Bronchopulmonary dysplasia (BPD) is a chronic lung disease that primarily affects premature infants who require mechanical ventilation and supplemental oxygen for respiratory distress. First described in 1967, BPD has evolved over time due to advancements in neonatal care and technology.
Today, it remains one of the most common long-term complications of preterm birth, especially in infants born before 28 weeks of gestation. For respiratory therapists, understanding BPD is crucial because they play a direct role in both its prevention and management.
What is Bronchopulmonary Dysplasia?
Bronchopulmonary dysplasia (BPD) is a chronic lung disease that primarily affects premature infants, especially those born before 28 weeks of gestation, who require prolonged mechanical ventilation and supplemental oxygen. It occurs when immature lungs are exposed to injury from oxygen toxicity, high airway pressures, or infections, leading to inflammation, scarring, and abnormal lung development.
Instead of forming numerous small alveoli for efficient gas exchange, the lungs develop fewer and larger air sacs, reducing surface area and impairing oxygen delivery. Infants with BPD often experience difficulty breathing, persistent oxygen needs, wheezing, and recurrent respiratory infections. While there is no cure, treatment focuses on supportive care, minimizing lung injury, and promoting growth to improve long-term respiratory outcomes.
Causes and Risk Factors
Bronchopulmonary dysplasia (BPD) develops when an infant’s lungs are underdeveloped or injured, most often in babies born prematurely. Because their lungs are fragile and not fully mature, they are more vulnerable to irritation, inflammation, and long-term breathing complications after birth.
Several factors increase the likelihood of BPD, including:
- Premature birth, which often leads to respiratory distress syndrome and the need for breathing support
- Prolonged mechanical ventilation or high oxygen levels, which can strain and damage delicate lung tissue
- Infections, such as neonatal sepsis, that trigger inflammation
- Inflammation before birth, sometimes linked to placental infections like chorioamnionitis
- Genetic predisposition and intrauterine growth restriction
Understanding these causes and risk factors is essential because it highlights the complex nature of BPD and why prevention is so challenging.
Respiratory therapists and healthcare teams must balance providing life-saving oxygen and ventilation while minimizing potential lung injury. Recognizing these risks early allows for tailored strategies that protect fragile lungs and improve long-term outcomes for premature infants.
Why is BPD Relevant to Respiratory Care?
Respiratory therapists are on the front lines of managing neonates at risk for or diagnosed with BPD. Their role includes:
- Ventilation management: Using lung-protective strategies to minimize barotrauma and volutrauma.
- Oxygen titration: Maintaining safe oxygen levels to reduce hypoxemia while avoiding hyperoxia.
- Airway clearance: Implementing techniques to reduce mucus plugging and infection risk.
- Long-term follow-up: Assisting in home oxygen therapy, monitoring growth, and educating caregivers.
Note: For respiratory therapists working in neonatal intensive care units (NICUs), a deep understanding of BPD is essential to improving outcomes and reducing complications.
Management Strategies
While there is no cure for BPD, treatment focuses on supportive care and prevention of further lung injury. Management often includes:
- Supplemental oxygen (sometimes required long-term)
- Noninvasive ventilation when possible to reduce ventilator-associated injury
- Bronchodilators and corticosteroids in selected cases
- Nutritional support to promote lung growth and overall development
- Preventive strategies, such as minimizing oxygen exposure and using surfactant therapy in premature infants
Bronchopulmonary Dysplasia Practice Questions
1. What is bronchopulmonary dysplasia (BPD)?
A chronic lung disease in premature infants caused by arrested lung development, often due to mechanical ventilation and oxygen exposure during the late canalicular or early saccular stage
2. What is the most common morbidity associated with extremely preterm infants?
Bronchopulmonary dysplasia
3. How is BPD best described?
An inflammatory lung disease of premature infants that leads to disrupted alveolar development and can be fatal in severe cases
4. Why is the incidence of BPD considered highly variable among different centers?
Due to inconsistent definitions, variable oxygen administration protocols, and differences in defining oxygen dependency
5. What is the most significant risk factor for developing BPD in neonates?
Degree of prematurity—the earlier the gestational age, the higher the risk
6. What are some intrauterine risk factors associated with BPD?
Genetic predisposition, chorioamnionitis, and preterm labor
7. What are common postnatal risk factors that contribute to BPD development?
Mechanical ventilation, supplemental oxygen, postnatal infections, and an exaggerated inflammatory response
