|
 Altitude Related Disease States*
Altitude sickness
Atmospheric pressure decreases as altitude increases, while the percentage of
O2 in air remains constant; thus, the partial pressure of O2
decreases with altitude and at 18,000 ft (5500 m) is about 1/2 that at sea
level. About 20% of persons ascending above 8000 ft (2500 m) in < 1 day
develop some form of altitude sickness. Persons who have had one attack are
slightly more susceptible to another if conditions are similar, but the effects
of high altitude vary greatly among and within individuals. Young children are
most susceptible, and incidence decreases linearly with increasing age. Abrupt
exposure to high altitude (eg, depressurization of aircraft, balloon ascent)
causes acute severe hypoxia and loss of consciousness rather than altitude
sickness.
Most persons acclimatize to altitudes of up to 10,000 ft (3000 m) in a few
days. The higher the altitude, the longer full acclimatization takes.
Acclimatization is an integrated series of responses that gradually restore
tissue oxygenation toward normal in persons exposed to altitude. Features of
acclimatization include sustained hyperventilation with persistent partially
compensated alkalosis, an initial increase in cardiac output (which is lower
than normal maximum cardiac output), increased RBC mass, and increased tolerance
for anaerobic work. After many generations at altitude, some ethnic groups have
acclimatized in slightly different ways.
Hypoxia stimulates breathing, increasing tissue oxygenation but also causing
respiratory alkalosis, which contributes to symptoms until loss of HCO3
in urine partially compensates. The basic pathophysiology of altitude sickness
is disturbance of water and electrolyte balance. Capillary permeability is
increased, allowing fluid to accumulate in various locations; the cause is
thought to be vascular endothelial damage. In susceptible persons, increased ADH
secretion results in tissue fluid retention, and plasma volume is decreased,
simulating an increase in Hct. A low hypoxic ventilatory response is not
associated with altitude sickness. The roles of atrial natriuretic peptide,
aldosterone, renin, and angiotensin are unclear.
Hypoxia increases pulmonary vascular resistance and pulmonary artery
pressure, but systemic resistance and arterial pressure usually change little.
Cerebral blood flow is decreased by hypocapnia, is increased by hypoxia, and
consequently varies with the balance between arterial CO2 and O2.
The role of this variation in symptomatology is unclear.
Peripheral or facial edema may be due to high altitude or, as at sea level,
to strenuous exertion. Thrombophlebitis may occur at extremely high altitude,
especially if a person is dehydrated and inactive. Dimmed vision, hemianopsia,
scotomata, and even transient blindness have been reported. Persons who have had
radial keratotomy may have significant visual disturbances at altitudes >
16,000 ft (> 5000 m) or even as low as 10,000 ft (3000 m). These alarming
symptoms disappear rapidly after descent. Retinal
hemorrhages may develop at altitudes as low as 9000 ft (2700 m); they are common
above 16,000 ft. They are usually asymptomatic unless in the macular region and
resolve rapidly without sequelae. Small hemorrhages may also occur under the
nails, in the kidneys, and in the brain.
The various clinical forms of altitude sickness are not separate entities but
parts of a spectrum in which one or more may be present in different degrees.
CNS dysfunction is considered a factor in several forms. No test can reliably
predict development of altitude sickness.
Acute mountain sickness (AMS):
This form is the most common and may develop at altitudes as low as 6500 ft
(2000 m). It is characterized by headache, fatigue, nausea, dyspnea, and sleep
disturbance. Exertion aggravates the symptoms. AMS usually subsides in 24 to 48
h but occasionally evolves into high-altitude pulmonary edema, high-altitude
cerebral edema, or both. Laboratory studies are nonspecific and are not helpful
in diagnosis.
High-altitude pulmonary
edema (HAPE):
This form is less common but more serious, usually developing 24 to 96 h
after rapid ascent above 8000 ft (2500 m). When most persons ascend above 8000
ft, fluid accumulates in lung interstitial tissues and is usually drained away
by the lymphatics. When fluid accumulates more rapidly than it is drained, frank
alveolar edema develops. Persons who have had one episode of HAPE are likely to
have another and should be so warned. Respiratory infections, even minor ones,
appear to increase the risk of HAPE. Recently identified persons who have
repeated episodes of HAPE are described as HAPE-S (susceptible); the reason for
their susceptibility is unknown. Men are 5 times more likely than women to
develop HAPE, but AMS and high-altitude cerebral edema affect men and women
equally. Children appear to be at a slightly greater risk, as are longtime
high-altitude residents when they return after a brief stay at low altitude. The
absence of one pulmonary artery is a rare congenital anomaly that greatly
increases the risk of HAPE, even at altitudes as low as 5000 ft (1500 m).
Persons who develop HAPE repeatedly or at an unusually low altitude should be
evaluated for pulmonary artery pathology or old pulmonary embolism.
