Volume of Aneurysmal Subarachnoid Hematoma Measured Quantitatively by 3D Slicer to Predict Symptomatic Cerebral Vasospasm.

Background and Objectives: Aneurysmal subarachnoid hemorrhage is strongly associated with symptomatic cerebral vasospasm. This study aims to investigate whether a quantitative measure of aneurysmal subarachnoid hematoma by 3D Slicer is more valuable for vasospasm risk prediction compared with modified Fisher scale and the new scale by Eagles. Materials and Methods: We performed a retrospective research of Digital Imaging and Communications in Medicine format (DICOM) in aneurysmal patients treated at our institution from 2019 to 2020. Association between vasospasm and hematoma volume by 3D Slicer was explored by univariate and multivariate analyses. Value of risk prediction was compared through area under the receiver operator characteristic curve (AUC) among the modified Fisher scale, the new scale by Eagles, and hematoma volume by 3D Slicer. Results: Hematoma volume by 3D Slicer had a significant relationship with vasospasm both by one-way analysis of variance (ANOVA; F = 19.37, P < 0.001) and a binary logistic regression analysis (odds ratio [OR] = 1.05, P = 0.016). Hematoma volume by 3D Slicer had a significantly higher AUC (0.708; 95% confidence interval [CI]: 0.618-0.798, P < 0.001) than the modified Fisher scale and the new scale by Eagles. The optimal diagnostic threshold for hematoma volume by 3D Slicer was 15.98 ml, and the sensitivity and specificity were 73.5% and 58.6%, respectively. Conclusions: Volume of aneurysmal subarachnoid hematoma measured quantitatively by 3D Slicer can improve the predictive value for symptomatic cerebral vasospasm.

Baveno-VII criteria to predict decompensation and initiate non-selective beta-blocker in compensated advanced chronic liver disease patients.

BACKGROUND/AIMS: The utility of Baveno-VII criteria of clinically significant portal hypertension (CSPH) to predict decompensation in compensated advanced chronic liver disease (cACLD) patient needs validation. We aim to validate the performance of CSPH criteria to predict the risk of decompensation in an international real-world cohort of cACLD patients. METHODS: cACLD patients were stratified into three categories (CSPH excluded, grey zone, and CSPH). The risks of decompensation across different CSPH categories were estimated using competing risk regression for clustered data, with death and hepatocellular carcinoma as competing events. The performance of "treating definite CSPH" strategy to prevent decompensation using non-selective beta-blocker (NSBB) was compared against other strategies in decision curve analysis. RESULTS: One thousand one hundred fifty-nine cACLD patients (36.8% had CSPH) were included; 7.2% experienced decompensation over a median follow-up of 40 months. Non-invasive assessment of CSPH predicts a 5-fold higher risk of liver decompensation in cACLD patients (subdistribution hazard ratio, 5.5; 95% confidence interval, 4.0-7.4). "Probable CSPH" is suboptimal to predict decompensation risk in cACLD patients. CSPH exclusion criteria reliably exclude cACLD patients at risk of decompensation, regardless of etiology. Among the grey zone, the decompensation risk was negligible among viral-related cACLD, but was substantially higher among the non-viral cACLD group. Decision curve analysis showed that "treating definite CSPH" strategy is superior to "treating all varices" or "treating probable CSPH" strategy to prevent decompensation using NSBB. CONCLUSION: Non-invasive assessment of CSPH may stratify decompensation risk and the need for NSBB in cACLD patients.