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Joel Zonszein Call Iris Carrasquillo RN, CDE for Diabetes Issues 718 904-2883 The Conundrum of Diabetes In hospitalized patients.

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Presentation on theme: "Joel Zonszein Call Iris Carrasquillo RN, CDE for Diabetes Issues 718 904-2883 The Conundrum of Diabetes In hospitalized patients."— Presentation transcript:

1 Joel Zonszein Call Iris Carrasquillo RN, CDE for Diabetes Issues The Conundrum of Diabetes In hospitalized patients

2 The Conundrum of Diabetes In hospitalized patients Joel Zonszein, MD, CDE, FACP, FACE Albert Einstein College of Medicine Montefiore Medical Center Bronx, New York

3 HYPERGLYCEMIA MICROVASCULOPATHY INSULIN SECRETION COMPLICATIONS IGT T y p e 2 d I a b e t e s CARDIOVASCULAR DISEASE Zonszein J. in Hursts the Heart (Ch 78) 1998; INSULIN RESISTANCE

4 DISEASE PROGRESSION CARDIOVASCULAR RISK NG IGTT2DM 2-hr PG mg/dl FG mg/dl mg/dl STRESS HYPERGLYCEMIA METABOLIC SYNDROME BP (mmHg) >130/85 TG (mg/dl) > 150 HDL-C (mg/dl) Men < 40 Women < 50 WAIST CIRCUMF (inches) Men > 40 Women > 35 Pantaleo A, Zonszein J. Heart Dis. 2003;5:323-33

5 HbA 1c Retinopathy Nephropathy Neuropathy CVD Mortality 10 years letter DCCT 9 7% 76% 54% 60% 57% p=.02* Kumamoto 9 7% 69% 70% - UKPDS 8 7% 17-21% 24-33% - 13% p=.007** ** N Eng J Med September 10, 2008 Glycemic Control and Complications Older 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, 1995 DCCT Study Group: N Engl J Med 329:977-86, 1993

6 Is Tighter Glycemic Control Better? Newer Studies CharacteristicsADVANCEVADTACCORD No. participants Mean age (yr) Median study duration (yr) 11, , , Baseline A1c Outcome A1c (intensive /control) vs vs vs. 7.5 Major Hypoglycemia (% yr)2.7 vs vs vs. 5.1 Weight gain (Kg)0.1 vs vs vs. 0.4 HR Primary outcomes (95% CI) HR Mortality (95% CI) 0.94 ( ) 0.93 ( ) 0.88 ( ) 1.07 ( ) 0.90 ( ) 1.22 ( ) ACCORD. N Engl J Med 2008;358 ADVANCE. N Engl J Med 2008;358 VADT N Engl J Med 2009;360

7 Del Prato S Diabetologia 2009;52:1259 VADT in the context of the natural history of Type 2 Diabetes HbA1c (%) TIME (years since diagnosis)

8 Del Prato S Diabetologia 2009;52:1259 VADT in the context of the natural history of Type 2 Diabetes HbA1c (%) TIME (years since diagnosis)

9 HbA1c (%) 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

10 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 ConventionalIntensive Blood Pressure <160/95<140/85 HbA1c <7.5%<6.5% Total Chol <250 mg/dL<190 mg/dL ACE-Inhibitor NoYes Aspirin with known CAD YesYes with PVDNoYes No PVD or CAD NoYes Gaede P et al. N Engl J Med. 2003;348:

11 Multiple Risks Interventions in Type 2 Diabetes (STENO -2 Trial) Relative Risk End PointsReduction Cardiovascular Composite53% (P=0.007) Nephropathy61% (P=0.003) Retinopathy58% (P=0.02) Autonomic neuropathy63% (P=0.002) Gaede P et al. N Engl J Med. 2003;348: *Gaede P et al. N Engl J Med. 2008;358: Lower CVD mortality years) 43% (P=0.04) *

12 Smoking cessation + Treatment of: Hypertension Dyslipidemia Hyperglycemia

13 Mortality in People With Diabetes: Causes of Death Diabetes and mortality closer to home… During the last decade in NYC: All cause mortality: by 12% Diabetes related mortality: by 50% Diabetes related Hospitalizations: by 44% Fang J, Alderman MH. Diabetes 2006;55:768

