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Bronchopulmonary dysplasia (BPD) is considered to be present when there is need for supplemental oxygen in premature infants who do not have other conditions requiring oxygen.
Infants with bronchopulmonary dysplasia begin their childhood with low functioning lung function and have airway obstruction and alveolar simplification which can contribute to spirometrically diagnosed COPD early in adulthood, especially if there is a second injury such as tobacco smoking.
A chronic disease of the preterm lung that has lasting effects on respiratory health in infancy and childhood, and may be associated with a greater risk of neurodevelopmental disability throughout childhood and adolescence.
BPD Is prevalent after extremely preterm birth.
The disease increases early childhood mortality, and impairs long-term pulmonary and neurodevelopmental outcomes.
It occurs most commonly in very premature born infants with the arrest of lung development (Alveolar hypoplasia what dysmorphic pulmonary vasculature and pulmonary inflammation).
It is associated with long-term respiratory problems and neurodevelopmental impairment.
Infants with bronchopulmonary dysplasia have long-term diminished FEV1.
In the most severely affected supplemental oxygen is required at home and pulmonary hypertension may develop.
It has increased in prevalence in the post surfact and error due to the increase resuscitation and survival of extremely premature infants.
It is a multifactorial disease, and ventilation-induced lung injuries are an important factor in its pathogenesis.
Inflammation associated with mechanical ventilation may contribute to its development.
In the most severely affected patients with BPD health consequences can persist through adulthood.
Optimal nutrition is a fundamental process to prevent BPD.
Affects almost half of infants born at gestational age is of less than 28 weeks.
Infants with BPD are more likely to die early, and those who survive have an increased risk of long-term pulmonary and neurodevelopmental morbidity.
Risk factors include:
Prolonged mechanical ventilation
High concentrations of inspired oxygen
Presence of nfection
Degree of prematurity
Pulmonary interstitial emphysema
High peak inspiratory pressures
Large end-tidal volumes
Repeated alveolar collapse
Increased airway resistance
Increased pulmonary artery pressures
Male sex
Intrauterine growth restriction
Genetic susceptibility
Maternal smoking
Premature infant lungs are more vulnerable to the inflammatory changes that result from mechanical ventilation.
Pulmonary inflammation is an important risk factor in the development of BPD, providing rationale for treating at risk infants with corticosteroids.
Normal lung architecture is interrupted..
Fewer and larger alveoli develop, and the interstitium is thickened.
The pulmonary vasculature develops abnormally.
Fewer and/or abnormally distributed alveolar capillaries result.
Pulmonary hypertension can develop as a result of increased pulmonary resistance.
The diagnosis is suspected when a ventilated infant is unable to wean from oxygen therapy, mechanical ventilation, or both.
Clinically Infants develop worsening hypoxemia, hypercapnia, and increasing oxygen requirements.
Diagnostic criteria require at least 28 days of > 21% oxygen or has to have continued need for supplemental oxygen at or ≥ 36 wk postmenstrual age.
Lung magnetic resonance imaging with hyperpolarized gas can identify lung abnormalities in patients with bronchopulmonary dysplasia and chronic airflow limitation, who meet the spirometry criteria for early onset COPD.
Chest x-ray evolves from a diffuse haziness due to accumulation of exudative fluid, to then multicystic or spongelike changes with alternating areas of emphysema, pulmonary scarring, and atelectasis.
The tracheal aspirate may show sloughed epithelium, with macrophages, neutrophils, and inflammatory markers.
Prognosis varies with severity, with most infants transitioning from mechanical ventilation to continuous positive airway pressure to low-flow oxygen over 2 to 4 mo.
Infants who still depend on mechanical ventilation at 36 wk gestation have a 20 to 30% mortality rate in infancy.
Infants who develop pulmonary arterial hypertension also are at higher risk of mortality during the first year of life.
Infants have a 3- to 4-fold increased rate of growth failure and neurodevelopmental problems.
For several years, infants are at increased risk of lower respiratory tract infections (particularly viral pneumonia or bronchiolitis) and may quickly develop respiratory decompensation if pulmonary infection occurs.
The threshold for hospitalization should be low if signs of a respiratory infection or respiratory distress develop.
Treatment
Nutrition supplementation
Fluid restriction
Diuretics
Oxygen supplementation as needed
Respiratory syncytial virus (RSV) monoclonal antibody (palivizumab)
Treatment: supportive and includes nutritional supplementation, fluid restriction, diuretics, and perhaps inhaled bronchodilators.
Inhaled corticosteroid therapy is considered only as a last resort.
Among mechanically ventilated very premature infants, administration of hydrocortisone between seven and 14 days after birth, compared with placebo, did not improve the outcome of death for BPD at 36 weeks post menstrual age: these findings do not support the use of hydrocortisone for this indication (STOP-BPD study group).
A metaanalysis of 32 randomized controlled studies should glucocorticoids given in the first six days reduced the incidence of BPD but not death and was associated with an increased incidence of cerebral palsy.
Very premature infants exposed to dexamethasone may be at risk for premature onset of COPD.
Continuous positive airway pressure (CPAP) to avoid intubation and mechanical ventilation is considered to prevent BPD and is the standard of care for preterm infants with respiratory distress after birth.
Pulmonary infections must be diagnosed early and treated aggressively.
Daily fluid intake is often restricted to about 120 to 140 mL/kg/day, because pulmonary congestion and edema may develop.
Inhaled bronchodilators do not appear to improve long-term outcome and are not used routinely.
Inhaled bronchodilators may be helpful for acute episodes of bronchoconstriction.
Weeks- months of additional ventilator support, supplemental oxygen, or both may be required for advanced disease.
Ventilator pressures or volumes and fraction of inspired oxygen (Fio2) should be reduced as rapidly as possible.
The degree of lung inflation carries a higher risk of BPD than does the degree of airway pressure.
Arterial oxygenation is continuously monitored during management with a pulse oximeter and maintained at ≥ 89% saturation.
Passive immunoprophylaxis with palivizumab, a monoclonal antibody to RSV is indicated primarily in high-risk infants.
Systemic and inhaled corticosteroids only in cases where there is thought to be no other alternative.
Systemic glucocorticoids initiated during the first post week reduce the risk of BPD but increase the risk of gastrointestinal perforation and cerebral palsy:similar findings occur within inhaled corticosteroids.
In a trial involving preterm infants, hydrocortisone treatment starting on postnatal day 14 to 28 did not result in a higher survival without moderate or survival without moderate to severe bronchopulmonary dysplasia than placebo.
Many extremely preterm infants need intubation for surfactant administration via an endotracheal tube to treat respiratory distress syndrome, because early surfactant administration is effective in BPD prevention.
The administration of surfactant by a catheter as a minimally invasive surfactant therapy (MIST) for preterm infants with respiratory distress syndrome did not result in a significant reduction in the likelihood of outcome of death or bronchopulmonary dysplasia.
In a randomized trial of preterm infants, with respiratory distress syndrome, supported with CPAP, minimally invasive surfactant therapy in preterm infants had lower rates with adverse respiratory outcomes during their first two years of life (OPTIMIST Trial).
In extremely preterm infants receiving surfactant for respiratory distress syndrome, early intratracheal budesonide may have little to no effect on the survival free of BPD (PLUSS Investigators).