Impact of Perihematomal Edema on Infectious Complications after Spontaneous Intracerebral Hemorrhage: Perihematomal edema on infectious complications

Objective: Intracerebral hematoma involves two mechanisms leading to brain injury: the mechanical disruption of adjacent brain tissue by the hematoma and delayed neurological injury. Delayed neurological injury involves perihematomal edema (PHE) formation. Infectious complications following intracerebral hemorrhage (ICH) are a significant contributor to post-ICH recovery. We sought to identify a correlation between PHE volumes and infectious complications following ICH. We also sought to explore the clinical impact of this association. Materials and Methods: This retrospective study included 143 patients with spontaneous ICH. CT scans were performed on admission, and 3 h, 24 h, and 72 h following admission. Hematoma and PHE volumes were calculated using a semi-automatic method. The absolute PHE volume at each time point and changes in PHE volume (ΔPHE) were calculated. Neutrophil to lymphocyte ratio (NLR) and serum C-reactive protein (CRP) levels were measured from the obtained blood samples. Neurological deterioration (ND) was assessed in all patients. Results: Infectious complications were associated with ΔPHE_72-24 (P < 0.01), whereas there was no association between infectious complications and ΔPHE_24-3 (P = 0.09) or ΔPHE_3-ad (P = 0.81). There was a positive correlation between ΔPHE_72-24 and NLR (r = 0.85, 95% CI: 0.79–0.90, P < 0.01) and between ΔPHE_72-24 and CRP levels (r = 0.89, 95% CI: 0.84–0.92, P < 0.01). The ND rate in the group of patients with infectious complications comorbid with high ΔPHE_72-24 was higher than the other patient groups (P < 0.01). Conclusions: This study revealed a correlation between ΔPHE_72-24 and infectious complications after spontaneous ICH, which was associated with markers of systemic inflammation. This phenotype linkage is a negative cascade that drives ND.