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Anästhesiol Intensivmed Notfallmed Schmerzther 1999; 34(6): 334-339
DOI: 10.1055/s-1999-193
ÜBERSICHT
Georg Thieme Verlag Stuttgart ·New York

Intensivpolyneuropathie

Critical illnes polyneuropathy E.  Hund
  • Neurologische Universitätsklinik, Heidelberg
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Publication History

Publication Date:
31 December 1999 (online)

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Zusammenfassung.

Muskuläre Schwäche und Atrophie beim Intensivpatienten beruhen im Gegensatz zu früheren Auffassungen nicht auf einer Inaktivitätsatrophie (disuse myopathy), sondern sind Folge de novo entstehender neuromuskulärer Erkrankungen. Hauptmanifestationen sind die verzögerte Entwöhnung vom Respirator und Verlängerung der neurologischen Rehabilitation. Nach den bisher vorliegenden Untersuchungen ist die Intensiv-Polyneuropathie die häufigste Ursache solcher sekundärer neuromuskulärer Probleme auf der Intensivstation. Differentialdiagnostisch kommen prolongierte Blockaden der neuromuskulären Übertragung sowie verschiedene Myopathien in Betracht. Die Pathogenese der Intensiv-Polyneuropathie ist unbekannt. Vermutet werden Einflüsse der gleichen Mediatoren, die für die systemischen Manifestationen des septischen Syndroms (systemic inflammatory response syndrome) verantwortlich sind. Eigene Untersuchungen weisen auf das Vorhandensein einer neurotoxischen Aktivität im Serum betroffener Patienten hin, die durch NMDA-Antagonisten kompetitiv hemmbar ist. Die Primärerkrankung per se hat keine Bedeutung. Bei den Intensiv-Myopathien gibt es darüber hinaus Hinweise auf Einflüsse exogener Faktoren, insbesondere von Steroiden und Muskelrelaxantien. Eine detaillierte elektrophysiologische Untersuchung langliegender Intensivpatienten ist wünschenswert, möglichst im Sinne eines wöchentlichen Monitorings. Bei unklaren Befunden kann eine Muskelbiopsie erforderlich sein, um die zugrundeliegende Störung genauer zu klassifizieren.

Contrary to earlier belief, muscle weakness and atrophy in critically ill patients is not due to inactivity or disuse but rather caused by neuromuscular disorders arising de novo during the stay in the ICU. Clinical manifestations include delayed weaning from the respirator and prolongation of the rehabilitation phase. The available data indicate that critical illness polyneuropathy is the most frequent cause of such secondary neuromuscular problems. For differential diagnosis prolonged neuromuscular blockade and several myopathies have to be taken into consideration. The pathogenesis of critical illness polyneuropathy is unknown. It has been suggested that the factors mediating the systemic inflammatory response are also responsible for axonal damage in critical illness polyneuropathy. We recently described a neurotoxic activity present in the sera of affected patients, which can be reversed completely by NMDA antagonists. The critical illness per se is unrelated to the development of neuropathy. By contrast, occurrence of myopathies may be triggered by exogenous factors such as high-dose glucosteroids and non-depolarizing muscle blocking agents. Detailed electrodiagnostic studies are desirable in patients with long-lasting ICU stays, whenever possible as weekly monitoring. In doubtful cases, muscle biopsy might be necessary for proper diagnosis and management.

Schlüsselwörter:

Sepsis - Komplikationen, neuromuskulär - Neuropathie - Myopathie

Keywords:

Sepsis - Critical illness - Neuropathy - Myopathy - Complications

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Dr. PD Ernst Hund

Neurologische Universitätsklinik

Im Neuenheimer Feld 400

69120 Heidelberg

Email: ernst_hund@ukl.uni-heidelberg.de

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