Prevention of necrotizing enterocolitis in preterm infants

Necrotizing enterocolitis (NEC) and intestinal perforation are very common emergencies in very low birth weight (VLBW) infants and are associated with high mortality and morbidity. It has been suggested that prematurity and feeding with nonhuman milk may be pecursors of NEC, because these factors could make the immature intestine sensitive to atrophy. Another risk factor may be the exposure to indomethacin: in extremely low birth weight infants, intestinal perforation was reported in association with indomethacin and high endogenous cortisol levels, and, in a large analysis, indomethacin was identified as an independent risk factor for spontaneous bowel perforation.

On these basis, an American group reported on Pediatrics its experience in treating preterm infants, over a period of 20 years (1986-2005). Usually, infants were not exposed to indomethacin or early dexamethasone treatment. In addition, this group adopted late-onset, slow, continuous drip (LOSD) enteral feeding protocol.

VLBW infants (501-1500 g) were evaluated for morphologic parameters, NEC, bowel perforation, use of the LOSD feeding protocol, and indomethacin therapy. Overall morbidity rates were compared with the Vermont Oxford Network (VON) database data for the last 4 years. During the analyzed periodod, 1158 infants received the LOSD feeding protocol, and were not exposed to indomethacin or early use of dexamethasone (group I), whereas 81 infants had at least one modification in these parameters (group II). The rate of NEC in group I (0.4%) was significantly lower than that in group II (6%). The comparison of group I with the VON database indicates that the LOSD feeding protocol, with no exposure to indomethacin or early use of dexamethasone, is associated with significantly lower rates of NEC (0.4% vs 5.9%), surgical NEC (0.4% vs 3.1%), and bowel perforation (0.35% vs 2.2%).

Although these findings do not support causal relationships between diet, exposure to indomethacin or early use of dexamethasone and NEC, it can be suggested that the LOSD feeding protocol and the lack of indomethacin exposure may contribute to the prevention of NEC and bowel perforation. In fact, the LOSD feeding protocol is based on longer initiation time, small and continuos feeding, and monitoring for residuals and abdominal distension; therefore, it does not challenge strongly the immature intestine and also offer total intestinal hygiene. Moreover, because the use of indomethacin has been implicated in spontaneous bowel perforations, the delicate handling of the gastrointestinal tract and the lack of exposure to indomethacin and early dexamethasone might have contributed to lower rates of intestinal morbidity. This protocol may also help in keeping systemic vascular resistance low, thus improving infants ability to tolerate a patent ductus arteriosus.

In conclusion, results from a 20-year experience with 1239 very low birth weight infants suggests that the LOSD feeding protocol and avoidance of indomethacin and early dexamethasone treatment may contribute to the prevention of NEC.

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