High-altitude pulmonary edema

High-Altitude Pulmonary Edema (HAPE)
Classification and external resources
Specialty emergency medicine
ICD-10 T70.2
ICD-9-CM 993.2

High-altitude pulmonary edema (HAPE) (HAPO spelled oedema in British English) is a life-threatening form of non-cardiogenic pulmonary edema (fluid accumulation in the lungs) that occurs in otherwise healthy mountaineers at altitudes typically above 2,500 meters (8,200 ft).[1] However, cases have also been reported at lower altitudes (between 1,500–2,500 metres or 4,900–8,200 feet in highly vulnerable subjects), though what makes some people susceptible to HAPE is currently unknown. HAPE remains the major cause of death related to high-altitude exposure, with a high mortality rate in the absence of adequate emergency treatment.

Signs and symptoms

Physiological and symptomatic changes often vary according to the altitude involved.[2]

The Lake Louise Consensus Definition for High-Altitude Pulmonary Edema has set widely used criteria for defining HAPE symptoms:[3]

Symptoms: at least two of:

Signs: at least two of:

The initial cause of HAPE is a shortage of oxygen caused by the lower air pressure at high altitudes.[1][4] The mechanisms by which this oxygen shortage causes HAPE are poorly understood, but two processes are believed to be important:

  1. Increased pulmonary arterial and capillary pressures (pulmonary hypertension) secondary to hypoxic pulmonary vasoconstriction.[5]
  2. An idiopathic non-inflammatory increase in the permeability of the vascular endothelium.[6]

Although higher pulmonary arterial pressures are associated with the development of HAPE, the presence of pulmonary hypertension may not in itself be sufficient to explain the development of edema: severe pulmonary hypertension can exist in the absence of clinical HAPE in subjects at high altitude.[7]

Incidence

The incidence of clinical HAPE in unacclimatized travelers exposed to high altitude (~4,000 m or 13,000 ft) appears to be less than 1%. The U.S. Army Pike's Peak Research Laboratory has exposed sea-level-resident volunteers rapidly and directly to high altitude; during 30 years of research involving about 300 volunteers (and over 100 staff members), only three have been evacuated with suspected HAPE.

Predisposing factors

Individual susceptibility to HAPE is difficult to predict. The most reliable risk factor is previous susceptibility to HAPE, and there is likely to be a genetic basis to this condition, perhaps involving the gene for angiotensin converting enzyme (ACE). Recently, scientists have found the similarities between low amounts of 2,3-BPG (also known as 2,3-DPG) with the occurrence of HAPE at high altitudes. Persons with sleep apnea are susceptible due to irregular breathing patterns while sleeping at high altitudes.

Research

To help understand factors that make some individuals susceptible to HAPE, the International HAPE Database was set up in 2004.[8] Individuals who have previously suffered from HAPE can register with this confidential database to help researchers study the condition. The standard and most important treatment is to descend to lower altitude as quickly as possible, preferably by at least 1000 metres.[1][9] Oxygen should also be given if possible. Symptoms tend to quickly improve with descent, but more severe symptoms may continue for several days. The standard drug treatments for which there is strong clinical evidence are dexamethasone[10] and nifedipine.[11] Phosphodiesterase inhibitors such as sildenafil and tadalafil are also effective[10] but may worsen the headache of mountain sickness.[12]

See also

References

  1. 1 2 3 Roach, James M.; Schoene, Robert B. (2002). "High-Altitude Pulmonary Edema". In Pandolf, Kent B.; Burr, Robert E. Medical Aspects of Harsh Environments (PDF) 2. Washington, DC: Borden Institute. pp. 789–814. OCLC 64437370.
  2. ↑ "Why do low oxygen levels cause altitude sickness?". Altitude.org.
  3. ↑ "The Lake Louise Consensus on the Definition of Altitude Illness". High Altitude Medicine Guide. Thomas E. Dietz. Retrieved 2012-11-10.
  4. ↑ Kenneth Baillie and Alistair Simpson. "Barometric pressure calculator". Apex (Altitude Physiology EXpeditions). Retrieved 2006-08-10.
  5. ↑ Bärtsch, P; Maggiorini, M; Ritter, M; Noti, C; et al. (October 1991). "Prevention of high-altitude pulmonary edema by nifedipine". The New England Journal of Medicine 325 (18): 1284–9. doi:10.1056/NEJM199110313251805. PMID 1922223.
  6. ↑ Swenson, ER; Maggiorini, M; Mongovin, S; et al. (May 2002). "Pathogenesis of high-altitude pulmonary edema: inflammation is not an etiologic factor". JAMA 287 (17): 2228–35. doi:10.1001/jama.287.17.2228. PMID 11980523.
  7. ↑ Maggiorini, M; Mélot, C; Pierre, S; et al. (April 2001). "High-altitude pulmonary edema is initially caused by an increase in capillary pressure". Circulation 103 (16): 2078–83. doi:10.1161/01.cir.103.16.2078. PMID 11319198.
  8. ↑ "International HAPE database". Apex (Altitude Physiology EXpeditions). Retrieved 2006-08-10.
  9. ↑ Luks, AM (2008). "Do we have a 'best practice' for treating high altitude pulmonary edema?". High Altitude Medicine & Biology 9 (2): 111–4. doi:10.1089/ham.2008.1017. PMID 18578641.
  10. 1 2 Maggiorini, M; Brunner-La Rocca, HP; Peth S; et al. (October 2006). "Both tadalafil and dexamethasone may reduce the incidence of high-altitude pulmonary edema: a randomized trial". Annals of Internal Medicine 145 (7): 497–506. doi:10.7326/0003-4819-145-7-200610030-00007. PMID 17015867.
  11. ↑ Bärtsch, P; Swenson, Erik R.; Maggiorini, ER; Maggiorini, M (2001). "Update: High altitude pulmonary edema". Advances in Experimental Medicine and Biology. Advances in Experimental Medicine and Biology 502: 89–106. doi:10.1007/978-1-4757-3401-0_8. ISBN 978-1-4419-3374-4. PMID 11950158.
  12. ↑ 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.

External links

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