eMedicine Specialties > Pediatrics: Cardiac Disease and Critical Care Medicine > Neonatology

Bronchopulmonary Dysplasia

Author: William Driscoll, DO, Associate Professor, Department of Pediatrics, Division of Neonatology, University of Florida at Jacksonville
Coauthor(s): Jonathan Davis, MD, Professor of Pediatrics, Chief of Newborn Medicine, Department of Pediatrics, Tufts University School of Medicine
Contributor Information and Disclosures

Updated: Apr 23, 2007

Introduction

Background

Bronchopulmonary dysplasia (BPD) is a form of chronic lung disease that develops in preterm neonates treated with oxygen and positive-pressure ventilation (PPV). Originally describing BPD in 1967, Northway reported clinical, radiographic, and histologic changes in the lungs of preterm infants who had respiratory distress syndrome (RDS) and who were treated with oxygen and mechanical ventilation.

Northway's original definition has been extensively modified over the last 4 decades. Bancalari’s definition involves ventilation criteria, oxygen requirement at 28 days to maintain arterial oxygen tensions >50 mm Hg, and abnormal findings on chest radiographs. In 1988, Shennan et al proposed that an additional need for supplemental oxygenation at 36 weeks' postmenstrual age may be the most accurate indicator of pulmonary outcome; this criterion decreased the large number of relatively healthy preterm infants Bancalari and others included in their definitions.

In 2001, Jobe and Bancalari summarized proceedings of a National Institute of Health consensus conference on BPD. Investigators from the National Institute of Child Health and Human Development (NICHD) recently validated their recommendations. This group improved the definition of BPD and attempted to assign a severity score based on oxygen requirements and the need for respiratory support. However, many physicians set different standards for oxygen requirements and for target ranges for oxygen saturation. This variation in practice may notably influence the incidence and severity of BPD in a particular neonatal ICU (NICU).

Pathophysiology

The pathogenesis of BPD remains complex and poorly understood. BPD results from a variety of toxic factors that can injure small airways and that can interfere with alveolarization (septation), leading to alveolar simplification with a reduction in the overall surface area for gas exchange. The developing pulmonary microvasculature can also be injured. Many strongly believe that alveolar and vascular development are intimately related. Damage to the lung during a critical stage of lung growth can result in clinically significant pulmonary dysfunction. The lungs (alveolar and vascular compartments), heart, and brain are the major organs affected.

Frequency

United States

BPD occurs infrequently in infants who had a  birth weight of >1250 g and in infants who were born at >30 weeks' gestation. Antenatal glucocorticosteroids, early surfactant therapy, and gentle modalities of ventilation have minimized the severity of lung injury, particularly in relatively mature infants. However, improved survival has increased the prevalence of BPD, especially in small infants who may have been exposed to in utero infection (eg, chorioamnionitis).

Several trials of surfactants revealed that incidences of BPD range widely from 17-57%, and no substantial difference between placebo- and surfactant-treated survivors was found. In 1998, Kresch and Clive performed a meta-analysis of surfactant-replacement therapy for infants weighing <2 kg. Infants receiving modified natural surfactant had improved survival, without BPD. In 2001, Van Marter and associates described the wide variation in the prevalence of BPD in different NICUs using various ventilatory strategies. This variation has also been noted among sites in the Vermont Oxford Network (VON) and in the NICHD research network, suggesting that different populations and practices may directly affect outcomes. Infants with severe BPD are often extremely immature and had a very low birth weight, though term infants with clinically significant respiratory failure may also be at increased risk.

International

Studies similar to those in the United States have been conducted to compare rates of BPD in different NICUs in Europe. Results have been similar despite the relatively homogeneous population.

Mortality/Morbidity

Since the introduction of surfactant replacement, survival of the most immature infants has improved. However, the stable 25-50% survival rates in preterm infants at 23-24 weeks likely reflect the lack of alveolarization and vascular development. Survival and morbidity improved in infants >24 weeks after the widespread administration of antenatal corticosteroids was introduced in 1994.

Along with other advances in technology and an improved understanding of neonatal physiology, infants with BPD appear to have milder disease today than in years past.

Infants with severe BPD remain at high risk for pulmonary morbidity and mortality during the first 2 years of life. Infants with BPD are at risk for repeated pulmonary infections and asthma requiring repeated hospital admissions and physician visits.

