High-altitude illness
Introduction
As barometric pressure falls with increasing altitude, the partial pressure of inspired oxygen (PiO2) falls. At approximately 5,500 m PiO2 is roughly half that at sea level and by the summit of Everest (≈8,900 m) it is less than one third. The resulting hypoxaemia provokes predictable physiological responses (hyperventilation, sympathetic activation) but in susceptible individuals clinical syndromes develop.
The principal clinical entities are acute mountain sickness (AMS), high‑altitude cerebral oedema (HACE) and high‑altitude pulmonary oedema (HAPE). All are driven by hypoxia but differ in pathophysiology, presentation and immediate management priorities.
Emergency clinicians must recognise these conditions quickly, begin life‑saving measures (oxygen, descent), start first‑line pharmacotherapy when indicated and arrange urgent evacuation when required.
Altitude categories and timing
- High altitude: ~1,500-3,500 m.
- Very high altitude: ~3,500-5,500 m.
- Extreme altitude: >5,500 m.
Most altitude illness occurs within hours to a few days of ascent. Risk rises with rapid ascent and elevations above ~2,500-3,000 m.
Pathophysiology (concise)
Hypoxaemia from reduced PiO2 leads to increased ventilation and sympathetic activity. Key mechanisms include:
- AMS: mild cerebral swelling and altered cerebral blood flow regulation.
- HACE: vasogenic cerebral oedema from increased cerebral blood flow and blood-brain barrier disruption, causing raised intracranial pressure and focal dysfunction.