Description
- Hyperglycaemia first detected in pregnancy that does not meet criteria for overt diabetes
- A stress test of pancreatic beta-cell reserve unmasked by the insulin resistance of pregnancy - not a benign pregnancy quirk
Classification of hyperglycaemia in pregnancy
| Criteria | |
|---|---|
| Overt diabetes in pregnancy | FPG >=7.0 mmol/L, OR 2 h PG >=11.1 mmol/L on 75 g POGTT, OR HbA1c >=6.5% (48 mmol/mol) - at any gestation |
| Gestational diabetes | Values above the GDM thresholds but below overt DIP |
| Early GDM | GDM detected <20 weeks |
- Overt DIP is treated as pre-existing type 2 diabetes: needs retinal and renal assessment, tighter targets, and definite postpartum follow-up
Epidemiology
- ~15-20% of Australian pregnancies under the previous (2014) criteria; the 2025 threshold rise reduces this
- Rising with maternal age and obesity
- Markedly higher prevalence in Aboriginal and Torres Strait Islander, South Asian, South-East Asian, Pacific Islander, Middle Eastern and Māori women
- Recurrence in a subsequent pregnancy ~35-50%
- Lifetime risk of type 2 diabetes ~50% (up to 10x the background rate), most within 10 years
Aetiopathogenesis
- Placental hormones drive progressive insulin resistance from the second trimester
- Human placental lactogen, placental growth hormone, progesterone, cortisol, TNF-alpha
- -> ~50-60% fall in insulin sensitivity by the third trimester
- Normal pregnancy compensates with beta-cell hyperplasia and a 2-3x rise in insulin secretion
- GDM = failure of that compensation - pre-existing beta-cell dysfunction unmasked
- Hence the high subsequent T2DM risk: the defect predated the pregnancy and persists after it
- Insulin requirements rise through the second and third trimesters and fall abruptly at delivery
- Fetal consequences - Pedersen hypothesis
- Maternal glucose crosses the placenta freely; maternal insulin does not
- -> fetal hyperglycaemia -> fetal hyperinsulinaemia (a growth factor)
- -> macrosomia, organomegaly, increased adiposity, delayed surfactant production, polycythaemia
- -> at delivery the glucose supply stops but hyperinsulinaemia persists -> neonatal hypoglycaemia
Risk factors
- Previous GDM (the strongest), previous macrosomic infant, previous stillbirth
- BMI >=30, age >=40, family history of diabetes in a first-degree relative
- High-risk ethnicity, PCOS, corticosteroid or antipsychotic therapy
- Previous bariatric surgery (OGTT poorly tolerated - use glucose monitoring instead)
- Multiple pregnancy
Diagnosis
ADIPS 2025 diagnostic thresholds - these changed in 2025; the older numbers are wrong
75 g 2-hour pregnancy OGTT - GDM if ANY one value is met or exceeded:
| ADIPS 2025 | (previous 2014) | |
|---|---|---|
| Fasting | >=5.3 mmol/L | 5.1 |
| 1 hour | >=10.6 mmol/L | 10.0 |
| 2 hour | >=9.0 mmol/L | 8.5 |
- Overt diabetes in pregnancy if FPG >=7.0, 2 h >=11.1, or HbA1c >=6.5%
- Rationale: the 2014 IADPSG-derived thresholds labelled ~1 in 5 pregnancies without commensurate benefit; the 2025 thresholds align diagnosis with the level of hyperglycaemia where treatment demonstrably helps
- Adopted across Australian pathology services from 2025
When to test
- All women: 75 g POGTT at 24-28 weeks
- Early testing (<20 weeks, ideally 10-14 weeks) with a POGTT if:
- Previous GDM, OR
- Early-pregnancy HbA1c 6.0-6.4% (42-47 mmol/mol) without known diabetes
- Clinician may offer it for other individual risk factors
- *A normal early test does not exclude GDM - repeat the POGTT at 24-28 weeks*
- Early HbA1c at booking in high-risk women, to detect undiagnosed overt diabetes
Practical
- Test requires a fasting sample (8-14 h), seated, no smoking; the fasting sample must be processed promptly (glycolysis in the tube falsely lowers the result - fluoride-citrate tubes)
- Do not use HbA1c to diagnose GDM after the first trimester - red cell turnover and dilutional anaemia make it unreliable
- Early GDM treatment (TOBOGM) modestly reduces the perinatal composite outcome - the basis for early testing in the high-risk group
Management1 exam ›
Phase-based: antenatal glycaemic control -> delivery planning -> postpartum reclassification and lifelong risk.
