Classic Bronchopulmonary Dysplasia Research Articles

Analysis of interleukins 6, 8, 10 and 17 in the lungs of premature neonates with bronchopulmonary dysplasia

Bronchopulmonary dysplasia (BPD) is an abnormality that occurs in premature neonate lung development. The pathophysiology is uncertain, but the inflammatory response to lung injury may be the responsible pathway. The objective of this study is to evaluate the role of interleukins 6, 8, 10, and 17 through the anatomopathological and immunohistochemical study of the lungs of premature neonates with BPD. Thirty-two cases of neonatal autopsies from the Pathology Department of the Clinics Hospital of the Universidade Federal do Paraná, who presented between 1991 and 2005 were selected. The sample included neonates less than 34 weeks of gestational age who underwent oxygen therapy and had pulmonary formalin-fixed paraffin-embedded (FFPE) samples. Pulmonary specimens were later classified into three groups according to histopathological and morphometric changes (classic BPD, new BPD, and without BPD) and subjected to immunohistochemical analysis. The antibodies selected for the study were anti-IL-6, anti-IL-8, anti-IL-10, and anti-IL-17A monoclonal antibodies. IL-6, IL-8, and IL-10 showed no significant differences in tissue expression among the groups. IL-17A had higher tissue immunoreactivity in the group without BPD compared with the classic BPD group (1686 vs. 866 μm2, p = 0.029). This study showed that the involvement of interleukins 6, 8, and 10 might not be significantly different between the two types of BPD. We speculated that IL-17A could be a protective factor in this disease.

Новая форма бронхолегочной дисплазии: реалии сегодняшнего дня

Study Objective: to analyse the dynamics in morbidity of the classic and New forms of bronchopulmonary dysplasia (BPD) in children hospitalised to the National Medical Research Centre of Children Health during previous 8 years. Study Design: retrospective analysis of medical records. Materials and Methods. In 2012–2019, we analysed 369 cases of children with the new BPD and 231 cases of children with the classic disease. Study Results. The article contains the information on the 8-year observation demonstrating prevalence of the new BPD and describes disease characteristics and course in premature infants. The retrospective analysis of 2012–2019 data shows that the number of paediatric patients with the new BPD is gradually increasing. Whereas in 2012 the classic BPD prevailed (156 (68.4%) out of 228 children with confirmed diagnosis), later the new form accounted for more BPD cases (p < 0.05). According to information available, an equal ratio (50% for the classic form and 50% for the new form) is demonstrated in 2013, the period when the Russian Federation started using the live birth and dead birth criteria proposed by the World Health Organisation (WHO). Conclusion. Improved neonatal intensive care methods and transition of the Russian Federation to the WHO live birth and dead birth criteria in 2012 were pre-conditions for BPD pathomorphism. The of rate of the classic form in the Russian Federation has been decreasing year after year. It is essential to identify the long-term complications from the new BPD, especially functional capabilities of the respiratory tract in older patients with the history of disease. Study of the features and long-term complications from this new form is a burning issue of paediatric pulmonology and requires careful attention. Keywords: bronchopulmonary dysplasia, new form, classic form, premature infants.

