Ultra-early neurological deterioration following a brain arteriovenous malformation rupture.

Purpose: This study aims to explore the impact of ultra-early neurological deterioration (U-END) on the outcome (mortality and poor neurological status) following a brain arteriovenous malformation (BAVM) rupture and identify determinants of U-END. Methods: Patients with BAVM ruptures admitted to a single tertiary care center were retrospectively reviewed. U-END was defined as a worsening by two or more points on the Glasgow Coma Scale (GCS). U-END was tested as a potential predictor of in-hospital mortality and poor outcomes. Univariate and multivariate analyses were performed to identify determinants of U-END. Patients with U-END were also matched and compared with BAVM rupture controls presenting with a GCS close or equal to either their initial or their lowest GCS. Results: A total of 248 patients with BAVM ruptures met the inclusion criteria, with 39 (15.7%) patients presenting with U-END. U-END was not associated with and was not an independent predictor of in-hospital mortality (12.8 vs. 10.5% in the rest of the study population; p = 0.67) or poor outcomes (39.5 vs. 36.9%; p = 0.77). The only independent determinants of U-END were hydrocephalus (OR 2.6 [95%CI, 1.1-6.4]; p = 0.03) and intraventricular hemorrhage (IVH; OR 3.5 [95%CI, 1.1-11.7]; p = 0.04). When compared to the initial GCS control group, U-END patients more often presented with IVH (89.5 vs. 64.1%; p = 0.009) and hydrocephalus (73 vs. 38.5%; p = 0.003). When compared to the lowest GCS control group, U-END patients had lower early S100B serum levels (0.35 ± 0.37 vs. 0.83 ± 1; p = 0.009) and a lower rate of poor outcome (39.5 vs. 64.9%; p = 0.03). Conclusion: Ultra-early neurological deterioration in ruptured BAVMs did not result in increased mortality or poor outcomes and was most often related to IVH and hydrocephalus.

Secondary S100B Protein Increase Following Brain Arteriovenous Malformation Rupture is Associated with Cerebral Infarction.

Early S100B protein serum elevation is associated with poor prognosis in patients with ruptured brain arteriovenous malformations (BAVM). The purpose of this study is to determine whether a secondary elevation of S100B is associated with early complications or poor outcome in this population. This is a retrospective study of patients admitted for BAVM rupture. A secondary increase of S100B was defined as an absolute increase by 0.1 µg/L within 30 days of admission. Fisher's and unpaired t tests followed by multivariate analysis were performed to identify markers associated with this increase. Two hundred and twenty-one ruptures met inclusion criteria. Secondary S100B protein serum elevation was found in 17.1% of ruptures and was associated with secondary infarction (p < 0.001), vasospasm-related infarction (p < 0.001), intensive care (p = 0.009), and hospital length of stay (p = 0.005), but not with early rebleeding (p = 0.07) or in-hospital mortality (p = 0.99). Secondary infarction was the only independent predictor of secondary increase of S100B (OR 9.9; 95% CI (3-35); p < 0.001). Secondary elevation of S100B protein serum levels is associated with secondary infarction in ruptured brain arteriovenous malformations.

S100B Serum Elevation Predicts In-Hospital Mortality After Brain Arteriovenous Malformation Rupture.

Background and Purpose- S100B protein serum elevation has been associated with poor prognosis in neurologically ill patients. The purpose of this study is to determine whether elevation of S100B is associated with increased in-hospital mortality after brain arteriovenous malformation rupture. Methods- This is a retrospective study of patients admitted for brain arteriovenous malformation rupture. The study population was divided into derivation and validation cohorts. Univariate followed by multivariate logistic regression was used to determine whether elevation of S100B serum levels above 0.5 µg/L during the first 48 hours after admission (S100Bmax48) was associated with in-hospital mortality. Results- Two hundred and three ruptures met inclusion criteria. Twenty-three led to in-hospital mortality (11%). Mean S100Bmax48 was 0.49±0.62 µg/L. In the derivation cohort (n=101 ruptures), multivariate analysis found Glasgow coma scale score ≤8 (odds ratio, 21; 95% CI, 2-216; 0.001) and an S100Bmax48>0.5 µg/L (odds ratio, 19; 95% CI, 2-188; P=0.001) to be associated with in-hospital mortality. When applied to the validation cohort (n=102 ruptures), the same model found only S100Bmax48>0.5 µg/L (odds ratio, 8; 95% CI, 1.5-44; P=0.01) to be associated with in-hospital mortality. Conclusions- Elevated S100B protein serum level is strongly associated with in-hospital mortality after brain arteriovenous malformation rupture.