Bronchopulmonary dysplasia

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Bronchopulmonary dysplasia
CXR - Bronchopulmonary dysplasia.jpg
Radiograph of bronchopulmonary dysplasia
Specialty Pediatrics   OOjs UI icon edit-ltr-progressive.svg
CausesLong-term high oxygen supplementation

Bronchopulmonary dysplasia (BPD; part of the spectrum of chronic lung disease of infancy) is a chronic lung disease which affects premature infants. Premature (preterm) infants who require treatment with supplemental oxygen or require long-term oxygen are at a higher risk. [1] The alveoli that are present tend to not be mature enough to function normally. [2] It is also more common in infants with low birth weight (LBW) and those who receive prolonged mechanical ventilation to treat respiratory distress syndrome. It results in significant morbidity and mortality. The definition of bronchopulmonary dysplasia has continued to evolve primarily due to changes in the population, such as more survivors at earlier gestational ages, and improved neonatal management including surfactant, antenatal glucocorticoid therapy, and less aggressive mechanical ventilation. [3]

Contents

Currently the description of bronchopulmonary dysplasia includes the grading of its severity into mild, moderate and severe. This correlates with the infant's maturity, growth and overall severity of illness. [4] The new system offers a better description of underlying pulmonary disease and its severity. [5]

"The term 'bronchopulmonary dysplasia' was first used by [William] Northway et al. in 1967 to describe a chronic form of injury to the lungs caused by barotrauma and oxygen injury in preterm infants requiring mechanical ventilation." [6]

Presentation

Complications

Feeding problems are common in infants with bronchopulmonary dysplasia, often due to prolonged intubation. Such infants often display oral-tactile hypersensitivity (also known as oral aversion). [7]

Physical findings:[ citation needed ]

Cause

Prolonged high oxygen delivery in premature infants causes necrotizing bronchiolitis and alveolar septal injury, with inflammation and scarring. This results in hypoxemia. Today, with the advent of surfactant therapy and high frequency ventilation and oxygen supplementation, infants with BPD experience much milder injury without necrotizing bronchiolitis or alveolar septal fibrosis. Instead, there are usually uniformly dilated acini with thin alveolar septa and little or no interstitial fibrosis. It develops most commonly in the first four weeks after birth. [8] Bronchopulmonary dysplasia is now known to be due to abnormal wound healing in response to injury; [9] it has been linked to alterations in the Wnt/beta-catenin pathway. [10] [11]

Diagnosis

Earlier criteria

The classic diagnosis of bronchopulmonary dysplasia may be assigned at 28 days of life if the following criteria are met:[ citation needed ]

  1. Positive pressure ventilation during the first two weeks of life for a minimum of three days.
  2. Clinical signs of abnormal respiratory function.
  3. Requirements for supplemental oxygen for longer than 28 days of age to maintain PaO2 above 50 mm Hg.
  4. Chest radiograph with diffuse abnormal findings characteristic of bronchopulmonary dysplasia.

Newer criteria

The 2006 National Institute of Health (US) criteria for BPD (for neonates treated with more than 21% oxygen for at least 28 days) [12] is as follows:, [13] [14]

Mild
Moderate
Severe

Management

Infants with bronchopulmonary dysplasia are often treated with diuretics that decrease fluid in the alveoli where gas exchange occurs and bronchodilators that relax the airway muscles to facilitate breathing. [15] To alleviate bronchopulmonary dysplasia, caffeine is another commonly used treatment that reduces inflammation and increases lung volume thereby improving extubation success and decreasing the duration of mechanical ventilation. [16] Viral immunization is important for these children who have a higher risk of infections in the respiratory tract. [17]

Corticosteroid treatment

There is evidence that steroids (systemic corticosteroid treatment) given to babies less than seven days old can prevent bronchopulmonary dysplasia. [18] This treatment increases the risk of neurodevelopmental sequelae (cerebral palsy) and gastrointestinal perforation. [18]

For babies seven days old and older, "late systemic postnatal corticosteroid treatment" may reduce the risk of death and of bronchopulmonary dysplasia. [19] There is some evidence that this treatment does not increase the risk of cerebral palsy, however, long-term studies considering the neurodevelopmental outcomes is needed to further understand the risk of this treatment option. [19] Late systemic postnatal corticosteroid treatment is therefore only recommended for babies seven days old or older who cannot be taken off of a ventilator. [19] The benefit and risks of systemic corticosteroid treatment in older babies who are not intubated (on a ventilator) is not known. [19]

