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Dr. Kanakamani Madhivanan, M.D., D.M. (Endocrinology), Assistant Professor Department of Endocrinology, Diabetes, Metabolism Christian Medical College,

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Presentation on theme: "Dr. Kanakamani Madhivanan, M.D., D.M. (Endocrinology), Assistant Professor Department of Endocrinology, Diabetes, Metabolism Christian Medical College,"— Presentation transcript:

1 Dr. Kanakamani Madhivanan, M.D., D.M. (Endocrinology), Assistant Professor Department of Endocrinology, Diabetes, Metabolism Christian Medical College, Vellore

2 Plan of presentation  Introduction  Physiology of fuel metabolism in normal pregnancy  Pathophysiology of GDM  Epidemiology of GDM  Screening and diagnosis  Maternal and fetal risks  Management of GDM  Obstetric management


4 Introduction  Global increase in prevalence of DM  Individual importance - Hyperglycemia in pregnancy has adverse effects on both mother and fetus  Public health importance – rising epidemic of DM in part attributed to the diabetic pregnancies  Prevention of type 2 DM should start intrauterine and continue throughout life

5 Introduction  Gestational diabetes (GDM) is defined as any degree of impaired glucose tolerance of with onset or first recognition during pregnancy. Many are denovo pregnancy induced Some are type 2 ( 35-40%) 10% have antibodies

6 Introduction  Difficult to distinguish pregestational Type 2 DM and denovo GDM Fasting hyperglycemia blood glucose greater than 180 mg/dL on OGT acanthosis nicgrans HbA1C > 5.3% a systolic BP > 110 mm Hg BMI > 30 kg/m2 Fetal anomalies  Clues for Type 1 Lean DKA during pregnancy Severe hyperglycemia with large doses of insulin


8 Fuel metabolism in pregnancy  Goal is uninterrupted nutrient supply to fetus  The metabolic goals of pregnancy are 1) in early pregnancy to develop anabolic stores to meet metabolic demands in late pregnancy 2) in late pregnancy to provide fuels for fetal growth and energy needs.

9 Glucose metabolism in pregnancy  Early pregnancy E2/PRL stimulates b cells –Insulin sensitivity same and peripheral glucose utilisation – 10% fall in BG levels  Late pregnancy ○ Fetoplacental unit extracts glucose and aminoacids, fat is used mainly for fuel metabolism ○ Insulin sensitivity decreases progressively upto 50-80% during the third trimester ○ variety of hormones secreted by the placenta, especially hPL and placental growth hormone variant, cortisol, PRL,E2 and Prog

10 Glucose metabolism in pregnancy Fetus Fat GlucoseAminoacids Insulin resistance Hyperinsuli nemia FASTING accelerated starvation and esxaggerated ketosis (maternal hypoglycemia, hypoinsulinemia, hyperlipidemia, and hyperketonemia) FED hyperglycemia, hyperinsulinemia, hyperlipidemia, and reduced tissue sensitivity to insulin

11  24-hour insulin requirement before conception is approximately 0.8 units / kg.  In the first trimester, the insulin requirement rises to 0.7units / kg of the pregnant weight – more unstable glycemia with a tendency to low fasting plasma glucose and high postprandial excursions and the occurrence of nocturnal hypoglycemia  By the second trimester, the insulin requirement is 0.8 units per kilogram. From 24 th month onwards steady increase in insulin requirement and glycemia stabilises  By third trimester the insulin requirement is unit /kg pregnant weight per day  Last month – may be a decrease in insulin and hypoglycemias esp. nocturnal


13 Magnitude of problem: Global  Prevalence of GDM varies worldwide and among different racial and ethnic groups within a country ○ America – white women (3.9%) and Asian (8.7%) ○ Europe – 0.6% to 3.6% ○ Australia – 3.6% to 4.7% (Indian women – 17.7%) ○ China – 2.3%; Japan – 2.9%  Variability is partly because of the different criteria and screening regimens

14 Magnitude of the problem - India  Chennai, hospital based, universal screening – 18.9% had FPG ≥ 126 and PPPG ≥ 140. Trivandrum – 15% Bangalore – 12% Erode – 18.8%  Chennai, community based, universal screning, 17.8% in urban, 13.8% in semi urban and 9.9% in rural areas.  Chennai : 0.56%  Mysore Parthenon Study: 6%  Maharashtra, hospital based, selective screening – 7.7% had GDM; 13.9% had IGGT.

