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REVIEW ARTICLE
Year : 2013  |  Volume : 2  |  Issue : 1  |  Page : 19-25

Peri-operative management of hyperglycemia in obese diabetic patients


1 Director and Consultant Endocrinologist, Excel Center, Guwahati, India
2 Department of Medicine, Regional Institute of Medical Sciences, Imphal, Manipur, India

Date of Web Publication1-Jan-2013

Correspondence Address:
Salam Ranabir
Singjamei, Chingamakha, Liwa Road, Imphal - 795 008, Manipur
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/2278-019X.105327

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  Abstract 

The prevalence of overweight and obesity has increased to epidemic proportion across the globe. With it the prevalence of metabolic syndrome and type diabetes mellitus has also increased tremendously. Hyperglycemia as a consequence of associated type 2 diabetes mellitus, or stress response facilitated by counter-regulatory hormone surge is encountered quite commonly in obese patients during pre-operative assessment. There are reports of increased peri-operative complications with higher glucose levels in some studies, while evidence derived from some other studies are inconclusive. There are conflicting data regarding the benefit of a very tight intra-operative glucose control. There is clinical trial evidence that should help the operative team to develop some locally derived threshold near a reasonable blood glucose cut-off; for e.g., blood glucose level of 180 mg/dL for an elective major (i.e., requiring general anesthesia) procedure and 250 mg/dL for an emergency major or any sort of minor (not requiring general anesthesia) procedure.

Keywords: Diabetes mellitus, obese, peri-operative


How to cite this article:
Baruah MP, Ranabir S. Peri-operative management of hyperglycemia in obese diabetic patients. J Med Nutr Nutraceut 2013;2:19-25

How to cite this URL:
Baruah MP, Ranabir S. Peri-operative management of hyperglycemia in obese diabetic patients. J Med Nutr Nutraceut [serial online] 2013 [cited 2019 Sep 21];2:19-25. Available from: http://www.jmnn.org/text.asp?2013/2/1/19/105327


  Introduction Top


In a very simplistic and basic way, obesity can be best defined as a heterogeneous complex disorder of multiple etiologies characterized by excess body fat. What is the extent of this problem? Is there an Obesity epidemic? More than one billion adults world wide were over weight in 2002 with BMI > 25 kg/m2, and at least 300 million were clinically obese with BMI > 30 kg/m2.[1],[2] Significantincreasein the prevalence of obesity has been observed more particularly in developing nations including India [Figure 1].[3]
Figure 1: Highlighting high prevalence of obesity in different geographical region of India. No data was available in the female population from Bombay. Source: Mohan et al. [3]

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Although body mass index (BMI) has been used extensively to classify obesity, it appears to be an in adequate tool to predict the actual fat content of the body. A person of Asian origin is expected to have significantly more body fat content (especially visceral fat) than person of European line age with comparable BMI. This phenomenon is typically described as 'The Y-Y paradox.[4] Indians and people from other Asian nations tend to develop cardiovascular mortality and morbidity at a lower BMI possibly because of the presence visceral adiposity.[5]

Recent consensus have suggested lower cut-off both for BMI as well as waist circumference for Indians in particular and Asians in general [Table 1].[6]
Table 1: Current consensus highlighting lower cut off for Asians with regard to both body mass index and waist circumference

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Risks due to obesity

The metabolic syndrome is a complex condition including obesity, hypertension, hyperlipidemia, and glucose intolerance, is attributable mainly to underlying insulin resistance. High prevalence of morbidity and mortality from cardiovascular and cerebrovascular disease is the hallmark of this condition.The clinical relevance of obesity is underscored by the very fact that it exists in most instances as a part and partial of the metabolic syndrome.[7] The interplay of defective genes or improper expression of so called protective (during starvation) genes along with certain environmental factorspredisposes a persons to the risk of development of single or multiple component of metabolic syndrome, which eventually lead to the adverse outcomes like stroke, diabetes mellitus, myocardial infarction, and peripheral vascular disease [Figure 2].[8]
Figure 2: Multiple genetic and environmental factors contributes to the development of metabolic syndrome. Modified from Razani B et al.[8]

