Abstract Body: Approximately 30% of aneurysmal subarachnoid hemorrhage (aSAH) patients who survive the rupture develop delayed cerebral ischemia (DCI) 4 to 10 days following aSAH. Multiple clinical studies indicate the cause of DCI is multifactorial, but identifying which patients are at-risk for developing DCI is lacking. Previous studies have identified numerous biomarkers, such as coagulation and platelet factors, which may predict patients at-risk for DCI, but to-date, no markers are widely utilized in the clinical setting. Thus, we sought to investigate various biomarkers of platelets to identify which factors are predictive of patients at-risk for DCI. aSAH patients were prospectively enrolled and had blood collected 1, 2, 4, 7, and 10 days post-aSAH. DCI was adjudicated by three independent clinicals. Blood was used from 148 aSAH patients (n=101 no DCI, N=47 DCI) for analysis of TEG, platelet receptors for activation (CD62p) and aggregation (PAC-1) via flow cytometry, platelet aggregation via Chrono-log, and 22 aSAH (n=17 no DCI, n=5 DCI) patients were used to analyze the platelet activation status (i.e. morphology, see Figures) via microscopy. Six healthy patients were used as controls. aSAH caused hypercoagulability in all aSAH patients. However, neither TEG nor Chrono-log parameters were reliable in predicting which aSAH patients would develop DCI. Similarly, the markers for platelet activation (CD62p) and aggregation (PAC-1) were not able to distinguish which aSAH patients would get DCI. Interestingly, morphological analysis of platelets revealed significantly higher platelet activation two days after aSAH in the aSAH patients who later developed DCI (see Figure). Although this preliminary study involves a small sample size of 22 patients, the results suggest that platelet morphology rather than other platelet tests may identify individuals at-risk for DCI following aSAH. However, further research with a larger patient cohort is necessary to validate these findings.