Diabetes in pregnancy

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

Maternal hyperglycaemia around conception increases congenital-malformation and miscarriage risk; later exposure contributes to fetal overgrowth, polyhydramnios, shoulder dystocia, operative birth and neonatal hypoglycaemia. Diabetes also increases pre-eclampsia, retinopathy progression and kidney risk.

Insulin requirements often fall early in pregnancy, rise with placental insulin resistance later, and drop rapidly after placental delivery. A pre-written dose and monitoring plan is therefore safer than reacting to isolated glucose values.

The central decisions are whether pregnancy is being prepared safely, whether gestational diabetes needs medicine after initial lifestyle treatment, and whether maternal or fetal findings require earlier escalation, delivery planning or inpatient management. Exact thresholds and timing belong to current NICE and local maternity protocols.

Key points

Pre-existing type 1 or type 2 diabetes and gestational diabetes are distinct pathways, but all need joint obstetric–diabetes care and explicit postpartum planning.
Offer preconception review before pregnancy where possible: optimise glucose safely, prescribe high-dose folic acid, review medicines, assess retina and kidneys, and discuss pregnancy-specific risks.
NICE advises aiming for preconception HbA1c below 48 mmol/mol when achievable without problematic hypoglycaemia and strongly advises avoiding pregnancy when HbA1c exceeds 86 mmol/mol.
Stop ACE inhibitors, angiotensin-receptor blockers and statins before conception or promptly when pregnancy is confirmed; replace them through specialist advice.
Metformin may be used before and during pregnancy when benefit outweighs harm; other oral glucose-lowering medicines are usually stopped and insulin substituted under the specialist pathway.
NICE diagnoses gestational diabetes on a 75-g oral glucose tolerance test when fasting plasma glucose is at least 5.6 mmol/L or the 2-hour value is at least 7.8 mmol/L; HbA1c is not the standard later-pregnancy diagnostic test.
If safely achievable, NICE pregnancy capillary targets are fasting below 5.3 mmol/L and either 1-hour post-meal below 7.8 or 2-hour post-meal below 6.4 mmol/L; people using insulin should keep glucose above 4 mmol/L.
For gestational diabetes with fasting glucose below 7.0 mmol/L, start diet and exercise; offer metformin if targets are unmet after 1–2 weeks, and offer immediate insulin with or without metformin at 7.0 mmol/L or above.
Offer real-time continuous glucose monitoring to pregnant people with type 1 diabetes and provide specialist education on sensor limitations, insulin adjustment and ketone testing.
Gestational diabetes medication usually stops after birth, but persistent hyperglycaemia must be excluded and lifelong type 2 diabetes surveillance arranged.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Pre-existing diabetes

Type 1 or type 2 diabetes may predate conception, exposing early embryonic development to maternal hyperglycaemia unless glucose is optimised beforehand.

Gestational insulin resistance

Placental hormones progressively increase insulin resistance later in pregnancy; pancreatic reserve may be insufficient to maintain maternal glucose within the pregnancy range.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Maternal glucose rises
Insulin deficiency or pregnancy-related resistance raises maternal glucose, which crosses the placenta and increases fetal glucose exposure.
2
Fetal insulin secretion increases
The fetal pancreas responds with greater insulin secretion, promoting growth and fat deposition and increasing oxygen and metabolic demands.
3
Insulin needs change across pregnancy
Requirements may fall early, rise with later placental resistance and drop rapidly after placental delivery, making pre-written adjustment and monitoring plans important.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Pre-existing diabetes

Type 1 or type 2 diabetes predates conception or is identified as overt diabetes early in pregnancy. Look for complications, medicines unsafe in pregnancy and prior hypoglycaemia or ketoacidosis.

Gestational diabetes risk

Previous gestational diabetes or macrosomic baby, first-degree family history, BMI at or above the NICE threshold and higher-risk ethnic background trigger formal testing at the recommended gestation.

Gestational hyperglycaemia

The 75-g oral glucose tolerance test establishes the diagnosis using current fasting and two-hour thresholds; fasting glucose severity and ultrasound findings influence whether insulin begins immediately.

