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Gestational dm

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  • Memory-based self-monitoring of blood glucose (SMBG). <br />
  • See comment <br />
  • Carbohydrate CHO <br />
  • plasma value is approximately 12% higher than a whole blood value. A finger stick yields arterialized blood, which does not influence the fasting glucose concentration because in the fasting state there is little glucose uptake by muscle tissue. After eating, however, muscle glucose utilization becomes a factor. Measurement of glucose concentrations in blood samples obtained by a finger stick yields higher values than if a venous sample had been obtained. This is because the arterialized blood has not yet traversed muscles and hence glucose removal by this tissue has not occurred. <br />
  • Levels of HbA1c are related to the rate of congenital anomalies and spontaneous early abortions in pre-existing diabetes, but the use of this measure, which retrospectively reflects glycemic profile in the last 10 weeks, for treatment evaluation in GDM is questionable. In addition, the association between glycosylated hemoglobin and pregnancy outcome in GDM or prediction of macrosomia is poor <br />

Gestational dm Gestational dm Presentation Transcript

  • DM in Pregnancy Dr.Sushma Sharma Prof.,Dept. of ObGyn, MIMER Medical college, Talegaon
  • Increasing Prevalence of GDM  Abnormal maternal glucose regulation occurs in 3-10% of pregnancies  GDM accounts for 90% of cases of DM in pregnancy  Overt - 35% type 1 DM, and 65% type 2 DM
  •  Not limited to western countries  Increase is noted in India and China  3.8-20% in different part of India, more in urban – DIPSI  Compared with white women the RR of GDM in Indian women is 11.3
  • Increase is attributable to:  Sedentary lifestyles  Changes in diet  Immigration from high-risk populations  Childhood and adolescent obesity
  • CLASSIFICATION  GESTATIONAL DIABETES: 1 abnormal value on GTT or hgbA1c - 5.7 to 6.4%.  A1 - Euglycemia achieved with diet and exercise.  A2 - Require medication  PREEXISTING DIABETES   Type I. No endogenous insulin, ketosis prone Type II. Late onset,insulin resistant
  • Gestational Diabetes Mellitus Glucose intolerance with onset or first recognition during pregnancy.  Many are denovo pregnancy induced  Some are type 2 ( 35-40%) Whether insulin or only diet modification is needed Persists or not after Delivery.
  • DM Incipient type 2 Preexisting type 2 True GDM delivery conception 10 type 1 Follow up 20 30 40
  • Maternal-fetal Metabolism in Normal Pregnancy
  • Metabolism in Pregnancy   Goal is uninterrupted nutrient supply to fetus Metabolic goals of pregnancy are   In early pregnancy to develop anabolic stores to meet metabolic demands in late pregnancy In late pregnancy to provide substrate for fetal growth and energy needs.
  • Metabolic Changes
  • Meal sets in motion a complex series of hormonal actions, Increase in blood glucose Sec. secretion of pancreatic insulin, glucagon, somatomedins, & adrenal catecholamines. These adjustments ensure that an ample, but not excessive, supply of glucose is available to mother & fetus.
  • Placental steroid & peptide hormones (eg, E, P, chorionic somatomammotropin) ↑se linearly throughout 2nd & 3rd trimesters. ↑se insulin resistance ↑sed insulin secretion.  24 hr mean insulin levels are 50% higher in 3rd trimester compared with nonpregnant state
  • Glucose Metabolism in Pregnancy FASTING accelerated starvation FED hyperglycemia, (maternal hypoglycemia, hypoinsulinemia, hyperlipidemia, hyperketonemia) hyperinsulinemia, Fat Hyperins ulinemia Insulin resistance Glucose Aminoacids hyperlipidemia, reduced sensitivity to Fetus insulin
  • GDM  Precise mechanisms unknown  Hallmark is ↑sed insulin resistance  Inability to secrete sufficient insulin to compensate for the increased nutritional needs of gestation due to: ↑sed adiposity of pregnancy,   ↑sed anti-insulin hormones, such as HPL, HPGH, prolactin, cortisol (potent), P & E (weak)  enzymes with insulinase activity  Oxytocinase, histaminase, alkaline phosphatase
  • Compartment Mother Metabolic Effect Placental Hormones HPL HPGH Cortisol Oestrogen Progesterone Glucose Placenta Mode of transport Facilitated Diffusion By GLUT3 carriers Insulin resistance Impaired insulin action Aberrant Fuel Mixture Amino acids Active Cholesterol TG Lipase Ketones Diffusion FFA Glycerol Diffusion Diffusion Aberrant fuel mixture Foetus Hyperinsulinemia Fuel Mediated Teratogenesis Fuel Mediated Teratogenesis
  • Perinatal Mortality, Morbidity & Birth Injury
