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- Herausgeber: John Wiley & Sons
- Kategorie: Fachliteratur
- Sprache: Englisch
Clinical Canine and Feline Respiratory Medicine provides reliable information on the diagnosis and management of respiratory disease in a user-friendly format. With an emphasis on the features of the history and physical examination that aid in efficient diagnostic planning, the book is an accessible, readable resource for optimizing treatment of patients with diseases of the respiratory tract. Offering comprehensive, accessible coverage of respiratory disorders, Clinical Canine and Feline Respiratory Medicine is a useful practice guide and study aid for general practitioners and veterinary students. Beginning with introductory chapters on the localization of disease, diagnostics, and therapeutics, the heart of the book focuses on the full range of respiratory diseases, including nasal disorders, diseases of airways, parenchymal diseases, pleural and mediastinal diseases, and vascular disorders. Each chapter takes a common format with diseases subdivided by etiology into structural, infectious, inflammatory, and neoplastic disorders. Clinical Canine and Feline Respiratory Medicine is a useful tool for students and practitioners engaged in studying, diagnosing, and treating respiratory disease.
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Veröffentlichungsjahr: 2013
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Contents
1 Localization of Disease
Nasal Discharge
Loud Breathing
Cough
Tachypnea
Exercise Intolerance
2 Respiratory Diagnostics
General
Imaging
Airway Sampling
Respiratory Endoscopy
Sample Analysis
3 Respiratory Therapeutics
Drug Therapy
Routes of Administration
Adjunct Therapy
4 Nasal Disorders
Structural Diseases
Infectious Diseases
Inflammatory Diseases
5 Diseases of Airways
Structural Disorders
Infectious Diseases
Inflammatory Disorders
6 Parenchymal Disease
Structural Diseases
Infectious Diseases
Inflammatory Disorders
7 Pleural and Mediastinal Disease
Structural Disorders
Infectious Disorders
Neoplastic Disorders
Miscellaneous Disorders
8 Vascular Disorders
Structural Disorders
Infectious Disorders
Miscellaneous Disorders
Edition first published 2010
©2010 Blackwell Publishing
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The contents of this work are intended to further general scientific research, understanding, and discussion only and are not intended and should not be relied upon as recommending or promoting a specific method, diagnosis, or treatment by practitioners for any particular patient. The publisher and the author make no representations or warranties with respect to the accuracy or completeness of the contents of this work and specifically disclaim all warranties, including without limitation any implied warranties of fitness for a particular purpose. In view of ongoing research, equipment modifications, changes in governmental regulations, and the constant flow of information relating to the use of medicines, equipment, and devices, the reader is urged to review and evaluate the information provided in the package insert or instructions for each medicine, equipment, or device for, among other things, any changes in the instructions or indication of usage and for added warnings and precautions. Readers should consult with a specialist where appropriate. The fact that an organization or Website is referred to in this work as a citation and/or a potential source of further information does not mean that the author or the publisher endorses the information the organization or Website may provide or recommendations it may make. Further, readers should be aware that Internet Websites listed in this work may have changed or disappeared between when this work was written and when it is read. No warranty may be created or extended by any promotional statements for this work. Neither the publisher nor the author shall be liable for any damages arising herefrom.
Library of Congress Cataloging-in-Publication Data
Johnson, Lynelle R.
Clinical canine and feline respiratory medicine / Lynelle R. Johnson. p.; cm.
Includes bibliographical references and index. ISBN 978-0-8138-1671-5 (pbk. : alk. paper) 1. Respiratory organs–Diseases. 2. Dogs–Diseases.
3. Cats–Diseases. I. Title.
[DNLM: 1. Dog Diseases–therapy. 2. Respiratory Tract Diseases–veterinary. 3. Cat Diseases–therapy.
4. Clinical Medicine–methods. SF 992.R47 J67c 2010] SF992.R47J64 2010
636.089'62—dc22
2009049308
A catalog record for this book is available from the U.S. Library of Congress.
1 2010
With special thanks to the clients and patients who have furthered my knowledge of respiratory medicine and fueled my passion for discovery. I remain indebted to my mentor Brendan McKiernan for all that he has taught me over the years.
