Gestational Diabetes Mellitus

Dr. Hema Divakar

Dr. Seshiah V

Dr. Susheela Rani B S

Introduction

The prevalence of obesity, diabetes, and impaired glucose tolerance (IGT) in the general

population is increasing and with an earlier onset. This means that even young adults in the

reproductive age are diabetic and even more are becoming diabetic during pregnancy. The

adverse health impact of Gestational Diabetes Mellitus is not limited to mother and her fetus in

the current pregnancy. Apart from the increased risk of developing Type 2 diabetes in the mother

and metabolic syndrome in subsequent years, the intrauterine programming of this fetus places it

at a high risk of developing diabetes, obesity and metabolic syndrome in later life. Identifying

and treating gestational diabetes plays a key role in the primary prevention of Diabetes.

Definition

Gestational Diabetes is any degree of glucose intolerance with onset or first recognition during

pregnancy’. The definition is applicable even if the condition persists after pregnancy. It does not

exclude the possibility that unrecognized glucose intolerance may have antedated or begun

concomitantly with the pregnancy.

Prevalence

The prevalence rate of diabetes during pregnancy varies between 3% and 15% of pregnancies

based on the background rates of diabetes. Almost 90% of all cases of diabetes during pregnancy
are gestational diabetes. The prevalence of GDM1 in urban area is 17.8% , Semi-urban area Commented [S1]: Seshiah V, Balaji V, Madhuri S Balaji,
Panneerselvam A, Kapur A. Pregnancy and Diabetes Scenario
around the World: India. International Journal of Gynaecology &
is13.8% and in rural area 9.9% respectively. The average prevalence of GDM irrespective of Obsteterics 2009 Mar; 104 suppl 1: S35-8.

area is 13.4%. The risk factors are Age ≥ 25 years, BMI >25 and family history of diabetes

Diagnosis

The earlier diagnostic thresholds (O’Sullivan and Mahan, NDDG, Carpenter & Coustan) were

based on data from women who were diagnosed with diabetes after gestation and not on any

short-term adverse pregnancy outcomes. The results of the Hyperglycemia and Adverse

Pregnancy Outcome (HAPO) and Australian Carbohydrate Intolerance Study in Pregnant

Women2 (ACHOIS) studies indicate that maternal glucose levels much lesser than those used to

diagnose diabetes were associated with maternal and perinatal problems. The International

Association of Diabetes and Pregnancy Groups3 (IADPSG) proposed a new set of criteria. A

diagnosis of GDM is made if one value of plasma glucose concentration is equal to or exceeds

the thresholds of 92, 180 and 153 mg/dl (for fasting, one-hour and 2-hour post glucose load

glucose values respectively), after performing a 75 g OGTT. Though one value is recommended,

it is mandatory to perform OGTT. A cost-utility analysis found that screening based on IADPSG

criteria was not cost effective4

Disadvantages of the IADPSG criteria: In this HAPO study, on which IADPSG criteria is

based did not include population from India, China, South Asian countries (except city of

Bangkok, Hong Kong), Middle East and Sub Saharan countries. Thus HAPO is ethnically

Caucasian based study.

Generally pregnant women do not visit antenatal clinic in a fasting state because of

commutation and a belief not to fast for long hours. For a pregnant woman, the request to attend

fasting for a blood test may not be realistic because of the long travel distance to the clinic in

many parts of the world, and increased tendency to nausea in the fasting state. Consequently

nonfasting testing may be the only practical option5. The dropout rate is very high when a

pregnant woman is asked to come again for the glucose tolerance test. In all GDM, FPG values

do not reflect the 2-hour post glucose with 75 g oral glucose, which is the hallmark of GDM.

Ethnically Asian Indians have high insulin resistance and as a consequence, their 2-hour PG is

higher compared to Caucasians. The insulin resistance during pregnancy escalates further and

hence FPG is not an appropriate option to diagnose GDM in Asian Indian women. Asian and

South Asian ethnicity are both independently associated with increased insulin resistance in late

pregnancy. A diagnostic FPG was present in only 24% of those with GDM in Bangkok and 26%

in Hong Kong.

