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Bronchopulmonary dysplasia (BPD): Prevention

Bronchopulmonary dysplasia (BPD): Prevention
Literature review current through: Jan 2024.
This topic last updated: Nov 14, 2023.

INTRODUCTION — Bronchopulmonary dysplasia (BPD; also known as neonatal chronic lung disease [CLD]) is a major cause of respiratory illness in preterm infants. It is an important contributing factor in the increased risk of mortality and morbidity in the preterm population.

This topic will provide an overview of strategies used to prevent BPD. Other related topics include:

(See "Antenatal corticosteroid therapy for reduction of neonatal respiratory morbidity and mortality from preterm delivery".)

(See "Postnatal use of glucocorticoids for prevention of bronchopulmonary dysplasia (BPD) in preterm infants".)

(See "Bronchopulmonary dysplasia (BPD): Clinical features and diagnosis".)

(See "Bronchopulmonary dysplasia (BPD): Management and outcome".)

(See "Complications and long-term pulmonary outcomes of bronchopulmonary dysplasia".)

(See "Pulmonary hypertension associated with bronchopulmonary dysplasia".)

TERMINOLOGY

Prematurity – Different degrees of prematurity are defined by gestational age (GA), which is calculated from the first day of the mother's last period, or birth weight (BW), as summarized in the table (table 1) and discussed in detail separately. (See "Preterm birth: Definitions of prematurity, epidemiology, and risk factors for infant mortality", section on 'Definitions'.)

BPD – BPD is a chronic lung disease characterized disruption of pulmonary development and/or lung injury in the context of preterm birth. Clinically, BPD is defined as an ongoing need for supplemental oxygen and/or respiratory support at either 28 days postnatal age or 36 weeks postmenstrual age (PMA) in a preterm neonate with radiographic evidence of parenchymal lung disease (image 1). Various criteria are used to define BPD, as summarized in the (table 2) and discussed in detail separately. (see "Bronchopulmonary dysplasia (BPD): Clinical features and diagnosis", section on 'Definitions and severity of BPD').

OUR APPROACH — The following is a summary of the strategies that we use to reduce the incidence of BPD in infants who are at risk for developing BPD. The combination of interventions addresses the multiple risk factors implicated in the pathogenesis of BPD (algorithm 1). (See "Bronchopulmonary dysplasia (BPD): Clinical features and diagnosis", section on 'Risk factors'.)

Initial general measures — General measures are provided to all infants who are at risk for BPD (extremely preterm [EPT] infant, gestational age <28 weeks).

Antenatal steroids – Antenatal glucocorticoids are appropriate for pregnant woman at 23 to 34 weeks of gestation at high risk for preterm delivery within the next seven days. This is discussed separately. (See "Antenatal corticosteroid therapy for reduction of neonatal respiratory morbidity and mortality from preterm delivery".)

Fluid management – After the first week of life, fluid intake is generally restricted to 130 to 140 mL/kg per day to maintain neutral or slightly negative fluid balance. Fluid status and nutritional status is monitored frequently, and fluid intake modified to avoid dehydration and overhydration and to ensure adequate growth. (See "Respiratory distress syndrome (RDS) in preterm infants: Management", section on 'Fluid management'.)

Nutrition – In our centers, nutritional goals are set to provide adequate caloric intake to promote somatic and lung growth [1]. Mother's breast milk is the preferred nutritional source, and if not available, we use donor breast milk. (See "Approach to enteral nutrition in the premature infant".)

Caffeine – We administer caffeine to all EPT infants within the first 24 hours of life. These neonates have the highest risk for BPD. (See "Management of apnea of prematurity", section on 'Caffeine'.)

Vitamin A – One of the authors of this topic routinely uses vitamin A (if available) in ventilator-dependent extremely low birth weight (ELBW) infants (birth weight <1000 g). (See 'Vitamin A' below.)

Respiratory support — The goal for respiratory support for infants at risk for BPD is to maintain adequate oxygenation and ventilation while minimizing respiratory intervention that may lead to lung injury. Our approach is briefly summarized here. These interventions are discussed in greater detail separately. (See "Respiratory distress syndrome (RDS) in preterm infants: Management" and "Approach to mechanical ventilation in very preterm neonates".)