HAPE is a high-pressure edema with increased microvascular permeability.
Excessive vasoconstriction in some areas causes overperfusion in others, and the
resulting ventilation/perfusion mismatch is considered the precipitating cause.
There is new evidence that a decrease in alveolar nitric oxide, perhaps due to
absence of nitric oxide synthase, is an important factor in susceptibility to
HAPE.
HAPE is characterized by increasing dyspnea; irritative cough that produces
frothy, often bloody sputum; weakness; ataxia; and, later, coma. Cyanosis,
tachycardia, and low-grade fever are common and, with fine or coarse pulmonary
rales (often audible without a stethoscope), may lead to a misdiagnosis of
pneumonia. Chest x-ray shows Kerley lines and patchy edema unlike that in heart
failure. Atrial pressure is normal, but pulmonary artery pressure is greater
than that in healthy persons experiencing hypoxia. HAPE may worsen rapidly; coma
and death may occur within hours.
High-altitude cerebral
edema (HACE):
Cerebral edema is believed to be present to a mild degree in all forms of
altitude sickness. Diffuse or patchy edema of the brain, seen on CT scans, is
thought to contribute to HACE and to AMS. Severe edema is manifested as ataxia,
headache, mental confusion, and hallucinations. Stiff neck does not occur, and
papilledema is not necessary for diagnosis. CSF pressure may be elevated, but
the fluid is normal. Gait ataxia is a reliable early warning sign. Coma and
death may develop within a few hours of the first symptoms. HACE must be
differentiated from other causes of coma (eg, infection, vascular accident,
ketoacidosis) by the history, absence of significant fever or paralysis, and
normal blood and CSF studies.
Altitude sickness is best prevented by slow ascent, but the safe rate of
ascent varies among individuals. Most can ascend to 5000 ft (1500 m) in 1 day
without symptoms, but many are affected by ascending to 8000 ft (2500 m). Above
this level, a rate of 1500 ft (460 m)/day is advisable. Climbers should learn
how fast they can ascend without developing symptoms; a climbing party should be
paced for its slowest member. Although physical fitness enables greater exertion
with less O2 consumption, it does not protect against any form of
altitude sickness. Strenuous effort should be avoided for 24 to 36 h after the
ascent is completed, but bed rest is less beneficial than mild exercise.
Drinking much more water than usual is important, because overbreathing dry
air at altitude greatly increases water loss, and dehydration with some degree
of hypovolemia aggravates symptoms. Additional salt should be avoided. Alcohol
seems to worsen AMS and diminishes nocturnal ventilation, thus accentuating
sleep disturbance. Eating frequent small meals that are high in easily digested
carbohydrates improves altitude tolerance and is recommended for the first few
days.
Acetazolamide 125 mg at bedtime (for most persons) or 125 mg q 8 h is an
effective prophylactic for AMS. Sustained-release capsules (500 mg once daily)
are also available. Starting acetazolamide before the ascent has no advantage.
Acetazolamide inhibits carbonic anhydrase, increasing ventilation and allowing
better O2 transport with less alkalosis; it eliminates periodic
breathing (almost universal during sleep at high altitude), thus preventing
sharp falls in blood O2. Acetazolamide should not be given to
patients allergic to sulfa
drugs. Low-flow O2 during sleep has the
same effect but is inconvenient. Analogs of acetazolamide offer no advantage.
Antacids are useless for prevention. Dexamethasone, which minimizes symptoms of
AMS, is not recommended for prevention.
Retinal hemorrhages require no treatment, generally
resolving while the climber remains at high altitude.
Acute Mountain Sickness seldom requires treatment other than
fluids, analgesics, a light diet, mild activity, and (rarely) descent. Dexamethasone4 mg po q 6 h is effective;
Acetazolamide250 mg po q 6 h may
alleviate symptoms. Ibuprofen, which decreases platelet aggregation, is more
effective than aspirin for altitude headache but may also cause easy bruising.
When HAPE is suspected, bed rest and O2 may be
tried, but if the condition worsens, immediate descent is essential. If
descent is not possible, the person can be placed in a large hyperbaric bag in
which the pressure can be increased, simulating descent. This measure helps buy
time in an emergency but is not a substitute for descent. Nifedipine 20 mg
sublingually followed by a 30-mg slow-release tablet lowers pulmonary artery
hypertension and is beneficial. Strong diuretics (eg,
furosemide) are
contraindicated. Although morphine is effective, the resulting respiratory
depression may outweigh the drug's value. Because the heart is normal in HAPE,
digitalis is of no value; however, in the subacute form of infantile and adult
mountain sickness, the heart fails, and
digitalis and descent are necessary to
save life. Once the patient is hospitalized, other causes of pulmonary disease
are ruled out, and the patient is treated with adequate oxygenation (sometimes
by intubation and positive end-expiratory pressure), bed rest, judicious
diuresis, postural drainage, and, if superimposed infection is suspected,
antibiotics. When promptly treated, patients usually recover from HAPE within 24
to 48 h.