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The Endocrine obesity

The common garden variety of obesity is usually describedas simple or primary obesity, not so much because itis a disorder with simple mechanism, but more so because such a terminology helps clinician to differentiate this condition from so called endocrine or secondary obesity. While the etio-pathogenesis of the former is polygenic in nature, and that of the later is monogenic, i.e. due to excess or deficiency of a particular hormone. For common etiologies of endocrine obesity are described in [Table 2].
Table 2: Showing some common endocrine conditions associated with obesity

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It is of paramount importance to remember the causes of Endocrine obesity in preoperative evaluation, as such factors, if ignored, may lead to grave outcomes. Of all etiologies of Endocrine obesity, clinician must be at ease to differentiate a Cushing's syndrome from primary hypothyroidism as these two conditions are not too uncommon. Difference between Cushing's syndrome and Primary hypothyroidism is described in [Table 3].
Table 3: Highlights the easily identifiable differentiating points between the two conditions

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Peri-operative evaluation of obesity pertains to three major issues: [1] Whether obesity is the result of some serious medical syndromes (e.g., Cushing's syndrome, hypothyroidism), [2] Whether concomitant and predominant components of metabolic syndrome (such as diabetes mellitus, hypertension, coronary artery disease, cerebrovascular disease) are present or not and [3] Any system involved as outcome of obesity or not (such as sleep apnoea).

Obesity and other modulator of perioperative hyperglycemia

Presence of insulin resistance as a component of metabolic syndrome in obese patient is a rule barring a few exceptions. Apart from this, various other factors operating alone or in combination can contribute to peri-operative hyperglycemia [Figure 3]. Those who are particularly prone to develop hyperglycemia are the patients already having diabetes, obesity, metabolic syndrome, preexisting undiagnosed beta cell dysfunction.So called stress hyperglycemia which so often seen in non-diabetic perioperative patients is the result of excessive release of counter-regulatory hormones than actual insulin deficiency. These counter-regulatory hormones namely glucagon, epinephrine and cortisol (and to lesser extent growth hormone) work in concert to maintain hyperglycemia as an exaggerated physiological defense mechanism to overcome stress.[9]
Figure 3: Factors modulating peri-operative hyperglycemia. Modified from Akhtar et al [9]

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Pre-operative assessment in obese patients with hyperglycemia

It is now clear that hyperglycemia as a consequence of associated type 2 diabetes mellitus, or stress response facilitated by counter-regulatory hormone surge encountered quite commonly in obese patients during pre-operative assessment. There are reports of increased peri-operative complications with higher glucose levels in some studies, while evidence derived from some other studies are inconclusive. Not surprisingly, there is no consensus as to what should be the specific pre-operative glucose threshold for case cancellation. There are conflicting data regarding the benefit of avery tight intra-operative glucose control. One has to remember the fact that patient characteristic and the nature of the surgical procedure may play a bigger role than the bold glucose level alone. As regards glycated haemoglobin(HbA1c), which is considered as a gold standard for assessing glycemic control in chronic care setting, no consensus has been developed so far. While some propose <6% as cut-off for acceptance of a patient for anesthesia (based on data from a single study on vascular surgery patients, a more robust study on general surgical patient population found no such correlation.[10],[11] The American Diabetic Association (ADA) however recommends that for those patients known to have diabetes mellitus for long time, but without sufficient information of glycemic control in recent past in their history, HbA1c should be an useful tool to assess the glycemic status that may be crucial to the clinical decision making.[12]

It is most usual for obese T2DM patients to have been prescribed other medications for co- morbidities. One such group of medications is antiplatelet agents, which has to be discontinued prior to surgery.

Presence of insulin resistance as a component of metabolic syndrome in obese patient is a rule barring a few exceptions. Pre-operative environment is quite stressful for all patients. Moreover, metformin, a useful drug to combat insulin resistance, is to be stopped prior to major surgery to avoid precipitating lactic acidosis. These factors together contribute to increase requirement of insulin in this category patient, which is an important consideration for the clinician.

The authors feel that wisdom supported by some favorable clinical trial evidence should help the operative team to develop some locally derived threshold near a reasonable blood glucose cut-off; for e.g., blood glucose level of 180 mg/dL for an elective major (i.e., requiring general anesthesia) procedure and 250 mg/dL for an emergency major or any sort of minor (not requiring general anesthesia) procedure [Table 4]. Surgeries which involve prolonged soft tissue handling and deeper penetration should be considered as major from the glycemic point of view irrespective of the type of anesthesia (general, regional, spinal). This is because such procedures expose the patient to the risk of post-operative infections.
Table 4: Proposed blood glucose threshold for carrying out surgical procedures in different situations.

