Bronchopulmonary Dysplasia (BPD)

Last updated date: 27-Aug-2023

Originally Written in English

Bronchopulmonary Dysplasia (BPD)

Bronchopulmonary Dysplasia


Bronchopulmonary dysplasia is a kind of chronic lung illness that occurs in premature infants who are given oxygen and positive-pressure ventilation. The pathophysiology of this illness is complicated and poorly understood; nonetheless, a variety of causes can not only harm tiny airways but also interfere with alveolarization (alveolar septation), resulting in alveolar simplicity and a reduction in total surface area for gas exchange. Injuries to the developing pulmonary microvasculature are also possible.


Bronchopulmonary Dysplasia definition

The term "bronchopulmonary dysplasia" (BPD) presents a chronic form of lung injury produced by barotrauma and oxygen injury in premature newborns requiring mechanical ventilation. Despite considerable breakthroughs in preterm baby care over the last few decades, such as the discovery of surfactants and improved and gentler means of breathing, the prevalence of BPD remains high.

These new tactics have resulted in the survival of very low birth weight infants and a shift in the features of BPD. In 1999, Jobe created the term "new BPD" to characterize the chronic lung illness that was prevalent in preterm newborns at the time. When opposed to "old BPD," which was characterized by dysmorphic microvasculature and alveolar simplification, this "new BPD" showed significantly less airway injury and alveolar septal fibrosis.



Because to disparities in prenatal methods, management approaches, and a lack of an uniform classification of BPD, the prevalence of BPD varies greatly between centers. Infants born at a lower gestational age (GA) and birth weight had the greatest observed rate of BPD. According to neonatal research network statistics, the incidence of BPD in extremely low birth weight newborns (birth weight less than 1500 grams) ranges from 40 to 68 percent, depending on the criteria of BPD utilized.

This incidence was discovered to be inversely linked to the infant's GA. Male sex, low birth weight, white race, restricted development for GA, and a family history of asthma are among of the additional demographic risk factors for BPD.


What causes bronchopulmonary dysplasia?

Bronchopulmonary dysplasia is a complex illness caused by a number of prenatal and postnatal events affecting both the mother and the newborn. The following are some of the prenatal risk factors that impact the development of BPD:

  1. Lack of antenatal steroids
  2. Maternal smoking
  3. Pregnancy-induced hypertension/preeclampsia
  4. Hypoxia
  5. Maternal infection, including chorioamnionitis
  6. Genetic susceptibility
  7. Congenital anomalies causing pulmonary hypoplasia

Similarly, various postnatal factors predispose premature infants to develop BPD including:

  1. Lung immaturity
  2. Poor nutrition
  3. Need for mechanical ventilation
  4. Oxygen injury
  5. Infection/sepsis



Pathophysiology of Bronchopulmonary Dysplasia

The pathophysiology of BPD in preterm neonates is based on injury from mechanical ventilation and reactive oxygen species to premature lungs in the context of prenatal variables predisposing the lungs to BPD. This cascade of events results in an exaggerated inflammatory response with an increase in proinflammatory cytokines such as interleukin(IL)-6, IL-8, tumor necrosis factor alpha, and others, as well as growth factors (transforming growth factor) and angiogenic factors (vascular endothelial growth factor, angiopoietin 2), which leads to abnormal tissue repair and lung development arrest. The pathology found in "new BPD" is characterized by dysregulated vascular and delayed alveolar development.


Clinical presentation

Clinical presentation of Bronchopulmonary Dysplasia


A history of extremely premature birth is commonly present, which is frequently accompanied with chorioamnionitis, preterm labor, preterm rupture of membranes, or the requirement for iatrogenic delivery (due to maternal preeclampsia or other complications). Infants with bronchopulmonary dysplasia (BPD) frequently have a history of needing a high degree of respiratory assistance from birth, typically requiring mechanical ventilation or CPAP soon after delivery.


Physical examination

Physical examination, chest radiography, pulmonary function tests, and histopathologic examination all reveal aberrant findings in infants with BPD. The first observations made immediately after birth are consistent with respiratory distress syndrome (RDS). The persistence of these anomalies has been linked to a greater risk of bronchopulmonary dysplasia.

During the first 10 days of life, physical examination may indicate tachypnea, tachycardia, increased labor of breathing (including retractions, nasal flaring, and grunting), frequent desaturations, and considerable weight loss.

Infants born with severe bronchopulmonary dysplasia are frequently severely immature and have a low birth weight. During the first two weeks of life, their oxygen and ventilatory support requirements often increase. To ensure appropriate breathing and oxygenation, oxygen supplementation, ventilator support, or both are frequently increased in weeks 2-4.




Diagnosis of Bronchopulmonary Dysplasia

BPD evaluation includes a blood gas analysis, a chest x-ray, and an assessment of the patient's nutritional state. A blood gas analysis may detect hypoxia, hypercarbia, or acidosis. These patients continue to be monitored with continuous pulse oximetry in order to achieve appropriate oxygen saturation. Many clinics additionally use transcutaneous carbon dioxide monitoring to assess the infant's ventilation.

