to localize the disease process to the prostate and/or the urinary bladder.
ALTERNATIVES AND THEIR RELATIVE MERITS Prostatic washings are done infrequently since the advent of ultrasound-guided prostate biopsy procedures; however, washings do provide a representative prostate tissue sample. AUTHOR: DONALD R. KRAWIEC
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Porcupine Quill Removal
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Porcupine Quill Removal OVERVIEW AND GOAL To safely remove all porcupine quills embedded in the tissues of a patient (almost always dogs). Although most patients are brought to veterinary attention within 24 hours of exposure to quills, extensive migration can occur in just 1-2 days; therefore, immediate removal is appropriate.
INDICATIONS Any witnessed or unwitnessed encounter with a porcupine Suspected prior porcupine encounter, presenting with signs of quill migration (ocular, thoracic, abdominal, or other site of discomfort, possibly with draining tract). In regions where porcupines are part of the natural fauna, a history of prior porcupine quill trauma should always be investigated when evaluating a patient weeks or months later for vague, nonspecific signs.
CONTRAINDICATIONS None
EQUIPMENT, ANESTHESIA General anesthesia is almost always required both for accessing remote (oral) quills and for pain control during the procedure. Quills routinely penetrate the mouth and pharynx; therefore, complete oral exam under general anesthesia is required even if quills initially appear to be confined to the muzzle.
ANTICIPATED TIME 30 minutes to 3 hours or more, depending on number of quills and depth of penetration
PREPARATION: IMPORTANT CHECKPOINTS Prior to beginning the procedure, advise owners that even with diligent removal of all visible quills, some may have penetrated beyond the point where they can be seen and can cause health problems in the future. Prior to induction, the clinician should be sure to inspect the surface of the face/body on which the dog will be lying once anesthetized to avoid having quills inadvertently driven more deeply into tissue during anesthesia.
POSSIBLE COMPLICATIONS AND COMMON ERRORS TO AVOID Failing to remove all quills: Remaining quills can migrate to deeper tissues and body cavities, including lungs and heart. The number and location of quills at initial presentation do not appear to be associated with the risk of quill retention and infection. Time from quill injury to the development of complications can range from days to months. Quill breakage during extraction. Requires dissection to remove the retained fragment.
PROCEDURE It is important to perform a full oral exam on the patient, as quills can be embedded in the oropharyngeal region and hard palate (see p. 1295). Quills are extracted one at a time with hemostats or needle drivers, beginning on the exterior (skin) and working into the mouth and pharynx. Removal is safest when grasping the quill as close to the skin as possible and pulling straight out. Doing so minimizes the likelihood of breaking the quill. If the quill should break, careful dissection to retrieve the remainder of the quill should be performed while attempting to minimize soft-tissue trauma. Placing quills in a bowl with gauze and water facilitates the removal process and minimizes risks of injury to those removing the quills. Quill removal in locations other than skin depend on the location: Thoracoscopy or thoracotomy is needed to remove quills from the thoracic cavity. An ophthalmologist should be consulted if there are quills embedded in the ocular or periorbital areas. Ultrasonography can be useful in identifying migrating quills in the eye, joint space, thorax and abdomen. A quill appears as two distinct hyperechoic lines.
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Additional diagnostic tests such as thoracic radiographs, echocardiography, MRI, and complete blood work may be indicated on a case-by-case basis, generally if a chronically retained quill is suspected to be causing persistent problems.
POSTPROCEDURE Many dogs do not learn from their previous encounters with porcupines. Therefore, it is important to educate owners to avoid repeat events. After quill removal, antibiotic administration may be indicated (e.g., amoxicillin-clavulanate, 13.75 mg/kg PO q 12 h): Porcupine quills themselves possess antibiotic properties, and infections after quill removal are not common. However, if significant trauma of the skin or subcutaneous tissues has occurred secondary to dissection, or if the quill has migrated to an atypical location, broad-spectrum antibiotics may be warranted. A longer course of antibiotics is indicated in certain situations, such as migration to the pleural space or central nervous system. Analgesia: opiates (e.g., buprenorphine, 0.01-0.02 mg/kg IV or IM) and/or nonsteroidal antiinflammatories (e.g., meloxicam, 0.1 mg/kg PO q 24 h)
ALTERNATIVES AND THEIR RELATIVE MERITS There are no humane alternatives to removing the quills.
SUGGESTED READING Grahn BH, Szentimrey D, Pharr JW, et al: Ocular and orbital porcupine quills in the dog: a review and case series. Can Vet J 36:488–493, 1995. Johnson MD, Magnusson KD, Shmon CL, et al: Porcupine quill injuries in dogs: a retrospective of 296 cases (1998-2002). Can Vet J 47:677–682, 2006. McCarthy TC: Porcupine quill retrieval with thorascopy. Vet Med 99:15–16, 2004. AUTHOR: CASS ROGERS
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Physical Rehabilitation
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Physical Rehabilitation SYNONYMS Physical therapy, physiotherapy Note: In some U.S. states, the term physical therapy (and possibly physiotherapy) is a protected term reserved only for human physical therapists. Therefore, claiming to practice such therapy without being a licensed physical therapist is potentially misleading and illegal. The term physical rehabilitation is safe and recommended for veterinary medicine.
OVERVIEW AND GOALS Using modalities, manual therapies, and therapeutic exercises to increase function by strengthening an animal's muscles, accelerating the healing of damaged tissues, increasing flexibility and ranges of motion, and decreasing pain. These therapies are becoming more common in veterinary medicine.
INDICATIONS Postoperative orthopedic/joint surgery (e.g., fractures, cranial cruciate ligament tears, total hip replacements, femoral head and neck ostectomy) Postoperative laminectomy/hemilaminectomy or other spinal surgery Acute neurologic diseases (fibrocartilaginous embolism/stroke, trauma, intervertebral disk disease [IVDD]) Osteoarthritis/spondylosis Vestibular disease and other balance/proprioceptive problems Postoperative amputation Soft-tissue injuries (e.g., sprains and strains, tendon repairs, muscle tears) Obesity/conditioning
CONTRAINDICATIONS Unstable and/or infected fractures and joints Therapeutic ultrasound is contraindicated over metal implants, tumors, growth plates, eyes, heart, and pregnant uteruses. Neuromuscular electrical stimulation may be contraindicated in animals with seizure disorders. Heat is contraindicated over acutely inflamed tissues. Swimming and underwater treadmill exercise are contraindicated in animals with diarrhea.
EQUIPMENT, ANESTHESIA Physical rehabilitation can be successfully performed with a minimal amount of equipment. The practitioner's hands are the greatest asset. The following are, however, recommended for optimal results, depending on the case: Manual restraint at times Goniometer to measure angles of joints Gulick II tape measure (to measure limb circumference/muscle mass) Heat packs Cold/ice packs Inflatable exercise/yoga balls and/or rolls Therapeutic ultrasound unit (with ultrasound gel) Neuromuscular electrical stimulation (NMES) unit Treadmills (underwater or land) Swimming area (pools for larger animals, tubs for smaller animals) Canine life vests Various slings and carts Cavaletti rails (horizontal bars or poles at varying heights for the animal to walk over; a ladder lying flat works well) Stairs Balance boards (“wobble” and “rocker” boards) Elastic resistance bands Leg weights Extracorporeal shockwave therapy unit (usually requires sedation) Low-level (“cold”) lasers Various splints and orthotics
ANTICIPATED TIME
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About 20-90 minutes Usually performed several times a week Note: Most postop orthopedic cases require an average of 1 month of rehabilitation, neurologic cases average 2-3 months, and osteoarthritis cases may continue indefinitely (or may benefit from intermittent rehabilitation such as 1-2 month stints several times a year).
PREPARATION: IMPORTANT CHECKPOINTS Be sure that any surgical repair is stable. Watch for any swelling or signs of infected tissues, which could contraindicate treatment. Be sure that the animal's condition is not deteriorating with rehabilitation. Exercise animals on an empty stomach (subjectively, doing so may decrease risk of gastric dilation/volvulus). Take joint range-of-motion measurements (goniometry) in flexion and extension using a goniometer: Normal values are published for some breeds. The measurements should be rechecked every 2-4 weeks to monitor progress. Measure thigh or forearm circumference as a rough measure of muscle mass. The measurement of this circumference is done with a tape measure, preferably the Gulick II to decrease margin of error. This measurement also should be monitored every few weeks for progress.
POSSIBLE COMPLICATIONS AND COMMON ERRORS TO AVOID Do not institute hydrotherapy (e.g., swimming, underwater treadmill) until skin incisions have successfully sealed (at least 5 days). It is easy to overwork the animal, especially in the initial treatments. Be sure the animal can easily handle the work regimen in the beginning. As a general rule, exercise can be increased about 20% per week if the animal is improving. Do not stress the tissues too much (remember time frames for tissue healing): For example, bone healing (fracture, surgical osteotomy) takes 8-12 weeks to be complete under ideal conditions. A classic pitfall would be applying too much force too early or allowing the dog to apply too much via inappropriate exercise. Signs of pain and palpable instability could be warning signs. Consultation with the surgeon on the stability of the repair is recommended. In the immediate postoperative period, therapeutic exercise may be contraindicated. These animals may still benefit from cryotherapy and gentle passive range-of-motion exercises three to four times daily.
PROCEDURE Thermal treatments (cryotherapy, heat therapy) are applied to the affected area and should not create discomfort. If acute inflammation is present (e.g., first few days after surgery, flare-up of chronic conditions), initiate cryotherapy with an ice pack or cold pack first. Apply for 10-15 minutes over the site of the inflammation. Cryotherapy aims to decrease edema, inflammation, and pain. For chronic situations, heat therapy is indicated. This is accomplished by massage, warm packs for superficial areas, or therapeutic ultrasound for deeper tissues (2-5 cm under the skin). Heat will increase blood flow to the tissues, increasing flexibility and decreasing the chance of injury with exercise. It can also reduce pain. After the warm-up period, stretching can be instituted if the procedure does not contribute to tissue injury. Tissue injury is avoided through precautions, including heeding the normal time frame of bone healing if relevant (as already described) and using an appropriately limited degree of force during healing, such as avoiding excessive force (animal vocalizes or resists). If the animal is vocalizing, then the practitioner may be going too far. Of course, some animals will squirm or vocalize without even being touched, so individual personalities are taken into consideration. The individual joints are brought to a comfortable end range in flexion and then extension for 10-15 seconds each. This is repeated 6-15 times. Passive range-of-motion (PROM) exercises are also instituted at this point. The entire limb is cycled through its ranges of motion, being sure to incorporate all desired joints. This will increase flexibility and minimize adhesions and contractures. NMES can be used for artificially eliciting a muscle contraction: Electrical current is delivered by pads through the skin to the motor end plate, thereby causing the muscle belly to contract. NMES is primarily used for strengthening muscles and increasing endurance as well as to attenuate atrophy. This modality is most helpful in animals that are paralyzed and paretic. After successfully undergoing such treatments, the animal (depending on the individual case) may now be ready for therapeutic exercises. These are designed to increase strength, balance, and proprioception as well as encourage weight bearing on affected limbs as indicated. Therapeutic exercise is also helpful in improving active range-of-motion (AROM) in joints, flexibility, and overall function. Therapeutic exercises include the following: Assisted standing exercises, using slings or exercise balls and rolls, are used in the early stages, especially for patients that are paralyzed or paretic. These exercises are designed to encourage the patient to bear as much of his/her own weight as possible.
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The patient is supported in a standing position with the assistance of either slings or yoga balls under the trunk. The patient can be rocked side to side or front to back. If the patient begins to collapse, he/she is then lifted back up to the original position, and the exercise begins anew. Weight-shifting exercises are designed to shift the patient's weight onto the affected limb(s) to encourage weight bearing. This is achieved with balls and rolls, balance boards, wheelbarrowing and dancing exercises, or simply discouraging use of the contralateral limb in a normal standing position. Sit-to-stand exercises are used for increasing ranges of motion and strength in the hind limbs. The dog is commanded to sit squarely on its rear end and then to stand up. Small treats can be used. Note: To get the dog to flex the hind limb squarely, the affected limb can be positioned against a wall to prevent “cheating.” Stair climbing is used for improving strength, coordination, and flexibility. Underwater treadmills are valuable tools that can be used in most cases: Water height can be adjusted to different levels to change the animal's buoyancy and thereby the amount of weight the limbs are bearing. Changing water heights also changes the active ranges of motion for all the joints of the limbs, depending on which ones are breaking the plane of the water. Most units will also allow variations in speed, time, and incline. Resistance jets can be installed. Life vests and slings for assistance should be used as needed. Land treadmills can also be used. Cavaletti rails are used for increasing AROM, strength, balance, and coordination: These are typically created with traffic cones with holes drilled through at different heights. PVC pipes can then be inserted at the desired heights to create an obstacle course for the dog to negotiate. The dog must lift its limbs to walk over these rails, thus encouraging active range of motion. The cones and poles can be arranged to also force the dog to weave in and out of the cones, further strengthening the patient's balance and coordination skills. Elastic resistance bands and leg weights can be used to further challenge the dog with many activities. Be careful where these are placed—do not put undue stress or torque on susceptible tissues; usually reserved for advanced cases, when a patient has progressed from simpler exercises: Can be used for a postoperative patient with cranial cruciate ligament repair toward the end of its treatments or a patient with osteoarthritis that has successfully progressed to a point that it needs to be further challenged Balance boards are used for increasing proprioceptive awareness and balance as well as strength: These are typically flat wooden boards with a fulcrum underneath, on which the dog stands and tries to balance itself. Indications in some animals with vestibular disease, ataxia of various causes, amputees.
PHYSICAL REHABILITATION Dog on underwater treadmill. Treadmill speed and depth of water can be adjusted to optimize level of activity.
POSTPROCEDURE Stretching after exercise is usually indicated. Cryotherapy (10-15 minutes) is also frequently indicated after the treatment to reduce muscle spasms, pain, and swelling. Any progression of lameness or signs of pain must be noted. If observed, reduce the next treatment by about 50%. Note: Be
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careful to differentiate orthopedic pain from muscle soreness. Muscle soreness is expected after the first few treatments. Palpate the muscle bellies and move the joints to identify the source of pain. Antiinflammatory medications can be used as needed: Carprofen: 2.2 mg/kg PO q 24 h to q 12 h Deracoxib: 1-2 mg/kg PO q 24 h Firocoxib: 5 mg/kg PO q 24 h
ALTERNATIVES AND THEIR RELATIVE MERITS Acupuncture (see p. 1195 ) may also be helpful with pain control and neurologic diseases. Chiropractic therapy may be helpful in some cases.
SUGGESTED READING Bockstahler B, Levine D, Millis D: Essential facts of physiotherapy in dogs and cats. Lifelearn, 2004, Guelph. Gross DM: Canine physical therapy: orthopedic physical therapy. Wizard of Paws, 2002, East Lyme, CT. Marsolais GS, Dvorak G, Conzemius MG: Effects of postoperative rehabilitation on limb function after cranial cruciate ligament repair in dogs. J Am Vet Med Assoc 220:1325–1330, 2002. Millis DL, Levine D, Taylor RA: Canine rehabilitation and physical therapy. St Louis, 2004, WB Saunders. Smarick SD, Rylander H, Burkitt JM, et al: Treatment of traumatic cervical myelopathy with surgery, prolonged positive-pressure ventilation, and physical therapy in a dog. J Am Vet Med Assoc 230:370–374, 2007. AUTHOR: TIMOTHY V. HATT
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Phlebotomy SYNONYM Venipuncture
OVERVIEW AND GOAL To obtain blood with minimal stress to the patient for diagnostic or monitoring purposes, treatment of certain blood disorders, transfusion, or to administer medications
INDICATIONS Diagnostic testing Blood transfusion Polycythemia Hemochromatosis
CONTRAINDICATIONS Infection or injury at the sampling site Jugular venipuncture in animals with coagulopathy
EQUIPMENT, ANESTHESIA Alcohol Clippers (+/−) Needle and syringe/Vacutainer collection system: Method used depends on vessel size, blood volume required, operator's preference. Tourniquet (+/−) Sample tubes Gauze and tape/bandage wrap (+/−) Sedation is dependent on the disposition and the health of the animal.
ANTICIPATED TIME 1-5 minutes
PREPARATION: IMPORTANT CHECKPOINTS Ensure that the proper criteria have been meet prior to diagnostic testing (e.g., animal fasted) and the required sampling containers are on hand. Using jugular veins spares the cephalic veins for IV catheterization and allows for a larger volume to be collected faster. Experienced restrainers reduce the stress to the patient and improve the chance for successful venipuncture.
POSSIBLE COMPLICATIONS AND COMMON ERRORS TO AVOID Hematoma An insufficient amount of sample can produce an incorrect blood-to-anticoagulant ratio and result in erroneous values: Use 0.5-mL pediatric containers for neonates/exotics (e.g., BD Microtainer tubes) Blood collection for coagulation profiles should be drawn with minimal trauma (first attempt) to prevent tissue thromboplastin from entering the sample. Improper handling of the specimen can alter results.
PROCEDURE Positioning of the patient depends on the ability to restrain the patient and operator preference.
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Apply isopropyl alcohol to the area. In animals with dense hair coats, it may be necessary to clip the area if the vein is neither visible or palpable. Jugular vein: Occlude the vein by inserting pressure with your thumb at the thoracic inlet. Using the same hand, palpate the vein with your index finger. Cephalic or saphenous vein: Hold the leg and apply slight traction to help stabilize the skin and vein while the restrainer uses one hand to create a tourniquet effect at the elbow. Placing your thumb alongside the vein may prevent it from moving. Insert the needle through the skin with bevel up: If using a syringe, apply gentle negative pressure. If you do not have blood in the hub of the needle, draw back your needle (do not come out of the skin) and advance towards where you can palpate the vein. After obtaining the sample, release the pressure on the vein before withdrawing the needle. If using a Vacutainer collection system, push in the Vacutainer tube with your thumb after you have penetrated the skin. Carefully watch for blood while you are advancing, and stop when blood enters the tube. If you get a flashback of blood and then it stops, you may have gone through the vein. Slowly back your needle out until blood flows. When changing Vacutainer tubes (needle still in the vein), be sure to firmly stabilize the plastic Vacutainer holder. Often the act of changing the tubes will push the needle ahead. If no blood flows after changing tubes, slowly back the needle out 1-2 mm until you see blood flow. If this is unsuccessful, withdraw (not out of the skin) and redirect the needle. After obtaining the sample, remove the tube and release the pressure on the vein before withdrawing the needle from the skin. In veins that roll laterally and are difficult to penetrate, an assertive forward movement will aid in successful venipuncture. If blood flow stops during aspiration, rotate the needle slightly in the vein. Excessive negative pressure can cause the vein to collapse and hemolysis to occur. After the desired amount of blood has been drawn and the needle is removed, the restrainer applies digital pressure until hemostasis occurs. Marginal ear vein prick: Puncture marginal ear vein with a needle or lance. Some apply a thin film of petroleum jelly or other hydrophobic substance to the surface being pricked, which can help the blood bead rather than run. Collect blood onto test strip or capillary tube. Apply pressure to puncture site afterwards to aid hemostasis.
POSTPROCEDURE Patients with coagulopathy require that pressure be applied to the vein for at least 5 minutes after venipuncture.
ALTERNATIVES AND THEIR RELATIVE MERITS Central venous catheter: technically challenging, expensive, facilitates multiple blood draws for monitoring in clinic patients AUTHOR: ELAINE REVELER
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Peritoneal Dialysis
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Peritoneal Dialysis OVERVIEW AND GOAL Exchange of dialyzable solutes and fluid between the peritoneal capillary vessels and the dialysate solution. Exchange occurs across the semipermeable peritoneal membrane as a result of diffusion, ultrafiltration, and convection.
INDICATIONS Acute renal failure unresponsive to conventional medical management Hyperkalemia or hypercalcemia (severe) Intoxication from dialyzable toxin or drugs (e.g., ethylene glycol 1 cm). In the absence of ultrasound guidance, the site of entry is at the level of the costochondral junction, right fifth intercostal space. The area is widely clipped of hair and aseptically prepared. The wide clipping of hair should allow the procedure to be done without a sterile drape. The designated site of centesis is again confirmed with ultrasound. Lidocaine is infused subcutaneously, intramuscularly (intercostal muscle), and subpleurally. Doing so requires that the needle be repeatedly withdrawn until almost out of the skin and then redirected and reinserted until a region at least 2 cm square and spanning the entire thickness of the chest wall has been infiltrated. The clinician puts on sterile gloves and makes a 3-mm skin incision in the center of the site using the scalpel blade. The catheter, which covers a metal stylet, is attached to the 6-mL syringe, and the tip of the catheter-stylet combination is inserted into the skin incision. The clinician advances the syringe-catheter-stylet combination (which is grasped in the palm as a handle to advance the catheter and stylet) while drawing back on the syringe plunger to create negative pressure. The orientation is perpendicular to the chest wall and is neither cranially nor caudally directed. When a flashback of effusion is seen to enter the syringe, the syringe-styletcatheter apparatus is advanced only 2-3 mm farther into the chest. With continuing negative pressure on the syringe (effusion flowing into syringe), the syringe and stylet are kept in the same position, while the catheter is advanced several centimeters farther. In this way, the catheter is seated well within the pericardial space. Using a large-volume syringe (35 or 60 mL), the effusion is withdrawn. Ideally, an assistant helps by emptying one syringe while the clinician is filling the other with pericardial effusion; thus, two syringes can aseptically be traded back and forth until the pericardium is empty. When the effusion has partially or completely been removed, the catheter is withdrawn, and the skin incision is closed with tissue glue.
PERICARDIOCENTESIS Pericardiocentesis in a dog with severe cardiac tamponade and hemorrhagic pericardial effusion. Left lateral recumbency; head is beyond the lower right corner of the image. The syringe-catheter-stylet combination has been advanced to the point of entering the pericardium, and effusion is seen in the hub of the stylet and the syringe. Next, the catheter will be advanced off the stylet.
POSTPROCEDURE Ascites caused by cardiac tamponade should resolve spontaneously over the 12- to 36-hour period following pericardiocentesis. A recheck echocardiogram immediately post centesis and another echocardiogram 12-24 hours later are recommended
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(assess remaining volume, and note in record). Rapid reaccumulation of effusion suggests malignancy, atrial rupture from stretch, or coagulopathy.
ALTERNATIVES AND THEIR RELATIVE MERITS Pericardiectomy: long-term palliation Diuretic: contraindicated in acute treatment (does not mobilize effusion but does deplete circulating blood volume, worsening cardiac filling); advocated by some for chronic treatment to delay of recurrence of idiopathic or malignant effusions AUTHOR: ETIENNE CÔTÉ
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Parenteral Nutrition
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Parenteral Nutrition SYNONYMS PN, partial parenteral nutrition (PPN), total parenteral nutrition (TPN)
OVERVIEW AND GOALS Parenteral nutrition (PN) is nutrition delivered by the IV route. It can be life saving in animals that cannot tolerate enteral feeding. Used when no other feeding option exists, and the need for nourishment is a critical factor in clinical outcome.
INDICATIONS Animals in need of nutritional support when: Enteral nutrition is contraindicated (e.g., gastrointestinal [GI] dysfunction or risk of pulmonary aspiration). Sufficient nutrition cannot be provided by the enteral route alone (e.g., severe malabsorptive disease).
CONTRAINDICATIONS Animals that can be fed safely and effectively by the enteral route Animals that are at risk with catheter placement: Central venous catheters in animals at high risk of thromboembolic disease (e.g., protein-losing nephropathy or enteropathy, hyperadrenocorticism, disseminated intravascular coagulopathy) Jugular catheters in animals with increased cerebral pressure (e.g., head trauma) Animals experiencing fluid overload (e.g., animals with heart failure, oliguria, or severe hypoproteinemia)
EQUIPMENT, ANESTHESIA Venous access: A dedicated catheter is required for delivery of the nutrient solution to avoid septic complications and drug-nutrient interactions. Treat catheter placement as a surgical procedure (surgical prep, draping, and the use of sterile gloves) (see p. 12935/19/2011). Place a central venous catheter to deliver TPN, because the nutrient solution is hyperosmolar. Solutions that are more dilute can be prepared, but the resulting large volume that must be infused can become a limiting factor. Catheters made of nonthrombogenic materials (polyurethane or silicone) are preferred, particularly for peripheral infusion. Multilumen central or peripherally placed central catheters (PICC lines) can be used if one of the ports is dedicated for PN. Nutrient admixture: Amino acid solutions (3%-10%) are used for providing protein. These solutions come with and without added electrolytes. Nonprotein calories can be provided by a combination of lipid emulsions (10% or 20%) and dextrose (10%-50%) or dextrose alone. Electrolytes can be added to the nutrient solution as needed or provided separately in the animal's crystalloid fluid therapy. The latter allows greater flexibility. Alternatively, a combination amino acid and electrolyte solution can be used. Special parenteral vitamin and mineral preparations are available. However, because most companion animals receive PN for relatively short periods of time (30 kg, and have a normal physical exam and negative heart-worm and rickettsial serologies. Butorphanol, 0.1-0.2 mg/kg for IV use Sterile 450-mL collection bag with tubing, needle, and anticoagulant (commercially available) Digital gram scale Hemostat forceps Scissors Hemoclips and stripper sealer (optional) Cats: Donor cats should be healthy adults, weigh >4 kg, have a normal physical exam and normal blood smear, and be negative for feline leukemia and feline immunodeficiency virus serologies. Ketamine HCl, 1-2 mg/kg for IV use Two 35-mL syringes (a 60-mL syringe may collapse the vein). Anticoagulant (citrate-phosphate-dextrose-adenine-1 or adenine-citrate-dextrose) A 19-gauge butterfly needle Note: Heparin (300 units per 50 mL blood collected) can be used as an anticoagulant in an emergency. Dilute heparin in 3 mL of saline to facilitate mixing. Heparin contains no preservatives: administer blood within 24 hours. Heparin activates platelets: avoid in thrombocytopenic animals. BLOOD ADMINISTRATION: IV or intraosseous (IO) catheter Transfusion set with filter (dogs) A 170-µm syringe filter and an IV extension set (cats)
ANTICIPATED TIME Whole blood collection: 20-40 minutes Administration: minutes to maximum of 4 hours, depending on animal's condition
PREPARATION: IMPORTANT CHECKPOINTS Check PCV of recipient and donor prior to transfusion. Save hematocrit tube containing recipient plasma for future comparison if hemolytic reactions occur. Aseptic technique is essential. See Cross-Match and Blood Typing, .
POSSIBLE COMPLICATIONS AND COMMON ERRORS TO AVOID TRANSFUSION REACTIONS (see p. 1111): Monitor temperature, heart rate, and respiratory rate every 10 minutes for 30 minutes, then every 60 minutes until transfusion completed. Uncommon (3%) and rarely fatal (30 cm H2O): Can cause acute deterioration in ventilatory parameters Auscultation usually reveals dull breath sounds in upper parts of thorax (i.e., dorsally when animal is in sternal recumbency). The absence of a “glide sign” with thoracic focused assessment of sonography for trauma (TFAST) is strongly suggestive of pneumothorax. Perform thoracocentesis in suspected cases. Tension pneumothorax is associated with a severe decrease in cardiac output and hypotension; check for tension pneumothorax in ventilated animals that suddenly develop shock. Oral and ocular ulcers: usually avoided with good nursing care: Lubricate eyes with sterile eye lubricant, and cleanse mouth with 0.1% chlorhexidine solution–soaked gauze sponges every 4 hours.
PROCEDURE Note: Step-by-step guidelines to initiate PPV are beyond the scope of this text, and clinicians should consult more extensive reviews to become familiar with different ventilator modes and their indications. The following are suggested guidelines for starting PPV. Most cases do better in sternal recumbency. Ambu bag: Bag size (in milliliters) should be at least 15 × BW (kilograms) to be able to deliver adequate tidal volumes. Set oxygen flow rates at 10-15 L/min (delivers 50%-90% oxygen levels). Attach adjustable PEEP valve to exhaust limb if PEEP desired (requires compatible attachment site). Adjust PEEP by turning valve to the desired level (start with 5 cm H2O). If an oxygen reservoir bag is used, higher (90%-100%) inspired oxygen levels can be achieved. Animals can breathe spontaneously while connected to Ambu bags, although airway resistance is higher. Anesthetic machine with manual ventilation: Insert adjustable PEEP valve in the expiratory limb of tubing (bidirectional valves eliminate the risk of occlusion associated with backward insertion of unidirectional valves) if PEEP is desired. SUGGESTED INITIAL PPV SETTING GUIDELINES (see figure): Inspired oxygen concentration (Fio2): Start with 100% Fio2. For long-term (many hours) use, decrease to the lowest Fio2 that maintains desired Pao2/SaO2 to reduce the risk of oxygen toxicosis. Respiratory rate (RR): 8-20 breaths per minute (bpm) Increase the RR to decrease the PacO2 if >50 mm Hg. New RR = RR × PacO2/desired PacO2 RR often >20 breaths/minute if underlying pulmonary disease is present. Oxygen flow rates: Start with 0.5-1 L/kg/min. Often need to increase if underlying pulmonary disease is present. Tidal volume: Amount of air delivered with each breath Normal values: 10-15 mL/kg Values of 4-6 mL/kg are associated with fewer lung injuries in people. Volumes in excess of 20 mL/kg are likely to cause lung injury (barotrauma and volutrauma). May need to increase tidal volume if PacO2 does not respond to increased RR General rule: use lowest volume possible to achieve oxygen and carbon dioxide goals. Airway pressure: If pressure gauge available Normal airway pressures reach 15-20 cm H2O. Values that are >30 cm H2O are to be avoided (likely to result in lung injury). Inspiratory time: Inspiratory time is normally between 1.5 and 2.5 seconds. Inspiratory to expiratory (I:E) ratio: Start with values of 1:2-1:4. Try to stay >1:2 to prevent the next breath being delivered before exhalation is complete. Increasing RR or tidal volume will decrease I:E ratio.
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Increasing oxygen flow rates will increase I:E ratio. Changing one parameter may require a change in another to maintain desired I:E ratio. PEEP: Healthy lungs do not require PEEP. Adding PEEP to diseased lungs often improves oxygenation, prevents further alveolar collapse, and reduces ventilator-induced lung injury. A common starting value is 3 cm H2O. If 3 cm H2O does not achieve desired results (based on Pao2/SaO2), increase the PEEP by 2-4 cm H2O until desired values are achieved. Exceeding 15 cm H2O of PEEP increases the risk of lung injury and may decrease cardiac output.
VENTILATION, POSITIVE PRESSURE Potential ventilator settings for a 40- to 60-kg animal. Volume control ventilation (VCV) with synchronized intermittent mandatory ventilation (SIMV) is shown. The inspired oxygen content is 21% (room air). The peak inspiratory pressure (PIP) is high (34 cm H2O), and efforts should be made to decrease this value by decreasing tidal volume, increasing peak flow rate, or decreasing positive end-expiratory pressure (PEEP).
VENTILATION, POSITIVE PRESSURE Ventilator in use.
POSTPROCEDURE Supplemental oxygen is often required after weaning from ventilation (seep. 1318).
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Oxygen supplementation should be set up prior to extubation (nasal oxygen is frequently used).
ALTERNATIVES AND THEIR RELATIVE MERITS Liquid ventilation using perfluorocarbons shows promise in managing some forms of respiratory failure in people but is cost prohibitive to most veterinary practices and clients.
SUGGESTED READING Campbell VL, King LG: Pulmonary function, ventilator management, and outcome of dogs with thoracic trauma and pulmonary contusions: 10 cases (1994-1998). J Am Vet Med Assoc 217(10):1505–1509, 2000. Drellich S: Principles of mechanical ventilation. Vet Clin North Am Small Anim Pract 32(5):1087–1100, 2002. Mueller ER: Suggested strategies for ventilatory management of veterinary patients with acute respiratory distress. J Vet Emerg Crit Care 11(3):191–198, 2001 AUTHOR: SØREN R. BOYSEN
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Vaginoscopy OVERVIEW AND GOAL Visual inspection of the surface of the vaginal mucosa. This can be accomplished through a plastic or metal speculum, or is most rewarding with a fiberoptic endoscope.
INDICATIONS Examining the physical changes associated with hormonal events of the canine reproductive cycle Evaluating abnormal conditions of the caudal reproductive tract (vestibule, vagina, and caudal cervix). Common disorders of the caudal reproductive tract include vaginal septa, vestibulovaginal stenosis (strictures), paramesonephric septal remnants, tumors, foreign bodies, lymphoid inflammation or hyperplasia, and ectopic ureters. To facilitate catheterization of the cervix for intrauterine artificial insemination
EQUIPMENT, ANESTHESIA Bitches in estrus tolerate vaginal procedures well; bitches in early proestrus or anestrus may need sedation or even general anesthesia, depending on the medical reasons to perform the vaginoscopy. Equipment: Endoscope or speculum: if using a rigid endoscope, its size should be compatible with the size of the bitch. Sterile water-soluble lubricant Light source if not integral part of endoscope/speculum Swabs Microscope slides
VAGINOSCOPY Endoscopic view of the canine vagina in midestrus.
ANTICIPATED TIME 5-20 minutes
PREPARATION: IMPORTANT CHECKPOINTS Be sure to apply lubricant copiously to the endoscope before introducing it. Position: if in estrus, most bitches will remain standing while vaginoscopy is being performed, especially if transcervical insemination is to be performed. In anestrous or spayed dogs, care should be taken to not traumatize the vaginal walls,
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especially if a rigid endoscope is being used. Anesthetized dogs may be positioned in lateral, ventral, or dorsal recumbency; the latter prevents inadvertent fecal contamination of the perineovulvar area.
PROCEDURE Once the perineum is cleansed and excessive hair clipped, the vulvar labia are separated, and the instrument is introduced at a craniodorsal angle to avoid the clitoral fossa until the vestibule and vagina are visualized. Areas to be inspected: urethral opening, vestibulovaginal junction, vagina, vaginal dorsal median fold that leads to the narrow cranial vagina, vaginal fornix and paracervical area, and cervical caudal os (ostium uteri externum) Physical changes due to circulating hormones cause dramatic changes in the appearance of the vaginal mucosa, especially during proestrus and estrus: Under the influence of estrogens produced by ovarian follicles, the vaginal epithelium undergoes hyperplasia and metaplasia during proestrus. The vaginal mucosa becomes edematous, swollen, and appears smooth, round, and plump. As the bitch advances into late proestrus and estrus, declining concentrations of serum estrogens result in a wrinkling and shrinking of the vaginal mucosal folds, progressing to a markedly angulated and crenulated outline during mid to late estrus.
POSTPROCEDURE Submission of samples, microscopic review of smears
ALTERNATIVES AND THEIR RELATIVE MERITS Digital vaginal palpation (see p. 1292): conveys the changes in texture of the vaginal mucosa but does not demonstrate lesions Serum progesterone assay: often used in conjunction with vaginoscopy; the appearance of the mucosa (and cornification of cells; see p. 1202) indicate when to begin measuring serum progesterone. AUTHOR: CARLOS PINTO
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Vaginal Palpation in the Bitch SYNONYM Digital vaginal examination
OVERVIEW AND GOALS Minimally invasive digital examination of the vagina to evaluate the vaginal anatomy. Possible lesions in bitches include: Vaginal strictures Vaginal tumors Trauma during breeding Congenital anatomic anomalies
INDICATIONS Vaginal discharge Poor breeding experience Urinary incontinence (urine pooling) Dystocia
CONTRAINDICATIONS There are relatively few contraindications to this procedure. If infection of the reproductive tract is a consideration: Vaginal culture should be taken first. Culture is followed by vaginal cytologic analysis before a digital examination is performed.
