Altitude Illness¶
Chapter 475 | Harrison's 22e · Parts 15-16 – Genetics, Genomics & Precision Medicine
Detailed clinical reference synthesised from Harrison's Principles of Internal Medicine, 22nd Edition
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[PAGE 3754] 3754 PART 15 Disorders Associated with Environmental Exposures Implementing Actions Strengthening Public Implementing Policies and Political Support for Adaptation for Mitigation (Secondary Prevention) (Primary Prevention) Improving the Public’s Implementing Health Understanding of Climate Policymaking Process Change Adaptation Also supports Energy Policy Planning Healthy and GHG mitigation Building Movements for Sustainable Built Transportation Policy Addressing Climate Environments Change Agriculture Policy Promoting Nature-Based Promoting Climate Justice Climate Solutions* Health Impacts Climate Change Heat-related Disorders Increased Greenhouse Gas Levels Temperature Rise Respiratory Disorders Fossil Fuel Combustion Carbon Dioxide Sea-level Rise Vectorborne Diseases Other Greenhouse Gas Sources Methane Hydrologic Extremes: Waterborne Diseases Loss of Carbon Sinks Nitrous oxide • Droughts Food Insecurity & - Floods Malnutrition Other GHGs - Wildfires Mental Health Impacts Violence FIGURE 474-11 Conceptual framework of climate change and its health impacts. (Reproduced with permission from JA Patz, BS Levy.) ■ FURTHER READING Caminade C et al: Global risk model for vector-borne transmission of 475 Altitude Illness Zika virus reveals the role of El Niño 2015. Proc Natl Acad Sci USA 114:119, 2017. Buddha Basnyat, Geoffrey Tabin, Steven Roy Colón-González FJ et al: The effects of weather and climate change on dengue. PLoS Negl Trop Dis 7:e2503, 2013. Glass GE et al: Satellite imagery characteristics local animal reservoir ■ EPIDEMIOLOGY populations of Sin Nombre virus in the southwestern United States. Mountains cover one-fifth of the earth’s surface; 140 million people Proc Natl Acad Sci USA 99:16817, 2002. live permanently at altitudes ≥2500 m, and 100 million people travel to Goren A et al: The emergence and shift in seasonality of Lyme bor- high-altitude locations each year. Skiers in the Alps or Aspen; tourists reliosis in Northern Europe. Proc Biol Sci 290:20222420, 2023. to La Paz, Ladakh, or Lahsa; religious pilgrims to Kailash-Manasarovar Levy BS, Patz JA (eds): Climate Change and Public Health, 2nd ed. or Gosainkunda; trekkers and climbers to Kilimanjaro, Aconcagua, or Oxford University Press, 2024. Everest; miners working in high-altitude sites in South America; and Mora C et al: Over half of known human pathogenic diseases can be military personnel deployed to high-altitude locations are all at risk aggravated by climate change. Nat Climate Change 12:869, 2022. of developing acute mountain sickness (AMS), high-altitude cerebral Ogden NH: Risk maps for range expansion of the Lyme disease vec- edema (HACE), high-altitude pulmonary edema (HAPE), and other tor, Ixodes scapularis, in Canada now and with climate change. Int J altitude-related problems. AMS is the benign form of altitude illness, Health Geogr 7:1, 2008. whereas HACE and HAPE are life-threatening. Altitude illness is likely Paaijmans KP et al: Temperature-dependent pre-bloodmeal period to occur above 2500 m but has been documented even at 1500–2500 m. and temperature-driven asynchrony between parasite development In the Mount Everest region of Nepal, ~50% of trekkers who walk to and mosquito biting rate reduce malaria transmission intensity. PLoS altitudes >4000 m over ≥5 days develop AMS, as do 84% of people who One 8:e55777, 2013. fly directly to 3860 m. The incidences of HACE and HAPE are much Patz JA et al: Impact of regional climate change on human health. lower than that of AMS, with estimates in the range of 0.1–4%. Finally, Nature 438:310, 2005. reentry HAPE, which in the past was generally limited to highlanders Patz JA et al: Climate change and waterborne disease risk in the Great (long-term residents of altitudes >2500 m) in the Americas, is now Lakes region of the U.S. Am J Prev Med 35:451, 2008. being seen in Himalayan and Tibetan highlanders—and often mis- Ryan SJ et al: Warming temperatures could expose more than 1.3 billion diagnosed as a viral illness—as a result of recent rapid air, train, and new people to Zika virus risk by 2050. Glob Change Biol 27:84, 2021. motorable-road access to high-altitude settlements. Trtanj J et al: Climate impacts on water-related illness, in The Impacts of Climate Change on Human Health in the United States: A Scientific Assessment. U.S. Global Change Research Program, Washington, DC, ■ PHYSIOLOGY 2016, pp 157–188. Ascent to a high altitude subjects the body to a decrease in barometric pressure that results in a decreased partial pressure of oxygen in the inspired gas in the lungs. This change leads in turn to less pressure, driving oxygen diffusion from the alveoli and throughout the oxygen cascade. A normal initial “struggle response” to such an ascent includes increased ventilation—the cornerstone of acclimatization—mediated
