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On the Failure of Insulin to Affect Hyperglycemia During Cardiac Surgery

Schricker, Thomas, MD, PhD

doi: 10.1097/00000539-200212000-00080
LETTERS TO THE EDITOR: Letters & Announcements
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Department of Anesthesia

Royal Victoria Hospital McGill University

Montreal, QC, Canada

To the Editor:

I read with great interest the manuscript by Rassias et al. reporting a positive effect of insulin infusion on neutrophil phagocytic capacity after coronary artery bypass surgery (1). Notwithstanding the potential immunological significance of their results, the authors’ strategy to maintain normoglycemia and patient selection criteria deserve further comment.

Table 1 in the article shows that an average of 16.3 U of insulin was given and that the mean bypass time was 95 min in the study group. Accordingly, the authors’ statement in the discussion that insulin was infused at 10 U/h during extracorporal circulation can only be true if insulin was discontinued after separation from bypass. The methodology and algorithm shown in the appendix do not provide this information. If, contrary to the protocol published by Chaney et al., who continued insulin treatment until sternal closure (2), insulin was stopped immediately post bypass, why was the plasma glucose concentration on arrival in the ICU, more than 1 h later, lower than in the control group? In this context one would further appreciate information about how insulin was infused, i.e., centrally or peripherally and if corresponding tubing was preconditioned with albumin, blood or insulin prior to administration (to avoid delayed insulin delivery due to its binding to tubing material).

In order to better understand the failure of insulin to reduce hyperglycemia in this protocol, the reader also needs to know if the two groups were comparable with respect to preoperative medication, in particular β-adrenergic blocker therapy, actual blood loss and transfusion requirements, fluid replacement, cardioplegia, absolute temperatures during bypass, end-tidal isoflurane concentrations (isoflurane has a strong hyperglycemic effect) (3), antibiotic treatment (were antibiotics diluted in dextrose 5%?), and the amount and type of catecholamines that were actually used as well as the total doses of protamine and heparin. Heparin stimulates lipoprotein lipase in vivo leading to an increase in free fatty acids, which subsequently impair glucose utilization by the so called Randle mechanism (4). Assuming that heparin dosing was based on body weight, which appeared to be greater in the treatment group, one would expect that patients in the insulin group received more heparin.

By setting the upper body mass index (BMI) limit at 37 kg/m2 the authors admitted obese patients (BMI > 28 kg/m2) to their study protocol, thereby voluntarily accepting subjects, who likely have glucose intolerance and insulin resistance (5). Although the mean BMI in the insulin group at 29.8 kg/m2 was significantly greater than in the control group (25.7 kg/m2, P = 0.0043), which per se may account for the failure of insulin to affect hyperglycemia, the discussion totally ignores this important issue.

Finally, in light of the long-recognized detrimental effects of acute hyperglycemia in surgical patients and the most recent finding of a 40% reduction in mortality by maintaining plasma glucose concentration between 80 and 110 mg/dL in critically ill patients (60% after cardiac procedures) (6), it is surprising that patients in the control group had to develop severe hyperglycemia (400 mg/dL) in order to receive insulin treatment.

Thomas Schricker, MD, PhD

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References

1. Rassias AJ, Givan AL, Marrin CAS, et al. Insulin increases neutrophil count and phagocytic capacity after cardiac surgery. Anesth Analg 2002; 94: 1113–9.
2. Chaney MA, Nikolov MP, Blakeman BP, Bakhos M. Attempting to maintain normoglycemia during cardiopulmonary bypass with insulin may initiate postoperative hypoglycemia. Anesth Analg 1999; 89: 1091–5.
3. Horber FF, Krayer S, Miles J, et al. Isoflurane and whole body leucine, glucose and fatty acid metabolism in dogs. Anesthesiology 1990; 73: 82–92.
4. Baron AD, Brechtel G, Edelman SV. Effects of free fatty acids and ketone bodies on in vivo non-insulin-mediated glucose utilization and production in humans. Metabolism 1989; 38: 1056–61.
5. Tighe AP, Allison DB, Kral JG, Heymsfield SB. Nutritional support of obese patients. In: Rombeau JL, Caldwell MD, eds. Clinical nutrition: parenteral nutrition. Philadelphia: WB Saunders, 1993: 716–36.
6. Van den Berghe G, Wouters P, Weekers F, et al. Intensive insulin therapy in critically ill patients. New Engl J Med 2001; 345: 1359–67.
© 2002 International Anesthesia Research Society