Altitude sickness

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Altitude sickness
Classification and external resources
Sign displays "Caution! Your are at 17586 ft (5360 m)"
Altitude Sickness Warning - Indian Army
ICD-10 T70.2
ICD-9 E902.0
DiseasesDB 8375 29615
MedlinePlus 000133
eMedicine med/3225
MeSH D000532

Altitude sickness—also known as acute mountain sickness (AMS), altitude illness, hypobaropathy, "the altitude bends", or soroche—is a pathological effect of high altitude on humans, caused by acute exposure to low partial pressure of oxygen at high altitude. It commonly occurs above 2,400 metres (8,000 feet).[1][2] It presents as a collection of nonspecific symptoms, acquired at high altitude or in low air pressure, resembling a case of "flu, carbon monoxide poisoning, or a hangover".[3] It is hard to determine who will be affected by altitude sickness, as there are no specific factors that correlate with a susceptibility to altitude sickness. However, most people can ascend to 2,400 metres (8,000 ft) without difficulty.

Acute mountain sickness can progress to high altitude pulmonary edema (HAPE) or high altitude cerebral edema (HACE), which are potentially fatal.[2][4]

Chronic mountain sickness, also known as Monge's disease, is a different condition that only occurs after very prolonged exposure to high altitude.[5]

Causes[edit]

The available amount of oxygen to sustain mental and physical alertness decreases with altitude. Available oxygen drops as the air density itself, the number of molecules (of both oxygen and nitrogen) per given volume, drops as altitude increases.

However, the percentage of oxygen in air, at 21%, remains almost unchanged up to 21,000 metres (69,000 ft).[6] The RMS velocities of diatomic nitrogen and oxygen are very similar and thus no change occurs in the ratio of oxygen to nitrogen.

Dehydration due to the higher rate of water vapor lost from the lungs at higher altitudes may contribute to the symptoms of altitude sickness.[7]

The rate of ascent, altitude attained, amount of physical activity at high altitude, as well as individual susceptibility, are contributing factors to the onset and severity of high-altitude illness.

Altitude sickness usually occurs following a rapid ascent and can usually be prevented by ascending slowly.[4] In most of these cases, the symptoms are temporary and usually abate as altitude acclimatization occurs. However, in extreme cases, altitude sickness can be fatal.

Climbers on Mount Everest often experience Altitude Sickness.

Definitions[edit]

  • High altitude: 1,500 to 3,500 metres (4,900 to 11,500 ft) - The onset of physiological effects of diminished inspiratory oxygen pressure (PiO2) includes decreased exercise performance and increased ventilation (lower arterial PCO2). Minor impairment exists in arterial oxygen transport (arterial oxygen saturation (SaO2) at least 90%), but arterial PO2 is significantly diminished. Because of the large number of people who ascend rapidly to altitudes between 2,400 and 4,000 m, high-altitude illness is common in this range.[8]
  • Very high altitude: 3,500 to 5,500 metres (11,500 to 18,000 ft) - Maximum SaO2 falls below 90% as the arterial PO2 falls below 60mmHg. Extreme hypoxemia may occur during exercise, during sleep, and in the presence of high altitude pulmonary edema or other acute lung conditions. Severe altitude illness occurs most commonly in this range.[8]
  • Extreme altitude: above 5,500 metres (18,000 ft) - Marked hypoxemia, hypocapnia, and alkalosis are characteristic of extreme altitudes. Progressive deterioration of physiologic function eventually outstrips acclimatization. As a result, no permanent human habitation occurs above 6,000 m. A period of acclimatization is necessary when ascending to extreme altitude; abrupt ascent without supplemental oxygen for other than brief exposures invites severe altitude sickness.[8]

Signs and symptoms[edit]

People have different susceptibilities to altitude sickness; for some otherwise healthy people, acute altitude sickness can begin to appear at around 2000 meters (6,500 ft) above sea level, such as at many mountain ski resorts, equivalent to a pressure of 80 kPa.[9] This is the most frequent type of altitude sickness encountered. Symptoms often manifest themselves six to ten hours after ascent and generally subside in one to two days, but they occasionally develop into the more serious conditions. Symptoms include headache, fatigue, stomach illness, dizziness, and sleep disturbance.[4] Exertion aggravates the symptoms.

