HIGH-ALTITUDE ILLNESS
EPIDEMIOLOGY
• Altitude illness is likely to occur at >2500 m and has occurred even at 1500–2500 m.
• 100 million persons travel to high-altitude locations each year.
CLINICAL SYNDROMES
Acute Mountain Sickness (AMS), Including HACE
AMS represents a clinical continuum of neurologic disease, of which high-altitude cerebral edema (HACE) is the most severe form.
• Risk factors: rate of ascent, history of high-altitude illness, exertion
– Lack of physical fitness is not a risk factor.
– Exposure to high altitude within the preceding 2 months may be protective.
– Pts >50 years old may be less likely to develop AMS than younger pts.
• Pathophysiology: Although the exact mechanisms remain unknown, hypoxic cerebral vasodilatation and altered permeability of the blood-brain barrier contribute to cerebral edema in AMS.
• Clinical manifestations
– Nonspecific symptoms (headache, nausea, fatigue, and dizziness) with a paucity of physical findings, developing 6–12 h after ascent to a high altitude
– HACE: encephalopathy whose hallmarks are ataxia and altered consciousness with diffuse cerebral involvement but generally without focal neurologic deficits
• Retinal hemorrhages and, less commonly, papilledema may be seen.
• Retinal hemorrhages occur frequently at ≥5000 m irrespective of the presence of symptoms of AMS or HACE.
• Prevention: Gradual ascent with acclimation is the best measure to prevent AMS.
– At >3000 m, a graded ascent of ≤300 m each day is recommended.
– Taking an extra day for acclimation after 3 days of gain in sleeping altitude is helpful.
– Pharmacologic prophylaxis is warranted when the pt has a history of AMS or when flight to a high-altitude location is required.
• Acetazolamide (125–250 mg PO bid) or dexamethasone (8 mg/d in divided doses), administered 1 day before ascent and continued for 2–3 days, is effective.
• Gingko biloba is ineffective for prevention of AMS.
TREATMENT Acute Mountain Sickness
See Table 31-1.
TABLE 31-1 MANAGEMENT OF ALTITUDE ILLNESS
• Prognosis: With AMS, the pt may reascend gradually to a higher altitude after symptoms abate. In HACE, reascent after a few days is not advisable.
High-Altitude Pulmonary Edema (HAPE)
HAPE is primarily a pulmonary problem and not necessarily preceded by AMS.
• Risk factors: rapid rate of ascent, history of HAPE, respiratory tract infections, cold environmental temperatures, male sex, abnormalities of the cardiopulmonary circulation leading to pulmonary hypertension (e.g., patent foramen ovale, mitral stenosis, 1° pulmonary hypertension)
• Pathophysiology: noncardiogenic pulmonary edema characterized by patchy pulmonary vasoconstriction that leads to overperfusion in some areas. Hypoxia-induced impairment of nitric oxide release may play a role in vasoconstriction.
• Clinical manifestations: reduction in exercise tolerance greater than that expected at the given altitude; dry, persistent cough with blood-tinged sputum; tachypnea and tachycardia at rest
– Chest x-rays may reveal patchy or localized opacities or streaky interstitial edema.
– Kerley B lines or a bat-wing appearance typically is not seen.
• Prevention
– Gradual ascent with acclimation is the best measure to prevent HAPE.
– Pharmacologic prophylaxis with sustained-release nifedipine (30 mg PO qd or bid) is effective for pts who have a history of HAPE or who must ascend rapidly.
TREATMENT High-Altitude Pulmonary Edema
See Table 31-1.
• Prognosis: Pts may reascend slowly a few days after symptoms resolve. The architecture of the lung is well preserved, with rapid reversibility of abnormalities.
Other High-Altitude Problems
• Sleep impairment
– Increased periodic breathing and changes in sleep architecture (e.g., increased time in lighter sleep stages) lead to poor-quality sleep.
– Acetazolamide (125 mg PO qhs) decreases hypoxemic episodes and alleviates sleeping disruptions caused by excessive periodic breathing.
