Altitude illness develops at elevations above 2,000-2,400 m, the elevation of most ski resorts in the western United States.

Of lowland residents visiting these altitudes, approximately 25% develop acute mountain sickness.

Up to 54% of people traveling abruptly to altitudes above 4,000 meters develop AMS.

20% of experienced climbers develop symptoms of AMS.

Others at risk include balloon riders, campers, and passengers in unpressurized aircraft (eg, parachutists).

Children more susceptible than adults.

Alcohol consumption, smoking, and rigorous exercise upon arrival to altitude predispose to AMS.

Oxygen saturation drops below 90% at 2,500 m in most people.

Hypoxia leads to low arterial oxygenation in cerebral blood flow, which leads to hyperventilation and respiratory alkalosis.

Sodium retention resulting from hypoxia to the sodium pump leads to fluid retention.

Rapid ascent does not allow the body to acclimate to these changes.

Throbbing headache, malaise, lethargy, anorexia, sleep disturbances, nausea, vomiting, and a dry cough or mild dyspnea.

Typically develop within 8-24 hr of ascent and resolve without specific treatment in 24-72 hr.

Tachycardia.

Peripheral fluid retention (edema).

Generally benign, self-limited condition that resolves without sequelae.

Failure to improve within 24-48 hr and/or the development of pulmonary or neurologic symptoms may indicate the development of high-altitude cerebral edema (HACE) or high-altitude pulmonary edema (HAPE).

None; however, other causes of AMS symptoms should be entertained (toxins, hypoglycemia, meningitis, etc).

Stop the ascent and rest or plan acclimatization day in air travel to altitude.

Avoid alcohol and vigorous exercise early at altitude. Moderate exercise assists with acclimatization.

Acetaminophen or ibuprofen may help alleviate the headache.

Antiemetics may help alleviate the nausea.

Acetazolamide (Diamox) 250 mg tid is a carbonic anhydrase inhibitor that stimulates ventilation and can improve the symptoms of AMS:

Descent from altitude, oxygen therapy, and hyperbaric treatment are generally not necessary for AMS.

High-altitude cerebral edema (HACE) is associated with rising intracranial pressure brought on by an alteration of dynamic autoregulation of cerebral blood flow. This results in overperfusion of capillaries and vasogenic cerebral edema.

High-altitude pulmonary edema (HAPE) is caused by exaggerated pulmonary hypertension and high capillary pressure inducing a high permeability-type lung edema.

Risk factors include: elevation attained, speed of ascent, and a history of previous HAPE. Strenuous exercise performed immediately upon arrival to altitude may also contribute.

The reported incidence ranges from 0.01-15.5% of those ascending to high altitude.

Mortality of HACE approaches 60% if coma ensues.

A genetic predisposition may exist.

The mechanism of injury in HACE is not well understood, but is probably related to hypoxic cerebral vasodilation.

Sympathetic vasoconstrictor overactivity and endothelial dysfunction (impaired nitric oxide release and augmented endothelial-1 release) may contribute to pulmonary hypertension in HAPE-prone individuals.

Symptoms of AMS are present with all forms of altitude injury and include headache, nausea, vomiting, anorexia, lightheadedness, dizziness, and are worsened by exertion.

Typical symptoms of HACE include: unrelenting headache associated with vomiting, truncal ataxia, impaired mental status (confusion, poor judgment, delirium), and severe lassitude. Hemiparesis, hemiplegia, seizures, and coma are less common but suggest progression of this syndrome. HACE can develop within 24 hr of AMS, but typically will be delayed 1-3 d.

HAPE symptoms are mostly respiratory and include dyspnea, cough, fatigue, chest pain, weakness, and lethargy. Cough may be frothy or blood stained as a result of capillary distension and leakage.

Patients developing HACE may show nonspecific neurologic deficits (ranging from ataxia to coma) in addition to the signs of AMS (tachycardia, generalized edema).

HAPE patients can show tachypnea, orthopnea, tachycardia, low-grade fever, and cyanosis.

Lung auscultation may reveal rales, but the degree of crackles may not reflect the severity of pulmonary compromise.

While AMS is a generally benign, self-limiting condition that improves with acclimatization, HACE and HAPE are very dangerous clinical syndromes requiring prompt treatment as
pulmonary failure and death may occur within hr of symptom onset.

Symptoms of HACE or HAPE can resolve within a few days if immediate descent and treatment have occurred.

Previous episodes increase the risk for future recurrence.

Prevention is important:

Arterial blood gas (if available) may demonstrate hypoxia and may be useful to show improvement with therapy.

Other causes of altered mental status and cardiopulmonary disease should be ruled out with any means necessary (chemistry, CSF, CBC).

Chest radiograph may be normal or appear as mild congestive heart failure.

Descent from altitude is key.

Oxygen (2-4 L/min).

Dexamethasone (Decadron) 4-8 mg IV q 4 hr may be helpful in HACE, especially when descent is delayed.