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The finer points of clinical neurology may seem of little relevance when climbing in the Himalaya at 6000 metres or stormbound in a tent, but this is often the setting for high altitude cerebral oedema—the distinct, potentially fatal neurological sequel of chronic hypobaric hypoxia where there is overperfusion of the brain with widespread cerebral oedema, raised intracranial pressure, followed by coma and sometimes death. This brief review explains what is known about the condition, first recognised in climbers and trekkers above 4000 m, and summarises some other ways in which the brain may be affected at high altitude.
ACUTE AND CHRONIC HYPOXIA: ACUTE MOUNTAIN SICKNESS
The decline in atmospheric oxygen with altitude and the oxygen cascade from ambient air to venous blood are shown in figures 1 and 2. The arterial pO2 in mmHg corresponds closely to the percentages on the horizontal axis of figure 1—a useful aide memoire if you are unable to grasp kilopascals. For example, on many trekking peaks in Nepal, Tibet, or the Andes at around 6000 m there is 50% of sea level oxygen in the atmosphere. As a result, arterial pO2 is distinctly low—around 50 mmHg with oxygen saturation around 70%, decreasing further with exercise (fig 3). Above 8000 m (Everest is 8848 m) acclimatised man without an oxygen system is close to the limits of survival.1
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