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Pulmonary Emphysema: IntroductionOwn Your Copy Today

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 should be distinguished from alveolar hyperinflation, a common and temporary postmortem finding that occurs secondary to obstruction of air outflow. While the pathogenesis is not fully understood, at least 2 possibilities have been suggested: 1) there appears to be degradation and weakening of alveolar walls and interstitium by inflammatory cell protease activity, particularly neutrophil elastase, in patients with low antiprotease production; and 2) the condition develops secondary to chronic bronchitis or bronchiolitis ( bronchiolitis fibrosa obliterans) causing obstruction of airways on expiration. This creates a “check valve” lesion, in which air is able to enter alveoli on inspiration or through communicating pores in alveolar walls, but is unable to leave freely.
Emphysema is an important disease in humans; in other animals it typically occurs secondary to another pulmonary disease process. Chronic obstructive pulmonary disease (COPD) or “heaves” in horses ( Recurrent Airway Obstruction) can cause enlargement and destruction of airspaces secondary to chronic generalized bronchiolitis, which is characterized by epithelial hyperplasia, goblet cell metaplasia, peribronchiolar fibrosis, and lymphoplasmacytic inflammation. The association of high numbers of eosinophils with COPD suggests allergic, infectious, and/or toxicologic etiologies for the condition. Congenital lobar emphysema of dogs (as seen in the Pekingese breed) occurs secondary to aplasia or hypoplasia of bronchiolar cartilage. Due to well-developed interlobular septa and lack of collateral ventilation, sheep, pigs, and particularly cattle are susceptible to interstitial emphysema. Any pathologic process that results in forced expiration can cause air to be forced into interlobular septa. The condition may occur as a sequela of acute interstitial pneumonia in cattle. Severe interstitial emphysema can cause subcutaneous emphysema as air dissects along fascial planes from the lungs through the mediastinum and thoracic inlet to the subcutis of the back.
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.

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