Dr. Kanakamani Madhivanan, M.D., D.M.

(Endocrinology),
Assistant Professor
Department of Endocrinology, Diabetes, Metabolism
Christian Medical College, Vellore
Plan of presentation
Introduction
Physiology of fuel metabolism in normal
pregnancy
Pathophysiology of GDM
Epidemiology of GDM
Screening and diagnosis
Maternal and fetal risks
Management of GDM
Obstetric management
Introduction
Global increase in prevalence of DM
Individual importance - Hyperglycemia in
pregnancy has adverse effects on both
mother and fetus
Public health importance rising epidemic
of DM in part attributed to the diabetic
pregnancies
Prevention of type 2 DM should start
intrauterine and continue throughout life
Introduction
Gestational diabetes (GDM) is defined as
any degree of impaired glucose tolerance of
with onset or first recognition during
pregnancy .
Many are denovo pregnancy induced
Some are type 2 ( 35-40%)
10% have antibodies
Introduction
Difficult to distinguish pregestational Type 2 DM and
denovo GDM
Fasting hyperglycemia
blood glucose greater than 180 mg/dL on OGT
acanthosis nicgrans
HbA1C > 5.3%
a systolic BP > 110 mm Hg
BMI > 30 kg/m2
Fetal anomalies
Clues for Type 1
Lean
DKA during pregnancy
Severe hyperglycemia with large doses of insulin
Fuel metabolism in pregnancy
Goal is uninterrupted nutrient supply to
fetus
The metabolic goals of pregnancy
are
1) in early pregnancy to develop
anabolic stores to meet metabolic
demands in late pregnancy
2) in late pregnancy to provide fuels
for fetal growth and energy needs.
Glucose metabolism in
pregnancy
Early pregnancy
E2/PRL stimulates b cells Insulin sensitivity
same and peripheral glucose utilisation 10% fall
in BG levels
Late pregnancy
Fetoplacental unit extracts glucose and
aminoacids, fat is used mainly for fuel
metabolism
Insulin sensitivity decreases progressively upto
50-80% during the third trimester
variety of hormones secreted by the placenta,
especially hPL and placental growth hormone
variant, cortisol, PRL,E2 and Prog
 Glucose metabolism in
pregnancy

FASTING FED
accelerated Fat hyperglycemia,
starvation and hyperinsulinemia,
esxaggerated Insulin resistance Hyperinsuli hyperlipidemia,
ketosis nemia and reduced
(maternal tissue sensitivity
hypoglycemia, Glucose Aminoacids to insulin
hypoinsulinemia,
hyperlipidemia,
and Fetus
hyperketonemia)
 24-hour insulin requirement before conception is approximately 0.8 units /
kg.
In the first trimester, the insulin requirement rises to 0.7units / kg of the
pregnant weight more unstable glycemia with a tendency to low fasting
plasma glucose and high postprandial excursions and the occurrence of
nocturnal hypoglycemia
By the second trimester, the insulin requirement is 0.8 units per kilogram.
From 24th month onwards steady increase in insulin requirement and
glycemia stabilises
By third trimester the insulin requirement is 0.9 - 1.0 unit /kg pregnant
weight per day
Last month may be a decrease in insulin and hypoglycemias esp.
nocturnal
Magnitude of problem: Global
Prevalence of GDM varies worldwide and
among different racial and ethnic groups
within a country
America white women (3.9%) and Asian (8.7%)
Europe 0.6% to 3.6%
Australia 3.6% to 4.7% (Indian women 17.7%)
China 2.3%; Japan 2.9%