Vitamin A

Vitamin A treatment in low birth weight babies may improve the 36-week mortality risk, decrease the days of mechanical ventilation, and decrease the incidence of bronchopulmonary dysplasia. [20]

Other

Oxygen therapy at home is recommended in those with significant low oxygen levels. [21]

Hypercarbia (too much carbon dioxide in the blood) may contribute to the development of bronchopulmonary dysplasia. [22] Monitoring the level of carbon dioxide in neonatal infants to ensure that the level is not too high or too low (hypocarbia) is important for improving outcomes for neonates in intensive care. [23] Carbon dioxide can be monitored by taking a blood sample (arterial blood gas), through the breath (exhalation), and it can be measured continuously through the skin by using a minimally invasive transcutaneous device. [23] The most effective and safest approach for measuring carbon dioxide in newborn infants is not clear. [23]

It is not clear if treatment with superoxide dimutase supplementation is effective at preventing bronchopulmonary dysplasia in infants born preterm or at reducing preterm infant mortality. [24]

Epidemiology

The rate of BPD varies among institutions, which may reflect neonatal risk factors, care practices (e.g., target levels for acceptable oxygen saturation), and differences in the clinical definitions of BPD. [25] [26] [27]

Long-term

Adult survivors may have asthma-like symptoms and have a higher risk of developing obstructive lung disease. [10] Phenotypes in adult survivors have been "broadly categorized as predominantly asthma-like, emphysematous, or consistent with pulmonary hypertension." [10]

See also

Related Research Articles

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Intrauterine growth restriction (IUGR), or fetal growth restriction, is the poor growth of a fetus while in the womb during pregnancy. IUGR is defined by clinical features of malnutrition and evidence of reduced growth regardless of an infant's birth weight percentile. The causes of IUGR are broad and may involve maternal, fetal, or placental complications.

<span class="mw-page-title-main">Preterm birth</span> Birth at less than a specified gestational age

Preterm birth, also known as premature birth, is the birth of a baby at fewer than 37 weeks gestational age, as opposed to full-term delivery at approximately 40 weeks. Extreme preterm is less than 28 weeks, very early preterm birth is between 28 and 32 weeks, early preterm birth occurs between 32 and 34 weeks, late preterm birth is between 34 and 36 weeks' gestation. These babies are also known as premature babies or colloquially preemies or premmies. Symptoms of preterm labor include uterine contractions which occur more often than every ten minutes and/or the leaking of fluid from the vagina before 37 weeks. Premature infants are at greater risk for cerebral palsy, delays in development, hearing problems and problems with their vision. The earlier a baby is born, the greater these risks will be.

<span class="mw-page-title-main">Oxygen toxicity</span> Toxic effects of breathing oxygen at high partial pressures

Oxygen toxicity is a condition resulting from the harmful effects of breathing molecular oxygen at increased partial pressures. Severe cases can result in cell damage and death, with effects most often seen in the central nervous system, lungs, and eyes. Historically, the central nervous system condition was called the Paul Bert effect, and the pulmonary condition the Lorrain Smith effect, after the researchers who pioneered the discoveries and descriptions in the late 19th century. Oxygen toxicity is a concern for underwater divers, those on high concentrations of supplemental oxygen, and those undergoing hyperbaric oxygen therapy.

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<span class="mw-page-title-main">Infant respiratory distress syndrome</span> Human disease affecting newborns

Infant respiratory distress syndrome (IRDS), also called respiratory distress syndrome of newborn, or increasingly surfactant deficiency disorder (SDD), and previously called hyaline membrane disease (HMD), is a syndrome in premature infants caused by developmental insufficiency of pulmonary surfactant production and structural immaturity in the lungs. It can also be a consequence of neonatal infection and can result from a genetic problem with the production of surfactant-associated proteins.

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<span class="mw-page-title-main">Neonatal intensive care unit</span> Intensive care unit specializing in the care of ill or premature newborn infants

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<span class="mw-page-title-main">Respiratory disease</span> Disease of the respiratory system

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Palivizumab, sold under the brand name Synagis, is a monoclonal antibody produced by recombinant DNA technology used to prevent severe disease caused by respiratory syncytial virus (RSV) infections. It is recommended for infants at high-risk for RSV due to conditions such as prematurity or other medical problems including heart or lung diseases.

