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Lynelle R. Johnson

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A fully updated edition of the essential comprehensive resource on diagnosing and treating respiratory diseases in dogs and cats

Canine and Feline Respiratory Medicine, Third Edition is a thorough, comprehensive reference for respiratory medicine in dogs and cats. Focusing on the entire respiratory tract, the book presents detailed coverage of diagnostics and therapeutics. Now fully updated to incorporate the latest clinical data and case studies, this Third Edition continues to be an indispensable resource for all small animal veterinary practitioners involved with respiratory disease.

Covering a wide range of respiratory diseases, the book draws on extensive research and clinical practice. Readers of the third edition of Canine and Feline Respiratory Medicine will also find:

  • Clinical photographs and illustrations accompanying every major concept discussed
  • New clinical case examples for diseases in specific locations of the respiratory tract and new sections in almost every chapter
  • Discussion of the full range of disease processes

Canine and Feline Respiratory Medicine is ideal for any veterinary practitioner or specialist with an interest in respiratory disease, including internal medicine specialists and residents.

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Table of Contents

Cover

Table of Contents

Title Page

Copyright Page

Dedication Page

Preface

Acknowledgments

1 Localization of Disease

Nasal Discharge

Loud Breathing

Cough

Tachypnea versus Panting

Exercise Intolerance

Differentiating Cardiac from Respiratory Disease

Additional Considerations

References

2 Respiratory Diagnostics

General

Diagnostic Imaging

Airway Sampling

Respiratory Endoscopy

Sample Analysis

References

3 Respiratory Therapeutics

Considerations in Drug Therapy

Routes of Administration

Adjunct Therapy

References

4 Nasal Disorders

Structural Diseases

Infectious Diseases

Inflammatory Diseases

Other Nasal Diseases

References

5 Diseases of Airways

Structural Disorders

Infectious Diseases

Inflammatory Disorders

Neoplastic Disorders

References

6 Parenchymal Disease

Structural Diseases

Infectious Diseases

Inflammatory Disorders

References

7 Pleural and Mediastinal Disease

Structural Disorders

Infectious Disorders

Other Pleural Disorders

References

8 Vascular Disorders

Structural Disorders

Infectious Disorders

Miscellaneous Disorders

References

Glossary

Index

End User License Agreement

List of Tables

Chapter 1

Table 1.1 Causes of nasal discharge in dogs and cats.

Table 1.2 Respiratory causes of cough in dogs and cats.

Chapter 2

Table 2.1 Normal coagulation parameters for dogs and cats (University of Ca...

Table 2.2 Normal blood gas values for dogs and cats.

Table 2.3 Respiratory causes of hypoxemia.

Table 2.4 Airway sampling techniques for various lung patterns.

Table 2.5 Select anesthetic agents that can be considered to facilitate res...

Table 2.6 General guidelines for performing bronchoalveolar lavage (BAL).

Table 2.7 Lower respiratory tract flora found in healthy dogs and cats.

Table 2.8 Characteristics of pleural fluid.

Chapter 3

Table 3.1 Gram‐stain characteristics and antibiotic susceptibility for comm...

Table 3.2 Drug dosages of antibiotics commonly used for respiratory tract i...

Table 3.3 Side effects of commonly used antibiotics.

Table 3.4 Antifungal drug therapy.

Chapter 5

Table 5.1 Congenital forms of laryngeal paralysis.

Table 5.2 List of pathogens currently identified as involved in canine infe...

Table 5.3 Clinical characteristics, diagnostic methods, and treatment for p...

Chapter 6

Table 6.1 Bacterial organisms commonly found in dogs with lower respiratory...

Table 6.2 Bacterial organisms commonly found in cats with lower respiratory ...

Table 6.3 Characteristics of common fungal organisms.

Chapter 7

Table 7.1 Organisms commonly identified in animals with pyothorax.

List of Illustrations

Chapter 1

Figure 1.1 Nasal airflow can be assessed by occluding one nostril and assess...

Figure 1.2 Palpation during ocular retropulsion can suggest the presence of ...

Figure 1.3 In the normal animal, palpation of the soft palate will readily d...

Figure 1.4 Prior to thoracic auscultation, the laryngeal and cervical trache...

Figure 1.5 Each region of the thorax should be percussed to detect regional ...

Chapter 2

Figure 2.1 Coagulation cascade. FDPs, fibrin degradation products.

Figure 2.2 Pulse oximetry measures hemoglobin saturation with oxygen, which ...

Figure 2.3 (a and b) The urinary catheter used to collect an airway sample d...

Figure 2.4 During instillation of fluid to the airways, the three‐way stopco...

Figure 2.5 A sterile suction trap can be secured below the patient during th...

Figure 2.6 An over‐the‐needle catheter (lower half of the slide) can be used...

Figure 2.7 (a) To initiate a transtracheal wash, the over‐the‐needle cathete...

Figure 2.8 The short catheter has been seated between the tracheal rings and...

Figure 2.9 Visualization of the choanae is obtained by inserting a flexible ...

Figure 2.10 Image of the normal nasopharynx in (a) a dog and (b) a cat. The ...

Figure 2.11 The sheath (~5 mm outer diameter) for the telescope portion of t...

Figure 2.12 Normal nasal turbinates in (a) the dog and (b) the cat.

Figure 2.13 Prior to entering the nasal cavity, the cytology brush should be...

Figure 2.14 Diagnostic yield of a nasal biopsy sample is improved when the s...

Figure 2.15 Nasal flush can be performed in a cat by inserting a syringe tip...

Figure 2.16 (a) Right‐angle forceps can be used to place a Foley catheter ab...

Figure 2.17 A periodontal probe is inserted along the gum lines surrounding ...

Figure 2.18 Endoscopic image of the larynx showing the palate (P), cornicula...

Figure 2.19 A bronchoscopy adapter allows passage of a ~5.0 mm endoscope thr...

Figure 2.20 Endoscopic view of the normal canine trachea.

Figure 2.21 Endoscopic view of the carina illustrating the openings into the...

Figure 2.22 Distal airways in the dog exhibit relatively sharp bifurcations ...

Figure 2.23 Bronchoalveolar lavage (BAL) is performed by gently wedging the ...

Figure 2.24 (a) To initiate thoracocentesis, the skin is tented and the cath...

Figure 2.25 Ultrasound guidance is used to obtain a lung biopsy using a Temn...

Figure 2.26 Cytocentrifuge of a normal BAL sample (40×) reveals primarily ma...

Chapter 3

Figure 3.1 Nebulization is administered in a cat carrier covered in plastic ...

Figure 3.2 Chest coupage is performed after nebulization by using cupped han...

Figure 3.3 Transected skull shows placement of a nasal oxygen catheter throu...

Figure 3.4 For removal of viscid pleural fluid associated with pyothorax, ad...

Figure 3.5 This cat is in left lateral recumbency with the head to the right...

Figure 3.6 (a) The red rubber catheter and stabilizing catheter are assemble...

Figure 3.7 A purse‐string suture and finger cot pattern are used to close th...

Figure 3.8 Mila small‐bore chest tube kit contains (from top to bottom) 14 a...

Figure 3.9 The plastic sheath used to deploy the J wire contains a groove to...

