Inpatient
Glucose
Control
Resident’s conference
Ghana Kang, R2
9/13/2011
Hyperglycemia and hospitalization
 A recent survey estimated that 22% of all hospital
inpatient days were incurred by people with diabetes
and that hospital inpatient care accounted for half of the
$174 billion total US medical expenditures for this
disease
 It’s estimated that 12-25% of patients who are in
hospital beds have diabetes or some degree of
hyperglycemia.
 Of patients in the cardiac care unit, one out of two may
have diabetes or glucose intolerance.
Glucose measurement
Glucose Measurement
Methodologies
 The small and colorless glucose molecule is very difficult to
measure directly. Therefore, all marketed glucose
measurement devices use indirect measurement methods.
 All techniques are enzymatic, with measurement of
byproducts by optical or electrochemical methods.
Byproduct formed is directly proportional to the amount of
glucose present.
 Hexokinase: used most commonly in central laboratory devices.
 Glucose oxidase (GO)
 Glucose-1-dehydrogenase (GDH)
 A second GDH-based measurement system with steadily
increasing market share, Glucose-1-dehydrogenase
pyrroloquinolinequinone (GDH-PQQ) is more nonspecific for
glucose.
 May yield falsely high glucose readings in the presence of
maltose, xylose, or galactose
Andrew D. Pitkin, et al., Challenges to Glycemic Measurement in the Perioperative and Critically Ill Patient: A Review, J
Diabetes Sci Technol 2009;3(6):1270-1281
Factors affecting accuracy of glucose measurement
1. Terminology
 A potential error in current practice arises from the use of
blood and plasma glucose as interchangeable terms, with
the consequent risk of misinterpretation.
 The glucose concentration in plasma is approximately 11%
higher than that in whole blood because plasma is denser
than whole blood
A mutiplier of 1.11
for the conversion of glucose
in blood to plasma
has been recommended.
(55%)
(<1%)
(45%)
Factors affecting accuracy of glucose measurement
1. Terminology
 The physiologic activity of glucose corresponds more
closely with plasma concentration than whole blood
glucose concentration, which varies considerably with
hematocrit.
 Most of the POC devices measure glucose in whole
blood and self correct internally, reporting results as
plasma glucose.
Factors affecting accuracy of glucose measurement
2. Sampling site
 ADA and WHO recommend the use of venous plasma
glucose for measuring and reporting.
 The widespread use of capillary blood sampling despite
evidence that this may lead to measurement error (fingertip
blood samples ≈ capillary blood samples)
 The difference between capillary and venous glucose is
typically small in non-hypotensive fasting subjects, but can
be up to 8% higher in capillary blood after meals or glucose
challenge.
 Compared to capillary blood, arterial sampling is generally
accepted to be a more accurate measurement.
Factors affecting accuracy of glucose measurement
3. Patient and Environmental Factors
Hematocrit
hematocrit  glucose
High oxygen tension (ie, pO2 >100 mm Hg)
can falsely decrease glucose readings on
some glucose oxidase-based blood
glucose meters, especially when patients
are receiving oxygen therapy.
The enzyme GDH is less specific for
glucose than glucose oxidase and but is
not as susceptible to variations in oxygen
concentration
Andrew D. Pitkin, et al., Challenges to Glycemic Measurement in the
Perioperative and Critically Ill Patient: A Review, J Diabetes Sci Technol
2009;3(6):1270-1281
FDA Public Health Notification: potentially fatal errors with GDH-PQQ glucose monitoring technology. August 13, 2009. Available at
http://www.fda.gov/MedicalDevices/Safety/AlertsandNotices/PublicHealthNotifications/ucm176992.htm. Accessed August 30, 2009.
Insulin Analogues
History
1922
Banting and Best use bovine insulin extract on human
Porcine insulin has only a single amino acid variation from the
human insulin, and bovine insulin varies by three amino acids.
Both are active on the human receptor with approximately the
same strength.
