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A FEW THINGS can really put a damper on a well-planned mountain vacation: Travel difficulties, rain, or an unpleasant surprise in lodging accommodations often top the list. While these conditions may create difficulties, they all pale in comparison with the greatest danger for high-altitude vacationers both within the United States and abroad: altitude illness.
In the Western United States, millions of people visit travel destinations above 8,202 ft (2,500 m).1 These higher destinations include Alaska, California, Colorado, Idaho, Montana, New Mexico, Nevada, Oregon, Washington, and Wyoming. Popular high-altitude destinations outside of the United States include the Canadian Rockies, Mt. Kilimanjaro in Tanzania, Machu Picchu and the Inca Trail in Peru, the European Alps, and the Himalayas.
Altitude illness should be a chief concern for anyone on a vacation in the mountains, particularly those who normally reside at sea level. People venturing above 8,202 ft (2,500 m) at any time of year should have adequate knowledge regarding altitude illness.2 This article will provide up-to-date information on preventing, recognizing, and treating altitude illness.
People can succumb to altitude illness at varying degrees of elevation (see Defining high altitude). Elevation is a concern because barometric pressure decreases with increasing altitude, which decreases the partial pressure of oxygen dissolved in blood.3
Regardless of the altitude, the percentage of oxygen in the atmosphere is always the same (21%). But with increasing altitude, barometric pressure decreases and fewer oxygen molecules are present in any given volume of air. Thus, as air becomes less compressed from the weight of air above (Boyle's Law), fewer oxygen molecules are inspired per breath, increasing the risk of hypoxia and altitude illness.4
The degree of hypoxia is directly related to barometric pressure.3 For example, the barometric pressure at 19,028 ft (5,800 m), or roughly the elevation at the summit of Mt. Kilimanjaro, is half that of sea level.5 Environmental factors such as geographical distance from the equator (barometric pressure is higher at the equator due to a cold air mass in the stratosphere) and season (the influence of temperature on the barometric pressure equation) influence barometric pressure and, consequentially, the potential for hypoxia.4
The body attempts to minimize the effects of hypoxia through a gradual process known as acclimatization, which is the adjustment to changes in the amount of oxygen inspired at higher altitudes.4 These changes begin at elevations as low as 4,921 ft (1,500 m).5 Ascending quickly to altitude, usually by driving or flying, increases the chance a traveler will become hypoxic and experience altitude illness because the body has no time to adapt and acclimatize to the decreased barometric pressure.4
Acclimatization occurs through multiple physiologic changes that increase the movement of oxygen to the cells and the efficiency by which the oxygen is utilized.4 The most rapid response of acclimatization is an increase in respiratory rate. Peripheral chemoreceptors in the carotid bodies sense the decrease in inspired oxygen and stimulate the respiratory centers in the brainstem to increase ventilation.4 This response is known as hypoxic ventilatory response (HVR).5 Over time, the increased respiratory rate results in a respiratory alkalosis that triggers a braking mechanism, limiting any further increase in ventilation.5 This occurs because the subsequent decrease in serum carbon dioxide is sensed by central chemoreceptors, creating a negative feedback mechanism that suppresses respiratory drive.4
By now internal metabolic adaptations have begun, and the kidneys compensate for the respiratory alkalosis by excreting more bicarbonate (HCO3-).5 As the blood pH becomes more normalized, the ventilation braking mechanism is overcome, allowing further increases in respiratory rate and arterial oxygen content. This process can take 4 to 7 days to be effective but can be altered by extrinsic factors such as the administration of acetazolamide, a carbonic anhydrase inhibitor and nonbacteriostatic sulfonamide that helps speed up the acclimatization process.5
Acetazolamide acts as a respiratory stimulant by causing the kidneys to diurese more bicarbonate, leading to a renal loss of HCO3- ions that carry out sodium, water, and potassium. This lessens the severity of respiratory alkalosis in an attempt to return blood pH to a normal range, overcoming the negative feedback that's suppressing the HVR and stimulating the central chemoreceptors to continue increasing respiratory rate.5
Other pathophysiologic alterations involve hematocrit concentrations and metabolic changes that alter the oxygen binding capacity of hemoglobin, which occurs over days to months.4 Hypoxia stimulates an increased production of red blood cells that usually occurs after a week at high altitude.4 The increase in red blood cells is due to renal and hepatic erythropoietin production, resulting in erythropoiesis and greater red blood cell mass.4 The increase in hemoglobin concentration (which occurs as a result of initial plasma volume contraction due to diuresis and less frequently by movement of fluid from blood vessels to cells and tissues) and increased erythropoiesis increase arterial oxygen content and improve tissue oxygenation to something similar to that occurring at sea level.4 However, travelers who have a trip length of less than 7 days will experience only the increased hematocrit due to initial fluid loss. Over weeks to months, red blood cells and plasma volume both increase.5
