PULMONARY PATHOLOGY IN SURFACTANT-TREATED PRETERM INFANTS WITH RESPIRATORY-DISTRESS SYNDROME - AN AUTOPSY STUDY

Citation
P. Toti et al., PULMONARY PATHOLOGY IN SURFACTANT-TREATED PRETERM INFANTS WITH RESPIRATORY-DISTRESS SYNDROME - AN AUTOPSY STUDY, Biology of the neonate, 70(1), 1996, pp. 21-28
Citations number
34
Categorie Soggetti
Pediatrics
Journal title
ISSN journal
00063126
Volume
70
Issue
1
Year of publication
1996
Pages
21 - 28
Database
ISI
SICI code
0006-3126(1996)70:1<21:PPISPI>2.0.ZU;2-L
Abstract
The present study examines the histological features of the lungs of n eonates who died of respiratory distress syndrome or related complicat ions after surfactant therapy. Our aim was to determine whether these lungs showed any unusual histological findings. Complete autopsies wer e performed 6-12 h after death in 10 surfactant-treated preterm infant s and in 30 infants who died before surfactant therapy was available. Representative paraffin sections of all pulmonary lobes, stained with haematoxylin and eosin, were examined microscopically. A few selected slides were also stained with periodic acid-Schiff, Vierhoff-van Gieso n, and Mallory trichrome. Hyaline membrane disease and bronchopulmonar y dysplasia were present in each group, although there was an increase d incidence of intra-alveolar haemorrhage in surfactant-treated babies (in 8 of 10 surfactant-treated as compared with 7 of 30 untreated bab ies). Amongst those treated with surfactant, we observed the persisten ce of acute alveolar damage with unresolved hyaline membrane disease i n 5 infants who died at the ages of 5, 6, 10, 12, and 13 days, respect ively, and histological evidence of pneumocyte type 2 hyperplasia and dysplasia in 2 infants who died at 22 and 41 days of age, respectively . These observations reveal that surfactant-treated infants who fail t o respond to therapy have continuing alveolar injury and an increased incidence of intra-alveolar haemorrhage. Since oxygen radicals can ind uce pneumocyte damage and necrosis and since free radicals provoke alv eolar haemorrhage in animal models, we propose that the lesions we obs erved may stem from a lack, in some preterm babies, of specific mechan isms that detoxify oxygen radicals.