Step 2 CK · Obstetrics & Gynecology

Preconception Care & Pregestational Diabetes

Name: Preconception Care & Pregestational Diabetes
Creator: Veli Bakalov, MD

The best time to prevent a birth defect is before the pregnancy test turns positive

Obstetrics & Gynecology·Medical Disorders of Pregnancy·5 min read·9 high-yield points·Reviewed by Veli Bakalov, MD @HemeOncBuddy

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Every woman who could conceive takes folic acid 0.4 mg daily from at least 1 month before conception; a prior NTD-affected pregnancy calls for 4 mg daily.
MMR and varicella are live vaccines: give them to nonimmune women before pregnancy and avoid conception for 1 month.
Before conception switch ACE inhibitors/ARBs to labetalol or nifedipine, warfarin to LMWH, and valproate to lamotrigine or levetiracetam.
Wash out methotrexate (1–3 months), mycophenolate (≥6 weeks, switch to azathioprine) and isotretinoin (≥1 month) before conception.
Anomaly risk in pregestational diabetes rises with HbA1c (target <6.5% before conception); heart defects are most common and caudal regression is most specific.
Insulin is preferred in pregnancy; needs dip in the first trimester, climb with hPL-driven resistance and fall abruptly after placental delivery.
Surveillance in pregestational diabetes: baseline retinal exam and urine protein, aspirin from 12 weeks, fetal echo at ~20–22 weeks, testing from 32 weeks.
Deliver at 39 0/7–39 6/7 weeks if well controlled, at 36–38 weeks with vasculopathy or poor control; offer cesarean if estimated fetal weight is ≥4,500 g.
Fetal hyperinsulinemia causes macrosomia, RDS, polycythemia and neonatal hypoglycemia after cord clamping.

The preconception visit

Why before. Organogenesis spans roughly weeks 3–8 after conception, and the neural tube closes about 28 days after conception, often before a woman knows she is pregnant. Anything meant to prevent anomalies must be in place before conception.

0.4 mgdaily folic acid for every woman who could conceive

4 mgdaily after a prior pregnancy affected by a neural tube defect

Folic acid. Take 0.4 mg daily from at least 1 month before conception through the first trimester; a woman with a previous NTD-affected pregnancy takes 4 mg daily, ideally starting about 3 months before conception.

Chronic disease. Aim for HbA1c <6.5% in diabetes, control blood pressure with pregnancy-safe drugs, make hypothyroid women euthyroid (then raise levothyroxine by about 25–30%, for example two extra doses per week, once pregnancy is confirmed), wait for at least 6 months of lupus quiescence, and restart a phenylalanine-restricted diet in phenylketonuria, because high maternal phenylalanine causes microcephaly, intellectual disability and heart defects. Weight, smoking, alcohol and drug use are addressed at the same visit.

Vaccines. Check rubella and varicella immunity. Nonimmune women receive MMR and varicella vaccines before pregnancy and avoid conception for 1 month because both are live; inadvertent vaccination in early pregnancy is not a reason for termination. Inactivated vaccines such as influenza, Tdap and hepatitis B are safe during pregnancy.

Carrier screening. Cystic fibrosis and spinal muscular atrophy carrier screening and a CBC (with hemoglobin electrophoresis when indicated) for hemoglobinopathies are offered to all; fragile X testing is added with a family history of intellectual disability or early ovarian insufficiency, and ancestry-based or expanded panels are acceptable. A carrier's partner is tested next. Screening before conception widens options such as IVF with preimplantation genetic testing or donor gametes.

Teratogens to switch or wash out

Common teratogens and preconception plans

Drug	Fetal harm	Plan
ACE inhibitors, ARBs	Renal dysgenesis, oligohydramnios, skull hypoplasia, growth restriction	Switch to labetalol or nifedipine
Warfarin	Nasal hypoplasia, stippled epiphyses; later fetal bleeding	Switch to LMWH (mechanical valves need individualized plans)
Valproate	Neural tube defects, lower IQ, autism	Gradual supervised switch to lamotrigine or levetiracetam
Methotrexate	Miscarriage, craniofacial and limb defects	Stop 1–3 months before conception; hydroxychloroquine, sulfasalazine or a TNF inhibitor can substitute
Mycophenolate	Miscarriage, microtia, cleft lip and palate	Stop ≥6 weeks before; switch to azathioprine
Isotretinoin	CNS, ear, conotruncal heart and thymic defects	Stop ≥1 month before; two contraceptive methods during therapy
Leflunomide	Active metabolite persists up to 2 years	Cholestyramine washout before conception

Uncontrolled seizures threaten mother and fetus more than most antiepileptic drugs, so an anticonvulsant is never stopped abruptly; it is replaced before conception and kept at the lowest effective dose.

Pregestational diabetes before and early in pregnancy

Glycemia and anomalies. Hyperglycemia during organogenesis raises the rates of miscarriage and major anomalies in proportion to HbA1c. Congenital heart disease is the most common anomaly (transposition of the great arteries, VSD and other conotruncal defects), followed by neural tube defects, renal anomalies and small left colon; caudal regression (sacral agenesis) is rare but the most specific. The goal is HbA1c <6.5% before conception if it can be reached without hypoglycemia, with effective contraception until then.

Baseline evaluation. A dilated retinal exam (retinopathy can progress in pregnancy, particularly with rapid tightening of control, and is re-examined during pregnancy), urine protein/creatinine ratio and serum creatinine (nephropathy raises the risks of preeclampsia and growth restriction), an ECG with long-standing disease or vascular risk, and TSH in type 1 diabetes because of associated autoimmune thyroid disease.

Drug therapy and targets. Insulin does not cross the placenta and is preferred for both type 1 and type 2 diabetes; metformin crosses the placenta but may be continued as an adjunct in type 2, and other oral agents are replaced. Targets are fasting glucose <95 mg/dL, 1-hour postprandial <140 mg/dL, 2-hour postprandial <120 mg/dL, and HbA1c <6% if achievable without hypoglycemia.

Insulin needs and surveillance

Changing requirements. Insulin needs dip in the first trimester, when nausea and greater insulin sensitivity invite hypoglycemia. They climb through the second and third trimesters as human placental lactogen, progesterone, cortisol and placental growth hormone create insulin resistance, then fall abruptly once the placenta is delivered, so doses are cut immediately postpartum (type 1 patients still need basal insulin).

Pregnancy predisposes to diabetic ketoacidosis at lower glucose levels, sometimes below 200 mg/dL, and DKA endangers the fetus; check ketones in any unwell pregnant woman with type 1 diabetes.

First visitDating ultrasound, HbA1c, retinal exam, urine protein/creatinine, creatinine, ECG as indicated, TSH in type 1
12 weeksStart low-dose aspirin 81 mg, ideally before 16 weeks, to lower preeclampsia risk
About 20–22 weeksDetailed anatomy scan and fetal echocardiogram
Third trimesterGrowth ultrasounds for macrosomia or, with vasculopathy, growth restriction
From 32 weeksAntenatal testing with NST or BPP; earlier with poor control or vasculopathy

Other maternal risks. Preeclampsia, polyhydramnios from fetal polyuria, preterm birth, infection and stillbirth are all more common, especially with poor control or vasculopathy.

Delivery and the newborn

Timing. Well-controlled diabetes without vascular disease is delivered at 39 0/7–39 6/7 weeks; vascular complications, poor control or a prior stillbirth move delivery to 36 0/7–38 6/7 weeks. Cesarean is offered when estimated fetal weight is ≥4,500 g because of shoulder dystocia. During labor an insulin-dextrose infusion keeps maternal glucose about 70–110 mg/dL, since intrapartum hyperglycemia stimulates fetal insulin and worsens neonatal hypoglycemia.

Why the newborn struggles. Maternal glucose crosses the placenta but insulin does not, so the fetus responds with β-cell hyperplasia and hyperinsulinemia. Insulin acts as a growth factor, producing macrosomia, organomegaly and septal hypertrophy, and it delays surfactant production, causing respiratory distress syndrome. Polycythemia with hyperbilirubinemia and hypocalcemia are also common. When the cord is clamped the glucose supply stops while insulin persists, so hypoglycemia appears in the first hours; plan early feeding and glucose checks.