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PubMed2003

Vascular changes play a role in the pathogenesis of necrotizing enterocolitis in asphyxiated newborn pigs.

Necrotizing enterocolitis (NEC) is the most common acquired gastrointestinal emergency in neonates. We have developed an animal model of NEC in asphyxiated newborn pigs and investigated the effects of asphyxia on blood flow in superior mesenteric artery and abdominal aorta, cardiovascular data, arterial acid-base and blood gas parameters, and endothelial cytoskeletal structure in mesenteric microvasculature. Anesthetized, mechanically ventilated newborn pigs were included in two groups: piglets underwent severe asphyxia, and sham-operated control animals. A cardiovascular and metabolic failure developed in asphyxiated piglets approximately 1 h after the induction: severe hypotension and bradyarrhythmia were seen and significant reductions of the blood flow were measured in the superior mesenteric artery and abdominal aorta during the critical phase. Rearrangement of cytoskeletal actin structure corresponding to enhanced vascular permeability was seen with bodipy phallacidin in mesenterial endothelium of asphyxiated piglets after a 24-h recovery period. In conclusion, severe vasomotor changes during asphyxia may result in mesenteric endothelial dysfunction implicated in increased vascular permeability, edema formation, and development of NEC in asphyxiated piglets.

Animals↗
PubMed2005

Protective effect of tumor necrosis factor alpha antibody on experimental necrotizing enterocolitis in the rat.

BACKGROUND: Necrotizing enterocolitis (NEC) is a common and devastating disorder of premature infants. Elevated proinflammatory cytokines, especially tumor necrosis factor alpha (TNF-alpha), have been implicated in the pathogenesis of NEC. The aim of this study was to evaluate the effects of TNF-alpha on the inflammatory response in NEC by immunoneutralizing TNF-alpha with a selective antibody. METHODS: Neonatal Sprague-Dawley rats were divided in 3 groups: group 1 (n = 20), a NEC-like enterocolitis was induced by formula feeding, asphyxia, and cold exposure; group 2 (n = 9), animals were treated like in group 1 and additionally received TNF-alpha antibody intraperitoneally; and group 3 (n = 17), animals were dam-fed (controls). Animals were killed in case of imminent death or after 96 hours. Specimens from small bowel were processed for blinded histologic (H&E) and immunhistologic (myeloperoxidase [MPO]) analysis. RESULTS: In group 1, animals developed severe NEC (mean NEC score, 3.28 +/- 0.32; mean MPO, 65.85 +/- 9.46). In group 2, animals developed mild NEC (mean NEC score, 1.72 +/- 0.41; mean MPO, 34.33 +/- 9.69; P < .05). In group 3, no NEC was induced (mean NEC score, 0.0 +/- 0; mean MPO, 6 +/- 1.32; P < .05). CONCLUSION: Tumor necrosis factor alpha antibody may have an attenuating effect on experimental NEC in rats.

Animals↗
PubMed2005

The role of PAF, TLR, and the inflammatory response in neonatal necrotizing enterocolitis.

The pathogenesis of neonatal necrotizing enterocolitis remains poorly understood. Recent evidence suggests that PAF (platelet activating factor) and human toll-like receptors (TLRs) contribute to the pro-inflammatory response that is characteristic of NEC pathology. Understanding the regulation of these molecular interactions may provide new approaches for prevention or treatment of this dreaded condition.

Bacteria↗
PubMed2005

Epidermal growth factor reduces hepatic sequelae in experimental necrotizing enterocolitis.

BACKGROUND AND AIM: Neonatal necrotizing enterocolitis (NEC) is the most common gastrointestinal disease of premature infants. We recently demonstrated that the gut/liver axis plays an important role in the pathophysiology of NEC through the release of inflammatory mediators into the intestinal lumen. We have also shown that supplementation of formula with epidermal growth factor (EGF) dramatically decreases ileal pathology associated with experimental NEC. In this study, we examined the effects of EGF on the liver portion of the gut/liver axis in the neonatal rat model of NEC. METHODS: Newborn rats were divided into three experimental groups, NEC, hand-fed with growth-factor free formula; NEC + EGF, hand-fed with formula supplemented with 500 ng/ml rat EGF; or DF, dam fed. All animals were exposed to asphyxia and cold stress twice daily for 4 days to develop NEC. RESULTS: EGF receptor expression was significantly (p <or= 0.01) decreased in the NEC+EGF group compared to the NEC group. EGF supplementation significantly decreased Kupffer cell numbers (p <or= 0.01) as well as hepatic tumor necrosis factor (TNF)-alpha and interleukin-18 production (p <or= 0.05). Further, TNF-alpha in the intestinal luminal contents of the NEC+EGF group were normalized to levels observed in DF controls compared to the NEC group (p <or= 0.05). Activated nuclear factor-kappaB was also substantially decreased in the NEC+EGF group versus the NEC group. CONCLUSION: The results of this study indicate that EGF normalizes cytokine overproduction in the liver of neonatal rats with NEC, which contributes to diminished intestinal damage during the development of experimental NEC. These data suggest that supplementation of formula with EGF can have beneficial effects on the gut/liver axis during NEC pathogenesis.

