Contribution of dehydration to END in acute ischemic stroke not mediated via coagulation activation

Abstract

Objective: Dehydration is a risk factor for early neurological deterioration (END) after ischemic stroke, yet the underlying mechanism is unclear. Outbalanced coagulation activation may contribute to ischemia progression, concurrently with dehydration-induced blood viscosity change. We aimed to investigate whether the contribution of dehydration to END was mediated by blood coagulation activation. Methods: We retrospectively evaluated consecutive patients presenting with mild or moderate stroke (National Institutes of Health Stroke Scale score ≤14) within 24 hr of onset between Jan 2016 and Dec 2017. Dehydration was defined by a serum nitrogen to creatinine ratio (BUN/Cr) of ≥15 and blood coagulation activity was assessed with thromboelastography (TEG). The correlations between BUN/Cr and TEG parameters were assessed and their relationship in the development of END was analyzed. Results: Of 244 patients, 64 (26.2%) developed END within 3 days after admission. Patients with END had significantly higher BUN/Cr (19.2 ± 5.7 vs. 15.3 ± 2.9, p = 0.008), shorter R and K on TEG test (R: 3.9 ± 1.0 vs. 4.6 ± 1.1, p = 0.001; K: 1.3 ± 0.5 vs. 1.5 ± 0.4, p = 0.005). Comparison between patients with and without dehydration revealed no significant differences in TEG parameters. Multivariate regression suggested that dehydration status (OR 3.91, 95%CI 2.17–8.67, p = 0.008) and shorter R tercile on TEG (OR 3.18, 95% CI 1.23–7.90, p = 0.016) were independently associated with END; however, the odds ratio of R for END remained unchanged after adjustment for dehydration status. Conclusion: Our findings suggested that the contribution of dehydration to END after ischemic stroke was mediated by blood coagulation activation.