DIPSI test –A single test to diagnose GDM (Diabetes in Pregnancy Study Group India6

Procedure

In the antenatal clinic, a pregnant woman after undergoing preliminary clinical examination, has

to be given a 75 g oral glucose load, irrespective of whether she is in the fasting or non-fasting

state and without regard to the time of the last meal. A venous blood sample is collected at 2

hours for estimating plasma glucose by the GOD-POD method. GDM is diagnosed if 2-hour PG

is ≥ 140 mg/dL . If 75 g glucose packet is not available, remove and discard 5 level teaspoons

(not heaped) of glucose from a 100 g packet which is freely available. Performing this test in the

non-fasting state is rational, as glucose concentrations are affected little by the time since the last
meal in a normal glucose tolerant woman, whereas it will, in a woman with gestational diabetes.

After a meal, a normal glucose tolerant woman would be able to maintain euglycemia despite

glucose challenge due to brisk and adequate insulin response, whereas, in a woman with GDM

who has impaired insulin secretion, the glycemic level increases with a meal and with glucose

challenge, the glycemic excursion exaggerates further. This cascading effect is advantageous as

this would not result in false-positive diagnosis of GDM.

This single-step procedure serves both as screening and diagnostic procedure and has been

approved by Ministry of Health, Government of India and also recommended by the new WHO

criteria (2013).

DIPSI diagnostic criteria 2-hour PG ≥ 140 mg/dL is similar to WHO criteria 2-hour PG ≥ 140

mg/dL to diagnose GDM, the only difference being DIPSI test does not require pregnant woman

to be in the fasting state.

Selective versus universal screening

Countries in South Asia have shown a high prevalence of Diabetes and universal screening of all

pregnant women is required. According to new recommendations all women should be screened

for GDM, even if they have no symptoms7.

Gestational age at Screening

DIPSI guidelines recommend screening once in the first trimester to look for Pregestational

Diabetes and if normal, again at 24-28 weeks and 32-34weeks of pregnancy.

Pathophysiology of Gestational Diabetes

As a result of increase in estrogens and progesterone in the first half of pregnancy, there is β cell

hyperplasia and increased insulin secretion by the mother. This results in increased peripheral

glucose utilization and glycogen storage and a reduced glucose production. In the second and

third trimester progressive increase of cortisol and placental hormones like Human Placental

Lactogen, Prolactin and Human Somatommaotropin, there is an increase in insulin resistance

which is three times normal. The result of these adjustments is a ‘diabetogenic’ effect resulting in

reduction of glycogen stores, increased hepatic glucose production. At this time a facilitated

anabolism during feeding co-exists with an accelerated starvation during fasting. This stimulates

the maternal system to use other sources, other than glucose for its functioning. Free fatty acids

whose levels have increased due to the Insulin resistance provide the fuel for maternal

functioning while glucose is preferentially diverted to the fetus by a process of simple diffusion.

Pancreatic cells increase their insulin secretion to meet the demands due to increased insulin

resistance. Thus, despite large changes in Insulin sensitivity, maternal blood glucose levels

remain normal.

GDM results when the insulin secretion is unable to match the insulin resistance of pregnancy.

Risk Factors

The most common risk factors include:

 Maternal Age >35yrs,

 Macrosomia (birth weight >90th centile) in a previous pregnancy

 Member of an ethnic group with a higher rate of type II diabetes. Asians especially from

South Asia, African Americans, Hispanics, Native Americans

  Polycystic ovarian syndrome

 Pregnancy-related hypertension

 History of spontaneous abortions and unexplained stillbirths

 Family history of diabetes (especially in first-degree relatives)

 Being overweight, obese or severely obese GDM in a previous pregnancy

 Genetic risk factors

It is important to note that no known risk factors are identified in 50% of GDM women.

Complications of GDM

Effects on the Mother

Hypertensive disorders of Pregnancy

At least 20% of pregnant diabetic women will develop Gestational Hypertension and/or

preeclampsia, with the most at-risk patients being those with underlying microvascular

complications, pre-existing hypertension, or poor glycemic control. Glycemic control,

particularly during the first half of pregnancy, is a strong predictor of preeclampsia in women

with type 1 diabetes mellitus

Cesarean Section and Instrumental Deliveries

GDM is a risk factor for cesarean sections and operative deliveries and is associated with

cesarean delivery rate of up to approximately 30%.

