1. DM in Pregnancy
Dr.Sushma Sharma
Prof.,Dept. of ObGyn,
MIMER Medical college,
Talegaon

2. 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

3. 
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

4. Increase is attributable to:

Sedentary lifestyles

Changes in diet

Immigration from high-risk populations

Childhood and adolescent obesity

5. 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

6. 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.

7. DM
Incipient type 2
Preexisting type 2
True GDM
delivery
conception
10
type 1
Follow up
20
30
40

8. Maternal-fetal
Metabolism in Normal
Pregnancy

9. 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.

10. Metabolic Changes

11. 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.

12. 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

13. 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

14. 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

15. 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

16. Perinatal Mortality,
Morbidity & Birth Injury

17. 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

18. 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

19. MACROSOMIA

20. SHOULDER DYSTOCIA

21. 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%

22. 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

23. 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

24. RDS
Hypoglycemia
Hypocalcemia
Hypomagnesemia
Thrombocytopenia
Neonate
Polycythemia
heel-stick blood
Renal vein
thrombosis
Hyperbilirubinemia
Child
Adult
Behavior - Intellect deficit
Obesity
Diabetes mellitus
Diabetes mellitus

25. 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

26. 






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%

27. MANAGEMENT
Interdisciplinary team effort

Patient education

Medical Nutrition therapy

Glycemic monitoring: SMBG and targets

Pharmacological therapy

Fetal monitoring: ultrasound

Planning on delivery

28. PRENATAL
MANAGEMENT

29. Screening Tests for GDM
Best method still controversial

30. Criteria of Diagnosis

ADA recommendations

WHO criteria

Urine Glucose

Spot Test

HbA1C, Serum fructosamine

31. 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

32. 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

33. 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

34. 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.

35. 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

36. 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

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. Dietary Therapy

Avoid single large meals with large % of
simple CHOs

6 feedings/day, with 3 major & 3 snacks

39. 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

40. 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 .

41. Exercise
Absolute Contraindication







Preterm Labor
PROM
Incompetent Cervix
Persistent 2nd or 3rd trimester bleeding
IUGR
Placenta Previa beyond 26 week
PIH

42. INSULIN
MEDICATION
ORAL DRUGS

43. 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.

44. 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

45. 
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.

46. 
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

47. 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 %)

48. 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%

49. OHA in Pregnancy

Cross placenta.

Fetal hperinsulinemia.

Prolonged fetal hypoglycemia

51. 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

52. 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

53. 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.

54. 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

55. 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

56. Postpartum Care

Prevent infection

Insulin infusion is discontinued

GDM on diet-no monitoring

GDM on insulin /Pre-gestational DM-Monitor BS

57. 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

58. 
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

59. Contraception

Low dose EP can be used

Progestin only pills shown to ↑se risk of
T2DM in GDM

IUCD – ↑sed PID

60. Women and Diabetes

Diabetes no longer
means
›
›
›
›
›
Abstinence
Amenorrhea
Inability to
conceive
Inability to deliver
healthy children
Death during
pregnancy

61. 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.