joel zonszein call iris carrasquillo rn, cde for diabetes issues 718 904-2883 the conundrum of...
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The Conundrum of DiabetesIn hospitalized patients
Joel Zonszein, MD, CDE, FACP, FACE
Albert Einstein College of Medicine Montefiore Medical Center
Bronx, New York
HYPERGLYCEMIA
MICROVASCULOPATHY
INSULINSECRETION
CO
MP
LIC
AT
ION
S
IGT T y p e 2 d I a b e t e s
CARDIOVASCULAR DISEASE
Zonszein J. in Hurst’s the Heart (Ch 78) 1998;2117-2142
INSULIN RESISTANCE
HbA1c
Retinopathy
Nephropathy
NeuropathyCVD Mortality10 years letter
DCCT9 7%
76%
54%
60%
57% p=.02*
Kumamoto9 7%
69%
70%
-
-
UKPDS8 7%
17-21%
24-33%
-
13% p=.007**
** N Eng J Med September 10, 2008
Glycemic Control and ComplicationsOlder Studies -10 years latterGlycemic Control and ComplicationsOlder Studies -10 years latter
UKPDS Study Group: Lancet 352:837-53, 1998 *DCCT/EDIC Study Research Group, N Engl J Med December 353:2643-, 2005
Ohkubo Y: Diabetes Res Clin Prac 28:103-17, 1995DCCT Study Group: N Engl J Med 329:977-86, 1993
Is Tighter Glycemic Control Better?Newer Studies
Characteristics ADVANCE VADT ACCORD
No. participants
Mean age (yr)
Median study duration (yr)
11,140
66
5
1,791
60
5.6
10,251
62
3.4
Baseline A1c
Outcome A1c (intensive /control)
7.2
6.3 vs. 7.0
9.4
6.9 vs. 8.5
8.1
6.4 vs. 7.5
Major Hypoglycemia (% yr) 2.7 vs. 1.5 21.2 vs. 9.9 16.2 vs. 5.1
Weight gain (Kg) 0.1 vs. 1.0 7.8 vs. 3.4 3.5 vs. 0.4
HR Primary outcomes (95% CI)
HR Mortality (95% CI)
0.94 (0.84-1.06)
0.93 (0.83-1.06)
0.88 (0.74-1.05)
1.07 (0.81-1.42)
0.90 (0.78-1.04)
1.22 (1.01-1.46)
ACCORD. N Engl J Med 2008;358ADVANCE. N Engl J Med 2008;358 VADT N Engl J Med 2009;360
Del Prato S Diabetologia 2009;52:1259
VADT in the context of the “natural history of Type 2 Diabetes
Hb
A1c
(%)
TIME (years since diagnosis)
Del Prato S Diabetologia 2009;52:1259
VADT in the context of the “natural history of Type 2 Diabetes
Hb
A1c
(%)
TIME (years since diagnosis)
TIME (years since diagnosis)
Hb
A1c
(%)
Drive risk for complications
Build up “bad” metabolic memory
Del Prato S Diabetologia 2009;52:1259
VADT in the context of the “natural history of Type 2 Diabetes
Multiple Risk Interventions in Type 2 Diabetes (STENO-2 Trial)• 160 patients with type 2 diabetes and microalbuminuria, randomized
to conventional or intensive treatment for multiple risks for 8 years
Conventional IntensiveBlood Pressure <160/95 <140/85HbA1c <7.5% <6.5%Total Chol <250 mg/dL <190
mg/dLACE-Inhibitor No YesAspirin with known CAD Yes Yes with PVD No Yes No PVD or CAD No Yes
Gaede P et al. N Engl J Med. 2003;348:383-393.
Multiple Risks Interventions in Type 2 Diabetes (STENO -2 Trial)
Relative Risk End Points Reduction
Cardiovascular Composite 53% (P=0.007)
Nephropathy 61% (P=0.003)
Retinopathy 58% (P=0.02)
Autonomic neuropathy 63% (P=0.002)
Gaede P et al. N Engl J Med. 2003;348:383-393.
*Gaede P et al. N Engl J Med. 2008;358:580 -591.
