Post-term Pregnancy & Stillbirth
Date it right, test at 41, deliver by 42—and work up every loss
Definitions, dating, and why pregnancies run long
Terminology. Term is split by completed weeks: early term 37+0–38+6, full term 39+0–40+6, late term 41+0–41+6, and post-term ≥42+0 weeks. Perinatal risk rises steadily across the late-term window, so these labels drive surveillance and delivery decisions.
Dating comes first. The most common reason a pregnancy looks post-term is a wrong due date. Crown-rump length measured before 14 weeks is the most accurate dating method (within about 5–7 days); the ultrasound date replaces the LMP date when they differ by more than 5 days before 9 weeks or more than 7 days at 9+0–13+6 weeks. Later biometry is far less precise (up to ±3 weeks in the third trimester), so a late growth scan should not move the due date.
Who goes post-term. Nulliparity, a prior post-term pregnancy (the strongest predictor), obesity, and a male fetus. Rare fetal causes show how labor starts: in anencephaly (no functioning fetal hypothalamic–pituitary–adrenal axis) and X-linked placental sulfatase deficiency (low maternal estriol), the fetal adrenal DHEA-S → placental estrogen signal that helps trigger labor is missing.
Risks of prolonged pregnancy
Two processes create the danger: an aging placenta that cannot keep pace (chronic fetal hypoxia) or one that keeps working (continued growth).
| Problem | Mechanism | Consequences |
|---|---|---|
| Oligohydramnios | Reduced placental perfusion → less fetal urine | Cord compression, variable decelerations, intolerance of labor |
| Meconium passage | Mature fetal gut plus hypoxic stress | Meconium aspiration syndrome: airway obstruction, chemical pneumonitis, pulmonary hypertension |
| Dysmaturity | Chronic uteroplacental insufficiency | Wasted newborn; hypoglycemia, polycythemia; stillbirth |
| Macrosomia | Continued growth with a functioning placenta | Shoulder dystocia, brachial plexus injury, operative delivery |
| Maternal morbidity | Large fetus, prolonged labor | Labor dystocia, cesarean, 3rd/4th-degree lacerations, postpartum hemorrhage, infection |
Postmaturity (dysmaturity) syndrome. The newborn of chronic placental insufficiency is thin with little subcutaneous fat, has dry, cracked, peeling skin, long nails, and scant vernix and lanugo, and is often stained yellow-green by meconium (skin, nails, cord). Depleted glycogen causes early hypoglycemia, and chronic hypoxia drives erythropoietin → polycythemia.
A nonvigorous meconium-stained newborn gets standard resuscitation; routine intubation for tracheal suctioning is no longer recommended, and amnioinfusion does not prevent meconium aspiration.
Surveillance and timing of delivery
Antenatal testing. From 41+0 weeks, weekly or twice-weekly nonstress testing plus amniotic fluid assessment (the modified biophysical profile) screens for placental insufficiency. Oligohydramnios—deepest vertical pocket <2 cm (preferred: same outcomes, fewer unnecessary inductions) or AFI ≤5 cm—or a nonreassuring test calls for delivery, not repeat testing. A reactive NST does not cancel oligohydramnios.
- Confirm datingfirst-trimester CRL; review IVF or early-ultrasound records
- 39+0 weekselective induction reasonable for low-risk patients who choose it; offer membrane sweeping
- 41+0 weeksweekly or twice-weekly NST + fluid assessment; offer induction (41+0–41+6)
- 42+0 weeksinduction recommended; delivery completed by 42+6
- At any pointoligohydramnios or nonreassuring testing → deliver
Why 41 weeks. The Swedish SWEPIS trial (induction at 41 vs waiting to 42 weeks) stopped early for excess perinatal deaths with waiting; pooled trials show induction at ≥41 weeks lowers perinatal mortality without raising cesarean rates.
ARRIVE. In low-risk nulliparas, induction at 39+0–39+4 weeks lowered cesarean and hypertensive-disorder rates versus expectant management, with no worse composite perinatal outcome—a reasonable option, not a mandate.
Preparing the cervix and inducing labor
Membrane sweeping. At term (about 38–41 weeks) a finger passed through the internal os separates the membranes from the lower uterine segment, releasing endogenous prostaglandins. It increases spontaneous labor and reduces post-term pregnancy and formal induction; expect cramping, spotting, and irregular contractions.