The first commercial insulin preparations contained numerous impurities and varied
in potency from lot to lot by as much as 25 percent
1936
Hagedorn discovers that adding protamine to insulin prolongs the
effect of insulin
1946
Nordisk formulates Isophane porcine insulin (Neutral Protamine
Hagedorn or NPH insulin) by adding Neutral Protamine to regular
insulin
Protamine
1953
NPH
Novo formulates Lente porcine and bovine insulins by adding
zinc for longer-lasting insulin
Zinc
Lente
1981
1983
Novo Nordisk chemically and enzymatically converts porcine
insulin to 'human' insulin
Lilly produces synthetic, recombinant 'human' insulin,
branded Humulin
By the early 1980s, the development of purified pork insulin and then recombinant
human insulin virtually eliminated insulin allergy and immune-mediated lipoatrophy.
These achievements marked a slowdown in the innovation of insulin products until
the 1990s, when the reports of the Diabetes Control and Complications Trial4 and the
United Kingdom Prospective Diabetes Study5 confirmed the value of glycemic control
in the delay or prevention of complications of diabetes.
1996
Lilly Humalog "lispro" insulin analogue
approved by the U.S. FDA
2000
”Aspart” Insulin analogue
2004
”Glulisine” Insulin analogue
2003
2006
”Glargine” Insulin analogue
”Detemir” Insulin analogue
AHRQ Pub. No. 08(09)-EHC017-3 March 2009
???Risk of cancer in patients receiving
insulin analogues
 In spite of the clinical superiority, the potential mitogenic
effect of some analogues remains to be clarified and
constitutes a fundamental safety issue.
 Insulin and IGF-1 receptors display >50% of amino acid
sequence homology and even >84% in the tyrosine kinase
domain, while both ligands bind to both receptors.
 So far, no reliable date on this has been published.
 In 2000, adenocarcinoma with the use of insulin AspB10 in
laboratory animals.
 In 2009, glargine  ???cancer
 The FDA, ADA, AACE, and EASD have formally stated
that patients should continue to use insulin analogues
until more information is available.
QUESTION 1:
Does improving glycemic
control improve clinical
outcomes for inpatients with
hyperglycemia?
A) Yes
B) No
Era of unawareness
 A decade ago, there was a general lack of recognition
of the need to identify and treat hyperglycemia among
hospitalized patients.
 Acute hyperglycemia was often considered to be
benign and even a physiological reaction to acute
illness.
 There were no published guidelines or glycemic targets
for the inpatient setting, so hyperglycemia in the
hospital setting was essentially ignored.
 There is substantial observational evidence linking
hyperglycemia in hospitalized patients (with or without
diabetes) to poor outcomes
 Diabetes contributes to longer hospital length of stay
regardless of the reason for admission.
Completed Intensive Insulin Interventions
Studies showing benefit
Study
Patient
Methodolog
Populations y
Intervention
Outcome
Malmberg
1995
(DIGAMI I)
AMI in diabetes
Prospective, case IV insulin therapy followed
control study
by multiple insulin
injections (126-196mg/dl)
1-year mortality
29%
Van Den
Berghe
2001
Surgical ICU
Prospective,
randomized
controlled
Glucose level 80110mg/dl vs.
conventional tx.
Mortality 34%
Furnary
2003
Diabetes-CABG
surgery
Case/control
study
IV insulin maintains a
glucose<200 compared
with SQ insulin
Mortality 50%
with IV insulin
Krinsley
2004
Mixed
medical/surgical
ICU
Case/control
study
(historical control
group)
Compared preprotocol
with postprotocol to
maintain glucose<140
Mortality 29.3%
The varying glucose target levels of these studies make it difficult to compare
their results
Van den Berghe G, et. al. Intensive insulin therapy in critically ill patients.
N Engl J Med. 2001; 345: 1359-1367
Prospectively evaluated 1500 patients in the surgical ICU.
For the first time, patients’ BG was controlled to a very low target (80-110mg/dL)
Intensive insulin therapy reduced overall in-hospital mortality by 34%,
bloodstream infections by 46%, acute renal failure requiring dialysis by 41 %.
In response……
 Because of the dramatic reduction in mortality with normalization of glucose
levels in the single center, the Van den Berghe study led to widespread
adoption of this practice in ICUs worldwide.