Preface
Management of small animal patients with respiratory disease is challenging, in part because clinical signs of disease can appear similar across a large number of respiratory disorders. In addition, respiratory signs can mimic those caused by cardiac or systemic diseases, and respiratory disorders can develop secondary to these diseases. I believe that localizing disease through a comprehensive physical examination, acquiring a thorough appreciation of the most current and appropriate respiratory procedures, understanding respiratory therapeutics, and using a resource that offers descriptions of the most common respiratory syndromes are all important for making us better diagnosticians and clinicians in respiratory medicine. The goal of this textbook is simple. It is to impart that knowledge in a logically developed, easy-to-read, and well-indexed manner from the perspective of a clinician whose first love is respiratory medicine and one who is fortunate to subspecialize in this aspect of internal medicine. Throughout this book, I have organized the text for the busy practitioner wanting to practice at “the cutting-edge” of veterinary medicine and for the veterinary student looking for a thoughtful integration of clinically relevant anatomy, physiology, and disease.
I approached this task recognizing that all the comprehensive medicine textbooks contain excellent chapters on respiratory disorders. This textbook aims to provide an authoritative, cohesive, and complete discussion of all the elements needed to diagnose and treat small animal respiratory diseases specifically in a user-friendly, single-author volume. The first section deals with the common presenting signs for patients with respiratory disease: nasal discharge, loud breathing, cough, tachypnea, and exercise intolerance. This is intended as a quick reference for immediate localization of the site of disease in order to guide diagnostic investigations. The next section contains detailed how-to descriptions of all those important diagnostic methods. I then devote an extensive chapter to therapeutic options. All medical options are covered in detail with canine and feline dose rates for the drugs that I find useful in the management of simple and complex respiratory diseases. 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: structural, infectious, inflammatory, and neoplastic disorders.
I hope that this textbook will instill confidence in students and practitioners as they identify and manage respiratory conditions in dogs and cats.
Lynelle R. Johnson
Acknowledgments
I am indebted to my colleagues in medicine, radiology, cardiology, critical care, clinical pathology, and pathology at the University of California, Davis, who provided me with the intellectual stimulation, collegiality, and wisdom to create this book. Special thanks to the faculty in Small Animal Internal Medicine, who provided clinical coverage during my sabbatical leave thereby providing me the time needed to focus on this endeavor. I am thankful for the staff at the UC Davis Veterinary Medical Teaching Hospital who ensured that my patients were evaluated safely, effectively, and efficiently. A special thank you to John Doval for his expert assistance in generating images for this book.
I am also exceptionally grateful to my colleagues at the University of Melbourne, Australia, who hosted my sabbatical leave. The generosity, enthusiasm, and encouragement that they offered were unsurpassed, and they provided me with the utmost support in all my academic and scholarly endeavors.
1
Localization of Disease
Clinical signs that provide clues to the existence of respiratory disease include nasal discharge, cough, respiratory noise, tachypnea, difficulty breathing, or exercise intolerance. The first step toward making a diagnosis requires accurate localization of the anatomic origin of disease within the respiratory tract: the nasal cavity, upper or lower airway, lung parenchyma, or pleural space. This will allow construction of an accurate list of differential diagnoses, will facilitate efficient diagnostic testing, and will allow rational empiric therapy while waiting for test results.
Nasal Discharge
History
Nasal discharge is almost always a sign of local disease within the nasal cavity. One exception is eosinophilic bronchopneumopathy, an inflammatory condition of the lung and airways that can also involve the nasal epithelium. A second exception can be found in the dog or cat with lower respiratory tract disease (usually bacterial pneumonia) that coughs airway material into the nasopharynx, which subsequently drains from the nose. In both situations, animals usually have a combination of cough and nasal discharge. The most common 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.
Table 1.1. Causes of nasal discharge in dogs and cats
Dog
Cat
Infectious
Canine infectious respiratory disease complex
a
Aspergillus
Penicillium
Rhinosporidium
Acute upper respiratory tract disease complex
b
Cryptococcus
Aspergillus
Inflammatory
Lymphoplasmacytic rhinitis
Feline chronic rhinosinusitis
Neoplastic
AdenocarcinomaSarcomasLymphoma
LymphomaAdenocarcinomaSarcomas
Local
Tooth root abscessOronasal fistulaTraumaForeign bodyNasal or nasopharyngeal polyp
Nasal or nasopharyngeal polypTooth root abscessOronasal fistulaForeign bodyTrauma
Other
Primary ciliary dyskinesiaNasal mitesXeromycteria (dry nose syndrome)
Primary ciliary dyskinesia
aReported causes include canine adenovirus-2, canine parainfluenza-3 virus, canine respiratory coronavirus, canine herpesvirus, canine distemper virus, Bordetella and Mycoplasma. Canine influenza virus is a new addition to the list of etiologic agents.
bReported causes include feline herpesvirus-1, feline calicivirus, Chlamydophila, Bordetella, and Mycoplasma.