Chest radiographs can reveal reduced lung volumes, hyperinflation, atelectasis, pulmonary edema, and pulmonary interstitial emphysema. High-resolution CT may reveal abnormalities that are not seen on regular chest radiography. At 36 PMA, infants with moderate or severe BPD must be evaluated for pulmonary hypertension (PH) by an echocardiography. Because the morbidity and mortality associated with the diagnosis of PH in BPD are relatively high, several institutions choose to test all patients with BPD.

BPD is clinically diagnosed based on the GA, postmenstrual age (PMA), oxygen exposure, and oxygen need at 36 weeks PMA. The current definition was proposed in 2001 at a National Institute of Child Health and Human Development (NICHD) workshop, where infants born at less than or equal to 32 weeks GA with 28 days of oxygen exposure are diagnosed with mild, moderate, or severe BPD at 36 weeks PMA based on their respiratory support at the time.

This definition still has several flaws and does not reliably predict respiratory outcomes; hence, the NICHD workshop on BPD advocated a change of this classification in 2016. The proposed improvement calls for the use of radiographic confirmation and takes into consideration newer ways of non-invasive ventilation. Although this new classification further categorizes BPD, it does not solve the basic problem of using therapy as the major criterion identifying the disorder and its severity.



 Management of Bronchopulmonary Dysplasia

The overall goal of managing babies with BPD is to maintain them as their lungs expand, minimize future lung damage, maximize lung function, and recognize problems associated with BPD. The following are the many measures used in the care of these infants:

  1. Fluid restriction: Infants are limited to a total fluid amount of 120 to 150 ml/kg/day, depending on the severity of their lung illness. Fluid restriction improves pulmonary function by minimizing pulmonary edema and promoting gas exchange. Despite being widely used, there is inadequate data to support this practice.
  2. Minimize ventilator-associated lung injury: Wherever possible, non-invasive ventilation is the recommended technique of ventilation. If mechanical breathing is required, caution should be exercised to avoid barotrauma and volutrauma. Early extubation has been demonstrated to reduce the incidence of BPD.
  3. Minimize oxygen associated injury: One of the most important elements in the etiology of BPD is hyperoxia exposure. There is much disagreement over SpO target ranges. One method tries to achieve a SpO of 88-94 percent by setting a lower alert limit of 88 percent and a higher alarm limit of 96 %.
  4. Pharmacological interventions:
  • Corticosteroids: In BPD, systemic corticosteroids have been used to enhance lung function, reduce inflammation, and decrease the requirement for mechanical ventilation. Concerns regarding long-term neurodevelopmental outcomes, however, have led to recommendations that they be limited to babies with severe BPD who are ventilator dependent and have high oxygen demands. Despite several clinical trials, it is unknown which corticosteroid gives the greatest effect and at what dose. Despite the conflicting results, low-dose dexamethasone and hydrocortisone are still utilized in the treatment of BPD. The available evidence does not support the usual use of inhaled corticosteroids to prevent BPD.
  • Diuretics: Thiazides and loop diuretics are the most often utilized diuretics in the treatment of BPD's short-term pulmonary mechanics. These medicines are most typically utilized in ventilator-dependent babies who have an increasing need for positive end-expiratory pressure despite fluid restriction. A systematic evaluation of the literature found no improvement in long-term clinical outcomes in babies with established or developing BPD.
  • Bronchodilators: - The use of beta-2 agonists can reduce airway resistance and enhance compliance. Their routine usage, however, is not suggested in BPD since it has not been proved to enhance long-term results. They should only be used to treat acute bouts of bronchoconstriction in older babies who are still ventilator dependent.



Diet for Bronchopulmonary Dysplasia

Infants with bronchopulmonary dysplasia have higher energy needs. Although excessive fluid administration (and inability to lose weight) in the first week of life may raise the risk of patent ductus arteriosus (PDA) and bronchopulmonary dysplasia, early parenteral feeding is frequently utilized to alleviate the catabolic condition of the premature newborn.

It is vital to increase the patient's intake of protein, carbs, lipids, vitamins, and trace metals to avoid additional lung damage and to aid tissue recovery. Excessive administration of non-nitrogen calories, on the other hand, should be avoided since it may result in excessive carbon dioxide generation and hinder weaning.

Antioxidant enzymes may preserve the lungs and aid in the prevention or treatment of bronchopulmonary dysplasia. Deficiency of trace elements such as copper, zinc, and manganese in premature infants may predispose them to lung damage, and supplementation may give protection.

Vitamins A and E are dietary antioxidants that may aid in the prevention of lipid peroxidation and the maintenance of cell integrity. However, vitamin E supplementation in premature infants does not prevent bronchopulmonary dysplasia. Preterm newborns may be vitamin A deficient, and several trials of vitamin A treatment to prevent bronchopulmonary dysplasia in preterm infants have been undertaken. Data from meta-analyses published in a Cochrane Database review of vitamin A supplementation show that it lowers the incidence of bronchopulmonary dysplasia in preterm newborns.