Wilson–Mikity syndrome, a form of chronic lung disease (CLD) that exists only in premature infants, leads to progressive or immediate development of respiratory distress. This rare condition affects low birth babies and is characterized by rapid development of lung emphysema after birth, requiring prolonged ventilation and oxygen supplementation. It is closely related to bronchopulmonary dysplasia (BPD), differing mainly in the lack of prior ventilatory support. All the initial patients described with Wilson–Mikity syndrome were very low birth weight infants that had no history of mechanical ventilation, yet developed a syndrome that clinically resembled BPD. Upon the death of some of these infants, autopsies showed histologic changes similar to those seen in BPD.

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<span class="mw-page-title-main">Pulmonary interstitial emphysema</span> Collection of air outside of the normal air space of the pulmonary alveoli

Pulmonary interstitial emphysema (PIE) is a collection of air outside of the normal air space of the pulmonary alveoli, found instead inside the connective tissue of the peribronchovascular sheaths, interlobular septa, and visceral pleura. This collection of air develops as a result of alveolar and terminal bronchiolar rupture. Pulmonary interstitial emphysema is more frequent in premature infants who require mechanical ventilation for severe lung disease. Infants with pulmonary interstitial emphysema are typically recommended for admission to a neonatal intensive care unit.

Bubble CPAP is a non-invasive ventilation strategy for newborns with infant respiratory distress syndrome (IRDS). It is one of the methods by which continuous positive airway pressure (CPAP) is delivered to a spontaneously breathing newborn to maintain lung volumes during expiration. With this method, blended and humidified oxygen is delivered via short binasal prongs or a nasal mask and pressure in the circuit is maintained by immersing the distal end of the expiratory tubing in water. The depth to which the tubing is immersed underwater determines the pressure generated in the airways of the infant. As the gas flows through the system, it "bubbles" out and prevents buildup of excess pressures.

Surfactant therapy is the medical administration of exogenous surfactant. Surfactants used in this manner are typically instilled directly into the trachea. When a baby comes out of the womb and the lungs are not developed yet, they require administration of surfactant in order to process oxygen and survive. This condition that the baby has is called newborn respiratory distress syndrome, and it is treatable. Surfactant coat the smallest parts of the lungs called the alveoli and helps for oxygen to go in and for carbon dioxide to go out. How surfactant does this is by not allowing the alveoli to collapse and to retain their inflated shape when the baby exhales.

Christian P. Speer is a German pediatrician and Professor of Pediatrics specialized in neonatology at the Julius Maximilian University of Würzburg. Speer is known for his scientific and educational contributions in neonatal medicine.

<span class="mw-page-title-main">Henry Halliday (paediatrician)</span> British neonatologist (1945–2022)

Henry Lewis Halliday was a British-Irish paediatrician and neonatologist. In 2021, Halliday was awarded the James Spence Medal for research into neonatology, for coordinating two of the largest neonatal multicentre trials for prevention and treatment of a number of neonatal respiratory illnesses and for a breakthrough in the development of a new lung surfactant that brought relief to very small babies suffering from infant respiratory distress syndrome (RDS).

