High-altitude pulmonary oedema (HAPE / HAPO)
Overview
High-altitude pulmonary oedema (HAPE) is a non-cardiogenic pulmonary oedema caused by hypoxia-induced pulmonary vasoconstriction, which raises pulmonary arterial and capillary pressures and leads to leakage of proteinaceous fluid into the alveoli.
It is a life‑threatening complication of ascent to high altitude that may follow acute mountain sickness (AMS) but can occur without preceding AMS or cerebral involvement (HACE). Untreated HAPE has a high case fatality in historical series, so early recognition and prompt treatment are essential.
Epidemiology and risk factors
- Typical altitude of onset is classically greater than 2,500-3,000 m, but individual susceptibility varies.
- Most cases present within 2-4 days after ascent, although onset can be earlier or later depending on rate of ascent, exertion and individual predisposition.
- Important risk factors include rapid ascent and inadequate acclimatisation, a prior history of HAPE (the strongest single risk factor), heavy exertion on arrival, cold exposure, and an exaggerated hypoxic pulmonary vasoconstrictive response.
- Pre-existing pulmonary hypertension or significant cardiac disease increases risk.
Pathophysiology (concise)
Hypoxic pulmonary vasoconstriction causes uneven vasoconstriction and raised pulmonary arterial and venous pressures. Overdistension and mechanical stress of pulmonary capillaries produce “stress failure” with leakage of proteinaceous fluid and sometimes red cells into the interstitium and alveoli.
This is a haemodynamic process rather than volume overload; therefore diuretics are generally not helpful...