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Dexamethasone and blood glucose during surgery
- Pol C. Hans, A. Vanthuyne, P. Y. Dewandre, J. F. Brichant, and V. Bonhomme (25 August 2006)
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Re: Abdominal Surgery, Morbid Obesity, Age, Dexamethasone, Diabetes Mellitus and Glucose Metabolism
- Pol C. Hans, Vincent L. Bonhomme (22 August 2006)
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Does Dexamethasone Increase Blood Glucose Concentration?
- Fabian O Kooij, Jasper E. Kal (22 August 2006)
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Abdominal Surgery, Morbid Obesity, Age, Dexamethasone, Diabetes Mellitus and Glucose Metabolism
- Thomas Schricker, George Carvalho (8 August 2006)
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Pol C. Hans , A. Vanthuyne, P. Y. Dewandre, J. F. Brichant, and V. Bonhomme
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Editor- We thank Drs Kooij and Kal for their interest and comments regarding our paper on blood glucose concentration profile after dexamethasone administration in diabetic and non diabetic patients undergoing abdominal surgery. They first noted that several risk factors including abnormal glucose homeostasis, obesity, duration of fasting and type of surgery, may be responsible for hyperglycaemia in the peri-operative period. We completely agree with that comment for two reasons: 1) as mentioned in their letter, this particular point has already been highlighted and published 2) we demonstrated and confirmed in our study that severe obesity is a determinant factor of glucose increase, regardless of the metabolic status of patients. Second, they considered 10 mg of dexemethasone as a low dose. As a matter of fact, there is still some controversy in the literature regarding the optimal dose of dexamethasone to be used for PONV prophylaxis and a 10 mg injection is probably in the upper part of the prophylactic range. They also noted that surgical stress is another very important contributing factor to the increase in blood glucose concentration. Once again, we do agree with that point which was clearly mentioned and discussed in our paper. In our study, we addressed this issue by looking at the CRP level measured in all patients the day after surgery and failed to find any difference between groups. However, given the disparity of surgery in our patients, we think that surgical stress can not be definitely consider as a minor risk factor and agree that it should be evaluated specifically and in a different way in a further study. Finally, the last and most important comment questions the role of dexamethasone as the primary cause of hyperglycaemia and stresses the importance of including a control group in the design of the study. As mentioned in the paper, our study was not designed to investigate the effect of dexamethasone on blood glucose level. This question has already been answered in the literature, even if dexamethasone is certainly not the only factor that should be incriminated. We did not conclude that dexamethasone was responsible for hyperglycaemia. We actually demonstrated that after dexamethasone administration, blood glucose profile significantly differs in non-diabetic and type2 diabetic patients undergoing day morning scheduled abdominal surgery. In addition, the main message the reader should keep in mind is that in the course of dexamethasone injection, severe obesity and poor-controlled diabetes rather than diabetes per se are determinant factors of hyperglycaemia and should incite to a close monitoring of blood glucose level. Pol C. Hans and Vincent L. Bonhomme Conflict of Interest:None declared |
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Pol C. Hans, Associated Head University Dpt of Anaesthesia and ICM, CHR Citadelle, Liege, Belgium, Vincent L. Bonhomme
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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, we have to mention that non- bariatric laparoscopies were performed for cholecystectomies and gynaecological surgery. Bariatric surgery mainly included open gastric bypass laparotomies and was the group with the highest magnitude of surgical trauma. CRP, which has been reported to be reliable to quantify this particular point, was not discriminative in our study despite a high statistical power. All patients received a standard dose of low molecular weight heparine the day before surgery. A 5 h preoperative fasting was observed in all patients. Epidural anaesthesia was deliberately excluded in the study protocol. Several patients were given 5 mg ephedrine in case of 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 post-operative analgesic regimen was chosen according to the type of surgery and adjusted to patients’ requests. All of them felt reasonably comfortable in the post-operative period. Without denying the potential importance of the above considerations, we would like to stress the following points. The study was designed to compare 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 poor controlled diabetes, rather than diabetes per se, and severe obesity were determinant factors of 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 incite anaesthesiologists to carefully monitor blood glucose in poorly controlled diabetic and in severely obese patients who are candidates for receiving dexamethasone in the perioperative period. Pol Hans and Vincent Bonhomme Conflict of Interest:None declared |
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Fabian O Kooij , Jasper E. Kal
