Bronchopulmonary

Dysplasia (BPD)

Abdulwahhab S
Learning objectives
 After completion of this lesson, learners will be able to:
 Define bronchopulmonary dysplasia
 Describe risk factors for bronchopulmonary dysplasia
 Describe pathological changes of bronchopulmonary
dysplasia
 Explain management of bronchopulmonary dysplasia
Bronchopulmonary Dysplasia (BPD)
 BPD is a form of chronic lung disease that
develops almost in preterm neonates treated with
oxygen and positive-pressure ventilation (PPV).
 BPD is usually defined as a need for supplemental
oxygen at 28 days or 36 weeks' postconceptional
age for infants less than 32 weeks' GA.
Cont’d
 For infants born at <32 weeks' gestation who
received supplemental oxygen for their first 28
days, the NIH defined BPD at 36 weeks'
postmenstrual age (PMA) as
 Mild: no supplemental O2 requirement
 Moderate: supplemental O2 requirement
<30%
 Severe: supplemental O2 requirement
≥30% and/or continuous positive airway
pressure (CPAP) or ventilator support
Cont’d
 For infants born at ≥32 weeks, the NIH defined BPD as
supplemental O2 requirement for the first 28 days with

severity level based on O2 requirement at 56 days.

 Operationally, many clinicians simply define BPD as

requirement for oxygen supplementation at 36 weeks’ PMA.
 Lung parenchyma usually appears abnormal on chest
radiographs.
Incidence
 Incidence is inversely related to the gestational age
and birthweight.
 Infants <28 weeks' gestation or <1,000 g birth weight
are most susceptible, with incidence rates of 35% to
50%.
 However, full-term infants with meconium aspiration,
pneumonia and certain cardiac and GIT anomalies
that require chronic ventilator support may also
develop BPD.
Risk factors
 Immature lung substrate

 Volutrauma and lung injury from mechanical ventilation or

BMV
 Oxygen toxicity
 Genetic factors
 Excessive early IV fluid administration
 Persistent L-R shunt through PDA
 Intrauterine or perinatal infection (e.g., Ureaplasma urealyticum)
 Intrauterine growth restriction
 Pathogenesis
Acute lung injury

 Caused by the combination of O 2 toxicity, barotrauma, and volutrauma from MV.

 Airway and vascular tone may be altered.

 Sloughed cells and accumulated secretions not cleared adequately by the

damaged mucociliary transport system cause inhomogeneous peripheral airway

obstruction

 Leads to alternating areas of collapse and hyperinflation and proximal airway

dilation.

 Inflammation may also lead to impaired alveolarization and emphysematous

changes in the lung.

Cont’d
Chronic phase of lung injury

 The interstitium may be altered by fibrosis and cellular hyperplasia that

results from excessive release of growth factors and cytokines, leading

to dysregulated repair.

 Interstitial fluid clearance is disrupted, resulting in pulmonary fluid

retention.

 Airways develop increased muscularization and hyperreactivity.

 The physiologic effects are decreased lung compliance, increased

airway resistance, and impaired gas exchange with resulting

ventilation -perfusion mismatching and air trapping.

Cont’d
 Necrotizing bronchiolitis
 Obstruction of the small airway lumens by
debris and edema
 Areas of peribronchial, interstitial fibrosis, and

 Areas of atelectasis alternating with areas of

emphysema.
Clinical manifestations
 Tachypnea,

 Tachycardia,

 Increased work of breathing (with retractions, nasal

flaring, and grunting),
 Frequent desaturations,

 Wheezing or prolongation of expiration and rales.

 In severe cases, right-sided heart failure may occur.

Investigations
 Blood gas analysis may show hypoxemia and hypercarbia.
 Chest x-ray: radiographic findings may be quite variable

 Early: appears as diffuse haziness and lung hypoinflation

with small round radiolucencies dispersed throughout the
lungs.
 Later: shows streaky interstitial densities, patchy
atelectasis, and cyst formation with concomitant
hyperinflation.
Management
 Prevention of BPD is the cornerstone of management
by avoiding, as much as possible, factors that
predispose to injury.
 Goals of treatment:

 Minimize further lung injury (barotrauma and

volutrauma, O2 toxicity, inflammation)

 Maximize nutrition

 Diminish O2 consumption
Cont’d
 Respiratory support

 Mechanical ventilation

 Supplemental oxygen

 PDA management

 Fluid management

 Diuretics

 Bronchodilators

 Corticosteroids

 Nutritional support

 Blood transfusion
Complications
 Upper airway obstruction

 Pulmonary hypertension
 Metabolic imbalance r/t diuretics

 Infection

 Hearing loss: ototoxic drug, ischemic CNS injury

 ROP
 Early growth failure
Prognosis
 Good for infants who have been weaned from
oxygen before discharge from the NICU.
 The first 2 years are the dangerous periods for
airways disease.
 Mortality in infants with BPD ranges from 10-25%.
 Cardiorespiratory failure and acquired infection
(respiratory syncytial virus) are common causes of
death.