INFLUENCE OF INFECTION ON PATENT DUCTUS-ARTERIOSUS AND CHRONIC LUNG-DISEASE IN PREMATURE-INFANTS WEIGHING 1000 GRAMS OR LESS

Objective: To test the hypotheses that (1) infection increases ductal dilatory prostaglandins and inflammatory mediators that may influence the closure of a patent ductus arteriosus (PDA), increasing the incide nce of late episodes of PDA (after 7 days) and the rate of closure fai lures, and (2) the concurrence of PDA and infection increases the risk of chronic lung disease (CLD). Methods: One hundred fourteen prematur e infants (birth weight, 500 to 1000 gm) were prospectively assessed f or PDA and infection, Serum levels of 6-ketoprostaglandin F-1 alpha an d tumor necrosis factor alpha were measured routinely in all infants a nd when PDA or infection was present, Multivariate assessment of risk factors for PDA closure failure and for CLD was done by logistic regre ssion, and expressed as an odds ratio and as 95% confidence intervals. Results: Late PDA episodes were more frequent in infants with infecti on than in those without infection. A temporally related infection (<5 days between both diagnoses) was associated with an increased risk of PDA closure failure (odds ratio, 19.1 confidence interval, 4 to 90)), In addition to birth weight and the severity of initial respiratory f ailure, PDA and infection increased the risk of CLD (odds ratio, 11.7 (confidence interval, 1.7 to 81) for PDA; odds ratio, 3.1 (confidence interval, 1 to 11) for infection), Furthermore, when both factors were temporally related, they further increased the risk of CLD (odds rati o, 29.6 (confidence interval, 4.5 to >100)), Infants with infection an d those with PDA had higher levels of 6-ketoprostaglandin F-1 alpha th an did control subjects, Levels of tumor necrosis factor alpha were al so elevated in infants with infection and in those with late PDA. Conc lusions: Infection adversely influences PDA outcome by increasing the risk of late ductal reopening and PDA closure failures, Increased leve ls of prostaglandins and tumor necrosis factor alpha in infants with i nfection may explain the poor PDA outcome. The concurrence of PDA and infection potentiates their negative effects on the risk of CLD.