Bin ich anfällig für Höhenkrankheiten?

Zusammenfassung

Absolute Höhe, Vorakklimatisation, Aufstiegsgeschwindigkeit und individuelle Anfälligkeit sind die wichtigsten Prädiktoren der akuten Bergkrankheit (ABK), des Höhenhirnödems (HHÖ) und des Höhenlungenödems (HLÖ). Die Anfälligkeit für akute Höhenkrankheiten lässt sich am besten durch anamnestische Angaben abschätzen. Messungen der Sauerstoffsättigung und der Ventilation in akuter Hypoxie zur Beurteilung der Anfälligkeit für ABK sind aufgrund der ungenügenden Trennschärfe nicht sinnvoll. Obwohl der überschießende pulmonal-arterielle Druckanstieg in Hypoxie ein entscheidender pathophysiologischer Faktor des HLÖ ist, kann er nicht zur Identifizierung von HLÖ-Anfälligkeit im Tiefland herangezogen werden, weil noch weitere (unbekannte) Faktoren in der Pathogenese dieser Krankheit eine Rolle spielen. Ob Tests in Hypoxie bei fehlender Höhenanamnese eine Verbesserung der Vorhersage bringen und zu einer größeren Reduktion von Höhenkrankheiten führen als Beratungen ohne Hypoxietests wurde bisher nicht untersucht. Deshalb können Hypoxietests außerhalb von kontrollierten Studien nicht empfohlen werden. Die Bestimmung genetischer Polymorphismen zur Erfassung der individuellen Anfälligkeit ist wegen fehlender Aussagekraft nicht sinnvoll. Eine gute aerobe Leistungsfähigkeit schützt nicht vor ABK und HLÖ, ist aber eine wichtige Voraussetzung für das Bergsteigen in großen Höhen (> 4000 m). Aus Berganamnese, geplanter Präakklimatisation und Aufstiegsprofil können das individuelle Risiko abgeschätzt und entsprechende Empfehlungen ausgesprochen werden.

ABSTRACT

Final altitude, degree of pre-acclimatization and individual susceptibility as well as rate of ascent are the major determinants of acute mountain sickness (AMS), high altitude cerebral edema (HACE) and high altitude pulmonary edema (HAPE). Susceptibility to acute high altitude illnesses can best be judged from the history of previous exposures. Measuring arterial oxygen saturation or ventilation in acute hypoxia at low altitude for evaluating susceptibility to AMS adds little to an assessment based on history, because of a large overlap of individual results. Although the exaggerated rise of pulmonary artery pressure (PAP) in hypoxia is a prerequisite for HAPE measuring PAP in acute hypoxia at low altitude does not reliably identify HAPE susceptible individuals because other (unknown) factors contribute to the pathophysiology of HAPE. Whether hypoxic testing is helpful in individuals without a history of altitude exposure for risk assessment and whether it prevents acute high altitude illnesses better than a purely history based approach needs to be determined yet in controlled studies. Therefore, such testing cannot be recommended outside controlled studies. Susceptibility to AMS and HAPE has a polygenic basis and controversial results regarding associations of susceptibility with various gene polymorphisms had been reported. At present, there is no clinically useful, comprehensive genetic approach for assessing susceptibility to acute high altitude illnesses. A good aerobic performance does not protect form AMS, HACE and HAPE. It is, however, an important prerequisite for successful mountaineering at altitudes above 4000 m. Exercise testing is, however, not necessary for assessment of aerobic performance, because, in healthy individuals, it can be judged from the mountaineering history. State of the art is to give advice based on a risk assessment that relies on the mountaineering history and information about degree of pre-acclimatization and the planned ascent profile.

Key words

acute mountain sickness - high altitude cerebral edema - high altitude pulmonary edema - individual susceptibility - risk assessment

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