Severe HACE requires immediate descent. Supplementary oxygen or
pressurization in a hyperbaric bag buys time but does not cure. Dexamethasone 8
mg IV q 4 h helps but not dramatically. Its value in an altitude emergency is
dubious.
Decompression Sickness
Aviation Decompression Sickness (DCS) may occur at any time within an
unpressurized flight, an unexpected aircraft depressurization, altitude chamber
operations or high altitude high opening parachute operations. DCS does not
generally occur with exposure to altitudes below 18,000 feet. Aviators are
generally protected from DCS by maintaining cabin altitudes at lower levels by
cabin pressurization, by use of pressure suits, by pre-oxygenation to reduce
total body nitrogen or a combination of these measures. Currently, the largest
numbers of DCS cases seen in Naval Aviation operations involve low pressure
chamber activities at the rate of about 1 case per 1000 chamber exposures.
Effects of bubble formation
There are two pathophysiologic effects attributed to the formation
of nitrogen bubbles with altitude exposure (or upon decompression from diving):
-
A direct mechanical effect of the bubble in
distortion of tissue or in vascular obstruction, causing pain, ischemia,
infarction or dysfunction.
-
Tissue-bubble interface activity resulting in
denaturation of proteins, platelet aggregation and other biochemical
mechanisms causing tissue damage and release of pain mediating substances.
Because these bubbles may form at different locations, there may be
multifocal symptoms that may not necessarily following dermatomal or anatomic
distributions. Once bubbles are formed, they expand as dissolved gases continue
to come out of solution. Carbon dioxide is highly diffusible and contributes to
bubble enlargement, especially if formed in excess by vigorous exercise. For
this reason, DCS patients should be kept at rest.
Clinical syndromes of DCS
Type I DCS
Limb
pain (musculoskeletal symptoms) :
The most common presenting symptom, accounting for 60-70% of altitude
related cases and 80-90% of diving cases. Pain usually begins gradually and is
poorly localized, but increases in intensity and localizes with time as a
throbbing ache. Sometimes the pain is sharp and clearly localized. Pain may be
mild or intermittent at first but may increase steadily and can become very
severe. Often poorly localized, the pain is characteristically hard to describe,
but "deep" and "like something boring into the bone" are
expressions sometimes used. Local inflammation and tenderness are often absent,
and the pain may not be affected by motion. Guarding may be seen. If the painful
area is accessible, inflation of a blood pressure cuff over the site may relieve
the pain and help distinguish it from pain of ischemia or nerve entrapment which
would be made worse by such pressure. Sharp, shooting or encircling pain,
migratory pain and tingling or burning trunk pains arise from CNS involvement
and should be considered Type II DCS and treated accordingly.
Cutaneous bends:
The skin is often affected during and after the
decompression event. There are two distinct manifestations; The most common
symptom is a transient, multifocal itching, often associated with a
scarlatiniform rash, and is not an indication of development of serious sequelae.
Itching or crawling sensations usually occur in hyperbaric chamber dives and do
not require recompression as a rule. Cutis Marmorata results from venous
obstruction and vasospasm and presents as confluent rings of pallor, surrounded
by areas of cyanosis which blanche to the touch. This may be the harbinger of
more serious forms of DCS and should be treated by recompression.
Lymphatic bends:
Rare. Recompression usually provides prompt relief
of pain, but swelling of lymphatic tissue may persist after treatment.
Type II DCS
The most severe form of DCS, and may present as neurological,
cardiorespiratory or inner ear symptoms, pain or shock. There may be concurrent
Type I symptoms in 30-40% of cases. About 10-15 of all altitude DCS cases will
be type II.
Early Type II DCS symptoms may seem inconsequential. Fatigue is a very common
and early symptom, progressing to weakness, dyscoordination and other
difficulties. Many symptoms of Type II DCS are the same as those of arterial gas
embolism (AGE), although AGE presents very early, usually within 10 minutes
after exposure. Treatment of AGE is also appropriate for DCS.
Neurological symptoms may
accompany pain or occur independently. They occur in > 50% of patients with
decompression sickness. Neurologic symptoms and signs vary from mild paresthesia
to major cerebral problems. Seemingly minor early manifestations, such as
weakness or numbness in the extremities, may have serious consequences, such as
paraplegia, which may be irreversible if treatment is delayed or inappropriate.
Spinal cord DCS may present with numbness, weakness and paralysis or urinary
dysfunction, and occurs in about 10% of Type II altitude DCS cases. Cerebral DCS
is the most common of Type II DCS. Fatigue is a very common symptom.