Another physiologic change that helps combat hypoxia is an increase in production of 2,3 diphosphoglycerate, which decreases the affinity of oxygen for hemoglobin and allows more oxygen to be transferred to the tissues.5 Additionally, acute exposure to high altitudes results in an increase in heart rate and cardiac output, both at rest and with physical activity.4 These increases dissipate and return toward sea-level values over time once acclimatization has occurred.4
If ascent is too rapid and the body isn't given the time to allow these physiologic changes to occur, altitude illness will often result.2
Altitude illness becomes common above 8,202 ft (2,500 m) and presents in three forms: acute mountain sickness (AMS), high altitude cerebral edema (HACE), and high altitude pulmonary edema (HAPE).3 These forms of altitude illness can vary from mild to severe and may develop rapidly over hours or more slowly over days.4 These factors increase the risk of acquiring any form of altitude illness:
* rapid ascent
* history of altitude illness
* substantial physical exertion at altitude
* preexisting lung or cardiovascular disease
* a genetic susceptibility
* other preexisting conditions such as sleep apnea, neuromuscular disease, chronic obstructive pulmonary disease, restrictive lung disease, pneumonia, cystic fibrosis, pulmonary hypertension, or congenital heart abnormalities that involve right-to-left shunts.6
Travelers often are unaware or deny they have altitude illness and blame their symptoms on various other causes, such as the cold or heat, infection, alcohol use, insomnia, exercise, lack of fitness, or migraine.4 This denial of symptoms associated with altitude illness can delay treatment and risks further exacerbation with continued ascent.
The most common altitude illness, AMS afflicts otherwise healthy travelers who ascend rapidly to high altitudes.3 It's almost universal among those flying directly to altitudes above 12,467 ft (3,800 m). AMS affects both men and women of any age and fitness level.4 Signs and symptoms typically begin 6 to 12 hours following arrival at an altitude above 8,202 ft (2,500 m).4
The most accepted definition for AMS was developed in 1991 during the International Hypoxia Symposium in Lake Louise, Alberta, Canada. The Lake Louise Consensus Committee definition of AMS is the presence of a headache and at least one of the following signs and symptoms after a recent arrival to a high altitude:
* sleep disturbance
The signs and symptoms of AMS usually resolve within 3 days if altitude isn't increased.4
One common differential diagnosis to consider when identifying AMS is the person's hydration status. A balanced approach to hydration at altitude is essential due to insensible loss of fluids from sweat, which evaporates quickly, and respiratory loss in cool, dry air. Overhydration without adequate food intake could lead to hyponatremia with signs and symptoms similar to AMS.4 Early identification of AMS is important because it's often a precursor to HACE or HAPE.4
The best treatment for AMS is to stop further ascent and/or to descend. AMS is first treated with rest without an increase in elevation and administration of acetazolamide along with warmth, food, and rehydration.6 If the patient doesn't improve with treatment at this altitude, descending 984 to 3,281 ft (300 to 1,000 m) is the next step in treatment. Aspirin or ibuprofen may relieve headache and antiemetics can help manage nausea.3
Any deterioration in the patient's condition makes descent necessary. If weather or other conditions prevent descent, the following treatment protocol should be followed:
* Administer oxygen.
* Place the patient in a portable hyperbaric chamber.
* Administer oral acetazolamide and consider I.M. dexamethasone if the patient begins to exhibit signs and symptoms bordering on HACE.4 The mechanism of action for dexamethasone isn't completely understood, but it's thought that glucocorticoids trigger changes to capillary permeability and cause cytokine release.8
Closely monitor a patient with AMS because the condition may quickly progress to a more severe form of AMS or to HACE, making an earlier descent to alleviate symptoms and/or evacuation for definitive care essential.4 With the above treatments, signs and symptoms of AMS may disappear, only to reappear upon further ascent.4
The most common cause of death related to altitude illness, HAPE involves movement of fluid from the intravascular to extravascular space in the alveoli, impairing gas exchange. HAPE typically occurs at an altitude greater than 8,202 ft (2,500 m), usually develops between 48 and 96 hours at altitude, and may develop rapidly or gradually depending on the individual.4 It's usually a result of very rapid ascent to high altitude combined with extreme physical exertion.4
This condition isn't completely understood, but experts believe hypoxia causes an abnormally profound hypoxic pulmonary vasoconstrictive response (HPVR), resulting in leaking capillaries and alveolar hemorrhage.4 This vasoconstriction is uneven and the pulmonary vessels that aren't downstream of the constricted vessels become exposed to higher pressures and hyperperfusion, leading to stress failure of these vessels.4,9 This failure allows proteins and blood cells to leak into the interstitial space and, eventually, the alveolar space.4 Pulmonary edema is enhanced and exacerbates the poor gas exchange.4
Travelers with a genetic defect in normal nitric oxide synthesis may be more susceptible to HAPE. Experts believe that nitric oxide synthesis normally modifies the HPVR and is protective in nature.4 While nitric oxide isn't a commonly requested lab test, it's possible to measure for travelers who've previously experienced HAPE to identify a possible genetic predisposition.
