Chronic Subdural Hematoma: Role of Vascular Endothelial Growth Factor and Craniotomy in Pathophysiology and Prevention of Recurrence

Abstract

Current body of evidence suggests that the maintenance or enlargement of chronic subdural hematoma (cSDH) is caused by multiple factors. Inflammatory and vascular endothelial growth factor (VEGF)–induced accumulation of hematoma plays an important role in pathophysiology of cSDH. If neomembrane is implicated in the propagation of inflammatory mediators, excision of the culprit membrane becomes essential to treat and prevent recurrence of cSDH. This retrospective study was conducted in a service hospital where 48 cases of cSDH were operated in 2 years. Patients were evaluated clinically and radiologically. Surgical procedure offered included burr hole craniotomy (BHC), twist drill craniotomy (TDC), or craniotomy (Cr) with excision of neomembrane. Cr was offered whenever there was suspicion or evidence of reaccumulation, solid or calcified hematoma formation, nonobliteration of the subdural space, or numerous thick membranes as were demonstrated in imaging. In Cr maximum part of outer neomembrane was excised and margins were coagulated. The excised outer neomembrane was sent for immunohistochemical examination to assess the VEGF expression. Depending on the VEGF expression as seen on the microscope, these expressions were grouped into weak, moderate, or strong VEGF expression. The study showed that cSDH patients with neomembrane formation benefit from Cr. The strong VEGF expression from the excised neomembrane further strengthens the proinflammatory VEGF theory propagation of cSDH. It further proves that excision of the culprit membrane is essential to prevent recurrences.

Keywords

chronic subdural hematoma - vascular endothelial growth factor - neomembrane

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