Tracheobronchial disease represents a series of problems covering disorders of the upper and lower airways.
Tracheobronchial disease represents a series of problems covering disorders of the upper and lower airways. Patients with inflammatory disease of the larynx and trachea should be evaluated for evidence of lower airway disease. The extensive defense mechanisms in the lungs can carry mucus, inflammatory cells and debris up the trachea to the pharynx. These inflammatory cells can recruit more cells and lead to secondary inflammation of the upper airways.
Laryngeal paralysis can be either congenital or acquired and is a common cause of emergency visits in large breed dogs. The paralysis may be either unilateral or bilateral. Congenital laryngeal paralysis has been reported in the Bouvier des Flanders and the Siberian husky. Acquired laryngeal paralysis is more common with many proposed etiologies. The recurrent laryngeal nerve innervates the arytenoid processes of the larynx. One of the longest nerves in the body, it is susceptible to a variety of degenerative processes. Damage to the nerve anywhere along its course by trauma, surgery, neoplasia, polyneuropathy or possibly hypothyroidism can lead to a loss of innervation of the intrinsic laryngeal muscles.
Animals with laryngeal paralysis will present with varying degrees of exercise intolerance, stridor, voice change, inspiratory effort, cyanosis and hyperthermia. They will have a pronounced inspiratory stridor with a slow, deep (obstructive) breathing pattern. Often an obvious inspiratory wheeze will be heard loudest over the larynx. Diagnosis is by direct examination under a light plane of anesthesia. A low dose of a short acting barbiturate (thiopental) or propofol is administered to allow the mouth to be held open while visualizing the glottis. Normally the arytenoid cartilages abduct on inspiration. With laryngeal paralysis the arytenoids may actually be drawn together during inspiration causing inflammation and edema. Laryngeal paralysis may be unilateral or bilateral. Increased airway pressures can lead to everted laryngeal saccules further compromising the laryngeal lumen.
Large breed dogs with laryngeal paralysis may present in extreme distress. Because panting is such an important method of controlling body temperature, subclinical laryngeal paralysis may only become evident on hot days or following strenuous exercise. The body temperature can quickly climb to dangerous levels, necessitating treatment for heat stroke. Dyspnea from upper airway obstruction can cause the animals to become anxious and more dyspneic. A vicious cycle begins as the more distressed they become, the harder they try to breathe. Handling these animals can be difficult and often the best treatment is sedation.
Patients with prolonged hyperthermia should be hospitalized and observed for complications. The kidneys, GI tract, liver and nervous tissue can all be damaged by excessive heat. Disseminated intravascular coagulation is another common complication. Once the patient is stable and signs of heat stroke have resolved definitive treatment for laryngeal paralysis can proceed.
Collapsing trachea occurs most commonly in middle aged to older, obese, toy breeds. It develops due to weakening of cartilage rings and redundant dorsal longitudinal ligament of the trachea, or chronic inflammatory disease of the small airways. Increased airway resistance in the small airways predisposes to tracheal collapse. Small airway disease associated with chronic bordetellosis, mycoplasmosis, or allergic disease is most common. Intrathoracic tracheal collapse, extrathoracic tracheal collapse, and collapsing main stem bronchi can occur together or independently. Tracheal collapse leads to chronic coughing with or without a terminal retch. Severe tracheal collapse can induce dyspnea and syncope. Affected dogs are generally healthy between coughing episodes.
Tracheal cough is easy to induce on physical examination. Softened tracheal rings can be palpated in some cases with extrathoracic collapse. Pharyngeal inflammation is common. Crackles are present in some dogs with small airway disease. Many affected dogs also have mitral valve endocardiosis and a heart murmur making it difficult to differentiate between respiratory cough and cardiac cough on physical examination alone.
Inspiratory and expiratory cervical and thoracic radiographs should be done on all dogs with suspected tracheal collapse. Intrathoracic tracheal collapse is more evident on expiratory films and extrathoracic collapse is more evident on inspiratory films. Fluoroscopy aids in the diagnosis of tracheal collapse but requires specialized equipment. With bronchoscopy the clinician can visualize dynamic changes in airway diameter. Bronchial compression by an enlarged left atrium can also be seen with the bronchoscope. All dogs with collapsing trachea and radiographic evidence of alveolar, bronchial or interstitial disease should be assessed with a TTW. Many dogs with collapsing trachea have chronic bronchitis due to bacterial disease or allergic disease and the underlying inflammation and increased small airway resistance potentiates the tracheal collapse.
Heart failure can be differentiated from collapsing trachea and small airway disease by assessing the thoracic radiographs and correlating to physical examination findings. Dogs with left heart failure most commonly have a combination of elevated heart rate, pale mucous membranes, poor pulse character, left atrial enlargement, pulmonary venous hypertension, and perihilar interstitial or alveolar edema. Dogs with collapsing trachea or small airway disease usually have normal heart rates, normal pulse character, normal mucous membrane color, bronchial pattern, pulmonary arterial hypertension, and cor pulmonale. Some dogs with left heart disease will have an enlarged left atrium that presses on mainstem bronchi inducing cough. However, unless pulmonary venous hypertension or perihilar interstitial or alveolar edema is present, the animal is probably not in heart failure.
Animals may aspirate a variety of foreign objects. Small grass-awns can often migrate into the deeper respiratory passages causing severe coughing fits, pulmonary granulomas and even pyothorax. Larger foreign objects may present with signs of upper airway obstruction causing respiratory distress as described for laryngeal paralysis. Sedation or anesthesia may be required to calm the animal and allow removal of the object.
Pulmonary edema is a complication of acute upper airway obstruction. Edema is primarily related to in increased alveolar capillary permeability. This form of non-cardiogenic pulmonary edema may show up hours after the cause of the upper airway obstruction has been removed. Patients that become more dyspneic or those whose dyspnea doesn't resolve should be monitored closely. Treatments will be discussed in the next section under pulmonary edema.
Infectious tracheobronchitis is a syndrome induced by a number of viral and bacterial agents. Adenovirus-2 and parainfluenza are the common viral agents; Bordetella bronchiseptica and Mycoplasma spp. are the common bacterial agents. Affected dogs are generally healthy except for coughing. The cough is dry and is usually accompanied by a terminal retch. There is usually a history of exposure to other dogs. Clinical signs of disease develop within 3-9 days post-exposure. Physical examination generally reveals a healthy animal with a tracheal cough, increased phlegm in the oral pharynx, and enlarged, red tonsils. Chest auscultation is usually normal except for referred tracheal sounds. Occasionally, polysystemic illness including fever, depression, and anorexia will occur if secondary bacterial bronchopneumonia develops. These dogs usually have lower respiratory crackles and wheezes. Viral Inflammation predisposes to colonization by normal bacterial flora. Bordetella and Mycoplasma reside on the surface of the mucociliary apparatus and inhibit normal clearance functions predisposing to the development of bacterial pneumonia.
A presumptive diagnosis or infectious tracheobronchitis is made on historical and physical examination finding in dogs with cough as the only problem. Dogs that present with fever or crackles should be assessed with a CBC, thoracic radiographs, and TTW. Vaccination against bordetellosis may decrease the incidence of infectious tracheobronchitis in kennel or show situations. Intranasal products are probably superior to injectable products but due to the short-lived nature of Ig-A, twice yearly vaccination is necessary to maintain local immunity.