EQUIPMENT, ANESTHESIA Minimal restraint usually required Antiseptic cleanser Sterile exam glove Sterile water-soluble lubricant
ANTICIPATED TIME With a cooperative bitch, the procedure should take less than 5 minutes, from gentle cleansing of the vulvar lips to finishing the exam.
POSSIBLE COMPLICATIONS AND COMMON ERRORS TO AVOID Urethral opening lies on the ventral surface of the vestibule and should be avoided: This is not difficult if the finger is passed up to the vestibulovaginal junction perpendicularly to the ground in the standing bitch. Vestibulovaginal junction is one barrier to the entrance of the uterus and should not be mistaken for the cervix or a stricture: The canine vagina is very long (up to 12 inches [29 cm] in giant-breed dogs), and thus the cervix is unlikely to be palpated on digital examination of the vagina. The junction acts a barrier to pathogens and will be narrower than the vestibule or vagina. If the examiner proceeds slowly, he or she should be able to pass the finger beyond the junction in most bitches (depending on the size of the bitch and the size of the finger).
PROCEDURE Animal should be restrained in standing position.
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Vulvar lips should be gently wiped with a mild antibacterial cleanser. Examiner should wear sterile gloves. After coating the gloved index finger with the sterile lubricant, the finger is passed into the vulva and turned directly upward (90° angle to the floor in the standing animal). The upward direction is important so the urethral opening is avoided. When the finger cannot go any farther dorsally, it is turned directly cranially (parallel to the floor) and advanced over the ischium and into the vaginal vault: As the finger passes over the ischium into the vagina, there may be a slight tightening at the vestibulovaginal junction. Depending on the size of the bitch and the size of the hand, most fingers should pass through this junction. If the finger is well lubricated and it does not pass this point, a vaginal stricture should be considered.
VAGINAL PALPATION Anatomic relationship of vestibule and vagina in the bitch. Dorsal is toward top of image, cranial to left.
ALTERNATIVES AND THEIR RELATIVE MERITS Speculum examination (vaginoscopy; seep. 1361) may be performed for the visualization of the vaginal walls and vault: Inflamed walls in vaginitis cases Urine on the floor of the vagina in urine-pooling disorders Evidence of trauma in difficult breeding Evaluation of vaginal folds and mucosa for timing of estrus Vaginoscopy with an endoscope to visualize vagina and potentially the cervix AUTHOR: CAROL A. MCCLURE
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Vagal Maneuver SYNONYMS Carotid sinus massage Ocular pressure Valsalva maneuver
OVERVIEW AND GOALS A physical manipulation that temporarily increases parasympathetic tone, mainly for diagnostic—and occasionally therapeutic —cardiac rhythm effects
INDICATIONS Tachycardia in which the rate is so rapid that it is unclear on the electrocardiogram (ECG) whether the rhythm is ventricular or supraventricular (e.g., heart rate is >260 bpm)
CONTRAINDICATIONS Ocular disease (for ocular pressure) Disorders of the ventral neck (for carotid sinus massage) Bradycardia, including the bradycardia-tachycardia syndrome (sick sinus syndrome)
EQUIPMENT, ANESTHESIA No anesthetic requirement; procedure is performed when the animal is awake. Procedure requires ECG machine with printer to assess and record initial cardiac rhythm and to record effect of vagal maneuver.
ANTICIPATED TIME Normal
Regular
Positive, negative, absent, or buried
Same as P wave
Regular
Normal
1:1
Atrial flutter
>300
Regular
Positive (F waves; sawtooth baseline)
Same or less than P wave rate
Regular or irregular
Normal
Generally more P waves than QRS complexes
Atrial fibrillation
>500
Irregular
None to baseline undulation (F waves)
Less than P wave rate (100-280)
Irregular
Normal
No P waves; more undulations than QRS complexes
Accelerated idioventricular rhythm
Normal
Regular
Normal (often buried in QRS complex)
70-150
Fairly regular; may be irregular
Wide
Dissociated; more QRS complexes than P waves
Ventricular flutter
Not Not Not discernible discernable discernable
>350
Regular
Sine wave
Dissociated; more QRS waves than P waves
Ventricular fibrillation
Not Not Not discernible discernable discernable
>400
Grossly irregular
No QRS complexes
Dissociated; no QRS complexes
Second-degree AV block
Normal
Regular
Normal
100/cmm
Small increase: 100 mg/dL
Small increase: 24 hours after temperature decrease to 15 minutes Strong contractions >30 minutes without delivery No fetus produced after 4-6 hours of onset of stage II labor
Dystocia
More than 3 hours between fetal delivery
Dystocia in canine
Vaginal discharge
Dystocia, metritis, pyometra
Temperature >39.7°C in the bitch
Dystocia, metritis, pyometra, uterine torsion, mastitis
Profuse vomiting, diarrhea, and toxemia in the bitch Incessant crying of offspring Anorexia, lethargy, depression >24 hours postpartum
Metritis, mastitis
Hot, painful, swollen mammary glands
Mastitis
Extreme restlessness, panting, tremors, and stiff gait
Eclampsia
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Dyspnea Causes From Ettinger S, Feldman E: Textbook of veterinary internal medicine, ed 5, St Louis, 2000, Saunders.
Upper Airway Disorders *
Nasal cavity Stenotic nares Obstruction (infection, inflammation, neoplasia, trauma, bleeding disorders) Pharynx, larynx Elongated or edematous soft palate Pharyngeal polyp (cat) Laryngeal edema, collapse, foreign body, inflammation, trauma, paralysis, spasm, neoplasia, vocal-fold webbing Everted laryngeal saccules Cervical trachea Collapse, stenosis Trauma, foreign body Neoplasia, osteochondral dysplasia Parasites (Oslerus osleri)
Lower Airway Disorders Thoracic trachea (see Cervical Trachea, above) Extraluminal compression (lymphadenopathy, heart-based tumors, enlarged left atrium) Bronchial disease (allergic, infectious, parasitic, chronic obstructive pulmonary disease)
Pulmonary Parenchymal Disorders Edema (cardiogenic, noncardiogenic) Pneumonia (infectious, parasitic, inhalation) Neoplasia Allergy (allergic pneumonitis, including heartworm; eosinophilic granuloma; eosinophilic bronchopneumopathy) Embolism (dirofilariasis, hyperadrenocorticism, disseminated intravascular coagulation) Trauma, bleeding disorders
Pleural/Body Wall Disorders Pneumothorax Pleural effusion Congenital body wall disorders (pectus excavatum) Thoracic wall trauma Thoracic wall neoplasia Thoracic wall paralysis Diaphragmatic hernia (congenital, acquired)
Mediastinal Disorders Infection Trauma, including pneumomediastinum Neoplasia
Peritoneal Cavity Disorders Organomegaly, obesity Effusion Gastric torsion, dilatation/volvulus
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Hemoglobin Disorders Anemia Methemoglobinemia Cyanosis
Miscellaneous Central nervous system (brain, spinal cord) Peripheral nerve, neuromuscular, muscular Metabolic (acidemia; severe hypokalemia in cats) Anxiety Fear Pain
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Dysphagia Causes From Ettinger S, Feldman E: Textbook of veterinary internal medicine, ed 6, St Louis, 2005, Saunders.
Anatomic or Mechanical Lesions Pharyngeal inflammation (e.g., abscess, inflammatory polyp, oral eosinophilic granuloma) Foreign-body obstruction (oral, pharyngeal, nasopharyngeal, proximal esophagu) Neoplasia Retropharyngeal lymphadenomegaly Sialocele Mandibular fracture Lingual frenulum disorder Cricopharyngeal achalasia or asynchrony TMJ disorder (e.g., luxation, fracture) Cleft palate Pharyngeal trauma
Pain Stomatitis/glossitis/pharyngitis (FIV, FeLV, immune-mediated disease, uremic glossitis, ingestion of a caustic substance) Tooth-related problems (tooth root abscess, fracture, periodontitis) Trauma Electric cord burns Retrobulbar abscess
Neuromuscular Disorders Myasthenia gravis (focalized or generalized) Acute polyradiculoneuritis Masticatory myositis Tick paralysis Botulism Polymyositis TMJ disease
Neurologic Disorders Rabies Trigeminal paralysis or neuritis Neuropathies of CN VII, IX, X, or XII CNS disease (brainstem lesion) CN, Cranial nerve; CNS, central nervous system; FeLV, feline leukemia virus; FIV, feline immunodeficiency virus; TMJ, temporomandibular joint.
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Disseminated Intravascular Coagulation (DIC) Associated Conditions Modified from Bonagura J: Kirk's current veterinary therapy XIII, St Louis, 2000, Saunders.
Intravascular Hemolysis Hemolytic transfusion reaction Hemolytic anemia
Septicemia Gram-negative bacteria (endotoxin) Gram-positive bacteria (bacterial coat mucopolysaccharide)
Viremia
Parasitic Infections Protozoal infection Metazoal infection
Obstetric Complications
Miscellaneous Gastric dilatation/volvulus Diabetes mellitus
Neoplasia
Massive Tissue Injury Burns Trauma Surgical procedures Heatstroke
Venoms and Toxins Snakebites Insect stings Aflatoxin
Hepatic Disease
Pancreatitis While a cause-and-effect relationship has not been established for most cases of DIC in dogs and cats, the conditions listed here are suspected to contribute to the onset, perpetuation, or both, of DIC.
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Diskospondylitis: Microorganisms Infectious Agents Associated With Diskospondylitis in Dogs and Cats Modified from Greene C: Infectious diseases of the dog and cat, ed 2, St Louis, 1999, Saunders.
Dogs Bacterial Staphylococcus pseudintermedius Bruceila canis Nocardia Actinomyces Streptococcus canis Escherichia coli Alcaligenes Micrococcus Proteus Mycobacterium Corynebacterium Fungal Aspergillus terreus Paecilomyces varioti Fusarium Mucor
Cats S. canis Actinomyces E. coli
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Discolored Urine From Willard M, Tvedten H: Small animal clinical diagnosis by laboratory methods, ed 4, St Louis, 2004, Saunders. RBCs, Red blood cells.
Potential Causes in Dogs and Cats Urine Color
Causes
Dark yellow
Concentrated urine
Pale yellow
Normal urochromes, urobilin
Yellow-brown
Bile pigments
Yellow-orange Bilirubin Fluorescein Concentrated urine Phenazopyridine Red
Hemoglobin RBCs Myoglobin Dyes Phenazopyridine Phenolsulfonphthalein
Green-blue
Methylene blue Dithiazanine Biliverdin
Brown-black
Bile pigments Myoglobin Methemoglobin
Milky
Pyuria Lipiduria Phosphate crystals
Colorless
Dilute
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Dilated Cardiomyopathy Differential Diagnosis: Myocardial Failure Modified with permission from Kittleson M: Small animal cardiovascular medicine, St Louis, 1998, Mosby, p 320. †
These causes constitute less than 10% of the clinical cases of severe myocardial failure seen clinically. The remainder are idiopathic.
*
Clinically documented causes of myocardial failure in veterinary medicine.
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Potential Causes of Ventricular Dilation and Poor Contractility (Myocardial Failure) Viral Parvovirus* Distemper virus Canine herpesvirus
Fungal Rickettsial Ehrlichia canis Rickettsia rickettsii Bartonella elizabethae
Spirochetal Borrelia burgdorferi
*
Parasitic Trypanosoma cruzi Toxoplasma gondii Toxocara canis
*
Endocrinologic Severe hypothyroidism Hyperthyroidism* Pheochromocytoma
Drugs and Toxins Adriamycin* Cobalt Gossypol
Physical Injury Electric shock Trauma Heatstroke
Nutritional Deficiencies *
Taurine
Carnitine*
Ischemia/Infarction Septic coronary artery embolus* *
Atherosclerosis
Muscular Dystrophy
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Diet: Assessment Relevant Considerations Inquire about specific varieties and amounts of what the patient is typically fed and what it is currently being fed, including: Commercial pet foods Home-prepared diets Table foods or scraps Treats Dietary supplements Foods used to deliver medications or supplements Establish who lives in the household and whether there have been any recent changes, including: People and other pets Inquire about how the patient is fed and whether there have been any recent changes, including: Who feeds the pet Timing of meals Free choice versus meal feeding Ask about the patient's feeding behavior. AUTHOR: KATHRYN MICHEL
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Diarrhea Major Categories and Causes for Acute Diarrhea in Dogs and Cats From Willard M, Tvedten H: Small animal clinical diagnosis by laboratory methods, ed 4, St Louis, 2004, Saunders.
Intestinal Parasites Hookworms Roundworms Whipworms Coccidia Giardia intestinalis (sometimes difficult to diagnose) Strongyloides Trichomoniasis
Dietary Problems Poor-quality food or food poisoning Sudden dietary change (especially in young animals) Food intolerance or allergy
Acute Viral or Bacterial Enteritis Parvovirus (canine and feline) Coronavirus (canine and feline) Clostridium perfringens–associated enteritis Campylobacteriosis Salmonellosis Escherichia coli–associated enteritis (verotoxin-producing strains)
Intussusception
Intoxication Garbage Food poisoning Heavy metal Organophosphate
Hemorrhagic Gastroenteritis
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Diarrhea, Small Versus Large Intestine Modified from Willard M, Tvedten H: Small animal clinical diagnosis by laboratory methods, ed 4, St Louis, 2004, Saunders.
Differentiation of Chronic Small-Intestinal from Chronic Large-Intestinal Diarrhea Small-Intestinal Diarrhea
Large-Intestinal Diarrhea
Weight loss (most important criterion)
Expected
Uncommon except with histoplasmosis, pythiosis, or cancer
Polyphagia
Often present
Uncommon
Vomiting
Common
Occurs in 10%-20% of animals
Volume of feces
May be normal or larger than normal
May be normal or smaller than normal
Frequency of defecation
Normal to slightly increased
Normal to markedly increased; may have many small defecations per bowel movement
Slate-gray feces (steatorrhea) Occasionally
No
Hematochezia
No
Sometimes present
Melena
Sometimes
No
Mucoid stools
Rare (unless ileum is diseased)
Often present
Tenesmus/dyschezia
Rarely present
Sometimes present
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Diarrhea, Neonatal Modified from Bonagura J: Kirk's current veterinary therapy XIII, St Louis, 2000, Saunders. FeLV, Feline leukemia virus; FIP, feline infectious peritonitis; FIV, feline immunodeficiency virus.
Causes of Neonatal Diarrhea in Puppies and Kittens Dietary Abrupt change in diet Overfeeding Indiscretion: garbage ingestion Ingestion of abrasive or indigestible material Food intolerance Intolerance of lactose ingested as milk
Endoparasitic Helminths: ascarids, hookworms, whipworms, Strongyloides Others: cestodes, trematodes, Trichinella Protozoa: coccidia (Cystoisospora), Cryptosporidium, Giardia lamblia Others: Pentatrichomonas, Entamoeba, Balantidium, rickettsial organisms Salmon poisoning disease
Obstructive Intestinal foreign body Intussusception Intestinal volvulus
Idiopathic Chronic Diarrhea in Young Cats Drug- and Toxin-Induced Antiinflammatory drugs Antimicrobials Anthelmintics Heavy metals: lead, arsenic, thallium Insecticides: organophosphates Plants
Infectious Viral: parvoviruses, coronaviruses, rotaviruses, canine distemper, FeLV, FIV, FIP Bacterial: Salmonella spp., Campylobacter spp., Yersinia enterocolitica, Bacillus piliformis, Escherichia coli, Clostridium spp.
Extraintestinal Renal failure Hepatic disease Hypoadrenocorticism Acute pancreatitis Diabetes mellitus
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Diarrhea, Chronic Large Intestinal: Causes From Bonagura J: Kirk's current veterinary therapy XIII, St Louis, 2000, Saunders.
Diagnosis in 74 Cases of Chronic Large-Bowel Diarrhea Diagnosis
Number of Cases
Idiopathic
19
Plasmacytic lymphocytic colitis
15
Clostridium perfringens enterotoxicosis 10 Malignant neoplasia
10
Pyogranulomatous colitis
6
Histiocytic ulcerative colitis
3
Eosinophilic granulomatous colitis
2
Trichuris vulpis
1
Histoplasmosis
1
Miscellaneous
7
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Diabetes, Ketoacidosis Triggers and Predisposing Conditions Acromegaly Chronic kidney disease Congestive heart failure Epinephrine release Glucagonoma Glucocorticoid treatment Hepatitis/cholangiohepatitis Hyperadrenocorticism Infection Abscess (subcutaneous, other) Periodontal/oral Pneumonia Pyoderma Pyometra Urinary tract infection Pancreatitis Progesterone (diestrus; progestagen treatment)
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Diabetes Mellitus Complications in Dogs and Cats Modified from Feldman E, Nelson R: Canine and feline endocrinology and reproduction, ed 3, St Louis, 2004, Saunders.
Common Iatrogenic hypoglycemia Persistent polyuria and polydipsia (PU/PD) Weight loss Cataracts (dogs) Bacterial infections, especially in the urinary tract Pancreatitis Ketoacidosis Hepatic lipidosis Peripheral neuropathy (cat)
Uncommon Peripheral neuropathy (dog) Glomerulonephropathy, glomerulosclerosis Retinopathy Systemic hypertension Exocrine pancreatic insufficiency Gastric paresis Diabetic diarrhea Diabetic dermatopathy (dog) (i.e., superficial necrolytic dermatitis/hepatocutaneous syndrome)
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Diabetes Insipidus, Nephrogenic Causes From DiBartola S: Fluid, electrolyte, and acid-base disorders in small animal practice, St Louis, 2000, Saunders.
Congenital (Primary)
Acquired (Secondary)Functional Drugs Glucocorticoids Lithium Demeclocycline Methoxyflurane Escherichia coli endotoxin (e.g., pyelonephritis, pyometra) Diuretics Electrolyte/mineral disturbances Hypokalemia Hypercalcemia Altered medullary hypertonicity Hypoadrenocorticism Multifactorial or unknown mechanism Hepatic insufficiency Hyperthyroidism Hyperadrenocorticism Postobstructive diuresis Acromegaly
Structural Medullary interstitial amyloidosis (e.g., in cats, shar-pei dogs) Polycystic kidney disease Chronic pyelonephritis Chronic interstitial nephritis
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Dermatosis, Periocular Dogs Parasitic: Demodicosis Sarcoptic acariasis Trombiculiasis Fungal: Dermatophytosis Malassezia dermatitis Bacterial: Staphylococcal folliculitis Mucocutaneous pyoderma Protozoal: Leishmaniasis Allergic: Atopic dermatitis Food allergy Contact allergic dermatitis Angioedema Autoimmune/immune-mediated: Pemphigus (foliaceus, erythematosus, vulgaris) Lupus erythematosus (cutaneous, systemic) Bullus pemphigoid Canine familial dermatomyositis Erythema multiforme Uveodermatologic syndrome Vitiligo Neoplastic: Epitheliotropic lymphoma Miscellaneous: Juvenile cellulitis Superficial necrolytic dermatitis (hepatocutaneous syndrome) Zinc-responsive dermatosis Actinic dermatitis
Cats Parasitic: Notoedric acariasis Demodicosis Trombiculiasis Fungal: Dermatophytosis Bacterial: Staphylococcal folliculitis Allergic: Atopic dermatitis Food allergy Contact allergic dermatitis Autoimmune/immune-mediated: Pemphigus (foliaceus, erythematosus, vulgaris) Cutaneous lupus erythematosus Systemic lupus erythematosus Erythema multiforme Periocular leukotrichia (Siamese) Miscellaneous: Actinic dermatitis Idiopathic facial dermatitis (Persian, Himalayan, exotic short hair)
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Dermatoses, Scaling and Crusting Modified from Ettinger S, Feldman E: Textbook of veterinary internal medicine, ed 6, St Louis, 2005, Saunders. BC, Bacterial culture; Bx, skin biopsy; C, common; CS, clinical signs; Cyt, cytology; DTM, dermatophyte test medium fungal culture; Hx, history; IDST, intradermal skin test; IgE, allergen-specific serum IgE assay; MDB, minimum database; NSF, no significant findings; R, rare; SS, skin scraping; U, uncommon; +, positive; −, negative.
Scaling and Crusting Dermatoses of Dogs and Cats Lesion Distribution
Frequency Pruritus
Diagnosis
Varies
Trunk
C
− to + +
CS, Cyt, BC, Bx
Dog > cat
Varies
Trunk, feet
C
+
CS, Cyt, BC, Bx
Crusts, ulcers
Dog
German shepherd or Lips, others peribuccal
U
+ (painful) CS, Bx
Moist crust, exudation, erythema
Dog
Any (often flea related)
Face, neck, caudal trunk
C
+++
CS
Dermatophytosis
Crusts, scales, alopecia, erythema
Cat > dog
Young most frequently
Head, extremities, trunk
C
− to + +
DTM, Wood's light
Malassezia dermatitis
Crusts, scales, erythema, lichenification
Dog > cat
Adult most frequently Axillary, groin, interdigital, facial
C
+++
Cyt
Ctenocephalides felis Scales, erythema (flea)
Dog > cat
Any
Lumbosacral, neck
C
+
CS, parasite exam
Sarcoptes scabiei
Crusts, scales, excoriations, alopecia, erythema
Dog
Any
Pinnal margins, C lateral elbows, ventrum
+++
SS, response to therapy
Demodex canis
Crusts, scales, exudation, alopecia, erythema
Dog
Young or From single immunocompromised lesions on the adults head to generalized
C
− to +
SS
Cheyletiella spp.
Scales
Dog, cat
Young, most frequently
Dorsal trunk to generalized
U
− to + + + SS, tape impression
Notoedres cati
Crusts, scales
Cat
Any
Head, feet, generalized
U
− to + + + SS
Crusts, scales, erosions
Cat
Any
Face, pinnae, perioral, feet, trunk
U
++
Disease
Lesions
Species Signalment
Superficial folliculitis
Crusts, scales, collarettes, pustules
Dog > cat
Deep pyoderma
Crusts, ulcers
Mucocutaneous pyoderma Acute moist dermatitis
Bacterial
Fungal
Parasitic
Viral Feline leukemia virus (FeLV)
Serology, Bx
Allergic Reaction
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Species Signalment
Lesion Distribution
Disease
Lesions
Frequency Pruritus
Diagnosis
Atopic dermatitis
Erythema, Dog > alopecia, crusts cat (excoriation), scales, and others
All, dogs often 1-5 years old
Face, ears, feet, ventrum
C
+ to + + + CS, IDST, IgE
Food hypersensitivity
Erythema, crusts (excoriation), and others
Dog, cat
All, any age
Any
C
+ to + + + Food trial
Flea bite hypersensitivity
Erythema, crusts (excoriation), and others
Dog, cat
All
Caudal C dorsum, ventrum, thighs
+ + to + + Response + to flea control
Miliary dermatitis
Small hemorrhagic crusts
Cat
All (often associated with fleas)
Dorsum
C
++
Hyperadrenocorticism Alopecia, Dog > cutaneous cat atrophy, calcinosis cutis, crusts (pyoderma)
Middle-aged, older animals
Trunk
C
− (occ. +) MDB, hormone assays, imaging, Bx
Hypothyroidism
Scaling, dry skin, pyoderma, ± alopecia
Dog
Middle-aged, often large breeds
Generalized
C
−
MDB, thyroid assay
Superficial necrolytic dermatitis (hepatocutaneous syndrome)
Severe adherent crusting
Dog (cat)
Old
Muzzle, R footpads, pressure points
+ to ++ (painful)
Bx, MDB, liver assays, imaging
Dog, cat
Any age and sex; Akita, chow chow, and others
Nasal planum, U muzzle, pinnae, footpads, trunk
− to +
Bx
Nasal planum, muzzle
−
Bx
CS
Endocrine and Metabolic
Immune-Mediated Disease Pemphigus foliaceus
Crusts, pustules
Discoid lupus erythematosus (DLE)
Crusts, Dog, depigmentation, cat erosions, ulcers
Collies, Shetland sheepdog, and others
Exfoliative cutaneous lupus erythematosus
Excessive scaling
German short-haired Generalized pointer
Erythema multiforme
Crusts, vesicles Dog, cat erythema, target lesions, erosions, ulcers
Dog
U
U
Bx
Any
Axillae, groin, U mucocutaneous junctions
−
Bx
Onset before 6 months of age; American cocker spaniel and others
Generalized
Bx − to + +, especially with secondary infections
Congenital and Hereditary Primary seborrhea
Excessive scaling or greasy skin
Dog (cat)
U
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Disease
Lesions
Species Signalment
Lesion Distribution
Frequency Pruritus
Diagnosis
Ichthyosis
Excessive scaling
Dog
Golden retriever, Norfolk terrier, American Bulldog and others
Generalized
U
Bx
Schnauzer comedo syndrome
Comedones that may become crusted
Dog
Miniature schnauzer
Dorsum
C
−
CS, Bx
Familial canine dermatomyositis
Alopecia, scaling, depigmentation
Dog
Onset before 6 months of age, collie, Shetland sheep dog, and others
Face, pressure U points
−
Cx, Bx
Secondary seborrhea Excessive scaling or greasy skin
Dog, cat
Any age
Depends on primary cause
C
− to + + + CS, any depending appropriate on cause tests for primary disease
Vitamin A–responsive Marked dermatosis follicular plugging, hyperkeratotic plaques
Dog
Cocker spaniel and others; Adult onset
Generalized, more pronounced on ventrum
U
− to + +
CS, Bx
Ear margin dermatosis
Follicular casts and scaling
Dog
Dachshund and others
Ear margins, lateral and medial
U
− may become painful
CS, Bx
Erythema, scaling, may progress to exudation and crusting
Dog > cat
Light-haired animals, Pinnae, nasal C outdoor exposure planum (cat), bridge of nose, ventrum (dog)
− to +
CS, Bx
Zinc-responsive dermatosis
Crusts, scales, erythema, alopecia
Dog
Siberian husky, Alaskan malamute; young adults
Periocular, U perioral mucocutaneous junctions, pressure points
− to +
Bx
Fatty acid deficiency
Scales
Dog, cat
Any
Generalized
U
− to + +
Dietary hx
Dog > cat
Older animals
Generalized or localized
U
− to + + + Bx
Young to middleaged, standard poodle, Akita, vizsla, and others
Face, trunk, pinnae, become generalized
C
− to + +
Cornification Defects
Environmental Solar dermatitis
Nutritional
Others Cutaneous lymphoma Lesions highly variable but may include severe scaling Granulomatous sebaceous adenitis
Hyperkeratosis, Dog (cat) alopecia, follicular casts, may be erythematous
CS, Bx
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Disease
Lesions
Species Signalment
Lesion Distribution
Otitis externa
Scale, erythema otic exudate
Dog > cat
Pinnae, ear canal
Any
Frequency Pruritus
Diagnosis
C
Otoscopic examination, Cyt, BC
++
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Eosinophilia Potential Causes of Eosinophilia in Dogs and Cats From Feldman E, Nelson R: Canine and feline endocrinology and reproduction, ed 3, St Louis, 2004, Saunders, 2004. Parasitism Heartworm disease Gl Dermatologic Other Asthma Nonparasitic dermatologie disease Mast cell tumor Hypoadrenocorticism (Addison's disease) Uterine disease Eosinophilic myositis Eosinophilic pneumonitis/rhinitis/conjunctivitis Eosinophilic enterocolitis (allergic colitis) Eosinophilic leukemia Eosinophilic granuloma complex Eosinophilic vasculitis Drug reaction Gl, Gastrointestinal.
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Enteropathies: Breed-Related Modified from Ettinger S, Feldman E: Textbook of veterinary internal medicine, ed 6, St Louis, 2005, Saunders.
Suspected and Confirmed Breed Susceptibilities for Small-Intestinal Disease in Dogs and Cats Breed
Condition
Basenji
Lymphocytic-plasmacytic enteritis (also called immunoproliferative disease)
Beagle
Cobalamin deficiency
Border collie
Cobalamin deficiency
Boxer
Histiocytic ulcerative colitis
German shepherd
Idiopathic antibiotic-responsive, inflammatory bowel disease (lymphoplasmacytic, eosinophilic)
Giant schnauzer
Defective cobalamin absorption
Irish setter
Gluten-sensitive enteropathy
Lundehund
Lymphangiectasia
Retrievers
Dietary allergy
Rottweiler
Susceptibility to parvovirus
Soft-coated wheaten terrier
Protein-losing enteropathy/nephropathy
Shar-pei
Lymphocytic-plasmacytic enteritis, cobalamin deficiency
Toy breeds
Hemorrhagic gastroenteritis
Yorkshire terrier
Lymphangiectasia
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Endocarditis Modified with permission from Greene C: Infectious diseases of the dog and cat, ed 2, St Louis, 1999, Saunders, p 568.
Frequency of Isolation of Bacteria from Positive Blood Culture Bacteria
Canine Endocarditis (% of Cases)
Gram Positive Staphylococcus intermedius 6–33 Streptococcus spp.
12–26
Gram Negative Escherichia coli
6–30
Anaerobic Propionibacterium acnes
6
Erysipelothrix rhusiopathiae 19 Corynebacterium spp.
19
Other Bartonella spp.
28
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Electrocardiogram (ECG) Abnormalities Common Associations
Baseline Sawtooth: atrial flutter versus artifact (panting, purring, electrical interference).
P waves Tall (>0.4 mV [dog], >0.2 mV [cat]): P pulmonale. Rule out right atrial enlargement. Tall P waves are normal if R-R interval is short (i.e., normal during sinus tachycardia), but P wave height should normalize when heart rate slows. Wide (>0.05 sec [dog], >0.04 sec [cat]): P mitrale. Rule out left atrial enlargement. Cyclical increase and decrease in P-wave amplitude: wandering pacemaker. Absent: isoelectric to that lead (P waves are present but visible only in other leads), atrial standstill due to hyperkalemia, atrial standstill due to atrial myocardial disorder (rare), atrial fibrillation (fine, wavy baseline and irregularly irregular R-R interval must be present also).
PR Association Long PR interval (>0.13 sec [dog], >0.09 sec [cat]): first-degree atrioventricular (AV) block. Progressive lengthening of PR interval until longest one is followed by P wave without QRS complex: second-degree AV block, Mobitz type I. Two or more consecutive P waves without QRS complexes, then a P wave triggers a QRS complex: second-degree AV block, Mobitz type II. P waves and QRS complexes occur independently: third-degree AV block (normal or high atrial [P wave] rate, ventricular escape rhythm [wide, bizarre QRS complexes] slower than atrial rate) or ventricular tachycardia (wide, bizarre QRS complexes occur at a faster rate than P waves, which are often buried within the QRS complexes). Short PR interval (0.04 sec [cats]): diagnostic of left bundle branch block. Strongly suggests left ventricular enlargement; also occurs with severe hyperkalemia, quinidine toxicity. Small (low amplitude): rule out hypothyroidism, pericardial effusion, pleural effusion, ascites, obesity, pneumothorax, intrathoracic mass, hypothermia (dogs); rule out normal (cats).
Q Waves (Lead II) Deep: generally normal, especially in young, large-breed dogs; has been loosely associated with interventricular septal hypertrophy in dogs.
R Waves (Lead II) Tall (>2.5 mV [dogs that are small or medium breeds], >3.0 mV [dogs that are large breeds], >0.9 mV [cats]): left ventricular enlargement.
S Waves (Lead II) Deep: rule out right ventricular enlargement. S1S2S3 (S wave present in leads I, II, and III): strongly suggests right ventricular enlargement.
ST Segment Elevation (>0.15 mV [dog], any [cat]) or depression (>0.2 mV [dog], any [cat]): myocardial hypoxia, electrolyte disturbances. Slurring/coving: myocardial hypoxia.
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T Waves Tall (>1 mV or >¼ of height of R wave [dog]; >0.3 mV [cats]): commonly normal. If onset of tall T waves is noted during ECG monitoring over time: rule out hyperkalemia, myocardial hypoxia, movement artifact (change in limb position). Different from rest of T waves: indicates abnormal repolarization, which in turn suggests abnormal ventricular depolarization of that heartbeat (e.g., premature ventricular complex). Widespread availability of echocardiography has demonstrated that ECG is of limited accuracy for inferring cardiac structure. Indications of abnormal cardiac chamber size based on ECG features should be considered tentative and are best confirmed or ruled out using echocardiography.
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Effusions Modified with permission from Kittleson MD, Kienle RD, editors: Pericardial disease and cardiac neoplasia. In Small animal cardiovascular medicine, St Louis, 1998, Mosby, p 420. FIP, Feline infectious peritonitis; GI, gastrointestinal.
Characteristics of Effusions Parameter
Transudate
Modified Transudate
Exudate
Hemorrhage
Specific gravity
1.025
>1.025
Protein (g/dL)
2.5
>2.5
Appearance
Clear and watery
Clear to serosanguineous
Turbid, serosanguineous, serofibrinous
Serosanguineous, sanguineous
Cellularity 3 (cells/mm )
2500
>5000
>5000
Cytologic examination
Macrophages, mesothelial cells, and occasional neutrophils
Macrophages, mesothelial cells, and occasional neutrophils and erythrocytes
Variable
Primarily erythrocytes
Examples
Hypoalbuminemia (renal loss, GI loss, hepatic synthetic failure, massive skin wound/burn loss), prehepatic congestion/obstruction (e.g., portal vein thrombosis)
Heart failure, posthepatic vascular obstruction (e.g., caudal vena caval thrombosis), neoplasia, chyle
Septic (bacterial infection [aerobic, anaerobic]), nonseptic (e.g., FIP)
Anticoagulant rodenticide toxicosis, ruptured neoplasm, trauma
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Effusions, Bicavitary* Conditions Associated With Bicavitary Effusions Modified from Willard M, Tvedten H: Small animal clinical diagnosis by laboratory methods, ed 4, St Louis, 2004, Saunders. Cardiovascular conditions Pericardial effusion of any cause (neoplastic, idiopathic, toxic [anticoagulant], other) causing cardiac tamponade Constrictive pericardial disease Right-sided congestive failure: dilated cardiomyopathy, tricuspid regurgitation of any cause (tricuspid dysplasia, myxomatous tricuspid valve disease/endocardiosis, other), severe pulmonic stenosis, cor pulmonale of any cause (heartworm disease/caval syndrome, idiopathic pulmonary hypertension, other), tricuspid valve stenosis Caudal vena cava thromboembolism Congenital obstruction: caudal vena cava Hypoalbuminemia: protein-losing nephropathy, protein-losing enteropathy, advanced hepatic disease, pancreatitis, extensive burns Bile peritonitis Vasculitis (e.g., FIP) Neoplastic conditions Right atrial fibroma Metastatic adenocarcinoma Lymphoma Hemangiosarcoma Mesothelioma Cholangiocellular carcinoma Chemodectoma Prostatic adenocarcinoma Diffuse carcinomatosis FIP, Feline infectious peritonitis.
