Acute altitude sickness
The incidence of acute altitude sickness varies
with the altitude, the rate of ascent, and the individual’s susceptibility.
Several studies have been conducted to determine the incidence of acute
altitude sickness in groups of hikers and climbers. Results vary widely,
ranging from a frequency of less than 1% to 53% at altitudes of 3,000 to 5,500m
(9,840 – 18,045 ft). Forster, however, reported that 80% of those who ascended
to the top of Mauna Kea(4,205m, or 13,976ft) on the island of Hawaii
experienced some symptoms of acute altitude sickness. At elevations of 2,500 to
3,500m(8,202 – 11,483ft), altitudes commonly experienced by recreational skiers
and hikers, the incidence of acute altitude sickness is about 7% for men and
22% for women, but the reason for this sex difference is unclear.
Although the precise underlying cause of acute
altitude sickness is not fully understood, it appears that those people who
experience the greatest distress also have a low ventilatory response to
hypoxia. This inadequate ventilation allows PO2 to decrease further and carbon
dioxide to accumulate in the tissues, and these two factors may induce most of
the symptoms associated with altitude sickness.
Headache is the most common symptom associated
with ascent to high altitude. Headache is rarely experienced below 2,500m(under
8,000ft), but ascent to 3,600m(12,000ft) results in headache in the majority of
people. The headache at altitude, which many sufferers describe as continuous
and throbbing, is typically worse in the morning and after exercise. Alcohol
consumption worsens the symptoms. The precise mechanism is unknown, but hypoxia causes dilation of the cerebral
blood vessels, so stretching of pain receptors in these structures is a likely
cause. Related problems associated with central nervous systemhypoxia include
impaired visual acuity and night vision. At extreme altitudes, example Mount Everest , verbal expression, reasoning, and mood may
all be affected. There is no evidence of permanent mental impairment associated
with cerebral hypoxia.
Another side effect of acute altitude sickness
is an inability to sleep despite marked fatique. Studies have shown that the
inability to achieve satisfying sleep at altitude is associated with an
interruption in the sleep stages. In addition, some people suffer a pattern of
interrupted breathing, called Cheyne-Stokes
breathing, which prevents them from falling to sleep and remaining
asleep. Cheyne-Stokes breathing is characterized by alternate rapid
breathing and slow, shallow breathing, usually including intermittent periods
in which breathing completely stops. The incidence of this irregular
breathing pattern increases with altitude, occurring 24% of the time at
2,440m(8,005ft), 40% of the time at 4,270m(14,009ft), and 100% of the time at
altitudes above 6,300m(20,669ft).
How can athletes avoid acute altitude sickness?
No evidence indicates that superior physical conditioning prevents the symptoms
of altitude sickness. Even athletes who are highly endurance trained before
altitude exposure seem to have little protection against the effects of
hypoxia, and some data suggest that young, fit individuals may be more prone to
experiencing symptoms. Currently, it is difficult to determine which athletes
may be susceptible to these symptoms, unless suggested by a prior history of
acute altitude sickness.
People can usually prevent acute altitude
sickness by gradually ascending to altitude, spending periods of a few days at
several lower elevations. A gradual ascent of no more than 300m(984ft) per day
at elevations above 3,000m(9,840ft) has been suggested to minimize the risks of
altitude sickness. Of the drugs that have been used to reduce the symptoms of
those who develop acute altitude sickness, acetazolamide started the day before
ascent is the only established preventive measure. Acetazolamide is sometimes
combined with steroids such as dexamethazone. Both drugs must be used with
medical supervision. Of course, the definitive treatment for severe acute
mountain sickness is a retreat to lower altitude, but high-flow oxygen and the
use of hyperbaric rescue bags are also effective in severe cases.
High-altitude pulmonary edema
Unlike acute mountain sickness, high-altitude pulmonary edema(HAPE),
which is the accumulation of fluids in the lungs, is life threating. The cause
of HAPE is unknown, but may be related to the pulmonary vasoconstriction
resulting from hypoxia, causing blood clots to form in the lungs. Remaining
tissue becomes overperfused, and fluid and protein leak out of the capillaries.
This seems to occur most frequently in unacclimatized people who rapidly ascend
to altitudes above 2,500m(8,202ft). The disorder occurs in otherwise healthy
people and has been reported more often in children and young adults. The fluid
accumulation interferes with air movement into and out of the lungs, leading to
shortness of breath, a persistent cough, chest tightness, and excessive
fatique. Disruption of normal breathing impairs blood oxygenation, causing
cyanosis(a bluish tint) of the lips and fingernails, mental confusion, and loss
of consciuousness. High-altitude pulmonary edema is treated via
administration of supplemental oxygen and movement of the victim to a lower
altitude.
High-altitude cerebral edema
Rare cases of high-altitude cerebral edema(HACE), which is fluid accumulation in
the cranial cavity, have been reported. The condition is often a subsequent
complication of HAPE. This neurological condition is characterized by mental
confusion, lethargy, and ataxia(difficulty walking), progressing to
unconsciousness and death. Most cases have been reported at altitudes
greater than 4,300m(14,108ft). The cause of HACE is unknown, but the treatment
is administration of supplemental oxygen, a hyperbaric bag, and prompt descent
to a lower altitude. If descent is delayed, permanent impairment may ensue.
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