[Acute altitude-induced edema of the lung]

High-altitude pulmonary edema has the following clinical features: it occurs in young healthy subjects exposed to altitudes usually above 3,000 m; it is favored by rapid ascent, exercise, cold, and sleep; it can give a deceptive clinical picture because of the patchy distribution of the edema. Hemodynamically, severe pulmonary arterial hypertension (PAH) occurs without increase in wedge pressure or left atrial pressure. Under treatment (rest, oxygen, diuretics), the condition rapidly improves. The physiopathological mechanism of this non-cardiogenic edema is complex and not yet fully defined: PAH essentially stems from hyperreactivity of the pulmonary circulation towards hypoxic arteriolar vasoconstriction, increase in pulmonary blood volume, and pulmonary microthrombosis. Postulated mechanisms involving mixed intra-alveolar edema with high pressure and increased permeability are based on transarterial leakage, over perfusion with endothelial injury, and an increase of permeability in relation to histamine and vasoactive polypeptides. Prevention relies, for a large part, on the identification of HAPE-prone subjects, slow ascent to high altitude, moderate physical activity, warm clothing, and prior administration of acetazolamide.