In infants who require supplemental oxygen, we set a peripheral oxygen saturation (SpO2) target range of 90 to 95 percent. (See 'Ventilation strategies to minimize lung injury' below and "Neonatal target oxygen levels for preterm infants".)

In most preterm infants, we use early positive airway pressure support (typically with continuous positive airway pressure [CPAP]). (See "Respiratory distress syndrome (RDS) in preterm infants: Management", section on 'Early positive pressure'.)

In preterm infants who require intubation soon after birth, we provide early surfactant therapy. (See "Respiratory distress syndrome (RDS) in preterm infants: Management", section on 'Surfactant therapy'.)

In preterm infants with respiratory failure, we use a mechanical ventilation strategy that aims to minimize ventilator-induced lung injury (VILI). The approach is summarized in the table (table 3) and is discussed in detail separately. (See "Approach to mechanical ventilation in very preterm neonates", section on 'Clinical approach'.)

In infants with severe persistent respiratory failure despite optimal settings on conventional ventilation, a trial of high-frequency ventilation (HFV) is used to minimize VILI. This is discussed separately. (See "Approach to mechanical ventilation in very preterm neonates", section on 'Transition to HFV'.)

The role that mechanical ventilation and oxygen toxicity play in the pathogenesis of BPD is discussed separately. (See "Bronchopulmonary dysplasia (BPD): Clinical features and diagnosis", section on 'Risk factors'.)

Postnatal glucocorticoids — We do not routinely administer postnatal systemic or inhaled glucocorticoids to prevent BPD. Systemic glucocorticoids are reserved for EPT infants who remain ventilator-dependent and/or require oxygen supplementation >50 percent at two to four weeks postnatal age. This is discussed in detail separately. (See "Postnatal use of glucocorticoids for prevention of bronchopulmonary dysplasia (BPD) in preterm infants".)

INTERVENTIONS

Overview

Measures that are routinely used – The following interventions are generally used in combination to improve outcomes (including a reduction in the risk of BPD) in at-risk preterm infants, especially extremely preterm infants (EPT; gestational age [GA] <28 weeks) (algorithm 1):

Antenatal glucocorticoid therapy (see "Antenatal corticosteroid therapy for reduction of neonatal respiratory morbidity and mortality from preterm delivery").

Protective ventilatory strategies that minimize barotrauma or volutrauma in infants who require respiratory support for neonatal respiratory distress (RDS) (table 3) (see "Respiratory distress syndrome (RDS) in preterm infants: Management", section on 'Early positive pressure' and "Approach to mechanical ventilation in very preterm neonates").

Mother's breast milk (see "Approach to enteral nutrition in the premature infant" and "Infant benefits of breastfeeding").

Caffeine (see "Management of apnea of prematurity", section on 'Caffeine').

Modest fluid restriction (see "Fluid and electrolyte therapy in newborns" and "Respiratory distress syndrome (RDS) in preterm infants: Management", section on 'Fluid management').

Measures that are used selectively – Preterm infants who remain ventilator-dependent at one week after birth are at high risk for developing BPD. Such neonates may benefit from additional preventive measures, including:

Selective us of postnatal glucocorticoid therapy in high-risk EPT infants (see "Postnatal use of glucocorticoids for prevention of bronchopulmonary dysplasia (BPD) in preterm infants").

Some centers use vitamin A supplementation (if available) in EPT infants who require mechanical ventilation support (see 'Vitamin A' below).

Selective use of a trial of diuretic therapy (see "Bronchopulmonary dysplasia (BPD): Management and outcome", section on 'Diuretics' and "Respiratory distress syndrome (RDS) in preterm infants: Management", section on 'Fluid management').

Measures that are not used – These include:

Routine use of postnatal glucocorticoid therapy in all at-risk preterm infants. This is because of concerns of adverse effects, particularly adverse neurodevelopmental outcome, with early glucocorticoid therapy, as discussed separately. (See "Postnatal use of glucocorticoids for prevention of bronchopulmonary dysplasia (BPD) in preterm infants", section on 'Adverse effects'.)

Routine use of inhaled nitric oxide (iNO), since this does not appear to be effective. (See "Respiratory distress syndrome (RDS) in preterm infants: Management", section on 'Inhaled nitric oxide'.)

Late surfactant administration, since this does not appear to be effective. (See "Respiratory distress syndrome (RDS) in preterm infants: Management", section on 'Timing'.)

