***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
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    Input: Background and Purpose — We aim ed to analyze the frequency of  persistent hyperglycemia ( PH ) , its implication s for outcome , and to document the inpatient management of hyperglycemia . Methods — Post hoc analysis of the GLIAS ( Glycemia in Acute Stroke ) study , a multicenter , prospect i ve , and observational cohort study of 476 acute ischemic stroke patients . Capillary finger-prick glucose was determined on admission and during the first 48 hours . We defined PH was defined as at least 2 values ≥155 mg/dL. Outcome ( modified Rankin Scale ) was evaluated at 3 months . Results —  PH  developed in 117 patients ( 24.7 % ) .  PH was associated with poorer outcome ( modified Rankin Scale score > 2 : 56.2 % vs 28.1 % ; P<0.01 ) and higher mortality ( 26.7 % vs 5.9 % ; P<0.01 ) than those with glycemia < 155 mg/dL. PH ≥155 mg/dL was associated with a 4-fold increase in the odds of poor outcome at 3 months ( odds ratio , 4.7 ; 95 % confidence interval , 2.2–10.2 ) after adjustment for age , gender , hypertension , diabetes , stroke severity , admission glycemia , and infa rct volume . Only 20 % of patients with hyperglycemia ≥155 mg/dL received insulin on admission , with a progressive increase in the use  of insulin  during the following 48 hours . However , 114 ( 39.1 % ) out of 291 patients who received corrective treatment for hyperglycemia still had levels ≥155 mg/dL. Conclusions — PH ≥155 mg/dL is a common observation in acute ischemic stroke patients that is associated with poorer outcome and higher mortality . Almost 40 % of patients maintained levels ≥155 mg/dL despite corrective treatment Background and Purpose — Hyperglycemia is common after subarachnoid hemorrhage ( SAH ) . The extent to which prolonged hyperglycemia contributes to in-hospital complications and poor outcome after SAH is unknown . Methods — We studied an inception cohort of 281 SAH patients with an initial serum glucose level obtained within 3 days of SAH onset and who had at least 7 daily glucose measurements between SAH days 0 and 10 . We defined mean glucose burden ( GB ) as the average peak daily glucose level > 5.8 mmol/L ( 105 mg/dL ) . Hospital complications were recorded prospect ively , and 3-month outcome was assessed with the modified Rankin scale . Results — The median GB was 1.8 mmol/L ( 33 mg/dL ) . Predictors of high-GB included age ≥54 years , Hunt and Hess grade III – V , poor Acute Physiology and Chronic Health Evaluation (APACHE)-2 physiological subscores , and a history of diabetes mellitus ( all P≤0.001 ) . In a multivariate analysis , GB was associated with increased intensive care unit length of stay ( P=0.003 ) and the following complications : congestive heart failure , respiratory failure , pneumonia , and brain stem compression from herniation ( all P<0.05 ) . After adjusting for Hunt-Hess grade , aneurysm size , and age , GB was an independent predictor of death ( odds ratio , 1.10 per mmol/L ; 95 % CI , 1.01 to 1.21 ; P=0.027 ) and death or severe disability ( modified Rankin scale score of 4 to 6 ; odds ratio , 1.17 per mmol/L ; 95 % CI 1.07 to 1.28 , P<0.001 ) . Conclusions — Hyperglycemia after SAH is associated with serious hospital complications , increased intensive care unit length of stay , and an increased risk of death or severe disability Introduction Hyperglycaemia following aneurysmal subarachnoid hemorrhage ( SAH ) is associated with complications and impaired neurological recovery . The aim of this study was to determine the effect of insulin treatment for glucose control on cerebral metabolism in SAH patients . Methods This prospect i ve , nonr and omized study was conducted in 31 SAH patients in an intensive care unit ( age 52 ± 10 years , World Federation of Neurological Surgeons grade 2.9 ± 1.6 ) . A microdialysis catheter was inserted into the vascular territory of the aneurysm after clipping . Blood glucose levels above 140 mg/dl were treated with intravenous insulin and the microdialysates were