High altitude disease can be divided into acute mountain sickness
(AMS), high altitude pulmonary edema (HAPE) and high altitude
cerebral edema (HACE). AMS is essentially a benign and limited
disease, while HAPE and HACE can be potentially lethal. The most
common form of altitude disease is acute mountain sickness. ACUTE MOUNTAIN SICKNESS
The incidence of AMS is about 25% at 9,000 ft and 67% at 14,000
SYMPTOMS
Symptoms usually consist of headache, nausea, vomiting, anorexia,
weakness, fatigue, light headedness, dizziness, difficulty sleeping,
chilliness, irritability, difficulty in concentration, tinnitus, visual and
auditory disturbances, dyspnea, palpitations, tachycardia, weight
loss and Cheyne Stokes breathing. HEADACHES. Headache is usually the first manifestation and may
be mild to severe, bitemporal, throbbing, worse at night and on
awakening. These symptoms may occur at altitudes as low as 6500
feet (2000 m). The more common symptoms are usually attributable
to cerebral edema and occur within the first 24 hours of rapid ascent,
and tend to improve over 3-7 days in the majority of patients. EDEMA. Some patients may develop peripheral and visceral
edema, weight gain, proteinuria and oliguria. As individuals
ascend to high altitude, there is a shift of fluid from the intravascular
space into the interstitial or intracellular space, and a tendency toward
TREATMENT MILD SYMPTOMS. Treatment of AMS is descent. However, mild
symptoms can be treated with rest, acetaminophen, ibuprofen, and
acetazolamide (250 mg BID). MODERATE SYMPTOMS. Moderate symptoms can be treated with
rest, dexamethasone (4 mg q6h for 1-3 days, tapered over 5 days),
and acetazolamide 250-500 mg BID-TID.
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SEVERE SYMPTOMS. Severe symptoms must be treated with
oxygen, dexamethasone (8 mg followed by 4 mg q6h PO or IM), and
acetazolamide up to 1.5 grams daily. Acetazolamide functions by
increasing ventilation, preventing periodic breathing, improving
oxygenation, increasing diuresis, and creating a metabolic acidosis
by urinary loss of bicarbonate, potassium and sodium. PREVENTION. Prevention of AMS may be effected by common
sense measures such as avoiding alcohol, sedatives, excessive
exertion on the first day, and slow ascent. Individuals should eat
frequent small meals that are high in easily digested carbohydrates
such as jams, fruits, and starches. Extra salt should be avoided, but
drinking more water than usual is important in preventing water
loss created by over breathing the dry air at high altitudes. If
ascending to 6-7000 feet (2,000 m), take 2-3 days to ascend to this
level. Above 10,000 feet (3,000 m) ascend 1,000 feet per day. ACETAZOLAMIDE. Acetazolamide may be started the day before the
ascent at 250-500 mg and taken every h.s. for 3-5 days. NIFEDIPINE. Nifedipine may be started 2 days before the ascent at
20 mg daily, followed by 20 mg q8h starting on the day of ascent and
continued for 3 days. DEXAMETHASONE. Dexamethasone may also be started on the day
of ascent at 2-4 mg q6h and continued for 3 days, and then tapered
over 5 days. PENTOXIFYLLINE. Pentoxifylline has been used in some countries to
improve cerebral function, and prochlorperazine at 10 mg PO q6h has
also been used as a preventive measure in some countries. These
latter two drugs have not been widely used in the USA. CHRONIC MOUNTAIN SICKNESS
This illness is also known as Monge's disease. It is uncommon and
results from chronic alveolar hypoventilation in residents of high
altitude settlements. It resembles alveolar hypoventilation
(Pickwickian syndrome). It apparently is due to a loss of
ventilatory acclimatization. The hallmarks of the disease are a low or
absent ventilatory response to hypoxia, excessive hypoxemia,
pulmonary hypertension, secondary polycythemia and cor pulmonale.
It was first described in 1928 as an illness occurring in indigenous
Quechua Indian residents in the Andes.
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SYMPTOMS
It is characterized by hypoxemia, cyanosis, somnolence, mental
depression, clubbing of the fingers, polycythemia, and right
LABORATORY HEMATOCRIT. The hematocrit commonly is greater than 75%. ECG. The ECG may show right axis deviation, right atrial and
ventricular hypertrophy. CHEST X-RAY. Chest x-ray will show right heart enlargement and
central pulmonary vessel prominence. HEART CATHETERIZATION. Heart catheterization may show
pulmonary hypertension. PULMONARY FUNCTION TESTING. Pulmonary function testing will
show alveolar hypoventilation and elevated PCO2. TREATMENT
The treatment of CMS is simple. Descent to lower altitudes causes a
rapid improvement in the symptoms and reversal of the abnormal
physical findings and laboratory abnormalities. Patients that are
unable to move to lower altitudes may be treated with
medroxyprogesterone and other respiratory stimulants. Phlebotomy
may be used, but is not the treatment of choice. HIGH ALTITUDE PULMONARY EDEMA (HAPE)
HAPE usually occurs after a rapid ascent to above 9000 feet (2700
CONTRIBUTING FACTORS
Contributing factors include strenuous exercise and exposure to
cold. Long term residents at high altitude may develop reentry
pulmonary edema when they return to high altitude after a short
visit at lower altitudes. Patients that have a congenital absence of
one pulmonary artery are particularly at risk for HAPE, and tend to
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develop the syndrome at altitudes as low as 5000 feet (1500 m).