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 or bilateral signs. Acute nasal discharge is often accompanied by sneezing and is most commonly associated with viral upper respiratory tract disease or a foreign body. Animals with acute nasal discharge usually have dramatic clinical signs that either resolve within a week without treatment or are so severe that animals are rapidly evaluated by a veterinarian. More frustrating cases are those with chronic nasal discharge, which often have low level but progressive signs from weeks to months to years before the severity of disease prompts veterinary care.
With many causes of nasal disease 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 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. Pure epistaxis has been associated with local causes of disease, including inflammatory rhinitis, canine aspergillosis, and neoplasia; however, systemic vascular disorders must also be considered including coagulopathies and systemic hypertension.
Nasal discharge that is strictly unilateral is most suspicious for local disease due to a foreign body, trauma, tooth root abscess or oronasal fistula, or an early fungal infection or neoplasm. However, systemic vascular disease or a coagulopathy can result in unilateral signs. Also, inflammatory diseases such as lymphoplasmacytic rhinitis in the dog and feline chronic rhinosinusitis can also present with lateralizing clinical signs, although in most cases, imaging and histology reveal that both sides of the nasal cavity are affected.
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. Primary ciliary dyskinesia is a defect of innate immunity that results in effectual mucociliary clearance, failure to clear secretions, and recurrent infection. Therefore, this condition would be more frequently recognized in a younger animal. Affected dogs are often purebred, with an increased prevalence in the Bichon Frise, although any breed of dog or cat can be affected. While neoplastic disease most typically affects older animals, it also occurs in animals 2–4 years of age and can be particularly aggressive, especially in dogs. Canine aspergillosis is most often encountered in younger dogs and older cats. Cryptococcus and inflammatory rhinitis can affect dogs or cats of any age.
Nasal disease of most types (fungal, neoplastic, and inflammatory) is most commonly found in dolicocephalic dog breeds. An unusual combination of rhinitis and bronchop-neumonia has been reported in the Irish wolfhound, where a genetic defect in respiratory immunity is suspected.
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, lack of soft palate depression, 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 nasal diseases, particularly nasal neoplasia, feline cryptococcosis, and nasopharyngeal polyps, and because these findings can detect local extension or metastasis.
Nasal airflow can be assessed by holding a chilled microscope in front of each nostril to show fogging of the glass or by using a wisp of cotton (from a cotton ball or Q-tip) to watch for air movement. The mouth should be held closed during the procedure, 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). An animal with a mass effect in the nasal cavity or nasopharynx will fail to fog the glass or move the cotton wisp and will often object to this manipulation because it obstructs airflow. Conversely, even animals with heavy mucus accumulation in the nasal cavity will 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. 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 or retrobulbar abscess) will cause a lateralizing difference in the resistance to depression. Similarly, 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 nasopharyngeal region (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.
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 within the optic tract.
Figure 1.3. In the normal animal, palpation of the soft palate will readily depress tissue into the nasopharyngeal region. The presence of a mass lesion in the nasopharynx will result in resistance to depression.
Neoplastic disease, fungal infection, or inflammatory diseases within the nasal cavity can involve mandibular lymph nodes and the disease process can sometimes be identified by cytology of a lymph node aspirate, even when there is no palpable enlargement. Nasal depigmentation 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.
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 loud breathing. Stertor is a gurgling or snoring sound that is produced as air flows past a soft tissue obstruction. It can be caused by narrowing of the nasal cavity, by elongation or thickening of the soft palate, or by edema or eversion of laryngeal saccules. It varies in tone and pitch, and it may be audible on both inspiration and expiration. 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 effect, or occasionally in an animal with nasopharyngeal stenosis or fixed cervical tracheal collapse or stenosis.
Signalment
Stertor is commonly encountered in brachycephalic dog breeds such as bulldogs (English and French), Pugs, and Boston Terriers and is also seen in Himalayan and Persian cats. Loud breathing is often present early in life and becomes worse with 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 the disease is manifest. Affected breeds include the Dalmatian, Rottweiler, Great Pyrenees, Bouvier des Flandres, Siberian Husky, White German Shepherd, and some cats (see Chapter 5). Acquired laryngeal paralysis is most commonly found in older large breed dogs such as Labrador and Golden retrievers. 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, age varies depending on the severity of disease.
Physical Examination
In a normal animal, breathing is quiet at rest. Stertor and stridor can 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 and to improve detection of heart sounds. 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 may be evident.