14 Approved Antidiabetic Medications in the US MedicatonRouteYear (FDA approved) Insulin Inhaled Parenteral Pulmonary SulfonylureasOral1946 Biguanides Phenphormin Metformin Oral Alpha-glycosidase inhibitorsOral1995 Thiazolidinediones Troglitazone Rosiglitazone Pioglitazone Oral GlinidesOral1997 GLP analogues Byetta®Parenteral2005 Amylin analogues Symlin® Parenteral2005 DPP-IV inhibitors Januvia® and Onglyza Oral2006 and 2009 Modified from Nathan D. N Eng J Med 2007;356:

15 Combination Therapy; Different Sites of Action Muscle and adipose tissue: Peripheral glucose uptake THIAZOLIDINEDIONES Liver: Glucose production BIGUANIDES Pancreas: Insulin secretion SULFONYLUREAS MEGLITINIDES Intestine: Digestion and absorption of carbohydrates -GLUCOSIDASE INHIBITORS Injectables: INSULINS EXENATIDE and PRAMLINTIDE glucagon, insulin, gastric, orectins SITAGLIPTIN

16 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: Yes*No A1C7% Diagnosis Lifestyle Intervention + Metformin Add Basal Insulin – Most effective Add Sulfonylurea – Least expensive Add Glitazone – No hypoglycemia Intensify InsulinAdd GlitazoneAdd Basal InsulinAdd 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%

17 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:

18 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:

19 * Check A1C every 3 months until <7% and then at least every 6 months thereafter. Nathan DM, et al. Diabetes Care. 2006;29: Yes*No A1C7% Diagnosis Lifestyle Intervention + Metformin Add Basal Insulin – Most effective Add Sulfonylurea – Least expensive Add Glitazone – No hypoglycemia Intensify InsulinAdd GlitazoneAdd Basal InsulinAdd 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

20 Lifestyle + MET + Basal/Bolus Insulin Lifestyle + MET + Basal/Bolus Insulin Lifestyle + MET + Basal Insulin Lifestyle + MET + Basal Insulin At 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 hypoglycemia Weight loss Nausea/vomiting Lifestyle + MET + GLP-1 Agonist No hypoglycemia Weight loss Nausea/vomiting Lifestyle + MET + Pio No hypoglycemia Edema/CHF Bone loss Lifestyle + MET + Pio No hypoglycemia Edema/CHF Bone 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: 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…

21 Lifestyle + MET + Basal/Bolus Insulin Lifestyle + MET + Basal/Bolus Insulin Lifestyle + MET + Basal Insulin Lifestyle + MET + Basal Insulin At 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 hypoglycemia Weight loss Nausea/vomiting Lifestyle + MET + GLP-1 Agonist No hypoglycemia Weight loss Nausea/vomiting Lifestyle + MET + Pio No hypoglycemia Edema/CHF Bone loss Lifestyle + MET + Pio No hypoglycemia Edema/CHF Bone 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: 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…

22 Management of Hyperglycemia in Hospitalized patients

23 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: 424 Diaz R, 1998 Circulation 24:2227–2234 Kjellman UW, 2000 Scand Cardiovasc J 34:321–330 Van Den Berghe G, 2001 N Engl J Med 345:1359 –1367 SepNet. Study. N Engl J Med 2008;358: NICE-SUGAR Study. N Engl J Med 2009;360:

24 Dr. Demetrio Sodi Pallares Glucose Insulin and Potassium Infusion (GIK)

25 Overview of Glucose-Insulin-Potassium Therapy for AMI: A 40-Year Prospective Overview of GIK Therapy for AMI: A 30-Year Prospective

26 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

27 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 (%) Intensive treatment Conventional treatment Days After Admission RR 43% (95% CI ) Intensive insulin therapy in SICU patients: Improves survival

28 Intensive insulin therapy in SICU patients baseline characteristics Conventional n 783 Intensive n 785 Age BMI Cardiac surgery (%)6362 History of Diabetes13 Glucose >110 (%) Glucose >200 (%) Van den Berghe G. New Engl J Med 2001;345:

29 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/D3371<0.001 Morning glucose173103<0.001 % BG < 40 mg/dL 639<0.001 Van den Berghe G. New Engl J Med 2001;345:

30 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: 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): American Diabetes Association. Diabetes Care. 2005;28(suppl 1):S4-S36.

