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Abstract
Clinical and basic experimental approaches to pediatric acute lung injury (ALI), including acute respiratory distress syndrome (ARDS), have historically focused on acute care and management of the patient. Additional efforts have focused on the etiology of pediatric ALI and ARDS, clinically defined as diffuse, bilateral diseases of the lung that compromise function leading to severe hypoxemia within 7 days of defined insult. Insults can include ancillary events related to prematurity, can follow trauma and/or transfusion, or can present as sequelae of pulmonary infections and cardiovascular disease and/or injury. Pediatric ALI/ARDS remains one of the leading causes of infant and childhood morbidity and mortality, particularly in the developing world. Though incidence is relatively low, ranging from 2.9 to 9.5 cases/100,000 patients/year, mortality remains high, approaching 35% in some studies. However, this is a significant decrease from the historical mortality rate of over 50%. Several decades of advances in acute management and treatment, as well as better understanding of approaches to ventilation, oxygenation, and surfactant regulation have contributed to improvements in patient recovery. As such, there is a burgeoning interest in the long-term impact of pediatric ALI/ARDS. Chronic pulmonary deficiencies in survivors appear to be caused by inappropriate injury repair, with fibrosis and predisposition to emphysema arising as irreversible secondary events that can severely compromise pulmonary development and function, as well as the overall health of the patient. In this chapter, the long-term effectiveness of current treatments will be examined, as will the potential efficacy of novel, acute, and long-term therapies that support repair and delay or even impede the onset of secondary events, including fibrosis.
Highlights
Since first described by Ashbaugh and colleagues in 1967 as “Adult Respiratory Distress Syndrome in Children,” Pediatric Acute Respiratory Distress Syndrome (Pediatric acute respiratory distress syndrome (ARDS)) has been recognized as a distinct syndrome, with hallmarks and outcomes that differ from those of patients suffering from adult ARDS or neonatal RDS [1,2,3]
Studies singled out lung surfactant deficiency that can be caused by a large variety of pulmonary and extra-pulmonary insults as an underlying factor in Pediatric ARDS, Pediatric ARDS Fibrosis versus Repair but the pathophysiology has since been recognized as much more complex [3]
Since identification of the pathways involved in lung injury, most of the literature has been focused on the use of therapies aimed at truncating the inflammatory response
Summary
Since first described by Ashbaugh and colleagues in 1967 as “Adult Respiratory Distress Syndrome in Children,” Pediatric Acute Respiratory Distress Syndrome (Pediatric ARDS) has been recognized as a distinct syndrome, with hallmarks and outcomes that differ from those of patients suffering from adult ARDS or neonatal RDS [1,2,3]. It may be that slower patient responses allow a cascade of signaling events to occur that promotes long-term, pro-fibrotic remodeling Though this hypothesis has yet to be completely tested, multiple studies in animal models and on cadaveric human tissue have demonstrated potential mechanisms and intervention points for the development of fibrosis following ALI resulting in Pediatric ARDS. The fibrotic phase of Pediatric ARDS is identified by the deposition of excess collagen and other extracellular matrix material and is associated with intra-alveolar, alveolar septal wall and alveolar ductal fibrosis as there is an attempt by the body to recreate the alveolar basement membrane that overlies collapsed and atelectatic regions of the lung [30, 38] Together, these pathologic changes result in the impaired lung physiology characteristic of Pediatric ARDS, which includes decreased functional residual capacity, diminished compliance accompanied by an increase in the work of breathing, increased deadspace and shunt fraction, and impaired gas exchange [39,40,41]. This mechanical intervention has a well-known capacity to feed forward to create further injury via mechanical stretch and mesenchymal activation, thereby exacerbating the development of fibrosis
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