A. Antenatal - glycaemic targets
- Fasting/pre-meal <=5.0-5.3 mmol/L
- 1 h postprandial <=7.4 mmol/L
- 2 h postprandial <=6.7 mmol/L
- Self-monitoring 4x/day (fasting + post-meals)
B. First-line: medical nutrition therapy and activity
- Dietitian referral for every woman - carbohydrate quantity and distribution, low glycaemic index, adequate energy for fetal growth
- Physical activity 30 min most days (post-meal walking targets the postprandial rise specifically)
- Appropriate gestational weight gain by BMI category
- ~70-85% achieve target on diet and activity alone
C. Pharmacotherapy - if targets are not met within 1-2 weeks
- Insulin is first-line and the preferred agent
- Isophane/NPH or a basal analogue (detemir) for fasting hyperglycaemia
- Rapid-acting analogue (aspart, lispro) with meals for postprandial hyperglycaemia
- Dose escalation is expected - requirements rise steeply through the second and third trimesters
- Does not cross the placenta
- Metformin - crosses the placenta; used in Australia where insulin is declined or impractical
- Often still needs supplemental insulin (~40-50%)
- Long-term offspring data reassuring but not complete - counsel and document
- Glibenclamide is not recommended - more neonatal hypoglycaemia and macrosomia
- *Screen for and manage a rapidly falling insulin requirement in late pregnancy - it may indicate placental insufficiency*
D. Fetal surveillance and delivery
- Serial growth ultrasound (macrosomia, polyhydramnios)
- Timing of delivery:
- Diet-controlled with normal growth: await spontaneous labour, generally deliver by 40-41 weeks
- On insulin/metformin, or with macrosomia or other complications: deliver around 38-39 weeks
- Mode is obstetric; discuss elective caesarean if estimated fetal weight >4.5 kg (shoulder dystocia)
- Intrapartum: hourly BSL, insulin-dextrose infusion if on insulin or BSL >7
- Stop all GDM medication immediately after delivery
E. Neonatal
- Early feeding and BSL monitoring for the first 24 h - neonatal hypoglycaemia is the commonest complication
- Watch for jaundice, polycythaemia, hypocalcaemia, respiratory distress
F. Postpartum - the step most often missed
- 75 g 2-hour OGTT at 6-12 weeks postpartum to reclassify (HbA1c is unreliable this early)
- Then HbA1c or fasting glucose at least every 1-3 years for life
- Test before every subsequent pregnancy and in early pregnancy
- Breastfeeding reduces subsequent maternal T2DM and childhood obesity - actively support it
- Weight, diet, exercise; consider metformin for prevention in those with persisting prediabetes
- Contraception and pre-pregnancy planning advice
- Register with the National Gestational Diabetes Register (NDSS) for recall
Associations
- Obesity, PCOS, metabolic syndrome, non-alcoholic fatty liver disease
- Pre-eclampsia and gestational hypertension - shared endothelial and metabolic pathways
- Polyhydramnios, preterm birth, caesarean delivery, perineal trauma, shoulder dystocia
- Subsequent maternal type 2 diabetes (~50%) and cardiovascular disease
- Offspring: macrosomia, neonatal hypoglycaemia, jaundice, later childhood obesity and impaired glucose tolerance (intergenerational transmission)
- Corticosteroids given for fetal lung maturity - transient marked hyperglycaemia requiring insulin cover
- High-risk ethnic groups; socioeconomic disadvantage; rural and remote access barriers
- Antipsychotics, protease inhibitors
Natural history & complications
- Hyperglycaemia resolves at delivery in the great majority - because the placenta is the driver
- Recurrence 35-50% in a subsequent pregnancy
- Type 2 diabetes in ~50% over 10-20 years - the single most important long-term message
- Highest risk: early diagnosis in pregnancy, insulin requirement, obesity, high-risk ethnicity, persisting postpartum dysglycaemia
- Cardiovascular disease risk approximately doubled, partly independent of subsequent diabetes
- ~5-10% of "GDM" is actually undiagnosed type 2 diabetes - which is why the postpartum OGTT matters
- Consider type 1 diabetes or MODY if lean, young, ketosis-prone, strong family history, or persistent hyperglycaemia postpartum (check GAD/IA-2 antibodies)
Complications to anticipate
- Maternal: pre-eclampsia, polyhydramnios, operative delivery, birth trauma
- Fetal/neonatal: macrosomia, shoulder dystocia and brachial plexus injury, neonatal hypoglycaemia, hyperbilirubinaemia, polycythaemia, respiratory distress, stillbirth (uncontrolled)
- Congenital malformation risk belongs to pre-existing/overt diabetes with first-trimester hyperglycaemia, not to GDM diagnosed at 24-28 weeks
7 of 7 sections written · drafted 2026-09-12