Long term Morbidity

Recurrence in subsequent pregnancies GDM recurrence rate is 30-84% based on the

ethnicities and GDM diagnostic criteria used.

Type 1 and Type 2 Diabetes

20% to 30% of women with GDM will develop T2DM8 within the first 5 years postpartum. Risk

factors are BMI, weight gain after pregnancy, family history of diabetes, fasting and post

challenge glucose levels during and after pregnancy, postpartum insulin resistance and βcell

secretion, and the need for pharmacological treatment during pregnancy.

Cardiovascular disease and Metabolic syndrome

Women with GDM show numerous cardiovascular risk factors such as abdominal obesity,

insulin resistance, abnormal glucose tolerance, dyslipidemia, high blood pressure, metabolic

syndrome, impairments of endothelial dysfunction and inflammation markers9. Their risk for

developing CV disease is increased 1.7 folds.

Effects on the Fetus

Each fetal islet cell functions as an endocrine organ appears at 11th week of gestation recognises

and responds to maternal glycemia at 15-16 weeks of gestation. Thus when fetuses are

exposed to increased amniotic fluid glucose around these weeks of gestation, the

metabolic perturbations are underway and earlier screening and intervention is

recommended. After 20 weeks’ gestation, the fetus has a functioning pancreas and is

responsible for its own glucose homeostasis. Most, but not all, of the fetal and neonatal sequelae

of diabetes during gestation are a function of maternal glycemic control. This concept has its

ontogeny in the Pedersen hypothesis, which states that maternal hyperglycemia results in fetal

hyperglycemia. Unchecked fetal hyperglycemia results in hypertrophy of fetal pancreatic islets

and hyperinsulinemia. The pathologic conditions in the late gestation fetus and newborn IDM are

the result of fetal hyperglycemia, hyperinsulinemia, or the combined effects of the two.

Diabetes during the periconceptional period.

Miscarriage

Uncontrolled Diabetes is associated with double the incidence of miscarriage. The incidence of

miscarriage increases linearly with the blood sugars, with an incidence of 44% in women with

HbA1C >11%. Conversely, excellent glycemic control normalizes the miscarriage rate.

Birth defects

Pregestational diabetes which is poorly controlled in the peri-conceptional period is associated

with increased congenital anomalies 10 (Table 1). In women with overt diabetes and suboptimal

glycemic control before conception, the likelihood of a structural anomaly is increased 4- to 8-

fold.. Two-thirds of birth anomalies involve the cardiovascular and central nervous systems.

Neural tube defects occur 13-20 times more frequently in diabetic pregnancies, and

genitourinary, gastrointestinal, and skeletal anomalies are also more common.

Meticulous preconceptional care to control sugars have shown reduce the incidence of

congenital abnormalities to that of non-diabetic population

Chromosomal abnormalities

Some women who develop gestational diabetes may have underlying biochemical changes that

induce nondisjunction and the development of chromosomal defects. Women with gestational

diabetes are 7.7 times as likely to have an infant with a numeric sex chromosome defect as those

without gestational diabetes11.

The effect of maternal diabetes on the developing fetus

Growth restriction

This is a feature of pregnancies associated with type 1 diabetes and vascular disease.

Specifically, pregnant patients with diabetes-associated retinal or renal vasculopathies and/or

chronic hypertension are most at risk for growth restriction.

Macrosomia

The potent combination of fetal hyperinsulinemia, a major anabolic hormone, and

hyperglycemia, a major anabolic fuel, results in a striking increase in fat stores and a modest

increase in protein stores. Hepatomegaly, splenomegaly, and cardiomegaly (caused by

intraventricular septal hypertrophy) are particularly prominent. Macrosomia by definition is birth

weight above 4000-4500g, regardless of the gestational age. The incidence of Macrosomia is

increased 3 fold in diabetic women in comparison to non- diabetic and occurs in 15-45% of

babies born to diabetic women. With increasing postprandial glucose values there is an increase

in the macrosomia rate. Neonates of diabetic mothers have a larger shoulder and extremity

circumference, a decreased head-to-shoulder ratio, significantly higher body fat, and thicker

upper extremity skin folds compared with non-diabetic control infants of similar weights. Birth

injury, including shoulder dystocia and brachial plexus trauma, are more common among infants

of diabetic mothers, and macrosomic fetuses are at the highest risk. Macrosomia is associated

with a 5-fold higher rates of severe hypoglycemia and a 2-fold increase in neonatal jaundice

relative to infants of mothers without diabetes12..