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It is generally advisable to start the surgery during early morning in obese patients who are diabetic or who have had hyperglycemia documented during immediate pre-operative evaluation. Those patients with type 2 diabetes already on insulin, the scheduled basal insulin dose to provide basal coverage should be administered on the night before surgery to assure optimum fasting blood glucose for the operating room. In case the surgery is not planned during the first 6 hours of the day, basal insulin has to be injected in the morning, and the dose should usually be 50-100% depending on the patient. In such situation lower dose should be chosen for lean patients and higher dose for the obese counterparts. Correction dose should be injected if the morning blood glucose exceeds 180 mg/dl. This can be in the form of an intravenous bolus. For insulin sensitive patient one unit of short acting insulin IV can reduce blood glucose upto 50 mg/dl. However, obese patient may need higher doses to reduce the blood glucose to the same extent.

Intra and post-operative glycemic control

Due to insulin resistance, and increased baseline metabolic activity mostly under the influence of catecholamines, hyperglycemia is encountered quite often in critically ill patients in hospital setting. One hypothesis claims that hyperglycemia is a beneficial adaptive response, while another considers it as harbinger of complication adversely influencing outcome.

During the last decade, a number of studies were performed to examine both the hypothesis. One study particularly including surgical post-operative ICU patients showed benefit, while two other mostly including critically ill patients from medical ICUs failed to do so.[13],[14],[15] Current guidelines on the targets of inpatient hyperglycemia are mainly the outcome of evidence generated by these studies. American Association of Clinical Endocrinologists(AACE)[16] recommends a glucose range of 140-180 mg/dl for most hospitalized persons with hyperglycemia provided these targets can be safely achieved [Table 5]. American College of Physician[17] even recommends a less stringent cut off to ensure safety to the patient [Table 5]. The ADA[12] is more forthcoming in its view towards management of critically ill inpatients with hyperglycemia [Table 5]. To quote their expert panel-"Goals for blood glucose levels in critically ill patients: Insulin therapy should be initiated for treatment of persistent hyperglycemia starting at a threshold of no greater than 180 mg/dl (10mmol/l). Once insulin therapy is started, a glucose range of 140-180 mg/dl (7.8 to 10 mmol/l) is recommended for the majority of critically ill patients. More stringent goals, such as 110-140 mg/dl (6.1-7.8 mmol/l) may be appropriate for selected patients, as long as this can be achieved without significant hypoglycemia."
Table 5: Glycemic targets as suggested by different expert panels

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There is no denying of the fact that insulin remains the sole modality of treatment in inpatient hyperglycemia control. It is more physiological than any other agent included in the armamentarium to treat hyperglycemia. Insulin is potent anti-hyperglycemic agent. However judicious use of insulin is imperative to getting the desired effect, and at the same time avoiding the major undesirable side effect, i.e., hypoglycemia. Many oral anti-diabetic drugs which are used successfully in out-patients are not at all suitable in pre-operative setting, except very few occasions where minor surgery is contemplated. There prolonged action may lead to undesired hypoglycemia during intra and post-operative period and Hyperglycemia.

Glucose monitoring is strongly advocated in all surgical patients who are diabetic.It is also advisable to initiate monitoring in obese patient even without the history of diabetes, especially those receiving glucocorticoid, octreotide, being initiated on high calorie parenteral or enteral nutrition. If hyperglycemia documented, its persistence have to be established by repeated tests before a strategy to control the same is undertaken.[12]

During the intra-operative and immediate post-operative period it is prudent to use an intravenous insulin protocol[18] which has demonstrated efficacy and safety in clinical trial settings [Table 6]. A standard practice is to start insulin infusion at the rate of 1 unit per hour. One of the important determinants of insulin dose is pre-surgical ambulatory insulin dose of which approximately 50% will be the basal requirement in the peri- and post-operative stage. In a patient who is not stressed, and does not have insulin resistance (lean patient) the estimated dose can be divided by 24 to set the insulin infusion rate (unit per hour). However this can be hugely altered if the patient is under stress, or there is significant insulin resistance. Any obese patient with hyperglycemia will be in the latter category. For such patients, adopting a weight based regimen such as 0.02 units/kg body weight/hour is quite a reasonable step. For patients with renal or hepatic impairment the dose has to be lowered. In most instances, the maximum biologic effect of insulin can achieved with an infusion rate of 10 units per hour or less. But in obese patients, specially requiring intensive care, the rate of insulin infusion can go up to 50 units per hour.[19]
Table 6: Suggested insulin infusion and additional intravenous bolus protocol for intra and immediate post-operative period