Men are more susceptible to HAPE than women. Other factors that increase the risk include young age, cold environmental temperatures, fast ascent, strenuous physical exertion, preexisting infection, and history of HAPE.10 AMS may or may not precede HAPE.4
Signs and symptoms of HAPE manifest first with reduced exercise tolerance with dyspnea on exertion that eventually deteriorates to dyspnea at rest.11 Early signs and symptoms of HAPE include a dry cough that often progresses to a productive cough with frothy white or pink-tinged sputum.4 In the late stages, hemoptysis is present and the lips and nail beds may become cyanotic.4 Other signs and symptoms may include:
* chest pain.4
Descent is the primary treatment for HAPE and shouldn't be delayed.12 Ideally the patient should avoid any exertion and be carried in a sitting position. Keep the patient warm because exertion and cold exacerbate HAPE by increasing sympathetic drive, causing further pulmonary vasoconstriction.4 In addition to descent, adjunct treatments include the use of oxygen, sitting the patient upright, administering slow-release oral nifedipine and, if AMS is coexistent, oral dexamethasone. The use of nifedipine results in a reduction of mean pulmonary artery pressure and pulmonary vascular resistance and improves oxygenation.12 If descent must be delayed, a hyperbaric chamber can be used.4
Phosphodiesterase inhibitors, including tadalafil and sildenafil, have been used by healthcare providers in rescue situations. The ability of this class of drugs to decrease pulmonary arterial pressure and cause pulmonary vasodilatation makes their use seem logical to address HAPE-related symptoms, but their effectiveness hasn't been studied in great detail.2
Prevention, the best strategy, can be achieved with adequate acclimatization, slow ascent, and oral acetazolamide starting 1 day before ascent.4
HACE is rare but life threatening and has occurred at altitudes as low as 8,202 ft (2,500 m).4 HACE and AMS are thought to be opposite ends of the same disease spectrum. HACE usually follows the development of AMS that doesn't resolve in the usual 3- to 4-day period after identification with no additional ascent.4 While often progressing from AMS, HACE can occur independently or in conjunction with HAPE. The mechanisms of development occur from hypoxia, causing increased vascular permeability.4 This results in cerebral edema within the restrictive confines of the cranium.4 Risk factors for HACE are similar to those of AMS and HAPE, with fast ascent being the most significant.4
The patient with HACE will often have a combination of the following signs and symptoms:
While these are similar to those experienced in AMS, they're more severe and will progress to even more severe signs and symptoms such as ataxia, unreasonable behavior, neurologic deficits, cranial nerve palsies, retinal hemorrhages, confusion, stupor, coma, and pulmonary edema.4
Immediate descent is the definitive treatment. Oxygen and oral, I.V., or I.M. dexamethasone administration will facilitate symptomatic relief. If descent is impossible due to weather or terrain, a hyperbaric chamber could be implemented as a bridge therapy until descent is possible.2 Again, as with AMS and HAPE, prevention is the best policy and can be achieved by adhering to a slow ascent profile, avoiding hard physical exertion, taking oral acetazolamide 1 day before ascent, and ensuring proper rest and hydration.
See Quick guide to altitude illness for an overview of preventing, identifying, and treating these three types of altitude illness.
Acclimatization takes time, and if a traveler ascends quickly there's a greater chance of developing altitude illness. Virtually all travelers will experience some of the signs and symptoms of altitude illness, and their chance of being affected doesn't depend on age, gender, or fitness.13 To acclimatize, the traveler must ascend gradually and slowly and ease into physical exertion.11 Knowing the signs, symptoms, and treatment of altitude illness will better prepare the traveler to prevent such conditions and help nurses and other potential rescuers to respond appropriately. Preparation and prevention are the key elements to enjoying a trip at high altitudes.
