Clinical overview
Preterm birth — delivery before 37 completed weeks (259 days) of gestation — is the single largest direct cause of neonatal death and long-term neurodevelopmental disability worldwide, and a dominant driver of perinatal mortality in South Africa. The registrar's task is rarely glamorous: it is the unglamorous, high-leverage work of buying gestational weeks, protecting the brain and lungs, and getting the baby born in the right place. Two related but distinct clinical problems dominate this objective. The first is preterm labour with intact membranes — regular contractions with cervical change before term. The second is preterm prelabour rupture of membranes (PPROM) — rupture of the fetal membranes before 37 weeks and before the onset of labour, which precedes roughly a third of preterm births and shifts the whole calculus towards infection.
The central tension in both is the same: every additional day in utero improves survival and reduces morbidity, but the intrauterine environment may itself become dangerous (chorioamnionitis, abruption, cord compression). Management is therefore a continuous risk–benefit negotiation between prolonging the pregnancy and delivering the baby — and in the South African setting, that negotiation is profoundly shaped by where the woman is. A 28-week delivery at a tertiary centre with a NICU and surfactant is a survivable event; the same delivery in a district hospital without ventilation or a neonatal team is frequently not. Decisions about tocolysis, transfer, and resuscitation cannot be separated from the level of care. The NDoH National Integrated Maternal and Perinatal Care Guideline (NDoH, 2024) frames this explicitly, and Saving Mothers/Saving Babies (NCCEMD) repeatedly identifies failure to refer in utero and failure to give antenatal steroids as avoidable contributors to preterm perinatal death.
Core knowledge
Definitions and gestational thresholds
- Preterm birth: delivery from viability up to 36⁺⁶ weeks. Subcategories matter clinically: extremely preterm (<28 weeks), very preterm (28 to 31⁺⁶), moderate (32 to 33⁺⁶), and late preterm (34 to 36⁺⁶). The bulk of births are late preterm, but the bulk of mortality and morbidity sits below 32 weeks.
- Threshold of viability: a moving line set by neonatal capability. South African resource realities mean the locally agreed threshold (commonly framed around ~26 weeks or a birth weight ~750–800 g in many public units, lower in well-resourced centres) is not identical to high-income thresholds. The 5th-edition NDoH guideline and local neonatal protocols define the institution's viability cut-off; the registrar must know the local one, because it determines whether active intervention (steroids, tocolysis, caesarean for fetal indication) is offered at all.
- PPROM: rupture of membranes before labour and before 37 weeks. Pre-viable PPROM (before the local viability threshold, classically <24 weeks) carries an additional burden of pulmonary hypoplasia and limb contractures from prolonged oligohydramnios and warrants honest, individualised counselling.
Why babies are born too early
Preterm birth is a syndrome, not a single disease, with overlapping pathways: intrauterine infection/inflammation (the dominant mechanism in early PPROM and very preterm labour — ascending genital tract organisms trigger prostaglandin-driven membrane weakening and myometrial activation); uteroplacental ischaemia/abruption; uterine overdistension (multiple pregnancy, polyhydramnios); cervical insufficiency; decidual senescence; and iatrogenic/indicated preterm birth for maternal or fetal disease (pre-eclampsia, growth restriction). Recognising the pathway reframes management — see Multiple pregnancy, Intrauterine growth restriction and Antepartum haemorrhage.
Membrane physiology in PPROM
The membranes maintain the sterile amniotic compartment. Once ruptured, the latency period (rupture-to-delivery interval) is inversely related to gestation — earlier PPROM tends to have longer latency, but every day of latency raises the cumulative risk of chorioamnionitis, cord prolapse (especially with malpresentation or high presenting part), placental abruption, and fetal/neonatal sepsis. Oligohydramnios from ongoing loss adds cord compression and, if prolonged from early gestation, pulmonary hypoplasia.
Figure J18.1 — PPROM and preterm-birth mechanism map showing the shared inflammation-to-contractions pathway, latency trade-off, speculum-first diagnosis and the local-viability/NICU check.
Assessment
Preterm labour — is it real labour?
Most women presenting with threatened preterm labour will not deliver imminently, and over-treatment carries its own harms (unnecessary transfer, tocolytic side-effects, iatrogenic delivery). The assessment seeks to separate true preterm labour from a false alarm.
- History: gestation (re-confirm dating — see Gestational age assessment), contraction frequency and painfulness, any fluid loss or bleeding (which changes everything — see Antepartum haemorrhage), fever, dysuria, decreased fetal movements (Decreased fetal movements), and risk factors (previous preterm birth, multiple pregnancy, infection, smoking, short interpregnancy interval).
- Examination: maternal temperature, pulse, BP; abdominal palpation for tenderness (abruption), presentation, and contraction frequency; sterile speculum examination to look for cervical dilatation, visible membranes, pooling of liquor, and to take swabs. Avoid digital vaginal examination if PPROM is suspected — it introduces organisms, shortens latency, and adds nothing the speculum did not.
- Cervical assessment: cervical length on transvaginal ultrasound and, where available, fetal fibronectin help triage — a short cervix or positive fibronectin raises the probability of imminent delivery, while a long closed cervix and negative test reassure. These tools rule out better than they rule in; in many SA public units they are unavailable and clinical judgement plus serial assessment governs.