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  HIGH ALTITUDE ILLNESS By Larry Rigsby M.D. (also an Everest climber)

High altitude illness describes several syndromes that can occur in unacclimatized individuals shortly after ascent to high altitude.  These illnesses usually occur at altitudes of greater than 2,500 meters (8,200 feet) but can occur as low as 2,000 meters (6,560 feet).  There are three well-recognized high altitude illnesses. 

  • Acute mountain sickness (AMS).
  • High altitude cerebral edema (HACE).
  • High altitude pulmonary edema (HAPE).

Other high altitude conditions include

  • High altitude periodic breathing of sleep.
  • High altitude retinal hemorrhage (HARH).
  • Chronic mountain sickness.
  • Subacute mountain sickness.

High altitude affects the human body due to oxygen deprivation.  Oxygen is critical to normal cellular function.  The main physiologic effects of hypoxia (low oxygen) alter physical performance, mental performance and sleep.  

As one gains altitude, there is a drop in the barometric pressure with a corresponding drop in the oxygen pressure.  At an altitude of 3,000 meters (9,840 feet), commonly an altitude encountered at ski resorts, the barometric pressure and the inspired oxygen pressure are 70% that noted at sea level.  At 5,000 meters (16,400 feet) the inspired oxygen pressure is 50% that at sea level.  On the summit of Mt. Everest 8,848 meters (29,021 feet) the inspired oxygen is 29% that at sea level.

Acclimatization is an adaptive process that allows human beings to tolerate high altitude.  It is a great example of how the human body can adapt and respond to a hostile environment.  The process of acclimatization begins immediately but requires several days to be notable and requires weeks to be near complete.   Climbers at extreme altitude require over a month for the acclimatization process to be near complete.  Hyperventilation is the most important feature in the acclimatization process.  There is an increase in the depth and the rate of breathing; an extreme example is on the summit of Mt. Everest where the pressure of inspired oxygen is 29% that of sea level.  The ventilation is increased five-fold.  Another adaptive process is polycythemia or an increase in the red blood cell mass.  This occurs over the course of weeks.  Other factors include acid-base changes with the loss of bicarbonate, or base from the kidneys.  The ability to acclimatize may improve with successive exposures to high altitude over years.  Himalayan climbers note improvement in symptoms and physical performers with each visit.  A misconception of the acclimatization process is that the body returns to its sea level condition or that the hypoxia of high altitude can be nullified by acclimatization.  This is not the case.   For example, on arrival at 14,000 feet maximum physical performance is 80% that at sea level.  At two weeks of acclimatization it is just slightly above 85%.

Persons over 50 years of age seem to be less susceptible to altitude illness.  Women are equally prone to AMS but seem to be less susceptible to HAPE.  Physical fitness is not protective against high altitude illness, although obesity may be a risk factor.  Medical conditions such as mild COPD, hypertension, coronary artery disease and diabetes do not seem to affect the susceptibility of high altitude illness.  Genetics seem to play an important role. 


AMS is the most common altitude related illness.  It can occur in 40-50% of individuals who ascend to 4,200 meters (approximately 14,000 feet).  It has been reported to occur at an altitude as low as 2,000 meters.

AMS is defined as the presence of a headache in an unacclimatized individual who ascends to 2,500 meters or greater plus the presence of one or more of the following symptoms:  Anorexia, nausea, vomiting, insomnia, dizziness, lassitude or fatigue.  The symptoms generally develop over 2-3 hours and generally resolve in 2-3 days. 

The cause of AMS is unknown.  Brain edema and increased cerebrospinal fluid pressure has been postulated as a cause however recent MRI studies did not confirm this.  It was also found that cerebrospinal fluid pressures were unchanged. 

Oxygen free radicals have also been postulated as a cause and there is some data to suggest that antioxidants may help. 

Other common conditions that can be confused with AMS include migraine headache and dehydration.  A good diagnostic trial is to have the individual drink one liter of fluids and use a mild pain reliever such as aspirin, ibuprofen or acetaminophen (paracetamol).  If symptoms resolve rapidly it is probably not AMS.

The best prevention of AMS is slow ascent.  A popular rule of thumb among trekkers is that above 3,000 meters (9,840 feet) each day’s ascent should not average more than 300 meters.  This is conservative and most climbers adhere to 400 to 600 meters per day.  For every increase of 600 to 1,200 meters an extra rest day should be added.  Even a brief recent exposure to high altitude affords some protection against AMS.  If rapid ascent is inevitable acetazolamide or Diamox is helpful.  The dose is 250 mg twice daily and some recommend doses as low at 125 mg twice daily.  Diamox should not be given to persons with a history of sulfa or sulfphonamide allergy.  Common side effects are increased urination, paresthesia or tingling of the fingers and toes and an unpleasant taste to carbonated beverages.  Diamox should be started 24 hours before ascent and may be discontinued 2-3 days after arrival at maximum altitude.  In patients allergic to Diamox dexamethasone in doses of 2 mg every six to eight hours can be used.  Individuals using dexamethasone should be cautioned against further ascent as severe rebound of AMS can occur on discontinuation of this drug. 

