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Pediatrics · Chapter 2. Neonatology

Bronchopulmonary dysplasia

Dysplasia bronchopulmonalis

Bronchopulmonary dysplasia (BPD) is a chronic polyetiological lung disease affecting predominantly premature newborns against the background of morphological immaturity of the respiratory system. The pathology arises as a consequence of intensive care in the neonatal period and is characterized by prolonged oxygen dependence, respiratory failure, and impaired normal lung tissue growth.

ICD-10 codeP27.1 — Bronchopulmonary dysplasia originating in the perinatal period.
Key markerThe need for supplemental oxygen persists at 28 days of life and older.
Main triggerToxic effects of high oxygen concentrations and aggressive mechanical ventilation (in the classic form).
Clinical courseSymptoms of respiratory failure regress with the natural growth of the lungs.
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

Morphological substrate and clinical core

The disease develops as an iatrogenic or post-infectious complication after treatment for respiratory distress syndrome (RDS) or neonatal pneumonia. The basis of pathogenesis is specific damage to the bronchioles and pulmonary parenchyma.

Morphologically, this manifests as the development of emphysema, proliferation of fibrous tissue, and in the case of extreme prematurity, arrest of the development and replication of new alveoli. Clinically, the process is accompanied by persistent oxygen dependency, signs of bronchial obstruction, and respiratory failure (RF). In a favorable course, the symptoms gradually diminish as the patient grows older and the lung tissue undergoes compensatory growth.

Diagnostic criteria of BPD

The diagnosis is established comprehensively. Specialists analyze anamnestical data, the clinical picture, and specific radiological findings.

Clinical and anamnestic markers:

  • Respiratory support: mechanical ventilation (MV) or nasal continuous positive airway pressure (NCPAP) during the first week of the child's life.
  • Duration of oxygen therapy: the need for a breathing mixture with an oxygen concentration greater than 21% persists by 28 days of life and longer.
  • Symptomatology: presence of respiratory failure and bronchial obstruction syndrome at an age older than one month against the background of ongoing oxygen supplementation.

Radiological picture: In the first months of life, a characteristic "mottled" pattern is observed on the radiograph. Zones of interstitial edema alternate with areas of hypertranslucency (increased aeration). Fibrous cords and ribbon-like parenchymal opacities are also defined.

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Disease Classification

The pathology is systematized along several vectors to accurately determine management tactics and prognosis:

  1. By gestational age and form: BPD in term infants and BPD in preterm infants are distinguished. In premature infants, the disease is additionally divided into two fundamentally different forms — classic and new. In term infants, the pathology proceeds clinically and radiologically identically to the classic form.
  2. By severity: mild, moderate, and severe.
  3. By course phase: periods of exacerbation alternate with periods of remission.

Classic and new forms of BPD: what is the difference?

Understanding the differences between forms of BPD in premature infants is critically important. They differ cardinally in etiology, clinical course, and structural changes in the lungs.

SignClassic ("old") formNew form
Essence of pathogenesisIatrogenic injury, inflammation, and fibrosis due to baro- and volutrauma.Arrest of lung tissue development, impaired alveologenesis and vascular growth.
EtiologyMechanical ventilation with "harsh" parameters. Absence of surfactant prophylaxis.Intrauterine inflammation (chorioamnionitis), extreme prematurity.
Gestational ageAny gestational age of prematurity.Less than 32 weeks (typically 24–28 weeks).
Association with RDSAlways an outcome of prior RDS.Preceding RDS is not mandatory.
Respiratory supportMandatory aggressive mechanical ventilation in anamnesis.Mechanical ventilation is not mandatory; gentle therapy was often used (NCPAP, diffuse O2).
ClinicSevere course. Obstruction and pulmonary hypertension frequently occur.Usually a mild course. Bronchial obstruction and pulmonary hypertension are rare.
X-rayInterstitial edema, hyperinflation, bullae, ribbon-like opacities, and fibrosis.Homogeneous opacification ("haziness"), small opacities. Hyperinflation is not characteristic.
OutcomesRecovery, or emphysema, chronic bronchitis, bronchiolitis obliterans.Currently considered unclear and require study.
How to memorize

For quick memorization of the essence of BPD forms, use the association: "Classic breaks, New-form freezes". The classic form is a breakdown (iatrogenic trauma, inflammation, and severe fibrosis from harsh mechanical ventilation), while the new form is a freeze (arrest of alveolar and vascular development in extremely premature infants).

Class and exam questions

Does BPD always develop only in extremely premature infants?

No, the disease can develop in children with any gestational age, including term newborns. In the case of term infants, the clinical picture and X-ray changes fully correspond to the classic ("old") form of BPD.

What role does respiratory distress syndrome (RDS) play in the development of the new form of the disease?

Unlike the classic form, in which prior RDS is an obligatory trigger, the development of the new form of BPD can occur without a preceding episode of respiratory distress syndrome.

Do the symptoms resolve with age?

Yes, the disease is characterized by a gradual reverse development (regression) of respiratory failure and oxygen dependency. This occurs naturally as the child's lung volume increases and new lung tissue grows.

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What else to study on this topic

  • Specific criteria for determining BPD severity grades (mild, moderate, severe).
  • Pathogenetic mechanisms of pulmonary hypertension formation in the classic form of the disease.
  • Outpatient management tactics for patients with BPD during periods of remission.
  • Mechanisms of the influence of intrauterine inflammation (chorioamnionitis) on alveologenesis processes.
  • Long-term consequences of the new form of BPD and assessment of patients' quality of life.

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