11830 Westline Industrial Drive St. Louis, Missouri 63146
SAUNDERS MANUAL OF SMALL ANIMAL PRACTICE, THIRD EDITION Copyright © 2006, 2000, 1994 by Saunders, an imprint of Elsevier Inc.
ISBN-13: 978-0-7216-0422-0 ISBN-10: 0-7216-0422-6
All rights reserved. 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. Permissions may be sought directly from Elsevier’s Health Sciences Rights Department in Philadelphia, PA, USA: phone: (+1) 215 239 3804, fax: (+1) 215 239 3805, e-mail:
[email protected]. You may also complete your request on-line via the Elsevier homepage (http://www.elsevier.com), by selecting “Customer Support” and then “Obtaining Permissions.”
Notice Knowledge and best practice in this field are constantly changing. As new research and experience broaden our knowledge, changes in practice, treatment and drug therapy may become necessary or appropriate. Readers are advised to check the most current information provided (i) on procedures featured or (ii) by the manufacturer of each product to be administered, to verify the recommended dose or formula, the method and duration of administration, and contraindications. It is the responsibility of the practitioner, relying on their own experience and knowledge of the patient, to make diagnoses, to determine dosages and the best treatment for each individual patient, and to take all appropriate safety precautions. To the fullest extent of the law, neither the Publisher nor the Editors assumes any liability for any injury and/or damage to persons or property arising out or related to any use of the material contained in this book. ISBN-13: 978-0-7216-0422-0 ISBN-10: 0-7216-0422-6
Publishing Director: Linda Duncan Acquisitions Editor: Liz Fathman Senior Developmental Editor: Jolynn Gower Editorial Assistant: Stacy Beane Publishing Services Manager: Julie Eddy Senior Project Manager: Joy Moore Designer: Jyotika Schroff
Printed in the United States of America Last digit is the print number:
9 8 7 6 5 4 3 2 1
We dedicate this book to our families: To my wife, Susan Crisp; my children, Justin and Mary; my parents, Robert and Sandy; and my brother, Thomas. (SJB) To my wife, Sherrie, and my son, Cameron. (RGS)
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Contributors
Nancy L. Anderson, DVM, PhD, ABUPC (Avian) Director of Wildlife Services, Lindsay Wildlife Museum, Walnut Creek, California Pet Rodents Basic Husbandry and Medicine of Pet Reptiles Francisco J. Alvarez, DVM Chief Resident, Clinical Oncology Service, Veterinary Medical Teaching Hospital, Department of Veterinary Clinical Services, The Ohio State University, Columbus, Ohio Respiratory Neoplasia Laura J. Armbrust, DVM, Diplomate ACVR Assistant Professor, Radiology, Clinical Sciences, Kansas State University College of Veterinary Medicine, Manhattan, Kansas Radiographic and Ultrasonographic Techniques Dennis N. Aron, DVM, Diplomate ACVS Professor, Small Animal Surgery, Department of Small Animal Medicine, College of Veterinary Medicine, University of Georgia, Athens, Georgia Luxation, Subluxation, and Shearing Injuries of the Tarsal Joint Shane W. Bateman, DVM, DVSc, Diplomate ACVECC Associate Professor-Clinical, Head of Emergency and Critical Care, Department of Veterinary Clinical Sciences, The Ohio State University, Columbus, Ohio Emergency and Critical Care Techniques and Nutrition Fluid Therapy for Dogs and Cats
Jamie R. Bellah, DVM, Diplomate ACVS Staff Surgeon, Affiliated Veterinary Specialists, Orange Park, Florida Surgery of Intertriginous Dermatoses Larry Berkwitt, DVM, Diplomate ACVIM Chief of Staff, Internal Medicine, Veterinary Referral and Emergency Center, Norwalk, Connecticut Diagnostic Methods in Respiratory Disease Sonya V. Bettenay, BVSC (Hons), FACVSc (Dermatology), Diplomate ECVD Dermatopathology, Laboklin, Munich, Germany Skin Cytology and Biopsy David S. Biller, DVM, Diplomate ACVR Professor and Head of Radiology, Department of Clinical Sciences, College of Veterinary Medicine, Kansas State University, Manhattan, Kansas Radiographic and Ultrasonographic Techniques Stephen J. Birchard, DVM, MS, Diplomate ACVS Associate Professor, Small Animal Surgery, Department of Veterinary Clinical Sciences, The Ohio State University, Columbus, Ohio Diseases of the Thyroid Gland Selected Skin Graft and Reconstructive Techniques Surgery of the Liver and Biliary Tract Diseases and Surgery of the Exocrine Pancreas Peritonitis Pleural Effusion Principles of Thoracic Surgery
Karin Muth Beale, DVM, Diplomate ACVD Staff Dermatologist, Gulf Coast Veterinary Specialists, Houston, Texas Dermatology Consultant, ANTECH Diagnostics, Irvine, California Dermatophytosis
Dale E. Bjorling, DVM, MS Diplomate ACVS Professor and Chair, Surgical Sciences, Affiliate Professor, Division of Urology, Department of Surgery, School of Veterinary Medicine, University of Wisconsin, Madison, Wisconsin Surgery of the Kidney and Ureter Surgery of the Urethra Thoracic Trauma
Richard M. Bednarski, DVM, MS, Diplomate ACVA Associate Professor of Anesthesiology, Hospital Director, Department of Veterinary Clinical Sciences, The Ohio State University, Columbus, Ohio Pain Management in the Surgical Patient
Mark W. Bohling, DVM Resident, Small Animal Surgery, Department of Clinical Sciences, Auburn University, Auburn, Alabama Management of the Traumatic Wound by Primary Closure vii
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John D. Bonagura, DVM, MS, Diplomate ACVIM (Internal Medicine, Cardiology) Professor, Cardiology and Internal Medicine, Department of Veterinary Clinical Sciences, The Ohio State University, Columbus, Ohio Cardiovascular Radiography Cardiovascular Drugs Heart Failure in Dogs Syncope Valvular Heart Disease Cardiomyopathy Pericardial Diseases Vascular Diseases Congenital Heart Disease Respiratory Infections Jennifer Bonczynski, DVM, Diplomate ACVS Staff Surgeon, Department of Surgery, The Animal Medical Center, New York, New York Pancreatic Beta Cell Neoplasia Harry W. Boothe, DVM, MS Professor, Small Animal Surgery, Department of Clinical Sciences, College of Veterinary Medicine, Auburn University, Auburn, Alabama Surgery for Otitis Media and Otitis Interna Surgery of the Prostate Gland Surgery of the Testes and Scrotum Surgery of the Penis and Prepuce Randy J. Boudrieau, DVM, Diplomate ACVS Professor, Surgery, Clinical Sciences, Tufts University School of Veterinary Medicine, North Grafton, Massachusetts Section Head, Small Animal Surgery, Henry & Lois Foster Hospital for Small Animals, North Grafton, Massachusetts Delayed Union, Nonunion, and Malunion Heather L. Bowles, DVM, Diplomate ABVP Fallston Veterinary Clinic, Fallston, Maryland Avian Reproductive Tract Disorders Ronald M. Bright, DVM, MS, Diplomate ACVS Affiliate Professor, Department of Clinical Sciences, College of Veterinary Medicine, Colorado State University Staff Surgeon, Surgical Referral Services, Fort Collins, Colorado Staff Surgeon, Veterinary Consultation Services, Inc., Knoxville, Tennessee Surgery of the Esophagus Diseases of the Stomach Surgery of the Stomach Surgery of the Intestines Anorectal Surgery
Marjory B. Brooks, DVM, Diplomate ACVIM Associate Director, Comparative Coagulation Laboratory, Animal Health Diagnostic Center, Population Medicine and Diagnostic Science, College of Veterinary Medicine, Cornell University Ithaca, New York Coagulation Diseases Steven C. Budsberg, DVM, MS, Diplomate ACVS Professor, Department of Small Animal Medicine and Surgery, University of Georgia, Athens, Georgia Orthopedic Disorders of the Distal Extremities C. Anthony Buffington, DVM, PhD, Diplomate ACVN Professor, Department of Veterinary Clinical Sciences, College of Veterinary Medicine, The Ohio State University, Columbus, Ohio Emergency and Critical Care Techniques and Nutrition Clay A. Calvert, DVM, Diplomate ACVIM Professor, Department of Small Animal Medicine and Surgery, College of Veterinary Medicine, University of Georgia, Athens, Georgia Heartworm Disease Marcia A. Carothers, DVM, Diplomate ACVIM (Internal Medicine) Staff Veterinarian, Akron Veterinary Referral and Emergency Center, Akron, Ohio Respiratory Neoplasia Sue Chen, DVM Gulf Coast Veterinary Specialists, Houston, Texas Avian Reproductive Tract Disorders Rabbits Dennis J. Chew, DVM, Diplomate ACVIM Professor, Department of Veterinary Clinical Sciences, College of Veterinary Medicine, The Ohio State University, Columbus, Ohio Fluid Therapy for Dogs and Cats Diseases of the Parathyroid Gland and Calcium Metabolism Diseases of the Urinary Bladder Lynette K. Cole, DVM, MS, Diplomate ACVD Assistant Professor, Dermatology, College of Veterinary Medicine, Veterinary Teaching Hospital, The Ohio State University, Columbus, Ohio Diseases of the Pinna Otitis Media and Otitis Interna Carmen M. H. Colitz, DVM, PhD, Diplomate ACVO Assistant Professor, Ophthalmology, Department of Veterinary Clinical Sciences, The Ohio State University, Columbus, Ohio Diseases of the Lacrimal System
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Sarah Colombini Osborn, DVM, MS, Diplomate ACVD Co-Owner, Dermatology, Gulf Coast Veterinary Dermatology & Allergy, Houston, Texas Consultant, Dermatopathology/Dermatology, Antech Diagnostics, Phoenix, Arizona Canine and Feline Demodicosis Paul A. Cuddon, DVM, Diplomate ACVIM (Neurology) Neurological Center for Animals, Lakewood, Colorado Disorders of the Spinal Cord Támara M. Costa-Gómez, DVM Arboretum View Animal Hospital, Downers Grove, Illinois Surgery of the Kidney and Ureter Surgery of the Urethra Kechia M. Davis, DVM Resident, Small Animal Surgery, Department of Clinical Sciences, Veterinary Teaching Hospital, North Carolina State University, Raleigh, North Carolina Mammary Gland Neoplasia
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William R. Fenner, DVM, Diplomate ACVIM (Neurology) Emeritus Faculty, College of Veterinary Medicine, The Ohio State University, Columbus, Ohio Diagnostic Approach to Neurologic Disease Roger B. Fingland, DVM, MS, MBA, Diplomate ACVS Associate Dean, Clinical Programs, Professor and Director, Veterinary Medical Teaching Hospital, College of Veterinary Medicine, Kansas State University, Manhattan, Kansas Surgery of the Urinary Bladder Surgery of the Ovaries and Uterus Surgery of the Vagina and Vulva Obstructive Upper Airway Disorders Richard B. Ford, DVM, MS, Diplomate ACVIM, Diplomate (Hon) ACVPM Professor, Medicine, Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University, Raleigh, North Carolina Vaccination Guidelines for the Dog and Cat
Charles E. DeCamp, DVM, MS, Diplomate ACVS Professor, Michigan State University, East Lansing, Michigan Open Fractures
S. Dru Forrester, DVM, MS, Diplomate ACVIM (Small Animal Internal Medicine) Professor, College of Veterinary Medicine, Western University of Health Sciences, Pomona, California Diseases of the Kidney and Ureter
R. Tass Dueland, DVM, MS, Diplomate ACVS Professor, Orthopedic Surgery, Affiliate Professor, Division of Orthopedic Surgery, Medical School, University of Wisconsin-Madison, Madison, Wisconsin Orthopedic Disorders of the Stifle
Linda A. Frank, MS, DVM, Diplomate ACVD Professor, Dermatology, Small Animal Clinical Sciences, College of Veterinary Medicine, University of Tennessee, Knoxville, Tennessee Sex Hormone and Endocrine Look-alike Dermatoses
Joan Dziezyc, DVM, Diplomate ACVO Associate Professor, Department of Small Animal Medicine and Surgery, College of Veterinary Medicine Staff Ophthalmologist, Veterinary Medical Teaching Hospital, Texas A&M University, College Station, Texas Diseases of the Retina, Choroid, and Optic Nerve
Rance M. Gamblin, DVM, Diplomate ACVIM (Oncology) Staff Oncologist, Akron Veterinary Internal Medicine Oncology Practice, Metropolitan Veterinary Hospital, Akron, Ohio Principles of Oncology
Erick L. Egger, DVM, Diplomate ACVS Special Appointment, Small Animal Orthopedics, Veterinary Clinical Sciences, Colorado State University, Fort Collins, Colorado Fractures of the Tibia and Fibula Christine Ellis, DVM Exotic Animal Veterinary Service, Fort Collins, Colorado Ferrets
Jennifer Gieg, DVM Resident, Internal Medicine, Department of Veterinary Clinical Sciences, The Ohio State University, Columbus, Ohio Diseases of the Urinary Bladder Stephen D. Gilson, DVM, Diplomate ACVS Sõnorã Veterinary Specialists, Scottsdale, Arizona Principles of Oncology
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Mary B. Glaze, DVM, MS, Diplomate ACVO Professor, Veterinary Ophthalmology, Louisiana State University, Veterinary Clinical Sciences Veterinary Ophthalmologist, Veterinary Teaching Hospital and Clinic, Louisiana State University, Baton Rouge, Louisiana Diseases of the Orbit Joanne C. Graham, DVM, MS, Diplomate ACVIM (Oncology) Assistant Professor and Staff Oncologist, Iowa State University, Ames, Iowa Soft Tissue Sarcomas and Mast Cell Tumors David Grant, DVM, MS, Diplomate ACVIM (Small Animal Internal Medicine) Clinical Instructor, Department of Small Animal Clinical Sciences, Virginia-Maryland Regional College of Veterinary Medicine, Blacksburg, Virginia Diseases of the Kidney and Ureter Thomas K. Graves, DVM, PhD, Diplomate ACVIM Assistant Professor, Small Animal Medicine, Veterinary Clinical Medicine, University of Illinois, Urbana, Illinois Diseases of the Testes and Scrotum Diseases of the Penis and Prepuce Diseases of the Ovaries and Uterus Deborah S. Greco, DVM, PhD Staff Internist and Endocrinologist, Department of Medicine, The Animal Medical Center, New York, New York Diabetes Mellitus Henry W. Green, III, DVM, Diplomate ACVIM (Cardiology) Assistant Professor, Department of Veterinary Clinical Sciences, Purdue University School of Veterinary Medicine, West Lafayette, Indiana Congenital Heart Disease Tia B. Greenberg, DVM Westminster Veterinary Group, Westminster, California Avian Dermatology Craig E. Griffin, DVM, Diplomate ACVD Partner, Clinician, Animal Dermatology Clinic, San Diego and Garden Grove, California Flea Allergy Dermatitis Amy M. Grooters, DVM, Diplomate ACVIM Associate Professor and Chief, Companion Animal Medicine, Veterinary Clinical Sciences, School of Veterinary Medicine, Louisiana State University, Baton Rouge, Louisiana Deep Fungal Infections
Robert L. Hamlin, DVM, PhD, Diplomate ACVIM (Cardiology) Professor, Veterinary Biosciences and Biomedical Engineering, The Ohio State University, Columbus, Ohio Auscultation and Physical Diagnosis Don J. Harris, DVM Owner and Director, Avian and Exotic Animal Medical Center, Miami, Florida Avian Infectious Diseases Callum W. Hay, BVMS, Diplomate ACVS President, Veterinary Surgical Services, Inc., Tampa, Florida Osteomyelitis Osteoarthritis Immune-Mediated Arthritis Cheryl S. Hedlund, DVM, MS, Diplomate ACVS Professor, Surgery, Veterinary Clinical Sciences, School of Veterinary Medicine, Louisiana State University, Baton Rouge, Louisiana Surgery of the Nasal Cavity and Sinuses Karen Helton-Rhodes, DVM, Diplomate ACVD Veterinary Referral Centre, Little Falls, New Jersey Immune-Mediated Dermatoses Andrew Hillier, BVSc Associate Professor, Veterinary Clinical Sciences, The Ohio State University, Columbus, Ohio Mycobacteriosis Scabies, Notoedric Mange, and Cheyletiellosis Atopic Dermatitis Feline Symmetrical Alopecia Cheryl Holloway, RVT Animal Health Technician, College of Veterinary Medicine, The Ohio State University, Columbus, Ohio Emergency and Critical Care Techniques and Nutrition Robert V. Hitchinson, DVM Co-director, Animal Clinic Northview, Inc., North Ridgeville, Ohio Infertility and Breeding Disorders John A. E. Hubbell, DVM, MS, Diplomate ACVA Professor, Department of Veterinary Clinical Sciences, The College of Veterinary Medicine, The Ohio State University, Columbus, Ohio Practical Methods of Anesthesia Richard M. Jerram, BVSc, Diplomate ACVS Specialist, Small Animal Surgery, Veterinary Specialist Group, Auckland, New Zealand Fractures and Dislocations of the Mandible Fractures of the Maxilla
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Lynelle R. Johnson, DVM, PhD, Diplomate ACVIM (Small Animal Internal Medicine) Assistant Professor, VM: Medicine & Epidemiology, University of California, Davis, California Bronchopulmonary Disease
William C. Kisseberth, DVM, PhD, Diplomate ACVIM Assistant Professor, Department of Veterinary Clinical Sciences, The Ohio State University, Columbus, Ohio Diseases of the Spleen
Susan E. Johnson, DVM, MS, Diplomate ACVIM (Internal Medicine) Associate Professor, Veterinary Clinical Sciences, The Ohio State University, Columbus, Ohio Diseases of the Esophagus and Disorders of Swallowing Diseases of the Stomach Diseases of the Intestines Diseases of the Liver and Biliary Tract Diseases and Surgery of the Exocrine Pancreas
David W. Knapp, DVM, Diplomate ACVS Staff Surgeon, Angell Animal Medical Center, Boston, Boston, Massachusetts Management of the Open Wound
Matthew S. Johnston, VMD, DABVP (Avian) Assistant Professor, Zoological Medicine, Clinical Sciences, Colorado State University, Fort Collins, Colorado Avian Respiratory System Disorders Denise Jones, DVM, BS Partner and Staff Veterinarian, Findlay Animal Hospital, Findlay, Ohio History and Physical Examination Nancy D. Kay, DVM, Diplomate ACVIM Staff Internist, Animal Care Center of Sonoma County, Rohnert Park, California Diseases of the Prostate Gland Bruce W. Keene, DVM, MSc, Diplomate ACVIM (Cardiology) Professor, Cardiology, Department of Clinical Sciences, North Carolina State University, Raleigh, North Carolina Heart Failure in Dogs Thomas J. Kern, DVM, Diplomate ACVO Associate Professor, Ophthalmology, Department of Clinical Sciences, College of Veterinary Medicine Cornell University, Ithaca, New York Diseases of the Cornea and Sclera Peter P. Kintzer, DVM, Diplomate ACVIM Staff Internist, Boston Rood Animal Hospital, Springfield, Massachusetts Diseases of the Adrenal Gland Susan E. Kirschner, DVM, Diplomate ACVO Ophthalmologist, The Animal Eye Doctor, Beaverton, Oregon Diseases of the Eyelid
Shianne L. Koplitz, DVM, PhD Diplomate ACVIM (Cardiology) Cardiology Resident, Department of Veterinary Clinical Sciences, The Ohio State University, Columbus, Ohio Syncope Michael P. Kowaleski, DVM, Diplomate ACVS Assistant Professor, Small Animal Orthopedic Surgery, Department of Veterinary Clinical Sciences, The Ohio State University, Columbus, Ohio Fractures and Dislocations of the Carpus Osteochondrosis Gail A. Kunkle, DVM, Diplomate ACVD Professor, SACS-CVM, University of Florida, Gainesville, Florida Necrotizing Skin Diseases Kenneth W. Kwochka, DVM, Diplomate ACVD Vice President for Research and Development, DVM Pharmaceuticals, Miami, Florida Keratinization Defects Mary Anna Labato, DVM, Diplomate ACVIM (Small Animal) Clinical Associate Professor, Department of Clinical Sciences, Cummings School of Veterinary Medicine at Tufts University Staff Veterinarian, Small Animal Medicine, Foster Hospital for Small Animals, North Grafton, Massachusetts Disorders of Micturition Linda B. Lehmkuhl, DVM, MS, Diplomate ACVIM (Cardiology) Staff Cardiologist, Cardiology, Med Vet, Medical Center for Pets, Worthington, Ohio Cardiomyopathy Patricia J. Luttgen, DVM, MS, Diplomate ACVIM (Neurology) Staff Neurologist, Neurological Center for Animals, Denver, Colorado Disorders of the Spinal Cord
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Paul A. Manley, DVM, MSc, Diplomate ACVS Professor, Chief of Small Animal Services, Surgical Sciences, School of Veterinary Medicine, University of Wisconsin, Madison, Wisconsin Osteoarthritis Immune-Mediated Arthritis Philip A. March, DVM, MS, Diplomate ACVIM (Neurology) Associate Professor, Department of Veterinary Clinical Sciences, The Ohio State University, Columbus, Ohio Diagnostic Approach to Neurologic Disease Diseases of the Brain and Cranial Nerves Sandra Manfra Marretta, DVM, Diplomate ACVS, Charter Dipolomate AVDC Professor and Head, Small Animal Surgery and Dentistry, Veterinary Clinical Medicine, College of Veterinary Medicine, University of Illinois, Urbana, Illinois Dentistry and Diseases of the Oropharnyx Hilary K. Matthews, DVM, PhD, Diplomate ACVIM Section Head, Internal Medicine, Capital Veterinary and Referral Center, Columbus, Ohio Diseases of the Urethra Margaret C. McEntee, DVM, Diplomate ACVIM (Medical Oncology), Diplomate ACVR (Radiation Oncology) Assistant Clinical Professor, University of California, Davis, School of Veterinary Medicine, Davis, California Diseases of the Spleen Mary A. McLoughlin, DVM, MS, Diplomate ACVS Assisstant Professor Department of Veterinary Clinical Sciences, The Ohio State University, Columbus, Ohio Diseases of the Urinary Bladder Diseases of the Vagina and Vulva Michael S. Miller MS, VMD, Diplomate, ABVP Co-owner and Cardiology Consultant, Veterinary Specialty Center of Delaware, Wilmington, Delaware, Director, Cardiology-Ultrasound Referral Service, Thornton, Pennsylvania Electrocardiography Disorders of the Cardiac Rhythm Nicholas J. Millichamp, BSC, BVM, PhD, DVOpthal, Diplomate ACVO, Diplomate MRCS Associate Professor, Small Animal Medicine and Surgery, College of Veterinary Medicine, Staff Opthalmologist, Veterinary Teaching Hospital, Texas A&M University, College Station, Texas Diseases of the Retina, Choroid, and Optic Nerve
Darryl L. Millis, DVM, MS, Diplomate ACVS Professor, Orthopedic Surgery, Small Animal Clinical Sciences, University of Tennessee, Knoxville, Tennessee Postoperative Physical Rehabilitation Milan Milovancev, DVM Resident, Small Animal Surgery, University of Wisconsin, Madison, Wisconsin Neoplasia of Thoracic and Pelvic Limbs Cecil P. Moore, DVM, MS, Diplomate ACVO Professor and Chairman, Department of Veterinary Medicine and Surgery, University of Missouri, Columbia, Missouri Diseases of the Conjunctiva Daniel O. Morris, DVM, Diplomate, ACVD Assistant Professor and Chief, Dermatology and Allergy, Clinical Studies-Philadelphia, University of Pennsylvania, Philadelphia, Pennsylvania Malassezia Dermatitis Ralf S. Mueller, DMV, DMVH, Diplomate ACVD, FACVs Chief, Dermatology Service, Medizinische Tierklinik, Universität München, Munich, Germany Disorders of the Claw William W. Muir III, DVM, PhD, Diplomate ACVA, Diplomate ACVECC Professor, Department of Veterinary Clinical Sciences, College of Veterinary Medicine, The Ohio State University Columbus, Ohio Cardiopulmonary Cerebral Resuscitation Alan C. Mundell, DVM Animal Dermatology Service, Seattle, Washington Mycobacteriosis Rhett Nichols, DVM, ACVIM Endocrinology and Internal Medicine Consult, Antech Diagnostics, Lake Success, New York Diseases of the Hypothalamus and Pituitary James O. Noxon, DVM, Diplomate ACVIM (Internal Medicine) Professor, Department of Veterinary Clinical Sciences, Iowa State University, Ames, Iowa Adjunct Professor, Department of Companion Animals, Atlantic Veterinary College, University of Prince Edward Island, Charlottetown, Prince Edward Island, Canada Otitis Externa
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Barbara L. Oglesbee, DVM, Diplomate ABVP (Avian Practice) Adjunct Associate Professor, Department of Veterinary Clinical Sciences, The Ohio State University, Columbus, Ohio and Westminster Veterinary Group, Westminster, California Avian Techniques Avian Infectious Diseases Avian Digestive System Disorders
Anthony Pilny, DVM The Center for Avian and Exotic Medicine, New York, New York Avian Neurologic Disorders
Marvin L. Olmstead, DVM, MS, Diplomate ACVS Emeritus Professor, Small Animal Orthopedics, Department of Veterinary Clinical Sciences, The Ohio State University, Columbus, Ohio Oregon Veterinary Associates, Springfield, Oregon Disorders of the Coxofemoral Joint
Michael Podell, DVM, MSc, Diplomate ACVIM (Neurology) Adjunct Professor, Veterinary Clinical Medicine, University of Illinois, Champaign-Urbana, Illinois Medical Director and Staff Neurologist, Animal Emergency and Critical Care Center, Northbrook, Illinois Adjunct Professor, Veterinary Biosciences, The Ohio State University, Columbus, Ohio Seizures
Rodney L. Page, DVM, MS, Diplomate ACVIM (Internal Medicine, Oncology) Professor, Oncology, North Carolina State University, Raleigh, North Carolina Principles of Oncology Matthew Palmisano, DVM, MS, Diplomate ACVS Veterinary Referral and Emergency Center, Norwalk, Connecticut Neoplasia of the Maxilla and Mandible Fractures and Dislocations of the Spine Orthopedic Disorders of the Stifle Surgery of the Skeletal Muscle and Tendon Neoplasia of Thoracic and Pelvic Limbs Pediatric Fractures
Lauren R. Pinchbeck, DVM Clinical Instructor, Veterinary Clinical Sciences, Department of Dermatology, The Ohio State University, Columbus, Ohio Scabies, Notoedric Mange, and Cheyletiellosis
James C. Prueter, DVM, Diplomate ACVIM Hospital Director, The Veterinary Referral Clinic, Cleveland, Ohio Diagnostic Methods in Respiratory Disease Katherine E. Quesenberry, DVM, Diplomate ABVP (Avian Practice) Avian and Exotic Pet Service, The Animal Medicine Center, New York, New York Avian Neurologic Disorders Rabbits
David L. Panciera, DVM, MS, Diplomate ACVIM (Small Animal Internal Medicine) Professor, Department of Small Animal Clinical Sciences, Virginia-Maryland Regional College of Veterinary Medicine, Viginia Tech, Blacksburg, Virginia Diseases of the Thyroid Gland
John F. Randolph, DVM, Diplomate ACVIM Professor of Medicine, Cornell University Hospital for Animals, Department of Clinical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, New York Diseases of the Hypothalamus and Pituitary
Robert B. Parker, DVM, Diplomate ACVS Chairman, Department of Surgery, Animal Medical Center, New York, New York Fractures of the Humerus
Rose E. Raskin, DVM, PhD, Diplomate ACVP Professor, Veterinary Clinical Pathology, Department of Veterinary Pathobiology, School of Veterinary Medicine, Purdue University, West Lafayette, Indiana Erythrocytes, Leukocytes, and Platelets
Janet L. Peterson, DVM, Diplomate ACVIM (Oncology) Staff Veterinarian, Mission MedVet, Mission, Kansas Tumors of the Skin and Subcutaneous Tissues Mark E. Peterson, DVM, Diplomate ACVIM Head, Division of Endocrinology, Department of Medicine, The Animal Medical Center, New York, New York Diseases of the Thyroid Gland Diseases of the Adrenal Gland Diseases of the Hypothalamus and Pituitary
Nyssa J. Reine, DVM Diplomate ACVIM Department of Medicine, The Animal Medical Center, New York, New York Pancreatic Beta Cell Neoplasia Laura G. Ridge, DVM, Diplomate ACVIM Internal Medicine Resident, Department of Small Animal Medicine and Surgery, University of Georgia, Athens, Georgia Heartworm Disease
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Mark C. Rochat, DVM, Diplomate ACVS Associate Professor and Chief, Small Animal Surgery, Department of Veterinary Clinical Sciences, College of Veterinary Medicine, Oklahoma State University, Stillwater, Oklahoma Fractures of the Pelvis Amputation of the Digit Wayne S. Rosenkrantz, DVM, Diplomate ACVD Partner, Animal Oncology Clinic, Tustin and San Diego, California Miliary Dermatitis and Eosinophilic Granuloma Complex Edmund J. Rosser, Jr., DVM, Diplomate ACVD Professor, Dermatology, Small Animal Clinical Sciences, Michigan State University, College of Veterinary Medicine, East Lansing, Michigan Pyoderma James K. Roush, DVM, MS, Diplomate ACVS Professor and Section Head, Small Animal Surgery, Veterinary Clinical Sciences, Kansas State University, Manhattan, Kansas Fractures of the Shoulder Miscellaneous Diseases of Bone John E. Rush, DVM, MS, Diplomate ACVIM (Cardiology), Diplomate ACVECC Professor and Associate Department Chair, Department of Clinical Sciences, Cummings School of Veterinary Medicine at Tufts University, North Grafton, Massachusetts Valvular Heart Disease Valerie F. Samii, DVM, Diplomate ACVR Associate Professor, Department of Veterinary Clinical Sciences, The Ohio State University, Columbus, Ohio Cardiovascular Radiolography Diagnostic Imaging in Respiratory Disease Randall H. Scagliotti, DVM Associate Clinical Professor, Department of Surgical and Radiological Sciences, University of California, Davis, California Neuro-opthalmology Vicki J. Scheidt, DVM, Diplomate ACVD Hanover Veterinary Clinic, Hanover, New Hampshire Feline Symmetrical Alopecia Patricia A. Schenck, DVM, PhD Assistant Professor, Diagnostic Center for Population and Animal Health, Endocrine Diagnostic Section, Michigan State University, Lansing, Michigan Diseases of the Parathyroid Gland and Calcium Metabolism
Eric R. Schertel, DVM, PhD, Diplomate ACVS COO, Surgery, MedVet, Worthington, Ohio Surgical Correction of Patent Ductus Arteriosus Shock Principles of Thoracic Surgery Karsten E. Schober, DVM, PhD, Diplomate ECVIM-CA Clinical Assistant Professor, Veterinary Teaching Hospital, The Ohio State University, Columbus, Ohio Cardiovascular Drugs Linda G. Shell, DVM, Diplomate ACVIM (Neurology) Editor and Consultant, Veterinary Information Network, Davis, California Neurology and Internal Medicine Consultant, Veterinary Neurology Education and Consulting, Pilot, Virginia Peripheral Nerve Disorders G. Diane Shelton, DVM, PhD, Diplomate ACVIM (Internal Medicine) Professor, Director, Comparative Neuromuscular Laboratory, Department of Pathology, University of California, San Diego, La Jolla, California Disorders of the Muscle and Neuromuscular Junction Robert G. Sherding, DVM, Diplomate ACVIM Professor, Small Animal Internal Medicine, Department of Veterinary Clinical Sciences, The Ohio State University, Columbus, Ohio Feline Leukemia Virus Feline Immunodeficiency Virus Feline Infectious Peritonitis (Feline Coronavirus) Feline Infectious Respiratory Disease Canine Infectious Tracheobronchitis (Kennel Cough) Canine Distemper Intestinal Viruses Rabies and Pseudorabies Miscellaneous Viral Diseases Rickettsiosis, Ehrlichiosis, Anaplasmosis, and Neorickettsiosis Borreliosis (Lyme Disease) Systemic Bacterial Infectious Diseases Systemic Mycoses Toxoplasmosis and Other Systemic Protozoal Infections Diseases of the Esophagus and Disorders of Swallowing Diseases of the Stomach Diseases of the Intestines Diseases of the Liver and Biliary Tract Diseases and Surgery of the Exocrine Pancreas Constipation and Anorectal Diseases Respiratory Infections Pleural Effusion
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Peter Shires, BVSc, MS, Diplomate ACVS Professor, Small Animal Surgery, Director, Veterinary Educational Technologies, Virginia-Maryland Regional College of Veterinary Medicine, Virginia Polytechnic Institute and State University, Blacksburg, Virginia Fractures of the Femur Gretchen K. Sicard, DVM Assistant Professor, Small Animal Surgery, College of Veterinary Medicine, Kansas State University, Manhattan, Kansas Surgery of the Urinary Bladder Surgery of the Ovaries and Uterus Surgery of the Vagina and Vulva Daniel D. Smeak, DVM, Diplomate ACVS Professor, Small Animal General Surgery, Head, Small Animal Surgery, Department of Veterinary Clinical Sciences, The Ohio State University, Columbus, Ohio Selected Skin Graft and Reconstructive Techniques Surgery of the External Ear Canal and Pinna Francis W. K. Smith Jr., DVM, Diplomate ACVIM (Cardiology, Small Animal Internal Medicine) Clinical Assistant Professor, Clinical Sciences, Tufts University School of Veterinary Medicine, North Grafton, Massachusetts Vice-President, VetMed Consultants, Inc., Santa Fe, New Mexico Electrocardiography Disorders of the Cardiac Rhythm Mark M. Smith, VMD, Diplomate ACVS, Diplomate AVDC Center for Veterinary Dentistry and Oral Surgery, Gaithersburg, Maryland Fractures of the Skull Neoplasia of the Axial Skeleton
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Michael Stone, DVM, Diplomate ACVIM (Small Animal Internal Medicine) Assistant Clinical Professor, Department of Clinical Studies, Cummings School of Veterinary Medicine at Tufts University, North Grafton, Massachusetts Ultrasonographer, Veterinary Internal Medicine Mobile Specialists, North Woodstock, Connecticut Systemic Immune-Mediated Diseases Steven F. Swaim, DVM, MS Professor, Small Animal Surgery, College of Veterinary Medicine, Auburn University, Auburn, Alabama Management of the Traumatic Wound by Primary Closure Robert A. Taylor, BS, DVM, MS, Diplomate ACVS Clinical Affiliate, Veterinary Teaching Hospital, Colorado State University, Fort Collins, Colorado Chief Surgeon, Alameda East Veterinary Hospital, Denver, Colorado Scapulohumeral Luxation Larry P. Tilley, DVM, Diplomate ACVIM (Internal Medicine) VetMed Consultants, Inc., Santa Fe, New Mexico Electrocardiography Disorders of Cardiac Rhythm James Tomlinson, DVM, MVSc, Diplomate, ACVS Professor, Orthopedic Surgery, Veterinary Medicine and Surgery, College of Veterinary Medicine, University of Missouri, Columbia, Missouri Fractures and Growth Deformities of the Radius and Ulna, Luxation of the Elbow David M. Vail, DVM, Diplomate ACVIM (Oncology) Professor, Oncology, Animal Cancer Center, Department of Clinical Sciences, Colorado State University, Fort Collins, Colorado Lymphoid Neoplasia
Rebecca L. Stepien, DVM, MS, Diplomate ACVIM Clinical Associate Professor, Cardiology, Clinical Cardiologist, Department of Medical Sciences, University of Wisconsin School of Veterinary Medicine, Madison, Wisconsin Vascular Diseases
Raymund F. Wack, DVM, Diplomate ACZM Assistant Clinical Professor, Medicine and Epidemiology, College of Veterinary Medicine, University of California, Davis, California Basic Husbandry and Medicine of Pet Reptiles
Elizabeth A. Stone, DVM, Diplomate ACVS Dean and Professor, Surgery, Ontario Veterinary College/University of Guelph, Guelph, Ontario, Canada Mammary Gland Neoplasia
Stephen D. White, DVM, Diplomate ACVD Professor, Medicine and Epidemiology, School of Veterinary Medicine, University of Califonia Davis, California Food Hypersensitivity David A. Wilkie, DVM, MS, Diplomate ACVO Associate Professor, Department of Veterinary Clinical Sciences, The Ohio State University, Columbus, Ohio Ophthalmic Equipment and Techniques Diseases of the Lens Diseases of the Uvea Glaucoma
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Preface
The world of small animal veterinary medicine continues to grow in scope and complexity. Practicing veterinarians and veterinary students are continuously bombarded with new information on the diagnosis and treatment of diseases affecting pet animals. Busy veterinarians have precious little time to keep up with current developments in the profession. We recognize that challenge, and thus we attempt to provide a comprehensive book that covers the commonly encountered disorders seen in small animal practice. Although difficult to include all the pertinent material in a one-volume text, the semi-outline format used in the Manual allows our authors to be concise, yet thorough. As in the first two editions, we continue to make information user friendly by including many key points, condensing information into tables and bulleted lists, and illustrating procedures and surgical techniques with many simple line drawings. However, it is impossible to provide an exhaustive discussion of all small animal diseases in one book. Pathophysiology of disease, rare conditions, and infrequently used diagnostic and treatment methods are not included. Readers are directed to many well-written veterinary textbooks or journals that cover various subjects in greater detail than what we have space for in the Manual. But the Manual seems to have found a niche. From what countless practitioners and students have told us, it is a text that is not kept on a bookshelf gathering dust, but is open on a counter, desk, or exam table where it is almost constantly being used to update or review important clinical information. This is exactly how we hoped the book would be used. Although we have stayed true to the book’s original style, we have added some new authors, section editors, and chapters. New chapters include Pain Management, Vaccination Guidelines, Disorders of the Claw, Postoperative Physical Rehabilitation, and Syncope. Examples of other new areas covered in the third edition are: new emerging infectious diseases; skin cytology for diag-
nosis of skin disorders; an overview of current imaging techniques such as digital radiography, computed axial tomography, and magnetic resonance imaging; technique for laser declaw; indications for laparoscopic and thorascopic surgery; and a brief discussion of arthroscopic procedures for certain joint disorders. Additionally, all chapters, even if rewritten by the same author, have been thoroughly and meticulously revised and updated, and several new illustrations have been added. The Appendix of Drug Dosage Guidelines has also been updated and many new drugs included. We are very grateful to all those who have contributed to the third edition of the Manual. The section editors and chapter authors have done an excellent job organizing and presenting information in their areas of expertise. They have correlated their own clinical experience with information available in the literature and have provided useful and practical information. We also wish to thank the faculty, residents, and students at The Ohio State University College of Veterinary Medicine for their support and advice on the preparation of this edition. The Manual is the result of a tremendous amount of organizing, copyediting, proofreading, and attending to details. We are indebted to the staff at Elsevier for all their hard work, particularly Ms. Jolynn Gower, Managing Editor. Thanks also to Ms. Joy Moore, Senior Project Manager. We also thank Ms. Sarah Self, Production Editor and the staff at Graphic World Publishing Services. Finally, we appreciate the work of our very talented medical illustrator, Ms. Felecia Paras. As we have indicated in both of the previous editions of the Manual, we are striving for continued improvement of our work. We welcome any comments or criticisms that will help make future editions an even more valuable part of the small animal clinicians’ library. Stephen J. Birchard, DVM, MS Robert G. Sherding, DVM
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Section
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Patient Management Stephen J. Birchard
History and Physical Examination Denise Jones
Veterinarians are faced with many diagnostic challenges on a daily basis. By far the most important diagnostic tool that veterinarians possess is their ability to obtain a complete history and perform a thorough physical examination. This information, when accurately interpreted, lays the foundation for a logical diagnostic and therapeutic plan. A systematic and thorough history and physical examination prevents unnecessary diagnostic testing and needless cost to the owner.
GENERAL HISTORY Obtain both objective and subjective information when collecting the history.
•
• Objective data consist of the signalment, environ-
•
ment, diet, and medical history. For a patient’s first visit, determine the length of ownership and the place of origin. Subjective data include a description of the primary complaint and a historical overview of the patient’s general health. The owner often may not realize how a seemingly unimportant observation may be related to the primary problem. Tailor specific questions to the individual case.
Signalment • The signalment consists of the patient’s age, species, breed, and gender. Note whether the patient is intact
or neutered. The patient’s breed will sometimes become a key factor when formulating differential diagnoses. Congenital or hereditary disorders should be considered. For example, familial renal disease should be a primary differential for a young Shih Tzu presenting with polydipsia and polyuria. In other cases the disease process may not be congenital or hereditary, but it may be more prevalent in certain breeds than others. For example, a small-breed dog that presents with lameness that is localized to the hip is more likely to have avascular necrosis of the femoral head (Legg-Perthes disease) than hip dysplasia. Verify that previously recorded data are correct and up-to-date. For example, the patient may have been neutered since its last visit or the physical examination may indicate that the recorded age is questionable.
Environment • Gather environmental information as a routine part •
of the patient’s history. In many circumstances, where the pet is kept provides a vital clue in diagnosis. Determine whether the pet is free roaming or confined to a yard or house. If the patient is confined to a yard, ask the owner if the yard is fenced, if the pet is chained, and if an escape has been possible in the recent past. The free-roaming or recently escaped pet may have had access to toxins or have been 1
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subject to trauma, which is less likely for an indoor pet. For example, in a dyspneic patient, diaphragmatic hernia ranks higher on the differential diagnosis list for a free-roaming pet than for a strictly indoor pet. Determine the geographic origin of the pet and any record of recent travels. This becomes paramount if the patient has been exposed to diseases endemic to certain regions but not prevalent in the current environment, such as systemic mycoses and vector-borne diseases. Determine the pet’s water source. This may be important if the pet has access to contaminated outdoor water, toilet-bowl water treated with deodorants or cleansers, or if the pet has limited access to water. Question the owner if there has been any potential exposure to toxins such as antifreeze, pesticides, or insecticides if the patient’s clinical presentation is indicative of intoxication. Exposure to houseplants or outdoor vegetation may also provide a clue. For a vomiting or anorexic patient, questions should include access to potential ingested foreign bodies.
Dietary History • Always include dietary information in the routine
•
database. Question the owner about the patient’s appetite and noticeable weight gain or loss. Also note whether the owner watches the pet eat. Determine the following pertinent facts in the dietary history: • Type of diet (e.g., dry, moist, semimoist, or table food) • Brand name of food • Type of snacks • Method of feeding (i.e., free-choice or individual meals) • Amount
Preventive Health Care Status • Evaluate the patient’s preventive health care status.
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Prior Medical History: Previous Illnesses and Surgeries • Often the patient’s prior or ongoing health problems
• • •
•
dates of each. Avoid simply asking if the patient is current on vaccinations because many clients are unfamiliar with vaccination recommendations. Inform the client about what vaccinations are available as well as the indications and booster intervals for each (see Chapter 7). For a feline patient, discuss the subjects of feline leukemia virus (FeLV) and feline immunodeficiency virus (FIV), including the dates and results of previous testing. Exposure to stray cats or cats known to be FeLV-positive or FIV-positive may also be relevant. History of previous cat fight wounds may warrant repeat testing for FIV. However, if the patient has been previously vaccinated for FIV, then further FIV
play a role in its presenting ailment; therefore, review the information previously recorded in the medical record and discuss previous problems managed by other veterinarians. Record the dates of the previous illness or surgery, followed by a brief description of the problem, how it was managed, and the response to treatment. Discern the relevance of prior illnesses before obtaining extensive details; otherwise, the history may become unnecessarily lengthy and confusing. Specifically question the owner as to any medications the patient is currently or has recently been given. Over-the-counter products as well as prescription medications should be noted.
Primary Complaint • Use the history to identify and localize the primary
• •
Review the patient’s prior medical record.
• Record all previous vaccinations received and the
testing will be invalid since the FIV test is an antibody test. For a canine patient, record heartworm test dates and results. If the patient is receiving heartworm preventive therapy, note the type, frequency, and dose (see Chapter 152).
•
problem. Much of this information is subjective, based mostly on the owner’s interpretation of the pet’s clinical signs and behavior. Be aware that some owners are extremely observant of their pet and others are not. Prompt owners to describe the pet’s behavior and clinical signs in their own words. An astute clinician collects all data and subjectively analyzes this information in context of an owner’s perceptivity. Encourage the owner to describe the patient’s problem from its onset so that a chronologic picture is obtained. Avoid leading questions that might result in a deceptive history. For example, ask if there has been any change in frequency of defecation. Do not ask if the patient is defecating more frequently than normal. Determine the last period of normalcy or the duration of the clinical signs. This will help determine how acute or chronic the problem may be and will guide the ranking of differential diagnoses. Some differentials are more likely for an acute problem; others are more likely for a chronic problem. For example, intestinal intussusception or an intestinal foreign body are likely differentials for a puppy presenting with an acute episode of persistent vomiting. A gastric foreign body or inflammatory bowel disease are more likely in a similar patient with chronic intermittent vomiting. The onset and severity of the illness influences how rapidly or aggressively the problem should be approached.
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• Determine the progression of the clinical signs. Once
•
•
•
again, this may help not only in formulating a list of differentials but also in developing a treatment plan. For example, a patient presenting with a history of seizures is managed more aggressively when the seizures are increasing in frequency and length than when they have been the same for months or years. Question the owner as to any intervening signs that might provide a clue to the most likely differential diagnosis. For example, a cat with chronic diarrhea and intermittent episodes of fever is considered a more likely candidate for infectious disease than for dietary intolerance. Attempt to further define and localize the problem. For example, characterize diarrhea as originating in the small or large bowel before proceeding to a diagnostic or therapeutic plan. Ask questions regarding frequency, appearance (color and consistency), and presence or absence of straining to help localize this problem. Specific questions oriented by body systems follow in the next section. Determine treatments and response. For example, a dog presenting with pruritus unresponsive to previous treatment with corticosteroids is a more likely candidate for food allergy dermatitis than for atopy. Record what medication was given, the dose, the duration of treatment, and the level of response observed.
HISTORY ORIENTED BY BODY SYSTEMS For a complete history, include a system-by-system review of the patient’s general health. This can be accomplished by the experienced clinician as the physical examination is performed. The novice may prefer to obtain the entire history before proceeding with the physical examination. Develop a consistent and systematic method. One method is to begin with questions concerning the patient’s head and proceed caudally, as demonstrated in the following text. It is left to the clinician’s discretion as to how in-depth the client is questioned about systems that do not appear to affect the primary complaint. Apply the general principles described in the previous section in the approach to all body systems (e.g., onset and duration).
Eyes • Ask if any ocular discharge has been noted. If so,
•
describe the discharge (serous, mucoid, or mucopurulent) and determine if it has been unilateral or bilateral. Determine if ocular pain or discomfort is present as indicated by blepharospasm, face rubbing or pawing, or photophobia. These signs may be seen with anterior uveitis, glaucoma, corneal ulcerations, or foreign bodies.
3
• Ask about ocular redness, swelling, and asymmetry. • Ask if the owner has noticed a color change in the pet’s
•
eye. This change can occur with anterior uveitis and iriditis, in which hyphema may be present or the iridial color may be altered. A localized pigment change in the iris may occur with an iris cyst or melanoma. Ask the owner if their pet seems to be experiencing any loss of vision. If there is an apparent problem, does it seem to be affected by daylight or darkness? Also ask if decreased vision appears to be a unilateral or bilateral problem. See also Section 10.
Head, Neck, Ears, Nose, and Oral Cavity • Record any history of swelling or asymmetry of the head and neck region.
• Inquire about head shaking, ear scratching, and otic
•
•
discharge or odor that may indicate the possibility of otitis or a foreign body in the ear. Determine if any loss of hearing has been evident. Ask if any nasal discharge has been present. Note the character of any nasal discharge (serous, mucoid, mucopurulent, or hemorrhagic) and whether it has been unilateral or bilateral. Note any history of sneezing, nose rubbing, nasal asymmetry, or stridor. Request information relating to the oral cavity, such as odor, difficulty eating or drinking, abnormal swellings involving the gingiva or tongue, and changes in gingival pigmentation. Ask if there has been any change in the patient’s ability to vocalize. The patient’s voice can be affected either by a mass in the laryngeal region or by laryngeal paralysis.
Cardiopulmonary System • Ask if cough, exercise intolerance, weakness, or fainting have been observed. These may indicate cardiopulmonary disease. ▼ Key Point Attempt to differentiate syncope from seizures based on the owner’s description of the event.
• Syncope is a transient loss of consciousness that may be precipitated by exercise in patients with underlying cardiac disease (see Chapter 148). During a syncopal episode the patient usually demonstrates very little motor movement. The episode typically lasts less than a minute, and usually the patient returns to normal within a short period of time. Seizures vary greatly in severity. They are often preceded by a preictal phase during which the patient may be anxious or disoriented. The actual seizure usually involves a loss of consciousness and active motor activity such as tonic-clonic limb movements and rapid jaw movements. The postictal phase may last from minutes to days. The patient may be either overly agitated or depressed during this time. Seizure disorders are discussed in Chapter 127.
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Section 1 / Patient Management
• Characterize coughing as productive or nonproduc-
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tive, moist or dry, and harsh or honking. Some owners may confuse a productive cough with vomiting; therefore, ask whether abdominal heaving occurs prior to the production of fluid or foam or whether coughing and gagging are more typical. Yellow or green fluid is indicative of vomitus. The circumstances surrounding the cough are often relevant. For example, cough associated with tracheal collapse is often elicited with excitement or pulling on the patient’s collar. Coughing secondary to congestive heart failure may be exacerbated with the pet in a sternal position. Is the pet routinely exposed to cigarette smoke? This can play a role in chronic bronchitis or feline asthma. Determine if dyspnea has been observed. It may be difficult for an owner to differentiate between heavy panting and true dyspnea. Ask if the pet is breathing the same during the exam as it was at home. Also inquire if the pet seems reluctant to exercise or lie down, as would be expected with most dyspneic animals. Open-mouth breathing for a cat is always considered abnormal except when it is excessively stressed. See also Chapter 142.
Digestive System Most problems related to the digestive system are clinically manifested as anorexia, regurgitation, vomiting, diarrhea, constipation, weight loss, or a combination of these. Determine which clinical sign is being exhibited, because the owner may incorrectly interpret what is observed. For example, owners often assume that their pet is constipated if it is observed straining to defecate, when diarrhea may be the actual cause. Ask specific questions to differentiate between vomiting and regurgitating. Regurgitation is characterized as a passive ejection of ingested material from the esophagus. It typically occurs soon after a meal is eaten. The regurgitated material is usually undigested and tubular in form. Vomiting frequently involves an abdominal heave movement or retching. Time of vomiting in relation to eating should be noted and is variable depending on the underlying disorder. Vomitus is not tubular in form and may consist of froth, fluid, yellow-green bile, food, or ingested foreign material. Include the following specific information in approaching a digestive system problem:
• Review dietary history, as previously described. Specifically ask about treats or access to garbage. environmental history, as previously described. • Has there been any exposure to toxins, drugs, or plants? • Are there any toys or other foreign objects that the pet may have ingested? Note vaccination status.
• Record
•
• Ask how the patient’s appetite has been and how it compares with its normal appetite.
• Has any vomiting been noted (onset, frequency,
•
progression)? • Has the owner actually observed the pet vomiting? In a multi-pet household, verify that it is the presenting patient that is actually vomiting. • Does the pet exhibit any retching or abdominal heaving when “vomiting”? • How frequently is the pet vomiting? • What is the relationship of vomiting to eating, if any? • What is produced when the pet vomits? Describe the vomitus—digested or undigested food, fluid, foam, and color. Green or yellow fluid is typical of bile. Has the owner witnessed the patient defecating, and are there any abnormalities? • How long since the last observed bowel movement? • Has any diarrhea been observed (onset, progression)? • Has the stool been persistently loose? • How frequently does the animal defecate? • What volume of stool is typically produced? Small amounts of stool produced frequently are indicative of large bowel disease, and larger amounts of stool produced less frequently are more typical of small bowel disease. • What is the color and consistency of the stool (formed but soft, cow patty–like, watery)? • What is the consistency of the last stool produced? • Is there any blood or mucus present? (These are indicative of large bowel disorders.) • Does the animal strain while defecating? Straining is typical of diseases localized to the colon, rectum, or anus. • Does the owner witness all eliminations (i.e., is the pet walked on a leash, does it have access to a fenced yard. or does it roam free)? Consider that owners may not be fully aware of what their pet is eliminating. See also Section 6.
Urinary System Often, the owner complaint may be that the pet is urinating excessively. The following questions help distinguish whether excessive urination is due to polyuria or pollakiuria:
• Has there been any change in the quantity of water that the pet consumes?
• Are there other pets in the household that have access to the same water source?
• Is the pet urinating inside the house (i.e., having “accidents”)?
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•
• •
•
• Are these urinations observed? (The owner should verify that this is the pet having the accidents versus another pet in the household.) • Does the owner know if the accidents occur while the animal is awake or asleep? If the owner has not observed the act, there may be other clues to pursue. Where has the owner found the accidents (where the pet sleeps, next to a door, etc.)? A patient that is experiencing urinary incontinence may be dribbling urine while resting in its sleeping area. Dogs that are well house-trained may urinate close to an outside door if they are unable to hold their urine until allowed access to the outside yard. Another clue to urinary incontinence is the presence of urine on the pet’s perineal region or rear legs. • Does the animal seem to be consciously aware of the act, or does the animal dribble urine without seeming to be aware? Has there been any change in frequency of urination? If the patient is urinating frequent small amounts (pollakiuria), then differentials should include lower urinary tract disorders such as cystitis, urolithiasis, and neoplasia. Does the animal appear to strain while urinating? (This is typical of lower urinary tract disease.) What quantity of urine is produced? Larger quantities of urine are indicative of polyuria, which occurs with a large number of underlying metabolic disorders (renal disease, liver disease, diabetes, mellitus, diabetes insipidus, hyperadrenocorticism, hypercalcemia, etc.). Has the owner noticed any blood in the urine? If so, is it before, during, or after urination? Bleeding only at the beginning of urination is more likely to be from the urethra. Hematuria present throughout the urination is most typical of bleeding of renal origin. Blood seen at the end of urination usually originates from the urinary bladder. Remember to consider the genital system as a potential source for the blood, as with prostatic disease or vaginal masses. See also Section 7.
Genital System Females
• Verify if the patient is intact or spayed. • Note any vulvar discharge and describe the amount, •
consistency, color, and odor. This type of discharge may be valid for spayed pets as well as intact ones. If the patient is intact, ask the following questions: • When did the owner last observe a heat cycle for the patient? Was it a normal cycle? How long did it last? • Have the heat cycles been at regular intervals? • Has the pet been intentionally bred or is there any possibility of an accidental breeding? Is there any
5
previous history of pregnancy? If so, were there any complications (e.g., dystocia, abortions, mastitis, metritis, etc.)? • If there is a history of successful pregnancy, how many puppies were whelped? • Has the patient been tested for brucellosis? When? Was the mate previously tested?
Males
• Verify if the patient is intact or neutered. • Has the patient exhibited any evidence of difficulty urinating or defecating?
• Has any preputial or penile discharge been noted? (Describe the amount, consistency, color, and odor.)
• The following questions apply to intact males: • Has the patient been used for breeding? If so, when was he last bred? Was there any difficulty in breeding? • Were any litters sired? If so, how many puppies were in each litter? • Has the patient been tested for brucellosis? When? Was the mate previously tested? See also Section 7.
Swelling or Masses Ask if any abnormal masses or swellings have been observed that have not been previously mentioned. Note the location, how long the mass or swelling has been present, and any change in appearance, character, or size. If the patient has not been examined in your practice before, ask if the mass has been previously sampled by either a fine needle aspirate or a surgical biopsy. Obtain a fine needle aspirate from masses that have not been previously investigated. ▼ Key Point Perform diagnostics on masses that are changing rapidly since there is a higher incidence of malignancy associated with these.
Skin An accurate and detailed history is essential for successful management of dermatologic problems. Remember that some systemic disease processes may manifest themselves in cutaneous changes, such as hyperadrenocorticism or systemic lupus erythematosus (SLE). Some clinicians prefer to have the owner fill out a standardized dermatologic history form prior to specific questioning. Include the following questions on such a form, or directly ask the owner:
• Has any hair loss been observed? Did hair loss involve the undercoat or the main coat?
• Is there evidence of pruritus (scratching, biting, or licking)?
• Where does the pet seem to be most pruritic? Many atopic and food-allergic patients may rub their faces
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and lick their feet excessively. Flea-allergic patients predominantly chew the dorsal tail-base region. • If the pet is pruritic, how severe is it? Have the owner grade the degree of pruritus on a scale of 1 to 10, with 10 being the most severe. This helps subsequent evaluation of treatment response. • Is the skin problem continuous or seasonal? If seasonal, then determine when the pet is most severely affected. • Has the owner noticed fleas? What flea products have been used? Has the pet been on monthly preventive treatment? If so, which product? • What type of bedding does the pet use? • Is there any exposure to feathers? • What type of carpet is in the house (wool, synthetic, cotton)? • What is the diet? What treats are given? • Are there any indoor plants? • Is the pruritus worse indoors or outdoors? • Is there any exposure to tobacco smoke? • Has the pet ever had any drug reactions? (describe) Describe odors, pigment changes, or texture changes of the skin or hair coat. Does the pet have any dandruff? If so, what areas are involved? How often is the patient groomed (clipped, brushed, combed)? How often is the patient bathed? When was the pet last bathed, and what products were used? Are there other pets in the household? Has the pet been exposed to other animals outside of the household? Did any of these animals exhibit signs of skin disease? Do any members of the household have skin problems? Do any of the pet’s close relatives have a history of skin problems? Has there been any previous treatment? When was the pet last treated? What was the name of the drug, the dose, the route of administration, and the frequency of treatment? What level of response was noted? See also Section 5.
Musculoskeletal System • History relating to the musculoskeletal system generally focuses on lameness or discomfort.
• Remember to correlate the age and breed of the individual to the lameness observed. There are numerous examples in which the signalment may provide a clue to the underlying disorder. Many musculoskeletal disorders occur predominantly in young, large-breed dogs. These include but are not limited to osteochondritis dissecans, ununited anconeal process, panosteitis, and hypertrophic osteodystrophy. Middle-aged to older large-breed patients are more at risk for neoplasia such as osteosarcoma.
•
• •
•
• •
•
Small-breed individuals have a higher tendency toward medial patellar luxation and avascular necrosis of the femoral head. When lameness has been observed, discern if the patient has been bearing weight on the affected leg. Determine if lameness has been previously observed in this limb or other limbs. For example, panosteitis is often considered a shifting leg lameness. Ask if there are any other signs of illness in addition to the lameness. The lameness may be a manifestation of systemic disease such as SLE or Lyme disease. Has the owner noticed any swelling or masses associated with the affected limb? Is the lameness intermittent, progressive, or static? Is the lameness worse before or after exercise? Arthritic patients often “warm out” of their lameness. Question owner in regard to routine daily activity such as running, jumping, hunting, jumping on and off furniture, etc. Has the pet engaged in any activities out of the ordinary lately? These patients are more at risk for traumatic injuries such as a cranial cruciate ligament tear or a ruptured intervertebral disc. Ascertain any possibility of trauma that could have resulted in a fracture. In some cases, the owner may have witnessed the traumatic incident. In others, the patient may have been unsupervised during the time in question. Specifically ask if the patient was confined to the house or a fenced area. If the animal was free roaming and unobserved, determine how long it was unsupervised to help assess the possibility of a traumatic incident. Determine if the owner has observed loss of muscle mass, asymmetry of the limbs, or swollen joints. Ask if the patient has demonstrated any difficulty rising, climbing stairs, or descending stairs. These problems are frequently noted in patients with hip dysplasia, intervertebral disc disease, or neurologic diseases such as degenerative myelopathy. In regions endemic for Lyme disease, ask if any ticks have been observed on the pet. Check vaccination status regarding Lyme disease. In nonendemic areas, obtain a travel history. See also Section 8.
Nervous System Many questions related to the nervous system may have been previously asked while taking the history of the other body systems. Once again, consider the age and breed to help provide clues to the differential diagnoses. Small-breed dogs are more commonly seen with portosystemic shunts and may present with neurologic signs. Hypoglycemia and congenital diseases are prime differentials for seizuring puppies. Epilepsy typically has an onset in young adults. For seizures with an onset during middle age or geriatric years, consider metabolic disease or neoplasia. Diseases of the central nervous
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system (CNS) may be reflected by abnormalities in other systems (e.g., blindness, hearing loss, or urinary incontinence). With a presenting complaint of rear limb “weakness,” differentiate between disorders of the musculoskeletal system and those of the nervous system with the history and physical examination. Consider the following points in regard to the nervous system:
• Verify vaccination history for distemper and rabies. • Focus on obtaining a good environmental history,
• •
• •
•
such exposure to toxins or plants. Is there any possibility of a traumatic accident resulting in head trauma or spinal injury? Ask if any behavioral changes, such as aggression or dementia, have been observed. If these signs are present, are they intermittent or persistent? Is there any evidence of pain when the patient is touched or picked up? Does the pet cry or yelp when it moves? These signs can occur in a patient with intervertebral disc protrusion. Record any history of seizures, including their duration and the time interval between them. Obtain a description of the seizure. If behavioral changes or seizures have been observed, ask if there is any relationship between when the pet eats and when these signs occur. Neurologic signs may be exacerbated postprandially in patients with a portosystemic shunt. Ask if there has been any evidence of weakness in the patient. If present, is the weakness generalized or localized (i.e., to one side of the body, in the forelegs, or to the rear)? Determine if any abnormalities in posture or ambulation have been observed, such as the pet’s tendency to fall to one side, to circle to one side, to knuckle over, or to drag its toes. Be sure to note the acuteness of onset and the progression of the neurological signs.
•
cat. The most commonly used systems utilize either a 5- or 9-point scale. I prefer the 5-point scale, where score 1 correlates to an emaciated body condition and score 5 indicates a grossly obese state. Score 3 is considered an ideal weight for the patient. Those body conditions that fall between two scores are assigned a half score. For example, a patient that is just over its ideal weight would be scored as 3.5. Refer to Tables 1-1 and 1-2 for details of body condition scoring in dogs and cats, respectively. Record the patient’s body condition score (BCS) in the patient’s record each visit. If the collection of the history and the physical exam result in a vague, poorly defined illness, consider hospitalizing the patient for observation. Sometimes owners may find it difficult to accurately describe the pet’s behavior or clinical signs. Also, some patient’s may mask their depression or pain when they initially arrive in a new environment. A nervous patient should be reevaluated once it has adjusted to the hospital surroundings. Occasionally, animals become more agitated the longer they are away from their owner. Finally, many disease processes become more evident with time, so the physical should be repeated on any undiagnosed or hospitalized patient.
Table 1-1. BODY CONDITION SCORING FOR DOGS Score
Body Condition
Parameters Evaluated
1
Emaciated
2
Thin
3
Ideal
4
Overweight
5
Obese
Skeletal in appearance with no obvious body fat and minimal muscle mass. Boney prominences visible. Ribs slightly visible and easily palpable. Prominent waist and abdominal tuck from side and dorsal views. Ribs not visible but palpable with only a slight fat covering. Abdominal tuck present from side view, and waist present from dorsal view. Smooth contour over tail base. Difficult to palpate ribs because of moderate fat layer. Loss of abdominal tuck from side view, and wide waist from dorsal view. Thickening over tail base. Excessive fat cover over entire body. Ribs extremely difficult to palpate. No waist present from dorsal view. Fat skin folds droop from caudal abdomen on side view. Thick fat roll at tail base.
See also Section 9.
PHYSICAL EXAMINATION: GENERAL OBSERVATION • To begin the physical examination, watch the patient as it enters the room.
• Continue the visual evaluation of the patient while
•
the history is collected. Observe the general body condition and any abnormalities in behavior, attitude, posture, ambulation, and respiratory pattern. During this time, the patient may be placed on the examination table or allowed to roam the examination room. During the general observation of the patient, evaluate its body condition. Several body condition scoring systems have been developed to aid in assessing the amount of body fat present in the individual dog or
7
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Table 1-2. BODY CONDITION SCORING FOR CATS Score
Body Condition
Parameters Evaluated
1
Emaciated
2
Thin
3
Ideal
Skeletal in appearance in the shorthaired cat. Boney protrusion of the wing of ilia and lumbar vertebra. Ribs easily palpable with only slight fat covering. Waist prominent caudal to ribs. Minimal abdominal fat present. Uniform distribution of body fat. Ribs palpable but not prominent. Slight waist present caudal to ribs. Minimal abdominal fat pad present ventrally. Ribs difficult to palpate. Loss of visible waist and some abdominal distention present. Moderate abdominal fat pad present ventrally. Ribs not palpable. Excessive fat deposits generalized but especially noted in abdominal region.
4
Overweight
5
Obese
PHYSICAL EXAMINATION: VITAL SIGNS Initially, record the vital signs and current body weight of every patient.
Body Temperature • Obtain the rectal temperature early in the course of
• •
the examination to help avoid an elevation of temperature that may result from anxiety or excitement. If you are unsure whether the elevated temperature is the result of environmental factors, then consider hospitalizing the patient to recheck the body temperature in a few hours. In emergency situations, attend to hypothermia or hyperthermia early in the course of the examination. Normal rectal temperature for dogs range from 99.5°F to 102.5°F. For cats the range is 100.5°F to 102.5°F. Note any blood or melena that is evident on the thermometer.
Pulse and Heart Rate • Record the pulse rate and evaluate the pulse quality. • Normal heart rate values (beats per minute) are as follows: • Large dogs—60 to 100 bpm • Medium-size dogs—80 to 120 bpm
•
• Small dogs—90 to 140 bpm • Domestic cats—140 to 250 bpm Determine if arrhythmias or pulse deficits are present.
Capillary Refill Time • Lift up the upper lip, press on the buccal mucous membranes, and determine how long it takes for the membranes to resume normal pink color (normal is 30
3.0–5.0 5.0–7.5 7.5–9.5 9.5–12.0 2.5–4.0
Dogs
Cats
Table 2-2. NORMAL VALUES Dogs Awake Temperature (°F) Heart rate (bpm) Respiratory rate (breaths/minute) Capillary refill time (sec) Packed cell volume (%) Total plasma protein (g/100 ml) Total leukocytes (6,000–17,000/ml) Albumin (g/100 ml) Sodium (mEq/L) Potassium (mEq/L) Chloride (mEq/L) Calcium (mg/100 ml) Creatinine (mg/100 ml) Blood urea nitrogen (mg/100 ml) Arterial pH Arterial pCO2 (mm Hg) Arterial pO2 (mm Hg) Arterial HCO3 (mEq/L) Arterial base excess (mEq/L) CO2 combining power (mEq/L)
99.5–102.5 70–180 20–40 50% inspired O2)
Cats Awake 100.0–102.5 145–200 20–40 50% inspired O2)
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Table 2-4. ANESTHETIC DRUGS AND DOSES IN DOGS Drug
Intravenous Dose (mg/kg)
Intramuscular or Subcutaneous Dose (mg/kg)
Anticholinergic Atropine Glycopyrrolate
0.02–0.04 0.005–0.010
0.02–0.04 0.005–0.010
Tranquilizer/Sedative Acepromazine Xylazine Medetomidine Diazepam Midazolam
0.05–0.20 0.3–0.8 0.007–0.020 0.10–0.25 0.05–0.20
0.1–0.3 0.5–1.5 0.01–0.04 0.10–0.25 0.1–0.2
Analgesic Morphine Oxymorphone Fentanyl Meperidine Butorphanol Nalbuphine Buprenorphine Hydromorphone
NR* 0.05–0.10 0.002–0.005 0.4–2.0 0.1–0.2 0.5–2.0 0.005 0.05–0.2
0.2–0.5 0.1–0.3 0.004–0.008 1.0–4.0 0.1–0.4 0.5–2.0 0.005 0.1–0.4
Anesthetic Tiletamine/zolazepam (Telazol) Thiopental Etomidate Propofol
0.5–4.0 6–10 1–4 2–6
4–10 NR NR NR
Combination Acepromazine/oxymorphone Acepromazine/butorphanol Ketamine/acepromazine Ketamine/xylazine Ketamine/diazepam (50 : 50)
0.05–0.10/0.01–0.02 0.05–0.10/0.1–0.2 2–5/0.05–0.10 1–5/0.1–0.8 1 ml/10 kg
0.1–0.2/0.1–0.2 0.1–0.2/0.1–0.2 5–10/0.1–0.2 5–10/0.3–1.5 NR
*NR, not recommended.
• Not an analgesic itself, but it may potentiate other
• Produces profound cardiopulmonary depression,
drugs that are analgesics. Produces hypotension through an a-adrenergic blockade, particularly in large doses. Potentiates hypothermia. Epinephrine reversal (i.e., hypotension after epinephrine administration) can occur. Calms excitable dogs. Aggressive dogs or cats may not become tractable. Combine with opioids or cycloheximides to produce the desired effect (see Tables 2-4 and 2-5). Avoid in animals with epilepsy, shock, bleeding disorders (inhibition of platelet function), or liver disease. Reduce the dose or choose another agent in stressed or older animals because effects may be exaggerated. Cats are calmed but usually still resist restraint.
including bradycardia, first- and second-degree atrioventricular blockade, catecholamine sensitization, and decreased respiratory rate. Combine with an anticholinergic (atropine or glycopyrrolate), particularly if large doses are administered. Do not use in patients with preexisting cardiac, liver, or kidney disease or with shock. Reverse effects with yohimbine, tolazoline, or atipamezole (see “Recovery and Reversal” for doses). Vomiting occurs in approximately 25% of dogs and 50% of cats. See Tables 2-4 and 2-5 for doses.
• • • •
• •
Xylazine
• An a -adrenergic agonist that produces sedation with
• • • • •
Medetomidine
• An a -adrenergic agonist that produces sedation with 2
•
2
muscle relaxation and analgesia.
• Produces an obtunded state from which the patient is difficult to arouse.
• Produces analgesia for minor procedures. Is not usually sufficient for surgery.
• •
muscle relaxation and analgesia (see Tables 2-4 and 2-5 for doses). Similar to but approximately 100 times more potent than xylazine with a longer duration of action. Produces analgesia for minor procedures. Combine with ketamine or opioids to enhance analgesia. Produces dose-dependent cardiopulmonary depression including bradycardia, decreased arterial blood pressure, and slowing of respiratory rate.
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Table 2-5. ANESTHETIC DRUGS AND DOSES IN CATS Drug
Intravenous Dose (mg/kg)
Intramuscular or Subcutaneous Dose (mg/kg)
Anticholinergic Atropine Glycopyrrolate
0.02–0.04 0.005–0.010
0.02–0.04 0.005–0.010
Tranquilizer/Sedative Acepromazine Xylazine Medetomidine Diazepam Midazolam
0.05–0.20 0.4–1.0 0.01–0.03 0.10–0.25 0.05–0.20
0.1–0.3 0.8–1.8 0.03–0.08 0.10–0.25 0.1–0.2
Analgesic* Oxymorphone Butorphanol Nalbuphine Buprenorphine Hydromorphone
0.01–0.04 0.05–0.20 0.5–1.5 0.005 0.05–0.1
0.05–0.10 0.1–0.3 0.5–1.5 0.005 0.1–0.3
Anesthetics Ketamine Tiletamine/zolazepam (Telazol) Thiopental Etomidate Propofol
4–10 0.5–4.0 6–10 1.0–4.0 2–6
10–20 4–12 NR† NR NR
Combination Acepromazine/oxymorphone Acepromazine/butorphanol Ketamine/acepromazine Ketamine/xylazine Ketamine/diazepam (50 : 50)
0.05–0.07/0.01–0.04 0.05–0.07/0.07–0.15 4–8/0.05–0.10 4–8/0.1–0.8 1 ml/10 kg
0.1–0.2/0.05–0.20 0.1–0.2/0.1–0.2 7–15/0.1–0.2 7–15/0.3–1.5 NR
*Higher doses can be associated with nervousness and excitement. † NR, not recommended.
• Combine with an anticholinergic (atropine or • • •
glycopyrrolate), particularly if large doses are administered. Do not use in patients with preexisting cardiac or kidney disease or with shock. Reverse effects with yohimbine, tolazoline, or atipamezole (see “Recovery and Reversal” for doses). Vomiting, diuresis, and muscle jerking may occur.
Diazepam and Midazolam
• Benzodiazepine derivatives that produce mild seda-
• • • •
tion in dogs and cats. Neither is effective in calming an excited patient when used alone. Both are anticonvulsants. Use to enhance tractability in depressed patients or in combination with other agents (primarily opioids). Administer diazepam IM or slowly IV with caution. The drug is solubilized in a propylene glycol base that can produce bradycardia and hypotension. Administer water-soluble midazolam IV, SC, or IM. Use in patients with cardiorespiratory compromise or another metabolic disease. Both agents produce minimal cardiopulmonary side effects and provide muscle relaxation.
• Use both drugs as premedicants to parenteral or inhalation anesthesia.
• Occasionally, paradoxical responses occur, including disorientation and aggression.
• Diazepam can be given as an appetite stimulant in cats.
• See Tables 2-4 and 2-5 for doses and suggested combinations.
Analgesic Drugs (see also Chapter 6) Nonsteroidal Anti-inflammatory Drugs
• Use nonsteroidal anti-inflammatory drugs (NSAIDs)
• •
• •
for acute and chronic pain associated with inflammation. They reduce pain by inhibiting prostaglandin formation and through central effects. Potentiate the action of other analgesics. Use NSAIDs orally or by injection to provide analgesia, antipyresis, and as an anti-inflammatory in the perioperative period and for chronic pain. Analgesia produced is equivalent to opioids for some types of pain. NSAIDs can cause gastrointestinal injury and renal damage. See Table 2-6 for doses.
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Table 2-6. NONSTEROIDAL ANTI-INFLAMMATORY DRUG USE IN DOGS Nonsteroidal Anti-inflammatory Drug Carprofen Deracoxib Etodolac Ketoprofen Meloxicam Phenylbutazone Tepoxalin
Dosage 2 mg/kg twice daily or 4 mg/kg once daily orally (injectable 4 mg/kg SC once daily) 3–4 mg/kg once daily orally for 7 days 10–15 mg/kg once daily orally 2.2 mg/kg IV, SC, or IM for dogs and cats, single dose 0.1 mg/kg (0.2 mg/kg loading dose) once daily, SC, PO (cats: if given SC, dose of 0.3 mg/kg is used one time only) 40 mg/kg daily in three divided doses for 2 days then reduce 10 mg/kg once daily orally
Opioids
Dissociative Anesthetics
•
Ketamine and Tiletamine/Zolazepam
• • •
• • • •
Use in dogs and cats to augment the effects of sedatives and tranquilizers and to provide analgesia. Minimal or no sedation is produced when administered alone, except for morphine and meperidine. Use in combination with tranquilizers or sedatives. Use lower doses in cats compared with dogs (see Tables 2-4 and 2-5), because higher doses have the potential to cause excitement and disorientation. Morphine, oxymorphone, fentanyl, hydromorphone, and meperidine are opioid agonist drugs frequently used in small animal practice. Regulations require rigorous recordkeeping and security. Vagal tone is increased (bradycardia), and respiration is depressed. Sensations of touch or vision are not diminished. Sensitivity to sound may be increased. May cause vomiting and defecation. Reverse agonists and agonist-antagonists with naloxone. Partial reversal of the respiratory and central nervous system (CNS) depressant effects of agonists can be accomplished with agonist-antagonists (e.g., butorphanol), which reverse the deleterious effects of the agonists and provide the animal with some analgesia.
Fentanyl
• Fentanyl can be administered transdermally using a
•
patch developed for human use. Time from patch application until full effect is 2 to 6 hours in cats and 12 to 24 hours in dogs. The skin must be clipped (or shaved) to facilitate absorption, but absorption varies considerably. Duration of action may be as long as 5 days. Prevent ingestion by the animal or humans.
Other Opioids
• Ketamine and tiletamine/zolazepam (Telazol, Ft.
• • • •
•
Dodge Animal Health, Ft. Dodge, Iowa) produce a unique form of sedation or anesthesia that has been called dissociative anesthesia. These maintain swallowing and ocular reflexes, increase muscle tone, and produce amnesia, superficial analgesia, and catatonia. They stimulate the cardiovascular system, resulting in increased heart rate and arterial blood pressure. They produce an apneustic (breath-holding) respiratory pattern. The intensity is dose related. Use low doses of ketamine (up to 6 mg/kg IM) in the cat to produce an obtunded state with malleable rigidity of the limbs, dilated pupils, and hypersalivation. Higher doses (14–20 mg/kg IM) have been used, but analgesia is not an appropriate level for visceral surgery. Using ketamine with other drugs (xylazine, medetomidine, diazepam, or midazolam) is a better approach in both dogs and cats. Do not give ketamine alone in the dog because of resultant muscle rigidity and seizure activity. See Tables 2-4 and 2-5 for doses. Use tiletamine/zolazepam (Telazol) to produce a state similar to that of ketamine with the addition of muscle relaxation. The drug is approved for IM use in both the dog and the cat. At low doses (2–4 mg/kg IM) it provides helpful restraint in both the dog and the cat. It is also used in small doses IV (0.5– 1.5 mg/kg) in a manner similar to ketamine/ diazepam for induction and short-duration restraint (see Tables 2-4 and 2-5 for doses).
INJECTABLE DRUGS FOR SHORT-TERM ANESTHESIA
• Butorphanol, nalbuphine, and buprenorphine are
•
opioid agonist-antagonist or partial agonist drugs. This classification means that these compounds produce analgesia but have less addictive potential. Degree of analgesia may be sufficient for mild to moderate pain but not for severe pain.
A variety of injectable drugs and drug combinations can be used for short-term anesthesia or restraint in dogs (Table 2-7) and cats (Table 2-8). Many of these combinations employ the drugs previously described. Prior administration or coadministration of sedatives or
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Table 2-7. SUGGESTED ANESTHETIC PROTOCOLS FOR DOGS Patient (Agent)
Dose
Comments
Healthy (Elective Procedure) Acepromazine Thiopental Isoflurane* (or) Sevoflurane*
0.02 mg/kg SC or IM 6–10 mg/kg IV 0.5%–3.5%, inhaled 2.0%–4.5%, inhaled
Total dose not to exceed 4 mg Give 6 mg/kg initially, increase in 2 mg/kg increments Adjust to anesthetic depth Adjust to anesthetic depth
Aged Patient Intravenous fluids Ketamine/diazepam (50 : 50) (or) Propofol Isoflurane* (or) Sevoflurane*
1 ml/10 kg IV 2–4 mg/kg IV 0.5%–3.5%, inhaled 2.0%–4.5%, inhaled
Short duration of action
Patient in Pain Intravenous fluids Acepromazine Oxymorphone Thiopental Isoflurane* (or) Sevoflurane*
0.01–0.02 mg/kg IM 0.05–0.02 mg/kg IM 4–8 mg/kg IV 0.5%–3.5%, inhaled 2.0%–4.5%, inhaled
Can be mixed with oxymorphone Watch for bradycardia Dose is reduced after premedicant; start with 4 mg/kg
Critical Patient Intravenous fluids Diazepam and Propofol (or) Ketamine/diazepam (50:50) Isoflurane* (or) Sevoflurane*
0.02 mg/kg IV 2–4 mg/kg IV 1 ml/10 kg IV 0.5%–3.5%, inhaled 2.0%–4.5%, inhaled
Give slowly Give to effect
*Concentration required depends on fresh gas flow rate. The lower the flow rate, the higher the concentration required.
Table 2-8. SUGGESTED ANESTHETIC PROTOCOLS FOR CATS Patient (Agent)
Dose
Healthy (Elective Procedure) Acepromazine (with)
0.01–0.02 mg/kg SC or IM
Ketamine (and) Thiopental (or) Tiletamine/zolazepam (with) Thiopental Isoflurane* (or) Sevoflurane*
4–8 mg/kg IM 5–10 mg/kg IV 3–5 mg/kg IM 3–7 mg/kg IV 0.5%–3.5%, inhaled 2.0%–4.5%, inhaled
Aged or Renally Compromised Patient Intravenous fluids Midazolam with oxymorphone Ketamine (or) Thiopental (or) Propofol Isoflurane* (or) Sevoflurane*
0.05 mg/kg IM 0.1–0.2 mg/kg IM 1–2 mg/kg IV 3–7 mg/kg IV 2–4 mg/kg 0.5%–3.5%, inhaled 2.0%–4.5%, inhaled
Critical Patient Intravenous fluids Ketamine/diazepam (50:50) Isoflurane* (or) Sevoflurane*
0.5 ml/5 kg IV 0.5%–3.5%, inhaled 2.0%–4.5%, inhaled
*Use a non-rebreathing anesthetic system (Bain or Ayres T-piece).
Comments Mix acepromazine with ketamine; add opioid for analgesia Give to effect Tiletamine/zolazepam may be sufficient for intubation
Drugs can be mixed Give slowly to effect
Administer slowly
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tranquilizers with drugs that produce anesthesia allows a reduction in the dose of the anesthetic drug. Anesthetic drugs tend to produce more depression of cardiopulmonary function than do sedatives or tranquilizers; thus the patient benefits from the decreased dose. Thiobarbiturates are the primary addition to the list of drugs already discussed. Other drugs, such as etomidate and propofol, offer potential advantages, such as fewer cardiopulmonary effects and lack of cumulative effects, but are expensive. Although endotracheal intubation is not required for the delivery of injectable anesthetic drugs, patients can benefit from intubation for protection of the airway and for oxygen supplementation.
Thiobarbiturates (Thiopental) • Sedative or hypnotic agents that produce short-term IV anesthesia.
• Barbiturates produce CNS depression that ranges
Propofol • A phenolic compound that produces hypnosis similar to thiopental.
• Depresses hemodynamics comparable to thiobarbi• • • • •
from drowsiness to coma.
• Not good analgesics at subhypnotic doses. When • • •
•
doses are increased to produce unconsciousness, anesthesia is produced. Cause respiratory depression and some arterial blood pressure depression. Sensitize the heart to catecholamine-induced arrhythmias. Ventricular bigeminy is often noted but resolves without treatment. Duration of effect is primarily determined by redistribution away from the brain into muscle and lean body tissues. Level and duration of anesthesia produced by a given dose depends on what other drugs have been administered, the rate of administration, and the level of awareness of the animal at the time of administration. Use with caution in patients with preexisting cardiovascular disease, hypotension, or shock.
turates, but does not sensitize the myocardium to epinephrine-induced arrhythmias. Depresses respiration. Administer slowly IV over a 30- to 60-second period to minimize the potential for apnea. Use with analgesics for painful procedures. Anesthesia can be maintained using propofol as a continuous IV infusion (0.4–0.8 mg/kg/min). Noncumulative, so recovery following multiple doses or an infusion occurs within the same time frame as that following a single dose. Relatively insoluble. Supports microbial growth if contaminated. Discard unused drug. Useful for induction of anesthesia in sighthounds and patients requiring cesarean section. Useful in compromised patients because of the lack of residual effects.
Ketamine Mixtures Use ketamine in combination with sedatives and tranquilizers to provide short-term injectable anesthesia.
Ketamine/Diazepam
• Administer ketamine with diazepam in a 50:50
•
▼ Key Point Do not use thiobarbiturates in greyhounds or other sighthounds because of prolonged elimination.
(volume-to-volume) mixture at a dose of 1 ml/10 kg IV. Give for brief periods (5–10 minutes) of restraint. Provides enough analgesia for minor surgical procedures. Readminister as needed to effect. Works well in depressed or geriatric patients. May not be effective in young, excited, or aggressive animals. Produces moderate muscle relaxation, cardiopulmonary support, and increased salivation. Ocular and swallowing reflexes are maintained, but orotracheal intubation can be accomplished.
Ketamine/Acepromazine
• •
•
•
Administer to effect, beginning with doses in the range of 4 to 6 mg/kg, increasing in 2 mg/kg increments. Onset of action is within 30 seconds. Can be mixed 50:50 (volume to volume) with propofol to allow a reduction in the dose of both drugs as a way to reduce cost. Can cause sloughing of tissues if administered perivascularly. Use for induction to inhalation anesthesia. Compatible with all agents previously described. Reduce the dose by approximately half if sedatives or tranquilizers are given prior to administration. Duration of action is prolonged by hypoproteinemia and acidosis. Administer IV fluids to shorten duration by promoting diuresis, and administer NaHCO3 (2 mEq/kg) to shorten duration by alkalinizing the urine.
• Use ketamine with acepromazine to produce a quieter recovery than that with ketamine/diazepam but less muscle relaxation. Usually produces enough anesthesia for minor peripheral surgery, but visceral analgesia is not sufficient for abdominal surgery.
Ketamine/Xylazine and Ketamine/Medetomidine
• These combinations produce muscle relaxation, •
sedation, and analgesia that are improved over other combinations. Bradycardia and depression of cardiac contractility and respiration occur. Coadminister an anticholinergic. Use in young animals with good cardiopulmonary reserve. Avoid in animals with preexisting
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cardiovascular disease, particularly those with cardiac conduction abnormalities. The combination of medetomidine (60–80 mg/kg), butorphanol (0.2 mg/kg), and ketamine (5 mg/kg) administered IM is a useful preanesthetic in cats that is sufficient for some surgery and is easily augmented with inhalants.
and endotracheal intubation. The injectable drugs and drug combinations previously described, with the possible exception of ketamine/xylazine combinations, can be used to induce anesthesia. Ketamine/xylazine combinations produce significant cardiopulmonary depression that can be extreme when inhalant anesthetic drugs are added.
Tiletamine/Zolazepam • Use IV or IM to produce anesthesia. • Produces muscle relaxation and support of hemody-
Inhalant Anesthetics • Inhalant anesthetics have several advantages, includ-
•
• •
namics, but also produces respiratory depression. Maintains oropharyngeal reflexes. Recovery is prolonged with increasing doses. Recovery is usually uneventful in the cat but may be stormy in the dog. Administer low doses of acepromazine to quiet a difficult recovery.
Etomidate • A nonbarbiturate hypnotic that can be used for shortterm IV anesthesia.
• Produces a hypnotic state with little cardiovascular • •
effect. Etomidate is expensive. Limit to patients with significant cardiovascular and respiratory disease. Recovery can be stormy, with vomiting and muscle tremors. Premedicate the animal with sedatives or tranquilizers to minimize these effects.
Anticholinergics • Used to reduce salivation, block vagal inhibition of
ing the coadministration of oxygen, the ease with which anesthesia depth is changed, and the fact that recovery does not depend on metabolism. The agents are primarily eliminated by exhalation. Administer via breathing circuits, with circle anesthetic systems being the most common.
Equipment Circle Anesthetic Systems
• A carbon dioxide absorber removes carbon dioxide from the exhaled gas.
• Exhaled gas is rebreathed, making the system an economic one.
• Use 4 to 7 ml/kg/min as the minimum fresh gas flow rate for oxygen. This rate matches the animal’s metabolic need for oxygen. Increase the fresh gas flow rate for oxygen to 10 to 20 ml/kg/min if nitrous oxide is given. Add the nitrous oxide flow to the oxygen flow rate. The pop-off valve in the circle system needs to be open to vent the excess gas at this flow rate.
the heart, and quiet the digestive tract if indicated.
• Not innocuous. Respiratory dead space is increased • • • •
(bronchodilation). Ventricular arrhythmias are more likely to occur. Use if bradycardia occurs or is likely to occur. Not routinely indicated in anesthesia. Myocardial oxygen consumption is increased owing to tachycardia. Secretions become more viscous. Glycopyrrolate is more potent and has a longer duration of action than atropine. It does not cross the placental or blood-brain barrier. Give IM, SC, or IV when expediency is important. Atropine dose is 0.02 to 0.04 mg/kg. Glycopyrrolate dose is 0.01 mg/kg.
Non-rebreathing Anesthetic Systems
• Bain and Modified Jackson Rees (Hudson RCI; Temecula, California) (SurgiVet; Waukesha, Wisconsin).
• Use for patients less than 2 to 4 kg, because less resistance to respiration is produced.
• Use a fresh gas flow of 1.5 times the minute ventilation (approximately 150 ml/kg/min). Fresh gas flow rates are higher because the fresh gas removes carbon dioxide from the system.
Scavenging Equipment ▼ Key Point Use of inhalation anesthetics mandates
ANESTHESIA FOR MAJOR PROCEDURES Anesthesia for major procedures, requiring optimal hypnosis, analgesia, and muscle relaxation for relatively long periods, usually incorporates the inhalant anesthetics (see Tables 2-7 and 2-8). Although inhalant drugs can be given as the sole source of anesthesia, injectable drugs are usually given to facilitate induction
the removal of expired and waste gases from the operating room environment.
• Exhaust waste gases using suction systems or vent them to the outside via a hole in an exterior wall.
• Directing gases to the floor is insufficient. • Use activated charcoal canisters as alternatives to absorb halogenated compounds. This is not effective for nitrous oxide.
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Isoflurane
• The combination of morphine, lidocaine, and ketamine can be used to supplement analgesia and reduce the requirement for inhalant anesthetics. Add 15 ml of 2% lidocaine (300 mg), 0.6 ml ketamine (60 mg), and 1.6 ml morphine (24 mg) to 1 L balanced electrolyte solution. Administer the combination at the standard rate (10 ml/kg/hour IV).
• Halogenated ether that produces anesthesia when inhaled in concentrations of 1.0% to 3.0%.
• Produces very rapid induction and recovery; relatively insoluble in blood.
• Maximal attainable concentration at room temperature is 30%.
• Use in precision out-of-the-circle vaporizers. • Produces dose-dependent cardiopulmonary depres• •
sion. Adequate ventilation is usually maintained. Ventricular arrhythmias are not enhanced. Use in patients with metabolic disease, in geriatric patients, and in patients prone to cardiac arrhythmias. Is minimally metabolized (50% of total kcal) to delay gastric emptying.
Parenteral Nutrition
trolled with insulin therapy as needed (see “Glucose Monitoring”).
Calorie and Protein Content Estimate energy needs of PN patients as previously described. Attempt administration of nutrients at rates exceeding resting energy needs only after the initial goal has proved tolerable for the animal. Provide 2.5 g of protein per kilogram of body weight. Restrict protein intake to approximately 2 g/kg/day in animals with severely compromised liver or kidney function.
Minerals and Vitamin Content
• Parenteral nutrition (PN), or intravenous feeding,
•
allows the provision of short-term metabolic and immune system support to animals with severe GI disease or pancreatitis. Because PN therapy is relatively expensive and is associated with more complications than feeding through the GI tract, use enteral feeding whenever the GI tract can tolerate it. PN is also not indicated when the patient’s prognosis is hopeless. The high osmolality of PN solutions requires the use of a central venous catheter inserted in the external jugular vein or placed in a peripheral catheter and advanced into a central vein. Proper insertion and maintenance of the PN catheter is one of the keys to successful PN therapy. Use aseptic technique when placing the intravenous catheter. If well cared for, central vein catheters may be used for prolonged periods. Do not remove the catheter unless a specific indication for removal exists.
▼ Key Point Once a catheter is placed and designated for PN therapy, do not use it for other purposes, such as drawing blood samples, administering medications, or measuring central venous pressure.
Adverse drug-nutrient reactions and clogged catheters are serious potential complications of these practices.
Glucose Content
• Formulate glucose-based PN solutions based on the
•
patient’s estimated nutrient needs. The most commonly used PN solution for patients at Ohio State University contains 17.5% glucose. Glucose-based PN solutions are filterable, bacteriostatic because of the high osmolality, relatively easy to prepare, and relatively inexpensive. On the other hand, their hyperosmolality necessitates central venous access, and thrombophlebitis may result if solutions are infused at high rates into small veins. Hyperglycemia, usually less than 600 mg/dl, is also more common with glucose-based solutions than with lipid-based solutions. This has minimal pathophysiologic significance but needs to be monitored and con-
49
The macromineral portion of the solution is provided by an amino acid-electrolyte solution. Zinc, copper, manganese, and chromium, as well as water-soluble vitamins, are routinely added to PN solutions. The essential fatty acids, fat-soluble vitamins, and minerals necessary for prolonged PN therapy do not appear to be necessary for the short-term PN more typically provided to veterinary patients.
Apparatus and Delivery
• The apparatus required for PN administration
•
includes the solution, the solution container, an administration set, a 0.22-mm filter, a dedicated central venous catheter, and, preferably, an infusion pump. Provide PN at a rate intended to meet resting energy needs by the end of the first 24 hours, then advance to slightly higher rates of intake, if necessary, over the next 24 to 48 hours as patient tolerance allows.
Glucose Monitoring
• During the initiation phase, measure blood glucose every 4 to 6 hours until stable. Once goals are reached, monitor the patient as described subsequently. At the end of therapy, wean the patient from the solution over 4 to 24 hours as tolerance permits by progressively halving of the infusion rate to avoid hypoglycemia, particularly if insulin has been infused. If the patient is able to eat, offer food and record the food intake. As soon as signs of appetite are observed, decrease the PN administration rate to approximately half the previous rate to encourage the animal to begin eating on its own. ▼ Key Point The most important monitoring parameter for patients receiving glucose-based PN is blood glucose, which is monitored closely during initiation of therapy.
• Treat patients when blood glucose concentrations exceed 250 mg/dl with intramuscular administration of 0.25 U of regular insulin per kilogram of body weight every 4 to 6 hours as necessary. Insulin therapy
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is not commonly required for dogs, although consider it for cats during the first 36 hours to control hyperglycemia. Diabetic animals placed on PN often require continuous infusions of higherthan-expected quantities of insulin to control their blood glucose concentration effectively. When insulin is used, caution must be exercised with regard to the central venous catheter, which is presumed to be in place continually. If insulin is given and then vascular access is lost, give a 5% glucose infusion through a peripheral vein immediately to prevent severe rebound hypoglycemia.
Complications of PN The most common PN-related complications are mechanical, technical, and related to glucose abnormalities. Use a strict protocol for prevention, diagnosis,
and treatment of sepsis. PN-related infections occur only rarely.
Returning to Normal Food Intake
• In general, discontinue assisted feeding when patients begin eating a quantity of food that contains at least half of their calculated daily energy needs. Ideally, the weaning process should take place gradually over at least a day or two before the feeding tube is removed or PN administration stopped.
SUPPLEMENTAL READING Buffington CAT, Holloway C, Abood SK: Manual of Veterinary Dietetics. St. Louis: WB Saunders, 2004.
Chapter
▼
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4
Radiographic and Ultrasonographic Techniques David S. Biller / Laura J. Armbrust
The purpose of the radiograph is to provide a lasting record of maximum information. The sequence of the major operations involved in transforming the altered morphology and tissue density within a diseased animal into a two-dimensional, black-and-white radiograph and then reaching a diagnosis is complex and includes the following steps: (1) making a properly exposed and positioned radiograph; (2) recording the x-ray picture with the assistance of accessory equipment; (3) reviewing radiographs in proper conditions and in a systematic and detailed manner; (4) recognizing lesions—therefore [requiring] a knowledge of normal radiographic anatomy and its variation by age, species, and breed and the ability to recognize and understand artifacts; and (5) evaluating radiographic abnormalities with respect to clinical and laboratory findings.
•
Recommendations • The 300-mA machine may have adjustable mA stations
Dr. Peter Suter
• X-RAY MACHINE
•
Milliampere-Second and Kilovolt Peak • mA (milliampere) ¥ seconds (time) = mAs (milliampere-
•
second), which affects the degree of blackness (density) of the radiograph with no effect on contrast. A direct relationship exists between mA and radiographic density. Time and mA both influence the number of x-rays produced but have no effect on the penetrating ability of the beam. To quickly check the adequacy of the mAs on a film, hold the film up to room light and place a white sheet of paper about 1 inch behind the film. Place a finger between the film and the paper. If the finger can be readily seen through the film in the black area (the most exposed), increase the mAs. kVp (kilovolt peak) is the only machine factor that influences radiographic contrast and has some control over the amount of radiographic density (blackness). The contrast can be expressed as being low, which means that there are many shades of gray (long scale) between the extremes of black and white. The term high contrast means that there are few shades of gray
(short scale). Lowering the kVp increases the contrast, and raising the kVp reduces the contrast. To adjust the technique to alter film contrast while maintaining the same radiographic density, consider the following: • The mAs and the kVp have to be in balance. • As the mAs increases, the kVp must decrease. • As the kVp increases, the mAs must decrease. • Doubling radiographic density requires doubling the mAs or increasing the kVp by 10% in the 40- to 100-kVp range or 15% in the 100-kVp or greater range.
• •
• •
•
of 25, 50, 100, 200, and 300 and two (1 and 2 mm or smaller) focal spots. An ideal kVp range is 40 to 120 and is adjustable in 1 or 2 kVp per step. A timing device is necessary to control the duration of an x-ray exposure. Modern x-ray machines have electronic timers with ranges that can control motion in the patient and prevent blurring. With a timed exposure of 1/120 second, all significant motion is stopped. The line voltage compensator is automatic or manual. The tube stand moves along the full length of the table and has an adjustable height from 0 to 60 inches (152 cm). The tube is able to rotate 90 degrees around the vertical axis and 180 degrees around the horizontal axis. The table is 5 to 6 feet in length with a top that has floating motion in four directions. The collimator decreases scatter radiation and human and patient exposure as it increases film quality. Always leave a clear margin of collimation on every film. The collimator is lighted and has a centering mark. A high-quality, dial-adjustable, multileaf lead shutter collimator is highly recommended. Filters have the primary function of reducing patient radiation dose by removing scatter radiation and increasing (mean beam energy) quality. Most x-ray equipment has inherent filtration equal to 1.5- to 51
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•
• •
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2.0-mm aluminum. Increased film quality can be obtained by adding an additional 2.0-mm aluminum filtration. Total filtration must be at least 2.5-mm aluminum. Grids consist of a flat plate with a series of lead foil strips separated by transparent spacers. They are made in various sizes and improve the diagnostic quality of radiographs by absorbing the greater part of the scatter radiation. Position grids between the patient and the cassette, usually under the table. Use only for body parts thicker than 10 cm. The reciprocating grid (Potter-Bucky diaphragm) includes a mechanism that moves the grid during exposure to eliminate grid lines from the radiograph. This grid is optional equipment but recommended for the bestquality radiographs. • Grids can be classified in three ways: the lead content (g/cm2), the number of lines per inch, and the ratio of lead strip height to the space between the lead strips. In general, high-ratio grids absorb scatter better but are more expensive. More lines per inch give better quality, because the lead strips are narrower and therefore lines become less prominent; however, they cost more. The most common grid is an 8:1 with 103 lines per inch. • The higher the grid ratio, the more critical the x-ray tube alignment. Always stay within the focal zone of the grid. This is usually written on the grid and is 36 to 42 inches (90–105 cm) in most instances. Exposure switches include the two-position exposure switch on the console and the two-position exposure foot switch, with a cord of sufficient length. High-frequency x-ray machines have a few advantages over single-phase x-ray machines. A 150-mA highfrequency generator can produce a quantity of x-rays equal to that of a 300-mA, single-phase x-ray
•
machine. Many of the units use 110 volts. They are reliable, with less downtime than single-phase machines. Their cost, at present, is greater than that of single-phase machines but most likely will decrease in the future. For a list of x-ray machine manufacturers, see Table 4-1.
ACCESSORY RADIOGRAPHIC EQUIPMENT Intensifying Screens The screen is a suspension of phosphor crystals in a binder. The phosphor in the screen converts x-ray photons into visible light, to which the film is more sensitive. A latent image is created by exposure of the film to this light. This technique reduces x-ray exposure to the patient by at least 10 times and the time of x-ray exposure, thus decreasing the chance of blurring.
• Screen speed depends on the thickness of the phos-
•
•
phor layer, the size of phosphor crystals, and the efficiency of phosphor crystals at absorbing x-rays and converting them to light. Screen classification varies because each company has a slightly different system for labeling screen speed. Resolution ability of the screen is inversely related to speed. Increased speed gives decreased resolution. Have a technique chart available for each screen speed. Par speed is the starting point for comparison of screens. High speed has a speed 2 times that of par speed. Ultraspeed is 4 times par speed. High detail speed is half that of par speed. Types of Screens • Calcium tungstate screens reduce the amount of radiation necessary to expose film by 10 times com-
Table 4-1. X-RAY MACHINE MANUFACTURERS Company Bennett X-Ray Technologies Continental X-ray Control-X Medical Fischer Imaging Corp. MinXray Summit Industries Universal (Del Medical Systems)
Address 445 Oak St. Copiague, NY 11726-2719 2000 S. 25th Ave. Broadview, IL 60153 West Pointe Business Park 2289 W. Brooke Dr. Columbus, OH 43228 12300 North Grant St. Denver, CO 80241-3120 3611 Commercial Ave. Northbrook, IL 60062-1822 2901 W. Lawrence Ave. Chicago, IL 60625 11550 W. King St. Franklin Park, IL 60131
Phone Number
Website
800-922-9399 708-345-3050 800-777-9729
www.cxmed.com
800-825-8257
www.fischerimaging.com
847-564-0323
www.minxray.com
800-729-9729
www.summitindustries.net
800-800-6006
www.delmedical.com
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•
•
pared with film exposed without a screen. They are also less expensive than rare-earth screens. Calcium tungstate emits a broad spectrum of light in the ultraviolet and blue range. • Rare-earth screens are more expensive than calcium tungstate screens. The light emitted is in the ultraviolet, green, or blue range. The major advantage of rare-earth over calcium tungstate screens is that rare-earth screens are fast, because of a more efficient production of light. Therefore, they decrease the production of scatter, the exposure time, the radiation dose, the chance of motion and subsequent blurring, and the wear and tear on the x-ray tube. System speed is the speed of film and screen in combination. It is not an additive system. A very low system speed results when screens and films with different color spectrum sensitivities are put together. Ask the film dealer what system speed you have with your particular screens and film. The higher the system speed number, the more sensitive the system and the less radiation necessary to make an exposure. System speeds can vary from 50 to 3200 and higher. The higher the system speed number, the less radiation to the patient and to personnel within the room; however, the lower the system speed number, the better the resolution qualities. When you know the system speed, changing the technique chart is simpler. If the system speed doubles, change the mAs on the technique chart by half. If the system speed decreases by 50%, double the mAs on the technique chart. Exposure time
▼ Key Point Always use the shortest exposure times possible to eliminate blurring.
•
• For thoracic radiographs, exposure times of 1/60 second or shorter stop the effects of respiratory and heart motion. • For abdominal radiographs, employ exposure times of 1/40 second or shorter to eliminate gastrointestinal motion. • For extremity radiographs, exposure times of 1/20 second or shorter eliminate the effects of patient motion. Rare-earth screens have a system speed that allows the shortest exposure times possible to eliminate motion problems and to lower radiation exposure to patient and personnel. In general, when using a 300-mA machine and a 400 to 800 speed system, with an 8:1 grid, good-quality radiographs are attainable even for large-breed dogs. In a feline practice, a slower system, such as a 100 to 250 speed system, provides excellent quality. As the crystal size gets larger, the system gets faster but resolution is reduced.
53
• Clean screens with the product recommended by the manufacturer on a regular schedule (monthly) and whenever debris is noted on the radiographs.
Film Radiographic film provides a permanent record containing the maximum amount of diagnostic information.
• Film is made of a light-sensitive emulsion, composed
•
•
•
•
•
•
of gelatin and silver halide with other ingredients attached to a plastic (polyester) base. The silver halides are sensitive to light and change when exposed to light to produce a latent image. The process of developing changes silver ions into black silver, thus producing the radiographic image. Fixer removes all unexposed silver from the film. The emulsion may be attached to one or both sides of the base. X-ray film may be most sensitive to direct x-ray exposure (nonscreen film) or to blue, green, or ultraviolet light. Films vary in their contrast. Some films appear more black and white after exposure and development. Use the film that is recommended by your screen manufacturer to match the spectrum of light produced by your screens. Choose a film that results in the contrast range most pleasing to you. Use a film that gives you a system speed that results in quality radiographs. Make sure to match film, screens, and processing chemicals. Film must be sensitive to the type of light emitted by the screens in use. Film speed determines the amount of light required to produce an image on the radiograph. Fast film has large crystals (silver halide), requires less exposure, and produces a grainy image. Slow film has small crystals, requires greater exposure, and produces a sharper image. Screen film is manufactured with crystals that are sensitive to fluorescent light. Nonscreen film is a direct exposure–type film and is manufactured to be sensitive to x-rays. Nonscreen film requires 10 to 25 times more radiation than screen film. Film is available in both metric and nonmetric measurements. The most common sizes used in small animal practice are 8 ¥ 10 inches, 10 ¥ 12 inches, and 14 ¥ 17 inches. X-ray film is sensitive not only to light and x-ray photons but also to humidity, chemicals, and physical stress. Film is stored on end to reduce pressure on the face of the film. High humidity causes film fogging, and low humidity causes film static; therefore, between 30% and 40% humidity is appropriate for film storage. Storage temperature should not exceed 50°F to 70°F (10°C to 21.1°C). Store the film away from developing chemicals and ionizing radiation. Do not put pressure on the film when loading or unloading film. Film and screen companies are provided in Table 4-2.
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Table 4-2. FILM AND SCREEN COMPANIES Company AGFA Eastman Kodak Co. Fuji Medical Systems Konica Minolta Medical Imaging Picker International 3M Medical Imaging System
Address
Phone Number
100 Challenger Rd. Ridgefield Park, NJ 07660 Health Sciences Division Rochester, NY 14650 90 Viaduct Rd. Stamford, CT 06907 411 Newark Pompton Turnpike Wayne, NJ 07470 595 Miner Rd. Highland Heights, OH 44143 3M Center St. Paul, MN 55144-1000
Cassettes Cassettes are used primarily to contain and protect film. Two basic types are available: rigid cassettes that contain both the film and the screen and cardboard cassettes that hold nonscreen film.
• • •
• Rigid cassettes protect both screens and film from
• •
physical damage and film from exposure to light. The cassette provides snug contact between the film and the screens. The front of the cassette is usually a rigid plastic, aluminum, or other substance that absorbs relatively few x-ray photons. Usually, a small rectangle in the corner of the cassette shields the film from x-rays to allow an unexposed area for film identification. The back of the cassette is lined with lead to absorb backscatter radiation. The back of the cassette is also equipped with latches to provide a lightproof seal. Cassettes for a nonscreen film only protect the film from light exposure. They are usually made from cardboard. Cassettes are numbered. When defects are noted on a radiograph, they can be traced to the correct cassette. Dropping a cassette causes warping and results in poor film-screen contact and a distorted radiographic image.
Miscellaneous Accessories • Use the screen cleaner that is recommended by your screen manufacturer.
• Use safety devices (lead aprons, lead gloves, glasses, •
• •
and lead thyroid shield) when personnel are required in the x-ray room for patient positioning. Film markers consist of right and left lead film markers, Mitchell markers (for horizontal radiographs), and time markers (for upper gastrointestinal and intravenous urography radiographs). A device capable of measuring body-part thickness and determining the kVp for exposure is needed. Positioning devices include sponge wedges, sandbags, Plexiglas or foam trough, rope, tape, and agents for
•
Website
877-777-2432
www.agfa.com
800-926-1519
www.kodak.com
800-431-1850
www.fujimed.com
800-934-1034
www.medical.konicaminolta.us
800-635-972 888-364-3577
www.3m.com
chemical restraint to avoid human exposure associated with hand-holding whenever possible. Film filing envelopes are needed. Contrast media are required (see “Contrast Studies” and Table 4-6). Monitoring devices (film badges) for employees and room monitoring, a film viewer (at least one double bank), and a hot light (high-intensity light) are needed. Radiographic accessory companies are listed in Table 4-3.
CHECKING X-RAY MACHINE ACCURACY Milliampere Station Check • Use an aluminum step wedge to check mA station (setting) accuracy. Use the step wedge to determine if your mA stations are linear. It cannot determine if all your mA stations are off by the same amount. A step wedge (see Table 4-3 for sources) gives a general idea about the mA stations. A step wedge is inexpensive ($100) and easy to use. Place the step wedge on a loaded cassette; make many separate exposures of the step wedge, changing the mA but always having the same mAs and kVp. If you cannot keep the same mAs throughout all mA stations, do as many as possible at one mAs setting then go back and check the rest at another mAs. Example 25 mA 50 mA 100 mA 300 mA 100 mA 200 mA
1
/10 second /20 second 1 /40 second 1 /120 second 1 /60 second 1 /120 second 1
2.5 2.5 2.5 2.5 1.7 1.7
mAs mAs mAs mAs mAs mAs
70 70 70 70 70 70
kVp kVp kVp kVp kVp kVp
Compare the densities of all exposures. They should be the same for all mA stations taken at the same mAs. An exposure that varies from the average shows that there is a problem with that mA station. This test
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Table 4-3. RADIOGRAPHIC ACCESSORY COMPANIES Company
Address
Bar-ray Products
P.O. Box 36 Monarch St. Littlestown, PA 17340 5201 8th Ave. South St. Petersburg, FL 33707 5201 Naimen Parkway Solon, OH 44139 P.O. Box 570 2630 Kaneville Ct. Geneva, IL 60134 3954 SE 44th St. Grand Rapids, MI 49512 595 Miner Rd. Highland Heights, OH 44143 4131 S.W. 47th Ave., Ste. 1404 Davie, FL 33314 10625 Telge Rd. Houston, TX 77095 182 NW Earl St. Madras, OR 97741-0069 3M Center St. Paul, MN 55144-1000 420 Hempstead Turnpike West Hempstead, NY 11552
Burkhart Cone Instruments Fischer Industries Medical I.D. Systems Picker International Pulse Medical (Radiation Concepts) S&S Technology Shielding International 3M Animal Care Products Wolf X-ray Corp.
does not tell you if all mA stations are accurate, but it does tell you if a particular station has a problem.
• A digital, electronic mA-checking device is the most accurate way to compare your mA stations.
▼ Key Point The only accurate way to check the kVp is the Wisconsin test cassette ($1300; see Table 4-3 for sources).
• The Wisconsin test cassette has many kVp settings listed on the front of the cassette. Under each of these settings is a certain amount of material to attenuate the beam. After exposure and processing, this film provides information to determine if the kVp settings are accurate. Another less accurate way to obtain a general check of kVp accuracy is to vary mAs and kVp. Go through all kVp settings, employing density-changing factors to keep the densities the same throughout all these exposures.
Example 100 mAs at 50 kVp 50 mAs at 55 kVp 25 mAs at 61 kVp 12.5 mAs at 67 kVp 6.2 mAs at 74 kVp
Website
888-422-7729
www.bar-ray.com
800-872-9729
www.usaxray.com
800-321-6964
www.coneinstruments.com
800-356-5911
www.fischerind.com
800-262-2399
www.medid.com
800-635-9729 800-342-5973
www.rci-pulsemed.com
800-231-1747
www.ssxray.com
800-292-2247
www.shieldingintl.com
888-364-3577
www.3m.com
800-356-9729
www.wolfxray.com
If your mA stations and kVp settings are working correctly, each exposure has the same density but a different contrast range. Remember to employ densitychanging factors when necessary.
Exposure Timer Check (Single-Phase Machine)
Kilovolt Peak Check
•
Phone Number
3.1 1.5 0.8 0.4 0.2
mAs mAs mAs mAs mAs
at at at at at
81 90 99 108 124
kVp kVp kVp kVp kVp
Use a spinning-top test tool. It can be purchased from the same company as the machine (see Table 4-1) or from an accessory company (see Table 4-3). This tool is inexpensive ($50) and easy to use. It is a flat metal spinning top with a hole in one side. The top is set on a loaded cassette and spun. Take an exposure at 1 /120 second. Move the top to another corner of the film, spin again, and expose at 1/60 second. This maneuver is repeated at 1/40 and 1/30 second. At 1/120 second, only one dot should be seen; at 1/60, two dots; at 1/40, three dots; and at 1/30, four dots. If more or less dots are on the film than expected, the timer is not accurate.
Line Voltage Line voltage is the amount of current coming into the machine. The amount of current may vary, depending on electrical wiring, consistency of voltage in the area, and usage of current on the same circuit in the particular practice. Almost all machines used for small animals have a line voltage-check device. Some have a meter and a dial to adjust line voltage and do not permit exposure until the voltage is manually adjusted. Other machines have an automatic line voltage adjustment.
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Almost all equipment in small animal practice uses 120 volts (i.e., right out of the socket).
FILM PROCESSING Manual Processing Film developing is a chemical process and therefore depends on both time and temperature.
Advantages and Disadvantages
• Advantages
•
• Less expensive setup costs than those of an automatic processor. • No special electrical or structural changes are necessary for the darkroom. Disadvantages • Valuable technician time to develop films and maintain chemical baths (i.e., increased labor costs). • Quality is not consistent, due to human error, compared with automatic processors. • Longer time to prepare diagnostic films compared with automatic processors.
Accessories
• • • • • • • •
Developing tanks Two stirring paddles Two thermometers Film developing hangers of different sizes Chemicals Adjustable mixing valve for measuring temperature Timer Dust-free drying cabinet or area
water
Darkroom Safelight Darkroom safelights must produce enough illumination in the darkroom so that a person can see to process radiographic film (load and unload cassettes) without unwanted density (fog) to the film. Safelights utilize a wavelength of light different from that to which the film is sensitive. A Wratten 6B filter is adequate for bluesensitive film. A GBX-2 filter is employed with greensensitive or both green- and blue-sensitive films. Usually, 15-watt bulbs are used with safelights. The safelight is about 4 feet from the film-handling area. No system is 100% safe; therefore, expose the film no longer than necessary.
Radiograph Labeling
• A radiograph is a legal document and must therefore have permanent labeling. On the label, include the hospital or veterinarian’s name, the date the radiograph was taken, and the owner’s name or the
animal’s file number. Label the radiograph with right or left, dorsoventral or ventrodorsal (DV/VD), a time marker on contrast studies, and a Mitchell marker when a horizontal beam is used. Basic types of permanent marking systems are available: • Lead letters and numbers in a holder with the hospital or veterinarian’s name, placed on the cassette during exposure. • Radiopaque marking tape (lead-impregnated tape). Information may be written on the tape, and the tape is placed on the cassette before exposure. • A darkroom printer transfers data from a card to the corner of the x-ray film that was shielded from radiation during exposure. This system requires cassettes with special windows. The film is removed from the cassette, and the corner of the film where it was blocked from light exposure is imprinted by exposing the patient information on a 5 ¥ 7-inch card onto the film.
Silver Recovery Recover silver from fixer solutions by either manual or automatic systems. Fixer solutions may be sold to companies for silver recovery. Alternatively, you may purchase a system (metallic replacement process, electrolytic recovery, or chemical precipitation) for silver recovery in your practice. Exposed developed and undeveloped film may also be sold for silver recovery. Usually, the supplier of the x-ray films or processing solutions can be consulted to determine if silver recovery is feasible and who to contact.
Procedure for Manual Film Processing
• Check temperatures, turn off room lights, use safelights, and agitate (mix) solutions well.
• Place the film on development hangers, making sure all four corners are attached.
• Set and start time depending on the temperature in the developing tank.
• Place the hanger with the film into the developing tank. Rap hard against the tank wall to dislodge air bubbles. Agitate by pulling film out of the developer, and let the developer drain to one lower corner. Return film to the developer. Repeat agitation every minute. Manufacturers recommend a specific temperature for the developed solution that they produce, usually 68°F (20°C). Adjust for change in temperature (increased temperature, decreased time, and vice versa). The chemical manufacturer can provide a time-temperature development chart. Example 60∞F 65∞F 68∞F 70∞F 75∞F
(15.5∞C) (18.3∞C) (20.0∞C) (21.1∞C) (23.8∞C)
8.5 6.0 5.0 4.5 3.5
minutes minutes minutes minutes minutes
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• At the end of the developing time, remove the hanger • • • • • • • • • •
from the developer and drain over the rinse tank. Agitate film in rinse water for 30 seconds. Place the hanger with film in fixer at the end of the developing time. Set the timer. Fixer time equals twice the development time. Agitate film every 2 to 3 minutes while in the fixer. At the end of fixation time, remove film from fixer and drain. Place the hanger in wash water at the end of fixer time. Agitate after 2 to 3 minutes. Wash for 15 to 30 minutes, depending on water flow and temperature in wash tank. Provide no less than four water changes per hour in the wash tank. At the end of the wash, remove from water and drain. Place film in a drier cabinet or hang up to dry.
Automatic Processing • Processors are a good investment for most veterinary practices. New, small, tabletop models are priced from $3500. Most of these processors develop an excellent quality film in 90 to 210 seconds. They can use cold water for processing; therefore, no special needs exist for plumbing. They are also easy to maintain.
•
• •
•
•
•
▼ Key Point If your small animal practice is processing 7 to 10 films a day, consider an automatic processor.
• Advantages • Highly repeatable results • Short waiting time for diagnostic films • Ability to process large quantity of films quickly and accurately
• •
57
• Good quality control • Smaller darkroom necessary Disadvantages • Machine is expensive. • Darkroom structural changes are expensive. • Needs daily and weekly maintenance. • Repairs can be expensive. Equipment includes processor, safelight, water for processing, chemicals, sponges to clean rollers of processor, and processor cleaning solution. Tabletop film processors are easy to install (no special plumbing or wiring). Different models process films as fast as 90 seconds or as long as 31/2 minutes. Most are made for easy care and cleaning. They are relatively inexpensive (from $3000 to $7000). Large, hard-wired, 90-second film processors need special plumbing and electrical wiring, but they are able to process many films. They need special cleaning and repairs and are expensive ($15,000– $25,000). The more a processor is used, the fewer problems it will have. It is made to be used on a 24-hour basis. Chemical buildup on rollers can cause film artifacts. Rollers age and crack if oxidized chemicals are left on them. Clean processors often. • All processors need cleaning daily when not in use. Take out the rollers and wash them down with a sponge and water. Dry and replace the rollers. Clean the chemical tanks. Once a month, clean with processor cleaning solution. Cleaning a processor takes about 15 minutes a day but saves in wasted film and time. Consider purchasing a processor with a standby mechanism. This function helps conserve water, energy, and chemicals. Automatic processor companies are listed in Table 4-4.
Table 4-4. AUTOMATIC PROCESSOR COMPANIES Company AFP Imaging Corp. AGFA All Pro Imaging Corp. Eastman Kodak Co. Fischer Industries Konica Minolta Medical Imaging Picker International
Address 250 Clearbrook Rd. Elmsford, NY 10523 100 Challenger Rd. Ridgefield Park, NJ 07660 70 Cantiague Rock Rd. P.O. Box 870 Hicksville, NY 11801-1127 Health Sciences Division Rochester, NY 14650 P.O. Box 570 2630 Kaneville Ct. Geneva, IL 60134 411 Newark Pompton Turnpike Wayne, NJ 07470 595 Miner Rd. Highland Heights, OH 44143
Phone Number
Website
914-592-6100
www.afpimaging.com
877-777-2432
www.agfa.com
800-247-8324
www.allproimaging.com
800-926-1519
www.kodak.com
800-356-5911
www.fischerind.com
800-934-1034
www.medical.konicaminolta.us
800-635-9729
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Darkroom
Technique Chart (with Grid) (Fig. 4-3)
Recommendations
Thorax with Grid
• Darkroom location: Locate the darkroom close to
1. Use a dog of average size and body condition for all measurements. 2 Take a lateral measurement across the chest at the widest point. 3. Find that measurement on your technique chart. 4. Underneath this lateral measurement, set your kVp at 95—a value in the middle of the ideal kVp parameters for a thorax. 5. Fill out your chart according to the kVp per centimeter increments. 6. Once the kVp values have been assigned, take three chest films at different mAs values. You may begin with 0.8, 1.6, and 3.2 mAs for a rare-earth system and 5, 10, and 20 mAs for calcium tungstate, for example. Select the mAs value at 95 kVp that provides you with the best technique.
•
water and drains for plumbing purposes, and close to radiographic area to reduce unnecessary walking and to increase efficiency. Darkroom layout (Figs. 4-1 and 4-2): Darkrooms do not have to take up much room but are at least 6 ¥ 8 feet. Many darkrooms are located where a bathroom might have been. This eliminates the process of bringing in new plumbing and electrical outlets. Try to include a sink for cleanup and processor maintenance. Keep wet and dry areas separate to eliminate contamination of screens and unexposed film by chemicals. Always have good ventilation to keep heat, humidity, and chemical fumes from destroying film and to reduce exposure of personnel to chemical fumes. Paint all walls white to reflect light from the safelights and for a brighter working environment. Use an adequate number and type of safelights. Make sure all safelights are 40 inches from the working area to prevent film fogging.
TECHNIQUE CHARTS • Have a working knowledge of equipment (tube rating
•
charts and anode cooling curves). A constant focal film distance is recommended. The same film, screens, and darkroom technique are used, as described previously. The technique chart is set up to take radiographs of normal animals. Different animals may have the same lateral thoracic measurement but different body types (obese, emaciated, etc.). The emaciated animal may be overexposed with the technique from the chart; therefore, you will need to decrease the exposure (kVp). The obese animal may be underexposed following the chart technique; therefore, you will have to increase the exposure (kVp). • The technique may need to be increased (2– 30%) for numerous reasons (e.g., obesity, pregnancy, ascites, pleural effusion, or disease processes that increase lung opacity, such as pneumonia and atelectasis) and for positive-contrast studies. • The technique may need to be decreased (2– 30%) for numerous reasons, including emaciation, pneumothorax, emphysema, gastric dilatation, and volvulus.
Abdomen with Grid 1. Follow the first three steps under “Thorax with Grid.” 2. Set your kVp at 85. 3. Fill out the chart according to the kVp per cm increments. 4. Double the mAs value used in the thorax technique.
Spine with Grid 1. Follow the first three steps under “Thorax with Grid.” 2. Set your kVp at 65. 3. Fill out the chart according to the kVp per cm increments. 4. Set the mAs value 4 times that used for the abdomen. This setting also works for femur, humerus, shoulder, and pelvis.
Technique Chart (Tabletop without Grid) (Fig. 4-4) Thorax, Abdomen, and Spine 1. On the grid chart for thorax, abdomen, and spine, find the last kVp setting for 11 cm. 2. Decrease the kVp as the thickness decreases. For example, if 74 kVp is at 11 cm, use 72 kVp at 10 cm, 70 kVp at 9 cm, and so forth. 3. Adjust the mAs by reducing to half (possibly more depending on the type of grid) the mAs value for the base techniques for the thorax, abdomen, and spine. If films are still overexposed, reduce the mAs by half again.
Extremity ▼ Key Point Always select the shortest possible exposure times. This entails choosing the highest mA value to achieve the shortest exposure times.
1. Measure a normal dog carpus. The average is 4 to 5 cm. 2. Underneath that measurement, set your kVp at 60 (a value in the middle of your ideal kVp parameters for extremities).
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Figure 4-1. processing.
Floor plan for a darkroom using manual (wet tank)
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Figure 4-2. processing.
Floor plan for a darkroom using automatic
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Figure 4-3. with a grid.
Technique chart to use
Figure 4-4. Technique chart. For tabletop exposures, take the Buckey grid technique and reduce the mAs by 50% to 75%. Continue kVp down from Buckey chart.
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3. Fill out the chart, according to the kVp per cm increments. 4. Take films at three different mAs values (0.8, 1.6, and 3.2 with rare earth; 5, 10, and 20 with calcium tungstate). Continue selecting the mAs values until an appropriate exposure has been made. Your tabletop extremity chart is now complete. Employ this chart for all extremities distal to and including the elbow and stifle.
Nonscreen Film Technique Chart • For the nonscreen film technique chart, the mAs in
• Need to have computers and a software package to integrate with medical records
DIGITAL RADIOGRAPHY Direct digital radiography (DR) uses specialized x-ray equipment that has a digital imaging sensor. Once the image is transferred to the computer system, image analysis and storage are similar to those previously listed for CR.
your technique chart may vary up or down from the example shown in Figure 4-5.
Advantages • A digital image is generated (these can easily be sent
COMPUTED RADIOGRAPHY
• Excellent image quality. • Film, processor, and darkroom can be eliminated.
to specialists if needed).
Computed radiography (CR) is an indirect digital imaging technology in which a plate (which looks similar to a cassette but is filmless) is used to record the image. A reader is required to extract the data, which is converted to a digital image and viewed on a computer screen. CR utilizes standard x-ray machines. Components of CR include both the hardware described previously and the software (for display, storage, and archiving). New technique charts must be developed when switching from a traditional film-screen system to CR. CR software allows image manipulation that can adjust for exposure and contrast. Images can also be drawn, and measurements can be taken. ▼ Key Point The ability of the viewer to appreciate the image quality provided by CR depends on the quality of the computer monitor.
Disadvantages • Currently more expensive than CR systems (cannot be used with existing x-ray equipment).
• Few current systems allow horizontal beam radiography.
• Need to have computers and a software package to integrate with medical records.
POSITIONING AND TECHNIQUE Measuring for Radiographic Studies • Measure all animals standing. • Measurements for the thorax, abdomen, and thora-
Advantages • A digital image is generated (these can easily be sent • • • •
to specialists if needed). Existing radiography equipment can be used. Excellent image quality. Initially less expensive than digital radiography. Film, processor, and darkroom can be eliminated.
Disadvantages • Still have to use an imaging plate • Need to purchase new plates and a reader
•
• •
columbar spine are all taken at the same location on the animal. Observe the animal from above, taking the lateral measurement from the widest point across the ribs. The DV/VD measurement is made at the same point. The widest point is usually at the thoracolumbar junction. Measure the pelvis across the wings of the ilium. This is a very accessible area to measure, giving highly repeatable results. The same measurement is used for both the lateral and the VD. Measure extremities at the widest point. Make sure all personnel measure all areas at the same point; otherwise, the technique will vary from one study to the next.
Figure 4-5. Technique chart to use with nonscreen film. Use a lateral measurement across the skull to set technique. Always use 50 kVp for the best contrast.
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• For a lateral (right or left) radiograph, pull the legs
Thorax Obtain thoracic films at full inspiration. Include from the thoracic inlet to behind the diaphragm. In a large dog, this may take two radiographs for both lateral and DV/VD views. Short exposure times of 1/60 second or less decrease motion artifact from cardiac and respiratory motion. A high-kVp, low-mAs technique increases latitude (increased shades of gray). • For the lateral (right or left) measurement, elevate the sternum to the same plane as the spine. Pull the animal’s legs cranially to reduce soft tissue over the cranial thorax. Include the sternum, and take the radiograph during peak inspiration (Fig. 4-6). • For the DV/VD view, the sternum is superimposed over the spine. Center the beam at the caudal border of the scapula; center the beam on the spine. Take the radiograph during peak inspiration. VD radiographs are preferable to DV for evaluation of the accessory lung lobe and the caudal mediastinum. DV radiographs are preferred if evaluation of the caudal pulmonary vessels is important. The dog’s disposition, clinical status (e.g., heart failure, pulmonary edema, or pleural effusion), or position of previous radiographs help choose between VD and DV thoracic radiographs (Fig. 4-7). A Plexiglas or foam trough is useful for positioning for the VD view (add 10% kVp to your technique when using a trough). • Take both right and left lateral views of the thorax with a DV/VD view to evaluate for pulmonary metastases or focal disease.
•
•
•
caudally but not enough to stretch the abdominal musculature taut. Place the edge of the cassette 1 to 2 inches cranial to the xiphoid and at the coxofemoral joint (palpate for the greater trochanter). Take the radiograph at peak expiration (Fig. 4-8). The DV/VD is the same as that for the lateral abdomen (Fig. 4-9). A Plexiglas or foam trough is useful for positioning for the VD view (add 10% kVp to your technique when using a trough). A horizontal beam radiograph can be used to check for free abdominal air. Place the animal in left lateral recumbency for 10 minutes before radiography. Air is demonstrated around the right liver lobes. The technique is similar to the vertical beam technique in that distance remains at 40 inches. Remember to reduce the mAs if a grid is not used. In compression radiography, a wooden spoon can be used to compress the abdomen for separation of
Abdomen Withhold food for at least 12 hours for optimal abdominal radiographs. Encourage the animal to defecate and urinate before being radiographed. Radiographs include the diaphragm to the coxofemoral joints. For large-breed dogs, this may require two 14 ¥ 17-inch films for both the lateral and DV/VD views. Use a 1/40-second or less exposure time to reduce motion; use a kVp in the 70 to 90 range for maximum latitude.
Figure 4-7. radiograph.
Positioning for dorsoventral or ventrodorsal thoracic
Center beam over caudal scapula
Sternum
Figure 4-6.
Positioning for lateral thoracic radiograph.
Figure 4-8.
Positioning for lateral abdominal radiograph.
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Mediolateral (ML) The animal is in lateral recumbency, with the down side to be radiographed. Extend the leg about 45 degrees from the vertebral column. Flex the opposite leg and place it over the thorax. Pull the head and neck back so that the cervical spine and trachea are not overlapping the joint space.
Humerus Caudocranial The animal is in dorsal recumbency, with the legs extended. Rotate the sternum away from the side being radiographed. Center the x-ray beam at the midhumerus. The radiograph includes both the shoulder and the elbow joints.
Mediolateral Figure 4-9.
Positioning for ventrodorsal abdominal radiograph.
structures. The spoon can separate the colon from the urinary bladder to demonstrate the uterus, for example. Remember to reduce the kVp, because you are decreasing the thickness of the tissue being radiographed.
Extremities For radiography of the extremities, the animal needs a clean, dry haircoat. Remove splints and bandages if possible. Place the limb to be radiographed closest to the film. Employ a high-mAs, low-kVp (50–70) technique to produce high-contrast radiographs. Collimate closely. Use tabletop (nongrid) techniques on parts less than 10 cm thick. Administer anesthesia or tranquilizers whenever needed. Use positioning devices. Measure the part to be radiographed over the thickest area. If the part thickness varies greatly, two exposures (e.g., lateral pelvis and femur) may be necessary. In the case of moderate variation, choose the greater measurement to set the exposure and “hot light” the slightly overexposed areas when reading the film. When long bones are being radiographed, include the joints proximal and distal. ▼ Key Point Radiograph the opposite limb for comparison to determine normal from abnormal.
Scapula and Shoulder Joint
Place the animal in a position similar to that for the ML view of the scapula and the shoulder joint. Center the x-ray beam at the mid-humerus. The radiograph includes both the shoulder and the elbow joints.
Elbow Joint Craniocaudal The animal is in sternal recumbency, with the elbow joint in full extension. If the elbow cannot be completely extended, angle the x-ray beam 10 degrees to 20 degrees, craniodistal to caudoproximal.
Mediolateral The animal is in lateral recumbency, with the elbow slightly flexed. Pull the opposite leg caudally. Center the beam on the palpable medial epicondyle. The elbow is in extreme flexion if identification of the anconeal process is of importance.
Craniolateral-Caudomedial Oblique This aids in imaging of the lateral aspect of the medial coronoid.
Antebrachium Craniocaudal Place the animal in sternal recumbency. Extend the leg and position the elbow for a true craniocaudal projection. The film includes both elbow and carpus.
Caudocranial
Mediolateral
The animal is in dorsal recumbency, with the sternum rotated away from the side being radiographed. The leg is fully extended. Center the x-ray beam at the midscapula. For the shoulder joint, center the beam at the point of flexion for the joint.
The animal is in lateral recumbency, with the leg in the neutral position. Move the opposite limb caudally; center the beam on the midshaft radius. It may be easier to obtain the radiograph if the elbow is slightly flexed. Include the elbow and carpal joint on the film.
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Carpus or Metacarpus
Lateral
Dorsopalmar
The animal is in lateral recumbency, with the dependent leg pulled cranially. Elevate the nondependent leg with a foam block parallel to the tabletop.
By convention, positional terms change from cranial and caudal to dorsal and palmar distal to the radius. Place the animal in sternal recumbency, with the extremity extended. Allow the elbow to abduct slightly so that the carpus is in true dorsopalmar (DP) view. Center the x-ray beam on the carpus or metacarpus.
Mediolateral Place the animal in lateral recumbency, with the affected leg down. Slightly flex the carpus; center the xray beam on the carpus. A lateral view of the metacarpus is often unrewarding.
Lateral Oblique Place the animal in lateral recumbency. Place a foam wedge to elevate the pelvis approximately 20 degrees. Push the upper leg proximally to rotate.
Ventrodorsal Flexed Hip (Frog-Leg Position) Place the animal in dorsal recumbency, and flex and abduct the femurs so that the stifles are lateral to the abdomen. Place the femurs at an angle of 45 degrees to the spine.
Oblique Views
Femur
Place the animal in sternal recumbency, with the carpus/metacarpus in DP. Rotate the extremity 45 degrees in both directions for the two oblique views (dorsolateral to palmar medial oblique and dorsomedial to palmar lateral oblique).
Craniocaudal
Digits
Mediolateral
Dorsopalmar
Place the animal in lateral recumbency with the leg to be examined on the cassette. Abduct the opposite leg and rotate out of the x-ray beam’s path. Center the x-ray beam at mid-femur. Include the hip and stifle on the film.
Place the paw flat against the cassette.
Mediolateral Place the animal in lateral recumbency. Pull the specific digit to be examined dorsally with tape.
Place the animal in dorsal recumbency or in the erect sitting position, with the leg extended. Center the x-ray beam at mid-femur. Include the hip and stifle on the radiograph. Measure at the proximal femur.
Stifle
Oblique Views
Caudocranial
Place the animal in sternal recumbency, with the carpus/metacarpus in DP. Rotate the extremity 45 degrees in both directions for the two oblique views (dorsolateral to palmar medial oblique and dorsomedial to palmar lateral oblique). Cotton can be placed between the digits to help with separation.
Place the animal in ventral recumbency with the leg to be examined pulled caudally into maximum extension. In large dogs, angle the x-ray beam 15 degrees caudodistal to cranioproximal. Center the x-ray beam at the joint space.
Pelvis
Position the animal as for the mediolateral femur view, with the x-ray beam centered on the joint space. Usually, the tarsus is away from the cassette, so you need to place a foam wedge under the hip and femur.
Tranquilization may be necessary for routine VD and lateral radiographs. General anesthesia is recommended for Orthopedic Foundation for Animals (OFA) or Penn-Hip radiographs.
Mediolateral
Tibia and Fibula
Ventrodorsal Extended Hip
Caudocranial
The animal is in dorsal recumbency, with the legs extended. The pelvis is straight; the femurs are parallel and as close to the cassette as possible. Patellae are superimposed over the distal femurs. Center the x-ray beam on the hip joints. Include the stifles on the radiographs. Legs are the same distance apart as the acetabula.
Position the animal as for the caudocranial stifle view. The x-ray beam remains vertical and centered at the mid-tibia. Include stifle and tarsus on the film.
Mediolateral Place the animal in lateral recumbency with the tibia and fibula included on the film.
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• In the average-size dog, five vertebral segments can be
Tarsus Dorsoplantar Place the animal in dorsal recumbency. Extend the leg, and center the x-ray beam at the proximal intertarsal joint.
Mediolateral Place the patient in lateral recumbency. Slightly flex the tarsocrural joint. Center the x-ray beam at the proximal intertarsal joint.
adequately evaluated per film. Because of the divergence of the x-ray beam, all areas of interest have to be centered to evaluate intervertebral disc spaces. ▼ Key Point Poor patient positioning and poor radiographic quality commonly occur when animals are not anesthetized or heavily sedated for spinal films. Many radiographic lesions can be obscured by poor technique. Conversely, a normal structure can be falsely identified as a lesion.
• Ideal spinal survey studies are listed in Table 4-5.
Oblique Views Dorsolateral to palmar medial oblique and dorsomedial to palmar lateral oblique. Position the animal in dorsal recumbency, then rotate 45 degrees in each direction (lateral and medial) for the two oblique views.
Cervical Spine
Metatarsus and Digits
For radiography, the spine must be parallel to the cassette. In many cases, support the center of the neck with radiolucent positioning blocks (sponges). Place the head in a normal position (neither flexed nor extended) relative to the neck. The head must be lateral because it controls the position of the proximal neck. Pull the front legs back over the thorax to allow thinning of the tissues over the caudal neck. The thorax must be in the accurate lateral position because it controls the position of the caudal neck. Extending the entire neck may help open up the caudal cervical disc spaces. Include both occipital and cervicothoracic areas on the radiograph.
Position the animal as for the metacarpus and digits of the forelimbs.
Spinal Positioning and Technique: General Principles • Materials needed include sandbags, foam wedges, •
• •
markers (right and left), and a Plexiglas trough to aid in positioning the animal without anyone in the room. Use general anesthesia or heavy sedation in all but the most subdued animals. Exceptions are suspected fracture, congenital malformation with instability, and other diseases in which the animal’s condition or protective mechanisms that have maintained stability will be compromised. Short-scale, high-contrast (high-mAs, low-kVp) technique provides good detail. Use a grid and collimate to include only the spine. At least two radiographic views of the area of interest are needed: lateral and VD.
Measure at the caudal cervical spine for all views.
Lateral View
Ventrodorsal View The spine is not parallel to the cassette because of the anatomic variation between the head and the thorax. The spine inclines away from the cassette at the thorax. Place the head in normal position (hard palate and dorsal nose at a 60 degree angle to the cassette). If the head is in a true VD position, an undesirable arch is pro-
Table 4-5. SPINAL SURVEY STUDIES Study
Centering—Lateral
Cervical spine (C1-5) Cervical spine (C6-T2)
C3-4 C6-7
Occipitoatlantoaxial
C1 C1 flexion, C1 oblique T6-7 T12-13 L3-4 LS LS flexion LS extension Center on area of suspected lesion
Thoracic spine (cranial) Thoracolumbar spine (T12-13) Lumbar spine Lumbosacral spine Post-trauma
Centering—Ventrodorsal C3-4 C6–T1 (x-ray beam angled 15 degrees ventrocaudal to dorsocranial) C1 (rostrocaudal open mouth to visualize the dens) T6-7 T12-13 L3-4 LS Cross-table (horizontal beam); center on area of suspected lesion
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duced in the cervical spine. The midplane of the head and thorax must be perpendicular to the cassette. Tilting the x-ray tube ventrocaudal to dorsocranial approximately 10 to 20 degrees permits imaging of the intervertebral disc spaces.
Thoracolumbar Spine Lateral View The midplane of the entire body must be parallel to the cassette. Most animals must have the sternum elevated for good lateral views of the spine. Pull the front legs cranially and the rear legs caudally to straighten the spine. Extending the entire neck may help open up the cranial thoracic disc spaces.
Ventrodorsal View
Nonscreen packet
Figure 4-10. Positioning for dorsoventral occlusal (intraoral) radiograph of the skull.
The midplane of the entire spine must be perpendicular to the cassette. When the dorsal spines are prominent, as in thin animals, radiolucent positioning blocks may be beneficial. The body may be held by placing tension on the legs.
Skull Radiography • General anesthesia or deep tranquilization of the patient is essential, if not specifically contraindicated by the patient’s physical condition, to obtain radiographs of good diagnostic quality. ▼ Key Point The lack of proper patient restraint is the most common cause of skull radiographs of nondiagnostic quality.
• The highest-resolution (detail) radiographic image
•
of the skull is produced with a nonscreen film or an ultradetail film-screen combination. Nonscreen film necessitates a 10- to 20-fold increase in the mAs compared with film in par speed screen cassettes. The positioning of the patient and the number of projections needed for a complete study depend upon the area of the skull being evaluated. A minimum of two views is necessary.
Figure 4-11. Positioning for the ventrodorsal (20∞ to 30∞ tube angle), open-mouth view of the skull.
Routine Skull Lateral and DV views are used.
Nasal Cavity and Paranasal Sinuses Lateral and DV occlusal (Fig. 4-10), VD open mouth (extraoral film) (Fig. 4-11), frontal (primary beam parallel to the hard palate) (Fig. 4-12), and lateral oblique (right and left) (Fig. 4-13) are used to evaluate small frontal sinuses.
Figure 4-12. skull.
Positioning for the rostrocaudal (frontal) view of the
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Figure 4-13. Positioning for the open-mouth lateral oblique (20∞ to 30∞) view of the frontal sinuses.
Figure 4-15. Positioning for the open-mouth lateral oblique (20∞ to 30∞) view of the mandible.
Figure 4-16. Positioning for the ventrodorsal occlusal (intraoral) view of the mandible. Figure 4-14. Positioning for the open-mouth lateral oblique (20∞ to 30∞) view of the maxilla.
Central beam
Dental Arches
• Maxillary: Right and left lateral obliques (20–30 •
degrees) (Fig. 4-14), VD open mouth (extraoral film), and DV occlusal. Mandibular: Right and left lateral obliques (20–30 degrees), open mouth (Fig. 4-15), and VD occlusal (Fig. 4-16).
Long axis of tooth 90 Bisecting angle Film Bisecting angle technique for radiographing the
Bisecting Angle Technique
Figure 4-17. teeth.
Project the central beam perpendicular to an imaginary plane that bisects the angle formed by the long axis of the tooth (or teeth) and the plane of the film (Fig. 4-17).
Foramen Magnum
Tympanic Bullae (Middle Ears) DV, open mouth frontal. The primary beam bisects the angle of the opened temporomandibular joint (TMJ) (Fig. 4-18); right and left lateral obliques (30 ¥ 30 degrees) (Fig. 4-19). Palpate the jugular processes; when these processes are oblique, the bullae will also be properly oblique.
Rostrodorsal-caudoventral oblique (fronto-occipital). The central beam passes between the eyes and exits through the foramen magnum (Fig. 4-20).
Temporomandibular Joint DV, open mouth frontal (see Fig. 4-18). The primary beam bisects the angle of the opened temporomandibular joint; right and left lateral obliques (20–30 degrees) (see Fig. 4-13).
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Mandible DV, lateral, and lateral oblique (right and left).
Maxilla DV occlusal, VD open mouth, lateral, and lateral oblique (right and left).
Zygomatic Bone and Orbit DV, lateral, and lateral oblique (right and left); frontal; and VD open mouth. Figure 4-18. Positioning for the open-mouth rostrocaudal (basilar) view of tympanic bullae.
CONTRAST STUDIES Contrast Medium • Positive-contrast medium: iodine (ionic, nonionic), barium (liquid, paste) (Table 4-6)
• Negative-contrast medium: room air, carbon dioxide, nitrous oxide
Excretory Urogram (Intravenous Pyelogram, Intravenous Urogram) • A well-prepared animal is important for this contrast study (excretory urogram[EU], intravenous pyelogram, and intravenous urogram are synonymous terms). Withhold food for 12 to 24 hours. Give enemas the night before and at least 2 hours before the study. Determine renal function (blood urea nitrogen and serum creatinine) before initiating the study. ▼ Key Point Always take scout films before performing contrast studies of the urinary tract.
Figure 4-19. Positioning for the lateral oblique (30∞ nose elevated, then 30∞ oblique) view of tympanic bullae.
• The primary contraindication in animals is dehydra-
•
• Figure 4-20. Positioning for (fronto-occipital) view of the skull.
the
rostrodorsal-caudoventral
tion. Contrast medium is hypertonic and will compromise an already unstable patient. Make sure the patient is properly hydrated before EU. Other contraindications in people include diabetes mellitus, multiple myeloma, heart failure, and known hypersensitivity to the contrast medium. Use a water-soluble, iodinated ionic contrast media (Renografin, Conray, Hypaque, Renovist, etc.). Dose is 2 ml/kg intravenously (approximately 300–400 mg/ml of iodine), not to exceed 90 ml or 35 g of iodine. For animals with impaired renal function, the dose may need to be doubled (4 ml/kg). Place an indwelling catheter to help avoid perivascular injections and to allow intravenous access if complications occur. Give the bolus as fast as possible. Increase radiographic technique (mAs) 5% to 10% over scout films. Keep the kVp approximately 70 to produce better differentiation between the kidney and the contrast medium.
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Table 4-6. RADIOGRAPHIC CONTRAST AGENTS Type of Contrast Agent Barium products
Iodinated gastrointestinal contrast agent Iodinated contrast agent Myelographic contrast agent
Brand Names
Manufacturers
Intropaste (barium paste) Barosperse (barium suspension) Novopaque (barium suspension) E-Z-ML- 196 (barium suspension) Gastrografin Omnipaque (iohexol) Renografin 60 or 76 Hypaque-76 Conray 30 or 400 Omnipaque (iohexol) Isovue (iopamidol)
Lafayette Pharmacal (Lafayette, IN) Mallinckrodt (St. Louis, MO) Lafayette Pharmacal (Lafayette, IN) E-Z-EM (Westbury, NY) Bracco Diagnostics (New Brunswick, NJ) Amersham Health (Piscataway, NJ) Bracco Diagnostics (New Brunswick, NJ) Amersham Health (Piscataway, NJ) Mallinckrodt (St. Louis, MO) Amersham Health (Piscataway, NJ) Bracco Diagnostics (New Brunswick, NJ)
Technique 1. Immediate postinjection VD film demonstrates nephrographic phase. 2. VD and lateral films at 5 minutes. 3. In some cases, if there is poor filling of the renal pelvis, between 10 and 20 minutes following contrast administration place an abdominal wrap between the bladder and the kidney to compress the ureters, causing the pelvis and diverticula of the kidney to completely distend for better evaluation. This is contraindicated in cases of severely diseased bladder walls or mass lesions, in which it may cause rupture. 4. VD and lateral films at 15 minutes for evaluation of the pyelographic stage. 5. VD and lateral films at 30 minutes. 6. Remove the compression wrap and take lateral and VD radiographs. 7. Modify this technique as needed for the suspected disease entity. For example, to evaluate for ectopic ureters, take oblique films off lateral at the bladder trigone between 15 and 20 minutes. A pneumocystogram may also be helpful for identifying the distal ureters and vesicoureteral junctions. • Complications include perivascular injection, which can be treated by instilling saline into tissues to dilute; nausea or vomiting; adverse systemic (anaphylactoid) reaction; and contrast-induced renal failure. The study may be nondiagnostic when the kidneys become bright (contrast enhanced) and remain that way, but there is no opacification of the collecting system, ureters, or bladder. Be careful in VD positioning to avoid aspiration.
Cystography • Contrast medium: For negative contrast, use nitrous
• •
oxide, room air, or carbon dioxide; for positive contrast, use a water-soluble iodinated ionic contrast medium (not barium). Catheters: Foley, tom cat, male dog, or metal female catheters Sterile lubricant gel
• Three-way stopcock • Contrast studies • Negative-contrast cystogram (pneumocystogram) • Positive-contrast cystogram (technique of choice for identifying urinary bladder location and tears) • Double-contrast cystogram (superior for demonstrating lesions involving the urinary bladder wall and intraluminal filling defects)
Technique (Double Contrast) 1. Withhold food for 12 to 24 hours. 2. Administer warm-water cleansing enemas the night before and 3 to 4 hours before the procedure if needed. 3. Sedation or tranquilization may be necessary for catheterization, especially in cats and female dogs. 4. A small amount of 2% lidocaine (2–5 ml) infused into the urinary bladder before the contrast agent may reduce urinary bladder spasm. 5. Place the catheter tip within the bladder neck. 6. Empty the urinary bladder. 7. Infuse the positive-contrast medium (1–3 ml in cats and dogs 25 pounds), rotate the patient, and massage the bladder to distribute the contrast medium and coat the entire mucosal surface. 8. Slowly infuse negative-contrast material (approximately 10 ml/kg, but range is extremely variable). Complete distention is desirable and can be judged by palpation, back pressure felt on syringe plunger, or reflux of gas around catheter. 9. Take a lateral, two lateral obliques, and a VD radiograph to examine the bladder full on doublecontrast cystograms. 10. Evacuate contrast material from the bladder after the study.
Technique (Positive Contrast)
• Increase exposure technique by 10% for a positivecontrast study.
• Only lateral and VD views are necessary for positivecontrast cystograms.
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• Use the technique described previously for catheter •
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taken if needed. Follow-up radiographs may be helpful if a bolus of contrast material is retained within the esophagus.
placement. Administer 3 to 5 ml/kg of positive-contrast medium.
Complications
Complications
• Fatal air embolism (rare cases). An increased risk
• Aspiration. • Leakage of barium into mediastinum. Low osmolal-
•
exists with ulcerative or erosive cystitis. Carbon dioxide is more soluble than room air in blood and thus less likely to cause this problem. Air embolism occurs immediately after the administration of negative-contrast medium. Place the animal in left lateral recumbency, and lower the head to maintain normal blood circulation through the heart. The air is trapped in the right ventricle. Iatrogenic trauma (hematuria or rupture) and infection (bacterial contamination or cystitis).
Urethrography • Retrograde positive-contrast study of the urethra using iodine.
• Equipment includes catheter (Foley, metal, male dog), sterile gel, lidocaine, and water-soluble iodinated contrast medium.
Technique 1. Evacuate the colon with an enema, if needed, before the study; take scout films before the study to evaluate technique and preparation. 2. Pass a urinary catheter into the distal urethra. Inflate the balloon if a Foley catheter is used (in distal urethra for female dogs or cats and proximal to the os penis in male dogs when possible). 3. Administer 2 to 5 ml of 2% lidocaine before injecting contrast material to reduce urethral spasm. 4. Position male dogs with their legs drawn cranially. 5. Administer 10 to 20 ml of contrast medium for male dogs and 5 to 10 ml for female dogs and cats. Inject as a bolus and take radiographs during the last few milliliters of injection. 6. A lateral radiograph may be sufficient, but subsequent lateral and VD oblique views may be helpful.
Complications
• Iatrogenic trauma and bacterial contamination Esophagography Technique 1. Take survey cervical and thoracic radiographs. 2. Position the animal in lateral recumbency. 3. Administer contrast medium (see Table 4-6) (barium sulfate suspension, Esophotrast, barium burger) slowly into the buccal pouch. 4. Dose is variable (5–20 ml); use enough to induce swallowing and coat esophagus. 5. Obtain radiographs following swallows. The lateral view is most informative; additional views can be
ity, nonionic iodinated contrast medium (iohexol) may be indicated if perforation is suspected.
Gastrography ▼ Key Point Before contrast studies of the gastrointestinal tract, discontinue all drugs that may influence motility.
Technique 1. Fast patient 12 to 24 hours before the study. 2. Give cleansing enema the night before and 3 to 4 hours before the study, especially if complete upper gastrointestinal study is to be done. 3. Take plain films before the study. Then pass a stomach tube for administration of contrast medium. 4. Obtain negative-contrast gastrogram (pneumogastrogram) by administering 6 to 16 ml of room air per kilogram of body weight using a stomach tube. Immediately take four views (right and left lateral, VD, and DV). This is often valuable in the diagnosis of radiolucent foreign bodies. 5. Obtain positive-contrast gastrogram using barium (suspension, 30% weight-to-volume) at a dose of 6 to 12 ml/kg (see Table 4-6). Administer through a stomach tube, and take films immediately (right and left lateral, VD, and DV). Use this procedure to document gastric displacement, certain gastric foreign bodies, and gastric perforation. Barium begins leaving the stomach within 5 to 15 minutes. The stomach is emptied by 30 to 60 minutes in cats and 1 to 2 hours in dogs. 6. A double-contrast gastrogram can be done as a separate study or during an upper gastrointestinal study. Give barium, 60% weight-to-volume at a dose of 1.5 to 3 ml/kg, and insufflate with room air at 10 ml/kg. Immediately take DV, VD, and right and left lateral films. This study is indicated in cases of suspected gastric wall and mucosal lesions.
Upper Gastrointestinal Study • Preparation requires a 12- to 24-hour fast and an • •
enema the night before and 3 to 4 hours before the study. Use barium suspension, 30% to 60% weight-tovolume, for routine studies (see Table 4-6). Dose is 8 to 16 ml/kg. Use iodinated contrast (ionic and nonionic) agents (see Table 4-6) with suspected perforation for quick determination of small intestine patency and location
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and when endoscopy is planned immediately following the contrast study. For restraint in canines use acepromazine, and in felines use ketamine/acepromazine preparations. See Chapter 2 for doses. These sedatives have less effect on motility than do many others.
Technique 1. Take survey radiographs (right lateral and VD). 2. Immediately after administration of barium, take right and left lateral and DV and VD views. Obtain right lateral and VD radiographs at 15, 30, and 60 minutes. Be consistent unless a lesion is identified that is better evaluated by repositioning the animal. Then, proceed at hourly intervals until the contrast material reaches the colon. 3. Modify this protocol for each individual depending on the suspected disease entity or the lesions visualized during the procedure. 4. Expected transit time to the colon is 3 to 4 hours for dogs and 1 hour for cats.
Complications
• Aspiration of barium with or without gastric contents. • Leakage of barium indicates a gastrointestinal (GI) perforation, which is a surgical emergency. Barium itself induces a chemical peritonitis that may make treatment of GI perforation more difficult. ▼ Key Point Whenever GI perforation is suspected, use nonionic iodinated contrast medium (e.g., iohexol) instead of barium.
Myelography • Myelography is the radiographic evaluation of the •
•
•
spinal cord by injection of a positive-contrast agent into the subarachnoid space. Indications • To evaluate transverse myelopathy • To determine nature, location, and extent of a lesion prior to surgery • To identify multiple lesions when one lesion might be masked by another and therefore not detected clinically Contraindications • Diffuse myelopathy that is not amenable to surgery • Meningitis, which may be aggravated by contrast medium • Not indicated when survey radiographs and clinical signs are adequate for diagnosis Contrast medium (see Table 4-6) • Dose for cisternal tap: Cervical study (0.2– 0.3 ml/kg); thoracolumbar study (0.45 ml/kg) • Dose for lumbar tap: Cervical study (0.45 ml/kg); thoracolumbar study (0.3 ml/kg)
▼ Key Point Always obtain survey spinal radiographs before myelography.
Basic Technique 1. Animals must be under general anesthesia. 2. Perform sterile preparation of the puncture site. 3. Collect and analyze cerebrospinal fluid (CSF) if deemed necessary.
Cisternal Tap Procedure 1. Position the animal in lateral recumbency. 2. Place the nose parallel to the tabletop and perpendicular to the spine. 3. Use a 20- or 22-gauge, 1.5- to 2.5-inch spinal needle with the bevel directed caudally. 4. Insert the needle on the dorsal midline between the occipital protuberance and the wings of the atlas. 5. Direct the needle toward the mandible. 6. If the needle hits bone, move the needle cranially or caudally until it falls into the atlanto-occipital (AO) space. 7. Remove the stylet and check for CSF flow often while advancing the needle. 8. Inject contrast material slowly after seeing CSF in the needle. Prior to injection, collect a specimen if CSF for later analysis is indicated. 9. Elevate the head for 5 minutes before taking radiographs. 10. Take lateral and VD radiographs (also VD oblique if necessary). Remove the endotracheal tube, if necessary, for the VD radiograph.
Lumbar Tap Procedure 1. Position the animal in lateral or sternal recumbency, and flex the rear legs to help open the interarcuate spaces. 2. Use a 20- or 22-gauge, 1.5- to 3.5-inch spinal needle. 3. Insert the needle through the L5-6 interarcuate space for small dogs and cats and L4-5 for large dogs. Place the needle on the dorsal midline just lateral to the dorsal spinous processes of L6 at a 50 to 60 degree angle in a cranioventral direction toward the interarcuate space at L5-6. In cats, insert the needle off the cranial edge of the L6 dorsal spinous process perpendicular to the long axis of the spine. Direct the needle ventrally through the interarcuate space. 4. Inject in either the dorsal or the ventral subarachnoid space. Always check for CSF flow before injection; however, it is not always obtained. Increase the likelihood of obtaining CSF by elevating the head and shoulders before placing the needle. 5. Perform a small test injection (0.25–0.50 ml) followed by a radiograph to check needle placement. 6. Slowly inject total dose. Take radiograph views based on localization determined by neurologic examination.
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Complications
• Seizures (incidence is reduced with new contrast • • • • •
agents, e.g., iohexol) Exacerbation of clinical signs Hyperesthesia Apnea during injection Epidural injection will not negatively affect the health of the animal but negatively affects the quality of the myelogram. Central canal filling occurs when the needle is placed through the center of the cord. It usually appears thin on radiograph and sharply defined in the normal animal.
Interpretation Lesions are divided into three categories (Fig. 4-21): 1. Extradural, characterized by a. Displacement of the spinal cord b. Narrowing or compression of the subarachnoid space c. Deviation of the subarachnoid space d. Spinal cord may appear wide on opposite view 2. Intradural extramedullary, characterized by a. Filling defect within the subarachnoid space (“golf tee” sign) b. Possibly associated extradural or intramedullary component 3. Intramedullary, characterized by a. Spinal cord widening in all views
Extradural
Intradural Extramedullary
Intramedullary
Lateral
Ventrodorsal
RADIATION SAFETY Basic Radiation Safety The objectives of radiation safety are to obtain the maximum amount of diagnostic information while keeping the radiation exposure to personnel and animals to a minimum. ▼ Key Point The responsibility for radiation safety lies solely with the owners of the practice.
Radiation protection in veterinary medicine is the subject of the National Council on Radiation Protection and Measurements (NCRP) Report No. 36, titled Radiation Protection in Veterinary Medicine. This report specifically outlines when radiation protection surveys are made. The report makes recommendations concerning tube housing, aluminum filtration, collimation types, and centering devices. A special section discusses radiography with portable and mobile diagnostic equipment. All practices need a copy of this report. Other NCRP reports that may be pertinent are No. 116, which discusses protection devices and provides recommendations for the maximum permissible dose (MPD); No. 107, which explains the concept of ALARA (as low as reasonably achievable) for medical and dental personnel; and No. 35, which discusses dental applications of diagnostic radiology. The MPD was established to keep the radiation exposure of workers below a level at which adverse effects might be observed during a lifetime and to minimize the incidence of genetic effects in the entire population. The MPD does not apply to animal patients, to radiation emitted from natural background sources, or to radiation therapy. The actual risk to an individual exposed to MPD is small, but the risk is directly proportional to the received dose. Therefore, radiation exposure must be kept as low as possible. Radiation can cause both tissue and genetic damage. The effects of radiation can be demonstrated in a short time, or they can be cumulative and not observed for a long time. Federal regulations regarding use of x-ray equipment and radiation protection are published in the Code of Federal Regulations, available at university and public libraries. Individual states publish radiation control regulations that are reprinted from the state codes. These regulations include information concerning the licensing of x-ray machines, the licensing fee, and the procedure to be followed in obtaining licensing. The goal in diagnostic radiology is to obtain radiographs with minimum exposure to both patient and personnel.
Maximum Permissible Dose Figure 4-21.
Radiographic patterns of myelographic lesions.
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The MPD is currently 5 rem per year.
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▼ Key Point Be familiar with federal, state, and local regulations regarding use of x-ray equipment and radiation safety.
Reducing Exposure Three methods reduce radiation exposure: (1) increased distance between the individual and the radiation source, (2) decreased duration of exposure, and (3) protective barriers between the individual and the radiation source.
• •
• Limiting radiation exposure • Limit the number of individuals within the room where the procedure is taking place. Use positioning devices, such as sandbags, sponges, tape, and Plexiglas or foam trough. Use chemical restraint whenever possible. ▼ Key Point When you must be present within the radiographic room during film taking, always wear protective clothing.
• Protective lead apparel includes apron, gloves, thyroid shield, and protective goggles. Lead apparel is usually 0.5-mm lead equivalent. Hang aprons up to prevent the lead from cracking. Store gloves so that liners can dry. Check all protective clothing at least twice a year for cracks and tears. Place the items on a film cassette and radiograph them at an exposure of approximately 85 kVp. ▼ Key Point Never permit any portion of the body to be within the primary beam, even if covered with protective clothing.
• •
• Never hand-hold any x-ray tube. All x-ray tubes leak radiation from the housing. • Use a shielding device whenever possible to protect all or part of your body. Lead glass may be part of this shield so that you may continue to see the patient. When using a horizontal x-ray beam, never position any part of your body behind the cassette. Use collimation. An unexposed border on the radiograph demonstrates that the primary beam did not
•
•
exceed the size of the cassette (film). This practice helps reduce scatter radiation by decreasing the interaction between the primary beam and the tissue, therefore increasing radiographic quality. Check the collimator light for accuracy; replace the bulb as needed. Use fast film, fast rare-earth screens, and high-kVp techniques to lower the exposure factors and the amount of radiation produced. Use a 2.0-mm aluminum filter installed at the tube housing port to remove the softer (less energetic) radiation portion of the x-ray beam. This aids in the reduction of scatter radiation and exposure to the patient. Individuals within the room should always stand as far from the radiation source as possible. If you double the distance from the source of radiation, you decrease your exposure level by a factor of 4 (inverse square law). All personnel working with radiation are required to wear a film badge or some other method of monitoring the amount of exposure if they have the potential to receive greater than 1/4 MPD. Remember that wearing the device does not protect the individual, but it serves as a reminder of working in a potentially hazardous environment. For a monitoring device to be most helpful in determining exposure to radiation, wear it consistently in the same location on the body outside the apron at the neck. Film badges register when exposed to heat, light, water, or pressure. They can be purchased through companies listed in Table 4-7.
▼ Key Point Never permit anyone under the age of 18 or a pregnant woman in the room during a diagnostic procedure.
• Rotate personnel, thus reducing the amount of exposure to each person.
• Do not direct the x-ray beam into adjacent rooms that may be occupied.
• Use a gonadal shield for the patient. • Always plan radiographic procedures (e.g., proper position and technique), thus reducing the number of films needed, which ultimately reduces the exposure to patient and personnel.
Table 4-7. SOURCES OF FILM BADGES Company Landauer Teledyne Brown Engineering
Address
Phone Number
Website
2 Science Rd. Glenwood, IL 60425 50 Van Buren Ave. Westwood, NJ 07675
800-323-8830
www.landauerinc.com
201-664-7070
www.tbe.com
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Clinic Construction • Check with your state’s health department (radiation • •
•
protection division) for the latest laws on radiation safety and clinic construction. Register your x-ray machine with the state. Many states are now conducting “surprise spot checks” of x-ray machines and radiographic records. Maintain film and technique logs for complete records (Figs. 4-22 and 4-23). If constructing a new clinic, a drawing of the layout must be sent to the state radiation protection department. This drawing indicates the location of the x-ray machine and demonstrates how the space in the room where the x-ray machine is located will be used. The use of the adjoining rooms and an estimate of the degree of traffic in these areas are determined. The radiation safety department then sends a computerized layout of wall, ceiling, and floor materials to be used in certain areas of your clinic.
From the differential list, additional tests can be done to help formulate a definitive diagnosis.
• Successful interpretation of radiographs depends on many factors. ▼ Key Point The most important factor in the successful interpretation of radiographs is the quality of the radiographs being examined.
• At least two views at right angles to each other are
• • • •
RADIOGRAPHIC INTERPRETATION Radiology is a valuable adjunctive diagnostic tool. Do not interpret radiographs without considering the history, clinical signs, physical examination findings, and laboratory data. Radiographic signs are rarely pathognomonic; therefore, a specific diagnosis is seldom possible. History + Physical exam + Lab findings + Radiographs = Differential list
Figure 4-22. inventory log.
Film usage and
75
• • • • • •
needed. The use of right or left lateral radiographs is based on the preference of the individual reading the radiographs. The same holds true for VD and DV views, but be consistent. Maximize viewing conditions. Dark, quiet room. At least two view boxes to evaluate two views simultaneously. Always place the film on the view boxes such that the anatomic structures are in the same position and direction: DV/VD radiograph with the animal’s right to your left; lateral radiograph with the head to your left. Have a shielded, high-intensity (hot) lamp available. Read films slowly and thoroughly. Always have radiology and anatomy texts nearby. Evaluate the radiographs using a systematic approach. Evaluate the entire film before concentrating on obvious lesions. Use an area method, evaluating the radiograph either peripheral to center or center to peripheral. Use an organ system method. Evaluate all parts of a system before examining the next system.
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Figure 4-23. nique log.
• However you choose to evaluate films, be consistent •
from case to case. Knowledge of normal radiographic anatomy is essential.
Radiographic Signs • Radiopacity: Various radiographic opacities are caused
• •
by the differential absorption of x-rays. The opacity of surrounding material also influences the observed opacity of a structure. The five radiopacities in decreasing order (white to black) are those of metal, bone, soft tissue (fluid), fat, and gas. Metal is the only one that is not a biologic opacity. Geometry: Size, shape, position, margination, and number. Function: Excretion (intravenous urography), motility (upper gastrointestinal), patency, and integrity. Evaluation of function often requires contrast medium and multiple films.
