HAPE was first defined according to clinical criteria at the International Hypoxia Symposium in Canada in 1991 (Offner 2001).
High altitude pulmonary oedemaT70.2
HistoryThis section has been translated automatically.
DefinitionThis section has been translated automatically.
High-altitude pulmonary edema (HAPE) is a massive leakage of fluid from the pulmonary capillaries into the alveolar space and the interstitium at altitudes above approx. 1,500 m (Herold 2020).
ClassificationThis section has been translated automatically.
Pulmonary edema is divided into 4 different stages:
- 1. interstitial pulmonary edema, in which fluid leaks into the lung tissue.
- 2. alveolar pulmonary edema. Here, both exudation and transudation of serous fluids into the alveoli and bronchioles take place.
- 3. foam formation with expansion of the original amount of fluid occurs in this stage.
- 4 Finally, in the last stage, asphyxia occurs (Herold 2020).
Occurrence/EpidemiologyThis section has been translated automatically.
High-altitude pulmonary edema can occur from an altitude of approx. 1,500 - 2,000 m. However, there are large individual and geographical/climatic fluctuations (Herold 2020). From an altitude of 3000 - 4500 m, 70% of mountaineers experience HAPE cases (Offner 2001). Men are affected more frequently than women (Kasper 2015).
The prevalence is higher in cold countries than in southern areas, as the air pressure decreases at low temperatures and towards both poles (Offner 2001).
EtiopathogenesisThis section has been translated automatically.
HAPE is caused by a reduced availability of oxygen at high altitudes, as atmospheric pressure decreases with increasing altitude. (Luks 2022)
HAPE develops within 2 - 4 days after arrival at high altitude (Kasper 2015).
Risk factors for HAPE are:
- Anamnestic evidence of HAPE already present
- Rapid ascent
- Low outside temperatures (these increase pulmonary intravascular pressure)
- Infections of the respiratory tract
- Existing heart defects such as patent foramen ovale, primary pulmonary hypertension, mitral stenosis, unilateral absence of the pulmonary artery (Kasper 2015)
- Male gender (Offner 2001)
- Living near sea level (Luks 2022)
PathophysiologyThis section has been translated automatically.
High-altitude pulmonary oedema is a non-cardiogenic oedema characterized by patchy pulmonary vasoconstriction. The exact mechanism of this vasoconstriction is not yet known. In some areas this leads to hyperperfusion. This increases pulmonary capillary pressure and leads to capillary stress failure (Kasper 2015).
People at risk of HAPE also have lower levels of nitric oxide in their exhaled breath at high altitudes (Kasper 2015).
The reduced alveolar pressure, together with a lack of oxygen, leads to pulmonary vasoconstriction, the so-called Euler-Liljestrand reflex (Herold 2020).
Clinical featuresThis section has been translated automatically.
The main symptoms are
- Headache
Other symptoms also occur, such as:
- fatigue
- weakness
- nausea
- dizziness
- Sleep disorders (Herold 2020)
-fever
In the later course, the following may also occur:
- Tachycardia
- tachypnea
- vomiting
- Oliguria (Antwerpes 2024)
A dry cough, possibly with bloody sputum, also often occurs at high altitudes. However, this pathomechanism has not yet been clarified (Kasper 2015).
In the most severe form of high altitude pulmonary edema, also known as HACE, the following symptoms occur:
- Ataxia
- Severe headache
- Impaired consciousness
- vomiting
- Visual disturbances
- Hallucinations (Herold 2020)
DiagnosticsThis section has been translated automatically.
The diagnosis is primarily made clinically, if only for the reason that instrumental examinations are not available at high altitude (Luks 2022).
At least 2 symptoms and 2 clinical signs must be present during exposure to altitude:
- Resting dyspnoea
- cough
- General weakness
- Decreased performance
- Thoracic tightness
- Rattling noises
- Whistling breath
- Central cyanosis
- Tachypnea
- Tachycardia (Offner 2001)
Physical examination:
- Auscultatory rales are present
ImagingThis section has been translated automatically.
