1058. Complement Activation Associated With Edema Formation in Intracerebral Hemorrhage
Authors: Nina Teresa Yoh; Natasha Ironside; Trae Robison; Victoria Dreyer; Martin Schmidt, PhD; Brandon Christophe; E. Connolly, MD (New York, NY)
Stroke is the second leading cause of death and disability in the US with intracerebral hemorrhage (ICH) causing 50% of stroke-related deaths. In patients surviving the initial event, secondary injury triggered by the presence of hematoma plays a significant role in pathophysiological changes leading to poor outcomes. In murine studies, a strong association has been shown between complement overactivation and increased neurological damage and edema following ICH. In this study we assess and compare the concentrations of iC3b, a cleavage product of complement activation, to relative hematoma size, edema formation and clinical outcome following ICH.
This is a prospective, observational IRB-approved study of patients admitted to the NYP-Columbia neurological intensive care unit from March 2017 to February 2018 for the treatment of ICH. Arterial whole blood on post-ictal days 0-14 were collected along with clinical and imaging data from patients’ charts. Complement activation was measured via iC3b using a novel rapid lateral flow assay. Patients were included for analysis for whom imaging and complement data were available at presentation and at week 2. Seven patients met this criteria.
Comparison of hematoma volume and edema volume from presentation to two weeks post-ictal showed that increases in complement activation correlated with a statistically significant increase in absolute edema volume (R² = 0.82, p = 0.02) and a relative decrease in absolute hematoma size (R² = 0.61, p = 0.15).
Our data suggests that complement activation is involved in the robust inflammatory response that follows ICH and is associated with an increase in edema volume. Further studies can be aimed at elucidating specific mechanisms of secondary injury related to complement pathways. Furthermore, the association of the complement with edema and direct tissue damage following ICH makes complement activation an intriguing therapeutic target.