Lower CVD mortality (@7.8 years) 43% (P=0.04) *
Smoking cessation
+
Treatment of:
HypertensionDyslipidemia
Hyperglycemia
Approved Antidiabetic Medications in the US
Medicaton Route Year (FDA approved)
Insulin Inhaled
ParenteralPulmonary
19212006-2007
Sulfonylureas Oral 1946
Biguanides Phenphormin Metformin
OralOral
1957- 19771995
Alpha-glycosidase inhibitors Oral 1995
Thiazolidinediones Troglitazone Rosiglitazone Pioglitazone
OralOralOral
1997-200019991999
Glinides Oral 1997
GLP analogues Byetta® Parenteral 2005
Amylin analogues Symlin® Parenteral 2005
DPP-IV inhibitors Januvia® and Onglyza Oral 2006 and 2009
Modified from Nathan D. N Eng J Med 2007;356:437-440
Combination Therapy; Different Sites of Action
Muscle and adipose tissue:Peripheral glucose uptakeTHIAZOLIDINEDIONES
Liver: GlucoseproductionBIGUANIDES
Pancreas: InsulinsecretionSULFONYLUREASMEGLITINIDES
Intestine: Digestion and absorption of carbohydratesa-GLUCOSIDASE INHIBITORS
Injectables: INSULINS EXENATIDE and PRAMLINTIDEglucagon, insulin, gastric, orectins
SITAGLIPTIN
The 2006 ADA Treatment Algorithm
*Check A1C every 3 months until <7% and then at least every 6 months thereafter. Nathan DM, et al. Diabetes Care. 2006;29:1963-1972.
Yes*No A1C7%
Diagnosis
Lifestyle Intervention + Metformin
Add Basal Insulin – Most effective
Add Sulfonylurea– Least expensive
Add Glitazone– No hypoglycemia
Intensify Insulin Add Glitazone Add Basal Insulin Add Sulfonylurea
Yes*No A1C7%Yes*No A1C7%
Add Basal or Intensify Insulin
Intensive Insulin + Metformin Glitazone
Yes*No A1C7% Yes*No A1C7% Yes*No A1C7%
How are we managing hyperglycemia in 2008… What drug to use when combination of SUO and Metformin fails?
• Patient: Maria
• Age: 51
• Height: 5' 3“, Weight: 224 lbs
• FBG between 110 and 140 mg/dl A1c 8.1%
• Treatment: maximum doses of MET (5 y) and an SFU (2 y)
• Patient goal: motivated;
• Choices:– Add pioglitazone– Add neutral protamine Hagedorn (NPH) h,s.– Add exenatide twice daily
N Engl J Med 2008;358:293-297.
• Patient: Maria● USA Diabetologist:
● 53% add exenatide twice daily● 32 % add NPH insulin before bedtime● 15% add pioglitazone (15%)
● USA other specialties:● 52% add NPH before bedtime● 24% add exenatide twice daily● 24% add pioglitazone
How are we managing hyperglycemia in 2008… What drug to use when combination of SUO and Metformin fails?
N Engl J Med 2008;358:293-297.
*Check A1C every 3 months until <7% and then at least every 6 months thereafter. Nathan DM, et al. Diabetes Care. 2006;29:1963-1972.
Yes*No A1C7%
Diagnosis
Lifestyle Intervention + Metformin
Add Basal Insulin – Most effective
Add Sulfonylurea– Least expensive
Add Glitazone– No hypoglycemia
Intensify Insulin Add Glitazone Add Basal Insulin Add Sulfonylurea
Yes*No A1C7%Yes*No A1C7%
Add Basal or Intensify Insulin
Intensive Insulin + Metformin Glitazone
Yes*No A1C7% Yes*No A1C7% Yes*No A1C7%
The 2006 ADA Treatment Algorithm
Lifestyle + MET+
Basal/Bolus Insulin
Lifestyle + MET+
Basal/Bolus Insulin
Lifestyle + MET+
Basal Insulin
Lifestyle + MET+
Basal InsulinAt Diagnosis:
Lifestyle+
MET
At Diagnosis:
Lifestyle+
MET
STEP 1 STEP 2 STEP 3
Tier 1: Well-validated core therapies*
Lifestyle + MET+
SFU†
Lifestyle + MET+
SFU†
Lifestyle + MET + GLP-1 Agonist‡
No hypoglycemiaWeight loss
Nausea/vomiting
Lifestyle + MET + GLP-1 Agonist‡
No hypoglycemiaWeight loss
Nausea/vomiting
Lifestyle + MET + PioNo hypoglycemia
Edema/CHFBone loss
Lifestyle + MET + PioNo hypoglycemia
Edema/CHFBone loss
Lifestyle + MET+
Pio + SFU†
Lifestyle + MET+
Pio + SFU†
Lifestyle + MET+
Basal insulin
Lifestyle + MET+
Basal insulin
Tier 2: Less well-validated therapies*
†SFUs other than glybenclamide (glyburide) or chlorpropamide. ‡Insufficient clinical use to be confident regarding safety.Adapted from Diabetes Care. 2009;32:193-203 For Important Safety Information about exenatide (GLP-1 agonist), see slides 9-11 and the accompanying full Prescribing Information.