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Edema Modified from Mitchell RN, Cotran RS: Hemodynamic disorders, thrombosis, and shock. In Cotran RS, et al, editors: Robbins pathologic basis of disease, ed 6, Philadelphia, 1999, Saunders.
Cause
Contributing Factor
Specific Clinical Syndromes
Increased hydrostatic pressure
Impaired venous return
Congestive heart failure (CHF) Pericardial disease (pericardial effusion, constrictive pericarditis, pericardial cyst or neoplasm) Portal hypertension Venous obstruction or compression (thrombosis, external pressure, extremity inactivity)
Small-caliber arteriolar dilation
Heat Neurohumoral dysregulation
Reduced plasma oncotic pressure
Hypoproteinemia
Protein losing nephropathy (amyloidosis, glomerulonephritis) Synthetic failure (chronic liver disease) Malnutrition Protein-losing gastroenteropathy
Lymphatic obstruction
Decreased lymphatic drainage of interstitium
Various inflammatory conditions Congenital (lymphedema) Neoplastic Postsurgical Postirradiation
Sodium retention
Excess dietary intake with renal insufficiency Increased tubular sodium resorption
Inflammation
Renal hypoperfusion Increased renin-angiotensin-aldosterone secretion
Acute inflammation Chronic inflammation Angiogenesis
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Fever of Unknown Origin Associated Conditions Modified with permission from Greene C: Table 96-3: Conditions associated with fevers of unknown origin. In Greene C, editor: Infectious diseases of the dog and cat, ed 2, St Louis, 1999, Saunders, p 696.
Systemic Infections
Dogs Bacterial endocarditis, bacteremias from an inapparent focus (e.g., secondary to persistent neutropenia or a congenital/acquired immunodeficiency syndrome); Lyme borreliosis (acute); leptospirosis; brucellosis; mycobacterial infections; rickettsial disease (e.g., ehrlichiosis, RMSF); protozoal infections (e.g., babesiosis, leishmaniasis, disseminated toxoplasmosis, neosporosis); disseminated mycotic infections (e.g., histoplasmosis, blastomycosis, cryptococcosis, coccidioidomycosis, aspergillosis)
Cats FIV infection; FeLV infection; feline hemotropic mycoplasma infection; feline infectious peritonitis; bacteremias from an inapparent focus; systemic mycoses (e.g., histoplasmosis, cryptococcosis); mycobacterial infections (often atypical); atypical calicivirus infection
Localized Infections
Dogs Bacterial endocarditis; urogenital infections (e.g., pyelonephritis, chronic prostatitis/prostatic abscess, stump pyometra); pyothorax and lung infections (e.g., inhaled pulmonary foreign bodies/pulmonary abscess, bronchopneumonia); occult hepatic abscess or cholangitis; localized peritonitis; diskospondylitis; juvenile metaphyseal osteomyelitis; retrobulbar or tooth root abscess; oropharyngeal stick injuries, septic thrombi
Cats Pyothorax and lung infections (e.g., pulmonary abscess, bronchopneumonia), upper respiratory infections; occult hepatic abscess or cholangiohepatitis; urogenital infections (e.g., pyelonephritis); localized peritonitis; osteomyelitis; cat bite abscess/cellulitis
Immune-Mediated Diseases
Dogs SLE; immune-mediated polyarthropathies: rheumatoid arthritis (erosive); nonerosive, nonseptic polyarthritis; idiopathic diseases; polyarthritis-meningitis complex (weimaraner, Newfoundland, German shorthaired pointer, boxer, beagle); polyarthritis-polymyositis complex (spaniel breeds); polyarthritis of Akitas; polyarthritis and amyloidosis of the Chinese shar-pei (shar-pei hock/fever); polyarteritis nodosa; autoimmune hemolytic anemia and immune-mediated thrombocytopenia; steroid-responsive meningitis; immunodeficiency syndromes
Cats SLE (rare in cats); chronic progressive polyarthropathy, including the ankylosing (periosteal proliferative) and luxating (erosive) forms; autoimmune hemolytic anemia (uncommon; may be FeLV associated); immune-mediated thrombocytopenia (rare; may be FeLV associated)
Neoplasia
Dogs
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Solid neoplasms (especially those that are necrotic, elicit an inflammatory response or have widespread metastases); lymphoproliferative or myeloproliferative disease
Cats FeLV-related lymphoproliferative and myeloproliferative disorders
Miscellaneous
Dogs Metaphyseal osteopathy, panosteitis; inflammatory-granulomatous bowel disease; liver disease (e.g., hepatic necrosis, cirrhosis, portosystemic shunts); pulmonary emboli; nodular panniculitis; drug reactions (tetracyclines, penicillin, sulfonamides, amphotericin B, quinidine)
Cats Pansteatitis (cats on fish-rich diets); hypervitaminosis A; drug reactions (e.g., tetracycline, levamisole) FeLV, Feline leukemia virus; FIV, feline immunodeficiency virus; RMSF, Rocky Mountain spotted fever; SLE, systemic lupus erythematosus.
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Feline Leukemia Virus and Feline Immunodeficiency Virus: Associated Disorders Associated Diseases From Ettinger S, Feldman E: Textbook of veterinary internal medicine, ed 5, St Louis, 2000, Saunders. Immunosuppression with opportunistic infections Gingivitis/stomatitis (FIV > FeLV) Myeloproliferative disease/erythroleukemia (FeLV ≫ FIV) Lymphosarcoma/lymphoid leukemias (FeLV ≫ FIV) Diarrhea/panleukopenia-like syndrome Weight loss/cachexia Chronic fever Glomerulonephritis Anterior uveitis/pars planitis/glaucoma (FIV ≫ FeLV) Behavioral changes/dementia/peripheral neuropathies Hypergammaglobulinemia (FIV > FeLV) Hemolytic anemias/aplastic anemias (FeLV ≫ FIV) Lymphopenia/neutropenia Thrombocytopenia (FeLV ≫ FIV) Abortion/fetal resorption/thymic atrophy (FeLV ≫ FIV) Chronic progressive polyarthritis FeLV, Feline leukemia virus; FIV, feline immunodeficiency virus.
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Glucosuria From Willard M, Tvedten H: Small animal clinical diagnosis by laboratory methods, ed 4, St Louis, 2004, Saunders.
Causes in Dogs and Cats Blood glucose concentration exceeding renal threshold (common)
Diabetes mellitus Stress (especially in cats) Infusion of dextrose-containing fluids Hyperadrenocorticism (rarely causes glucose >180 mg/dL) Pheochromocytoma (rare)
Abnormal proximal renal tubular function
Aminoglycoside toxicity Acute renal failure Fanconi syndrome Primary renal glucosuria
Contamination
Urinary hemorrhage in an animal with mild hyperglycemia
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Glomerular Diseases, Dogs Associated Diseases Reported in Dogs Modified from Ettinger S, Feldman E: Textbook of veterinary internal medicine, ed 6, St Louis, 2005, Saunders.
Infectious Bacterial Bartonellosis (G) Borreliosis (G) Brucellosis (G) Endocarditis (G) Pyometra (A, G) Pyoderma (A, G) Other chronic bacterial infections (A, G) Protozoal Babesiosis (MPGN) Hepatozoonosis (G) Leishmaniasis (A, MN, P-E, and P-M) Trypanosomiasis (G) Rickettsial Ehrlichiosis (G) Viral Canine adenovirus type 1 (P-M) Parasitic Dirofilariasis (A, MN) Fungal Coccidioidomycosis (A, G) Blastomycosis (G)
Inflammatory Chronic dermatitis (A, G) Inflammatory bowel disease (G) Pancreatitis (A, G) Periodontal disease (A, G) Polyarthritis (A, G) SLE (A, MN, P-E, and P-M) Other immune-mediated diseases (G)
Neoplastic Leukemia (G) Lymphosarcoma (A, G) Mastocytosis (G) Primary erythrocytosis (MCD?) Systemic histiocytosis (G) Other neoplasms (A, G, MN)
Miscellaneous Corticosteroid excess (G) Trimethoprim-sulfa therapy (G) Hyperlipidemia (?) Congenital C3 deficiency
Familial
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Idiopathic (A, G, MN, MCD, P-E, or M) A, Amyloidosis; G, glomerulonephritis, uncharacterized; MCD, minimal change disease; MN, membranous nephropathy; MPGN, membranoproliferative (mesangiocapillary) glomerulonephritis; P, proliferative (E, endocapillary; M, mesangial); SLE, systemic lupus erythematosus; ?, association uncertain.
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Glomerular Diseases, Cats Associated Diseases Reported in Cats From Ettinger S, Feldman E: Textbook of veterinary internal medicine, ed 6, St Louis, 2005, Saunders.
Systemic Disease (Glomerular Disease) Infectious Bacterial Chronic bacterial infections (G) Mycoplasmal polyarthritis (G) Viral FIV (G) FIP (MN) FeLV (G, MN)
Inflammatory Pancreatitis (G) Cholangiohepatitis (G) Chronic progressive polyarthritis (G) SLE (MN) Other immune-mediated diseases (G)
Neoplastic Leukemia (MN) Lymphosarcoma (MN) Mastocytosis (G) Other neoplasms (G)
Miscellaneous Acromegaly (?) Mercury toxicity (MN)
Familial (MN)
Idiopathic (MN) FeLV, Feline leukemia virus; FIP, feline infectious peritonitis; FIV, feline immunodeficiency virus; G, glomerulonephritis, uncharacterized; MN, membranous nephropathy; SLE, systemic lupus erythematosus; γ, uncertain association.
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Gastrointestinal Ulceration Conditions and Drugs Associated With Gl Ulceration in Small Animals From Bonagura J: Kirk's current veterinary therapy XII: small animal practice, St Louis, 1995, Saunders.
Impaired Mucosal Defense Drugs *
NSAIDs Corticosteroids Stress Shock Sepsis Trauma Major surgery Neurologic disease Head trauma Intervertebral disk disease† Metabolic disorders Liver disease Renal disease Pancreatitis Inflammatory bowel disease GI neoplasia Mastocytosis Gastric motility disorders
Hyperacidity Gastrinoma Mastocytosis Gl, Gastrointestinal; NSAIDs, nonsteroidal antiinflammatory drugs. *
NSAIDs that have been associated with GI ulcers in small animals include aspirin, indomethacin, phenylbutazone, flunixin, ibuprofen, deracoxib, meloxicam, naproxen, and piroxicam. †
Treated with corticosteroids.
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Gastrointestinal Endocrine Diseases Disease
Main Clinical Abnormality
Glucagonoma
Persistent hyperglycemia; hepatocutaneous syndrome possible
Gastrinoma
Gastric ulceration
Carcinoma
Liver; lethargy, anorexia; metastasis; no vasoactive amine signs
Pancreatic polypeptidoma Chronic vomiting
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Gastric Outflow Obstruction From Slatter D: Textbook of small animal surgery, ed 3, Philadelphia, 2003, Saunders. AAPH, Acquired antral pyloric hypertrophy; CHPG, chronic hypertrophic pyloric gastropathy.*Condition is secondary to CHPG/AAPH, gastric motility disorders, chronic gastritis, gastric or duodenal ulcers, gastric neoplasia, or extragastric causes.
History, Physical Findings, and Laboratory Findings in Animals With Gastric Retention or Outflow Obstruction
History
Chronic Gastritis Related
Ulcer Related or Gastric Neoplasia
Vomiting present: variable chronicity; intermittent occurrence
Vomiting present: progressive increase in frequency
CHPG/AAPH
Motility Disorder
Vomiting present: variable chronicity
Vomiting present: variable chronicity
Partially digested food
Partially digested food Partially digested food or bile-stained fluid
Partially digested food or bile-stained fluid
Occurs anytime after eating
Occurs anytime after eating
Hematemesis common
Exacerbated by eating or drinking
*
Extragastric Vomiting present
Hematemesis may be present Dietary modifications affect frequency Abdominal distention present
Abdominal distention present
Abdominal distention present
Abdominal distention present
Abdominal distention present
Appetite good
Appetite good
Appetite variable to poor
Appetite variable to poor
Appetite variable to poor
Body weight variable
Body weight variable
Weight loss, unthrifty
Weight loss, unthrifty
Body weight variable
May have history of acute or gastric dilatation with volvulus or other gastric disease or surgery
Melena may be present
Melena common; abdominal pain present
History compatible with specific extragastric disease
Normal to decreased body condition
Slight to significant Slight to significant Signs decreased body decreased body consistent with condition condition extragastric disease
Bright, responsive
Bright, responsive
Normal to depressed
Normal to depressed
No abdominal pain
No abdominal pain
Variable cranial abdominal pain
Variable cranial abdominal pain
Cranial abdominal distention
Cranial abdominal distention
Cranial abdominal distention
Cranial abdominal distention
Physical Normal to Examination decreased body condition
Appetite variable to poor
Cranial abdominal distention
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Laboratory Findings
Chronic Gastritis Related
Ulcer Related or Gastric Neoplasia
CHPG/AAPH
Motility Disorder
Extragastric
No abnormalities unless severe vomiting
No abnormalities Variable acid-base Variable acid-base Variable unless severe vomiting status status acid-base status
Alkalosis
Alkalosis
Hypokalemia
Hypokalemia
Hypokalemia
Hypokalemia
Anemia (chronic disease, blood loss, or iron deficiency)
Anemia (chronic disease, blood loss, or iron deficiency)
Hypochloremia
Hypochloremia
Hypoproteinemia
Hypoproteinemia
Hemoconcentration
Hemoconcentration
Laboratory findings consistent with extragastric disease
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Hypoxemia Causes
Hypoventilation* Acute barbiturate toxicosis, CNS lesion, neuromuscular disease (e.g., botulism, polyradiculoneuritis), pneumothorax, flail chest, pleural effusion, upper airway obstruction (e.g., laryngeal paralysis, foreign body, large airway trauma, large airway mass), anesthetic circuit problems
Diffusion/Gas Exchange Disorder* Pneumonia, pulmonary edema, pulmonary hemorrhage
Ventilation/Perfusion Mismatch* Pulmonary thromboembolism, prolonged recumbency
Right-to-Left Cardiovascular Shunt Tetralogy of Fallot, right-to-left shunting patent ductus arteriosus, other forms of Eisenmenger's physiology CNS, Central nervous system.
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Hypothyroidism Neurologic Associations (Confirmed or Suspected) Neuromuscular weakness (slowly progressive) Muscle atrophy (scapular, masticatory) Facial nerve paralysis Vestibular signs (peripheral) Laryngeal paralysis Megaesophagus
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Hypothermia Causes Modified with permission from Bonagura J: Kirk's current veterinary therapy XII small animal practice, St Louis, 1995, Saunders, p 159.
Iatrogenic Surgery Anesthesia Overzealous treatment of hyperthermia
Systemic Disease Cardiac Hypothyroidism Sepsis Chronic kidney disease Hypoadrenocorticism Malnutrition Hypoglycemia Neurologic: Head trauma Neoplasia Cerebrovascular accident
Environmental Exposure Trauma
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Hypotension, Systemic Causes Modified from Ettinger S, Feldman E: Textbook of veterinary internal medicine, ed 6, St Louis, 2005, Saunders.
Decreased PreloadHypovolemia Hemorrhage Trauma Gastrointestinal losses Polyuria Hypoadrenocorticism Effusions or other third spacing of fluid Burns Heatstroke Pulmonary arterial hypertension (severe)
Decreased Venous Return Pericardial effusion/cardiac tamponade Constrictive pericarditis Severe pneumothorax Positive-pressure ventilation Gastric dilatation/volvulus Heartworm disease (cavai syndrome)
Decreased Cardiac Function Cardiomyopathy Valvular disease Bradyarrhythmias Tachyarrhythmias Electrolyte abnormalities Acid-base disturbances Severe hypoxemia
Decreased Vascular Tone SIRS Anaphylaxis Neurogenico Drug-induced (anesthetic agents, vasodilators, β-blockers, calcium channel blockers) Electrolyte abnormalities Acid-base disturbances Severe hypoxemia SIRS, Sepsis/systemic inflammatory response syndrome.
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Hypophosphatemia Causes Modified from DiBartola S: Fluid, electrolyte, and acid-base disorders in small animal practice, St Louis, 2000, Saunders.
Maldistribution (Translocation) Treatment of diabetic ketoacidosis Carbohydrate load or insulin administration Respiratory alkalosis or hyperventilation Parenteral nutrition or nutritional recovery Hypothermia
Increased Loss (Reduced Renal Resorption) Primary hyperparathyroidism Renal tubular disorders (e.g., Fanconi syndrome) Proximally acting diuretics (e.g., carbonic anhydrase inhibitors) *(?) Eclampsia Hyperadrenocorticism (?)
Decreased Intake (Reduced Intestinal Absorption) Dietary deficiency (?) Vomiting (?) Malabsorption (?) Phosphate binders Vitamin D deficiency
Laboratory Error Example: mannitol administration
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Hyponatremia Causes From DiBartola S: Fluid, electrolyte, and acid-base disorders in small animal practice, St Louis, 2000, Saunders.
With Normal Plasma Osmolality Hyperlipidemia Hyperproteinemia
With High Plasma Osmolality Hyperglycemia Mannitol infusion
With Low Plasma Osmolality Including Hypervolemia Severe liver disease Congestive heart failure Nephrotic syndrome Advanced renal failure Including Normovolemia Psychogenic polydipsia Syndrome of inappropriate antidiuretic hormone secretion Antidiuretic drugs Myxedema coma of hypothyroidism Hypotonie fluid infusion Including Hypovolemia Gastrointestinal loss: Vomiting Diarrhea Third-space loss: Pancreatitis Peritonitis Uroabdomen Pleural effusion (e.g., chylothorax) Peritoneal effusion Cutaneous loss: Burns Hypoadrenocorticism Diuretic administration
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Hypomagnesemia Causes of Magnesium Depletion in Humans Modified from DiBartola S: Fluid, electrolyte, and acid-base disorders in small animal practice, St Louis, 2000, Saunders.
Inadequate Dietary Intake Protein-calorie malnutrition Magnesium-free fluids and total parenteral nutrition
Gastrointestinal Disorders Prolonged nasogastric suction Chronic diarrhea Malabsorption syndromes Extensive bowel resection Intestinal and biliary fistulas Primary infantile hypomagnesemia
Renal Loss Chronic parenteral fluid therapy with magnesium-free fluids Intrinsic tubular disorders: Chronic interstitial nephritis, pyelonephritis, glomerulonephritis Acute tubular necrosis (diuretic phase) Postobstructive diuresis Renal tubular acidosis Congenital magnesium wasting Drug injury: Aminoglycosides Amphotericin B Cisplatin Cyclosporine Loop diuretics Osmotic diuretics: glucose, mannitol, urea Hypercalcemia Hypokalemia Alcohol
Metabolic Hypercalcemia Hypophosphatemia
Endocrine Diabetes mellitus Hyperthyroidism Primary hyperparathyroidism Hyperadrenocorticism Syndrome of inappropriate antidiuretic hormone secretion
Redistribution Pancreatitis Hyperadrenergic states Massive blood transfusion Insulin therapy Refeeding syndrome
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Hypothermia Acute respiratory alkalosis Sepsis Cardiopulmonary bypass
Miscellaneous Severe burns Excessive lactation Excessive sweating
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Hypokalemia: Associated Disorders (Cats) Conditions Associated With Hy pokalemia in Cats Modified from Bonagura J: Kirk's current veterinary therapy XIII, St Louis, 2000, Saunders. Thyrotoxicosis Chronic kidney disease Metabolic acidosis Dietary Potassium deficient Acidified diets Insulin overdose Diuretic therapy (furosemide) Metabolic alkalosis Chronic vomiting/diarrhea Fluid administration (plasma dilution and volume-induced diuresis) Idiopathic (Burmese breed) Systemic diseases Hepatic disease Infectious disease Hyperaldosteronism (adrenocortical tumor) Renal tubular acidosis
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Hypokalemia: Causes Causes Modified from DiBartola S: Fluid, electrolyte, and acid-base disorders in small animal practice, St Louis, 2000, Saunders.
Decreased Intake Alone, unlikely to cause hypokalemia unless diet is aberrant Administration of potassium-free fluids (e.g., 0.9% NaCl, 5% dextrose in water)
Translocation (ECF to ICF) Alkalemia Insulin/glucose-containing fluids Catecholamines Hypothermia (?) Hypokalemic periodic paralysis (Burmese cats)
Increased LossGI (FEk < 4%-6%) Vomiting of stomach contents Diarrhea
Urinary (FEk > 4%-6%) Chronic kidney disease in cats Diet-induced hypokalemic nephropathy in cats Distal (type I) RTA Proximal (type II) RTA after NaHco3 treatment Postobstructive diuresis Dialysis Mineralocorticoid excess: Hyperadrenocorticism Primary hyperaldosteronism (adenoma, hyperplasia)
Drugs Loop diuretics (e.g., furosemide, ethacrynic acid) Thiazide diuretics (e.g., chlorothiazide, hydrochlorothiazide) Amphotericin B Penicillins Albuterol overdosage ECF, Extracellular fluid; FEk, urinary fractional excretion of potassium; GI, gastrointestinal; ICF, intracellular fluid; RTA, renal tubular acidosis.
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Hypoglycemia Causes Modified from Willard M, Tvedten H: Small animal clinical diagnosis by laboratory methods, ed 4, St Louis, 2004, Saunders. Beta-cell tumor (insulinoma)* Extrapancreatic neoplasia Hepatocellular carcinoma, hepatoma Leiomyosarcoma, leiomyoma Hemangiosarcoma (rarely) Hepatic insufficiency* Portocaval shunts* Chronic fibrosis, cirrhosis Sepsis* Hypoadrenocorticism Hypopituitarism Idiopathic hypoglycemia* Neonatal hypoglycemia Juvenile hypoglycemia (esp. toy breeds) Hunting dog hypoglycemia Renal failure (rarely) Exocrine pancreatic neoplasia Hepatic enzyme deficiencies von Gierke's disease (type 1 glycogen storage disease) Cori's disease (type 3 glycogen storage disease) Severe polycythemia Prolonged starvation Prolonged sample storage* Iatrogenic* Insulin therapy Sulfonylurea therapy Ethanol Ethylene glycol Artifact Glucometers Laboratory error
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Hypochloremia Causes Adapted from de Morais: Chloride ion in small animal practice: the forgotten ion. J Vet Emerg Crit Care 2:11-24, 1992. Pseudohypochloremia Lipemic samples (titrimetric methods) Excessive loss of chloride relative to sodium Vomiting of stomach contents* *
Therapy with thiazides or loop diuretics Chronic respiratory acidosis Hyperadrenocorticism Exercise Therapy with solutions containing high sodium concentration relative to chloride Sodium bicarbonate Sodium penicillin (extremely high doses)
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Hypocapnia Causes Modified with permission from King L: Textbook of respiratory disease in dogs and cats, St Louis, 2004, Saunders, 183. Hypotension Fever Sepsis Excitement Exercise Pain Pulmonary thromboembolism Early pulmonary parenchymal disease Cytokine release in the systemic inflammatory response syndrome Inappropriate ventilator settings Compensation for metabolic acidosis Definition of hypocapnia: abnormally decreased arterial carbon dioxide tension (e.g., in dogs: Pco2 4 weeks
Severe Dental Disease Infection
Chronic Infections or Inflammation Pyelonephritis, chronic dermatitis (examples)
Inflammatory Bowel Disease (IBD) Lymphoplasmacytic Eosinophilic
Neoplasia Lymphoma, other
Disorders Influencing Lipid Metabolism Diabetes mellitus Idiopathic hyperlipidemia (e.g., schnauzer, Shetiland sheepdog, other)
Pancreatitis, Chronic Hypothyroidism, Severe Congestive Heart Failure (CHF)
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Hepatic Neoplasia From Ettinger S, Feldman E: Textbook of veterinary internal medicine, ed 6, St Louis, 2005, Saunders.
Dogs *
Primary Hepatic Tumors (26%) Hepatocellular carcinoma Hepatocellular adenoma Hepatic hemangiosarcoma Biliary carcinoma Other Leiomyosarcoma Liposarcoma Myxosarcoma Fibrosarcoma Biliary adenoma Hepatic carcinoid Hemolymphatic Neoplasia (28%) Lymphoma MCT Plasma cell tumor Metastatic Neoplasia (46%)
Cats *
Primary Hepatic Tumors (20%) Biliary carcinoma Hepatocellular carcinoma Hepatic hemangiosarcoma Other Biliary cystadenoma Myelolipoma Hepatic carcinoid Hemolymphatic Neoplasia (60%) Lymphoma MCT Plasma cell tumor Metastatic Neoplasia (20%) MCT, Mast cell tumor Primary tumors: in order of prevalence.
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Hepatic Infections and Abscesses Bacteria Isolated from Hepatobiliary Suppurative Inflammation and Abscesses Modified with permission from Greene C: Infectious diseases of the dog and cat, ed 2, St Louis, 1999, Saunders, p 616.
Aerobic Cultures (Positive Cultures: n = 54) n ≥ 3 each Escherichia coli Staphylococcus pseudintermedius S. aureus S. epidermidis Streptococcus group D enterococci Streptococcus β-hemolytic Enterococcus Enterobacter aerogenes E. agglomerans Pseudomonas aeruginosa n = 1 each Pseudomonas fluorescens Klebsiella pneumoniae Bacillus spp. Acinetobacter calcoaceticus Citrobacter freundii Moraxella phenylpyruvica Pasteurella multocida Bordetella bronchiseptica Nocardia Salmonella Campylobacter jejuni
Anaerobic Cultures (Positive Cultures: n = 26) Propionibacterium acnes Clostridium perfringens Clostridium Bacteroides melaninogenicus Corynebacterium spp. Actinomyces Peptostreptococcus Fusobacterium Anaerobic streptococci
Additional Microbes Reported Elsewhere Bacillus piliformis Corynebacterium spp. Proteus spp. Francisella tularensis Listeria monocytogenes Eugenic fermenter-4 bacilli In order from most to least common. Data acquired from case records, Companion Animal Hospital, College of Veterinary Medicine, Cornell University, Ithaca, NY, 1985–1996.
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Hepatic Fibrosis Causes in Dogs From Bonagura J: Kirk's current veterinary therapy XIII, St Louis, 2000, Saunders. Chronic hepatitis Hepatic copper accumulation Primary (Bedlington terriers, West Highland white terriers) Secondary (Doberman pinschers, Skye terriers) Infectious Drug-induced Primidone Metabolic α1-Antitrypsin deficiency Others Lobular dissecting hepatitis Idiopathic chronic hepatitis Toxins, chemicals Pyrrolizidine alkaloids, CCI4 Postnecrotic fibrosis Chronic congestive heart failure Chronic cholangiohepatitis Chronic biliary obstruction Idiopathic hepatic fibrosis Perivenous Diffuse pericellular Periportal
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Hepatic Failure, Acute Clinically Relevant Causes Modified from Ettinger S, Feldman E: Textbook of veterinary internal medicine, ed 4, St Louis, 1994, Saunders.
Category of Injury
Examples
Trauma
Automobile accident High-rise syndrome
Toxin
Environmental agents: Aflatoxin Amanita pantherina, Amanita phalloides Cycadaceae Heavy metals Drugs: Thiacetarsemide Mebendazole Diethylcarbamazine-oxibendazole Acetaminophen Methoxyflurane, halothane Diethylcarbamazine Tetracycline Trimethoprim-sulfadiazine Griseofulvin Diazepam (cats)
Infectious agents
Infectious canine hepatitis Leptospirosis Toxoplasmosis Heartworm caval syndrome Bacterial sepsis
Thermal Extension of abdominal inflammation
Metabolic disorder
Heatstroke Pancreatis Peritonitis Inflammatory bowel disease
Lipidosis (cats)
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Hemothorax Causes of Hemothorax and Sanguineous Pleural Effusion Modified with permission from King L: Textbook of respiratory disease in dogs and cats. St Louis, 2004, Saunders, p 611. Trauma Malignancy Coagulopathy Diaphragmatic hernia Lung lobe torsion Pulmonary infarction Pulmonary abscessation Recent surgery Aortic aneurysm Swan-Ganz catheter placement* Tube thoracostomy
*
Hemopneumothorax* *
Costal exostosis *
Endometriosis Foreign body Heartworm disease Central venous catheter placement * Reported only in human literature.
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Hemoptysis Causes From Ettinger S, Feldman E: Textbook of veterinary internal medicine, ed 6, St Louis, 2005, Saunders.
Pulmonary Pulmonary thromboembolism: secondary to neoplastic, endocrine, cardiac, metabolic disease Pulmonary hypertension: secondary to heartworm disease; congenital or acquired cardiac defects that result in shunting of blood Chronic bronchitis/bronchiectasis Bacterial pneumonia Nocardiosis Pulmonary abscess Kennel cough (rarely causes hemoptysis) Fungal pneumonia: blastomycosis, histoplasmosis, coccidioidomycosis Parasites: Paragonimus kellicotti, Capillaria aerophila, Aelurostrongylus abstrusus Eosinophilic bronchopneumopathy Neoplasia, lung: primary adenocarcinoma, undifferentiated carcinoma, SCC, chondrosarcoma; metastatic; primary tracheal tumors Lung lobe torsion
Cardiovascular Heartworm disease Cardiogenic pulmonary edema Arteriovenous fistula Bacterial endocarditis
Systemic Bleeding disorder: primary (quantitative or qualitative platelet defects) or secondary hemostatic (factor deficiencies, anticoagulant rodenticide toxicity, DIC) abnormalities Trauma: pulmonary contusion, tracheal rupture, FB Iatrogenic: endotracheal intubation; complication of lung biopsy/aspirate, transtracheal wash, or bronchoscopy DIC, Disseminated intravascular coagulopathy; FB, foreign body; SCC, squamous cell carcinoma.
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Hematuria Causes Modified from Ettinger S, Feldman E: Textbook of veterinary internal medicine, ed 6, St Louis, 2005, Saunders.
Urinary Tract Origin (Kidneys, Ureters, Bladder, Urethra) Trauma Traumatic collection (e.g., catheter, cystocentesis) Renal biopsy Blunt trauma (e.g., automobile accident) Urolithiasis Neoplasia Inflammatory disease Urinary tract infection Feline lower urinary tract signs/disease/interstitial cystitis Chemically-induced inflammation (e.g., cyclophosphamide-induced cystitis) Parasites Dioctophyma renale Capillaria plica Bleeding disorder Warfarin intoxication Disseminated intravascular coagulation Hemophilia Thrombocytopenia Renal infarction Renal pelvic hematoma Vascular malformation Renal telangiectasia (Welsh corgi) Idiopathic renal hematuria
Genital Tract Contamination (Prostate, Prepuce, Vagina) Estrus Inflammatory, neoplastic, and traumatic lesions of the genital tract
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Hematochezia Causes Modified from Tams TR: Gastrointestinal symptoms. In: Handbook of small animal gastroenterology, Philadelphia, 1996, Saunders.
Anal Disease Perianal fistulas Anal sacculitis or abscess Stricture Neoplasia (e.g., anal sac tumor) Trauma (e.g., bite wound) Perianal hernia Foreign body
Rectum and Colon Proctitis (inflammation of the rectal mucosa) Colitis Idiopathic Inflammatory bowel disease Stress Infectious Campylobacter spp. Clostridium perfringens Parvovirus Parasitism Hookworms Whipworms Coccidia Roundworms Neoplasia Rectal polyp Adenocarcinoma Lymphoma Rectal prolapse Mucosal trauma Movement of foreign material (e.g., hairballs) Iatrogenic (e.g., thermometers, enemas, fecal loops) Automobile trauma Ileocecocolic area: intussusception Bleeding disorder Constipation often can cause excessive straining which can result in formed stools with blood on the surface.
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Hematemesis Causes Modified with permission from Kirk RW, Bonagura JD, editors: Kirk's current veterinary therapy XI: small animal practice, St Louis, 1992, Saunders, p 133.
Bleeding Disorders Disseminated intravascular coagulation Anticoagulant rodenticide toxicity Thrombocytopenia Congenital or acquired coagulation factor deficiencies/defects
Heavy Metal Toxicity Arsenic Lead Zinc
Infectious Disorders GI parasitism Viral gastroenteritis Bacterial gastroenteritis
Perioperative Hemorrhage Gastric dilatation/volvulus Gastrectomy Gastrostomy
Gastric/Duodenal Erosions/UlcerationsInfiltrative Disease Neoplasia Inflammatory bowel disease Phycomycosis
Metabolic Disorders Renal disease Liver disease Hypoadrenocorticism
Stress Erosions/Ulcerations Burns (Curling's ulcer) Neurologic disorders Head trauma (Cushing's ulcer) Spinal cord disorders Sepsis/septic shock Hypovolemic shock Multiple trauma
Drug AdministrationGlucocorticoids
NSAIDs
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Aspirin Indomethacin Phenylbutazone Naproxen Sulindac Deracoxib Ibuprofen Flunixin meglumine Meclofenamic acid Piroxicam
Gastric/Duodenal Foreign Bodies
Neoplasia Mast cell tumor Gastrinoma (Zollinger-Ellison syndrome) Pancreatic polypeptide–secreting tumor Basophilic leukemia
Hemorrhagic Gastroenteritis
Esophageal Disorders Esophagitis Esophageal neoplasia Esophageal foreign bodies Gl, Gastrointestinal: NSAIDs, nonsteroidal antiinflammatory drugs.
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Heartworm: Clinical Severity With permission from Fox P: Textbook of canine and feline cardiology: principles and practice, St Louis, 2000, Saunders, p 707.
Classification of Heartworm Disease Severity Based on Signs, Physical Examination, and Radiographic Findings Examination Findings
Class
Clinical Signs
Radiographic Findings
1
None to occasional cough
Normal examination
No lesions
2
Occasional cough and mild-tomoderate exercise intolerance
Increased lung sounds
Slight pulmonary arterial enlargement
Fair general condition
Circumscribed perivascular density plus mixed alveolar- interstitial lesions
3
Persistent cough, moderate to severe exercise intolerance
Increased lung sounds
Moderate-to-severe pulmonary arterial enlargement
Caval syndrome
Weight loss, cachexia
Accentuated or split S2
RV enlargement
Respiratory distress
Right apical gallop Diffuse and severe pulmonary infiltrates
Overt right heart failure
Tachypnea, dyspnea
General loss of condition
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Heartworm Disease: Complications Complications Untreated Eosinophilic granulomatosis Eosinophilic pneumonitis Right-sided congestive heart failure* Hemoglobinuria, “pigment nephropathy”
*
Hemolytic anemia* Pulmonary thromboembolism
During or Shortly After Treatment Period Acute (Surgical Removal) Anaphylaxis Hypotension Cardiac arrest Subacute (Medical Treatment) Eosinophilic pneumonitis Pain at injection site (melarsomine) Pulmonary thromboembolism (possibly massive, especially if inadequate exercise restriction) Sudden death (especially if inadequate exercise restriction) * Together, comprise the “caval syndrome” of heartworm disease
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Heartworm Dirofilaria Versus Acanthocheilonema Modified from Ettinger S, Feldman E: Textbook of veterinary internal medicine, ed 6, St Louis, 2005, Saunders.
