BRONCHOPULMONARY DYSPLASIA
Category: Child Health
Abstract : Bronchopulmonary dysplasia (BPD) is a chronic lung disease (CLD) that develops
in preterm neonates treated with oxygen and positive pressure ventilation (PPV).
Northway originally described BPD in 1967 with clinical, radiographic, and
histologic lung changes in preterm infants who had respiratory distress syndrome
(RDS) and were treated with oxygen and ventilator therapy. Currently, BPD is
Bronchopulmonary dysplasia (BPD) is a chronic lung disease (CLD) that develops
in preterm neonates treated with oxygen and positive pressure ventilation (PPV).
Northway originally described BPD in 1967 with clinical, radiographic, and
histologic lung changes in preterm infants who had respiratory distress syndrome
(RDS) and were treated with oxygen and ventilator therapy.
Currently, BPD is
infrequent in infants with birth weight greater than 1200 g and in infants of
greater than 30 weeks' gestation. Antenatal glucocorticosteroids, early
surfactant therapy, and gentler modalities of ventilation have minimized the
severity of lung injury, particularly in more mature infants. However, in some
smaller infants who may have been exposed to chronic chorioamnionitis, its
pathogenesis remains enigmatic.
bronchopulmonary dysplasia
Pathophysiology: The pathophysiology of BPD is multifactorial. Major organ
systems affected include the lungs and the heart. The alveolar stage of lung
development in the human is from about 36 weeks' gestation to 18 months
postnatally, with most alveolarization occurring within 5 to 6 months of term
birth. Although primary septation forms saccules and secondary septal crests
indicate alveolarization, some investigators think that septations are a
continuous process. The intense pulmonary
microvasculature branching runs
parallel with lung development; however, detailed understanding of their
interactions and interactions with various growth factors is elusive.
In
contrast to the findings of Northway, in the postsurfactant era, the lungs of
infants dying of BPD show less fibrosis and more uniform inflation. The large
and small airways are remarkably free of epithelial metaplasia, smooth muscle
hypertrophy, and fibrosis. However, alveoli are less numerous and are larger,
indicating an interference with septation, despite an increase in elastic tissue
that is proportionate to the severity of the respiratory disease before death.
Some specimens also have decreased pulmonary microvasculature development.
Because most infants survive, the pathologic progression of the disease and the
healing process are not fully understood.
Mechanical ventilation and
oxygen interferes with alveolar and vascular development in preterm baboons and
in lambs. Infants with severe BPD have pulmonary hypertension and abnormal
pulmonary vascular development.
bronchopulmonary dysplasia
Frequency: The frequency of BPD is dependent on the definition used and can
be quite different between neonatal intensive care units (NICUs). An analysis of
several surfactant trials reveals an incidence of BPD (ie, oxygen requirement at
age 28 d with an abnormal finding on chest radiography) ranging widely from
17-57%; no significant difference between placebo- and surfactant-treated
survivors was found. In 1998, Kresch et al performed a more recent meta-analysis
of surfactant replacement therapy for infants weighing less than 2 kg, which
demonstrated improved survival without BPD in infants receiving modified natural
surfactant. Infants with severe BPD are often extremely immature and of very low
birth weight, although term infants with significant respiratory failure may
also be at increased risk. In fact, since the survival of very low birth weight
infants has improved by surfactant supplementation, the actual prevalence of BPD
has increased.
bronchopulmonary dysplasia Mortality/Morbidity: Since the
routine use of surfactant replacement has begun, survival of the most immature
infants has improved. Along with other advances in technology and improved
understanding of neonatal physiology, infants with BPD today appear to have less
severe disease as compared to infants with BPD in years past. Infants with
severe BPD remain at high risk for pulmonary morbidity and mortality during the
first 2 years of life.
• Pulmonary mechanics
o Pulmonary complications
include increased airway resistance, decreased lung compliance, increase in
airway reactivity, and increase in airway obstruction. Increased resistance and
airway activity may be evident in the early stages of BPD. With worsening
severity, airway obstruction can become significant, with expiratory flow
limitations. In the early and mild stages of BPD, functional residual capacity
(FRC) can be increased; however, increases in FRC are noted in severe BPD
secondary to air trapping and hyperinflation.
o Lung compliance is reduced in
infants with BPD. Changes on pulmonary function tests (PFTs) correlate with
radiographic findings. Compliance is often reduced in infants with BPD secondary
to increased resistance, resulting in frequency dependence and tachypnea often
observed in these infants. Serial PFTs may help assess therapeutic modalities
employed to treat BPD, but they are fraught with variability and error related
to excessive chest wall distortion and the location from which measurements are
made.
bronchopulmonary dysplasia Physical:
• Infants with BPD have
abnormal findings on physical examination, chest radiography, pulmonary function
testing, and histopathologic examination.
• Infants with severe BPD are
often extremely immature and of very low birth weight.
o They frequently
respond to conventional ventilation and surfactant administration.
o
Extraordinary therapeutic modalities, such as HFV and inhaled NO, have been
employed to improve survival of these infants with mixed success.
o Oxygen
and ventilator requirements often increase within the first 2 weeks of
life.
• Other infants initially respond well to surfactant and various
forms of ventilation strategies.
o Over the course of the second to fourth
weeks of life, oxygen assistance, ventilator assistance, or both often increases
to maintain adequate oxygenation and ventilation.
o Chest radiographs
obtained in these infants may demonstrate decreased lung volumes, areas of
atelectasis and hyperinflation, lung haziness, and PIE.
• Arterial blood
gases may reveal acidosis, hypercarbia, and hyperoxia.
• Physical
examination may reveal the following:
o Tachypnea
o Tachycardia
o
Increased work of breathing, with retractions, nasal flaring, and
grunting
• Poor weight gain and increased energy intake requirements are
frequently noted.
• Different scoring systems have been developed and
studied to predict BPD, to gauge the severity of illness, and to predict the
survival of patients with BPD.
bronchopulmonary dysplasia Causes:
•
Volutrauma and barotrauma
• Oxygen toxicity
• Inflammation
•
Infection
• Nutrition
bronchopulmonary dysplasia Lab Studies:
• Arterial blood gases may reveal
acidosis, hypercarbia, and hyperoxia.
Imaging Studies:
• Chest
radiography is helpful in distinguishing BPD severity and in differentiating BPD
from atelectasis, pneumonia, and air leak syndrome.
• More recently, CT
scanning and MRI studies of infants with BPD have provided more detailed images
of the damaged airway and lung.
bronchopulmonary dysplasia Histologic
Findings: In 1996, Cherukupalli and colleagues completed morphologic and
biochemical lung analyses of infants with BPD. Four distinct pathologic stages
have been identified, which are acute lung injury, exudative bronchiolitis,
proliferative bronchiolitis, and obliterative fibroproliferative
bronchiolitis.
bronchopulmonary dysplasia Staging: In 1967, Northway and
associates first described 4 different stages of severity. Stage 1 was similar
to uncomplicated RDS. Stage 2 revealed pulmonary parenchymal opacities and a
bubbly appearance to lungs. In stages 3 and 4, patients had areas of
atelectasis, hyperinflation, bleb formation, and fibrosis. Edwards in 1979 and
Toce in 1984 subsequently refined Northway's original findings and correlated
BPD score with illness severity.
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