Bronchopulmonary dysplasia (BPD), the most chronic lung disease in infants, is a complex disorder with a multifactorial etiopathogenesis, a variable clinical course, with serious long‐term pulmonary and neurodevelopmental consequences. Notwithstanding… Click to show full abstract
Bronchopulmonary dysplasia (BPD), the most chronic lung disease in infants, is a complex disorder with a multifactorial etiopathogenesis, a variable clinical course, with serious long‐term pulmonary and neurodevelopmental consequences. Notwithstanding the multiple challenges associated with this disease, a critical and annoying problem has been the very definition of BPD. The initial pathological description of babies dying of severe “hyaline membrane disease” was reported in the early 1960s; however, the use of the term “bronchopulmonary dysplasia” with a correlative description of the clinical, pathologic, and radiographic features was first described in 1967. In 1979, the National Heart, Lung, and Blood Institute (NHLBI)—based on a workshop conducted a year prior—suggested a purely clinical definition focusing on the requirement of supplemental oxygen at 28 days, along with “characteristic” radiographic features. This was followed by the Shennan et al suggested definition of utilizing the supplemental oxygen requirement at 36 weeks corrected gestational age (GA). Continuing the trend of focusing entirely on the clinical requirement of supplemental oxygen and the degree of respiratory support, the National Institute of Child Health and Human Development, NHLBI, and Office of Rare Diseases, in 2000, proposed the current (NIH consensus) definition of BPD: infants requiring supplemental oxygen for at least 28 days and at 36 weeks postmenstrual age. The disease was further categorized as mild, moderate, or severe. The major fallacy of the above approach was using a therapy for the diagnosis of a disease, given that the therapy per se did not have standardized guidelines for its use in this population of premature neonates. In an attempt to mitigate the above situation, a “physiological” definition of BPD was proposed. Recently, a further refinement of the definition of BPD incorporates specific supplemental oxygen requirement with oxygen saturation targeting, along with the mode of respiratory (invasive/noninvasive) support, with radiographic changes, assessed at 36 weeks postmenstrual age. It is too early to tell if this newer definition will be an improvement as there are no published correlations of this definition with short or long‐term outcomes. There is a marked variability in the practice parameters by physicians (neonatologists) of using the multiple modes of ventilatory support and oxygen supplementation in the management of preterm infants. Given the subjective nature and the range of the “acceptable/ adequate response” to the above therapy in such scenarios, it would be expected that a more robust and objective measure of the need for such pulmonary support could potentially improve on defining the actual need for such therapy. In the manuscript in this issue of Pediatric Pulmonology by Nobile et al, the authors utilized the ratio of noninvasive pulse oximetry (oxygen saturation or SatO2) to the fraction of inspired O2 (FiO2)—designated as SFR—to characterize the O2 diffusion capability in the lungs. As stated by the authors, the SFR has been shown to be a reliable surrogate marker for the P/F ratio (arterial oxygen concentration [PaO2] to inspired oxygen concentration [FIO2] ratio) in multiple clinical settings. 9
               
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