Prevention of Preterm (Premature) Labor

Preterm (premature) labor is labor that begins before the 37th week of pregnancy; it is responsible for 85% of neonatal illnesses and deaths. The onset of labor is a result of a complex sequence of biologic events involving regulatory factors that are still poorly understood. Significant risk factors for the onset of preterm labor are a past history of preterm delivery, premature rupture of the membranes, urinary tract infection, exposure to diethylstilbestrol, multiple gestation, and abdominal or cervical surgery. In high-risk women (prior preterm birth), ultrasound measurement of cervical length (< 25 mm) in the second trimester may also identify a significant risk.

Low rates of preterm delivery are associated with success in educating patients to identify regular, frequent uterine contractions and in alerting medical and nursing staff to evaluate these patients early and initiate treatment if cervical changes can be identified.

Distinguishing true from false labor in patients with a history of previous preterm births can be facilitated by the use of fetal fibronectin measurement in cervicovaginal specimens. This ubiquitous protein can be released by several different stimuli. Its absence (< 50 ng/mL) in the face of uterine contractions in a patient with a previous preterm birth has a negative predictive value of 93-97% for delivery within 7-14 days. Despite initial promising findings, several prospective randomized controlled trials have failed to demonstrate a benefit of home uterine activity monitoring in preventing preterm birth. On the other hand, a recent study has suggested that weekly injections of 17a-hydroxyprogesterone caproate from 16 to 36 weeks of gestation in women with a history of preterm delivery can substantially reduce the rate of recurrent preterm birth.

In more acute situations, intravenous magnesium sulfate is effective, as are intravenous ß-adrenergic drugs. Magnesium sulfate is given as a 4- or 6-g bolus followed by a continuous infusion of 2-3 g/h. The rate may be increased by 1 g/h every 30 minutes to 2 hours until contractions cease or a blood magnesium concentration of 6-8 mg/dL is reached. Magnesium levels are determined every 4-6 hours to monitor the therapeutic blood level. After contractions have ceased for 12-24 hours, magnesium can be stopped and the situation reassessed.

Uterine smooth muscle is largely under sympathetic nervous system control, and stimulation of ß2-adrenergic receptors relaxes the myometrium. Consequently, inhibition of uterine contractility often can be accomplished by the administration of ß-adrenergic drugs such as ritodrine or terbutaline. Alternatively, use of an oxytocin receptor antagonist might also be expected to inhibit uterine contractility. However, trials of one such antagonist, atosiban, have shown only minimal efficacy.

Ritodrine is no longer manufactured. Terbutaline can be given as an intravenous infusion starting at 2.5 ug/min and increased by 2.5 ug/min every 20 minutes until contractions cease or to a maximum dose of 20 ug/min. Terbutaline can also be administered as subcutaneous injections of 250 ug every 3 hours. Oral terbutaline therapy following parenteral treatment is often elected and consists of giving 2.5-5 mg every 2-4 hours. With terbutaline, a dose-related elevation of heart rate of 20-40 beats/min may occur. An increase of systolic blood pressure up to 10 mm Hg is likely, and the diastolic pressure may fall 10-15 mm Hg during the infusion. Nifedipine has also been used in doses of 10-20 mg orally every 4-6 hours. Blood pressure may fall with nifedipine, but cardiac output increases considerably. Transient elevation of blood glucose, insulin, and fatty acids together with slight reduction of serum potassium have been reported with ß-adrenergic drugs. Fetal tachycardia may be slight or absent. No drug-related perinatal deaths have been reported with ß-agonists. Maternal side effects requiring dose limitation are tachycardia (= 120 beats/min), palpitations, and nervousness. Fluids should be limited to 2500 mL/24 h. Serious side effects (pulmonary edema, chest pain with or without electrocardiographic changes) are often idiosyncratic, not dose-related, and warrant termination of therapy.

One must identify cases in which untimely delivery is the sole threat to the life or health of the infant. An effort should be made to eliminate (1) maternal conditions that compromise the intrauterine environment and make premature birth the lesser risk, eg, preeclampsia-eclampsia; (2) fetal conditions that either are helped by early delivery or render attempts to stop premature labor meaningless, eg, severe erythroblastosis fetalis; and (3) clinical situations in which it is likely that an attempt to stop labor will be futile, eg, ruptured membranes with chorioamnionitis, cervix fully effaced and dilated more than 3 cm, or strong labor in progress.

In pregnancies of less than 34 weeks’ duration, betamethasone, 12 mg intramuscularly, or dexamethasone, 16 mg intramuscularly, repeated in 12-24 hours, is administered to hasten fetal lung maturation and permit delivery 48 hours after initial treatment when further prolongation of pregnancy is contraindicated.

ACOG practice bulletin. Assessment of risk factors for preterm birth. Clinical management guidelines for obstetrician-gynecologists. Number 31, October 2001. Obstet Gynecol 2001;98:709. 

Goldenberg RL: The management of preterm labor. Obstet Gynecol 2002;100(5 Part 1):1020.

Meis PJ et al: Prevention of recurrent preterm delivery by 17 alpha-hydroxyprogesterone caproate. N Engl J Med 2003; 348:2379.

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Revision date: June 18, 2011
Last revised: by David A. Scott, M.D.