High-altitude pulmonary edema (HAPE) is a life-threatening form of non-cardiogenic pulmonary edema that occurs in otherwise healthy people at altitudes typically above . HAPE is a severe presentation of altitude sickness. Cases have also been reported between in people who are at a higher risk or are more vulnerable to the effects of high altitude.

Classically, HAPE occurs in people normally living at low altitude who travel to an altitude above .

There are many factors that can make a person more susceptible to developing HAPE, including genetic factors. The understanding of the risk factors and how to prevent HAPE is not clear. HAPE remains the major cause of death related to high-altitude exposure, with a high mortality rate in the absence of adequate emergency treatment.

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

The Lake Louise Consensus Definition for high-altitude pulmonary edema has set widely used criteria for defining HAPE symptoms.

In the presence of a recent gain in altitude, the presence of the following:

Symptoms: at least two of:

  • Shortness of breath at rest
  • Cough
  • Weakness or decreased exercise performance
  • Chest tightness or congestion

Signs: at least two of:

  • Crackles or wheezing (while breathing) in at least one lung field
  • Central blue skin color
  • Tachypnea (rapid breathing)
  • Tachycardia (rapid heart rate)

Acute mountain sickness and high altitude cerebral edema may also be present in conjunction with HAPE, however these symptoms may be subtle or not present at all. The most reliable sign of HAPE is severe fatigue or exercise intolerance, especially in someone that was previously not displaying this symptom.

Risk factors

There are multiple factors that can contribute to the development of HAPE, including sex (male), genetic factors, prior development of HAPE, ascent rate, cold exposure, peak altitude, intensity of physical exertion, and certain underlying medical conditions (e.g., pulmonary hypertension). The resultant hypoxemia is then thought to precipitate the development of:

  1. Increased pulmonary arterial and capillary pressures (pulmonary hypertension) secondary to hypoxic pulmonary vasoconstriction.
  2. Increased capillary pressure (hydrostatic pressure) with over-distention of the capillary beds and increased permeability of the vascular endothelium, also known as "stress failure." This leads to subsequent leakage of cells and proteins into the alveoli, aka pulmonary edema.

Diagnosis

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|+Expected SpO<sub>2</sub> and PaO<sub>2</sub> levels at altitude The suggested rate of ascent is the same that applies to the prevention of acute mountain sickness and high-altitude cerebral edema.

The Wilderness Medical Society (WMS) recommends that, above , climbers

  • not increase the sleeping elevation by more than a day, and
  • include a day with no additional ascent every 3–4 days. a pulmonary vasodilator which prevents the altitude induced pulmonary hypertension. The recommendation for its use is strongest for individuals with a history of HAPE. According to published data, treatment is most effective if given one day prior to ascent and continued for four to five days, or until descent below . Acetazolamide has proven to be clinically effective, but formal studies are lacking. Salmeterol is considered an adjunctive therapy to nifedipine, though only in highly susceptible climbers with clearly demonstrated recurrence of HAPE.

Treatment

thumb|Demonstrating the use of a [[Portable hyperbaric bag|portable hyperbaric chamber.]]

The recommended first line treatment is descent to a lower altitude as quickly as possible, with symptomatic improvement seen in as few as . However, descent is not mandatory in people with mild HAPE and treatment with warming techniques, rest, and supplemental oxygen can improve symptoms. although its use is best in combination with and does not substitute for descent, hyperbaric therapy, or oxygen therapy. and can be considered as add-on treatment if first-line therapy is not possible; however, they may worsen the headache of mountain sickness. There is no established role for the inhaled beta-agonist salmeterol, though its use can be considered.

This condition was subsequently noticed in otherwise healthy climbers who would die shortly after arriving at high altitudes.

See also

  • Hazards of outdoor recreation
  • High-altitude cerebral edema (HACE)
  • High-altitude flatus expulsion (HAFE)

References