Acute high-altitude sickness

Abstract

At any point 1-5 days following ascent to altitudes ≥2500 m, individuals are at risk of developing one of three forms of acute altitude illness: acute mountain sickness, a syndrome of nonspecific symptoms including headache, lassitude, dizziness and nausea; high-altitude cerebral oedema, a potentially fatal illness characterised by ataxia, decreased consciousness and characteristic changes on magnetic resonance imaging; and high-altitude pulmonary oedema, a noncardiogenic form of pulmonary oedema resulting from excessive hypoxic pulmonary vasoconstriction which can be fatal if not recognised and treated promptly. This review provides detailed information about each of these important clinical entities. After reviewing the clinical features, epidemiology and current understanding of the pathophysiology of each disorder, we describe the current pharmacological and nonpharmacological approaches to the prevention and treatment of these diseases.

FIGURE 1

Susceptibility-weighted magnetic resonance imaging in a) axial and b) sagittal planes shows microhaemorrhages (arrows) in the corpus callosum of a 65-year-old female who had suffered from severe high-altitude cerebral oedema 7 weeks previously at 3450 m. Reproduced from [1] with permission from the publisher.

FIGURE 2

a) Chest radiograph of a 37-year-old male mountaineer with high-altitude pulmonary oedema (HAPE) showing a patchy to confluent distribution of oedema, predominantly on the right side; b) computed axial tomography scan of 27-year-old mountaineer with recurrent HAPE showing patchy bilateral nodular distribution of oedema. Reproduced from [61] with permission from the publisher.

FIGURE 3

Individual bronchoalveolar lavage a) red blood cell counts and b) albumin concentrations plotted against pulmonary artery systolic pressures at high altitude (4559 m). Reproduced from [56] with permission from the publisher.