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CORTICOSTEROID THERAPY
Maternal corticosteroid treatment with betamethasone and dexamethasone has been shown in several controlled trials to decrease the incidence of respiratory distress syndrome. Antenatal corticosteroid therapy decreased the risk of respiratory distress syndrome, intraventricular hemorrhage, and mortality in infants born prematurely. Antenatal therapy with corticosteroids should be considered for all fetuses at risk for preterm delivery between 24 and 34 weeks of gestational age, regardless of race, gender, or availability of surfactant therapy. Antenatal corticosteroids should be considered in the presence of preterm PROM in pregnancies less than 30-32 weeks of gestation unless there is evidence of clinical chorioamnionitis.
There has been hesitation to use corticosteroids in some patients because of the impression that delivery will occur before a full course of therapy (ie, less than 24 hours). However, treatment with corticosteroids for less than 24 hours still appears to be associated with a significant reduction in neonatal mortality, respiratory distress syndrome, and intraventricular hemorrhage. The most commonly used regimens of antenatal corticosteroids would appear to be either two doses of 12 mg of betamethasone given intramuscularly 24 hours apart or four doses of 6 mg of dexamethasone intramuscularly 12 hours apart.
METHOD OF DELIVERY
Retrospective studies show that the singleton breech of less than 32-34 weeks of gestation or weighing less than 1,500 g has less morbidity and mortality if delivered by the cesarean method, particularly if the breech presents as a footling. There are no convincing data to indicate that cesarean delivery is indicated for cephalic presentations if labor is progressing in a normal fashion. Factors associated with intraventricular hemorrhage are the prematurity of the fetus, shock, and respiratory distress syndrome, but not the mode of delivery for cephalic presentations.

Methods to arrest preterm labor include bed rest and tocolytics. The most widely used tocolytic drugs are magnesium sulfate, beta-mimetics, calcium channel blockers, and prostaglandin synthetase inhibitors. Recently, atosiban (an oxytocin analog) and nitric oxide donor drugs have been used.
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Magnesium sulfate is frequently used as a first-line drug for tocolysis, particularly in patients with diabetes. It is initiated by a loading dose of 4-6 g intravenously, followed by a continuous maintenance dose of 2-4 g per hour, in an attempt to achieve serum concentrations of 6-8 mg/dL. After successful tocolysis, oral beta-adrenergic agents are usually used until near term (approximately 36 weeks). Deep-tendon reflexes should be checked routinely to ensure their presence, and fluid intake and output should be monitored because pulmonary edema can occur with this agent. Fetal serum levels equilibrate with maternal concentrations, and occasional transient depression caused by hypermagnesemia in newborns has been reported. Long-term magnesium therapy markedly increases calcium losses, which could ultimately affect bone mineralization.
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Calcium channel blocking drugs are used because of their ability to cause a decrease in intracellular free calcium and, hence, inhibition of myometrial contractility. In all studies, nifedipine was more successful or as good as ritodrine in stopping contractions. These adverse effects include hypercapnia, hypoxia, and acidosis.
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Beta-adrenergic tocolysis is usually initiated by the parenteral route either by a continuous intravenous infusion, titrating the infusion rate against contractions and side effects, or the intermittent intramuscular or subcutaneous approach. After cessation of uterine contractions, oral medication is often used in a dose and at a frequency that results in a mild maternal tachycardia until near term.
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Maternal side effects, such as hypotension, excessive tachycardia or cardiac arrhythmias, myocardial ischemia, and pulmonary edema, may be serious. Strict intake and output of fluids are necessary while the patient is on intravenous therapy and for 24 hours thereafter. Fluid restriction to less than 2,500 mL/d is recommended. Colloid osmotic pressure determinations may be useful because pulmonary edema is rare if the colloid osmotic pressure is above 15 mm Hg. Any symptoms of significant chest pain should be evaluated by electrocardiographic studies and should lead to a search for evidence of myocardial ischemia. Hypokalemia and hyperglycemia tend to revert toward normality after 24-36 hours of treatment, but they can be a significant problem if superimposed on underlying abnormal carbohydrate metabolism.
The benefits of pregnancy prolongation with the use of beta-adrenergic receptor antagonists are not clearly proven beyond the initial 24-48 hours. Several meta-analyses show that beta-mimetics given to prevent preterm birth delay delivery no more than 36-48 hours.