Because of increased insensible water loss via their thin, immature skin, extremely preterm newborns may require substantial quantities of free water. Excessive fluid administration raises the likelihood of symptomatic PDA and pulmonary edema (PE). The higher ventilator settings and oxygen needs required to treat PDA and PE may aggravate lung damage and raise the development of bronchopulmonary dysplasia. Although early PDA therapy improves pulmonary function, it has little effect on the incidence of bronchopulmonary dysplasia. Oh et al. discovered in a retrospective research that reducing fluid intake immediately after delivery helped minimize the risk of mortality and oxygen need at 36 weeks' corrected gestational age.

Supplementation of protein and fat is gradually increased to deliver around 3-3.5 g/kg/day. Rapid and early injection of high lipid concentrations may aggravate bronchopulmonary dysplasia by depleting pulmonary vascular lipid. Excessive glucose loading can cause an increase in oxygen demand, respiratory drive, and glucosuria. Preterm newborns have much higher calcium and phosphorus needs.

The fetus's mineral reserves are depleted throughout the third trimester, leaving the severely preterm newborn lacking in calcium and phosphorus and at danger of rickets. Furosemide medication plus restricted intravenous calcium delivery may exacerbate bone mineralization and lead to secondary hyperparathyroidism.

Bronchopulmonary dysplasia is reduced by vitamin A intake. Trace minerals (e.g., copper, zinc, manganese) must be supplemented since they are important cofactors in antioxidant enzymes.



The multifactorial etiology of bronchopulmonary dysplasia complicates its prevention. Note the following:

  • Prenatal steroid medication and postnatal surfactant therapy have increased survival and reduced the severity of bronchopulmonary dysplasia. Preterm delivery and chorioamnionitis prevention should minimize the incidence of bronchopulmonary dysplasia.
  • Optimized oxygenation, ventilation (early extubation, greater use of continuous positive airway pressure [CPAP]), and hydration management may reduce the incidence and severity of bronchopulmonary dysplasia.
  • Maximizing nutritional assistance, carefully controlling fluid intake, and using diuretics sparingly all help to enhance lung recovery.
  • There is insufficient evidence to support the use of high-frequency ventilation, inhaled nitric oxide (iNO), and antioxidants (other than vitamin A) to prevent bronchopulmonary dysplasia.


Long-Term Monitoring


Infants with bronchopulmonary dysplasia (BPD) are at high risk of respiratory infections in the first 2 years of life. Note the following:

  • Infection with a respiratory syncytial virus (RSV) can cause serious sickness and even death in newborns with bronchopulmonary dysplasia.
  • Monthly RSV antibody injections may prevent or minimize the likelihood of rehospitalization in babies with bronchopulmonary dysplasia, as well as lessen the severity of sickness.
  • The American Academy of Pediatrics (AAP) has produced a policy statement regarding the use of RSV antibody shots in preterm infants discharged from the NICU during RSV season (November to March).


Growth and development

Poor growth and delayed development are common in newborns with bronchopulmonary dysplasia, particularly those with significantly impaired pulmonary function. Furthermore, with increased fluid consumption and frequent lung infections, many babies' pulmonary function may deteriorate. The cornerstones of therapy in and out of the hospital include diuretics, high-energy formulas, and breast-milk supplements.

Infants suffering from bronchopulmonary dysplasia are at a greater risk of poor neurodevelopment. Abnormal growth occurred in 50-60% of babies with bronchopulmonary dysplasia at 18-22 months corrected age in severely low birth weight infants. When comparing newborns with severe bronchopulmonary dysplasia to infants with moderate bronchopulmonary dysplasia, the risk of neurodevelopmental disability, cerebral palsy, and low intelligence quotient (IQ) more than quadrupled.



BPD is a chronic condition that lasts long after you leave the hospital and into adulthood. During their first year of life, infants with BPD have a 50% likelihood of being readmitted to the hospital. They are more likely to develop reactive airway disease, asthma, emphysema, and RSV bronchiolitis. BPD also has an impact on their growth and neurodevelopment. Infants with BPD who are born at a low birth weight are more likely to suffer impairments in fine and gross motor abilities, as well as language.

Infants with BPD are at a significant risk of developing cardiopulmonary complications such as pulmonary hypertension (PH), cor pulmonale, and systemic hypertension. According to a recent meta-analysis, the cumulative estimated prevalence of PH in BPD is 20%, and it can be as high as 40% in severe BPD. According to a recent, prospective research, BPD-associated pulmonary hypertension (BPD-PH) affects at least 8 to 25% of children with extremely low birth weight (birth weight less than 1000g). Retrospective studies show that individuals with BPD-PH had a 2-year morbidity rate ranging from 26 to 47 %.



Bronchopulmonary dysplasia (BPD) is a serious condition that affects premature newborns that require NICU care. It causes breathing issues in newborns since their lungs are not fully grown and ready to perform the function of breathing. To help them breathe, these newborns frequently require a breathing tube and are attached to a breathing machine.

Several drugs may be required throughout their hospital stay to treat this lung illness. Some newborns may also require home oxygen and may require hospitalization if they develop respiratory infections. Babies with BPD require more energy and may require additional nutrients.