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GO! Diabetes Program

GO! Diabetes Program. Goals For Today. Review evidence based guidelines and equip you to deliver state of the art care to your diabetic patients Introduce the role of a diabetes educator Understand tools that support practice performance and improvement . (In)Adequacy of Care.

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GO! Diabetes Program

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  1. GO! DiabetesProgram

  2. Goals For Today • Review evidence based guidelines and equip you to deliver state of the art care to your diabetic patients • Introduce the role of a diabetes educator • Understand tools that support practice performance and improvement

  3. (In)Adequacy of Care • US NHANES Databases 1988 – 2002 • Glycemic control improved minimally • Blood pressure distribution unchanged • Improvements in lipids, ASA use, vaccinations • Why such slow improvement • Clinical inertia • Chronic illness • Lack of team approach • Reactive vs. proactive care

  4. Control of CV Risk Factors in Diabetic Hypertensive Patients in Academic Medical Centers • A1C <7% • 27% • LDL <100 • 36% • BP <130/85 mmHg • 27% • Daily Aspirin (ASA) Use • 46% • BP, Lipids and A1C • 3% • BP, Lipids, A1C + ASA • 2% McFarlane SI. DiabetesCare 2002;25:718

  5. Glycemic Control • Does glycemic control matter? • Diabetes Complications and Control Trial (DCCT) • 1441 type 1 diabetics randomized into two groups • Conventional treatment (HgbA1C =9%) • Intensive treatment (HgbA1C = 7%) • Epidemiology of Diabetes and Complications (EDIC) • Continuation of DCCT in which groups were intensively managed • Previous intensive group had reduced macrovascular events Diabetes Complications and Control Trial (DCCT) N Engl J Med; 1993; 329: 977-986.

  6. Effect of Tighter Glycemic Control on Progression of Retinopathy DCCT

  7. Effect of Intense Glycemic Control on Nephropathy from DCCT

  8. United Kingdom Prospective Diabetes Study • Study summary – 10 years • Type 2 diabetics – convention vs. intense control • Glycemic control – 7.0 vs. 7.9 • Hypertension control – 144/82 vs. 154/87 • Glycemic control • metformin, sulfonylureas, and insulin • Hypertension • captopril, atenolol

  9. UKPDS Blood Pressure Study:Tight vs. Less Tight Control • 1148 type 2 patients • BP lowered to avg. 144/82 (controls-154/87); 9 yr follow-up Endpoint Risk Reduction(%) P Value______ Any diabetes related endpoint 24 0.0046 Diabetes related deaths 32 0.019 Heart failure 56 0.0043 Stroke 44 0.013 Myocardial infarction 21 NS Microvascular disease 37 0.0092 UKPDS. BMJ. 317: 703-713. 1998.

  10. Glycemic Control Reduces Complications Diabetes Control and Complications Trial (DCCT) Research Group. N Engl J Med 1893:329:977-988 UK Prospective Diabetes Study (UKPDS) Group. Lancet 1993; 352:837-853.

  11. ABCs Of Diabetes Management Diabetes Care 2009;32:S6-12

  12. Recommendations for Adults with Diabetes Mellitus • Goals should be individualized • Certain populations (children, pregnant females and elderly) require special considerations • Set less intensive goals in patients with severe or frequent hypoglycemia • Most patients should target their HgbA1C to be less than 7%. The ACCORD trial has suggested more stringent targets aren’t beneficial and may be harmful

  13. Type 1 Vs Type 2:How To Tell Them Apart

  14. Diabetes: Early Detection and Lifestyle Monitoring

  15. Metabolic Syndrome • Requires 3 or more: • Triglycerides > 150 • HDL < 40 • Waist size >40” men, >35” women • BP > 130/85 • Fasting glucose > 100 • Caveat: Treatment counts for requirements… (Grundy, Circulation, 2005)

  16. “Pre-Diabetes” • Key Point: You have to predict the emergence of diabetes and head it off before it evolves in a patient • Cut-off values: • Fasting sugars between 100-126 • 2-hr GTT of 140-200 • Which would catch a problem earlier?

  17. Pre-Diabetes Definition If FBG >100 there is a 10-15% risk of DM within 7 years… or Fasting GTT

  18. Who and When to Screen? • Family history • Overweight (BMI 25) • Dyslipidemia • HTN • High risk ethnicity • Vascular disease • Prior glucose elevation • Hx or exam findings • Starting at age 45, a fasting blood glucose every three years • More frequent screening if:

  19. Benefits of Diagnosis • Seven trials showed a reduction of 32-62% in relative risk from behavioral or pharmacologic interventions • Numbers needed to treat were in the 4-14 range • Cost/benefit analysis clearly favors early diagnosis and intervention. [Currently ~50 million prediabetics] (CDC)

  20. Role of Obesity in Diabetes • Obesity (specifically abdominal) has one of the highest associations with insulin resistance and glucose intolerance • Numerous studies have tied weight loss to diabetes prevention

