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Propofol-Infusionssyndrom

Propofol infusion syndrome

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Zusammenfassung

Das Propofol-Infusionssyndrom ist sowohl bei Langzeitsedierung als auch bei einer Propofolanästhesie von 5 h Dauer beobachtet worden. Pathophysiologisch vermutet man, dass eine durch Propofol induzierte Hemmung der Fettsäureoxidation und eine Störung der oxidativen Phosphorylierung in den Mitochondrien durch Entkoppelung der Atmungskette zu einem intrazellulären Energiedefizit mit einer Laktatazidose und Muskelnekrose führt. Propofol kann eine Triggersubstanz darstellen, wenn bestimmte „Primer“ vorliegen. Als „Primer“ wurden schwere Grunderkrankungen identifiziert, bei denen die Patienten hohen Katecholamin- und/oder Kortisolspiegeln ausgesetzt waren. Wenn Verdacht auf Propofol-Infusionssyndrom besteht, muss die Zufuhr von Propofol beendet werden. Die weitere Therapie umfasst den Ausgleich der metabolischen Azidose und die Stabilisierung der Hämodynamik. Zur beschleunigten Elimination von Propofol und von potenziell toxischen Metaboliten wird die Hämodialyse oder Hämofiltration empfohlen. Aufgrund des Risikos von potenziell tödlichen Nebenwirkungen sollte der Einsatz von Propofol zur Langzeitsedierung schwerstkranker Patienten kritisch überdacht werden. Bei unter kontinuierlicher Propofolinfusion auftretender, ungeklärter Laktatazidose muss ein Propofol-Infusionssyndrom in Erwägung gezogen werden.

Abstract

Propofol infusion syndrome has not only been observed in patients undergoing long-term sedation with propofol, but also during propofol anesthesia lasting 5 h. It has been assumed that the pathophysiologic cause is propofol’s impairment of oxidation of fatty acid chains and inhibition of oxidative phosphorylation in the mitochondria, leading to lactate acidosis and muscular necrosis. It has been postulated that propofol might act as a trigger substrate in the presence of priming factors. Severe diseases in which the patient has been exposed to high catecholamine and cortisol levels have been identified as trigger substrates. Once the development of propofol infusion syndrome is suspected, propofol infusion has to be stopped immediately and specific therapeutic measures initiated, including cardiocirculatory stabilization and correction of metabolic acidosis. To increase elimination of propofol and its potential toxic metabolites, hemodialysis or hemofiltration are recommended. Due to its possible fatal side effects, the use of propofol for long-term sedation in critically ill patients should be reconsidered. In cases of unexplained lactate acidosis occurring during continuous propofol infusion, propofol infusion syndrome must be taken into consideration.

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  1. Klinik für Anästhesiologie, Universitätsklinikum Heidelberg

    J. Motsch & J. Roggenbach

  2. Klinik für Anästhesiologie, Universitätsklinikum Heidelberg, Im Neuenheimer Feld 110, 69120 , Heidelberg

    J. Motsch

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  1. J. Motsch
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  2. J. Roggenbach
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Correspondence to J. Motsch.

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Motsch, J., Roggenbach, J. Propofol-Infusionssyndrom. Anaesthesist 53, 1009–1024 (2004). https://doi.org/10.1007/s00101-004-0756-3

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