Do Early Prognostic Measures Differentiate Mechanisms of ICU Death in Aneurysmal Subarachnoid Hemorrhage? An Analysis of Fatal Outcomes

Background/Objectives: In aneurysmal subarachnoid hemorrhage (aSAH), intensive care unit (ICU) deaths may follow neurological or systemic pathways, but the relationship between early prognostic measures and the mechanism of death is unclear. Methods: We retrospectively reviewed 261 consecutive adults with aSAH admitted to the ICU between January 2020 and June 2026. World Federation of Neurosurgical Societies (WFNS) grade, modified Fisher scale and Subarachnoid Hemorrhage Early Brain Edema Score (SEBES) were assessed at admission; the neutrophil-to-lymphocyte ratio (NLR) and C-reactive protein (CRP)-to-albumin ratio (CAR) came from the first routine blood sample; and Acute Physiology and Chronic Health Evaluation II (APACHE II) and Sequential Organ Failure Assessment (SOFA) came from the first 24 h. Brain death was assigned to the neurological category by a predefined rule; the remaining deaths were adjudicated independently by two intensivists. Results: Eighty-six patients (33.0%) died: 45 (52.3%) neurological, 37 (43.0%) systemic/medical and 4 (4.7%) mixed/undetermined; 94.6% of systemic/medical deaths were sepsis-related. Agreement among the 54 independently adjudicated deaths was high (κ = 0.829). CAR discriminated toward systemic/medical death (AUC 0.671; 95% CI 0.552–0.791), whereas APACHE II (0.702) and SOFA (0.682) discriminated toward neurological death; WFNS (0.643) and SEBES (0.638) showed the same direction. NLR did not discriminate mechanism of death in this cohort (0.449). CAR was very highly correlated with CRP (ρ = 0.994). Conclusions: Among aSAH decedents, early prognostic measures were associated with the mechanism of death in opposite directions; the systemic/medical association predominantly reflected sepsis-related deaths. Because the analysis was restricted to decedents and time to death differed by mechanism (7 versus 26 days), the findings are exploratory and do not establish cause-specific risk prediction in the overall aSAH population.