Intrauterine Fetal Demise

Fresh still birth, Intrauterine death, common features in diabetic pregnancies earlier, are now rare

complications of diabetic pregnancy. Good glycemic control and better fetal monitoring have

drastically reduced fetal loss. One of the mechanisms that could cause fresh still birth is fetal

hyperglycemia causing fetal hyper insulinemia. The resulting need for increased oxygen

consumption may be unmet in some leading to fetal hypoxia and acidosis. Another mechanism

could be reduced uteroplacental perfusion due to maternal vasculopathy giving rise to fetal

growth restriction.

Neonatal effects

Hypoglycemia

The newborn IDM undergoes a sudden interruption of glucose delivery in the postpartum period,

which, when accompanied by high neonatal insulin levels, results in neonatal hypoglycemia. Up

to 50% of IDMs experience significant hypoglycemia after birth. Hypoglycemia is more

common in macrosomic or growth-retarded IDMs than in IDMs who are of appropriate size for

gestational age. The nadir in the IDM’s blood sugar usually occurs between 1 and 3 hours of life.

Neonatal Hypocalcemia and Hypomagnesaemia

Hypocalcemia and hypomagnesemia occur within the first 72 hours of birth in up to 50% of

IDMs. Abnormalities in calcium metabolism most likely represent a delayed transition from fetal

to neonatal parathyroid control.

Polycythemia defined as hemoglobin concentrations more than 20 g/dL and hematocrit levels

more than 65%, is present in 20% to 30% of IDMs at birth.

Bilirubinemia
IDMs are at increased risk for hyperbilirubinemia because of an expanded red cell mass,

ineffective erythropoiesis, and relative immaturity of hepatic bilirubin conjugation and excretion.

Respiratory Disease Syndrome (RDS)

IDMs are more likely to have respiratory symptoms in the newborn period from either RDS

(surfactant deficiency) or retained fetal lung fluid (transient tachypnea of the newborn) after

operative delivery. They are more prone to developing RDS than neonates born to mothers

without diabetes. This increased risk persists until approximately 38 weeks’ gestation. RDS

occurs more frequently in IDMs because of later onset of maturity of the type II alveolar cells

leading to surfactant deficiency.

Neurologic function

IDMs can present with acute neurologic abnormalities secondary to CNS dysfunction which can

occur as a result of perinatal asphyxia, glucose and electrolyte abnormalities, polycythemic

vascular sludging, and birth trauma. Cerebral symptoms may include seizures, jitteriness,

lethargy, changes in tone, and movement disorders.

Long term effects on the Offspring

Offspring of diabetic mothers have been shown to have increased incidence of Diabetes, Obesity,

Cardiovascular risk and neuro-behavioral problems in childhood and adolescence.

Management during pregnancy

If the diagnosis of GDM is established in the first trimester, an estimation of HbA1C will throw

light on the glycemic status in the peri-conceptional period. Additional investigations include,
  Blood urea nitrogen (BUN), Serum Creatinine, Protein-to-creatinine ratio to evaluate

Renal function

 Fundoscopic examination for Retinopathy

 Thyroid-stimulating hormone

 Plasma Sugars or Capillary blood sugar by using plasma glucose standardized

Glucometers

 Serum screening for Aneuploidy

Biochemical screening for Aneuploidy and NTD

Levels of MSAFP, unconjugated estriol (uE3), and inhibin A, which are components of some

second trimester Down syndrome screening tests, are significantly reduced in women with

diabetes, thereby mimicking the pattern suggestive of Down syndrome. Therefore, MoM

values should be adjusted in women with diabetes13.

Ultrasonography

 First trimester - Ultrasonographic assessment for pregnancy dating and viability.