15 Risk factors  A family history of diabetes, especially in first degree relatives  Prepregnancy weight ≥110% of ideal body weight or body mass index over 30 kg/m2 or significant weight gain in early adulthood, between pregnancies, or in early pregnancy  Age greater than 25 years  Previous delivery of a baby greater than 4.1 kg  Personal history of abnormal glucose tolerance  Member of an ethnic group with higher than the background rate of type 2 diabetes (in most populations, the background rate is approximately 2 percent)  Previous unexplained perinatal loss or birth of a malformed child  Maternal birthweight greater than 4.1 kg or less than 6 pounds 2.7 kg  Glycosuria at the first prenatal visit  Polycystic ovary syndrome  Current use of glucocorticoids  Essential hypertension or pregnancy-related hypertension


17 Maternal complications  Worsening retinopathy – 10% new DR, 20% mild NPDR and 55% mod-severe NPDR progresses  Worsening proteinuria. GFR decline depends on preconception creatinine and proteinuria  Hypertension and Cardiovascular disease  Neuropathy – No worsening (gastroparesis, nausea, orthostatic dizziness can be worsened)  Infection

18 Maternofetal complications  Macrosomia: 63 percent  Cesarean delivery: 56 percent  Preterm delivery: 42 percent  Preeclampsia: 18 percent  Respiratory distress syndrome: 17 percent  Congenital malformations: 5 percent  Perinatal mortality: 3 percent  Spontaneous abortion, third trimester fetal deaths, Polyhydramnios, preterm birth, ?adverse neurodevelopmental outcome  Risk for type 2 DM

19 Neonatal complications  Morbidity associated with preterm birth  Macrosomia ± birth injury (shouldeer dystocia, brachial plexus injury)  Polycythemia and hyperviscosity  Hyperbilirubinemia  Cardiomyopathy  Hypoglycemia and other metabolic abnormalities (hypocalcemia, hypomagnesemia)  Respiratory problems  Congenital anomalies

20 Congenital anomalies  2/3 rd CVS or CNS,– times common  Cardiac( including great vessel anomalies) : most common  Central nervous system (spina bifida/anencephaly) : 7.2%  Skeletal: cleft lip/palate, caudal regression syndrome  Genitourinary tract: ureteric duplication  Gastrointestinal : anorectal atresia

21  Skeletal and central nervous system Caudal regression syndrome Neural tube defects excluding anencephaly Anencephaly with or without herniation of neural elements Microcephaly  Cardiac Transposition of the great vessels with or without ventricular Ventricular septal defects Coarctation of the aorta with or without ventricular septal defects or patent ductus arteriosus Atrial septal defects Cardiomegaly  Renal anomalies Hydronephrosis Renal agenesis Ureteral duplication  Gastrointestinal Duodenal atresia Anorectal atresia Small left colon syndrome

22 Caudal regression syndrome



25 Whom to screen ?  No consensus recommended screening ranges from selective screening of average- and high-risk individuals to universal diagnostic testing of the entire population dependent on the risk of diabetes in the population. Risk stratification based on certain variables Low risk : no screening Average risk: at weeks High risk : as soon as possible


27 To satisfy all these criteria  Age <25 years  Not a member of an ethnic group with high prevalence of GDM  Not a member of an ethnic group with high prevalence of GDM ( not Hispanic, Native American/Alaskan, Asian/Pacific Islander, African American)  Normal prepregnancy body weight (not 20% or more over desired body weight or BMI 27 kg/m2 or more)  No family history of diabetes in first-degree relatives.  No history of abnormal glucose tolerance  No history of poor obstetric outcome Low risk for GDM

28 High risk  Marked obesity  Prior GDM (30-50% risk for recurrence)  Glycosuria  Strong family history

29 When and how to screen?  weeks  High risk First prenatal visit  50 g glucose loading test  High risk women – 3 hr GTT with 100 g glucose


31 50 g GTT  A 50-g oral glucose load is given without regard to the time elapsed since the last meal and plasma or serum glucose is measured one hour later  A value ≥130 mg/dL is considered abnormal ; we use ≥130 mg/dL as the threshold for our patients.  Capillary blood should not be used for screening unless the precision of the glucose meter is known, it has been correlated with simultaneously drawn venous plasma samples, and has met federal standards for laboratory testing.

32 100 g GTT  Oral glucose tolerance test ( OGTT) with 100 gm glucose  Overnight fast of at least 8 hours  At least 3 days of unrestricted diet and unlimited physical activity  > 2 values must be abnormal Fasting > 95 mg/dl 1-h > 180 mg/dl 2-h > 155 mg/dl 3-h > 140 mg/dl

33 75 g GTT Fasting > 95 mg/dl 1-h > 180 mg/dl 2-h > 155 mg/dl Fasting > 95 mg/dl OR 2-h > 140 mg/dl ADAWHO

34 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 weeks and then at 32 – 34 weeks


36 MANAGEMENT ISSUES  Patient education  Medical Nutrition therapy  Pharmacological therapy  Glycemic monitoring: SMBG and targets  Fetal monitoring: ultrasound  Planning on delivery

37 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

38 Calorie allotment  30 kcal per kg current weight per day in pregnant women who are BMI 22 to 25.  24 kcal per kg current weight per day in overweight pregnant women (BMI 26 to 29).  12 to 15 kcal per kg current weight per day for morbidly obese pregnant women (BMI >30).  40 kcal per kg current weight per day in pregnant women who are less than BMI 22.