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One note of caution is regarding the use of subcutaneous sliding scale. Although it is the most widely used protocol for insulin administration in hospital setting, ADA has opined to the contrary, and describes it as "retrospective" form of insulin replacement which is inherently illogical and which has been associated with increased glycemic excursions.[20] The results of such an arbitrary regimen can not only be quite unsatisfactory but also, at times dangerous due to sharp rise and fall within short intervals [Figure 4]. Moreover, evidence also suggests that hypoglycemia resulting from continuous insulin infusion not short lived and hence much less critical than repeated subcutaneous insulin. The main reason of hypoglycemia is due to 'stacking' of insulin effect in sliding scale. If insulin infusion cannot be initiated in type 2 diabetic during anesthesia, repeated intravenous bolus therapy also has been advocated.[21]
Figure 4: Patterns of blood glucose following two different insulin protocols: Subcutaneous (SC) sliding scale versus protocol driven intra venous (IV) infusion. The green lines indicate the range of blood glucose which is considered as ideal in hospital setting

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Sliding scale results in wide fluctuations ranging from critically low blood glucose to severe hyperglycemia (resulting in so called "saw-tooth' curve) within short intervals. Blood glucose values usually settle near the attempted range of blood glucose within 4-5 hrs of initiation of the infusion. During subsequent hours it fluctuates nominally within a narrow range of 100 mg/dl. [Figure 4]

Management in transition period

Conventionally, random blood glucose target of 140-180 mg/dl is considered optimal in non-critically ill patient (ADA). Such a value is quite acceptable in patients coming out of post-operative intensive care units and being taken into general inpatient care. However unlike in critically ill patients, there is no clear evidence for specific blood glucose goals. If treated with insulin, the pre-meal blood glucose target should generally be below 140 mg/dl with random blood glucose target around 180 mg/dl. Hypoglycemia remains the main concern. A tighter control should only be aimed in stable patients with history of tight glycemic control. In the pre-operative period, clinicians should aim for less stringent targets in those with multiple co-morbidities.[12] Insulin requirement for obese post-operative patients are definitely more as almost all of them have insulin resistance.

Subcutaneous short acting or rapid acting insulin should be started at least 1-2 hrs infusion to maintain an effective plasma level of insulin. If a transition to intermediate or long acting insulin from IV insulin is planned, the former should be started 3-4 hour prior to discontinuation of IV insulin.

Clinician and the caretakers should practice the use of scheduled subcutaneous insulin to fulfill the three components of physiological insulin requirement namely-basal, nutritional/prandial, and correction which is the method for achieving and maintaining glucose control in non-critically ill patients.[19] These nomenclatures are furthere laborated below and pictorially depicted in [Figure 5].
Figure 5: Insulin requirement through various postoperative stages. These estimations are for illustrative purposes only; actual requirements may vary widely. Adopted and modified from Clement, et al. [19]

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Basal insulin requirement

It is the amount of exogenous insulin per unit time necessary to prevent unchecked gluconeogenesis and ketogenesis. In absence of basal insulin, blood glucose may increase upto 45 mg/dl per hour after insulin withdrawal in insulin-deficient patients.[19]

Nutritional insulin requirement

It is the amount of insulin necessary to cover intravenous dextrose, TPN, enteral tube feedings, nutritional supplements and/or discrete meals.[19]

Prandial insulin requirement

Also referred to as "bolus" or "mealtime" insulin, prandial insulin is usually administered before eating. There are occasional situations when this insulin may be injected immediately after eating, such as when it is unclear how much food will be eaten.[19]

Correction/Supplemental

It is also described as illness or stress related insulinincrease in daily insulin requirement attributed to illness, stress, or treatment. There is wide individual variation. It is basically apportioned between basal, nutritional and correction doses and need to be decreased as clinical condition improves.[19]

