Airway collapse is a common cause of cough in dogs. It may occur in any age of dog and occurs in both small and large breed dogs. The etiology is unknown. Tracheal collapse is associated with reduction in cartilaginous constituents that provide rigidity to the cartilage rings, and it is not entirely certain whether this is a congenital or acquired lesion. The role of inflammation versus mechanical stress in progression of the disease is unclear. Similarly, bronchial collapse, or bronchomalacia, has an uncertain cause and progression. Some clinicians believe it is caused by airway inflammation; however, clinically, it appears that it may be identified with or without concurrent airway inflammation. For example, airway collapse has been reported as part of eosinophilic bronchopneumopathy.
Intrathoracic airway collapse (tracheal or bronchial) can be seen in conjunction with cervical tracheal collapse, but can also be present as a sole entity. In some dogs, the intrathoracic trachea collapses dynamically with expiration, while in other dogs, the left cranial lobar bronchus and others may be found to be collapsed at rest. Finally, some dogs display diffuse or generalized airway collapse during the respiratory cycle.
Recognition of airway collapse is challenging without advanced imaging such as fluoroscopy or bronchoscopy; however, some physical examination and radiographic findings are suggestive. Dogs with intrathoracic airway collapse associated with either tracheal collapse or inflammatory airway disease typically display a honking or snapping cough and may show an expiratory push during breathing. Expiratory crackles can be a finding with diffuse airway collapse but may also be present with chronic bronchitis or eosinophilic lung disease.
Plain radiographs will sometimes show evidence of large airway collapse, particularly when the thoracic trachea or mainstem bronchi are collapsing during expiration; however, it is much easier to see collapse in the cervical trachea. Obtaining inspiratory and expiratory lateral views can help identify dynamic change. Fluoroscopy during a cough is a better way to demonstrate collapse of the large bronchi. However, this only allows visualization of changes in caliber of the larger airways, just beyond lobar bifurcations. Bronchoscopy allows a more complete evaluation of changes in airway caliber during respiration; however, not all dogs with airway collapse are stable enough for the anesthesia required for the procedure, and some dogs destabilize during bronchoscopy. In particular, dogs that are obese, dogs with intractable cough, and dogs with marked expiratory effort are poor candidates for anesthesia. Owners should be informed of the possibility for worsening of signs following anesthesia for any procedure, and in some instances, severely affected animals cannot resume respiratory efforts following anesthesia. If the animal is stable for bronchoscopy, all airways should be evaluated for the presence of airway collapse and the degree (or percentage) of airway obstruction. In addition, markers of inflammation, such as hyperemia, mucus, or mucosal nodules should be noted and bronchoalveolar lavage is recommended in order to diagnose infectious or inflammatory lung disease.
When airway collapse is diagnosed definitively or is highly suggested by physical exam and radiographs, initial therapy might include a bronchodilator in hopes of improving expiratory airflow. Bronchodilators in common use include methylxanthine derivatives (theophylline) and beta agonists (terbutaline or albuterol). Extended-release theophylline products are recommended because they can be administered twice daily. Bioavailability and pharmacodynamic effects for most products on the market are unknown, and animals treated with theophylline should be monitored closely for therapeutic effect and adverse reactions. Side effects include vomiting, diarrhea, nervousness, agitation, or anxiety. A dosage of 10 mg/kg PO BID can be safely used in most dogs. Many drugs and medical conditions alter theophylline metabolism (most notably enrofloxacin), and in some dogs, administration of half the recommended dose for the first week of treatment is advisable. If the drug is tolerated, the dosage can be increased to the appropriate amount.
Beta agonists cause airway relaxation by direct stimulation of receptors on airway smooth muscle and are more potent bronchodilators than methylxanthine derivatives. However, since dogs do not bronchoconstrict, these drugs are not used as commonly in dogs as in cats.
When a primary airway disease, such as inflammatory bronchitis or eosinophilic lung disease, is diagnosed, glucocorticoid therapy would also be indicated. Inhaled steroids are preferred to avoid side effects associated with oral steroids. Obviously, antibiotic therapy is indicated for dogs with concurrent bacterial infection, although this seems to occur rarely.
In obese dogs, weight loss is essential to reduce the work of breathing and decrease pressure on the thorax. Clinical signs can be dramatically reduced by weight loss alone. Owners should be taught how to feed an appropriate amount of good quality food and to monitor for 1% weight loss per week. In severely obese dogs, it may take 4–6 months to achieve the ideal body weight.
Finally, when infection and inflammation have been controlled, cough suppressants can be helpful in reducing the cycle of cough-induced injury and perpetuation of cough. Generally, narcotic cough suppressants are required. Dosing with a high dose frequently in the initial stages of disease, with tapering of the dose to effect tends to work best. This also helps to avoid tolerance. Hycodan (0.55–1.1 mg/kg q 6 hours initially) and butorphanol (0.22 mg/kg q 6 hours initially) are most commonly employed in the US. Owners should be aware that this dose may cause sedation.
The prognosis for control of clinical signs in dogs with airway collapse is guarded. Owners should be advised that a cough will likely always be present to some degree and signs can wax and wane over time, requiring repeat diagnostic evaluation to determine whether infection, inflammation, or progressive airway collapse has developed. The goal of therapy is to reduce clinical signs to an acceptable level and decrease intractable or paroxysmal episodes that lead to hospitalization or collapse.