  • PATHOGENIC EVENTS Maternal Hyperglycemia Fetal Hyperglycemia Hypotrophy Pancreatic islet & B cells Fetal Hyperinsulinemia ↑Oxygen uptake ↑BMR ↑Fetal substrate uptake Lung Surfactant↓ Lipids / Amino acid ↑ Hypoxemia ? SB ↑Erythropoieti n Polycythemia Marosomia Respiratory Distress Syndorme
  • PEDERSEN THEORY Maternal Diabetes Glucose crosses placenta Carbohydrate surplus of fetus Increased secretion of insulin Free amino acid Stimulation of protein, lipid & glycogen synthesis Stimulatory effect on development of B cells Release Insulin like growth factor MACROSOMIA
  • MACROSOMIA
  • SHOULDER DYSTOCIA
  • Perinatal Mortality to Maternal Blood Glucose During Last Weeks of Pregnancy Mean glucose level Perinatal mortality >150 mg% 100–150 mg% <100 mg% 24% 15% 4%
  • Fetal Consequences First Trimester Second Trimester Third Trimester -Malformations -Growth Restriction -Fetal Wastage -Hypertrophic cardiomyopathy -Polyhydramnios -Erythraemia -Placental Insufficiency -Preeclampsia -Fetal loss -Low IQ -Hypoglycemia -Hypocalcemia -Hyperbilirubinemia -Respiratory distress syndrome -Macrosomia -Hypomangnesmia -Intrauterine Death
  • Malformations in infants of Diabetic Mothers, No Risk in GDM Anomaly Caudal regression Spina bifida Anencephaly Myelocele Hydrocephalus Dextrocardia Conus arteriosus defects VSD Renal agenesis/hypoplasia Onset 3 wks 6 wks 4 wks 4 wks 5 wks 4 wks 5 wks 6 wks 6 wks
  • RDS Hypoglycemia Hypocalcemia Hypomagnesemia Thrombocytopenia Neonate Polycythemia heel-stick blood Renal vein thrombosis Hyperbilirubinemia Child Adult Behavior - Intellect deficit Obesity Diabetes mellitus Diabetes mellitus
  • Maternal Complications  Worsening retinopathy – 10% new DR, 20% mild NPDR and 55% mod-severe NPDR progresses  Worsening proteinuria.  Hypertension and Cardiovascular disease  Neuropathy – No worsening  Infection
  •        Hypoglycemia Diabetic Ketoacidosis Preeclampsia: 18 % Preterm delivery: 42 % Cesarean delivery: 56 % 50% lifetime risk in developing Type II DM in GDM Recurrence risk of GDM is 30-50%
  • MANAGEMENT Interdisciplinary team effort  Patient education  Medical Nutrition therapy  Glycemic monitoring: SMBG and targets  Pharmacological therapy  Fetal monitoring: ultrasound  Planning on delivery
  • PRENATAL MANAGEMENT
  • Screening Tests for GDM Best method still controversial
  • Criteria of Diagnosis  ADA recommendations  WHO criteria  Urine Glucose  Spot Test  HbA1C, Serum fructosamine
  • Whom and When to Screen? Indian Scenario - The DIPSI Guidelines  75 gm GCT with single PG at 2 hrs   ≥ 140 mg/dL is GDM ≥ 120 mg/dL is DGGT  Universal screening  First trimester, if negative at 24 – 28 wks and then at 32 – 34 weeks
  • First visit Hb A1C   Collect 24 hr urine (protein, creatinine clearance, creatinine)  CVS status - ECG and echocardiogram  Eye exam  Bl urea nitrogen, serum creatinine,  TSH, and free thyroxine levels
  • 2nd Trimester Laboratory Testing     Spot urine protein-to-creatinine study in women with elevated value in first trimester MSAFP HbA1C Capillary blood sugar 4-7 times daily
  • Ultrasound      Dating scan at 8 – 12 wks Nuchal translucency 11-14 wks Targeted scan including fetal echo at 18-20 wks Growth scan at 26 wks and every 4 wks thereafter NST + AFI twice wkly starting at 32 wks; 28 -wks if poorly controlled or class D- T.
  • Fetal Evaluation Procedure Low risk High risk Fetal kick counts 28 28 USG for fetal growth 28 & 37 weeks Monthly NST In GDM 36weeks Semiweekly 28-34 weeks, Semiweekly FHS/BPP/Doppler 36 weeks, weekly 27 weeks-1-3/week Amniocentesis For lung maturity - 35 - 38 wks
  • Tx Targets - Controversial  ACOG       F venous plasma ≤ 95 mg/dl 1 hr PP ≤ 140 mg/dl 2 hr PP ≤ 120 mg/dl Pre-meal ≤ 100 mg/dl A1C ≤ 6% ADA   Premeal 80-110 2 hr PP not >155 These are venous plasma targets, not glucometer targets
  • Medical Nutrition Therapy   Goals  Achieve normoglycemia  Prevent ketosis  Provide adequate weight gain  Contribute to fetal well-being Nutritional plan  Calorie allotment  Calorie distribution  CH2O intake
  • Dietary Therapy  Avoid single large meals with large % of simple CHOs  6 feedings/day, with 3 major & 3 snacks
  • Artificial Sweeteners and Caffeine:  Avoid saccharin as it crosses the placenta.  Aspartame , acesulfame-K and sucralose allowed in limited amounts. Artificial sweeteners containing CHO counted as part of total CHO  Caffeine is allowed in moderation. <300 mg/day is allowed to limit potential harm to the fetus
  • Exercise     ACOG recommends – 30 min/day of moderate exercise . Begin with 5 – 10 min of warm up period involving stretching exercises. In sedentary women, exercise HR should not exceed 140 bpm. Exercising lowers maternal glucose conc in GDM .
