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New concepts in necrotizing enterocolitis.

Abstract

Necrotizing enterocolitis is an overwhelming gastrointestinal emergency that primarily afflicts premature infants born weighing less than 1500 g. Despite years of investigation, the etiology remains unclear, and accepted prevention and treatment strategies are lacking. Studies published over the last year have provided new insight into several aspects of this complex disease. In this review, novel information is presented on (1) the epidemiology; (2) methods of early diagnosis, such as abdominal magnetic resonance imaging; (3) the importance of risk factors, including assessment of feeding strategies and role of bacterial colonization; (4) the pathophysiology, highlighting experimental and clinical trials evaluating the role of inflammatory mediators and growth factors on the disease; (5) preventive strategies, such as anaerobic bacterial supplementation; and (6) surgical interventions, including peritoneal drainage. Understanding some of these important aspects of necrotizing enterocolitis may help improve the outlook of patients with this dreaded disease. Although the incidence of neonatal necrotizing enterocolitis (NEC) and the mortality stemming from this disease have not significantly improved over the last 30 years, there is exciting new information that may significantly improve the outlook of patients with this overwhelming intestinal emergency in the near future.

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BibTeXRIS

M S Caplan, T Jilling. 2001. New concepts in necrotizing enterocolitis.. https://doi.org/10.1097/00008480-200104000-00004

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Necrotising enterocolitis.

Necrotising enterocolitis is one of the most common gastrointestinal emergencies in newborn infants. Here we review the epidemiology, clinical presentation, and pathophysiology of the disease, as well as strategies for diagnosis, management, and prevention. Necrotising enterocolitis is one of the most devastating and unpredictable diseases affecting premature infants. Despite decades of research, its pathogenesis remains unclear; diagnosis can be difficult; and treatment is challenging. We will need to improve our understanding of intestinal defences in premature infants, dietary and bacterial factors, and genetic effects that could predispose infants to necrotising enterocolitis before we can develop new strategies for prevention and treatment.

Enterocolitis, Necrotizing↗

Intestinal immune defences and the inflammatory response in necrotising enterocolitis.

Necrotising enterocolitis is a devastating neonatal gastrointestinal emergency predominantly affecting low birth weight, premature infants and is accompanied by significant mortality and morbid sequelae. The pathophysiology remains obscure and the management of infants with necrotising enterocolitis has not changed since the recognition of this disease. Necrotising enterocolitis is most likely the clinical culmination of multiple different risk factors interacting with each other to produce bowel injury through a final, common inflammatory pathway. Here, we review intestinal immunity and the specific inflammatory mediators involved in this disease process.

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Laboratory parameters predictive of developing necrotizing enterocolitis in infants born before 33 weeks of gestation.

PURPOSE: The aim of this study was to identify laboratory findings predictive of necrotizing enterocolitis (NEC). METHODS: Prospective follow-up of 140 infants of less than 33 weeks of gestation. Twenty-six infants developed NEC (grades I to III, criteria of Bell et al [Ann Surg 1978;187:1-7]) (NEC group). For each, 2 birth-weight, gestational age- and postnatal age-matched controls were selected (control group). Blood counts, glucose and electrolyte levels, C-reactive protein, and acid-base balance 3 days, 2 days, and 1 day before and at the onset of NEC and at corresponding ages from the controls were recorded. RESULTS: Metabolic acidosis occurred, the platelet levels decreased, and the blood glucose increased on successive days in the infants with grade NEC II-III. At the onset of NEC, the infants had significantly lower platelet and higher blood glucose levels compared with controls. More than half of infants with intestinal perforation had leukocyte levels above 30 x 10(9)/L and pH less than 7.25, and their mean blood glucose levels increased to more than 1.5 mmol/L in 24 hours. The remaining parameters were not useful. CONCLUSION: A persistent metabolic acidosis, decreasing platelet, and increasing blood glucose level on several successive days might predict a developing NEC, and leukocyte values above 30 x 10(9)/L, pH less than 7.25, and a blood glucose rise by 1.5 mmol/L or more within 24 hours predict NEC with intestinal perforation. Such findings should alert the physician to look for signs of NEC in a preterm infant.

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