PEDIATRICS Vol. 111 No. 3 March 2003, pp. 671-672
COMMENTARY |
The Relationship of Neonatal Feeding Practices and the Pathogenesis and Prevention of Necrotizing Enterocolitis
Abbreviations: NEC, necrotizing enterocolitis
Enteral alimentation is critical to the pathogenesis of necrotizing enterocolitis (NEC).1 In 1978, Brown and Sweet2 proposed that aggressive feeding protocols contributed to the pathogenesis of NEC. By instituting a very conservative feeding protocol with modest daily enteral volume increments and stopping feedings with the slightest suggestion of feeding intolerance, they were able to reduce the incidence of NEC. Other studies also suggested that affected infants were fed either too rapidly or with excessive daily increments.3–8
Because NEC is primarily a disease of premature infants, it seems logical to suggest that immature gastrointestinal functions (digestion, motility, defense mechanisms, vascular and microvascular circulation, and mucosal integrity) may contribute to its pathogenesis.1–8 Enteric bacteria may ferment malabsorbed carbohydrates to various gases, producing distension and increased intraluminal pressure, which could decrease mucosal blood flow. Short chain fatty acid products of fermentation could be toxic to enterocytes. Alternately, nutritionally induced inflammation (increased growth of bacteria with release of endotoxin) together with impaired mucosal barrier function and an imbalance between inflammatory versus antiinflammatory mediators could contribute to NEC. Poor gastrointestinal motility (from immaturity, ileus, inflammation) may produce stasis and bacterial overgrowth, thus exacerbating the abnormal states discussed above.
Nonetheless, randomized trials have not demonstrated that fast versus slow or early versus delayed feedings have altered the incidence of NEC.9–11 Indeed, the incidence of NEC was not affected in one randomized study, which achieved full enteral feedings within 7 or 10 days. However, no study has fed infants at the rates or volumes present before the onset of NEC.4
In an attempt to improve gastrointestinal function and avoid the risk of intravenous alimentation, many neonatologists use gut stimulation protocols. Also called gut priming, minimal enteric feedings, hypocaloric feeds, or trophic feeds, this method has demonstrated important benefits when compared with infants kept nothing per os.8,12–15 These studies reported no effect on the incidence of NEC, but have demonstrated a decreased incidence of direct and indirect hyperbilirubinemia as well as signs of osteopenia. In addition, glucose tolerance and feeding tolerance were improved as well as the maturation of antral-duodenal motility. Theoretically, gut stimulation could also prevent fasting-induced mucosal atrophy, thus preventing bacterial translocation and episodes of endotoxemia, mucosal inflammation, or sepsis.
In an exciting and novel approach to the disappointment that previous gut stimulation protocols did not prevent NEC, Berseth and colleagues16 compared their gut stimulation protocol with a traditional enteral feeding protocol using standard rates of volume advancement. The authors had to close the study early because the incidence of NEC in the advancing volume group was 10% versus 1.4% in those receiving the gut stimulation protocol.
This study raises several important questions, such as is gut stimulation protective or do early advancing protocols contribute to the development of NEC? Both may be correct. Regardless, the study reinforces previous conclusions that gut stimulation protocols are beneficial to very low birth weight infants and should be routine in all neonatal intensive care units. There are very few contraindications to using these protocols, even in infants weighing 500 to 600 g with indwelling umbilical catheters while on ventilators.12,14 The initiation of a gut stimulation protocol for 7 to 10 days followed by modest advancement of feedings, particularly with human milk, may greatly reduce the incidence of NEC.13,16
Department of Pediatrics
Medical College of Wisconsin
Milwaukee, WI 53226
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FOOTNOTES
Received for publication Dec 3, 2002; Accepted Dec 3, 2002.
Reprint requests to (R.M.K.) Medical College of Wisconsin, Department of Pediatrics, MACC Fund Research Center, 8701 Watertown Plank Rd, Milwaukee, WI 53226. E-mail: bobkay{at}mcw.edu
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[Abstract/Free Full Text]
PEDIATRICS (ISSN 1098-4275). ©2003 by the American Academy of Pediatrics
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