Glucose Control

Abstract

Stress-related hyperglycemia is a common finding in acutely ill patients, and is related to the severity and outcome of the critical illness. The pathophysiology of stress hyperglycemia includes hormonal and neural signals, leading to increased production of glucose by the liver and peripheral insulin resistance mediated by the translocation of transmembrane glucose transporters. In one pioneering study, tight glycemic control by intensive insulin therapy in critically ill patients was associated with improved survival. However, this major finding was not confirmed in several other prospective randomized controlled trials. The reasons underlying the discrepancy between the first and the subsequent studies could include nutritional strategy (amount of calories provided, use of parenteral nutrition), case-mix, potential differences in the optimal blood glucose level (BG) in different types of patients, hypoglycemia and its correction, and the magnitude of glucose variability. Therefore, an improved understanding of the physiology and pathophysiology of glycemic regulation during acute illness is needed. Safe and effective glucose control will need improvement in the definition of optimal BG and in the measurement techniques, perhaps including continuous monitoring of insulin algorithms and closed-loop systems.

Hyperglycaemia in criticaly ill patients

“…Таким образом, несмотря на наличие ГГ, инсу-линзависимые ткани испытывают недостаток энергети-ческих субстратов. Преобладание анаэробного распада глюкозы над аэробным приводит к истощению запасов гликогена в печени, гиперлактатемии и усилению окси-дативного стресса [10], который, в свою очередь, способ-ствует поддержанию гипергликемии.…”

Hypoglycaemia, hypoglycorrhachia, neuroglycopenia and glycaemic thresholds

“…Various and sequential homoeostatic mechanisms are normally activated in order to maintain normoglycaemia (Preiser 2013). Lowering of the rate of insulin secretion by pancreatic beta cells represents the earliest response to decreasing plasma glucose concentrations (reacting within the reference range for plasma glucose concentrations).…”