The very question of future development of extremely preterm infants

The survival rates for extremely preterm infants, born at <28 weeks of gestation, have markedly improved over the past two decades and this has raised concern over a possible increase in morbidity. Due to advances in perinatal, neonatal and paediatric care, our greatest fears have not materialised. Instead, most infants born preterm these days function in the same way as their term-born counterparts 1. The clinical challenge is to recognise those preterm infants who face a higher risk of a wide range of disabilities, and the most common issues at the moment are cognitive and behavioural problems. A systematic review that was published online in January 2018 looked at 30 studies covering a total of 10 293 preterm infants born before 32 weeks of gestation and/or with very low birthweights of <1500 g after 2006. It estimated that 20.6% had motor delays at approximately two years of corrected age, with a 95% confidence interval of 13.9–29.4, and that the figures for cognitive delays were 16.9% (10.4–26.3) on the basis of developmental scales 2. Despite extensive meta-analyses and outcome research after very preterm births, the clinician at the bedside of an extremely preterm infant in an individual neonatal intensive care unit is still uncertain about the extent to which they will face these delays. One of the major challenges of interpreting the results of any outcome studies or systematic reviews on preterm infants is the heterogeneity of research designs 2. There are wide differences in reporting active treatment policies at birth 3, background mortality rates 3, inclusion and exclusion criteria such as genetic disorders, sociodemographic characteristics, parental education, length of follow-up and the exact measures used and definitions of outcome. All of this might result in flaws with regard to the clinical impact of the study. Brain imaging protocols, magnetic resonance imaging (MRI) settings and expertise levels differ between centres, resulting in a wide variation in sensitivity and specificity of brain MRI findings, for example as predictors of cerebral palsy 4. It is also evident that the landscape of classical phenotypes of preterm morbidity and outcomes is changing. In this issue of Acta Paediatrica, Brumbaugh et al. 5 use the National Institute of Health consensus definition of bronchopulmonary dysplasia (BPD) to define modern BPD. Using this classification by severity, they report that modern BPD may not, in itself, translate to poor early cognitive outcomes that are similar to classic BPD. This is a concrete message that tells clinicians like me that we need to prepare to change our thinking about the causal connections between neonatal morbidities and outcome. The decreasing trend of cerebral palsy, even among extremely preterm infants 2, has already changed our perceptions of the outcomes of prematurity. At the same time, the severity of cerebral palsy in preterm infants has decreased 6. As a clinical observation, it has also been commented that the main type of cerebral palsy in preterm survivors has changed from bilateral spastic type to unilateral spastic cerebral palsy. There is strong demand for harmonising outcome studies to enhance the accumulation of accurate prognostic information. The 2016 paper by Rysavy et al. 7 provided recommendations for reporting outcomes of extremely preterm births to improve the dialogue about the topic and enable us to compare outcomes between different studies. This distinctive paper serves as a valuable resource for everyone carrying out outcome studies of preterm infants. When the parents of an extremely preterm infant who has a severe BPD and unilateral periventricular haemorrhagic infarction ask me about their child's future development, which is the most important factor after their survival, what valid evidence do I use as the basis for my answer? Despite the research that has been carried out to date, the question still remains under debate. We still need to know so much more.

Inhaled dry salt micro particles in the treatment of bronchopulmonary dysplasia: a five case series report

Background. Despite current medical ad-vances, to this day there is no single medi-cal intervention to effectively prevent or treat bronchopulmonary dysplasia (BPD) in both preterm and term infants. Along with protective ventilation strategies, vari-ous drugs are being used or are being re-searched at this very moment, with the sole purpose of improving the general outcome for these patients. Inhaled dry salt micro particles therapy is now one of them. Materials and methods. This report pre-sents five patients, diagnosed with severe BPD. All of them received, complemen-tary to classical BPD management and respiratory support, continuous inhaled dry salt micro particles, via SaltMed car-tridges, for a period of 12 to 30 days. After only 24 hours of administration, we were able to observe a significant improvement in respiratory function and dynamics. It was possible to use a lower fraction of in-spired oxygen (FiO2), mean airway pres-sure (MAP) and peak inspiratory pressure (PIP) in all mechanically ventilated pa-tients. Higher tidal volumes were recorded and we observed improvement in oxygen-ation indexes.Conclusion. Continuously inhaled dry salt micro particles, administered complemen-tary to classic BPD management, could improve respiratory and overall morbid-ity and mortality in infants with any form of BPD. Further study of these possible effects is needed, as there is no data pub-lished on this matter so far.

Blood Cytokine Profiles Associated with Distinct Patterns of Bronchopulmonary Dysplasia among Extremely Low Birth Weight Infants

To explore differences in blood cytokine profiles among distinct bronchopulmonary dysplasia (BPD) patterns. We evaluated blood spots collected from 943 infants born at ≤1000g and surviving to 28days on postnatal days 1, 3, 7, 14, and 21 for 25 cytokines. Infants were assigned to the following lung disease patterns: (1) no lung disease (NLD); (2) respiratory distress syndrome without BPD; (3) classic BPD (persistent exposure to supplemental oxygen until 28days of age); or (4) atypical BPD (period without supplemental oxygen before 28days). Median cytokine levels for infants with BPD were compared with the IQR of results among infants with NLD. The distribution of enrolled infants by group was as follows: 69 (NLD), 73 (respiratory distress syndrome), 381 (classic BPD), and 160 (atypical BPD). The remaining 260 infants could not be classified because of missing data (104) or not fitting a predefined pattern (156). Median levels of 3 cytokines (elevated interleukin [IL]-8, matrix metalloproteinase-9; decreased granulocyte macrophage colony-stimulating factor) fell outside the IQR for at least 2 time points in both infants with atypical and classic BPD. Profiles of 7 cytokines (IL-6, IL-10, IL-18, macrophage inflammatory protein-1α, C-reactive protein, brain-derived neurotrophic factor, regulated on activation, normal T cell expressed and secreted) differed between infants with classic and atypical BPD. Blood cytokine profiles may differ between infants developing classic and atypical BPD. These dissimilarities suggest the possibility that differing mechanisms could explain the varied patterns of pathophysiology of lung disease in extremely premature infants.

