Gestational diabetes is a form of diabetes that develops during pregnancy and usually resolves after giving birth. It occurs when hormones produced during pregnancy interfere with the mother's body's ability to produce and use insulin properly. This can cause high blood glucose levels. Left untreated, gestational diabetes can increase the risk of complications for both mother and baby, such as preeclampsia in the mother, and macrosomia, shoulder dystocia, and jaundice in the baby. It is diagnosed through a glucose tolerance test between 24-28 weeks of gestation. Treatment may involve lifestyle modifications like diet and exercise or insulin therapy if needed. Close monitoring during pregnancy and screening for diabetes after pregnancy is important.

1. Gestational
Diabetes
Presented by: Dr. Neville M.G & Dr. Jonas L.F ( O&G Housemen SGH)
Supervisor: Dr Muniswaran Ganeshan (MRCOG, M MED O&G)

2.  Gestational diabetes is carbohydrate intolerance of
variable severity, with onset or first recognition of
hyperglycaemia during pregnancy.
 Gestational diabetes is a condition in which women
without previously diagnosed diabetes exhibit high blood
glucose levels during pregnancy (especially during third
trimester).

3. Introduction
• Represents most common metabolic complication during
pregnancy; early manifestation of type 2 diabetes
• Studies have shown that gestational hyperglycaemia is associated with highe
incidence of adverse maternal and fetal outcomes than is seen in normal
pregnancy
• High proportion (>50%) have GDM in the subsequent pregnancy
• Increased risk of subsequent T2DM
- approx. 50 % of women with GDM progressed to DM within 5 years duration
- 35 to 60% of women develop T2DM within 10 years after being diagnosed w
GDM.

4. PATHOPHYSIOLOGY
 Early in pregnancy, maternal estrogen and progesterone increase and promote
pancreatic ß-cell hyperplasia and increased insulin release
 As pregnancy progresses, increased levels of human placental lactogen,
cortisol, prolactin, progesterone, and estrogen lead to insulin resistance in
peripheral tissues.
 Table 1 describes the diabetogenic potency and time of peak effect of these
hormones. The timing of these hormonal events is important in regard to
scheduling testing for GDM
Hormone Peak elevation (weeks) Diabetogenic potency
Prolactin 10 Weak
Estradiol 26 Very weak
HPL 26 Moderate
Cortisol 26 Very strong
Progesterone 32 Strong
Adapted from Jovanovic-Peterson L, Peterson C: Review of gestational diabetes mellitus and low-calorie diet
and physical exercise as therapy. Diabetes Metab Rev 12:287-308, 1996.

5.  GDM results when there is delayed or insufficient insulin secretion in the
presence of increasing peripheral resistance

6. Risk factors (WHO/NICE)
Patients were considered to be risk-factor positive if any of the
following is present:
 age 35 years and above
 previous macrosomic baby with birth weight 4.0kg or more
 previous unexplained still birth
 previous baby with congenital abnormally
 previous pregnancy with gestational diabetes mellitus
 history of Diabetes Mellitus in first degree relatives
 Obese or pre-pregnancy weight more than 80kg, BMI > 30
 Ethnicity

7.  In the public health service in Malaysia, screening for
gestational diabetes is done selectively where only
patients with risk factors are screened and
diagnosed using a 1-step 75g OGTT.
 This is done at least once at or around 24-28 weeks
gestation, unless there are indications for it to be
done earlier.
 However, as Asian ethnicity is considered a risk
factor, selectively screening our women without
regard to their Asian background may results in gross
under-detection of gestational diabetes (~50%)
 On the other hand, to have all pregnant women
undergo the 75g OGTT may be cumbersome and have
some economic implications, particularly in low
resource areas.

8. Effects on Pregnant Women
 Pre-eclampsia
 Polyhydramnios
 Operative delivery in pregnancies complicated with
GDM/length of hospital stay, risks of infection.
 significant risk of developing diabetes later in life
 higher triglycerides,free fatty acids,and lower high-density
level (HDL) cholesterol. (cardiovascular risk)

9. Effects on Fetus
• increased rate of stillbirths in untreated GDM
• increased risk of macrosomia
(fetal weight >90th percentile
for gestational age or >4 kg)
• fetal hyperinsulinemia and subsequently increase fetal
growth
• shoulder dystocia is increased 2-6X; brachial plexus injury
• Neonatal hypoglycemia. In severe case, intravenous (IV)
glucose solution may needed or else the baby will suffer
brain damage

10.  Respiratory distress symptom
 Neonatal jaundice/hyperbilirubinemia
Long Term Outcome:
 IGT in adolescent children
 By 8 years of age, 50% of children of diabetic mothers
had weights above the 90th percentile compared to
children of women without diabetes
 high incidence of obesity
 neurodevelopmental course- child’s poorer
performance on standard measures of psychomotor
development at 6 and 9 years of age.

