Acute respiratory distress syndrome (ARDS) is an acute respiratory
failure syndrome caused by non-cardiogenic pulmonary edema of various
etiologies.[1](#ref-0001) When the fetus encounters asphyxia,
acidosis, infection, meconium inhalation, et al. during childbirth, the
inflammatory pathway will be activated. The systemic inflammatory
response can remove pathogens, but the excessive inflammatory response
will prompt pulmonary surfactant (PS) inactivation and increase the
permeabilities of alveolar epithelial and endothelial cells, resulting
in the accumulation of edema fluid in the alveoli and eventually leading
to severe hypoxemia, respiratory distress and decreased lung
compliance.[1,2](#ref-0001) Population-based studies in the United
States, Australia, Europe, and New Zealand reported that the incidence
of ARDS in children is 2.0-12.8 per 100000
person-years,[3](#ref-0003) and according to the interim report of
the International Neonatal ARDS Multicenter Study, the mortality of
neonatal ARDS (NARDS) is approximately 20%.[4](#ref-0004) Due to
the high mortality of NARDS, the researchers try to explore potential
new treatments to limit the incidence and mortality of NARDS. Systemic
inflammatory response plays a significant role in the occurrence and
development of NARDS, budesonide, a non-halogenated corticosteroid, has
a potent local pulmonary anti-inflammatory effect, therefore, it may be
an effective treatment option for NARDS. This article reviews the
evolution of ARDS definition and diagnosis, pathophysiological
mechanisms of NARDS, and gives an outlook on the application of
budesonide in NARDS.