4.2 Article

Leukocytosis in Patients with Neurologic Deterioration after Acute Ischemic Stroke is Associated with Poor Outcomes

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JOURNAL OF STROKE & CEREBROVASCULAR DISEASES
卷 22, 期 7, 页码 E111-E117

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ELSEVIER
DOI: 10.1016/j.jstrokecerebrovasdis.2012.08.008

关键词

Deterioration; leukocytosis; National Institutes of Health Stroke Scale; outcome; prognosis; stroke

资金

  1. AHRQ HHS [T32 HS013852] Funding Source: Medline

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Background: Neurologic deterioration (ND) after acute ischemic stroke (AIS) has been shown to result in poor outcomes. ND is thought to arise from penumbral excitotoxic cell death caused in part by leukocytic infiltration. Elevated admission peripheral leukocyte levels are associated with poor outcomes in stroke patients who suffer ND, but little is known about the dynamic changes that occur in leukocyte counts around the time of ND. We sought to determine if peripheral leukocyte levels in the days surrounding ND are correlated with poor outcomes. Methods: Patients with AIS who presented to our center within 48 hours of symptom onset between July 2008 and June 2010 were retrospectively identified by chart review and screened for ND (defined as an increase in National Institutes of Health Stroke Scale score >= 2 within a 24-hour period). Patients were excluded for steroid use during hospitalization or in the month before admission and infection within the 48 hours before or after ND. Demographics, daily leukocyte counts, and poor functional outcome (modified Rankin Scale score 3-6) were investigated. Results: Ninety-six of the 292 (33%) patients screened had ND. The mean age was 69.5 years; 62.5% were male and 65.6% were black. Patients with a poor functional outcome had significantly higher leukocyte and neutrophil levels 1 day before ND (P = .048 and P = .026, respectively), and on the day of ND (P = .013 and P = .007, respectively), compared to patients with good functional outcome. Conclusions: Leukocytosis at the time of ND correlates with poor functional outcomes and may represent a marker of greater cerebral damage through increased parenchymal inflammation.

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