8. How does barotrauma from positive-pressure ventilation affect the developing lung?
It disrupts septal development, reducing the number of alveoli and impairing lung growth
9. What is the most common antenatal infection associated with preterm delivery and BPD?
Ureaplasma infection
10. What are the major postnatal insults that increase the risk of developing BPD?
Mechanical ventilation and oxygen toxicity
11. What is the first step in the pathogenesis of arrested lung development seen in BPD?
Acute lung injury (ALI)
12. How does lung injury in premature infants differ from that in adults?
It involves a reduced early inflammatory response but a prolonged late phase with fibrosis and decreased lung compliance
13. What is the initial cellular injury during acute lung injury in BPD?
Microfractures and necrosis of Type I pneumocytes caused by mechanical stretch or pressure
14. What happens after Type I pneumocyte destruction in BPD?
Cytokines are released, recruiting neutrophils and macrophages to the lungs
15. Which proinflammatory cytokines are elevated following acute lung injury in BPD?
TNF-α, IL-1, IL-6, and IL-8
16. Which anti-inflammatory cytokine is notably diminished during the response to acute lung injury in premature lungs?
IL-10
17. What cellular event increases reactive oxygen and nitrogen species (ROS and RNS) in BPD, even without hyperoxia?
Cyclic stretch from mechanical ventilation
18. What enzyme is primarily responsible for generating free radicals in this context?
NADPH oxidase
19. What damaging enzymes are released by neutrophils during BPD progression?
Elastases and matrix metalloproteinases (MMPs)
20. How do elastases and MMPs contribute to BPD pathology?
They lead to interstitial remodeling, elastin accumulation, and scarring
21. Why is the premature lung especially vulnerable to free radical damage?
It lacks sufficient antioxidant defenses like superoxide dismutase, catalase, glutathione peroxidase, and G6PD
22. What long-term effect does BPD have on lung structure?
Fibrosis due to disrupted septal development and reduced alveolar formation
23. What clinical intervention most commonly precedes the development of BPD?
Prolonged mechanical ventilation
24. What is severe acute lung injury in adults commonly called?
Acute Respiratory Distress Syndrome (ARDS)
25. What is the long-term outcome of acute lung injury in premature infants?
Chronic lung disease, also known as bronchopulmonary dysplasia
26. What developmental stage is affected when mechanical ventilation disrupts alveolar formation?
The saccular stage of lung development
27. Why does BPD result in fewer alveoli?
Primary and secondary septa are damaged, preventing normal alveolar development
28. What role does oxygen toxicity play in the development of BPD?
It promotes inflammation, oxidative stress, and cellular injury in the immature lung
29. What term describes lung damage caused by pressure during ventilation?
Barotrauma
30. How can early interventions reduce the risk of BPD?
By minimizing ventilator time, avoiding oxygen overexposure, and managing infections early
31. Why does airway resistance increase in infants with bronchopulmonary dysplasia (BPD)?
Due to a reduced number of developing bronchioles and impaired lung compliance, which narrows the cross-sectional area of the airways
32. What is the single most important intervention for improving outcomes in premature infants?
Providing adequate nutrition, including Vitamin A supplementation, which has been shown to reduce the incidence of BPD
33. How does oxygen concentration during delivery room resuscitation impact BPD risk?
Using 30% oxygen instead of 90% is associated with a lower incidence of BPD in preterm infants
34. What antenatal intervention has been proven to reduce the incidence of BPD in premature infants?
Antenatal steroid administration
35. What is a serious potential side effect of steroid use in premature infants?
Increased risk of spontaneous bowel perforation, especially when used in conjunction with NSAIDs within the first two weeks of life
36. How does caffeine therapy affect mechanical ventilation duration in preterm infants?
It reduces the duration of mechanical ventilation by approximately one week
37. What is the most common reason extremely low birth weight infants (<1000g) fail to wean from mechanical ventilation?
Apnea of prematurity due to immature respiratory centers
38. How does caffeine therapy help prevent ventilator dependency in premature infants?
It stimulates the central respiratory drive and helps reduce apnea of prematurity