Glucocorticoids

Antenatal glucocorticoids — Antenatal glucocorticoid therapy is an effective intervention for prevention of respiratory distress syndrome (RDS) resulting in less need for mechanical ventilation and oxygen supplementation (risk factors for BPD). Antenatal glucocorticoids are appropriate for pregnant individuals from 23 to 34 weeks of gestation who are at risk for preterm delivery within the next seven days. This is discussed separately. (See "Antenatal corticosteroid therapy for reduction of neonatal respiratory morbidity and mortality from preterm delivery".)

Postnatal glucocorticoids — We do not routinely administer postnatal systemic or inhaled glucocorticoids to prevent BPD. Systemic glucocorticoids are reserved for EPT infants who remain ventilator-dependent and/or require oxygen supplementation >50 percent at a postnatal age of two to four weeks. This is discussed in detail separately. (See "Postnatal use of glucocorticoids for prevention of bronchopulmonary dysplasia (BPD) in preterm infants".)

Surfactant — Exogenous surfactant therapy given within the first 30 to 60 minutes after birth is effective in the prevention and treatment of RDS and reduces the need for mechanical ventilation and oxygen supplementation (risk factors for BPD). The use of early surfactant to prevent and treat RDS is discussed separately. (See "Respiratory distress syndrome (RDS) in preterm infants: Management", section on 'Surfactant therapy'.)

Fluid management — The goal of fluid management is to maintain neutral or slightly negative fluid balance. Our usual practice is to restrict total fluid intake to 130 to 140 mL/kg per day after the first week of life. However, the fluid status of the patient must be monitored frequently to avoid dehydration or overhydration as fluid needs widely vary in preterm infants due to differences in insensible fluid loss. Caloric intake and growth should be closely monitored. (See "Fluid and electrolyte therapy in newborns".)

The available evidence does not support the routine use of diuretic therapy in maintaining a neutral or negative fluid balance to prevent BPD. However, it may be reasonable to selectively use diuretic therapy as a trial in chronically ventilator-dependent infants with moderate to severe pulmonary impairment despite adequate fluid restriction. This is discussed in greater detail separately. (See "Respiratory distress syndrome (RDS) in preterm infants: Management", section on 'Fluid management'.)

Use of diuretics in the management of infants with established BPD is discussed separately. (See "Bronchopulmonary dysplasia (BPD): Management and outcome", section on 'Diuretics'.)

Ventilation strategies to minimize lung injury — Mechanical ventilation (MV) has been a lifesaving intervention in the care of preterm infants at risk for RDS due to premature lung development. However, mechanical ventilation causes tissue injury and inflammation due to volutrauma that contributes to BPD. As a result, MV strategies aim to minimize lung injury while achieving adequate oxygenation and ventilation. These strategies include:

Avoidance of MV through preferential use of noninvasive respiratory support (eg, nasal continuous positive airway pressure [nCPAP]) when possible. (See "Respiratory distress syndrome (RDS) in preterm infants: Management", section on 'Early positive pressure'.)

Use of volume-targeted ventilation (VTV) using low tidal volumes (4 to 6 mL/kg). (See "Approach to mechanical ventilation in very preterm neonates", section on 'Clinical approach'.)

Use of high-frequency oscillatory or jet ventilation (HFOV or HFJV) as a rescue therapy. (See "Approach to mechanical ventilation in very preterm neonates", section on 'Transition to HFV'.)

The approach is summarized in the table (table 3), and discussed in greater detail separately. (See "Approach to mechanical ventilation in very preterm neonates".)

Caffeine — For most ELBW infants (BW <1000 g), we suggest prophylactic caffeine starting on the first day of life. The available clinical trial data suggest this intervention is safe and effective for reducing BPD and perhaps other long-term complications. This is discussed separately. (See "Management of apnea of prematurity", section on 'Caffeine'.)

Vitamin A — EPT infants may have vitamin A deficiency, which may promote the development of BPD [2]. However, data are conflicting as to whether vitamin A supplementation reduces the incidence of BPD. If there is a benefit, it appears to be modest.