COMPUTED TOMOGRAPHY Computed tomography (CT) is a cross-sectional imaging technique that allows identification of structures without the superimposition present with radiographs. Like radiographs, CT uses x-rays to produce an image. There are many different types of CT
Radiology tech-
machines, but all produce a thin fan of x-rays that are directed through the patient and strike a row of radiation detectors. The amount of radiation going through a specific part of the patient, and therefore reaching the detector, is related to the density of the body part. Based on numerous views of each part and the image density of different areas, a computer is used with various algorithms to form a cross-sectional, gray-scale image. Similar to radiographs, when looking at a CT: bone = white, air = black, fat = dark gray, and soft tissues/fluid = various shades of gray. Once the image has been acquired, post-processing parameters can be adjusted to optimize viewing of certain areas (i.e., bone, soft tissue, lung, and brain). Thus, the term soft-tissue or bone window is commonly used when evaluating CT images. Often, the same study is viewed in multiple windows for a complete evaluation. For example, a CT of the thorax would need to be viewed in a soft-tissue window (for the mediastinum), a lung window (for the pulmonary parenchyma), and a bone window (for the ribs and spine). The adjustment in a bone versus a soft-tissue window is made by changing the window width and window level. The window width defines how many shades of gray are seen over a given density of tissue (providing a long or short scale of contrast). The window level is the midpoint of the window width. CT studies are normally performed with slices in the transverse (axial) plane through the area of interest. This information can then be used to reformat the area
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of interest into a different plane (sagittal, coronal, or oblique), therefore maximizing interpretation. Common areas to use CT in veterinary medicine are the nasal cavity, middle ears, skull (bone changes or trauma), skeletal (elbows and spine), thorax, abdomen, and areas of neoplasia (for surgical or radiation planning). Magnetic resonance imaging (MRI) is considered best for soft-tissue structures, particularly the brain and spinal cord.
Advantages • The cross-sectional image is provided without
•
superimposition of structures, allowing more accurate detection and assessment of the extent of disease. CT is considered better than MRI for evaluation of bone abnormalities (MRI is best for soft tissue).
Disadvantages • Higher cost compared with radiographs (less expen-
77
termed the Tesla. Low-field magnets are less than 0.5 Tesla, mid-field magnets are 0.5 to 1 Tesla, and highfield magnets are more than 1 Tesla. Although all types of magnets are utilized, the cost of the machine and the time needed to acquire the image depend on field strength. In general, high-field magnets are more expensive, but images are acquired more quickly than from low-field units. Images are acquired using different pulse sequences (imaging acquisition parameters). These different sequences are used because the signal intensity (appearance of the image) will vary depending on primarily the water, fat, and mineral content of the area being imaged. Typical sequences are termed T1-weighted, T2weighted, and proton density. There are a variety of fat saturation techniques and variations in the sequences that are also utilized. Contrast material is generally given to patients and the T1-weighted sequences are repeated. The contrast material is a ferromagnetic substance that enhances signal intensity on T1-weighted sequences.
sive than MRI).
• The animal must not move during the CT study, so the patient must undergo general anesthesia in most cases.
MAGNETIC RESONANCE IMAGING MRI is a cross-sectional imaging technique that is considered excellent for imaging soft tissues. CT is still considered the best cross-sectional imaging modality when assessment of bone is required. MRI utilizes a magnetic field, radiofrequency (RF) waves, and the hydrogen protons in the patient for creation of the images. The equipment consists of a magnet, receiving coils, and hardware and software of the control station. MRI technology utilizes a magnet to polarize hydrogen atoms in the tissues and monitor the summation of the spinning energies within living cells. When a patient is put in a strong magnet, some of the atoms become aligned with the magnetic field. If an RF pulse is sent into the patient, the vector direction of the hydrogen protons can be changed. As the atoms realign themselves with the magnetic field, they give off an RF pulse that can be detected by the receiver coil. The amount of RF signal given off and the time at which it is released are characteristic for certain tissues. This information is again processed by a computer to provide a cross-sectional image with various shades of gray. The shade of gray of a certain tissue depends on the acquisition parameters. In other words, fluid may be dark gray in one acquisition and bright white in a different acquisition. Cortical bone and air will always be black with MRI. The images can be acquired in any plane without reformatting. There are different types of magnets, ranging from low- to mid- to high-field units. The unit strength is
Advantage • MRI is useful for areas that cannot be evaluated by more conventional methods (radiographs or ultrasound) such as the central nervous system, particularly the brain.
Disadvantage • Limited access • High cost ULTRASOUND Ultrasound is rapidly becoming an accepted imaging modality in small animal practice. New and used equipment is available at reasonable prices, and usefulness has increased to include ophthalmic, cardiac, abdominal, and reproductive disease diagnosis. It is a safe, noninvasive diagnostic technique that provides information about the internal architecture of organs within the abdomen and thorax. Functional information can also be obtained with echocardiography. Ultrasound is not meant to replace diagnostic radiography but to complement it. Ultrasound is operator dependent. The quality of the image and the information gained are directly related to the ability of the person doing the study.
Equipment The major components of the diagnostic ultrasound imaging system are pulser, transducer, receiver, memory, and display. Electrical pulses are produced by the pulser, and these drive the transducer. The transducer produces ultrasound pulses for each electrical
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pulse it receives. The transducer also produces electrical pulses for each ultrasound pulse (reflection) it receives from tissues. The electrical pulses go to the receiver, where they are converted to information that the memory can utilize. Information from the memory drives the display, which produces an image. Suppliers of ultrasound equipment are listed in Table 4-8.
• Mechanical: In a mechanical (sector) scanner, the
•
Machines
• Questions to consider before purchasing or leasing ultrasound equipment:
• What kind of scanning will I be doing (e.g., heart,
•
abdomen, real-time, B-mode, or M-mode)? • How large or small are my patients? • Is someone in the practice willing to accept primary responsibility for learning and doing the procedures? • How much money can I invest? There are multiple types of transducers • A linear array scanner produces a rectangular image and can be used to evaluate broad areas, where no bony or gas-filled structures interfere. These scanners are usually less expensive. The major drawback is the transducer contact zone, which makes intercostal and subcostal (heart, liver, biliary tract, and right kidney) imaging difficult. • A sector scanner produces a pie-shaped image. A smaller contact zone is used, which makes intercostal and subcostal imaging less difficult.
•
sound wave is focused a certain distance from the transducer (focal point). The sound wave is within focus for some distance on both sides of the focal point (focal zone). Resolution is best within this fixed focal zone. The scanner contains moving parts. Electronic: These are linear or sector scanners with no moving parts; therefore, they are more durable than mechanical scanners. The beam is formed by adding together many small beams from an array of small crystals. The scanner has variable (dynamic) focusing. The focal zone therefore can be placed anywhere in the image depth. Image display • M-mode (motion-mode): Documents motion, especially that of the heart (echocardiography). A thin ultrasound beam is directed into the heart, is reflected back, and then is shown on the screen as numerous moving lines. Motion is indicated along the side, and time is shown along the bottom of the screen. • B-mode (brightness-mode): Echoes are displayed as dots. The brightness of the dot changes with the amplitude of reflection. The larger the reflection, the brighter the dot—no reflection, black dot. The location of the dot corresponds to the location of the reflector in the body. • Real time: The image is continually updated during the entire examination. This permits direct observation of moving structures (e.g., heart or bowel peristalsis).
Table 4-8. ULTRASOUND COMPANIES Company Aloka Alliance Medical U.S.A. Classic Medical Supply Hitachi Medical Corp. Jorgensen Laboratories Medelex Products Group International Sound Technologies SoundVision Ultrasource Universal Medical Systems
Address 10 Fairfield Blvd. Wallingford, CT 06492-7502 112 N. Bridge St. Smithville, MO 64089 19900 Mona Road, Ste. 105 Tequesta, FL 33469 1959 Summit Commerce Park Twinsburg, OH 44087 1450 N. Van Buren Ave. Loveland, CO 80538 732 N. Pastoria Ave. Sunnydale, CA 94086 447 Main St. P.O. Box 1807 Lyons, CO 80504 5939 Darwin Ct, Ste. 101 Carlsbad, CA 92008 417 Tory Dale Ct. Roseville, CA 95747 5241 Plainfield Ave. NE, Ste. Q Grand Rapids, MI 49525 299 Adams St. Bedford Hills, NY 10507
Phone Number 800-442-5652
Website www.aloka.com
888-689-3070 800-722-6838
www.classicmedical.com
800-800-3106
www.hitachimed.com
800-525-5614
www.jorvet.com
800-644-0692
www.medelex.com
800-336-5299
www.productsgroup.com/vet_index.html
800-268-5354
www.soundvet.com
800-957-5565
www.soundvisionweb.com
888-680-6989
www.ultrasource.net
800-842-0607
www.u-m-s.com
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• New versus used equipment • New equipment purchase is ideal because some companies offer training (in-house or continuing education course) and a year-long warranty with service and parts (in-house service or another unit is made available while your unit is serviced by the company). Manufacturer-reconditioned units may provide a year-long or shorter warranty. The major disadvantage of new equipment obviously is the higher cost. • A great deal of used equipment is available with the advent of newer technology. Older, used, outdated equipment is being replaced with new equipment based on new technology. The price of old equipment is very attractive, sometimes as low as $1000. Although initial cost is low, some significant expense may be required, including service, maintenance, transducers, and accessories. If the appropriate frequency transducers do not come with the unit (often only 2- and 3-MHz transducers come with units that were used on human patients), the cost can increase 3 to 4 times to purchase 5- and 7.5-MHz transducers.
Transducers
• Transducers are available in a variety of frequencies
• •
(2–15 MHz). Low-frequency transducers provide greater depth of penetration, but because of large wavelength, resolution is poorer. High-frequency transducers provide excellent resolution, but the beam is rapidly attenuated in tissue. They are therefore used to evaluate superficial tissues. Use as high a frequency transducer as possible to maximize resolution but still allow penetration to the depth needed. For transducer uses, see Table 4-9.
• • • •
There are various methods of preserving the image for inclusion in the animal’s medical record: • Polaroid camera—Heat-sensitive, thermal-paper recorder • Multiformat camera—Can record multiple images on x-ray film • Videotape—Images are recorded, allowing evaluation by others at a later time • Digital images or digital video
Ultrasound Technique • Patient preparation
This may include a guided biopsy attachment for the transducer, calipers, a screen-labeling device, and an Mmode/B-mode split screen. Portability of the machine must also be considered.
Ultrasonographic Accessories
•
• Positioners • V-trough is easily constructed from wood or Plexiglas. Table 4-9. TRANSDUCER SELECTION Transducer Type 7.5 MHz 5.0 MHz 3.5 MHz
Use Eye, feline heart and abdomen, small canine abdomen (8 is conclusive evidence of local ocular or CNS antibody production. ▼ Key Point The combination of antibody titers (especially IgM) and PCR assay on aqueous humor or CSF is the most accurate way to diagnose ocular or CNS toxoplasmosis.
Polymerase Chain Reaction and Antigen Assays
• PCR assay can be used to detect T. gondii DNA in
•
blood, CSF, or aqueous humor. The PCR assay in blood can be positive in cats with and without clinical disease; thus, a positive PCR by itself does not confirm clinical toxoplasmosis. Toxoplasma antigen can be detected in cats initially 1 to 4 weeks after exposure and then intermittently for up to 1 year. This does not distinguish active from past infection and thus has no advantage over antibody titers.
Identification of Toxoplasma Organisms Detection of Tachyzoites Characteristic intracellular inclusions are occasionally identified in aspirate and impression smear cytologies stained routinely or in biopsies.
Detection of Oocysts in Feces Fecal oocysts are rarely detected because most cats are past the transient stage of oocyst shedding by the time clinical signs occur (see under “Stages of Infection”); thus, this is not a suitable method for diagnosis of clinical toxoplasmosis.
• Procedure: Use Sheather’s sugar centrifugation-
•
flotation (Sheather’s solution: 500 g of table sugar, 320 ml of distilled water, and 6.5 g of phenol crystals melted in a hot water bath). Make a fecal suspension with 5–10 g of feces and water, then centrifuge one part fecal suspension with two parts Sheather’s solution for 10 minutes at 1000 g and examine one to two drops from the meniscus. Disadvantages: Oocysts are small, easily overlooked, and morphologically indistinguishable from certain other coccidia (Hammondia spp., Besnoitia spp.) without specialized animal inoculation studies. Nevertheless, assume coccidian oocysts 10 ¥ 12 mm in size in feline feces to be Toxoplasma until proved otherwise.
▼ Key Point Detection of fecal oocysts is not a reliable diagnostic test for clinical toxoplasmosis because oocyst shedding occurs only briefly and usually ends before clinical signs begin.
Treatment Toxoplasmosis can be treated with clindamycin, trimethoprim-sulfonamide, or azithromycin. Localized ocular infection is most responsive. Approximately 60% of animals with generalized toxoplasmosis recover with treatment; thus, the prognosis is guarded. Mortality rate is highest in neonates and in animals that are severely immunosuppressed. ▼ Key Point Clindamycin is the initial drug of choice for treating clinical toxoplasmosis, and it penetrates the blood-brain and blood-eye barriers. It also reduces oocyst shedding.
• Clindamycin (Antirobe, Upjohn): 12.5 mg/kg PO or IM q12h for 28 days.
• Trimethoprim-sulfadiazine: 15 mg/kg PO q12h for 28 days.
• Azithromycin (Zithromax): 10 mg/kg PO q12h for 7 days.
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• For uveitis, use 1% prednisone drops topically every 6 to 8 hours for 2 weeks.
Prevention in Cats
sure to oocysts is very unlikely from petting cats or from cat licks, bites, and scratches. ▼ Key Point Because of the way cats defecate, bury their feces, and keep their haircoats clean, transmission of Toxoplasma oocysts to humans by touching and caring for a pet cat is very unlikely.
Prevent cats from ingesting tissue cysts in meat and prey animals.
• Do not feed cats raw meat, viscera, or bones, and do • • •
not allow them to scavenge these from garbage. Do not allow cats to ingest raw (unpasteurized) milk, especially from goats. Do not allow cats to roam free where they can hunt prey (mice, birds) for food. Do not allow cats to eat transport vectors (cockroaches, flies, earthworms).
• The question often is raised, how dangerous is a
•
Public Health Considerations Toxoplasmosis is an important zoonosis in humans. Infection in immunocompetent people is inapparent or causes a self-limiting, flu-like illness. Infection during pregnancy can cause fetal toxoplasmosis, leading to stillbirth or severe ocular or CNS disease. Approximately 10% of people with AIDS develop toxoplasma encephalitis from reactivation of encysted bradyzoites.
Preventive Measures in Humans Prevention of human infection is based on avoiding ingestion of sporulated oocysts in the environment or tissue cysts in undercooked meat. Contaminated drinking water has caused some outbreaks.
oplasma antibodies has little public health benefit and is not recommended.
Environmental Control Measures
• Control the stray cat population to reduce contami-
•
compromised people should avoid contact with soil, cat feces, litter boxes, and raw meat.
• Do not eat raw or undercooked meat. Cook meat to • • • • • •
Risks of Owning an Infected Cat Direct contact with cats is highly unlikely to pose a risk of human infection. Oocysts shed in cat feces are the only means of transmission from cat to human. Expo-
healthy pet cat with a positive Toxoplasma antibody titer? Most seropositive cats and cats with clinical toxoplasmosis have completed oocyst shedding by the time they develop a positive titer. Repeat exposure of a seropositive cat results in little or no shedding. Most cats that are shedding infective oocysts are seronegative and preclinical. Seronegative cats are non-immune and would be more likely to shed oocysts if exposed, thus posing a greater risk to its owner than a seropositive cat.
▼ Key Point Serologic testing of healthy cats for Tox-
▼ Key Point Pregnant women and severely immuno-
160∞F to kill tissue cysts. Use good kitchen hygiene. Wash hands, cutting boards, sink tops, and utensils that come in contact with raw meat. Change the litter box daily to remove oocysts before they have 24 hours to become infective. Disinfect with boiling or scalding water. Wear gloves while gardening, or wash hands after gardening to prevent exposure to oocysts in soil. Wash fruits and vegetables thoroughly before eating to remove soil particles with oocysts. Boil or filter surface water before drinking if contamination is possible. Keep sandboxes covered when not in use so that cats cannot defecate in them.
225
nation of the environment, soil, and water with oocysts. Cats that defecate in the soil are likely to be the same cats that must hunt for their food and thereby have a high risk of infection. To reduce entry of Toxoplasma into the food chain, prevent cats from roaming where food-producing animals and livestock feed are kept. Pork is the most likely source of cyst ingestion in people in the United States.
NEOSPOROSIS Etiology Neosporosis is a protozoan disease of dogs caused by Neospora caninum, a coccidian parasite that resembles the appearance of Toxoplasma and has a similar life cycle. Dogs and wild canids are definitive hosts, and other animals (especially cattle) are intermediate hosts.
• Dogs are infected by ingesting meat infected with •
•
tissue cysts containing bradyzoites or by transplacental transmission. Rapidly replicating tachyzoites disseminate and produce necrotizing lesions in many tissues or cause transplacental infection of a developing fetus. Clinical disease in dogs primarily reflects neuromuscular infection. As the definitive host, the dog completes the life cycle in its intestines and sheds fecal oocysts that become infective in the environment within 24 hours of passage.
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• Clinical disease has not been seen in cats, but exper•
imentally infected kittens develop encephalomyelitis and polymyositis. N. caninum has worldwide economic importance as a major cause of abortion in dairy cattle.
Clinical Signs Multifocal, progressive neuromuscular signs predominate as a result of non-suppurative encephalomyelitis, polyradiculoneuritis, and fibrosing polymyositis.
• Clinical signs can include hind-limb paresis and
•
ataxia progressing to ascending paralysis, hind-limb extensor rigidity, and muscle atrophy and contracture. Dysphagia and masticatory muscle involvement can be seen. Less common manifestations include myocarditis (arrhythmias), pneumonia (fever, dyspnea, cough), ulcerative or pruritic dermatitis, chorioretinitis, and multifocal intra-abdominal dissemination (hepatitis, pancreatitis).
▼ Key Point Subclinically infected bitches can transmit Neospora in utero to successive litters of puppies. Congenital neosporosis is particularly severe and often leads to in utero or neonatal puppy mortality.
Laboratory and Radiographic Findings • Muscle involvement may cause increased serum levels •
•
of muscle enzymes (CK, AST) and abnormal electromyographic findings. CSF shows a moderately increased protein (20 to 150 mg/dl) and increased leukocytes (10 to 100 cells/ml) composed of a mixture of small and large mononuclear cells and neutrophils. Thoracic radiographs may show interstitial and alveolar infiltrates.
Diagnosis • Presumptive diagnosis is based on the combination
•
of compatible clinical signs and a Neospora antibody titer of >1:200 using immunofluorescent antibody (IFA) or ELISA. Serologic crossreactivity with Toxoplasma is minimal. Rarely, the diagnosis can be confirmed by identification of Neospora tachyzoites in cytologies of CSF, skin lesions, or BAL or in biopsies of infected tissues (e.g., muscle). Oocysts can be detected by fecal flotation or PCR, but oocyst shedding is not found in dogs with overt clinical disease. Neospora organisms can be distinguished from Toxoplasma by PCR, immunohistochemistry, or electron microscopy.
Treatment Neosporosis is treated similar to toxoplasmosis using one or a combination of both of the following regimens.
• Clindamycin (15 mg/kg PO q12h) for 28 days • Trimethoprim-sulfadiazine (15–20 mg/kg PO q12h) combined with pyrimethamine (0.5 mg/kg PO q12h) for 28 days Treat all littermates of infected puppies. The prognosis for dogs with severe neurologic involvement is grave, and animals that recover usually have residual neurologic deficits.
Prevention and Public Health • Do not breed dogs with a history of whelping infected puppies.
• Avoid glucocorticoids in seropositive dogs because of the potential for activating encysted infection.
• Neospora is seroprevalent in white-tailed deer; thus, do not let dogs have access to deer carcasses.
• Do not allow dogs to have access to bovine placental tissues (afterbirth) or aborted fetuses.
• Because Neospora infection has a large economic •
impact as a cause of bovine abortion, prevent dog feces from contaminating livestock feed and water. Neospora caninum antibodies have been detected in people, but it is not yet clear whether Neospora is a cause of zoonotic disease.
HEPATOZOONOSIS Etiology Hepatozoonosis is a tick-transmitted protozoan disease of dogs caused by Hepatozoon americanum or Hepatozoon canis. Ticks become infected during feeding on an infected dog. The infection is then transmitted to a new canine host when the tick is ingested, not by the tick bite.
• H. americanum is most common in North America
•
and is transmitted by the Gulf Coast tick, Amblyomma maculatum. Infection is endemic in southern states in the Gulf Coast region (Texas, Oklahoma, Louisiana, Mississippi, Alabama, Florida, and Georgia). H. canis is transmitted by the brown dog tick, Rhipicephalus sanguineous, and occurs in Southern Europe, the Middle East, Africa, and Asia.
▼ Key Point H. americanum, the etiology of American hepatozoonosis, causes a more severe form of clinical disease than H. canis, which usually causes subclinical or mild disease.
• Uncharacterized Hepatozoon spp. have been reported sporadically in cats.
Pathogenesis After an infected tick is ingested, H. americanum organisms disseminate widely and form numerous distinctive tissue cysts, especially in the muscles. The organisms
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most pronounced on the pelvis, long bones of the limbs, and vertebrae. The periosteal lesions may appear as smooth, lamellar thickening of the bone or irregular proliferations.
replicate until cysts rupture, eliciting a severe pyogranulomatous inflammatory response and disseminating more organisms to form new cysts. ▼ Key Point American hepatozoonosis is a chronic debilitating illness characterized by waxing and waning fever, extreme leukocytosis, polymyositis, proliferative periosteal bone lesions, and severe cachexia.
In contrast, H. canis has relatively low pathogenicity; clinical signs are absent or mild in many infected dogs. Severe disease is mostly limited to dogs with concurrent disease or immunosuppression. Muscle and periosteal involvement do not occur with H. canis, but organisms are frequently seen in circulating leukocytes.
Clinical Signs Clinical signs begin within 4 weeks of ingesting an infected tick and continue to wax and wane as more organisms are released into muscle tissue, exacerbating myositis, muscle pain, and fever.
• Fluctuating fever (>104∞F) and lethargy • Myalgia, stiffness, lameness, painful gait, reluctance to move
• Hyperesthesia over the paraspinal muscles • Progressive weight loss, weakness, and muscle • • •
atrophy Mucopurulent ocular discharge with each flare-up Transient bloody diarrhea Possible protein-losing glomerulonephropathy (due to immune complex glomerulonephritis or amyloidosis) in advanced cases
Diagnosis ▼ Key Point Muscle biopsy is the most reliable means of confirming American hepatozoonosis.
• Definitive diagnosis is based on visual identification
•
• The most characteristic hematologic finding is
•
•
extreme neutrophilic leukocytosis (mean 75,000 to 85,000/ml; range 20,000 to 200,000/ml), consisting of mostly mature neutrophils with a mild left shift. Mild normocytic-normochromic nonregenerative anemia is also common. The platelet count is usually normal to increased. Dogs with thrombocytopenia should be evaluated for other concurrent tick-borne infections (see Chapter 17). Common serum chemistry abnormalities are increased alkaline phosphatase, hypoglycemia (in vitro artifact of high white blood cell count), hypoalbuminemia, and hyperglobulinemia. Radiographically, most dogs infected with H. americanum develop diffuse periosteal bony proliferations,
of tissue stages of H. americanum organisms, which are most reliably found in skeletal muscle biopsies and rarely in circulating leukocytes on Giemsa-stained blood smears. In contrast, blood smears are usually diagnostic for H. canis infection. An ELISA-based serologic test for H. americanum has a sensitivity of 93% and specificity of 96%.
Treatment No treatment has been found to effectively eliminate H. americanum from infected tissues in dogs. However, the following treatment has been shown to prolong survival and control clinical signs for extended periods, even years. Pain and fever improve within 48 hours of initiating treatment.
• For H. americanum, use the combination of clin-
Laboratory and Radiographic Findings The presumptive diagnosis of hepatozoonosis in dogs from endemic areas is based on the combination of typical clinical signs (fever, pain, and muscle wasting), extreme leukocytosis, typical serum chemistry abnormalities, and characteristic periosteal bone lesions on radiographs.
227
• • •
damycin (Antirobe) (10 mg/kg PO q8h), trimethoprim-sulfadiazine (Tribrissen or Ditrim) (15 mg/kg PO q12h), and pyrimethamine (Daraprim) (0.25 mg/ kg PO q24h) for 2 weeks to establish remission; and follow this with decoquinate (Deccox, Alpharma) (10–20 mg/kg PO q12h, mixed with food) for 2 years and possibly lifelong to maintain remission and prevent relapses. Decoquinate, an anticoccidial livestock feed additive, decreases recurrences by inhibiting development of the organisms released from tissue cysts, thereby preventing repeated cycles of reinfection and illness. Use nonsteroidal anti-inflammatory drugs as needed for pain and fever. Avoid corticosteroids because they can worsen the disease. For H canis, imidocarb dipropionate (Imizol) (5– 6 mg/kg IM or SC, two doses 2 weeks apart) is highly effective and considered the drug of choice. It may be effective for H. americanum. Pretreatment with atropine (0.04 mg/kg SC), 30 minutes prior to imidocarb injections, reduces the parasympathomimetic side effects of imidocarb.
Prevention and Public Health • Prevention depends on minimizing tick exposure, using an effective tick preventative product on dogs in endemic areas, and routinely checking dogs for ticks and removing them promptly.
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• Zoonotic transmission from dogs to people does not appear to occur.
LEISHMANIASIS
Laboratory Findings • Hematologic findings are thrombocytopenia, anemia, •
Etiology Leishmania spp. are flagellated protozoan parasites that cause vector-transmitted cutaneous and visceral diseases in dogs, humans, and other mammals. In most areas of the world, rodents and dogs serve as reservoir hosts, and infection is transmitted by sand fly vectors. Leishmaniasis occurs worldwide and is endemic in the Mediterranean region of Europe and South America. Leishmania infantum, a member of the Leishmania donovani complex, is the most frequently reported cause of visceral leishmaniasis in dogs. ▼ Key Point Visceral leishmaniasis is endemic in
Diagnosis Presumptive diagnosis of leishmaniasis is based on clinical signs, international travel history, breed (foxhound), and antibody titer. Confirmation is based on cytologic identification of organisms (especially bone in marrow), detection of Leishmania DNA by PCR assay, or protozoal culture.
• Antibody titers develop 2 to 4 weeks after infection
North American foxhounds and foxhound kennels.
• Other dog breeds have also been infected sporadi-
• •
cally in North America. The source of infection in most of these cases has been traveling or living in an endemic country or importation from an endemic country. Cats are usually subclinically infected or only develop cutaneous leishmaniasis. Infection can also be transmitted iatrogenically by transfusion of contaminated blood.
•
• Clinical Signs Sand flies transmit infection during feeding on the host. Intracellular organisms (amastigotes) are disseminated by macrophages and cause cutaneous lesions, polysystemic vasculitis, lymphoreticular hyperplasia, hyperglobulinemia, and immune complex disease of the kidneys and joints. Dogs have subclinical infection for months to several years before developing clinical signs. Visceral leishmaniasis with cutaneous involvement is the most common form of disease in dogs.
• Fever, chronic weight loss, muscle wasting (despite normal appetite)
• Vomiting, diarrhea, melena • Hepatosplenomegaly, generalized lymphadenopathy • Ulcerative or granulomatous dermatitis characterized
• • • • • •
by non-pruritic facial alopecia, hyperkeratosis, scaling, mucocutaneous ulcers, and intradermal nodules on the muzzle, pinnae, ears, and foot pads Elongated brittle toe nails Anterior uveitis, conjunctivitis, blepharitis Cough; sneezing (rhinitis), epistaxis Neutrophilic polyarthritis (lameness, swollen painful joints) Glomerulonephritis, polyuria-polydipsia, renal failure Icterus
lymphopenia, leukocytosis with a left shift, and occasional positive Coombs test. Other lab findings are polyclonal hyperglobulinemia (sometimes monoclonal), hypoalbuminemia, proteinuria, azotemia, increased serum liver enzymes, and the presence of antinuclear antibodies (ANAs).
•
and decline 1 to 3 months after treatment. Infections are considered persistent; thus, a positive IFA antibody titer (≥1:64) is indicative of current “active” infection. Dogs occasionally have false-negative titer results. Trypanosoma causes crossreacting antibodies. Definitive diagnosis can be established in some dogs by cytologic identification of organisms (amastigotes; 2.5 to 5 mm ¥ 1.5 to 2 mm) in aspirates of bone marrow (60% of cases), lymph nodes (30% of cases), or spleen; in impressions of skin lesions; or by the presence of organisms in biopsies of skin or infected organs. Confirmation can also be based on PCR detection of Leishmania DNA in aspirates of bone marrow (the specimen of choice), lymph nodes, or spleen. Blood PCR is useful but less reliable than bone marrow. Both antibody titers and PCR assay are available to practicing veterinarians through the Vector Borne Disease Diagnostic Lab at North Carolina State University. Submission requirements and forms are available at http://www.cvm.ncsu.edu/docs/ tickbornediseaselab.html. The U.S. Centers for Disease Control, Division of Parasitic Diseases (CDC, Atlanta, GA; telephone: 770-488-4475) also provides diagnostic confirmation, including protozoal culture using bone marrow or lymph node aspirates.
Treatment ▼ Key Point Treat leishmaniasis with an antimonial drug plus allopurinol for inducing remission, followed by long-term allopurinol to prevent relapse.
Leishmania infection can often be controlled with medical therapy, but it is usually not curable in dogs. Since the organisms are not eliminated by treatment, relapses are common a few months after treatment is stopped. The prognosis for remission is variable. Dogs
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with renal disease have a poor prognosis. The following drug regimens are recommended:
• Allopurinol (Zyloric, Glaxo): 15 to 20 mg/kg PO
•
•
•
q12–24h, initially combined with sodium stibogluconate or meglumine antimonite, then continued alone for several months to maintain remission. Sodium stibogluconate (Pentostam, Wellcome): 30 to 50 mg/kg IV or SC q24h, combined with allopurinol, for 3 to 4 weeks or until resolution of signs and lab abnormalities; available in the United States through the CDC at http://www.cdc.gov/ncidod/srp/drugs/drugservice.html. Meglumine antimonite (Glucantime, Merial; available in Europe): 100 mg/kg IV or SC q24h, combined with allopurinol, for 4 weeks or until resolution of signs and lab abnormalities. Amphotericin B lipid complex (ABLC) (Abelcet, Enzon) at 3 mg/kg IV q48h (3 times weekly) for a minimum of five treatments. ABLC can be used as an alternative to antimonials in animals with good renal function. Dilute in 5% dextrose to a concentration of 1 mg/ml and infuse over 1 to 2 hours (see Chapter 20). Liposome-encapsulated amphotericin (AmBisome, Gilead Sciences) is a more expensive alternative.
Prevention and Public Health • In endemic regions, avoid sand flies, especially at
• •
night when they feed, and use insecticides as premise sprays and topical applications to dogs. Deltamethrin collars are highly effective. Permethrin spray is also effective. Screen potential blood donors to prevent iatrogenic transmission. Direct contact with infected dogs is unlikely to pose a risk of human infection; however, dogs serve as a reservoir for infection of sand flies that can transmit infection to people. In highly endemic countries, control of canine infections is key to reducing leishmaniasis in people.
OTHER PROTOZOAL INFECTIONS Other systemic protozoal infections are summarized in Table 21-1.
SUPPLEMENTAL READING Toxoplasmosis Brown RR, Elston TH, Evans L, et al: Feline zoonoses guidelines from the American Association of Feline Practitioners. Compend Contin Educ Pract Vet 25:936–965, 2003.
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Dubey JP: Toxoplasmosis and other coccidial infections. In Sherding RG (ed): The Cat: Diseases and Clinical Management, 2nd ed. New York: Churchill Livingstone, 1994, p 565. Dubey JP, Carpenter JL: Histologically confirmed clinical toxoplasmosis in cats: 100 cases (1952–1990). J Am Vet Med Assoc 203:1556, 1993. Dubey JP, Lappin MR: Toxoplasmosis and neosporosis. In Greene CE (ed): Infectious Diseases of the Dog and Cat, 3rd ed. St. Louis: Elsevier, 2006, pp 749–769. Lappin MR: Protozoal and miscellaneous infections. In Ettinger SJ (ed): Textbook of Veterinary Internal Medicine, 6th ed. St. Louis: Elsevier, 2005, pp 638–646. Lappin MR, Greene CE, Winston S, et al: Clinical feline toxoplasmosis: Serologic diagnosis and therapeutic management of 15 cases. J Vet Intern Med 3:139, 1989.
Neosporosis Lappin MR: Protozoal and miscellaneous infections. In Ettinger SJ (ed): Textbook of Veterinary Internal Medicine, 6th ed. St. Louis: Elsevier, 2005, pp 638–646. Lindsay DS, Dubey JP, McAllister M: Neospora caninum and the potential for parasite transmission. Compend Contin Educ Pract 21:317–321, 1999.
Leishmaniasis Ciaramella P, Corona M: Canine leishmaniasis: Clinical and diagnostic aspects. Compend Contin Educ Pract 25:358–369, 2003. Ciaramella P, Corona M: Canine leishmaniasis: Therapeutic aspects. Compend Contin Educ Pract 25:370–375, 2003. Rosypal AC, Zajac AM, Lindsay DS: Canine visceral leishmaniasis and its emergence in the United States. Vet Clin North Am Small Anim Pract 33:921–937, 2003. Schantz PM, Steurer FJ, Duprey, ZH, et al: Autochthonous visceral leishmaniasis in dogs in North America. J Am Vet Med Assoc 226:1316–1322, 2005.
Hepatozoonosis Macintire DK, Vincent-Johnson NA, Kane CW, et al: Treatment of dogs infected with Hepatozoon americanum: 53 cases (1989–1998). J Am Vet Med Assoc 218:77–82, 2001. Vincent-Johnson NA: American canine hepatozoonosis. Vet Clin North Am Small Anim Pract 33:905–920, 2003.
Trypanosomiasis (Chagas Disease) Meurs KM, Anthony MA, Slater M, Miller MW: Chronic Trypanosoma cruzi infection in dogs: 11 cases (1987–1996). J Am Vet Med Assoc 213:497, 1998.
Other Protozoa Lappin MR: Protozoal and miscellaneous infections. In Ettinger SJ (ed): Textbook of Veterinary Internal Medicine, 6th ed. St. Louis: Elsevier, 2005, pp 638–646.
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▼
Section
Chapter
▼
3
22
Hematology/Oncology Janet L. Peterson
Erythrocytes, Leukocytes, and Platelets Rose E. Raskin
splenomegaly, and hepatomegaly from extravascular hemolysis or extramedullary hematopoiesis and discolored urine from the effects of hemoglobin or excess bilirubin excreted.
ERYTHROCYTE DISORDERS Anemia: Overview Anemia is characterized by a reduction in the overall erythrocyte content, number of erythrocytes, or hemoglobin concentration. It is one of the most frequent hematologic abnormalities encountered in practice. Anemia is not a disease but rather the reflection of a disease state. Causes of anemia may be divided into three general categories: blood loss, hemolysis, and decreased erythrocyte production. ▼ Key Point Determine the cause of the anemia before giving supportive treatment.
Clinical Signs
• Primary signs of anemia relate to the reduction in
•
•
oxygen-carrying capacity of the blood. The patient may present with lethargy, weakness, anorexia, heart murmur, tachypnea, and pale mucous membranes. Occasionally, the animal may appear normal, but routine blood evaluation before an elective surgical procedure may uncover the abnormality. Sedentary animals, especially cats, often have moderate anemia that goes unnoticed for long periods. Secondary signs of anemia often relate to the effects of increased blood cell destruction, such as icterus,
Principles of Diagnosis Several tests can be used to document and characterize the anemia morphologically or etiologically.
History and Physical Examination Use the history and physical examination to determine the following:
• • • •
Occurrence of trauma or surgery Drug, chemical, or toxin exposure Underlying infectious, parasitic, or neoplastic disease Duration of disease, sites of blood loss, and presence of organomegaly
Complete Blood Count (Table 22-1)
• Packed cell volume (PCV) is the most accepted and least expensive method of documenting anemia. Spin microhematocrit tubes 5 minutes at a rate of 12,000 to 15,000 ¥g and measure the proportion of the concentrated cell population of the total plasma volume. Evaluate the plasma color after centrifugation. Alternatively, the hematocrit (Hct) can be calculated by multiplying the number of the erythrocytes in mil231
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Table 22-1. HEMATOLOGY REFERENCE RANGES FOR DOGS AND CATS* Parameter
Canine
Feline
PCV or Hct (%) Hemoglobin (g/dl) RBCs (¥106/ml) MCV (fl) MCHC (g/dl) Reticulocytes (¥103/ml) Platelets (¥103/ml) WBCs (¥103/ml) Segmented neutrophils (¥103/ml) Band neutrophils (/ml) Lymphocytes (/ml) Monocytes (/ml) Eosinophils (/ml) Basophils (/ml) Plasma protein (g/dl) Fibrinogen (mg/dl)
37–55 12–18 5.5–8.5 60–75 32–36 75%; FDP < 5 mg/ml; D-dimer < 250 ng/ml.
• Prothrombin time (PT) detects deficiencies in extrinsic • • •
and common pathways. Fibrinogen concentration (mg/dl) is a quantitative measure of plasma fibrinogen. Thrombin clotting time (TCT) detects both deficiency and dysfunction of fibrinogen. Based on the pattern of abnormalities detected in coagulation screening assays, individual clotting factor analyses identify specific single or multiple coagulation factor deficiencies.
platelet count do not detect abnormal vWF. Three subtypes of vWD occur in dogs: Type 1 vWD is a mild to moderate form characterized by low vWF concentration and normal vWF structure. Type 2 vWD causes a severe bleeding diathesis, with low vWF concentration and abnormal structure. Type 3 vWD is a severe form caused by a complete lack of vWF.
• Measurement of vWF antigen is a specific measurement of plasma vWF concentration.
• Patients with vWF below the normal range (estab-
Specific von Willebrand Factor Assays Specific tests must be performed to establish diagnosis of vWD. Clotting time tests, coagulation assays, and
•
lished at each testing laboratory) are considered at risk for carrying and/or expressing the vWD trait. In addition to low or absent plasma vWF, affected individuals have prolonged in vivo bleeding time.
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Diagnosis of Disseminated Intravascular Coagulation
Transfusion Therapy
Definitive diagnosis of DIC cannot be based on one diagnostic test but depends on a combination of clinical signs and laboratory abnormalities. The DIC process is dynamic, and an early thrombotic or pro-coagulant phase may be followed by later signs of hemorrhage. Serial evaluations are useful to monitor response to therapy and determine prognosis.
Transfusion therapy to supply active factors is required for patients with severe, inherited coagulation factor deficiencies and severe vWD and for patients with acquired disorders that are not responsive to correction of an underlying disease process. Table 23-6 lists blood product(s) and dosages for treating specific coagulation disorders (see Chapter 22 for a description of crossmatching protocol).
• The presence of high plasma concentration of
•
fibrin or fibrinogen degradation products or of crosslinked fibrin fragments (D-dimer) is compatible with ongoing systemic fibrinolysis usually caused by DIC. Additional laboratory criteria of DIC include the following: • Falling platelet count • Low antithrombin activity • Low or high fibrinogen • Prolongation of coagulation screening assays (aPTT, PT, TCT) • Presence of schistocytes on stained peripheral blood smears • Elevated values of plasma-soluble fibrin monomer and thrombin-antithrombin complex are believed to be sensitive tests of DIC; however, these assays are not readily available in clinical human or veterinary practice
• Transfusion of whole blood, administered within 4 to
TREATMENT
•
▼ Key Point Successful management of patients with coagulation disorders requires establishing an accurate diagnosis and then administering appropriate transfusion and non-transfusion support. Pretreatment samples are invaluable for establishing definitive diagnosis early in the course of disease.
•
•
6 hours of collection, supplies active coagulation factors and vWF, as well as red blood cells (RBCs). Transfusion of plasma products (fresh plasma, fresh frozen plasma, plasma concentrate), rather than whole blood, reduces the risk of immunologic transfusion reactions, most importantly RBC sensitization. Plasma components also can be transfused preoperatively and repeatedly in 1 day without causing volume overload. Stored whole blood and packed red cells do not contain replacement levels of coagulation factors or vWF, but the administration of red cells is indicated for patients with signs of acute or chronic blood loss anemia. Packed cells, in combination with an appropriate plasma product, are the therapeutic equivalent of fresh whole blood. The use of blood components, rather than fresh whole blood, provides a more convenient, rapid, and often safer means of transfusion support. Do not routinely pretreat with antihistamine or corticosteroid before transfusion of any blood product. Acute immune reactions directed against RBCs can be prevented in cats by using donors that are blood type and cross-match compatible with the recipient. Anti-RBC reactions are prevented in dogs by using type-compatible or “universal donor”–type dogs. Dogs negative for dog erythrocyte antigen (DEA) 1 (1.1 and 1.2) and negative for DEA 7 are unlikely to
Table 23-6. GUIDELINES FOR TRANSFUSION* Product
Volume †
Fresh whole blood Packed red cells Fresh plasma† Fresh frozen plasma‡ Plasma cryoprecipitate§ Cryosupernatant
*
§
Frequency
12–20 ml/kg 6–10 ml/kg 6–12 ml/kg
q24h q12–24h q8–12h
1 U¶/10 kg
q4–12h (as needed)
6–12 ml/kg
q8–12h
Indications Signs of anemia accompanying coagulation factor deficiencies, von Willebrand disease, disseminated intravascular coagulation Coagulation factor deficiencies, von Willebrand disease, hemorrhagic disseminated intravascular coagulation Hemophilia A (factor VIII deficiency), fibrinogen deficiency, von Willebrand disease Hemophilia B (factor IX deficiency); Factor VII, X, and XI deficiency; vitamin K deficiency
Transfuse at a rate of 1–2 ml/min for cats and puppies, 3–6 ml/min for adult dogs. Collected in citrate anticoagulant, transfused within 4–6 hours of collection. ‡ Frozen within 4–6 hours of collection, stored below -20∞C. § Supernatant remaining after thawing fresh frozen plasma for separation of cryoprecipitate. ¶ 1 unit = cryoprecipitate produced from 200 ml of fresh frozen plasma. †
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•
sensitize recipients and can be considered universal donors. Cross-species transfusions of any blood product are contraindicated because fatal anaphylaxis can result.
• Give transfusions for patients with severe anemia, •
Nursing Care
•
Nursing care practices that reduce hemorrhage include the following:
•
• • • •
Confinement to limit activity Feeding soft food Avoidance of neck leads and intramuscular injections Use of peripheral veins for sampling or intravenous catheter placement
Do not give platelet inhibitory drugs, including sulfas and nonsteroidal anti-inflammatory agents.
• •
Drug Therapy Vitamin K Therapy Vitamin K therapy improves hemostasis only in vitamin K-deficient patients. It often is initiated pending test results, but maintenance of vitamin K therapy is not indicated when diagnosis of inherited factor deficiency, non-obstructive liver disease, vWD, or DIC is made. Anticoagulant rodenticide toxicities are the most common cause of vitamin K deficiency in dogs and cats. Vitamin K reverses the anticoagulant effect of rodenticides over a period of 24 to 48 hours from initiation of therapy.
the preferred parenteral route of administration because intravenous vitamin K can cause anaphylaxis, and hematomas may form at intramuscular injection sites. Vitamin K3 (Synkayvite) is not effective for treating rodenticide toxicity because of its delayed onset of action.
Hormonal Therapy Endocrine imbalance (hypercortisolism or hypocortisolism, hypothyroidism, and hyperestrogenism) can impair hemostasis and complicate the management of acquired or hereditary platelet and coagulation disorders. Diagnosis and correction of the endocrinopathy can prevent or minimize transfusion requirements.
Thyroxin Thyroid insufficiency (see Chapter 31) is common in many breeds with the vWD trait, including Doberman pinscher, Bernese mountain dog, golden retriever, and standard poodle.
• Treat hypothyroid dogs with L-thyroxine at a standard replacement dosage of 0.02 mg/kg PO q12–24h, with post-pill monitoring to ensure attainment and maintenance of normal T4 values.
Treatment for Warfarin Toxicity Warfarin is a relatively short-acting poison, and treatment for a total of 1 week usually is adequate. Standard treatment is as follows:
• Administer an initial dose of vitamin K1 (AquaMe• •
phyton, Merck, Sharp, Dohme), 2.2 mg/kg subcutaneously (SC). Follow with a dose of 1.1 mg/kg SC or by mouth (PO), q12h, until active bleeding subsides. Continue therapy with an oral preparation (Mephyton) at the same twice-daily dosage for a total of 1 week.
Desmopressin Acetate Desmopressin acetate (DDAVP, USV Pharmaceutical), a vasopressin analogue, has shown efficacy in transiently improving hemostasis in some dogs affected with type 1 vWD.
• Its activity probably is the result of release of vWF
•
Treatment for Long-acting Rodenticide Toxicity The following steps are taken to treat toxicity from second-generation or long-acting rodenticides (diphacinone, pindone, bromadiolone, and brodifacoum):
pulmonary, or CNS hemorrhage at presentation (see Table 23-6). Initiate parenteral vitamin K1 as for warfarin (2.2 mg/kg SC). Administer vitamin K1 at 1.1 mg/kg SC, q12h, until the hematocrit value stabilizes and active bleeding subsides. Maintain oral vitamin K1 at 1.1 mg/kg PO, q12h, for a total of 2 weeks. Taper the maintenance dose by one-half every 2 weeks during treatment. To prevent relapse, continue therapy for 4 to 6 weeks.
▼ Key Point Subcutaneous injection of vitamin K is
Wound Management Good management reduces the need for transfusion in some patients with coagulation disorders and mucosal or cutaneous hemorrhage. The best treatment, for even small wounds, is usually suture and/or pressure bandages. Application of tissue adhesive (Vetbond, 3M Co.) to focal areas of bleeding also can limit local blood loss.
263
•
from intracellular stores, and its effectiveness depends on the patient’s ability to produce functional vWF protein. Duration of action, after a dose of 1 mg/kg SC, is 3 to 4 hours; repeated dosage within 24 hours does not prolong response time. The onset of action is 15 to 30 minutes. Desmopressin is often given as preoperative prophylaxis to dogs with mild to moderate type 1 vWD.
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Plasma products should be available in case the patient does not respond.
Heparin Therapy
• Unfractionated heparin therapy (100–300 U/kg SC
•
•
q6–8h) is often used to manage thrombotic DIC and other acute thrombotic syndromes. Because of extensive protein and cell binding, unfractionated heparin (UFH) anticoagulant effect varies widely among patients and requires close monitoring to prevent overdosage and iatrogenic bleeding. Prolongation of aPTT to approximately 1.5 to 2 times the patient’s baseline or the assay’s mean value is a common therapeutic target. Low molecular weight heparins are newer anticoagulant drugs with a more predictable pharmacologic profile than UFH. Safe and effective dosage guidelines have not yet been developed for dogs and cats. The target therapeutic range for high-dose anticoagulant effect in human patients is 0.5 to 1.0 Units of anti-Xa activity per milliliter. Transfusion therapy with fresh blood or blood products to replace active coagulation factors, fibrinogen, and platelets is more likely than heparin therapy to benefit patients presenting with severe hemorrhage in association with DIC.
▼ Key Point The critical factor for successfully managing all patients with DIC is identification and correction of the underlying disorder.
SUPPLEMENTAL READING Dodds WJ: Bleeding disorders. In Morgan RV (ed): Handbook of Small Animal Practice. New York: Churchill Livingstone, 1988, pp 773–785. Madewell BR: Sample preparation for the laboratory. In Kirk RW (ed): Current Veterinary Therapy X. Philadelphia: WB Saunders, 1989, pp 410–419. Forsythe LT, Willis SE: Evaluating oral mucosa bleeding times in healthy dogs using a spring-loaded device. Can Vet J 30:344, 1989. Kristensen AT, Feldman BF: General principles of small animal blood component administration. In Feldman BF, Kristensen AT (eds): Veterinary Clinics of North America: Canine and Feline Transfusion Medicine. Philadelphia: WB Saunders, 1995, pp 1277–1290. Wardrop KJ: Medical indications for plasma therapy. Proceedings of the American College of Veterinary Internal Medicine, 14th Annual Forum 1996, pp 31–33. Brooks MB: Von Willebrand Disease. In Feldman BF, Zinkl JG, Jain NC. (eds): Schalm’s Veterinary Hematology, 5th ed. Philadelphia: Lippincott Williams & Wilkins, 2000.
Chapter
▼
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24
Systemic Immune-Mediated Diseases Michael Stone
Immune-mediated diseases may affect multiple body systems; for example, polyarthritis may be associated with thrombocytopenia or proteinuria. A CBC, platelet count, chemical profile and urinalysis are considered the minimum database for any suspected immunemediated disease. The diagnosis of “idiopathic immunemediated disease” remains a diagnosis of exclusion. Infectious/parasitic, neoplastic, and toxic causes must always be excluded with appropriate testing and/or therapeutic trials. Since many immune-mediated diseases are treated similarly, this chapter begins with a general discussion of treatment and commonly used drugs. This is followed by a discussion of immune-mediated hemolytic anemia, immune-mediated thrombocytopenia, and systemic lupus erythematosus.
TREATMENT OF IMMUNE-MEDIATED DISEASES
▼ Key Point Some cats do not effectively respond to prednisone. These cats may be “poor converters” that cannot metabolize inactive prednisone to the active form, prednisolone. Thus, when cats don’t respond well to prednisone, try using an alternate steroid (see Table 24-1).
• Corticosteroids are generally administered at full doses until the disease is in complete remission. Complete remission may be defined as resolution of signs of disease along with radiographic or laboratory changes that were initially present. After remission is attained the dose is cut, generally in half, for 4 weeks. Reevaluation is then performed, and if signs of disease are absent (on physical or laboratory data), the dose is again halved. This protocol is followed monthly until the animal either relapses or stops medication. ▼ Key Point The minimum duration of therapy for any immune-mediated disease is 6 months.
Corticosteroids Corticosteroids are effective immunosuppressive agents. Many animals tolerate their administration with only mild side effects, or the disease goes into remission and the corticosteroid treatment may be stopped. For many animals with immune-mediated disease, single agent therapy with corticosteroids is adequate.
• Prednisone is always included initially in immunosuppressive protocols. The dosage is approximately 2.2 mg/kg once daily in most cases; however 1 mg/kg/day may be used in less severe diseases. The dose may be divided into twice daily administration, but there is no obvious benefit from the division. Some dogs are intolerant to prednisone and will develop side effects (polyuria, polydipsia, polyphagia, panting, and/or lethargy) that are unacceptable to the owner. ▼ Key Point Therapy with an equipotent dose of a different steroid (prednisolone, methylprednisolone, triamcinolone, or dexamethasone) often resolves unacceptable side effects of prednisone (Table 24-1).
• Many patients will experience a relapse as the dose is tapered. Relapse is treated with return to full dose administration, again with monthly tapering, but as the dose is approached that previously allowed relapse, the dosage may then either be held constant or tapered more slowly. If signs of relapse are mild, the dose may instead be increased to the most recently effective dose and held there for a few months before it is tapered again.
Combination Immunosuppression Therapy Combination immunosuppression therapy is very useful, because the addition of another agent may allow a lower dose of corticosteroid to be used (prednisonesparing effect). Additional medications may also increase the strength of immunosuppression because they work by different mechanisms. The drug most frequently used in combination with corticosteroids in dogs is azathioprine. ▼ Key Point Combination immunosuppressive therapy is often more effective and has less side effects than prednisone therapy alone. 265
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Table 24-1. INITIAL IMMUNOSUPPRESSIVE DOSES OF CORTICOSTEROID AND THEIR AVAILABLE STRENGTHS IN THE UNITED STATES Available Oral Strengths Prednisone Prednisolone Methylprednisolone Triamcinolone Dexamethasone
1, 2.5, 5, 10, 20, 50 mg tablets; 5 mg/5 ml syrup 5, 20 mg tablets; 15 mg/5 ml syrup 2, 4, 8, 16, 24, 32 mg tablets 4, 8 mg tablets 0.25, 0.5, 0.75, 1, 1.5, 4, 6 mg tablets
Azathioprine
•
•
•
Initial Canine Dose (Oral)
10 mg/day
2.2 mg/kg/day
10 mg/day
2.2 mg/kg/day
8 mg/day
2.2 mg/kg/day
2–4 mg/day 1–2 mg/day
0.4 mg/kg/day 0.2 mg/kg/day
not recommended. Instead, the use of chlorambucil is recommended for cats that require immunosuppression in addition to prednisolone.
• Azathioprine (Imuran) is administered orally. Adverse side effects are infrequent in dogs. The dose is approximately 2.2 mg/kg once daily until remission occurs, then the same dose is administered every other day. A potential side effect is bone marrow suppression, and a complete blood count (CBC) should be evaluated after 7 days, and then every 2 weeks while the patient is receiving daily treatment. Once the patient is receiving every other day therapy, a CBC should be evaluated every 3 months, but bone marrow suppression is unusual at this dose. Prednisone and azathioprine are frequently used in combination. The drugs are administered together once daily and then tapered after remission is attained. The method of tapering is somewhat arbitrary; if signs of prednisone intolerance are experienced then the prednisone is tapered first; if bone marrow disease is encountered the azathioprine should be tapered or discontinued first. If the disease was difficult to get into remission then only one drug should be tapered at a time; if the disease easily went into remission, then both drugs may be tapered concurrently. Tapering should be performed every 4 weeks, with the minimum duration of therapy being 6 months. It is important to have a therapeutic plan to follow. Notations in the medical record should include the intended date of recheck, with the tests to be performed and the expected decrease of dose if tests return results within normal limits. Relapse is treated with the administration of full dosage of both medications with gradual taper to the lowest effective dose. As the dose that allowed relapse is approached, the dosage may then either be held constant or tapered more slowly. Cats often develop life-threatening neutropenia with the use of azathioprine, and its use in this species is
Initial Feline Dose (Oral)
Chlorambucil
• Chlorambucil (Leukeran) is an oral drug, used in •
•
cats at 15 mg/m2 (4 mg total dose for most cats) once daily for 4 days, repeated every 3 weeks. Potential side effects include anorexia and bone marrow suppression. A CBC should be evaluated 5 to 7 days after the last dose. If after two or more evaluations the CBC remains normal (no leukopenia), further monitoring may not be necessary. If leukopenia is detected (absolute neutrophil count < 3,000/ml), the dose of the next administration should be decreased by 25%. Signs of infection (loss of appetite along with fever) during the expected white blood cell count (WBC) nadir (3–10 days after administration) should be aggressively treated. Physical examination, CBC, and treatment with amoxicillin and enrofloxacin are indicated if severe neutropenia (22% and bilirubin 3 mg/dl): treatment with intravenous fluids, heparin, prednisone or dexamethasone, and azathioprine is indicated. More aggressive therapy may be considered: intravenous human immunoglob-
•
ulin (0.5g/kg IV once daily for 3 days), cyclosporine (Sandimmune 10 mg/kg IV or PO twice daily; Neoral or Atopica 5 mg/kg PO twice daily), or methylprednisolone sodium succinate pulse therapy (11 mg/kg IV once daily for 3 days). Monitor blood counts daily until stabilization occurs, then at least weekly until the PCV is >25%. Full doses of immunosuppressive medications are administered until the hematocrit normalizes, and then they are tapered as discussed in the Treatment section. It is not necessary to normalize the hematocrit to eliminate clinical signs of disease, and in some cases it may be preferable to allow a low grade of anemia to persist in order to decrease medications to tolerable levels. The minimum length of treatment is 6 months.
Prognosis ▼ Key Point Mild IMHA may respond well to treatment, whereas rapidly progressive cases are associated with a high rate of mortality.
The prognosis is guarded to fair for mild cases and very guarded for aggressively hemolytic cases. Many patients are able to taper completely off medications, however, relapses occur unpredictably. Relapses may be associated with immune stimulation due to vaccination, infection, or stress, and avoidance of these causes may be prudent. Monitoring for control, recurrence, and infection should be performed at least 3 to 4 times per year for the life of the patient.
IMMUNE-MEDIATED THROMBOCYTOPENIA Immune-mediated thrombocytopenia (IMT) is usually suspected when cutaneous petechiae or bleeding from mucosal surfaces are discovered in an otherwise healthy-appearing animal. Severe thrombocytopenia associated with other causes is more often associated with overt clinical illness.
Etiology A specific cause of IMT is not known. Many other causes of thrombocytopenia exist (Table 24-4) that must be differentiated from IMT; these are usually associated with less severe thrombocytopenia (>25,000/ml). Any drug the patient is receiving must be considered as a potential cause of hapten-mediated thrombocytopenia and stopped, if possible.
Clinical Signs • Epistaxis, oral cavity hemorrhage, cutaneous petechiation or ecchymoses, hematuria, hematochezia and/or melena are common presenting complaints. Hematomas, hemothorax, hemoperitoneum and
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hyperactivity of the mononuclear-phagocytic cell system). • Bone marrow evaluation is not routinely necessary, but may reveal increased or decreased megakaryocytes and mild plasmacytosis. Tests for detection of antiplatelet antibodies are not necessary in most cases.
Table 24-4. CAUSES OF THROMBOCYTOPENIA IN THE DOG AND CAT Sequestration in spleen (splenic neoplasia, torsion, hematoma, thrombosis/infarction) Drugs (cytotoxic, antibiotics, estrogen, nonsteroidal antiinflammatory drugs, albendazole, griseofulvin, propylthiouracil, ketoconazole, others) Neoplasia (hematopoietic, histiocytic, hemangiosarcoma) Infectious agents (Ehrlichia canis, E. ewingii, E. chafeensis, Anaplasma phagocytophila, A. platys, Rickettsia rickettsii, parvovirus, distemper, feline leukemia virus, feline immunodeficiency virus, cytauxzoonsis, systemic mycoses, leptospirosis, Babesia canis, B. gibsoni, sepsis, endotoxemia) Bone marrow disease (myelofibrosis, myelodysplasia, necrosis, myelophthesis) Recent vaccination Vasculitis Disseminated intravascular coagulation/systemic thrombosis (thoracic, abdominal, peripheral) Hemolytic uremic syndrome Severe hemorrhage (anticoagulant rodenticide, trauma) Idiopathic, immune-mediated thrombocytopenia
Concurrent Diseases IMT may coexist with other immune-mediated diseases. Anemia may be caused by blood loss or concurrent IMHA. The presence of spherocytosis, or severe anemia in the face of normal blood protein levels, is suggestive of concurrent IMHA (see Figure 24-1).
Treatment • Most cases of IMT respond to immunosuppressive •
•
hemarthroses are more commonly associated with anticoagulant poisonings or hemophilia. Physical examination may reveal pale gums, splenomegaly, and cutaneous, mucosal, or ocular hemorrhages. Fever is occasionally present. Fundic examination may reveal retinal hemorrhages. Rectal examination may reveal melena or hematochezia.
Diagnosis • The presence of severe thrombocytopenia (11.0 mg/dl (2.75 mmol/L) Serum ionized calcium concentration • Dogs: >5.8 mg/dl (1.45 mmol/L) • Cats: >5.6 mg/dl (1.40 mmol/L) Young dogs may have a mild hypercalcemia (usually 18 mg/dl.
Etiology Hypercalcemia may be parathyroid-dependent (primary hyperparathyroidism) or parathyroid-independent (normal functioning of the parathyroid gland).
• In parathyroid-independent hypercalcemia, elevated
•
ionized calcium concentration causes suppression of PTH production. On analysis, ionized calcium concentration is elevated, and PTH concentration is in the lower part of or below the reference range. PTHrP concentration may be elevated if there is a tumor producing PTHrP. Concentration of 25hydroxyvitamin D3 may be elevated in cases of vitamin D toxicity. Parathyroid-dependent hypercalcemia (primary hyperparathyroidism) is characterized by elevated ionized calcium concentration without the appropri-
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ate suppression of PTH production due to a PTHsecreting tumor of the parathyroid gland.
• Anorexia, vomiting, and constipation can result from
See Table 32-3 for a list of hypercalcemia-related conditions.
•
Clinical Signs
•
Clinical signs in hypercalcemia depend on the magnitude of the calcium elevation, how quickly the hypercalcemia developed, and the duration of the hypercalcemia. Serum total calcium concentrations of 4.5 mmol/L) are often associated with severe life-threatening signs. Soft tissue mineralization may occur with prolonged hypercalcemia when the product of total calcium (mg/dl) times serum phosphorus (mg/dl) equals 70 or greater.
•
• Polydipsia and polyuria are the most common signs of hypercalcemia in dogs due to direct stimulation of the thirst center and a decreased ability of the kidneys to concentrate urine.
Table 32-3. CONDITIONS ASSOCIATED WITH HYPERCALCEMIA Nonpathologic Conditions Hyperlipemia Non-fasted serum samples Young growing dogs Laboratory error or improper handling of sample Transient Conditions Hemoconcentration Hyperproteinemia Pathologic Conditions Parathyroid-dependent hypercalcemia Primary hyperparathyroidism Parathyroid-independent hypercalcemia Malignancy-associated hypercalcemia Lymphoma Adenocarcinoma of the apocrine glands of the anal sac Multiple myeloma Metastatic bone tumors Miscellaneous tumors (lymphocytic leukemia, mammary carcinoma, fibrosarcoma, pancreatic adenocarcinoma, testicular interstitial cell tumor, lung carcinoma, squamous cell carcinoma, thyroid adenocarcinoma, osteosarcoma) Hypoadrenocorticism Renal failure Hypervitaminosis D Cholecalciferol (rodenticide) toxicity Dovonex ingestion Iatrogenic due to dietary supplementation Houseplants (Cestrum diurnum, Solanum malacoxylon, Trisetum flavescens) Granulomatous disease (blastomycosis, schistosomiasis) Grape toxicity Bone lesions (sepsis, disuse osteoporosis) Severe hypothermia Idiopathic hypercalcemia in cats
decreased excitability of gastrointestinal smooth muscle. Generalized weakness may develop from decreased muscle excitability. Depression, muscle twitching, and seizures can occur as neurologic manifestations. Cardiac arrhythmias can develop from direct effects on the myocardium or secondary to cardiac mineralization.
▼ Key Point Polydipsia and polyuria are the most common clinical signs of hypercalcemia.
Diagnosis Abnormalities depend on the underlying cause, severity, and duration of hypercalcemia (see later under “Conditions Associated with Hypercalcemia”).
History and Physical Examination
• A complete history and thorough physical examination are essential for diagnosing the cause of hypercalcemia. Obtain dietary history to assess the possibility of over-supplementation or under-supplementation with vitamin D.
Laboratory Tests
• Perform a complete blood count (CBC) and serum chemistry profile, and consider tests such as serum ionized calcium, PTH, 25-hydroxyvitamin D, and PTHrP concentrations. Collect samples for diagnostic testing prior to treatment.
Radiography and Ultrasound
• Soft tissue mineralization of the kidneys, heart, lungs stomach, and other tissues may be detected.
• Abdominal masses, mediastinal masses, pulmonary lesions suggestive of metastasis, or lymph node enlargement especially in the tracheobronchial region may be visualized.
Electrocardiography
• Prolongation of the PR interval, shortening of the QT interval, and cardiac arrhythmias (ventricular fibrillation) may develop with severe hypercalcemia.
Principles of Treating Hypercalcemia ▼ Key Point The definitive treatment for hypercalcemia is to remove the underlying cause.
Unfortunately, the etiology may not be apparent, and supportive measures must be taken to decrease the serum calcium concentration (see Table 32-4 for specific drugs and dosage recommendations). Supportive measures may include the following.
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Table 32-4. TREATMENT OF HYPERCALCEMIA Treatment
Dose
Indications
Comments
Volume Expansion SQ saline (0.9%)
75–100 ml/kg/day
Mild hypercalcemia
IV saline (0.9%)
100–125 ml/kg/day
Moderate to severe hypercalcemia
Contraindicated if peripheral edema is present Contraindicated in congestive heart failure and hypertension
Diuretics Furosemide
2–4 mg/kg q8–12h IV, SC, PO
Moderate to severe hypercalcemia
Volume expansion is necessary prior to use of this drug
Glucocorticoids Prednisone Dexamethasone
1–2.2 mg/kg q12h PO, SC, IV 0.1–0.22 mg/kg q12h IV, SC
Moderate to severe hypercalcemia
Use of these drugs prior to identification of etiology may make definitive diagnosis difficult
Inhibition of Bone Resorption Calcitonin
4–6 IU/kg q8–12h SC
Hypervitaminosis D toxicity
Response may be short lived; vomiting may occur
Bisphosphonates Etidronate (EHDP)
5–15 mg/kg daily to q12h
Moderate to severe hypercalcemia
Expensive; use in dogs limited
Clodronate
20–25 mg/kg in 4-hr IV infusion
Pamidronate
1.3 to 2.0 mg/kg in 150-ml 0.9% saline in 2-hr IV infusion; can repeat in 1–3 wks
Approved in Europe; availability in U.S. limited
EHDP, ethane-1-hydroxy-1,1-diphosphonate.
Volume Expansion
Glucocorticoids
Volume expansion with IV 0.9% NaCl solution decreases hemoconcentration and encourages renal calcium loss by improving glomerular filtration rate and sodium excretion, resulting in less calcium resorption.
• Glucocorticoids decrease bone resorption of calcium,
Loop Diuretics
•
• Diuretics such as furosemide increase calcium excre-
•
tion; however, high doses may be needed. Diuretic use in a dehydrated patient is contraindicated because volume contraction and further hemoconcentration may worsen the hypercalcemia. Thiazide diuretics, which decrease calcium excretion by the kidneys, are contraindicated.
decrease intestinal calcium absorption, and increase renal calcium excretion. These effects are nonspecific and lead to a mild decrease in the magnitude of hypercalcemia. Glucocorticoids often cause a substantial decrease in serum calcium concentration when hypercalcemia is secondary to lymphoma, myeloma, hypervitaminosis D, or hypoadrenocorticism.
▼ Key Point The use of glucocorticoids prior to determination of the etiology of hypercalcemia may make definitive diagnosis difficult, especially for lymphoma and myeloma.
Sodium Bicarbonate Sodium bicarbonate given as an IV bolus or as a continuous infusion has been shown to decrease serum total and ionized calcium concentration. Although the magnitude of calcium reduction is mild, alkalosis favors the binding of ionized calcium to protein, resulting in a decrease in ionized calcium. Sodium bicarbonate therapy is more beneficial when combined with other treatments and is reserved for life-threatening situations.
Calcitonin Calcitonin can be useful during treatment of cholecalciferol toxicity. For calcitonin to decrease serum calcium, multiple injections per day are required. Long-term side effects include anorexia and vomiting, and diminished effectiveness of calcitonin treatment may occur over time. Use calcitonin only when other treatments have not adequately lowered serum calcium.
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Bisphosphonates (Diphosphonates)
▼ Key Point A normal (or negative) concentration
These compounds inhibit osteoclastic bone resorption.
of PTHrP does not rule out the presence of a malignancy.
• Etidronate (Didronel, Norwich Eaton) has been used •
•
with some success as an oral agent for long-term control of hypercalcemia, but it is not well absorbed. Intermittent IV injections of pamidronate (Aredia, Novartis) are effective for the control of vitamin D toxicity, hyperparathyroidism, and malignancy-associated hypercalcemia. Clodronate is an alternative. Since bisphosphonates have nephrotoxic potential, use these after rehydration. Use IV fluids during and for several hours after treatment with bisphosphonates.
Lymphoma
• Lymphoma is the most common tumor associated
•
Mithramycin This drug is a potent inhibitor of osteoclastic bone resorption; however, mithramycin has been associated with many serious side effects, such as thrombocytopenia, hepatic necrosis, renal necrosis, and hypocalcemia, and is no longer recommended.
•
Peritoneal Dialysis Using a calcium-free dialysate, this procedure can be considered as a last resort when other methods fail to decrease serum calcium concentration.
with hypercalcemia in the dog. Of dogs with lymphoma, 10% to 40% have concurrent hypercalcemia, and a large number of these have mediastinal lymphoma. Although lymphadenopathy is usually detected, hypercalcemia may be the first abnormality noted. A thorough physical examination, together with thoracic and abdominal radiography, abdominal ultrasonography, multiple lymph node aspirates or biopsies, and multiple bone marrow aspirates or core biopsies, may be necessary to confirm a diagnosis of lymphoma. Treatment with corticosteroids decreases serum calcium concentration; however, their lympholytic effect makes subsequent identification of lymphoma very difficult. The return of hypercalcemia may precede clinical evidence of tumor regrowth in animals undergoing chemotherapy. Treatment of lymphoma is discussed in Chapter 27.
▼ Key Point Lymphoma is the most common tumor
CONDITIONS ASSOCIATED WITH HYPERCALCEMIA For a complete list of conditions associated with hypercalcemia, see Table 32-3.
associated with hypercalcemia in the dog.
Apocrine Gland Adenocarcinoma of the Anal Sac
• This tumor usually occurs in older female dogs, with
Hypercalcemia Associated with Malignancy ▼ Key Point Malignancy-associated hypercalcemia is the most common cause of persistent hypercalcemia in dogs and the third most common cause in cats.
Hypercalcemia primarily results from increased osteoclastic bone resorption and increased renal tubular resorption. Rarely, increased intestinal absorption also may play a role. Factors that may be produced by tumors and result in humoral hypercalcemia of malignancy include PTH, PTHrP, transforming growth factor, calcitriol, prostaglandin E2, osteoclast-activating factor, and other cytokines (interleukin-1, interleukin2, and gamma interferon).
• In dogs, lymphoma, adenocarcinoma of the apocrine •
glands of the anal sac, and multiple myeloma are the most common tumors associated with hypercalcemia. In cats, lymphoma, and squamous cell carcinoma each account for one-third of the cases of malignancy-associated hypercalcemia.
•
hypercalcemia developing in approximately 50% of cases. Humoral mechanisms are typically responsible for hypercalcemia, as PTHrP has been identified from tumor tissue in dogs. The tumor is usually malignant and has metastasized to regional lymph nodes by the time of diagnosis. Surgical resection is associated with reduction of serum calcium. Failure to remove all of the tumor or recurrence of the tumor usually results in the return of hypercalcemia. Despite surgical excision, radiation, and various chemotherapy protocols, the tumor usually recurs, and reported survival times range from 2 to 21 months.
Multiple Myeloma
• Multiple myeloma in dogs has been associated with
•
hypercalcemia in 10% to 15% of cases. Humoral factors as well as direct lysis of bone may account for the increased serum calcium. Long-term survival has been reported following treatment of multiple myeloma with chemotherapy, but associated hypercalcemia, light-chain proteinuria, and extensive bony lesions are associated with a shorter survival time.
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Hypoadrenocorticism • Approximately 30% of dogs with hypoadrenocorti-
•
•
cism (Addison’s disease) have mild to moderate hypercalcemia (total calcium concentration 85%) but moderate sensitivity (500/ml is consid-
• Give special attention to any history of trauma or prior abdominal surgery.
• Determine if the animal recently ate any foreign •
•
bodies that could have caused bowel perforation. Determine if the animal has had any signs of gastric or colonic ulceration. A history of hematemesis, melena, or hematochezia is indicative of a more serious lesion of the GI tract and increases the suspicion of perforation. Determine if the signalment and history are typical of pancreatitis.
Physical Examination • Look for the clinical signs listed previously. • Carefully palpate the abdomen for evidence of pain,
•
fluid, ileus, or masses. Perform a rectal examination to evaluate for evidence of pelvic trauma, prostate or urethral problems, or hematochezia. Evaluate for fever.
•
Hematology
• Neutrophilia may be present with or without toxic
• •
neutrophils. A left shift (an increase in the number of band neutrophils) indicates more significant inflammation. A degenerative left shift (more bands than segmented neutrophils) indicates an overwhelming, life-threatening inflammatory process. Chronic blood loss or chronic infection may result in anemia. Hypoproteinemia due to loss or sequestration of albumin is very common in peritonitis.
Serum Chemistry Profile
Diagnostic Tests
• Many parameters may be altered, depending on the
Fluid Analysis Abdominocentesis
• Electrolytes (sodium, potassium, and chloride) may
See Chapter 3 for a description of the technique for abdominocentesis.
• Animals with peritonitis will have many neutrophils
•
•
(>500/ml) and may have bacteria on cytologic examination. Absence of bacteria suggests a sterile peritonitis, such as can occur with chemical peritonitis. The presence of bacteria within phagocytes confirms septic peritonitis. Bacteria within and outside phagocytes suggest that the infection is overwhelming the defense mechanisms. The presence of cocci and rods indicates mixed infection, such as can occur with GI perforation. Gram stain of the fluid can differentiate gram-negative rods (usually aerobes such as Escherichia coli) from gram-positive rods (usually anaerobes such as Clostridium spp.). Large numbers of red blood cells (RBCs) indicate hemorrhage associated with the peritonitis. This can
type of peritonitis and the associated clinical signs.
• •
•
•
be depleted in animals that are vomiting. Acidotic animals may be hyperkalemic. Dehydration can artificially elevate electrolyte concentrations. Hypoglycemia may be present in animals with septic peritonitis. Serum urea nitrogen is elevated in animals with uroperitoneum and in animals suffering from prerenal azotemia due to dehydration or shock. Hyperkalemia may also be seen in animals with uroperitoneum. Serum pancreatic enzymes (amylase, lipase, trypsin) frequently are mildly elevated in all types of peritonitis, and they are moderately to markedly elevated when underlying pancreatitis is the cause of peritonitis. Serum liver enzymes and bilirubin are variably increased in all types of peritonitis and may be markedly increased in sepsis, biliary tract rupture, liver abscess, and pancreatitis.
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Radiography
• In most cases, use lactated Ringer’s solution supple-
Plain Radiography
• Plain abdominal radiography usually reveals a loss of
•
contrast and lack of soft tissue detail either focally or throughout the abdomen. Fluid may be present in the peritoneal cavity. Pneumoperitoneum may be seen if any portion of the GI tract has perforated or there has been penetrating abdominal trauma. Radiographs obtained using horizontal projection can confirm air in the peritoneal space, because it rises to the dorsum of the cavity (see Chapter 4).
Contrast Studies
•
•
Ultrasonography • Ultrasonography can confirm the presence of peri-
•
toneal fluid and can be used to assist in sampling the fluid for analysis. It is especially valuable for evaluating the pancreas as a potential cause of peritonitis. Soft tissue masses or abscesses may be detected (see Chapter 4).
TREATMENT Management of peritonitis consists of supportive care and definitive measures to eliminate or correct the cause. The decision to treat the animal medically or surgically depends on the cause and the animal’s response to treatment. If a surgical disease is not suspected and the peritonitis is mild, medical treatment alone may suffice. However, promptly initiate surgical treatment if the peritonitis is moderate or severe, is not improving with medical treatment, or is due to a surgical lesion such as a perforated intestine or biliary or urinary rupture.
Medical Management Fluids IV fluids are probably the most important supportive treatment. The type of fluids used depends on the type of peritonitis and the metabolic alterations present in the patient.
mented with potassium to prevent or correct hypokalemia. After correcting the dehydration, give fluids at a maintenance rate, plus continuing losses, until the animal is able to maintain hydration with oral intake. (See Chapter 5 for fluid therapy details.)
Antibiotics Systemic antibiotics are indicated in bacterial peritonitis. Choose antibiotics based on culture and sensitivity testing of peritoneal fluid.
• In the absence of culture results, use broad-spectrum
• Perform positive-contrast urethrography, cystography, and/or intravenous (IV) pyelography if uroperitoneum is suspected (see Chapter 4). Perform positive-contrast GI studies to diagnose perforation (see Chapter 4). Avoid using barium as the contrast agent when perforation is suspected, because barium leakage into the peritoneal cavity can be devastating (treat with immediate laparotomy, peritoneal lavage, and drainage). Instead, use a watersoluble, non-ionic, iodinated contrast agent, such as iohexol (Omnipaque).
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•
bactericidal drugs. Results of Gram stain of abdominal fluid (see under “Diagnosis”) can be used to guide antibiotic choice. Combinations of antibiotics may be necessary if a mixed population of bacteria is present. For example, combine ampicillin or one of the cephalosporins (e.g., cefazolin) with enrofloxacin for peritonitis due to a mixed bacterial population. Alternatively, if the animal has normal renal function, combine ampicillin with an aminoglycoside (e.g., amikacin or gentamicin). Other options include penicillins, clindamycin, or metronidazole for anaerobes and other fluoroquinolones for gram-negative rods.
Lavage and Drainage ▼ Key Point One of the most important treatments for peritonitis is drainage of fluid and debris from the peritoneal cavity.
Abdominal drains such as Penrose drains or sump drains (e.g., a fenestrated Brunswick catheter inside a fenestrated Penrose drain) are ineffective for draining the entire peritoneal cavity for any longer than a few hours. However, these types of drains can be effective for the initial drainage of the abdomen or for animals that are producing large amounts of abdominal fluid.
• Open abdominal drainage has been used successfully in experimental and clinical peritonitis and is described under “Surgical Management.” ▼ Key Point Recent
studies have found closed suction drains (e.g., Jackson Pratt drains) to be effective in the treatment of generalized peritonitis (see description under “Surgical Management”).
• Lavage of the peritoneal cavity has been recommended but is controversial. Addition of fluid to the peritoneal cavity may potentiate generalized peritonitis and should only be used when all of the lavage fluid can be drained. Therefore, lavage should be reserved for those patients that undergo surgical treatment of the problem. Lavage consists of copious
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•
•
•
Section 6 / Digestive System
amounts of warm, sterile saline. Continue lavage until the fluid removed from the peritoneal cavity appears clear. Addition of antibiotics or antiseptics to the lavage fluid has not been shown to have any benefit over the use of saline alone in conjunction with systemic antibiotics. Do not use aminoglycosides in peritoneal lavage during anesthesia, especially if systemic neuromuscular blocking agents are being used. Aminoglycosides can potentiate the effect of these agents. Also, aminoglycosides will be absorbed and can reach toxic blood levels if they also are being given parenterally. Avoid using povidone-iodine (Betadine) in lavage fluid in animals with peritonitis, because it can also be absorbed and cause severe toxicity, possibly due to absorption of large amounts of iodine.
Surgical Management Correction of lesions resulting in peritonitis is covered in the appropriate chapters.
Preoperative Considerations
• As discussed under “Medical Management,” correct •
fluid and electrolyte disorders, when possible, before surgery. Begin antibiotic treatment before surgery if contamination is present or is likely to occur during the surgery.
Closed versus Open Peritoneal Drainage A key decision for the surgeon is whether to use closed or open drainage methods for peritonitis. Closed suction drains are reasonably effective for septic peritonitis. Complications with the use of these drains are less than with open drainage. Consider the following factors when deciding which type of peritoneal drainage to use:
• Type and severity of the peritonitis
• • • •
• If the source of the peritonitis can be definitively corrected at surgery, consider choosing closed peritoneal drainage. Ability of the patient to withstand the complications of open drainage Financial considerations (closed drainage patients tend to require less intensive therapy) Hospital facilities and personnel Personality of the patient • Open peritoneal drainage would be very difficult in a fractious animal.
Technique for Closed Peritoneal Drainage 1. After the laparotomy has been performed and the cause of the peritonitis has been corrected, lavage the abdominal cavity with warm, sterile saline. Use copious amounts of saline to flush bacteria and
2.
3. 4. 5. 6. 7.
debris from the cavity. Discontinue flushing when the lavage solution appears clear on removal from the abdomen. Place the drain(s) (e.g., Jackson Pratt drain) either directly adjacent to the source of the peritonitis or along the ventral midline to facilitate drainage of fluid from the entire abdomen. If necessary, use absorbable sutures to tack the omentum to the peritoneum away from the drain to prevent occlusion. Exit the drain from the abdominal cavity through separate stab incisions lateral to the ventral midline abdominal incision. Close the abdominal incision routinely. Frequently empty the drain reservoir, and characterize the type and amount of fluid. Remove the drain when little or no fluid is being recovered and the patient’s other clinical parameters are significantly improved (usually 3–5 days postoperatively).
Technique for Open Peritoneal Drainage 1. After the laparotomy has been performed and the cause of the peritonitis has been corrected, lavage the abdominal cavity with warm, sterile saline. Use copious amounts of saline to flush bacteria and debris from the cavity. Discontinue flushing when the lavage solution appears clear on removal from the abdomen. 2. Partially close the abdominal incision. Place large horizontal mattress or simple continuous sutures of monofilament polypropylene or nylon (1-0 or 2-0) in the linea alba to reduce the incisional gap to approximately 3 to 4 cm in width. Leave the remaining tissue layers open (Fig. 76-1A). 3. Cover the incision with a sterile dressing consisting of (from inside out) sterile petrolatum-impregnated gauze, sterile laparotomy sponges or towels, cotton, conforming gauze, and tape. Make the bandage large enough to extend several centimeters beyond the cranial and caudal aspect of the incision, and construct it so that slippage will not occur. a. Large monofilament polypropylene eyelet sutures can be placed, and umbilical tape “laces” used to hold the laparotomy pads or towels in place (Fig. 76-1B). 4. Change the bandage aseptically two or more times daily, depending on the quantity of fluid drainage. Sedate the patient if necessary for bandage changes. Gently break down omental or falciform ligament adhesions to the sutures with a sterile-gloved hand between bandage changes. If necessary, obtain samples of peritoneal fluid periodically for cytology and culture. a. Weigh the bandage before and after placement on the animal to estimate fluid loss (500 ml = 1 lb). Use this information to help
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• Overall progress of the patient • Quantity, character, and cytology of fluid drainage
Linea alba
from the abdomen
• Resolution of fever and neutrophilia with a left shift Subcutaneous fat
Postoperative Care and Complications
• Keep the bandage as clean as possible. Indwelling
•
A
Eyelet sutures
B Figure 76-1. Partial closure technique for open abdominal drainage. A, Partially close the linea alba with a loosely placed, simple continuous suture using a monofilament non-absorbable material. B, To hold the primary layer of the abdominal bandage in place, put several eyelet sutures in the skin, then use umbilical tape to “lace” through the eyelets over the abdominal sponge.
calculate fluid requirements and to monitor the trend of abdominal fluid production. 5. In most patients, the abdomen can be closed within 5 to 7 days of the original surgery (see below). Perform abdominal closure by removing the original sutures in the fascia and proceeding with routine closure. Additional culture samples from the peritoneum may be obtained just before closure. The decision on when to close the abdominal incision is subjective. Base this decision on several factors:
urinary catheterization may be necessary in a male dog, or the animal can be kept on an elevated grate to prevent urine soaking of the bandage. Open drainage of the abdomen can cause several complications: • Loss of fluid and protein from the peritoneal cavity—Supportive care with IV fluids and colloids is very important. Hyperalimentation (or total parenteral nutrition) also is necessary if the animal is not eating adequately (see Chapter 3 for nutritional management of the critical care patient). • Electrolyte depletion, especially potassium—Supplement IV fluids with potassium if necessary (see Chapter 5). • Discomfort from the peritonitis and from the open abdomen—Administer analgesics as necessary (e.g., morphine, butorphanol, buprenorphine, or oxymorphone) (see Chapter 6). • Herniation of abdominal viscera or omentum—This may occur if the bandage slips or is damaged by the animal. Gently lavage any tissue that becomes contaminated with sterile saline or remove surgically. Restrict exercise.
SUPPLEMENTAL READING Bjorling DE, Crowe DT, Kolata RJ, Rawlings CA: Penetrating abdominal wounds in dogs and cats. J Am Anim Hosp Assoc 18:742, 1982. Bjorling DE, Latimer KS, Rawlings CA, et al: Diagnostic peritoneal lavage before and after abdominal surgery in dogs. Am J Vet Res 44:816, 1983. Crowe DT, Bjorling DE: Peritoneum and peritoneal cavity. In Slatter DH (ed): Textbook of Small Animal Surgery, 2nd ed. Philadelphia: WB Saunders, 1993, p 407. MacCoy, D: Peritonitis. In Bojrab MJ (ed): Pathophysiology in Small Animal Surgery. Philadelphia: Lea & Febiger, 1981, p 142. Mueller MG, Ludwig LL, Barton LJ: Use of closed-suction drains to treat generalized peritonitis in dogs and cats: 40 cases (1997–1999). J Am Vet Med Assoc 219:789–794, 2001. Staatz AJ, Monnet E, Seim HB: Open peritoneal drainage versus primary closure for the treatment of septic peritonitis in dogs and cats: 42 cases (1993–1999). Vet Surg 31:174–180, 2002.
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Section
7
Disorders of the Urogenital System
Chapter
▼
Mary A. McLoughlin
77
Diseases of the Kidney and Ureter David Grant / S. Dru Forrester
ACUTE RENAL FAILURE Acute renal failure (ARF) is a syndrome caused by an abrupt decline in renal function that occurs over a period of hours to days. Clinical signs result from inability of the kidneys to excrete metabolic wastes and adequately regulate fluid, acid, base, and electrolyte balance. Consistent laboratory findings include azotemia with decreased urine concentrating ability (urine specific gravity usually 1.035 in dogs and >1.040 in cats). In addition, prerenal azotemia quickly resolves when the cause of decreased renal perfusion is corrected (e.g., fluid therapy).
• Renal azotemia is caused by renal failure and occurs
•
when 75% of nephrons are nonfunctional. Dogs and cats with renal failure have concomitant azotemia and inability to adequately concentrate urine. Isosthenuria (specific gravity of 1.008–1.012) often exists, and urine specific gravity (USG) is almost always 30 to 60 minutes without expulsion of a fetus
• Resting phase between delivery of a fetus >4 hours with known retained fetuses
• Intermittent weak contractions for >2 hours without delivery of a fetus
• Systemic signs of illness (e.g., fever, severe weakness, and vomiting)
• Signs of severe pain during parturition • Purulent or hemorrhagic vaginal discharge • Evidence of fetal death Treatment Medical Management
• If both mother and offspring appear healthy, and
• •
there is no obstruction, consider oxytocin therapy. Oxytocin (0.25 U/dog IM or SC) increases the frequency of uterine contractions. A pup should be delivered within 30 minutes of oxytocin administration. Animals not responding to oxytocin within 30 minutes are candidates for cesarean section.
▼ Key Point Repeated doses of oxytocin are usually not helpful and are not recommended because the hormone can cause placental separation and fetal death. Sustained uterine contractions induced by oxytocin can also cause decreased fetal blood supply.
• Calcium gluconate is sometimes given prior to oxytocin because calcium is necessary for muscle contraction, and calcium administration can increase uterine contraction even if the measured serum calcium concentration is normal.
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• 10% Calcium gluconate is given as a very slow intravenous bonus (through an indwelling catheter to avoid the risk of extravasation) at a dosage of 0.2 ml/kg.
• Perform abdominal ultrasound to detect a dead fetus, •
▼ Key Point Do not administer calcium salts subcutaneously because they are irritating and can cause tissue necrosis and subcutaneous calcium deposition.
retained placenta, uterine enlargement, and abdominal effusions associated with peritonitis. Obtain abdominal radiographs to detect retained dead fetuses.
Treatment
• Fluid therapy is essential, and shock doses of intravenous fluids are often needed.
Indications for Caesarian Section (see Chapter 91)
• Add potassium and glucose to the fluids as needed
• No response to medical management • Uterine inertia • Maternal pelvic or vaginal abnormality or systemic
• Administer broad-spectrum antibiotics (see under
illness
• Oversized fetus • Evidence of fetal death • Owners concerned about loss of newborns during a
(indicated by serum chemistry profile results).
•
difficult parturition (e.g., brachycephalic dog)
• Hypocalcemia or hypoglycemia in the bitch or queen; parturition rarely resumes following correction of these biochemical abnormalities, so perform cesarean section along with treatment for hypoglycemia or hypocalcemia
POSTPARTUM UTERINE DISORDERS
•
“Pyometra”). Choose antibiotics based on antimicrobial sensitivity testing if possible. Oxytocin therapy has been recommended to evacuate uterine contents, but this hormone is not effective more than 48 hours after parturition. Endogenous oxytocin should have already maximally stimulated its receptors, so there is little rationale for its use. Because of the risk of sepsis and death, exploratory laparotomy and ovariohysterectomy are necessary (see Chapter 91).
Uterine Prolapse • Rarely, the uterus can prolapse immediately following parturition.
Bacterial Metritis
• The condition is diagnosed by the finding of tissue
Etiology
• Treatment involves manual reduction of the pro-
protruding from the vulva following parturition. lapsed tissue, or, if tissue is devitalized, amputation. For a discussion of surgical treatment of uterine prolapse, see Chapter 91.
Bacteria can ascend into the uterus and cause severe, life-threatening infection following normal parturition, prolonged dystocia, parturition with retained fetus or placenta, or abortion.
Clinical Signs
• History of recent parturition (usually within a week). • Hemorrhagic, fetid, mucopurulent vaginal discharge • •
•
is common. Depression, lethargy, anorexia, vomiting, and any sign of systemic illness can be present. The abdomen can be painful on palpation, and a turgid uterus can be palpated. Uterine involution in a normal postpartum period is not complete by this time, so palpation findings are subjective. Patients can present in septic shock.
Subinvolution of Placental Sites Etiology
• The process of uterine involution occurs for up to
•
Diagnosis
•
• Urinalysis, complete blood count, and serum chem-
•
• •
istry can show results consistent with sepsis, dehydration, and, if advanced, multiple organ failure. Vaginal cytology yields degenerate neutrophils and bacteria. Bacterial culture of the vaginal discharge is useful in selecting an antibiotic.
3 months postpartum but is usually essentially complete by 6 weeks. During that period, a hemorrhagic, sometimes brownish, and mucoid discharge from the vagina is normal. Early in the process of uterine involution, the discharge can seem quite copious. In some bitches, placental attachment sites are invaded by trophoblastic cells, these sites fail to regress normally, and hemorrhage persists. Subinvolution of placental sites (SIPS) is most common in younger bitches. SIPS is not known to occur in the cat.
Clinical Signs Persistent vaginal bleeding for more than 6 weeks postpartum in an otherwise normal bitch is the typical clinical sign of SIPS.
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Diagnosis
• Examination of a vaginal smear from a bitch with • •
SIPS reveals hemorrhage, parabasal cells, and, sometimes, the presence of trophoblastic cells. Blood loss due to SIPS is rarely clinically significant. Monitor red blood cell count or packed cell volume if indicated. If clinical anemia develops, other causes of blood loss should be investigated.
• In rare cases, cytology of vaginal discharge may yield tumor cells.
• A suspected uterine mass can be confirmed by
• •
Treatment
• SIPS eventually resolves without treatment. • Bitches are commonly fertile following an episode SIPS, and the condition does not necessarily develop following subsequent pregnancies.
UTERINE NEOPLASIA Etiology • Tumors of the uterus are rare in dogs and cats, •
•
probably because of the high prevalence of ovariohysterectomy. Endometrial adenocarcinoma is the most common uterine tumor of the queen, and leiomyoma and leiomyosarcoma are the most common uterine tumors of the bitch. A variety of other tumors have been reported in dogs and cats, but they are very uncommon.
Clinical Signs • Uterine tumors are most often found incidentally at ovariohysterectomy.
• Vaginal discharge may be present in some animals •
with invasive uterine tumors. Tumors of the cervix may cause bleeding. In cats, endometrial adenocarcinoma is typically associated with local and distant metastases to many different organs, and clinical signs referable to any organ system can be seen.
Diagnosis • Uterine masses may be detected by abdominal palpation.
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•
abdominal ultrasound, whereas it is difficult to localize a mass to the uterus on plain abdominal radiographs. Ultrasound-guided fine-needle aspiration of a uterine mass may yield a cytopathologic diagnosis. Perform preoperative evaluation consisting of urinalysis, complete blood count, serum chemistry, three-view thoracic radiographs, and abdominal ultrasound to evaluate for metastatic disease. Definitive diagnosis is made by histopathology of surgically obtained tissues.
Treatment • Ovariohysterectomy is the recommended treatment (see Chapter 91).
• Most bitches can be cured by complete excision of a uterine mass.
SUPPLEMENTAL READING Biddle D, Macintire DK: Obstetrical emergencies. Clin Tech Small Anim Pract 15(2):88–93, 2000. Brodey RS, Roszel JF: Neoplasms of the canine uterus, vagina, and vulva: A clinicopathologic survey of 90 cases. J Am Vet Med Assoc 151(10):1294–1307, 1967. Gilbert RO, Nothling JO, Oettle EE: A retrospective study of 40 cases of canine pyometra-metritis treated with prostaglandin F2-alpha and broad-spectrum antibacterial drugs. J Reprod Fertil Suppl 39:225–229, 1989. Kyles AE, Vaden S, Hardie EM, Stone EA: Vestibulovaginal stenosis in dogs: 18 cases (1987–1995). J Am Vet Med Assoc 209(11):1889–1893, 1996. Noakes DE, Dhaliwal GK, England GC: Cystic endometrial hyperplasia/pyometra in dogs: A review of the causes and pathogenesis. J Reprod Fertil Suppl 57:395–406, 2001. Root MV, Johnston SD, Olson PN: Estrous length, pregnancy rate, gestation and parturition lengths, litter size, and juvenile mortality in the domestic cat. J Am Anim Hosp Assoc 31(5):429–433, 1995. Watts JR, Wright PJ, Lee CS: Endometrial cytology of the normal bitch throughout the reproductive cycle. J Small Anim Pract 39(1):2–9, 1998. Zone MA, Wanke MM: Diagnosis of canine fetal health by ultrasonography. J Reprod Fertil Suppl 57:215–219, 2001.
Chapter
▼
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91
Surgery of the Ovaries and Uterus Gretchen K. Sicard / Roger B. Fingland
Surgical procedures performed on the uterus and ovaries include ovariohysterectomy, cesarean section, uterine biopsy, and rarely, ovariectomy. Uterine surgery usually is straightforward but requires sound basic surgery skills and a thorough understanding of the anatomy and physiology of the reproductive tract.
• The uterine branch of the internal iliac artery is the main artery to the uterus. The uterine branch of the urogenital artery supplies the caudal portion of the uterus, the cervix, and part of the vagina. The uterine branch of the ovarian artery supplies the cranial part of the uterine horns.
ANATOMY (Fig. 91-1) Ovaries • The ovaries are located 1 to 3 cm caudal to the kidneys.
OVARIOHYSTERECTOMY Preoperative Considerations • Elective sterilization is the most common indication for ovariohysterectomy. Ovariohysterectomy is the treatment of choice for most uterine diseases including pyometra, uterine torsion, cystic endometrial hyperplasia, uterine rupture, and uterine neoplasia (see Chapter 90 for a description of these diseases).
• The ovaries are attached to the abdominal wall by the mesovarium, a part of the broad ligament.
• The suspensory ligament is the cranial continuation
• •
•
of the broad ligament and extends between the ventral third of the last two ribs and the ventral surface of the ovary. The proper ligament is a continuation of the suspensory ligament and extends from the caudal end of the ovary to the cranial end of the uterine horn. The ovarian arteriovenous complex (OAVC) lies on the medial side of the broad ligament and supplies the ovaries and the cranial portion of the uterine tube. The distal two-thirds of the OAVC is convoluted in the dog, similar to the pampiniform plexus in males. The left ovarian vein drains into the left renal vein; the right ovarian vein drains into the caudal vena cava.
▼ Key Point Ovariohysterectomy before the first or second estrus provides a definitive protective factor against development of mammary neoplasia. After the third estrus (or approximately 2.5 years), there is no significant effect of ovariohysterectomy for the prevention of mammary neoplasia.
• An alternative method of sterilization of a female dog
Uterus • The uterus consists of the cervix, body, and two •
•
uterine horns. Oviducts (uterine tubes) connect the uterine horns and ovaries. The uterus is attached to the dorsolateral wall of the abdominal cavity and the lateral wall of the pelvic cavity by paired double folds of peritoneum called broad ligaments. The round ligament is the caudal continuation of the proper ligament. The round ligament extends caudally and ventrally in the broad ligament and passes through the inguinal canal, terminating subcutaneously near the vulva.
992
•
or cat is ovariectomy without hysterectomy. Studies have shown no difference in long-term results, or complications, between ovariectomy and ovariohysterectomy. Ovariectomy may also be considered for the surgical treatment of small animal patients with a mass lesion involving the ovary, particularly if the owner wishes to maintain the reproductive status of the animal. However, if ovarian neoplasia is suspected, ovariohysterectomy coupled with a complete abdominal exploratory is indicated to ensure complete resection of the neoplasm and examination of all abdominal viscera for evidence of metastasis. Whether the procedure is elective or not, perform an appropriate preoperative evaluation, including a complete history, physical examination, and appropriate blood work.
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Suspensory ligament
993
Cervix
Uterine vessels Figure 91-1.
Anatomy of the uterus and ovaries.
Ovarian bursa Ovarian arteriovenous complex
Uterine horn
Ovary
Surgical Procedure Objective
• To remove the uterus and ovaries Equipment
• Standard general surgery instrument pack and suture • Ovariohysterectomy (Snook) hook (optional) Technique 1. After anesthetizing the animal, manually express the urinary bladder. 2. Position the animal in dorsal recumbency. 3. Prepare the entire ventral abdominal region for aseptic surgery. 4. Skin incision: a. Dog: Make a ventral midline incision extending from the umbilicus to a point halfway between the umbilicus and the brim of the pubis. b. Cat: Begin the ventral midline incision approximately 1 to 2 cm caudal to the umbilicus and extend the incision caudally 3 to 5 cm. c. A longer abdominal incision is required to remove an enlarged uterus (e.g., pyometra). d. Attempt to incise exactly on midline in lactating bitches to avoid trauma to the mammary glands. 5. Enter the abdominal cavity through the linea alba. 6. Locate the left uterine horn using the ovariohysterectomy hook or index finger. Displace the omentum and bowel cranially if necessary to find the uterus. 7. Place a small hemostat across the proper ligament to aid in caudal retraction of the ovary. 8. Grasp the ovary between the thumb and the middle fingers. Place the index finger as far proximal as possible on the suspensory ligament (Fig. 91-2A). 9. Place tension on the suspensory ligament by rotating the index finger caudally. Gradually increase
Proper ligament of the ovary
tension on the suspensory ligament until the ligament stretches or ruptures. ▼ Key Point Avoid placing tension on the OAVC during manipulation of the suspensory ligament or when placing ligatures.
10. Identify the OAVC. Using a Rochester-Carmalt hemostatic forceps (clamp), make an opening in the mesovarium immediately caudal to the OAVC in an area clear of vessels and fat (Fig. 91-2B). 11. Triple-clamp and transect the OAVC (Fig. 91-2C). a. Double-clamp the OAVC with RochesterCarmalt hemostatic forceps. Place the first clamp immediately proximal (toward the aorta) to the ovary and the second clamp approximately 5 mm proximal to the first. Place a third clamp across the proper ligament between the ovary and the uterine horn. Transect the OAVC between the middle clamp and the ovary (Fig. 91-2D). b. Alternatively, place all three clamps across the OAVC proximal to the ovary. Transect the OAVC between the middle clamp and the clamp adjacent to the ovary (Fig. 91-2E). ▼ Key Point Place the hemostatic forceps on the OAVC as close as possible to the ovary to prevent accidental inclusion of the ureter, but be sure to remove all of the ovarian tissue.
12. Loosely place a circumferential ligature around the proximal clamp (Fig. 91-2F). Tighten the ligature as the clamp is removed. In this manner, the circumferential ligature is tightened in the groove of crushed tissue created by the clamp (Fig. 91-2G). ▼ Key Point The clamp adjacent to the ligature may need to be loosened before knotting to ensure proper tightness of the knot.
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Figure 91-2. Ovariohysterectomy. A, Separate the suspensory ligament. B, Open the mesovarium immediately caudal to the ovarian arteriovenous complex (OAVC). C, Triple-clamp the OAVC. D, Transect the OAVC between the ovary and the clamp. E, Alternative clamp and transection method.
13. Place a transfixing ligature between the circumferential ligature and the transected end of the OAVC (Fig. 91-2H and I). A full ligature (circumferential) may be used instead of a transfixing ligature in young cats or small dogs. ▼ Key Point Never include ovarian tissue in the ligatures.
14. Grasp the OAVC distal to the ligature (without grasping the ligature) with thumb forceps, remove the middle clamp, and inspect the OAVC for bleeding. If bleeding occurs, place a second circumferential ligature on the OAVC proximal to the first. 15. Follow the left uterine horn distally to the bifurcation, locate the right uterine horn, and follow the right uterine horn proximally to the right OAVC. 16. Ligate and transect the right OAVC, as described previously. 17. Transect the broad ligament. a. In most preparturient animals, the broad ligament can be manually separated. Make an opening in the broad ligament adjacent to the uterine artery and vein close to the cervix (Fig. 91-2J). Place four fingers through the opening
18. 19. 20.
21.
in the broad ligament and grasp the entire broad ligament, including the round ligament (Fig. 912K). Pull the broad ligament cranially (not ventrally) until the broad ligament and the round ligament are free (Fig. 91-2L). b. If the broad ligament is highly vascular, large vessels may be ligated individually or mass ligation of the broad ligament or portions of the ligament may be ligated. Exteriorize the uterine body and locate the cervix. Divide the uterine body after two ligatures are placed (Fig. 91-2M through O). Remove the entire uterus proximal to the cervix. Evaluate the OAVC pedicles and the uterine body for bleeding prior to abdominal closure. The left and right OAVC are located immediately caudal to the caudal pole of each respective kidney. a. Locate the left OAVC pedicle by retracting the descending colon medially, exposing the left paralumbar gutter. b. Locate the right OAVC pedicle by retracting the duodenum medially, exposing the right paralumbar gutter. c. Retroflex the bladder. The ligated uterine body lies ventral to the descending colon and dorsal to the bladder. Close the abdominal incision routinely.
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Figure 91-2. Continued F, Place circumferential suture around the proximal clamp. G, Tighten the suture in the groove of crushed tissue. H and I, Ligature pattern for transfixing ligature. J, Open the broad ligament adjacent to the uterine artery and vein close to the cervix. K, Grasp the broad ligament. L, Pull the broad ligament cranially until it and the round ligament are free. M, Place the first transfixing suture. N, Place the second transfixing suture. O, Transect the uterine body.
Postoperative Care • Administer postoperative analgesics as needed (see
• Dogs with pyometra may be toxemic or septicemic (see Chapter 90). Administer broad-spectrum antibiotics during surgery, and continue antibiotics after surgery if the animal is toxemic or septicemic or if peritonitis was present at surgery.
Chapter 6).
• Restrict exercise and monitor for wound complications or hemorrhage after ovariohysterectomy.
• Postoperative care following ovariohysterectomy for pyometra: • Dogs with pyometra frequently have renal dysfunction without associated morphologic abnormalities, and they may be azotemic, oliguric, or anuric. Monitor renal function and maintain hydration after surgery. Diuresis with crystalloid fluids administered intravenously for at least 24 to 36 hours after surgery is advisable. Placement of a urinary catheter will assist with monitoring urine output (see Chapter 90 for more information on pyometra).
Postoperative Complications Complications following elective ovariohysterectomy are rare and may include the following.
Hemorrhage
• Hemorrhage is the most common complication fol•
lowing ovariohysterectomy in dogs weighing more than 25 kg. Common causes of hemorrhage include failure to adequately tighten circumferential or transfixion
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ligatures, tearing of the OAVC while breaking the suspensory ligament, failure to ligate large vessels in the broad ligament, tearing of the uterine artery due to excessive traction on the uterine body and premature removal of a clamp during ligation. In addition, persistent hemorrhage after surgery can occur in patients with undiagnosed or untreated coagulation disorders such as von Willebrand disease or specific coagulation factor deficiency (see Chapter 23). The incidence of hemorrhage can be reduced by maintaining meticulous surgical technique. Avoid becoming complacent during routine ovariohysterectomy.
•
•
Fistulous Tracts and Granulomas
• Sublumbar draining sinus tracts in spayed female
Uterine Stump Pyometra Uterine stump pyometra can occur if a portion of the uterine body or uterine horn is not removed and the animal has increased serum progesterone. The source of the increased serum progesterone can be endogenous from residual ovarian tissue or exogenous from progestational compounds administered for treatment of dermatitis.
•
Ovarian Remnant Syndrome (Recurrent Estrus)
• This condition results from retained functional resid-
dogs may develop when non-absorbable multifilament suture material, such as polymerized caprolactam (Braunamid, B. Braun Melsungen) used for ligating the OAVC or uterine body becomes contaminated. Treatment is exploratory celiotomy and removal of suture material.
▼ Key Point Do not use non-absorbable multifilament suture material for ligation of the OAVC or uterine body.
▼ Key Point Complete excision of the uterine body and ovaries reduces the incidence of uterine stump pyometra.
and secretion of follicle-stimulating hormone and luteinizing hormone. Additional structural causes of urinary incontinence may include adhesions or granulomas of the uterine stump that interfere with urinary bladder sphincter function and, rarely, vaginoureteral fistula from common ligation of the vagina and ureter. Prudent administration of exogenous estrogens or alpha-adrenergic drugs may be indicated for estrogenresponsive urinary incontinence (see Chapter 83).
Body Weight Gain Weight gain may occur after ovariohysterectomy; the cause is poorly understood.
ual ovarian tissue.
• Treatment is removal of residual ovarian tissue. ▼ Key Point To increase the likelihood of identifying residual ovarian tissue, perform exploratory celiotomy to find ovarian remnants when the dog is showing signs of recurrent estrus.
• If ovarian tissue is not located, identify both ureters and resect remnants of the OAVC pedicles bilaterally. Submit the tissue for histopathologic analysis.
Ligation of Ureter
• This complication is more likely to occur when
• • •
ovariohysterectomy is associated with hemorrhage, pyometra, or cesarean section. It may also occur when the urinary bladder is distended and the trigone and ureterovesical junction are displaced cranially. Hydronephrosis and occasionally pyelonephritis can result. Ureteronephrectomy may be required. Avoid by careful placement of ligatures on the OAVC and uterine body.
Urinary Incontinence
• Urinary incontinence after ovariohysterectomy can occur in susceptible individuals (approximately 20% of canine patients) due to a combination of low systemic estrogen levels and increase production
Eunuchoid Syndrome This is a rare complication identified in working dogs after ovariohysterectomy. Clinical signs include decreased aggression, loss of interest in work, and decreased stamina.
Complications Related to Celiotomy The most common complications associated with celiotomy are the following:
• • • • •
Self-mutilation of the abdominal wound Seroma formation Dehiscence Failure to remove gauze sponges from the abdominal cavity Laceration of the spleen or urinary bladder
CESAREAN SECTION Preoperative Considerations Indications for Cesarean Section
• Dystocia from primary uterine inertia • Protracted dystocia resulting in secondary uterine inertia
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• Obstructive dystocia (oversized fetus or narrow pelvic • • •
canal) Prolonged gestation Dystocia from fetal malpositioning Fetal death with putrefaction
Certain breeds (Chihuahuas, English bulldogs) frequently require cesarean section because of a high incidence of dystocia. (See Chapter 90 for further discussion of dystocia.)
Anesthesia
• Animals that require cesarean section may have fluid •
•
• • • •
and metabolic disturbances that place them at greater risk for general anesthesia. Correction of fluid and metabolic abnormalities should be well under way prior to induction of anesthesia. Administer intravenous fluid therapy and a prophylactic broad-spectrum antibiotic such as cefazolin, 22 mg/kg IV. Various regimens for induction and maintenance of anesthesia (see Chapter 2 for general principles of anesthesia) have been recommended. The objective is to administer an appropriate level of anesthesia and analgesia to the dog or cat without causing excessive depression of the puppies or kittens. Epidural anesthesia using a local anesthetic with or without an opioid can be attempted in dogs. Intravenous narcotics or propofol combined with local anesthesia may be used in dogs. Ketamine and local anesthesia may be used in cats. Administer standard inhalation anesthesia after the puppies or kittens are removed.
▼ Key Point Minimize time from induction to delivery by fully preparing the surgical site prior to anesthesia.
• Induce anesthesia and intubate the animal on the surgery table, preferably after the initial skin preparation. ▼ Key Point Inform the owner prior to surgery that ovariohysterectomy may be necessary if the uterus is not viable.
Surgical Procedure Objective
• To remove all fetuses from the gravid uterus as quickly and safely as possible
Equipment
• • • • •
Standard general surgery instrument pack and suture Laparotomy sponges Clean towels Doxapram (Dopram, Robins) and naloxone (Narcan, Elkins-Sinn) (if narcotics are used for induction) Incubator or heat lamp
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Technique 1. Position the animal in standard dorsal recumbency. 2. Perform the final skin preparation and place surgical drapes. 3. Incise skin, subcutaneous tissue, and linea alba on the ventral midline beginning cranial to the umbilicus and extending as far caudally as necessary to exteriorize the uterus. ▼ Key Point Avoid incising mammary tissue when making the initial skin incision. Enter the abdominal cavity cautiously to avoid lacerating the gravid uterus.
4. Exteriorize the uterus. 5. Isolate the uterus from the abdominal viscera with moist laparotomy sponges. 6. Identify an avascular area on the dorsal or ventral midline of the uterine body. Make a small incision in the uterine body with a scalpel by tenting the tissue of the uterine wall to avoid inadvertently lacerating a fetus with the scalpel. a. Extend the incision with Metzenbaum scissors to a sufficient length to accommodate the largest fetus. The uterus may tear during extraction of a fetus if the length of the incision is not adequate. 7. Move a fetus to the incision by gently squeezing the uterine horn (Fig. 91-3A). 8. Grasp the fetus and gently remove it from the uterus. 9. Open the amniotic sac as the fetus is removed (Fig. 91-3B). Direct fetal fluids away from the operative field to minimize contamination. 10. Clamp and transect the umbilical vessels approximately 2 cm from the fetal abdominal wall (Fig. 91-3C). 11. Place the neonate on a sterile towel and pass it to an assistant. Alternatively, the neonate can be passed to the assistant before the umbilical vessels are transected, leaving this responsibility to nonsterile operating room assistants. 12. Remove the placenta by separating the placental attachment from the endometrium using gentle traction. To decrease the potential for severe postoperative uterine hemorrhage, do not remove the placenta if placental separation is difficult. 13. Extract the remaining fetuses by gently manipulating them toward the site of the uterine incision. 14. Palpate the uterus from the pelvic canal to the ovaries to make certain that no fetuses remain. 15. The uterus will contract rapidly after all fetuses have been removed and occasionally during extraction of the last few fetuses. Administration of oxytocin rarely is necessary to initiate uterine involution. 16. Close the uterus with 2-0 or 3-0 absorbable suture material in a one- or two-layer inverting suture pattern (e.g., Cushing and Lembert).
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Figure 91-3. Cesarean section. A, Move the fetus toward the incision. B, Break the amniotic sac as the fetus is removed. C, Clamp and transect the umbilical vessels.
17. Locally lavage the uterus with warm physiologic saline solution prior to returning it to the abdominal cavity. 18. Lavage the abdominal cavity with warm physiologic saline solution and aspirate all lavage fluid if contamination or spillage of uterine contents occurred.
Postoperative Care and Complications
▼ Key Point En bloc ovariohysterectomy (rapid re-
• Clamp the umbilical vessels and remove the fetal
moval of the uterus and ovaries before hysterotomy and removal of the neonates) is associated with a neonatal survival rate that is similar to other techniques for medical and surgical management of dystocia.
Care of Neonates ▼ Key Point Remove the fetal membranes from the neonate’s mouth and nose immediately after delivery.
membranes if this was not done by the surgeon.
• Clear mucus from the mouth and nares with gentle suction or cotton swabs.
• Assess the viability of the neonate. Neonates often are bradycardic and apneic.
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• Dry the neonate briskly with a soft towel because skin • • •
• •
• •
stimulation reflexly stimulates respiration. Mucus can be cleared from the upper airway by grasping the neonate firmly and slowly swinging it downward. Administer a respiratory stimulant such as doxapram (Dopram, Robins), 0.5 to 2.0 mg/kg PO or IM, if the neonate does not respond to mechanical stimulation. Poor neonatal viability can be due to anesthetic agents administered to the dam for induction of anesthesia. Administer a narcotic antagonist such as naloxone (Narcan, Elkins-Sinn), 0.01 mg/kg PO or IM, if the dam was given a narcotic for induction of anesthesia. Alternately, medications can be given topically on the neonate’s tongue to be absorbed through the mucous membranes. Some neonates may not breathe spontaneously for 30 to 60 minutes after delivery. Be persistent with resuscitation efforts. Neonates that do not breathe spontaneously can be intubated with a sterile puppy feeding tube for assisted ventilation. Place neonates in an environmental temperature of approximately 32∞C. Examine neonates for congenital abnormalities such as cleft palate, imperforate anus, hernias, and limb deformities.
Care of the Dam
• Clean residual antiseptic solution, blood, and fetal • •
fluids from the dam’s mammary glands prior to allowing the neonates to nurse. Place the dam with neonates after anesthetic recovery so that neonates receive colostrum as soon as possible after birth. Make certain that the dam has adequate milk and that each neonate nurses. • Oxytocin (0.5 U/kg IM or SC) can be administered to stimulate milk letdown.
▼ Key Point Ovariohysterectomy performed in conjunction with cesarean section should not interfere with the dam’s mothering instincts or ability to produce milk. Ovarian hormones are not important for maintenance of lactation.
• Consider discharging the dam and neonates as soon as the dam has recovered from anesthesia and has demonstrated appropriate behavior toward the neonates.
Complications Short Term
• These include hemorrhage, hypovolemia, and hypothermia.
• Place the dam in a warm, quiet environment and administer intravenous crystalloid or colloid fluids as needed.
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Long Term
• Potential long-term complications include peri• • •
tonitis, wound dehiscence, agalactia, and uterine hemorrhage. Prolonged severe endometrial hemorrhage may require administration of oxytocin or, in nonresponsive cases, emergency ovariohysterectomy. Monitor serum calcium levels if hypocalcemia is suspected. See Chapter 32 for diagnosis and treatment of eclampsia. Although multiple cesarean sections can be performed on a dam, uterine scarring may prevent future placentation, and peritoneal adhesions may complicate subsequent celiotomies.
UTERINE PROLAPSE Preoperative Considerations • Uterine prolapse is a rare condition that can occur anytime during or up to several days after parturition.
• Animals presented with uterine prolapse may be clin-
• •
• • •
ically stable or may have mild to severe metabolic imbalances. Treat disturbances in fluid, electrolyte, or acid-base balance before managing the uterine prolapse. Assess the viability of the prolapsed uterus. Treatment options include manual reduction, manual reduction with immediate ovariohysterectomy, internal reduction via celiotomy, and amputation of the uterus externally. Manual reduction of the prolapsed uterus is the treatment of choice, although an episiotomy may be required. Ovariohysterectomy may be necessary after manual reduction if the uterus is devitalized. Consider external amputation only if the uterus cannot be reduced. Then remove ovaries through a celiotomy incision.
Manual Reduction Technique 1. Epidural anesthesia is preferred, but standard general anesthesia can be used. 2. Clean the uterus and wrap it with sterile gauze sponges soaked in physiologic saline. Soaking the sponges with a hypertonic dextrose solution may help reduce swelling. 3. Apply sterile water-soluble lubricating jelly to the uterus and attempt gentle reduction with a gloved finger or with a sterile, smooth syringe case. 4. If manual reduction is unsuccessful, prepare the perineum and the prolapsed uterus for aseptic surgery and perform an episiotomy (see Chapter 93 for technique). Reduction is facilitated by episiotomy. If manual reduction still is not possible,
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consider internal reduction via celiotomy or external amputation.
Surgical Procedure for External Amputation of Prolapsed Uterus Objectives
• To resect the prolapsed uterine horns and, if possible, the ovaries
• To avoid contamination of the abdominal cavity • To minimize uterine hemorrhage
UTERINE BIOPSY Uterine biopsy and culture is most commonly indicated in female patients of breeding age with a clinical history of reproductive failure or persistent vaginal discharge arising from the uterus. Uterine biopsy is performed for the purposes of diagnosis and prognosis.
Surgical Procedure for Uterine Biopsy Objectives
Equipment
• To obtain a full thickness tissue sample and culture
• Standard general surgical instrument pack
• To minimize contamination of the peritoneal cavity
Technique
Equipment
1. Administer epidural or general anesthesia. 2. Position the animal in dorsal recumbency with the rear limbs tied forward. 3. Prepare the ventral abdominal and perineal areas for aseptic surgery. Place a purse-string suture in the anus. 4. Incise the uterine body near the vulva. Place stay sutures in the incised proximal wall of the uterine body to prevent retraction into the vagina. Be careful not to damage the urethra if the vagina has prolapsed with the uterus. 5. Identify the uterine horns. 6. Apply gentle caudal traction on the uterine horns to expose the ovaries. Ligate the right and left OAVC. 7. If the ovaries cannot be exposed, place two circumferential ligatures around each uterine horn as far cranial as possible. Transect the uterine horns between the two ligatures. 8. Double-ligate and transect the uterine vessels. 9. Close the proximal stump of the uterine body with synthetic absorbable suture material in a simple interrupted pattern and reduce the remaining tissue into the abdomen. 10. If the ovaries remain, perform a ventral midline celiotomy and bilateral ovariectomy.
• Standard general surgical instrument pack
Postoperative Care and Complications • Recurrence after successful manual reduction of a
•
uterine prolapse is rare. However, warn owners that recurrence is possible with subsequent whelping, particularly if dystocia occurs. Complications seldom occur after manual reduction or external amputation of the uterus. Lifethreatening hemorrhage can occur rarely after external amputation.
sample from the uterus
Technique 1. Follow the surgical technique described under “Cesarean Section,” steps 1 to 5, to expose the uterus. 2. Palpate the uterus for abnormalities such as mass lesions, cystic areas, or fluid accumulation. 3. Use a 4- to 6-mm skin biopsy punch to obtain a full thickness biopsy sample of either one of the uterine horns or the uterine body. 4. Insert a small sterile swab into the uterine lumen to obtain a sterile culture sample. 5. Close the biopsy site using 4-0 or 5-0 synthetic absorbable monofilament suture (Monocryl, PDS) in an interrupted or cruciate pattern. ▼ Key Point The submucosa is the holding layer of the uterus. Avoid placing suture material within the lumen of the uterus.
SUPPLEMENTAL READING Berzon JL: Complication of elective ovariohysterectomies in the dog and cat at a teaching institution: Clinical review of 853 cases. Vet Surg 8:89, 1979. Gaudet DA: Canine dystocia. Compend Contin Educ 7:406, 1985. Gaudet DA: Retrospective study of 128 cases of canine dystocia. J Am Anim Hosp Assoc 21:813, 1985. Moon PF, Erb HN, Ludders JW: Perioperative management and mortality rates of dogs undergoing cesarean section in the United States and Canada. J Am Vet Med Assoc 213:365, 1998. Richler IM, Hubler M, Jöchle W, et al: The effect of GnRH analogs on urinary incontinence after ablation of the ovaries in dogs. Theriogenology 60:1207, 2003. Robbins MA, Mullen HS: En bloc ovariohysterectomy as a treatment for dystocia in dogs and cats. Vet Surg 23:48, 1994. Roberts DD, Straw RC: Uterine prolapse in a cat. Compend Contin Educ 10:1295, 1988.
Chapter
▼
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Diseases of the Vagina and Vulva Mary A. McLoughlin
Small animals with diseases of the vulva and vagina can present with clinical signs of lower urinary tract disease (urgency, pollakiuria, stranguria, and hematuria), intermittent or continuous urinary incontinence, vaginal discharge, perivulvar dermatitis, excessive licking, and foul odor. Because the vulva and the vestibule form a common orifice for the lower urinary and reproductive systems, careful examination of associated diseases is warranted. See Chapter 93 for discussion of the anatomy of the vagina and vulva.
•
DISEASES OF THE VULVA Congenital Abnormalities Congenital abnormalities of the vulva are uncommon and are often detected because of the secondary problems they cause. Abnormalities of the anatomic structure, size, or positioning of the vulva have been shown to be contributing factors to the development several disorders, including chronic or recurrent urinary tract infections, cystitis, vaginitis, vestibulitis, urine pooling or urinary incontinence, perivulvar dermatitis, and difficulty with natural mating. Diagnosis of vulvar disorders is made by physical examination of the vulva and perivulvar region, as well as digital palpation and vaginoscopy.
Vulvar Hypoplasia or “Juvenile” Vulva Etiology
• Vulvar hypoplasia has been described as a small or
•
•
infantile vulva, which is frequently retracted and obscured by the perivulvar skin folds. The patient’s weight or body condition score should not bias the diagnosis of vulvar hypoplasia. The vulva should not be covered or obscured by regional skin folds dorsally or laterally. It should not be necessary to pull upward on the perineal skin between the anus and the vulva to expose the complete extent of the vulva. Tremendous variation in size, structure, and position of the vulva exists among various breeds of dogs, as
•
•
well as within specific breed standards. The vulva should be located on the perineal midline directly ventral to the anus. Although the size of the vulva varies among dogs, it should be readily visible in the standing dog when viewed from behind. The vulva should not be positioned ventrally between the rear legs so that it is no longer visible. Perivulvar skin folds may obscure both hypoplastic and normal-sized vulvas. There are a number of breeds of dogs that appear to be conformationally predisposed to perivulvar skin folds as young dogs without being overweight, including Newfoundland, Labrador retriever, mastiff, German shepherd, Akita, basset hound, Staffordshire terrier, and bull terrier. It is well recognized that the anatomic characteristics of the vulva are altered due to the hormonal influence of the estrus cycle in unspayed females. The vulva becomes swollen and enlarged during proestrus and estrus. As the vulva enlarges, it is generally assumes a more dorsal position in the perineal region to facilitate mating. The size of the vulva generally does not change in spayed female dogs. It has been theorized that vulvar hypoplasia results from ovariohysterectomy at an early age prior to development of secondary sex characteristics. However, there is no scientific literature to support this statement.
Clinical Signs
• A small or hypoplastic vulva is common and frequently not associated with any clinical abnormalities. However if the vulva is small and recessed by the surrounding perivulvar skin folds, body heat and moisture from vaginal secretions or urine can accumulate between local skin folds, creating an environment conducive to skin maceration, inflammation, and bacterial overgrowth. Microtrauma to the skin surfaces from friction between the opposing skin folds, combined with tissue maceration and inflammation, causes normal skin defense mechanisms to be overwhelmed, allowing secondary bacterial infections to occur. 1001
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• Superficial dermatitis in the perivulvar region can •
result in a foul odor and discharge. Secondary clinical signs of chronic vestibulitis, vaginitis, cystitis, and ascending urinary tract infection have also been reported.
Treatment
Clitoral Hypertrophy The clitoris is located on the ventral floor of the vulva, normally recessed within the clitoral fossa. The clitoral fossa demarcates the cranial edge of the vulva at the transition of the vulva to the vestibule. The clitoris is described as the female homologue to the penis and may contain an os clitidoris.
• Medical management of perivulvar dermatitis with
•
systemic antibiotics or topical therapies such as antimicrobials, antiseptic, cleansing, or drying agents can be performed (see Chapter 38). However, this approach is typically only palliative and often unrewarding for long-term resolution. Episioplasty, the surgical excision of the excessive perivulvar skin folds to expose and reposition a small or recessed vulva, is the treatment of choice for perivulvar dermatitis, chronic or recurrent urinary tract infections, or vestibulitis secondary to ascending infection or chronic local inflammation (see Chapter 54).
Etiology
• Clitoral enlargement is typically associated with any
• •
one of a number of developmental or acquired etiologies, including disorders of sexual differentiation (see Chapter 90), exposure to anabolic steroids, or hyperadrenocorticism (see Chapter 33). Enlargement of the clitoris may result in exposure of the clitoris by its protrusion through the vulvar cleft. Clitoral enlargement has been documented in normal female dogs.
Clinical Signs Vulvar Stenosis Etiology
• The clinical signs associated with clitoral hypertrophy
• Abnormal fusion of the genital folds and genital
•
•
swellings can result in narrowing or stenosis of the vulva, vestibule, or vestibulovaginal junction. Vulvar stenosis has been most frequently reported in the collie and Shetland sheepdog breeds.
•
Clinical Signs
• There are frequently no clinical signs if the affected •
• •
animal has been spayed. This abnormality may be overlooked unless the affected female is intended for breeding or a digital examination of the vulva, vestibule, and vestibulovaginal junction is indicated. Affected females may experience pain when mating is attempted, requiring the deposition of semen by artificial insemination. If pregnancy does occur, vulvar stenosis can result in dystocia. A planned cesarean section can be performed to avoid this complication, or an episiotomy can be performed at the time of delivery of the first fetus.
Treatment
• Enlargement of the vulvar orifice, rima vulvae, by •
permanent episiotomy (episiostomy) can be performed (see Chapter 93). Increasing the size of the vulvar orifice may result in an increased exposure of the vestibule, vagina, and lower urinary tract to ascending environmental contaminants, resulting in secondary vestibulitis, vaginitis, and urinary tract infection.
are variable. Animals may be presented for purely cosmetic reasons rather than specific health concerns. Enlargement of the clitoris and exposure through the vulvar cleft can result in clitoritis from environmental exposure, drying, and mechanical irritation. Inflammation of the clitoris can also result in secondary urinary tract infection, vestibulitis, or vaginitis with discharge due to drainage around the enlarged clitoris.
Treatment
• Symptomatic therapy with systemic antimicrobials,
•
anti-inflammatory drugs, or local treatment with topical therapies is typically unrewarding for longterm resolution of clinical signs. Determination of an underlying etiology is essential to direct treatment at an inciting cause. Withdrawal of all anabolic steroids or treatment of hyperadrenocorticism may result in regression of the clitoral enlargement.
▼ Key Point Surgical treatment of clitoral hypertrophy is not indicated if a patient does not have any associated clinical signs.
• Perform clitoral resection for patients with persistent clinical signs associated with clitoral enlargement.
Surgical Procedure: Clitoral Resection Technique 1. Perform an episiotomy to expose the clitoris and clitoral fossa. The external urethral orifice is identified and catheterized (see Chapter 93).
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2. Dissect the base of the clitoris, which may include an os, from the fossa and surrounding vulvar and vestibular mucosa using sharp dissection. 3. Control hemorrhage with electrocautery or a laser. Larger “phalluses” present in dogs with intersex disorders may bleed profusely. Control of local hemorrhage is essential. 4. Close the incised edges of the vulvar and vestibular mucosa with a monofilament absorbable suture, eliminating the clitoral fossa. 5. Close the episiotomy in a routine manner (see Chapter 93).
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be evident in the region of the ovaries at the caudal pole of either kidney. Treatment Exploratory laparotomy and biopsy: Direct identification, excision, and biopsy of a mass lesion in the region of either or both ovarian pedicles will definitively diagnose the presence of estrogen-secreting ovarian tissue and distinguish among ovarian remnant syndrome, neoplasia, and cystic ovaries (see Chapter 91). Surgical identification of ovarian remnants is easier if the exploratory is performed while the animal is in estrus.
Postoperative Care
• Place an Elizabethan collar to prevent self-trauma. • Consider administration of nonsteroidal antiinflammatory drugs after surgery for swelling, pain, and discomfort (see Chapter 6).
Vulvar Enlargement
Vulvar Trauma Etiology. Injury to the vulva is relatively uncommon but can occur as a result of blunt or penetrating trauma, dog fights, injury during breeding, attempts to disrupt a mating, or difficulty whelping.
Etiology
Diagnosis
• Edema or swelling of the vulva is a normal response
• Evaluation of the injury requires a complete physical
•
•
to estrogenic stimulation during the follicular stages of the estrus cycle in intact dogs and cats. Typically, vulvar swelling resolves on its own as the female enters diestrus. Persistent or prolonged swelling of the vulva in cycling females may represent prolonged estrogenic stimulation from cystic ovaries or an estrogenproducing ovarian neoplasm, such as a granulosa cell tumor (see Chapter 90). Vulvar swelling in a spayed female dog is also associated with estrogenic stimulation and may be a result from the presence of functional ovarian tissue after ovariohysterectomy (ovarian remnant syndrome; see Chapter 90). • Ovarian remnants are reported more frequently in cats than in dogs, with remnant ovarian tissue more frequently retained at the site of the right ovarian pedicle.
• •
examination, digital vulvar and vestibular examination, episiotomy, or vaginoscopy. Complete examination of the vulva to determine the extent of the injury may require sedation or general anesthesia when the patient is stable. Placement of a urethral catheter and closed urinary collection system may be necessary with severe trauma or swelling of the vulvar or perivulvar region.
Treatment
• Standard care and treatment of local wounds is indi-
Clinical Signs
cated. Flushing of the wounds and surgical debridement may be necessary (see Chapter 56). Primary closure or reconstruction of the vulva may be necessary to prevent narrowing or stenosis as a result of second-intention healing. Placement of a urinary catheter attached to a closed collection system will aid management of wounds in this location.
The vulvar lips appear edematous and turgid on physical examination. A serosanguineous discharge may be noted.
DISEASES OF THE VESTIBULE AND VAGINA
• •
Diagnosis
Congenital Abnormalities
• Vaginal cytology: Evidence of estrogenic stimulation.
Abnormalities in the embryologic development of the urogenital sinus may result in structural malformations affecting the vagina and vestibule, including vaginal septum, persistent hymen, septal remnants, or persistent paramesonephric remnant and vestibulovaginal stenosis. Any of these conditions may prohibit or prevent natural mating or may contribute to the susceptibility of the local environment to chronic or recur-
• •
Smears should contain mostly superficial and anuclear squamous cells. Hormonal evaluation: Evaluation of serum concentrations of estradiol and progesterone may be warranted (see Chapter 90). Abdominal ultrasound examination: Cystic ovarian tissue, ovarian remnants, and ovarian neoplasia may
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rent ascending infections of the urinary or reproductive tracts.
Persistent Hymen, Septal Remnants, Paramesonephric Remnants, and Vestibulovaginal Stenosis Many names are currently being used to describe the persistent vertical bands of tissue located at the opening of the vestibulovaginal junction, including persistent hymen, septal remnants, paramesonephric remnants, and vaginal septum.
Etiology
• If the paramesonephric ducts fail to unite with each
•
•
• •
other or fail to fuse or cannulate with the urogenital sinus, it can result in a vertical septum or annular fibrous stricture at the vestibulovaginal opening. Incomplete fusion of the caudal paramesonephric ducts with retention of a medial partition results in an elongated vertical vaginal band, a vaginal septum, or rarely a bifid vagina. Vertical bands of tissue of varying width are commonly identified at the cingulum, which is the circular opening at the vestibulovaginal junction. These bands can be found in normal female dogs and those with developmental abnormalities of the lower urinary and reproductive tracts. Vertical bands of tissue at the cingulum of the vestibulovaginal junction are seen in almost all patients diagnosed with ureteral ectopia. Vertical or annular bands that narrow or partition the vestibulovaginal junction result in clinical signs associated with mating difficulties.
Clinical Signs Clinical signs of chronic vaginitis, vestibulitis, vaginal discharge, urine pooling, chronic cystitis, or urinary tract infection have been attributed to narrowing of the vestibulovaginal junction in dogs. However, no cause and effect has been clearly identified.
Diagnosis
• A number of diagnostic techniques can be used to eval-
•
uate the vestibulovaginal anatomy, including digital vaginal examination, urogenital endoscopy, and positive-contrast retrograde vaginourethrography. Digital examination can be performed with the patient awake or sedated. • Diagnosis of a hymen or persistent septal remnant is made when two small openings are identified on either side of a centrally oriented band. • For female dogs with an annular or stenotic opening at the vestibulovaginal junction, digital penetration of the cranial vaginal vault is not pos-
•
•
sible. If vestibular or vaginal stenosis is of concern, the bitch should be evaluated under the effects of sedation during estrus, when this opening should be at it widest. Rigid or flexible endoscopy allows examination of the vestibule, vestibulovaginal junction, and cranial vaginal vault region. Fluid insufflation will provide an optically clear environment and provide distension of the local tissues to improve visualization. • Definitive diagnosis of a septum, septal remnant, or annular narrowing at the vestibulovaginal junction is made by endoscopic examination. Positive-contrast retrograde vaginourethrography has recently been advocated as a method to diagnosis vestibulovaginal stenosis in dogs. Controversy exists regarding the specific radiographic measurements necessary to accurately make this diagnosis. No effort has been made to correlate clinical signs and endoscopic and radiographic findings in female dogs with suspected vestibulovaginal stenosis.
Treatment Persistent Hymen or Septal Remnant. Surgical correction of persistent vertical bands of tissue located at the vestibulovaginal junction is indicated in bitches with persistent clinical signs or failure to successfully breed or whelp. ▼ Key Point Surgical excision of the vertical band of tissue at the vestibulovaginal junction is not indicated in asymptomatic patients.
Surgical Procedure: Removal of Persistent Hymen or Septal Remnant 1. Thin and moderately thick bands of tissue can be easily removed using cupped biopsy forceps while examining the area through a rigid or flexible endoscope. 2. Grasp the band with the forceps at its base and separate it from its attachment along the vestibulovaginal junction. 3. Separate the tissue remnant from the opposite base of attachment and remove. 4. Remove thick or broad-based septa via a direct surgical approach using an episiotomy (see Chapter 93) or using a surgical laser.
Annular Bands or Vestibulovaginal Stenosis Complete resection of an annular stricture at the vestibulovaginal junction and anastomosis of the remaining vagina and vestibule is an extremely difficult and time-consuming surgery. A short (2.5 ng/dl is needed to maintain the canine pregnancy. Consider premature luteolysis in bitches having problems with premature loss of puppies when other causes cannot be found. Perform serum progesterone testing periodically (the frequency of testing depends on the results obtained). A drop below 5 ng with greater than 5 days of gestation remaining may require progesterone supplementation. Treat with progesterone in oil, as an injection (2.2 ng/kg IM), or altrenogest (Regu-Mate, Hoechst). Regu-Mate will not show on a serum progesterone test as it is a synthetic product. Progesterone in oil will show on a progesterone test and can be monitored to determine if and when further supplementation is needed.
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▼ Key Point There can be associated birth defects of the vaginal tract in female pups if progesterone supplementation is not used judiciously.
Pyometritis Pyometritis is a disease of the uterus caused by an inflammation of the uterine lining, allowing a secondary bacterial infection. Pyometritis can also be caused by the misuse use of estrogen for mismating while the uterus is under the effects of progesterone. See Chapter 90 for a complete discussion of pyometra in dogs and cats.
Vaginal Wall Edema (Vaginal Hyperplasia)
• Vaginal wall edema occurs during the estrogen phase • • • • •
of estrous cycle is due to fluid uptake by the vaginal tissue. Brachiocephalic breeds, Labradors, and coonhounds are more frequently affected. Ovulation and subsequent decrease in serum estrogen causes regression of tissues. Vaginal edema typically does not cause whelping problems. It may recur during subsequent heat cycles. Treatment consists of preventing trauma and keeping tissue from drying until edema regresses (see Chapters 92 and 93).
• •
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roidism are evident, perform a diagnostic evaluation (see Chapter 31). Be aware of genetic defects associated with any given breed. Individuals to be used for breeding should be tested for as many genetic diseases as possible. Assure adequate immunity for reproductive diseases.
Brucella canis
• Brucella canis is the bacterial organism most com•
• • •
monly associated with abortion in the bitch and orchitis in the male (also see Chapter 19). Since Brucella canis is passed through all body discharges, including urine, individuals should be blood tested for brucellosis even if they are being bred for the first time. Test the bitch for brucellosis before each mating. Test frequently-used males every 6 months, even if only bred to Brucella canis-negative bitches. The rapid slide agglutination test (RSAT) commonly performed as a screening test can have falsepositive results in the 20% range. A negative RSAT does confirm the Brucella-negative status.
▼ Key Point Isolate individuals testing Brucella positive on the RSAT from other dogs until further testing. Agar-gel immunodiffusion, immunofluorescent antibody, and blood culturing for Brucella canis are confirmatory tests for brucellosis.
Pregnancy Diagnosis
Diagnosis See Chapters 90 to 93 for discussion of diagnosis and treatment of diseases of the ovaries, uterus, vagina, and vulva.
Prebreeding Evaluation
• Perform a complete physical examination of both the
•
•
•
brood bitch and the stud dog, including evaluation of the external genitalia. The bitch and stud should be in good health and of good weight. Overweight bitches are associated with conception, whelping, and nursing problems when compared with nonoverweight bitches. The bitch should be free of parasites, appropriately vaccinated, and on heartworm-preventative medication. Heartworm-preventative medication should be continued during pregnancy and after whelping. Routine vaginal culturing without abnormal discharge or signs of inflammation is not justified. • Mycoplasma and ureaplasma are considered normal flora in the vagina. Obtaining routine bacteriologic cultures and treating for mycoplasma or ureaplasma without clinical signs is of no value. Serum thyroid levels are of minimal importance in canine reproduction, whether discussing the male or the female. However, if clinical signs of hypothy-
There is currently no early pregnancy diagnostic test for the canine. Available midgestation techniques include the following:
• Ultrasound—After day 19 post-ovulation • Palpation—Between day 23 and day 30 post-ovulation • Relaxin testing (Witness Test, Synbiotics, San Diego, California)—After day 26 post-ovulation
• Radiography—After day 47 post-ovulation Ultrasound Ultrasound confirms pregnancy and fetal viability. It is typically the earliest method to accurately confirm a pregnancy. Ultrasound is not considered an accurate method for predicting exact litter size.
Palpation Palpation of the caudal abdomen in a relaxed patient can accurately determine pregnancy in many breeds of dogs.
• Palpation is most commonly performed between 21 and 30 days after ovulation.
• Palpation of distinct uterine swellings dorsal and cranial to the bladder typically signifies pregnancy.
• There is a narrow window of opportunity to accurately diagnose pregnancy by palpation. As the
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pregnancy progresses, the uterus enlarges and the individual fetal swellings become less distinct. Palpation as a method of pregnancy diagnosis can be difficult in large or nervous bitches.
Relaxin Evaluation of serum relaxin levels, a hormone produced by the placenta, can accurately confirm pregnancy. However, false negatives can occur in litters of small numbers.
Abdominal Radiography
• Plain abdominal radiographs can accurately determine pregnancy but not until 47 days after ovulation.
• Optimal time for radiographs is 52 to 56 days •
•
A number of methods have been devised based on the type semen being used, the semen quality, the age of the bitch, and the expertise of the veterinarian performing the insemination. Methods of artificial insemination include vaginal, transcervical, and endoscopic or surgical intrauterine deposition of semen.
Collection of Semen Collection of semen from male dogs is routinely performed for vaginal or intrauterine artificial insemination, cryopreservation, extension, and chilling for the purposes of shipping for a distant breeding or for evaluation as a part of the breeding soundness examination.
• Male dogs can be easily collected manually.
post-ovulation to assure mineralization of all fetal skeletons. Abdominal radiography are more commonly performed to determine litter numbers and size of pups. Litter size is determined by evaluating both the lateral and the ventrodorsal views and by counting the skeletal structures of each fetus (spine or calvarium). Radiographic signs indicating possible fetal death or problems include collapsed calvarium, reversed “c” sign, and gas within fetuses.
Treatment Treat any underlying diseases or problems (also see Chapters 90 to 93). Improve management strategies, such as timing of breeding, using the recommendations previously discussed under “Etiology of Nonconception.” If vaginal anomalies are present, correct them if possible (see Chapter 93).
•
•
Estrus Induction
• Clinical research is currently being done using • • •
various categories of drugs to induce ovulatory cycles in the bitch. An interval of 4 months is the minimum anestral interval required. Cabergoline (5 mg/kg PO q24h), a dopaminergic agonist will shorten anestrus by lowering prolactin levels. Desorelin, a gonadotropin-releasing hormone (GnRH) analogue, either as an injection or an implant has shown particularly promising results.
Artificial Insemination Due to disease concerns, cost, and restrictions of airline travel, the shipping of fresh chilled and frozen semen has dramatically increased. Knowledge of techniques for collection, handling, and shipping of semen, as well as methods of artificial insemination, has become essential for successful canine breeding.
•
• The male is stimulated using a non-intimidating female demonstrating clinical signs of estrus. • Semen collection should be performed in a quiet environment. • The ejaculate is collected into a polyvinyl chloride sheath with an attached calibrated collection container. • Manual stimulation of the glans bulbous of the penis permits a semen sample to be obtained. Parasympathetic stimulation produces erection of the penis, and sympathetic stimulation results in ejaculation. The male dog ejaculates three distinct fractions: • First fraction—Prostatic fluid containing no spermatozoa. • Second fraction—Thicker milky white volume that contains spermatozoa. • Third fraction—Clear fluid containing prostatic secretions and no spermatozoa. It is not necessary to collect this fraction. Male dogs can be collected every other day, daily for 5 to 6 days, or twice on 1 day without affecting sperm numbers. Evaluation of semen is essential. Abnormal sperm cannot fertilize ova.
Characteristics of Normal Semen
• Volume—0.5 to 30 ml or more (depends on the length • • • •
of the collection, breed of dog, and size of the prostate) Total count—22 million/kg of body weight Motility—>80% Morphology—60–70%).
Sperm Morphology
• The queen does not show vaginal bleeding during
Microscopic examination of the spermatozoa morphology should be performed as part of the semen evaluation.
• The male cat mounts the queen, biting her neck
this time.
• Primary defects—Greater than 20% of morphologic
•
abnormalities involving the head, neck, and tail can result in reduced fertility. Primary defects occur in the seminiferous tubules during development. Secondary defects—Greater than 20% of morphologic abnormalities that occur after collection, including bent or coiled tails, can also result in reduced fertility. Review collection techniques and sample handling in this situation.
Diagnosis and Treatment See Chapters 86 to 89 for discussion of diagnosis and treatment of testicular and penile diseases in dogs and cats.
• •
•
for stabilization as the erect penis penetrates the vulva. Penile spines on the penis of an intact male stimulate the vaginal receptor sites, triggering LH release. Multiple breedings are needed for complete ovulation and for the best chance of pregnancy. The female cat presents herself to the male with the rear elevated and the tail moved to one side. After the breeding act, the female normally vocalizes and rolls on the floor. The period of male acceptance can vary considerably based on the number of breedings and the LH release. The period of male acceptance can persist for a prolonged period of time (up to 2 weeks or longer) depending on the availability and the breeding aggressiveness of the male.
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Interestrous
• An unbred female will have a normal interestrous •
period of 5 to 14 days before returning to proestral signs. The estrous cycle repeats itself until the female becomes pregnant or the length of daylight shortens enough to return the female to anestrus.
•
Diestrus
• The period of elevated progesterone will last for 45 to 50 days in the pseudo-pregnant female and 60 to 65 days in the pregnant queen.
Diseases of the Breeding Queen See Chapters 90 and 93 for discussion of diseases of the ovaries, uterus, vaginal, and vulva.
Stimulation of Estrus Numerous medical therapies have been described to induce estrus in cats.
• Administration of 2 mg of FSH intramuscularly daily
Diagnosis and Prebreeding Evaluation See “Prebreeding Evaluation” under the canine section in this chapter.
•
• The female should be of good flesh without being •
• •
overweight. A balanced commercial diet should be fed. Females to be bred should be free of viral diseases including feline leukemia virus (FeLV), feline immunodeficiency virus (FIV) and feline infection peritonitis (FIP) (see Chapters 8, 9, and 10, respectively). Vaccinations for upper respiratory diseases and panleukopenia should be current. A good quarantine protocol should be established in a cattery to prevent the introduction of outside pathogens when new individuals are introduced.
prevent injury to the handler when stimulating the female. Vasectomized tom cat—This is the most reliable method of stimulation for the queen to ovulate as the vasectamized tom cat completes the natural breeding act without placing sperm cells in the female. Repeat breedings are necessary (multiple over an 8–24-hour period) to ensure ovulation. Confirm ovulation by detecting a serum progesterone rise, usually 48 to 72 hours after breeding.
until estrus is exhibited (up to 7 days), followed by mating to induce LH release or by injecting human chorionic gonadotropin (250 IU) intramuscularly on day 2 and 3 of estrus or by injecting 25 mg of GnRH intramuscularly. A non-medical method used to induce estrus in the queen may include the use of full spectrum light bulbs to mimic the equivalent of 14 hours of daily sunlight.
Feline Artificial Insemination Collection of Semen
• Collection of the semen for insemination, freezing, •
or evaluation is normally accomplished with an electroejaculator. Electroejaculation is performed under general anesthesia, and the male is pretreated with an antihistamine to diminish the retrograde movement of sperm into the bladder.
Vaginal Insemination
Treatment Inducing Ovulation
• Insemination can be performed using a lacrimal
In situations that require the female to ovulate (e.g., artificial insemination), numerous methods have been attempted.
•
• Hormonal stimulation—Injecting 25 mg of GnRH once
•
a day (Cystorelin, Ceva Labs) or 250 IU of luteinizing hormone or human chorionic gonadotropin (HCG). Administer when the queen shows peak receptivity to a male. The injection may be repeated 24 to 36 hours later. If successful, the queen should show signs of reduced sexual activity in 24 to 48 hours. Vaginal stimulation—Use a moistened Q-Tip or glass rod for repeated stimulation of the vaginal tract receptors to mimic natural breeding may induce ovulation. Vaginal stimulation is most successful when an intact tom is housed nearby as this may have a psychic effect on the female to help stimulate ovulation. Restrain the female (i.e., wrapped in towel) to
catheter with a conical tip or a shortened plastic artificial insemination rod similar to those used in bitches. A maximum volume of less than 0.1 to 0.2 ml is most desirable due to the relative size of the feline vaginal cavity.
Intrauterine Insemination
• Surgical exposure of the uterus for direct deposition
• •
of semen should be considered in queens for which uterine or ovarian disease may be suspected and direct examination is desired. The use of frozen semen has been shown to have the greatest chance of success with direct insemination into the uterus. Intrauterine insemination is performed through a 3to 4-cm caudal abdominal incision to expose the uterus or laprascopically.
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• The semen is injected into the uterine lumen through a 22-gauge hypodermic needle.
Estrus Suppression Progestogens and androgens have been used to suppress the estrous cycle in the queen. However, both methods are associated with negative behavior and deleterious side effects.
•
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toxoplasmosis). Potential surgical examination of the uterus and ovaries may be required to achieve a diagnosis. See Chapter 90 for more information on etiologies, diagnosis, and treatment of abortion in dogs and cats.
SUPPLEMENTAL READING
• The administration of GnRH (25 mg IM) or LH (HCG at 250 IU IM) will induce ovulation in a queen at peak estrus and delay the next cycling for 45 to 50 days.
MALE CAT See Chapters 86 to 89 for diagnosis and treatment of diseases of the testicle, penis, and prepuce.
ABORTION • Fetuses and placentas of the aborted fetuses should
• •
be evaluated grossly, histopathologically, and microbiologically. Microorganisms, genetic defects, toxins, drugs, progesterone deficiencies, and diet have all been described as agents leading to litter loss. The histopathologic evaluation of the placenta for inclusive bodies, dehydration, and signs of inflammation is critical. Culture vaginal discharges and perform serum titers for viral diseases and other microbial agents (i.e.,
Davidson AP, Feldman, EC: Ovarian and estrous cycle abnormalities in the bitch. In Ettinger SJ, Feldman EC (eds): Textbook of Veterinary Internal Medicine. Philadelphia: WB Saunders, 1995, p 1607. Johnston SD: Breeding management of the bitch. In Ettinger SJ, Feldman EC (eds): Textbook of Veterinary Internal Medicine. Philadelphia: WB Saunders, 1995, p 1604. Johnston SD: Infertility in the bitch. In Kirk RW, Bonagura JD (eds): Current Veterinary Therapy XI. Philadelphia: WB Saunders, 1992, p 954. Meyers-Wallen VN: Semen analysis, artificial insemination, and infertility in the male dog. In Ettinger SJ, Feldman EC (eds): Textbook of Veterinary Internal Medicine. Philadelphia: WB Saunders, 1995, p 1649. Oettle EE: Sperm abnormalities and fertility in the dog. In Bonagura JD, Kirk RW (eds): Current Veterinary Therapy XII. Philadelphia: WB Saunders, 1995, p 1060. Shille VM, Sojka NJ: Feline reproduction. In Ettinger SJ, Feldman EC (eds): Textbook of Veterinary Internal Medicine. Philadelphia: WB Saunders, 1995, p 1690. Soderberg SF: Infertility and disorders of breeding. In Birchard SJ, Sherding RG (eds): Saunders Manual of Small Animal Practice. 2nd edition. Philadelphia: WB Saunders, 2000, pp 1050–1059. Verstegen JP, Onclin K, Silva LD, Concannon PW: Effect of stage of anestrus on the induction of estrus by the dopamine agonist cabergoline in dogs. Theriogenology 51(3):597, 1999.
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▼
Section
Chapter
▼
8
95
Skeletal System Matthew Palmisano
Postoperative Physical Rehabilitation Darryl L. Millis
The appropriate postoperative management of small animals undergoing orthopedic or neurologic surgery is critical for a successful outcome. Inadequate surgical and postoperative treatment may result in fracture disease. The appropriate use of physical rehabilitation techniques in combination with pharmaceutical agents is necessary to achieve an optimal outcome.
GOALS OF POSTOPERATIVE PHYSICAL REHABILITATION • Prevent loss of joint range of motion and stiffness • Reduce the deleterious effects of disuse of muscu• • • •
loskeletal tissues Improve the rate of recovery Improve the quality and quantity of movement Enhance the ultimate outcome Enhance performance, conditioning, and endurance
PREOPERATIVE CONSIDERATIONS IN THE REHABILITATION PLAN • Patient’s age and physical condition. Obese patients •
and those with poor cardiovascular condition will require a less aggressive rehabilitation plan. Surgical condition and the repair technique. The stability of the surgical repair helps determine how aggressive the rehabilitation plan may be.
• Presence of concurrent injuries. Animals with multi• •
ple injuries generally undergo a less aggressive rehabilitation plan. Owner compliance. The therapist must consider the ability and willingness of the owner to participate in the rehabilitation plan. Expertise of the rehabilitation team.
PERIOPERATIVE PAIN MANAGEMENT Institute preemptive pain management to allow postoperative therapy to be as comfortable and pain free as possible (see Chapter 6). Effective control of pain and postoperative inflammation allow rehabilitation to begin earlier with more rapid progress to functional activities.
Medications and Techniques • Preoperative butorphanol or morphine. • Epidural opioid analgesia. • Intra-articular administration of local anesthetic agents such as bupivacaine.
• Morphine or buprenorphine are commonly used for immediate postoperative analgesia.
• Nonsteroidal anti-inflammatory drugs (NSAIDs), such as deracoxib or carprofen may be administered prior to or immediately after surgery and continued in the postoperative period in healthy patients free of renal and gastrointestinal disease or bleeding 1027
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tendencies. Knowledge of NSAID pharmacokinetics is important so that dosing strategies take advantage of peak drug effects. Medication is continued for 7 to 14 days after surgery. See Chapter 6 for further discussion of postoperative pain management.
REHABILITATION IN THE IMMEDIATE POSTOPERATIVE PERIOD ▼ Key Point The main objectives in the first 24 to 72 hours after surgery are to provide pain control, reduce joint effusion and tissue edema using cryotherapy, and reestablish normal joint range of motion (ROM) as soon as possible.
If normal motion is not established by 2 weeks, dogs may permanently lose some ROM. Prevention of muscle atrophy is also critical. Early use of the limb with functional weight bearing is the key to returning the patient to function as soon as possible.
Cryotherapy (Cold Packs) • Cryotherapy is the therapeutic use of cold. • The effects of cryotherapy include the following: • • • •
Vasoconstriction Decreased blood flow Reduced cellular metabolism and permeability Attenuation of traumatic or exercise-induced edema • Decreased muscle spasm • Analgesia as a result of decreased sensory and motor nerve conduction velocity
Cryotherapy Devices
• Place crushed ice in a sealed plastic bag and wrap the bag in a thin cloth, such as a pillowcase or towel.
7. A compression bandage, such as a modified Robert Jones bandage, may be applied after cryotherapy to help prevent swelling and edema.
Range of Motion and Stretching Exercises Perform ROM and stretching exercises to help maintain or improve flexion and extension of joints; improve flexibility of muscles, tendons, and ligaments; and help enhance awareness of neuromuscular structure and function. ROM exercises are important in dogs undergoing any joint surgery, especially cranial cruciate ligament rupture stabilization, elbow fractures, and fracture of the distal femoral physis in skeletally immature dogs.
Range of Motion Exercise Technique 1. Place the patient on soft padding in lateral recumbency. 2. Stabilize the limb proximal to the joint. 3. Gently grasp the limb below the affected joint. The closer the hands are placed to the joint, the lower the forces will be that are applied to the joint. 4. Slowly flex the joint over several seconds until there is the first indication of discomfort, such as tensing the limb, turning the head in recognition, or trying to gently push away. Under no circumstances should the animal vocalize in pain or attempt to bite. In general, joint flexion is more comfortable than joint extension. 5. Slowly extend the joint over several seconds until there is the first indication of discomfort. 6. Other motions may be appropriate, such as abduction and adduction or rotary motions, especially of the shoulder and hip. 7. Repeat for 10 to 30 repetitions depending on the animal’s reaction to the motion, 3 to 6 times daily. 8. Do all joints in the affected limb, including the digits.
• Prepare a mixture consisting of two parts water and
▼ Key Point Over-aggressive ROM exercises will
one part alcohol in a double-sealed plastic bag and place it in a freezer. The resulting pack is a frozen slush that conforms to any surface. Use commercially available cold packs. Use circulating cold water cryotherapy units.
result in pain, reflex inhibition, delayed use of the limb, and ultimately more fibrosis of the tissues around the joint.
• •
Cryotherapy Technique 1. Apply to the affected area immediately after surgery during recovery from anesthesia. 2. Apply the cold pack for 15 to 20 minutes. 3. Use caution when applying cold packs to hypothermic or small patients. 4. Apply for 15 to 30 minutes every 6 to 8 hours for the first 3 or 4 days after surgery. 5. Monitor the patient for discomfort. 6. Do not use cryotherapy in patients with poor or absent pain sensation.
The primary objective is to gently flex and extend individual joints through their comfortable ROM. As the animal nears full ROM, more natural gait movement may be instituted by putting all of the joints of a limb through a ROM simultaneously, similar to the motion of riding a bicycle.
Stretching Technique 1. Stretching is often combined with ROM exercises in stiff joints with decreased ROM. 2. Stabilize the limb proximal to the joint, and grasp the limb below the affected joint and gently move it.
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3. At the end range of flexion, hold the position for 15 to 30 seconds. Gradually attempt to increase flexion as long as the patient remains comfortable. 4. Extend the joint, and at the end range of extension, hold the position for 15 to 30 seconds. Gradually attempt to increase extension as long as the patient remains comfortable. 5. The main idea is to stretch and realign soft tissues and collagen, not to tear or damage tissues. 6. Repeat for two to five repetitions, 1 to 3 times daily.
• •
• THERAPEUTIC EXERCISES Therapeutic exercises are an essential part of a physical rehabilitation program, whether a patient is being treated immediately after surgery or for chronic conditions. Therapeutic exercises may be performed by the therapist or as part of a home treatment program with owner involvement. ▼ Key Point When a home exercise program is prescribed, always demonstrate the exercise first and then have the owner demonstrate the exercises for you to ensure that they are properly performed.
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healing tissues. This is especially relevant with the modern analgesic and surgical techniques used, which may result in less pain and attempts to do more activity. Conversely, some patients may need some encouragement if they are not progressing as expected. Do not hurt a patient during exercises or increase the activity level too rapidly. This may result in reflex inhibition and decreased use of the limb, which will ultimately slow progress. Pathologic reasons for delayed recovery should always be ruled out prior to increasing the level of activity.
Assisted Standing These exercises bridge the gap between passive ROM and stretching exercises and more active exercises. They are useful for dogs recovering from neurologic conditions, such as intervertebral disk rupture, or severe musculoskeletal trauma, such as bilateral pelvic injuries. Assisted standing is useful for patients that have adequate strength to bear some weight but are too weak to bear complete weight.
• Position the dog with the feet squarely underneath the body.
Objectives • Improve active pain-free ROM and flexibility • Improve use of limb and reduce lameness • Improve muscle mass and muscle strength • Improve daily function • Help prevent further injury
• Support the animal with a towel or sling. Allow the
Considerations
Proprioceptive Exercises
▼ Key Point It is most important that exercises be
These exercises help animals regain their ability to appropriately use and place their limbs, and they include weight shifting, balance board activities, and Swiss balls or PhysioRolls.
performed correctly, rather than performing many repetitions incorrectly.
• Begin with standing exercises, assisted walking, and
• • • • •
proprioceptive exercises in patients that have serious musculoskeletal injuries, neurologic conditions, or multiple limb involvement. Progress to slow, low-impact activities as the patient gains strength and stamina and is able to support its own weight. As the animal continues to recover, the speed, duration, and number of repetitions may be increased, and more challenging exercises may be added. Vary the routine so that the therapist and patient do not become bored with repetitive exercises. Try different activities to determine what works best in an individual patient. Allow the patient to guide an increase in activity, within reasonable limits. Increased activity must always be considered in response to the time frame of expected tissue healing and the strength of the
dog to bear as much weight as it is able.
• As the animal weakens and begins to slowly collapse, •
lift it back to a standing position with the limbs squarely placed under the body. Start with 10 to 15 repetitions bid–tid, and gradually increase to 5 minutes per session.
Weight Shifting and Perturbation Exercises
• Stand the dog squarely on firm footing. • Place the hands on the side of the dog for support. • Push the dog gently from side to side. In severely
•
affected dogs, some support may be necessary to avoid falling. As the animal regains proprioceptive ability, the shifts may be more challenging. It may be necessary in some dogs to place mild pressure over the pelvis or shoulders to encourage greater stability and weight bearing.
Balance Boards
• Dogs may be placed on a traditional balance board with either the front or the hind limbs on the board, or special balance boards designed for quadruped animals may be made (Fig. 95-1).
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conditions, but they are also frequently performed incorrectly.
• Perform leash walks very slowly to allow the dog an •
• •
• Figure 95-1. A specially made balance board may be used for proprioceptive training.
• Support the dog to avoid injury from falls. • The balance board may be manipulated to rock the dogs from side to side, back and forth, or in all directions.
Side Bending and Cervical Flexion and Extension With the dog standing squarely, use a treat so that the dog follows it from side to side and up and down. The ability to actively move while maintaining balance is the goal.
Swiss Balls and PhysioRolls
• Dogs with severe proprioceptive disability may be • •
•
placed over a properly sized and inflated, large PhysioRoll to help provide support during weight bearing. As strength and ability return, the front half of the dog may be placed on the PhysioRoll, allowing some weight bearing and balancing to occur. To help aid limb awareness and neuromuscular activity, perform rhythmic stabilization exercises by standing the dog on a properly sized ball or PhysioRoll and gently “bouncing” the dog while maintaining support to prevent falling. Animals returning to good function may be challenged by standing the dog on a properly sized PhysioRoll and allowing it to bear weight while maintaining support to prevent falling.
Treadmill Walking Treadmill walking is a useful modality to encourage use of the limb and early gait patterning. The ground moving under the dog often encourages a non–weightbearing patient to begin using limb. Most dogs trained to leash will walk on a treadmill.
• Use a harness or sling to provide support and prevent
• •
•
therapeutic exercise for patients recovering from surgery or affected with chronic musculoskeletal
falls. Sidewalls to prevent stepping off the treadmill, variable speed of the treadmill, a timer, and the ability to change the incline angle are all useful features for canine treadmills. Do not face the treadmill toward a wall. One person may be in front of the dog to encourage it. A person may stand beside the dog to lift and advance an affected limb during the normal gait sequence to encourage proper use of the limb for those patients with severe conditions (gait patterning training). Dogs may initially walk for 1 to 3 minutes, 2 to 3 times per day at a slow speed. If lameness is not worse after activity, increase the exercise increased 10% to 20% per week.
Stair Climbing
• This exercise is useful to improve power in the rearlimb muscles.
• Stair climbing may begin if the repair is stable and •
Slow Walks ▼ Key Point Slow leash walks are the most important
opportunity to bear weight; perform at the speed of the dog, not the handler. For difficult situations, dogs may be gently “bumped” to challenge their balance and encourage touching the limb to the ground at the end of the swing phase of gait for the affected limb. Behavior modification is encouraged to train the dog to use the limb. Praise the dog when it touches the limb down. Initially perform leash walks for 2 to 5 minutes, 2 to 3 times daily. If lameness or limb use is not worse after the first couple of days, gradually increase the length and time of the walks 10% to 20% each week. Dogs may be walked up and down inclines, hills, or ramps to add more challenges and to encourage muscular and cardiovascular fitness.
•
the dog is consistently using the limb at a walk with decreasing lameness over time. Walk the dog slowly up the stairs, being certain that the dog steps up with each limb rather than skipping up steps or jumping up steps by using both rear limbs (“bunny hopping”). If possible, begin with low, gradually rising steps, and progress to increasingly steeper steps.
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• Begin with 5 to 7 steps, and increase to two to four flights 1 to 3 times daily.
• Be certain that lameness is not worse after jogging. • The dog may jog up hills for greater effect if there are no problems jogging on flat surfaces.
Sit-to-Stand Exercises These exercises may be beneficial for dogs with hip dysplasia, a condition in which full extension of the hips is painful (see Chapter 108). Sit-to-stand exercises strengthen the gluteal muscles, but the hip joints only extend to a normal standing position, with no overextension of the hip.
• Back the dog into a corner, with the affected leg
•
•
against a wall. This will encourage the dog to push up evenly with both rear limbs when rising, and not pushing up with a good leg, while pushing the affected leg out from the body. Concentrate on having the dog sit and stand correctly, with both rear limbs flexing equally while sitting, and pushing off evenly with both rear limbs to stand. Start with 5 to 10 repetitions once or twice daily, and work up to 15 repetitions 3 to 4 times daily.
Cavaletti Rails
• Cavaletti rails are raised rails or poles that are spaced
• • •
• These exercises are useful for encouraging lateral
• Wheelbarrowing exercises are designed to improve use of the forelimbs.
• •
dog forward. Dogs with normal proprioception will move the forelimbs so they do not fall. Some dogs with weakness of the forelimbs may require support to prevent them from collapsing. As dogs become stronger and endurance improves, dogs may be wheelbarrowed up and down inclines for greater effect.
Dancing Exercises
• Dancing exercises are designed to improve use and strengthening of the rear limbs.
• Because of the proximity of the handler to the dog’s mouth, apply a muzzle.
• Lift the forelimbs off the ground and move the dog • •
forward or backward. Dogs with normal proprioception will move the limbs so that they do not fall. In some situations, the handler should get behind the dog and place the arms under the axillary region of the dog to support it and walk forward. As dogs become stronger and endurance improves, dogs may dance up and down inclines for greater effect.
Jogging
• Jogging may be initiated in cases in which the fixa•
tion is stable and the dog is walking on the limb with minimal lameness and pain. Begin jogging slowly to improve muscle strength and cardiovascular fitness; 2 to 3 minutes, 2 to 3 times daily, and increase up to 20 minutes, 2 to 4 times daily.
apart on the ground to help increase stride length, limb use, and active ROM of joints. A ladder that is lying on the ground may act as Cavaletti rails. The height of the rails is raised to encourage greater active flexion and extension of the joints (Fig. 95-2). As the animal improves, the rails may be spaced at varying distances to provide challenges to proprioception. Begin with slow walking over the rails, and progress to trotting to add additional challenges to the patient.
Circling, Figure of Eight, Serpentine, and Pole Weaving
Wheelbarrowing
• Lift the rear limbs off of the ground, and move the
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•
•
flexion of the spinal column, proprioceptive training, and weight shifting during gait in preparation for more challenging exercises, such as turning sharply while running. Walk the dog slowly in the desired pattern with frequent changes in direction, encouraging the dog to flex the body and spinal column and pivot on the affected limb. If vertical poles are used, the distance between the poles should be less than the length of the dog to encourage lateral bending of the spinal column and weight shifting.
Muscle Strengthening Activities These exercises concentrate on strengthening muscles to improve power and speed. They include carrying weights, playing ball, and running for short distances at high speed.
• Place strap-on leg weights relatively proximal on the • • •
limb to reduce the muscle force and stress on joints during the early rehabilitation period. As strength and stamina improve, move the weights further distally to provide more challenges. In general, use 0.25-kg, 0.5-kg, 1-kg, and 2-kg weights for small, medium, large, and very large dogs, respectively. Use the weights 2 to 3 times per week during normal walking. Dogs may initially resist the leg weights, but most become accustomed to them and will walk with the weights.
Controlled Ball Playing
• Begin on a relatively short leash or in an enclosed kennel or room to avoid overly explosive activity in the early postoperative period.
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Figure 95-2. Walking over raised Cavaletti rails encourages increased active range of motion of joints and proprioceptive training of the limbs.
