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Anästhesiol Intensivmed Notfallmed Schmerzther 2007; 42(6): 432-438
DOI: 10.1055/s-2007-984549
Fachwissen: Topthema: Pädiatrische Neuroanästhesie

© Georg Thieme Verlag Stuttgart · New York

Pädiatrische Neuroanästhesie - Physiologie und Pathophysiologie des kindlichen Zerebrums

Klaus U. Klein, Kristin Engelhard, Christian Werner
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Publication Date:
09 July 2007 (online)

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Wenn es um intrakranielle Pathologien im Kindesalter geht, sind für ein optimales anästhesiologisches Management substanzielle Kenntnisse von Anatomie, Physiologie und Pathophysiologie des kindlichen Zerebrums unverzichtbar. Dieser Beitrag stellt zerebrale Entwicklung und altersabhängige Grundlagen von zerebraler Perfusion, Metabolismus und intrakraniellem Druck dar. Dabei geht er auf den Pathomechanismus einer hypoxisch-ischämischen kindlichen Hirnschädigung mit Exzitotoxizität, Ödembildung und Immunmodulation bis hin zum Zelltod ein.

Kernaussagen

  • Die erhöhte Vulnerabilität des frühkindlichen Gehirns begründet sich in der besonderen Anatomie des Neurokraniums und dem hohen Metabolismus während der Entwicklung. Reflexprüfungen sind hilfreich für die Beurteilung der Reife des frühkindlichen zentralen Nervensystems.

  • Die altersabhängigen Unterschiede der intrakraniellen Druck-Volumen-Verhältnisse sind für die Beurteilung einer Kapazitätsänderung des kindlichen Hirngewebekompartiments (80 %), Blutvolumenkompartiments (12 %) und Liquorkompartiments (8 %) von Bedeutung.

  • Die zerebrale Durchblutung und der Metabolismus sind im Neugeborenenalter vermindert, im Klein- und Schulkindalter im Vergleich zur adulten Situation hingegen erhöht. Die Kopplung von zerebraler Durchblutung und Metabolismus ist vom Alter unabhängig.

  • Die zerebrovaskuläre Autoregulation zum Erhalt einer konstanten zerebralen Perfusion ist bei Früh- und termingerechten Neugeborenen wahrscheinlich existent, wobei die untere Grenze zu niedrigeren Werten verschoben ist. Analog zum Erwachsenen kann die zerebrovaskuläre Autoregulation beim Vorliegen intrakranieller Läsionen aufgehoben und direkt vom zerebralen Perfusionsdruck abhängig sein. In dieser Situation kann eine Reduktion des zerebralen Perfusionsdruckes zur zerebralen Ischämie bzw. eine Steigerung zum Hirnödem führen.

  • Mit einer Erhöhung des arteriellen Kohlendioxid-Partialdruckes steigt die kindliche zerebrale Durchblutung linear bzw. exponentiell beim Vorliegen einer arteriellen Hypoxämie (CO2-Vasoreaktivität). Im Falle einer ausgeprägten arteriellen Hyperoxie kann sie reduziert sein (O2-Vasoreaktivität).

  • Der Erhalt der Homöostase des kindlichen Flüssigkeitshaushalt ist für eine konstante zerebrale Perfusion und Oxygenierung von wesentlicher Bedeutung (Normotonie, Normovolämie, Normoxämie, Normokapnie, Normoglykämie, Normothermie).

  • Multiple pathophysiologische Mechanismen führen nach einem hypoxisch-ischämischen Geschehen durch Exzitotoxizität, Ödemformation und Inflammation des Gewebes zum apoptotischen oder nekrotischen Zelltod im ischämischen Hirnareal.

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Dr. med. Klaus U Klein

Email: kuklein@uni-mainz.de

PD Dr. med. Kristin Engelhard

Email: engelhak@mail.uni-mainz.de

Prof. Dr. med. Christian Werner

Email: werner@anaesthesie.klinik.uni-mainz.de

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