Two cases of bronchopulmonary dysplasia of similar appearance in adult monozygotic twin: pathology and computed tomographic findings.

Bronchopulmonary dysplasia (BPD) is related to decreased lung function throughout life. However, the pathology and radiology pattern of BPD of adults are not documented well yet. In this case report, we present BPD case of an adult monozygotic twin showing nearly identical lesions on chest computed tomography (CT). CT images showed mixed areas of ground-glass and reticular opacities in both lungs. They had common histories of pneumonias requiring mechanical ventilations in period of infants. Pulmonary function test of one patient showed a pulmonary insufficiency with airway obstruction. Pathologic findings showed bronchiolar hyperplasia and peribronchiolar fibrosis which was similar to classic BPD patients. Our twin case report might help provide distinguishing pathology and radiology pattern of an adult pulmonary sequelaes of BPD. It might be reasonable to make close follow-up for BPD patients to evaluate the long-term outcomes of BPD survivors.

КЛІНІЧНІ ОСОБЛИВОСТІ ПЕРЕБІГУ РІЗНИХ ФОРМ БРОНХОЛЕГЕНЕВОЇ ДИСПЛАЗІЇ.

&lt;p&gt; Під спостереженням знаходилась 131 дитина (269 спостережень) віком від 1 місяця до 3 років з діагнозом бронхолегенева дисплазія. Для нової форми бронхолегеневої дисплазіїхарактерно формування гострого бронхіоліту (р&amp;lt;0,001) дихальною недостатністю ІІ-ІІІ ступенів (р&amp;lt;0,001) під час&lt;br /&gt;загострення захворювання. Клінічними маркерами даної форми захворювання в стадіїремісії можна вважати задишку при фізичному навантажені (р&amp;lt;0,01), акроціаноз при занепокоєнні (р&amp;lt;0,01), втягнення поступливих місць грудної'клітки (р&amp;lt;0,01)та розгорнення нижньої'апертури (р&amp;lt;0,001). Загострення класичної' бронхолегеневої'дисплазії'характеризується частими&lt;br /&gt;обструктивними бронхітами (р&amp;lt;0,001), бронхіолітами (р&amp;lt;0,01), пневмоніями (р&amp;lt;0,01). Виявлені маркери обструктивнорестриктивної'дихальної'недостатності при класичній бронхолегеневїй дисплазії: задишка у спокої'та при фізичному навантаженні&lt;br /&gt;(р&amp;lt;0,01), бочкоподібна грудна клітка (р&amp;lt;0,01) та втягнення поступливих місць (р&amp;lt;0,001), розгорнута нижня апертура (р&amp;lt;0,001), бочкоподібна грудна клітка (р&amp;lt;0,05), притуплення, що чергується з коробковим звуком (р&amp;lt;0,01) та жорстке дихання (р&amp;lt;0,001) і крепітація (р&amp;lt;0,01). Для пацієнтів з бронхолегеневою дисплазією доношених загострення проявлялося частими пневмоніями (р&amp;lt;0,001), що корелювало з порушеннями нейро-респіраторного драйву (г=0,678; р&amp;lt;0,05). Клінічними маркерами бронхолегеневої'&lt;br /&gt;дисплазії'доношених під час ремісії'захворювання являються задишка (р&amp;lt;0,01), недостатнє додавання у масі тіла (р&amp;lt;0,001), тахіпноє (р&amp;lt;0,01), акроціаноз (р&amp;lt;0,001), притуплення в нижніх відділах грудної' клітки (р&amp;lt;0,001), жорстке дихання (р&amp;lt;0,001). Крепітація та ослаблене дихання нехарактерні для бронхолегеневої'дисплазії'доношених.&lt;br /&gt;&lt;br /&gt;&lt;/p&gt;

