Hypoglycemia has been shown in the critically ill pateint to be independently associated with a 3-fold increase in mortality. In a trial of intensive insulin therapy, severe hypoglycemia occurred in up to 28% of patients.5 It is further speculated that the incidence of hypoglycemia is likely to be higher outside of clinical trials if intensive insulin protocols are used. The main consequences of acute and persistent hypoglycemia are neurologic deficits, which at times can be quite difficult to detect but remain a true concern. Hypoglycemia has been shown to cause acute electroencephalographic alterations. In a 4-year follow-up of patients treated with intensive insulin therapy (target blood glucose 80-110 mg/dL), this population was found to have impairments in quality of life and social functioning as compared to patients who received conventional insulin therapy.6
The relationship between hypoglycemia and outcome may be explained by an association with severity of illness and an increased risk of death, or a true deleterious biologic effect in critically ill patients. Hypoglycemia might exert biologic toxicity by increasing the systemic inflammatory response, inducing neuroglycopenia, inhibiting the corticosteroid response to stress, impairing sympathetic nervous system responsiveness, causing cerebral vasodilatation or by unidentified mechanisms. Furthermore, many experimental studies have demonstrated that both insulin and hypoglycemia can induce hypotension, vasodilatation, nitric oxide release, sympathetic system response exhaustion, and decreased ability to respond to repeated stress.