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Acute mountain sickness (or altitude sickness) affects climbers who rapidly ascend to heights of at least 2500 meters. The symptoms of acute mountain sickness include headache, fever, fatigue, nausea, dizziness, anorexia, and sleep disturbances. This article describes the management of acute mountain sickness. Acetazolamide, which reduces the formation of CSF, is the main drug therapy, and additional drugs include nonsteroidal antiinflammatory drugs for headache and dexamethasone for cerebral edema. Oxygen inhalation at 1 L/minute and descent to lower altitudes is recommended. The role of a portable hyperbaric chamber is also described.
• Acute mountain sickness occurs after ascent to an altitude of at least 2500 meters. | |
• Symptoms include headache, fever, fatigue, nausea, dizziness, anorexia, and sleep disturbances. | |
• If symptoms are not relieved, or with further ascent, cerebral and pulmonary edema may occur. | |
• Treatment is medical, with supplementary oxygen therapy. | |
• If symptoms persist, the affected person should descend to a lower altitude. |
Acute mountain sickness (or altitude sickness) affects climbers who rapidly ascend to heights of at least 2500 meters. Altitude-related health problems have been known to humans ever since they started to cross high mountains. The first documented report of mountain sickness was by a Chinese official, Too-Kin, between 37 and 32 BC when he encountered difficulties crossing the Kilik Pass (4827 m) into what is present-day Afghanistan (14). He described headache and vomiting and gave names such as "the Great Headache Mountain" and "the Little Headache Mountain" to the mountains on his route. In the year 403, a Chinese man crossing into Kashmir, a companion of the monk Fa Hsien, died with difficulty in breathing and foam at his mouth, now known as high-altitude pulmonary edema (14). Similar cases were described by the Jesuit priest Father Acosta in 1590 in the high Andes of Peru (01). Paul Bert, the French pioneer in the investigation of the effects of atmospheric pressure on body function, recognized hypoxia as the cause of altitude sickness in 1877 (06). An Italian physiologist, Angelo Mosso, documented a case of mountain illness at an altitude of 4559 m on the Italian Alps bordering Switzerland in 1894 (33). A cerebral form of mountain sickness in which cerebral edema predominated was described in a series of patients in 1975 (18).
There are 2 well-known high-altitude syndromes: (1) acute mountain sickness, which occurs within a few hours to a few days at high altitude; and (2) chronic mountain sickness, also called Monge disease, which develops after several years of residence at high altitude (32). Acute mountain sickness may develop into high-altitude cerebral edema or high-altitude pulmonary edema. A subacute form of mountain sickness was described in Indian soldiers in Kashmir who developed pulmonary hypertension and congestive heart failure within a few months of living at altitudes of 5800 to 6700 m (02).
The Lake Louise Consensus on the Definition of Altitude Illness defined acute mountain sickness as a syndrome occurring in the setting of a recent gain in altitude, consisting of headache and at least 1 of the following: (1) gastrointestinal symptoms, such as anorexia, nausea, or vomiting; (2) fatigue or weakness; (3) dizziness or lightheadedness; and (4) difficulty sleeping. Acute mountain sickness without headache has been reported at an altitude of below 3000 m and be triggered by chronic stress or excessive exertion (12). Persons who are not acclimatized to high altitudes and who ascend to 2500 m are at risk for acute high-altitude illnesses (05).
• Initial symptoms of acute mountain sickness are headache, fever, fatigue, nausea, dizziness, anorexia, and sleep disturbances. | |
• If untreated, acute mountain sickness may proceed to high-altitude cerebral edema or high-altitude pulmonary edema. | |
• Chronic mountain sickness manifests by hypoxemia, polycythemia, high hemoglobin levels, and migraine headaches in permanent residents at altitudes above 4000 m. | |
• Acute mountain sickness is a benign condition, but the more advanced forms can be accompanied by severe morbidity and death. |
Symptoms of acute mountain sickness. These include headache, fever, fatigue, nausea, dizziness, anorexia, and sleep disturbances. These are observed with a rapid ascent to 2500 m or higher; similar symptoms may be observed during high-altitude flights if the cabins are not adequately pressurized. If untreated, acute mountain sickness may proceed to high-altitude cerebral edema or high-altitude pulmonary edema.
