Bronchopulmonary Dysplasia
Bronchopulmonary dysplasia (BPD) is a chronic lung disease that occurs in preterm infants who
are treated with oxygen and positive-pressure ventilation. The incidence and severity of BPD
differ by institution, according to the standards used for diagnosis.
The pathogenesis of BPD is poorly understood at this time. Various toxic factors injure the small
airways and interfere with alveolarization, which reduces the overall surface area available for
gas exchange. In some patients, the developing pulmonary microvasculature also is injured.
Premature birth, combined with oxygen treatment, mechanical ventilation, inflammatory agents,
and/or infection, is presumed to lead to premature lung maturation, which in turn is associated
with arrest in development of the lung alveolar and vascular growth.
BPD most often occurs in infants who weigh less than 1250 grams (g) and were born prior to 30
weeks’ gestation. About 25% of infants who weigh less than 1500 g develop BPD.
Infants with severe BPD will remain at high risk for pulmonary morbidity until they are ≈2 years
old. These infants are at risk for recurrent pulmonary infections and asthma. Abnormal long-term
neurodevelopmental outcome, muscular development, and slow growth are common among
infants with BPD. More severe disease and worse neurodevelopmental outcomes are seen in
male infants with BPD.
Examination and workup of an infant with BPD may reveal:
 Tachypnea
 Tachycardia
 Increased work of breathing
 Frequent desaturations
 Significant weight loss during the first 10 days of life
 Acidosis, hypercarbia, and hypoxia
 Airway resistance, decreased lung compliance, increased airway reactivity, and increased
airway obstruction
 Pulmonary hypertension and cor pulmonale
 Persistent right ventricular hypertrophy or fixed pulmonary hypertension
Medical intervention includes:
 Mechanical ventilation
 Surfactant replacement
 Continuous positive airway pressure
 Transfusion of packed red blood cells (if patient is anemic)
Potential complications include:
 Trauma secondary to positive pressure ventilation, generally referred to as barotraumas
 Atrophy and fatigue of the respiratory muscles may lead to atelectasis and extubation failure
 Prolonged and repeated intubations, as well as mechanical ventilation, sometimes is associated
with severe upper airway abnormalities, such as vocal cord paralysis, subglottic stenosis, and
laryngotracheomalacia
 Preterm birth exposes the neonate to high oxygen concentrations, increasing the risk of injury
because of oxygen free radicals
 Repeated episodes of desaturation and hypoxia
 Forced exhalation efforts because of infant agitation may cause atelectasis and recurrent
hypoxic episodes
 Increased risk for pneumonia, bronchiolitis, and respiratory syncytial virus continues after
discharge from the hospital
Nutrition considerations:
 Extremely low-birth-weight infants often are catabolic for the first few days of life
 Research has shown that patients who receive suboptimal amounts of calories and protein
during the first weeks to months of life are at increased risk for developing BPD; infants who
receive excessive amounts of fluid are also at a higher risk
 Extremely preterm infants have high insensible water losses and might need large amounts of
free water, but excessive fluids increase the risk of symptomatic patent ductus arteriosus and
pulmonary edema
 BPD increases energy requirements; infants may require 120-150 kilocalories/kilogram (kg) to
gain weight
 It often is necessary to concentrate formula to provide 24, 27, or 30 calories per ounce; the
addition of Microlipid®, Polycose®, or Caloreen® can increase the nutrients provided
 Maximizing intake of macronutrients and micronutrients is crucial to preventing further lung
injury; however, excessive administration of non-nitrogen calories might cause excessive
formation of carbon dioxide:
– Excessive glucose loads may increase oxygen consumption, the respiratory drive, and
glucosuria
– Maximum neonatal glucose oxidative capacity is 12-13 milligrams/kg/minute, or 18 grams
(g)/kg/day
 Recently, standard practice is to administer amino acid-containing solutions beginning at birth
 Supplementation of copper, zinc, and manganese in preterm infants might help to protect
against lung injury
 Calcium and phosphorus requirements are high in preterm infants:
– These infants are at risk for developing rickets and secondary hyperparathyroidism
– Lasix® may worsen bone mineralization
 Vitamin A supplementation reduces the risk of BPD in premature neonates
 It is necessary to increase protein and fat supplementation incrementally until the infant is
receiving 3-3.5 g/kg/day
 Rapid and early administration of high concentrations of lipids may worsen BPD by depleting
pulmonary vascular lipid
 Standard supplementation schemes with commercial human-milk fortifiers sometimes are
inadequate to meet infants’ needs
 Gastroesophageal reflux, impaired suck-swallow coordination, and feeding resistance are
common among infants with BPD
References and recommended readings
Ambalavanan N. Bronchopulmonary dysplasia. Medscape Reference Web site.
http://emedicine.medscape.com/article/973717-overview. Accessed March 13, 2013.
Bronchopulmonary dysplasia (BPD). Children’s Hospital of Eastern Ontario Web site.
http://www.cheo.on.ca/en/bpdnutrition. Accessed March 13, 2013.
Wemhöner A, Ortner D, Tschirch E, Strasak A, Rüdiger M. Nutrition of preterm infants in
relation to bronchopulmonary dysplasia. BMC Pulm Med. 2011;11:7. doi:10.1186/1471-246611-7.
Wilson DC, McClure G, Halliday HL, Reid MM, Dodge JA. Nutrition and bronchopulmonary
dysplasia. Arch Dis Child. 1991;66(1):37-38.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1590361/. Accessed March 13, 2013.
Young TE. Nutritional support and bronchopulmonary dysplasia. J Perinatol. 2007;27:S75-S78.
doi:10.1038/sj.jp.7211725.
Contributed by Elaine Koontz, RD, LD/N
Review Date 3/13
K-0657