High-altitude pulmonary edema: a collective review

In summary, HAPE is a potentially fatal form of noncardiogenic PE seen in a small number of individuals visiting above 9,000 ft in elevation. The pathophysiology is uncertain but is probably due, at least in part, to hydrostatic and capillary permeability abnormalities of the pulmonary vascular bed in response to hypobaric hypoxia. A subclinical form above 14,000 ft is common (15% to 23% incidence), but the incidence of HAPE itself is unclear. Possible risk factors include rapid ascent, strenuous activity on arrival, reascent to altitude by highlanders after a short stay lower, previous HAPE, cold, respiratory tract infections, sedation, youth, and the peripheral edema of AMS. Clinical presentation is similar to that of pneumonia: tachypnea, tachycardia, cyanosis, cough, fever, and chest discomfort. Symptoms often worsen with sleep. WBC count is usually elevated, and arterial blood gases reveal a respiratory alkalosis and an alarmingly low hemoglobin saturation. Chest radiographs reveal bilateral patchy infiltrates. Radiographic findings are dissimilar to those from cardiogenic PE. Differential diagnosis includes pneumonia, PE and HAB. Treatment modalities include early descent, bed rest, oxygen therapy, and EPAP. Mortalities range from 4% to 27% depending on the rapidity of descent and evacuation.