A Lyon1. 1. Simpson Memorial Maternity Pavilion, Edinburgh, Scotland. andy.lyon@ed.ac.uk
Abstract
UNLABELLED: The clinical, radiological and pathological features of chronic lung disease 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 ventilation and low concentrations of inspired oxygen. The underlying pathophysiology of long-term lung damage appears to be a disturbance of the normal alveolar 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, steroids and both antenatal and post-natal infection. A final common pathway for many of these insults is persistence of an acute inflammatory response in the airways. There is good evidence that intra-uterine exposure to pro-inflammatory cytokines, as a consequence of ascending infection, induces both preterm labour and inflammation in the airways which triggers the lung injury sequence before birth. These cytokines have also been shown to have major effects on other organs in the body, in particular their association with brain damage and cerebral palsy. Treatment with antibiotics from birth has not been shown to affect the incidence or severity of chronic lung disease. CONCLUSION: Intra-uterine infection is not only a common cause of preterm onset of labour but also a trigger to lung injury which significantly increases the risk of development of long-term respiratory disease in the newborn infant.
UNLABELLED: The clinical, radiological and pathological features of chronic lung disease 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 ventilation and low concentrations of inspired oxygen. The underlying pathophysiology of long-term lung damage appears to be a disturbance of the normal alveolar 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, steroids and both antenatal and post-natal infection. A final common pathway for many of these insults is persistence of an acute inflammatory response in the airways. There is good evidence that intra-uterine exposure to pro-inflammatory cytokines, as a consequence of ascending infection, induces both preterm labour and inflammation in the airways which triggers the lung injury sequence before birth. These cytokines have also been shown to have major effects on other organs in the body, in particular their association with brain damage and cerebral palsy. Treatment with antibiotics from birth has not been shown to affect the incidence or severity of chronic lung disease. CONCLUSION:Intra-uterine infection is not only a common cause of preterm onset of labour but also a trigger to lung injury which significantly increases the risk of development of long-term respiratory disease in the newborn infant.
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