Gestational Diabetes

Introduction

Gestational diabetes is carbohydrate intolerance of variable severity first recognised during pregnancy. It complicates approximately 4-5% of pregnancies in the UK and accounts for around 87% of all cases of diabetes seen in pregnancy, the remainder being pre-existing type 1 and type 2 disease.¹ Its incidence is rising in parallel with maternal obesity and increasing maternal age.

It matters because it is a treatable cause of avoidable perinatal harm. Maternal hyperglycaemia crosses the placenta freely; maternal insulin does not. The fetus responds with its own hyperinsulinaemia, and since insulin is a fetal growth factor the result is macrosomia, organomegaly and delayed pulmonary maturation. Treating the mother's glucose reduces macrosomia, shoulder dystocia and pre-eclampsia, which is why screening and treating a largely asymptomatic condition is justified.²

Gestational diabetes is also a window on future health. It is best understood not as a disease of pregnancy but as a stress test of pancreatic reserve, unmasking women whose beta cell function is already marginal. Around half will develop type 2 diabetes within ten years, and this is the single most useful piece of information to convey at the postnatal appointment.

Pathophysiology

Normal pregnancy is deliberately insulin resistant. The placenta secretes human placental lactogen, placental growth hormone, progesterone and cortisol, all of which antagonise insulin action at the level of the insulin receptor and its downstream signalling. Insulin sensitivity falls by 50-60% by the third trimester. The teleological purpose is to divert glucose towards the fetus after maternal meals.

A woman with normal beta cell reserve compensates by increasing insulin secretion two- to threefold and remains euglycaemic. Gestational diabetes occurs when that compensation fails. Because placental hormone output rises with placental mass, the condition characteristically appears in the late second and third trimesters and resolves within hours of delivery of the placenta. Hyperglycaemia detected in the first trimester is therefore usually pre-existing diabetes that was never diagnosed, not gestational diabetes.

Screening and diagnosis

The UK uses risk-factor based screening rather than universal testing. Any woman with one or more of the following is offered a 75 g oral glucose tolerance test at 24-28 weeks:

• BMI above 30 kg/m2
• Previous macrosomic baby weighing 4.5 kg or more
• Previous gestational diabetes
• First-degree relative with diabetes
• A family origin with a high prevalence of diabetes, including South Asian, Black Caribbean and Middle Eastern origin

A woman with previous gestational diabetes is offered testing as early as possible after booking, either by an early OGTT or by self-monitoring of blood glucose, and again at 24-28 weeks if the early test is normal. Testing should also be arranged at any point in pregnancy if glycosuria of 2+ or above is found on one occasion, or 1+ on two occasions, or if the fetus is found to be macrosomic or there is polyhydramnios.¹

Management

A woman with a new diagnosis should be seen in a joint diabetes and antenatal clinic within one week. She is taught capillary blood glucose monitoring, given dietary advice from a specialist dietitian, and given clear numerical targets. The treatment ladder then escalates over short intervals, because there is limited time in which to influence fetal growth.

Diet and exercise

Where the fasting plasma glucose at diagnosis is below 7.0 mmol/L, a trial of diet and exercise is offered first. The advice centres on replacing high glycaemic index carbohydrate with low glycaemic index alternatives, distributing carbohydrate across the day, and taking moderate exercise such as 30 minutes of walking after meals. Around a third of women achieve target on this alone. Response is reviewed after one to two weeks, not months.

Metformin

Metformin is added if targets are not met within one to two weeks of dietary change. It reduces hepatic gluconeogenesis and improves peripheral insulin sensitivity, does not cause maternal hypoglycaemia, and is associated with less maternal weight gain than insulin. It crosses the placenta but has a reassuring safety record in pregnancy. Gastrointestinal side effects are the main limitation and are reduced by starting at a low dose with food and titrating upwards.

Insulin

Insulin is added when metformin plus diet fails to achieve target, and is started immediately alongside diet at diagnosis if the fasting plasma glucose is 7.0 mmol/L or above. Where the fasting glucose is between 6.0 and 6.9 mmol/L and there are already complications such as macrosomia or polyhydramnios, immediate insulin is also considered. Isophane (NPH) insulin is the usual first choice; rapid-acting analogues such as aspart and lispro are used for postprandial excursions. Insulin requirements rise steadily through the third trimester as the placenta enlarges.

