gms | German Medical Science

58. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie e. V. (DGNC)

Deutsche Gesellschaft für Neurochirurgie (DGNC) e. V.

26. bis 29.04.2007, Leipzig

Cerebrospinal fluid leakage through arachnoideal tears influences the pathogenesis and progression of chronic subdural hematoma

Liquorleckage durch Arachnoidearisse beeinflussen die Entstehung und Progredienz von chronischen subduralen Hämatomen

Meeting Abstract

  • corresponding author R.A. Kristof - Neurochirurgische Universitätsklinik Bonn
  • J. M. Grimm - Neurochirurgische Universitätsklinik Bonn
  • B. Stoffel-Wagner - Institut für Klinische Biochemie der Universität Bonn

Deutsche Gesellschaft für Neurochirurgie. 58. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie e.V. (DGNC). Leipzig, 26.-29.04.2007. Düsseldorf: German Medical Science GMS Publishing House; 2007. DocFR.02.03

The electronic version of this article is the complete one and can be found online at: http://www.egms.de/en/meetings/dgnc2007/07dgnc068.shtml

Published: April 11, 2007

© 2007 Kristof et al.
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Outline

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Objective: To clarify whether cerebral spinal fluid (CSF), presumably leaking through an arachnoid tear into the subdural space, is involved in the genesis of chronic subdural hematoma (CSDH) and subdural hygroma (SH), and to clarify whether this leakage of CSF into the subdural space influences the postoperative recurrence rate of CSDH and SH.

Methods: In this prospective observational study, 78 patients treated surgically for CSDH (n=68) or SH (n=10) were evaluated regarding their clinical and radiological findings at presentation, the content of beta-trace protein (βTP) in the evaluated subdural fluid (βTPSF) and serum (βTPSER), and the CSDH/SH recurrence rate. The βTPSF was considered to indicate an admixture of cerebrospinal fluid to the subdural fluid if βTPSF/βTPSER>2.

Results: The median of βTPSF was 4.17 mg/l (range 0.33-51 mg/l) in the whole patient group. An arachnoid tear, as indicated by βTPSF/βTPSER>2, was found to be present in 88% of the patients with CSDH and in 100% of the patients with SH (p=0.26). In patients that later had to be re-operated for recurrences of CSDH/SH, the βTPSF concentrations (median 6.69 mg/l, range 0.59-51 mg/l) and the βTPSF/βTPSER ratios (median 10.82, range 1.36-83.88) were significantly higher (p=0.04 and p=0.048, respectively) than in patients not requiring re-operation (βTPSF: median 4.12 mg/l, range 0.33-26.8 mg/l and βTPSF/βTPSER: median 5.89, range 1.1-67.68, respectively).

Conclusions: As indicated by the presence of βTP in the subdural fluid, CSF leakage into the subdural space, probably through arachnoid tears, is present in the vast majority of patients with CSDH and SH. Patients with recurrences of CSDH and SH are presenting have significantly higher concentrations of βTPSF at their first surgery than patients not requiring a re-operation for recurrences of CSDH/SH. These findings are presented in the literature for the first time and have to be confirmed in detail by further studies.