Animals↗
PubMed2003

Neonatal necrotizing enterocolitis: an overview.

PURPOSE OF REVIEW: Necrotizing enterocolitis represents a disease entity that remains quite challenging for neonatologists all around the world, in that its aetiology has yet to be revealed, but it is the cause of death for many premature infants each year, affecting up to 28% of very low birthweight infants. This is an attempt to improve the management of affected babies and stimulate more research concerning new diagnostic tools. RECENT FINDINGS: Current trends in the field of (early) diagnosis, such as: (1) imaging techniques, e.g. contrast radiography, portal vein ultrasonography, magnetic resonance, radionuclide scanning; (2) gastrointestinal tonometry; (3) the detection of biochemical markers, cytokines, growth factors; and (4) the determination of the mean peak hydrogen: carbon dioxide ratio excreted in breath, are only some of those mentioned. Various novel preventive techniques are also presented, among which platelet-activating factor acetyl hydrolase activity enhancement, platelet-activating factor receptor antagonists and probiotics, such as Bifidobacterium infantis and Lactobacillus acidophilus, seem quite promising. Regarding treatment, the use of oxygenated perfluorocarbon has added to the limited alternatives available. These data along with other recent discoveries concerning the risk factors and pathogenesis of this disease create a full picture of the current opinion on this topic. SUMMARY: Keeping in mind that the key to confronting such a devastating disorder as necrotizing enterocolitis is early diagnosis and prevention, both clinically applicable and experimental advances are presented with the hope of improving the survival rates of patients affected.

Enterocolitis, Necrotizing↗
PubMed2004

Concentrations of IL-10 in preterm human milk and in milk from mothers of infants with necrotizing enterocolitis.

BACKGROUND: Despite the protective effects of human milk against necrotizing enterocolitis, the incidence is highest in the extremely premature infant, and only minimally decreased with feeding human milk. This suggests that certain protective agents may be lower in milk from mothers delivering extremely premature infants. The anti-inflammatory cytokine IL-10 was one possibility. AIM: We hypothesized that low concentrations of IL-10 in preterm milk contribute to the development of necrotizing enterocolitis in extremely premature infants. METHODS: IL-10 in human milk collected at weeks 1, 2, and 4 postpartum was measured by ELISA in mothers of infants born extremely premature at 23-27 wk gestation (group EP), premature at 32-36 wk gestation (group P), and term at 38-42 wk gestation (group T). Single milk samples were collected from a separate group of mothers whose infants developed necrotizing enterocolitis. RESULTS: There were no significant differences in concentrations of milk IL-10 among groups EP, P, or T. Concentrations of IL-10 declined as lactation progressed (p < 0.001). IL-10 in milk was frequently undetected in all groups, but even more so in the milk of the group of women whose infants had necrotizing enterocolitis (86%) than in groups EP (40%) and P (27%) (p < 0.01). CONCLUSION: IL-10 was present in preterm milk from most women, and the concentrations in preterm and term milk were not significantly different. A paucity of IL-10 in human milk was found in certain mothers in each group, especially in those whose infants developed necrotizing enterocolitis.

Adult↗
PubMed1984

Hexosaminidase: a biochemical marker for necrotizing enterocolitis in the preterm infant.

To evaluate hexosaminidase as a biochemical marker for the early detection of necrotizing enterocolitis in preterm infants, 33 preterm infants without necrotizing enterocolitis and 18 preterm infants with necrotizing enterocolitis had hexosaminidase activity measured during the course of their hospitalization. Although hexosaminidase activity could not identify those preterm infants with necrotizing enterocolitis who had impending perforation, the data strongly suggest that measurements of serum hexosaminidase activity may provide an early biochemical indication of the presence of necrotizing enterocolitis in the preterm infant. Hopefully, early detection of necrotizing enterocolitis in these infants will reduce the morbidity and mortality of this disease.

Clinical Enzyme Tests↗
PubMed1994

Tocolysis with indomethacin increases the incidence of necrotizing enterocolitis in the low-birth-weight neonate.