 On the basis of initial studies, the American Association of Clinical
Endocrinologists (AACE) convened a consensus conference and published
the first inpatient glycemic targets in 2004.
 Tight glycemic control for the critically ill patient
 In 2005, for the first time, the American Diabetes Association (ADA) published
recommendations for inpatient glycemic care in its yearly standards of care.
 Very quickly it was recognized that implementing inpatient glycemic control
was not a simple task and that there were many barriers to overcome.
 In 2006, conference was held to address some of the barriers and make
recommendations on how to overcome them.
 Call for creation of inpatient multidisciplinary steering committees
Completed Intensive Insulin Interventions
Studies showing no benefit
 Most recent studies have not shown a major benefit
from controlling BG to a target of 80-110mg/dL.
Study
Patient
Populations
Methodology
Intervention
Outcome
Malmberg
2005
(DIGAMI 2)
AMI in diabetes
Prospective,
randomized,
multicenter trial
3 distinct insulin strategies
including IV insulin
No difference in
mortality
Van Den
Berghe
2006
Medical ICU
Prospective,
randomized,
controlled study
Glucose level 80-110mg/dl
vs conventional treatment
No significant
decrease in
mortality
NICESUGAR
2009
Mixed
medical/surgical
ICU
Prospective,
randomized,
controlled, multicenter trial
Glucose of 81-108ml/dl vs
conventional
glucose<180mg/dl
Mortality 2.6% in
the intensive-control
group
Data on Blood Glucose Level, According to Treatment Group
Conventional control group
Target<180mg/dL
Intensive control group
target: 81-108mg/dL
achievement of a glucose level
modestly above the target range
in a substantial proportion of patients
in the intensive-control group.
The NICE-SUGAR Study Investigators. N Engl J Med 2009;360:1283-1297
Probability of Survival and Odds Ratios for Death, According to Treatment Group
hazard ratio, 1.11; 95% CI, 1.01 to 1.23; P=0.03
-The 90-day mortality was significantly higher in the intensively treated versus the
conventionally treated group (78 more deaths; 27.5% versus 24.9%; P = .02) in both surgical
and medical patients.
-Mortality from cardiovascular causes was more common in the intensively treated group (76
more deaths; 41.6% versus 35.8%; P = .02).
-Severe hypoglycemia was also more common in the intensively treated group (6.8% versus
0.5%; P<.001).
The NICE-SUGAR Study Investigators. N Engl J Med 2009;360:1283-1297
Severe hypoglycemia
in NICE-SUGAR study
 Glucose levels were measured using either Point-ofcare (POC) devices or Central laboratory devices
(CLD) with samples obtained from either arterial
catheters or capillary sites.
 The recorded number of episodes of severe
hypoglycemia (defined as a blood glucose level
≤40mg/dL) was 272 in the intensive control group, as
compared with 16 in the conventional-control group;
173 of all 288 episodes (60.1%) were confirmed by a
laboratory measurement.
Hyperglycemia in Hospitalized Medical and
Surgical Patients in Non-ICU Settings
 No RCTs have examined the effect of intensive glycemic
control on outcomes in hospitalized patients outside ICU
settings.
 Several observational studies, however, point to a strong
association between hyperglycemia and poor clinical
outcomes, including prolonged hospital stay, infection,
disability after discharge from the hospital, and death
QUESTION 1:
Does improving glycemic control improve clinical outcomes for
inpatients with hyperglycemia?
 Overall, although a very tight glucose target (80 to 110
mg/dL) was beneficial in a predominantly surgical ICU
population, this target has been difficult to achieve in
subsequent studies, including NICE-SUGAR study, without
increasing the risk for severe hypoglycemia.
 There has been no consistent reduction in mortality with
intensive control of glycemia, and increased mortality was
observed in the largest published study to date.
 The reasons for this inconsistency are not entirely clear.
QUESTION 2:
What glycemic targets can be
recommended in hospitalized
patients?