[PAGE 3755] Altitude Illness 3755 CHAPTER 475 by the carotid bodies. Hyperventilation may cause respiratory alkalosis phenomenon at high altitude—is associated with AMS. Debilitating and dehydration. Respiratory alkalosis may be extreme, with an arterial fatigue consistent with severe AMS on descent from a summit is an blood pH of >7.7 (e.g., at the summit of Everest). Alkalosis may depress important risk factor for death in mountaineers. A prospective study the ventilatory drive during sleep, with consequent periodic breathing involving trekkers and climbers who ascended to altitudes between and hypoxemia. During early acclimatization, renal suppression of car- 4000 and 8848 m showed that high oxygen desaturation and low venti- bonic anhydrase and excretion of dilute alkaline urine combat alkalosis latory response to hypoxia during exercise are independent predictors and tend to bring the pH of the blood to normal. Other physiologic of severe altitude illness. However, because there may be a large overlap changes during normal acclimatization include increased sympathetic between groups of susceptible and nonsusceptible individuals, accu- tone; increased erythropoietin levels, leading to increased hemoglobin rate cutoff values are hard to define. Prediction is made more difficult levels and red blood cell mass; increased tissue capillary density and because the pretest probabilities of HAPE and HACE are low. Neck mitochondrial numbers; and higher levels of 2,3-bisphosphoglycerate, irradiation or surgery damaging the carotid bodies, respiratory tract enhancing oxygen utilization. Even with normal acclimatization, how- infections, and dehydration appear to be other potential risk factors ever, ascent to a high altitude decreases maximal exercise capacity (by for altitude illness. Unless guided by clinical signs and symptoms, pulse ~1% for every 100 m gained above 1500 m) and increases susceptibility oximeter readings alone on a trek should not be used to predict AMS. to cold injury due to peripheral vasoconstriction. If the ascent is made Pathophysiology Hypobaric hypoxia is the main trigger for alti- faster than the body can adapt to the stress of hypobaric hypoxemia, tude illness. In established AMS, raised intracranial pressure, increased altitude-related disease states can result. sympathetic activity, relative hypoventilation, fluid retention and ■ GENETICS redistribution, and impaired gas exchange have all been well noted; Hypoxia-inducible factor, which acts as a master switch in high- these factors may play an important role in the pathophysiology of altitude adaptation, controls transcriptional responses to hypoxia AMS. Severe hypoxemia can lead to a greater than normal increase throughout the body and is involved in the release of vascular in cerebral blood flow. However, the exact mechanisms underlying endothelial growth factor (VEGF) in the brain, erythropoiesis, and AMS and HACE are unknown. Evidence points to a central nervous other pulmonary and cardiac functions at high altitudes. In particular, system process. Magnetic resonance imaging (MRI) studies have sug- the gene EPAS1,
Figures & Illustrations¶
Reproduced from Harrison's 22nd Edition.
Figure 1¶
Caption: FIGURE 475-1 T2 magnetic resonance image of the brain of a patient with high- to altitude cerebral edema (HACE) shows marked swelling and a hyperintense posterior body and splenium of the corpus callosum (area with dense opacity). The patient, a climber, went on to climb Mount Everest about 9 months after this episode of HACE. (From B Basnyat et al: Clinical images. A mystery. Wilderness Environ Med 15: 53, 2004. Reused with permission from the Wilderness Medical Society. ©2004 Wilderness Medical Society.)
Figure 2¶
Caption: FIGURE 475-3 Chest radiograph of a patient with high-altitude pulmonary edema shows opacity in the right middle and lower zones simulating pneumonic FIGURE 475-2 A hyperbaric bag. The cylindrical, portable (<7 kg) nylon bag has consolidation. The opacity cleared almost completely in 2 days with descent and a one-way valve to prevent carbon dioxide buildup. A patient with severe acute supplemental oxygen. mountain sickness (AMS), high-altitude cerebral edema (HACE), or high-altitude pulmonary edema (HAPE) is zipped inside the bag, which is continuously inflated with a foot pedal. The increased barometric pressure (2 psi) inside the bag simulates taking acetazolamide, in which case metabolic acidosis may super- descent; for example, at 4250 m, the equivalent “elevation” inside the bag is ~2100 m. vene. Assessment of arterial blood gases is not necessary in the evalu- No supplemental oxygen is required. ation of HAPE; an oxygen saturation reading with a pulse oximeter is generally adequate. The existence of a subclinical form of HAPE has
Figure 3¶
Caption: FIGURE 474-11 Conceptual framework of climate change and its health impacts.
Figure 4¶
Caption: FIGURE 475-3 Chest radiograph of a patient with high-altitude pulmonary edema shows opacity in the right middle and lower zones simulating pneumonic FIGURE 475-2 A hyperbaric bag. The cylindrical, portable (<7 kg) nylon bag has consolidation. The opacity cleared almost completely in 2 days with descent and a one-way valve to prevent carbon dioxide buildup. A patient with severe acute supplemental oxygen. mountain sickness (AMS), high-altitude cerebral edema (HACE), or high-altitude pulmonary edema (HAPE) is zipped inside the bag, which is continuously inflated with a foot pedal. The increased barometric pressure (2 psi) inside the bag simulates taking acetazolamide, in which case metabolic acidosis may super- descent; for example, at 4250 m, the equivalent “elevation” inside the bag is ~2100 m. vene. Assessment of arterial blood gases is not necessary in the evalu- No supplemental oxygen is required. ation of HAPE; an oxygen saturation reading with a pulse oximeter is generally adequate. The existence of a subclinical form of HAPE has
Generated from Harrison's Principles of Internal Medicine, 22nd Edition.