• Progress to ball playing in an enclosed area, such as a small dog run or room. As the animal nears full return to function, begin activity on a long leash, and if there are no problems, begin off-leash activity in a safe environment.
• The goal is to exercise for 30 to 40 minutes twice daily, with some of the time spent jogging.
• Initiate swimming at a later time, generally 4 to 8 weeks after surgery. Swimming may be too stressful for some surgical procedures to begin earlier than this.
Aquatic Exercises
• Begin aquatic exercises when the incision is sealed.
• • •
Gently test the incision to be certain that the edges do not separate. Do not perform aquatic exercises in patients with drainage from the incision, active infections, or if the incision is not sealed. Walking on an underwater treadmill may begin by day 5 to 7 after surgery in many patients. Fill the water level to the level of the elbow, and set the treadmill at a slow, comfortable walking pace for the dog. Initially walk dogs at a slow speed for 1 to 5 minutes, 2 to 3 times per day, gradually increasing the speed and length of activity as the patient allows.
SUPPLEMENTAL READING Bockstahler B, Levine D, Millis DL (eds): Essential Facts of Physiotherapy in Dogs and Cats. Vet Verlag, 2004. Levine D, Millis DL, Marcellin-Little D, Taylor RA (eds): Small Animal Physical Rehabilitation. Veterinary Clinics of North America: Small Animal Practice. Elsevier, scheduled publication November 2005. Millis DL, Levine D, Taylor RA (eds): Canine Physical Therapy and Rehabilitation. WB Saunders (Elsevier), 2004.
Chapter
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96
Fractures of the Skull Mark M. Smith
Fractures of the zygomatic arch require surgery if they interfere with mastication or compress ocular structures. The most common extracranial fracture requiring surgery is a depression fracture of the frontal sinus. Intracranial fractures that require surgery are those that depress into brain parenchyma, causing significant compromise of cerebral function. Most skull fractures are amenable to conservative management. Weigh the complications of general anesthesia in a neurologically compromised patient against the positive effects of surgical intervention. Fine motor movement is not necessarily required of small animal pets; therefore, intracranial surgery rarely is performed.
ZYGOMATIC ARCH FRACTURE Preoperative Considerations • Before anesthesia and surgery, perform a complete neurologic examination on all head trauma patients.
• General anesthesia may alter intracranial pressure •
• ANATOMY Zygomatic Arch • The cranial portion of the zygomatic arch is formed
•
by the zygomatic bone, and the caudal portion is formed by the zygomatic process of the temporal bone. The zygomatic arch forms the ventral and lateral rim of the orbit.
Calvarium • The dorsal sagittal crest courses craniocaudal over • • • • •
the calvarium. The nuchal crest courses mediolateral over the caudal edge of the skull. The frontal sinus of the frontal bone comprises the frontal encasement of the brain. The diploic calvarium has two distinct cortical bone layers between which is an interstitial layer of honeycombed bone and vessels. The brain is encased by the frontal, parietal, temporal, and occipital bones. The temporalis muscles cover almost the entire calvarium.
•
•
(ICP), leading to exacerbation of intracranial edema and/or hemorrhage. To reduce ICP, consider hyperventilation (to reduce PaCO2), osmotic agents, corticosteroids, and an anesthetic protocol including barbiturates (see Chapter 2). Obtain skull radiographs to document fracture displacement and to screen for other, less apparent fractures. If possible, perform radiography immediately before surgery, thus avoiding the necessity for, and risk of, two separate anesthetic procedures. If available, computed tomography (CT) provides the most accurate assessment of the presence and severity of skull and cranial fractures. CT views avoid superimposition of overlying bone that makes the interpretation of plain skull radiographs difficult. Confirm the presence of an intact optic nerve and vision before surgery. Surgery for a zygomatic arch fracture may be contraindicated if ocular function is irreversibly impaired.
▼ Key Point Acepromazine may lower the central nervous system (CNS) seizure threshold, and ketamine increases cerebral blood flow. Do not use these drugs in patients with a history of brain trauma.
Surgical Procedure Objectives
• Reduce fractures that can cause compression of the eye or cosmetic deformity.
• Avoid trauma to the zygomaticotemporal and zygomaticofacial nerves.
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▼ Key Point Non-displaced fractures of the zygo-
• If normal function is inhibited or pain persists, resection of the affected segment of the zygomatic arch is indicated. Reconstruction of the muscle tissue provides acceptable appearance and function.
matic arch have a good prognosis for uncomplicated healing with conservative management.
Equipment
• • • • •
Standard general surgical pack and sutures Gelpi or Weitlaner self-retaining retractors Sharp periosteal elevator Small Steinmann pins and orthopedic wire (multiple sizes, 18–24 gauge) Small malleable retractor
Prognosis • The prognosis is good with conservative management.
• With operative management, the prognosis is good to excellent.
Technique 1. Place the patient in ventral recumbency with the head supported. Attach tape to the mandibular canines and the table to secure the head position. 2. Prepare the periocular area for aseptic surgery. Ocular lubricating ointment avoids corneal damage from antiseptic agents. 3. Incise the skin directly over the zygomatic arch. 4. Incise and elevate the periosteum using a sharp periosteal elevator. Be careful to avoid the zygomaticotemporal and zygomaticofacial nerves (medial to the zygomatic bone). 5. Use a small malleable retractor to protect the orbit. 6. Reduce and secure fracture fragments using orthopedic wire (18–24 gauge, depending on the size of the animal). Small pins may be used to make holes in the bone for wire placement. Small orthopedic plates may be required to maintain reduction in extremely comminuted fractures or when cosmesis is of paramount importance. ▼ Key Point Do not use small pins as a component of the definitive repair, because pin migration following surgery may cause ocular and intracranial trauma.
7. Appose subcutaneous tissues in a simple interrupted pattern (absorbable suture). 8. Subcuticular sutures (absorbable suture) provide skin apposition and avoid suture irritation of ocular structures.
Postoperative Care and Complications Short Term
• Perform serial neurologic examinations to monitor changes in neurologic status.
• Monitor for clinical signs of seroma and infection. Long Term
• Excessive bony callus may compress ocular structures and interfere with mastication.
• Periarticular fractures may lead to degenerative joint disease of the temporomandibular joint (TMJ) and bony ankylosis.
EXTRACRANIAL FRACTURES Extracranial fractures include fractures of the nuchal crest, sagittal crest, and frontal sinus.
Preoperative Considerations See “Zygomatic Arch Fracture.”
Surgical Procedure Objective
• Maintain reduction of severely displaced fractures of the nuchal crest, sagittal crest, and frontal sinus. ▼ Key Point The cranial muscle mass usually prevents severe fracture displacement and provides enough fracture stability to allow conservative management of most extracranial fractures.
Equipment
• • • •
Standard general surgical pack and sutures Gelpi or Weitlaner self-retaining retractors Sharp periosteal elevator Small Steinmann pins and orthopedic wire (multiple sizes, 20–24 gauge)
Technique 1. Place the patient in ventral recumbency with the head supported. Attach tape to the mandibular canines and table to secure the head position. 2. Prepare the fracture area for aseptic surgery. 3. Make a skin incision directly over the fractured bony prominence. 4. Elevate the periosteum to allow anatomic reduction. 5. Frontal sinus fractures usually are depressed, requiring elevation and fixation with orthopedic wire. 6. Reduce and fix nuchal and sagittal crest fractures with orthopedic wire. ▼ Key Point Do not use small pins as a component of the definitive repair because pin migration following surgery may cause ocular or intracranial trauma.
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7. Appose muscle fascia and subcutaneous tissues in individual layers, using absorbable suture in a simple interrupted pattern. 8. Close the skin similarly, using non-absorbable suture.
Postoperative Care and Complications
• Comminuted calvarial fractures may lacerate meninges, venous sinuses, or the cerebral cortex.
• Calvarial fractures usually are associated with CNS
•
Short Term
• Perform serial neurologic examination to monitor for change in neurologic status.
• Monitor for clinical signs of seroma and infection. • Subcutaneous emphysema may occur secondary to frontal sinus fracture. Whether management of the fracture is surgical or conservative, a compressive bandage minimizes continued formation of subcutaneous emphysema until organized hematoma and fibrin deposition provide a functional barrier to air migration from the frontal sinus. Thus, bandaging is recommended for 2 to 4 days.
compromise. Medical management of CNS trauma is indicated before diagnostic procedures requiring anesthesia. Progressive deterioration in CNS status despite intensive medical management is an indication for skull radiography to determine fracture severity.
Surgical Procedure Objectives
• Elevate depressed calvarial fractures that may cause extensive functional loss of cerebral mass.
• Remove large comminuted fragments of the calvarium that may cause cerebral laceration. ▼ Key Point Linear and minor depressed intracranial fractures are best managed conservatively.
Long Term
Equipment
• Fractures usually heal without complications, provid-
• • • •
•
ing acceptable cosmesis. Most complications are related to CNS trauma, such as seizures (see Chapter 127).
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Standard general surgical pack and sutures Gelpi or Weitlaner self-retaining retractors Sharp periosteal elevator Pneumatic or electric bur drill
Technique
INTRACRANIAL FRACTURES Preoperative Considerations • Preoperative anesthetic and neurologic concerns are similar to those for zygomatic arch fractures.
• Fractures may be linear cracks, depressed bony fragments, or comminuted separate bony fragments.
• Intracranial fractures are usually closed fractures.
1. Place the patient in ventral recumbency with the head supported. Attach tape to the mandibular canines and table to secure the head position. 2. Prepare the dorsal skull area for aseptic surgery. 3. Make a dorsal incision (Fig. 96-1A). 4. Incise the superficial temporal fascia and elevate the temporalis muscle ventrally to expose the fracture area (Fig. 96-1B). Skin incision
A
B
Figure 96-1. Procedure for repairing intracranial fracture. See text for explanation.
Reflection of temporalis muscle to expose defect
D Bur holes placed around fragment
C
Elevation of fragments
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5. Drill multiple small bur holes through the calvarium around the periphery of the fracture area to allow elevation of the fracture fragments (Fig. 96-1C). 6. Elevate fragments with a small, blunt elevator (Fig. 96-1D). 7. Remove any large comminuted fragments that may cause laceration. Despite the potential for large calvarial defects, replacement of the temporalis muscle provides adequate coverage. 8. Replace the temporalis muscle and appose the superficial fascia using absorbable suture in a simple interrupted pattern. 9. Close the subcutaneous layers similarly, followed by skin closure using non-absorbable suture in a simple interrupted pattern. ▼ Key Point Meticulous, atraumatic surgical technique, prevention of cerebral edema, and removal of hematoma if calvarial fragments are removed are of the highest priority when operating on intracranial fractures.
Postoperative Care and Complications Short Term
• Perform serial neurologic examinations to monitor for change in neurologic status.
• Monitor for clinical signs of seroma and infection.
Long Term
• Bony healing occurs without complication; however, neurologic recovery depends on the location and severity of the original traumatic incident.
Prognosis • With cranial fracture repair, the prognosis is good. • For neurologic recovery there is a guarded prognosis. SUPPLEMENTAL READING Dulisch ML: Skull and mandibular fractures. In Slatter DH (ed): Textbook of Small Animal Surgery. Philadelphia: WB Saunders, 1985, p 2286. Newton CD: Fractures of the skull. In Newton CD, Nunamaker DM (eds): Textbook of Small Animal Orthopaedics. Philadelphia: JB Lippincott, 1985, p 287. Oliver JE: Craniotomy, craniectomy, and skull fractures. In Bojrab MJ (ed): Current Techniques in Small Animal Surgery. Philadelphia: Lea & Febiger, 1975, p 359.
Chapter
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97
Fractures and Dislocations of the Mandible Richard M. Jerram
Mandibular fractures account for approximately 2% of all fractures in dogs and 15% of all fractures in cats. Most mandibular fractures occur as a result of automobile trauma, although dog bites and gunshots are also reported causes. Pathologic fractures can occur with severe dental or metabolic disease. Young cats and dogs (F Palate
30–40 12 M>F Buccal Mucosa Common Common Poor Poor–fair Poor
5 9 F>M Rostral Mandible Never Never Excellent Excellent Excellent
Rare Occasional Fair Fair Fair
FSA; fibrosarcoma; MM, malignant melanoma; SCC, squamous cell carcinoma.
study, 40% of dogs with oral melanoma had normalsized lymph nodes and had evidence of metastasis to the lymph nodes on cytologic evaluation.
cal planning. These imaging modalities are especially helpful in evaluating caudal maxillary tumors or tumors involving the orbit, zygoma, TMJ, or vertical ramus of the mandible.
TUMOR TYPES
Biopsy
• Perform an incisional biopsy before surgery to obtain a definitive diagnosis. ▼ Key Point Obtain a tissue biopsy of any suspicious oral lesions. Early detection is critical to successful treatment.
• Biopsy is very important in determining the treat-
•
ment, as well as the long-term prognosis, for the pet. Many oral tumors do not exfoliate easily, so fineneedle aspiration is usually not helpful. A wedge biopsy for histopathologic examination is necessary for a definitive diagnosis. Obtain fine-needle aspirates for cytology or histopathologic evaluation via biopsy of all enlarged, submandibular, or pharyngeal lymph nodes to look for metastatic disease. Perform fine-needle aspiration even on normal-sized regional lymph nodes. In one
Benign Non-odontogenic Neoplasms Epulis Epulides are fibrous tumors originating from the periodontal ligament. They are rarely seen in the cat but are one of the most common oral tumors seen in the dog. There is no sex predisposition, and a familial predisposition has been noted in the boxer. Three types of epulides are characterized, based on histopathologic evaluation:
• Fibromatous epulis is a benign, noninvasive growth in
•
which the periodontal ligament stroma is the predominant cell type. These epulides are pedunculated and often multiple. Ossifying epulides have a similar biologic behavior to fibromatous epulides, but histopathologically they have an osteoid component. Malignant transformation to osteosarcoma has been reported.
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• Acanthomatous epulis is the most aggressive of the epulides. This type of epulis is characterized by extensive bony invasion into the alveolar bone and is most often seen in the rostral mandible. Acanthomatous epulides can become quite large but do not metastasize. However, approximately 30% of acanthomatous epulides undergo malignant transformation.
Treatment and Prognosis
• Since epulides are local tumors, they can be treated
•
with aggressive curettage of the alveolar socket (with fibromatous and ossifying epulides). However, a better outcome can be achieved with en bloc resection of the tumor and surrounding bone. En bloc resection is recommended with acanthomatous epulides due to their extensive bony involvement. Recurrence rate is high if the tumor is only debulked, and a complete resection is considered curative. Radiation therapy of epulides without surgery can be effective and is often curative. Large or incompletely excised epulides can be treated with surgery, followed by postoperative radiation therapy. Chemotherapy is generally not effective for epulides.
Other Benign Non-odontogenic Neoplasms Other rarely seen, benign non-odontogenic neoplasms include fibroma, hemangioma, lipoma, chondroma, osteoma, and histiocytoma. These tumors look grossly similar and require biopsy for histopathologic evaluation.
Malignant Non-odontogenic Neoplasms Malignant Melanoma Malignant melanoma is characterized by local invasion and early metastasis. They can be darkly pigmented (melanotic) or non-pigmented (amelanotic). Oral melanomas are often ulcerated and necrotic, so clinical signs frequently seen are halitosis and oral bleeding. Dogs with more heavily pigmented oral mucosa, such as the chow, are predisposed to malignant melanoma. Malignant melanoma is found (in order of decreasing frequency) on the gingival, buccal and labial mucosa, hard palate, and tongue.
• Newer therapies, such as immunotherapy, have shown some promise in treatment. ▼ Key Point Overall prognosis with oral melanomas is poor, with a 30 degrees (often occurring in miniature breeds) indicates lateral retinacular laxity and the need for lateral imbrication. Patellar luxation procedures vary; some animals require only one step, whereas others need combined procedures. In some cases, combined parapatellar arthrotomy and release is necessary (to release means to diminish the pull or tension on tissue, often accomplished by incising perpendicularly to the line of tension). In other cases, combined arthrotomy and imbrication is needed (to imbricate means to tighten, either by suturing alone or by excision and subsequent closure of tissue).
Surgical Procedures Objective
• Stabilize the patella anatomically in the trochlea while maintaining the full range of pain-free motion.
Equipment
• Standard orthopedic surgical pack and suture
• • •
•
•
patella luxates and whether the tissues opposite the luxated side are very lax. If the former is present, perform combined parapatella arthrotomy and release to diminish the pull of the tissues. If the latter is present, combined arthrotomy and imbrication is indicated to tighten the lax side. With an adequately deep trochlear groove and no excessive tibial rotation, a release may be the only step needed to maintain the patella in its anatomic position. With a shallow trochlea, deepening can be accomplished by trochleoplasty, chondroplasty, or wedge resection. Techniques in which the articular cartilage is preserved (e.g., wedge resection) are preferred over those in which articular cartilage is not preserved. Correct excessive medial rotation of the tibia with a lateral antirotational nylon suture (fabella to tibial tuberosity drill hole; see Fig. 110-4) or by translocation of the tibial tuberosity laterally.
Techniques Trochleoplasty 1. Following arthrotomy and inspection of the stifle, mark the medial and lateral boundaries of the planned trochlear groove by longitudinal cuts in the trochlear cartilage using a scalpel blade. To prevent fracture, try to obtain as much width and height as possible without weakening the remaining condylar bone. 2. Remove the articular cartilage within the marked lines by power burring or with a rongeur. 3. Reduce the luxated patella for a trial fit and, if necessary, smooth the new surface with a fine, halfround file, or rasp. The depth of the new trochlea should accommodate the patella so that one-half to two-thirds of the patella’s height is in the groove. 4. Verify depth, smoothness, and stability by palpating the patella while putting the joint through its range of motion (flexion and extension with internal and external rotation of the tibia). 5. Close the synovia and joint capsule with appropriately sized monofilament nylon sutures in an interrupted cruciate pattern. If possible, perform partial-thickness closure whereby the suture is not within the joint. Close skin and subcutis routinely.
material
• Preferably power bur, oscillating saw, and drill or • Double-action rongeur, bone curettes, and fine •
handsaw (hacksaw or Exacto saw #236), file, or rasp Sharp osteotomes and mallet
Postoperative Care
• Begin physical therapy, consisting of ice packs and
Surgical Principles
• Reduce the patellar luxation and determine whether the tissues are tight on the side toward which the
•
gentle, passive flexion and extension to half the normal range of motion on the day of surgery. Twenty repetitions 4 to 6 times daily are recommended. Swimming after suture removal is permitted. Restricted activity (leash walking only, no stairs, no ball playing, etc.) for 1 month.
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• Give analgesics as needed (Bufferin, 10 mg/kg PO bid; Carprofen, Rimadyl, 2.2 mg/kg PO bid; Deracoxib, Deramaxx, 2–4 mg/kg PO sid, with food). (See Chapter 6.)
Chondroplasty 1. Make a trochlear outline, as described for trochleoplasty, down to subchondral bone (Fig. 110-3). 2. Using a thin, sharp, curved osteotome (Zimmer #2881-00-01, #2881-00-02) perform an osteotomy and create a rectangular cartilage flap with the hinge either proximally or distally. Include 1 to 2 mm of bone in the thickness of the flap. 3. Remove underlying bone with power burring, a bone curette, or a rongeur. 4. After adequate depth is obtained, press the flap manually into the new groove. Pressure from the patella helps keep the flap in position. 5. Close the skin and subcutis routinely.
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3. The shallowness of the trochlea determines the width of the next two saw cuts, which are parallel and peripheral to the first cuts. Remove these two pieces of bone. Place the trochlear segment with its intact cartilage into the recess; this results in a deeper trochlea with preservation of most of the articular surface. 4. Pressure of the articulating patella ensures good contact of the osteotomized segment. 5. Close the skin and subcutis routinely. Postoperative Care
• Perform physical therapy and administer analgesics, as described for trochleoplasty. ▼ Key Point Use caution with this technique in immature animals with open physes. Premature closure may occur; therefore, it is better suited for animals older than 8 months.
▼ Key Point This technique is best used in dogs less than 6 months of age in which the mineralized tissue is relatively soft and pliable for creating a flap.
Postoperative Care
• Perform physical therapy and administer analgesics, as described previously for trochleoplasty.
Wedge Resection 1. Make a trochlear outline as described for trochleoplasty. 2. With a power saw or fine handsaw, make two pieshaped cuts at the peripheral borders previously outlined. Medial and lateral condylar osteotomies should meet centrally. Remove this central piece of bone and articular cartilage and place it in a bloodsoaked sponge.
Imbrication After the depth of the trochlear groove is reestablished, reevaluate the status of tibial rotation. If there is medial or lateral rotary instability, perform imbrication of the lax side using one of several techniques. 1. DeAngelis technique (fabella to patellar tendon; Fig. 110-4, left): Using non-absorbable monofilament suture, place mattress pattern sutures around the medial and lateral fabellae and running extracapsularly, engaging the distal patellar tendon. 2. Flo technique (see Fig. 110-4, right): Place the proximal aspect of the sutures similarly, but distally engage the proximal tibia through a transverse drill hole in the tibial tuberosity. 3. Place additional sutures, if needed, in a fan-like pattern, originating at the fabella and engaging the parapatellar tissue.
Fabella
Patellar tendon
Figure 110-3.
Chondroplasty procedure. See text for details.
Figure 110-4. Imbrication techniques of DeAngelis (left) and Flo (right). These techniques are used for cruciate stabilization and for antirotation purposes with patella luxations.
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Alternative method Figure 110-5. Tibial tuberosity transposition: A, Area of partial osteotomy of tibial tuberosity is shown in color; the cranial tibial muscle is reflected. B, The newly positioned segment is wired in place. Alternate fixation method: (inset) Kirschner wires holding osteotomized tibial tuberosity in transposed position.
A
B
4. Alternatively, scarify the retinacular tissue with the scalpel blade and use a Lembert suture pattern to place several bilateral parapatellar sutures. 5. If there is redundant tissue on one side of the patella after reduction, make two elliptical incisions through retinaculum, capsule, and synovia. Remove the redundant tissue and imbricate using routine closure or a vest-over-pants suture pattern.
new location of the insertion of the patellar tendon should realign the forces to maintain the patella in position, assuming other disruptive forces have been corrected. 6. If the new position is not closely adjacent to the osteotomy site, insert Kirschner wires (Fig. 110-5B), a tension band, or a lag screw obliquely for stable fixation.
▼ Key Point As a rule, when suturing is the main com-
▼ Key Point Exercise great care in young animals not
ponent of imbrication, physical therapy should be gentle to diminish stress upon the suture material and allow adequate time for tissue healing.
Tibial Tuberosity Translocation Equipment
• Osteotome and mallet or a dental molar cutter • Orthopedic Kirschner wires Technique 1. Perform medial and lateral parapatellar arthrotomies. For lateral translocation, reflect cranial tibial muscle. 2. With an osteotome, mallet, or molar cutter, make an osteotomy of the tibial tuberosity, leaving the soft tissue still attached distally if possible (Fig. 110-5, center). 3. Hold the osteotomized tibial tuberosity in position with a bone clamp (Synthes 399.07) after creating a bed in the tibia by roughening the site with a rongeur or curette. 4. Using a power or hand drill, make two small holes through the newly positioned osteotomized segment and through the base of the tibial tuberosity (see Fig. 110-5). 5. Place an appropriately sized (20–22 gauge) orthopedic wire through the holes in a mattress pattern and twist tightly medially to secure the bone in the new site. Cut the wire, leaving two to three twists. The
to cause physeal growth arrest by inappropriate placement of Kirschner wires through the proximal tibial growth plate.
7. If the wire ends cause skin irritation, they may be removed after bony union has occurred. ▼ Key Point Because
medial and lateral rotary instability and laxity contributes significantly to malalignment of the tibial tuberosity, correction of the laxity by imbrication (Flo technique) may eliminate the need for transposition of the tuberosity.
CRANIAL CRUCIATE LIGAMENT RUPTURE Diagnosis • The history usually reveals an acute onset of rear-limb lameness, particularly during exercise.
• Chronic and persistent lameness may also be seen, especially in older, overweight dogs.
• Firm swelling of the medial aspect of the joint can be palpated when a chronic cruciate ligament (CL) rupture is present.
Diagnostic Manipulations Two diagnostic manipulations can confirm abnormal cranial movement of the tibia at the stifle.
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Cranial Drawer
• Position the thumbs on the caudolateral aspect of the
• •
•
• • •
stifle so that the lower thumb engages the head of the fibula while the upper thumb is placed in the region of the lateral fabella or the edge of the lateral femoral condyle. Wrap the other fingers of the upper hand around the cranial aspect of the lower thigh, keeping the femur motionless and the patella in the trochlear groove. Test the cranial laxity of the stifle joint with the tibia in modest flexion (15–30 degrees) (Lachman test) and in 45 to 90 degrees (or more) of flexion (cranial drawer sign). Do not test for cranial drawer with the stifle in full extension. The medial and lateral collateral ligaments will tighten in this position, thereby limiting cranial translation of the tibia. With complete rupture of both bands of the cranial CL, cranial laxity is detected at each position. With partial rupture, laxity may be detectable at only one of these positions. Severity of laxity is subjectively ranked in 2-mm increments (e.g., 1+ = 2 mm, 2+ = 4 mm, 3+ = 6 mm, and 4+ = 8 mm) of cranial displacement (translation) of the tibia on the femur.
Tibial Compression
• Use one hand to hold the femur motionless, with the • •
index finger resting on the tibial tuberosity; gently dorsiflex the hock with the other hand. The gastrocnemius muscle will tighten and, when cranial CL laxity is present, the tibia can be felt to move cranially under the index finger. In our experience, the cranial drawer test is more consistent than the tibial compression test. However, perform both tests. A diagnostic impression is obtainable in 90% of anesthetized dogs if proper positioning and a calm approach are used.
Preoperative Considerations • Obtain preoperative stifle radiographs to document
•
joint effusion, extent of degenerative joint disease, normal fabellae, and avulsions of the ligamentous attachments. To rule out predisposing or concurrent diseases, consider obtaining a routine laboratory database of complete blood count (CBC), serum chemistry profile, and urinalysis.
Comparison of Surgical Techniques for Cranial Cruciate Ligament Repair Much debate currently exists regarding the optimal method for cranial CL repair. Subjectively, more surgeons are turning to tibial plateau leveling osteotomy (TPLO) for repair due to the perceived earlier return to function and more complete weight bearing.
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However, objective studies showing a statistically significant difference between the lateral imbrication techniques and the TPLO are lacking. Some studies have shown an improved return to function with the lateral imbrication and TPLO procedures over intracapsular repairs. The choice of surgical techniques largely depends on surgeon preference, which is related to success with the various techniques and comfort level. One study showed 36% of surgeons use the lateral retinacular imbrication technique as the primary method of repair, while 13% routinely performed the fascial strip “over-the-top” technique and 25% performed the TPLO.
Surgical Procedures • The procedures to correct CL rupture are broadly
•
•
classified as either intracapsular (stabilization from within the joint) or extracapsular (stabilization outside the joint). Intra-articular repairs utilize autogenous or synthetic materials to re-create an intact cranial CL. Examples of intracapsular repairs include patellar tendon techniques, over-the-top repairs, and under-and-over repairs. While many intracapsular repairs are still performed today, subjective and more recent objective data suggests that these repairs may be inferior to the extracapsular techniques, such as the lateral imbrication technique and TPLO. This is especially true in largebreed dogs.
Objectives
• Visually assess the extent of joint damage. • Slow the progression of degenerative joint disease by stabilizing the joint.
• Reduce or eliminate the drawer sign. • Inspect the meniscus for tears (usually caudal horn of medial meniscus).
Equipment
• Standard orthopedic pack and suture • Intramedullary pin pack • Orthopedic wire passer Techniques Fascial Strip Over-the-Top Technique 1. The fascial strip over-the-top technique is an intracapsular repair and is most suitable for dogs weighing less than 40 lb. 2. Place the dog in dorsal or lateral recumbency and prepare the stifle for aseptic surgery. 3. Make a cranial skin incision extending from 2 inches above the patella to the tibial crest. 4. Perform a craniolateral arthrotomy with formation of a distally based fascial strip. For adequate bio-
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5. 6.
7.
Figure 110-6. Fascial strip over-the-top technique for repair of cranial cruciate rupture. See text for details.
mechanical strength, make the width of the strip 2 to 3 times the width of the patellar tendon. The length needed is twice the distance from the proximal patella to the tibial tuberosity. The base of the strip is at the level of the joint line. 5. Cut the fascial strip proximally and insert it, lateral to medial, through a fat pad tunnel made with a hemostat (Fig. 110-6). Enter the caudolateral joint capsule caudal to the lateral fabella and gently advance the hemostat through the intercondylar notch, keeping the hemostat tip lateral to the caudal CL. Grasp the proximal end of the graft in the joint and pull it through the intercondylar notch lateral to the caudal CL and over the top of the lateral condyle. Make a small incision through the joint capsule, pull the fascial strip through it, and secure it to the capsular reflection onto the lateral femoral condyle with six to eight monofilament nylon sutures (2-0) with the appropriate tension to achieve a minimal drawer sign. 6. Close the arthrotomy incision with interrupted absorbable suture material. Complete closure may not be possible distally, depending on the width of the graft harvested. 7. Routinely close the remaining tissues.
Lateral Retinacular Imbrication Technique The lateral retinacular imbrication technique is the most common extracapsular technique performed in practice and can be performed in any size patient. 1. Place the dog in lateral recumbency and prepare the stifle for aseptic surgery. 2. Make a lateral parapatellar skin incision. 3. Perform a lateral arthrotomy. The cranial CL and meniscus are evaluated and debrided if torn. 4. Separate the lateral joint capsule from the biceps femoris muscle. Severe the distal insertion, and
8.
reflect the biceps femoris fascia caudally as far back as the lateral head of the gastrocnemius muscle. Close the joint capsule using interrupted absorbable suture material. Drill a hole in the tibial tuberosity with an intramedullary pin that is larger than the diameter of the suture material chosen. Drill the hole medial to lateral, just caudal to the tibial insertion of the straight patellar ligament. Pass an orthopedic wire passer (Small Graft Passer, Jorgensen Labs, Loveland, CO) around the lateral fabella. The pointed tip of the wire passer is started between the gastrocnemius muscle and the lateral femoral condyle just distal to the lateral fabella. It is pushed around the fabella and allowed to penetrate through the musculature just proximal to the fabella. Placed appropriately sized nylon leader line (NLL) through the slot in the wire passer, and pull the passer around the fabella, taking the suture material with it. One to two strands of either 80 or 125-lb test NLL are most suitable for elimination of cranial drawer.
▼ Key Point Use one strand of 80-lb test NLL in dogs 8 years of age). Therefore, identify other concurrent diseases and treat accordingly. Amputation of a limb is often difficult for owners to accept. Prior to surgery, explain the functional and cosmetic changes resulting from amputation. Most patients function very well after amputation, and cosmesis is acceptable. One study found a direct relationship between owner satisfaction and long-term survival. Most clients were happy with their decision to amputate their pet’s limb if the pet lived a longer, goodquality life.
6.
7. 8.
Surgical Procedures Thoracic Limb Amputation with Removal of the Scapula Use this technique when the tumor involves the humerus or scapula. Scapulohumeral joint disarticulation can be performed when the scapula is not involved, but it is technically harder to perform than amputation with scapula removal. Thoracic limb amputation at midhumerus is technically easier to perform and causes less blood loss than removal of the scapula because it requires no major muscle belly transection. However, owners often find this procedure cosmetically unacceptable, because both the proximal humerus and scapula are easily visible as the muscles atrophy after surgery.
Objectives
• Complete tumor resection with wide margins of normal tissue
• Minimize blood loss • Close or drain large areas of dead space Equipment
• Standard general surgery instruments and suture • Electrocautery • Closed suction drainages (preferable) or Penrose
9. 10. 11.
scapula, and abduct the latter from the chest wall (Fig. 116-2C,D). Sever the common insertion of the latissimus dorsi, teres major, and cutaneous muscles from the teres tubercle of the humerus. The axillary lymph node can be identified at this location, and should be removed and submitted for evaluation of metastasis. Ligate and divide the thoracodorsal artery and vein and cut the thoracodorsal nerve. Further abduct the scapula and rotate it medially. Ligate and divide the axillary and lateral thoracic arteries and the brachial and axillary veins. a. To avoid pooling of large amounts of blood in the limb, double-ligate arteries before veins. Ligate veins first if dissemination of disease is a major concern (Fig. 116-3, top). Transect the brachial plexus of nerves with scissors or a scalpel. Complete the amputation by cutting the pectoral and cleidobrachialis muscles away from the humerus (Fig. 116-3, bottom). If dead space cannot be closed, place a closed suction drain (e.g., Jackson-Pratt) or passive drain (Penrose). Routinely close the muscles, subcutaneous tissues, and skin (Fig. 116-4). Make sure to eliminate dead space during closure, and do not close tissues under tension.
Pelvic Limb Amputation at Midfemur Use this procedure when the tumor does not involve the femur. This method provides a stump, which provides lateral protection of genitalia in males.
Objectives
• Same as for thoracic limb amputation. Equipment
• Same as for thoracic limb amputation, plus
drains
• Bone cutting instrument (oscillating saw, Gigli wire, bone cutting forceps)
Technique
Technique
1. Place the dog in lateral recumbency and aseptically prepare the entire leg and chest wall for surgery. 2. Incise the skin along the spine of the scapula to the greater tubercle of the humerus. Carry the incision circumferentially to the medial side of the shoulder joint. 3. Ligate and divide the cephalic vein as it runs deep to the cleidobrachialis muscle. 4. Sharply separate the omotransversarius and the cervical and thoracic parts of the trapezius muscles from the scapular spine (Fig. 116-2A,B). 5. Subperiosteally elevate the rhomboideus and serratus ventralis muscles from the medial aspect of the
1. Place the dog in lateral recumbency and aseptically prepare the entire limb and pelvis for surgery. 2. Incise the skin in two connected semicircles; ventrolaterally from the tuber ischii down to the patella and up to the flank and ventromedially from the ends of the lateral incision to midthigh. 3. Transect the caudal belly of the sartorius and gracilis muscles at midthigh. 4. Isolate, ligate, and divide the saphenous nerve and femoral artery and vein. 5. Transect the pectineus muscle at its insertion on the femur, and the cranial sartorius and quadriceps muscles proximal to the patella.
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A Trapezius m. Cleidocervicalis m.
B
Clavicular tendon
Trapezius m.
Omotransversis m.
Cleidobrachialis m.
Omotraversus m.
Cleidocervicalis m.
C Rhomboideus m.
D
Trapezius m.
Rhomboideus m. Seratus ventralis m.
Deep pectoral m.
Figure 116-2.
Initial dissection of muscles for thoracic limb amputation.
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Latissimus dorsi m.
axillary a. Scalenus m. Thoracodorsal a. and v. Axillary and accessory lymph nodes
Omotransversus m.
Trapezius m. (reflected)
Cleidocervicalis m.
Serratus ventralis m.
Deep pectoral m.
Superficial pectoral m.
Cleidobrachialis m.
Figure 116-3.
Ligation and severing of axillary artery and continued dissection for thoracic limb amputation.
6. Incise the tensor fasciae latae and biceps femoris muscles along the skin incision. 7. Isolate the sciatic nerve trunk and sever it at the greater trochanter. 8. Transect the abductor cruris caudalis, semitendinosus, semimembranosus, and adductor magnus et brevis muscles at midthigh. 9. Complete the amputation by osteotomy of the femur using a Gigli wire or oscillating bone saw, leaving the proximal one-third of the femur. Bone wax is packed into the cut end of the osteotomy.
10. If necessary, place a closed suction drain (e.g., Jackson-Pratt) or passive drain (e.g., Penrose) to drain dead space. Routinely close the muscles, subcutaneous tissues, and skin.
Pelvic Limb Amputation by Hip Disarticulation Use this procedure when there is tumor involvement of the mid- to distal femur. Tumors of the proximal femur and hip joint may require en bloc resection of the acetabulum and part of the pelvis (subtotal
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Figure 116-4.
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Muscle closure after thoracic limb amputation.
hemipelvectomy) with the femur to ensure complete removal.
Objectives
• Same as for thoracic limb amputation. Equipment
• Same as for thoracic limb amputation Technique 1. Place the dog in lateral recumbency and aseptically prepare the entire limb and pelvis for surgery. 2. Incise the skin in two connected semicircles, ventrolaterally from the tuber ischii down to the midthigh and up to the flank, and ventromedially from the ends of lateral incision down to the inguinal fold. 3. Isolate, ligate, and divide the femoral and superficial circumflex femoral arteries and femoral vein. 4. Transect the sartorius, pectineus, gracilis, and adductor magnus et brevis muscles 2 cm from their origin (Fig. 116-5A,B). 5. Ligate and divide the medial circumflex femoral artery and vein. 6. Elevate the iliopsoas muscles from the lesser trochanter of the femur. 7. Sever the saphenous and femoral nerves. 8. Cut the medial coxofemoral joint capsule and round ligament. 9. Transect the tensor fasciae latae, biceps femoris, abductor cruris caudalis, semitendinosus, and semimembranosus muscles in their proximal one-third.
10. Sever the sciatic nerve distal to its branches to the upper thigh muscles (Fig. 116-5C). 11. With the limb in flexion and abduction, sever the hip rotator muscles, including the internal and external obturator and gemellus muscles. 12. Complete the amputation by severing the three gluteal muscles (superficial, middle, and deep), and the lateral joint capsule and by elevating the rectus femoris muscles from the iliopubic eminence (Fig. 116-5D). 13. If necessary to drain excessive dead space, place a closed suction drain (e.g., Jackson-Pratt) or passive drain (e.g., Penrose). Routinely close the muscles, subcutaneous tissue, and skin.
Postoperative Care and Complications Short Term
• Always submit the amputated limb for histopathologic confirmation of the preoperative diagnosis.
• Monitor the patient closely for pain, hemorrhage, hypotension, or electrolyte disturbances.
• Routinely administer analgesics (see Chapter 6). • With proper surgical technique minimizing dead
• •
space, seroma formation should be minimal but can be managed with pressure bandages, warm compresses three to four times daily, or drain placement. Remove drains when drainage is minimal. Nursing and supportive care will be required until the patient has recovered and adapted enough to function well on three limbs. Start chemotherapy after skin suture removal.
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Section 8 / Skeletal System Vastus medialis muscle
Caudal and cranial sartorius muscle
Pectineus muscle Gracllis muscle Semitendinosus muscle External abdominal oblique muscle
Adductor magnus and brevis muscles Semimembranosus muscle External obturator muscle Pectineus muscle (origin)
Tensor fasciae latae muscle
Femoral artery (ligated and transected) and vein
A
B Internal obturator muscle
Sclatic nerve (transected)
Quadratus femoris muscle
Vastus lateralis muscle Cranial and caudal sartorius muscles
External obturator muscle Biceps femoris muscle (retracted)
C
Vastus medialis muscle
Gracilis muscle Semimembranosus muscle Quadratus femoris muscle
D Figure 116-5. lateral views.
lliopsoas muscle External obturator muscle
Dissection of muscles, vessels, and nerves for pelvic limb amputation by hip disarticulation. A and D, medial views; B and C,
Long Term
• Evaluate the patient clinically and radiographically •
Rectus femoris muscle Femoral head
every 8 to 12 weeks to look for tumor recurrence at the surgical site and pulmonary metastasis. Institute a strict weight loss program, especially with forelimb amputation in overweight patients.
metastasis secondary to OSA. In some cases, lung lobectomy to remove metastatic tumors can significantly prolong survival time (see Chapter 167). Patients that are candidates for removal of lung metastasis should satisfy the following criteria:
• Primary tumor in complete remission for >300 days. • No greater than two nodules visible on plain radiographs.
MANAGEMENT OF METASTATIC DISEASE As a general rule, chemotherapy is ineffective in patients with radiographically detectable pulmonary
• Metastatic disease restricted to the lung only (negative bone scan or survey radiographs). Median survival time in 36 dogs after removal of lung metastasis was approximately 6 months.
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LIMB-SPARING PROCEDURES • Limb-sparing procedures are indicated in patients
•
that are not good candidates for limb amputation, or when clients refuse amputation. With this procedure, the affected bone is resected and is replaced with a normal bone allograft. The site that is most amenable to limb-sparing surgery is the distal radius. Other sites (proximal humerus, proximal tibia) are not amenable to limb-sparing surgery because complication rates are unacceptably high. In addition, patients typically have poor limb function because the procedure requires arthrodesis of the joint closest to the tumor. Limb-sparing procedures are associated with a higher complication rate than limb amputation, are technically difficult to perform, and requires access to a bone bank, which limits its use in private practice. Consult a surgical specialist.
Indications • Tumor involving 50% or less of the length of the bone.
• Tumor that does not extend across the joint, into the adjacent ulna, or into the surrounding soft tissues.
• A patient that is free of metastatic or other concurrent diseases.
Complications • Infection (45–55% of cases) • Recurrence (25% of cases)
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• Plate breakage • Host bone fracture • Sequestrum formation In patients with a failed limb-sparing procedure, limb amputation can be performed as a salvage procedure.
SUPPLEMENTAL READING Berg J, Weinstein MJ, Schelling SH, et al: Treatment of dogs with osteosarcoma by administration of cisplatin after amputation or limb-sparing surgery: 22 cases (1987–1990). J Am Vet Med Assoc 200:2005–2008, 1992. Davis GJ, Kapatkin AS, Craig LE, et al: Comparison of radiography, computed tomography, and magnetic resonance imaging for evaluation of appendicular osteosarcoma in dogs. J Am Vet Med Assoc 220:1171-1176, 2002. Evans HE: Miller’s Anatomy of the Dog, 3rd ed. Philadelphia: WB Saunders, 1993. Green EM, Adams WM, Forrest LJ: Four fraction palliative radiotherapy for osteosarcoma in 24 dogs. J Am Anim Hosp Assoc 38:445–451, 2002. Liptak JM, Dernell WS, Ehrhart N, et al: Canine appendicular osteosarcoma: diagnosis and palliative treatment. Compend Contin Educ Pract Vet 26:172–182, 2004. Liptak JM, Dernell WS, Ehrhart N, et al: Canine appendicular osteosarcoma: Curative-intent treatment. Compend Contin Educ Pract Vet 26:186–196, 2004. Watson CL, Lucroy MD: Primary appendicular bone tumors in dogs. Comp Contin Educ Pract Vet 24:128–138, 2002. Withrow SJ, MacEwen EG: Small Animal Clinical Oncology, 3rd ed. Philadelphia: WB Saunders, 2001, pp 378–417. Withrow SJ, Powers BE, Straw RC, et al: Comparative aspects of osteosarcoma—dog versus man. Clin Orthop Rel Res 270:160–167, 1991.
Chapter
▼
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117
Miscellaneous Diseases of Bone James K. Roush
Some of the diseases affecting bone are discussed in this chapter. See respective chapters for other bone and cartilage diseases, such as hip dysplasia, avascular necrosis of the femoral head, and osteochondrosis.
Lameness
• There is acute onset of weight-bearing lameness without a history of recent trauma. ▼ Key Point Lesions often resolve in one bone and develop in another, resulting in the classic history of “shifting leg” lameness.
PANOSTEITIS Panosteitis is a disease of young large-breed dogs manifested by intermittent lameness of one or more limbs. Onset usually occurs in the first year of life. The disease is self-limiting, but clinical signs may persist in one or more limbs for months. Differentiate panosteitis from other causes of lameness in young dogs, such as hip dysplasia and osteochondritis dissecans.
Etiology • The etiology of panosteitis is unknown. • Panosteitis may have a polygenetic origin, because •
•
German shepherd dogs are commonly affected. Contributing causes include stress, transient vascular abnormalities, metabolic disorders, allergies, hyperestrogenism, and autoimmune reaction following viral infection. The characteristic histopathologic lesion is degeneration of medullary adipocytes, followed by stromal cell proliferation, intramembranous ossification, and regeneration of the adipose bone marrow.
Clinical Signs Signalment
• Panosteitis usually is seen in large and giant-breed
• •
dogs, most often 5 to 12 months of age; however, it has been reported in dogs up to 5 years of age, and I have seen it in a 7-year-old dog. Male dogs are affected more frequently than females (4:1 ratio). In females, the first episode of the disease often occurs in association with the first estrus. Panosteitis has been reported in the German shepherd, Great Dane, Irish setter, St. Bernard, Doberman pinscher, Airedale, basset hound, and miniature schnauzer.
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• Pain due to the disease is of intermittent duration •
•
and severity, but the dog rarely, if ever, is completely non–weight bearing on the affected limb or limbs. Lameness or radiographic lesions may occur simultaneously in multiple limbs or bones, or lameness may resolve for a period of time, only to recur in another limb. After a bone passes through the lesion cycle, it is unlikely that it will be affected again, but lameness may occur in that limb if the disease affects another bone in the limb. Clinical signs often continue for several months and usually resolve by 18 to 20 months of age.
Diagnosis ▼ Key Point Diagnosis of panosteitis is established by eliciting pain on firm palpation of a long bone and by characteristic radiographic lesions.
Physical Examination
• Applying firm pressure to the diaphyses of the affected bone results in clinical signs of discomfort.
Laboratory Evaluation
• Hematology and serum chemistry profiles usually are normal.
• Eosinophilia occurs inconsistently (this disease was previously referred to as eosinophilic panosteitis).
Radiography Confirm suspected cases by survey radiography of the affected bone(s).
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Table 117-1. CHARACTERISTIC RADIOGRAPHIC LESIONS SEEN IN DISEASES AFFECTING BONE Disease
Lesion
Panosteitis
Increased opacity in medullary cavity of diaphysis Radiolucent metaphyseal line adjacent to physis Periosteal reaction beginning on metacarpals or metatarsals, bilaterally symmetric Bony proliferation on ventral mandible and skull Large, smooth bony protuberance in metaphyseal area Well-circumscribed, radiolucent metaphyseal defect Longitudinal, linear radiolucent cartilaginous core defect in distal ulna
Hypertrophic osteodystrophy Hypertrophic osteopathy Craniomandibular osteopathy Cartilaginous exostosis Bone cyst Retained enchondral
• Early radiographic lesions are characterized by areas • • • • •
of increased density and accentuated trabecular pattern within the medullary cavity (Table 117-1). These areas may be focal or multifocal and commonly occur near the nutrient foramen. Bone cortices may be thickened, and progressive mottling and opacification of the medullary cavity occur. A smooth, linear periosteal proliferation may develop. During resolution, sclerotic areas gradually decrease in size and density. Radiographic signs may persist for several months after lameness resolves. There is no correlation between the radiographic lesions and severity of clinical signs.
Differential Diagnoses
• Differentiate panosteitis as a cause of lameness from
•
other diseases that are characterized by onset during or shortly after the rapid-growth phase in large-breed dogs. In particular, eliminate hypertrophic osteodystrophy, osteochondritis dissecans of the shoulder or elbow (see Chapter 118), ununited anconeal process (see Chapter 118), and hip dysplasia (see Chapter 108) as a cause of lameness before ascribing clinical signs to panosteitis.
Treatment ▼ Key Point Panosteitis is a self-limiting disease.
• No specific therapy for panosteitis exists. • Administer a nonsteroidal anti-inflammatory drug approved for dogs, as needed, to alleviate pain (see Chapter 6).
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• Restrict exercise in severely affected animals. • Inform clients that the lameness may shift to other limbs and that the animal may be intermittently lame for 6 to 18 months.
HYPERTROPHIC OSTEODYSTROPHY Hypertrophic osteodystrophy (HOD) is a developmental disease of young, rapidly growing large- and giantbreed dogs. Dogs with HOD exhibit lameness in one or more limbs in association with swelling and inflammation of the metaphyseal regions of long bones. Complications related to prolonged recumbency, anorexia, and hyperthermia have been reported in severely affected animals. The overall prognosis for HOD is guarded. Although many dogs recover spontaneously, permanent bone changes and physical deformities may develop.
Etiology • The etiology of HOD is unknown. • Historically, the disease has been attributed to
• •
vitamin C deficiency, but decreased levels of ascorbic acid in the serum or urine do not appear to be related to the disease. Skeletal lesions similar to those of HOD have been produced experimentally by feeding a free-choice diet abnormally high in protein, calories, and calcium. Canine distemper virus may be involved as a causative agent.
Clinical Signs Signalment ▼ Key Point HOD occurs only in growing animals with open physes.
• Onset of clinical signs usually occurs at 3 to 4 months of age (range, 2–8 months).
• HOD has been reported in the Great Dane, Irish wolfhound, St. Bernard, Irish setter, Labrador retriever, basset hound, greyhound, German shepherd, German short-haired pointer, borzoi, boxer, Dalmatian, Weimaraner, Doberman pinscher, and collie.
Systemic Signs
• The severity of HOD varies, ranging from an absence •
of systemic signs to severe anorexia, weight loss, fever, and depression. Clinical signs are episodic in nature, and lameness often is bilaterally symmetric.
Lameness
• Lameness varies from a mild limp in minimally affected dogs to non–weight bearing lameness in severely affected animals.
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• Affected long bone metaphyses are extremely •
swollen, warm, and painful in animals with severe disease. Multiple long bones and limbs are affected, and, in extreme cases, dogs are reluctant to stand or move.
• Irregular widening of the physis may be seen in later stages of the disease.
• Subperiosteal or extraperiosteal bone formation is seen in metaphyseal regions and may involve the diaphysis.
Diagnosis
Differential Diagnoses
History/Physical Examination
• Differentiate HOD from other causes of lameness in
• The history may include recent weight loss, reluctance to move, and anorexia.
immature large- or giant-breed dogs.
• Other diseases that result in metaphyseal swelling or in signs of pain during palpation of long bones include panosteitis, bone-associated neoplasms, and hypertrophic osteopathy. Radiographic lesions in these diseases are distinct and allow easy differentiation; the last two diseases are unlikely to be the cause of lameness in young dogs.
• Affected metaphyses are warm and swollen on palpation.
• Signs of pain may be elicited on palpation of the metaphyseal areas.
• Pyrexia of up to 106°F may be present. Laboratory Evaluation
• Laboratory data are normal, or mild abnormalities related to anorexia and stress may be present.
Radiography
▼ Key Point There is no specific treatment for HOD.
• In mild or moderately affected dogs, there is often
• Radiographic changes usually occur in the metaphy-
•
Treatment
ses of the long bones and are bilaterally symmetric. Other bones, including the mandible, ribs, and scapula, may be affected. The characteristic radiographic lesion is generalized sclerosis and enlargement of the metaphysis.
spontaneous remission.
• Correction of dietary imbalances and decreased caloric intake may be beneficial.
• Good supportive care of severely affected dogs is
▼ Key Point Radiolucent areas form in the metaph-
•
ysis and coalesce to form an area of radiolucency parallel to the growth plate, called a double physeal line (Fig. 117-1).
•
Radius
•
Ulna
Metaphyseal radiolucent line
Sclerosis Metaphyseal radiolucent line
Normal physes Figure 117-1. Metaphyseal radiolucent lines and metaphyseal sclerosis proximal to distal radial and ulnar physis in a dog with hypertrophic osteodystrophy.
essential to prevent decubital ulcers, provide nutrition (see Chapter 3), and maintain hydration (see Chapter 5). Give nonsteroidal anti-inflammatory analgesics, as needed, to relieve discomfort (see Chapter 6). Severely affected animals may require nutritional intake via force-feeding or gastrostomy tube (see Chapter 3). Parenteral fluids may be needed to prevent dehydration in these animals (see Chapter 5). There is no evidence that mineral, vitamin C, or vitamin D supplements are beneficial; these substances actually may accelerate the rate of dystrophic calcification.
HYPERTROPHIC OSTEOPATHY Hypertrophic osteopathy (HO) is a pathologic disease process affecting long bones secondary to a space-occupying mass in the abdominal or thoracic cavities. The disease has been reported in many species, including dogs, cats, and humans. HO is characterized by bilateral symmetric swelling of the distal limbs accompanied by periosteal bone formation. HO has been referred to as hypertrophic pulmonary osteoarthropathy, pulmonary osteoarthropathy, and hypertrophic pulmonary osteopathy. Hypertrophic osteopathy is the term that most accurately reflects the rare joint involvement and the variable site of the primary space-occupying lesion.
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Etiology • Hypertrophic osteopathy occurs secondary to a •
•
variety of diseases and occurs in dogs and cats of all breeds and ages. HO is most often secondary to metastatic pulmonary neoplasia, although it has been reported with primary pulmonary neoplasia, pulmonary abscesses, pulmonary tuberculosis, chronic bronchopneumonia, spirocercosis, dirofilariasis, rib tumors, bacterial endocarditis, hepatic adenocarcinoma, and various primary bladder neoplasms (neurofibrosarcoma, botryoid rhabdomyosarcoma, and transitional cell sarcoma). The pathogenic mechanisms underlying the bone pathology are unknown. Evidence points to an increased peripheral vascular supply secondary to the pulmonary lesion. This increased peripheral blood flow has been observed both in dogs and humans and may be related to irritation of afferent nerve pathways and stimulation of a nervous reflex.
Figure 117-2. Smooth periosteal proliferation (arrows) on radius and ulna characteristic of hypertrophic osteopathy.
Clinical Signs ▼ Key Point Signs of HO may be present months before onset of clinical signs relating to the underlying disease; early recognition is important for diagnosis and treatment of the primary disease.
Signalment
• Dogs and cats with HO may be of any breed and
•
•
usually are affected late in life.
• A reported increased incidence of the disease in female and large-breed dogs may be due to the increased incidence of mammary tumor metastasis in female dogs, and of primary bone tumors in largebreed dogs.
Lameness
• Most animals present with acute or gradual lameness of all four limbs and with reluctance to move.
Diagnosis Physical Examination
• The distal limbs are swollen, firm, and warm. • Signs of pain may be elicited on deep palpation of the long bones.
•
affecting the long bones of the appendicular skeleton (Fig. 117-2). Endosteal bone proliferation does not occur. Distal portions of the limbs, especially the metatarsals and metacarpals, are involved first, but periosteal proliferation eventually may involve the more proximal long bones and occasionally the mandible, pelvis, ribs, and vertebrae. In very early cases, periosteal new-bone formation is not evident, but symmetric soft tissue swelling is present. If the primary disease resolves, the bony and soft tissue radiographic abnormalities regress.
▼ Key Point Thoracic and abdominal radiographs are essential to evaluate the underlying disease process and to confirm the diagnosis of HO. Abdominal ultrasound may also be helpful in identifying a mass lesion.
Differential Diagnoses The bony periosteal reactions of hypertrophic osteopathy are similar to those of panosteitis and hypertrophic osteodystrophy, but HO will not exhibit the increased medullary opacities of panosteitis, nor the radiolucent metaphyseal line characteristic of HOD. It is rare to see HO in a young (adolescent) animal.
Laboratory Evaluation
Treatment
• Laboratory findings reflect the underlying disease
▼ Key Point Removal of the underlying primary
process and are not characteristic of HO.
Radiography
lesion usually results in regression of the lameness and distal limb lesions.
• Survey radiographs demonstrate a bilateral, sym-
• Resection of primary or metastatic pulmonary neo-
metric, generalized periosteal proliferative reaction
plasms provides temporary relief of signs related to
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• •
•
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HO, but long-term survival is dependent on the type of neoplasm. Appropriate treatment of dirofilariasis, spirocercosis, and primary lung disease may increase the chances for long-term survival. Inflammation and clinical signs of pain resolve 1 to 2 weeks after removal of the thoracic or abdominal mass. Periosteal reactions regress in 3 to 4 months, but residual radiographic changes may persist in severe cases. Lameness may persist in some animals even after removal of the mass. When resection of the primary mass is not feasible, unilateral vagotomy (on the side of the lesion) may provide temporary regression of clinical signs.
Figure 117-3. Bony proliferation (arrows) on the ventral mandible of a dog with craniomandibular osteopathy.
Radiography
CRANIOMANDIBULAR OSTEOPATHY Craniomandibular osteopathy (CMO) is a non-neoplastic, noninflammatory proliferative bony disease in growing dogs that affects bones of endochondral origin, most commonly the mandibles, occipital bones, or temporal bones. Bony lesions are bilateral and symmetric. CMO occurs predominantly in terriers, especially Scottish, West Highland white, and Cairn terriers, but the disease also has been reported in the boxer, Labrador retriever, Great Dane, and Doberman pinscher.
Etiology • CMO is likely of heritable origin, with recent reports
Diagnosis of CMO is confirmed by radiographic evidence of the bony proliferative lesions.
• Obtain survey radiographs of the skull and mandible, •
•
•
of likely autosomal recessive heritance.
• Osteoclastic resorption of mandibular bone occurs, followed by production of woven bone on both the periosteal and endosteal surfaces of the bone. Cyclic episodes of bone resorption and proliferation result in the formation of mature fibrous bone that may remain permanently.
Clinical Signs • Disease onset occurs at 4 to 10 months of age. Both •
sexes are affected equally. Presenting clinical signs include pain on manipulation or opening of the mouth, mandibular swelling, ptyalism, inability to open the mouth, intermittent fever, and lethargy.
Diagnosis Physical Examination Signs of pain are elicited during direct palpation of the swelling or attempts to open the mouth. In advanced cases, the clinician may be unable to open the mouth more than 1 or 2 cm. Dogs may be febrile during the period of bone proliferation. Lymphadenopathy or temporal muscle atrophy may be present.
•
including oblique, dorsoventral, and lateral views, to assess the extent of the disease. A non-neoplastic, bilaterally symmetric bony proliferation is seen projecting from the periosteal surfaces of the mandible or other bones of the cranium (Fig. 117-3). Angular processes of the mandible and bullae may fuse and obstruct jaw motion. Lesions may also involve the occipital bone, parietal bone, frontal bone, maxilla, and appendicular bones. The proliferation of new bone decreases as growth slows, and becomes radiographically static when the animal is approximately 1 year old. Partial or complete regression of bony lesions occurs, but moderate or severe cases result in permanent bone proliferation to varying degrees. The prognosis is poor for dogs with radiographic evidence of partial or complete bony ankylosis of the temporomandibular joints (TMJs).
Differential Diagnoses
• Lesions of CMO in the appendicular skeleton may •
appear radiographically similar to HOD, but CMO lacks the metaphyseal radiolucent line of HOD. Radiographic appearance differentiates CMO from bony neoplasia and osteomyelitis.
Treatment • There is no specific therapy for CMO. • Administer nonsteroidal anti-inflammatory analgesic •
therapy at manufacturer recommended dosage as needed (see Chapter 6). Nutritional support by gastrostomy or enterostomy tube or parenteral supplementation may be necessary (see Chapter 3). As the condition stabilizes, most animals have impaired mouth function but are capable of maintaining normal nutritional status.
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• Surgical intervention to reduce new bone mass and
• Removal of MCE sometimes is requested to improve
increase TMJ range of motion has met with limited success.
• Malignant transformation of exostoses to chon-
MULTIPLE CARTILAGINOUS EXOSTOSIS Multiple cartilaginous exostosis (MCE) is a disease of dogs and cats in which multiple ossified protuberances arise from the bone in metaphyseal regions. Vertebrae, ribs, and long bones commonly are affected. The exostosis ceases to grow when the physis nearest the exostosis ossifies.
Etiology • MCE probably is heritable in dogs, horses, and humans.
• The accepted pathogenesis is that the exostosis is derived from displaced chondrocytes that separate from the physis during development.
Clinical Signs • The animal often is presented with a firm, distinct swelling on the involved bone.
• Lameness or limb dysfunction develops only when
•
adjacent structures such as the tendons or nerves are compressed or mechanically distorted by the exostoses. Other clinical signs, including pain, lameness, mechanical dysfunction, and neurologic deficits, depend on the structure affected.
cosmetic appearance.
•
drosarcomas or osteosarcomas has been reported. Continued growth of the exostosis after the animal is mature suggests malignant transformation. In general, the prognosis is good after removal of uncomplicated MCE.
BONE CYSTS Bone cysts are smooth radiolucent cavities found rarely in the long bones of dogs. Flat bones (e.g., mandible, ribs) also may be affected. Four types of bone cysts have been described in dogs:
• • • •
Monostotic (affecting one bone) Polyostotic (affecting more than one bone) Aneurysmal Subchondral
Aneurysmal bone cysts are extremely rare in dogs and are locally aggressive. Bone cysts found in young, large-breed dogs usually do not produce clinical signs until they attain a large size.
Etiology • The etiology of monostotic, polyostotic, and aneurysmal bone cysts is unknown.
• Subchondral bone cysts often are not primary lesions and may be the result of chronic osteoarthritis or diseases leading to osteoarthritis (e.g., rheumatoid arthritis, systemic lupus erythematosus).
Diagnosis Physical Examination
Clinical Signs
• A smooth, immovable bony swelling is visible and pal-
Signalment
pable near a metaphysis.
• Pain may be elicited on palpation of the mass or sur-
• The age of affected animals ranges from 4 to 30
rounding soft tissues.
Radiography
• Obtain skeletal survey radiographs of animals with suspected cartilaginous exostosis.
• Radiographic lesions are juxtacortical masses at or adjacent to the metaphysis.
• Large, scattered radiolucent areas of hyaline cartilage •
may be present within the exostosis. The exostotic growths may involve any bone except the skull. Surgical biopsy of the lesion confirms the diagnosis.
Treatment
•
months, but most animals are less than 1 year of age. Breeds reported to develop bone cysts include the German shepherd, Weimaraner, Irish wolfhound, Afghan, saluki, Great Dane, and Doberman pinscher.
Presentation
• Pain, swelling, and stiffness of the nearest joint may be present.
• Acute lameness or swelling may occur at the site of the cyst owing to a pathologic fracture.
Diagnosis Radiography
▼ Key Point Removal of the exostosis relieves asso-
• Survey radiographs establish a diagnosis of bone
ciated pain, mechanical dysfunction, and neurologic deficits.
cysts. A benign, expansive, radiolucent area in the metaphysis is characteristic.
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• The metaphyseal cortex may be thinned by expand•
ing cysts. Pathologic fractures may be evident radiographically.
Histopathology
• The cyst is lined by fibrous connective tissue. • Aneurysmal bone cysts are filled with blood, and the
•
blood spaces are lined by connective tissue trabeculae. Multinucleate giant cells and mature bone may be present in these cysts. Monostotic and polyostotic cysts may fill with blood after pathologic fracture.
Differential Diagnoses
• Differentiate bone cysts from more aggressive lesions such as chondrosarcoma, osteosarcoma, and giant cell tumors.
Treatment • Curettage of the walls and filling of the defect with • •
cancellous bone is the definitive treatment in most animals. Treat pathologic fractures through cysts by debridement of the cyst wall, cancellous graft, and fracture fixation. Consider cyst resection if the lesion is located in flat bones (e.g., rib resection or mandibulectomy).
Treatment • No treatment is necessary for animals without forelimb deformity.
• Immature animals with forelimb deformities may
•
LABRADOR RETREIVER SKELETAL DYSPLASIA Skeletal dysplasia is a heritable disease of Labrador retrievers characterized by forelimb achondroplasia and ocular effects. It demonstrates autosomal recessive transmission of skeletal effects and is linked with an incomplete dominant heritable ocular dysplasia in these dogs.
Etiology • The skeletal defects are heritable via autosomal recessive transmission.
• Linked ocular defects are heritable via incomplete dominant transmission.
• The disease is only recognized in Labrador retrievers. Clinical Signs • The forelimbs of affected immature Labs appear
RETAINED ENCHONDRAL CARTILAGINOUS CORES Retained enchondral cartilaginous cores occur in the distal ulnar metaphysis of young, large-breed dogs. Radiographically, the retained enchondral cartilage is seen as a central, longitudinal radiolucent cone in the distal ulnar metaphysis and usually is an incidental finding of no clinical significance. These lesions, however, may interfere with normal growth of the ulna, resulting in forelimb deformities.
Etiology • The etiology is unknown. Clinical Signs • Signs may include valgus deviation, external rotation of the carpus, and cranial bowing of the radius.
Diagnosis • Survey radiographs establish the diagnosis in animals with appropriate forelimb deformities.
• The lesion also may be an incidental finding unrelated to clinical lameness if normal growth of the ulna is apparent.
benefit from distal ulnectomy, which may allow spontaneous correction of radial and ulnar deformities during continued growth (see Chapter 105). Mature animals require ulnar and radial osteotomies to correct forelimb deformity (see Chapter 105).
• •
shorter and exhibit achondroplastic conformation. The disease is often first noted during rapid growth phases from 8 to 16 weeks of age. Abnormal conformation of the coxofemoral joints also occurs and is visible radiographically. Ocular changes include cataracts, retinal dysplasia, and rhegmatogenous retinal detachments. Dogs are often visually impaired at presentation.
Diagnosis ▼ Key Point The combination of forelimb achondroplasia associated with the linked ocular diseases of cataracts, dysplasia, or retinal detachment in immature animals leads to the diagnosis.
• The history or presence of other full siblings with similar signs is indicative of the heritable condition.
• Radiograph the forelimb to demonstrate the achondroplastic changes of the disease and demonstrate asynchronous growth of the radius and ulna. Comparison of radial length with heterozygote siblings is diagnostic.
Differential Diagnosis
• Differentiate the skeletal lesions from traumatic shortening of the radius and ulna due to previous
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damage to the distal radial or ulnar growth plates. In the latter, the radiographic changes will most likely be unilateral and visible evidence of early closure of the growth plates may be evident.
Treatment • There is no treatment for individual animals affected by the disease.
• Monitor breeding lines of Labrador retrievers for evidence of the disease. Remove probable carriers of the trait from breeding stock.
SUPPLEMENTAL READING Alexander JW: Selected skeletal dysplasias: Craniomandibular osteopathy, multiple cartilaginous exostoses, and hypertrophic osteodystrophy. Vet Clin North Am Small Anim Pract 13:55, 1983.
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Alexander JW: Orthopedic diseases. In Slatter DH (ed): Textbook of Small Animal Surgery. Philadelphia: WB Saunders, 1985, p 2312. Goldschmidt MH, Biery DN: Bone cysts in the dog. In Newton CD, Nunamaker DM (eds): Textbook of Small Animal Orthopaedics. Philadelphia: JB Lippincott, 1985, p 611. Lenehan TM, Fetter AW: Hypertrophic osteodystrophy. In Newton CD, Nunamaker DM (eds): Textbook of Small Animal Orthopaedics. Philadelphia: JB Lippincott, 1985, p 597. Lenehan TM, Fetter AW: Hypertrophic osteopathy. In Newton CD, Nunamaker DM (eds): Textbook of Small Animal Orthopaedics. Philadelphia: JB Lippincott, 1985, p 603. Lenehan TM, Van Sickle DC, Biery DN: Canine panosteitis. In Newton CD, Nunamaker DM (eds): Textbook of Small Animal Orthopaedics. Philadelphia: JB Lippincott, 1985, p 591. Muir P, Dubielzig RR, Johnson KA, Shelton GD: Hypertrophic osteodystrophy and calvarial hyperostosis. Compend Cont Ed Pract Vet 18:143, 1996. Riser WH, Newton CD: Craniomandibular osteopathy. In Newton CD, Nunamaker DM (eds): Textbook of Small Animal Orthopaedics. Philadelphia: JB Lippincott, 1985, p 603.
Chapter
▼
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118
Osteochondrosis Michael P. Kowaleski
Osteochondrosis refers to a group of diseases that are characterized by aberrant development of the epiphyseal or physeal cartilage in growing animals. The cause of osteochondrosis appears to be multi-factorial; some of the factors that have been implicated include nutrition (overnutrition, excess dietary calcium, excess protein), genetics, exercise, environmental factors, and trauma (excessive mechanical loading), as the lesions frequently occur at the point of greatest loading of the joint.
ETIOLOGY ▼ Key Point Osteochondrosis is a failure of endochondral ossification, and this term refers to the disease in general. Osteochondritis dissecans (OCD) refers to the combination of dissecting lesions of articular cartilage, communication of synovial fluid into the subchondral bone, and the resulting synovitis. Most commonly large- or giantbreed dogs are affected.
• Osteochondrosis at the physeal growth plate begins
•
as an abnormal accumulation of viable hypertrophic chondrocytes that subsequently fail to undergo matrix mineralization, causing a slowing of growth, not complete cessation. In the dog, this primarily occurs at the distal ulnar physis (retained cartilage core or radius curvus), leading to the characteristic antebrachial deformities seen with asynchronous growth of the radius and ulna, namely shortening of the ulna, cranial bowing of the radius, valgus angulation, external rotation, shortening of the radius, and variable amounts of elbow and carpal incongruity. Elbow dysplasia is a collection of diseases presumed to be a result of osteochondrosis, including ununited anconeal process (UAP), OCD of the medial portion of the humeral condyle, and fragmented medial coronoid process (FMCP) (Fig. 118-1).
1194
OSTEOCHONDRITIS DESSICANS OF THE SHOULDER, HOCK, AND STIFLE In dogs, OCD lesions can occur in the shoulder on the caudal humeral head, in the hock on the trochlear ridges of the talus (medial more commonly than lateral), and in the stifle on the femoral condyle (lateral more commonly than medial).
Anatomy • See the respective chapters on shoulder, hock, and stifle disorders (Chapters 102, 112, and 110).
Pathophysiology • A defect in endochondral ossification results in a focal area of abnormal subchondral bone formation.
• The overlying cartilage fails to undergo endochon• • •
• •
dral ossification resulting in focal retention of cartilage instead of conversion to bone. This thickened region of cartilage becomes necrotic and weak, resulting in cartilage breakdown under normal loading conditions or secondary to trauma. Early in the disease process, the lesions of osteochondrosis affect only the epiphyseal cartilage, and the animal is asymptomatic. Once a fissure occurs in the thickened cartilage, it extends through the necrotic cartilage into the subchondral bone, allowing access of the synovial fluid to the subchondral bone. • This stage seems to correspond to the onset of clinical signs, at which time it is called osteochondritis dissecans. OCD results in two distinct joint abnormalities: joint incongruity secondary to malformation of cartilage and subchondral bone, and joint mouse formation. Cartilage flaps that remain attached may ossify, and the resulting bone remains viable as long as the flap is attached. • Detached cartilage flaps may survive in the joint fluid and grow in size.
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A
ununited ancaneal process
C B OCD of humeral condyle
fragmented medial coronoid process
Figure 118-1. The various manifestations of elbow dysplasia include (A) ununited anconeal process, (B) fragmentation of the medial portion of the coronoid process of the ulna, and (C) OCD of the medial portion of the humeral condyle.
•
•
• If these cartilage flaps attach to the joint capsule, they may become mineralized or ossified. Curettage of the chondral and subchondral lesion stimulates neochondrogenesis; however, the resultant fibrocartilage does not have the same material properties as the original hyaline cartilage, and is not as durable. The new cartilage rarely attains the height or density required to reestablish joint congruity.
Clinical Signs Shoulder
• Large-breed dogs, 4 to 8 months of age, 2:1 to 3:1 male/female ratio.
• Bilateral in 27% to 68% of cases; many are clinically • •
affected in only one limb. Lameness is initially noted after exercise or after rest preceded by exercise. Pain with shoulder extension, crepitus, deltoid and spinatus muscle atrophy.
Hock
• Large-breed dogs, 5 to 8 months of age, commonly Rottweiler, Labrador retriever, and bullmastiff.
• Lateral trochlear ridge OCD is seen most commonly in the Rottweiler.
• Hind limb lameness characterized by a shortened stride and hyperextension of the tarso-crural joint.
• Thickening of the tarsus especially if the medial trochlear ridge of the talus is involved.
Stifle
• Large-breed dogs, 5 to 7 months of age. • Lameness varies from mild to severe. • Joint effusion, muscle atrophy, and crepitus may be evident.
Diagnosis • The radiographic signs of osteochondrosis are well characterized and easily recognized in most cases;
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high-quality, well-positioned radiographs are necessary for an accurate diagnosis (see Chapter 4). Normal cartilage is not visible radiographically unless significant dystrophic calcification has occurred. Since OCD lesions consist of areas of relatively thicker cartilage than the surrounding cartilage and a failure of endochondral ossification of the underlying bone, the lesion is observed as a flattened or saucer-like “divot” in the subchondral bone.
•
with large lesions and severe osteoarthritis are less likely to benefit from surgery. Dogs with OCD of the hock may fare as well with or without surgery; this is likely due the relatively large size of the typical lesion in the hock, as well as the tendency for osteoarthritis to be significant in this joint preoperatively.
Surgical Procedures
Shoulder
Objectives
• Radiographs reveal a flattening of the humeral head
• The goals of surgery are to debride the osteochon-
•
in a properly positioned lateral view. An arthrogram may be needed of the lesion is not evident or a cartilage has migrated into the biceps tendon sheath.
Hock
dral defect with minimal damage to the joint during the surgical approach and procedure.
Equipment
• Same as for OCD of the humerus, discussed later in this chapter.
• Radiographic identification of the lesion may be • • •
difficult due to the location of the lesion on the trochlear ridge. Extended dorsoplantar projection may reveal a defect in the trochlear ridge. A dorsolateral-plantaromedial 45-degree oblique projection in full extension outlines the medial trochlear ridge of the talus. A skyline view of the talus may identify a lesion on the center of the trochlear ridge of the talus.
Stifle
• Slight flattening and sclerosis of the subchondral •
bone of the femoral condyle is evident in a caudocranial view of the stifle. Avoid confusing the extensor fossa for an OCD lesion.
Preoperative Considerations • As the relative size of the osteochondral defect to the total joint surface area increases, the resulting joint incongruity also increases. Thus, a small defect in a large joint (shoulder) has less of an impact than in a small (hock) or complex (elbow or stifle) joint. ▼ Key Point Surgical treatment of OCD lesions can result in normal or near-normal function in large joints with relatively small lesions (shoulder); however, function is improved but clinical signs are not always alleviated in complex or small joints (elbow, hock, and stifle).
• The degree of osteoarthritis in the joint prior to
•
surgery has an impact on long-term function; as the degree of osteoarthritis increases, function is diminished. Patients with small lesions and minimal osteoarthritis will have the best surgical result; conversely, patients
Technique
• An arthrotomy or arthroscopy can be employed. • See respective chapters on shoulder, hock, and stifle • • •
disorders for a description of surgical approaches (see Chapters 102, 112, and 110). Debride the lesion to the level of subchondral bleeding bone utilizing a curette, a hand bur, or a motorized shaver. Debride the edges of the lesion peripherally to normal cartilage, and perpendicular to the subchondral bed. Microfracture can be utilized to create vascular access channels from the lesion to the underlying subchondral bone.
Postoperative Care and Complications • Apply a soft padded bandage for 3 to 5 days from the • •
digits to the mid-diaphysis proximal to the incision to minimize postoperative swelling. Remove skin sutures in 10 to 14 days. Confine the dog to leash walks only for 6 weeks to allow neochondrogenesis to occur. Allow gradual return to normal activity over the next 6 weeks to allow cartilage remodeling to occur.
Prognosis ▼ Key Point The prognosis for return to normal function in dogs with OCD of the shoulder is good to excellent; over 95% of patients are sound at 4 to 8 weeks.
• Early treatment of OCD of the hock (4–6 months of age) is indicated; otherwise the prognosis is poor due to a tendency for progressive degenerative joint disease (DJD) to develop.
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• OCD of the stifle carries a more guarded prognosis than that of the shoulder OCD; 75% will be normal if treated early.
CANINE ELBOW DYSPLASIA Elbow dysplasia is a collection of diseases, which were initially presumed to be a result of osteochondrosis. Recently, asynchronous growth or uneven joint loading has been implicated in the pathogenesis of this disorder.
Pathophysiology • Canine elbow dysplasia (CED) is a collection of
•
• • • •
•
developmental diseases of the canine elbow, which is believed to be caused by a primary incongruity between the humerus, radius, and ulna. Manifestations include fragmented medial coronoid process (FMCP) of the ulna, ununited anconeal process (UAP) of the ulna, and osteochondritis dissecans (OCD) of the medial portion of the humeral condyle. Classically, a decreased radius of curvature of the ulnar trochlear notch was suggested as the cause. A second theory is that elbow incongruity in CED is caused by asynchronous growth between the radius and ulna. Lagging radial growth and a relatively long ulna may stress the medial coronoid process and humeral condyle, resulting in FMCP and OCD, respectively. In an experimental study, surgical shortening of the radius in normal dogs resulted in altered intraarticular contact potentially stressing the medial coronoid process. Dogs with unilateral UAP have been shown to have a slightly longer radius on the affected side.
Ununited Anconeal Process
Pathophysiology
• UAP may be secondary to abnormal loading of the
• •
stabilizer of the canine elbow, particularly in extension during the stance phase of the gait. Instability or detachment of the process leads to synovitis and eventually osteoarthritis.
• In chondrodystrophic breeds, UAP may result from premature closure of the distal ulnar physis and asynchronous growth of the radius and ulna.
Clinical Signs
• Large-breed dogs, especially the German shepherd, basset hound, and St. Bernard, are affected.
• Signs including forelimb lameness, elbow abduction, •
• •
and external rotation of the foot become apparent at 5 to 8 months of age. Crepitus, joint effusion, and peri-articular thickening of the elbow may be noted.
Diagnosis
• Clinical signs, age, and breed form the basis for a provisional diagnosis.
• A flexed lateral radiographic view reveals an irregu•
• Ununited anconeal process (UAP) is a failure of the
•
elbow joint secondary to elbow incongruity or an abnormal size or shape of the trochlear notch; it has not been definitively proven to be secondary to OCD. Physeal closure of the anconeal process initially occurs distally, and then progresses proximally along the physis. Incomplete endochondral ossification along the physis can result in foci of retained cartilage within a closed physis mimicking UAP.
▼ Key Point The anconeal process is an important
Anatomy ossification center of the anconeal process to fuse with the proximal ulna by 20 to 24 weeks of age. Thus, a diagnosis of UAP prior to 24 weeks of age may be premature. The blood supply to the anconeal process is via the dorsal joint capsule attachment; therefore the bone remains viable and capable of endochondral ossification unless these attachments are disrupted. Physeal closure of the anconeal process initially occurs distally, and then progresses proximally along the physis. The anconeal process is an important stabilizer of the canine elbow, particularly in extension during the stance phase of the gait. Instability or detachment of the process leads to synovitis and eventually osteoarthritis.
1197
lar radiolucent line between the anconeal process and the olecranon. Radiographs of the contralateral elbow may be useful for comparison; bilateral UAP occurs in about 30% of cases.
Preoperative Considerations
• Removal of the anconeal process is an acceptable
•
•
method of treatment. However, the anconeal process is an important stabilizer of the elbow, and its removal may lead to elbow instability and osteoarthritis. Surgical reconstruction, such as procedures that enhance fusion of the anconeal process, may be the preferred method of management, since these procedures preserve the function of this intra-articular stabilizing structure. A dynamic proximal ulnar osteotomy alone may be sufficient to allow fusion of the anconeal process in young (6–12 months) dogs, while a dynamic proximal ulnar osteotomy and lag screw fixation may be required in older (over 1 year) dogs, or in dogs
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•
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with loose attachment of the anconeal process to the olecranon. Four categories of UAP have been defined, and the type of union may be used to guide treatment. • Cartilage retention nest. In this lesion (usually an incidental finding) the anconeal process is united; however, an area of cartilage remains along part of the fusion site. This lesion is not likely to be a cause of lameness. • Delayed union. A normal union may occur in young dogs (5–6 months) if cage rest and exercise restriction are employed. If union fails to occur after 4 to 6 weeks of conservative treatment, surgical treatment is indicated. • Non-displaced nonunion. The anconeal process is apposed to the proximal ulna by fibrous or fibrocartilaginous tissue. Such fragments can be successfully reconstructed if the fragment size, bone density (screw holding power), viability of the tissue interface and fragment, and degree of interfragmentary compression achieved are adequate. • Displaced nonunion. The anconeal process is physiologically (due to lack of blood supply or viable interface tissue) or anatomically separated from the proximal ulna. These loose fragments act as foreign bodies and interfere with normal joint function, and should be removed.
Surgical Procedures Objectives
• Remove or reconstruct the anconeal process. • Identify and treat concurrent conditions such as OCD/FMCP.
Equipment
• • • • • • •
Standard surgical pack and suture Gelpi self-retaining retractors Suction and cautery Periosteal elevator Drill, drill bits, taps, depth gauge, screws, and screwdriver Small bone curette Small osteotome and mallet, gigli wire or oscillating bone saw
Technique The anconeal process may be removed via a caudolateral arthrotomy. 1. Place the patient in lateral recumbency, with the affected limb up; prepare for aseptic surgery using the hanging limb technique. 2. Perform a caudo-lateral approach to the elbow, placing the incision in the anconeus muscle at its insertion on the ulna, and elevate the muscle using the periosteal elevator. 3. Retract the anconeus muscle and lateral head of the triceps with the gelpi retractor.
4. Externally rotate the antebrachium and slightly flex the elbow to gain adequate exposure of the anconeal process. 5. Remove the anconeal process and close. The quality of attachment of the anconeal process can be evaluated with arthroscopy or following an arthrotomy. If the anconeal process is firmly attached, perform a dynamic proximal ulnar osteotomy to normalize loading within the joint; this may allow the anconeal process to fuse spontaneously. If the anconeal process is loosely attached, perform interfragmentary compression with lag screw fixation, and a dynamic proximal ulnar osteotomy can be performed to normalize loading within the joint. 1. Explore the joint and the quality of attachment of the anconeal process with arthroscopy or following an arthrotomy. 2. If the anconeal process is loosely attached, attempt lag screw fixation of the UAP. a. Drill a thread hole either freehand from the apex of the anconeal process to the caudal ulna, or from the caudal ulna to the apex of the anconeal process (the latter is facilitated by using an aiming device). b. Drill a glide hole in the caudal ulna by overdrilling the thread hole. c. Measure the screw length. d. Tap the thread hole in the anconeal process. e. Insert the screw from caudal to cranial observing the degree of compression (Fig. 118-2). f. Do not allow the screw tip to protrude beyond the apex of the anconeal process. 3. Perform a caudo-lateral approach to the ulnar diaphysis by elevating the extensor carpi ulnaris and abductor pollicis longus from the lateral aspect of the ulna, and the flexor carpi ulnaris and deep digital flexor from the medial aspect. 4. Perform an ulnar osteotomy just distal to the level of the radial head, oriented cranio-distal to caudo-proximal 30 to 40 degrees (Fig. 118-3). The angle of the osteotomy prevents caudal tipping of the proximal segment due to the pull of the triceps muscle. 5. An intramedullary pin placed from the olecranon to the distal ulnar diaphysis can be used to increase stability of the proximal segment (see Fig. 118-3). 6. Do not hesitate to remove the anconeal process if a. Technical difficulties prevent successful internal fixation. b. Bone quality is poor resulting in poor screw purchase or compression. c. The shape of the anconeal process results in poor joint congruency following internal fixation.
Postoperative Care and Complications
• Apply a soft padded bandage for 3 to 5 days from the digits to the mid-diaphysis proximal to the incision to minimize postoperative swelling.
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lateral annular ligament
caudal crus of ulnar collateral lig.
interosseous lig.
Figure 118-3. An oblique osteotomy of the ulna can be performed to equalize forces within the elbow joint. The placement of an intramedullary pin in the ulna is optional. Perform this technique if internal fixation of the anconeal process is utilized, in order to decrease the likelihood of implant failure due to cyclical stress. Figure 118-2. Rigid internal fixation of the anconeal process utilizing a screw placed in lag fashion.
OCD OF THE MEDIAL PORTION OF THE HUMERAL CONDYLE AND FRAGMENTATION OF THE MEDIAL PORTION OF THE CORONOID PROCESS (FMCP) OF THE ULNA
• Remove skin sutures in 10 to 14 days. • Confine the dog to leash walks only for 6 weeks to
• •
allow neochondrogenesis to occur at the site of removal, or anconeal process fusion to occur, depending on the technique that has been performed. Repeat radiographs in 4 to 6 weeks to assess fusion of the anconeal process and healing of the ulnar osteotomy if performed. Allow gradual return to normal activity over the next 6 weeks to allow cartilage remodeling to occur.
Prognosis
• Good results were obtained with dynamic proximal
•
•
ulnar osteotomy in a group of young dogs 6 to 12 months old; less favorable results were obtained in a group of dogs 1 to 2 years old. In animals with anconeal process removal the prognosis is good to fair; resolution of lameness occurs postoperatively. However, most animals begin to be lame at 6 to 7 years of age secondary to osteoarthritis. The prognosis is good to excellent if the anconeal process fuses following surgical reconstruction.
OCD and FMCP affect the distal humerus in the same dog populations that are affected by OCD of the shoulder, and may be bilateral. OCD and FMCP coexist in as many as 37% of cases.
Anatomy • FMCP is separation of the medial coronoid process from the ulna; the etiology is unknown.
• OCD usually occurs on the medial portion of the humeral condyle.
Pathophysiology FMCP
• OCD of the medial coronoid may play a role; a defect •
in endochondral ossification may lead to degeneration of the process and fissure formation. Developmental elbow incongruity has also been implicated; a relatively long ulna and short radius may result in an increase of weight-bearing forces on
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the medial coronoid process, which may precipitate fragmentation. Fragmentation of the coronoid results in a separate piece of cartilage and trabecular bone, which is attached to the annular ligament with fibrous tissue. Separation occurs through calcified trabeculae that are then covered, in part, with fibrous connective tissue. The end result is joint instability and development of DJD. Cartilage on the opposing medial humeral condyle may be eroded by the loose coronoid fragment (kissing lesion). Peri-articular osteophytes and soft-tissue fibrosis develop progressively over time.
OCD
Radiographs
• Obtain lateral and cranio-caudal views, and a flexed • • • • •
• A failure of endochondral ossification results in an OCD lesion in the medial portion of the humeral condyle.
Clinical Signs • Forelimb lameness, initially evident at 5 to 8 months •
• •
•
•
of age, is seen in retrievers, Bernese mountain dogs, and Rottweilers. Clinical signs usually become apparent at 5 to 7 months of age; however, the dog may not be presented until 1 to 2 years of age after development of DJD. Lameness is worse after exercise, and joint effusion and peri-articular fibrosis may be palpable. Lameness is usually unilateral even if both joints are affected; a stiff or stilted gait may be observed if bilateral forelimb lameness is present due to shortened stride. Pain with flexion and extension of the joint is evident, especially with supination or pronation; discomfort may be noted with palpation of the medial coronoid process. Avoid shoulder motion during manipulation to avoid mistaking shoulder pain for elbow pain.
•
lateral exposed anconeal process to assess for osteophytosis. A craniolateral-caudomedial 15-degree oblique with 30 degrees flexion may help visualize the medial coronoid. A mediodistal-lateroproximal oblique (MEDLAP) view has recently been shown to enhance visualization of the medial coronoid process. Blunting of the coronoid, visible fragments, and osteophytes associated with the coronoid process, anconeal process, or radial head may be visible. The earliest radiographic sign is commonly the presence of osteophytes on the anconeal process. Later signs include subchondral bone sclerosis, articular and peri-articular osteophytosis, joint space narrowing, joint effusion, and peri-articular soft-tissue thickening indicating secondary DJD. Definitive diagnosis can be made with arthroscopy, computed tomography, magnetic resonance imaging, or arthrotomy.
OCD
• Radiographically a triangular subchondral bone defect is evident in the medial portion of the humeral condyle in the cranio-caudal projection.
Differential Diagnosis • Other conditions affecting the elbows of young dogs • •
produce similar signs, and can be differentiated radiographically. Consider UAP, combinations with OCD/FMCP and UAP, and subluxation resulting from premature physeal closure. Other diseases of the forelimb in young dogs should be considered such as OCD of the shoulder and panosteitis.
Treatment
Diagnosis
Medical Management
FMCP
• Asymptomatic dogs or those with severe DJD may be
• The radiographic findings of FMCP are nonspecific. • Evaluate both elbows radiographically, as the disease is commonly bilateral.
• A presumptive diagnosis is made based on typical
•
history and clinical signs. ▼ Key Point The FMCP cannot always be observed, and the diagnosis may be made by inference due to the presence of osteoarthritis.
• Osteophytosis and superimposition of the radial head on the coronoid process make identification of the FMCP difficult.
•
treated medically; all surgically treated dogs are also treated with lifelong medical management, as surgical treatment does not halt the progression of DJD. Weight loss, exercise moderation, nonsteroidal antiinflammatory drugs (NSAIDs), and chondroprotective agents are the cornerstones of treatment. Rest (2–3 weeks) and NSAIDs are utilized to treat episodes of lameness, followed by return to moderate regular exercise.
Preoperative Considerations Persistent lameness and mild DJD are indications for surgery; however, some dogs with moderate or severe
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DJD may benefit from loose fragment removal. It is important to note that surgical treatment does not halt the progression of DJD.
Equipment
• Arthroscopy tower, arthroscope and camera, hand
Surgical Procedure Objectives
•
• The goals of surgery are to remove the FMCP and to
• • •
•
•
debride the osteochondral defect with minimal damage to the joint during the surgical approach and procedure. An arthrotomy or arthroscopy can be employed. • Elbow arthroscopy via medial portals allows identification and removal of the FMCP with graspers or a shaver. Arthroscopy improves intra-articular identification with recognition of cartilage defects, and allows eburnated cartilage to be treated by abrasion arthroplasty and/or microfracture. The ability to treat bilaterally, as well as identify and manage coexistent cartilage defects, supports arthroscopic management. See respective chapters on elbow disorders for a description of surgical approaches (see Chapter 105).
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instrumentation, and motorized shaver if arthroscopy is to be performed Standard surgical pack and suture if arthrotomy is to be performed Gelpi self-retaining retractors Suction and cautery Small bone curette
Technique
• Perform either arthroscopy via the medial portals, or
• •
an open approach. • If arthroscopy is performed, both elbows may be treated in a single session. • If an arthrotomy is performed, operate on the more symptomatic elbow first, followed by the second in 4 to 6 weeks. Several open approaches are suitable, including the muscle splitting approach (Fig. 118-4), and osteotomy of the medial epicondyle of the humerus. In FMCP, remove the fragment(s) and debride the fragment’s bed to the level of subchondral bleeding
medial coronoid process
median nerve
incision into joint capsule
C
superficial digital flexor
A
flexor carpi radialis
B
Figure 118-4. Medial approach to the elbow joint by an intermuscular incision. Incise the intermuscular septum between the flexor carpi radialis and deep digital flexor muscles or the flexor carpi radialis and the pronator teres muscles. Retraction of the muscles allows exposure and incision of the joint capsule parallel to the muscles. Note the proximity of the ulnar and median nerves.
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•
•
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bone utilizing a curette, a hand bur, or a motorized shaver. In OCD, debride the lesion to the level of subchondral bleeding bone utilizing a curette, a hand bur, or a motorized shaver, ensuring that the edges of the lesion are debrided peripherally to normal cartilage, and are perpendicular to the subchondral bed. Microfracture can be utilized to create vascular access channels from the lesion to the underlying subchondral bone. If arthroscopy is performed, identify and treat concurrent conditions such as cartilage eburnation or kissing lesions with microfracture or abrasion arthroplasty. • Perform microfracture with specially designed chondropicks. Place the pick within the lesion, and gently tap it into the surface using a mallet. Treat the entire lesion in a grid-like pattern; space the holes 2 to 3 mm apart and 1 to 2 mm deep. • Perform abrasion arthroplasty as for an OCD lesion; debride the lesion to the level of subchondral bleeding bone utilizing a curette, a hand bur, or a motorized shaver, ensuring that the edges of the lesion are debrided peripherally to normal cartilage, and are perpendicular to the subchondral bed.
Postoperative Care and Complications • Arthroscopy: • Apply a soft padded bandage for 24 hours.
•
• Institute strict exercise restriction for 4 to 6 weeks, followed by gradual return to normal activity. • Long-term medical management of osteoarthritis should be employed. Arthrotomy: • Obtain postoperative and 6-week follow-up radiographs if implants are used (osteotomy of the epicondyle). • Apply a soft padded bandage for 5 to 7 days. • Institute strict exercise restriction for 4 to 6 weeks, followed by gradual return to normal activity. • Administer long-term medical management of osteoarthritis.
Prognosis • The prognosis for full function is guarded because • • •
of progressive DJD regardless of the treatment method. Most dogs are functional pets with intermittent lameness. Osteoarthritis is usually present and requires lifelong medical management. In a recent study of surgical management of 429 dogs, approximately 50% had a resolution of lameness, 30% had a diminished severity of lameness, and in 20% severity of lameness was not affected by surgery.
Chapter
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119
Pediatric Fractures Matthew Palmisano
Fractures occurring in immature animals (1 year of age. ▼ Key Point The prognosis for continued growth of the physis with Salter-Harris type I through III fractures may be more favorable than type IV through VI due to preservation of the growing zones of the physis. However, warn owners of the possibility of premature physeal closure with limb shortening or angular limb deformity with any fracture of the long bones involving the physis.
PREOPERATIVE CONSIDERATIONS • High-quality, orthogonal radiographic views of the •
fractured bone are a must when characterizing the type of fracture and determining method of repair. Consider external coaptation, either by splinting or casting, in fractures that are simple, transverse, minimally displaced, easily reduced, and distal to the stifle or elbow. Some Salter-Harris I and II physeal
turnover and deposition associated with growth. External coaptation has the advantage of preserving blood supply with minimal soft tissue disruption, which will allow a bony union by 3 to 4 weeks. Consider open reduction and internal fixation (bone plates, pins, or screws) of fractures with unstable fractures, intra-articular fractures, or fractures >48 hours old. Immature bone is very soft and easily fractured with aggressive manipulation. Particular care should be taken with the growth plate. The proliferative zone of cartilage is usually with the epiphyseal segment, so particular care should be taken with this segment so as not to cause premature physeal closure. Gentle tissue handling and preservation of blood supply are important. A balance should be made between rigid stabilization of implants and maintenance of the soft tissues.
SURGICAL PROCEDURES Operative Considerations • In most physeal fractures, use the smallest Kirschner
•
wires, pins, or screws that will provide sufficient stabilization, while causing the least amount of physeal trauma. Refer to the following chapters for specific fixation techniques of commonly seen physeal fractures: • Salter-Harris IV distal humeral fracture: Chapter 104. • Salter-Harris I or II capital femoral physeal fracture: Chapter 109. • Salter-Harris I proximal humeral fracture: Chapter 104. • Salter-Harris I or II distal femoral fracture: Chapter 109. • Salter-Harris I or II proximal tibial fracture: Chapter 111.
POSTOPERATIVE CARE AND CONSIDERATIONS Postoperative Care • Elimination of high-impact activity is a must, since immature bone is soft and implants used in fixation are relatively small and susceptible to bending and loosening.
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• If postoperative immobilization is required using a
• •
•
bandage or cast, reevaluate the coaptation weekly. A cast may need to be changed every 2 weeks in young, large- or giant-breed dogs, because they may quickly outgrow the cast. Obtain radiographs of the repair every 2 weeks in order to assess healing. Radiograph the contralateral limb for comparison. Exuberant callus formation with muscle and tendon entrapment, muscle atrophy, and joint contracture may be minimized using postoperative physical therapy (see Chapter 95). In some cases, remove the implants in 4 weeks in order to minimize the potential for premature physeal closure.
Complications • Exuberant bony callus is a problem in younger
•
patients and is seen in unstable fixations or external coaptation of distal femoral fractures. Bony callus can entrap muscle and tendon. Bony callus can also cause fusion between bones. If this occurs between the radius and ulna, asynchro-
•
•
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nous growth and resultant angular limb deformity can occur. Angular limb deformity caused by premature physeal closure should be identified and addressed early. Corrective osteotomies are often required in order to correct the angular limb deformity (see Chapter 105). Limb shortening caused by premature physeal closure may alter limb gait, but limb length discrepancies of 25% or less are often well tolerated in dogs and cats due to their relatively flexed stance.
SUPPLEMENTAL READING Brinker WO, Piermattei DL, Flo GL: Handbook of Small Animal Orthopedics and Fracture Treatment, 2nd ed. Philadelphia: WB Saunders, 1990. Johnson JM, Johnson AL, Eurell J: Histological appearance of naturally occurring canine physeal fractures. Vet Surg 23:81–86, 1994. Manfra Marretta S, Scrader SC: Physeal injuries in the dog: A review of 135 cases. JAVMA 182:708–710, 1983. Manley P: Principles of fracture fixation in growing animals. Sem Vet Med Surg (SA) 7:36–43, 1992. Salter RB, Harris WR: Injuries involving the epiphyseal plate. J Bone Joint Surg 45A:587-621, 1963.
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120
Open Fractures Charles E. DeCamp
An open fracture is one that has been exposed to the environment and contaminated by or infected with bacteria. The soft tissue injury that accompanies an open fracture may be a simple puncture wound or a complex injury with vascular compromise and tissue necrosis. Successful management of open fractures depends on proper treatment of soft tissue wounds and fracture fixation. If soft tissue wounds are properly managed, the morbidity of wound infection is reduced and fracture healing can proceed at a normal rate.
CLASSIFICATION OF OPEN FRACTURES Open fractures are classified as type I, II, or III, based on the mechanism and severity of soft tissue injury (Fig. 120-1). The purpose of classification is to determine the likelihood of serious infection. The type of wound management and the choice of fracture fixation partly depend on the classification.
• Type I develops when a fracture fragment penetrates
•
•
•
the skin, exposing the fracture to bacterial contamination. Soft tissue injury is minor, and wound infection is unlikely with proper care. Type II develops when an external object forcefully penetrates the skin and soft tissues, creating a fracture and contaminating the wound. Fracture severity is highly variable, but soft tissue injury is relatively minimal and usually is not complicated by vascular compromise and tissue necrosis. Bacterial contamination generally is more extensive than for type I injuries. Type III develops when an external object forcefully penetrates the skin and soft tissues, creating a fracture, contaminating the wound, and severely damaging the soft tissues. The ability of the body to combat soft tissue infection commonly is complicated by vascular compromise and necrosis. The risk of bacterial infection is very high. Some authors describe an additional class of open fracture, type IV, where the trauma has caused amputation or near amputation of the limb.
1206
▼ Key Point Type I open fractures are least likely to develop wound infections; type III open fractures almost always have some level of infection.
• In all fracture types, if the wound has been neglected and infection develops, manage the injury as though it were a type III injury.
PREOPERATIVE CONSIDERATIONS • Perform a complete physical examination to rule out injury to other organs.
• The diagnosis of an open fracture may be made by direct inspection, palpation, and radiography.
• If skin penetration, laceration, or avulsion is present, • •
•
assume that the fracture is open and contaminated until proven otherwise. Cover all open wounds with a sterile dressing. Obtain radiographs after dressing placement. • Radiographic signs of air within the soft tissues adjacent to a fracture are diagnostic of an open fracture. Use aseptic technique when manipulating the wound.
▼ Key Point Violating the rules of strict asepsis during early wound management increases the probability of nosocomial infection.
• If preparation of the wound cannot proceed imme-
•
diately, use external coaptation for temporary stabilization of the fracture. Apply a reinforced Robert Jones bandage for injuries below the stifle or elbow. Use a spica splint for open fractures of the femur or humerus. To prepare the wound, remove the sterile bandage and carefully clip surrounding hair to avoid contamination. If necessary, cover the wound with sterile gauze sponges moistened with sterile saline or sterile water soluble lubricant gel to prevent introduction of the clipped hair into the wound.
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• Reconstruct soft tissue to cover bone and provide •
limb function. It may be necessary to defer this aspect if a large tissue defect or necrosis is present. Provide temporary or definitive fracture fixation.
Equipment • Two standard general orthopedic packs and suture material
• Bone curette and brush • Sterile saline or lactated Ringer’s solution • Fracture fixation equipment: • • • •
Materials for external coaptation External skeletal fixation pins and clamps Power drills Bone plating equipment
Surgical Debridement Techniques Type I Open Fracture Figure 120-1. Types of open fractures. Type I (top): Fracture fragment penetrates skin. Type II (center): Penetrating object causes minor injury to soft tissue. Type III (bottom): Penetrating object causes extensive damage to soft tissue.
1. Little or no surgical debridement is required. 2. If the bone is not visibly exposed and the wound is small, copiously lavage the wound with sterile lactated Ringer’s solution. 3. Sharply excise necrotic tissue, if present, from the wound before fracture fixation.
Type II Open Fracture
• Lavage the wound with copious amounts of sterile
• •
•
saline or lactated Ringer’s solution to remove small particulate matter from the wound interstices (see Chapter 56). Betadine and alcohol may be used on the skin surrounding the wound; however, avoid contact of detergents or alcohol with the open wound. Remove a sample of fluid from the fracture site for laboratory tests, using a swab if the size and type of wound permit its introduction. Base definitive antibiotic treatment on culture and sensitivity tests. A Gram stain may reveal the organism type and aid the initial choice of antibiotics. Consider giving broad-spectrum systemic antibiotics while waiting for results of culture and sensitivity.
▼ Key Point Systemic antibiotics are less important than proper wound care for prevention and treatment of wound infection.
SURGICAL DEBRIDEMENT, FRACTURE FIXATION, AND SOFT TISSUE RECONSTRUCTION Objectives • Improve wound environment to reduce the risk of infection.
1. Surgical debridement generally is not extensive; however, be careful to remove all non-viable tissue. 2. Copiously lavage the wound with sterile lactated Ringer’s solution before fracture fixation.
Type III Open Fracture (Extensive Debridement and Lavage) 1. Prepare the limb and wound for aseptic surgery. If a surgical approach to a bone is anticipated, extend the skin preparation to the appropriate anatomic field. 2. Drape the limb using standard aseptic technique and water-impermeable drapes. 3. Sharply excise necrotic skin, fat, fascia, and muscle from the wound. 4. Remove any loose, dirty, small fragments of bone. 5. To preserve the blood supply and prevent development of bone sequestra, maintain tissue attachments to bone fragments. Point ▼ Key
Clean large, attached bone fragments with a bone curette or brush if necessary. Do not remove them.
6. Clean, but do not debride, tendons, ligaments, intact blood vessels, and nerves unless they are necrotic. 7. If necessary, extend access to the bone by a surgical approach for fracture fixation. If severe contamina-
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tion or infection is present, apply external skeletal fixation with minimal or no surgical approach (see Chapter 111).
Fracture Fixation • Do not carry out fracture fixation until initial wound management is complete (as described previously).
• If the fracture is stable and non-articular and involves a bone distal to the stifle or elbow joint, external coaptation may be effective. Most other fractures require surgically applied orthopedic fixation.
Techniques
2. In general, do not use metallic implants at the fracture site unless adequate wound drainage is assured. Do not use intramedullary pins because of the difficulty in providing surgical drainage from the medullary canal. 3. Bone plates may be used in conjunction with delayed or secondary wound closure techniques, unless severe infection is present. 4. If possible, use external skeletal fixation (see Chapter 111) because a fixator may be constructed that avoids placement of metallic implants directly in the fracture site. However, anatomic considerations may contraindicate their use.
If a surgical approach is made, obtain samples of fluid from the fracture site and submit for culture and sensitivity.
▼ Key Point Regardless of the type of orthopedic
▼ Key Point To avoid bacterial contamination from
5. If an external fixator cannot be used, a type I external fixator, transarticular external fixator, or external coaptation may be used as temporary fixation so that local wound care and resolution of infection may proceed. When the wound environment has improved, other methods of internal fixation such as bone plates and lag screws may be applied with less risk of infection.
debrided tissues, use a new, sterile pack for the surgical approach and fracture fixation.
Type I Open Fracture 1. Repair with the appropriate method of external or internal fixation. 2. If a surgical approach is made to the bone, avoid contact with the traumatic wound to prevent bacterial contamination. Skin drapes may be used. 3. After fracture fixation, close the wound routinely. Penrose drains or delayed wound closure techniques usually are not necessary.
Type II Open Fracture 1. Repair with the appropriate method of external or internal fixation. 2. If a surgical approach is made to the bone, avoid contact with the traumatic wound. Skin drapes may be used. 3. Because bacterial contamination of the wound can be more severe than for type I fractures, provide proper drainage of exudates. 4. If the surgical wound is closed, place Penrose drains to exit the wound at a site ventral to the surgical incision. Alternatively, in medium to large dogs, consider placement of closed suction drains. 5. If bacterial contamination is severe, perform delayed or partial wound closure to ensure proper drainage (see Chapters 55 and 56).
implant, rigid fixation is mandatory for definitive treatment of the fracture.
Reconstructive Soft Tissue Surgery • Primary, delayed primary, or secondary closure tech• •
•
•
niques (see Chapters 55 and 56) may be used to treat traumatic wounds in open fractures. Wounds may be allowed to heal by second intention. Some wounds may not heal because of their large size or because they are located at a site of active motion or a pressure point (e.g., elbow). In these cases, reconstruct the skin wound with a skin flap or graft (see Chapter 57). Skin flaps or grafts may be constructed at the time of fracture fixation but often are delayed until a healthy bed of granulation tissue indicates that wound infection is resolved. If arthrodesis is the primary method of orthopedic fixation for the carpus or tarsus, perform skin reconstruction 1 month before arthrodesis. This allows full resolution of soft tissue infection and good soft tissue cover over the proposed arthrodesis site.
POSTOPERATIVE CARE
Type III Open Fracture ▼ Key Point Treatment of most type III open fractures proceed in the following order: wound care, fracture fixation, and skin reconstruction.
• Administer postoperative analgesics as necessary (see Chapter 6).
• Continue appropriate postoperative wound care to prevent and control infection.
• Keep open wounds bandaged, and replace the 1. Carefully choose a method that reduces the risk and severity of wound infection.
bandage daily to prevent accumulation of exudates at the wound site.
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• Lavage open wounds daily with sterile saline or lac• • • • •
tated Ringer’s solution until healthy granulation tissue indicates resolution of infection. Restrict activity, depending on the fracture type and method of fixation. Use an Elizabethan collar, if necessary, to prevent the animal from licking its wounds or removing the bandages. Stage implant removal to provide optimal bone healing and to minimize risk of long-term wound or bone infection. Perform a physical examination and obtain radiographs at appropriate intervals to evaluate proper bone healing and resolution of infection. Administer postoperative physical therapy as needed to restore function in the affected limb (see Chapter 95).
COMPLICATIONS • Continued infection suggests the presence of •
necrotic soft tissue or bone, an unstable fracture site, or unstable orthopedic implants. Delayed healing of a fracture may develop from prolonged infection at the fracture site, poor reduction,
1209
unstable fixation, or bone loss due to trauma or infection (see Chapters 121 and 122). ▼ Key Point Most complications can be avoided with proper wound management, orthopedic fixation, and postoperative care. Serial examinations to assess progress are essential to avoid development of major problems.
SUPPLEMENTAL READING Brinker WO, Piermattei DL, Flo GL: Handbook of Small Animal Orthopedics and Fracture Treatment. Philadelphia: WB Saunders, 1990, p 50. Dueland RT: Open (compound) fractures. In Brinker WO, Hohn RB, Prieur WD (eds): Manual of Internal Fixation in Small Animals. Berlin: Springer-Verlag, 1984, p 108. Grant GR, Olds RB: Treatment of open fractures. In Slatter DH (ed): Textbook of Small Animal Surgery, 3rd ed. Philadelphia: WB Saunders, 2003, p 1793. Nunamaker DM: Open fractures and gunshot injuries. In Newton CD, Nunamaker DM (eds): Textbook of Small Animal Orthopaedics. Philadelphia: JB Lippincott, 1985, p 481. Richardson DC: Fracture first aid: The open (compound) fracture. In Slatter DH (ed): Textbook of Small Animal Surgery. Philadelphia: WB Saunders, 1985, p 1945.
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121
Osteomyelitis Callum W. Hay
Osteomyelitis is caused by infection of bone and associated structures (soft tissue, periosteum, and endosteum). Osteomyelitis is invariably caused by an infectious agent such as bacteria or fungi. Acute onset osteomyelitis is rare and generally does not show detectable radiographic changes until 5 to 10 days after bone inoculation. Chronic osteomyelitis is seen as a complication from orthopedic surgery, extension of tooth infection into bone (with periodontal disease), or from nail bed infections. Osteomyelitis can mimic other diseases such as panosteitis, hypertrophic osteodystrophy, and neoplasia and should be differentiated from these.
ETIOLOGY Bacteria • The common routes of bacterial infection are outlined in Table 121-1. ▼ Key Point Chronic bacterial osteomyelitis is the most common form seen in veterinary medicine.
bone or soft tissue, foreign material such as metallic orthopedic implants or methyl methacrylate, and especially fracture instability.
• Beta-lactamase–producing Staphylococcus aureus bacte-
•
ria cause a large majority of infections. Other common bacteria are Pseudomonas aeroginosa; Escherichia coli; and Streptococcus, Bacteroides, Actinomyces, and Clostridium species. Bacteria produce a mucopolysaccharide coating called glycocalyx, which protects bacteria from phagocytes, antibiotics, and antibodies. Bacterial colonization of orthopedic implants or necrotic bone allows reinfection once antibiotic therapy is stopped.
Fungi Fungal entry into the respiratory tract can lead to osteomyelitis from hematogenous spread. Direct contamination through an open wound is possible, but rare. Most infections will occur in the vertebral bodies/disks or in the bones of the skull. Coccidioides, Blastomyces, Histoplasma, Cryptococcus, and Aspergillus spp. can all cause fungal osteomyelitis.
• Orthopedic surgical procedures allow introduction
•
•
of bacteria from the patient’s skin or from implants placed in the wound (bone plates, suture). Direct inoculation from the surgeon’s skin or apparel is also possible. Chronic periodontal disease with extension of infection into the mandible or maxilla can lead to chronic osteomyelitis and bone weakening. The mandible of small dogs can be susceptible to iatrogenic fracture during tooth extraction, if significant osteomyelitis is present. Nail bed infections acquired from trauma and the environment can extend into phalanges and digits (see Chapter 63).
▼ Key Point Osteomyelitis is often propagated by local tissue environmental factor(s), which over whelm the body’s own natural defense mechanisms. These include poor vascularity, necrotic 1210
DIAGNOSIS History • Osteomyelitis can be preceded by orthopedic surgery, penetrating trauma, chronic dental disease, injury to the toes/foot pads, or possibly known travel to an endemic fungal region.
Physical Examination • The patient may have evidence of lameness, inappe-
•
tence, malaise, elevated body temperature, muscle atrophy, and pain on direct palpation of affected area(s). Patients who have had orthopedic surgery may have obvious instability at the fracture site or exterior migration of pins. A draining tract may develop distal
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Table 121-1. ROUTES OF INFECTION IN OSTEOMYELITIS Open reduction and internal fixation of fractures; other orthopedic intervention Open fractures Extension from soft tissue infection (periodontal disease, rhinitis, otitis media) Traumatic injuries and bite wounds Penetrating foreign bodies, including sticks and grass awns Gunshot injury Hematogenous Prosthetic joint replacement surgery
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• Mucopurulent nasal discharge, coughing, or pulmonary crackles/wheezes may be observed in patients with disseminated fungal infections (see Chapter 20).
Hematology • Acute systemic infection may cause a neutrophilic leukocytosis; however, chronic osteomyelitis may not cause significant hematologic abnormalities.
Diagnostic Imaging Survey Radiography
• Acute osteomyelitis will not be readily apparent for 10 to 14 days after initial inoculation.
• Focal bone lucencies and aggressive periosteal proliferation may be seen.
• Bone sequestra are diagnostic of chronic osteomyelitis.
• Evidence may be seen of implant migration/failure. • It can be difficult to differentiate hypertrophic non-
• • Sinus tract
union from chronic osteomyelitis with survey radiographs (also see Chapter 122). Both processes can be associated with an aggressive periosteal response with apparent lucent areas. In the case of mild fracture instability, both can be present simultaneously. Fungal osteomyelitis generally involves flat bones and the metaphyses of long bones and may have multiple lytic and proliferative lesions. Acute osteomyelitis can be difficult to distinguish from acute postoperative infection because radiographic changes are minimal.
Contrast Radiography
• It may be useful to inject soluble iodinated contrast
• Figure 121-1. Chronic osteomyelitis with sequestrum, loose unstable implants, and involucrum walling off the focus of infection. These conditions favor chronic bacterial infection, and purulent exudate drains through a dependent sinus.
•
•
to the surgical site (Fig. 121-1). Exudate from a tract is not necessarily copious and can appear minimal, especially if the patient is frequently licking the site. Small-breed dogs with severe dental disease with mandibular involvement may be very painful on oral manipulation. Pathologic fractures (either precipitated iatrogenically from tooth extraction or from trauma) are easily palpable under general anesthesia. Swelling, heat, pain, and possibly a draining tract may be seen in patients with digital osteomyelitis.
media (e.g., iohexal) into a draining tract to determine the location and extent of chronic osteomyelitis. This can be especially useful in trying to differentiate the location of necrotic bone encased in more vascular periosteal bone formation. Perform the fistulogram by injection of contrast media into the draining tract. Use an appropriate-size rubber feeding catheter, or Foley catheter, and place in the tract under aseptic conditions. Occlusion of the exterior of the tract with digital pressure or using an atraumatic instrument may be necessary to allow proper contrast flow. Try not to allow significant outward leakage, which could hinder the ability to interpret radiographic abnormalities.
Laboratory Evaluation Cytology
• Smears of aspirates or swabs can be useful for diagnosing fungal infections. They are probably of limited use for presumed bacterial causes since the sensitivity and specificity of cytology is likely to vary widely between cases of osteomyelitis.
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Bacteriology
Acute Osteomyelitis
• Obtain samples using appropriate asepsis (clipping,
▼ Key Point Open fractures, especially in the upper
•
•
disinfecting skin, and using sterile gloves) with appropriate restraint (heavy sedation or general anesthesia). Submit aspirates of affected tissue for aerobic and possibly anaerobic culture and sensitivity. Obtain surgical samples from bone, implants, or tissue; these should be taken preferably before perioperative antibiotic prophylaxis has been administered. Obtain samples for fungal cultures. However, these may take weeks to yield results.
limbs or with extensive soft tissue loss and bone exposure in any bone, are considered surgical emergencies. Appropriate equipment and experience are necessary to minimize complications. Consider expedient referral to a specialist if these resources are not readily available.
Preoperative Considerations Antibiotic Prophylaxis
Histopathology
• Administer antibiotics after appropriate samples have
• Histopathology is likely to be useful if neoplasia is
• Parenteral use: consider using ampicillin (20 mg/kg
suspected.
been obtained.
• Specialized fungal stains can be requested on pathology samples submitted to any laboratory.
TREATMENT The treatment goals in osteomyelitis are to provide a suitable local environment that is conducive to granulation tissue formation, soft callus formation, and ultimately new bone regeneration. Chronic bacterial osteomyelitis is much more common than acute osteomyelitis and fungal osteomyelitis. However, open fractures, acute postoperative orthopedic infection, and deep bite wounds should be considered predisposing factors to acute osteomyelitis, which if inappropriately treated could lead to chronic osteomyelitis.
Surgical Procedures Objectives
• • • • • •
Identify pathogenic organisms. Determine antibiotic sensitivity. Drain infected tissue. Remove avascular bone (sequestrectomy). Stabilize the fracture. Implant a bone graft to aid osseous union of fractures.
Equipment
• Standard orthopedic instrument pack and suture. • Rongeurs to debride bone. • Fracture repair instruments and equipment (e.g., • • •
plates, screws, external fixator, and possibly interlocking nails). Orthopedic power equipment. Curettes for bone graft collection and debridement. Retractors: hand-held or self-retaining, such as gelpi retractors.
•
q6–8hr IV) with either amikacin (15 mg/kg q24hr IV) or enrofloxacin (5–10 mg/kg q24hr SC). Use metronidazole (15 mg/kg q12hr IV) for suspected anaerobes; however, ampicillin will be effective against most anaerobic organisms. Cefazolin, while effective against S. aureus, is generally not effective against Enterococcus, which is likely to be present in a wound contaminated from the environment. Oral use: consider amoxicillin/clavulanate (20 mg/ kg q12hr PO) and/or enrofloxacin (5–10 mg/kg q24hr PO). Analgesia
• Patients with acute osteomyelitis are extremely painful. Consider using injectable narcotics such as morphine, butorphanol, buprenorphine, or other similar drugs. If not contraindicated, ketoprofen, meloxicam, carprofen, or flunixin can be given parenterally. Consider epidural administration of morphine and/or bupivacaine for hind limbs where there is no involvement of tissue over the lumbosacral junction (see Chapter 6 for discussion of pain management).
Technique 1. Administer general anesthesia and then clip and aseptically prepare the surgical site. 2. While good exposure is necessary, avoid unnecessary disruption of blood supply or soft tissue attachments to bone. 3. Debride necrotic and infected tissue and remove any foreign material involved in the infection. 4. Lavage the wound thoroughly with sterile saline under pressure from a 20- to 60-cc syringe with an 18-gauge needle. ▼ Key Point Pulsatile pressure with a syringe and needle is more effective at removing bacteria from a wound than simple low-pressure lavage.
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5. Replace loose implants and provide rigid fracture fixation. 6. External fixation is useful for temporary and definitive stabilization of open fractures, especially on the tibia, radius/ulna, and mandible. It may be preferable to stabilize the femur and humerus with plates/screws or interlocking nails depending on the surgeon’s preferences. 7. Consider leaving wounds on the distal limbs open if there is severe loss of skin, muscle, or bone. With appropriate care these wounds will form granulation tissue and can possibly be closed in a delayed manner.
Postoperative Care and Complications
• If the wound is left open, cover it with sterile
• • •
petrolatum-impregnated gauze with sterile sponges. Use cast padding, stretch gauze, and a stretch bandage to cover the wound (see Chapter 56 for open wound management). Irrigate daily (sterile saline) for 3 to 10 days until there is healthy granulation tissue present. Continue with antibiotics, based on the results of culture, for 4 to 6 weeks. Obtain radiographs at 3- to 6-week intervals to determine the progression of healing.
Chronic Osteomyelitis Preoperative Considerations ▼ Key Point Chronic antibiotic therapy alone will fail
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ment and antibiotic therapy and will not require stabilization. ▼ Key Point Bone will heal in an infected environment with internal fixation as long as there is adequate stability.
Technique 1. Expose the fracture site and identify non-viable bone and remove it using rongeurs. 2. Remove and replace implants with either internal fixation (plate/screws or interlocking nail) or external fixation. 3. Irrigate the wound with sterile saline using pulsatile lavage through a 30- to 60-cc syringe and 18-gauge needle. 4. Harvest a cancellous bone graft from the proximal humerus and pack into the bone defect. Larger defects can be filled with a mixture of cancellous bone and cortical/cancellous bone from a rib or ilium. 5. If the wound is to be left open, delay bone graft application until granulation tissue has formed (3–10 days). Manage the wound as outlined in acute osteomyelitis (also see Chapter 56). 6. Highly resistant infections (such as Pseudomonas aeroginosa or E. coli) can be treated with antibioticimpregnated methylmethacrylate beads; these can be impregnated with amikacin, gentamycin, or tobramycin and left temporarily in the wound for 7 to 14 days.
unless the other underlying causes are identified and corrected.
Postoperative Care
• Select antibiotics on the basis of microbiologic Consider amputation of the affected limb if treatment carries a poor prognosis, especially if there is considerable muscle contracture, neurologic damage, soft tissue loss, and financial constraints from the owner. Treat phalangeal osteomyelitis by digital amputation (see Chapter 114). Chronic mandibular or maxillary osteomyelitis can pose a therapeutic challenge due to the lack of bone present in these cases. Obviously infected or necrotic bone should be removed (see Chapter 99); however, iatrogenic fractures created during tooth extraction will generally heal with debride-
culture and continue for 4 to 6 weeks.
• Obtain radiographs at 3- to 6-week intervals to assess the progression of healing.
• Consider physiotherapy and swimming to maintain •
range of motion in joints and to promote controlled use of the limb (see Chapter 95). If continued poor healing is present, assess fracture stability, look for sequestra, and reevaluate microbiologic sensitivities. If none of these factors are present, the fracture may be biologically inactive. Place a bone graft in the bone defect to accelerate healing.
Chapter
▼
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Delayed Union, Nonunion, and Malunion Randy J. Boudrieau
DELAYED UNION AND NONUNION Healing times for similar fractures in any single group of patients are fairly uniform; however, a small number of fractures have longer than normal healing times, or may fail to heal at all. The particular type of fracture (comminuted or simple), the bone involved and its location (e.g., distal radius/ulna in small-breed dogs), the age of the animal, and the type of fixation use all influence normal healing times.
• Classification: • When the fracture requires longer than normal time to heal but shows definitive signs of progression in healing, it is classified as a delayed union. • A fracture that does not heal over a similar period and that has no tendency toward further healing is classified as a nonunion (Table 122-1). Other classifications are based on fracture site, fragment displacement, and presence or absence of infection, but are not routinely used.
Definitions
can be classified into two groups: those with callus formation (the hypertrophic viable nonunions) and those without callus formation (both viable oligotrophic and non-viable nonunions). Most fractures unite within a reasonable time despite systemic factors such as malnutrition, generalized metabolic or endocrine abnormalities, and acute or chronic generalized disease states. ▼ Key Point Nonunion results from local factors at the fracture site.
Most commonly these local factors can be identified as inadequate fracture fixation, resulting in instability (Table 122-3). Motion within a fracture site creates interfragmentary strain at the site, and if this strain exceeds tissue tolerance, the tissue will not form within the gap. For example, essential fragile capillaries will not be able to cross the fracture gap within the early granulation tissue formation, or later, with the subsequent stages of tissue differentiation (cartilage and bone).
• This concept has mistakenly been thought to be a
Delayed Union Radiographic evaluation of the fracture site will reveal callus formation and progressive bone healing, but complete healing has yet to occur over a longer than expected time frame. Delayed union usually needs no other therapy than continuation of ongoing treatment of the fracture. Continued immobilization (assuming stable fixation) allows healing to occur in the majority of cases. A delayed union may, however, be preliminary to a nonunion.
• •
Nonunion Radiographic evaluation of the fracture site reveals a lack of progression of fracture healing (i.e., bone healing has stopped). Variable amounts of callus may be present depending upon a further subclassification of viable (biologically active) or non-viable (biologically inactive) nonunion (Table 122-2). These nonunions 1214
• •
greater problem in highly comminuted fractures as opposed to simple fractures. The problem has greater significance in a two-piece fracture. This situation most often occurs in transverse fractures, where greater difficulty is encountered in attaining appropriate stability. This is important in fracture fixation and the achieving of stability when anatomically reconstructing a fracture. A two-piece fracture has the interfragmentary strain concentrated at the single fracture site. A comminuted fracture has this same amount of interfragmentary strain distributed throughout the many fracture sites (or less strain at each individual site). The result is that in a single fracture there is high strain, whereas in a comminuted fracture there is low strain at each fracture site. Resultant motion in a two-piece fracture will have potentially greater adverse effects on bone healing than in a more comminuted fracture.
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Table 122-1. EXPECTED APPROXIMATE HEALING TIMES OF UNCOMPLICATED DIAPHYSEAL FRACTURES WITH MINIMAL LOSS OF CORTICAL BONE
Age of Animal 1 yr
External Skeletal and Intramedullary Pin Fixation
Bone Plate Fixation*
2–3 wk 4–6 wk 5–8 wk 7–12 wk
4 wk 2–3 mo 3–4 mo 5–8 mo
*Fractures stabilized by this method may not be considered clinically healed (have sufficient strength) as early as fractures stabilized by other means of fixation, because direct cortical union (primary bone healing by Haversian remodeling) is not supported by periosteal callus. This is of primary importance when considering timing of implant removal. Clinical function is not adversely affected by this method of fixation because plates provide rigid fixation.
Table 122-2. VIABLE AND NON-VIABLE NONUNION Viable Nonunion (Biologically Active) Hypertrophic (“elephant foot,” or abundant callus) Moderately hypertrophic (“horse’s hoof,” or moderate callus) Oligotrophic (little or no callus)
Non-viable Nonunion (Biologically Inactive) Dystrophic (poor vascularity of one or both sides of the fracture) Necrotic (avascular areas, or bone fragments, within the fracture, i.e., sequestra) Defect (large bone defect at the fracture) Atrophic (defect at the fracture with resorption of the adjacent bone)
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Table 122-3. FACTORS ASSOCIATED WITH DELAYED UNION AND NONUNION Local Factors* Fracture location Fracture gap Soft tissue interposition Bone loss secondary to trauma Soft tissue trauma Loss of blood supply as a result of initial trauma Contamination, infection Neoplasia
Treatment Factors† Malposition (inadequate reduction) Fracture gap Soft tissue interposition Distraction (by implants or external fixation devices) Bone loss due to intraoperative removal Soft tissue trauma Loss of blood supply due to surgical trauma Inadequate Fixation (Internal or External)‡ Instability Postoperative infection *Related to the fracture. † Related to the reduction and fixation. ‡ Most common factor.
Finally, a very common local factor identified in the etiology of nonunions is in miniature or toy breed dogs, where there is a limited vascular supply to the distal radius. Fractures of this bone in these breeds of dogs have a high propensity for developing into a nonunion. Therefore, obtain rigid fixation using bone plates and place cancellous bone grafts. ▼ Key Point Regardless of the etiology of the nonunion, it requires some form of surgical intervention in order for healing to progress.
The most common local factor is a fracture gap (with or without interposition of soft tissues) that exceeds the regenerative capacity of the bone. There is a critical distance over which bone will not form within a gap, resulting in a nonunion. ▼ Key Point Soft tissue trauma also is an important local factor for bone healing, as damage to the vascular supply will impede healing.
This may occur at the time of fracture, but also at the time of surgery. The importance of the surrounding soft tissues cannot be overemphasized as it is these tissues that are the source for the early revascularization of the bone (transient extraosseous circulation). Therefore, the surgical approaches must be anatomic and atraumatic in nature in order to best preserve this surrounding soft tissue envelope.
Problems Related to Non-healing Fractures Patients with non-healing fractures may have additional problems related to function, such as disuse muscle atrophy, decreased range of joint motion and stiffness related to scar tissue contraction, neurovascular dysfunction, and limb angulation and/or shortening. These functional deficiencies will be the ultimate determinant of the success or failure of treatment, not whether the bone eventually can be made to unite.
Bone Healing
• Bone heals by either primary (Haversian remodeling) or secondary (periosteal callus) union.
• Secondary bone healing, with formation of visible periosteal callus, begins with connective tissue formation that progresses to form fibrocartilage and finally bone.
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• Primary bone healing occurs without formation of
• Radiography may reveal the etiology of the problem.
connective tissue; bone disposition occurs directly (direct Haversian remodeling, or by gap healing, with fracture gaps 60,000; degenerate neutrophils
*Isolation or observation of significant numbers of any microorganism from joint fluid is highly supportive of an infectious or septic etiology, regardless of cell count. Cell counts in immune-mediated and septic joints may be similar in many cases. WBC, white blood cell; +, positive; ±, can be positive or negative; -, negative.
•
•
(one for cytology, one for a Gram stain) and place some synovial fluid in a blood culture bottle to enrich small numbers of bacteria that may be present if sepsis is suspected. Then place the rest of the synovial fluid in a blood tube with ethylenediaminetetraacetic acid (EDTA) shaken out (frequently the synovial fluid volume is small, so there is a relative excess of EDTA). EDTA interferes with the mucin clot test, making interpretation difficult. The predominant cell type seen on cytology in immune arthropathy is usually non-degenerate neutrophils, but mononuclear cells can sometimes be predominant. See Table 124-1 for comparison of joint fluid analysis in various arthropathies.
Synovial Biopsy • May be indicated in diagnostically challenging cases • • •
of immune-mediated joint disease. Requires open biopsy using strict aseptic technique. Harvest synovium at the cartilage-bone margin. Histology shows plasma cell and lymphocyte infiltration.
TREATMENT A dilemma in the treatment of polyarthropathy is whether the process is infectious or non-infectious. The treatment for a non-infectious problem (i.e., immunosuppression) exacerbates an infectious cause of polyarthropathy. If intracellular bacteria are seen on synovial fluid analysis or if bacterial culture is positive, the process is likely septic. However, in endemic areas for Lyme disease and ehrlichiosis it can be difficult to distinguish these from immune-mediated joint disease. Some prefer to initially treat with tetracyclines (e.g., for 1 week) and change to corticosteroids if no response is seen, or after results of diagnostic testing are available. The cyclic nature of many of the immune-mediated diseases, however, makes interpreting a response to treatment difficult.
Nonerosive Forms ▼ Key Point The initial treatment for all nonerosive immune-mediated arthropathies is similar. Use either nonsteroidal anti-inflammatory drugs (NSAIDs) or corticosteroids.
• The lowest dose of drugs to control signs should be used.
• Recurrences are possible after cessation of therapy. Initial Therapy (2 to 4 Weeks of Therapy)
• Buffered aspirin at the higher (anti-inflammatory)
• •
•
dose range (25–40 mg/kg q8h PO) could be tried. Carprofen (2 mg/kg q12h PO) could be administered as an alternative because of its lower risk of gastrointestinal side effects. If sepsis has been ruled out, prednisone at 1 to 3 mg/kg q12h PO may be given. It is best to use either NSAIDs or steroids, but not both. The higher doses of these drugs together may potentiate each other’s side effects. It is feasible to use prednisone on alternate days with NSAIDs, at low doses. Besides clinical signs, repeat aspiration of joint fluid may allow monitoring of the effectiveness of therapy. A cell count of less than 4000/mm3 is ideal. In cases in which the cell count does not decrease and the clinical signs are present, other immunosuppressive drugs may be needed (Table 124-2).
Long-Term Therapy (Months to Years)
• Preferably, the patient should be weaned off therapy after 2 to 4 months of treatment.
• If signs reappear after several attempts to discontinue therapy, the patient will likely require long-term corticosteroid therapy at the lowest possible dose. Base the decision to proceed with long-term therapy on the severity of the problem. Cases nonresponsive to glucocorticoids may require more aggressive immunosuppression as outlined in the next section.
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Table 124-2. DRUG REGIMENS USED FOR CONTROL OF IMMUNE-MEDIATED ARTHRITIS Drug
Dose
Action
Comments
Acetylsalicylic acid (aspirin)
25–40 mg/kg q8h PO
Analgesic; anti-inflammatory
Glucocorticoids (prednisone, prednisolone)
1–3 mg/kg q12h PO until remission achieved; then decrease to lowest effective maintenance dose 1.5–2.5 mg/kg PO q24h 4 days/ week Dogs: 2 mg/kg q48h PO
Anti-inflammatory; immunosuppressive
Generally more effective for degenerative joint disease First choice for nonerosive forms; can be used alone or in combination with other drugs
Cyclophosphamide* (Cytoxan, Mead Johnson) Azathioprine† (Imuran, Burroughs Wellcome) Gold sodium thiomalate (Solganal, Schering)
Immunosuppressive Immunosuppressive
0.5–1 mg/kg IM once weekly
Unknown
Monitor WBC count; watch for hemorrhagic cystitis Monitor WBC count; relatively toxic in cats Used in erosive forms; limited clinical experience
*Glucocorticoids are commonly administered concurrently with this drug. †Glucocorticoids are commonly administered on alternating days with this drug. WBC, white blood cell.
Erosive Forms ▼ Key Point Canine
rheumatoid arthritis usually requires immunosuppression in addition to prednisone for a response.
• Cyclophosphamide is often used along with prednisone in treating rheumatoid arthritis.
• The side effect of hemorrhagic cystitis associated with
• •
• •
cyclophosphamide can be devastating to the patient. Discontinuing cyclophosphamide after 4 months of therapy minimizes the chances of hemorrhagic cystitis. Note that cyclophosphamide is used for 4 days during each week of therapy. Gold sodium thiomalate can be used to maintain remission after cessation of cyclophosphamide. Gold salt is a slow-acting antirheumatic drug and is unsuitable for inducing remission. Azathioprine can be used instead of cyclophosphamide to induce remission in dogs only, since it is toxic to cats. Additional treatment information is in Table 124-2.
Surgery • Surgery has a limited role in managing immune• •
mediated arthropathies. Pancarpal arthrodesis could be considered in some patients with localized disease to the carpi (see Chapter 106). Surgery for cranial cruciate ligament rupture in immune-mediated polyarthropathies should be considered with a very guarded prognosis due to ongoing joint destruction.
Supportive Care • As in osteoarthritis, lifestyle modification, weight reduction, and exercise restriction aid in managing immune-mediated arthropathies.
PROGNOSIS Nonerosive Forms The prognosis for Type I to III forms is favorable; it is guarded for Type IV due to the presence of neoplasia. The breed-specific diseases differ in prognosis. The arthritis of Akitas and Shar-Peis has a poor prognosis. SLE patients may frequently relapse. The polyarthritismyositis syndrome of spaniels has a guarded to good prognosis, and the polyarthritis-meningitis syndrome in other dogs has a good prognosis. Drug-induced polyarthropathies usually respond to cessation of drug therapy. The nonerosive form of feline progressive polyarthritis has a guarded prognosis.
Erosive Forms Canine rheumatoid arthritis can be difficult to treat successfully and may be expensive, especially if gold salt therapy is needed. Greyhound polyarthritis and the erosive forms of feline progressive polyarthritis have poor prognoses.
SUPPLEMENTAL READING Bennet D: Immune-based non-erosive inflammatory joint disease of the dog. Part 3: Canine idiopathic polyarthritis. J Small Anim Pract 28:909, 1987. Bennet D: Treatment of the immune-based inflammatory arthropathies of the dog and cat. In Kirk RW (ed): Current Veterinary Therapy: Small Animal Practice, 12th ed. Philadelphia: WB Saunders, 1995, pp 1188–1195. Goring RL, Beale BS: Immune-mediated arthropathies. In Bojrab MJ (ed): Pathophysiology in Small Animal Surgery, 2nd ed. Philadelphia: Lea & Febiger, 1993, pp 742–757.
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Section
Chapter
▼
9
125
Nervous System Philip A. March
Diagnostic Approach to Neurologic Disease William R. Fenner / Philip A. March
PRINCIPLES OF NEUROLOGIC EXAMINATION Objectives • Confirm that neurologic disease is present. • Localize the site of any lesion(s). • Determine the extent to which the nervous system is
• Begin by evaluating the level of consciousness. A
•
involved.
• Guide the choice of diagnostic aids. • Determine the prognosis. Approach • Perform the examination in a logical, methodical, and consistent manner.
• Develop a consistent sequence and follow it with all patients.
• Begin with the general and advance to the specific. • Perform painful portions of the examination last. PROCEDURES FOR THE NEUROLOGIC EXAMINATION General Observations Mental Status Mental status is regulated by the brain stem and cerebrum and consists of level and content of consciousness.
normal animal is alert; an abnormal animal is depressed, stuporous, or comatose, depending on the severity of the mental depression. Abnormal levels of consciousness may result from lesions of the brain stem or diffuse cerebral disease. In addition to the level of consciousness, evaluate the patient for mentational disorders. Behavior of a normal animal is described as appropriate; an animal with abnormal behavior is considered demented. • A demented animal is unaware and unconcerned with its surroundings. It may head-press, walk off tables, and in other ways show a complete disregard for its own safety and well-being. • Dementia is a sign of a cerebral disorder.
Head Posture Head posture is regulated by the vestibular system and the strength of neck muscles.
• A normal animal holds its head in a plane parallel to the ground.
• If an animal holds one ear closer to the ground than •
the other ear, it is described as having a head tilt, which suggests a vestibular injury. In some animals, the chin is tucked under or pulled tightly toward the sternum; this postural abnormality (ventroflexion) may be seen in cats with polymyopathies (e.g., hypokalemia) or thiamine 1233
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deficiency and in dogs with cervical vertebral malformations.
Coordination of Head Movement
• Abnormal posture may be caused by diminished position sense (proprioception), weakness, or pain.
• Many animals present with abnormal posture as a result of pain from orthopedic disorders rather than neurologic disturbances.
This is regulated primarily by the cerebellum. Disturbances of head coordination appear as head tremors.
Tests of Postural Reactions Circling
Gait and Stance
Attitudinal and postural (A-P) reactions test the integrity of the interconnecting pathways that regulate posture and movement as an extension of the evaluation of gait and stance. These tests evaluate the proprioceptive fibers of peripheral nerve, spinal cord, brain stem, cerebrum, and cerebellum. Some tests also evaluate special proprioception. The upper motor neurons and their connections to lower motor neurons are also evaluated. Because so many portions of the nervous system are evaluated, A-P reactions are good screening tools for detecting nervous system disorders but are not very helpful with specific localization.
Gait
• With lesions of the cerebrum, the postural deficit
Circling is a nonspecific finding in animals with brain disease.
• A lesion in any part of the brain may cause circling; the animal usually circles toward the diseased side.
• Circling in brain stem and cerebellar injury usually is •
a result of a vestibular dysfunction; therefore, circling is accompanied by a head tilt. Animals with cerebral injury circle, but they rarely have head tilts.
A normal gait requires integration of almost the entire nervous system; therefore, abnormal gaits may result from injury to almost any part of the nervous system.
• Sensory disturbances, such as loss of proprioception,
•
usually result in ataxia or loss of coordination of limb movements. Signs of loss of coordination of the limbs include swaying, veering, crossing over of the limbs, and scuffing of the toes.
•
▼ Key Point Ataxia may be seen with disease or
•
injury of the cerebellum, brain stem, spinal cord, and injuries to cranial nerve 8 (vestibular nerve). Cerebral and peripheral nerve lesions rarely cause ataxia.
• Cerebellar lesions cause ataxia in most patients. • Cerebral lesions may produce mild weakness characterized by intermittent stumbling, tripping, and reluctance to initiate or sustain activity. More obvious signs of weakness may be caused by an injury to the brain stem, spinal cord, or peripheral spinal nerves. When classifying the weakness, also consider the resting muscle tone in the limbs. • Spasticity is an increase in muscle tone resulting in decreased flexion of the limbs during movement. The resultant gait is rigid and choppy. • Spasticity may be seen with injuries to the cerebrum, the brain stem, and some levels of the spinal cord.
Stance Normal animals stand with their limbs at about shoulder or hip width, with the weight equally distributed on all four limbs.
•
normally is seen in the limbs on the opposite side of the body (contralateral) from the diseased hemisphere. With brain stem lesions, the clinical signs usually are bilateral but are worse on the same side (ipsilateral) as the brain stem injury. With lesions of the cerebellum, spinal cord, and peripheral nerves, the clinical signs are almost always on the same side of the body as the nervous system injury. With cerebellar injuries, A-P reactions usually are present but are ataxic. With peripheral vestibular injuries, A-P reactions are preserved, but the animal tends to lean, fall, and roll to the diseased side when the maneuvers are performed. Hemihopping may be slightly delayed on the same side as the vestibular lesion.
Proprioceptive Positioning Abnormally abduct or adduct a limb, or turn the paw so that the animal bears weight on the dorsal surface of its paw (stands knuckled over). If A-P reactions are intact, the animal briskly brings the limb back to a normal resting position.
Hemihopping Hold the limbs on one side off the ground while the patient is hopped sideways on its other two limbs. A normal animal has no trouble initiating a brisk hopping response without buckling or collapsing on the limb if conscious proprioception and strength are normal in that limb. Hemistanding the animal on one or two limbs can also be used to assess limb strength.
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cats) in a stressful environment may have an absent menace (false-negative finding).
Wheelbarrowing Hold the thoracic or pelvic limbs off the ground while the patient is walked forward and then backward on its other two limbs. A normal animal has no trouble maintaining itself and walking normally during this test.
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Pupillary Light Reflex (see also Chapter 141)
Additional A-P reactions include the extensor postural thrust reaction, the righting reaction, visual placing reactions, tactile placing reactions, and tonic neck reactions. All these tests evaluate the same basic pathways, although each may test one portion of the nervous system more completely than another. These tests are well described in standard neurology texts.
This tests the reflex portion of the optic nerve (CN2) and the autonomic function of the oculomotor nerves (CN3). The test is performed by illuminating the eye with a bright light source. The normal response is rapid constriction of both pupils. The pupillary constriction in the eye being illuminated is called the direct pupillary response. The constriction in the opposite pupil (the one being illuminated indirectly) is called the consensual response. Failure of one or both pupils to constrict is an abnormal pupillary light reflex (PLR).
Cranial Nerve Examination
• A lesion of CN2 produces loss of constriction in both
Other Attitudinal and Postural Reactions
The cranial nerve (CN) examination tests the function of each CN. Often a CN deficit confirms the presence of a lesion above the foramen magnum. The CN examination allows precise localization of intracranial diseases in many cases. Because many CNs supply only the motor or the sensory component of a CN reflex, the testing of a CN reflex generally involves testing more than one nerve. This is unlike spinal reflexes in which generally the sensory and the motor components of a reflex are carried by the same nerve. Many of the CN reflexes also are under higher control. Therefore, a CN reflex evaluates the following:
• Two peripheral CNs (one motor and one sensory) • A central connection (usually the brain stem) • A higher regulatory center (usually the cerebrum) A lesion in any one of these sites may cause loss or depression of the reflex being tested. For a more complete review of the neuroanatomy of CNs, consult a neuroanatomy textbook.
•
•
•
Pupillary Symmetry In this test the eyes are observed for equal pupil size.
• If CN3 and the sympathetic nerve to the eye are normal, the two pupils will be equal in size.
• If the pupils are unequal (anisocoria), this indicates
Menace Response (see also Chapter 141) The menace response tests CN2 (sensory) and CN7 (motor) and their central connections in the cerebrum, brain stem, and cerebellum. The test is performed by making a menacing gesture toward an animal. The normal response is an avoidance response (e.g., an eye blink or turning of the head).
• Loss of the menace response normally indicates a
• •
lesion in one of the following sites: retina (ipsilateral), optic nerve (ipsilateral), optic tract (contralateral), cerebrum (contralateral), brain stem (ipsilateral), cerebellum (ipsilateral), or facial nerve (CN7) (ipsilateral). False-positive menace responses also occur, most commonly when the movement of the hand produces air currents that stimulate the corneal reflex. Sounds and other distractions may make the menace response difficult to evaluate. Animals (especially
pupils when the affected eye is illuminated; however, when the normal eye is illuminated, both pupils constrict. If the lesion is in CN3 or the brain stem, the affected pupil fails to constrict regardless of which eye is being illuminated, but the unaffected eye constricts normally when each eye is illuminated. Because ophthalmic diseases such as posterior synechia or severe iris atrophy may also produce loss of pupillary responsiveness, a thorough eye examination is essential in any patient with abnormal pupils. Other causes of a misleading PLR are increased sympathetic tone and a weak light source, both of which will slow the PLR.
•
•
possible damage to one of these two nerves. • If CN3 is abnormal, the large pupil is denervated and the PLR will be absent in that eye. • If the sympathetic nerve is abnormal, the small pupil is abnormal and the PLR will be normal in both eyes. Cats may have mild physiologic anisocoria if one eye is receiving more light than the other. For this reason, ensure that both eyes receive equal illumination when evaluating for anisocoria. A number of ophthalmic disorders may produce anisocoria, including glaucoma, iritis, uveitis, and synechia. Because of this, perform a complete ophthalmic examination on all patients with anisocoria.
Pupillary Size The size of the pupil is determined by the amount of ambient light (CN2) and the integrity of the innervation of the pupillary muscles (CN3 and sympathetic nerve).
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• Abnormally large pupils may be caused by excitement •
(sympathetic stimulation), bilateral optic nerve injury, CN3 paralysis, or ophthalmic disease. Abnormally small pupils may be associated with loss of sympathetic tone, excess parasympathetic tone, or ophthalmic disease.
Ocular Position In normal dogs and cats, both eyes look in the same direction at any given time (normally straight ahead). This normal resting position is determined by the influence of the cerebrum and CN8 on the extraocular muscles (CN3, CN4, and CN6). If one of these portions of the nervous system is not functioning, deviation of one or both of the eyeballs may occur. Strabismus is deviation of only one globe.
• Medial strabismus may result from an injury to CN6 (abducens nerve).
• Ventrolateral strabismus may result from injury to CN3 or CN8 (vestibulocochlear nerve).
• A lesion to CN4 (trochlear nerve) results in intorsion
•
(a form of rotation) of the eye, which can be recognized only in animals with oval pupils or on ophthalmic examination. Passive deviation of both eyes in the same direction (gaze paresis) is sometimes seen in cerebral injuries.
Ocular Motility Voluntary Eye Movement
tion of the head turn. This recurring slow-fast, slow-fast oscillation continues as long as the head is moving.
• A lesion of CN8 or its central connections may result
•
Pathologic Nystagmus When a normal animal’s head is not moving, it does not display any involuntary eye movements. If nystagmus is present when the head is at rest, this is a sign of nervous system disease and is called pathologic nystagmus. This usually is the result of an imbalance in the special proprioceptive system, which includes CN8, the brain stem, and the cerebellum. A lesion of any of these structures can cause pathologic nystagmus. Features of pathologic nystagmus that may help localize its origin include the direction, method of induction, and persistence of the nystagmus.
• Direction of nystagmus: • In horizontal nystagmus, the eyes move in a plane parallel to the head (i.e., the eyes move from side to side). ▼ Key Point Horizontal nystagmus is most commonly seen in peripheral vestibular disease but can occur in central vestibular disease (see Chapter 61). The fast component of the nystagmus usually is away from the diseased side.
Voluntary eye movement is initiated by cerebral stimulation of CN3, CN4, and CN6. As the animal looks around the examination room, observe to see if it appears unable to move the eyes in one or more directions.
• In vertical nystagmus, the eyes move in a plane perpendicular to the head (e.g., the eyes move up and down).
• With a cerebral lesion, both eyes are involved, and •
there is a tendency for the eyes to look toward the diseased cerebral hemisphere. With a lesion of the CNs, only one eye is usually involved. The involved eye will tend to have strabismus at rest and lack the ability to move.
▼ Key Point Vertical nystagmus is most commonly seen in central vestibular disease. The fast component of the nystagmus is usually away from the diseased side; therefore, brain stem disease causes up-going nystagmus, and cerebellar disease causes down-going nystagmus.
Involuntary Eye Movements: Nystagmus Involuntary rhythmic oscillations of the eyes, termed nystagmus, can be induced by turning the head. This maneuver stimulates CN8, which in turn stimulates CN3, CN4, and CN6, which innervate the extraocular muscles. This involuntary eye movement is called physiologic nystagmus. Physiologic Nystagmus Physiologic nystagmus is characterized by a “slow phase,” in which the eyes move slowly away from the direction in which the head is turning, followed by a “fast phase,” in which the eyes rapidly move in the direc-
in loss of the ability to initiate physiologic nystagmus so that neither eye will move when the head is turned toward the side of the vestibular lesion. A lesion of one or more of the CNs that innervate the extraocular muscles (CN3, CN4, or CN6) paralyzes only that eye, resulting in loss of physiologic nystagmus in the paralyzed eye.
•
• In rotatory nystagmus, the eyes rotate in a clockwise or counterclockwise direction in the orbit, with components of both horizontal and vertical movement. This type of nystagmus may occur with a peripheral or central vestibular lesion. Method of induction of nystagmus: • Resting nystagmus occurs when the head is at rest and in a normal position. This type of nystagmus is most characteristic of peripheral vestibular disease but can be seen with central vestibular disease.
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•
• Positional or induced nystagmus occurs when the head is still but is in an abnormal position (e.g., on its side or upside down). Positional nystagmus is most characteristic of central vestibular dysfunction (e.g., brain stem and cerebellar lesions). It is also seen during the recovery phase of peripheral vestibular diseases. Persistence of nystagmus: • Permanent nystagmus persists over time. It may have any direction and method of induction, but it is consistently present. Permanent nystagmus is characteristic of most brain stem diseases and of progressive peripheral vestibular and cerebellar diseases. • Resolving nystagmus disappears over a period of time (days to weeks). It does not recur unless there is new damage to the vestibular system. Resolving nystagmus is characteristic of nonprogressive peripheral vestibular and cerebellar diseases. In the recovery period of these diseases, nystagmus may become positional.
Facial Symmetry Facial weakness (CN7) may result from injury to the contralateral cerebrum, ipsilateral brain stem, and ipsilateral peripheral nerve.
• Clinical signs include drooping of the lip, deviation
•
of the nasal philtrum, increases in palpebral fissure size (pseudoptosis), and in some animals, drooping of the eyelid (true ptosis). Confirm the diminished muscle function by testing the palpebral and/or corneal reflexes.
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• Initiate the reflex by lightly touching the cornea, which produces retraction of the eye into the orbit.
• Lack of the reflex usually is a sign of neurologic dysfunction of CN5 or CN6.
• In some animals with loss of the retrobulbar fat pad, the eye may be enophthalmic and incapable of retraction, whereas in others, a retrobulbar mass may prevent retraction.
Facial Sensory Examination This tests CN5 and its cerebral connections.
• Lightly stimulate the nasal mucosa, which should •
produce an avoidance response such as head turning or withdrawal. The nasal mucosa is a more reliable site for stimulation than the lips, which are relatively insensitive in some animals.
Gag Reflex The gag reflex, which is easier to test in dogs than in cats, tests CN9 (glossopharyngeal nerve) and CN10 (vagus nerve) and their brain stem connections.
• To initiate the test, lightly stimulate the oropharynx,
•
which should produce a swallowing reflex. Loss or depression of the reflex usually indicates brain stem or peripheral nerve dysfunction. Examine the pharynx for evidence of paralysis of the soft palate, and look at the larynx for evidence of laryngeal paralysis (may be difficult in an awake animal). Either condition may result from brain stem injuries or peripheral nerve injuries to CN9 or CN10.
Palpebral Reflex
Tongue Examination
This reflex tests CN5 and its brain stem connection to CN7.
• Look for atrophy of the tongue, which can be pro-
• Initiate the reflex by touching the palpebral margins,
•
•
which produces an eye blink. Loss of the eye blink reflex is usually complete if there is an injury to CN5 or CN7. In some animals with contralateral cerebral disease or myasthenia gravis, lagophthalmos or incomplete closure of the palpebral margins is observed.
Corneal Reflex Like the palpebral reflex, this reflex tests CN5 and its brain stem connection to CN7.
• Initiate the reflex by lightly touching the cornea, which produces an eye blink.
Retractor Oculi Reflex This reflex tests CN5 and its brain stem connection to CN6 (abducens nerve).
duced by brain stem or peripheral nerve injury to CN12. Also look for deviation of the tongue, which can be caused by cerebral injuries, as well as brain stem and peripheral nerve injuries. The tongue will deviate toward the side of the lesion.
Spinal Reflex Examination The spinal segmental reflexes directly test the reflex arcs of the spinal cord. They also indirectly test the higher centers in the brain that regulate the spinal reflexes. ▼ Key Point If an injury occurs within the reflex arc, it will cause loss or depression of the reflex. Such a reflex loss allows precise localization of a nervous system injury. Because a lesion in the lower motor neuron (LMN) is involved, loss of reflexes is called an LMN sign or an LMN reflex change.
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▼ Key Point If a lesion occurs cranial to a reflex arc, it disconnects the reflex from its higher (brain) regulation. This regulation tends to be inhibitory over specific proprioceptive reflexes such as the patellar and triceps reflexes. Loss of regulation results in exaggeration of these reflexes, especially the patellar reflex. Because this exaggeration reflects a lesion in the central nervous system (CNS) involving upper motor neuron (UMN) pathways, these reflex changes are called UMN signs or UMN reflexes.
• This reflex is easier to elicit than the triceps reflex, but its significance is often uncertain since it can often be elicited even with lesions of the LMN pathways. Biceps Reflex This reflex evaluates the musculocutaneous nerve, which arises from spinal cord segments C6 to C7.
• Initiate by striking the tendon of insertion of the biceps tendon, causing a slight flexion of the elbow.
• This reflex is more difficult to obtain than the triceps reflex and is difficult to interpret.
UMN changes are not as precisely localizing as LMN reflexes. Spinal reflexes are classified into three groups:
• Proprioceptive reflexes • Nociceptive reflexes • Special (released) reflexes This division is based on the type of sensory stimulation required to elicit the first two reflexes and on the special conditions required to elicit the third reflex.
Proprioceptive Reflexes These myotatic reflexes are initiated by stretch of tendons or muscle spindles. The patellar reflex is strongly influenced by UMN pathways and, therefore, may be exaggerated with UMN lesions. Other proprioceptive reflexes either are not influenced or are weakly influenced by the UMN system. Increases and decreases in the force of reflex activity are both components of proprioceptive reflexes; thus, be sure to grade the strength of these reflexes. A standard grading scale is as follows: 0 = Absent reflex 1 = Diminished reflex 2 = Normal reflex 3 = Increased reflex 4 = Increased reflex with clonus
Pelvic Limb Proprioceptive Reflexes Patellar Reflex This reflex tests the femoral nerve and its spinal cord segments (L4–L6).
• Elicit by striking the patellar tendon. This action produces extension of the stifle.
• This reflex is very obtainable and reliable in all animals.
• An exaggerated reflex may be present if a UMN lesion is present.
• When testing this reflex, a phenomenon known as a false localizing sign sometimes occurs if a sciatic nerve or L6 to S2 injury is present. Paralysis of the sciatic nerve results in a hyperactive patellar reflex. This may be due to functional loss of the antagonist muscles that oppose the extensor muscles of the stifle. Cranial Tibialis Reflex This reflex tests the peroneal branch of the sciatic nerve, which originates from spinal cord segments L6 to S2.
• Initiate by striking the belly of the cranial tibial
Thoracic Limb Proprioceptive Reflexes
muscle. The normal response is flexion of the tarsus. This reflex is readily obtainable in most animals.
Triceps Reflex
Gastrocnemius Reflex
This tests the radial nerve that arises from spinal cord segments C7 to T2.
This reflex tests the tibial branch of the sciatic nerve, which originates from spinal cord segments L6 to S2.
• Elicit by striking the tendon of insertion of the triceps
• Elicit by striking the belly of the gastrocnemius
•
muscle. A normal response is a slight extension of the elbow. This reflex is difficult to obtain in a normal animal. A reflex may be present if a UMN lesion is present. Extensor Carpi Radialis Reflex
Like the triceps reflex, this tests the radial nerve and spinal cord segments C7 to T2.
• Elicit by striking the muscle belly of the extensor carpi radialis muscle. The normal response is extension of the carpus.
•
muscle or its tendon of insertion. The expected normal response is extension of the tarsus. This reflex is very difficult to obtain in dogs and cats and is considered unreliable.
Nociceptive Spinal Reflexes The nociceptive reflexes are initiated by nociceptive (painful) stimuli, such as pinching, compression, and pin pricks. These nociceptive stimuli induce withdrawal of the limb or some other reflex action. These reflexes only test the integrity of the spinal reflex arc.
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▼ Key Point The fact that a reflex withdrawal reflex is present tells nothing about the health of the nociceptive pathways traveling cranially to the brain. Loss of a nociceptive reflex indicates an LMN lesion.
These reflexes do not have a large UMN influence; therefore, they do not become exaggerated with UMN lesions.
Thoracic Limb Flexor Reflex This reflex utilizes all the peripheral nerves of the thoracic limb and tests spinal cord segments C6 to T2.
• Elicit by digital compression. The normal response •
is withdrawal of the limb from the source of the stimulus. Loss of the reflex indicates a lesion in the reflex arc.
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Crossed Extensor Reflex This abnormal reflex may be seen in any limb.
• Initiate by eliciting a flexor reflex in an animal in
•
lateral recumbency. In a normal animal, the limb being stimulated flexes and the contralateral, paired limb is unaffected. In UMN disease, when the stimulated limb flexes, the contralateral limb will involuntarily extend.
▼ Key Point When present, the crossed extensor reflex is a sign of UMN dysfunction.
Nociceptive Evaluation Nociceptive evaluation (testing pain responses) tests for cerebral recognition of pain perception after digital compression. Cerebral recognition must be in the form of a purposeful directed response to the stimulus (turning, vocalizing, biting, struggling).
Pelvic Limb Flexor Reflex This reflex tests the sciatic nerve and the L6 to S2 spinal cord segments and nerve roots.
• Initiate by digital compression. The normal response •
is withdrawal of the limb from the source of the stimulus. Loss of this reflex indicates a lesion in the reflex arc.
Perineal Reflex The perineal reflex tests the pudendal nerve, spinal cord segments S1 to S3, and the cauda equina.
• Initiate by lightly pricking or stroking the perianal •
skin or perineum area. The expected response is constriction of the anal sphincter and flexion of the tail. If mild weakness is suspected, it is best to test the reflex during a digital rectal examination to estimate the strength of contracture of the sphincter.
Decreased Pain Perception A mild loss in pain perception is called hypalgesia or hypoesthesia. If the loss is total, it is referred to as analgesia or anesthesia.
• Loss of pain perception is tested by producing •
This evaluation tests peripheral nerves, spinal cord, brain stem, and cerebrum. The cerebellum is not involved in the nociceptive pathways. ▼ Key Point Peripheral nerve lesions usually cause focal sensory loss, confined to the distribution of the involved nerve(s). Severe spinal cord lesions cause a bilateral, symmetrical sensory loss proceeding caudally from the approximate level of the injury.
Special (Released) Reflexes These are reflexes that are suppressed by the UMN in normal animals. When disconnection between the reflex arc and the UMN occurs, these reflexes become released or uninhibited. Thus, the presence of these reflexes indicates loss of UMN inhibition to a reflex arc.
Babinski Reflex This occurs only in the pelvic limbs.
• Elicit by lightly stroking the plantar aspect of the • •
metatarsus. In a normal animal, the toes either are unaffected or flex slightly. In the presence of UMN disease, the toes may spread apart and elevate (dorsiflex), which is known as a positive Babinski reflex. This reflex is often absent even with UMN lesions.
enough pain so that cerebral recognition occurs and a reaction is produced. To elicit a reaction, compress the digits vigorously. The expected response is turning of the head and/or vocalization.
• Brain stem lesions rarely produce detectable analge• •
sia, because a lesion of that severity would result in the death of the animal. Cerebral lesions produce only hypalgesia. The sensory deficit with a cerebral lesion is usually contralateral to the diseased hemisphere.
Increased Sensitivity or Exaggerated Response to Pain Hyperesthesia refers to increased sensitivity; hyperpathia is an exaggerated response to pain. In veterinary medicine these two terms are used interchangeably. Exaggerated responsiveness to pain is tested by digital manipulation of the dorsal spinous processes
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and paraspinal muscles. Alternatively, the paraspinal region can be stimulated with a hemostat or safety pin.
• The objective is to produce a recognizable stimulus that is not normally bothersome to the patient.
• The stimulus is applied up and down the spine, •
looking for an area where the patient shows an unusually acute response to the stimulus. An exaggerated response usually is an indication of an extradural, nerve root, or meningeal lesion (e.g., herniated disc or meningitis).
▼ Key Point Paraspinal stimulation is valuable for localizing spinal cord lesions because a hyperpathic response indicates that the problem is extramedullary and establishes the location of the lesion.
INTERPRETATION OF THE NEUROLOGIC EXAMINATION The neurologic examination will usually demonstrate neurologic abnormalities if the patient has neurologic disease. Listing the neurologic abnormalities and then answering the following questions will aid lesion localization (Fig. 125-1).
•
• Is the disease in the CNS or peripheral nervous system (PNS)?
•
•
Figure 125-1. Localization flow chart. (CNS, central nervous system; PNS, peripheral nervous system.)
• If conscious and unconscious proprioceptive deficits (knuckling, ataxia) are present, the lesion is probably in the CNS. • If UMN signs are present (paresis with UMN reflex changes), the lesion is probably in the CNS. • If there are lateralizing signs of paresis or proprioceptive loss, the lesion is probably in the CNS. • If diffuse weakness and diminished reflexes in all four limbs are present (usually without postural deficits), the lesion is probably in the PNS. (See Chapters 129 and 130 for localization of PNS lesions.) • If the animal has CN deficits and limb signs (postural deficits, weakness, ataxia), the lesion is usually in the CNS. • If the animal has CN deficits and no other signs, the lesion is probably in the PNS portion of those CNs. • If the animal has a history of seizures, a depressed level of consciousness, and/or a head intention tremor, the lesion is probably in the CNS. Is the disease above or below the foramen magnum? • If the animal has a CN abnormality, a history of seizures, an abnormal head posture, abnormal head coordination, or an abnormal level of consciousness, the lesion is likely to be above the foramen magnum. (See Chapter 126 for localization of brain lesions.) • If the lesion involves the limbs alone, the lesion is most likely below the foramen. (See Chapter 128 for localization of spinal cord lesions.) After you have localized the lesion (above or below the foramen; CNS or PNS), try to localize the lesion more precisely. • Use CN deficits, cerebellar signs, cerebral signs, spinal reflex changes, and areas of spinal hyperpathia to determine a more specific localization (see Chapters 126 and 128). • Make every effort to attribute all neurologic abnormalities to one focal lesion. If this is not possible, the lesion is probably multifocal or diffuse. Information gained by localizing the lesion includes the following: • Ability to rule out etiologies that would not cause lesions at the site of your localization. • Improved ability to select appropriate diagnostic tests based on your localization. For example, myelography is appropriate if the lesion localization is in the spinal cord. A cerebrospinal fluid (CSF) analysis would be appropriate if the lesion localization was multifocal since the primary cause of multifocal CNS disease is inflammatory disease. • Prognostic information for the animal’s likely outcome. For example, UMN tetraplegia with no deep pain sensation after severe trauma has a very guarded to poor prognosis.
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SELECTION OF DIAGNOSTIC AIDS Diagnostic aids are laboratory tests and procedures that help determine which differential diagnosis is the most likely cause of the patient’s signs. The primary purpose of a diagnostic aid is to provide etiologic information. As a consequence of establishing a diagnosis, these tests may also provide prognostic information. In addition, some tests provide anatomic information, allowing “finetuning” of the results of the neurologic examination. Diagnostic aids used in evaluation of the nervous system include general screening tests such as routine serum biochemistries and complete blood counts that identify metabolic and toxic injuries to the nervous system. More specific tests that aid in lesion localization and diagnosis include neuroimaging, CSF analysis, and electrodiagnostic tests. Electrodiagnostic tests will also more specifically localize lesions causing neurologic dysfunction. To select the most appropriate diagnostic aids, combine historical information with neurologic examination findings. After interpreting results of the diagnostic aids, the diagnosis should be evident.
GENERAL SCREENING TESTS Hematology In the majority of patients with nervous system disease, there are minimal hematologic changes. There are exceptions, such as some forms of infectious encephalitis and toxic diseases that secondarily affect the nervous system (e.g., lead poisoning).
White Blood Cell Changes Elevation of white blood cell (WBC) numbers often indicates an inflammatory disease process; however, a low WBC count may be seen in viral infections.
Red Blood Cell Changes Anemia, if profound, may result in hypoxia and cerebral signs. An abnormally high red blood cell (RBC) count (polycythemia) with increased serum viscosity can cause diminished blood flow to muscles and produce a myasthenia-like syndrome. It also may result in sludging of CNS blood flow with subsequent CNS infarction.
Biochemical Tests These tests help evaluate animals with metabolic illness. Because the cerebrum has very high metabolic demands, it is affected by many generalized metabolic disorders. The motor unit also appears susceptible to a wide variety of generalized metabolic insults. Examples of biochemical abnormalities that have an impact
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on the nervous system include hypoglycemia and hyperglycemia, hypocalcemia and hypercalcemia, hypokalemia and hyperkalemia, hyponatremia and hypernatremia, acidosis and alkalosis, uremia, hyperammonemia, hyperlipidemia, and hyperviscosity from dysproteinemia.
Urinalysis and Urine Culture and Sensitivity Many metabolic diseases that may affect the nervous system (diabetes mellitus, diabetes insipidus, renal disease, liver disease) produce changes in the urine. An increased urine protein-to-creatinine ratio due to protein-losing nephropathy could predispose the patient to CNS thromboembolic events secondary to hypercoagulability. In addition, some CNS infections (discospondylitis, etc.) are associated with concurrent urinary tract infections; therefore, evaluation of urinalysis and urine culture and sensitivity may be helpful in CNS infections. Urine and blood cultures are recommended if discospondylitis is present.
Ophthalmologic Examination An ophthalmologic examination is indicated in patients with inflammatory neurologic disease. Many CNS infectious diseases can cause a concurrent anterior uveitis and chorioretinitis. A retinal exam may also be a useful screening test for hypertension (detached retinas and retinal hemorrhage) and raised intracranial pressure (papilledema). (See Chapter 138.)
Blood Pressure Measurement Hypertension can be associated with hypothyroidism, hyperthyroidism, hyperadrenocorticism, renal insufficiency, hepatic insufficiency, and pheochromocytoma. Hypertension can also be idiopathic (essential hypertension). An elevated blood pressure can predispose the patient to CNS vascular disease. If hypertension is present, appropriate blood tests, especially for underlying endocrine or renal disease, should be performed. (See Chapter 153 for more information on hypertension.)
