High-Altitude Pulmonary Oedema

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Introduction[edit | edit source]

Factors that can contribute to High-Altitude Pulmonary Oedema (HAPE) include altitude, speed and mode of ascent, and individual variability. [1]

HAPE usually develops 2-5 days after a person ascends to altitudes above 2500-3000m. It hardly occurs at an altitude below 2500-3000m, and after 1 week of acclimatisation at a given altitude. [1] As mentioned on the Acclimatisation page, this is considered 'moderate altitude', where mountain sickness can occur, and acclimatization would be essential for athletic performance. [2]

There are two different scenarios in which HAPE can occur. The first involves individuals who live at high altitude, and are returning from a journey at low altitude, while the second scenario involves individuals who live at low elevation or sea level and are rapidly ascending altitude. [1]

The first type can be elicited with returning to HAPE conditions, and indicated as pulmonary oedema with electrocardiographic (ECG) signs of right-ventricular overload. This was reported in Peru. The type with unacclimatised individuals was reported in the Rocky Mountains. It is seen that both types may share the same pathophysiology. [1]

Epidemiology[edit | edit source]

HAPE can occur in healthy individuals. It most commonly occurs in mountain climbers and trekkers. [1]

In this population, when the ascent to an altitude of 4559m, takes 3 or more days, the prevalence of HAPE is <0.2%. However, when an ascent to the same altitude is completed within 22 hours, the incidence increases to 7% in individuals without radiographically proven HAPE, and increases to 62% in individuals with radiographically proven HAPE. [1]

The incidence of HAPE also increases from 2.5-15.5% when an altitude of 5500m is ascended by airlift, rather than trekking, and having gradual exposure to changing conditions over 4-6 days. [1]

HAPE can also occur at lower elevations ranging from 2500-3000m, which can be found in the Japanese Alps and North America. There is an estimated incidence of 0.01-0.1% in visitors of the ski resorts in the Rocky Mountains of Colorado. Re-entry HAPE (the first scenario) is seen to occur in the Rocky Mountains, which is also seen to occur in the Andes. It is common in vulnerable families, and commonly affects children. [1]

It is interesting to note that HAPE has been found to occur at Alpine resorts at elevations of 1400 to 2400m, which have areas for skiing up to 3200m. Individuals who my be more prone to HAPE at these elevations may have had previous or unknown underlying conditions. It is possible that affected individuals may have had diastolic heart failure rather than HAPE caused by hypertensive heart disease. [1]

In addition, Women are seen to be more prone to HAPE than Men. [1]

Pathophysiology[edit | edit source]

Who is most at risk?[edit | edit source]

Prevention[edit | edit source]

Individuals who are susceptible to HAPE can avoid the risk of such a condition if ascent is gradual, with an average ascent of 300-350m per day when at an altitude greater than 2500m. [1]

Sings & Symptoms[edit | edit source]

In many cases, HAPE is preceded by symptoms of Acute Mountain Sickness (AMS). Feel free to read about AMS in the 'Risks' section of the Acclimatisation page.

Primary symptoms of HAPE include dyspnoea on exertion, cough, and reduced exercise performance. As the pulmonary oedema condition increases, the cough can worsen, as well as breathlessness at rest and orthopnoea may result. Further progression may be indicated by gurgling in the chest, and pink frothy sputum.

Clinical features can include cyanosis, tachypnoea, tachycardia, and an increased body temperature though below 38.5 degrees. Rales can be noticed, and would specifically be located over the middle lung fields.

The degree of pulmonary oedema seen on a chest x-ray may outweigh the findings that can be noticed on auscultation.

In serious and progressed cases, there may be signs of cerebral oedema associated with the pulmonary oedema, such as ataxia or reduced levels of consciousness.

Subclinical HAPE may occur, but cause none to minimal symptoms, which can be ignored. I tis possible that people may have subclinical pleural oedema in the lung, which can vaguely represent oedema, and resolve on its own, even with the individuals at high altitude.

Treatment[edit | edit source]

When a person is at ascent, there may be limited medical facilities or supplies available. If there is access to a medical facility, supplemental oxygen would be the primary choice of treatment. [1]

Without any medical facilities available, immediately descending to a lower elevation would be indicated. [1]

However, if neither of these options are viable, treatment with nifidipine would be recommended until descent becomes an available option. [1]

Resources[edit | edit source]

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References[edit | edit source]

  1. 1.00 1.01 1.02 1.03 1.04 1.05 1.06 1.07 1.08 1.09 1.10 1.11 1.12 1.13 Bärtscha P, Mairbäurla H, Swensonb E R, Maggiorinic M. High altitude pulmonary oedema. Swiss Medical Weekly. 2003:133:377-384.
  2. Bergeron MF, Bahr R, Bartsch P, Bourdon L, Calbet JAL, Carlsen KH, Castagna O, Gonazalez-Alonso J, Lundby C, Maughan RJ, Millet G, Mountjoy M, Racinais S, Rasmussen P, Singh DG, Subudhi AW, Young AJ, Soligard T, Engebretsen L. International Olympic Committee consensus statement on thermoregulatory and altitude challenges for high-level athletes. British Journal of Sports Medicine. 2012:46:770-779.