GESTATIONAL DIABETES MELLITUS

GDM- COMPLICATIONS AND
PREVENTION
Dr.Shikha Singh
Associate Professor
Deptt. Og OBGYN
S.N.Medical College
AGRA.

• Pregnancy is characterized by insulin resistance and
hyperinsulinemia. The resistance stems from
placental secretion of diabetogenic hormones
including GH, CRH, hpl, and progesterone, as well as
increased maternal adipose deposition, decreased
exercise, and increased caloric intake.

TWO TYPES:TWO TYPES:
• Preexisting DM and pregnancy
• Gestational diabetes

Diabetes in pregnancy
Pre-existing diabetes Gestational diabetes
Pre-existing diabetes
IDDM
(Type1)
NIDDM
(Type2) True GDM

Preexisting diabetes inPreexisting diabetes in
pregnancypregnancy
• Type 1 DM ( IDDM)
• Type 2 DM (NIDDM)

Preexisting DM inPreexisting DM in
pregnancypregnancy
Effect of pregnancy on pre-existing DM
• Increase requirement for insulin doses
• Nephropathy , autonomic neuropathy may
deteriorate
• Progress in diabetic retinopathy (2X)
• Hypoglycemia
• Diabetic ketoacidosis

Preexisting DM InPreexisting DM In
PregnancyPregnancy
Effect of preexisting DM on pregnancy
(1) Maternal
1. increase risk of miscarriage
2. increase risk of preclampsia
3. increase risk of infection eg vaginal candidiasis,
UTI, endometrial or wound infection
4. increase LSCS rate

PregnancyPregnancy
(2) Fetal
1. increase risk of congenital abnormalities
sacral agenesis, congenital heart disease,
neural tube defects
Hba1c level Risk
normal not increased
<8% 5%
>10% 25 %

PregnancyPregnancy
2. Perinatal mortality (excluding congenital
abnormality ) 2 fold increased
3. Increase risk of sudden unexplained intrauterine
fetal death.

Complications of pregnancy in pre-Complications of pregnancy in pre-
existing DMexisting DM
Maternal:
Increase insulin requirment
Hypoglycemia
Infection
Ketoacidosis
Deterioration in retinopathy
Increased proteinuria+edema
Miscarriage
Polyhydramnio
Shoulder dystocia
Preeclampsia
Increased caesarean rate

Fetal:
Congenital abnormalities
Increased neonatal and perinatal
mortality
Macrosomia
Late stillbirth
Neonatal hypoglycemia
Polycythemia
jaundice

Gestational diabetesGestational diabetes
Definition
Carbohydrate intolerance resulting in hyperglycemia
of variable severity with onset or first recognition
during pregnancy
• This includes women with preexisting but previously
unrecognized diabetes

Diagnostic Criteria forDiagnostic Criteria for
Gestational DiabetesGestational Diabetes

Screening and diagnosis
In general, the test is performed btn 24-28 wk
because at this point in gestation the diabetogenic
effect of pregnancy is manifest and there is
sufficient time remaining in pregnancy for therapy
to exert its effect

• Screening and diagnosis
In general, risk factor includes:
1. age>25y
2. BMI > 25
3. previous GDM
4. Family hx of DM in 1st
degree relative
5. previous macrosomic baby (<4 kg)
6. polyhydramnio
7. large for date baby in current pregnancy
8. previous unexplained stillbirth

Screening
Fasting / random glucose/ glucose challenge
test(50gm)
Diagnosis
Glucose challenge test
(75gm/100gm ?)

• Diagnosis
WHO criteria 1998,
75 gm glucose
fasting 2 hr(mmol/L)
Impaired fasting glucose 6.1-6.9
IGT <or =7 and 7.8-11
DM >or = 7 or > or=11.1

• Incidence
2-9%
more common in Asian and Indian women
In developed countries, increasing trend because of
epidemic of obesity

Clinical significance of GDM
1. High incidence of macrosomia, and adverse
pregnancy outcomes,
2. A significant proportion(30%) identified as GDM in
fact have DM before pregnancy

• Women with glucose intolerance just above normal
range are at low risk for pregnancy complications,
those with more severe glucose intolerance
approaching the criteria of diabetes are at risk of
neonatal complications

