High Altitude Sickness

Acute mountain sickness (AMS)
Acute mountain sickness (AMS) occurs when the traveler ascends too high too fast. AMS is the most common form of altitude sickness and usually occurs in abrupt ascents to above 9000 feet.  The symptoms may resemble those of an alcohol hangover; however, since symptoms are often vague, any feeling of being unwell at high altitude should be considered AMS until proven otherwise.

Symptoms usually begin 2-12 hours after arrival at the higher elevation, often during or after the first night*.  The symptoms are due to a mild swelling of the brain tissue that results from acute hypobaric hypoxia. It is believed that the swelling is due to hemodynamic changes (vasodilation) that increase blood flow to the brain. Vasodilation combined with increased cardiac output cause vessel walls to thin and leak fluid into the surrounding tissue.

Headache at high elevation is common, but it must not be considered “normal.” Headache, is the universal symptom and should always be considered a sign of AMS. There are a number of other symptoms depending upon the severity of the AMS.  

AMS is classified according to severity:

Complications associated with AMS include: 

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Headaches should never be considered a “normal” result of high altitude.

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Mild AMS

Mild AMS does not interfere with normal activities and usually subsides within 1 to 3 days*, but it serves as a warning to stop or slow ascent until further acclimatization takes place.  Symptoms include:

Symptoms may worsen at night because of alterations in breathing.

Moderate AMS

With moderate AMS, normal activity becomes more difficult, and the person may have difficulty walking.  Symptoms include:

When these symptoms occur, the person requires advanced medications or descent.  Usually descending 1000 feet will result in improvement within 24 hours.  Alternatively, supplemental oxygen at 2 L per minute will relieve headache quickly and resolve AMS over hours, but it is rarely available.* The person should remain at the lower altitude until all symptoms have subsided, up to 3 days. 

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People with moderate AMS often have severe headaches, unrelieved by medications.

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Severe AMS

If the symptoms associated with mild and moderate AMS increase in severity it is cause for concern.  Symptoms include:

Having the person walk a straight line, heel to toe, is a good test to determine whether there is ataxia.  If the person is unable to walk the straight line, then ataxia is present, and this is an indication that the complication of high altitude cerebral edema (HACE) is present. The person suffering from severe AMS should immediately descend 2000 feet to a lower level.  Failure to do so could result in life-threatening HACE or high altitude pulmonary edema (HAPE), both of which are complications of severe AMS.

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The person with severe AMS should remain at the same elevation and not ascend.

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High altitude cerebral edema (HACE)
HACE results from fluid leakage that swells brain tissue. The signs and symptoms of HACE have been reported in historical literature going back about to 32 BC.  Indeed, an area of the Himalayan Mountains became known as “Big Headache and Little Headache Mountains.”  However, HACE was only recognized in medical literature in 1975.  HACE is now generally considered to be endstage AMS rather than a separate disorder. It is thought to be the result of increased cerebral edema, caused by increased cerebral blood flow due to increased permeability of cerebral vasculature when exposed to hypoxia. Hypoxia increases cerebral blood flow, causes increased intracranial pressure and most of the clinical symptoms associated with HACE.  HACE usually occurs after a week or more at high altitude in about 5% of those with AMS.  HACE is a progression of AMS that includes increasingly serious symptoms:

Descent is absolutely critical, and anyone suffering from HACE must be sent to a medical facility for proper follow-up treatment.  One problem with HACE is that the neurological complications may impair mental state, perception, and judgment, and those suffering from the disorder may not be aware or able to articulate their problems.  HACE may be fatal in 1 to 2 days if not treated promptly.  CT of the head can be useful to rule out other disorders, such as stroke, but will not indicate HACE.  MRI of the head can show changes specific to HACE. 
Emergency treatment of HACE includes:

High altitude pulmonary edema (HAPE)
High altitude pulmonary edema (HAPE) can occur by itself, but sometimes occurs in conjunction with HACE. For reasons that are not clear, HAPE occurs 5 times more frequently in males than females. The symptoms of HAPE include:

HAPE is associated with marked pulmonary hypertension that is not related to preexisting pulmonary or cardiac disease. This pulmonary hypertension results from vasoconstriction of pulmonary arterioles. Hypoxia is known to cause contraction of pulmonary arterial smooth muscle.

