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
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