High-Altitude Travel - Clinical Tree

Increasing numbers of people are traveling to high altitude for work or pleasure. While the rewards of such travel are often great and include opportunities to see places of great beauty or historical and cultural significance, to accomplish lifelong objectives, or to simply have an enjoyable vacation, there are risks associated with such travel. Unacclimatized lowlanders are at risk for one of several forms of acute altitude illness within the first several days of ascent, while individuals with underlying medical problems may be at risk for worsening control of those problems or other complications.

This chapter provides information for counseling individuals seeking advice about how to prevent such problems. After defining the term “high altitude” and describing features of the high-altitude environment and the physiologic responses to hypobaric hypoxia, the chapter describes a general approach to three types of patients who may present for evaluation: the traveler who has never been to high altitudes before and seeks advice on ensuring a safe trip, the returning traveler who had a problem on a prior trip and seeks advice on how to avoid repeating such problems in the future, and the potentially at-risk traveler with underlying medical problems that may be exacerbated by hypobaric hypoxia or may predispose to acute altitude illness.

What Constitutes “High Altitude”?

Although there are no firm definitions, the term “high altitude” generally refers to regions located above 1500 m (~5000 ft) in elevation. While some physiologic responses to hypoxia begin just above this threshold, acute altitude illness does not generally occur until an individual ascends above 2340 m (~8000 ft). For most healthy individuals, it is only when traveling above this latter threshold that the altitude should be taken into account with trip planning. For individuals with underlying medical conditions, however, the effect of the altitude may need to be considered at lower elevations. Regardless of underlying health status, the further an individual travels above these thresholds, the greater the potential for altitude-related problems.

The majority of high-altitude travelers will not ascend above 5500-6500 m, a range that includes common trekking destinations such as Mt. Kilimanjaro (5895 m) and Everest base camp (5350 m). Select individuals, typically those engaged in mountaineering expeditions, do ascend above this range and are exposed to extreme degrees of hypoxia that pose significant physiologic challenges and markedly increase the risk of acute altitude illness if proper acclimatization measures are not undertaken.

The Environment at High Altitude

The defining environmental feature at high altitude is the nonlinear decrease in barometric pressure with increasing elevation. This change, which is more pronounced at higher latitudes and during the winter months, leads to decreased ambient partial pressure of oxygen (PO ₂ ) that, in turn, lowers the PO ₂ throughout the body and triggers several important physiologic responses (described later).

Other important environmental changes include lower air density, increased ultraviolet (UV) light exposure, decreased humidity, and decreased ambient temperature. The lower air density is likely too small to be of clinical significance, while the increased UV exposure decreases the time necessary to develop sunburn and ultraviolet keratitis (“snow blindness”), particularly with travel on snow-covered terrain. The decrease in humidity increases insensible water losses through the respiratory tract and the risk of dehydration, particularly when individuals engage in physical exertion, while the decrease in temperature may increase the risk of hypothermia and frostbite depending on the full range of environmental conditions at the time of travel.

Air quality often improves in the mountains, but this is not always the case. Greater solar radiation increases smog potential, while extensive valley systems can trap pollutants during temperature inversions, particularly when near urban centers. Finally, wood and yak-dung stoves are common heat sources in rural areas of the Himalaya and elsewhere, leading to poor air quality when these stoves are in high use.

Physiologic Responses to Hypobaric Hypoxia

The decrease in PO ₂ at all points along the oxygen transport cascade from inspired air to the alveolar space, arterial blood, and tissues causes physiologic responses across multiple organ systems, which facilitates adaptation to the hypobaric hypoxia ( Table 10.1 ). Some of the responses, such as the increase in minute ventilation, start within minutes of exposure, while other responses, such as erythropoiesis, take several weeks before their full effect is realized. The magnitude of these responses varies considerably between individuals, and this variability plays a large role in determining tolerance of hypobaric hypoxia and susceptibility to acute altitude illness.