Treatment of GDM reduces serious
perinatal morbidity
30
1 1
10
4 3
21
0
10
20
Serious
perinatal
complication
Shoulder
dystocia
Macrosomia
Infants(%)
Intervention
Routine care

Fetal complicationsFetal complications
• Macrosomia (>4 kg)
risk is 16-29% as compared to 10% in control
• Increase in caesarean delivery, instrumental
deliveries ( forceps/vacuum), birth trauma, such as
brachial plexus injuries , clavicular fractures
• Increase in neonatal hypoglycemia (24% ),
hyperbilirubinemia, hypocalcemia, polycythemia
• Children are at risk of type 2 DM and obesity in life

Maternal complicationsMaternal complications
• Increase risk of hypertensive disorders
• Increase risk of caesarean and instrumental
deliveries
• Increased Risk (40-60%) of developing type 2 DM
within10-15 yr.

Outpatient Glucose TargetsOutpatient Glucose Targets
for Pregnant Womenfor Pregnant Women

Glucose Levels for Insulin Initiation in GDM
Fasting plasma glucose ≤105 mg/dL (5.8 mmol/L)
1-hour postprandial plasma glucose ≤155 mg/dL (8.6
mmol/L)
2-hour postprandial plasma glucose ≤130 mg/dL (7.2
mmol/L)
Gestational Diabetes Mellitus (GDM):
Initiation of Insulin
1. ADA. Diabetes Care. 2004;27(suppl 1):S88-90.

• Large randomized study on going
HAPO trial in USA
(Hyperglycemia and Adverse Pregnancy
Outcome study)

Management
• Management similar as preexisting DM
• Need for glucose monitoring
• Start with Diet control
• Commence insulin for poor control
• Delivery plan individualised

• In view of risk of developing type 2 DM
the woman should be screened annually for DM on
yearly basis.

Maternal hyperglycemia
|
Fetal hyperglycemia
|
Fetal pancreatic beta-cell
hyperplasia
|
Fetal hyperinsulinaemia
|
Macrosomia,organomegaly,
polycythaemia, hypoglycemia, RDS

GDM- Can we make aGDM- Can we make a
difference?difference?
• Screening is easy and not costly.
• Interventions are low key for the majority.
• Treatments make a difference.
• Future maternal Type 2 DM can be prevented.
• Future maternal CVS risk can be addressed.
• Family health can influence offspring health.

ManagementManagement
Aim
Achieve maternal near normoglycemic level
to prevent adverse perinatal outcomes

Management ofManagement of
Gestational DiabetesGestational DiabetesAt home:
1. Self-monitoring (BG) 2. Controlled diet 3. Metformin and/or insulin
(6 times daily)
In clinic:
•Blood glucose review (every
2-4 weeks)
•Dietary advice and
medication adjustments
Challenge
Treatment is difficult to
predict
Demanding for patient
and for the NHS

Regular Blood SugarRegular Blood Sugar
monitoringmonitoring

DietDiet
• Low-carbohydrate diet , high fibre with caloric
restriction
• Frequent small snacks may be needed between
meals
• Avoid starvation

Medical nutrition therapy (MNT)Medical nutrition therapy (MNT)
• MNT and lifestyle changes can effectively
manage 80% to 90% of mild GDM cases
• As pregnancy progresses, glucose
intolerance typically worsens; patients
may ultimately require insulin therapy
1. Chitayat, L, et al. Diabetes Technology & Therapeutics. 2009;11:S105-111. 2. ADA. Diabetes Care. 2013;36(suppl 1):S11-66.
3. ADA. Diabetes Care. 2004;27(suppl 1):S88-90. 4. Castorino K, Jovanovic L. Clin Chem. 2011;57(2):221-30.
5. Jovanovic L, et al. Mt Sinai J Med. 2009;76(3):269-80. 6. Mathiesen ER, et al. Endocrinol Metab Clin N Am. 2011;40:727-738.