31 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 :976

32 3054 received IIT goal: 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, ) Odds ratio for death with IIT: 1.14 (95% CI, ; P=.02) Finfer S, et al. N Engl J Med. 2009;360::1283 BG, mg/dL Base- line Days After Randomization Conventional Intensive Days After Randomization Conventional Intensive P=.03 Probability of Survival NICE-SUGAR: Outcomes

33 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: mg/dL (target, 110 mg/dL) Postprandial <180 mg/dL Glycemic Targets (ADA) and (ACE) ICU (target, 140 to 180 mg/dL) Medical/Surgical Units Preprandial: target < 140 mg/dL Postprandial 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): American Diabetes Association. Diabetes Care. 2005;28(suppl 1):S4-S Consensus: Inpatient Hyperglycemia. Endocr Practice 2009;15 (No.4)

34 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 = Standard treatment Follow-up (years) 2345 Low-risk and not previously on insulin (N = 272) Risk reduction (51%) P = IV insulin 48 hours, then 4 injections daily Follow-up (years) 2345 DIGAMI = Diabetes and Insulin-Glucose Infusion in Acute Myocardial Infarction. Mortality (%)

35 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 = Standard treatment Follow-up (years) 2345 Low-risk and not previously on insulin (N = 272) Risk reduction (51%) P = IV insulin 48 hours, then 4 injections daily Follow-up (years) 2345 DIGAMI = Diabetes and Insulin-Glucose Infusion in Acute Myocardial Infarction. Mortality (%) DIGAMI: Intensive insulin therapy improves mortality: AMI in patients with Diabetes

36 DIGAMI 2: Intensive insulin therapy during AMI n1253 European Heart Journal 2005;26: Grup 1 n=474 Intensive Insulin Control IV insulin + glucose Grup 2 n=473 Standard Control IV insulin + glucose Grup 3 n=306 Routine use of insulin HbA1c 7.2% 7.3% ~6.8% FG mg/dl Admision 24hrs Final

37 DIGAMI 2: Time to first major event Death, Reinfarction, or Stroke European Heart Journal 2005;26:

38 Mean Glucose & In-Hospital Mortality in Patients with AMI (Reference: Mean BG mg/dl) Kosiborod M et al. Circulation 2008:117:1018 N= 16,871

39 Hypoglycemia & Mortality in Hyperglycemic AMI Patients: Influence of Insulin Therapy Kosiborod M, et al. JAMA. 2009;301:1556 Hypoglycemia No hypoglycemia P=.92 P<.001 Mortality, % No Insulin TreatmentInsulin Treatment Is hypoglycemia simply a marker of the sickest patients? N=7338 no hypo N=482 hypo (BG <60) N=7338 no hypo N=482 hypo (BG <60)

40 TREATING THE PATIENT, NOT THE BLOOD SUGARS Insulin replacement therapy in type 1 diabetes Insulin supplementation in type 2 diabetes INSULIN DOSE IS RELATED TO THE DEGREE OF ISENSITIVITY NOT GLYCEMIC LEVEL

41 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: 59; 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

42 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

43 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

44 Programmed Insulin Therapy (PIT): Insulin therapy Insulin replacement in T1DM Intravenous insulin in acute care Avoid continuation or initiation of oral agents Avoid combination (cocktail) therapies Replace RISSC for PIT Use of intermediate or long acting insulin vs. rapid or short acting insulins

45 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

46 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

47 Insulins Peak (duration) hrs RAPID-ACTING –Humalog lispro1-2 (2-6) –Novolog aspart1-2 (2-6) –Apidra glulisine1-2 (2-6) SHORT-ACTING –Regular2-4 (3-6) INTERMEDIATE-ACTING –NPH6-12 (10-24) LONG ACTING –Lantus glargine none (24) –Levemir detemirnone (20-24) Insulin analogues Modified from: Ragucci E, Zonszein J, Frishman WH. Heart Dis. 2003;5:18-33 BASAL BOLUS

