Neonates bronchopulmonary dysplasia

Amin SB, Sinkin RA, McDermott MP, Kendig JW. Lipid intolerance in neonates receiving dexamethasone for bronchopulmonary dysplasia. Arch Pediatr Adolesc Med 1999 153(8) 795-800. 

Huysman WA, de Ridder M, de Bruin NC, et al. Growth and body composition in preterm infants with bronchopulmonary dysplasia. Arch Dis Child Eetal Neonatal Ed 2003 88 F46-F51. 

Robertson CMT, Etches PC, Goldson E, Kyle JM. Eight-year school performance, neurodevelopmental, and growth outcome of neonates with bronchopulmonary dysplasia A comparative study. Pediatrics 1992 89 365-372. 

Fungal Infections Although fxmgal upper respiratory tract colonisation and infections are known adverse effects of inhaled corticosteroids, only recently a fxmgal lower respiratory fracf infection, and more specifically a case of Candida pneumonia in a neonate, was attributed to ICS [11 ]. The neonate received inhaled beclomethasone therapy (400 xg, six times a day) for bronchopulmonary dysplasia. After 20 days of freafment, the patient developed a lower respiratory tract infection. Klebsiella pneumoniae was isolated in fhe fracheal aspirate and treated with amnxirillin-clavulanate without clinical improvement. A week later, bronchoscopy was performed and extended candidiasis was found and treated successfully with fluconazole. Candida pneumonia secondary to airway colonisation is rare and in this case, it was likely provoked by the ICS treatment. 

Dexamethasone has been used to diminish the inflammatory injury which contributes to the chronic lung disease in oxygen- and ventilator-depen-dent neonates with bronchopulmonary dysplasia (BPD) (22,23). The use of corticosteroids in high doses would seem to create an additional risk for infection in these vulnerable children. There does not appear to be any definite increase in risk for the development of nosocomial LRI in dexamethasone-treated neonates (22-25). 

Figure 2 Neonatal rat model of bronchopulmonary dysplasia reproduces the human disease. (A) EvG stain for matrix deposition and (B) H E stain in rat lung 28 days after treatment with Ad vector expressing active TGF-p 1 (29 days old). (A) demonstrates a combination of fibrosis (dark stain) and large alveoli and (B) demonstrates inhibition of alveolarization with large alveoli and a lack of any interstitial infiltrate. (C) and (D) H E stain of human infant, (C) 120 days old and (D) 790 days old, showing midstage (C) and late-stage (D) BPD with combination of fibrosis and enlarged alveoli. A,B, lOOx magnification C, 20>< D50x (C and D from Ref. 96.)...

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