Necrotizing Enterocolitis In Full‐Term Neonates

Abstract

22 February 2001 Dear Editor NECROTIZING ENTEROCOLITIS IN FULL-TERM NEONATES We read with interest the review article on necrotizing enterocolitis (NEC) in full-term neonates.1 Although the author mentioned various risk factors that are associated with NEC in term neonates, we call your attention to some of the more recent data we have published on this topic. First of all, NEC in term infants is a rare event, at least in this part of the world. The incidence quoted as 5–;25% of NEC infants came from the studies published in the 1970s and 1980s. We published more recent figures derived from a detailed population-based study on the incidence and aetiology of NEC in full-term neonates born in New South Wales and Australian Capital Territory in Australia.2 The incidence in our region was 0.05 per 1000 live births which was similar to the crude estimation (0.06 per 1000) in > 2500 g infants based on the CDC hospital diagnosis information in the United States. With regards to risk factors, one important message is missing in this article. There is a great difference in aetiological factors between full-term and premature infants. Earlier institutional studies suggested the association of congenital diseases in term infants.3 The major finding in our recent regional study was that about two-thirds of the 29 NEC neonates had an underlying congenital disease, which included congenital heart lesions in 35% and endocrine lesions in 17%. This contrasts with prematurity being the major underlying risk factor in premature infants, who have an inherent gastrointestinal immaturity and other illnesses associated with prematurity. The role of T-cryptantigen screening in the management of NEC was discussed in this review. We would like to caution that the literature on antigen screen was derived primarily from the preterm population. NEC aetiological factors appear very different between the preterm and term infants. The mortality of our series is low and both deaths were not associated with haemolysis (circulatory collapse with panhypopituitarism and the other due to congenital anomaly). Furthermore, in the largest series of T-cryptantigen reported in preterm infants (27 antigen positive cases in 200 NEC infants) we have not been able to demonstrate reduced mortality since the introduction of routine screening,4 so the benefit of screening is yet to be proven in preterm infants, let alone in term infants. The author’s suggestion of exploring cytokine modulation therapy in the prevention of NEC in term infants is unlikely to be effective given the different aetiological factors, in particular the high incidence of associated congenital diseases in term infants. Furthermore, with the rarity of disease and low mortality in term neonates, even if we restrict the preventive therapy to high-risk term neonates such as infants with congenital heart disease it is extremely difficult to justify the expenditure involved. For example, during our study period of 6.5 years with over 539 000 live births, we would expect about 1300 cases born with major heart defects based on National Perinatal Statistics Unit data.5 Only 10 of these developed NEC! In short, NEC in term and preterm infants are very different in many aspects and the knowledge derived from preterm infants may not be applicable in term infants.