One topic of hot conversation given the recent release of the movie “Everest” is that of acute mountain sickness. In the movie they recount numerous instances where the climbers heading for the 8848m high summit experience confusion, a hacking productive cough, vision problems and some serious frostbite. But what exactly is this acute mountain sickness (AMS) business?
The exact pathophysiology of AMS is not completely worked out, but the best way to think about it is a pathologic, disordered response of the body and brain to the specific situation of hypobaric hypoxia. A previous study performed found that AMS occurred quickest and most reliably in hypobaric hypoxia (vs. normobaric hypoxia or hypobaric normoxia), but did occur at a slower rate in normobaric hypoxia. One might postulate then that the hypoxia part of the equation is most important, and the hypobaria has an additive effect. In general, the correct response of the body in this environment is to increase the respiratory rate (via carotid body stimulation by hypoxia) and diuresis in order to hemoconcentrate and carry more oxygen per mL blood. Eventually, the body produces increased amounts of red blood cells and hemoconcentrates in this way. However, in persons predisposed to AMS, studies have found either profoundly impaired respiratory responses and/or diuresis. Use of alcohol or sleep aids have been found to further depress the respiratory response and can increase the severity of AMS. In one study, all subjects with AMS were found to have increased levels of serum epinephrine (due to increased activation of the sympathetic nervous system (SNS)), and this was thought to contribute to vasoconstriction of the renal arterioles, impairing their ability to diuresis properly. The increase in fluid load on the body leads to both vasogenic and intracellular edema, which is thought to be behind an increase in intracranial pressure (ICP) that is believed to contribute, if not cause, some of the various symptoms of AMS. ICP is also affected by the relative increase in cerebral blood flow that occurs early in an ascent due to hypoxia induced vasodilation. The role of SNS activation in AMS is further supported by a study that found that symptoms of AMS were lessened with administration of a beta-adrenergic blocker prophylactically.
The most common symptom experienced in AMS is high altitude headache, which is more intense both at night and during exertion. The second most common symptom reported is insomnia or sleep disturbance that is disproportional to the days activities and expected loss of sleep due to environmental stressors. Other symptoms that can occur include GI distress (mainly nausea), fatigue and dizziness. It is experienced mainly at altitudes > 2500m and the incidence depends on rate of ascent, final altitude achieved, exertion and a person’s susceptibility.
Currently, AMS can only be diagnosed clinically and there are no objective tests used for diagnosis. Multiple studies in the past have looked at using ultrasound to monitor the optic nerve sheath diameter as a surrogate for increased ICP, and see if it correlates to the severity or incidence of AMS symptoms. Although the studies did show a correlation of both increasing optic nerve sheath diameter and severity of AMS symptoms with increasing altitude, a direct comparison of optic nerve sheath diameter to AMS severity score showed great intersubject variability as well as great overlap. Therefore, currently this cannot be used as a reliable measure or objective test to confirm or refute the diagnosis of AMS in a patient.
What is the best way to treat a patient diagnosed with AMS? First-line for these patients are Oxygen (35% at 4300m) and descent >300m as soon as possible. Pharmacological management includes both acetazolamide and glucocorticoids. Acetazolamide (a carbonic anhydrase inhibitor) is used both for prophylaxis and treatment of AMS, acting both as a respiratory stimulant, a diuretic and an inhibitor of CSF production. Glucocorticoids are mainly reserved for the more severe forms of AMS and high altitude cerebral edema.