There is also an increased incidence of HAPE in individuals that
SYMPTOMS
The symptoms begin after about 6-96 hours after arriving at the high
altitude level. The symptoms consist of a dry irritating cough that may
become bloody and frothy, dyspnea, substernal pain, wheezing,
orthopnea, cyanosis, tachycardia, weakness, ataxia, and coma. The
incidence of HAPE varies from .01-2%. It is uncommon, but
potentially much more serious than acute mountain sickness. Most of
the complicated cases occur at altitudes beyond 10,000 ft. It is not
unusual to see 1-2 deaths from HAPE at Colorado ski resorts
LABORATORY CHEST X-RAY. Chest x-rays will show unilateral or bilateral alveolar
infiltrates with enlargement of the pulmonary arteries. The pulmonary
edema is a noncardiogenic form of pulmonary edema, and
cardiomegaly and Kerley B lines are not seen in HAPE.
Recurrent episodes of pulmonary edema usually do not show
the same radiographic distribution of infiltrates. The atrial pressure
is normal, but there is elevation of the pulmonary artery pressure. The
pulmonary wedge pressure is normal, while the pulmonary vascular
resistance is elevated. BLOOD TESTS. The white count is occasionally elevated, but the
sedimentation rate is usually normal. Patients with HAPE have a
relative thrombocytopenia and prolonged prothrombin time. ECG. ECG findings may reveal right ventricular strain. The mortality
of HAPE ranges from between 0-50% depending on several factors. TREATMENT
Treatment of HAPE consists of oxygen, descent to a lower altitude,
and rest. OXYGEN. By administering 100% oxygen, the pulmonary artery
pressure will drop, arterial oxygen saturation will increase, and
respiratory rates will decrease. High flow rates should be given by
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mask to maintain arterial oxygen saturation greater than 90% in
patients with severe HAPE. DESCENT. Descent of about 1500-3000 feet is usually effective. REST. Exertion should be kept to a minimum. EPAP. Expiratory positive airway pressure (EPAP) up to 10 cm
H2O will improve the hypoxia, increase tidal volume and decrease
the respiratory rate without a change in the minute ventilation. DEXAMETHASONE. Dexamethasone at 8 mg initially, followed by
4 mg q6h PO may be useful, but its effectiveness has not been
established. ACETAZOLAMIDE. Likewise acetazolamide may be helpful by
increasing diuresis and stimulating ventilation, but its efficacy has not
been established. FUROSEMIDE. Furosemide should not be given, as it has no benefit,
and may lead to pulmonary embolism. NIFEDIPINE. Nifedipine has been shown to lower pulmonary
hypertension and improve oxygenation. It is initially given as 10 mg
sublingually plus 20 mg PO, followed by 20 mg PO q6h. Nifedipine
may be used as a prophylactic agent for HAPE. HIGH ALTITUDE CEREBRAL EDEMA
High altitude cerebral edema (HACE) is the least common of all of
the syndromes, but can be potentially severe. HACE usually occurs
SYMPTOMS
After about 1-3 days at altitudes greater than 8250 feet (2500 m), the
patient will develop severe headaches, confusion, staggering gait,
truncal ataxia, seizures, hallucinations, mental confusion, slurred
speech, nausea and vomiting, which can progress to coma. The
development of cerebellar ataxia is a sensitive symptom,
prompting immediate treatment. Retinal hemorrhages may be seen
in about 50% of patients. They are very common at altitudes greater
than 16,000 feet (5000 m). They usually are of no concern unless
they appear in the macular area. Nosebleeds are rare, but subungual
splinter hemorrhages are occasionally seen at altitudes greater than
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HOW TO INTERPRET THROMBOPHILIA RISK TEST RESULTS Factor II Gene (Prothrombin) Mutation Absent. Normal or “Wild Type”Risk for thrombosis increased three to five times. Mutation: 20210G>A Mutant. Risk for thrombosis increased fifteen fold. Individuals with one copy of the 20210G>A mutation (i.e., heterozygous) are at a two to four-fold relative increased risk for venous
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