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Diabetes in Pregnancy Martin L Gimovsky MD Division of Maternal Fetal Medicine

Diabetes in Pregnancy Martin L Gimovsky MD Division of Maternal Fetal Medicine Newark Beth Israel Medical Center Newark, New Jersey. Learning Points. Importance - 17 million diabetics in US + 6 million undiagnosed, 6 – 8% of population

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Diabetes in Pregnancy Martin L Gimovsky MD Division of Maternal Fetal Medicine

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  1. Diabetes in Pregnancy Martin L Gimovsky MD Division of Maternal Fetal Medicine Newark Beth Israel Medical Center Newark, New Jersey

  2. Learning Points • Importance - 17 million diabetics in US + 6 million undiagnosed, 6 – 8% of population • Pathophysiology - A diabetic has metabolic changes that adversely affect blood vessels • Pregnancy - Accelerates/predisposes these metabolic derangements. • Treatment - Seeks to minimize maternal and fetal/neonatal M&M by correcting/compensating for fluctuations in blood glucose.

  3. Overview: Diabetes • Hyperglycemic state fasting and/or postprandial • Due to relative/absolute deficiency of insulin • Results in significant changes in intermediary metabolism with striking clinical effects

  4. Beta cells Storage granules Nucleus Endoplasmic reticulum

  5. The Islet of a Type 1 Diabetic Beta Cells (Injured and then) Destroyed

  6. Islet cells and Isle of Langerhans Beta cells in blue Alpha cells in red Delta cells unmarked

  7. Type 2 and GDM • Tissue becomes insulin resistant • Hyperglycemia • Inhibits glucose uptake • Results in inadequate insulin response • Disrupts pulsatile insulin release • Enhances lipolysis in visceral fat • Increases FFA, increases insulin resistance • Impaired glucose tolerance  elevated FBS and increases PP hyperglycemia

  8. Diabetes alters intermediary metabolism

  9. Insulin Effects Glucose, aa  glycogen Glycogen  glucose X • Protein synthesis • Protein catabolism Glucose, amino acid uptake  Inhibits glucose, amino acid uptake X X • Fatty acid synthesis • Fatty acid release X

  10. Comparison of Diabetic Types

  11. Diabetes in Pregnancy • Common medical complication • 2-5% (2.6%) of live births • 90% are gestational diabetics, White class A1, A2 (GDM & NIDDM) • 10% are overt diabetics, White class B-H (IDDM)

  12. Diabetes and Pregnancy • Pregnancy is a “diabetogenic state.” • Placenta has passive control of glucose to fetus, but is impermeable to insulin. • Maternal intermediary metabolism is under control of hormonal influences that insure fetal needs for glucose are met.

  13. Pregnancy as a Diabetogenic State Increasing glucose (&insulin) demand both maternal and fetal • Increasing insulin resistance  hormone driven • Maternal hyperglycemia fetal excess of nutrients  fetal hyperglycemia & insulinemia, neonatal hypoglycemia • Teratogenesis • Catabolism consumes energy & oxygen and  episodic fetal hypoxemia, results in fetal hypertension, cardiac remodeling, polycythemia, increased blood viscosity, heart failure, stillbirth

  14. Insulin Resistance in Pregnancy • More insulin demand: Increased basal level and response to blood glucose, increased overall demand for glucose • Insulin is less efficient (resistance) • HCS, Prolactin, E&P •  Hyperglycemia •  Facilitate a continuous supply of glucose for placental transfer

  15. Effect of Pregnancy Hormones on Maternal Carbohydrate Metabolism HCS = decreases glucose tolerance Prolactin = insulin resistance Glucocorticoids = glycogenolysis, gluconeogenesis

  16. IDDM, NIDDM (I,II) Poly-dipsia, uria, phagia, glycosuria Infections Vascular damage FBS > 140 mg/dL Random BS > 200 GESTATIONAL(III) Hyperglycemia first seen in pregnancy Screening: 50 gram 1 hr > 140 Diagnosis: 100 gram GTT 2 abnormal values, or a single value > 200 Overview: Recognition Clinical Preclinical

  17. Classification of Overt Diabetes (IDDM) in PregnancyHare and White, Diabetes Care 3:394 1980

  18. Fetal Anomalies Stillbirth Macrosomia Neonatal Resp distress Hypoglycemia Hyperbilirubinemia Hypocalcemia Hypertrophic Cardiomyopathy Maternal Infections, DKA, HyperOsm Vascular damage results in Retinopathy Benign Neovascularization Renal failure Microalbuminuria <300 Nephropathy >300 Myocardial infarction Neuropathy Peripheral Autonomic Effects of Diabetes in Pregnancy

  19. Monitoring Blood Sugar • Blood glucose levels both fasting and postprandial are the key indicators • AGP ambulatory blood glucose profile • SMBG self monitored blood glucose • HbA1c glycosylated hemoglobin 4-6 week intervals