Bishop score. Dilation, effacement, station, consistency, and position. A score ≤6 is unfavorable and needs ripening before oxytocin; a score >8 predicts vaginal delivery rates similar to spontaneous labor.
| Method | Action | Key points |
|---|---|---|
| Misoprostol | PGE1 analog, vaginal or oral | Cheap, effective; tachysystole; not for term ripening after a cesarean or transmural myomectomy |
| Dinoprostone | PGE2 gel or vaginal insert | Insert can be pulled if tachysystole develops |
| Balloon catheter | Mechanical dilation of the internal os | Little tachysystole; preferred ripening method with a uterine scar |
| Oxytocin ± amniotomy | Uterotonic once the cervix is ripe | Standard agent for induction and augmentation |
Do not ripen a scarred uterus with misoprostol in the third trimester—uterine rupture risk. Use a balloon catheter, then oxytocin, for induction during a trial of labor after cesarean.
Tachysystole (>5 contractions in 10 minutes, averaged over 30 minutes) is the main prostaglandin hazard: stop or remove the agent and give terbutaline if the fetal heart rate is affected.
Stillbirth: diagnosis and evaluation
Definition and diagnosis. In the United States stillbirth is fetal death at ≥20 weeks (or ≥350 g if gestational age is unknown). Patients usually report absent fetal movement; absent Doppler heart tones raise suspicion, and absent cardiac activity on real-time ultrasound confirms it. The Spalding sign (overlapping skull bones) is a late radiographic finding.
Risk factors and causes. Black race, age ≥35, obesity, smoking and substance use, pregestational diabetes, chronic hypertension, SLE/antiphospholipid syndrome, multiple gestation, fetal growth restriction, and prior stillbirth. Leading causes are obstetric complications such as abruption, placental disease, fetal genetic or structural anomalies, infection, cord accidents, and hypertensive disorders; many remain unexplained despite full evaluation.
| Test | Looks for | Notes |
|---|---|---|
| Fetal autopsy | Anomalies, infection, growth pattern | High yield; if declined, external exam by a pathologist, photos, X-ray or MRI |
| Placenta, cord, membranes | Abruption, infarction, chorioamnionitis, cord lesions | Among the most informative tests |
| Chromosomal microarray | Aneuploidy, copy-number variants | Preferred over karyotype (no dividing cells needed); amniocytes, placental block, cord, or internal fetal tissue |
| Kleihauer-Betke / flow cytometry | Fetomaternal hemorrhage | Draw promptly, ideally before delivery; also sets anti-D dose |
| Antiphospholipid antibodies | Lupus anticoagulant, anticardiolipin, anti-β2-glycoprotein I | APS causes placental insufficiency and fetal death |
| Syphilis, parvovirus B19 | Congenital infection, fetal anemia and hydrops | Serology; tissue PCR if available |
| HbA1c or glucose tolerance test; toxicology | Occult diabetes; cocaine and other drugs | Cocaine → abruption |
Inherited thrombophilia panels (factor V Leiden, prothrombin mutation, protein C/S, antithrombin) and TORCH titers are not part of the routine workup; test for inherited thrombophilia only with a personal or family history of VTE.
Delivery, aftercare, and the next pregnancy
Route. Most women labor spontaneously within about 2 weeks, but most choose prompt delivery. Options depend on gestational age, preference, and provider skill: dilation and evacuation in the second trimester (limits intact autopsy) or induction with misoprostol, ideally after mifepristone 200 mg orally 24–48 hours earlier to shorten the induction. From 28 weeks, standard obstetric induction protocols apply. Cesarean is reserved for maternal indications—it adds maternal risk with no fetal benefit.
A fetus retained >4 weeks releases tissue factor (thromboplastin) → slow consumption of fibrinogen and platelets → DIC. Check fibrinogen, platelets, and PT/PTT at diagnosis and serially during expectant management; a falling fibrinogen means deliver, with blood products available.
Aftercare. Give anti-D immune globulin to unsensitized Rh(D)-negative women; the 300 μg dose covers about 30 mL of fetal whole blood, with extra vials if the Kleihauer-Betke shows more. Suppress lactation with a supportive bra, ice, and NSAIDs; cabergoline (a dopamine agonist) is an option, whereas bromocriptine is no longer used (stroke, MI, seizures). Offer seeing and holding the baby, naming, and mementos (photos, footprints); screen for depression and PTSD, and schedule a visit to review results.
The next pregnancy. Recurrence risk is several-fold above baseline and depends on the cause. Plan a first-trimester dating ultrasound, aneuploidy screening, a detailed anatomy scan, serial growth scans, daily kick counts, and NST/BPP from 32 weeks (or 1–2 weeks before the gestational age of the prior loss). Address modifiable risks: smoking cessation, weight, glucose and blood pressure control, and heparin plus low-dose aspirin when antiphospholipid syndrome is confirmed.