Describe the definitions, causes and management of preterm Labour and Premature Rupture of Membranes.

Antenatal corticosteroids reduce neonatal mortality most effectively.

Definition

Preterm labour is the onset of regular uterine contractions with progressive cervical change occurring after viability and before 37 completed weeks. Premature rupture of membranes (PROM) is spontaneous rupture of the membranes before the onset of labour; when this happens before 37 weeks it is preterm PROM (PPROM).

Preterm Labour - Management Pathway

Causes and Risk Factors

Previous preterm birth, infection (urinary, genital, chorioamnionitis), polyhydramnios and multiple pregnancy (over-distension), cervical incompetence, antepartum haemorrhage, pre-eclampsia, uterine anomalies and fibroids, low socio-economic status, smoking and a short inter-pregnancy interval. Many cases are idiopathic.

Diagnosis

• Preterm labour — documented uterine contractions with cervical dilatation/ effacement
• a short cervix on transvaginal ultrasound and a positive fetal fibronectin test support the diagnosis and predict risk.
• PROM — a history of sudden gush of fluid, with pooling of liquor in the posterior fornix on sterile speculum examination
• supported by a positive nitrazine test (alkaline pH) and ferning on microscopy, and by oligohydramnios on ultrasound.
• Digital examination is avoided in PROM to reduce infection.

Management of Preterm Labour

• Confirm the diagnosis, assess gestation and fetal wellbeing, and exclude contraindications to continuing the pregnancy (chorioamnionitis, abruption, fetal distress, lethal anomaly).
• Tocolysis to gain 48 hours for steroid action and in-utero transfer — nifedipine (calcium-channel blocker), atosiban (oxytocin antagonist) or isoxsuprine; contraindicated when prolonging pregnancy is unsafe.
• Antenatal corticosteroids — betamethasone (12 mg IM, two doses 24 h apart) or dexamethasone — to accelerate fetal lung maturity and reduce RDS, intraventricular haemorrhage and necrotising enterocolitis.
• Magnesium sulphate for fetal neuroprotection when birth before 32 weeks is imminent.
• Group-B-streptococcus prophylaxis (intrapartum penicillin) as indicated, and in-utero transfer to a unit with neonatal intensive care.

Management of Prom / Pprom

• Confirm rupture and gestation; assess for chorioamnionitis (maternal fever, tachycardia, uterine tenderness, offensive liquor, fetal tachycardia, raised white-cell count/CRP).
• At term, if labour does not start spontaneously, induce (risk of infection rises with the latent period).
• In PPROM without infection, manage expectantly with monitoring, latency antibiotics (e.g. Erythromycin) to prolong pregnancy and reduce infection, and corticosteroids ± magnesium; deliver if chorioamnionitis, fetal distress or abruption supervene, or once a safe gestation is reached.

WHY Tocolysis Buys Time Rather Than Stops Labour

A concept that clarifies the whole management of preterm labour is why tocolytics are given at all, when they rarely prevent preterm birth. Tocolysis does not cure the underlying cause (infection, overdistension, cervical weakness), and by itself does not significantly improve perinatal outcome. Its value lies entirely in the 48 hours it buys — and those hours are golden, because they permit the two interventions that genuinely save babies: a course of antenatal corticosteroids (betamethasone or dexamethasone), which take about 24–48 hours to act and reduce respiratory distress syndrome, intraventricular haemorrhage, necrotising enterocolitis and neonatal death; and in-utero transfer to a centre with neonatal intensive care — the fetus being the safest incubator for transport. Magnesium sulphate may also be given for fetal neuroprotection before 32 weeks. Understanding that tocolysis is a means to an end — a window for steroids and transfer — rather than an end in itself explains why it is used only for a strictly limited period, why it is pointless once these have been achieved, and why it is withheld when prolonging the pregnancy would be dangerous (chorioamnionitis, severe pre-eclampsia, fetal distress).

WHY Pprom Is a Balance Between Infection and Prematurity

The management of preterm prelabour rupture of membranes turns on one dilemma: the risk of infection weighed against the risk of prematurity. Once the membranes rupture, the protective barrier is gone and ascending infection becomes progressively more likely with time — chorioamnionitis threatens the mother with sepsis and the fetus with pneumonia, sepsis and neurological injury; oligohydramnios adds cord compression and, if very early and prolonged, pulmonary hypoplasia. Yet delivering immediately at, say, 30 weeks exposes the baby to every hazard of prematurity. The resolution is a balance based on gestation: before 34 weeks, if there is no infection and the fetus is well, manage expectantly — with corticosteroids, prophylactic antibiotics (erythromycin, which prolongs latency and reduces infection) and close surveillance for chorioamnionitis (maternal fever, tachycardia, uterine tenderness, offensive discharge, fetal tachycardia, rising leucocyte count and CRP); after 34 weeks, or at any gestation once infection or fetal compromise appears, deliver. Recognising that time is both friend (maturity) and enemy (infection) explains why digital examination is avoided (a sterile speculum is used instead) and why vigilance for infection must be constant.

• Preterm labour = labour before 37 completed weeks — the leading cause of perinatal mortality and morbidity.
• Tocolytics (nifedipine, atosiban) buy ~48 hours; their value is to allow corticosteroids to act and to permit in-utero transfer.
• Antenatal corticosteroids reduce RDS, IVH, NEC and neonatal death; MgSO4 gives fetal neuroprotection before 32 weeks.
• PPROM: manage expectantly before 34 weeks with steroids and erythromycin, watching closely for chorioamnionitis; deliver if infection or compromise appears.
• Avoid digital vaginal examination in PPROM (it introduces infection) — use a sterile speculum.