A)
B)
C)
D)
Fasting <140
Random 140-180
None of the above
A and B
Recommendation of Glycemic
targets in different patient
populations in the hospital
setting
-Review of guidelines
AACE-ADA guideline (2009)
Moghissi,et.al., Consensus: Inpatient Hyperglycemia, Endocr Pract. 2009;15(No. 4)
Amir Qaseem, et.al., 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; 154:260-267
ACC/AHA Guidelines (2007)
 “The usefulness of strict control of blood glucose
concentration during the perioperative period is uncertain in
patients with diabetes mellitus or acute hyperglycemia who
are undergoing noncardiac surgical procedures without
planned ICU admission.”
 “It is reasonable that blood glucose concentration be
controlled during the perioperative period in patients with
diabetes mellitus or acute hyperglycemia who are at high
risk for myocardial ischemia or who are undergoing
vascular and major noncardiac surgical procedures
with planned ICU admission.”
J Am Coll Cardiol 2007:50:e242
Question 2.
What glycemic targets can be recommended in
different patient populations in the hospital setting?
 All experts now seem to agree that a target of nearnormalization of blood glucose levels in hospitalized patients
is inappropriate but also that hyperglycemia can have
adverse consequences and should be treated in a
substantial fraction of hospitalized patients.
 AACE/ADA guidelines
 ICU patients: 140-180
 non-ICU patients: Fasting<140, random <180
 ACP guidelines
 ICU patients: 140-200
 There is difference of opinion revolving around the details of
the specific target range for blood glucose in hospitalized
patients, a subject that is evolving as the research base
increases.
Tailoring insulin use to the
clinical scenario
Sliding Scale Insulin
 To date, since the discovery of insulin in 1921, no study has shown
a benefit of SSI in improving glycemic control or clinical outcome.
 “cookbook” approach to hyperglycemia
 Simple and convenient, avoids telephone calls to the physicians
 Retroactive and inefficient therapy that allows wide glycemic
fluctuation, putting patients on a roller coaster of fluctuations in
blood glucose.
 In a prospective RCT(RABBIT 2 Trial)*, it was found that basalbolus insulin resulted in lower mean fasting and random blood
glucose levels in comparison with SSI alone without the use of
basal insulin.
*Umpierrez GE , Smiley D, Zisman A, et al., Randomized study of basal-bolus insulin therapy in the
inpatient management of patients with type 2 diabetes (RABBIT2 trial), Diabetes Care. 2007; 30;2181-2186
AACE-ADA guideline (2009)
Moghissi,et.al., Consensus: Inpatient Hyperglycemia, Endocr Pract. 2009;15(No. 4)
Physiologic Subcutaneous
Insulin Protocols
 Basal insulin
 glargine, detemir, or NPH
 Prevents gluconeogenesis and ketogenesis
 Bolus insulin (nutritional or prandial)
 Lispro, aspart, or regular
 Attempts to control the prandial glucose excursion
 Correction insulin (supplemental)
 Lispro, aspart, or regular
 Fine tunes suboptimal glycemic control by offering the flexibility
of adding insulin beyond the calculated nutritional dose.
 Needs to be distinguished from SSI, which refers to an insulin
regimen that is given alone with the sole purpose of “resolving”
hyperglycemia and is not scheduled in combination with basal
insulin.
Correction or Supplemental Insulin Algorithms
Blood
glucose
(mg/dL)
Low-dose
algorithm for pts
taking≤0.5U/kg
daily
Moderate-dose
algorithm for pts
taking>0.5U/kg
daily
High-dose
algorithm for pts
taking>1U/kg daily
Ac
Hs
Ac
Hs
Ac
Hs
150-200
1
0
2
0
3
0
201-250
2
1
4
2
6
3
251-300
3
2
6
4
9
6
301-350
4
3
8
6
12
9
351-400
5
4
10
8
15
12
>400
6
5
12
10
18
15
Ariana R. Pichardo-Lowden, et.al., Management of hyperglycemia in the non-intensive
care patient: Featuring subcutaneous insulin protocols, Endocrine practice vol 17 No.2
March/April 2011
 Total Daily Dose (TDD)
 Can be determined by considering preadmission insulin
needs, overall glycemic control, body weight, or
intravenous insulin requirements.
 When a dose is selected on the basis of weight,
 0.5U/kg is an adequate starting dose for most patients.
