Bronchopulmonary dysplasia

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A chronic lung disease affecting premature infants


Bronchopulmonary dysplasia
Synonyms BPD
Pronounce
Field Pulmonology, Neonatology
Symptoms Tachypnea, retractions, hypoxemia, need for prolonged oxygen therapy
Complications Pulmonary hypertension, growth failure, recurrent respiratory infections
Onset Typically within the first 4 weeks of life
Duration Chronic; may persist into childhood
Types Mild, moderate, severe (based on oxygen requirement at 36 weeks postmenstrual age)
Causes Lung injury from mechanical ventilation and/or oxygen therapy
Risks Prematurity, low birth weight, infection, PDA, high oxygen exposure
Diagnosis Clinical criteria, oxygen requirement at 28 days and 36 weeks PMA, chest X-ray
Differential diagnosis Respiratory distress syndrome, congenital pneumonia, pulmonary hypoplasia
Prevention Antenatal corticosteroids, non-invasive ventilation, surfactant therapy
Treatment Respiratory support, nutrition, bronchodilators, diuretics, corticosteroids
Medication Albuterol, furosemide, dexamethasone
Prognosis Variable; some resolve over time, others have long-term respiratory issues
Frequency ~10,000–15,000 cases/year in the U.S.
Deaths Associated with severity; improved survival with neonatal care advances


Bronchopulmonary dysplasia (BPD) is a chronic lung disease that primarily affects premature infants who have received mechanical ventilation or supplemental oxygen therapy to treat respiratory distress syndrome (RDS). It is characterized by abnormal development of the alveoli, inflammation, and pulmonary fibrosis, leading to long-term respiratory difficulties.

History[edit | edit source]

The term "bronchopulmonary dysplasia" was first described in 1967 by Dr. William Northway to characterize the chronic lung damage observed in premature infants treated with high levels of oxygen and prolonged mechanical ventilation. Advances in neonatal intensive care have since altered the presentation and understanding of BPD, shifting from scarring to more developmental arrest in alveolarization.

Pathophysiology[edit | edit source]

BPD results from a combination of factors that injure the immature lungs, including:

  • Barotrauma from mechanical ventilation
  • Oxygen toxicity from high inspired oxygen concentrations
  • Inflammatory responses to infection or ventilation
  • Poor postnatal nutrition

These injuries disrupt the normal development of alveoli and pulmonary vasculature. The lungs of infants with BPD show fewer, larger alveoli with thickened septa, impaired gas exchange, and increased airway resistance.

Risk Factors[edit | edit source]

Risk factors for developing BPD include:

Clinical Presentation[edit | edit source]

Signs and symptoms may include:

Diagnosis[edit | edit source]

BPD is diagnosed based on:

  • The need for oxygen supplementation at 28 days of life and at 36 weeks postmenstrual age (PMA)
  • Severity classification (mild, moderate, severe) depends on oxygen dependency and respiratory support at 36 weeks PMA or 56 days of life
  • Chest X-ray may show areas of:
    • Atelectasis
    • Hyperinflation
    • Linear opacities or cystic changes
  • Pulmonary function testing and echocardiography may aid in assessment

Management[edit | edit source]

Management of BPD involves a multidisciplinary approach:

  • Respiratory support: Minimize further lung injury using non-invasive methods like CPAP or nasal cannula when possible
  • Pharmacologic therapy:
  • Nutrition: High-calorie feeds and possible gastrostomy to support growth and healing
  • Treatment of complications: Monitor for and manage pulmonary hypertension, tracheomalacia, and infections

Complications[edit | edit source]

Long-term complications of BPD may include:

Prognosis[edit | edit source]

Prognosis depends on:

  • Degree of prematurity
  • Severity of lung damage
  • Presence of comorbidities

With modern neonatal care, survival rates have improved, and many infants recover lung function over time. However, some children continue to have respiratory and developmental issues into adolescence.

Prevention[edit | edit source]

Preventive measures include:

  • Antenatal corticosteroids to accelerate fetal lung maturation
  • Early use of surfactant therapy
  • Minimizing invasive ventilation using CPAP or NIPPV
  • Targeted oxygen saturation goals to reduce oxygen toxicity
  • Infection control and nutritional support

See also[edit | edit source]

External links[edit | edit source]






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