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Einfluss des Schädel-Hirn-Traumas auf Zeitpunkt und Technik der Frakturversorgung

Traumatic brain injury: impact on timing and modality of fracture care

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Zusammenfassung

Das Schädel-Hirn-Trauma (SHT) ist bei Patienten <45 Jahren die häufigste Todesursache. Patienten mit schwerem SHT, die das initiale Trauma überleben, sind für sekundäre zerebrale Insulte besonders anfällig. Diese „Sekundärschäden“ sind vorwiegend durch eine transiente Hypotension und/oder Hypoxämie in der frühen Behandlungsphase bedingt und beeinflussen entscheidend die Prognose nach schwerem SHT. Im Rahmen der direkten Traumafolge kommt es zu einer massiven endogenen Entzündungsreaktion im intrakraniellen Kompartment, die die Entwicklung des posttraumatischen Hirnödems und des verzögerten neuronalen Zelltodes zur Folge hat. Diese „überschießende“ neuroinflammatorische Reaktion, deren eigentlicher phylogenetischer Sinn es ist, Schadenszonen abzugrenzen, nekrotisches Gewebe zu entfernen und eine Reparation der entstandenen Defekte zu vermitteln, bestimmt wesentlich das Ausmaß der sekundären Hirnschäden. Es ist deshalb bei Mehrfachverletzungen von entscheidender Bedeutung, diese pathophysiologischen Implikationen zu erkennen und einen iatrogenen, potentiell letalen, „2nd hit“ für das verletzte Gehirn durch ein optimales Management zu vermeiden.

Das bei isolierten Verletzungen übliche Konzept einer sofortigen, definitiven Frakturbehandlung muss bei mehrfachverletzten Patienten mit SHT durch ein modifiziertes Versorgungskonzept im Sinne einer „orthopedic damage control“ mit temporärer externer Frakturfixation ersetzt werden. Hierbei werden biomechanische Gesichtspunkte der Frakturversorgung kompromisslos der Prioriät einer frühzeitigen intensivmedizinischen SHT-Therapie mit dem Ziel der Vermeidung sekundärer zerebraler Insulte untergeordnet.

Die vorliegende Übersichtsarbeit soll den aktuellen Stand der pathophysiologischen Erkenntnisse der neuroinflammatorischen Kaskade nach SHT darstellen und aufzeigen, wie durch ein prioritätenorientiertes Behandlungskonzept der „letalen Entität“ SHT adäquat Rechnung getragen wird.

Abstract

Traumatic brain injury (TBI) represents the major “killing factor” after trauma in young individuals. Those patients who survive the initial injury are highly susceptible to secondary insults to the injured brain which are mainly caused by hypotension and/or hypoxia in the early resuscitative period. Furthermore, a potent inflammatory cascade is initiated within the injured brain which leads to the development of brain edema and delayed neuronal cell death. This profound endogenous neuroinflammatory response after TBI, which is phylogenetically aimed at repairing lesioned tissue and defending the brain from invading pathogens, is in large part responsible for the extent of secondary brain damage and adverse outcome. Thus, the optimal management of the multiply injured patient, based on a thorough understanding of the pathophysiological alterations after TBI, should avoid an iatrogenic “second hit” which may be devastating to the injured brain.

The standard approach of “early total care” for isolated fractures should be strictly avoided in brain-injured patients in favor of an “orthopedic damage control” concept with temporary external fixation of long bone fractures and priority given to early transfer to intensive care.

The present review provides an up-to-date overview on the neuroinflammatory pathophysiology of brain injury and its implications for an optimized concept of fracture care in TBI patients.

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  1. Klinik für Unfall- und Wiederherstellungschirurgie, Charité, Universitätsmedizin, Campus Benjamin Franklin, Berlin

    P. F. Stahel, W. Ertel & C. E. Heyde

  2. Klinik für Unfall- und Wiederherstellungschirurgie, Charité, Universitätsmedizin, Campus Benjamin Franklin, Hindenburgdamm 30, 12200, Berlin

    P. F. Stahel

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Stahel, P.F., Ertel, W. & Heyde, C.E. Einfluss des Schädel-Hirn-Traumas auf Zeitpunkt und Technik der Frakturversorgung. Orthopäde 34, 852–864 (2005). https://doi.org/10.1007/s00132-005-0844-3

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