Análises histopatológica e morfométrica no diagnóstico da "nova" displasia broncopulmonar e comparação clinicopatológica com a forma clássica da doença

INTRODUÇÃO: A displasia broncopulmonar (DBP) continua sendo a principal complicação nos recém-nascidos (RN) prematuros. Com o uso de surfactante exógeno e da prevenção de doenças respiratórias no período neonatal a incidência de DBP clássica vem diminuindo, porém uma nova forma de DBP tem surgido, mais branda e associada aos desenvolvimentos pulmonar alveolar e vascular incompletos. Do ponto de vista anatomopatológico a DBP clássica é caracterizada por processos de lesão e reparação, e os achados da "nova" DBP são de hipoplasia alveolar com nenhuma fibrose. OBJETIVOS: Demonstrar as alterações histopatológicas e morfométricas em pulmões de prematuros que foram a óbito, com quadro clínico compatível com "nova" DBP, comparando-as com um grupo controle (sem DBP) e com a forma clássica da doença, além de correlacionar os três grupos com o tempo de uso de oxigênio entre outros fatores de risco da DBP. MATERIAL E MÉTODOS: A população foi composta por 59 amostras de pulmões de prematuros com idade gestacional (IG) menor que 34 semanas e submetidos à oxigenioterapia. Fatores de risco para DBP foram coletados por meio da revisão de prontuários. Amostras pulmonares foram separadas em dois grupos, o com DBP clássica e o sem DBP clássica. O segundo grupo foi então submetido à análise morfométrica para contagem do número de alvéolos, medidas as áreas e os perímetros dos alvéolos. Após esta análise a população estudada ficou dividida em grupo com DBP clássica; com "nova" DBP (casos com mais de sete dias de oxigenioterapia); e grupo controle ou sem DBP clássica ou "nova" (casos com menos de sete dias de oxigenioterapia). RESULTADOS: o primeiro grupo apresentava inflamação e fibrose septal evidentes. Já os segundo e terceiro grupos apresentavam alterações histopatológicas mínimas, sendo então necessária a análise morfométrica para separá-los. O grupo com "nova" DBP apresentou número de alvéolos, sua área e perímetro diminuídos (p < 0,005) quando comparados ao grupo controle. Não houve diferença estatisticamente significativa entre os três grupos com relação aos fatores de risco para desenvolvimento de DBP. CONCLUSÃO: As formas de DBP clássica e "nova" são de etiologia multifatorial, porém distintas entre si. Para diagnóstico anatomopatológico da "nova" DBP pode ser necessária a análise morfométrica. As alterações histopatológias e morfométricas deste estudo antecederam a necessidade de oxigenioterapia por mais de 28 dias. Portanto, instituir terapêutica para DBP antes do 28º dia de vida em RN prematuro em oxigenioterapia estaria justificado pelos nossos achados histopatológicos e morfométricos.

Lung Disease in Premature Neonates: Radiologic-Pathologic Correlation

Pulmonary disease is the most important cause of morbidity in preterm neonates, whose lungs are often physiologically and morphologically immature. Surfactant deficiency in immature lungs triggers a cascade of alveolar instability and collapse, capillary leak edema, and hyaline membrane formation. The term respiratory distress syndrome (RDS) has come to represent the clinical expression of surfactant deficiency and its nonspecific histologic counterpart, hyaline membrane disease. Historically, chest radiographs of infants with RDS predictably demonstrated decreased pulmonary expansion, symmetric generalized reticulogranular lung opacities, and air bronchograms. Refinements in perinatal medicine, including antenatal glucocorticoid administration, surfactant replacement therapy, and increasingly sophisticated ventilatory strategies have decreased the prevalence of RDS and air leak, altered familiar radiographic features, and lowered the threshold of potential viability to a gestational age of approximately 23 weeks. Alveolar paucity and pulmonary interstitial thickness in these profoundly premature neonates impair normal gas exchange and may necessitate prolonged mechanical ventilation, increasing the risk of lung injury. Bronchopulmonary dysplasia (BPD), alternatively termed chronic lung disease of infancy, is a disorder of lung injury and repair originally ascribed to positive-pressure mechanical ventilation and oxygen toxicity. Before the advent of surfactant replacement therapy, chest radiographs of infants with classic BPD demonstrated coarse reticular lung opacities, cystic lucencies, and markedly disordered lung aeration that reflected alternating regions of alveolar septal fibrosis and hyperinflated normal lung parenchyma. In the current era of surfactant replacement, BPD is increasingly a disorder of very low-birth-weight neonates with arrested alveolar and pulmonary vascular development, minimal alveolar septal fibrosis and inflammation, and more subtle radiographic abnormalities.

