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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, congenital heart disease).
Etiology
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.
Diagnosis
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 and nursery-acquired pneumonia, should be sought.
For diagnosis, the patient has to have required at least 28 days of > 21% O2. Specific additional diagnostic criteria (see Table 2: Respiratory Disorders in Neonates, Infants, and Young Children: 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.
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Table 2
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| National Institute of Child Health and Human Development Criteria for Diagnosis of Bronchopulmonary Dysplasia* |
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< 32 Wk Gestational Age†
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≥ 32 Wk Gestational Age‡
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Diagnosis
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Breathing room air at 36 wk PMA or discharge, whichever comes first
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Breathing room air by 56 days postnatal age or discharge, whichever comes first
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Mild BPD
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Need for < 30% O2 at 36 wk PMA or discharge, whichever comes first
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Need for < 30% O2 at 56 days postnatal age or discharge, whichever comes first
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Moderate BPD
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Need for ≥ 30% O2, positive pressure, or both at 35 wk PMA or discharge, whichever comes first
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Need for ≥ 30% O2, positive pressure, or both at 56 days postnatal age or discharge, whichever comes first
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Severe BPD
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*These criteria are in addition to the baseline requirement of > 21% O2 for at least 28 days.
†Assessed at 36 wk PMA.
‡Assessed at age 29 to 55 days.
BPD = bronchopulmonary dysplasia; PMA = postmenstrual age.
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Prognosis
Prognosis varies with severity. Infants who still depend on mechanical ventilation at 36 wk gestation have a 20 to 30% mortality rate in infancy. 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
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; 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 is sometimes used: chlorothiazide 10 to 20 mg/kg po bid plus spironolactone 1 to 3 po mg/kg once/day or split into twice-daily doses. 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.
Weeks or months of additional ventilator support, supplemental O2, or both may be required for advanced BPD. Ventilator pressures 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 ≥ 88% 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 Miscellaneous Viral Infections in Infants and Children: 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.
Prevention
Practices for prevention of BPD include
Inhaled nitric oxide seems to be promising and is under investigation.
Last full review/revision March 2009 by Anand D. Kantak, MD; John T. McBride, MD
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