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As more people enjoy the outdoors, high-altitude illness is increasingly becoming a problem that family physicians across the country must treat. High-altitude illness, which usually occurs at altitudes of over 1,500 m (4,921 ft), is caused primarily by hypoxia but is compounded by cold and exposure. It presents as one of three forms: acute mountain sickness (AMS), high-altitude pulmonary edema (HAPE) and high-altitude cerebral edema (HACE). But high-altitude illness can have many other manifestations. Cardinal symptoms include dyspnea on exertion and at rest, cough, nausea, difficulty sleeping, headache and mental status changes. Treatment requires descent, and gradual acclimatization provides the most effective prevention. Acetazolimide is an effective preventive aid and can be used in certain conditions as treatment.
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PMID:High-altitude medicine. 957 28

Headache is known to be the predominant symptom in acute mountain sickness which is also frequently accompanied by nausea, vomiting and insomnia. Nowadays, every year millions of skiers and mountaineers are attracted to mountains all over the world. At altitudes between 2500 m and 5000 m about 20% to 90% of those who are not adapted to high altitude will experience high altitude headache (HAH). It is well documented that HAH can be best prevented by observance of the golden rule: not to go too high too fast. Although many mountaineers are aware of this rule, its observance is complicated by unknown individual susceptibility, the location of mountain huts, the use of cable cars, limited holiday time, unfavorable weather or avalanche conditions. Therefore, there is a widespread use of drugs for the treatment and prevention of HAH. In the past, the increase in cerebral blood flow during acute hypoxia was thought to be the main cause of HAH. More recent findings, however, have caused this hypothesis to be reduced in importance and have supported the pathogenetic consequence of sensitization of intracranial pain-sensitive structures. The effectiveness of cyclooxygenase inhibition for the treatment and prevention of HAH suggests that especially prostaglandins may be an important mediator between hypoxia and HAH. Besides oxygen, acetazolamide, dexamethasone and especially inhibitors of prostaglandin synthesis such as ibuprofen and naproxen are approved for the treatment of HAH. Acetazolamide, dexamethasone, and aspirin were also found to prevent HAH. The most beneficial effects however, may be achieved by the combined application of acetazolamide and aspirin. This combination increases oxygenation and reduces prostaglandin synthesis.
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PMID:[High altitude headache: epidemiology, pathophysiology, therapy and prophylaxis]. 1058 87

Almost every second trekker or climber develops two to three symptoms of the high altitude illness after a rapid ascent (> 300 m/day) to an altitude above 4000 m. We distinguish two forms of high altitude illness, a cerebral form called acute mountain sickness and a pulmonary form called high altitude pulmonary edema. Essentially, acute mountain sickness is self-limiting and benign. Its symptoms are mild to moderate headache, loss of appetite, nausea, dizziness and insomnia. Nausea rarely progresses to vomiting, but if it does, this may anticipate a progression of the disease into the severe form of acute mountain sickness, called high altitude cerebral edema. Symptoms and signs of high altitude cerebral edema are severe headache, which is not relieved by acetaminophen, loss of movement coordination, ataxia and mental deterioration ending in coma. The mechanisms leading to acute mountain sickness are not very well understood; the loss of cerebral autoregulation and a vasogenic type of cerebral edema are being discussed. High altitude pulmonary edema presents in roughly twenty percent of the cases with mild symptoms of acute mountain sickness or even without any symptoms at all. Symptoms associated with high altitude pulmonary edema are incapacitating fatigue, chest tightness, dyspnoe at the minimal effort that advances to dyspnoe at rest and orthopnoe, and a dry non-productive cough that progresses to cough with pink frothy sputum due to hemoptysis. The hallmark of high altitude pulmonary edema is an exaggerated hypoxic pulmonary vasoconstriction. Successful prophylaxis and treatment of high altitude pulmonary edema using nifedipine, a pulmonary vasodilator, indicates that pulmonary hypertension is crucial for the development of high altitude pulmonary edema. The primary treatment of high altitude illness consists in improving hypoxemia and acclimatization. For prophylaxis a slow ascent at a rate of 300 m/day is recommended, if symptoms persist, acetazolamide at a dose of 500 mg/day is effective. Mild acute mountain sickness may also be treated with the same dose acetazolamide. Glucocorticoids are the first line treatment of the malignant form of acute mountain sickness. Nifedipine is effective only for the prophylaxis and treatment of high altitude pulmonary edema.
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PMID:[Mountaineering and altitude sickness]. 1144 1