Pulmonary arterioles normally function as low pressure vessels. Their musculature is relatively thin and unevenly dispersed. Abnormally high pressure can cause fluid to escape through these thin walls. The fluid collects in the alveoli, preventing efficient exchange of oxygen. Oxygen desaturation can lead to impaired cerebral function, cyanosis and sometimes death. HAPE can become life-threatening very quickly, so it is imperative that the person have treatment to relieve symptoms and descend to a lower altitude immediately. The person must be sent to a medical facility for proper medical follow-up treatment.

Emergency treatment includes:

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HAPE occurs when fluid leaks from the blood vessels into the lungs.

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Subacute infantile mountain sickness
Subacute infantile mountain sickness has been reported only in places of very high altitude, above 11,000 feet.  This disorder typically affects infants who were born at low altitude and were subsequently brought to reside in a higher altitude.  Little is known of this disorder in the West because most cases are in China and Tibet, but it has occurred in other areas of high elevation, such as Peru.   The disorder gained prominence after a large-scale migration of Han Chinese moved from the low altitude of mainland China to the high altitudes of Tibet.

The disorder is characterized by evidence of severe hypoxic pulmonary hypertension and heart failure.  It affects the heart and lungs with extreme medial hypertrophy of muscular pulmonary arteries and muscularization of pulmonary arterioles, together with dilatation of the pulmonary trunk and massive hypertrophy and dilatation of the right ventricle. This is a condition known as high altitude heart disease (HAHD), also associated with chronic mountain sickness. This disorder is usually fatal within a few weeks or months and appears to be the human equivalent of brisket disease (also known as high mountain disease) in cattle, to which 30 to 40% of lowland cattle brought to high elevations succumb.

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Subacute infantile mountain sickness affects infants in places of very high altitude.

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Chronic mountain sickness  (CMS) (Monge’s disease)
Carlos Monge in Peru first described chronic mountain sickness in 1928, but, as in subacute infantile mountain sickness, most people in the West are not familiar with the disorder since it almost exclusively occurs in very high elevations, such as in Tibet, Peru, and India. CMS appears to also be similar to brisket disease in cattle.  Recent reports have involved Indian soldiers living at extremely high altitudes for prolonged periods of time. Many people become acclimatized to the higher elevation, but some long-term residents of high altitudes may lose their acclimatization, usually immigrants to the area rather than people born there. CMS is the result of excessive desensitization to chronic hypoxia with depression of the respiratory center leading to chronic hypercapnia (excess carbon dioxide).   Chronic mountain sickness is a syndrome that includes the following:

High altitude polycythemia is often referred to as excessive erythrocytosis (EE). Many people can function well with hematocrits in the 55% to 70% range if they don’t develop further symptoms. 

HAHD as a clinical form of CMS was first reported  in China in 1955.  The major characteristics of HAHD are enlarged heart, right ventricular hypertrophy, and right heart failure due to severe pulmonary hypertension, resulting in structural changes to the small pulmonary arteries.  With early diagnosis and removal of the affected person to a lower elevation, the symptoms usually subside; however, remaining at a high elevation with HAHD may result in death. HAHD affects both children and adults. More than 2000 cases of HAHD have been reported in Tibet and China, but most reports have been published only in Chinese medical journals. HAHD is an increasing problem in China because large numbers of people have migrated to higher altitudes in order to exploit natural resources.   One problem with diagnosis in the West is that some pre-existing lung diseases, such as cor pulmonale with right ventricular failure, mimic HAHD.  Additionally mild pulmonary hypertension and right ventricular hypertrophy are part of the compensatory mechanisms for acclimatization developed by people who live at high altitudes and are common findings, especially among people who have moved to the areas.

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CMS occurs when people lose their acclimatization and develop changes in the heart and excessive erythrocytosis.

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