*Validation based on clinical trials and clinical judgment
A1c ≥7%
Another Day….. another new Consensus Algorithm the 2009…
Lifestyle + MET+
Basal/Bolus Insulin
Lifestyle + MET+
Basal/Bolus Insulin
Lifestyle + MET+
Basal Insulin
Lifestyle + MET+
Basal InsulinAt Diagnosis:
Lifestyle+
MET
At Diagnosis:
Lifestyle+
MET
STEP 1 STEP 2 STEP 3
Tier 1: Well-validated core therapies*
Lifestyle + MET+
SFU†
Lifestyle + MET+
SFU†
Lifestyle + MET + GLP-1 Agonist‡
No hypoglycemiaWeight loss
Nausea/vomiting
Lifestyle + MET + PioNo hypoglycemia
Edema/CHFBone loss
Lifestyle + MET+
Pio + SFU†
Lifestyle + MET+
Basal insulin
Tier 2: Less well-validated therapies*
†SFUs other than glybenclamide (glyburide) or chlorpropamide. ‡Insufficient clinical use to be confident regarding safety.Adapted from Diabetes Care. 2009;32:193-203 For Important Safety Information about exenatide (GLP-1 agonist), see slides 9-11 and the accompanying full Prescribing Information.
*Validation based on clinical trials and clinical judgment
A1c ≥7%
Another Day….. another new Consensus Algorithm the 2009…
Management of Hyperglycemia in Hospitalized patients
Intensive insulin therapy in critically ill patients. • NON-DIABETES
– Sodi-Pallares “polarizing GIK solution”– Metabolic control in SICU patients– Metabolic control in MICU patients– Intensive insulin therapy in sepsis (German SepNet)– NICE-SUGAR
• DIABETES– DIGAMI– DIGAMI 2
Sodi-Pallares D, 1963 Dis Chest 43: 424Diaz R, 1998 Circulation 24:2227–2234
Kjellman UW, 2000 Scand Cardiovasc J 34:321–330Van Den Berghe G, 2001 N Engl J Med 345:1359 –1367
SepNet. Study. N Engl J Med 2008;358:125-139NICE-SUGAR Study. N Engl J Med 2009;360:1283-1297
Dr. Demetrio Sodi Pallares1913 - 2003
Glucose Insulin and Potassium Infusion (GIK)
Overview of Glucose-Insulin-Potassium Therapy for AMI: A 40-Year Prospective
Overview of GIK Therapy for AMI: A 30-Year Prospective
CREATE-ECLA: Effect of GIK Therapy on Mortality in Patients With STEMI*
Glucose Insulin and Potassium Infusion (GIK)in STEMI: Death at 30 Days by Predefined Subgroups
van den Berghe G, et al. N Engl J Med. 2001;345:1359–1367.
Conventional: insulin when blood glucose > 215 mg/dL.Intensive: insulin when glucose > 110 mg/dL and maintained at 80–110 mg/dL
Survival in ICU (%)
100
96
92
88
80
0
84
0 20 40 60 80 100 120 140 160
Intensive treatment
Conventional treatment
Days After Admission
RR 43% (95% CI 15 - 62)
Intensive insulin therapy in SICU patients: Improves survival
Intensive insulin therapy in SICU patientsbaseline characteristics
Conventional
n 783
Intensive
n 785
Age 62.2 63.4
BMI 25.8 26.2
Cardiac surgery (%) 63 62
History of Diabetes 13 13
Glucose >110 (%)
Glucose >200 (%)
76
13
73
11
Van den Berghe G. New Engl J Med 2001;345:1359-1367
Intensive insulin therapy in SICU patients
Conventional
n 783
Intensive
n 785
p
value
Insulin therapy n
(%)
307
(39.2)
755
(98.7)
<0.001
Median Insulin does IU/D 33 71 <0.001
Morning glucose 173 103 <0.001
% BG < 40 mg/dL 6 39 <0.001
Van den Berghe G. New Engl J Med 2001;345:1359-1367
Glycemic Targets in Hospital Patients 2004
Glycemic Targets (ACE)1
ICU
110 mg/dL
Medical/Surgical Units
Preprandial: 110 mg/dL
Maximal glucose: 180 mg/dL
Glycemic Targets (ADA)2
ICU
<180 mg/dL (target, 110 mg/dL)
Medical/Surgical Units
Preprandial: 90-130 mg/dL(target, 110 mg/dL)
Postprandial <180 mg/dL
ACE indicates American College of Endocrinology; ADA, American Diabetes Association; ICU, intensive care unit.1. Garber AJ, Moghissi ES. Endocr Pract. 2004;10(suppl 2):4-9.2. American Diabetes Association. Diabetes Care. 2005;28(suppl 1):S4-S36.
