18th February 2025

High altitude pulmonary oedema

High altitude pulmonary oedema (HAPE) occurs after rapid ascent to altitudes above 2500-3000 m and typically occurs 2-5 days after the ascent. It is the most common cause of death in high altitude sickness, with a mortality rate of more than 10% when treated and 50% when untreated. This is thought to occur due to reduced environmental FiO2 at higher altitudes, which leads to uneven hypoxia-driven vasoconstriction to physiologically address ventilation-perfusion mismatch. This increases vascular resistance in the pulmonary arteries, causing pulmonary hypertension. Increased hydrostatic pressure leads to capillary leak and pulmonary oedema.

Symptoms include breathlessness (particularly reduced exercise tolerance), cough and chest tightness. Acute altitude sickness and cerebral oedema may occur at the same time.

Risk factors include: male sex, prior high altitude pulmonary oedema, fast ascent rate, high peak altitude, cold exposure, high intensity of exertion, pre-existing pulmonary hypertension and genetic factors.

The most important management strategy is to descend until there is resolution of symptoms. Oxygen may be a temporising measure if descent is delayed. Nifedipine and phosphodiesterase inhibitors may be used as adjuncts.