INCIDENCE AMS occurs in the setting of more gradual and less severe hypoxic insult than with acute hypoxic syndrome. Its incidence varies by location, depending on ease of access, rate of ascent, and sleeping altitude reached. A recent study at 2100 m (6900 ft) found a 25 percent incidence of AMS in physicians attending a continuing-education meeting in Colorado. Other studies at resorts between 2220 and 2700 m (7200 and 9000 ft, respectively) claimed an incidence between 17 and 40 percent, and a sleeping altitude of 2750 m (9000 ft) seemed to be a threshold for increased attack rate. 1 Approximately 40 percent of trekkers in Nepal on the path to Mt. Everest suffer AMS, while climbers on Mt. Rainier have the very-high incidence of 70 percent because of the rapidity of ascent.
SUSCEPTIBILITY In addition to rate of ascent and sleeping altitude, inherent factors determine individual susceptibility to acute mountain sickness. Factors identified so far are low hypoxic ventilatory response and low vital capacity. Age has little influence on incidence, with children being as susceptible as adults. Women are just as likely, if not more so, to develop mountain sickness but appear to have less pulmonary edema. Susceptibility to AMS is generally reproducible in an individual on repeated exposures. Persons living at intermediate altitudes of 1000 to 2000 m already are acclimatized partially and do much better than lowlanders upon ascent to higher altitudes. There is no relationship of susceptibility to AMS and physical fitness.
CLINICAL PRESENTATION The diagnosis of AMS is based on the setting, symptoms, and physical findings. The setting is rapid ascent of an unacclimatized person to 2000 m (6600 ft) or higher. Typically, the person on arrival feels lightheaded and slightly breathless, especially with exercise. One to six hours later, but sometimes delayed for one day or more (and especially after a night's sleep), the typical symptoms of mild AMS develop; they are similar to an alcohol hangover. The headache usually is described as bifrontal and worsened with bending over and the Valsalva maneuver. Gastrointestinal symptoms include anorexia, nausea, and sometimes vomiting, and the chief constitutional symptoms are lassitude and weakness. The person with AMS is often irritable and wants to be left alone. Sleepiness and a deep inner chill, also are common. If the illness progresses, the headache becomes more severe, and vomiting, oliguria, and increased dyspnea develop. Lassitude may progress to the victim requiring assistance for eating and dressing. The most severe form of AMS, high altitude cerebral edema (HACE), is heralded by onset of ataxia and altered level of consciousness; coma may ensue within 12 h if treatment is delayed. The diagnosis can be difficult in preverbal children. 2
Physical findings in mild AMS are nonspecific. Heart rate and blood pressure are variable, and usually in the normal range, although postural hypotension may be present. Localized rales are detectable in up to 20 percent of persons with AMS. Body temperature may be slightly elevated (up to 38.5°C) in AMS, and more so in high altitude pulmonary edema (HAPE) and HACE.3 Funduscopy reveals venous tortuosity and dilatation, and retinal hemorrhages are common over 5000 m or in those with pulmonary and cerebral edema. Fluid retention is a hallmark of AMS, in contrast to the usual diuresis of acclimatization, and may result in peripheral edema, especially of the face. Differential diagnosis in this setting includes hypothermia, carbon monoxide poisoning, pulmonary or CNS infection, dehydration, and exhaustion.
The natural history of AMS at a Colorado resort (3000 m or 10,000 ft) recently was documented. Mean duration of symptoms was 15 h, with a range to 94 h, despite the fact that one-half of those with symptoms self-medicated.4 At higher sleeping altitudes, the illness may last much longer, even weeks if untreated, and is more likely to progress to pulmonary or cerebral edema. Eight percent of those with AMS at 4243 m (14,000 ft) in Nepal developed cerebral or pulmonary edema, or both.
PATHOPHYSIOLOGY AMS is due to hypobaric hypoxia, but the exact sequence of events leading to illness is unclear. Figure191-1 offers a schema for the pathophysiology. The symptoms indicate a neurologic etiology; scans confirming cerebral edema have been obtained in persons severely ill. Whether the more common mild illness of headache, anorexia, and malaise is due to mild cerebral edema has yet to be confirmed, but seems likely. Two types of cerebral edema have been proposed. One is cytotoxic edema, due to failure of the sodium-potassium pump with subsequent intracellular accumulation of sodium and water. The other is a vasogenic edema, due to a leaky blood-brain barrier.
