Chapter 2 The Pre-Travel Consultation Self-Treatable Conditions
For the Record: A History of the Definition & Management of Altitude Illness
As explorers began to challenge the higher parts of the Earth, first in Europe in 1786 with the ascent of Mont Blanc and later in Asia and South America, the high-altitude environment occasionally proved unexpectedly fatal. Deaths in otherwise healthy young men were attributed to “heart failure” or “pneumonia,” and a specific syndrome associated with rapid ascent was not suspected. The first detailed clinical descriptions of high-altitude pulmonary edema (HAPE) and high-altitude cerebral edema (HACE) were published in 1913 by Thomas Ravenhill, based on his work with high-altitude miners in Chile. Scottish physiologist A. M. Kellas also provided detailed descriptions of “mountain sickness” in papers that were a prelude to the British attempts on Mount Everest in the 1920s.
These early descriptions were overlooked until the syndromes of altitude illness were rediscovered in the early 1960s. Herbert Hultgren, a Stanford cardiologist, documented HAPE in the Andes in 1959. A year later, Charles Houston, a physician and mountain climber noted for an epic attempt on K2 in 1953, documented a case of pulmonary edema in a healthy 21-year-old backcountry skier in Aspen, Colorado, in which a cardiac cause was definitively ruled out. The first modern description of HACE is credited to Fitch in 1964. Originally, the spectrum of altitude illness was thought to include 3 syndromes: acute mountain sickness (AMS), along with HAPE and HACE. In recent times, however, AMS is understood to represent early HACE, although the term is still used. All the syndromes are classified under the term “altitude illness.”
China, having annexed Tibet in the 1950s, invaded a remote corner of northern India in 1962 at altitudes of 15,000–18,000 ft. Chinese troops, attacking from the Tibetan plateau, had no problems with the altitude, but the Indian troops transported rapidly to those heights experienced considerable rates of altitude illness. The Indian physician treating these troops, Inder Singh, reported on almost 2,000 cases of altitude illness during the brief war. One of his key observations was that the severity of illness was not related to the altitude at which the symptoms began. Illness could be just as severe at 11,000 ft as at 18,000 ft. His insightful 1969 paper in the New England Journal of Medicine is well worth reading today.
The advent of high-altitude trekking in Nepal in the late 1960s and early 1970s opened up a new group of people—nonmountaineers—to the risk of altitude illness. The trekking route to Mount Everest involves walking on trails that range in altitude from 5,000 to 18,000 ft (1,525 to 5,500 m). The technical ease encouraged trekkers to ascend faster than they could acclimatize, and an estimated 5–10 people per year died of altitude illness in the Everest region in the early 1970s. In 1974, Dr. Peter Hackett trekked to Mount Everest and stayed to run an aid post at 14,000 ft on the way to Everest Base Camp. He remained in Nepal for 18 months and brought back detailed correlations between the risk of altitude illness and the rate of ascent.
At that time, trekkers had the choice of walking over several high passes on the way to Everest Base Camp, starting from close to Kathmandu, or flying into Lukla, an airstrip located at 9,000 ft. The trekkers who walked experienced altitude illness at a rate of 42%, while those who flew were ill at a rate of 60%. Dr. Hackett recommended 2 extra acclimatization days in the upper portions of the trek, which decreased the rate of altitude illness to <40%. His recommendations are still the basis of the itineraries for trekking to Everest Base Camp, even though the rate of altitude illness on this schedule remains approximately 35%.
In addition to trekkers walking into high-altitude destinations, travelers increasingly fly to a number of cities where they risk altitude illness, including Cusco, Peru (11,150 ft, 3,400 m); Lhasa, Tibet (12,000 ft, 3,660 m); and La Paz, Bolivia (12,400 ft, 3,780 m). Tourists who fly from a low altitude to any of these destinations should consider taking acetazolamide to help prevent altitude illness.
In the 1930s, the antibiotic sulphanilamide was noted to cause metabolic acidosis and compensatory hyperventilation, an effect later attributed to inhibition of renal carbonic anhydrase. Another sulfonamide, acetazolamide, was a more potent carbonic anhydrase inhibitor. Inducing healthy people to breathe more was postulated to improve acclimatization to altitude, and in an article published in 1968, acetazolamide was shown to prevent altitude illness. To this day, acetazolamide remains the best drug to prevent altitude illness.
Because of variations in individual susceptibility and the modern tendency to take short trips that do not permit gradual acclimatization, altitude illness will continue to occur in travelers. However, there is no longer any reason why high-altitude sojourners should die of altitude illness. Education on acclimatization, recognition of symptoms, and appropriate response can ensure that an otherwise inconvenient and uncomfortable illness does not turn into a tragedy.
- Forwand SA, Landowne M, Follansbee JN, Hansen JE. Effect of acetazolamide on acute mountain sickness. N Engl J Med. 1968 Oct 17;279(16):839–45.
- Hackett PH, Rennie D, Levine HD. The incidence, importance, and prophylaxis of acute mountain sickness. Lancet. 1976 Nov 27;2(7996):1149–55.
- Singh I, Khanna PK, Srivastava MC, Lal M, Roy SB, Subramanyam CS. Acute mountain sickness. N Engl J Med. 1969 Jan 23;280(4):175–84.
- Swenson ER. Carbonic anhydrase inhibitors and ventilation: a complex interplay of stimulation and suppression. Eur Res J. 1998 Dec;12(6):1242–7.
- West JB. High life: a history of high-altitude physiology and medicine. New York: Oxford University Press; 1998.
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