The clinical, radiological and pathological features of chronic lung diseas
e have changed from those seen when the condition was first described. Most
babies who now develop chronic lung disease have a birth weight below 1000
g and have only mild early respiratory disease, requiring minimal ventilat
ion and low concentrations of inspired oxygen. The underlying pathophysiolo
gy of long-term lung damage appears to be a disturbance of the normal alveo
lar development which is continuing after birth, resulting in emphysematous
like lungs with fewer and larger alveoli. Alveolarisation is affected by a
number of insults including ventilation, oxygen, nutritional problems, ste
roids and both antenatal and post-natal infection. A final common pathway f
or many of these insults is persistence of an acute inflammatory response i
n the airways. There is good evidence that intra-uterine exposure to pro-in
flammatory cytokines, as a consequence of ascending infection, induces both
preterm labour and inflammation in the airways which triggers the lung inj
ury sequence before birth. These cytokines have also been shown to have maj
or effects on other organs in the body, in particular their association wit
h brain damage and cerebral palsy. Treatment with antibiotics from birth ha
s not been shown to affect the incidence or severity of chronic lung diseas
e.
Conclusion Intra-uterine infection is not only a common cause of preterm on
set of labour but also a trigger to lung injury which significantly increas
es the risk of development of long-term respiratory disease in the newborn
infant.