Preterm labor and birth

• Preterm labor: regular uterine contractions with cervical effacement, dilation, or both before 37 weeks’ gestation
• Preterm birth
  • Live birth between 20 0/7 weeks’ and 36 6/7 weeks’ gestation
  • WHO subcategories
    • Extremely preterm (< 28 weeks)
    • Very preterm (28 to < 32 weeks)
    • Moderate to late preterm (32 to < 37 weeks)

Epidemiology

---

Etiology

Risk factors

• Prior spontaneous PTB (single strongest risk factor).
• Short cervical length (CL <25 mm on TVUS prior to 24 wks). c
• Multiple gestations (uterine overdistension).
• Cervical trauma/surgery (e.g., LEEP, cold knife conization).
• Infections: Intra-amniotic infection, STIs, asymptomatic bacteriuria, BV.
• Uterine anomalies or large leiomyomas.
• Low SES, maternal age <18 or >35, cigarette/substance use, short interpregnancy interval (<18 mos).

Pathophysiology

---

Clinical features

---

Diagnostics

---

Treatment

---

• Secondary Prevention (Asymptomatic High-Risk Patients):

  • Prior sPTB: Serial TVUS CL monitoring every 1–2 weeks from 16 to 24 weeks GA + vaginal progesterone (or IM 17-OHPC).
    • If CL shortens to ≤ 25 mm before 24 weeks $\to$ place cervical cerclage.
  • Incidental Short Cervix (CL ≤ 25 mm at ≤ 24 weeks, no prior sPTB): Initiate daily vaginal progesterone (cerclage not routinely indicated).

• Acute Active Preterm Labor Management (by Gestational Age):

  1. < 32 Weeks GA:

     • Antenatal Corticosteroids: Betamethasone (12 mg IM q24h $\times$ 2 doses) or Dexamethasone (6 mg IM q12h $\times$ 4 doses) to accelerate fetal lung maturity (reduces RDS, IVH, NEC, and neonatal mortality). c
     • Tocolytic Therapy (48 hours): Indomethacin (first-line < 32 wks; COX inhibitor). Limit use to < 48 hours to prevent oligohydramnios and premature closure of fetal ductus arteriosus.
     • Neuroprotection: Magnesium Sulfate ($MgS{O}_4$) IV bolus + maintenance infusion to reduce risk and severity of cerebral palsy.
     • GBS Prophylaxis: IV Ampicillin (or Penicillin G) administered until delivery or until GBS culture returns negative.

  2. 32 0/7 to 33 6/7 Weeks GA:

     • Antenatal Corticosteroids: Betamethasone or Dexamethasone.
     • Tocolytic Therapy (48 hours): Nifedipine (first-line $\ge$ 32 wks; CCB).
     • GBS Prophylaxis: IV Ampicillin/Penicillin.
     • $MgS{O}_4$ is NOT indicated for neuroprotection at $\ge$ 32 weeks.

  3. 34 0/7 to 36 6/7 Weeks GA (Late Preterm):

     • Antenatal Corticosteroids: Betamethasone (if not previously administered and delivery expected within 7 days).
     • No Tocolytics: Allow labor to progress; risks of tocolysis outweigh benefits at $\ge$ 34 weeks.
     • GBS Prophylaxis: IV Ampicillin/Penicillin if GBS status is positive or unknown.

• Contraindications to Tocolysis:

  • Absolute: Intrauterine fetal demise (IUFD), lethal fetal anomaly, non-reassuring fetal status, severe preeclampsia/eclampsia, maternal hemodynamic instability/abruption, intra-amniotic infection.

Complications

---

• Neonatal Complications:
  • Respiratory Distress Syndrome (RDS) (surfactant deficiency).
  • Intraventricular Hemorrhage (IVH) (fragile subependymal germinal matrix). c
  • Necrotizing Enterocolitis (NEC).
  • Patent Ductus Arteriosus (PDA).
  • Bronchopulmonary Dysplasia (BPD) & Retinopathy of Prematurity (ROP).
  • Neonatal sepsis, hypothermia, hypoglycemia, hyperbilirubinemia.
  • Long-term: Cerebral palsy, developmental delay, chronic lung disease.
• Maternal Complications:
  • Intra-amniotic infection (chorioamnionitis) and postpartum endometritis.
  • Postpartum hemorrhage (PPH) due to uterine atony.
  • Increased rate of operative interventions (Cesarean delivery, vacuum/forceps-assisted birth).

Intraventricular hemorrhage (IVH)

• Definition: Bleeding into the ventricles from the germinal matrix, a highly vascularized region within the subventricular zone of the brain from which cells migrate out during brain development.
• Etiology: associated with a number of risk factors
  • Birth weight < 1500 g and delivery before 32 weeks’ gestation due to the fragility of the germinal matrix and/or impaired autoregulation of blood pressure
  • Maternal chorioamnionitis
• Pathophysiology
  • Immaturity of the basal lamina and lack of astrocytic glial fibrillary acidic protein within the germinal matrix leads to abnormal cerebral autoregulation.
  • Alterations in an infant’s blood pressure (e.g., during birth, intubation) → failure of cerebral autoregulation to compensate for the change in blood pressure → rupture of and bleeding from vessels in the germinal matrix → rupture of ependyma → blood flows into the ventricles
• Clinical features
  • Usually occurs within the first days of life (up to day 5)
  • Most infants are asymptomatic, but saltatory (for several days) or, more rarely, catastrophic (over minutes to hours) courses are also possible.
  • Lethargy, hypotonia, irregular respirations, seizures, bulging anterior fontanelle c
  • Cranial nerve abnormalities (e.g., pupils react sluggishly to light) and changes in eye movement (e.g., roving eye movements)