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Pharmacology for Preterm Labor Lindsey Garfield, Phd; Emily Chin, Phd

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Pharmacology for Preterm Labor Lindsey Garfield, Phd; Emily Chin, Phd DOI: 10.1097/JPN.0000000000000474 Continuing Education r r J Perinat Neonat Nurs Volume 34 Number 2, 155–161 Copyright C 2020 Wolters Kluwer Health, Inc. All rights reserved. Pharmacology for Preterm Labor Lindsey Garfield, PhD; Emily Chin, PhD ABSTRACT includes uterine contractions with accompanying cer- Preterm birth occurs with 10% of deliveries and yet ac- vical dilation greater than 2 cm or changes in dilation counts for more than 85% of perinatal morbidity and mor- or effacement.3 Many women presenting with preterm tality. Management of preterm labor prior to delivery in- labor will give birth at term (50%); in addition, 30% cludes a multipronged pharmacologic approach targeting of preterm labor resolves spontaneously.4,5 Preterm la- utilization of reproductive hormones for continuation of bor is generally not treated prior to neonatal viabil- pregnancy, advancement of fetal lung maturity, and the ity and only when delay of neonatal birth will benefit decrease of uterine contractility (tocolysis). This article will the newborn.3 Current pharmacologic management for review and compare guidelines on pharmacologic manage- premature labor consists of advancing fetal lung ma- ment of preterm labor as recommended by the American turity, decreasing uterine contractility, and utilizing re- College of Obstetricians and Gynecologists and the Euro- productive hormones for continuation of pregnancy.6 pean Association of Perinatal Medicine. The classifications Guidelines on the use of pharmacologic management of drugs discussed include exogenous progesterone, of preterm labor are disputed among obstetricians corticosteroids, and tocolytics (β-adrenergic agonists, mag- throughout the world and professional organizations nesium sulfate, calcium channel blockers, prostaglandin have established various guidelines for practice.6–8 This inhibitors, nitrates, and oxytocin receptor blockers). For article will explore pharmacologic management for pre- each of these drug classes, the following information will mature labor and compare pharmacologic guidelines be presented: mechanism of action, maternal/fetal side written by the American College of Obstetricians and effects, and nursing implications. Gynecologists (ACOG) and the European Association Key Words: pharmacology, preterm, tocolytics of Perinatal Medicine. EXOGENOUS PROGESTERONE TO MAINTAIN urrently in the United States, preterm births PREGNANCY 1 account for 10% of live births. Preterm birth Maternal progesterone is vital to the establishment Cis defined as birth between 20 weeks’ gesta- and continuation of pregnancy.9 Progesterone increases tion and less than 37 weeks’ gestation and accounts for blood flow to the uterus, stimulates the endometrium 2 more than 85% of all perinatal morbidity and mortality. to thicken, and helps establish the placenta.10 Proges- Preterm labor usually precedes preterm birth and terone also is necessary for fetal development, sup- presses uterine contractions, and strengthens the pelvic Author Affiliation: Marcella Niehoff School of Nursing, Loyola wall. Low maternal progesterone is associated with University Chicago, Chicago, Illinois. preterm labor and exogenous progesterone is a prophy- Disclosure: The authors have disclosed that they have no significant lactic therapy used for pregnant women who have ex- relationships with, or financial interest in, any commercial companies perienced a preterm birth prior.11 Progesterone admin- pertaining to this article. istration should be initiated between 16 and 20 weeks Each author has indicated that he or she has met the journal’s require- and only in women with intact membranes. Proges- ments for Authorship. terone reduces the risk of preterm birth by maintain- Corresponding Author: Lindsey Garfield, PhD, Marcella Niehoff 12 School of Nursing, Loyola University Chicago, 1032 W Sheridan Rd, BVM ing uterine acquiescence. Studies suggest that proges- 13 Hall 1007—Lake Shore Campus, Chicago, IL 60660 (lgarfi[email protected]). terone reduces the risk of preterm birth by up to 50% Submitted for publication: September 17, 2019; accepted for publication: and may decrease the incidence of respiratory distress, January 20, 2020. neonatal morbidity, and neonatal mortality in pregnant The Journal of Perinatal & Neonatal Nursing www.jpnnjournal.com 155 Copyright © 2020 Wolters Kluwer Health, Inc. Unauthorized reproduction of this article is prohibited. women with a shortened cervix. Confounding research long-term follow-up leave questions related to effects of suggests that in a subset of individuals, those with cer- corticosteroids in pregnancy and long-term infant health tain genetic factors or women with premature