FIG. 191-1. High altitude illnesses. Central role of elevated sympathetic activity in the edemas of altitude: Hypoxemia ("Pa O2) elevates cerebral blood flow (CBF), which in turn raises cerebral capillary hydrostatic pressure (P cap) such that a transcapillary fluid shift occurs. The resulting high-altitude cerebral edema (or AMS) reduces brain compliance. Elevated intracranial pressure and distortion of CNS structures provokes elevation of peripheral sympathetic activity above levels normally produced by stimulation of peripheral chemoreflexes. Hypoxia raises pulmonary vascular resistance, which raises pulmonary artery pressure (P ap). Elevated sympathetic activity to the lungs decreases compliance of pulmonary arteries and provokes pulmonary venous constriction and increased capillary permeability. The precise influence of hypoxic pulmonary vascular responses combined with increased pulmonary sympathetic activity on pulmonary hydrostatic pressure is unclear. The relative importance of pulmonary capillary stress failure is uncertain (?). Only small elevations of P cap are required to cause large fluid fluxes if permeability is increased such that HAPE occurs. Increased sympathetic activity is associated with a neurogenic anti-natriuresis such that fluid retention and peripheral edema occur. Increased aldosterone from sympathetic stimulation of renin or from ACTH, and increased vasopressin from stimulation of chemoreflexes add to the tubular a-adrenergic antinatriuresis and opposes natriuretic effects from atrial natriuretic peptide (ANP) released by elevated central blood volume. However, ANP could contribute to peripheral edema, HAPE, or HACE. Renal fluid retention contributes to elevated P cap in lung, brain, and peripheral tissues. (From Krasney JA: A neurogenic basis for acute altitude illness. Med Sci Sport Exerc 26:195, 1994.)
No direct evidence for cytotoxic edema in humans at altitude has been reported, but a large shift of fluid into the total intracellular space, presumably including the brain, was demonstrated to take place over the first three days at altitude, when AMS occurs. The time required for fluid shift and overhydration of the brain may explain the time lag in onset of symptoms, which distinguishes AMS from acute hypoxia. In support of the vasogenic theory, white-matter brain edema on magnetic resonance imaging (MRI) recently was demonstrated in persons with high altitude cerebral edema, and it may also occur in AMS.5 The leaky blood-brain barrier is due either to loss of autoregulation and overperfusion or to hypoxia-induced increased permeability. The fact that corticosteroids so effectively treat AMS also supports the notion of vasogenic edema, since this is the only type of cerebral edema responsive to steroids. Further research is likely to reveal that brain swelling is due to both cytotoxic and vasogenic mechanisms.
The cerebral edema, interstitial pulmonary edema, peripheral edema, and the antidiuresis observed in AMS all point to an abnormality of water handling by the body. The mechanism is thought to be increased renin-angiotensin, aldosterone, and ADH in contrast to the normal ADH and aldosterone suppression at high altitude, and usual diuresis. A decrease in glomerular filtration also has been observed. The effectiveness of diuretics in prevention and treatment of AMS reinforces the importance of fluid retention in the pathophysiology. Increased sympathetic activation is thought to play a role in the pulmonary and renal circulations contributing to the pathophysiology6 (see Fig 191-1).
Relative hypoventilation due to a sluggish hypoxic ventilatory response is a characteristic of AMS-susceptible individuals and has been linked to fluid retention. Hypoventilation, of course, results in greater hypoxic stress and is equivalent to being at a higher altitude. Higher Pa CO2 and lower PaO2 also increases cerebral blood flow and aggravates brain swelling. Less hypocapnia also may reduce the stimulus for bicarbonate diuresis and aggravate fluid retention.
TREATMENT (Table 191-2) Descent and Oxygen The goals of treatment are to prevent progression, abort the illness, and improve acclimatization; early diagnosis is essential. Initial clinical presentation does not predict eventual severity, and all persons with AMS must be observed carefully for progression. The three principles of treatment are: (1) to not proceed to a higher sleeping altitude in the presence of symptoms; (2) to descend if symptoms do not abate or become worse despite treatment; and (3) to descend and treat immediately in the presence of a change in consciousness, ataxia, or pulmonary edema. Mild AMS is self-limited and generally improves with an extra 12 to 36 h of acclimatization if ascent is halted. Descent is the definitive treatment for all forms of altitude illness, although it is not always an option, nor always necessary. Remarkably, a drop in altitude of only 500 to 1000 m usually is effective promptly. Evacuation to a hospital or to sea level is unnecessary except in the most severe cases. To simulate descent, portable hyperbaric bags are being used in various locations to treat AMS. The patient is inserted into the fabric chamber, and a pressure of 2 psi is achieved by means of a manual or automated pump; the pressure is equivalent to a drop in altitude of 1500 m (5000 ft). A valve system creates sufficient ventilation to avoid CO 2 accumulation or O2 depletion.
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