SURG-72. Ischemia Predicts Poorer Survival in Glioblastoma Independent of Neurological Deficits

Abstract INTRODUCTION Tissue ischemia and hypoxia are recognized contributors to glioblastoma (GBM) pathophysiology in preclinical and in vitro models. However, the prognostic significance of postoperative tissue ischemia in patients with GBM remains poorly defined. This study aims to investigate the association between postoperative ischemia and survival outcomes in GBM patients. METHODS A retrospective analysis was performed on patients with GBM treated between 2013 and 2024 who had postoperative imaging available within 72 hours. Postoperative ischemic changes were defined as new areas of diffusion restriction and dichotomized as small and large, confluent ischemic changes based on median infarct volume (5 cm3). RESULTS Postoperative ischemic changes were observed in 203 patients (45%), with 96 (21.3%) exhibiting rim restriction only. The incidence of new or worsened neurological deficits was significantly higher in patients with small (25.5%) or large (46.4%) ischemic changes (p < 0.001). Patients with large ischemic changes had significantly shorter progression-free survival (PFS: 6 months [4.4–7.6]) and overall survival (OS: 14 months [7.6–20.4]) compared to those with smaller or no ischemic injury (PFS: p = 0.02; OS: p < 0.001). Increasing infarct volume was independently associated with reduced PFS (HR = 1.02, 95% CI: 1.01–1.03; p = 0.005) and OS (HR = 1.02, [1.01–1.032]; p = 0.002), after adjusting for neurological function and other confounders. When infarct volume was treated as a categorical variable, large ischemic changes remained independently predictive of shorter PFS (HR =1.4, [1.02–1.9]; p = 0.03) and OS (HR = 1.8, [1.3–2.4]; p < 0.001). CONCLUSION Increasing infarct volume is associated with a stepwise decline in both PFS and OS, with the most pronounced effects observed in patients with large, confluent ischemic changes—independent of postoperative neurological deficits. These findings highlight the critical importance of minimizing ischemic injury during maximal safe resection. Elucidating the cellular and molecular mechanisms underlying ischemia in glioblastoma may offer novel avenues for refining surgical approaches and developing adjunctive therapies.