Abstract

The role of inflammatory response in the pathophysiology of subarachnoid hemorrhage (SAH) is being increasingly recognized. This study analyzed the impact of cellular and biochemical markers of early inflammatory response to ictus on outcome after SAH. Patients with SAH were prospectively studied for markers of early cellular, biochemical, and cytotoxic inflammatory response, including total leukocyte count (TLC), high-sensitivity C-reactive protein (hs-CRP), and lactate dehydrogenase. The relationship of these markers to delayed cerebral ischemia (DCI), new infarct, and Glasgow Outcome Scale (GOS) score at 3 months was studied. The study comprised 246 patients. Of patients, 94 who developed DCI had a significantly higher TLC [± SD] (11.2× 10(3)/mm(3) [± 4.0] vs. 9.4× 10(3)/mm(3) [± 2.9], P= 0.001) and 62 with new infarct had significantly higher TLC (11.0× 10(3)/mm(3) [± 3.6] vs. 9.8× 10(3)/mm(3) [± 3.4], P= 0.05). GOS score had a significant inverse relationship to TLC at admission. The mean TLC [± SD] was 12.7× 10(3)/mm(3) [± 4.2], 11.7× 10(3)/mm(3) [± 3.1], 10.2× 10(3)/mm(3) [± 3.4], and 9.3× 10(3)/mm(3) [± 2.8] among patients with GOS scores of 1, 3, 4, and 5 (P < 0.001). hs-CRP showed a trend of an inverse relationship to GOS score in univariate analysis. Lactate dehydrogenase had no relationship with any outcome parameter. In multivariate analysis, higher admission TLC had a significant association with DCI (P= 0.01) and poorer GOS score (P < 0.001), and higher hs-CRP had a significant association with poorer GOS score (P= 0.05). A leukocytosis response to ictus seems to have a significant independent association with both DCI and poor GOS score, and hs-CRP level had a significant independent association with poor GOS score, indicating preeminence of early cellular response in SAH pathophysiology.

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