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. 2011 Oct;25(5):813-24.
doi: 10.1016/j.beem.2011.05.004.

Glycemic control in non-diabetic critically ill patients

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Glycemic control in non-diabetic critically ill patients

Farnoosh Farrokhi et al. Best Pract Res Clin Endocrinol Metab. 2011 Oct.

Abstract

Hyperglycemia is a common and costly health care problem in hospitalized patients. In hospital hyperglycemia is defined as any glucose value >7.8 mmol/l (140 mg/dl). Hyperglycemia is present in 40% of critically ill patients and in up to 80% of patients after cardiac surgery, with ∼ 80% of ICU patients with hyperglycemia having no history of diabetes prior to admission. The risk of hospital complications relates to the severity of hyperglycemia, with a higher risk observed in patients without a history of diabetes compared to those with known diabetes. Improvement in glycemic control reduces hospital complications and mortality; however, the ideal glycemic target has not been determined. A target glucose level between 7.8 and 10.0 mmol/l (140 and 180 mg/dl) is recommended for the majority of ICU patients. This review aims to present updated recommendations for the inpatient management of hyperglycemia in critically ill patients with and without a history of diabetes.

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Figures

Fig. 1
Fig. 1
Pathogenesis of stress hyperglycemia Stress hyperglycemia results from increased hepatic glucose production and impaired glucose utilization in peripheral tissues. Excess counterregulatory hormones (glucagon, cortisol, catecholamines, and growth hormone) increases lipolysis and protein breakdown (proteolysis), and impaired glucose utilization by peripheral tissues. Hyperglycemia causes osmotic diuresis that leads to hypovolemia decreased glomerular filtration rate and worsening hyperglycemia. At the cellular level increased blood glucose levels results in mitochondrial injury by generating reaction oxygen species and endothelial dysfunction by inhibiting nitric oxide production. Hyperglycemia increases levels of pro-inflammatory cytokine such as TNF-α, and IL-6 leading to immune system dysfunction, also increases plasminogen activator inhibitor-1 and fibrinogen causing platelet aggregation and hypercoagulable state. These changes can eventually lead to increased risk of infection, impaired wound healing, multiple organ failure, prolonged hospital stay and death.

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