Regular uterine contractions with cervical change before 37 weeks gestation.
Also known as: preterm labor, PTL, premature labor, threatened preterm labor
Overview
Regular uterine contractions accompanied by a change in cervical dilation and/or effacement, or initial presentation with regular contractions and cervical dilation of at least 2 cm, before 37 0/7 weeks gestation (ACOG). Older criteria specified at least 4 contractions per 20 minutes or 8 per 60 minutes.
Epidemiology
Preterm birth occurs in ~10% of US pregnancies and is the leading cause of neonatal morbidity and mortality. Approximately half of preterm births are preceded by spontaneous preterm labor.
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Question 1ReproductiveMedium
A 27-year-old woman at 30 weeks gestation presents with rhythmic uterine cramping and increased watery vaginal discharge. She reports a 2-day history of low-grade fevers. On exam she has a temperature of 38.2°C (100.8°F), uterine fundal tenderness, and contractions every 4 minutes. Cervical exam shows 3 cm dilation and 70% effacement. Amniotic fluid analysis reveals an elevated white blood cell count and a positive Gram stain. She is diagnosed with preterm labor secondary to intra-amniotic infection. Which of the following best explains this patient's preterm labor?
AUteroplacental ischemia activates the renin-angiotensin system, inducing vasoconstrictive uterine spasm
BUterine overdistension stretching the myometrium and triggering premature contractions
Intra-amniotic infection activates the final common pathway of preterm labor: microbial products and pro-inflammatory cytokines (IL-1, IL-6, TNF-alpha) upregulate phospholipase A2 and cyclooxygenase-2, increasing prostaglandin synthesis in the decidua and myometrium.
Prostaglandins drive coordinated myometrial contractions, oxytocin receptor upregulation, and cervical collagen breakdown (ripening), matching the contractions plus dilation/effacement seen here.
This inflammatory cascade is the dominant mechanism in infection-triggered preterm labor; because prolonging the pregnancy leaves mother and fetus exposed to the infection, ACOG lists intra-amniotic infection as a contraindication to tocolysis, even as a temporizing measure.
Why the others are wrong
Estrogen from the maturing placenta directly triggers synchronized myometrial gap junction formation — estrogen does promote gap junctions and contractility, but this describes normal term parturition physiology, not the cytokine-driven cascade caused by intra-amniotic infection.
Decidual hemorrhage generates thrombin, directly stimulating myometrial contraction — thrombin-mediated preterm labor follows abruption or decidual bleeding, and she has no vaginal bleeding or abruption findings; her fever, fundal tenderness, and positive amniotic fluid Gram stain identify infection as the trigger.
Uteroplacental ischemia activates the renin-angiotensin system, inducing vasoconstrictive uterine spasm — uteroplacental ischemia is one trigger of preterm labor, but it acts through decidual hemorrhage and thrombin generation, not renin-angiotensin-mediated vasoconstrictive spasm, and it does not fit the febrile, infected picture here.
Uterine overdistension stretching the myometrium and triggering premature contractions — overdistension is a recognized pathway to preterm labor, but it arises from multiple gestation or polyhydramnios, neither of which is described here; her fever, fundal tenderness, and positive amniotic fluid Gram stain identify intra-amniotic inflammation as the trigger.
Per ACOG, intra-amniotic infection (chorioamnionitis) drives preterm labor through inflammatory prostaglandin production, and management is antibiotics and delivery; tocolysis is contraindicated.
Question 2ReproductiveMedium
A 27-year-old woman at 30 weeks gestation presents with regular painful contractions every 4 minutes and pelvic pressure. Exam shows the cervix is 4 cm dilated and 90% effaced, and fetal monitoring is reassuring. Despite nifedipine tocolysis and a first dose of betamethasone, contractions intensify and she delivers a liveborn infant 6 hours later. Which of the following complications is the neonate most likely to develop in the immediate neonatal period?
ARetinopathy of prematurity
BBronchopulmonary dysplasia
CIntraventricular hemorrhage
DNecrotizing enterocolitis
EHyaline membrane disease
Reveal answer & full explanation
Correct answer: E — Hyaline membrane disease
ARetinopathy of prematurity
BBronchopulmonary dysplasia
CIntraventricular hemorrhage
DNecrotizing enterocolitis
EHyaline membrane disease✓
Why Hyaline membrane disease is correct
Hyaline membrane disease (neonatal respiratory distress syndrome) results from surfactant deficiency in immature type II pneumocytes and is the most common acute complication of preterm birth, with incidence rising sharply as gestational age falls below 34 weeks.
