Abnormal Uterine Contractions

Overview

Physiology of Normal Uterine Contractions

• Prostaglandins (PGF₂α, PGE₂) from uterine decidual cells act on adjacent myometrial cells to stimulate contraction
• Oxytocin (OT) from the maternal posterior pituitary stimulates uterine decidual cells to increase PGF₂α synthesis; PGs and OT act synergistically
• Gap junctions form between myometrial smooth-muscle cells, coordinating contractions
• A functional shift from progesterone dominance → estrogen dominance (via increased estrogen receptor expression) transforms the myometrium into the laboring phenotype

Medical Physiology (Boron & Boulpaep), p. ~3502–3519

Classification of Abnormal Uterine Contractions

1. Inadequate (hypotonic) uterine contractions — most common
2. Mismatch of fetal and pelvic size (cephalopelvic disproportion)
3. Abnormal fetal position (malpresentation)

Miller's Anesthesia, 10e, p. 8828

Types of Abnormal Labor Patterns

1. Prolonged Latent Phase

• Latent phase > 20 hours in primipara (Friedman's criteria)
• Associated with increased risk: cesarean delivery, 3rd/4th degree lacerations, febrile morbidity, intrapartum blood loss
• Management: therapeutic narcosis (morphine sulfate 15–20 mg) or oxytocin augmentation

2. Protraction Disorders

• Labor progressing, but slower than expected
• Reduced oxytocin receptor density in the lower uterine segment may explain failure to respond to oxytocin augmentation

3. Active-Phase Arrest (Arrest of Dilation)

• No cervical change for ≥4 hours despite adequate uterine contractions (>200 Montevideo units)
• Recommended: minimum 6 hours of oxytocin augmentation before proceeding to cesarean delivery

4. Arrest of Descent (Second-Stage Failure)

• Failure of the presenting part to descend despite complete cervical dilation

Creasy & Resnik's Maternal-Fetal Medicine, p. 940–941, 3094–3124

Risk Factors for Failure to Progress

Creasy & Resnik's Maternal-Fetal Medicine, Table 40.5

Hypotonic vs. Hypertonic Contractions

Molecular Basis of Variability

• OT receptor polymorphisms → poor response to intrinsic or extrinsic oxytocin → inadequate contractility
• β₂-adrenergic receptor polymorphisms → exaggerated response to β₂-agonists → inhibited contractility
• Multiparity → faster labor; greater maternal weight, older age, larger fetus → slower labor

Miller's Anesthesia, 10e, p. 8828

Management

Augmentation of Dysfunctional Labor

• Oxytocin IV infusion (10 mIU/min typical; up to 40 mIU/min)
• Avoid uterine hyperstimulation: >5 contractions/10 min requires stopping the infusion
• Because oxytocin t½ is 12–15 min, hyperstimulation resolves rapidly after discontinuation; restart at half the previous dose
• Complications of overstimulation: uterine rupture, fetal hypoxia (decreased uteroplacental perfusion), forced passage through incompletely dilated cervix

Active Management of Labor (Dublin Protocol)

1. Admit only when painful contractions + complete cervical effacement present
2. Amniotomy soon after admission
3. Oxytocin augmentation if no adequate progress

Goodman & Gilman's Pharmacological Basis of Therapeutics, p. 1001 Creasy & Resnik's Maternal-Fetal Medicine, p. 941

Fetal Consequences

• Late FHR decelerations (uteroplacental insufficiency pattern)
• Fetal hypoxia and acidemia
• Sinusoidal FHR pattern (fetal anemia in severe cases)

Textbook of Family Medicine, 9e; Miller's Anesthesia, 10e