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  • Updated 07.07.2021
  • Released 07.13.1999
  • Expires For CME 07.07.2024

Mountain sickness: neurologic aspects



Acute mountain sickness (or altitude sickness) affects climbers who rapidly ascend to heights of at least 2500 meters. The symptoms of acute mountain sickness include headache, fever, fatigue, nausea, dizziness, anorexia, and sleep disturbances. This article describes the management of acute mountain sickness. Acetazolamide, which reduces the formation of CSF, is the main drug therapy, and additional drugs include nonsteroidal antiinflammatory drugs for headache and dexamethasone for cerebral edema. Oxygen inhalation at 1 L/minute and descent to lower altitudes is recommended. The role of a portable hyperbaric chamber is also described.

Key points

• Acute mountain sickness occurs after ascent to an altitude of at least 2500 meters.

• Symptoms include headache, fever, fatigue, nausea, dizziness, anorexia, and sleep disturbances.

• If symptoms are not relieved, or with further ascent, cerebral and pulmonary edema may occur.

• Treatment is medical, with supplementary oxygen therapy.

• If symptoms persist, the affected person should descend to a lower altitude.

Historical note and terminology

Acute mountain sickness (or altitude sickness) affects climbers who rapidly ascend to heights of at least 2500 meters. Altitude-related health problems have been known to humans ever since they started to cross high mountains. The first documented report of mountain sickness was by a Chinese official, Too-Kin, between 37 and 32 BC when he encountered difficulties crossing the Kilik Pass (4827 m) into what is present-day Afghanistan (14). He described headache and vomiting and gave names such as "the Great Headache Mountain" and "the Little Headache Mountain" to the mountains on his route. In the year 403, a Chinese man crossing into Kashmir, a companion of the monk Fa Hsien, died with difficulty in breathing and foam at his mouth, now known as high-altitude pulmonary edema (14). Similar cases were described by the Jesuit priest Father Acosta in 1590 in the high Andes of Peru (01). Paul Bert, the French pioneer in the investigation of the effects of atmospheric pressure on body function, recognized hypoxia as the cause of altitude sickness in 1877 (06). An Italian physiologist, Angelo Mosso, documented a case of mountain illness at an altitude of 4559 m on the Italian Alps bordering Switzerland in 1894 (33). A cerebral form of mountain sickness in which cerebral edema predominated was described in a series of patients in 1975 (18).

There are 2 well-known high-altitude syndromes: (1) acute mountain sickness, which occurs within a few hours to a few days at high altitude; and (2) chronic mountain sickness, also called Monge disease, which develops after several years of residence at high altitude (32). Acute mountain sickness may develop into high-altitude cerebral edema or high-altitude pulmonary edema. A subacute form of mountain sickness was described in Indian soldiers in Kashmir who developed pulmonary hypertension and congestive heart failure within a few months of living at altitudes of 5800 to 6700 m (02).

The Lake Louise Consensus on the Definition of Altitude Illness defined acute mountain sickness as a syndrome occurring in the setting of a recent gain in altitude, consisting of headache and at least 1 of the following: (1) gastrointestinal symptoms, such as anorexia, nausea, or vomiting; (2) fatigue or weakness; (3) dizziness or lightheadedness; and (4) difficulty sleeping. Acute mountain sickness without headache has been reported at an altitude of below 3000 m and be triggered by chronic stress or excessive exertion (12). Persons who are not acclimatized to high altitudes and who ascend to 2500 m are at risk for acute high-altitude illnesses (05).

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