This document discusses gestational diabetes mellitus (GDM). It begins by defining GDM as an endocrine disease involving faulty carbohydrate metabolism that complicates 3-5% of pregnancies. The document then discusses the pathophysiology of GDM, screening and diagnostic methods including oral glucose tolerance tests, maternal and fetal complications, and management approaches including careful antenatal supervision and control of blood sugar levels. Key goals of management are finding the optimal time and method of delivery and arranging newborn care.

2. Contents
 Introduction.
 Definition and incidence.
 Pathophysiology
 Screening and diagnostic methods.
 Maternal and fetal complications.
 Management.
 You should know now.

3.  Diabetes mellitus is an endocrine
disease, involving faulty carbohydrate
metabolism, probably of genetic
origin.
 DM complicates 3 – 5% of all
pregnancies, and is a major cause of
perinatal morbidity, mortality as well
as maternal mortality.

4. Altered carbohydrate metabolism of the mother, because
a) Placental insulinase breakdown the maternal insulin
a) Placenta releases contra insulin hormones like
- human placental lactogen
- Oestrogen & progesterone
Blunting the action of insulin
c) Increased insulin destruction by kidney

5. d)Increased Lipolysis – The mother uses fat for her caloric
needs and saves glucose for foetal needs.
e) Changes in glucose – The foetus uses preferentially
alanin and other aminoacids and deprive the mother
of a major gluconeogenic source.

6. Repeat and random urine samples taken on one or more
occasion through out pregnancy reveal glycosuria in 5 – 50%
cases.
Renal Glycosuria :
During pregnancy renal threshold is diminished due to
combined effect of increased GFR and impaired tubular
reabsorption of glucose.
Present most commonly in mid pregnancy.
Glycosuria is seen with blood sugar is much below 180mg%.
No Rx required, condition disappears after delivery.

7. A diabetic pregnancy is more prone to certain
complications like.
1) Spontaneous Abortions :
Insulin dependant women with initial glycosylated Hb
above 12% or persistent plasma glucose level more than
120mg/100ml have increased risk abortion.

8. 2) Polyhydraminos :
Usually associated with a large placenta and macrosomia.
 Might be due to foetal polyuria due to fetal
hyperglycimia.
3) Pre-eclamptic toxaemia & hypertension :
 10 – 20% of pregnant diabetic women have toxaemia or
hypertension
 Incidence of increased preterm delivery, and increased
perinatal morbidity and mortality.
(As high as 20%)

9. 4) Infections :
 Urinary tract infection and monilial vulvovaginitis more
likely to occur
 Also high incidence of chorioaminitis, endometriosis.
(Mostly in poorly glycaemia controlled diabetic patients)

10. CAUSE : Over distended uterus due to
 Associated polyhydraminos or
 Macrosomic baby
 Infection
 Associated PIH
 Increased operative delivery
CAESAREAN SECTION :
 Elective CS rate higher due to increased perinatal loss after 38 wks
of gestation.
KETOACIDOSIS :
 Affects only 1% of diabetic pregnancies, but it is one of the most
serious complications.
 Foetal loss can be as high as 20%.

11. Pregnancy imposes a heavy burden on diabetic
patient.
 More insulin is necessary to achieve metabolic
control.
 Progression of diabetic retinopathy.
 Worsening of diabetic nephropathy.
 Increased risk of death for patients with diabetic
cardiomyopathy.

12. CENTRAL NERVOUS SYSTEM :
 Anencephally
 Holoprosencephally
 Encephalocele
HEART AND GREATVESSELS :
 Transposition of the great vessels
 Ventricular septal defect
 Aortic coarctation
 Atrial septal defect
SKELETAL AND SPINAL :
 Caudal regression syndrome
GENITOURINARY :
 Renal Agencies
 Ureteral duplication
GASTRO-INTESTINAL :
 Oesophagial atresia
 Anal atresia

13. RDS :
Neonates of the diabetic have delayed lung maturity, so
increased risk of RDS.
FETAL DEATHS :
placental insufficiency, abruption, foetal growth restriction or
oligo hydramnios present.
Hypothesis proven with foetal blood sampling by decreased
foetal pH and increased foetal PCO2.
Macrosomia :
Macrosomia – Diff. Delivery – shoulder dystocia

14. HYPERBILIRUBINAEMIA :
 Pathogenesis might be due to prematurity and polycythaemia with
haemolysis.
HYPOGLYCEMIA :
 Hypoglycemia of < 30mg% leads to hypotonia, hypothermia,
apnoea, convulsion.
 Hypocalcaemia – seen in 50% of infants.
 Predisposition to diabetes – IDM have a 1 – 3%, risk of developing
insulin dependant diabetes.
If only father – 6%, If both parents – 20%.