 0.4U/kg for patients at risk for hypoglycemia (advanced age,
hemodialysis, low body weight) or with type1 diabetes
 0.7U/kg or higher for more insulin-resistant patients
1. Patients Eating
(an intake of at least 50% of the scheduled meals)
Basal insulin
Nutritional or
prandial insulin
Detemir or Glargine: 50%
of TDD as a single
injection in the morning or
bedtime
50% of TDD divided
equally between meals.
Supplemental or
correctional
insulin
NPH: 50% of TDD (70%
of basal dose in the
morning ac and 30% ac
supper or hs)
Most patients
0.5U/kg (TDD)
Low dose ac & hs
Risk of
hypoglycemia
0.4U/kg (TDD)
Low dose ac & hs
Insulin resistant
0.7U/kg (TDD)
Moderate dose ac & hs
Example
 A 50 y.o man with diabetes who is 180cm (71in) tall and weighs
90kg(198 lb) is admitted for pneumonia treatment with a random blood
glucose level of 300mg/dL and an A1c level of 10.8%. Oral diabetic
agents are discontinued, and blood glucose testing is ordered before
meals and at bedtime.
 Calculate total daily dose of insulin
 0.5U/kg X 90kg = 45 units.
50%
50%
Basal insulin
Nutritional or
prandial insulin
Supplemental or
correctional
insulin
23 units of insulin
glargine taken once daily
(50% of TDD)
7-8 units of insulin
aspart (Novolog) taken
zero to 15 minutes before
meals (50% of TDD, in
three divided doses)
Based on glucose
readings, give additional
aspart (novolog) per
standard correctional
insulin schedule
2. Patients Fasting
Basal insulin
Nutritional or
prandial insulin
Detemir or Glargine: 50%
of TDD as a single
injection in the morning or
bedtime
None if entirely fasting.
NPH: 50% of TDD (Divide
amount in 3 equal doses
to be given q 8h if
GFR>50ml/min or divide
in 2 equal doses to be
given q 12h if
GFR<50ml/min)
Supplemental or
correctional
insulin
If glucose>180mg/dL X 2
days and taking clear
liquids, start 25% of TDD
divided equally between
meals.
Most patients
0.5U/kg (TDD)
Low dose q6h
Risk of
hypoglycemia
0.4U/kg (TDD)
Low dose q6h
Insulin resistant
0.7U/kg (TDD)
Moderate dose q6h
3. Transition from IV to SC insulin
 Patients who receive IV insulin infusions will usually require transition
to subcutaneously administered insulin when they begin eating
regular meals or are transferred to lower intensity care.
 Typically, a percentage (usually 75% to 80%) of the total daily IV
infusion dose is proportionately divided into basal and prandial
components
 Amount used in last 6 hours X 4.
 If insulin drip rate is fluctuating >1U/h within past 6 hours, consider
continuing the drip and reassess, or calculate TDD= 80% of 6 stable doses
(insulin units/h) within the last 12 hours X 4.
 Subcutaneously administered insulin must be given 2 to 3 hours
before discontinuation of IV insulin therapy in order to prevent
hyperglycemia.
Example
1AM
2AM
3AM
4AM
5AM
6AM
7AM
8AM
9AM
10AM
11AM
Noo
n
7U/h
8U/h
6U/h
5U/h
5U/h
5U/h
4U/h
4U/h
5U/h
4U/h
3U/h
2U/h
Insulin requirement in the past 6 hours
= 4+4+5+4+3+2= 22 units
TDD =0.8 X (22 units X 4) = 70 units.
Basal = 50% of TDD = 35 units
Prandial= 50% of TDD in 3 divided doses=35 units/3 =12 units each meal.
Specific clinical situations
4. Patients Receiving high dose steroids
 Hyperglycemia is a common complication of corticosteroid
therapy.
 Several approaches have been proposed for treatment of
this condition, but no published protocols or studies have
investigated the efficacy of these approaches.
 A reasonable approach is to institute glucose monitoring for
at least 48 hours in all patients receiving high-dose
glucocorticoid therapy and to initiate insulin therapy as
appropriate.
Patients receiving high-dose steroids
 Corticosteroids has an effect on the overall insulin
requirements several hours after their administration, and
they notoriously exaggerate postprandial glucose.