Thoracic Radiographs and Abdominal Ultrasound Thoracic radiographs and abdominal ultrasound are often indicated if either neoplastic or infectious conditions of the nervous system are suspected. They may also be indicated if an underlying endocrine or renal disorder exists. Transcranial ultrasonography in young toy breeds with open fontanelles is a useful screening test for hydrocephalus.
Fecal Analysis Severe parasitism has been reported as a cause of CNS disease in young animals.
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reason, plain radiographs provide minimal information regarding actual spinal cord compression.
Serology Viral (distemper, feline infectious peritonitis), fungal (cryptococcosis, blastomycosis, histoplasmosis, coccidioidomycosis), protozoal (toxoplasmosis, neosporosis), and rickettsial (Rocky Mountain spotted fever and ehrlichiosis) infections of the nervous system result in the development of antibodies. These antibodies may be assayed in the patient’s serum. CSF serology is more reliable than serum antibody assays for some of these infectious disease agents. (See the CSF serology section, Chapter 126, and Section 2 for more specific information.)
Myelography • For myelography of the spine, positive (radiopaque)
•
Immunofluorescence Some viral infections that affect the nervous system may be diagnosed by using immunofluorescent techniques to detect antigen in CSF or nervous tissue (the latter is reserved for postmortem examination).
•
Toxicology Blood can be assayed for many toxins known to affect the nervous system (e.g., lead poisoning).
• NEURORADIOGRAPHY AND SPECIAL IMAGING Radiography and special imaging can be used to evaluate the supporting structures of the nervous system and in some cases the nervous system itself. These studies provide information about CNS anatomy and can reveal structural abnormalities but generally do not provide information about neurologic function. (See Chapter 4 for additional information about neuroradiography and appropriate radiographic techniques.)
Plain Radiography of the Spine • Plain radiographs can be very helpful in identifying
•
bony lesions of the spine. Disorders that can cause changes in the vertebrae include vertebral body tumors, osteomyelitis, degenerative joint disease, fractures and luxations, soft tissue tumors that cause secondary bony lysis or pressure necrosis, mucopolysaccharidosis, hypervitaminosis A, and congenital vertebral body disorders (spina bifida, hemivertebrae, atlantoaxial malformation, etc.). Changes in the intervertebral disc space (collapse, calcification, foraminal opacification, discospondylitis) can also be identified (see Chapter 128). The major disadvantage of plain radiographs is the inability to image the spinal cord itself and soft tissues that may be impinging on the spinal cord. For this
contrast material is delivered into the subarachnoid space to outline the spinal cord and radiographs are taken (see Chapter 4). Myelography is very useful for imaging extradural or intradural/extramedullary lesions that are causing secondary spinal cord compression. Myelography can be used to localize areas of intervertebral disc herniation, spinal tumors, and other compressive lesions. It is also extremely effective in identifying areas of dynamic spinal cord compression. Post-myelogram computed tomography aids in determining the extent of lesion lateralization in the spinal canal. Myelography requires lengthy anesthetic times, provides marginal to no information about intramedullary diseases, is contraindicated in the presence of meningomyelitis, and is contraindicated in the presence of elevated intracranial pressure. Epidural leakage of contrast material can diminish the diagnostic information obtained. See Chapter 4 for proper myelographic technique and interpretation.
Skull Radiography • Skull radiography provides very limited information
• •
• • • •
•
about potential intracranial lesions. Bony structures of the cranial vault are visualized, but the brain itself is not. Loss of convolutional markings (gyral and sulcal markings) on the inside of the skull may be seen with hydrocephalus. Foramen magnum occipital dysplasia or “keyhole malformation” can be diagnosed using special rostrocaudal and caudorostral views of the foramen magnum. Bony or intranasal tumors and infections may be characterized by focal areas of bony lysis and/or proliferation. Occasionally, focal areas of the calvarium will show either hyperostosis (bony thickening) or lysis adjacent to a slowly expanding meningioma. Fractures of the skull can usually be identified with the appropriate views. Soft tissue or fluid densities within the tympanic bullae, bulla wall thickening and lysis, or a combination of both is usually evidence of chronic otitis media. See Chapter 4 for more details of the positioning techniques, imaging procedures, and image interpretation for skull radiography.
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Computed Tomography • Computed tomography (CT) provides adequate •
• •
•
imaging of forebrain structures and large spaceoccupying lesions. CT provides excellent imaging of bony lesions such as skull fractures, skull and vertebral tumors, bulla osteitis secondary to otitis media, and discospondylitis. Intraparenchymal brain hemorrhage in the acute stages can also be identified. Post-myelogram CT of the spinal cord is very useful for defining axial locations of spinal cord lesions (see Chapter 128). Disadvantages of CT include poor resolution of brain stem, cerebellar, and spinal cord parenchyma and limited abilities to image CNS structures in more than one plane. Axial images can be reformatted to provide a limited series of low-resolution images in different planes. See Chapter 4 for more details on CT.
Magnetic Resonance Imaging • Magnetic resonance imaging (MRI) provides supe-
• • •
•
•
rior imaging of brain and spinal cord parenchyma but poor imaging of bony structures. For brain lesions, MRI provides more precise lesion localization than CT (see Chapter 126). Brain edema is also more clearly identified using MRI than using CT. MRI sequences can be manipulated to give more information regarding primary lesions and CSF characteristics. Magnetic resonance images can easily be obtained in three planes to provide additional information about lesion size and extent. Extra-axial versus intra-axial location and pattern of contrast enhancement often aid in establishing a tentative diagnosis of brain tumors. The precise neuroanatomic information provided by MRI facilitates surgical planning for either biopsy or resection and radiation therapy planning. MRI also provides excellent resolution of intramedullary inflammatory, vascular, and congenital lesions. Some neurodegenerative conditions including cerebellar abiotrophy and lysosomal storage diseases may have characteristic MRI features. Syringohydromyelia and caudal occipital malformation syndrome in toy breeds and Cavalier King Charles spaniels are readily identified using MRI (see Chapter 128). MRI is less invasive than myelography and is an alternative imaging technique for intervertebral disc herniation and spinal cord tumors. MRI is the imaging modality of choice for peripheral nerve sheath tumors because it enables simultaneous visualization of the peripheral and central (spinal cord) components of the tumor (see Chapters 128 and 129). See Chapter 4 for more details on MRI.
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CEREBROSPINAL FLUID COLLECTION AND ANALYSIS Indications • CSF collection and analysis are indicated if an inflam-
•
matory (infectious or non-infectious) CNS condition is suspected. Signs of inflammatory meningoencephalomyelitis may include rapidly progressive focal or multifocal neurologic deficits, recurrent seizures, neck or multifocal spinal pain, and chronic or recurrent “fevers of unknown origin.” CSF analysis is less useful for non-inflammatory CNS conditions. CSF abnormalities in non-inflammatory conditions are often mild and nonspecific.
Contraindications CSF collection is contraindicated in the presence of elevated intracranial pressure. Increased intracranial pressure can usually be recognized in the unanesthetized patient as a declining or depressed level of consciousness. In a patient with these signs, MRI is indicated prior to the CSF tap in order to assess the extent of brain swelling and early signs of brain herniation. (See Chapter 126 for a more detailed discussion of signs of brain herniation.) A cisternal or lumber CSF tap in a patient with elevated intracranial pressure can lead to severe brain herniation and death.
Technique • Perform CSF collection under general anesthesia
•
in dogs and cats. For brain disorders, collect CSF at the cerebellomedullary cistern. For spinal cord disorders, collect CSF at the L4 to L5 or L5 to L6 site. The lumbar space, however, can be more difficult to enter, yields smaller amounts of CSF, and has a higher rate of blood contamination in very small animals. The average distance between the skin and the cerebellomedullary cistern varies with the size of the patient. Reported distances for dogs and cats are 1/ inch for cats and dogs < 4.5 kg, 3/ inch for 2 4 dogs 4.5 to 9.1 kg, 1 inch for dogs 9.1 to 22.7 kg, 11/2 inches for dogs 22.7 to 50.9 kg, and 2 inches for dogs > 50.9 kg.
Cerebrospinal Fluid Analysis CSF analysis includes gross visual examination, cytologic analysis, biochemical analysis, and culture. In addition, serologic procedures may be indicated. There are slightly different normal values for fluid collected from cerebellomedullary and lumbar spaces; thus, note the
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collection site. Fluid from the cerebellomedullary cistern tends to have slightly more cells and lower protein than fluid from the lumbar space.
Gross Examination Normal CSF is clear and colorless. With inflammation, CSF generally becomes turbid and assumes an off-white to grayish color. Pink discoloration is usually caused by blood contamination. Yellow-orange–colored CSF (xanthochromic) generally indicates either breakdown of hemoglobin from previous hemorrhage or severe elevations of CSF protein (>100 mg/dl).
Cytology
• Cytologic evaluation consists of a total cell count on unconcentrated CSF and preparation of a slide from a concentrated CSF sample for evaluation of cell types and differential numbers. ▼ Key Point Perform the total cell count quickly (within 1 hour or less of the tap) because cells from CSF begin to degenerate rapidly following collection.
• The type and number of cells may reflect the cause of the inflammation and thus provide etiologic information. Normally there are 5 WBCs per microliter are definitively abnormal if no RBCs are present. • A finding of 50 to 200 WBCs per microliter suggests a moderate inflammation, as seen with fungal, protozoal, and immune diseases, but this number may also be seen with meningiomas. • More than 200 WBCs per microliter indicates a marked inflammatory process, as seen with bacterial meningitis and some immune diseases.
Cerebrospinal Fluid Cytologic Interpretation Suppurative Meningitis Suppurative meningitis is diagnosed if the number of cells in the CSF is increased and the cells are predominantly neutrophils. Suppurative meningitis is the most common pathologic response to idiopathic meningitis or vasculitis in young dogs, bacterial encephalitis, feline infectious peritonitis, and some tumors (e.g., meningiomas). Mild increases in CSF neutrophils may be seen following CNS trauma, acute intervertebral disc herniation, fibrocartilaginous embolic myelopathy, and other acute vascular insults.
Mixed Inflammation Mixed inflammation is diagnosed when the increased number of cells in the CSF are composed of multiple cell types, including macrophages, lymphocytes, neutrophils, and sometimes plasma cells. Although a mixed cytology is generally the result of fungal, protozoal, and idiopathic encephalitis, this cytologic change may also be seen in chronic bacterial infections that are being inadequately treated. Idiopathic granulomatous meningoencephalitis (GME) is typically characterized by granulomatous inflammation (lymphocytes, monocytes, macrophages), but neutrophils may sometimes be present in the acute stages. Nonsuppurative Inflammation Nonsuppurative inflammation is diagnosed when the number of cells in the spinal fluid is increased and it is composed primarily of mononuclear cells, especially lymphocytes. It is most characteristic of idiopathic immune-mediated forms of encephalitis, rickettsial infections, and some viral infections. Although this type of CSF abnormality is least likely to be due to an acute bacterial infection of the nervous system, it may occur. Chronic compressive spinal cord lesions may cause a mild elevation of lymphocytes and monocytes. Eosinophilic Inflammation Increased eosinophils in CSF may be observed secondary to immune-mediated eosinophilic meningoencephalitis, fungal infections, protozoal infections, and aberrant parasite migrations. Red Blood Cell Pleocytosis Increased RBC numbers are usually due to iatrogenic blood cell contamination during the CSF tap procedure. RBCs may also be increased due to previous hemorrhage due to trauma, coagulopathy, or inflammation. Erythrophagocytosis and xanthochromia may be observed if there has been previous hemorrhage. Tumor Cells, Infectious Agents, and Intracellular Inclusions Tumor cells are rarely identified in CSF with the exception of neoplastic lymphocytes in some forms of CNS lymphoma. Cryptococcal and other fungal organisms may occasionally be identified (see Chapter 20). Rarely, intracellular rickettsial organisms, distemper inclusions, and bacteria may be observed. Absence of intracellular bacteria and degenerative changes in neutrophils do not rule out a bacterial CNS infection. Some lysosomal storage diseases are characterized by intracellular storage bodies within WBCs. (See Chapters 126 and 128 for further discussion of CSF abnormalities in brain and spinal cord diseases.)
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Cerebrospinal Fluid Biochemical Evaluation When evaluating the chemical composition of the CSF, remember that CSF is produced both by active transport and by ultrafiltration. As a result, CSF contains essentially the same constituents as plasma, but they are present in different concentrations. Generally, the levels of CSF constituents are lower than the serum levels. The two constituents measured most commonly for diagnostic purposes are protein and glucose.
Protein Levels The concentration of protein is quite low in CSF compared to plasma. In dogs and cats, protein from a cerebellomedullary cisternal tap is usually less than 25 mg/dl, whereas that from a lumbar puncture may be as high as 45 mg/dl. This difference may be the result of an increase in the permeability of the blood-brain barrier, production of immunoglobulins in the intrathecal space, or a combination of both. Conditions known to elevate CSF protein include encephalitis, meningitis, neoplasms, CNS infarctions, chronic neurodegenerative conditions, and trauma. CSF protein can be analyzed qualitatively and quantitatively by electrophoresis or immunoelectrophoresis. In normal CSF, albumin composes about 75% of the protein, and most of the remainder is globulin. An increase in CSF globulin without a parallel increase in albumin suggests local immunoglobulin production and encephalitis.
Glucose Levels Normal CSF glucose levels are about 60% to 80% of those in blood. In humans with CNS bacterial infections, the CSF glucose is decreased. There does not appear to be a similar relationship between bacterial encephalitis and decreased CSF glucose in dogs. Plasma glucose can decrease dramatically in the presence of septicemia and bacteremia. A meningitic patient that is also bacteremic will likely have a drop in CSF glucose.
Cerebrospinal Fluid Serologic Examination The CSF may be tested serologically for antibodies against infectious agents. Cryptococcal antigen can also be measured in CSF. Detection of CSF antibodies may be especially helpful in the diagnosis of canine distemper, feline infectious peritonitis, and toxoplasmosis. Paired or single serum titers are usually sufficient for diagnosis of neosporosis, rickettsial diseases, and some fungal disorders.
• The presence of CSF antibody usually indicates an •
active CNS infection and production of intrathecal antibody. False-positive CSF antibody titers can occur due to either iatrogenic blood contamination or blood-CSF barrier breakdown secondary to inflammation. CSF titer correction formulas are available and can be performed by some diagnostic testing laboratories if
•
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both CSF and serum are submitted (see Chapter 126). False-negative CSF antibody titers can occur with feline infectious peritonitis and cryptococcosis.
ELECTROENCEPHALOGRAPHY Electroencephalography (EEG) is the graphic recording of shifts in resting membrane potential of the dendritic network in the cerebral cortex. This network is influenced and modulated by the activity of subcortical nuclear centers such as the reticular formation. Changes in EEG wave frequency and amplitude and occurrence of paroxysmal epileptiform complexes (spikes, sharp waves, and spike-slow wave complexes) are abnormalities that indicate a corticocerebral disturbance.
Indications • EEG can be a useful screening test for any cortico-
•
•
cerebral lesion. The procedure is noninvasive, relatively inexpensive, and can occasionally be performed without chemical restraint in the dog. Sedation or anesthesia is often required to minimize patient movement and to maintain a constant level of consciousness. In the awake state, normal variations in wakefulness can change EEG waveform frequency and amplitude. A montage (specific arrangement) of scalp electrodes allows patterns of abnormal activity to be localized to specific cortical areas. Focal slowing and paroxysmal activity suggests a focal neoplastic, infectious, traumatic, or vascular lesion. Diffuse slowing and changes in amplitude are suggestive of diffuse cerebral injury or metabolic disorders. EEG can be useful for confirming seizure activity in patients with atypical or subclinical seizures.
Disadvantages • Disadvantages include recording artifacts due to
•
patient movement, muscle activity, equipment malfunction, electrical interference, and drugs used to sedate or anesthetize the patient. These artifacts can obscure EEG recording and make it difficult to interpret. EEG provides little definitive information concerning the etiology of the underlying cerebral lesion. Neuroimaging with CT or MRI provides more definitive information about what is causing the cerebral dysfunction (see Chapter 126).
BRAIN STEM AUDITORY EVOKED RESPONSE The brain stem auditory evoked response (BAER) tests the nervous system pathways for hearing. A normal
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Table 125-1. INTERPRETATION OF ABNORMAL ELECTRODIAGNOSTIC EXAMINATION Procedure
Abnormal Finding
Interpretation
Electromyography
Increased insertional activity
Neuropathies Myopathies Myotonia Cramp Electrolyte disorders Myopathies Neuropathies (axon or cell body) Electrolyte disorders Myopathies Acute denervation Reinnervation Myopathies Neuropathies (myelinopathies or combined axonopathy and myelinopathy) Junctionopathies
Spontaneous activity Motor unit action potentials
Diminished size Increased size
Nerve conduction studies
Decreased velocity
Repetitive nerve stimulation
Incremental or decremental response
BAER depends on normal function of hearing receptors (cochlear receptors), CN8 (cochlear branch), the cochlear nucleus, and other “relay” nuclei for auditory signal transmission in the brain stem. An audible click produced by headphones or inserts in the ear triggers electrical activity in the structures above. The sequential neural activity is detected by scalp electrodes after each click stimulus. Several hundred amplified responses are “signal averaged,” and the averaged waveform is displayed as a consecutive series of four to five waveforms. Wave I is generated by the cochlear receptors and cochlear nerve. Waves II through V are generated by relay nuclei in the brainstem.
ELECTRODIAGNOSTIC EXAMINATION OF THE MOTOR UNIT The electrodiagnostic examination of the motor unit consists of three parts:
• Needle electromyography • Nerve conduction studies • Repetitive nerve stimulation Each test evaluates different aspects of the motor unit. Interpretation of abnormal electrodiagnostic findings is summarized in Table 125-1.
Interpretation • In congenital “sensorineural” deafness, the cochlear
Needle Electromyography • Electromyography (EMG) provides information
receptors degenerate perinatally. The resulting BAER is a “flat line” tracing. Injury to the cochlear receptors in the inner ear by otitis interna, neoplastic processes, or ototoxic drugs can also result in sensorineural deafness and an absent BAER. Middle ear effusions or soft tissue masses may inhibit normal sound transmission to the inner ear. This can result in lower amplitude, delayed BAER waveforms, or if severe, complete absence of the BAER. This form of hearing loss is called conductive hearing loss. A brain stem lesion affecting the auditory relay nuclei may decrease amplitudes and delay onset latencies (time to onset of wave) of waves II to V. Since the vestibular receptors and vestibular branch of CN8 are close to the cochlear system, the BAER may provide indirect localizing information in patients with vestibular disease secondary to otitis or neoplasia. In idiopathic geriatric vestibular syndrome, the auditory pathways and BAER are not affected.
about the functional status of motor unit innervation and muscle membrane ion conductance. A recording needle is inserted into a muscle and spontaneous muscle potentials are recorded and evaluated. Electrical activity is “audible,” and the sound of the potentials can be amplified to produce characteristic sounds from a loudspeaker. Persistent spontaneous activity in a resting muscle under anesthesia is abnormal. Normal muscle is “electrically silent” in the resting state with the exception of very low–amplitude miniature endplate potentials. In veterinary patients, general anesthesia is usually necessary to avoid patient discomfort and minimize patient movement. In humans and in extremely cooperative animal patients, awake studies may be performed to assess motor unit action potentials (MUAPs) normally generated during a voluntary muscle contraction. During sustained contractions, patterns of “recruitment” of these potentials can be observed to determine if they are normal or abnormal. Individual MUAP waveform characteristics
•
•
• •
•
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contraction produces a signal called a compound muscle action potential (CMAP) that can be recorded with a recording needle placed in the muscle. The CMAP is typically biphasic and approximately 25 mV in amplitude if the nerve is stimulated supramaximally. The CMAP is also called the M wave. Amplitude, duration, and number of phases of the CMAP can be altered in different neuromuscular diseases and should be measured and evaluated in all nerve conduction studies.
(amplitude, duration, number of phases) can also be altered in neuropathies and myopathies. Neuromuscular junction disorders may cause a reduction in MUAP amplitude.
Interpretation
• Fibrillation potentials, positive sharp waves, and
•
• •
•
complex repetitive discharges are examples of abnormal spontaneous activity. Fibrillation potentials and positive sharp waves are brief isolated potentials that range from 40 to 1000 mV in amplitude. The presence of any of these potentials indicates a neuropathy or myopathy but does not distinguish between them. Both neuropathies and myopathies cause functional denervation of the myofiber. Myopathic injury and necrosis disrupt normal muscle membrane integrity and the membrane receptors that are post-synaptic to nerve axon terminals. Complex repetitive discharges are several-second bursts of high-amplitude potentials (500–1000 mV) that may increment, decrement, or remain consistent in amplitude over time. These potentials may be observed in chronic neuropathies, myopathies, and in congenital myotonia. In congenital myotonia, the high-frequency repetitive discharges that wax and wane in frequency and amplitude are called myotonic discharges and may cause a characteristic “divebomber” sound. Spontaneous activity in neuromuscular junction disorders is rare but can occur sporadically with tick paralysis and botulism. In most polyneuropathies and polymyopathies, EMG activity is generalized and can be observed in most muscle groups. With focal nerve or muscle injuries, EMG can be very useful in localizing the distribution and extent of nerve and/or muscle injury. Occasionally, the resting EMG will be normal (no spontaneous activity) in peracute neuropathies and in some chronic neuropathies and myopathies. Nerve conduction tests and repetitive nerve stimulation should still be performed in these cases. If nerve conduction studies are abnormal or if clinical signs are suggestive of a neuropathy or myopathy, muscle and nerve biopsies should also be performed.
Interpretation
• The speed of conduction primarily evaluates the
•
•
Nerve Conduction Studies • Motor nerve conduction studies measure the velocity
•
of action potential conduction between two points along a motor nerve. Conduction velocity is calculated as the difference in distance divided by the difference in conduction latency of the action potential between these two points. Latency is the amount of time that elapses between the stimulus and the onset of the electrical response in the innervated muscle. Electrical stimulation of a normal motor nerve proximally results in electrical activation and contraction of the innervated muscle distally. The distal muscle
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•
•
health of the myelin sheath. Myelin injury results in slowed conduction velocity and, often, a lower amplitude and polyphasic CMAP due to temporal dispersion. Temporal dispersion refers to the prolonged duration of the CMAP due to the presence of nerve fibers that conduct at widely different velocities as a result of varying degrees of demyelination. Conduction block (no conduction) can occur if myelin injury is severe. The amplitude of the CMAP is also affected by the number of healthy motor units (nerve fibers with their respective neuromuscular junctions and myofibers). The greater the number of normal motor units activated, the greater the amplitude of the CMAP. With axonal injury that spares the myelin sheath, nerve conduction may be normal or mildly decreased. There is a reduction in the number of available motor units; this reduction leads to the reduced size of the CMAP. As the neurogenic lesion becomes chronic, there is axon sprouting of the terminal branches of surviving neurons. These axon sprouts reinnervate some of the denervated muscle fibers. The evoked potential will then have a prolonged duration (temporal dispersion) and may become polyphasic. This occurs because the axon sprouts conduct more slowly than the normal fibers, so the muscle fibers receive their impulses at different times. In addition, because the motor unit now has more fibers, the evoked potential will be increased in amplitude. In most acute and chronic neuropathies, a combined axon and myelin injury is the general rule. Furthermore, axonal degeneration will inevitably lead to myelin degeneration over time. For this reason, most neuropathies are characterized by slowed conduction velocity, reduced amplitude of the CMAP, and increased duration and number of phases of the CMAP. Myopathic conditions reduce the number of healthy myofibers in the motor unit and thus will result in reduced amplitude of the CMAP. Nerve conduction velocity is normal. Neuromuscular junction disorders in which acetylcholine release is reduced (tick paralysis and botu-
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lism) are characterized by normal conduction velocity but severely reduced amplitude of the CMAP. Sensory nerve conduction is similar to motor nerve conduction testing, except that the stimuli are applied to the nerve distally and the recordings are made directly from the nerve proximal to the site of stimulation.
•
Repetitive Nerve Stimulation Repetitive nerve stimulation (RNS) refers to nerve stimulation by 5 or 10 consecutive supramaximal stimuli with concurrent recordings made of the consecutive CMAPs produced by these stimuli. The amplitudes of each CMAP are then compared with the amplitude of the first CMAP. A normal patient will show no changes in the amplitudes of the successive CMAPs in the series. Neuromuscular junction diseases often cause a progressive change in the amplitudes during the first five stimuli. An increase in amplitude is called an incremental response; a decrease in amplitude is called a decremental response. RNS should be performed at a stimulation rate of 4 months) and is not associated with early clinical improvement. Complications of radiation therapy include ocular (conjunctivitis, keratoconjunctivitis sicca, cataracts) and dermatologic (erythema, alopecia, otitis) changes. A potential late, delayed reaction may occur 9 to 24 months after radiation and is characterized by white matter necrosis.
Stereotactic Radiosurgery
• Stereotactic radiosurgery is the application of a single •
• •
high dose of radiation delivered to a stereotactically defined target volume. The procedure utilizes multiple, non-coplanar beams originating from a radiation source that rotates in an arc around the patient’s tumor. All beams are focused on the target in non-intersecting planes using a stereotactic image-based system. This radiation procedure reduces radiation exposure of normal brain tissue and so avoids adverse effects associated with conventional radiation therapy. Delivery of the entire radiation treatment as a single dose minimizes anesthetic events and reduces costly repeat visits associated with conventional radiation therapy.
INFLAMMATORY BRAIN DISEASES Inflammation of brain parenchyma and its meninges (meningoencephalitis) occurs secondary to infectious or idiopathic insults. ▼ Key Point Idiopathic inflammatory conditions are more common than infectious conditions in dogs, but the reverse is true in cats.
Idiopathic disorders frequently have an immunemediated component. Most infectious agents reach the brain hematogenously. Local extension from extraneural sites, usually due to erosion through bone, is a mechanism used by some fungal and bacterial organisms. Other sources of infection include foreign body migration, previous trauma, and iatrogenic contamination during neurosurgery. An unusual but important mode of entry into CNS is that used by rabies and pseudorabies viruses and by Listeria bacteria. These agents are inoculated into a peripheral site, enter peripheral nerve axons, and then undergo retrograde axonal transport into the CNS. The cascade of inflammatory changes that occurs after brain injury leads to a self-perpetuating process of brain tissue ischemia, necrosis, and edema. Inflammatory brain disorders are usually associated with multifocal clinical signs and lesions are often disseminated throughout the CNS. Clinical signs, however, may indicate a focal neurolocalization for the most prominent lesion. Some inflammatory disorders have a predilection for the cerebral cortex, whereas many others have a predilection for brain stem sites and frequently cause central vestibular signs. The onset and progression of clinical signs is usually rapid (days to weeks) but can be prolonged. Infectious diseases may be accompanied by systemic signs, but idiopathic brain conditions are usually characterized by signs referable to the CNS only. As in the case of neoplastic conditions, inflammatory diseases can lead to the formation of large, spaceoccupying lesions, increased ICP, and herniation of brain structures.
Infectious Meningoencephalitis Etiology
• Infectious diseases are a common cause of acute to •
subacute, rapidly progressive neurologic dysfunction in dogs and cats and tend to occur in young adults. Major etiologic categories include viral, fungal, rickettsial, and protozoal agents. Bacterial diseases of the CNS can also occur but are less common. Klebsiella, Escherichia coli, Streptococcus, Enterococcus, Staphylococcus, Pasteurella, Actinomyces, Nocardia, and various
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Table 126-1. INFLAMMATORY BRAIN DISEASE CAUSED BY INFECTIOUS AGENTS IN THE CAT
Disease/Agent
Typical Age of Onset
Onset/ Progression
FIP (coronavirus)
Young (1 year) on combined phenobarbital and bromide therapy • Unacceptable quality of life on combined phenobarbital and bromide therapy with a seizure-free status period of >3 months • Infrequent initial seizures (3000 mg/L. Caution should be used in treating dogs with underlying renal insufficiency, due to reduced renal elimination of bromide. Therapy of bromide intoxication consists of IV normal saline administration to enhance bromide renal excretion. Careful monitoring is advised as dogs may become more susceptible to seizure activity with lowering of the serum concentration.
New Antiepileptic Drugs with Potential for Use in Dogs Several AEDs that have recently been approved for use in people offer exciting potential for use in dogs. Unfortunately, complete information is unavailable on the pharmacokinetic or therapeutic properties of these
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drugs in controlled studies in dogs. Most of these medications are still quite expensive. The drugs are listed in alphabetical order and not in preference of use.
▼ Key Point A major benefit of gabapentin is that there is minimal hepatic metabolism thus it will not induce drug–drug interactions with other AEDs with hepatic metabolism (e.g., phenobarbital).
Felbamate (Felbatol) Felbamate is a dicarbamate with proven ability to block seizures induced by a variety of methods. Felbamate is believed to increase seizure threshold and prevent seizure spreading by reducing excitatory neurotransmission in the brain. Neuroprotective effects have also been shown through this ability to alter excitatory neurotransmission. In clinical trials in people, felbamate has been shown to be most useful as monotherapy in the treatment of uncontrolled partial epilepsy. The drug is metabolized by the hepatic microsomal P450 enzymes and with increased clearance in younger dogs. In dogs, the drug has a high bioavailability and proteinbinding capability.
• Effective control of focal seizure activity with docu• •
•
•
•
mented therapeutic serum concentrations has been shown with felbamate therapy in dogs. The recommended dosage in dogs is 20 mg/kg q8h PO initially; increase as necessary up to a maximum of 3000 mg/day. Felbamate is a non-sedating drug but has been reported with a higher incidence of aplastic anemia and liver toxicity in people. These adverse effects have not been documented in dogs. Avoid concurrent use of felbamate and phenobarbital due to the possibility of increased hepatotoxicity and alteration of serum phenobarbital concentrations (felbamate increases serum phenobarbital concentration by 25%). Serial monitoring of the complete blood count and chemistry panel is recommended at 1 month and then every 3 months during treatment for the first year and then every 6 months thereafter. Trough serum drug concentration is typically done 1 to 2 weeks after initiation of treatment, with a therapeutic range between 25 and 100 mg/L.
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• Dosage: 30 to 60 mg/kg/day (divided every 8–12
• •
hours). Gradual increase in dose over 1 to 2 weeks is recommended to allow adaptation to the sedating effects. Reduced doses may be needed in patients with renal insufficiency. Serum monitoring is not recommended, as the drug has a very high therapeutic index and little drug–drug interactions. Gabapentin is particularly useful in epileptic dogs with underlying hepatic disease.
Levetiracetam (Keppra) Levetiracetam is the S-enantiomer of the ethyl analogue of piracetam that has broad-ranging, unique, and not completely known mechanisms of action against seizures. The drug is well absorbed but is more rapidly metabolized in people as compared with other drugs. The pharmacodynamic effect (i.e., the effect of the drug at the target organ) is believed to outlive the known half-life of the drug. Levetiracetam was the best tolerated of all new AEDs currently in human clinical trials, with adverse reactions equal to that of the placebo. Overall, this drug is proven to be an effective adjunctive therapy to control partial seizures previously refractory in treatment in people.
• Initial dosage: 500 to 1500 mg/day divided every 8 to 12 hours with gradual incremental dose titration.
• In my experience, the best response to this drug has
•
been in dogs exhibiting automatisms and generalized seizures as an add-on medication to phenobarbital and/or bromide. The serum trough therapeutic range in epileptic people is reported to be 3 to 37 mg/ml.
Gabapentin (Neurontin) Gabapentin is a novel AED whose mechanism of action is still not fully understood. Initially designed to mimic gamma-aminobutyric acid (GABA) in the brain, gabapentin can readily pass through the blood-brain barrier. Once in the brain, however, gabapentin does not mimic the pharmacologic properties of GABA, nor does it bind to GABA receptors. In preclinical studies, gabapentin effectively blocked seizures induced by a variety of proconvulsant methods. New evidence suggests that gabapentin may facilitate the extracellular transport of GABA out of cells to act on the GABA-alpha receptor. The dog is the only known species to partially biotransform the drug to N-methyl-gabapentin.
Topiramate (Topamax) Topiramate is a sulphamate-substituted monosaccharide with a mechanism of action of blockade of seizure spread by rapidly potentiated GABA activity in the brain. In people, topiramate is well absorbed and is primarily renal excreted as an unchanged drug. With a relatively long half-life of 20 to 30 hours, twice daily dosing is recommended. With a relatively broad-spectrum activity against many seizure types and minimal adverse effects, topiramate is approved for use in both adult and pediatric human patients. The dosage range is between 25 and 50 mg/kg/day, but gradual dose titration is better tolerated.
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Diazepam (Valium)
• Initial dosage: 2 to 10 mg/kg q12h with gradual incre• •
mental dose titration. I have used topiramate most successfully in dogs with partial and generalized seizures unresponsive to phenobarbital and bromide therapy. The serum therapeutic range is unknown in dogs but is between 2 and 25 mg/L in people.
Zonisamide (Zonegran) Zonisamide is a substituted 1,2-benzisoxazole derivative that works by both blocking the propagation of epileptic discharges and suppressing focal epileptogenic activity. Pharmacokinetic information on the dog is limited to a very small population of normal beagles. In general, zonisamide is well absorbed, has a relatively long half-life, and has high protein-binding affinity. The drug is highly concentrated in red blood cells due to high binding to carbonic anhydrase and other red cell protein components. Zonisamide is hepatic metabolized and thus is influenced by concurrent administration of similarly metabolized drugs. Broad-spectrum antiepileptic activity has been reported against a variety of seizure types, with particular improvement in the treatment of adult myoclonus epilepsy. Major adverse effects in people include a higher incidence of renal calculi formation, sedation, and gastrointestinal disorders.
• Initial dosage: 5 to 10 mg/kg/day divided every 8 to •
•
12 hours with gradual incremental dose titration. In my experience, zonisamide can be an efficacious and well-tolerated drug in the dog with recurrent generalized seizures refractory to phenobarbital and/or bromide therapy. The major adverse effects include sedation, ataxia, and inappetence. Phenobarbital dosages should be reduced by 25% at the time of starting zonisamide. The serum trough therapeutic range is reported from 10 to 40 mg/ml.
Drugs with Increased Risk or Inappropriate Pharmacokinetics in the Dog ▼ Key Point Since both primidone and phenytoin have been proved not to provide effective seizure control and are potentially hepatotoxic in the dog, do not use these drugs to treat seizures in the dog.
Lamotrigine (Lamictal) The drug is converted to a cardiotoxic 2-N methyl metabolite in dogs, which is not found in people.
Phenytoin (Dilantin)
• There is a high risk of hepatotoxicity with this drug. • It is difficult to maintain adequate steady-state serum concentrations due to the very rapid elimination halflife (approximately 2 hours).
• Functional tolerance develops very quickly to
• •
diazepam, which results in inability to use diazepam as an effective emergency drug to stop cluster seizures or status epilepticus. There is potential for causing physical dependence and withdrawal seizures. It is difficult to maintain adequate steady-state serum concentrations.
Gamma-vinyl-gamma-aminobutyric acid (Vigabatrin)
• Potential for causing hemolytic anemia • Potential for causing central nervous system vacuolation with chronic use
• Ineffective for stopping seizures Carbamazepine (Tegretol) It is difficult to maintain adequate steady-state serum concentrations due to the very rapid elimination halflife (approximately 2 hours).
Benzodiazepines Benzodiazepines are a class of AEDs that interact with specific central nervous system benzodiazepine receptors, which activate the GABA-alpha chloride channel to hyperpolarize neuronal membranes.
• Diazepam is the most widely used benzodiazepine in veterinary medicine and is best used for the treatment of emergency seizures by IV and per rectal administration (see below). ▼ Key Point Chronic oral administration of diazepam is not recommended in the dog due to lack of effectiveness to stop seizures, very short half-life, potential for increased hepatic enzyme inhibition, physical dependence, and cross-tolerance to prevent effective use of IV diazepam to stop emergency seizures.
• A long-acting benzodiazepine, clorazepate, is a diazepam prodrug with more suitable pharmacokinetic properties for chronic use in the dog. However, similar problems may arise as with chronic oral diazepam, especially the potential for severe withdrawal seizure activity.
Treatment of Refractory Epilepsy in Cats Since cats have an extremely high prevalence of symptomatic epileptic seizures, epileptic cats may not respond to phenobarbital alone. Moreover, the often focal nature of the underlying pathologic condition (e.g., meningioma or cerebrovascular accident) may predispose cats to focal seizure activity, which can be difficult to control with phenobarbital, in my experience. Unfortunately, cats are quite sensitive to the sedative
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effects of many of the AEDs. Therefore, most combination therapies require a delicate balance of drug dosing. The following drugs may be tried in addition to or as replacement of phenobarbital therapy in cats. ▼ Key Point Adding a second AED or changing to a different therapy should be considered in cats whose seizures continue despite persistent trough serum phenobarbital concentrations above 20 mg/ml.
Benzodiazepines Diazepam
• Cats appear to be resistant to developing functional tolerance to diazepam.
• Initial dosage: 0.5 mg/kg PO divided every 8 to 12 •
hours. Serum concentrations of nordiazepam can be monitored, but a therapeutic range has not been determined for the cat.
Clorazepate Clorazepate is a long-acting benzodiazepine, similar in action to diazepam.
• Initial dosage: 2 to 3.75 mg total dose per cat q12–24h •
PO. Start at a low dose (1–2 mg per cat) and gradually increase over time. Serum concentrations of nordiazepam can be monitored, but a therapeutic range has not been determined for the cat.
Clonazepam Clonazepam is a long-acting benzodiazepine, similar in action to diazepam.
• Initial dosage: 0.5 mg total dose once to twice daily. Gabapentin (Neurontin) Gabapentin is a useful AED in the cat due to its predominant renal excretion, similar to the dog. Cats, however, may exhibit increased sedation and will benefit by a gradual increment in dosing over 1 to 2 weeks.
• Initial dosage: 5 to 10 mg/kg daily for 3 to 5 days, •
then increase to every 12 hours. Further increases are dependent on response to therapy. Both solution (250 mg/5 ml) and capsular formulations of the drug are available. The drug can be used as both a monotherapy and an add-on medication.
Topiramate (Topamax) In my experience, a number of cats with focal seizures, exclusive or with secondary generalization of seizures, will improve with the addition of topiramate to phenobarbital therapy. The key to success is gradual adapta-
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tion and eventual lowering of the phenobarbital dosage. The latter should be performed to acquire a trough level of approximately 10 mg/ml.
• Initial dosage: 12.5 mg total dose per cat per day, with incremental dosing up to 25 mg every 12 hours.
• Both breakable tablet (25 mg) and sprinkle (15 mg) formulations are available.
• Metabolic acidosis has been associated with chronic dosing in people. Periodic venous blood gas monitoring is recommended in addition to routine evaluation of complete blood counts and serum chemistry panels.
Drugs with Increased Risk or Inappropriate Pharmacokinetics in the Cat Benzodiazepines Fatal, acute idiosyncratic hepatotoxicity after diazepam administration has been reported in the cat. Thus, obtain a liver chemistry panel in all cats 3, 7, and 14 days and then every 3 to 6 months after initiation of therapy.
Bromide Bromide therapy in cats is not recommended as a standard therapy due to the relatively high prevalence of adverse respiratory problems. Cats can develop cough and more severe respiratory signs suggestive of an allergic asthmatic disease. I no longer recommend the use of bromide in cats.
Hospital Emergency Treatment for Seizures ▼ Key Point A reliable protocol for rapid treatment is necessary for the emergency management of seizuring patients.
The physiologic sequelae of clustered or continuous seizure activity (status epilepticus) leading to increased intracranial pressure and neuronal necrosis include systemic arterial hypertension, loss of cerebrovascular regulation, disruption of the blood-brain barrier, and cerebral edema. If not treated appropriately, the seizuring patient may develop serious neurologic complications due to these events.
Guidelines for When to Administer Emergency Therapy for Seizures
• A single seizure that persists >5 minutes from the time the seizure is identified
• Status epilepticus • More than one seizure per hour, regardless of seizure length
• Three or more seizures per day, regardless of seizure length
Protocol for Emergency Management of Seizures A protocol for the emergency treatment of seizures in the dog and cat is outlined in Table 127-4. Two main
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Table 127-4. PROTOCOL OF THE MEDICAL MANAGEMENT OF STATUS EPILEPTICUS AND CLUSTER SEIZURES IN THE DOG AND CAT Phase 1 The goals of this initial phase are to stabilize the patient, institute short-acting AEDs with minimal adverse effects to immediately control active seizures, and to rapidly establish serum concentrations of a maintenance AED to preserve seizure control. 1. ABC: Establish a patent airway, maintain adequate breathing, and provide circulatory support. 2. Start a continuous IV infusion of 0.9% saline at a dosage of 5 to 10 ml/kg/hour. 3. Evaluate STAT blood glucose, PCV/TP, BUN, and AED serum concentration (if appropriate). Treat for hypoglycemia only if the blood glucose is £60 mg/dl. 4. Administer a bolus dose of DZ 0.5 mg/kg IV if a seizure episode lasts £1 minute, there have been at least two seizures (regardless of duration), or an intracranial etiology is suspected (regardless of duration). a. Alternate treatment: DZ per rectal injection (5 mg/ml of parenteral DZ) (1) No prior PB therapy: 1 mg/kg (2) Prior PB therapy: 2 mg/kg 5. Administer PB after DZ to provide a sustained antiepileptic effect as serum levels of DZ decline. a. Drug-naïve patients: (1) Give a loading dose of PB to rapidly establish therapeutic drug levels. Use this formula: Loading dose (total mg) = Desired serum level (mg/ml) ¥ Body weight (kg) ¥ 0.8 L/kg. Use an IV injection at a rate of £100 mg/min. (2) Desired serum concentration: Dogs = 20 mg/ml, cats = 10 mg/ml. b. PB-treated patients: (1) Give 1 mg/kg IV for each microgram per milliliter of desired increase in patient serum level. (2) Dogs: Raise serum concentration at increments of 5 mg/ml up to 30 mg/ml. (3) Cats: Raise serum concentration at increments of 3 mg/ml up to 20 mg/ml. 6. Alternative treatment with BR after DZ in dogs only: a. Drug-naïve patients: (1) Oral loading (NaBr or KBr): 200-mg/ml solution Target Css ¥ Vd = Total dose administered = 2000 mg/L ¥ 0.45 L/kg = 900 mg/kg/day divided into equal doses every 4 hours for 24 hours (2) IV loading (NaBR): 3% NaBR in sterile water Target Css ¥ Vd = Total dose administered by continuous rate infusion in a central vein = 2500 mg/L ¥ 0.45 L/kg = 900 mg/kg every 24 hours b. BR-treated patients: (1) New added oral dose over 24 hours: (Target Css - Actual Css) ¥ Vd L/kg = (Target Css - Actual Css) ¥ 0.45 L/kg = mg/kg doses in 4 equal doses every 6 hours (2) Target Css: Monotherapy BR treatment = 2000 mg/L; BR plus PB = 1500 mg/L Phase 2 The goals of this phase are to institute maintenance AED therapy and monitor for further seizures activity. 1. Institute maintenance PB either PO or IM. a. Drug-naïve patients: After IV loading dose, initiate oral therapy at 2.5 mg/kg q12h starting in 12 hours. b. Established epileptic patients: Increase dose to an amount higher than that being administered on admission. (1) New total mg/day = (Desired concentration/Established concentration) ¥ Total mg current dose c. Dogs: Increase the desired concentration in the maintenance dose formula at increments of 5 mg/ml up to 30 mg/ml. d. Cats: Increase the desired concentration in the maintenance dose formula at increments of 3 mg/ml up to 25 mg/ml. 2. BR therapy (dogs only) if BR is to be used as monotherapy: a. Drug-naïve patients: (1) Maintenance dose: Target Css ¥ (Clearance/Bioavailability) = mg/kg/day = 2000 mg/L ¥ 0.02 = 40 mg/kg/day divided bid b. Previous BR-treated patients: (1) New maintenance dose: (Target Css - Actual Css) ¥ (Clearance/Bioavailability) = mg/kg/day = (2500 mg/L - Actual Css) ¥ 0.02 = added mg/kg/day 3. BR therapy (dogs only) if BR is to be used as combined therapy with PB: a. Drug-naïve patients: (1) Maintenance dose: Target Css ¥ (Clearance/Bioavailability) = mg/kg/day = 1500 mg/L ¥ 0.02 = 30 mg/kg/day given daily or divided BID b. Previous BR-treated patients: (1) New maintenance dose: (Target Css - Actual Css) ¥ (Clearance/Bioavailability) = mg/kg/day = (2000 mg/L - Actual Css) ¥ 0.02 = added mg/kg/day 4. If seizures continue: a. At a rate of less than one per 3 hours: Use DZ 0.5 mg/kg IV bolus up to three doses and then proceed to phase 3. b. At a rate of more than one per hour: Proceed to phase 3.
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Table 127-4. PROTOCOL OF THE MEDICAL MANAGEMENT OF STATUS EPILEPTICUS AND CLUSTER SEIZURES IN THE DOG AND CAT—cont’d Phase 3 The goal of this phase is to treat recurrent seizures in patients that fail to respond to an initial course of IV bolus doses of DZ and PB. 1. Begin continuous rate IV infusion of DZ at an initial rate of 0.25 mg/kg/hour in a 0.9% NaCl (or 0.45% NaCl/2.5% dextrose if on BR) at a maintenance fluid rate. 2. If seizures continue (less than three total), increase the rate up to 0.5 mg/kg/hour. 3. If a total of three or more seizures occur while on the DZ infusion, administer one of the following for 6 hours: a. For pentobarbital: Initial bolus to induce general anesthesia at 2 mg/kg IV slowly to effect (if patient has been on PB prior to admission, a higher dose may be needed due to induction of the hepatic P450 system). Continuous infusion of approximately 5 mg/kg/hour to effect. b. For propofol: Initial slow infusion of 4 to 8 mg/kg IV to effect, followed by continuous infusion to maintain general anesthesia (8 to 12 mg/kg/hour). (1) Advantages: Primarily renal excreted (safer to use in dogs with liver disease), rapidly metabolized to allow rapid recovery, and does not induce biochemical changes. (2) Disadvantages: Can induce apnea, cause hypovolemia, and is relatively expensive for prolonged use. 4. Maintenance PB therapy should be administered IM throughout the anesthesia to provide sustained therapeutic serum concentration upon emergence from anesthesia. 5. Appropriate supportive care and monitoring should be provided for general anesthesia. 6. After 4 to 6 hours, if any further seizures occur, proceed to phase 4. Phase 4 The goal of this phase is induction of prolonged general anesthesia. 1. Barbiturate a. Maintain general anesthesia as established in phase 3 for an additional 12 hours, followed by a tapering of anesthesia every 2 to 4 hours. 2. Gas anesthesia a. Indications: Refractory seizures to above steps or contraindication to use of benzodiazepine or barbiturate drugs (hepatotoxicity or hepatic encephalopathy). b. Isoflurane offers the following advantages: Rapid induction and adjustable anesthetic depth with smooth emergence from anesthesia, no hepatotoxicity, less perfusion problems, and less effect on elevation of intracranial pressure than halothane. c. Obtain arterial blood gases every 4 to 8 hours to ensure adequate oxygenation. AED, antiepileptic drug; BR, bromide; BUN, blood urea nitrogen; Css, steady-state concentration; DZ, diazepam; PB, phenobarbital; PCV/TP, packed cell volume and total protein; Vd, volume of distribution.
components are listed in this protocol: restoring homeostatic conditions and providing specific seizure treatment. Many drugs used to control seizures have the potential to cause serious adverse effects, including death. Specific seizure treatment is divided into four successive phases.
• Phases 1 and 2 involve using a short-acting AED to
• •
stop immediate seizure activity and a long-acting AED to prevent further seizures. Diazepam is currently the drug of choice in treating prolonged seizures, including status epilepticus and cluster seizures. Phases 3 and 4 outline steps to follow if a dog continues to seizure despite prior treatment. To implement this protocol, be sure to have injectable diazepam, phenobarbital, pentobarbital, propofol, and a 24-hour monitoring facility.
cost, decrease patient morbidity, and contribute positively to the overall AED therapy. Per rectum administration of the IV formulation of diazepam allows rapid absorption of active drug into the bloodstream through the rectal mucosa in 0.06 second (dog) or 0.04 second (cat)
• Tall R waves • Dog: R greater than 3.0 mV in leads II, aVF, V6LU (V4), CV6LL (V2), and CV5RL (rV2). R greater than 1.5 mV in lead I. Sum of R wave amplitude in leads I and aVF greater than 4.0 mV.
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• Cat: R > 1.0 mV in CV6LU (V4). R > 0.9 mV in lead II or aVF. R wave or Q wave > 1.0 in V10.
Right Atrial Enlargement Right atrial enlargement is characterized by taller-thannormal P waves in lead II (Fig. 144-14).
• Dog: P > 0.4 mV (or prolonged P wave in some dogs). • Cat: P > 0.2 mV (tall P waves may also indicate left atrial enlargement in cats).
Right Ventricular Enlargement Right ventricular enlargement is characterized by one or more of the following (Fig. 144-15):
• Right axis orientation (dog > +100 degrees; cat > +160 degrees)
• S wave in leads I, II, III, and aVF • S wave in lead I greater than 0.05 mV (dog) • Chest leads • Dog: S greater than 0.8 mV in CV6LL (V2). S greater than 0.7 mV in CV6LU (V4). R/S ratio less than 0.87. T positive (except for the Chihuahua) and W-shaped QRS complex in V10. • Cat: Prominent S waves in CV6LL (V2) and CV6LU (V4); T positive in V10.
SPECIAL DIAGNOSTIC PROCEDURES Postexercise Electrocardiography
Figure 144-14. Tall P waves suggestive of right atrial enlargement. (From Tilley LP: Essentials of Canine and Feline Electrocardiography, 3rd ed. Philadelphia: Lea & Febiger, 1992.)
Patients with suspected cardiac disease or arrhythmia, based on auscultation or history of syncope or exercise intolerance, may have normal resting ECGs. Sometimes, an arrhythmia can be documented by repeating an ECG after vigorous exercise. T wave changes or S-T segment abnormalities may become apparent following exercise, suggesting underlying myocardial disease.
Figure 144-15. Marked right axis deviation in a dog with advanced heartworm disease and evidence of right-sided heart failure. (From Tilley LP: Essentials of Canine and Feline Electrocardiography, 3rd ed. Philadelphia: Lea & Febiger, 1992.)
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episodes may be discovered, although an event monitor is more specific in this situation (see below).
Vagal Maneuvers Indications
• Vagal maneuvers are sometimes useful in evaluating
•
supraventricular tachycardias. A sudden surge of vagal tone may slow or block conduction down the AV node. This effect may terminate reentrant supraventricular tachycardia or “uncover” atrial flutter or tachycardia when there is regular AV conduction and atrial activity is buried within the ST-T. Vagal maneuvers may also help evaluate baroreceptor and sinus node functions.
▼ Key Point The veterinarian cannot be certain that an arrhythmia identified on a Holter recording of an animal with syncope is the cause of the animal’s problem, unless the animal has a syncopal episode or related clinical signs at the same time the arrhythmia is recorded.
• Holter monitoring is also used as a screening tool for
Technique
• While running a lead II rhythm strip, vigorously • •
massage the carotid sinuses that are located under the mandible in the jugular furrow. If this maneuver does not break the tachycardia, apply gentle, progressive ocular pressure. If still unsuccessful, apply ocular pressure and carotid sinus massage.
Interpretation
• If a supraventricular tachycardia breaks abruptly and
• • • •
the rhythm remains normal for at least a short time after stopping the vagal maneuver, the arrhythmia was probably reentrant atrial (supraventricular) tachycardia. If the rate gradually slows during the vagal maneuver and then speeds up again after the vagal maneuver, the rhythm is probably sinus tachycardia. If multiple P waves (>300/min) are observed, related to vagal-induced AV block, either atrial tachycardia or flutter is likely. If there is no change during the vagal maneuver, no conclusion can be made regarding the nature of the supraventricular tachycardia. Another area in which a vagal maneuver may be helpful is in trying to rule out bradyarrhythmia as a cause of syncope. If the vagal maneuver results in prolonged periods of sinus arrest or produces AV block, this supports sinus or AV nodal disease as a cause of syncope.
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•
•
the diagnosis of arrhythmogenic right ventricular cardiomyopathy (boxer cardiomyopathy) in boxers and occult cardiomyopathy in Doberman pinschers. • While in most breeds normal animals will have fewer than 25 VPCs in 24 hours, the threshold for normal may be higher in boxers The presence of greater than 100 VPCs, couplets, or runs is highly suggestive of arrhythmogenic right ventricular cardiomyopathy in boxers. • In Doberman pinchers, the presence of VPCs is a risk factor for development of dilated cardiomyopathy. In one study of Doberman pinschers with normal echocardiograms, all animals with greater than 50 VPCs per 24 hours, 94% with greater than 10 VPCs per 24 hours, and 94% with couplets or triplets of VPCs developed echocardiographic evidence of dilated cardiomyopathy within 1 year. However, not all Dobermans pinschers with VPCs develop cardiomyopathy and the absence of VPCs on a 24-hour Holter study does not rule out the subsequent development of dilated cardiomyopathy. When using Holter monitoring of antiarrhythmic therapy, a greater than 85% reduction in the frequency of VPCs in an indication of effective arrhythmia suppression. Holter monitoring is offered by some veterinary cardiologists and transtelephonic ECG services, and it sometimes can be arranged through a local medical cardiologist. Holter recordings should be reviewed by a veterinary cardiologist, as technicians trained to read human Holter studies often overinterpret atrial premature complexes on canine ECGs.
Holter Monitoring
Event Recorders
Holter monitors provide a 24-hour ECG recording (Fig. 144-16). These recordings are ideal for identifying intermittent arrhythmias, determining the frequency and severity of arrhythmias, and monitoring the efficacy of antiarrhythmic drug therapy.
Event or loop recorders are the best diagnostic tool for identifying arrhythmias as the cause of syncope. These are small digital ECG recorders that can easily be worn by even small dogs and cats.
• Holter monitoring may be helpful in patients with
ECG. After the veterinarian attaches the system, the animal is sent home. When the animal has an event (e.g., syncope, collapse, or seizure) the owner pushes a button to activate the memory feature, which preserves the ECG in memory for a preprogrammed
syncope in which routine ECGs and laboratory evaluation do not confirm a diagnosis. If arrhythmias are identified on Holter monitoring of a patient with a history of syncope, the cause of the collapsing
• These units record a continuous 5-minute loop of an
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Figure 144-16. Printouts of three displayed time segments from a 24-hour electrocardiographic recording (Holter monitoring). The period of ventricular tachycardia can be easily recognized and correlated with the times of occurrence by referring to the digital time entries displayed adjacent to the electrocardiographic data. Detected ventricular ectopic activity can be efficiently enlarged, especially on the 15-second time segment (bottom frame) for more complete analysis and documentation. (From Tilley LP: Essentials of Canine and Feline Electrocardiography, 3rd ed. Philadelphia: Lea & Febiger, 1992.)
•
time before, during, and following the event. After the recording is made, it can be transmitted transtelephonically for printing and interpretation of the ECG. In animals with frequent syncopal episodes, an event monitor is preferable to a Holter monitor for making a diagnosis because the event recording is timed with the clinical signs. In a study of 60 collapsing animals, 51 tracings (85%) were diagnostic, ruling out arrhythmias in 65% and confirming arrhythmias in 35%.
Atropine Response Test Patients with symptomatic bradyarrhythmia may be administered a test dose of atropine (0.05 mg/kg IM or SC) and undergo an ECG 30 minutes later. This test is helpful in determining the role of vagal tone in the bradyarrhythmia and whether or not oral anticholinergic drugs (e.g., hyoscyamine) might alleviate some symptoms associated with the bradycardia, particularly when pacing is not an option.
Lidocaine Response Test Patients with sustained, wide, complex tachycardia (ventricular tachycardia or atrial tachycardia with a bundle branch block) may be administered lidocaine (2–4 mg/ kg IV) to help establish a diagnosis. Termination of the arrhythmia suggests the disturbance is a lidocaineresponsive, ventricular tachycardia. Occasionally, an atrial tachycardia will break following the administration of lidocaine.
SUPPLEMENTAL READING Bonagura JD: Cardiovascular diseases. In Sherding RG (ed): The Cat, Diseases and Clinical Management. New York: Churchill Livingstone, 1989, p 649. Calvert CA, Wall M: Results of ambulatory electrocardiography in overtly healthy Doberman pinschers with equivocal echocardiographic evidence of dilated cardiomyopathy. J Am Vet Med Assoc 219(6):782–784, 2001.
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Chapter 144 / Electrocardiography Harpster NK: The cardiovascular system. In Holzworth J (ed): Diseases of the Cat: Medicine and Surgery. Philadelphia: WB Saunders, 1987, p 820. Kittleson MD, Kienle RD: Electrocardiography: basic concepts, diagnosis of chamber enlargement, and intraventricular conduction disturbances. In Kittleson MD, Kienle RD (eds): Small Animal Cardiovascular Medicine. St. Louis, Mosby, 1998, p 72. Meurs KM, Spier AW, Wright NA, Hamlin RL: Use of ambulatory electrocardiography for detection of ventricular premature com-
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plexes in healthy dogs. J Am Vet Med Assoc 218(8):1291–1292, 2001. Miller MS, Tilley LP, Smith FWK Jr, Fox PR: Electrocardiography. In Fox PR, Sisson D, Moise NS (eds): Canine and Feline Cardiology, 2nd ed. Philadelphia: WB Saunders, 1999. p 67. Tilley LP: Essentials of Canine and Feline Electrocardiography, 3rd ed. Philadelphia: Lea & Febiger, 1992.
Chapter
▼
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145
Disorders of Cardiac Rhythm Michael S. Miller / Larry Patrick Tilley / Francis W.K. Smith, Jr.
Cardiac arrhythmias include disorders of cardiac impulse formation, conduction, rate, and regularity. Terms such as dysrhythmia, ectopia, and ectopy also are used to identify arrhythmias. Cardiac arrhythmias can be benign and clinically insignificant, or they can cause clinical signs. They can even progress to malignant arrhythmias that lead to heart failure, syncope, or sudden death. Causes of cardiac arrhythmias include heart disease and disorders involving the autonomic nervous system, endocrine system, electrolytes, and other body systems. Anesthetic agents and other drugs can precipitate rhythm disturbances. Cardiac arrhythmias are diagnosed and classified electrocardiographically; see Chapter 144 for additional pertinent information regarding electrocardiography. A summary of the clinical pharmacology of drugs used in the treatment of congestive heart failure (CHF) is found in Chapter 146.
ETIOLOGY • Cardiac arrhythmias are classified in Table 145-1. • •
They occur with congenital or acquired cardiac disease or systemic disorders (Table 145-2). Cardiac pathology does not necessarily correlate with the type and severity of arrhythmias. Arrhythmia variation in animals with cardiac or systemic disorders may be explained by the complex interactions among cardiac cell transmembrane potentials, the autonomic nervous system, and body fluids.
MECHANISMS • The normal cardiac impulse is generated automati-
•
cally in the sinus node and is spread through the atria rapidly and sequentially via the His bundle, the bundle branches, and the intraventricular conduction system to the ventricular myocardium. The normal atrioventricular (AV) node serves as a bridge between the atria and the ventricles and slows
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• •
•
•
•
the cardiac impulse prior to rapid impulse conduction through the ventricles. Cardiac rhythm disturbances develop from diverse electrophysiologic mechanisms. Enhanced automaticity in sinus node or subsidiary pacemaker cells can generate tachycardias or ectopic rhythms. Such activity may be influenced by sympathetic activity. Triggered activities are common causes of ectopic rhythms and tachycardias. Early or late afterdepolarizations follow a previously driven (sinus) depolarization. The premature impulses occur when the cell spontaneously depolarizes during or just after repolarization. Reentry, a common arrhythmia mechanism, typically is caused by functional dissociation of cardiac tissue, a unidirectional block in one pathway, and slowed conduction in the other pathway. The impulse then returns to the origination point by retrograde conduction through the unidirectionally blocked pathway. Electrophysiologic mechanisms, arrhythmia manifestations and accompanying clinical signs and symptoms may vary widely among dogs with specific inherited cardiac diseases. Arrhythmogenic mechanisms can be modified (for better or for worse) by autonomic activity, heart rate, and many cardiac and non-cardiac drugs.
DIAGNOSTIC APPROACH Systematic Evaluation of the Electrocardiographic Strip See also Chapter 144.
• Is sinus rhythm or an arrhythmia present? • Is the heart rate rapid, slow, or normal? • Are P waves present? • Yes. Do the P (atria) waves occur at regular or irregular intervals? What are the height, width, and direction? • No. What reason or abnormality explains the absence of the P wave? Is the P wave superimposed
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Table 145-1. CLASSIFICATION OF CARDIAC ARRHYTHMIAS Supraventricular Rhythms Sinus rhythm Sinus arrhythmia Sinus bradycardia Sinus tachycardia Atrial premature complexes Sinus block and/or arrest Atrial tachycardia Atrial/supraventricular tachycardia (reentrant) Atrial flutter Atrial fibrillation Atrioventricular junctional rhythm Ventricular Rhythms Ventricular escape (rhythm) Ventricular premature complexes Idioventricular tachycardia Ventricular tachycardia Ventricular asystole Ventricular fibrillation Conduction Disorders Atrial standstill First-degree AV block Second-degree AV block Complete (third-degree) AV block Arrhythmias and Conduction Disturbances Sick sinus syndrome Ventricular preexicitation and the Wolff-Parkinson-White syndrome
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SUPRAVENTRICULAR RHYTHMS Sinus Rhythm Definition
• Impulses originate in the sinus node. • The rhythm is regular with less than a 10% variation in the R-R interval.
• There is a normal P wave for each QRS complex, with a constant P-R interval.
• The heart rate is between 60 and 180 beats per minute (bpm) in dogs and between 120 and 240 bpm in cats.
Etiology and Clinical Significance
• Sinus rhythm is a normal resting rhythm in dogs and cats and requires no therapy.
• Animals with symptomatic cardiac disease or noncardiac disease may show a sinus rhythm.
Sinus Arrhythmia Definition
• Impulses originate in the sinus node. • The rhythm is irregular with more than a 10% variation in the R-R interval.
• There is a normal P wave for each QRS complex, with a constant P-R interval.
• A wandering pacemaker (a change in the morphol-
•
• •
on a portion of the QRS complex, S-T segment, or T wave? Is the arrhythmia atrial standstill, atrial fibrillation, atrial flutter, AV junctional escape rhythm, or atrial tachycardia? Do the QRS (ventricular) complexes occur with regularity and uniformity? What is their morphology? If wide and bizarre, is this due to a ventricular arrhythmia or caused by a premature atrial impulse that is aberrantly conducted, or is bundle branch block evident? What is the relationship between the P waves and the QRS complexes? Is the relationship consistent? If AV dissociation is present, from where does the QRS complex evolve? Are AV junctional and/or Purkinje or idioventricular foci involved?
Questions To Be Answered in the Interpretation of Cardiac Arrhythmia • What is the possible mechanism for the arrhythmia? • Is it sinus, atrial, AV junctional, or ventricular in • •
origin? Is there a conduction abnormality? What is the severity and frequency of the arrhythmia?
•
ogy of the P wave due to a change in pacemaker location or conduction) is often present. Heart rates are similar to those for sinus rhythm.
Etiology and Clinical Significance
• Sinus arrhythmia is a normal rhythm variation in the
• •
resting dog, often correlated with varying levels of sinus node vagal tone, which changes with respiration (decreased vagal tone and increased heart rate during inspiration). Sinus arrhythmia is unusual in cats. Pronounced sinus arrhythmia occurs in the normal resting dog and in dogs and cats with respiratory disease.
Treatment
• No treatment is required unless there is symptomatic bradycardia, in which case anticholinergics or sympathomimetics may be helpful.
Sinus Bradycardia Definition
• Impulses originate in the sinus node but at a slowerthan-normal frequency.
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Table 145-2. CAUSES OF CARDIAC ARRHYTHMIAS Cardiac Causes in Dogs
Cardiac Causes in Cats
Heredity (genetics not documented in all cases) Doberman (His bundle degeneration) English springer spaniel (persistent atrial standstill) Miniature schnauzer, dachshund, cocker spaniel, West Highland white terrier (sick sinus syndrome) Pug, Dalmatian (sinus node disease) Pug (stenosis and degeneration of the His bundle) Wolff-Parkinson-White syndrome Golden retriever (Duchenne muscular dystrophy) German shepherd (ventricular tachyarrhythmia) Atrial and/or ventricular arrhythmias Atrial enlargement, secondary to congenital defects or acquired disease Cardiomyopathy Congenital heart disease Congestive heart failure Mitral valve disease (congenital and acquired) Myocarditis, endocarditis Myocardial ischemia Trauma Drugs Conduction system disease Acquired sinus and AV node disease (sick sinus syndrome) Cardiomyopathy Neoplasia Surgical damage to conduction tissue Trauma Vascular (e.g., microscopic intramural myocardial infarction) Ventricular septal defect and other congenital defects Infection (Lyme disease) Drugs Degeneration
Heredity (rare) Wolff-Parkinson-White syndrome Atrial and ventricular arrhythmias Cardiac enlargement secondary to congenital heart defects Cardiomyopathy Neoplasia Trauma Systemic diseases Conduction system disease Cardiomyopathy Neoplasia Idiopathic fibrosis in older cats
Noncardiac Causes in Dogs and Cats Dogs and Cats Acidosis or alkalosis Autonomic nervous system imbalance (parasympathetic or sympathetic); central nervous system (pain, excitement, fear); respiratory, gastrointestinal, organic brain disease Drug toxicity (e.g., digitalis, preoperative sedatives, anesthetic agents, catecholamines, antiarrhythmic agents, bronchodilators) Electrolyte disorders (hyperkalemia, hypercalcemia, hypokalemia, hypocalcemia, hypomagnesemia) Endocrinopathies (hypothyroidism, hyperthyroidism, Addison’s disease, pheochromocytoma) Hypothermia Hypovolemia Hypoxia, anemia Mechanical stimulation (cardiac catheterization, intravenous catheter) Neoplasia Shock Toxemia, sepsis Trauma
Adapted from Miller MS, Tilley LP: Treatment of arrhythmias and conduction disturbances. In Miller MS, Tilley LP, eds.: Manual of Canine and Feline Cardiology. Philadelphia: WB Saunders, 1995, with permission.
• The rhythm is regular. • There is a normal P wave for each QRS complex, with •
a constant P-R interval. The heart rate is 240 bpm in cats.
Etiology and Clinical Significance
• Sinus tachycardia may be a normal physiologic • •
Etiology and Clinical Significance
• Sinus arrest may be consistent with an increase in
•
•
vagal tone (e.g., ocular pressure, irritation of the vagus nerve, brachycephalic breeds, or respiratory disease). Diseases of the atria (including fibrosis, cardiomyopathy, and neoplasia) and drug toxicity (e.g., digitalis, propranolol, quinidine, xylazine, and acepromazine) may result in sinus arrest. Sinus arrest is one of the arrhythmias of the sick sinus syndrome.
rhythm resulting from high sympathetic tone occurring with exercise or excitement. Sinus tachycardia may also occur with conditions such as stress, anxiety, pain, shock, fever, anemia, CHF, hyperthyroidism, and pheochromocytoma. Drugs (e.g., atropine, sympathomimetic agents, theophylline, ketamine, and light anesthesia) and intoxicants (caffeine, chocolate, cocaine) also can cause sinus tachycardia.
Electrocardiographic Differentials
• Other supraventricular tachyarrhythmias confused
•
with sinus tachycardia include paroxysmal (atrial or AV junctional) tachycardia, atrial flutter with 2:1 AV block, and ventricular tachycardia when sinus tachycardia is associated with wide QRS complexes. A vagal maneuver (e.g., carotid sinus or ocular stimulation for 5 to 10 seconds) may result in a transient, gradual slowing of the sinus tachycardia.
Electrocardiographic Differentials
Treatment
• Sinus block and/or sinus arrest can be confused with
• Identify and treat the underlying cause of the sinus
marked sinus arrhythmia or with sinus bradycardia
tachycardia.
Tab: 25, 50, 100 mg OS: 25 mg/ml Inj: 0.5 mg/ml Inj: 0.05, 0.1, 0.3, 0.4, 0.5, 0.8, 1.0 mg/ml Tab: 0.125, 0.25, 0.5 mg Inj: 0.25 mg/ml Elixir: 0.05 mg/ml Cap: 0.05, 0.1, 0.2 mg
Tab: 30, 60, 90, 120 mg Inj: 5 mg/ml Cardizem: 120, 180, 300 mg Dilacor: 120, 180, 240 mg Inj: 1 : 1000 conc (1 mg/ml) 1 : 10000 conc (0.1 mg/ml) Inj: 10, 250 mg/ml
Inj: 0.2 mg/ml Inj: 1 : 5000 (0.2 mg/ml) Inj: 5, 10, 15, 20 mg/ml (without epinephrine)
Atenolol (Tenormin)
Atropine sulfate*
Digoxin* (Lanoxin)
Diltiazem (Cardizem, Dilacor)
Epinephrine* (Adrenalin)
Glycopyrrolate* (Robinul)
Isoproterenol (Isuprel)
Lidocaine* (Xylocaine)
Esmolol (Brevibloc)
Tab: 200 mg
Formulation
Ventricular arrhythmias
Short-term management of sinus bradycardia, AV block, sick sinus syndrome
Sinus bradycardia, AV block, sick sinus syndrome
Supraventricular tachyarrhythmias, ventricular tachycardia, dynamic outflow tract obstruction
Cardiac arrest
Supraventricular arrhythmias, hypertrophic cardiomyopathy, hypertension
Supraventricular arrhythmias, myocardial failure
Sinus bradycardia, AV block, sick sinus syndrome, cardiac arrest
Atrial and ventricular arrhythmias, hypertrophic cardiomyopathy, hypertension, aortic stenosis
Class III antiarrhythmic agent; indicated for severe refractory atrial and ventricular arrhythmias
Indications
Dog: 50–500 (usually 50–100) mg/kg IV bolus every 5 minutes (up to 500 mg/kg) 50–200 mg/kg/min CRI Cat: Same Dog: 0.005–0.01 mg/kg IV, IM 0.01–0.02 mg/kg SC Cat: Same Dog: 0.04–0.09 mg/kg/min IV (titrate up to effect) 10 mg/kg/min IM, SC qid Cat: Same Dog: 2–8 mg/kg slowly IV or IO (double the dose IT) in 2-mg/kg boluses followed by IV drip at a dosage of 25–75 (occasionally up to 100) mg/kg/min CRI Cat: 0.25–0.75 mg/kg IV over 5 min
Dog: 0.01–0.04 mg/kg IV, IM, IO 0.02–0.04 mg/kg SC tid–qid (IT: double dose) Cat: Same Dog: Maintenance dose—0.22 mg/m2 PO bid, 0.0055–0.01 mg/kg PO bid IV loading dose—0.0025 mg/kg IV bolus repeated hourly 3–4 times (total up to 0.01 mg/kg). Begin oral therapy 12 hours later Oral loading dose—Twice maintenance dose for first 24–48 hours Cat: 0.01 mg/kg PO qod (Tab preferred) 0.007 mg/kg PO qod (with furosemide and aspirin) Dog: 0.5–2.0 mg/kg PO tid (consider higher dose of 5 mg/kg based on recent studies) 0.1–0.2 mg/kg IV bolus, then 2–6 mg/kg/min IV CRI Dilacor—1.5–6 mg/kg PO sid Cat: 1.0–2.5 mg/kg PO tid 0.1–0.2 mg/kg IV bolus, then 2–6 mg/kg/min IV CRI Dilacor—30–60 mg PO sid Dog: 0.2 mg/kg IV, IO q3–5min Double dose for IT administration Cat: Same
Dog: 0.25–1.0 mg/kg PO sid–bid Cat: 6.25–12.5 mg total dose PO sid–bid
Dog: 10–20 mg/kg PO q12h Cat: None
Dosages
Use with caution in cats Drug of choice for initial control of ventricular tachycardia Effects increased by high potassium and decreased by low potassium Seizures controlled with diazepam
Longer duration of action with less of a chronotropic effect than atropine
Monitor with ECG Previously recommended dose of 0.02 mg/kg may be safer starting dose if defibrillator is not available Ultra–short-acting beta1-selective beta-adrenergic blocker
Less myocardial depression than verapamil Dilacor capsules contain 60-mg tablets used for dosing cats
Toxicity potentiated by hypokalemia, hyponatremia, hypercalcemia, thyroid disorders, hypoxia Dose on lean body weight; reduce dose 10%–15% with elixirs Therapeutic range 1–2 ng/ml 8 hours after a dose Rapid digitalization not recommended except in emergency Reduce dose 50% with quinidine
Use as last resort for recurrent hemodynamically unstable ventricular tachycardia Takes weeks to achieve therapeutic levels Less bronchoconstriction, vasoconstriction, interference with insulin therapy than with non-selective beta-blockers Taper dose when discontinuing therapy Decrease dose with renal disease May transiently worsen bradyarrhythmia More potent chronotropic effects than glycopyrrolate
Comments
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Amiodarone (Cordarone)
Drug Trade Name
Table 145-3. COMMON ANTIARRHYTHMIC DRUGS: FORMULATIONS, INDICATIONS, AND DOSAGES
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Cap: 150, 200, 250 mg
Cap: 250, 375, 500 mg Tab: 250, 375, 500 mg Tab Procan, Pronestyl SR; 250, 500, 750, 1000 mg Inj: 100, 500 mg/ml Tab: 10, 20, 40, 60, 80, 90 mg Inj: 1 mg/ml OS: 4, 8, 80 mg/ml Tab: 324 mg Inj: 80 mg/ml
Mexiletine (Mexitil)
Procainamide* (Procan SR, Pronestyl SR, Procainamide CR)
Propranolol* (Inderal)
Quinidine gluconate* (Quinaglute Dura-Tabs) Quinidine polygalacturonate (Cardioquin) Quinidine sulfate* (Quinidex)
Tab: 400, 600 mg Tab: 40, 80, 120 mg Inj: 2.5 mg/ml
Tocainide (Tonocard) Verapamil* (Calan, Isoptin)
Supraventricular arrhythmias, hypertrophic cardiomyopathy
Ventricular arrhythmias
Ventricular arrhythmias
Ventricular and supraventricular arrhythmias, WPW syndrome, conversion of atrial fibrillation
Atrial and ventricular arrhythmias, hypertrophic cardiomyopathy, hypertension, thyrotoxicosis
Ventricular and supraventricular arrhythmias, WPW syndrome
Ventricular arrhythmias
Atrial and ventricular arrhythmias cardiomyopathy
Dog: 10–20 mg/kg PO bid–tid Cat: None Dog: 0.05–0.20 mg/kg slow IV (1–2 minutes) in boluses of 0.05 mg/kg given at 10- to 30-minute intervals (to effect) Cat: None
Dog: 1–3.5 mg/kg PO bid Cat: 1/8 of 80-mg Tab PO bid
Dog: 0.2–1.0 mg/kg PO tid 0.02–0.06 mg/kg IV over 5–10 minutes C < 4.5 kg: 2.5–5 mg PO bid–tid C > 4.5 kg: 5 mg PO tid–tid 0.02–0.06 mg/kg IV over 5–10 minutes D:† 6–20 mg/kg PO, IM qid 6–20 mg/kg PO tid with sustained release products 5–10 mg/kg IV (very slowly) Cat: None
Dog: 10–30 mg/kg IM PO qid (Procan SR, Pronestyl SR, Procainamide CR; tid) 2 mg/kg IV over 3–5 min up to total dose of 20 mg/kg 20–50 mg/kg/min CRI Cat: 3–8 mg/kg PO, IM tid–qid
Dog: 5–8 mg/kg PO bid–tid Cat: None
Dog: 0.25–1.0 mg/kg PO tid Cat: Same
Decrease digoxin dose 50% when using quinidine Effects increased by high potassium and decreased by low potassium Monitor ECG: 25% prolongation of QRS is sign of toxicity Has vagolytic, negative inotropic, vasodilating properties Reduce dose in CHF, hepatic disease, hypoalbuminemia Quinidine base (%) in each quinidine salt Quinidine gluconate (62%): 324-mg Tab = 200 mg of quinidine Antiarrhythmic agent with class II (beta-blocking) and class III effects May be proarrhythmic when administered as sole agent in young German shepherds with inherited ventricular arrhythmias Oral analogue of lidocaine Giving with food may decrease GI upset Diltiazem is safer alternative in heart failure Potent vasodilator and negative inotrope
Less bronchoconstriction, vasoconstriction, interference with insulin therapy than with nonselective beta-blockers Taper dose when discontinuing therapy Reduce dose with liver disease Take with food to reduce GI side effects Synergistic effect when combined with beta-blockers Beware of hypotension with IV administration Effects increased by high potassium and decreased by low potassium Monitor ECG: 25% prolongation of QRS is sign of toxicity Fewer GI and CV side effects than quinidine Use with caution in cats Reduce dose with severe renal and liver disease Non-selective beta-blocker Start with low dose and titrate to effect Taper dose when discontinuing therapy Reduce dose with liver disease
Chapter 145 / Disorders of Cardiac Rhythm
*Available in a generic preparation. † Note: Dosage calculated for quinidine base equivalent, which varies with each quinidine salt. See Comment column. AV, atrioventricular; Cap, capsules; CHF, congestive heart failure; conc, concentration; CRI, constant rate infusion; ECG, electrocardiogram; GI, gastrointestinal; Inj, injectable; IT, intratracheal; OS, oral solution; Tab, tablets; WPW, Wolff-Parkinson-White.
Tab: 80, 120, 160, 240 mg
Sotalol (Betapace)*
Tab: 200, 300 mg Tab SR: 300 mg Inj: 200 mg/ml
Tab: 275 mg
Tab: 50, 100 mg/kg Inj: 1 mg/ml
Metoprolol (Lopressor)
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Figure 145-2.
Atrial premature complexes in a dog. (Lead II rhythm strip, paper speed 50 mm/sec; 1 cm = 1 mV.)
• Antiarrhythmic drugs are seldom required. • Administer atenolol (6.25 mg total dose q12–24h PO)
•
or propranolol (2.5 mg total dose q8–12h PO) to hyperthyroid cats with intractable tachycardia (i.e., unresponsive to antithyroid medication). Administer digitalis for sinus tachycardia in CHF. Digoxin will reestablish normal baroreceptor function and lessen sympathetic tone.
Atrial Premature Complexes (Fig. 145-2)
•
Electrocardiographic Differentials
• Sinus rhythm with APCs may be confused with
Definition
• Impulses originate from an atrial focus, often other than the sinus node.
• The rhythm is irregular and the heart rate varies with
•
the sinus node rate.
• There is usually an abnormal P’ wave (premature P
•
•
•
wave) followed by a normal QRS complex. The P’-R interval of the APC may vary from the sinus rhythm P-R interval. The P’ wave may have various morphologies and may be fused with the T wave of the preceding beat. The P¢ wave may occur so early in the cardiac cycle that the AV conduction system will be refractory and the impulse will not be conducted to the ventricles (e.g., APC with physiologic AV block). The pause following the APC is often less than fully compensatory because of premature depolarization and resetting of the sinus node. Full compensatory pause occurs when the R wave-to-R wave interval surrounding the APC is equal to two normal R-R intervals. The QRS complex is usually normal, but the intraventricular conduction system may be, in a relative or absolute refractory period, causing a bizarre (abnormal shape or direction) QRS complex. This abnormality is termed an APC with aberrant ventricular conduction.
chronic valvular fibrosis, cardiomyopathy, congenital
marked sinus arrhythmia and ventricular premature complexes during auscultation, and with ventricular premature complexes on the ECG, when APCs are conducted with aberrant ventricular conduction. A P¢ wave preceding the abnormal QRS complex and a similarity of the initial deflection of the QRS complex compared with a preceding normal beat supports the diagnosis of aberrant conduction.
Treatment
• Infrequent APCs may be a normal variation and do not require treatment.
• If this arrhythmia is associated with CHF, treat the arrhythmia with digoxin.
• If the APCs are associated with poor hemodynamic status without myocardial failure, prescribe digoxin, diltiazem, or a beta-blocker (e.g., propranolol or atenolol) (see Table 145-3).
Atrial Tachycardia (Figs. 145-3 and 145-4) Definition
• Atrial tachycardia indicates rapid, abnormal impulses •
Etiology and Clinical Significance
• APCs often indicate underlying cardiac disease (e.g.,
defect, or cor pulmonale) resulting in atrial enlargement. Other causes include electrolyte disturbances, thyrotoxicosis, hypoxia, anemia, drug toxicity (e.g., digitalis, dobutamine, or dopamine), toxemia, and increased sympathetic tone.
•
originating from an atrial site other than the sinus node. The atrium and/or AV junctional areas may be involved in a reentrant circuit that allows the impulse to restimulate the atrium, as well as to pass to the ventricles. (A vagal maneuver may abolish this arrhythmia.) An abnormal automatic focus in the atrium may also be responsible for this arrhythmia. (A vagal maneu-
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Figure 145-3. Paroxysmal atrial tachycardia (left) and after termination by a vagal maneuver (right) in a cat. (Lead II rhythm strip, paper speed 50 mm/sec; 1 cm = 1 mV.)
Figure 145-4. Paroxysmal atrial tachycardia terminated after a ventricular premature complex in a dog. (Lead II rhythm strip, paper speed 50 mm/sec; 1 cm = 1 mV.)
• • • • • •
ver will cause AV block but not abolish the atrial tachycardia.) The heart rate is >140 to 180bpm in dogs and >240bpm in cats, in which it often approaches 300bpm. The rhythm is usually regular but may be slightly irregular. There is a P¢ wave for each QRS complex, although the P¢ wave is usually of different morphology than the sinus P wave. The P-R interval is constant. The P¢ wave may not be evident because it may be fused with the preceding T wave or occur simultaneously with the preceding QRS complex. The QRS complex may also be of different morphology because of aberrant ventricular conduction. An irregular R-R interval may be caused by concurrent AV block or by multifocal atrial tachycardia (P’ waves varying in shape, the firing of two or more ectopic atrial foci).
Etiology and Clinical Significance
• Atrial tachycardia suggests severe myocardial or con-
Differential Diagnosis
• Atrial tachycardia can be confused with sinus tachycardia, AV junctional tachycardia, and atrial flutter.
• A vagal maneuver may be helpful diagnostically. Abrupt termination suggests AV nodal reentry, whereas transient AV block may develop with atrial tachycardia or atrial flutter, allowing abnormal P¢ waves or atrial flutter waves to be identified at the baseline.
Treatment
• Sustained (non-paroxysmal) atrial tachycardia often •
•
duction system disease.
• This arrhythmia also may be secondary to digitalis toxicity or may occur under general anesthesia.
• Systemic disease that results in autonomic nervous systemic abnormalities also may be a cause.
• In cats, this arrhythmia is correlated with cardiomyopathy and hyperthyroidism.
•
is associated with weakness, hypotension, CHF, and syncope and requires immediate therapy. A vagal maneuver (ocular pressure or carotid sinus pressure) (see Chapter 144) may terminate an atrial tachycardia but generally only causes transient block of ectopic P’ waves. If CHF is present, administer digitalis for the arrhythmia. IV digoxin, given cautiously, may slow the ventricular response and improve the clinical status (see Table 145-3). If digoxin is ineffective, IV diltiazem, verapamil, esmolol, or propranolol may convert supraventricular tachycardia (or atrial tachycardia) to sinus rhythm or slow the ventricular response rate. Use propranolol and verapamil with great caution because they
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Figure 145-5.
• •
•
•
•
Atrial fibrillation in a dog. (Lead II rhythm strip, paper speed 50 mm/sec; 1 cm = 1 mV.)
may depress cardiac contractility and exacerbate CHF. For atrial tachycardia without CHF, initiate therapy with diltiazem, verapamil, or a beta-blocker (e.g., esmolol, atenolol, propranolol, or sotalol). Intramuscular procainamide or quinidine gluconate also have been used to convert atrial tachycardia to normal sinus rhythm in dogs with refractory atrial tachycardia. Atrial (supraventricular) tachycardia associated with accessory pathways (most commonly reported in Labrador retrievers) may respond acutely to IV therapy with diltiazem, verapamil, or procainamide. For long-term management, oral procainamide with or without a beta blocker is recommended. Digoxin is generally not recommended as it may preferentially direct current to the accessory pathway, which can be dangerous should atrial fibrillation develop. A class III antiarrhythmic such as sotalol or amiodarone can be tried in refractory cases. Radiofrequency catheter ablation following electrophysiologic mapping of reentrant or accessory pathway circuits is available at select referral centers for refractory symptomatic atrial tachyarrhythmias as a potential arrhythmia cure without permanent implantation devices. Reserve electrical cardioversion for refractory cases, to be administered only by an experienced veterinary cardiologist possessing the proper equipment.
Atrial Fibrillation (Fig. 145-5) Definition
• A high number of disorganized atrial impulses,
•
•
caused by a disorder of reentry within the atria, bombard the AV node, leading to an irregular rhythm. Many of these impulses approach the AV node in a refractory period and are not conducted to the ventricles, or they affect the conduction of subsequent impulses (concealed conduction). The heart rate is usually rapid (often >180 bpm in dogs and >240 bpm in cats), and the rhythm is irregular.
▼ Key Point The lack of P waves, an irregularly irregular rhythm on all ECGs leads, and an arterial pulse deficit are the hallmarks of atrial fibrillation.
• No P waves are seen, but there are normally shaped •
QRS complexes. Instead of P waves, small or large oscillations (f waves) are present. There may be some variation and widening of the QRS complexes due to aberrant ventricular conduction or bundle branch block. Subtle beat-to-beat variation may be observed in cats with atrial fibrillation.
Etiology and Clinical Significance
• Atrial fibrillation commonly occurs in patients with
•
• •
•
cardiomyopathy, advanced chronic valvular heart disease, pericarditis, and progressive congenital heart disease. Other rare etiologies include severe ischemia or shock (gastric dilatation-volvulus after cardiac arrest), atrial tumor (hemangiosarcoma), and electrolyte disturbances (hyperkalemia). Loss of atrial contraction decreases the stroke volume and cardiac output. The rapid ventricular rate also results in poor cardiac output. “Slow” atrial fibrillation (ventricular response rate 60 bpm but 100 bpm in the dog). The rhythm usually is regular. The negative P¢ wave may occur before, during, or after the normal QRS complex. The P¢-R or R-P¢ interval is constant. The P¢ wave location depends on the area of impulse generation and the relative speed of retrograde conduction through the atrium compared with antegrade conduction through the AV node, His bundle, and ventricular conduction system.
Treatment
• Since most dogs and virtually all cats with this arrhyth-
•
•
•
mia have heart failure, digoxin is the initial treatment of choice to slow the ventricular response (see Table 145-3). Rarely, a sinus rhythm will return. After approximately 3 to 7 days, if the ventricular rate is not controlled, add a calcium channel antagonist such as diltiazem (begin with 0.5 mg/kg q8h) and increase the dose slowly until the resting ventricular rate is adequately controlled. The optimal ventricular response rate for dogs or cats with CHF and atrial fibrillation has not been determined, but most clinicians aim for rates of 20–30 bpm) • Repetitive complexes or runs of VPCs at very rapid rates (e.g., >180 bpm), especially if causing signs or hypotension • Multifocal QRS configurations (not a definite indication) • R on T phenomena (vulnerable period for development of ventricular fibrillation), in which the VPC occurs during the Q-T interval of the previous complex • Associated clinical signs of poor cardiac output (e.g., weakness, dyspnea, and syncope) are probably the clearest indication for therapy. Do not treat ventricular escape complexes (while the QRS complex is similar to a VPC in configuration, these are not premature but occur at the end of
pauses). Escapes represent a safety mechanism for maintaining cardiac output. Antiarrhythmic drugs commonly used to control VPCs in the hospital setting include IV lidocaine and parenteral procainamide (rarely quinidine) (see Table 145-3). Electrolyte imbalances and pain should be managed as these issues may contribute to VPCs in hospitalized patients. For chronic therapy of VPCs, the choice depends a great deal on the concern about repetitive rhythms and risk, as well as the appreciation of drug cost and toxicity. Beta-blockers such as atenolol, sotalol, and propranolol are often chosen for isolated VPCs, and in cats are the beta-blockers are the principle drugs used. Mexiletine, procainamide, and (rarely) tocainide are other options, but they have more side effects and are probably better reserved for more malignant arrhythmias (see Table 145-3 for dosages and Chapter 146 for a discussion of the clinical pharmacology of these drugs).
Ventricular Tachycardia (Figs. 145-8–145-10)
• VPCs can be confused with APCs with aberrant ventricular conduction and right or left bundle branch block.
1465
•
VPCs in a row) are discharged from one or more ventricular foci and capture the ventricles. This arrhythmia may be paroxysmal (non-sustained) or sustained. The rate usually is >100 bpm in dogs and >150 bpm in cats. Once established, the rhythm tends to be regular unless the arrhythmia is intermittent or variable exit block develops (between Purkinje cells and ventricular myocardium). The P waves that are seen are normal in shape but have no fixed relationship to wide and bizarre QRS complexes. This independence is described as AV dissociation. Rarely, retrograde P waves are observed in the S-T segment because of ventricular to atrial conduction. A sustained ventricular rhythm faster than an escape (idioventricular) rhythm but slower than the above mentioned rates is termed an idioventricular tachycardia.
Etiology and Clinical Significance ▼ Key Point Ventricular tachycardia can be welltolerated or represent a life-threatening arrhythmia that, if sustained, may lead to hypotension, myocardial ischemia, syncope or seizures, shock, and sudden death. Each case must be individually evaluated.
• Some patients with ventricular tachycardia show no clinical signs, especially if there is no underlying
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Figure 145-9. 1 cm = 1 mV.)
Paroxysmal ventricular tachycardia showing fusion beat (F) in a dog. (Lead II rhythm strip, paper speed 50 mm/sec;
Figure 145-10.
•
Ventricular tachycardia-flutter in a dog. (Lead II rhythm strip, paper speed 50 mm/sec; 1 cm = 1 mV.)
primary cardiac disease and the rate is not too rapid. All etiologies of VPCs (e.g., primary and secondary cardiac disease; see Table 145-2) may lead to a ventricular tachycardia; however, not all are dangerous to the patient.
• Acid-base or electrolyte disturbances, such as hypomagnesemia, hypokalemia, or hyperkalemia, that may respond to specific electrolyte or fluid therapy. • Hypomagnesemia can cause or potentiate ventricular tachycardia. Magnesium chloride (1–2 mg/ kg/min for 20–30 minutes) can also exert a primary antiarrhythmic effect.
Differential Diagnosis
• Ventricular tachycardia can be confused with
▼ Key Point Cats with ventricular tachycardia associ-
supraventricular rhythms—sinus tachycardia, atrial tachycardia, or atrial fibrillation—when ventricular conduction is abnormal (as with left or right bundle branch block).
ated with hypokalemia may respond to simple KCl therapy (IV in fluids, oral) (see Chapter 5).
Treatment
• Antiarrhythmic therapy is required for some patients with sustained ventricular rhythms. Exceptions include patients with the following: • Complete heart block in which the ventricular rhythm may be an escape mechanism • “Slow” ventricular rhythms (also called idioventricular tachycardias) in which the ectopic rate is 90 mm Hg. In atrial fibrillation, heart rate control can be gained by up-titration of the oral dosage. For initial oral therapy, 0.5 mg/kg q8h is appropriate. Provided CHF is under control, the dose of diltiazem can be rapidly increased (increasing each successive dose by about 0.25 mg/kg) to a target of about 1.5 mg/kg PO, q8h. Some patients require even higher doses (up to 2 mg/kg q8h, or greater), but care must be taken to prevent hypotension or excessive myocardial depression, particularly in the setting of CHF. The optimal target examination heart rate response in atrial fibrillation is between 100 and 150/min during clinical examination (or ECG). An alternative to three times daily dosing with standard diltiazem is twice daily treatment with a longacting diltiazem preparation such as Cardizem-CD or Dilacor. These sustained release drugs may be compounded. Dilacor comes in tablet form (within a capsule that is readily opened), and can be cut in half. The same total daily dose of diltiazem should be given but now in two divided doses. The effects of breaking tablets on long-acting drug effects is uncertain. In cats under therapy for HCM, the usual dose of standard diltiazem is 7.5 mg (1/4 of a 30-mg tablet), PO q8h. This dosing interval is generally impractical for cat owners, and an alternative approach is to administer Dilacor, 1/2 of a 60-mg tablet, once daily. Some clinicians use this drug on a bid. basis in cats, but there is a higher incidence of adverse effects. Cardizem-CD can be compounded into a palatable syrup, starting at 30-mg per cat once daily. However, preliminary pharmacokinetic studies reported a lower bioavailability and suggest the tolerated dosage might be as high as 10 mg/kg once daily. Unfortunately, detailed clinical studies with sustained release preparations are unavailable. Overall, diltiazem should reduce myocardial oxygen demand in HCM by decreasing contractility, blood pressure, and heart rate. (Though heart rate is less effectively controlled when compared to atenolol.) Effects on reducing dynamic outflow tract gradients have been disappointing at the doses commonly used. (Atenolol appears better for this purpose in HCM with obstruction.) Thus, the main reason to choose diltiazem therapy in cats with HCM is for potential improvement of diastolic function and for prevention or treatment of CHF in HCM. In a recent multicenter study of cats with recent onset CHF, the addition of diltiazem to background furosemide therapy did not provide any clear shortterm benefits; however, some clinicians will establish diltiazem therapy at the time of follow-up, after initial stabilization of CHF with furosemide and an ACEI.
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• As for beta-blockers, the long-term benefit of diltiazem in feline HCM has not been demonstrated.
Combined therapy of Calcium-Channel Blockers and Beta-Blockers On occasion, the combination of a beta-blocker and a CCB will be considered. Since many of the pharmacologic effects on the heart are similar, the clinician must be mindful of adverse effects (see below).
• Diltiazem and carvedilol may be used in combination
•
•
in dogs with CHF and atrial fibrillation. Initially digoxin and diltiazem are used to control heart rate; subsequently, carvedilol is up-titrated as described above. This may permit a dose reduction in diltiazem. Diltiazem and atenolol is sometimes considered for cats with HCM and severe dynamic LV outflow tract obstruction. This combination of drugs must be used with great care because of additive depressive effects on heart rate, AV conduction, contractility, and blood pressure. In patients with unresponsive hypertension, the addition of a beta-blocker (atenolol, carvedilol) to amlodipine or ACEI-amlodipine is generally well tolerated.
on their electrophysiologic characteristics (the Vaughan– Williams classification); however, this ordering is not ideal, and other schemes have been proposed. The Vaughan-Williams classification places antiarrhythmic drugs in one of four classes (or subclasses). As with any classification, it is limited and does not consider other potentially useful drugs with anti-arrhythmic effects. For example, the anti-cholinergic effects of atropine; the parasympathetic effects of digoxin; the delayed AV nodal conduction caused by (potassiumchannel opening with) adenosine; and the membrane stabilizing effects of the magnesium salts are not included.
• Class I anti-arrhythmic drugs reduce the rate of Na+
Adverse Effects of Calcium Channel Blockers The adverse effects of CCB are extensions of their pharmacologic activities. Treatment involves withdrawing the drug or lowering the dose. Bradycardia and cardiac depression can generally be overcome by administration of atropine or infusion of dopamine. Hypotension from excessive vasodilation responds to infusion of an alpha-adrenergic or mixed alpha/beta agonist (phenylephrine, ephedrine, adrenaline). Calcium infusions may be beneficial but are proarrhythmic. Common adverse effects of CCB include
•
• Depression and weakness, usually from hypotension • Hypotension from vasodilation or depression of
•
•
cardiac output
• Worsening or precipitation of CHF from cardiac depression (reduced contractility and heart rate)
• Bradycardia from sinus or AV nodal depression (sinus bradycardia; AV block)
• Anorexia, salivation, and weight loss (cats) • Skin reactions, including erythema and localized edema
• Constipation is often reported in human patients and may occur in some animals
ANTI-ARRHYTHMIC DRUGS Overview The anti-arrhythmic drugs are used to treat disorders of heart rhythm. These drugs can be classified based
•
influx by blocking the rapid sodium channel. These drugs generally decrease the rate of depolarization, slow conduction, and increase overall refractory period of cells; these are subdivided as follows: • IA (e.g., quinidine, procainamide, disopyramide) lengthen the action potential duration and the refractory period. • IB (e.g., lidocaine and mexiletine) shorten the action potential duration but increase the refractory period;. • IC (e.g., flecainide, propafenone) produces little effect on action potential duration but slows conduction. The Class II anti-arrhythmic drugs block beta adrenoceptors and decrease sinus node rate, slow AV nodal conduction, and reduce arrhythmias related to high sympathetic tone. Central effects may also be evident with some lipophilic drugs. The Class III anti-arrhythmic drugs prolong action potential duration by blocking potassium channels and also increase cell refractoriness. These include the drugs amiodarone and sotalol. These drugs generally do not change automaticity or conduction velocity. The Class IV drugs block the movement of calcium ions across the slow calcium dependent channel and include verapamil and diltiazem. Effects are a decreased heart rate, slowing of AV nodal conduction, and other less well-defined anti-arrhythmic effects. Effective use of any anti-arrhythmic drug depends on clinical response and experience. There is very little published information regarding anti-arrhythmic therapy of cats.
▼ Key Point Every drug used to treat arrhythmias is considered an extra-label drug use in veterinary practice, and treatment recommendations are based mainly on clinical experience with various arrhythmias.
Hypokalemia and hypomagnesemia decrease or nullify the beneficial effects of many anti-arrhythmic
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drugs, especially class I agents. Electrolyte disorders can also predispose to pro-arrhythmic effects with Class IC and III agents. The indications and drugs of choice for various arrhythmias are quite varied and are summarized in Chapter 145. Lidocaine, mexiletine, procainamide, sotalol, amiodarone, diltiazem, and the beta-blockers have been used most often in clinical practice with varying degrees of effectiveness and toxicity. Typical dosages of these drugs are summarized in Table 146-1 and “essential use” is summarized below. Anti-arrhythmic drugs not only affect electrical activity of cardiac tissues but can also negatively reduce myocardial contractility. Additional effects may develop indirectly related to activation of the autonomic nervous system. Aside from the beta-blockers, most anti-arrhythmic drugs demonstrate a pro-arrhythmic effect in a small percentage of patients. This and other potential adverse effects make the use of anti-arrhythmic therapy a true risk-benefit proposition.
• Commonly used: sotalol, mexiletine, beta-blockers
▼ Key Point Anti-arrhythmic drugs must be used cau-
•
tiously in the setting of CHF. Most anti-arrhythmic drugs are negative inotropes and are likely to worsen CHF.
for chronic therapy in dogs
• Less often used: procainamide, amiodarone, propafenone in dogs
• Commonly used: beta-blockers for chronic therapy in cats
• Less often used: sotalol or procainamide in cats Arrhythmias in setting of CHF
• For atrial fibrillation, begin with digoxin and then •
•
•
Common Indications for Anti-arrhythmic Drugs As discussed under the individual anti-arrhythmic drugs, more than one agent may be indicated for the treatment of a specific arrhythmia. Selection of one drug over another often is based on clinical experience, published trial, or simply personal preference. Some drugs are more likely to depress heart function and ABP, while others have a better adverse-risk profile. These various effects are often considerations in anti-arrhythmic drug choice. Some guidelines are indicated below:
The clinical pharmacology and clinical use of specific anti-arrhythmic drugs, based on the Vaughan Williams Classification (I–IV), are summarized below.
Procainamide • Procainamide (Class IA) is a “broad–spectrum” anti-
Sinus bradycardia
• Atropine, glycopyrrolate, or catecholamines in the hospital; oral anti-cholinergic or sympathomimetic drugs can be tried for chronic oral management (cardiac pacing is better)
•
Supraventricular tachycardias
• Commonly used: digoxin (with CHF), diltiazem, beta-blockers
•
• Less often used: sotalol, amiodarone, procainamide AV block
• Atropine or catecholamines can be tried for hospital
•
management (cardiac pacing is preferred)
Ventricular arrhythmias
• Commonly used: lidocaine, procainamide, esmolol, magnesium salts for hospital therapy
add diltiazem; with control of CHF, a beta-blocker can be considered. Boxers, Doberman pinschers, and other breeds often develop CHF complicated by complex ventricular ectopy. Mexiletine or procainamide (+/– betablocker such as carvedilol) is most often used to control ventricular tachycardia in the CHF patient. Sotalol is an effective anti-arrhythmic, but demonstrates prominent beta-blocking properties, and should not be prescribed in the setting of uncontrolled CHF. Amiodarone is also a negative inotropic drug, but is probably preferable to sotalol in the setting of CHF and also may be better tolerated than mexiletine in some dogs. Mexiletine often leads to GI or neurological side effects in dogs with CHF.
•
arrhythmic agent with potential value for the treatment of acute atrial fibrillation; suppression of atrial, junctional, and ventricular premature complexes; control of atrial and ventricular tachycardias; and potential suppression of AV nodal bypass tracts. The drug is available for injection, oral administration (capsules), and sustained release products. The short elimination half-life of 2 to 4 hours in the dog necessitates frequent administration. Limited sustained-release oral preparations of these drugs are available, allowing q6–8h oral dosing. Dosing guidelines are indicated in Table 146-1. Procainamide is sometimes administered to control PVC’s and to maintain sinus rhythm following conversion of sustained or paroxysmal ventricular tachycardia in the dog and infrequently in the cats. Procainamide can be given to dogs already receiving or unresponsive to a lidocaine infusion. The drug is particularly versatile as it can be given IV, IM, or SQ, and then orally to maintain sinus rhythm. The long-term use of procainamide is considered in some dogs needing chronic treatment for ventricular tachycardia, though less often than for sotalol or
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mexiletine. A sustained release preparation must be prescribed to maintain blood levels, and it is suggested that the drug be co-administered with a betaadrenergic blocker unless there is CHF.
Adverse effects
• Procainamide is hypotensive when given too rapidly
•
•
•
•
by intravenous bolus. This is explained by depressive effects on myocardial contractility and by peripheral vasodilation. As with other class IA drugs (and class III drugs), the prolongation of the action potential can serve as a proarrhythmic stimulus, worsening the ventricular rhythm. Atrioventricular block can occur (from the direct depressive effect on the infranodal bundle of His and bundle branches). Do not use procainamide in the setting or pre-existent AV block. Prolongation of the QRS and QT intervals can occur with eventual development of a polymorphic ventricular tachycardia or ventricular fibrillation (pro-arrhythmia). If the QRS complex prolongs to >25% of baseline, stop the drug and reduce the dosage. Procainamide can lead to lupus erythematosus in dogs and has been associated with immune mediated reactions and changes in hair color.
• •
• •
smaller boluses with constant intravenous infusion is the usual method for controlling acute ventricular tachycardia in the dog. Lidocaine is relatively easy to control, and compared to other anti-arrhythmics, has minimal adverse hemodynamic effects, making it the drug of choice for hospital management of ventricular tachycardia. The cat is quite sensitive to the neuroexcitatory side effects of lidocaine, which must be given to this species slowly and at lower dosages. It is common for arrhythmias to become less responsive to lidocaine. This is particularly true when there is inattention to potassium (and magnesium) supplementation in hospitalized patients. When lidocaine does fail, it can be combined with procainamide if another injectable medication is required and may still provide anti-fibrillatory and analgesic effects to the patient. When long-term therapy is needed, lidocaine may be followed by treatment with sotalol or mexiletine and a beta-blocker. Mexiletine is used to suppress ventricular arrhythmias; unlike lidocaine, it can be given orally. The drug is often combined with a beta-blocker for chronic management of severe ventricular arrhythmias in the dog. Mexiletine can be effective but carries a higher sideeffect profile than sotalol, an alternative treatment for chronic ventricular tachycardia.
Lidocaine and Mexiletine
Adverse effects
Lidocaine, mexiletine, and the rarely used tocainide (Class IB) have similar electrophysiologic properties. (Chronic tocainide use causes numerous side effects in dogs including renal failure and ocular injury; this drug should not be prescribed). Lidocaine (IV) and mexiletine (oral) are the drugs in Class IB most often administered for control of ventricular tachycardia in dogs. These drugs decrease automaticity of cardiac tissues by a class I effect (see above). Refractoriness is minimally prolonged. Lidocaine also reduces disparities in action potential duration preferentially in ischemic tissue, making it suitable for preventing re-entrant ventricular arrhythmias in the setting of myocardial ischemia. Lidocaine may also be used for acute cardioversion of atrial fibrillation into normal sinus rhythm in vagally induced atrial fibrillation.
• CNS excitation including anxiety and twitching,
• Lidocaine has a very rapid onset of action after IV
Indications, contraindications, and clinical pharmacology of the beta-blockers (Class II) have been described previously. Sotalol is a beta-blocker with powerful Class III effects and is described below. The beta-blockers are “broad spectrum” anti-arrhythmic drugs, and key points regarding arrhythmia control of these drugs are summarized below:
• •
administration and a terminal halflife in dogs of 0.9 hours. It is then quickly metabolized by the liver (1–3 hours). Intravenous boluses must be repeated (every 10–20 minutes) or supplemented with a constant rate IV infusion (see Table 146-1). Dosing guidelines are indicated in Table146-1. Effectiveness of therapy depends on the extracellular K+, which must be maintained in the normal range. Initial administration of lidocaine as a bolus (or loading infusion) followed by simultaneous use of
often followed by depression
• Focal or generalized convulsions (control with diazepam)
• Depression of sinus or AV nodal function, particularly in the cat
• Hypotension is uncommon but can occur with toorapid injection.
• Drug interactions • Both propranolol and cimetidine reduce liver blood flow and delay excretion of lidocaine and mexiletine.
• CHF, hypotension, and halothane anesthesia may reduce lidocaine clearance and require lower dosages to prevent toxicity.
Beta-Adrenergic Blockers
• Treatment of severe sinus tachycardia in drug toxicities or hyperthyroidism.
• Suppression of atrial premature complexes and some atrial tachycardias.
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• Depression of AV nodal conduction, decreasing the
• Both sotalol and amiodarone depress myocardial
ventricular rate response to atrial flutter/fibrillation. Used as monotherapy to control isolated ventricular PVCs or combination with a Class I anti-arrhythmic drug for management of ventricular tachycardia or complex ventricular rhythms. Ultra-short acting IV beta blockade (esmolol) or graded IV doses (propranolol) can be used to control ventricular arrhythmias in the critical care setting (following trials of lidocaine and procainamide). Oral administration of a beta-blocker (atenolol, metoprolol, or propranolol) may be useful for longterm therapy of PVCs. Adverse effects have been discussed previously. Of highest importance is the negative inotropic effect of beta-blockers in the setting of uncontrolled CHF or hypotension.
contractility so use these drugs in CHF with caution. Sotalol in particular should be avoided in the setting of CHF or pronounced myocardial dysfunction. Amiodarone appears better tolerated in dogs with CHF. Lengthening of the QT interval from prolongation of the action potential duration offers both anti-arrhythmic benefit and proarrhythmic risk with all Class III drugs. A highly malignant form of polymorphic ventricular tachycardia (of the torsade de pointes variety) may develop.
•
•
• •
Sotalol and Amiodarone Sotalol and amiodarone (Class III) prolong the action potential duration by blocking potassium channels and also exert beta-blockers effects (sotalol > amiodarone).
• The principal indications for these agents are life•
•
•
•
threatening or refractory ventricular arrhythmias. Class III drugs, particularly amiodarone, also have been used to prevent recurrence of atrial fibrillation in dogs following successful electrical cardioversion. Conversion of atrial fibrillation to sinus rhythm is possible, but relatively uncommon with either drug. Sotalol is the drug of choice for many clinicians for the long-term treatment of malignant ventricular arrhythmias. It is eliminated by the kidneys. In dogs peak plasma concentrations are attained within 2 hours. Oral dosages of 1 to 2 mg/kg q12h are well tolerated in dogs with normal ventricular function. Sotalol has been used occasionally in cats. Malignant ventricular arrhythmias can be exacerbated by hypokalemia in sotalol-treated patients. Amiodarone is a complicated drug (exhibiting varying degrees of class I, II, III, and IV activities) and considered an effective anti-arrhythmic drug with a prolonged duration of action (days) and an extremely long elimination half-life and hepatic metabolism. Bretylium and ibutilide are other drugs with class III properties. Bretylium tosylate is used in humans for prevention of ventricular fibrillation. Ibutilide has been used in people to rapidly convert atrial fibrillation to normal sinus rhythm; use in animals has been limited mainly to experimental models.
Adverse effects
• Amiodarone has an arm’s length of side effects associated with chronic use, including impaired thyroid dysfunction, hepatotoxicity, neutropenia, corneal microdeposits, and potentially fibrosis of the lung. Lower dosages may be safer.
•
Calcium Channel Blockers (Diltiazem) The calcium channel blockers (Class IV) have been discussed previously. Diltiazem and the prototype drug verapamil block the L-type calcium channel and alter membrane responsiveness of SA and AV nodal cells, as these are highly dependent on slow (calcium) current for depolarization. The following comments pertain mainly to anti-arrhythmic effects of these drugs.
• Diltiazem is the CCB most often used in dogs and in
•
cats with supraventricular tachyarrhythmias. Diltiazem has profoundly depressant effects on AV nodal conduction and therefore slows the ventricular response rate to ectopic atrial tachycardia, atrial flutter, and atrial fibrillation. This effect is typically greater than for beta-blockers at equivalent negative inotropic doses. Infrequently CCB therapy leads to conversion to sinus rhythm. Calcium channel blockers are also useful for supraventricular tachycardias that use the AV node as part of the re-entrant tachycardia circuit. By blocking the orthodromic (downward) path of current, the electrical circuit is abolished and sinus rhythm may resume.
Adverse Effects Adverse effects have been described previously.
• Reflex sinus tachycardia, secondary to vasodilation
•
may develop; however, diltiazem directly depresses sinoatrial nodal function so the effect may be blunted. Accordingly, a CCB should be used cautiously in sick sinus syndrome or in dogs with sinus node dysfunction. In the setting of pre-existent AV block, diltiazem (or verapamil) is contraindicated.
SUPPLEMENTAL READING Brown SA, Brown CA, Jacobs G, Stiles J, Hendi RS, Wilson S: Effects of the angiotensin converting enzyme inhibitor benazepril in cats with induced renal insufficiency Am J Vet Res 62:375–383, 2001.
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Bulmer BJ, Sisson DS: Therapy of heart failure. In Ettinger and Nelson (eds): Textbook of Veterinary Internal Medicine, 6th ed. Philadelphia, WB Saunders, 2005, pp 948–972. COVE Study Group: Controlled clinical evaluation of enalapril in dogs with heart failure: Results of the Cooperative Veterinary Enalapril Study Group. J Vet Intern Med 9:243–252, 1995. Ettinger SJ, Benitz AM, Ericsson GF, Cifelli S, et al: Effects of enalapril maleate on survival of dogs with naturally acquired heart failure. The Long-Term Investigation of Veterinary Enalapril (LIVE) Study Group. J Am Vet Med Assoc 213:15731577, 1998. Fuentes VL, Corcoran B, French A, Schober KE, Kleemann R, Justus C: A double-blind, randomized, placebo-controlled study of pimobendan in dogs with dilated cardiomyopathy. J Vet Intern Med 16:255–261, 2002. IMPROVE Study Group: Acute and short-term hemodynamic, echocardiographic, and clinical effects of enalapril maleate in dogs with naturally acquired heart failure: Results of the Invasive Multicenter PROspective Veterinary Evaluation of Enalapril study. J Vet Intern Med 9:234–242, 1995.
Kvart C, Haggstrom J, Pedersen HD, Hansson K, et al: Efficacy of enalapril for prevention of congestive heart failure in dogs with myxomatous valve disease and asymptomatic mitral regurgitation. J Vet Intern Med 16:80–88, 2002. Opie LH, Gersh BJ: Drugs for the heart, 6th ed. Philadelphia, WB Saunders, 2005. Pouchelon JL for the BENCH investigators: The effects of benazepril on survival times and clinical signs of dogs with congestive heart failure: Results of a multicenter, prospective, randomized, doubleblinded, placebo-controlled, long term clinical trial. J Vet Cardiol 1:7–18, 1999. Smith PJ, French AT, Van Israel N, Smith SGW, Swift ST, et al: Efficacy and safety of pimobendan in canine heart failure caused by myxomatous mitral valve disease. J Small Anim Pract 46:121–130, 2005. Quinones M, Dyer DC, Ware WA, Mehvar R: Pharmacokinetics of atenolol in clinically normal cats. Am J Vet Res 57:1050–1053, 1996.
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147
Heart Failure in Dogs John D. Bonagura / Bruce Keene
Heart failure (HF) is a state wherein the cardiac output is inadequate to meet the perfusion needs of the metabolizing tissues and exercise capacity is limited. The causes of HF in dogs are diverse, but there are stereotypical cardiovascular and systemic responses to impaired cardiac function, regardless of cause. This chapter provides a brief overview of HF; considers the causes and diagnoses of HF in dogs; and reviews treatment plans for management of the cardiac failure patient. The clinical pharmacology and pathophysiologic rationale for drugs used in treatment of HF are detailed in Chapter 146. Management of HF in cats is discussed in the chapter “Cardiomyopathy” (Chapter 150).
OVERVIEW
• Vasoconstriction is a prominent feature of HF and is
•
•
Heart failure is a not a specific disease but a pathophysiologic disorder. Some of the key abnormalities of this condition are summarized below, and the pathophysiologic rationale for using particular cardiovascular drugs is summarized in Chapter 146. The reader is directed to other textbooks for a detailed review of pathophysiology of HF.
• HF is triggered by a cardiac lesion (or injury) that
• •
•
leads to systolic or diastolic dysfunction of the heart. Decreased cardiac output and blood pressure (often called “arterial underfilling”) are pivotal events that initiate the syndrome of HF. The decrease in blood pressure is countered by adaptations of the neuroendocrine system, kidney, heart muscle, and blood vessels. There is increased activity of vasoconstrictor and sodium-retaining control systems; attenuation of vasodilator and natriuretic systems; activation of fetalgene programs within the heart; and increased activity of tissue mediators that lead to myocardial and vascular hypertrophy, fibrosis, and inflammation. The well-compensated cardiac patient often maintains basal (resting) cardiac output and blood pressure within the normal range. This is achieved through vasoconstriction, mild volume expansion, and redistribution of blood flow.
•
•
• •
mediated by sympathetic nervous system activation, the renin-angiotensin system, release of arginine vasopressin, and local endothelial mediators such as endothelin. These systems represent therapeutic targets for both current and for future drug developments. The excess sodium and water retention characteristic of the syndrome of congestive heart failure (CHF) is mediated by sympathetic stimulation that alters renal blood flow, the release of aldosterone and vasopressin, and inhibition of natriuretic hormones that are released from the stretched heart. The need for diuretics and dietary sodium restriction in CHF stems from activation of these compensatory responses. The heart itself changes in structure and function in a process called cardiac remodeling. As heart disease progresses there is increasing dependence on myocardial hypertrophy, cardiac dilatation, and heart rate to maintain cardiac output. At the same time, structural alterations in the intercellular matrix of collagen and connective tissue impair the filling and pumping functions of the myocardium. Key mediators of cardiac injury include norepinephrine, angiotensin II, aldosterone, and pro-inflammatory cytokines. The increased use of “cardioprotective” drugs in HF are aimed at blunting these mediators and the tissue damage caused by them. Despite the effectiveness of these combined compensations for maintaining arterial blood pressure, these systems become increasingly maladaptive. This concept is central to the progression and the treatment of HF. Compensatory mechanisms activated in advanced heart disease are so effective that clinical signs of cardiac failure may be evident only with exercise when pulmonary venous pressure increases and perfusion of skeletal muscles becomes limited. With worsening cardiac function hemodynamic abnormalities become prominent. Decreases in cardiac output, systemic arterial blood pressure (ABP), and tissue perfusion develop, accompanied by increases in systemic and pulmonary vascular resistances. 1495
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Table 147-1. OVERVIEW OF MORPHOLOGIC/ANATOMIC DIAGNOSES Developmental disorder or malformation Vascular change: congestion, edema, hemorrhage, thrombosis, infarction Inflammation Degeneration Necrosis Apoptosis (programmed cell death) Hypertrophy Neoplasia Disruptive defects such as trauma These lesions may be encountered in the pericardium, myocardium, endocardium-valves, conduction system, or blood vessels of the heart or circulation.
Table 147-2. OVERVIEW OF ETIOLOGIC DIAGNOSES D = developmental disorders; degenerative lesions A = anomalies, autonomic dysfunction, anemia M = metabolic diseases (endocrine diseases, electrolyte disturbances, renal failure), mechanical problems (such as a foreign body) N = neoplasia or nutritional disorder I = infectious, inflammatory, ischemic, immune, iatrogenic and idiopathic diseases T = tumor, trauma or toxin
• The etiologic diagnosis indicates the putative cause of • Inadequate tissue perfusion contributes to exercise • •
•
intolerance, azotemia, and metabolic disturbances such metabolic acidosis. Elevations in pulmonary arterial, venous, and capillary hydrostatic pressures lead to clinical signs of CHF. While hemodynamics may explain many clinical signs, morbidity and mortality of HF are related strongly to the tissue effects of accentuated neurohormonal and cytokine activities that develop in response to the failing heart. Chronic therapy of CHF is aimed at modulating and countering these responses to minimize clinical signs of CHF, protect tissues, and prolong life.
ETIOLOGY Next in this chapter we will consider the key causes of heart disease in dogs, as well as an overview of cardiac disease classification and applicable diagnostic studies. The following are salient points regarding cardiac diagnosis and the clinical workup.
Classification
•
Causes The most important causes of canine heart disease involve a limited number of acquired disorders and a handful of important congenital heart defects. These conditions, as well as usual diagnostic findings, are summarized in Table 147-4 and in other chapters across this section. The most important acquired cardiac disorders responsible for HF in dogs are:
• Mitral and tricuspid valvular endocardiosis, which is
Identifying the predominant form and cause of heart disease and classifying the pathophysiologic mechanism of cardiac failure allows the clinician to direct appropriate therapy and render a more accurate prognosis. Cardiac diagnoses can be classified in a number of ways.
• The morphologic or anatomic diagnosis refers to the lesions one might observe during gross or microscopic examination of the heart or blood vessels (Table 1471). It is also helpful to classify CV diseases relative to the anatomic components of the system affected; this is often included into the anatomic diagnosis as follows: pericardial diseases; myocardial diseases; valvular and endocardial diseases; disorders of the impulse forming and conduction system (arrhythmias); and vascular diseases.
cardiovascular disease and includes genetic disorders and errors of metabolism (Table 147-2). A sub-classification of the etiologic diagnosis includes general designations of “congenital” heart disease and “acquired” heart disease. The physiologic diagnosis represents the disruption in cardiovascular function that results from cardiovascular disease, including the clinical signs observed in the patient. This diagnosis can be general or relatively specific. For example, contractility failure, hemodynamic overloads, diastolic failure, and arrhythmia are considered general pathophysiologic mechanisms for reduced cardiac output and heart failure. Examples of more specific cardiovascular diagnoses include syncope, valvular regurgitation, left to right shunt, and cardiac murmur (Table 147-3).
•
•
characterized by progressive and chronic atrioventricular valve degeneration often with valve prolapse and ruptured mitral valve chordae tendineae. Atrial arrhythmias, left mainstem bronchial compression, CHF, left atrial rupture, and systemic hypertension may complicate the picture. Dilated cardiomyopathy, which is a primary myocardial disorder of progressive contractility failure leading to heart failure. Often associated with cardiac arrhythmias such as atrial fibrillation and ventricular tachycardia; the condition is “idiopathic” but certainly genetically predisposed in many dogs. Sudden death is common. Pericardial effusion causing cardiac tamponade (impaired filling of the heart from compression) is under-recognized. The main causes in dogs are idio-
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Table 147-3. OVERVIEW AND DEFINITION OF PHYSIOLOGIC CV DIAGNOSES Arrhythmia (dysrhythmia)—disorder of electrical impulse formation or conduction leading to an abnormal heart rate or rhythm. Bradyarrhythmia—a cardiac arrhythmia characterized by a slow heart rate as with sinus bradycardia, sinus arrest, atrial standstill, or atrioventricular block. Cardiac murmur: functional—a prolonged audible vibration associated with blood flow in the heart or great vessels but unrelated to structural heart disease (also termed physiologic or innocent murmur); functional murmurs are often caused by anemia, fever, thyrotoxicosis, elevated sympathetic tone, or protracted bradycardia. Cardiac murmur: organic—audible vibration associated with abnormal blood flow in the heart or great vessels associated with structure disease; these murmurs typically indicate pathology affecting the heart valves or a congenital shunt. Congestive heart failure—an advanced pathophysiologic state of heart failure characterized by renal sodium retention, elevated venous pressures, and fluid accumulation in the lung, subcutaneous tissues, or body cavities. Contractility failure—a general mechanism of ventricular dysfunction; see myocardial failure. Diastolic heart failure (diastolic dysfunction)—impairment of ventricular diastolic filling or distensibility as with concentric hypertrophy of the ventricle or pericardial disease; the ventricle must be filled by higher than normal filling (venous and atrial) pressures. Heart failure—a pathophysiologic state caused by systolic or diastolic failure of the heart and characterized by neurohormonal activation and inadequate cardiac output relative to exercise and tissue perfusion demands. Hemodynamic overload—a condition characterized by increased demand on the ventricle to pump a greater stroke volume or a higher pressure than normal; typically these are subdivided into volume overloads and pressure overloads (see the following). Hypertension—elevated systemic arterial blood pressure; in dogs systolic values exceeding 160 mm Hg are suspicious and those >180 mm Hg are considered elevated Hypotension—reduced systemic arterial blood pressure; when systolic ABP is 90 mm Hg). This upward adjustment is especially important in
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•
•
• •
sideration should be given to additional “cardioprotection” therapy with a beta-blocker such as carvedilol (Coreg) or metoprolol-long acting. Initial doses of carvedilol (also an alpha blocker and potent antioxidant) is about 0.05 to 0.1 mg/kg, PO, q12h. The dose can be increased every 2 to 4 weeks with a target of 0.2 to 0.4 mg/kg q12h for dogs with CHF due to dilated cardiomyopathy. The benefits of beta-blockade in small-breed dogs with valvular endocardiosis are uncertain and a topic of current study See Cardiovascular Drugs (Chapter 146) for a more complete discussion of beta-blockers, as well as side effects of these drugs. Weakness, bradycardia (HR 1 year following the first signs of
•
•
CHF provided they receive optimal veterinary and home care, including extra-label drugs such as carvedilol and pimobendan combined with “standard” therapy of furosemide-spironolactone, an ACEI, and dietary modifications. The prognosis for DCM is always more guarded, especially in Doberman pinschers. Once CHF has progressed to severe (“functional class IV”) failure, the outlook is generally guarded-to-poor and a 3- to 9month prognosis is typical. There are no critical studies that prospectively examine prognostic criteria across all groups. The multicenter enalapril (North America) and benazepril (European) studies clearly indicate improved survival and
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reduction of clinical signs in canine CHF caused by DCM or chronic valvular disease when an ACEI is added to background therapy of furosemide +/digoxin. Where pimobendan is available to treat canine DCM or advanced valvular heart disease, the long-term outcome also appears more favorable when compared to “conventional” therapy with furosemide and digoxin or even furosemide and an ACEI. (Though it is illogical not to combine pimobendan with furosemide and an ACEI.) Beta-blockers slow the progression of cardiac dilatation and HF in experimental canine myocardial diseases, and a drug like carvedilol should be part of the long-term treatment regimen, especially in DCM, provided it is tolerated.
Causes of Death The causes of death in chronic CHF vary but are most often related to one of the following:
• Sudden electrical event (such as asystole or ventricu• • • •
lar fibrillation) Hypoxemia (pulmonary edema, pleural effusion) Pulmonary embolism leading to fatal hypotension Multi-systemic organ failure Client desire for euthanasia. This is a particularly common ending and pertains to many factors that include effectiveness of therapy, severity of signs, client (and veterinarian) perceptions about quality of life, and issues of care (medication frequency, visits to the veterinary hospital, costs) among other factors.
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148
Syncope John D. Bonagura / Shianne L. Koplitz
OVERVIEW Syncope, or fainting, is a sudden and unexplained loss of consciousness and postural tone usually related to inadequate delivery of oxygen to the brain. This chapter outlines a general approach to the diagnosis of the syncopal patient. Effective therapy of syncope is predicated on identifying and managing the underlying disorder.
Characteristics of Syncope • The event is often precipitated by exercise, sudden
•
• • • •
•
•
activity, or excitement (sympathetic stimulation). However, syncope can occur during rest or even sleep, especially in cats. Along with a loss of consciousness, there is a failure to maintain postural tone, causing falling. If the dog or cat is recumbent at the onset of the event, it is common for the patient to fall backwards or to roll to lateral recumbency. Brief stiffening is common along with forelimb rigidity and opisthotonus. Minor convulsive activity may be observed, such as focal head twitching. This is more common in cats wherein syncope often resembles a true seizure event. Urination during the event is a frequent observation. Defecation may occur but is far less common. Mucous membrane color is initially pale pink to white when the cause is low blood pressure; subsequently, cyanotic, normal, or flushed membranes may be observed. If hypoxemia from respiratory disease or a right-to-left shunt is the cause of fainting, cyanosis may precede the spell. Following recovery of blood pressure and cerebral function, mentation and behavior are typically normal. However, if the syncope is related to a protracted cardiac arrhythmia or ongoing or progressive pathology, as with a stroke, there may be a longer period of listlessness, stupor, or profound weakness. Some patients with syncope also demonstrate pre- or near-syncope. This is characterized by a sudden jerk of the head and body. This apparent “lightheadedness” abates just in time to prevent falling.
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Differential Diagnosis • The differential diagnosis of syncope includes seizure disorder or epilepsy; sleep disorder, including narcolepsy; stroke or transient ischemic attack of the CNS; metabolic disease affecting the CNS; and drug intoxication. • Syncope is readily confused with seizure disorders or epilepsy (see Chapter 127). Facial fits, generalized tonic-clonic movements, and postictal behavioral abnormalities are more typical of true seizures. However, clients can readily confuse the two, and even after obtaining a careful history, an experienced clinician may remain uncertain about the nature of the event. • Sleep disorders such as narcolepsy are rare (see Chapter 127) but may be precipitated in dogs by eating. The event appears similar to actual sleep, and in some cases, dogs may chew their food and literally fall asleep on the food bowl. Cataplexy, a loss of postural tone with maintenance of consciousness, is rare in dogs and cats. • Strokes or transient ischemic attacks can cause true syncope or, more commonly, lead to progressive or episodic neurological dysfunction (see Chapter 126). • Central nervous system disorders, such as primary brain lesions, may lead to altered consciousness and episodic falling, which might be misinterpreted as a syncopal attack (see Chapter 126). Acute vestibular syndromes may lead to falling, but mentation is normal, and the signs are generally obvious during neurological examination (see Chapters 61 and 126). • Metabolic diseases may alter cerebral function and be associated with staggering or falling; these include hypoglycemia, hepatic encephalopathy, and hypoadrenocorticism when it causes profound hypotension. • Overdose of prescribed drugs or ingestion of human drugs or toxins in the household can at times lead to altered cerebral function as well as hypotension, ataxia, or weakness. The resulting fall may be interpreted as syncope. In some cases, drugs cause profound hypotension leading to true fainting.
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Chapter 31); transient ischemic attacks also have been reported in cats.
ETIOLOGY General Mechanisms • Syncope is generally caused by insufficient oxygen
•
•
•
delivery to the brain. • The arterial oxygen content of the blood depends on pulmonary function (arterial pO2) and the hemoglobin concentration (PCV, hematocrit). • Delivery of oxygen-containing blood is achieved by cerebral blood flow, which depends on arterial blood pressure (ABP) and the integrity of the vascular supply to the brain. From a pathophysiologic perspective, general causes of impaired cerebral oxygen delivery include: • Low arterial pO2 • Anemia • Cerebrovascular disease • Hypotension (low ABP) The most common cause of syncope is a sudden fall in ABP. This is typically caused by a cardiac arrhythmia, impairment of cardiac filling, or malfunction of the baroreceptor reflex arc. Blood pressure depends on cardiac output and systemic vascular resistance. • Cardiac output is the product of heart rate and stroke volume. • Stroke volume is modified by ventricular preload (venous return), myocardial contractility (inotropic state), valvular function, and ventricular afterload (impedance to ejection). • Stroke volume also is influenced by heart rhythm. Arrhythmias can alter ventricular filling or reduce the effectiveness of ventricular contraction. • Systemic vascular resistance depends on autonomic tone to arterioles, local (metabolic) factors that dilate or constrict the vessels, and the baroreceptor reflex systems. • Vasoactive drugs also can affect vascular tone.
Non-Cardiovascular Causes of Syncope Syncope may be caused by disorders other than heart disease. Non-cardiovascular etiologies include:
Cerebral Hypoxia
• Anemia—in particular, moderate to severe or acute anemia.
• Respiratory disease—such patients are usually cyanotic from airway obstruction, pulmonary disease, or pleural effusion.
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Stroke
• This is a disruption in cerebral function related to sudden loss of blood supply.
• Hemorrhagic stroke—this is most commonly related to systemic hypertension in dogs and cats.
• Ischemic (thrombotic) stroke—a rare cause of syncope, but it has been observed in cats with feline cardiomyopathy and with bacterial endocarditis in dogs.
Metabolic Disorders
• Hypoglycemia is a relatively uncommon cause of
• •
syncope and is more likely to cause weakness, seizures, or coma. However, hypoglycemia can also affect autonomic function, blood vessel tone, and vascular response to changes in posture, predisposing to true syncopal attacks. Addison’s disease may lead to syncope, likely related to volume depletion (see Chapter 33). Plasma volume depletion from any cause, including vomiting and diarrhea, can reduce cardiac output and ABP.
Drugs
• Drugs that affect heart rate, rhythm, plasma volume, or vascular tone may lead to hypotension and syncope. Examples include inadvertent ingestion of a beta-blockers or illicit drugs (cocaine); over-zealous treatment with diuretics; and administration of vasodilator drugs.
Cardiac and Vascular Causes of Syncope Among the many cardiovascular causes of syncope are the following disorders:
Right-to-Left Shunting
• This can occur with congenital heart malformations including tetralogy of Fallot (see Chapter 154).
Bradyarrhythmias
• Sinus arrest; persistent atrial standstill; high-grade, second-degree, or complete AV block; ventricular asystole (see Chapter 145).
Tachyarrhythmias
• Ventricular tachycardias (often >300 bpm); less often supraventricular tachycardias or atrial fibrillation.
Reduced Cardiac Preload Cerebrovascular Disease
• This is relatively uncommon in dogs but can occur with severe hypothyroidism and accompanying atherosclerosis of the cerebral vessels in dogs (see
• This can be due to structural heart disease or reduced venous return.
• Pericardial disease—cardiac tamponade. • Intracardiac tumor with obstruction to cardiac filling.
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• Caudal vena cava obstruction. • Severe plasma volume depletion.
• Autonomic control mechanisms are central to blood
Valvular Heart Disease
• If sufficiently severe, outflow tract stenosis, atrioventricular valvular stenosis, or mitral or tricuspid regurgitation can limit cardiac output sufficiently to cause or contribute to syncope.
Cardiomyopathy
• Syncope is related to limited cardiac output, development of arrhythmias, or obstruction to blood flow (hypertrophic cardiomyopathy) (see Chapter 150).
Pulmonary Hypertension
• Acquired and congenital causes of pulmonary hypertension represent a common cause of syncope, especially in dogs. This may relate to obstruction of blood flow from the right ventricle, arrhythmias, and inappropriate activation of the baroreceptor reflex.
Congestive Heart Failure
• As with pulmonary hypertension, there may be mul•
tiple reasons for syncope in dogs and cats with CHF (see Chapter 147). Ischemia as a trigger for inappropriate activation of the baroreceptor reflex is a potential cause of syncope.
Hemorrhage
• Sudden hemorrhage is more likely to lead to hypotension and collapse but can also lead to syncope, as with rupture of a splenic tumor or traumatic injury with blood loss.
Thromboembolism
• A cerebral embolus may lead to a stroke that may include loss of consciousness and falling. The likely cardiac causes would be bacterial endocarditis or, in cats, a form of feline cardiomyopathy.
Loss of Vascular Tone
• Inappropriate vasodilation may follow administration of drugs, hypoglycemia, or activation of the cardiac baroreceptors (see below).
Reflex-Mediated Syncope Syncope can be caused by inappropriate and prolonged activation of the baroreceptor reflex; this is termed reflex-mediated syncope. A variety of other names for reflex-mediated syncope are encountered including: “vasovagal,” “neurocardiogenic,” “neural-mediated,” “vasodepressor,” “cardioinhibitory,” and “situational” syncope. While seemingly common, this form of syncope is poorly described in veterinary medicine.
•
pressure control: • The baroreceptor reflex controls heart rate, ventricular contractility, and systemic vascular resistance via the autonomic nervous system. • Baroreceptors located in the systemic arteries (aortic and carotid sinuses) are well appreciated, but pressure receptors are also present within the ventricular myocardium (unmyelinated C-fibers). The sudden stimulation of these myocardial receptors is capable of triggering a baroreceptor reflex. One of the main reasons for activation of these cardiac receptors is sudden vigorous contraction of the myocardium as might occur with surges of sympathetic tone, excitement, or exercise. • Activation of the baroreceptor reflex slows the heart rate and causes vasodilation (reduced vascular resistance) through increased vagal and reduced sympathetic tone. Inappropriate activation of this reflex can lead to excessive vasodilatation and bradycardia, reducing ABP markedly. • Syncope can occur when a baroreceptor reflex is triggered inappropriately by sudden sympathetic stimulation of the heart, especially with excitement, or by situations such as coughing, urinating, or vomiting. The reflex can be predominately that of sinus arrest/bradycardia (“cardioinhibitory syncope”), vasodilation (“vasodepressor syncope”), or a mixed response (“vasovagal syncope”). • In people, this inappropriate reflex activation is most often related to sudden sympathetic surges (as with pain or fright) or from postural (orthostatic) changes that develop with sudden or protracted standing. The sympathetic surge stimulates the heart to maintain ABP and perfuse the elevated head. However, postural activation for this reflex in quadrupeds seems less important than other triggers. • Common disease associations for reflex-mediated syncope in dogs include aortic and pulmonic stenosis, pulmonary hypertension, acquired valvular heart disease, and congestive heart failure. The reflex is often triggered by excitement, activity, or coughing (a type of situational syncope). • There can be a “disconnect” between the recovery of the sinus node function and the return to normal systemic vascular resistance (which can be delayed). This point is pivotal because on first examination the owner or veterinarian may identify a heart rate that is more than sufficient to maintain ABP (generally >40 beats per minute). However, the arterioles may be persistently dilated, producing an unconscious or very weak animal, with pale or cyanotic mucous membranes. Multiple reasons for syncope may be operative in a patient. For example, in a dog with tight congenital subaortic stenosis, possible mechanisms for excitement- or exercise-induced syncope might include: (1) reflex-mediated from stimulation of ventricular
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baroreceptors; (2) myocardial ischemia leading to ventricular tachycardia; (3) outflow tract stenosis limiting stroke volume and cardiac output; and (4) effects of a cardiovascular drug, such as high-dose enalapril, that leads to peripheral vasodilation and reduced vascular resistance.
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Electrocardiography ▼ Key Point It is pivotal that the clinician understands the cardiac rhythm occurring during a syncopal episode.
There are a number of ways to determine the rhythm.
DIAGNOSIS A number of diagnostic studies are needed to establish a diagnosis of syncope and identify the underlying cause for fainting.
• Resting (baseline) ECG —this is rarely diagnostic. If aus•
History and Physical Examination The history should include a medication history and full description of the event(s) as discussed in the Overview.
• Perform a complete physical, ophthalmic, neurolog•
•
•
ical, and cardiovascular examination. Measure resting ABP to identify pre-existent hypotension or hypertension. If the patient is taking cardiovascular drugs, measure the ABP a number of times during the day. If the patient is currently affected by CHF and receiving potentially hypotensive drugs (diuretics, ACEinhibitors, vasodilators, beta-blockers), it may be helpful to hospitalize the patient, administer medications, and record the ABP throughout the day. Systolic pressures 10.8) with left atrial enlargement, and pulmonary venous distention. With the possible exception of catastrophic CHF, the diagnosis of endocardiosis should not be
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Treatment Therapy of chronic valvular disease depends on the stage of disease and severity of clinical signs. Combination drug therapy and dietary management is indicated once CHF has developed. Surgical repair or replacement of a cardiac valve is rare in veterinary practice. The aims of medical therapy are to control clinical signs of CHF, mitigate neurohormonal activation, reduce mitral regurgitant fraction, and prolong life. Diuretics, ACEIs, direct vasodilators, digoxin, pimobendan, pulmonary medications, and dietary measures may be prescribed at various times during the course of the disease. Anti-arrhythmic drugs are required in selected dogs, especially those with atrial fibrillation and serious ventricular arrhythmias. Atrial fibrillation is usually managed with digoxin combined with either a betablocker or calcium channel blocker (see Chapter 145). The clinical pharmacology of these cardiac medications is reviewed in Chapter 146. Specific management strategies for the hospital and home treatment of heart failure are discussed in Chapter 147 and summarized in this section. The following is a summary of general therapeutic approaches.
The Asymptomatic Dog
• The ideal approach to the management of the asymp-
•
tomatic dog has not been determined. While ACEI use is still a subject of some debate, the two published clinical trials examining their use in asymptomatic dogs have failed to demonstrate appreciable clinical benefit. Some clinicians withhold all therapy until there are objective signs of CHF. Others prefer to prescribe an ACEI, empirically, if there is concurrent systemic
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hypertension or evidence of marked cardiomegaly or clearly progressive disease on radiographs or echocardiography. There is no evidence that early enforcement of a very low sodium-restricted diet is of benefit. Early diuretic use and/or severe salt restriction activate the reninangiotensin-aldosterone system and may be counterproductive. Moderation of sodium intake is often recommended at this stage, especially limitation of high sodium treats.
•
•
Coughing in the Dog with Mitral Regurgitation
• A harsh cough is often the initial clinical sign of
•
advanced MR. Coughing is a frequent complication of left bronchial compression, a condition that often precedes the onset of overt pulmonary edema. The lack of clear-cut clinical or radiographic evidence of pulmonary edema in the dog with a mitral murmur and cough complicates determination of the cause of cough. Many dogs exercise well (except for an exertional cough) and sleep comfortably without tachypnea. It is unlikely that these dogs have overt CHF unless transient bouts of pulmonary edema develop with exertion. The best therapeutic approach to bronchial compression is unresolved. • One approach is prescription of an ACEI, possibly combined with a once daily diuretic. Such therapy can decrease cardiac size and blood pressure, which in turn may decrease regurgitant fraction. This therapy also is likely to mitigate transient, exercise-induced pulmonary edema and to delay the onset of more overt signs of CHF. • If the cough continues, medications effective for primary airway disease may be helpful. This can include a cough suppressant (butorphanol 0.55 mg/kg, PO, q8–12h or hydrocodone 0.22 mg/kg, PO, q8–12h). An empiric course of a theophylline salt can be tried (10–20 mg/kg of a sustained release preparation, PO, q12h; beware of excitement as a side effect). This should be discontinued if a clear response is not evident within 2 weeks. In dogs with suspected concurrent respiratory disease, consider a brief course of prednisolone (0.5 mg/kg daily for 5–7 days) to reduce inflammation and break the coughing cycle.
•
Home Therapy of Left-Sided CHF
• Chronic therapy of heart failure caused by mitral
Hospital Treatment of Left-Sided CHF
• Once CHF has developed, the initial course of management is based on the severity of clinical signs of pulmonary edema. Initial therapy generally includes cage rest, oxygen if required, and furosemide (2– 4 mg/kg, q6–q12h, IV or IM). Some clinicians also add nitroglycerin paste (1/2 to 1-1/2 inches cutaneously q8–12h) as a venodilator. Others administer aminophylline (10 mg/kg, q8h) if there is a concern about bronchospasm. The efficacy of bronchodilators has
not been established, and they may induce tachycardia, arrhythmia, or anxiety in some dogs. Moderate to large volume pleural effusion should be removed by thoracentesis. Dogs with concurrent respiratory distress and large volume ascites may benefit from abdominocentesis. Life-threatening pulmonary edema requires more aggressive treatment beyond oxygen and high-dose furosemide (also see Chapter 147). Consider a constant rate IV infusion of furosemide. Drugs that reduce left ventricular afterload should be administered unless the patient is hypotensive. The direct arterial vasodilator, hydralazine (1–2 mg/kg, PO), or IV administration of sodium nitroprusside (1–5 mg/ kg/min) will promptly lower blood pressure and LV load. Administration of an ACEI such as enalapril (0.5 mg/kg, PO) also reduces load, but the onset of action is slower. • The dose of these vasodilators should be titrated to a systolic arterial blood pressure of 85–95 mmHg. Aggressive afterload reduction significantly decreases the mitral regurgitant fraction. Such therapy is especially important in cases of peracute regurgitation caused by ruptured mitral valve chordae tendineae. Some patients in severe CHF exhibit marked anxiety and air hunger. Treatment with morphine may be useful if it does not induce vomiting (0.1 mg/kg, administer 25% IM; administer the balance SC 15 minutes later). Alternatively, consider subcutaneous administration of acepromazine (0.025 mg/kg) mixed with buprenorphine (0.005 mg/kg). Some clinicians find that butorphanol (0.25 mg/kg, IM) is an effective sedative with the advantage of not inducing vomiting.
•
valvular disease includes a maintenance dose of furosemide (2–5 mg/kg, q8–24h), an ACEI such as enalapril or benazepril (0.5 mg/kg, PO, q12–24h), and dietary sodium restriction. Titrate the daily doses of furosemide and the ACEI to clinical signs, objective measures of fluid accumulation, arterial blood pressure (to maintain a systolic pressure of 90– 120 mm Hg), and renal function. Reduce dosages if hypotension or progressive azotemia develops. Pimobendan, a potent inotropic drug with vasodilating properties (see Chapter 146), has not been approved in the United States at the time of writing; however, it is available in many countries and represents a valuable drug for management of dogs with CHF due to MR. Digoxin also is prescribed by many cardiologists. Use an initial conservative dose (0.005 mg/kg, q12h), and adjust based on serum digoxin concentrations (target is 0.8–1.2 ng/ml at a 10–12 hour trough).
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• Atrial fibrillation or frequent atrial ectopic beats represent clear indications for digitalization. Once CHF is controlled and digoxin has been initiated, co-therapy with a beta-blocker or diltiazem may be required to attain better ventricular rate control. • Digoxin also may be useful to reduce syncopal episodes in dogs where no clear clinical cause for syncope can be established. Digoxin is contraindicated in the setting of complicated ventricular rhythm disturbances or ventricular tachycardia.
•
▼ Key Point Combination therapy is preferred in the management of CHF. Monotherapy with a diuretic or a diuretic and sodium-restricted diet is no longer considered appropriate treatment for most dogs because volume depletion activates the reninangiotensin-aldosterone system.
• Treat progressive or refractory pulmonary edema first by optimizing current therapy. Should q12h ACEI therapy, q8h doses of furosemide, and pimobendan (where available) fail to control this problem, consider adding another vasodilator, digoxin, or a second diuretic. • Combination therapy with an ACEI and hydralazine (0.5–1 mg/kg, PO, q12h) or amlodipine (0.05– 0.2 mg/kg, PO, q24h daily) can more effectively reduce the mitral regurgitant fraction. Such treatments are best initiated in the hospital, where arterial blood pressure can be monitored frequently. Many dogs can tolerate a systolic blood pressure as low as 80–85 mm Hg initially without overt clinical signs of hypotension, allowing time for further adaptive responses. Blood pressure in this 80– 85 mmHg range during chronic management of CHF is sometimes associated with lethargy or weakness. A second vasodilator is also critical in dogs with MR and concurrent systemic hypertension despite full ACEI and diuretic therapy. Amlodipine, hydralazine, carvedilol, or compounded prazosin may be effective for individual patients (Chapter 153). • An alternative approach to progressive CHF is the addition of another diuretic, which is described in a following section.
•
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often demonstrates minimal pulmonary edema, whereas Doppler echocardiography may show signs of pulmonary hypertension, such as high-velocity tricuspid regurgitation. Management of dogs with a prominent component of right-sided CHF includes treatment with an ACEI (q12h), furosemide (q8h), pimobendan (if available), and a restricted sodium diet. Digoxin is also useful to control fluid accumulation in many dogs. Should these methods fail then a variety of other strategies can be attempted. Initially, the dog may be hospitalized, treated with subcutaneous furosemide (or other loop diuretic), and receive judicious paracentesis for tense ascites (removing between 1/4 to 1/2 of the fluid accumulation). Treat atrial fibrillation if present. Two or 3 days of enforced cage rest and parenteral diuretic therapy may alleviate most of the retained fluid. At that point, treatment strategies can include any (or all) or the following: • Markedly increasing the oral dose of furosemide to effect (because poor absorption of the medication may be partially responsible for the refractory ascites). • Using flexible subcutaneous diuretic dosing (having the client substitute a subcutaneous dose of furosemide for the usual oral dose). • Adding spironolactone (2 mg/kg, PO, q12 to 24h) or another potassium-sparing diuretic to the regimen. • Adding hydrochlorothiazide and spironolactone (2–4 mg/kg, PO, q12–24h of the combined product) to the regimen. This approach is especially aggressive because electrolyte reabsorption is blocked at sequential points along the nephron. Accordingly, the potential for volume depletion and electrolyte disturbances is very high and must be monitored carefully (reevaluate the patient, blood pressure, and serum biochemistries at 3 days, 7 days, and 14 days after starting this treatment). Pleural effusion in valvular heart disease is often a poor prognostic sign. A neoplastic cause for the effusion should be excluded, and treatment of pleural effusion due to CHF is as discussed previously for right-sided heart failure. Periodic thoracocentesis may be required.
Treatment of Right-Sided Congestive Heart Failure
Other Respiratory Complications in Advanced MR
• Right-sided CHF with ascites or biventricular CHF
• A persistent, nonresponsive cough in animals with
with pleural effusion is more likely to occur in dogs in which pulmonary hypertension, tricuspid regurgitation, or atrial fibrillation. Pulmonary hypertension usually is a consequence to chronic elevation in left atrial pressure or pulmonary vascular narrowing secondary to chronic CHF or primary lung disease. When right-sided CHF dominates the clinical picture, it is not uncommon to notice a reduction of dyspnea and an increase in exercise intolerance. Radiography
otherwise well-controlled CHF can be a vexing problem. Bronchial compression or intercurrent airway disease may be the culprit in many of these cases. Provided there is no radiographic evidence of pulmonary edema, it is reasonable to continue the current cardiac medications and to add a cough suppressant, such as hydrocodone or butorphanol, or even a brief course of prednisolone, to control the cough.
•
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• In other dogs, signs develop that suggest accelerated
•
pulmonary fibrosis. These dogs have exercise intolerance, some may faint, and some are persistently tachypneic but generally sleep well without any resting dyspnea. Auscultation reveals diffuse inspiratory crackles that might be easily confused with those caused by pulmonary edema. Hypoxemia and pulmonary hypertension may be present, however radiography indicates “clear” lung fields or minimal interstitial density despite marked cardiomegaly. Escalation of diuretic or vasodilator therapy often does not improve the respiratory signs and may predispose the animal to syncope by reducing blood pressure. Other reasons for persistent respiratory signs in dogs with MR include tracheal collapse, chronic bronchitis, pulmonary neoplasia, pneumonia, and recurrent pulmonary thromboembolism.
cardiac disease might not be the leading differential diagnosis. In order to diagnose this disease the clinician must maintain a high index of suspicion in animals with multisystemic clinical signs, especially when the differential diagnoses include serious infection or immune mediated disease.
Etiology • Pathogenic bacteria identified in dogs and cats with
•
Patient Follow-Up Follow-up examinations and complications are described in Chapter 147. In general, a repeat examination should be performed 5 to 10 days after initiation of CHF therapy. Testing at the recheck should include historical and physical examination, blood pressure, evaluation of serum BUN, creatinine and electrolytes, and possibly thoracic radiographs. In dogs with stable CHF, follow-up examinations every 2 to 4 months are recommended to titrate therapy and insure owner compliance.
Prognosis
• •
Pathogenesis • The pathogenesis of infective endocarditis involves
The prognosis for longevity is highly variable. Dogs with heart murmurs but without clinical signs of heart disease may survive for many years and often succumb from a non-cardiac disorder. Clinical signs associated with bronchial compression indicate that sufficient volume overload has developed to compress the airways, but this alone is not an indication of CHF. Once overt pulmonary edema or ascites develops, the prognosis for life becomes guarded. Assuming initial stabilization is successful, a survival range of between 3 months and 2 years should be discussed with the client. With good veterinary and home care and a dedicated client, many dogs live for 9 to 12 months or longer before spontaneous death or euthanasia.
BACTERIAL (INFECTIVE) ENDOCARDITIS Bacterial endocarditis (BE) is a bacterial infection of the valvular or mural endocardium. The mitral and aortic valves are the most common sites of cardiac bacterial infection in dogs and cats. Establishment of a cardiac infection requires a portal of bacterial entry into the circulation, subsequent bacteremia, and colonization of the endocardium. In most cases, bacterial endocarditis is manifested as a multisystemic disorder, and
bacterial endocarditis include streptococci, staphylococci, corynebacteria, Escherichia coli, Enterobacter aerogenes, and Pseudomonas, Pasteurella, Erysipelothrix, and Bartonella spp. Many of these bacteria are normal inhabitants of the skin, oral cavity, and respiratory and intestinal tracts. Bartonellosis is discussed in Chapter 19. Bacteria can gain access to the circulation via external wounds, established infections, and a variety of surgical procedures and invasive medical interventions; however, in many cases, there is no evidence of these sources. Endocarditis may be a sequela to septic arthritis, osteomyelitis, prostatitis, infected catheters, and other infections. Immunosuppressive drugs (e.g., corticosteroids, anticancer chemotherapy) also predispose to infection. Injudicious use of antibiotics may predispose to infection by resistant or virulent organisms.
•
entry of bacteria into the circulation and invasion of the valve endocardium by direct extension from the bloodstream. • Virulent bacteria may attach themselves to the valve surface, ulcerate the endocardium, and invade the valve stroma. • Previously diseased valves are believed to be more susceptible, particularly when the endocardium is disrupted. Dogs with subaortic stenosis are at increased risk for endocarditis, presumably because of jet lesions on the aortic valve. Conversely, for uncertain reasons, dogs with endocardiosis are rarely affected with BE. • High titers of agglutinating antibodies that cause clumping of bacteria, thereby increasing the size of the infectious inoculum, are thought to play a role in some cases. Collagen is exposed once micro-organisms colonize and ulcerate the endocardium, causing platelet aggregation and the local accumulation of fibrin. • Vegetations resembling thrombi form on the valve surface. These vary in color from yellowish red to gray and are covered by a thin layer of clotted blood. • Lesions usually are localized to the valve but can extend to the mural endocardium, chordae tendineae (causing rupture), or sinuses of Valsalva
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• Arrhythmia.
Immune complexes
• Ventricular and supraventricular arrhythmias may be related to endomyocarditis, myocardial infarction from bland thrombi, cardiac dilation, or “toxemia.” Extension of aortic root abscesses into the conduction system can cause AV block.
Abscess AV block
Emboli Bacteremia (fever)
LA
CHF M-R
VC
RA RV
LV
Aortic regurgitation
S1 S2 Aortic stenosis
Bacteremia and Metastatic Infection S1 S 2
Infarct Myocarditis
S 1 S2 Figure 149-2. Diagrammatic representation of endocarditis. Consult the text for an explanation of abbreviations and symbols.
•
•
•
•
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(this may hasten the spread of septic foci via the coronary arteries to the myocardium). Chronic valvular infections are established when layers of fibrin are deposited repeatedly at the site of infection, “protecting” the bacterial colonies from host responses and from many antibacterial agents. Deformation of the valve usually results in valvular insufficiency. Exuberant vegetation or fibrotic healing may form in such a way as to produce valve stenosis, but this is less common. Parts of the vegetation may break off, seeding the various tributaries of the systemic circulation, including the coronary arteries. • Intermittent bacteremia causes persistent or recurrent fever. • Thromboemboli, which can be septic or “bland” (aseptic), can also be shed from the infected valve. Formation of immune complexes is an important host response; these may be filtered into the joints, kidneys, or other tissues; attract complement and leukocytes; and cause inflammation in these tissues.
• Bacteremia causes fever, shivering, malaise, and anorexia.
• Other tissues may be seeded, resulting in brain • •
abscesses, splenitis, osteomyelitis, septic arthritis, pyelonephritis, myositis, or other remote infections. In advanced cases, it is difficult to distinguish a primary infection (portal of entry) from a metastatic infection. Bacteremia and sepsis may be associated with disseminated intravascular coagulopathy (DIC) and lead to death from septic shock or organ failure.
Immune-Mediated Disease Immune complexes may form and be trapped in many organs or tissues, with the following effects:
• The kidneys, leading to glomerulonephritis • The brain and meninges, causing meningoencephalitis
• The joints, causing polyarthritis • The skeletal muscles, causing myositis and myalgia • The small blood vessels, leading to vasculitis, thrombosis, or hemorrhage
• The eye, leading to chorioretinitis ▼ Key Point Do not confuse the clinical findings seen in endocarditis of recurrent fever, multisystemic involvement, polyarthritis, and DIC with those of primary immunologic or neoplastic diseases; such an assumption may prompt inappropriate therapy with corticosteroids.
Pathophysiology
Thromboembolic Complications
The clinical signs of infective endocarditis result from cardiac injury, bacteremia and sepsis, thromboembolic complications, and immune-mediated processes (Fig. 149-2).
Septic or bland (sterile) thrombi derived from the vegetation may be carried to distant tissues. Consequences include
Cardiac Injury A variety of cardiac manifestations are possible, including
• • • • • •
Mitral and aortic valvular regurgitation. Valvular stenosis (less common). Coronary occlusion with myocardial infarction. Secondary myocardial invasion, causing myocarditis or myocardial abscessation. Pericarditis. Left-sided CHF (from advanced valvular injury).
• Myocardial infarction and myocarditis. • Renal infarcts, abscess, pyelonephritis, and glomeru• • • • •
lonephritis. Stroke, meningitis, and encephalitis. Bone infarcts and osteomyelitis. Vascular obstruction including aortic-iliac occlusion. Splenic infarcts. Intestinal ischemia.
Because of the low incidence of right-sided endocarditis in small animals, pulmonary embolism and pneumonia are rare. The notable exceptions are BE secondary to infection from patent ductus arteriosus
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surgery and infection of a central venous catheter, dialysis catheter, or transvenous pacing lead.
Clinical Signs and Diagnosis Signalment Endocarditis is more common in certain large-breed male dogs (e.g., German shepherds) and in dogs with congenital subaortic stenosis.
Serum Biochemistries Biochemical alterations may reflect organ injury from infection, thrombosis, infarction, or poor perfusion from heart failure. Azotemia or liver enzyme elevations are often present, and elevation of serum alkaline phosphatase is common in dogs with gram negative infections. Hyperglycemia or hypoglycemia, hypoalbuminemia, and elevated bilirubin can also be noted.
Tests for Autoimmune Disease
History
• The history may suggest previous or concurrent infec• •
tion (especially of the skin, oral cavity, gut, bone, or urogenital tract). Certain diagnostic and therapeutic procedures predispose to BE by causing bacteremia (e.g., surgical implants, endoscopy, and dental extractions). Persistent use of corticosteroids or antineoplastic drugs or improper use of antibiotics may predispose to BE.
Rheumatoid factor test, Coombs’ test, or antinuclear antibody (ANA) assays can be positive in patients with BE.
Blood Cultures Two or more positive blood cultures, obtained from a patient with compatible clinical signs, strongly suggest BE.
• Cultures are most rewarding if taken near febrile
Physical Examination Physical examination findings may include
• Fever which may or may not be antibiotic-responsive, • • • •
depression, anorexia, and shaking “chills.” Polyarthritis (shifting lameness) with or without joint effusion and myalgia. Signs of vasculitis with hemorrhages (skin, eye, mucous membranes). Multifocal neurological deficits from meningitis or encephalitis. Signs of cardiac injury: • A cardiac murmur, particularly a “new” or changing murmur. • BE destroys portions of the valve; therefore, regurgitant murmurs (MR, aortic regurgitation) usually are present in dogs and cats with BE. A systolic ejection murmur often accompanies the diastolic murmur of aortic insufficiency due to increased LV stroke volume. Large vegetation(s) on the valves also may contribute to valve stenosis murmurs. • The pulse pressure increases with aortic insufficiency, which causes hyperkinetic femoral pulses with rapid run-off of diastolic pressure. Always consider BE when aortic regurgitation, which is uncommon in dogs and cats, is present. • Signs of overt left-sided CHF or arrhythmias (especially ventricular premature complexes) may develop from cardiac injury.
Laboratory Tests Complete Blood Count (CBC) Mild anemia and leukocytosis with neutrophilia and monocytosis may be present. Thrombocytopenia is often present, and red blood cell (RBC) fragments may suggest vasculitis (see Chapter 153) or DIC.
•
•
•
•
bouts when the animal is not receiving antibiotics. Cultures may be positive before, during, or after bouts of fever. Serial positive blood samples, taken 1 to 2 hours apart from different sites, help to rule out the possibility of skin contamination. (Aseptically prepare the skin before obtaining the sample.) Transfer sufficient blood (5–10 ml) into special broth media tubes (usual blood : medium ratio of 1 : 10). Aerobic and anaerobic culture and sensitivity are indicated. Special antibiotic adsorbing media are available for patients who have received antibiotic therapy. Some microorganisms are difficult to culture (e.g., Bartonella spp.), leading to so-called “culturenegative” endocarditis. Serologic testing and/or PCR testing can help establish a diagnosis of Bartonella in these cases. Dogs with culture negative endocarditis, especially those with aortic valve disease, should be suspected of having Bartonella (see Chapter 19). If a primary source of infection is suspected then cultures should be obtained from this location (i.e., urine culture, bone culture in suspected osteomyelitis, etc.).
Urinalysis Hematuria, proteinuria, pyuria, or casts may be shown if pyelonephritis or glomerulitis is present. Culture the urine if there are any abnormalities, but do not automatically assume that organisms cultured from urine are responsible for the cardiac infection.
Cardiac Studies Cardiac studies may substantiate the diagnosis and indicate the degree of cardiac injury. Serial studies after successful antimicrobial therapy are useful,
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although complete resolution of valvular pathology is uncommon.
• Radiographs may indicate cardiomegaly, valve calcifi•
•
•
cation (from chronic BE), CHF, or (rarely) embolic pneumonia. Electrocardiograms can be normal, but they may indicate chamber enlargement or arrhythmias (most often ventricular premature contractions). • ST-T changes, indicating ischemia or infarction, may be present (check precordial leads for these). • AV block in endocarditis likely indicates aortic valve involvement with a perivalvular inflammation affecting the bundle of His. Echocardiography is useful, especially for diagnosis and prognosis. • Routine 2-D or M-mode echocardiography may demonstrate a recent vegetation (oscillating thrombus) or more chronic lesion (thick, hyperechoic valve). Echocardiography is also helpful for identifying hemodynamic overload (cardiomegaly). A negative examination of the valves does not rule out BE. • Echocardiography alone may not be sufficient to distinguish mitral BE from advanced mitral endocardiosis. • Doppler studies can document both abnormal valvular regurgitation and stenosis. Hemodynamically significant aortic regurgitation is associated with an adverse outcome. Progressive cardiomegaly demonstrated by echocardiography or radiography indicates clinically significant valvular injury and is a poor prognostic finding.
Other Studies Other studies may be abnormal depending on the organ involved. Cerebrospinal fluid (CSF) and joint fluid cytology and culture may show evidence of septic or aseptic (immune complex) suppurative inflammation.
Treatment Consider the following principles:
• Use bactericidal antibiotics. Because the bacteria
• • • •
are sequestered within the vegetation, normal defense and healing processes (e.g., granulation) are impeded. Because the drug must penetrate fibrin, do not use most sulfa drugs. Long-term (1–3 months) therapy is needed to ensure sterilization of the vegetation. Ideally, use IV therapy to obtain the highest possible plasma concentrations for the first 5 to 7 days. (This is sometimes impractical.) Guide antibiotic therapy by blood cultures. It is appropriate to delay antibiotic therapy for 2 to 4
•
•
•
•
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hours while blood cultures are being obtained, unless the patient is demonstrating signs of septic shock. Empirical therapy for BE often includes the following drugs: • Penicillins (high doses) are safe and useful for streptococcal infections but have limited efficacy against many staph and other microorganisms. • Aminoglycosides, combined with a synthetic penicillin or cephalosporin, provide wider antimicrobial coverage. Use of these drugs requires good patient hydration and careful monitoring for nephrotoxicity. Aminoglycosides should be withheld from animals with concurrent CHF that require furosemide administration. • A patient with renal failure may be treated with a newer-generation cephalosporin in lieu of an aminoglycoside. • In cases of suspected Bartonella, a combination of gentamicin (for 15 days) and doxycycline is recommended, with careful monitoring for nephrotoxicity. Azithromycin, 5 to 10 mg/kg q24h for the first 7 days, then every other day for 6 to 12 weeks, represents another approach to treating patients with confirmed Bartonella infection. Treat for at least 4 weeks (at least 10–14 days when using an aminoglycoside, with continuation of the penicillin or cephalosporin for the full 4 weeks). Some cardiologists recommend treatment for 6 to 8 weeks. Repeat blood cultures following discontinuation of therapy or if fever should recur. If left-sided CHF develops, treat according to guidelines described above for valvular endocardiosis. Remember that vasodilator therapy is contraindicated for dogs with septic shock. Use prophylactic antibiotics if the patient undergoes any procedure that may cause bacteremia. (The general subject of prophylactic therapy of BE is unresolved, and no firm recommendations can be made.)
Prognosis The prognosis for BE is guarded. Negative prognostic predictors include large vegetations with accompanying marked cardiomegaly, CHF, marked aortic regurgitation, gram-negative infections, elevation of serum alkaline phosphatase or hypoalbuminemia, treatment with corticosteroids, delayed diagnosis or treatment with bacteriostatic antibiotics, and premature termination of antibiotics.
• Acute, ulcerative BE may cause dramatic clinical signs • •
but, if promptly treated, may leave only mild cardiac dysfunction. Chronic BE with severe valvular destruction is more difficult to treat because severe CHF may develop. Echocardiographic evidence of diffuse, large vegetative lesions and documentation of volume overload imply a poor prognosis. The likelihood of CHF is high in these instances.
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SUPPLEMENTAL READING Griffiths LG, Orton EC, Boon JA: Evaluation of techniques and outcomes of mitral valve repair in dogs. J Am Vet Med Assoc 224:1941–1945, 2004. Smith PJ, French AT, Van Israel N et al: Efficacy and safety of pimobendan in canine heart failure caused by myxomatous mitral valve disease. J Small Anim Prac 46:121–130, 2005. MacDonald KA, Chomel BB, Kittleson MD et al: A prospective study of canine infective endocarditis in northern California
(1999–2001): Emergence of Bartonella as a prevalent etiologic agent. J Vet Int Med 18:56–64, 2004. Häggström J, Kvart C, Pedersen HD: Acquired valvular heart disease. In: Ettinger SJ and Feldman EC (eds): Textbook of Veterinary Internal Medicine, 6th ed. St. Louis: WB Saunders, 2005, pp 1022–1039. Kvart C, Häggström J, Pedersen HD et al: Efficacy of enalapril for prevention of congestive heart failure in dogs with myxomatous valve disease and asymptomatic mitral regurgitation. J Vet Int Med 16:80–88, 2002.
Chapter
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150
Cardiomyopathy John D. Bonagura / Linda B. Lehmkuhl
OVERVIEW
• Taurine deficiency in cats is a classic example of a reversible dilated cardiomyopathy.
