Amy Bieda


Bronchopulmonary dysplasia (BPD) is a multifactorial disorder that evolves in infants born prematurely. These infants require some degree of mechanical ventilation and have an oxygen requirement because of respiratory distress (Davidson & Berkelhamer, 2017). Extremely premature infants are at the highest risk of developing BPD because it usually occurs at a pivotal stage of lung development. With the advent of postnatal corticosteroids, surfactant therapy, and improved ventilator management, the survival rate has increased, resulting in infants with this long-term morbidity. Infants with BPD may have prolonged hospitalizations and multiple hospital readmissions, especially during the first year of life. Approximately 10,000 to 15,000 infants are diagnosed yearly in the United States with a prevalence of males over females (Jensen & Schmidt, 2014).


Northway, Rosan, and Porter (1967) first described BPD in a group of moderate to late premature infants who developed pulmonary changes on chest radiograph with respiratory failure related to long-term mechanical ventilation and prolonged exposure to high levels of oxygen. These changes included areas of atelectasis and marked scarring with hyperinflation, pulmonary fibrosis, and smooth muscle hypertrophy in the pulmonary vasculature. This description is referred to as “classic” BPD.

The introduction of surfactant therapy in the early 1990s, increased use of antenatal steroids, and improvements in ventilator technology changed the clinical presentation of BPD (Jensen & Schmidt, 2014) and a new pathophysiology emerged. In this group of infants, alveoli formation may stop or there may be a decrease in alveolar growth. Lung changes include less pulmonary fibrosis, inflammation, and smooth muscle hypertrophy with an increase in lung fluid and damage to vascular development. These changes are derived from an interruption in lung development rather than barotrauma and volutrauma from mechanical ventilation and was labeled the “new” BPD.

In 2001, the National Institute of Child Health and Human Development (NICHD) proposed a change in the definition of BPD in infants less than 32 weeks gestational age. This definition was based on the severity of lung disease and the need for supplemental oxygen at 28 days of life and/or method of ventilatory support at 36 weeks postmenstrual age. However, because of the wide practice variations in neonatal intensive care units (NICUs) and the spectrum of the severity of this disease, the new definition has limitation (Davidson & Berkelhamer, 2017).

131Antenatal risk factors, such as chorioramnionitis, lack of antenatal steroids, and fetal growth restriction have been implicated as prenatal risks for the development of BPD. The risk factor of chorioramnionitis is controversial because of its complex nature. Empirical research suggests that inflammation increases surfactant production and promotes lung maturation (Davidson & Berkelhamer, 2017), whereas animal models suggest lung injury. There are multiple confounders making it difficult to determine a causal relationship.

Antenatal steroids are a primary prophylactic treatment of women who are in preterm labor (American College of Obstetricians and Gynecologists, 2011) and their use has contributed to decreased respiratory distress syndrome (RDS) and morbidities common in premature infants. Although antenatal steroids stimulate lung maturation in the fetus, they have not decreased the rate of BPD.

Low birth weight is a robust predictor of BPD especially in infants less than 28 weeks gestational age. Increased rates of BPD and aberrant pulmonary outcomes have also been demonstrated in preterm infants who are small for gestation age (SGA) or have intrauterine growth restriction (IUGR) at delivery (Poindexter & Martin, 2015).

Clinical Aspects


Infants born extremely premature are in the canalicular stage of lung growth and mechanical ventilation interferes with normal lung development. Mechanical ventilation can contribute to volutrauma (increased lung volume or lung stretching) and barotrauma (excessive ventilator pressures) resulting in lung overdistention. As a result, there is a cycle of continuous injury to the lung with healing and rehealing (Gardner, Hines, & Nyp, 2016).

In addition, very sick infants may be exposed to high levels of supplemental oxygen therapy for prolonged periods of time. Hyperoxia causes acute pulmonary injury to the developing lung resulting in inflammation, pulmonary edema, and thickening of the alveolar membrane. In addition to hyperoxia, preterm infants lack antioxidant mediators contributing to cytotoxic oxygen free radical production resulting in oxidative stress and further lung injury (Glen & Kinsella, 2011).

Infants with a patent ductus arteriosis (PDA) and persistent left to right (systemic to pulmonary) shunting of blood may have increased pulmonary circulation resulting in increased interstitial fluid. Increased interstitial fluid results in impaired pulmonary function and prolongs the need for mechanical ventilation as well as increases the need for supplemental oxygen, which contribute to the pathology of BPD (Glen & Kinsella, 2011). Infants with severe BPD may also develop pulmonary hypertension and cor pulmonale (right-sided heart failure).

An increased incidence of BPD has also been associated in infants with RDS who receive large volumes of fluid in the first few days of life. In a Cochrane review (Bell & Acarregui, 2014), careful regulation of fluid intake in premature infants may reduce the risk of BPD.

132BPD in premature infants has been associated with postnatal nosocomial infection. Gram positive and gram negative bacteria, cytomegalovirus (CMV), and adenovirus have been shown to increase the systemic inflammatory response in the lungs resulting in the production and release of proinflammatory cytokines. Prolonged antibiotic use especially during the first week of life has also been implicated (Novitsky et al., 2015).


