Chapter 162 Bronchopulmonary Disease
Diseases of the tracheobronchial tree and pulmonary parenchyma are very common in canine and feline patients and are responsible for substantial morbidity in the pet animal population. Determining the underlying disease responsible requires an understanding of clinical signs, interpretation of laboratory and radiographic findings, and collection and analysis of airway samples. Individualized therapy will be most likely to lead to amelioration of signs. Many respiratory tract diseases are chronic in nature, and the goals of therapy become controlling clinical signs and avoiding progression of disease.
CLINICAL SIGNS
• As disease progresses, shortness of breath and decreased ability to exercise may become more evident. Parenchymal disorders usually are associated with abnormal respiratory rate and effort as well as exercise intolerance and signs of systemic illness.
• In chronic airway disease or parenchymal lung disorders, complications such as syncope and cyanosis may arise from progressive respiratory disease.
Overview in Dogs
• Common causes of respiratory disease in dogs include tracheal or bronchial collapse, chronic bronchitis, and infectious or inflammatory lung disease. Clinical signs of cough and exercise intolerance are common to all three conditions, and further diagnostic testing is needed to further define the underlying disorder. Isolated cervical tracheal collapse may be suspected by the observation of a high-pitched, honking cough in a small breed dog in combination with inspiratory difficulty; however, lower-airway inflammatory disease may complicate the clinical picture and will be easily missed unless a full evaluation is completed. Additionally, some dogs with tracheal collapse have concurrent laryngeal paralysis, detected by the presence of dramatic stridor over the larynx along with voice change. Chronic bronchitis is a very common disease of small-breed dogs; however, large breed dogs are equally affected.
• Acute respiratory distress, characterized by extreme tachypnea, cyanosis, or collapse, may be observed in animals with decompensated chronic tracheobronchial or interstitial disease. This should be distinguished from other causes of acute respiratory signs such as pulmonary edema (cardiogenic and noncardiogenic), pulmonary thromboembolism, and disease of the pleural space (pneumothorax or pleural effusion).
Overview in Cats
• The most common cause of respiratory signs in cats is lower-airway inflammatory disease (chronic bronchitis and asthma). These airway diseases have many features that parallel the same disorders in people, including spontaneous airflow limitation, airway inflammation, and bronchial hyper-responsiveness.
• Cats are susceptible to pulmonary infection with bacteria, although bacterial infection of feline airways is a relatively uncommon phenomenon. Similarly, aspiration pneumonia, which is common in the dog, occurs relatively uncommonly in the cat. Isolation of Mycoplasma spp. from the lower airways of a cat should be considered indicative of infection since this organism is not found in the lower airways of healthy cats. This is important to recognize because isolation requires special culture techniques, and, in some studies, this organism is the most common cause of primary lung infection in the cat. Yersinia pestis, the cause of bubonic and pneumonic plague, is an additional primary pathogen to consider in cats from New Mexico (see Chapter 19).
• Other infectious agents to consider as causes of respiratory signs in cats include systemic mycoses (particularly cryptococcosis, blastomycosis, and histoplasmosis), parasites (lungworms and heartworm), viruses (calicivirus, herpesvirus, feline infectious peritonitis), and protozoa (toxoplasmosis).
• Additional causes of cough that should be considered are tracheobronchial foreign body, tracheal neoplasm, and chylothorax. Other differential diagnoses for cats with primarily shortness of breath include pleural effusion (chylothorax, pyothorax, hydrothorax, hemothorax), pneumothorax, pulmonary thromboembolism, neoplasia, and cardiac failure.
TRACHEAL COLLAPSE
Etiology
• Hypocellular tracheal cartilage with deficient production of glycosaminoglycans and chondroitin sulfate has been found in some dogs with tracheal collapse. These metabolic deficiencies cause a reduction of bound water within tracheal cartilage and result in decreased turgidity of the ring structure. The abnormalities in chondrogenesis that result in tracheal collapse may be congenital or inherited, or may be related to dietary deficiencies.
