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Outpatient Management of Diabetes Mellitus

Outpatient Management of Diabetes Mellitus. Gary L. Francis, MD, PhD Professor and Associate Chair for Research USUHS. The Face of IDDM In 1920 was not Encouraging. 1921 – Banting and Best Began to Isolate the “Internal Secretion of the Pancreas”. 1923 Banting and Best Awarded

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Outpatient Management of Diabetes Mellitus

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  1. Outpatient Management of Diabetes Mellitus Gary L. Francis, MD, PhD Professor and Associate Chair for Research USUHS

  2. The Face of IDDM In 1920 was not Encouraging

  3. 1921 – Banting and Best Began to Isolate the “Internal Secretion of the Pancreas”

  4. 1923 Banting and Best Awarded Nobel Prize for Discovery And Use of Insulin in the Treatment of IDDM

  5. b-cell destruction Insulin Deficiency Decreased Glucose Utilization Islets of Langerhans Glucagon Excess Muscle Increased Protein Catabolism Liver Increased Ketogenesis Gluconeogenesis Adipo- cytes IncreasedLipolysis Polyuria Volume Depletion Ketonuria Hyperglycemia Ketoacidosis

  6. Classification of Different Forms of Diabetes Mellitus

  7. Type 1 DM • Autoimmune destruction of the pancreatic islet cell • Hallmark = lymphocytic infiltration of islets • Progresses over years • Leads to insulin deficiency • Later may also be associated with glucagon deficiency

  8. Progression to Type 1 DM Autoimmune markers (ICA, IAA, GAD Autoimmune destruction Honeymoon 100% Islet loss “Diabetes threshold”

  9. Disease-Free Survival is Shortened with More Numerous Antibodies

  10. EPIDEMIOLOGY • Most common metabolic disease in childhood • Annual incidence 15 new cases per 100,000 in children < 18 yrs • Frequency increases with increasing age. • 1: 1400 at age 5 yrs • 1: 400 at age 16 yrs • Males and females equally affected • No correlation with socioeconomic status

  11. IDDM RISK OF CONCORDANCE • Offspring of IDDM parent: 2-5% overall risk • Offspring of diabetic mother: 2% risk • Offspring of diabetic father: 5% risk

  12. 1.9/100,000 school age children 1/1430@ 5 yr of age 1/360 @ 16 yr of age ID twins 50% concordance risk Dizygotic twins 20% concordance risk Two shared HLA haplotypes (DR3 + DR4) 12-20% risk One shared HLA haplotype (DR3 or DR4) 5-7% risk No shared HLA haplotypes 1-2% risk HLA DQ(beta) Asp57 virtual protection HLA DQ(beta) non-Asp57 100 X increased risk Type I - IDDM

  13. DIABETES MELLITUSCLINICAL MANIFESTATIONS • Classic Presentation: • Polyuria • Polydipsia • Polyphagia • Weight loss. • Insidious • Onset of lethargy and weakness. • Duration of symptoms usually < 1 month.

  14. DIABETES MELLITUS - TYPE IBody Systems Involved • GU Urinary frequency • GI Nausea, vomiting, constipation abdominal pain • Respiratory Acidosis, Kussmaul breathing • Cardiovascular Vascular collapse, dehydration tachycardia • CNS Cerebral edema • Musculoskeletal Glycogen depletion, K loss muscle weakness

  15. DIABETES MELLITUS - TYPE 1THERAPEUTIC OBJECTIVES • Achieve metabolic control • Maintain normal growth and sexual Maturation • Prevent acute and chronic complications • Prevent ketoacidosis

  16. Hypoglycemia: May be unaware School grades Early am symptoms Headache Nightmares Look for at camp Reduce dose 10% Hyperglycemia: Few symptoms Nocturia Dawn phenomenon Adolescent insulin resistance Increase dose 10% IDDM: OPTIMIZING GLYCEMIC CONTROL

  17. Treatment of T1 DM • Insulin • 1 u/kg/day – 1.3 u/kg/day in puberty • Standard 2 – 3 injections (NPH / Reg) / day • Intensive Therapy • long acting at bedtime + short acting at meals • 4 – 6 shots / day • Insulin Pump • Diet – adequate calories / limit fat / complex CHO • Exercise • GOAL – Optimal glycemic control