High-altitude cerebral edema. This is characterized by the presence of a change in mental status or ataxia in a person with acute mountain sickness or the presence of both mental status changes and ataxia in a person without acute mountain sickness. The clinical manifestations are severe headaches, ataxic gait, hallucinations, cranial nerve palsies, hemiplegia, and seizures. Various degrees of impairment of consciousness may occur, from drowsiness to coma. Neurologic symptoms can progress from mild symptoms to unconsciousness within 12 to 72 hours. Several transient focal neurologic signs may manifest at high altitude without associated acute mountain sickness or other concurrent illness. Seizures may occur at high altitude without any clinical evidence of acute mountain sickness. At high altitude, seizure risks in a seizure-prone person may be higher than for normal individuals. Transient global amnesia can occur at high altitude. An explanation for this is that marked hyperventilatory response to hypoxia in some individuals can cause significant hypocapnic cerebral vasoconstriction leading to local ischemia of certain regions of the brain and resulting in transient focal neurologic impairment.
Neuropsychological effects of high altitude. Impairment of short-term memory and deficits in verbal fluency, language production, and cognitive fluency are noticeable in most individuals on ascent to altitudes above 6000 meters. Those who survive a comatose state may have memory and gait deficits that persist for months.
High-altitude pulmonary edema. Although some degree of pulmonary edema is present in high-altitude cerebral edema, it may be overshadowed by more dramatic neurologic symptoms. Symptoms of high-altitude pulmonary edema are dyspnea and dry cough that changes to productive cough. Signs are tachycardia, cyanosis, and pink-tinged frothy sputum. High-altitude pulmonary edema is diagnosed in the presence of at least 2 of 4 symptoms (dyspnea at rest, cough, weakness or decreased exercise performance, chest tightness or congestion) and 2 of 4 signs (crackles or wheezing in at least 1 lung field, central cyanosis, tachypnea, or tachycardia).
Chronic mountain sickness. This is manifested by hypoxemia, polycythemia, high hemoglobin levels, and migraine headaches in those who live permanently in altitudes above 4000 m. Cardiovascular complications of living at very high altitude are pulmonary hypertension, right heart enlargement, and congestive heart failure. These patients usually have cognitive impairment.
Acute mountain sickness is a relatively benign condition, but the more advanced forms with high-altitude cerebral edema and high-altitude pulmonary edema can be accompanied by severe morbidity, and death may result if prompt treatment measures are not instituted. Complications of acute mountain sickness include thromboembolic events and retinal hemorrhages.
• Acute mountain sickness is caused by an ascent to high altitude without acclimatization. | |
• Hypoxia is a contributing factor in the pathogenesis. | |
• High-altitude cerebral edema is likely due to vasogenic as well as cytotoxic mechanisms, and venous hypertension is a possible contributory factor. | |
• Cerebral edema increases peripheral sympathetic activity that acts neurogenically in the lungs to cause high-altitude pulmonary edema. |
The process of acute acclimatization to high altitude is mediated by the endocrine system and involves hemoconcentration through diuresis to increase the oxygen carrying capacity of the blood as compensation for reduced partial pressure of oxygen (40). Disturbance of this mechanism may lead to the development of mountain sickness.
Acute mountain sickness is caused by ascent to high altitude without acclimatization, and chronic mountain sickness may result after prolonged residence at high altitude even in acclimatized persons. There is no agreement as to the height at which symptoms of acute mountain sickness appear consistently, as it depends on the state of acclimatization of a person. Gender, age, or level of physical fitness plays no significant role in the susceptibility to acute mountain sickness.
Cerebral blood flow increases in acute hypoxia, but there is no difference between white matter and grey matter, irrespective of susceptibility to acute mountain sickness. Therefore, acute phase differences in regional cerebral blood flow during acute hypoxia are not a primary feature of susceptibility to mountain sickness. Vasogenic and cytotoxic mechanisms are proposed for high-altitude cerebral edema, and venous hypertension is a possible contributory factor (39).
Symptoms of acute mountain sickness are often attributed to raised intracranial pressure resulting from cerebral edema. However, diffusion-weighted MRI studies have shown only slight astrocytic swelling caused by redistribution of fluid from the extracellular space to the intracellular space without any evidence for further barrier disruption or increase in cerebral edema or pressure. Cerebral edema is not a valid explanation of symptoms because some vasogenic edema occurs with as well as without symptoms of acute mountain sickness. Findings of a study in human volunteers indicate that hypoxia stimulates cerebral oxidative-nitrative stress, which may be a risk factor for acute mountain sickness by a mechanism that appears to be independent of impaired blood-brain barrier function and cerebral oxidative metabolism (04).