Differentiating Characteristics of Acanthocheilonema (formerly Dipetalonema) reconditum and Dirofilaria immitis
Acanthocheilonema reconditum
Number in Blood
Motion
Usually few
Progressive Curved body
Shape
Length (Modified Knott Test) 263 µm (250-288 µm)
Blunt head Curved or “buttonhook” tail
Dirofilaria immitis
Usually many
Stationary
Straight body and tail
308 µm (295-325 µm)
Tapered head
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Heart Murmurs: Congenital Heart Defect-Associated Modified with permission from Kittleson M: Small animal cardiovascular medicine, St Louis, 1998, Mosby, p 197. PDA, Patent ductus arteriosus; VSD, ventricular septal defect.
Auscultatory Abnormalities in Dogs With Congenital Cardiac Disease Point of Maximal Intensity
Abnormality
Timing of Murmur
Quality of Murmur
Comments
Aortic regurgitation
Diastolic
Decrescendo; usually soft
Left base
May occur in association with a VSD
Atrial septal defect
Systolic
Soft
Left base
Result of relative pulmonic stenosis
Eisenmenger's Absent (a systolic syndrome (right-to-left murmur may still be shunting PDA or VSD) present in a PDA with bidirectional shunting)
—
Left axillary region for a bidirectional PDA
Split second heart sound may be present
Mitral dysplasia
Systolic
Holosystolic or pansystolic; plateau
Left apex
May radiate widely
Left-to-right shunting PDA
Continuous
Wind tunnel
Cranial to the left base
Peaks in intensity at S2
Pulmonic stenosis
Systolic
Crescendodecrescendo
Left base
Possible ejection sound
Subaortic stenosis
Systolic
Crescendodecrescendo
Left-base (occasionally right base and occasionally apex)
May radiate up into carotid arteries
Tetralogy of Fallot
Systolic
Crescendodecrescendo
Left base
Murmur may rarely be absent
Tricuspid dysplasia
Systolic
Holosystolic or pansystolic; plateau
Right apex
May be soft or absent in cats with severe disease
VSD
Systolic
Holosystolic or pansystolic; plateau
Cranial to or at right apex; left base
Second heart sound may be split
VSD and aortic regurgitation
Systolic and diastolic (to-and- fro murmur)
Pansystolic murmur Left base or cranial followed by a diastolic to right apex decrescendo murmur
May sound as if it is continuous and may be confused with a PDA murmur
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Heart Murmurs Characteristics and Clinical Signs Associated With “Innocent” Murmurs Versus Murmurs Associated With CHD Modified from Bonagura J: Kirk's current veterinary therapy XIII, St Louis, 2000, Saunders.
Innocent Murmur Grade usually TIBC) ↓ or N —
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Insulin Resistance Recognized Causes of Insulin Ineffectiveness or Insulin Resistance in Diabetic Dogs and Cats From Feldman E, Nelson R: Canine and feline endocrinology and reproduction, ed 3, St Louis, 2004, Saunders.
Caused by Insulin Therapy Inactive insulin Diluted insulin Improper administration technique Inadequate dose Somogyi effect Inadequate frequency of insulin administration Impaired insulin absorption, especially Ultralente insulin Antiinsulin antibody excess
Caused by Concurrent Disorder Diabetogenic drugs Hyperadrenocorticism Diestrus (bitch) Acromegaly (cat) Infection, especially of oral cavity and urinary tract Hypothyroidism (dog) Hyperthyroidism (cat) Renal insufficiency Liver insufficiency Cardiac insufficiency Glucagonoma (dog) Pheochromocytoma Chronic inflammation, especially pancreatitis Pancreatic exocrine insufficiency Severe obesity Hyperlipidemia Neoplasia
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Inflammatory Bowel Diseases Causes of Chronic Small Bowel Inflammation From Ettinger S, Feldman E: Textbook of veterinary internal medicine, ed 6, St Louis, 2005, Saunders.
Chronic Infection Giardia sp. Histoplasma sp. Toxoplasma sp. Mycobacteria sp. Protothecosis Pythiosis Pathogenic bacteria (Campylobacter, Salmonella spp., pathogenic Escherichia coli)
Food Allergy
Small Bowel Inflammation Associated With Other Primary Gastrointestinal Diseases Lymphoma Lymphangiectasia
Idiopathic Causes Lymphocytic-plasmacytic enteritis (LPE) Eosinophilic gastroenterocolitis (EGE) Granulomatous enteritis (same as regional enteritis?)
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Infertility, Male Based on Inability to Sire a Litter Modified from Feldman E, Nelson R: Canine and feline endocrinology and reproduction, ed 3, St Louis, 2004, Saunders.
Congenital InfertilityHormonal Hypopituitarism Hypothyroidism
Chromosomal aberration
Developmental Cryptorchidism Penis, prepuce, os penis anomaly Testicular hypoplasia Duct aplasia
Motility defect Kartagener's syndrome Retrograde ejaculation
Acquired InfertilityHormonal Hypopituitarism Hypothyroidism Hyperadrenocorticism
Metabolic Uremia Hepatic
Neoplasia Compression Hormonal secretion
Stress
Infection
Fever
Duct obstruction
Immune-mediated orchitis
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Drugs, exogenous hormone therapy
Retrograde ejaculation
Idiopathic testicular degeneration
Sexual overuse?
Psychological?
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Infertility With Preserved Libido Drugs and Exogenous Hormones That Affect Fertility in Humans and Possibly Dogs From Feldman E, Nelson R: Canine and feline endocrinology and reproduction, ed 3, St Louis, 2004, Saunders.
Chemotherapeutic Drugs Busulfan Chlorambucil Cisplatin Cyclophosphamide Methotrexate Vinblastine Vincristine
Miscellaneous Drugs Amphotericin B* Alloxan Cimetidine* Clomipramine *
Ketoconazole Spironolactone Sulfasalazine
HormonesAnabolic Steroids Methyltestosterone* *
Testosterone esters
Estrogens Estradiol 17B* *
Diethylstilbestrol KABI 1774*
Progestogens Medroxyprogesterone acetate
*
*
Megestrol acetate
*
Delmadinone acetate
Others *
Glucocorticoids
*
Tamoxifen citrate *
Gossypol
*
GnRH antagonists *
GnRH agonists
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Incontinence, Urinary Causes Modified from Ettinger S, Feldman E: Textbook of veterinary internal medicine, ed 6, St Louis, 2005, Saunders. Urethral sphincter mechanism incompetence Ectopie ureters Neurologic disorders Urge incontinence (secondary to urinary tract infection [UTI] or uroliths) Idiopathic detrusor instability Paradoxic (overflow) incontinence Ureterocele Pelvic bladder Ureterovaginal or urethrorectal fistula Patent urachus
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Incontinence, Fecal Causes From Ettinger S, Feldman E: Textbook of veterinary internal medicine, ed 6, St Louis, 2005, Saunders.
Neurologic DiseaseSacral Spinal Cord Congenital vertebral malformation Meningomyelocele Sacrococcygeal hypoplasia of Manx cats Sacral fracture Sacrococcygeal subluxation Lumbosacral instability Viral meningomyelitis Diskospondylitis Degenerative myelopathy Neoplasia
Peripheral Neuropathy Trauma Repair of perineal hernia Perineal urethrostomy Penetrating wounds Dysautonomia Hypothyroidism Diabetes mellitus
Nonneurologic DiseaseColorectal Causes Inflammatory bowel disease Neoplasia Constipation
Anorectal Causes Trauma Surgery (anal sac, perineal hernia, rectal resection) Perianal fistula Neoplasia
Miscellaneous Causes Severe diarrhea Irritable bowel syndrome Decreased mentation Old age/cognitive disfunction
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Immunodeficiency-Related Complications Organisms and Medical Problems Commonly Implicated in Immunocompromised Hosts Modified with permission from Greene C: Infectious diseases of the dog and cat, ed 2, St Louis, 1999, Saunders, p 684.
Opportunistic Organisms Viruses: feline herpesvirus, feline infectious peritonitis, feline calicivirus, canine papillomavirus, canine herpesvirus Rickettsia: Haemobartonella Bacteria: Citrobacter sp., Escherichia coli, Enterobacter, Klebsiella pneumoniae, Mycobacterium spp., Nocardia asteroides, Proteus, Pseudomonas aeruginosa, Serratia marcescens, Staphylococcus pseudintermedius Fungi: Aspergillus sp., Candida sp., Cryptococcus, Histoplasma, Mucor Protozoa: Pneumocystis carinii, Toxoplasma gondii, Cryptosporidium Metazoa: Demodex canis, Otodectes, Notoedres, Sarcoptes scabiei
Medical Problems Recurrent skin infections Recurrent mucosal infections Neonatal sepsis and mortality Reactive amyloidosis Vasculitis, arteritis, polyarthritis Recurrent bacteremia Granulomatous infections Chronic hypersensitivity reactions Autoimmune diseases Persistent intracellular rickettsial or bacterial infections Disproportional leukocytosis Persistent lymphopenia
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Immunodeficiency Syndromes: Congenital With permission from Greene C: Infectious diseases of the dog and cat, ed 3, St Louis, 2006, Saunders, p 1015–1016. In addition to the listed syndromes, bone marrow dyscrasia has been described in miniature and toy poodles and transient hypogammaglobulinemia in Samoyeds, but less is known of these disorders. AD, autosomal dominant; AR, autosomal recessive; GI, gastrointestinal; HOD, hypertrophic osteodystrophy; Ig, immunoglobulin; IL, interleukin; RAMP, resistance against mycobacterial protein; U, unknown; XR, X-linked recessive; γ, suspected.*(E.g., springer spaniel, Old English sheepdog, English setter, West Highland white terriers, pointers.)
Primary or Hereditary Immunodeficiencies Disease (Synonyms) Inheritance Breeds
Defect
Characterization
Functional/morphologic cilia abnormalities
Rhinosinusitis, bronchopneumonia with bronchiectasis, situs inversus
Dog *
Ciliary dyskinesia (immotile cilia syndrome)
AR
Many breeds
Respiratory infections
U
Irish wolfhound
Unknown, IgA defect?
Rhinitis, pneumonia
Bactericidal neutrophil U defect
Doberman pinscher
Unknown
Upper respiratory tract infections, reduced bactericidal activity, ciliary dyskinesia not excluded
Cyclic hematopoiesis (cyclic neutropenia)
AR
Gray collie
Hematopoietic growth factors
Severe neutropenia every 12-14 days, reactive amyloidosis
Leukocyte adhesion deficiency (canine granulocytopathy)
AR
Irish setter
CD11/18 deficiency, B-chain (CD18) deficiency
Severe leukocytosis, limited pus formation, lack of neutrophil adhesion
Complement component 3 (C3) deficiency
AR
Brittany spaniel
C3 deficiency
Pyogenic infections, lack of C-mediated phagocytosis in colony of dogs with neuromuscular disease
Selective cobalamin malabsorption
AR
Giant schnauzerBorder collie
Ileal cobalamin receptor defect
Weight loss, inappetence, leukopenia with hypersegmentation, megaloblastic bone marrowMethylmalonic aciduria
Increased susceptibility to avian mycobacteriosis
U
Basset hound
RAMP deficiency?
Increased susceptibility to
XR
Dachshund
Unknown
Pneumocystis carinii pneumonia Pelger-Huët anomaly
AD
Australian shepherd, foxhound, others
Unknown
Susceptibility to fungal and rickettsial infections, pyoderma
U
German shepherd
Macrophage? T cell?
No immunodeficiency, hyposegmented granulocytes
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Disease (Synonyms) Inheritance Breeds
Defect
Characterization
Severe combined immunodeficiency
XR
Basset hound, Cardigan, Welsh corgi
Common gamma chain of Severe bacterial/viral infections, IL-2 and other cytokines no IgG and IgA, deficient lymphocyte blastogenesis
Selective IgA deficiency
U
Beagle, shar-pei, German shepherd
IgA deficiency
Respiratory and GI infections
Thymic abnormalities and dwarfism
U
Weimaraner
Unknown
Reduced growth (thymosin responsive)
Recurrent infections
U
Weimaraner
Reduced IgG
Pyoderma, severe abscess formation, bleeding tendency (HOD)
Combined immunodeficiency
U
Shar-pei
T cell, B cell, low IL-6 and IL-2
Skin, respiratory, and GI infections
Amyloidosis
U
Shar-pei
Elevated IL-6
Arthritis, amyloidosis, renal failure, hepatic rupture, hypoproteinemia
Lethal acrodermatitis
AR
Bull terrier
Zinc metabolism defect
Zinc deficiency, hyperkeratosis
Increased susceptibility to parvoviral infection
U
Rottweiler, Doberman
Unknown
Vaccine-exacerbated immunity
U
Akita
Unknown
Variable meningitis, polyarthritis
Hypotrichosis, congenital and thymic aplasia
AR
Birman
Unknown
Nude kittens, neonatal death, no thymus
Thymic and lymphoid atrophy
U
Ragdoll
Unknown
Neonatal death or fatal infections at weaning, lack of lymph nodes and thymus
Leukocyte granulation U
Birman
Unknown
No immunodeficiency, acidophilic granules
Pelger-Huët anomaly
AD
Domestic shorthair
Unknown
No immunodeficiency, hyposegmented granulocytes
Chédiak-Higashi syndrome
AR
Persian
Unknown
No immunodeficiency, large granules in phagocytes, bleeding tendency
Reactive AA amyloidosis
U
Abyssinian, Siamese, Oriental shorthair
Unknown
Reactive AA amyloidosis, renal or hepatic failure
Cat
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Immunodeficiency Syndromes: Acquired Common Acquired Causes of Compromised Immune Sy stem Function From Bonagura J: Kirk's current veterinary therapy XIII, St Louis, 2000, Saunders.
Drugs Antineoplastics Corticosteroids Other immunosuppressive agents (e.g., azathioprine, gold salts)
Malnutrition Intestinal parasitism Inflammatory bowel disease Protein-calorie deficiency Obesity
Infections Viral infection (FeLV, FIV, FIP, CDV, parvovirus) Ehrlichia canis
Endocrine Disease Hyperadrenocorticism Diabetes mellitus
Neoplasia
Miscellaneous Neonatal colostrum deprivation CDV, Canine distemper virus; FeLV, feline leukemia virus; FIP, feline infectious peritonitis; FIV, feline immunodeficiency virus.
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Ileus Causes From Ettinger S, Feldman E: Textbook of veterinary internal medicine, ed 6, St Louis, 2005, Saunders.
Physical Intestinal obstruction Overdistention by aerophagia
Neuromuscular Anticholinergic drugs Dysautonomia Spinal cord injury Visceral myopathies
Metabolic Hypokalemia Uremia Endotoxemia
Functional Abdominal surgery Ischemia Inflammatory causes Peritonitis Pancreatitis Parvovirus
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Icterus Modified from Ettinger S, Feldman E: Textbook of veterinary internal medicine, ed 4, St Louis, 1994, Saunders. DIC, Disseminated intravascular coagulation; FeLV, feline leukemia virus; FIP, feline infectious peritonitis; ICH, infectious canine hepatitis; SLE, systemic lupus erythematosus.
Differential Diagnosis of Icterus Prehepatic or Hemolytic Icterus
Extrahepatic Icterus
Hepatic Icterus
Hemolytic Anemias
Bile Duct Occlusion
Miscellaneous Disorders
Erythrocyte parasitemia:
Cholecystitis
Endotoxemia/sepsis
Babesia
Cholangitis
Shock
Anoxia → cholestasis
Mycoplasma haemofelis Secondary peribiliary disease
Chronic passive congestion
DIC
Incompatible blood transfusion
Congenital malformations
Hyperthyroidism (cat, rare)
Neonatal isoerythrolysis
Choledochal cysts
Microangiopathic hemolytic Multiple biliary cysts (cat) anemia
Intrahepatic Cholestasis
DIC
Intraluminal bile duct occlusion Infectious
Vasculitis
Inspissated bile syndrome (cat)
Neoplasia:
Dirofilariasis
Cholelithiasis
Mechanical infiltrativesinusoids, peribiliary
Vascular neoplasia (hemangiosarcoma)
Trauma → blood clots
Congenital erythrocyte defects
Neoplasia:
Paraneoplastic effects
Pyruvate kinase deficiency (basenji dog)
Primary and secondary biliary involvement
Viral (FIP, ICH, parvovirus)
Phosphofructokinase deficiency
Hemolytic disease → cholestasis
Bacterial (leptospirosis, septicemia)
Hereditary stomatocytosis (malamute)
Pancreatic disease
Mycotic
Immune-mediated hemolytic anemia
Parasitic infection (flukes)
Drug associated:
SLE
Ruptured biliary tract (bile duct or gallbladder)
Methyltestosterone Impeded androgens (danazol)
Carprofen
Idiopathic
Trauma
Sulfa antibiotics
Mebendazole
Drug associated
Cholelithiasis
Thiacetarsemide
Infectious:
Cholangitis/cholecystitis
Anticonvulsants (phenytoin, primidone, phenobarbital)
FeLV
Iatrogenic: hepatic biopsy
Infectious disease associated
Diltiazem (sustainedrelease formulation)
Acetaminophen
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Prehepatic or Hemolytic Icterus
Extrahepatic Icterus
Hepatic Icterus
Ehrlichia
Specific hepatic disorders:
Dirofilariasis
Cholangitis
Leptospirosis
Cirrhosis
Septicemia
Chronic idiopathic hepatitis of dogs
Lobular dissecting hepatitis
Onion toxicity, zinc toxicity
Hepatic lipidosis (cat)
Breed-specific disorder:
Benzocaine (cat), methionine
Idiopathic lipidosis secondary to other disorders
Bedlington terrier
Vitamin K1, acetaminophen
Diabetes mellitus
Doberman pinscher
Phenazopyridine
Hepatic necrosis: many causes
West Highland white terriers
Propylene glycol
Infiltrative disease (neoplasia, amyloid, infectious agents)
Heinz body anemia
Cholangiohepatitis syndrome (cat)
Cetacaine (cat), methylene blue
Increased Hemoprotein Liberation
Cocker spaniels
Body cavity hemorrhage
Severe steroid hepatopathy (dogs only)
Large hematoma formation and absorption Ineffective erythropoiesis Congenital porphyria (cat, rare)
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Joint Effusion From Willard M, Tvedten H: Small animal clinical diagnosis by laboratory methods, ed 4, St Louis, 2004, Saunders. LE, Lupus erythematosus; RBC, red blood cell; WBC, white blood cell.
Analysis of Joint Effusions NONINFLAMMATORY INFLAMMATORY JOINT DISEASE JOINT DISEASE Degenerative Joint Disease
Neoplastic Joint Involvement
Hemarthrosis
Infectious Inflammation
Noninfectious Inflammation NORMAL
Color
Light yellow
Light yellow, blood-tinged
Bloody, xanthochromic
Variable: yellow, bloodtinged, bloody
Variable: yellow, bloodtinged
Turbidity
Clear, slightly turbid
Mild to moderate turbidity
Turbid
Turbid to purulent
Variable: slight Clear to moderate turbidity
Viscosity
Normal
Normal to reduced
Reduced
Reduced
Reduced
Viscous
Mucin clot test
Normal firm
Normal firm
Normal to slightly friable
Friable
Friable
Firm
Few to moderate
Rare
Strawcolored
Cytologic Analysis RBC
Few
Few to many
Many, Moderate erythrophagocytosis
WBC/µL
5%-10% body weight, anorexia >2-3 days' duration, early satiety
Any tumors
Syndrome of inappropriate antidiuretic hormone secretion
Hyponatremia, polyuria and polydipsia, edema
Pulmonary carcinoma (dog)
Fever
Persistent pyrexia >39.7°C (103°F) without infection
Lymphoproliferative and myeloproliferative neoplasms; mast cell, hepatic, and brain tumors
Polycythemia
Exercise intolerance, seizures, red mucous membranes, packed cell volume >60
Renal tumors, lymphoma, polycythemia vera, hepatic tumors
Hypertrophic osteopathy
Painful, hard, swollen distal limbs, reluctance to walk
Primary lung tumors, rhabdomyosarcoma (bladder), esophageal sarcomas, pulmonary metastasis, carcinoma, renal carcinomas, hepatic adenocarcinoma, renal papillary adenoma (cat), Sertoli cell tumor, transitional cell carcinoma of bladder, adrenocortical carcinoma
Dermatologic disorders Nodular dermatofibrosis, erythema, flushing, necrolytic migratory erythema
Renal cystadenocarcinoma, mast cell tumor, pheochromocytoma, pancreatic adenocarcinoma
Renal disorders
Many tumors, including lymphoma, plasma cell tumors, mast cell tumors
Amyloid deposition, glomerulonephritis, concentrating defects, proteinuria, nephrotic syndrome
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Paraneoplastic Disorder
Clinical Features
Central nervous system Tissue hypoxia with or without dysfunction thromboembolism, due to hyperviscosity syndrome (seizures, dementia)
Associated Neoplasms in Companion Animals Lymphoma, plasma cell tumors
Peripheral nervous system disorders: Neuromuscular junction
Myasthenia gravis (weakness with exercise that improves with rest)
Thymoma, hepatocellular carcinoma, osteosarcoma, mammary adenocarcinoma, pheochromocytoma, pulmonary adenocarcinoma
Neuropathy
Weakness, cranial nerve abnormalities
Lymphoma, bronchogenic carcinoma, insulinoma, leiomyosarcoma, hemangiosarcoma, and undifferentiated sarcomas
Neuromyopathy
Weakness, muscle pain, proprioception deficits
Pulmonary carcinoma
Myopathy
Myositis
Thymoma
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Panting Causes Modified with permission from King L: Textbook of respiratory disease in dogs and cats, St Louis, 2004, Saunders, p 47. Elevated ambient temperature Overweight/obesity Fever, hyperthermia Anxiety, nervousness Pain Hyperadrenocorticism Glucocorticosteroid therapy Pheochromocytoma Hyperthyroidism Hypocalcemia Narcotic administration Cardiac disease/tachyarrhythmias Brain disease
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Retinopathies Common Sy stemic Disorders Affecting the Retina Modified from Slatter D: Fundamentals of veterinary ophthalmology, St Louis, 2001, Saunders.
Dog Blastomycosis Coccidioidomycosis Cryptococcosis Distemper Ehrlichiosis Rocky Mountain spotted fever Histoplasmosis Systemic hypertension Larva migrans (Toxocara spp.) Leishmaniasis Lymphoma Multiple myeloma Toxoplasmosis Uveodermatologic syndrome
Cat Blastomycosis Cryptococcosis FIP Histoplasmosis Multiple myeloma Systemic hypertension Lymphoma (both FeLV positive and negative) Toxoplasmosis Tuberculosis FeLV, Feline leukemia virus; FIP, feline infectious peritonitis.
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Respiratory Parasites Parasite (Host)
Comment
Aelurostrongylus abstrusus (cats)
Coughing, sneezing, lethargy possible but usually no signs
Capillaria aerophila (dogs, cats)
Chronic cough or no clinical signs
Crenosoma vulpis (wild canids; rarely dogs) Chronic cough clinically mimicking chronic sterile bronchitis Eucoleus boehmi (dogs, cats)
Chronic sneezing, nasal discharge, facial rubbing
Filaroides hirthi (dogs only)
Breeding kennels; zinc sulfate flotation is best (not Baermann)
Oslerus osleri (wild canids; rarely dogs)
Nodules in large airway mucosa; treatment difficult
Paragonimus kellicotti (dogs, cats)
Chronic cough ± pneumothorax; rust-colored pharyngeal phlegm
Pneumonyssoides caninum (dogs)
Nasal mite; sensitive to parenteral (and presumably oral) ivermectin
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Renal Failure, Acute Causes of Intrinsic Acute Renal Failure From Ettinger S, Feldman E: Textbook of veterinary internal medicine, ed 6, St Louis, 2005, Saunders.
Renal Ischemia Progression of prerenal azotemia Renal vascular disease (avulsion, thrombosis, stenosis)
Nephrotoxicosis Exogenous toxins Endogenous toxins Drugs
Primary Renal Diseases Infections: pyelonephritis, leptospirosis, infectious canine hepatitis Immune-mediated disease: acute glomerulonephritis, SLE, renal transplant rejection Neoplasia: lymphoma Miscellaneous: “Alabama rot”
Systemic Diseases With Renal Manifestations Infections: FIP, borreliosis, babesiosis, leishmaniasis, bacterial endocarditis Pancreatitis SIRS, sepsis, multiple organ failure, DIC Heart failure SLE Hepatorenal syndrome Malignant hypertension Hyperviscosity syndrome: polycythemia, multiple myeloma DIC, Disseminated intravascular coagulopathy; FIP, feline infectious peritonitis; SIRS, systemic inflammatory response syndrome; SLE, systemic lupus erythematosus.
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Renal Failure, Acute Versus Chronic From Bonagura J: Kirk's current veterinary therapy XIII, St Louis, 2000, Saunders. ARF, Acute renal failure; CKD, chronic kidney disease; PCV, packed cell volume; PU/PD, polyuria and polydipsia.*The clinician should be aware that there are many caveats to using these aids.
Diagnostic Aids for the Differentiation of Acute Renal Failure and Chronic Kidney Disease
*
Acute Renal Failure
Chronic Renal Failure
Caveats
History
Ischemic episode, toxicant exposure, nephrotoxic drug use, acute illness
Long-standing signs of weight loss, PU/PD, nocturia, vomiting, diarrhea; prior episodes of illness; prior renal disease/insufficiency
Animals with ARF developing secondary to another disease may have long-standing signs; urine output does not differentiate ARF from CKD.
Body condition
Good
Poor
Some animals with ARF have a poor body condition from another disease process; some animals with CKD look fine.
Kidneys
Normal to large, smooth contour, may be painful
Small, irregular contour
Some chronic renal diseases cause renal enlargement.
Osteodystrophy
Absent
Sometimes present
PCV
Normal to increased
Decreased (nonregenerative)
Animals with ARF may have nonregenerative anemia.
Urine sediment
May be active
Often inactive
Many animals with ARF have inactive urine sediments.
Serum creatinine
Recently within reference range
Previously increased
Previous prerenal and postrenal factors could also have caused increase.
Serum potassium Normal to increased
Normal to decreased
Metabolic acidosis
More severe
Less severe
Urine output is a major determinant of serum potassium concentration.
Histopathologic features
Acute tubular necrosis, acute inflammation
Interstitial fibrosis, glomerulosclerosis, chronic inflammation
Carbamylated hemoglobin
Normal to mild increase
Increased
Chronic renal lesions can be an incidental finding.
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Regurgitation Causes From Ettinger S, Feldman E: Textbook of veterinary internal medicine, ed 6, St Louis, 2005, Saunders. AChE, Acetylcholinesterase; SLE, systemic lupus erythematosus.
Esophageal Disease Megaesophagus (primary or secondary) Esophagitis Mechanical obstruction (foreign body, stricture, vascular ring anomaly)
Alimentary Disorders Pyloric outflow obstruction Gastric dilatation/volvulus Hiatal hernia
Neuropathies Peripheral (polyradiculitis, giant-cell axonal neuropathy, polyneuritis, lead poisoning) Central (distemper, brainstem lesion, neoplasia, trauma)
Neuromuscular Junction Abnormalities Myasthenia gravis (focal or generalized) Botulism Tetanus AChE toxicity
Immune-Mediated Causes SLE Polymyositis Dermatomyositis
Endocrine Hypothyroidism Hypoadrenocorticism
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Red Eye: Differential Diagnosis With permission from Lavignette AM: Differential diagnosis and treatment of anterior uveitis. Vet Clin North Am 3:504, 1973. Modified from Slatter D: Fundamentals of veterinary ophthalmology, St Louis, 2001, Saunders. Note: These disorders often do not exist in isolation, and features of two or more disorders may be present simultaneously, may negate each other, or may be additive.
Parameter
Anterior Uveitis
Conjunctivitis
Superficial Keratitis
Glaucoma
Conjunctiva
Not thickened, vessels easily seen
Thick, folded, and hyperemic, vessels concealed
Not thickened
Not thickened
Conjunctival vessels
Circumcorneal and straight, not movable with conjunctiva
Superficial, diffuse, and tortuous
Diffuse, vessels form fine network in vicinity of cornea
Diffuse, superficial and prominent
Secretion or discharge
None
Moderate to copious
Serous to purulent
None
Pain
Moderate
Severe
Moderate to severe
Severe to acute
Photophobia
Moderate
None
Severe
Slight
Cornea
Clear to steamy
Clear
Clouded to opaque
Steamy
Pupil size
Small, sluggish, irregular, or fixed
Normal
Normal
Dilated, moderate to complete, and fixed
Pupillary light reflex
Poor
Normal
Normal
Absent
Intraocular pressure
Variable; typically low/diminished acutely
Normal
Normal
Elevated
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Systemic Inflammatory Response and Multiple Organ Dysfunction With permission from Fox P: Textbook of canine and feline cardiology: principles and practice, St Louis, 2000, Saunders, p 275. MODS, Multiple organ dysfunction syndrome; SIRS, systemic inflammatory response syndrome; Y, yes, usually present; +, possibly present; +/++/+++, mild, moderate, severe.
Clinical Manifestations of SIRS and MODS SIRS
MODS
Anorexia
+/++
++/+++
Lethargy
+/++
++/+++
Historic Abnormalities
Diarrhea (hemorrhagic)
+
Physical Examination Mental depression
+/++
Fever
Y
Hypothermia Vasodilation (red mucous membranes, accelerated capillary refill time)
Y Y
Vasoconstriction (pale mucous membranes, prolonged capillary refill time) Heart murmur
+++
Y Y
+
Arterial pulse quality: “Bounding”
Y
Normal or decreased
Y
Tachycardia, arrhythmias
+
Y
Tachypnea, hyperventilation
Y
Y
Petechiae or bleeding
+
+/Y
Clinical Pathologic Findings Hyperglycemia
+/Y
Hypoglycemia Leukocytosis (possibly following transient leukopenia; left shift, mild toxic changes)
+/Y Y
Leukopenia or rapid decrease in leukocytes, with marked left shift, toxic neutrophils
Y
Coagulation parameters: Normal to hyperactive
Y
Hypoactive
Y
Increased liver enzymes (particularly alkaline phosphatase)
Y
Hyperbilirubinemia
+/Y
Hypoalbuminemia
+/Y
+/Y
Azotemia
+/++
+/++/+++
Acidosis (lactic/metabolic)
+
+/++
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SIRS
MODS
Hemodynamic Changes Cardiac output: Normal to high
Y
Low
Y
Arterial blood pressure; central venous pressure: Normal
+/++
+
Low
+/++/+++ +/++
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Syncope Differential Diagnoses for Syncope and Episodic Weakness From Fox P: Textbook of canine and feline cardiology: principles and practice, St Louis, 2000, Saunders, 447.
Primary Cardiac Causes Arrhythmias Obstruction to cardiac filling Obstruction of ventricular ejection
Hypotension Inadequate cardiac output (e.g., dilated cardiomyopathy) Inadequate vascular tone (e.g., vasodilators, b-blockers) Inadequate blood volume: Blood loss: Internal (e.g., splenic hemangiosarcoma, GI blood loss) External (e.g., trauma) Diuresis (e.g., furosemide) Hypoadrenocorticism Fluid loss (e.g., emesis, diarrhea)
Hypoxemia Respiratory failure Pulmonary thromboembolism
Abnormalities of Blood Constituents Hypoglycemia Hypokalemia Anemia Hepatoencephalopathy
Neurologic and Neuromuscular Disorders Epilepsy Structural CNS disorders: Neoplasia Cerebral arterial disease Thromboembolism Narcolepsy Myasthenia gravis
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Syncope, Disease Associations With permission from Fox P: Textbook of canine and feline cardiology: principles and practice, St Louis, 2000, Saunders, p 451.
Cardiovascular Causes of Syncope and Breed Predispositions Causes of Syncope
Breed Predispositions
Structural Heart Diseases Dilated cardiomyopathy
Doberman pinscher, boxer, cocker spaniel, giant-breed dogs
Chronic valvular disease
Small-breed dogs (middle-aged to geriatric)
Pulmonic stenosis
English bulldog, Samoyed, beagle, Chihuahua, cocker spaniel, others
Subaortic stenosis
Newfoundland, boxer, golden retriever, German shepherd, others
Right-to-left shunting congenital defects
English bulldog
Hypertrophic cardiomyopathy
Cats (Maine coon, Ragdoll, Sphynx, Himalayan)
Pericardial effusion Intracardiac mass lesions (neoplasia; thrombus)
German shepherd, golden retriever, others
Cardiac Arrhythmias Sick sinus syndrome
Miniature schnauzer, dachshund, West Highland white terrier, cocker spaniel
Advanced AV block
German shepherd, dachshund, pug, Doberman pinscher
Asystole Sinus bradycardia Supraventricular tachycardia
Labrador retriever
Ventricular tachycardia
German shepherd, boxer, Doberman pinscher, cocker spaniel
Cor Pulmonale Pulmonary embolism Pulmonary hypertension Heartworm disease Tussive “Cough Drop” Syncope
Small-breed dogs with combined cardiopulmonary disease
Vasovagal Syncope
Boxer, brachycephalic breeds?
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Stunted Growth Potential Causes of Small Stature in Dogs and Cats From Feldman E, Nelson R: Canine and feline endocrinology and reproduction, ed 3, St Louis, 2004, Saunders.
Endocrine Hyposomatotropism Hypothyroidism Hyperadrenocorticism Hypoadrenocorticism Diabetes mellitus
Nonendocrine Malnutrition Gastrointestinal: Maldigestion Pancreatic exocrine insufficiency Malabsorption Heavy intestinal parasitism Hepatic: Portosystemic vascular shunt Glycogen storage disease Renal disease Cardiovascular disease (especially congenital heart defects) Skeletal dysplasia; chondrodystrophy Mucopolysaccharidosis Hydrocephalus
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Storage Disorders From Ettinger S, Feldman E: Textbook of veterinary internal medicine, ed 5, St Louis, 2000, Saunders. CNS, Central nervous system; DSH, domestic shorthair; PNS, peripheral nervous system.
Lysosomal Storage Disorders Species/Breed
Age of Onset
Duration
Signs/Pathologic Examination
Neuronal Disorders GM1 Gangliosidosis (Betagalactosidase Deficiency) Feline
4-6 months
6-10 months
Ataxia, tremors, paresis, visual loss, seizures, behavioral changes; corneal and retinal lesions; CNS, liver, pancreatic acinar cells involved
2-4 months
4-6 months
Visual signs, tremors, dysmetria, paresis, behavioral changes; CNS, liver, kidney, spleen, lymph nodes
Siamese, Korat, mixed breeds Canine Beagle/mixed Canine German shorthaired pointers Feline
6 months 18 months
Behavioral changes, seizures, ataxia, weakness, visual signs, coma; CNS
4-10 weeks
Tremors, dysmetria, ataxia, paresis; dwarfism, corneal opacity; CNS, liver, endothelium, bone marrow, spleen, kidney
DSH Sphingomyelin Lipidosis (Sphingomyelinase Deficiency) Feline
3-6 months
3-6 months
Siamese, DSH
Stunted growth, ataxia, dysmetria, tremors; CNS, liver, lung, spleen, lymph nodes, kidney, bone marrow, adrenal gland
Sphingomyelin in Lipidosis (Glucocerebrosidase Deficiency) Canine
7 months 1 month
CNS, liver
Sidney silkie Mannosidosis (α-Mannosidase Deficiency) Neuronal Ceroid Lipofuscinosis Canine
14-18 months
8-12 months
Visual, mental, behavioral changes, cerebellar signs, seizures; CNS, lymph nodes, salivary gland, prostate, kidney
11-30 weeks
2-3 months
Tremor, dysmetria, paresis, muscle atrophy, visual changes, mental changes
English setters Leukodystrophies: Globoid Cell Canine Cairn and West Highland white terriers, beagles, blue tick hound, poodles Feline
CNS, PNS
Metachromatic Leukodystrophy: Cavitating leukodystrophy Canine Dalmatians
3-6 months
Decreased vision, ataxia, paresis
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Stomatitis Modified from Slatter D: Textbook of small animal surgery, ed 3, Philadelphia, 2003, Saunders. FeLV, Feline leukemia virus; FIV, feline immunodeficiency virus.
