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
Acute mountain sickness (AMS).
High altitude cerebral
High altitude pulmonary
Other high altitude
High altitude periodic
breathing of sleep.
High altitude retinal
Chronic 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
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.
ACUTE MOUNTAIN SICKNESS
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
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
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).
HIGH ALTITUDE CEREBRAL EDEMA (HACE)
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.
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.
HIGH ALTITUDE PULMONARY EDEMA (HAPE)
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
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
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
Treatment of HAPE
Descent, descent, descent!
Keep warm. Cold weather increases
pulmonary artery pressures and makes HAPE worse.
Nifedipine 10 mg swallow or chew
followed by 20 mg every six to 12 hours.
Hyperbaric treatment with Gamow
HIGH ALTITUDE PERIODIC BREATHING OF SLEEP
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.
HIGH ALTITUDE RETINAL HEMORRHAGE (HARH)
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.
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