39. What is the diagnostic criterion for bronchopulmonary dysplasia (BPD)?
Treatment with >21% oxygen for at least 28 days after birth
40. How is mild BPD defined in preterm infants born before 32 weeks?
Breathing room air by 36 weeks postmenstrual age or at discharge
41. How is mild BPD defined in infants born after 32 weeks?
Breathing room air by 56 days postnatal age
42. How is moderate BPD defined in infants born before 32 weeks?
Requiring <30% FiO₂ at 36 weeks postmenstrual age
43. How is moderate BPD defined in infants born after 32 weeks?
Requiring <30% FiO₂ by 56 days postnatal age
44. How is severe BPD defined in infants born before 32 weeks gestation?
Needing >30% FiO₂ and/or positive pressure or CPAP at 36 weeks postmenstrual age
45. How is severe BPD defined in infants born after 32 weeks?
Needing >30% FiO₂ and/or positive pressure or CPAP by 56 days postnatal age
46. What is the most common chronic lung disease of infancy?
Bronchopulmonary dysplasia (BPD)
47. What are three alternative names for BPD?
Chronic lung disease of infancy, neonatal chronic lung disease, evolving chronic lung disease
48. What respiratory condition do most babies with BPD initially have?
Respiratory distress syndrome (RDS), often due to a deficiency in surfactant
49. What structural abnormalities may be present in the lungs and heart of infants with BPD?
Fewer alveoli, fewer blood vessels, and underdevelopment of the heart, kidneys, brain, stomach, intestines, and eyes
50. What is respiratory distress syndrome (RDS)?
An acute lung injury in neonates characterized by alveolar and interstitial edema, hyaline membrane hemorrhage, epithelial swelling, and collagen proliferation
51. What are some additional causes or risk factors for BPD?
Barotrauma, endotracheal intubation, oxygen toxicity, pulmonary interstitial edema, nutritional deficits, infections, and patent ductus arteriosus (PDA)
52. How does endotracheal intubation affect BPD risk?
It increases the risk of BPD by approximately five times
53. What are the clinical signs and symptoms of BPD?
Tachypnea, cyanosis, nasal flaring, expiratory grunting, oral-tactile hypersensitivity, and suprasternal/intercostal/subcostal retractions
54. What is oral-tactile hypersensitivity, and why is it relevant in BPD?
It refers to heightened sensitivity around the mouth, often seen in infants with prolonged intubation or respiratory distress
55. Why is the patent ductus arteriosus (PDA) a risk factor for BPD?
It contributes to pulmonary overcirculation and edema, exacerbating lung injury
56. What role does pulmonary interstitial edema play in the pathogenesis of BPD?
It impairs gas exchange and contributes to lung inflammation and fibrosis
57. How does oxygen toxicity contribute to BPD development?
By generating reactive oxygen species (ROS) that damage lung tissues in oxygen-sensitive premature infants
58. Why is surfactant deficiency significant in the development of RDS and BPD?
It leads to alveolar collapse, impaired gas exchange, and increased susceptibility to ventilator-induced injury
59. What role do nutritional deficits play in BPD progression?
Poor nutrition delays lung healing and development, increasing vulnerability to lung injury
60. Why is early identification of BPD severity important in clinical management?
It guides respiratory support strategies and nutritional interventions to improve long-term outcomes
61. What is a characteristic chest X-ray finding in an infant with bronchopulmonary dysplasia (BPD)?
A ground-glass appearance, resembling pulmonary fibrosis
62. What are the four main components of treatment for BPD?
Breathing support, surfactant replacement, medications, and nutritional support
63. Which form of respiratory support may be used in the treatment of BPD?
High-frequency mechanical ventilation, CPAP, or supplemental oxygen
64. How is surfactant typically delivered in the treatment of BPD?
Via endotracheal tube
65. What types of medications may be used in the management of BPD?
Bronchodilators, diuretics, potassium supplements, and antibiotics
66. What type of medication, when given within 24 hours of birth, can be beneficial in reducing BPD severity?
Corticosteroids
67. What maternal interventions can help prevent BPD in preterm infants?
Regular prenatal care, healthy nutrition, avoiding smoking and alcohol, infection prevention, and possible progesterone or corticosteroid therapy
68. How do corticosteroids help prevent BPD in preterm infants?
They speed up fetal lung maturity and promote surfactant production
69. What factors influence the outcomes of infants diagnosed with BPD?
Severity at diagnosis, susceptibility to infections, long-term oxygen or ventilator dependency, and developmental complications
70. What long-term complications are associated with BPD in children?
Developmental delays, persistent lung issues, and ongoing susceptibility to respiratory infections
71. Which neonate is at the highest risk for developing BPD?
A premature infant born at 28 weeks who requires high-pressure mechanical ventilation
