Travel to a high altitude requires that the human body acclimatize to hypobaric hypoxia. Failure to acclimatize results in three common but preventable maladies known collectively as high-altitude illness: acute mountain sickness (AMS), high-altitude cerebral edema (HACE), and high-altitude pulmonary edema (HAPE). Capillary leakage in the brain (AMS/HACE) or lungs (HAPE) accounts for these syndromes. The morbidity and mortality associated with high-altitude illness are significant and unfortunate, given they are preventable. Practitioners working in or advising those traveling to a high altitude must be familiar with the early recognition of symptoms, prompt and appropriate therapy, and proper preventative measures for high-altitude illness.

High-altitude illness.

The incidence, importance, and prophylaxis of acute mountain sickness

https://www.thelancet.com/pdfs/journals/lancet/PIIS0140-6736(03)13591-X.pdf

High-altitude illness

https://www.emed.theclinics.com/article/S0733-8627(04)00015-X/pdf

Cellular hypoxia is the common final pathway of brain injury that occurs not just after asphyxia, but also when cerebral perfusion is impaired directly (eg, embolic stroke) or indirectly (eg, raised intracranial pressure after head injury). We Review recent advances in the understanding of neurological clinical syndromes that occur on exposure to high altitudes, including high altitude headache (HAH), acute mountain sickness (AMS), and high altitude cerebral oedema (HACE), and the genetics, molecular mechanisms, and physiology that underpin them. We also present the vasogenic and cytotoxic bases for HACE and explore venous hypertension as a possible contributory factor. Although the factors that control susceptibility to HACE are poorly understood, the effects of exposure to altitude (and thus hypobaric hypoxia) might provide a reproducible model for the study of cerebral cellular hypoxia in healthy individuals. The effects of hypobaric hypoxia might also provide new insights into the understanding of hypoxia in the clinical setting.

https://www.thelancet.com/pdfs/journals/laneur/PIIS1474-4422(09)70014-6.pdf

The cerebral effects of ascent to high altitudes

Observations on acute mountain sickness occurring between 11,000 and 18,000 feet, in 1925 men, 18, to 53 years old, showed no direct relation between altitude and severity of illness; mild, moderate and severe cases occurred at all altitudes. A time lag of six to 96 hours between arrival and onset of symptoms ruled out any direct relation between hypoxia and acute mountain sickness. During this period there was clinical evidence of respiratory dysfunction with slow, irregular or Cheyne—Stokes breathing, pulmonary congestion and antidiuresis. In one biopsy and two autopsy studies there was evidence of cerebral edema. Diuresis induced with furosemide provided effective routine therapy. Morphine and betamethasone were used as additional aids in severe cases. Clinical features of acute mountain sickness were ascribed to hypoxia, pulmonary congestion, increased cerebral blood flow, increased cerebrospinal-fluid pressure and cerebral edema.

C. S. V. Subramanyam

Papers

Acute Mountain Sickness