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Bronchopulmonary dysplasia

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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.

BPD is a chronic disease that affects approximately half of infants born between 29 weeks of gestation.

The disease increases early childhood mortality, and impairs long-term pulmonary and neurodevelopmental outcomes.

It is associated with long-term respiratory problems and Neurodevelopmental impairment.

It is a multifactorial disease, and ventilation-induced lung injuries are an important factor in its pathogenesis.

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.

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).

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.

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.

 

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