1. Tight glycemic control through medical nutrition therapy, exercise, blood glucose monitoring, and potentially insulin is important to manage diabetes in pregnancy. 2. Close fetal surveillance through growth scans and tests are needed to monitor for complications like macrosomia. 3. Delivery timing and type (vaginal vs c-section) depends on maternal and fetal status and risks like macrosomia. 4. Neonatal risks include hypoglycemia, jaundice, and respiratory distress which requires close monitoring after birth. 5. Counseling on future diabetes risk and appropriate contraception is important in postpartum care.

1. DIABETES IN PREGNANCY
KISHORE SR
CH 26- SHEILA BALAKRISHANAN

2. Contents
Introduction
Gestational Diabetes
Pregestational Diabetes
Complications of Diabetes in Pregnancy

3. Introduction
• Diabetes is a state of physiological Insulin
resistance.
• Estrogen, Progesterone and Human placental lactogen
act as insulin antagonists causing insulin resistance.

4. • Human Placental Lactogen
 Affects protein, fat & carbohydrate metabolism.
 Increase lipolysis  increased FFA  increase in
insulin resistance
 FFA used for maternal metabolism so that glucose &
amino acids are available for the fetus.
• Plasma cortisol also increases leading to insulin
resistance.
• So pancreas is forced to produce more insulin and
plasma glucose level fall.

5. • Pregnancy is characterized by “Fasting Hypoglycemia”
and “Post-prandial Hyperglycemia”.
• Insulin resistance in late pregnancy is a normal
physiological adaptation that shifts maternal energy
metabolism from carbohydrate to lipid oxidation &
thereby spares glucose for the fetus.
• Gestational diabetes occurs when the pancreas despite
increased insulin production cannot counter the insulin
resistance caused by pregnancy hormones.

6. Types of Pregnancy Diabetes
• Pregestational or Overt Diabetes (10%)
• Gestational diabetes (90%)

7. GESTATIONAL DIABETES
• Carbohydrate intolerance of variable severity, with
onset or first recognition during the present
pregnancy.
• GDM usually manifests in the latter half of
pregnancy so no effect on organogenesis and does
not cause congenital defects.
• The main problem is macrosomia
• Reverts to normal following delivery.

8. Screening
• Universal screening- all the women are screened
• Selective screening- only women with the risk factors.
Advantage of screening:
• Reduces perinatal mortality & morbidity
• Picks up those women likely to develop type II diabetes in
the future.

9. Risk factors
PREGNANCYPREPREGNANCY
Obesity
Polyhydramnios
Repeated infections
Macrosomia
Glycosuria
Age >30
Previous GDM
Family history of DM
Previous macrosomic baby
Bad obstetric history
Polycystic ovary syndrome

10. • OGTT (oral glucose tolerance test)
▫ Done at 24-28 weeks
▫ Done after an overnight fasting of atleast 8hours
▫ 75g of glucose in 100ml water
▫ Two readings taken after 1hr and the next 1hr
Diagnosis:
• Fasting > or equal 5.1 mmol/L
• 1 hour > or equal 10 mmol/L
• 2 hours > or equal 8.5 mmol/L
Women with GDM should be screened for persistant diabetes
6-12weeks post partum. They have high risk of life long diabetes
so screen every 3 yrs.

11. • One Step Test or Spot Test
▫ No need for fasting.
▫ Given 75g of glucose in 300ml water irrespective of last meal.
▫ Blood glucose assessed at 2 hours
▫ Diagnosis of GDM if > 7.7 mmol/L
• Two Step procedure
•50 g glucose challenge test followed by a 100 g OGTT if the 1 hour
plasma glucose is 7.7 mmol/L or more.
• The fasting plasma glucose level is determined following 100 g of oral
glucose and plasma glucose level estimated at 1,2 & 3hours
•FBS 5.2 mmol/L 1 hour 10 mmol/L
•2 hour 8.6 mmol/L 3 hour 7.7 mmol/L

12. Management
• Tight glycemic control is the cornerstone in the
management
• Divided into Medical and Obstetric management.

13. Medical management
Medical Nutrition Therapy (MNT)
• Recommended calorie intake is about 30 cal/kg/day
divided over 3 meals and 3 snacks. The aim is to blunt
the post prandial hyperglycemia.
• Bed time snack should contain complex carbohydrate
and protein to prevent late night hypoglycemia and
early morning starvation ketosis.

14. Components of dietCalories
Carbohydrates: 40-
45% of calories
30 Kcal/kg/dayNormal weight
Fat: <35% of calories40 Kcal/kg/dayUnderweight
Protein: 12-20% of
calories
24 Kcal/kg/dayOverweight

15. Exercise
• Light exercise especially of the upper part of the
body.
• 20min daily atleast
• Least mechanical stress should be on the trunk.

