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. 1995 Apr;126(4):605-10.
doi: 10.1016/s0022-3476(95)70362-4.

Changing trends in the epidemiology and pathogenesis of neonatal chronic lung disease

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Changing trends in the epidemiology and pathogenesis of neonatal chronic lung disease

M A Rojas et al. J Pediatr. 1995 Apr.

Abstract

Objective: To assess the role of specific risk factors that may predispose preterm infants with mild or no initial respiratory distress syndrome to the development of chronic lung disease (CLD).

Study design: Clinical data were collected prospectively from 119 ventilator-supported preterm infants with birth weights between 500 and 1000 gm, who survived more than 28 days and required fewer than 3 days of treatment with fraction of inspired oxygen > 25% during the first 5 days of life. Logistic regression analysis was used in a multivariate assessment of risk factors for CLD.

Results: Chronic lung disease occurred in 44 of the patients (37%). The analysis showed that low birth weight, patent ductus arteriosus (PDA), and sepsis were significant risk factors for CLD. The corresponding odds ratios for CLD and their 95% confidence intervals (CI) were as follows: 2.9 per 100 gm birth weight decrement (CI, 1.7 to 4.8); 6.2 (CI, 2.1 to 18.4) for PDA; and 4.4 (CI, 1.3 to 14.5) for sepsis. When sepsis and PDA occurred simultaneously, the odds ratio for CLD increased to 48.3 (CI, 6.3 to > 100) in comparison with infants without these conditions. Episodes of PDA were categorized as either early (occurring during the first week of life) or late (after the first week), and the respective odds ratios for CLD were 2.8 (CI, 0.8 to 9.4) and 21.1 (CI, 5.6 to 80) in comparison with infants without PDA. For the duration of symptomatic PDA, the odds ratio for CLD was 3.5 per week that the PDA remained open (CI, 1.9 to 6.5).

Conclusion: CLD is a frequent sequela in very low birth weight infants with mild or no respiratory distress syndrome. In this population, the development of late episodes of PDA, usually in association with a nosocomial infection, seems to play a primary role in the pathogenesis of CLD.

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