Original Article
Neonatal Complications after the Administration of Indomethacin for Preterm Labor
N Engl J Med 1993; 329:1602-1607November 25, 1993
- Abstract
Background
The use of indomethacin as a tocolytic agent in pregnant women appears to be accompanied by a low incidence of neonatal complications. However, the neonatal effects of indomethacin have been studied primarily in infants born after 32 weeks' gestation. This study was designed to examine the incidence of neonatal complications in very premature infants.
Methods
We identified 57 infants delivered at or before 30 weeks' gestation whose mothers had been treated with indomethacin for preterm labor and matched them with 57 infants whose mothers had not received indomethacin. The infants in the two groups were matched for sex, gestational age at delivery (mean [±SD], 27.6 ±2.0 weeks), exposure to betamethasone for 24 hours or more before delivery, and rupture of membranes 24 hours or more before delivery.
Results
There were no significant differences between the two groups in birth weight, Apgar scores, cord-blood gas values, frequency of multiple gestation, or incidence of respiratory distress syndrome. The proportion of infants who required exogenous surfactant was similar, as were ventilator settings at 24 hours, the incidence of chronic lung disease, and the incidence of sepsis. The infants exposed to indomethacin had a lower urine output and higher serum creatinine concentrations during the first three days after delivery. More indomethacin-exposed infants had necrotizing enterocolitis (29 percent vs. 8 percent, P = 0.005), intracranial hemorrhage grade II to IV (28 percent vs. 9 percent, P = 0.02), and patent ductus arteriosus (62 percent vs. 44 percent, P = 0.05). More indomethacin-exposed infants with a patent ductus arteriosus required surgical ligation because of either a lack of initial response or a reopening of the duct after postnatal indomethacin therapy (50 percent vs. 20 percent of the unexposed infants, P = 0.05).
Conclusions
Antenatal indomethacin therapy for preterm labor appears to increase the risk of serious neonatal complications in infants born at or before 30 weeks' gestation.
Media in This Article
Figure 1
Incidence of Necrotizing Enterocolitis among Infants Delivered at or before 30 Weeks' Gestation Who Were Exposed to Indomethacin Antenatally and among Infants Who Were Not Exposed.Figure 2
Incidence of Intracranial Hemorrhage among Infants Delivered at or before 30 Weeks' Gestation Who Were Exposed to Indomethacin Antenatally and among Infants Who Were Not Exposed.Article Activity
- Article
Indomethacin, a potent inhibitor of prostaglandin synthesis, has been used as a tocolytic agent since the mid-1970s. It crosses the placenta freely1 and can inhibit the synthesis of prostaglandins in fetal tissues. The use of indomethacin during pregnancy can cause constriction of the fetal ductus arteriosus and oligohydramnios due to decreased fetal urine output2-5.
Indomethacin has profound effects on platelet and neutrophil function,6 cerebral, mesenteric, and renal hemodynamics,7-9 renal tubular function,9 and gastrointestinal oxygen consumption in both animals and premature infants7. However, the neonatal complications most frequently associated with these effects -- sepsis, intracranial hemorrhage, renal dysfunction, and necrotizing enterocolitis2,10 -- have not occurred consistently in controlled trials of antenatal indomethacin therapy, in which the mean gestational age of the newborns was more than 32 weeks11-15. Because these complications occur most frequently among infants delivered at or before 30 weeks' gestation, we hypothesized that the rarity of neonatal complications after antenatal exposure to indomethacin was due to the advanced gestational age of the infants studied. We therefore performed a matched retrospective cohort study to determine the incidence of neonatal complications among infants exposed to indomethacin in utero and delivered at or before 30 weeks' gestation.
Methods
We identified 57 infants born from 24 through 30 weeks of gestation whose mothers had been treated with indomethacin for preterm labor between January 1986 and January 1991. These infants were chosen from a computerized data base containing information on the mothers, from which we obtained no information about neonatal outcome. Each infant was matched with an infant not exposed to indomethacin, according to sex, gestational age at delivery, exposure to betamethasone for 24 hours or more before delivery, premature rupture of membranes 24 hours or more before delivery, and year of delivery. Gestational age was determined as the best obstetrical estimate based on early ultrasonography or information supplied by the mother and was confirmed by examination of the infants. Infants with serious congenital anomalies were excluded.
