Managing laryngeal and tracheal problems (Proceedings)
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.
Tracheal collapse and hypoplastic trachea
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.