Overview of Pulmonary Emphysema
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. While the pathogenesis of pulmonary emphysema is not fully understood, at least three mechanisms have been suggested: 1) an imbalance between protease secreted by neutrophils and macrophages, and antiprotease activity results in destruction of alveolar walls and interstitial matrix; 2) inappropriate maintenance of lung structure and repair follows injury; and 3) the condition develops secondary to obstruction of airways on expiration due to chronic bronchitis/bronchiolitis or congenital abnormality of the airway wall. This 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.
Recurrent airway obstruction, or “heaves” in horses (see Recurrent Airway Obstruction in Horses), is associated with chronic bronchitis and bronchiolitis, resulting in alveolar hyperinflation by air trapping. The condition is partially reversible with bronchodilators; however, a small subset 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. Because of well-developed interlobular septa and lack of collateral ventilation, cattle are particularly susceptible to interstitial emphysema. 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 (see Acute Bovine Pulmonary Emphysema and Edema), and moldy sweet potato toxicity (see 4-Ipomeanol Toxicity (Moldy Sweet Potato) and Perilla Ketone Toxicity (Purple Mint Toxicity) in Cattle) 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.
Clinical signs depend on the primary disease process. Often, affected animals present with labored breathing, and auscultation reveals abnormal breath sounds such as wheezes and crackles due to airway disease. The area of thoracic auscultation is typically enlarged due to lung hyperinflation. 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. Pulmonary emphysema affects a small percentage of horses with recurrent airway obstruction (~12%). Lesions may develop as subpleural bullae or emphysema localized to a lobe or diffused lesions.
Minor degrees of emphysema may precede death if there was a prolonged struggle or exaggerated respiration. These agonal changes should be differentiated from antemortem lesions.