Two major forms of pulmonary emphysema are generally recognized. Alveolar emphysema is abnormal, permanent enlargement of air spaces distal to the terminal bronchiole and destruction of alveolar septal walls without apparent fibrosis. Interstitial emphysema is the presence of air within the supporting connective tissue stroma of the lung (interlobular, subpleural, mediastinal, subcutaneous).
Emphysema affects ~10% of people with chronic obstructive pulmonary disease; the main risk factors are tobacco smoke exposure and α1-antitrypsin deficiency. In animals, it typically occurs secondary to a primary obstructive pulmonary disease process.
Although the pathogenesis of pulmonary emphysema is not fully understood, at least three mechanisms have been suggested:
an imbalance between protease secreted by neutrophils and macrophages, and antiprotease activity results in destruction of alveolar walls and interstitial matrix
inappropriate maintenance of lung structure and repair following injury
the condition develops secondary to obstruction of airways on expiration due to chronic bronchitis/bronchiolitis or congenital abnormality of the airway wall
This last mechanism creates a “check valve” lesion, in which air is able to enter alveoli on inspiration or through collateral ventilation but is unable to leave freely and causes air trapping.
Pulmonary diseases associated with airway obstruction and dyspnea, such as bovine respiratory syncytial virus infection, acute respiratory disease syndromes, such as acute pulmonary edema and emphysema, and moldy sweet potato toxicity are commonly associated with interstitial emphysema. Severe interstitial emphysema can cause large gas bullae in all parts of the lung and subcutaneous emphysema as air dissects along fascial planes from the lungs through the mediastinum and thoracic inlet to the subcutis of the back. Because of well-developed interlobular septa and lack of collateral ventilation, cattle are particularly susceptible to interstitial emphysema.
Recurrent airway obstruction, or “heaves,” in horses is associated with chronic bronchitis and bronchiolitis, resulting in alveolar hyperinflation by air trapping. The condition is partially reversible with bronchodilators; however, about 12% of horses develop alveolar emphysema presumably from chronic overdistention of alveolar walls and protease/antiprotease imbalance associated with pulmonary inflammation.
Congenital lobar emphysema of dogs (as seen in the Pekingese breed) occurs secondary to aplasia or hypoplasia of bronchiolar cartilage that collapses during expiration, leading to air trapping. In cats, overdistention of the alveoli can occur during end-stage asthma conditions or as a result of chronic obstructive pulmonary disease. Airway irritants commonly associated with this in cats (particularly indoor cats) are tobacco smoke, allergens, and air pollution. Obesity and dental disease are thought to exacerbate this condition in cats, and the Siamese breed may be at higher risk.
Animals with pulmonary emphysema may present with labored breathing and coughing, and physical examination may reveal abnormal breath sounds such as wheezes and crackles. The area of thoracic auscultation is typically enlarged due to lung hyperinflation. Pulse oximetry or arterial blood gas may show nonspecific oxygen deficiency. Thoracic radiographs and CT may show hyperlucent lungs with a flattened diaphragm. Pulmonary function tests, though rarely available, can provide a definitive diagnosis.
At necropsy, the lungs do not collapse and stay overinflated. Histology is the only method to differentiate lung overinflation secondary to pulmonary emphysema from air trapping due to airway obstruction from chronic bronchiolitis or bronchitis. Air bubbles (bullae) of various sizes may be seen in the subpleural space and interstitium, as well as around the kidneys and pericardial sac in cattle with emphysema. Lesions may develop as subpleural bullae or emphysema localized to a lobe or diffused lesions.
Acute therapy for animals that are hypoxemic (eg, PaO2<80), hypoxic (eg, lactate above reference range), or struggling to breathe includes oxygen, injectable anti-inflammatory medications, and aerosolized bronchodilators if available. If the primary disease process is known, therapy directed toward that is essential and may result in significant improvement of clinical signs. Treatment for chronic disease includes administration of bronchodilator and anti-inflammatory drugs, along with air quality control measures.
With the exception of congenital forms, the majority of pulmonary emphysema cases are secondary to an inflammatory condition, and the condition is irreversible.
Treatment includes bronchodilators, anti-inflammatory medications, and addressing the primary disease process when possible.
Keeping air quality high and eliminating or minimizing pulmonary irritants is the key to prevention.