Abnormal long-term neurodevelopmental outcome, muscular development, slow growth, and chronic pulmonary morbidity are common in infants with BPD. Whether abnormal neurodevelopmental outcomes are directly related to BPD or to the patients' marked immaturity and disease severity is hard to determine.

Sex

Male infants with BPD tend to have more severe disease and worse neurodevelopmental outcome.

Age

BPD is most common in the most immature neonates born at 22-32 weeks' gestational age. These patients frequently weigh <1000 g at birth.

Clinical

Physical

Infants with BPD have abnormal findings on physical examination, chest radiography, pulmonary function testing, and histopathologic examination. Initial findings observed shortly after birth are consistent with RDS. Persistence of these abnormalities can be associated with an increased risk of BPD.

Physical examination may reveal tachypnea, tachycardia, increased work of breathing (with retractions, nasal flaring, and grunting), frequent desaturations, and significant weight loss during the first 10 days of life.

Infants with severe BPD are often extremely immature and had a very low birth weight. Their requirements for oxygen and ventilatory support often increase in the first 2 weeks of life. At weeks 2-4, oxygen supplementation, ventilator support, or both are often increased to maintain adequate ventilation and oxygenation.

Causes

More on Bronchopulmonary Dysplasia

Overview: Bronchopulmonary Dysplasia
Differential Diagnoses & Workup: Bronchopulmonary Dysplasia
Treatment & Medication: Bronchopulmonary Dysplasia
Follow-up: Bronchopulmonary Dysplasia
Multimedia: Bronchopulmonary Dysplasia
References
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Further Reading

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Keywords

BPD, chronic lung disease, CLD, respiratory distress syndrome, RDS, synchronized intermittent mechanical ventilation, SIMV, intermittent mechanical ventilation, IMV, high-frequency jet ventilation, HFJV, antioxidant enzyme, AOE

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Contributor Information and Disclosures

Author

William Driscoll, DO, Associate Professor, Department of Pediatrics, Division of Neonatology, University of Florida at Jacksonville
William Driscoll, DO is a member of the following medical societies: American Academy of Pediatrics
Disclosure: Nothing to disclose.

Coauthor(s)

Jonathan Davis, MD, Professor of Pediatrics, Chief of Newborn Medicine, Department of Pediatrics, Tufts University School of Medicine
Jonathan Davis, MD is a member of the following medical societies: American Academy of Pediatrics, American Medical Association, American Thoracic Society, European Society for Paediatric Research, and Society for Pediatric Research
Disclosure: Nothing to disclose.

Medical Editor

Steven M Donn, MD, Professor of Pediatrics, Director, Neonatal-Perinatal Medicine, Department of Pediatrics, University of Michigan Health System
Steven M Donn, MD is a member of the following medical societies: American Pediatric Society
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine.com, Inc
Disclosure: Pfizer Inc Stock Investment from broker recommendation; Avanir Pharma Stock Investment from broker recommendation

Managing Editor

Arun K Pramanik, MD, MBBS, Professor of Pediatrics, Director of Neonatal Fellowship, Louisiana State University Health Sciences Center
Arun K Pramanik, MD, MBBS is a member of the following medical societies: American Academy of Pediatrics, American Thoracic Society, National Perinatal Association, and Southern Society for Pediatric Research
Disclosure: Nothing to disclose.

CME Editor

Carol L Wagner, MD, Professor of Pediatrics, Medical University of South Carolina
Carol L Wagner, MD is a member of the following medical societies: American Academy of Pediatrics, American Chemical Society, American Medical Women's Association, American Public Health Association, American Society for Bone and Mineral Research, American Society for Clinical Nutrition, Massachusetts Medical Society, National Perinatal Association, and Society for Pediatric Research
Disclosure: Nothing to disclose.

Chief Editor

Ted Rosenkrantz, MD, Head, Division of Neonatal-Perinatal Medicine, Professor, Departments of Pediatrics and Obstetrics/Gynecology, University of Connecticut School of Medicine
Ted Rosenkrantz, MD is a member of the following medical societies: American Academy of Pediatrics, American Medical Association, American Pediatric Society, Connecticut State Medical Society, Eastern Society for Pediatric Research, and Society for Pediatric Research
Disclosure: Nothing to disclose.

 
 
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