• GI issues: abdominal bloating, distension, and excessive flatus can result from decreased atmospheric pressure. Diarrhea is not associated with high altitude but may indicate bacterial or parasitic infection, which is common in many high-altitude locations in the developing world.
• High-altitude cough: Hypoxia and bronchoconstriction (due to cold and exercise) lead to a debilitating cough that is sometimes severe enough to cause rib fractures, especially above 5000 m.
• High-altitude neurologic events unrelated to “altitude illness”: Even without other symptoms of AMS, transient ischemic attacks, strokes, subarachnoid hemorrhage, transient global amnesia, delirium, and cranial nerve palsies can occur, particularly in pts with few traditional risk factors for these conditions.
PREEXISTING MEDICAL CONDITIONS
Few medical conditions influence susceptibility to altitude illness, and no evidence-based guidelines exist regarding the advisability of high-altitude travel by pts with these conditions.
• Cardiac disease: Pts with ischemic heart disease, previous myocardial infarction, angioplasty, and/or bypass surgery should have an exercise treadmill test. A strongly positive treadmill test is a contraindication for high-altitude trips. Pts with poorly controlled arrhythmias also should avoid high-altitude travel.
• Asthma: Severely asthmatic pts should be cautioned against ascending to high altitudes.
• Pregnancy: Although there are no relevant data, it is unadvisable for pregnant women to travel to altitudes >3000 m, given the steep drops in oxygen saturation at these altitudes.
• Sickle cell disease: High altitude is one of the rare environmental exposures that occasionally provoke a crisis in persons with the sickle cell trait, even at 2500 m.
• Diabetes mellitus: Trekking at high altitudes may enhance sugar uptake. Pts taking insulin may require lower doses on trekking/climbing days than on rest days.
• Chronic lung disease: Pts with preexisting pulmonary hypertension should be discouraged from ascending to high altitudes. If such travel is necessary, treatment with sustained-release nifedipine (20 mg PO bid) should be considered.
• Chronic kidney disease: Acetazolamide should be avoided by pts with preexisting metabolic acidosis and by pts with a glomerular filtration rate (GFR) ≤10 mL/min; the dose of acetazolamide should be adjusted if the GFR is ≤50 mL/min.
DECOMPRESSION SICKNESS (DCS)
DCS is caused by the formation of bubbles from dissolved inert gas (usually nitrogen) during or after ascent (decompression) from a compressed gas dive.
• Incidence: 1:10,000 recreational dives. Risk factors are deeper and longer dives and too rapid of an ascent.
• Pathophysiology: Bubbles may form within tissues themselves, leading to symptoms by mechanical distraction of pain-sensitive or functionally-important structures. Bubbles also appear in the venous circulation where they can incite inflammatory and coagulation cascades, damage endothelium, activate formed elements of blood such as platelets, and cause symptomatic vascular obstruction (also in arterial beds when a patent foramen ovale is present).
• Clinical manifestations: Most cases present with mild symptoms of pain, fatigue, and minor neurologic illnesses such as patchy paresthesias. Pulmonary and cardiovascular manifestations can be life-threatening including dyspnea, chest pain, arrhythmia, coagulopathy, and hypotension.
• Diagnosis
– Based on integration of findings and examination of the dive profile while correlating relationship of symptoms temporally to the dive.
TREATMENT Decompression Sickness
Horizontal positioning to prevent bubble entry into the cerebral circulation, IV fluids, and 100% oxygen. Definitive treatment with hyperbaric oxygen administered in a compression chamber with stepwise decompression over variable periods adjusted to treatment response. If recovery is complete, diving can be resumed after a period of at least 1 month; if residual symptoms exist, diving is discouraged.
For a more detailed discussion, see Basnyat B, Tabin G: Altitude Illness, Chap. e51; and Bennett MH, Mitchell SJ: Hyperbaric and Diving Medicine, Chap. e52 in HPIM-18.