  18. DIABETES MELLITUS - TYPE 1MONITORING STRATEGIES • Self Blood Glucose Monitoring – 4-6 / day • Urine Testing – Ketones - PRN • Glycosylated Hemoglobin - HbA1 C - quarterly • Blood lipids - annually • Thyroid function – annually • Urine microalbumin – quarterly after 5 yr • Dilated fundoscopic – age 10 yr + 3-5 yr Hx

  19. TYPE I - DIABETES MELLITUSMONITORING STRATEGIES • Glycosylated hemoglobin - HbA1c • Average blood glucose 3-4 months • Affected by anemia, hemoglobinopathy • Age dependent target range • Probably HbA1c < 8% for most • school age children • adolescents • Beware of hypoglycemia (80% risk in DCCT)

  20. Definition of Various Levels of Glycemic Control

  21. DIABETES MELLITUS-TYPE ICOMPLICATIONS Acute Chronic • Hypoglycemia Neuropathy • Hyperglycemia Retinopathy • Ketosis Nephropathy • Ketoacidosis

  22. Hyperglycemia: Microangiopathic complications Hypoglycemia: Neuronal loss Poor school performance seizures

  23. Microangiopathic complications from DM can occur by the time of diagnosis but typically 10 – 15 yr

  24. Nephropathy • Diabetes #1 cause of end-stagerenal disease (ESRD) • 1st manifestation = microalbuminuria (low but abnormal, 30 mg/day or 20 µg/min urine albumin) • Without intervention • In 80% albumin excretion increases 10–20% / year to overt nephropathy (albumin = 300mg/24 h or 200 µg/min) over 10–15 yr • Once nephropathy occurs • GFR falls over severalyears (2–20 ml · min-1 · year-1). • ESRD develops • in 50% of type 1 DM with nephropathywithin 10 years • and in 75% by 20 yr. • Microalbuminuria is rare with short duration of type 1 DM • Screening in type 1 DM should begin after5 yr of disease

  25. Retinopathy • After 20 yr, nearly all patients with T1 DM and >60%with T2 DM have some retinopathy • In patients with T1 DM • 3.6% of young-onset patients (aged <30 yr at dx) were legally blind • 86% of blindness was due to diabetic retinopathy • 1.6% of old-onsetpatients (aged 30 yr at dx) were legally blind. • Vision-threatening retinopathy almost never occurs with T1 DM in the first 3–5 years of diabetesor before puberty. • Dilated funduscopic – age 10 yr + 3-5 yr Hx

  26. Typical Split-Dose NPH-REG BID Regimen

  27. BID NPH / REG AM NPH / REG DINNER REG HS NPH

  28. School Individual treatment plan Glucagon Administer for severe low BG Nutrition 55% CHO Complex CHOs 30% FAT < 10% Saturated 15% Protein OPC Management Tools

  29. SICK DAY MANAGEMENT • NEVER omit your insulin, even if you can't eat. • Test your blood sugar every 4 hours. If you need help, ask for it! • If you have T1 DM, test your urine for ketones every 4 hours. • Drink clear liquids (at least ½ cup / hr), and eat light foods • Rest. Do not exercise during an illness. • Call your doctor or diabetes educator if: • You have an obvious infection • Your illness lasts longer than 2 days • You have vomiting or diarrhea more than 8 hours • Your blood sugar is over 400 mg in two consecutive tests • All urine tests are positive for large amounts of sugar • You have moderate to large urine ketones with a blood glucose level over 200 mg for more than 8 hours • You feel very ill or experience pain • You have extreme fatigue, shortness of breath, or dizziness

  30. Total usual AM dose of insulin • NPHRegular • 22 units4 units • Total usual PM dose of insulin • NPHRegular • 10 units4 units • GRAND TOTAL: • 40 Units • For blood sugar over 150 mg/dl, add 10% of your total daily dose as Regular insulin every 4-6 hours. • Here is an example: Blood sugar is 210 mg and urine ketones are negative. • 10% of the total dose = 4 units. • Add 4 units regular insulin to usual dose every 4-6 hours, when blood sugar is over 150 mg.

