(1)
Acute Mountain Sickness
Acute mountain sickness (AMS) is associated with ascent to
altitudes above 8000 ft, particularly with ascent rates greater than 1000 ft per
day. Common symptoms include
tachycardia, insomnia, headache, nausea, vomiting, anorexia, retinal
hemorrhages, dizziness, and fatigue. It
may be considered a mild form of cerebral edema. Symptoms are partially relieved by resting and are completely
relieved by return to lower altitudes.
Cheyne-Stokes (periodic) breathing occurs in most persons
with increasing altitude and is more
pronounced during sleep.
Several respiratory cycles of increasing depth and frequency are followed
by cycles of decreasing depth and frequency until short periods of apnea result.
After a few seconds, the cycle begins again.
At higher elevations bizarre and colorful dreams may occur during sleep.
While these symptoms may be disturbing and interfere with rest they occur
commonly and are not harbingers of more serious disorders.
Central nervous system (CNS) depressants or tranquilizers should not be
used.
The primary stimulus for ventilation at sea level is carbon
dioxide acting on the peripheral chemoreceptors (carotid) and the medullary
respiratory center. The higher
concentration of oxygen provides little drive to breathe.
With ascent to altitude, there is a progressive decrease in inspired and
arterial partial pressures of oxygen and in arterial oxygen saturation.
This hypoxemia results in hypoxic stimulation of the peripheral
chemoreceptors leading to increased minute ventilation which increases arterial
oxygen saturation and proportionately reduces the arterial partial pressure of
carbon dioxide and leads to alkalosis. These
changes reduce the CO2 dependent component of the respiratory drive,
blunting the increased ventilation resulting from hypoxemia.
Respiratory acclimatization to altitude occurs when the CSF
re-establishes its usual pH and the medullary respiratory center ventilatory
drive increases to levels associated with sea-level partial pressures of carbon
dioxide in the arterial blood. This allows the full hypoxic stimulus to ventilation to
manifest, further raising arterial oxygen saturation.
The resetting of central carbon dioxide and pH sensitivity can be
accelerated by the carbonic anhydrase activity of acetazolamide, reducing
altitude symptoms and sleep disturbance. Peripheral
chemoreceptor stimulation also results in redistribution of the cardiac output,
reducing gut blood flow and increasing vital organ flows.
Barometric pressure and the partial pressure of oxygen are
reduced as altitude increases. At a
given altitude barometric pressure varies with latitude (high latitudes, lower
pressures) and with season, weather, and temperature. As a result of the adiabatic lapse rate, so important in
weather, temperature is reduced about 6.5° C per thousand meters of elevation.
Cold and hypothermia are associated with higher elevations and should be
considered for their contribution to altitude illness, as should dehydration,
which results from increased respiratory and skin water losses if not adequately
noted and replaced.
Respiratory and circulatory acclimitizations take place
relatively quickly. Hormonal,
hematopoietic and metabolic adaptations may take longer to maximize. The more
rapid acclimatization responses protect against acute mountain sickness.
Longer term acclimatization improves aerobic exercise capability.
Excessive aerobic exercise at altitude may predispose to severe hypoxemia
through reduction of the pulmonary capillary transit time of hemoglobin below
that required for equilibration of hemoglobin saturation with alveolar partial
pressure of oxygen. Strenuous exercise increases cardiac output and pulmonary
blood flow velocity resulting in more severe hypoxemia, unlike sea level
exercise, where hemoglobin saturation occurs in the higher alveolar partial
pressures of oxygen. This may
partially explain why the incidence of AMS is indifferent to the level of
physical conditioning and is increased with more strenuous climbing,
(i.e., carrying packs, increased pace, etc).
Hypoxemia may be worsened by carbon monoxide poisoning in
poorly ventilated sleeping tents, sleep apnea, and high altitude pulmonary edema
(HAPE).
(2)
Prevention of AMS
Airlifting personnel to high altitudes increases the
incidence of AMS, as does rapid rates of ascent on foot. Continued
ascent in the face of symptoms of AMS results in increased incidence of high
altitude cerebral edema (HACE) and high altitude pulmonary edema (HAPE).