Variability is partly because of the

different criteria and screening regimens
Magnitude of the problem -
India
Chennai, hospital based, universal screening
18.9% had FPG 126 and PPPG 140.
Trivandrum 15%
Bangalore 12%
Erode 18.8%
Chennai, community based, universal screning,
17.8% in urban, 13.8% in semi urban and 9.9% in rural
areas.
Chennai : 0.56%
Mysore Parthenon Study: 6%
Maharashtra, hospital based, selective
screening 7.7% had GDM; 13.9% had IGGT.
Risk factors
A family history of diabetes, especially in first degree relatives
Prepregnancy weight 110% of ideal body weight or body mass index over
30 kg/m2 or significant weight gain in early adulthood, between
pregnancies, or in early pregnancy
Age greater than 25 years
Previous delivery of a baby greater than 4.1 kg
Personal history of abnormal glucose tolerance
Member of an ethnic group with higher than the background rate of type 2
diabetes (in most populations, the background rate is approximately 2
percent)
Previous unexplained perinatal loss or birth of a malformed child
Maternal birthweight greater than 4.1 kg or less than 6 pounds 2.7 kg
Glycosuria at the first prenatal visit
Polycystic ovary syndrome
Current use of glucocorticoids
Essential hypertension or pregnancy-related hypertension
Maternal complications
Worsening retinopathy 10% new DR, 20%
mild NPDR and 55% mod-severe NPDR
progresses
Worsening proteinuria. GFR decline depends
on preconception creatinine and proteinuria
Hypertension and Cardiovascular disease
Neuropathy No worsening (gastroparesis,
nausea, orthostatic dizziness can be
worsened)
Infection
Maternofetal complications
Macrosomia: 63 percent
Cesarean delivery: 56 percent
Preterm delivery: 42 percent
Preeclampsia: 18 percent
Respiratory distress syndrome: 17 percent
Congenital malformations: 5 percent
Perinatal mortality: 3 percent
Spontaneous abortion, third trimester fetal deaths,
Polyhydramnios, preterm birth, ?adverse
neurodevelopmental outcome
Risk for type 2 DM
Neonatal complications
Morbidity associated with preterm birth
Macrosomia birth injury (shouldeer dystocia, brachial
plexus injury)
Polycythemia and hyperviscosity
Hyperbilirubinemia
Cardiomyopathy
Hypoglycemia and other metabolic abnormalities
(hypocalcemia, hypomagnesemia)
Respiratory problems
Congenital anomalies
Congenital anomalies
2/3rd CVS or CNS, 13-20 times common
Cardiac( including great vessel anomalies) : most
common
Central nervous system (spina bifida/anencephaly) :
7.2%
Skeletal: cleft lip/palate, caudal regression syndrome
Genitourinary tract: ureteric duplication
Gastrointestinal : anorectal atresia
 Skeletal and central nervous system
Caudal regression syndrome
Neural tube defects excluding anencephaly
Anencephaly with or without herniation of neural elements
Microcephaly
Cardiac
Transposition of the great vessels with or without ventricular
Ventricular septal defects
Coarctation of the aorta with or without ventricular septal defects or patent ductus arteriosus
Atrial septal defects
Cardiomegaly
Renal anomalies
Hydronephrosis
Renal agenesis
Ureteral duplication
Gastrointestinal
Duodenal atresia
Anorectal atresia
Small left colon syndrome
Caudal regression syndrome
Caudal regression syndrome
Whom to screen ?

No consensus
recommended screening ranges from
selective screening of average- and high-risk
individuals to universal diagnostic testing of
the entire population dependent on the risk
of diabetes in the population.
Risk stratification based on certain variables
Low risk : no screening
Average risk: at 24-28 weeks
High risk : as soon as possible
 Low risk for GDM
To satisfy all these criteria

Age <25 years

Not a member of an ethnic group with high prevalence of GDM
(not Hispanic, Native American/Alaskan,
Asian/Pacific Islander, African American)
Normal prepregnancy body weight (not 20% or more
over desired body weight or BMI 27 kg/m2 or more)
No family history of diabetes in first-degree relatives.

No history of abnormal glucose tolerance

No history of poor obstetric outcome

High risk
Marked obesity
Prior GDM (30-50% risk for recurrence)
Glycosuria
Strong family history
When and how to screen?
24-28 weeks
High risk
First prenatal visit
50 g glucose loading test
High risk women 3 hr GTT with 100 g
glucose
50 g GTT
A 50-g oral glucose load is given without
regard to the time elapsed since the last
meal and plasma or serum glucose is
measured one hour later
A value 130 mg/dL is considered
abnormal ; we use 130 mg/dL as the
threshold for our patients.
Capillary blood should not be used for
screening unless the precision of the
glucose meter is known, it has been
correlated with simultaneously drawn
venous plasma samples, and has met
100 g GTT
Oral glucose tolerance test ( OGTT) with 100 gm
glucose
Overnight fast of at least 8 hours
At least 3 days of unrestricted diet and unlimited
physical activity
> 2 values must be abnormal

Fasting > 95 mg/dl

1-h > 180 mg/dl
2-h > 155 mg/dl
3-h > 140 mg/dl
75 g GTT

ADA WHO
Fasting > 95 mg/dl Fasting > 95 mg/dl
1-h > 180 mg/dl OR
2-h > 155 mg/dl 2-h > 140 mg/dl
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
weeks and then at 32 34 weeks
MANAGEMENT ISSUES

