gms | German Medical Science

63. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC)
Joint Meeting mit der Japanischen Gesellschaft für Neurochirurgie (JNS)

Deutsche Gesellschaft für Neurochirurgie (DGNC) e. V.

13. - 16. Juni 2012, Leipzig

Evaluation of surgical treatment for cerebral contusion in the Japan neurotrauma data bank

Meeting Abstract

Suche in Medline nach

  • T. Maeda - Japan Neurotrauma Data bank, Japan Society of Neurotraumatology, Nihon University School of Medicine, Tokyo, Japan; Department of Neurological Surgery, Nihon University School of Medicine, Tokyo, Japan
  • T. Hirayama - Department of Neurological Surgery, Nihon University School of Medicine, Tokyo, Japan
  • Y. Katayama - Japan Neurotrauma Data bank, Japan Society of Neurotraumatology, Nihon University School of Medicine, Tokyo, Japan; Department of Neurological Surgery, Nihon University School of Medicine, Tokyo, Japan

Deutsche Gesellschaft für Neurochirurgie. Japanische Gesellschaft für Neurochirurgie. 63. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC), Joint Meeting mit der Japanischen Gesellschaft für Neurochirurgie (JNS). Leipzig, 13.-16.06.2012. Düsseldorf: German Medical Science GMS Publishing House; 2012. DocMI.04.06

doi: 10.3205/12dgnc012, urn:nbn:de:0183-12dgnc0123

Veröffentlicht: 4. Juni 2012

© 2012 Maeda et al.
Dieser Artikel ist ein Open Access-Artikel und steht unter den Creative Commons Lizenzbedingungen (http://creativecommons.org/licenses/by-nc-nd/3.0/deed.de). Er darf vervielfältigt, verbreitet und öffentlich zugänglich gemacht werden, vorausgesetzt dass Autor und Quelle genannt werden.


Gliederung

Text

Objective: Early massive edema caused by severe cerebral contusion results in progressive intracranial pressure elevation and clinical deterioration within 24–72 hours after trauma. Our clinical studies, including diffusion magnetic resonance imaging, demonstrated that the central (core) area of the contusion undergoes necrosis, whereas the peripheral (rim) area shows cellular swelling caused by ischemia during this period. We suggest that the early massive edema is attributable to a high osmolality within the necrotic brain tissue which may generate an osmotic potential across the central and peripheral areas.

Methods: We analyzed the effects of surgical excision of the necrotic brain tissue in patients with cerebral contusion registered on the Japan Neurotrauma Data Bank.

Results: A group of patients treated conservatively demonstrated a clearly higher mortality at 6 months after trauma, when compared to a group of patients treated by surgery (44% vs. 23%; p = 0.004; n = 198; 2004–2006). The most striking differences were observed in patients who demonstrated “talk and deteriorate” (64% vs. 22%; p = 0.0099; n = 54; 2004–2006).

Conclusions: These findings support our hypothesis that early massive edema is caused by the cerebral contusion through the presence of necrotic brain tissue, and indicate that surgical excision of the necrotic brain tissue is the only therapy which can avoid clinical deterioration in many cases.