 A strategy to address persistent hyperglycemia related to
a single dose of a corticosteroid, typically given in the
morning, is the initiation of NPH insulin, taking advantage
of similar peak and duration effects of NPH and
prednisone/prednisolone.
 0.1U/kg for every 10mg of prednisone a day up to 0.4U/kg.
(Clore and Thurby-Hay)
Patients receiving high-dose steroids
 The administration of multiple high doses of
glucocorticoids throughout the day.
 In this situation, NPH alone may fail to achieve and
maintain glycemic control, usually because of
postprandial hyperglycemia.
Basal insulin
Nutritional or
prandial insulin
Supplemental or
correctional
insulin
30% of the TDD for
patients eating
70% of the TDD divided
equally between meals.
Moderate dose q ac & hs
if eating or q 6h if NPO for
taking<0.5U/kg TDD or at
risk of hypoglycemia.
High dose for
taking>0.5U/kg TDD
Patients receiving high-dose steroids
 During corticosteroid tapers, insulin dosing should be
proactively adjusted to avoid hypoglycemia.
 Percentage of insulin decrease or increase should be half
the percent steroid decrease or increase. (i.e., if steroid
dose is reduced or increased 50%, insulin dose is
reduced or increased 25% simultaneously-basal and
nutritional)
Specific clinical situations
5. Patients Receiving TPN
 The high glucose load in standard parenteral nutrition
frequently results in hyperglycemia, which is associated
with a higher incidence of complications and mortality
in critically ill patients in the ICU.
 Insulin therapy is highly recommended, with glucose
targets as defined previously on the basis of the
severity of illness.
Patients receiving TPN
Basal insulin
Nutritional or prandial
insulin
Supplemental or
correctional insulin
Use insulin drip X 24 h.
None if entirely fasting
Low dose q ac & hs if eating or q
6h if NPO for taking<0.5U/kg TDD
or at risk of hypoglycemia.
Calculate TDD as per IV to SQ
protocols.
Incorporate 80% of the new TDD
as regular insulin in the TPN bag.
When TPN bag containing insulin
is started, discontinue insulin
infusion.
Daily dose adjustment:
If BG>180, insulin in the TPN by
20% (most patients) or 10% if risk
of hypoglycemia.
May use SQ long- or
intermediate-acting insulin while
waiting for insulin dose
adjustment in subsequent TPN
bag.
Initiate preprandial insulin if
daytime glucose>180mg/dl X 2
days.
If taking clear liquids: give
0.05U/kg ac
If taking food: give 0.1U/kg ac
If at risk for hypoglycemia, give
0.05U/kg ac
Moderate dose for taking>0.5U/kg
TDD
Specific clinical situations
6. Patients Using an Insulin Pump
 Patients who use continuous subcutaneous insulin
infusion (pump) therapy in the outpatient setting can be
candidates for diabetes self-management in the
hospital, provided they have the mental and physical
capacity to do so.
 Of importance, nursing personnel must document basal
rates and bolus doses on a regular basis (at least
daily).
 The availability of hospital personnel with expertise in
continuous subcutaneous insulin infusion therapy is
essential
Daily dose adjustment
Basal insulin
Nutritional or
prandial insulin
If fasting and morning
BG>140mg/dL
If eating and
random/postprandial
BG>180mg/dL
Patients on≤0.5U/kg
or *at risk for
hypoglycemia
 By 10%
 By 10%
Patients on
>0.5U/kg
 By 20%
 By 20%
If fasting and morning
BG<100mg/dL X 2 or
B<70mg/dL anytime
If eating and
random/postprandial
BG<100mg/dL X 2 or
B<70mg/dL anytime
 By 20%
 By 20%
For all patients
Supplemental or
correctional
insulin
*at risk for hypoglycemia: insulin naïve, Elderly (>75 years), underweight-BMI<18.5kg/m2,
renal dysfunction (GFR<50ml/min), severe hepatic or cardiac dysfunction,
known gastroparesis (consider using regular insulin instead of lispro or Aspart)
Transition to outpatient care
 Preparation for transition to the outpatient setting
should begin at the time of hospital admission.
