Bronchopulmonary dysplasia (BPD) is a condition which now principally occurs in babies born before 30 weeks’ gestation (time in the womb), being more commonly observed in the most immature of these babies.
Medical text written November 1991 by Contact a Family. Approved November 1991 by Professor M Patton, Professor of Medical Genetics, St George’s Hospital Medical School, London, UK and Dr J E Wraith. Consultant Paediatrician, Royal Manchester Children’s Hospital, Manchester, UK. Last updated October 2010 by Dr R Rivers, Consultant Neonatologist (Emeritus), Imperial College Healthcare Trust, St Mary’s Hospital, London.
BPD is thought to reflect an imbalance between factors promoting inflammation in the very immature lungs and the factors that are designed to inhibit excessive inflammation. The healing and repair that follows the inflammation is also poorly organised so that the lungs do not always grow normally afterwards. Factors which predispose these babies to develop BPD include exposure to infections in the womb before birth, the need for breathing support from a ventilator and for oxygen supplementation in the air they are being given after birth.
There may be a continuing need for the baby to have some form of breathing support. The amount of added oxygen they are receiving at the age of 28 days and, if still needed, when they reach the equivalent of 36 weeks’ gestation, are used to define the severity of the BPD. The need for additional oxygen may persist for some weeks or even months, with a few babies actually going home on oxygen therapy.
Babies who have been affected by the more severe forms of BPD are more prone to wheezing episodes requiring medication and some may require later re-hospitalisation for breathing difficulties. Viral infections during the first years of life are often triggers for wheezing episodes and those babies who are receiving additional oxygen at home may be offered a series of injections of specific antibody to give them some protection against one of these viruses, the human respiratory syncytial virus, during their first winter at home.
Any genetic predisposition to BPD development is likely to involve several gene interactions in the pro-inflammatory, inhibitory and repair pathways in the lung along with genes affecting the types of chemicals produced to stabilise lung aeration and help in the fight against infections. These components of inheritance interact with the complex environmental factors mentioned above and, as yet, no distinct inherited gene patterns predisposing to BPD in the human baby have been identified.
Not applicable for this condition.
Information and support in the UK for bronchopulmonary dysplasia is available from BLISS – the premature baby society (see entry Prematurity and Sick Newborn).