 Second trimester - Detailed anatomic ultrasonogram at 18-20 weeks and a fetal

echocardiogram if the blood sugars were elevated in the first trimester

 Third trimester –

From 28 weeks’ gestation on, progressive growth is monitored using fetal biometry,

 in women with diabetic vascular disease to detect growth restriction

 in other group of diabetic patients to detect LGA fetuses

Abdominal circumference is the best parameter which correlates with the nutritional state of

the fetus. Abdominal circumference more than 75th centile and a rising trend in the fetal

growth pattern of scans done at 24-27weeks and at 28-31 weeks predict fetal macrosomia14.
Doppler studies are not useful for macrosomic fetuses seen in GDM and their role is restricted

to GDM pregnancies with growth restricted fetuses.

Monitoring Glycemic Control

The main focus of treatment in a woman with GDM is achieving glycemic control. A 2-hour

post-meal monitoring is as the fetus is more sensitive to postprandial excursions of glucose than

fasting hyperglycemia

Target:

Mean plasma glucose (MPG) level ~105–110 mg/ dL

FPG ~90 mg/dL

2-hour postprandial peaks ~120 mg/dL

Monitoring based on Fetal growth

Recent studies15 have shown that GDM management predominantly based on fetal growth

provided the same perinatal outcome as management based on strict glycemic control. Instead of

administering Insulin to all women who qualified to receive it, it was withheld in women with

normal fetal growth; even though their glucose levels would have qualified them for insulin

under standard care. There was no adverse outcome, but the ultrasound approach reduced the

SGA ( due to over correction of the glycemic status) rate by more than half.

SMBG Self-measurement of blood glucose levels (SMBG) by finger stick measurement is the

mainstay of glucose monitoring. This technique of glucose monitoring is simpler, accessible and
therefore possible in all women. If SMBG is not possible, laboratory venous plasma glucose has

to be estimated.

Frequency of glucose monitoring: Though it would be ideal to estimate glucose levels 7 times

a day, a more practical method would be a staggered assessment of 2-3 glucose estimations per

day with fasting, post breakfast, post lunch, post dinner and 3am.

Continuous Glucose Monitoring (CGM) measures interstitial glucose levels in subcutaneous

tissue within a range of 50-400 mg/dl. Unlike SMBG which gives a snapshot of glucose profile,

CGM monitors glucose every 5 min and can accurately detect high postprandial blood glucose

levels and nocturnal hypoglycemic events that may go unrecognized by intermittent blood

glucose monitoring.

Treatment

Medical Nutrition Therapy

Diet

Most of the women with GDM are managed with diet alone. Diet is modified in such way that

excess weight gain and postprandial hyperglycemia are avoided while providing adequate

nutrition to the mother and fetus. Caloric composition includes 40-50% from complex, high-fiber

carbohydrates, 20% from protein, and 30-40% from primarily unsaturated fats. The calories may

be distributed 10-20% at breakfast, 20-30% at lunch, 30-40% at dinner and 30% with snacks,

especially a bedtime snack in order to reduce nocturnal hypoglycemia. Food for the day is

distributed in 3 small meals and 3 snacks. Typically, breakfast is split into two equal halves taken

at an interval of 2 hours since insulin resistance is found to be highest in the mornings.

Weight gain

The Fifth International Workshop-Conference on GDM recommends a relatively small gain

during pregnancy of 7 kg (15 lb) or more for obese women (BMI ≥ 30 kg/m2) and a

proportionally greater weight gain (up to 18 kg or 40 lb) for underweight women (BMI < 18.5

kg/m2) at the onset of pregnancy. It is important to record pre-pregnancy height and weight,

charting women’s weight gain throughout pregnancy, and sharing the results with them so they

are aware of their progress towards weight gain goal.

Exercise

Since GDM is associated with Insulin resistance and Insulin resistance is known to improve with

physical activity, it is prudent to assume that exercise is the most suitable intervention for women

with GDM. ACOG and ADA recognize exercise as “a helpful adjunctive therapy” for GDM and

suggest 30 minutes or more of moderated exercise a day on most, if not all, days of the week.

Thus, in the short term, exercise could help avoid insulin or reduce its dosage while in the long

term it can provide a healthy lifestyle with its added benefits.

