Letter: Systemic Immune-Inflammation Index Predicts Delayed Cerebral Vasospasm After Aneurysmal Subarachnoid Hemorrhage

To the Editor: We read with great interest the article by Geraghty et al1 on “Systemic Immune-Inflammation Index Predicts Delayed Cerebral Vasospasm After Aneurysmal Subarachnoid Hemorrhage.” The hypothesis and the work done by the authors on the same are commendable. The authors1 have used the retrospective study design to present an unbiased and well-balanced study comparing those presenting with and without delayed cerebral vasospasm after aneurysmal subarachnoid hemorrhage and its correlation with the Systemic Immune Inflammation Index (SII). The authors have been able to conclusively and objectively prove their hypothesis with significant results. The univariate and multivariate models have proven the hypothesis true. Furthermore, the authors have shown that even SII in addition to age, anterior circulation aneurysms, diabetes and Modified Fischer scale, predicts increased risk of vasospasm.1 However, there is limited number of patients in the study. In addition, the authors have mentioned that SII was assessed at admission. However, the time from ictus to measurement of SII or admission has not been mentioned. Furthermore, the measurement of SII was at a single point of time; there was no repeat measurement to indicate whether the SII value was increasing or decreasing. In addition, SII is elevated in case of other pathologies such as cancer, gliomas, and cerebral ischemia.2-6 The authors while evaluating for other factors at admission should have mentioned the exclusion of those patients with additional pathologies at admission. Although the SII multivariate model in this study has been shown to have an excellent Odds Ratio of 1.386 and P = .003, the predictive sensitivity of the same using the Youden Index is just 58.9%.1 Furthermore, digital subtraction angiography (DSA) is the gold standard for determining vasospasm.7 The authors state that DSA could not be performed in all patients and that transcranial Doppler ultrasonography values were used to establish vasospasm.1 Furthermore, there were a few patients in whom only DSA was performed and not transcranial Doppler ultrasonography. All patients with vasospasm irrespective of the method of assessment were, however, included in the same group. The authors should have accounted for the same or presented a further subgroup analysis of the same to prove that SII is elevated in patients with delayed cerebral vasospasm after aneurysmal subarachnoid hemorrhage. In conclusion, the authors have presented objective evidence to prove their hypothesis. We would like to congratulate the authors for a well-researched and analyzed study.