Graded ascent is the most certain prevention, particularly for sleeping
altitudes. Prevent over-exertion
and dehydration. Acetazolamide
prophylaxis speeds ventilatory acclimatization, increases minute ventilation and
hemoglobin saturation, counters the fluid retention of AMS, and decreases
cerebral spinal fluid (CSF) production. It
is particularly useful if rapid ascent cannot be avoided.
A single 500 mg sustained-action capsule daily, beginning 24 hours before
ascent and continued for 2-4 days, is probably the optimal dosage.
Acetazolamide is a sulfonamide derivative and may cause allergic
reactions in persons allergic to sulfa drugs.
Paresthesias of the extremities and of the lips are common.
Visual effects may result from its mild diuretic action by lowering the
production of aqueous humor. Dexamethasone, 4 mg, followed 6 hours later with
4mg is frequently effective in improving AMS, in conjunction with acetazolamide.
(3)
Treatment
(a)
Mild AMS:
Rest, stop ascent and strenuous activities, acclimatize at same altitude,
acetazolamide, 500 mg sustained release capsule daily, analgesics as needed, and
antiemetics as needed. Or: descent 1000 ft or more.
(b)
Moderate AMS:
Low-flow oxygen to relief or 90 percent saturation by pulse oximetry,
acetazolamide as above plus dexamethasone, 4 mg, any route, every 6 hours, and
hyperbaric therapy, or immediate descent to relief.
(4)
High Altitude Cerebral Edema (HACE)
HACE is a potentially fatal altitude illness, which may
develop in the presence of AMS or HAPE. HACE
presents with altered mental status, progressing to ataxia, coma, and death.
Less common symptoms include hallucinations and seizures and progression
to fatal outcome may take from 12 hours to 1-3 days.
Early focal signs suggest other neurologic problems since cerebral edema
results in a generalized encephalopathy; but severe edema may produce focal
deficits and particularly cranial nerve palsies.
HACE usually occurs in persons with AMS, thus respiratory alkalosis and
severe hypoxemia exist, and HAPE and/or cyanosis is common.
Retinal hemorrhages and fever may be present.
(5)
Treatment of HACE
Administration of increased partial pressure of oxygen is
critically important in survival, either by use of supplemental oxygen,
immediate return to lower elevation, or use of a (portable) pressure chamber,
such as the Gamow bag. Pending
descent, dexamethasone, 8 mg, IV, IM or orally followed by 4 mg QID should be
started. Oxygen at 4 liters per
minute (lpm) or as required for 90 percent saturation by pulse oximetry, should
be instituted. Rapid descent is
critical. Patients should be
hospitalized ASAP. MRI studies
point to a reversible vasogenic etiology, most prominent in the corpus callosum
with edema of white matter. If not
corrected, cytotoxic neurologic
damage follows with permanent neurologic deterioration and death.
Hospitalization is usually required for 1-2 weeks (return
to normal neurologic exam) and full recovery by MRI may require several weeks to
months.
(6)
High Altitude Pulmonary Edema
(HAPE)
Personnel at higher altitudes have increased
ventilation/perfusion inequalities and increased lung water.
With AMS there is increased pulmonary interstitial edema and elevated
pulmonary artery pressures. Hypoxemia
probably leads to increased pulmonary vascular endothelium permeability which
can progress to HAPE, the most common cause of death related to high altitude. The incidence of HAPE in troops may reach 15 percent,
depending upon rate of ascent, final altitude, severity of cold weather, level
of exertion, and use of depressant sleeping medications. HAPE is more common in young persons, particularly males.
It most commonly occurs on the second night of exposure, manifested by
fatigue, dyspnea on exertion, dry cough, and need for longer rest periods.
Some peripheral edema is common. A
close examination for HAPE and HACE is absolutely necessary.
As the condition worsens, tachypnea, dypsnea at rest, and audible
pulmonary rales may be present. Signs
of HACE may also appear and may obscure symptomatology of HAPE (more than half
show HACE on autopsy). Increases in
pulmonary artery pressure and pulmonary vascular resistance are present.