Levels of arterial norepinephrine are significantly higher at baseline and during the first hour of hypoxia in subjects who later develop acute mountain sickness, and this may be a possible biomarker for individuals who may be relatively susceptible to the illness (23). Results of a study of cortical excitability using transcranial magnetic stimulation suggest that high altitude deeply changes cortical excitability by affecting both inhibitory and excitatory circuits and that this is reflected in acute mountain sickness symptoms (31).
In a study of acute mountain sickness, headache fulfilling the criteria of migraine increased in frequency, and this association may be due to common nonspecific symptoms, although a common underlying pathophysiology cannot be excluded (34). However, a history of migraine or other headache at low altitude is not a major risk factor for acute mountain sickness.
Stormy weather is another aggravating factor because a low-pressure front on the weather map is equivalent to several hundred feet of additional altitude. Hypoxia is an important factor in the etiology of acute mountain sickness, and a decrease in barometric pressure is the main cause of hypoxia at high altitude. Partial pressure of oxygen falls 30%, from 159 mm Hg at sea level to 112 mm Hg at a height of 2900 m, and a 50% decrease occurs at an altitude of 5500 m, which is the highest level of continuous human habitation (20). Residence above this level leads to some manifestations of chronic mountain sickness.
Various studies suggest that genotype contributes to capacity to rapidly and efficiently acclimatize to altitude, but the mechanism by which this occurs has not been elucidated (28). There is a wide variation among individuals regarding performance at high altitude and susceptibility to high-altitude illness, which may occur as a result of genetic variation. Only limited information is available about the genetic basis of high-altitude illness. No clear associations between gene polymorphisms and susceptibility to mountain sickness have been discovered.
A higher than anticipated occurrence of acute mountain sickness (42.85%) has been noted among athletes with neurologic impairments due to spinal cord injury, multiple sclerosis, and traumatic brain injury. Neurologic disability groups, history of acute mountain sickness, and prior occurrence of headache at high altitude could be used as predictors for the development of symptoms of acute mountain sickness (22).
Altitude sickness has been reported to occur in air force pilots flying above 5000 m in unpressurized aircrafts. Symptoms are subtle and often involve cognitive impairment or lightheadedness. The most common cause of hypoxia in these aircraft is the failure of the mask or regulator, or a mask leak. Rapid accidental decompression did not feature as a cause of hypoxia in these cases.
The pathomechanism of acute mountain sickness is not clear. Hypoxia at high altitude appears to be a triggering factor. Increased free plasma vascular endothelial growth factor, a hypoxia-induced protein that produces vascular permeability on ascent to altitude, is associated with acute mountain sickness and may play a role in its pathophysiology. Physiological and pathophysiological responses to extreme environmental challenges such as hypoxia of high altitude are like responses seen in critical illness. Study of human responses to hypobaric hypoxia may offer important insights into the pathophysiology of critical illness.
Both hypoxia as well as hyperoxia may alter reactive oxygen species (ROS) production by changing mitochondrial Po2 (PmO2), and high ROS levels may cause oxidative stress and cell damage. Altitude triggers high mitochondrial ROS production in muscle regions with high metabolic capacity but limited O2 delivery. Because PmO2 depends on the balance between O2 transport and utilization, a mathematical model of O2 transport and utilization in skeletal muscle can be used to predict conditions that cause abnormally high ROS generation (08). According to this model, ROS generation in exercising normal muscle switches to high levels at approximately 5000 meters, which is the altitude above which permanent human residence is impossible.
Another study has shown that increases in severity of acute mountain sickness is independently related to normobaric hypoxia, hypobaric hypoxia, and duration of exercise, suggesting that hypobaric hypoxia may affect development of acute mountain sickness above the level induced by normobaric hypoxia alone and that the 2 conditions are not interchangeable for studying acute mountain sickness (11). However, the duration of exercise has an impact on physiological responses.