Causes of Stomatitis Conditions associated with immune system depression or dysfunction
Necrotizing ulcerative gingivostomatitis Mycotic infections (commonly candidiasis) Neutrophil dysfunction, gray collie syndrome, drug therapy, viral infection (e.g., FeLV)
Autoimmune disorders
Vesiculobullous skin diseases (e.g., pemphigus and pemphigoid) Systemic or discoid lupus erythematosus Sjögren-like syndrome
Hypersensitivity
Drug eruptions Insect stings
Viral infections
FeLV FIV Calicivirus
Miscellaneous conditions
Eosinophilic granuloma complex Feline chronic gingivostomatitis
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Splenomegaly Causes of Splenomegaly Modified from Bonagura J: Kirk's current veterinary therapy XIII, St Louis, 2000, Saunders.
Generalized SplenomegalyInflammation Infectious Granulomatous condition
Neoplasia Primary: Lymphoma Mastocytosis Histiocytosis Leukemias (acute, chronic) Metastatic
Hyperplasia Extramedullary hematopoiesis
Amyloidosis
Congestion Pharmacologic: Phenothiazine tranquilizer Barbiturates Torsion of splenic pedicle: Isolated With gastric dilatation/ volvulus Portal vein/caudal vena cava hypertension: Vascular anomaly Congestive heart failure Hepatic cirrhosis Neoplasia
Localized SplenomegalyNeoplasia Hemangiosarcoma Hemangioma Lymphoma Leiomyosarcoma Fibrosarcoma Osteosarcoma
Other Hematoma Nodular hyperplasia Abscess
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Splenic Diseases: Infectious Infectious Causes of Splenomegaly/Splenitis
*
*Infectious disease may affect the spleen directly or indirectly cause splenomegaly by causing chronic anemia, chronic antigen stimulation, or disturbances in blood flow (e.g., endotoxemia). From Ettinger S, Feldman E: Textbook of veterinary internal medicine, ed 6, St Louis, 2005, Saunders.
Viral Diseases FIP (C) FeLV (C) FIV (C) Infectious canine hepatitis (D)
Rickettsial and Mycoplasmal Diseases Ehrlichiosis (canine and feline) RMSF (Rickettsia rickettsii) Q fever (Coxiella burnetii) Hemotropic mycoplasmosis (Mycoplasma haemofelis)
Bacterial Infections Canine brucellosis Mycoplasmosis Florida borreliosis Plague Tularemia Streptococcosis Staphylococcosis Salmonellosis Francisella infection Endotoxemia
Fungal Diseases Cryptococcosis Histoplasmosis Blastomycosis
Protozoal Diseases Toxoplasmosis Cytauxzoonosis (C) Babesiosis (Babesia canis and B. gibsoni) Leishmaniasis (D) C, Cats; D, dogs; FeLV, feline leukemia virus; FIP, feline infectious peritonitis; FIV, feline immunodeficiency virus; RMSF, Rocky Mountain spotted fever.
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Shock With permission from Fox P: Textbook of canine and feline cardiology: principles and practice, St Louis, 2000, Saunders, p 273.
Clinical Classification of Shock: Mechanism or Primary Cause Shock Classification Primary Mechanism
Examples
Cardiogenic
Dilated cardiomyopathy
Poor ventricular contractility
Toxins/drugs Myocardial infarction Pericardial effusion/cardiac tamponade Distributive
Vasomotor dysfunction
Arteriovenous shunting Hypotension (expanded venous capacitance) High or normal resistance Hypodynamic late septic shock
Hypoxemic
Lack of oxygen
Anemia Hypoxemia
Metabolic
Inability to utilize energy substrates
Sepsis Cyanide poisoning Heatstroke Hypoglycemia
Obstructive
Inadequate cardiac preload
Pericardial tamponade Restrictive pericarditis Intracardiac masses
Hypovolemic
Inadequate circulating blood volume Dehydration (any cause) Hypoproteinemia Blood loss
Septic
Bacteremia
Sepsis
Endotoxemia
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Serotonin Syndrome–Inducing Agents From Crowell-Davis SL, Poggiagliolmi S: Understanding behavior: serotonin syndrome. Compend Contin Educ Vet 30:490–493, 2008 and Mohammad-Zadeh LF, Moses L, Gwaltney-Brant SM: Serotonin: a review. J Vet Pharmacol Ther 31:187–199, 2008.
Substances That Potentially May Cause Serotonin Syndrome Agent
General Comments for Each Category of Agent Foods or supplements: L-5-HTP, L-tryptophan, Griffonia seed extract Aged cheese, chicken liver
L-5-HTP is an OTC supplement used in humans for depression, insomnia; serotonin syndrome (SS) reported as a result of accidental ingestion in dogs. Tyramine present in certain foods can interfere with MAO inhibitors' action and enhance their toxicity.
Medications that increase presynaptic release of serotonin: Amphetamine Methylphenidate Ecstasy (MDMA; 3,4 methylenedioxymethamphetamine) Bromocriptine l-dopa
In addition to CNS excitation from amphetamine, signs of confusion, disorientation, hallucination, and rigidity may be due to SS. Cyproheptadine, 1.1 mg/kg for dogs and 2-4 mg/cat PO or per rectum q 6-8 h, can be used for treating signs of SS; discontinue after 2-3 treatments if no relief. Chlorpromazine and other phenothiazines possess some antiserotonin effects.
Presynaptic reuptake inhibitors, selective serotonin reuptake inhibitors (SSRIs), and tricyclic antidepressants: Fluoxetine Bupropion Duloxetine Fentanyl Pethidine Paroxetine Sertraline Citalopram Fluvoxamine Amitriptyline Clomipramine (Clomicalm) Tramadol Chlorpheniramine Venlafaxine Dextromethorphan Meperidine
SS is a clinical entity characterized by presence of some GI signs, CNS signs (hyperreflexia, tremors, rigidity, confusion, agitation, excitation, seizures), and mydriasis, tachycardia, hyperthermia. SS can be seen with acute large overdose or with repeated therapeutic treatment. Cyproheptadine, 1.1 mg/kg for dogs and 2-4 mg/cat PO or per rectum q 6-8 h, can be used for treating signs of SS; discontinue after 2-3 treatments if no relief. Chlorpromazine and other phenothiazines possess some antiserotonin effects.
Serotonin metabolism inhibitors: Selegiline (MAO-B inhibitor; Anipryl) Amitraz
Selegiline recommended for use in dogs for cognitive dysfunction Interaction likely when selegiline used concurrently with tricyclic antidepressants, amitraz, meperidine, and SSRIs
Serotonin agonists at postsynaptic membrane: Buspirone Lithium LSD (lysergic acid diethylamide)
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Seizures: Characteristics and Differentiation Modified from Ettinger SJ, Feldman EC: Textbook of veterinary internal medicine, ed 6, St Louis, 2005, Saunders, p 27. Convulsive syncope (anoxic or anoxic-epileptic seizures) are syncopal events generally caused by cardiac arrhythmias that produce profound syncope, temporary cerebral hypoxia, and seizures. Therefore, clarification of the type of event observed by the owner (syncope versus seizure) may be difficult and generally rests on the observation of an episode, the presence of heart disease, and the documentation of a severe bradycardia or tachycardia during the event. Videotaping of an episode by the owner and cardiac event monitoring (pager-size portable electrocardiographic [ECG] unit that is triggered by the owner when an event occurs) can be invaluable in clarifying whether an animal is experiencing seizures versus syncope.
Seizures, Differentiation from Other Events Seizure (Grand Mal) Precipitating Usually none event
Seizure (Partial) Usually none
Episodic Weakness
Narcolepsy/Cataplexy
Exertion, pain, micturition, defecation, cough, stressful event
Exertion or none
Excitement, feeding
Seconds; acute weakness, staggering, vocalization, autonomic stimulation
None (disorder is neuromuscular)
None
None
None
None
Syncope
Prodrome
Minutes to days; atypical behavior (e.g., anxious, more withdrawn, attention-seeking) ± vomiting
Aura
None
Event features
Chomping, Localized hypersalivation, signs tonic-clonic limb motion; duration often 1-2 minutes; duration > 5 minutes is consistent with seizure and highly inconsistent with syncope
Motionlessness; flaccid or rigid extension of limbs; opisthotonos possible; no tonicclonic activity; duration generally transient (3 months of age have high titers of naturally occurring type A antibodies that act as strong hemagglutinins and hemolysins. Type A or AB kittens born to type B queens are at risk of developing neonatal isoerythrolysis. Generally higher incidence of type B blood: British shorthair, Devon Rex, Cornish Rex breeds, DSH and DLH on U.S. west coast, Europe, Japan, and Australia (see p. 1379).
SPECIMEN AND PROCESSING CONSIDERATIONS SPECIMEN EDTA whole blood (lavender-top tube) Typing cards are species specific. Dog blood typing cards can be used for determining DEA 1.1 antigen status, and cards for cats can be used for determining type A, B, or AB. Marked anemia, marked hemolysis, or autoagglutination can interfere with results. RELATIVE COST: $$$
PEARLS Dogs: blood groups that have the most clinical relevance are DEA 1.1 and DEA 1.2, also called Al and A2. Because DEA 1.1 is the most antigenic, DEA 1.1-negative dogs are recommended as donors for patients with unknown blood types. Cats: because of the widespread prevalence of naturally occurring erythrocyte antigens, blood from blood donor cats and the recipient cat should be typed, and a cross-match performed (see p. 1234) prior to any blood transfusion. Blood types should be compatible (acceptable: A into A; B into B; A, B, or AB into AB) and the cross-match should not show incompatibility. AUTHOR: DEBORAH G. DAVIS
Pricing Information $: $150
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Blood pH DEFINITION +
Measure of the hydrogen ion (H ) concentration (acidity) of the blood
TYPICAL NORMAL RANGE Dogs, 7.31-7.42; cats, 7.24-7.40
PHYSIOLOGY Blood pH is inversely related to H+ concentration; increased [H+ ] = decreased pH. Hydrogen ions are continuously produced by metabolic processes and excreted via the kidneys or bound to buffers.
CLINICAL APPLICATIONS CAUSES OF ABNORMALLY HIGH LEVELS: Increased pH indicates alkalosis, either respiratory (decreased Pco2) or metabolic (increased bicarbonate). Metabolic causes: vomiting, diuretics, overadministration of bicarbonate. Respiratory alkalosis is caused by hyperventilation due to pulmonary disease, direct stimulation of central nervous system (pain, anxiety), septicemia. NEXT DIAGNOSTIC STEP TO CONSIDER IF LEVELS HIGH: Respiratory: thoracic radiography/ultrasound, evaluate mentation and respiratory rate and depth, blood cultures. Metabolic: evaluate for vomiting, review treatment history. CAUSES OF ABNORMALLY LOW LEVELS: Decreased pH indicates acidosis, either metabolic (low bicarbonate) or respiratory (increased Pco2). Metabolic causes: bicarbonate loss (and/or production of endogenous acids) due to diarrhea, lactic acidosis, ketoacidosis, uremia, ingestion of exogenous toxins (ethylene glycol). Respiratory causes: pulmonary parenchymal disease, pulmonary restrictive disease (pleural effusion, pneumothorax, diaphragmatic hernia), central nervous system depression (anesthesia, narcotics, brainstem disease), airway obstruction. NEXT DIAGNOSTIC STEP TO CONSIDER IF LEVELS LOW: Consider serial blood lactate measurements to monitor progression if clinically indicated. Metabolic: calculate anion gap to determine if due to loss of bicarbonate (anion gap normal) or accumulation of organic acid (high anion gap). Evaluate serum biochemistry profile and urinalysis for renal disease, diabetes mellitus, and other systemic causes. Respiratory: ensure patent airway, thoracic radiography/ultrasound, evaluate mentation.
SPECIMEN AND PROCESSING CONSIDERATIONS DRUG EFFECTS ON LEVELS: Decrease: sedative, narcotic, general anesthetics causing respiratory depression. Increase: bicarbonate or diuretic administration. LAB ARTIFACTS THAT MAY INTERFERE: Decrease: delayed analysis of sample, excessive heparin in syringe. Increase: sample exposure to room air. SPECIMEN: Whole blood collected and maintained in heparinized syringe, 0.05-0.1 mL of heparin/mL blood. Cap syringe end to limit exposure to room air. Specimens analyzed within 15 minutes of collections are preferred. Storage in a capped syringe on ice at 4°C for up to 2 hours is acceptable. RELATIVE COST: $$ (reported as part of blood gas analysis)
PEARLS Disturbances of pH can be life threatening. Periodic monitoring during prolonged anesthesia and in patients with severe metabolic illness (vomiting, diarrhea, shock) is critical. AUTHOR: LOIS ROTH-JOHNSON 1ST EDITION AUTHOR: JAMES H. MEINKOTH
Pricing Information
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Blood Gas Analysis DEFINITION Evaluation of blood pH, Pco2, Po2, and bicarbonate. Other calculated parameters may be included. A blood pH lower than normal indicates acidosis, whereas a blood pH higher than normal indicates alkalosis. The acidosis is considered metabolic if a low Hco− 3 is a predominant coabnormality; conversely, is considered respiratory if high Pco2 is a predominant coabnormality.
SYNONYM Acid-base analysis
TYPICAL NORMAL RANGE Arterial pH: dog, 7.35-7.45; cat, 7.30-7.42 Pco2 (mm Hg): dog, 31-42; cat, 25-37 Po2 (arterial, breathing room air; mm Hg): dog, 90-100; cat, 90-100 Hco− 3 (mEq/L): dog, 19-26; cat, 14-21
PHYSIOLOGY Blood pH is maintained within narrow limits by a variety of buffers acting in concert. Pco2 and bicarbonate (Hco3) are the main parameters used for detecting respiratory and metabolic derangements (respectively) altering pH. Arterial Po2 is used for evaluating pulmonary function. Normal respiration maintains high Po2 and relatively low Pco2 concentration. General interpretive steps are to determine whether the pH has changed significantly and then evaluate the Hco− 3 and Pco2 to determine whether the change is due to metabolic or respiratory abnormalities, respectively.
CLINICAL APPLICATIONS CAUSES OF ABNORMALLY HIGH LEVELS: See individual tests, particularly pH. CAUSES OF ABNORMALLY LOW LEVELS: See individual tests, particularly pH.
SPECIMEN AND PROCESSING CONSIDERATIONS DRUG EFFECTS ON LEVELS: Diuretics such as furosemide can cause metabolic alkalosis. LAB ARTIFACTS THAT MAY INTERFERE: Exposure to room air will result in falsely increased Po2 and decreased Pco2. Failure to analyze samples promptly can result in decreases in pH and Po2. SPECIMEN: Whole blood collected and maintained in heparinized syringe (0.05-0.1 mL of heparin [1000 units/mL] per mL blood). Cap end of syringe to limit exposure to room air. Specimens analyzed within 15 minutes of collection are preferred. Storage in a capped syringe on ice at 4○C for up to 2 hours is acceptable. RELATIVE COST: $$
PEARLS Alterations in pH can be life threatening. Handheld point-of-care analyzers are available for use in clinics. Venous blood samples are sufficient for routine evaluation of pH, Pco2, and Hco− 3. Arterial samples are more difficult to obtain but are needed for meaningful interpretation of Po2 levels. Submission of specimens to a reference lab may not be practical because of specimen sensitivity to environmental influence. AUTHOR: LOIS ROTH-JOHNSON 1ST EDITION AUTHOR: JAMES H. MEINKOTH
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Blastomyces Testing DEFINITION Blastomycosis is a systemic fungal infection caused by the dimorphic fungus Blastomyces dermatitidis.
SYNONYMS Agar-gel irnmunodiffusion (AGID) test for antibody, enzyme immunoassay (EIA) test for antigen
PHYSIOLOGY Following inhalation of Blastomyces spores, a primary lung infection develops, with subsequent dissemination via blood and lymphatics to multiple tissues, most notably skin, eye, bone, lymph nodes, and brain.
TYPICAL NORMAL RANGE Consult the laboratory conducting the test for information regarding reference range for AGID. Reference range for EIA antigen test is 1.055 specific gravity). Negative in healthy dogs, trace or +1 in normal dogs with moderately or highly concentrated urine.
PHYSIOLOGY Bilirubin is a byproduct of erythrocyte hemoglobin metabolism. Increased bilirubin production/release is caused by hemolytic states and abnormalities in hepatobiliary excretion of bilirubin. Water-soluble conjugated bilirubin is readily filtered through the glomerulus; dogs have especially low renal thresholds, with minimal tubular resorption of bilirubin such that bilirubinuria precedes hyperbilirubinemia (icterus). Also, canine renal tubular epithelial cells are capable of bilirubin production from hemoglobin resorbed from urine. Cats have higher thresholds and greater tubular resorption of conjugated bilirubin; therefore, bilirubinuria is more clinically significant than in dogs and usually indicates hepatobiliary disease. Albumin-bound unconjugated bilirubin does not pass the glomerulus readily, but animals with albuminuria/proteinuria may have enough albumin/protein in urine to get measurable amounts of unconjugated bilirubin in urine.
CLINICAL APPLICATIONS CAUSES OF ABNORMALLY HIGH LEVELS: Hemolytic diseases and decreased hepatobiliary excretion of bilirubin NEXT DIAGNOSTIC STEP TO CONSIDER IF LEVELS HIGH: Assess urine specific gravity, hematocrit (if very low, likely bilirubinuria secondary to hemolytic crisis), liver enzymes (alanine aminotransferase, alkaline phosphatase, ± γ-glutamyl transferase; if significantly increased, bilirubinuria likely caused by decreased hepatobiliary excretion), and serum total bilirubin concentration. IMPORTANT INTERSPECIES DIFFERENCES: In health, only dogs are expected to have bilirubinuria; however, cats with extremely concentrated urine may have trace or +1 reaction on dipstick.
SPECIMEN AND PROCESSING CONSIDERATIONS DRUG EFFECTS ON LEVELS Indican (a substance that may occur in the urine of normal animals) and etodolac metabolites may cause spurious increase. Ascorbic acid may cause spurious decrease. LAB ARTIFACTS THAT MAY INTERFERE: Ultraviolet light causes bilirubin degradation. It is best if the urine sample has less than 30 minutes of direct ultraviolet light exposure prior to analysis. SPECIMEN: Urine (minimum 5 mL) in clean/sterile container collected by free catch, catheterization, or cystocentesis RELATIVE COST: $ (reported as part of urinalysis) AUTHOR: ELIZABETH G. WELLES
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Bilirubin DEFINITION A pigment produced by the degradation of the heme portion of hemoglobin (and to a lesser extent, other porphyrin-containing compounds)
TYPICAL NORMAL RANGE Dogs: approximately 0-0.3 mg/dL Cats: approximately 0-0.1 mg/dL. Specific values vary among laboratories. For mmol/L, multiply mg/dL × 17.1.
PHYSIOLOGY During the breakdown of red blood cells (either senescent or pathologic hemolysis), heme is split to iron and protoporphyrin; protoporphyrin is converted to biliverdin then to unconjugated bilirubin predominately in macrophages of the spleen, bone marrow, and liver. Unconjugated bilirubin is released into the circulation, where it is bound to carrier proteins (albumin, globulins) and transported to the liver for uptake, conjugation, and secretion into bile. Conjugation renders bilirubin water soluble. Laboratory assays include total serum bilirubin, direct (conjugated) bilirubin, and indirect (unconjugated) bilirubin, which is a calculated value.
CLINICAL APPLICATIONS CAUSES OF ABNORMALLY HIGH LEVELS: Hemolysis, decreased hepatic uptake, decreased functional liver mass, decreased bile excretion (intrahepatic or extrahepatic) NEXT DIAGNOSTIC STEP TO CONSIDER IF LEVELS HIGH: Assess for hemolytic disease (CBC, saline prep for autoagglutination, Coombs’ test), bile obstruction (alkaline phosphatase [ALP], imaging), hepatic disease (alanine aminotransferase, ALP, liver biopsy).
SPECIMEN AND PROCESSING CONSIDERATIONS LAB ARTIFACTS THAT MAY INTERFERE Hemolysis interferes with (either increases or decreases, depending on the method) measurement. Lipemia falsely increases bilirubin. Light degrades bilirubin (up to 50% in 1 hour in direct sunlight or fluorescent light). SPECIMEN: Nonhemolyzed serum (red top tube). Separate serum from red blood cells as soon as possible. Store at 2°C-8°C (refrigeration). Protect from light. RELATIVE COST: $$ (Typically part of chemistry profile); $ (as an individual test)
PEARLS Determination of conjugated and unconjugated forms of bilirubin is not usually useful in differentiating hemolytic from hepatic/biliary causes of icterus in dogs and cats. AUTHOR: LOIS ROTH-JOHNSON 1ST EDITION AUTHOR: FONZIE QUANCE-FITCH
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Bile Acids (Blood, Urinary) DEFINITION Family of detergent-like compounds (predominately cholic acid and chenodeoxycholic acid) synthesized in the liver from cholesterol and secreted in bile to aid in digestion and absorption of fat and fat-soluble vitamins.
TYPICAL NORMAL RANGE Fasting bile acids normally 20 mmol/L, postprandial samples >25 mmol/L, and/or urine bile acid/creatinine ratio >7.1 indicate liver disease. Urine: urine sulfated bile acids (USBA)/creatinine (crt) and total BA: crt are considered diagnostically useful. Dogs: USBA:crt > 1.0 and total BA:crt > 7 suggest liver disease Cats: USBA: crt > 2.0 and total BA:crt > 4 suggest liver disease
PHYSIOLOGY Bile acids are stored in the gallbladder; released as a bolus into the small intestines upon feeding. In health, an efficient enterohepatic circulation exists, and up to 95% of bile acids are recycled via this cycle. Serum bile acids are evaluated in paired samples (fasting, postprandial). When portal blood clearance or biliary excretion is impaired, urinary excretion of BA increases. Urinary bile acid/creatinine ratios reflect an average serum bile acid concentration. Only a single urine sample is required.
CLINICAL APPLICATIONS CAUSES OF ABNORMALLY HIGH LEVELS: Decreased clearance from blood (decreased functional liver mass, compromised portal circulation [congenital or acquired portosystemic shunt]). Cholestasis due to obstruction, cirrhosis, inflammation. Specific causes are many. NEXT DIAGNOSTIC STEP TO CONSIDER IF LEVELS HIGH: Assess for cholestasis (bilirubin, alkaline phosphatase), portosystemic shunt (imaging), other liver diseases (alanine aminotransferase, imaging, liver biopsy). CAUSES OF ABNORMALLY LOW LEVELS: Low bile acid values are not clinically significant.
SPECIMEN AND PROCESSING CONSIDERATIONS LAB ARTIFACTS THAT MAY INTERFERE Decrease: hemolysis, lipemia (spectrophotometric method), no effect on radioimmunoassay Increase: hypertriglyceridemia (spectrophotometric method), no effect on radioimmunoassay
SPECIMEN Serum (red-top tube): 12-hour fasting sample and 2-hour postprandial sample recommended separate serum from red blood cells as soon as possible. Store at 2°C-8°C (refrigeration). Urine: fresh urine, avoid blood contamination. RELATIVE COST: Serum (single), $$ serum (paired), $$; urine bile acid/crt, $$
PEARLS If cholestasis is present (e.g., patient is icteric without evidence of hemolysis), bile acids do not provide any additional information on hepatic function. Bile acids are a good indicator of hepatobiliary function but are not specific for the type of underlying disease. Extrahepatic disorders (e.g., gastrointestinal disease) can elevate bile acid concentrations. Urine bile acids are more specific for canine liver dysfunction than serum bile acids. Occasional preprandial values that exceed postprandial values are attributed to spontaneous gallbladder contraction. Urine test has low diagnostic sensitivity (false negatives common) but good specificity (few false positives).
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AUTHOR: LOIS ROTH-JOHNSON 1ST EDITION AUTHOR: FONZIE QUANCE-FITCH
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Bicarbonate DEFINITION An anion that is the major extracellular buffer in blood
TYPICAL NORMAL RANGE Dogs and cats: 17-24 mEq/L (mEq/L = mmol/L).
PHYSIOLOGY Bicarbonate is formed from the conversion of carbon dioxide and water to carbonic acid by carbonic anhydrase. Carbonic acid dissociates into bicarbonate and hydrogen ion. During metabolic acidosis, bicarbonate minimizes pH changes by binding to excess +
+
−
H . Binding excess H decreases measurable Hco 3.
CLINICAL APPLICATIONS CAUSES OF ABNORMALLY HIGH LEVELS: Metabolic alkalosis (causes: vomiting, diuretics, overadministration of bicarbonate) or respiratory acidosis (causes: pulmonary parenchymal disease [pneumonia, pulmonary edema], pulmonary restrictive disease [pleural effusion, pneumothorax, diaphragmatic hernia], hypoventilation/central nervous system depression [anesthesia, narcotics, brain stem disease], airway obstruction) NEXT DIAGNOSTIC STEP TO CONSIDER IF LEVELS HIGH: Evaluate arterial blood gas profile (particularly pH and Pco2) to −
differentiate between metabolic alkalosis (high pH, high Hco 3, high Pco2) and metabolic compensation for respiratory acidosis (low −
pH, high Pco2, high Hco 3). Evaluate for underlying causes listed above. CAUSES OF ABNORMALLY LOW LEVELS: Metabolic acidosis (causes: bicarbonate loss due to diarrhea, lactic acidosis, ketoacidosis, uremia, and ingestion of ethylene glycol) or compensation for respiratory alkalosis (causes: pulmonary disease [pneumonia, pulmonary edema], direct stimulation of central nervous system [pain, anxiety], septicemia) NEXT DIAGNOSTIC STEP TO CONSIDER IF LEVELS LOW: Evaluate arterial blood gas profile to differentiate between metabolic −
−
acidosis (low pH, low Hco 3, low Pco2) and metabolic compensation for respiratory alkalosis (high pH, low Pco2, low Hco 3). Evaluate for underlying causes listed above.
SPECIMEN AND PROCESSING CONSIDERATIONS LAB ARTIFACTS THAT MAY INTERFERE: Decrease: processing delay. Specimens analyzed within 15 minutes of collections are ○
preferred. Storage in a capped syringe on ice at 4 C for up to 2 hours is acceptable. SPECIMEN: Bicarbonate is a calculated value provided as part of a blood gas analysis. Whole blood in a heparinized syringe, avoiding exposure to room air, is used as described for blood gas analysis. RELATIVE COST: $$ (part of blood gas analysis, not available as a separate test)
PEARLS Total carbon dioxide (Tco2) estimates plasma bicarbonate, which is part of most serum biochemistry profiles. Tco2 is the total amount of co2 gas that can be released from serum. At physiologic pH (7.4), about 95% of the potential gas is co2 and 5% is Hco−3. Therefore, although Tco2 is usually slightly higher (1-2 mEq/L) than bicarbonate on a blood gas profile, it is considered a clinically accurate assessment of bicarbonate. May not be practical to submit to a reference laboratory, owing to sensitivity of specimen to environmental influences and time constraints for accurate test results AUTHOR: LOIS ROTH-JOHNSON 1ST EDITION AUTHOR: JAMES H. MEINKOTH
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Bence Jones Urinary Proteins DEFINITION Unassociated immunoglobulin light chains produced in excess by abnormal plasma cells, typically with malignant plasma cell neoplasia (multiple myeloma).
SYNONYMS Free immunoglobulin light chains, M-proteins, myeloma proteins, paraproteinuria
TYPICAL NORMAL RANGE Reported as negative or positive
PHYSIOLOGY Light chains are a component of immunoglobulins. Increased production occurs with increased immunoglobulin production or catabolism, as with multiple myeloma or (rarely) plasma cell tumors, the benign counterpart. Bence Jones proteins precipitate when heated, followed by redissolving when boiled and precipitation again when cooled.
CLINICAL APPLICATIONS CAUSES OF ABNORMALLY HIGH LEVELS: Multiple myeloma; less often associated with extramedullary plasmacytoma or chronic lymphocytic leukemia; rarely associated with chronic infectious diseases NEXT DIAGNOSTIC STEP TO CONSIDER IF LEVELS HIGH: Confirm monoclonal gammopathy with plasma immunoelectrophoresis. Assess for osteolytic bone lesions (radiographs); bone marrow plasmacytosis or plasma cell neoplasia (cytologic analysis of aspirate, or biopsy); urine protein electrophoresis (monoclonal spike in β or d regions).
SPECIMEN AND PROCESSING CONSIDERATIONS LAB ARTIFACTS THAT MAY INTERFERE: False positives can occur with marked proteinuria. SPECIMEN: Urine: Store at 2°C-8°C (refrigeration). RELATIVE COST: $$
PEARLS Heat precipitation method is not highly sensitive. Urine protein dipstick tests do not detect Bence Jones protein. The presence of Bence Jones proteins in the urine does not indicate glomerular disease (the molecules are sufficiently small to pass through normal glomerular fenestrations). AUTHOR: LOIS ROTH-JOHNSON 1ST EDITION AUTHOR: FONZIE QUANCE-FITCH
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Basophils DEFINITION White blood cell (granulocytic leukocyte) that has a segmented nucleus and metachromatic (purple) granules in cytoplasm. Basophils are rarely encountered in the blood of healthy animals.
TYPICAL NORMAL RANGE Dogs and cats: 0-0.1 × 103 basophils/µL.
PHYSIOLOGY Basophilic precursors undergo differentiation in the bone marrow, enter peripheral blood circulation for a few hours, and then enter tissue. Basophils produce leukotrienes and release histamine, heparin, and other mediators from their granules. Basophils participate in immunoglobulin E-mediated hypersensitivity reactions. They are similar in morphology to mast cells, but mast cells have a nonsegmented nucleus and primarily reside in tissue.
CLINICAL APPLICATIONS CAUSES OF ABNORMALLY HIGH LEVELS: Allergic reactions (e.g., food, insect sting); parasitism (e.g., dirofilariasis/heartworm disease, flea infestation): mast-cell neoplasm; basophilic leukemia; myeloproliferative neoplasms (e.g., essential thrombocythemia, polycythemia vera) NEXT DIAGNOSTIC STEP TO CONSIDER IF LEVELS HIGH: Additional tests directed by history, physical exam findings, and results of ancillary diagnostic tests to rule out causes of high values listed above IMPORTANT INTERSPECIES DIFFERENCES: The granules in feline basophils stain lavender or light violet. The metachromatic staining of granules in feline basophilic myelocytes diminishes as the basophilic precursors undergo maturation in the marrow. Because canine basophils have comparatively low numbers of metachromatic granules, a grey basophilic cytoplasm, and are large, they can be misidentifled as monocytes on blood smear.
SPECIMEN AND PROCESSING CONSIDERATIONS SPECIMEN: EDTA whole blood (lavender-top tube) and freshly prepared blood smear RELATIVE COST: $$ (reported as part of CBC)
PEARLS Basophilia often accompanies eosinophilia, a further indication of allergic or parasitic disease. Careful examination is necessary to identify basophils; when stained with the rapid Romanowsky stains (e.g., Diff-Quik), the cytoplasmic granules of canine basophils may be even less apparent. AUTHOR: STEPHEN D. GAUNT
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Bartonellosis Testing DEFINITION Bartonella spp. are a group of vector-transmitted, intraerythrocytic bacterial organisms that can induce persistent infections in dogs, cats, and humans.
TYPICAL NORMAL RANGE Consult laboratory for information regarding reference ranges. Some general guidelines include: Immunofluorescence antibody (IFA) test for B. vinsonii and B. henselae. Negative titer is 200,000 U/L) are strongly suggestive of muscular dystrophy. AUTHOR: RUANNA GOSSETT
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Cortisol DEFINITION Cortisol is a glucocorticoid hormone produced by the adrenal gland cortex. It initiates synthesis of proteins and receptors for hormones and cytokines involved in gluconeogenesis, protein catabolism, lipolysis, immune responses, and water balance.
TYPICAL NORMAL RANGE Baseline cortisol concentration in health is 0.4-6 µg/dL or 10-160 nmol/L in dogs and 0.4-4 µg/dL or 10-110 nmol/L in cats.
PHYSIOLOGY Identification of a naturally occurring, abnormally high concentration of cortisol is helpful towards making a diagnosis, because concentrations fluctuate numerous times daily. Increased concentrations may need to be provoked or suppressed for diagnostic purposes. ACTH released from pituitary adenomas/adenocarcinomas stimulates adrenal cortical release of cortisol. Adrenocortical adenoma/adenocarcinoma in dogs and most cats overproduce cortisol. In ferrets and some cats, adrenocortical tumors produce other steroid hormones such as estrogen or progesterone and may result in clinical signs of hyperadrenocorticism. Ovarian/Sertoli cell tumors in dogs can produce cortisol-like compounds. Stress of systemic disease causes increased release of ACTH from the pituitary gland, with subsequent increased release of cortisol from adrenal glands. Administration of exogenous ACTH for use in the diagnosis of hyperadrenocorticism causes increased adrenal gland production and release of cortisol. Administration of exogenous corticosteroids (specifically dexamethasone) is used for suppressing production/release of ACTH, with subsequent decrease in adrenal release of cortisol. Dexamethasone is used for this test because it cross-reacts with cortisol minimally [350 (cats) have suboptimal to poor glycemic control. NEXT DIAGNOSTIC STEP TO CONSIDER IF LEVELS HIGH: Review history and physical exam for findings indicative of diabetes mellitus. Check serum glucose level and urine for the presence of glucose +/− ketones.
CAUSES OF ABNORMALLY LOW LEVELS Animals with hypoproteinemia and hypoalbuminemia may have lowered fructosamine. If hypoalbuminemia is concurrent with diabetes mellitus, the fructosamine level may appear falsely low. Hyperthyroid cats have lower fructosamine than healthy cats because of accelerated protein (albumin) turnover. NEXT DIAGNOSTIC STEP TO CONSIDER IF LEVELS LOW: Check serum albumin and globulin concentrations. In cats >6 years old, test for hyperthyroidism. IMPORTANT INTERSPECIES DIFFERENCES: Glucose has a higher affinity for albumin in dogs and globulins in cats, and conection methods are used by reference laboratories. SPECIMEN AND PROCESSING CONSIDERATIONS SPECIMEN: Serum (red-top tube) or heparinized plasma (green-top tube) RELATIVE COST: $$
PEARLS Fructosamine is not typically used for assessing persistent hypoglycemia, as would occur in patients with insulinoma. AUTHOR: ELIZABETH G. WELLES
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Folate DEFINITION The anionic form of folic acid. Part of B-vitamin complex.
