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Management of blood glucose and diabetes in critically ill patient receiving enteral feeding. Pamela Charney, et al. Nutrition in Clinical practice.

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Presentation on theme: "Management of blood glucose and diabetes in critically ill patient receiving enteral feeding. Pamela Charney, et al. Nutrition in Clinical practice."— Presentation transcript:

1 Management of blood glucose and diabetes in critically ill patient receiving enteral feeding Pamela Charney, et al. Nutrition in Clinical practice 19: , April 2004. 報告者:賴美足

2 ˇ1.Mechanics of glucose regulation 2.Evaluation of energy source
Management of blood glucose and diabetes in critically ill patient receiving enteral feeding. ˇ1.Mechanics of glucose regulation 2.Evaluation of energy source 3.Selection of enteral formulas and infusion routes 4.Glycemic control in patients receiving tube feeding

3 Insulin The β-cells secrete 40 to 50 units of insulin daily.
Endocrine sensors located in the GI tract signal the pancreas. Parenteral nutrition dose not stimulate the early insulin secretion. (∵dextrose bypasses the GI tract)

4 Table 1 Metabolic effects of insulin and its action on specific enzymes or proteins
Target enzyme or protein Increase glucose uptake (muscle) Increase glucose transporter (liver) Increase glucokinase Increase glycogen synthesis (liver, muscle) Increase glycogen synthase Decrease glycogen breakdown Decrease glycogen phosphorylase Increase glycolysis, acetyl CoA production (liver, muscle) Increase phosphofructokinase-1 Increase fatty acid production Increase acetyl CoA carboxylase Increase triacylglycerol synthesis (adipose tissue) Increase lipoprotein lipase

5 Glucagon The liver is the main site of glucagon action.
In the fasting, blood glucose is maintained via hepatic gluconeogenesis and glycogenolysis. Lipolysis and ketogenesis are also stimulated by glucagon.

6 Catecholamines epinephrine and norepinephrine
Catecholamines epinephrine and norepinephrine act in the periphery to stimulate muscle glycogenolysis.

7 During stress or illness, hyperglycemia may cause by:
Stress、illness Cytokines、Inflammatory mediators Increased gluconeogenesis、 Insulin resistance hyperglycemia

8 1.Mechanics of glucose regulation ˇ2.Evaluation of energy source
Management of blood glucose and diabetes in critically ill patient receiving enteral feeding. 1.Mechanics of glucose regulation ˇ2.Evaluation of energy source 3.Selection of enteral formulas and infusion routes 4.Glycemic control in patients receiving tube feeding

9 Diet and diabetes: the energy substrate controversy
Monounsaturated fatty acids Alternate carbohydrate sources

10 Monounsaturated fatty acids
30% of total calories as MUFA have improvement in lipoprotein and glycemic control in DM patients. High MUFA diet and low GI diet had similar impact on PC glucose in IGT patients.

11 Alternate carbohydrate sources
Fructose Modifying starch Fructooligosaccharides (FOS) Induced-viscosity complexes Natural glucose-lowering agents

12 Fructose (GI of fructose=19)
Small dose (5~10g) : eg, a piece of fruit beneficial for reducing the acute. postprandial glycemic response. (fig 1.) Large dose (50g) : increase serum TG. malabsorptive diarrhea and intolerance. only small dose had the effect of lower glucose level.

13 Figure 1. The effect of fructose on the release of glucokinase from its regulatory protein in the hepatocyte. GKRP, glucokinase regulatory protein. Glucose Fructose Fructokinase Fructose-1-phosphate Glucose-6-phosphate Glucose Inactive glucokinase Active glucokinase Fructose-6-phosphate Fructose-6-phosphate GKRP GKRP Nucleus Glycolysis Cytosol

14 Modifying starch Slowly digested
Raw corn starch: cannot be added to liquid formulas. (∵high temp. gelatinization, increase digestibility) OSA-esrerified starch (1-octenyl succinic anhydride-esterified starch): reduced PC glucose. (heat stable, slowly digested)

15 FOS (Fructooligosaccharides)
Not absorbed from the small intestine no increase in PC glucose. As a prebiotic for healthy bacteria in the large intestine.

16 Induced-viscosity complexes
Lower glycemia similar to soluble dietary fibers. Outside the body: free-flowing, low-viscosity solution In the GI tract: increase viscosity. (∵acid and amylase) Can reduce the tube clogging that occurs with fiber-containing formulas.

