High altitude pulmonary edema

Publisher Website
Google Scholar
Abstract
High altitude pulmonary edema (HAPE) is a non-cardiogenic edema which afflicts susceptible persons who ascend to altitudes above 2500 meters and remain there for 24 to 48 h or longer. Incidence varies with the rate of ascent and the altitude, while contributing factors include exertion and perhaps cold. Individuals susceptible to HAPE have low hypoxic ventilatory drive and an increased pulmonary vasoconstrictor response to hypoxia. Pathophysiologically, excessive pulmonary hypertension is the sine qua non of HAPE, but other factors must also be present to produce permeability edema. Clinical manifestations of mild HAPE are dyspnea with exertion, decreased exercise ability, and dry cough. Symptoms of more advanced HAPE are dyspnea, tachycardia, and tachypnea at rest, cyanosis, ataxia, change in consciousness and productive cough. Coma may rapidly ensue. Death usually follows misdiagnosis and lack of prompt treatment. Therapy consists of improving oxygenation and reducing pulmonary hypertension either by giving supplemental oxygen or descending to a lower altitude. Positive airway pressure devices, morphine, and diuretics may be adjunctive therapy, primarily when oxygen and/or descent are not possible. The leak rapidly reverses with treatment, and without residual lung damage. Slow, gradual ascent is the best prevention of HAPE, but acetazolamide has been anecdotally effective for HAPE-susceptibles. The capricious nature of the disorder mandates better public education efforts so that HAPE can be correctly recognized and treated.

This publication has 69 references indexed in Scilit: