Obstetrics and Gynaecology chapters
Diabetes in pregnancy: pre-existing and gestational diabetes
Why pregnancy makes glucose control harder, how pre-existing and gestational diabetes affect mother and baby, the OGTT cut-offs, glucose targets, metformin and insulin, timing of delivery and care of the baby after birth.
- Pregnancy is diabetogenic: placental hormones (especially human placental lactogen) cause insulin resistance in the second half. Diabetes is either pre-existing (type 1 or 2) or gestational (GDM), diagnosed by a 75 g OGTT at 24-28 weeks.
- Poor control early causes miscarriage and congenital anomalies (cardiac, neural tube, caudal regression); poor control later causes macrosomia, polyhydramnios, shoulder dystocia, stillbirth and neonatal hypoglycaemia.
- Treat with diet, then metformin and/or insulin, aim for fasting under 5.3 and 1-hour under 7.8 mmol/l, deliver at 38-39 weeks, and retest the mother after birth.
On this page
Overview
Diabetes complicates pregnancy in two ways:
- Pre-existing diabetes: type 1 or type 2 diabetes present before pregnancy.
- Gestational diabetes mellitus (GDM): glucose intolerance that first appears in pregnancy. It affects about 10-15% of pregnancies depending on the criteria used.
Pakistan has a very high rate of type 2 diabetes, so many women enter pregnancy with undiagnosed diabetes. Good control before and during pregnancy prevents most of the harm to the baby.
Why pregnancy is diabetogenic
- In the first half of pregnancy, insulin sensitivity is fairly normal.
- In the second half, placental hormones cause insulin resistance, so the mother uses less glucose and more passes to the fetus.
- The main hormone is human placental lactogen (human chorionic somatomammotropin), which rises with placental size; progesterone, cortisol and oestrogen add to it.
- A woman whose pancreas cannot raise insulin output enough develops GDM; a woman already on treatment needs more insulin or metformin in the second half.
- After delivery of the placenta, insulin needs fall back at once to pre-pregnancy levels.
Placental lactogen is the hormone most responsible for insulin resistance in late pregnancy.
The Pedersen hypothesis (why babies grow big)
Maternal glucose crosses the placenta, but insulin does not. High maternal glucose makes the fetal pancreas produce more insulin. Fetal hyperinsulinaemia drives growth and fat deposition (macrosomia), and after birth, when the maternal glucose supply stops, the still-high insulin causes neonatal hypoglycaemia.
Effects of diabetes on pregnancy
| Stage | Problem |
|---|---|
| Early (organogenesis, first 42 days) | Miscarriage (an HbA1c over 85 mmol/mol carries about 30% pregnancy loss); congenital anomalies 2-4 times more common, with a threefold rise in cardiac and neural tube defects |
| Later pregnancy | Macrosomia, polyhydramnios (fetal polyuria), pre-eclampsia (three times the risk), infection, stillbirth (about five times the risk), preterm delivery |
| Labour | Shoulder dystocia, birth trauma, operative delivery (caesarean rate can approach 50%) |
| Baby | Hypoglycaemia, polycythaemia, jaundice, hypocalcaemia, hypomagnesaemia, birth asphyxia |
Congenital anomalies in infants of diabetic mothers
- Cardiac: VSD, ASD, transposition of the great arteries, truncus arteriosus, coarctation.
- Neural: neural tube defects, holoprosencephaly.
- Caudal regression (lumbosacral agenesis): rare but strongly linked with maternal diabetes.
- Renal anomalies (duplex ureter, renal agenesis).
Anomalies come from high glucose around conception, so they are a problem of pre-existing diabetes, not of GDM that appears at 24-28 weeks.
GDM does not usually cause congenital anomalies. If a "GDM" mother has a baby with a major anomaly, she probably had unrecognised pre-existing diabetes.
How pregnancy affects diabetes
- Morning sickness upsets control in early pregnancy.
- Rising insulin needs in the second half.
- More severe hypoglycaemia (and less awareness of it).
- Retinopathy may worsen: retinal checks at booking, again at 16-20 weeks, and at 28 weeks.
- Nephropathy may worsen, with higher risk of pre-eclampsia and preterm delivery.
- Diabetic ketoacidosis develops faster and is dangerous to the fetus.
Pre-existing diabetes: care
Before pregnancy
- Aim for HbA1c below 42 mmol/mol without hypoglycaemia; use contraception until control is good.
- High-dose folic acid 5 mg daily (instead of the usual 400 micrograms) to lower the neural tube defect risk.
- Stop ACE inhibitors and statins; switch to drugs safe in pregnancy.
- Check for retinopathy, nephropathy and neuropathy.
- Pre-meal glucose target 4-7 mmol/l before conception.
During pregnancy
- Multidisciplinary team: obstetrician, physician, diabetes nurse or midwife, dietitian.
- Self-monitoring of capillary glucose up to 7 times a day.
- Targets: fasting or pre-meal below 5.3 mmol/l; 1 hour after meals below 7.8 mmol/l.
- Insulin (doses rise in the second half); metformin where suitable.
- Low-dose aspirin from 12 weeks to reduce pre-eclampsia.
- Anomaly scan at 19-20 weeks including the cardiac outflow tracts.
- Serial growth scans for macrosomia and polyhydramnios.
- If steroids are needed for preterm delivery, give extra insulin (steroids raise glucose).
Gestational diabetes
Risk factors (screen these women)
- BMI 30 or more.
- Previous macrosomic baby (4.5 kg or more).
- Previous GDM.
- First-degree relative with diabetes.
- Ethnic origin with a high diabetes rate (South Asian, black Caribbean, Middle Eastern).
- Also suspect GDM with glycosuria on repeated testing, polyhydramnios or a large-for-dates fetus, or a previous unexplained stillbirth.
Some countries (for example the USA and Australia) test all pregnant women rather than only those with risk factors; Pakistani units vary, so check local practice.
Screening and diagnosis
- 75 g oral glucose tolerance test at 24-28 weeks.
- Previous GDM: test early (about 16-18 weeks) and repeat at 24-28 weeks if normal.
| Guideline | Fasting | 1 hour | 2 hours |
|---|---|---|---|
| NICE (UK) | 5.6 mmol/l or more | Not used | 7.8 mmol/l or more |
| WHO 2013 | 5.1 mmol/l or more | 10.0 mmol/l or more | 8.5 mmol/l or more |
One abnormal value is enough for diagnosis.
Glycosuria alone does not diagnose GDM. The kidney's threshold for glucose falls in pregnancy because GFR rises, so glycosuria is common in normal pregnancy.
Fasting 5.4 mmol/l (cut-off 5.6) → below
2-hour 8.1 mmol/l (cut-off 7.8) → above
One value at or over the cut-off → GDM diagnosed
Treatment
- Diet and lifestyle change first.
- If targets are not met, add metformin.
- Add or switch to insulin if metformin is not enough or not tolerated, or if glucose is very high at diagnosis.
Treatment reduces the number of large-for-gestational-age babies and shoulder dystocia.
Labour and delivery
- If all is well, aim for delivery at 38-39 weeks (induction or caesarean as indicated); earlier if macrosomia, pre-eclampsia or poor control.
- Macrosomia may need caesarean to avoid shoulder dystocia.
- In labour, women on insulin get an IV insulin and glucose sliding scale, keeping glucose at 4-7 mmol/l to cut neonatal hypoglycaemia.
- After delivery: stop treatment for GDM; return to pre-pregnancy insulin doses in pre-existing diabetes; watch for hypoglycaemia, especially while breastfeeding.
The baby
- Early feeding and blood glucose checks for neonatal hypoglycaemia.
- Watch for respiratory problems, jaundice, polycythaemia, hypocalcaemia and birth injury.
Long-term follow-up after GDM
- Fasting glucose or HbA1c at 6-13 weeks after birth to exclude persisting diabetes.
- High lifetime risk of type 2 diabetes: annual testing, weight control, exercise.
- High chance of GDM in the next pregnancy.
Expect: human placental lactogen and insulin resistance; risk factors for GDM; the 75 g OGTT at 24-28 weeks and the NICE and WHO cut-offs; folic acid 5 mg and HbA1c targets before pregnancy; cardiac and neural tube defects and caudal regression with pre-existing diabetes; macrosomia, polyhydramnios, shoulder dystocia and stillbirth; fetal hyperinsulinaemia causing neonatal hypoglycaemia; metformin and insulin; delivery at 38-39 weeks; glucose 4-7 mmol/l in labour; postnatal glucose test at 6-13 weeks and the future risk of type 2 diabetes.
Quick revision
- Pregnancy causes insulin resistance in the second half (placental lactogen).
- GDM: 75 g OGTT at 24-28 weeks; NICE fasting 5.6 or 2-hour 7.8; WHO 5.1, 10.0, 8.5.
- Pre-existing diabetes: folic acid 5 mg, HbA1c below 42, aspirin from 12 weeks.
- Early hyperglycaemia: miscarriage, cardiac and neural tube defects, caudal regression.
- Late hyperglycaemia: macrosomia, polyhydramnios, shoulder dystocia, stillbirth.
- Fetal hyperinsulinaemia causes neonatal hypoglycaemia.
- Targets: fasting under 5.3, 1-hour under 7.8; diet, then metformin, then insulin.
- Deliver 38-39 weeks; retest mother at 6-13 weeks.
Written by The House Job from standard references (Obstetrics by Ten Teachers; Guyton and Hall Textbook of Medical Physiology; Nelson Essentials of Paediatrics).
FAQ
Why does gestational diabetes appear in the second half of pregnancy?
Placental hormones such as placental lactogen rise as the placenta grows and steadily reduce insulin sensitivity, unmasking women whose insulin reserve is limited.
Why is the baby of a diabetic mother at risk of low blood sugar?
High maternal glucose made the fetal pancreas produce extra insulin; when the cord is cut, glucose supply stops but insulin stays high for a while.
Does gestational diabetes cause birth defects?
Usually not, because it develops after organs have formed; anomalies point to high glucose around conception, as in pre-existing diabetes.
What follow-up does a woman need after gestational diabetes?
A fasting glucose or HbA1c a few weeks after birth and regular checks afterwards, because she is at high risk of type 2 diabetes.