• Collapse may be present in the cervical region, intrathoracic region, or both. In some dogs, collapse of smaller airways supported by cartilage can be seen. Collapse may be found solely at rest, or it may be dynamic, varying with the phases of respiration. In these situations, cervical collapse is found on inspiration, while intrathoracic collapse occurs on expiration. Inflammation within the airways may exacerbate airway collapse.
Pathophysiology
• Loss of structural support in the cartilage of the tracheal ring allows fluctuations in airway diameter in association with changes in airway pressure that occur during respiration or cough.
• The trachea generally collapses in a dorsoventral orientation. Tracheal rings become flattened, leading to narrowing of airway diameter, elongation of the dorsal tracheal membrane, and prolapse into the airway. Concussive trauma between the dorsal tracheal membrane and the ventral epithelial surface of the trachea results in airway injury, mucus production, and perpetuation of cough. Reduction in the radius of the airway increases the resistance to airflow, which necessitates an increase in driving pressure to maintain normal air movement into and out of the lungs. Increased airflow can perpetuate airway inflammation and injury.
• Collapse is isolated to the cervical trachea in some dogs, but many dogs also have disease in the intrathoracic region.
Clinical Signs
Signalment
Small-breed dogs are typically affected with tracheal collapse, and an increased prevalence is generally seen in the Yorkshire terrier, poodle, Pomeranian, and chihuahua. Any breed of dog can be affected by lower-airway collapse, although typically smaller breed dogs are affected. Animals of any age may present with signs related to tracheal and/or lower-airway collapse.
History
• Coughing, gagging, and retching can be reported with tracheal collapse and may be mistaken for vomiting. Owners might also suspect a tracheal foreign body or “kennel cough” as a cause for signs.
• Paroxysms of coughing often occur and may lead to cough syncope. In general, cough and respiratory distress progress over time until the animal becomes debilitated or unable to function.
• Animals with tracheal collapse can have long periods of normalcy between episodes of apparent acute disease. Exacerbations of clinical signs may be associated with any additional respiratory-related complication including inflammation or infection (bronchitis or pneumonia), upper-airway obstruction (laryngeal paralysis or everted saccules), or congestive heart failure (CHF). A common cause for exacerbation of disease is intubation for a procedure under anesthesia. Finally, weight gain appears to worsen clinical signs of disease in affected animals.
Physical Examination
• Obesity is very common in dogs with tracheal and airway collapse. Hepatomegaly has also been reported, which may be a result of fat deposition in the liver.
• Dogs with tracheal collapse can appear normal at rest. Excitement induces a honking cough, and in more severe cases can result in airway obstruction and respiratory distress. Animals typically have marked tracheal sensitivity, and even gentle palpation can precipitate a crisis.
• High-pitched inspiratory noises are sometimes heard over the narrowed trachea in animals with cervical collapse. The presence of stridor indicates that concurrent laryngeal paralysis should be considered.
• An end-expiratory snap may be heard over the thorax with collapse of the intrathoracic trachea or mainstem bronchi.
Diagnosis
Radiography
• Inspiratory and expiratory lateral views and a ventrodorsal view are recommended to evaluate tracheal luminal diameter, pulmonary infiltrates, and cardiac size.
• The trachea can appear radiographically normal in more than 50% of cases, and false-positive results are also common. Performing fluoroscopy during the induction of a cough can be used to aid in the diagnosis, although even this technique cannot identify all cases of collapsed trachea.
Transtracheal Wash
• Use sedation and oral intubation when performing a tracheal wash on a patient with tracheal collapse. To avoid tracheal irritation, use a sterile endotracheal tube of small diameter. Lidocaine gel applied lightly to the tube can lessen induction of cough. It is not necessary to expand the inflatable cuff during the short procedure, and this can also lessen the tendency for worsening of cough after the procedure.