It manifests within minutes to hours of delivery with tachypnea, grunting, retractions, and nasal flaring, making it the earliest and highest-yield complication in the immediate neonatal period at 30 weeks.
This is exactly why antenatal betamethasone is given between 24 0/7 and 33 6/7 weeks to accelerate fetal lung maturity and reduce respiratory distress; only one dose was received before delivery, so the protective effect is incomplete.
Why the others are wrong
Bronchopulmonary dysplasia is a chronic lung disease defined by oxygen dependence at 36 weeks corrected age; it is a downstream consequence of prolonged ventilation and oxygen exposure used to treat the acute lung disease, not the immediate complication at birth.
Necrotizing enterocolitis is ischemic/inflammatory bowel injury that usually appears over the first days to weeks of life with feeding intolerance and is most common in very-low-birth-weight infants, so it is less likely than respiratory distress in the immediate period at 30 weeks.
Retinopathy of prematurity is abnormal retinal vascularization driven largely by oxygen exposure; it is screened for and detected weeks later, not an acute peripartum event.
Intraventricular hemorrhage — germinal matrix bleeding is a classic complication of prematurity, and incomplete antenatal steroid exposure raises its risk, but its risk climbs steeply at lower gestational ages, especially below 28 weeks, many bleeds are clinically silent and found on screening cranial ultrasound, and at 30 weeks it is far less common than surfactant-deficient respiratory distress, which begins within minutes to hours of delivery.
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Smoking, substance use, short interpregnancy interval, low BMI, Black race, low socioeconomic status
Pathophysiology
Final common pathway involves activation of decidua, myometrium, and cervix. Triggers include inflammation/infection (microbial products and cytokines such as IL-1, IL-6, and TNF-alpha increase decidual prostaglandin synthesis), uteroplacental ischemia, uterine overdistension, decidual hemorrhage (thrombin directly stimulates myometrial contraction, as in abruption), and stress. Progesterone withdrawal at the local level, prostaglandin release, and oxytocin receptor upregulation drive coordinated contractions and cervical ripening.
Clinical presentation
Symptoms
Rhythmic uterine cramping or low back pain
Pelvic pressure, 'feels like the baby is going to fall out'
Change in vaginal discharge (mucousy, watery, bloody)
Signs / physical exam
Palpable contractions, cervical change on exam
Cervical dilation >=3 cm or effacement >=80% strongly supports diagnosis
Fetal heart tones reassuring or with variable decelerations
Differential diagnosis
Braxton-Hicks contractions — Irregular, painless, not associated with cervical change; resolve with hydration and rest
Round ligament pain — Sharp groin pain with movement; not rhythmic; no cervical change
UTI / pyelonephritis — Dysuria, frequency, CVA tenderness; UA positive; can precipitate preterm contractions
Constipation / GI distress — Abdominal cramping not localized to uterus; no cervical change
Diagnostic workup
Diagnostic criteria
Persistent regular contractions plus cervical change (dilation/effacement), or regular contractions with cervical dilation of at least 2 cm at presentation. Equivocal cases triaged with transvaginal CL and fFN.
Labs
Urinalysis and urine culture; GBS culture if not current; cervical cultures (GC/CT) as indicated
CBC, basic metabolic panel
Fetal fibronectin (fFN) from posterior fornix between 22 0/7 and 34 6/7 wk: most useful negative predictive value (<1% delivery within 7-14 days if negative)
Imaging
Transvaginal ultrasound cervical length: <25 mm raises concern; >=30 mm reassuring
Obstetric ultrasound for fetal biometry, presentation, AFI, placental location
Continuous external fetal monitoring
Diagnostic algorithm
flowchart TD
A[Contractions <37 wk] --> B[Speculum + TVUS cervical length]
B --> C{Cervical change<br/>or CL <20 mm?}
C -->|No, CL >=30 mm| D[Likely false labor<br/>discharge with precautions]
C -->|Equivocal 20-29 mm| E[Fetal fibronectin]
E -->|Negative| D
E -->|Positive| F[Admit, treat as PTL]
C -->|Yes| F
F --> G[Antenatal steroids<br/>24-34 wk]
F --> H[Tocolysis x 48 h<br/>nifedipine or indomethacin]
F --> I[MgSO4 neuroprotection<br/>if <32 wk]
F --> J[GBS prophylaxis<br/>if delivery imminent]
Triage and management algorithm for suspected preterm labor.