• MNT nutritional goals and
recommendations:
o Choose healthy low-carbohydrate, high-fiber
sources of nutrition, with fresh vegetables as the
preferred carbohydrate sources
o Count carbohydrates and adjust intake based
on fasting, premeal, and postprandial SMBG
measurements
o Avoid sugars, simple carbohydrates, highly
processed foods, dairy, juices, and most fruits
o Eat frequent small meals to reduce risk of
postprandial hyperglycemia and preprandial
starvation ketosis

• In clinical practice, women often require 1800 to
2500 kcal per day.
• For IBW the caloric requirement is 30 kcal/kg/day;
• overweight, 22 to 25 kcal/kg/day;
• morbidly obese women is 12 to 14 kcal/kg/day
(present pregnant weight).
• underweight, the caloric requirement may be up to
40 kcal/kg/day to achieve recommended weight
gains, blood glucose goals, and nutrient intake

Diabetes in Pregnancy:Diabetes in Pregnancy:
Pharmacologic TherapyPharmacologic Therapy
• When MNT alone fails, pharmacologic therapy
is indicated
o AACE guidelines recommend insulin as the optimal approach1
o Insulin therapy is required for the treatment of T1DM during
pregnancy2
• Metformin and the sulfonylurea glyburide are
the 2 most commonly prescribed oral
antihyperglycemic agents during pregnancy
• Due to efficacy and safety concerns, the ADA
does not recommend oral antihyperglycemic
agents for gestational diabetes mellitus (GDM)
or preexisting T2DM

1. AACE. Endocr Pract. 2011;17(2):1-53. 2. Castorino K, Jovanovic L. Clin Chem. 2011;57(2):221-30.
3. ADA. Diabetes Care. 2004;27(suppl 1):S88-90. 4. Jovanovic L, et al. Mt Sinai J Med. 2009;76(3):269-80.
5. Micronase PI. Pifizer. Division of Pifizer, NY, NY, 2010. 6. Diabeta PI. Sanofi-Aventis U.S. Bridgewater, NJ, 2009.
Medication Crosses
Placenta
Classification Notes
Metformin Yes Category B Metformin and glyburide may be
insufficient to maintain normoglycemia at
all times, particularly during
postprandial periods2Glyburide Minimal
transfer
Some formulations
category B, others
category C

Oral HypoglycemicOral Hypoglycemic
agentsagents
• Implicated as teratogeneic in animal studies esp
first generation sulfonyureas
• In humans, scattered case reports of congenital
abnormality
• Risk of congenital abnormality related to maternal
glycemic control rather than mode of the anti-DM
agents

Oral hypoglycemic agentsOral hypoglycemic agents
• For Type 2 DM patients,
to stop oral hypoglycemic agents and change to
insulin
Reassure that the risk of congenital abnormality due
to drug is small

• Biguanides ( metformin)
• Cat B drug
• Commonly used in Polycystic Ovarian
Disease (PCOD) to treat insulin resistance
and normalize reproductive function
• Not teratogeneic
• Reduce first trimester miscarriage
• 10X reduce gestational diabetes

Sulfonylureas
• 1st
generation drug increase risk of neonatal
hypoglycemia
• 2nd
generation drug (Glyburide) no such effect
and other morbidities .
• Cat C drug
• 4%-20% patients failed to achieve glucose
control with maximum dose of drug
• Increase risk of preeclampsia and need for
phototherapy

Insulin Use During PregnancyInsulin Use During Pregnancy
1. Jovanovic L, et al. Mt Sinai J Med. 2009;76(3):269-80. 2. AACE. Endocr Pract. 2011;17(2):1-53.
3. Castorino K, Jovanovic L. Clin Chem. 2011;57(2):221-30. 4. ADA. Diabetes Care. 2004;27(suppl 1):S88-90.

• ONLY insulin could be considered safe so far
considering below types of insulin:
o Crystal human insulin(Regular)
o Neutral Protaminated Hagedorn (NPH) insulin
o Aspart insulin
o Lispro insulin
DatePresentation title Slide no 47
Control of GDM

Insulin AnaloguesInsulin Analogues
• 1. rapid-acting insulin analogs
(lispro) Cat B
concerns about teratogenesis, antibodies formation,
growth-promoting properties
majority of evidence showed that it does not cross
placenta, and has no adverse maternal or fetal
effects

Insulin AnaloguesInsulin Analogues
2. Long acting analogs
glargine
Cat C drug
Not well studied systemically

1. AJ Farmer et al (2005), Diabetes Care, vol. 28, 11, pp. 2697-
2702
2. ME Larsen et al (2010), J Telemed Telecare, 16, pp.433-440

Healthcare professionals
use the website to:
•Review submitted data
•Automatic prioritization of
patients
•Feedback via text
messages