16. Insulin
• Indicated when MNT fails.
• Self administration should be encouraged
• Ideally, 3 premeal injections of rapid acting regular
insulin (aspart and lispro)
• The requirements increase and pregnancy advances
• Mild cases, mixture of rapid and intermediate acting,
given twice daily (30:70)

19. Monitoring
• Self monitoring by glucometer and capillary blood
glucose or venous plasma levels.
• Aim is to keep the fasting plasma level at 5.1 mmol/L
(95mg/dl)
• 2 hours post prandial 6.6mmol/L
• Women using daily self monitoring had less
macrosomic infants.
• Ideal monitoring is 4 times a day including fasting,
post breakfast, post lunch and post dinner with
additional testing whenever she is symptomatic

21. Oral hypoglycemic agents
• Metformin
• Glyburide

22. Obstetric Management
Antepartum
• Nuchal translucency is assessed at 11-14 weeks
• Anomaly scan at 18-20 weeks
• Growth scan done monthly at third trimester (28,32,36
weeks)
• Look for macrosomia (increased in abdominal
circumference with increased fetal subcutaneous fat)
and polyhydramnios

24. • Antepartum fetal surveillance and non stress
testing and biophysical profile may help prevent
still birth and unnecessary preterm delivery and detect
fetal compromise.
• Antepartum corticosteroid to enhance lung maturity
are not contraindicated in pregnancy
• Doppler studies is indicated in case of diabetes
complicated by preeclamsia and growth restriction.

25. Intrapartum
▫ Timing of delivery
 Early delivery is indicated if there is presence of fetal or
maternal complications or if the glycemic index control
is poor.
 Women on insulin are best delivered after 38 weeks.
 Previous term still birth is an indication for early
delivery.

26. ▫ Type of Delivery
 Diabetes per se is not an indication for C-section and VD
maybe allowed if no complications.
 Vaginal delivery:
 No maternal or fetal complications
 The cervix is favorable, average baby size, vertex presentation with no
CPD
 Induction of labour.
 Continuous CTG monitoring is mandatory.
 Shoulder dystocia should be anticipated
 Caesarean:
 If there is maternal or fetal complications
 Macrosomia (On US increasing AC or fetal weight > 4000g)

27. ▫ Intrapartum Glycemic control:
 Euglycemic state should be maintained.
 Morning dose of insulin is skipped in elective CS
 Mother should get a limited amount of glucose during
labour
 Hourly glucose monitoring is done.
 Once into active labour, she can be started on the sliding
scale of insulin using an Insulin & Dextrose infusion
regimen.
▫ Neonatal Care
 Blood glucose levels closely monitored for 48hrs
 Early breastfeeding is advocated
 Cord clamped early to prevent neonatal polycythemia.
 Avoid heat loss and look for congenital abnormalities.

28. Postpartum care
▫ Prophylactic antibiotics to minimize infections
▫ Most women with GDM will no longer require insulin
▫ At 6-12 weeks do OGTT
▫ Lifelong screening at least every 3 years

29. Counseling and Contraception
• Counseled about the risk of future diabetes and
receive lifestyle advice.
• Encouraged to continue on diet and exercise.
• Annual OGTT
• Barrier methods are safe.
• Low dose Combined OCPs, injectable progestogens
and IUD can all be safely used in women who had
GDM.

30. SUMMARY: PRINCIPLES OF MANAGEMENT
OF GDM
1. Tight glycemic control
2. Antepartum fetal surveillance
3. Timing of delivery
4. Good neonatal care
5. Counselling for the future.

31. Q. For a 12 week pregnant lady with FBS of 9.4mmol/L,
the anti diabetic drug of choice is?
a) Mixtard
b) Metformin
c) Glipizide
d) Glibenclamide
e) Aspart

32. PREGESTATIONAL OR OVERT
DIABETES
• To remember that women are already diabetic at the
time of conception
• Hence, prove for congenital abnormalities
• Management is similar to GDM
• Preconceptional and early pregnancy care is
important.

33. Complications
MATERNAL
• Ketoacidosis
▫ Rare but high fetal loss
• Diabetic retinopathy
▫ Laser photocoagulation done
during pregnancy can prevent
blindness
• Diabetic nephropathy
• Post partum thyroiditis
FETAL
• Miscarriage
• Congenital malformations
• IUGR

34. Management
Investigations
Mandatory for all overt diabetics
▫ Fundoscopy to rule out retinopathy
▫ Renal function tests to look for nephropathy
▫ ECG
▫ Urine culture
▫ Glycosylated Hb (at end of first trimester)

35. Preconceptional Management:
• Planned pregnancy
• Good glucose control
• HbA1c should be within normal limit (<6%)
• Folic acid preconceptionally and in the first trimester
• Evaluate for retinopathy and nephropathy

36. Medical Management
• Insulin needs increase as pregnancy advances.
• Three pre-meal injections of rapid acting regular
insulin along with a shot of intermediate acting insulin
at bedtime
• Self monitoring of glucose is important
• Continuous glucose monitoring system (CGMS) is
needed in certain cases
• If blood sugar very high, test for ketone bodies in
urine

37. Obstetric Management
Same as for GDM
• In addition to the scan at 11-14 weeks and the anomaly
scan, a FETAL ECHOCARDIOGRAPHY is also
advised due to high incidence of cardiac anomalies.