Treatment
First-line
Antenatal corticosteroids (accelerate fetal type II pneumocyte maturation and surfactant synthesis; reduce RDS, IVH, NEC, and neonatal death) 24 0/7 to 33 6/7 wk (consider 34 0/7 to 36 6/7 wk in late preterm if not previously given): betamethasone 12 mg IM x 2 doses 24 h apart or dexamethasone 6 mg IM x 4 doses 12 h apart
Magnesium sulfate for fetal neuroprotection when delivery anticipated <32 wk (4-6 g IV loading dose then 1-2 g/h)
Tocolysis (generally 24 0/7 to 33 6/7 wk, for up to 48 h) to delay delivery for steroid effect, magnesium neuroprotection, and maternal transfer to higher level of care; contraindicated with intra-amniotic infection, maternal hemorrhage with hemodynamic instability (e.g., abruption), nonreassuring fetal status, preeclampsia with severe features or eclampsia, fetal demise or lethal anomaly, PPROM (except short-term for steroids or transfer without infection), or a maternal contraindication to the drug
First-line tocolytics: nifedipine (CCB) or indomethacin (NSAID, restrict to <32 wk and <48 h to avoid ductal closure and oligohydramnios)
Beta-agonist (terbutaline) limited to short-term use; FDA boxed warning against prolonged use (>48-72 h) due to maternal cardiac toxicity
GBS intrapartum antibiotic prophylaxis if delivery imminent and culture positive/unknown
Prevention in women with prior spontaneous PTB
17-OH progesterone caproate IM weekly from 16-36 wk historically used; recent PROLONG trial led to FDA withdrawal of Makena — current recommendations favor vaginal progesterone in setting of short cervix
Vaginal progesterone (100-200 mg nightly) for women with short cervix (<25 mm) <24 wk
Cervical cerclage for women with prior spontaneous PTB AND short cervix <25 mm before 24 wk
Second-line / adjunct
Atosiban (oxytocin receptor antagonist) — not available in US
Magnesium sulfate as tocolytic (less effective than nifedipine; primary role is neuroprotection)
Complications
Preterm birth with prematurity-related morbidity: RDS, BPD, IVH, NEC, retinopathy of prematurity, neurodevelopmental impairment; RDS (surfactant deficiency) presents within minutes to hours of birth, whereas NEC, BPD, and ROP develop days to weeks later
Maternal: tocolytic side effects (pulmonary edema with beta-agonists, hypotension with nifedipine, ductal closure with indomethacin)
Magnesium toxicity (loss of DTRs, respiratory depression) — treat with IV calcium gluconate
PANCE pearls
Indomethacin tocolysis is contraindicated after 32 wk because it can cause premature ductal closure in utero and oligohydramnios.
Magnesium sulfate for fetal neuroprotection can be given to a patient receiving nifedipine; concurrent use has not been shown to increase serious magnesium-related adverse effects, but the combination can add hypotension and neuromuscular or cardiac depression, so monitor BP, reflexes, and respirations.
Fetal fibronectin is most useful for its strong negative predictive value — a negative fFN supports outpatient management.
Magnesium for neuroprotection (<32 wk) is given regardless of whether the patient is also receiving it as a tocolytic.
Cervical length <25 mm + prior spontaneous PTB is the cerclage indication; isolated short cervix without prior PTB is treated with vaginal progesterone, not cerclage.
References
ACOG PB 234 — ACOG Practice Bulletin 234: Prediction and Prevention of Spontaneous Preterm Birth (Obstet Gynecol 2021)
ACOG PB 171 — ACOG Practice Bulletin 171: Management of Preterm Labor (Obstet Gynecol 2016)
PROLONG — Blackwell et al., Am J Perinatol 2020 — 17-OHPC efficacy
BEAM Trial — Rouse et al., NEJM 2008 — MgSO4 for fetal neuroprotection
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