Background The optimal target range for blood glucose in critically ill patients remains unclear. Methods Within 24 hours after admission to an intensive care unit(ICU), adults who were expected to require treatment in the ICU on 3 or more consecutive days were randomly assigned to undergo either intensive glucose control, with a target blood glucose range of 81 to 108 mg per deciliter(4.5 to 6.0 mmol per liter), or conventional glucose control, with a target of 180 mg or less per deciliter(10.0 mmol or less per liter). We defined the primary end point as death from any cause within 90 days after randomization. Results Of the 6104 patients who underwent randomization, 3054 were assigned to undergo intensive control and 3050 to undergo conventional control; data with regard to the primary outcome at day 90 were available for 3010 and 3012 patients, respectively. The two groups had similar characteristics at baseline. A total of 829 patients(27.5%) in the intensive-control group and 751(24.9%) in the conventional-control group died(odds ratio for intensive control, 1.14; 95% confidence interval, 1.02 to 1.28; P=0.02). The treatment effect did not differ significantly between operative(surgical) patients and nonoperative(medical) patients(odds ratio for death in the intensive-control group, 1.31 and 1.07, respectively; P = 0.10). Severe hypoglycemia(blood glucose level, <40 mg per deciliter>[2.2 mmol per liter]) was reported in 206 of 3016 patients(6.8%) in the intensive-control group and 15 of 3014(0.5%) in the conventional-control group(P<0.001). There was no significant difference between the two treatment groups in the median number of days in the ICU(P = 0.84) or hospital(P = 0.86) or the median number of days of mechanical ventilation(P = 0.56) or renal-replacement therapy(P=0.39). Conclusions In this large, international, randomized trial, we found that intensive glucose control increased mortality among adults in the ICU: a blood glucose target of 180 mg or less per deciliter resulted in lower mortality than did a target of 81 to 108 mg per deciliter.(ClinicalTrials.gov number, NCT00220987.)
In critically ill patients with acute kidney injury, treatment with higher-intensity continuous renal-replacement therapy did not reduce mortality at 90 days. (ClinicalTrials.gov number, NCT00221013.)
Background and Purpose-The Intensive Blood Pressure Reduction In Acute Cerebral Haemorrhage Trial (INTERACT) study suggests that early intensive blood pressure (BP) lowering can attenuate hematoma growth at 24 hours after intracerebral hemorrhage. The present analyses aimed to determine the effects of treatment on hematoma and perihematomal edema over 72 hours. Methods-INTERACT included 404 patients with CT-confirmed intracerebral hemorrhage, elevated systolic BP (150 to 220 mm Hg), and capacity to start BP-lowering treatment within 6 hours of intracerebral hemorrhage. Patients were randomly assigned to an intensive (target systolic BP 140 mmHg) or standard guideline-based management of BP (target systolic BP 180 mm Hg) using routine intravenous agents. Baseline and repeat CTs (24 and 72 hours) were performed using standardized techniques with digital images analyzed centrally. Outcomes were increases in hematoma and perihematomal edema volumes over 72 hours. Results-Overall, 296 patients had all 3 CT scans available for the hematoma and 270 for the edema analyses. Mean systolic BP was 11.7 mm Hg lower in the intensive group than in the guideline group during 1 to 24 hours. Adjusted mean absolute increases in hematoma volumes (mL) at 24 and 72 hours were 2.40 and 0.15 in the guideline group compared with Ϫ0.74 and Ϫ2.31 in the intensive group, respectively, an overall difference of 2.80 (95% CI, 1.04 to 4.56; Pϭ0.002). Adjusted mean absolute increases in edema volumes (mL) at 24 and 72 hours were 6.27 and 10.02 in the guideline group compared with 4.19 and 7.34 in the intensive group, respectively, for an overall difference of 2.38 (95% CI, Ϫ0.45 to 5.22; Pϭ0.10). Conclusion-Early intensive BP-lowering treatment attenuated hematoma growth over 72 hours in intracerebral hemorrhage. There were no appreciable effects on perihematomal edema. (Stroke. 2010;41:307-312.)
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