There may be confusion, odd behavior and personality changes. Headache, tremor,
hemiplegia, hemisensory losses and scotomata may also occur. These signs and
symptoms may range from mild and seemingly inconsequential to fulminant and life
threatening. Vestibular involvement may produce severe vertigo by imitating a
round or oval window rupture with, tinnitus and hearing loss. The occurrence of any
neurological symptom after a dive or flight should be considered a symptom of
Type II DCS or AGE.
The “Chokes”
is the respiratory form of decompression sickness. It results from
massive bubble embolization of the pulmonary vascular tree and account for 5-10%
of altitude DCS. In some patients, the condition resolves spontaneously, but
without prompt recompression, it can rapidly progress to circulatory collapse
and death. Substernal discomfort and coughing during deep inspiration or during
inhalation of tobacco smoke are often early manifestations. In animal studies,
the chokes are strongly associated with exposure to altitude soon after diving.
The chokes and other serious manifestations developing at altitude are not
necessarily cured by return to ground level and may require prompt chamber
recompression. If not treated promptly, the result may be circulatory collapse
and death.
Significant bubble formation can usually be avoided by restricting the uptake
of gas--eg, by limiting the depth and duration of dives to a range that does not
require decompression stops during ascent. Decompression sickness seldom
develops when dives are kept within appropriate no-stop limits or when
decompression tables are followed. Repeated dives may cause decompression
sickness. Because excess inert gas remains in the body after every dive, the
amount of excess gas increases with each dive. If the interval between dives is
< 12 h, repetitive dive tables must be used.
Flight after diving
OPNAVINST 3710.7
prohibits flight or low pressure chamber exposure within 24 hours of a SCUBA or
compressed air dive or high pressure chamber run. This may be reduced to 12
hours for urgent operational requirements provided there are no symptoms
following the dive and the subject is examined and cleared by a flight surgeon.
Diving at altitude
This refers to
dives at elevations, such as in mountain lakes and may be a factor in increasing
risk for DCS. U.S. Navy dives above 2300 ft. MSL require CNO approval.
Triage and referral
of altitude DCS cases
Type I DCS
If symptoms
appear at altitude and resolve on descent, use 100% 02 for two hrs
and observe for recurrence. If none, light duty only and ground for 1 week. Warn
the patient to return promptly if symptoms recur for hyperbaric therapy.
If symptoms develop at altitude and persist, or
develop after flight, place the patient on 100% 02 while arranging
evacuation or recompression. If evacuation is delayed and symptoms resolve,
leave on oxygen for 24 hrs. Then, place the patient on limited duty for 1 week,
and no physical training for 72 hrs. Recurrence must be treated by hyperbaric
therapy.
Current U. S. Navy diving medicine protocols are to
treat all patients referred for altitude DCS regardless of whether or not
symptoms have resolved.
Type II DCS
All must be
recompressed urgently or evacuated promptly for treatment.
Aeromedical evacuation of
DCS cases
-
Contact your local Hyperbaric Center facility
prior to transport. Any known or suspected cases of DCS should be discussed
with a trained hyperbarics physician, They can provide valuable information
and advice regarding treatment and patient transportation options
-
Continue to provide 100% oxygen delivery via a
tight fitting mask.
-
If air transportation is required it must be at
or near sea level (14.7psi) pressure, the use of a pressurized aircraft is
ideal, but if a helicopter or other unpressurized aircraft is used, a
maximum flying altitude of 1,000 feet (14.17psi) should never be
exceeded.
-
Oxygen should be administered by a tight fitting
mask and used continuously during the transport to the Hyperbaric facility.
-
Place patient in supine position (unless
unconscious) , neutral head position and uncrossed extremities for
transport.
-
Obtain a complete history and perform a complete
physical exam Including a detailed neurologic exam, do not ignore seemingly
minor symptoms, they can quickly become major. Also, Do not allow patient to
sleep in order to monitor mental status
-
Ensure adequate IV hydration with either N.S.
or
Ringers Lactate to prevent hemoconcentration which can occur with
intravascular volume loss. Urine output should be at least 60cc/hr so
consider Foley catheterization.
-
Inflatable cuffs should be filled with WATER
rather than air.
-
Dexamethasone is controversial, but may be given
10 mg. IV if indicated.
References:
24 Hour Points of Contact:
Naval
Medical Research Institute (NMRI) Bethesda, MD
DSN: 295-1839/5875 Com: (306) 295-1839/5875
This section was contributed by CDR Jay S. Dudley, MC, USN (FS).
*Source:
Operational Medicine 2001, Health
Care in Military Settings, NAVMED P-5139, May 1, 2001, Bureau
of Medicine and Surgery, Department of the Navy, 2300 E Street NW, Washington,
D.C., 20372-5300 |
