Glycemic management in critically ill patients
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摘要
Hyperglycemia associated with critical illness,also called "stress hyperglycemia" or "stress diabetes",is a consequence of many pathophysiologic hormonal responses including increased catecholamines,cortisol,glucagon,and growth hormone.Alterations in multiple biochemical pathways result in increased hepatic and peripheral insulin resistance with an uncontrolled activation of gluconeogenesis and glycogenolysis.Hyperglycemia has a negative impact on the function of the immune system,on the host response to illness or injury,and on infectious and overall outcomes.The degree of glucose elevation is associated with increased disease severity.Large randomized controlled trials including the Van den Berghe study,the NICE-SUGAR trial,VISEP and GLUCONTROL have shown that the control of glucose levels in critically ill patients has implications on outcome and that both hyperglycemia and hypoglycemia are detrimental and should be avoided.Glucose variability has also been shown to be detrimental.Aggressive glucose control strategies have changed due to the concerns of hypoglycemia and therefore intermediate target glucose control strategies are most often adopted.Different patient populations may vary with regards to optimal glucose targets,timing and approach for glucose control,and with regards to the prognostic significance of glucose excursions and variability.Medical,surgical,and trauma patients may benefit at different rates from glucose control and the approach may need to be adapted to various medical settings and to correspond to the workflow of health providers.Effect modifiers for the success of insulin therapy for hyperglycemia include the methods of nutritional supplementation and exogenous glucose administration.Further research is required to improve insulin protocols for glucose control,to further define glucose targets,and to enhance the accuracy of glucose measuring technologies.
Hyperglycemia associated with critical illness,also called "stress hyperglycemia" or "stress diabetes",is a consequence of many pathophysiologic hormonal responses including increased catecholamines,cortisol,glucagon,and growth hormone.Alterations in multiple biochemical pathways result in increased hepatic and peripheral insulin resistance with an uncontrolled activation of gluconeogenesis and glycogenolysis.Hyperglycemia has a negative impact on the function of the immune system,on the host response to illness or injury,and on infectious and overall outcomes.The degree of glucose elevation is associated with increased disease severity.Large randomized controlled trials including the Van den Berghe study,the NICE-SUGAR trial,VISEP and GLUCONTROL have shown that the control of glucose levels in critically ill patients has implications on outcome and that both hyperglycemia and hypoglycemia are detrimental and should be avoided.Glucose variability has also been shown to be detrimental.Aggressive glucose control strategies have changed due to the concerns of hypoglycemia and therefore intermediate target glucose control strategies are most often adopted.Different patient populations may vary with regards to optimal glucose targets,timing and approach for glucose control,and with regards to the prognostic significance of glucose excursions and variability.Medical,surgical,and trauma patients may benefit at different rates from glucose control and the approach may need to be adapted to various medical settings and to correspond to the workflow of health providers.Effect modifiers for the success of insulin therapy for hyperglycemia include the methods of nutritional supplementation and exogenous glucose administration.Further research is required to improve insulin protocols for glucose control,to further define glucose targets,and to enhance the accuracy of glucose measuring technologies.
Hyperglycemia associated with critical illness,also called "stress hyperglycemia" or "stress diabetes",is a consequence of many pathophysiologic hormonal responses including increased catecholamines,cortisol,glucagon,and growth hormone.Alterations in multiple biochemical pathways result in increased hepatic and peripheral insulin resistance with an uncontrolled activation of gluconeogenesis and glycogenolysis.Hyperglycemia has a negative impact on the function of the immune system,on the host response to illness or injury,and on infectious and overall outcomes.The degree of glucose elevation is associated with increased disease severity.Large randomized controlled trials including the Van den Berghe study,the NICE-SUGAR trial,VISEP and GLUCONTROL have shown that the control of glucose levels in critically ill patients has implications on outcome and that both hyperglycemia and hypoglycemia are detrimental and should be avoided.Glucose variability has also been shown to be detrimental.Aggressive glucose control strategies have changed due to the concerns of hypoglycemia and therefore intermediate target glucose control strategies are most often adopted.Different patient populations may vary with regards to optimal glucose targets,timing and approach for glucose control,and with regards to the prognostic significance of glucose excursions and variability.Medical,surgical,and trauma patients may benefit at different rates from glucose control and the approach may need to be adapted to various medical settings and to correspond to the workflow of health providers.Effect modifiers for the success of insulin therapy for hyperglycemia include the methods of nutritional supplementation and exogenous glucose administration.Further research is required to improve insulin protocols for glucose control,to further define glucose targets,and to enhance the accuracy of glucose measuring technologies.