Pharmacotherapy

A. Insulin. If the glucose levels at diagnosis of diabetes are FPG >120mg/dL and/or 2 hour PPG

>200mg/dL Insulin is started along with MNT. Insulin is also indicated in women with GDM in

whom MNT after 2 weeks of initiation is ineffective in maintaining target glucose levels. Some

studies16 recommend starting insulin therapy when the fetal abdominal circumference (AC)

measured by ultrasound is higher than the 75th percentile for gestational age. Fetal AC as a

measure for insulin initiation should be used in conjunction with GDM severity parameters and

level of glycemic control throughout pregnancy.

Initiating Insulin

Preferable to start with Premix insulin 30/70 of any brand*

Starting dose: 4 units before breakfast

Every 4th day increase 2 units till 10 units

If FPG remains > 90 mg/dL advise → 6 units before breakfast and 4 units before dinner

Review with blood sugar test → Adjust dose further

Total insulin dose per day can be divided as two-thirds in the morning and one-third in the

evening.

*Initially if post-breakfast plasma glucose is high → Start Premix 50/50

If GDM is diagnosed in the third trimester; MNT is advised for a week. Insulin is initiated if

MNT fails.

If 2-hour PG > 200 mg/dL at diagnosis, a starting dose of 8 units of Premixed insulin could be

administered straightaway before breakfast and the dose has to be titrated on follow-up.

Human Insulins are the most extensively studied and favored Insulins. Regular insulin has

some drawbacks. It starts its action from 30 to 60 min after subcutaneous injection and it

peaks too late (2-3 h after injection) to be very effective in postprandial control. Also, it lasts

too long (duration of 8-10 h), with an increased risk of postprandial hypoglycemia. Insulin

analogues are useful in reducing the risk of hypoglycemia, mainly during the night, and in
 promoting a more physiologic glycemic profile in pregnant women with diabetes. Insulin

Lispro and Aspart have been approved for use in pregnancy.

Insulin administration: Conventionally, there are two methods for administering insulin:

subcutaneous multiple daily injections (MDI) and continuous subcutaneous insulin infusion

pump (CSII). Insulin Pens provide convenience and ease of use. The dosing is more accurate.

31G pen needles and shorter (4mm) needles have overcome some of the barriers for insulin use

thereby increasing the acceptability of Insulin therapy.

B. Oral Antidiabetic agents

Though Insulin is the perfect pharmacologic agent for treatment of GDM, it is not the preferred

agent always. The use of insulin is often associated with hypoglycaemia and increased weight.

Moreover, this treatment is inconvenient and expensive because it requires refrigerated storage

and skilled handling, which are not always available in low-resource countries. Oral alternatives

to insulin that achieve similar glycemic control without these drawbacks17 include Glyburide

Metformin and Acarbose. Glyburide, a sulfonyl urea which does not cross the placenta in

significant amount, increases insulin secretion and decreases insulin resistance by reducing

glucose toxicity. The starting dose is 2.5 mg orally in the morning increased by 2.5mg to a

maximum total dose of 20mg/day. Glyburide is as effective as Insulin in achieving glycemic

targets with comparable pregnancy outcomes.

Acarbose an oral α – glucosidase inhibitor is used in the dosage of 25mg three times daily to a

maximum of 300mg/day. Use is associated with high frequency of abdominal cramping.

Metformin, a biguanide, is an “insulin sensitizer” that increases tissue sensitivity to insulin

without increasing insulin production, thereby minimizing the risk of hypoglycemia. Since

Metformin crosses the placenta there were concerns about possibilities of fetal abnormalities.

The cornerstone Metformin in Gestational Diabetes18 (MiG) a prospective study of women with

mild GDM randomly assigned to metformin or insulin, demonstrated no increase in perinatal

complications compared with insulin.

Regulatory authorities around the globe have not approved any oral anti-diabetic agents for use

in GDM.

Antepartum fetal surveillance

GDM managed with Diet and exercise with well controlled sugars and no other risk factors are

monitored similar to non-diabetic women with no risk factors19. All other GDM need intense

monitoring.