Since the incidence of BPD varies among neonatal intensive care units (NICUs), the decision to use vitamin A supplementation may depend upon the local incidence of BPD and the availability and cost of the drug [3]. For example, one of the authors of this topic routinely uses vitamin A supplementation at their center as a preventive measure in EPT infants who require mechanical ventilation (if the drug is available); whereas the other author does not routinely use it at their center. At most centers where vitamin A is used, its use is limited to EPT infants who require mechanical ventilation.

When vitamin A is given, it is administered within 24 hours after birth as an intramuscular (IM) injection of 5000 international units. This dose is then provided three times per week for four weeks.

Enteral water-soluble vitamin A is not used for this purpose because, although it may increases plasma retinol levels in EPT infants, it does not appear to reduce the severity of BPD [4,5].

Evidence supporting IM vitamin A supplementation includes the following:

In a meta-analysis of five trials (884 neonates), IM vitamin A supplementation compared with control modestly reduced rates of BPD; however, the finding did not achieve statistical significance (68 versus 74 percent; relative risk [RR] 0.93, 95% CI 0.86-1.01) [6].

A subsequent multicenter retrospective study from the Pediatrix Medical Group of neonates from 2010 to 2012 reported that the shortage of vitamin A in the United States that began in 2010 did not affect the incidence of mortality or BPD in the participating NICUs [7]. During the study period, vitamin A supplementation in patients decreased from a level of 27 percent to 2 percent as the supply of vitamin decreased. A multivariable analysis demonstrated that vitamin A supplementation was not an independent risk factor for death or BPD.

Vitamin A may be beneficial in a subset of preterm infants, as suggested by a post-hoc subgroup analysis of data from the largest placebo-controlled trial [8]. In this report, the benefit of vitamin A therapy was greater for infants at a lower risk for BPD than those at a higher risk. However, as noted by the authors, data used for this study was from 1996 to 1997 and other aspects of clinical care have changed, which may have impacted these results.

Breast milk — Mother's own milk is the preferred form of nutrition for preterm infants as it offers several advantages over formula, including prevention of BPD. (See "Human milk feeding and fortification of human milk for premature infants", section on 'Benefits of mother's milk'.)

A meta-analysis of 17 cohort studies and 5 RCTs (8661 neonates) demonstrated that human milk compared with formula is associated with a lower incidence of BPD, although the certainty of this finding is low [9]. In addition, an observational study found breast milk from the mother reduced the risk of BPD and reported a dose-response relationship with an increased reduction in BPD as the volume of consumed breast milk increased [10]. However, the results of this study are limited by the potential of confounding factors.

Other interventions — Interventions that are ineffective in preventing BPD include inhaled nitric oxide alone or in combination with surfactant, supplementation with docosahexaenoic acid, and sustained inflation in the delivery room for infants requiring respiratory support.

Inhaled nitric oxide (iNO) – The available data do not support the use of iNO (either alone or in combination with surfactant) as an intervention to prevent BPD. We agree with the guidance of the expert panel convened by the National Institute of Health and a 2014 American Academy of Pediatrics clinical report that recommend against the use of iNO in the routine management of preterm infants below 34 weeks gestation who require respiratory support [11,12].

Data on the use of iNO in the management of preterm neonates with RDS are discussed separately. (See "Respiratory distress syndrome (RDS) in preterm infants: Management", section on 'Inhaled nitric oxide'.)

However, iNO is a well-established treatment for term or late preterm infants with persistent pulmonary hypertension, as discussed separately. (See "Persistent pulmonary hypertension of the newborn (PPHN): Management and outcome", section on 'Inhaled nitric oxide (iNO)'.)

Late surfactant therapy – Late deficiency of postnatal surfactant production or surfactant dysfunction has been proposed as a contributor for the pathogenesis of BPD because it may be associated with episodes of respiratory deterioration in ventilator-dependent preterm infants. However, late administration of surfactant does not appear to reduce the risk of BPD, as discussed separately. (See "Respiratory distress syndrome (RDS) in preterm infants: Management", section on 'Timing'.)

Combination of steroid and surfactant – Data on the use of combination surfactant plus budesonide are limited. This therapy cannot be recommended until there are more definitive data establishing its safety and efficacy. The data supporting this intervention are discussed separately. (See "Postnatal use of glucocorticoids for prevention of bronchopulmonary dysplasia (BPD) in preterm infants", section on 'Intratracheal glucocorticoids'.)