39 Carb intake  Postprandial blood glucose concentrations can be blunted if the diet is carbohydrate restricted. Complex carbohydrates, such as those in starches and vegetables, are more nutrient dense and raise postprandial blood glucose concentrations less than simple sugars.  Carbohydrate intake is restricted to % of calories, with the remainder divided between protein (about 20%) and fat (about 40%).  With this calorie distribution, 75 to 80 percent of women with GDM will achieve normoglycemia.

40 Calorie distribution  Variable opinion  Most programs suggest three meals and three snacks; however, in overweight and obese women the snacks are often eliminated Breakfast — The breakfast meal should be small (approximately 10%of total calories) to help maintain postprandial euglycemia. Carbohydrate intake at breakfast is also limited since insulin resistance is greatest in the morning. Lunch — 30% of total calories Dinner — 30% of total calories Snacks — Leftover calories (approximately 30% of total calories) are distributed, as needed, as snacks.

41 Monitoring BG  Atleast 4 times Fasting and 3 one hr postprandial  Pre vs postprandial monitoring Better glycemic control (HbA1c value 6.5 versus 8.1 percent) A lower incidence of large-for-gestational age infants (12 versus 42 percent) A lower rate of cesarean delivery for cephalopelvic disproportion (12 versus 36 percent)

42 Monitoring BG  Home monitoring Maintain log book Use a memory meter Calibrate the glucometer frequently  HbA1C Ancillary test for feedback to the patient Lower values when compared to nonpregnant state – lower BG and increase in red cell mass and slight decrease in life span – measured every 2-4 weeks Target < 5.1%

43  Studies report no to moderate correlations between HbA1 and different components of the glucose profile when an HbA1 result of 4% to 5% includes a capillary blood glucose range of 50 to 160 mg/dL.  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  Glycosylated protein and fructosamine widely variable and not yet established

44 Glycemic targets (ACOG)  ACOG Fasting venous plasma ≤ 95 mg/dl 1 hour postprandial ≤ 140 mg/dl 2 hour postprandial ≤ 120 mg/dl Pre-meal ≤ 100 mg/dl A1C ≤ 6%  ADA premeal hr postmeal not more than 155 These are venous plasma targets, not glucometer targets

45 PHARMACOLOGICAL INTERVENTION  If the FPG at diagnosis is ≥ 120, can consider immediate therapy.  Otherwise, MNT for 2 weeks If majority FPG (4/7) > 95 or PP > 120 then to start on insulin.

46 Insulin  ≈ 15% need insulin  Total dose varies. ≈ 0.7 to 2 units per kilogram (present pregnant weight)  FBG high – Night NPH ≈ 0.2 units/kg  PPBG high – bolus ≈ 1.5 units/10 gm CH2O for breakfast and ≈ 1 unit /10 gm CH2O for lunch and dinner  If both pre and postprandial BG high or if the woman's postprandial glucose levels can only be blunted if starvation ketosis occurs - four injection/day regimen. Total 0.7 unit/kg up to week unit/kg for weeks 18 to unit/kg for weeks 26 to unit/kg for weeks 36 to term. In a morbidly obese woman, the initial doses of insulin may need to be increased to 1.5 to 2. units/kg to overcome the combined insulin resistance of pregnancy and obesity.

47 OHA in pregnancy  Systematic review by John Hopkins University maternal glucose levels did not differ substantially between gravidae treated with insulin versus those treated with oral glucose-lowering agents there was no consistent evidence of an increase in any adverse maternal or neonatal outcome with use of glyburide, acarbose, or metformin compared with use of insulin  Inconsistent data. ADA, ACOG, USFDA do not endorse.

48 OHA in pregnancy  Tolbutamide and chlorpropamide Cross placenta. Fetal hperinsulinemia. Prolonged fetal hypoglycemia  Glibenclamide Minimal transplacental transport Observational studies – no excess anomalies or hypoglycemia Only RCT – 404 women. Glib vs insulin. No difference

49  second-generation sulfonylureas especially glyburide, do not significantly cross the diabetic or nondiabetic placenta. Fetal concentrations reached no more than 1% to 2% of maternal concentrations.  tolbutamide diffused across the placenta most freely, followed by chlorpropamide, then glipizide, with glyburide crossing the least.  Metformin crosses placenta – not teratogenic in rat models