The mothers' records were reviewed to determine the total dose of indomethacin administered and the duration of treatment, the lengths of time from the first and last doses to delivery, the duration of any antenatal betamethasone treatment, and whether they received treatment with other tocolytic agents. Neonatal data, obtained from the medical records by a separate investigator, included birth weight, Apgar scores, umbilical-cord blood gas values, presence or absence of intrauterine growth retardation, incidence of fetal anomalies, use of neonatal surfactant therapy, ventilator settings 24 hours after delivery, and the incidence of respiratory distress syndrome, chronic lung disease, or neonatal death. Respiratory distress syndrome was defined as a typical clinical presentation with characteristic x-ray findings and a need for inspired oxygen at a fraction of 0.25 or more for more than 24 hours. Chronic lung disease was defined as a need for oxygen or ventilatory support at 28 days of age for reasons other than apnea.
We specifically examined the infants' charts for neonatal complications potentially associated with indomethacin exposure: sepsis, necrotizing enterocolitis, intracranial hemorrhage, patent ductus arteriosus, and renal dysfunction. Sepsis was diagnosed only when the infant had positive blood or cerebrospinal fluid cultures. The diagnosis of confirmed necrotizing enterocolitis required either bowel perforation or intramural intestinal air (pneumatosis intestinalis) on abdominal radiography. Suspected necrotizing enterocolitis was defined as persistently abnormal radiographic findings (but without pneumatosis intestinalis or free air) with guaiac-positive stools or abdominal distention and symptoms that required the discontinuation of oral feedings and treatment with antibiotics for 10 days. All the infants underwent cranial ultrasonography within the first week after delivery and weekly thereafter until 36 weeks' gestation (postconceptional age) to detect intracranial hemorrhage. The images were graded according to the criteria of Papile et al16. Patent ductus arteriosus was diagnosed when the clinical suspicion of this condition was confirmed by echocardiography. Evaluation of renal function included measurements of serum creatinine concentrations at 24, 48, and 72 hours of age and of urine output at these same times.
The results were analyzed with two-tailed Student's t-tests, chi-square tests, or McNemar's test, as appropriate. In addition, the categorical outcome variables (presence or absence of necrotizing enterocolitis, intracranial hemorrhage, and patent ductus arteriosus) were analyzed with use of hierarchical logistic regression, and the numerical outcomes (urine output and serum creatinine concentration) by repeated-measures analysis of variance to examine the possible effects and interactions with the other variables, such as multiple gestation, sex, gestational age, birth weight, prolonged rupture of membranes, betamethasone administration, cesarean section, and administration of other tocolytic agents, specifically magnesium sulfate, ritodrine, and terbutaline17. The results are presented as means ±SD. P values below 0.05 were considered to indicate statistical significance.
Results
All infants were delivered at or before 30 weeks' gestation. As intended, the groups were similar in weight and gestational age at birth (according to the pediatric examination) (Table 1Table 1
Characteristics of Infants Delivered at or before 30 Weeks' Gestation According to Antenatal Indomethacin Exposure.). They were also similar in the incidence of multiple gestation, delivery by cesarean section, and use of other tocolytic agents, specifically magnesium sulfate and beta-sympathomimetic drugs (terbutaline or ritodrine). The indication for indomethacin treatment was preterm labor that was unresponsive to these other agents. Whether indomethacin was used in such cases depended solely on the discretion of the attending physician.The mothers of the infants exposed to indomethacin received 50 to 6000 mg of the drug (median, 425). The infants' mean gestational age at the time of initial exposure was 25.7 ±1.8 weeks, and the median duration of therapy was 3 days (range, 1 to 79). Sixty-five percent of the mothers received indomethacin for 4 days or less, 81 percent for 7 days or less, and 88 percent for 10 days or less. Sixty-five percent of the mothers received their last dose of indomethacin within 24 hours of delivery, and 81 percent received their last dose within 48 hours.
