In the last decade, it has become
increasingly clear that necrotizing enterocolitis (NEC) is neither a uniform
nor a well-defined disease entity. There are many factors that are forcing this
unwelcome realization upon the neonatal and Pediatric surgery communities. In
the course of this manuscript we will review the acquired neonatal intestinal
diseases (ANIDs), some which do lead to the common final pathology of NEC and
some which do not. During the late 1970s, Necrotizing
Enterocolitis (NEC) was most commonly seen in preterm
infants >30 weeks of gestation an association between excessive fluid intake
and the increasing incidence of NEC was noted.
Although there were a dozen or so preterm case reports of spontaneous
intestinal perforation (SIP) in the literature, it was in 1988 that heralded
the coming epidemic in neonatology by linking its prevalence to a case series
of six very low birth weight infants. It was 10 years later, when surfactant
was universally available and researchers began exploring the use of early
postnatal dexamethasone as means to attenuate chronic lung disease, that SIP
began to move from an infrequent complication to a regular part of the
differential for every extremely low-birth-weight infant were the first to
demonstrate the deleterious relationship between early postnatal steroids and
SIP in a retrospective cohort. Since this initial report, many controlled trials have been stopped or altered because of an
increased rate of SIP in neonates being treated with steroids. We now know that
this perturbation is accentuated when steroids are given concomitantly with
early indomethacin, making this the first clear example of harmful drug synergy
in neonatology.
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