Long-chain fatty acids – Docosahexaenoic acid (DHA) and other omega-3 long-chain polyunsaturated fatty acids (LCPUFAs) are integral components of the brain and retinal phospholipid membrane. Preterm infants miss some of the fetal accretion of DHA, which normally occurs during the third trimester of pregnancy. Based upon the available evidence, direct or indirect LCPUFA supplementation does not appear to prevent BPD. However, LCPUFA supplementation appears to have other beneficial effects in preterm infants, particularly on neurocognitive and visual development. Recommendations regarding maternal and infant LCPUFA supplementation are provided separately. (See "Long-chain polyunsaturated fatty acids (LCPUFA) for preterm and term infants".)

Sustained inflation in the delivery room – Sustained lung inflation during neonatal resuscitation in the delivery room may be harmful and should be avoided, as discussed separately. (See "Neonatal resuscitation in the delivery room", section on 'Sustained inflation'.)

Superoxide dismutase – Superoxide dismutase is a naturally occurring enzyme that provides defense against oxidative injury, which has been implicated in the pathogenesis of BPD. In the available clinical trials, postnatal administration of superoxide dismutase did not have any apparent benefit in terms of reducing the incidence of BPD, other morbidities, or mortality [13]. Superoxide dismutase is not available for clinical use, and it remains an investigational drug.

PentoxifyllinePentoxifylline is a xanthine derivative with anti-inflammatory properties. The use of nebulized pentoxifylline as a preventive measure for BPD was studied in a single small pilot randomized trial [14,15]. As such, additional data are needed before pentoxifylline can be recommended as a routine measure to prevent or treat BPD in neonates. Studies investigating the use of pentoxifylline in the treatment of neonatal sepsis are discussed elsewhere. (See "Treatment and prevention of bacterial sepsis in preterm infants <34 weeks gestation", section on 'Pentoxifylline'.)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Bronchopulmonary dysplasia".)

INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

Basics topics (see "Patient education: Bronchopulmonary dysplasia (The Basics)")

SUMMARY AND RECOMMENDATIONS

Effective interventions – Interventions that are effective for reducing the risk of bronchopulmonary dysplasia (BPD) in extremely preterm (EPT) infants (gestational age [GA] <28 weeks) who are at risk for BPD include (algorithm 1):

Antenatal glucocorticoid therapy – Antenatal glucocorticoid therapy for pregnant individuals <34 weeks gestation who are at high risk for preterm delivery, which is discussed in detail separately. (See "Antenatal corticosteroid therapy for reduction of neonatal respiratory morbidity and mortality from preterm delivery".)

Nutrition and fluid management – In all preterm infants, nutritional goals are set to provide adequate caloric intake to promote somatic and lung growth, and fluid intake is adjusted to maintain neutral or slightly negative water balance. Mother's breast milk is the preferred nutritional source, and if not available, donor breast milk is used. These issues are discussed separately. (See "Approach to enteral nutrition in the premature infant" and "Parenteral nutrition in premature infants" and "Fluid and electrolyte therapy in newborns" and "Human milk feeding and fortification of human milk for premature infants" and "Respiratory distress syndrome (RDS) in preterm infants: Management", section on 'Fluid management'.)

Oxygen targets – In preterm infants who require supplemental oxygen, target oxygen saturation (SpO2) levels are set for values between 90 and 95 percent, as discussed separately. (See "Neonatal target oxygen levels for preterm infants", section on 'Oxygen target levels'.)

Ventilation strategies that minimize lung injury – Use of ventilation strategies that minimize lung injury, including preferential use of noninvasive modalities. The approach to mechanical ventilation in preterm infants is summarized in the table (table 3) and discussed in detail separately. (See "Respiratory distress syndrome (RDS) in preterm infants: Management", section on 'Clinical approach' and "Approach to mechanical ventilation in very preterm neonates".)

Caffeine therapy – Early caffeine therapy is routinely given to all EPT infants, as discussed separately. (See "Management of apnea of prematurity", section on 'Caffeine'.)

Vitamin A supplementation – The use of vitamin A supplementation is center-dependent. If vitamin A is available, practitioners may consider its administration to EPT infants who require ventilatory support; however, the relative benefit of vitamin A supplementation in this setting appears to be small. (See 'Vitamin A' above.)

