Abdominal surgery, morbid obesity, age, dexamethasone, diabetes mellitus and glucose metabolism
*E-mail: thomas.schricker{at}mcgill.caEditor—We read, with interest, the paper by Hans and colleagues1 showing moderately increased capillary blood glucose concentrations during and after abdominal surgery in type 2 diabetic morbidly obese patients when compared with a younger group of non-diabetic obese patients. All patients in this protocol had received a bolus of 10 mg of dexamethasone for the prophylaxis of postoperative nausea and vomiting at the induction of general anaesthesia. The peak mean glucose concentration, 2 h after the administration of dexamethasone, was 8.7 mmol litre–1 in the diabetic and 7.5 mmol litre–1 in the non-diabetic group. These are slightly higher than peak circulating blood glucose concentrations (7.0 mmol litre–1) previously observed in non-diabetic, normal weight for height women undergoing abdominal hysterectomy with sevoflurane anaesthesia and who had not received dexamethasone.2 Some aspects of this study merit further comment.
Notwithstanding the lack of control groups and the fact that the diabetic patients had a significantly greater body mass index than non-diabetic subjects, which per se can explain the small difference in glycemia, the manuscript by Hans does not provide certain information concerning patient characteristics and study design that are pertinent for the understanding of perioperative glucose metabolism. As hyperglycemia depends on the magnitude of surgical tissue trauma, which is not necessarily reflected by CRP-levels obtained 24 h after surgery, it is relevant to define ‘bariatric surgery’, ‘non-bariatric laparoscopy’ and ‘non-bariatric laparotomy’. For example, did patients in the bariatric surgery group undergo open, laparoscopic Roux-en-Y gastric bypass surgery, sleeve gastrectomy, gastric banding or abdominal liposuction? The duration of preoperative fasting has been demonstrated to have an impact on insulin sensitivity and glycemia after surgery.3 Therefore, it would be interesting to know whether some procedures necessitated bowel cleaning and whether preoperative fasting periods were comparable in the two groups.
As the type of analgesia has significant effects on glucose metabolism4 it needs to be explained how pain was controlled after surgery. Apparently none of the patients had epidural anaesthesia or analgesia for procedures that, in many centres, are routinely performed under combined general/epidural anaesthesia. One may, therefore, appreciate a more detailed explanation of the patient selection process, that is were patients who were eligible and opted for epidural anaesthesia excluded from recruitment? In this context one would also appreciate more details about the patients' co-morbidities and medication with a potential impact on glucose metabolism, in particular the use of ß-adrenergic blockers or thyroid hormone replacement therapy. Did the patients intraoperatively receive vasopressors with known metabolic effects such as ephedrine, epinephrine or norepinephrine? Hypotension must have occurred frequently after premedication with 300 µg clonidine.
No information was provided regarding the fluid replacement strategy and transfusion practice. What was the actual blood loss? Did some patients require transfusion of packed red blood cells or fresh frozen plasma both of which contain high concentrations of glucose? It also needs to be stated which and how much crystalloid solution was administered during the study period, because, for example, the lactate content of Hartmann's solution may affect the blood glucose levels in surgical patients. Finally, it is unknown if subcutaneous heparin was used. Heparin stimulates lipoproteinlipase in vivo leading to an increase in free fatty acids, which subsequently impair glucose utilization by the so-called Randle mechanism.5 Assuming that heparin dosing was based on body weight, which was significantly greater in the diabetic group, one would expect that patients in the insulin group received more heparin.
These questions are relevant for the interpretation of small changes in glycemia, particularly when fingerprick capillary blood glucose instead of circulating blood glucose measurements are performed; a technique that is inadequate to assess glucose metabolism during and after surgery.
Montreal, Canada
Editor—We would like to thank Drs Schricker and Carvalho for their interest in our work. Basically we agree with the majority of concerns they addressed regarding missing data and their potential implications either on perioperative blood glucose levels or on the mechanisms of their disturbances.
In an attempt to answer their comments; non-bariatric laparoscopies were performed for cholecystectomy and gynaecological surgery, bariatric surgery was mainly for open gastric bypass laparotomies and was the group with the highest magnitude of surgical trauma. CRP, which has been reported to be reliable in quantifying this, was not discriminative in our study despite a high statistical power. All patients received a standard dose of low molecular weight heparin the day before surgery. All patients were fasted for 5 h before operation. Epidural anaesthesia was deliberately excluded in the study protocol. Several patients were given 5 mg ephedrine for arterial hypotension but no statistical difference was observed between groups. No patient required transfusion of red blood cells during the study period and crystalloids consisted in free glucose plasmalyte solutions. The postoperative analgesic regimen was chosen according to the type of surgery and adjusted to patients' requests. All of them felt reasonably comfortable in the postoperative period.
Without denying the potential importance of the above considerations, we would like to stress the following points. The study was designed to compare the blood glucose profile in diabetic and non-diabetic patients after dexamethasone administration, and not for investigating the effect of dexamethasone on blood glucose in surgical patients. The peak glucose level was recorded 120 min after dexamethasone administration and not later during or after surgery. We demonstrated that poorly controlled diabetes (rather than diabetes per se) and severe obesity were determinant factors for a glucose increase. The significant correlation between maximum blood glucose concentration and BMI was obtained in the whole group of patients whatever their clinical status. Consequently, the factors mentioned by Drs Schricker and Carvalho probably deserve further investigation in studies including more patients in an attempt to achieve a high statistical power and draw definitive conclusions regarding their potential implication. In the meanwhile, we consider that our results should encourage anaesthetists to carefully monitor blood glucose in poorly controlled diabetic and in severely obese patients who may receive dexamethasone in the perioperative period.
Liege, Belgium
*E-mail: pol.hans{at}chu.ulg.ac.be
References
1 Hans P, Vanthuyne A, Dewandre PY, Brichant JF, Bonhomme V. Blood glucose concentration after 10 mg dexamethasone in non-diabetic and type 2 diabetic patients undergoing abdominal surgery. Br J Anaesth 2006; 97:164–70
2 Geisser W, Schreiber M, Hofbauer H, et al. Sevoflurane versus isoflurane-anaesthesia for lower abdominal sugery. Effects on perioperative glucose metabolism. Acta Anaesthesiol Scand 2003; 47:174–9[CrossRef][ISI][Medline]
3 Nygren J, Thorell A, Soop M, et al. Perioperative insulin and glucose infusion maintains normal insulin sensitivity after surgery. Am J Physiol 1998; 275:E140–8
4 Kehlet H and Nolte K. Effect of postoperative analgesia on surgical outcome. Br J Anaesth 2001; 87:62–72
5 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[CrossRef][ISI][Medline]
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