Increasing proteinaceous interstitial exudate, sometimes
resembling bronchopneumonia, develops as pulmonary edema worsens.
The exudate contans vasoactive eicosanoids and complement proteins.
Autopsy frequently shows thrombi, pulmonary hemorrhage, and infarcts. However, left-sided cardiac function is maintained.
The hypoxic ventilatory response is thought to play a role in
susceptibility to AMS, and the hypoxic pulmonary vascular resistance response
probably also plays a role in susceptibility to HAPE.
(7)
Treatment of HAPE
Treatment consists of oxygen and immediate descent of at
least 1000 meters, if possible. Bed
rest and oxygen are helpful; exercise should be minimized until recovered.
Hyperbaric treatment can substitute for low-flow oxygen.
Oxygen rapidly reduces pulmonary artery pressure, respiratory rate, and
other symptoms. In severe cases, if
immediate descent is not possible, request an airdrop of oxygen rather than wait
for rescue teams or helicopter evacuation.
Nifedipine, 30 mg slow release capsule, one every 12-24 hours or 10 mg
sublingually (remove the gel from the capsule) as needed is an effective adjunct
in reducing pulmonary vascular resistance and pressure.
Hospitalization is indicated until functionally recovered, but hypocapnic
alkalosis and some hypoxemia persist for days.
Oxygen saturation of 90 percent or higher is satisfactory for discharge,
usually in several days. Subsequent ascents should be more gradual, but are not
contraindicated. Prophylactic
acetazolamide is effective in preventing repeat HAPE upon subsequent altitude
exposure and both acetazolamide and nefedipine should be carried by the
individual on subsequent ascents.
(8)
Other Altitude Related Illnesses
Altitudes conducive to AMS are frequently also cold.
Thermal insulation is less effective at altitude because of the reduction
in density of the insulating air. The
metabolic generation of heat is also reduced because of hypoxia.
Symptoms of hypothermia may be confused with AMS and HACE.
Ultraviolet radiation exposure increases about 4 percent per 1,000 feet
of altitude and reflection from snow and ice increases this exposure further.
Snowblindness, sunburn, and hyperthermia during vigorous exercise may
occur. The later contributes to dehydration, which is common at
altitude, where greater respiratory and sensory losses occur.
Alcohol and CNS depressant medications should be avoided.
Breathing cold air may trigger asthma in some, but has not been reported
and is not a contraindication to ascent. High
altitude retinal hemorrhages usually resolve spontaneously in 7-14 days.
Current data suggests normal pregnancy is not a contraindication to
moderate ascents.
References
(a)
High Altitude Medicine Guide, (http://www.gorge.net/hamg/),
(excellent, physician-oriented.)
(b)
Wilderness Medicine, Management of Wilderness and Environmental
Emergencies, 3rd Ed., Paul
S. Auerbach, Ed., Mosby, St. Louis 1995, (excellent, every doc should own this)
(c)
Altitude Illness, Prevention
and Treatment,
http://www.mindspring.com/~treeline/altitu~1.htm,
(d)
Outdoor Action Guide to High Altitude: Acclimatization and Illness, http://www.princeton.edu/~oa/altitude.html
(e)
Hackett, PH et al, High-altitude cerebral edema evaluated with magnetic
resonance imaging, clinical correlation and pathophysiology, JAMA 1998;
280(22):1920-1925
(f)
Cox, GR, Danger in the Mountains: Pathophysiology and treatment of
altitude-related illnesses, Proc of 13th Ann Emer Med Symposium,
July, 1996, (excellent review by Navy Doc)
(g)
Murdoch, DR, Symptoms of infection and altitude illness among hikers in
the Mount Everest region of Nepal, Aviat Space Environ Med 1995; 66:148-51
(h)
Cox, GR, NAMI Flight Surgeon Program Instructor Guide, Environmental
Physiology 7: Altitude Related Illnesses
(i)
The Gamow Bag,
http://spot.colorado.edu/~gamow/research/bag.html
Written by CDR David B. Gillis, MC, USNR,
Naval Operational Medicine Institute, Pensacola, Florida, (1999)
|