Treating hyperglycemia aggressively “may be beneficial” and should be done in a sane and cost effective manner
Counterpoint: Inpatient management.A premature call to arms
Inzucchi and Rosenstock Diabetes Care April 2005 28:976
3054 received IIT goal: 81-108 mg/dL(time weighted BG = 118 mg/dL)
3050 received CIT goal: <180 mg/dL(time-weighted BG = 145 mg/dL)
• 90-day mortality: IIT: 829 patients (27.5%), CIT: 751 (24.9%)
• Absolute mortality difference: 2.6% (95% CI, 0.4-4.8)
• Odds ratio for death with IIT: 1.14 (95% CI, 1.02-1.28; P=.02)
Finfer S, et al. N Engl J Med. 2009;360::1283
BG
, mg
/dL
180
160
140
120
100
800
1 2 3 4 5 86 7 9 10 11 12 13 14Base-line
Days After Randomization
Conventional
Intensive
108
1.0
0.9
0.8
0.7
0.60
10 20 30 40 50 8060 70 900
Days After Randomization
Conventional
Intensive
P=.03
Pro
bab
ility
of
Su
rviv
al
NICE-SUGAR: Outcomes
Glycemic Targets in Hospital Patients 2009
Glycemic Targets (ACE)1
ICU
110 mg/dL
Medical/Surgical Units
Preprandial: 110 mg/dL
Maximal glucose: 180 mg/dL
Glycemic Targets (ADA)2
ICU
<180 mg/dL (target, 110 mg/dL)
Medical/Surgical Units
Preprandial: 90-130 mg/dL(target, 110 mg/dL)
Postprandial <180 mg/dL
Glycemic Targets (ADA) and (ACE) 3 2009
ICU
(target, 140 to 180 mg/dL)Medical/Surgical Units
Preprandial: target < 140 mg/dLPostprandial or random <180 mg/dL
ACE indicates American College of Endocrinology; ADA, American Diabetes Association; ICU, intensive care unit.1. Garber AJ, Moghissi ES. Endocr Pract. 2004;10(suppl 2):4-9.2. American Diabetes Association. Diabetes Care. 2005;28(suppl 1):S4-S36.3. Consensus: Inpatient Hyperglycemia. Endocr Practice 2009;15 (No.4) 353-369
DIGAMI: Intensive insulin therapy improves mortality: AMI in patients with Diabetes
Malmberg K, et al. BMJ. 1997;314:1512–1515. (Reproduced with permission from the BMJ Publishing Group.)
All subjects
(N = 620)Risk reduction (28%) P = 0.011
Standard treatment
0
30
20
40
70
10
50
60
0 1
Follow-up (years)
2 3 4 5
Low-risk and not previously on insulin
(N = 272)Risk reduction (51%) P = 0.0004
IV insulin 48 hours, then 4 injections daily
0
30
20
40
70
10
50
60
0 1
Follow-up (years)
2 3 4 5
DIGAMI = Diabetes and Insulin-Glucose Infusion in Acute Myocardial Infarction.
Mortality(%)
Malmberg K, et al. BMJ. 1997;314:1512–1515. (Reproduced with permission from the BMJ Publishing Group.)