• After intubation, pass a sterile polypropylene urinary catheter or feeding tube to the level of the carina (the fourth intercostal space), and inject sterile nonbacteriostatic saline (4-5 ml), and then aspirate back into the syringe. Stimulating a cough and performing coupage during aspiration will increase the return of fluid as will a sterile mucus trap system attached to a controlled suction device. Only 1 to 2 ml of fluid are required for sample processing (cultures and cytology), and a second and third aliquot can be instilled if the sample recovered is inadequate. Alternatively, culture can be performed using a guarded swab passed through the endotracheal tube. This system will not be contaminated by the tip of the endotracheal tube.
Bronchoscopy
• When available, bronchoscopy is useful both for collection of airway samples and for grading the extent and severity of tracheal collapse. In small dogs, a bronchoscope with a diameter smaller than 5 mm diameter is most useful for assessing the airways. Flexible bronchoscopy has an advantage over rigid bronchoscopy because of the ability to assess lower airways as well. Bronchoscopy can confirm the presence of isolated cervical tracheal collapse and can identify passive or dynamic collapse of lower airways. Determining the extent of disease is important when deciding whether surgical correction or placement of an intraluminal stent is feasible.
• Bronchoalveolar lavage can be used to collect lower-airway samples. Culture can be obtained from the lavage fluid or from a guarded endoscopic microbiology brush. Veterinarians performing respiratory endoscopy and bronchoscopic-guided airway lavage should be intimately familiar with respiratory tract anatomy and trained in the procedures of bronchoscopy. Particular attention must be paid to coordinating the airway examination with anesthesia methods, and assuring sufficient ventilation and delivery of oxygen during the procedure.
Treatment
General
• Weight loss is beneficial for most patients. Reducing the amount of fat on the thoracic cage improves chest wall compliance and decreases the work of breathing. Many dogs will experience substantial reduction in cough and improvement in respiratory health with weight loss alone.
• Efforts should be made to limit exposure to environmental stressors such as high humidity and heat during exercise. A harness should be used in place of a collar.
Antitussives
• Opiates such as hydrocodone (0.2 mg/kg PO q6-12h) or butorphanol (0.5-11 mg/kg PO q6-12h) are most effective. The dosing regimen must be sufficiently flexible to control cough without inducing nausea or excessive sedation.
Bronchodilators
Dogs that have intrathoracic airway collapse and evidence of small airway disease may benefit from the use of bronchodilators (Table 162-1). Bronchodilators have no clinically significant effect on the large airways and do not result in an increased diameter in the tracheal lumen. Instead, these drugs act primarily on small airways, making it easier for air to flow out of the lungs and lessening the tendency for dynamic collapse of large airways.
Table 162-1 BRONCHODILATORS COMMONLY USED IN CANINE AND FELINE BRONCHOPULMONARY DISEASE.
| Drug | Dosage | Side effects |
|---|---|---|
| Methylxanthines | ||
| Sustained-release theophylline | Dog: 10 mg/kg PO q12h | Multiple drug interactions, gastrointestinal upset, tachycardia |
| Cat: 10 mg/kg PO q24h (PM) | ||
| Beta agonists | ||
| Terbutaline | Dog and cat: 0.01 mg/kg SC, IV | Tachycardia, hypotension |
| Dog: 1.25–5.0 mg/dog PO q12h | ||
| Cat: 0.625 mg PO q12h | ||
| Terbutaline MDI | 200 μg/puff q12h by aerosol | |
| Albuterol | Dog: 50 μg/kg PO q12h | |
| Albuterol MDI | 90 μg/puff q12h by aerosol | |
| Epinephrine | 20 μg/kg IV, IM, SC, IT | Cardiac arrhythmias, hypertension, vasoconstriction |
MDI, metered dose inhaler
Surgical Stabilization
• Surgical placement of tracheal ring prostheses has been successful in reducing clinical signs in dogs with focal cervical tracheal collapse. The surgery is technically demanding and is associated with occasionally serious complications. However, most owners report that the surgery is beneficial in improving the quality of life for their pet (see Chapter 161).