引文
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2 Turina M,Fry DE,Polk HC.Acute hyperglycemia and the innate immune system:clinical,cellular,and molecular aspects.Crit Care Med 2005;33:1624-1633[PMID:16003073 DOI:10.1097/01.CCM.0000170106.61978.D8]
3 Turina M,Christ-Crain M,Polk HC.Diabetes and hyperglycemia:strict glycemic control.Crit Care Med 2006;34:S291-S300[PMID:16917434 DOI:10.1097/01.CCM.0000231887.84751.04]
4 Marfella R,Nappo F,De Angelis L,Siniscalchi M,Rossi F,Giugliano D.The effect of acute hyperglycaemia on QTc duration in healthy man.Diabetologia 2000;43:571-575[PMID:10855531DOI:10.1007/s001250051345]
5 Khaodhiar L,Mc Cowen K,Bistrian B.Perioperative hyperglycemia,infection or risk?Curr Opin Clin Nutr Metab Care 1999;2:79-82[PMID:10453334 DOI:10.1097/00075197-199901000-00013]
6 Perner A,Nielsen SE,Rask-Madsen J.High glucose impairs superoxide production from isolated blood neutrophils.Intensive Care Med 2003;29:642-645[PMID:12552364 DOI:10.1007/s00134-002-1628-4]
7 Finfer S,Chittock DR,Su SY,Blair D,Foster D,Dhingra V,Bellomo R,Cook D,Dodek P,Henderson WR,Hébert PC,Heritier S,Heyland DK,Mc Arthur C,Mc Donald E,Mitchell I,Myburgh JA,Norton R,Potter J,Robinson BG,Ronco JJ.Intensive versus conventional glucose control in critically ill patients.N Engl JMed 2009;360:1283-1297[PMID:19318384 DOI:10.1056/NEJMoa0810625]
8 Preiser JC,Devos P,Ruiz-Santana S,Mélot C,Annane D,Groeneveld J,Iapichino G,Leverve X,Nitenberg G,Singer P,Wernerman J,Joannidis M,Stecher A,Chioléro R.A prospective randomised multi-centre controlled trial on tight glucose control by intensive insulin therapy in adult intensive care units:the Glucontrol study.Intensive Care Med 2009;35:1738-1748[PMID:19636533DOI:10.1007/s00134-009-1585-2]
9 Brunkhorst FM,Engel C,Bloos F,Meier-Hellmann A,Ragaller M,Weiler N,Moerer O,Gruendling M,Oppert M,Grond S,Olthoff D,Jaschinski U,John S,Rossaint R,Welte T,Schaefer M,Kern P,Kuhnt E,Kiehntopf M,Hartog C,Natanson C,Loeffler M,Reinhart K.Intensive insulin therapy and pentastarch resuscitation in severe sepsis.N Engl J Med 2008;358:125-139[PMID:18184958 DOI:10.1056/NEJMoa070716]
10 Van den Berghe G,Wilmer A,Hermans G,Meersseman W,Wouters PJ,Milants I,Van Wijngaerden E,Bobbaers H,Bouillon R.Intensive insulin therapy in the medical ICU.N Engl J Med 2006;354:449-461[PMID:16452557 DOI:10.1056/NEJMoa052521]
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