Patients use the phone app
to:
•Annotate SMBG data with
meal tags, medication doses
and other comments
•Review previous data
graphically
•Request a call back from the
midwife

Real-time managementReal-time management
(GDm-Health)(GDm-Health)

Diabetes in Pregnancy: InsulinDiabetes in Pregnancy: Insulin
Insulin Options Shown to Be Safe During Pregnancy
Name Type Onset
Peak
Effect
Duration
Recommended
Dosing Interval
Aspart
Rapid-acting
(bolus)
15 min 60 min 2 hrs Start of each meal
Lispro
Rapid-acting
(bolus)
15 min 60 min 2 hrs Start of each meal
Regular
insulin
Intermediate-
acting
60 min 2-4 hrs 6 hrs
60-90 minutes
before meal
NPH
Intermediate-
acting (basal)
2 hrs 4-6 hrs 8 hrs Every 8 hours
Detemir
Long-acting
(basal)
2 hrs n/a 12 hrs Every 12 hours
1. Castorino K, Jovanovic L. Clin Chem. 2011;57(2):221-30.
2. Kitzmiller JL, et al. Diabetes Care. 2008;31(5):1060-79.
Following a positive pregnancy test, patients with preexisting
diabetes being treated with insulin or oral antihyperglycemic
medications should be transitioned to one of the above options2

MonitoringMonitoring
• Regular home glucose monitoring with h’stix
• Insulin may be need to be adjusted as gestation
advances
• Hba1c monitoring
• Fetal monitoring with USG
• Refer ophthamologist

DeliveryDelivery
• Timing and mode of delivery individualised
• Intrapartum insulin infusion with glucose monitoring
• no contraindication for Breast feeding either with
insulin or oral hypoglycemic agents

Pre-conceptionPre-conception
CounsellingCounselling
• Allows for optimisation of diabetic control prior to
conception, and assessment of the presence of
complications like hypertension, nephropathy, and
retinopathy
• Should counsel that good control and lower hba1c
lower the risk of congenital abnormalities and
improve outcome
• If necessary, proliferative retinopathy may be
treated with photocoagulation prior to conception
• Contraindications to pregnancy only :ischemic
heart dx, untreated proliferative retinopathy, severe
renal impairment(creatinine>250 mmol/L)

Diabetes and PregnancyDiabetes and Pregnancy
ConclusionConclusion
(1) Preexisting DM in pregnancy
• Good glucose control is important for decreasing
morbidities
• Insulin is still the gold standard of tx in pregnancy
• Increasing evidence for clincial effectiveness for
treatment with oral hypoglycemic agents

Diabetes and pregnancyDiabetes and pregnancy
conclusionconclusion
(2) Gestational diabetes
• The morbidities increases as glucose level
approaching the diagnosis as DM
• Possible that treatment improves outcomes
• Overlap with preexisting DM, esp type2
• Long term implication for health of the
mother and baby

• GDM is common.
• Dietary intervention works.
• Breast feeding should be encouraged.
• Diabetes post GDM is a public health concern
but can be prevented.
• Metabolic syndrome and future CVS risk post
GDM is a public health concern and requires
F/U.
• A strong screening programme is essential.
• Integrated care is required.

Plan of presentationPlan 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

IntroductionIntroduction
 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

• Gestational diabetes (GDM) is defined as any
degree of impaired glucose tolerance of
with onset or first recognition during
pregnancy .
o Many are denovo pregnancy induced
o Some are type 2 ( 35-40%)
o 10% have antibodies

• Difficult to distinguish pregestational Type 2 DM and
denovo GDM
o Fasting hyperglycemia
o blood glucose greater than 180 mg/dL on OGT
o acanthosis nicgrans
o HbA1C > 5.3%
o a systolic BP > 110 mm Hg
o BMI > 30 kg/m2
o Fetal anomalies
• Clues for Type 1
o Lean
o DKA during pregnancy
o Severe hyperglycemia with large doses of insulin

Fuel metabolism inFuel metabolism in
pregnancypregnancy

Fuel metabolism inFuel metabolism in
pregnancypregnancy
• Goal is uninterrupted nutrient supply to fetus
• The metabolic goals of pregnancy are
o 1) in early pregnancy to develop anabolic stores to meet metabolic
demands in late pregnancy
o 2) in late pregnancy to provide fuels for fetal growth and energy needs.