The Lake Louise assessment system of AMS is based on a self-report questionnaire as well as a quick clinical assessment.[10]

Those individuals with the lowest initial partial pressure of end-tidal pCO2 (the lowest concentration of carbon dioxide at the end of the respiratory cycle, a measure of a higher alveolar ventilation) and corresponding high oxygen saturation levels tend to have a lower incidence of acute mountain sickness than those with high end-tidal pCO2 and low oxygen saturation levels.[11]

Primary symptoms[edit]

Headaches are the primary symptom used to diagnose altitude sickness, although a headache is also a symptom of dehydration. A headache occurring at an altitude above 2,400 metres (8,000 feet = 76 kPa), combined with any one or more of the following symptoms, may indicate altitude sickness:

Severe symptoms[edit]

Symptoms that may indicate life-threatening altitude sickness include:

Pulmonary edema (fluid in the lungs)
    • Symptoms similar to bronchitis
    • Persistent dry cough
    • Fever
    • Shortness of breath even when resting
Cerebral edema (swelling of the brain)
    • Headache that does not respond to analgesics
    • Unsteady gait
    • Gradual loss of consciousness
    • Increased nausea
    • Retinal hemorrhage

The most serious symptoms of altitude sickness arise from edema (fluid accumulation in the tissues of the body). At very high altitude, humans can get either high altitude pulmonary edema (HAPE), or high altitude cerebral edema (HACE). The physiological cause of altitude-induced edema is not conclusively established. It is currently believed, however, that HACE is caused by local vasodilation of cerebral blood vessels in response to hypoxia, resulting in greater blood flow and, consequently, greater capillary pressures. On the other hand, HAPE may be due to general vasoconstriction in the pulmonary circulation (normally a response to regional ventilation-perfusion mismatches) which, with constant or increased cardiac output, also leads to increases in capillary pressures. For those suffering HACE, dexamethasone may provide temporary relief from symptoms in order to keep descending under their own power.

HAPE can progress rapidly and is often fatal. Symptoms include fatigue, severe dyspnea at rest, and cough that is initially dry but may progress to produce pink, frothy sputum. Descent to lower altitudes alleviates the symptoms of HAPE.

HACE is a life-threatening condition that can lead to coma or death. Symptoms include headache, fatigue, visual impairment, bladder dysfunction, bowel dysfunction, loss of coordination, paralysis on one side of the body, and confusion. Descent to lower altitudes may save those afflicted with HACE.

Physiology[edit]

The physiology of altitude sickness is based on the following equation:

Vgas=A/TDk(P1-P2)

Where Vgas is the diffusion rate, A is the area of the lung, T is the thickness of the lung membranes, P1 and P2 are the differences in partial pressure of any gas-but most importantly CO2 and O2-where in high altitudes the partial pressure differences for O2 are low and the differences in partial pressures for CO2 are high. Thus CO2 will have a high diffusion out and O2 will have a low diffusion though the alveolar membranes and into the blood.

The body's response to high altitude includes the following:

  • ↑Erythropoietin → ↑hematocrit and hemoglobin
  • ↑2,3-DPG (allows ↑ release of O2 and a right shift on the Hb-O2 disassociation curve)
  • ↑renal excretion of bicarbonate (use of acetazolamide can augment for treatment)
  • Chronic hypoxic pulmonary vasoconstriction (can cause Right Ventricular Hypertrophy)

Prevention[edit]

Ascending slowly is the best way to avoid altitude sickness.[4] Avoiding strenuous activity such as skiing, hiking, etc. in the first 24 hours at high altitude reduces the symptoms of AMS. Alcohol and sleeping pills are respiratory depressants, and thus slows down the acclimatization process and should be avoided. Alcohol also tends to cause dehydration and exacerbates AMS. Thus, avoiding alcohol consumption in the first 24–48 hours at a higher altitude is optimal.

