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Pediatrics · Chapter 2. Neonatology

Etiology and Pathogenesis of Bronchopulmonary Dysplasia

Bronchopulmonary dysplasia

Bronchopulmonary dysplasia (BPD) is a multifactorial disease of immature lungs that occurs in premature infants. The basis of the pathology is the arrest of normal lung tissue development against the background of morphofunctional immaturity and aggressive external impacts (inflammation, mechanical ventilation, oxidative stress).

Risk groupExtremely premature infants (gestation < 32 weeks, weight < 1500 g, more often < 1000 g)
Main factorMorphofunctional immaturity and surfactant deficiency
Iatrogenic triggersProlonged mechanical ventilation (barotrauma, volutrauma) and hyperoxia (FiO2 > 50%)
Severity assessmentPerformed at 36 weeks of postconceptional age (for <32 weeks) or on the 56th day of life
3 min readFor medical studentsUpdated Sep 20, 2026
Material prepared by WhiteCoat Pro editorial team based on platform study guidesReviewed by medical editor: Aulov A. A., general practitioner · 09/24/2026

Concept evolution and disease forms

Historically, BPD was associated exclusively with iatrogenic lung injury: the toxic effects of high oxygen concentrations and mechanical trauma during mechanical ventilation. This led to inflammation and fibrosis.

Today, BPD is considered a group of diseases. The key cause is the disruption (arrest) of normal growth and maturation of lung tissue, including alveoli and small pulmonary circulation vessels. There are two main forms:

  • Classical ("old"): develops due to aggressive respiratory support (mechanical ventilation) and hyperoxia. Accompanied by prominent inflammation and fibrosis.
  • "New": occurs in extremely premature infants (gestation < 32 weeks, extremely low birth weight). It can develop even without the use of harsh mechanical ventilation parameters, against the background of surfactant administration. The essence is the arrest of the alveolarization process.

Key risk factors and triggers

The pathogenesis of BPD is caused by a combination of morphofunctional immaturity and external aggressive influences. Triggers are divided into several groups:

  • Immaturity: gestation less than 30 weeks, surfactant and antioxidant system deficiency.
  • Iatrogenic (respiratory): mechanical ventilation for more than 3 days, barotrauma (peak inspiratory pressure > 30 cm H2O), hyperoxia (oxygen fraction > 50%).
  • Infectious and inflammatory: chorioamnionitis, cytomegalovirus infection, Ureaplasma urealyticum, sepsis, ventilator-associated pneumonia.
  • Mechanical and hemodynamic: air leak syndromes (pneumothorax), pulmonary edema due to fluid overload or patent ductus arteriosus.
  • Nutritional and metabolic: calorie deficit, hypovitaminosis (A, E, C), selenium deficiency.
  • Genetic and local: male sex, family history of asthma, proteolysis imbalance (excess elastase), microaspiration in reflux.
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Stages of development of classical BPD (according to W.H. Northway)

The classical form goes through four successive stages, reflecting the transition from acute distress syndrome to irreversible changes:

  1. Acute injury (2–3rd day): picture of neonatal RDS. Radiologically: air bronchogram and nodular-reticular network.
  2. Exudative phase (4–10th day): destruction of the alveolar epithelium and capillary endothelium, interstitial edema, bronchiolar necrosis. Beginning of tissue remodeling (squamous metaplasia). On the radiograph — "opacification" of the lung fields.
  3. Proliferative phase (11–20th day): active inflammation (macrophages, fibroblasts), progression to obliterating bronchiolitis. Vascular muscle hypertrophy leads to pulmonary hypertension (cor pulmonale). Radiologically, the "sponge" symptom (cysts and atelectasis) is formed.
  4. Fibrous-obliterative phase (from 21–28th day): predominance of sclerosis. Foci of fibrosis alternate with compensatory emphysema (macroscopically — cobblestone pattern). On X-ray — fibrous cords and areas of emphysema.

Class and exam questions

What is "new" BPD and how does it differ from the classical one?

"New" BPD occurs in extremely premature infants (less than 32 weeks) and represents an arrest in the development of alveoli and pulmonary vessels. Unlike the classical form, it can develop without prolonged harsh mechanical ventilation and high doses of oxygen.

What criteria are used to assess the severity of BPD?

Severity is assessed by three parameters: anamnestic (oxygen requirement), clinical (severity of respiratory failure), and radiological (structural changes).

At what time frames is the severity of BPD assessed?

For infants under 32 weeks of gestation — at 36 weeks of postconceptional age; for those born after 32 weeks — on the 56th day of life (or at discharge).

What role does inflammation play in the pathogenesis of BPD?

Auto-alteration due to generalized inflammation (hypercytokinemia) damages the lungs, worsens malnutrition, and causes a specific anemia distinct from the anemia of prematurity.

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What else to study on this topic

  • Diagnostic criteria for respiratory failure in BPD
  • Radiological signs of BPD at various stages
  • Pulmonary hypertension and cor pulmonale in BPD
  • Specific anemia in hypercytokinemia in infants with BPD

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