11. How to Diagnose GDM
 FBS??
 RBS??
 Glucosuria??
 MOGTT??

12.  ANSWER:
MOGTT
So how’s it done??
Screening for GDM is performed with a 75-g oral
glucose load given between 24 and 28 weeks
gestation, with venous plasma glucose level
taken pre and 2 hours post. The screening
test is performed at a time when the
diabetogenic effects of pregnancy are
peaking.

13. WHO HAPO ADA IADPSG
Fasting 7.0 5.1 5.3 5.1
2 hours 7.8 8.5 8.6 8.5
notes One abnormal Two abnormal One abnormal
value required value required value required

14. HAPO STUDY:
 This was an international multicentre observation
study in which over 23,000 pregnant women
were assessed for glucose intolerance using the
75 g OGTT. The results remained blinded,
providing fasting glucose <5.8 mmol/l and 2-h
glucose <11.1 mmol/l.
 The study showed relation between high blood
glucose levels with macrosomia n neonatal
hypoglycemia
 Other outcomes: caesarean section, shoulder
dystocia,
birth injury, pre-eclampsia, premature delivery,
admission to neonatal intensive care and neonatal
hyperbilirubinaemia

15. ACHOIS
 Women with gestational diabetes (WHO criteria)
were randomized either to an intervention group
which received dietary advice, glucose
monitoring and insulin therapy if required, or a
control group receiving usual care.
 The intervention group showed a significantly
lower rate (1% vs 4%) of serious perinatal
complications including death, shoulder dystocia,
bone fracture and nerve palsy.
 rates of caesarean section were similar between
the intervention and the control group
 however there was an increased incidence of
induction of labour in the intervention group (39%
vs 29%).

16. MANAGEMENT:
Exercise
 . Jovanovic-Peterson and associates studied 19 women
with GDM, assigning 9 to dietary treatment and 10 to
diet plus 20 minutes of monitored exercise 3 times a
week for 6 weeks.
 They found a significantly lower OGTT and fasting
blood glucose in patients assigned to the exercise
group beginning 6 weeks after initiating therapy.
 What type of exercise??
Non weight bearing (ex: swimming, cycling, brisk
walking)

17. Diet control
 ADA has recommended dietary therapy to
start with 2,000–2,500 kcal/day (35 kcal/kg
present pregnancy weight), with 50–60%
carbohydrates (complex, high fiber), 10–
20% protein, and 25–30% fat (<10%
saturated). New ADA recommendations
specify a protein level of 10–20% of calories
but now allow greater flexibility in the levels
of carbohydrate and fat.

18. Insulin
 The ACOG criteria for initiating insulin therapy
include a fasting plasma glucose level 5.8 mmol/l and
2-hour plasma postprandial levels 6.6 mmol/l.
 Total insulin doses can be calculated and given with
split dosing by three injections. If insulin is required,
the target plasma glucose levels are:
fasting 1hour 2 hours 2-6 am
3.3-5.8 mmol/l Not > 7.2-7.8 < 6.7 mmol/l 3.3- 5.0 mmol/l
mmol/l

19. OHA
 1) Gilbenclamide (sulphonylurea): MOA: enhance insulin secretion
by beta cells. Older sulphonylurea medications such as tolbutamide
and chlorpropamide can cause fetal hyperinsulinaemia. Glibenclamide
has minimal passage across the placenta.
Study: A trial published in 2000 randomized 404 women with
gestational diabetes to receive either glibenclamide or insulin
treatment.
Results: no difference in the glycaemic control achieved between the
two groups and no significant differences in rates of macrosomia or
metabolic neonatal complication.
 2) Metformin: MOA: increase insulin sensitivity.
Study: MiG trial randomized 751 women to insulin or metformin
treatment with insulin supplementation if required.
Results:There was no difference in peri-natal morbidity between the
two groups. 46% of the metformin group received supplemental
insulin to meet glucose targets.

20. Timing and mode of delivery
Timing:
-Uncomplicated, well controlled DM not requiring insulin with
normal fetal growth- 38 to 40 weeks
-GDM requiring insulin therapy- 38 weeks/earlier if indicated
Mode Of Delivery:
 Studies have documented an increase in the rate of shoulder
dystocia when macrosomia is suspected. Consequently,
estimated fetal weight plays an important role in the decision-
making process for route of delivery. When it is suspected that
the fetus is macrosomic, cesarean delivery should be
considered. Providers must remember that ultrasonography has
a range of error of ±10–15% in estimating fetal weight at term.

21.  Look for unrecognized DM2 or GDM at 1st prenatal
visit if risk factors
 New criteria for diagnosing GDM ’ 2-hr, 75 g OGTT
 Increased no. of women with GDM
 Rx hyperglycemia in pregnancy to prevent maternal &
fetal complications
 Lifestyle modifications: diet & exercise (during & after
pregnancy)
 Pharmacologic options: MFM, Glyburide, Insulin
 Screen for DM2 or pre-diabetes at 6-12 wks post-
partum

22. The end