TABLE 10.1

Physiologic Responses to Hypobaric Hypoxia

System	Responses
Pulmonary responses	Arterial hypoxemia triggers increased peripheral chemoreceptor output, leading to an increase in minute ventilation and a respiratory alkalosis. The respiratory alkalosis blunts the initial ventilatory responses. With continued time at high altitude, minute ventilation rises further due to renal compensation for the respiratory alkalosis and increased sensitivity of the peripheral chemoreceptors. Alveolar hypoxia triggers hypoxic pulmonary vasoconstriction, leading to an increase in pulmonary vascular resistance and pulmonary artery pressure.
Cardiac responses	Cardiac output increases, largely due to an increase in heart rate. Stroke volume declines due to a decrease in plasma volume. Myocardial contractility is preserved. Systemic blood pressure increases to a variable extent.
Renal responses	Variable increase in diuresis and natriuresis following ascent leads to a decrease in circulating plasma volume. Arterial hypoxemia triggers increased secretion of erythropoietin (EPO) within 24-48 hours of ascent. There is an increase in bicarbonate excretion, as compensation for the acute respiratory alkalosis.
Hematologic responses	There is an initial increase in hemoglobin concentration and hematocrit due to reduction in plasma volume. Over days to weeks, there are further increases in red blood cell mass, hemoglobin concentration, and hematocrit due to increased EPO concentrations.

Because of these environmental changes and physiologic responses to hypobaric hypoxia, high-altitude travelers are at risk for a range of problems they might not experience at lower elevations and may present for evaluation with one of several possible concerns:

The altitude-naïve traveler who has never ascended to high altitude before and seeks advice on how to ensure a safe trip
The returning traveler who had problems on a prior high-altitude trip and seeks information about what happened and how to prevent such problems in the future
The potentially at-risk traveler who has underlying medical problems that may worsen at high altitude or predispose to acute altitude illness.

The remainder of this chapter describes an approach to each of these situations.

The Altitude-Naïve Traveler

Many travelers have never been to high altitude and seek advice about what to expect in this environment and how to prevent problems. Alternatively, individuals who have traveled to high altitude before without difficulty may be going to significantly higher elevations and are now concerned about similar issues. Effective counseling of such travelers encompasses a range of topics described in detail below.

Normal Responses to High Altitude

Even if they avoid acute altitude illness, individuals feel different at high altitude than at lower elevations as a result of the environmental changes and physiologic responses to hypobaric hypoxia. These differences ( Table 10.2 ) should be reviewed as part of pre-trip counseling, as this can prevent misinterpretation of normal responses as evidence of illness and facilitate identification of those individuals who are truly becoming ill.

TABLE 10.2

How Travelers Feel Different at High Altitude Compared with the Altitude of Residence

Heart rate at rest and with any level of exertion higher than at altitude of residence
Increased respiratory rate and tidal volume
More frequent sighs
Increased frequency of urination
Dyspnea on exertion that resolves quickly with rest
Difficulty sleeping, including frequent arousals, insomnia, vivid dreams
Transient lightheadedness on rising to a standing position

High-altitude travelers who are otherwise well commonly report poor sleep quality, insomnia, vivid dreams, and frequent awakenings. A major contributor to these problems is periodic breathing, in which periods of crescendo-decrescendo breathing movements are punctuated by apneas lasting from 5 to 20 seconds. While overall sleep quality tends to improve over time, periodic breathing can persist or worsen during long stays at high altitude.

Exercise is also challenging at high altitude. At any given level of work, heart rate and minute ventilation are higher than at sea level, and, unlike at sea level, arterial oxygen saturation decreases with progressive exercise. Even following extensive pre-trip physical training, individuals experience more intense breathlessness during exertion, particularly during the first few days at altitude. Importantly, however, on stopping to rest, dyspnea typically resolves within a short time (~1-2 min).

Recognition of Acute Altitude Illness

All high-altitude travelers should be able to recognize the three main forms of acute altitude illness: acute mountain sickness (AMS), high-altitude cerebral edema (HACE), and high-altitude pulmonary edema (HAPE). The clinical features of these diseases are described in Table 10.3 , while information about their underlying pathophysiology is described in several excellent reviews listed at the end of this chapter. Of these entities, AMS is by far the most common and the most likely to be encountered during high-altitude travel. HACE and HAPE are uncommon but potentially fatal if not recognized promptly and warrant attention in pre-travel counseling.