All the indomethacin-exposed infants were delivered after spontaneous preterm labor. In the control group, 3 infants were delivered after labor was induced because of maternal preeclampsia; the remaining 54 infants were delivered after spontaneous preterm labor.
The characteristics of the infants after delivery are shown in Table 2Table 2
Neonatal Characteristics of Infants Exposed to Indomethacin Antenatally and of Unexposed Infants.. There were no significant differences in the frequency of Apgar scores below 6 at five minutes, in the mean umbilical-cord blood pH, or in the incidence of intrauterine growth retardation, minor fetal anomalies, or use of surfactant therapy. The incidence of respiratory distress syndrome, the ventilator settings at 24 hours, and the frequency of the ultimate development of chronic lung disease were similar in the two groups. The rate of culture-proved sepsis was identical in the two groups (19 percent), and the lowest white-cell counts (9700 ±4700 per cubic milliliter in the indomethacin group vs. 8700 ±4800 per cubic milliliter in the unexposed group) and the lowest platelet counts (221,000 ±100,000 per cubic milliliter vs. 228,000 ±78,000 per cubic milliliter) during the first seven days after delivery were similar. There was a trend toward higher mortality in the indomethacin group (P = 0.15). In addition, the incidence of death due to causes unrelated to necrotizing enterocolitis (four in the unexposed group vs. six in the indomethacin group) was similar in the two groups.The infants exposed to indomethacin had a significantly higher incidence of necrotizing enterocolitis (P = 0.005) (Figure 1Figure 1
Incidence of Necrotizing Enterocolitis among Infants Delivered at or before 30 Weeks' Gestation Who Were Exposed to Indomethacin Antenatally and among Infants Who Were Not Exposed.), primarily because of the increased incidence of confirmed necrotizing enterocolitis (19 percent in the indomethacin group vs. 2 percent in the unexposed group, P = 0.005). There was a significant independent association of necrotizing enterocolitis with low gestational age, low birth weight, and the absence of antenatal betamethasone therapy (P = 0.025). However, there was no significant interaction between these or other risk factors and the effect of antenatal indomethacin exposure on the frequency of necrotizing enterocolitis. The excess incidence of necrotizing enterocolitis was not attributable to the postnatal use of indomethacin, because this was comparable in the two groups (47 percent of the indomethacin-exposed group received postnatal indomethacin, as compared with 36 percent of the unexposed group). In addition, there was no significant difference in the incidence of necrotizing enterocolitis in the group with antenatal indomethacin exposure between the infants who received indomethacin postnatally (19 percent of whom had necrotizing enterocolitis) and those who did not (35 percent had necrotizing enterocolitis). Among the infants exposed to indomethacin who required surgical exploration for confirmed necrotizing enterocolitis, four had typical intestinal necrosis and three had isolated perforation. The one infant in the control group with confirmed necrotizing enterocolitis did not have a perforation or require surgery. Nine percent of the infants exposed to indomethacin died of complications of necrotizing enterocolitis, as compared with 2 percent of the infants in the unexposed group.The infants who were exposed to indomethacin also had an increased incidence of grade II to IV intracranial hemorrhage (P = 0.02) (Figure 2Figure 2
Incidence of Intracranial Hemorrhage among Infants Delivered at or before 30 Weeks' Gestation Who Were Exposed to Indomethacin Antenatally and among Infants Who Were Not Exposed.), primarily because of an increase in the incidence of grade II intracranial hemorrhage (21 percent, vs. 6 percent among the unexposed infants; P = 0.03). There was a significant (P = 0.025) independent interaction among early gestational age, low birth weight, and intracranial hemorrhage. There was no significant interaction, however, between these or other risk factors and the effect of antenatal indomethacin exposure on intracranial hemorrhage.The infants exposed to indomethacin in utero had significantly more renal dysfunction, as evidenced by elevated serum creatinine concentrations and decreased urine output during the first three days after birth (Figure 3Figure 3
Serum Creatinine Concentration, Fluid Intake, and Urine Output in Infants Delivered at or before 30 Weeks' Gestation Who Were Exposed to Indomethacin Antenatally and in Unexposed Infants.). The mean serum creatinine concentration was significantly higher among the infants exposed to indomethacin on days 1, 2, and 3. Urine output was significantly lower among the indomethacin-exposed infants on days 1 and 2, but not day 3. Fluid intake did not differ significantly between the two groups. There was no significant interaction between the other risk factors and the effect of antenatal indomethacin exposure on the serum creatinine concentration or urine output.The infants exposed antenatally to indomethacin had a significantly higher incidence of patent ductus arteriosus (62 percent, vs. 44 percent among the unexposed infants; P = 0.05) (Table 3Table 3