 Early assessment of a patient’s cognitive abilities,
literacy level, visual acuity, dexterity, cultural context,
and financial resources for acquiring outpatient diabetic
supplies allows sufficient time to prepare the patient
and address problem areas.
 Discharge planning, patient education, and clear
communication with outpatient providers are critical for
ensuring a safe and successful transition to outpatient
glycemic management.
THD Practice
AS-IS
THD Insulin Sliding Scale
------------------------------------------ Universal SSI in EPIC unless
Glucose
AC
HS
physicians create their own SSI.
60-120
NO insulin NO insulin
 No consideration of the degree of
121-150
2 units
NO insulin
insulin resistance.
151-200
4 units
NO insuiln
 SSI (novolog) +/- Long acting
201-250
6 units
3 units
(Lantus)
251-300
8 units
4 units
 Does this novolog SSI include
5 units
prandial and correctional components 301-350 10 units
351-400 12 units
6 units
or is it just correctional without
prandial component?
> 400 15 units
7 units
--------------------------------------------
TO-BE??
 SSI-L, SSI-M, SSI-H in order set.
 Prandial component based on
individual patient’s TDD should be
incorporated
CONCLUSIONS
 Hyperglycemia in hospitalized patients is extremely common.
Hospitalization is an opportunity to evaluate long-term diabetes control
and initiate new therapy.
 Think about various factors that may affect accuracy of glucose
measurement, if there are discrepancies between venous and capillary
readings.
 A target of near-normalization of blood glucose levels in most hospitalized
patients is inappropriate.
 Different targets for different patient populations. Always use your clinical
judgment.
 Stringent targets for patients with high risk of MI, vascular and noncardiac major
surgery with planned ICU admission
 Do more than SSI. Physiologic Insulin protocol is the preferred method.
 Always reassess and adjust accordingly.
References
1.Ven den Berghe G, et. al. Intensive insulin therapy in critically ill patients. N Engl J Med. 2001; 345: 1359-1367
2. Moghissi ES, Reexamining the evidence for inpatient glucose control: New recommendations for glycemic targets,
Am J Health-Syst Pharm, vol 67, Aug 15, 2010 Suppl 8
3. The nice-sugar study investigators, Intensive versus Conventional Glucose Control in Critically Ill Patients, N Engl
J Med Volume 360(13):1283-1297
4. Moghissi,et.al., Consensus: Inpatient Hyperglycemia, Endocr Pract. 2009;15(No. 4)
5. Amir Qaseem, et.al., 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; 154:260267
6. Ariana R.Pichardo-Lowden, et.al., Management of hyperglycemia in the non-intensive care patient: Featuring
subcutaneous insulin protocols, Endocr Pract. 2011; 17 (No.2)
7. Visiliki Valla, Review article: Therapeutics of diabetes mellitus: Focus on insulin analogues and insulin pumps,
Hindawi Publishing corporation Esperimental diabetes research volume 2010, article ID 178372, 14 pages
8. Leile K.Dawson and et.al., Risk of cancer in patients receiving insulin glargine, Am J Health-Syst Pharm Vol 67
Dec 1, 2010, 2025-2031
References
9. I.B. Hirsch, Insulin analogues, N Engl J Med 2005;352:174-83
10. Umpierrez GE , Smiley D, Zisman A, et al., Randomized study of basal-bolus
insulin therapy in the inpatient management of patients with type 2 diabetes
(RABBIT2 trial), Diabetes Care. 2007; 30;2181-2186
11. Ariana R. Pichardo-Lowden, et.al., Management of hyperglycemia in the nonintensive care patient: Featuring subcutaneous insulin protocols, Endocrine
practice vol 17 No.2 March/April 2011
12. Konrad C.Nau, et.al., Glycemic control in hospitalized patients not in intensive
care: beyond sliding-scale insulin, Americal Family Physician, volume 81,
number 9, 1130-1135
13. Andrew D. Pitkin, et al., Challenges to Glycemic Measurement in the
Perioperative and Critically Ill Patient: A Review, J Diabetes Sci Technol
2009;3(6):1270-1281
14. http://www.medscape.org/viewarticle/714742