A historical perspective on high altitude pulmonary edema.

Acute pulmonary edema, a potentially fatal clinical condition, represents a serious complication of so-called "Acute mountain sickness". The overt clinical picture of high altitude pulmonary edema (HAPE) includes clinical signs, serious hypoxemia, pulmonary hypertension, and alveolar edema on chest radiography. The first case of HAPE, documented by postmortem, is probably that of doctor Jacottet, who died during the building of an observatory on Mont Blanc in 1891. In 1913, TH Ravenhill, a pioneer in mountain medicine, wrote a fundamental paper that provided a first diagnostic framework for HAPE, and, in the course of the twentieth century, H Hultgren, among his various observations on HAPE, some of which documented through cardiac catheterization, hypothesized an acute failure of the left ventricle as the cause of HAPE. Hultgren also reported, during the sixties, clinical cases in which the left atrial pressure was normal, even in the presence of an increase in pulmonary pressure. Acute pulmonary hypertension has since then been considered a basic pathophysiological factor in the genesis of HAPE, and recently Swiss Authors have provided evidence that elevated arterial pressure extends to pulmonary microcirculation, so as to determine a fluid overload in the pulmonary district. Current views of HAPE indicate that it is a kind of hydrostatic acute pulmonary edema with a modification of alveolar-capillary permeability, even if it is still not known what is the precise mechanism leading to the pathological vasoconstriction in some individuals and not in others. The potential seriousness of HAPE needs preventive and therapeutic measures whose relevance was long ago recognized and documented by different physicians, as our historical survey shows.