Alexander E. Merkler, MD
Intracerebral hemorrhage (ICH) is a catastrophic type of stroke with a one-month mortality of 40%. Although initial ICH volume is the strongest predictor of mortality, hematoma expansion is a potentially modifiable risk factor that correlates well with both functional outcome and death and occurs in up to 40% of patients with ICH. Research has therefore focused on 1) identification of factors that predict hematoma expansion and 2) methods to reduce hematoma expansion.
The relationship between neuroinflammation, WBC count, and ICH pathophysiology is complex with prior studies suggesting that a higher WBC count predicts worse outcome. On the other hand, acute leukocytosis is associated with coagulation and consequently may lead to an arrest hematoma expansion in ICH. In this study, Dr. Morotti et al. evaluate the relationship between admission leukocytosis and hematoma expansion in patients with ICH. Hematoma expansion was defined as an increase in ICH volume of >30% or >6mL. WBC count was analyzed in quartiles.
The authors retrospectively evaluated 1302 prospectively collected patients with non-traumatic ICH. Of these patients, 15.9% experienced a hematoma expansion. The median WBC count on admission was 9200 cells/uL. Overall, after adjustment for demographics and other risk factors for hematoma expansion, higher admission WBC was independently associated with a reduced risk of hematoma expansion (OR for 1000 cells increase 0.91, 95% CI 0.86-0.96). In secondary analyses, the authors evaluated the effect of WBC subtypes on hematoma expansion; higher admission neutrophil count was associated with a lower risk of hematoma expansion (OR for 1000 cells increase 0.90, 95% CI 0.85-0.96) whereas higher admission monocyte count was associated with hematoma expansion (OR for 1000 cells increase, 2.71, 95% CI 1.08-6.83). Lymphocyte count was not associated with hematoma expansion.
Despite certain limitations such as lack of information regarding baseline infectious/inflammatory conditions that may have affected admission WBC counts, the study is certainly suggestive that acute inflammation plays a role in modulating the coagulation cascade following ICH. Perhaps identification of methods to acutely alter neuroinflammation may prove to be a salient method to halt hematoma expansion.