References

  1. ↑ Merck Manual, Professional Edition, Bronchopulmonary Dysplasia.
  2. ↑ "Bronchopulmonary Dysplasia". American Lung Association. Retrieved 2020-03-12.
  3. ↑ Northway Jr, WH; Rosan, RC; Porter, DY (Feb 16, 1967). "Pulmonary disease following respirator therapy of hyaline-membrane disease. Bronchopulmonary dysplasia". The New England Journal of Medicine. 276 (7): 357–68. doi:10.1056/NEJM196702162760701. PMID   5334613.
  4. ↑ Sahni, R; Ammari, A; Suri, MS; Milisavljevic, V; Ohira-Kist, K; Wung, JT; Polin, RA (Jan 2005). "Is the new definition of bronchopulmonary dysplasia more useful?". Journal of Perinatology. 25 (1): 41–6. doi:10.1038/sj.jp.7211210. PMID   15538399. S2CID   22550494.
  5. ↑ Ehrenkranz, RA; Walsh, MC; Vohr, BR; Jobe, AH; Wright, LL; Fanaroff, AA; Wrage, LA; Poole, K; National Institutes of Child Health and Human Development Neonatal Research, Network (Dec 2005). "Validation of the National Institutes of Health consensus definition of bronchopulmonary dysplasia". Pediatrics. 116 (6): 1353–60. doi:10.1542/peds.2005-0249. PMID   16322158. S2CID   21228956.
  6. ↑ Sahni, Mitali; Mowes, Anja K. (2023), "Bronchopulmonary Dysplasia", StatPearls, Treasure Island (FL): StatPearls Publishing, PMID   30969701 , retrieved 2023-09-18
  7. ↑ Gaining & Growing. "Bronchopulmonary dysplasia", Gaining & Growing, March 20, 2007. (Retrieved June 12, 2008.)
  8. ↑ National Heart, Lung, and Blood Institute (1998). Bronchopulmonary Dysplasia. National Institutes of Health. p. 2.{{cite book}}: CS1 maint: multiple names: authors list (link)
  9. ↑ Thébaud, Bernard; Goss, Kara N.; Laughon, Matthew; Whitsett, Jeffrey A.; Abman, Steven H.; Steinhorn, Robin H.; Aschner, Judy L.; Davis, Peter G.; McGrath-Morrow, Sharon A.; Soll, Roger F.; Jobe, Alan H. (2019-11-14). "Bronchopulmonary dysplasia". Nature Reviews Disease Primers . 5 (1): 78. doi:10.1038/s41572-019-0127-7. ISSN   2056-676X. PMC   6986462 . PMID   31727986.
  10. 1 2 3 Wozniak, Phillip S.; Makhoul, Lara; Botros, Mena M. (5 December 2023). "Bronchopulmonary dysplasia in adults: Exploring pathogenesis and phenotype". Pediatric Pulmonology . 59 (3): 540–551. doi:10.1002/ppul.26795. ISSN   8755-6863.
  11. ↑ Liu, Jiaqi; Xiao, Qing; Xiao, Jiani; Niu, Chenxi; Li, Yuanyuan; Zhang, Xiaojun; Zhou, Zhengwei; Shu, Guang; Yin, Gang (2022-01-03). "Wnt/β-catenin signalling: function, biological mechanisms, and therapeutic opportunities". Signal Transduction and Targeted Therapy . 7 (1): 3. doi:10.1038/s41392-021-00762-6. ISSN   2059-3635. PMC   8724284 . PMID   34980884.
  12. ↑ Kinsella, JP; Greenough, A; Abman, SH (Apr 29, 2006). "Bronchopulmonary dysplasia". Lancet. 367 (9520): 1421–31. doi:10.1016/S0140-6736(06)68615-7. PMID   16650652. S2CID   23716814.
  13. ↑ "Bronchopulmonary Dysplasia". Patient.info. Retrieved 2 February 2014.
  14. ↑ Jobe, AH; Bancalari, E (June 2001). "Bronchopulmonary dysplasia". Am J Respir Crit Care Med. 163 (7): 1723–9. doi:10.1164/ajrccm.163.7.2011060. PMID   11401896.
  15. ↑ American Lung Association Scientific; Medical Editorial Review Panel. "Diagnosing and Treating Bronchopulmonary Dysplasia". American Lung Association. Retrieved 4 December 2020.
  16. ↑ Yuan, Yuan; Yang, Yang; Lei, Xiaoping; Dong, Wenbin (June 2022). "Caffeine and bronchopulmonary dysplasia: Clinical benefits and the mechanisms involved". Pediatric Pulmonology. 57 (6): 1392–1400. doi:10.1002/ppul.25898. PMID   35318830. S2CID   247616415.
  17. ↑ American Lung Association Scientific; Medical Editorial Review Panel. "Diagnosing and Treating Bronchopulmonary Dysplasia". American Lung Association. Retrieved 4 December 2020.