All subjects
(N = 620)Risk reduction (28%) P = 0.011
Standard treatment
0
30
20
40
70
10
50
60
0 1
Follow-up (years)
2 3 4 5
Low-risk and not previously on insulin
(N = 272)Risk reduction (51%) P = 0.0004
IV insulin 48 hours, then 4 injections daily
0
30
20
40
70
10
50
60
0 1
Follow-up (years)
2 3 4 5
DIGAMI = Diabetes and Insulin-Glucose Infusion in Acute Myocardial Infarction.
Mortality(%)
DIGAMI: Intensive insulin therapy improves mortality: AMI in patients with Diabetes
DIGAMI 2:Intensive insulin therapy during AMI n1253
European Heart Journal 2005;26:650-661
Grup 1 n=474 Intensive Insulin Control IV insulin + glucoseGrup 2 n=473 Standard Control IV insulin + glucoseGrup 3 n=306 Routine use of insulin
HbA1c7.2%7.3%7.3%
~6.8%
FG mg/dlAdmision 24hrs Final230 164 144225 164 150232 180 150
DIGAMI 2: Time to first major event Death, Reinfarction, or Stroke
European Heart Journal 2005;26:650-661
TREATING THE PATIENT, NOT THE BLOOD SUGARS
Insulin replacement therapy in type 1 diabetesInsulin supplementation in type 2 diabetes
INSULIN DOSE IS RELATED TO THE DEGREEOF ISENSITIVITY NOT GLYCEMIC LEVEL
Case 1: 52-year-old male
• Hospitalized with atypical chest pain ROMI
• Reports previous good health, on no meds,
no prior Hx of DM, his 57-year-old brother has T2DM
• Ht: 5’9”; Wt: 221 lb Abdominal obesity, Acanthosis
• BP: 130/92 mm Hg
• Random plasma glucose: 219 mg/dL
• Lipids: – TG: 380 mg/dL – HDL-C: 28 mg/dL– LDL-C: 170 mg/dL
• What tests will your order?
• What diet will your order?
• How will you treat his hyperglycemia?
• Continuity of care…..
Case 1: 52-year-old male
Programmed Insulin Therapy
• Insulin replacement therapy in type 1 diabetes Basal Bolus
• Insulin supplementation in type 2 diabetes
Change RISSC for PIT– Avoid oral antidiabetic agents– Use basal insulin for supplementation– Avoid insulin meal coverage in T2DM
• Intensive Intravenous Insulin Therapy
Programmed Insulin Therapy (PIT): Goals
• Provide education and improve patient care
• Better but less intensive and cost effective glycemic control– Optimize Point of care CBG– Avoid HYPOGLYCEMIA– Avoid HYPERGLYCEMIA– Avoid “glucose toxicity”
• Continuity of care
• Improve LOS
Programmed Insulin Therapy (PIT):Insulin dose
• Use intermediate or long-acting insulins:– Lantus (glargine) can be given at AM, bed time, or at any time,
but should be “synchronized to the same hour every day– NPH, 7AM (50% of daily dose) and bed-time (50% of daily dose)
• Starting dose by weight and other factors– 0.3 units/Kg/day in end-organ failure– 0.5 units/Kg/day in stable medical patients– 0.7 units/Kg/day in surgical interventions or acute illnesses
• Constant dose adjustments
Insulins Peak (duration) hrs• RAPID-ACTING
– Humalog lispro 1-2 (2-6)– Novolog aspart 1-2 (2-6)– Apidra glulisine 1-2 (2-6)
• SHORT-ACTING– Regular 2-4 (3-6)
• INTERMEDIATE-ACTING– NPH 6-12 (10-24)
• LONG ACTING– Lantus glargine none (24)– Levemir detemir none (20-24)
Insulin analoguesModified from: Ragucci E, Zonszein J, Frishman WH. Heart Dis. 2003;5:18-33
BA
SA
L
B
OL
US
Insulins Peak (duration) hrs• RAPID-ACTING
– Humalog lispro 1-2 (2-6)– Novolog aspart 1-2 (2-6)– Apidra glulisine 1-2 (2-6)
• SHORT-ACTING– Regular 2-4 (3-6)
• INTERMEDIATE-ACTING– NPH 6-12 (10-24)
• LONG ACTING)– Lantus glargine none (24)– Levemir detemir none (20-24)