High altitude: elevation from 4,921 ft (1,500 m) to 11,483 ft (3,500 m) above sea level
Very high altitude: elevation from 11,483 ft (3,500 m) to 18,046 ft (5,500 m)
Extreme altitude: elevation above 18,046 ft (5,500 m).
Acute Mountain Sickness (AMS)
Prevent: ascend slowly, take acetazolamide prophylactically
Identify: assess for headache plus one of following: anorexia, nausea, vomiting, lethargy, fatigue, weakness, sleep disturbance, dizziness
Treat: descend (best treatment); rest at current altitude, administer acetazolamide, oxygen, and antiemetics as prescribed; use portable hyperbaric chambers; rehydrate, encourage eating; and in extreme cases of AMS bordering on HACE, administer dexamethasone as prescribed4,7
High Altitude Pulmonary Edema (HAPE)
Prevent: ascend slowly, take nifedipine prophylactically only for those with a history of HAPE
Identify: assess for dyspnea with exertion, dyspnea at rest, dry cough that progresses to productive (white frothy or pink-tinged sputum), hemoptysis, cyanosis of lips/nail beds, nausea, insomnia, headache, dizziness, confusion, orthopnea, chest pain
Treat: descend (best treatment); sit patient upright, administer oxygen and nifedipine as prescribed, place patient in hyperbaric chamber; if signs and symptoms of AMS/HACE are present, consider administering dexamethasone as prescribed4,7,11
High Altitude Cerebral Edema (HACE)
Identify: assess for headache plus one of following: anorexia, nausea, vomiting, lethargy, fatigue, weakness, sleep disturbance, dizziness progressing to ataxia, unreasonable behavior, neurologic deficits, cranial nerve palsies, retinal hemorrhages, confusion, stupor, coma, pulmonary edema
Treat: descend (best treatment); administer oxygen, dexamethasone, and acetazolamide as prescribed; place patient in hyperbaric chamber4,7
1. Hatzenbuehler J, Glazer J, Kuhn C. Awareness of altitude sickness among visitors to a North American ski resort. Wilderness Environ Med. 2009;20(3):257-260. [Context Link]
2. Luks AM, McIntosh SE, Grissom CK, et al. Wilderness Medical Society consensus guidelines for the prevention and treatment of acute altitude illness. Wilderness Environ Med. 2010;21(2):146-155. [Context Link]
3. Simon RB, Simon DA. Preparing for travel to high altitudes. Nursing. 2012;42(9):66-67. [Context Link]
4. West JB, Schoene RB, Milledge JS, Luks AM. High Altitude Medicine and Physiology. 5th ed. London, UK: CRC Press; 2012. [Context Link]
5. Hackett PH, Roach RC. High-altitude medicine. In: Auerbach PS, ed. Wilderness Medicine. 6th ed. Philadelphia, PA: Mosby Elsevier; 2012. [Context Link]
6. Gallagher SA, Hackett P, Rosen JM. High altitude illness: physiology, risk factors, and general prevention. UpToDate. 2013. http://www.uptodate.com. [Context Link]
7. Kupper T, Gieseler U, Angelini C, et al. Consensus statement of the UIAA Medical Commission Vol 2: Emergency field management of acute mountain sickness, high altitude pulmonary oedema, and high altitude cerebral oedema. The International Mountaineering and Climbing Federation (UIAA). 2009;V2.2:1-13. [Context Link]
8. Imray C, Wright A, Subudhi A, Roach R. Acute mountain sickness: pathophysiology, prevention, and treatment. Prog Cardiovasc Dis. 2010;52(6):467-484. [Context Link]
9. Scherrer U, Rexhaj E, Jayet PY, Allemann Y, Sartori C. New insights in the pathogenesis of high-altitude pulmonary edema. Prog Cardiovasc Dis. 2010;52(6):485-492. [Context Link]
10. Jones BE, Stokes S, McKenzie S, Nilles E, Stoddard GJ. Management of high altitude pulmonary edema in the Himalaya: a review of 56 cases presenting at Pheriche Medical Aid Post (4240 m). Wilderness Environ Med. 2013;24(1):32-36. [Context Link]
11. Stream JO, Grissom CK. Update on high-altitude pulmonary edema: pathogenesis, prevention, and treatment. Wilderness Environ Med. 2008;19(4):293-303. [Context Link]
12. Deshwal R, Iqbal M, Basnet S. Nifedipine for the treatment of high altitude pulmonary edema. Wilderness Environ Med. 2012;23(1):7-10. [Context Link]
13. Richardson A. Mountaineering: Essential Skills for Hikers and Climbers. New York, NY: Skyhorse Publishing; 2010. [Context Link]
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