  21. Obesity cont. • A 5-10% weight loss yields a 58% reduction in the incidence of diabetes! • At the end of four years • Diet and exercise regimens average a 4kg loss after two years • Advice alone results in a 1kg gain (Franz, Journal Amer. Diabetes Assoc, 2007)

  22. Quantifying Obesity • Easiest is by waist circumferences. • 40” males, 35” females • Some variation by ethnicity (35” and 31” for Asians) • Measured across iliac crest in the back and the umbilicus in the front

  23. Healthcare Maintenance • Latest ADA guidelines (2009) • Lab surveillance • Diabetic education • Vaccinations/routine healthcare • Smoking cessation • Foot exams • Eye exams

  24. Reasons to Look at Feet • Up to 70% of diabetics eventually develop a neuropathy • Up to 25% develop foot ulcers • Diabetes doubles your risk of LE disease (vascular, neuro, skin) • More than half of the foot ulcers become infected at some point

  25. The real morbidity… • 10-20% of infected ulcers lead to amputation • Diabetes accounts for the vast majority of non-traumatic amputations • One amputation increases the likelihood of another • 5-year mortality rates approach 80%

  26. Foot Surveillance • Examine the feet at every visit • Annual comprehensive evaluation • Sensation • Pulses • Skin condition (ulcers, hair, nails) • Anatomic deformities • Shoe evaluation

  27. Sensory Exam • 10-gram monofilament • Patient should not watch • Five sites per foot • Apply filament perpendicular to skin • Allow slight buckle of filament in one motion • Each site should take 1-2 sec • Do not apply to ulcers or calluses

  28. Foot Exam Sites • Fewer sites than 10 years ago…

  29. Procedures/Billing • Foot exams • Protective footwear • Nail trimming • Debridement of corns and calluses

  30. Diabetic Foot Examination G0245 - Initial physician evaluation of a diabetic patient with diabetic sensory neuropathy resulting in a loss of protective sensation (LOPS) which must include: • 1. the diagnosis of LOPS; • 2. a patient history; • 3. a physical examination that consists of at least the following elements: • (a) visual inspection of the forefoot, hindfoot, and toe web spaces,

  31. Diabetic Foot Examination • 3.Exam cont: • (b) evaluation of a protective sensation, • (c) evaluation of foot structure and biomechanics, • (d) evaluation of vascular status and skin integrity, • (e) evaluation and recommendation of footwear, and • 4. patient education

  32. Diabetic Foot Examination G0246 -Follow-up evaluation of a diabetic patient with diabetic sensory neuropathy resulting in a loss of protective sensation (LOPS) to include at least the following: • 1. a patient history; • 2. a physical examination that includes: • (a) visual inspection of the forefoot, hindfoot, and toe web spaces, • (b) evaluation of protective sensation, • (c) evaluation of foot structure and biomechanics, • (d) evaluation of vascular status and skin integrity, • (e) evaluation and recommendation of footwear, and • 3. patient education.

  33. Diabetic Foot Examination G0247- Routine foot care of a diabetic patient with diabetic sensory neuropathy resulting in a loss of protective sensation (LOPS) to include if present, at least the following: • (1) local care of superficial wounds, • (2) debridement of corns and calluses, and • (3) trimming and debridement of nails. NOTE: Code G0247 must be billed on the same date of service with either G0245 or G0246 in order to be considered for payment.

  34. Medicare Protective Footwear One pair of depth shoes and three pairs of inserts One pair of custom-molded shoes (including inserts) and two additional pairs of inserts

  35. Eye Care • Diabetic retinopathy is the leading preventable cause of blindness • Prevalence of DR increases with duration of diabetes (100% Type 1, 60% Type 2 after 20 years) • Of all recommendations, eye screening is the least likely to get done

  36. Pathogenesis • Increased circulating glucose leads to weakness of capillary walls • Microaneurysms and leakage occurs causing eventual infarction of the nerve fiber layers (cotton wool spots) • The localized hypoxia then leads to vasoproliferation • Extension into the vitrea (+/- hemorrhage) leads to fibrosis and vision loss

  37. Diabetic Retinopathy Normal Retina (left) contrasted with Proliferative Diabetic Retinopathy (right) Refer patients for ophthalmologist evaluation

  38. Glycemic Control – Oral Agents

  39. PANCREAS GLUCAGON GLUCAGON GLUCAGON AMYLIN INSULIN INSULIN How The Body Handles Glucose (Fed State) LIVER BRAIN Glucose 90-140 mg/dL Blood Glucose 60-90 mg/dL FAT GI TRACT MUSCLE

  40. PANCREAS GLUCAGON GLUCAGON GLUCAGON AMYLIN AMYLIN INSULIN INSULIN INSULIN GI TRACT Pathophysiology of Type 2 Diabetes LIVER Metformin (Glitazone) Insulin Sulfonylureas Insulin Analogs Glinides Exenatide BRAIN INSULIN INSULIN A1C < 7% Premeal ~ 100mg/dL PPG < 200 mg/dL Hyperglycemia FAT Weight Loss Exercise Glitazones (Metformin) Pramlintide Dietary Composition Portion Control -Glucosidase Inhibitors MUSCLE

