High Altitude illness

Individuals who are not acclimatized and ascend rapidly to high altitude environments are at risk for a number of the debilitating and potentially lethal illnesses.

High altitude illnesses include: high altitude headache, acute mountain sickness, high altitude cerebral edema, and high altitude pulmonary edema.

Symptoms may occur in the first days after arrival at high altitudes.

2500 m is the traditional threshold for high altitude illnesses.

Rarely mild illness may occur in persons who have ascended above 2000 m but below 2500 m.

Cerebral and pulmonary syndromes that can develop after ascent to high altitude.

Nausea and vomiting may progress acute mountain sickness to high-altitude cerebral edema.

The absence of headache or other symptoms of acute mountain illness does not rule out the development of high altitude cerebral edema.

High-altitude cerebral edema usually develops after two days at altitudes above 4000 m, and the prevalence is estimated to be 0.5-1% among persons at that elevation.

High-altitude cerebral edema Is associated with MRI changes of cerebral vasogenic edema and micro hemorrhages primarily in the corpus callosum.

Increased serum levels of IL-6, IL-6 receptor, and C reactive protein at elevtions higher than 3400 m.

At 8400 m healthy individuals have severe hypoxia.

Surveys show that individuals who travel to high altitude: 15% are over age 60 and 33% reported pre-existing medical problems.

The most common pre-existing medical conditions include hypertension, thyroid disease, asthma, and diabetes.

Decreased humidity in the air temperature and increased exposure to UV light occur in the mountain environment, but its most important environmental variable is a decrease in barometric pressure that occurs with ascent.

Barometric pressure decrease reduces the Po2 along the oxygen transport chain from inspiration of air to organ and tissue oxygenation.

This sets in motion physiological responses to restore the concentration of oxygen and support metabolic demand.

A key mediator in responses of decreased PO2 is the hypoxia-inducible factor, a gene transcription factor that regulates cellular responses to hypoxia including cellular metabolism, angiogenesis, and erythropoiesis.





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