BACKGROUND: Many ICUs have implemented protocols for tight glucose control, but there are few data on hypoglycemia and neurologic outcomes in patients with subarachnoid hemorrhage (SAH). METHODS: We prospectively ascertained 172 patients with SAH, who were treated according to a standard protocol for target glucose 80-110 mg/dl. Outcomes were assessed with the modified Rankin scale (mRS) at 14 days, 28 days, and 3 months. RESULTS: Worse neurologic injury at admission (P < 0.001) and a history of diabetes (P = 0.002) were associated with increased glucose variance. There was lower nadir glucose in patients with radiographic cerebral infarction (81 +/- 15 vs. 87 +/- 16 mg/dl, P = 0.02), symptomatic vasospasm (78 +/- 12 vs. 84 +/- 16 mg/dl, P = 0.04) and angiographic vasospasm (79 +/- 14 vs. 86 +/- 16 mg/dl, P = 0.01), but maximum and mean glucose values were not different. Glucose < 80 mg/dl was earlier and more frequent in patients with worse functional outcome at 3 months (P < 0.001). Progressive reductions in nadir glucose were associated with increasing functional disability at 3 months (P = 0.001) after accounting for neurologic grade and mean glucose. Severe hypoglycemia (<40 mg/dl) occurred in one patient. CONCLUSIONS: In patients with SAH, nadir glucose < 80 mg/dl is associated with cerebral infarction, vasospasm, and worse functional outcomes in multivariate models. Protocols for target glucose 80-110 mg/dl effectively control hyperglycemia, but may place patients with SAH at risk for vasospasm, cerebral infarction, and poor outcome even when severe hypoglycemia does not occur.
BACKGROUND: Many ICUs have implemented protocols for tight glucose control, but there are few data on hypoglycemia and neurologic outcomes in patients with subarachnoid hemorrhage (SAH). METHODS: We prospectively ascertained 172 patients with SAH, who were treated according to a standard protocol for target glucose 80-110 mg/dl. Outcomes were assessed with the modified Rankin scale (mRS) at 14 days, 28 days, and 3 months. RESULTS: Worse neurologic injury at admission (P < 0.001) and a history of diabetes (P = 0.002) were associated with increased glucose variance. There was lower nadir glucose in patients with radiographic cerebral infarction (81 +/- 15 vs. 87 +/- 16 mg/dl, P = 0.02), symptomatic vasospasm (78 +/- 12 vs. 84 +/- 16 mg/dl, P = 0.04) and angiographic vasospasm (79 +/- 14 vs. 86 +/- 16 mg/dl, P = 0.01), but maximum and mean glucose values were not different. Glucose < 80 mg/dl was earlier and more frequent in patients with worse functional outcome at 3 months (P < 0.001). Progressive reductions in nadir glucose were associated with increasing functional disability at 3 months (P = 0.001) after accounting for neurologic grade and mean glucose. Severe hypoglycemia (<40 mg/dl) occurred in one patient. CONCLUSIONS: In patients with SAH, nadir glucose < 80 mg/dl is associated with cerebral infarction, vasospasm, and worse functional outcomes in multivariate models. Protocols for target glucose 80-110 mg/dl effectively control hyperglycemia, but may place patients with SAH at risk for vasospasm, cerebral infarction, and poor outcome even when severe hypoglycemia does not occur.
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