Impaired structural remodelling of pulmonary arteries in newborns with congenital diaphragmatic hernia: A histological study of 29 cases

Congenital diaphragmatic hernia (CDH) is associated in many cases with lung hypoplasia and pulmonary hypertension (PH). The pathogenetic mechanisms un derlying the pulmonary hypertension in CDH are not completely understood. I n order to alleviate the pulmonary hypertension, new therapeutic modalities have been introduced including extracorporeal membrane oxygenation (ECMO), This paper reports a study of the histology of the lungs of 29 CDH autopsy cases, with special attention to the pulmonary arteries, and relating the findings to gestational age and ECMO treatment, Formalin-fixed and paraffin -embedded specimens were stained with haematoxylin and eosin (H&E) and elas tic van Gieson (EvG) stains, followed by morphometric measurements of the a rterial media and adventitia, As expected, there was a significant decrease in adventitial percentage and total wall thicknesses of small pulmonary ar teries with an external diameter less than or equal to 150 mu m in term con trol newborns compared with pre-term controls (p=0.0004 and 0.05). In CDH n ewborns, all the measured values of the arterial wall remained significantl y higher. The increase of adventitial thickness also affected the supernume rary arteries in CDH neonates, CDH newborns subjected to ECMO treatment sho wed a significantly thinner arterial adventitia than CDH cases who did not receive ECMO (p=0.0001), the former approaching normal values. These result s indicate that in CDH, there is failure of the normal arterial remodelling processes occurring in the perinatal period. The adventitial thickening, w hich has been reported previously in term CDH patients only, was related in the present study to differences in gestational ages. This appears to be p artially reversed by ECMO treatment, thus constituting one of the mechanism s by which ECMO treatment aids in alleviating the associated PH in CDH newb orns, Copyright (C) 1999 John Wiley & Sons, Ltd.