72. What is the priority nursing intervention for an infant with BPD?
Monitoring oxygen saturation via pulse oximetry
73. What intervention helps facilitate gas exchange in infants with BPD?
Providing or arranging for chest physiotherapy
74. What is another commonly used name for bronchopulmonary dysplasia?
Chronic lung disease
75. How is BPD defined?
A persistent lung disease that develops in premature infants after receiving respiratory support during the neonatal period
76. What are two important interventions for preventing or treating lung immaturity in preterm infants?
Antenatal corticosteroids and postnatal surfactant therapy
77. What is the primary cause of BPD in premature infants?
Lung damage from positive-pressure ventilation and prolonged oxygen exposure
78. What are common causes of BPD in term or near-term infants?
Pneumonia, sepsis, meconium aspiration, diaphragmatic hernia, and lung hypoplasia
79. What are typical clinical manifestations of BPD in infants?
Tachypnea, wheezing, grunting, nasal flaring, retractions, cyanosis, crackles, and signs of respiratory distress
80. What are expected chest X-ray findings in a patient with BPD?
Hyperinflation, areas of atelectasis, and interstitial thickening
81. What long-term therapy may be required for severe cases of BPD?
Tracheostomy with ongoing respiratory support and infection management
82. Which class of medication is not recommended for routine use in managing BPD?
Systemic corticosteroids
83. What medication is administered monthly to high-risk infants to prevent respiratory syncytial virus (RSV)?
Palivizumab (Synagis), a monoclonal antibody
84. What are the main focuses of BPD management in infants?
Managing acute respiratory episodes, providing adequate nutrition, and supporting growth and development
85. What should be included in the routine assessment of an infant with BPD?
Monitoring for infection, checking vital signs, pulse oximetry, assessing airway patency, respiratory status, color, and behavior
86. Bronchopulmonary dysplasia (BPD) is most commonly seen in preterm infants born at less than how many weeks of gestation?
Less than 32 weeks
87. What two structural abnormalities characterize bronchopulmonary dysplasia in the lungs?
Alveolar hypoplasia and impaired pulmonary vascular growth
88. Bronchopulmonary dysplasia is commonly associated with which abnormal respiratory rate pattern?
Tachypnea
89. What findings are typically seen on a chest radiograph of an infant with bronchopulmonary dysplasia?
Air trapping, focal atelectasis, interstitial changes, and peribronchial thickening
90. Up to what percentage of infants with BPD are re-admitted for acute respiratory illness within the first two years of life?
Up to 50%
91. To support proper growth and development, the target oxygen saturation for infants with BPD outside the NICU should be at or above what percentage?
92%
92. Which two inhaled medications may help treat symptoms like wheezing and chronic cough in BPD?
Inhaled corticosteroids and β2 agonists
93. Pulmonary hypertension is a common complication of which neonatal lung condition?
Bronchopulmonary dysplasia (BPD)
94. What is the minimum number of days postnatally that an infant must require supplemental oxygen to meet the diagnostic criteria for BPD?
28 days
95. How is bronchopulmonary dysplasia typically classified in terms of severity?
Mild, moderate, or severe based on oxygen and ventilation needs at specific timepoints
96. What is the main pathophysiologic feature of bronchopulmonary dysplasia?
Abnormal development of the alveoli and pulmonary vasculature
97. What condition frequently precedes the development of bronchopulmonary dysplasia in preterm infants?
Respiratory distress syndrome (RDS)
98. What is the term used for thickening around the airways commonly seen on imaging in BPD?
Peribronchial thickening
99. Why are β2 agonists used in the treatment of BPD?
To relieve bronchospasm and improve airflow
100. What structural lung change contributes to poor gas exchange in infants with BPD?
Alveolar simplification and reduced surface area
Final Thoughts
Bronchopulmonary dysplasia (BPD) is a complex chronic lung disease that highlights the importance of specialized respiratory care in neonates. As neonatal survival improves, the prevalence of BPD remains significant, making it a vital area of focus for respiratory therapists.
By applying lung-protective strategies, carefully managing oxygen therapy, and providing long-term support, respiratory therapists can play a critical role in improving the quality of life and long-term outcomes for affected infants.
Written by:
John Landry is a registered respiratory therapist from Memphis, TN, and has a bachelor's degree in kinesiology. He enjoys using evidence-based research to help others breathe easier and live a healthier life.
References
- Thébaud B, Goss KN, Laughon M, Whitsett JA, Abman SH, Steinhorn RH, Aschner JL, Davis PG, McGrath-Morrow SA, Soll RF, Jobe AH. Bronchopulmonary dysplasia. Nat Rev Dis Primers. 2019.