48 Insulins Peak (duration) hrs RAPID-ACTING –Humalog lispro1-2 (2-6) –Novolog aspart1-2 (2-6) –Apidra glulisine1-2 (2-6) SHORT-ACTING –Regular2-4 (3-6) INTERMEDIATE-ACTING –NPH6-12 (10-24) LONG ACTING) –Lantus glargine none (24) –Levemir detemirnone (20-24) Insulin analogues Modified from: Ragucci E, Zonszein J, Frishman WH. Heart Dis. 2003;5:18-33 BASAL BOLUS

49 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

50 Addition of Biphasic, Prandial, or Basal Insulin to Oral Therapy; Primary and Secondary Outcomes at 1 Year Holman R et al. N Engl J Med 2007;357: Biphasic Prandial Basal A1c (%) <6.5(%) Hypo pt/yr Wt gain (Kg)

51 Mean A1C Levels During a 24-Week Study (N=756) Study End A1C 1.7% Lantus ® (insulin glargine [rDNA origin] injection) vs NPH in Insulin-naïve Patients: Mean Reduction in A1C 1,2 Lantus ® (n=367) NPH (n=389) P=NS vs NPH Week of Treatment 8.56 Mean A1C (%) Please see Important Safety Information for Lantus (insulin glargine [rDNA origin] injection) at the end of the presentation. Please see accompanying Full Prescribing Information for Lantus. 1. Adapted from Riddle M et al. Diabetes Care. 2003;26: Data on file. Aventis Pharmaceuticals Inc.

52 Comparison of Insulin Regimens Among Oral Treatment Failures Change in HbA 1c (%) Weight Change (kg) Yki-Jarvinen H et al. N Engl J Med. 1992;327: * -1.9* -1.8* -1.6* -0.5 *P 0,001 vs. control group P < 0.05 vs. other insulin treatment groups 2.2 * 1.2* 1.8 * 2.9 * -0.9

53 Pathophysiology of Type 1 Diabetes ADA. Diabetes Care. 2002;25(suppl 1):S1 Loss of -cell mass Insufficient insulin Absolute insulin deficiency

54 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

55 T1DM Insulin replacement 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 U/K/D –Bedtime only (h.s.) –AM + h.s. –If elevated postprandials: change to insulin replacement Insulin Dosage Schedules

56 mg % or U/ml GLUCOSE INSULIN Breakfast Lunch Tea Dinner Difficult to replicate prandial basal Normal insulin secretion

57 Plasma Insulin ( U/mL) Time 4:008:0012:0016:0020:0024:004:008:00 BreakfastLunchDinner T1DM a state of insulin deficiency Insulin as replacement basal/bolus pattern Glucose Bolus Insulin Base Insulin Skyler J, Kelleys Textbook of Internal Medicine 2000.

58 T1DM Insulin replacement 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 U/K/D –Bedtime only (h.s.) –AM + h.s. –If elevated postprandials: change to insulin replacement Insulin Dosage Schedules

59 Adapted from Kahn SE et al. Diabetes. 1993;42: Insulin Secretion Insulin Sensitivity Obese Type 2 Diabetes Lean High Low High Hyperbolic Relationship Between Insulin Secretion and Insulin Sensitivity

60 Insulin Secretion Insulin Sensitivity High Low High Treating according to degree of insulin resistance SENSITIZERS + PROVIDERS + INCRETINOMIMETICS sensitizers Insulin or Insulin-providers Incretinomimetics

61 GLUCOSE INSULIN Breakfast Lunch Dinner Glucose and insulin in T2DM and acute illness 300 mg/dl 100 mg/dl 5-20 mcu/L mcu/L

62 GLUCOSE Breakfast Lunch Dinner Insulin therapy in T2DM and acute illness 300 mg/dl 100 mg/dl BG mg/dl Insulin units < >40010 Regular Insulin 30 units/D in 100 K

63 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:

64 Mean Blood Glucose Levels During Insulin Therapy * p<0.01 ¶ p<0.05 ¶ * * * ¶ ¶ ¶ Day 3: P=0.06

65 GLUCOSE Breakfast LunchDinner Insulin therapy in T2DM Long-acting insulin Fewer POC glucose monitoring 300 mg/dl 100 mg/dl Insulin Glargine units/D in 100 K CBG

