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Division of Maternal Fetal Medicine Newark Beth Israel Medical Center

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Presentation on theme: "Division of Maternal Fetal Medicine Newark Beth Israel Medical Center"— Presentation transcript:

1 Division of Maternal Fetal Medicine Newark Beth Israel Medical Center
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 X 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 Overview: Recognition
Clinical Preclinical 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

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

18 Effects of Diabetes in Pregnancy
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

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 120 AGP 70 Relatively flat, narrow limits

21 IDDM in Third Trimester 3 Injection Regimen Mean 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 Oral Hypoglycemics Fast Acting Secretagogues, and Sensitizers
Second Generation (Pregnancy category B) Glyburide, Glipizide, Glimepride Biguanides Metformin Fast Acting Secretagogues, and Sensitizers Short duration of action

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 >< mgs, 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: Insulin N=203 Glyburide N=201 Mean glucose FBS, Pre, Postpr 114,104,104 116,108,107 Hba1c 1T Hba1c 3T 5.7% 5.4 5.6% 5.5 Dose 85+/ -48 units 9 +/- 6 mgs Results No difference in neonatal or PN outcome

33 Glyburide vs Insulin Langer et al 2000
LGA 12% 13 Anomalous 2 > 4 delivery 7 4 NN low BS NICU admit RDS/pulmonary 9 6 8

34 Glyburide After ADA Diet Failure Carolinas Medical Center, 2004
4/5 gravidas were controlled, 1/5 insulin Neonatal Outcome 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 Outcomes Summary, multiple studies
Indicator Threshold/Goal Perinatal Mortality Mean BS < 115 mg/dL Spontaneous Abortion HgA1c < 7% Malformations Postprandial < 140 Macrosomia Mean BS < 100 Neonatal Metabolic Problems Mean neonatal BS > 1 SD below the mean

36 Malformations Postprandial BS < 140 mgs/Dl

37 Perinatal Mortality Mean BS < 115 mg/Dl

38 Neonatal Morbidity in Diabetic Pregnancy
GDM (III) Type I Type II Hyperbilirubin 29% 55 44 Hypoglycemia 9 29 24 RDS 3 8 4 Cardiomyopathy 1 2 Polycythemia Neonatal BG > 1 SD below the mean Neonatal hypoglycemia =

39 Maternal Morbidity Class DM A1, A2 B, C D,F,R PIH 10% 8 16 Chronic HBP
17 DKA 8% 7 9 C/S 12% 44 57

40 Guidelines for Diabetic Pregnancy
Preconception Optimal glycemic control Folic acid x 3 months, GC 1st Trimester Fetal Viability CRL 2nd Trimester Fetal Development Level 2 scan Fetal growth baseline 24 weeks MMS 3rd Trimester Fetal Growth and Well-being Kick 28wks NST/BPP 36 weeks EFW, Deliver at with amnio, without

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

42 Diabetes and Obesity

43 Fetal surveillance first 28 weeks
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

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: 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 weeks Can reduce the risk

49 Comorbidity with Hypertension Blood Pressure during Gestation

50 Fetal Growth Abnormalities in Diabetic Pregnancy by White Class California Diabetes Project, 1991
GDM Class A,B,C Class D,F,R Total >90th% 22% 31 22 24 <10th% 4 5

51 Big Babies Macrosomia – > 4500 gms ACOG, >4250 Langer
Infants of diabetics (IDM) – 15-45% macrosomic Large for Gestational Age (LGA) > 90th% 30% diabetes in pregnancy, 70% are constitutional Hard to predict fetal weight, easy to measure neonatal weight

52 Traumatic Birth & Shoulder Dystocia
Risk is > for diabetic fetus/neonate, at any EGA Suspected macrosomia- size>dates by FH, EFW> 4500 gms (Tech Bull # 30, 2001) Induction or prophylactic C/S unlikely to reduce the rate of permanent injury By ultrasound EFW above 4500, actual bwt for ½ is within 10% of estimate At EFW 4500 gms, then estimate 333 – 1667 C/S to prevent a single permanent Erb’s palsy

53 Respiratory Distress Syndrome
Abnormal timing of phospholipid production delay in PG+ Higher levels of myoinositol  persistence of PI+ PG/PI less favorable at same EGA Effect is magnified with mean plasma glucose > 110 mgs < 38.5 wks w/amnio; >38.5 with > 3% PG

54 Intrapartum Decisions
@ 40 wks with good 38 with PG:PI Active phase must be adequate Protracted descent best managed by C/S Avoid mid-pelvic operative delivery absolutely Outlet/low pelvic delivery with great care Liberal use of C/S

55 Conclusions Regulation of blood glucose needs to begin prior to conception for best result. Treatment includes diet, exercise, oral hypoglycemics and insulin. Comorbidities- Obesity, HBP, CAD Fetal growth and well being, timing of delivery require attention in 3rd trimester.


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