Pre acclimatization[edit]

Pre Acclimatization is when the body develops tolerance to low oxygen concentrations before ascending to an altitude. It significantly reduces risk because less time has to be spent at attitude to acclimatize in the traditional way. Additionally, because less time has to be spent on the mountain, less food and supplies have to be taken up. Several commercial systems exist that use altitude tents, so called because they mimic altitude by reducing the percentage of oxygen in the air while keeping air pressure constant to the surroundings. This technology was invented by Hypoxico, Inc. in the 1990s and has received a strong following from climbers and athletes the world over.

Altitude acclimatization[edit]

Altitude acclimatization is the process of adjusting to decreasing oxygen levels at higher elevations, in order to avoid altitude sickness.[12] Once above approximately 3,000 metres (10,000 feet = 70 kPa), most climbers and high-altitude trekkers take the "climb-high, sleep-low" approach. For high-altitude climbers, a typical acclimatization regimen might be to stay a few days at a base camp, climb up to a higher camp (slowly), and then return to base camp. A subsequent climb to the higher camp then includes an overnight stay. This process is then repeated a few times, each time extending the time spent at higher altitudes to let the body adjust to the oxygen level there, a process that involves the production of additional red blood cells.[citation needed] Once the climber has acclimatized to a given altitude, the process is repeated with camps placed at progressively higher elevations. The general rule of thumb is to not ascend more than 300 metres (1,000 ft) per day to sleep. That is, one can climb from 3,000 (10,000 feet = 70 kPa) to 4,500 metres (15,000 feet = 58 kPa) in one day, but one should then descend back to 3,300 metres (11,000 feet = 67.5 kPa) to sleep. This process cannot safely be rushed, and this is why climbers need to spend days (or even weeks at times) acclimatizing before attempting to climb a high peak. Simulated altitude equipment that produces hypoxic (reduced oxygen) air can be used to acclimate to high altitude, reducing the total time required on the mountain itself.[citation needed]

Altitude acclimatization is necessary for some people who move rapidly from lower altitudes to intermediate altitudes (e.g., by aircraft and ground transportation over a few hours), such as from sea level to 8,000 feet (2,400 m) as in many Colorado, USA mountain resorts. Stopping at an intermediate altitude overnight can alleviate or eliminate occurrences of AMS.

Medical treatment[edit]

The drug acetazolamide (trade name Diamox) may help some people making a rapid ascent to sleeping altitude above 2,700 metres (9,000 ft), and it may also be effective if started early in the course of AMS.[13] Acetazolamide can be taken before symptoms appear as a preventive measure at a dose of 125 mg twice daily. The Everest Base Camp Medical Centre cautions against its routine use as a substitute for a reasonable ascent schedule, except where rapid ascent is forced by flying into high altitude locations or due to terrain considerations.[14] The Centre suggests a dosage of 125 mg twice daily for prophylaxis, starting from 24 hours before ascending until a few days at the highest altitude or on descending;[14] with 250 mg twice daily recommended for treatment of AMS.[15] The Centers for Disease Control and Prevention (CDC) suggest the same dose for prevention of 125 mg acetazolamide every 12 hours.[16] Acetazolamide, a mild diuretic, works by stimulating the kidneys to secrete more bicarbonate in the urine, thereby acidifying the blood. This change in pH stimulates the respiratory center to increase the depth and frequency of respiration, thus speeding the natural acclimatization process. An undesirable side-effect of acetazolamide is a reduction in aerobic endurance performance. Other minor side effects include a tingle-sensation in hands and feet, and it can make carbonated drinks taste "flat". Although a sulfonamide, acetazolamide is a non-antibiotic and has not been shown to cause life-threatening allergic cross-reactivity in those with a self-reported sulfa allergy.[17][18][19] Dosage of 1000 mg/day will produce a 25% decrease in performance, on top of the reduction due to high-altitude exposure.[20] The CDC advises that Dexamethasone be reserved for treatment of severe AMS and HACE during descents, and notes that Nifedipine may prevent HAPE.[16]

A single randomized controlled trial found that sumatriptan may help prevent altitude sickness.[21] Despite their popularity, antioxidant treatments have not been found to be effective medications for prevention of AMS.[22] Interest in phosphodiesterase inhibitors such as sildenafil has been limited by the possibility that these drugs might worsen the headache of mountain sickness.[23] A promising possible preventive for altitude sickness is myo-inositol trispyrophosphate (ITPP), which increases the amount of oxygen released by hemoglobin.