  • Exercise Absolute Contraindication        Preterm Labor PROM Incompetent Cervix Persistent 2nd or 3rd trimester bleeding IUGR Placenta Previa beyond 26 week PIH
  • INSULIN MEDICATION ORAL DRUGS
  • When to Start Insulin Therapy in GDM Fastinga Postprandial Reference 105b None Metzger >95 2 h> 120 Langer et al. >100 1 h > 130 Ramus and Kitzmiller >90 1 h> 120 Jovanovic–Peterson a – Glucose concentrations (mg/dl) measured in finger–stick wholeblood samples unless designated otherwise. b – Venous plasma sample.
  • Why Insulin? Gold standard because of its safety and efficacy it can not cross placenta because large mol wt (6000Da)  NPH insulin is the only basal insulin that has been adequately studied in pregnancy
  •  Insulin regimen should:    Result in a smooth glucose profile throughout the day, with no hypoglycemic reactions bet meals or at night. HbA1C is (< 6.5%) at least 3 months before conception 1.0 mg/day of folic acid for at least 3 months before conception to minimize the risk of neural tube defects in the fetus.
  •  Regimen and timing of insulin injections different from non-pregnant state because as pregnancy progress:   Progressive lowering of maternal F & PPBG  . ↑sing fetal demand for glucose ↑ses the risk of symptomatic hypoglycemia
  • Monitoring BG  At least 4 times (SMBG)   Fasting and 3 one hr postprandial Pre vs. postprandial monitoring    Better glycemic control (HbA1c value 6.5 vs. 8.1 %) ↓ incidence of LGA infants (12 vs. 42 %) ↓rate of CS delivery for CPD (12 vs. 36 %)
  • Monitoring BG   Home monitoring  Maintain log book  Use a memory meter  Calibrate the glucometer frequently HbA1C  Ancillary test for feedback to the pt  Lower values when compared to non-pregnant state – lower BG – measured every 2-4 weeks  Target < 5.1%
  • OHA in Pregnancy  Cross placenta.  Fetal hperinsulinemia.  Prolonged fetal hypoglycemia
  • WHEN TO DELIVER    Class A1  Labor spontaneously or induce 40-42 weeks, Cochrane review-”little evidence to support elective induction at 38wks Class A2 -C ( good control with nl antepartum testing)  Induce at 39 – 40 weeks Class D - T or class A2 - C with poor control  Deliver at 37-38 weeks
  • Mode of Delivery  Vaginal route – preferred  Indications of C.S. -EFW->4.5 Kg [ACOG ] -H/O shoulder Dystocia, previous stillbirth -other obstetric indications  EFW - 4 - 4.5Kg - Role of CS controversial
  • Scheduled C-Section       Usual medication (insulin or glyburide) at bedtime Eat nothing after midnight Do not take morning medication Check blood glucose Perform CS within 2 hrs If unable to perform surgery immediately or pt in poor control, start insulin drip, Perform CS after 4-6 hrs euglycemia.
  • Vaginal delivery : Management • • • • • • Strict asepsis Restrict number of PV examinations Electronic fetal heart rate monitoring Partogram Obstetrician to be well versed with the Mx of SHOULDER DYSTOCIA Call Paediatrician
  • Insulin During Labor      Tight control of maternal glycaemia is essential throughout labor. In labor no extra insulin is required because labor is a form of exercise Monitor BS- 1 hourly Target BS-70-100 mg/dl Monitor urine sugar & ketone 2-4 hourly
  • Postpartum Care  Prevent infection  Insulin infusion is discontinued  GDM on diet-no monitoring  GDM on insulin /Pre-gestational DM-Monitor BS
  • Postpartum Care Continued  Type 1 DM-restart insulin [0.5-0.6U/Kg] on day 2-5 post delivery.  Breast feeding: helps in weight loss.  Insulin, tolbutamide compatible.  Chlropropamide secreted small amounts  Glyburide and glipizide not secreted  Metformin secreted - no adverse effects
  •  Check BG before discharge  Lifestyle modification: exercise, weight reduction & healthy diet  75 OGTT at 6-12 wks postpartum: classify patients into normal/impaired glucose tolerance and diabetes
  • Contraception  Low dose EP can be used  Progestin only pills shown to ↑se risk of T2DM in GDM  IUCD – ↑sed PID
  • Women and Diabetes  Diabetes no longer means › › › › › Abstinence Amenorrhea Inability to conceive Inability to deliver healthy children Death during pregnancy
  • Teachable Moments  Women with a history of GDM present an ideal group for diabetes prevention, not only in preventing diabetes in themselves, but for their family, for whom they are often the gatekeepers for nutrition and exercise.  Pregnancy is a teachable moment when women are usually very focused on their own health and the health of their baby.