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
Definition

 it is a chronic metabolic disorder

(Carbohydrate, fat, protein metabolism)
characterized by hyperglycemia
resulting from either relative deficiency
of pancreatic insulin production,
ineffective use of insulin in the cellular
level.
Incidence

 About 1-4% all pregnancies and 90% out

of them are GDM
 50% of women with GDM will become
Overt Diabetic (Type 2) over period of 5-
20 year.
Classification
Classification Characteristic Treatment
Type I: Insulin Juvenile ,Onset, Diet control and
dependent PRONE TO insulin
DM(IDDM) Ketosis, pancreatic
B cells do not produce
insulin
Type II: Non Insulin Adult onset pancreatic Diet control and
dependent DM B cells in Islets of insulin Therapy
(NIDDM) Langerhans unable to
meet increased
demand of insulin
overtime or in time of
stress.
Type III: Gestational During pregnancy in Diet control alone or
DM (GDM) which carbohydrate diet control and
intolerance that insulin therapy.
develop during
pregnancy regardless
of severity.
Types of DM in pregnancy
1. pre-gestational DM
a. Type I (IDDM)
b. Type II(NIDDM)

2. Gestational DM
3. Overt DM -(plasma glucose level ≥200
mg/dl) may be preexisting or first time
during pregnancy
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 hyperinsulinemi
esxaggerated Insulin resistance Hyperinsuli a,
ketosis nemia hyperlipidemia,
(maternal and reduced
hypoglycemia, Glucose Aminoacids tissue sensitivity
hypoinsulinemia to insulin
, 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
Pathogenesis of pregestational
DM
Pathophysiology of GDM
Cont..
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
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
federal standards for laboratory testing.
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 22.
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 percent of
women with GDM will achieve normoglycemia.
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% of total
calories) are distributed, as needed, as snacks.
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
 Glycosylated protein and fructosamine widely variable and
not yet established
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
insulin resistance of pregnancy and obesity.
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 teratogenic
in rat models
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
5–15 % optimally controlled GDM

 Starts when the cord is clamped

 Exaggerated insulin release secondary to

pancreatic ß-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
 Both parents - 1 in 2.
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