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 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, and environmental features that appear to trigger cough.
Animals with a wet- or moist-sounding cough most likely have excessive airway secretions due to infectious or inflammatory airway or parenchymal disease. Observant owners of the animal with a productive cough may note that the animal swallows after coughing or retches to remove secretions from the airway. However, infectious, inflammatory, and structural diseases of the airway can also result in a dry cough when secretions are minimal or early in the course of disease. Cough in animals with airway disease is often harsh and can be chronic, intermittent, or paroxysmal in nature. Animals with pneumonia may have a softer cough along with a vague history of illness characterized by anorexia and lethargy.
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 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 may have foreign body pneumonia. Fungal pneumonia should be suspected in animals with cough that have traveled to endemic regions. In those animals, 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.
Table 1.2. Respiratory causes of cough in dogs and cats
Dog
Cat
Infectious tracheobronchitis
Canine infectious respiratory disease complex
a
Mycoplasma
Bordetella
Pneumonia
BacterialAspirationForeign bodyFungalEosinophilicInterstitial
BacterialAspirationForeign bodyFungalInterstitial
Inflammation
Chronic bronchitisEosinophilic bronchopneumopathy
Asthma/chronic bronchitis
Neoplasia
PrimaryMetastatic
PrimaryMetastatic
Structural
BronchiectasisAirway collapse
Bronchiectasis
aReported causes include canine adenovirus-2, canine parainfluenza-3 virus, canine respiratory coronavirus, canine herpesvirus and canine distemper virus along with Bordetella and Mycoplasma. Canine influenza virus can also be included in the list of etiologic agents.
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 examination should include the larynx and trachea, followed by auscultation of all lung fields. 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 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) can be heard on inspiration more than expiration.
Lung sounds in animals with airway or parenchymal disease are often increased in loudness or harshness. Adventitious (abnormal) lung sounds (crackles and wheezes) are discontinuous noises that should always be taken as an indicator of disease. Crackles are thought to result from rapid opening 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. Wheezes result from air passing through airways narrowed by intraluminal mucus, extraluminal compression, or by collapse or constriction, and are usually heard on expiration. 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.
Fine crackles are suggestive of pulmonary edema, particularly if ausculted in the hilar region of a dog, whereas coarse crackles are more suggestive of pneumonia or airway disease. Dogs or cats with pulmonary fibrosis can display either fine or coarse crackles that are auscultable diffusely across the chest. Auscultation in dogs with airway collapse can reveal diffuse crackling sounds because of the presence of concurrent bronchitis or because of small airways that suddenly pop open. A loud snapping sound over the hilar region at end expiration is suggestive of collapse of the intrathoracic trachea, carina, or mainstem bronchi.
Tachypnea
History
Tachypnea is most often associated with parenchymal or pleural disease, although in the cat, tachypnea can also be seen with bronchial disease. Therefore, in the cat, tachypnea can be found in conjunction with historical features of cough and decreased activity. Parenchymal diseases that lead to tachypnea are primarily pneumonia and pulmonary edema, and these disorders can be acute or chronic and insidious in onset. They are typically associated with systemic signs of illness such as lethargy, anorexia, and weight loss. Tachypnea due to with 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 for filling of the pleural space.
Physical Examination
Cervical and thoracic auscultation as described for evaluation of animals with cough is important for animals that present with tachypnea since many diseases will result in both clinical signs. In addition to listening for increased sounds, it is important to determine if there is an absence of lung sounds, which might indicate either lung consolidation or the presence of fluid or air in the pleural space.
A notable clinical sign associated with parenchymal or pleural disease is a rapid, shallow breathing pattern, although with pleural disease, exaggerated chest wall motion can sometimes be present. 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 lung sounds or detection of adventitious sounds. 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 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 rapidly striking them with fingers of the opposite hand (Figure 1.5). The sound that develops varies depending on whether an air or fluid density is present within the thoracic cage. 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.
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.
Careful auscultation of the heart is also indicated in animals with parenchymal or pleural disease because congestive heart failure can lead to respiratory signs due to pulmonary edema or pleural effusion. In such a case, a heart murmur or gallop would be expected along with tachycardia, and jugular veins are often distended in an animal with right ventricular failure. If the apical impulse is poorly audible, this is an additional clue to the presence of pleural effusion.
Exercise Intolerance
History
In general, 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 bronchitis, 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 may 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 or inflammation may 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.
