Transcript Management of blood glucose in the critically ill patient

Management of blood glucose
and diabetes in critically ill
patient receiving enteral feeding.
Pamela Charney, et al. Nutrition in Clinical
practice 19:129-136, April 2004.
報告者:賴美足
93.10.21
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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
2
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)

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Table 1 Metabolic effects of insulin and its action on specific
enzymes or proteins
Metabolic effect
Target enzyme or protein
Increase glucose uptake
(muscle)
Increase glucose transporter
Increase glucose uptake
(liver)
Increase glucokinase
Increase glycogen synthesis
(liver, muscle)
Increase glycogen synthase
Decrease glycogen breakdown
(liver, muscle)
Decrease glycogen phosphorylase
Increase glycolysis, acetyl CoA
production (liver, muscle)
Increase phosphofructokinase-1
Increase fatty acid production
(liver)
Increase acetyl CoA carboxylase
Increase triacylglycerol synthesis
(adipose tissue)
Increase lipoprotein lipase
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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.

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Catecholamines epinephrine and
norepinephrine

Catecholamines epinephrine and
norepinephrine act in the periphery to
stimulate muscle glycogenolysis.
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During stress or illness,
hyperglycemia may cause by:
Stress、illness
↓
Cytokines、Inflammatory mediators
↓
Increased gluconeogenesis、
Insulin resistance
↓
hyperglycemia
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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
8
Diet and diabetes: the energy
substrate controversy

Monounsaturated fatty acids

Alternate carbohydrate sources
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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.

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Alternate carbohydrate sources
Fructose
 Modifying starch
 Fructooligosaccharides (FOS)
 Induced-viscosity complexes
 Natural glucose-lowering agents

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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.

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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
Inactive
Active
glucokinase
glucokinase
Fructose-6GKRP
GKRP
phosphate
Nucleus
Glucose-6phosphate
Fructose-6phosphate
Glycolysis
Cytosol
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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)

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FOS (Fructooligosaccharides)
Not absorbed from the small intestine
no increase in PC glucose.
 As a prebiotic for healthy bacteria in the
large intestine.

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Induced-viscosity complexes
Lower glycemia similar to soluble dietary
fibers.
 Outside the body: free-flowing, lowviscosity solution
 In the GI tract: increase viscosity. (∵acid
and amylase)
 Can reduce the tube clogging that occurs
with fiber-containing formulas.

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Natural glucose-lowering agents
American ginseng
 Organic acid (lactic and acetic acids)
 Fenugreek seeds
 Clausena anisata extract

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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
18
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↑)
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Polymeric formulas
PT
Fat
CHO
Fructose
%of
calories
%of
calories
%of
calories
Jevity
16.7
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Glucerna
16.8
Glucerna
SR
Resource
diabetic
Othe
r
MUFA
D.Fiber
calories)
%of
calories
g/L
54.3
-
16.5
14.4
49
34.2
17.7
(6.3)
34.7
14.3
20
33
47
28.6
(11)
24.6
7.6
Resista
nt
starch,
FOS
24
40
36
27
(10)
26.8
12.7
Guar
gum
g/L (%of
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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.

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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
22
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.

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Serum glucose goals

Critically ill patients : 80~120 mg/dl

Non-critically ill patients: 100~150 mg/dl
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Effects of hypoglycemia(≦60mg/dl)
Adrenergic:
sweating, palpitations, anxiety,
tachycardia, hunger.
 Neuroglycopenic:
headache, visual change, seizures,
confusion.

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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.
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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.
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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.
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hyperglycemia and hypoglycemia:
common causes

Hyperglycemia:
Illness/infection, Overfeeding, Medications,
Insufficient insulin, Volume depletion

Hypoglycemia:
excess insulin dose, severe stress, renal
dysfunction, severe hepatitis, sepsis,
diabetic gastroparesis
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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

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Insulin preparation pharmacokinetics
Insulin
Route
Onset
Peak
Effective
duration, h
Rapid-acting
SQ
Lispro
5-15 min
30-90 min
5
Aspart
5-15 min
30-90 min
5
30-60 min
2-3 h
0.5 h
5-8
3-5
NPH
2-4 h
4-10 h
10-16
Lente
2-4 h
4-10 h
10-16
Ultralente
6-10 h
10-16 h
18-24
Glargine
2-4 h
No peak
20-24
Short-acting
Regular
Intermediateacting
Long-acting
SQ, subcutaneous
SQ
IV
SQ
SQ
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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.

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Reference
M. Molly McMahon.
Management of parenteral nutrition in acutely ill
patients with hyperglycemia.
Nutrition in Clinical practice 19:120-128, April 2004.
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