gms | German Medical Science

70. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC)
Joint Meeting mit der Skandinavischen Gesellschaft für Neurochirurgie

Deutsche Gesellschaft für Neurochirurgie (DGNC) e. V.

12.05. - 15.05.2019, Würzburg

Oxidative stress correlates to haemorrhage volume and clinical outcome of patients with intracerebral haemorrhage

Oxidativer Stress korreliert mit dem Blutungsvolumen und dem klinischen Zustand von Patienten mit intrazerebraler Blutung

Meeting Abstract

  • presenting/speaker Julia Masomi-Bornwasser - Universitätsmedizin, Neurochirurgie, Mainz, Deutschland
  • Christina Frenz - Universitätsmedizin, Neurochirurgie, Mainz, Deutschland
  • Jan Schmitt - Universitätsmedizin, Neurochirurgie, Mainz, Deutschland
  • Harald Krenzlin - Universitätsmedizin, Neurochirurgie, Mainz, Deutschland
  • Johannes Lotz - Universitätsmedizin, Institut für klinische Chemie und Laboratoriumsmedizin, Mainz, Deutschland
  • Thomas Kerz - Universitätsmedizin, Neurochirurgie, Mainz, Deutschland
  • Florian Ringel - Universitätsmedizin, Neurochirurgie, Mainz, Deutschland
  • Naureen Keric - Universitätsmedizin, Neurochirurgie, Mainz, Deutschland

Deutsche Gesellschaft für Neurochirurgie. 70. Jahrestagung der Deutschen Gesellschaft für Neurochirurgie (DGNC), Joint Meeting mit der Skandinavischen Gesellschaft für Neurochirurgie. Würzburg, 12.-15.05.2019. Düsseldorf: German Medical Science GMS Publishing House; 2019. DocV135

doi: 10.3205/19dgnc150, urn:nbn:de:0183-19dgnc1502

Published: May 8, 2019

© 2019 Masomi-Bornwasser et al.
This is an Open Access article distributed under the terms of the Creative Commons Attribution 4.0 License. See license information at http://creativecommons.org/licenses/by/4.0/.


Outline

Text

Objective: Oxidative stress (OS) plays an important role in the development of secondary injury after intracerebral hemorrhage (ICH). OS, a result of the destruction of the balance between oxidation and antioxidant system, causes overproduction of malondialdehyde (MDA), a decrease of antioxidative enzymes like superoxide dismutase (SOD), glutathione peroxidase (GPx), total and free glutathione-sulfhydryl (GSH) and total antioxidant status (TAS). The aim of this study is to assess the impact of OS on clinical outcome after ICH.

Methods: In this prospective observational study ICH patients with an ICH volume >30 cc who were equipped with an external ventricular drain were included (2017 until 2018). Blood and cerebrospinal fluid (CSF) samples were obtained from 16 patients with ICH (5 female, 11 male, mean age 65±12 years) and 24 controls (14 female, 10 male, mean age 59±14 years). Neurological outcome (modified ranking scale, mRS) was determined 6 weeks after ICH. ICH volume was calculated before and after treatment using the I-plan software. Antioxidative activity measurements were performed at day 1 and 3 in serum (GPx, GSH) as well as in serum and in CSF (TAS, SOD, MDA).

Results: Mean ICH volume was 61.9±61.1 cm3 before and 12.5±29.8 cm3 after treatment. At day 1, total (83.2±17.9 mg/l) and free (78.8±21.1 mg/l) GSH levels were significant higher in the control group compared to the ICH group (5.6±2.4 mg/l; 5.7±1.8 mg/l; p<0.0001). TAS decreased significantly in CSF from 217.1±58.9 µmol/l at day 1 to 106.1±123 µmol/l at day 3 (p=0.0129). The 6 weeks mRS of the ICH group was 4.5±1.3 and 1.1±1.0 in the control group. Low levels of TAS in CSF on day 3 do correlate with impaired neurological outcome (r=-0.68; p=0.0205). Lager ICH volumes significantly correlate with lower levels of TAS in CSF at day 1 (r=-0.8; p=0.003), of MDA in CSF (r=-0.75; p=0.0322) and of free GSH in serum (r=-0.75; p=0.0322).

Conclusion: Larger ICH volumes lead to a reduction of antioxidant properties demonstrated by lower TAS levels in CSF and reduced free GSH concentrations in serum and correlate with lower MDA levels in CSF. Decreasing levels of TAS in CSF predicted an unfavorable clinical outcome. We found that oxidative stress is a result of ICH and increases with the initial ICH size. It seems to contribute to secondary brain injury and impaired neurological outcome.