Management of Preterm labour

Women who have spontaneous preterm labour ( 24- 34weeks) are given antenatal

glucocorticoids. All women with GDM will experience hyperglycemia despite ongoing care and

increases in insulin administration. Increasing the dose of insulin earlier i.e. when the steroids are

administered as opposed to waiting for glucose levels to deteriorate, may prevent the increase in

serum glucose levels. Among tocolytics used for the management of preterm labour

betamimetics are best avoided as they are known to cause hyperglycemia.

Timing of delivery
Elective cesarean section for suspected macrosomia results in a high number of unnecessary

procedures, and early induction of labor to limit fetal growth may result in a substantial increase

in the cesarean section rate because of failed inductions. Pregnancies complicated by fetal

macrosomia are best managed expectantly. When labor fails to progress as expected, the

possibility of fetopelvic disproportion should be considered within the context of the best

estimate of the fetal weight20. GDM managed on diet and exercise with good glycemic control,

fetal monitoring reassuring and no other risk factors are delivered at term21. GDM with risk

factors are delivered earlier based on the risk involved.

Induction of labour

The idea of inducing labour in women with suspected fetal macrosomia is to achieve vaginal

delivery before the fetus reaches a size that would imply increased risk of fetal and maternal

injuries. However, trials have shown cesarean section rate to be higher when induction is done

for macrosomia without any reduction in perinatal morbidity22. Hence, routine induction of

labour for macrosomia is not found to be beneficial.

Mode of Delivery

Elective Cesarean Section

Since macrosomia is associated with increased risk of birth injuries it is appropriate to discuss

and offer elective cesarean delivery as an option when the estimated birth weight is 4500gm or

above.

Management of labour

During labour, good glycemic control needs to be maintained while avoiding hypoglycemia.

Insulin requirements are low or often no insulin is required due to the strenuous exercise of

labour. .
Fetal surveillance in uncomplicated diet controlled GDM is like that of any other woman in

labour.

GDM on Insulin and GDM with other risk factors need continuous electronic fetal monitoring

A pediatrician is required to be in attendance at delivery

Vaginal delivery should be supervised by an experienced accoucheur with anticipation and

preparation for prolonged labour and shoulder dystocia.

Glucose monitoring in labour – 2hourly and 4 hourly for women on Insulin and diet alone

respectively

Intrapartum targets for Glucose - 70 and 110 mg/dl

Insulin

Dosage is based on sliding scale - 2-hourly (Table 2)

Intravenous insulin infusion

Suitable for patients requiring intensive therapy and/or poor control on a sliding scale, for

example severe preeclampsia.

50U of Actrapid in 50ml of Normal saline given at the rate of 1-2U/hour

Elective caesarean section

Usual insulin the night before caesarean section and none next morning. Surgery first on the

theatre list in the morning. Glucose level is monitored in theatre prior to anaesthetic

Postop- sliding scale of Insulin

Postpartum
Insulin requirements fall dramatically postpartum. Glucose levels need to be monitored to avoid

profound and/or prolonged hypoglycaemia.

GDM

GDM on diet – Blood sugars are checked on the day of discharge

GDM on Insulin - No Insulin required. Blood glucose monitoring twice daily for 48 hours

If blood glucose levels are persistently elevated after 72 hours – Anti - diabetics to be started. All

types of insulin, glyburide, or glipizide can be safely used by breastfeeding women. Metformin,

while excreted into breast milk, does not appear to have harmful neonatal effects nevertheless it

is safer to use insulin during lactation.

Neonatal management

Watch for hypoglycemia, hypocalcemia and hyperbilirubinemia, polycythemia and RDS

Commence feeding within one hour of birth and feed 3 - 4 hourly.

Blood sugars are measured at four hours of age or before the second feed (whichever comes first)

and every 4th hourly until 3 consecutive readings ≥ 46mg/dL

Early Postpartum Care

Breast feeding

Breastfeeding by women who had GDM is beneficial both for the mother and the offspring.

Breast feeding is associated with a >40% long-term reduction of the risk of developing

postpartum diabetes.

In children of mothers who have GDM, a population previously shown to have a high risk of

infant overweight, breast-feeding for >3 months appears to be negatively associated with

overweight in early childhood. type 1 and type 2 diabetes.