17 Natural glucose-lowering agents
American ginseng Organic acid (lactic and acetic acids) Fenugreek seeds Clausena anisata extract

18 1.Mechanics of glucose regulation 2.Evaluation of energy source
Management of blood glucose and diabetes in critically ill patient receiving enteral feeding. 1.Mechanics of glucose regulation 2.Evaluation of energy source ˇ3.Selection of enteral formulas and infusion routes 4.Glycemic control in patients receiving tube feeding

19 Enteral formula selection
Most “standard” polymeric formulas can be used. For critically ill patients, total calorie may be more importance. Overfeeding should be avoid. (↑insulin requirement) Special formulas specific for DM patients. (↑MUFA, ↓CHO) Most formulas do not contain >15g fiber per liter. (viscosity↑)

20 Polymeric formulas PT Fat CHO Other Jevity MUFA D.Fiber 16.7 29 54.3 -
%of calories Fat CHO Fructose g/L (%of calories) MUFA D.Fiber g/L Other Jevity 16.7 29 54.3 - 16.5 14.4 Glucerna 16.8 49 34.2 17.7 (6.3) 34.7 14.3 Glucerna SR 20 33 47 28.6 (11) 24.6 7.6 Resistant starch, FOS Resource diabetic 24 40 36 27 (10) 26.8 12.7 Guar gum

21 Enteral formula infusion: continuous vs intermittent feeding
Continuous feeding allows for improved blood glucose control. Postpyloric feeding be used in patient who have a history of gastroparesis or are at risk for developing delayed gastric emptying. Postpyloric feedings should be initiated on a continuous basis.

22 1.Mechanics of glucose regulation 2.Evaluation of energy source
Management of blood glucose and diabetes in critically ill patient receiving enteral feeding. 1.Mechanics of glucose regulation 2.Evaluation of energy source 3.Selection of enteral formulas and infusion routes ˇ4.Glycemic control in patients receiving tube feeding

23 Goals for glycemic control during enteral feeding
As close to normal as possible. Hyperglycemia ↑risk of infection. A prospective, randomized, controlled trial comparing standard care vs tight blood glucose control in surgical ICU patients showed that morbidity and mortality were significantly reduced if blood glucose goals were set at 110 mg/dL or lower. Avoidance of hypoglycemia is important.

24 Serum glucose goals Critically ill patients : 80~120 mg/dl
Non-critically ill patients: 100~150 mg/dl

25 Effects of hypoglycemia(≦60mg/dl)
Adrenergic: sweating, palpitations, anxiety, tachycardia, hunger. Neuroglycopenic: headache, visual change, seizures, confusion.

26 Treatment of hypoglycemia in hospitalized adult patients treated with insulin or oral diabetic agents I. Presumed symptomatic hypoglycemia should be treated without waiting to check plasma or blood glucose level. A. if the patient is able to swallow safely, administer ~15g of CHO in one of the following forms: 1. 5 sugar packets dissolved in 4 ounces (1/2cup) of water. 2. 4 ounces (1/2cup) of fruit juice. 3. glucose oral gel (glucose 15) 15g orally must be used for those receiving Acarbose (Precose) or Miglitol (Glyset). B. if the patient has a functioning feeding tube, administer one of the following by feeding tube: 1. 4 ounces (1/2cup) of fruit juice. (not orange juice or other pulp-containing juice) 2. 5 sugar packets dissolved in 4 ounces (1/2cup) of water.

27 Treatment of hypoglycemia in hospitalized adult patients treated with insulin or oral diabetic agents (續) C. if the patient is not able to take oral feeding or is NPO: 1. if IV access is available, administer D50W 25ml (12.5g). 2. if no IV access is present, administer Glucagon 1mg by subcutaneous injection. After glucogen treatment, for those patients who are not NPO, provide a snack in order to prevent subsequent hypoglycemia. D. contact either the primary service or the diabetes consulting service, whichever is responsible for the patient’s diabetes management.

28 Treatment of hypoglycemia in hospitalized adult patients treated with insulin or oral diabetic agents (續) II. For treatment of asympomatic hypoglycemia (glucose ≦60mg/dl), follow steps A through C above. III. Glucose monitoring after treatment: measure reflectance meter glucose in 15 minutes. If glucose level is not >80mg/dl, repeat the treatment outlined above. Recheck the glucose level in 15 minutes. Repeat further treatment (and glucose checks at 15 minutes intervals) until the glucose level is >80mg/dl.

29 hyperglycemia and hypoglycemia: common causes
Illness/infection, Overfeeding, Medications, Insufficient insulin, Volume depletion Hypoglycemia: excess insulin dose, severe stress, renal dysfunction, severe hepatitis, sepsis, diabetic gastroparesis

30 Glycemic management during enteral feeding
Type 1 DM patient: Basal insulin should be provided with CHO, even during periods of no oral intake. Renal dysfunction patients: OHA may be contraindicated in critical. 50% of preillness insulin requirements during initiation of feeding. “Sliding scale” + basal insulin

31 Insulin preparation pharmacokinetics
Route Onset Peak Effective duration, h Rapid-acting SQ Lispro 5-15 min 30-90 min 5 Aspart Short-acting Regular IV 30-60 min 2-3 h 0.5 h 5-8 3-5 Intermediate-acting NPH 2-4 h 4-10 h 10-16 Lente Long-acting Ultralente 6-10 h 10-16 h 18-24 Glargine No peak 20-24 SQ, subcutaneous

32 Conclusion Special formulas for DM have not shown improved outcomes when compared with standard formulas. Close monitoring and judicious use of insulin are keys to maintaining control and avoiding complications.

33 Reference M. Molly McMahon.
Management of parenteral nutrition in acutely ill patients with hyperglycemia. Nutrition in Clinical practice 19: , April 2004.


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