2
Respiratory Diagnostics
General
Laboratory Testing
Basic blood work (complete blood count and biochemical panel) are often performed during the workup of a respiratory patient and may help support the presence of an underlying respiratory tract disease. In local diseases associated with inflammation or infection such as rhinitis and tracheobronchitis, hematologic changes are rarely found. With parenchymal diseases such as bacterial or aspiration pneumonia, a neutrophilic leukocytosis is often found. Neutrophilia or eosinophilia is reported in eosinophilic pneumonia/bronchopneumopathy and feline bronchial disease. Fungal pneumonia is anticipated to result in neutrophilia and monocytosis, reflecting the chronic nature of disease. Chronic hypoxemia can result in polycythemia.
Biochemical abnormalities in respiratory diseases are usually nonspecific. Hyperglobulinemia can be found in feline bronchial disease, fungal pneumonia, chronic foreign body or aspiration pneumonia, or bronchiectasis due to chronic antigenic stimulation, and concurrent hypoalbuminemia is occasionally present as a negative acute phase reactant.
Molecular diagnostics are increasingly used to document the presence of an infectious organism, such as feline herpesvirus-1, Bordetella, or Mycoplasma, in either upper or lower respiratory tract disease; however, there are important limitations to interpretation of results (see sections on specific diseases). Also, it is critical to realize that a positive molecular assay does not confirm that the organism is responsible for the clinical disease identified.
Pulse Oximetry
Pulse oximetry provides an estimate of hemoglobin saturation with oxygen and is inexpensive, noninvasive, and easy to perform. The technique relies on detection of the optical density of the pulse wave as blood passes through the arterial system. The sensor subtracts the signal between pulses from the height of the pulse wave to determine oxygenation of inflowing blood only. Because of this feature, pulse oximetry can provide a falsely low measurement in a hypotensive patient with weak pulses or in an animal with anemia. This technique cannot differentiate between methemoglobin and oxyhemoglobin.
Pulse oximetry is useful prior to anesthetizing the patient for a respiratory procedure or as a monitoring tool during therapy. Sites that can used to obtain a measurement include the lip, tongue, between the toes, on the ear pinna, and sometimes on the abdomen. The probe can be applied to various sites several times to obtain a signal, and detection of a strong pulse rate indicates that the reading is likely accurate. A pulse oximeter reading below 95% correlates with a PaO2 of less than 80 mm Hg (Figure 2.1). When such a reading is obtained, an arterial blood gas analysis should be performed, if available, to confirm the degree of hypoxemia. It is important to remember that the pulse oximeter measures only oxygenation. It provides no information on ventilatory status and thus cannot detect hypoventilation (increased PaCO2) in an animal.
Figure 2.1. Pulse oximetry measures hemoglobin saturation with oxygen, which has a sigmoidal relationship with the partial pressure of arterial oxygen. A hemoglobin saturation <95% equates to a PaO2<80 mm Hg and indicates hypoxemia.
Pulse oximetry can be valuable in determining response to therapy in hypoxemic patients because improvements in oxygenation occur prior to radiographic changes. However, because of the sigmoidal relationship between hemoglobin saturation and arterial oxygen, oximetry remains a somewhat crude estimate of lung function.
Arterial Blood Gas Analysis
Arterial samples are obtained by direct puncture of the dorsal metatarsal artery in dogs and the femoral artery in cats and small dogs. A small needle (23–25 gauge) on a heparinized syringe is used, or a self-filling syringe can be used. The artery is palpated and stabilized with two fingers of one hand while the syringe is firmly placed through the wall of the artery. Approximately 0.5-mL blood is needed for analysis and the sample must be stoppered and stored on ice until analyzed. After withdrawal of the syringe, firm pressure is applied to the artery for 3–5 minutes. An arterial blood gas analysis measures PaO2, PaCO2, pH, total CO2, and hemoglobin saturation with oxygen, and allows calculation of bicarbonate, base excess and deficit, and oxygen content (Table 2.1).
Alveolar–arterial oxygen gradient and PF ratio
The alveolar–arterial (A–a) oxygen gradient estimates the difference between the calculated alveolar oxygen level expected for the animal and the measured arterial oxygen level. Thus, the A–a gradient corrects for the level of ventilation performed by the animal and allows comparison of blood gas data through the course of disease that is not impacted by the effect of an increase or a decrease in PaCO2 on PaO2. The A–a oxygen gradient is calculated as
where FiO2 is the fraction of inspired oxygen (0.21 on room air), PB is the barometric pressure (inmmHg), PH2O is the water vapor pressure (47 mm Hg at 37°C), and R is the respiratory quotient (ratio of CO2 production to O2 consumption, usually assigned a value between 0.8 and 1.0). PaO2 and PaCO2 are obtained from blood gas analysis. Normal value is <15.
