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Altitude illness is a term encompassing a group of subacute and chronic syndromes, the underlying pathophysiology of which is triggered by continuous exposure to hypoxia. These conditions are described in the following sections. Further information can be obtained from detailed reviews.[227] [228]
Acute exposure to altitude often results in a constellation of signs and symptoms known as acute mountain sickness (AMS). The most common symptoms are headache, decreased appetite, nausea and vomiting, insomnia, ataxia, and peripheral edema.[229] AMS can occur after several hours of exposure to elevations greater than 2500 to 3000 m, although susceptibility to AMS is subject to interindividual variation. AMS develops in approximately 25% of visitors to ski resorts in the American Rockies (altitude, 1920 to 2960 m).[230] Effective prophylactic measures against AMS in mountaineers include slow ascent (around 300 m/day) or "staging" in which several days are spent at an intermediate altitude of around 2000 m.[229] Pharmacologic prophylactic measures include the administration of acetazolamide,[231] which is believed to work by augmenting the ventilatory response to hypoxia as a result of the metabolic acidosis that occurs after its administration. An effective dose range is 125 to 250 mg orally twice daily begun the day before ascent.[227] Dexamethasone has also been shown to be effective in a dosage of 4 mg every 6 hours, although symptoms may occur as soon as use of the drug is discontinued.[59] [232] One published study suggests that Gingko biloba prevents AMS,[233] but contrary evidence has also been presented.[234] Despite its value in preventing high-altitude pulmonary edema (HAPE; see the next section), nifedipine does not prevent AMS symptoms.[235] Insomnia associated with AMS responds to treatment with acetazolamide. Sedative/hypnotic drugs can depress ventilation and exacerbate hypoxia and should therefore be used cautiously. It has been reported that zolpidem does not depress ventilation at high altitudes and may thus be preferred for insomnia in persons with AMS, although its use for this indication has not been studied in clinical trials.[227]
Most individuals recover spontaneously from AMS after several days at altitude. If treatment is required, time-honored methods are descent and supplementary oxygen. A descent of only 500 to 1000 m usually leads to resolution of AMS. Simulated descent using a portable inflatable hyperbaric chamber (Gamow bag) operated by foot pump is also effective. Depending on the altitude, inflation of such a chamber to only 2 psi (100 mm Hg) produces a decrease in equivalent altitude of 1500 to 2000 m.[227]
AMS symptoms could conceivably exist at sea level. It is possible that the headache that frequently occurs in patients receiving narcotic analgesia after surgery may be due to a form of "AMS" caused by mild hypoxemia.
A less frequent, but more serious complication of hypoxia is HAPE. [227] [228] [236] A hemodynamic pathophysiology for HAPE is suggested by its tendency to occur when pulmonary vascular flow or pressure is particularly high (e.g., primary pulmonary hypertension[227] [237] ) or in individuals with an exaggerated pulmonary hypertensive response to hypoxia and in the lung contralateral to unilateral absence of the PA.[238] In addition, in HAPE-susceptible individuals, the probability of recurrence can be reduced by the administration of slow-release nifedipine.[239] On the other hand, bronchopulmonary lavage in subjects with HAPE has revealed that the protein content of the edema fluid is high, thus implicating an increase in permeability. [240] [241] Paradoxically, measurement of the transcapillary escape rate of albumin has revealed no altitude-related increase.[242] A hypothesis that connects mechanical forces in the pulmonary circulation with increased pulmonary capillary permeability suggests that HAPE may be caused by stress failure of pulmonary capillaries as a result of the acute elevation in PA pressure.[243] In a group of 262 recreational climbers who ascended from 1200 to 4559 m over a 18- to 24-hour period, severe HAPE developed in only 1 climber, who was evacuated, but 40 had radiologic or physical diagnostic evidence supportive of increased pulmonary extravascular lung water (rales or edema on chest radiography).[244]
Prophylaxis against HAPE includes slow ascent. Perhaps above an altitude of 2500 m, the altitude at which one sleeps should not be increased by more than 600 m per 24 hours, and an extra day of acclimatization should be added for each increase of 600 to 1200 m.[227] People with known predisposing factors such as unilateral absence of the PA should avoid high altitudes. For climbers with known susceptibility to HAPE, nifedipine (20 to 30 mg of a slow-release formulation every 12 hours) can lower PA pressure and provide prophylaxis.[227] Inhaled salmeterol has also been shown to prevent HAPE,[245] possibly by accelerating clearance of fluid from the lung.
Treatment of HAPE consists of descent or supplemental oxygen, or both.[227] If either descent is impossible or oxygen is unavailable, pharmacologic reduction of PA pressure should be initiated. Nifedipine, 10 mg sublingually, followed by 20 mg of a slow-release preparation administered orally every 6 hours, has been successful in HAPE.[246] PA pressure can also be lowered in patients with HAPE by administering hydralazine, phentolamine, or NO.[246] [247] [248] [249] Administration of 40 ppm NO (inspired O2 concentration, 20%) by inhalation to individuals with HAPE at an altitude of 4559 m (barometric pressure, 440 mm Hg) induced a reduction in PA pressure and improvement in arterial Hb O2 saturation (67% before inhalation to 73% after breathing NO for 15 minutes).[248] Other suggested treatments include drugs that can lower PA pressure, such as prostaglandins [250] and NO donors such as sildenafil,[250] [251] or treatments that facilitate clearance of alveolar fluid, such as β2 -adrenergic agonists,[245] recompression in a Gamow bag,[227] and application of expiratory airway pressure.[252]
Individuals with a previous history of HAPE who wish to travel to altitude should ascend slowly and consider nifedipine prophylaxis. A history of HAPE at low altitude (≤2500 m) should prompt an investigation for an underlying cause.[227]
The rarest form of high-altitude illness, but the most lethal, is high-altitude cerebral edema (HACE). HACE is
Treatment of HACE is a medical emergency and ideally should include evacuation or descent and administration of supplemental O2 . Although a reduction in altitude of 500 to 1000 m is usually effective for AMS, treatment of HACE may require descent to a lower altitude. Use of a Gamow bag may also be effective. Recommended adjunctive treatment includes dexamethasone, 8 mg immediately and then 4 mg every 6 hours. If descent is delayed, acetazolamide 250 mg twice daily, is recommended.[227]
A small percentage of high-altitude residents develop symptoms consisting of headaches, bone pain, confusion, sleeplessness, and a sensation of congestion in the head, often accompanied by extreme polycythemia, a constellation of findings known as chronic mountain sickness or Monge's syndrome.[257] Clinical improvement and increased work capacity often result from phlebotomy, and descent to lower altitudes relieves the symptoms completely.
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