Figure 3.10 (a) Right lateral and (b) dorsoventral radiographs in a dog, sho...

Chapter 4

Figure 4.1 Retroflex view of the choanae in a Pug shows hyperemic and swolle...

Figure 4.2 Stenotic nares in a brachycephalic cat.

Figure 4.3 Position of the soft palate in a brachycephalic dog. E represents...

Figure 4.4 Everted laryngeal ventricles (S) are evident at the ventral‐most ...

Figure 4.5 Laryngeal collapse in a 2‐year‐old Norwich Terrier. Cuneiform pro...

Figure 4.6 Rhinoscopic view of the left nasal cavity of a dog that had acute...

Figure 4.7 An adult cat evaluated for chronic nasal discharge was placed und...

Figure 4.8 An adult DMH cat has obvious facial swelling on the left side of ...

Figure 4.9 Retroflex view of the choanae in a 17‐year‐old spayed female dome...

Figure 4.10 Computed tomography images from a young dog with nasopharyngeal ...

Figure 4.11 (a) The dorsal portion of the nose is distorted by a mass lesion...

Figure 4.12 Cytology of an impression smear from a nasal mass in a cat. Wrig...

Figure 4.13 Depigmentation at the entrance to the right nasal cavity.

Figure 4.14 Open mouth radiographic view (a) of the nasal cavity in a 2‐year...

Figure 4.15 Computed tomography (CT) images from two dogs with confirmed sin...

Figure 4.16 Fungal plaques identified during endoscopy in a dog with sino‐na...

Figure 4.17 New methylene blue staining of an impression smear from the samp...

Figure 4.18 Placement of nasal catheters for treatment of sino‐nasal aspergi...

Figure 4.19 CT image of the rostral nasal cavity from a cat presented for a ...

Figure 4.20 Retroflex view of the choanae in a 10‐year‐old spayed female (FS...

Figure 4.21 Cervical radiograph from a 4‐year‐old spayed female domestic sho...

Figure 4.22 Endoscopic view of the choanae reveals a nasopharyngeal polyp.

Figure 4.23 Open mouth views of the nasal cavity of a cat taken under genera...

Figure 4.24 Computed tomography image of the nasal cavity in a cat with righ...

Figure 4.25 Computed tomography image through the frontal sinus and nasophar...

Figure 4.26 Rhinoscopic image in a cat with chronic rhinosinusitis reveals m...

Figure 4.27 Computed tomography findings in a dog with lymphoplasmacytic rhi...

Figure 4.28 Rhinoscopic image from a dog with idiopathic LPR reveals mucosal...

Figure 4.29 Facial asymmetry is evident in this 9‐year‐old male castrated do...

Figure 4.30 Computed tomography image from a 9‐year‐old spayed female (FS) D...

Figure 4.31 Rhinoscopic image from a dog with nasal neoplasia reveals a soft...

Figure 4.32 Nasal mite found in the nose of a dog presented for reverse snee...

Case Figure 1 Computed tomography.

Case Figure 2 Rhinoscopy.

Chapter 5

Figure 5.1 Right lateral cervical radiograph of a 9‐year‐old male castrated ...

Figure 5.2 Endoscopic image of an 11‐year‐old male castrated (MC) Labrador R...

Figure 5.3 Laryngoscopic image from a 1‐year‐old Norwich Terrier with inspir...

Figure 5.4 Laryngoscopic image from an 11‐year‐old Maltese with intermittent...

Figure 5.5 The airways are exposed to atmospheric pressure in the cervical r...

Figure 5.6 Inspiratory (a) and expiratory (b) fluoroscopic images from a 13‐...

Figure 5.7 Fluoroscopic image from a 15‐year‐old spayed female (FS) Pug demo...

Figure 5.8 (a) Grade I: The cartilage ring structure of the trachea remains ...

Figure 5.9 Bronchoscopic image demonstrating 70–100% collapse of lobar bronc...

Figure 5.10 Prosthetic rings used for external support in dogs with cervical...

Figure 5.11 Catheter delivery system and close‐up of a distal deployment ste...

Figure 5.12 (a) Right lateral and (b) ventrodorsal radiographs from an 8‐yea...

Figure 5.13 Sagittal reconstruction of a computed tomography (CT) image from...

Figure 5.14 Bronchoscopic image of the lungs from a cat with bronchiectasis....

Figure 5.15 Right lateral (a), left lateral (b), and ventrodorsal (c) radiog...

Figure 5.16 Bronchoscopic visualization of the distal airways in a 1 year ol...

Figure 5.17 Bronchoscopy in a 6 year old Golden‐Doodle with a 1 month histor...

Figure 5.18 (a) Right lateral and (b) dorsoventral radiographs from a 12‐yea...

Figure 5.19 Bronchoscopic images from two dogs with chronic bronchitis. (a) ...

Figure 5.20 Neutrophilic airway cytology from a dog with chronic bronchitis ...

Figure 5.21 (a) Right lateral and (b) dorsoventral radiographs from a 2‐year...

Figure 5.22 Right lateral radiograph from a 4‐year‐old male castrated (MC) R...

Figure 5.23 (a) Left lateral and (b) ventrodorsal radiographs from a 9‐year‐...

Figure 5.24 Bronchoalveolar lavage cytology from two cats with feline bronch...

Figure 5.25 Right lateral radiographs from (a) an 11‐year‐old cat with a lar...

Figure 5.26 Bronchoscopic image from a 10‐year‐old cat with an adenocarcinom...

Case Figure 1 Cervical radiograph (a). Thoracic radiographs (b–d).

Case Figure 2 Bronchial collapse at the left cranial and caudal lobar bronch...

Chapter 6

Figure 6.1 Electron microscopy image showing two abnormal cilia in cross‐sec...

Figure 6.2 (a) Right lateral and (b) dorsoventral radiographs from a dog wit...

Figure 6.3 Bronchoscopic image demonstrating torsion of the right middle lun...

Figure 6.4 Fluoroscopic image demonstrates barium being coughed or regurgita...

Figure 6.5 (a) Right lateral, (b) left lateral, and (c) dorsoventral radiogr...

Figure 6.6 Bronchoscopy image from a dog with

Mycoplasma

pneumonia reveals a...

Figure 6.7 Airway cytology from bronchoalveolar lavage (BAL) fluid confirms ...

Figure 6.8 Right lateral thoracic radiographs from a dog with (a) coccidioid...

Figure 6.9 (a) Right lateral and (b) dorsoventral radiographs from a 2‐year‐...

Figure 6.10 (a) Right lateral and (b) dorsoventral radiographs from a 3‐year...

Figure 6.11 BAL cytology from a dog with

Pneumocystis

pneumonia reveals clas...

Figure 6.12 Gross necropsy findings from a dog with pyogranulomatous pneumon...

Figure 6.13 (a) Right lateral and (b) dorsoventral radiographs from a 1‐year...

Figure 6.14 (a) Dorsoventral radiograph and (b) cross‐sectional computed tom...

Figure 6.15 Bronchoscopic images from dogs with eosinophilic lung disease ca...

Figure 6.16 Airway cytology from a dog with eosinophilic lung disease confir...