rupture outcomes. Corticosteroids are considered an adjunct to of membranes, progesterone injections do not prolong other therapies targeted to prolong pregnancy and stop pregnancy.14 In addition, progesterone given intramus- preterm labor.21 Appropriate use of corticosteroids for cularly has been found to increase the incidence of preterm lung development should also consider poten- gestational diabetes by threefold.15 tial short- and long-term outcomes. CORTICOSTEROIDS TO IMPROVE FETAL TOCOLYTICS TO DECREASE UTERINE LUNGS CONTRACTIONS Corticosteroids are a class of steroid hormones natu- Tocolytics are a group of medications used to decrease rally produced in the adrenal cortex.16 Corticosteroids uterine contractions in women experiencing preterm la- are anti-inflammatory, immunosuppressant and used bor between 23 and 34 weeks’ gestation, though they to treat a wide range of conditions.16 Corticosteroids, have not been proven to stop preterm labor.31 Tocolytic such as betamethasone or dexamethasone, are recom- therapy is not considered in all preterm labor patients 6 32 mended for pregnant women between 24 and 33 /7 due to maternal and fetal complications. Maternal weeks’ gestation and may be considered for pregnant contraindications to tocolytics include chorioamnioni- 0 6 women 34 /7 to 36 /7 weeks’ gestation who are at risk of tis, placental abruption, severe preeclampsia, cardiac delivery within 7 days.17 Corticosteroids promote fetal disease, poorly controlled diabetes or hypertension, lung maturity18 and consistently improve outcomes of and medical conditions necessitating pregnancy preterm birth such as reduction and severity of respira- termination.32 Fetal contraindications to tocolytics in- tory distress syndrome, decreased mortality, improved clude intrauterine growth restriction, intrauterine fe- stability of neonates, reduced rates of intraventricular tal demise, and lethal fetal anomalies.31 Tocolytics hemorrhage, and decreased rates of necrotizing ente- include β-adrenergic agonists (terbutaline, ritodrine), rocolitis compared with preterm neonates not exposed magnesium sulfate, calcium channel blockers (nifedip- to corticosteroids.19 Corticosteroids’ mechanism of ac- ine), prostaglandin inhibitors (indomethacin, ketoro- tion includes the accelerated development of type 1 lac), nitrates (nitroglycerine), and oxytocin receptor and type 2 pneumocytes, which improves lung me- blockers (atosiban).8,33,34 Recent meta-analysis suggests chanics and gas exchange.20 In addition, corticosteroids prostaglandin inhibitors (indomethacin, ketorolac) as increase surfactant production, surfactant release, and the best first-line tocolytic therapy,35 though experts in upregulation of epithelial Na+ channels that absorb lung the field do not all agree on the most effective tocolytic fluid after birth.8,21 Corticosteroids increase the number for delaying preterm birth.21 Tocolytic therapy is recom- of β receptors in the lung, aiding in the lungs transi- mended only for short prolongation of pregnancy to al- tion to air breathing.20 Although the positive effects of low for the administration of corticosteroids.4 Long-term lung maturity with corticosteroids are well established, tocolytic therapy is not effective in preventing preterm negative effects of corticosteroids pose risks to the de- birth or improving neonatal outcomes.35 veloping neonate.22 The most prominent negative effect β-Adrenergic agonists stimulate the β receptors of corticosteroid treatment on lung development is the in smooth muscle cells causing uterine relaxation.36 decrease in numbers of alveoli and decrease in lung β-Adrenergic agonists mostly affect β2 receptors in growth.22 This adverse effect has been studied in the smooth muscle of the myometrium (middle layer of animal model using rats, sheep, and monkeys but not uterine wall), bronchioles, and blood vessels, though 23–25 extensively studied in humans. It has been posited they may also exhibit a small effect on β1 recep- that mechanical ventilation and prematurity also con- tors in the heart and small intestines causing cardio- tribute to the decrease in pulmonary growth.26 Cur- vascular and metabolic responses.8,33 Caution should rent recommendations specifically state using a single be exercised with administration of β-adrenergic ag- course of corticosteroids in pregnant women as cumu- onists to mothers with cardiovascular disorders, glau- lative treatment remains speculative.21 Further concern coma, diabetes mellitus, placenta previa, and placen- on antenatal corticosteroid use and its effects on brain tal abruption.37 In fetuses, the density of β-adrenergic development and neuromotor function is evidenced in receptors is low compared with adults, resulting in a animal models with mice, rats, and sheep.27–29 However, less powerful fetal cardiovascular response.38 These fe- in human studies,
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