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Bronchopulmonary Dysplasia (BPD)
Bronchopulmonary dysplasia is chronic lung disease of the neonate that typically is caused by prolonged ventilation and is further defined by age of prematurity and extent of O2 requirement.
Bronchopulmonary dysplasia (BPD) is considered present when there is need for supplemental O2 in premature infants who do not have other conditions requiring O2 (eg, pneumonia [see Neonatal Pneumonia], congenital heart disease).
BPD has a multifactorial etiology
Significant risk factors include
Additional risk factors include
The lungs of premature infants are more vulnerable to the inflammatory changes that result from mechanical ventilation. The development of normal lung architecture is interrupted; fewer and larger alveoli develop, and the interstitium is thickened. Also, the pulmonary vasculature develops abnormally, with fewer and/or abnormally distributed alveolar capillaries; pulmonary resistance may be increased and pulmonary hypertension (see Persistent Pulmonary Hypertension of the Newborn ) can develop.
BPD typically is suspected when a ventilated infant is unable to wean from O2 therapy, mechanical ventilation, or both. Infants typically develop worsening hypoxemia, hypercapnia, and increasing O2 requirements. Additionally, when an infant cannot be weaned within the expected time, possible underlying disorders, including patent ductus arteriosus (see Patent Ductus Arteriosus (PDA) ) and nursery-acquired pneumonia (see Neonatal Pneumonia), should be sought.
For diagnosis, the patient has to have required at least 28 days of > 21% O2. Specific additional diagnostic criteria (see National Institute of Child Health and Human Development Criteria for Diagnosis of Bronchopulmonary Dysplasia*) have been developed by the NICHD.
Chest x-ray initially shows diffuse haziness due to accumulation of exudative fluid; appearance then becomes multicystic or spongelike, with alternating areas of emphysema, pulmonary scarring, and atelectasis. Alveolar epithelium may slough, and macrophages, neutrophils, and inflammatory mediators may be found in the tracheal aspirate.
National Institute of Child Health and Human Development Criteria for Diagnosis of Bronchopulmonary Dysplasia*
Prognosis varies with severity. Most infants gradually transition from mechanical ventilation (see Soft-Tissue Injuries : Mechanical ventilation) to continuous positive airway pressure (see Soft-Tissue Injuries : Continuous positive airway pressure (CPAP)) to low-flow O2 (see Soft-Tissue Injuries : 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 with BPD 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 is supportive and includes nutritional supplementation, fluid restriction, diuretics, and perhaps inhaled bronchodilators. Respiratory infections must be diagnosed early and treated aggressively. Weaning from mechanical ventilation and supplemental O2 should be accomplished as early as possible.
Feedings should achieve an intake of 150 calories/kg/day including protein 3.5 to 4 g/kg/day; caloric requirements are increased because of the increased work of breathing and to aid lung healing and growth.
Because pulmonary congestion and edema may develop, daily fluid intake is often restricted to about 120 to 140 mL/kg/day. Diuretic therapy transiently improves pulmonary mechanics but not long-term clinical outcome. Thiazide or loop diuretics can be used for short-term benefit in patients who do not respond adequately to or cannot tolerate fluid restriction. Chlorothiazide 10 to 20 mg/kg po bid with or without spironolactone 1 to 3 mg/kg po once/day or split into twice-daily doses is often tried first. Furosemide (1 to 2 mg/kg IV or IM or 1 to 4 mg/kg po q 12 to 24 h for neonates and q 8 h for older infants) may be used for short periods, but prolonged use causes hypercalciuria with resultant osteoporosis, fractures, and renal calculi. If long-term diuretic use is required, chlorothiazide is preferred because it has fewer adverse effects. Hydration and serum electrolytes should be monitored closely during diuretic therapy.
Inhaled bronchodilators (eg, albuterol) do not appear to improve long-term outcome and are not used routinely. However, they may be helpful for acute episodes of bronchoconstriction.
Weeks or months of additional ventilator support, supplemental O2, or both may be required for advanced BPD. Ventilator pressures or volumes and fraction of inspired O2(Fio2) should be reduced as rapidly as tolerated, but the infant should not be allowed to become hypoxemic. Arterial oxygenation should be continuously monitored with a pulse oximeter and maintained at ≥ 89% saturation. Respiratory acidosis may occur during ventilator weaning and treatment and is acceptable as long as the pH remains > 7.25 and the infant does not develop severe respiratory distress.
Passive immunoprophylaxis with palivizumab, a monoclonal antibody to RSV, decreases RSV-related hospitalizations and ICU stays but is costly and is indicated primarily in high-risk infants (see Respiratory Syncytial Virus (RSV) and Human Metapneumovirus Infections : Prevention for indications). During RSV season (November through April), children are given 15 mg/kg IM q 30 days until 6 mo after treatment of the acute illness. Infants > 6 mo also should be vaccinated against influenza.
Systemic or inhaled corticosteroids are discouraged except as a last-resort therapy for established BPD with rapidly worsening pulmonary status and impending death. Informed parental consent is required.
Practices for prevention of BPD include
Use of antenatal corticosteroids
Prophylactic use of exogenous surfactant in selected high-risk infants (eg, weighing < 1000 g and requiring ventilator support)
Early therapeutic continuous positive airway pressure
Early use of surfactant for treatment of RDS
Prophylactic use of methylxanthines (eg, caffeine 5 to 10 mg/kg po once/day), particularly when birth weight is < 1250 g
Permissive hypercarbia and hypoxemia to achieve low ventilator pressures, volumes, or both
Prophylactic use of vitamin A (5000 units IM 3 times/wk for a total of 12 doses) for infants with birth weight < 1000 g
Avoidance of large volumes of fluid
Inhaled nitric oxide has been studied and may help prevent of BPD. However, optimal dosage, duration, and timing are unclear, so nitric oxide is not yet recommended outside of research protocols.
Bronchopulmonary dysplasia (BPD) is chronic lung disease of premature infants.
BPD develops in neonates who required prolonged mechanical ventilation and/or O2 supplementation, which can disrupt normal lung development.
Diagnosis is based on prolonged (≥ 28 days) need for O2 supplementation and sometimes ventilatory support.
Wean from respiratory support as soon as possible and use nutritional supplementation, fluid restriction, and sometimes diuretics.
Prevent by using antenatal corticosteroids, surfactant, caffeine, and vitamin A and use lowest Fio2 and airway pressure as possible.
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