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PubMed · 17027734

Necrotising enterocolitis.

Patricia W Lin·Barbara J Stoll
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Abstract

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.

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Enterocolitis, NecrotizingFemaleHospital MortalityHumansInfant, Low Birth WeightInfant, NewbornInfant, PrematureLength of StayMalePrevalenceJournal ArticleReview

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Patricia W Lin, Barbara J Stoll. 2006-10-07. Necrotising enterocolitis.. https://doi.org/10.1016/s0140-6736(06)69525-1

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PubMed2006

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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PubMed2006

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.

Enterocolitis, Necrotizing↗
PubMed2006

Impact of gestational age on the clinical presentation and surgical outcome of necrotizing enterocolitis.

OBJECTIVE: This investigation tests the hypothesis that the clinical presentation and the outcome of necrotizing enterocolitis (NEC) vary with gestational age (GA). METHODS: All infants admitted to our center between October 1991 and September 2003 were evaluated weekly to identify confirmed cases of NEC. Based upon GA, these infants were divided into five groups: Extremely premature (EP, 23 to 26 weeks), very premature (VP, 27 to 29 weeks), moderately premature (MP, 30 to 34 weeks), near-term (NT, 35 to 36 weeks), and term (T, 37 to 42 weeks). RESULTS: A total of 202 infants developed NEC. The most common sign of NEC among EP infants was ileus (77%), followed by abdominal distention (71%), emesis (58%), pneumoperitoneum (54%), fixed intestinal loop (52%), gasless abdomen (42%) and bloody stools (17%). Intramural gas was detected in 100% of T but was present in only 29% of EP infants (P < 0.0001). Similarly, portal venous gas was common in T but infrequent in the EP infants (47 vs 10%, P < 0.0001). Despite a higher peritoneal drain insertion rate (31 vs 5%, P < 0.001) and a higher mortality rate (33 vs 10%, P = 0.05) in EP compared to T infants, other clinical outcomes were not different. CONCLUSIONS: The clinical presentation of NEC is different in EP compared to more mature infants; however, outcome among NEC survivors is similar across all GA. Reliance solely on observation of intramural or on portal venous gas in EP infants may lead to a delay or failure in the diagnosis.

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