Impact of Perihematomal Edema on Infectious Complications after Spontaneous Intracerebral Hemorrhage.

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 ΔPHE72-24 (P < 0.01), whereas there was no association between infectious complications and ΔPHE24-3 (P = 0.09) or ΔPHE3-ad (P = 0.81). There was a positive correlation between ΔPHE72-24 and NLR (r = 0.85, 95% CI: 0.79-0.90, P < 0.01) and between ΔPHE72-24 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 ΔPHE72-24 was higher than the other patient groups (P < 0.01).

CONCLUSIONS

This study revealed a correlation between ΔPHE72-24 and infectious complications after spontaneous ICH, which was associated with markers of systemic inflammation. This phenotype linkage is a negative cascade that drives ND.