• Regression of left ventricular hypertrophy may occur The left and right ventricles are capable of undergoing significant morphologic change in response to stresses and stimuli. Reaction to increased volume or pressure work frequently leads to chamber dilatation and hypertrophy, along with alterations in the cytoskeletal matrix of the ventricle. Myocardial and chamber responses develop with chronic valvular heart disease, cardiac shunts, systemic and pulmonary hypertension, thyrotoxicosis, and chronic anemia. These responses to stress are directed by various neural, hormonal, and genetic messages acting on the myocardium. These signals influence genetic expression in the cardiomyocyte and interstitial cells, and remodel the ventricle. “Cardiomyopathy” refers to disease of the myocardium and, by extension, the cardiomyocyte and the supporting collagen and interstitial matrix. Idiopathic or primary cardiomyopathies are those that cannot be explained by a malformation, acquired cardiac lesion, dysrhythmia, or coronary artery disease. Many idiopathic cardiomyopathies are genetic diseases. A more expansive definition of cardiomyopathy accepts that some myocardial diseases can be explained by other disorders, and in such cases, the term secondary cardiomyopathy can be used. When myocardial failure develops from chronic volume or pressure overload of the ventricle, the term cardiomyopathy of overload has been proposed to explain the remodeling associated with increased ventricular work. Although there are many known causes of cardiomyopathy, most cases in cats and dogs are idiopathic and thought to represent a genetic disorder. This is particularly true of dilated cardiomyopathy in dogs and hypertrophic cardiomyopathy in cats. What stimulates these genetic factors to cause heart muscle disease is poorly understood, and most cases of cardiomyopathy are irreversible and progressive. But there are special examples that demonstrate that some cardiomyopathic states can be postponed, arrested, or even reversed. For example:
• Chronic tachyarrhythmias cause a cardiomyopathy with loss of myocardial contractility that is reversible if the arrhythmia is resolved.
after successful treatment of systemic hypertension or hyperthyroidism. Cardiomyopathies often are classified by the postmortem anatomic appearance of the left (or right) ventricle and by the correlative echocardiographic features of ventricular anatomy and function. The most important forms of cardiomyopathy can be classified as follows (see Table 150-1):
• Myocarditis—An inflammation of the heart muscle
•
•
•
• •
•
observed most often in cats. It may be responsible for premature ventricular complexes, sudden death, or progressive heart failure. Dilated cardiomyopathy (DCM)—A dilated, poorly contracting left ventricle (LV) usually associated with development of congestive heart failure (CHF), cardiac arrhythmias, and sudden death. DCM is a common disease of dogs but is very uncommon in cats. Hypertrophic cardiomyopathy (HCM)—A thickening of the LV walls of unknown or genetic cause and displaying considerable phenotypic heterogeneity. HCM is mainly a disorder of cats and often leads to cardiac murmurs, CHF, or thromboembolic disease. Restrictive cardiomyopathy (RCM)—A heterogeneous and poorly characterized disorder defined by extensive fibrosis in the LV. It is encountered mainly in mature or older cats and is a recognized cause of arrhythmias, CHF, and arterial thromboembolism. Right ventricular cardiomyopathy—A disorder that affects mainly (or initially) the right ventricle resulting in either CHF or ventricular arrhythmias. Unclassified cardiomyopathy—Primary LV diseases that are not easily classified as HCM, DCM, or RCM. Some cases are probably related to myocardial infarction. Cardiotoxicity—The heart also can be damaged by a number of cardiotoxins, some of which are listed in Table 150-1. The outcome of cardiotoxicity is often an arrhythmia, conduction disturbance, sudden death, or development of a secondary dilated cardiomyopathy. 1527
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Table 150-1. CAUSES OF CARDIOMYOPATHY (CM) Disorder* Myocarditis Noninfective Infective
Feline
Canine
Idiopathic Thymoma (immune-mediated) Toxoplasmosis Feline infectious peritonitis?
Idiopathic Trauma Bacterial Parvovirus Distemper virus Systemic mycoses Lyme carditis (Borrelia) Chagas disease (Trypanosoma cruzi) Idiopathic† Carnitine or Taurine deficiency Breed-“specific” DCM† Doberman pinscher Boxer dog Cocker spaniel “Giant” purebred dogs Springer spaniel muscular dystrophy Sustained ventricular or supraventricular tachycardia Idiopathic Hypertension Hyperthyroidism (iatrogenic)
Dilated CM (DCM)‡
Taurine deficiency Idiopathic Potassium iodide toxicity Hyperthyroidism Sustained ventricular or supraventricular tachycardia Chronic hypokalemia (causes taurine deficiency?)
Hypertrophic CM Left ventricular concentric hypertrophy
Idiopathic† (familial?) Acromegaly (rare) Hypertension† Hyperthyroidism† Idiopathic* Idiopathic
Restrictive-intermediate CM Arrhythmogenic right ventricular cardiomyopathy Cardiotoxicity
Boxer dog (genetic)† English bulldog (genetic?)† Catecholamines including brain-heart syndrome and pheochromocytoma Doxorubicin Digitalis purpurea (foxglove) and Strophanthus spp. Toad (Bufo) toxicity Chocolate toxicity
Sodium iodide
*Both primary (idiopathic) and secondary causes of cardiomyopathy are considered here. † Most important types. ‡ Also see infective and noninfective myocarditis because DCM can develop secondary to severe inflammatory disease.
This chapter will next describe the clinical features of feline cardiomyopathies and the therapy of related complications. Following this is a consideration of canine DCM and arrhythmogenic cardiomyopathy.
FELINE HYPERTROPHIC CARDIOMYOPATHY Overview and Pathophysiology of Feline HCM • Feline idiopathic HCM is characterized by hypertro-
•
•
phy and thickening of the left ventricle unexplained by congenital heart disease, systemic hypertension, or an endocrinopathy. The condition is genetic in a number of feline breeds, including the Maine coon cat, Persian cat, and the Ragdoll. Thus far, one sarcomeric mutation has been identified. The pattern of ventricular hypertrophy in this disease is variable as demonstrated at necropsy or by 2D echocardiography. • Symmetrical concentric hypertrophy of the LV walls and papillary muscles is considered typical of
•
•
•
feline HCM, but there is substantial variation in the location and severity of hypertrophy in this disease. • The main histologic finding is of myocardial cell hypertrophy with fiber disarray. Small, intramural coronary arteries are often narrowed. Microscopically, there is fibrosis between myocytes. Focal areas of infarction or inflammation may be observed. • The left atrium (LA) is usually dilated and the wall may be hypertrophied from increased pressures needed to fill the LV. Atrial or auricular clots are found attached to the chamber wall in some cases. The natural history of untreated feline HCM is quite variable following a benign or lethal course; a brief or protracted clinical disease; and sometimes remarkable recovery from life-threatening complications. Some cats remain asymptomatic for many years before succumbing (if ever) to the disease. Clinical signs in HCM are explained by left-sided CHF, complications of arterial thromboembolism (ATE), LV outflow tract obstruction, or arrhythmias capable of causing syncope or sudden cardiac death. The differential diagnosis for the clinical signs of HCM in cats is extensive (Tables 150-2 and 150-3),
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Table 150-2. DIFFERENTIAL DIAGNOSIS OF FELINE CARDIOMYOPATHY AND HEART FAILURE* Other Causes of Dyspnea/Tachypnea Airway obstruction Nasopharyngeal polyp Laryngeal paresis Tracheal or esophageal foreign body, neoplasm, granuloma, abscess Mediastinal masses Lymphoma or thymoma Primary bronchopulmonary disease Bronchial asthma/bronchitis Lungworms and lung flukes Pneumonia (viral, bacterial, fungal, toxoplasmic) Neoplasia Aspiration Pulmonary vascular disease/embolism Heartworms/spontaneous worm death Noncardiogenic pulmonary edema Electrocution Trauma (shock lung) Anaphylaxis Trauma Diaphragmatic hernia Pulmonary hemorrhage/edema Pneumothorax Hemothorax Pleural effusion Pyothorax Hemothorax Feline infectious peritonitis (FIP) Lymphoma-associated effusion Chylothorax Hyperthermia/fever Anemia Methemoglobinemia Acetaminophen toxicity Cetacaine Abnormal ventilatory pattern Metabolic acidosis Central nervous system disease Other Causes of Acute Lameness/Paresis/Gait Abnormality Musculoskeletal pain or injury Bite wounds Hypokalemia (weakness) Peripheral neuropathy Related to diabetes mellitus
Spinal cord disease Injury Neoplasia FIP infection Extradural mass/granuloma Urinary obstruction Causing abdominal pain and reluctance to move Other Causes of Cardiac Murmurs/Gallops/Arrhythmias/ Cardiomegaly Congenital heart disease Especially spetal defects and mitral valve dysplasia Congenital peritoneopericardial-diaphragmatic hernia Bacterial endocarditis Pericarditis FIP infection Idiopathic Bacterial Neoplastic Lymphoma Mesothelioma Cardiac neoplasia Lymphoma Cor pulmonale Heartworms Severe chronic respiratory disease Chronic degenerative valvular disease (mitral, aortic) Dilation of the aortic root with aortic regurgitation Cardiac arrhythmias (primary electrical disturbances) Chronic bradyarrhythmias Atrioventricular block in aged cats Tachyarrhythmias and premature complexes Sedatives, tranquilizers, anesthetic drugs Chronic or severe anemia Hyperthyroidism Acromegaly Systemic hypertension Chronic renal disease Hyperthyroidism Idiopathic Electrolyte abnormalities Hyperkalemia Urinary obstruction Hypokalemia Renal disease
*The most common clinical presentations of feline cardiomyopathy are dyspnea from congestive heart failure, rear-limb paresis from aortic thromboembolism and inactivity. The veterinarian often detects a murmur, gallop rhythm, arrhythmia, or cardiomegaly during examination.
and includes congenital heart disease, myocarditis, and other forms of primary cardiomyopathy (RCM, DCM). When an echocardiogram demonstrates thickening of the LV, specific disorders causing LV hypertrophy must be excluded including • Mitral valve malformation causing dynamic obstruction of the LV outflow tract with secondary hypertrophy. • Congenital aortic or subaortic stenosis. • Hyperthyroid heart disease (thyrotoxicosis). • Hypertensive heart disease. • Focal basilar septal hypertrophy associated with aortic dilatation (aortoannular ectasia). • Acromegaly (growth hormone excess).
• The pathophysiology of feline HCM (Figure 150-1) is relevant to the diagnosis and drug therapy of this disease. The presumptive cause of CHF is ventricular diastolic dysfunction, because most cats with HCM have a normal to hyperdynamic LV ejection fraction. • Diastolic dysfunction is the inability to fill the left ventricle with normal LA pressures. • Early diastolic dysfunction is characterized by abnormal myocardial relaxation with a vigorous LA contraction to support late diastolic filling. This situation is associated with the atrial (S4) gallop so often detected in these cats. • Progressive ventricular disease is associated with reduced chamber compliance with loss of passive
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Table 150-3. COMMON FELINE CARDIAC DISEASES Disorder Pericardial effusion and pericardial disease
Septal defects—VSD, ASD, ECD Dilated cardiomyopathy (DCM) phenotype
Hypertrophic cardiomyopathy (HCM) phenotype
Restrictive cardiomyopathy phenotype
Unclassified or “Intergrade” cardiomyopathy Congenital mitral valvular disease
Heartworm disease
Arrhythmias: PACs, PVCs; AV block
Necropsy and Echo (Anatomic Diagnosis)
Typical Clinical Problems
• Peritoneopericardial diaphragmatic hernia (PPDH) • Secondary to CHF • Infection (including FIP) secondary to infection • Neoplastic related (LSA) • Echo: echo-free space around heart; +/- mass lesions; often observe left-sided cardiomyopathy; Liver and fat in PPDH • Ventricular or atrial septal defect • AV valve malformation (ECD) • Echo: above lesions with volume overload of affected chambers • Cardiac chamber dilatation (typically left sided chambers +/- right sided) • Echo: cardiac dilatation & loss of myocardial contractility
• Unexplained cardiomegaly (PPDH) • CHF as a cause of PE • CHF as consequence of PE and cardiac tamponade • Systemic illness (infection, neoplasia)
• • • •
• • • • • • • • • • •
• Congenital • Genetic?
• Left ventricular hypertrophy that is concentric or regional • Focal septal LVH (aged cats; dilated aortic root) • Echo: LV hypertrophy; variable; possible LA dilation • Left ventricular endomyocardial fibrosis or myocardial fibrosis (multifocal or generalized) • LV wall infarction • Echo: Marked bi-atrial dilatation; variable LV anatomy, wall motion, and systolic function • Left ventricular myocardial disease with variable morphologic characteristics with Echo showing systolic and diastolic LV function • Mitral valve dysplasia (MV malformation; generally causes MR; rarely MS) • Echo: Mitral valve malformation; LA and LV dilatation • Pulmonary vascular disease • Pulmonary thromboembolism, pneumonitis, and fibrosis • Aberrant infection • Echo: parasites in the PA Necropsy or Echo may demonstrate cardiac lesions but often there is no overt structural lesion
• • • • • • • • • • • • • • •
Systolic heart murmur Cardiomegaly CHF Cyanosis (reversed shunt) CHF—left-sided; biventricular Arterial thromboembolism Arrhythmias Sinus bradycardia Hypotension Soft heart sounds Secondary AV valvular regurgitation Abnormal auscultation: heart murmur, gallop, arrhythmia Thyroid adenoma in cases of hyperthyroidism Target organ injury: brain, eyes, kidneys, and heart in systemic hypertension Abnormal auscultation: gallop, arrhythmia, heart murmur CHF—biventricular Chylothorax (from CHF) Arterial thromboembolism Arrhythmias Sudden cardiac death CHF—left sided or biventricular Arterial thromboembolism Arrhythmias Sudden cardiac death Systolic heart murmur Development of CHF
• Signs related to pulmonary disease (cough), vomiting • Dyspnea and lung infiltrates due to thromboembolism or spontaneous worm death • CHF—chylothorax (uncommon) • Syncope • Sudden cardiac death • CHF
Etiologic diagnosis
• • • •
Congenital (?genetic)—PPDH Infectious (coronavirus) Lymphosarcoma Immunosuppression (?)
Idiopathic DCM Taurine deficiency DCM Moderate to severe anemia Fulminant myocarditis
• Primary HCM: genetic or idiopathic cardiomyopathy
• Idiopathic RCM • Antecedent myocarditis • Chronic HCM with myocardial injury from coronary thromboembolism, coronary vascular disease, or neurohormonal injury • Prior HCM with progressive myocardial failure or infarction (?) • Myocarditis (?) • Congenital • Genetic?
• Dirofilaria immitis—adult parasites found in the pulmonary arteries and heart
• Cardiomyopathy • Degeneration of conduction system • Metabolic disorders • Hypoxia
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echocardiographic studies. The presence of significant SAM is invariably associated with an eccentric jet of mitral regurgitation (MR), readily seen by color Doppler examination. • Some chronic cases of HCM appear to evolve into a restrictive form of cardiomyopathy with either regional wall dysfunction (suggestive of myocardial infarction) or globally reduced LV systolic function (suggesting fibrosis or ischemia). Rarely, a cat will progress to a grossly dilated form of disease.
Normal AP A
Venous P( ) ⫽ edema PH RV failure LAP( ) ⫽ LAE
PA LA RA LV LVPW RV
IVS
Gallop 1
2
Hypertrophy ⫽ compliance Contractility (N, ) EDV( ) EDP( )
⫾LV gradient
Ischemia ⫽ poor relaxation HR ⫹ Arrhythmias ⫽ filling time
Figure 150-1. Diagrammatic representation of hypertrophic cardiomyopathy. Explanation of abbreviations can be found in text.
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Clinical Findings in Feline HCM The clinical presentation and examination findings in feline HCM are variable.
• Male cats are predisposed in some reports, and cats
•
•
•
•
•
LV ventricular distensibility. Tissue injury and fibrosis increase myocardial and chamber stiffness, requiring elevated LA filling pressures. This creates a situation of rapid early diastolic filling that becomes restricted as the stiff ventricle is distended. This correlates to a ventricular (S3) or summation (S3+4) gallop. As the left atrium distends, a loss of atrial contractility may develop. This reduces filling effectiveness and also predisposes to stagnant flow, formation of atrial thrombi, and atrial fibrillation. The roles of myocardial ischemia, infarction, and neurohormonal activation in the pathogenesis of progressive tissue injury and cardiac dysfunction are possible therapeutic targets because b-blockers and angiotensin system inhibitors blunt these detrimental responses. Demand ischemia—the sudden increase in myocardial oxygen demand that outstrips coronary blood supply—may contribute to the sudden development of left-sided CHF (flash pulmonary edema) so often observed in stressed cats with HCM. Ischemia impairs myocardial filling and contraction. For this reason, drugs with anti-ischemic effects (atenolol, diltiazem) are often prescribed in this disease. Systolic abnormalities are identified in some cats with HCM. These include subtle abnormalities detected only by tissue Doppler echocardiography; identification of apical or free wall-infarcts; regional wall motion abnormalities; or rarely, a global loss of LV systolic function. Dynamic and labile pressure gradients between the LV and aorta are often identified during ejection across the LV outflow tract. In most cases, systolic gradients stem from either septal and papillary muscle hypertrophy (midventricular obstruction) or systolic anterior motion (SAM) of the mitral valve causing mitral septal contact. These abnormalities can be documented on high-quality
•
of any age, including young cats, may be affected. As previously noted, certain breeds are at genetic risk for this disease, and it is not uncommon to examine affected cats that are related. Most often, the idea of HCM is prompted by auscultation of a murmur or gallop sound in a cat that has no other signs of heart disease. Nonspecific signs such as lethargy or anorexia may be reported.
▼ Key Point Most cats with HCM are healthy and asymptomatic for the disease.
• When symptomatic for left-sided CHF, a cat will
• •
•
demonstrate tachypnea and dyspnea, signs attributable to pulmonary edema or pleural effusion. Cough can occur but is an inconsistent sign. • Stress, fever, moderate-to-severe anemia, thyrotoxicosis, anesthesia, surgical procedures, trauma, or fluid therapy may precipitate CHF in a previously stable cat. • Prior therapy with corticosteroids may be another risk factor, though cause and effect are not firmly established. Urgent presentation may follow ATE to the terminal aorta, a forelimb, or cerebrum. Syncope or sudden cardiac death can occur but are less common than in the human disease. Sudden death may be explained by a coronary embolus, a ventricular arrhythmia, or if signs of CHF are unrecognized and the cat succumbs to hypoxia. Typical physical examination features of HCM include various combinations of the following: • Gallop rhythm—This is related to ventricular diastolic dysfunction or heart failure. • Systolic murmur—Murmurs are commonly due to MR or dynamic LV outflow obstruction. These murmurs can vary, often increasing in intensity with higher heart rates (and higher sympathetic tone). This finding is not specific because functional ejection murmurs also become more intense with increasing sympathetic drive, and functional
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murmurs are extremely common in cats of all ages. • Clinical signs of ATE—These are discussed below. • Auscultatory evidence of pulmonary edema or pleural effusion include increased bronchovesicular sounds, crackles or a fluid line, indicating CHF. • Prominent left apical impulse is a sign of possible LV hypertrophy. • Arrhythmias may be detected in some cats with HCM. ABP is usually normal in cats with HCM; however, some cats demonstrate profound hypotension associated with cardiogenic shock (along with hypothermia and bradycardia). • Low ABP also may be detected in the cat receiving diuretic and ACEI therapy for CHF. • Systemic hypertension may cause secondary LV hypertrophy; but HCM does not cause systemic hypertension.
Diagnostic Tests in HCM A number of routine diagnostic tests are helpful in recognizing and staging HCM.
• The electrocardiogram may be abnormal, but results are very inconsistent. Increased amplitude R-waves in lead II (exceeding 0.7–1.0 mV.) or a left axis deviation compatible with concentric hypertrophy or left anterior fascicular block may be observed. ▼ Key Point A normal ECG does not exclude a diagnosis of cardiomyopathy.
• Thoracic radiographs can be normal, but in moderate
•
to severe disease will demonstrate abnormalities. • Cardiomegaly (elongation), apex shifting (to the right or left), and LA enlargement (most evident as an auricular bulge on the DV view) are common findings. • In cats with CHF, the cardiac silhouette may be further enlarged by a small to moderate pericardial effusion caused by CHF. Cardiac silhouette size may be reduced considerably after diuretic therapy. • Prominent pulmonary vascular patterns may indicate pulmonary hypertension secondary to elevated LV diastolic pressure or fluid retention. • Increased lung densities are compatible with pulmonary edema and may be focal, patchy, diffuse, and often in more dependent areas than is typical for dogs with CHF. • Pleural effusion is common in acute CHF and in chronic, longstanding cases of heart failure. Evaluation of the effusion typically reveals a modified transudate and sometimes chylothorax. Routine CBC and clinical chemistries are unremarkable in most cases unless there is thromboembolism or intercurrent disease. The creatine kinase (CK), AST, and ALT all derived from skeletal muscle origin are
markedly elevated in thromboembolism to the limb(s). • Renal function may become impaired in cats with concurrent renal disease or in those treated for heart failure with diuretics and ACEIs. In many cases of advanced, treated CHF there will be mild to moderate azotemia. • Serum thyroxine is normal in cats with idiopathic HCM (unless they are manifesting two diseases). • A number of recent reports indicate the potential value of measuring serum or plasma cardiac troponin-I (cTN-I) since this protein increases in cats with HCM. This may become a useful screening test for identifying cats with HCM. ▼ Key Point In a large percentage of cats with systolic murmurs, echocardiography demonstrates a normal heart or trivial cardiac pathology. Heart murmurs in these cases are considered functional, likely related to sympathetic stimulation of the heart.
• Echocardiography —Definitive diagnosis and staging of HCM relies on echocardiography and Doppler studies interpreted in light of clinical findings. • Typical HCM is characterized echocardiographically by papillary muscle thickening, generalized thickening of the LV walls (generally to 6 mm or more in diastole), normal to decreased intraluminal size, and normal or increased systolic shortening fraction. • There is a marked heterogeneity to the pattern of hypertrophy, and not all wall segments may be involved. There may be generalized involvement with greater involvement of the septal or free wall segments. Some cats demonstrate markedly asymmetric hypertrophy mainly affecting the LV free wall. This finding usually portends development of CHF. Conversely, focal midventricular hypertrophy, even with midventricular obstruction, is usually benign. In older cats, isolated, focal, dorsal septal hypertrophy is a common finding. Whether this represents true HCM, or a growth response to aortic dilation and altered subaortic blood flow, is uncertain, but the condition is generally benign. • Increased left atrial size is a strong indicator of risk for ATE or CHF. • Doppler studies may demonstrate MR, dynamic obstruction, or abnormal LV filling patterns. Early diastolic dysfunction is characterized by abnormal myocardial relaxation, shown on Doppler studies as delayed LV relaxation in early diastole with a vigorous LA contraction to support late diastolic filling. • Progressive ventricular disease is associated with reduced chamber compliance. Doppler studies
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A PA LA
Venous P( ) Edema PH
( )LAP ⫽ LAE
RA ( )RA ⫾TR ( )RV
RV failure
LV RV
⫾MR ⫾Hypertrophy Fibrosis ⳱ stiffness N to ( ) contractility PVCs
•
Figure 150-2. Diagrammatic representation of restrictive cardiomyopathy. Explanation of the abbreviations can be found in the text.
•
often show a prominent early filling (E-) wave with trivial atrial contraction (A-) wave. These findings generally precede development of CHF. The differential diagnosis of feline cardiomyopathy is extensive (Table 150-2), including other cardiovascular and noncardiac disorders.
FELINE RESTRICTIVE CARDIOMYOPATHY (RCM) Feline RCM represents a heterogeneous disorder, and some latitude is used in placing cats within this category. The disorder described below might be interpreted by others as “intermediate cardiomyopathy” or as “unclassified cardiomyopathy.”
Overview and Pathophysiology of Feline RCM • The key pathologic feature is diffuse or multifocal endomyocardial or myocardial fibrosis.
•
• A common feature of RCM is striking biatrial dilation. • Systemic thromboemboli are common and LA and ventricular mural thrombi may be observed. • Histologic lesions include endocardial thickening, endomyocardial fibrosis, myocardial interstitial fibrosis, myocyte hypertrophy, and focal myocytolysis and necrosis. Arteriosclerosis of intramural coronary arteries may be recognized. The pathophysiology of RCM in the cat is unresolved but in many ways fits the “intermediate” label initially suggested by Harpster (Figure 150-2). • Echocardiography generally demonstrates mild systolic dysfunction, regional LV wall dysfunction, mild mitral or tricuspid valvular regurgitation, elevated LA pressures, and impaired LV distensibility with a “restrictive” filling pattern (tall but abbreviated E-wave; small A-wave). • Myocardial or endomyocardial fibrosis is the most likely explanation for these abnormalities. • Progressive increases of LA pressure develop, and the combination of ventricular dysfunction, atrial stiffness, and renal retention of sodium elevate pulmonary venous pressures and predispose to CHF and to pulmonary hypertension. • Pulmonary edema, pleural effusion, jugular venous distention, and hepatic congestion are typical manifestations of CHF in this disease. Clinically a diagnosis of “biventricular” CHF is often made. • Stasis of blood and the stretched LA places affected cats at risk for atrial thrombi and systemic thromboembolism.
Clinical Findings in Feline RCM • The clinical findings and diagnostic studies of RCM
• The pathogenesis of these lesions is undetermined. Antecedent myocarditis seems a likely, though unproven, initiating cause. In other cats, RCM clearly represents a late stage of HCM complicated by myocardial fibrosis or myocardial infarction. A variety of necropsy lesions have been observed in cats demonstrating clinical features of RCM. • LV endomyocardial fibrosis may be patchy, multifocal, or diffuse in distribution. • The left ventricle can exhibit regional hypertrophy, but overall the walls are not thickened. Often there is regional thinning or infarction of the LV free wall or apex interspersed with focal hypertrophy. Prominent papillary muscle hypertrophy or fibrosis is evident in some cats. • The LV cavity may be dilated but is usually normal to reduced in size. • Extreme endocardial fibrotic scarring can involve the mitral valve apparatus, lead to mid-ventricular stenosis, or obliterate the LV apex.
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• •
are in many ways similar to those of HCM with a few notable differences. • Most cats with RCM are middle aged or older and present with signs of CHF or ATE. • Some have previously been diagnosed with HCM. • The most consistent physical auscultatory finding is a loud gallop sound; murmurs are variable and less common than in HCM. • Premature ventricular or atrial beats are common, leading to an irregular rhythm and arterial pulse. • Signs of elevated systemic venous pressure, including hepatomegaly, pleural effusion, and elevated jugular venous pressure, are common. This may indicate RV dysfunction from RV involvement, pulmonary hypertension, or simply the generalized response of fluid retention in compensation for chronic left heart failure. The electrocardiogram is frequently abnormal showing cardiomegaly patterns, axis deviations, or conduction disturbances along with atrial or ventricular ectopy. Thoracic radiography is often impressive and characterized by LA dilation and cardiac elongation that is typical of LV enlargement.
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• The cardiac apex can be pointed or rounded. • Some cats manifest astounding biatrial enlargement. Pericardial effusion may further enhance cardiac silhouette size. • Pleural effusion is typical. Echocardiography demonstrates a number of possible abnormalities. The most characteristic feature of RCM viewed by echocardiography is marked LA or biatrial dilation, mildly reduced shortening fraction, and irregular or hyperechoic ventricular walls, +/bands spanning the LV. Often there is marked wall thinning typical of myocardial infarction. Infarction or severe myocardial fibrosis often creates a segmental, hypocontractile wall. Clinical laboratory tests of cats with RCM are not specific and most abnormalities are attributable to CHF, diuretic therapy, or thromboembolism as described above for HCM. A plasma or whole blood taurine should be measured in cats with decreased LV ejection fraction. Analysis of pleural effusates indicates a transudate, modified transudate, or chyle. The predominant cells present are macrophages, mesothelial cells, and small lymphocytes unless there is chylothorax, in which case, well-preserved neutrophils may be more numerous in response to the irritation.
•
• •
CHF. Exceptional cases are seen prior to onset of CHF. Cats with DCM are very likely to present in “cardiogenic shock” with sinus or junctional bradycardia, marked hypothermia, and severe hypotension (systolic ABP 240/min); cardiomegaly (increased QRS voltages); axis deviation (to the left or right); and premature atrial or ventricular complexes. • In most cases, the cardiovascular complications of hyperthyroidism regress following successful treatment of the underlying condition. LV hypertrophy usually decreases except in the cat with concurrent diseases of uncontrolled hypertension or with primary (idiopathic) HCM. Hypertension may improve or resolve as cardiac output decreases with reduction of thyroid concentration; however, other causes of hypertension may endure (especially primary renal disease), requiring medical management with amlodipine. Sinus tachycardia and premature beats usually resolve with initiation of anti-thyroid medication (methimazole, Tapazole). Persistent tachycardia may indicate concurrent CHF or a need for lowdoses of a beta-blocker (atenolol, 1/4 of a 25-mg tablet PO, once or twice daily). • In a small percentage of cats, the cardiac effects of hyperthyroidism are manifested in a more clinically significant manner. Thoracic radiographs will demonstrate that the heart is moderately to severely enlarged, and careful scrutiny may indicate a small (or even a large) pleural effusion. In these patients, a full cardiac workup is indicated. Re-examination of the patient may indicate prominent jugular pulses or overt jugular venous
•
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distension, compatible with plasma volume expansion and heart disease. In advanced hyperthyroidism, there can be sufficient cardiac dysfunction and volume expansion to cause more generalized cardiomegaly. Echocardiography often shows biatrial dilatation with normal or even reduced LV shortening fraction despite thickened LV wall measures. Affected cats should be evaluated for concurrent hypertension, anemia, or renal failure. Great care must be taken when administering fluid therapy as large pleural effusions may occur. Thoracocentesis may be needed. In cats with advanced cardiac disease, anti-thyroid medication should be initiated without delay; beta-blockers avoided to prevent cardiac depression; and an ACEI prescribed for cardiac protection, control of incipient (or overt) CHF, and for antihypertensive effects. • Therapy of hyperthyroid heart disease is predicated on controlling the underlying disorder and is discussed in Chapter 31. Treatment of CHF as a complication of hyperthyroidism is discussed below. Systemic hypertension—Cats with systemic hypertension may develop progressive LV disease with concentric ventricular hypertrophy. The left ventricle and small coronary arteries represent one of the “target organs” of high blood pressure. • Most healthy cats have systolic ABP measurements of 42 mm, are highly predictive of DCM. • Before accepting a diagnosis of occult DCM, the clinician should request more detailed echocardiographic measures of systolic function including LV short-axis shortening area (normally >48%), apical-to-basilar mitral annular motion, and volumetric estimates of LV ejection fraction (normally >45–50% in single plane models). Advanced Doppler methods of assessment are also available but require further definition. • Serial echocardiographic examinations are very helpful in establishing a downward trend in LV function. One should accept however that a 5% to 8% day-to-day variation is not uncommon in measured or calculated echocardiographic variables, so that large differences and trends are more meaningful than tiny up or down movements. Holter ECG—The 24-hour ambulatory ECG is a useful adjunct in the diagnosis of occult DCM or arrhythmogenic cardiomyopathy. The Holter recording may help establish the diagnosis in breeds highly prone to DCM with cardiac arrhythmias, such as Doberman pinschers. Most cardiologists consider >50 VPCs per day clearly abnormal. Some consider even lower numbers of VPCs abnormal. In dogs in which ventricular ectopy is evident from auscultation and routine ECG, a Holter recording provides more objective information about the severity of the rhythm disturbance. Other diagnostics—Future directions are likely to lead to more dependence on biomarkers (troponins, natriuretic peptides) for identification of myocardial disease in breeds at risk or when screening echocardiograms return ambiguous results. • Breeders are always hoping for tests that will provide the earliest recognition of disease, but it is unrealistic to expect phenotype testing, no matter how sophisticated, to identify all genetically affected animals within a breeding line.
•
•
• Many dogs that develop DCM do not demonstrate any signs until their later years, long after breeding has ceased. • In this regard, genetic testing will be a better answer for this particular group of clients and dogs. Management of occult DCM involves protection of the myocardium and management of serious arrhythmias. • An ACEI is prescribed for dogs with documented occult DCM based on echocardiography. Enalapril or benazepril at 0.5 mg/kg PO once or twice daily is appropriate. If LV function is very poor, b.i.d. dosing should be attained over a 2-week time. In the report of O’Grady and colleagues, in Doberman pinschers, treatment with enalapril roughly doubled the time duration between diagnosis of occult DCM and onset of overt signs of heart failure. • Beta-blockade with carvedilol or metoprolol also is cardioprotective and should be considered in dogs with occult DCM. In large breed dogs, long-acting metoprolol is usually well tolerated (1/2 of a 25-mg tablet, q12h). Carvedilol (Coreg) is relatively expensive, but dogs with occult DCM are more likely to tolerate it than dogs with overt CHF. Optimal target dosages are unknown, but initial dosing of 0.1 mg/kg PO q12h can be increased every 2 to 4 weeks to a target of 0.4 to 0.5 mg/kg q12h. If lethargy or exercise intolerance develops, insure that CHF has not been precipitated. • Blood pressure and renal function tests should be followed with these medications. • If cardiac arrhythmias are also present, a 24-hour Holter ECG should be done to assess arrhythmia severity (unless a routine ECG already shows that it is severe) and antiarrhythmic therapy considered. This is discussed more fully below under arrhythmogenic cardiomyopathy. Prognosis—Prediction of survival in occult DCM is difficult • One of the problems relates to that of precisely establishing a diagnosis of occult DCM. • Once unambiguous evidence of LV systolic dysfunction is identified (LVSF typically 15% or less in a dog with sinus rhythm and normal ventricular conduction), the development of CHF is likely within 6 to 12 months, even in the setting of cardioprotective drugs. • When less stringent criteria are set for diagnosis of occult DCM, many dogs will still be alive 2 to 4 years later.
DCM with Congestive Heart Failure Advanced cases of DCM usually present with a history of exercise intolerance and clinical signs of CHF.
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• Syncope related to ventricular arrhythmia or neural •
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mediated syncope (inappropriate bradycardia and vasodilation) may be reported by the owner. Physical examination reveals signs typical of CHF: • There can be marked weight loss and cachexia. • The arterial blood pressure usually is normal owing to vasoconstriction and neurohormonal activation, but it will be decreased in profound DCM with cardiogenic shock. • Auscultation may reveal atrial and ventricular gallops, systolic murmurs, or arrhythmias. • The intensity of the first heart sound and strength of the arterial pulse is often diminished, indicating reduced LV contractility and stroke volume. • Crackles of pulmonary edema or a pleural fluid line may be evident. • Clinical signs of left-sided CHF include tachypnea, respiratory distress, abnormal breath sounds, and coughing related to pulmonary edema. • Right-sided CHF is characterized by jugular pulses and jugular venous distension, hepatomegaly, and ascites. • Pleural effusion is common in biventricular failure. Diagnostic studies in advanced cases of DCM. • The standard 6-lead ECG may demonstrate a number of abnormalities: Cardiomegaly (wide or tall P-waves; wide or increased amplitude QRS complexes). Myocardial disease (wide QRS, slurred R-wave descent with ST-segment coving, small complexes in boxers and English bulldogs; left bundle branch block). Atrial or ventricular premature complexes; atrial fibrillation; or ventricular tachycardia. • The signal averaged ECG may demonstrate late potentials indicating increased risk for ventricular fibrillation. • Thoracic radiography reveals cardiomegaly and typical vascular and pulmonary parenchymal features of heart failure. Pleural effusion is common. • The echocardiogram shows left ventricular dilation with reduced LV shortening fraction. Other common findings include: Increased mitral E-point to septal separation. Decreased LV or septal wall excursions. LA dilation. Variable right-sided cardiomegaly. Doppler evidence of mitral regurgitation and tricuspid regurgitation. Possible evidence for pulmonary hypertension. Diastolic ventricular dysfunction with a restrictive filling pattern. Routine chemistry laboratory tests are usually normal or reflect intercurrent disease, consequences of CHF, or complications of CHF therapy. • Specialized blood tests for taurine may be performed in selected cases (mainly in American
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cocker spaniels, golden retrievers, Newfoundlands, breeds atypical for DCM, and in dogs receiving all lamb and rice diets). • Cardiac troponin-I is usually elevated along with increased plasma ANP and BNP. Therapy of CHF associated with DCM is discussed in detail in Chapter 147. Principles of Hospital Management of CHF include • Administer furosemide (2–5 mg/kg IV); follow this with repeated IV or IM injections. Alternatively begin a constant rate infusion of furosemide. • Provide supplemental oxygen by nasal prongs or other method appropriate for the size of the dog. If oxygen is unavailable, direct a fan to the facial region to minimize dyspnea. • Administer nitroglycerin ointment topically (1–1.5 inches for a large breed dog q12h). • Treat life-threatening pulmonary edema with afterload reduction using an infusion of sodium nitroprusside (0.5–2.5 mcg/kg/min is the typical dosage range) with careful attention paid to arterial blood pressure. Titrate the infusion to a systolic value of 90 to 100 mm Hg. A less effective alternative for load reduction is enalapril at 0.25 to 0.5 mg/kg PO q12h. • Perform thoracocentesis if there is a moderate to large pleural effusion. • For CHF with systemic hypotension begin an infusion of dobutamine (2.5–10 mcg/kg/min) for 24 to 48 hours. Dobutamine can have benefits beyond the period of infusion. In the setting of hypotension, arterial vasodilators such as nitroprusside or an ACEI should be avoided until the pressure is stabilized by dobutamine. In dogs with AF, digoxin (0.01mg/kg PO q12h for the first two doses; 0.005 mg/kg PO q12h thereafter) is prescribed to control the ventricular rate response. Principles of long-term home management of CHF include • Furosemide (2–4 mg/kg PO q8-12h) • Spironolactone (1–2 mg/kg PO once or twice daily) • Enalapril or benazepril (0.25 mg/kg PO q12h; increase to 0.5 mg/kg PO q12h after the first reevaluation) • Digoxin (0.003–0.005 mg/kg PO q12h) unless there are contraindications for therapy such as ventricular ectopy or renal failure. • Pimobendan (Vetmedin, 0.2–0.3 mg/kg PO q12h) if available, generally supplants digoxin except in AF when both drugs are administered. • A sodium-restricted diet. • A b-blocker may be considered to blunt the cardiotoxic effects of the sympathetic nervous system; however, heart failure must be well controlled first. Consider carvedilol (Coreg), starting at 0.05 to 0.1 mg/kg PO q12h; up-titrate the dose every 2 to 4 weeks to a target of 0.2 to 0.4 mg/kg PO q12h.
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Having pimobendan on-board facilitates uptitration of the beta-blocker. Unfortunately, the prescription drug (Coreg) is expensive. Dosing can be difficult in that dogs may not tolerate the negative inotropy of any b-blocker. When AF complicates CHF, diltiazem (up-titrate from 0.5–2.0 mg/kg PO q8h) is prescribed to control ventricular rate (see details in next section). Once heart rate is controlled, a long-acting form of diltiazem can be substituted (using the same total daily dose, but administered once or twice daily). Fish oil supplements containing omega-3 fatty acids may improve appetite and reduce cardiac cachexia (EPA—30–40 mg/kg PO daily; DHA—20–25 mg/ kg PO daily). In dogs with a diagnosis of hypothyroidism, ensure that the plasma level is checked to prevent iatrogenic hyperthyroidism, a condition that increases the demand for cardiac output and is arrhythmogenic. In general, even a giant breed dog with hypothyroidism should not receive more than 0.6 to 0.8 mg of L-thyroxin daily. For serious ventricular arrhythmias in the setting of CHF: mexiletine (5–8 mg/kg tid) plus a low dose beta-blocker. Amiodarone or procainamide are alternatives, but results have not always been favorable. Optimally, a Holter ECG should be used to assess therapy.
Arrhythmogenic Cardiomyopathy The term “arrhythmogenic cardiomyopathy” is a useful expression that refers to recurrent or persistent ventricular or atrial arrhythmias in the setting of a normal echocardiogram. The most commonly observed rhythm disturbances are PVCs and ventricular tachycardia (VT). However, atrial rhythm disturbances may be recognized including atrial fibrillation, paroxysmal or sustained atrial tachycardia, and atrial flutter.
• As discussed above, some dogs affected with arrhyth-
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mogenic cardiomyopathy clearly progress to classic DCM; however, many others do not. Thus, in some dogs, the key to clinical management of cardiomyopathy is control of the cardiac arrhythmia. ARVC—Arrhythmogenic cardiomyopathy with ventricular arrhythmias is particularly common in the boxer dog (and also in English bulldogs), where the term arrhythmogenic right ventricular cardiomyopathy (ARVC) is used to indicate the putative origin of arrhythmia. This term has largely replaced the “boxer cardiomyopathy” designation, but Harpster’s original classification is still useful. • Many boxers demonstrate only isolated PVCs (upright or with a left bundle branch block morphology in leads I and II). Many boxers carry this Type I designation for years without incident.
• Boxers often collapse or faint due to sustained VT; these were classified as Type II. • Some boxers will progress to develop more “classic” DCM as well, often with marked biventricular CHF. Ventricular and atrial arrhythmias are common in these Type III dogs. • Doberman Pinschers—The Doberman pinscher is another breed that often manifests ventricular ectopics prior to the development of overt myocardial failure (DCM). Many of these dogs die suddenly, without premonitory bouts of syncope and before the onset of heart failure. Others progress to classic DCM with left-sided or biventricular CHF. • Lone AF—The Irish wolfhound, Great Dane, and Newfoundland are giant breeds prone to AF without obvious impairment of LV contractility. Frequently, onset of AF is preceded by atrial premature complexes or paroxysmal atrial tachycardia or flutter. • This can be considered another form of arrhythmogenic cardiomyopathy, though it is more often designated as lone AF or occult DCM. • In one report, the average time interval between recognition of AF and CHF in Irish wolfhounds was about 2 years, but progressive DCM was a common feature of many dogs. • The results of other reports indicate that a relationship between AF and DCM is less clear. • Clinical Assessment—A data base should be obtained from dogs with suspected arrhythmogenic cardiomyopathy, including • Careful review of clinical signs relevant to the arrhythmia. • Medication history. • Complete physical examination. • CBC and serum biochemical profile (including electrolytes). • Serum troponin-I (cTn-I). • Routine ECG with a long rhythm strip. • Ambulatory (Holter) ECG, especially when the rhythm is characterized by only isolated atrial or ventricular premature complexes and there are no related clinical signs. The Holter ECG is particularly important in the asymptomatic patient with a rhythm strip that does not indicate a clear need for therapy. • Echocardiogram. • Thoracic radiograph (optional). From this information, the clinician should determine the most likely etiology of the rhythm disturbance and also attempt to judge the overall clinical significance of the arrhythmia. This assessment is pivotal to any therapeutic decisions.
• Differential Diagnosis—Arrhythmogenic cardiomyopathy must be distinguished from other causes of cardiac arrhythmias with normal left ventricular function.
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• Other recognized disorders associated with cardiac arrhythmias should be excluded, for example: Cardiac tumors (hemangiosarcoma) Electrolyte imbalance (hypokalemia, calcium disturbances) Systemic hypertension Splenic tumor Postoperative or traumatic ventricular arrhythmia (caused by ischemia and reperfusion injury). • A drug history should be obtained to ensure the arrhythmia is not caused by drugs or hormones that increase sympathetic tone (including excessive supplementation of L-thyroxin). • In those cases where LV systolic function is reduced, a revised diagnosis of DCM with arrhythmia is appropriate, so long as a tachycardiainduced cardiomyopathy is eliminated. Sustained tachyarrhythmias can cause a reversible tachycardia-induced dilated cardiomyopathy; this is most likely when the tachycardia is relentless, with few intervals of sinus rhythm. In such cases, it is valuable to assess LV function before and 3 to 4 weeks after control of the tachyarrhythmia. Once the rhythm or heart rate response has been controlled, a more objective assessment of ventricular function can be obtained. Management Approach —Successful management of isolated arrhythmias in dogs is similar to that associated with treatment of arrhythmias in CHF, but with the advantage that normal ventricular function allows a wider selection and higher dosages of anti-arrhythmic drugs to be used. Most of the drugs used to control heart rhythm also depress cardiac function. This effect limits anti-arrhythmic drug use in heart failure. In this regard, the clinician should be vigilant, since an arrhythmia may be the first sign of progressive myocardial disease, and DCM and CHF may develop in the future. • The first question to address is whether the arrhythmias should even be treated. For example, isolated PVCs or atrial premature complexes probably should not be treated with potent anti-arrhythmic drugs unless there have been signs related to collapse or syncope. • The goals of therapy are three: prevent sudden death; prevent or reduce clinical signs; and protect the ventricle from tachycardia-induced cardiomyopathy. • When anti-arrhythmic therapy is prescribed, discuss the adverse drug effects with the owner, the importance of follow up ECGs (including Holter recordings), and discuss the potential for pro-arrhythmia (worsening of the rhythm). • Remember that the duration of therapy depends on the likely etiology of disease. In many cases of arrhythmogenic cardiomyopathy, treatment will be lifelong.
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• Have the client record any symptoms that might be related to the arrhythmias or possible adverse effects of the drugs. • Follow up with the patient at regular intervals. Begin with a client interview and routine auscultation. Follow with a standard ECG (if an arrhythmia is detected). Consider the use of a Holter ECG. • When a patient is stable on routine ECGs and is receiving a consistent dose of medication, perform another Holter ECG. ▼ Key Point Evaluate the response to therapy with both a routine ECG and a Holter ECG.
• Lone Atrial Fibrillation —In dogs with lone AF, Holter data provide insight about the daily heart rate and the exercise heart rate. Average daily heart rates that exceed 90 to 95/min or moderate-level exercise heart rates that exceed 200/min are reasonable grounds for slowing the heart rate response to AF or referring for cardioversion. • Beta-blocker therapy for heart rate control—Control of the ventricular rate response can be achieved with atenolol (0.5–1 mg/kg PO q12h) or metoprolol (12.5 mg PO twice daily in giant breeds). These drugs are also potentially cardioprotective if the AF is a premonitory sign of future DCM. For the first three days, the initial dose of the betablocker should be 50% of the prescribed dose, to prevent undue lethargy. Thereafter, the drug dose can be titrated up over 2 to 4 weeks to achieve an appropriate average daily heart rate (generally in the range of 70– 80/min). • Diltiazem therapy for heart rate control—The use of this calcium channel blocker (dosed at 1–2.0 mg/ kg PO q8h) is effective in controlling heart rate but does not confer the “cardioprotection” of betablockers should the arrhythmia represent early DCM. An initial dose of 0.6 mg/kg PO q8h for the first day is recommended before increasing the dose. Diltiazem can be used in combination with a beta-blocker. A long-acting preparation of diltiazem can also be used if q8h dosing is difficult (using the same total daily dosage, divided q12h). • Digoxin therapy—While digoxin can be prescribed for lone AF, cardiac glycosides are less effective for controlling excessive exercise-related rates and are not recommended by us when there is no evidence of heart failure. • Cardioversion —The conversion of AF back to sinus rhythm is definitely possible in dogs with lone AF. The use of procainamide, sotalol, or amiodarone for this purpose has met with mixed, and generally unfavorable, results. However, electrical DC biphasic cardioversion is highly successful in the setting of lone AF, especially in giant breeds, provided lowdose amiodarone is administered following the
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procedure to maintain normal rhythm. This procedure requires referral to a cardiologist. Ventricular arrhythmias and ventricular tachycardia— Grading the severity of ventricular arrhythmias in terms of relative risk for sudden death is difficult but highly pertinent to management of these dogs. Once this had been done, and if a decision is made to treat the arrhythmia, a long-term plan for management should be established. • Relative Risk—Clearly the presence of clinical signs (collapse, syncope) is an indication to control ventricular tachycardia if the clinician is certain that a tachyarrhythmia is the basis for the episodes. In most cases, the situation is less clear cut, and the clinician must “grade” the arrhythmia in terms of severity. Isolated PVCs or runs of monomorphic, “slow” VT (usually 10,000 per day or about 7 PVCs per minute) they may be difficult to ignore. One well tolerated
approach is to prescribe a beta-blocker such as atenolol (0.5–1 mg/kg PO q12h), which will likely reduce the total number of ectopics but not create a pro-arrhythmic situation. • Ventricular Tachycardia —When treatment is elected, the choice of drug depends largely on personal preference, but some recommendations can be advanced. The Chapter “Cardiovascular Drugs” describes the clinical pharmacology, use, and adverse effects of these drugs. Sotalol (1–2 mg/kg PO q12h) is generally well tolerated in dogs and clearly improves Holter ECG recordings in some breeds (such as boxers). This drug should not be used in German shepherds with inherited ventricular ectopy. Mexiletine—An oral drug related to lidocaine, mexiletine (Mexitil) is an effective ventricular antiarrhythmic in many dogs (5–8 mg/kg PO q8h). We combine it with a b-blocker such as propranolol (0.5–1 mg/kg PO q8h) or atenolol (0.5– 1 mg/kg PO q12h). Anorexia, tremors, and vomiting are adverse effects. For unresponsive patients, sotalol (1 mg/kg PO q12h) can be substituted for the other beta-blocker. Amiodarone (Cordarone) is an effective drug for VT, but may be more pro-arrhythmic and carries a higher incidence of adverse effects than sotalol. With a long elimination half-life, a loading dose is used initially (5–10 mg/kg PO q12h) followed by a lower maintenance dose (4–6 mg/kg PO once daily). Procainamide —The use of a long-acting procainamide preparation (15–20 mg/kg PO q8h) is recommended as procainamide HCl has a very short elimination half-life in dogs. As with mexiletine, it may be more effective when combined with a beta-blocker.
SUPPLEMENTAL READING Basso C, Fox PR, Meurs KM, Towbin JA, Spier AW, Calabrese F, Maron BJ, Thiene G: Arrhythmogenic right ventricular cardiomyopathy causing sudden cardiac death in boxer dogs: A new animal model of human disease. Circulation 109(9):1180–5, 2004. Ferasin L, Sturgess CP, Cannon MJ, Caney SM, Gruffydd-Jones TJ, Wotton PR: Feline idiopathic cardiomyopathy: A retrospective study of 106 cats (1994–2001). J Feline Med Surg 5:151–9, 2003. Meurs KM: Boxer dog cardiomyopathy: An update. Vet Clin North Am Small Anim Pract 34:1235–44, 2004. O’Grady MR, O’Sullivan ML: Dilated cardiomyopathy: An update. Vet Clin North Am Small Anim Pract 34:1187–207, 2004. Smith SA, Tobias AH: Feline arterial thromboembolism: An update. Vet Clin North Am Small Anim Pract 34(5):1245–71, 2004.
Chapter
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Pericardial Diseases John D. Bonagura
The pericardium consists of two mesothelial-lined membranes: the visceral layer (epicardium) that is tightly adhered to the myocardium and the reflection of this membrane that forms the parietal pericardium. Between these is a space that contains the heart, origins of the major arteries, and terminations of the vena cava and pulmonary veins. The normal pericardial space also contains a very small amount of serous, lubricating pericardial fluid. The normal pericardium limits acute cardiac dilatation, maintains cardiac geometry, contributes to ventricular compliance and interdependence, reduces friction, and provides a barrier from inflammation. The pericardium is not essential to survival and can be removed surgically.
• The most important congenital forms of pericardial
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disease are congenital peritoneopericardial diaphragmatic hernia (PPDH) and the relatively rare congenital pericardial cysts (which will not be discussed in this chapter). The main acquired pericardial diseases in dogs and cats are pericardial effusion (PE), constrictive pericarditis, and constrictive-effusive pericardial disease. In many cases, PE is related to the presence of a cardiac or heart-base neoplasm. PE is the accumulation of excessive or abnormal fluid within the pericardial space. Cardiac tamponade refers to a state of cardiac compression and impaired filling from increased intrapericardial pressure. While mass lesions and cysts can compress the heart, the majority of cases are caused by a PE. The total volume within the pericardial space is finite. Pericardial fluid accumulation can occur only if the parietal pericardium stretches (increasing the volume of the pericardial space) or the volume within the cardiac chamber shrinks. Since the parietal pericardium contains few elastic fibers, it is not easily distended in the setting of acute fluid accumulation. For this reason, even small volumes of acute intra-pericardial hemorrhage can produce cardiac tamponade. When parietal effusion develops more gradually, the parietal pericardium and pericardial space expand substantially. Progressive pericardial stretching, combined with increases in venous pressure, permit a sit-
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uation in which large volumes of PE may develop. Effusions exceeding one liter may accumulate in larger dogs. Pericardial constriction occurs secondary to pericardial inflammation or scarring. The normally strong pericardium becomes thicker and fluid within the space is reabsorbed. Eventually the pericardial membranes act as a “shrink wrap” about the heart. Constrictive-effusive pericardial disease is a condition that includes both pericardial restriction and a small volume of pericardial fluid. Pericardial diseases can eventually cause congestive heart failure (CHF).
▼ Key Point Pericardial disease is one of the most common causes of right-sided heart failure in the dog. In older dogs, cardiac or heart-base neoplasia is a common etiology.
PERITONEOPERICARDIAL DIAPHRAGMATIC HERNIA PPDH is a defect in the embryologic septum transversum that separates the peritoneal from the pericardial space. Defects permit direct communication of abdominal organs or tissue with the heart. PPDH is relatively common in cats and also can develop in dogs. (Weimaraner dogs and schnauzers are predisposed.) Males may be predisposed. Himalayan and domesticated long-haired cats were more likely to be affected by PPDH in one study. In cats, it is typical for the hernia to contain mainly fat with one or more lobes of liver. In the dog the hernia may be subtle, containing only falciform fat, or there may be liver or loops of intestine contained.
Clinical Signs Many affected dogs and cats are without overt clinical signs, unless the hernia is large and there is a large volume of herniated abdominal content within the thorax. Infrequently, liver strangulation may lead to signs of discomfort. 1549
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Cardiac tamponade is a rare complication of PPDH. Entrapment of a loop of bowel or strangulation of the liver requires prompt recognition and surgical management.
PERICARDIAL EFFUSION Etiology • Acquired PE is very common in dogs and is observed sporadically in cats. Figure 151-1. Representation of the enlarged cardiac silhouette and double-density cardiac shadow caused by omental fat in a patient with peritoneopericardial diaphragmatic hernia. Arrows indicate the edge of the heart.
• Transudation into the pericardial space occurs sec-
Diagnosis Physical Examination
• The diagnosis may first be suspected during routine • • •
examination as heart sounds may be muffled or displaced. Often there is a systolic murmur, which may be functional or represent a concurrent cardiac defect. Abdominal palpation may reveal a concurrent umbilical hernia. In a small percentage of patients, there are clear anomalies of the sternum; these may be palpable or evident by radiography.
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Diagnostic Imaging
• Careful radiographic examination leads one to suspect the diagnosis (Fig. 151-1).
• One typically observes altered radiographic density in
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the caudoventral portion of the pericardial space. The heart and carina are usually displaced craniodorsally, as are pulmonary venous entries to the left atrium. Ventral to the caudal vena cava there may be a soft tissue shadow, the persistent mesothelial remnant that delineates the dorsal border of the hernia. Intestinal loops may create an unusual gas pattern within the mediastinum (pericardial space). Ultrasonography of the thorax, or a barium swallow (if intestinal loops are present) will be diagnostic.
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Treatment Treatment of PPDH is surgical and optimally accomplished at the time of spay/neuter. Surgical results have indicated a very favorable outcome. However, a PPDH often is an incidental finding in mature animals, and in these cases, surgical intervention may not be warranted unless intestines are contained within the thorax or the risk of herniation is deemed high. Consultation with an experienced surgeon can be helpful in these patients.
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ondary to PPDH, right-sided CHF, cysts, hypoalbuminemia, infections/toxemia, and causes of increased vascular permeability. These fluid accumulations tend to be relatively small and are often incidental necropsy or ultrasound findings. Small effusions do not to impair heart function. There are two noteworthy clinical situations that do merit comment. • Mass lesions at the heart base, including chemodectomas, can obstruct lymphatic drainage leading to a large and compressive transudative PE. • In cats with severe CHF, a very large PE may develop which may resolve with successful medical therapy of heart failure. Exudation into the pericardial space is usually caused by infective or non-infective pericarditis; these conditions are relatively uncommon in small animals. • Nocardia infection and perforating foreign bodies are potential causes of septic pericarditis in dogs and cats. • Fungal involvement of the pericardium is recognized with coccidiomyocosis in the dog or with opportunistic fungi in immunosuppressed dogs (e.g., aspergillosis). • Idiopathic, sterile (inflammatory) pericarditis can develop occasionally in the dog and also may be a consequence of recurrent, idiopathic intrapericardial hemorrhage. • Pericarditis in cats has been associated infrequently with feline cardiomyopathy but does occur in the polyserositis form of infection with feline infectious peritonitis virus. Idiopathic intrapericardial hemorrhage (with or without secondary pericardial reaction) is relatively common in dogs. This is a disorder of dogs typically less than 7 or 8 years of age, though it can occur in older dogs. As the name suggests, the etiology is unknown. Recurrent bleeding evokes an inflammatory reaction with pericardial thickening that can be difficult to distinguish from mesothelioma. Constrictive or constrictive-effusive pericardial disease can develop. Neoplasia of the heart, heart base, or pericardium frequently leads to a hemorrhagic effusion in dogs. • Hemangiosarcoma of the right atrium is especially common in dogs >7 years of age. Tumors can be isolated to the heart or multicentric with splenic
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involvement and pulmonary or distant metastasis. Metastatic disease is very common. • Aortic body tumor (or chemodectoma) originates from the base of the aorta and grows along the heart base, often along the path of least resistance. Metastatic disease is very unusual. • Ectopic (heart-base) thyroid carcinoma can cause a large heart base mass that is more likely to invade the myocardium. • Mesothelioma of the pericardium also occurs frequently, but the diagnosis is often difficult as discussed below. Progressive growth is typical and the pericardium may scar or constrict. • Lymphosarcoma of the right atrium and ventricles is an important cardiac neoplasm in the cat but is considered a rare cause of PE in dogs. It is frequently multicentric. • Metastatic carcinoma to the heart or pericardium is rare in dogs or cats. • Other cardiac tumor types (e.g., fibrosarcoma) have been reported but are rare. Left atrial rupture can occur in dogs with mitral regurgitation from chronic valvular endocardiosis. Linear tears develop within the stretched left atrial wall and occasionally transmural separation occurs leading to sudden cardiac tamponade. Uncommon causes of pericardial hemorrhage include blunt chest trauma; puncture of the heart (knife, bullet, and missile); coagulopathy, and as a complication of thoracocentesis. Chyle is a very rare fluid type in the pericardial space.
• Inflammatory disease within the pericardial space
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Pathophysiology • The cause and underlying pathophysiology of a pericardial disorder influences the clinical presentation. An understanding of these processes (Fig. 151-2) is instructive relative to diagnostic studies and therapy.
Cardiac and output Liver VC Ascites
A PA CVP JVP VC
ABP
LAP RAP
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LVDP LV
Filling RVDP Effusion Tamponade Pericarditis
Pr
Figure 151-2. Diagrammatic representation of pericardial effusion. See text for explanation. A, aorta; ABP, arterial blood pressure; CVP, central venous pressure; JVP, jugular venous pressure; LAP, left atrial pressure; LV, left ventricle; LVDP, left ventricular diastolic pressure; PA, pulmonary artery; Pr, pressure; RAP, right atrial pressure; RVDP, right ventricular diastolic pressure; VC, vena cava.
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may create clinical signs related to localized chest discomfort or constitutional signs of systemic inflammation. This is especially true in cases of septic pericarditis. Cardiac tamponade is the major pathophysiologic event in PE and represents the state of cardiac compression caused by increased intrapericardial fluid pressure. The normally negative inspiratory pericardial pressure becomes positive. This can be documented in clinical cases by a simple fluid manometer attached to a drainage catheter that has entered the pericardial space. • Tamponade is the mechanism by which low cardiac output and congestive heart failure (CHF) develop with PE. • Intrapericardial pressures can rise rapidly as the elastic limits of the membrane are exceeded (a steep pressure to volume relationship). • Increased (positive) intrapericardial pressure develops leading to diastolic collapse of the right atrium and the right ventricle along with compression of the vena cava. • Reduced right ventricular filling decreases preload and cardiac output; systemic hypotension occurs if sympathetic and fluid-retaining compensatory mechanisms are insufficient. • Syncope, collapse, or sudden death may occur if systemic hypotension is severe. • However, given sufficient time ABP is reestablished by combinations of heightened sympathetic discharge, systemic vasoconstriction, renal retention of sodium and water, and elevated venous pressures. • Extremely high venous pressures are characteristic of chronic pericardial diseases. Congestive heart failure, with a predominately right-sided component (ascites, pleural effusion, subcutaneous edema) is the consequence of chronic cardiac tamponade or constriction. • Additional hemodynamic features include equilibration of diastolic pressures in the ventricles, atria and great veins, and accentuated respiratory variation in ABP (pulsus paradoxicus). Diastolic equilibration of pressures requires cardiac catheterization for documentation. Pulsus paradoxicus is readily identified by palpation or ABP measurement with a Doppler flow system and is defined as an exaggerated fall in the ABP and pulse pressure during inspiration (see “Physical Examination”). Pulsus paradoxicus is explained by exaggeration of the normal respiratory-induced variation in right and left-sided cardiac filling. Left ventricular filling and systemic arterial pressure fall as right ventricular filling is augmented by negative inspiratory pleural pressures. Since the total volume with the pericardial space is finite, the increased venous return shifts the ventricular septum into the left
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ventricle during inspiration, reducing LV preload and stroke volume. As a result, palpable pulse pressure and measured systolic ABP decline during inspiration and increase with expiration as the process is reversed.
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Diagnosis The clinical diagnosis of PE follows a logical course from history and physical examination to selection of diagnostic tests. These studies should establish the diagnosis, etiology, and clinical significance of a PE. The electrocardiogram, thoracic radiography, fluoroscopy, abdominal ultrasonography, and echocardiography offer complementary information.
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▼ Key Point Echocardiography is the clinical gold standard for diagnosis of PE.
Pericardiocentesis can be both diagnostic and therapeutic in this disorder. Diagnosis in some patients requires surgical exploration with biopsy of the pericardium or surrounding tissues.
Signalment PPDH is more common in young dogs and cats but may be an incidental finding in older animals. Dogs >7 years of age are more likely to develop cardiac or heart base neoplasia. Golden retrievers and St. Bernard dogs are predisposed to idiopathic pericardial hemorrhage; brachycephalic breeds to chemodectoma; golden retrievers, Labrador retrievers, German shepherds, and many other breeds to hemangiosarcoma; golden retrievers to mesothelioma.
▼ Key Point Pulsus paradoxicus is an often-overlooked physical examination finding of cardiac tamponade.
• Right-sided CHF is more typical of PE and is associ-
• •
History Collapse or syncope are particularly common signs with acute cardiac tamponade (e.g., sudden hemorrhage). Dogs with a history of sudden collapse are more likely to have an underlying neoplastic cause. Syncope also can occur after diuretic therapy of right-sided congestive heart failure (because elevated venous pressures are needed to maintain cardiac filling and cardiac output and this compensation is lost with volume depletion).
• Clients may note abdominal distension from CHF. • Signs of illness may be present when there is underlying multicentric or metastatic neoplasia, septic pericarditis, or abdominal disease.
Physical Examination
• Patients with acute cardiac tamponade may be
•
hypotensive with palpable distention of the jugular vein. A systolic ABP 160 mm Hg (by the Doppler-flow method) are suspicious for hypertension. Values persistently greater than 180 mm Hg are diagnostic of hypertension, provided the dog is quiet, does not have tachycardia, and is not struggling. In cats, pressures >150 mm Hg are suspicious for hypertension, and values persistently greater than 160 mm Hg are considered diagnostic for hypertension (although some authors propose 170 mm Hg as the cutoff). Although “white-coat hypertension” related to the stress of examination has been reported in cats more frequently than dogs, both cats and dogs may have stress- or excitement-related elevations of blood pressure. In some animals, systolic pressures measured by oscillometric methods are about 10 to 20 mm Hg lower than those measured by Doppler-flow or direct arterial puncture methods. Thus, a systolic pressure of 170 mm Hg by an oscillometric method in a dogs is probably indicative of hypertension.
Diastolic Blood Pressure
• Diastolic ABP depends on systemic vascular resistance, heart rate, and cardiac output.
• Vasodilation associated with systemic diseases (anemia, hyperthyroidism) or arterial vasodilator therapy often lowers diastolic pressure. Conversely, spontaneous or
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• •
drug-induced vasoconstriction increases diastolic (as well as systolic) ABP. Diastolic pressure is detected with variable accuracy by oscillometric recording devices, but is more difficult to estimate with the Doppler flow method. Diastolic pressures exceeding 100 to 110 mm Hg are generally considered to be high, assuming that the animal is not excited during the recording. Values exceeding 120 mm Hg are generally treated for hypertension.
Mean Blood Pressure
• The mean arterial pressure is the geometric mean •
pressure during the cardiac cycle and is closer to the diastolic than the systolic reading. Oscillometric ABP devices measure this variable by detecting maximum oscillations in the blood vessel wall that correspond to the mean ABP. Provided the systolic and diastolic pressures can be recorded, the mean can be estimated as: 1
MAP = (diastolic pressure) + ( /3 [systolic pressure – diastolic pressure])
Arterial Pulse Pressure
• The pulse pressure, or difference between systolic
•
•
and diastolic ABP, is the basis for the palpable pulse identified during physical examination. The systolic and diastolic pressures are closely related in most circumstances so that each will increase or decrease proportionately. However, as indicated above, there are differences in the determinants of each pressure and situations are encountered where maximal and minimal pressures diverge. Aortic input impedance affects systolic ABP. For example, a potential reason for isolated systolic hypertension in older cats is the increase in aortic stiffness associated with idiopathic aortic dilation. Stroke volume has a marked effect on systolic ABP. Stroke volume is increased in cases of increased left ventricular filling (Frank-Starling effect) and increased sympathetic activity. Simply increasing stroke volume usually increases both systolic and diastolic pressures. But there are situations in which stroke volume increases but diastolic pressure decreases. This is especially likely in the setting of peripheral vasodilation, abnormal run-off of aortic blood flow, or when the heart rate is especially slow. Examples include: • Anemia • Thyrotoxicosis • Administration of arterial vasodilator drugs • Patent ductus arteriosus • Moderate to severe aortic regurgitation • Large arteriovenous fistula • Bradycardia (from drugs or chronic heart block)
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• In these situations the arterial pulse is often bounding and measurement of systolic pressure does not provide a comprehensive picture of ABP or perfusion pressure.
Etiology The precise mechanisms underlying hypertension in animals are not well understood except in experimental cases. Inability to regulate plasma volume (renal disease or hyperadrenocorticism), excessive adrenergic activity (pheochromocytoma), increased cardiac output (hyperthyroidism), and activation of the reninangiotensin system (glomerular disease) are likely candidates. The clinical associations of systemic hypertension should be appreciated because some disorders are treatable and management may minimize the need for antihypertensive therapy. While systemic hypertension is considered idiopathic or “essential” in some dogs and cats, a number of well defined clinical disorders have been associated with increases in ABP.
• Renal disease (particularly glomerular disease) • Hyperadrenocorticism—both Cushing’s disease in
• • • • • •
dogs (with glucocorticoid excess) and Conn’s disease in cats (associated with mineralocorticoid excess and hypokalemia) can lead to hypertension. Pheochromocytoma—a catecholamine-producing tumor of the adrenal medulla. Hyperthyroidism—both spontaneous disease in cats and iatrogenic disease in dogs Diabetes mellitus—in both dogs and cats Drugs—particularly the alpha-adrenergic agonists (such as phenylpropanolamine) that lead to vasoconstriction. Central nervous system (CNS) disorders—if associated with excessive sympathetic output. Idiopathic or “essential” hypertension—hypertension of undetermined cause.
▼ Key Point Systemic hypertension should be approached initially as a symptom or complication of another disease condition rather than a disease in itself. Only after underlying diseases have been excluded by appropriate testing can systemic hypertension be deemed “idiopathic.”
Clinical Signs Injury to arterioles or larger arteries or the direct transmission of pressure across the microcirculation is responsible for many of the clinical signs of hypertension. Additionally, the left ventricle must hypertrophy to maintain an increase in pressure work. Other clinical signs may be attributed to the underlying disease responsible for elevated ABP. ▼ Key Point The eyes, brain, heart, and kidneys are the main target organs of injury in cases of systemic hypertension.
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Brain Abnormalities
may be difficult to discern if hypertension is the cause or the consequence of renal disease and hypertension secondary to chronic renal disease promotes further glomerular damage.
• Cerebral or brainstem injury can result from hypertension owing to brain edema or hemorrhagic stroke. Clinical signs include signs of intracranial abnormalities, including abnormal mentation, neurologic deficits, head tilt, seizures, and coma. Presumably, as with human patients with hypertension, dogs and cats also develop “headaches” and this may account for some of the inactivity observed in affected small animals.
Ocular Abnormalities
Other Manifestations
• Other blood vessels can be injured in patients with hypertension.
• Epistaxis or bleeding from other sites also has been •
• Ocular abnormalities include retinal edema, hemorrhage, and detachments. These lesions can progress to blindness. Sudden blindness also may develop due to intraocular hemorrhage and hyphema. Recognition requires careful ophthalmic examination. Acute lesions are often superimposed on chronic retinal changes.
Cardiac Abnormalities
Diagnosis • When evaluating the hypertensive patient, search for •
• The heart generates the pressure in hypertension and •
•
• •
may also be injured by work and the high pressures distributed across the coronary vascular system. A systolic cardiac murmur of uncertain cause or an atrial (S4) gallop sound may indicate hypertensive heart disease. A systolic heart murmur may represent mitral regurgitation, flow into a dilated aorta, or dynamic ventricular outflow tract obstruction related to the hypertrophic disease. Concentric left ventricular hypertrophy and resultant cardiomegaly are the markers for chronic hypertension and can be identified by an echocardiogram (most sensitive), electrocardiogram (increased voltages or left-axis deviation), or thoracic radiograph (least sensitive). Coronary arteries also are injured from high arterial pressures. While congestive heart failure (CHF) stemming from hypertensive heart disease is relatively uncommon in dogs and cats, distinguishing left ventricular hypertrophy due to systemic hypertension from primary hypertrophic cardiomyopathy or hyperthyroid heart disease in cats can be a challenge. In dogs with chronic mitral valve disease, systemic hypertension increases the load on the left ventricle and increases the regurgitant volume. Persistent hypertension may prevent effective drug control of CHF in these dogs.
Kidney Abnormalities
• The kidneys are both a source and target of hypertension. Abnormal renal contour or size, proteinuria, and mild-to-moderate azotemia often are found in hypertensive animals. Hypertension injures glomerular vessels and damages renal tissues. In some cases it
reported with hypertension, especially the labile hypertension of pheochromocytoma. Chronic systemic hypertension can lead to aortic dilatation even in relatively young animals. Rarely, the aorta can tear leading to a dissection of blood between layers.
•
•
•
•
•
an underlying cause, as treatment may reduce the need for antihypertensive drugs. Consider the history, and determine if any medications that might increase ABP have been prescribed (such as thyroid hormone; alpha-adrenergic agonists; antihistamine combinations with vasoconstricting properties). At a minimum, perform routine diagnostic studies that include a full serum biochemical profile; complete urinalysis; serum thyroxin; and either abdominal radiographs or optimally an abdominal ultrasound examination with particular attention to the kidneys and adrenal glands. Diagnosis of hypertension requires measurement of ABP using either an arterial puncture attached to a pressure transducer or an indirect determination that uses a reliable technology and consistent technique. Both oscillometric methods and Doppler flow methods have been used successfully for measuring ABP in dogs. Systolic ABP is slightly underestimated by the oscillometric technique. Systolic pressures can be readily determined in cats using Doppler flow meter and occlusion cuff on a fore or hind limb. Oscillometric measurements can be obtained from cats using an appropriately-sized cuff at the tailhead in the sternal animal. Oscillometric measurements using a tail cuff may underestimate Doppler-obtained blood pressure. Care must be taken to consider normal variation in excited animals. Slight differences (5–10 mm Hg) between front and back limbs are normal in many animals, and the cuff size (diameter) is critical to prevent overestimation (too small a cuff) or underestimation (too wide a cuff).
▼ Key Point Since the development of systemic hypertension is usually an indication for life-long therapy, the diagnosis should be as certain as pos-
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sible. One or two high pressure readings in the setting of overt target-organ injury are sufficiently conclusive. However, in otherwise healthy animals, repeated measures—preferably over a number of days—should be obtained before establishing a diagnosis.
•
Technique for Measuring Blood Pressure Because technical details are very important in establishing a correct diagnosis, consider the following technical pointers for measuring blood pressure:
• Understand your recording unit and how it works. • Practice on numerous animals of different sizes. Prac-
•
•
• •
•
•
• •
•
tice improves skill and confidence. Train others to measure ABP and compare results. When using Doppler methods, learn to evenly decrease the pressure in the cuff and manometer. Measure ABP in calm animals that are comfortably restrained—in many clinical situations, it is advantageous to let the pet rest in its caretaker’s arms or lap for the measurements. Avoid measuring ABP in sedated animals. Have a supply of different-sized pediatric cuffs (e.g., #1–#6 pediatric cuffs) available. Place nonelastic, selfadhesive tape (such as Vetwrap) around the cuff to prevent slippage. Do not allow the cuff tubing leading to the manometer to kink. Measure the limb and use an appropriate sized cuff. The cuff must compress the limb evenly and occlude the artery with the approximate pressure recorded by the manometer. Use the smallest cuff appropriate for the limb size. Cuff diameter should be 40% of the limb circumference in dogs and between 30% and 40% of the limb circumference in cats. There is often a 10- to 20-mm Hg difference between next sized cuffs; wider variations suggest a technical error in recording or a cuff problem. Place the cuff around the distal radius (antebrachium), metatarsus or tailhead, around a relatively cylindrical portion of the appendage. Secure the cuff with wrap and attach it to the manometer. The inflatable bladder of the cuff should be positioned directly over the underlying artery. Place the patient in either lateral or sternal recumbency on a padded table, in a quiet room, with calm people. Gently restrain the patient, and give the pet time to acclimatize to the environment. Measure heart rate (HR). If it is high (e.g., >160 in a dog; >240 in a cat), try to help the animal relax before proceeding. Consider the site of measurement relative to heart level. The cuff should be at the level of the heart during measurement. ABP should not be measured in a standing animal unless a tail cuff is used. Inflate the cuff one or two times, slowly and gently, and allow the animal to experience what
•
•
•
•
• •
•
•
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will happen during measurement. Then record the pressure. With a Doppler method, place the crystal palmar (or plantar) and just distal to the large carpal (metatarsal) pad. Use subtle medial-lateral; anteriorposterior movements to detect the arterial signal. In cats and small dogs, or in patients with low blood pressure, use a light touch and copious ultrasound gel (not rectal jelly) to obtain an optimal acoustic signal. Clipping the hair can be helpful. Once a reading is obtained, repeat the measurement two more times noting the values and the concurrent HR. For Doppler flow systems, consider using earphones attached to the available output plug to reduce the loud, popping on/off sound of crystal movement, a noise that may startle the patient. At a minimum, do not place the audio speaker near the patient’s head. If using an automated oscillometric device, attach the cuff at the tail base, the antebrachium, or the metatarsus. Place the two cuff lines on either side of the artery (which is generally ventral and slightly medial). Measure HR with a stethoscope. It should correspond almost exactly with the automated monitor. If it does not, do not accept the displayed values. If the ABP value is “low” (systolic pressure < 90 mm Hg) try the next smaller cuff. If it is still low, go to the hind limb to verify the value. If the animal is not symptomatic, interpret the clinical situation and determine the most likely cause (for example, volume depletion, sedatives, or cardiovascular drugs). If the ABP is high (systolic pressures of >180 mm Hg in dogs; >160 mm Hg in cats), try the next sized larger cuff, as this will more easily compress the artery. If ABP is still high (or 200 mm Hg) or if target organ injury is evident (especially if there is ocular or cerebral disease), treat the hypertension before addressing the underlying disorder. Modest dietary sodium restriction is reasonable in treating hypertension, however, there is little evidence that severe sodium restriction will benefit most dogs and cats with hypertension. Attempting to control significant hypertension by diet alone is illadvised, and diet should be viewed as simply an adjunct to antihypertensive drug therapy. Drug therapy is generally required to treat hypertension. ABP can be lowered pharmacologically by reducing cardiac output or reducing systemic vascular resistance by dilating systemic arterioles. Therapy of systemic hypertension usually involves a stepwise approach, starting with a moderate dosage of one drug, increasing the dose to the desired effect as needed, or adding other drugs if required. Consider possible drug interactions when prescribing multiple drugs. There are also some particular situations wherein a specific regimen of drugs is more desirable, for example, in glomerular disease or in hypertension associated with pheochromocytoma. A variety of drugs can be prescribed for treatment of hypertension. These and specific pointers for clinical use, are described below (also see Chapter 146 for more details).
• The starting dose in cats is 1/4 of a 2.5-mg tablet PO •
•
•
•
•
•
•
once daily. In some cases, higher doses, up to 1.25 mg PO q12h, may be needed. In hypertensive dogs, amlodipine is dosed initially at 0.1 to 0.2 mg/kg PO q12h. Response is variable in dogs, though it tends to be very good at higher dosage ranges of 0.2 to 0.5 mg/kg PO q12h. Amlodipine has a relatively slow onset in dogs, and a prolonged duration of action. Unless urgent control of ABP is needed, increase the dose gradually, over several weeks to target ABP levels (usually 200 mm Hg systolic ABP) or associated with overt target organ injury (retinal or CNS signs). Comparison to ACEI: amlodipine is more effective than benazepril in lowering ABP, but is not considered directly renoprotective (aside from reducing ABP) in patients with significant proteinuria. The combination of amlodipine with benazepril or enalapril is reasonable in cats or in dogs with documented renal disease with proteinuria. Optimal ABP control may be facilitated by the amlodipine besylate, whereas benazepril may reduce proteinuria and delay progression of renal disease, especially in cats. Amlodipine is relatively expensive, compared to generic or veterinary enalapril or benazepril, and this may be an important issue in large dogs wherein combined therapy may allow for dose reduction of amlodipine. One approach to combination therapy is administration of amlodipine once daily in the morning and the ACEI once daily after noon. If higher doses of both drugs are needed, they can be administered together, twice daily. In addition, there is a combination capsule of 10 mg amlodipine/2.5 mg benazepril (Lotrel) that may be useful in some larger patients or might be compounded for individual use.
Drug Therapy for Systemic Hypertension Calcium Channel Blockers
▼ Key Point In most feline patients, amlodipine besylate is the drug of choice for treatment of severe systemic hypertension and is generally effective as a single therapy when dosed appropriately.
• Most clinicians initiate treatment of systemic hyper-
•
tension in cats with the calcium-channel antagonist/vasodilator amlodipine besylate (Norvasc). Dihydropyridines such as amlodipine and felodipine are more vascular selective than other calcium channel blockers such as diltiazem. Although diltiazem may slow heart rate, it is not recommended as a primary therapy for systemic hypertension. Amlodipine is an effective and well-tolerated therapy for hypertension in cats, based on a number of small, but convincing, clinical studies. Clinical experience indicates amlodipine at higher doses is effective for blood pressure control in dogs.
Angiotensin-Converting Enzyme Inhibitors
• Hypertension in dogs or cats can be treated with an
• •
ACEI, typically benazepril (human Lotensin in the United States; veterinary Fortecor in many other countries) or enalapril (veterinary Enacard). The initial dose of an ACEI for cats is between 0.5 and 1 mg/kg PO once daily. Dogs are usually treated at 0.5 mg/kg PO q12h.
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• An ACEI is particularly reasonable therapy in dogs
• In dogs with functional pheochromocytoma to
and cats with mild hypertension and concurrent glomerular disease (see Chapter 77). As indicated above, in patients with moderate to severe hypertension, an ACEI is best added to the calcium channel blocker amlodipine besylate.
control heart rate, arrhythmias, and blood pressure, a beta blocker (propranolol starting at 0.25 mg/kg PO q8h) should be administered only after initial therapy with the nonselective alpha-blocker phenoxybenzamine or the alpha1-adrenergic blocker prazosin (see below). If there is concern about beta-blockage, a brief infusion of the ultra–short-acting nonselective blocker esmolol (500 mcg/kg/minute infusion over 10 minutes) can be given as a test. In canine patients with concurrent non-cardiogenic pulmonary edema (“pheo-lung”) or a catecholamine-induced dilated cardiomyopathy, beta-blockers must be used with great care if at all to prevent further impairment of pulmonary or cardiac function.
•
Diuretics
• In comparison to human patients, diuretic therapy of •
•
• •
hypertension of dogs and cats is inferior and rarely undertaken. Diuretics decrease cardiac filling and cardiac output and lower ABP. However, diuretic monotherapy is rarely successful in controlling hypertension in small animals, and the resulting volume contraction can worsen azotemia and activate the renin-angiotensin system. Diuretics are more appropriate as adjunctive therapy in urgent hypertensive situations or in patients with where hypertension and congestive heart failure are both evident. A loop diuretic such as furosemide (1–2 mg/kg q12–24h) is most often used. This can be combined with spironolactone (0.5–1 mg/kg daily). If diuretics are used, they may be combined with an ACEI to limit further activation of the reninangiotensin-aldosterone system.
Other Vasodilators
• Sodium nitroprusside—an infusion of nitroprusside
• • •
Beta-Adrenergic Blockers
• Beta blockers decrease heart rate, cardiac output, • •
•
•
and plasma renin activity. These and possibly other (central) effects are antihypertensive. Currently, these drugs are used mainly in co-therapy of four conditions: As an add-on drug to amlodipine and an ACEI in the rare case of unresponsive hypertension that requires “triple therapy” for control. Atenolol is chosen in cats; atenolol or carvedilol in dogs. In cats, as an initial management for mild hypertension associated with protracted sinus tachycardia and high cardiac output due to hyperthyroidism, atenolol (1–2 mg/kg PO q12–24h) is typically chosen. The daily dose often requires down-adjustment (or drug discontinuation) to prevent bradycardia once the hyperthyroid state is controlled with methimazole. In hyperthyroid cats with severe hypertension, a combination of amlodipine and atenolol can be used. In dogs with degenerative valvular heart disease and systemic hypertension caused by hyperadrenocorticism or chronic renal disease, the use of carvedilol (Coreg; dosed at 0.5–1 mg/kg PO q12h) may control hypertension and provide cardioprotection. Carvedilol is also an alpha-adrenergic blocker. The drug is expensive, and cost may limit its use. In dogs with concurrent CHF, first control the condition with diuretics and an ACEI before starting carvedilol.
•
•
• •
•
represents aggressive antihypertensive therapy in the setting of severe target organ injury, hemorrhagic stroke, and uncontrolled CHF. This drug is used mainly in dogs. Dosing in systemic hypertension is generally higher than that required for treatment of CHF (see Chapter 147). Initially begin at 2.5 mcg/kg/min; the infusion rate can be increased every 15 minutes by 1 mcg/kg/min to a maximum of 20 mcg/kg/min. Some dogs are highly resistant to even high-rate infusions. Hydralazine—The direct-acting arterial vasodilator hydralazine (1–3 mg/kg PO q12h) can be used in unresponsive systemic hypertension. In animals receiving other antihypertensive medications, hydralazine therapy should be initiated at the low end of the dosing range and titrated up slowly as needed to control ABP. Prazosin—the alpha-adrenergic blocker prazosin is an older medication that is not used very often today. While somewhat inconvenient to dose (coming in only 1-mg, 2-mg, and 5-mg capsules), it can be highly effective in dogs unresponsive to other medications, particularly in the case of pheochromocytoma (when phenoxybenzamine or Dibenzyline is unavailable). The initial dose of prazosin may result in profound drop in ABP. Blood pressure should be monitored carefully during therapy. An initial dose of 0.5 mg (discard 1/2 of the capsule contents) can be given to most dogs. The usual dose in dogs is one 1-mg capsule, q8–12h; if higher doses are needed, the 2-mg capsule can be used. In cats, prazosin can be dosed at 0.5 mg PO, twice daily.
Follow-Up of Drug Therapy
• Reevaluate blood pressure regularly to ensure efficacy and prevent further organ injury.
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• Be diligent in looking for signs of drug toxicity, includ-
• Pulmonary embolism alters the normal relationship
ing hypotension (weakness, depression, syncope, progressive renal failure). Follow serum biochemistries with particular attention to indicators of renal function. Continue to manage the underlying condition if known. As there are no large, prospective studies to guide therapy, treat each patient individually.
between lung perfusion and ventilation, impairs right ventricular function, and may produce considerable pulmonary parenchymal damage.
• • •
THROMBOSIS AND THROMBOEMBOLISM General Concepts • Thrombosis refers to the local formation of a blood clot
• • •
•
• •
•
•
• •
within a blood vessel. Thrombi are potentially dangerous owing to obstruction of blood flow. Thrombi may develop in arteries or veins. Embolism is the sudden occlusion of an artery that occurs when an organized substance is carried from one point to another by the vascular system. A thrombus that is dislodged from the site of formation and is carried by the blood to another location is termed a thromboembolus. Systemic thromboembolism occurs when a thrombus is carried from a formation site in the left side of the heart to the termination of an artery within the systemic circulation. Pulmonary thromboembolism indicates that a thrombus formed within a systemic vein and dislodged, traveling with venous return across the right side of the heart and into the pulmonary arteries. Thrombosis may be initiated by different mechanisms (see Chapter 23). A systemic arterial thrombus typically starts with activation and aggregation of platelets (white thrombus). Arterial thrombosis frequently is initiated by injury to vascular endothelium or atrial endocardium. Stasis of blood and activation of clotting factors is thought to cause systemic venous thrombosis (red thrombus). Deficiencies of plasma antithrombin appear to predispose to venous thrombosis. Frequently venous thrombosis is associated with trauma, systemic inflammation, neoplasia, or other disorders favoring a pro-coagulant environment. A thrombus or embolus obstructs blood flow. Consequences of vascular obstruction include ischemia (lack of blood flow), infarction (necrosis of tissues nourished), and associated inflammatory reactions. Systemic arterial thrombi can be clinically silent or lifethreatening, depending on the specific vessels, tissues, or organ injured. Systemic venous thrombi obstruct systemic venous return, typically leading to local edema from impaired venous drainage.
Etiology A number of clinical disorders are associated with the development of thrombi or emboli in systemic arteries or veins (Table 153-1).
Pathophysiology • The pathogenesis of clinical signs depends on the
•
•
acuteness of injury, location of vascular obstruction, magnitude of thrombosis, collateral circulation, the tissue affected, and inflammatory mediators. The pathological consequences of ischemia or infarction of the systemic circulation include: Bone—Infarcts and zones of bone necrosis Brain—Ischemia-induced neuronal damage, edema, cell necrosis, hemorrhagic necrosis Limbs—Muscle ischemia, rhabdomyocytolysis, pain, peripheral neuropathy Myocardium—Myocardial ischemia or infarction, arrhythmias, abnormal ventricular wall motion, ventricular dysfunction, heart failure, sudden cardiac death Spinal cord—Neuronal degeneration, ischemic or hemorrhagic necrosis Kidney, adrenal gland, liver, spleen, or gut—Infarcts, hemorrhages, and parenchymal necrosis may occur with subsequent organ dysfunction Skin—Infarcts or cutaneous hemorrhages Pathological consequences of ischemia or infarction of the systemic venous or pulmonary arterial circulation include: • Lung—Pulmonary embolism and pulmonary parenchymal injury leading to ventilation-perfusion inequality in the lung. • A massive pulmonary embolus can obstruct the left or right pulmonary artery, severely limit cardiac output, and lead to hypotension, myocardial ischemia, and cardiac arrest. • Embolization of smaller pulmonary vessels can cause pulmonary infarction and also initiate the release of vasoactive chemicals that cause lung edema and inflammation. • Recurrent pulmonary thromboembolism reduces vascular cross-sectional area, increases pulmonary vascular resistance, and predisposes patients to chronic pulmonary hypertension. Acute or chronic pulmonary hypertension may result in signs of right-sided congestive heart failure (e.g., ascites, jugular distention). • Systemic veins—Obstruction of venous return, elevation of venous and capillary pressures, and edema of dependent tissues.
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Table 153-1. CAUSES OF THROMBOSIS AND THROMBOEMBOLISM Systemic Venous or Pulmonary Arterial Thrombosis/Thromboembolism
Systemic Arterial Thrombosis/Thromboembolism Cardiac Disease/Origin Feline cardiomyopathy (from the left atrium) Bacterial endocarditis (thrombi shed from the vegetation) Penetrating foreign body (needle, porcupine quill)
Hypercoagulable states Deficiency of antithrombin III (protein-losing nephropathies) Venous stasis Systemic inflammatory reaction
Atrial fibrillation (rare, except in cats) Missile—gun bullets or pellets that directly penetrate the vascular system Aberrant filarial parasites within systemic arteries (Dirofilaria immitis) Cartilaginous embolism of the spinal cord vessels Inflammation of the blood vessel wall (arteritis or vasculitis) Direct trauma or iatrogenic injury to arterial blood vessels Polycythemia Disseminated intravascular coagulopathy Torsion of a vascular pedicle (splenic torsion, mesenteric torsion) Artificial heart valve
Specific Disorders (Multiple Mechanisms) Cushing’s disease Immune-mediated hemolytic anemia Pheochromocytoma Verminous pulmonary arteritis (Dirofilariasis; Angiostrongylosis) Heartworm embolus from adulticide therapy (dogs) or spontaneous worm death (cats) Invasive neoplasm Diseases of veins Venous inflammation (phlebitis) from catheters, trauma, or drugs Thrombophlebitis—phlebitis with localized thrombus formation Fat emboli (from long bone fractures) Air emboli (from catheters or procedures such as cystography or cryosurgery) Retrograde venous embolus of the spinal cord Cardiac Disease/Origin Tricuspid valve thrombus Intracardiac tumor Intracardiac catheter Central line dialysis catheter Pacing lead
Diagnosis • The clinical diagnosis of thrombosis or embolism
•
•
•
requires a high level of suspicion. A sudden onset of clinical signs is typical of some conditions; other disorders are chronic in nature. The physical examination and laboratory signs of embolism depend on a number of factors, including the: • Vascular system involved and the tissues served by affected vessels. • Acuteness of the obstruction and magnitude of tissue injury. • Degree of collateral circulation available to support the affected region. Clinical abnormalities of thrombosis/thromboembolism range from subtle to obvious. Table 153-2 indicates some of the typical clinical and laboratory findings of various thrombotic or embolic diseases. Advanced imaging studies can be useful in confirming the diagnosis of arterial thrombosis or embolism. (see Chapter 4) The optimal examination varies with the suspected cause and tissues injured. In some cases the thrombus may be imaged directly; in others, perfusion deficits may be identified. Specialists should be consulted regarding specialized radiographic, ultrasonographic, echocardiographic, angiographic, and radionuclide studies.
• Clinical laboratory tests may demonstrate changes • • • • • •
•
attributable to decreased blood flow, organ ischemia, or tissue necrosis. The diagnosis of cutaneous and appendicular thrombosis/embolism usually can be made from physical examination. Cutaneous vasculitis usually leads to hemorrhages and edema. Aortoiliac thrombosis (Chapter 150) causes typical clinical signs (see Table 153-2) along with marked elevations in skeletal muscle enzymes. A diagnosis of superficial venous thrombosis or thrombophlebitis is made from inspection and palpation of superficial veins and tissues. Duplex Doppler ultrasound can be used to examine the vessel lumen and interrogate blood flow patterns in ambiguous cases. Myocardial infarction is diagnosed by characteristic ECG changes, progressive elevations of cardiac troponin-I, and by echocardiographic wall motion studies. Diagnosis of abdominal thrombosis or embolism may be difficult and require surgical exploration in the case of an acute abdomen. In many cases, however, abdominal ultrasound with Doppler studies may show the presence of a thrombus and associated obstruction to flow from the aorta.
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Table 153-2. CLINICAL FINDINGS IN THROMBOSIS AND THROMBOEMBOLISM Organ or Tissue Brain Spinal cord Limbs
Myocardium
Possible Clinical Findings Ischemic neuropathy or “thrombotic stroke” Fainting, falling, persistent neurologic deficits, coma, or seizures Rapidly progressive segmental spinal cord disease Signs depend on the level and extent of cord injury Sudden onset of limb weakness or paresis Affected limb(s) are pale, cold, and pulseless Absence of Doppler flow signals in affected arterial system Signs of ischemic lower motor neuron sensory and motor neuropathy Ischemic myopathy (pain, muscle contracture, possible late-onset edema) Bone infarcts may be associated with diffuse or shifting lameness or pain Discomfort, anxiety, tachypnea Premature ventricular complexes Hypotension Progressive heart failure Sudden cardiac death
Mesenteric and splanchnic vessels*
Possible abdominal pain (colic) Severe abdominal pain if aortic thrombus or mesenteric ischemia Acute onset of hindlimb weakness or paralysis if thrombus is in caudal aorta Acute renal failure if thrombus is cranial to kidneys Shock
Skin
Cutaneous hemorrhages, petecchiae, or ecchymosis may be evident Sudden onset of tachypnea or dyspnea Possible mild pyrexia Variable heart rate, but may be increased Acute, severe: hypotension from impaired right-ventricular function sudden death Chronic: clinical signs of pulmonary hypertension; possible right-sided CHF Loud S2; tricuspid regurgitation murmur in pulmonary hypertension
Pulmonary embolism
Systemic venous thrombosis
Cutaneous veins are swollen and may be “knobby” in appearance Superficial veins do not collapse, and may be warm and painful (thrombophlebitis) Subcutaneous edema in the tissues drained by the venous system Deep venous thrombosis involving the external iliac veins may lead to bilateral limb edema Bilateral jugular thrombosis can lead to intermandibular edema Thrombosis of the cranial vena cava causes intermandibular and pectoral edema, pleural effusion, or chylothorax There may be signs of pulmonary thromboembolism with any venous thrombus
*Thrombosis or volvulus of renal, adrenal gland, splenic, or splanchnic arteries
Laboratory Examination—Possible Findings MRI or contrast CT can demonstrate imaging abnormalities Secondary changes in CSF MRI or contrast CT can demonstrate imaging abnormalities Secondary changes in CSF Myelogram negative for extradural compression Duplex Doppler studies show lack of blood flow in affected system Angiogram positive for obstruction (rarely necessary) Elevated muscle enzymes (CK > > > AST > > ALT) Increased blood lactate Hyperkalemia and hypermagnesemia (with reperfusion)
ECG abnormalities (acute ST-T segment deviation, infarction patterns, ventricular arrhythmias) Elevated creatine kinase-MB Elevated serum troponin-I (cTn-I) Echocardiographic abnormalities (regional ventricular wall hypokinesis) Serum biochemical abnormalities may reflect end-organ injury (azotemia or an Addisonian crisis) Abdominal ultrasound can frequently identify the presence and location of the thrombus Duplex Doppler studies of abdominal vessels may be revealing Arteriography positive for obstruction (rarely done) Exploratory surgery may indicate vascular obstruction Ancillary testing in dogs with aortic thrombi often reveals protein losing nephropathy or Cushing’s disease Laboratory tests compatible with vasculitis Thoracic radiographs may show nonspecific parenchymal changes, localized pleural effusion, or redistribution of blood flow (away from affected areas), but may be normal Radiographic signs of heartworm infection when due to dirofilariais Large proximal thrombi and heartworms may be identified by echocardiography with imaging of the pulmonary arteries in some cases Distal thrombi must be diagnosed from radionuclide scans (perfusion defects) or pulmonary arteriography Normal d-dimer test argues against pulmonary thromboembolism Positive heartworm tests when due to dirofilariasis Duplex Doppler echocardiography positive for thrombus or altered pattern of blood flow pattern of blood flow
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• Pulmonary thromboembolism is a difficult diagnosis.
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It may be suspected from the history and medical workup, but there are no readily available tests for definitive diagnosis (see Table 153-2). Radionuclide scans that show perfusion deficits may be highly suggestive in the absence of concurrent lung infiltration or a history of chronic respiratory disease (as parenchymal disease may affect perfusion). Dopplerechocardiographic studies documenting acute, high velocity tricuspid and pulmonic insufficiency is suggestive of pulmonary thromboembolism in a patient at risk for this complication. D-dimer assay may be positive in patients with pulmonary embolism; however, this result is not specific and may be positive in other disorders. A negative ddimer test is more likely to be helpful in excluding pulmonary embolism.
•
• Heparin therapy—either unfractionated or fraction-
•
Principles of Therapy
• Principles of therapy for thrombosis and throm-
•
•
•
•
• Heparin is contraindicated in overt bleeding, particularly in cases of CNS hemorrhage. Effects of heparin on platelets are complex and thrombocytopenia may occur. Heparin is teratogenic and long-term use may lead to other adverse effects such as bone loss. Overdoses can be reversed with protamine sulfate.
Administration
• Recommended doses of unfractionated heparin vary
Formulations
• Unfractionated sodium and calcium heparin contain higher and lower molecular weight fractions. Unfractionated heparin binds with antithrombin (formerly AT-III) and inactivates a number of coagulation enzymes, most prominently activated thrombin (factor IIa) and activated factor X (Xa). This inactivation and the effects of the chosen doses can be measured using standard prothrombin and activated
ated (LMWH)—is indicated in patients known to be at high risk for development of thrombosis. Heparin does not dissolve clots but reduces the expansion of existing clots and may prevent new thrombus formation. Common disorders managed by heparin include arterial thromboembolism in feline cardiomyopathy, pulmonary thromboembolism, catheter thrombosis of central lines, thrombophlebitis, thrombosis of the jugular vein, suspected deep venous thrombosis in the limb or abdomen, protein-losing nephropathy (provided plasma transfusion has been administered to replenish antithrombin), and some cases of acute bacterial endocarditis. In severe heartworm disease, the use of heparin during the post-adulticide period may reduce adverse effects and limit secondary thrombosis around dead worms. Heparin is also used for short-term prevention of thrombosis in patients at high risk for delayed thromboembolism after surgery, trauma, or during recovery from systemic inflammatory diseases. Low-dose heparin is often used in the management of disseminated intravascular coagulopathy (discussed more fully in Chapter 23)
Contraindications
Heparin Therapy Heparin is a heterogeneous anticoagulant that inhibits coagulation and is used in the prevention and management of systemic venous and arterial thrombosis and thromboembolism. Heparin is administered by injection, either subcutaneously or intravenously (as a bolus or constant rate infusion).
partial thromboplastin times; both values are prolonged with unfractionated heparins. Low-molecular weight heparin (LMWH), including enoxaparin (Lovenox) and dalteparin (Fragmin) preferentially inhibit factor Xa. These anticoagulants do not prolong the standard coagulation tests, and dosing must be assessed by less-available anti-Xa assays.
Indications
Treatment
boembolism include prevention of further thrombosis, treatment of the underlying disorder, removal or disintegration of the clot when possible, and supportive care to damaged tissues. Thrombolytic therapy with tissue plasminogen activator has not been evaluated adequately in veterinary medicine. Although potentially effective in clot lysis, the high cost of the drug, the high incidence of adverse effects (including severe reperfusion hyperkalemia), the narrow window of time in which the medication must be delivered, and the high mortality associated with therapy of some conditions have limited the use of this medication in veterinary patients. A specialist with experience in thrombolysis should first be consulted. See Chapter 150 for details about treating thromboembolism associated with feline cardiomyopathies.
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widely, ranging from 10–75 IU/kg SC q8h for “prevention” of thrombosis or treatment of disseminated intravascular coagulation to 200 to 300 IU/kg SC q8h or by constant rate IV infusion for cases of established thrombosis (e.g., aortoiliac thromboembolism in cats). In management of acute thromboembolism, an initial IV dose of 250 to 300 IU/kg IV can be administered, followed by 150 to 200 IU/kg SC q8h (do not administer IM).
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• Obtain a baseline clotting profile and adjust the dose
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• •
to maintain the activated partial thromboplastin time (APTT) or prothrombin time at approximately 2 to 21/2 times baseline; alternatively, the international normalization ratio (INR) prothrombin time can be prolonged to a value of 2.0 to 3.0. Doses of LMWH for veterinary medicine require further definition, but for dalteparin and for enoxaparin consider 100 IU/kg SC q12h, though oncedaily dosing with dalteparin might be successful in some cases. In dogs dosages of 100 IU/kg to 200 IU/kg of enoxaparin have been used clinically. While LMWH can be used long term, drug expense and the need for one to two injections daily has limited the use of these drugs for long-term prevention of thromboembolism in dogs and cats.
•
•
• Aspirin Therapy
• Aspirin inhibits cyclooxygenase and blocks the for-
•
• • •
•
mation of thromboxane A2 in platelets. Aspirin has been recommended for the prevention of arterial thromboembolism in a number of conditions including feline cardiomyopathy, canine heartworm disease, bacterial endocarditis, and after cardiac valve repair in dogs. However there is little objective published information regarding risk/benefit of therapy. Aspirin probably has little, if any, role in the therapy of established thrombotic disease aside from a single dose administered within 2 hours of an acute arterial thromboembolic event. Doses of aspirin are empirical, and there are doubts regarding efficacy in preventing clots. Commonly used doses in dogs with heartworm disease are 5 mg/kg PO q12–24h. In cats with cardiomyopathy, the traditional dose is one coated, adult, low-dose regimen aspirin of 81 mg per cat, PO every three days. However, ultra-low dosages of 5 mg per cat daily may be equally effective. Gastric ulceration is a concern with any dose of aspirin. Do not use aspirin with other anticoagulants or with corticosteroids because of the risk of fatal GI bleeding. Concurrent gastric protection with famotidine may be helpful in animals with signs of gastric irritation on aspirin therapy. The use of buffered aspirin is preferred to limit gastrointestinal upset.
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•
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Other Drugs to Prevent Coagulation
• Clopidogrel bisulfate (Plavix) has been studied in
•
Warfarin Therapy
• Warfarin (Coumadin) inhibits vitamin K-dependent
•
factors important in coagulation. Extra-label warfarin has been used in home care of dogs and cats to prevent recurrent pulmonary thromboembolism in dogs and to inhibit arterial thromboembolism in cats with cardiomyopathy. There is more experience using warfarin in the cardiomyopathic cat that either has survived
an embolic episode or is at high risk for future thromboembolism. Tablets can be crushed and 1/2 of a 1-mg tablet PO daily is recommended. The second 1/2 of the same tablet should be used on the subsequent day (as the tablet formulation may not be uniform). Ideally, when initiating warfarin therapy the cat should first receive heparin at 100 IU/kg q8h for 24 to 48 hours because warfarin initially creates a hypercoagulable state. Dosing is difficult in cats because 1/2 of a tablet is often insufficient and 3/4 of a tablet may be too much! The use of split dosing (alternating 1/2 and 3/4 tablet dosages) may be useful; alternatively, it is reasonable to ask a compounding pharmacy to dissolve a number of tablets into a solution so long as the drug remains stable. The initial dosage for dogs is approximately 0.1 to 0.2 mg/kg, PO daily. As in cats, split dosing may be needed to obtain benefit while limiting risk of hemorrhage. The optimal dose of warfarin should prolong the prothrombin time; for example, the INR should be prolonged to a value of 2.0 to 3.0 when a standard value is available for cats in the testing laboratory. Otherwise, a 2x to 3x prolongation over the baseline time may be used. The urine and stool should be carefully evaluated for fresh blood, a finding that indicates a need for downward dosage adjustment. Because of difficulties in dosing, numerous drug and food interactions, and the need to frequently test the clotting times, the overall use of warfarin in small animals is very low. Animals receiving warfarin therapy should not be allowed outside exercise without supervision.
healthy cats. The drug inhibits ADP receptors on platelets. Based on studies in healthy cats, a possible dose of 1/2 of the human Plavix 75 mg tablet (containing 97.8 mg of clopidogrel bisulfate = 75 mg of clopidogrel base) may be a reasonable daily dose for a cat. There are no published studies of efficacy in cardiomyopathic cats or long-term studies of toxicity. Use is strictly extra-label. Abciximab is a glycoprotein IIb/IIIa receptor antagonist that inhibits aggregation of platelets. There are limited feline data regarding this drug and no published studies of clinical use.
Surgery or Catheter Intervention
• Surgical intervention is recommended infrequently in •
the management of vascular thrombosis. Some blood vessels are simply inaccessible. Surgery in cats with iliac thrombosis due to cardiomyopathy is complicated by the risk of anesthesia,
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•
•
•
development of disseminated intravascular coagulation, and the severe reperfusion hyperkalemia that can develop following revascularization. When suprarenal aortic thrombosis is suspected, abdominal ultrasound should be performed to evaluate the aorta and renal vessels. A positive study is an indication for surgery. Monitor ECG and serum potassium carefully intra-operatively and postoperatively. Other indications for surgery of arterial thrombosis include multiple splenic thromboses, suspected bowel infarction or volvulus, and bleeding/thrombosis with associated mechanical compression (e.g., extradural bleeding). Catheter-based interventions for the management of systemic or pulmonary arterial thrombosis/ thromboembolism have not advanced in veterinary medicine. The use of embolectomy (Fogarty) catheters has not been evaluated satisfactorily in animals, but this technique often is limited by the small size of many veterinary patients. Similarly, the cost and risks of localized thrombolytic therapy delivered via an intracardiac catheter has deterred advancement of this area.
VASCULITIS Etiology • There are a number of causes of arteritis (inflamma•
•
tion involving arterioles or arteries) and phlebitis (inflammation of veins). Arteritis may develop as a component of multisystemic infections, including infectious canine hepatitis, (see Chapter 16), feline infectious peritonitis (see Chapter 10), and Rocky Mountain spotted fever (see Chapter 17). Immune-mediated arteritis is believed to be important in feline infectious peritonitis, systemic lupus erythematosus, idiopathic vasculitis in Akita, spitz, and Doberman pinscher dogs, and following some drug reactions. Cutaneous manifestations of vasculitis are discussed in other chapters in this text. Phlebitis is generally related to injection of irritating drugs or chemicals or physical trauma caused by indwelling catheters, often with secondary infections. Thrombophlebitis indicates a situation of vein inflammation with accompanying thrombosis.
•
• Cutaneous hemorrhages • Coagulation disorders including thrombocytopenia and disseminated intravascular coagulopathy • Thrombosis and ischemic injury (see previous discussion of thrombosis) • Thrombocytopenia Vasculitis syndromes—Specific clinical vasculitis syndromes commonly seen in cats and dogs include: • Feline infectious peritonitis (see Chapter 10) • Verminous arteritis associated with dirofilariasis and Angiostrongylus vasorum infection (uncommon in the United States) • Rocky Mountain spotted fever, a tick-borne infection caused by Rickettsia rickettsii that affects dogs and human beings. Invasion of vascular endothelial cells causes vasculitis with mononuclear inflammation, microscopic thrombosis, and microinfarction. The condition is a multisystemic disorder that can affect the heart (myocarditis and arrhythmias), brain, blood (thrombocytopenia, neutropenia), and skin (edema, rash). Fever is common, and death may occur (see Chapter 17 for details).
Treatment • Treatment of vasculitis depends on the underlying cause.
• Management of FIP (see Chapter 10), systemic lupus
• • • •
Clinical Signs • Clinical signs of vasculitis are related to local and systemic release of inflammatory mediators, increased vascular permeability, and interruption of the vascular endothelial lining; potential signs include: • Fever • Subcutaneous edema
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erythematosus (see Chapter 24), immune-mediated vasculitis (see Chapter 24), and Rocky Mountain spotted fever (see Chapter 17) are discussed elsewhere in this text. Antimicrobials such as doxycycline are often administered empirically while awaiting results of serologic tests. Immunosuppressive doses of glucocorticoids are indicated for the management of some vasculitides. Thrombotic complications may require prophylactic heparin to prevent disseminated intravascular coagulation (see under “Heparin Therapy”). Treatment of thrombophlebitis of superficial veins is supportive. • Remove any catheters from the affected vein or limb. • Hot-pack the area and gently wrap the limb to reduce edema and self-trauma. • If there is risk of infection, select a broad-spectrum antibiotic. • If there is a concern about extension of the thrombus centrally, examine the vessel using duplex Doppler ultrasound. • Therapy with unfractionated heparin or LMWH should be instituted, especially if there is a likelihood of pulmonary embolism (see above). For home therapy either long-term LMWH or warfarin should be considered until the problem has resolved.
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• Chemical phlebitis can be treated with topical dimethyl sulfoxide (DMSO) and a corticosteroid ointment (q8–12h) with concurrent administration of prednisolone (0.5 mg/kg PO q12h).
ARTERIOSCLEROSIS AND ATHEROSCLEROSIS Etiology Arteriosclerosis
• Arteriosclerosis is a chronic arterial metamorphosis
•
•
•
characterized by loss of elasticity, luminal narrowing, and proliferative and degenerative lesions of the intima and media. Coronary arteriosclerosis, prominent in older dogs with endocardiosis, has been related to small and microscopic areas of myocardial fibrosis. Presumably this is due to ischemic necrosis and infarction of myocytes secondary to reduced perfusion. Similar lesions also have been observed in dogs with congenital subaortic stenosis, in dogs with diabetes mellitus, and in cats with hypertrophic cardiomyopathy. Small-vessel (intramural) arteriosclerosis may contribute to the morbidity of other cardiac disorders by causing ischemia-induced arrhythmias (e.g., premature ventricular contractions) or increased myocardial stiffness (e.g., hypertrophic cardiomyopathy, subaortic stenosis).
Atherosclerosis
• Atherosclerosis pertains to the arteriosclerotic state that
•
also includes fatty degenerative changes in the arterial wall. This is the typical underlying lesion of coronary artery disease in human patients, but is quite rare in small animals. Naturally occurring atherosclerosis occurs in severe canine hypothyroidism (see Chapter 31) when serum cholesterol concentrations are very high (generally >750 mg/dl).
•
Treatment • Treatment of arteriosclerosis includes treatment of
• •
•
Diagnosis • The diagnosis of arteriosclerosis and atherosclerosis
•
in clinical patients is difficult. Suspect this condition in patients with severe hypercholesterolemia and in association with the aforementioned cardiac disorders. Suspect acute myocardial infarction due to extramural coronary thrombosis with respiratory distress,
the underlying disease and the complications of ischemia. There are no published studies regarding management of acute coronary syndromes in dogs or cats. Drugs used in management of cardiovascular disease are discussed in Chapter 146. In cases of presumed myocardial infarction, administer oxygen and nitroglycerin ointment. Beta blockers such as carvedilol or atenolol decrease myocardial oxygen consumption and may be cardioprotective in animals with multifocal small vessel coronary arteriosclerosis. Their use in acute myocardial infarction is appropriate provided the patient does not demonstrate bradycardia, hypotension or signs of congestive heart failure. Calcium channel blockers (e.g., diltiazem, 0.5– 2.0 mg/kg, q8h PO) may act as a coronary vasodilator and prevent coronary vascular spasm.
VASCULAR NEOPLASIA Etiology • Vascular tumors can be primary or metastatic. The
▼ Key Point In canine and feline patients, clinically important hyaline arteriosclerosis is primarily related to the intramural coronary vasculature. The overall clinical significance of arterial degenerative changes in animals is relatively small compared with that in human beings.
ventricular arrhythmias, and severe ST-T segment changes on the ECG (particularly ST-T segment elevation). Echocardiography may reveal regional hypokinesis of the left ventricular free wall. Diagnosis is presumptive because coronary angiography is rarely performed in animals, but any of the above findings in conjunction with an elevated cardiac troponin-I (cTnI) concentration is suggestive of acute myocardial infarction. In some animals, acute myocardial infarction, superimposed on other heart disease, may lead to acute congestive heart failure. In the differential diagnosis of extramural coronary artery obstruction or thrombosis, rule out embolic complications of bacterial endocarditis.
•
•
•
endocardium and vascular elements of the heart also may become neoplastic. Primary arterial and venous tumors are uncommon: Carotid and aortic body tumors (chemodectomas) can act as space-occupying lesions in the neck, cranial thorax, or in the area of the ascending aorta and base of the main pulmonary artery. Aortic body tumors are an important cause of pericardial effusion in older dogs. These tumors also may be an incidental finding at necropsy (see Chapter 151). Tumors from vascular elements (e.g., hemangiosarcoma) and malignancies metastatic to blood vessels are described in detail in Chapter 28. Hemangiosarcoma is the most common intracardiac tumor. Multicentric involvement (e.g., liver, spleen, heart) is common. Pulmonary metastasis is frequent.
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• Tumor-related hemorrhage into the pericardial space •
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can cause cardiac tamponade. Intraluminal obstruction to venous return (usually of the caudal vena cava) causes ascites. This is most common with intracardiac hemangiosarcoma; however, other primary intracardiac tumors, such as myxoma and fibrosarcoma, can cause similar problems. When neoplastic lesions impinge on the cranial vena cava, jugular distention and subcutaneous edema of the head and neck may be seen. Extravascular neoplasms may invade blood vessels; for example, obstruction of the caudal vena cava can develop secondary to ingrowth of a pheochromocytoma from the adrenal medulla (see Chapter 33).
Clinical Signs • Clinical signs depend on the type and location of the
Treatment • Treatment of vascular neoplasia is complicated and requires surgery, and possibly chemotherapy (see Chapter 26). Most patients should be transferred to a referral hospital for advanced imaging, staging, and management.
ARTERIOVENOUS FISTULA Etiology • An arteriovenous (AV) fistula is a congenital or acquired communication between artery and vein.
• Congenital lesions tend to be multiple and involve the limbs or the thorax.
• A post-traumatic fistula is usually a single direct con-
tumor
• Signs of cardiac or vena caval neoplasia are usually
•
those of right-sided CHF (hepatomegaly, ascites, pleural effusion) or acute cardiac tamponade (hypotension and collapse). Compression of the cranial vena cava (e.g., from mediastinal lymphoma) can cause intermandibular and ventrocervical subcutaneous edema.
Diagnosis • The differential diagnosis of caudal vena cava • • • • • • • •
obstruction includes idiopathic sclerosis, neoplasia, kinking, or trauma of the caudal vena cava. Imaging studies are very useful in diagnosis. (see Chapter 4) Radiographic studies may demonstrate mass lesions; however, the cardiac silhouette may be radiographically normal when the obstruction is intraluminal. Nonselective angiography (peripheral venous injection) or selective angiography may demonstrate vascular obstruction or interruption. Ultrasound studies may demonstrate dilated hepatic veins typical of obstructed hepatic venous drainage or solid tissue mass lesions around blood vessels. Echocardiography can reveal intracardiac mass lesions. Computerized tomography and magnetic resonance imaging angiography are advanced methods to evaluate vascular mass lesions. Radiopharmaceutical studies may be helpful to identify tumors of neural crest origin (chemodectoma, pheochromocytoma). Although blood tests are not diagnostic for vascular tumors, an elevated cTnI concentration in an animal with pericardial effusion is supportive of the presence of hemangiosarcoma. Patients may be anemic due to blood loss in cases of severe hemopericardium, or exhibit the nonregenerative anemia of chronic illness. Evidence of disseminated intravascular coagulopathy may be noted.
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nection associated with abnormal healing of the injured blood vessels; a limb, an ear, or even the tail may be affected. Rarely, declawing operations and tumors have been associated with AV fistula formation in the feline paw. Thyroid carcinoma may lead to a cervical AV communication in dogs. AV fistulas also have been reported secondary to other tumors. An hepatic AV fistula is a special type of congenital vascular malformation. This condition usually is associated with portal hypertension and ascites (see Chapter 71). Multiple congenital aortic to pulmonary fistulas may create a pathophysiology similar to patent ductus arteriosus.
Clinical Signs • Clinical signs of an AV fistula include local vascular
•
•
changes (due to venous hypertension) and cardiac manifestations (due to increased cardiac output required to perfuse the shunt). Any combination of the following signs may be observed: AV fistulas are most common in a limb; associated signs may include: subcutaneous edema, pain, inability to use the limb, a warm or cool extremity, distended and tortuous superficial veins, and abnormal tissue growth. A continuous murmur (bruit) may be detected by auscultation over the affected area as blood shunts continuously through the fistula.
▼ Key Point A positive Branham sign may be present in large AV shunts; slowing of the heart rate follows digital occlusion of the artery as the result of a sudden increase in arterial resistance and pressure.
• Multiple aortic-to-pulmonary AV fistulas usually lead to left heart enlargement from increased venous return. Pulmonary overcirculation may be evident.
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However, due to the low resistance of multiple shunts (that eventually enter the pulmonary veins), a heart murmur may be absent making the initial diagnosis very difficult. A large AV fistula will increase cardiac output (equal to the shunt flow). Compensation may be manifested by tachycardia, cardiomegaly, and increased pulmonary vascularity Increased cardiac work, cardiac dilation, renal retention of sodium and water, elevation of venous filling pressures, and eventually congestive heart failure (in the case of large shunts).
• The prognosis is good for animals with acquired AV
Diagnosis • Diagnosis of AV fistula is made by clinical signs, ultra-
Fox PR, Petrie JP, Hohenhaus A: Peripheral vascular disease. In Ettinger SJ, Feldman E, (eds.). Textbook of Veterinary Internal Medicine, 6th ed. Philadelphia: Saunders, 2005. Henik RA: Diagnosis and treatment of feline systemic hypertension. Compend Cont Educ Pract Vet 19:163, 1997. Littman MP: Spontaneous systemic hypertension in 24 cats. J Vet Intern Med 8:79–86, 1994. Olivier NB: Pathophysiology of arteriovenous fistulae. In Slatter DH, ed.: Textbook of Small Animal Surgery. Philadelphia: WB Saunders, 1985, p 1051. Smith CE, Rozanski EA, Freeman LM, Brown DJ, Goodman JS, Rush JE: Use of low molecular weight heparin in cats: 57 cases (1999–2003). J Am Vet Med Assoc 225:1237-1241, 2004. Smith SA, Tobias AH, Jacob KA, Fine DM, Grumbles PL: Arterial thromboembolism in cats: acute crisis in 127 cases (1992–2001) and long-term management with low-dose aspirin in 24 cases. J Vet Intern Med. 17:73-83, 2003. Smith SA, Tobias AH. Feline arterial thromboembolism: an update. Vet Clin North Am Small Anim Pract. 34:1245–1271, 2004. Stepien RL, Rapoport GS, Henik RA, Wenholz L, Thomas CB: Comparative diagnostic test characteristics of oscillometric and Doppler ultrasonographic methods in the detection of systolic hypertension in dogs. J Vet Intern Med 17:65–72, 2003.
•
•
sonography (including Doppler studies), and selective angiography if necessary. These studies may generally require transfer of the patient to a referral hospital.
Treatment • Ligation or removal of the shunt is the treatment of choice.
• The surgical approach usually is guided by imaging and vascular contrast studies.
• Other methods of vessel occlusion (e.g., catheterdelivered “umbrellas” or “coils”) have not been used routinely in veterinary practice but can be useful in single fistulas that are clearly demarcated by angiography.
fistulas that are not associated with malignancy.
• Congenital AV fistulas may be problematic and involve difficult surgical procedures.
• Limb amputation may be necessary if the exact loca•
tion of the shunt cannot be isolated and ligated or if the limb becomes devitalized (see Chapter 116). Management of hepatic AV fistulas may require partial hepatectomy of the involved lobe.
SUPPLEMENTAL READING
Chapter
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154
Congenital Heart Disease Henry W. Green / John D. Bonagura
ETIOLOGY
•
• Congenital heart disease (CHD) is a general term
•
•
indicating malformation of the heart or great vessels. CHD is present at birth and represents the most common cause of cardiovascular disease in animals younger than 1 year of age. Diagnosis, staging, and management of CHD can be complicated, and the purpose of this chapter is to offer a framework for recognition and understanding of common cardiac malformations in dogs and cats. Common defects based on prevalence in referral centers include: • In dogs: patent ductus arteriosus (PDA), subvalvular aortic stenosis (SAS), pulmonic stenosis (PS), atrial and ventricular septal defects (ASD, VSD), mitral and tricuspid valvular dysplasia (malformation), persistent right aortic arch, tetralogy of Fallot, and cor triatriatum dexter. • In cats: atrial and ventricular septal defects, mitral and tricuspid valve dysplasia, patent ductus arteriosus, tetralogy of Fallot, and aortic stenosis. • Congenital peritoneopericardial diaphragmatic hernia is a common defect of the diaphragm and pericardium (see Chapter 151).
CLINICAL APPROACH The vast majority of CHD cases are recognized initially by cardiac auscultation. A routine 6-lead electrocardiogram (ECG) and thoracic radiographs will also provide diagnostic information in cases of moderate to severe CHD; however, these studies are likely to be negative in mild disease. Definitive diagnosis requires advanced echocardiography with Doppler studies. The general approach to diagnosis based on initial auscultation findings is summarized in Figure 154-1 along with typical ECG and radiographic features. The following are some pointers regarding diagnosis and assessment of CHD in dogs and cats.
• As a general rule, soft ejection type murmurs in
▼ Key Point Most congenital heart defects are considered to have a genetic basis, but the mode of inheritance is most often unknown or impacted by multiple genes.
• Even in cases of suspected autosomal dominant inheritance, the penetrance of the lesion may be incomplete, making clinical recognition difficult or impossible. Furthermore, there are no genetic tests available for detection of carriers. This situation makes genetic counseling difficult. • Animals with even mild CHD should not be bred. • Dogs or bitches with normal cardiac phenotype that produce CHD-affected puppies in more than one litter should be removed from breeding programs. • Breeding dogs with equivocal cardiac status based on echocardiography and Doppler studies should
be bred only if other important characteristics are considered strong or outstanding. Other factors—including environmental, chromosomal, infectious, toxicologic, nutritional, and drugrelated—may result in CHD; however, little is known concerning the direct cause and effect relationships in dogs and cats.
•
otherwise healthy puppies or kittens can be followed through the vaccine sequence. Increasing murmur intensity, other physical abnormalities (stunted growth, cyanosis), or any suggestion of clinical signs (exercise intolerance, dyspnea) should prompt immediate evaluation by a veterinarian with experience in congenital heart disease. A loud systolic murmur, a diastolic murmur, or a continuous murmur is not likely to be innocent and should be evaluated promptly. The signalment, physical examination findings, 6- or 9-lead ECG, and thoracic radiographs may provide a provisional diagnosis and help to guide any initial treatment plans. • PDA, VSD, SAS, and mitral valve malformation are more likely to lead to left-sided cardiomegaly, a finding that may be evident on ECG or thoracic radiographs. With ASD, PS, and tricuspid valve malformation, right-sided cardiomegaly might be identified. 1589
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Figure 154-1. Typical findings in congenital heart disease; exceptions to these findings are common. ASD, atrial septal defect: ECD, endocardial cushion defect; IVCD, intraventricular conduction defect; LAE, left atrial enlargement; LVE, left ventricular enlargement; LVH, left ventricular hypertrophy; MPA, main pulmonary artery; PDA, patent ductus arteriosus; PMI point of maximal intensity; RAE, right atrial enlargement; RBBB, right bundle branch block; RV, right ventricle; RVE, right ventricular enlargement; RVH, right ventricular hypertrophy; SAS, subaortic stenosis; VSD, ventricular septal defect.
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• Radiographs are particularly helpful for recognizing pulmonary vascular changes and congestive heart failure (CHF). However, such examinations are not definitive in terms of diagnosis, and do not substitute for expert evaluation using echocardiographic techniques.
bronchoesophageal collateral vessels that mix lowoxygen venous return with pulmonary venous blood. • A typical consequence of shunt reversal is progressive secondary polycythemia, a complication that can lead to a markedly elevated hematocrit and hyperviscosity syndrome. • Advanced pulmonary vascular disease changes the examination findings to that of marked RV hypertrophy, pulmonary artery dilation, and reduced size of the left heart chambers. In the case of shunt lesions, the right-to-left shunt serves as a needed pressure-relief valve for the right side, but predisposes to arterial desaturation and polycythemia. This situation is generally irreversible and explains why a “reversed” PDA cannot be corrected surgically without fatal consequences.
▼ Key Point Definitive diagnosis and staging of CHD requires advanced imaging with echocardiography and Doppler studies. In ambiguous cases, cardiac catheterization and angiocardiography are necessary. Advanced cardiac evaluations are best obtained by referral to a cardiologist.
• When a dog or cat is suspected of having CHD con-
•
sider the following points: • Animals presenting with one defect may have concurrent or complicating cardiac issues. For example, combinations of outflow tract obstruction and atrioventricular valvular dysplasia generate a less favorable prognosis. In chronic volume overload, as with uncorrected PDA, progressive myocardial failure or development of atrial fibrillation can impact prognosis negatively. • Young animals with relatively severe lesions often appear totally normal to the client and may remain compensated for months to years. The presence of exertional symptoms is generally an indication of serious CHD. Delaying cardiac evaluation until the onset of clinical signs is a serious clinical error, as by that time therapeutic options may be limited or less effective. • Early therapeutic intervention may slow or eliminate irreversible myocardial damage and prevent heart failure. For example, after successful closure of a PDA, most dogs will live a normal life without need for cardiac follow-up. • CHF or arrhythmic death may occur suddenly and unexpectedly in dogs or cats with CHD. Progressive pulmonary vascular disease develops in some patients with left-to-right shunts (PDA, VSD, ASD, aorticopulmonary window) or congenital mitral stenosis. Elevated vascular resistance can cause severe pulmonary hypertension (PH) in these patients. • PH due to vascular injury and high resistance increases pulmonary artery, right ventricular (RV), and right atrial pressures; reduces left-to-right shunting; and limits venous return to the left atrium. • This development usually improves symptoms (and facilitates growth), but the benefit is temporary. Severe pulmonary vascular disease eventually limits cardiac output, causes progressive exercise intolerance, and often leads to arterial desaturation (a reduced oxygen content due to low partial pressure of oxygen). Desaturation is related to either right-to-left shunting of blood across a defect (Eisenmenger’s physiology) or development of
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DIAGNOSIS The balance of this chapter discusses the general approach to recognition of cardiac malformations from the perspective of the first examiner. Key points about prevalence, physical examination, and interpretation of diagnostic studies is presented along with an overview of management options for common defects. The reader is referred to the supplemental reading for a more complete review of specific defects and various complications of CHD. Despite the technical advances in cardiology, a thorough history and physical examination is an essential part of the diagnostic process. In the evaluation of CHD, cardiac auscultation is especially important (Fig. 154-1), and experienced examiners can often establish a tentative diagnosis based on auscultation and breed predisposition (Table 154-1).
Signalment and History Age, breed, and sex should be considered when evaluating animals for suspected CHD. As many specific breed predilections are identified—especially in dogs— a predisposition can be useful in formulating the differential diagnoses. Table 154-1 is a guide to breed for the most commonly recognized disorders, but is not a comprehensive listing.
• CHD is most often an incidental finding, discovered at the time of initial immunization.
• Most animals with CHD are asymptomatic when first
•
examined, often in the face of hemodynamically severe defects. Thus do not conclude that the defect is mild in a patient with an unremarkable history. Stunted growth often indicates a patient with CHF or a right-to-left shunt (cyanotic heart disease). Signs of CHF may include coughing, exercise intolerance, orthopnea, tachypnea, respiratory distress, or abdominal distension.
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Table 154-1. BREED AND SEX PREDILECTIONS FOR CERTAIN CONGENITAL CARDIAC DEFECTS* Defect Patent ductus arteriosus (PDA) Pulmonic stenosis (PS) Subaortic stenosis (SAS)
Ventricular septal defect (VSD) Atrial septal defect (ASD) Mitral dysplasia Tricuspid dysplasia Tetralogy of Fallot
• A precordial heave is an apical impulse that is
Predilection Poodle, Bichon friese, collie, Pomeranian, German shepherd, Shetland sheepdog, and many other breeds (female : male, 2.2 : 1) Beagle, bulldog, fox terrier, miniature schnauzer, Chihuahua, Samoyed, Labrador retriever Newfoundland, boxer, German shepherd, German shorthaired pointer, golden retriever, rottweiler, bull terrier English bulldog, springer spaniel
•
Cardiac Murmurs
• Murmur characteristics may be suggestive of a par-
Samoyed, boxer, Doberman pinscher Great Dane, German shepherd, bull terrier (male > female) Great Dane, German shepherd, Weimaraner, Labrador retriever (male > female) Keeshond, English bulldog
*Note: SAS, PDA, and PS are the most common defects in dogs. ASD/VSD and atrioventricular valve dysplasias are the most common defects in cats.
•
• Exercise intolerance is usually a sign of advanced CHD. • Syncope and exertional collapse are usually signs of severe CHD and may be related to: • Right-to-left shunts (hypoxemia) • Ventricular outflow tract obstruction (e.g. aortic and pulmonic stenosis) • Intermittent ventricular arrhythmias • Inappropriate activation of cardiac baroreceptors following sympathetic stimulation (reflex-mediated syncope) • CHF
•
Physical Examination Exam findings of particular importance in CHD include palpation of the precordium, auscultation of the heart, evaluation of the femoral arterial and jugular venous pulses, and inspection of mucous membranes. In addition, perform a careful respiratory and abdominal evaluation for signs of left- or right-sided CHF.
stronger than normal and often indicates hypertrophy or enlargement of the underlying ventricle. RV hypertrophy is suggested by a right-sided impulse of greater intensity than that on the left. Caudal displacement of the left apical impulse beyond the 6th intercostal space (ICS) may indicate cardiac dilatation. A precordial thrill is a palpable vibration, a manifestation of a loud heart murmur that identifies the point of maximum intensity (PMI).
•
ticular cardiac defect (see Fig. 154-1 and Chapter 142). Most murmurs associated with CHD are systolic. A continuous murmur is due to PDA or, rarely, from an aorticopulmonary window. A diastolic murmur is most likely due to aortic regurgitation, a condition that may coexist with VSD, aortic valvular malformation, or SAS complicated by aortic valvular endocarditis. Atrioventricular valvular stenosis (or supravalvular stenotic ring) is a rare cause of diastolic heart murmurs. Distinguishing an innocent (functional) murmur from one caused by CHD, especially in the case of mild aortic stenosis or trivial mitral malformation, may be difficult if not impossible. • Murmurs caused by clinically-significant CHD are typically louder and of longer duration than innocent murmurs. • Innocent murmurs are often intermittent, may be musical, and usually diminish or resolve by 16 to 24 weeks of age. Murmurs that persist are more likely to suggest cardiac malformation. • A particularly difficult issue for breeders is the persistence of a soft ejection murmur in the absence of an echocardiographic imaging lesion. It may be impossible to determine if CHD is present or not. With the exception of ventricular outlet obstruction (SAS or PS), murmur intensity or duration does not correlate reliably with the severity of the cardiac lesion. For example, dogs with severe tricuspid valve dysplasia may have soft murmurs, whereas a small and restrictive VSD can create a very loud murmur. A murmur may be soft or absent in the following serious situations: right-to-left shunting defects with polycythemia, pulmonary or aortic atresia, large unrestrictive VSD, tricuspid dysplasia, or severe PH.
Precordial Palpation
Pulse Evaluation
The left and right apical impulses—the points of the strongest cardiac movements on each side of the thorax—identify the relative mitral valve area on the left and the tricuspid valve area on the right. Palpation is useful in localizing normal and abnormal cardiac sounds.
Inspect the jugular venous pulse and palpate the femoral arterial pulse. The arterial pulse character depends on the pulse pressure (systolic minus diastolic pressure), the stroke volume of the left ventricle (LV), and the rate of pressure rise during LV ejection.
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• Jugular venous distension or pulsations suggest right•
• Left-Ventricular Hypertrophy—Tall R waves >2.5 to 3.0 mV in lead II in dogs or >0.9 mV in cats usually indicate eccentric hypertrophy of the LV. A left axis deviation is also compatible with concentric LV hypertrophy, though septal defects may lead to a similar axis shift. Common causes of LV enlargement include PDA, SAS, VSD, and mitral valve dysplasia. • Right-Ventricular Hypertrophy—Right axis deviation with S waves in leads I, II, III, aVF, and V2 to V6 suggest RV hypertrophy. Common causes include PS, tetralogy of Fallot, ASD, tricuspid dysplasia, and PH. Splintered R-waves also may be observed with tricuspid valve malformation. • Atrial Enlargement—a P wave duration of >0.04 seconds is suggestive of left or right atrial dilation; a P wave >0.4mV in dogs indicates right atrial dilation.
sided heart disease, for example, PS, tricuspid regurgitation, or right-sided CHF. Weak, hypokinetic, or late-rising arterial pulses suggest outflow obstruction as in significant subaortic stenosis, LV dysfunction, volume depletion, or heart failure. Conversely, bounding (hyperkinetic or waterhammer) pulses are most commonly associated with PDA or aortic regurgitation, as these situations create a wide pulse pressure.
Mucous Membranes
• Normal membranes are pink with a capillary refill
•
time of 5g/dl of desaturated hemoglobin. Pulmonary dysfunction due to left-sided CHF or concurrent bronchopneumonia is the most common cause of cyanosis in CHD. Lesions that allow right-to-left shunting, such as tetralogy of Fallot, can lead to persistent or exerciseinduced cyanosis in the absence of pulmonary dysfunction. • Right-to-left shunting requires a source of high rightsided resistance, and a communication or shunt proximal to the obstruction. With this combination, desaturated right-sided blood may enter the left side of the circulation. • Reasons for high resistance include PH from high vascular resistance, PS, mid-RV obstruction, and tricuspid valve disease (either stenosis or severe regurgitation that raises right atrial pressure). • The lesion allowing shunting can be a patent foramen ovale, ASD, VSD, or PDA. Additionally, in certain complex defects, there may be only a single great vessel exiting the heart; one ventricle that serves each great vessel; or transposition of the great vessels. Each of these situations allows mixing of pulmonary venous and systemic venous blood and may lead to cyanosis. • The term “differential cyanosis” generally refers to the condition of pink oral membranes and cyanotic caudal membranes (best seen in the vulva or prepuce). This is most typical of reversed PDA caused by a large ductus and severe PH.
Electrocardiography The ECG is of little value in recognition of mild CHD. Diagnostic yield increases when evaluating rhythm disturbances or identifying cardiac chamber enlargement in the presence of moderate to severe cardiomegaly (see Chapter 144). Common chamber enlargement patterns are summarized below.
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Thoracic Radiography Routine thoracic radiography is used for evaluation of cardiac size and chamber enlargement; assessment of the great vessels; and evaluation of pulmonary circulatory dynamics (see Chapter 143).
• Determination of left-sided vs. right-sided cardio-
• • • •
• •
megaly is informative in the differential diagnosis of CHD. While echocardiography is a more accurate method for assessing chamber size and wall thicknesses, the radiograph may be helpful. In particular, marked elongation of the heart is suggestive of LV dilatation, as with PDA. Conversely, concentric hypertrophy of a ventricle secondary to outflow obstruction may be underestimated by radiography. Remember that young puppies have a relatively dominant RV shadow until approximately 8 to 12 weeks of age. Dilation of the main pulmonary artery is suggestive of PS, a left-to-right shunt, or PH. Dilatation of the ascending aorta is typical of subaortic stenosis and pulmonary atresia; dilation in the descending aorta is typical of PDA (ductus bump). Radiographs are especially helpful for observing pulmonary vascular changes as with left-to-right shunts (overcirculation) or right-to-left shunts or severe PS (undercirculation). Radiographs also provide objective proof for the presence or absence of CHF. Radiographic changes associated with common malformations are summarized in Figure 154-1.
Echocardiography Echocardiography represents a noninvasive method for obtaining detailed images of cardiac anatomy and assessment of cardiac function. Supplemented with Doppler studies of blood flow, the echocardiographic examination has largely replaced invasive cardiac
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catheterization and angiocardiography for definitive diagnosis of CHD. Echocardiography provides information that is not only diagnostic but also supportive of surgical and catheter-based therapeutic interventions.
• Two-dimensional (2D) echocardiography allows identification of the anatomical defect(s). Among lesions that can be imaged are patent foramen ovale, ASD, VSD, PS, SAS, mitral valvular malformation, tricuspid valvular malformation, and the internal structure of a PDA. An estimate of the size and severity of a defect can also be obtained with high quality 2D images.
•
▼ Key Point Trivial or mild lesions of CHD may not be evident by 2D imaging.
•
• With 2D and M-mode imaging, the degree of myocar-
•
dial hypertrophy or chamber dilation can be assessed as well as subsequent functional changes in heart function. This allows evaluation of overall significance of the cardiac lesion. Mild disease usually causes few anatomic or functional changes in the heart. Color and spectral Doppler echocardiography are used to detect normal and abnormal blood flow and measure the direction and velocity of blood flow in the heart and great vessels. Doppler studies can be
used to provide estimates of intracardiac pressures. Combined with 2D imaging, these modalities provide highly accurate, noninvasive quantitation of the severity of a cardiac lesion. Doppler methods also may allow estimation of pulmonary arterial pressure, shunt ratio, magnitude of stenosis, and regurgitant fraction. Contrast echocardiography can be performed by injecting agitated saline or other gas-containing microbubbles into a peripheral vein to improve detection of cardiac shunting defects (particularly right-to-left shunts). These studies can be performed when Doppler technology isn’t available or to improve Doppler echocardiographic studies. A summary of common echocardiographic findings in CHD is found in Table 154-2.
Cardiac Catheterization Cardiac catheterization is an invasive procedure useful for diagnosing structural malformation and assessing physiologic abnormalities when echocardiographic Doppler studies are equivocal or when therapeutic, catheter-based intervention is beneficial. Because of its relatively invasive nature and the necessity for general anesthesia, catheterization has limited applications. These include:
Table 154-2. ECHOCARDIOGRAPHIC AND DOPPLER FEATURES OF SELECT CONGENITAL HEART DEFECTS Defects Patent ductus arteriosus (PDA) Pulmonic stenosis (PS) Subaortic stenosis (SAS) Ventricular septal defect (VSD)
Atrial septal defect (ASD) Mitral valve dysplasia Tricuspid valve dysplasia Tetralogy of Fallot
Pulmonary hypertension (PH)
Echocardiographic and Doppler Features Dilated left atrium, left ventricle, and pulmonary trunk; possible identification of PDA; turbulent flow in main pulmonary artery, with retrograde diastolic flow and increased transmitral and aortic flow velocities, reduced LV systolic myocardial function Right ventricular hypertrophy, right atrial and pulmonary artery enlargement, outflow tract obstruction, thickened valve leaflets, septal flattening and/or paradoxical septal motion, high-velocity flow (>15 m/sec) across the pulmonic valve Left ventricular (LV) hypertrophy, dilated aorta, subvalvular narrowing, high-velocity flow (>2.0 m/sec) across the aortic valve Variable chamber enlargement, most commonly left atrial and ventricular, possible identification of defect, right ventricular hypertrophy if pulmonary hypertension (PH) or very large defect, visualization of flow across defect, may be bidirectional; increased transmitral and PA flow velocity, right-to-left shunt in the case of PH (Doppler or bubble study) Right atrial and ventricular enlargement, possible identification of defect, main pulmonary artery enlargement, flow across defect, increased velocity flow across tricuspid (diastole) and pulmonic (systole) valves Left atrial and left ventricular enlargement, abnormal mitral valve anatomy, increased transmitral diastolic flow velocity, turbulent retrograde systolic transmitral flow Right atrial and ventricular enlargement, abnormal tricuspid valve anatomy, increased transtricuspid diastolic flow velocity, turbulent retrograde systolic transtricuspid flow Right ventricular hypertrophy, right ventricular outflow tract obstruction, identification of VSD, overriding aorta, small left heart, contrast study indicating right-to-left shunting, septal flattening and flattening and/or paradoxical septal motion, right-to-left flow across VSD (Doppler or bubble study), decreased diastolic transmitral flow, possibly increased transaortic systolic flow, increased flow velocity across the pulmonic valve Right ventricular hypertrophy, right atrial enlargement, dilated main pulmonary artery, visualization of associated shunt, right-to-left shunt by Doppler or bubble study, increased flow acceleration across pulmonary valve
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• Delineating ambiguous anatomic lesions. • Identifying vascular abnormalities that evade ultrasound studies, such as some systemic to pulmonary shunts or multiple arteriovenous fistulas. Facilitating interventions such as balloon valvuloplasty for PS, balloon dilation for severe SAS, or transcatheter occlusion of shunts.
•
These procedures require referral to a cardiologist or a clinical specialist with advanced training, equipment, and expertise in the diagnosis and management of CHD.
•
•
TREATMENT OF COMPLICATIONS OF CONGENITAL HEART DISEASE Definitive or palliative therapy for CHD often requires surgery or a catheter-based intervention. Prior to such treatments, establish a definitive diagnosis. Symptomatic medical therapy can be directed for complications of severe CHD such as CHF or arrhythmias. PH is a problematic complication to address. Severe polycythemia also requires management.
Congestive Heart Failure • Most forms of CHD lead to progressive volume or
•
• •
pressure overload of the affected ventricle. With time, diastolic and systolic ventricular function decline and cardiac output becomes limited. This situation is worsened by development of mitral or tricuspid valvular regurgitation or atrial fibrillation. The end-result is development of left- or right-sided CHF. An important differential diagnostic consideration for right-sided CHF in a puppy or a young dog is cor triatriatum dexter. This disorder is characterized by the partitioning of the right atrium by an obstructive membrane that impairs venous return from the caudal vena cava. When CHD progresses to CHF, the medical therapy is very similar to that used for acquired heart disease (detailed in Chapter 147). Initial management of left-sided CHF involves treatment with furosemide (2–4 mg/kg IV, IM, or SC), oxygen, and 2% nitroglycerine ointment. Sedation with butorphanol (0.25 mg/kg IM or SC) may be added if necessary. • If this approach fails to control the CHF, and the cause is a left-to-right shunt, sodium nitroprusside (0.5–2.5 mcg/kg/min infusion) can be used to reduce the arterial pressure and magnitude of shunting. • Alternatively, enalapril or another angiotensinconverting enzyme inhibitor (ACEI) can be initiated to reduce afterload and reduce left-to-right shunting (see Chapter 147). • Maintain systolic blood pressure in the 80 to 120 mm Hg range, particularly in cases of aortic
•
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stenosis where hypotension can reduce coronary perfusion. Chronic medical therapy of CHF in dogs with CHD is identical to that described in Chapter 147 and includes furosemide, an ACEI, spironolactone, and often digoxin or (where available) pimobendan. In cats, the initial use of furosemide and an ACEI is appropriate. The use of beta-blockers in treatment of dogs with CHF is unresolved, and care must be used to avoid bradycardia, especially in dogs with fixed obstructions such as SAS and PS, as cardiac output in these conditions is relatively heart-rate dependent. For dogs already taking beta-blockers as cardioprotection, once CHF develops, the beta-blocker should be continued, the dosage reduced if needed to obtain a target examination heart rate in the 100 to 140/min range. In some cases, medical therapy for CHF may be discontinued if definitive repair of the defect can be successfully performed. This is particularly true in young dogs or cats with PDA.
Arrhythmias • Controlling arrhythmias in the setting of severe CHD •
•
•
may help to maintain a compensated state and to prevent sudden death. Atrial fibrillation is particularly destabilizing to dogs with CHF; treat to achieve heart rate control with digoxin, diltiazem, and a beta-blocker. Electrical cardioversion is another option to restore sinus rhythm. Specific therapy of arrhythmias is discussed in Chapter 145. Re-entrant supraventricular tachycardia due to an accessory pathway may be encountered in some dogs with tricuspid dysplasia, particularly Labrador retrievers. Ventricular arrhythmias have been particularly associated with SAS and PS. Holter ECG monitoring may be indicated to screen for rhythm disturbances, especially in dogs with exertional symptoms. Chronic therapy of clinically significant ventricular tachycardia may include sotalol, mexiletine plus a betablocker, amiodarone, or procainamide.
Pulmonary Hypertension • The presence of PH due to high vascular resistance
•
is difficult to manage, as the vascular changes responsible are typically irreversible. The evaluation of PH usually requires referral to a specialist experienced in CHD. PH usually develops rapidly in dogs with large left-toright shunts. In cats it is more gradual and, if caught, can be arrested by closure of a left-to-right shunt. Drugs that reduce pulmonary vascular resistance such as sildenafil (Viagra) at initial doses of 0.5 to 2 mg/kg q12h PO may be beneficial in cases of
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advanced PH. Currently this therapy is very expensive. Arterial blood pressure must be monitored, as reduced systemic resistance will lead to greater rightto-left shunting. Controlled exercise is important to prevent exertional collapse or dyspnea. This may be difficult to achieve in puppies or kittens.
Polycythemia • In cases of right-to-left shunting due to obstructive
•
•
•
lesions of the right heart (PS, tricuspid stenosis), balloon valvuloplasty or surgery may decrease rightsided pressures and control the cause of shunting. Care must be exercised with a large ventricular septal defect, since florid left-to-right shunting may develop across the VSD. Phlebotomy may be required in patients with rightto-left shunting and secondary polycythemia. A packed cell volume (PCV) of 62% to 65% is often well tolerated, but values exceeding 68% to 70% are likely to cause exercise difficulties or stroke-like signs. Usual treatment measures for polycythemia include periodic phlebotomy with replacement by IV or subcutaneous crystalloid fluid (see Chapter 22 for a discussion of management of polycythemia). When the need for phlebotomy becomes too frequent, bone marrow suppression can be attempted using hydroxyurea. Treatment may not work, and anorexia, gastrointestinal disturbances, and skin rash may limit tolerability of the drug. A regular complete blood count and platelet count should be performed.
•
•
•
•
Ventricular and Atrial Septal Defects • Surgical closure of septal defects is the definitive
TREATMENT AND PROGNOSIS OF SPECIFIC DEFECTS In addition to management of complications of CHD discussed above, the potential to more definitely treat the specific malformation is inviting. Unfortunately, many of these conditions require an operation during cardiopulmonary bypass by a highly skilled cardiothoracic surgeon. Even extracardiac procedures such as PDA ligation or catheter-based treatments for PDA or PS can end badly if the clinician is inexperienced.
•
•
▼ Key Point Surgical or interventional management of cardiac defects should be performed only by properly trained and experienced clinicians in a fully equipped and staffed hospital.
Patent Ductus Arteriosus • Closure is strongly recommended in left-to-right shunting defects as the 1-year mortality for untreated dogs exceeds 60%. In the reversed (right-to-left) shunting PDA, closure of the defect is contraindicated and therapy is focused on reducing complica-
tions of PH and polycythemia by periodic phlebotomy (see above). Thoracotomy and surgical ligation of the ductus is very successful with perioperative mortality that should be 4mm) defects. The prognosis following isolated closure of a PDA is excellent. A normal lifespan can be anticipated, and most cases do not require any cardiac follow-up. Exceptions to this rule include dogs with marked LV systolic dysfunction (determined by echocardiography), dogs with prior CHF, or dogs with atrial fibrillation. Refer these patients to a cardiologist for evaluation. Reversed PDA has a poor prognosis, though with vigilant therapy some patients live beyond 5 years of age, affected mainly by rear limb weakness during exercise.
•
•
treatment but requires cardiopulmonary bypass and open heart surgery. While this has been successfully performed, it is not commonly practiced in veterinary medicine. Palliative pulmonary arterial banding, creating a supravalvular PS, has been used successfully to reduce the left-to-right shunt of a VSD. This procedure is recommended only for those animals with rapidly progressive cardiomegaly and overt or impending CHF. Simple cardiomegaly is not an indication for banding, as very few of these patients ever develop CHF. Transcatheter occlusion devices have been developed for closure of septal defects, but are still experimental. Right-to-left shunting may develop in dogs or cats with VSD due to PH, valvular or subvalvular PS, or progressive, mid-ventricular fibromuscular obstruction (so-called double-chambered RV). Exercise intolerance and polycythemia may develop. Treatment is as described above for polycythemia. The prognosis for septal defects is variable. • CHF associated with ASD is rare in dogs, but may develop in cats, especially in those with endocardial cushion defects and large communications.
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• A small, restrictive VSD carries an excellent prognosis for longevity. CHF associated with VSD is actually quite rare because most patients are “naturally-selected” for smaller defects and rarely require any intervention. Thus, the prognosis for dogs that attain 16 weeks of age without signs of CHF is good. • The exception is the dog with a VSD and aortic root prolapse or aortic malalignment defects because severe (audible) aortic regurgitation may occur, and CHF can develop in middle age from LV volume overload. • Cats with VSD are more likely to develop CHF, especially if the detect is large (50% of aortic diameter).
Tetralogy of Fallot • Definitive surgical treatment for tetralogy of Fallot •
•
• • •
•
includes closure of the VSD and removal or bypass of the stenosis under cardiopulmonary bypass. Palliative surgery involves creation of an extra-cardiac shunt between the systemic and pulmonary circulations (e.g., Blalock-Tausig shunt). Such shunts increase pulmonary flow, improve arterial saturation, and may produce significant clinical improvement. The major limitation is the extent to which these shunts will remain patent. Animals with a sedentary lifestyle will often tolerate this disease well, especially if the PS is not too severe. Some will live for 5 or more years. Exercise creates vasodilation in skeletal muscle and increases tissue oxygen demands; accordingly, most tetralogy of Fallot patients have signs of tachypnea and exercise intolerance with exertion. Sudden death is common consequent to progressive hypoxemia, polycythemia and cardiac arrhythmias. Avoid drugs that cause systemic vasodilation in these patients, as right-to-left shunting may be exacerbated. Beta-blockage with the nonspecific beta-blocker propranolol (start at 0.25 mg/kg PO q8h and up-titrate over 4 weeks to 1 mg/kg PO q8h) may be beneficial by reducing exercise-induced RV hyper-contractility, an event that can add a dynamic component to RV outflow obstruction. The beta2 blocking effect should theoretically benefit by preventing some exerciseinduced peripheral vasodilation. Manage polycythemia as described above (see Chapter 22).
•
•
• • •
of choice for PS when the lesion is characterized by valvular thickening with commissural fusion. In experienced hands the procedure mortality is 4 years has been reported in dogs with even very severe SAS (>120 mm Hg). Atenolol is recommended for all dogs with a gradient >50 mm Hg.
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Beta-blockade is particularly helpful in the specific situation of dynamic SAS caused by mitral valve malformation wherein beta-blockade may completely alleviate the obstruction and allow regression of LV hypertrophy. Unfortunately, severe SAS carries a discouraging prognosis owing to premature death. Sudden arrhythmic cardiac death and progressive LV dysfunction with development of CHF are typical outcomes. Mature dogs with mild SAS are more likely to live normal lives, though some still experience sudden death. Dogs with even mild disease are at higher risk for development of bacterial endocarditis. Therefore, administer prophylactic antibiotics during elective surgical procedures or whenever wound contamination is an issue.
Atrioventricular Valve Dysplasia (Stenosis) • Balloon valvuloplasty has been performed with vari• •
able success in dogs with tricuspid and mitral valvular or supravalvular stenosis. Surgical repair of affected valves can be attempted. Replacement of dysplastic valves has been performed successfully with cardiopulmonary bypass. Most cases are treated medically when signs of CHF or atrial fibrillation develop. Consideration should be given to ACEI (enalapril) and to beta-blocker
• •
•
(carvedilol or metoprolol) therapy for establishing cardioprotection in dogs with severe mitral regurgitation and associated cardiomegaly. Tricuspid malformation, associated with an ASD, may lead to right-to-left shunting; secondary polycythemia should be managed (see under “Polycythemia”). Mild mitral or tricuspid valvular dysplasia is often well tolerated; however, severe lesions lead to CHF and arrhythmias such as atrial fibrillation. Dogs with severe mitral disease usually develop CHF in early to middle age, particularly when the valve is both stenotic and incompetent. Many dogs with relatively severe tricuspid regurgitation survive for 7 or 8 years before CHF ensues. Tricuspid stenosis is typically associated with an ASD or patent foramen ovale, leading to secondary polycythemia.
SUPPLEMENTAL READING Bonagura JD, Lehmkuhl LB: Congenital heart disease. In Fox PR, Sisson DD, Moise NS (eds): Textbook of Canine and Feline Cardiology: principles and clinical practice, 2nd ed. Philadelphia: WB Saunders, 1999. Oyama MA, Sisson DD, Thomas WP, Bonagura JD: Congenital heart disease. In: Ettinger SJ, Feldman EC (eds): Textbook of Veterinary Internal Medicine, 6th ed. St Louis: WB Saunders, 2005.
Chapter
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Surgical Correction of Patent Ductus Arteriosus Eric R. Schertel
Ligation of the patent ductus arteriosus (PDA) in dogs and cats is a rewarding surgical procedure. When performed by an experienced surgeon, the combined operative/postoperative mortality rate is relatively low (8–10%) compared with surgery of other forms of congenital heart disease. The long-term prognosis after correction is excellent. However, like any thoracic or cardiovascular procedure, special attention to the details of anesthetic and surgical techniques is necessary for success. An accurate diagnosis is important, as is a thorough knowledge of the anatomy and physiology of the cardiovascular system.
PREOPERATIVE AND PERIOPERATIVE CONSIDERATIONS • Consult the chapter on congenital heart disease (see •
•
ANATOMY AND PHYSIOLOGY • The ductus arteriosus is a remnant of the left sixth
• •
•
•
aortic arch and connects the pulmonary artery and the descending aorta in the fetus and newborn. Its continued patency after birth results in left-to-right shunting of blood causing volume overload of the left atrium and ventricle. In severe cases, left ventricular failure may be present. The relationship of the descending aorta, main pulmonary artery, and right and left pulmonary arteries with the PDA must be appreciated (Fig. 155-1). The PDA may vary in size and shape but generally is approximately one-fifth to one-fourth the diameter of the aorta, or slightly smaller than the left main pulmonary artery. The PDA is usually short (0.5–1.0 cm), bridging the small distance between the aorta and pulmonary artery. The left vagus nerve lies over the ductus and is immediately underneath the visceral pleura. The recurrent laryngeal nerve arises from the vagus and courses caudal and medial to the PDA. Rarely, a persistent left cranial vena cava may be found coursing over the pulmonary artery. This does not pose a surgical problem in PDA ligation.
• • •
Chapter 154) for details of diagnosis and medical management. Institute conservative medical management before surgery when there is evidence of heart failure. More aggressive medical management may not benefit the patient as much as surgery. Mortality with surgery is higher when congestive heart failure (CHF), atrial fibrillation, or substantial myocardial failure is present. The mortality of nonsurgically managed PDA patients also is high. Thus, if conservative therapy for heart failure is not effective in 24 to 48 hours, surgery combined with intensive medical management is the appropriate course of action in most patients. Administer IV fluids judiciously during anesthesia and surgery, especially in animals with heart failure. Perioperative mortality is 8% to 10% according to published reports. Perioperative complications occur in 10% to 15% of cases.
LIGATION OF THE PATENT DUCTUS ARTERIOSUS Objectives • Careful exposure and definition of the ductus
•
arteriosus through a left fourth intercostal space thoracotomy. (The left fifth space may be indicated in cats.) Double ligation of the ductus without trauma to the vessels or other surrounding structures.
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Vagus nerve Recurrent laryngeal nerve Aorta Ductus Plane of cut Right pulmonary artery
Aorta Ductus
Thymus Phrenic nerve
Left pulmonary artery
Figure 155-1. Retraction of the left cranial lobe of the lung allows exposure of the region of the ductus.
Correct D+
Incorrect D
Equipment • General surgery pack and standard suture, plus • • • •
instruments required for thoracic surgery (see Chapter 167). Assorted sizes of right-angle forceps Vascular clamps, preferably pediatric/infant ductus clamps (three pairs) Multipurpose peripheral vascular clamps (two pairs) Suture; silk, sizes 3-0 up to 1-0, and non-absorbable, 5-0 or 6-0, on a cardiovascular needle
Technique 1. Use an appropriate anesthetic regimen based on the preoperative assessment of cardiac function (see Chapter 2 for discussion of anesthesia techniques). Positive pressure ventilation is required during the majority of the procedure. 2. Place the patient in right lateral recumbency. Clip and aseptically prepare the left thorax from the cranial border of the scapula to rib 13, and from the dorsal to the ventral midline. Include the left shoulder and axilla, and extend past the elbow. 3. Perform a standard left fourth intercostal space thoracotomy (see Chapter 167). 4. Identify the region of the ductus following caudal retraction of the left cranial lung lobe (see Fig. 1551). Retract the lobe with a moist sponge or laparotomy pad. 5. Elevate the vagus nerve and encircle with silk suture or umbilical tape for retraction to expose the PDA. Identify the location of the recurrent laryngeal nerve as it courses from the vagus to the caudal aspect of the ductus. 6. Palpate the thrill in the main pulmonary artery for reference.
Figure 155-2. Exposure of the ductus. Top, Initial area of dissection. Bottom, Use of closed right-angle forceps to dissect the region behind the patent ductus arteriosus. See text for further details.
7. Begin blunt and sharp dissection cranial and caudal to the PDA. Extend the dissection caudally between the aorta and left main pulmonary artery for a distance of at least 1.5–2 times the diameter of the ductus (Fig. 155-2, top). Extend the dissection cranioventrally between the aorta and main pulmonary artery a similar distance. The depth of the dissection should be at least equal to the width of the ductus (Fig. 155-2, inset). Dissect adjacent to the relatively thick-walled aorta. 8. Consider preparing the craniodorsal aspect of the aorta just distal to the left subclavian artery by reflecting the pleura and adjacent mediastinal tissues. This requires a small amount of time and ensures a clear path for clamp placement if hemorrhage control is necessary (see below). 9. The pericardium has a variable insertion at the level of the ductus. It may be inserted on the aortic side or on the main pulmonary artery side of the ductus. Thus, the ductus occasionally is within the pericardium. In these circumstances, incise the pericardium at its insertion on the ductus or aorta.
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10. Once the cranial and caudal aspects of the ductus are exposed, initiate blunt dissection behind the PDA using right-angle forceps (Fig. 155-2, bottom). Take care to identify the depth of the ductus. Accomplish dissection behind the ductus by inserting closed forceps, spreading gently, and removing the forceps. Carry out dissection adjacent and parallel to the surface of the aorta. 11. I prefer caudal to cranial dissection to avoid repeated work in the cranial aspect of the ductus. The vascular structures of the cranial region are more readily damaged and are most prone to hemorrhage. However, minor medial dissection in this area often is necessary. 12. When the majority of the medial dissection is complete, gently separate the aorta and main pulmonary artery cranial to the ductus to allow identification of the tips of the right-angle forceps as they are passed from caudal to cranial. When the tips are visible, carefully incise the remaining fascia over the tips of the forceps with a #15 blade. This is preferable to repeated efforts at pressing through this fascia. ▼ Key Point Do not cut any tissue unless you are certain that it is fascia and not vessel wall.
13. Individually pass two strands of 1-0, 2-0, or 3-0 silk or polyester suture, depending on the size of the dog or cat, and the size of the ductus (Fig. 155-3, top). 14. Attenuate the ductus prior to ligation to observe the hemodynamic effects. If bradycardia is observed, atropine may be given. Double-ligate the ductus, aortic side first. Palpate the pulmonary artery again for ductal-related thrill or turbulence. 15. If hemorrhage is encountered from perivascular structures, control with pressure, ligation, or cautery. If the ductus ruptures and aggressive hemorrhage is encountered, first use digital pressure to control blood loss. Next, place vascular clamps on the aorta in the previously prepared region just caudal to the left subclavian artery and cranial to the ductus (Fig. 155-3, bottom). Also place clamps caudal to the ductus on the aorta and across the base of the ductal origin from the pulmonary artery. Identify the region of hemorrhage and suture with 5-0 or 6-0 nonabsorbable suture on a cardiovascular needle. A recent study evaluated the use of deliberate hypotension for dogs with hemorrhage during PDA dissection. Intravenous nitroprusside was used to lower blood pressure and reduce bleeding, allowing continued dissection and ligation of the ductus. See Supplemental Reading for more information. 16. Subcutaneously tunnel a #5 or 8 Fr. red rubber tube from a small wound made caudal to the skin incision. Place the tube in the thorax through the
Figure 155-3. Top, Suture placement for double ligation of the ductus. Bottom, Procedure for controlling hemorrhage after ductus rupture.
thoracotomy. Close the thorax in a routine manner, incorporating the temporary thoracic tube (see Chapter 167). 17. After evacuating air and fluid from the thorax, remove the temporary thoracic tube. If hemorrhage or inadvertent lung injury occurs, place a standard indwelling thoracic tube (see Chapter 3).
POSTOPERA TIVE CARE AND COMPLICA
TIONS
Short T erm ▼ Key Point Close postoperative monitoring in an intensive care setting is of the utmost importance.
• Monitor the following parameters/signs: • Mucous membrane color, capillary refill time, respiratory rate, blood pressure • Dyspnea, urine output • Recovery of body temperature, pulse, thoracic auscultation
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should be no diastolic murmur if ligation was successful.
• Analgesic therapy is indicated in animals with pain •
•
• •
(see Chapter 6 for discussion of postoperative analgesia). Some surgeons treat routinely with furosemide (1–2 mg/kg) during the preoperative and immediate postoperative periods. This may be guided by the preoperative status, course of surgery, patient size, and operative fluid balance. If preoperative medical management was instituted, continue it postoperatively until clinical signs resolve. Perform frequent intermittent evacuation of the thorax (e.g., q2h) if a tube was left in place. Remove the thoracic tube when negative pressure is achieved or fluid or air production has subsided. Limit fluid therapy but maintain a sterile intravenous catheter for 24 hours. Auscultate the heart postoperatively for persistent murmur. A systolic murmur of mitral insufficiency, caused by left ventricular dilation, may be present. This murmur generally abates within 10 days. There
Long Term • Reevaluate heart sounds at 2 weeks when sutures are • •
removed, at 6 months, and then yearly thereafter to detect the uncommon occurrence of recanalization. Recanalization of the PDA occurs rarely (1–2% of cases) and is treated by relegation or division of the ductus and oversewing of the cut ends. PDA ligation has excellent long-term results if ligation is complete.
SUPPLEMENTAL READING Hunter SL, Culp LB, Muir WW 3rd, et al. Sodium nitroprussideinduced deliberate hypotension to facilitate patent ductus arteriosus ligation in dogs. Vet Surg. 2003, 32(4):336–340.
Chapter
▼
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Shock Eric R. Schertel
▼ Key Point Shock is the clinical state resulting from an inadequate supply of oxygen to the tissues or an inability of the tissues to utilize oxygen properly.
Shock involves numerous physiologic disturbances and pathologic changes that affect multiple organ systems in different ways. Veterinarians often are alerted to the presence of shock in their patients by the physical findings of depressed mentation, pale mucous membranes, tachycardia, and weak pulse pressure. These clinical signs are the manifestations of a complex process and do not represent the full extent of the problem. The objective of this chapter is to provide a simplified approach to the diagnosis, monitoring, and treatment of shock. Information on the various manifestations, mechanisms, and temporal patterns of shock is beyond the scope of this book, but nonetheless is considered important to appropriate and successful therapy. Therapy for shock caused by acute heart failure is discussed in Chapter 147. See appropriate chapters for discussion of specific diseases that can cause shock.
ETIOLOGY AND CLASSIFICATION Shock generally is classified by etiology because each cause of shock may produce distinct primary and secondary pathophysiologic changes and temporal patterns. Shock etiologies can be organized into those forms that result from:
• An abnormality or inadequacy of the vehicle of •
oxygen transport (blood) An abnormality of the transport system (cardiovascular system)
Hypovolemia and hypoxemia (anemic, hypoxic) are examples of the first category (Table 156-1). Diseases that disrupt the cardiovascular system and its control mechanisms (circulatory control mechanisms) also cause shock. The three important circulatory control mechanisms regulate:
• Blood pressure and blood flow distribution • Blood volume distribution • Cardiac function Shock may also develop from the presence of one or more of these conditions.
• Sepsis is an example of a condition in which shock is caused by a loss of control of blood flow distribution.
• Endotoxemia and gastric dilatation-volvulus also •
cause shock by interfering with the distribution of blood volume, but via different mechanisms. Heart failure creates shock due to inadequate cardiac function (see Table 156-1).
CLINICAL SIGNS Mental Attitude Depressed mentation often is the most apparent physical finding in a patient with shock. This parameter is subjective and may be complicated by head injury.
• Causes: Decreased cerebral blood flow and oxygen delivery, circulating toxins, or head injury.
Arterial Pulse Pressure A weak pulse is common but not necessary for shock to exist. The pulse feels weak at mean arterial pressures 140 beats per minute (bpm) in large-breed dogs, >160 bpm in small-breed dogs, and >180 bpm in cats. Begin monitoring with electrocardiography (ECG) if an irregular rhythm is detected.
