Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27066462
&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests
in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215
Pediatric Acute Respiratory Distress Syndrome: Fibrosis versus Repair
#MMPMID27066462
Im D
; Shi W
; Driscoll B
Front Pediatr
2016[]; 4
(?): 28
PMID27066462
show ga
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.