Postnatal glucocorticoids – We do not routinely administer postnatal systemic or inhaled glucocorticoids to prevent BPD. Systemic glucocorticoids are reserved for EPT infants who remain ventilator-dependent and/or require oxygen supplementation >50 percent at a postnatal age of two to four weeks. This is discussed in detail separately. (See "Postnatal use of glucocorticoids for prevention of bronchopulmonary dysplasia (BPD) in preterm infants".)

Ineffective interventions – Interventions that do not appear to be effective for prevention of BPD in EPT infants include (see 'Other interventions' above):

Inhaled nitric oxide (iNO) (see "Respiratory distress syndrome (RDS) in preterm infants: Management", section on 'Inhaled nitric oxide')

Late surfactant therapy (see "Respiratory distress syndrome (RDS) in preterm infants: Management", section on 'Timing')

Sustained lung inflation during neonatal resuscitation (see "Neonatal resuscitation in the delivery room", section on 'Sustained inflation')

ACKNOWLEDGMENT — The editorial staff at UpToDate acknowledge James Adams, Jr., MD, who contributed to an earlier version of this topic review.

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  2. Tyson JE, Wright LL, Oh W, et al. Vitamin A supplementation for extremely-low-birth-weight infants. National Institute of Child Health and Human Development Neonatal Research Network. N Engl J Med 1999; 340:1962.
  3. Darlow BA, Graham PJ. Vitamin A supplementation for preventing morbidity and mortality in very low birthweight infants. Cochrane Database Syst Rev 2000; :CD000501.
  4. Rakshasbhuvankar AA, Simmer K, Patole SK, et al. Enteral Vitamin A for Reducing Severity of Bronchopulmonary Dysplasia: A Randomized Trial. Pediatrics 2021; 147.
  5. Manapurath RM, Kumar M, Pathak BG, et al. Enteral Low-Dose Vitamin A Supplementation in Preterm or Low Birth Weight Infants to Prevent Morbidity and Mortality: a Systematic Review and Meta-analysis. Pediatrics 2022; 150.
  6. Darlow BA, Graham PJ, Rojas-Reyes MX. Vitamin A supplementation to prevent mortality and short- and long-term morbidity in very low birth weight infants. Cochrane Database Syst Rev 2016; :CD000501.
  7. Tolia VN, Murthy K, McKinley PS, et al. The effect of the national shortage of vitamin A on death or chronic lung disease in extremely low-birth-weight infants. JAMA Pediatr 2014; 168:1039.
  8. Rysavy MA, Li L, Tyson JE, et al. Should Vitamin A Injections to Prevent Bronchopulmonary Dysplasia or Death Be Reserved for High-Risk Infants? Reanalysis of the National Institute of Child Health and Human Development Neonatal Research Network Randomized Trial. J Pediatr 2021; 236:78.
  9. Huang J, Zhang L, Tang J, et al. Human milk as a protective factor for bronchopulmonary dysplasia: a systematic review and meta-analysis. Arch Dis Child Fetal Neonatal Ed 2019; 104:F128.
  10. Patel AL, Johnson TJ, Robin B, et al. Influence of own mother's milk on bronchopulmonary dysplasia and costs. Arch Dis Child Fetal Neonatal Ed 2017; 102:F256.
  11. Cole FS, Alleyne C, Barks JD, et al. NIH Consensus Development Conference statement: inhaled nitric-oxide therapy for premature infants. Pediatrics 2011; 127:363.
  12. Kumar P, Committee on Fetus and Newborn, American Academy of Pediatrics. Use of inhaled nitric oxide in preterm infants. Pediatrics 2014; 133:164.
  13. Albertella M, Gentyala RR, Paraskevas T, et al. Superoxide dismutase for bronchopulmonary dysplasia in preterm infants. Cochrane Database Syst Rev 2023; 10:CD013232.
  14. Lauterbach R, Szymura-Oleksiak J, Pawlik D, et al. Nebulized pentoxifylline for prevention of bronchopulmonary dysplasia in very low birth weight infants: a pilot clinical study. J Matern Fetal Neonatal Med 2006; 19:433.
  15. Schulzke SM, Kaempfen S, Patole SK. Pentoxifylline for the prevention of bronchopulmonary dysplasia in preterm infants. Cochrane Database Syst Rev 2014; :CD010018.
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