Hypoxia also leads to capillary leak and vasogenic cerebral edema, which is a major operating factor in high-altitude cerebral edema. This has been demonstrated by MRI studies that show reversible white matter edema. The flux of the fluid is influenced by the hydrostatic pressure in presence of an opening of the blood-brain barrier. With progression of extracellular vasogenic edema, the intercapillary distance is increased, rendering the cells ischemic. They may swell further, increasing the intracranial pressure. This cytotoxic mechanism, which has been used in the past to explain high-altitude cerebral edema, may become operational at a later stage and may be preventable by the earlier treatment of vasogenic edema. This concept is supported by the effectiveness of dexamethasone in treating high-altitude cerebral edema. Cerebral edema has been investigated by MRI in volunteers exposed to normobaric hypoxia and shown to be aggravated by exercise (29). Edema was associated with accumulation of water in the extracellular space but independent of development of acute mountain sickness, casting doubt on the concept that acute mountain sickness and high-altitude cerebral edema share a common mechanism.
Animal experimental studies have shown that hypoxia-induced cerebral edema and neuronal apoptosis are associated with increased expression of the neuropeptide corticotrophin releasing factor (CRF), which acts on type 1 receptor (CRFR1) to trigger signaling of cAMP/PKA in cortical astrocytes, leading to activation of water channel aquaporin-4 (AQP4) and cerebral edema (09). These effects can be blocked by a CRFR1 antagonist.
High-altitude anterior ischemic optic neuropathy is likely due to inadequate autoregulatory response of the retinal vascular system.
Fever in acute mountain sickness is attributed to systemic inflammatory reaction. Rise of temperature may be correlated with reduction in arterial oxygen saturation at high altitude.
The pathophysiology of high-altitude pulmonary edema is unclear, but hypoxia-induced pulmonary artery hypertension is well documented. Pulmonary capillary pressure remains normal, indicating that high-altitude pulmonary edema is not cardiac in origin. The edema fluid has a high content of protein, red cells, and leukocytes, resembling the fluid characteristics in neurogenic pulmonary edema. The accumulation of this protein-rich fluid in the alveolar space implies an increase in the permeability of the pulmonary vascular epithelium that overwhelms the lung's capacity for removing fluid from the alveoli. Hypoxia, in addition to pulmonary hypertension, plays a part in the increased permeability. The role of pulmonary hypertension is supported by the effectiveness of nifedipine and nitric oxide in relieving pulmonary edema by reducing pulmonary hypertension. Sodium-driven clearance of alveolar fluid may also have a pathogenic role in pulmonary edema. This forms the basis of beta-adrenergic agonists therapy, which upregulates the clearance of alveolar fluid and attenuates pulmonary edema.
Primary intracranial events in high-altitude cerebral edema (cerebral edema, hypoxic cerebral vasodilatation, and elevated cerebral capillary hydrostatic pressure) elevate peripheral sympathetic activity that acts neurogenically in the lungs to cause high-altitude pulmonary edema. These events also act on the kidneys to promote salt and water retention.
Predisposing factors. Various factors that may predispose to acute mountain sickness include the following.
Genetic. In a case-control study, sequencing showed a significant association between the rs1008348 polymorphism and susceptibility to acute mountain sickness in a Han Chinese population, suggesting that this particular single nucleotide polymorphism might be a risk factor (25). This study provides a basis for further elucidation of the genetic mechanisms underlying acute mountain sickness.
Physical exercise at high altitude. This increases the incidence and severity of acute mountain sickness, probably by exercise-induced exaggeration of arterial hypoxemia. Increased ventilatory response to a hypoxic environment is a normal acclimatization response, and alterations in the response, such as inappropriate hypoventilation, have been implicated in the pathogenesis of acute mountain sickness. Support for this hypothesis comes from the prophylactic effectiveness of acetazolamide, a drug that increases ventilation.
Preexisting medical conditions. Persons with preexisting medical conditions, such as chronic obstructive pulmonary disease and sickle cell anemia, may face increased risks at high altitude.
Predisposing factors for acute mountain sickness are obesity, alcohol or sedative consumption, and physical exhaustion. The use of oral contraceptives at high altitudes is associated with an increased risk for the development of acute mountain sickness (15). The reason for this is lowering of circulating progesterone, which has antiinflammatory and antidiuretic effects, in addition to respiratory smooth muscle relaxation.