Prior to the onset of altitude sickness, ibuprofen is a suggested non-steroidal anti-inflammatory and painkiller that can help alleviate both the headache and nausea associated with AMS. It has not been studied for the prevention of cerebral edema (swelling of the brain) associated with extreme symptoms of AMS.[24]

For centuries, indigenous peoples of the Americas such as the Aymaras of the Altiplano, have chewed coca leaves to try to alleviate the symptoms of mild altitude sickness. In Chinese and Tibetan traditional medicine, an extract of the root tissue of Radix rhodiola is often taken in order to prevent the same symptoms, though neither of these therapies has been proven effective in clinical study.

Oxygen enrichment[edit]

In high-altitude conditions, oxygen enrichment can counteract the hypoxia related effects of altitude sickness. A small amount of supplemental oxygen reduces the equivalent altitude in climate-controlled rooms. At 3,400 meters (11,155 feet = 67 kPa), raising the oxygen concentration level by 5 percent via an oxygen concentrator and an existing ventilation system provides an effective altitude of 3,000 metres (10,000 feet = 70 kPa), which is more tolerable for surface-dwellers.[25]

Other methods[edit]

Increased water intake may also help in acclimatization[26] to replace the fluids lost through heavier breathing in the thin, dry air found at altitude, although consuming excessive quantities ("over-hydration") has no benefits and may cause dangerous hyponatremia. It’s a good idea to limit alcohol intake the first day or so at higher elevation as well.

Oxygen from gas bottles or liquid containers can be applied directly via a nasal cannula or mask. Oxygen concentrators based upon pressure swing adsorption (PSA), VSA, or vacuum-pressure swing adsorption (VPSA) can be used to generate the oxygen if electricity is available. Stationary oxygen concentrators typically use PSA technology, which has performance degradations at the lower barometric pressures at high altitudes. One way to compensate for the performance degradation is to utilize a concentrator with more flow capacity. There are also portable oxygen concentrators that can be used on vehicular DC power or on internal batteries, and at least one system commercially available measures and compensates for the altitude effect on its performance up to 4,000 meters (13,000 ft). The application of high-purity oxygen from one of these methods increases the partial pressure of oxygen by raising the FiO2 (fraction of inspired oxygen).

Treatment[edit]

The only reliable treatment and in many cases the only option available is to descend. Attempts to treat or stabilize the patient in situ at altitude is dangerous unless highly controlled and with good medical facilities. However, the following treatments have been used when the patient's location and circumstances permit:

  • Oxygen may be used for mild to moderate AMS below 3,700 m (12,000 ft) and is commonly provided by physicians at mountain resorts. Symptoms abate in 12–36 hours without the need to descend.
  • For more serious cases of AMS, or where rapid descent is impractical, a Gamow bag, a portable plastic hyperbaric chamber inflated with a foot pump, can be used to reduce the effective altitude by as much as 1,500 meters (5,000 ft). A Gamow bag is generally used only as an aid to evacuate severe AMS patients, not to treat them at altitude.
  • Acetazolamide 250 mg twice daily dosing assists in AMS treatment by quickening altitude acclimatization.[27] A study by the Denali Medical Research Project concluded: "In established cases of acute mountain sickness, treatment with acetazolamide relieves symptoms, improves arterial oxygenation, and prevents further impairment of pulmonary gas exchange."[28]
  • The folk remedy for altitude sickness in Ecuador, Peru and Bolivia is a tea made from the coca plant. See mate de coca.
  • Steroids can be used to treat the symptoms of pulmonary or cerebral edema, but do not treat the underlying AMS.
  • Two studies in 2012 showed that Ibuprofen 600 milligrams three times daily was effective at decreasing the severity and incidence of AMS. But it was not clear if this affected HAPE or HACE.[29][30]