  20. Normal glucose tolerance in pregnancy Mean BS 85, range 70 - 106 120 AGP 70 Relatively flat, narrow limits

  21. IDDM in Third Trimester3 Injection RegimenMean 137, Range 100 - 165 Wider limits, increase in mean value

  22. Overview: Management of Diabetes • Dietary modifications • Caloric content, distribution of food types, frequency of meals, snacks in context of “Glycemic Index, Load” • Interventional Exercise • Insulin • Oral hypoglycemics

  23. Dietary Modification

  24. Considerations in Diabetic Diet • Kcal/kg/d (30 kcal/kg/d) • CHO=50%, Protein 25%, Fat 25% (ADA 2002) • Decrease kcal for BMI > 30, increase for BMI<25 (ADA 2002) • Low glycemic foods (slow absorption) • Avoid nocturnal hypoglycemia • Avoid ketonemia

  25. Glycemic Index • Pro: Measures how rapidly BG is elevated in response to eating a specific food. • Con: Values not necessarily reflective of how foods are really consumed • Total calories may be more important

  26. RCT: diet + exercise > diet alone Bung et al, 1993

  27. Glycemic Response to Exercise: Nonpregnant and Pregnant Exercise lowers BG further and faster in pregnancy Nonpregnant Pregnant

  28. Insulin preparations vary by time to peak action and total duration of action • Lispro- 1h/2h • Regular- 2h/4h • NPH- 4h/8h • Ultralente- 8h/20h Insulin pen

  29. Oral Hypoglycemics • First generation: Sulfonylureas (diabinase)-freely crossed placenta  High level in neonate Severe & prolonged hypoglycemia Sporadic reports of anomalies

  30. Fast Acting Secretagogues, and Sensitizers Short duration of action Oral Hypoglycemics • Second Generation (Pregnancy category B) • Glyburide, Glipizide, Glimepride • Biguanides Metformin

  31. Oral Hypoglycemics • Glyburide • Rx of adult onset diabetes • Transplacental dose small • No known fetotoxicity, teratogenicity • Effect is mildly hypoglycemic to gravida and fetus • Dosed by BMI >< 25 2.5mgs, 5 mgs • Similar effect to a 70:30 mix (NPH:Reg)

  32. Control: Insulin vs Glyburide Langer et al: Comparison of glyburide and insulin in women with GDM. NEJM 2000;343:1134-8.

  33. Glyburide vs InsulinLanger et al 2000

  34. Glyburide After ADA Diet Failure Carolinas Medical Center, 2004 • 4/5 gravidas were controlled, 1/5 insulin • NeonatalOutcome • 23% had hypoglycemic episode • 11% had polycythemia • 38% were LGA (> 90th centile) • 13% were macrosomic (> 4000 gm) • 7% needed (any) respiratory support

  35. Glycemic Control: Fetal OutcomesSummary, multiple studies

  36. Malformations Postprandial BS < 140 mgs/Dl

  37. Perinatal Mortality Mean BS < 115 mg/Dl

  38. Neonatal Morbidity in Diabetic Pregnancy Neonatal BG > 1 SD below the mean Neonatal hypoglycemia =

  39. Maternal Morbidity

  40. Guidelines for Diabetic Pregnancy

  41. Preconception Counseling Maternal medical risks Fetal and neonatal risks Obstetric complications Family/social supports Economic

  42. Diabetes and Obesity

  43. 1st Trimester Dx: up to 20% GDM Fetal viabilty Accurate dates 2nd Trimester Mult marker screen Level 2 scan, Fetal cardiac echo 24 weeks fetal growth 28 fetal kick counts Fetal surveillance first 28 weeks

  44. Diabetic Ketoacidosis • Type 1 diabetic, 2nd trimester • Infections • Limited prenatal care • Unrecognized new onset of diabetes • Inadequate insulin  excessive hepatic glucose production

  45. Diabetic Ketoacidosis

  46. Treatment of DKA • Recognition: hyperventilation, dehydration, hypotension, fruity odor to breathe, elevated BS, + serum ketones 1:4 • Infection, poor compliance, unrecognized onset of DM • Treatment: Vigorous fluid resuscitation (NS) until base deficit is < -4; anion gap is < 12 • Small bolus (10u) then continuous infusion of low dose insulin 5u/hr; Potassium 20 meq/hr, bicarbonate replacement < 1 amp, pH < 7.2

  47. 3rd Trimester • Fetal growth by 32 week scan, • Fetus may be IUGR or LGA, EFW • Fetal Testing: 28-32 wks BPP, NST 2X • Comorbidity with PIH, Chronic HBP • Timing of delivery: term or close • Confirmation of fetal lung maturity

  48. Fetal Demise in-Utero • Increased glucose is catabolized consumes energy & oxygen. • The greater the fluctuation in BS, the more fetal hyperglycemia & hyperinsulinemia • Decrease testing intervals in A2 or >, test twice weekly after 30-32 weeks • Can reduce the risk

  49. Comorbidity with HypertensionBlood Pressure during Gestation

  50. Fetal Growth Abnormalities in Diabetic Pregnancy by White ClassCalifornia Diabetes Project, 1991

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