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Editor - With interest, we have read the article by Hans and co- workers entitled “Blood glucose concentration profile after 10 mg dexamethasone in non-diabetic and type 2 diabetic patients undergoing abdominal surgery” [1]. In recent years, an increasing amount of attention has been directed at perioperative and critical illness hyperglycaemia, since hyperglycaemia has been associated with higher morbidity and mortality rates [2,3]. Several risk factors have been identified that increase the risk of hyperglycaemia in the perioperative period, including abnormal glucose homeostasis, obesity, duration of fasting and type of surgery [4]. In addition, administration of dexamethasone may affect normal glucose homeostasis resulting in hyperglycaemia. To date the effect of the low dose of dexamethasone that is commonly used for PONV prophylaxis on blood glucose concentration is not known. Therefore, the conclusion of the study by Hans et al. that 10 mg dexamethasone may increase blood glucose concentration in non-diabetic and type 2 diabetic patients is potentially very relevant. However, we feel that Hans’ conclusion is not entirely justified by the data that are presented. Besides the possible effect of dexamethasone, several other factors may have contributed to the increase in blood glucose concentration, of which surgical stress is probably the most important. The mere fact that blood glucose concentration has previously been shown to increase significantly over the course of surgery in patients who did not receive dexamethasone may by itself explain the results, whether patients had diabetes or not [5,6]. Therefore, the lack of a control group of patients that did not receive dexamethasone or preferably a control group receiving a placebo precludes any conclusion about the effect of dexamethasone on blood glucose concentration. Hence, the hyperglycaemia Hans et al found could have been caused by other factors than the low dose dexamethasone. This is supported by others showing that in normal subjects, high dose dexamethasone indeed increased insulin resistance, but did not increase blood glucose concentration [7]. Once more, this illustrates the importance of including a control group in the design of the study. Without such a control group, interpretation of the data of this study remains difficult. Fabian O. Kooij* Jasper E. Kal Amsterdam, The Netherlands * Email: f.o.kooij@amc.uva.nl References 1. Hans P, Vanthuyne A, Dewandre PY, et al. Blood glucose concentration profile after 10 mg dexamethasone in non-diabetic and type 2 diabetic patients undergoing abdominal surgery. Br J Anaesth 2006;97:164- 70. 2. Van den Berghe GH, Wouters P, Weekers F, et al. Intensive insulin therapy in the critically ill patients. N Engl J Med 2001;345:1359-67. 3. McCowen KC, Malhotra A, Bistrian BR. Stress-induced hyperglycemia. Crit Care Clin 2001;17:107-24. 4. Cely CM, Arora P, Quartin AA, et al. Relationship of baseline glucose homeostasis to hyperglycemia during medical critical illness. Chest 2004;126:879-87. 5. Pasternak JJ, McGregor DG, Lanier WL. Effect of single-dose dexamethasone on blood glucose concentration in patients undergoing craniotomy. J Neurosurg Anesthesiol 2004;16:122-5. 6. Sicardisalomon Z, Rodhe P, Hahn RG. Progressive decrease in glucose clearance during surgery. Acta Anaesthesiol Scand 2006;50:848-54. 7. Nicod N, Giusti V, Besse C, Tappy L. Metabolic adaptations to dexamethasone-induced insulin resistance in healthy volunteers. Obes Res 2003;11:625-31. Conflict of Interest:None declared |
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Thomas Schricker , George Carvalho
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Editor-- We read, with interest, the paper by Hans et al. 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 (1). 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, two hours after the administration of dexamethasone, was 8.7 mmol/l in the diabetic and 7.5 mmol/l in the non- diabetic group. These values are slightly higher than peak circulating blood glucose concentrations (7.0 mmol/l) previously observed in non-diabetic, normal weight for height women who underwent abdominal hysterectomy under sevoflurane anaesthesia and who had not received dexamethasone (2). Some aspects of the present 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 hours 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 metabolism (4) 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, i.e. were patients who were eligible and opted for epidural anesthesia 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 ?-adrenergic blockers or thyroid hormone replacement therapy. Furthermore, did patients intraoperatively receive vasopressors with known metabolic effects such as ephedrine, epinephrine or norepinephrine? Hypotension must have occurred frequently after premedication with 300 ?g clonidine. Furthermore 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. All these questions should have been addressed in the manuscript because they 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. T. Schricker * G. Carvalho Montreal, Canada *E-mail: thomas.schricker@mcgill.ca 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, Lattermann R, Füssel S, Georgieff M, Schricker T. Sevoflurane versus isoflurane-anaesthesia for lower abdominal sugery. Effects on perioperative glucose metabolism. Acta Anaesthesiol Scand 2003; 47: 174-9 3. Nygren J, Thorell A, Soop M, Efendic S, Brismar K, Karpe F, Nair K, Ljungqvist O. Perioperative insulin and glucose infusion maintains normal insulin sensitivity after surgery. Am J Physiol 1998; 275: E140-8 4. Kehlet H, 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 Conflict of Interest:None declared |
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