SYNONYM Folic acid
TYPICAL NORMAL RANGE Dogs: 6.5-11.5 mg/L. Cats: 9.7-21.6 mg/L.
PHYSIOLOGY Primary source is diet; also produced by enteric bacteria. Ingested folate is released from food and hydrolyzed in proximal small intestine. Dietary and bacterial-origin folate is taken up by intestinal epithelium, metabolized, and systemically absorbed (blood).
CLINICAL APPLICATIONS CAUSES OF ABNORMALLY HIGH LEVELS: Intestinal bacterial overgrowth, exocrine pancreatic insufficiency (EPI), excessive gastric acid production, over-supplementation NEXT DIAGNOSTIC STEP TO CONSIDER IF LEVELS HIGH: Test for bacterial overgrowth, EPI. Evaluate diet. CAUSES OF ABNORMALLY LOW LEVELS: Small-intestinal mucosal disease, dietary deficiency, medication (sulfasalazine, phenytoin, antibiotics that deplete gastrointestinal flora, causing decreased folate production), extensive intestinal neoplasia NEXT DIAGNOSTIC STEP TO CONSIDER IF LEVELS LOW: Evaluate diet, medication history. Assess for intestinal mucosal disease (endoscopy or surgery). IMPORTANT INTERSPECIES DIFFERENCES: Different reference ranges for dogs and cats. High serum concentration in cats is of no known clinical significance. Cobalamin deficiency has been associated with decreased folate utilization and resultant increased folate values in cats. Increased serum folate (due to bacterial overgrowth) associated with low immunoglobulin A in German shepherd dogs.
SPECIMEN AND PROCESSING CONSIDERATIONS DRUG EFFECTS ON LEVELS: Decrease: associated with sulfasalazine, phenytoin, and antibiotics that disturb intestinal flora. LAB ARTIFACTS THAT MAY INTERFERE: False increase: hemolyzed specimens (released from red blood cells). SPECIMEN: Nonhemolyzed serum (red-top tube; separate serum from clot immediately, and place in fresh red-top tube for submission). Stable at ○
○
4 C for 1 day, −20 C for 6-8 weeks. Avoid repeated freezing, thawing. RELATIVE COST: $$
PEARLS Folate should be evaluated in conjunction with cobalamin and trypsinlike immunoreactivity for best interpretation. Low cobalamin concentration may result in a functional folate deficiency, with measured folate concentration within the reference interval. Maternal folate deficiency is associated with congenital malformations (neural tube and conotruncal cardiac defects) in humans, but there is no evidence of a similar problem in dogs and cats. AUTHOR: LOIS ROTH-JOHNSON
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Fluid Analysis DEFINITION Biochemical and Cytologie analysis of fluid aspirated from body cavities (abdominal, pleural, pericardial) or joints (see p. 1519). Typically includes assessment of color, turbidity, viscosity, protein concentration, total cell counts (may include differential), and Cytologie description.
TYPICAL NORMAL RANGE Body cavity effusions are classified as: *Conversion: for mg/mL, multiply g/dL by 10.
Protein (g/dL) Transudate
7.5
PHYSIOLOGY Transudates: decreased plasma osmotic pressure, usually due to hypoalbuminemia, results in fluid movement from vasculature to body cavities. Causes include protein-losing enteropathy and nephropathy, severe chronic liver disease with decreased protein production. Modified transudate: results from increased hydrostatic pressure or increased vascular permeability; causes are numerous, including congestive heart failure, inflammation, and neoplasia. Exudate: due to inflammation with increased vascular permeability
CLINICAL APPLICATIONS CAUSES OF ABNORMALLY HIGH LEVELS: Altered plasma protein osmotic pressure, hypoproteinemia, vascular obstruction, inflammation, neoplasia NEXT DIAGNOSTIC STEP TO CONSIDER IF LEVELS HIGH: Assessment of history and physical examination findings in combination with serum biochemical changes and Cytologie appearance of fluid help determine if fluid accumulation is the result of metabolic, inflammatory, orneoplastic disease.
SPECIMEN AND PROCESSING CONSIDERATIONS DRUG EFFECTS ON LEVELS: Peritoneal lavage, IV or subcutaneous fluid administration may alter protein concentration and cell counts. Corticosteroid administration may have adverse affect on cell morphology.
SPECIMEN Obtain specimens using sterile technique. Fill EDTA (lavender-top) tube to prevent clotting. A sterile tube (red top) or other container should be used for specimens to be cultured. Submission of direct or sediment smears prepared when the specimen is obtained is suggested to allow evaluation of cells before autolytic changes occur. RELATIVE COST: $$
PEARLS Clear, colorless fluids are usually transudates; increasing turbidity is associated with increased protein concentration and/or cell counts and classified as modified transudates or exudates. Sediment smears should be prepared if low cellularity is suspected. Fluid analysis from cysts or abscesses is not diagnostically useful. Fluid from these sources should be submitted only for Cytologie analysis.
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AUTHOR: LOIS ROTH-JOHNSON
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Fibrinogen DEFINITION A glycoprotein important in hemostasis; a positive acute-phase protein that increases due to inflammation or tissue injury; important in tissue repair
TYPICAL NORMAL RANGE Dogs: 150-300 mg/dL; cats: 150-300 mg/dL
PHYSIOLOGY Made in the liver; production is upregulated with inflammation or tissue damage (due to cytokines interleukin [IL]-1, IL-6, and tumor necrosis factor [TNF]). It is a nonenzymatic coagulation factor (factor I), cleaved (activated) by thrombin to form fibrin and promote stable clot formation.
CLINICAL APPLICATIONS CAUSES OF ABNORMALLY HIGH LEVELS: Two major causes include dehydration (hemoconcentration) and increased production by the liver (positive acute-phase protein) in response to cytokines IL-1, IL-6, and TNF due to inflammation or tissue damage. Can also increase with physiologic stress (pregnancy). NEXT DIAGNOSTIC STEP TO CONSIDER IF LEVELS HIGH: Look for source of inflammation/tissue injury: review history and physical exam; CBC (determine if inflammatory leukogram is present), serum biochemistry profile; if hyperglobulinemia, serum protein electrophoresis is warranted to document a polyclonal gammopathy supportive of an inflammatory process. CAUSES OF ABNORMALLY LOW LEVELS: Increased consumption in disseminated intravascular coagulation or increased fibrinogenolysis, decreased hepatic fibrinogen synthesis, inherited/congenital disorders (documented in bichon frise, Bernese mountain dogs, Lhasa apso, vizsla, and collie). NEXT DIAGNOSTIC STEP TO CONSIDER IF LEVELS LOW: Full coagulation profile (activated partial thromboplastin time, prothrombin time, thrombin time, platelet count, and fibrinogen degradation products) to assess for disseminated intravascular coagulation. Serum biochemistry profile to evaluate hepatic parameters. Serum bile acids to evaluate hepatobiliary function.
SPECIMEN AND PROCESSING CONSIDERATIONS SPECIMEN: Citrated plasma (blue-top tube). Centrifuge and remove plasma within 1 hour of collection and transfer to plain red-top tube. Label as plasma. Test as soon as possible. Stable at 2-8°C for 24 hours; freeze if there is a longer time interval before testing. RELATIVE COST: $$ AUTHOR: DEBORAH G. DAVIS
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Fibrin or Fibrinogen Degradation Products DEFINITION Fibrin or fibrinogen degradation products (FDPs) are protein fragments of fibrin or fibrinogen that have been cleaved by plasmin as part of fibrinolysis. Assays to detect FDPs are used for identifying increased fibrin or fibrinogen breakdown that is seen with excessive coagulation (disseminated intravascular coagulation [DIC]). Plasmin can act on both fibrinogen and fibrin, and assays for FDPs do not differentiate between fibrinolysis and fibrinogenolysis.
TYPICAL NORMAL RANGE Semiquantitative normal values: dogs, 0-10 mg/mL; cats, 0-8 mg/mL. Abnormal values are reported as moderately increased or markedly increased. Exact values are laboratory dependent.
PHYSIOLOGY Formed by plasmin breakdown of non-cross-linked fibrin and fibrinogen. FDPs are potent inhibitors of coagulation; they compete with fibrinogen for the active sites on thrombin and interfere with the conversion of fibrinogen to fibrin. Interfere with platelet aggregation; they bind to the fibrinogen-binding site on platelets. Eliminated by the liver and kidney, so patients with hepatic or renal disease can have elevated FDPs in the absence of significantly elevated levels of fibrin(ogen) breakdown.
CLINICAL APPLICATIONS CAUSES OF ABNORMALLY HIGH LEVELS Increased fibrinolysis: internal hemorrhage, local or disseminated intravascular coagulation, sepsis or other severe inflammation Decreased FDP clearance: hepatic disease, renal failure
NEXT DIAGNOSTIC STEP TO CONSIDER IF LEVELS HIGH CBC with platelet count/serum chemistry profile/urinalysis Coagulation profile: activated partial thromboplastin time, prothrombin time, thrombin time, angiotensin III and D-dimer levels
SPECIMEN AND PROCESSING CONSIDERATIONS LAB ARTIFACTS THAT MAY INTERFERE: False increases can occur when FDP generation occurs during collection (traumatic venipuncture). SPECIMEN: Serum assay: use tubes filled with thrombin, or reptilase (snake venom) with soybean trypsin inhibitor or aprotinin (light blue-top tubes with yellow label). Plasma assays: citrated (light blue top-tube). Tubes should be completely filled. RELATIVE COST: $$
PEARLS Serum (plain red-top tube) specimens cannot be used because clot formation consumes FDPs, lowering measurement. A clot in the citrate tube will interfere with accuracy of the plasma assay. D-dimer assays continue to be evaluated in small-animal medicine and may prove to be more sensitive and/or specific than FDP assays for detecting coagulation and clot lysis. AUTHOR: DEBORAH G. DAVIS
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Feline Leukemia Virus Immunofluorescent Antibody (IFA) DEFINITION Feline leukemia virus (FeLV) is a retrovirus of cats that causes hematopoietic neoplasia, immunosuppression, and/or anemia.
TYPICAL NORMAL RANGE Reported as positive or negative
PHYSIOLOGY Following exposure to FeLV via the oronasal route, the virus replicates in oropharyngeal lymphoid tissue. The virus may be cleared with an effective immune response. An ineffective immune response results in viremia and replication in bone marrow and lymphoid cells. Affected cats may be transiently viremic with latent virus residing in the marrow, may become persistently viremic, or may be overtly healthy carriers. Persistent viremia may result in immunosuppression, myelosuppression, hematopoietic neoplasia, immune complex diseases, or reproductive disorders.
CLINICAL APPLICATIONS CAUSES OF ABNORMALLY HIGH LEVELS: IFA detects the cell-associated FeLV core antigen, p27, in cells; therefore, a positive IFA indicates infection with FeLV and probable bone marrow infection. A positive IFA with a negative ELISA is always a false result, and both tests should be repeated. NEXT DIAGNOSTIC STEP TO CONSIDER IF LEVELS HIGH: Correlate with history, clinical findings, and laboratory data. CAUSES OF ABNORMALLY LOW LEVELS: A negative IFA with a positive ELISA indicates either uninfected (false-positive ELISA) or early infection. NEXT DIAGNOSTIC STEP TO CONSIDER IF LEVELS LOW: If positive ELISA and negative IFA, repeat both tests in 6-8 weeks to determine effective clearance of virus versus persistent infection.
SPECIMEN AND PROCESSING CONSIDERATIONS LAB ARTIFACTS THAT MAY INTERFERE: Marked thrombocytopenia, marked leukopenia, eosinophilia, or poor-quality buffy coat or bone marrow smear may cause false-negative or false-positive results.
SPECIMEN 1 mL EDTA-anticoagulated whole blood (lavender-top tube); stable at 4°C for 4 days. Air-dried buffy coat smears or bone marrow smears: store at room temperature. RELATIVE COST: $$
PEARLS Vaccination for FeLV involves a different component of the virus (gp70 protein) than the one detected by IFA. Therefore, prior vaccination does not affect test results. The FeLV IFA test is less sensitive (does not catch all FeLV-positive cases) but more specific (positive result is reliably positive) compared to the FeLV ELISA. Therefore, FeLV IFA is not a good initial screening test but is an excellent confirmatory test. AUTHOR: PATTY J. EWING
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Feline Leukemia Virus (ELISA) DEFINITION Feline leukemia virus (FeLV) is a retrovirus of cats that causes hematopoietic neoplasia, immunosuppression, and/or anemia.
SYNONYMS FeLV enzyme-linked immunosorbent assay
TYPICAL NORMAL RANGE Reported as positive or negative
PHYSIOLOGY Following exposure to FeLV via the oronasal route, the virus replicates in oropharyngeal lymphoid tissue. The virus may be cleared with an effective immune response. An ineffective immune response results in viremia and replication in marrow and lymphoid cells. Affected cats may be transiently viremic with latent virus residing in the marrow, may become persistently viremic, or may be overtly healthy carriers. Persistent viremia may result in immunosuppression, myelosuppression, hematopoietic neoplasia, immune complex diseases, or reproductive disorders.
CLINICAL APPLICATIONS CAUSES OF ABNORMALLY HIGH LEVELS: ELISA detects the free soluble FeLV core antigen, p27; therefore, a positive ELISA indicates that the cat is viremic (infected with FeLV). False-positive results due to technical error can occur, but this occurs infrequently (sensitivity and specificity are reported to be 99.9%). NEXT DIAGNOSTIC STEP TO CONSIDER IF LEVELS HIGH: Confirm with FeLV IFA test. CAUSES OF ABNORMALLY LOW LEVELS: A negative ELISA indicates that either the cat is not infected or has an early infection. NEXT DIAGNOSTIC STEP TO CONSIDER IF LEVELS LOW: If the cat was recently exposed to an FeLV positive cat but the ELISA is negative, early infection is possible and retesting in 30-90 days is recommended.
SPECIMEN AND PROCESSING CONSIDERATIONS LAB ARTIFACTS THAT MAY INTERFERE: Hemolysis may cause a false-positive or false-negative result. SPECIMEN: 1 mL serum (red-top tube) or EDTA plasma (lavender-top tube) RELATIVE COST: $
PEARLS Vaccination for FeLV involves a different component of the virus (gp70 protein) than the one detected by ELISA. Therefore, prior vaccination does not affect test results. The FeLV ELISA test is more sensitive (more likely to catch all FeLV-positive cases) but less specific (may also erroneously identify a few FeLV-negative cases as positive) compared to the FeLV IFA. Therefore, FeLV ELISA is a good initial screening test, but positive results may or may not be true positives and need to be confirmed with IFA. AUTHOR: PATTY J. EWING
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Feline Immunodeficiency Virus Testing DEFINITION Feline immunodeficiency virus (FIV) is a retrovirus (lentivirus) that attacks the immune system of cats and results in progressive immunosuppressive disease.
TYPICAL NORMAL RANGE Reported as positive or negative
PHYSIOLOGY FIV is inoculated via saliva or blood from bite wounds. There are three stages of infection. Acute phase: FIV initially infects T lymphocytes and salivary glands, with subsequent spread to other mononuclear cells; cats may have fever, leukopenia, and lymphadenopathy. Subclinical phase: cats may be without clinical signs for years. Chronic phase: progressive immunosuppression with development of a wide variety of clinical disorders, including stomatitis/gingivitis, anemia and leukopenia, neurologic signs, enteritis, weight loss, and opportunistic infections. A cat may have no clinical signs for years, owing to a prolonged subclinical phase that follows acute infection. Available tests measure circulating FIV antibody levels, not viral antigen. The extended natural course of lentivirus infections makes the presence of antibody essentially equivalent to infection (exceptions: maternal antibody, vaccination).
CLINICAL APPLICATIONS CAUSES OF ABNORMALLY HIGH LEVELS: Screening test: ELISA (SNAP) or rapid immunomigration assay—positive indicates possible exposure to FIV or FIV vaccine; positive or equivocal result requires confirmatory testing. Due to maternally transferred antibody, FIV testing of kittens 5 mg/kg/d in cats (permanent retinal lesions); caution in seizure patients; drug interactions (inhibits theophylline catabolism).
5.7, 22.7, 68, 136 mg T; 22.7 mg/mL I
2.5-5 mg/kg PO q 24 h (this dose is the maximum in cats)
VM, HM
VM
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Generic Name (Trade Name)
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Indications/Drug Type
Enteric probiotic supplement Nonspecific benign (FortiFlora) diarrhea Entocort
(see budesonide)
Epakitin
(see chitosan-based phosphate binder)
Ephedrine
Bronchodilator Urinary incontinence
Canine Dose
Feline Dose
1 packet PO (on food or as treat) q 24 h
Same
1-2 mg/kg PO q 8-12 h; 0.3-1 mg/kg IV, IM for hypotension
2-5 mg per cat PO q 8-12 h
1. α-adrenergic agent and β-adrenergic agent used for inotropic and chronotropic support: 2. Cardiac arrest 3. Bronchodilation 4. Anaphylaxis 5. Hemostasis (topical)
Epirubicin (Ellence, Pharmorubicin, 4′-epidoxorubicin)
Anthracycline antineoplastic
EPO
(see erythropoietin)
Epoetin-α
(see erythropoietin)
Epogen
(see erythropoietin)
Epsiprantel (Cestex)
Tapeworms (cesticide)
How the Drug Is Supplied 1 gram/packet P VM
For bronchospasm: usually combine with sedative +/− bronchodilator; caution if heart disease or hypertension; CNS stimulation, restlessness
25, 50 mg C; 50 mg/mL I
Arrhythmogenic; VO ; increases M 2 avoid high doses (tachycardia); vasoconstriction; avoid direct sunlight exposure; Note: 1:1000 and 1:10,000 solution both commonly available, so use caution (10-fold difference)
1:1000 (1 mg/mL) I; 1:10,000 0.1 mg/mL) Epipen: 0.15 mg (0.15 mL) or 0.3 mg (0.3 mL), one-time dose I
— Same as for doxorubicin according to chemo protocol 2 (e.g., 30 mg/m IV CRI q 21 days)
Same as for doxorubicin but with generally fewer adverse effects (especially lesser incidence and extent of cardiotoxicity)
10, 50, 200 mg I (2 mg/mL) HM
5.5 mg/kg PO once
GI signs possible
12.5, 25, 50, 100 mg, T
Hypotension
Epinephrine (Adrenalin)
Comments
1. 0.0025 mg/kg IV, Same repeated to effect (= 1 mL of 1 : 10,000 per 40 kg BW); triple if administering intratracheally 2. 2, 3. 0.025 mg/kg IV, IM, SQ 3. Topical use: place 1 or 2 drops after applying pressure to, and dabbing blood from, a persistently bleeding wound
2.75 mg/kg PO once
HM
HM
VM
Ergocalciferol (vitamin D2, calciferol, Drisdol)
Hypocalcemia
500-2000 IU/kg PO q 24 h
Second or third choice after calcitriol, DHT
400 IU T 50 000 IU (1.25 mg) C 500 000 IU/mL (12.5 mg/mL) I HM
Erythromycin
1. Macrolide antibiotic, G+ drug, Campylobacter, Mycoplasma, Rickettsia, Chlamydia 2. GI prokinetic
Erythropoietin (EPO, Recombinant human Epoetin, Epogen, r-Hu EPO, erythropoietin
1. 10-20 mg/kg PO q Same 8h 2. 0.5-1 mg/kg PO q 8h
Hypersensitivity; GI upset
200, 250, 333 400, 500 mg T; 100 mg/mL I HM
100 U/kg 3× per week SQ until RBC levels
Same
Anaphylaxis, hypertension, GI
2000, 3000, 4000, 10,000, 20,000 I
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Generic Name (Trade Name)
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Indications/Drug Type
Procrit)
Canine Dose
Feline Dose
increase; then 1× per week thereafter, titrated based on response
Eskalith
(see lithium carbonate)
Esmolol (Brevibloc)
β-blocker with very rapid onset and offset
0.05-0.1 mg/kg/min (50-100 mcg/kg/min) IV CRI, titrated to effect
Esomeprazole (Nexium)
Proton pump inhibitor
1 mg/kg PO q 24 h
Same
Gastric ulceration
—
Comments
How the Drug Is Supplied
signs; autoantibodies may develop
HM
Contraindicated with preexisting bradycardia, CHF
10, 20 mg/mL HM
S-enantiomer of omeprazole (hence “S-omeprazole”), which may provide increased potency
20, 40 mg T, C (both ER) HM
Repeatedly shown to be toxic to BM; unpredictable abortifacient; not recommended
—
0.3, 0.625, 0.9, 1.25, 2.5 mg T
Estradiol cyclopentanepropionate (ECP, estradiol cypionate)
Estradiol to terminate pregnancy
—
Estrogen—conjugated (Premarin)
Estrogen derived from pregnant mare serum; used for treating postovariohysterectomy estrogen insufficiency causing urinary incontinence
0.625 mg = 1 mg DES; — use PO for urinary incontinence (see diethylstilbestrol)
May induce signs of estrus
HM
Estrumate
(see cloprostenol)
Ethanol 20%
Ethylene glycol toxicosis
Dilute to 20% ethanol in saline; administer 5 mL/kg IV q 6 h × 5 Tx, then q 8 h × 4 Tx (see p. 369)
Dilute to 20% ethanol in saline; administer 5 mL/ kg IV q 6 h × 5 Tx, then q 8 h × 4 Tx (see p. 369)
May cause or exacerbate CNS depression; monitor hydration, electrolytes, acid-base status, perivascular damage. If alternatives are lacking, an 80-proof alcoholic beverage (40% ethanol) such as vodka may be diluted 1:1 in sterile 0.9% NaCl to create a 20% ethanol solution
Etidronate (Didronel)
Bisphosphonate antihypercalcemic agent
5-10 mg/kg PO q 12-24 h
Same
200, 400 mg T 50 Main indication is severe paraneoplastic mg/mL I hypercalcemia; renal HM excretion, avoid in renal hyper-PTH
Etodolac (EtoGesic, Lodine) NSAID; selective COX-2 inhibitor for DJD in dogs
EtoGesic
(see etodolac)
Etretinate (Tegison)
Synthetic retinoid used to treat disorders of keratinization in specific breeds (primarily cocker
10-15 mg/kg PO q 24 h
1 mg/kg PO q 24 h
Total dose: 10 mg per cat PO q 24 h
—
GI and renal toxicity; if long-term, use low dose; do not administer with ASA or corticosteroids; may cause KCS in dogs
150, 300 mg T
Vomiting, anemia KCS, increased liver enzymes, expensive
10, 25 mg C HM
VM; 200, 300 mg C; 400, 500 mg T HM
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Generic Name (Trade Name)
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Indications/Drug Type
Canine Dose
Feline Dose
Comments
0.5-1 mg/kg PO, IV q 12-24 h
0.5 mg/kg PO, IV q 24 h
Advantages over other similar agents: once-a-day dosage, minimal P450 inhibition
How the Drug Is Supplied
spaniels) Excedrin
(see acetaminophen)
Famotidine (Pepcid)
H2 receptor antagonist
10, 20, 40 mg T; 8 mg/mL S; 10 mg/mL I HM, OTC
Factrel
(see gonadotropin releasing hormone)
Fatty acid nutritional supplement (Derm Caps)
Dietary supplement, allergic skin disease, dry skin
1 regular capsule PO q — 24 h per 9 kg BW; one ES capsule PO q 24 h per 25-30 kg BW; 1 “100s” capsule PO q 24 h per 45 kg BW
Regular, ES, GI upset, increased bleeding times, “fishy” 100s, C breath
Acaricidal, phenylguanidine, antiparasitic
10-15 mg/kg PO q 24 h for 3 days
Is metabolized to fenbendazole and oxfendazole
27.2, 163.3 mg T
Antiseizure drug used when seizures are refractory to phenobarbital and bromide
15 mg/kg PO q 8 h; can increase to 60 mg/kg PRN
Monitor for BM suppression; hepatotoxic; expensive
400, 600 mg T; 600 mg/tsp S
222 mg/g granules; 100 mg/mL S
Febantel (Rintal)
Felbamate (Felbatol)
Same
VM
VM
HM
Felbatol
(see felbamate)
Feldene
(see piroxicam)
Felimazole
(see methimazole)
Feliway
(see pheromones, feline synthetic)
Fenbendazole (Panacur)
Hookworm, whipworm, roundworm, Taenia, Paragonimus, Filaroides, Giardia, Capillaria, lungworm (Aelurostrongylus)
50 mg/kg PO q 24 h Same; not FDA for 3 days; repeat in 3 approved weeks; whipworms, also repeat in 3 months; lungworms: 50 mg/kg PO q 24 h for 10 days
Vomiting (rare); safe in dogs with heartworms
Transdermal opioid patch, usually lasts at least 72 hours; requires 12 hours to be effective; injectable is ultrashort acting
Patches: 5-10 kg = 25 mcg/h; 10-20 kg = 50 mcg/h; 20-30 kg = 75 mcg/h; >30 kg = 100 mcg/h
2.5-mg patch
Apply a patch to a small clipped area on thorax; never cut patch; prevent human contact with gel surface of patches; avoid heat exposure (e.g., heating pad), increases absorption; respiratory depression and hypoventilation
2.5 mg (25 mcg/h), 5 mg (50 mcg/h), 7.5 mg (75 mcg/h), 10 mg (100 mcg/h) patches; 0.05 mg/ mL (50 mcg/mL) I, HM; former VM injectable (Innovar) was 8× more concentrated than human injectable; do not confuse.
None
Do not use with other cholinesterase inhibiting agents; do not use in puppies or sick or debilitated dogs
5.6% and 13.8% solution VM
Fentanyl (Duragesic, Sublimaze)
Injectable: 0.01-0.04 mg/kg SQ, IM, IV; CRI: 0.003-0.006 mg/kg/hr (3-6 mcg/kg/hr) IV
Fenthion (Prospot, Spot-on)
Organophosphate insecticide
4-8 mg/kg topically to unbroken skin; follow instructions; do not apply more than once every 2 weeks
VM
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Generic Name (Trade Name)
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How the Drug Is Supplied
Indications/Drug Type
Canine Dose
Feline Dose
Comments
Ferric cyanoferrate (Prussian blue, Radiogardase)
Thallium poisoning
100-200 mg/kg PO q 8 h
None
Administer as capsule 500 mg C or in a glucose HM solution orally; constipation, vomiting
Ferrous sulfate
Iron supplementation
Total dose: 100-300 mg per dog PO q 24 h
Total dose: 50-100 mg per cat PO q 24 h
Common side effects: minor GI upset; overdose: severe GI signs, hypotension, collapse; delayed toxicity = pulmonary edema, liver failure (see deferoxamine)
325 mg (65 mg Fe) T; 18, 44 mg Fe/5 mL S
Antibodies develop after several days of therapy
300 mcg/mL I
HM, OTC
Fertagyl
(see gonadotropin releasing hormone)
Feverall
(see acetaminophen)
Fiber (soluble dietary)
(see psyllium mucilloid)
Filaribits
(see diethylcarbamazine)
Filgrastim (Neupogen, r-Hu G-CSF)
Recombinant human granulocyte colonystimulating factor; used for chemotherapy-induced neutropenia
1-5 mcg/kg per day SQ for 3-5 days maximum
Finasteride (Proscar)
Used for treating benign prostatic hyperplasia by inhibiting enzyme that changes testosterone to active dihydroxytestosterone
Total dose: 5 mg per — dog (BW 10-40 kg) PO q 24 h
1, 5 mg T Little published objective information HM about use, efficacy, or side effects in canine medicine
Fipronil (Frontline)
Topical parasiticide for fleas and ticks
9.7% solution; apply topically by weight once monthly
Same
Keep away from 9.7% solution, children, food, water; 0.29% spray avoid contact with pet VM if fipronil is still wet on skin; use on puppies only if >10 weeks old, kittens if >12 weeks old
Firocoxib (Previcox)
Nonsteroidal antiinflammatory drug, COX-2 inhibitor type
5 mg/kg PO q 24 h
1.5 mg/kg PO once only
57, 227 mg T Used mainly for osteoarthritis in dogs; VM safety not established for repeated dosing in cats
Flagyl
(see metronidazole)
Fleet
(see phosphate enemas)
Flomax, Flomaxtra
(see tamsulosin)
Florinef
(see fludrocortisone)
Flovent
(see fluticasone)
Fluconazole (Diflucan)
Imidazole antifungal compound: especially useful for cryptococcosis or CNS/ ocular mycoses
Flucort
(see flumethasone)
Flucytosine (Ancobon, Ancotil)
Aspergillosis, cryptococcosis, candidiasis
1-5 mcg/kg per day SQ for 3-5 days maximum
HM
2.5-5 mg/kg PO q 24 h Same; up to 50 or divided q 12 h mg PO total dose per cat q 12 h
Historically was expensive, though generic form now available (cheaper)
50, 10, 200 mg T; 2 mg/mL I
100 mg/kg PO q 12 h, Same or 25-50 mg/kg PO q 6 h
Renal, BM, and hepatotoxicity; may cause GI upset; do not administer to pregnant animals;
250, 500 mg C; 75 mg/mL S
HM
HM
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Generic Name (Trade Name)
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Indications/Drug Type
Canine Dose
Feline Dose
Comments
How the Drug Is Supplied
neurologic side effects in cats Fludrocortisone (Florinef)
Flumazenil (Romazicon)
Flumethasone (Flucort)
Hypoadrenocorticism, mineralocorticoid replacement therapy
0.1 mg/5 kg PO q 24 h or q 12 h; adjust dosage by need and laboratory testing
0.1 mg/5 kg per day PO; adjust dosage by need and laboratory testing
Systemic hypertension, PU/PD, weight gain. Cushing's-like side effects possible (some glucocorticoid activity)
0.1 mg T
Benzodiazepine antagonist, possibly management of hepatic encephalopathy
0.01-0.02 mg/kg IV (titrate depending on benzodiazepine dose)
Same
—
0.1 mg/mL I
Antiinflammatory, corticosteroid
Total dose: 0.06-0.25 mg PO, IV, IM, SQ q 24 h per dog; intralesional, intraarticular
Total dose: 0.03-0.125 mg PO, IV, IM, SQ q 24 h per cat
Glucocorticoid-related 0.0625 mg T; 0.5 mg/mL I side effects
0.25-1 mg/kg IV, IM, SQ q 24 h; maximum 3-5 days dosage
0.25 mg/kg IV, IM q 24 h; maximum 3-5 days dosage
Platelet dysfunction, ulcerative gastritis, kidney damage; multiple safer alternative drugs
50 mg/mL I
2-4 drops applied topically to ear, q 12 h
Systemic corticosteroid effects; wear gloves (to avoid transcutaneous absorption by owner/ tech/vet)
0.1% otic solution
Do not use
Part of a chemotherapy protocol; BM toxicity, GI toxicity, and neurotoxicity possible
50 mg/mL I
Used for treating behavioral disorders (e.g., acral lick dermatitis)
8, 16, 32, 64 mg chewable T VM
HM
Flunixin meglumine (Banamine)
NSAID analgesic agent
Fluocinolone 0.01% with 60% DMSO (Synotic)
Topical corticosteroid plus DMSO for severe otic inflammation
2-12 drops applied topically to ear, q 12 h
Fluorouracil (Adrucil)
Chemotherapy agent for carcinomas
150 mg/m IV weekly or 2-10 mg/kg IV weekly
Serotonin reuptake inhibitor
0.5-2 mg/kg PO q 24 h 0.5 mg/kg PO q 24 h
Fluoxetine (Prozac, Reconcile)
2
HM
VM
VM
VM
HM
10 mg T; 10, 20, 40 mg C; 4 mg/ mL S HM
Flurbiprofen 0.03% solution (Ocufen)
Topical ocular NSAID
1 drop instilled in eye q 12 h, adjusted PRN
—
Caution with corneal ulcers; contraindicated in infected corneal ulcers
2.5, 5, 10 mL OS HM
Fluticasone (Flovent)
Inhaled glucocorticoid
1 puff PRN, up to q 12-24 h
Same
Need inhaler apparatus; some patients are reluctant to accept placement of a mask at first; maximum effect only after 7-14 days of use; see p. 1289
7.9 g and 13 g inhalation canisters (0.044, 0.11, or 0.22 mg [44, 110, or 220 mcg] per puff) HM
Folate
B vitamin
Total dose: 2.5-5 mg PO per dog q 24 h
Total dose: 2.5 mg PO per cat q 24 h
—
0.4, 0.8, 1 mg/mL I; 5 mg T
—
Dilute drug properly; monitor renal, electrolyte, and hydration status
Fomepizole (Antizol-Vet, 4-methylpyrazole, 4-MP)
Treatment of known or suspected ethylene glycol toxicity
22 mg/kg IV; then 15, 15, and 5 mg/kg IV at 12, 24, and 36 hours following initial dose;
HM 1.5-g kit I VM, HM
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Generic Name (Trade Name)
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Indications/Drug Type
Canine Dose
How the Drug Is Supplied
Feline Dose
Comments
0.06 mg/kg SQ q 12 h
Selectively binds antithrombin III, inactivating factor Xa. No effect on platelet function. No clinical trials to establish safety or efficacy in cats at this time.