analyzed hourly for the first 12 hours of infusion . Results No hypoglycaemia occurred . Twenty-four patients were treated with insulin for glucose control . Higher age and World Federation of Neurological Surgeons score were risk factors for need for insulin treatment ( P < 0.05 ) . Although blood glucose remained stable after initiation of insulin infusion , insulin induced a significant decrease in cerebral glucose at 3 hours after onset of the infusion until the end of the observation period ( P < 0.05 ) , reflecting high glucose utilization . The lactate : pyruvate ratio and glutamate did not increase , excluding ischaemia as possible cause of the decrease in glucose . Glycerol tended toward higher values at the end of the observation period ( 9 to 12 hours ) , reflecting either tissue damage after SAH or the beginning of cellular distress after insulin infusion . Conclusion Higher SAH grade was among the risk factors for need for insulin . Intensive glycaemic control using insulin induced a decrease of cerebral glucose and a slight increase in glycerol , though blood glucose remained normal . Future studies might detect relevant metabolic derangements when insulin treatment starts at low cerebral glucose levels , and may allow us to design a strategy for avoidance of insulin-induced metabolic crisis in SAH patients BACKGROUND AND PURPOSE Hyperglycemia following acute stroke is strongly associated with subsequent mortality and impaired neurological recovery , but it is unknown whether maintenance of euglycemia in the acute phase improves prognosis . Furthermore , the safety of such intervention is not established . METHODS In an explanatory , r and omized , controlled trial to test safety , 53 acute ( within 24 hours of ictus ) stroke patients with mild to moderate hyperglycemia ( plasma glucose between 7.0 and 17.0 mmol/L ) were r and omized to receive either a 24-hour infusion of 0.9 % ( 154 mmol/L ) saline or a glucose potassium insulin ( GKI ) infusion at 100 mL/h . The GKI consisted of 16 U human soluble insulin and 20 mmol potassium chloride in 500 mL 10 % glucose . Blood glucose was measured every 2 hours with Boehringer Mannheim Glycaemie test strips , pulse and blood pressure were measured every 4 hours , and plasma glucose sample s were taken every 8 hours . Insulin concentration in the GKI was altered according to BM glucose values . RESULTS There were no statistically significant differences between the 2 groups at baseline . Twenty-five patients received GKI , 1 of whom required intravenous glucose for symptomatic hypoglycemia . Plasma glucose levels were nonsignificantly lower in the GKI group throughout the infusion period . Four-week mortality in the GKI group was 7 ( 28 % ) , compared with 8 ( 32 % ) in the control group . CONCLUSIONS GKI infusions can be safely administered to acute stroke patients with mild to moderate hyperglycemia producing a physiological but attenuated glucose response to acute stroke , the effectiveness of which remains to be eluci date BACKGROUND The role of intensive insulin therapy in patients with severe sepsis is uncertain . Fluid resuscitation improves survival among patients with septic shock , but evidence is lacking to support the choice of either crystalloids or colloids . METHODS In a multicenter , two-by-two factorial trial , we r and omly assigned patients with severe sepsis to receive either intensive insulin therapy to maintain euglycemia or conventional insulin therapy and either 10 % pentastarch , a low-molecular-weight hydroxyethyl starch ( HES 200/0.5 ) , or modified Ringer 's lactate for fluid resuscitation . The rate of death at 28 days and the mean score for organ failure were co primary end points . RESULTS The trial was stopped early for safety reasons . Among 537 patients who could be evaluated , the mean morning blood glucose level was lower in the intensive-therapy group ( 112 mg per deciliter [ 6.2 mmol per liter ] ) than in the conventional-therapy group ( 151 mg per deciliter [ 8.4 mmol per liter ] , P<0.001 ) . However , at 28 days , there was no significant difference