Individuals with low baseline insulin sensitivity levels are more susceptible to the development of acute mountain sickness (36). Potential diabetogenic side effects should be considered when using dexamethasone for treatment in these persons.
• Acute mountain sickness affects more than 25% of individuals ascending to 3500 m and more than 50% of those ascending above 6000 m. |
Acute mountain sickness affects more than 25% of individuals ascending to 3500 m (11,500 ft) and more than 50% of those above 6000 m (19,700 ft); for each 1000-m (3300-ft) increase in altitude above 2500 m (8200 ft), the prevalence increases 13% (30). It is estimated that of the 20 million visitors to ski resorts in the western United States every year, approximately 5 million have some symptoms of acute mountain sickness. The incidence of severe acute mountain sickness in UK military personnel performing adventure training on Mount Kenya at an altitude of 4985 m was 34% (17). For trekkers to Nepal, the death rate from altitude illness was 0.0036% (35).
• Gradual ascent and acclimatization are the cornerstones of prevention. | |
• Prophylactic medications against headache in acute mountain sickness are aspirin and sumatriptan. |
Gradual ascent and acclimatization are the cornerstones of prevention. Ideally, one should take a break for a couple of days at the altitude of 2500 m and then repeat the breaks at every 500 m ascent. High carbohydrate diet and moderate physical activity help in acclimatization. Efficacy of acetazolamide, which is commonly used for prevention of acute mountain sickness, remains controversial.
Cognitive deficits tend to decrease in subjects pretreated with dexamethasone. One explanation for this trend is that cognitive deficits in otherwise asymptomatic subjects exposed to high altitude are caused by subclinical cerebral edema.
Aspirin has a prophylactic effect against headache, the main symptom of acute mountain sickness. Aspirin may support adaptation to high altitude by reducing sympathetic activity mediated by prostaglandins. Sumatriptan prophylaxis is effective in preventing development of acute mountain sickness.
Prophylactic use of lipid-soluble antioxidant vitamins at the prescribed doses is a safe and effective measure that may attenuate acute mountain sickness.
A preliminary randomized, double-blinded, placebo-controlled trial suggests that intravenous iron supplementation may protect against the symptoms of acute mountain sickness in healthy volunteers, possibly because of the ability of iron to influence cellular oxygen sensing pathways (37).
It is possible to determine a subject's susceptibility to mountain sickness by testing response to altitude at sea level using a hypobaric chamber in a laboratory with a range of simulated altitudes. Prophylactic measures may be recommended for such individuals prior to ascent to high altitudes.
Elevated serum concentrations of low-density lipoprotein (LDL) are protective against the development of acute mountain sickness. The use of statins, although they lower serum LDL concentrations, may provide protection against development of acute mountain sickness because of their antiinflammatory properties (16).
Some of the subjective symptoms of acute mountain sickness, such as headache and sleep disturbances, are also seen in study subjects at sea level, indicating the role of travel-related stress in the causation of these symptoms. In cases of fever at moderate altitude, the differential diagnosis must include acute mountain sickness.
Acute mountain sickness should be differentiated from altitude decompression sickness, which usually affects aviators ascending to high altitude rapidly in nonpressurized airplanes and is characterized by symptoms due to embolization of gas bubbles released from the blood circulation. This condition is like decompression sickness affecting the divers who ascend to the ocean surface rapidly, and both these conditions are managed by recompression. Altitude decompression sickness is not encountered during mountain climbing unless an aviator affected by this condition happens to make an emergency landing on a mountain.
High-altitude cerebral edema needs to be distinguished from cerebral edema associated with other intracranial disorders, but the temporal association with ascent to high altitude, absence of history of neurologic disorders or head injury, and relief of symptoms on descent help in differentiating high-altitude cerebral edema from other conditions. Patients with intracranial space-occupying lesions may show manifestations of increased intracranial pressure on ascent to high altitude. Other focal neurologic disturbances at high altitude are transient ischemic attacks, cerebral venous thrombosis, seizures, syncope, and diplopia. A young male with no prior history of high-altitude sickness experienced a severe headache associated with nausea, difficulty sleeping, loss of appetite, and fatigue on ascent to 5200 m and received medical treatment with diagnosis of acute mountain sickness (10). He failed to improve on descent to lower level and neurologic investigations revealed hemorrhage in a pituitary tumor. It is important to recognize neurologic conditions that are precipitated by altitude and not to consider them as part of mountain sickness because treatment may be different. Neurologic conditions that should be considered in the differential diagnosis of acute mountain sickness include the following:
• Arteriovenous malformation |
Similarly, high-altitude pulmonary edema needs to be differentiated from pulmonary hypertension and pulmonary edema due to cardiac diseases. Again, the history of absence of previous cardiac disease, temporal association with ascent, and response to agents such as acetazolamide help in differentiation. Right ventricular enlargement and heart failure may develop in patients with subacute mountain sickness. Erythrocytosis or secondary polycythemia in chronic mountain sickness needs to be differentiated from polycythemia vera.