Insulin analoguesModified from: Ragucci E, Zonszein J, Frishman WH. Heart Dis. 2003;5:18-33
BA
SA
L
B
OL
US
Fixed-Mixed Insulins
HUMULIN (NPH/REG)– 70/30– 50/50
HUMALOG (Prot-lispro/free lispro)– 75/25– 50/50
NOVOLIN (NPH/REG)– 70/30
NOVOMIX (Prot-aspart/aspart)– 70/30
Insulin analogues
Pathophysiology of Type 1 Diabetes
ADA. Diabetes Care. 2002;25(suppl 1):S1
Loss of -cell mass
Insufficient insulin
Absolute insulin deficiency
Insulin Therapy “Basal – Bolus” Concept
· Some insulin is secreted at all times – the basal insulin
· Incremental amounts of insulin are secreted in response to rising postprandial glucose levels –the bolus insulin
• T1DM Insulin replacement 0.3-0.5 U/Kg/D – 2/3 given in the AM, 1/3 in the PM– 2/3 long acting, 1/3 short acting
• T2DM Insulin supplementation 0.5-1.0 U/K/D– Bedtime only (h.s.)– AM + h.s.– If elevated postprandials: change to “insulin
replacement”
Insulin Dosage Schedules
mg
% o
r
U/m
l
100
0
12 6 12 6 12
GLUCOSE
INSULIN
Breakfast Lunch Tea Dinner
Difficult to replicate
prandial
basal
Normal insulin secretion
PlasmaInsulin(U/mL)
Time
4:00 8:00 12:00 16:00 20:00 24:00 4:00 8:00
Breakfast Lunch Dinner
T1DM a state of insulin deficiencyInsulin as replacement basal/bolus pattern
75
50
25
0
GlucoseBolus InsulinBase Insulin
Skyler J, Kelley’s Textbook of Internal Medicine 2000.
• T1DM Insulin replacement 0.3-0.5 U/Kg/D – 2/3 given in the AM, 1/3 in the PM– 2/3 long acting, 1/3 short acting
• T2DM Insulin supplementation 0.5-1.0 U/K/D– Bedtime only (h.s.)– AM + h.s.– If elevated postprandials: change to “insulin
replacement”
Insulin Dosage Schedules
GLUCOSE
INSULIN
Breakfast Lunch Dinner
Glucose and insulin in T2DM and acute illness
300 mg/dl
100 mg/dl
5-20 mcu/L
20-200 mcu/L
GLUCOSE
Breakfast Lunch Dinner
Insulin therapy in T2DM and acute illness
300 mg/dl
100 mg/dl
BG mg/dl Insulin units
<250 0
251-300 4
301-350 6
351-400 8
>400 10
Regular Insulin30 units/D in 100 K
GLYCEMIC CONTROL “REGULAR INSULIN SLIDING SCALE” (RISSC)
• HYPERGLYCEMIA ……………...40% – severity of illness– high admission glucose level– infection disorders– corticosteroids
• HYPOGLYCEMIC EPISODES……23% – African-American– low serum albumin
Queale WS. Arch Intern Med 1997;157:545-552
Blood Glucose Levels During Isulin Treatment
Days of Therapy
Blo
od
glu
cose
(m
g/d
L)
100
120
140
160
180
200
220
240
Admit 1 2 3 4 5 6 7 8 9 10
SSRI
Lantus + glulisine
Mean Blood Glucose Levels During Insulin Therapy
* p<0.01
¶ p<0.05
¶* * *
¶ ¶ ¶
Day 3: P=0.06
GLUCOSE
Breakfast Lunch Dinner
Insulin therapy in T2DM Long-acting insulinFewer POC glucose monitoring
300 mg/dl
100 mg/dl
Insulin Glargine50-70 units/D in 100 K
CBG CBG
GLUCOSE
Breakfast Lunch Dinner
300 mg/dl
100 mg/dl
Insulin therapy in T2DM Intermediate-acting insulinFewer POC glucose monitoring
NPH50-70 units/D in 100 K
CBGCBG
• Indications*
1. AMI
2. Revascularization
3. Selective surgical cases
• Labor intensive and expensive– More feasible in acute care units
• Changed early to aggressive subcutaneous insulin regimens
Montefiore: Intravenous Insulin Protocol
* Not for DKA and or HHC
Montefiore Length of Stay –LOS
MOSES WEILER NORTH
NONDIABETES DIABETES
NONDIABETES DIABETES
NONDIABETES DIABETES
2002 5.9 5.3 5.9 5.7
2007 4.3 4.8 5.4 4.6
2008 5.7 4.6 5.2 4.2 6.9 6.3
THANKSQUESTIONS ?