1. ¹Institute for Neurosurgical Pathophysiology, University Medical Center of the Johannes Gutenberg-University Mainz, Mainz, Germany
2. ²Clinic of Neurosurgery, University Hospital Basel, Switzerland
3. ³Department of Nuclear Medicine, University Medical Center of the Johannes Gutenberg-University Mainz, Mainz, Germany

Correspondence: Dr B Alessandri, Insitute for Neurosurgical Pathophysiology, University Medical Center of the Johannes Gutenberg-University Mainz, Langenbeckstrasse 1, Mainz D-55131, Germany. E-mail: alessandri@nc-patho.klinik.uni-mainz.de

Received 22 July 2009; Revised 2 September 2009; Accepted 28 September 2009; Published online 4 November 2009.

Abstract

Outcome from acute subdural hematoma is often worse than would be expected from the pure increase of intracranial volume by bleeding. The aim was to test whether volume-independent pathomechanisms aggravate damage by comparing the effects of blood infusion with those of an inert fluid, paraffin oil, on intracranial pressure (ICP), cerebral perfusion pressure (CPP), local cerebral blood flow (CBF), edema formation, glucose metabolism ([18F]-deoxyglucose, MicroPET ), and histological outcome. Rats were injured by subdural infusion of 300 L venous blood or paraffin. ICP, CPP, and CBF changes, assessed during the first 30 mins after injury, were not different between the injury groups at most time points (n=8 per group). Already at 2 h after injury, blood caused a significantly more pronounced decrease in glucose metabolism in the injured cortex when compared with paraffin (P<0.001, n=5 per group). Ipsilateral brain edema did not differ between groups at 2 h, but was significantly more pronounced in the blood-treated groups at 24 and 48 h after injury (n=8 per group). These changes caused a 56.2% larger lesion after blood when compared with paraffin (48.123.0 versus 21.111.8 mm³; P<0.02). Blood constituent-triggered pathomechanisms aggravate the immediate effects due to ICP, CPP, and CBF during hemorrhage and lead to early reduction of glucose metabolism followed by more severe edema and histological damage.