• Placement of intraluminal stents has resulted in alleviation of clinical signs in dogs with severe tracheal collapse that failed to respond to medical management. Stents made from a nitinol metal alloy are placed fluoroscopically. Once placed, stents are generally not removable. Complications associated with obstruction of a principal bronchus, device fracture, and granuloma formation have been reported.
CHRONIC BRONCHITIS
Etiology
• Smoking remains the major cause of chronic bronchitis in people, and exposure to air pollution or particulate matter may play a role in the canine disease.
Pathophysiology
• Chronic airway inflammation results in characteristic changes in lower-airway structure and function. Neutrophilic infiltration of the airway results in release of proteases and oxidant species that damage the mucosa, stimulating a chronic cycle of injury and repair of the epithelium.
• Chronic bronchitis is characterized by hypertrophy and hyperplasia of mucous glands and goblet cells. These changes result in accumulation of mucus within the airway with obstruction of airflow, leading to clinical signs of cough and exercise intolerance.
• Histopathologic changes reported in dogs with chronic bronchitis include inflammatory cells in the lamina propria, goblet cell proliferation, enlargement of mucous glands, epithelial erosion with healing by basal cell proliferation, and squamous metaplasia. Mild emphysema, characterized by increased alveolar air space and loss of interalveolar septae is occasionally seen, although dogs do not display clinical manifestations of emphysema.
Clinical Signs
History
• The characteristic historical finding in chronic bronchitis is the presence of a chronic cough for at least 2 months’ duration, in the absence of other disorders that can cause cough. An acute exacerbation of disease may cause the owner to seek veterinary attention, but often it is discovered that the dog has coughed for years when a careful history is obtained.
• The cough associated with chronic bronchitis can be a dry hacking cough or may be reported as moist or harsh. Swallowing or licking the lips after a cough suggests that the cough is productive, which is probably due to excessive mucus production.
• Exercise intolerance, fatigue, or increased panting may be reported in addition to cough, however, the typical dog with bronchitis is not systemically ill. This characteristic helps distinguish chronic bronchitis from other causes of cough including infective pneumonia, CHF, and thoracic neoplasia.
Physical Examination
• Chronic bronchitis is classified as an obstructive airway disease that classically results in a slow, deep respiratory pattern in order to decrease the work of breathing. When observed carefully, animals severely affected by chronic bronchitis may show prolonged expiration and an expiratory push. These animals may also be intermittently cyanotic or syncopal. Dogs with chronic bronchitis may also pant or appear short of breath when excited or agitated during an examination.
• Tracheal sensitivity is usually present but this is a nonspecific finding associated with airway inflammation. Concurrent tracheal or airway collapse is commonly present and may be detected by the characteristic goose-honk cough or as a snapping sound over the thoracic cage when intrathoracic airways collapse on expiration.
• The presence of normal lung sounds does not rule out the diagnosis of chronic bronchitis. Stimulating a large inspiration by causing breath holding or inducing a cough will increase the detection of abnormal lung sounds in many cases.
• Adventitious lung sounds are often found in dogs with chronic bronchitis. Coarse or harsh, diffuse crackles are reported along with expiratory wheezes.
• Cardiac auscultation may reveal concurrent mitral-valve insufficiency in older, small-breed dogs. Heart rate and rhythm may be helpful in ruling out CHF as a cause of cough, because these dogs typically exhibit a regular sinus rhythm or sinus tachycardia, whereas dogs with respiratory disease usually have a normal to slow heart rate, often with sinus arrhythmia due to increased vagal input from pulmonary disease.
