There are three main types of altitude-related disorders: acute mountain sickness (AMS), which may progress to high altitude pulmonary oedema (HAPE) or high altitude cerebral oedema (HACE). All three conditions are due to the chronic hypobaric hypoxia which develops at high altitudes
Acute mountain sickness is generally a self-limiting condition. Features of AMS start to occur above 2,500 - 3,000m, developing gradually over 6-12 hours and potentially last a number of days:
Prevention and treatment of AMS
- the risk of AMS may actually be positively correlated to physical fitness
- gain altitude at no more than 500 m per day
- acetazolamide (a carbonic anhydrase inhibitor) is widely used to prevent AMS and has a supporting evidence base
- it causes a primary metabolic acidosis and compensatory respiratory alkalosis which increases respiratory rate and improves oxygenation
- treatment: descent
A minority of people above 4,000m go onto develop high altitude pulmonary oedema (HAPE) or high altitude cerebral oedema (HACE), potentially fatal conditions
- HAPE
- mechanism: hypobaric hypoxia → uneven hypoxic pulmonary vasoconstriction → uneven blood flow in the lungs → areas of the lung receiving more blood experience an increase in capillary pressure → more fluid leakage. Hypoxia may also directly increase capillary permeability, exacerbating fluid leakage into the alveolar space.
- presents with classical pulmonary oedema features
- HACE
- in contrast to the above, cerebral vasodilation is the problem. Hypoxia → cerebral vasodilation → elevated cerebral blood volume
- also, hypoxia → increase in the permeability of the blood-brain barrier → capillaries in the brain more leaky → leading to fluid accumulation in the extracellular spaces
- both these factors → cerebral oedema
- presents with headache, ataxia, papilloedema
Management of HACE
Management of HAPE
- descent
- nifedipine, dexamethasone, acetazolamide, phosphodiesterase type V inhibitors*
- oxygen if available