Adult Bronchopulmonary Dysplasia: The Similarity in Roentgen and Histopathologic Appearance Between Some Cases of Oxygen Toxicity, Radiation Pneumonitis, and Postcytotoxic Nonspecific Bronchopneumonia

Bronchopulmonary dysplasia (BPD) was first described by Northway et al in 1967. This article describes the evolution of our understanding of the pathophysiology of BPD and the approaches to treatments of this illness developed over the past fifty years. These interventions had their roots in the understanding of the principles of the surface tension present at air- liquid interfaces, which were developed over 150 years before BPD’s initial description. Improving outcomes in neonatal care have led to greater survival of preterm and very preterm infants, and to an evolution of the pathogenesis and pathology of BPD, from an illness caused primarily by barotrauma and oxygen toxicity to one of interruption of lung development. While the incidence of BPD has remained about the same in recent decades, this is because survival of infants born at lower gestational ages is increasing. Understanding of molecular, genetic and physiologic mechanisms has led to newer treatments that have mitigated some of the harmful effects of prolonged mechanical ventilation. Recognition of BPD as a chronic multi-system disease has resulted in further improvements in care after discharge from neonatal intensive care. Since many of the origins of chronic obstructive lung disease in adults are based in childhood respiratory illnesses, improving outcomes of BPD in infancy and childhood will undoubtedly lead to improved respiratory outcomes in the adults that these children will become.

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Recent advances in late lung development and the pathogenesis of bronchopulmonary dysplasia

AJP Lung Cellular and Molecular Physiology ◽

10.1152/ajplung.00267.2013 ◽

2013 ◽

Vol 305 (12) ◽

pp. L893-L905 ◽

Cited By ~ 100

Author(s):

Alicia Madurga ◽

Ivana Mižíková ◽

Jordi Ruiz-Camp ◽

Rory E. Morty

Keyword(s):

Gas Exchange ◽

Surface Area ◽

Bronchopulmonary Dysplasia ◽

Lung Development ◽

Oxygen Toxicity ◽

Structural Development ◽

Vascular Structure ◽

Recent Developments ◽

Immature Lung ◽

Prematurely Born Infants

In contrast to early lung development, a process exemplified by the branching of the developing airways, the later development of the immature lung remains very poorly understood. A key event in late lung development is secondary septation, in which secondary septa arise from primary septa, creating a greater number of alveoli of a smaller size, which dramatically expands the surface area over which gas exchange can take place. Secondary septation, together with architectural changes to the vascular structure of the lung that minimize the distance between the inspired air and the blood, are the objectives of late lung development. The process of late lung development is disturbed in bronchopulmonary dysplasia (BPD), a disease of prematurely born infants in which the structural development of the alveoli is blunted as a consequence of inflammation, volutrauma, and oxygen toxicity. This review aims to highlight notable recent developments in our understanding of late lung development and the pathogenesis of BPD.

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Radiographic Features of Pulmonary Oxygen Toxicity in the Newborn: Bronchopulmonary Dysplasia

Radiology ◽

10.1148/91.1.49 ◽

1968 ◽

Vol 91 (1) ◽

pp. 49-58 ◽

Cited By ~ 79

Author(s):

William H. Northway, ◽

Robert C. Rosan

Keyword(s):

Bronchopulmonary Dysplasia ◽

Oxygen Toxicity ◽

Radiographic Features

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Therapy for bronchopulmonary dysplasia in premature infants focuses on reducing the effects of oxygen toxicity and mechanical ventilation

Drugs & Therapy Perspectives ◽

10.2165/00042310-200521070-00004 ◽

2005 ◽

Vol 21 (7) ◽

pp. 11-14

Author(s):

&NA;

Keyword(s):

Mechanical Ventilation ◽

Bronchopulmonary Dysplasia ◽

Premature Infants ◽

Oxygen Toxicity

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Complications in the Treatment of the Respiratory Distress Syndrome: Bronchopulmonary Dysplasia, Oxygen Toxicity, and the Wilson-Mikity Syndrome

Pediatric Clinics of North America ◽

10.1016/s0031-3955(16)32852-8 ◽

1973 ◽

Vol 20 (2) ◽

pp. 419-431 ◽

Cited By ~ 23

Author(s):

Victor G. Mikity ◽

Paddy Taber

Keyword(s):

Respiratory Distress Syndrome ◽

Respiratory Distress ◽

Bronchopulmonary Dysplasia ◽

Distress Syndrome ◽

Oxygen Toxicity

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Late Breaking Abstract - Role of shear stress and oxygen toxicity on central nervous system comorbidities in bronchopulmonary dysplasia

10.1183/13993003.congress-2021.pa2256 ◽

2021 ◽

Author(s):

Lena Haist ◽

Sophia Stöcklein ◽

Juan David Henao Sanchez ◽

Benjamin Schubert ◽

Anne Hilgendorff

Keyword(s):

Central Nervous System ◽

Shear Stress ◽

Nervous System ◽

Bronchopulmonary Dysplasia ◽

Oxygen Toxicity

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Etiology of Bronchopulmonary Dysplasia

PEDIATRICS ◽

10.1542/peds.96.4.796 ◽

1995 ◽

Vol 96 (4) ◽

pp. 796-797

Author(s):

Paola Papoff ◽

Lucia Pacifico ◽

Giovanni Bucci

Keyword(s):

Preterm Infants ◽

Bronchopulmonary Dysplasia ◽

Inflammatory Reaction ◽

Lung Fibrosis ◽

Risk Group ◽

Oxygen Toxicity ◽

Control Group

We read with great interest the article by Groneck et al (Pediatrics. 1994;93:712-718). The authors concluded that an inflammatory reaction is present in the lungs of preterm infants prone to develop bronchopulmonary dysplasia (BPD), and they suggested that this concept of inflammation could link the pathophysiological gap between barotrauma- and oxygen toxicity-induced injury and subsequent lung fibrosis. In their study, a total of 12 neonates developed BPD: 11 of 24 neonates in the BPD-risk group and 1 of 35 in the control group.

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