• Michael Hugelshofer, Christopher M Sikorski, Martin Seule, Jeremy Deuel, Carl I Muroi, Martina Seboek, Kevin Akeret, Raphael Buzzi, Luca Regli, Dominik J Schaer, and Emanuela Keller.
• Department of Neurosurgery, Clinical Neuroscience Center, University Hospital and University of Zurich, Zurich, Switzerland. Electronic address: michael.hugelshofer@usz.ch.
• World Neurosurg. 2018 Dec 1; 120: e660-e666.

BackgroundAneurysmal subarachnoid hemorrhage (aSAH) is often complicated by the occurrence of delayed ischemic neurologic deficits (DIND), which impairs the clinical outcome of patients. The release of oxyhemoglobin (oxyHb) from lysing erythrocytes into cerebrospinal fluid (CSF) may critically contribute to the development of DIND.MethodsVentricular CSF of 18 high-grade (Fisher 3 and 4) aSAH patients was sampled daily from external ventricular drains between days 0 and 14 after bleeding. CSF was spectrophotometrically analyzed with precise quantification of cell-free oxyHb levels.ResultsOxyHb levels in CSF showed a delayed peak reaching the highest levels in the high-risk period for developing of DIND between days 3 and 14 after aneurysm rupture. Patients with DIND had a significantly higher cumulative oxyHb exposure within the first week after bleeding.ConclusionsOxyHb levels in CSF may be useful as a biomarker to predict DIND in aSAH patients. The contribution of oxyHb in CSF to the pathogenesis of DIND should be further investigated as a potential therapeutic target.Copyright © 2018 Elsevier Inc. All rights reserved.

32 keywords...

hide…