Incidence of Patent Ductus Arteriosus According to Antenatal Indomethacin Exposure.). Lower gestational age and lower birth weight were independently associated with a higher incidence of patent ductus arteriosus. Both these risk factors also had a significant (but opposite) effect on the action of antenatal indomethacin on the ductus arteriosus -- that is, the more mature the infant, the more likely antenatal indomethacin exposure was to be associated with patent ductus arteriosus. For example, among infants with birth weights of 1000 g or less, 68 percent of the infants in the unexposed group had a patent ductus arteriosus, as compared with 71 percent of the infants with antenatal indomethacin exposure. In contrast, among infants with birth weights above 1000 g, the incidence was 15 percent in the unexposed group and 52 percent in the group with antenatal indomethacin exposure (P = 0.03).The response to neonatal treatment of patent ductus arteriosus also differed in the two groups. One infant in each group had a patent ductus arteriosus that was not hemodynamically important and did not require treatment. Seven infants in the indomethacin group and three in the unexposed group had a patent ductus arteriosus that was treated with surgical ligation; these infants were never given indomethacin as neonates. The indication for direct surgical management was abnormal renal function, which was considered to be a contraindication to indomethacin therapy. Indomethacin was the most frequent initial form of therapy in the neonatal period for a patent ductus arteriosus (used in 76 percent of those with a patent ductus arteriosus who had antenatal indomethacin exposure and 83 percent of those without such exposure). Neonatal indomethacin therapy was significantly less successful, however, in closing the patent ductus arteriosus in infants delivered after exposure to indomethacin in utero; 50 percent of such neonates treated with indomethacin after birth ultimately required surgical ligation, as compared with 20 percent in the unexposed group (P = 0.05).
None of the complications in the indomethacin group were related to the length of time between the last dose of indomethacin and delivery or to the total dose of indomethacin given to the mother.
Discussion
We found a significantly increased risk of necrotizing enterocolitis, patent ductus arteriosus, intracranial hemorrhage, and renal dysfunction in preterm infants after the administration of indomethacin to their mothers for treatment of preterm labor. This study was retrospective and thus subject to unanticipated biases in case selection. The use or nonuse of indomethacin in the mothers was not randomly assigned but depended solely on the decision of the attending physician to use another agent to treat persistent labor in women in whom standard tocolytic therapy had failed. Careful review of all maternal charts did not reveal other indications for the use of indomethacin. Under these conditions, 70 percent of the mothers who received indomethacin at our institution nonetheless delivered at or before 30 weeks' gestation.
Obviously, tocolytic therapy was unsuccessful in both groups. The groups were closely matched in terms of factors known to influence neonatal outcome. The fact that we studied very premature infants, who are much more susceptible to neonatal complications than infants born later, may explain why other investigators have not found similar results. In addition, 81 percent of the infants in our study were delivered within 48 hours after their exposure to indomethacin. Such recent exposure would not be expected among infants delivered closer to term. We did not find a significant relation between neonatal complications and the length of time from the last dose of indomethacin to delivery. However, the majority of infants were delivered within a short interval after the last dose, making it difficult to examine this relation. Similarly, the majority of infants were exposed to a narrow range of indomethacin doses, making it difficult to examine the relation of neonatal complications to the amount of indomethacin administered to the mother.
Gastrointestinal complications, including intestinal perforation, are known side effects of indomethacin therapy in adults and newborn infants18,19. Indomethacin decreases mesenteric blood flow,20-22 blocks autoregulation of oxygen consumption in the terminal ileum,7 and increases the risk of bowel necrosis after temporary ischemia23. Prenatal intestinal perforation has not been reported after exposure to indomethacin. Germ-free rats are resistant to indomethacin-induced small-bowel perforations; thus, the sterile fetal intestine may explain the delayed appearance, after delivery, of gastrointestinal lesions in human neonates exposed to indomethacin in utero10,24.
