Pathology of Pulmonary Edema

Abstract

Pulmonary edema is a common finding in many clinical conditions and is the result of increased fluid leakage from the pulmonary microcirculation. The increased leakage may occur at the level of the pulmonary capillaries or from the small intraacinar arteries and veins (these are sometimes referred to as extraalveolar or corner vessels). The protein concentration of th fluid varies with the type of edema. When fluid leakage is the result of increased pressure, it is protein-poor; when it is the result of increased permeability of the pulmonary vascular endothelium, it is protein-rich. In the lung, some fluid normally escapes from the microcirculation into the interstitial space. This fluid provides nutrients to the cells and to structures within the interstitium. Excess fluid drains through the interstitium to the lymphatics in the loose connective tissue sheaths surrounding the airways and larger arteries and veins (the penbronchovascular sheaths) and in the interlobular septae. This process also occurs in the pleura, the excess fluid here draining to the hilar lymph nodes by way of the interlobular septae. It is only when these pathways are overwhelmed that pulmonary edema develops. Initially, fluid accumu]ation is in the peribronchovascular sheaths; then, if fluid accumulation continues, edema of the alveolar wall is seen. Jntraalveolar edema occurs only when there is damage to the alveolar epithelial layer. Thus, Unless there is direct damage to the epithelial cell layer, intraalveolar edema represents a late, and often end-stage, finding. This review starts with a brief description of the structure and ultrastructural appearance of the cells that are involved or damaged when pulmonary edema develops. The second part deals with experimental studies that give insights into the mechanisms that contribute to or cause the various types of pulmonary edema.