  31. Total usual AM dose of insulin • NPHRegular • 14 units2 units • Total usual PM dose of insulin • Regular • 4 units • Total usual bedtime dose of insulin • NPH • 10 units • GRAND TOTAL: • 30 Units • For blood sugar over 150 mg/dl PLUS moderate to large ketones in the urine, add 20% of your total daily dose as Regular insulin every 4-6 hours. • Example: Blood sugar is 300 mg, urine ketones - positive. • 20% of the total dose = 6 units. • Add 6 units regular insulin to usual dose every 4-6 hours, when blood sugar is over 150 mg and urine ketones are positive.

  32. DCCT Study Findings Lowering blood glucose reduces risk: Eye disease 76% reduced risk Kidney disease 50% reduced risk Nerve disease 60% reduced risk The DCCT is a clinical study conducted from 1983 to 1993 by the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK). The study showed that keeping blood glucose levels as close to normal as possible slows the onset and progression of eye, kidney, and nerve diseases caused by diabetes. NEJM 342:381-389, 2000

  33. RS is a 12 yr old female with T1 DM for 6 yrs. A1C = 7.3, insulin dose is AM: 8 Reg / 18 NPH; Dinner: 7Reg; HS: 20 NPH. BGs

  34. Continuous Glucose Monitor - Overnight Unsuspected and Asymptomatic Hypoglycemia – Common up to 85% of episodes are nocturnal

  35. Continuous GlucoseMonitoring Device • Worn like the pump • Inserted with similar tubing and catheter • Records continuously for three days • Downloaded to your computer • Data not yet available for patient use • Chase et al Pediatrics 107: 222 (2001) • 5 patients, 10 – 17 yr old, DM 3.8 – 9.3 yr • 12.8 hypoglycemic episodes / patient / month • 85% asymptomatic nocturnal • 15% symptomatic nocturnal

  36. Continuous Glucose Monitoring in Children with IDDM • Majority have unsuspected, nocturnal hypoglycemia • Current insulin regimens are non-physiologic despite what we teach the residents • We need to develop new paradigms that incorporate designer insulins and pumps into management strategies for our patients

  37. Breakfast Lunch Dinner BG Insulin

  38. Currrent Insulins • Regular • Supposed to be “fast” • Onset is ½ - 1 hr • Peak 2 – 3 hr • Lasts 6 – 8 hrs • Hexamers in bottle delay absorption • Mis-match meal – insulin results in lows • NPH • Precipitated with protamine • Requires 45 inversions to mix and achieve same bioavailability • Peak 4 – 10 hr • Lasts 12-18 hr • Patient and site variability

  39. BID Split-Dose / MixedNPH / REG • Induces fasting hyperinsulinemia and frequent hypoglycemia • Requires between meal snacks • Predisposes to obesity • Can NOT mimic pancreatic ß-cell insulin secretion • Limited day-to-day variability

  40. “Designer” Insulins • Glargine • GLY21/ARG31/ARG32 • Ultra-long acting • No “peak effect” • Could be used to provide “basal” insulin secretion like pump therapy • Lispro • Invert lysine/proline • Currently in use • Ultra-short acting • Onset 15 minutes • Duration – < 4 hrs • Excellent for meal bolus, “correction” bolus, bedtime highs, toddlers

  41. Glargine / Lispro • Avoids fasting hyperinsulinemia and hypoglycemia • Can mimic pancreatic ß-cell insulin secretion • 36% had hypoglycemia vs 50% on NPH

  42. Insulin Pump Therapy • 6,500 in 1990 – 46,500 in 1998 • Uses Lispro Insulin ONLY • NO DEPOT • Reduces hypoglycemia • Shortens time to DKA • Can mimic pancreatic ß-cell insulin secretion • Improves life-style variability • Reduces need for snacks

  43. INSULIN PUMP THERAPY IN CHILDREN • First US Attempts: Yale University – 1970s • Increased short term mortality • Presumed: unrecognized hypoglycemia • Abandoned for several years • Problems: • Patients selected for poor compliance • Limited home BG technology • Regular insulin infused

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