High altitude pulmonary edema

Altitude, speed and mode of ascent, and, above all, individual susceptibili ty are the most important determinants for the occurrence of high altitude pulmonary edema (HAPE). This illness usually occurs only 2-5 d after acute exposure to altitudes above 2500-3000 m. Chest radiographs and CT scans sho w a patchy predominantly peripheral distribution of edema. Wedge pressure i s normal at rest, and there is an excessive rise of pulmonary artery pressu re (PAP) that precedes edema formation and appears to be a crucial pathophy siologic factor for HAPE. Additional factors such as an inflammatory respon se and/or a decreased fluid clearance from the lung may, however, be necess ary for the development of this noncardiogenic pulmonary edema. Bronchoalve olar lavage in patients with mostly advanced HAPE shows evidence of inflamm atory response with increased capillary permeability. There are, however, n o prospective data to decide whether the inflammatory response is a primary cause of HAPE. or a consequence of edema formation. Supplemental oxygen is the primary treatment in areas with medical facilities whereas the treatme nt of choice in remote mountain areas is immediate descent. When this is im possible and supplemental oxygen is not available, treatment with nifedipin e is recommended until descent is possible. Even susceptible individuals ca n avoid HAPE when they ascend slowly with an average gain of altitude not e xceeding 300-350 m.d(-1) above an altitude of 2500 m.