gms | German Medical Science

Cerebral vasospasm is a common and potentially devastating complication in patients who have sustained aneurysmal subarachnoid hemorrhage (SAH). Recently, convincing data have implicated a role of inflammation in the development and maintenance of cerebral vasospasm. Several studies suggest that various constituents of the inflammatory response, including adhesion molecules, cytokines, leukocytes, immunoglobulins, and complement, may be critical in the pathogenesis of cerebral vasospasm. Some of these inflammatory mediators are induced by acute phase proteins such as the C-reactive protein (CRP). The aim of this study was to evaluate the relationship of the C-reactive protein to the likelihood of a delayed neurological deficit after aneurysmal SAH.

Eighty-eight patients suffering from aneurysmal SAH were included in our study. The serum CRP, blood counts and TCD measurements were evaluated on a daily basis until day 8 after SAH. General clinical data, data concerning the treatment as well as the presence of a ischemic lesion on the discharge CT scan were recorded. Furthermore outcome data and data concerning infections such as pneumonia, ventriculitis etc. were collected.

Thirty-seven patients (42%) developed delayed ischemic lesions. 59 patients showed a relevant infection (67%) but only 2 patients developed bacterial infections before day 7 after SAH. Serum CRP values increased from initially 16.6µg/l (range 0-68 µg/l) to 100.2µg/l (range 40.9µg/l-342µg/l) In the correlation analysis there was a statistically significant correlation of an increase of the serum CRP of day 3 to 4 after SAH to the development of a ischemic lesion on the discharge CT scan (p< 0.003). This increase did not correlate to the development of a bacterial infection. Serum leucocyte counts did not correlate to the serum CRP. However the increase correlated to the outcome data according to the Glasgow outcome Scale on discharge as well as the increase of flow velocities in the transcranial doppler measurements.

It is plausible that the inflammatory response may indeed represent a critical common pathway in the pathogenesis of cerebral vasospasm after SAH. Investigations into the nature of the inflammatory response accompanying SAH are needed to elucidate the precise role(s) of inflammatory events in SAH-induced pathologies.