Intensive insulin therapy in the intensive care unit

This association is thought to be causal based on potential glucose toxicity in the context of ischemia‐reperfusion. Studies in patients and animals support the hypothesis of toxicity induced by excess glucose, specifically toxicity to the mitochondria of cells that take up glucose independent of insulin and in proportion to the circulating levels of glucose. 3‐5 However, the level at which blood glucose becomes toxic in the clinical context of critical illness is unclear. Several studies with heterogeneous designs and outcome measures have tested the hypothesis that tight control of blood glucose levels improves outcomes in critically ill patients. The first such randomized trial targeted a “strictly normal” level for fasting glucose (i.e., 4.4‐6.1 mmol/L), compared with usual care, in adult patients in surgical intensive care units (ICUs). 6 Usual care, at that time, was to initiate insulin only when a patient’s blood glucose level exceeded the renal threshold (12 mmol/L) and to discontinue insulin when the level decreased below 10 mmol/L. The intervention comprised insulin infused continuously via an accurate syringe-driven infusion pump to patients in a nonfasting state. Dose modifications were performed frequently by well-trained bedside nurses who used accurate blood gas analyzers to measure glucose and potassium levels. The intervention was labelled “intensive insulin therapy” and was found to reduce morbidity and mortality. A subsequent study in a medical ICU setting 7