50 OHA in pregnancy  Metformin Category B No adverse outcome after first trimester Second, third trimester safe and effective Vs. insulin – no serious adverse effects No studies vs. glibenclamide  Acarbose Two prelim studies  Thiazolidinediones and GLP-1 Not studied


52 Fetal monitoring  Baseline ultrasound : fetal size  At weeks: major malformations fetal echocardiogram  26 weeks onwards: growth and liquor volume  III trimester: frequent USG for accelerated growth ( abdominal: head circumference)

53 Timing of delivery  Small risk of late IUD even with good control  Delivery at 38 weeks – to avoid late still birth and fetal growth leading to shoulder dystocia  Vaginal delivery: preferred  Caesarian section only for routine obstetric indication just GDM is not an indication !  Unfavorable condition of the cervix is a problem  4500 grams, cesarean delivery may reduce the likelihood of brachial plexus injury in the infant (ACOG). Assessing fetal weight accurately is a problem

54 Management of labor and delivery  Maternal hyperglycemia in labor: fetal hyperinsulinemia, worsen fetal acidosis and neonatal hypoglycemia  Insulin requirements come down  Maintain sugars: mg/dl  Routine GDM diet  Maintain basal glucose requirements  Monitor sugars 1-4 hrly intervals during labour  Give insulin as infusion only if sugars more than 120 mg/dl

55 Glycemic management during labour  Later stages of labour: start dextrose to maintain basal nutritional requirements: ml/hr of 5% dextrose  Elective LSCS: check FBS, if in target no insulin, start dextrose drip  Continue hourly SMBG  Post delivery keep patients on dextrose-normal saline till fed  No insulin unless sugars more than normal nonpregnant levels

56 Post partum follow up  Check BG before discharge  Breast feeding: helps in weight loss. Insulin, tolbutamide compatible. Chlropropamide secreted small amounts – watch for hypoglycemia in infant. Glyburide and glipizide not secreted Metformin secreted - no adverse effects  Lifestyle modification: exercise, weight reduction  OGTT at 6-12 weeks postpartum: classify patients into normal/impaired glucose tolerance and diabetes  Contraception – low dose EP can be used. Progestin only pills shown to increase risk of T2DM in GDM  Preconception counseling for next pregnancy

57 Immediate management of neonate  Hypoglycemia : 50 % of macrosomic infants 5–15 % optimally controlled GDM  Starts when the cord is clamped  Exaggerated insulin release secondary to pancreatic ß-cell hyperplasia  Increased risk : blood glucose during labor and delivery exceeds 90 mg/dl Anticipate and treat hypoglycemia in the infant

58 Management of neonate  Hypoglycemia <40 mg/dl  Encourage early breast feeding  If symptomatic give a bolus of 2- 4 ml/kg, IV 10% dextrose  Check after 30 minutes, start feeds  IV dextrose : 6-8 mg/kg/min infusion  Check for calcium, if seizure/irritability/RDS  Examine infant for other congenital abnormalities


60 Future risks - Mother  Atleast 6 weeks post delivery, 75 g OGTT for all GDM  ≥ 90% normoglycemic  Recurrence of GDM – 30-60% Older Multipara Weight gain interpregnancy Higher infant BW in index pregnancy  IGT and T2DM 20% IGT postpartum 6m, 15m and 9 y

61 Who will progress to DM?  WC and BMI – stronset predictors  Autoantibodies  DM at earlier gestational age  Gestational requirement of insulin  Higher FBG  Higher BG on OGTT  Neonatal hypoglycemia  Recurrent GDM

62 Preconception counselling  Diabetic mother : glycemic control with insulin/SMBG Target: HbA1c < 7%  Folic acid supplementation: 5 mg/day  Ensure no transmissible diseases: HBsAg, HIV, rubella  Try and achieve normal body weight: diet/exercise  Stop drugs : oral hypoglycemic drugs, ACE inhibitors, beta blockers

63 Risk of developing DM in offspring  Type 1 - Father - 1 in 17 risk Mother - 1 in 25 risk if, at the time of pregnancy, the mother is < 25 years of age but a 1 in 100 risk if the mother is 25 years of age or older. These risks are doubled if the affected parent developed diabetes before age 11. Both parents have type 1 diabetes - 1 in in 4.  Type 2 polyglandular autoimmune syndrome – 50%  Type 2 Single parent - 1 in 7 if the parent was diagnosed before age 50 and 1 in 13 if the parent was diagnosed after age 50. There is some evidence that the offspring's risk is greater when the parent with type 2 diabetes is the mother. I Both parents - 1 in 2.

64 Conclusion  Gestational diabetes is a common problem in India  Risk stratification and screening is essential in all Indian pregnant women  Tight glycemic targets are required for optimal maternal and fetal outcome  Patient education is essential to meet these targets  Long term follow up of the mother and baby is essential


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