• Testing in a simulated hypobaric chamber for susceptibility to acute mountain sickness | |
• Chest X-ray | |
• Blood gases | |
• Visual analog scale for the assessment of subjective phenomena, such as headache | |
• EEG | |
• Ultrasound, which measures the increase of optic nerve sheath, is a surrogate biomarker for raised intracranial pressure. | |
• Intracranial pressure monitoring | |
• MRI | |
• Psychological testing |
Acute mountain sickness by itself does not require any diagnostic workup, as the symptoms subside spontaneously by acclimatization, therapeutic measures, or descent to a lower altitude. A 100 mm visual analog scale, which is commonly used to assess subjective phenomena such as pain, has been found to be reliable for the self-assessment of acute mountain sickness (AMS) as applied to the Lake Louise AMS Self-report Score. This scale uses a categorical numeric rating scale to answer 5 questions addressing symptoms, such as headache.
There are no validated biomarkers of mountain sickness. The mainstay of prediction for susceptibility to acute mountain sickness is testing of a person in a simulated hypobaric chamber. A study has compared plasma cytokine profiles of acute mountain sickness–susceptible individuals with acute mountain sickness–resistant individuals at low altitude by cytokine array analysis, and the results were as follows (27).
• Compared to acute mountain sickness–resistant individuals, the level of insulin-like growth factor binding protein 6 (IGFBP-6) was significantly lower in acute mountain sickness–susceptible individuals. | |
• Conversely, the levels of serum amyloid A1, dickkopf WNT signaling pathway inhibitor 4, and interleukin 17 receptor A were significantly higher in acute mountain sickness–susceptible individuals than in acute mountain sickness–resistant individuals. |
The following diagnostic measures are useful in patients with high-altitude cerebral edema:
• MRI. This can be used for assessment of cerebral edema in the acute, convalescent, and recovered phases of high-altitude cerebral edema, as well as for exclusion of other intracranial pathology. | |
• Intracranial pressure monitoring | |
• Increase of optic nerve sheath diameter as measured by ultrasound is a surrogate biomarker for raised intracranial pressure and is associated with the presence and severity of acute mountain sickness. However, in a controlled study, individual responses to altitude and oxygen varied greatly, and the results do not support a role for increased intracranial pressure in mild to moderate acute mountain sickness (24). A review of 6 studies has shown that variability in optic nerve sheath diameter across the included studies and within each study limits the utility of this method in the diagnosis of acute mountain sickness in individual subjects (26). | |
• In a prospective study on subjects with acute mountain sickness, optical coherence tomography of optic nerve head enabled detection of subtle increases in the peripapillary retinal nerve fiber layer in some cases, even in absence of high-altitude cerebral edema and papilledema (03). | |
• EEG. Amplitude change, particularly in the alpha band, on quantitative EEG analysis performed at moderate altitude may possibly predict the risk of developing acute mountain sickness. | |
• Neuropsychological testing. Cognitive deficits may be assessed by impairment of reaction time on psychomotor performance tests. |
The following investigations are relevant to high-altitude pulmonary edema:
• Chest x-rays |
• For acute mountain sickness management, use oxygen inhalation, nonsteroidal antiinflammatory drugs for headache, antiemetics for nausea, and acetazolamide. If there is no relief, descend to lower altitudes. | |
• For cerebral edema management, evacuate to a hospital. |
Management varies according to the type of clinical presentation.