Traditionally, scientists and clinicians have explored peripheral physiological responses to acute hypoxia to explain the pathophysiological processes that lead to acute mountain sickness (AMS) and high-altitude cerebral edema (HACE). After more than 100 years of investigation, little is yet known about the fundamental causes of the headache and nausea that are the main symptoms of AMS. Thus, we review the evidence supporting a change in focus to the role of the central nervous system in AMS. Our justification is (i) that the symptoms of AMS and HACE are largely neurological, (ii) that HACE is considered to be the end-stage of severe AMS and was recently identified as a vasogenic edema, opening the door for a role for blood-brain barrier permeability in AMS, (iii) that new, non-invasive techniques make measurement of brain water levels and cerebral blood volume possible and (iv) that the available experimental evidence and theoretical arguments support a significant role for brain swelling in the pathophysiology of AMS. We believe that an examination of the responses of the central nervous system to acute hypoxia will reveal important new pathophysiological processes that may help explain AMS and HACE.
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PMID:Frontiers of hypoxia research: acute mountain sickness. 1158 30

A significant portion of the world's geography lies above 10,000 feet elevation, an arbitrary designation that separates moderate and high altitude. Although the number of indigenous people living at these elevations is relatively small, many people travel to high altitude for work or recreation, exposing themselves to chronic or intermittent hypoxia and the associated risk of acute mountain sickness (AMS) and less frequently, high altitude pulmonary edema (HAPE) and high altitude cerebral edema (HACE). The symptoms of AMS (headache, nausea, anorexia, fatigue, lassitude) occur in those who travel too high, too fast. Some investigators have linked the development of these symptoms with the condition of altered blood-brain barrier permeability, possibly related to hypoxia induced free radical formation. The burden of oxidative stress increases during the time spent at altitude and may even persist for some time upon return to sea level. The physiological and medical consequences of increased oxidative stress engendered by altitude is unclear; indeed, hypoxia is believed to be the trigger for the cascade of signaling events that ultimately leads to adaptation to altitude. These signaling events include the generation of reactive oxygen species (ROS) that may elicit important adaptive responses. If produced in excess, however, these ROS may contribute to impaired muscle function and reduced capillary perfusion at altitude or may even play a role in precipitating more serious neurological and pulmonary crisis. Oxidative stress can be observed at altitude without strenuous physical exertion; however, environmental factors other than hypoxia, such as exercise, UV light exposure and cold exposure, can also contribute to the burden. Providing antioxidant nutrients via the diet or supplements to the diet can reduce oxidative stress secondary to altitude exposure. In summary, the significant unanswered question concerning altitude exposure and antioxidant supplementation is when does oxidative stress become potentially damaging enough to merit antioxidant therapy and conversely, what degree of oxidative stress is necessary to foster the adaptive response of altitude exposure?
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PMID:Work at high altitude and oxidative stress: antioxidant nutrients. 1232 88

Acute mountain sickness and high altitude cerebral edema are specific pathologies of high altitude exposure. The usual symptoms of acute mountain sickness are headache, nausea, vomiting, insomnia, lassitude, dizziness and ataxia. High altitude cerebral oedema is a severe state of acute mountain sickness with, in addition, alteration of mental status and consciousness. The pathophysiology of these 2 diseases are essentially due to an increase of intracranial pressure directly dependent of an increase of cerebral volume. Molecular and cellular mechanisms underlying acute mountain sickness and high altitude cerebral oedema are still poorly understood. The regulation of cerebral blood flow by nitric oxide seems to play a major role.
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PMID:[High altitude cerebral oedema]. 1281 24

Cerebral blood flow is thought to increase at high altitude and in subjects suffering from acute mountain sickness (AMS); however, data from the literature are contentious. Blood flow velocity in the middle cerebral artery (MCAv) may be used as a proxy measure of cerebral blood flow. Using transcranial Doppler sonography, MCAv was measured during normo- and hyper-ventilation in subjects who participated in a trial that tested the effect of magnesium supplementation on the prevention of AMS. First, MCAv was recorded at 353 m (baseline). Subjects were then randomized to receive oral magnesium citrate and matching placebo. A second measurement was taken after a 24 +/- 2 h ascent from 1130 m to 4559 m (altitude I), and a third after a 20-24 h stay at 4559 m (altitude II). Using multivariate linear regression, an association was sought between MCAv and magnesium supplementation, subjects' age and gender, altitude itself, a temporary stay at altitude, and the presence of AMS (Lake Louise Score >6 with ataxia, nausea and/or headache). Subjects with AMS had additional Doppler recordings immediately before and after rescue medication (oxygen, dexamethasone and acetazolamide). Forty-seven subjects had measurements at baseline, 39 (21 receiving magnesium and 18 placebo) at altitude I and 26 (13 receiving magnesium and 13 placebo) at altitude II. During hyperventilation, MCAv decreased consistently (for each measurement, P<0.001). Magnesium significantly increased MCAv by 8.4 cm.s(-1) (95% confidence interval, 1.8-15), but did not prevent AMS. No other factors were associated with MCAv. Eleven subjects had severe AMS [median score (range), 11 (8-16)] and, after rescue medication, the median score decreased to 3 (range, 0-5; P=0.001), but MCAv remained unchanged (65 +/- 18 cm.s(-1) before compared with 67 +/- 16 cm.s(-1) after rescue medication; P=0.79). MCAv was increased in subjects who received magnesium, but was not affected by exposure to high altitude or by severe AMS.
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PMID:Effect of magnesium, high altitude and acute mountain sickness on blood flow velocity in the middle cerebral artery. 1457 4