Patient education
Medical Nutrition therapy
Pharmacological therapy
Glycemic monitoring: SMBG and targets
Fetal monitoring: ultrasound
Planning on delivery
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
Calorie allotment
30 kcal per kg current weight per day in
pregnant women who are BMI 22 to 25.
24 kcal per kg current weight per day in
overweight pregnant women (BMI 26 to
29).
12 to 15 kcal per kg current weight per
day for morbidly obese pregnant women
(BMI >30).
40 kcal per kg current weight per day in
pregnant women who are less than BMI
Carb intake
Postprandial blood glucose concentrations
can be blunted if the diet is carbohydrate
restricted. Complex carbohydrates, such as
those in starches and vegetables, are more
nutrient dense and raise postprandial
blood glucose concentrations less than
simple sugars.
Carbohydrate intake is restricted to 33-
40% of calories, with the remainder divided
between protein (about 20%) and fat
(about 40%).
With this calorie distribution, 75 to 80
Calorie distribution
Variable opinion
Most programs suggest three meals and three
snacks; however, in overweight and obese women
the snacks are often eliminated
Breakfast The breakfast meal should be small
(approximately 10%of total calories) to help
maintain postprandial euglycemia.
Carbohydrate intake at breakfast is also limited
since insulin resistance is greatest in the
morning.
Lunch 30% of total calories
Dinner 30% of total calories
Snacks Leftover calories (approximately 30%
Monitoring BG
Atleast 4 times
Fasting and 3 one hr postprandial
Pre vs postprandial monitoring
Better glycemic control (HbA1c value 6.5
versus 8.1 percent)
A lower incidence of large-for-gestational
age infants (12 versus 42 percent)
A lower rate of cesarean delivery for
cephalopelvic disproportion (12 versus 36
percent)
Monitoring BG
Home monitoring
Maintain log book
Use a memory meter
Calibrate the glucometer frequently
HbA1C
Ancillary test for feedback to the patient
Lower values when compared to nonpregnant state
lower BG and increase in red cell mass and slight
decrease in life span measured every 2-4 weeks
Target < 5.1%
 Studies report no to moderate correlations
between HbA1 and different components of the
glucose profile when an HbA1 result of 4% to 5%
includes a capillary blood glucose range of 50 to
160 mg/dL.
Levels of HbA1c are related to the rate of
congenital anomalies and spontaneous early
abortions in pre-existing diabetes, but the use of
this measure, which retrospectively reflects
glycemic profile in the last 10 weeks, for treatment
evaluation in GDM is questionable. In addition,
the association between glycosylated hemoglobin
and pregnancy outcome in GDM or prediction of
macrosomia is poor
Glycemic targets (ACOG)

ACOG
Fasting venous plasma 95 mg/dl
1 hour postprandial 140 mg/dl
2 hour postprandial 120 mg/dl
Pre-meal 100 mg/dl
A1C 6%

ADA
premeal 80-110
2 hr postmeal not more than 155

These are venous plasma targets, not glucometer targets

PHARMACOLOGICAL
INTERVENTION
If the FPG at diagnosis is 120, can
consider immediate therapy.
Otherwise, MNT for 2 weeks
If majority FPG (4/7) > 95 or PP > 120 then
to start on insulin.
Insulin
15% need insulin
Total dose varies. 0.7 to 2 units per kilogram (present
pregnant weight)
FBG high Night NPH 0.2 units/kg
PPBG high bolus 1.5 units/10 gm CH2O for
breakfast and 1 unit /10 gm CH2O for lunch and
dinner
If both pre and postprandial BG high or if the woman's
postprandial glucose levels can only be blunted if
starvation ketosis occurs - four injection/day regimen.
Total 0.7 unit/kg up to week 18
0.8 unit/kg for weeks 18 to 26
0.9 unit/kg for weeks 26 to 36
1. unit/kg for weeks 36 to term.
In a morbidly obese woman, the initial doses of insulin may need
to be increased to 1.5 to 2. units/kg to overcome the combined
OHA in pregnancy
Systematic review by John Hopkins
University
maternal glucose levels did not differ
substantially between gravidae treated with
insulin versus those treated with oral
glucose-lowering agents
there was no consistent evidence of an
increase in any adverse maternal or neonatal
outcome with use of glyburide, acarbose, or
metformin compared with use of insulin
Inconsistent data. ADA, ACOG, USFDA
do not endorse.
OHA in pregnancy
Tolbutamide and chlorpropamide
Cross placenta. Fetal hperinsulinemia.
Prolonged fetal hypoglycemia
Glibenclamide
Minimal transplacental transport
Observational studies no excess anomalies
or hypoglycemia
Only RCT 404 women. Glib vs insulin. No
difference
 second-generation sulfonylureas
especially glyburide, do not significantly
cross the diabetic or nondiabetic
placenta. Fetal concentrations reached
no more than 1% to 2% of maternal
concentrations.
tolbutamide diffused across the placenta
most freely, followed by
chlorpropamide, then glipizide, with
glyburide crossing the least.
Metformin crosses placenta not
OHA in pregnancy
Metformin
Category B
No adverse outcome after first trimester
Second, third trimester safe and effective
Vs. insulin no serious adverse effects
No studies vs. glibenclamide
Acarbose
Two prelim studies
Thiazolidinediones and GLP-1
Not studied
Fetal monitoring
Baseline ultrasound : fetal size
At 18-22 weeks: major malformations
fetal echocardiogram
26 weeks onwards: growth and liquor volume
III trimester: frequent USG for accelerated growth
( abdominal: head circumference)
Timing of delivery
Small risk of late IUD even with good control
Delivery at 38 weeks to avoid late still birth and fetal
growth leading to shoulder dystocia
Vaginal delivery: preferred
Caesarian section only for routine obstetric indication
just GDM is not an indication !
Unfavorable condition of the cervix is a problem
4500 grams, cesarean delivery may reduce the
likelihood of brachial plexus injury in the infant
(ACOG). Assessing fetal weight accurately is a problem
Management of labor and delivery
Maternal hyperglycemia in labor: fetal hyperinsulinemia,
worsen fetal acidosis and neonatal hypoglycemia
Insulin requirements come down
Maintain sugars: 70-90 mg/dl
Routine GDM diet
Maintain basal glucose requirements
Monitor sugars 1-4 hrly intervals during labour
Give insulin as infusion only if sugars more than 120 mg/dl
Glycemic management during
labour
Later stages of labour: start dextrose to maintain
basal nutritional requirements: 150-200 ml/hr of
5% dextrose
Elective LSCS: check FBS, if in target no insulin,
start dextrose drip
Continue hourly SMBG
Post delivery keep patients on dextrose-normal
saline till fed
No insulin unless sugars more than normal
nonpregnant levels
Post partum follow up
Check BG before discharge
Breast feeding: helps in weight loss. Insulin,
tolbutamide compatible. Chlropropamide secreted small
amounts watch for hypoglycemia in infant. Glyburide
and glipizide not secreted Metformin secreted - no
adverse effects
Lifestyle modification: exercise, weight reduction
OGTT at 6-12 weeks postpartum: classify patients into
normal/impaired glucose tolerance and diabetes
Contraception low dose EP can be used. Progestin only
pills shown to increase risk of T2DM in GDM
Preconception counseling for next pregnancy
Immediate management of neonate
Hypoglycemia : 50 % of macrosomic infants
515 % optimally controlled GDM