Figure 6.17 (a) Left lateral and (b) dorsoventral radiographs from a 12‐year...

Figure 6.18 (a) Right lateral and (b) dorsoventral radiographs of a 2‐year‐o...

Figure 6.19 (a) Right lateral and (b) dorsoventral radiographs from a 12‐yea...

Figure 6.20 (a) Right lateral and (b) dorsoventral radiographs from a 17‐yea...

Figure 6.21 (a) Right lateral and (b) dorsoventral radiographs from a 10‐yea...

Figure 6.22 Pulmonary metastasis of a thyroid carcinoma in a 13‐year‐old spa...

Figure 6.23 (a) Right lateral radiograph and (b) gross necropsy findings in ...

Figure 6.24 Bronchoscopic image from a 10‐year‐old male castrated domestic s...

Figure 6.25 Cytology from a BAL sample in a 13‐year‐old castrated male (MC) ...

Case Figure 1 Lateral (a and b) and dorsoventral (c) thoracic radiographs.

Case Figure 2 Bronchoscopy.

Case Figure 3 BAL fluid was hypercellular.

Chapter 7

Figure 7.1 (a) Right lateral and (b) dorsoventral radiographs from a 7‐year‐...

Figure 7.2 Computed tomographic slice through the caudal thorax of a 6‐year‐...

Figure 7.3 Thoracic radiographs with red markings outlining the boundaries o...

Figure 7.4 Right lateral radiograph from an 18‐month‐old spayed female domes...

Figure 7.5 (a) Right lateral and (b) dorsoventral radiographs of a 2‐year‐ol...

Figure 7.6 (a) Right lateral and (b) ventrodorsal radiographs from a 6‐year‐...

Figure 7.7 Pleural fluid cytology from a cat with pleural effusion reveals d...

Figure 7.8 (a) Lateral scout image from computed tomography and (b) a cross‐...

Figure 7.9 This 9‐year‐old spayed female (FS) Mix breed dog demonstrates pto...

Figure 7.10 Dorsoventral radiograph from a Bulldog demonstrates widening of ...

Figure 7.11 Right lateral radiograph from an 11‐year‐old Labrador reveals a ...

Figure 7.12 (a) Right lateral and (b) dorsoventral radiographs from a 7‐year...

Figure 7.13 (a) Right and (b) left lateral radiographs show rounding of the ...

Figure 7.14 Chylous effusion is typically opaque due to the presence of chyl...

Figure 7.15 (a) Right and (b) left lateral radiographs from a cat with chylo...

Figure 7.16 Necropsy image from a 5‐year‐old spayed female domestic short ha...

Case Figure 1 Thoracic radiographs.

Case Figure 2 Lymphoscintigraphy.

Chapter 8

Figure 8.1 Dorsoventral film radiograph from a dog documented to have a pulm...

Figure 8.2 Perfusion scan from the dog depicted in Figure 8.1 indicates a la...

Figure 8.3 (a) Right lateral and (b) dorsoventral radiographs from a 4‐year‐...

Figure 8.4 Echocardiographic image from the dog depicted in Figure 8.3 demon...

Figure 8.5 (a) Right lateral and (b) dorsoventral radiographs from a 5‐year‐...

Figure 8.6 (a) Right lateral and (b) dorsoventral radiographs from a 13‐year...

Figure 8.7 Doppler echocardiography reveals tricuspid regurgitation with an ...

Figure 8.8 Two‐dimensional Doppler image from the right parasternal short‐ax...

Figure 8.9 Type I (normal), type II, and type III pulmonary velocity profile...

Figure 8.10 This right parasternal short‐axis view through the left (L) and ...

Figure 8.11 (a) Right lateral and (b) dorsoventral radiographs from a 10‐yea...

Case Figure 1 Dorsoventral (a) and lateral (b and c) thoracic radiographs.

Case Figure 2 Echocardiography demonstrating the right pulmonary artery inde...

Guide

Cover Page

Table of Contents

Title Page

Copyright Page

Dedication Page

Preface

Acknowledgments

Begin Reading

Glossary

Index

WILEY END USER LICENSE AGREEMENT

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Canine and Feline Respiratory Medicine

Third Edition

Lynelle R. Johnson, DVM, MS, PhD, Diplomate ACVIM

Department of Medicine and Epidemiology

University of California School of Veterinary Medicine

Davis, California, USA

Copyright © 2025 by John Wiley & Sons, Inc. All rights reserved, including rights for text and data mining and training of artificial technologies or similar technologies.

Published by John Wiley & Sons, Inc., Hoboken, New Jersey.Published simultaneously in Canada.

No part of this publication may be reproduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, photocopying, recording, scanning, or otherwise, except as permitted under Section 107 or 108 of the 1976 United States Copyright Act, without either the prior written permission of the Publisher, or authorization through payment of the appropriate per‐copy fee to the Copyright Clearance Center, Inc., 222 Rosewood Drive, Danvers, MA 01923, (978) 750‐8400, fax (978) 750‐4470, or on the web at www.copyright.com. Requests to the Publisher for permission should be addressed to the Permissions Department, John Wiley & Sons, Inc., 111 River Street, Hoboken, NJ 07030, (201) 748‐6011, fax (201) 748‐6008, or online at http://www.wiley.com/go/permission.

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Limit of Liability/Disclaimer of WarrantyWhile the publisher and author have used their best efforts in preparing this book, they make no representations or warranties with respect to the accuracy or completeness of the contents of this book and specifically disclaim any implied warranties of merchantability or fitness for a particular purpose. No warranty may be created or extended by sales representatives or written sales materials. The advice and strategies contained herein may not be suitable for your situation. You should consult with a professional where appropriate. Further, readers should be aware that websites listed in this work may have changed or disappeared between when this work was written and when it is read. Neither the publisher nor authors shall be liable for any loss of profit or any other commercial damages, including but not limited to special, incidental, consequential, or other damages.

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Wiley also publishes its books in a variety of electronic formats. Some content that appears in print may not be available in electronic formats. For more information about Wiley products, visit our website at www.wiley.com.

Library of Congress Cataloging‐in‐Publication Data Applied for:Hardback ISBN: 9781394233366

Cover Design: Wiley Cover Images: Courtesy of Lynelle R. Johnson

This book would not have been possible without the support of my husband and life partner, David Maggs, who will forever be my inspiration in teaching, in research, and in writing.

Preface

Patients with respiratory disease often represent a diagnostic challenge because clinical signs are so similar among different disease processes that affect the respiratory system. Nasal discharge is typical with many upper respiratory conditions, cough encompasses infectious, inflammatory, and neoplastic diseases, and difficulty breathing can result from a disorder anywhere along the respiratory tract. In addition, animals with cardiac and systemic diseases often present with respiratory signs, which means that all cases require thought and introspection on appropriate localization of disease as well as the underlying pathophysiology. The most critical piece of the puzzle is a comprehensive respiratory examination, which provides the key to a rational diagnostic work‐up. This book has been designed to provide easily understood pathways to a clinical diagnosis in an expeditious fashion. It is my hope that this contribution to the veterinary literature conveys highly specific details on respiratory examination, diagnostics, and diseases in a clinically relevant, logical, and easy‐to‐read fashion. This extensively updated edition includes new knowledge that has been generated on respiratory diseases and diagnostic testing and provides case examples to illustrate diagnostic pathways.