Strategies to minimize lung injury in extremely low birth weight infants

To review the main causes of new bronchopulmonary dysplasia and the strategies utilized to decrease its incidence in extremely low birth weight infants. For this review a MEDLINE search from 1966 to October 2004, the Cochrane Database, abstracts from the Society for Pediatric Research and recent meetings on the topic were used. The survival of extremely low birth weight infants has increased significantly due to improvement in both scientific knowledge and technology. This improvement in survival has therefore resulted in an increased incidence of bronchopulmonary dysplasia. The characteristics of bronchopulmonary dysplasia in extremely low birth weight infants, the so called "new" bronchopulmonary dysplasia are quite different from the classic bronchopulmonary dysplasia described by Northway. This new bronchopulmonary dysplasia has a multifactorial etiology, which includes volutrauma, atelectrauma, oxygen toxicity and lung inflammation. Therapy such as prenatal corticosteroids, exogenous surfactant, nasal continuous positive airway pressure, new mechanical ventilation modalities and gentle ventilation have been used in attempts to decrease lung injury severity. In order to prevent lung injury in extremely low birth weight infants, it is necessary to minimize several factors that induce bronchopulmonary dysplasia and to utilize less aggressive therapeutic strategies. In addition to the current therapy used to decrease lung injury, knowledge of these causative factors may create new therapies that may be fundamental in improving the clinical outcomes of premature infants.

165 The “New” Bronchopulmonary Dysplasia. Epidemiological Study on The Euroneonet Database

Background: Bronchopulmonary dysplasia (BPD) has classically been related to the use of high oxygen concentrations and mechanical ventilation in infants with respiratory distress syndrome (RDS). However, an increasing number of very low birth weight infants (VLBWI) develop BPD without having acute RDS, which has been termed “new” BPD.Aim: To identify the characteristics of VLBWI who develop this “new ” form of BPD.Methods: This is a multicenter, prospective, longitudinal study of a cohort of 1798 VLBWI born in 2001 and 2002, at one of the 30 Spanish NICU included in EuroNeoNet initiative. The database, including demographic characteristics, risk factors, interventions and outcomes, was searched to identify babies alive at 36 weeks PMA (n=1549). BPD was diagnosed (need of oxygen at 36 PMA) in 221(14%) babies, 32 of who did not have RDS. An univariate and logistic regression analysis was used to asses the risk factors for BPDResults: In comparison to the classical BPD, babies with the “new” BPD were more mature, had a higher birthweight, needed less resuscitation manoeuvres and respiratory support, had a lower incidence of PCA, but a higher one of early sepsis (7.4 vs. 12.5%) and NEC (6.9 vs. 21.9 %). Multifactorial analysis in infants without RDS (n=804), showed an increased risk for BPD related to use of CPAP (OR 3.6; 95% IC 1.5– 8.8) and mechanical ventilation (4.8; 1.9–11.8), and to the presence of both, early sepsis (9.1; 1.9– 42.4) and late sepsis (4.8; IC 2–11.1). However, in patients with RDS (n=745) we showed an increased risk related to CPAP, mechanical ventilation, late sepsis and PDA (1.7, 1.1–2.6), but not with early onset sepsis.Conclusion: As previously reported (1), we showed risk factors of developing DBP in infants with and without RDS are CPAP, mechanical ventilation, and late sepsis. Nevertheless, in babies without RDS, BDP is associated with early sepsis, and in those with RDS with PDA. Despite the small number of patients without RDS who developed BPD in our cohort, the higher incidence of early sepsis and NEC point out toward prenatal factors related to fetal inflammatory disease (2).

Relationship between Wilson-Mikity syndrome and the new bronchopulmonary dysplasia.

