Objective: To review intestinal complications associated with ibuprofen treatment of patent ductus arteriosus (PDA).Study Design: Data from preterm infants treated with ibuprofen were retrospectively reviewed. w 2 test and Fischer's exact test were used for univariate analyses. Multivariate analyses with logistic regression modeling were used to identify risk factors.Result: One hundred and two infants were treated with ibuprofen for PDA. Nine (9/102, 8.8%) infants developed spontaneous intestinal perforation (SIP), whereas 93/102 (91.2%) did not. The mean (±s.d.) gestational age (GA) at birth in infants with and without SIP was 25.2 ( ± 1.3) vs 27.6 ( ± 2.4) weeks (P ¼ 0.02) and the median (interquartile) length of stay (LOS) was 109.5 (91.0 to 116.5) vs 75.0 (53.0 to 94.5) days (P ¼ 0.002), respectively. The mean ( ± s.d.) age at starting ibuprofen was 3.3 ( ± 1.3) vs 5.8 (±3.5) days in infants with and without SIP, respectively (P ¼ 0.03). In logistic regression analyses, increasing GA and later initiation of ibuprofen treatment were protective against risk of SIP; odds ratio, 95% confidence interval (OR, 95% CI) ¼ 0.26 (0.09 to 0.75), P ¼ 0.01 and 0.63 (0.41 to 0.95), P ¼ 0.03, respectively.Conclusion: Infants at lower GA are at risk of SIP when treated early with ibuprofen for symptomatic PDA.
THE DUCTUS ARTERIOSUS IS a vascular shunt that exists before birth to enable blood flow to bypass the lungs, which are not yet functional, and direct it instead to the systemic circulation and to vital organs such as the kidney and the gastrointestinal (GI) tract. In the term infant, this shunt should start to close within the first few hours after birth; it should close functionally within 72 hours and anatomically within 2 weeks after birth.1 In the preterm infant, functional and subsequent anatomic closure frequently does not take place. Failure of ductal closure occurs in as many as 60 percent of all infants who are less than 28 weeks gestation at birth.1 Causes for patency of the ductus arteriosus in preterm infants include decreased smooth muscle fibers in the duct and continued responsiveness of the ductus arteriosus to prostaglandins produced within it.
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