HIGH-ALTITUDE PULMONARY-EDEMA

Altitude, speed and mode of ascent and, above all, individual suscepti bility are the most important determinants for the occurrence of high- altitude pulmonary edema (HAPE). This illness usually occurs only 2-5 days after acute exposure to altitudes above 2,500-3,000 m. Chest radi ographs and CT scans show a patchy predominantly peripheral distributi on of edema. Wedge pressure is normal at rest, and there is an excessi ve rise in pulmonary artery pressure (Ppa) which precedes edema format ion. Bronchoalveolar lavage in patients with advanced HAPE shows evide nce of inflammatory response with increased capillary permeability. Th ere are, however, no prospective data indicating whether the inflammat ory response is a primary cause of HAPE or a consequence of edema form ation. Excessive rise in Ppa appears to be a crucial pathophysiologic factor for HAPE. Recent observations of high Ppa in HAPE-susceptible s ujects who did not develop pulmonary edema after rapid ascent to high altitude suggest either that Ppa does not necessarily reflect capillar y pressure in these individuals or else that additional factors, such as an inflammatory response and/or a decreased fluid clearance from th e lung, are necessary for the development of pulmonary edema. The trea tment of choice is immediate descent. When this is impossible and supp lemental oxygen is not available, treatment with nifedipine is recomme nded until descent is possible.