Glucose metabolism inGlucose metabolism in
pregnancypregnancy
 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 inGlucose metabolism in
pregnancypregnancy
Fetus
Fat
Glucose Aminoacids
Insulin resistance Hyperinsuli
nemia
FASTING
accelerated
starvation and
esxaggerated
ketosis
(maternal
hypoglycemia,
hypoinsulinemia,
hyperlipidemia,
and
hyperketonemia)
FED
hyperglycemia,
hyperinsulinemia,
hyperlipidemia,
and reduced
tissue sensitivity
to insulin

• 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

EPIdemiology AND RiskEPIdemiology AND Risk
factorsfactors

Magnitude of problem:Magnitude of problem:
GlobalGlobal
• 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 problemMagnitude of the problem
- India- 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 factorsRisk 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 and Fetal risksMaternal and Fetal risks

Maternal complicationsMaternal 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

MaternofetalMaternofetal
complicationscomplications
• 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 complicationsNeonatal 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 anomaliesCongenital 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
o Caudal regression syndrome
o Neural tube defects excluding anencephaly
o Anencephaly with or without herniation of neural elements
o Microcephaly
• Cardiac
o Transposition of the great vessels with or without ventricular
o Ventricular septal defects
o Coarctation of the aorta with or without ventricular septal defects or patent ductus
arteriosus
o Atrial septal defects
o Cardiomegaly
• Renal anomalies
o Hydronephrosis
o Renal agenesis
o Ureteral duplication
• Gastrointestinal
o Duodenal atresia
o Anorectal atresia
o Small left colon syndrome

SCREENING ANDSCREENING AND
DIAGNOSISDIAGNOSIS

Whom to screen ?Whom to screen ?
• No consensus
o 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

To satisfy all these criteriaTo satisfy all these criteria
 Age <25 yearsAge <25 years
 Not a member of an ethnic group with high prevalence of GDMNot 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 toleranceNo history of abnormal glucose tolerance
 No history of poor obstetric outcomeNo history of poor obstetric outcome
Low risk for GDMLow risk for GDM

High riskHigh risk
• Marked obesity
• Prior GDM (30-50% risk for recurrence)
• Glycosuria
• Strong family history

When and how to screen?When and how to screen?
• 24-28 weeks
• High risk
o First prenatal visit
• 50 g glucose loading test
• High risk women – 3 hr GTT with 100 g glucose

50 g GTT50 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

100 g GTT100 g GTT
 Oral glucose tolerance test ( OGTT) with 100 gm
glucose
 Overnight fast of at least 8 hoursOvernight fast of at least 8 hours
 At least 3 days of unrestricted diet and unlimitedAt least 3 days of unrestricted diet and unlimited
physical activityphysical activity
 >> 2 values must be abnormal2 values must be abnormal
FastingFasting > 95 mg/dl> 95 mg/dl
1-h1-h > 180 mg/dl> 180 mg/dl
2-h2-h > 155 mg/dl> 155 mg/dl
3-h3-h > 140 mg/dl> 140 mg/dl

75 g GTT75 g GTT
FastingFasting >> 95 mg/dl95 mg/dl
1-h1-h >> 180 mg/dl180 mg/dl
2-h2-h >> 155 mg/dl155 mg/dl
FastingFasting >> 95 mg/dl95 mg/dl
OROR
2-h2-h > 140 mg/dl> 140 mg/dl
ADAADA WHOWHO

Whom and when to screen? IndianWhom and when to screen? Indian
Scenario -The DIPSI GuidelinesScenario -The DIPSI Guidelines
• 75 gm GCT with single PG at 2 hrs –
o ≥ 140 mg/dL is GDM
o ≥ 120 mg/dL is DGGT
• Universal screening
• First trimester, if negative at 24 – 28 weeks and then
at 32 – 34 weeks

Management of gdmManagement of gdm

MANAGEMENT ISSUESMANAGEMENT ISSUES
• Patient education
• Medical Nutrition therapy
• Pharmacological therapy
• Glycemic monitoring: SMBG and targets
• Fetal monitoring: ultrasound
• Planning on delivery

Medical nutrition therapyMedical nutrition therapy
• Goals
o Achieve normoglycemia
o Prevent ketosis
o Provide adequate weight gain
o Contribute to fetal well-being
• Nutritional plan
o Calorie allotment
o Calorie distribution
o CH2O intake