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Prostaglandin synthetase inhibitors have been reported to be effective tocolytic agents in isolated reports. Concern related to adverse fetal effects, however, has limited their use to patients who are early in gestation and are showing signs of difficulty. Narrowing of the ductus arteriosus has been observed in some pregnancies during their use, and oligohydramnios may be induced after a few days. It has been suggested that the effect on the ductus is less evident before 32 weeks of pregnancy. Importantly, long-term use is associated with pulmonary hypertension. Thus, if these agents are used, it is recommended that they be used only at 20-32 weeks, for only 1-3 days, and that the fetus and amniotic fluid volume be evaluated daily.
Atosiban, an oxytocin inhibitor, competitively inhibits oxytocin. Its use in humans is currently experimental; therefore, its benefit is still unproved.

Initial evaluation of patients with suspected preterm labor should include asssment of the presence and frequency of uterine contractions, the cervical status, and an assessment of gestational age. Before considering whether to use tocolysis, a search should be made for treatable factors of preterm labor, such as pyelonephritis, and an evaluation should be made to determine whether there are any maternal or fetal contraindications to a specific tocolytic treatment. Relative contraindications include mild hypertension, fetal growth restriction, and cervical dilatation greater than 4 cm. A urine culture is often obtained, and cultures of the lower genital tract for group B hemolytic streptococci, Chlamydia trachomatis, and Neisseria gonorrhoeae are recommended. Amniocentesis for fetal lung maturity and Gram stain as well as culture are frequently obtained, depending on the gestational age and the presenting clinical situation.
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Preterm birth is defined as any birth occurring before the end of 37 weeks of gestation. The incidence is between 8% and 10% of all births, and preterm births account for more than 60% of non-anomalous-related neonatal mortality and morbidity. Most neonatal mortality occurs in those preterm deliveries that occur between 20 and 30 weeks of gestation (or in infants weighing less than 1,500 g). Survival of neonates delivered at tertiary care centers has improved yearly, particularly for those pregnancies ending at 25-32 weeks of gestation. Significant increases in survival rates occur at 25-26 weeks (20% at 24 weeks to 50% at 26 weeks.) Long-term impairment has remained high for those survivors delivered at 25 weeks of gestation and earlier.
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The cause of preterm labor is unknown in most patients. Multiple risk factors, however, have been reported to be associated with an increased likelihood of subsequent preterm labor: multiple gestation (40-50%), previous preterm labor or delivery (20-50% recurrence), diethylstilbestrol exposure, hydramnios, uterine anomalies, previous cone biopsy, previous second-trimester losses, cervical dilatation and effacement before 32 weeks of gestation, excessive preterm uterine activity, and placenta previa. Risk factors include low socioeconomic status and extremes of age (less than age 18 and greater than age 40 years). In addition, it is now recognized that perhaps as many as one fifth of spontaneous preterm births may be complicated by intrauterine or extrauterine infections. Finally, cervical vaginal infections such as bacterial vaginosis, if untreated, also place the patient at greater risk.
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Subclinical chorioamnionitis has emerged as a possible significant cause of preterm birth. Many cases of preterm PROM, as well as up to one fourth of cases of idiopathic preterm birth, may be due to subclinical intraamniotic infection. Bacterial products such as lipopolysaccharide can be identified in the amniotic fluid without other evidence of infection. Furthermore, endogenous host products (cytokines) secreted in response to infection can also be identified in the amniotic fluid of these pregnancies. These cytokines, including interleukin-1, interleukin-6, interleukin-8, and tumor necrosis factor (cachectin), are secretory products of macrophage activation. Additionally, amniotic fluid platelet-activating factor may be synergistically involved in activating the cytokine network.
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Numerous risk-scoring systems based on the aforementioned factors have been proposed but found to be of no benefit in identifying women who deliver preterm. There are no biochemical tests currently proven to predict preterm labor, although preliminary studies suggest cervicovaginal fetal fibronectin may be a marker for impending preterm labor. Intermittent daily monitoring of uterine activity in the outpatient setting has shown that otherwise silent contractions of more than six per hour are associated with preterm labor, but monitoring did not prevent preterm birth.