Management of hypoglycemia

One must not overlook perils of hypoglycemia in an intra-operative patient undergoing general anesthesia. Frequent monitoring with glucometer may be immense help during such situation. The most ideal approach would be to adopt and implementa hypoglycemia management protocol which is based on wisdom and logic. It is of paramount importance to train the nursing staff to detect hypoglycemia, offer preliminary treatment and finally alert the physician in charge. Major risk factors for hypoglycemia aredecreased carbohydrate intake, reduction of corticosteroids, deteriorating renal function, underlying undiagnosed endocrinopathy like hypothyroidism, and prior hypoglycemia. More frequent monitoring may be required in such situation. A tendency to overcorrect hypoglycemia is to be avoided at all cost.[22] A practically useful algorithm is described in [Figure 6]. The sequence of events and interventions from the onset till recovery from the episode, and even beyond in special situation must be recorded meticulously in the hospital records.[12]
Figure 6: A practical algorithm showing the vital steps in management of hypoglycemia in peri-operative period

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Role of bedside glucose monitoring

Advent of portable bedside glucose meters has revolutionized the quality of diabetes management.Judicious use of computers significantly enhanced the efficiency of this system. The role of bedside blood glucose monitoring is immense and such measures have been describes as an "additional vital sign".[19] Modern glucometers are designed for capillary whole blood testing which roughly matches with venous plasma in basal condition (not in post prandial). Caution is however particularly required in interpreting the values in critically ill patients with hypotension, dehydration, anemia, and other interfering chemicals in blood. In such situations, arterial or venous (not capillary) drawn from lines in situ can be used with the glucometer. Arterial concentrations are 5 mg/dl higher than the capillary concentration.[19]

Post hospitalization follow-up and risk re-assessment

Intravenous insulin infusion during intra and post-operative recovery is changed to basal bolus insulin therapy during transition phase when patient is shifted from intensive treatment ward to general care facilities. Once the patient is stable enough for discharge, the surgical team should consult the physician/diabetologist and also diabetes educator whenever and wherever possible. The diabetes care team should reassess the ongoing regimen, paying special attention to factors such as cost of medications, the patient's ability to monitorand self-manage, previous control of diabetes, and contraindications to medications. The medical history of the medications which were used prior to surgery may come quite handy at this situation. In all obese patients, metformin must be included in the oral regimen if not contraindicated for specific reasons. As regards the secretagogues, newer agents belonging to the incretin mimetic class are preferred agents for obese type 2 diabetic patients.

Newly diagnosed diabetic patients require diabetes self-management education (DSME). While planning and executing the discharge in this group of patients, assessment of the patient's ability to pay for diabetes supplies and medications should be done. Another group with no prior history of hyperglycemia, but found to have single or multiple reading(s) of random blood glucose >125 mg/dl are at increased risk of developing diabetes in future. They should be advised to undertake a standard glucose tolerance test as per ADA guidelines[23] within a month of hospital discharge and yearly thereafter.

 
  References Top

1.World Health Organization. Global strategy on diet, physicalactivity and health, 2003. Available from: http://www.who.int/hpr/NPH/docs/gs_obesity.pdf. [Last accessed on 2003 Nov 11].  Back to cited text no. 1
    
2.International Obesity Task Force. Available from: http://www.iotf.org. [Last accessed on 2003 Nov 13].  Back to cited text no. 2
    
3.Mohan V, Deepa R. Obesity and abdominal obesity in Asian Indians. Indian J Med Res 2006;123:593-6.  Back to cited text no. 3
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4.Yajnik CS, Yudkin JS. The Y-Y paradox (Clinical picture). Lancet 2004;363:163.  Back to cited text no. 4
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5.Wasir JS, Misra A, Vikram NK, Pandey RM, Gupta R. Comparison of definitions of the metabolic syndrome in adult Asian Indians. J Assoc Physicians India 2008;56:158-64.  Back to cited text no. 5
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6.Misra A, Chowbey P, Makkar BM, Vikram NK, Wasir JS, Chadha D, et al. Consensus Statement for Diagnosis of Obesity, Abdominal Obesity and the Metabolic Syndrome for Asian Indians and recommendations for physical activity, Medical and Surgical Management. J Assoc Physicians India 2009;57:163-70.  Back to cited text no. 6
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7.Leroith D. Foreword. Control of feeding behavior and the peripheral metabolism by the hypothalamus. Endocrinol Metab Clin North Am 2008;37:11-2.  Back to cited text no. 7
    