•
• Causes: Hypotension, hypovolemia, pain, stress, and
•
fever may cause tachycardia. Irregular rapid heart rhythms result from ventricular tachycardia and atrial tachyarrhythmias, including atrial fibrillation (see Chapter 145).
surement that reflects blood volume. It may be obtained via a jugular catheter positioned so that its tip is within the thorax (see Chapter 3). CVP is approximately equivalent to the right atrial pressure and reflects the function of the systemic circulation and the right heart (Fig. 156-1). CVP is easily measured by a water manometer attached to the jugular catheter (see Chapter 3). Normal CVP ranges from 0 to 5 cm H2O. In shock, CVP usually is -3 to 2 cm H2O but may be as low as -5 cm H2O. The goal of fluid therapy in shock is to optimize blood volume by administering fluid in an amount that increases CVP to between 5 and 12 cm H2O. Plasma proteins, particularly albumin, maintain plasma volume. Assess total plasma proteins prior to fluid therapy and frequently during treatment to ensure that values remain above 4.0 g/dl (albumin >1.5 g/dl).
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12 11 10 9 8 7 6 5
Figure 156-1.
Determinants of CVP Cardiac Heart rate Contractility Pulmonary artery pressure Tricuspid regurgitation Pericardial pressure Pleural pressure Circulatory Blood volume Flow distribution A-V shunt Volume distribution Venomotor tone Venous resistance (obstruction)
Treatment Preliminary Measures
• Establish an airway and ventilate if necessary. Admin•
•
Determinants of central venous pressure (CVP).
Arterial Pressure
• Digital palpation may be used to assess mean arterial
•
pressure (MAP). Strong pulse pressure usually reflects a MAP of >70 mm Hg. A weak pulse is detected when MAP is 30%.
ister 100% oxygen via an endotracheal tube, mask, nasal tube, or tracheal catheter. To evaluate the patient for the cause of shock, obtain a history and perform a physical examination. The time allotted for these efforts depends on the condition of the patient. Place and secure a large-gauge intravenous (IV) catheter, preferably jugular. The jugular catheter should be long enough to reach the thoracic cavity. • Jugular catheterization has the advantages of allowing the use of a large-gauge catheter even in small patients, ease of placement, access for blood sampling, rapid fluid administration, CVP measurement, and catheter security. The major disadvantage is that jugular catheters are slightly more expensive. Obtain blood for storage in ethylenediaminetetraacetic acid (EDTA) and clot tubes. Measure hematocrit and total protein, serum electrolytes, serum creatinine, blood glucose, and a complete blood count.
Optimize Blood Volume
Cardiac Output tion are the physical findings that best reflect cardiac output. However, these are not always accurate. Urine output is a good indicator of cardiac output. When cardiac output is reduced, sympathetic nervous system activity may maintain blood pressure within normal limits but may decrease renal blood flow. Consequently, urine output will be decreased (130 mEq/L. Administration of 7% NaCl (hypertonic saline) is an alternative resuscitation regimen in patients that are not hydrated. Deliver the initial dosage of 4 to 6 ml/kg over 5–10 minutes (Table 156-3). The hypertonic saline may be combined with 6% dextran 70 or hetastarch and given at the same dosage. Supplement this form of initial treatment by giving isotonic crystalloid fluids at a minimum rate of 20 ml/kg/hr. The goal of the initial rapid rate of fluid administration is to establish a normal arterial pressure and optimize blood volume. An adequate arterial pressure is easily determined by palpation of pulse pressure. Physical signs, including pulse pressure, may be normal despite continuing tissue hypoxia and less than optimal or unstable blood volume. Blood volume is optimized when CVP is 5 to 12 cm H2O. To treat hypoproteinemia, fresh or frozen plasma may be administered at a dosage of 10 to 20 ml/ kg/day IV. Alternatively, synthetic colloids may be used to treat hypoproteinemia. Those useful in small animal patients include 6% dextran 70 and 6% hetastarch. The dosages are similar to those for plasma
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Table 156-2. TREATMENT OF SHOCK Therapeutic Goal
Therapy
Specific Objectives
Optimize blood volume
Crystalloids Isotonic Hypertonic Colloids Whole blood
CVP 5–12 cm H2O Wedge pressure 7–20 mm Hg Total protein >4.0 g/dl Albumin >1.5 g/dl Normal skin turgor
Optimize blood flow
Fluids Inotropic agents
Optimize oxygen delivery and consumption
Fluids Whole blood Packed red cells O2 supplementation Mechanical ventilation Respiratory care Fluids Vasopressors
Urine output >1 ml/kg/hr CRT 35 torr Cardiac index 150–200 ml/min/kg Pao2 >70 torr Pvo2 >35 torr Hct >25 Pink mucous membranes Patient bright, alert, responsive
Optimize blood pressure
Optimize heart rate/rhythm
Fluids Antiarrhythmics
Arterial pressure: Systolic, 100–160 mm Hg Mean, 70–120 mm Hg Diastolic, 50–100 mm Hg Strong pulse 70–160 bpm Sinus rhythm
Correct acid-base imbalance
NaHCO3
pH >7.3 and C] Parasitic infections [F, C] Aelurostrongylus abstrusus [F] Paragonimus kellicotti [C, F] Capillaria aerophilia [C, F] Osleri (Filaroides) infection (F. milksi, F. hirthi) [C] Aspergillosis (endobronchial infection) Viral infections: feline calicivirus; canine distemper virus Chlamydia psittaci [F] Rickettsial infections (Ehrlichia canis; Rocky Mountain spotted fever) [C >> F] Toxoplasma gondii [F > C] Hematogenous bacterial infection Nocardia spp., Actinomyces, anaerobes¶ Leishmania donovani [C] Systemic mycoses: Histoplasma encapsulatum, Blastomyces dermatitidis, Coccidioides immitis, Cryptococcus neoformans [C > F] Response to parasitic infection: migrating nematodes [C] Dirofilaria immitis [C > F] Lungworms and flukes [F, C]
• • •
•
Pleuritis and Pleuropneumonia Feline infectious peritonitis Anaerobic bacteria Aerobic bacteria (Pasteurella spp., E. coli, etc.) Nocardia asteroids Actinomyces spp. Blastomyces dermatitidis [C >> F] Toxoplasma gondii [F >> C] *This list is not comprehensive; important clinical conditions are indicated with the most commonly affected species designated as [C] = canine; [F] = feline. † Infection commonly extends to the larynx and trachea. ‡ Infection commonly extends to the bronchi and may cause pneumonia. § Alveolar involvement may develop in some cases of interstitial pneumonia. ¶ Pulmonary abscess, pleuropneumonia, and pyothorax may develop with these agents.
•
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of or discharge into the nasopharynx may cause reversed sneezing or gagging. Contagion is an issue with some causes of upper respiratory infections, especially with agents associated with the feline upper respiratory infections (see Chapter 11). Acute viral rhinitis is usually self-limiting within 1 to 2 weeks. • Persistence of viral or bacterial rhinitis or sinusitis can occur in immunocompromised cats infected with feline leukemia virus (FeLV) or feline immunodeficiency virus (FIV). • In addition, feline herpesvirus persists in a latent subclinical carrier form in recovered cats, and this occasionally recrudesces to result in episodic or persistent rhinitis (or conjunctivitis). Primary bacterial rhinitis and sinusitis are uncommon (except with Bordetella bronchiseptica); however, secondary bacterial infection can develop as a sequel to mucosal injury or obstructed nasal passages caused by upper respiratory viral infection, foreign body, periodontal disease and root abscesses, oral-nasal fistula or cleft palate, trauma (sequestrum), allergic rhinitis, lymphocytic-plasmacytic rhinitis, congenital ciliary dyskinesia (including the Kartagener syndrome), polyps, neoplasia, and fungal infection. B. bronchiseptica infection can lead to significant rhinitis as well as tracheobronchitis. Chronic bronchitis or lobar pneumonia can predispose to sinusitis, and vice versa. It is likely that a sinubronchial route of migration reinforces each infection. Bacterial isolates in rhinitis/sinusitis are variable and typify bacteria normally encountered in the nasopharynx, including gram-positive, gram-negative, and anaerobic organisms. Recently Bartonella spp. has been incriminated as a possible cause of nasal cavity discharge, including epistaxis, in dogs. Fungal infection of the nasal cavity or sinuses (see Table 163-1) can also be associated with immunosuppression; however, this immunodeficiency may be difficult to demonstrate in dogs. Aspergillus flavus, for example, is a normal inhabitant of the nasal cavity, but may invade respiratory epithelium in dogs with altered immunity or preexistent inflammation (e.g., lymphocytic-plasmacytic rhinitis, foreign body, or trauma). Nasal parasites, such as the nasal mite, Pneumonyssus (Pneumonyssoides) caninum, and the nasal nematode, Eucoleous, are uncommon in most localities, but are a potentially treatable cause of upper nasal/ nasopharyngeal signs; this should be considered, especially in young dog with rhinitis and reversed sneezing.
Clinical Signs • Sneezing, nasal discharge, and gagging or retching from postnasal drip are the typical signs of infectious rhinitis and sinusitis.
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Table 163-2. DIAGNOSIS OF RESPIRATORY INFECTIONS Nasal Cavity and Paranasal Sinuses Signalment (age, breed, sex), vaccination status, history Physical examination (emphasis: head, eyes, nose, oral cavity, regional lymph nodes, skin) Auscultation Serologic tests (aspergillosis, FeLV, FIV, and cryptococcus) Skull, dental, and nasal radiographs CT or MRI of the nasal cavity and paranasal sinuses Examination of the teeth, oral cavity, oropharynx, and tonsils under anesthesia (inspection, palpation, examination with dental probes and mirrors) Rhinoscopy (nasal cavity and retroflex rhinoscopy of the nasopharynx and posterior choanae) Nasal culture (bacterial, fungal) Aspiration biopsy/cytology (swab or nasal flush) of nasal exudate Mucosal biopsy of the nasal cavity Fine-needle aspiration biopsy/cytology of enlarged regional lymph nodes or mass lesions Surgical exploration of the nasal cavity and paranasal sinuses for culture, biopsy, and debridement Virology: Immunocytologic identification of viruses (e.g., immunofluorescence for canine distemper, feline herpes) and virus isolation (e.g., feline calicivirus)
Larynx Ultrasonography of larynx Visual examination of the larynx during light anesthesia Radiography
Trachea Radiography (cervical and thoracic) Fluoroscopy Tracheoscopy (endoscopy) Cytologic examination of tracheal lesions (brush cytology of the tracheal mucosa)
Bronchopulmonary Diseases History and physical examination (observation, auscultation, percussion of the thorax) Thoracic radiography Complete blood count Heartworm (HW) tests (enzyme-linked immunosorbent assay [ELISA] antigen tests for dogs and cats, microfilaria tests for dogs, HW antibody test for cats) Fecal examinations (flotation and Baermann sedimentation to detect lung parasites) Serologic testing (e.g., immunodiffusion or other tests for systemic mycoses, IgM ELISA for toxoplasmosis) Arterial blood gas Pulse oximetry Bronchoscopy Culture of tracheobronchial secretions (transtracheal wash, endotracheal approach using a guarded culture swab, or aspiration through sterile tubing advanced through a sterilized endoscopic port) Cytologic examination of the bronchi or lower airways Transtracheal wash of tracheobronchial secretions Endotracheal aspiration cytology Via a catheter placed in the trachea or bronchial tree Via an endotracheal tube (method sometimes used in cats and very small dogs) Brush cytology of the bronchial mucosa Bronchial aspiration cytology (selective, via a bronchoscope catheter) Bronchoalveolar lavage with a wedged bronchoscope Fine-needle aspiration (FNA) of the lung or a mass lesion Lung biopsy Pulmonary function testing
Diseases of the Pleural Space History and physical examination (observation, auscultation, percussion of the thorax) Thoracic radiography (pre- and post-thoracentesis) Thoracentesis Cytology of pleural effusate Culture and sensitivity of pleural effusate Serological testing when appropriate (FIV, FIP) Biochemical tests (e.g., serum/pleural effusion triglyceride concentration) Ultrasound examination Computed tomography (CT) or magnetic resonance imaging (MRI) of thorax Lymphangiography
Diseases of the Mediastinum History and physical examination (observation, auscultation, percussion of the thorax) Thoracic radiography Ultrasound examination CT or MRI of mediastinum FNA of mediastinal masses Barium swallow and esophagram Tracheoscopy/bronchoscopy
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• Reversed sneezing (violent, inspiratory movements •
• • • •
against a closed glottis) may occur with nasopharyngeal irritation from any source. Involvement of the ocular conjunctiva is not uncommon with contagious causes of rhinitis. Corneal involvement may suggest herpesvirus infection. Chorioretinitis may develop consequently to infectious canine distemper virus or cryptococcosis. Cough may indicate postnasal drip with pharyngeal irritation or concurrent involvement of the larynx, trachea, or bronchial tree. Some dogs retch and expectorate secretions that have accumulated in the pharynx. A serous discharge is typical of acute viral disease, whereas mucopurulent nasal exudate suggests a bacterial or fungal component. Other clinical findings such as fever, enlargement of the tonsils, bony swelling, regional lymphadenopathy, oral ulceration, and ocular or neurological involvement may be evident depending on the underlying causes of disease.
and over-interpretations of positive cultures must be avoided.
• The typical canine work-up for signs of nasal disease
Diagnosis • The differential diagnosis of upper respiratory infec-
•
•
•
•
tions is extensive (Table 163-3), including primary infectious diseases, secondary infections, and a large number of non-infective disorders. The age, vaccination status, history, and physical examination tend to focus the diagnostic considerations in most cases. The diagnostic studies chosen depend on the presumptive diagnosis and response to initial therapy (see Table 163-2). Primary infectious diseases, nasal mites, and foreign bodies with secondary infection are the important cause of rhinitis and sinusitis in younger dogs and cats. Older pets (older than 8 years of age) tend to be afflicted with nasal tumors complicated by secondary nasal infection. The poorly understood, idiopathic, lymphocytic-plasmacytic rhinitis of dogs and cats is a very common biopsy diagnosis that may be associated with allergy or infection. This disorder may allow for opportunistic secondary mucosal invasion by bacteria or fungi. Suppurative rhinitis is a less common biopsy diagnosis of the nasal mucosa. Primary and secondary bacterial infection may be involved; infection by Bartonella spp. should be considered. Infections caused by Aspergillus spp. and Penicillium spp. require histologic examination of nasal tissue, sometimes with special staining (e.g., silver stains) to detect hyphae. A positive agar gel immunodiffusion (AGID) test may also be supportive of the diagnosis. Routine culture is nonspecific because these fungi can be normal inhabitants of the nasal cavity.
▼ Key Point Because bacteria and fungi can be cultured normally from the nasal cavities, a careful exclusion of an underlying condition is essential
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•
requires general anesthesia. Routine laboratory tests can be obtained including a complete blood count (CBC) and serologic tests for aspergillosis and polymerase chain reaction (PCR) for Bartonella. Regional lymph nodes can be aspirated if enlarged, and routine thoracic films exposed to exclude concurrent bronchopulmonary infection. However, most diagnoses are made under general anesthesia. • At a minimum, diagnostic imaging should include an open mouth radiograph of the nasal cavity. Abnormal findings include focal or multifocal lesions, increased soft tissue or fluid density, loss of turbinate detail, nasal septal deviation, and boney destruction. These findings are not diagnostic of any specific condition, and each is compatible with some form of chronic infection. • Optimally computed tomography (CT) of the nasal cavity, paranasal sinuses, and nasopharynx should be done and interpreted by an expert in this form of imaging. • After radiological procedures, initiate anesthetic examination with careful inspection of the oral cavity, oropharynx, tonsils, and larynx. Follow this with antegrade rhinoscopy via the nostrils and retrograde rhinoscopy across the nasopharynx using a retroflexed endoscope. Unfortunately, rhinoscopy is limited in small dogs (and cats) related to availability of appropriate sized endoscopes. Visual findings of disease may include abnormal mucosal color (hyperemic, white); plaque formation (fungus or lymphocytic-plasmacytic rhinitis); puff ball (rhinosporidiosis) or nasal mites; and destruction of turbinate structure or friable mucosa. An obvious foreign body or mass lesions may be observed in some cases. Hemorrhage may obscure the examination field. • Then undertake mucosal biopsy of the nasal cavity, preferably guided by findings at endoscopy or radiography/CT. Blind biopsy based on location of clinical signs is also appropriate. In some cases of chronic rhinitis, large chunks of nasal turbinate bone may be obtained during this procedure. Request special stains (e.g., silver stains) for suspected cases of fungal rhinitis. At the end of the procedure the nasal cavity is flushed bilaterally with cooled saline (ensure that the endotracheal tube is inflated and the caudal airways packed with sponges; put the nose “down” to prevent aspiration and swallowing of fluid). Inspect the collection sponges at the conclusion of the procedure for any foreign material or tissue that may be appropriate for cytologic or histopathologic examination.
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Table 163-3. DIFFERENTIAL DIAGNOSIS OF UPPER AIRWAY INFECTIONS Causes of Nasal Discharge
Causes of Epistaxis
Infectious causes of nasal discharge in dogs and cats (see Table 163–1) Inflammatory causes of nasal discharge Lymphocytic plasmacytic rhinitis Idiopathic, including “allergic” rhinitis Postinflammatory scars at posterior choanae Congenital diseases predisposing to nasal discharge Ciliary dyskinesis Congenital—cleft palate Imperforate posterior choanae openings Immunodeficiency disease (IgA) Physical disorders leading to nasal discharge Foreign body Acquired—oro-nasal defect Trauma leading to nasal bleeding or fracture/sequestrum Abnormal drainage from the nasal cavity due to inflammatory or congenital webs, tumors, or polyps Neoplastic causes of nasal discharge
Thrombocytopenia from any cause Thrombocytopathia Ehrlichiosis Hyperglobulinemia or other hyperviscosity syndromes Polycythemia (serous discharge or epistaxis) Hypertension (including pheochromocytoma) Coagulopathy with normal platelets (not typical; usually due to platelet problems) Neoplasms Foreign bodies Violent sneezing from any cause Some chronic infections
Dogs—Malignant Tumors Adenocarcinoma (most common) Chondrosarcoma Fibrosarcoma Mast cell tumor Osteosarcoma Squamous cell carcinoma Transmissible venereal tumor
Cats—Malignant Tumors
Other Upper Airway Disorders Inflammatory polyps Disease of the tonsils Laryngeal edema consequent to inflammation, trauma, or increased work of breathing Unilateral or bilateral laryngeal paresis Inflammatory nodules on the vocal folds Eversion of the laryngeal saccules Airway obstruction Collapse of the glottic opening Congenital tracheal lesions (segmental lesions) Tracheal collapse Relentless barking Foreign body or foreign material Swallowing disorders, esophageal masses, or megaesophagus Trauma leading to hematoma, edema, fracture, perforation, laceration, or disruption Iatrogenic injury (traumatic intubation, excessive cuff inflation) Mass lesions: granulomas, tumors, and neoplastic conditions
Other Respiratory Disorders Squamous cell carcinoma Adenocarcinoma Lymphoma
Benign Tumors (Dogs and Cats) Polyps (more common in cats) Adenoma Fibroma
Mediastinal lymphadenopathy or heart base tumors causing airway compression Primary bronchial collapse Left main bronchus compression by an enlarged left atrium Primary chronic bronchitis (noninfectious) Heartworm disease Lungworms Pulmonary neoplasm Granulomatous disease
• Positive fungal cultures for aspergillosis are not nec-
•
•
essarily diagnostic for the disease, but invasion of nasal mucosa with hyphae or a positive immunodiffusion or enzyme linked immunosorbent assay (ELISA) test are supportive of the diagnosis. Mucosal biopsies can be cultured for bacteria. A positive culture is more likely to be significant when compared to a flush or swab (superficial) culture, but results must be interpreted carefully. • Rarely, surgical exploration of the nasal cavity and paranasal sinuses is needed for definitive diagnosis. The typical feline work-up for signs of nasal disease is often completed in two stages: • Initially, submit a CBC and feline leukemia virus (FeLV), feline immunodeficiency virus (FIV), and Cryptococcus ELISA tests to the laboratory.
• Obtain a chest radiograph if the condition is chronic or there are lower airway signs. • Send a swab of nasal discharge to the lab with specific instructions to stain the smear for Cryptococcus neoformans. • Submit advanced virus diagnosis tests (immunofluorescence; PCR) for herpesvirus infection. • Following this first set of treatments, treat the cat empirically with a single course of antibiotics (amoxicillin, clavulanate, or doxycycline with food) and lysine (for possible herpesvirus infection) while awaiting the test results. Clients are instructed to provide good home nursing care and a stress-free environment for the cat. • If these studies fail to yield a diagnosis and empiric therapy is not curative, then anesthetic procedures
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including nasal cavity imaging, rhinoscopy, and biopsy are needed, as described above for the dog. • When clients cannot pursue advanced imaging and rhinoscopy, an “intermediate” and less costly (but more superficial) approach can be taken using a very short period of general anesthesia. Premedicated the cat with butorphanol (0.25 mg/ kg, IM) with acepromazine (0.1 mg/kg, unless contraindicated), accomplish IV anesthetic induction, and intubate the cat with a cuffed endotracheal tube. If permitted, obtain one open-mouth radiograph of the nasal cavity. Use a warmed dental mirror and a strong focal light source to evaluate the retropharyngeal space to rule out a polyp or obvious foreign body. Pull the soft palate in a rostral and ventral direction using a spay hook, and place the mirror in the caudal oropharynx to direct reflected light into the nasopharynx. Then obtain two or three empiric nasal mucosal biopsies from the affected side(s) using 2- to 3mm biopsy forceps. At the conclusion of the procedure, flush the nasal cavity gently with sterile saline using a soft red-rubber tube to dislodge accumulated secretions or foreign material. The glottis should be protected by inflation of the cuff, packing with clean sponges (inspect at end of procedure), and by keeping the cat in a nose-down position so that most fluid exits the pharynx via the mouth.
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• For cats with chronic bacterial rhinitis of uncertain
•
•
cause, a recurring cycle of intermittent antibiotics may be needed. Amoxicillin-clavanalate, doxycycline (5–10 mg/kg PO daily, always followed by food), and a 5-day course of azithromycin (5–10 mg/kg daily for 5 days; thereafter 10 mg/kg q72h) may provide symptomatic relief. A course of clindamycin also may be considered as it has some efficacy against Mycoplasma spp. Lysine (250 mg/day once or twice daily, crushed in food) can be tried if herpesvirus is thought to be a predisposing cause. Treat immunosuppressed cats with secondary bacterial rhinitis with broad-spectrum antibiotics if clinical signs worsen or if lower respiratory infection develops. For cats with FIV or FeLV viral-related immunosuppression, the empiric use of diluted human interferon alpha 2a (30 units, PO for 7 days, every other week) or of recombinant feline alpha interferon has been advocated, but more studies are needed. Cats do form antibodies against human interferon, which may limit effectiveness long term. In bacterial rhinitis associated with tooth root abscesses, management of the dental disease, along with a long-term course of antibiotics, may be curative. Any oronasal fistula should be closed.
Treatment of Fungal Rhinitis A variety of treatments have been suggested for welldefined fungal rhinitis/sinusitis. Treatment recommendations depend on the specific agent, and protocols can be complicated and, in many cases, unsuccessful.
• General principles of therapy Treatment of Viral and Bacterial Rhinitis • Treatment of acute upper respiratory infection depends
•
on the underlying condition. In cases of viral rhinitis, supportive nursing care, maintenance of hydration, and prevention of secondary bacterial infections by administration of a broad-spectrum antibiotic represent a typical therapy (avoid tetracyclines in puppies, enrofloxacin in growing animals, and chloramphenicol in cats). Ophthalmic medications may be useful for conjunctivitis or in cases of herpesvirus associated corneal ulcers (avoid corticosteroids). Dogs or cats with respiratory infection caused by bacterial infection may respond to doxycycline. This is especially true for B. bronchiseptica or Bartonella infections, which may be primary. Tetracyclines should not be used in pregnant bitches or in young dogs or cats if permanent teeth have not yet erupted (as staining will occur). Because B. bronchiseptica is an inhabitant of the mucosal brush-border, it can be difficult to eradicate infection with systemic antibiotics. In welldefined cases, empiric therapy with nebulized gentamicin can be considered (for details, see “Infectious Tracheobronchitis”).
• Patients with fungal rhinitis represent complicated cases, and the clinician should consult detailed textbooks or current literature before embarking on any course of therapy for these serious conditions. It may be helpful to discuss options with an internist or a surgical specialist. • Oral medical therapy with an azole antimicrobial represents the least complicated approach to treatment. However, the drugs are expensive and many patients will not respond. Furthermore, these drugs may have significant adverse effects, such as hepatotoxicity, that must be discussed with the client. • The use Foley-type balloon catheters or red-rubber tubes, placed by endoscopy or by surgery, allows for instillation of antifungal medication. Some imidizoles are available in liquid form and can be infused directly into the nasal cavity and frontal sinus. • Surgical debridement may be considered a possible adjunct to therapy. Non-surgical debridement can be done via an endoscope or with devices used for dental cleaning (Water-pik) dislodge infected material.
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• Rhinosporidiosis is associated with “puff-ball granulo•
•
mas” in the nose. These can be treated by surgical extraction. Aspergillus flavus and Penicillium spp. are most commonly treated with nasal tubes placed by endoscopy or surgery. • The endoscopic method involves general anesthesia; placement of two infusion catheters in the nasal cavity (or frontal sinus if visible); multiple Foley or balloon catheters within the nostrils rostrally and in the cranial soft palate (via the nasopharynx); and infusion of antifungal medication with the dog placed in varying recumbent positions during the procedure. Before treatment, the balloons are inflated to create a nearly sealed nasal cavity. A onetime treatment of liquid enilconazole is administered (1% or 10 mg/ml, enilconazole) or clotrimazole (approximately 120 ml of a 1% solution) for 1 hour. A slow, constant infusion process maintains continual filling of the space and contact with the mucosa. This may be preceded by debridement of affected tissues (controversial). Enilconazole is also effective as a vapor, which may enhance its local effect. • One-treatment cures with enilconazole and clotrimazole have been reported. In one study of 24 dogs an 80% response rate was observed. In another study of 36 dogs, almost 95% responded to local treatment of enilconazole (about 55% responded to a single treatment). A second treatment 3 to 4 weeks later provided a positive outcome for most dogs that did not respond to a single infusion. One study of 60 dogs treated with clotrimazole reported about a 90% response rate. • An alternative method is placement of nasal tubes in the frontal sinus either surgically or by use of an endoscope to instill enilconazole (10 mg/kg, in 10 ml of solution divided between each nasal cavity) for 10 to 14 days. This approach is more labor intensive and may have a higher success rate, but has largely been supplanted by the endoscopic method. • Oral therapy of nasal aspergillosis may be attempted as a primary treatment or as a supplement to local therapy. A number of drugs have been used with varying success. Itraconazole at 5 mg/kg PO q12h for 2 to 3 months. Thiabendazole, which is less effective (40–50% positive response) and is more hepatotoxic, but can be administered at a dose of 10 to 20 mg/kg PO q12h with food (start at lower dose) for 6 to 8 weeks. The main advantage is a lower drug cost. Ketoconazole (Nizoral 5–10 mg/kg PO q12h for 6–8 weeks) is about as effective as thiabendazole. Cryptococcus neoformans infection of the upper airways is treated with fluconazole, itraconazole, ketoconazole, or amphotericin B (alone or in combination with flucytosine). Fluconazole seems to be useful at 50 mg total dose per cat q24h for 2 to 4 months. Itra-
conazole at 5 mg/kg q12h may be an alternative and needs to be continued even after the control of nasal discharge. Occasionally, higher doses are needed.
INFECTIOUS TRACHEOBRONCHITIS General Points • Acute tracheobronchitis refers to an inflammation of •
•
• •
•
•
•
•
•
the trachea and bronchial tree of recent onset and short duration. Canine infectious tracheobronchitis (ITB), also known as the kennel cough complex, refers to a group of acute contagious infections in dogs that cause inflammation of the larynx, trachea, and bronchi. ITB is discussed in Chapter 12. Feline upper respiratory infection (URI) complex refers to a group of acute contagious upper respiratory diseases in the cat that may also involve the trachea or bronchial tree (see Chapter 11). In some cases the lung is involved as well. The clinical signs of tracheobronchitis typically include a paroxysmal, harsh, dry cough that can last for days to weeks. The condition may be accompanied by other signs of upper respiratory infection such as nasal discharge and sneezing (which are typical in cats and may be noted in dogs with Bordetella infection). In many cases, signs are isolated to the tracheobronchial tree. Common canine infectious agents include B. bronchiseptica, canine parainfluenza virus, canine adenoviruses (types 1 and 2), canine distemper virus, canine reoviruses (types 1 and 2), and canine herpesvirus. B. bronchiseptica is the most common bacterial infection, and canine parainfluenza virus is the most common viral isolate noted in the dog with canine infectious tracheobronchitis (ITB). Recently a new canine influenza virus, mutated from an equine strain, has been identified in dogs. This virus can cause signs identical to those of other “kennel cough” agents. In cats, feline herpesvirus and calicivirus are considered the most common causes of contagious upper respiratory disease. Calicivirus is more likely to involve the lower airways. Mycoplasma infection and bordetellosis should also be in the differential diagnosis for lower airway disease in cats. Many of these infectious diseases are very contagious and associated with high-density populations. The infectious agents can be transmitted by aerosol or fomite. Incubation periods are typically between 3 and 10 days. Vaccinations confer partial to complete protection against many of the ITB agents in most cats and dogs. In addition to infectious (contagious) causes, other conditions may predispose to tracheobronchial infection or inflammation. Some of these include:
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•
• Abnormal local immunity • Boarding kennels/catteries • Racetracks • Ciliary dyskinesis (rare) • Contagious diseases • Debilitation/poor nutrition • Drying of the mucous membranes • General anesthesia (intubation; aspiration) • Poor vaccination history • Recurrent or chronic bronchial disease Acute tracheobronchitis indicates an inflammatory reaction. The usual consequences of this inflammation are variable increases in tracheobronchial secretions and cough. If respiratory clearance mechanisms or immunity is insufficient, pneumonia may develop from the primary agent (e.g., bordetellosis) or from secondary bacterial invaders.
•
•
•
•
Diagnostic Tests • Routine hematologic tests and radiographs are
• • • • •
usually unremarkable; however, the client must understand that a number of other conditions can lead to similar clinical signs and should be prepared to support further examinations if indicated. If the patient is very ill, or if the clinical course of expected improvement is not met, additional tests are indicated. A CBC and serum chemistry panel (especially renal function, glucose) is appropriate for sick animals. Fecal flotation and empiric deworming with pyrantel is recommended for puppies and kittens. If significant ocular signs such as photophobia or anisocoria are noted, stain the cornea for ulcers; if results are positive, give antibiotics (without steroids). In previously untested cats, perform FeLV and FIV tests to screen for immunosuppressive diseases. Radiography of the thorax is probably the most indicated of studies and can be justified to rule out bron-
chiopneumonia and other causes of acute cough. The right middle lung lobe is predisposed to secondary infection in upper respiratory diseases, and pulmonary involvement is best seen on a VD or DV projection. Culture and cytology of the tracheobronchial airway secretions are indicated in unresponsive cases or those with confounding bacterial pneumonia. A transtracheal wash in cooperative dogs or an endotracheal wash in puppies or cats can be used to obtain a diagnostic sample. Other diagnostic tests may be considered in ruling out the differential diagnosis. These are indicated in Table 163-3.
Therapy of Infectious Tracheobronchitis • The viral causes of these diseases are usually self-
Diagnosis of Tracheobronchitis • In general, one diagnoses feline upper respiratory infections and canine infectious tracheobronchitis from the history and physical examination. The long list of potential causes of signs of acute tracheobronchitis includes the conditions listed in the lower portion of Table 163-3. Some conditions (e.g., noninfective bronchitis, neoplasia) are more likely in mature animals and should be excluded initially by examination and thoracic radiography. The duration of signs and the response to supportive treatment will largely determine which diagnostic considerations are pursued. In classic kennel cough with no constitutional signs, diagnostic studies are generally negative and are not indicated. Poor responders should be worked up.
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•
limiting, and often no treatment is necessary. This is especially true in mild, uncomplicated cases with minimal constitutional signs (i.e., animals that are without fever, still eating, and not acting sick). Specific supportive, symptomatic, and antimicrobial therapy for infectious tracheobronchitis is described in Chapters 11 (cats) and 12 (dogs).
Prevention of ITB • Vaccination in dogs can be performed routinely with the following antigens: B. bronchiseptica, canine parainfluenza virus, canine adenovirus type 2, and canine distemper virus (see Chapter 7). Cats can be vaccinated against herpes-, calici-, and panleukopenia (parvo) viruses and bordetellosis (see Chapter 7).
BRONCHOPNEUMONIA Etiology • Pulmonary infections are common in dogs and in •
• • •
cats. Bacterial pneumonia is an important cause of morbidity and mortality in dogs and cats. Though numerous infectious agents (viruses, rickettsia, and systemic mycoses) can cause interstitial pneumonia, most cases of bronchopneumonia are bacterial in origin. Common microorganisms responsible for pneumonia are indicated in Table 163-1. The route of infection is typically inhalation. Hematogenous spread of bacterial pneumonia to the lungs is less common and can be very difficult to treat. The clinician should appreciate possible risk factors and predisposition for pneumonia, including: • Contagious upper respiratory infection (e.g., infective tracheobronchitis after boarding) • Preexistent bronchopulmonary disease (including noninfectious bronchitis, lung contusion, heartworm disease, smoke inhalation, pulmonary atelectasis, thromboembolic disease)
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• Inhalation or aspiration of pharyngeal or gastric fluid or contents (due to anesthesia, swallowing disorders, megaesophagus, neuromuscular disease, laryngeal paralysis, posterior fossa lesion, stupor, vomiting, prolonged recumbency), or opiates and postoperative sedatives • Oro-nasal sources of infection (sinusitis, dental disease) • Immunosuppression caused by another virus (FeLV, FIV, canine distemper, parvovirus) or disease (e.g., hyperadrenocorticism, diabetes mellitus, generalized demodecosis) • Immunosuppressive drug therapy (glucocorticoids, anticancer chemotherapy) • Abnormal respiratory defense mechanisms (Cushing’s disease, chronic bronchitis, ciliary dyskinesia, neutrophil dysfunction syndromes) • Bronchial foreign body • Foreign body aspiration pneumonia (e.g., food, mineral oil in cats) • Debilitation, hospitalization, nosocomial infection Sedation with opiates. • Indwelling intravenous catheter sepsis (hematogenous spread) • Contaminated endotracheal tube, tracheostomy tube, or bronchoscope • Aspiration or inhalation of liquid foreign material during diagnostic or therapeutic procedures (barium sulfate, medications, mineral oil, nutritional supplements) • Following thoracic surgery Prompt recognition and treatment of bronchopneumonia is important. It is equally important to identify the predisposing cause so that further episodes can be prevented or anticipated.
• Thoracic radiographs are key to the diagnosis of
•
Clinical Signs • The history often indicates a predisposing factor for bronchopneumonia.
• Tachypnea, respiratory distress, productive cough, and fever are typical findings.
• Constitutional signs—depression, anorexia, and list• •
lessness—may be observed as the only features of disease. Mucopurulent nasal exudate may be present. Pulmonary adventitious sounds—especially rhonchi and crackles—may be ausculted; however, loud or asymmetric bronchial sounds can be the only auscultatory finding.
•
•
Diagnosis of Bacterial Bronchopneumonia ▼ Key Point Point Clinical signs, radiography, and the CBC are usually sufficient to make a presumptive diagnosis of bacterial pneumonia.
•
bronchopneumonia. • The typical findings are increased lung density that is most commonly alveolar in nature leading to border effacement (silhouetting) of the heart. The lobe may become consolidated, producing a fluid density lobar sign. • The right middle lung lobe is most prone to bacterial infection; the cranial lobes also are frequently involved. In contrast, dorso-caudal pulmonary infiltrates are very unlikely to be associated with bacterial infection of the lung with the exception of atypical microorganisms (mycoplasmas, fungal infections, mycobacteria), or hematogenous pneumonia (from sepsis), which is diffuse, beginning as an interstitial pattern and progressing to alveolar. • A cranioventral distribution of bacterial bronchopneumonia is typical. • With some foreign bodies, the intermediate lobe may be involved. • Lung consolidation may occur, leading to an eventual loss of air bronchograms except in the most proximal portion of the lobe. Radiographic differential diagnosis is important. • Hilar or sternal lymphadenopathy is uncommon with bacterial infection. • Nodular densities are more typical of fungal disease, granulomatosis, or pulmonary neoplasia. • The combination of bronchopneumonia with concurrent septic pleural effusion (pyothorax) is very uncommon in dogs and cats. These findings are suggestive of an atypical infectious agent such as Nocardia asteroides or actinomycosis, presence of a foreign body, concurrent malignancy, or pulmonary embolus. • Pneumonia caused by viral, protozoal (e.g., toxoplasmosis), rickettsial, or fungal infection is typically interstitial in distribution. Fungal and Toxoplasma infections produce granulomatous lesions in the lung, and with systemic mycoses, hilar lymphadenopathy can be pronounced. • Esophageal air or dilatation may indicate simple air swallowing or a more serious condition such as megaesophagus or myasthenia gravis. CBC—Leukocytosis, left shift, and monocytosis are typical abnormalities on the CBC; however, the magnitude of change is not consistently related to the extent of infection. Overwhelming fulminant bacterial pneumonia may cause a neutropenia with degenerative left shift. Serology—Infected cats also may be FIV or FeLV positive. FIV infection has also been associated with nonbacterial alveolitis and interstitial pneumonia. Airway cytology and culture can confirm the diagnosis. • Transtracheal or endotracheal aspiration cytology demonstrates neutrophilic inflammation, often with degenerative PMNs and intracellular bacteria.
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• Cocci are usually streptococcus, and rods are usually gram-negative bacteria. • The culture is typically positive for bacterial growth (see Table163-1). • Special media are needed for effective culturing of Myocoplasma spp.; mycoplasma culture should be requested in most cases, and especially in cats. • While a fine-needle aspiration of a collapsed lung can provide diagnostic tissue, in general, one should avoid percutaneous needle aspiration of a consolidated lung in order to prevent inoculation of the pleural space. ▼ Key Point Bronchopneumonia is typically a complication related to another disorder, general anesthesia, or medical or surgical treatments. The precipitating cause should be identified.
Treatment of Bacterial Bronchopneumonia • Keep the patient well hydrated and warm. Fluid • • •
therapy is often required to prevent dehydration and inspissated respiratory secretions. Perform thoracic coupage 4 to 6 times daily. Once the patient feels better, brief walks, followed by coupage, help to mobilize tracheobronchial secretions. Airway humidification may assist in expectoration of secretions. Expectorants like guaifenesin are of uncertain merit and are not usually prescribed. Bronchodilator therapy (sustained release theophylline at 10–20 mg/kg PO q12h for dogs) is of unproven efficacy but may reverse irritative bronchoconstriction and strengthen respiratory muscle effort in dyspneic animals.
•
▼ Key Point Cough suppressants are contraindicated in bronchopneumonia.
• Humidified oxygen should be administered to dyspneic, cyanotic, or hypoxemic animals.
• Antibiotics should be prescribed for at least 3 weeks. •
•
The duration of therapy may be longer pending clinical results and radiographs. Antibiotic choice should be based on culture and sensitivity (obtained by transtracheal or endotracheal washing) and with consideration of current or prior antibiotic therapy. Request a Gram stain on expectorated material or a cytoprep from an airway washing. Initial/Empiric antibiotic therapy is initiated when culture results are pending, when cultures are reported as “no growth,” or when airway culture is simply unavailable. An extended or broad-spectrum antibiotic is generally indicated in dogs and in cats. The choice depends on a number of factors including the species, age of the patient, severity of pneumonia radiographically, respiratory status (oxygen
•
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saturation, respiratory rate and depth), previous antibiotic therapy, and suspected source and type of microorganism. In cases of nosocomial (hospitalacquired) infection, a more aggressive antibiotic protocol may be indicated. There is no one best choice for antibiotic therapy in pneumonia, and the best approach is to culture fluid from the lung and target a specific microorganism based on sensitivity testing. • Cephalosporins and amoxicillin-clavulanic acid are generally effective with activity against gram-positive and gram-negative bacteria, as well as against anaerobes. They are generally well tolerated by dogs and cats, including most young animals. Rapid IV administration of cefazolin can cause vomiting. These drugs do not demonstrate significant activity against mycoplasma spp. • Sulfadiazine-trimethoprim is a reasonable drug for first-line therapy of bronchopneumonia in dogs. • Azithromycin is increasingly used for treatment of infections in dogs and cats, and is proabably a good drug for empiric therapy of pneumonia. There is demonstrated activity against mycoplasma spp. • Fluoroquinolones (enrofloxacin or orbifloxacin) are broad-spectrum drugs available for both parenteral and oral use. These antibiotics should not be used for trivial infections. There is some activity against mycoplasma spp. Resistant or complicated bronchopneumonia • Doxycycline is an excellent choice for unresponsive pneumonia, in part related to strong activity against bordetellosis and myoplasma infection. However, the overall spectrum is limited and it is not generally chosen as a single drug for empirical therapy. In resistant pneumonia in cats, doxycycline is a good choice because of the high probability of mycoplasma infection. • In cases of life-threatening or poorly responsive pneumonia, the spectrum of a cephalosporin or amoxicillin-calvulanic acid can be extended with parenteral amikacin, once daily (provided hydration and renal function are satisfactory). This combination does not affect mycoplasma spp. • In cases of pulmonary consolidation, a combination of a fluoroquinolone combined with clindamycin, metronidazole, or amoxicillin is a reasonable choice. • In life-threatening bronchopneumonia, consider a combination of IV enrofloxacin plus IV amoxicillin or a third generation cephalosporin. Management of bacterial pyothorax requires thoracostomy tube drainage and antibiotics. Because anaerobic organisms are commonly involved in pyothorax, treatment with penicillin (20,000–40,000 units/kg PO or IV q6–8h), alone or in combination with sulfadiazine-trimethoprim, or clindamycin is recommended.
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Follow-Up • Obtain thoracic radiographs to ensure resolution of
•
infection. Areas of lobar consolidation may take 2 to 6 weeks to become totally clear. Failure of steady clinical and radiographic improvement indicates a need to reevaluate the patient and to consider a tracheal wash or bronchoscopy with bronchial fluid aspiration. Recurrent pneumonia also is common, particularly in those animals with persistence of predisposing factors, including swallowing disorders, chemotherapy, ciliary dyskinesis, and acquired or congenital immune deficiencies. Infrequently, an unresponsive or refractory single lobe infection requires surgical lobectomy for resolution of the problem. Surgery is also indicated in cases of lung abscess or pneumonia due to a foreign body that cannot otherwise be retrieved. Surgical results are generally rewarding in this clinical situation.
• Parasites of the nasal cavity include cuterebra and other grubs, the microscopic nematode Eucoleus boehmi, nasal mite Pneumonyssus (Pneumonyssoides) caninum, and the gapeworm (S. ierei).
Clinical Signs • Signs depend on the specific parasite, site and • • • •
• RESPIRATORY PARASITES Etiology • A number of respiratory parasites have been identified in dogs and cats. The life cycle of some respiratory parasites is complex and involves intermediate and transport hosts. Some of the more important infections include: • Aelurostrongylus abstrusus is a parasite of cats. This nematode requires a snail or slug as an intermediate host. Cats are often infected by eating transport hosts including birds, small mammals, and reptiles. • Paragonimus kellicotti is a fluke parasitic to dogs and cats. Infection follows ingestion of an intermediate host (crayfish, aquatic snail) or a transport host (e.g., raccoon). • Capillaria aerophilia is a nematode parasite of the dog and cat that has a direct life cycle. Pathogenic potential appears very low. • Crenosoma vulpis, the fox lungworm, infrequently infects dogs. • Osleri/Filaroides spp. are nematodes that invade the respiratory tract of the dog. Transmission is direct, often from bitch to pups. Three related species have been associated with respiratory disease, O. osleri (found in granulomas near the tracheal bifurcation), F. milksi (a bronchopulmonary parasite), and F. hirthi (a lung parasite of importance to research colonies). • Dirofilaria immitis infects the pulmonary arteries, causing secondary pulmonary injury (see Chapter 152). • Toxoplasma gondii is a protozoan capable of multisystemic infection that is usually subclinical, but occasionally can cause pneumonia (see Chapter 21). Immunosuppression predisposes to toxoplasmosis.
•
severity of infection, and the magnitude of the host reaction. Mild cases are asymptomatic and only detected if ova are identified during routine fecal examination. Clinically apparent infections occur most often in younger animals (300 days], no other metastatic sites, slow doubling time, and less than three metastatic lesions).
▼ Key Point Always submit lung tumors for histopathologic evaluation to establish diagnosis and prognosis.
Chemotherapy
• Chemotherapy may be beneficial in some tumors, mainly if used as an adjunctive therapy.
• Lymphomatoid granulomatosis may respond to com-
• •
bination chemotherapy with prednisone, vincristine, and cyclophosphamide. Eosinophilic granulomas may respond to immunosuppressive doses of prednisone alone. Carboplatin and gemcitabine are two drugs used for adjunctive therapy for excised primary pulmonary tumors. Malignant pleural effusion can be treated with intrapleural chemotherapy. 5-fluoruracil is an inexpensive drug that can be used safely in dogs. Cisplatin
is other drug that can be used in dogs but is nephrotoxic. Cisplatin and 5-fluoruracil are fatal if used in cats. Some metastatic tumors that are responsive to chemotherapy include hemangiosarcoma (VAC protocol; vincristine, doxorubicin, and cyclophosphamide), lymphoma (COP with or without doxorubicin or L-asparaginase), and some malignant histiocytosis (lomustine with prednisone). Specific protocols for these types of tumors are described in the literature.
•
tumor burden, thoracic lymph node involvement, and other metastases. Absence of lymphatic invasion by the lung tumor has been associated with increased survival times. Small (1 year). Even large lobar masses can be removed successfully with a reasonable (>6 months) survival time. In cats, based in the histologic grade, poorly differentiated tumors have a median survival time of 2.5 months and those tumors that are moderately differentiated without evidence of metastasis have a median survival time of 23 months after surgery. Following treatment, monitor with routine thoracic radiographs every 1 to 3 months.
SUPPLEMENTAL READING Allen HS, Broussard J, Noone K: Nasopharyngeal diseases in cats: a retrospective study of 53 cases (1991–1998). J Am Anim Hosp Assoc 35:457–461, 1999. Brown MR, Rogers KS, Mansell KJ, et al: Primary intratracheal lymphosarcoma in four cats. J Am Anim Hosp Assoc 39:468–472, 2003. Gottfried SD, Popvitch CA, Goldschmidt MH, et al: Metastatic digital carcinoma in the cat: a retrospective study of 36 cats (1992–1998). J Am Anim Hosp Assoc 36:501–509, 2000. Hahn KA, McEntee MF: Primary lung tumors in cats: 86 cases (1979–1994). JAVMA 211(10):1257–1260, 1997. Hahn KA, McEntee MF: Prognosis factors for survival in cats after removal of a primary lung tumor: 21 cases (1979–1994). Veterinary Surgery 27:307–311, 1998. Henry CJ, Brewer WG, Tyler JW, et al: Survival in dogs with nasal adenocarcinoma: 64 cases (1981–1995). J Vet Intern Med 12(6):436–439, 1998: Evaluation of prognosis factors for dogs with primary lung tumors: 67 cases (1985–1992). JAVMA 211(11): 1422–1427, 1997. Mukaratirwa S, Van der Linde-Sipman JS, Gruys E: Feline nasal and paranasal sinus tumors: clinicopathological study. Histomorphological description and diagnostic immunohistochemistry of 123 cases. J Feline Medical Surg 3(4): 235–245, 2001. Ogilvie GK, Weigel RM, Haschek WM, et al: Prognostic factors for tumor remission and survival in dogs after surgery for primary lung tumor: 76 cases (1975–1985). JAVMA 195(1):109–112, 1989. Rogers KS, Walker MA, Helman RG: Squamous cell carcinoma of the canine nasal cavity and frontal sinus: eight cases. J Am Anim Hosp Assoc 32(2):103–110, 1996.
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Thoracic Trauma Dale E. Bjorling
Thoracic trauma in dogs and cats most often is the result of automobile accidents. The lack of apparent external injuries may be misleading; the diaphragm, thoracic wall, heart, or lungs may be severely damaged with little apparent damage to the overlying skin. Evaluate animals presented for treatment of thoracic trauma thoroughly but rapidly; if necessary, institute treatment prior to completing a full patient assessment. Animals with thoracic trauma may suffer concurrent abdominal or skeletal injuries. Surgical correction of injuries associated with thoracic trauma may be required on an emergency basis; however, in general veterinary practice it is preferable to avoid emergency surgery of animals suffering thoracic trauma unless absolutely necessary. This chapter discusses the major disorders caused by thoracic trauma: pulmonary and myocardial contusions, pneumothorax, rib fractures and flail chest, hemothorax, and diaphragmatic hernia; see Chapter 164 for discussion of chylothorax. Injuries to abdominal viscera are discussed in respective organ-system chapters.
• Blunt trauma can cause pneumothorax, hemothorax, pulmonary contusions, fractured ribs, or any combination of these.
Penetrating Trauma • Penetrating trauma usually is the result of a gunshot.
•
•
•
It may also result from a sharp instrument (e.g., a knife, screwdriver, stick, or arrow) or from deep bite wounds inflicted by a big dog on a smaller dog or cat. Consider the type of projectile, point of entry, and path of the penetrating object when attempting to diagnose thoracic trauma, even if wound entry is distant to the thoracic cavity. The path of a projectile may be altered if it strikes bony structures. It is often unclear whether thoracic injuries have resulted from penetrating wounds. Depending on the extent of injury, signs of cardiovascular collapse or respiratory distress may develop more slowly in patients suffering penetrating injuries of the thorax. In at least one study, mortality subsequent to bite wounds only occurred with thoracic or abdominal trauma, and exploratory thoracotomy failed to improve survival.
ETIOLOGY CLINICAL SIGNS
Blunt Trauma • Blunt trauma to the thoracic cavity usually is the
• Tachypnea or dyspnea (difficulty breathing) is a typical
result of automobile accidents. It may also be the result of being kicked by a human or farm animal (horse, cow), being struck by a heavy object, or falling from heights (e.g., falling from a window of a highrise building). The severity of injury depends on the mass of the object delivering the blow, the velocity of the object, and the area to which the blow is delivered. It has been shown experimentally that when a blow equivalent to that delivered by a car is administered to the thorax of anesthetized dogs, the thoracic viscera may be compressed until the opposing parietal pleural surfaces underlying the ribs may almost be brought into contact. The ribs of young animals are pliable and tend to fracture less often than those of older animals.
presenting sign in dogs and cats that suffer thoracic trauma. The animal may have an anxious or distressed appearance. The owner may or may not have observed the injury. Clinical signs of thoracic trauma may be delayed in onset, especially those associated with diaphragmatic hernia. Hypovolemic shock may result from internal or external hemorrhage or accumulation of fluid within tissue spaces. An animal suffering from hypovolemic shock has an increased heart rate, weak peripheral arterial pulses, cold extremities, and pale mucous membranes, and it often appears depressed or stuporous (see Chapter 156 for further discussion of shock). Gastrointestinal signs (diarrhea or vomiting due to obstruction) may be observed if a portion of the gastrointestinal tract has been displaced into the tho-
•
•
•
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racic cavity through a diaphragmatic hernia. These signs are not commonly present immediately after the injury has occurred.
DIAGNOSIS
•
and abnormal location of the cardiac apex beat (displaced by herniation of abdominal viscera). Also palpate the abdominal cavity for concurrent intra-abdominal injuries. The absence of viscera suggests their displacement into the thoracic cavity.
Auscultation
▼ Key Point Treatment of hypovolemic shock or
• Carefully auscultate the entire thoracic cavity to
other life-threatening disorders takes precedence over patient evaluation.
determine whether breath sounds can be identified throughout the thoracic cavity. The absence of respiratory sounds strongly suggests displacement of the lungs by air, fluid (e.g., blood), or abdominal viscera. Crackles suggest intrapulmonary fluid accumulation. Auscultate the heart as well. A change in the location or pitch of heart sounds suggests displacement of the heart by air, fluid, or viscera. Ventricular arrhythmias may occur as the result of traumatic myocarditis or myocardial ischemia; however, their onset is more frequently observed 24 to 48 hours after the traumatic episode. See also Chapter 142.
History • Attempt to identify recent or past traumatic episodes. • Question the owner regarding the onset and pro-
•
gression of the current clinical signs.
• Take the history while initial evaluation of vital signs is in progress so that life-threatening injuries (e.g., tension pneumothorax) can be detected and treated immediately.
Physical Examination
•
After initially determining the animal’s vital signs (e.g., heart rate, respiratory rate, mucous membrane color and refill, temperature, and level of consciousness), examine the respiratory system using the following:
Percussion
• • • • •
Observation (of breathing) Palpation Auscultation Percussion Radiography
• Perform percussion of the thoracic wall to determine
•
Observation
• Observe the rate, depth, and effort of respirations. • Rapidly developing dyspnea usually is the result • •
• •
of pneumothorax, pulmonary contusion, or hypovolemia. Rapid, shallow, choppy breathing can result from restriction of the thoracic wall because of painful rib fracture. Paradoxical motion of the chest wall is caused by collapse of a portion of the rib cage on inspiration when multiple rib fractures create an unstable flail chest wall. Decreased hemithorax movement (fixation) can be seen on the side into which abdominal viscera have herniated through a ruptured diaphragm. Herniation of the lung into the intercostal space countercurrent with each respiration indicates torn intercostal muscles.
Palpation
• • •
Fractures
• Thoracic injuries may occur in more than 30% of dogs and cats sustaining traumatic fractures.
• Examine the animal for the presence of fractures; do
•
• Palpate the thoracic wall for rib fractures, unstable (flail) segments, hematomas (usually adjacent to rib fractures), subcutaneous emphysema (crepitus), intercostal muscle tears (usually under intact skin),
increased or decreased resonance. By placing one hand flat on the thoracic wall and tapping the knuckle of the middle finger with a percussion hammer or the tips of the fingers of the opposite hand, a sound of consistent frequency is produced in normal animals. In animals with air or air-filled viscera underlying the thoracic wall, the pitch is deeper and more resonant, whereas the sound produced in animals with fluid or solid viscera immediately under the thoracic wall is dull and less resonant. Percussion aids detection of pneumothorax, pleural effusion (e.g., hemothorax and chylothorax), diaphragmatic hernia, and consolidation of lung lobes. Skilled use of this technique requires frequent practice on normal animals to allow a distinction between normal and abnormal sounds. See also Chapter 142.
•
not be distracted by the obvious presence of broken bones but continue searching for evidence of more serious internal injuries. If spinal fractures are suspected, handle the animal with great care until these have been stabilized or it is determined radiographically that the spine is intact. The presence of fractures suggests that trauma of sufficient force to inflict injury to the thorax and its con-
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tents has occurred. A survey of dogs injured in motor vehicle accidents found that more than 50% of animals with intrathoracic injuries also had fractured bones.
Surface Wounds and Abrasions
• Clip hair from the thoracic wall area as necessary to •
identify abrasions, bruises, or wounds that may point to likely sites of intrathoracic injury. Open wounds that freely communicate with the pleural space can cause progressive pneumothorax; unless the animal is stable, seal these immediately.
• If a diaphragmatic hernia is suspected but unconfirmed by plain radiographs, consider positivecontrast celiography or abdominal ultrasonography (see Chapter 4).
Thoracocentesis If indicated, perform thoracocentesis to obtain a sample of pleural fluid or to drain air from the pleural space (see Chapter 3 for technique).
• Analyze the fluid for the presence and concentration
Thoracic Radiography Take radiographs to evaluate the heart, lungs, pleural space, and thoracic wall (see Chapters 143 and 159 for a discussion of thoracic radiography).
•
• It is sometimes advisable to delay thoracic radiography of the injured animal until after higher priority conditions such as shock have been stabilized by emergency treatment. Pulmonary contusion, characterized by hemorrhage and fluid accumulation within the lungs, may not reach its greatest extent for 6 to 12 hours and then often may not appear radiographically to be improved for 7 to 10 days after injury.
•
▼ Key Point The full severity of pulmonary contusions may not be apparent on thoracic radiographs made within 1 to 2 hours of injury.
• A narrowed cardiac silhouette may suggest • •
• • •
•
hypovolemia. Evaluate the pleural space carefully for fluid, air, or abdominal viscera, and evaluate the integrity of the diaphragmatic outline. Look for radiographic evidence of fracture or dislocation of skeletal structures and subcutaneous emphysema, which indicates leakage of air into the subcutaneous space from the environment, the thoracic cavity, or a major airway. Pneumomediastinum is seen as air outlining the mediastinal contents and is indicative of tracheobronchial rupture. If the animal’s condition does not preclude this, obtain two radiographic projections. Often it is difficult to identify a diaphragmatic hernia on thoracic radiographs, particularly if obscured by accumulation of fluid within the pleural space. If a large quantity of pleural fluid is present, remove it and repeat the radiographs (see Chapter 159) or obtain an ultrasound examination, if readily available. Observations suggesting a diaphragmatic hernia include cranial displacement of the stomach, the loss of the caudal outline of the liver, and the presence of gas-filled viscous organs within the thoracic cavity.
1717
of red blood cells (RBCs) and plasma protein. The fluid may be whole blood, or it may be a combination of transudate, exudate, chyle, and blood, depending on the severity and duration of injury and the organs affected. Centrifuge an aliquot of the fluid and examine the cellular portion microscopically for degenerative neutrophils, bacteria, and organic matter (see Chapter 164). These findings may suggest a severe inflammatory process and possibly perforation of the esophagus or gastrointestinal tract. On rare occasions, the biliary tract may be ruptured in the presence of diaphragmatic hernia, and this can be identified by determining the concentration of bilirubin within pleural fluid. Biliary-pleural fistula has also been reported secondary to gunshot in a dog.
Blood Samples • Draw blood and store the sample in anticoagulant •
and serum tubes (preferably before initiating treatment), unless analyzed immediately. Although these samples may not be needed, it is often helpful to determine the biochemical status of the animal at the time of hospital admission when attempting to distinguish between preexistent disease and that which has developed acutely after injury. These same considerations apply to the collection and storage of urine samples.
Packed Cell Volume and Plasma Protein Concentration • Determine the packed cell volume (PCV) and plasma • •
•
protein concentration (PPC) as soon as possible after the initial examination. It is critical to record these values because the diagnosis of continuing hemorrhage often relies on comparison of serial determinations of PCV and PPC. If hemorrhage is ongoing, these two values continue to decline at a similar rate. If, however, hemorrhage has ceased, it is not uncommon for the PPC to stabilize while the PCV continues to decline. The administration of IV fluids may further decrease these values; consider this when evaluating these parameters.
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Arterial pH and Blood Gas Tensions • These values give an indication of ventilatory func-
• Supplemental oxygen may be provided by an incu-
tion and gas exchange.
• Satisfactory oxygenation of the blood by the lungs requires adequate cardiac output, and decreased cardiac output caused by hypovolemic shock or depressed cardiac function may profoundly affect blood gas values.
Electrocardiography • If available, obtain serial electrocardiograms to check
• • •
for arrhythmias associated with myocardial injury.
bator or oxygen cage, face mask, nasal catheter (see Chapter 3), transtracheal cannula or catheter, or endotracheal or tracheostomy tube. When supplemental oxygen is administered to the animal in such a manner that it does not pass through the nasal passages, prewarm and humidify the air. A transtracheal catheter may be placed using a largegauge (12–18) jugular catheter passed between the rings of the trachea. Secure the catheter to the skin and attach to the oxygen source. Deliver oxygen via the transtracheal catheter at an initial rate of 10 to 20 ml/kg/min.
• If electrocardiography is not available, closely monitor the animal’s heart rate and rhythm and the occurrence of pulse deficits.
TREATMENT Modify treatment to suit the individual needs of each trauma patient. Place and maintain at least one IV catheter for administration of fluids and drugs early in the course of treatment. In severely traumatized animals, place two IV catheters (one may be a central venous line) to allow more rapid infusion of IV fluids. When confronted with a seriously injured animal, it is often difficult to develop a logical, disciplined treatment plan. The airway, breathing, and circulation (ABC) approach is a consistent, comprehensive plan for initial treatment of animals with thoracic trauma.
Airway, Breathing, and Circulation Approach Airway
Circulation If myocardial function is satisfactory, administer IV fluids as needed to increase the circulating blood volume and cardiac output.
• In most cases of hypovolemic shock, administer a • •
• • •
Be sure that the animal has a patent airway.
• Remove debris from the trachea and bronchi by •
forceps or suction or by passing an endotracheal tube. If the pharynx, larynx, or cranial portion of the trachea is severely damaged, consider performing a tracheostomy (see Chapter 3).
Breathing (Spontaneous or Assisted) and Oxygen Therapy Restore thoracic wall integrity by sealing open (“sucking”) chest wounds with an occlusive dressing and stabilizing flail segments so that the animal can ventilate effectively. Fluid and air should be removed from the pleural space. If the animal is not able to ventilate satisfactorily, institute assisted breathing.
•
Assisted breathing requires an endotracheal or tracheostomy tube and may necessitate anesthetizing the animal or giving neuromuscular blocking drugs to paralyze the animal (see Chapter 2).
•
•
blood volume of IV fluids (90 ml/kg in dogs and 65 ml/kg in cats) as rapidly as gravity flow allows. In the presence of significant ongoing hemorrhage, fluid bags may be pressurized to increase the rate of administration. After the rapid infusion of a bolus of IV fluids equivalent to one blood volume, reassess the status of the patient and determine the need for ongoing fluid administration. If signs of hypovolemic shock have abated and hemorrhage has ceased, continue to administer fluids at a rate of 30 to 50 ml/kg q24h (see Chapter 156). If the animal’s condition does not stabilize, continue rapid fluid administration. Auscultate the lungs for evidence of pulmonary edema and carefully monitor for other signs of edema (e.g., tachypnea, chemosis, tearing, tissue swelling, decreasing PCV and PPC). If necessary, monitor the central venous pressure (CVP) to determine the ability of the right side of the heart to eject the volume of blood presented to it (see Chapter 3 for CVP techniques). The relative change in CVP is more significant than the absolute value, and an increase of 7 to 10 cm of water indicates that the rate of fluid administration should be slowed. Because the low oncotic pressure of crystalloid fluids may contribute to fluid loss into the tissue space, a general rule for replacement of blood loss by crystalloid fluids is as follows: • For every 1 ml of blood lost, administer 3 ml of crystalloid fluid.
Pleural Space Drainage • The pleural space may be drained intermittently by thoracocentesis using a hypodermic needle.
• If continuous or prolonged pleural drainage for removal of fluid or air is required, place a thora-
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• • •
•
costomy tube (see Chapter 3 for thoracic drainage techniques). Attach thoracostomy tubes to a three-way stopcock to allow intermittent aspiration of the tube (e.g., q2–4h) or to a continuous suction device. If continuous suction is used, carefully control the negative pressure; it should not be less than -5 to -10 cm of water. Alternatively, attach the thoracostomy tube to a Heimlich one-way flutter valve. • If using this valve, carefully monitor the animal for complications. • Be aware that if the valve becomes cracked or the valve’s diaphragm becomes wet, the one-way function of the valve may be lost and severe pneumothorax may develop. • This valve is available in two sizes, and animals weighing 15 Days Old
• Isolate all birds testing positive for PBFDV to prevent • Isolate all birds with feather lesions caused by PBFDV
and oronasal and oral secretions. These contaminated materials may be inhaled or ingested by susceptible birds. Infected hens may pass the virus to offspring through the egg. Latent infections are common in budgerigars and are believed to be responsible for spread of this virus. Clinically normal parents may transmit polyomavirus to their offspring, some of which also become inapparent carriers. There is currently no evidence to support the existence of persistent infections in larger psittacine birds. However, some psittacine birds may become infected without demonstrating clinical signs and shed virus before eliminating the infection. Thus, birds with subclinical infections may be responsible for viral outbreaks, especially in pet stores and breeding facilities where susceptible neonates are exposed.
Clinical Signs Hatchling Budgerigars 3–5 days Effective against many anaerobic bacteria Good against many gram-negative and gram-positive isolates Excellent for hand-feeding neonates May cause emesis in some birds, especially macaws
CNS, central nervous system; IM, intramuscularly; IV, intravenously PO, orally (per os).
•
•
•
• Because it may not be possible to achieve these high levels in pet birds, this test may not accurately predict the efficacy of the antibiotic chosen in vivo. Determining the minimum inhibitory concentration (MIC) of antibiotics allows a more accurate assessment of antimicrobial efficacy in pet birds; however, this test is not readily available. For this reason, the Kirby Bauer test still is commonly used. When choosing an antibiotic based on standard Kirby Bauer testing check the following: • The bacterial isolate should be susceptible to the antibiotic. • The antibiotic preferably should be bactericidal, known to penetrate into the site of infection, and effective at very low serum concentrations. Antibiotics and dosages commonly used in pet birds are listed in Table 169-1.
• Addition of medications to a small amount of favorite •
•
food is a stress-free method and generally effective as long as the entire portion is readily consumed. Administration of antibiotics via drinking water is the least preferred method because most antibiotics are unpalatable and are not water soluble and because ingestion of the medication is sporadic and effective concentrations at the site of infection are rarely achieved. When a bird is hospitalized and the intestinal tract is functioning properly, oral medications may be administered via gavage tube. Parenteral Administration
• Many antibiotics commonly used in avian medicine •
Route of Administration Oral Administration
• Direct oral administration of medications often is
•
used in pet birds, especially for palatable solutions or suspension. However, this method is difficult for some owners. Instruct owners on the proper restraint techniques. Even after this, birds sometimes spit out the medication, and aspiration is a possibility.
•
are poorly absorbed when given orally, necessitating parenteral administration. Use injectable antibiotics in the following cases: • When a bird is unwilling to take oral medications • When GI motility is altered • In critically ill or septicemic birds The advantages of this method include precise dosing, rapid development of therapeutic serum concentrations, and relatively stress-free administration. Some practitioners teach their clients to administer IM injections to their pets (the technique for IM injection is described in Chapter 168).
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Monitoring Assess antibiotic effectiveness by monitoring the resolution of clinical signs, serial hemograms, cytology, and culture. Serial fecal or cloacal Gram stains during and after antibiotic administration are important because development of secondary infections, especially candidiasis or aspergillosis, are common.
Gram-Positive Infections Gram-positive infections occur less frequently in pet birds. Pathogens include beta-hemolytic Streptococcus, Staphylococcus aureus, and Clostridium spp. Follow the same principles for diagnosis and treatment as outlined previously for gram-negative infections.
• Abdominal distension due to hepatomegaly and dilated, fluid-filled, thickened intestines is common.
• Subcutaneous and periorbital masses may be seen. • Lameness due to endosteal bone proliferation occasionally is reported.
• Signs often are nonspecific and slowly progressive. Diagnosis Hematology and Serum Biochemistry
• Severe leukocytosis (>20,000) with marked heterophilia and monocytosis is common.
• Anemia and polychromasia usually are present. • AST levels usually are elevated with hepatic involvement.
Histopathologic Lesions
Avian Tuberculosis Etiology
• On postmortem examination, in addition to the
Tuberculosis in psittacines, unlike that in mammals, usually is a primarily alimentary disease.
• Although a few cases of Mycobacterium tuberculosis and M. bovis have been reported in pet birds, the causative agent usually is M. avium.
•
• These gram-positive, acid-fast granulated rods are
•
•
capable of causing disease in birds, pigs, guinea pigs, rabbits, and humans. Brotogeris parakeets (especially gray-checked parakeets) are particularly susceptible, followed by Amazon parrots, budgerigars, and Pionus parrots.
•
Transmission
• Transmission occurs primarily by ingestion of fecal-
• •
•
contaminated food, water, or soil; an aerosol route or wound contamination also is possible. The organism is capable of surviving in soil for up to 2 years. After ingestion, the organisms penetrate the GI mucosa and colonize under the serosa. A primary bacteremia occurs (usually without clinical signs), and the organisms are phagocytized (but not killed) by mononuclear phagocyte cells of the liver, spleen, and bone marrow. Multiplication within these cells causes a local reaction by the cell-mediated immune system and the formation of nodules, which may calcify with time. Release of the organisms from the liver results in a secondary bacteremia, with localization in lungs, kidneys, gonads, and intestines. Tubercles in the intestinal wall may open into the intestinal lumen, resulting in shedding of large numbers of organisms in the feces.
Clinical Signs
• Clinical signs include chronic weight loss (often despite a good appetite), depression, chronic diarrhea, polyuria, and poor feathering.
• •
grossly visible nodules previously described, diffuse infiltration of epithelioid or giant cells may result in a grossly thickened firm intestine, hepatomegaly, or splenomegaly. Histologically, the intestinal villi may be club shaped, swollen, and filled with epithelioid cells containing acid-fast rods. Definitive diagnosis is based on identification of acidfast rods and epithelioid cells on biopsy or postmortem slide preparations. The liver is generally the most reliable source. Acid-fast staining or culture of feces also may demonstrate the organism, although false-negative results are common owing to intermittent shedding of organisms. Cultures require 3 to 6 weeks for results. Indirect diagnosis with intradermal tuberculin and slide agglutination tests also frequently produce falsenegative results.
Treatment
• Euthanasia often is recommended because of the •
potential human health hazard, especially to immunocompromised owners. Successful treatment of pet birds with M. avium, mimicking human treatment protocols, has been reported.
SUPPLEMENTAL READING Aguilar RF, Redig PT: Diagnosis and treatment of avian aspergillosis. In Bonagura JD, Kirk RW (eds): Current Veterinary Therapy XII: Small Animal Practice. Philadelphia: WB Saunders, 1995, pp 1294–1299. Aranaz A, Liebana E, Mateos A, Dominguez L: Laboratory diagnosis of avian mycobacteriosis. Semin Avian Exot Pet Med 6:9–17, 1997. Cross GM: Viral diseases. Semin Avian Exot Pet Med 4(2), 1995.
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Chapter 169 / Avian Infectious Diseases Dorrestein GM: Bacteriology. In Altman RB, Clubb SL, Dorrestein GM, Quesenberry K (eds): Avian Medicine and Surgery. Philadelphia: WB Saunders, 1997, pp 225–280. Flammer K: Chlamydia. In Altman RB, Clubb SL, Dorrestein GM, Quesenberry K (eds): Avian Medicine and Surgery. Philadelphia: WB Saunders, 1997, pp 364–379. Gerlach H: Viruses. In Ritchie BW, Harrison GJ, Harrison LR (eds): Avian Medicine: Principles and Application. Lake Worth, FL: Wingers Publishing, 1994, pp 862–948. Gregory CR, Latimer KS, Niagro FD, et al: A review of proventricular dilatation syndrome. J Assoc Avian Vet 8:69–75, 1994.
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Ritchie BW: Papovaviridae. In Ritchie RW (ed): Avian Viruses: Function and Control. Lake Worth, FL: Wingers Publishing, 1995, pp 127–170. Ritchie BW: Herpesviridae. In Ritchie RW (ed): Avian Viruses Function and Control. Lake Worth, FL: Wingers Publishing, 1995, pp 171–218. VanDerHeyden N: New strategies in the treatment of avian mycobacteriosis. Semin Avian Exot Pet Med 6:25–33, 1997.
Chapter
▼
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170
Avian Dermatology Tia B. Greenberg
Skin and feather disorders are common in companion avian species. Since many of these disorders have a psychological basis, either as the primary cause or as a contributing component, diagnosis and treatment can often be frustrating. A detailed history, physical examination, and assessment of a wide range of diagnostic tests are generally required for diagnosis.
• Provide a balanced diet including a wide variety of • •
ANATOMY
fresh fruits and vegetables, a pelleted diet, and limited access to seeds. Allow exposure to unfiltered natural sunshine daily, if possible. Bathe or mist feathers daily with water to help promote healthy skin and feathers.
GENERAL HISTORY AND EXAMINATION
A basic understanding of normal structure and function of the skin is important.
History
• The avian skin consists of the epidermis, dermis, and
A complete, detailed history is essential to the diagnosis of birds presenting with dermatologic disorders. Include questions such as the following:
subcutis tissue.
• The epidermis is composed of three layers: the basal •
•
or germinative layer, the intermediate layer, and the cornified layer. The dermis consists of the superficial layer and the dermal layer. • The dermal layer varies in thickness depending on its location on the body. For example, the face is a non-feathered area and therefore is thicker than feathered areas. • During breeding season, females and some males will develop dermal thickening and neovascularization in the ventral abdominal area. This area is referred to as the brood patch or incubation patch since it contributes to egg incubation. The area should not be confused with an area of feather loss and is a normal finding. The subcutis is composed of the fascia superficialis, the superficial layer, and the favia profunda. • The subcutis is a very thin layer and therefore not amenable to suturing. • Because this layer is so thin, it can be difficult to maintain a needle in the subcutaneous space while administering subcutaneous injections.
GUIDELINES FOR HEALTHY SKIN AND FEATHERS Provide the bird owner with information on proper nutrition and husbandry guidelines to keep the bird’s skin and feathers healthy. 1758
• How long have you owned the bird, and where was it acquired?
• Are there any new birds in the house? If so, are they • • • • • • • • • • • • • •
sick? Has this bird had any contact with other birds? Has anything changed in the bird’s environment? What type of cage is used, and where is it located? What diet is normally fed and, of this, what does the bird actually consume? Have there been any changes in the diet? Has appetite or water consumption changed? Are there any behavioral changes? Is there any change in droppings? What is the bird’s reproductive status? Have the bird’s feathers changed in the past 6 months? Does the bird seem itchy? When was the onset of the presenting complaint? Has the problem progressed? Has the bird been examined by or treated by another veterinarian? Has there been any previous illness? Is the bird currently on any medications, including over-the-counter medications?
Physical Examination Perform a thorough physical exam.
• Notice the distribution and severity of skin or feather lesions.
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Table 170-1. COMMON DERMATOLOGIC CONDITIONS IN SPECIFIC SPECIES Canaries Knemidokoptes Feather cysts Scaly leg syndrome Genetic baldness Papilloma virus Chlamydophila Mites Budgerigars Knemidokoptes Lipomas Fibrosarcomas Feather cysts Uropygial gland problems Polyfolliculitis Cockatiels Giardia Genetic baldness Feather cysts Conures Feather picking Self-mutilation
Amazons Amazon foot necrosis Lipomas Feather picking Cockatoos Feather picking PBFDV Papillomas Rose-Breasted Cockatoos Lipomas Macaws PBFDV Feather picking Lovebirds PBFDV Feather picking Ulcerative dermatitis
• Lesions begin as hyperkeratosis, crusting, and •
• Gross appearance of characteristic honeycomb lesions is usually diagnostic.
• If in doubt, perform a gentle skin scraping to confirm the presence of mites. Treatment
• Give ivermectin at 0.2 mg/kg SQ, PO, or topically every 2 to 4 weeks for three to four treatments.
• Do not administer ivermectin by an IM route. • For birds weighing 2 years of age.
• Adrenal gland disease in ferrets is not Cushing’s disease. Excessive sex steroids, not corticosteroids, are produced by a hyperplastic or neoplastic adrenal gland.
▼ Key Point Perform a complete abdominal exploratory; insulinomas can metastasize to the regional lymph nodes, liver, and spleen (uncommon). Concurrent adrenal tumors (see Adrenal Gland Disease) are common.
Etiology • The etiology is unknown. Possible causes of adrenal
• If the spleen is enlarged and appears irregular or mottled, consider performing a complete or partial splenectomy and submit for histopathology.
Postoperative Care and Complications
• Postoperatively monitor the blood glucose concen-
• • •
•
•
tration bid–tid until the ferret is discharged from the hospital. Many ferrets become euglycemic immediately after surgery. Some ferrets may remain hypoglycemic. Rarely, ferrets may become transiently hyperglycemic after surgery. Most ferrets will require resumption of medical therapy 2 to 6 months after surgery. Some ferrets will need medical therapy immediately postoperatively. Monitor blood glucose levels for 10 to 14 days after surgery and at 60 to 90 day intervals. Iatrogenic pancreatitis is rarely a problem in ferrets; however, as a precaution, withhold food and water for 12 hours postoperatively; give 2.5% to 5.0% dextrose IV during this period. Monitor blood glucose 1 to 4 times daily. Transient diabetes mellitus may occur postoperatively. Hyperglycemia and glucosuria may be present for 1 to 21 days postoperatively; generally no treatment is required. Histopathologic examination of the pancreatic mass may reveal hyperplasia, adenoma, and/or adenocarcinoma of the pancreatic beta cells, even within a single tissue specimen.
Prognosis • The prognosis is guarded, but with surgery and medical treatment, ferrets have had a good quality of life for more than 1 year after diagnosis of insulinoma. The median survival time was 17 months (range, 0.5–40 months) in one study of 53 ferrets treated with surgery, medical management, or both.
1833
•
•
disease in ferrets include early neutering, genetic factors, and lack of exposure to normal seasonal photoperiods. The incidence of adrenal neoplasia is higher in ferrets in the United States. In the U.S., ferrets are typically neutered at 6 weeks of age, and are housed indoors under artificial light cycles. Ferrets in Europe and Australia are typically housed outside, and are not neutered until 6 months of age. Adrenal neoplasia in ferrets causes a variety of clinical signs, and appears to be the result of excessive secretion of estrogens and androgens, not cortisol. Pituitary-dependent hyperadrenocorticism has not been documented in ferrets. Adrenal tumors most commonly arise from the adrenocortical tissue. Common histopathological findings include hyperplasia, adenoma, and adenocarcinoma.
Clinical Signs • Signs include progressive, bilaterally symmetric
• •
•
alopecia, usually starting at the tail base and progressing cranially. Hair loss often starts in the early spring or fall. There may be a history of alopecia and spontaneous hair regrowth as well. Pruritis often is reported, along with excessive dryness of the skin and small excoriations. Thinning of the skin is common. An enlarged vulva, mimicking estrus, may be the only clinical sign in spayed females. Mucoid or mucopurulent vulvar discharge may be noted. Castrated males may exhibit territorial marking and sexual behaviors, and may develop the strong body odor and oily hair coats of intact males. Mammary hyperplasia can occur in either sex. Male ferrets may present with partial to complete urinary obstruction. Persistent elevation of adrenalderived androgenic hormones may cause development of prostatic hypertrophy, prostatic cysts, or periurethral cysts, which cause narrowing of the
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• • • •
• • •
Section 12 / Diseases of Avian and Exotic Pets
urethra. Affected ferrets may present with stranguria, dysuria, azotemia, and severe metabolic derangement. Male ferrets that are described as straining to urinate should be treated as an emergency (see “Urinary System”). Atrophy of abdominal musculature and mobilization of fat to the ventral abdomen, leading to a pendulous appearance, may be seen. Atrophy of hind limb musculature and rear limb paresis can occur. Polyuria/polydipsia is uncommon but has been reported. Collapse, anemia, and petechiation resembling estrogen toxicity have been described in male and female ferrets with chronic or advanced adrenal disease (see Hematopoietic System). Enlarged adrenal glands may occasionally be noted on the physical examination. The left adrenal gland is easier to palpate than the right. Radiographs are not typically helpful in confirming this disease. Ultrasonography may be useful for identification of adrenalmegaly. CBC is typically unremarkable unless estrogen toxicity-like anemia is present. The serum chemistry profile is typically within normal limits unless insulinoma is present.
Diagnosis ▼ Key Point A history of symmetric truncal hair loss suggests the diagnosis. Differential diagnosis includes seasonal alopecia, which typically appears in the spring or fall, affects only the tail, and resolves after several weeks.
Table 175-4. STEROID HORMONE CONCENTRATIONS IN FERRETS Steroid
Range
Androstenedione (nmol/L) Estradiol (pmol/L) 17-hydroxyprogesterone (nmol/L)
0–15 30–180 0–0.8
From Clinical Endocrinology Laboratory, University of Tennessee College of Veterinary Medicine.
• Perform exploratory surgery to confirm the diagnosis.
Treatment • Adrenal tumors can be managed medically or surgi•
Medical Therapy The goal of medical treatment is to decrease or eliminate the clinical signs of adrenal gland disease. Medical therapy will not stop or prevent the growth of an existing tumor, and should be reserved for ferrets that are poor surgical candidates, ferrets with inoperable bilateral adrenal tumors, or ferrets with recurrent adrenal gland disease.
• Medical treatments described in the literature
• Female ferrets often present with a swollen vulva. Dif-
•
•
ferential diagnoses include an intact female ferret, a female ferret with an ovarian remnant, and seasonal alopecia. Perform a serum steroid panel or administer human chorionic gonadotropin (100 IU) IM to determine if a female ferret is unspayed or has an ovarian remnant. A plasma steroid hormone assay may be used to support the diagnosis. Elevated plasma concentration of estradiol, androstenedione, and/or 17-hydroxyprogesterone is a reliable indicator of adrenal gland disease (see Table 174-4). A hormone panel is commercially available through the Clinical Endocrinology Laboratory of the Department of Comparative Medicine at the University of Tennessee. The adrenocorticotropic hormone (ACTH) stimulation test and the low-dose dexa-methasone suppression test are not useful in ferrets. Ferrets with adrenal gland disease do not produce abnormal concentrations of cortisol, and adrenal gland disease in the ferret appears to be independent of ACTH. Urine cortisol/creatinine ratio does not appear to be a specific indicator of adrenal gland disease.
cally. Surgical management is preferred and recommended. Medical treatment may cause clinical signs to regress, but will not stop growth of the adrenal tumor.
•
•
include mitotane, ketoconazole, androgen receptor blockers, aromatase inhibitors, and gonadotropinreleasing hormone analogs. Gonadotropin-releasing hormone analogs. There are two general types of GnRH analogs: GnRH agonists and GnRH antagonists. To date only GnRH agonists such as leuprolide acetate (Lupron Depot, TAP Pharmaceuticals Inc., Lake Forest, IL) have been used to control the signs of adrenal disease in the ferret. Of the medical treatments described, anecdotal reports suggest that leuprolide acetate has been most effective in alleviating dermal and urogenital signs of adrenal disease. Administer the 1 month depot formulation of leuprolide acetate at a dose of (250 µg/kg) IM every 30 days. Androgen receptor blockers theoretically block the actions of androgens at the receptor site, and decrease or reverse the signs of adrenal gland disease. In human medicine these drugs are used to treat men with prostatic carcinoma or prostatic hyperplasia. Flutamide (Eulexin, Schering Corporation, Kenilworth, NJ) and bicalutamide (Casodex, AstraZeneca Pharmaceuticals LP, Wilmington, DE) have been used, primarily in male ferrets. Results are variable.
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• Aromatase inhibitors such as anastraozole (Arimidex,
•
AstraZeneca Pharmaceuticals LP) inhibit aromatase, an enzyme involved in estrogen production. Some ferrets show decreased evidence of adrenal gland disease symptoms when treated with this drug. Mitotane (0,p’-DDD) (Lysodren, Bristol-Myers Squibb Oncology, Princeton, NJ) is rarely effective in ferrets with adrenal gland disease, presumably because ferrets do not develop pituitary-dependent hyperadrenocorticism. If clinical signs do resolve, they will often recur as soon as the mitotane therapy is withdrawn.
▼ Key Point Perform a fasting blood glucose test before starting mitotane therapy. Do not use mitotane if blood glucose is low (indicative of concomitant insulinoma). Mitotane causes a decrease in endogenous cortisol production; if insulinoma is present, serum glucose levels also may fall, causing a hypoglycemic crisis.
• Give mitotane (50 mg/kg) PO q24h for 7 days, then
•
•
• •
q48h until clinical signs start to resolve. At that time decrease to q72h until signs are fully resolved, then maintain the ferret on 50 mg/kg once q7–30d as necessary. Mitotane must be compounded in 50-mg aliquots in #1 capsules. Capsules must be administered intact. Have owners coat the capsules with vegetable oil, push into the back of the throat, and follow with a palatable liquid or blenderized cat food to promote swallowing. The most common side effect of mitotane is hypoglycemia. Teach owners to recognize the signs of hypoglycemia, and have prednisone available at home. If side effects occur, discontinue mitotane and administer prednisone (1.0–1.25 mg) PO. If continuation of mitotane therapy is desired after a hypoglycemic crisis, administer concomitantly with prednisone (see Insulinoma). Ketoconazole is not effective in the treatment of adrenal disease in the ferret.
Surgical Therapy Follow the adrenalectomy preoperative described for dogs (see Chapter 33).
•
•
•
exploratory. Observe and palpate the pancreas at surgery for insulinomas, which often are found concurrently with adrenal neoplasia.
Postoperative Care and Complications • Monitor fasting serum glucose levels every 60 to 90 days during mitotane therapy and after adrenalectomy, even if no pancreatic nodules were evident during surgery.
Prognosis • The prognosis following successful surgery is good. A •
•
indwelling IV or IO catheter preoperatively, and administer fluids pre-, intra-, and postoperatively. If insulinoma is present concurrently treat and monitor appropriately. Perform a ventral midline laparotomy. Palpate and visualize both adrenal glands carefully. Normal adrenal glands are 5 to 8 mm ¥ 2–3 mm in size, are pale pink in color, and are typically surrounded by fat. The left adrenal gland lies in a fat pad cranial to the left kidney. The right adrenal gland is located cranio-
medial to the right kidney under the caudate liver lobe adjacent to the vena cava. It may be necessary to transect the hepatorenal ligament to fully visualize and palpate this gland. Adrenal changes may be subtle, especially in younger ferrets and because the adrenal glands are surrounded by fat. Visual changes, such as dark circular lesions and small raised cysts, may be present instead of gross enlargement. One or both adrenal glands may be affected. If only the left adrenal gland is affected, removal is relatively straightforward. If the right adrenal gland is affected, removal can be difficult because of the gland’s proximity to the vena cava and liver (see Chapter 33). If both adrenal glands are affected, remove the left adrenal gland and debulk the right adrenal gland. Bilateral adrenalectomy has been described in the ferret, but should be done with caution. Monitor postoperatively for development of acute adrenal hypocorticism. If acute AHC develops, treat as described for dogs (see Chapter 33).
▼ Key Point Always perform a complete abdominal
protocol
• Fast the ferret 4 to 6 hours preoperatively. Place an
•
•
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•
full resolution of clinical signs can be expected in many cases. Recurrent or continued symptoms of adrenal gland disease may be associated with development of a tumor on the remaining adrenal gland, or recurrence of an adrenal tumor due to metastasis (which is rare). Even without treatment, ferrets may survive up to 2 years or longer after diagnosis, although the hair loss is generally progressive. Potential sequelae to chronic adrenal gland disease include prostatic disease, bone marrow suppression, or mechanical interference with the vena cava (right adrenal gland).
Pheochromocytoma Pheochromocytomas are adrenal tumors that arise from the adrenal medulla and produce excessive amounts of catecholamines. Pheochromocytomas have been reported in ferrets, but are rare. Treatment of choice is surgical removal of the affected gland.
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LYMPHOSARCOMA Lymphosarcoma (lymphoma) is common in ferrets of all ages, and is similar in presentation to the disease in cats and dogs (see Chapter 27). Three presentations may occur in the ferret and include lymphosarcoma, lymphocytic, and lymphoblastic forms.
• Often the CBC and differential WBC counts are not
•
Etiology • A viral etiology has been hypothesized. Clinical Signs Clinical signs are variable, depending on the form of lymphoma present and the organ system involved.
• •
• Lymphosarcoma: Solid tissue tumors are present in the organs or lymph nodes.
• Lymphocytic lymphoma: Adult ferrets are most com-
•
• •
• •
monly affected. The course and survival time can be long. Peripheral lymphadenopathy is typically present and metastasis to visceral organs may occur. The neoplastic cell identified on cytology or histopathology is a mature, well-differentiated lymphocyte. Lymphoblastic lymphoma: Young ferrets are most commonly affected. Leukemia and neoplasia in visceral organs occur early in the course of this form of the disease. Large immature lymphocytes are noted on cytology or histopathology. Other forms: Cutaneous lymphoma may occur in the ferret. Clinical signs that may accompany any form of lymphoma include: • Inappetence, lethargy, splenomegaly, and weight loss despite a normal appetite • Dyspnea, tachypnea, and exercise intolerance • Peripheral lymphadenopathy and/or abnormal CBC • Acute collapse, often with pyrexia • Fever of unknown origin • Cutaneous masses • Chronic diarrhea and/or rectal prolapse Some ferrets are asymptomatic; lymphoma may be an incidental finding during evaluation for another medical problem. Lymphoma tends to be a more acute, fulminant disease in younger animals.
•
•
•
Treatment Splenectomy
• If the spleen is involved, perform a splenectomy (see Chapter 25) to reduce the overall tumor load.
Chemotherapy Chemotherapy for lymphoma may be successful (approximately 10% remission rate). In general, protocols have been adapted from feline medicine (see Chapters 26 and 27).
• Success of chemotherapy may be affected by the age
Diagnosis The method of diagnosis depends on the organ system involved.
• Obtain a thorough history and physical examination. • Perform a CBC, platelet count, and a serum biochemistry profile. If the ferret is anemic, perform a reticulocyte count.
diagnostic for lymphoma. The CBC may be normal or may reveal an absolute or relative lymphocytosis. Anemia, leukopenia, and thrombocytopenia may be seen. Abnormal lymphocytes may occasionally appear in the differential count. Persistent absolute lymphocyte counts greater than 3500 or a relative lymphocytosis (>60%) are considered suspicious; repeat the CBC in 4 to 6 weeks and perform a bone marrow biopsy and/or lymph node biopsy if the CBC results are repeatable or if lymphadenopathy is present. The serum chemistry profile may disclose elevated liver enzymes if the liver is involved; paraneoplastic syndromes are uncommon in the ferret. Perform thoracic and abdominal radiography and ultrasonography to evaluate for intra-thoracic and intra-abdominal masses. Perform fine-needle aspiration or biopsy of affected tissues for histological and cytological examination. Fine-needle aspiration of the spleen is usually inconclusive. Lymph node biopsy is often the most helpful diagnostic tool for diagnosis of lymphoma. If possible, biopsy an enlarged lymph node. When lymphadenopathy is not present, biopsy the popliteal lymphnode. The popliteal lymph node is the most accessible peripheral node for biopsy. Avoid biopsy of intra-abdominal lymph nodes if possible. Perform bone marrow aspiration to identify infiltration by neoplastic cells and the disease (see “Clinical Techniques”).
• • •
of the ferret, concurrent disease (e.g., adrenal gland disease, insulinoma), concurrent medication, inappropriate use of and resistance to chemotherapeutic agents (ferrets treated with prednisone prior to chemotherapy), and the type of lymphoma present. Ferrets with bone marrow involvement or with solid tumors involving organs typically have a poor prognosis. Longer periods of remission tend to occur in individuals with adult onset or lymphocytic lymphoma. IV chemotherapeutic agents are given via butterfly catheter or small-gauge needle with the ferret under
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cell tumor, mesothelioma, osteoma, osteosarcoma, schwannoma, squamous cell carcinoma, thymoma, and renal and pancreatic carcinomas.
Table 175-5. CHEMOTHERAPY PROTOCOL II FOR LYMPHOMA* Week
Drug
Dose
1
Vincristine Asparaginase Prednisone
2 3 4–6
Cyclophosphamide Doxorubicin As weeks 1–3 above but discontinue asparaginase Vincristine Cyclophosphamide Vincristine Methotrexate
0.07 mg/kg, IV 400 IU/kg, IP 1 mg/kg, PO, q24h and continued throughout therapy 10 mg/kg, SC 1 mg/kg, IV
8 10 12 14
0.07 mg/kg, IV 10 mg/kg, SC 0.07 mg/kg, IV 0.5 mg/kg, IV
IV, intravenously; IP, intraperitoneally; PO, per os; SC, subcutaneously. *Protocol is continued in sequence biweekly after week 14. From Rosenthal KE: Ferrets. Vet Clin North Am 24:19–20, 1994.
•
sedation; face-mask administration of isoflurane is the most convenient and rapid method of sedation. One chemotherapy protocol is outlined in Table 175-5.
▼ Key Point Monitor the CBC weekly. If the WBC falls below 2000 WBC/ml, or the RBC falls below 4 ¥ 106/ml discontinue vincristine for 1 week or more until the WBC count increases to at least 3000 WBC/ml.
Dermatologic Diseases SEASONAL CHANGES IN THE SKIN AND HAIRCOAT Ferrets may experience dramatic seasonal changes in the haircoat triggered by photoperiod changes. This change is most apparent in the intact animal. If one is unfamiliar with these changes, normal coat changes may be interpreted incorrectly as a medical problem. ▼ Key Point Individual animals may exhibit different patterns of coat change each successive year.
Haircoat • A normal, diffuse, gradual thinning of the coat typi-
• • •
• Palliative therapy may be attempted by administering oral prednisone (2.2 mg/kg) PO q24h.
• Supportive care is important (see “Nutritional
•
Support for Insulinoma”).
• Consider referral to an oncologist if experience with chemotherapeutic agents is limited.
•
OTHER TYPES OF NEOPLASIA
•
• Chordoma: Chordomas are tumors that arise from
• •
• •
notochord remnants. Tumors occur most often at the tip of the tail, but may occur in the cervical region as well. GIT: Gastric adenocarcinoma. Reproductive tract: Tumors include granulosa cell tumors, luteomas, and leiomyomas in intact females and in remnant tissue in spayed females. Sertoli cell tumors have been reported in intact males. Skin and Subcutis: See Dermatologic Diseases in this chapter. Other tumors reported in ferrets include chondroma, chondrosarcoma, fibroma, fibrosarcoma, hepatic adenocarcinoma, hemangioma, hemangiosarcoma, mast
1837
•
•
cally occurs in the spring when the photoperiod is increasing and continues through the summer. The coat typically becomes shorter and darker at this time, and the face mask may appear or disappear. Focal alopecia should not be present. Some ferrets may experience a dramatic 1-day loss of the undercoat. A normal, but dramatic, loss of body weight (up to 40%) may occur at this time as well. Hair growth will reverse in the fall and winter. Coats typically become longer, thicker, and lighter. Body weight may change (up to 40%) as well. Females in estrus and males “in season” may show an even more marked hair loss but should not have areas of alopecia. Males typically lose hair in the inguinal area because of constant rubbing to mark territory; the mid- and caudal abdomen is often wet with urine. Neutered ferrets or ferrets kept under artificial lighting conditions often experience no coat changes. Neutering or spaying may cause temporary, diffuse alopecia hair thinning postoperatively, particularly if the animal was reproductively active at the time of surgery. The preoperative color pattern may not return. At any time of the year, regrowth of hair that has been shaved for medical procedures is slow. This is particularly true in the winter and summer when no active hair growth is occurring.
Skin • Hair regrowth (regardless of the cause of alopecia) is often preceded by a blue to purple discoloration of the skin that can alarm the owner. This discoloration
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•
•
Section 12 / Diseases of Avian and Exotic Pets
is caused by new hairs growing through the dermis, and is most noticeable on the abdomen and face. Intact jills may exhibit a bluish discoloration of the skin during estrus. If ovariohysterectomy is performed while a jill is in estrus, this discoloration may occur approximately 10 days postoperatively. Pseudonails associated with hyperkeratosis of the footpads may occur in ferrets older than 2 years of age that are housed on carpet or linoleum surfaces. Trim pseudonails as necessary. Rub a small amount of petroleum jelly or vitamin E oil into the pads daily to help prevent lesions.
• Topical treatments include twice-weekly cleansing
INFECTIOUS DISEASES
•
Bacterial Infections Cutaneous bacterial infections in ferrets are typically manifested as abscesses or as a diffuse, ulcerative pyoderma.
Abscesses • Abscesses may develop secondary to puncture wounds, bites, or may develop in the inguinal fat after traumatic injury (e.g., being stepped on). For diagnosis and treatment of abscesses, see “Infectious Diseases.”
Ulcerative Pyoderma Ulcerative pyoderma is the second most commonly encountered form of bacterial dermatitis in the ferret.
with an antibacterial shampoo containing chlorhexidine or benzoyl peroxide. Daily application of an antibacterial cream may be beneficial if the lesion is small and localized.
Canine Distemper Virus Infection Dermatologic lesions are quite prominent with CDV infection in ferrets.
• Dermatologic signs typically begin with hyperemia
•
Dermatophytosis • Microsporum canis and Trichophyton mentagrophytes are •
most common agents are Staphylococcus and Streptococcus spp.
Fleas • Flea infestation may be encountered in pet ferrets. Clinical signs are similar to those seen in cats (see Chapter 45).
Treatment
• Flea shampoos, dips, or powders containing
Clinical Signs
• Focal alopecia with diffusely hyperemic, thickened,
•
ulcerated skin may occur over any area of the body.
Diagnosis
• Perform a cutaneous punch biopsy (see Chapter 37) •
to rule out diffuse cutaneous mast cell tumor, which may have a similar gross appearance. Perform bacterial culture and sensitivity testing.
Treatment
• Administer systemic antibiotics based on culture and sensitivity testing. Antibiotics effective in the treatment of pyoderma in ferrets often include amoxicillin-clavulanate (Clavamox, SmithKline) (13– 25 mg/kg) q12h PO and cephalosporins (use feline dosages).
the most common causes of superficial mycotic infections in the ferret. See “Infectious Diseases” in this chapter for diagnosis and treatment.
EXTERNAL PARASITES
Etiology
• Various bacteria can cause ulcerative pyoderma. The
around the lips, chin, eyes, and sometimes the inguinal area. With time, crusts and skin thickening may appear. Hyperkeratosis of the foot pads occurs as the disease progresses. See Infectious Diseases in this chapter for a detailed discussion of CDV in ferrets; also see Chapter 13 for a discussion of CDV in dogs.
•
•
•
pyrethrin may be used. Products containing lindane or organophosphates are not recommended for use in the ferret. Imidacloprid (Advantage, Bayer Corporation, Shawnee Mission, KS) (0.4ml) topically every 3 weeks has been reported to be effective. No adverse effects have been noted. This drug may be used in conjunction with lufenuron. Lufenuron (Program, Norvartis Animal Health, Greensboro, NC) (45 mg) PO every 4 weeks has been anecdotally reported to be effective. Advise clients that there is a 6- to 8–week period before flea numbers are observed to decline. Fipronil (Frontline, Merial LTD., Iselin, NJ). Half the cat dose has been anecdotally reported to be effective. This drug may be used in conjunction with lufenuron. Selamectin (Revolution, Pfizer, New York, NY). Administration of the cat dosage has been anecdotally reported to be effective.
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• Flea collars are not recommended because they come •
• Bathe the ferret within 24 to 48 hours after treatment.
off easily and small pieces can be ingested. Treat the environment for fleas.
•
Ear Mites Ear mite infection in ferrets is caused by Otodectes cyanotis, the same parasite that infects cats and dogs.
1839
•
Clinical Signs
• Ferrets rarely exhibit pruritis, even with heavy mite
Wash all bedding and treat all other potential hosts in the household (see Chapter 59). Topical treatments may not be effective due to the narrow size of the ear canal, and patient resistance to treatment. Persistent infections may be due to the presence of ear mites on the body, or failure to deliver the topical agent effectively. In such cases, parenteral administration of ivermectin (0.5 mg/kg) SC every 7 to 10 days for 2 treatments may be necessary. Do not use topical and parenteral ivermectin together.
infestation.
• Ferrets normally have large volumes of dark reddish-
•
•
•
brown ear wax present in the ear canal, which resembles the debris present with O. cyanotis infestation. If ear mite infestation is present, wax production may become excessive and cause occlusion of the external ear canal. O. cyanotis infestation may be accompanied by secondary bacterial infection, leading to otitis media or otitis interna. Neurological signs such as head tilt and circling may occur (see Chapter 61 for techniques for the management of otitis media in cats). When chronic ear mite infestation is present, lichenification and a bluish pigment may appear on the inner surface of the pinnae. These changes are caused by a response to chronic irritation, and usually regress after treatment. Rarely, O. cyanotis may colonize other parts of the body.
Sarcoptic Mange Etiology Sarcoptes scabiei mites are transmissible between dogs and ferrets via contact with the infected hosts or their bedding. (See Chapter 44 for discussion about sarcoptic mange in dogs and cats.)
Clinical Signs
• Lesions are typically confined to the feet, which
•
become hyperemic, swollen, and intensely pruritic. Crusting often occurs around the nails, and in severe cases the nails may slough. Generalized alopecia, accompanied by intense pruritis, occurs rarely.
Diagnosis
Diagnosis
• Examine all ferrets for ear mites; the incidence of
• A positive diagnosis is based on clinical signs, exclu-
•
•
infestation is high in some populations. Mites in the ear canal can often be visualized using an otoscope; however, otoscopic examination is often difficult because of the uncooperative nature of the patient and small size of the ear canal. Confirm the diagnosis by microscopic examination of ear debris.
•
sion of differential diagnoses, and positive skin scrapings obtained from several sites (false negative results do occur). A common differential diagnosis is contact allergy. Similar lesions have been observed in ferrets housed on plastic-floor cages. These lesions resolve when the cage bottom is changed to wire or wood.
Treatment
Treatment
• Thoroughly clean the ears. • Administer ivermectin (Ivomec, Merck-Sharp &
• Advise clients of the zoonotic potential of this
•
•
Dohme Agvet), (1 mg/kg) divided into two doses. Instill one dose into each ear. Repeat in 2 weeks. Tresaderm (Merck Agvet, Rahway, NJ) may be used to treat ear mites in ferrets. Administer 2 drops in each ear q24h for 7 days, stop for 7 days, then repeat. This medication has been reported to be effective in treatment of ear mites in the ferret. Selamectin may be used for treatment of ear mites in the ferret. Use at the dose described for treatment of fleas.
parasite.
• Treatment may need to be based on differential • • •
diagnoses; mites may be difficult to identify on skin scrapings. Administer ivermectin (0.5 mg/kg) SC every 2 weeks for three treatments. Lime sulfur dips may be used instead of ivermectin. Dip ferrets in 2% lime sulfur every 7 days until signs have resolved for 2 weeks. Wash all bedding and treat all potential contact hosts in the household.
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Demodectic Mange
Treatment
Etiology
• No treatment is necessary. Hair regrowth will occur
Demodicosis is rare in the ferret.
• Artificially lengthening the photoperiod may speed
Clinical Signs
• If the tail exhibits excessive amounts of waxy scaling
when the photoperiod changes. hair regrowth, although not reliably. or comedones, clean the tail weekly with a mild shampoo.
• Otitis externa has been associated with demodicosis. This may be the only presenting sign.
• Localized alopecia accompanied by pruritis may occur.
Diagnosis
Estrus Alopecia Alopecia may be seen in intact females that have been in estrus for 1 month or longer.
• Mites may be identified on routine skin scrapings and examination of ear canal debris.
Treatment
Clinical Signs
• Bilaterally symmetrical hair loss over the shoulders
• Treatment can be difficult. Use ivermectin at the daily dose described for dogs (see Chapter 43).
• Do not use mitotane. ENDOCRINE ALOPECIA Tail Alopecia
•
and flanks, which eventually progresses to involve the entire body. Hairs epilate easily, and the underlying skin appears normal. A grossly enlarged vulva indicates a state of estrus. Be aware that the ferret also may be anemic and thrombocytopenic (see “Anemia”).
Diagnosis
• Diagnosis is based on clinical signs in an intact female.
Etiology The etiology of tail alopecia in the ferret is unknown but is suspected to be caused by hormonal fluctuations because the disease responds to changes in the photoperiod. Hair loss occurs most commonly at the time of the fall molt, when the photoperiod is becoming shorter, but may be seen any time of year under artificial lighting conditions. Hair regrowth usually occurs in 2–8 weeks. The same pattern of alopecia is not always repeated annually.
Treatment
Clinical Signs
Adrenal Gland Disease • Bilateral, symmetrical alopecia is a common sign of
• Hair loss, ranging from diffuse hair thinning to complete alopecia, occurs from the base of the tail to the tip. ▼ Key Point Alopecia occurs only on the tail. If alopecia extends to the body, suspect another form of endocrine disease, such as adrenal gland disease.
• Perform an ovariohysterectomy (see Chapter 91) if
•
the ferret is stable enough for the procedure, or induce ovulation with HCG (see “Termination of Estrus”; “Anemia”). Hair regrowth will recur rapidly after surgery or ovulation; however, changes in hair length, color, or thickness are common.
adrenal disease in the ferret (see “Adrenal Gland Disease”).
Hypothyroidism • Hypothyroidism has not been documented in ferrets.
• Comedones and a brown, waxy scale may accompany the alopecia.
Diagnosis
• Diagnosis is based on clinical signs. • Differential diagnoses include the early stages of adrenal gland disease; however, hair loss on the body typically occurs as well when this condition is present.
NEOPLASIA Neoplasia of the skin is the third most common neoplasia reported in the ferret and commonly occurs in ferrets 1 year of age and older. Complete removal of skin masses using wide surgical excision followed by histopathology is recommended.
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Chapter 175 / Ferrets
Mast Cell Tumors
• Cardiac disease is relatively common in the ferret. Quality of life and long-term prognosis for ferrets with cardiac disease depends on the type and severity of cardiac disease present, and the initial response to treatment. Many ferrets do well for months on the appropriate medications.
Mast cell tumors are the most common skin masses encountered and are typically benign in the ferret.
• Individual tumors typically appear as slightly raised,
• •
flat, button-like cutaneous masses ranging in size from 2 to 10 mm. The tumors are often tan in color or may be hyperemic with a dark flaky crust. Tumors may also appear as raised, ulcerated areas, or as diffuse areas of erythema and crusting. Pruritis may be present at the site. Mast cell tumors have occasionally been associated with diffuse or generalized areas of alopecia that resolve with surgical removal of the tumor. Metastasis is rare but has been reported in the lung and gallbladder (see Chapter 28 for information about mast cell tumors in dogs and cats).
Sebaceous Epitheliomas • These tumors may also be referred to as haral cell • •
tumors or sebaceous adenomas and are common in the ferret. Tumors may appear as wart-like, ulcerated, or cystic masses ranging in size from 0.5 to 2 cm. Excision is usually curative. Recurrence is rare, and metastasis is not reported.
Other Neoplasms • Other, less common neoplasms of the skin and sub-
• •
cutaneous tissues include: basal cell carcinoma, basi-squamo-sebaceous carcinoma, hemangioma, histiocytoma, leiomyosarcoma, lymphoma, myxosarcoma, neurofibrosarcoma, perianal gland adenocarcinoma, sebaceous gland adenocarcinoma, and squamous cell carcinoma. Adenocarcinomas often metastasize to regional lymph nodes, liver, and lungs. Diagnosis, treatment, and prognosis for these tumors in ferrets are the same as for dogs and cats (see Chapter 30).
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Congestive Heart Failure Clinical Signs
• Ferrets appear to compensate well for early cardiac •
• • • • •
insufficiency, perhaps because a slight decrease in activity is not readily apparent to owners. Ferrets with congestive heart failure (CHF) may present with clinical signs that resemble symptoms associated with other disease entities, such as anorexia, ascites, coughing, dehydration, dyspnea, exercise intolerance, generalized weakness, hindlimb weakness, hypothermia, lethargy, tachypnea, and weight loss. Pale or cyanotic mucus membranes and a prolonged capillary refill time (CRT) may be noted on physical examination. Jugular pulses may be present when right-sided CHF is present. Femoral pulses may be weak, irregular, or normal. Ascites, hepatomegaly, or splenomegaly may be noted on abdominal palpation. Murmurs may be noted on auscultation, and are typically associated with valvular insufficiency.
Diagnosis
• History and physical examination findings are important in the diagnosis of heart disease.
• Perform a complete physical examination, including auscultation of the heart, and evaluation of the capillary refill time. Observe for tachypnea or dyspnea and auscult the lungs. Palpate the abdomen and examine for ascites. ▼ Key Point Proceed with further testing only if the ferret is stable. Otherwise, administer furosemide and oxygen therapy.
Cardiovascular Diseases
• Diagnosis requires information obtained by radioCHARACTERISTICS OF THE NORMAL FERRET HEART
graphy, ECG, and echocardiography.
• Obtain whole-body radiographs. The cardiac silhou-
• Cardiac auscultation is centered more caudally in the thorax than are auscultations in cats.
• The heart extends from the sixth rib to the caudal
• •
border of the seventh or eighth rib (compared with cats, where it extends from the second to the sixth rib). The heart rate averages 180 to 250 beats per minute. A pronounced sinus arrhythmia and pronounced bradycardia are common during auscultation.
•
•
ette typically appears enlarged and globoid in shape with rounded right and left ventricles. Ascites, hepatomegaly, pleural effusion, and pulmonary edema may be present as well. Evaluate a CBC, serum biochemical profile, and urinalysis to determine if azotemia, electrolyte abnormalities, or other systemic diseases are present. Perform a heartworm test if the history is supportive for potential exposure. If thoracic or abdominal effusion is present, perform thoraco- or abdominocentesis and submit fluid for
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Table 175-6. ELECTROCARDIOGRAPHIC DATA FOR 52 CLINICALLY NORMAL FERRETS* Parameter
Mean ± SD (Range)† (n = 25)
Age (mo) Male:female ratio Body weight (kg) Heart rate (beats/min) Rhythm Normal sinus Sinus arrhythmia Frontal plane MEA (degrees) Lead II P amplitude (mV) P duration(s) PR interval(s) QRS duration(s) R amplitude (mV) QT interval(s)
10–20 All male 1.4 ± 0.2 196 ± 26.5 (140–240)
Average, 5.2 1.25 NA 233 ± 22
NA NA 86.13 ± 2.5 (79.6–90)
67% 33% 77.22 ± 12
NA NA 0.056 ± 0.0086 (0.04–0.08) 0.044 ± 0.0079 (0.035–0.06) 2.21 ± 0.42 (1.4–3) 0.109 ± 0.018 (0.08–0.14)
0.122 ± 0.007 0.024 ± 0.004 0.047 ± 0.003 0.043 ± 0.003 1.46 ± 0.84 0.12 ± 0.04
Value‡ (n = 27)
NA, not available; MEA, mean electrical axis. *All ferrets were sedated with ketamine-xylazine. †Data from Bone L, Battles AH, Goldfarb RD, et al: Electrocardiographic values from clinically normal, anesthetized ferrets (Mustela putorius furo). Am J Vet Res 49:1884–1887, 1988. ‡Data adapted from Fox JG: Biology and diseases of the ferret. Philadelphia, Lea & Febiger, 1988, p 170; and Edwards J: Unpublished data, 1987.
•
cytologic examination. Perform centesis as described for cats; take into consideration the relatively caudal position of the heart in ferrets. Sedation is usually necessary. A modified transudate is typically associated with CHF. Perform standard six-lead electrocardiography (ECG) if possible (Table 175-6 lists normal ferret ECG parameters). Sedation may be necessary. Electrocardiography may reveal atrial premature contractions, atrial tachycardia, atrial fibrillation, ventricular premature contractions, and ventricular tachycardia.
▼ Key Point Sedation with isoflurane is recommended when necessary. Sedation with ketamine or a ketamine-diazepam combination raises the heart rate. The heart rate tends to decrease with ketamine-xylazine sedation; therefore, avoid using xylazine in ferrets with suspected cardiac disease.
• Echocardiography is the most useful diagnostic tool in the ferret. The same echocardiographic changes observed in the dog and cat are seen in the ferret. (Table 175-7).
Treatment ▼ Key Point Treatment of acute CHF should focus on improving oxygenation and reducing cardiac preload and afterload.
Table 175-7. MEAN ECHOCARDIOGRAPHIC VALUES FOR 34 NORMAL ADULT FERRETS Parameter Left ventricle, end-diastolic Left ventricle, end-systolic Left ventricular posterior or free wall Fractional shortening End-point septal separation
Mean Value 11.0 mm 6.4 mm 3.3 mm 42% None
From Sitinas N, Beeber N, Skeels M: Unpublished data, 1992.
• Place the ferret in an oxygen-rich environment.
• • •
Administer supportive care such as subcutaneous fluids (e.g. 0.45% saline and 2.5% dextrose), and provide nutritional support for ferrets that are anorexic. Administer diuretics such as furosemide (1–4 mg/kg) IM or IV bid–tid. Nitroglycerin 2% ointment may be applied to the skin in the axilla, inguinal area, or on a hairless body surface. Angiotensin-converting enzyme (ACE) inhibitors may be given to reduce afterload and preload. Give enalapril (Enacard, Merck Agvet Division) (0.5 mg/kg) PO q48h, then titrate up to q24h if possible. ACE inhibitors may cause hypotension in ferrets, titrate to effect.
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• When diuretics and ACE inhibitors are used together • •
it is important to monitor for azotemia. Perform thoracocentesis or abdominocentesis when indicated. Monitor body weight, CRT, heart rate and rhythm, hydration status, mucous membrane color, respiratory rate, respiratory effort, BUN, creatinine, and serum electrolytes.
▼ Key Point Chronic therapy typically includes the use of ACE inhibitors, and diuretics with the addition of digoxin in ferrets with dilated cardiomyopathy. Whenever possible, try to titrate the diuretic dose to the lowest possible dose without recurrence of pleural effusion or pulmonary edema.
• Administer digoxin elixir (0.01 mg/kg) PO sid–bid to ferrets with dilated cardiomyopathy.
• Side effects associated with digoxin include anorexia, •
•
•
•
arrhythmias, diarrhea, lethargy, and vomiting. Serum digoxin levels should be monitored every 4 to 8 weeks. Normal values have not been published for the ferret; reference values for dogs and cats are used for interpretation. Use of antiarrhythmic drugs such as atenolol or diltiazem is not well documented in the ferrets, but may be useful in the treatment of ferrets with hypertrophic cardiomyopathy. Salt-free diets may be beneficial; however, they are often unpalatable to ferrets. Instruct the owner to avoid feeding snacks, treats, or food items with a highsalt content. Management includes periodic reevaluation of heart rate and rhythm, serum electrolytes, and renal values. Radiographs should be used to monitor for the development of pulmonary edema or changes in the cardiac silhouette. ECG and echocardiography should be repeated periodically as well.
Cardiomyopathy Cardiomyopathy may occur in ferrets 2 years of age or older. Dilated (congestive) and hypertrophic forms can occur; the dilated form is more common.
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• Moist rales and increased respiratory sounds may be noted when pulmonary edema is present.
• Pleural effusion may be present, and may cause an •
increased inspiratory effort. The heart may sound muffled on auscultation. Coughing generally is not noted.
Diagnosis
• See the CHF section in this chapter. Treatment
• Treatment is the same as that described for CHF. • Taurine supplementation does not appear to have any effect on DCM in the ferret.
Follow-Up Care
• See the CHF section in this chapter. Hypertrophic Cardiomyopathy Etiology The cause of hypertrophic cardiomyopathy (HCM) is unknown.
Clinical Signs
• Clinical signs may be compatible with those described for CHF or DCM (see above).
• Other clinical signs are similar to those described for the cat, and include acute onset of congestive heart failure and/or sudden death.
Diagnosis
• Follow the same guidelines described for DCM. • Include HCM on the rule-out list when evidence of • •
cardiac disease is noted on the physical examination or diagnostic evaluation. Radiographs may not be beneficial in the diagnosis of HCM. Echocardiography should be used for definitive diagnosis.
Treatment
Dilated Cardiomyopathy Etiology
• Treatment should be aimed toward alleviating signs
The cause of dilated cardiomyopathy (DCM) in the ferret is unknown.
•
Clinical Signs
• Abdominal enlargement secondary to ascites, •
anorexia, dyspnea, lethargy, and weight loss are often noted. Ascites, heart murmur, pale mucous membranes, tachycardia, and weakness may be noted on physical examination.
• •
of CHF and improving the diastolic efficiency of the left ventricle. Administer beta-adrenergic blocking drugs such as atenolol (3.125–6.25 mg) PO sid. Titrate to effect. Administer calcium channel blockers such as diltiazem (3.75–7.5 mg) PO bid. Titrate to effect. Diuretics are indicated if symptoms of CHF are present (see above).
Follow-Up Care
• Follow-up is the same as that described for CHF and DCM.
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Heartworm Disease Natural and experimental heartworm infections have been reported in ferrets (see Chapter 152). The clinical presentation of heartworm disease typically resembles that of cats; however, the life cycle of Dirofilaria immitis in ferrets is similar to the life cycle present in the dog. Reported adult worm burdens range from 1 to 10. The presence of only one adult worm in the heart can be lethal.
Etiology
• Heartworm disease is caused by the canine heart•
worm Dirofilaria immitis, a filarial nematode that is transmitted via mosquitoes. Ferrets that are housed outdoors in endemic areas are at greatest risk of infection; however, ferrets kept indoors also can become infected.
• Submit blood for an enzyme-linked immunosorbent
• • •
Clinical Signs
• Clinical signs include coughing, dyspnea, hepato-
•
megaly, inappetence, lethargy, melena, weakness, and symptoms associated with right-sided CHF (pulmonary edema, pleural effusion, ascites). Sudden death due to pulmonary artery obstruction may also occur. Microfilaria may be present in the blood of approximately 50% of infected ferrets.
Diagnosis
Treatment
• Treatment of heartworm disease in ferrets is difficult.
• •
• Diagnosis is based on the history, clinical signs, heart• •
worm test results, radiographs, and echocardiography. If the history is compatible with cardiac failure, inquire about possible mosquito exposure. Physical examination findings resemble those of heart failure (see above).
▼ Key Point Minimize stress in ferrets suspected of heartworm disease. If symptoms of congestive heart failure are present, delay further diagnostic evaluation until the patient is stabilized (see “Treatment of Congestive Heart Failure”).
• Obtain whole body radiographs. Thoracic changes
•
may include cardiomegaly with enlargement of the right atrium, caudal vena cava, and right ventricle. Pleural edema and pleural effusion may be present as well. Radiographic changes in the peripheral pulmonary arteries are not typically noted because the worms tend to reside in the right side of the heart and in the main pulmonary artery. Abdominal changes often include hepatomegaly, splenomegaly, and ascites. If possible, draw blood for the modified Knott’s test for microfilaria. Microfilaria are identified in approximately 50% of infected ferrets.
assay (ELISA) for Dirofilaria antigen. Antigen is produced by adult female heartworms; there is a potential for false negative test results in ferrets with low worm burdens. A commercial assay (Snap Heartworm Antigen Test Kit; IDEXX Laboratories Inc., Portland, ME) has been used to detect heartworm infection in the ferret. Perform a CBC, serum biochemical profile, and urinalysis to rule out the presence of other systemic diseases. If pleural or abdominal effusion is present, submit fluid for cytology. A modified transudate is typically noted when CHF is present. Echocardiography may be used to visualize heartworm(s) in the pulmonary artery, right ventricle, and right atrium; dilation of the right ventricle and right atrium may be assessed as well. Doppler echocardiography may be used to evaluate the patient for the presence of pulmonary hypertension.
• • • • •
• •
Success is dependent on early diagnosis, diligent supportive care, and long-term antithrombotic therapy in conjunction with adulticide therapy. If signs of CHF are present, treat this first, and stabilize the patient (see the CHF section). If the patient is symptomatic and microfilaremia positive: • Administer microfilaricidal therapy: Ivermectin (50 µg/kg) SC every 30 days until clinical signs and microfilaremia resolve. • Follow with adulticide therapy: melarsomine (Immiticide, Rhone Merieux, Athens, GA) using a two-stage protocol: Stage 1: Administer a single dose of melarsomine (2.5 mg/kg) IM. Stage 2: 1 month later, administer two injections of melarsomine (2.5 mg/kg) IM given 24 hours apart. Transient swelling at the site of injection is common. Administer prednisone (0.5 mg/kg) PO sid–tid during adulticide treatment and for as long as clinical signs persist. If pleural effusion is present administer diuretics (see the CHF section). Cage confinement is important for 4 to 6 weeks after treatment. Perform a post-treatment ELISA for heartworm antigen 3 months after adulticide therapy. Repeat every 30 days if results are positive. Most ferrets become seronegative 4 months after treatment. Begin heartworm prevention 1 month after adulticide treatment. If ferrets are microfilaria negative, administer adulticide therapy as described above.
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Prevention ▼ Key Point Because of the high mortality associated with heartworm disease, recommend preventive therapy for all ferrets in heartworm-endemic areas.
• Ivermectin may be given as preventive therapy begin-
• •
ning 1 month before and continuing 2 months after mosquito season. Liquid ivermectin 1% may be diluted in propylene glycol (0.3 ml ivermectin in 30 ml propylene glycol) and administered at a dose of (0.2 ml/kg) PO every month. This solution must be stored in an amber glass bottle out of sunlight. Feline Heartguard (Merck Agvet) may be administered using the dose appropriate for a 1- to 5-lb cat. If possible, house all ferrets in endemic areas within structures with mosquito-proof screening. Follow the same recommended guidelines for heartworm prevention in dogs and cats.
Valvular Heart Disease Valvular heart disease may occur in ferrets >3 years of age.
Clinical Signs
• Clinical signs depend on the severity of the underly• • •
ing disease process. Mitral regurgitation may be ausculted as a systolic murmur in the left apical region. Tricuspid regurgitation is ausculted in the right parasternal region. Dyspnea and moist rales may be noted on auscultation of the lungs if CHF is present.
Diagnosis
• Obtain thoracic radiographs to evaluate the size of
• • •
the heart and to determine if CHF is present. Pulmonary edema typically appears as a mixed alveolar and interstitial pattern in the caudodorsal lung lobes. Electrocardiography (ECG) may be normal or may demonstrate evidence of atrial arrhythmias. Echocardiography typically demonstrates thickening of affected valves and atrial enlargement. Doppler echocardiography may be used to identify and quantify the degree of regurgitation present. Aortic regurgitation is often noted in ferrets and is considered an incidental finding.
Treatment
• Treatment is recommended if CHF is present, or if cardiac enlargement is significant (see the CHF section).
Myocarditis Myocarditis occurs when the myocardium is infiltrated with inflammatory cells, resulting in the development of reduced myocardial function, arrhythmias, and
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replacement of the normal myocardial tissue with fibrous tissue.
Etiology
• Causes include sepsis, systemic vasculitis, parasitic, bacterial or viral infection, and autoimmune disorders.
• Aleutian disease can cause fibrinoid necrosis and mononuclear cell infiltration of the arterioles of the heart.
Clinical Signs
• Antemortem diagnosis is difficult. • Suspect myocarditis if arrhythmia and/or acute •
myocardial dysfunction is noted in association with multisystemic illness. Definitive diagnosis is made by histopathological evaluation of affected myocardial tissue.
Treatment
• Treatment should be directed at identifying and treating the underlying systemic disease.
• Cardiovascular support should be provided and may include the use of diuretics or antiarrhythmic drugs (see the CHF section).
Other Cardiac Diseases As clinical experience with pet ferrets increases, other types of cardiac disease are likely to be recognized. Third-degree heart block (of unknown etiology) and various forms of valvular disease, including mitral and tricuspid insufficiency and endocarditis, have been seen in ferrets.
• The approach to these conditions in ferrets is the same as for other companion animals; use the drug dosages given previously for cardiac myopathies.
Gastrointestinal System CHARACTERISTICS OF THE NORMAL FERRET DIGESTIVE TRACT Teeth • The permanent teeth erupt between 50 and 74 days of age.
• The dental formula is 2 (I3/3, C1/1, Pm3/3, M1/2). • The third upper premolar (carnassial tooth) has three roots. The second lower molar has one root. All other premolars and molars have two roots.
Gastrointestinal Tract • The ferret is an obligate carnivore with a simple stomach, short intestinal tract, no cecum or ileocolic valve, and a short colon.
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• The duodenum terminates at the jejunoileum; there • •
is no gross anatomic distinction between the jejunum and the ileum. The junction of the jejunoileum and the colon is determined by evaluating the pattern of anastomosis between the jejunal artery and the ileocolic artery. GI transit time is approximately 3 to 4 hours.
•
Anal Sacs • The anal sacs are located between the external and internal anal sphincter muscles at 4 and 8 o’clock. The ducts are located near the mucocutaneous junction.
Diet • The exact nutritional requirements of the ferret have not been determined.
• The diet of the ferret must contain predominantly animal protein and fat.
• Due to the short digestive tract and rapid GI transit
• • •
• •
•
•
• •
time, the ferret requires a concentrated maintenance diet high in protein (30–35%) and fat (15–18%), and low in fiber. The protein quality should be 85% to 90% digestible. Breeding ferrets and kits may require diets higher in protein and fat. Meat, poultry, meat and poultry meals, and other animal-based proteins should appear first, then several more times on the food ingredient list. Complex carbohydrates (starch, fiber) are not readily digested by the ferret. High–fiber diets can induce a relative protein-calorie deficiency; the ferret cannot eat enough of a low-density food to meet its high maintenance requirements. Premium cat foods and ferret diets typically meet the ferret’s nutritional requirements for growth and reproduction. Treats and supplements should not exceed more than 10% of the daily diet. Acceptable treats include meat baby foods, and moist cat or ferret diets. High–sugar or carbohydrate treats should be limited, especially if insulinoma is present. Fatty acid supplements should be given in measured amounts (a few drops per day). Administration of large quantities of fatty acid supplements may reduce the intake of the balanced diet. Canine diets should not be fed to ferrets; the protein, fat, and carbohydrate content is not appropriate, and the diets often contain high percentages of grain and vegetable matter. The long–term effect of formulated dry and canned diets on the long–term health of ferrets is controversial among some practitioners. Some practitioners feel that feeding commercial diets containing large quantities of plant-based ingredients contributes to the development of eosinophilic gastroenteritis, inflammatory bowel disease, insulinoma,
urolithiasis, and general untriftiness. For example, most ferrets in the United States are fed dry kibbled diets, and the incidence of insulinoma is high. Many ferrets in Europe and Australia are fed whole prey items (e.g., a “natural diet), and the incidence of insulinoma is low. A correlation between diet and the development of certain diseases in ferrets is hypothetical at this time; however, this controversy demonstrates the need for longer–term diet studies in the ferret.
DENTAL DISEASE • The canine teeth are often worn or broken at the tips due to biting and gnawing.
• Broken canine teeth typically are not painful unless the dental pulp is exposed.
• Dental tartar and periodontal disease are common in ferrets over 2 years of age.
• Soft, moist diets may predispose ferrets to the development of dental disease.
• Tartar typically accumulates first on the second and third upper premolars.
• Dental abscesses are not common, but may be noted, even in young ferrets.
• Follow the basic medical and surgical treatment principles described for dental diseases in dogs and cats (see Chapter 64).
SALIVARY MUCOCELE • Ferrets have five major pairs of salivary glands: the • •
• •
parotid, submandibular, sublingual, molar, and zygomatic. Salivary mucocele occurs secondary to trauma or infection of a salivary gland. Salivary mucocele typically presents as a soft to firm swelling in the region of the orbit, oral commissure, or mandibular lymph node. Aspiration of the swelling often yields a clear to serosanguinous or mucinous fluid; microscopic examination demonstrates amorphous debris and occasional RBCs. Treatment of choice is surgical excision of the affected gland (see Chapter 64). Advise clients that recurrence is possible.
MEGAESOPHAGUS Megaesophagus is rare in ferrets.
Etiology • The etiology of megaesophagus in ferrets is unknown (see list of possible causes in dogs in Chapter 65).
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Clinical Signs • Clinical signs resemble those described for the dog •
and include: lethargy, anorexia, dysphagia, coughing, choking, dyspnea, weight loss, and regurgitation. Clients may indicate that the ferret vomits up large boluses of food.
Diagnosis • Diagnosis may be based on clinical signs and radiographic evidence of megaesophagus.
• Obtain thoracic radiographs. The esophagus is often
• •
dilated and filled with air in the cervical and thoracic regions. Food may be present within the lumen of the esophagus. Perform a barium contrast study to delineate the esophageal mucosa and to identify potential mural lesions, strictures, or obstructions. Aspiration pneumonia may be visible radiographically.
GASTROINTESTINAL PARASITES • GI parasites are uncommon in the ferret. Coccidiosis • • •
protocols and dosages used for cats (see Chapter 69).
GASTRITIS, AND GASTRIC AND DUODENAL ULCERS
poor; response to therapy is usually not successful.
•
• •
(Reglan, AH Robins Company, Inc., Richmond VA) (0.2–1mg/kg) PO tid–qid may be helpful. Administer H2-receptor blocking drugs such as cimetidine, ranitidine (Zantac, Glaxo Pharmaceuticals, Research Triangle Park, NE), or famotidine (Pepcid AC, Johnson and Johnson, Fort Washington, PA). Administer antibiotics if indicated for aspiration pneumonia. Supportive care includes feeding high-calorie, highprotein slurried diets 3 to 4 times per day, and elevating the ferret for 15 to 30 minutes immediately after feeding.
NAUSEA AND VOMITING • Ferrets, like other carnivores, are able to vomit. • Differential diagnoses to consider for vomiting •
• •
include esophageal and gastroenteric disorders (see below). Ferrets often demonstrate symptoms associated with nausea or vomiting when gastroenteritis, GI disease, gastric ulcers, Helicobacter mustelae gastritis, or GI foreign bodies are present. Hypoglycemia may cause signs of nausea as well (see discussion of Insulinoma in this chapter). Signs of nausea include hypersalivation and pawing at the mouth. Ferrets may demonstrate bruxism (grinding of the teeth) when abdominal discomfort is present.
and giardiasis are occasionally seen. Nematodiasis is rare. Routine fecal testing is still recommended, especially in young animals and ferrets with diarrhea or rectal prolapse. Young ferrets with coccidiosis may have diarrhea and may be severely dehydrated. Cryptosporidiosis may occur in ferrets, but typically does not result in clinical disease. The zoonotic potential is unknown; however, it may be prudent to warn immunosuppressed owners of the potential for zoonosis.
Treatment • Treat with appropriate anthelmentics following the
Treatment • Follow canine treatment protocols. The prognosis is • GI promotility agents such as metoclopramide
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Gastric and duodenal ulcers have been documented in laboratory ferrets and reported occasionally in pet ferrets. Clinical signs are often vague, making the diagnosis difficult.
Etiology • The etiology is unknown but may include stress, GI
•
foreign body, H. mustelae gastritis, administration of ulcerogenic drugs, GI neoplasia, and azotemia secondary to renal disease. H. mustelae is similar to H. pylori, the bacteria associated with gastritis and ulceration in humans. H. mustelae infection in the ferret can be an incidental finding, or can induce gastritis, duodenitis, and GI ulceration.
Clinical Signs • Gastritis and ulcers may be acute or chronic. • Clinical signs include anorexia, lethargy, hypersalivation, bruxism (tooth grinding), weight loss, vomiting, and melena.
Diagnosis • Presumptive diagnosis may be made based on the history and clinical signs.
• Perform a CBC and serum biochemistry profile to rule out systemic and metabolic disease.
• Obtain fasting whole-body radiographs to help rule out the presence of a GI foreign body or trichobezoar.
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• A barium study may be used to demonstrate GI • •
ulceration. Exploratory laparotomy/gastrotomy is often required for a definitive diagnosis. Diagnosis of H. mustelae gastritis is often a diagnosis of exclusion. Definitive diagnosis requires the finding of organisms along typical histological lesions on gastric biopsy specimens.
Treatment • Debilitated, anorexic ferrets may require hospitaliza•
• • •
•
tion for supportive care. If the patient is vomiting, withhold food for 6 to 12 hours. Administer IV fluids containing dextrose, and monitor for signs of hypoglycemia. When vomiting has resolved begin to offer small, bland meals. Feed small meals of a bland, moist diet tid–qid (see diet recommendations in “Insulinoma” section). Avoid feeding high-fiber dry foods. Administer broad spectrum antibiotics if the ferret is debilitated. Administer a gastric protectant. Options include: • Bismuth subsalicylate (Pepto Bismol, Procter & Gamble) (1 ml/kg) PO tid. • Sucralfate (Carafate, Marion Merrell Dow, Inc., Kansas City, MO) (100 mg/kg) PO tid–qid. • Systemic H2-receptor antagonists such as cimetidine and famotidine. • Omeprazole (Prilosec, Astra Merck, Inc., Wayne PA) (_ the contents of a 10-mg capsule mixed with soft food) PO sid-bid. If H. mustelae infection is suspected, administer the following three drugs concurrently for at least 2 weeks (“triple therapy”): • Amoxicillin (10 mg/kg) PO, SC bid. • Metronidazole (20 mg/kg) PO bid. • Bismuth subsalicylate (Pepto-Bismol, Procter & Gamble) (see dosage information above).
GASTROINTESTINAL FOREIGN BODIES GI obstruction caused by foreign body ingestion or hairballs is one of the most common problems in pet ferrets.
Etiology • Foreign bodies typically occur in ferrets younger than 1 year of age; trichobezoars (hairballs) are common in ferrets older than 2 years of age. ▼ Key Point Suspect the presence of a GI foreign body in any young ferret presented for anorexia, even if no vomiting is reported.
• Rubber and foam objects are the most common foreign bodies. Obstruction with a hairball (older ferrets), cloth, or plant material also may occur.
Clinical Signs • Lethargy, partial or total anorexia, hypersalivation,
•
bruxism, pawing at the mouth, weight loss, and diarrhea are the most common clinical signs of GI foreign body. Hindlimb weakness, dehydration, and melena may be noted as well. Vomiting is uncommon; however, if the ferret is vomiting, be suspicious that a GI foreign body may be present.
Diagnosis • Diagnosis is based on the history, physical examination findings, radiographs, or exploratory laparotomy.
• History: Identify possible types or causes of foreign • •
• •
body ingestion. Ask the owners if hairball preventative is used routinely. Physical Examination: Large gastric foreign bodies are often palpable. Small foreign bodies in the small intestine may be associated with localized pain. Obtain fasting (4–6 hours) plain whole body radiographs. Radiographs may reveal segmental ileus, and marked gaseous distention of the stomach and/or bowel. Occasionally a foreign body or trichobezoar can be identified. Obtain a GI barium contrast study to identify small foreign bodies and to rule out GI ulceration. Perform a CBC and serum biochemical panel to rule out hepatic lipidosis and other systemic diseases.
Treatment Surgical removal is the treatment of choice. If the ferret is debilitated, begin supportive therapy, and perform surgery as soon as possible.
• Surgery: Follow routine preoperative, operative, and
• • •
postoperative procedures for gastrotomy or enterotomy (see Chapters 68 and 70). Ferret tissues are more delicate than those of a puppy or kitten of equivalent weight. Use 4-0 or 5-0 suture material to close the GI tract. Perform gastric biopsy to rule-out underlying H. mustelae infection, and other GI diseases. Perform biopsy of the liver. Evaluate the entire abdominal cavity prior to closure. Older ferrets often have concurrent diseases such as insulinoma or adrenal gland disease. The prognosis following gastrotomy is good with prompt therapy.
Prevention ▼ Key Point Instruct owners to “ferret proof” the house if ferrets are allowed to roam. In particular, restrict access to rubber toys and rubber objects.
• To prevent trichobezoars, administer a feline hairball laxative product (2–4 cm) PO 2 to 3 times per week.
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EPIZOOTIC CATARRHAL ENTERITIS Epizootic catarrhal enteritis (ECE, “green slime disease”) is a highly infectious diarrheal disease that first appeared in 1993.
• Loperamide (Imodium A-D, McNeil Consumer) • •
Etiology The etiological agent is thought to be a coronavirus. ECE can spread rapidly through a ferret population, often affecting 100% of ferrets within 48 hours. Histological examination of intestinal biopsy samples reveals lymphocytic enteritis with villous atrophy and blunting, and degeneration of the apical epithelium.
Clinical Signs • The history often includes recent exposure of an
•
•
older ferret to a new or young ferret that appears healthy. Often within 48 hours the older ferret becomes anorexic and lethargic. Four clinical syndromes are typically seen: 1. ECE may cause relatively mild diarrhea that lasts several days in young ferrets with no underlying disease. 2. ECE may cause severe diarrhea lasting for several days that may be followed by an acute onset of severe bloody diarrhea in older ferrets or ferrets with concomitant disease. Anemia may develop as a sequelae. 3. A wasting disease with abnormal stools that have the appearance of bird-seed or of being grainy. These stools may develop in ferrets that initially appear to have recovered from the diarrheal phase. 4. Voluminous green, watery diarrhea and occasional vomiting followed by chronic wasting may occur in some ferrets. The clinical course of disease can be prolonged in some ferrets, and may last weeks to months. Affected ferrets typically appear to recover, but continue to have persistent, intermittent diarrhea.
Treatment • No one specific treatment is consistently effective. • Supportive care, including fluid therapy and nutri• • • •
tional support, is very important in the treatment of ECE. Treat sick ferrets with aggressive fluid therapy. Administer fluids IV, IO, PO, or SC depending on the ferret’s status. Administer broad-spectrum parenteral antibiotics. Feed a bland, high-calorie diet, such as a mixture of Science Diet A/D (Hills Science Diet, Topeka, KS) mixed with Deliver 2.0 (Mead Johnson Nutritionals). Intestinal adsorbents or protectants (e.g., Kaopectate, UpJohn) may help in some ferrets.
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•
(0.2 mg/kg) or (1 ml/kg) PO bid every 1 to 3 days may be helpful. Administration of prednisone (1mg/kg) PO bid every 14 days may alleviate the chronic, intermittent diarrhea in ferrets with long-term symptoms. The disease may recur in previously affected ferrets; an asymptomatic carrier state appears to be possible. Do not house ferrets that have had ECE with ferrets that have not had the disease.
ROTAVIRUS • Rotavirus has been associated with several outbreaks
• • •
of diarrhea and high mortality in ferret kits 2 to 6 weeks of age; it is often referred to as “ferret kit disease.” Rotavirus also causes diarrhea in the young of several other species, including humans, cattle, swine, sheep, and rats. In adult ferrets, rotavirus infection is rarely fatal, but may cause bright green mucoid diarrhea that lasts for several days. There is no readily available antemortem test for the rotavirus infection; rotavirus particles can be identified in feces by electron microscopy.
Treatment • Treatment consists of supportive care. Administer fluids, antibiotics, and nutritional support.
SALMONELLA Salmonellosis is rare in the ferret, and is typically associated with exposure to contaminated raw meat and meat by-products. Salmonella typhimurium, S. newport, and S. choleraesuis may be associated with clinical disease.
• Clinical signs include anorexia, lethargy, fever, and • •
•
diarrhea (usually bloody). Conjunctivitis and anemia have also been reported. Diagnosis is based on clinical signs and a positive fecal culture. Multiple fecal samples must be collected, and selective media is used for culture. Treatment includes aggressive supportive care and antibiotic therapy. • Ferrets may be presented in shock. IV fluids and administration of rapidly acting intravenous corticosteroids may be necessary for treatment of these patients. Other details of salmonellosis, including its public health significance, are discussed elsewhere in this text.
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biopsy specimens from affected skin were consistent with allergic dermatitis. These ferrets were treated with corticosteroids, and did respond to treatment. One also responded to diet change.
EOSINOPHILIC GASTROENTERITIS Eosinophilic gastroenteritis (EGE) is an inflammatory bowel disease that occurs in ferrets and other animals.
Etiology No specific etiological agent has been identified in the ferret, but food allergy is implicated in humans and other animals.
Clinical signs • Chronic diarrhea with or without mucus or blood,
• •
and weight loss are the most common signs. Inappetence, intermittent vomiting, and skin lesions may be seen as well. On physical examination, the mesenteric lymph nodes may be enlarged and the intestines may feel thickened. A marked peripheral eosinophilia is often present on the CBC differential.
Diagnosis • Presumptive diagnosis is based on history, clinical
•
signs, physical examination findings, the presence of a peripheral eosinophilia, and/or the presence of eosinophils on fecal cytology. Definitive diagnosis is based on histological examination of intestinal biopsy specimens. Mild to extensive eosinophilic infiltration of the mucosa, submucosa, and muscularis of the stomach and small intestines are noted. Focal eosinophilic granulomas maybe identified in the mesenteric lymph nodes.
Treatment • Treatment is similar to that described for treatment •
•
•
of dogs and cats. Begin corticosteroid therapy with prednisone (1.0–2.5 mg/kg) PO sid every 14 days. Perform a recheck examination and CBC 2 weeks after the last dose. If the ferret has improved clinically and the peripheral eosinophilia is resolving, decrease the prednisone dose by 50% every 14 days, and recheck again. Continue the prednisone taper at 2-week intervals until the ferret is tapered to the lowest possible dose, or withdrawn from the steroids altogether. Although food allergy has not been identified as a definitive etiological cause of EGE, changing the ferret to a hypoallergenic diet, such as a feline lamb and rice-based diet may be helpful in resolution of signs. There have been reports of ferrets with peripheral eosinophilia (up to 40%), and erythema and crusting of the feet, ears, and face. Histological lesions in
INFLAMMATORY BOWEL DISEASE Inflammatory bowel disease (IBD) can occur in the ferret.
Etiology The etiology is unknown; dietary factors, hypersensitivity reactions, or an immune-mediated cause have been considered.
Clinical Signs • Clinical signs can be subtle and include diarrhea;
• • •
nausea; occasional vomiting; soft, malformed stools that resemble bird seed; and weight loss. These signs often resemble ECE, EGE, and Helicobacter gastroenteritis. Affected ferrets are often young or middle-aged adults. Elevation of liver enzymes and serum globulins may be noted on serum biochemistry analysis. Lymphocytosis may be noted on the CBC.
Diagnosis • Diagnosis is based on the history, clinical signs, and diagnostic work-up.
• Definitive diagnosis is made by histological examination of gastric and intestinal biopsy samples. Mild to severe lymphoplasmacytic gastritis and enteritis are noted on histopathology.
Treatment • Administer corticosteroids such as prednisone
• •
(1.0–2.5 mg/kg) PO sid every 14 days initially, and taper in a manner similar to that described for EGE. Some ferrets respond poorly to steroid therapy. Azathioprine (Imuran, Prometheus Laboratories, San Diego, CA) (0.9 mg/kg) PO q24–72h may be used as an alternative to steroid treatment. Hypoallergenic diets may offer some benefit.
PROLIFERATIVE BOWEL DISEASE (PBD) Proliferative bowel disease (PBD) in ferrets was first reported in 1982, and is similar to the PBD that occurs in swine and hamsters. PBD was a commonly encountered disease in the late 1980s and early 1990s, but is relatively uncommon now.
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Etiology PBD is caused by Lawsonia intracellularis, an intracellular bacteria that cannot be propagated by routine culture methods.
Clinical Signs • This disease affects primarily young ferrets 4 to 14
• Metronidazole (20 mg/kg) q12h, PO may be effective.
Prevention and Prognosis • The prognosis is good with timely therapy. • Some ferrets improve temporarily and then relapse at the end of the treatment period. Use a long-term course of antibiotic therapy in these animals.
months of age.
• Acute and chronic forms of the disease can occur. • Diarrhea is present and often contains mucus and
• • •
blood. Defecations are frequent and small; ferrets often cry out when they defecate. The rectum may be partially prolapsed. Other signs include lethargy, depression, inappetence, weight loss, dehydration, and pyrexia. Neurologic signs such as ataxia and muscle tremors may be present. The intestines may feel firm or thickened on abdominal palpation.
Diagnosis • A tentative diagnosis of proliferative bowel disease is
• •
•
based on clinical signs and physical examination. Definitive diagnosis requires intestinal or colonic biopsy, but this rarely is warranted because response to therapy usually is good if initiated early. A polymerase chain reaction (PCR) assay specific for the swine isolate, and an indirect fluorescent antibody test (IFA) are available. Necropsy lesions include gross thickening and discoloration of the small intestine and/or colon. Ridges of proliferative tissue that are distinct from normal adjacent tissues are present on the mucosal surface. Histological examination of biopsy samples or necropsy specimens typically demonstrate epithelial proliferation, hypertrophy of the muscularis, and infiltration of the bowel wall with monocytic or granulocytic inflammatory cells. Silver-stained tissues reveal intracellular, comma-shaped organisms in crypt epithelial cells. Glandular hyperplasia consisting of irregular, branching proliferative glands that lack goblet cells, and necrotic debris may be identified in the crypts. Severe glandular hyperplasia may resemble neoplasia and can metastasize.
Treatment • Treat mild cases on an outpatient basis. • Hospitalization for supportive care (fluid therapy, •
nutritional support) may be necessary when severe disease is present. Administer Chloramphenicol (50 mg/kg) q12h, PO, IV, IM, or SC as the drug of choice. Treat for at least 2 weeks; longer therapy often is necessary to prevent relapse.
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RECTAL PROLAPSE • Rectal prolapse is usually a disease of young ferrets, and is often associated with diarrhea.
• Possible causes of rectal prolapse include colitis, diar• • • • • •
rhea, GI parasitism (e.g., coccidiosis), PBD, and other diseases that may cause straining or diarrhea. Other differentials include GI lymphoma, benign intestinal polyps, and postoperative complications of anal gland removal. Perform direct fecal and fecal flotation tests to screen for parasites. Medical treatment is similar to that described for other species. Administer anthelmentics and antibiotics when indicated. The prolapse may resolve without surgical intervention when the underlying disease process is resolved. Surgical correction is usually unnecessary (see below). If indicated, perform a biopsy of the prolapsed tissue to rule out lymphoma.
Surgical Therapy • Flush the prolapsed tissues with sterile saline and replace them into the rectum.
• Place a purse-string suture in the anus with a small •
opening to allow passage of feces. Keep the pursestring suture in place for 2 to 5 days. In ferrets with chronic prolapse, surgery may be necessary to reduce the size of the anal opening. Excise a small triangular wedge of anal mucosa and routinely close the defect by suturing. Alternatively, consider abdominal exploratory surgery and colopexy (see Chapter 75)
ANAL SAC ABSCESS • Clinical signs and physical examination findings in •
ferrets with an abscessed anal sac are the same as those described in dogs and cats. The recommended treatments include antibiotic therapy, lancing and drainage of the abscess, or surgical removal of both anal sacs (see Chapter 75).
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Anal Sacculectomy
Females
Anal sacculectomy is performed as a treatment for anal sac abscesses, or to decrease the musky “ferret” odor. For odor reduction, neutering should be performed simultaneously because the apocrine, perianal, sebaceous, and scent glands in the skin are under hormonal control and contribute to the overall musky odor. Some clinicians believe that neutering is sufficient to decrease odor and that routine anal sacculectomy should be discouraged.
• Female ferrets (jills) are seasonally polyestrous and
Surgical Technique 1. Grasp the anal sac duct and hold it closed with mosquito forceps. Make a circumferential skin incision around the duct opening. 2. Apply gentle caudal traction to the anal sac, and use a scalpel blade or gauze to tease away the surrounding fascia. 3. Leave the surgical sites open, and allow to heal by second intention.
Alternative Technique 1. Make small, arc-like incisions just lateral to the duct openings. 2. Dissect the subcutaneous tissues bluntly to reveal the neck of the anal sac; grasp the opening and hold it closed with mosquito forceps. 3. Dissect the sac free of surrounding tissues, using gentle traction. 4. Do not suture the incisions.
Urogenital System
•
• •
• •
are induced ovulators. Ovulation typically occurs 30 to 40 hours after mating. The vulva is located in the perineal region ventral to the anus. In non-estrous females the vulva is small, and looks like a slit; during estrus (or when adrenal gland disease is present), the vulva becomes swollen and is easily visualized. If mating is unsuccessful, pseudopregnancy results and lasts 41 to 43 days. Approximately 50% of females remain in estrus if they are not bred. The resultant prolonged elevation of serum estrogens can cause bone marrow toxicity and pancytopenia (see the discussion of anemia under “Hematopoietic System” in this chapter). Submit blood for a CBC and platelet count if the ferret has been in estrus for more than 28 days. Termination of estrus is recommended (see “Termination of Estrus in the Hematopoietic”.)
Castration
• Most pet male ferrets in the United States have already been neutered prior to 8 weeks of age.
• Castrate intact male ferrets at 6 to 8 months of age in order to reduce aggressive behavior and odor.
• Castration is performed using techniques similar to those used in cats (see Chapter 87). • Make an incision in the scrotum over each testicle. • Remove the testicles using an open or closed technique. • Incisions may be left open to heal by second intention.
Ovariohysterectomy
REPRODUCTIVE SYSTEM
• Most pet female ferrets in the United States have already been spayed prior to 8 weeks of age.
Characteristics of the Normal Ferret Reproductive System
• Spaying intact female ferrets is recommended to
Ferrets reach sexual maturity during the first breeding season after birth. The breeding season runs from March to August under natural lighting conditions.
• Ovariohysterectomy is similar to the procedure per-
Males
• The opening of the prepuce is located just caudal to the umbilical area.
• Males (hobs) have a J-shaped os penis. • During the breeding season (March–August), testicle
prevent estrogen-induced bone marrow hypoplasia. formed in cats (see Chapter 91). • The ventral midline incision is made approximately 1 cm caudal to the umbilicus, and may be extended as necessary. • The uterus is bicornuate, and is located dorsal to the bladder. • Ovarian vasculature may be difficult to locate due to the large amount of body fat typically present in this region.
size is twice that noted in the fall and winter months.
• Prostatic tissue is located at the base of the urinary bladder and surrounds the urethra. Prostatic disease associated with adrenal gland disease may occur in middle-aged and geriatric male ferrets (see “Adrenal Gland Disease” and “Prostatic Disease”).
Pyometria/Metritis • Pyometra and metritis are uncommon in pet ferrets in the United States because they are usually spayed prior to being sold as pets.
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• Clinical signs may include anorexia, lethargy, pyrexia,
• Treatment includes aggressive supportive care
and vulvar discharge. Polyuria and polydipsia are not usually noted. Persistent estrus may predispose ferrets to pyometra. Preoperatively perform a CBC and a serum biochemical analysis to rule out estrogen-induced bone marrow hypoplasia (see “Anemia” in “Hematopoietic System”). Provide appropriate supportive care pre- and postoperatively. Perform ovariohysterectomy when the patient is stable (see Chapter 91). Start the ferret on broad-spectrum antibiotic therapy preoperatively, and continue postoperatively for 10 to 14 days. Use broad-spectrum antibiotics. Organisms commonly associated with pyometra include Staphylococcus spp, Streptococcus spp, Corynebacterium spp, and E. coli.
including IV or IO fluids containing dextrose. Perform an immediate cesarean section (see Chapter 91). Postoperative care includes continued supportive care, including frequent feedings of high-calorie critical care diets. Jills that survive pregnancy toxemia often do not produce milk. Kits can be difficult to hand rear; if a foster jill is not available, attempts may be made to hand rear the kits using a kitten milk replacer (see below). Kits born before 40 days of gestation often do not survive. The prognosis is usually poor, even with aggressive treatment.
• •
• • •
Vulvar Swelling in Spayed Females • Vulvar swelling is an external sign of estrus in female
• •
•
Mastitis • Do not breed females with a history of mastitis. • Abrasions to the mammary tissue and nipples can
ferrets.
• In a spayed female, a swollen vulva indicates a
• •
• •
remnant of ovarian tissue, or another source of estrogens and estrogen precursors such as adrenal gland disease (see “Adrenal Gland Disease”). Ovarian remnants typically induce signs of estrus in ferrets younger than 2 years of age. Administer HCG (100 IU) IM. Vulvar swelling should subside if an ovarian remnant is present. If no changes occur, adrenal gland disease is probably the cause of the clinical signs. Perform exploratory laparotomy to remove the ovarian remnant (see Chapter 91). Evaluate for uterine remnants and adrenal gland disease as well. Preoperatively evaluate a CBC to rule out estrogeninduced bone marrow hypoplasia.
• •
Pregnancy Toxemia • Pregnancy toxemia is a potentially life-threatening • • •
• •
•
condition that occurs in late pregnancy. Primiparous females are most commonly affected. The disease results in high mortality of jills and kits. Toxemia can be induced if an accidental fast occurs in the last week of gestation. Pregnancy toxemia may also develop in primiparous jills that are carrying large litters due to nutritional compromise induced by the size of the gravid uterus and the resultant reduced capacity of the stomach. Advise owners that pregnant jills must have access to food and water al lib during pregnancy. Suspect pregnancy toxemia if acute lethargy develops in the last week of gestation. Other clinical sings include dehydration, melena, hypoglycemia, ketonuria, and azotemia. Affected ferrets usually are presented in an acute state of shock.
•
cause mastitis. Prevent trauma from occurring by providing a large nest box opening with smooth edges that allows the jill to pass through easily. Mastitis may be acute or chronic. Acute mastitis typically occurs immediately after whelping or during the third week of lactation. • Affected glands appear swollen, firm, red to purple in color, and are painful. Gangrene can develop within hours of clinical signs. • Treatment must be aggressive. Administer broadspectrum antibiotics, and apply hot packs to the affected area 2 to 3 times per day for 2 days. Debride necrotic tissue if present. Provide supportive care and analgesic therapy. • Submit a sample for bacterial culture and sensitivity testing. Modify antibiotic therapy based on test results. • If there is no clinical response to medical therapy in 2 days, or if gangrene rapidly develops, consider surgical removal of the affected mammary tissue. Because of the potential for severe toxicity and life-threatening disease, do not delay surgery if gangrene is already present, or if there is no improvement with medical therapy. • If the jill continues to lactate, leave the kits with her. Supplement feed the kits with a kitten milk replacer if necessary. Do not foster the kits with another jill because this may result in mastitis in the foster jill. • Ingestion of infected milk may cause gastroenteritis in the kits; kits may need to be treated with antibiotics as well. Chronic mastitis is often difficult to diagnose. The affected jill often appears normal, while the kits lose weight or fail to thrive. • Mammary glands appear firm but are not painful or discolored; often the glands are presumed to be full of milk.
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• Affected mammary glands become scarred and are no longer functional. Affected jills should be culled from the breeding program.
Foster Care of Kits • Hand-rearing kits from birth is difficult. Prognosis is • • • • • •
poor for survival. It may be necessary to provide supplemental feeding for kits if the jill’s milk production is reduced, or if the litter size is large. Whenever possible, foster kits with another lactating jill. Most jills will accept kits of any size or age. Kits require a milk supplement that contains a high fat content (20%). Kitten milk replacers mixed with cream may be used. Feed kits as much as they will eat 4 times per day with a dropper or small pet nurser. Begin to mix solid food with the enriched milk replacer when kits are 4 weeks of age. This mixture may be offered in a shallow dish or bowl. Kits may be weaned onto a solid diet at 5 to 6 weeks of age. Feline or ferret growth diets are recommended.
URINARY SYSTEM Characteristics of the Normal Ferret Urinary System • The right kidney lies cranial to the left kidney. The • • •
cranial end of the right kidney often lies under the caudate lobe of the liver. The bladder is small, and can hold up to 10 ml of urine. Male ferrets have a small prostate gland that surrounds the urethra at the base of the bladder. Urinalysis: • The normal urine pH is 6.0 for ferrets on a meatbased diet. • Normal values for urine-specific gravity have not been reported. • There is evidence that proteinuria may be normal in ferrets (7–33 mg/dl in males; 0–32 mg/dl in females) and that bilirubinuria can occur in the absence of liver disease.
the kidneys, pale mucous membranes, and oral ulceration.
Diagnosis and Treatment
• Diagnosis is based on clinical signs, physical examination, and CBC, serum biochemical analysis, and urinalysis results. ▼ Key Point Hyperphosphatemia, hypocalcemia, and high BUN may be noted on serum biochemical analysis. Serum creatinine concentration is often normal or only moderately elevated.
• Treatment should address the underlying cause, if possible.
• Nonspecific treatment includes fluid therapy, nutri•
tional supportive care, and antibiotic therapy based on culture and sensitivity when indicated. Prognosis is guarded, depending on laboratory findings and response to treatment.
Renal Cysts Unilateral or bilateral renal cysts are relatively common in ferrets (see Chapter 77 for a description of this disease in dogs and cats). The condition is usually an incidental finding in middle-aged and older ferrets, although clinical signs associated with this condition can occur at any age.
Etiology
• The cause of renal cysts in the ferret is unknown. • Heredity does not appear to be a factor. Renal cysts are not associated with hepatic or biliary cysts.
• Renal cysts typically present as one or more smooth
•
masses on the surface of the kidney. On abdominal palpation affected kidneys feel smoothly enlarged or irregular. Polycystic disease is unusual in the ferret. When present, affected kidneys appear rough and irregular; multiple cysts are often distributed throughout the renal tissue. Cysts may be present in other organs as well.
Clinical Signs
Renal Disease
• Usually there are no clinical signs associated with
Renal disease in not common in ferrets, but may occur.
• Rarely, there may be enough disruption of normal
Clinical Signs
• Clinical signs are similar to those described in other
•
animals, and include ataxia, bruxism, halitosis, hindlimb weakness, inappetence, melena, mucus membrane ulceration, polyuria/polydipsia, vomiting, and weight loss. Physical examination findings may include cachexia, dehydration, irregularity in the shape and size of
renal cysts. renal parenchyma to lead to renal failure, and subsequent clinical signs.
Diagnosis
• Palpate the kidneys for irregular shape. • Perform a CBC, serum biochemical profile, and urinalysis.
• Abdominal radiography usually is not helpful unless the kidneys are very irregular.
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• Perform an abdominal ultrasound to detect renal • •
cysts, to evaluate renal architecture, and to rule out other conditions such as renal neoplasia. Intravenous pyelography or nuclear scintigraphy may be used to evaluate renal function. Renal cysts may be an incidental finding during abdominal surgery.
tent wetness in the perineal region, and frequent licking of the perineum.
• Urethral calculi may cause obstruction in both male and female ferrets. • Ferrets with urethral obstruction often strain and cry as they attempt to urinate. • If complete obstruction is present ferrets often appear lethargic and anorexic, and may not demonstrate obvious signs of dysuria.
Treatment
• There is no specific treatment for renal cysts. No treatment is necessary in asymptomatic animals.
• Monitor affected ferrets by periodic abdominal pal• • •
pation, serum biochemical profile, urinalysis, and ultrasound, if indicated. If an affected kidney becomes very large, consider unilateral nephrectomy (if the opposite kidney is functional) (see Chapter 78). Symptomatic ferrets may be managed using the same supportive care methods used in dogs and cats with chronic renal failure. The prognosis is grave for ferrets in renal failure.
Hydronephrosis • Hydronephrosis is uncommon in ferrets. Iatrogenic hydronephrosis may occur as the result of inadvertent ligation of a ureter during ovariohysterectomy (see Chapter 77 for information about hydronephrosis in dogs and cats).
Cystitis • Bacterial cystitis without urinary calculi is rare in pet
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Diagnosis
• Palpate the bladder to identify cystic calculi. The
•
urinary bladder wall may be thickened; in ferrets with urethral obstruction, the bladder is distended and firm. Obtain abdominal radiographs to confirm the presence of radiopaque urinary calculi. Cysteine calculi are not radiopaque and require contrast radiography or ultrasonography for diagnosis.
▼ Key Point Small stones located at the base of the os penis can be very hard to identify.
• Renal calculi may be an incidental finding on whole body radiographs, or may be associated with renal failure.
Treatment ▼ Key Point Urethral obstruction is an emergency. Severe metabolic derangement, coma, and death may occur if urethral obstruction is not diagnosed and treated quickly.
ferrets. Follow treatment protocols for cystitis in dogs (see Chapter 79).
Urolithiasis Urinary calculi was a common cause of stranguria in ferrets at one time; improvement in the quality of ferret diets has decreased the incidence of calculi. Calculi are usually composed of calcium oxalate or struvite (magnesium ammonium phosphate hexahydrate). Cysteine calculi also have been reported.
Etiology
• The cause of urinary calculi is unknown; however, diet is believed to be a factor.
• Diets containing plant proteins or poor quality meat-
•
based proteins may be associated with the development of urinary calculi. Urolithiasis is uncommon in ferrets maintained on a high-quality feline or ferret diet containing high-quality animal-based proteins. Other factors may include urinary tract infection, metabolic, genetic, and congenital factors.
Clinical Signs Clinical signs depend on the location of the urolith(s) and may include dysuria, stranguria, hematuria, persis-
• Stabilize non-obstructed ferrets by providing sup-
•
• •
•
•
portive care, fluids, analgesics, and antibiotics (if indicated) prior to performing cystotomy to remove the urolith(s). Cystic calculi may be removed surgically via cystotomy; the procedure is similar to that used in cats and dogs (see Chapter 80). Close the bladder wall with 4-0 or 5-0 absorbable sutures. Submit a urolith sample for analysis and bacterial culture/sensitivity testing. Administer antibiotics for a minimum of 10 to 14 days. Use results of follow-up urinalysis, and urine culture/sensitivity testing to determine when to discontinue antibiotic therapy. Begin conversion to a high-quality–animal, proteinbased feline or ferret diet. Urinary acidifies are not usually necessary once the ferret is on a high-quality animal, protein-based diet, since this diet alone will cause the urine to be acidic. Feline calculi-dissolving diets and preventative diets may be offered to ferrets; however, many ferrets do not find these diets palatable.
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• Renal calculi can often be managed medically by administering antibiotic therapy and changing the diet.
Urethral Obstruction ▼ Key Point The bladder is very fragile in ferrets.
static carcinoma have also been reported in the ferret, but are rare.
Diagnosis History and Clinical Signs
• Clinical signs associated with prostatic disease may
Handle ferrets with obstruction gently to avoid bladder rupture.
• Urinary obstruction in the male ferret can be difficult
•
•
• •
•
to manage. Catheter placement is challenging due to the small size of the urethra and the J-shaped os penis. (See Urinary Catheterization in the Techniques section of this chapter.) To facilitate placement of the urinary catheter, empty the bladder via cystocentesis prior to catheterization. Submit urine samples for urinalysis and bacterial culture/sensitivity testing. Use either a ferret urinary catheter (Slippery Sam Ferret Urinary Catheter, Cook Veterinary Products), a standard tom cat catheter, or a 3.5-Fr red rubber catheter for catheterization. Inhalant anesthesia with isoflurane or sevoflurane is strongly recommended to facilitate catheter placement. If the urinary catheter placement is not successful, consider emergency cystotomy, and attempt to perform anterograde flushing of the urethra via the cystotomy site. Perineal urethrostomy may be considered if cystotomy is unsuccessful (see Chapter 82).
Prevention
•
include symptoms associated with a urinary tract infection, urethral obstruction, or urinary incontinence. Signs of adrenal gland disease are often present (see “Adrenal Gland Disease”).
Physical Examination
• On physical examination, a large, firm, often painful caudal abdominal mass is usually palpable. With careful palpation, this mass is found to be bilobed, representing the urinary bladder and a cystic structure. Ferrets with mild to moderate prostatic disease may appear to have a normal-sized prostate on abdominal palpation, yet are still symptomatic.
Diagnostic Tests It is important to remember that adrenal gland disease is usually the cause of prostatic disease. Perform a complete diagnostic work-up that includes whole-body radiography, CBC, serum biochemistry analysis, and urinalysis. A plasma steroid hormone assay, and abdominal ultrasound may be indicated as well.
• Obtain abdominal radiographs; prostatic enlarge•
• Feed a high-quality, animal protein-based feline or
ment or prostatic cysts appear as mass lesions dorsal to the bladder. Perform abdominal exploratory surgery for a definitive diagnosis.
ferret diet.
PROSTATIC DISEASE/PROSTATIC CYSTS Prostatic disease and subsequent urethral obstruction is a potentially life-threatening condition of middle-aged and geriatric male ferrets. This condition typically occurs in association with adrenal gland disease.
Etiology • Prostatic disease and prostatic cyst formation are pre-
•
•
sumed to be the effect of excessive androgens on the prostate. Excessive androgen production occurs with adrenal gland disease. Squamous metaplasia of prostatic glandular epithelium occurs and may subsequently lead to the development of cysts ranging in size from 1 to 6 cm or larger. Secondary bacterial infection and abscessation may occur. Prostatic abscesses associated with transitional cell tumor of the bladder, prostatic seminoma, and pro-
Treatment • Address urethral obstruction if present (see “Urolithiasis”).
• Manage medically until the ferret is stable for adrenalectomy and surgical drainage of the cysts.
• Medical management includes maintenance of
• •
•
urinary catheterization for several days, administration of fluids, antibiotic therapy, anti-inflammatory and analgesic therapy, and nutritional support as needed. Consider administration of an androgen receptor blocker (see “Adrenal Gland Disease”). Consider administration of leuprolide acetate 30-day depot formulation (Lupron Depot, Bristol-MyersSquibb Oncology, Princeton, NJ) (250 ug/kg) IM; prostatic tissue shrinkage may occur within 48 hours in some individuals. Some ferrets have been maintained successfully on monthly injections of this drug, although results are highly variable. Perform adrenalectomy and drainage of the cysts. Large cysts may require debulking.
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• Perform bacterial culture and sensitivity testing of the cyst contents. ▼ Key Point Omental pull-through procedures and marsupialization have been described as means of prostatic abscess management in the ferret. These procedures should be used with some caution. Prostatic abscesses and prostatic cysts can be difficult to differentiate from paraurethral cysts. Paraurethral cysts communicate with the urethra or bladder neck. Consider performing contrast radiography to determine if there is communication between the cyst/abscess and the bladder prior to performing these procedures.