My goal with this text was to integrate relevant anatomy, physiology, and pathophysiology in a rational and readable manner that is immediately clinically applicable for the busy practitioner and inquiring student. I approached this task recognizing that the major comprehensive textbooks in veterinary medicine contain excellent chapters on respiratory disorders. My book aims to provide a cohesive and complete discussion in a user‐friendly, single‐author volume. The first section deals with the common presenting signs demonstrated by patients with respiratory disease (nasal discharge, loud breathing, cough, tachypnea versus panting, and exercise intolerance) as well as a section on differentiating cardiac from respiratory disease. The next chapter contains detailed how‐to descriptions of the most important diagnostic methods needed to confirm a respiratory disease as well as interpretation of the results. I then devote an extensive chapter to therapeutic options, addressing concerns about appropriate antibiotic stewardship with recognition of knowledge gaps in the field. The remainder of the book has thorough explanations of individual diseases, divided into chapters dealing with disorders of the nose, airways, lung parenchyma, pleura, and pulmonary vasculature. Each chapter follows the same easy‐to‐read order, with diseases subdivided by etiology into structural, infectious, inflammatory, and neoplastic disorders.

I hope that this third edition of my textbook will instill confidence in students and practitioners as they identify and manage respiratory conditions of dogs and cats.

Acknowledgments

I am indebted to my clients and patients at the University of California, Davis, Veterinary Medical Teaching Hospital, who taught me so much about respiratory medicine and continually challenged me to find answers to their problems.

This work was completed with the support of my colleagues at UC Davis, who have afforded me the opportunity and freedom to pursue respiratory medicine as my passion for the past 24 years. Clinicians and house officers in all services have supported my clinical efforts as well as my research, and my departmental colleagues and the School's leadership have been both encouraging and accommodating. In particular, I am grateful for assistance from Drs. Alessia Cenani, Philipp Mayhew, and Lance Visser in completion of this edition.

This book is the result of years of discovery and clinical effort, and it would not have been possible without the inspiration from colleagues and collaborators in the USA and worldwide, who share a fascination with and great knowledge of respiratory medicine. The veterinarians I have met through the American and European Colleges of Veterinary Internal Medicine and the Veterinary Comparative Respiratory Society have motivated me to continue my search for knowledge and to share what I have learned.

1Localization of Disease

Nasal Discharge

History

Nasal discharge is almost always a sign of local disease within the nasal cavity, however there are some instances when nasal discharge can occur with lower respiratory, gastrointestinal, or systemic disease. One exception to a purely nasal localization of nasal discharge is eosinophilic bronchopneumopathy, an inflammatory condition of the epithelial lining of the airways and lungs that can also involve the nasal epithelium. Affected animals can have nasal signs that last longer or are more noticeable to owners than are lower respiratory signs. Interestingly, cats with eosinophilic lower airway disease do not display this clinical finding. Nasal discharge can also accompany infectious lower respiratory tract disease in the dog that coughs airway material into the nasopharynx, which subsequently drains from the nose. This happens less commonly in the cat. Thirdly, some animals with vomiting or regurgitation will display nasal discharge because of nasopharyngeal regurgitation of gastrointestinal contents. This might be more common in brachycephalic breeds, which frequently develop pharyngeal collapse associated with increased inspiratory respiratory effort (Pollard et al. 2018). Brachycephalic animals also are prone to oral mishandling of food due to excessive pharyngeal folds and because of multiple gastrointestinal diseases, including hiatal hernia, gastroesophageal reflux, and mild inflammatory intestinal disease that leads to vomiting or regurgitation. All of these features contribute to nasal discharge in brachycephalic animals, with brachycephalic dogs affected more often than cats. Finally, nasal discharge, particularly sanguinous nasal discharge, can be encountered in systemic diseases associated with coagulopathies (thrombocytopenia, thrombocytopathy, coagulation factor defects), hypertension, or hyperviscosity syndrome, such as encountered with leishmaniasis and chronic ehrlichiosis.

The most common respiratory causes of nasal discharge include infectious, inflammatory, and neoplastic disorders as well as dental‐related nasal disease and foreign bodies (Table 1.1). Additional clinical signs that can be seen in animals with nasal disease include sneezing or reverse sneezing, pawing or rubbing at the face, noisy breathing or mouth breathing, facial pain, or an unexplained odor near the head.

When evaluating the animal with nasal discharge, important considerations include the duration of signs, the type of discharge as well as changes in its character over time, and the presence of unilateral, bilateral, or progressive signs. Acute onset of nasal discharge is often accompanied by sneezing, is frequently paroxysmal in nature, and is most commonly associated with infectious upper respiratory tract disease or a foreign body. Affected animals can have signs that resolve within a week without treatment, however some dogs or cats are so severely affected that they are rapidly taken to the veterinarian to determine a plan for intervention. Occasionally, dogs with nasal foreign bodies will have resolution of signs despite continued presence of organic matter within the nose. This represents a diagnostic and therapeutic dilemma, particularly in the dog that has an appropriate signalment and exposure history for a nasal foreign body. Failure to investigate signs and potentially retrieve a foreign body can have long‐term consequences due to migration of the foreign body into the central nervous system or development of a secondary fungal infection. The most frustrating cases are those with chronic, slowly progressive nasal discharge and sneezing over weeks to months to years before the severity of disease prompts veterinary care. Prioritizing various empiric therapies requires an assessment of the top differential diagnoses likely in each case and determining what treatment is least likely to worsen signs, to interfere with further diagnostic testing, or to hamper the owner from pursuing specific work‐up.

Table 1.1 Causes of nasal discharge in dogs and cats.

Dog

Cat

Infectious

Canine infectious respiratory disease complex

a

Acute upper respiratory tract disease complex

b

Aspergillus

Cryptococcus

Cryptocococcus

Aspergillus

Penicillium

Rhinosporidium

Leishmania

Ehrlichia

Inflammatory

Lymphoplasmacytic rhinitis

Feline chronic rhinosinusitis

Neoplastic

Adenocarcinoma

Lymphoma

Sarcoma

Adenocarcinoma

Lymphoma

Sarcoma

Local

Tooth root abscess

Nasal or nasopharyngeal polyp

Oronasal fistula

Tooth root abscess

Trauma

Oronasal fistula

Foreign body

Foreign body

Nasal or nasopharyngeal polyp

Trauma

Other

Primary ciliary dyskinesia

Primary ciliary dyskinesia

Nasal mites

Xeromycteria (dry nose syndrome)

a Reported causes include canine adenovirus‐2, canine parainfluenza‐3 virus, canine respiratory coronavirus, canine herpesvirus, canine distemper virus, canine influenza viruses (H3N8, H3N2, H1N1), pneumovirus, Bordetella, Mycoplasma cynos, Mycoplasma canis, and Streptococcus equi subsp. zooepidemicus. Novel viral organisms are continually being identified.

b Reported causes include feline herpesvirus‐1, feline calicivirus, Chlamydia, Bordetella, and Mycoplasma.