2.5, 5. 7.5, 10 mg prefilled syringes I
—
100 mg T
then 3-5 mg/kg IV, q 12 h, until recovery Fondaparinux (Arixtra)
Anticoagulant; prophylaxis for prevention of thromboembolism in feline cardiomyopathy
Fortaz
(see ceftazidime)
Fortekor
(see benazepril)
FortiFlora
(see enteric probiotic supplement)
Fosamax
(see alendronate)
Fragmin
(see heparin-low molecular weight)
Frontline
(see fipronil)
Fulvicin
(see griseofulvin)
Fungizone
(see amphotericin B)
Furadantin
(see nitrofurantoin)
Furazolidone (Furoxone)
Furosemide (Lasix, Salix)
1. Amebiasis 2. Enteric coccidiosis 3. Giardiasis
Potent loop diuretic agent; used in acute renal failure; hypercalcemia; hypertension, CHF (especially pulmonary edema), ascites, and fluid retention
Furoxone
(see furazolidone)
Gabapentin (Neurontin)
Pain, paresthesias; refractory seizures
Gammagard S/D
(see immunoglobulin)
Garamycin
(see gentamicin)
G-CSF
(see filgrastim)
Gemcitabine (Gemzar)
Various forms of neoplasia
1. 2.2 mg/kg PO q 8 h for 7 days 2. 8-20 mg/kg PO q 24 h for 7 days 3. 4 mg/kg PO q 12 h for 7 days
0.5-6 mg/kg PO, SQ, IM, IV q 8-12 h
10 mg/kg PO q 8 h
10 mg/kg IV CRI over 30 minutes; 275 mg/ 2 m IV CRI
Same
HM
HM
0.5-4 mg/kg PO, SQ, IM, IV q 8-12 h
5-10 mg/kg PO q8h
2
25 mg/m diluted and given IV slowly twice weekly, according to chemo protocol
Use lowest effective dosage; high doses reserved for IV use in acute severe pulmonary edema; monitor for hypokalemia, hyponatremia, and hypochloremic alkalosis; caution: azotemia and dehydration
12.5, 20, 40, 50, 80 mg T; 10 mg/ mL S; 50 mg/mL I
Used for pain associated with caudal occipital malformation and other neurologic disorders
100, 300, 400, 600, 800 mg C, T 50 mg/mL S
VM, HM
HM
200 mg, 1 g vials Emerging drug in veterinary oncology at I time of this writing, VM, HM with dosage, efficacy, and side effects still being characterized
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Generic Name (Trade Name)
Indications/Drug Type
Canine Dose
Feline Dose
Comments
How the Drug Is Supplied
Gemfibrozil (Lopid)
Lipid-lowering agent
7.5 mg/kg PO q 12 h
—
—
300, 600 mg T HM
Gemzar
(see gemcitabine)
Genoptic
(see gentamicin, ophthalmic)
Gentamicin (Garamycin, Gentocin)
Broad-spectrum aminoglycoside antibiotic most effective against G− bacteria
6 mg/kg IV, q 24 h, or 2-4 mg/kg IM, SQ, IV q 8 h, max 7 days
Same
Higher dosage given q 50 mg/mL I 24 h is preferred (less VM, HM nephrotoxic); not effective orally; do not use in renal failure or dehydrated/ hypovolemic patients; reserved for serious identified infections only; not for anaerobic infections; nephrotoxic-ototoxic
Gentamicin, otic (Gentocin otic)
Ear infections, especially Pseudomonas or Proteus
Apply q 8 h
Apply q 8 h
Includes betamethasone 1 mg/mL, which can have topical and/or systemic corticosteroid effects; ototoxic risk (aminoglycoside)
3 mg/mL otic solution VM, HM
Gentamicin, ophthalmic (Gentocin, Genoptic)
Conjunctival/corneal infections, especially Pseudomonas
Apply q 4-8 h
Apply q 4-8 h
Rarely irritating; a preparation that contains corticosteroids also exists in nearly identical packaging; use caution when selecting product
3 mg/g OO; 3 mg/ mL OS VM, HM
Gentocin
(see gentamicin)
Geocillin
(see carbenicillin)
Geopen
(see carbenicillin)
Glargine
(see insulin)
Glipizide (Glucotrol)
Oral hyperglycemic agent; useful in some type II diabetes mellitus in cats
0.25-0.5 mg/kg PO q 12 h generally not recommended
0.25-0.5 mg/kg PO q 12 h
Hypokaemia, GI effects, hepatopathy; eventual loss of efficacy (very common); no objective information available on extended-release formulation in veterinary diabetic patients
5, 10 mg T
None
May induce hypokalemia; 1 unit = 1 mg
1 mg/mL I HM
Glucagon
1. Provocative testing agent for insulinoma, diabetes mellitus, and hyperadrenocorticism 2. Insulinoma
Glucantime
(see meglumine)
Glucosamine-chondroitin sulfate (Cosequin)
Chondroprotective agent for osteoarthritis
1. 0.03 mcg/kg IV 2. 5 ng (0.005 mg)/kg/ min IV CRI
HM
Rare case report data but very positive response
Small- and medium-size dogs: 1-2 RS capsules PO q 24
1 RS capsule PO q 24 h
—
RS and DS, C VM
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Generic Name (Trade Name)
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Indications/Drug Type
Canine Dose
How the Drug Is Supplied
Feline Dose
Comments
0.625 mg/cat PO q 24 h
In most cases, insulin therapy eventually becomes necessary
1.25, 2.5, 5 mg T
Same
50% solution = 500 mg/ mL; do not use if anuria, CHF, severe dehydration
220 mL S
h; big dogs: 1-2 DS capsules PO q 24 h, or 2-4 RS capsules PO q 24 h Glucotrol
(see glipizide)
Glyburide (Diabeta, Micronase, Glynase)
Oral hypoglycemic drug; diabetes mellitus
0.2 mg/kg PO q 24 h
Glycerin 50% solution (oral) (Osmoglyn)
Glaucoma
1-2 mL/kg PO once
Glycerin suppositories
Constipation
1 suppository per rectum
Same or 3 mL — liquid per rectum
OTC, HM
Glycopyrrolate (Robinul)
Anticholinergic preanesthetic agent
0.01 mg/kg SQ, IM, IV
Same
Tachycardia, arrhythmias, intestinal ileus, mydriasis, and photophobia; avoid in narrow-angle glaucoma
0.2 mg/mL I VM,
100 mg/mL I
Glycosaminoglycanpolysulfated Chondroprotective agent; (Adequan)
slows ± helps heal noninfectious, degenerative, and traumatic arthritis
2-4 mg/kg IM twice weekly for 4 weeks; then once every 2-4 weeks
2 mg/kg IM q 4 days for 6 doses; then PRN
Occasional pain at injection site; possibly
HM
HM
HM
VM
Glynase
(see glyburide)
GoLYTELY (polyethylene glycol-electrolyte solution)
Large bowel evacuant/ cathartic
22-33 mL/kg via stomach tube
20-30 mL/kg via stomach tube
Withhold food; Powder or administer twice q 2 h concentrate for apart, 12 hours prior dilution HM to GI endoscopic procedure
Gonadotropin-releasing hormone (GnRH, gonadorelin, Fertagyl, Factrel, Cystorelin)
Male infertility; cryptorchidism/ testicular descent
2.2-3.3 mcg/kg IM
25 mcg/cat IM
Response may be clinical (overt physical signs) or endocrine (2- to 4-fold increase in serum testosterone levels)
50 mcg/mL I VM,
Goodwinol (Rotenone)
Demodicosis (localized)
Apply topically q 24 h
Rotenone, orthophenyl phenol, and benzocaine mixture; efficacy not demonstrated
1.24% Rotenone O
Granisetron (Kytril)
Serotonin 5-HT3 inhibitor antiemetic
0.01 mg/kg IV
Same
HM
VM
1 mg T 1 mg/mL I 0.2 mg/mL S
Same
HM
Gravol
(see dimenhydrinate)
Griseofulvin (Fulvicin)
Dermatophytoses
50-150 mg/kg PO q 24 h to q 12 h; 25-50 mg/kg q 24 h if using microsize product (U/F); 5-15 mg/kg PO q 12 h, if using ultramicrosize product (P/G)
Same
U/F prep better absorbed than regular: therefore, dosage is 50% lower for this formulation; P/G even more so: therefore, dosage is a further 30% lower for this formulation; GI signs, teratogen, granulocytopenia, anemia, hepatopathy
125, 250, 500 mg T; 250, 500 mg microsize formulation T; 125, 165, 250, 330 mg ultramicrosize formulation T; 125 mg/5 mL S VM/HM
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Generic Name (Trade Name)
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Indications/Drug Type
Canine Dose
Growth hormone, human (Protropin, somatrem)
Pituitary dwarfism
0.1 IU SQ q 48-72 h × 4-6 weeks
hCG
(see chorionic gonadotropin, human)
Havidote
(see Calcium EDTA)
Heartgard-30
(see ivermectin)
Hemoglobin glutamer (Oxyglobin)
Bovine hemoglobin-based oxygen-carrying fluid; used for hemolytic, blood loss, or ineffective erythropoietic anemias
Heparin
Heparin, low-molecular-weight
1. Anticoagulation 2. DIC therapy
Anticoagulant
(Dalteparin [Lovenox], Enoxaparin [Fragmin])
10-30 mL/kg IV at 10 mL/kg/h in a one-time single infusion; some administer partial dosages daily instead
Feline Dose
Limited efficacy in dogs because human product often induces autoantibody formation; 3 IU = 1 mg
Not licensed; used IV by some at 15 mL/ kg IV in a slow single dose or daily split doses
1. 200-300 IU/kg SQ 75-150 IU/kg q or IV, q 8 h to q 6 6-8 h h, for thromboembolism; SQ increase PTT to 1.5-2.5 times normal or ACT to 1.2-1.4 times normal 2. 50-100 IU/kg SQ, q 6-8 h
Dalteparin (Fragmin): 100-150 IU/kg SQ q 6-12 h
Dalteparin (Fragmin): 100-150 IU/kg SQ q 6-12 h Enoxaparin (Lovenox): 1 mg/ kg SQ q 6-12 h
Herplex
(see idoxuridine)
Hespan
(see hetastarch)
Hetacillin (Hetacin)
Similar to penicillin
10-20 mg/kg PO q 8 h
Comments
Same
How the Drug Is Supplied 5, 10 mg vials I HM
Overdosage may 125 mL I; cause single-use bags cardiopulmonary VM signs; hemoglobinuria; has no clotting factors; interferes with clinical pathologic testing; half-life in vivo = 18-43 hours Prolongs bleeding time; not thrombolytic; ineffective in the absence of antithrombin III (e.g., protein-losing diseases); “regular” heparin is unfractionated heparin (versus low-molecular-weight heparin)
1000, 2000, 5000, 10,000, 20,000, 40,000 mg/mL I
Outpatient (owneradministered) SQ anticoagulant; main differences versus unfractionated heparin: low-molecular-weight heparin is less antigenic (seemingly not important in VM), and much more expensive; clinical efficacy and advantages not yet proven in VM
Enoxaparin: 100 mg/mL I; 30, 40, 60, 80, 100, 120, 150 mg I (prefilled syringes)
Penicillin reactions
50, 10, 200 mg T
HM
Dalteparin: 10,000 or 25,000 IU/mL I; 2500, 5000, 10,000 IU I (prefilled syringes) HM
VM
Hetacin
(see hetacillin)
Hetastarch 6% (Hespan)
Colloid and plasma volume expansion, shock, sepsis, head trauma
Hu G-CSF
(see filgrastim)
10-20 mL/kg per day IV
10-15 mL/kg per day IV
Rapid IV bolus initially over 5-10 minutes; titrate crystalloids slowly; volume overload possible
500 mL package of 6% hetastarch in 0.9% NaCl I HM
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Generic Name (Trade Name)
Indications/Drug Type
Human chorionic gonadotropin
(see chorionic gonadotropin, human)
Human growth hormone
(see growth hormone, human)
Humulin
(see insulin)
Hycodan
(see hydrocodone)
Hydralazine (Apresoline)
Arteriolar vasodilator, CHF
Canine Dose
Feline Dose
Comments
How the Drug Is Supplied
0.5-3 mg/kg PO q 8-12 2.5-5 mg/cat h total dose PO q 12 h
Hypotension, tachycardia malaise, depression, anorexia
10, 25, 50, 100 mg T; 20 mg/mL S HM
Hydrea
(see hydroxyurea)
Hydrochlorothiazide (HydroDIURIL)
Diuretic, nonhormonal therapy for CDI and NDI, urolithiasis (calcium containing)
2-4 mg/kg PO q 12 h, initially; then decrease by 50% or to q 24 h
1-2 mg/kg PO q 12 h, initially; then decrease by 50% or to q 24 h
Hypokalemia; exacerbates digitalis toxicity; dehydration
25, 50, 100 mg T
Hydrochlorothiazide/ Diuretic plus aldosterone spironolactone (Aldactazide) blocker
Use on basis of 1 mg/ kg of spironolactone PO q 12-24 h
Rarely used
Often used in conjunction with furosemide in chronic, recurrent CHF
25/25 mg T; 50/50 mg T
0.22 mg/kg PO q 6-24 h PRN
Rarely used
Sedation; C-III substance; Hycodan contains hydrocodone 5 mg/tab and homatropine 1.5 mg/ tab; constipation (rare)
5 mg T; 1 mg/mL S
Prolonged use may result in iatrogenic Cushing's syndrome
1% O
Hydrocodone bitartrate (Hycodan)
Narcotic antitussive
HM
HM
HM
Hydrocortisone acetate 1% cream
Topical corticosteroid for focal dermatitis
Apply topically q 6-12 h Same
Hydrocortisone sodium succinate (Solu Cortef)
Intravenously injectable corticosteroid; hypoadrenal crisis
4-5 mg/kg IV acutely and/or 0.5 mg/kg/h IV CRI
HydroDIURIL
(see hydrochlorothiazide)
Hydrogen peroxide 3%
Emetic
0.25-0.5 mL/kg PO (3% solution); repeat once in 5-15 minutes PO if emesis does not occur
Same
Do not use if a caustic 3% topical agent was ingested, if solution HM level of consciousness OTC is decreased, or if the patient is unable to swallow; see Vomiting, Induction of, p. 1364
Hydromorphone (Dilaudid)
Analgesia, preanesthetic
0.1-0.2 mg/kg SQ, IM, or IV once or PRN up to q 2-4 h
Same
Vomiting common immediately postinjection, bradycardia, seconddegree AV block, dysphoria in some cats
1, 2, 4, 10 mg/mL I
Chemotherapeutic compound; disorders of RBC excess, especially polycythemia vera and right-to-left cardiac shunts
20-25 mg/kg PO q 12-24 h; when PCV decreases, then 25-50 mg/kg PO q 48 h and adjust based on PCV
10-15 mg/kg PO q 24 h; then q 48 h based on PCV
Anorexia, vomiting, BM suppression possible; monitor CBC regularly
500 mg C
H1 receptor antihistamine for allergic skin disorders
1-2 mg/kg PO q 8-12 h 0.5-1 mg/kg PO q 12 h to q 8 h
Sedative, anticholinergic side effects
10, 25, 50, 100 mg T; 10 mg/5 mL S; 25, 50 mg/mL I
Hydroxyurea (Hydrea)
Hydroxyzine (Atarax)
HM
100, 250, 500, 1000 mg vials I HM
HM
HM
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Generic Name (Trade Name)
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Indications/Drug Type
Canine Dose
Feline Dose
Comments
How the Drug Is Supplied HM
Hyoscyamine (Levsin)
Antimuscarinic, inhibits propulsive GI motility
Hytakerol
(see dihydrotachysterol)
Ibafloxacin (Ibaflin)
Fluoroquinolone antibiotic
0.003-0.006 mg/kg PO q 8 h
15 mg/kg PO q 24 h
Same; infrequently used
Same
Useful in irritable bowel syndrome and functional intestinal disorders; dry mouth; urinary retention; tachycardia
0.125 mg T; 0.125 mg/5 mL S; 0.375 mg C ER; 0.5 mg/mL I
Packaged as dial-syringe for oral dosing
3% oral gel in 15 mL preloaded syringe
HM
VM
Ibuprofen (Advil, Motrin, Nuprin)
Nonsalicylate, NSAID
Idoxuridine (Herplex, Stoxil)
Used for treating feline herpesviral keratitis, KCS
Ifex
(see ifosfamide)
Ifosfamide (Ifex)
Various neoplasms
Imaverol
(see enilconazole)
Imferon
(see iron dextran injection)
Imidacloprid (Advantage)
Topical treatment for adult and larval stage of fleas
Imidapril (Prilium)
Imidocarb (Imizole)
Imipenem-cilastatin (Primaxin)
Imipramine (Tofranil)
Not recommended
Not recommended
Frequently cause GI OTC, HM bleeding and irritation; many safer alternatives
1 drop q 4 h initially, then q 6-8 h
Occasional ophthalmic irritation
0.1% OS
2 — 350-375 mg/m IV once every 3 weeks for 3 treatments maximum
Efficacy under investigation; dosing interval according to chemo protocol; pretreat with mesna and IV diuresis to reduce risk of hemorrhagic cystitis; neutropenia possible
50 mg/mL I
Apply topically to intact skin; dose monthly by BW from prepackaged cards
Avoid contact with skin, food, or water; avoid eye exposure
9.1% topical solution
Oral liquid formulation (reconstituted lyophilized powder) Veterinary form not available in the United States
2.5, 5, 10 mg/mL S
Painful injection; give IM; cholinergic side effects
120 mg/mL I
Adverse effects possible: GI, CNS, hypersensitivity; reduce dose if renal compromise; different formulations for IV and IM use
250, 500 mg vials I
Same
ACE inhibitor; treatment of heart failure caused by dilated cardiomyopathy or mitral regurgitation
0.25 mg/kg PO q 24 h
Babesia gibsoni, Ehrlichia canis; hepatozoonosis
5-7.5 mg/kg IM or SQ once, repeat in 2-3 weeks
—
Broad-spectrum bactericidal carbapenem antibacterial
2-10 mg/kg slow IV (over 30 minutes), q 6-8 h for 3-5 days
Same
Tricyclic antidepressant; behavioral changes, narcolepsy, cataplexy, inappropriate elimination
0.5-2 mg/kg PO q 8-12 0.5 mg/kg PO q Prolonged onset of h 12-24 h, or total action, drowsiness, dose 2.5-5 mg behavioral changes per cat PO q 12 h
HM
VM
VM
VM
HM
10, 25, 50 mg T; 125 mg/mL I HM
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Generic Name (Trade Name)
Indications/Drug Type
Imizole
(see imidocarb)
Immiticide
(see melarsomine)
Immunoglobulin (Gammagard S/D, human intravenous immunoglobulin G, IVIG)
Treatment of primary immunodeficient states; also IHA, ITP, and CLL
ImmunoRegulin
(see Propionibacterium acnes)
Imodium
(see loperamide)
Impavido
(see miltefosine)
Imuran
(see azathioprine)
Inderal
(see propranolol)
Inocor
(see amrinone)
Insulin (Humulin R, N, U, PZI, Vetsulin, Caninsulin, Glargine)
Diabetes mellitus, diabetic ketoacidosis, severe hyperkalemia
Feline Dose
Comments
0.5-1.5 g/kg slow IV infusion
—
Must be given IV; very 2.5, 5, 10 g single-dose vials I expensive; hypersensitivity; not HM reported as first-line therapy
Regular: 0.5-1 U/kg initially IM or SQ; then q 4-6 h. NPH: 0.5-1 U/kg q 12-24 h SQ. IV CRI protocol: 0.05-0.1 U/kg/h, using regular insulin (Humulin R) only
NPH, Lente, Ultralente, glargine: Total dose (starting): 1-2 U per cat SQ q 24 h to q 12 h
100 U/mL I Dosage variable: adjust and monitor HM, VM accordingly; these are average approximate dosages; maintain hydration; avoid hypoglycemia and hypokalemia
CRI: same
Interceptor
(see milbemycin)
Interferon-alfa (Roferon)
Immune modulator with antiviral and antiproliferative effects; used for FeLV and FAIDS, leukemia, lymphoma, FIP
Interferon-omega (Virbagen) Immunomodulator; parvoviral enteritis, FeLV, FIV Intropin
(see dopamine)
Iodides
(see sodium iodide 20%)
Ipecac syrup
Induce vomiting
Ipodate (Oragrafin)
Irbesartan (Avapro)
How the Drug Is Supplied
Canine Dose
1 IU/5 kg BW, PO every 2 weeks to stimulate appetite
Total dose: 30 IU per cat PO: 7 days on, then 7 days off
Dosages of up to 20,000 IU/cat IM and 2 2 million IU/m SQ (dogs) have been used
3, 5, 6, 9, 10, 18, 36 million IU per vial I HM
2.5 million IU/kg IV q 24 h × 3 d
1 million IU/kg SQ q 24 h × 5 d
10 million IU/vial I
0.25-0.5 mL/kg PO; can repeat once after 5-15 minutes if not vomiting
Not Do not use with recommended in activated charcoal cats; use 3% (ineffective) hydrogen peroxide PO instead
70 mg/mL S; OTC, HM; many oral OTC; 50 mg/mL I
Total dose: 15-100 mg per cat PO q 12 h; titrated based on clinical response and T3
500 mg C
Oral radiographic contrast agent with antithyroid effects; used for hyperthyroidism
—
Angiotensin receptor antagonist
5-60 mg/kg PO q 12 h
VM
Blocks T4 conversion to T3; therefore, blood monitoring = serum T3 levels
HM
HM
75, 150, 300 mg Used in humans T intolerant to ACE inhibitors; efficacy of HM irbesartan has been demonstrated in the dog (RAAS effect) but clinical proof and long-term safety not yet determined
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Generic Name (Trade Name) Iron-dextran injection (Imferon)
Isoproterenol (Isuprel)
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Indications/Drug Type
Canine Dose
Feline Dose
Comments
Iron-deficiency anemia
10 mg/kg in divided doses IM or total dose 100-300 mg PO per day for one dog
Same: IM or total dose 50-100 mg PO per day for one cat
Irritating IM
0.2 mg in 250 mL 5% dextrose, IV CRI at a rate of 0.05-0.1 mcg/ kg/min; titrate to effect, adequate HR
0.2 mg in 250 mL 5% dextrose, IV to effect, adequate HR
Increased HR, increased or decreased BP, CNS stimulation, arrhythmogenic
β-adrenergic agonist
Isoptin
(see verapamil)
Isosorbide dinitrate
Orally administered vasodilator
0.5-2 mg/kg PO q 12 h Same
How the Drug Is Supplied Many oral OTC; 50 mg/mL I HM
0.2 mg/mL (= 200 mcg/mL) I HM
5, 10, 20, 30, 40 No recognized therapeutic efficacy in mg T small animals HM
Isotretinoin (Accutane)
Sebaceous adenitis, keratinization disorders, mycosis fungoides, feline acne
1-2 mg/kg PO q 12 h; reduce dosage after 1 month if improving
Total dose: 5-10 GI and CNS effects mg PO q 24 h may occur, if so, per cat reduce dosage by 50% or stop; teratogen; KCS in dogs; other mucocutaneous side effects
10, 20, 40, mg C HM
Isuprel
(see isoproterenol)
Itraconazole (Sporanox)
Antimycotic fungistatic imidazole compound for blastomycosis, coccidioidomycosis, cryptococcosis; histoplasmosis M. canis, dermatophytosis, candidiasis
5-10 mg/kg PO q 24 h
Same
100 mg C; 10 Long-term therapy mg/mL S (months or more) often required; must HM be taken with food; open capsules and place pellets in food if necessary; antacid GI drugs will reduce efficacy (decrease absorption); monitor liver status
Ivermectin (Heartgard-30, Heartgard Plus, Ivomec)
GABA agonist, antiparasiticide
1. HW prophylaxis: 0.006 mg/kg (6 mcg/ kg) PO, once monthly
HW prophylaxis: 0.024 mg/kg (24 mcg/kg) SQ; repeat in 3-4 weeks (usually under 0.1 mL)
Do not use in collies or other dogs sensitive to drug (exception: collies and similar breeds usually tolerate low [HW prophylaxis] dose); CNS, vomiting, anaphylaxis; can give injectable solution PO; of questionable value in treating feline heartworm disease; consider testing individual patients prior to treatment for the MDR-1 gene mutation if ivermectin is the treatment of choice in patients where susceptibility to toxicosis is possible (see pp. 706 and 625)
1. Heartworm prophylaxis, microfilaricide 2. Heartworm 3. Endoparasites 4. Sarcoptic mange 5. Demodectic mange 6. Otodectic mange 7. Cheyletiellosis
2. HW microfilaricide; 0.05 mg/kg (50 mcg/ kg) once PO, 2-4 weeks after adulticide Tx 3. 0.2 mg/kg (200 mcg/ Same kg) PO 4. 0.3 mg/kg (300 mcg/ Same kg) PO or 0.2 mg/kg (200 mcg/kg) SQ 2 times, 14 days apart 5. 0.05 mg/kg (50 mcg/ Same kg) PO; increase to 0.3 mg/kg (300 mcg/ kg) by day 5; increase to 0.6 mg/kg (600 mcg/kg) once daily PO after 30 days if necessary
68, 136, 272 mcg T or chewables; 10 mg/mL (= 10,000 mcg/ mL) I VM
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Generic Name (Trade Name)
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Indications/Drug Type
Canine Dose
Feline Dose
Comments
How the Drug Is Supplied
6. 0.3 mg/kg (300 mcg/ Same kg) PO, SQ 2 times at 14 days apart 7. 0.3 mg/kg (300 mcg/ Same kg) SQ 2 times at 21 days apart Ivomec
(see ivermectin)
Jenotone
(see aminopropazine)
Kaolin Pectin
GI tract protectant
Kabikinase
(see streptokinase)
Kaon
(see potassium salts oral supplement)
KBr
(see bromide)
Keflex
(see cephalosporin antibiotics)
Kenalog
(see triamcinolone)
Keppra
(see levetiracetam)
Ketamine HCl (Ketaset, Vetalar)
Dissociative anesthetic agent; short-action when given IV in healthy dogs/cats: 10-20 minutes
Ketaset
(see ketamine)
Ketoconazole (Nizoral)
Ketoprofen (Orudis KT; Ketofen)
1-2 mL/kg PO q 2-6 h
Same
May limit absorption of other medications; limited efficacy
Many OTC preparations; T/S
100 mg/mL I
VM, HM
When diazepam (at diazepam dose of 0.5 mg/kg) given IV first: immediately follow with ketamine 5-7 mg/kg IV bolus for sedation and minor procedures (diazepam [5 mg/mL]: ketamine combination in ratio of 1:1 → use 0.5 mL/10 kg of each [in separate syringes] IV)
Restraint: 11 mg/kg IM; anesthesia (but does not provide deep analgesia): 22-33 mg/kg IM or 2.2-4.4 mg/kg IV
Eyes remain open: use ophthalmic ointment; salivation, seizures, respiratory depression, laryngospasm, hypothermia; do not use with renal failure or glaucoma; reduce dose by 50%-75% if stable but systemically ill; avoid if hypertrophic cardiomyopathy; controlled drug
Antifungal agent; protothecosis; inhibits glucocorticoid synthesis
10-15 mg/kg PO q 12 h; long-term 10 mg/kg PO q 24 h; hyperadrenocorticism Rx: 15 mg/kg PO q 12 h
5-10 mg/kg q 12 h PO or q 24 h; long term: 10 mg/kg q 48 h PO
200 mg T Anorexia, nausea, vomiting, constipation, HM hepatotoxicity; monitor liver status; begin lower and titrate upwards to reduce risk of side effects; must be given with food (for good absorption); drug interaction potential: DMSO inhibitor; antacids decrease absorption
NSAID
0.5-1 mg/kg PO q 12 Same h; 1-2 mg/kg SQ, IM, or IV once or q 24 h up to 3 days maximum
GI ulceration, renal effects possible
VM, HM
25, 50, 75 mg C; 12.5 mg T, HM, OTC; 5, 10, 20 mg T; 10, 100 mg/mL I, VM (not approved in United States) OTC, VM
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Generic Name (Trade Name)
Indications/Drug Type
Canine Dose
Feline Dose
Comments
How the Drug Is Supplied
Kitten Milk Replacer (KMR)
Milk replacement
—
30 mL per ¼ lb BW PO daily, divided into 3-6 meals
—
OTC, VM
Klonopin
(see clonazepam)
KMR
(see kitten milk replacer)
Kytril
(see granisetron)
Lactulose (Cephulac, Chronulac)
Hepatic encephalopathy is treated by acidifying colon contents, trapping NH4 that is then expelled; the drug is also a stool softener
0.25-0.5 mL/kg
Total dose: 1-5 mL PO q 8 h per cat
666 mg/mL S Loose stools/diarrhea; HM flatulence; cramping; may use per rectum in patients with hepatic coma
Lacrilube
(see artificial tears ointment)
Lamprene
(see clofazimine)
Lanoxin
(see digoxin)
Lansoprazole (Prevacid)
Proton pump inhibitor; gastric ulceration
PO q 8-12 h As a retention enema: total volume = 10-20 mL/kg (consisting of 3 parts lactulose plus 7 parts water) per rectum
Enema: same as for dog
1 mg/kg IV q 24 h
Same
Usage less well-documented in VM compared to omeprazole
15, 30 mg C
Generally effective and potent; may combine with oral carbonic anhydrase inhibitor; 1 drop = approximately 0.0015 mg
0.05 mg/mL OS
Large amounts daily could result in malabsorption (e.g., fat-soluble vitamins)
OTC, S, VM
6 mg/mL I HM
Lantus
(see insulin glargine)
Lasix
(see furosemide)
Latanoprost (Xalatan)
Topical prostaglandin analog used in the treatment of glaucoma
1 drop to affected eye, q 12-24 h
—
Laxative paste (Laxatone, Cat-a-Lax, etc.)
Oral laxative, hairball Tx
½-2 inches PO daily until not constipated, then weekly or PRN
Same
Leflunomide (Arava)
Autoimmune disorders (IHA, ITP, sterile meningitis, systemic histiocytosis)
1.5-4 mg/kg PO q 24 h —
10, 20, 100 mg T Beneficial and adverse effects HM variably documented to date; GI and BM effects possible; seek trough serum level of 20 mcg/mL
Leucovorin
Reversal of methotrexate activity; sulfa-associated myelotoxicosis
5-15 mg per dog PO
Higher/repeated doses may be indicated for methotrexate toxicosis; can assess plasma methotrexate levels
Leukeran Levamisole (Levasole, Ripercol, Tramisol)
1 mg/kg q 24 h
HM
5, 15, 25 mg T 3, 10 mg/mL I 50, 100, 350 mg vials I HM
(see chlorambucil) 1. Heartworm microfilaricide 2. Immune stimulant 3. Feline lungworm
1. 10 mg/kg PO q 24 h 7-14 days as a microfilaricide 2. 2.5-5 mg/kg PO q 48 h for immune modulation
2.5-5 mg/kg PO q 48 h for immune modulation;
Salivation, vomiting, shock-like syndrome with excessive microfilaricide death, 10-20 mg/kg PO q neurotoxic, sudden 48 h for death; not FDA
184 mg T; 136 mg/ mL S; 11.5% gel VM
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Generic Name (Trade Name)
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Indications/Drug Type
Canine Dose
Feline Dose
Comments
How the Drug Is Supplied
Aelurostrongylus and Capillaria
approved for small animal medicine
50 mg T HM
Levarterenol
(see norepinephrine)
Levasol
(see levamisole)
Levetiracetam (Keppra)
Third-line anticonvulsant for refractory seizures
20 mg/kg PO q 8 h, in addition to KBr and phenobarbital
—
Few adverse effects reported; can be up-titrated if starting dose ineffective; expensive
250, 500, 750, 1000 mg T 100 mg/mL S 100 mg/mL I HM
Levophed
(see norepinephrine)
Levothyroxine sodium (Soloxine, Synthroid, thyroxine)
Synthetic thyroid hormone replacement therapy
0.04 mg/kg PO q 12 h Myxedema coma: 0.005 mg/kg slow IV q 12 h
Total dose: 0.05-0.1 mg PO q 24 h per cat
Thyrotoxicosis; do not give only on basis of low T4 (assess clinical signs and other lab results); adjust dose based on response and blood levels; concurrent antiepileptics (e.g., phenobarbital) may affect levels; maximum dose for largest dog: 0.8 mg PO q 12 h
0.025, 0.05, 0.075, 0.125, 0.15 mg T HM 0.2, 0.5 mg/mL I 0.1, 0.2, 0.3, 0.4, 0.5, 0.6, 0.8 mg T VM
Levsin
(see hyoscyamine)
Lidocaine (Xylocaine)
Ventricular arrhythmias, local anesthesia
2-4 mg/kg IV over 1-2 minutes, then 0.5-2 mg/kg every 20-60 minutes, or 0.04-0.08 mg/kg/min (40-80 mcg/kg/min) CRI IV; inject up to 4 mg/kg SQ for local anesthesia
0.25-1 mg/kg slowly over 5 minutes; give 1-4 mg bolus maximum over 5 minutes; use diluted solution as CRI 0.01-0.04 mg/ kg/min (10-40 mcg/kg/min)
20 mg/mL I Give initial bolus slowly; seizures, HM hypotension; use lidocaine preparations without epinephrine for cardiac arrhythmia therapy; use only for life-threatening arrhythmias
Lime sulfur solution (LymDyp, Sulfodip)
Bacterial and fungal dermatosis, sarcoptic mange
Dip once to twice weekly; let air dry; use 4-6 weeks (ideally until 2-3 fungal cultures are negative)
Same
Offensive odor; stains 2% dip furniture; wear gloves VM to avoid hypersensitivity
Lincocin
(see lincomycin)
Lincomycin (Lincocin)
Staphylococcal and 15-25 mg/kg PO, IV, anaerobic infections, some IM q 8-12 h Mycoplasma infections
Same
Vomiting, hepatotoxicity; do not use in combination with chloramphenicol or erythromycin
100, 200, 500 mg T; 50 mg/mL S; 100 mg/mL I
Monitor BUN, creatinine; lethargy, anorexia
2.5, 5, 10, 20, 40 mg T
Liothyronine, T3
(see triiodothyronine)
Liquiprin
(see acetaminophen)
Lisinopril (Zestril, Prinivil)
ACE inhibitor; CHF, protein-losing nephropathy
Lithane
0.5-0.75 mg/kg PO q 24 h
0.25 mg/kg PO q 24 h
HM, VM
HM
(see lithium carbonate)
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Generic Name (Trade Name)
Indications/Drug Type
Canine Dose
Feline Dose
Comments
Lithium carbonate (Eskalith, Lithane, Lithotabs)
Increased production of all cell lines by BM
21-26 mg/kg per day PO
Unknown
Nausea, diarrhea, vertigo
How the Drug Is Supplied 300 mg C; 450 mg T ER HM
Lithotabs
(see lithium carbonate)
Lodine
(see etodolac)
Lomotil
(see diphenoxylate with atropine)
Lomustine (CCNU, CeeNu)
Nitrosourea alkylating agent for brain tumors, mast cell tumors, relapse or failure to respond to lymphoma therapy
60-90 mg/m PO once every 3 weeks
—
Opiate antidiarrheal, acute colitis
0.1-0.2 mg/kg
0.1-0.15 mg/kg
PO q 8 h
PO q 12 h
0.02-0.1 mg/kg PO q 8-24 h PRN
0.125-0.25 mg/cat PO q 12-24 h
Loperamide (Imodium)
Lopid
(see gemfibrozil)
Lopressor
(see metoprolol)
Lorazepam (Ativan)
Benzodiazepine; anxiolytic. Phobias, anxiety disorders
2
Neutropenia may develop after 7 days; GI adverse effects, anemia; its active metabolites reach the CNS
10, 40, 100 mg C
Discontinue if not effective within 48 hours; collie sensitivity; CNS adverse effects possible in dogs and cats (see p. 706)
2 mg C;
HM
1 mg/5 mL S HM, OTC
0.5, 1, 2 mg T 2 mg/mL S 2, 4 mg/mL I HM
Losec
(see omeprazole)
Lotensin
(see benazepril)
Lotrimin
(see clotrimazole)
Lovenox
(see heparin-low molecular weight)
Lufenuron (Program)
Insect development inhibitor; inhibits chitin synthesis 1. Prevents flea eggs from developing into adults 2. Coccidioidomycosis 3. Dermatophytosis
Lutalyse
(see prostaglandin F2-α)
Lym-DYP
(see lime sulfur solution)
Lyrica
(see pregabalin)
Lysine
Herpesviral keratitis palliation
Administer PO in conjunction with food. 1. 10 mg/kg PO once every 30 days 2. 5-10 mg/kg PO q 24 h 3. 54-100 mg/kg PO once q 2-4 wk
30 mg/kg PO once monthly or 10 mg/ kg once every 6 months by SQ injection 51-266 mg/kg PO once
Expensive as long-term daily Tx for fungal disease; efficacy in dermatophytosis questionable; may be combined with milbemycin for control of fleas, heartworms, roundworms, whipworms
250-500 mg/day Lifelong therapy for in food lifelong infection
Sold in packets for varying BW by T, S, or 10 mg/mL T or I
Many sizes and formulations OTC VM, HM
Lysodren
(see o,p′-DDD)
Macrobid
(see nitrofurantoin)
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Generic Name (Trade Name)
Indications/Drug Type
Macrodantin
(see nitrofurantoin)
Magnesium hydroxide (Milk of Magnesia)
Antacid, laxative
Magnesium sulfate
Hypomagnesemia
Mannitol 20%
Marbofloxicin (Zeniquin)
How the Drug Is Supplied
Canine Dose
Feline Dose
Comments
Total dose: 5-10 mL PO q 4-6 h per dog
—
Cathartic agent at 3-5× the antacid dosage; rarely used because high dosing frequency and rebound acid secretion
77.5 mg/g S
0.75-1 mEq/kg/d as IV Same CRI; for hypomagnesemiaassociated life-threatening ventricular arrhythmias: 0.15-0.3 mEq/kg slow IV (15-30 minutes) while monitoring for adverse effects
Monitor for acute toxicosis: increased QT interval on ECG; lethargy, hypotension, weakness, collapse
100 mg/mL
Osmotic diuretic used for treating acute glaucoma, cerebral edema, and oliguria/ anuria; aids in elimination of certain toxins (e.g., ethylene glycol)
0.5-1 g/kg IV slowly over 15-20 minutes for anuria; double dosage for acute glaucoma or cerebral edema
Same
Rehydrate patient prior to use; can repeat twice if urine output is not increased; resolubilize (by warming) if crystallized, ensuring to cool to body temperature before administering; overzealous use: circulatory overload/ pulmonary edema
100 mg/mL (10%); 200 mg/mL (20%) I
Fluoroquinolone class antibiotic
2-4 mg/kg PO q 24 h
Same
Anorexia and vomiting; not recommended for rapidly growing dogs (possible arthropathy); caution in seizure patients (as with all fluoroquinolones)
25, 50, 100, 200 mg T
Marin
(see silymarin)
Maropitant (Cerenia)
Antiemetic (motion sickness, enteritis, etc.); neurokinin-1 antagonist
Marquis
(see ponazuril)
Matulane
(see procarbazine)
Maxitrol
(see dexasporin)
MCT oil
(see medium chain triglycerides)
Mebendazole (Telmintic)
Hookworm, whipworm, and roundworm
1 mg/kg SQ or 2 mg/ kg PO; up to 5 days
22 mg/kg with food once daily for 3 days
OTC, HM
(0.8 mEq/mL), 125 mg/mL (1 mEq/mL), 500 mg/mL (4 mEq/mL) I HM
HM, VM
VM
Not approved; experimental report: single dose 1 mg/kg PO, SQ, or IV was safe and effective in cats
16, 24, 60, 160 Pain at injection site common; refrigeration mg T may help.
