Abstract TP547: Peripheral Blood Indices for Platelet Reactivity and Systemic Inflammation Correlate With Coated-Platelet Trends After Aneurysmal Subarachnoid Hemorrhage

Introduction: Cerebral micro-thrombosis and neuroinflammation are important mechanisms causing delayed cerebral ischemia (DCI) after aneurysmal subarachnoid hemorrhage (aSAH). Apart from these local events, aSAH also mounts a systemic inflammatory response that may be reflected through various systemic markers. Mean platelet volume to platelet count (MPV:PLT), platelet count to lymphocyte count ratio (PLR), neutrophil count to lymphocyte count ratio (NLR) are established markers for platelet reactivity and systemic inflammation, respectively. Hypothesis: We assessed if peripheral blood indices (PBI) correlated with an established marker for platelet reactivity, coated-platelets, in predicting DCI after aSAH. Methods: A prospective cohort of 44 patients presenting with varying grades of aSAH were enrolled to assess coated-platelet levels in predicting DCI. Non-linear regression analysis was performed to assess the association correlation between coated-platelets and PBI trends in predicting DCI. Results: Twenty-nine (65.9%) of the enrolled patients developed DCI, and a higher rise in coated-platelets from patient’s baseline predicted development of DCI. Using non-linear regression models MPV:PLT showed a rise in ratio during the first 3 days followed by progressive decline. In contrast, PLR and NLR showed initial declines in their respective ratios until 4.2 and 5.8 days respectively followed by a gradual rise. Although slope differences for patients developing DCI as compared to those without DCI for MPV:PLT showed a trend towards significance (p=0.06), intergroup difference for PLR or NLR was not statistically significant. However, a significant relationship between MPV:PLT and coated-platelets (p<0.0001) was observed: with every unit rise in MPV:PLT ratio, coated-platelet levels increased by 0.04%. Similarly, a significant relationship was observed between PLR and coated-platelets (p=0.0001), with every unit rise in PLR, coated-platelets decreased by 2.06%. Conclusion: An early rise in MPV:PLT ratio with corresponding parallel rise in coated-platelet levels allude to presence of prothrombotic factors after aSAH. Also, a fall in PLR and NLR suggest a possible immunosuppressed state during the early phase after aSAH.