See also[edit]

References[edit]

  1. ^ Baillie, Kenneth; Simpson, Alistair. "Altitude Tutorials - Altitude Sickness". Apex (Altitude Physiology Expeditions). Archived from the original on 9 January 2010. Retrieved 26 January 2010. 
  2. ^ a b Roach, Robert; Stepanek, Jan; and Hackett, Peter. (2002). "24". Acute Mountain Sickness and High-Altitude Cerebral Edema. In: Medical Aspects of Harsh Environments 2. Washington, DC: Borden Institute. Archived from the original on 11 January 2009. Retrieved 5 January 2009. 
  3. ^ The Mountaineers. Mountaineering: The Freedom of the Hills, 7th Edition. Seattle, WA: Mountaineers Books, 2003
  4. ^ a b c d A.A.R. Thompson. "Altitude Sickness". Apex. Retrieved 8 May 2007. 
  5. ^ A.J. Giannini, H.R. Black, R.L. Goettsche. The Psychiatric, Psychogenic and Somatopsychic Disorders Handbook. New Hyde Park, NY. Medical Examination Publishing Co.,1978. pp.190,192. ISBN 0-87488-596-5.
  6. ^ FSF Editorial Staff (May–June 1997). "Wheel-well Stowaways Risk Lethal Levels of Hypoxia and Hypothermia". Human Factors and Aviation Medicine (Flight Safety Foundation) 44 (3): 1–5. Archived from the original on 28 November 2010. Retrieved 28 October 2010. 
  7. ^ Hackett, P H; R C Roach (12 July 2001). "High-altitude illness". The New England Journal of Medicine 345 (2): 107–114. doi:10.1056/NEJM200107123450206. ISSN 0028-4793. PMID 11450659. Retrieved 25 March 2009. 
  8. ^ a b c d Auerbach, Paul (2007). Wilderness Medicine. Fifth ed. Mosby Elsevier. ISBN 0-323-03228-1. 
  9. ^ K. Baillie and A. Simpson. "Acute mountain sickness". Apex (Altitude Physiology Expeditions). Retrieved 8 August 2007.  — High altitude information for laypeople
  10. ^ Savourey, G; Guinet, A,; Besnard, Y; Garcia, N; Hanniquet, AM; Bittel, J (October 1995). "Evaluation of the Lake Louise acute mountain sickness scoring system in a hypobaric chamber". Aviation, Space, and Environmental Medicine (Alexandria, VA: Aerospace Medical Association) 66 (10): 963–7. PMID 8526833. 
  11. ^ Douglas, Danielle; Robert Schoene (2010). "End-tidal partial pressure of carbon dioxide and acute mountain sickness in the first 24 hours upon ascent to cusco, peru (3326 meters)". Wilderness and Environment Medicine 21 (2): 109–113. doi:10.1016/j.wem.2010.01.003. 
  12. ^ Muza, S.R.; Fulco, C.S.; Cymerman, A. (2004). "Altitude Acclimatization Guide". U.S. Army Research Inst. of Environmental Medicine Thermal and Mountain Medicine Division Technical Report (USARIEM–TN–04–05). Retrieved 5 March 2009. 
  13. ^ World Health Organization (1 January 2007). "CHAPTER 3 Environmental health risks" (PDF). International travel and health. p. 31. Retrieved 21 November 2009. 
  14. ^ a b Himalayan Rescue Association - Everest Medical Clinic. "Prophylaxis". ExplorersWeb. Retrieved 21 November 2009. 
  15. ^ Himalayan Rescue Association - Everest Medical Clinic. "Treating AMS". ExplorersWeb. Retrieved 21 November 2009. 
  16. ^ a b Hackett P, Shlim D (2009). "Chapter 2 The Pre-Travel Consultation - Self-Treatable Diseases - Altitude Illness". In Turell D, Brunette G, Kozarsky P, Lefor A. CDC Health Information for International Travel 2010 "The Yellow Book". St. Louis: Mosby. ISBN 0-7020-3481-9. Retrieved 21 November 2009. 
