Define and describe the screening, effects on pregnancy and management of gestational Diabetes Mellitus.

Screening by OGTT is done at 24–28 weeks.

Definition

Gestational diabetes mellitus (GDM) is carbohydrate intolerance of variable severity with its onset or first recognition during the present pregnancy, irrespective of whether insulin is used or whether it persists after delivery. It must be distinguished from pre-gestational (overt) diabetes, which exists before conception.

Screening & Diagnosis of GDM

Classification (white's)

White's classification grades diabetes in pregnancy by onset, duration and vascular complications. Class A is gestational diabetes — A1 (controlled by diet) and A2 (requiring insulin). Pre-gestational diabetes is graded B–T (Class B onset > 20 years/duration < 10 years, through to classes with retinopathy, nephropathy and transplantation).

Screening and Diagnosis

Universal screening is recommended in high-prevalence populations such as India.

• DIPSI (Diabetes in Pregnancy Study Group of India) — a single-step test: 75 g oral glucose irrespective of the last meal, with a venous plasma glucose at 2 hours of > 140 mg/dL diagnosing GDM.
• IADPSG / WHO (fasting 75 g OGTT) — GDM if any value is met or exceeded: fasting ≥ 92 mg/dL, 1 hour ≥ 180 mg/dL, 2 hours ≥ 153 mg/dL.
• Overt diabetes is diagnosed by fasting ≥ 126 mg/dL, random/2-hour ≥ 200 mg/dL or HbA1c ≥ 6.5%.

Effects on Pregnancy

Maternal — increased pre-eclampsia, polyhydramnios, recurrent infections (urinary, vaginal), preterm labour, increased operative and instrumental delivery, recurrence in later pregnancies and a high lifetime risk of type-2 diabetes. Fetal/neonatal — macrosomia with shoulder dystocia and birth trauma, sudden unexplained intra-uterine death, congenital malformations (mainly with pre-gestational diabetes, not GDM), and neonatal hypoglycaemia, respiratory distress syndrome, hypocalcaemia, polycythaemia and hyperbilirubinaemia.

Management

Medical nutrition therapy and exercise

The mainstay is a diabetic diet (≈ 30–35 kcal/kg with controlled carbohydrate, split into three meals and snacks) and regular moderate exercise. Most A1 cases are controlled by these measures alone.

Glucose monitoring and targets

Self-monitoring of blood glucose with targets of fasting < 95 mg/dL, 1-hour post-prandial < 140 mg/dL and 2-hour < 120 mg/dL.

Drug therapy

Insulin is the drug of choice when diet fails to achieve targets (it does not cross the placenta); metformin is an accepted alternative in selected women. Doses are titrated to the glucose profile.

Fetal surveillance and timing of delivery

Serial growth scans, amniotic-fluid assessment and antenatal fetal monitoring (NST/biophysical profile) in the third trimester. Well-controlled GDM is usually delivered at term (around 38–39 weeks); earlier delivery for poor control or complications. Caesarean section is considered for an estimated fetal weight suggesting macrosomia (≥ 4–4.5 kg) or for the usual obstetric indications.

Intrapartum and postpartum

Maintain maternal blood glucose with an insulin–dextrose infusion during labour. Anticipate and treat neonatal hypoglycaemia. Insulin requirement falls sharply after delivery; perform a 75 g OGTT at 6 weeks postpartum to detect persisting diabetes, counsel on lifestyle and future risk, and advise contraception.

WHY GDM Harms the Fetus — One Mechanism Explains Everything

Understanding why maternal hyperglycaemia harms the fetus makes every complication of gestational diabetes coherent. Glucose crosses the placenta freely, but maternal insulin does not. The fetus is therefore exposed to the mother's high glucose and responds by producing its own insulin — becoming hyperinsulinaemic (the Pedersen hypothesis). Since insulin is the principal fetal growth hormone, this drives macrosomia — but of a particular kind: fat is deposited on the shoulders and trunk while the head grows normally, which is precisely why these babies suffer shoulder dystocia (and brachial plexus injury) even when the head delivers easily. Fetal hyperinsulinaemia also delays surfactant production (so respiratory distress may occur even near term) and, at birth — when the maternal glucose supply is abruptly cut off while the baby's high insulin persists — produces profound neonatal hypoglycaemia within hours, along with polycythaemia, hypocalcaemia and jaundice; fetal polyuria causes polyhydramnios. Recognising that a single mechanism — fetal hyperinsulinaemia driven by maternal glucose — explains macrosomia, shoulder dystocia, RDS and neonatal hypoglycaemia makes the whole subject intelligible, and explains why tight glycaemic control is the goal.

WHY Screening and Postpartum Follow-up Both Matter

A useful concept is why GDM is screened for universally in India, and why the story does not end at delivery. GDM is usually asymptomatic — the mother feels perfectly well — so it is missed unless actively sought; yet its complications are largely preventable by treatment, beginning with diet and exercise and, if targets are not met, insulin (or metformin). This is why India uses a simple, single-step, non-fasting 75 g oral glucose test (DIPSI: a 2-hour value ≥140 mg/dL is diagnostic), applicable at any time of day — designed for practicality in a population that cannot easily attend fasting. Equally important is what follows: GDM is a window into the woman's future, revealing a beta-cell reserve that failed under stress — and around half of such women develop type 2 diabetes within a decade. She must therefore be re-tested at about 6 weeks postpartum, screened regularly thereafter, and counselled about weight, diet and exercise; her child, too, carries a raised lifetime risk of obesity and diabetes. Understanding that GDM is both an immediate obstetric risk and a lifelong metabolic warning explains why screening and long-term follow-up are equally essential.

• GDM = carbohydrate intolerance first recognised in pregnancy, caused by the insulin resistance of placental hormones (hPL, cortisol).
• India screens universally with the DIPSI test: 75 g oral glucose (non-fasting); a 2-hour value ≥140 mg/dL diagnoses GDM.
• Fetal effects follow fetal hyperinsulinaemia: macrosomia → shoulder dystocia, polyhydramnios, RDS, and neonatal hypoglycaemia.
• Treatment: medical nutrition therapy and exercise first; insulin (or metformin) if targets are not achieved.
• Re-test at 6 weeks postpartum — about half develop type 2 diabetes within 10 years.