Pregnancy ketoacidosisRed flag

Nausea, vomiting, abdominal pain, dehydration, deep breathing or malaise with blood ketones can represent DKA even when glucose is not markedly raised, particularly with pump interruption or SGLT2 exposure.

Severe hypoglycaemiaRed flag

Reduced awareness, nocturnal episodes, seizure or third-party assistance is especially concerning early in type 1 pregnancy. Review targets, insulin, CGM alarms and glucagon access immediately.

Microvascular progressionRed flag

New visual symptoms, worsening albuminuria, hypertension or declining renal function may represent pregnancy-accelerated retinopathy, kidney disease or pre-eclampsia and needs joint specialist assessment.

Fetal or obstetric concernRed flag

Reduced fetal movement, abnormal growth, polyhydramnios, hypertension, proteinuria or threatened preterm birth changes surveillance and delivery planning; glucose control alone does not determine safety.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
Preconception HbA1c and glucose reviewFirst step
Why
Quantify recent exposure and identify a safer route into pregnancy.
Interpretation and limitations
Use the NICE preconception target as an aspiration only when achievable without problematic hypoglycaemia. Any improvement helps, but HbA1c above 86 mmol/mol carries sufficiently high risk for strong advice to defer conception.
02
Capillary glucose or continuous glucose monitoring
Why
Guide daily insulin, meals and activity throughout pregnancy.
Interpretation and limitations
Agree individualised targets that avoid problematic hypoglycaemia. NICE advises fasting capillary plasma glucose below 5.3 mmol/L and either 1-hour post-meal below 7.8 or 2-hour post-meal below 6.4 mmol/L; if using insulin, keep glucose above 4 mmol/L. Confirm unexpected sensor values by capillary testing.
03
Blood ketones
Why
Detect pregnancy DKA promptly during illness or hyperglycaemia.
Interpretation and limitations
Follow the person's type 1 sick-day plan and maternity threshold; rising beta-hydroxybutyrate with vomiting or malaise needs urgent clinical assessment even at near-normal glucose.
04
Seventy-five gram oral glucose tolerance test
Why
Diagnose gestational diabetes in those meeting the screening pathway.
Interpretation and limitations
Diagnose gestational diabetes if fasting plasma glucose is at least 5.6 mmol/L or the 2-hour value is at least 7.8 mmol/L. Test other NICE risk-factor groups at 24–28 weeks; after previous gestational diabetes, offer early testing and repeat at 24–28 weeks if the early result is normal.
05
Retinal assessment with digital imaging
Why
Establish baseline disease and detect progression during pregnancy.
Interpretation and limitations
Arrange at preconception or early antenatal review and at NICE-defined intervals according to findings. Rapid glucose improvement can transiently worsen established retinopathy, but is not a reason to withhold necessary control.
06
Renal profile and urinary albumin assessment
Why
Measure baseline kidney disease and pre-eclampsia risk.
Interpretation and limitations
Significant albuminuria or reduced eGFR needs nephrology or renal–obstetric input before conception where possible. Later proteinuria must be interpreted against baseline, blood pressure and pre-eclampsia features.
07
Serial fetal growth and wellbeing assessment
Why
Detect growth acceleration, restriction, fluid abnormality and placental compromise.
Interpretation and limitations
Ultrasound timing and fetal surveillance follow the specialist maternity plan. Normal maternal glucose logs do not overrule reduced movements or abnormal growth trajectory.
08
Postnatal fasting plasma glucose or HbA1c
Why
Detect persistent diabetes after gestational diabetes and establish long-term surveillance.
Interpretation and limitations
Use the NICE test and timing: fasting plasma glucose is usually offered 6–13 weeks after birth, with HbA1c used later when needed. An oral glucose tolerance test is not routinely required in the NICE postnatal pathway.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Previously unrecognised type 2 diabetes

Marked hyperglycaemia early in pregnancy, prior risk factors or persistent postpartum disease may indicate diabetes that preceded gestation rather than transient gestational diabetes.

Autoimmune type 1 diabetes

Weight loss, ketones or rapid deterioration suggests insulin deficiency requiring urgent specialist treatment rather than routine gestational-diabetes escalation.

Transient stress hyperglycaemia

Acute illness or glucocorticoid exposure can temporarily raise glucose; trajectory and follow-up clarify whether an enduring pregnancy-related disorder is present.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01PreconceptionPrepare pregnancy with diabetesFirst stepA person with diabetes could become pregnant or is actively planning conception.

1Discuss contraception until ready, pregnancy risks, glucose targets, hypoglycaemia and ketone plans, and refer promptly to the joint diabetes–pregnancy service.
2Start folic acid 5 mg daily through 12 weeks of pregnancy, optimise HbA1c safely and arrange retinal, renal, blood-pressure and medication review.
3Stop or replace ACE inhibitors, ARBs, statins and unsuitable glucose-lowering medicines through authorised prescribers; never withdraw insulin from type 1 diabetes.
4Provide meter or CGM supplies, blood-ketone equipment, glucagon where appropriate and written contacts for positive pregnancy test, vomiting, ketones or severe hypoglycaemia.

02GestationalNew gestational diabetesA 75-g oral glucose tolerance test shows fasting plasma glucose at least 5.6 mmol/L or 2-hour glucose at least 7.8 mmol/L.

1Arrange joint diabetes–antenatal review within one week, explain fetal and maternal risks without blame, teach glucose monitoring, use the pregnancy targets, and offer dietitian-led eating and physical-activity advice.
2If fasting glucose at diagnosis is below 7.0 mmol/L, trial diet and exercise and offer metformin if targets are unmet after 1–2 weeks; offer insulin if metformin is contraindicated, unacceptable or insufficient. At 7.0 mmol/L or above offer immediate insulin with or without metformin; at 6.0–6.9 with macrosomia or hydramnios consider immediate insulin.
3EscalationReview fasting and post-meal patterns frequently, escalating therapy by the agreed algorithm while protecting against hypoglycaemia and inadequate gestational weight gain.
4Coordinate growth surveillance, birth timing, intrapartum glucose and neonatal feeding plans with the maternity service rather than allowing HbA1c alone to dictate delivery.

03EmergencyIllness and ketones in pregnancyVomiting, inability to eat, rising ketones, pump failure or symptoms compatible with DKA.

1Contact maternity triage and the diabetes team immediately, check capillary glucose and blood ketones, continue basal insulin and use the person's emergency correction plan while travelling for assessment.
2In hospital obtain venous gas, electrolytes, ketones, renal function and infection assessment, start pregnancy-adapted DKA treatment and involve obstetrics, anaesthesia and critical care early.
3Treat maternal physiology first with carefully monitored fluids, insulin and potassium; fetal compromise often improves with maternal correction and delivery is not the automatic first intervention.
4Identify the trigger, including infection, steroid exposure, vomiting, pump interruption or inappropriate SGLT2 use, and revise equipment and sick-day education before discharge.

04PostnatalAfter birth and future riskDelivery after pre-existing or gestational diabetes.

1Reduce pre-existing insulin immediately according to the written postpartum plan and monitor closely because insulin requirement and hypoglycaemia risk fall rapidly after placental delivery.
2Stop gestational diabetes medication unless persistent hyperglycaemia or pre-existing disease requires continued treatment; check glucose before transfer to routine community care.
3Support early feeding and neonatal glucose observation under the local neonatal pathway, while ensuring maternal meals and insulin timing remain safe.
4Arrange 6–13-week diabetes testing after gestational diabetes and annual HbA1c thereafter, plus lifestyle and future-preconception support because recurrence and type 2 diabetes risks remain substantial.

Key medicines and prescribing safety4 treatments · regimens, roles and cautions

Reduces neural-tube-defect risk in pregnancies complicated by pre-existing diabetes.

Folic acid

Take 5 mg orally once daily before conception until 12 weeks' gestation.

Begin before conception when possible; this high-dose preparation requires prescription and does not replace broader preconception nutrition, medicine review or anomaly screening.

Can be an adjunct or alternative to insulin before and during pregnancy and treats gestational diabetes after lifestyle measures.

Metformin

Initiate and titrate under the pregnancy diabetes protocol with meals as tolerated.

Discuss placental transfer, gastrointestinal effects and individual benefit; check renal function and pause during severe dehydration or tissue hypoxia. Other oral agents are generally stopped.

Essential for type 1 diabetes and used when pregnancy targets cannot be met safely with lifestyle or metformin.

Insulin

Regimen and dose are individualised repeatedly from glucose patterns by the specialist team.

Requirements change across gestation and fall abruptly postpartum. Prevent identification and device errors, review injection sites, ensure hypoglycaemia treatment and never stop basal insulin during illness.

Allows a trained companion to treat hypoglycaemia when oral carbohydrate cannot be taken safely.

Glucagon rescue

Use the supplied preparation and device exactly as taught for severe hypoglycaemia.

Call emergency services after severe events, place the person safely, give carbohydrate after recovery and arrange urgent insulin and awareness review; nausea and vomiting may follow.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Early pregnancy loss or malformation

Maternal hyperglycaemia around conception increases miscarriage and congenital-malformation risk during a period when fetal organs are developing.

Fetal overgrowth and birth injury

Fetal hyperinsulinaemia promotes excessive growth, increasing polyhydramnios, operative birth, shoulder dystocia and neonatal complications, particularly when maternal hyperglycaemia persists.

Maternal vascular complications

Pregnancy can amplify pre-eclampsia, kidney disease and retinopathy risk, particularly when diabetes or microvascular damage predates conception.

Neonatal hypoglycaemia

After delivery, placental glucose supply stops abruptly while fetal insulin remains elevated, predisposing the newborn to early low glucose.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Review glucose or CGM patterns at frequent pregnancy contacts, including hypoglycaemia, sensor use, insulin delivery, food intake, ketones and psychosocial burden.
Check blood pressure and urine at antenatal visits and respond to headache, visual symptoms, upper-abdominal pain, oedema or fetal growth change through the pre-eclampsia pathway.
Repeat retinal assessment and renal review at NICE-defined points, with faster ophthalmology or nephrology escalation for established disease or deterioration.
Use serial ultrasound and local fetal-surveillance protocols; ask about fetal movement at every relevant contact and provide same-day instructions for reduction.
After birth, track maternal glucose, insulin reduction, breastfeeding-related hypoglycaemia, neonatal feeding and glucose, and completion of the mother's long-term diabetes test.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Lower glucose does not exclude DKA

Placental and fasting physiology can produce ketoacidosis with only modest hyperglycaemia. Symptoms and blood ketones should drive urgent assessment rather than a reassuring glucose value.

The first weeks matter

Organogenesis occurs before many first antenatal appointments, which is why contraception, folic acid and medicine review belong in routine diabetes care before pregnancy is declared.

Retinopathy can transiently worsen

Rapid improvement in glucose may accelerate established retinal change. Arrange surveillance and specialist treatment rather than leaving dangerous hyperglycaemia untreated.

Gestational diabetes is not over at delivery

Medication may stop, but future type 2 diabetes and recurrent gestational diabetes risks persist. Postpartum testing and annual surveillance must have a named owner.

Breastfeeding changes insulin need

Energy use and irregular feeds can increase maternal hypoglycaemia risk. Keep rapid carbohydrate available and adapt insulin with the diabetes team.

Terminology should follow the person

Use pregnancy-capable, respectful language while retaining terms needed for guideline navigation; clinical eligibility depends on organs, physiology and treatment, not assumptions about identity.

11Common pitfallsFrequent interpretation and management errors.

01
Waiting until pregnancy is confirmed to review teratogenic or fetotoxic medicines.
02
Using HbA1c instead of the recommended oral glucose tolerance test for gestational diagnosis.
03
Assuming near-normal glucose excludes ketoacidosis during pregnancy.
04
Withholding basal insulin because a pregnant person is vomiting or fasting.
05
Treating rapid fetal growth without reviewing post-meal glucose patterns.
06
Failing to arrange postnatal diabetes testing after gestational diabetes.