Epidemiology of bronchopulmonary dysplasia
Introduction
More than 40 years ago, Northway et al. provided the seminal description of Bronchopulmonary dysplasia (BPD):1 the report of a case series of 32 preterm infants who developed chronic lung disease and characteristic clinical, radiographic and pathological features following mechanical ventilation for respiratory distress syndrome (RDS). Subsequent improvements in neonatal intensive care that have reduced mortality among even the most preterm infants have been unaccompanied by reduced rates of BPD, a form of chronic lung disease that primarily affects preterm infants treated with mechanical ventilation for structural and/or biochemical lung immaturity. BPD remains the most prevalent and one of the most serious long-term sequelae of preterm birth, affecting, in the USA alone, approximately 14 000 preterm infants born each year.2, 3
Childhood impairments of health, neurodevelopment, and quality of life are common among preterm infants with BPD and these include increased risk of post-neonatal mortality4, 5, *6, 7 and higher rates of rehospitalization.8, 9 Adverse health consequences of BPD also include long-term pulmonary impairments10, 11, *12 such as asthma13, 14 and emphysema,10 pulmonary hypertension,15, 16, 17, 18 cardiovascular compromise,19, 20 undernutrition21, 22 and growth failure.23, 24 In addition, many infants with BPD suffer cognitive impairment,25, *26, 27 cerebral palsy (CP),28, 29, *30 and global neurodevelopmental deficits.31
Section snippets
Evolution of BPD: population at risk and histologic features
In the four decades since the first description of BPD, extremely preterm infants have been surviving in greater numbers and this trend has been accompanied by evolution in the epidemiology and pathological features of a new form of BPD. Currently, infants born at ≤26 weeks of gestation are at the greatest risk of developing BPD. The histologic features of ‘new’ BPD reflect the developmental immaturity of this high risk population born at the intersection of the canalicular and saccular phases
Incidence of BPD
BPD rates vary by the definition applied,34 gestational age distribution and other characteristics of the population, as well as by medical center. Data from the Eunice Kennedy Shriver National Institutes of Child Health and Human Development Neonatal Research Network (NICHD Neonatal Network)2 and others*35, 36 suggest that stable or increasing BPD rates are closely linked with progressively improving survival of extremely low birth weight2, *35, 36 and extremely preterm37 infants. The highest
Clinical and physiologic definitions of BPD
Northway described four stages of BPD, defined by clinical characteristics and radiographic findings: Stage I (2–3 days) RDS; Stage II (4–10 days) regeneration; Stage III (11–20 days) transition to chronic disease; Stage IV (> 1 month) chronic lung disease. Later, Bancalari39 defined BPD clinically as a disorder occurring among infants who received mechanical ventilation for at least 3 days in the first postnatal week and had characteristic radiographic findings and persistent respiratory
Epidemiologic antecedents of BPD
Pulmonary immaturity, consisting of structural underdevelopment and insufficiency of biochemical components or protectants such as surfactant, antioxidants, and proteinase inhibitors, constitutes the primary risk factor for BPD.52, 53 Northway et al. speculated that oxygen toxicity and barotrauma were responsible for the lung injury leading to BPD and subsequent epidemiologic studies supported their hypothesis. Early studies of the antecedents of classical BPD were narrowly focused on these and
Laboratory contributions to the epidemiology of ‘new’ BPD
Preterm infants are especially susceptible to lung injury due to mechanical, oxidant, and inflammatory factors because of the extreme structural and biochemical immaturity of the preterm lung.86 Volutrauma, inflammation, and deficiencies of endogenous protectors are recognized as important factors in the development of ‘new’ BPD.
The extremely preterm baboon (born at 125 days of a normal 180 day gestation)87, 88 and the preterm lamb89, 90, 91 models of BPD have contributed a great deal of
BPD prevention
Marked variation among medical centers in risk-adjusted BPD rates51 and demonstrated success in reducing BPD rates within individual institutions through quality improvement efforts42, 43 suggest that specific care practices modify BPD occurrence. Quality improvement interventions, however, have not proven uniformly successful125 and a single modifiable care practice that will prevent BPD is unlikely to be identified.
The search for preventive therapies and treatment strategies has included
Summary
In the four decades since its discovery by Northway et al.,1 BPD has evolved pathologically and epidemiologically yet remains a prevalent major morbidity among preterm infants. ‘New’ BPD likely results from exposure of a developmentally immature lung to sequential insults, some of which might begin in prenatal life. This multi-hit pathogenesis results in aberrant pulmonary development characterized by inadequate formation of parenchymal microvasculature and alveoli. Extreme pulmonary immaturity
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