Calorie allotmentCalorie 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 intakeCarb 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%).
•

Calorie distributionCalorie distribution
• Variable opinion
• Most programs suggest three meals and three
snacks; however, in overweight and obese women
the snacks are often eliminated
o 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.
o Lunch — 30% of total calories
o Dinner — 30% of total calories
o Snacks — Leftover calories (approximately 30% of
total calories) are distributed, as needed, as

Monitoring BGMonitoring BG
• Atleast 4 times
o Fasting and 3 one hr postprandial
• Pre vs postprandial monitoring
o Better glycemic control (HbA1c value 6.5 versus 8.1 percent)
o A lower incidence of large-for-gestational age infants (12 versus 42
percent)
o A lower rate of cesarean delivery for cephalopelvic disproportion (12
versus 36 percent)

Monitoring BGMonitoring BG
• Home monitoring
o Maintain log book
o Use a memory meter
o Calibrate the glucometer frequently
• HbA1C
o Ancillary test for feedback to the patient
o 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
o 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

Glycemic targets (ACOG)Glycemic targets (ACOG)
• ACOG
o Fasting venous plasma ≤ 95 mg/dl
o 1 hour postprandial ≤ 140 mg/dl
o 2 hour postprandial ≤ 120 mg/dl
o Pre-meal ≤ 100 mg/dl
o A1C ≤ 6%
• ADA
o premeal 80-110
o 2 hr postmeal not more than 155
These are venous plasma targets, not glucometer targets

PHARMACOLOGICALPHARMACOLOGICAL
INTERVENTIONINTERVENTION
• If the FPG at diagnosis is ≥ 120, can consider
immediate therapy.
• Otherwise, MNT for 2 weeks
o If majority FPG (4/7) > 95 or PP > 120 then to start on insulin.

InsulinInsulin• ≈ 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.
o Total 0.7 unit/kg up to week 18
o 0.8 unit/kg for weeks 18 to 26
o 0.9 unit/kg for weeks 26 to 36
o 1. unit/kg for weeks 36 to term.

OHA in pregnancyOHA in pregnancy
• Systematic review by John Hopkins University
o maternal glucose levels did not differ substantially between gravidae
treated with insulin versus those treated with oral glucose-lowering agents
o 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 pregnancyOHA in pregnancy
• Tolbutamide and chlorpropamide
o Cross placenta. Fetal hperinsulinemia. Prolonged fetal hypoglycemia
• Glibenclamide
o Minimal transplacental transport
o Observational studies – no excess anomalies or hypoglycemia
o 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 pregnancyOHA in pregnancy• Metformin
o Category B
o No adverse outcome after first trimester
o Second, third trimester safe and effective
o Vs. insulin – no serious adverse effects
o No studies vs. glibenclamide
• Acarbose
o Two prelim studies
• Thiazolidinediones and GLP-1
o Not studied

Obstetric managementObstetric management

Fetal monitoringFetal 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 deliveryTiming 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 deliveryManagement 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 labourGlycemic 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 upPost 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 neonateImmediate 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 infantAnticipate and treat hypoglycemia in the infant

Management of neonateManagement 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

Future risks in mother andFuture risks in mother and
childchild

Future risks - MotherFuture risks - Mother
• Atleast 6 weeks post delivery, 75 g OGTT for all GDM
• ≥ 90% normoglycemic
• Recurrence of GDM – 30-60%
o Older
o Multipara
o Weight gain interpregnancy
o Higher infant BW in index pregnancy
• IGT and T2DM
o 20% IGT postpartum
o 3.7% @ 6m , 4.9% @ 15m and 18.9% @ 9 y

Who will progress to DM?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 counsellingPreconception 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 inRisk of developing DM in
offspringoffspring
• Type 1 -
o Father - 1 in 17 risk
o 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.
o These risks are doubled if the affected parent developed
diabetes before age 11.
o Both parents have type 1 diabetes - 1 in 10 - 1 in 4.
• Type 2 polyglandular autoimmune syndrome – 50%
• Type 2
o 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.
o There is some evidence that the offspring's risk is greater
when the parent with type 2 diabetes is the mother. I

ConclusionConclusion
• 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

GESTATIONAL DIABETES MELLITUS

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