ECG
ECG may show a strain on the right ventricle (Kasper 2015).
Sonography
Even in the early stages, B-lines may be detectable as a sign of interstitial fluid accumulation (Antwerpes 2024).
Chest X-ray
The chest X-ray may show patchy or localized opacities. Sometimes a streaky, interstitial edema can also be seen (Kasper 2015).
LaboratoryThis section has been translated automatically.
Blood gas analysis:
This shows hypoxia and respiratory alkalosis. If the patient has taken acetazolamide to prevent altitude sickness, metabolic acidosis may be seen instead (Antwerpes 2024).
Differential diagnosisThis section has been translated automatically.
Complication(s)This section has been translated automatically.
- High altitude cerebral edema (HACE)
TherapyThis section has been translated automatically.
At the first signs of altitude sickness, oxygen should be administered to the patient and descent or transportation to lower altitudes should be arranged (Herold 2020).
Analgesics in the form of non-opioids can also be administered (Luks 2022).
Symptomatic therapy can help the affected person:
- Positive pressure bag
- Administration of a calcium antagonist such as nifedipine
- Dexamethasone in the case of additional HACE = high altitude cerebral edema (Herold 2020)
- Nifedipine, recommended dosage: 30 mg prolonged-release tablets orally every 12 hours
- Acetazolamide, recommended dosage: 125 mg p.o. every 12 h
As an alternative to acetazolamide,:
- Dexamethasone 2 mg orally every 6 h (Luks 2022)
Progression/forecastThis section has been translated automatically.
After the descent and a few days of rest, the changes usually disappear completely The lung structure itself does not suffer any permanent damage after a HAPE (Antwerpes 2024).
However, this is not the case with high-altitude cerebral edema. Here the mortality rate is around 40 %, provided a rapid descent is possible. Otherwise, HACE is almost always fatal (Antwerpes 2024).
ProphylaxisThis section has been translated automatically.
It has been shown that dexamethasone can reduce the incidence of HAPE by 78% (Kasper 2015).
Nifedipine (recommended dosage: 30 mg 1 - 2 x / d) can also prevent HAPE, especially in people who have to ascend quickly or have a history of HAPE (Kasper 2015).
Another medication for the prevention of HAPE is tadalafil 10 mg orally 2 x / d (Luks 2022)
LiteratureThis section has been translated automatically.
- Antwerpes F, Fink B et al.(2024) High altitude pulmonary edema. DocCheck Flexikon. doi: https://flexikon.doccheck.com/en/H%C3%B6henlungen%C3%B6dem
- Antwerpes F, Fink B et al (2024) High altitude cerebral edema. DocCheck Flexikon. doi: https://flexikon.doccheck.com/en/Spezial:Artikel_Autoren/H%C3%B6henhirn%C3%B6dem
- Herold G et al (2020) Internal medicine. Herold Publishing House 406 - 408
- Kasper D L, Fauci A S, Hauser S L, Longo D L, Jameson J L, Loscalzo J et al. (2015) Harrison's Principles of Internal Medicine. Mc Graw Hill Education 247, 476e- 1 - 476e- 4
- Luks A M (2022) Altitude sickness. MSD Manual. Edition for medical professionals. doi: https://www.msdmanuals.com/de-de/profi/verletzungen-vergiftungen/h%C3%B6henkrankheit/h%C3%B6henkrankheite?query=h%C3%B6henkrankheit
- Offner K, Kopp K H (2001) High Altitude Pulmonary Edema (HAPE). Georg Thieme Verlag Stuttgart / New York 296 - 297
- Reh F, Fink B, Antwerpes F et al. (2024) Acetazolamide. DocCheck Flexikon doi: https://flexikon.doccheck.com/en/Acetazolamid