With many causes of nasal signs, including viral disease or foreign body, discharge is serous initially and then progresses to a mucoid character when inflammation induces mucus production or when secondary bacterial infection develops. Yellow‐green nasal discharge can be an indicator of eosinophilic disease, but is also encountered in other infectious or inflammatory conditions, while brown‐tinged discharge suggests the presence of blood within the mucus. Bright red blood can be found in combination with nasal discharge because of trauma to blood vessels associated with the primary disease process or due to the severity of sneezing. Epistaxis with or without nasal discharge has been associated with local causes of disease, including inflammatory rhinitis, canine aspergillosis, and neoplasia; however, in animals with pure epistaxis, systemic disorders must be considered, including coagulopathies, hyperviscosity syndrome, and systemic hypertension.

Nasal discharge that is strictly unilateral is most suspicious for local disease caused by a foreign body, trauma, tooth root abscess or oronasal fistula, or for an early fungal infection or neoplasm. However, arterial hypertension or a coagulopathy can also result in unilateral nasal bleeding despite being a systemic disease. Interestingly, inflammatory diseases such as lymphoplasmacytic rhinitis in the dog and feline chronic rhinosinusitis can present with lateralizing clinical signs, although in most of these cases, imaging and histology reveal that both sides of the nasal cavity are affected.

Non‐respiratory history that should be collected includes environmental exposure to foreign bodies, previous trauma, and evidence of vomiting or regurgitation. For animals with epistaxis, potential exposure to rodenticides or vector‐borne diseases that can result in thrombocytopenia, thrombocytopathy, or vasculitis (such as Ehrlichia or Rocky Mountain Spotted Fever) should be identified. In addition, history should be scrutinized for signs consistent with systemic diseases such as hyperthyroidism, renal disease, or adrenal disease, which can result in arterial hypertension.

Signalment

Young animals with nasal discharge are most often affected by infectious upper respiratory tract diseases. A nasopharyngeal polyp should be considered when discharge is accompanied by obstructed breathing, stertorous respirations, gagging, or retching. Primary ciliary dyskinesia is a defect of innate immunity inherited in an autosomal recessive fashion that causes ineffectual mucociliary clearance, trapping of secretions, and recurrent infection. Therefore, this condition is frequently recognized in a younger animal. Affected dogs are often purebred, with an increased prevalence in the Bichon Frise, Old English Sheepdog (Merveille et al. 2014), and Newfoundland (Watson et al. 1999); genetic mutations have also been reported in the Alaskan Malamute (Anderegg et al. 2019), and Rough Collie (Hug et al. 2019) although any breed of dog or cat can be affected. While neoplastic disease most typically affects older animals, it also occurs in young to middle‐aged animals (2–5 years of age) and can be particularly aggressive in these younger animals, especially in the canine population. Nasal aspergillosis is most often encountered in younger dogs and older cats. Cryptococcosis and inflammatory rhinitis can affect dogs or cats of any age.

Nasal disease of most types (fungal, neoplastic, and inflammatory, as well as dental‐related and foreign body disease) is most commonly encountered in dolichocephalic dog breeds, likely because of the large surface area available for foreign body entrapment, for metabolism of inhaled toxicants, or for neoplastic transformation. An unusual combination of rhinitis and bronchopneumonia has been reported in the Irish wolfhound, where a genetic defect in respiratory immunity is suspected but has not been confirmed (Clercx et al. 2003).

Physical Examination

A complete physical examination is essential in every animal presented for evaluation of respiratory disease. In animals with nasal discharge, important features to focus on include the presence or absence of nasal airflow, changes in ocular retropulsion, ability to depress the soft palate easily into the dorsal nasopharyngeal wall, regional local lymph node enlargement, and facial asymmetry or pain. These parts of the physical examination are most important because they can help identify the space‐occupying nature of some causes of nasal disease, particularly nasal neoplasia, feline cryptococcosis, feline aspergillosis, and nasopharyngeal polyps, and because these physical examination findings can indicate local extension or metastasis.

Nasal airflow can be assessed by holding a chilled microscope slide in front of each nostril to show fogging of the glass or by using a wisp of cotton (from a cotton ball or swab) to watch for air movement. The mouth should be held closed during this maneuver, and occlusion of the alternate nostril can be helpful for enhancing airflow through the side of the nasal cavity to be examined (Figure 1.1). Cats create minimal airflow and a very thin wisp of cotton should be used and held in front of the nostril from above and below to check for flow. Alternatively, a stethoscope can be used to listen for airflow from each nostril. An animal with a mass effect in the nasal cavity or nasopharynx will fail to fog the glass, to move the cotton wisp, or to generate a sound at the stethoscope, and will often object to having the nose partly obstructed because it inhibits airflow. Conversely, even animals with heavy mucus accumulation in the nasal cavity will typically retain nasal airflow.

Facial palpation is performed to assess for a pain response, to locate swellings and depressions in bony structures, and to check for symmetry of the skull. Neoplastic processes and fungal infections are most likely to result in abnormal findings. Ocular retropulsion is a part of the facial examination and is performed by placing each thumb over the closed lids and pressing gently backward, upward, medially, and laterally (Figure 1.2). Nasal lesions that are producing a mass effect behind the globe (primarily a neoplasm, fungal granuloma, or retrobulbar abscess) will cause a lateralizing difference in the resistance to depression. Altered retropulsion is difficult to assess in a brachycephalic animal because the eyes are naturally more protruberant than in other dogs or cats. Palpation within the oral cavity can reveal bony abnormalities in the hard palate or might suggest a mass lesion above the soft palate. To perform this examination, the mouth is held open, and the roof of the mouth is palpated from the front of the hard palate through to the end of the soft palate. In the normal animal, the soft palate is readily depressed upward into the dorsal nasopharyngeal wall (Figure 1.3). A mass in this area (most commonly a neoplasm, fungal granuloma, or polyp) will resist depression. The dental arcade should also be evaluated during the oral examination, although it is important to remember that tooth root disease can be present in the absence of external signs and dental probing requires anesthesia.

Figure 1.1 Nasal airflow can be assessed by occluding one nostril and assessing flow from the alternate nostril with a cotton wisp or chilled microscope slide.

Figure 1.2 Palpation during ocular retropulsion can suggest the presence of a mass lesion in the optic canal or retrobulbar space.

Figure 1.3 In the normal animal, palpation of the soft palate will readily depress tissue into the dorsal nasopharyngeal wall. The presence of a mass lesion in the nasopharynx will result in resistance to depression.

Neoplastic disease or cryptococcosis within the nasal cavity leads to ipsilateral mandibular lymph node involvement and the disease process can sometimes be identified by cytology of a lymph node aspirate, even when there is no palpable enlargement. Nasal aspergillosis can result in reactive lymphadenopathy, although no fungal elements will be found on aspiration cytology. Nasal depigmentation along the drainage path of nasal discharge is a relatively specific feature of canine nasal aspergillosis found in up to 40% of cases and is thought to result from elaboration of a dermonecrotic toxin by the fungus (see Chapter 4).

