Elsevier

Critical Care Clinics

Volume 17, Issue 1, 1 January 2001, Pages 107-124
Critical Care Clinics

Stress-Induced Hyperglycemia

https://doi.org/10.1016/S0749-0704(05)70154-8Get rights and content

Stress-induced hyperglycemia is a common problem in patients admitted to the ICU, even when glucose homeostasis has previously been normal. Hyperglycemia is a near-universal finding in diabetic persons suffering catabolic illnesses and may worsen prognosis, although this possibility is controversial. The presence of hyperglycemia is associated with an increased risk of infectious complications in surgical patients, and indirect evidence indicates that maintenance of euglycemia can reduce the risk of infection. The causes of stress hyperglycemia include the presence of excessive counterregulatory hormones (glucagon, growth hormone, catecholamine, and glucocorticoid, either endogenous or exogenous), high circulating or tissue levels of cytokine (in particular tumor necrosis factor-α [TNα] and interleukin-1). This metabolic milieu results in failure of insulin to suppress hepatic gluconeogenesis despite hyperglycemia; in addition, insulin-mediated glucose uptake into skeletal muscle is impaired. Patients given excessive nutritional support, especially by the intravenous route, are particularly likely to encounter hyperglycemia. Insulin remains the obvious treatment for hyperglycemia, although evidence documenting the clinical benefit of aggressive insulin therapy in the ICU is sparse.

Section snippets

PREVALENCE OF STRESS HYPERGLYCEMIA IN CRITICALLY ILL PATIENTS

Hyperglycemia (defined loosely as plasma glucose > 200 mg/dL) in the absence of a diagnosis of diabetes is quite common, although most incidence and prevalence studies are small and restricted to specific populations. In addition, in the absence of measurement of glycohemoglobin, the possibility of underlying but undiagnosed diabetes mellitus rather than pure stress hyperglycemia must be considered. The phenomenon of stress hyperglycemia results primarily from excessive release of

Overview

Critical illness is associated with increases in the principal counterregulatory hormones (Table 2). The combination of excessive counterregulatory hormone release and overproduction of TNF-α, interleukin-1, and interleukin-6 is a major factor responsible for stress hyperglycemia in the nondiabetic host. The most obvious immediate explanation is that the metabolic milieu results in significant insulin resistance. Exogenous infusion of the catecholamines epinephrine and norepinephrine, but

Infectious Complications

The incidence of postoperative wound infections is significantly increased in patients with hyperglycemia, diabetes, or both.14 In this retrospective comparison of diabetic with nondiabetic patients who underwent coronary artery bypass grafting, rates of wound infections were significantly higher in the diabetic participants (7.5% versus 0.9%). It is plausible, however, that diabetic persons suffer increased infection rates because of vascular dysfunction and local wound problems. A key

Avoidance of Hyperglycemia

The use of TPN in the ICU is a frequent contributor to poor glucose control. Modification of TPN protocols should be considered in patients with stress hyperglycemia at baseline, to avoid exacerbation of the condition. First and foremost should be consideration of hypocaloric TPN providing at least 1000 kcal and 1 g/kg protein, not to exceed measured energy expenditure and 1.5 g/kg protein per day. The former therapy in a preliminary trial in critically ill, nontrauma patients had no obvious

SUMMARY

Stress hyperglycemia is common and likely to be associated with at least some of the same complications as hyperglycemia in true diabetes mellitus, such as poor wound healing and a higher infection rate. The predominant cause is the intense counterregulatory hormone and cytokine responses of critical illness, often compounded by excessive dextrose administration, usually as TPN. Although randomized data suggesting benefit of controlling hyperglycemia in hospitalized patients are paltry,

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    Address reprint requests to Karen McCowen, MD, Department of Medicine/Division of Clinical Nutrition, Beth Isreal Deaconess West Campus, 1 Deaconess Road, Boston, MA 02215. e-mail: [email protected]

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