Abstract WP50: Stress Hyperglycemia And Early Neurological Deterioration In Patients With Acute LVO And Low NIHSS

Abstract

Introduction: Stress hyperglycemia is an essential survival response. However, it is associated with poor prognosis after ischemic stroke, and its contribution to collateral failure is not well defined. We investigated whether stress hyperglycemia would be associated with early neurological deterioration (END) in acute large vessel occlusion (LVO) patients who present with mild neurological deficit. Methods: From a multicenter stroke registry, ischemic stroke patients with acute anterior circulation LVO and mild symptoms (NIHSS<6) were included and were grouped by a history of diabetes before the index stroke. Stress hyperglycemia ratio (SHR) was calculated as a ratio of serum glucose at arrival over glycosylated hemoglobin. END was defined as an increase in total NIHSS≥2 or any increase in the NIHSS consciousness or motor sub-scores. Results: Among a total of 731 mild LVO patients (mean age 68.0±12.9 years; 62.7% male), 172 (23.5%) had a history of diabetes, and 73 (10.0%) were newly diagnosed with diabetes during admission. The SHR was higher in known diabetic patients compared to no-DM / newly diagnosed diabetic patients (24.3±8.5 vs. 21.8±5.6, p-value<0.01). END occurred in 94 (12.9%) patients. The second (T2) and third (T3) tertile groups of SHR were more likely to experience END than the lowest tertile group (adjusted odds ratio (aOR) 2.29 [95% confidence interval (CI), 1.26-4.17] for T2; aOR 1.85 [95% CI 1.01-3.39] for T3). The association was maintained in the no-DM / newly diagnosed diabetic subgroup but not in cases with a history of diabetes (p for interaction=0.047). [Figure] Conclusions: Stress hyperglycemia was associated with END in acute LVO patients with low NIHSS, especially in the subgroup of patients without or newly diagnosed diabetes. In patients without a history of diabetes, where the physiologic response to hyperglycemia may currently be preserved, intensive glycemic control may benefit in maintaining leptomeningeal collaterals.