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Published on: November 15, 2024
Metabolic Chaos After Aneurysmal Subarachnoid Haemorrhage: Longitudinal Glucose-Potassium Ratio Dynamics and Clinical
Adrianna Lebiedzińska1, Jarosław Kędziora2, Jowita Woźniak3
1Clinical Department of Anesthesiology and Intensive Therapy, University Clinical Hospital in Wroclaw, 50-556 Wroclaw, Poland.
Background: Hyperglycemia after aneurysmal subarachnoid hemorrhage (aSAH) is associated with poor outcome, but admission glucose may not reflect dynamic metabolic stress during neurocritical care. Unlike previous studies focused primarily on admission measurements, we evaluated longitudinal glycemic trajectories and repeated glucose-potassium ratio (GPR) assessment across multiple observation windows in relation to clinical outcomes after aSAH. Methods: This retrospective single-center cohort study included 199 consecutive adults with aSAH treated between 2014 and 2025. Serial glucose and potassium measurements obtained during intensive care unit (ICU) stay were used to calculate admission values, longitudinal means across predefined observation windows, glycemic variability, hyperglycemia burden, and GPR. Primary outcomes were 30-day mortality and poor functional outcome at discharge (modified Rankin Scale ≥ 3). Secondary outcomes included delayed cerebral ischemia (DCI), delayed neurological deterioration (DND), transcranial Doppler (TCD) vasospasm, neurological deficit at ICU discharge, and length of stay. Results: Thirty-day mortality occurred in 35 patients (17.6%). Longitudinal metabolic markers demonstrated stronger associations with outcomes than admission values. Mean 30-day GPR was independently associated with mortality (OR 2.56, 95% CI 1.66-4.16; p < 0.001) and poor functional outcome (OR 2.90, 95% CI 1.80-5.03; p < 0.001). Hyperglycemia burden was associated with mortality (OR 1.10 per additional hyperglycemic day, 95% CI 1.02-1.20; p = 0.020) and poor functional outcome (OR 1.39, 95% CI 1.19-1.71; p < 0.001). Early GPR during the early brain injury period was associated with DCI (OR 1.40, 95% CI 1.01-1.93; p = 0.043), whereas 30-day GPR was associated with DND (OR 1.47, 95% CI 1.08-2.07; p = 0.019). ICU-specific GPR was associated with neurological deficit at ICU discharge (OR 2.06, 95% CI 1.29-3.50; p = 0.004), but not with TCD-defined vasospasm. Addition of GPR improved mortality prediction compared with the clinical model alone (AUC 0.86 vs. 0.77; p = 0.002). Conclusions: Longitudinal metabolic dysregulation after aSAH is strongly associated with mortality and neurological outcomes. Persistent hyperglycemia and repeated GPR assessment provide prognostic information beyond admission glucose, with early abnormalities associated with DCI and sustained disturbances linked to mortality and disability.
Background: Hyperglycemia after aneurysmal subarachnoid hemorrhage (aSAH) is associated with poor outcome, but admission glucose may not reflect dynamic metabolic stress during neurocritical care. Unlike previous studies focused primarily on admission measurements, we evaluated longitudinal glycemic trajectories and repeated glucose-potassium ratio (GPR) assessment across multiple observation windows in relation to clinical outcomes after aSAH. Methods: This retrospective single-center cohort study included 199 consecutive adults with aSAH treated between 2014 and 2025. Serial glucose and potassium measurements obtained during intensive care unit (ICU) stay were used to calculate admission values, longitudinal means across predefined observation windows, glycemic variability, hyperglycemia burden, and GPR. Primary outcomes were 30-day mortality and poor functional outcome at discharge (modified Rankin Scale ≥ 3). Secondary outcomes included delayed cerebral ischemia (DCI), delayed neurological deterioration (DND), transcranial Doppler (TCD) vasospasm, neurological deficit at ICU discharge, and length of stay. Results: Thirty-day mortality occurred in 35 patients (17.6%). Longitudinal metabolic markers demonstrated stronger associations with outcomes than admission values. Mean 30-day GPR was independently associated with mortality (OR 2.56, 95% CI 1.66-4.16; p < 0.001) and poor functional outcome (OR 2.90, 95% CI 1.80-5.03; p < 0.001). Hyperglycemia burden was associated with mortality (OR 1.10 per additional hyperglycemic day, 95% CI 1.02-1.20; p = 0.020) and poor functional outcome (OR 1.39, 95% CI 1.19-1.71; p < 0.001). Early GPR during the early brain injury period was associated with DCI (OR 1.40, 95% CI 1.01-1.93; p = 0.043), whereas 30-day GPR was associated with DND (OR 1.47, 95% CI 1.08-2.07; p = 0.019). ICU-specific GPR was associated with neurological deficit at ICU discharge (OR 2.06, 95% CI 1.29-3.50; p = 0.004), but not with TCD-defined vasospasm. Addition of GPR improved mortality prediction compared with the clinical model alone (AUC 0.86 vs. 0.77; p = 0.002). Conclusions: Longitudinal metabolic dysregulation after aSAH is strongly associated with mortality and neurological outcomes. Persistent hyperglycemia and repeated GPR assessment provide prognostic information beyond admission glucose, with early abnormalities associated with DCI and sustained disturbances linked to mortality and disability.
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