  18. 1 2 Doyle, Lex W.; Cheong, Jeanie L.; Hay, Susanne; Manley, Brett J.; Halliday, Henry L. (2021-10-21). "Early (< 7 days) systemic postnatal corticosteroids for prevention of bronchopulmonary dysplasia in preterm infants". The Cochrane Database of Systematic Reviews. 10 (5): CD001146. doi:10.1002/14651858.CD001146.pub6. ISSN   1469-493X. PMC   8530019 . PMID   34674229.
  19. 1 2 3 4 Doyle, Lex W.; Cheong, Jeanie L.; Hay, Susanne; Manley, Brett J.; Halliday, Henry L. (2021-11-11). "Late (≥ 7 days) systemic postnatal corticosteroids for prevention of bronchopulmonary dysplasia in preterm infants". The Cochrane Database of Systematic Reviews. 2021 (11): CD001145. doi:10.1002/14651858.CD001145.pub5. ISSN   1469-493X. PMC   8580679 . PMID   34758507.
  20. ↑ Huang, Li; Zhu, Diqing; Pang, Gaofeng (2021). "The effects of early vitamin A supplementation on the prevention and treatment of bronchopulmonary dysplasia in premature infants: a systematic review and meta-analysis". Translational Pediatrics. 10 (12): 3218–3229. doi: 10.21037/tp-21-496 . ISSN   2224-4344. PMC   8753470 . PMID   35070836.
  21. ↑ Hayes D, Jr; Wilson, KC; Krivchenia, K; Hawkins, SMM; Balfour-Lynn, IM; Gozal, D; Panitch, HB; Splaingard, ML; Rhein, LM; Kurland, G; Abman, SH; Hoffman, TM; Carroll, CL; Cataletto, ME; Tumin, D; Oren, E; Martin, RJ; Baker, J; Porta, GR; Kaley, D; Gettys, A; Deterding, RR (1 February 2019). "Home Oxygen Therapy for Children. An Official American Thoracic Society Clinical Practice Guideline". American Journal of Respiratory and Critical Care Medicine. 199 (3): e5–e23. doi:10.1164/rccm.201812-2276ST. PMC   6802853 . PMID   30707039.
  22. ↑ Hochwald, Ori; Borenstein-Levin, Liron; Dinur, Gil; Jubran, Huda; Ben-David, Shlomit; Kugelman, Amir (July 2019). "Continuous Noninvasive Carbon Dioxide Monitoring in Neonates: From Theory to Standard of Care". Pediatrics. 144 (1). doi: 10.1542/peds.2018-3640 . ISSN   1098-4275. PMID   31248940.
  23. 1 2 3 Bruschettini, Matteo; Romantsik, Olga; Zappettini, Simona; Ramenghi, Luca Antonio; Calevo, Maria Grazia (2016-02-13). "Transcutaneous carbon dioxide monitoring for the prevention of neonatal morbidity and mortality". The Cochrane Database of Systematic Reviews. 2016 (2): CD011494. doi:10.1002/14651858.CD011494.pub2. ISSN   1469-493X. PMC   8720274 . PMID   26874180.
  24. ↑ Albertella, Martina; Gentyala, Rahul R; Paraskevas, Themistoklis; Ehret, Danielle; Bruschettini, Matteo; Soll, Roger (2023-10-09). Cochrane Neonatal Group (ed.). "Superoxide dismutase for bronchopulmonary dysplasia in preterm infants". Cochrane Database of Systematic Reviews. 2023 (10): CD013232. doi:10.1002/14651858.CD013232.pub2. PMC  10561150. PMID   37811631.
  25. ↑ Fanaroff AA, Stoll BJ, Wright LL, Carlo WA, Ehrenkranz RA, Stark AR, et al. (2007). "Trends in neonatal morbidity and mortality for very low birthweight infants". Am J Obstet Gynecol. 196 (2): 147.e1–8. doi:10.1016/j.ajog.2006.09.014. PMID   17306659. S2CID   27489509.
  26. ↑ Van Marter LJ, Allred EN, Pagano M, Sanocka U, Parad R, Moore M, et al. (2000). "Do clinical markers of barotrauma and oxygen toxicity explain interhospital variation in rates of chronic lung disease? The Neonatology Committee for the Developmental Network". Pediatrics. 105 (6): 1194–201. doi:10.1542/peds.105.6.1194. PMID   10835057.
  27. ↑ Ellsbury DL, Acarregui MJ, McGuinness GA, Eastman DL, Klein JM (2004). "Controversy surrounding the use of home oxygen for premature infants with bronchopulmonary dysplasia". J Perinatol. 24 (1): 36–40. doi: 10.1038/sj.jp.7211012 . PMID   14726936.

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