TABLE 10.3

Clinical Features and Management of Acute High-Altitude Illnesses

Acute Altitude Illness	Timing and Altitude of Onset	Clinical Features	Prevention	Treatment
Acute mountain sickness (AMS)	Seen at altitudes ≥2340 m Altitude of onset varies significantly between individuals Subacute onset of symptoms within 6-10 hr of ascent to a given elevation	Headache plus one or more of the following: nausea, vomiting, lethargy, sustained light-headedness Normal neurologic exam and normal mental status	Slow ascent (above 2500 m, limit increases in sleeping elevation to 500 m/day) Avoid overexertion Acetazolamide or dexamethasone with moderate- to high-risk ascent profiles	Stop ascending Acetaminophen or NSAIDs for headache Antiemetics Mild to moderate illness: acetazolamide Severe cases: dexamethasone Descend if symptoms do not improve in 1-2 days or worsen on appropriate treatment Further ascent possible if symptoms resolve
High-altitude cerebral edema (HACE)	Seen at altitudes ≥3000 m, with increasing incidence at higher elevations Subacute onset of symptoms. Sudden onset of symptoms should prompt search for alternative causes	Preexisting AMS or concurrent HAPE symptoms (not universally present) Ataxia, altered mental status Severe lassitude, somnolence, coma Focal neurologic deficits uncommon and should prompt consideration of other diagnoses Potentially fatal if not recognized and treated promptly	Slow ascent Avoid overexertion Acetazolamide or dexamethasone with moderate- to high-risk ascent profiles	Descend until symptoms resolve If descent not possible, supplemental oxygen or a portable hyperbaric chamber Dexamethasone
High-altitude pulmonary edema (HAPE)	Seen at altitudes ≥2500 m, with cases documented at lower elevations in patients with history of pulmonary vascular diseases Subacute onset within 2-5 days of ascent	Mild: dyspnea and arterial O ₂ desaturation out of proportion to that seen in normal individuals with similar ascent rates at a given elevation; decreased exertional tolerance, dry cough Severe: dyspnea with mild exertion or at rest; cough with pink, frothy sputum; cyanosis May see concurrent signs or symptoms of AMS or HACE but not universally present Potentially fatal if not recognized promptly	Slow ascent Avoid overexertion Nifedipine for individuals with prior history of HAPE (alternative: phosphodiesterase inhibitors)	Descend until symptoms resolve Avoid heavy exertion on descent If descent not possible, supplemental oxygen or a portable hyperbaric chamber Nifedipine or phosphodiesterase inhibitor (may not be necessary if supplemental oxygen available) Avoid concurrent use of nifedipine and phosphodiesterase inhibitor

NSAIDs, Nonsteroidal anti-inflammatory drugs.

For individuals ascending to and remaining at a given elevation, the risk for these problems lasts up to 5 days following ascent. Individuals ascending to steadily higher elevations, as on a climbing expedition, remain at risk until they begin to descend from their maximum elevation, at which point the risk of illness decreases significantly and eventually disappears entirely as descent continues.

A challenge in recognizing AMS is the nonspecific nature of the symptoms, as headache can be seen as a result of dehydration, carbon monoxide intoxication from cooking in a poorly ventilated tent, and other causes. Similarly, symptoms of HAPE can be present in other respiratory disorders such as pneumonia and pulmonary embolism. However, while it is always important to consider a broad differential diagnosis, compatible symptoms and signs arising following ascent should be considered altitude illness until proven otherwise.

Risk Factors for Acute Altitude Illness

The primary reason individuals develop acute altitude illness is they ascend too high, too fast, where “fast” refers to the number of meters ascended per day rather than the walking pace itself. For example, an individual ascending to 5000 m over 3 days and remaining at that elevation is more likely to get sick than an individual completing the same ascent over 7 days.

There is an important interaction between the altitude attained and the time spent at that altitude that affects risk; individuals who ascend rapidly but descend quickly after reaching the summit may avoid altitude illness, whereas individuals who complete the same ascent at the same rate but remain on the summit for many hours face a higher risk of problems.

There is considerable inter-individual variability in susceptibility to acute altitude illness, such that some individuals acclimatize well and tolerate seemingly fast ascents while others develop problems even with appropriate ascent profiles. While susceptibility to altitude illness is likely a multigenetic trait, the specific genetic polymorphisms have not been identified, and we lack a simple, reliable means of predicting which travelers face risk following ascent.

A common misperception is that being in good physical condition protects against acute altitude illness. To the contrary, highly fit endurance athletes are just as susceptible to AMS, HACE, and HAPE as unconditioned individuals and must adhere to the same principles of altitude illness prevention.

Prevention of Acute Altitude Illness

Effective prevention relies on a combination of both nonpharmacologic and pharmacologic measures.

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