Abstract
Altitude, speed and mode of ascent and, above all, individual susceptibility are the most important determinants for the occurrence of high altitude pulmonary oedema (HAPE). This illness usually develops only within the first 2-5 days after acute exposure to altitudes above 2500-3000 m. An excessive rise in pulmonary artery pressure preceding oedema formation is the crucial pathophysiological factor. Recent investigations using right heart catheterisation and bronchoalveolar lavage (BAL) in incipient pulmonary oedema have shown that HAPE is a hydrostatic oedema in the presence of normal left atrial pressure with non-inflammatory high permeability leakage of the alveolocapillary barrier and mild alveolar haemorrhage. An inflammatory response may develop later in more advanced cases, as has been documented by BAL. Furthermore, decreased fluid clearance from the alveoli may contribute to such non-cardiogenic pulmonary oedema. Supplemental oxygen is the primary treatment in areas with medical facilities, while the treatment of choice in remote mountain areas is immediate descent. When this is impossible and supplemental oxygen is not available, treatment with nifedipine is recommended until descent is possible. Even susceptible individuals can avoid HAPE if they ascend slowly with an average gain of altitude not exceeding 300-350 m/day above an altitude of 2500 m.
Published Version
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