between the two groups in the rate of death or the mean score for organ failure . The rate of severe hypoglycemia ( glucose level , < or = 40 mg per deciliter [ 2.2 mmol per liter ] ) was higher in the intensive-therapy group than in the conventional-therapy group ( 17.0 % vs. 4.1 % , P<0.001 ) , as was the rate of serious adverse events ( 10.9 % vs. 5.2 % , P=0.01 ) . HES therapy was associated with higher rates of acute renal failure and renal-replacement therapy than was Ringer 's lactate . CONCLUSIONS The use of intensive insulin therapy placed critically ill patients with sepsis at increased risk for serious adverse events related to hypoglycemia . As used in this study , HES was harmful , and its toxicity increased with accumulating doses . ( Clinical Trials.gov number , NCT00135473 . Objective To determine whether hyperglycemia exerts deleterious effects via cerebral energy metabolism and to illuminate the effects of cerebral high/low glucose in patients with aneurysmal subarachnoid hemorrhage . Design and setting Prospect i ve , nonr and omized single-center study over a 2-year period in an intensive care unit at a primary -level university hospital . Patients 28 subarachnoid hemorrhage patients ( age 53 ± 10 years , WFNS grade 2.8 ± 1.5 ) classified as asymptomatic ( n = 5 ) or symptomatic with acute focal or delayed ischemic neurological deficits ( n = 23 ) . Measurements and results Hyperglycemia ( > 7.8 mmol/l ; > 140 mg/dl ) was more frequent in symptomatic patients and was reflected in higher glycerol concentrations than in asymptomatic patients . In all patients a microdialysis catheter was inserted into the tissue at risk ; dialysates were collected hourly for 10 days . Cerebral low-glucose episodes ( < 0.6 mmol/l ) and high-glucose episodes ( > 2.6 mmol/l ) occurred independently of blood glucose levels . During high-glucose episodes cerebral microdialysate levels were normal , while cerebral low glucose , occurring more frequently in symptomatic patients , was associated with severe cellular distress ( increase in lactate/pyruvate ratio , glutamate , glycerol ) and with unfavorable outcome if combined with hyperglycemia . Conclusions Although hyperglycemia was more frequent in symptomatic patients and associated with high glycerol levels , hyperglycemia was not related to cerebral high glucose . It appears that the association of adverse outcome with acute-phase hyperglycemia is not mediated by cerebral glucose metabolism . Cerebral low glucose was associated with severe metabolic distress and may present a target for therapy to improve clinical outcome Background : In patients with acute ischaemic stroke , hyperglycaemia has been retrospectively associated with negative outcome . There is an ongoing discussion as to which treatment algorithm , if any , provides the most effective prospect i ve intervention . Here we test the safety and feasibility of an intravenous insulin-only infusion protocol design ed for pragmatic routine clinical use . Methods : 40 ischaemic stroke patients with onset < 24 h ago , admitted to our stroke unit , were r and omized either to the study regimen ( 50 IU insulin in 50 ml 0.9 % saline solution applied intravenously via a perfusor pump ) , with the aim of reaching and maintaining blood glucose levels between 4.44 mmol/l ( 80 mg/dl ) and 6.11 mmol/l ( 110 mg/dl ) , or were treated with insulin subcutaneously if concentrations were above 11.10 mmol/l ( 200 mg/dl ) . Treatment was continued for 5 days . Primary outcome was the number of hypoglycaemic ( < 3.33 mmol/l ; < 60 mg/dl ) and severe hyperglycaemic ( > 16.65 mmol/l ; > 300 mg/dl ) events . Results : Hypoglycaemic events were significantly more common in patients treated intensively ( total n = 25 ; incidence rate ratio , IRR = 5.3 ; 95 % CI 
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Conclusions Intensive insulin therapy significantly increases the risk of hypoglycemia and does not influence mortality  among neurocritical care patients .
Very loose glucose control is associated with worse neurological recovery and should be avoided .