  17. ^ Platt, D; Griggs RC (April 2012). "Use of acetazolamide in sulfonamide-allergic patients with neurologic channelopathies". Archives of Neurology 69 (4): 527–9. doi:10.1001/archneurol.2011.2723. PMID 22158718. 
  18. ^ Kelly, TE; Hacket PH (2010). "Acetazolamide and sulfonamide allergy: a not so simple story". High Altitude Medicine & Biology 11 (4): 319–23. doi:10.1089/ham.2010.1051. PMID 21190500. 
  19. ^ Lee, Andrew G; Randy Anderson; Randy H. Kardon; Michael Wall (July 2004). "Presumed "sulfa allergy" in patients with intracranial hypertension treated with acetazolamide or furosemide: cross-reactivity, myth or reality?". American Journal of Ophthalmology 138 (1): 114–118. doi:10.1016/j.ajo.2004.02.019. Retrieved 11/05/2013.  Check date values in: |accessdate= (help)
  20. ^ "Altitude Acclimatization Guide". 
  21. ^ Jafarian S., Gorouhi F., Salimi S., Lotfi J. (2007). "Sumatriptan for prevention of acute mountain sickness: randomized clinical trial". Annals of Neurology 62 (3): 273–277. doi:10.1002/ana.21162. PMID 17557349. 
  22. ^ Baillie JK, Thompson AA, Irving JB, Bates MG, Sutherland AI, Macnee W, Maxwell SR, Webb DJ (May 2009). "Oral antioxidant supplementation does not prevent acute mountain sickness: double blind, randomised placebo-controlled trial". QJM 102 (5): 341–348. doi:10.1093/qjmed/hcp026. PMID 19273551. 
  23. ^ Bates MG, Thompson AA, Baillie JK (March 2007). "Phosphodiesterase type 5 inhibitors in the treatment and prevention of high altitude pulmonary edema". Current Opinion in Investigational Drugs 8 (3): 226–31. PMID 17408118. 
  24. ^ John Sanford (March 2012). "Ibuprofen decreases likelihood of altitude sickness, researchers find". Retrieved 19 September 2012. 
  25. ^ West JB (February 1995). "Oxygen enrichment of room air to relieve the hypoxia of high altitude". Respir Physiol 99 (2): 225–232. doi:10.1016/0034-5687(94)00094-G. PMID 7777705. 
  26. ^ Dannen, Kent; Dannen, Donna (2002). Rocky Mountain National Park. Globe Pequot. p. 9. ISBN 0-7627-2245-2. "Visitors unaccustomed to high elevations may experience symptoms of Acute Mountain Sickness (AMS)[...s]uggestions for alleviating symptoms include drinking plenty of water[.]" 
  27. ^ Cain SM, Dunn JE (July 1966). "Low doses of acetazolamide to aid accommodation of men to altitude". J Appl Physiol 21 (4): 1195–200. PMID 5916650. 
  28. ^ Grissom CK, Roach RC, Sarnquist FH, Hackett PH (March 1992). "Acetazolamide in the treatment of acute mountain sickness: clinical efficacy and effect on gas exchange". Annals of Internal Medicine 116 (6): 461–5. doi:10.7326/0003-4819-116-6-461. PMID 1739236. 
  29. ^ Lipman, Grant S; Kanaan, Nicholas C; Holck, Peter S; Constance, Benjamin B; Gertsch, Jeffrey H (June 2012). "Ibuprofen prevents altitude illness: a randomized controlled trial for prevention of altitude illness with nonsteroidal anti-inflammatories". Annals of Emergency Medicine 59 (6): 484–490. doi:10.1016/j.annemergmed.2012.01.019. PMID 22440488. 
  30. ^ Gertsch, Jeffrey H; Corbett, B; Holck, Peter S; Mulcahy, A; Watts, M; et al (2012). "Altitude Sickness in Climbers and Efficacy of NSAIDs Trial (ASCENT): randomized, controlled trial of ibuprofen versus placebo for prevention of altitude illness". Wilderness and Environmental Medicine 23 (4): 307–315. doi:10.1016/j.wem.2012.08.001. PMID 23098412. 

External links[edit]