The Impact of Intracranial Blood Clearance on Brain Edema as a Predictor of Delayed Cerebral Infarction Following Subararachnoid Hemorrhage.

Introduction: Brain edema is a common finding after intracranial aneurysm rupture and the severity of brain edema has been associated with the risk for delayed cerebral infarction (DCI). In this retrospective comparative study, we investigate a) the role of brain edema for DCI development and b) the impact of active blood clearance on the association between brain edema and DCI.

Methods: This study included 799 aSAH patients treated between 10/2005 and 10/2019, excluding those with early mortality (<96h). The Subarachnoid Hemorrhage Early Brain Edema Score (SEBES) was recorded in all patients. Delayed Cerebral Infarctions (DCI) were determined by an independent rating board and neurological outcome was independently assessed by modified Rankin Scale at 6 months. Active blood clearance by cisternal lavage therapy was introduced in 10/2015. 609 patients were treated before and 190 after implementation of cisternal lavage, with 61 high-risk patients (32.1%) receiving lavage. Multivariable regression models were applied to analyzed the role of brain edema for DCI and a matched pairs analysis assessed the impact of cisternal lavage.

Results: DCI increased the risk of poor neurological outcome (mRS 4-6) by over 10 times (OR: 10.3, 95% CI 6.8 - 15.8, p<0.001). Poor WFNS scores on admission and high blood volume in the basal cisterns and ventricles were key DCI predictors. Brain edema raised the DCI risk by 2-3 times across all SEBES grades ≥1 (OR 1.90 to 2.80). Cisternal lavage was negatively associated with DCI development (OR: 0.23, 95% CI 0.13- 0.42, p<0.001). In patients selected for cisternal lavage, there was no association between brain edema severity and DCI risk.

Conclusion: Brain edema following aSAH is strongly linked to an increased risk of DCI. However, this association disappears once the underlying cause of DCI-intracranial blood-is cleared. Thus, brain edema serves as a marker of bleeding severity rather than a direct causal factor in the development of DCI.