15. • Obesity (>200 lbs or > 15% of non-pregnant
ideal body wt.)
• Positive family history of diabetes (Sibling or
parent)
• History of still birth.
• History of delivery of a large infant
• Glycosuria
• History of unexplained neonatal death
• History of congenital anomaly
• History of prematurity

16. Screening for diabetes during Pregnancy :
Best screening test is the measurement of plasma
glucose 1 hr after ingesting 50mg of glucose (GCT)
140 mg/dl screening positive for GDM
Confirmatory test done by 3 hours OGTT.

17. Time Whole blood Mg
%
Fasting 95
1 hr 180
2 hr 155
3 hr 140
If any 2 or more values elevated GTT is abnormal.

18. Class Age of
onset
Duration (yrs) Vascular
disease
Therapy
A
- A1
- A2
Gestational
Gestational
FBS
< 105mg%
> 105mg%
2 hr PPG
< 120mg%
> 120mg%
Diet
Insulin
B Over 20 < 20 None Insulin
C 10 –19 10-19 None Insulin
D Before 10 > 20 Benign
Retinopathy
Insulin
F Any Any Nephropathy Insulin
G Any Any Proliferative
Retinopathy
Insulin
H Any Any Arteriosclerotic
heart disease
Insulin

19. PRE-CONCEPTIONAL COUNSELLING :
 Joint consultation of endocrinologist, obstetrician,
dieticians
 Blood glucose, HbA1c, RFT, ophthalmoscopy done
 OHA changed to insulin.
PRINCIPLES OF MANGEMENT :
 Careful antenatal supervision and control of diabetes
 To find optimum time and method of delivery
 Arrangement for care of newborn.

21.  ANC at monthly intervals upto 20 weeks – 2 wks interval
upto 30 wks.
 Daily calorie requirement 30-35Kcal/kg body wt. + 200
Kcal.
 Diet – CHO-50%, Protein-20%, Fat 25-30%.
 4 meal regimen – Breakfast 25% of total calorie intake
Lunch 30%
Dinner 30%
Bed time snack 15%
 Frequent blood sugar estimation
 Glycosylated Hb estimation, at end of 1st
trimester and 2
monthly thereafter.

22.  Sonographic evaluation to exclude cong.
Anomalies, macrosomia and IUGR (Rare)
 Assessment of fetal well being is to be
made from 32 wks onwards.
 When abnormal CTG, biophysical profile
done.
 Doppler umbilical artery velocimetry useful
in vasculopathy

23.  For glycemic goals – A double mixed regime employed.
 3 – 4 daily inj. of a regular (Human Actrapid) and
intermediate acting insulin (Isophane) before dinner.
Guard for hypoglycemia for tight control of sugar.
oral antidiabetic drugs- Controversial.
ADMISSION :
 Early hospitalisation facilities
 Stabilisation of diabetes, minimise incidence of pre-
eclampsia, polyhydramnios and preterm labour and to
select out the appropriate time of termination of
pregnancy.

24.  Stable insulin dependant pregnant diabetic can reach
term but not beyond EDD.
 Unstable insulin dependant diabetes, should deliver
soon, after foetal lung maturity assessed.
 To prevent intra uterine deaths in last 2 wks patient
should be admitted after 37 wks.
.

25.  To control diabetes by hrly estimation of blood
glucose and split up dose of soluble insulin if
required.
 To control ketosis
 To maintain potassium level
 Foetal monitoring like constant watch on foetal
condition.

26.  Prophylactic antibiotics to minimise infection.
 Insulin requirement dramatically falls following
delivery due to low levels of insulin
antagonising hormones.
 Post partum assessment of carbohydrate
metabolism.
 Rpt GTT after 6 wks.

27. Things you should know
 Screening and diagnostic tests for diabetes in
pregnancy.
 Effect of diabetes on pregnancy an fetus
 Effect of pregnancy on diabetes.
 Risk factors.
 Antepartum surveillance.
 Mx during labour.