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INTRODUCTION

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A variety of medications are used in obstetric practice by both obstetricians and anesthesiologists. These medications may differ from those used in the surgical operating room. This chapter reviews the medications commonly used in obstetrics.

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TOCOLYTIC MEDICATIONS

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Tocolytics are used by obstetricians to treat preterm labor in an attempt to prevent premature birth. Preterm birth is the leading cause of perinatal morbidity and mortality and complicates approximately 12% of pregnancies in the United States.1 Recent Cochrane meta-analyses of tocolytic agents determined that calcium channel blockers and oxytocin antagonists can delay delivery by 2 to 7 days,2 that β-mimetic drugs delay delivery by 48 hours but carry greater side effects,3 that there is insufficient evidence regarding cyclooxygenase (COX) inhibitors,4 and that magnesium sulfate is ineffective.5 Anesthesiologists may be more involved with other uses of these drugs, including in the treatment of uterine tetany, uterine inversion, retained placenta, and fetal head entrapment.

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Magnesium Sulfate

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Indications
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Magnesium sulfate has been used for suppression of preterm labor and for seizure prophylaxis in patients with severe preeclampsia. However, it is no longer used as a tocolytic agent because it has not been shown to be more effective than placebo in preventing preterm labor and delivery.6 Although the primary indication for magnesium sulfate administration remains prevention of seizure activity in patients with severe preeclampsia, a newer use of magnesium administration during preterm labor involves benefit to the brain of the unborn fetus. Studies have demonstrated that premature infants as young as 23 weeks, born to mothers treated with magnesium sulfate, have improved developmental outcomes.7

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Mechanism of Action
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The systemic effects of magnesium sulfate administration are widespread and require the need for careful monitoring. Magnesium crosses the blood-brain barrier and decreases irritability of the central nervous system (CNS) and decrease N-methyl-D-aspartate activity. These effects likely account for the anticonvulsant and brain protection properties. Magnesium also competes with calcium for binding sites on the sarcoplasmic reticulum, reducing intracellular calcium levels and reducing the force and frequency of muscle contraction in both skeletal and smooth muscle.8 Magnesium decreases the presynaptic release of acetylcholine, thereby reducing activity at the neuromuscular junction and decreases sensitivity of postjunctional membranes to acetylcholine. In addition, magnesium increases endothelial production of prostaglandin I2 (PGI2), increases cyclic guanosine monophosphate (GMP) production, and decreases angiotensin-converting enzyme levels, actions that all promote smooth muscle relaxation and vasodilation,8 with concomitant increased uterine blood flow.

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Dosing
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Magnesium sulfate is usually administered as a 4-g IV bolus over 30 minutes, ­followed by an infusion of 1 g per hour.9 Therapeutic levels range between 4 and 9 mEq/L. Plasma levels and deep tendon reflexes must be followed rigorously to avoid overdose and complications associated with magnesium toxicity. The effects of increasing ...

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