Glibenclamide is reserved for women who cannot tolerate metformin and decline insulin, or who do not achieve target on metformin and decline insulin.¹

Fetal surveillance and timing of birth

Ultrasound monitoring of fetal growth and amniotic fluid volume is offered every four weeks from 28 to 36 weeks. The purposes are to detect macrosomia, which influences counselling about mode of birth, and to detect polyhydramnios, which reflects fetal polyuria from hyperglycaemia and is a marker of poor control.

Women with gestational diabetes are advised to give birth no later than 40+6 weeks, by induction of labour or by caesarean section where indicated. Birth is offered earlier if there are maternal or fetal complications. This contrasts with pre-existing type 1 or type 2 diabetes, where elective birth is offered between 37+0 and 38+6 weeks because the stillbirth risk is higher and rises earlier.¹

Where macrosomia is suspected, the risks and benefits of vaginal birth, induction and elective caesarean section should be discussed. Ultrasound estimation of fetal weight has a margin of error of around 10-15% at term, so counselling has to acknowledge that uncertainty rather than treat the estimate as a measurement.

Intrapartum care

• Monitor capillary blood glucose hourly during labour, aiming for 4-7 mmol/L
• Start a variable rate intravenous insulin infusion if glucose is not maintained in that range, and for all women with type 1 diabetes
• Continuous electronic fetal monitoring is recommended for women on treatment
• Anticipate shoulder dystocia: senior obstetric, anaesthetic and neonatal staff should be available for a macrosomic baby
• Antenatal corticosteroids may be given if preterm birth is anticipated, but require additional insulin and close glucose monitoring because they cause a predictable rise

Complications

Note that congenital anomaly is not a feature of gestational diabetes. Organogenesis is complete by 10 weeks, long before gestational diabetes develops, so the neural tube, cardiac and caudal regression anomalies associated with diabetes belong to pre-existing disease with poor periconceptional control. Confusing the two is a common exam error.

Neonatal care

Babies of mothers with diabetes should stay with their mother unless there is a clinical reason to separate them. Feed as soon as possible after birth, within 30 minutes, and then at 2-3 hourly intervals. Capillary blood glucose is checked at 2-4 hours of age. Additional testing is arranged for babies with clinical signs, and admission to the neonatal unit is indicated for hypoglycaemia unresponsive to feeding, respiratory distress, jaundice requiring treatment, signs of cardiac decompensation or birth injury.¹

Red flags

Postnatal care and follow-up

All hypoglycaemic agents given for gestational diabetes should be stopped immediately after birth, because insulin resistance falls off a cliff with delivery of the placenta. Blood glucose is checked before discharge to confirm it has normalised. Women with pre-existing diabetes need their pre-pregnancy insulin regimen reinstated at reduced doses, with particular care while breastfeeding, which itself lowers glucose.

• Fasting plasma glucose at 6-13 weeks postnatally; if this window is missed, use HbA1c from 13 weeks onwards
• Annual HbA1c thereafter, in primary care, for life
• A fasting glucose of 6.0-6.9 mmol/L indicates high risk of type 2 diabetes; 7.0 mmol/L or above suggests type 2 diabetes is likely and warrants confirmation
• Offer referral to a structured diabetes prevention programme where available
• Advise on weight, diet, exercise and smoking, and explain the roughly 50% ten-year risk of type 2 diabetes
• Explain the high recurrence risk in a future pregnancy and the need for early testing after booking
• Encourage breastfeeding, which reduces the mother's subsequent risk of type 2 diabetes and the child's risk of obesity

Contraception should be discussed before discharge. Gestational diabetes is not in itself a contraindication to any method, including combined hormonal contraception, provided there is no vascular disease and no other UKMEC restriction.⁴

Contrast with pre-existing diabetes

Distinguishing gestational from pre-existing diabetes is worth doing explicitly, because the management differs at almost every point.