Treatment of AMS

·        Descent is curative but usually not required.

·        Supplemental oxygen is very helpful but again is not usually required.

·        Rest and avoidance of further ascent until symptoms have resolved.

·        Acetazolamide or Diamox 250 mg three times a day.

·        Decadron 4 mg four times a day could be used in place of Diamox or could be used in conjunction with Diamox in severe AMS.

·        Remember, if Decadron is used wait at least 18 hours after the last Decadron dose to continue ascent.

·        Pain relievers such as acetaminophen, ibuprofen or aspirin.

·        Ambien may be useful for treating insomnia.  Ambien does not suppress respiration at high altitude (however this has not been studied in clinical trials). 


HACE is considered to be the end stage of AMS.  HACE is defined as the onset of ataxia (altered balance or coordination), altered consciousness or both in someone with AMS or HAPE.  The incidence is difficult to estimate but may be as high as 1 to 2% of people ascending to greater than 4,800 meters (15,700 feet).

The classis symptoms of HACE are the usual symptoms of AMS plus confusion, hallucination, diminished levels of consciousness progressing to coma.  Seizures are uncommon.  Incoordination and unsteady gait occur.  Ask the individual to walk a straight line.

Treatment of HACE

·        This is a medical emergency.

·        Immediate descent!!!

·        Oxygen.

·        Decadron 8 mg initially followed by 4 mg every six hours.

·        If immediate descent is not possible a hyperbaric or Gamow bag is very helpful.  Treatment is usually given in hour segments within the bag with brief periods of observation. 


HAPE is potentially fatal and accounts for most of the deaths from high altitude illness. 

HAPE is similar to AMS in that the incidence is related to the rate of ascent.  As many as 10% who ascend rapidly to 4,500 meters get HAPE whereas 1 to 2% with gradual ascent.  50% of those with HAPE also have AMS and 14% with HAPE also have HACE or high altitude cerebral edema.  HAPE can also be seen in residents of high altitude who travel to low altitude and then return to altitude.  This is termed re-ascent high altitude pulmonary edema.

HAPE typically occurs on the second night at a new altitude and rarely occurs more than four days at a given altitude.   

The predominant symptom is dyspnea or shortness of breath with reduced exercise tolerance or performance.  There is often a dry cough with subsequently progresses to a cough that produces frothy bloody sputum.  The heart rate and respiratory rate are increased and mild fever is common.  On exam of the lungs crackles can be detected by auscultation with a stethoscope.  If a pulse oximeter or oxygen sat monitor is available this will reveal a significantly lower oxygen saturation at a given altitude.  In early HAPE the low oxygen saturation may only be detected during exertion.

As with AMS, the best prevention of HAPE is slow and graded ascent.  Climbers or trekkers with a previous history of HAPE may wish to consider prophylaxis with nifedipine or Procardia Slow Release 20 mg every eight hours.  Salmeterol or Serevent inhalation was also shown to be effective in decreasing the incidence of HAPE in susceptible mountaineers.

Treatment of HAPE

·        Descent, descent, descent!

·        Keep warm.  Cold weather increases pulmonary artery pressures and makes HAPE worse.

·        Oxygen.

·        Nifedipine 10 mg swallow or chew followed by 20 mg every six to 12 hours.

·        Hyperbaric treatment with Gamow bag. 


This is a common phenomenon.  It is also called Cheyne-Stokes respiration.  This typically occurs during non-REM sleep.  This form of breathing consists of a period of hyperventilation followed by a period of apnea or not breathing.  This form of sleeping can awaken subjects from sleep they can feel like they are gasping for their breath.  It is felt that this periodic breathing of sleep may significantly alter sleep patterns and the quality of sleep at night at altitude. 

Acetazolamide or Diamox in a dose of 125-250 mg at night can help this. 


This is not an uncommon finding above 4,200 to 4,500 meters (14,00 to 15,000 feet).  It is usually asymptomatic.  These usually do not distort the vision significantly but occasionally can cause some minor blurring of vision.  These tend to resolve on their own. 


1.  West, J.B., The Physiologic Basis of High Altitude Disease.

Annals of Internal Medicine, 2004, Vol. 141, pages 789-800.

2.  Hultgren, Herb, High Altitude Medicine Copyright© 1997.

Hultgren Publications.

3.  Hackett, P.H. and Roach, A.C., High Altitude Illness. N Eng

J Med,  2001, Vol. 345, pages 107-114.

4.  Bärtsch, P. et al, Acute Mountain Sickness: Controversies and

Advances. High Altitude Medicine and Biology, Vol. 5, pages 110-124.

5.  Schoene, R.B., Unraveling the Mechanism of High Altitude

Pulmonary Edema.  High Altitude Medicine and Biology, Vol. 5, pages 125-135.

6.  Hackett, P.H., Roach, R.C., High Altitude Cerebral Edema.

        High Altitude Medicine and Biology, Vol. 5, pages 136-146.



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