Oxygen saturation in high-altitude pulmonary edema.

Abstract

High altitude, defined as elevations greater than or equal to 8000 feet (2438 m) above sea level, is responsible for a variety of medical problems both chronic and acute. The spectrum of altitude illness ranges from the common, mild symptoms of acute mountain sickness, such as insomnia, headache, and nausea, to severe and potentially fatal conditions, such as high-altitude pulmonary edema (HAPE) and high-altitude cerebral edema (RACE).l HAPE is a noncardiogenic form of pulmonary edema that predominantly affects young, physically active, previously healthy individuals who arrived at high altitude between 1 and 4 days before developing symptoms. Symptoms of early, milder cases include dry nonproductive cough, decreased exercise tolerance, and dyspnea on exertion. In more severe cases the victim experiences severe dyspnea at rest, orthopnea, and cough productive of pink, frothy sputum. In the most severe (and rare) cases, HAPE can be complicated by ataxia, lethargy, or coma indicative of concomitant RACE. Symptoms are typically accompanied by physical findings of rales, temperature of up to 38.8DC (l02F), tachypnea, tachycardia, and possibly cyanosis. Rales often begin in the right middle lobe and then spread diffusely.l-3 A chest radiograph is the reference standard for confirming the diagnosis of RAPE. Radiographic findings show a normal cardiac silhouette with asymmetrical, fluffy, patchy infiltrates.1,3,4 Demonstration of sufficiently low arterial oxygen saturations, however, is also thought to be adequate for confirming diagnosis.s,6 In this study, we attempted to determine whether infiltrative processes (such as HAPE) shown on chest radiographs are consistently associated with lower blood oxygen saturation.