  41. General RulesHypoglycemic Therapy • Normalize fasting glucose levels first • Many patients will achieve glycemic targets • When to target postprandial glucose levels? • Preprandial values are at goal • A1C levels are not met • Measure 1-2 hours after beginning of the meal • Glucose are generally at their peak

  42. Glycemic Goals of Therapy Verbal Target ~100 <<200 As low as possible w/o unacceptable adverse effects Goal Premeal plasma glucose (mg/dL) 2-h postprandial plasma glucose A1C ADA 90-130 <180* <7%** ACE <110 <140 <6.5% * Evaluation and treatment of postprandial glucose may be useful in the setting of suspected postprandial hyperglycemia, with the use of agents targeting postprandial hyperglycemia and for suspected hypoglycemia ** More stringent glycemic goals (i.e. a normal A1C, <6%) may further reduce complications at the cost of increased risk of hypoglycemia Diabetes Care 2009;32:S6-12

  43. Biguanides: Metformin Mechanism of action • Reduces hepatic glucose production • Depends upon presence of insulin Safety and efficacy • Decreases A1C 1-2% • Adverse effects: diarrhea and nausea; main risk: lactic acidosis • Discontinuation rate 5% • Contraindications: renal, cardiac, hepatic insufficiency; IV contrast • No direct effect on kidney Dosing • Initial dose: 500 mg once a day; dosing: usually BID • Maximum effective dose: 2,000 mg per day • Titration frequency: week(s) to months • Alternate formulations: “XR” and combinations

  44. Cochrane ReviewJuly 2005 “Metformin may be the first therapeutic option in the diabetes mellitus type 2 with overweight or obesity, as it may prevent some vascular complications, and mortality. Metformin produces beneficial changes in glycaemia control, and moderated in weight, lipids, insulinaemia and diastolic blood pressure. Sulphonylureas, alpha-glucosidase inhibitors, thiazolidinediones, meglitinides, insulin, and diet fail to show more benefit for glycaemia control, body weight, or lipids, than metformin.”

  45. Metformin Outperformed Other Meds in Obese Patients (UKPDS) Lancet 1998 Sep 12;352(9131):854-65.

  46. Insulin Secretagogues: Sulfonylureas (SFU) and “Glinides” Mechanism of action • Stimulate basal and postprandial insulin secretion • Require functioning beta cells (no effect on beta cell dysfunction) • Work quickly Safety and efficacy • Decrease A1Capproximately1-2% • Lower fasting glucose 20% • Adverse events: weight gain, allergy (rare); main risk, hypoglycemia Dosing • Initial dose: 1/8 to 1/4 maximum dose; dosing: 1-2 times/day (SFU), 3 times/day (glinides) • Maximum effective dose: 1/2 maximum(full dose with nateglinide) • Titration frequency: day(s) to weeks

  47. Preferred Sulfonylureas • All available as generic agents Glipizide ER 5-20 mg once per day • Once daily, flat profile, low plasma levels resulting in a low risk of weight gain and hypoglycemia Glipizide 2.5 to 20 mg twice a day • Twice daily. Half-life 2-4 hours, peaks in 2-3 hours. By taking it once a day at low dose it stimulates insulin secretion for 6-12 hours Glimepiride 1-8 mg per day • Once daily. Half-life 9 hours, peak action for 4 hours. Special utility like with glipizide but with longer half-life Buse J. Personal Opinion Melander A. Diabetes 2004;53 Suppl 3:S151

  48. Thiazolidinediones (TZD’s or Glitazones): Pioglitazone and Rosiglitazone Mechanism of action • Enhance insulin sensitivity in muscle, adipose tissue • Inhibit hepatic gluconeogenesis • Reduced rate of beta cell dysfunction Safety and efficacy • Decrease A1C1-2% • Adverse events: edema, weight gain, anemia; rare serious risk: liver failure Dosing • Initial dose (monotherapy): 1/2 to 2/3 maximum; dosing,1-2 x/day • Maximum effective dose: maximum dose • Titration frequency: weeks to month(s)

  49. TZDs: Weight Gain and Edema • Derived from an increase in body fat and possibly increased fluid retention • Severity appears to be proportional to level of glycemic control achieved • Not inevitable and diet helps • Accentuated by combination with secretagogues or insulin • Usually mild to moderate and well tolerated Patients should be instructed to inform their doctors of rapid or excessive weight gain Lebovitz H. Diabetes Metab Rev 2002;18:S23 Fonseca V. Am J of Med 2003;115:42S

  50. Oral Hypoglycemics TZD Lipid Effects • Rosiglitazone(Avandia) • +LDL • +HDL • +Triglycerides • Pioglitazone (Actos) • +LDL • +HDL • -Triglycerides • Rosiglitazone – Black box warning for CHF and ischemic heart disease; warnings about increased fracture risk in women • Pioglitzaone – Black box warning for CHF and warning about increase fracture risk. No evidence to suggest increased ischemic heart disease.

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