Moritz Scherer1, Jin-On Jung2, Jonas Cordes3, Lars Wessels2, Alexander Younsi2, Silvia Schönenberger4, Markus Alfred Möhlenbruch5, Klaus Maier-Hein3, Andreas Unterberg2, Klaus Zweckberger2. 1. Department of Neurosurgery, Heidelberg University Hospital, Im Neuenheimer Feld 400, 69120, Heidelberg, Germany. moritz.scherer@med.uni-heidelberg.de. 2. Department of Neurosurgery, Heidelberg University Hospital, Im Neuenheimer Feld 400, 69120, Heidelberg, Germany. 3. Division of Medical Image Computing, German Cancer Research Center (DKFZ), Heidelberg, Germany. 4. Department of Neurology, Heidelberg University Hospital, Heidelberg, Germany. 5. Department of Neuroradiology, Heidelberg University Hospital, Heidelberg, Germany.
Abstract
BACKGROUND: 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. RESULTS: 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. CONCLUSION: 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.
BACKGROUND: 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. RESULTS: 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. CONCLUSION: 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.