Loud Breathing

Definition

Loud breathing most commonly results from a disorder affecting the nasal cavity or upper airway (larynx, pharynx, or cervical trachea), although occasionally animals with lower airway disease will present for evaluation of breathing that is loud or audible to an owner. Stertor and stridor are loud sounds resulting from narrowing of upper or large airways and are often audible without a stethoscope, although subtle stridor can be missed without specific auscultation over the larynx. Importantly, some animals will suffer from both stertor and stridor, which can have important ramifications for documenting the extent and severity of the obstructive disease, as well as for defining optimal treatment.

Stertor is a discontinuous gurgling or snoring sound that is produced as air flows past a soft tissue obstruction in the upper airway. It can be caused by narrowing within the nasal cavity or nasopharynx (from a polyp, mass, caudal aberrant turbinates, or stenosis), by elongation or thickening of the soft palate, or by edema or eversion of laryngeal ventricles (saccules). Tonsillar enlargement or mass lesions in the oral cavity can also lead to stertor. In brachycephalic dogs and cats, it is not possible to localize the source of stertor on physical examination alone and stertor is often multi‐factorial. Stertor varies in tone and pitch, and it can be audible on inspiration, expiration, or both.

In contrast, stridor is classically an inspiratory noise of a single, high pitch that results from rapid flow of air past a rigid obstruction, such as a paralyzed or collapsed larynx. Stridor can also be heard in an animal with a laryngeal mass or occasionally in an animal with nasopharyngeal narrowing due to stenosis or a mass. It can also be ausculted in an animal with a fixed large airway obstruction due to stenosis, hypoplasia, compression, or a mass effect. The airway obstruction can be anywhere from the larynx to the cervical or intrathoracic trachea. In severe cases where a large mass is obstructing airflow, stridor can be present on both inspiration and expiration. Finally, cervical tracheal collapse can also result in stridor, typically on inspiration.

Epiglottic retroversion is a cause of intermittent airway obstruction in dogs in which sporadic respiratory distress is present in conjunction with stridor or stertor. Although rarely reported, it is increasingly recognized as a cause of serious clinical disease (see Chapter 5).

Signalment

Stertor is commonly encountered in brachycephalic dog breeds such as Bulldogs (English and French), Pugs, and Boston Terriers, and is also heard in Himalayan and Persian cats. Loud breathing is often present early in life and becomes worse with the development of additional respiratory disease or with weight gain. Some animals are not presented for evaluation of stertor and respiratory difficulty until late in life because of the perception that noisy respiration is “normal” for the breed.

Animals with stridor due to congenital laryngeal paralysis are usually young (6–12 weeks) when clinical signs are first apparent, although some breeds show signs at 4–6 months and others at 1–2 years of age. Affected breeds include the Dalmatian, Rottweiler, Great Pyrenees, Bouvier des Flandres, Siberian Husky, White German Shepherd, and some cats (see Chapter 5). Certain breeds have concurrent polyneuropathy (Table 5.1). Acquired laryngeal paralysis is most commonly found in older, large breed dogs such as Labrador and Golden Retrievers as part of a generalized polyneuropathy that affects primarily long nerves in the body such as the recurrent laryngeal nerve and spinal nerves to the limbs. Because the larynx is responsible for phonation and breathing, dysfunction of that nerve is often the first abnormality noticed by owners. Brachycephalic breed dogs that develop laryngeal collapse are usually older at the time of diagnosis; however, because this is an end‐stage manifestation of airway obstruction, the age at which the condition is recognized varies depending on the severity of the obstruction. Atypical breeds such as the Norwich terrier, can manifest signs at a young age.

Physical Examination

In a normal animal, breathing is quiet at rest. Stertor and stridor can often be heard without the use of a stethoscope; however, in some instances, careful auscultation over the neck region is needed to confirm stridor. Increasing respiratory flow rate by gentle exercise can improve detection of stridor; however, panting must be discouraged. In the normal animal, auscultation over the larynx and trachea will reveal loud, hollow sounds that are heard equally on inspiration and expiration. Because upper respiratory noises are typically loud and can obscure lung sounds, auscultation of the larynx and tracheal region is recommended in all patients prior to thoracic auscultation to improve differentiation of upper from lower respiratory sounds. Listening specifically to upper airway noises through the stethoscope can also train the mind to filter out those sounds while ausculting the heart; this will facilitate detection of heart sounds and murmurs. Simultaneous palpation of femoral pulses is also helpful in this situation to provide a tactile sensation in timing of heart sounds and murmurs. This is particularly helpful in brachycephalic breeds (Figure 1.4).

Brachycephalic breeds commonly have visible stenotic nares as part of the disease complex, and excessive oropharyngeal folds can be evident on oral examination, although it is difficult to assess palate length in the awake animal due to breed conformation and presence of excessive froth in the back of the throat. Confirming an appropriate gag reflex is important in evaluating the patient with stridor, because swallowing abnormalities can potentiate aspiration. Finally, detecting the presence of bilateral nasal airflow assists in ruling out the nasopharynx or both nasal cavities as the site for generation of stridor or stertor.

Figure 1.4 Prior to thoracic auscultation, the laryngeal and cervical tracheal regions are ausculted to define upper airway sounds.

Cough

History

Cough occurs because of activation of irritant receptors that lie between epithelial cells lining the airways, and it can be triggered by inflammatory products of neutrophils or eosinophils, by the presence of excess secretions, and by airway compression or collapse (Table 1.2). Important historical features to determine include the onset and duration of cough, the character of the cough, exposure to foreign material or potential infectious diseases, and environmental features that appear to trigger cough. For example, dogs that cough after drinking or in the middle of the night might be suffering from aspiration injury.

The character of the cough described by the owner is occasionally helpful when prioritizing a list of differential diagnoses, although substantial overlap exists among the causes of cough. Animals with a wet‐ or moist‐sounding cough can have excessive airway secretions due to infectious or inflammatory airway disease or as a result of parenchymal disease such as pneumonia. Observant owners of the animal with a productive cough might note that the animal swallows after coughing or retches to remove secretions from the upper airway. However, diseases of the airway can also result in a dry cough when secretions are minimal or early in the course of disease. Infectious respiratory disease in young puppies typically results in a hoarse, seal‐bark cough and this is often ascribed to bordetellosis, although any of the organisms associated with canine infectious respiratory disease could be responsible. Cough in animals affected only by airway collapse is often harsh and can be chronic, intermittent, or paroxysmal in nature. A honking cough is frequently described in dogs with tracheal or airway collapse and a brisk, snapping sound on expiration is suggestive of large airway (bronchial) collapse. Animals with pneumonia tend to have a softer cough along with a vague history of illness characterized by anorexia and lethargy. Dogs with heart disease also can have a soft cough associated with signs of tachypnea, exercise intolerance, or lethargy. With severe or fulminant pulmonary edema, a dog might expectorate pink foam because edema fluid has flooded the alveolar space and entered the airways. However, the common association of cough with congestive heart failure has been called into question (Ferasin et al. 2013), and it can be challenging to differentiate cardiac from respiratory disease (see later).

Table 1.2 Respiratory causes of cough in dogs and cats.