•
•
Prognosis • The long-term prognosis is good if prostatic changes •
regress, and if subsequent adrenal gland disease does not occur in the remaining adrenal gland. Some ferrets may need to be maintained on androgen receptor blockers or leuprolide acetate indefinitely.
PARAURETHRAL CYSTS Etiology Paraurethral cysts are thin-walled single or multiple cysts present on the dorsal aspect of the bladder and proximal urethra. These cysts appear to also be associated with adrenal gland disease and can cause urethral obstruction. It is important to differentiate between prostatic cysts and paraurethral cysts when planning the surgical protocol.
Clinical signs • Paraurethral cysts have been reported in male and female ferrets.
• Clinical signs are similar to those described for prostatic disease, and include symptoms associated with
a urinary tract infection, urethral obstruction, urinary incontinence. Clinical signs of adrenal gland disease are usually present (see “Adrenal Gland Disease”).
Diagnosis Physical Examination
• A large, firm caudal abdominal mass is often palpable dorsal to the bladder, just cranial to the pelvic inlet.
Diagnostic Tests
• Perform a complete diagnostic work-up that includes
• Administer postoperative antibiotic therapy for a minimum of 10 to 14 days, along with androgen receptor blockers or leuprolide acetate. Base the decision to discontinue antibiotic therapy and androgen receptor blocker/leuprolide acetate therapy by monitoring changes on physical examination, follow-up radiography, and follow-up urinalysis.
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• • •
whole-body radiography, CBC, serum biochemical analysis, and urinalysis. Because adrenal gland disease is usually the underlying etiology, consider performing a plasma steroid hormone assay. Radiographically, paraurethral cysts appear as mass lesions dorsal to the bladder. Ultrasonography may be useful in evaluation of the paraurethral cysts and adrenal glands.
Treatment • Surgical drainage and debulking of the cysts is the treatment of choice.
• Marsupialization is an alternative, but may lead to a formation of a permanent cystotomy.
• Do not perform an omental pull-through procedure. SUPPLEMENTAL READINGS Anderson NL: Intraosseous fluid therapy in small exotic animals. In Bonagura JD, Kirk RW (eds): Current Veterinary Therapy XII. Philadelphia: WB Saunders, 1997, pp 1331–1335. Carpenter JW, Mashima T, Rupiper DJ: Exotic animal formulary, 2nd ed. Philadelphia: WB Saunders, 2002. Fox JG: Biology and diseases of the ferret. Philadelphia: Lea & Febiger, 1988. Lewington JH: Ferret husbandry, medicine and surgery. Oxford, England: Butterworth & Heinemann, 2000. Purcell K, Brown SA: Essentials of pet ferrets: a guide for practitioners. Lakewood, CO: AAHA Press, 1999. Quesenberry KE, Carpenter JW (eds): Ferrets, rabbits, and rodents: clinical medicine and surgery, 2nd ed. Philadelphia: WB Saunders, 2004. Rosenthal K: Ferrets. Vet Clin North Am Small Anim Pract 24:1, 1994. Schilling K: Ferrets for dummies. Indianapolis, IN: Wiley Publishing, Inc., 2000.
Chapter
▼
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Rabbits Sue Chen / Katherine E. Quesenberry
Rabbits are popular pets for both children and adults. They are easily litter trained and require minimal maintenance. This chapter stresses diagnosis and management of problems commonly encountered in pet rabbits. Refer to the supplemental readings for more comprehensive information.
• Specific information concerning breeds can be obtained from the American Rabbit Breeders Association by mail (PO Box 426; Bloomington, IL 61702) or on their Website (www.arba.net).
Anatomic and Physiologic Characteristics • Females of several breeds of rabbits have a large pen-
BIOLOGIC CHARACTERISTICS Rabbits, hares, and pikas are members of the order Lagomorpha. Lagomorphs have six incisors, in contrast to the closely related rodents, which have four incisors. The additional incisors (peg teeth) are small, rounded teeth located directly behind the upper incisors. Currently, there are over 100 breeds of rabbits, which vary in size, ear and body conformation, and coat type, recognized by the House Rabbit Breeders Society.
• All domestic rabbits are descendants of European
•
•
wild rabbits, Oryctolagus cuniculus.
• The two main genera of rabbits are Oryctolagus, the
• • • • •
•
European wild rabbits, and Sylvilagus, the cottontail rabbits. These genera differ in chromosome number and cannot interbreed. Rabbits can range in size weighing from 2.5 lb in the dwarf breeds up to 28 lb in the giant breeds. Giant breeds, which average more than 5 kg in body weight, include the American Checkered Giant, the Flemish Giant, and the Giant Chinchilla rabbits. Medium breeds, which average from 3.5 to 5 kg in body weight, include the Californian, the Silver Marten, and the Rex rabbits. Small breeds, which average less than 3.5 kg in body weight, include the Netherland Dwarf, the Jersey Wooly, and the Polish rabbits. Ears vary in size and shape between the different breeds, and most rabbits have upright ears. However, there are breeds that have ears in a downward carriage, which are known as “lops.” Coats can be divided into normal, Rex, and Satin breeds. Normal fur coats have an undercoat with projecting guard hairs. Rex breeds have short guard hairs that do not project above the undercoat, thus producing a “velvety” fur coat. Satin breeds have a genetic mutation that results in a “shiny” haircoat.
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• •
• •
•
dulous dewlap under their chin. This area is a frequent site of moist dermatitis, especially in obese rabbits kept in humid, warm environments that may have difficulty grooming themselves. The sense organs of rabbits are well developed. Like other prey species, the eyes are laterally set. This provides a completely circular field of vision with the exception of the small area below the mouth. Thus, long sensory hairs around the snout and the sensitivity of the lips help rabbits discriminate food. Teeth are open rooted and grow continuously. The deciduous teeth are shed right around the time of birth and the permanent teeth complete eruption around 3 to 5 weeks of age. The dental formula is 2/1 incisors, 0/0 canines, 3/2 premolars, and 2–3/3 molars. Rabbits are distinguished from rodents by possessing an extra set of upper incisors, which are also known as “peg teeth.” The gastrointestinal (GI) tract has a simple glandular stomach, a long intestinal tract, and a large cecum. The stomach serves as a reservoir for ingesta and is rarely empty. It holds approximately 15% of the GI contents. The cardia and pylorus are well developed, and, due to the anatomic arrangement of the cardia to the stomach, rabbits are unable to vomit. The cecum is the largest organ in the abdominal cavity and holds approximately 40% of the GI contents. Rabbits exhibit cecotrophy, which means they consume soft cecotrophs, also known as “night feces.” Antiperistaltic contractions in the colon retrograde non-fiber particles and fluid back into the cecum for fermentation and the formation of cecotrophs, which are an important source of B-vitamins, electrolytes, and nitrogen. The skeletal system is light and delicate compared with most mammals. The skeleton makes up 8% of
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the total body weight in rabbits, as opposed to 13% of the total body weight in cats. ▼ Key Point Red, pink, or orange discoloration of the urine occurs periodically in healthy rabbits. The color may be caused by porphyrin pigments or food-related metabolites excreted in the urine. Cytologic examination of the urine for red blood cells will help distinguish porphyrinuria from hematuria.
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Table 176-1. REFERENCE RANGES FOR PHYSIOLOGIC VALUES IN RABBITS Temperature Heart rate Respiratory rate Life span Blood volume Food consumption Water consumption General population Breeding does
38–40ºC 130–325 beats/min 32–60/min 5–9 yrs 55–65 ml/kg 50 g/kg/day 50–100 ml/kg/day 20%).
• A soft mass palpable in the stomach area of an anorectic rabbit is evidence of a hairball. The stomach of a healthy rabbit is normally full. However, a rabbit that has been anorectic for several days should have an empty stomach.
• Routinely brush long-haired rabbits or heavy shedders.
• Some owners administer a petrolatum-based cat laxative to their rabbits every 1 to 2 months.
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• Encourage rabbits to exercise. Prevent obesity by
• Abdominal ultrasonography also can be used to iden-
restricting the amount of pellets fed and not feeding sweet “treats”.
tify an enlarged uterus or uterine masses and to detect liver or lymph node metastases.
UROGENITAL/REPRODUCTIVE DISEASES Uterine Adenocarcinoma/Hyperplasia Etiology ▼ Key Point Uterine adenocarcinoma is the most common tumor in domestic rabbits.
• Adenocarcinoma rarely occurs in does younger than
• • •
4 years of age. The incidence in rabbits older than 4 years of age ranges from 50% to 80% in certain breeds such as the Dutch, French Silver, and Havana, suggesting a genetic component to the disease. Occurrence is independent of breeding status. Endometrial changes such as atrophy of the glandular epithelial cells and increased collagen content are associated with development of uterine neoplasia. Endometrial changes that may precede neoplastic changes include endometriosis, endometritis, and papillary, cystic, or adenomatous hyperplasia. Local metastasis can extend through the uterine myometrium and invade adjacent structures in the peritoneum such as lymph nodes. Hematogenous spread to the liver, lungs, and brain occurs late in the clinical course, after 10 to 12 months.
Clinical Signs Uterine adenocarcinoma is a slow-growing tumor that can be multicentric and involve both horns of the uterus.
Treatment
• Ovariohysterectomy is successful if done before metastasis has occurred.
• Surgical resection of early focal abdominal metastasis
•
Prevention
• Routine ovariohysterectomy of does before 2 years of age is recommended.
• Educate owners with intact does about the early
•
Etiology Mastitis in rabbits can be either septic or nonseptic.
• Septic mastitis is most common in lactating does.
•
hyperplastic stages.
• • •
often the first clinical sign noted. Decreased reproductive performance such as small litter size, stillbirths, dystocia, litter desertion, and infertility are seen in breeding does. Cystic mastitis is associated with uterine changes in many does. Depression, anorexia, dyspnea, and ascites are often noted in late-stage cases, especially if metastasis to the lungs has occurred.
Diagnosis
• An enlarged, thickened uterus or multiple rounded
•
caudal abdominal masses may be palpable on physical examination. A mass may be difficult to differentiate from abdominal fat in small does. An enlarged uterus may be visible on abdominal radiographs. Thoracic radiographs should be taken to screen for pulmonary metastasis.
clinical signs of uterine adenocarcinoma and recommend yearly to semi-annual check-ups once the patient is 3 years of age. Consider ovariohysterectomy in does older than 3 years of age with evidence of cystic mastitis or increased aggressive behavior.
Mastitis
• Clinical signs are usually inapparent during the early • Hematuria or a serosanguineous vaginal discharge is
is the treatment of choice but carries a guarded prognosis because of metastasis that may not be visible at the time of surgery. Prognosis is poor after pulmonary metastasis has occurred. Euthanasia is recommended.
•
Trauma from abrasive bedding or caging, heavy lactation, and poor sanitation predispose the mammary gland to infection. Staphylococcus aureus and Pasteurella and Streptococcus spp. are the most commonly isolated bacteria. E. coli and Pseudomonas, Pasteurella, and Klebsiella spp. also may cause mastitis. Nonseptic, cystic mastitis is seen in both breeding and non-breeding females older than 4 years of age. It may be associated with high estrogen levels, uterine hyperplasia, and uterine adenocarcinoma. In some cases, malignant cellular changes may occur and develop into mammary adenocarcinoma.
Clinical Signs
• With septic mastitis, the affected gland is swollen, • • •
firm, erythematous to blue-tinged, and warm to the touch. Infection spreads until all glands are affected. Abcesses of the mammary gland can develop independent of lactation status. Systemic signs of septic mastitis include pyrexia, depression, anorexia, death of neonates, or death of the doe. With cystic mastitis, glands became swollen, firm, and blue-tinged with a clear-to-dark serosanguineous discharge from the teats. Rabbits are not systemically ill.
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Diagnosis
Clinical Signs
• Diagnosis of septic mastitis is based on clinical signs,
• Rabbits with urinary pigment changes or excessive
history of lactation or pseudocyesis, and isolation of bacteria on culture of gland tissue or exudate. Cystic mastitis must be differentiated from septic mastitis and mammary neoplasia. Culture and sensitivity testing of the discharge is negative for bacterial growth. Fine-needle aspiration and cytology is indicated to identify any neoplastic tissue.
calcium in the urine usually have no other clinical signs. Dysuria, stranguria, urine scald, lethargy, anorexia, and depression may be seen in rabbits with cystitis or cystic calculi. Rabbits may also exhibit teeth grinding or stay in a hunched position in response to abdominal pain.
•
•
Treatment
Diagnosis
• Administer antibiotics for septic mastitis. Base
• Differentiate hematuria from pigment changes in the
•
• •
therapy on results of culture and sensitivity testing. Pain medication such as buprenorphine is indicated if the rabbit appears to be in pain. Warm compresses 2 to 3 times daily may be helpful. Consider surgical drainage or excision of mammary abscesses. Suckling kits need to be removed from the doe as they may become infected with the bacteria and die from septicemia. Cystic mastitis usually resolves within 3 to 4 weeks after ovariohysterectomy. Severely affected glands may require surgical excision.
Prevention
• Keep lactating does in a clean environment. Make • •
sure no sharp surfaces or wire edges are present that can traumatize the teats. Routinely examine lactating does for evidence of inflammation or teat injuries. Cystic mastitis can be prevented by routine ovariohysterectomy of young, healthy does.
•
• •
•
Dysuria/Hematuria Etiology
• Red, pink, or orange discoloration of the urine
•
• •
occurs periodically in healthy rabbits. The color may be the result of porphyrin pigments or food-related metabolites excreted in the urine. Thick, creamy to sandy, white urine indicates the presence of excess calcium in the urine. Unlike most mammals, intestinal absorption of calcium does not depend on vitamin D. Increases in dietary calcium intake results in large amounts of calcium being excreted in the urine. Hematuria occurs commonly with cystitis. Frank blood independent of or at the end of urination may indicate uterine adenocarcinoma. Cystic calculi occur in both male and female rabbits. Calculi usually are composed of calcium carbonate or calcium oxalate and may be associated with high dietary calcium intake.
urine by simple dipstick analysis for blood. If urine discoloration is intermittent, dispense dipsticks for owners to check the urine at home. Submit a urine sample for urinalysis in rabbits with clinical signs of cystitis, cystic calculi, or hematuria. Calcium oxalate crystals are commonly present, though ammonium phosphate, calcium carbonate, and monohydrate crystals are also often seen. If bacteria are identified, a urine sample collected by cytocentesis should be submitted for culture and sensitivity testing. A serum biochemical analysis and a CBC are necessary to assess renal function. Distinguish between hematuria and hemorrhagic vaginal discharge occurring secondary to uterine adenocarcinoma by physical examination, history, urinalysis, abdominal radiographs, and abdominal ultrasonography. Uterine adenocarcinoma is likely in a doe older than 3 years of age with a thickened uterus or multiple abdominal masses. Obtain abdominal radiographs if cystic calculi are suspected. Calculi are usually radiopaque and therefore visible in the bladder or urethra. Calculi may also be visible in the ureters or kidneys. Large amounts of calcium sediment may be visible in the bladder in rabbits excreting large amounts of calcium.
Treatment Treatment is not necessary in rabbits with pigmentbased changes in urine color.
• Instruct owners to decrease the dietary calcium levels
•
in rabbits with hypercalciuria. Grass hay (e.g., timothy) has a lower calcium content than legume hay (e.g., alfalfa). Feed grass hay, green leafy vegetables, and timothy-based pellets. Treat rabbits with simple bacterial cystitis with antibiotics. A 3-week course of chloramphenicol or trimethoprim/sulfa is usually effective. Submit a second urine sample for bacterial culture and sensitivity testing after 4 to 6 weeks.
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• Cystic calculi must be removed surgically. Submit calculi for stone analysis. Decrease dietary calcium after surgery to help prevent recurrence.
Treatment
• T. paraluiscuniculi is susceptible to penicillin. Give
Prevention
• For prevention, decrease dietary calcium levels, especially in mature or aged rabbits.
•
• Many pelleted diets are derived from alfalfa and
•
exceed dietary calcium requirements. Change to timothy-based pellets and substitute grass or timothy hay for alfalfa hay in the diet. Discontinue any supplemental vitamins. Overweight rabbits are predisposed to hypercalciuria and urolithiasis. Decrease or eliminate pellets from the diet and encourage rabbits to exercise to prevent obesity.
injections of benzathine penicillin G (a long-acting penicillin) at 42,000 to 84,000 IU/kg IM at weekly intervals for 2 to 3 weeks. Response is rapid; lesions dramatically regress, usually after one injection. Tetracyclines and chloramphencol have also been effective against T. cuniculi.
Prevention
• Screen rabbits in breeding colonies for treponematosis.
• The incidence of disease in pet rabbits is low. Preventive serologic screening is not necessary.
NEUROMUSCULAR/SKELETAL DISEASES
Treponematosis Etiology
Mandibular and Joint Abscesses
• Treponema paraluiscuniculi is the causative agent of
Etiology
•
rabbit syphilis. T. paraluiscuniculi is a spiral-shaped bacterium transmitted by direct and venereal contact between breeding rabbits or from doe to offspring. It is not a zoonotic disease.
• Abscesses of the mandible and joints occur frequently
Clinical Signs
• Most lesions develop on the external genitalia and
• • •
perineum. Infection of the nose, eyelids, lips, and chin may result from autoinfection. Lesions initially consist of erythematous vesicles that progress to papules, ulcerations, scaliness, and dry crusty lesions. Nasal lesions in pet rabbits are commonly mistaken for dermatophyte lesions. Rabbits remain alert, responsive, and active. The incidence of abortions, metritis, and infertility may increase in breeding females.
Diagnosis
•
•
Clinical Signs
• Joint abscesses are most frequent in the distal limb
• Diagnosis is based on history, clinical signs, distribution of lesions, and response to therapy.
• Submit fur samples for fungal culture and do •
•
skin scrapings to rule out dermatophytes and ectoparasites. Treponema organisms can be identified by darkfield microscopic examination of skin scrapings. The organisms also can be demonstrated histologically with silver stains of skin biopsy sections. Serologic tests such as the rapid serum regain (RPR) are available commercially to determine the presence of antibodies against T. cuniculi. A fluorescent antibody test against treponemal antigen also is used, and an ELISA is available to screen for antibodies. These tests are used for screening in rabbit-breeding colonies.
in pet rabbits. Bacteria such as Pasteurella multocida, Staphyloccoccus aureus, Pseudomonas aeruginosa, Fusobacterium nucleatum, Peptostreptococcus micros, Strepcococcus milleri group, Actinomyces israelii, Arcanobacterium haemolyticum, Prevotella spp., Proteus spp., and Bacteroides spp. have been isolated. Bacteria can also spread hematogenously from the initial infection. Malocclusion and root elongation of the cheek teeth sometimes accompany mandibular abscesses. Infection may spread from the oral cavity along the tooth root. Soft-tissue abscesses can also occur in the oral cavity or joints secondary to a penetrating wound from a foreign body.
•
• •
joints. The swellings are large, firm, and warm to the touch. Rabbits may be lame, depending on which joints are involved. Mandibular abscesses occur as firm swellings in the ventral facial area. Abscesses are sometimes quite large before they are apparent to the owner. Excessive ptyalism may be an early symptom. Affected rabbits may refuse to eat if mandibular abscesses are accompanied by dental disease. Many rabbits remain active and alert with no other clinical signs.
Diagnosis
• Thick, white purulent exudate is present on fine-needle aspirate of the swelling. Cytologic examination of the exudate shows neutrophils and
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• •
proteinaceous debris; bacteria may or may not be visible. Obtain radiographs to check for and evaluate the extent of any bone involvement. Submit tissue samples for bacterial culture and sensitivity testing. Because the necrotic centers are often sterile, collect samples from the inside of the abscess capsule wall.
Treatment ▼ Key Point Simple lancing of mandibular and joint abscesses is ineffective because of the thick, caseous nature of the exudate.
1877
• Vascular lesions, infection with herpesvirus, cerebral nematodiasis, hypovitaminosis A, and toxicoses (e.g., lead poisoning) are less common causes of head tilt and uncoordination.
Clinical Signs
• Onset may be acute or slowly progressive. The head • •
tilt may be mild or accompanied by torticollis, incoordination, and the inability to stand. Some rabbits have no other clinical signs. Other rabbits become depressed, anorexic, and lethargic. Rabbits with severe depression, positional nystagmus, and facial nerve deficits may have brain or meningeal lesions.
• Complete enbloc surgical excision of the abscess is
• •
•
•
•
• •
the preferred treatment. However, depending on the extent of involvement, this may not be possible and aggressive surgical debridement is the next best option. Remove any molars or premolars that are loose or that have radiographic evidence of extensive infection of the roots. Flush the soft tissue with copious amounts of sterile saline. Abscesses often re-occur and multiple surgeries concomitant with antibiotic therapy may be required for resolution. Antibiotic-impregnated polymethylmethacrylate (AIPMMA) beads can improve the success rate of surgical treatment of mandibular abscesses if abscessed tissue cannot by completely excised. Amputating the affected limb may be the most effective therapy for abscesses involving the joint and surrounding bone. Rabbits adapt well to amputation of either a fore or rear limb. Disease may recur in other joints, even if amputation of the affected limb has been performed. Hematogenous spread of the bacterial infection to other joints may occur at any time during the clinical course. Long-term antibiotic therapy is necessary. Some rabbits respond to oral fluoroquinolone or injectable penicillin therapy in combination with surgical debridement or amputation. Owners must be able to do extensive nursing care at home. Have the owners flush open wounds with sterile saline once or twice daily. The prognosis for successful therapy is guarded. With bony involvement, the prognosis is poor.
Torticollis/Head Tilt/Ataxia Etiology
Diagnosis Diagnosis is based on clinical signs. Establishing the exact cause may be difficult.
• Carefully examine both ear canals for evidence of infection.
• Rabbits with severe otitis media may have swellings at
• • •
•
•
Treatment
• Give antibiotics long-term, usually a minimum of 4 to
• Bacterial infection of the inner ear, middle ear, or
•
meninges is the most common cause of torticollis in pet rabbits. Pasteurella multocida is often implicated as a primary cause, though other bacteria may also be involved. Encephalitozoon cuniculi is another common cause of torticollis and incoordination in rabbits.
the base of the ear. White, creamy, caseous debris can often be massaged out of the ear canal. Cultures and sensitivity testing can be helpful in identifying organisms and in directing antibiotic therapy. Results of a CBC may reveal an inflammatory response. Skull radiographs may aid in diagnosis. Anesthesia is usually necessary for proper positioning. Bony changes in the bulla may indicate osteomyelitis. Serologic tests can be used to detect antibodies against E. cuniculi or P. multocida. A positive result is not diagnostic of the specific agent but is helpful in ruling out some possible causes. Often, the cause cannot be established, and a tentative diagnosis is based on response to therapy. Rabbits with pasteurellosis often improve with long-term antibiotic therapy and supportive care. Rabbits with parasitic migration may remain unchanged or improve gradually. Rabbits with clinical signs secondary to encephalitozoonosis are usually unresponsive to treatment or they deteriorate clinically. The cause sometimes is determined only on postmortem examination.
•
6 weeks. Choose an antibiotic that penetrates the blood-brain barrier and is effective against pasteurellosis (e.g., chloramphenicol and enrofloxacin). If exudate is visible in the ear canal, clean and flush the ear thoroughly. Tranquilization or anesthesia may be necessary. Administer a topical antibiotic in the ear canal 3 to 4 times daily. Administer systemic antibiotics based on culture and sensitivity testing.
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• Administer an oral Lactobacillus supplement during •
•
•
long-term antibiotic therapy. Supportive care is necessary in rabbits that are laterally recumbent or that have severe torticollis. Recumbent rabbits should be turned every 6 to 8 hours or propped up sternally to prevent hypostatic congestion of the lungs. Apply eye lubricants several times daily if the blink reflex is diminished. Hand-feeding may be required. Keep rabbits on clean, dry bedding to prevent urine scalding and contact dermatitis. Inform owners about the amount of supportive care needed in recumbent rabbits. Many owners elect euthanasia when faced with the difficulties and the time required for long-term nursing care. Euthanasia often is selected in debilitated rabbits if no clinical improvement is seen after several days of therapy.
Treatment
• Several treatment protocols have been reported;
• •
•
Encephalitozoonosis (Encephalitozoan cunuculi)
however, results have been variable. Administer fenbendazole (20 mg/kg q24h for 28 days), oxibendazole (30 mg/kg PO q24h for 7–14 days, then reduced to 15 mg/kg q24h for 30–60 days), or albendazole (30 mg/kg PO q24h for 30 days, then 15 mg/kg PO q24h for 30 days or 10–15 mg/kg PO q24h for 3 months). Clinical signs may recur in some rabbits when drugs are stopped. These rabbits may require medications indefinitely to control clinical signs. For rabbits with suspected concurrent bacterial infection, antibiotic therapy with chloramphenicol (30– 50 mg/kg PO q12h for 7 days) can be administered while awaiting the results of serologic testing. Patients with severe neurologic signs are often anorectic and will require supportive care such as fluids and force feeding until clinical signs abate.
Etiology
Prevention
• E. cuniculi is an obligate, intracellular, microsporidian
• Identify carriers in rabbit colonies and breeding facil-
•
•
parasite prevalent in domestic and wild rabbits. The organism infects mice, rats, hamsters, and guinea pigs less commonly. The major route of transmission is by ingestion of spore-contaminated urine. Inhalation and vertical transmission can also occur. E. cuniculi spores are environmentally resistant and can survive for 4 weeks in mild environmental conditions. The organism can infect lungs, kidneys, liver, heart, brain, and eye. Many infected rabbits are asymptomatic, or may develop clinical signs after a stressful event or other immunosuppressive conditions.
•
•
ities through serologic testing. Cull animals that test positive. Eliminate urine contamination between cages through proper sanitation procedures. Most disinfectants, such as quaternary ammonium compounds, iodophors, phenolic derivatives, alcohols, and hydrogen peroxide, are effective in inactivating spores. Prevent possible contact between pet rabbits housed outdoors and wild rabbits or rodents by elevating cages off the ground or housing pets in a rodentproof enclosure.
Vertebral Fractures/Luxation
Clinical Signs
Etiology
• Depending on the site of infection, clinical signs can
• The rear leg muscles of rabbits are well developed for
vary and include: torticollis, ataxia, nystagmus, rolling, seizures, paresis, and death. Clinical signs of encephalitozoonosis are similar to those of the neurologic form of pasteurellosis.
strong kicking and thumping. ▼ Key Point If rabbits are restrained poorly with inadequate control of the rear legs, animals may kick suddenly, resulting in fracture of their spinal vertebrae.
Diagnosis
• Presumptive diagnosis is based on clinical signs and • •
results of diagnostic testing of rabbits exhibiting neurologic signs. Serologic tests are available to detect the presence of antibodies against E. cuniculi. These include ELISAs and indirect fluorescent antibody assays. Definitive diagnosis requires histopathologic examination of affected tissues. Spores can be seen in the tissue and lesions in the brain usually consist of multifocal areas of necrosis and granulomas with perivascular lymphoplasmacytic cuffing.
• The lumbosacral region (L7) is the most common site for fracture or luxation.
Clinical Signs
• Clinical signs of a fractured back depend on the
•
degree of spinal cord damage and can include partial or complete paralysis of the rear legs and loss of normal bladder and bowel function. Signs are acute in onset and directly related to a traumatic incident.
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• Other disease problems may cause clinical signs similar to a vertebral fracture. Multifocal infection of the spinal cord secondary to pasteurellosis, parasite migration, or vascular thrombosis within the cord can cause neurologic deficits. The clinical onset is usually more chronic and slowly progressive than that of a fracture.
Clinical Signs
• Rabbits with bone fractures or luxations are acutely lame.
• Rabbits have minimal soft tissue to protect the long bones below the elbow and stifle from penetrating the skin, thus open fractures are common at these sites. Fractures are usually palpable on physical examination. Joint luxations are palpable as firm swellings.
Diagnosis
•
• Diagnosis is based on history and clinical signs. • Obtain radiographs of the vertebral column to
Diagnosis
confirm a fracture or luxation.
Treatment
• If a diagnosis is made within 6 to 12 hours of the time
•
•
•
of the fracture, administer methylprednisolone sodium succinate, prednisolone sodium succinate, or dexamethasone at shock dosages. Conservative medical management such as cage rest and nonsteroidal anti-inflammatory agents can be used to manage mild cases. Anti-inflammatory and pain medication such as Carprofen (Rimadyl, Pfizer Animal Health, Exton, PA) or Meloxican (Metacam, Boehringer, Ingelheim Vetmedica, St. Joseph, MO) are often effective in making the patient more comfortable. Attempts to stabilize the fracture surgically are usually not practical because of the poor prognosis and degree of nursing care necessary. Some owners try long-term supportive care to see whether neurologic function returns. They must be instructed on manual expression of the bladder and general nursing care. The rabbit’s bedding should be changed multiple times a day to prevent urine scald. The patient will also need to be placed on alternating sides frequently prevent formation of pressure sores. Prognosis for recovery is guarded to poor. Euthanasia usually is recommended in rabbits with complete transaction of the cord resulting in complete rear limb paralysis and urinary and fecal incontinence.
Prevention
• Diagnosis is based on history, clinical signs, and physical examination.
• Obtain radiographs to evaluate fractures for surgical repair or to confirm joint luxations.
Treatment
• Splints used in combination with padded bandages
•
•
•
• See Figs. 176-1, and 176-2 for proper restraint of rabbits.
Bone Fractures/Joint Luxations Etiology
• The skeleton of the rabbit is light and fragile. The
•
tibia, radius, and ulna fracture easily with traumatic events such as getting a limb caught in wire caging or accidentally being dropped or stepped on. Traumatic joint luxations of the elbow or stifle joint occasionally occur.
1879
•
are usually adequate to stabilize metatarsal, metacarpal, and phalangeal fractures. Bandage the foot in a functional position. Contour a moldable splint or casting material such as Orthoplast (Johnson & Johnson, New Brunswick, NJ) or Vet-lite (Runlite SA, Micheroux, Belgium; see www.runlite.com for distributors) along the plantar surface. External coaptation can also be effective for closed, simple, long-bone fractures. Maintain the limb in a normal position and incorporate both the joints above and below the fracture into the splint. Ideally, there should be at least 50% cortical contact between the fragment ends. Intramedullary pins can be used for better axial alignment of long bone fractures and to minimize bending and rotational forces. The pins should occupy at least 60% to 70% of the medullary cavity. Cross-pins can be used for supracondylar humeral or femoral fractures. Bone plates are not usually recommended other than in large rabbits because the thin cortices of rabbit bones makes screw placement difficult. External skeletal fixation provides rigid stability with minimal soft tissue disruption. Because fixator pin diameter should not exceed 20% of the bone diameter, Kirschner wires are often used in smaller patients. Most metal bars and clamps are too large or heavy for rabbits; therefore, bone cement or acrylics injected into appropriately sized rubber tubing are effective as fixator bars. (see Chapter 111 for examples of external skeletal fixators) Severely comminuted or open fractures may be best managed with limb amputation. Rabbits usually adapt well to amputation and can ambulate easily on three limbs. Forelimb amputation is best performed by removing the scapula. Mid-femoral amputation
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•
Section 12 / Diseases of Avian and Exotic Pets
of the hind limb is preferred over coxofemoral disarticulation. With a joint luxation, anesthesia is needed to manipulate the joint into normal position. With the joint reduced and the limb in extension, apply a splint to allow the surrounding soft tissue to develop fibrosis and keep the luxation reduced. Some luxations may additionally require a transarticular pin to stabilize the joint.
See Section 8 for treatment of orthopedic disorders in dogs and cats.
Postoperative Care
• Obtain a radiograph of the leg after repair to assess bone alignment and placement of pins (if used).
• Postoperative management vital for successful
•
healing includes strict cage rest, a clean environment, a good diet, and frequent monitoring any bandages or fixators. Antibiotics are indicated in all open and contaminated fractures to prevent subsequent osteomyelitis and abscess formation.
SUPPLEMENTAL READING Harcourt-Brown F: Textbook of Rabbit Medicine. Oxford, Butterworth-Heinemann, 2002. Quesenberry KE, Carpenter JW (eds): Ferrets, Rabbits, and Rodents: Clinical Medicine and Surgery. 2nd edition. W.B. Saunders, St. Louis, 2004.
Chapter
▼
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177
Pet Rodents Nancy L. Anderson
Many small rodents are commonly kept for companionship and enjoyment. This chapter provides information needed to diagnose and treat the most frequently encountered problems of mice, rats, gerbils, hamsters, guinea pigs, and chinchillas.
HUSBANDRY Caging and Sanitation • Cages should be made of stainless steel, hard plastic,
•
•
•
•
•
or glass. These materials are cleaned and sanitized easily and are resistant to gnawing or corrosion from urine and fecal matter. Minimum floor space and height requirements are listed for each species in Table 177-1. With the exception of guinea pigs, all cages need secure lids. Guinea pigs can be housed in open-topped enclosures with walls higher than 10 inches. Ensure that dogs, cats, wild animals, and small children do not have unsupervised access to these cages. Clean cages as needed, usually 1 to 3 times per week for most rodents. A scrub brush, dish soap, and water work well. If cages are not kept clean, ammonia, other irritants, moisture, and bacteria concentrations rise to harmful levels, predisposing animals to disease. Disinfect the cage twice a month with 1 part sodium hypochlorite (household bleach) mixed in 30 parts water. Let the bleach solution stand for at least 15 minutes. Rinse the cage well afterward. All solid-floored cages need to be covered in bedding. Shredded paper, non-resinous wood shavings, wood wool, and corn cobs are all acceptable. Provide at least 2 inches of bedding. Most rodents enjoy burrowing in deeper bedding when it is provided in one corner of a cage. Do not, however, fill the entire cage with deeper bedding. This usually leads to poor sanitation as a result of owners’ failure to recognize buildup of hidden wastes such as moisture from leaking water bottles, cached foods, urine, and feces. Wire mesh floors can be used successfully only if the dimension of the mesh is correct. Size the openings to be just large enough for an adult to retract a tarsal
•
•
• •
joint back through the mesh. Larger holes make it difficult for the animals to walk and cause pressure sores. Smaller openings may cause injuries such as tibial fractures and self-mutilation while struggling to free trapped appendages. Bedding above the wire keeps waste from dropping through the wire and therefore is not recommended. Wire bottom cages do not work well for breeding animals because neonatal rodents must be surrounded by nesting material to maintain moisture in the nest and prevent dehydration. Young rodents often cannot walk correctly on mesh sized for adult feet. All pet rodents require visual security. Tubes, jars, or cans made of nontoxic, nonabrasive substances work well for this purpose. Also provide objects for gnawing. Rodents possess open-rooted teeth, and constant wear is necessary to maintain normal dentition. Mice, rats, gerbils, and hamsters enjoy and benefit from exercise wheels. A good room temperature range for most pocket pets is 70°F to 75°F. Keep rodents with disease at 85°F to 90°F unless hyperthermia is of concern (some chinchillas). Provide 10 to 12 hours of darkness to 12 to 14 hours of light. This light cycle is essential if breeding is desired. Hamsters, guinea pigs, and chinchillas that are exposed to temperatures below 65°F may hibernate for a few days or until the ambient temperature rises. Heart rates may be less than 5 bpm during hibernation.
Nutrition ▼ Key Point Feed pet rodents laboratory animal chow appropriate for their species (Table 177-2). Seed diets are deficient in protein and contain excessive fat.
• Seeds, as well as vegetables and other foods, may be
•
fed as treats but not to provide more than 15% of calories. Intermittent exposure to vegetables and seeds causes mild, transient diarrhea. Supplementation of vitamin C is recommended for all guinea pigs. 1881
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Table 177-1. CAGING AND ENVIRONMENTAL REQUIREMENTS FOR POCKET PETS Requirement Air changes/hour Minimum cage floor space/animal (square inches) Minimum cage height (inches) Recommended room temperature (°C) Maximum-minimum room temperature (°C) Room humidity (%) Cage-cleaning frequency (days) Light cycle-hours light : hours dark
Rat
Mouse
Guinea Pig
Chinchilla
Hamster
Gerbil
10–15 35
10–15 15
10–15 101
>6 288
>6 20
>6 36
>6 21.1–26.6
>5 21.1–29.4
>10 18.3–23.8
>12 15.5–21.1
>6 18.3–23.8
>6 21.1
18.3–29.4
18.3–31
12.7–32.2
10–23.8
12.7–23.8
18.3–29.4
50–70 2–7 12–14 : 10–12
30–70 2–7 12 : 12
40–70 3–4 12 : 12
40–60 7 >12.5 : 11.5
30–70 3–7 12 : 12
30–50 14 12 : 12
Hamster
Gerbil
Table 177-2. DIETARY INFORMATION FOR POCKET PETS Rat
Mouse
Guinea Pig
Recommended diet
Laboratory rodent chow
Laboratory rodent chow
Guinea pig chow
Chinchilla chow
Hamster chow
Supplements
45.8 kg: 180 mg Cat: safe dose not established Midazolam Versed 0.1–0.25 mg/kg IV, IM, or 0.1–0.3 mg/kg/h IV infusion Milbemycin oxime Interceptor Dog: 0.5 mg/kg q30d PO For demodex: 1–2 mg/kg q24h PO For scabies: 2 mg/kg PO twice at 14-day intervals Milk of magnesia See Magnesium hydroxide Milk thistle Marin 6–100 mg q24h PO Minocycline Minocin 5.0–12.5 mg/kg q12h PO Misoprostol Cytotec Dog: 3–5 mg/kg q6–8h PO Mitotane (o,p¢-DDD) Lysodren For pituitary-dependent hyperadrenocorticism: 50 mg/kg/d PO (may be given in divided doses) for 5–10 days, then 50–70 mg/kg/wk PO Adrenal tumor: 50–75 mg/kg/d for 10 days PO, then 75–100 mg/kg/wk PO (see Chap. 33) Mitoxantrone Novantrone 5–6 mg/m2 IV q3wk Morphine Dog: 0.2–0.6 mg/kg IM, SC (as needed); 0.1 mg/kg epidural Cat: 0.1 mg/kg IM, SC (as needed) Nadolol Corgard 0.25–0.5 mg/kg q12h PO Nafcillin sodium Unipen 10 mg/kg q6h IM, PO Nalbuphine Dog: 0.5–2.0 mg/kg IV, IM, SC Cat: 0.5–1.5 mg/kg IV, IM, SC Nalorphine Nalline 0.44 mg/kg IV, IM, SC (1 mg for every 10 mg of morphine) Naloxone Narcan 0.003–0.01 mg/kg IV, IM, for opiate reversal Naltrexone hydrochloride Trexan Behavior problems: 2.2 mg/kg q12h PO Nandrolone decanoate Deca-Durabolin Dog: 1.0–1.5 mg/kg qwk IM Cat: 1 mg/cat qwk IM
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Appendix
Neomycin Biosol 10–20 mg/kg q6–12h PO Neostigmine bromide Prostigmin bromide 2 mg/kg/d PO (in divided doses, to effect) Neostigmine methylsulfate Prostigmin Antimyasthenic: 10 mg/kg IM, SC, as needed (atropine may be administered to counteract side effects) Antidote for curiform block: 40 mg/kg IM, SC (administer with atropine) Diagnostic aid for myasthenia gravis: 40 mg/kg IM, or 20 mg/kg IV Nitrofurantoin Furadantin Macrodantin 4 mg/kg q8h PO Nitroglycerin ointment Nitrol Ointment Nitro-Bid Ointment Nitrostat Ointment (1 inch of ointment is approximately 15 mg) Dog: 1/4–1 inch topically q12–24h Cat: 1/4 inch topically q12–24h Nitroprusside Nipride 2.5–15 mg/kg/min constant IV infusion Nizatidine Axid 2.5–5 mg/kg q24h PO Norfloxacin Noroxin 22 mg/kg q12h PO Novobiocin See Delta-Albaplex Olsalazine Dipentum Dog: 20–30 mg/kg q8–12h PO Omega fatty acids See also Derm Caps 1 capsule q12h PO (see also Essential fatty acids) Omeprazole Prilosec Dog: 20 mg/dog or 0.7–1.0 mg/kg q24h PO Cat: Not recommended Ondansetron Zofran 0.1–0.5 mg/kg q6–12h IV, SC 0.5–1.0 mg/kg q6–12h PO o,p’-DDD See Mitotane Ormetroprim See Primor Oxacillin Prostaphlin Bactocill 22–40 mg/kg q8h PO Oxazepam Serax Appetite stimulant: 2.5 mg/cat q12h PO
Oxtriphylline Choledyl SA Dog: 47 mg/kg (equivalent to 30 mg/kg theophylline) q12h PO Oxybutynin chloride Ditropan 5.0 mg/dog q8–12h PO Oxymetholone Anadrol 1–5 mg/kg q24h PO Oxymorphone hydrochloride Numorphan Analgesia: Dog: 0.05–0.1 mg/kg IV 0.1–0.3 mg/kg IM, SC Cat: 0.01–0.04 mg/kg IV 0.05–0.1 mg/kg IM, SC For preanesthesia or sedation: see Chapter 2 Oxytetracycline Terramycin 20 mg/kg q8h PO; 7.5–10.0 mg/kg q8h IV Oxytocin Dog: 5–20 units/dog IM, repeat q30min for primary inertia Cat: 3–5 units/cat IM 2-PAM See Pralidoxime chloride Pamidronate Aredia 1.3–2.0 mg/kg in 150 ml 0.9% saline in 2-hour IV infusion; can repeat in 1–3 weeks Pancreatic enzyme (pancrelipase) Viokase Pancrezyme 2 tsp per 20 kg body weight, or 1–3 tsp/0.45 kg of food, mixed with food 20 minutes prior to feeding Pancuronium bromide Pavulon 0.1 mg/kg IV Pantoprazole Protonix 0.7–1.0 mg/kg q24h IV, PO Paregoric Corrective Mixture 0.05–0.06 mg/kg q12h PO (5 ml of paregoric corresponds to approximately 2 mg of morphine) D-Penicillamine Cuprimine 10–15 mg/kg q12h PO Penicillin G potassium 20,000–40,000 U/kg q6–8h, IV, IM Penicillin G procaine 20,000–40,000 U/kg q12–24h IM Penicillin G sodium 20,000–40,000 U/kg q6–8h IV, IM Penicillin V 10 mg/kg q8h PO Pentazocine Talwin Dog: 1.65–3.3 mg/kg q4h IM Cat: 2.2–3.3 mg/kg IV, IM, SC
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Appendix Pentobarbital Anesthesia: 25–30 mg/kg IV (first 1/2 of the dose administered rapidly, then remaining administered to effect) Pentoxifylline Trental 10–15 mg/kg q8h PO Petrolatum, white (flavored) Laxatone Cat: 1–5 ml/cat q24h PO Phenobarbital Luminal Dog: 2–8 mg/kg q12h PO Cat: 1–2 mg/kg q12h PO For seizures: Initially: 2.5 mg/kg q12h PO (see Chap. 127) and adjust by plasma concentration Status epilepticus (dog or cat): 10–20 mg/kg IV (to effect) or IV loading protocol (preferred; see Chap. 127) Phenoxybenzamine hydrochloride Dibenzyline Dog: 0.25–0.5 mg/kg q8h PO Cat: 2.5 mg/cat q8–12h PO Phentolamine mesylate Regitine (U.S.) Rogitine (Canada) 0.02–0.1 mg/kg IV (as needed to maintain normal blood pressure) Phenylbutazone Butazolidin Dog: 10–15 mg/kg q8h PO (maximum dose: 800 mg) Cat: not recommended Phenylephrine hydrochloride Neo-Synephrine 0.01 mg/kg q15min IV 0.1 mg/kg q15min IM, SC Phenylpropanolamine hydrochloride Propagest Dexatrim Dog: 1–2 mg/kg q12h PO Cat: 1 mg/kg q12h PO Phenytoin Dilantin Antiepileptic in dog: 20–35 mg/kg q8h PO Antiarrhythmic in dog: 30 mg/kg q8h PO or 10 mg/kg IV over 5 minutes Phytonadione See Vitamin K1 Phytomenadione See Vitamin K1 Pimobendan Vetmedin Dog: 0.3–0.6 mg/kg/d divided q12h PO Piperazine 44–66 mg/kg PO once Piroxicam Feldene Dog: 0.3 mg/kg q48h PO (use cautiously) Cat: dosage not established
1955
Polyethylene glycol electrolyte solution GoLYTELY 25 ml/kg, then repeat in 2–4 hours PO Polysulfated glycosaminoglycans Adequan 1–2 mg/kg IM once every 4 days for 7 injections Potassium bromide Dog and cat: 30 mg/kg q24h PO (in food) (see Chap. 127) Potassium chloride 0.5 mEq/kg/d (do not administer at a rate faster than 0.5 mEq/kg/h) 10–40 mEq/500 ml of fluids, depending on serum potassium (see Chap. 5) Potassium citrate Urocit-K Dog: 50–75 mg/kg q12h PO Potassium gluconate Kaon elixir Tumil-K 2.2 mEq/100 kcal of energy/day PO Cat: 2–6 mEq/cat daily PO Potassium iodide 30–100 mg/cat daily (in single or divided doses) for 10–14 days Potassium (or sodium) phosphate (potassium or sodium) 0.01–0.03 mmol phosphate/kg/hr for 3–6 hours (or, 2.5 mg/kg over 6 hours) (3 mmol/ml or 93 mg/ml phosphate) Pralidoxime chloride (2-PAM) Protopam Chloride Organophosphate toxicosis: 20 mg/kg q8–12h (initial dose slow IV, or IM; subsequent doses IM, SC) Praziquantel Droncit Dog (PO): 6.8 kg: 5 mg/kg once Dog (IM, SC): £2.3 kg: 7.5 mg/kg once 2.7–4.5 kg: 6.3 mg/kg once ≥5 kg: 5 mg/kg once Cat (PO): 1.8 kg: 5 mg/kg once Cat (IM, SC): 5 mg/kg IM, SC paragonimiasis: 25 mg/kg q8h for 2 days Liver flukes: 20 mg/kg qd for 3 days; PO, SC Prazosin Minipress 0.5–2.0 mg/animal q8–12h PO Prednisolone Anti-inflammatory: Dog: 0.5–1.0 mg/kg q12–24h IV, IM, PO initially then taper to q48h Cat: 2.2 mg/kg q12–24h IV, IM, PO initially, then taper to q48h Immunosuppressive (dog and cat): initially 2.2–6.6 mg/kg/d IV, IM, PO, then taper to 2–4 mg/kg q48h Prednisolone sodium succinate Solu-Delta-Cortef Shock: 15–30 mg/kg IV, then repeat in 4–6 h CNS trauma: 15–30 mg/kg IV, then taper to 1–2 mg/kg q12h
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Appendix
Prednisone See Prednisolone Primidone Mylepsin Mysoline Initial dosage: 5–10 mg/kg q8h PO Primor (ormetroprim plus sulfadimethoxine) 25 mg/kg on first day, followed by 12.5 mg/kg q24h PO Procainamide Pronestyl Dog: 10–20 mg/kg q6h PO (maximum dose: 40 mg/kg); 8–20 mg/kg IV, IM; 25–50 mg/kg/min IV infusion Cat: 3–8 mg/kg IM, PO q6–8h Procainamide (extended-release tablets) Procan-SR Dog: 20–50 mg/kg q8h PO Cat: 62.5 mg/cat q8h PO Prochlorperazine Compazine 0.25–0.5 mg/kg q6–8h IM, SC Progesterone, repositol See Medroxyprogesterone acetate Promazine Tranquazine 1–2 mg/kg q6–8h IV, IM, PO Promethazine hydrochloride Phenergan 0.2–0.4 mg/kg q6–8h IV, IM, PO (maximum dose: 1 mg/kg) Propantheline bromide For detrusor hyperreflexia and urge incontinence: Dog: 7.5–30.0 mg/dog q8–24h PO (start low) Cat: 7.5 mg/cat q24–72h PO For diarrhea: 0.25 mg/kg q8–12h PO Propofol 2–6 mg/kg IV for anesthesia (see Chap. 2) Propranolol hydrochloride Inderal Dog: 20–60 mg/kg over 5–10 min q8h IV, 0.2–1.0 mg/kg q8h PO Cat: 2.5–5.0 mg/cat (0.4–1.2 mg/kg) q8–12h PO Prostaglandin E See Misoprostol Prostaglandin F2a Lutalyse Pyometra: Dog: 0.1–0.25 mg/kg, once daily for 3–5 days SC (see Chap. 90) Abortion: (See Chap. 90 for protocol) Psyllium Metamucil Dog: 1–3 tbsp/d (added to food) Cat: 1–3 tsp/d (added to food) Pyrantel pamoate Nemex, Strongid Dog: 2.5 kg: 5 mg/kg PO Cat: 20 mg/kg PO Pyridostigmine bromide Mestinon
Regonol Antimyasthenic: 0.02–0.04 mg/kg q2h IV, or 0.5–3.0 mg/kg q8–12h PO Antidote (curariform): 0.15–0.3 mg/kg IM, IV Pyrimethamine Daraprim Dog: 1 mg/kg q24h PO for 14–28 days (5 days for Neosporum caninum) Cat: 0.5–1.0 mg/kg q24h PO for 14–28 days Quinacrine hydrochloride Atabrine hydrochloride Dog: 6.6 mg/kg q12h PO for 5 days Cat: 11 mg/kg q24h PO for 5 days Quinidine gluconate Quinaglute Duraquin Dog: 6–20 mg/kg q6h IM; 6–20 mg/kg q6–8h PO (of base) (324 mg quinidine gluconate = 202 mg quinidine base) Quinidine polygalacturonate Cardioquin Dog: 6–20 mg/kg q6h PO (of base) (275 mg quinidine polygalacturonate = 167 mg quinidine base) Quinidine sulfate Clin-Quin Quinora Dog: 6–20 mg/kg q6–8h PO (of base) (300 mg quinidine sulfate = 250 mg quinidine base) Ranitidine Zantac Dog: 2 mg/kg q8–12h IV, PO Cat: 2.5 mg/kg q12h IV; 3.5 mg/kg q12h PO Retinoids See Isotretinoin; Retinol; Etretinate Retinol Aquasol-A 625–800 IU/kg q24h PO Riboflavin (vitamin B2) Dog: 10–20 mg/d PO Cat: 5–10 mg/d PO Rifampin Rifadin 10–20 mg/kg q24h PO Ringer’s solution 40–50 ml/kg/d IV, SC, IP for maintenance requirements Salicylate See Acetylsalicylic acid (aspirin) Selegiline See Deprenyl (Anipryl) Senna Senokot Cat: 5 ml/cat q24h (syrup); 1/2 tsp/cat q24h with food (granules) SMS 201-995 Octreotide 10–20 mg q8–12h SC
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Appendix Sodium bicarbonate (NaHCO3) Acidosis: 0.5–1.0 mEq/kg IV, monitor blood gases (8.5% solution = 1 mEq/ml of NaHCO3) Renal failure: 10 mg/kg q8–12h PO (adjust as necessary) Alkalinization of urine: 50 mg/kg q8–12h PO (1 tsp is approximately 2 g) Sodium chloride (0.9%) 40–50 ml/kg/d IV, SC, IP Sodium chloride 7% (hypertonic saline) 2–8 ml/kg/ IV for shock therapy Sodium iodide (20%) 20–40 mg/kg q8–12h PO Sodium nitroprusside See Nitroprusside sodium Sodium thiomalate See Gold sodium thiomalate Sotalol Betapace Dog: 1–3.5 mg/kg q12h PO Cat: 1/8 of 80 mg tab q12h PO
1957
Salazopyrin (Canada) Dog: 10–30 mg/kg q8–12h PO Cat: 10–20 mg/kg q12–24h PO (See also Mesalamine, Olsalazine) Sulfisoxazole Gantrisin 50 mg/kg q8h PO (urinary tract infections) Tacrolimus Prototopic (ointment) Apply topically q24h Taurine Dog: 250–500 mg/dog q12h PO Cat: 250 mg/cat q12h PO Tegaserod Zelnorm Dog: 0.05–0.1 mg/kg q12h PO Telezol See Tiletamine plus zolazepam Temaril-P (Trimeprazine plus prednisolone) 0.7–1.1 mg/kg (of trimeprazine) q12–24h PO
Spironolactone Aldactone 1–2 mg/kg q12h PO
Tepoxalin Zubrin Dog: 10–20 mg/kg q24h PO then 10 mg/kg q24h PO
Stanozolol Winstrol-V Dog: 1–4 mg/dog q12h PO; 25–50 mg/dog/wk IM Cat: 1 mg/cat q12h PO; 25 mg/cat/wk IM
Terbinafine Lamasil Dog: 30 mg/kg q24h PO for 21–28 days Cat: 30–40 mg/kg q24h PO for 21–28 days
Streptozotocin (See Chapter 35 for administration protocol)
Terbutaline Brethine, Bricanyl Dog: 2.5–5.0 mg/dog q8h SC, PO Cat: 0.625 mg/cat q12h SC, PO
Sucralfate Carafate Dog: 0.5–1.0 g/dog q8–12h PO Cat: 0.25 g/cat q8–12h PO Sufentanil Sufenta 2 mg/kg IV, up to a maximum dose of 5 mg/kg (premedicate with acepromazine) Sulfadiazine 100 mg/kg IV, PO (loading dose), followed by 50 mg/kg q12h IV, PO (see also Trimethoprim) Sulfadimethoxine Albon, Bactrovet 55 mg/kg PO (loading dose), followed by 27.5 mg/kg q12h PO (see also Primor) Sulfaguanidine 100–200 mg/kg q8h PO for 5 days Sulfamethazine 100 mg/kg PO (loading dose), followed by 50 mg/kg q12h PO Sulfamethoxazole Gantanol 100 mg/kg PO (loading dose), followed by 50 mg/kg q12h PO
Testosterone cypionate Andro-Cyp 1–2 mg/kg q2–4wk IM (see also Methyltestosterone) Testosterone propionate Testex Malogen 0.5–1.0 mg/kg 2–3 times/wk IM (see also Methyltestosterone) Tetanus toxoid (equine antitoxin) 100–500 U/kg (maximum 20,000 U); IV slowly over 5–10 minutes Tetracycline Panmycin Achromycin 15–22 mg/kg q6–8h PO 4.4–11.0 mg/kg q8–12h IV, IM (See also Oxytetracycline, Doxycycline, Minocycline) Theophylline Dog: 9 mg/kg q6–8h PO Cat: 4 mg/kg q8–12h PO (See also Aminophylline)
Sulfamethoxazole plus trimethoprim Bactrim Septra See Trimethoprim plus sulfadiazine
Theophylline (long-acting) Theo-Dur Slo-bid Gyrocaps Dog: 20 mg/kg q12h PO (Theo-Dur) 30 mg/kg q12h PO (Slo-bid) Cat: 25 mg/kg q24h PO at night
Sulfasalazine (Sulfapyridine plus mesalamine) Azulfidine (U.S.)
Thiabendazole Omnizole
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Appendix
Equizole Dog: 50 mg/kg q24h for 3 days, repeat 1 month Cat (Strongyloides): 125 mg/kg q24h for 3 days
Triflupromazine Vesprin 0.1–0.3 mg/kg IM, PO q8–12h
Thiacetarsamine sodium Caparsolate 2.2 mg/kg IV twice daily for 2 days
Tri-iodothyronine See Liothyronine
Thiamine (vitamin B1) Dog: 10–100 mg/dog/d PO Cat: 5–30 mg/cat/d PO (up to a maximum dose of 50 mg/cat/d) Thiomalate sodium See Gold sodium thiomalate Thiopental sodium Pentothal Dog: 6–10 mg/kg IV (to effect) Thiotepa 0.2–0.5 mg/m2 intracavitary or IV Thyroid hormone See Levothyroxine, Liothyronine Thyrotropin (TSH) Thytropar Dog: collect baseline sample, followed by 0.1 IU/kg IV (maximum dose is 5 IU); collect post-TSH sample at 6 hours Cat: collect baseline sample, followed by 2.5 IU/cat IM and collect post-TSH sample at 8–12 hours Ticarcillin Ticar 33–50 mg/kg q4–6h IV, IM Tiletamine plus zolazepam Telezol 0.5–4.0 mg/kg IV, 4–10 mg/kg IM, SC Tobramycin Nebcin 2 mg/kg q8hr IV, IM, SC Tocainide Tonocard Dog: 10–20 mg/kg q8h PO Toluene 267 mg/kg PO (of Toluene), repeat in 2–4 weeks Topiramate 2–10 mg/kg q12h PO Tramadol Dog: 1 mg/kg q12h PO Triamcinolone Vetalog Aristocort Anti-inflammatory: 0.5–1.0 mg/kg q12–24h PO, taper dose to 0.5–1.0 mg/kg q48h PO
Trimeprazine Panectyl 0.5 mg/kg q12hr PO (also see Temaril-P) Trimethobenzamide Tigan, Trimazide Dog: 3 mg/kg q8h IM, PO Cat: not recommended Trimethoprim plus sulfadiazine Tribrissen 15 mg/kg q12hr IM, PO, or 30 mg/kg q12–24h SC, PO (for Toxoplasma: 30 mg/kg q12h PO) Tripelennamine Pelamine 1 mg/kg q12h PO TSH (thyroid-stimulating hormone) See Thyrotropin Tylosin Tylocine, Tylan 20–40 mg/kg q12h PO Urofollitropin Metrodin Cat: 2 mg/cat q24h IM Ursodiol (ursodeoxycholate) Actigall 10–15 mg/kg q24h PO Valproic acid Depakene Dog: 60–200 mg/kg q8h PO; or 25–105 mg/kg q24h PO when administered with phenobarbital Vancomycin Vancocin Dog: 15 mg/kg q6–8h IV Cat: 12–15 mg/kg q8h IV Vasopressin (ADH) Pitressin Aqueous (20 U/ml): 10 U IV, IM (see also Desmopressin acetate) Verapamil Calan Isoptin Dog: 0.05 mg/kg q10–30 min IV (maximum cumulative dose is 0.15 mg/kg); oral dose is not established Cat: 1.1–2.9 mg/kg q8h PO
Triamcinolone acetonide Vetalog 0.1–0.2 mg/kg IM, SC, repeat in 7–10 days Intralesional: 1.2–1.8 mg, or 1 mg for every cm diameter of tumor q2wk
Vermiplex See Toluene
Tribrissen: see Trimethoprim sulfadiazine
Vincristine Oncovin Antitumor: 0.5–0.75 mg/m2 q7d IV Thrombocytopenia: 0.025 mg/kg once/wk IV
Trientine hydrochloride Syprine 10–15 mg/kg q12h, PO (1 hr before meals, do not give concurrently with other medications).
Vinblastine Velban 2 mg/m2 q7–14d IV
Viokase (See Pancreatic enzyme)
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Appendix Vitamin A (Retinoids) See Isotretinoin (Accutane), Retinol (Aquasol A), or Etretinate (Tegison) Vitamin B complex Dog: 0.5–2.0 ml q24hr IV, IM, SC Cat: 0.5–1.0 ml q24hr IV, IM, SC Vitamin B1 See Thiamine Vitamin B2 See Riboflavin Vitamin B12 See Cyanocobalamin Vitamin C See Ascorbic acid Vitamin D See Dihydrotachysterol; Ergocalciferol Vitamin E (Alpha tocopherol) Aquasol E 100–400 IU q12h PO (or 400–600 IU q12h PO for immune-mediated skin disease, hepatitis, and copper-associated liver disease) Vitamin K1 AquaMEPHYTON Mephyton
1959
Short-acting rodenticide toxicity: 1 mg/kg/d SC, PO for 10–14 days; long-acting rodenticide toxicity: 3–5 mg/kg/d SC, PO for 3–4 weeks; birds: 2.5–5.0 mg/kg q24h Severe cholestatic liver disease: 1 mg/kg q12hr SC or IM Warfarin Dog: 0.1–0.2 mg/kg q24h PO (adjust dose by monitoring clotting time) Cat: 0.06–0.1 mg/kg (monitor clotting time) Xylazine Rompun Dog: 0.3–0.8 mg/kg IV, 0.5 –1.5 mg/kg IM, SC Cat: 0.4–1.0 mg/kg IV, 0.8–1.8 mg/kg IM, SC Yohimbine Yobine For xylazine reversal: 0.1–0.4 mg/kg IV Zinc Liver copper chelation: 5–10 mg/kg q12hr PO (1–2 hr separate from meals) Zidovudine (AZT) Retrovir Cat: 15 mg q12h to 20 mg/kg q8h PO Zolazepam See Tiletamine plus zolazepam Zonisamide 5–10 mg/kg/d PO (divide bid or tid)
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Note: Page numbers followed by f indicate figures; those followed by t indicate tables. Abciximab, thrombotic disease management, 1584 Abdomen physical examination intestines, 14 kidneys, 14, 14f liver, 13 palpation, 13, 14f prostate, 15 spleen, 13 stomach, 13 urinary bladder, 15 uterus, 15 radiography, 63–64, 63f, 64f Abdominocentesis complications, 36 contraindications, 35 equipment, 35 indications, 35 objectives, 35 peritonitis diagnosis, 856 technique, 35–36 Abducent nerve, oculomotor system abnormalities, 141 Abiotrophy cerebellar, 1271 definition, 1270 multisystem neuronal abiotrophies, 1271 Abortion Brucella canis induction, 1019 chemical induction after mismating, 1021–1022 examination, 1025 Abscess ferret anal sac, 1851–1852 liver clinical signs, 769 diagnosis, 769 etiology, 767–769 treatment, 769 orbit, 1397–1398 prostate gland, 949, 956 rabbit mandibular and joint abscess, 1876–1877 reptiles, 1935 spleen, 275 uropygial gland, 1764–1765 Acanthambiasis, systemic infection, 221t Acarbose, diabetes type 2 management, 387, 387t ACE inhibitors. See Angiotensin-converting enzyme inhibitors Acemannan feline leukemia virus management, 123 open wound management, 553 Acepromazine applications, 19–20 dosage guidelines cat, 21t, 23t dogs, 20t, 23t
Acepromazine (Continued) ferret, 1821t rabbit, 1863t rodent, 1890t idiopathic feline lower urinary tract disease management, 910 Acepromazine/butorphanol, dosage guidelines cats, 21t dogs, 20t Acepromazine/oxymorphone, dosage guidelines cats, 21t dogs, 20t Acetabulum. See Pelvis Acetylcysteine, hepatoprotection, 760t Acidophil cell hepatitis, features, 786 Acromegaly clinical signs, 399–400 diagnosis, 400–402 etiology, 399 treatment, 401–402 ACT. See Activated clotting time ACTH. See Adrenocorticotropic hormone Actinic keratoses, pinna, 571 Activated clotting time (ACT), coagulation disease diagnosis, 259 Activated partial thromboplastin time, coagulation disease diagnosis, 260 Acute hepatic failure clinical signs, 765 diagnosis biopsy, 766 history, 765 imaging, 766 laboratory testing, 766, 767t physical examination, 765–766 treatment, 766 etiology hepatotoxins, 761, 762t, 763–764t infectious agents, 761 systemic diseases, 761, 765 Acute lymphoblastic leukemia. See Lymphoid leukemia Acute myeloid leukemia. See Myeloid leukemia Acute renal failure (ARF) azotemia associated disorders, 861, 862t postrenal, 861 prerenal, 861 renal, 861 clinical signs, 862 diagnosis differential diagnosis, 863t history, 862 laboratory testing, 863–864 physical examination, 862–863 etiology, 861–862, 862t
Acute renal failure (ARF) (Continued) prevention, 868 treatment acid-base abnormalities, 867 dopamine, 866 electrolyte disturbances hyperkalemia, 866 hyperphosphatemia, 867 hypokalemia, 866–867 fluid therapy, 865–866 furosemide, 866 hemodialysis, 866 initial management, 864 mannitol, 865–866 monitoring, 867 oliguria reversal, 865 poison antidotes, 868 vomiting control, 867 Acute tubular necrosis. See Acute renal failure Acyclovir, reptile dosage guidelines, 1927t AD. See Atopic dermatitis Adenovirus adenovirus-2 vaccination protocols, 109t, 110t, 111t avian infection clinical signs, 1751 diagnosis, 1751 etiology, 1751 prevention, 1751 treatment, 1751 bearded dragon infection, 1937 ADH. See Antidiuretic hormone Adrenal gland. See also Hyperadrenocorticism; Hypoadrenocorticism; Pheochromocytoma adrenalectomy anesthesia, 372–373 complications, 374 equipment, 373 feline symmetrical alopecia management, 529 objectives, 373 postoperative care, 374 preoperative considerations, 372 prognosis, 374 technique, 373–374, 373f anatomy, 372, 372f ferret tumors clinical signs, 1833–1834 diagnosis, 1834 etiology, 1833 pheochromocytoma, 1835 prognosis, 1835 treatment, 1834–1835 Adrenocorticotropic hormone (ACTH) deficiency. See Hypoadrenocorticism excess. See Hyperadrenocorticism
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Index
Adrenocorticotropic hormone (ACTH) (Continued) plasma assay, 359, 370 stimulation test, 358–359, 362–363, 368–369 Aflatoxicosis, avian, 1793–1794 Aging canine idiopathic vestibular disease, 1274–1275 neurodegenerative changes, 1272–1273 Air bronchogram, 1636, 1636f Air sacculitis, features and management, 1778–1780 Air sac rupture, features and management, 1780 Alanine aminotransferase (ALT), liver function testing, 750 Alaskan malamute, hereditary polyneuropathy, 1308 Albinism, strabismus, 1403 Albumin, liver function testing, 751–752 Albuterol, dosage guidelines, 1669t Aleutian disease clinical signs, 1825 diagnosis, 1825 etiology, 1824–1825 prevention, 1825 treatment, 1825 Alkaline phosphatase (ALP) liver function testing, 750–751, 750f semen test, 966–967 Allergen-specific immunotherapy (ASIT) efficacy, 485 feline symmetrical alopecia management, 528 flea allergy dermatitis management, 480 indications, 485 miliary dermatitis and eosinophilic granuloma complex management, 535 protocols, 485 recheck evaluations, 485 Allergic dermatitis, avian, 1763 Allergic pneumonitis, management in heartworm infection, 1571 Allergy testing intradermal versus serum tests, 483–484 miliary dermatitis and eosinophilic granuloma complex, 533–534 negative test interpretation, 484 screening, 484 seasonal considerations, 483 Alligator. See Reptiles Allopurinol leishmaniasis management, 229 prolonged life support, 1619 Alopecia. See also Alopecia X; Cyclic flank alopecia; Feline symmetrical alopecia; Follicular dysplasias; Pattern baldness; Post-clipping alopecia ferrets adrenal disease, 1840 estrus alopecia, 1840 tail alopecia, 1840 rabbits, 1863–1864 rodents, 1894 Alopecia X clinical signs, 519 diagnosis, 519 etiology, 519 treatment, 519 ALP. See Alkaline phosphatase ALT. See Alanine aminotransferase Amazon foot necrosis, features and management, 1763–1764 Amazon tracheitis virus, infection features, 1749
Amebiasis, reptiles, 1931–1932 Amikacin reptile dosage guidelines, 1927t rodent dosage guidelines, 1895t Aminopentamide, diarrhea management, 711t, 712 Aminophylline. See also Methylxanthine toxicosis reptile dosage guidelines, 1927t 5-Aminosalicylic acid, inflammatory bowel disease management, 728t, 729 Amiodarone arrhythmia management, 1493 dosage guidelines, 1474t, 1458t formulations, indications, and dosages, 1458t ventricular tachycardia management in dogs, 1548 Amitraz canine demodicosis management, 461 cheyletiellosis management, 472 collar, 462 dip, 461–462, 468–469 notoedric mange management, 470 scabies management, 468–469 Amitriptyline atopic dermatitis management, 486t idiopathic feline lower urinary tract disease management, 910 Amlodipine administration, 1489 dosage guidelines, 1474t indications, 1488 Ammonia tolerance test, liver function testing, 754 Ammonium urate. See Urolithiasis Amoxicillin borreliosis management, 189 reptile dosage guidelines, 1927t Amphotericin B adverse effects, 215 avian administration, 1742 blastomycosis management, 209 cryptococcosis management, 213 formulations, dosage, and administration, 215 fungal cystitis management, 908 histoplasmosis management, 208 indications, 213 leishmaniasis management, 229 pharmacology, 213, 215 renoprotective measures, 215 Ampicillin reptile dosage guidelines, 1927t rodent dosage guidelines, 1895t Amrinone administration, 1479 dosage guidelines, 1474t indications, 1479 Amylase, pancreatic function testing, 822 Anagen defluxion, feline symmetrical alopecia, 525–526 Anal gland, infection in ferrets, 1826 Anal sac. See also Anorectal disease; Anorectal surgery adenocarcinoma features and management, 321 ferrets abscess, 1851 anal sacculectomy, 1850 features, 1846 Analgesia. See Pain; specific drugs Anaplasma phagocytophilum. See Anaplasmosis Anaplasma platys. See Canine cyclic thrombocytopenia
Anaplasmosis clinical signs, 182 diagnosis, 183 etiology, 182 feline Ehrlichia-like diseases, 185 human infection risks, 183 laboratory findings, 182 nonregenerative anemia, 238–239 prevention, 183 treatment, 183 Anastrazole, ferret adrenal disease management, 1834 Androgens. See Hyperandrogenism Anemia associated diseases, 241–242 blood loss anemia, 234 blood transfusion, 233–234 chronic renal failure, 872–873 clinical signs, 231 diagnosis, 231–233, 234f drug and toxin induction, 242 ferrets clinical signs, 1829 diagnosis, 1829–1830 etiology, 1829 history, 1829 prevention, 1831 treatment, 1830–1831 Heinz body anemia, 237 hemolytic anemia, 234–235 hereditary non-spherocytic hemolytic anemia, 235–236 immune-mediated hemolytic anemia clinical signs, 267 concurrent diseases, 268 diagnosis, 267–268 etiology, 267, 267t prognosis, 268 treatment, 268 nonregenerative anemia, 238–240, 239–240f nutritional deficiencies cobalamin, 241 folate, 241 iron, 240–241 pure erythrocyte aplasia, 243 radiation induction, 243 Anesthesia adrenalectomy, 372–373 cesarean section, 997 drugs. See also specific drugs analgesics, 21–22 dissociative anesthetics, 22 dosage guidelines cats, 21t dogs, 20t injectable drugs for short-term anesthesia, 22, 23t, 24–25 tranquilizers, 19–21 endotracheal intubation, 18 ferrets, 1822 intravenous catheterization, 18 local anesthesia administration, 105 drugs, 104t, 105 duration, 105 epidural, 106 intercostal nerve block, 105 mandible, 105 onychectomy, 105 overview, 26 upper jaw, 105 major procedures adjuncts, 26 equipment, 25 inhalant anesthetics, 26
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Index Anesthesia (Continued) monitoring anesthetic record, 26 capillary refill time, 27 equipment, 27 heart rate, 26–27 respiratory rate, 27 portosystemic shunt surgery, 813 preoperative assessment, 18, 19t rabbits, 1862–1863 reptiles, 1925–1926 reversal and recovery, 28, 28t rodents, 1889, 1890t, 1891 thoracic surgery, 1724–1725, 1724t Angiography, liver, 755 Angiotensin-converting enzyme (ACE) inhibitors adverse effects, 1483 congestive heart failure management cats, 1483 dogs, 1482–1483 overview, 1502–1505, 1539 feline hypertrophic cardiomyopathy management, 1538–1539 ferret administration, 1842 glomerulonephritis management, 877 hypertension control, 873 hypertension management, 1578–1579 indications, 1482 mitral regurgitation management, 1519–1521 monitoring, 1483 Anisocoria ambient light, 1413 darkness, 1413, 1415 differential signs and tests, 1414t eye neurologic disturbances, 1407 oculomotor dysfunction, 1415 oculosympathetic dysfunction, 1415 optic nerve dysfunction, 1415 Ankyloblepharon, features and management, 1333–1334 Anorectal disease. See also Constipation; Megacolon; Perianal fistula; Perineal hernia; Pseudocoprostasis anal sac disease classification, 841 clinical signs, 841 diagnosis, 841 etiology, 841 treatment, 841, 850–851, 851f anal spasm features and management, 840 apocrine gland adenocarcinoma, 844 atresia, 840 clinical signs, 831 dermatitis, 843 foreign bodies and fecaliths, 839 perianal gland adenocarcinoma, 844 adenoma, 843 polyps, 843 proctitis, 837 prolapse clinical signs, 838 diagnosis, 838 etiology, 837–838 treatment conservative treatment, 838 surgery, 838, 845–846 rectovaginal fistula, 840 stenosis features and management, 839 surgery. See Anorectal surgery Anorectal surgery anal sacculectomy equipment, 850 objectives, 850
Anorectal surgery (Continued) postoperative care and complications, 851 preoperative considerations, 850 prognosis, 851 technique, 850–851, 851f anatomy, 845 atresia ani surgery equipment, 847 objectives, 847 postoperative care and complications, 847–848 preoperative considerations, 847 technique, 847 perianal fistula, 848 perineal hernia equipment, 849 objectives, 848 postoperative care and complications, 850 preoperative considerations, 848 prognosis, 850 technique, 849–850, 849f prolapse resection and anastomosis equipment, 845 objectives, 845 postoperative care and complications, 846 preoperative considerations, 845 technique, 845–846, 846f stricture surgery equipment, 846 limited to anal ring, 847 objectives, 846 postoperative care and complications, 847 preoperative considerations, 846 prognosis, 847 technique, 846–847 Anorexia, boas and pythons, 1928–1929 Antacids, gastroduodenal ulceration management, 676t Antebrachium, radiography, 64 Antibiotic therapy. See also specific antibiotics avian administration, 1742, 1745, 1754–1755, 1754t bacterial cystitis, 906–908 bacterial endocarditis, 1525 bacterial prostatitis, 955, 955t bartonellosis, 198, 200–201 bronchiectasis, 1675 bronchitis, 1673 brucellosis, 196–197 canine leproid granuloma syndrome, 431–432 canine parvovirus sepsis management, 160 chronic gastritis management, 679–680 claw infection, 607 corneal ulceration, 1352, 1353t cutaneous atypical mycobacteriosis drug dosage recommendations, 433t diarrhea management, 712 emphysematous cystitis, 908 feline leprosy syndrome, 431 gastroduodenal ulceration management, 678 infectious meningoencephalitis, 1257–1258, 1257t intestinal surgery antibiotic prophylaxis, 739 kennel cough management, 152–153 keratoconjunctivitis sicca, 1392 leptospirosis, 194 neutrophilic cholangitis, 801 open wound management, 553–554 pancreatitis, 824 peritonitis, 857
1963
Antibiotic therapy (Continued) prolonged life support, 1619 pyelonephritis, 874, 874t pyodermas, 423, 423t, 425, 427–428 pyometra, 986 pyothorax, 1700, 1701t retinal degeneration in cats, 1384 rodents, 1893–1894, 1895t spinal cord disorders, 1300 tetanus, 1301 thoracic trauma, 1722 tracheal collapse, 1668 tracheobronchitis, 1689 Antidiuretic hormone (ADH) assay, 406 deficiency and diabetes insipidus clinical signs, 404 diagnosis, 404–406 etiology, 404 treatment, 406 replacement therapy, 406 response test, 405–406 Antifreeze toxicosis ethanol treatment, 868 4-methylpyrazole treatment, 868 Antifungal therapy. See specific drugs Antinuclear antibodies, neuromuscular disease evaluation, 1321 Aortic stenosis, canine heart disease, 1499 Apocrine gland adenocarcinoma, features and management, 321, 844 Apraclonidine, glaucoma management, 1376t, 1377 Arachnoid cysts, clinical features and management, 1269–1270 ARF. See Acute renal failure Arrhythmias. See Cardiac arrhythmias Arrhythmogenic right ventricular cardiomyopathy (ARVC) breed susceptibility, 1546 clinical features, 1542 differential diagnosis, 1546–1547 treatment, 1547 Arterial pulse pressure, 1575 Arterial sampling. See Blood gas analysis Arterial thromboembolism (ATE) clinical features in cats, 1536–1537 prevention, 1541 treatment, 1540–1541 Arteriosclerosis diagnosis, 1586 etiology, 1586 treatment, 1586 Arteriovenous fistula clinical signs, 1587–1588 diagnosis, 1588 etiology, 1587 liver. See Hepatic arteriovenous fistula orbital, 1401 pinna, 571 treatment, 1588 Arteriovenous malformation, exophthalmos, 1397 Arteritis. See Vasculitis Arthritis. See Immune-mediated arthritis; Osteoarthritis Artificial insemination cats intrauterine insemination, 1024–1025 semen collection, 1024 vaginal insemination, 1024 dogs intrauterine insemination, 1021 semen collection, 1020 vaginal insemination, 1020–1021 ARVC. See Arrhythmogenic right ventricular cardiomyopathy
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Ascarid nematodes clinical signs, 714–715 diagnosis, 715 life cycle, 714 species, 714 treatment, 715 Ascites clinical signs, 748 treatment, 759 Ascorbic acid. See Vitamin C ASIT. See Allergen-specific immunotherapy Aspartate aminotransferase (AST), liver function testing, 750 Aspergillosis avian clinical signs, 1740–1741 diagnosis, 1741 etiology, 1740 forms, 1740 prevention, 1742 prognosis, 1742 respiratory system, 1776–1777, 1779 treatment, 1742 dermatologic lesions, 443 systemic infection, 214t Aspermia, 1022 Aspiration pneumonia, avian, 1778 Aspirin arterial thromboembolism management, 1541 dosage guidelines, 104t ferret dosage guidelines, 1821 glomerulonephritis management, 877 heartworm adjunctive therapy, 1571 immune-mediated arthritis, 1231, 1232t osteoarthritis management, 1224 rabbit dosage guidelines, 1863t thrombotic disease management, 1584 AST. See Aspartate aminotransferase Asteroid hyalosis, features and management, 1382 Asystole, features and management, 1468 ATE. See Arterial thromboembolism Atenolol atrial fibrillation management, 1547 dosage guidelines, 1474t feline hypertrophic cardiomyopathy management, 1538 formulations, indications, and dosages, 1458t hyperthyroidism management, 336 pharmacology, 1486 Atherosclerosis diagnosis, 1586 etiology, 1586 treatment, 1586 Atipamazole dosage guidelines, 28t rabbit dosage guidelines, 1863t Atlantoaxial instability anatomy, 1055 clinical signs, 1055 diagnosis, 1055 etiology, 1055 surgery dorsal approach, 1056, 1056f equipment, 1056 objectives, 1056 postoperative care and complications, 1057 preoperative considerations, 1056 ventral approach, 1056–1057, 1057f Atopic dermatitis (AD) clinical signs, 482 diagnosis allergy testing, 483–484
Atopic dermatitis (AD) (Continued) approach, 483 differential diagnosis, 483 epidemiology age and sex differences, 481 breed differences, 481 incidence, 481–482 seasonal incidence, 481 etiology, 481 feline symmetrical alopecia, 524 pinna, 569 treatment allergy-specific immunotherapy, 485 anti-inflammatory drugs, 485–486 antihistamines, 485 cyclosporine, 487 fatty acids, 486 glucocorticoids, 487 guidelines, 484 misoprostol, 487 pentoxyfylline, 487 tacrolimus, 486 topical drugs, 486 triamcinolone, 486 tricyclic antidepressants, 485–486 Atrial fibrillation breed susceptibility, 1546 congestive heart failure association, 1504 features and management, 1462–1463, 1462f treatment, 1547 Atrial premature complexes, features and management, 1460, 1460f Atrial septal defect, treatment and prognosis, 1596–1597 Atrial standstill, features and management, 1468–1469, 1542 Atrioventricular block, features and management, 1469–1470, 1470f, 1491 Atrioventricular junctional rhythm, features and management, 1463 Atropine advanced life support, 1613, 1616 applications, 25 corneal ulceration, 1352 dosage guidelines cats, 21t, 1474t dogs, 20t, 1474t reptiles, 1927t rodents, 1890t formulations, indications, and dosages, 1458t response test, 1452 Auricular hematoma anatomy, 590 surgery equipment, 591 objectives, 591 postoperative care and complications, 591–592 preoperative considerations, 590 technique, 591, 592f Auscultation. See Cardiovascular physical examination Autoantibodies, serological testing, 1248 Avascular necrosis, reptiles, 1935 Avian dermatology allergic dermatitis, 1763 Amazon foot necrosis, 1763–1764 anatomy, 1758 bacterial diseases chronic ulcerative dermatitis, 1761 folliculitis, 1760–1761 tuberculosis, 1761 breed susceptibility to disease, 1759t feathers anatomy and function, 1765
Avian dermatology (Continued) broken blood feathers, 1766 coloration, 1765 endocrine diseases, 1767–1768 loss, 1764–1767 molting, 1765 nutritional diseases, 1767 picking behavioral, 1769–1771 non-behavioral, 1768–1769 pseudoproblems, 1766 fungal diseases, 1761 healthy skin and feather guidelines, 1758 history, 1758 hypovitaminosis A, 1764 mites biting lice, 1760 red mites, 1759 scaly leg and face mites, 1759 neoplasias, 1761–1763 oil effects and toxicity, 1771 physical examination, 1758–1759 uropygial gland disorders, 1764–1765 viral diseases, 1760 Avian respiratory system air sac rupture, 1780 sacculitis, 1778–1780 anatomy and physiology lower respiratory tract, 1773, 1773f upper respiratory tract, 1772 aspergillosis, 1776–1777, 1779 aspiration pneumonia, 1778 bacterial pneumonia, 1779–1780 choanal atresia, 1776 clinical signs of disorders, 1773–1774 hypersensitivity syndrome, 1777 hypovitaminosis A, 1774 mycoplasmosis, 1777 Newcastle disease, 1780 polytetrafluorene toxicosis, 1779 psittacosis, 1776, 1780 rhinitis, 1774–1775 rhinoliths, 1775 sarcocystosis, 1780 sinusitis, 1775 tracheal disorders extramural obstruction, 1778 foreign bodies, 1777 strictures, 1777–1778 tracheitis, 1777–1778 Axonotmesis, 1313 Azathioprine canine chronic hepatitis management, 779 chronic gastritis management, 679–680 immune-mediated arthritis management, 1232t immunosuppression therapy, 266 inflammatory bowel disease management, 728t, 729–730 pemphigus complex management, 495 Azithromycin borreliosis management, 189 mycobacteriosis management, 202 neosporosis management, 226 toxoplasmosis management, 224 Azotemia. See Acute renal failure AZT. See Zidovudine Babesiosis hemolysis, 236–237 systemic infection, 220–221t Babinski reflex, spinal reflex examination, 1239 Baclofen, micturition disorder management, 946t
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Index Bacterial endocarditis (BE) canine heart disease, 1497, 1499 clinical signs, 1524 diagnosis, 1524–1525 etiology, 1522 pathogenesis, 1522–1523 pathophysiology, 1522–1523, 1522f prognosis, 1525 treatment, 1525 Bacterial infection, 192t. See also specific diseases and pathogens avian Gram-negative infections, 1754–1756, 1755t Gram-positive infections, 1756 ferrets, 1825–1827, 1849 reptiles, 1928 Bacterial overgrowth syndrome clinical signs, 735 diagnosis, 735–736 etiology, 735 treatment, 736 Bacterial pneumonia, avian, 1779–1780 BAER. See Brain stem auditory evoked response Balanoposthitis clinical features, 974 treatment, 976–977 Balantidium diagnosis, 720 treatment, 720 Balloon catheter dilatation, esophageal stricture management, 648 Baroreceptor testing, syncope, 1512 Bartonellosis cats, 197–199 dogs, 199–201 Basal cell tumors, features and management, 320 Basophilia, etiology, 247–248 Basophilic leukemia, 253 BCS. See Body condition score BE. See Bacterial endocarditis Beagle, necrotizing vasculitis, 1261–1262 Beak environmental care, 1784 growth abnormalities, 1785 normal, 1782 overgrowth, 1782 trimming, 1782 infection, 1782 neoplasia, 1784 nutritional disorders, 1783 structure and function, 1782 trauma, 1783–1784 Bearded dragon. See Reptiles Bedlington terrier, copper-associated hepatitis clinical signs, 780 diagnosis, 780–781 etiology, 780 prevention, 781 prognosis, 781 treatment, 781, 782t Benazepril, dosage guidelines, 1474t Benign prostatic hyperplasia etiology, 949 treatment, 954–955 Benzathine, rabbit dosage guidelines, 1863t Benzodiazepines canine toxicity, 1288 cat administration, 1289 Bernese mountain dog, necrotizing vasculitis, 1261–1262
Beta-blockers. See also specific drugs adverse effects, 1487, 1493 arrhythmia management, 1492–1493 atrial fibrillation management, 1547 calcium channel blocker combination therapy, 1490 contraindications, 1485–1486 feline hypertrophic cardiomyopathy management, 1538 hypertension control, 873 hypertension management, 1579 hyperthyroidism management, 335–336 indications, 1484–1485 mechanism of action, 1483–1484 Beta-glucan inhibitors, fungal infection management, 218 Bethanechol, micturition disorder management, 946t BFD. See Budgerigar fledgling disease Bicarbonate, 380 arterial thromboembolism management, 1541 dose calculation, 92 hypercalcemia management, 347 indications, 92 precautions, 93 reptile dosage guidelines, 1927t Biceps reflex, spinal reflex examination, 1238 Biliary tract cancer. See Hepatobiliary neoplasia diseases. See also Cholecystitis; Cholelithiasis; Gallbladder mucocele; Liver disease extrahepatic biliary obstruction clinical signs, 807 diagnosis, 807–808 etiology, 807, 807t treatment, 808 rupture clinical signs, 809 diagnosis, 809 etiology, 808–809 repair. See Biliary tract surgery treatment, 809 Biliary tract surgery anatomy bile ducts, 815 gallbladder, 815 biliary rupture repair equipment, 817 objectives, 817 technique, 817 cholecystectomy equipment, 815 indications, 815 objectives, 815 technique, 815–816 cholecystoenterostomy equipment, 817 indications, 816 objectives, 817 technique, 817 cholecystotomy equipment, 816 indications, 816 objectives, 816 technique, 816, 816f preoperative considerations, 815 Bilirubin, liver function testing, 751 Bilirubinuria, liver disease, 747 Billroth procedures. See Distal stomach partial gastrectomy Biomicroscopy equipment, 1328 indications, 1327–1328 technique, 1328 Biopsy. See specific diseases and tissues
1965
Biotin, deficiency in reptiles, 1938 Birds abdominal air sac endoscopy, 1739, 1739f beak. See Beak breathing tube placement, 1739, 1739f cloaca. See Cloaca crop supporter, 1738, 1738f culture sample collection, 1734, 1735f digestive system disorders. See specific components and diseases eggs. See Egg laying esophagus and crop disorders, 1787–1790 gavage feeding, 1733–1734, 1735f infectious disease. See specific diseases intestinal disorders, 1791–1792 intramuscular injection, 1737, 1737f liver disorders, 1792–1794 mouth opening, 1733, 1735f neurologic disorders diagnosis, 1810–1811 epilepsy, 1815 infectious disease, 1812–1813 metabolic disorders, 1811–1812 neoplasia, 1812 toxicosis, 1813–1814 trauma, 1814–1815 treatment, 1811 oral cavity disorders, 1785–1787 pancreas disorders, 1794–1795 reproductive disorders anatomy, 1797f cloaca, 1806–1807 female, 1796–1806 male, 1806 respiratory system. See Avian respiratory system restraint, 1733, 1734f sinus injection or flush, 1737, 1738f skin. See Avian dermatology stomach. See Proventriculus; Ventriculus subcutaneous fluid injection, 1734 tracheal injection or wash, 1738 venipuncture sites, 1734, 1736f, 1737 Birman cat abnormal granulation syndrome, 245 neuropathy, 1310 Bisphosphonates, hypercalcemia management, 348 Blastomycosis dermatologic lesions, 443 geographic distribution, 206f systemic infection clinical signs, 208 diagnosis, 208–209 etiology, 208 prognosis, 210 treatment, 209–210 Blepharitis allergic, 1338 bacterial, 1337–1338 fungal, 1338 granulomatous, 1338 parasitic, 1338 Blindness brain stem blindness, 1412 cerebral blindness, 1413 cortical blindness, 1413, 1413t diagnostics, 1408–1412 eye neurologic disturbances, 1408 ocular blindness, 1412 Blink reflex, oculomotor system abnormalities, 1416 Blister disease, reptiles, 1934 Blood culture, bacterial endocarditis, 1524
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Blood gas analysis anesthesia monitoring, 27 arterial sampling complications, 32 contraindications, 31 equipment, 31 indications, 31 objectives, 31 technique, 32, 32f bronchopulmonary disease evaluation, 1627 dehydration detection, 87 Blood glucose curve ideal curve, 382, 383f preparation, 382 problem identification, 383, 383f Blood pressure. See also Hypertension anesthesia monitoring, 27 arterial pulse pressure, 1575 diastolic blood pressure, 1574–1575 mean blood pressure, 1575 measurement, 1577 neurologic disease assessment, 1241 shock management, 1607 systolic blood pressure, 1574 Blood transfusion advanced life support, 1616 anemia management, 872 coagulation disease management, 262–263 cross-matching, 233 ferret, 1819, 1930 guidelines, 262t whole blood transfusion, 233–234 Blood urea nitrogen (BUN), liver function testing, 752 Boa. See Reptiles Body condition score (BCS) cats, 8t, 45, 46f dogs, 7t, 45, 46f Body surface area, determination from body weight, 289t Body temperature physical examination, 8 reptiles, 1910–1911, 1911t Bone cysts classification, 1191 clinical signs, 1191 diagnosis, 1191–1192 etiology, 1191 treatment, 1192 Bone marrow aspiration in ferret, 1819 biopsy, 233 Borates, flea control, 477t, 478 Bordetella bronchisepta cat infection clinical manifestations, 146 diagnosis, 147 respiratory disease, 144 routes, 144 subclinical carriers, 145 treatment, 147–148 dog infection. See Kennel cough Bornavirus, transmission, 176 Borreliosis clinical signs, 187 diagnosis, 187–189 etiology, 186 human infection, 190 prevalence, 186 transmission, 186–187 treatment, 189 vaccination, 189–190 vector control, 190 Botulism, ferrets, 1827 Bougienage, esophageal stricture management, 648
Box turtle. See Reptiles Boxer arrhythmogenic right ventricular cardiomyopathy, 1546 corneal ulceration, 1351 progressive axonopathy, 1307 Brachial plexus avulsions, 1313–1314 neuritis, 1311 Brachycephalic syndrome etiology, 1651 treatment, 1654 Bradycardia management, 1617 sinus bradycardia, 1455–1457, 1491 syncope, 1509 Brain stem, lesions, 1249 Brain stem auditory evoked response (BAER) brain tumors, 1252 interpretation, 1246 principles, 1245–1246 Brain trauma clinical signs, 1263 diagnosis, 1263 pathophysiology, 1262 treatment, 1263 Brain tumors biopsy, 1253 clinical signs, 1252 diagnosis, 1252–1253 management, 1253–1254 primary tumors, 1251 secondary tumors, 1251 Brittany spaniel, motor neuron disease, 1308 Bromethalin poisoning, clinical features and management, 1268 Bromide. See Potassium bromide Bronchial disease, physical examination, 1428 Bronchiectasis clinical signs, 1674 diagnosis, 1674–1675 etiology, 1674 pathophysiology, 1674 prognosis, 1675 radiography, 1640, 1674 treatment, 1675 Bronchitis clinical signs, 1669–1670 diagnosis, 1670–1672 etiology, 1669 pathogens, 1672t pathophysiology, 1669 prognosis, 1673 treatment, 1672–1673 Bronchoalveolar lavage, technique, 1628 Bronchodilators bronchitis management, 1673 feline bronchial disease management, 1677 pulmonary fibrosis management, 1679 tracheal collapse management, 1668, 1669t Bronchopneumonia clinical signs, 1690 diagnosis, 1690–1691 etiology, 1690 follow-up, 1691–1692 radiography, 1637 treatment, 1691 Bronchoscopy bronchitis, 1671 feline bronchial disease, 1677 technique, 1628, 1668
Brucellosis abortion induction in dogs, 1019 clinical signs, 195–196 diagnosis, 196 etiology, 195 pathogenesis, 195 pregnancy, 987 prevention, 197 transmission, 195 treatment, 196–197 Buccal mucosa bleeding time test, coagulation disease diagnosis, 259–260 Budgerigar fledgling disease (BFD) clinical signs, 1747–1748 diagnosis, 1748 polyomavirus, 1747 prevention, 1748 transmission, 1747 treatment, 1748 vaccination, 1748 Bumetanide, prolonged life support, 1618 BUN. See Blood urea nitrogen Bupivacaine, dosage guidelines, 104t Buprenorphene applications, 22 arterial thromboembolism management, 1540 dosage guidelines cats, 21t, 103t dogs, 20t, 103t ferrets, 1821t Buprenorphine, rabbit dosage guidelines, 1863t Burn injury crop, 1789–1790 necrosis, 505–506 reptiles, 1934–1935 Butorphanol applications, 22 arterial thromboembolism management, 1540 dosage guidelines cats, 21t, 103t dogs, 20t, 103t ferrets, 1821t rabbits, 1863t reptiles, 1927t idiopathic feline lower urinary tract disease management, 910 vomiting management, 668 C6 antibody test, borreliosis diagnosis, 188 Cabergoline, abortion induction, 1022 Cacrycystitis, features and management, 1394 Caffeine. See Methylxanthine toxicosis Caging rabbits, 1860 reptiles, 1915–1918 rodents, 1881, 1882t Caiman pox, crocodilians, 1942 Calcitonin calcium regulation, 343 hypercalcemia management, 347 reptile dosage guidelines, 1927t Calcitriol calcium regulation, 343 primary idiopathic seborrhea management, 510 Calcium. See also Hypercalcemia; Hypocalcemia advanced life support, 1616 continuous intravenous infusion, 94 distribution, 343 dystocia management, 989–990 hypocalcemia management, 352–353 hypocalcemic tetany management, 93–94
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Index Calcium (Continued) metabolism tests, 344–345, 344t, 345t regulation, 343–344 reptile dosage guidelines, 1927t subcutaneous injection, 94 Calcium channel blockers (CCBs). See also specific drugs adverse effects, 1490, 1483 arrhythmia management, 1493 beta-blocker combination therapy, 1490 contraindications, 1488–1489 hypertension control, 873 hypertension management, 1578–1579 indications, 1488 mechanism of action, 1487–1488 prolonged life support, 1619 Calcium oxalate. See Urolithiasis Calcium phosphate. See Urolithiasis Calcivirus, vaccination protocols, 112t, 113t Calvarium anatomy, 1033 fracture. See Skull fracture Campylobacter clinical signs, 722 diagnosis, 722 epidemiology, 721 ferret infection, 1826 prognosis, 722 treatment, 722 Cancer. See also specific tissues and tumors clinical features, 283 diagnosis biopsy, 284–285 cytology, 284 imaging, 293–284 laboratory evaluation, 283 euthanasia, 291 nutrition, 290 pain management, 290–291 risk factors, 284t staging, 285, 285t treatment principles chemotherapy, 288–290, 288t, 289t hyperthermia, 290 immunotherapy, 290 monitoring, 290 photodynamic therapy, 290 radiotherapy, 287–288, 287t surgery, 286, 286f Candidiasis avian, 1785–1786, 1791 clinical signs, 441 diagnosis, 441–442 etiology, 441 systemic infection, 214t treatment, 442 Canine acidophil cell hepatitis clinical signs, 173 diagnosis, 173 etiology, 173 prevention, 173 treatment, 173 virus features, 173 Canine chronic hepatitis acidophil cell hepatitis, 786 cocker spaniel, 785 copper-associated hepatitis Bedlington terrier clinical signs, 780 diagnosis, 780–781 etiology, 780 prevention, 781 prognosis, 781 treatment, 781, 782t dalmatian, 784–785 Doberman pinscher, 783–784 overview, 779
Canine chronic hepatitis (Continued) Skye terrier, 785 treatment, 782t idiopathic chronic hepatitis clinical signs, 778 diagnosis, 778 differential diagnosis, 778 etiology, 777 prognosis, 779 treatment, 778–779, 778t lobular dissecting hepatitis clinical signs, 785 diagnosis, 786 treatment, 786 West Highland white terrier, 783 Canine coronavirus clinical signs of infection, 163 diagnosis, 163 diarrhea, 720 etiology, 162 features, 162–163 prevention, 163 treatment, 163 Canine cyclic thrombocytopenia clinical signs, 183 diagnosis, 183 etiology, 183 laboratory findings, 183 prevention, 183 treatment, 183 Canine distemper virus. See Distemper Canine ear margin dermatosis clinical signs, 515 diagnosis, 515 etiology, 515 treatment, 515–516 Canine elbow dysplasia (CED) fragmentation of the medial portion of the coronoid process anatomy, 1199 clinical signs, 1200 diagnosis, 1200 pathophysiology, 1199–1200 prognosis, 1202 treatment, 1200–1202, 1201f humeral condyle osteochondritis dessicans anatomy, 1199 clinical signs, 1200 diagnosis, 1200 pathophysiology, 1200 prognosis, 1202 treatment, 1200–1202, 1201f pathophysiology, 1197 ununited anconeal process anatomy, 1197 clinical signs, 1197 diagnosis, 1197 pathophysiology, 1197 prognosis, 1199 treatment, 1197–1199, 1199f Canine eosinophilic pinnal folliculitis clinical signs, 573 diagnosis, 573 treatment, 573 Canine herpesvirus (CHV) clinical signs, 173–174 diagnosis, 174 epidemiology, 173 etiology, 173 features, 173 prevention, 174 treatment, 174 Canine infectious tracheobronchitis. See Kennel cough Canine leproid granuloma syndrome (CLGS)
1967
Canine leproid granuloma syndrome (CLGS) (Continued) clinical signs, 431 diagnosis, 431 etiology, 431 treatment, 431–432 Canine lupus onychitis. See Lupus erythematosus complex Canine parainfluenza virus. See Kennel cough Canine parvovirus (CPV) age incidence, 158 breed incidence, 158 clinical signs, 158–159 complications, 161 diagnosis, 159–160 diarrhea, 720 exposure minimization, 162 incubation, 158 pathogenesis, 158 prognosis, 161 transmission, 158 treatment, 160–161 types, 158 vaccination overview, 162 protocols, 109t, 110t, 111t Canine rotavirus clinical signs of infection, 164 diagnosis, 164 diarrhea, 720 etiology, 163 features, 163 prevention, 164 treatment, 164 Canine viral papillomatosis clinical signs, 174 diagnosis, 174 epidemiology, 174 etiology, 174 treatment, 175 virus features, 174 Capillary refill time anesthesia monitoring, 27 physical examination, 8 Carbamate poisoning, clinical features and management, 1266–1267 Carbamazepine, canine toxicity, 1288 Carbenicillin reptile dosage guidelines, 1927t rodent dosage guidelines, 1895t Carbimazole, hyperthyroidism management, 335 Carbonic anhydrase inhibitors, glaucoma management, 1376–1377, 1376t Carboplatin chemotherapy guidelines, 288t limb neoplasia management, 1179 Carboprofen ferret dosage guidelines, 1821t osteoarthritis management, 1224–1225 rabbit dosage guidelines, 1863t Cardiac arrhythmias asystole, 1468 atrial fibrillation, 1462–1463, 1462f atrial premature complexes, 1460, 1460f atrial standstill, 1468–1469 atrial tachycardia, 1460–1462, 1461f atrioventricular block, 1469–1470, 1470f atrioventricular junctional rhythm, 1463 classification, 1455t congenital heart disease complication management, 1595 etiology, 1454, 1456t mechanisms, 1454 sick sinus syndrome, 1470–1471 sinus arrhythmia, 1455 sinus block, 1457, 1457f
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Cardiac arrhythmias (Continued) sinus bradycardia, 1455–1457 sinus tachycardia, 1457, 1460 thoracic surgery management, 1731 treatment antiarrhythmic drugs. See also specific drugs classification, 1490 formulations, indications, and dosages, 1458–1459t indications, 1491 principles, 1471–1472 valvular heart disease, 1516 ventricular fibrillation, 1467–1468, 1467f ventricular premature complexes, 1463–1465, 1464f ventricular tachycardia, 1465–1467, 1466f Wolff-Parkinson-White syndrome, 1471 Cardiac catheterization, congenital heart disease, 1594–1595 Cardiomyopathy. See also Dilated cardiomyopathy; Feline hypertrophic cardiomyopathy; Feline restrictive cardiomyopathy classification, 1527–1528, 1528t dogs, 1542–1546 Cardiopulmonary cerebral resuscitation (CPCR) advanced life support, 1613, 1616–1617 airway endotracheal tube placement, 1609, 1612f establishment, 1609 oxygen delivery systems, 1610 arrest signs, 1610t breathing, 1610 cardiac arrest problems and treatment, 1614–1615t chest compression, 1610, 1612f, 1613 decision-making flow chart, 1620f equipment, 1611t open-chest cardiac massage, 1617 outcome prediction, 1621 phases, 1609 prolonged life support, 1617, 1619, 1619t Cardiopulmonary system, history taking, 2–4 Cardiovascular physical examination auscultation heart, 1427–1428, 1426–1427f lungs, 1427 stethoscope, 1426 technique, 13, 1426 bacterial endocarditis, 1524 congestive heart failure management, 1502–1503 heart disease findings, 1428–1429 inspection attitude, 1421 body condition, 1421 cough, 1422–1423 edema, 1422 jugular vein evaluation, 1423, 1423f mucous membrane color, 1422 posture, 1421 ventilation pattern, 1422 palpation abdomen, 1424 femoral pulse, 1424, 1425t technique, 1423–1424 thorax, 12–13, 1424 percussion abdomen, 1426 thorax, 13, 1425, 1425f respiratory disease findings, 1428 valvular heart disease, 1517–1518 Cardioversion, atrial fibrillation management, 1547 Carmustine, brain tumor management, 1253
Carnitine feline hepatic lipidosis management, 772 hepatoprotection, 760t lipid storage myopathy management, 1324 neuromuscular disease evaluation, 1322 Carprofen, dosage guidelines, 22t, 104t Carpus accessory carpal bone fracture management, 1099, 1099f anatomy articulations, 1097 ligaments, 1097–1098 osseous structures, 1097, 1098f luxations, subluxations, and hyperextension injuries diagnosis, 1099–1100 pancarpal arthrodesis, 1100, 1101f, 1102, 1102f partial carpal arthrodesis, 1102–1103, 1102f postoperative care and complications, 1103 preoperative considerations, 1100 radial carpal bone fracture management, 1098–1099 radiography, 65 ulnar carpal bone fracture management, 1099 Cartilage supplements, osteoarthritis management, 1226 Carvedilol dosage guidelines, 1474t occult dilated cardiomyopathy management, 1544 pharmacology, 1487 Castration benign prostatic hyperplasia management, 954 ferrets, 1852 prostatic neoplasia management, 954–955 rodents, 1891–1892 Cataplexy clinical signs, 1292 diagnosis, 1292–1293 etiology, 1292 pathophysiology, 1292 prognosis, 1293 treatment, 1293 Cataract clinical signs and diagnosis, 1361–1362 development stages, 1362 dog breed susceptibility, 1361t etiology, 1360–1361 lens-induced uveitis, 1362 prevention, 1363 rodents, 1896 treatment, 1362–1363 Catheterization. See Intravenous catheterization; Tenckhoff peritoneal dialysis catheter placement; Thoracic catheter/tube placement Caudal cervical spondylomyelopathy anatomy, 1057 clinical signs, 1058 diagnosis, 1058–1059 etiology, 1057–1058 surgery dorsal laminectomy, 1060–1061 equipment, 1060 objectives, 1059–1060 postoperative care and complications, 1061 preoperative considerations, 1059, 1059t ventral distraction and fusion, 1050, 1050f ventral slot, 1060
Caudal cruciate ligament, rupture and repair, 1139–1140, 1140f Cavaletti rails, postoperative period rehabilitation, 1031, 1032f CBC. See Complete blood count CCBs. See Calcium channel blockers CEA. See Collie eye anomaly CED. See Canine elbow dysplasia Ceftazadime, reptile dosage guidelines, 1927t Ceftiofur, reptile dosage guidelines, 1927t Ceftriaxone, borreliosis management, 189 Cellulitis, orbit, 1397–1398 Central venous pressure (CVP) determinants, 1606f fluid therapy monitoring, 99 monitoring in shock, 1604 Cephaloridine, rodent dosage guidelines, 1895t Cephalothin, reptile dosage guidelines, 1927t Cerebellum abiotrophies, 1271 hypoplasia cats, 1270 dogs, 1270 lesions, 1249–1250 Cerebral hypoxia, syncope, 1509 Cerebrospinal fluid analysis biochemical evaluation, 1245 brain tumors, 1253 collection, 1243 contraindications, 1243 cytology, 1244 gross examination, 1244 indications, 1243 infectious meningoencephalitis, 1255–1256 peripheral nerve disorders, 1306 serologic examination, 1245 spinal cord disorders, 1299 Ceruminous gland tumors, features and management, 320–321 Cesarean section anesthesia, 997 complications, 999 equipment, 997 indications, 990, 996–997 neonatal care, 998–999 objective, 997 postoperative care, 998–999 technique, 997–998, 998f Chédiak-Higashi syndrome, features, 244 Chemical injury, necrosis, 505 Chemotherapy agents, 288t applications, 288–289 failure sources, 289–290 insulinoma, 396–397 lung cancer, 1712 lymphoma considerations, 295 cytopenia considerations, 296 induction protocols, 295–296, 296t reinduction therapy, 297 rescue therapy, 297 mammary gland tumor, 314 mast cell tumor, 308, 309t nasal cavity tumors, 1708 principles, 289 safe handling, 289t skin tumors, 320t soft tissue sarcoma, 305, 306t thyroid cancer, 338 Cherry eye, features and management, 1395
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Index Chest compression, 1610, 1612f, 1613 Cheyletiellosis clinical signs, 471 diagnosis, 471–472 etiology, 470–471, 471f prevention, 473 treatment, 472–473 CHF. See Congestive heart failure Chinchilla. See Rodents Chitin inhibitors, fungal infection management, 217–218 Chlamydiosis, avian clinical signs, 1743 diagnosis, 1743–1744 etiology, 1742–1743 prevention, 1745 treatment, 1744–1745 Chlamydophila felis clinical manifestations, 146 diagnosis, 147 infection routes, 144 respiratory disease, 144 subclinical carriers, 145 treatment, 147–148 Chlorambucil chemotherapy guidelines, 288t chronic gastritis management, 680 immunosuppression therapy, 266 leukemia management, 298–299 pemphigus complex management, 495 Chloramphenicol ferret dosage guidelines, 1821 rabbit dosage guidelines, 1863t reptile dosage guidelines, 1925t rodent dosage guidelines, 1895t Chlorothiazide, diabetes insipidus management, 406 Chlorpheniramine atopic dermatitis management, 486t feline symmetrical alopecia management, 528 flea allergy dermatitis management, 480 miliary dermatitis and eosinophilic granuloma complex management, 535 Chlorpromazine tetanus management, 1301 vomiting management, 667 Chlorpropamide, diabetes insipidus management, 406 Choana atresia features and management, 1776 culture sample collection, 1734, 1735f Cholangiohepatitis. See Lymphocytic cholangitis Cholecystectomy equipment, 815 indications, 815 objectives, 815 postoperative care and complications, 803–804 technique, 815–816 Cholecystitis clinical signs, 803 diagnosis, 803 etiology, 802–803 prognosis, 804 surgery postoperative care and complications, 803–804 techniques, 803 Cholecystoenterostomy equipment, 817 indications, 816 objectives, 817 technique, 817
Cholecystotomy equipment, 816 indications, 816 objectives, 816 technique, 816, 816f Cholelithiasis clinical signs, 806 diagnosis, 806–807 etiology, 805–806 prognosis, 807 treatment, 807 Cholesterosis bulbi, features and management, 1382 Chondrosarcoma, limb neoplasia, 1176 Choroid. See also Uvea acquired diseases, 1383–1388 chorioretinitis clinical signs, 1386 diagnosis, 1386 etiology, 1385, 1385t, 1386t treatment, 1386 congenital diseases, 1382–1383 evaluation, 1381 neoplasia, 1389 Chromium, diabetes type 2 management, 387t, 388 Chronic lymphocytic leukemia. See Lymphoid leukemia Chronic renal failure (CRF) clinical signs, 869 diagnosis biopsy, 870 history, 869 laboratory testing, 869–870 physical examination, 869 etiology, 868–869 hypercalcemia association, 350 treatment anemia, 872–873 diet, 870–871 fluid balance, 871 hyperphosphatemia, 871–872 hypertension, 873 metabolic acidosis, 871 monitoring, 873 potassium balance, 871 renal transplantation, 870 Chronic superficial keratitis (CSK), features and management, 1356–1357 CHV. See Canine herpesvirus Cimetidine gastroduodenal ulceration management, 673, 674t reptile dosage guidelines, 1927t Ciprofloxacin, rabbit dosage guidelines, 1863t Cisapride constipation management, 835t, 836 gastric motility disorder management, 685 gastroduodenal ulceration management, 673, 676t reflux esophagitis management, 646 reptile dosage guidelines, 1927t Cisplatin chemotherapy guidelines, 288t limb neoplasia management, 1179 CK. See Creatinine kinase Claw disease anatomy, 603, 604f clinical signs, 604 diagnosis biopsy, 606, 606f blood tests, 606 culture, 605 cytology, 605 history, 604–605 physical examination, 605
1969
Claw disease (Continued) radiography, 606 skin scrapings, 605 etiology, 603–604 terminology, 603, 604t treatment bacterial infection, 607 fungal infection, 607–608 general therapy, 606–607 lupoid onychomadesis, 607 neoplasia, 607 Clemastine, atopic dermatitis management, 486t CLGS. See Canine leproid granuloma Clindamycin hepatozoonosis management, 227 neosporosis management, 226 reptile dosage guidelines, 1927t toxoplasmosis management, 224 Clitoris hypertrophy, 1002 resection, 1002–1003 Cloaca cloacitis, 1808 culture sample collection, 1734, 1735f neoplasia, 1808 papilloma, 1807 prolapse birds, 1807–1808 reptiles, 1932–1933 Clofamazine, feline leprosy syndrome management, 430 Clomipramine, feather picking management, 1770 Clonazepam, cat administration, 1289 Clopidogrel, thrombotic disease management, 1584 Clorazepate cat administration, 1289 dog administration, 1285t, 1288 Clostridium difficile diagnosis, 721 epidemiology, 723 treatment, 723 Clostridium perfringens clinical signs, 722–723 diagnosis, 723 epidemiology, 722 treatment, 723 Closure. See Wound closure Clotrimazole, fungal cystitis management, 908 Clotting factors classification, 260t inherited deficiencies, 257t autosomal traits, 257 X-linked traits, 257 CMO. See Craniomandibular osteopathy Coagulation diseases clinical signs, 258 diagnosis, 258–262 etiology, 256–258, 257t liver disease, 747–748, 754–755 treatment, 262–264, 759 Cobalamin assay, 708 deficiency and anemia, 241 diarrhea management, 712–713 feline hepatic lipidosis management, 772 inflammatory bowel disease management, 727 pancreatic function testing, 828, 828t Coccidioidomycosis dermatologic lesions, 443 geographic distribution, 206f systemic infection clinical signs, 210
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Coccidioidomycosis (Continued) diagnosis, 210–211 etiology, 210 treatment, 211 Coccidiosis clinical signs, 717–718 crocodilians, 194 diagnosis, 718 life cycle, 717 prevention, 716 rabbits, 1871 reptiles, 1931 species, 717 treatment, 718 Cocker spaniel, chronic hepatitis, 785 Codeine, diarrhea management, 711t Coelomitis, reproductive-associated, 1804–1805 Colchicine amyloidosis management, 877–878 hepatic cirrhosis management, 788 Colectomy. See Intestinal surgery Collagen, urethral injection, 948 Collateral ligament, injury and repair, 1141–1142 Collie eye anomaly (CEA), features and management, 1382–1383 Coloboma features and management, 1334 uvea, 1367 Coloplexy complications, 742 equipment, 741 indications, 741 objectives, 741 postoperative care, 742 technique, 741–742, 742f Colotomy complications, 743 equipment, 743 indications, 742 objectives, 742 postoperative care, 743 preoperative considerations, 742 prognosis, 743 technique, 743 Complete blood count (CBC) bacterial endocarditis, 1524 bronchopulmonary disease evaluation, 1627 heartworm diagnosis, 1566 Computed tomography (CT) adrenal tumors, 362 advantages and disadvantages, 77 brain trauma, 1263 brain tumors, 1252–1253 caudal cervical spondylomyelopathy, 1059t nasal cavity diseases, 1623 neurologic disease assessment, 1242–1243 otitis media and otitis interna, 595 overview, 76 pituitary tumors, 400 respiratory disease, 1641–1642 spinal cord disorders, 129 Congenital heart disease. See also specific diseases breed predisposition, 1592t complication management arrhythmias, 1595 congestive heart failure, 1595 polycythemia, 1596 pulmonary hypertension, 1595–1596 diagnosis cardiac catheterization, 1594–1595 clinical approach, 1589, 1590f, 1591 echocardiography, 1593–1594, 1594t electrocardiography, 1593
Congenital heart disease (Continued) history, 1591–1592 physical examination, 1592–1593 radiography, 1593 etiology, 1589 treatment and prognosis atrial septal defect, 1596–1597 heart valve dysplasia, 1598 patent ductus arteriosus, 1596 pulmonic stenosis, 1597 subaortic stenosis, 1597–1598 tetralogy of Fallot, 1597 ventricular septal defect, 1596–1597 Congenital sensorineural deafness, clinical features and management, 1276 Congestive heart failure (CHF) angiotensin-converting enzyme inhibitor management cats, 1483 dogs, 1482–1483 arrhythmias, 1491 beta-blocker management, 1484 clinical signs, 1500 congenital heart disease complication management, 1595 diagnosis history, 1500 laboratory tests, 1501 physical examination, 1500–1501 dilated cardiomyopathy association and management, 1544–1545 feline management home care, 1539–1540 hospital care, 1538–1539 prognosis, 1540 ferrets clinical signs, 1841 diagnosis, 1841–1842 treatment, 1842–1843 follow-up, 1506 mortality causes, 1507 pleural effusion, 1703–1704 prognosis, 1507, 1522 progression, 1506–1507 syncope, 1510 treatment in dogs asymptomatic dog, 1519–1520 atrial fibrillation, 1504 cardiogenic shock, 1502–1503 coughing dog with mitral regurgitation, 1520 follow-up, 1522 F-O-N-S therapy plan, 1501–1502 home therapy, 1504–1505 inotropic agents in hospital therapy, 1503–1504 left-sided congestive heart failure, 1520–1521 progressive left-sided failure, 1505–1506 progressive right-sided failure, 1506 pulmonary edema, 1502 respiratory complications, 1521–1522 right-sided congestive heart failure, 1521 ventral tachycardia, 1504 Conjunctiva anatomy and physiology, 1339 biopsy, 1341–1342, 1344–1345 flap for cornea ulceration, 1354, 1354f surgery biopsy, 1344–1345 indications, 1342, 1344 laceration repair, 1344 mass removal, 1345 symblepharon repair, 1345–1346 Conjunctivitis clinical signs, 1340–1341
Conjunctivitis (Continued) diagnosis, 1341–1342 etiology, 1339–1340 ferrets, 1826 treatment by cause, 1342, 1343t Constipation clinical signs, 833 diagnosis history, 833 laboratory testing, 833–834 physical examination, 833 radiography, 833 etiology, 831–833, 832t prevention, 836–837 reptiles, 1932 terminology, 831 treatment adjunctive treatment, 836–837 enema, 834 laxatives bulk-forming laxatives, 835–836 classification, 834–835, 835t emollient laxatives, 836 lubricant laxatives, 836 osmotic laxatives, 836 stimulant laxatives, 836 manual extraction, 834 promotility drugs, 835, 836t rectal suppositories, 834 Constrictive pericarditis. See Pericardial constriction Contact dermatitis, pinna, 569 Coonhound paralysis, clinical features and management, 1311 Copper-associated hepatitis Bedlington terriers clinical signs, 780 diagnosis, 780–781 etiology, 780 prevention, 781 prognosis, 781 treatment, 781, 782t overview, 779 treatment, 782t Cornea chronic superficial keratitis, 1356–1357 dermoids, 1347 endothelial degeneration, 1350 endothelial dystrophy, 1349–1350 feline eosinophilic keratitis, 1357 fluorescein staining, 1329 melanosis, 1357 microcornea, 1347–1348 neoplasia, 1358–1359 opacities, 1348 reflex and cranial nerve examination, 1237 stromal degeneration, 1349 stromal dystrophy, 1349 ulceration clinical signs, 1351–1352 diagnosis, 1352 etiology, 1350–1351 medical treatment, 1352–1353, 1353t surgical treatment, 1353–1356, 1354f, 1355f Corticosteroids. See Glucocorticoids Cortisol assay, 362 creatinine ratio, 363, 370 Cough cardiopulmonary disease, 1422–1423 diagnostic evaluation, 1625–1629 differential diagnosis, 1652 overview cat, 1665–1666 dog, 1665
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Index Cough (Continued) history taking, 3–4 suppressants, 1673, 1689 Coxofemoral joint. See also Hip dysplasia anatomy, 1115 avascular necrosis of femoral head, 1118–1119 luxation closed reduction, 1116, 1116f diagnosis, 1116 open reduction, 1116–1118, 1117f, 1118f CPCR. See Cardiopulmonary cerebral resuscitation CPV. See Canine parvovirus Cranial cruciate ligament, rupture and repair, 1136–1139, 1138f Cranial nerves disorders. See also specific disorders canine idiopathic vestibular disease, 1274–1275 congenital degenerative disorders, 1275–1276 endocrine diseases, 1275 idiopathic disorders, 1273–1274 neoplasia, 1275–1276 examination, 1235–1237 vision control, 1405–1406, 1406t Cranial tibialis reflex, spinal reflex examination, 1238 Craniomandibular osteopathy (CMO) breed susceptibility, 1190 clinical signs, 1190 diagnosis, 1190, 1190f etiology, 1190 treatment, 1190–1191 Creatinine kinase (CK), neuromuscular disease evaluation, 1321 CRF. See Chronic renal failure Crichopharyngeal achalasia surgery equipment, 655–656 objectives, 655 postoperative care and complications, 656 preoperative considerations, 655 prognosis, 656 technique, 656, 656f Crocodile. See Reptiles Crop anatomy, 1787 burn injury, 1789–1790 foreign bodies, 1789 stasis clinical signs, 1787 diagnosis, 1787–1788 prevention, 1788–1789 treatment, 1788 supporter, 1738, 1738f Crossed extensor reflex, spinal reflex examination, 1239 Crown amputation. See Dental extraction Cryotherapy, immediate postoperative period rehabilitation, 1028 Cryptococcosis dermatologic lesions, 443 prevention, 218 systemic infection clinical signs, 211–212 diagnosis, 212 etiology, 211 prognosis, 213 treatment, 213 Cryptorchidism clinical features, 963 treatment, 967 Cryptosporidiosis. See Coccidiosis CSK. See Chronic superficial keratitis CT. See Computed tomography
Cushing disease. See Hyperadrenocorticism Cutdown. See Intravenous catheterization CVP. See Central venous pressure Cyclic flank alopecia clinical signs, 520 diagnosis, 520 etiology, 520 treatment, 520 Cyclocryosurgery, glaucoma management, 1378, 1378f Cyclophosphamide chemotherapy guidelines, 288t immune-mediated arthritis, 1232, 1232t immune-mediated thrombocytopenia management, 269 Cyclophosphamide-induced hemorrhagic cystitis clinical signs, 911 diagnosis, 911 etiology, 911 prevention, 911–912 treatment, 911 Cyclopia, 1397 Cyclosporine atopic dermatitis management, 486t, 487 dosage guidelines, 1677t flea allergy dermatitis management, 480 inflammatory bowel disease management, 728t, 730 keratoconjunctivitis sicca management, 1392 miliary dermatitis and eosinophilic granuloma complex management, 535 pemphigus complex management, 495 primary idiopathic seborrhea management, 510 Cyclothorax clinical signs, 1701 complications, 1702–1703 diagnosis, 1702 etiology, 1701 treatment, 1702 Cyproheptadine atopic dermatitis management, 486t dosage guidelines, 1677t Cystectomy, subtotal equipment, 919 objectives, 919 postoperative care and complications, 920 preoperative considerations, 919 technique, 919–920 Cystine. See Urolithiasis Cystinuria, features and management, 879–880 Cystitis, ferrets, 1855 Cystocentesis, ferret, 1819 Cystography complications, 71 double contrast, 70 equipment, 916–917 objectives, 916 positive contrast, 70–71 postoperative care and complications, 918 technique, 917–918, 917f tube cystostomy, 920–921, 921f urinary bladder disease, 896 Cytauxzoonosis, systemic infection, 221t Cytosine arabinoside brain tumor management, 1253 chemotherapy guidelines, 288t Dachshund, sensory neuropathy, 1308 Dalmatian copper-associated hepatitis, 784–785 laryngeal paralysis-polyneuropathy complex, 1310
1971
Dancing Doberman disease, clinical features, 1312 Dantrolene, micturition disorder management, 946t Dapsone, pemphigus complex management, 496 Dazzle reflex, eye neurologic disturbance evaluation, 1409, 1417 DDAVP. See Desmopressin acetate Declawing. See Onychectomy Decoquinate, hepatozoonosis management, 227 Decubitus ulcers, necrosis, 506 Deep mycosis candidiasis clinical signs, 441 diagnosis, 441–442 etiology, 441 treatment, 442 classification, 435, 436t dermatologic lesions aspergillosis, 443 blastomycosis, 443 coccidioidomycosis, 443 cryptococosis, 443 histoplasmosis, 443 diagnosis biopsy, 435 cytology, 435 laboratory assessment, 436 hyalohyphomycosis clinical signs, 442 etiology, 442 treatment, 442 lagenidiosis clinical signs, 438 diagnosis, 439 etiology, 438 treatment, 439 mycetoma clinical signs, 442–443 etiology, 442 treatment, 443 phaeohyphomycosis clinical signs, 442 diagnosis, 442 etiology, 442 treatment, 442 pythiosis clinical signs cutaneous, 437 gastrointestinal, 437 diagnosis, 437–438 etiology, 436 treatment, 438 rhinosporidiosis clinical signs, 441 diagnosis, 441 etiology, 441 sporotrichosis clinical signs, 440 diagnosis, 440–441 etiology, 440 treatment, 441 zygomycosis clinical signs, 439 diagnosis, 439–440 epidemiology, 439 etiology, 439 treatment, 440 Deep otic flush, otitis media and otitis interna management, 596 Dehydration causes, 85 correction failure, 98t detection anticipation in disease, 87
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Dehydration (Continued) history-taking, 85–86 laboratory assessment, 86–87, 87t physical examination, 86 signs, 85t enophthalmos, 1403 fluid therapy volume calculations, 87–88, 88f, 88t types, 85 Delayed union associated factors, 1215t clinical signs, 1216 definition, 1214 diagnosis, 1216–1217 postoperative care and complications, 1218–1219 preoperative considerations, 1216–1217 prognosis, 1219 surgery, 1217–1218, 1217–1218f Delmadinone acetate, benign prostatic hyperplasia management, 954–955 Demodicosis canine demodicosis clinical signs adult onset, 459–460 juvenile onset, 459 diagnosis, 460, 460f etiology, 459 pathogenesis, 459 treatment end point, 462 generalized demodicosis, 461–462 localized demodicosis, 461 recurrence, 462–463 Demodex mite features, 459 feline demodicosis clinical signs, 463 diagnosis, 463 etiology, 463 treatment, 463 feline symmetrical alopecia, 524–525 ferrets, 1840 pinna cat, 568 dog, 568 Dental disease, ferrets, 1846 Dental extraction anatomy, 609, 610f, 610t, 611t complicated extraction, 614, 614f crown amputation with root retention, 614–615, 615f dental materials, 612t disease etiology and clinical signs, 609 equipment and instrumentation, 613t indications decay, 611 deformation, 612 erosion, 611 fracture, 611 impaction, 611–612 malocclusion, 611 overly retained teeth, 610 periapical inflammation, 611 periodontitis, 611 multirooted extraction, 613–614, 614f ophthalmic manifestations of dental disease, 612 preoperative considerations, 612 simple extraction, 612–613, 613f Dental trimming, rodents, 1892, 1892f Deprenyl. See Selegiline Deracoxib dosage guidelines, 22t, 104t osteoarthritis management, 1225 Dermatitis. See Pyoderma Dermatoid inclusion cyst, features and management, 322
Dermatomyositis, familial canine dermatomyositis, 1317 Dermatophytosis clinical signs cats, 452 dogs, 451–452 onychomycosis, 452 diagnosis biopsy and histopathology, 455, 456f culture, 454–455, 455t differential diagnosis, 453, 453t hair microscopic examination, 454, 454f, 454t history, 453 physical examination, 453 Wood’s light, 453–454 etiology anthrophilic dermatophytes, 451 Microsporum canis, 451 Microsporum gypseum, 451 Trichophyton mentagrophytes, 451 feline symmetrical alopecia, 524 ferrets, 1838 pinna, 566, 572 prevention, 458 rodents, 1893 treatment monitoring, 458 systemic therapy, 456–457 topical therapy, 456 vaccination, 458 Dermoid, features and management, 1347 Desmopressin acetate (DDAVP), coagulation disease management, 263–264 Detrusor hyperreflexia. See Urge incontinence Detrusor-urethral dyssynergia clinical signs, 942–943 diagnosis, 943–945 treatment, 945, 947 Dewclaw anatomy, 1168 removal, 1171–1172 Dexamethasone. See also Glucocorticoids reptile dosage guidelines, 1927t suppression test high-dose, 363–364, 369–370 low-dose, 363, 369 Dextrose parenteral fluid supplementation, 93 shock management, 1608 Diabetes insipidus. See Antidiuretic hormone Diabetes mellitus classification, 376 clinical signs, 377–378 diabetes type 2 management diet, 386 exercise, 386 oral hypoglycemic drugs, 386–389, 387f, 387t, 388f diabetic ketoacidosis management bicarbonate, 380 fluid therapy, 378 insulin, 378, 380 magnesium, 380 phosphorous, 380 potassium, 380 stepwise treatment, 379t diagnosis, 378 neuropathy, 1309 pathophysiology diabetic ketoacidosis, 376–377 uncomplicated disease, 376, 377f prevention, 389 uncomplicated diabetes management diet, 382t, 385–386
Diabetes mellitus (Continued) insulin, 380–381, 381t monitoring, 381, 383–385 Diaphragm, radiography, 1634–1635 Diaphragmatic hernia pleural effusion, 1705 radiography, 1635 repair, 1721–1722 Diarrhea acute, 702 chinchilla, 1905 chronic, 702 diagnosis bacterial overgrowth tests, 709 biopsy, 710 breath hydrogen test, 708 endoscopy colonoscopy, 710 upper gastrointestinal endoscopy, 710 exocrine pancreatic insufficiency test, 708 fecal examinations bacteria, 707 fungi, 707 parasites, 705–707, 706t viruses, 707 fecal fat analysis, 708 fecal occult blood test, 707 fecal proteolytic activity, 708 fecal stains, 707 history, 704 intestinal motility tests, 709 laboratory findings, 705, 705t physical examination, 704–705, 704t protein-losing enteropathy tests, 709 radiography, 709 serum folate and cobalamin assays, 708 sugar absorption tests, 708–709 therapeutic trials, 710 ultrasound, 710 dietary diarrhea diagnosis, 713 etiology, 713 treatment, 713 drug- and toxin-induced diarrhea diagnosis, 713 etiology, 713 treatment, 713 fiber-responsive diarrhea. See Irritable bowel syndrome gerbil, 1904 guinea pig, 1908 hamster, 1902 large bowel diarrhea, 703, 703t management antibiotic therapy, 712 antidiarrheal drugs, 711–712, 711t cobalamin, 712–713 diet, 711 fenbendazole, 712 fluid therapy, 711 mouse, 1897 pathogens. See specific pathogens rabbit, 1868–1871 rat, 1900 reptiles, 1930–1931 small bowel diarrhea, 702–703, 703t Diastolic blood pressure, 1574–1575 Diatrizoate, hyperthyroidism management, 336 Diazepam applications, 21 brain trauma management, 1263 canine toxicity, 1288 cat administration, 1289 dosage guidelines
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Index Diazepam (Continued) cats, 21t dogs, 20t rabbits, 1863t rodents, 1890t micturition disorder management, 946t rectal administration at home, 1291–1292 tetanus management, 1301 Diazoxide, hypoglycemia management, 396 DIC. See Disseminated intravascular coagulation Dichlorophene, dosage guidelines, 714t Dichlorphenamide, glaucoma management, 1376–1377, 1376t Dicyclomine diarrhea management, 711t, 712 micturition disorder management, 946t Diet. See also Nutrition chronic gastritis management, 679 chronic renal failure management, 870–871 copper-associated hepatitis management, 781, 782t diabetes type 2 management, 386 diarrhea management, 711 elimination diet for miliary dermatitis and eosinophilic granuloma complex, 533–534 eosinophilic gastritis management, 681–682 gastric motility disorder management, 684 glomerular disease management, 878 history taking, 2 hypoallergenic diet, 527–528 hypoglycemia management, 395–396 inflammatory bowel disease diagnosis, 726–727 treatment, 727 restriction in canine parvovirus management, 160–161 restriction in food hypersensitivity diagnosis commercial diets, 489–490 home diets, 489 hydrolyzed protein diets, 490 interpretation, 490 uncomplicated diabetes management, 382t, 385–386 vomiting management, 667 Diethylcarbamazine dosage guidelines, 714t heartworm prevention, 1573 Digestive system, history taking, 4 Digital radiography. See X-ray Digits amputation, 1172–1172, 1172f anatomy, 1168 radiography, 65 Digoxin administration, 1478 adverse effects, 1478 atrial fibrillation management, 1547 congestive heart failure management, 1505 dosage guidelines, 1474t ferret administration, 1843 formulations, indications, and dosages, 1458t indications, 1477 mechanism of action, 1477 Dihydrocodone, dosage guidelines, 1474t Dilated cardiomyopathy canine heart disease, 1496 cats, 1534 congestive heart failure association and management, 1544–1545
Dilated cardiomyopathy (Continued) dogs clinical features, 1542–1543 pathophysiology, 1542–1543, 1543f ferrets, 1843 occult dilated cardiomyopathy, 1543–1544 Diltiazem administration, 1489 arrhythmia management, 1493 atrial fibrillation management, 1547 dosage guidelines, 1474t feline hypertrophic cardiomyopathy management, 1538 formulations, indications, and dosages, 1458t indications, 1488 Dimethyl sulfoxide (DMSO) amyloidosis management, 877 prolonged life support, 1619 Dioctophyma renale. See Kidney worm Diphenhydramine atopic dermatitis management, 486t flea allergy dermatitis management, 480 Diphenoxylate, diarrhea management, 711t Dipivefrin, glaucoma management, 1376t, 1377 Discoid lupus erythematosus. See Lupus erythematosus complex Discospondylitis, management, 1300 Disseminated intravascular coagulation (DIC) clinical features, 258 diagnosis, 262 erythrocyte fragmentation, 238 platelet consumption, 249 Distachiasis, features and management, 1336 Distal denervating disease, clinical features and management, 1312 Distal phalanx, anatomy in cats, 1168, 1169f Distal stomach partial gastrectomy Billroth I procedure, 693–694, 693f Billroth II procedure, 694–695, 694f equipment, 693 objectives, 693 postoperative care and complications, 695 preoperative considerations, 693 prognosis, 695 Distal symmetrical polyneuropathy, clinical features and management, 1312 Distemper canine distemper virus, 154 client education, 156–157 clinical signs, 155 diagnosis, 155–156 epidemiology, 154 ferrets clinical signs, 1822 diagnosis, 1822 etiology, 1822 prevention, 1823 treatment, 1822–1823 immune response, 154–155 infection stages, 154 pathogenesis, 154 prevention, 157 prognosis, 156 transmission, 154 treatment, 156 vaccination, 109t, 110t, 111t, 157 Diuretics. See also specific drugs adverse effects, 1475–1476 heart failure management left-sided congestive heart failure, 1520–1521 right-sided congestive heart failure, 1521
1973
Diuretics (Continued) hypercalcemia management, 347 hypertension management, 1578–1579 monitoring, 1476 prolonged life support, 1618–1619 DMSO. See Dimethyl sulfoxide Doberman pinscher arrhythmogenic cardiomyopathy, 1546 chronic hepatitis, 783–784 distal polyneuropathy, 1312 Dobutamine administration, 1478–1479 adverse effects, 1479 congestive heart failure management, 1503 dosage guidelines, 1474t indications, 1478–1479 prolonged life support, 1617–1618 DOCP, hypoadrenocorticism management, 360 Dolasetron, vomiting management, 668 Dopamine acute renal failure management, 866 administration, 1478–1479 adverse effects, 1479 dosage guidelines, 1474t indications, 1478–1479 prolonged life support, 1617–1618 Doramectin notoedric mange management, 470 scabies management, 469 Dovonex, hypercalcemia induction, 349 Doxapram, reptile dosage guidelines, 1927t Doxepin atopic dermatitis management, 486t feather picking management, 1770 Doxorubicin chemotherapy guidelines, 288t limb neoplasia management, 1179 Doxycycline anaplasmosis management, 183 avian administration, 1745 borreliosis management, 189 canine cyclic thrombocytopenia management, 183 ehrlichiosis management, 182 neorickettsiosis management, 184 Rocky Mountain spotted fever management, 179 salmon poisoning disease management, 184 Drug-induced necrosis clinical signs, 503 treatment, 503 Duction test, eye neurologic disturbance evaluation, 1411 Dwarfism clinical signs, 402 diagnosis, 402–403 etiology, 402 prevention, 403–404 treatment, 403 Dysautonomia, clinical features and management, 1311–1312 Dysplasia congenital, 250 drug induction, 251 infection, 250–251 nutritional, 251 Dyspnea diagnostic evaluation, 1625–1629 differential diagnosis, 1652 etiology, 1665 history taking, 4 Dystocia diagnosis, 989
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Dystocia (Continued) etiology, 988–989 reptiles, 1933 treatment, 989–990 Dysuria, rabbits, 1875–1876 Ear diseases. See specific diseases physical examination, 11, 11f Ear margin seborrhea clinical signs, 573 diagnosis, 573 treatment, 573 Ear mites ferrets, 1839 rabbits, 1864–1865 Ear surgery anatomy blood vessels, 583, 583f external ear canal, 582, 583f glands, 582, 583f horizontal ear canal, 582 nerves, 583, 583f vertical ear canal, 582 auricular hematoma anatomy, 590 equipment, 591 objectives, 591 postoperative care and complications, 591–592 preoperative considerations, 590 technique, 591, 592f indications, 582 lateral ear canal resection equipment, 585 objectives, 584 postoperative care and complications, 586 prognosis, 586 technique, 585–586, 585f preoperative considerations dermatologic examination, 583 ear palpation, 583 neoplasm staging, 584 neurologic examination, 584 otoscopic examination, 584 radiographic examination, 584 total ear canal ablation complications, 590 equipment, 588 indications, 587–588 objectives, 588 postoperative care, 588. 590 prognosis, 590 technique, 588, 589f vertical ear canal ablation equipment, 586 objectives, 586 postoperative care and complications, 586 prognosis, 586 technique, 586, 587f ECG. See Electrocardiography Echocardiography bacterial endocarditis, 1525 congenital heart disease, 1593–1594, 1594t feline hypertrophic cardiomyopathy, 1532–1533 ferrets, 1842t occult dilated cardiomyopathy in dogs, 1543–1544 pericardial constriction, 1559–1560 pericardial effusion, 1553–1554 principles, 1440 valvular heart disease, 1518
Eclampsia, hypocalcemia association, 353–354 Ectopic testes. See Testes Ectopic ureter. See Ureter Edrophonium chloride challenge test, 1321–1322 EEG. See Electroencephalography EGC. See Eosinophilic granuloma complex Egg laying egg binding and dystocia clinical signs, 1799 definition, 1798 diagnosis, 1799–1800 etiology, 1799 sites, 1799, 1799f treatment, 1800–1801 excessive diagnosis, 1796 etiology, 1796 treatment, 1796–1798 optimization of frequency, 1806–1807 reptiles, 1914 Ehrlichiosis canine acute phase, 180 chronic phase, 180–181 clinical signs, 180 diagnosis, 181–182 etiology, 180 human infection risks, 182 laboratory findings, 180 prevention, 182 prognosis, 182 transmission, 180 treatment, 182 feline Ehrlichia-like diseases, 185 nonregenerative anemia, 238–239 Ejaculate. See Semen Elbow dysplasia. See Canine elbow dysplasia radiography, 64 traumatic luxation reduction, 1095, 1095f Electrical alternans, electrocardiography, 1447, 1447f Electrocardiography (ECG) aberrant conduction, 1445–1446 advanced life support, 1616–1617, 1617f, 1618t anesthesia monitoring, 27 arrhythmias. See Cardiac arrhythmias atropine response test, 1452 bacterial endocarditis, 1525 bronchopulmonary disease evaluation, 1629 congenital heart disease, 1593 evaluation, 1443, 1443f, 1454–1455 event recorders, 1451 exercise testing, 1450 feline hypertrophic cardiomyopathy, 1532 feline restrictive cardiomyopathy, 1534 ferrets, 1842t heart enlargement left atrium, 1449, 1449f left ventricle, 1449–1450, 1449f right atrium, 1450, 1450f right ventricle, 1450, 1450f heartworm diagnosis, 1566 Holter monitoring, 1451, 1452f hypercalcemia, 1449 hyperkalemia, 1448–1449, 1449f hypoadrenocorticism, 358 hypocalcemia, 352, 1449 hypokalemia, 1449 indications, 1441 left anterior fascicular block, 1445, 1446f left bundle branch block, 1444–1445, 1445f
Electrocardiography (ECG) (Continued) lidocaine response test, 1452 normal tracing components, 1442–1443, 1442f, 1443f electrophysiology, 1442, 1442f findings, 1443, 1444t, 1455 pericardial effusion, 1553 QRS complex abnormalities electrical alternans, 1447, 1447f small complexes, 1447–1448 QT interval abnormalities, 1448 right bundle branch block, 1444, 1445f, 1446f ST segment depression, 1448 elevation, 1448 syncope, 1511–1512, 1512f technique, 1441–1442, 1442t thoracic trauma, 1718 T wave abnormalities, 1448 vagal maneuvers, 1451 valvular heart disease, 1518 ventricular preexcitation, 1446–1447, 1446f, 1447f Electroencephalography (EEG) brain tumors, 1252 disadvantages, 1245 indications, 1245 Electromyography (EMG) interpretation, 1246t, 1247 neuromuscular disease, 1322 peripheral nerve disorders, 1305 technique, 1246–1247 Electroretinography (ERG) eye neurologic disturbance evaluation, 1409 progressive retinal atrophy, 1385 ELISA. See Enzyme-linked immunosorbent assay EMG. See Electromyography Emphysema orbital, 1400–1401 radiography, 1641 Emphysematous cystitis clinical signs, 908 diagnosis, 908 etiology, 908 prevention, 908–909 treatment, 908 Enalapril, dosage guidelines, 1474t Encephalitis, necrotizing, 1259 Encephalitozoonosis rabbits, 1878 systemic infection, 221t Encephalopathy, metabolic, 1264, 1264t Endocardiosis. See Valvular heart disease Endocarditis. See Bacterial endocarditis Endodontic disease anatomy, 622 clinical signs, 623 diagnosis, 623 etiology, 623 surgery apexification, 624 apexogenesis, 624 endodontic therapy, 625 overview, 623, 624t postoperative care and complications, 625–626 preoperative considerations, 623 pulpotomy, 623–624 root canal, 624–625, 624f Endoscopy. See also specific techniques avian abdominal air sac endoscopy, 1739, 1739f
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Index Endoscopy (Continued) diarrhea evaluation colonoscopy, 710 upper gastrointestinal endoscopy, 710 foreign body removal stomach, 670 trachea, 1663 gastric outflow obstruction, 683 inflammatory bowel disease, 726 vomiting evaluation, 666 Endotracheal intubation anesthesia, 18 rodents, 1891 tube placement, 1609, 1612f sizes, 19t Enema dogs and cats, 834 reptiles, 1923 English pointer, motor neuron disease, 1308 Enophthalmos atrophy, 1403 breed-related, 1402 microphthalmos, 1402 neoplasia, 1403 orbital volume changes, 1402–1403 pain response, 1402 Enrofloxacin mycobacteriosis management, 202 rabbit dosage guidelines, 1863t reptile dosage guidelines, 1927t rodent dosage guidelines, 1895t Entamoeba diagnosis, 720 treatment, 720 Enteroenteroplexy complications, 742 equipment, 741 indications, 741 objectives, 741 postoperative care, 742 technique, 741–742, 742f Enterotomy complications, 740 equipment, 739 objectives, 739 postoperative care, 740 preoperative considerations, 739 prognosis, 740 technique, 739–740 Entropion classification, 1334 surgery heavy brow folds, 1335 lateral entropion, 1334–1335, 1335f medial entropion, 1335, 1335f temporary lid-everting sutures, 1335, 1335f ventral entropion, 1334, 1334f Environment, history taking, 1–2 Enzyme-linked immunosorbent assay (ELISA) borreliosis diagnosis, 188 ehrlichiosis diagnosis, 181 feline coronavirus diagnostics, 138 feline immunodeficiency virus diagnostics, 129 feline leukemia virus diagnostics, 120–121, 120t heartworm, 1564–1565 Eosinopenia, features, 247 Eosinophilia, etiology, 247 Eosinophilic gastritis. See Gastritis Eosinophilic gastroenteritis clinical signs, 730 diagnosis, 730
Eosinophilic gastroenteritis (Continued) etiology, 730 ferrets, 1850 treatment, 731 Eosinophilic granuloma complex (EGC) clinical signs, 532 diagnosis allergy testing, 533–534 blood tests, 533 history, 532–533 physical examination, 533 skin sampling and biopsy, 533 etiology, 531–532, 532t treatment allergen avoidance, 534 allergen-specific immunotherapy, 535 antihistamines, 535 antimicrobial therapy, 535 glucocorticoids, 534 immunomodulation, 535 progestational therapy, 535–536 Eosinophilic infiltration of airway clinical signs, 1680 diagnosis, 1680 etiology, 1680 pathophysiology, 1680 treatment, 1680–1681 Eosinophilic keratitis, feline, 1357 Eosinophilic leukemia, 253 Eosinophilic myositis, masticatory muscle and exophthalmos, 1397–1398 Ephedrine, micturition disorder management, 946t Epidermal dysplasia clinical signs, 511–512 diagnosis, 512 etiology, 511 treatment, 512 Epidermal inclusion cyst, features and management, 322 Epididymitis clinical signs, 964 infectious disease, 963–964 treatment, 967 Epilepsy. See Seizure Epinephrine advanced life support, 1613, 1616t dosage guidelines, 1474t, 1669t formulations, indications, and dosages, 1458t Epiphora, rodents, 1894, 1896 Episioplasty, 1011 Episiotomy equipment, 1010 indications, 1009 objective, 1009 postoperative care and complications, 1011 technique, 1010, 1010f Epizootic catarrhal enteritis, ferrets, 1846 Epsiprantel, dosage guidelines, 714t Epulis, oropharyngeal, 1048–1049 ERG. See Electroretinography Erythema multiforme clinical signs, 504 treatment, 504 Erythromycin gastric motility disorder management, 684 gastroduodenal ulceration management, 676t Erythropoietin administration, 872 monitoring of treatment, 872 side effects, 872–873 Esmolol dosage guidelines, 1474t
1975
Esmolol (Continued) formulations, indications, and dosages, 1458t pharmacology, 1487 Esophageal diseases avian anatomy, 1787 breed distribution, 636, 637t clinical signs, 636 diagnosis, 637–638 diverticula clinical signs, 649 diagnosis, 649 diverticulectomy. See Esophageal surgery etiology, 648–649 treatment, 649 esophagitis clinical signs, 646 diagnosis, 646 etiology, 656–656 prognosis, 647 treatment, 646–647 fistula clinical signs, 649 diagnosis, 649–650 etiology, 649 prognosis, 650 surgery. See Esophageal surgery treatment, 650 foreign bodies clinical signs, 644 diagnosis, 644 etiology, 644 prognosis, 645 removal, 644–645 hiatal disorders. See Gastroesophageal intussusception; Hiatal hernia hypomotility clinical signs, 641 diagnosis, 642–643 etiology, 641, 642t megaesophagus, 641 prognosis, 643 treatment, 643 neoplasia, 654 oropharyngeal dysphagia clinical signs, 638, 640 diagnosis, 640–641 etiology, 638 oral versus pharyngeal dysplasia, 638, 639–640t treatment, 641 perforation, 645 periesophageal obstruction, 653 stricture clinical signs, 647 diagnosis, 647–648 etiology, 647 surgical repair, 661 treatment, 648 vascular ring anomalies clinical signs, 650 diagnosis, 650–651 etiology, 650 persistent right aortic arch, 650, 651f surgery. See Esophageal surgery treatment, 651–652 Esophageal surgery anatomy body, 655 lower esophageal sphincter, 655 upper esophageal sphincter, 655 crichopharyngeal achalasia surgery equipment, 655–656 objectives, 655 postoperative care and complications, 656
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Esophageal surgery (Continued) preoperative considerations, 655 prognosis, 656 technique, 656, 656f diverticulectomy equipment, 660 objectives, 660 postoperative care and complications, 660 preoperative considerations, 660 prognosis, 661 technique, 660 esophagotomy equipment, 658 objectives, 658 postoperative care and complications, 658 preoperative considerations, 657 prognosis, 658 technique, 658 fistula surgery equipment, 660 objectives, 660 postoperative care and complications, 660 preoperative considerations, 659 prognosis, 660 technique, 660 hiatal hernia surgery equipment, 661 objectives, 661 postoperative care and complications, 662 preoperative considerations, 661 prognosis, 662 technique, 662, 662f, 663f resection and anastomosis equipment, 659 objectives, 659 postoperative care and complications, 659 preoperative considerations, 658–659 prognosis, 659 technique, 659, 659f stricture repair, 661 vascular ring anomaly surgery equipment, 657 objectives, 657 postoperative care and complications, 657 preoperative considerations, 656–657 prognosis, 657 technique, 657 Esophagography, technique, 71 Esophagostomy tube complications, 42 contraindications, 40 equipment, 40 indications, 40 objectives, 40 placement technique, 40–42, 41f postoperative care, 42 Estradiol, assay, 983 Estrogen. See also Hyperestrogenism benign prostatic hyperplasia management, 954–955 feline symmetrical alopecia management, 529 micturition disorder management, 946t prostatic neoplasia management, 955–956 Estrous cycle. See Ovarian cycle Ethanol, antifreeze toxicosis treatment, 868 Ethylene glycol. See Antifreeze toxicosis Ethylene glycol poisoning, clinical features and management, 1268 Etidronate, hypercalcemia management, 348
Etodolac dosage guidelines, 22t, 104t osteoarthritis management, 1225 Etomidate applications, 25 dosage guidelines cats, 21t dogs, 20t Etretinate, primary idiopathic seborrhea management, 510 Euthanasia, cancer patients, 291 Exercise diabetes type 2 management, 386 hypoglycemia management, 395–396 therapeutic exercise for postoperative rehabilitation aquatic exercise, 1032 assisted standing, 1029 ball playing, 1031–1032 Cavaletti rails, 1031, 1032f dancing exercises, 1031 jogging, 1031 objectives, 1029 proprioceptive exercises, 1029–1030, 1030f range of motion exercises, 1028 sit-to-stand exercises, 1031 stair climbing, 1030–1031 walking, 1030 wheelbarrowing, 1031 Exfoliative cutaneous lupus erythematosus. See Lupus erythematosus complex Exocrine pancreas insufficiency clinical signs, 827–828 diagnosis, 828, 828t etiology, 827 exocrine pancreas function, 819, 820t, 827 treatment enzyme replacement, 829 nutrition, 829 Exophthalmos abscess, 1397–1398 acquired disorders, 1397–1399 bilateral extraocular polymyositis, 1399 cystic disease, 1397, 1402 developmental disorders, 1397 masticatory muscle myositis, 1398–1389 neoplasia, 1399–1400 trauma, 1400–1402 Extensor carpi radialis reflex, spinal reflex examination, 1238 External ear canal. See Ear surgery; Otitis externa Extrahepatic biliary obstruction. See Biliary tract Extramedullary plasmacytoma, 300 Extraocular muscle myositis, 1318 Extrapleural space, radiography, 1632–1634 Eye. See also specific components anatomy, 1326f clinical signs with systemic disease, 1331t, 1332 culture, 1326 cytology, 1331–1332 enucleation, 1380 history taking, 3 intraocular prosthesis, 1379–1380, 1379f neurologic disturbances. See also Blindness; Nystagmus; Pupillary light reflexes anisocoria, 1413, 1414t, 1415 clinical signs, 1406–1408 diagnosis, 1408–1412 neuroanatomy, 1405–1406, 1406t, 1407f ocular motor system, 1416–1419 prognosis, 1419 treatment, 1419
Eye (Continued) neurologic examination, 1236 physical examination, 9 reptile disorders, 1936 ultrasound, 1332 Eyelid abnormalities and tear production defects, 1394–1395 anatomy, 1333 ankyloblepharon, 1333–1334 blepharitis allergic, 1338 bacterial, 1337–1338 fungal, 1338 granulomatous, 1338 parasitic, 1338 closure abnormalities, 1416–1417 coloboma, 1334 distachiasis, 1336 ectopic cilia, 1336 ectropion, 1336 entropion, 1334–1335 lagophthalmos, 1336 neoplasia, 1336–1337, 1337f neurologic control of movement, 1410–1411 opening abnormalities, 1417 surgical principles, 1333 treatment approaches, 1334t wedge resection, 1337, 337f Facial nerve eyelid responses, 1416–1417 lacrimation disorders, 1415 palsy clinical features and management, 1274 Facial symmetry, cranial nerve examination, 1237 FAD. See Flea allergy dermatitis Famotidine gastroduodenal ulceration management, 673, 674t reflux esophagitis management, 646 Fanconi-like syndrome, features and management, 879–880 Fasting serum bile acid, liver function testing, 752–753 Fatty acid supplements atopic dermatitis management, 486, 486t feline symmetrical alopecia management, 528 flea allergy dermatitis management, 480 lupoid onychomadesis management, 607 Fatty liver syndrome, avian, 1793 FCV. See Feline calcivirus Feather disorders. See Avian dermatology Febantel, dosage guidelines, 714t Fecal elastase, pancreatic function testing, 828, 828t Fecal occult blood test, 707 Feeding tubes. See Esophagostomy tube; Nasal catheter; Percutaneous endoscopic gastrostomy tube Felbamate dog administration, 1285t epilepsy management, 1287 Feline astrovirus clinical signs, 166 diagnosis, 166 etiology, 166 prevention, 166 treatment, 166 Feline bronchial disease clinical signs, 1676 diagnosis, 1676–1677 etiology, 1675
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Index Feline bronchial disease (Continued) pathophysiology, 1675 prognosis, 1678 treatment, 1677–1677, 1677t Feline calcivirus (FCV) clinical manifestations, 145t, 146 diagnosis, 147 infection routes, 144 respiratory disease, 144 subclinical carriers, 144–145 treatment, 147–148 Feline coronavirus. See Feline infectious peritonitis Feline foamy virus, clinical signs of infection, 176 Feline hepatic lipidosis clinical signs, 770 diagnosis, 770–771 etiology, 770 prognosis, 772 treatment, 771–772 Feline herpesvirus, corneal ulceration, 1351 Feline herpesvirus-144 (FHV-144) chronic disease, 146–147 clinical manifestations, 145, 145t diagnosis, 147 infection routes, 144 respiratory disease, 144 subclinical carriers, 144, 146 treatment, 147–148 vaccination and control, 148–149 Feline hypereosinophilic syndrome clinical signs, 731 diagnosis, 731 etiology, 731 prognosis, 731 treatment, 731 Feline hypertrophic cardiomyopathy clinical findings, 1528–1529, 1531–1532 diagnosis, 1532–1533 differential diagnosis, 1529t, 1530t pathophysiology, 1529, 1531, 1531f treatment of asymptomatic cat, 1537–1538 Feline immunodeficiency virus (FIV) age and sex distribution, 126 clinical signs acute infection, 127 chronic disease syndromes, 127–128 latent infection, 127 diagnosis enzyme-linked immunosorbent assay, 129 immunofluorescent antibody test, 129 polymerase chain reaction, 129 testing indications, 129 Western blot, 129 pathogenesis, 127 prevalence, 126 prevention, 131 prognosis, 131 public health risks, 126 risk factors, 126 structure, 126 subtypes, 126 transmission, 127 treatment goals, 129–130 immunomodulation, 130 interferons, 130 supportive therapy, 130, 131 zidovudine, 130 vaccination, 113t, 131 Feline infectious peritonitis (FIP) clinical course, 134 clinical signs, 133–134, 134t, 165, 1703 control of exposure and spread, 142, 166 coronavirus features, 132, 165
Feline infectious peritonitis (FIP) (Continued) diagnosis coronavirus detection, 136, 138–139, 166 features, 137t fluid analysis, 137–138 histopathology, 140 imaging, 136–137 immunohistochemistry, 140 laboratory evaluation, 136 dry form kidney disease, 135 liver disease, 135 neurologic disease, 135–136 ocular disease, 135 pulmonary disease, 136 reproductive disease, 136 etiology, 165, 1703 incubation, 134 pathogenesis, 132 prevalence, 133 risk factors, 133 transmission, 133 treatment, 141t, 166, 1703 antivirals, 140 immunomodulation, 140 interferons, 140–141 palliative therapy, 141 supportive measures, 141 vaccination, 142 wet form abdominal effusion, 134–135 pericardial effusion, 135 thoracic effusion, 135 Feline ischemic encephalopathy, 1261 Feline leprosy syndromes geographic distribution, 429 Mycobacterium lepraemurium disease clinical signs, 429–430 diagnosis, 430 etiology, 429 prevention, 431 treatment, 430–431 non-Mycobacterium lepraemurium disease clinical signs, 431 diagnosis, 431 etiology, 431 treatment, 431 Feline leukemia virus (FeLV) control, 124–125 diagnosis discordant results, 121 enzyme-linked immunosorbent assay, 120–121, 120t immunofluorescent antibody test, 121 neutralizing antibody tests, 122 polymerase chain reaction, 121–122 testing indications, 120, 120t virus isolation, 122 disease syndromes alimentary lymphoma, 117 anemia, 118–119 extranodal lymphomas, 118 immune-mediated disorders, 120 leukemias, 118 mediastinal lymphoma, 117 multicentric lymphoma, 118 myelodysplasia, 118 neutropenia, 119 nonspecific signs, 117 peripheral lymph node hyperplasia, 119 reproductive failure, 120 secondary infections, 119 thrombocytopenia, 119 immune response, 116
1977
Feline leukemia virus (FeLV) (Continued) infection classification latent infection, 116–117 persistent infection, 117 resistance, 116 transient infection, 116 sequence, 116 nonregenerative anemia, 238 prevalence, 115 structure, 115 transmission, 115–116 treatment acemannan, 123 general health care, 122 interferons, 122–123 palliative care, 123 PIND-ORF, 123 Propionibacterium acnes, 123 spread prevention, 122 staphylococcal A, 123 zidovudine, 123 vaccination administration, 124 adverse effects, 124 efficacy, 124 indications, 124 protocols, 112t, 113t Feline panleukopenia virus (FPV) clinical signs of infection, 164–165 diagnosis, 165 etiology, 164 features, 164 intestinal infection, 720 prevention, 165 treatment, 165 Feline poxvirus clinical signs, 175 diagnosis, 175 etiology, 175 treatment, 175 Feline restrictive cardiomyopathy clinical findings, 1533–1534 pathophysiology, 1533, 1533f Feline rotavirus clinical signs, 166 diagnosis, 166 etiology, 166 prevention, 166 subclinical infection, 166 treatment, 166 Feline spongiform encephalopathy (FSE), 176 Feline symmetrical alopecia (FSA) clinical signs, 526 diagnosis history, 526 laboratory tests, 526–527 physical examination, 526 etiology anagen defluxion, 525–526 atopic dermatitis, 524 demodicosis, 524–525 dermatophytosis, 524 flea allergy dermatitis, 524 food hypersensitivity, 524 Malassezia dermatitis, 525 notoedric mange, 525 otodectic mange, 525 psychogenic alopecia, 525 pyoderma, 525 systemic disease, 526 telogen effluvium, 525 trunk region disease, 523, 524t hair follicle growth and development factors, 524t normal shedding, 523
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Feline symmetrical alopecia (FSA) (Continued) treatment allergen-specific immunotherapy, 528 anti-inflammatory drugs, 528–529 antimicrobial therapy, 528 anxiolytics and tranquilizers, 529 flea control, 528 hormonal therapy, 529 hypoallergenic diet, 527–528 mite control, 528 Feline viral papillomatosis, features, 175 FeLV. See Feline leukemia virus Femoral pulse, evaluation, 1424, 1425t Femur. See also Coxofemoral joint anatomy diaphysis, 1126–1127 distal femur, 1128–1129 proximal femur, 1123 avascular necrosis of femoral head, 1118–1119 fracture management distal femur and patella, 1129–1131, 1129f, 1130f proximal femur, 1123–1126, 1124f, 1125f shaft, 1127–1128, 1127f, 1128f pelvic limb amputation at midfemur, 1180, 1182 radiography, 65 Fenbendazole diarrhea management, 712 dosage guidelines, 714t parasitic cystitis management, 908 rabbit dosage guidelines, 1863t reptile dosage guidelines, 1927t Fentanyl applications, 22 arterial thromboembolism management, 1540–1541 dosage guidelines cats, 21t, 103t dogs, 20t, 103t Ferret adrenal tumors, 1833–1835 alopecia, 1840 anemia, 1828–1831 anesthesia, 1822 bacterial infection, 1825–1827, 1849 blood collection cephalic vein, 1817 cranial vena cava, 1818 hematologic and biochemical values, 1817, 1817t, 1818t indications, 1816 jugular vein, 1818 saphenous vein, 1818 tail artery, 1718–1819 transfusion, 1819, 1930 bone marrow aspiration, 1819 catheterization intraosseous, 1820 intravenous, 1819–1820 urinary, 1821 cystocentesis, 1819 digestive tract features and diseases, 1845–1852 drug dosage guidelines, 1820–1821, 1821t fluid therapy, 1820 fungal infection, 1827 heart disease, 1841–1845 injection, subcutaneous and muscular, 1820 insulinoma, 1831–1833 lymphosarcoma, 1825, 1836–1837 neoplasia, 1836–1837, 1840–1841 nutrition, 1820 oral medication administration, 1820 parasites, 1847
Ferret (Continued) paraurethral cysts, 1857 prostatic disease, 1856–1857 radiography, 1819 reproductive system, 1852–1854 restraint, 1816 seasonal changes haircoat, 1837 skin, 1837–1838 sedation, 1821–1822, 1821t skin infection, 1838–1841 splenic aspiration, 1819 splenomegaly, 1827–1828 urinary system, 1854–1856 viral infection Aleutian disease, 1824–1825 canine distemper, 1822–1823, 1838 influenza, 1823–1824 rabies, 1824 rotavirus, 1825, 1849 FHV-144. See Feline herpesvirus-144 Fiber-responsive diarrhea. See Irritable bowel syndrome Fibrinogen, assay, 261 Fibrosarcoma avian, 1762–1763 biologic behavior, 302 clinical signs, 303–304 features and management, 323 oropharyngeal, 1049–1050 staging, 304, 304t treatment, 304–305 Fibula. See also Tarsus anatomy diaphysis, 1145 epiphysis, 1144 metaphysis, 1144–1145 physis, 1144 fracture management cross pin fixation, 1146–1147, 1147f external skeletal fixation, 1148–1150, 1149f interfragmentary lag screw fixation, 1146 intermedullary pin and wire fixation, 1147–1148, 1148f pin and tension wire band fixation, 1145–1146, 1146f plate and screw fixation, 1150, 1150f postoperative care and complications, 1150–1151 preoperative considerations, 1145 radiography, 65 Finasteride, benign prostatic hyperplasia management, 954 Fine-needle aspiration (FNA) cutaneous neoplasms, 414 inflammatory lesions, 414 liver, 755–756 lung, 1628 skin tumors, 316–318 soft tissue sarcoma, 304 splenic disease, 278–279 technique, 413–414 testes, 967 FIP. See Feline infectious peritonitis Fipronil cheyletiellosis management, 473 flea control, 477t scabies management, 468 FIV. See Feline immunodeficiency virus Flail chest, stabilization, 1720–1721, 1721f Flavoxate, micturition disorder management, 946t Flea ferrets, 1838–1839 rodents, 1892–1893
Flea allergy dermatitis (FAD) clinical signs, 475 diagnosis history, 475–476 laboratory assessment, 476 physical examination, 476 treatment response, 476 environmental sources of fleas, 475 epidemiology, 474 etiology, 474 feline symmetrical alopecia, 524 flea life stages, 474–475 prevention, 480 treatment affected pets, 479 allergic reaction blocking, 479–480 flea control, 476, 477t, 478 indoor area treatment, 478–479 outdoor area treatment, 479 unaffected pets, 479 Fluconazole adverse effects, 216 avian administration, 1742 blastomycosis management, 209–210 cryptococcosis management, 213 dosage and administration, 216 histoplasmosis management, 208 Malassezia dermatitis management, 449t reptile dosage guidelines, 1927t Flucytosine, features, 217 Fludrocortisone acetate, hypoadrenocorticism management, 360 Fluid therapy. See also Dehydration acute renal failure, 865–866 administration routes intraosseous, 97 intraperitoneal, 96 intravenous catheter care, 96 catheter selection, 96 vein selection, 96 subcutaneous, 96 advanced life support, 1616 brain trauma management, 1263 canine parvovirus management, 160 clinic stock solutions, 91 colloid solutions natural colloids, 89–90 synthetic colloids and composition, 90, 90t crystalloid solutions maintenance fluids, 88 osmolality, 89 replacement fluids, 89 decision-making, 82, 82f diabetic ketoacidosis management, 378 diarrhea management, 711 efficacy monitoring body weight, 98 central venous pressure, 99 databases, 98t electrolyte and acid-base status, 99 electrolyte distribution, 83 ferret, 1820 fluid compositions, 89t fluid selection, 95 hepatobiliary disease, 757, 757–758t, 771 indications, 82–83 infusion rate drip rate, 97 factors affecting, 97 infusion pumps, 98 ins and outs, 97–98 syringe pumps, 98 twenty four-hour infusion rate, 97 maintenance requirements, 83–84, 83f, 84t
