• Tomás Kotulák, Hynek Ríha, and Martin Haluzík.
• Institut klinické a experimentální medicíny Praha, Klinika anesteziologie a resuscitace, Kardiocentrum. tomas.kotulak@ikem.cz
• Cas. Lek. Cesk. 2011 Jan 1; 150 (1): 20-3.

AbstractIn the critically ill patient, hyperglycemia was believed to be a response by the body to a stressful situation. Stress-induced hyperglycemia is the consequence of increased levels of cortisol, cytokines, growth hormones, catecholamines, and glucagon resulting in the stimulation of endogenous glucose production through glycogenolysis and gluconeogenesis as well as other mechanisms including central and peripheral insulin resistance. Among other things, hyperglycemia has an effect on inflammation and function of the myocardium, kidney, central nervous system, and the immune system. The protective role of intensified insulin therapy (glycemia of 4.4-6.1 mmol/l) in the critically ill patient, as suggested by the Leuven trial, resulted in the quick and widespread adoption of this approach in practice. However, later studies did not support the Leuven trial results while pointing to the possibility of developing severe hyperglycemia. The large multicenter NICE-SUGAR study in 6,022 patients showed higher 90-day mortality in the group with tight glycemic control. The results of NICE-SUGAR led to revision of the guidelines for glycemic control in the critically, recommending to control glycemia below 10 mmol/l. The aim of this overview is to summarize available data on glycemic control in the critically ill patient.

15 keywords...

hide…