In 1960, Wilson and Mikity1 published a report of 5 cases of a new form of respiratory disease in the premature infant. An additional 29 cases were reported from our center in 1969.2 In the intervening years, similar cases had been reported from other centers in the United States, England, Canada, Australia, Switzerland, Italy, and Nigeria, indicating that these cases composed a definite clinical entity of wide geographic distribution. In the early 1960s, none of these infants had received assisted ventilation. Ventilatory support for premature infants became the standard of treatment in the late 1960s. The Wilson-Mikity syndrome (WMS) was swallowed up by bronchopulmonary dysplasia (BPD), the chronic effects of artificial ventilation first reported by Northway et al.3 These were a result of damage to the lung resulting in fibrosis, inflammation, and metaplasia. The reported infants of WMS all were premature with a medium weight of 1280 g.1,2 The smallest was 830 g, and 26 of the 35 were 2000 g. …

Bronchopulmonary dysplasia: changes in pathogenesis, epidemiology and definition

Bronchopulmonary dysplasia (BPD) continues to be one of the most common long-term complications associated with preterm birth. Its incidence is increasing as the survival of extreme premature infants improves, but its clinical presentation is milder than the original description of Northway and collaborators. In contrast to the classic BPD that was strongly related to mechanical injury and oxygen toxicity, current forms of the condition are more related to immaturity, perinatal infection and inflammation, persistent ductus arteriosus and disrupted alveolar and capillary development. Many different definitions of BPD have been proposed, most of which are based on the duration of supplemental oxygen requirement. The different definitions can produce strikingly different incidence figures, which may account for the wide variations in the condition reported in the literature. Some of the limitations of the criteria most commonly used to diagnose BPD are discussed in this article.

Bronchopulmonary dysplasia: an enduring challenge.

1. Yvonne E. Vaucher, MD, MPH* 1. *Clinical Professor of Pediatrics, Division of Neonatology, University of California, San Diego, Calif. After completing this article, readers should be able to: 1. Describe the most common cause of chronic lung disease during infancy. 2. Explain the importance of a history of bronchopulmonary dysplasia throughout childhood. 3. Identify infants at high risk for developing bronchopulmonary dysplasia. 4. List the adverse effects associated with postnatal corticosteroids. Despite clinical advances in antepartum, intrapartum, and neonatal care, bronchopulmonary dysplasia (BPD) continues to challenge infants who have been in neonatal intensive care units and their caretakers. BPD is the most common cause of chronic respiratory disease during infancy and remains a major cause of long-term medical, pulmonary, and neurodevelopmental morbidity, increasing the cost of health care and the utilization of medical and educational resources throughout childhood. BPD is a clinical diagnosis, defined by oxygen dependence for a specific period of time after birth and accompanied by characteristic radiographic findings that correspond to anatomic abnormalities. Thus far, a precise physiologic definition of BPD is lacking. As the clinical presentation has evolved over the past 30 years, so has the definition. As originally described by Northway in the 1960s, the diagnosis of classic BPD was based on progressive radiographic changes in preterm infants who were treated for severe respiratory distress syndrome (RDS) immediately after birth and had prolonged ventilator and oxygen dependence. This form of BPD occurred in larger, relatively mature preterm infants, who required treatment with high-pressure mechanical ventilation and high concentrations of oxygen. Although the acute respiratory disease initially improved in these infants, oxygen requirements increased 7 to 10 days after birth and persisted for at least 28 days. The definition of BPD subsequently was modified by Bancalari to include preterm infants who had less severe RDS that initially required short-term mechanical ventilation, but who also developed persistent respiratory symptoms and an oxygen requirement for at least 28 days after birth …

