Update on high-altitude pulmonary edema: pathogenesis, prevention, and treatment

Joshua O Stream, Colin K Grissom
Wilderness & Environmental Medicine 2008, 19 (4): 293-303
High-altitude pulmonary edema (HAPE) is a life-threatening noncardiogenic form of pulmonary edema (PE) that afflicts susceptible persons after rapid ascent to high altitude above 2500 m. Its pathogenesis is related to increased sympathetic tone, exaggerated hypoxic pulmonary vasoconstriction, uneven hypoxic pulmonary vasoconstriction with overperfusion of some regions of the pulmonary vascular bed, increased pulmonary capillary pressure, stress failure of pulmonary capillaries, and alveolar fluid leak across capillary endothelium resulting in interstitial and alveolar edema. Prevention of HAPE is most effectively achieved by gradual ascent with time for acclimatization, although recent small studies have highlighted a number of pharmacologic options. Inhaled salmeterol prevents HAPE presumably by increasing alveolar fluid clearance, the phosphodiesterase-5 inhibitor tadalafil works by acting as a pulmonary vasodilator, and dexamethasone seems to prevent HAPE by stabilizing the capillary endothelium, along with other potential effects. These investigations have yet to be validated in widespread clinical practice. Nifedipine, which prevents HAPE via its effects as a pulmonary vasodilator, has a longer history of clinical use. The most effective and reliable treatment of established HAPE is immediate descent and/or adequate flow supplemental oxygen to maintain arterial saturation above 90%, accompanied by rest from strenuous physical activity. Use of a portable hyperbaric chamber is an effective temporizing measure, and nifedipine may be used for treatment of HAPE, although only as an adjunct to descent and/or supplemental oxygen if these methods of treatment are not immediately available to a person with HAPE.

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