Contraception
Women with prior GDM generally can use all forms of contraception, following essentially the

same guidelines as other women. The only significant exception is that progestin- only methods

during lactation should be avoided or used with caution.

Diet & Exercise

Randomized controlled trials have proven that several interventions (diet and planned exercise

30 – 60 min daily at least 5 days per week and antidiabetic medications) can significantly delay

or prevent the appearance of type 2 diabetes in the women with impaired glucose tolerance (IGT)

in the postpartum period.

OGTT (Table 3)

All women with GDM whose sugars were normal in the immediate post partum[should undergo

a 75-g glucose tolerance test 6-12 weeks after delivery.

Reasons to perform OGTT after pregnancies complicated by GDM

1. The substantial prevalence of glucose abnormalities detected by 3 months postpartum.

2. Abnormal test results identify women at high risk of developing diabetes over the next 5–10

years.

3. Type 2 diabetes can be delayed or prevented by lifestyle interventions(diet and planned

exercise 30 – 60 min daily at least 5 days per week) and antidiabetic medications .

4. Interventions may also reduce subsequent CVD, which is the leading cause of death in both

types of diabetes.

5. Identification, treatment, and planning pregnancy in women developing diabetes after GDM

should reduce subsequent early fetal loss and major congenital malformations.
Women identified to have Impaired Glucose Tolerance are advised Diet and exercise.

Planned pregnancy

All the risks associated with Diabetes in Pregnancy are much higher in a woman with unplanned

pregnancy. Effective contraception helps to plan pregnancy.

Diet with all essential nutrients, avoidance of smoking, excessive coffee, alcohol, Folic acid to

prevent NTD and exercise for optimum pre-pregnancy BMI are important.

Woman should aim to achieve good Glycemic control with HbA1C of < 6.1

A change from Oral hypoglycemic agents to insulin and ACE inhibitors and angiotensin-II

receptor antagonists to suitable alternatives is warranted

Women who are on statins should discontinue.

Conclusion: Obstetricians are the gateway between two generations—mothers and infants. With

their key position of access to this sensitive group, they have the first opportunity to detect and

break the chain of “inheritance,” the passing on of the potential to develop diabetes from one

generation to another23. Pregnancy provides an opportunity to prevent the development of

diabetes in apparently healthy women who would not otherwise seek health care or receive

medical attention.
References

1. Seshiah V, Balaji V, Madhuri S Balaji, Panneerselvam A, Kapur A.

Pregnancy and Diabetes Scenario around the World: India. International

Journal of Gynaecology & Obsteterics 2009 Mar; 104 suppl 1: S35-8.

2. Crowther CA, Hiller JE, Moss JR, et al. for Australian Carbohydrate

Intolerance Study in Pregnant Women (ACHOIS) Trial Group, authors.

Effect of treatment of gestational diabetes mellitus on pregnancy

outcomes. N Engl J Med. 2005;352:2477–2486.

3. International association of diabetes and pregnancy study groups

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Table 1 Correlation between the levels of Hbeta A1-c in early pregnancy and the rate of

malformation

Hb A1-c Rate of Malformation

< 7.9% 6.9%

> 8.0% < 10% 19.0%

> 10% 31.5%

Table 2

For women requiring Insulin <40units/day

Blood glucose mg/dL Actrapid

90 nil

91-126 2 units

127 -– 180 4 units

180 -– 238 6 units

>238 8 units
Table 3

2006 WHO recommendations for the diagnostic criteria for Diabetes

Venous plasma glucose 2–h after ingestion of 75g oral glucose load

Fasting plasma glucose ≥7.0mmol/l (126 mg/dl)

or
Diabetes
2–h plasma glucose ≥11.1mmol/l (200mg/dl)

<7.0mmol/l (126mg/dl)
Fasting plasma glucose
and Impaired Glucose Tolerance

≥7.8 and <11.1mmol/l (IGT)

2–h plasma glucose
(140mg/dl and 200mg/dl)

6.1 to 6.9mmol/l
Fasting plasma glucose
(110mg/dl to 125mg/dl) Impaired fasting Glucose

and (if measured) (IFG)

2–h plasma glucose
<7.8mmol/l (140mg/dl)