Attempted control of hyperglycemia during cardiopulmonary bypass fails to improve neurologic or neurobehavioral outcomes in patients without diabetes mellitus undergoing coronary artery bypass grafting.

OBJECTIVE: Hyperglycemia worsens outcomes in critical illness. This randomized, double-blind, placebo-controlled clinical trial tested whether insulin treatment of hyperglycemia during cardiopulmonary bypass would reduce neurologic, neuro-ophthalmologic, and neurobehavioral outcomes after coronary artery bypass grafting. METHODS: Three hundred eighty-one nondiabetic patients undergoing isolated coronary artery bypass grafting were given infusions of insulin or placebo when their blood glucose concentration exceeded 100 mg/dL during cardiopulmonary bypass. The primary outcome measure was the combined incidence of new neurologic, neuro-ophthalmologic, or neurobehavioral deficits or neurologic death observed at 4 to 8 days postoperatively. This same measure was assessed secondarily at 6 weeks and 6 months. Length of hospital stay was also compared as a secondary assessment. RESULTS: The 2 groups were well matched at baseline. The insulin-treated group had significantly lower blood glucose concentrations during bypass. Sixty-six percent of subjects in the insulin-treated group and 67% of subjects in the control group demonstrated a new or worsening neurologic, neuro-ophthalmologic, or neurobehavioral deficit or neurologic death at the 4- to 8-day assessment. Outcomes were also similar in the 2 groups at 6 weeks (37% and 39% incidence, respectively) and 6 months (30% and 25%, respectively). Median lengths of stay were 7 and 6 days, respectively, in the treatment and control groups. None of these outcome differences was statistically significant. CONCLUSION: Attempted control of hyperglycemia during cardiopulmonary bypass had no significant effect on the combined incidence of neurologic, neuro-ophthalmologic, or neurobehavioral deficits or neurologic death and failed to shorten the length of hospital stay. These results do not contradict those of other studies showing that aggressive control of hyperglycemia in the postoperative period will improve outcome.

Intraoperative insulin therapy does not reduce the need for inotropic or antiarrhythmic therapy after cardiopulmonary bypass.

OBJECTIVE: To determine whether attempted glucose control through intraoperative insulin therapy reduces the need for inotropic or antiarrhythmic therapy after cardiopulmonary bypass (CPB). DESIGN: Post hoc analysis of a randomized, masked clinical trial of insulin therapy for prevention of neurobehavioral deficits. SETTING: Single university hospital. PARTICIPANTS: Nondiabetic patients undergoing elective coronary artery bypass graft surgery (n = 381). INTERVENTIONS: Patients received either insulin infusions in an attempt to maintain blood glucose at 80 to 120 mg/dL (n = 188) or placebo (saline; n = 193). Inotropic therapy was defined as the initiation of vasoactive support with epinephrine or amrinone infusions or mechanical support with the initiation of an intra-aortic balloon pump in the operating room or within 12 hours postoperatively. Antiarrhythmic therapy was defined as cardioversion, antiarrhythmic medications, or pacing. MEASUREMENTS AND MAIN RESULTS: Of patients, 64 in the placebo group and 71 in the insulin group required inotropic support after CPB (p = not significant). The use of cardioversion (55 in placebo group v 61 in insulin group), antiarrhythmic medications (64 in placebo group v 76 in insulin group), and pacing (118 in placebo group v 117 in insulin group) was similar between groups. Inotropic drug support was associated with age >60 years, female gender, reduced preoperative ejection fraction, history of angina, and increased duration of CPB. CONCLUSION: Intraoperative insulin therapy did not reduce the use of inotropic or antiarrhythmic support after cardiac surgery with CPB. The lack of benefit may be due to the inability to prevent hyperglycemia during the physiologic stress of CPB or a tribute to the effectiveness of modern myocardial preservation techniques.

Emboli and Neuropsychological Outcome Following Cardiopulmonary Bypass.

The dramatic decline in mortality related to cardiac surgery has resulted in over 330,000 surgeries involving cardiopulmonary bypass (CPB) being performed yearly in the United States. Although few patients die as a result of cardiac surgery, over two thirds of the patients demonstrate evidence of acute neuropsychological dysfunction postoperatively. The potential mechanisms contributing to post-CPB neuropsychological deficits are many, but two major inter-related etiologic factors, hypo-perfusion and emboli, are suggested as the probable culprits. If embolism is the cause of the deficits, increasing cerebral perfusion would deliver more emboli and increase the amount and severity of injury. Conversely, if hypoperfusion is the cause of the injury, then decreasing brain blood flow to minimize embolic delivery would increase the likelihood of perfusion injury. By monitoring the carotid arteries of patients undergoing coronary artery bypass graft surgery, we have determined the frequency and quantity of embolic signals that occur during CPB. Although we have not been able to determine the nature of the embolus, gaseous or solid, we have demonstrated a relationship between the overall embolic load and the probability of having NP dysfunction. (ECHOCARDIOGRAPHY, Volume 13, September 1996)