Association of Cerebrospinal Fluid Volume with Cerebral Vasospasm After Aneurysmal Subarachnoid Hemorrhage: A Retrospective Volumetric Analysis

NCJ_cover.jpgBy Moritz Scherer, Jin-On Jung, Jonas Cordes, Lars Wessels, Alexander Younsi, Silvia Schönenberger, Markus Alfred Möhlenbruch, Klaus Maier-Hein, Andreas Unterberg, Klaus Zweckberger

First Online: 26 November 2019

In aneurysmal subarachnoid hemorrhage (SAH), clot volume has been shown to correlate with the development of radiographic vasospasm (VS), while the role of cerebrospinal fluid (CSF) volume remains largely elusive in the literature. We evaluated CSF volume as a potential surrogate for VS in addition to SAH volume in this retrospective series.

Patients and Methods
From a consecutive cohort of aneurysmal SAH (n= 320), cases were included when angiographic evaluation for VS was performed (n= 125). SAH and CSF volumes were volumetrically quantified using an algorithm-assisted segmentation approach on initial computed tomography after ictus. Association with VS was analyzed using regression analysis. Receiver operating characteristic (ROC) curves were used to evaluate predictive accuracy of volumetric measures for VS and to identify cutoffs for risk stratification.

Among 125 included cases, angiography showed VS in 101 (VS+), while no VS was observed in 24 (VS−) cases. In volumetric analysis, mean SAH volume was significantly larger (26.8 ± 21.1 ml vs. 12.6 ± 12.2 ml, p= 0.001), while mean CSF volume was significantly smaller (63.0 ± 31.2 ml vs. 85.7 ± 62.8, p= 0.03) in VS+ compared to VS− cases, respectively. The absence of correlation for SAH and CSF volumes (Pearson R − 0.05, p= 0.58) indicated independence of both measures of the subarachnoid compartment, which was a prerequisite for CSF to act as a new surrogate for VS not related to SAH. Regression analysis confirmed an increased risk of VS with increasing SAH (OR 1.06, 95% CI 1.02–1.11, p= 0.006), while CSF had a protective effect toward VS (OR 0.99, 95% CI 0.98–0.99, p= 0.02). SAH/CSF ratio was also associated with VS (OR 1.03, 95% CI 1.01–1.05, p= 0.015). ROC curves suggested cutoffs at 120 ml CSF and 20 ml SAH for VS stratification. Combination of variables improved stratification accuracy compared to use of SAH alone.

This study provides a proof of concept for CSF correlating with angiographic VS after aneurysmal SAH. Quantification of CSF in conjunction with SAH might enhance risk stratification and exhibit advantages over traditional scores. The association of CSF has to be corroborated for delayed cerebral ischemia to further establish CSF as a surrogate parameter.

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