Dog

Cat

Infectious tracheobronchitis

Canine infectious respiratory disease complex

a

Mycoplasma

Bordetella

Pneumonia

Bacterial

Bacterial

Aspiration

Aspiration

Foreign body

Foreign body

Fungal

Fungal

b

Interstitial

b

Interstitial

b

Inflammatory disease

Chronic bronchitis

Asthma/chronic bronchitis

Eosinophilic bronchopneumopathy

Neoplasia

Primary

Primary

Metastatic

Metastatic

Structural disorders

Bronchiectasis

Bronchiectasis

Airway collapse

a Reported causes include canine adenovirus‐2, canine parainfluenza‐3 virus, canine respiratory coronavirus, canine herpesvirus, influenza viruses, and canine distemper virus along with Bordetella, Mycoplasma, and Streptococcus equi subsp. zooepidemicus.

b More commonly a cause of tachypnea than cough.

Determining environmental and travel history is important for animals with cough. Exposure to a high‐density dog population should raise concern for disease associated with canine infectious respiratory disease complex. If the cough is harsh and dry, Bordetella should be considered, while a soft, chronic cough could be suggestive of canine influenza virus infection. Sporting dogs that develop an acute onset of cough or have a chronic, antibiotic‐responsive cough could have foreign body pneumonia. Fungal pneumonia should be suspected in coughing animals have traveled to endemic regions. In those dogs or cats, cough is usually accompanied by tachypnea and systemic signs of illness. Finally, environmental history is important, because exposure to pollutants and airway irritants can exacerbate upper or lower airway diseases in both dogs and cats, although it remains unclear whether or not exposure to second‐hand smoke is an important factor in worsening cough in animals (Hawkins et al. 2010).

Signalment

In general, younger animals might be more likely to develop infectious or foreign body pneumonia, while older animals develop bronchitis, neoplasia, airway collapse, and perhaps aspiration pneumonia. Dogs with eosinophilic or fungal pneumonia also tend to be young to middle‐aged. Asthma/bronchitis seems to affect cats of all ages, although perhaps the eosinophilic form is more common in younger animals. Cervical tracheal collapse might be noted more commonly in younger dogs, while older dogs get both tracheal collapse and bronchomalacia.

The breeds affected depend on the underlying case of cough. For example, an older Retriever‐type dog is likely to develop laryngeal paralysis and subsequent aspiration pneumonia, while brachycephalic breeds can aspirate at a young or older age, developing either pneumonia or pneumonitis. Ciliary dyskinesia can result in antibiotic responsive cough and nasal discharge in breeds described earlier under nasal discharge. Tracheal collapse affects toy and small breed dogs, while chronic bronchitis and bronchomalacia can affect any size or breed of dog. Irish Wolfhounds seem to be predisposed to pneumonia and also develop a rhinitis/bronchopneumonia syndrome, while Standard Poodles and Cocker Spaniels appear to be prone to bronchiectasis.

Physical Examination

One of the more difficult challenges in assessing animals with respiratory disease is the development of good auscultation skills. Practice and patience are required because audible sounds are altered by age, body condition score, conformation, respiratory pattern, and the presence of disease. As mentioned earlier, careful auscultation should include the larynx and trachea, followed by listening to all lung fields (left, right, caudal, cranial, dorsal, and ventral). The anatomic origin for lung sounds has not been fully established; however, normal lung sounds are usually designated as bronchial, vesicular, or bronchovesicular. Bronchial sounds are loud and are heard best over the large airways near the hilus. Typically, they are louder and longer during expiration than inspiration and have a tubular character. Vesicular lung sounds are soft, heard best and longer on inspiration, and can be detected over the periphery of the chest in normal animals. The sound resembles a breeze passing through leaves on a tree. Bronchovesicular sounds (a mixture of bronchial and vesicular qualities) are typically louder on inspiration than expiration.

Lung sounds in animals with airway or parenchymal disease are often increased in loudness or harshness, and harsh bronchovesicular sounds can be the only physical examination finding in some animals with lower respiratory disease despite the presence of marked radiographic changes. Adventitious (abnormal) lung sounds (crackles and wheezes) are discontinuous noises and are not always present in respiratory patients, but should always be taken as an indicator of disease when ausculted. Adventitious lung sounds can be enhanced by inducing a cough or a deep breath, or by exercising the patient. In normal animals, it is difficult to induce a cough by palpating the trachea; however, animals with airway or parenchymal disease usually have increased tracheal sensitivity due to activation of irritant receptors by infection or inflammation.

Crackles are thought to result from rapid opening or closure of airways, but could also arise from equalization in pressure as air passes through fluid or mucus‐filled airways. They can be heard at any point during inspiration or expiration. Fine or soft crackles are suggestive of pulmonary edema, particularly if ausculted in the hilar region of a dog, whereas coarse crackles are more suggestive of airway or parenchymal disease. Dogs or cats with pulmonary fibrosis can display either fine or coarse crackles that are ausculted diffusely across the chest. Auscultation in dogs with airway collapse can reveal diffuse crackles, perhaps because of the presence of concurrent bronchitis or because of opening and closure of smaller airways during the phases of respiration. In the latter case, crackles are often present during both inspiration and expiration. A loud snapping sound over the hilar region at end expiration is suggestive of collapse of the intrathoracic trachea, carina, or mainstem bronchi. Wheezes are believed to arise from air passing through airways narrowed by intraluminal mucus, extraluminal compression, or by collapse or constriction, and are usually heard on expiration.

Tachypnea versus Panting

History

Tachypnea is most often associated with parenchymal or pleural disease, although in the cat tachypnea can also be encountered with inflammatory airway disease, particularly an asthma attack of bronchoconstriction. Parenchymal diseases that lead to tachypnea are primarily pneumonia and pulmonary edema. Pneumonia (infectious, aspiration, fungal, or interstitial) can be fulminant and acute, or it can be chronic and insidious in onset. Both pneumonia and pulmonary edema are typically associated with systemic signs of illness such as lethargy, anorexia, and weight loss. Tachypnea is also a characteristic of pulmonary vascular disease, particularly pulmonary embolic disease. This can be a reflection of vascular obstruction or alterations in central control of respiration.

Tachypnea due to pneumothorax is usually acute; however, pleural effusive disorders can result in either an acute presentation with respiratory distress or a more chronic development of signs due to slow accumulation of fluid. Usually, the degree of respiratory distress is associated with the rapidity of fluid or air accumulation rather than with the specific volume present. Cats seem to be particularly sensitive to addition of a final, critical volume of fluid that overcomes their ability to compensate.

Tachypnea must be differentiated from panting, which is typically characterized by rapid, open‐mouth breathing that does not result in abnormalities in gas exchange. Also, panting is not typically associated with a change in respiratory pattern or effort. Panting can be related to an upper airway or laryngeal disorder, but more often will reflect systemic illnesses such as cortisol or norepinephrine excess, or metabolic acidosis due to diabetic ketosis, diarrhea, uremia, or renal tubular acidosis. Central nervous system disorders that affect the respiratory center can result in panting as can abdominal distention due to organomegaly, neoplasia, pregnancy, obesity, ascites, gastric dilatation, or torsion. Finally, anxiety, pain, and hyperthermia can result in incessant panting.