38. Contraception
• Barrier method is safe
• Progesterone in the hormonal contraception may
increase insulin resistance
• COC is contraindicated in diabetics with vascular
disease and other risk factors
• IUDs in women with low risk of STDs
• Sterilization is an option for those who have
completed a family

39. Q. Which one of the following is a rare but serious
complication of Pregestational diabetes?
a) Nephropathy
b) Neuropathy
c) Thyroiditis
d) Ketoacidosis
e) Intrauterine Fetal death

40. COMPLICATIONS OF DIABETES
IN PREGNANCY
• Maternal complications
▫ Preeclampsia
▫ Polyhydramnios
 Due to maternal hyperglycemia in 20%
 Leads to fetal hyperglycemia and polyuria
 Osmosis is another factor
▫ Infections
▫ Risk of operative delivery
▫ Genital tract trauma (macrosomia)
▫ Puerperal sepsis and wound infections

41. • Fetal Complications
▫ Abortions and congenital anomalies are a major
problem of pregestational diabetes and GDM
usually appears only after 20 weeks.
▫ All the fetal and neonatal complications are due to
the fetal Hyperinsulinemia.
▫ This can be explained by the Pederson Hypothesis

43. • Miscarriage
▫ More in uncontrolled pregestational diabetes
• Congenital malformations
▫ More in uncontrolled pregestational diabetes
▫ Hyperglycemia, ketosis and O2 free radical toxicity are
the causative agents
 Cardiac defects (transposition of great vessels & VSD)
 Neural tube defects (anencephaly and spina bifida)
 Caudal regression syndrome or sacral agenesis (rare) but is
a congenital defect specific to diabetes.

44. • Unexplained intrauterine death (IUD)
▫ Due to fetal hypoxia
▫ Fetal hyperglycemia and hyperinsulinaemia increase the
O2 demand of fetus.
▫ Glycosylated Hb binds O2 more avidly but releases less O2
▫ Fetal polycythemia & hyperviscosity
▫ In overt DM with vasculopathy, placental insufficiency can
lead to IUD especially in association with preeclampsia.
• Prematurity

45. • Macrosomia
▫ Most common complication
▫ Increase in IGF I and II
▫ Increase adiposity in insulin dependent area as trunk and
shoulders.
▫ Good glycemic control reduces the risk
• Intrauterine Growth Restriction (IUGR)
• In Pregestational diabetes with vascular
complications (retinopathy & nephropathy).
• Disturbance in maternal fuels during organogenesis could
also be the cause.

46. • Neonatal complications
▫ Usually macrosomic, has increased adiposity, increased
skinfold thickness and visceromegaly (liver).
▫ Plethoric appearance because of polycythemia

47. • Respiratory Distress Syndrome:
▫ More common in overt diabetes delivered by CS
▫ Occur at all gestational ages.
▫ Fetal hyperinsulinemia impairs surfactant production in the
lung.
▫ This leads to delay in lung maturity and RDS.
▫ Hypoglycaemia:
▫ Fetal hyperinsulinemia causes hypoglycaemia (plasma
glucose level to be less than 2.2 mmol/L).
• Hypocalcaemia:
▫ Due to transient hypoparathyroidism, serum calcium level
below 0.38 mmol/L

48. • Hyerbilirubinaeimia :
• Due to Polycythaemia with hemolysis , can be due to
prematurity
• Hyperviscosity Syndrome:
• Due to increased erythropoiesis and polycythemia
• Renal vain thrombosis and necrotizing entrocolitis also result
from polycythemia.
• Hypertrophic cardiomyopathy:
• May progress to heart failure
• Echocardiography demonstrate Septal hypertrophy (transient
and resolve soon)
• If regress by 6 months  No permanent myocardial damage
• Rarely, it is severe and cause CCF in the first few days of life

49. • Birth trauma:
▫ Due to macrosomia and Shoulder dystocia due to
disproportionate growth of the shoulders
▫ Shoulder dystocia. This results in Erb’s and Klumpke’s
paralysis & fracture of the clavicle and humerus
Late effects:
• Obesity
• Early onset type II diabetes
• Cardiovascular disease

50. Thank you