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Index Fluid therapy (Continued) overhydration laboratory findings, 99 signs, 99 treatment, 99 pancreatitis, 824 parenteral fluid supplementation bicarbonate, 92–93 calcium, 94 dextrose, 93 magnesium, 93 phosphorous, 94–95 potassium, 91, 91t vitamins, 93 peritonitis, 857 preservatives, 95 pyometra, 986 shock, 1605, 1606t, 1607 vomiting, 666–667 water distribution, 82–83 Flumazenil, dosage guidelines, 28t Flunixin meglumine ferret dosage guidelines, 1821t osteoarthritis management, 1225 rabbit dosage guidelines, 1863t reptile dosage guidelines, 1927t Fluorescein, cornea staining, 1329 5-Fluorocytosine, avian administration, 1742 5-Fluorouracil, chemotherapy guidelines, 288t Flutamide, ferret adrenal disease management, 1834 Fly bite dermatitis clinical signs, 568 diagnosis, 568–569 treatment, 569 FMCP. See Fragmentation of the medial portion of the coronoid process FNA. See Fine-needle aspiration Focal subcutaneous emphysema. See Air sac rupture Folate, deficiency and anemia, 241 Follicular cysts, avian, 1763 Follicular dysplasias clinical signs, 521 diagnosis, 521 etiology, 521 treatment, 521 Food hypersensitivity clinical signs, 488–489 definition, 488 diagnosis, 489–490 etiology, 488 feline symmetrical alopecia, 524 pinna, 569 treatment, 490 Forebrain, lesions, 1250 Foreign bodies avian stomach impaction, 1790–1801 crop, 1789 ferret gastrointestinal tract, 1848 reptiles, 1930 trachea, 1663 Foreskin. See Penis FPV. See Feline panleukopenia virus Fractures. See Delayed union; Malunion; Nonunion; Open fractures; Pediatric fractures; see also specific bones Fragmentation of the medial portion of the coronoid process (FMCP) anatomy, 1199 clinical signs, 1200 diagnosis, 1200 pathophysiology, 1199–1200 prognosis, 1202 treatment, 1200–1202, 1201f
Free skin graft. See Skin graft and reconstruction Frostbite necrosis, 506 pinna, 570–571 Fructosamine diabetes diagnosis, 378 diabetes therapy monitoring insulin, 385 oral hypoglycemics, 388–389, 388f FSA. See Feline symmetrical alopecia FSE. See Feline spongiform encephalopathy Fucosidosis, clinical features, 1306 Fungal infection. See Deep mycosis; Dermatophytosis; Malassezia dermatitis; see also specific conditions Furosemide acute renal failure management, 866 administration, 1473, 1475 adverse effects, 1475–1476 brain trauma management, 1263 brain tumor management, 1253 congestive heart failure management, 1501–1502, 1504–1505, 1538–1539 dosage guidelines, 1474t ferret administration, 1842 formulations, 1473 mechanism of action, 1473 pericardial effusion management, 1559 prolonged life support, 1618 reptile dosage guidelines, 1927t Gabapentin cat administration, 1289 dog administration, 1285t epilepsy management, 1287 Gag reflex, cranial nerve examination, 1237 Gallbladder. See Biliary tract; Biliary tract surgery; Cholecystitis; Cholelithiasis; Gallbladder mucocele Gallbladder mucocele clinical signs, 804 diagnosis, 804–805 etiology, 804 prognosis, 805 treatment, 805 Gamma-glutamyltransferase (GGT), liver function testing, 750f, 751 Gangliosidosis, 244 Gastric dilatation-volvulus (GDV) clinical signs, 688 diagnosis, 688–689 etiology, 688 prevention, 689 surgery acute cases belt loop gastropexy, 699, 699f circumcostal gastropexy, 698–699, 699f equipment, 697 incisional gastropexy, 700 muscle flap gastropexy, 699, 700f objectives, 697 postoperative care and complications, 700 preoperative considerations, 697 prognosis, 700 prophylactic gastropexy, 700 tube gastropexy, 698, 698f overview, 689 partial gastrectomy, 692–693 treatment arrhythmias, 689 initial management, 689
1979
Gastric outflow obstruction clinical signs, 682 diagnosis endoscopy, 683 history, 682 physical examination, 682 radiography, 683 ultrasound, 683 etiology, 682 treatment, 683 Gastritis acute gastritis clinical signs, 668 diagnosis, 668–669 etiology, 668 treatment, 669 chronic gastritis clinical signs, 678 diagnosis, 678–679 etiology, 677–678 prognosis, 680 treatment, 679–680 eosinophilic gastritis clinical signs, 680–681 diagnosis, 681–682 epidemiology, 680 etiology, 680 prognosis, 682 treatment, 681–682 Gastrocnemius reflex, spinal reflex examination, 1238 Gastroduodenal ulceration clinical signs, 672 diagnosis, 672–673 etiology, 670–672 ferrets, 1847–1848 prevention, 677 risk factors, 671t treatment antibiotic therapy, 679 gastric acid secretion inhibitors, 673, 673f, 674–676t goals, 673 laparotomy, 679 mucosal cytoprotectants, 673, 677 Gastroesophageal intussusception clinical signs, 652 diagnosis, 652–653 etiology, 652 treatment, 653 Gastrography, technique, 71 Gastrointestinal stasis, rabbits, 1871–1872 Gastrotomy equipment, 692 objectives, 692 postoperative care and complications, 692 preoperative considerations, 691–692 prognosis, 692 technique, 692 GDV. See Gastric dilatation-volvulus Gecko. See Reptiles Genital system. See also Penis; Scrotum; Testes; Vagina; Vulva history taking females, 5 males, 5 physical examination, 15 Gentamicin rabbit dosage guidelines, 1863t reptile dosage guidelines, 1927t rodent dosage guidelines, 1895t Gerbil. See Rodents German shepherd, peripheral neuropathy in aging, 1309 German shorthaired pointer hereditary lupoid dermatosis, 572 necrotizing vasculitis, 1261–1262
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GGT. See Gamma-glutamyltransferase Giardiasis avian, 1791–1792 clinical signs, 718–719 diagnosis, 719 life cycle, 718 prevention, 719 treatment, 719 Gingivitis. See Periodontal disease; Stomatitis/gingivitis Glaucoma breed disposition, 1375t clinical signs, 1374, 1375t diagnosis, 1374–1375 prevention, 1380 primary versus secondary, 1374 treatment algorithm, 1375f medical treatment, 1376–1378, 1376t surgery, 1378–1380, 1379f Glimepiride, diabetes type 2 management, 387t Glipizide, diabetes type 2 management, 386–387, 387t, 388f Globoid cell leukodystrophy, clinical features, 1306 Glomerulonephritis associated conditions, 875t diagnosis, 875–877, 876f etiology, 875 treatment, 877–878 Glucocorticoid hepatopathy clinical signs, 773 diagnosis, 773–774 differential diagnosis, 772, 773t etiology, 773 treatment, 774 Glucocorticoids atopic dermatitis management cats, 487 dogs, 487 dosing, 486t brain trauma management, 1263 brain tumor management, 1253 bronchitis management, 1672–1673 canine chronic hepatitis management, 778–779 chronic gastritis management, 679 diarrhea management, 712 dosage guidelines, 266t eosinophilic gastritis management, 681 feline bronchial disease management, 1677, 1677t feline symmetrical alopecia management, 528–529 flea allergy dermatitis management, 479–480 heartworm adjunctive therapy, 1571 hepatic cirrhosis management, 788 histoplasmosis management, 208 hypercalcemia management, 347 hypoadrenocorticism management, 360 hypoglycemia management, 396 immune-mediated arthritis, 1232t immune-mediated disease management, 263 inflammatory bowel disease management, 728–729, 728t kennel cough management, 153 lupus erythematosus complex management, 498–499 miliary dermatitis and eosinophilic granuloma complex management, 534 monocytosis induction, 246 myasthenia gravis management, 1323 necrotizing vasculitis management, 1262
Glucocorticoids (Continued) neutrophilia induction, 245 neutrophilic cholangitis management, 801 osteoarthritis management, 1225 otitis externa management, 580 otitis media and otitis interna management, 597 pemphigus complex management, 495 primary idiopathic seborrhea management, 510 prolonged life support, 1619 pulmonary fibrosis management, 1679 reflux esophagitis management, 647 shock management, 1608 spinal cord trauma management, 1299–1300 tracheobronchitis management, 1690 uveitis management, 1370–1371, 1371t vasculitis management, 502 Glucosamines, osteoarthritis management, 1226 Glucose. See Dextrose Glycogen storage disorders, 1317 Glycopyrrolate advanced life support, 1613, 1616 applications, 25 dosage guidelines cats, 21t dogs, 20t rabbits, 1862t formulations, indications, and dosages, 1458t Glycosoaminoglycans, osteoarthritis management, 1225–1226 Goiter, avian, 1789 Golden retriever, hypomyelinating neuropathy, 1309 Gold salts immune-mediated arthritis management, 1232t pemphigus complex management, 496 Gout avian, 1814 reptiles, 1938–1939 Granulomatous meningioencephalomyelitis clinical signs, 1258 diagnosis, 1258 etiology, 1258 prognosis, 1259 treatment, 1258–1259 Granulomatous pulmonary disease clinical signs, 1681 diagnosis, 1681 etiology, 1681 pathophysiology, 1681 treatment, 1679–1680 Greyhound polyarthritis, 1228 Griseofulvin dermatophytosis management, 456–457, 457t onychomycosis management, 608 rabbit dosage guidelines, 1862t rodent dosage guidelines, 1895t Growth hormone assay, 400–401 deficiency. See Dwarfism excess. See Acromegaly replacement therapy, 403 Guinea pig. See Rodents Hair, microscopic examination for dermatophytosis, 454, 454f, 454t Hairball, rabbits, 1873
Haloperidol, feather picking management, 1770 Hamster. See Rodents Hantavirus, cat infection, 176 hCG. See Human chorionic gonadotropin Head and neck. See also Brain trauma; Brain tumors avian trauma, 1814 history taking, 3 physical examination, 9–12 Heart arrhythmias. See Cardiac arrhythmias electrocardiography. See Electrocardiography endocarditis. See Bacterial endocarditis feline disease differential diagnosis, 1529t, 1530t myocardial contusion, 1720 physical examination. See Cardiovascular physical examination radiography aortic enlargement, 1436, 1436f biventricular enlargement, 1435–1435 congestive heart failure, 1437–1438 echocardiography principles, 1440 interpretation heart disease features, 1439t initial approach, 1433 lateral radiograph cat, 1431 dog, 1430–1431, 1431f left atrium enlargement, 1434–1435, 1435f rupture, 1440 left ventricular enlargement, 1435, 1435f microcardia, 1436 pericardial effusion, 1440 pulmonary arteries and veins, 1432 pulmonary vasculature, 1437, 1437f right atrial enlargement, 1433, 1433f right ventricular enlargement, 1433–1434, 1434f technical considerations, 1430 valentine-shaped heart in cats, 1439–1440 ventrodorsal radiograph cat, 1431–1432 dog, 1431, 1431f vertebral heart score, 1438, 1438f valve disease. See Valvular heart disease Heart failure. See also Congestive heart failure etiology in dogs causes, 1496–1497, 1498–1499t, 1499–1500 classification, 1496, 1496t physiologic diagnosis, 1496, 1497t pathophysiology, 1495–1496 Heart rate anesthesia monitoring, 26–27 physical examination, 8 Heartworm clinical signs, 1563 diagnosis, 1563–1567 epidemiology, 1562 erythrocyte fragmentation, 237–238 ferrets clinical signs, 1844 diagnosis, 1844 etiology, 1844 treatment, 1844–1845 life cycle cats, 1562 dogs, 1561–1562 mosquito vectors, 1561 pathogenesis, 1562–1563
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Index Heartworm (Continued) prevention diethylcarbamazine, 1573 ivermectin, 1572 milbemycin oxime, 1572 missed doses, 1573 moxidectin, 1572 selamectin, 1572 radiography, 1639f reservoirs, 1561 severity classification, 1567 treatment adjunctive therapy, 1571 advanced disease, 1568–1570 cats, 1567 complications, 1569 contraindications, 1567 Immiticide, 1567–1568 microfilaria, 1570 monitoring, 1570 old dogs, 1567 sequelae, 1571 vena cava syndrome, 1567, 1569–170 Heineke-Mikulicz pyloroplasty. See Pyloroplasty Heinz body anemia, 237 Helicobacter pylori, chronic gastritis management, 680 Helminths. See Intestinal parasites Hemangiopericytoma biologic behavior, 302 clinical signs, 303–304 staging, 304, 304t treatment, 304–305 Hemangiosarcoma biologic behavior, 302 clinical signs, 303–304 management, 280, 280t, 304–305, 323 staging, 304, 304t Hematuria, rabbits, 1875–1876 Hemochromatosis, avian, 1794 Hemodialysis, acute renal failure management, 866 Hemoglobin, glycosylated diabetes diagnosis, 378 insulin therapy monitoring, 385 Hemoglobinuria, heartworm, 1563 Hemoplasmosis, hemolysis, 236 Hemothorax clinical signs, 1704 diagnosis, 1704 etiology, 1704 physical examination, 1429 thoracic surgery management, 1730–1731 treatment, 1704–1705, 1720 Heparin arterial thromboembolism management, 1541 coagulation disease management, 264 dosage guidelines, 1474t heartworm adjunctive therapy, 1571 inactivation, 256 prolonged life support, 1619 thrombotic disease management, 1583 Hepatic amyloidosis clinical signs, 777 diagnosis, 777 etiology, 777 hepatitis. See Canine chronic hepatitis treatment, 777 Hepatic arteriovenous fistula clinical signs, 795 diagnosis, 795–796 etiology, 795 treatment, 796 Hepatic cirrhosis clinical signs, 787
Hepatic cirrhosis (Continued) diagnosis, 787–788 etiology, 787 treatment, 788 Hepatic cysts clinical signs, 799 diagnosis, 799 etiology, 799 treatment, 799 Hepatic encephalopathy clinical signs, 748 treatment, 758–759 Hepatic fibrosis, avian, 1793 Hepatic microvascular dysplasia (HMD) clinical signs, 793 diagnosis, 793–794 etiology, 793 portosystemic shunt association, 792–793 prognosis, 794 treatment, 794 Hepatic nodular hyperplasia clinical signs, 798 diagnosis, 898–799 Hepatitis. See Canine chronic hepatitis Hepatobiliary neoplasia clinical signs, 797 diagnosis, 797–798 etiology, 797 treatment, 798 tumor types, 796, 796t Hepatocutaneous syndrome. See Superficial necrolytic dermatitis Hepatoprotectants, 759, 760t, 761 Hepatotoxins, 761, 762t, 763–764t Hepatozoonosis clinical signs, 227 diagnosis, 227 etiology, 226 pathogenesis, 226–227 prevention, 227–228 systemic infection, 220t treatment, 227 Herniation, space-occupying lesions, 1250–1251 Herpes hepatosplenitis. See Pacheco’s disease Herpesvirus pregnancy infection, 987 vaccination protocols, 112t, 113t Hiatal hernia clinical signs, 652 diagnosis, 652–653 etiology, 652 surgery equipment, 661 objectives, 661 postoperative care and complications, 662 preoperative considerations, 661 prognosis, 662 technique, 662, 662f, 663f treatment, 653 Hip dysplasia diagnosis, 1119 treatment femoral head and neck excision arthroplasty, 1120–1121, 1121f medical, 1119 pectineal myectomy, 1121 total hip replacement, 1121–1122 triple pelvic osteotomy, 1120 Histiocytic ulcerative colitis clinical signs, 732 diagnosis, 732 treatment, 732 Histiocytoma, features and management, 324
Histoplasmosis dermatologic lesions, 443 geographic distribution, 206f prevention, 218 systemic infection clinical signs, 205–206 diagnosis, 206–208 etiology, 205 pathogenesis, 205 treatment, 208 History taking acute hepatic failure, 765 body systems cardiopulmonary system, 2–4 digestive system, 4 eyes, 3 genital systems, 5 head and neck, 3 musculoskeletal system, 6 nervous system, 6–7 skin, 5–6 swelling or masses, 5 urinary system, 4–5 chronic renal failure, 869 claw disease, 604–605 coagulation diseases, 258 congenital heart disease, 1591–1592 constipation, 833 dehydration detection, 85–86 dermatophytosis, 453 diarrhea, 704 diet, 2 environment, 1–2 eye neurologic disturbances, 1408 feline symmetrical alopecia, 526 flea allergy dermatitis, 475–476 heartworm, 1564 liver disease, 748 miliary dermatitis and eosinophilic granuloma complex, 532–533 necrotizing dermatoses, 500 objective versus subjective data, 1 otitis externa, 575 otitis media and otitis interna, 594 pericardial effusion, 1552 peritonitis diagnosis, 856 preventive health care status, 2 previous illness and surgery, 2 primary complaint, 2–3 reptiles, 1920 rodents, 1883–1884 scabies, 466 signalment, 1 splenic disease, 277 syncope, 1511 thoracic trauma, 1716 valvular heart disease, 1517 vomiting, 665 HMD. See Hepatic microvascular dysplasia HO. See Hypertrophic osteopathy Hock osteochondritis dessicans clinical signs, 1195 diagnosis, 1195–1196 pathophysiology, 1194–1195 prognosis, 1196–1197 surgery, 1196 sore hock in rabbits, 1866–1867 HOD. See Hypertrophic osteodystrophy Holter monitoring, 1451, 1452f, 1544 Honey, open wound management, 553 Hookworm clinical signs, 715 diagnosis, 715 life cycle, 715 prevention, 715–716
1981
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Hookworm (Continued) species, 715 treatment, 715 Hormone-responsive incontinence clinical signs, 942–943 diagnosis, 943–945 treatment, 947 Human chorionic gonadotropin (hCG), excessive egg laying management, 1797, 1797t Humerus. See also Scapulohumeral luxation anatomy, 1080 condylar fracture management, 1083–1084, 1084f condyle osteochondritis dessicans anatomy, 1199 clinical signs, 1200 diagnosis, 1200 pathophysiology, 1200 prognosis, 1202 treatment, 1200–1202, 1201f diaphyseal fracture management, 1082–1083, 1082f intercondylar fracture management, 1084–1085, 1085f proximal humerus fracture complications, 1076 diaphyseal fracture management, 1081–1082, 1081f head, 1075 neck, 1075, 1076f physeal fracture management, 1080–1081 postoperative care, 1076 preoperative considerations, 1074–1075 prognosis, 1076 Salter-Harris fractures of proximal physis, 1075, 1075f tubercle, 1075 radiography, 64 supracondylar fracture management, 1083 Hyalohyphomycosis clinical signs, 442 etiology, 442 treatment, 442 Hyaloid artery, retention, 1381 Hydralazine adverse effects, 1482 dosage guidelines, 1474t hypertension management, 1578–1579 indications, 1482 Hydration, physical examination, 8 Hydrocephalus clinical signs, 1268 diagnosis, 1268–1269 etiology, 1268 prognosis, 1269 strabismus, 1403 treatment, 1269 Hydrochlorthiazide adverse effects, 1476 dosage guidelines, 1474t mechanism of action, 1476 Hydromorphone arterial thromboembolism management, 1540 dosage guidelines, 103t Hydronephrosis, ferrets, 1855 Hydropropulsion, urethral, 924–925 Hydroxyzine Amazon foot necrosis management, 1764 atopic dermatitis management, 486t feline symmetrical alopecia management, 528
Hyperadrenocorticism cats clinical signs, 369 diagnosis, 369–370 etiology, 368 treatment, 370–371 dogs atypical hyperadrenocorticism, 368 clinical signs, 361 diagnosis, 361–364 etiology, 360–361 prognosis, 367 treatment, 364–367 Hyperandrogenism clinical signs, 518 diagnosis, 518–519 etiology, 517 treatment, 519 Hypercalcemia clinical signs, 346 definition, 345 diagnosis, 346 electrocardiography, 1449 etiology, 345–346, 346t, 348–351 idiopathic hypercalcemia in cats, 350 malignancy association, 348 management in lymphoma, 297 treatment, 346–348, 347t Hyperestrogenism anemia, 242 clinical signs, 517–518 diagnosis, 518–519 etiology, 517 treatment, 519 Hyperkalemia acute renal failure management, 866 electrocardiography, 1448–1449, 1449f Hypernatremia, fluid therapy, 95 Hyperoxaluria, domestic shorthaired cats, 1307 Hyperparathyroidism clinical signs, 351 diagnosis, 350–351 etiology, 350 hypercalcemia association, 350 reptiles, 1937–1938 treatment, 351 Hyperphosphatemia acute renal failure management, 867 chronic renal failure, 871–872 Hyperprogesteronism clinical signs, 518 diagnosis, 518–519 etiology, 517 treatment, 519 Hypersensitivity syndrome, avian, 1778 Hypertension canine heart disease, 1497 cats, 1535–1536 chronic renal failure, 873 clinical signs, 1575–1576 definition, 1574 diagnosis, 1576–1577 etiology, 1575 glomerular disease management, 878 treatment angiotensin-converting enzyme inhibitors, 1578–1579 beta-blockers, 1579 calcium channel blockers, 1578 diuretics, 1579 follow-up, 1579–1580 general measures, 1578 vasodilators, 1579 Hyperthermia, cancer management, 290, 305
Hyperthyroidism, feline cardiac effects, 1535 clinical signs, 331–332, 331t diagnosis, 332–334 etiology, 331 treatment, 335–337 Hypertonicity syndromes, features and management, 1317–1318 Hypertrophic cardiomyopathy. See also Feline hypertrophic cardiomyopathy ferrets, 1843 Hypertrophic gastropathy clinical signs, 686 diagnosis, 686 etiology, 685 forms, 685 treatment, 686 Hypertrophic osteodystrophy (HOD) clinical signs, 1187–1188 diagnosis, 1188, 1188f etiology, 1187 treatment, 1188 Hypertrophic osteopathy (HO) clinical signs, 1189 diagnosis, 1189, 1189f etiology, 1189 nomenclature, 1188 treatment, 1189–1190 Hypoadrenocorticism anemia, 242 clinical signs, 357–358 diagnosis, 358–359 primary versus secondary, 357 treatment acute disease, 359–360 chronic disease, 360 Hypocalcemia avian, 1811–1812, 1814 clinical signs, 352 crocodilians, 1941–1942 definition, 351–352 diagnosis, 352 electrocardiography, 1449 etiology, 352–354, 352t ferrets, 1832–1833 reptiles, 1938 treatment, 352–353, 353t Hypodipsia diagnosis, 407 etiology, 407 treatment, 407 Hypoglycemia acute crisis management, 391–392 chronic management, 395–396 differential diagnosis, 391t seizure management, 392 syncope, 1509 Hypokalemia acute renal failure management, 866–867 electrocardiography, 1449 Hyponatremia, fluid therapy, 95 Hypoparathyroidism clinical signs, 354 diagnosis, 354 etiology, 354 treatment, 354–355 Hypophosphatemia, hemolysis, 238 Hypospadia, clinical features, 973 Hypothyroidism anemia, 241 avian, 1767–1768 cats clinical signs, 330–331 diagnosis, 331 etiology, 330 treatment, 331
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Index Hypothyroidism (Continued) dogs clinical signs, 328–329, 328t diagnosis, 329–330 etiology, 327 treatment, 330 neuropathy, 1309–1310 turtles, 1940 IBD. See Inflammatory bowel disease IBS. See Irritable bowel syndrome Ibuprofen osteoarthritis management, 1225 rabbit dosage guidelines, 1863t ICH. See Infectious canine hepatitis Ichthyosis clinical signs, 513 diagnosis, 513–514 etiology, 513 treatment, 514 Idiopathic feline lower urinary tract disease (IFLUTD) clinical signs, 909 diagnosis, 909 etiology, 909 prevention, 910 treatment acute crisis, 910 chronic therapy, 910 Idiopathic nasodigital hyperkeratosis clinical signs, 514 diagnosis, 515 etiology, 514 treatment, 515 IFLUTD. See Idiopathic feline lower urinary tract disease IGF-I. See Insulin-like growth factor-I Iguana. See Reptiles Ilidacloprid, flea control, 477t Ilium. See Pelvis Imidocarb diproprionate, ehrlichiosis management, 182 Imipramine, micturition disorder management, 946t Immiticide complications, 1569 heartworm management, 1567–1568 side effects, 1569 storage, 1569 Immune-mediated arthritis clinical signs canine erosive arthritis, 1228 canine non-erosive arthritis, 1227–1228 cats, 1228 greyhound polyarthritis, 1228 diagnosis, 1229, 1229f, 1230f, 1231, 1231f etiology, 1227 prognosis, 1232 treatment, 1232t erosive forms, 1232 non-erosive forms, 1231 Immune-mediated dermatoses. See Lupus erythematosus complex; Pemphigus complex; Subepidermal blistering dermatoses; Uveodermatologic syndrome; Vasculitis Immune-mediated hemolytic anemia. See Anemia Immune-mediated thrombocytopenia. See Thrombocytopenia Immunotherapy, cancer management, 290 Impetigo. See Pyoderma Inclusion body disease, reptiles, 1936–1937 Incontinence. See Diarrhea; Micturition disorders Infectious canine hepatitis (ICH) clinical signs, 172
Infectious canine hepatitis (ICH) (Continued) diagnosis, 172–173 etiology, 172 incidence, 172 pathogenesis, 172 prevention, 173 transmission, 172 treatment, 173 virus features, 172 Infectious meningoencephalitis. See Meningoencephalitis, infectious Infectious tracheobronchitis. See Tracheobronchitis, infectious Infective endocarditis. See Bacterial endocarditis Infertility algorithm for male infertility diagnosis, 965f cats, 1024–1025 dogs females diagnosis, 1019–1020 etiology, 1015–1019 treatment, 1020–1021 males, 1022–1023 Inflammatory bowel disease (IBD). See Eosinophilic gastroenteritis; Feline hypereosinophilic syndrome; Histiocytic ulcerative colitis; Lymphocyticplasmacytic inflammatory bowel disease; Neutrophilic enterocolitis; Regional granulomatous enterocolitis Influenza ferrets clinical signs, 1823 diagnosis, 1823 etiology, 1823 prevention, 1824 treatment, 1824 H5N1 transmission, 176 Injection-site sarcoma, feline, 303 Insulin diabetic ketoacidosis management, 378, 380 dosage guidelines, 381, 381t monitoring of therapy, 381, 383–385 oral hypoglycemic agent combination, 388 preparations, 380–381 resistance diagnosis and treatment, 384t uncomplicated diabetes management, 380–381, 381t Insulin-like growth factor-I (IGF-I), assay, 401, 403 Interceptor. See Milbemycin oxime Interferons canine parvovirus management, 161 feline immunodeficiency virus management, 130 feline infectious peritonitis management, 140–141 indications, 122–123 Interstitium radiography bronchial pattern, 1640, 1640f mixed patterns, 1640 nodular pattern, 1637–1638 pulmonary hyperlucency, 1640–1641 unstructured pattern, 1638–1639, 1639f vascular pattern, 1639 Intertarsal joint. See Tarsus Intertriginous dermatoses. See Skin fold pyoderma Intestinal lymphangiectasia. See Proteinlosing enteropathy Intestinal neoplasia clinical signs, 736 diagnosis, 736–737 etiology, 736 treatment, 737
1983
Intestinal obstruction clinical signs, 737 diagnosis, 738 etiology, 737 pathophysiology, 737 treatment, 738 Intestinal parasites antihelminthic drugs, 714t ascarid nematodes clinical signs, 714–715 diagnosis, 715 life cycle, 714 species, 714 treatment, 715 avian, 1792 Balantidium diagnosis, 720 treatment, 720 coccidiosis clinical signs, 717–718 diagnosis, 718 life cycle, 717 prevention, 716 species, 717 treatment, 718 Entamoeba diagnosis, 720 treatment, 720 fecal examination, 705–707, 706t, 714 giardiasis clinical signs, 718–719 diagnosis, 719 life cycle, 718 prevention, 719 treatment, 719 hookworm clinical signs, 715 diagnosis, 715 life cycle, 715 prevention, 715–716 species, 715 treatment, 715 Strongyloides clinical signs, 716–717 diagnosis, 717 life cycle, 716 species, 716 treatment, 717 tapeworm clinical signs, 717 diagnosis, 717 life cycle, 717 species, 717 treatment, 717 Tritrichomonas foetus clinical signs, 719 diagnosis, 719 treatment, 719–720 whipworm clinical signs, 716 diagnosis, 716 life cycle, 716 prevention, 716 species, 716 treatment, 716 Intestinal surgery anatomy, 739 antibiotic prophylaxis, 739 colotomy complications, 743 equipment, 743 indications, 742 objectives, 742 postoperative care, 743 preoperative considerations, 742 prognosis, 743 technique, 743
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Intestinal surgery (Continued) enteroenteroplexy/coloplexy complications, 742 equipment, 741 indications, 741 objectives, 741 postoperative care, 742 technique, 741–742, 742f enterotomy complications, 740 equipment, 739 objectives, 739 postoperative care, 740 preoperative considerations, 739 prognosis, 740 technique, 739–740 resection and anastomosis complications, 741 equipment, 741 indications, 740 objectives, 740 postoperative care, 741 preoperative considerations, 740 technique, 741 subtotal colectomy complications, 744–745 equipment, 743 indications, 743 objectives, 743 postoperative care, 744–745 preoperative considerations, 743 technique, 743–744, 744f typhlectomy equipment, 745 indications, 745 objectives, 745 postoperative care, 745 preoperative considerations, 745 prognosis, 745 technique, 745 Intestines, physical examination, 14 Intraocular pressure measurement. See Tonometry Intraosseous catheterization complications, 31 contraindications, 30 equipment, 31 ferret, 1820 fluid therapy, 97 indications, 30 reptiles, 1924, 1924f rodents, 1889 technique, 31, 31f Intravenous catheterization anesthesia, 18 cutdown contraindications, 29 equipment, 29 objective, 29 technique, 29–30, 30f ferret, 1819–1820 fluid therapy. See also Fluid therapy catheter care, 96 catheter selection, 96 vein selection, 96 Intravenous pyelogram, technique, 69–70 Intravenous urogram, technique, 69–70 Iodine, reptile dosage guidelines, 1927t Iopanoic acid, hyperthyroidism management, 336 Iris. See Uvea Iron, deficiency and anemia, 240–241 Irritable bowel syndrome (IBS) clinical signs, 732–733 diagnosis, 733 etiology, 732 treatment, 733
Ischemic encephalopathy, feline, 1261 Ischium. See Pelvis Isoflurane applications, 26 dosage guidelines cats, 23t dogs, 23t Isoproterenol, formulations, indications, and dosages, 1458t Isosorbide dinitrate, dosage guidelines, 1474t Isotretinoin ichthyosis management, 514 schnauzer comedo syndrome management, 513 Itraconazole adverse effects, 216 avian administration, 1742 blastomycosis management, 209 cryptococcosis management, 213 dermatophytosis management, 457, 457t dosage and administration, 216 feline symmetrical alopecia management, 528 fungal cystitis management, 908 histoplasmosis management, 208 Malassezia dermatitis management, 449, 449t onychomycosis management, 608 pharmacology, 216 Ivermectin avian administration, 1792 canine demodicosis management, 462 cheyletiellosis management, 472–473 dosage guidelines dogs, 714t ferrets, 1821 rabbits, 1863t reptiles, 1927t rodents, 1893t ferret administration, 1844 heartworm prevention, 1572 notoedric mange management, 470 otitis externa management, 580 scabies management, 468 toxicity features and management, 462, 1267 Jaundice, liver disease, 747 Joint fluid analysis, immune-mediated arthritis, 1229, 1231, 1231t Jugular vein bird venipuncture, 1737 evaluation, 1423, 1423f turtle venipuncture, 1922, 1922f Juvenile cellulitis clinical signs, 573 diagnosis, 573 treatment, 573 Kaopectate, diarrhea management, 712 Kennel cough clinical signs, 151–152 diagnosis, 152 etiology, 151 pathogenesis, 151 prevention, 153 transmission, 151 treatment, 152–153 vaccination, 153 Keratinization defects canine ear margin dermatosis, 515–516 epidermal dysplasia, 511–512 ichthyosis, 513–514 idiopathic nasodigital hyperkeratosis, 514–515 lichenoid-psoriasiform dermatosis, 512
Keratinization defects (Continued) primary defects of keratinization clinical signs, 508 diagnosis, 508–509 etiology, 508 primary idiopathic seborrhea, 509–510 schnauzer comedo syndrome, 512–513 sebaceous adenitis, 514 vitamin A-responsive dermatosis, 510 zinc-responsive dermatosis, 511 Keratoacanthoma, features and management, 322 Keratoconjunctivitis sicca etiology, 1391 qualitative tear deficiencies, 1392–1393 quantitative tear deficiencies clinical signs, 1391 diagnosis, 1391–1392 histology, 1391 treatment, 1392 Ketamine applications, 22 dosage guidelines cats, 21t, 103t dogs, 20t, 103t rabbits, 1863t reptile anesthesia, 1925 rodent dosage guidelines, 1890t Ketamine/acepromazine applications, 24 dosage guidelines cat, 21t dog, 20t ferret, 1821t rabbit, 1863t Ketamine/diazepam applications, 24 dosage guidelines cat, 21t, 23t dog, 20t, 23t ferret, 1821t rabbit, 1863t rodent, 1890t Ketamine/medetomidine applications, 24–25 rabbit dosage guidelines, 1863t Ketamine/midazolam, rabbit dosage guidelines, 1863t Ketamine/xylazine applications, 24 dosage guidelines cat, 21t dog, 20t ferret, 1821t rodent, 1890t Ketoconazole adverse effects, 217 blastomycosis management, 210 cryptococcosis management, 213 dermatophytosis management, 457, 457t dosage and administration, 217 fungal cystitis management, 908 histoplasmosis management, 208 hyperadrenocorticism management, 365–366, 370 Malassezia dermatitis management, 449, 449t onychomycosis management, 608 pharmacology, 217 prostatic neoplasia management, 955–956 reptile dosage guidelines, 1927t Ketoprofen dosage guidelines, 22t, 104t osteoarthritis management, 1225 rabbit dosage guidelines, 1863t Kidney anatomy, 889
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Index Kidney (Continued) biopsy equipment, 890 objectives, 889 postoperative care and complications, 890 preoperative considerations, 889 technique, 890 diseases. See Renal disease nephrectomy equipment, 892 objectives, 891–892 postoperative care and complications, 892 preoperative considerations, 891 technique, 892 nephrotomy equipment, 890 objectives, 890 postoperative care and complications, 891 preoperative considerations, 890 technique, 890–891, 890f physical examination, 14, 14f Kidney worm clinical signs, 883 diagnosis, 883 epidemiology, 883 prevention, 883 treatment, 883 Kilovolt peak check, X-ray machine, 55 King snake. See Reptiles Kirby Bauer susceptibility test, antibiotic selection, 1754–1755 Knott test, heartworm microfilaria detection, 1565 Labor. See Parturition Labrador retriever hereditary myopathy, 1316–1317 skeletal dysplasia, features and management, 1192–1193 Lacrimal system anatomy, 1390–1391 cherry eye, 1395 epiphora diseases, 1393–1395 keratoconjunctivitis sicca etiology, 1391 qualitative tear deficiencies, 1392–1393 quantitative tear deficiencies, 1391–1392 topical diagnosis of disorders, 1415–1416 Lactate, neuromuscular disease evaluation, 1321 Lagenidiosis clinical signs, 438 diagnosis, 439 etiology, 438 systemic infection, 214t treatment, 439 Lagophthalmos, features and management, 1336 Lamotrigine, canine toxicity, 1288 Larynx collapse features and management, 1651, 1658–1660, 1659f diagnostic evaluation, 1624 neoplasms clinical signs, 1709 diagnosis, 1709 prognosis, 1709 treatment, 1709 tumor types, 1708, 1708t paralysis features and management, 1651, 1656–1658, 1657f, 1658f sacculectomy, 1655–1656 Latanoprost, glaucoma management, 1377
Lateral bulla osteotomy equipment, 599 objectives, 599 postoperative care and complications, 600 preoperative considerations, 599 prognosis, 600 technique with total ear canal ablation, 600 technique without total ear canal ablation, 599–600, 600f Lateral ear canal resection (LECR) equipment, 585 objectives, 584 postoperative care and complications, 586 prognosis, 586 technique, 585–586, 585f Laxatives bulk-forming laxatives, 835–836 classification, 834–835, 835t emollient laxatives, 836 lubricant laxatives, 836 osmotic laxatives, 836 stimulant laxatives, 836 Lead anemia induction, 242 poisoning avian, 1813–1814 clinical features and management, 1265–1266 LECR. See Lateral ear canal resection Left anterior fascicular block, electrocardiography, 1445, 1446f Left atrium enlargement electrocardiography, 1449, 1449f radiography, 1434–1435, 1434f rupture, 1440, 1516–1517 Left bundle branch block, electrocardiography, 1444–1445, 1445f Left ventricle, enlargement electrocardiography, 1449–1450, 1449f radiography, 1435, 1435f Legg-Calvé-Perthes disease, 1118–1119 Leiomyoma, female genitalia, 1006 Leiomyosarcoma biologic behavior, 302 clinical signs, 303–304 female genitalia, 1007 staging, 304, 304t treatment, 304–305 Leishmaniasis clinical signs, 228 diagnosis, 228 etiology, 228 nonregenerative anemia, 239–240 prevention, 229 systemic infection, 220t treatment, 228–229 Lens. See also Cataract anatomy, 1360 congenital anomalies, 1360 luxation clinical signs, 1364 diagnosis, 1364 dog breed susceptibility, 1364t etiology, 1363–1364 prevention, 1365 treatment, 1364–1365 Leonberger dog, hereditary axonal polyneuropathy, 1308 Leprosy. See Feline leprosy syndromes Leptospirosis clinical signs, 193 diagnosis, 193–194 etiology, 191 hemolysis, 237
1985
Leptospirosis (Continued) human infection prevention, 195 pathogenesis, 191 prevalence, 191 prevention, 194–195 transmission, 191 treatment, 194, 868 vaccination protocols, 109t, 110t, 111t Leukemia. See Lymphoid leukemia; Myeloid leukemia; see also specific leukemias Leuprolide acetate excessive egg laying management, 1797, 1797t feather picking management, 1770–1771 ferret adrenal disease management, 1834 Levamisole avian administration, 1792 parasitic cystitis management, 908 reptile dosage guidelines, 1927t Levetiracetam dog administration, 1285t epilepsy management, 1287 Lichenoid-psoriasiform dermatosis clinical signs, 512 diagnosis, 512 etiology, 512 pinna, 571–572 treatment, 512 Lidocaine administration, 1492 advanced life support, 1616 adverse effects, 1492 dosage guidelines, 104t, 1474t formulations, indications, and dosages, 1458t response test, 1452 Limb neoplasia amputation anatomy, 1179 pelvic limb amputation hip disarticulation, 1182–1183, 1184f midfemur, 1180, 1182 postoperative care and complications, 1183–1184 preoperative considerations, 1179–1180 thoracic limb amputation with scapula removal, 1180, 1181–1183f biopsy, 1178, 1178f clinical signs, 1177 diagnosis, 1177–1178 etiology, 1176–1177, 1177t limb-sparing procedures, 1185 metastasis management, 1184 treatment chemotherapy, 1179 radiation therapy, 1179 surgery, 1178–1179 Lime sulfur dip cheyletiellosis management, 472 notoedric mange management, 470 rabbit dosage guidelines, 1863t rodent dosage guidelines, 1893t scabies management, 468 Lipase, pancreatic function testing, 822–823 Lipemia, avian, 1814–1815 Lipoma avian, 1762 features and management, 322–323 female genitalia, 1006 Liposarcoma avian, 1762 biologic behavior, 302 clinical signs, 303–304 staging, 304, 304t treatment, 304–305, 322–323 Lisinopril, dosage guidelines, 1475t
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Lissencephaly, clinical features and management, 1269 Little white shaker syndrome clinical signs, 1259–1260 diagnosis, 1260 etiology, 1259 prognosis, 1260 treatment, 1260 Liver disease amyloidosis. See Hepatic amyloidosis anemia, 241 arteriovenous fistula. See Hepatic arteriovenous fistula avian disorders, 1792–1794 cancer. See Hepatobiliary neoplasia canine vacuolar hepatopathies. See Glucocorticoid hepatopathy; Miniature Schnauzer vacuolar hepatopathy; Scottish terrier vacuolar hepatopathy; Superficial necrolytic dermatitis cholelithiasis. See Cholelithiasis cirrhosis. See Hepatic cirrhosis clinical signs acute versus chronic disease, 747 angiography, 755 ascites, 748 bilirubinuria, 747 biopsy analysis, 756 fine-needle aspiration, 755–756 laparoscopy, 756 laparotomy, 756 ultrasound guidance, 756 blood gas analysis, 755 coagulopathy, 747–748 hepatic encephalopathy, 748 history, 748 jaundice, 747 laboratory testing albumin, 751–752 ammonia tolerance test, 754 bilirubin, 751 blood ammonia concentration, 754 blood urea nitrogen, 752 cholesterol, 752 coagulation tests, 754–755 complete blood count, 749 electrolytes, 752 fasting serum bile acid, 752–753 globulin, 752 glucose, 752 liver enzymes, 749–751 postprandial serum bile acid, 753 protein C, 754 urinalysis, 749 urine bile acid, 753–754 nonspecific signs, 747 physical examination, 748 polyuria/polydipsia, 747 radiography, 755 ultrasound, 755 cysts. See Hepatic cysts failure. See Acute hepatic failure feline inflammatory liver disease. See Lymphocytic cholangitis; Lymphocytic portal hepatitis; Neutrophilic cholangitis hepatic lipidosis. See Feline hepatic lipidosis infectious disease abscess, 767–769 etiology, 766–767, 768t liver fluke, 769–770 microvascular dysplasia. See Hepatic microvascular dysplasia
Liver disease (Continued) nodular hyperplasia. See Hepatic nodular hyperplasia phenobarbital induction. See Phenobarbital-associated hepatic disease physical examination, 13 portal vein hypoplasia. See Primary portal vein hypoplasia portosystemic shunts. See Portosystemic shunt treatment ascites, 759 coagulopathy, 759 drug metabolism considerations, 757 gastrointestinal ulceration, 759 general therapy, 757–758t hepatic encephalopathy, 758–759 hepatoprotectants, 759, 760t, 761 infection, 759 nutrition, 758 objectives, 756–757 renal failure, 759 Liver fluke clinical signs, 769 diagnosis, 769 species, 769 treatment, 770 Liver surgery anatomy attachments, 810 blood supply, 810 lobes, 810 biopsy and partial hepatectomy equipment, 811 objectives, 811 postoperative care and complications, 812 technique, 811–812, 812f portosystemic shunt surgery. See Portosystemic shunt preoperative considerations, 810–811 Lizards. See Reptiles Lobular dissecting hepatitis clinical signs, 785 diagnosis, 786 treatment, 786 Lomustine brain tumor management, 1253 chemotherapy guidelines, 288t Loperamide diarrhea management, 711t inflammatory bowel disease management, 728t, 730 Lorikeet tetraparesis, features and management, 1815 Lower motor neuron bladder clinical signs, 941, 943 diagnosis, 943–945 treatment, 945 Lufenuron dermatophytosis management, 457 flea control, 477t Malassezia dermatitis management, 450 Lumpectomy, mammary gland tumor, 313 Lung auscultation, 1626 biopsy bronchoscopic biopsy, 1628 fine-needle aspiration, 1628 keyhole lung biopsy, 1628 risks, 1628–1629 lobe torsion, 1705 lobectomy, 1728–1730, 1729f neoplasms clinical signs, 1711 diagnosis, 1711–1712
Lung (Continued) epidemiology, 1710 prognosis, 1712 treatment, 1712 tumor types, 1710–1711, 1710t percussion, 1636 pulmonary contusion, 1719–1720 Lupus erythematosus complex canine lupus onychitis, 498 diagnosis, 498 discoid lupus erythematosus, 497–499 etiology, 497 exfoliative cutaneous lupus erythematosus, 498 pinna, 570 systemic lupus erythematosus, 498 treatment, 498–499 vesicular cutaneous lupus erythematosus, 498 Luteinizing hormone, timing of ovulation, 1015 Lyme disease. See Borreliosis Lymph nodes, physical examination, 12, 12f, 14 Lymphangiography, pleural effusion, 1699 Lymphangiosarcoma biologic behavior, 302 clinical signs, 303–304 staging, 304, 304t treatment, 304–305 Lymphocytic cholangitis, features, 802 Lymphocytic portal hepatitis, features, 802 Lymphocytic-plasmacytic inflammatory bowel disease clinical signs, 725 diagnosis dietary hypersensitivity, 726–727 endoscopy, 726 histopathology, 726 laboratory findings, 725–726 radiography, 726 ultrasound, 726 etiology, 725 prognosis, 730 treatment 5-aminosalicylic acid, 728t, 729 azathioprine, 728t, 729–730 cobalamin, 727 cyclosporine, 728t, 730 diet, 727 glucocorticoids, 728–729, 728t loperamide, 728t, 730 mesalamine, 728t, 729 metronidazole, 728t, 729 olsalazine, 728t, 729 sulfasalazine, 728t, 729 Lymphocytosis, etiology, 248 Lymphoid leukemia acute lymphoblastic leukemia, 298 chronic lymphocytic leukemia, 298–299 prognosis, 299 Lymphoma chemotherapy considerations, 295 cytopenia considerations, 296 induction protocols, 295–296, 296t reinduction therapy, 297 rescue therapy, 297 classification and clinical signs, 292–293 cutaneous therapy, 297 diagnosis, 293–295 etiology, 292 extranodal therapy, 297 hypercalcemia management, 297 peripheral nerves, 1310
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Index Lymphoma (Continued) prognosis cats, 298 dogs, 297–298 small cell variant, 297 staging, 293t Lymphopenia, etiology, 248 Lymphosarcoma, ferrets, 1825, 1836–1837 Lysosomal storage diseases, 242, 1273t Magnesium diabetic ketoacidosis management, 380 dosage guidelines, 1475t hypocalcemia management, 353 parenteral fluid supplementation, 93 Magnetic resonance imaging (MRI) adrenal tumors, 362 advantages and disadvantages, 77 brain trauma, 1263 brain tumors, 1252–1253 caudal cervical spondylomyelopathy, 1059t infectious meningoencephalitis, 1256–1257 nasal cavity diseases, 1623 neurologic disease assessment, 1243 neuromuscular disease, 1323 pituitary tumors, 400 principles, 77 respiratory disease, 1642 spinal cord disorders, 1299 Malassezia dermatitis (MD) clinical signs canine dermatitis, 447 canine otitis, 447 feline dermatitis and otitis, 447–448 diagnosis, 448–449 etiology, 445 feline symmetrical alopecia, 525 human zoonosis, 448 pathogenesis canine dermatitis, 445–446 canine mucositis, 447 canine otitis, 446–447 feline dermatitis and otitis, 447 pinna, 566–567 treatment immunotherapy, 450 systemic therapy, 449–450 topical therapy, 450 Malignant fibrous histiocytoma biologic behavior, 303 clinical signs, 303–304 staging, 304, 304t treatment cat, 305 dog, 304–305 Malignant hyperthermia syndrome, 1319 Malocclusion, rabbits, 1872–1873 Malunion closed wedge osteotomy, 1220, 1220f diagnosis, 1219 postoperative care and complications, 1221 preoperative considerations, 1219 prognosis, 1221 Mammary gland tumor (MGT) chemotherapy, 314 clinical signs, 311 diagnosis, 311–312 etiology, 311 prevention, 315 prognosis cats, 314–315 dogs, 314 risk factors, 311
Mammary gland tumor (MGT) (Continued) surgery biopsy, 314 lumpectomy, 313 mastectomy, 313 ovariohysterectomy, 314 pain control, 314 preoperative considerations, 312–313 technique, 313–314 Mandible anatomy, 1037, 1050–1051 fracture body fracture fixation acrylic bonding, 1040 acrylic splint, 1040 bone plating, 1041 external skeleton fixation, 1040–1041 tape muzzle, 1039, 1045f wiring, 1040 clinical signs, 1037 diagnosis, 1037 epidemiology, 1037 ramus fracture condylectomy, 1041 surgery, 1037–1038 mandibulectomy bilateral rostral mandibulectomy, 1053 hemimandibulectomy, 1053–1054 unilateral rostral mandibulectomy, 952–1053, 1053f neoplasia benign non-odontogenic neoplasms, 1048–1049 diagnosis, 1047–1048 malignant non-odontogenic neoplasms, 1049–1050 malignant odontogenic neoplasms, 1050 surgery, 1050–1051, 1053–1054 types, 1048t symphyseal separation wire fixation, 1038–1039 temporomandibular joint dislocation, 1042 dysplasia, 1042 Mange. See Notoedric mange Mannitol acute renal failure management, 865–866 brain trauma management, 1263 brain tumor management, 1253 glaucoma management, 1376, 1376t prolonged life support, 1619 MAP. See Mean arterial pressure Marsupialization, prostate, 960 Mast cell tumor (MCT) biologic behavior, 306–307 clinical signs, 307 diagnosis, 307–308 epidemiology, 305 etiology, 305–306 staging, 307t treatment, 308–309, 309t Mast cell tumor, ferrets, 1841 Mastectomy, mammary gland tumor, 313 Masticatory muscle myositis diagnosis, 1321 features, 1318 treatment, 1324 Mastitis chinchilla, 1905 ferrets, 1853 rabbits, 1874–1875 rodents, 1893 Maxilla anatomy, 1043, 1050–1051 fracture clinical signs, 1043 diagnosis, 1043
1987
Maxilla (Continued) surgery anesthesia, 1043–1044 body fractures, 1044–1046 complications, 1046 equipment, 1044 midline separations, 1044 objectives, 1044 postoperative care, 1046 preoperative considerations, 1043 maxillectomy bilateral premaxillectomy, 1051, 1052f hemimaxillectomy, 1051–1052, 1052f unilateral premaxillectomy, 1051 neoplasia benign non-odontogenic neoplasms, 1048–1049 diagnosis, 1047–1048 malignant non-odontogenic neoplasms, 1049–1050 malignant odontogenic neoplasms, 1050 surgery, 1050–1052, 1054 types, 1048t MCE. See Multiple cartilaginous exostosis MCS. See Muscle condition score MCT. See Mast cell tumor MD. See Malassezia dermatitis; Miliary dermatitis Mean arterial pressure (MAP), monitoring in shock, 1605 Mean blood pressure, 1575 Mebendazole reptile dosage guidelines, 1927t rodent dosage guidelines, 1893t Meclofenamic acid, osteoarthritis management, 1225 Medetomidine applications, 20–21 dosage guidelines cats, 21t, 103t dogs, 20t, 103t rabbits, 1863t reptiles, 1926 Mediastinal fluid, radiography, 1633 Mediastinal shift, radiography, 1633 Medroxyprogesterone acetate, excessive egg laying management, 1797, 1797t Megacolon clinical signs, 837 diagnosis, 837 etiology, 837 treatment, 837 Megaesophagus features and management ferrets, 1846–1847 physical examination, 13 Megestrol acetate benign prostatic hyperplasia management, 954 feline symmetrical alopecia management, 529 Meglumine antimonite, leishmaniasis management, 229 Melanoma eye, 1358–1359 features and management, 324–325 oropharyngeal, 1049 uvea, 1372–1373 Melanosis, corneal, 1357 Meloxicam dosage guidelines, 22t, 104t osteoarthritis management, 1225 reptile analgesia, 1926 Melphalan, chemotherapy guidelines, 288t
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Menace response cranial nerve examination, 1235 eye neurologic disturbance evaluation, 1409, 1417 Meningoencephalitis, infectious diagnosis, 1255–1257 etiology, 1254–1255, 1255t, 1256t treatment, 1257–1258, 1257t Meningioencephalomyelitis. See Granulomatous meningioencephalomyelitis Meningitis, management, 1300 Meniscus, injury and repair, 1140–1141 Meperidine applications, 22 dosage guidelines cats, 21t, 103t dogs, 20t, 103t Mesalamine, inflammatory bowel disease management, 728t, 729 Mesenteric portography, technique, 791 Metabolic encephalopathy, 1264, 1264t Metacarpal fracture anatomy, 1163 base and head fracture management, 1165 body fractures, 1163 surgical management, 1163–1165, 1164f, 1165f Metaldehyde poisoning, clinical features and management, 1266 Metatarsal fracture anatomy, 1163 base and head fracture management, 1165 body fractures, 1163 surgical management, 1163–1165, 1164f, 1165f Metformin, diabetes type 2 management, 387, 387t Methazolamide, glaucoma management, 1376–1377, 1376t Methemoglobinemia clinical features, 243–244 diagnosis, 244 treatment, 244 Methicillin-resistant staphylococcal skin infection, 428 Methimazole, hyperthyroidism management, 335 Methoprene, flea control, 477t, 478 Methotrexate, chemotherapy guidelines, 288t Methoxyflurane, dosage guidelines cats, 23t dogs, 23t Methylphenidate cataplexy management, 1293 narcoplexy management, 1293 Methylprednisolone. See Glucocorticoids 4-Methylpyrazole, antifreeze toxicosis treatment, 868 Methylxanthine toxicosis, clinical features and management, 1266 Methyridine, rodent dosage guidelines, 1893t Metoclopramide gastric motility disorder management, 685 gastroduodenal ulceration management, 673, 675t reflux esophagitis management, 646 reptile dosage guidelines, 1927t vomiting management, 667, 667f Metoprolol dosage guidelines, 1475t formulations, indications, and dosages, 1459t pharmacology, 1486–1487
Metritis avian, 1802–1803 ferrets, 1852–1853 Metronidazole avian administration, 1792 feather picking management, 1769 inflammatory bowel disease management, 728t, 729 reptile dosage guidelines, 1924t rodent dosage guidelines, 1895t toxicity features and management, 1267–1268 Metyrapone, hyperadrenocorticism management, 370 Mexiletine administration, 1492 adverse effects, 1492 dosage guidelines, 1475t formulations, indications, and dosages, 1459t ventricular tachycardia management in dogs, 1548 MGT. See Mammary gland tumor Microcornea, features and management, 1347–1348 Microphthalmos, 1402 Microsporum canis. See Dermatophytosis Microsporum gypseum. See Dermatophytosis Micturition disorders bladder function, 940 clinical signs, 943 diagnosis, 943–945 etiology, 941–943, 941t nervous control, 940–941 treatment endoscopic injection, 948 pharmacotherapy, 945, 946–947t, 947–948 surgery, 948 Midazolam applications, 21 dosage guidelines cats, 21t dogs, 20t rabbits, 1861t Milbemycin oxime (Interceptor), heartworm treatment and prevention, 1570, 1572 canine demodicosis management, 462 cheyletiellosis management, 472–473 dosage guidelines, 714t scabies management, 468 Miliary dermatitis (MD) clinical signs, 532 diagnosis allergy testing, 533–534 blood tests, 533 history, 532–533 physical examination, 533 skin sampling and biopsy, 533 etiology, 531–532, 532t treatment allergen avoidance, 534 allergen-specific immunotherapy, 535 antihistamines, 535 antimicrobial therapy, 535 glucocorticoids, 534 immunomodulation, 535 progestational therapy, 535–536 Milk snake. See Reptiles Milliampere station check, X-ray machine, 54–55 Milrinone administration, 1479 congestive heart failure management, 1503 indications, 1479
Miniature Schnauzer vacuolar hepatopathy clinical signs, 774–775 diagnosis, 775 differential diagnosis, 772, 773t etiology, 774 treatment, 775 Minimum database, neurologic patients, 1298 Misoprostil atopic dermatitis management, 486t, 487 gastroduodenal ulceration management, 673, 675t, 677 Mites. See Avian dermatology; Cheyletiellosis; Demodicosis; Notoedric mange; Scabies Mithramycin, hypercalcemia management, 348 Mitochondrial myopathy, 1317 Mitotane adverse effects, 367 ferret adrenal disease management, 1835 hyperadrenocorticism management, 364–367, 370 Mitoxantrone, chemotherapy guidelines, 288t Mitral valve disease chordae tendinae rupture, 1516 endocardiosis, 1496 left-sided cardiomegaly, 1515 malformation, 1499 physical examination, 1428–1429 prognosis, 1522 pulmonary venous pressure effects, 1516 radiography, 1438 regurgitant volume, 1515 treatment asymptomatic dog, 1519–1520 coughing dog with mitral regurgitation, 1520 follow-up, 1522 left-sided congestive heart failure, 1520–1521 respiratory complications, 1521–1522 Modafinil cataplexy management, 1293 narcoplexy management, 1293 Modified Sliding Scale of Scott, potassium supplementation, 91, 91t Monitor. See Reptiles Monocytosis corticosteroid induction, 246 inflammatory, 247 Morphine applications, 22 arterial thromboembolism management, 1540 dosage guidelines cats, 21t, 103t dogs, 20t, 103t rabbits, 1863t Morphine/lidocaine/ketamine, dosage guidelines, 103t Mouse. See Rodents Moxidectin heartworm prevention, 1572 scabies management, 469 MRI. See Magnetic resonance imaging Mucocele, exophthalmos, 1401 Mucopolysaccharidosis, 244 Multiple cartilaginous exostosis (MCE) clinical signs, 1191 diagnosis, 1191 etiology, 1191 treatment, 1191 Multiple myeloma clinical signs, 299 diagnosis, 299
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Index Multiple myeloma (Continued) epidemiology, 299 hypercalcemia association, 348 prognosis, 299 treatment, 299 Muscle. See Neuromuscular diseases; Skeletal muscle Muscle condition score (MCS), 45, 47f Muscular dystrophy dystrophin-deficient muscular dystrophy, 1315 merosin deficiency, 1315 sarcoglycan deficiency, 1315–1316 Musculoskeletal system history taking, 6 physical examination, 16 Myasthenia gravis acquired disease, 1318 autoantibody assay, 1321 congenital disease, 1318 edrophonium chloride challenge test, 1321–1322 treatment focal disease, 1324 generalized disease, 1323–1324 Mycetoma clinical signs, 442–443 etiology, 442 treatment, 443 Mycobacterial panniculitis clinical signs cats, 432 dogs, 432 diagnosis, 432–433 etiology, 432 prevention, 434 treatment, 433–434 Mycobacteriosis. See also Canine leproid granuloma syndrome; Feline leprosy syndromes; Mycobacterial panniculitis clinical signs, 201 diagnosis, 201 etiology, 201 human infection, 202 treatment, 201–202 Mycoplasma felis diagnosis, 147 infection routes, 144 respiratory disease, 144 treatment, 147–148 Mycoplasmosis avian, 1777 turtles, 1938 Myelitis, management, 1300 Myelofibrosis, idiopathic, 253–254 Myelography cisternal tap, 72 complications, 73 indications and contraindications, 72 interpretation, 73 lumbar tap, 73 spinal cord disorders, 1298–1299 Myeloid leukemia acute myeloid leukemias, 252 clinical signs, 251 diagnosis, 251 myelodysplastic syndrome, 251–252 treatment, 251 Myelophthisis myelofibrosis, 242 myelonecrosis, 243 neoplasia, 242 osteopetrosis, 243 Myiasis rabbits, 1865–1866 turtles, 1941 Myocardial contusion, treatment, 1720
Myocarditis cats, 1534–1535 dogs, 1542 ferrets, 1845 Myoptonia congenita, 1317 Myringotomy, otitis media and otitis interna management, 596 Myxosarcoma biologic behavior, 302 clinical signs, 303–304 staging, 304, 304t treatment, 304–305 Nalbuphine applications, 22 dosage guidelines cats, 21t dogs, 20t Nalorphine, rodent dosage guidelines, 1890t Naloxone, dosage guidelines, 28t Naltrexone, feather picking management, 1770 Naproxen, dosage guidelines, 104t Narcoplexy clinical signs, 1292 diagnosis, 1292–1293 etiology, 1292 pathophysiology, 1292 prognosis, 1293 treatment, 1293 Nasal catheter complications, 33 contraindications, 32 equipment, 32 indications, 32 objectives, 32 placement technique, 33, 33f Nasal cavity anatomy, 1643, 1644f neoplasms clinical signs, 1706–1707 diagnosis, 1706–1707 epidemiology, 1706 prognosis, 1708 treatment, 1707–1708 tumor types, 1706, 1707t polyp features and management, 1651, 1653, 1659–1660 radiography abnormalities, 1631–1632 anatomy, 1630 three-dimensional imaging, 1623 surgery bilateral carotid artery occlusion, 1646, 1646f complications, 1650 dorsal rhinotomy, 1646–1648, 1646f, 1647f equipment, 1646 objectives, 1645–1646 postoperative care, 1649–1650 preoperative considerations, 1643–1645 prognosis, 1650 sinus flushing, 1649 sinus obliteration, 1649 ventral rhinotomy, 1648–1649, 1648f, 1649f Nasal discharge, diagnostic evaluation, 1621–1623 Nasal wedge resection, 1654, 1654f Nasolacrimal duct congenital obstructions, 139 imperforate, 1393 irrigation, 1329–1330 Nasopharyngeal polyp surgery objectives, 601–602 postoperative care and complications, 602
1989
Nasopharyngeal polyp surgery (Continued) preoperative considerations, 601 prognosis, 602 technique, 602 NDV. See Newcastle disease virus Neck, physical examination, 11–12, 11f Necrotizing dermatoses burn injury, 505–506 chemical injury, 505 classification, 501t clinical signs, 500 decubitus ulcers, 506 diagnosis history, 500 laboratory testing, 500–501 physical examination, 500 skin biopsy, 501 drug-induced necrosis, 503 erythema multiforme, 504 frostbite, 506 immune-mediated dermatoses clinical signs, 506 treatment, 506–507 infection-induced necrosis, 507 neoplasia-related skin necrosis, 502–503 radiation injury, 505 snake bite, 505 spider bite, 505 superficial necrolytic dermatitis, 504–505 toxic epidermal necrolysis, 503–504 treatment principles, 502 vascular compromise, 507 vasculitis, 502 Necrotizing encephalitis, 1259 Necrotizing vasculitis, beagle, Bernese mountain dog, and German shorthaired pointer, 1261–1262 Nemalin rod myopathy, 1317 Neomycin, rodent dosage guidelines, 1895t Neoplasia-related skin necrosis clinical signs, 503 pathophysiology, 502–503 treatment, 503 Neorickettsiosis clinical signs, 184 diagnosis, 184 etiology, 183 feline Ehrlichia-like diseases, 185 laboratory findings, 184 Neorickettsia helminthoeca. See Salmon poisoning disease prevention, 184 treatment, 184 Neosporosis clinical signs, 226 diagnosis, 226 etiology, 225–226 prevention, 226 treatment, 226 Neostigmine, myasthenia gravis management, 1323 Nephrectomy equipment, 892 objectives, 891–892 postoperative care and complications, 892 preoperative considerations, 891 technique, 892 Nephrogenic diabetes insipidus, features and management, 879–880 Nephrolithiasis clinical signs, 881–882 diagnosis, 882 etiology, 881 prevention, 883 treatment, 882–883 Nephrotic syndrome, heartworm, 1563
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Nephrotomy equipment, 890 objectives, 890 postoperative care and complications, 891 preoperative considerations, 890 technique, 890–891, 890f Nerve biopsy, peripheral nerve disorders, 1305 Nerve conduction study interpretation, 1246t, 1247–1248 peripheral nerve disorders, 1305 technique, 1247 Nerve injury axonotmesis, 1313 clinical signs in limbs, 1313t nerve root avulsions, 1313–1314 neurapraxia, 1312 neurotmesis, 1313 Nerve sheath tumors biologic behavior, 302 clinical signs, 303–304 staging, 304, 304t treatment, 304–305 Nervous system history taking, 6–7 physical examination, 16 Nesiritide, canine applications, 1476 Neuroaxonal dystrophy, multisystem, 1271–1272 Neurologic examination birds, 1810 circling, 1234 cranial nerve examination, 1235–1237 gait, 1234 head posture, 1233–1234 interpretation, 1240, 1240f mental status, 1233 nociceptive evaluation, 1239–1240 postural reaction tests hemihopping, 1234 proprioceptive positioning, 1234 wheelbarrowing, 1235 principles, 1233 spinal cord disorders, 1298 spinal reflex examination, 1237–1239 stance, 1234 Neuromuscular diseases breed dispositions, 1316t clinical signs, 1320 diagnosis, 1320–1323 etiology acquired disorders, 1318–1320 hereditary disorders, 1315–1318 treatment, 1323–1324 Neurotmesis, 1313 Neutropenia congenital cyclic neutropenia, 245–246 drug and toxin induction, 246 immune mediation, 246 infectious, 246 paraneoplastic syndrome, 246 Neutrophilia corticosteroid induction, 245 inflammatory, 245 physiologic, 245 Neutrophilic cholangitis associations and predispositions, 800 clinical signs, 800 diagnosis, 800–801 etiology, 800 prognosis, 802 treatment, 801–802 Neutrophilic enterocolitis clinical signs, 732 diagnosis, 732 etiology, 732 treatment, 732
Neutrophilic leukemia, 253 Newcastle disease virus (NDV) clinical signs, 1751 diagnosis, 1751–1752 etiology, 1751 prevention, 1752 respiratory disease in birds, 1780 transmission, 1751 treatment, 1752 Niacinamide. See also Tetracycline/niacinamide lupus erythematosus complex management, 499 pemphigus complex management, 495 Niclosamide, rodent dosage guidelines, 1893t Nictitating membrane cherry eye, 1395 examination, 1327 movement abnormalities, 1417–1418 neurologic control of movement, 1411 Niemann-Pick disease, clinical features, 1306 Nitenpyram, flea control, 477t, 479 Nitroglycerine adverse effects, 1481 congestive heart failure management, 1501–1502, 1538–1539 dosage guidelines, 1475t indications, 1480–1481 Nitroprusside sodium adverse effects, 1481 congestive heart failure management, 1501–1502, 1539 dosage guidelines, 1475t hypertension management, 1579 indications, 1481 Nitrous oxide, applications, 26 Nizatidine chronic gastritis management, 679 constipation management, 835t, 836 gastric motility disorder management, 684 gastroduodenal ulceration management, 673, 674t Nociception, neurologic evaluation, 1239–1240 Nonsteroidal anti-inflammatory drugs (NSAIDs). See also Gastroduodenal ulceration; specific drugs applications, 21 dosage guidelines, 22t osteoarthritis management, 1224–1225 precautions, 106 uveitis management, 1371–1372, 1371t Nonunion associated factors, 1215t definition, 1214–1215 diagnosis, 1216–1217 expected fracture healing time, 1215t postoperative care and complications, 1218–1219 preoperative considerations, 1216–1217 prognosis, 1219 surgery, 1217–1218, 1217–1218f viable versus nonviable, 1214, 1215t Norwegian Forest cat, glycogen storage disease, 1306 Nose catheterization. See Nasal catheter physical examination, 10–11 Notoedric mange clinical signs, 469 diagnosis, 470 etiology, 469, 469f feline symmetrical alopecia, 525 treatment dips, 470 systemic therapy, 470
NSAIDs. See Nonsteroidal anti-inflammatory drugs Nutrition. See also Diet assessment, 45, 46f cancer patients, 290 delivery routes enteral feeding, 45–47 oral feeding, 45 diet selection in critical illness, 48 exocrine pancreas insufficiency, 829 feather diseases, 1767 feeding guidelines, 48–49 feeding tubes. See Esophagostomy tube; Nasal catheter; Percutaneous endoscopic gastrostomy tube ferret, 1820, 1846 hepatobiliary disease, 758, 771–772 pancreatitis, 825 parenteral nutrition apparatus, 49 calorie and protein content, 49 complications, 50 delivery, 49 glucose content, 49 glucose monitoring, 49–50 mineral and vitamin content, 49 normal food intake return, 50 rabbits, 1860 reptiles, 1918–1919 requirements calories, 47–48, 48f minerals and vitamins, 48 protein, 48 rodents, 1881–1883, 1882t superficial necrolytic dermatitis, 776 Nystagmus acquired, 1419 congenital, 1418–1419 cranial nerve examination, 1236–1237 eye neurologic disturbances, 1408 Nystatin, reptile dosage guidelines, 1927t OCD. See Osteochondritis dessicans Octreotide, hypoglycemia management, 396 Oculomotor nerve, anisocoria and dysfunction, 1415 Odontoma, 1050 Olecranon. See Ulna Oliguria, reversal, 865 Olsalazine, inflammatory bowel disease management, 728t, 729 Omentalization, prostate, 959, 959f Omeprazole gastroduodenal ulceration management, 673, 675t reflux esophagitis management, 647 Ondansetron, vomiting management, 668 Onychectomy carbon dioxide laser technique, 1170 closure and bandaging, 1170 equipment, 1169 nail trimmer technique, 1169–1170 objectives, 1169 postoperative care and complications, 1171 preoperative considerations, 1168–1169 scalpel technique, 1169, 1170f Open-chest cardiac massage, 1617 Open fractures classification, 1206, 1207f complications, 1209 debridement, 1207–1208 fixation, 1208 postoperative care, 1208–1209 preoperative considerations, 1206–1207 soft tissue reconstruction, 1208
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Index Open wound management advantages, 549–550 causes of open wounds, 549 daily management analgesia, 555 culture, 555 debridement, 555 frequency, 554–555 lavage, 555 rebandaging, 555 disadvantages, 550 indications, 549 initial management antibiotic therapy, 554 bandaging adherent dressings, 552 medications, 553 non-adherent dressings, 552–553 primary contact layer, 552 clipping, 551 debridement, 551–552 lavage delivery systems, 551 solutions, 551 patient evaluation, 550 secondary layer, 553 tertiary layer, 553 tie-over bandage, 553–554, 554f wound evaluation, 550–551 second intention healing, 555 Ophthalmic equipment diagnostics, 1325 surgery, 1325–1326 Ophthalmic nerve, lacrimation disorders, 1415 Ophthalmoscopy direct, 1328 indirect, 1328–1329 Optic nerve acquired diseases, 1388–1389 anisocoria and dysfunction, 1415 atrophy, 1389 congenital diseases, 1382–1383 evaluation, 1381 hypoplasia features and management, 1383 neoplasia, 1389 neuritis, 1388 papilledema, 1388–1389 Oral cavity, physical examination, 10, 10f Orbit abscess, 1397–1398 anatomy, 1396 enophthalmos, 1402–1404 exophthalmos, 1397–1402 globe-orbit relationship, 1396 neoplasia, 1399–1400, 1404–1405 strabismus, 1404–1405 trauma, 1400–1402 Orchidectomy cat, 971–972 dog closed technique, 970, 970f ectopic testes, 971 indications, 970t open technique, 970–971 postoperative care and complications, 971 preoperative considerations, 970 prognosis, 971 Orchitis avian, 1807 clinical signs, 964 immune-mediated, 964, 967, 1023 infectious disease, 963–964 treatment, 967 Organophosphate poisoning, clinical features and management, 1266–1267
Oronasal fistula anatomy, 616, 616f clinical signs, 617 diagnosis, 617 etiology, 617 surgery equipment, 617 objectives, 617 postoperative care and complications, 619 preoperative considerations, 617 techniques, 617–619, 618f, 619f Oropharyngeal dysphagia. See Esophageal diseases Orthodontic disease anatomy, 626 clinical signs, 626 diagnosis, 626 etiology, 626 surgery postoperative care and complications, 627 preoperative considerations, 626 technique, 627 Os penis deformity, clinical features, 973 Osteoarthritis anatomy and physiology, 1222, 1223f clinical signs, 1223 diagnosis, 1223 etiology, 1222 pathophysiology, 1222–1223 treatment medical treatment, 1224–1226 surgery, 1226 Osteochondritis dessicans (OCD) humeral condyle anatomy, 1199 clinical signs, 1200 diagnosis, 1200 pathophysiology, 1200 prognosis, 1202 treatment, 1200–1202, 1201f shoulder, hock, and stifle clinical signs, 1195 diagnosis, 1195–1196 pathophysiology, 1194–1195 prognosis, 1196–1197 surgery, 1196 Osteomyelitis diagnosis, 1210–1212, 1211f etiology, 1210, 1211f treatment acute osteomyelitis, 1212–1213 chronic osteomyelitis, 1213 Osteopetrosis, 241 Osteosarcoma, limb neoplasia, 1176 Otitis externa atopic dermatitis, 482 clinical signs, 575 diagnosis biopsy, 576 culture, 576 cytology, 576 history, 575 imaging, 576 otoscopic examination, 575–576 physical examination, 575 etiology, 574 pathogenesis, 574 prevention, 581 rodents, 1894 salivation abnormalities, 1416 treatment active ingredients in otic preparations, 577t drying, 579 external anal cleaning, 577–579, 579t
1991
Otitis externa (Continued) hyperplastic changes, 581 Malassezia infection, 580–581 principles, 576–577 Pseudomonas infection, 581 solutions for cleaning and drying, 579t surgery, 580 systemic therapy, 580 topical medications, 580 Otitis interna clinical signs, 594, 594t definition, 593 diagnosis biopsy, 596 computed tomography, 595 cytology and culture/susceptibility testing, 595 history, 594 physical examination, 594 pneumotoscopy, 595 positive contrast canalography, 595 ultrasound, 596 video otoscopy, 595 etiology, 593 neurologic sequelae, 598 rodents, 1894 surgical management anatomy, 599 lateral bulla osteotomy equipment, 599 objectives, 599 postoperative care and complications, 600 preoperative considerations, 599 prognosis, 600 technique with total ear canal ablation, 600 technique without total ear canal ablation, 599–600, 600f nasopharyngeal polyps objectives, 601–602 postoperative care and complications, 602 preoperative considerations, 601 prognosis, 602 technique, 602 ventral bulla osteotomy objectives, 601 postoperative care and complications, 601 preoperative considerations, 600 technique, 601, 601f treatment cleaning and drying agents, 597 deep otic flush, 596 glucocorticoids, 597 monitoring, 598 myringotomy, 596 recurrence prevention, 597 systemic antimicrobials, 596–597 topical antimicrobials, 597 Otitis media clinical signs, 593–594 definition, 593 diagnosis biopsy, 596 computed tomography, 595 cytology and culture/susceptibility testing, 595 history, 594 physical examination, 594 pneumotoscopy, 595 positive contrast canalography, 595 ultrasound, 596 video otoscopy, 595 etiology, 593
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Otitis media (Continued) lacrimation disorders, 1415 neurologic sequelae, 598 rodents, 1894 salivation abnormalities, 1416 surgical management anatomy, 599 lateral bulla osteotomy equipment, 599 objectives, 599 postoperative care and complications, 600 preoperative considerations, 599 prognosis, 600 technique with total ear canal ablation, 600 technique without total ear canal ablation, 599–600, 600f nasopharyngeal polyps objectives, 601–602 postoperative care and complications, 602 preoperative considerations, 601 prognosis, 602 technique, 602 ventral bulla osteotomy objectives, 601 postoperative care and complications, 601 preoperative considerations, 600 technique, 601, 601f treatment cleaning and drying agents, 597 deep otic flush, 596 glucocorticoids, 597 monitoring, 598 myringotomy, 596 recurrence prevention, 597 systemic antimicrobials, 596–597 topical antimicrobials, 597 Otodectic mange, feline symmetrical alopecia, 525 Otoscopic examination equipment, 575 otitis externa findings, 575–576 preoperative evaluation, 584 sedation, 575 Ovarian cycle canine cycle phases, 983t disorders anestrus, 982–983 diagnosis, 982–983 etiology, 982 overview, 1017–1018 prolonged estrus, 982–984 short interestrus intervals, 982 treatment, 983–984 ectopic ovulation in birds, 1803–1804 estrus induction, 1020 phases cat, 1023–1024 dog, 1016–1017 suppression in cat, 1025 timing of ovulation luteinizing hormone, 1015 progesterone, 1015–1016 Ovarian remnant syndrome clinical signs, 984 diagnosis, 984 etiology, 984 treatment, 984 Ovaries anatomy, 992, 993f avian cystic ovarian disease, 1804 neoplasia, 1806 oophoritis, 1805–1806
Ovaries (Continued) neoplasia clinical signs, 984 diagnosis, 984 etiology, 984 treatment, 984 resection. See Ovariohysterectomy Ovariohysterectomy complications celiotomy complications, 996 eunuchoid syndrome, 996 fistulous tracts and granulomas, 996 hemorrhage, 995–996 ovarian remnant syndrome, 996 ureter ligation, 996 urinary incontinence, 996 uterine stump pyometra, 996 weight gain, 996 equipment, 993 ferrets, 1852 mammary gland tumor, 314 objective, 993 postoperative care, 995 preoperative considerations, 992 technique, 993–994, 994f Overhydration laboratory findings, 99 signs, 99 treatment, 99 Oviduct, avian cystic hyperplasia, 1803 impaction, 1802 metritis, 1802–1803 neoplasia, 1806 prolapse, 1801 rupture, 1803 salpingitis, 1802–1803 Ovocentesis, birds, 1801 Oxybutynin, micturition disorder management, 946t Oxygen congestive heart failure management, 1501–1502, 1538–1539 heartworm adjunctive therapy, 1571 shock management, 1607–1608 Oxymorphone applications, 22 dosage guidelines cats, 21t, 103t dogs, 20t, 23t, 103t rabbits, 1863t Oxytetracycline, rodent dosage guidelines, 1895t Oxytocin dystocia management, 989 reptile dosage guidelines, 1927t Pacheco’s disease clinical signs, 1748 diagnosis, 1748–1749 etiology, 1748 prevention, 1749 transmission, 1748 treatment, 1749 vaccination, 1749 Packed cell volume (PCV) anemia diagnosis, 229 dehydration detection, 86–87, 87t fluid therapy monitoring, 99 thoracic trauma, 1717 Pain analgesics alpha-2 agonists, 104–105 nonsteroidal anti-inflammatory drugs, 106 opioids, 102, 102t, 103t, 104 assessment, 101, 101t
Pain (Continued) cancer patient management, 290–291 local anesthesia administration, 105 drugs, 104t, 105 duration, 105 epidural, 106 intercostal nerve block, 105 mandible, 105 onychectomy, 105 upper jaw, 105 pathways, 100–101 physical rehabilitation and management, 1027–1028 procedures with significant pain, 101t sample treatment protocols, 104t scoring system, 101–102, 102t terminology, 100 thoracic surgery management, 1730 Palatal defect anatomy, 616, 616f clinical signs, 617 diagnosis, 617 etiology, 617 surgery equipment, 617 objectives, 617 postoperative care and complications, 619 preoperative considerations, 617 techniques, 617–619, 618f, 619f Palpebral reflex, cranial nerve examination, 1237 Pamidronate, hypercalcemia management, 348 Pancreas anatomy, 392–393, 392f, 393f avian disorders, 1794–1795 exocrine pancreas function, 819, 820t, 827 insufficiency. See Exocrine pancreas insufficiency neoplasia clinical signs, 830 diagnosis, 830 epidemiology, 829 treatment, 830 surgery. See Pancreatic beta cell neoplasia Pancreatic beta cell neoplasia clinical signs, 390, 391t diagnosis, 390–391 etiology, 390 hypoglycemia. See Hypoglycemia insulinoma chemotherapy, 396–397 prognosis, 397 surgical treatment complications, 395 equipment, 393 intraoperative ultrasound, 394 methylene blue intravenous infusion, 394 neoplastic tissue removal, 394–395, 394f objectives, 393 postoperative care, 395 preoperative considerations, 393 visual examination and palpation, 394 Pancreatic insufficiency. See Exocrine pancreas insufficiency Pancreatic lipase immunoreactivity assay, pancreatic function testing, 823, 828, 828t Pancreatitis classification, 819, 820t clinical signs acute complications, 821 cats, 820–821 chronic complications, 821 dogs, 820
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Index Pancreatitis (Continued) diagnosis biopsy, 824 hematologic findings, 822 pancreatic function testing, 822–823 physical examination, 821–822 radiography, 823–824 ultrasound, 824 urinalysis, 822 etiology, 819 pathogenesis, 819–820, 821t pleural effusion, 1705 risk factors, 819 treatment acute complications, 825 bacterial complications, 824–825 chronic complications, 825 enzyme removal, 825 fluid therapy, 824 nutrition, 825 pain control, 824 recurrence prevention, 825–826 surgery equipment, 826 indications, 826 objectives, 826 postoperative care and complications, 827 preoperative considerations, 826 prognosis, 827 technique, 826–827 vomiting control, 824 Panleukopenia, vaccination protocols, 112t, 113t Panniculitis. See Mycobacterial panniculitis Panosteitis clinical signs, 1186 diagnosis, 1186–1187, 1187t etiology, 1186 treatment, 1187 Papilloma, features and management, 318–319 Papillomatosis, avian clinical signs, 1753 diagnosis, 1753 etiology, 1753 prevention, 1754 treatment, 1753 Paradoxical incontinence clinical signs, 942–943 diagnosis, 943–945 treatment, 948 Parainfluenza virus, vaccination protocols, 109t, 110t, 111t Paramyxovirus paramyxovirus-1. See Newcastle disease virus snake infection, 1937 transmission, 176 Paraneoplastic pemphigus. See Pemphigus complex Paraneoplastic syndrome, neutropenia, 246 Paraphimosis clinical features, 974 reptiles, 1933–1934 treatment, 977 Parathyroid gland anatomy, 339 parathyroidectomy equipment, 355 objectives, 355 postoperative care and complications, 356 preoperative considerations, 355 prognosis, 356 technique, 355
Parathyroid hormone (PTH). See also Hyperparathyroidism; Hypoparathyroidism assay, 345, 352 calcium regulation, 343 Parathyroid hormone-related protein (PTHrP), assay, 345 Parenteral nutrition (PN) apparatus, 49 calorie and protein content, 49 complications, 50 delivery, 49 glucose content, 49 glucose monitoring, 49–50 mineral and vitamin content, 49 normal food intake return, 50 Paromomycin, reptile dosage guidelines, 1927t Parturition, normal events, 988 Pasteurellosis, rabbits, 1868–1869 Patella fracture, 1130 luxation chondroplasty, 1134, 1135f classification, 1133–1134 diagnosis, 1134 imbrication, 1135–1136, 1135f preoperative considerations, 1134 tibial tuberosity translocation, 1136 trocheoplasty, 1134–1135 wedge resection, 1135 Patellar reflex, spinal reflex examination, 1238 Patent ductus arteriosus (PDA) anatomy and physiology, 1599 canine heart disease, 1499 physical examination, 1429 surgical correction equipment, 1600 ligation technique, 1600–1601, 1600f, 1601f objectives, 1599 postoperative care and complications, 1601–1602 preoperative considerations, 1599 treatment and prognosis, 1596 Patent urachus clinical signs, 896 diagnosis, 696 etiology, 896 treatment, 896 Pattern baldness clinical signs, 520 diagnosis, 520 etiology, 520 pinna, 571 treatment, 520–521 PBD. See Proliferative bowel disease PBFD. See Psittacine beak and feather disease PCR. See Polymerase chain reaction PCV. See Packed cell volume PDA. See Patent ductus arteriosus PDD. See Proventricular dilatation disease Pediatric fractures complications, 1205 physeal fracture classification, 1203–1204, 1204f physis histology, 1203 postoperative care, 1204–1205 preoperative considerations, 1204 surgery, 1204 PEG tube. See Percutaneous endoscopic gastrostomy tube Pelger-Huët anomaly, features, 244 Pelvic limb flexor reflex, spinal reflex examination, 1239
1993
Pelvis. See also Coxofemoral joint anatomy, 1104, 1105 fracture acetabulum, 1109–1111, 1110t, 1111f diagnosis, 1104–1105 healing and pelvic canal narrowing, 1113 ilium, 1106–1109, 1107f, 1108f, 1108t ischium, 1113 non-surgical treatment, 1105–1106 pubis, 1113 sacroiliac fracture or luxation, 1111–1113, 1112f, 1112t surgical indications, 1106 neoplasia biopsy, 1068 diagnosis, 1067–1068 prognosis, 1070 surgery, 1069–1070 radiography, 65 Pemphigus complex diagnosis, 493–494 differential diagnosis, 494 drug-related pemphigus, 493–494 etiology, 492 panepidermal pustular pemphigus, 493–494 paraneoplastic pemphigus, 493–494 pemphigus erythematosus, 493–494 pemphigus foliaceus, 492–494 pemphigus vegetans, 493–494 pemphigus vulgaris, 493–494 pinna, 569 prognosis, 496 treatment azathioprine, 495 chlorambucil, 495 cyclosporine, 495 dapsone, 496 general considerations, 494–495 glucocorticoids, 495 gold salts, 496 niacinamide, 495 sulfasalazine, 496 tacrolimus, 495 tetracycline, 495 Penicillamine copper-associated hepatitis management, 781, 782t hepatic cirrhosis management, 788 Penicillin, rabbit dosage guidelines, 1863t Penis acquired diseases, 974 amputation equipment, 979 objectives, 978 partial amputation, 979, 979f postoperative care and complications, 979 preoperative considerations, 978 prognosis, 979 subtotal amputation, 979 anatomy, 978 clinical signs of disease, 974–975 congenital diseases, 973 cranial advancement of prepuce, 980 diagnosis of disease, 975–976 foreign bodies, 974 neoplasms, 974, 976 persistent penile frenulum correction, 980–981 features, 973 preputial orifice enlargement, 979–980 prolapse in reptiles, 1933–1934 trauma, 974, 976 treatment of disease, 976–977
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Index
Pentastomiasis, features and management, 1929 Pentazocine, dosage guidelines, 103t Pentobarbital rodent dosage guidelines, 1890t tetanus management, 1301 Pentoxifylline atopic dermatitis management, 486t, 487 canine ear margin dermatosis management, 516 Pepto-Bismol, diarrhea management, 711t, 712 Percutaneous endoscopic gastrostomy (PEG) tube complications, 44 contraindications, 42 equipment, 42 indications, 42 objectives, 42 placement technique, 42–44, 43f postoperative care, 44 removal, 44 Perianal fistula clinical signs, 842 diagnosis, 842 etiology, 841 prognosis, 842 surgery, 848 treatment, 842 Perianal gland adenocarcinoma, 844 adenoma, 843 Perianal tumors, features and management, 319 Pericardial constriction diagnosis, 1559–1560 etiology, 1559 treatment, 1560 Pericardial effusion canine heart disease, 1496–1497 clinical signs, 1552 diagnosis, 1552–1555 etiology, 1550–1551, 1554–1555 pathophysiology, 1551, 1551f prognosis, 1554–1555 radiography, 1440 surveillance and evaluation, 1555–1556 treatment medical therapy, 1558 pericardiocentesis, 1556–1557 surgery, 1558–1559, 1559t Pericardiocentesis diagnostics, 1554 pericardial effusion management, 1556–1557 technique, 1556–1557 Perineal hernia clinical signs, 838–839 diagnosis, 839 etiology, 838 surgery, 848–850, 849f treatment, 839 Perineal reflex, spinal reflex examination, 1239 Periodontal disease anatomy, 619, 620f clinical signs, 620 diagnosis gingivitis, 620 periodontitis, 620 etiology, 620 surgery dental scaling subgingival scaling, 620–621, 621f supragingival scaling, 620 gingivectomy, 621–622, 621f open-flap curettage, 622, 622f
Periodontal disease (Continued) polishing technique, 621 postoperative care and complications, 622 preoperative considerations, 620 Peripheral nerve disorders anatomy and physiology, 1304 breed susceptibility. See specific breeds clinical signs, 1304, 1305t diagnosis, 1304–1306, 1305t idiopathic disorders, 1311 immune-mediated disorders, 1310–1311 metabolic/endocrine disorders, 1309–1310 neoplasias, 1310 nutritional disorders, 1310 toxic neuropathy, 1314 trauma, 1312–1314, 1313t treatment, 1306 Peritoneal dialysis. See also Tenckhoff peritoneal dialysis catheter placement hypercalcemia management, 348 Peritoneography pleural effusion, 1699 technique, 1635 Peritoneopericardial diaphragmatic hernia (PPDH) clinical signs, 1549 diagnosis, 1550, 1550f etiology, 1549 treatment, 1550 Peritonitis anatomy, 853 clinical signs, 855–856 diagnosis abdominocentesis, 856 hematology, 856 history, 856 peritoneal lavage, 856 physical examination, 856 radiography, 857 serum chemistry, 856 ultrasound, 857 diffuse peritonitis, 855 etiology bacterial, 853 bile leakage, 854 chemical, 854 chyle, 854 foreign bodies, 854–855 gastrointestinal tract, 854 iatrogenic, 854 pancreatitis, 854 trauma, 854 viral, 853 lethal factors, 855 local peritonitis, 855 treatment antibiotic therapy, 857 fluid therapy, 857 lavage and drainage, 857–858 surgery, 858–859, 859f Permethrin, flea control, 477t, 478 Persistent penile frenulum clinical features, 973 surgical correction, 980–981 Persistent right aortic arch. See Esophageal diseases Phacoemulsification, cataracts, 1363 Phaeohyphomycosis clinical signs, 442 diagnosis, 442 etiology, 442 systemic infection, 214t treatment, 442
Phalangeal fracture anatomy, 1166 management, 1166 Phenobarbital adverse effects, 1284 brain trauma management, 1263 brain tumor management, 1253 cat administration, 1283 dog administration, 1282–1283, 1285t intravenous loading, 1283 serum monitoring, 1283–1284 tetanus management, 1301 Phenobarbital-associated hepatic disease clinical signs, 786 diagnosis, 786–787 etiology, 786 prevention, 787 treatment, 787 Phenoxybenzamine, micturition disorder management, 946t Phenylbutazone dosage guidelines, 22t osteoarthritis management, 1225 Phenylpropanolamine, micturition disorder management, 946t Phenytoin, canine toxicity, 1288 Pheochromocytoma clinical signs, 371 diagnosis, 371 etiology, 371 ferrets, 1835 treatment, 371–372 Phimosis, clinical features, 973 Phlebitis. See Vasculitis Phosphofructokinase, deficiency, 235 Phosphorous diabetic ketoacidosis management, 380 parenteral fluid supplementation, 94 Photodynamic therapy, cancer management, 290 Physical examination acute hepatic failure, 765–766 body condition scoring cats, 8f dogs, 7f body systems abdomen intestines, 14 kidneys, 14, 14f liver, 13 palpation, 13, 14f prostate, 15 spleen, 13 stomach, 13 urinary bladder, 15 uterus, 15 ears, 11, 11f eyes, 9 genitalia, 15 head and neck, 9–12 lymph nodes, 12, 12f, 14 musculoskeletal system, 16 neck, 11–12, 11f nervous system, 16 nose, 10–11 oral cavity, 10, 10f rectal examination, 15 skin, 15–16 thorax auscultation, 13 palpation, 12–13 percussion, 13 cardiovascular system. See Cardiovascular physical examination chronic renal failure, 869 claw disease, 605 coagulation diseases, 258
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Index Physical examination (Continued) congenital heart disease, 1592–1593 constipation, 833 dehydration detection, 86 dermatophytosis, 453 diarrhea, 704–705, 704t endodontic disease, 623 eye neurologic disturbances, 1408–1412 feline symmetrical alopecia, 526 flea allergy dermatitis, 476 general observation, 7 heartworm, 1564 liver disease, 748–749 lungs, 1626 miliary dermatitis and eosinophilic granuloma complex, 533 necrotizing dermatoses, 500 otitis externa, 575 otitis media and otitis interna, 594 penis and prepuce, 975 pericardial effusion, 1552 peritonitis diagnosis, 856 reptiles, 1920–1921 rodents, 1885–1886 scabies, 466 splenic disease, 277 syncope, 1511 testes, 964–965 thoracic trauma, 1716–1717 vital signs body temperature, 8 capillary refill time, 8 heart rate, 8 hydration, 8 pulse, 8 respiratory rate, 8 vomiting, 665 Physical rehabilitation, postoperative goals, 1027 immediate postoperative period, 1028–1029 pain management, 1027–1028 preoperative considerations, 1027 therapeutic exercise, 1029–1032 Pilocarpine, glaucoma management, 1376t, 1377 Pimobendan administration, 1479–1480 adverse effects, 1480 congestive heart failure management, 1503–1505 dosage guidelines, 1475t indications, 1479 PIND-ORF, feline leukemia virus management, 123 Pinna dermatoses actinic keratoses, 571 arteriovenous fistula, 571 atopic dermatitis, 569 canine eosinophilic pinnal folliculitis, 573 contact dermatitis, 569 demodectic mange, 568 dermatophytosis, 566 ear margin seborrhea, 573 frostbite, 570–571 hereditary diseases, 571–572 juvenile cellulitis, 573 lupus erythematosus complex, 570 Malassezia dermatitis, 566–567 neoplastic disease, 571 overview, 566, 567t pemphigus complex, 569 sarcoptic mange, 567–568 sebaceous adenitis, 573 vasculitis, 570 zinc-responsive dermatosis, 572 Pinna surgery. See Ear surgery
Piperacillin, reptile dosage guidelines, 1927t Piperazine dosage guidelines, 714t rabbit dosage guidelines, 1863t rodent dosage guidelines, 1893t Piroxicam, osteoarthritis management, 1225 Pituitary gland anatomy, 398, 399f hormones and hypothalamic regulation, 399t lobe nomenclature, 398 Plague clinical signs, 203 diagnosis, 203 etiology, 202–203 transmission, 203 treatment, 203 Plasmacytoma extramedullary plasmacytoma, 300 solitary plasmacytoma of bone, 299 Plasma protein concentration, thoracic trauma, 1717 Platelet count, coagulation disease diagnosis, 259 Pleural effusion clinical signs, 1694 congestive heart failure, 1703–1704 cyclothorax, 1701–1703 diagnosis, 1694, 1696–1699, 1697t diaphragmatic hernia, 1705 etiology, 1694, 1695t feline infectious peritonitis, 1703 fluid analysis chylous effusion, 1698 hemorrhagic effusion, 1698 modified transudate, 1697–1698 nonseptic transudate, 1698 patterns, 1697t septic transudate, 1698 thoracentesis, 1697 transudate effusions, 1697 hemothorax, 1704–1705 lung lobe torsion, 1705 neoplasia, 1704 pancreatitis, 1705 physical examination, 1428 pulmonary thromboembolism, 1705 pyothorax, 1699–1701, 1701t radiography, 1634 thymic branchial cysts, 1705 Pleural thickening, radiography, 1634 PN. See Parenteral nutrition Pneumocystosis, systemic infection, 221t Pneumomediastinum, radiography, 1633–1634 Pneumonia ferrets, 1826 mice, 1896 rabbits, 1868 reptiles, 1929 turtles, 1938 Pneumonitis, radiography, 1638 Pneumothorax physical examination, 1428 radiography, 1634 thoracic surgery management, 1730 treatment simple pneumothorax, 1719 tension pneumothorax, 1719 Pneumotoscopy, technique, 595 Pollakiuria, history taking, 4–5 Polycythemia breed predisposition, 1592t congenital heart disease complication management, 1596 relative versus absolute, 241
1995
Polycythemia vera clinical signs, 253 diagnosis, 253 treatment, 253 Polydipsia antidiuretic hormone deficiency, 404 liver disease, 747 Polymerase chain reaction (PCR) borreliosis diagnosis, 189 conjunctivitis, 1341 ehrlichiosis diagnosis, 181 feline coronavirus diagnostics, 139 feline immunodeficiency virus diagnostics, 129 feline leukemia virus diagnostics, 121–122 Malassezia dermatitis diagnostics, 448–449 toxoplasmosis diagnosis, 224 Polymyositis bilateral extraocular polymyositis, 1398 features, 1318 treatment, 1318 Polyomavirus. See Budgerigar fledgling disease Polyostotic hyperostosis, features and management, 1798 Polyploid cystitis clinical signs, 910 diagnosis, 911 etiology, 910 treatment, 911 Polytetrafluorene toxicosis, avian, 1779 Polyuria antidiuretic hormone deficiency, 404 history taking, 4–5 liver disease, 747 Porphyria, feline, 235 Portosystemic shunt (PSS) clinical signs, 789 diagnosis, 789–791 etiology multiple shunts, 789, 789t single shunts extrahepatic shunts, 788 intrahepatic shunts, 788 prognosis, 792 surgery anatomy, 812–813, 813f anesthesia, 813–814 equipment, 814 objectives, 814 perioperative complications, 792 postoperative care and complications, 815 preoperative considerations, 813 techniques, 791, 814 treatment, 791–792 Post-clipping alopecia clinical signs, 521 diagnosis, 521 etiology, 521 treatment, 521 Postprandial serum bile acid, liver function testing, 753 Potassium. See also Hyperkalemia diabetic ketoacidosis management, 380 parenteral fluid supplementation, 91, 91t Potassium bromide brain tumor management, 1253 dog administration, 1285t, 1285–1286 feline toxicity, 1289 refractory epilepsy management, 1285–1286 Poxvirus, avian infection clinical signs, 1750 diagnosis, 1750 etiology, 1749 prevention, 1750
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Poxvirus, avian infection (Continued) transmission, 1750 treatment, 1750 PPDH. See Peritoneopericardial diaphragmatic hernia PPVH. See Primary portal vein hypoplasia Praziquantel avian administration, 1792 dosage guidelines dog, 714t reptile, 1927t rodent, 1893t salmon poisoning disease management, 184 Prazosin dosage guidelines, 1475t hypertension management, 1579 micturition disorder management, 946t Prednisolone. See Glucocorticoids Prednisone. See Glucocorticoids Pregnancy. See also Fertility abortion. See Abortion diagnosis, 1019–1020 toxemia in ferrets, 1853 Prepuce. See Penis Preventive health care status, history taking, 2 Preventricular contractions (PVCs), management, 1548 Priapism clinical features, 974 surgical management, 976 Primary idiopathic seborrhea clinical signs, 509 diagnosis, 509 etiology, 509 treatment, 509–510 Primary portal vein hypoplasia (PPVH) clinical signs, 794 diagnosis, 794–795 etiology, 794 portosystemic shunt association, 794 prognosis, 795 treatment, 795 Procainamide administration, 1491–1492 adverse effects, 1492 dosage guidelines, 1475t formulations, indications, and dosages, 1459t ventricular tachycardia management in dogs, 1548 Prochlorperazine, vomiting management, 667 Proctitis, features, 837 Progesterone. See also Hyperprogesteronism assay, 983 timing of ovulation, 1015–1016 Proliferative bowel disease (PBD), ferrets, 1850–1851 Propantheline diarrhea management, 711t, 712 micturition disorder management, 946t Propionibacterium acnes, feline leukemia virus management, 123 Propofol applications, 24 dosage guidelines cats, 21t, 23t dogs, 20t, 23t rabbits, 1863t reptiles, 1926 Propranolol dosage guidelines, 1475t formulations, indications, and dosages, 1459t
Propranolol (Continued) hyperthyroidism management, 336 pharmacology, 1486 Prostaglandin-E2, egg binding and dystocia management, 1797t, 1800 Prostaglandin-F2a abortion induction, 1022 egg binding and dystocia management, 1797t, 1800 pyometra management, 986 Prostate gland. See also Benign prostatic hyperplasia abscess, 949 anatomy, 957 biopsy complications, 953–954, 954t postoperative care and complications, 958 preoperative considerations, 957 punch biopsy, 957–958 wedge biopsy, 958 clinical signs, 950, 950t cystic hyperplasia, 949, 954–955 diagnostics imaging, 951 laboratory studies, 951–952 physical examination, 951 specimen collection brush specimen, 952–953, 953t ejaculate specimen, 952, 952t prostatic wash, 952, 952t ultrasound-guided prostatic aspirate, 953 drainage procedures drain tube placement, 959–960, 959f marsupialization, 960 objectives, 958 omentalization, 959, 959f postoperative care and complications, 960 preoperative considerations, 958 prognosis, 960 ultrasound-guided percutaneous drainage, 958–959 etiology, 949 ferret diseases, 1856 neoplasia, 949–950, 955–956 paraprostatic cysts, 949, 955 physical examination, 15 prostatectomy partial, 960–961, 961f postoperative care and complications, 961–962 total, 961–962 prostatitis treatment bacterial prostatitis, 955, 955t idiopathic prostatitis, 955 squamous metaplasia, 949, 955 Protein C, liver function testing, 754 Protein-losing enteropathy clinical signs, 733 diagnosis, 733–734 etiology, 733 prognosis, 734 treatment, 734 Prothrombin time, coagulation disease diagnosis, 261 Protothecosis, intestinal clinical signs, 724 diagnosis, 724 treatment, 725 Proventricular dilatation disease (PDD) clinical signs, 1752 diagnosis, 1752 prevention, 1753 treatment, 1753
Proventriculus bacterial proventriculitis, 1791 candidiasis, 1791 dilatation syndrome, 1791 foreign body impaction, 1790–1791 structure and function, 1790 Prucalopride constipation management, 835t, 836 gastric motility disorder management, 684 Pruritis atopic dermatitis, 482 parasite association, 465 Pseudocoprostasis clinical signs, 842 diagnosis, 842 etiology, 842 treatment, 843 Pseudorabies clinical signs, 170 diagnosis, 170–171 etiology, 170 prevention, 171 treatment, 171 virus features, 170 Psittacine beak and feather disease (PBFD) circovirus, 1745 clinical signs, 1746 diagnosis, 1746–1747 prevention, 1747 transmission, 1745 treatment, 1747 Psittacosis, respiratory disease, 1776, 1780 Psoriasiform dermatosis. See Lichenoidpsoriasiform dermatosis PSS. See Portosystemic shunt Psychogenic alopecia, 525 PTH. See Parathyroid hormone PTHrP. See Parathyroid hormone-related protein Pubis. See Pelvis Pulmonary contusion, treatment, 1719–1720 Pulmonary edema congestive heart failure management, 1502 mitral valve disease, 1516 non-cardiogenic clinical signs, 1682 diagnosis, 1682 etiology, 1682 pathophysiology, 1682 treatment, 1683 radiography, 1637–1638 Pulmonary fibrosis clinical signs, 1678 diagnosis, 1679 etiology, 1678 pathophysiology, 1678 prognosis, 1680 radiography, 1638, 1679 treatment, 1679 Pulmonary hypertension canine heart disease, 1497 congenital heart disease complication management, 1595–1596 syncope, 1510 Pulmonary thromboembolism, pleural effusion, 1705 Pulmonic stenosis canine heart disease, 1499 treatment and prognosis, 1597 Pulpotomy. See Endodontic disease Pulse anesthesia monitoring, 27 physical examination, 8
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Index Pulse oximetry anesthesia monitoring, 27 bronchopulmonary disease evaluation, 1627 Pupillary light reflexes anisocoria, 1413, 1414t, 1415 autonomic nervous system evaluation, 1409–1410 cranial nerve examination, 1235–1236 PVCs. See Preventricular contractions Pyelonephritis clinical signs, 873 diagnosis, 873–874 etiology, 873 treatment, 874, 874t Pyloromyotomy equipment, 695 objectives, 695 postoperative care and complications, 695–696 preoperative considerations, 695 prognosis, 695 technique, 695, 696f Pyloroplasty equipment, 696 Heineke-Mikulicz pyloroplasty, 696–697, 696f objectives, 696 postoperative care and complications, 697 preoperative considerations, 696 prognosis, 697 Y-U pyloroplasty, 697, 697f Pyoderma acute moist dermatitis clinical signs, 420 diagnosis, 420–421 etiology, 420, 421t prevention, 421 treatment, 421 deep pyodermas clinical signs, 425 diagnosis, 425 etiology, 424–425 treatment, 425–426 feline symmetrical alopecia, 525 ferrets, 1838 impetigo clinical signs, 423 diagnosis, 423 etiology, 423 treatment, 423, 423t methicillin-resistant staphylococcal skin infection, 428 recurrent disease clinical signs, 427 diagnosis, 427 etiology, 426–427 treatment, 427–428 skin fold pyoderma. See Skin fold pyoderma superficial folliculitis clinical signs, 423–424 diagnosis, 424 etiology, 423 treatment, 424 superficial pyodermas, 422–424 surface pyodermas, 420–422 Pyometra clinical signs, 985 diagnosis, 985–986 etiology, 985 ferrets, 1852–1853 risk factors, 985 treatment antibiotic therapy, 986 fluid therapy, 986
Pyometra (Continued) prostaglandin-F2a, 986 surgery, 986–987 Pyothorax clinical signs, 1700 complications, 1701 diagnosis, 1700 etiology, 1699–1700 treatment, 1700–1701, 1701t Pyrantel pamoate dosage guidelines, 714t rabbit dosage guidelines, 1863t reptile dosage guidelines, 1927t Pyrethrin cheyletiellosis management, 472 flea control, 477t, 478 rabbit dosage guidelines, 1863t Pyridostigmine bromide, myasthenia gravis management, 1323 Pyrimethamine, hepatozoonosis management, 227 Pyriproxyfen, flea control, 477t Pyruvate, neuromuscular disease evaluation, 1321 Pyruvate kinase, deficiency, 235 Pythiosis clinical signs cutaneous, 437 gastrointestinal, 437 diagnosis, 437–438 etiology, 436 intestinal clinical signs, 724 diagnosis, 724 treatment, 724 systemic infection, 214t treatment, 438 QRS complex. See Electrocardiography QT interval. See Electrocardiography Quinacrine, rodent dosage guidelines, 1893t Quinidine, formulations, indications, and dosages, 1459t Rabbit anatomy and physiology, 1858–1859 anesthesia, 1862–1863 breeds, 1858 caging, 1860 dermatologic problems, 1863–1867 drug administration, 1865, 1866t gastrointestinal disease, 1869–1874 neuromuscular/skeletal disease, 1876–1879 nutrition, 1860 radiography, 1861 reference ranges hematologic values, 1859t physiologic values, 1859t serum biochemical values, 1859t urinalysis values, 1860t reproduction, 1859 respiratory disease, 1867–1869 restraint, 1860–1861, 1861f sedation, 1862–1863 ultrasonography, 1861–1862 urogenital/reproductive disease, 1874–1876 venipuncture, 1861 Rabies clinical signs atypical rabies, 168–169 furious phase, 168 paralytic phase, 168 prodromal phase, 168 diagnosis direct fluorescent antibody test, 169
1997
Rabies (Continued) histopathology, 169 inoculation tests, 169 molecular diagnostics, 169 monoclonal antibody techniques, 169 epidemiology, 168 etiology, 168 ferrets clinical signs, 1824 diagnosis, 1824 etiology, 1824 prevention, 1824 treatment, 1824 human prevention and animal bite management, 170 pathogenesis, 168 postexposure management, 169–170 prevention, 169, 170 transmission, 168 treatment, 169 vaccination overview, 169 protocols cats, 112t, 113t dogs, 109t, 110t, 111t Radiation injury, necrosis, 505 Radiation safety clinic construction, 75 exposure minimization, 74 film badges, 74t maximum permissible dose, 73–74 records, 75f, 76f Radiation therapy applications, 287 brain tumor management, 1254 failure sources, 287–288 hyperadrenocorticism management, 366, 370 limb neoplasia management, 1179 mast cell tumor, 308 nasal cavity tumors, 1707–1708 principles, 287 soft tissue sarcoma, 305 tumor radiosensitivity, 287, 287t Radiography. See Computed tomography; Magnetic resonance imaging; X-ray Radioiodine, thyroid ablation, 336–338 Radius anatomy, 1086 fracture carpal bone fracture, 1098–1099 closed reduction, 1089–1090 external skeletal fixation, 1090, 1090f head fracture, 1088–1089 mid-shaft fracture, 1089 Monteggia fracture, 1089, 1089f plate fixation, 1090–1091 postoperative care and complications, 1087 preoperative considerations, 1086–1087 styloid process, 1091 growth deformity correction anatomy, 1091 distal radial physis closure, 1094–1095 postoperative care and complications, 1091 preoperative considerations, 1091 prognosis, 1092 proximal radial physis closure, 1093–1094, 1093f Range of motion exercises, immediate postoperative period rehabilitation, 1028 Ranitidine chronic gastritis management, 679 constipation management, 835t, 836 gastric motility disorder management, 684
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Ranitidine (Continued) gastroduodenal ulceration management, 673, 674t reflux esophagitis management, 646 Rat. See Rodents Rat snake. See Reptiles Ravuconazole, features, 217 Rectum. See also Anorectal disease; Anorectal surgery examination, 15 prolapse in ferrets, 1851 rectovaginal fistula, 840 Regional granulomatous enterocolitis (RGE) clinical signs, 731 diagnosis, 731–732 etiology, 731 treatment, 732 Relaxin, pregnancy diagnosis, 1020 Renal disease anemia, 241 biopsy. See Kidney cysts clinical signs, 880 diagnosis, 880–881 etiology, 880 treatment, 881 dog breed susceptibility, 869t failure. See Acute renal failure; Chronic renal failure ferrets, 1854–1855 glomerular disorders associated conditions, 875t diagnosis, 875–876 etiology, 875 treatment amyloidosis, 877–878 glomerulonephritis, 877 neoplasia diagnosis, 884 etiology, 884 prognosis, 884 treatment, 884 parasites. See Kidney worm pyelonephritis; Pyelonephritis stones; Nephrolithiasis surgery; Kidney trauma clinical signs, 885 diagnosis, 885 etiology, 884 treatment, 885 tubular disorders clinical signs, 879 cystinuria, 879–880 diagnosis, 879–880 Fanconi-like syndrome, 879–880 nephrogenic diabetes insipidus, 879–880 renal glucosuria, 879–880 renal tubular acidosis, 878–879 treatment, 880 Reovirus avian infection clinical signs, 1750–1751 diagnosis, 1751 etiology, 1750 prevention, 1751 transmission, 1750 treatment, 1751 reovirus type 2, feline diarrhea, 166 Repetitive nerve stimulation interpretation, 1246t, 1248 technique, 1248 Reptiles analgesia, 1926 anesthesia, 1925–1926 anorexia in boas and pythons, 1928–1929
Reptiles (Continued) bacterial infection, 1928 breeders, 1910 caging, 1915–1918 comparative anatomy and physiology body temperature, 1910–1911, 1911t cardiovascular system, 1913 endocrine system, 1915 gastrointestinal tract, 1911–1912, 1912f immune system, 1915 renal system, 1913–1914 reproductive system, 1914–1915 respiratory system, 1911–1912 skin and sense organs, 1911, 1915 crocodilian diseases, 1941–1942 dermatologic disorders, 1934–1936 drug therapy, 1926, 19257t enema, 1923 gastrointestinal disorders, 1930–1933 history taking, 1920 injection epicoelomic, 1923 intracoelomic, 1924 intramuscular, 1923–1924 intraosseous, 1924, 1924f sites, 1923f subcutaneous, 1923 mouth opening, 1912f neuromuscular disorders, 1936–1937 nutrition, 1918–1919 nutrition disorders, 1937–1938 ocular disorders, 1936 oral examination, 1921 physical examination, 1920–1921 radiography, 1924 reproductive disorders, 1933–1934 respiratory disorders, 1929–1930 restraint lizards, 1919, 1919f snakes, 1919–1920, 1920f turtles, 1920, 1920f sex determination lizards, 1914–1915 snakes, 1914 turtles, 1914 stomach intubation, 1922–1923 surgery, 1926 transportation, 1920 turtle diseases herpes virus infection, 1939–1940 mycoplasma pneumonia, 1938 myiasis, 1941 nutritional disorders, 1940 shell diseases, 1940–1941 urinary system disorders, 1938–1939 venipuncture, 1921–1922, 1922f Respiratory infection. See also specific infections classification anatomic, 1684t etiologic, 1683t diagnosis, 1685t differential diagnosis, 1686t parasites, 1692–1693 pathogens, 1682 Respiratory rate anesthesia monitoring, 27 physical examination, 8 Respiratory system. See Avian respiratory system; Respiratory infection; see also specific components and diseases Restraint birds, 1733, 1734f ferrets, 1816 rabbits, 1860–1861, 1861f reptiles lizards, 1919, 1919f
Restraint (Continued) snakes, 1919–1920, 1920f turtles, 1920, 1920f rodents, 1884, 1884f, 1885f Restrictive cardiomyopathy. See Feline restrictive cardiomyopathy Retained enchondral cartilaginous cores, features and management, 1192 Reticulocyte count, anemia diagnosis, 231 Retina acquired diseases, 1383–1388 chorioretinitis clinical signs, 1386 diagnosis, 1386 etiology, 1385, 1385t, 1386t treatment, 1386 congenital diseases, 1382–1383 degeneration clinical signs, 1385 diagnosis, 1385 etiology, 1384–1385 prevention, 1385 treatment, 1385 detachment, 1387–1388 evaluation, 1381 neoplasia, 1389 rodent degeneration, 1896 vascular disease, 1386–1387 Retractor oculi reflex, cranial nerve examination, 1237 Retrograde ejaculation, 1022 RGE. See Regional granulomatous enterocolitis Rhabdomyosarcoma biologic behavior, 302 clinical signs, 303–304 staging, 304, 304t treatment, 304–305 Rheumatoid arthritis. See Immune-mediated arthritis Rhinitis avian, 1774–1775 clinical signs, 1682–1683 diagnosis, 1683–1684 etiology, 1682 treatment, 1684, 1686–1687 Rhinoliths, features and management, 1775 Rhinoscopy, technique, 1623 Rhinosporidiosis clinical signs, 441 diagnosis, 441 etiology, 441 Ribs fracture stabilization, 1720–1721, 1721f neoplasia biopsy, 1068 diagnosis, 1067–1068 prognosis, 1070 surgery, 1068–1069 Rickettsiosis. See Rocky Mountain spotted fever Rifampin, mycobacteriosis management, 202 Right atrium, enlargement electrocardiography, 1450, 1450f radiography, 1433, 1433f Right bundle branch block, electrocardiography, 1444, 1445f, 1446f Right ventricle, enlargement electrocardiography, 1450, 1450f radiography, 1433–1434, 1434f RMSF. See Rocky Mountain spotted fever Rocky Mountain spotted fever (RMSF) clinical signs, 178–179 diagnosis, 179 etiology, 178 laboratory findings, 179
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Index Rocky Mountain spotted fever (RMSF) (Continued) pathogenesis, 178 prevention, 180 prognosis, 179 transmission, 178 treatment, 179 Rodents anesthesia, 1889, 1890t, 1891 caging and sanitation, 1881, 1882t chinchilla breeding, 1905 dermatology, 1904–1905 gastroenterology, 1905 general features, 1904 neurology, 1905 ophthalmology, 1905 drug administration injectable medications, 1907t intramuscular injection, 1888 intraosseous injection, 1889 intraperitoneal injection, 1888 intravenous injection, 1888–1889 oral, 1886–1888, 1887–1888f subcutaneous injection, 1888 euthanasia, 1891 gerbil breeding, 1904 dermatology, 1903 gastroenterology, 1904 general features, 1903 hematology, 1904 neurology, 1903 ophthalmology, 1903 urology, 1904 guinea pig breeding, 1908–1909 cardiology, 1907 dermatology, 1906 gastroenterology, 1907–1908 general features, 1906 hematology, 1909 musculoskeletal system, 1909 neurology, 1909 ophthalmology, 1906–1907 respiratory disease, 1907 urology, 1907 hamster breeding, 1902–1903 cardiovascular disease, 1902 dermatology, 1901 gastroenterology, 1902 general features, 1901 hematology, 1903 neurology, 1903 ophthalmology, 1901 respiratory disease, 1901–1902 urology, 1903 history taking, 1883–1884 mouse breeding, 1897 dermatology, 1892–1894 gastroenterology, 1896–1897 hematology, 1898 musculoskeletal disease, 1898 neurology, 1898 ophthalmology, 1894, 1896 respiratory disease, 1896 urology, 1897–1896 nutrition, 1881–1883, 1882t physical examination, 1885–1886 physiologic values, 1883t quarantine, 1883 radiology, 1886 rat breeding, 1900 cardiovascular disease, 1899
Rodents (Continued) dermatology, 1899 gastroenterology, 1900 hematology, 1900–1901 neurology, 1900 ophthalmology, 1899 respiratory disease, 1899 strains, 1899 urology, 1900 reference ranges hematologic values, 1887t serum biochemistry values, 1887t reproductive data, 1884t restraint, 1884, 1884–1885f skin and ear sample collection, 1886 surgery, 1891–1892, 1892f urine and fecal collection, 1886 venipuncture, 1886, 1886f Root canal. See Endodontic disease Ropivacaine, dosage guidelines, 104t Rotavirus, ferret infection, 1825, 1849 Rottweiler motor neuron disease, 1308 polyneuropathy, 1308 Sacrum. See Pelvis S-adenosylmethionine (SAM) feline hepatic lipidosis management, 772 hepatoprotection, 760t Salivary gland disease anatomy, 632, 632f clinical signs, 633 diagnosis, 633–634 etiology, 633 mucocele in ferrets, 1846 surgery drainage, 635 excision, 635, 634f marsupialization, 634 mucocele management, 635 postoperative care and complications, 635 preoperative considerations, 634 Salmon poisoning disease clinical signs, 184 diagnosis, 184 etiology, 184 laboratory findings, 184 prevention, 185 treatment, 184 Salmonellosis clinical signs, 721 diagnosis, 721 epidemiology, 720–721 ferrets, 1826, 1849 prognosis, 721 reptiles, 1928 treatment, 721 Salpingitis, 1802–1803 Salter-Harris classification, fractures, 1203–1204, 1204f SAM. See S-adenosylmethionine Sarcocystosis, avian, 1780 Sarcoptic mange ferrets, 1839 pinna, 567–568 SARD. See Sudden acquired retinal degeneration Scabies clinical signs, 466 diagnosis differential diagnosis, 466 history, 466 physical examination, 466 skin scrapes, 466–467 etiology, 465–46, 466f feline scabies. See Notoedric mange
1999
Scabies (Continued) treatment amitraz dip, 468–469 doramectin, 469 fipronil, 468 ivermectin, 468 lime sulfur dip, 468 milbemycin oxime, 468 moxedectin, 469 selamectin, 467–468 Scapula. See also Scapulohumeral luxation fracture body fractures, 1072–1073, 1073f glenoid fracture, 1074, 1074f neck fracture, 1073, 1074f sites, 1072, 1072f spine and acromion fractures, 1073–1074, 1073f surgery, 1072–1074 tubercle fracture, 1073–1074, 1074f thoracic limb amputation with scapula removal, 1180, 1181f–1183f Scapulohumeral luxation anatomy, 1077, 1078f closed reduction, 1077–1078 diagnosis, 1077 open reduction lateral luxation, 1079, 1079f medial luxation, 1078–1079, 1078f postoperative care, 1079 preoperative considerations, 1077 prognosis, 1079 Schirmer tear test equipment, 1327 eye neurologic disturbance evaluation, 1410t indications, 1326 keratoconjunctivitis sicca diagnosis, 1391–1392 technique, 1327 Schnauzer comedo syndrome clinical signs, 513 diagnosis, 513 etiology, 512–513 treatment, 513 Schwannoma biologic behavior, 302 clinical signs, 303–304 peripheral nerves, 1310 staging, 304, 304t treatment, 304–305 Sclera colobomatous defects, 1348 inflammation and trauma, 1358 neoplasia, 1358–1359 Scottish terrier vacuolar hepatopathy clinical signs, 774 diagnosis, 774 differential diagnosis, 772, 773t etiology, 774 treatment, 774 Scrotum ablation, 972, 972f anatomy, 969 diseases diagnosis, 968 etiology, 967–968 treatment, 968 Sebaceous adenitis clinical signs, 514, 573 diagnosis, 514, 573 etiology, 514 treatment, 514, 573 Sebaceous gland tumors, features and management, 319
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Sedation ferrets, 1821–1822, 1821t rabbits, 1862–1863 Seizure avian idiopathic epilepsy, 1815 cataplexy, 1292–1293 classification, 1277 clinical signs, 1279–1280 clinical stages, 1277–1278 diagnosis, 1281–1282 diagnostic scheme, 1277–1279, 1278t differential diagnosis, 1280, 1281t etiology, 1279 impairments, 1279 mouse, 1898 narcoplexy, 1292–1293 syncope differential diagnosis, 3 syndromes, 1278 treatment antiepileptics, 1282–1284, 1285t emergencies, 1289, 1290–1291t, 1291–1292 goals, 1282 initiation, 1282 refractory epilepsy cats, 1288–1289 dogs, 1285–1288 Selamectin cheyletiellosis management, 473 flea control, 477t heartworm prevention, 1571–1572 notoedric mange management, 470 otitis externa management, 580 rabbit dosage guidelines, 1863t scabies management, 467–468 Selegiline, hyperadrenocorticism management, 366 Semen artificial insemination. See Artificial insemination ejaculate collection, 952, 952t, 966 evaluation alkaline phosphatase test, 966–967 color and consistency, 966 culture, 967 sperm count, 966 sperm morphology, 966 sperm motility, 966 quality and conception, 1015, 1022–1023 Sendai virus, mouse infection, 1896 Sesamoid, injury and management, 1166 Sevoflurane, applications, 26 Sex hormone dermatoses clinical signs, 517–518 diagnosis, 518–519 etiology, 517 hyperandrogenism, 517–518 hyperestrogenism, 517–518 hyperprogesteronism, 517–518 look-a-like dermatoses, 519 Shell diseases pyramiding, 1941 rot, 1941 trauma, 1940–1941 Shock classification, 1603, 1604t clinical signs, 1603–1604 treatment, 1606t blood flow optimization, 1607 blood pressure optimization, 1607 blood volume optimization, 1605, 1606t, 1607 dextrose, 1608 electrolyte and acid-base disturbances, 1608 glucocorticoids, 1608
Shock (Continued) goals, 1604 monitoring, 1604–1605 oxygen therapy, 1607–1608 Shoulder. See also Scapulohumeral luxation anatomy, 1071 fracture diagnosis, 1071–1072 proximal humerus, 1074–1076, 1076f scapula, 1072–1074, 1072f, 1073f, 1074f osteochondritis dessicans clinical signs, 1195 diagnosis, 1195–1196 pathophysiology, 1194–1195 prognosis, 1196–1197 surgery, 1196 radiography, 64 Sick sinus syndrome (SSS), features and management, 1470–1471 Signalment, history taking, 1 Sildenafil adverse effects, 1481 indications, 1481 Silhouette sign, radiography, 1636, 1636f Silica. See Urolithiasis Silver sulfadiazine, open wound management, 553 Silybin, hepatoprotection, 760t Sinus block, features and management, 1457, 1457f Sinusitis avian, 1775 clinical signs, 1682–1683 diagnosis, 1683–1684 etiology, 1682 treatment, 1684, 1686–1687 Skeletal muscle anatomy, 1173 biopsy neuromuscular disease, 1322 peripheral nerve disorders, 1305 healing, 1173–1174 injury diagnosis, 1174 surgery equipment, 1174 objectives, 1174 postoperative care, 1175 technique, 1174–1175, 1175f Skin. See also specific diseases birds. See Avian dermatology ferret infection, 1838 seasonal changes, 1837–1838 history taking, 5–6 physical examination, 15–16 reptile disorders, 1911, 1934–1936 turgor and dehydration detection, 86 Skin biopsy equipment, 417 indications, 414–415 necrotizing dermatoses, 501 processing and submission, 418 sampling excisional biopsy, 415–416 incisional biopsy, 415 onychobiopsy, 416 principles, 415 punch biopsy, 415 shave biopsy, 416 sex hormone dermatoses, 518–519 site selection, 416–417 surgical technique, 417–418 Skin cytology indications, 409 interpretation ear cytology, 413
Skin cytology (Continued) fine-needle aspirates, 413–414 surface cytology, 412–413 processing of samples, 412 sampling techniques adhesive glass slide impression, 410 aspiration cytology, 411 direct glass slide impression, 410 Q-tip sample and smear, 411 Scotch tape impression, 410 surface skin scrape, 410 touch preparation, 411–412 Tzanck preparation, 411 Skin fold pyoderma body folds, 537–538 clinical signs, 422 diagnosis, 422 etiology, 421, 537 prevention, 422 sites, 422t surgical management complications, 540 equipment, 538 objectives, 538 postoperative care, 540 preoperative considerations, 538 technique, 538–540, 538f, 539f, 540f treatment, 422 Skin graft and reconstruction anatomy blood supply, 557–558 cutaneous muscle, 557 skin, 557 subcutaneous tissue, 557 axial pattern flaps indications, 561 objectives, 561 preoperative considerations, 561 technique caudal superficial epigastric axial pattern flap, 561 thoracodorsal axial pattern flap, 561–562 equipment for flaps, 560 free skin grafts mesh skin grafts equipment, 564 objectives, 564 postoperative care and complications, 565 preoperative considerations, 564 technique, 565, 565f pinch grafts equipment, 563 objectives, 563 postoperative care and complications, 564 preoperative considerations, 563 technique, 563–564, 564f indications, 557 postoperative care and complications of flaps, 562–563 random subdermal flaps indications, 558–559 objectives, 559–560 preoperative considerations, 559 technique advancement or transposition flaps, 560 direct distant flap, 560–561 types, 558, 558f, 559f Skin tumors anal sac adenocarcinoma, 321 apocrine gland adenocarcinoma, 321 basal cell tumors, 320 biopsy, 318 ceruminous gland tumors, 320–321
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Index Skin tumors (Continued) chemotherapy, 320t classification, 316, 317t dermatoid inclusion cyst, 322 diagnosis, 316–318 epidemiology, 316, 317t epidermal inclusion cyst, 322 keratoacanthoma, 322 papilloma, 318–319 perianal tumors, 319 sebaceous gland tumors, 319 squamous cell carcinoma, 321 Skull fracture anatomy, 1033 extracranial fracture surgery, 1034–1035 intracranial fracture surgery, 1035, 1035f zygomatic arch fracture surgery, 1033–1034 neoplasia biopsy, 1068 diagnosis, 1067–1068 prognosis, 1070 radiography, 67–69, 67f, 68f, 69f Skye terrier, copper-associated hepatitis, 785 SLE. See Systemic lupus erythematosus Snake bite hemolysis, 237 necrosis, 505 Snakes. See Reptiles Sneezing, diagnostic evaluation, 1621–1623 Snuffles, rabbits, 1867–1868 Sodium bicarbonate. See Bicarbonate Sodium chloride, hypoadrenocorticism management, 359–360 Sodium tibogluconate, leishmaniasis management, 229 Soft tissue sarcomas biologic behavior, 302–303 biopsy, 304 clinical signs, 303–304 etiology, 301–302 staging, 304, 304t treatment, 304–305, 306t Solitary plasmacytoma of bone, 299 Sotalol advanced life support, 1613 arrhythmia management, 1493 formulations, indications, and dosages, 1459t pharmacology, 1487 ventricular tachycardia management in dogs, 1548 Sperm. See also Semen morphology, 1023 motility, 1023 Spider bite, necrosis, 505 Spinal cord disorders classification, 1295t clinical signs, 1296–1297 diagnosis, 1298–1299 etiology anomalies, 1294 degenerative disorders, 1294 granulomatous meningoencephalitis, 1296 immune-mediated disorders, 1296 infection, 1295 neoplasia, 1296 toxins, 1296 trauma, 1294–1295 vascular disorders, 1296 prognosis, 1302–1303 treatment medical therapy, 1299–1301
Spinal cord disorders (Continued) physiotherapy and nursing care, 1302 surgical treatment, 1301–1302 Spindle cell carcinoma, uvea, 1373 Spine. See also Atlantoaxial instability; Caudal cervical spondylomyelopathy anatomy, 1062 fractures and dislocations clinical signs, 1063 diagnosis, 1063 etiology, 1062 surgery cervical fractures and luxations, 1064, 1064f equipment, 1063 indications, 1063 L6, L7. and sacral fractures, 1065–1066 postoperative care and complications, 1066 prognosis, 1066 thoracic/lumbar spinal fractures and luxations, 1064–1065, 1065f neoplasia biopsy, 1068 diagnosis, 1067–1068 prognosis, 1070 surgery, 1070 rabbit fracture and luxation, 1878–1879 radiography cervical spine, 67 principles, 66, 67t thoracolumbar spine, 67 Spironolactone congestive heart failure management, 1505, 1539 dosage guidelines, 1475t Spleen abscess, 275 anatomy, 272 biopsy, 279 ferret aspiration, 1819 function blood cell reservoir, 273 filtration, 273 hematopoiesis, 273–274 immunity, 273 hypersplenism, 276 hyposplenism, 276 neoplasia, 274 physical examination, 13 resection. See Splenectomy rupture, 274–275 Splenectomy partial splenectomy, 280–281 postoperative care and complications, 281 preoperative considerations, 280 total splenectomy, 281, 281t Splenomegaly clinical signs, 276, 276t diagnosis, 277–280 ferrets, 1827–1828 generalized, 275–276, 275t localized, 274, 274t platelet sequestration, 249–250 Spondylitis, snakes, 1937 Sporotrichosis clinical signs, 440 diagnosis, 440–441 etiology, 440 systemic infection, 214t treatment, 441 Squamous cell carcinoma avian, 1761–1762 features and management, 321 oropharyngeal, 1049 SSS. See Sick sinus syndrome
2001
ST segment. See Electrocardiography Staphylectomy anatomy, 1654 equipment, 1655 objectives, 1654–1655 postoperative care and complications, 1655 preoperative considerations, 1654 technique, 1655, 1655f Status epilepticus. See Seizures Stereotactic radiosurgery, brain tumor management, 1254 Stethoscope anesthesia monitoring, 27 auscultation. See Cardiovascular physical examination Stifle anatomy, 1132, 1133f caudal cruciate ligament rupture and repair, 1139–1140, 1140f collateral ligament injury and repair, 1141–1142 cranial cruciate ligament rupture and repair, 1136–1139, 1138f luxation, 1141–1142 meniscal injury and repair, 1140–1141 osteochondritis dessicans clinical signs, 1195 diagnosis, 1195–1196 pathophysiology, 1194–1195 prognosis, 1196–1197 surgery, 1196 palpation, 1132–1133 patellar luxation. See Patella radiography, 65 Stomach. See also Gastric dilatation-volvulus; Gastric outflow obstruction; Gastritis; Hypertrophic gastropathy; Vomiting anatomy omentum, 691 pylorus, 691 stomach, 691 foreign bodies clinical signs, 669 diagnosis, 669 etiology, 669 treatment, 669–670 motility disorders clinical signs, 684 diagnosis, 684 etiology, 683–684 treatment diet, 684 promotility drugs, 684–685 neoplasia clinical signs, 687 diagnosis, 687–688 etiology, 687 prognosis, 688 treatment, 688 physical examination, 13 reptile intubation, 1922–1923 surgery. See Distal stomach partial gastrectomy; Gastric dilatationvolvulus; Gastrotomy; Pyloromyotomy; Pyloroplasty ulceration. See Gastroduodenal ulceration Stomatitis/gingivitis clinical signs, 630 diagnosis, 630 etiology, 627, 628t, 629 reptiles, 1929–1930 treatment, 630–631 Stomatocytosis, hereditary, 235 Strabismus acquired, 1404 breed susceptibility, 1403
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Strabismus (Continued) developmental disorders, 1403–1404 eye neurologic disturbances, 1407 neoplasia, 1404 Streptozotocin, insulinoma management, 396–397, 397t Stress incontinence clinical signs, 942–943 diagnosis, 943–945 Stretching, immediate postoperative period rehabilitation, 1028–1029 Stroke, syncope, 1509 Strongyloides clinical signs, 716–717 diagnosis, 717 life cycle, 716 species, 716 treatment, 717 Struvite. See Urolithiasis Strychnine poisoning, management, 1301 Subaortic stenosis, treatment and prognosis, 1597–1598 Subarachnoid cysts, clinical features and management, 1269–1270 Subepidermal blistering dermatoses clinical signs, 496–497 diagnosis, 497 etiology, 496 treatment, 497 Sucralfate gastroduodenal ulceration management, 673, 675t reflux esophagitis management, 647 Sudden acquired retinal degeneration (SARD), 1384 Sugar, open wound management, 553 Sulfadiazine, reptile dosage guidelines, 1927t Sulfamethazine, rodent dosage guidelines, 1895t Sulfasalazine inflammatory bowel disease management, 728t, 729 pemphigus complex management, 496 Summation, radiography, 1636 Superficial folliculitis. See Pyoderma Superficial necrolytic dermatitis clinical signs, 504, 775–776 diagnosis, 776 differential diagnosis, 772, 773t etiology, 775 pathogenesis, 775 prognosis, 776 treatment, 504–505, 776 Suppurative cholangitis. See Neutrophilic cholangitis Swallowing disorders. See Esophageal diseases Symblepharon, repair, 1345–1346 Syncope clinical presentation, 1508 diagnosis, 1511–1512, 1512f differential diagnosis, 1508 etiology cardiac causes, 1509–1510 general mechanisms, 1509 non-cardiac causes, 1509 reflex-mediated syncope, 1510–1511 feline hypertrophic cardiomyopathy, 1531 heartworm, 1563 pericardial effusion, 1552 seizure differential diagnosis, 3–4 treatment, 1512 Synovial biopsy, immune-mediated arthritis, 1231
Synovial cell sarcoma biologic behavior, 302 clinical signs, 303–304 limb neoplasia, 1177 staging, 304, 304t treatment, 304–305 Systemic lupus erythematosus (SLE). See also Lupus erythematosus complex clinical signs, 270, 270t diagnosis, 270–271 etiology, 270 prognosis, 271 treatment, 271 Systolic blood pressure, 1574 Tachycardia atrial tachycardia, 1460–1462, 1461f sinus tachycardia, 1457, 1460 syncope, 1509 ventricular tachycardia cats, 1540 dogs, 1548 features, 1465–1467, 1466f, 1491, 1504 Tachypnea, diagnostic evaluation, 1625–1629 Tacrolimus atopic dermatitis management, 486, 486t keratoconjunctivitis sicca management, 1392 lupus erythematosus complex management, 499 miliary dermatitis and eosinophilic granuloma complex management, 535 pemphigus complex management, 495 Tapeworm clinical signs, 717 diagnosis, 717 life cycle, 717 species, 717 treatment, 717 Tarsus anatomy components, 1152, 1153f intertarsal joints, 1152–1153 tarsometatarsal joints, 1152–1153 tarsosacral joint, 1152, 1153f intertarsal luxation and subluxation distal intertarsal subluxation with dorsomedial instability management, 1161 overview, 1158 proximal intertarsal luxation with plantar instability management, 1159–1160, 1160f proximal intertarsal subluxation with dorsal instability management, 1160–1161 proximal intertarsal subluxation with plantar instability management, 1158–1159, 1159f talus head luxation management, 1162 tarsometatarsal subluxation with dorsomedial instability management, 1161 tarsometatarsal subluxation with plantar instability management, 1160–1161 radiography, 66 shear injury management ligament replacement, 1156–1157 postoperative care, 1157 preoperative considerations, 1155 prognosis, 1157 wound management and debridement, 1156
Tarsus (Continued) tarsocrural joint arthrodesis pantarsal arthrodesis, 1157–1158, 1158f postoperative care, 1158 preoperative considerations, 1157 tarsocrural luxation and subluxation double-prosthesis replacement, 1154–1155 Taurine, feline hepatic lipidosis management, 772 TBUT. See Tear breakup time Tear breakup time (TBUT), technique, 1327 Tear production. See Lacrimal system TECA. See Total ear canal ablation Teeth. See Dental extraction; Endodontic disease; Orthodontic disease; Periodontal disease; Stomatitis/gingivitis Teflon, urethral injection, 948 Tegaserod constipation management, 835t, 836 gastric motility disorder management, 684 Telogen defluxion clinical signs, 521–522 diagnosis, 522 etiology, 521 treatment, 522 Telogen effluvium, feline symmetrical alopecia, 525 Temporomandibular joint dislocation, 1042 dysplasia, 1042 Tenckhoff peritoneal dialysis catheter placement complications, 36–37 contraindications, 36 equipment, 36 indications, 36 objectives, 36 technique, 36 Tendons anatomy, 1173 healing, 1174 injury diagnosis, 1174 surgery equipment, 1175 postoperative care, 1175 preoperative considerations, 1175 technique, 1175, 1175f Tensilon test, 1248 Tepoxalin, dosage guidelines, 22t, 104t Terbinafine avian administration, 1742 dermatophytosis management, 457 features, 217 Malassezia dermatitis management, 449t, 450 onychomycosis management, 608 Terbutaline, dosage guidelines, 1669t Testes anatomy, 969 avian neoplasia, 1807 biopsy indications, 967 postoperative care and complications, 970 preoperative considerations, 969 prognosis, 970 technique, 969 diseases. See also Cryptorchidism; Epididymitis; Orchitis algorithm for male infertility, 965f clinical signs, 964 diagnosis, 964–967 etiology, 963–964 neoplasia, 964, 967
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Index Testes (Continued) testicular feminization syndromes, 963, 967 torsion, 964 treatment, 967 fine-needle aspiration, 967 orchidectomy cat, 971–972 dog closed technique, 970, 970f ectopic testes, 971 indications, 970t open technique, 970–971 postoperative care and complications, 971 preoperative considerations, 970 prognosis, 971 semen. See Semen Testosterone feline symmetrical alopecia management, 529 micturition disorder management, 946t Tetanus, management, 1301 Tetracycline anaplasmosis management, 183 canine cyclic thrombocytopenia management, 183 lupus erythematosus complex management, 499 neorickettsiosis management, 184 pemphigus complex management, 495 rabbit dosage guidelines, 1863t rodent dosage guidelines, 1895t salmon poisoning disease management, 184 Tetracycline/niacinamide, lupoid onychomadesis management, 607 Tetralogy of Fallot canine heart disease, 1499 treatment and prognosis, 1597 Theobromine. See Methylxanthine toxicosis Theophylline. See Methylxanthine toxicosis Thermal injury. See Burn injury Thiabendazole, rodent dosage guidelines, 1893t Thiamine deficiency clinical features and management, 1264–1265 reptiles, 1938 feline hepatic lipidosis management, 772 Thiopental applications, 24 dosage guidelines cats, 21t, 23t dogs, 20t, 23t rodents, 1890t Third eyelid. See Nictitating membrane Thoracentesis, pleural effusion, 1697 Thoracic catheter/tube placement complications, 40 contraindications, 38 equipment, 38 indications, 38 objectives, 38 postoperative care, 40 technique, 38–40, 39f Thoracic limb flexor reflex, spinal reflex examination, 1239 Thoracic surgery anatomy, 1723, 1726t anesthesia, 1724–1725, 1724t equipment, 1725, 1726t exploratory thoracotomy, 1722 lateral thoracotomy, 1725–1728, 1726–1728f
Thoracic surgery (Continued) lung lobectomy, 1728–1730, 1729f median sternotomy, 1728, 1729f postoperative care and complications, 1730 preoperative considerations, 1723–1724 thoracic tubes, 1730 Thoracic trauma blunt versus penetrating, 1715 clinical signs, 1715–1716 diagnosis, 1716–1718 treatment airway, breathing, and circulation, 1718 antibiotic therapy, 1722 diaphragmatic hernia repair, 1721–1722 exploratory thoracotomy, 1722 hemothorax, 1720 myocardial contusion, 1720 open chest wounds, 1721 pleural space drainage, 1718–1719 pneumothorax, 1719 pulmonary contusion, 1719–1720 rib fracture and flail chest stabilization, 1720–1721, 1721f Thoracocentesis complications, 37–38 contraindications, 37 equipment, 37 indications, 37 objectives, 37 technique, 37, 38f thoracic trauma, 1717 Thoracotomy. See Thoracic surgery Thorax physical examination. See also Cardiovascular physical examination auscultation, 13 palpation, 12–13 percussion, 13 radiography, 63, 63f Thrombin clotting time, coagulation disease diagnosis, 261 Thrombocythemia, primary, 253 Thrombocytopenia clinical signs, 248 diagnosis, 248–249 etiology, 249–250 immune-mediated thrombocytopenia clinical signs, 268–269 concurrent diseases, 267 diagnosis, 269 etiology, 268 prognosis, 269 treatment, 269 treatment, 249 Thrombocytosis clinical signs, 250 diagnosis, 250 etiology, 250 treatment, 250 Thromboembolism. See also Arterial thromboembolism diagnosis, 1581, 1582t etiology, 1581t features, 1580 pathophysiology, 1580 treatment abciximab, 1584 aspirin, 1584 clopidogrel, 1584 heparin, 1583 principles, 1583 surgery, 1584 warfarin, 1584 Thrombosis diagnosis, 1581, 1582t etiology, 1581t
2003
Thrombosis (Continued) features, 1580 pathophysiology, 1580 treatment aspirin, 1584 clopidogrel, 1584 heparin, 1583 principles, 1583 surgery, 1584–1585 warfarin, 1584 Thymic branchial cysts, features and management, 1705 Thyroid gland anatomy, 338–339, 338f neoplasia in dogs clinical signs, 337–338, 337t diagnosis, 338 treatment, 338 paratracheal palpation, 11–12, 11f radioiodine ablation cat, 336–337 dog, 338 radionuclide uptake and imaging, 334 thyroidectomy cat hyperthyroidism management, 336 technique cat, 339–340, 340f dog, 340–341, 341f Thyroid hormone. See also Hyperthyroidism; Hypothyroidism; Thyroxine feline symmetrical alopecia management, 529 laryngeal disease evaluation, 1624 tests, 329, 333 Thyrotropin-releasing hormone stimulation test, 329, 334 Thyroxine coagulation disease management, 263 free concentration analysis, 329, 333–334 hypothyroidism management cats, 331 dogs, 330 reptile dosage guidelines, 1927t Tibetan mastiff, hypertrophic neuropathy, 1307 Tibia. See also Tarsus anatomy diaphysis, 1145 epiphysis, 1144 metaphysis, 1144–1145 physis, 1144 fracture management cross pin fixation, 1146–1147, 1147f external skeletal fixation, 1148–1150, 1149f interfragmentary lag screw fixation, 1146 intermedullary pin and wire fixation, 1147–1148, 1148f pin and tension wire band fixation, 1145–1146, 1146f plate and screw fixation, 1150, 1150f postoperative care and complications, 1150–1151 preoperative considerations, 1145 radiography, 65 Ticks, reptiles, 1934 Tiletamine, reptile anesthesia, 1925–1926 Tiletamine/zolazepam applications, 22, 25 dosage guidelines cats, 21t dogs, 20t Timolol maleate, glaucoma management, 1376t, 1377
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Tocainide dosage guidelines, 1475t formulations, indications, and dosages, 1459t Toenail bleeding time test, coagulation disease diagnosis, 260 Tolazoline, dosage guidelines, 28t Tongue, cranial nerve examination, 1237 Tonometry applanation tonometry, 1330–1331 glaucoma diagnosis, 1375 indications, 1330 Schtz indentation tonometry, 1330 uveitis diagnosis, 1370 Tonsils neoplasia clinical signs, 632 diagnosis, 632 etiology, 632 treatment, 632 tonsillitis clinical signs, 631 diagnosis, 631 etiology, 631 treatment, 631–632 Topiramate cat administration, 1289 dog administration, 1285t epilepsy management, 1287–1288 Torovirus, feline diarrhea, 166 Torticollis, rabbits, 1877–1878 Tortoise. See Reptiles Total ear canal ablation (TECA) complications, 590 equipment, 588 indications, 587–588 objectives, 588 postoperative care, 588, 590 prognosis, 590 technique, 588, 589f Total plasma protein (TPP) dehydration detection, 86–87, 87t fluid therapy monitoring, 99 Toxic epidermal necrolysis clinical signs, 503–504 treatment, 504 Toxoplasmosis clinical signs, 222–223 diagnosis, 223–224 etiology, 219 prevention cats, 225 environmental control, 225 humans, 225 stages of infection, 219, 221–222 transmission, 219 treatment, 224–225 TPP. See Total plasma protein Tracheal disease avian disorders extramural obstruction, 1778 foreign bodies, 1777 injection or wash techniques, 1738 strictures, 1777–1778 tracheitis, 1777–1778 clinical signs, 1652–1653 collapse clinical features, 1651–1652, 1666–1667 diagnosis, 1667 etiology, 1666 medical therapy, 1667–1668, 1669t pathophysiology, 1666 prognosis, 1669 surgery, 1660–1663, 1661t, 1661f, 1668 diagnosis, 1624–1625, 1653–1654 fluoroscopy, 1654 foreign bodies, 1652, 1663
Tracheal disease (Continued) neoplasia, 1652 clinical signs, 1709–1710 diagnosis, 1709–1710 prognosis, 1710 treatment, 1710 tumor types, 1709, 1709t radiography, 1632, 1653 stenosis features and management, 1652, 1663–1664 Tracheobronchitis, infectious clinical features, 1687–1688 diagnosis, 1687–1688 prevention, 1690 treatment, 1688–1690 Tracheoscopy, technique, 1625, 1654 Tracheostomy complications, 35 contraindications, 34 equipment, 34, 1658 indications, 34 objectives, 34, 1658 postoperative care and complications, 35, 1659 preoperative considerations, 1658 technique, 34–35, 34f, 1658–1659, 1658f tube construction from endotracheal tube, 35f Tramadol, osteoarthritis management, 1226 Transfusion therapy. See Blood transfusion Transscleral photocoagulation, glaucoma management, 1378–1379 Transtracheal wash bronchitis, 1670–1671 technique, 1627, 1667–1668 Traumatic wound closure. See Wound closure Triamcinolone, atopic dermatitis management, 486, 486t Triceps reflex, spinal reflex examination, 1238 Trichomoniasis, avian, 1786–1787 Trichophyton mentagrophytes. See Dermatophytosis Tricuspid valve disease endocardiosis, 1496 malformation, 1499 right ventricular failure, 1516 Trientine, copper-associated hepatitis management, 781, 782t Trigeminal nerve eye function testing, 1412 neuritis clinical features and management, 1273–1274 neurofibroma clinical features and management, 1275 somatic sensory system of eye and orbit, 1419 trigeminolacrimal reflex and eye neurologic disturbance evaluation, 1410 Trigeminoabducent reflex, eye neurologic disturbance evaluation, 1411 Trilostane adverse effects, 365 hyperadrenocorticism management, 365, 367, 370 Trimethoprim hepatozoonosis management, 227 neosporosis management, 226 rabbit dosage guidelines, 1863t reptile dosage guidelines, 1927t toxoplasmosis management, 224 Triodothyronine suppression test, 334 Tritrichomonas foetus clinical signs, 719 diagnosis, 719 treatment, 719–720
Troglitazone, diabetes type 2 management, 387t, 388 Troponin-I, feline hypertrophic cardiomyopathy testing, 1532 Trypanosomiasis, systemic infection, 220t Trypsin-like immunoreactivity assay, pancreatic function testing, 822–823, 828, 828t Tube cystostomy. See Cystostomy Tuberculosis avian, 1756, 1761 ferrets, 1827 Tularemia clinical signs, 202 diagnosis, 202 etiology, 202 transmission, 202 treatment, 202 Turtles. See Reptiles T wave. See Electrocardiography Tylosin, rodent dosage guidelines, 1895t Typhlectomy equipment, 745 indications, 745 objectives, 745 postoperative care, 745 preoperative considerations, 745 prognosis, 745 technique, 745 Ulcerative pododermatitis, rabbits, 1866 Ulna carpal bone fracture, 1099 fracture closed reduction, 1089–1090 external skeletal fixation, 1090, 1090f mid-shaft fracture, 1089 Monteggia fracture, 1089, 1089f olecranon, 1087, 1087f plate fixation, 1090–1091 postoperative care and complications, 1087 preoperative considerations, 1086–1087 trochlear notch, 1088, 1088f growth deformity correction anatomy, 1091 distal ulnar physis closure, 1092–1093, 1092f postoperative care and complications, 1091 preoperative considerations, 1091 prognosis, 1092 Ultrasonography. See also Echocardiography adrenal gland, 362 applications, 80, 81t bronchopulmonary disease evaluation, 1629 echogenicity of organs, 80 equipment accessories, 79 ancillary equipment, 79 image storage, 79 machines, 78–79 suppliers, 78t transducers, 79, 79t eye, 1332 ferret, 1819 gastric outflow obstruction, 683 heartworm diagnosis, 1566–1567 inflammatory bowel disease, 726 interventional ultrasound, 80–81 liver, 755 neurologic disease assessment, 1241 otitis media and otitis interna, 596 ovaries, 983 pancreatitis, 823–824 pericardial effusion, 1553
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Page 2005
Index Ultrasonography (Continued) peritonitis diagnosis, 857 pleural effusion, 1699 pregnancy diagnosis, 1019 prostate gland, 951 rabbits, 1861–1862 respiratory disease, 1641 splenic disease, 278 technique, 79, 80f terminology, 80 testes, 966 vomiting, 666 Upper airway obstruction, physical examination, 1428 Upper gastrointestinal study, technique, 72 Upper motor neuron bladder clinical signs, 941–943 diagnosis, 943–945 treatment, 945 Urachal diverticulum clinical signs, 896–897 etiology, 896 Ureter anatomy, 889 ectopic clinical signs, 886, 942 diagnosis, 886, 945 etiology, 886 prevention, 886 treatment, 886, 948 obstruction clinical signs, 887 diagnosis, 887 etiology, 886–887 treatment, 887 stones. See Ureterolithiasis trauma clinical signs, 885 diagnosis, 885 etiology, 884 treatment, 885 ureteroneocystostomy equipment, 893 objectives, 893 postoperative care and complications, 894 preoperative considerations, 893 technique, 893–894, 893f ureterotomy and anastomosis equipment, 892 objectives, 892 postoperative care and complications, 893 preoperative considerations, 892 technique, 892–893 Ureterolithiasis clinical signs, 881–882 diagnosis, 882 etiology, 881 prevention, 883 treatment, 882–883 Urethra anastomosis equipment, 931 objectives, 931 postoperative care and complications, 931–932 preoperative considerations, 931 technique, 931 anatomy female, 930–931 male cat, 930 dog, 930 brush specimen collection, 952–953, 953t
Urethra (Continued) congenital disorders etiology, 922 clinical signs, 922 diagnosis, 922 treatment, 922–923 neoplasia clinical signs, 928 diagnosis, 928 etiology, 928 treatment, 928–929 obstruction clinical signs, 923 diagnosis, 923 etiology, 923 treatment hydropropulsion, 924–925 patient stabilization, 923–924 perineal urethrostomy, male cat equipment, 931 objectives, 935 postoperative care and complications, 936–937 preoperative considerations, 934–935 technique, 935–936 prepubic urethrostomy equipment, 937 objectives, 937 postoperative care and complications, 938 preoperative considerations, 937 technique, 937–938, 938f prolapse clinical signs, 927 diagnosis, 928 etiology, 927 surgery in male dog, 938–939 treatment, 928 stricture clinical signs, 927 diagnosis, 927 etiology, 927 treatment, 927 trauma clinical signs, 926 diagnosis, 926 etiology, 926 treatment, 926–927 urethritis bacterial urethritis, 925–926 proliferative urethritis, 925 urethrography, 71, 951 urethrostomy, male dog equipment, 933 objectives, 933 postoperative care and complications, 933–934 preoperative considerations, 933 technique, 933, 934f urethrotomy, male dog equipment, 932 objectives, 932 postoperative care and complications, 932–933 preoperative considerations, 932 technique, 932 Urge incontinence clinical signs, 942–943 diagnosis, 943–945 treatment, 947 Urinalysis bacterial endocarditis, 1524 dehydration detection, 87 glomerulonephritis, 876 neurologic disease assessment, 1241 urinary bladder disease, 895
2005
Urinary bladder catheterization in ferret, 1821 nervous control, 940–941 physical examination, 15 Urinary bladder disease. See also Cyclophosphamide-induced hemorrhagic cystitis; Emphysematous cystitis; Idiopathic feline lower urinary tract disease; Polyploid cystitis congenital diseases agenesis and malformations, 897–898 patent urachus, 896 urachal diverticulum, 896–897 diagnostic principles biopsy, 896 blood tests, 895 cystoscopy, 896 imaging, 895 residual urine volume, 895 urinalysis, 895 infection clinical signs, 905 diagnosis, 905–906, 906t etiology bacteria, 904–905 fungi, 905 parasites, 905 prevention, 908 recurrent disease, 907, 907t treatment, 906–907 neoplasia clinical signs, 912 diagnosis, 912–913 etiology, 912 prevention, 913 surgery. See Urinary bladder surgery treatment, 913 stones. See Urolithiasis trauma clinical signs, 913 diagnosis, 913–914 etiology, 913 prevention, 914 treatment, 914 Urinary bladder surgery anatomy, 915 cystectomy, subtotal equipment, 919 objectives, 919 postoperative care and complications, 920 preoperative considerations, 919 technique, 919–920 cystostomy equipment, 916–917 objectives, 916 postoperative care and complications, 918 technique, 917–918, 917f tube cystostomy, 920–921, 921f persistent urachus equipment, 915 objectives, 915 postoperative care and complications, 916 technique, 915–916 trauma equipment, 919 objectives, 918 postoperative care and complications, 919 preoperative considerations, 918 technique, 919 vesicourachal diverticulum excision equipment, 916 objectives, 916
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2006
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Urinary bladder surgery (Continued) postoperative care and complications, 916 technique, 916 Urinary system, history taking, 4–5 Urination. See Micturition disorders Urine bile acid, liver function testing, 753–754 Urolithiasis breed susceptibilities, 898t clinical signs, 899–900 diagnosis, 900 ferrets, 1855–1856 prevention, 902–904, 902t reptiles, 1939 treatment ammonium urate uroliths, 901, 902t calcium oxalate uroliths, 901, 902t calcium phosphate uroliths, 901 cystine uroliths, 901–902 medical versus surgical, 900–901 silica uroliths, 902 struvite uroliths, 901, 901t xanthine uroliths, 902 urolith types ammonium urate, 899 calcium oxalate, 899 calcium phosphate, 899 cystine, 899 silica, 899 struvite, 898–899 xanthine, 899 Uropygial gland anatomy and function, 1764 disorders, 1764–1765 Ursodiol canine chronic hepatitis management, 779 hepatoprotection, 760t Uterine inertia, features, 988 Uterus anatomy, 992, 993f biopsy, 1000 diseases bacterial metritis, 990 dystocia, 989 infection, 987 neoplasia, 991 parturition, 988–989 prolapse external amputation, 1000 features, 990 manual reduction, 999 pyometra, 985–987 subinvolution of placental sites, 990–991 physical examination, 15 rabbit adenocarcinoma/hyperplasia, 1874 resection. See Ovariohysterectomy torsion in birds, 1801–1802 Uvea anatomy, 1366 congenital abnormalities aniridia, 1367 coloboma, 1367 cyst, 1367 iris atrophy, 1367–1368 persistent pupillary membranes, 1366–1367 neoplasia, 1372–1373 Uveitis anterior uveitis clinical signs, 1369, 1369t diagnosis, 1369–1370, 1369f etiology, 1368–1369, 1368t prevention, 1372
Uveitis (Continued) sequelae, 1372 treatment, 1370–1372, 1371t classification, 1368 lens-induced uveitis, 1362 Uveodermatologic syndrome clinical signs, 497 diagnosis, 497 etiology, 497 treatment, 497 Vaccination. See also specific diseases annualized vaccination protocols cats high risk, 113t, 114t low risk, 112t, 113t moderate risk, 112t dogs high risk, 111t low risk, 110t moderate risk, 109t risk stratification, 108, 114 borreliosis, 189–190 budgerigar fledgling disease, 1748 core vaccines, 108 dermatophytosis management, 458 guidelines overview, 108 reassessment, 107–108 historical background, 107 immunity duration, 108 non-core vaccines, 108 Pacheco’s disease, 1749 polyneuropathy as complication, 1311 thrombocytopenia risks, 249 Vagina anatomy, 1009 annular bands, 1004 episiotomy. See Episiotomy hyperplasia features, 1005, 1019 surgical excision, 1012, 1013f neoplasia benign, 1006 malignant, 1007 persistent hymen features, 1004 surgical excision, 1011–1012 prolapse features, 1005–1006 surgical excision, 1013–1014, 1014f Vaginitis anatomy, 1009 diagnosis, 1007–1008 etiology, 1007 puppy vaginitis, 1018 treatment, 1008 Valvular heart disease. See also specific valves chronic disease pathology, 1514–1515 pathophysiology, 1515–1517, 1515f clinical signs, 1517 diagnosis, 1517–1519 differential diagnosis, 1519 etiology, 1514, 1514t ferrets, 1845 murmurs, 1513–1514 normal function, 1513 prognosis, 1522 stenosis, 1598 syncope, 1510 treatment asymptomatic dog, 1519–1520 coughing dog with mitral regurgitation, 1520 follow-up, 1522
Valvular heart disease (Continued) left-sided congestive heart failure, 1520–1521 respiratory complications, 1521–1522 right-sided congestive heart failure, 1521 valve structure, 1513 Vanadium, diabetes type 2 management, 387t, 388 Vascular encephalopathy clinical signs, 1260 diagnosis, 1260 etiology, 1260 prognosis, 1261 treatment, 1261 Vascular neoplasia clinical signs, 1587 diagnosis, 1587 etiology, 1586–1587 treatment, 1587 Vasculitis clinical signs, 499, 502, 1585 diagnosis, 499 etiology, 499, 502, 1585 infectious, 1262 necrotizing vasculitis of beagle, Bernese mountain dog, and German shorthaired pointer, 1261–1262 pinna, 570 reptiles, 1935 treatment, 499, 502, 1585 Vasotocin, reptile dosage guidelines, 1927t VECA. See Vertical ear canal ablation Vector-borne viruses, transmission of, 176 Vena cava syndrome. See Heartworm Venereal tumor, female genitalia, 1007 Ventral bulla osteotomy objectives, 601 postoperative care and complications, 601 preoperative considerations, 600 technique, 601, 601f Ventricular fibrillation defibrillation, 1617, 1618t features and management, 1467–1468, 1467f Ventricular preexcitation, electrocardiography, 1446–1447, 1446f, 1447f Ventricular premature complexes definition, 1463–1465 electrocardiogram, 1464f etiology, 1465 treatment, 1465 Ventricular septal defect (VSD) canine heart disease, 1499 treatment and prognosis, 1596–1597 Ventriculus candidiasis, 1791 foreign body impaction, 1790–1801 structure and function, 1790 Verapamil dosage guidelines, 1475t formulations, indications, and dosages, 1459t Vertebral heart score (VHS), cardiomegaly verification, 1438, 1438f Vertical ear canal ablation (VECA) equipment, 586 objectives, 586 postoperative care and complications, 586 prognosis, 586 technique, 586, 587f Vesicourachal diverticulum. See Urachal diverticulum Vesicular cutaneous lupus erythematosus. See Lupus erythematosus complex
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Index Vestibular syndrome, aging dog clinical features and management, 1274–1275 Vestibulo-ocular reflex, eye neurologic disturbance evaluation, 1412 VHS. See Vertebral heart score Vigabatrin, canine toxicity, 1288 Villous atrophy clinical signs, 734 diagnosis, 734 etiology, 734 prognosis, 735 treatment, 735 Vinblastine, chemotherapy guidelines, 288t Vincristine chemotherapy guidelines, 288t immune-mediated thrombocytopenia management, 269 Vital signs anesthesia, 19t, 26–27 body temperature, 8 capillary refill time, 8 heart rate, 8 hydration, 8 pulse, 8 respiratory rate, 8 Vitamin(s). See also specific vitamins parenteral fluid supplementation, 93–94 reptile dosage guidelines, 1927t Vitamin A deficiency in turtles, 1940 hypovitaminosis A in birds, 1764, 1774, 1785 toxicity in turtles, 1940 Vitamin A-responsive dermatosis clinical signs, 510 diagnosis, 510 etiology, 510 treatment, 510 Vitamin C hepatoprotection, 760t osteoarthritis management, 1226 Vitamin D assay of metabolites, 345 calcium regulation, 343–344 hypervitaminosis hypercalcemia, 349 reptiles, 1938 hypocalcemia management, 353 Vitamin E canine chronic hepatitis management, 779 copper-associated hepatitis management, 781, 782t feline hepatic lipidosis management, 772 hepatoprotection, 760t lupus erythematosus complex management, 499 Vitamin K deficiency crocodilians, 1942 dogs and cats, 256 therapy indications, 263 Vitreous humor diseases clinical signs, 1382 diagnosis, 1382 etiology, 1381–1382 treatment, 1382 evaluation, 1381 Vogt-Koyanagi-Harada syndrome. See Uveodermatologic syndrome Vomiting clinical signs, 664 diagnosis acute versus chronic vomiting, 664–665 endoscopy, 666 history, 665
Vomiting (Continued) laboratory evaluation, 666 laparoscopy, 666 physical examination, 665 radiography, 666 ultrasound, 666 etiology, 664, 665t ferrets, 1847 pathophysiology, 664 treatment, 824, 867 antiemetics, 667–668, 667f diet, 667 fluid therapy, 666–667 von Willebrand disease (vWD) antigen assay, 261 clinical features, 257–258 Voriconazole, features, 217 VSD. See Ventricular septal defect Vulva clitoral hypertrophy, 1002–1003 enlargement, 1003 episioplasty, 1011 ferrets and swelling, 1853 hypoplasia, 1001–1002 stenosis, 1002 trauma, 1003 vWD. See von Willebrand disease Warfarin arterial thromboembolism management, 1541 dosage guidelines, 1475t thrombotic disease management, 1584 Water deprivation test, 404–405 West Highland white terrier, chronic hepatitis, 783 West Nile virus (WNV) crocodilian infection, 1942 transmission, 175–176 Western blot borreliosis diagnosis, 189 feline immunodeficiency virus diagnostics, 129 Whipworm clinical signs, 716 diagnosis, 716 life cycle, 716 prevention, 716 species, 716 treatment, 716 WNV. See West Nile virus Wobbler’s syndrome. See Caudal cervical spondylomyelopathy Wolff-Parkinson-White syndrome, features and management, 1471 Wood’s light, dermatophytosis diagnosis, 453–454 Wound. See Open wound management; Wound closure Wound closure anatomy, 541 non-surgical. See Open wound management preoperative considerations, 541 with tension complications, 548 equipment, 542 objectives, 542 postoperative care, 547 technique, 542–547, 542f, 543f, 544f, 545f, 546f, 547f, 548f without tension complications, 542 equipment, 541 objectives, 541 postoperative care, 542 technique, 541
2007
Xanthine. See Urolithiasis Xanthoma, avian, 1763 Xeromycteria, lacrimation disorders, 1415–1416 X-ray accessories cassettes, 54 film, 53, 54t intensifying screens, 52–53 manufacturers, 55t miscellaneous accessories, 54 bird restraint, 1733, 1734f computed radiography, 62 congenital heart disease, 1593 contrast studies cystography complications, 71 double contrast, 70 positive contrast, 70–71 esophagography, 71 gastrography, 71 intravenous pyelogram, 69–70 intravenous urogram, 69–70 medium, 69, 70t myelography, 72–73, 73f upper gastrointestinal study, 71–72 urethrography, 71 digital radiography, 62 exposure time, 53 feline hypertrophic cardiomyopathy, 1532 feline restrictive cardiomyopathy, 1534 ferret, 1819 film processing automatic processing, 57, 57t darkroom layout, 58, 59f, 60f manual processing accessories, 56 advantages and disadvantages, 56 darkroom safelight, 56 radiograph labeling, 56 silver recovery, 56 technique, 56–57 fractures. See specific bones interpretation, 75–76 machine accuracy check exposure timer check, 55 kilovolt peak check, 55 line voltage, 55–56 milliampere station check, 54–55 components and recommendations, 51–52 kilovolt peak, 51 manufacturers, 52t milliampere-second, 51 nasal cavity abnormalities, 1631–1632 anatomy, 1630 neurologic disease assessment, 1242 pericardial effusion, 1553 peritonitis diagnosis, 857 positioning and technique abdomen, 63–64, 63f, 64f antebrachium, 64 carpus, 65 digits, 65 elbow, 64 extremities, 64 femur, 65 humerus, 64 measurements, 62 pelvis, 65 shoulder, 64 skull, 67–69, 67f, 68f, 69f
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2008
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X-ray (Continued) spine cervical spine, 66–67 principles, 66, 66t thoracolumbar spine, 67 stifle, 65 tarsus, 66 thorax, 63, 63f tibia and fibula, 665 pregnancy diagnosis, 1020 rabbits, 1861 radiation safety clinic construction, 75 exposure minimization, 74 film badges, 74t maximum permissible dose, 73–74 records, 75f, 76f reptiles, 1924 rodents, 1886 spinal cord disorders, 1298 technique chart with grid, 58, 61f nonscreen film technique chart, 62, 62f overview, 58 tabletop without grid, 58, 61f, 62 thoracic film anatomy, 1630–1631 aortic enlargement, 1436, 1436f biventricular enlargement, 1435–1436 congestive heart failure, 1437–1438 evaluation, 1626–1627 interpretation heart disease features, 1439t initial approach, 1433 lateral radiograph cat, 1431 dog, 1430–1431, 1431f
X-ray (Continued) left atrium enlargement, 1434–1435, 1435f rupture, 1440 left ventricular enlargement, 1435, 1435f lymph nodes, 1633, 1633f microcardia, 1436 pericardial effusion, 1440 pulmonary arteries and veins, 1433 pulmonary disease, 1635–1641 pulmonary vasculature, 1437, 1437f right atrial enlargement, 1433, 1433f right ventricular enlargement, 1433–1434, 1434f technical considerations, 1430, 1631 valentine-shaped heart in cats, 1439–1440 ventrodorsal radiograph cat, 1431–1432 dog, 1431, 1431f vertebral heart score, 1438, 1438f Xylazine applications, 20 dosage guidelines cats, 21t, 103t dogs, 20t, 103t rabbit dosage guidelines, 1863t Yohimbine, dosage guidelines, 28t Yolk emboli, features and management, 1815 Yorkshire terrier, melanoderma and alopecia, 572 Y-U pyloroplasty. See Pyloroplasty
Zidovudine (AZT) feline immunodeficiency virus management, 130 feline leukemia virus management, 123 Zinc copper-associated hepatitis management, 781, 782t hemolytic toxicity, 237 hepatoprotection, 760t Zinc-responsive dermatosis clinical signs, 511 diagnosis, 511 etiology, 511 pinna, 572 treatment, 511 Zonisamide dog administration, 1285t epilepsy management, 1288 Zygomatic arch anatomy, 1033 fracture surgery, 1033–1034 resection, 1042 Zygomatic mucocele, exophthalmos, 1401 Zygomycosis clinical signs, 439 diagnosis, 439–440 epidemiology, 439 etiology, 439 intestinal clinical signs, 724 diagnosis, 724 treatment, 724 systemic infection, 214t treatment, 440
