Uterine Relaxants

Many risk factors are associated with the triggering of premature labor, that is, labor that begins before the end of week 37 of gestation. These include maternal smoking or drug abuse, lack of prenatal care, multiple gestation, placental abnormalities, infection of the fetal membranes, cervical incompetence, and previous preterm birth. Although most episodes are of unknown origin, premature labor can develop spontaneously or may follow early rupture of fetal membranes, perhaps as a result of a genetically associated abnormality.

Uterine relaxants (tocolytic drugs) are administered where prolonged intrauterine life would greatly benefit the fetus or would permit additional time to allow treatment with drugs such as corticosteroids, which promote the production of fetal lung surfactant. Tocolytics are also used when temporary uterine relaxation is be desirable (e.g., intrauterine fetal resuscitation). While hydration, bed rest, and sedation have been used to inhibit uterine contractions, tocolytics are more likely to inhibit labor early in gestation, especially before labor is far advanced. Agents used in this regard include magnesium sulfate, alcohol, prostaglandin inhibitors, calcium channel blockers, hydroxyprogesterone, and (2-adrenergic agonists.

All tocolytic agents are powerful drugs that must be used with extreme care, since pulmonary edema, myo-cardial infarction, respiratory arrest, cardiac arrest, and death can occur during tocolytic therapy. Newborns of mothers given tocolytics have had respiratory depression, intraventricular hemorrhage, and necrotizing enterocolitis. Absolute contraindications to tocolysis include acute fetal distress (except during intrauterine resuscitation), chorioamnionitis, eclampsia or severe pre-eclampsia, fetal demise (of a singleton pregnancy), fetal maturity, and maternal hemodynamic instability.

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