The increased incidence of patent ductus arteriosus in the indomethacin-exposed neonates may seem puzzling. Between 60 percent and 80 percent of fetuses exposed to indomethacin antenatally have constriction of the ductus in utero, often with tricuspid regurgitation4,5. The frequency of this response to antenatal indomethacin exposure increases with advancing gestational age. The constriction of the fetal ductus usually resolves within 24 hours after the discontinuation of indomethacin5. However, after initial constriction, the ability of the ductus to contract actively in response to oxygen or indomethacin is limited25. This loss of responsiveness probably reflects early ischemic damage to the inner muscle wall. In infants who have had some degree of ductal constriction in response to indomethacin exposure in utero, the ductus probably has an impaired ability to contract in response to the normal increase in oxygen tension that occurs after birth. This phenomenon may account for the higher incidence of patent ductus arteriosus among the neonates in the indomethacin-exposed group. It may also explain why indomethacin was more likely to be associated with patent ductus arteriosus when it was given later in gestation. In addition, the loss of responsiveness of the ductus may explain why these infants had such a poor response to neonatal indomethacin therapy and required surgical ligation to treat the patent ductus arteriosus. The combination of betamethasone and indomethacin given antenatally causes an even greater constriction of the fetal ductus arteriosus26. Eighty-nine percent of the infants in this study were exposed antenatally to betamethasone, which may have contributed to the loss of ductal responsiveness and the increased rate of patent ductus arteriosus.
The increase in intracranial hemorrhage among indomethacin-exposed infants in our study contrasts with reports that indomethacin administered neonatally reduces the risk of severe intracranial hemorrhage in very premature infants27,28. The postnatal administration of indomethacin attenuates the cerebral hyperemic response that normally follows hypoxia and hypercapnia and in this way is thought to protect the fragile germinal matrix of the preterm infant29. On the other hand, indomethacin inhibits platelet aggregation, and previous studies have indicated an association between intracranial hemorrhage and hemostatic disorders6,30. In addition, maternal ingestion of other nonsteroidal antiinflammatory drugs has been associated with an increased incidence of intracranial hemorrhage in preterm infants31. Perhaps the extreme changes in fetal intracranial pressure that occur during preterm labor and delivery exacerbate this bleeding diathesis and cause intracranial hemorrhage.
Transient renal dysfunction has been reported as a complication of the administration of indomethacin in adults, newborns, preterm infants, and fetuses3,8. Our results confirm these earlier findings and demonstrate that when indomethacin is administered shortly before delivery, its renal effects can persist into the neonatal period. This alteration in renal function may result in metabolic and volume derangements.
Indomethacin is an effective tocolytic agent12-14. Nevertheless, it freely crosses the placenta, interferes with fetal prostaglandin production, and alters the normal fetal cardiovascular response to stress1. In our study, indomethacin appeared to increase the risk of several of the important complications associated with preterm birth. It is possible that a randomized, prospective trial of earlier use of indomethacin in the treatment of preterm labor might demonstrate that its efficacy as a tocolytic agent outweighs the risk of these complications. The dilemma that faces the obstetrician is that the fetuses most in need of effective tocolysis are also those at highest risk for indomethacin-induced neonatal complications when tocolysis fails to prevent preterm delivery.
Supported in part by a grant (HL 46691) from the National Heart, Lung, and Blood Institute and by a gift from Perinatal Associates Research Foundation.
We are indebted to Mr. Paul Sagan for his skillful editorial assistance.
Source Information
From the Cardiovascular Research Institute (R.I.C.) and the Departments of Pediatrics (J.M., R.I.C.) and Obstetrics, Gynecology and Reproductive Sciences (M.E.N., J.A.K.), University of California, San Francisco, and the California School of Professional Psychology, Alameda, Calif. (B.A.B.C.).
Address reprint requests to Dr. Clyman at Box 0544, Rm. 1403 HSE, University of California, San Francisco, CA 94143.
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