Starts when the cord is clamped

Exaggerated insulin release secondary to

pancreatic -cell hyperplasia

Increased risk : blood glucose during labor and

delivery exceeds 90 mg/dl

Anticipate and treat hypoglycemia in the infant

Management of neonate
Hypoglycemia <40 mg/dl

Encourage early breast feeding

If symptomatic give a bolus of 2- 4 ml/kg, IV 10%

dextrose

Check after 30 minutes, start feeds

IV dextrose : 6-8 mg/kg/min infusion

Check for calcium, if seizure/irritability/RDS

Examine infant for other congenital abnormalities

Future risks - Mother
Atleast 6 weeks post delivery, 75 g OGTT for
all GDM
90% normoglycemic
Recurrence of GDM 30-60%
Older
Multipara
Weight gain interpregnancy
Higher infant BW in index pregnancy
IGT and T2DM
20% IGT postpartum
3.7% @ 6m , 4.9% @ 15m and 18.9% @ 9 y
Who will progress to DM?
WC and BMI stronset predictors
Autoantibodies
DM at earlier gestational age
Gestational requirement of insulin
Higher FBG
Higher BG on OGTT
Neonatal hypoglycemia
Recurrent GDM
Preconception counselling
Diabetic mother : glycemic control with
insulin/SMBG
Target: HbA1c < 7%

Folic acid supplementation: 5 mg/day

Ensure no transmissible diseases: HBsAg, HIV,

rubella

Try and achieve normal body weight: diet/exercise

Stop drugs : oral hypoglycemic drugs, ACE

inhibitors, beta blockers
Risk of developing DM in
offspring
Type 1 -
Father - 1 in 17 risk
Mother - 1 in 25 risk if, at the time of pregnancy, the
mother is < 25 years of age but a 1 in 100 risk if the
mother is 25 years of age or older.
These risks are doubled if the affected parent developed
diabetes before age 11.
Both parents have type 1 diabetes - 1 in 10 - 1 in 4.
Type 2 polyglandular autoimmune syndrome 50%
Type 2
Single parent - 1 in 7 if the parent was diagnosed before
age 50 and 1 in 13 if the parent was diagnosed after age
50.
There is some evidence that the offspring's risk is greater
when the parent with type 2 diabetes is the mother. I
Conclusion
Gestational diabetes is a common problem in India

Risk stratification and screening is essential in all

Indian pregnant women

Tight glycemic targets are required for optimal

maternal and fetal outcome

Patient education is essential to meet these targets

Long term follow up of the mother and baby is

essential
THANKS