Magnesium is a physiological N-methyl-D-aspartate (NMDA) antagonist. The NMDA receptor may be involved in the pathogenesis of acute mountain sickness (AMS). In the present study, healthy subjects were randomized to receive either 400 mg of oral magnesium citrate (16 mmol) or matching placebo every 8 h for 5 days (prevention trial). Subjects then climbed to 4559 m in approx. 24 h and stayed there for 48 h. A Lake Louise Score <3 at any time was defined as the absence of AMS, whereas a score >6 (with ataxia, headache and nausea) was defined as a prevention failure. In a subsequent trial (treatment trial), subjects with a Lake Louise Score >6 (with ataxia, headache and/or nausea) were randomized to receive either 4 g of intravenous magnesium sulphate (16 mmol) or matching placebo. A decrease in the score >50% within 60 min was regarded as a treatment success. Dichotomous data were analysed using relative risk (RR) or odds ratio (OR), and continuous data using Student's t test or Wilcoxon's rank-sum test. In the prevention trial, data from 61 subjects (30 receiving magnesium and 31 placebo) were analysed. With oral magnesium, 20% of subjects had no AMS compared with 16.1% in the placebo group [RR (95% CI), 1.2 (0.4-3.6); where CI is confidence interval]. With magnesium, 40% were prevention failures compared with 35.5% in the placebo group [RR (95% CI), 1.13 (0.59-2.15)]. The mean time to failure and severity of AMS was similar between the two groups. With magnesium, 38.2% had loose stools compared with 11.8% in placebo group [RR (95% CI), 3.25 (1.18-8.97)]. In the treatment trial, 12 subjects received magnesium and 13 received the placebo. With intravenous magnesium, 25% were regarded as treatment successes compared with none in the placebo group [OR (95% CI), 9.71 (0.91-103.4)]. With magnesium, mean (+/- S.D.) scores decreased from 11.6 +/- 1.7 before treatment to 9.0 +/- 3.5 after treatment (P=0.009); scores remained unchanged in the placebo group. With magnesium, 75% of subjects experienced a transient flushing compared with 7.7% in the placebo group [RR (95% CI), 0.05 (0.01-0.25)]. In conclusion, oral magnesium does not prevent AMS. In subjects with established AMS, intravenous magnesium reduces the severity of symptoms to some extent, but this effect is of no clinical importance.
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PMID:Magnesium for the prevention and treatment of acute mountain sickness. 1457 5

As increasing numbers of people choose to sojourn or retire to the mountains, high-altitude illness is becoming a pathological phenomenon about which healthcare providers should have greater awareness. Hypoxia is the primary cause of high-altitude illness, but other stressors on the sympathetic nervous system, such as cold and exertion, also contribute to disease development and progression. Although variable across persons, symptoms of high-altitude disorders usually occur at altitudes over 7000 feet, and typically in 1 of 3 forms: acute mountain sickness (AMS), high-altitude cerebral edema (HACE), or high-altitude pulmonary edema (HAPE). Major symptoms include nausea, poor sleep, headache, lassitude, cough, dyspnea on exertion and at rest, ataxia, and mental status changes. As a rule, illness occurring at high altitude should be attributed to the altitude until proven otherwise. Treatment is best accomplished by descent and by oxygen or pharmacologic intervention if necessary. Under no circumstances should a person with worsening symptoms of high-altitude illness delay descent. As will be discussed in part II of this article, gradual ascent and subsequent acclimatization to altitude is the most effective prevention, though acetazolamide (Diamox) may be a useful prophylactic measure in some.
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PMID:High-altitude-related disorders--Part I: Pathophysiology, differential diagnosis, and treatment. 1513 83

Headache is the cardinal symptom of acute mountain sickness (AMS). The headache normally worsens, with increased cerebral affection and the development of high-altitude cerebral edema (HACE). A Norwegian expedition aimed to climb Baruntse (7129 m) in Nepal in 2003. At 5400 m a 35-year-old man felt exhausted. The next day he aborted his attempt at further climbing as a result of extreme fatigue. Over the next 24 hours he developed cough, dyspnea, and severe hypoxia before progressing to ataxia and blurred vision. At no point did he experience headache or nausea. The patient was evacuated by helicopter. He improved immediately after descent and recovered completely within a week. The speed of progression from AMS to HACE varies. Abrupt onset of HACE is occasionally reported. High-altitude pulmonary edema (HAPE) may induce severe hypoxia that can lead to rapid development of HACE. High-altitude cerebral edema in the setting of HAPE was the most likely diagnosis despite the unusual lack of headache. Rapid onset of HAPE with subsequent severe desaturation should raise awareness of the development of HACE, even in the absence of headache.
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PMID:High-altitude cerebral edema with absence of headache. 1744 14


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