—
Repeat as indicated; V/D may develop; hepatopathies have been incriminated in a small number of cases
10 mg/mL I
40 mg/g powder VM
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Generic Name (Trade Name)
Indications/Drug Type
Canine Dose
Feline Dose
Comments
Meclizine (Bonine, Dramamine II, Antivert)
Antiemetic, motion sickness
1.25 mg/kg PO q 24 h
12.5 mg per cat PO q 24 h
Lethargy, CNS depression possible
Medetomidine (Domitor)
Synthetic α-2 adrenoreceptor agonist; provides sedationanalgesia as chemical restraint for healthy exercise tolerant dogs; useful for sedation of cats that have compensated (“asymptomatic”) hypertrophic cardiomyopathy
0.005-0.02 mg/kg (5-20 µg/kg) IM as a single agent; used by some at half or quarter dose in combination with butorphanol, ketamine, morphine, or oxymorphone
0.02 mg/kg (20 µg/kg) IM
Do not use if 1 mg/ml I VM hypertensive; allow dog or cat to rest quietly after administration; do not use in older, younger (45 kg respectively. Begin 30 days before proestrus to suppress estrus.
100 mcg/mL S Do not use in pregnant dogs or in VM those with hepatic or renal disease. Pseudocyesis: multiply dosage by 10, and administer for 5 days.
Miconazole (Conofite)
Topical antifungal
Apply q 12 h to lesion; Same continue after resolution of lesions for 2 weeks
Contact hypersensitivity; caution: re. zoonosis if dermatophytosis (wear gloves)
Micro-K extencaps
(see potassium salts)
Micronase
(see glyburide)
Midazolam (Versed)
Benzodiazepine tranquilizer; 3-4× more potent than diazepam
Midol
(see acetaminophen)
Midriacyl
(see tropicamide)
Mifepristone (Mifeprex, RU-486)
Progesterone receptor antagonist
Milbemycin (Interceptor)
1. Anthelmintic action in HW prevention, HW microfilaricide, hookworm, and roundworm control 2. Demodicosis 3. Pneumonyssoides caninum
Canine Dose
Comments
How the Drug Is Supplied
OTC, topical cream, and solution HM
Preanesthetic dose: 0.1-0.3 mg/kg IV, IM, SQ (lower end of range if IV)
0.05-0.3 mg/kg Caution if liver IV, IM, SQ (mid- disease, avoid if to lower end of glaucoma range if IV and/or if combined with ketamine)
1 mg/mL, 5 mg/mL I
2.5 mg/kg PO
—
200 mg T
Abortifacient
q 12-24 h for 5 days 1. 0.5-1 mg/kg orally once monthly 2. 0.5-2.3 mg/kg PO q 12-24 h 2-4 weeks for demodicosis, longer if skin scrapings fail to clear mites; may use low dose for 30 days, twice after if necessary 3. 0.5-1 mg/kg per week for 3 weeks
Milk of Magnesia
(see magnesium hydroxide)
Milk thistle extract
(see silymarin)
Miltefosine (Miltex, Impavido)
Antiprotozoal; leishmaniasis
Minipress
(see prazosin)
Mintezol
(see thiabendazole)
Mirtazapine (Remeron)
Tricyclic antidepressant drug used for appetite stimulation, particularly in cats
0.6 mg/kg PO q 24 h
Prostaglandin E-1 analog; used for gastric ulcers
2-8 mcg/kg PO q 8-12 h
Misoprostol (Cytotec)
Feline Dose
HM
HM
—
2 mg/kg PO q 24 h × 4 weeks
Also available as otic formula (Milbemite) and compounded with lufenuron (Sentinel) and lufenuron plus nitenpyram (Sentinel with Capstar)
2.3, 5.75, 11.5, 23 mg T
Coadministered with allopurinol 20 mg/kg PO q 24 h (allopurinol for 6-12 months)
50 mg C
0.1% otic solution VM
HM
7.5, 15, 30, 45 mg T
3-4 mg/cat PO q 72 h maximum
HM
—
Secretory diarrhea, vomiting, anorexia;
100, 200 mcg T HM
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Indications/Drug Type
Canine Dose
Feline Dose
(especially those associated with NSAID use)
Mitaban
(see amitraz)
Mitotane
(see o,p′ DDD)
Mitoxantrone (Novantrone)
Chemotherapeutic agent closely related to doxorubicin but no cumulative cardiotoxicity
Mobic
(see meloxicam)
Morphine sulfate
Narcotic analgesic; acute CHF as adjunctive therapeutic agent to relieve anxiety
Comments
How the Drug Is Supplied
may induce abortion in pregnant mammals (also avoid client exposure); side effects are dose dependent
2
5 mg/m once every 3 weeks IV
2
6.25 mg/m once every 3 weeks IV
0.1-1 mg/kg q 2-6 h 0.05-0.2 mg/kg IM, SQ, IV, epidural; or IM, SQ q 2-6 h sustained-release 1.5-3 mg/kg PO q 12 h (ER)
Depression, GI signs, leukopenia, hepatotoxicity, extravasation injury
2 mg/mL I
Hyperexcitability in cats; vomiting, respiratory, and CNS depression; hypotension, especially if given IV; constipation
30 mg ER; 5, 10
HM
20 mg suppository; 10, 20 mg/5 mL S; 15, 30 mg T: 2, 4, 5, 8, 10, 15 mg/mL I HM
Motrin Moxidectin (Proheart)
(see ibuprofen) 1. Avermectin antiparasitic 2. Heartworm prophylaxis, demodicosis
Mucomyst
(see acetylcysteine)
Mycelex
(see clotrimazole)
Mycophenolate mofetil (CellCept)
Immunosuppression via inhibition of T- and B-cell proliferation; steroidresponsive meningitisarteritis, necrotizing encephalitis, other immune-mediated disorders
Mycostatin
(see nystatin)
Mydriacyl
(see tropicamide)
Mylepsin
(see primidone)
Myleran
(see busulfan)
Naloxone (Narcan)
Narcotic antagonist
Naltrexone (ReVia)
Nandrolone decanoate (Deca-Durabolin)
1. HW prevention: 3 mcg/ kg PO once monthly 2. Demodicosis: 0.2-0.4 mg/kg PO q 24 h
—
Available compounded with imidacloprid as Advantage Multi
30, 68, 136 mcg T; large animal product available as 11.3-g tube VM
20 mg/kg PO q 12 h; — reduce to 10 mg/kg PO q 12 h after 3-4 weeks if ongoing treatment
Reported adverse effects include hemorrhagic diarrhea, vomiting, and myelosuppression
250 mg C, 500 mg T, 250 mg/mL I
0.004-0.04 mg/kg IV, IM, SQ
Repeat dosing if prolonged action of narcotic
0.02, 0.4, 1 mg/mL I
25-50 mg PO q 24 h per cat
Contraindicated in hepatopathies; antagonizes opiate drugs (e.g., certain antitussives, antidiarrheals)
50 mg T
0.5-1 mg/kg per week IM
Give deep IM; do not administer to pregnant or hepato-
100 and
Partial opiate antagonist; certain behavioral disorders
1-2.2 mg/kg PO
Anabolic steroid and bone marrow stimulant (erythropoiesis only)
1 mg/kg/week IM
q 12-24 h
Same
HM
HM
HM
200 mg/mL I
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Indications/Drug Type
Canine Dose
Feline Dose
Comments insufficient animals or animals with hormone-sensitive tumors; C-III drug
Naprosyn
(see naproxen)
Naproxen (Naprosyn, Aleve)
NSAID
1.2-2.8 mg/kg PO q 24-96 h
Narcan
(see naloxone)
Naxcel
(see ceftiofur)
Nembutal
(see pentobarbital)
Nemex
(see pyrantel pamoate)
Neomycin (Biosol)
Aminoglycoside used orally 10-20 mg/kg PO q for SIBO, hepatic 8-12 h encephalopathy
Neoral
(see cyclosporinesystemic)
Neosar
(see cyclophosphamide)
Neostigmine (Prostigmin)
Anticholinesterase agent for myasthenia gravis
0.01-0.05 mg/kg IM, SQ PRN
Do not use
Severe GI ulceration/ perforation very common; renal, CNS; not a preferred drug; serum half-life is 32-92 hours in dogs; many safer alternatives
How the Drug Is Supplied HM
200, 250, 375, 500 mg T; 125 mg/5 mL S HM
Same
25, 200 mg/mL S; Ototoxicity and 100, 500 mg, T nephrotoxicosis are rare with oral dosage; VM, HM in severe intestinal disease, toxicosis may be more likely (systemic absorption)
Same
Muscarinic effects: vomiting, diarrhea, bradycardia are reversed by atropine
0.25, 0.5, 1, 2 mg/ mL I; 15 mg T HM
Neo-Synephrine
(see phenylephrine)
Neptazane
(see methazolamide)
Neupogen
(see filgrastim)
Neurontin
(see gabapentin)
New methylene blue
(see methylene blue)
Nexium
(see esomeprazole)
Niacinamide (nicotinamide)
Usually used in combination with a tetracycline for immunemediated dermatopathies
10 kg: 500 mg PO q 8 h
—
Niclosamide (Yomesan)
Tapeworm anthelmintic
154 mg/kg PO; fast 24 hours before; repeat in 2-3 weeks
Same
Occasionally soft stools; generally replaced by praziquantel
Nicotinamide
(see niacinamide)
Nilstat
(see nystatin)
Nipride
(see nitroprusside)
Nitenpyram (Capstar)
Flea adulticide; inhibits insect specific nicotinic receptors
Dogs up to 11 kg: total dose 11.4 mg PO per dog, maximum q 24 h;
Total dose: 11.4 mg PO per cat, max. q 24 h
Onset of action: rapid 11.4, 57 mg T (minutes to hours), VM but duration of activity
GI adverse effects possible
50, 100, 125, 250, 500 mg T HM
VM
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Indications/Drug Type
Canine Dose
Feline Dose
dogs >11 kg: total dose 57 mg PO per dog, maximum q 24 h Nitrofurantoin (Furadantin, Macrobid, Macrodantin)
UTIs
4 mg/kg PO q 8 h
Comments
How the Drug Is Supplied
limited (day[s])
Same
Oral form used only for UTIs; GI, hepatotoxicity
50, 100 mg T; 5 mg/mL S; 25, 50, 100 mg macrocrystals C HM
1
Apply /8- to ¼-inch strip q 8 h topically to skin
2% O May cause hypotension; apply HM with glove to hairless region (i.e., pinna or inguinal area); clinical efficacy questionable; nitrate tolerance/loss of efficacy in 48 hours
Arterial dilator, venodilator; 1-7 mcg/kg/min IV CRI reduces preload and afterload in CHF
1-2 mcg/kg/min IV CRI
Hypotension; use 2-3 days IV maximum; avoid extravasation
50 mg/vial I
H2 receptor antagonist
2.5-5 mg/kg PO q 24 h (for colonic motility effects)
Has GI prokinetic effects (via anticholinesterase activity)
75 mg T
Nitroglycerin 2% ointment (Nitrol ointment)
Transdermal venodilator for reducing cardiac preload in acute CHF
Nitrol ointment
(see nitroglycerin)
Nitroprusside (Nipride, Nitropress) Nizatidine (Axid)
Apply ¼-2 inch strip q 6-8 h topically to skin
5 mg/kg PO q 24 h
HM
150, 300 mg C 15 mg/mL S HM
Nizoral
(see ketoconazole)
Nolvasan
(see chlorhexidine)
Norepinephrine (Levophed, Levarterenol)
β1- and α-agonist; used for treating shock
Norpace
(see disopyramide)
Norvasc
(see amlodipine)
Novantrone
(see mitoxantrone)
Novin
(see dipyrone)
Numorphan
(see oxymorphone)
Nuprin
(see ibuprofen)
Nystatin (Nilstat, Mycostatin, Topical antifungal, oral Nystex) candidiasis
Nystex
(see nystatin)
Octreotide (Sandostatin)
Somatostatin analog with primary inhibitory effect on intestinal and pancreatic secretions; insulinoma, glucagonoma
Ocufen
(see flurbiprofen)
Ofloxacin (Ocuflox)
Topical fluoroquinolone antibiotic for ophthalmic use
1-2 mg in 250 mL of 0.9% NaCl, IV CRI to effect
None
50,000-150,000 IU PO q 6-8 h
100,000 IU PO q6h
Total dose: 10-40 mcg (0.01-0.04 mg) SQ q 8 h per dog
1 drop topically in affected eye q 12 h; adjust as necessary
Hypertension, tachycardia
1 mg/mL I
Fungicidal; not appreciably absorbed in GI tract, so useful for topical oral application
100,000 IU/mL S
Nausea, vomiting, abdominal discomfort
50, 100, 200, 500 mcg/mL I
HM
HM
HM
Same
Bactericidal G− and G+
3 mg/mL OS HM
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Indications/Drug Type
Canine Dose
Feline Dose
Comments
How the Drug Is Supplied
Salicylate; antiinflammatory activity in ulcerative colitis (5-ASA)
5-20 mg/kg PO q 8 h
Unknown
(see sulfasalazine)
250 mg C
Omeprazole (Prilosec, Losec)
Proton pump acid blocker; used in reflux esophagitis and hyperacidity syndromes
0.7 mg/kg PO q 24 h
Oncovin
(see vincristine)
Ondansetron (Zofran)
5-HT3 receptor antagonist (serotonin inhibitor); used in conjunction with emetogenic cancer chemotherapy; used in protracted vomiting unresponsive to other treatments
0.1-0.2 mg/kg IV bolus q 12 h
o,p′ DDD (Lysodren, Mitotane)
Hyperadrenocorticism; selective necrosis of the zonae fasciculata and reticularis of the adrenal gland
25 mg/kg PO q 12 h with food to effect (approximately 5-10 days); then 25-50 mg/kg once every 7-14 days to effect (based on monitoring adrenocortical function); give with food
None
Optimmune
(see cyclosporineophthalmic)
Oragrafin
(see ipodate)
Oral rehydration solution (ORS: Pedialyte)
Oral electrolyte and glucose replacement
Up to maintenance (60 mL/kg per day PO) and replacement (based on physical exam); PO divided into several doses as low-cost rehydration/ volume expansion
Same
Orbax
(see orbifloxacin)
Orbifloxacin (Orbax)
Fluoroquinolone antibacterial
Olsalazine (Dipentum)
Ormetoprimsulfadimethoxine
(see sulfadimethoxine/ ormetoprim)
ORS
(see oral rehydration solution)
Orthocide
(see captan powder 50%)
Orudis KT
(see ketoprofen)
Osaterone (Ypozane)
Benign prostatic hyperplasia
HM 10, 20, 40 mg C
Total dose: 5 mg per cat PO q 24 h
Few side effects noted
Same
4, 8 mg T; 2 Used before and for 48 h following specific mg/mL I; 1.25 mg/mL S IV cancer Tx
HM
HM
2.5-7.5 mg/kg PO q 24 Same h
2.5 mg/kg PO q 24 h × 7 days
Vomiting, diarrhea, weakness, glucocorticoid ± mineralocorticoid deficiency; hepatotoxicity; best if given in divided doses; insulin dose in diabetes may need to be altered (see p. 1566)
500 mg T
—
Many
VM
HM, OTC
May cause arthropathy in immature dogs; caution in seizure patients (as with all fluoroquinolones)
5.7, 22.7, 68 mg T
Remission of signs of benign prostatic hyperplasia for 6 months in approximately 83% of cases
1.875, 3.75, 7.5, 15 mg T
VM
VM
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Generic Name (Trade Name)
Indications/Drug Type
Canine Dose
Oseltamivir (Tamiflu)
Antiviral; canine influenza
1 mg/kg PO q 24 h
Osmoglyn
(see glycerin 50% solution [oral])
Ovaban
(see megestrol acetate)
Oxacillin (Prostaphlin)
Penicillin derivative used for staphylococcal skin infections
Feline Dose
22-40 mg/kg PO q 8 h; Same 15-20 mg/kg IV q 6-8 h
Comments
How the Drug Is Supplied
Not approved for dogs; controversial (viral resistance; may be needed in human outbreak)
30, 45, 75 mg C
Best if not given with food; GI upset possible
250 mg/5 mL S; 250, 500 mg C; 250, 500 mg 1, 2 gI
12 mg/mL S HM
HM
Oxazepam (Serax)
Oxtriphylline (Choledyl)
Appetite stimulant (oral benzodiazepine agent)
Bronchodilator (theophylline derivative)
—
4-10 mg/kg PO q 8 h
Total dose: 2.5 mg per cat PO once; do not use long term, can lead to hepatotoxicity
Overdosage results in 10, 15, 30 mg C; 15 mg T sedation and incoordination
4-10 mg/kg PO q8h
Vomiting, diarrhea, hyperexcitability
HM
100, 200 mg T; 400, 600 mg ER HM
Oxydex
(see benzoyl peroxide)
Oxyglobin
(see hemoglobin glutamer)
Oxymorphone (Numorphan)
Narcotic agonist for analgesia, anesthetic induction, and minor procedures
Preanesthesia: 0.1-0.2 mg/kg IM, SQ; 0.02-0.05 mg/kg IV; analgesia: 0.03-0.2 mg/kg IV, IM, SQ PRN
0.01-0.1 mg/kg IV, IM, SQ PRN
Respiratory and CNS depression; hypotension, sedation, bradycardia, feline hyperexcitability; panting (dogs); reverse with naloxone
1, 1.5 mg/mL I
Do not use in pregnancy (last trimester) or in first month of life (dental staining); GI side effects; photosensitivity; caution with liver and kidney disease; do not administer with antacids, dairy products, or intestinal adsorbents
50, 125 mg/mL I; 250 mg C
HM
Oxytetracycline (Terramycin) Broad-spectrum bacteriostatic agent; also used for rickettsiae, Mycoplasma spp., spirochetes, and chlamydiae; used for treating SIBO
10-20 mg/kg PO q 8 h to q 6 h; as OO, apply q 12 h to q 6 h
Same
Oxytocin (Pitocin, Syntocinon)
Obstetrics (uterine inertia): 5-25 U IM total dose, every 30 minutes, or 1-2 U/kg; milk production: 2-10 U IM or via intranasal spray
Obstetrics: 2 U/kg IM, every 30 minutes; milk production: 1 U IM
Do not use if birth canal obstructed; refrigerate vial and warm syringe before injection
10 U/mL I; 40 U/mL nasal spray
0.65-2 mg/kg diluted in 0.9% NaCl and give as IV CRI
—
Avoid calciumcontaining fluids like LRS
30, 60, 90 mg vials I
Pituitary hormone used for uterine inertia; to stimulate milk flow; vasopressive effects and as an antidiuretic
Oxtriphylline
(see choledyl)
Palladia
(see toceranib)
Pamidronate (Aredia)
Bisphosphonate compound; hypercalcemia (e.g., due to
HM
HM
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Indications/Drug Type
Canine Dose
Feline Dose
Comments
cholecalciferol intoxication) Pamprin
(see acetaminophen)
Panacur
(see fenbendazole)
Panadol
(see acetaminophen)
Pancreatic enzymes (Pancrelipase, Viokase)
Pancreatic exocrine insufficiency
Pancrelipase
(see pancreatic enzymes)
Pantoprazole (Protonix, Pantoloc)
Injectable proton pump inhibitor
Paracetamol
(see acetaminophen)
Paramite
(see phosmet dip)
Paraplatin
(see carboplatin)
Paregoric
Opiate antidiarrheal
Parlodel
(see bromocriptine)
Paroxetine (Paxil)
Selective serotonin reuptake inhibitor
How the Drug Is Supplied HM
½-2 tsp powder in 1 lb (500 g) of canned food or 2 cups of moistened dry food; allow to stand 15-30 minutes, then feed
Same proportional to size of feeding
0.7-1 mg/kg IV q 24 h
Avoid inhaling powder dust; Viokase brand has superior efficacy; gingival bleeding possible
VM, HM
Indicated for nonobstructive vomiting
40 mg vials I HM
0.05-0.06 mg/kg PO q 12 h to q 8 h
None
May cause constipation; controlled drug
HM, S
1 mg/kg PO q 24 h, usually for a minimum of several weeks
Total dose: 1.25-2.5 mg PO q 24 h per cat
Behavioral changes, anorexia possible; avoid combining with MAO inhibitors (Anipryl, amitraz, etc.)
10, 20, 30, 40, mg T; 12.5, 25 mg ER (Paxil CR) T HM
Paxil
(see paroxetine)
Pedialyte
(see oral rehydration solution)
D-penicillamine (Cuprimine, Depen)
10-15 mg/kg PO q 12 Orally active chelating agent for lead and copper; h used for aiding in the prevention of cysteine urolithiasis, copper storage disease
—
Penicillin, benzathine (Benzapen)
G+ infections; some 20,000-40,000 U/kg activity against anaerobes; IM, SQ q 48-72 h bactericidal
Same
Penicillin G potassium or sodium
G+ infections; some 20,000-40,000 U/kg IV, Same activity against anaerobes; IM, SQ q 4-6 h bactericidal
Administer on empty stomach if tolerable; may cause vomiting, skin eruptions, and vascular lesions; monitor CBC
250 mg (Depen) T; 125, 250 mg (Cuprimine) C HM
150,000 U/mL I Long-acting formulation; do not VM use with penicillin hypersensitivity; do not use if serious infection is suspected; IM or SQ injection only
Penicillin hypersensitivity contraindicates; may contain high levels K+ (administer judiciously and monitor); solution for injection should be completely transparent; not effective orally
1 million, 5 million, 10 million, and 20 million U vials I HM
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Indications/Drug Type
Canine Dose
How the Drug Is Supplied
Feline Dose
Comments
Same
Solution for injection is 300,000 U/mL I opaque = for IM/SQ VM injection only; penicillin hypersensitivity contraindicates
Penicillin G procaine (Wycillin, many others)
G+ infections; some 20,000-40,000 units/kg activity against anaerobes; IM, SQ q 12-24 h bactericidal
Penicillin-V
G+ infections; bactericidal; 5.5-11 mg/kg PO q 6-8 Same effective orally h
250 mg = 400,000 U; avoid if penicillin hypersensitivity; GI upset possible
250, 500 mg T; 125, 250 mg/5 mL S; many other sizes HM
Pentasa
(see mesalamine)
Pentazocine (Talwin)
Narcotic agonist/ antagonist used for short-term analgesia
Pentobarbital (Nembutal, pentobarbitone)
Status epilepticus, general anesthesia
Pentosan polysulfate (Elmiron)
Glycosaminoglycan-like agent; osteoarthritis (dogs); idiopathic cystitis (cats)
Pentostam
(see sodium stibogluconate)
Pentothal
(see thiopental)
Pentoxifylline (Trental)
Increases plasticity of RBC membranes; used in many dermatoses, including dermatomyositis
Pepcid
(see famotidine)
Pepto-Bismol
(see bismuth subsalicylate)
Percogesic
(see acetaminophen)
Percorten-V
(see desoxycorticosterone pivalate)
Periactin
(see cyproheptadine)
Persantine
(see dipyridamole)
PGF2-alpha
(see prostaglandin)
Pharmorubicin
(see epirubicin)
Phenobarbital
Long-acting barbiturate used for seizure control; occasionally used as a sedative
May cause salivation and/or sedation; reverse with naloxone; may cause dysphoria in cats
30 mg/mL I, HM; often combined with other Tx
Anesthesia: 10-30 mg/kg IV slowly to effect; seizures: 3-15 mg/ kg IV slowly to effect
Respiratory depression and hypotension may develop if used alone or especially with or after diazepam
50 mg/mL I; available as tablets, elixir, suppositories
10 mg/kg PO or 3 mg/ kg IM; given once weekly for 4 weeks
8 mg/kg PO q 12 h
Rare adverse effects (e.g., vomiting) in dogs; experimental drug with minimal clinical data in cats; efficacy and safety unproven
100 mg C
10-25 mg/kg PO q 12 h
—
Few adverse effects reported
400 mg T
Ataxia, sedation, PU/PD; long-term (especially if >35 mcg/mL serum levels) hepatotoxicity occurs; initial adjustment period is required (liver enzyme inducer); if using higher dose IV, monitor respirations; controlled
8, 16, 32, 65, 100 mg T; 15, 20 mg/5 mL S; 30, 60, 65, 130 mg/mL I
1-3 mg/kg IM, 2-6 mg/ kg PO
Anesthesia: 10-30 mg/ kg IV slowly to effect; seizures: 3-15 mg/kg IV slowly to effect
2-3 mg/kg SQ, IM, IV
1-2 mg/kg PO q 8-12 Same h; okay to titrate slowly up to 16 mg/kg per day in divided doses; may be given IV as a bolus of 2-15 mg/kg slowly for status epilepticus followed by 2-6 mg/h CRI if necessary; maintain trough serum
VM, HM
VM, HM
HM
HM
HM
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Generic Name (Trade Name)
http://www.clinicalvetadvisor2.com/html/bc/ch001s0019_s001.php#ch0...
Indications/Drug Type
Canine Dose
Feline Dose
Comments
How the Drug Is Supplied
substance; see also
levels at 15-45 mcg/mL
Phenobarbital: Adverse Effects/ Toxicosis, p. 871
Phenoxybenzamine HCl (Dibenzyline)
Adrenergic, α-receptor blocking agent; urinary incontinence due to detrusor sphincter dyssynergia
Phenylbutazone (Butazolidin) NSAID
Phenylephrine (Neo-Synephrine)
Phenylpropanolamine (Propalin, PPA)
0.25-1 mg/kg PO q 12 h
Total dose: 2.5-5 mg PO q 12-24 h per cat
May result in vomiting, 10 mg C hypotension/ HM hypertension, rapid HR, miosis; long (4-7 days) onset of action; no effect on postprostatic urethra of cats
10-15 mg/kg PO q 8-12 h
Not recommended
Use lowest effective dosage; do not exceed 800 mg per day; may cause vomiting, GI ulceration, BM suppression, nephrotoxicity; incidence of toxicosis is high; not generally recommended
100, 400, 1000 mg T
May cause nasal irritation if used chronically; vasoconstriction (systemic hypertension) and pupillary dilation if given parenterally (constant BP monitoring necessary); arrhythmogenic in combination with halothane
10 mg/mL I; OS and intranasal OTC products
Anxiety, dizziness, hypertension, tachycardia, urinary retention; no longer available as human OTC product
25, 50, 75 mg T
—
1. Postsynaptic 2. α-adrenergic stimulant used as the following: 3. As nasal drops for rhinitis 4. As IV infusion for treatment of hypotension
1. 1-2 drops intranasal pediatric solution, q 8-24 h 2. 1-3 mcg/kg per minute as IV CRI, adjusted to effect
Same
HM
α-adrenergic agonist used for treating hormoneresponsive urinary sphincter hypotonus (incontinence) by increasing urethral smooth muscle activity
1 mg/kg PO q 8 h
Anticonvulsant agent
—
—
No longer recommended
Pheromones, feline synthetic Behavioral disorders, facial (Feliway) acclimation to new environment
—
Topical application to surroundings
Spray may be applied Spray pump or to objects, or diffuser diffuser disseminates product VM in room
Phosmet dip (Paramite)
2 tbsp (1 oz) per gallon Do not use H2O; sponge on and let air dry
Phenytoin (Dilantin)
Organophosphate dip for fleas, ticks, and canine sarcoptic mange
1-2 mg/kg PO q 8-12 h
VM, HM
Wear gloves to use; use once weekly maximum; do not use in puppies 6 weeks old; for heartworm prevention: give within 1 month of first exposure to mosquitos and continue until within 1 month of last exposure
Prepackaged doses (topical liquid in plastic ampules)
Low level of effectiveness reported; not to be used with other MAO inhibitors (e.g., antidepressants, amitraz)
2, 5, 10, 15, 30 mg T, VM; 5 mg C, T
VM
HM
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Generic Name (Trade Name) Sertraline (Zoloft)
Sildenafil (Viagra)
http://www.clinicalvetadvisor2.com/html/bc/ch001s0019_s001.php#ch0...
Indications/Drug Type
Canine Dose
Feline Dose
Comments
Selective serotonin reuptake inhibitor
0.25-1 mg/kg PO q 24 h
0.5-1 mg/kg PO q 24 h
Anxiety, aggression, or obsessivecompulsive disorders; inappropriate elimination.
Pulmonary hypertension
0.5-1 mg/kg PO q 8 h
How the Drug Is Supplied 25, 50, 100 mg T 20 mg/mL S HM 25, 50, 100 mg T
—
HM
Silvadene cream
(see silver sulfadiazine)
Silver sulfadiazine (Silvadene cream)
Topical antiinfective preparation for complications of burns
Apply to burn area q 12 h as necessary
Same
Silymarin (milk thistle extract, Marin)
Hepatopathy
50-250 mg PO q 24 h
4-8 mg/kg PO q 24 h
Simplicef
(see cefpodoxime)
Sinequan
(see doxepin)
Slentrol
(see dirlotapide)
Slo-Bid
(see theophylline, sustained action)
Sodium bicarbonate
Metabolic acidosis, urine alkalinization (e.g., intoxication)
Sporotrichosis
Sodium iodide 20%
Sodium stibogluconate (Pentostam)
Leishmaniasis
Solganal
(see aurothioglucose)
Soloxine
(see levothyroxine sodium)
Solu-Cortef
(see hydrocortisone sodium succinate)
Solu-Delta-Cortef
(see prednisolone sodium succinate)
Solu-Medrol
(see methylprednisolone sodium succinate)
Somatrem
(see growth hormone, human)
Soriatane
(see acitretin)
Sotalol (Betapace)
Classes II and III antiarrhythmic agent; used primarily for treating ventricular
Hypersensitivity to sulfonamides; KCS; Dobermans
10 mg/g O
Nutraceutical; also compounded with SAMe (Denamarin); wide range of safety
9, 24, 70 mg T
mEq/day = (desired Same serum [HCO3] − present serum [HCO3]) × 0.3 × BW (kilograms); administer 50% over 15 minutes and recheck serum levels; then give the balance over 24 hours
Alkalosis, hypernatremia, CHF, hypokalemia; correct inciting factors concurrently (or prior to HCO3 Tx); 84 mg NaHCO3 contains 1 mEq HCO3
0.6, 1 mEq/mL I; 5, 10 grain T
15 mg/kg PO q 8 h; some higher doses reported
Same
Monitor for iodinism: fever, ptyalism, GI signs; contains 0.1 mg iodine/mL
20% (200 mg/mL) S
30-50 mg/kg SQ, IV q 24 h; or 10-20 mg/ kg IM q 24 h for 20-28 days
—
Not available in United 100 mL vials (100 States except through mg/mL) I the Centers for HM Disease Control and Prevention
1-3 mg/kg PO q 12 h
Total dose: 10-40 mg PO q 12 h per cat; very little
β-blocking effects seen at low dosages; type III effects at higher levels; begin
HM
VM
HM
VM
80, 120, 160, 240 mg T HM
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Generic Name (Trade Name)
http://www.clinicalvetadvisor2.com/html/bc/ch001s0019_s001.php#ch0...
Indications/Drug Type
Canine Dose
tachyarrhythmias
Spinosad (Comfortis)
Flea infestation
Spironolactone (Aldactone, Prilactone)
Potassium-sparing diuretic; 1-4 mg/kg PO q 12-24 inhibits aldosterone h
Sporanox
(see itraconazole)
Spot-on
(see fenthion)
Stadol
(see butorphanol)
Stanozolol (Winstrol)
Anabolic steroid used for treating anorexia, debilitation, and anemia
Stibogluconate
(see sodium stibogluconate)
Stoxil
(see idoxuridine)
Streptase
(see streptokinase)
Streptokinase (Kabikinase, Streptase)
Thrombolytic drug; arterial or pulmonary thromboembolism
Streptozotocin (streptozocin, Insulinoma chemotherapy Zanosar)
Strongid-T
(see pyrantel pamoate)
Sublimaze
(see fentanyl)
Succimer (meso-2, 3 dimercaptosuccinic acid, Chemet)
Lead toxicity chelating agent
Feline Dose
Comments
published experience with drug in cats
low and titrate upwards to effect
30-60 mg/kg PO q 30 days
Same
How the Drug Is Supplied
Acts within 30 minutes, duration of effect = 1 month. Side-effects can include vomiting, CNS signs; ensure dose