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Published on: October 23, 2020
The association between stress hyperglycemia ratio and cerebral edema in acute large vessel occlusion stroke
Li Zhang1, Xintian Xu2, Bailong Xin3
1Department of Neurology, Fifth Affiliated Hospital of Wenzhou Medical University (Lishui Municipal Central Hospital), Lishui, Zhejiang, China; Department of Neurology, The People's Hospital of Suichang County, Lishui, Zhejiang, China.
Background And Purpose:
Cerebral edema (CE) is a common complication of acute large vessel occlusion ischemic stroke (AIS-LVO). Stress-induced hyperglycemia may exacerbate brain damage, leading to adverse outcomes. Our study investigated the association between stress-induced hyperglycemia and CE after bridging therapy and achieved successful reperfusion (modified Thrombolysis in Cerebral Infarction [mTICI] score 2b-3) in AIS-LVO patients.
Methods:
This retrospective cohort study included 196 patients with AIS-LVO who underwent bridging therapy and achieved successful reperfusion at Lishui Central Hospital between January 2019 and December 2023. We calculated the Stress Hyperglycemia Ratio (SHR) using fasting blood glucose (FBG) and glycated hemoglobin (HbA1c) levels measured within 48 h of admission. The primary outcome was radiographically confirmed CE, and the secondary outcome was PH2-type hemorrhagic transformation (HT). Specifically, edema severity was graded 1-3 per SITS-MOST criteria, with grades CE1 and CE2 grouped as mild-to-moderate edema for comparison against the severe CE3 group. The associations between SHR and outcomes were analyzed using multivariable logistic regression, with restricted cubic splines (RCS) applied to explore nonlinear relationships. We also stratified analysesby diabetes status to validate the robustness of the findings.
Results:
The 196 enrolled patients were stratified into high-SHR (>0.94) and low-SHR (≤0.94) groups based on the median SHR value. Patients in the high-SHR group exhibited older age (71.1 ± 11.3 years), higher fasting blood glucose, and significantly increased risks of CE, CE3 and PH2 (all p < 0.05). Per-unit SHR increase was associated with significantly higher odds of PH2 (odds ratio [OR] = 4.01, 95 % confidence interval [CI]: 1.39-11.61), CE (OR = 3.31, 95 % CI: 1.73-6.31), and CE3 after stratification (OR = 2.65, 95 % CI: 1.38-5.08). RCS analysis demonstrated a linear dose-response relationship between SHR and CE (p < 0.001). Stratified analyses indicated stronger associations of SHR with PH2 (OR = 4.55, 95 % CI: 1.38-15.00) and CE (OR = 3.08, 95 % CI: 1.54-6.16) in non-diabetic patients, particularly for CE3 specifically demonstrated robust association (OR = 3.05, 95 % CI: 1.51-6.19) compared to attenuated effects in diabetic individuals.
Conclusion:
The SHR independently predicts poor functional outcomes in AIS-LVO. It shows significant association with CE (particularly CE3) in non-diabetic patients, suggesting that acute hyperglycemic stress has more pronounced effects in individuals without metabolic adaptation.
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