| High Altitude Pulmonary Edema | |
|---|---|
| Classification and external resources | |
| ICD-10 | T70.2 |
| ICD-9 | 993.2 |
High altitude pulmonary edema (HAPE) 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] Some cases, however, have been reported also at lower altitudes (between 1,500–2,500 metres or 4,900–8,200 feet in highly vulnerable subjects), although what makes some people susceptible to HAPE is not currently known. HAPE remains the major cause of death related to high-altitude exposure with a high mortality in absence of adequate emergency treatment.
Contents |
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][4]
Symptoms: at least two of:
Signs: at least two of:
Clinical symptoms are unlikely. Blood oxygen levels remain >90%.
Clinical symptoms are common and may develop after 2-3 days. Blood oxygen levels may drop below 90% or lower during exercise. Prior acclimation will decrease the severity of the symptoms.
Blood oxygen levels are <90%, even at rest. Progressive deterioration may occur despite acclimation.
The initial cause of HAPE is a shortage of oxygen which is caused by the lower air pressure at high altitudes.[1][5] The mechanisms by which this shortage of oxygen causes HAPE are poorly understood, but two processes are believed to be important:
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.[8]
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.
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.
In order to help understand the factors that make some individuals susceptible to HAPE, the International HAPE Database was set up in 2004.[9] Individuals who have previously suffered from HAPE can register with this confidential database in order 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][10] Oxygen should also be given if possible. Symptoms tend to quickly improve with descent, but less severe symptoms may continue for several days. The standard drug treatments for which there is strong clinical evidence are dexamethasone.[11] and nifedipine[12] Phosphodiesterase inhibitors such as tadalafil are also effective[11] but may worsen the headache of mountain sickness.[13]