In addition to surfactant therapy, which decreases the duration of mechanical ventilation and reduces the incidence of BPD, multiple modes of noninvasive respiratory modalities that do not require intubation/mechanical ventilation are available. Often infants are given surfactant via the endotracheal tube and then extubated to continuous positive airway pressure (CPAP), high-flow nasal cannula (HFNC), bi-level positive airway pressure (BiPAP), or nasal intermittent positive pressure ventilation (NIPPV). Permissive hypercapnia is a strategy that may reduce the risk of lung injury by accepting higher values of PaCO2 while using lower tidal volumes and inspiratory pressures. This is to evade pulmonary overdistention.

Corticosteroids such as dexamethasone, which reduce lung inflammation and improve gas exchange, may judiciously be used in the treatment of infants. Corticosteroids facilitate weaning and extubation from mechanical ventilation but the medication has side effects, including hyperglycemia, hypertension, infection, and gastrointestinal bleeding especially if given in the immediate postnatal period. Longitudinal studies have established that corticosteroids contribute to smaller head growth and abnormal neurological outcomes including cerebral palsy (CP; Khetan, Hurley, Spencer, & Bhatt, 2016). The type of corticosteroid, dose, and timing of initiation of therapy have not been determined (Onland, De Jaegere, Offringa, & van Kaam, 2017).

Other pharmacologic agents can be used in the treatment of BPD. Intravenous (IV) caffeine, if started in the first 3 days of life, helps in decreasing the incidence of BPD. Diuretics, such as furosemide (IV and oral), are loop diuretics used to treat the interstitial alveolar edema that is commonly seen. Thiazides, such as chlorothiazide and spironolactone, are also used. There is less electrolyte imbalance with the use of thiazides, which may decrease the need for furosemide.

Bronchodilators, such as albuterol and ipratropium bromide, can also be used to reduce reactive airway disease and help increase lung compliance. Premature infants at birth have low body stores of vitamin A, an antioxidant that is important in surfactant synthesis and the repair of lung epithelial cells. The administration of vitamin A starting after delivery may be useful in reducing oxygen use at 36 weeks postmenstrual age.

A PDA is usually treated either by surgical ligation, coil occlusion performed in a cardiac catheterization laboratory, or medically with either IV indomethacin or IV ibuprofen. All treatment modalities have associated risks. Current controversy exists whether to treat a PDA as the majority of them close spontaneously. 133Many centers are using a more cautious approach that includes clinical assessment of the infant, fluid restriction, and diuretic therapy.

Nutrition is an integral component in the management of premature infants. Postnatal growth is slower in infants with BPD and many have failure to thrive. These infants have high energy expenditure coupled with poor caloric intake, feeding difficulties (including oral aversion), and complications of respiratory disease, and may be fluid restricted on diuretic therapy resulting in poor linear growth and inadequate weight gain. Early enteral nutrition and increased protein in calorie dense formula or fortified maternal breast milk are of prime importance in improving lung growth, lung repair, decreasing the risk and severity of BPD, and improving neurologic outcomes (Poindexter & Martin, 2015).

Caring for the infant with BPD requires a strong interdisciplinary team of neonatologists, pulmonologists, nurses, nutritionists, physical therapists, occupational therapists, social workers, and child life specialists. Nurses must have in-depth knowledge of the pathophysiology of BPD, arterial and capillary blood gases, medications, oxygen therapy, ventilator management, nutrition, and growth and development.

This group of infants can be challenging to care for and should have a dedicated core of nurses who understand not only the infants’ physiologic status and recognition of any changes from baseline, but must also understand the infants’ nuances in behavior and responses to treatment.

Parental education is an ongoing process because these infants can be in the hospital for an extended period of time. Nurses must not only promote parent–infant bonding, but also help parents engage in socialization, language development, and emotional support of their infants.


BPD is a chronic condition that affects primarily premature infants. Current treatment modalities, such as noninvasive respiratory support, gentle ventilation, pharmacologic agents, and optimal nutrition are imperative. However, the prevention of BPD is challenging and at the core of this is preventing premature birth.

American College of Obstetricians and Gynecologists Committee on Obstetric Practice. (2011). Opinion No. 475: Antenatal corticosteroid therapy for fetal maturation. Obstetrics and Gynecology, 117(2, Pt. 1), 422–424. doi:10.1097/AOG.0b013e31820eee00

Bell, E., & Acarregui, M. (2014). Restricted versus liberal water intake for preventing morbidity and mortality in preterm infants. Cochrane Database of Systematic Reviews, 2014, 1–26. doi:10.1002/14651858.CD000503.pub3

Davidson, L., & Berkelhamer, S. (2017). Bronchopulmonary dysplasia: Chronic lung disease of infancy and long-term pulmonary outcomes. Journal of Clinical Medicine, 6(1), 4. doi:10.3390/jcm6010004


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Jun 30, 2018 | Posted by in NURSING | Comments Off on Dysplasia
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