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Erschienen in: Der Anaesthesist 12/2003

01.12.2003 | Leitthema

Toxikologie der Lokalanästhetika

Pathomechanismen—Klinik—Therapie

verfasst von: Dr. W. Zink, B. M. Graf

Erschienen in: Der Anaesthesist | Ausgabe 12/2003

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Zusammenfassung

Unabhängig von ihren physikochemischen Eigenschaften und ihrer chemischen Struktur blockieren sämtliche Lokalanästhetika spannungsgesteuerte Na+-Kanäle und verhindern somit die Erregungsweiterleitung in peripheren Nerven. Da derartige Ionenkanäle aber nicht nur an der Erregungsweiterleitung im peripheren Nerv beteiligt sind, kommt es bei exzessiver Anreicherung der Lokalanästhetika im menschlichen Organismus zu einer generalisierten Funktionseinschränkung erregbarer Membranen. Klinisch äußert sich die systemische Toxizität der Lokalanästhetika v. a. in einer Beeinträchtigung des zentralen Nervensystems (ZNS) sowie des kardiovaskulären Systems.
Hinsichtlich des ZNS zeigen sich die in charakteristischer Reihenfolge auftretenden Symptome als weit gehend unabhängig vom verwendeten Lokalanästhetikum; die jeweiligen toxischen Plasmaspiegel sind jedoch in hohem Maße substanzspezifisch. Neurophysiologisch beruhen diese Vorgänge zunächst auf einer selektiven Funktionseinschränkung kortikaler inhibitorischer Neuronengruppen; dies begünstigt die subkortikale Entstehung von Krampfpotentialen. Bei weiter steigenden zerebralen Lokalanästhetikakonzentrationen werden im Stadium der zentralnervösen Depression schließlich auch exzitatorische Neuronenverbände blockiert; was sich klinisch als Koma, Apnoe und Kreislaufkollaps manifestiert.
Direkte kardiotoxische Effekte der Lokalanästhetika beruhen hauptsächlich auf einer stereoselektiven Reizleitungsblockade und auf einer unspezifischen Blockade des myokardialen Energiestoffwechsels. Das Spektrum der in dieser Situation auftretenden Symptome ist uneinheitlich und reicht von extremen Bradykardien über (maligne) ventrikuläre Arrhythmien bis hin zum therapierefraktären Herz-Kreislauf-Stillstand.
Von der systemischen Toxizität bzw. von allergischen Reaktionen—letztere werden nach Sensibilisierung überwiegend durch Lokalanästhetika vom Estertyp ausgelöst—müssen lokale zytotoxische Effekte abgegrenzt werden. Substanzspezifisch kann es durch Lokalanästhetika direkt an der Applikationsstelle zu neuronalen und/oder skelettmuskulären Schädigungen kommen, die sich meist innerhalb weniger Tage bis Wochen zurückbilden. Während sich die zentralen neurotoxischen Erscheinungen oftmals klar definierbaren Krankheitsbildern zuordnen lassen („transiente neurologische Symptome“, Cauda-equina-Syndrom), ist die klinische Bedeutung skelettmuskulärer Schäden bislang noch weit gehend unklar.
Die „Therapie“ der zentralnervösen bzw. kardiovaskulären Intoxikation besteht in erster Linie darin, durch entsprechende Vorsichtsmaßnahmen eine systemische Akkumulation der Lokalanästhetika zu vermeiden. Die eigentliche Behandlung einer systemischen Intoxikation erfolgt streng symptomorientiert; hypoxische und azidotische Zustände sind auf jeden Fall zu vermeiden bzw. aggressiv zu korrigieren. Inwieweit experimentelle Therapieansätze auf den menschlichen Organismus zu übertragen sind, bleibt abzuwarten.
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Metadaten
Titel
Toxikologie der Lokalanästhetika
Pathomechanismen—Klinik—Therapie
verfasst von
Dr. W. Zink
B. M. Graf
Publikationsdatum
01.12.2003
Verlag
Springer-Verlag
Erschienen in
Der Anaesthesist / Ausgabe 12/2003
Print ISSN: 2731-6858
Elektronische ISSN: 2731-6866
DOI
https://doi.org/10.1007/s00101-003-0617-5

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