The PaO2/FiO2 ratio (PF or oxygenation ratio) provides a measure of the ability of the lung to oxygenate as the fraction of inspired oxygen changes from room air to 100% oxygen. This is calculated by dividing arterial oxygen by FiO2 (ranging from 0.21 to 1.0). Normal animals have a PF ratio of >500. Values between 300 and 500 indicate mild impairment of oxygenation, while values <200 indicate serious decrements in oxygenation. A PF ratio <200 is one of the requirements for a diagnosis of acute respiratory distress syndrome.
Table 2.1. Normal blood gas values for dogs and cats
Table 2.2. Respiratory causes of hypoxemia
Causes of hypoxemia
Obtaining an arterial blood gas, calculating the A–a gradient, and assessing response of hemoglobin saturation or PaO2 to exogenous oxygen supplementation allow assumptions to be made about the most likely mechanism causing hypoxemia (Table 2.2). This can help determine the most likely underlying cause of hypoxemia, although ventilation/perfusion mismatch contributes to the pathophysiology of hypoxemia in almost all lung diseases.
Imaging
Radiography is often the key to creating an appropriate list of differential diagnoses for the respiratory case and for determining the type of sampling method that is most likely to achieve a final diagnosis, such as endoscopy, fine-needle aspiration (FNA), or a tracheal wash (Table 2.3). It will also help determine the need for advanced imaging including fluoroscopy, ultrasound, nuclear scintigraphy, or computed tomography. Specific features of these tests are presented in the relevant disease sections.
Table 2.3. Airway-sampling techniques for various lung patterns
Airway Sampling
Transoral Tracheal Wash
Transoral tracheal wash is appropriate for use in large and small dogs or in cats. A sterile endotracheal tube and a sterile polypropylene or blunt-ended red rubber catheter (3.5–8 French) are needed. Prior to doing a tracheal wash, the catheter should be measured against the animal and marked at a position that estimates the location of the carina, which is approximately at the fourth intercostal space. Passing the catheter too far distally can result in airway damage. The animal is anesthetized with a short-acting anesthetic agent. Options include propofol, ketamine–valium, or a balanced protocol using a narcotic agent. Prior to intubation, the function of the larynx is assessed. In the cat, local lidocaine can be used to facilitate intubation and avoid contamination of the tube through contact with oropharyngeal or laryngeal mucosa. An assistant holds the tube in place during the lavage; however, if retrieval of fluid is less than desired, the cuff of the endotracheal tube can be inflated to improve suction.
With the endotracheal tube held in place, the polypropylene or red rubber catheter is passed sterilely to the level of the carina, and the three-way stopcock with syringe is attached to the outer port. An aliquot of saline (4–6 mL) is instilled into the airway, and suction is used to retrieve the fluid and cells from the lower airway. Either hand suction or house suction can be applied as needed. Retrieval of fluid can be enhanced by having the assistant compress the chest or by stimulating a cough during suction. Instillation and aspiration of fluid can be repeated several times until an adequate sample has been retrieved (0.5–1.0 mL is usually sufficient for culture and cytology).
A modification of the transoral tracheal wash can be performed, which yields a sample more closely approximating that of a bronchoalveolar lavage. In the dog, this is achieved using a 16-French ArgyleTM stomach tube (Sherwood Medical Co/Tyco Healthcare Kendall, Deland, FL) (Hawkins and Berry 1999). The dog must be large enough to accommodate an endotracheal tube that will not be fully occluded by the stomach tube. The stomach tube is shortened to remove any side holes on the distal end of the tube and to create a length that approximates the distance from the endotracheal tube to the last rib. The distal end of the tube can be tapered with a pencil sharpener to improve the ability to wedge within the airway, and the tube should be sterilized prior to use. Endotracheal intubation is carried out using a short-acting anesthetic agent (e.g., propofol) and a sterile endotracheal tube. The dog is placed in dorsal recumbency, and the modified stomach tube is passed through the lumen of the endotracheal tube until it meets resistance. Gentle pressure should be used when passing and wedging this tube to avoid perforating the lung. As soon as slight resistance is encountered, the tube is withdrawn 1–2 cm and lavage is initiated with 20 mL of sterile saline followed by 5 mL of air. Gentle hand suction is applied to retrieve the fluid, and a second aliquot can be instilled as needed.