66 GLUCOSE Breakfast Lunch Dinner 300 mg/dl 100 mg/dl Insulin therapy in T2DM Intermediate-acting insulin Fewer POC glucose monitoring NPH units/D in 100 K CBG

67 Montefiore Programmed Insulin Therapy: Continuous Intravenous Intensive Insulin Therapy Insulin replacement in T1DM Insulin supplementation in T2DM

68 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

69 DATETIMEHOURSGLUCOSEACTIONInfusion rate (ml/hr) = (Glucose – 80) x 0.03 (round to the nearest cc.) UNITS /HR X -80 X 0.03= *4* Insulin in acute illness: Continuous Intravenous Insulin Protocol (CIIP)

70 GLUCOSE INSULIN Breakfast Lunch Dinner 300 mg/dl 100 mg/dl 5-20 mcu/L mcu/L Insulin therapy in T2DM and acute illness Intravenous Insulin Therapy

71 GLUCOSE Breakfast Lunch Dinner Glucose and insulin in T2DM and acute illness Transition to Regular 300 mg/dl 100 mg/dl 5-20 mcu/L mcu/L IV Insulin Regular Insulin

72 GLUCOSE Insulin Glargine Breakfast Lunch Dinner Glucose and insulin in T2DM and acute illness Transition to Glargine 300 mg/dl 100 mg/dl 5-20 mcu/L mcu/L IV Insulin

73 39-year-old Hispanic female Hospitalized with abdominal pain and vomiting for 2 days 10-year history of hypertension, told to have T1DM No significant cardiac, vascular, or neurologic symptoms Readily admits to difficulty with diet and lifestyle. Current management: HCTZ (25 mg/d), NPH Insulin 20 units in AM 15 units h.s. Weight: 158 lbs; height: 55 (BMI 26 kg/m2) BP: 140/100 mm Hg without orthostatic changes EKG: T-wave flattening in V4-6, more pronounced since last EKG two years ago. No R-wave criteria for LVH. Random glucose 444 mg/dL; K: 3.6 mEq/L; BUN/CR: 38/1.6 mg/dL; urinalysis = trace protein

74 What tests will your order? What diet will your order? How will you treat his hyperglycemia? Continuity of care….. 39-year-old Hispanic female

75 Examples of Pen Insulin Delivery Devices

76 Case 2: 72-year-old African-American Hospitalized with pneumonia 18-year history of poorly controlled diabetes; obese Failed sulfonylureas; on increasing insulin for 10 years Current dose: 107 U/three divided doses Blood glucose (2-h pp): 265 mg/dL HbA 1c : 13.4% Urine albumin excretion: 492 mg protein/g creatinine Serum creatinine: 1.4 mg/dL BP: 148/94 mm Hg

77 What tests will your order? What diet will your order? How will you treat his hyperglycemia? Continuity of care….. Case 2: 72-year-old African-American

78 Montefiore Length of Stay –LOS MOSESWEILERNORTH NON DIABETES NON DIABETES NON DIABETES

79 THANKS QUESTIONS ?

80 Fuel dysregulation during acute illness and starvation. A state of further insulin resistance Glycogenolysis FFA Ketone bodies Hyperglycemia Lactate AA GluconeogenesisGluconeogenesis Glucose Pyruvate Lactate

81 Fuel dysregulation during acute illness Endogenous glucose production in a 100 Kg man I Liter of D5W = 50 g glucose 12 oz can of Coke = 39 g glucose Endogenous Glucose Production High Normal Fasting Rate Euglycemia Stress Rate Hyperglycemia Rate mg/kg/min Total grams/day D5W equivalent Coke equivalent 6 Liters 7 cans 12 Liters 14 cans

82 Fuel dysregulation during acute illness Endogenous glucose production in a 100 Kg man I Liter of D5W = 50 g glucose 12 oz can of Coke = 39 g glucose Endogenous Glucose Production High Normal Fasting Rate Euglycemia Stress Rate Hyperglycemia Rate mg/kg/min Total grams/day D5W equivalent Coke equivalent 6 Liters 7 cans 12 Liters 14 cans


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