Physical Examination

Cervical and thoracic auscultation, as described for evaluation of animals with cough, is important for animals that present with tachypnea, because many respiratory diseases will result in both cough and tachypnea. In addition to listening for increased sounds, it is important to determine if there is an absence of lung sounds, which might indicate the presence of fluid or air in the pleural space.

A notable clinical finding associated with parenchymal or pleural disease is a rapid, shallow breathing pattern, although with pleural disease, exaggerated chest wall motion or hyperpnea can sometimes be present in conjunction with a rapid respiratory rate. In animals with severe respiratory distress, elbows are abducted and the neck is extended to facilitate movement of air into the alveoli. Parenchymal diseases are characterized by increased or harsh lung sounds or by detection of adventitious sounds, particularly crackles. When pleural effusion is present, lung sounds are ausculted in the dorsal fields only and muffled sounds are heard ventrally; heart sounds are also muffled. Pneumothorax leads to an absence of lung sounds dorsally due to compression by air, and lung sounds are present in the ventral fields only. In some cases, a line of demarcation can be ausculted between normal and abnormal lung sounds, indicating a fluid line or the boundaries of air accumulation.

In addition to auscultation, thoracic percussion aids in determining if pleural disease is present. Percussion can be performed using a pleximeter and mallet or by placing the fingers of one hand on the chest and firmly striking them with fingers of the opposite hand (Figure 1.5). The sound that develops will vary depending on whether an air or fluid density is present within the thoracic cavity. Percussion of the chest in a region filled with fluid reveals a dull sound, while in an animal with pneumothorax or air trapping, percussion results in increased resonance. This technique is somewhat limited in a cat or small dog because of the small size of the thoracic cavity.

A general physical examination would include assessment of mucus membranes for pallor suggestive of anemia, tachycardia which could accompany stress or anxiety, and abdominal distention that would support organomegaly or neoplasia as causes for panting instead of tachypnea.

Figure 1.5 Each region of the thorax should be percussed to detect regional differences in the air/soft tissue sounds that are created. One hand is placed against the thorax and is rapped quickly and sharply with the curved fingers of the alternate hand.

Exercise Intolerance

History

Exercise intolerance can result from respiratory, cardiac, musculoskeletal, neurologic, or metabolic diseases. Respiratory disorders that result in exercise intolerance usually do so through airway obstruction in diseases such as laryngeal paralysis or bronchomalacia in the dog, asthma in the cat, or chronic bronchitis in either species, or through hypoxemia associated with parenchymal disease. Historical features in animals with airway obstruction can include loud breathing noises as well as progressive tiring and a reduced level of activity. Upper airway obstruction due to laryngeal disease can be accompanied by reports of dysphonia, decreased vocalization, gagging, or retching, while lower airway obstruction due to bronchoconstriction or inflammation is usually associated with cough.

Physical Examination

In the older, large breed dog presented for evaluation of exercise intolerance, careful attention should be paid to laryngeal auscultation for stridor suggestive of laryngeal paralysis. Increased tracheal sensitivity and loud or adventitious lung sounds in cats or dogs with exercise intolerance but no systemic signs of illness suggest that bronchial narrowing, collapse, or inflammation could be responsible for exercise intolerance. Animals that display tachypnea on physical examination, abnormal lung sounds, and systemic signs of illness likely suffer from some form of pneumonia, and if absence of lung sounds is detected, a pleural effusive disorder should be considered.

Differentiating Cardiac from Respiratory Disease

It can be difficult to distinguish animals with congestive heart failure from those with respiratory disease because of the similarity in clinical signs, physical examination findings, and sometimes even radiographic changes. In addition, some animals suffer from heart and lung or airway diseases concurrently, although in most situations one clinical syndrome predominates as the cause for presenting signs. Disorders of the respiratory tract that cause clinical complaints similar to those found in cardiac disease include asthma in cats and bronchitis in dogs, and pneumonia, pulmonary edema, and interstitial diseases in both species. In addition, respiratory or systemic causes of pleural effusion must be distinguished from hydrothorax due to biventricular heart failure. It is also important to understand that the presence of disease in one organ can lead to secondary disease in the other thoracic organ. For example, a number of respiratory disorders such as tracheobronchomalacia and pulmonary fibrosis can result in pulmonary hypertension and even right heart failure.

History

As suggested earlier, the presence and character of cough can sometimes be helpful in distinguishing cardiac from lung or airway disease. Typically, the cough in dogs with airway disease is chronic, harsh, and paroxysmal, but can be dry or productive. In contrast, dogs in congestive heart failure will have a soft, moist cough, as do some dogs with pneumonia. Cats with bronchial disease virtually always have a history of cough, while only 5–25% of cats with congestive heart failure might have cough in the history (Dickson et al. 2018). Cats with airway disease can present with rapid breathing, although in a study of cats presented to the veterinarian for respiratory distress, severe tachypnea was more common in cats with cardiac disease (Dickson et al. 2018). Pulmonary edema is often associated with an acute onset of clinical signs referable to the respiratory tract in association with constitutional signs of lethargy, inappetence, and depression. Animals with pneumonia frequently have a vague history of illness that can be acute or chronic but is also characterized by anorexia, malaise, and weight loss. Dogs with cardiac disease are often cachectic and lethargic, while dogs with chronic bronchitis are typically robust or obese and have a healthy appetite. Dogs or cats with pulmonary fibrosis generally display a gradual deterioration in exercise tolerance, and tachypnea or difficulty breathing is noted later during the course of disease.

Signalment

Signalment can be an important clue to determining whether cardiac or respiratory disease is more likely in a given case. A young animal with a heart murmur and clinical signs of cardiopulmonary disease is a likely candidate for congenital heart disease. Young to middle‐aged cats can be affected by hypertrophic cardiomyopathy or feline bronchial disease. It is more difficult to identify the primary cause of clinical signs in middle‐aged to older small breed dogs, because they can be affected by airway collapse, chronic bronchitis, and degenerative valvular disease concurrently. Exacerbation of any of these disease processes could be the cause for clinical presentation to the veterinarian.

Dobermans, Golden Retrievers, and giant breed dogs are commonly affected by cardiac disease, while primary respiratory conditions are less common in these dogs, with the exception of aspiration pneumonia associated with laryngeal paralysis, which is common in Retriever breeds. It is also important to recall that large breed dogs can be affected by airway collapse, chronic bronchitis, and pneumonia. Idiopathic pulmonary fibrosis is most commonly reported in older West Highland White Terriers, but other terrier breeds can be affected as well as cats, and younger dogs can also occasionally develop interstitial lung disease. A Maine Coon or Ragdoll cat is more often affected by hypertrophic cardiomyopathy, while a Siamese cat might be more likely to develop airway disease.

Physical Examination

Assessment of the respiratory pattern can be helpful in differentiating airway disease from cardiac disorders. In general, bronchomalacia and bronchitis in the dog or cat will be associated with increased effort on expiration or prolongation of the expiratory phase of respiration, while dogs or cats with pneumonia, pulmonary edema, or pleural effusion will more often display tachypnea.

Body temperature can be somewhat helpful in distinguishing cardiac from respiratory disease at least in cats, as a low body temperature in a cat is more typical with cardiac disease (Dickson et al. 2018