Epidemiology and Risk Factors for the “New” Bronchopulmonary Dysplasia

After completing this article, readers should be able to: 1. Explain the difference in clinical course between classic bronchopulmonary dysplasia (BPD) and “new BPD.” 2. Describe the potential role of inflammation in the pathogenesis of BPD. 3. Describe how patent ductus arteriosus may affect the development of BPD. 4. Delineate the role of infection in the pathogenesis of BPD. The classic severe form of bronchopulmonary dysplasia (BPD) described by Northway and colleagues is occurring less frequently, but there is an increasing number of small preterm infants who are surviving with a milder form of chronic lung damage (Fig. 1⇓ ). These two forms of chronic lung disease (CLD) differ not only in their clinical presentation but in pathogenic mechanisms and long-term consequences. Figure 1. Incidence of BPD by birthweight among infants weighing less than 1,500 g born in 1996 through 1998 at the University of Miami/Jackson Memorial Medical Center. Classic BPD was described in infants who had severe respiratory distress syndrome (RDS) and received aggressive ventilation with high positive airway pressures and inspired oxygen concentrations. The new form of BPD occurs in smaller preterm infants, most of whom receive antenatal steroids and postnatal surfactant therapy. Because of this therapy, they experience a mild initial respiratory course and, therefore, are not exposed to aggressive ventilation or high inspired oxygen concentrations. Accordingly, the lung damage they suffer must be caused in part by other factors. Most of these infants have extremely low birthweights and require prolonged ventilator support primarily for management of apnea and poor respiratory effort. They represent more than 75% of all infants diagnosed with CLD in our institution. In contrast to infants who have severe BPD, these patients initially require low concentrations of oxygen for treatment of mild RDS that usually responds favorably to exogenous surfactant. This often is followed by a few days …

Atypical chronic lung disease patterns in neonates.

To determine, in the postsurfactant era, the incidence and clinical characteristics of infants with atypical versus traditionally defined bronchopulmonary dysplasia (BPD) among premature infants with birth weights <1251 g. Retrospective cohort study. A single regional neonatal intensive care unit (level III/IV). Two hundred thirty-two premature infants <1251 g at birth consecutively admitted during a 2-year period. Incidence of classic BPD and atypical chronic lung disease (CLD) (occurring without preceding respiratory distress or after recovery from respiratory distress). Among 177 infants <1251 g who survived to 28 days, 27 (15%) had atypical CLD and 61 (34.5%) had classic BPD. Atypical CLD infants were significantly heavier and more mature than classic BPD infants (mean birth weights, 922 +/- 152 g vs 854 +/- 173 g; and mean gestational age, 26.8 +/- 1.3 weeks vs 26.1 +/- 1.6 weeks). Median duration of ventilator support (31 days; range, 2 to 127 vs 42 days; range, 4-145 days) and oxygen therapy (30 days; range, 11 to 163 vs 48 days; range, 19-180 days) were shorter in atypical CLD infants than in classic BPD infants. Atypical CLD comprised 31% of total cases of CLD. Atypical CLD appears to be less severe than classic BPD. These data suggest that initial, acute lung injuries are not the sole antecedents of neonatal CLD.

Bronchopulmonary dysplasia: prevention, management and long-term outlook

Despite major advances in neonatology over the last few years, neonatal intensive care units continue to care for a number of infants with ventilator and oxygen dependency or bronchopulmonary dysplasia (BPD). In 1967 Northway first described a chronic lung disease which developed after recovery from respiratory distress syndrome (RDS). 1 The original description was of a progressive illness culminating at 30 days in severe lung disease with oxygen dependency and a characteristic chest X-ray. The definition of BPD has evolved to the criteria currently used in Table 1. 36 weeks gestation is a more useful cut off when considering extremely preterm babies and is more predictive of final outcome than respiratory status at 28 days of life. The typical chest X-ray of BPD is seen in Figure 1. There are two variants which are sometimes seen in clinical practice. In the first the clinical criteria are similar but the lung appearance on chest radiograph is relatively normal or shows minor bilateral diffuse opacities. In the second the nonventilated preterm infant develops a persistent oxygen requirement commencing in the second week of life or later (Wilson Mikity syndrome). The prognosis in these two groups is better than in classical BPD. Although definitions of BPD are useful for statistics and comparisons, they are less useful clinically. BPD is more of a continuum of lung insult, injury and repair from birth. The absence of a diuresis classically present in the recovery phase of RDS, the development of pulmonary interstitial emphysema or pneumothoraces on the chest radiograph and the inability to wean the infant from the ventilator by day 7 of life are all early signs that chronic lung disease is likely to be established and the infant will continue to require respiratory support. The incidence of BPD from published studies varies considerably and is partly dependent on the definition. It varies from 3 0 4 0 % in mechanically ventilated newborns. 2~ Over the last 3 years a reduction in the number of babies with BPD on our Unit has been noted with an incidence of 15% in infants under 1500 g in 1995. Other units in the UK are reporting an increase. Good epidemiological studies are required to explain these differences.