• Determining the etiologic cause of cough in a dog with cardiomegaly, left atrial dilation, and collapse or compression of the mainstem bronchus can be challenging. In some dogs, increased left-atrial volume, causing compression of the bronchus is the primary problem, whereas in others, primary loss of cartilaginous support of the airway is the principal pathology resulting in cough. Some dogs might also suffer from airway inflammation that induces cough in conjunction with cardiac or airway structural abnormalities.
Diagnosis
Radiography
• Generalized peribronchial infiltrates are considered typical of chronic bronchitis. This pattern is usually characterized by “doughnuts” (end-on bronchi) or “tram lines” (airways seen in longitudinal section), which represent airway walls thickened by inflammation. In comparison to age-matched control dogs, dogs with bronchitis have thickening of bronchial walls and increased numbers of airway walls visible on chest radiographs. However, some older dogs demonstrate radiographic features of bronchial thickening without evident clinical signs of chronic bronchitis.
• Alveolar infiltrates are not typically found in chronic bronchitis and would suggest a diagnosis of pneumonia or pulmonary edema.
• Pulmonary infiltrates may be obscured by fat overlying the thoracic cage in obese animals. Obesity also leads to decreased thoracic compliance, which restricts expansion of the thorax and can lead to an apparent reduction in lung volume.
• Heart size can be difficult to interpret in patients with chronic bronchitis. True right-sided cardiomegaly may be seen in severely affected patients that develop pulmonary hypertension or cor pulmonale. However, many chondrodysplastic breeds will appear to have cardiomegaly due to breed conformation. Also, obesity can cause an enlarged cardiac silhouette as a result of intrapericardial deposition of fat. A vertebral heart score is a good method for objectively estimating heart size in many dogs (see Chapter 143).
Transtracheal Wash
• An endotracheal wash through a sterile endotracheal tube can be performed as described under “Tracheal Collapse.”
• A transtracheal wash can be performed by passing the needle of a jugular catheter between the tracheal rings (I prefer a puncture as low on the trachea as possible), and then threading a sterile catheter down the airway. Alternately, a through-the-needle catheter can be used to access the lower airways. After placement of the catheter and withdrawal of the needle, sterile tubing is passed through the catheter in order to collect the wash sample.
• A sterile preparation is performed in the site desired. Local anesthetic block can be achieved with SC infiltration with 2% lidocaine at the site of entry in the skin and in the trachea.
• The needle is placed into the skin several rings below the site where the trachea will be entered. By drawing the skin upward before penetrating the trachea, a SC tunnel will be created that lessens accumulation of air after the procedure. When the trachea has been entered, a slight “pop” is felt and the animal will usually cough. The catheter is threaded through the needle to the level of the carina (the fourth intercostal space).
• If a jugular catheter is used, the needle is withdrawn from the neck at this time, and the guard secured over the needle-catheter junction.
• When performing a transtracheal wash, the catheter should never be withdrawn back into the needle after the trachea has been entered, as this increases risk of shearing the catheter off into the airway.
Bronchoscopy
• Bronchoscopy is extremely useful in the diagnosis of chronic bronchitis, particularly in cases that lack typical radiographic findings. The procedure allows visualization of airway changes, localization of disease, collection of more specific airway samples, characterization of dynamic changes in airway caliber, and the opportunity to identify and biopsy lesions.
• Dogs with chronic bronchitis have variable degrees of airway hyperemia and a roughened appearance to the mucosa. The majority of dogs have increased mucus in the airways. Animals with long-standing bronchitis can have nodular proliferations of fibrous tissue protruding into the airway. These nodules are usually of varying size and are found throughout the airway. In some cases these must be differentiated from the nodules produced by the parasite Oslerus osleri, which are typically found on the floor of the airway just cranial to the carina.
Tracheobronchial Cytology
• Healthy dogs have primarily ciliated, columnar epithelial cells in tracheal wash fluid. Rare inflammatory cells or macrophages from the lower airway are seen.
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