Acute mountain sickness. The management of acute mountain sickness consists of 1 or more of the following measures:
• Nonsteroidal antiinflammatory drugs, eg, ibuprofen, for headache | |
• Oxygen inhalation at 1 L/minute | |
• Continuous positive airway pressure treatment reduces symptoms of acute mountain sickness and can be used with rechargeable battery for climbers at high altitudes (21). | |
• Antiemetics such as phenothiazine for nausea and vomiting | |
• Gabapentin may relieve high-altitude headaches but does not affect other symptoms of acute mountain sickness. | |
• Zolpidem for insomnia | |
• Acetazolamide 500 mg daily. Acetazolamide inhibits carbonic anhydrase. Acting on the proximal tubule cells of the kidney, acetazolamide causes bicarbonate diuresis, a consequent extracellular acidosis, and lowering of blood pH. It also stimulates respiration, increases partial pressure of oxygen in arterial blood, and lowers partial pressure of CO2 in the arterial blood, indicating an increase in ventilation. These effects improve oxygen supply to the tissues. Acetazolamide also reduces the bicarbonate content of the CSF by blocking carbonic anhydrase in the cells of the choroid plexus. This also reduces the rate of CSF formation and, combined with diuretic action of acetazolamide, contributes to reduction of cerebral edema. |
A systematic review of the literature, including 2 randomized trials, has concluded that it is not possible to establish clearly whether treatment with acetazolamide reduces the symptoms of acute mountain sickness or increases the risk of adverse effects because the certainty of the evidence is very low (38).
Clinical benefit of medroxyprogesterone, a respiratory stimulant, is unproven at high altitude. However, when medroxyprogesterone is given in combination with acetazolamide, it achieves the best PaO2 values.
• If symptoms persist, advise descent to lower altitudes. | |
• A transportable hyperbaric chamber may be used as an alternative to descent to a lower altitude. One such device is the Gamow bag, which can be carried in a backpack and pressurized when required. It is useful for treating acute mountain sickness, but the beneficial effects are temporary, within minutes after pressurization in the chamber. A multidisciplinary approach to the management of acute mountain sickness includes the use of a hyperbaric chamber capable of recompression to 3 atmosphere absolute (ATA) with vasoconstrictive effects of hyperbaric oxygen and elimination of the rebound after initial treatment (07). |
High-altitude cerebral edema. The patient must be evacuated immediately to a lower level, preferably to a hospital. The following measures may be used:
• Oxygen inhalation at 6 L/minute initially and 2 L/minute thereafter | |
• Administration of dexamethasone 10 mg intravenously and 4 mg intramuscularly every 6 hours. Dexamethasone likely reduces capillary wall permeability, thus, preventing the exudation of fluid into the extracellular space. It improves cerebral edema but does not correct the physiological abnormalities associated with exposure to high altitude. Dexamethasone is more effective if combined with a hyperbaric oxygenation. | |
• Hyperbaric chamber. The patient may be transported down the mountain in a Gamow bag or placed in a hyperbaric chamber at a medical center after evacuation. Hyperbaric oxygen therapy may be used because it is effective for cerebral edema (19). |
High-altitude pulmonary edema. The patient must be evacuated immediately to a lower altitude, preferably to a hospital. The following measures may be used:
• Evacuation in a Gamow bag to a lower altitude. | |
• Oxygen inhalation at 2 L/minute. | |
• Calcium channel blockers and phosphodiesterase inhibitors are the drugs of choice for the management of high-altitude pulmonary edema. | |
• Dexamethasone is used for the treatment of cerebral edema. |
Acute mountain sickness is a relatively benign condition, but the more advanced forms with high-altitude cerebral edema and high-altitude pulmonary edema can be accompanied by severe morbidity, and death may result if prompt treatment measures are not instituted. Complications of acute mountain sickness include thromboembolic events and retinal hemorrhages.
In recent years, the number of travelers aged 60 years or older has been increasing. A systematic review of various studies related to the effect of old age on the risk of acute mountain sickness reported conflicting results, but old age does not seem to be a contraindication for traveling at high altitude (13). However, the information provided by these studies will help health professionals tailor their care of the elderly traveling to high altitudes.
Pregnant women can usually tolerate travel up to an altitude of 4000 m with no change in delivery of oxygen to the placenta. Risk to the fetus is insignificant during short-term exposure to moderate altitudes. Women with high-risk and late-term pregnancies are advised not to travel to altitudes higher than 2500 m.
K K Jain MD
Dr. Jain was a consultant in neurology and had no relevant financial relationships to disclose.
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