8.Razani B, Chakrvarthy MV, Semenkovich CF. Insulin Resistance and Atherosclerosis. Endocrinol Metab Clin North Am 2008;37:603-21.  Back to cited text no. 8
    
9.Akhtar S, Barash PG, Inzucchi SE. Scientific principles and clinical implications of perioperative glucose regulation and control. Anesth Analg 2010;110:478-97.  Back to cited text no. 9
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10.Tung A. Anesthetic considerations with the metabolic syndrome. Br J Anaesth 2010;105:i24-33.  Back to cited text no. 10
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11.O′Sullivan CJ, Hynes N, Mahendran B, Andrews EJ, Avalos G, Tawfik S, et al. Haemoglobin A1c (HbA1C) in non-diabetic and diabetic vascular patients. Is HbA1C an independent risk factor and predictor of adverse outcome? Eur J Vasc Endovasc Surg 2006;32:188-97.  Back to cited text no. 11
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12.American Diabetic Association. Executive Summary: Standards of Medical Care in Diabetes-2011. Diabetes Care 2011;34:S4-9.  Back to cited text no. 12
    
13.Van den Berghe G, Wouters P, Weekers F, Verwaest C, Bruyninckx F, Schetz M, et al. Intensive insulin therapy in thecritically ill patients. N Engl J Med 2001;345:1359-67.  Back to cited text no. 13
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14.Van den Berghe G, Wilmer A, Hermans G, Meersseman W, Wouters PJ, Milants I, et al. Intensive insulin therapy in the medical ICU. N Engl J Med 2006;354:449-61.  Back to cited text no. 14
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15.The NICE-SUGAR Study Investigators. Intensive versus Conventional Glucose Control in Critically Ill Patients. N Engl J Med 2009;360:1283-97.  Back to cited text no. 15
    
16.HandelsmenY, Mechanick JL, Blonde L, Grunberger G, Bloomgarden ZT, Bray GA, et al. American Association of Clinical Endocrinologists medical guidelines for clinical practice for developing a diabetes mellitus comprehensive care plan. Enodocr Pract 2011;17:1-53.  Back to cited text no. 16
    
17.Qaseem A, Humphrey LL, Chou R, Snow V, Shekelle P; The Clinical Guidelines Committee of the American College of Physicians. Use of Intensive Insulin Therapy for the Management of Glycemic Control in Hospitalized Patients: A Clinical Practice Guideline from the American College of Physicians. Ann Intern Med 2011;154:260-7.  Back to cited text no. 17
    
18.Furnary AP, Gao G, Grunkemeier GL, Wu Y, Zerr KJ, Bookin SO, et al. Continuous insulin infusion reduces mortality in patients with diabetes undergoing coronary artery bypass grafting. J Thorac Cardiovasc Surg 2003;125:1007-21.  Back to cited text no. 18
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19.Clement S, Braithwaite SS, Magee MF, Hamann A, Smith EP, Schafer RG, et al. Hirsch IB, on behalf of diabetes in hospital writing committee. Management of diabetes and hyperglycemia in hospitals. Diabetes Care 2004;27:553-91.  Back to cited text no. 19
    
20.The ACE/ADA Task Force on Inpatient Diabetes. American College of Endocrinology and American Diabetes Association Consensus Statement on Inpatient Diabetes and Glycemic Control. Diabetes Care 2006;29:1955-62.  Back to cited text no. 20
    
21.Hemmerling TM, Schmid MC, Schmidt J, Kern S, Jacobi KE. Comparison of a continuous glucose-insulin-potassium infusion versus intermittent bolus application of insulin on perioperative glucose control and hormone status in insulin-treated type 2 diabetics. J Clin Anesth 2001;13:293-300.  Back to cited text no. 21
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22.Nobels F, Lecomte P, Deprez N, Van Pottelbergh I, Van Crombrugge P, Foubert L. Tightglycaemic control: Clinical implementation of protocols. Best Pract Res Clin Anaesthesiol 2009;23:461-72.  Back to cited text no. 22
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23.The Expert Committee on the Diagnosis and Classification of Diabetes Mellitus: Report of the Expert Committee on the Diagnosis and Classification of Diabetes Mellitus. Diabetes Care 2003;26:S5-20.  Back to cited text no. 23
    


    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6]
 
 
    Tables

  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5], [Table 6]



 

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