OBJECTIVE: The null hypothesis states that prolonged antenatal indomethacin exposure within 24 hours of delivery does not increase the incidence of necrotizing enterocolitis in the low-birth-weight neonate. STUDY DESIGN: The neonates of patients receiving indomethacin tocolysis admitted in preterm labor (N = 56) were compared with the neonates of preterm labor patients who received no indomethacin tocolysis (N = 703). These neonatal groups were then compared with regard to gestational age at delivery, birth weight, mode of delivery, antenatal magnesium and steroid exposure, incidence of respiratory distress syndrome, perinatal depression, sepsis, umbilical catheterization, and feeding rates and volumes. The overall incidence of necrotizing enterocolitis, mortality secondary to necrotizing enterocolitis, and the intervals from delivery and feeding to necrotizing enterocolitis diagnosis were also compared. The association between necrotizing enterocolitis and the duration of indomethacin exposure and the interval from exposure to delivery for both the indomethacin and control groups was determined. RESULTS: The incidence of necrotizing enterocolitis in neonates who were delivered within 24 hours of maternal indomethacin therapy was 20% compared with 9% in the control group (p = 0.005). The incidence of necrotizing enterocolitis in neonates with > 48 hours of antenatal indomethacin exposure was 26.4% compared with 4.1% in those with < 48 hours exposure (p = 0.042). The interval from first feeding to necrotizing enterocolitis development was significantly shorter in the indomethacin group versus the control group (2.1 +/- 3.0 vs 6.8 +/- 6.3 days) (p = 0.001), as was the mean interval from delivery to development of necrotizing enterocolitis (10.2 +/- 3.7 vs 15.2 +/- 3.8 days) (p = 0.019). CONCLUSIONS: Antenatal indomethacin exposure occurring within < or = 24 hours of delivery and of at least 48 hours' duration is associated with a significant increase in the incidence of necrotizing enterocolitis in the low-birth-weight neonate.

Birth Weight↗
PubMed1979

Asymptomatic cecal stenosis after necrotizing enterocolitis.

Survival of infants with necrotizing enterocolitis may be complicated by intestinal stricture(s) as a result of healing of ischemic segments of bowel. An asymptomatic cecal stenosis not visible on barium enema was identified at operation for reestablishment of intestinal continuity. Infants recovering from acute necrotizing enterocolitis deserve continued surveillance for mechanical and functional abnormalities of the gastrointestinal tract. Patency of the intestinal lumen distal to the ostomy site should be clearly demonstrated by the surgeon when continuity is reestablished.

Cecal Diseases↗
PubMed1976

Neonatal pneumatosis coli: a mild form of neonatal necrotizing enterocolitis.

A distinctive form of necrotizing enterocolitis was observed in seven newborn infants in a 4 1/2-year period. Characteristically these patients had gross blood in the stools, but other local and systemic signs were mild or absent. Radiography mainly revealed submucosal intramural intestinal gas which was limited to the colon (pneumatosis coli). There was no evidence of small bowel involvement as judged by the absence of small intestinal pneumatosis or distension. This form of colonic disease should be recognized as a benign variety of neonatal necrotizing enterocolitis that carries a favorable prognosis and responds to medical management without sequelae.

Enterocolitis, Pseudomembranous↗
PubMed1989

Severity of necrotizing enterocolitis: influence on outcome at 2 years of age.

The long-term outcome of very low birth weight (VLBW) infants with necrotizing enterocolitis has been reported to be similar to that of other VLBW infants. To examine the influence of disease severity on outcome, the growth and neurodevelopment of survivors of necrotizing enterocolitis were evaluated when the babies were 20 months' corrected age. Between 1975 and 1983, 1506 VLBW infants were admitted to the hospital, and necrotizing enterocolitis developed in 84 (5.6%). Forty infants (48%) survived to be 20 months' corrected age, and complete follow-up data were available for 36. Survivors were classified by modified Bell's criteria into four groups by increasing severity of disease; 13 had mild necrotizing enterocolitis (stage IIA, IIB), and 23 had severe necrotizing enterocolitis (stage IIIA, IIIB). The 36 survivors were compared with 766 surviving VLBW infants without necrotizing enterocolitis. There were no perinatal or socioeconomic differences between groups. Compared with infants with stage II necrotizing enterocolitis at 20 months, infants with stage III necrotizing enterocolitis had a higher rate of subnormal body weight (39% vs 15%) and subnormal head circumference (30% vs 0%). Thirty-three percent of necrotizing enterocolitis survivors had significant neurodevelopmental impairment; the majority of impaired infants (10 of 12) were survivors of stage III necrotizing enterocolitis. These findings highlight the importance of continued evaluations for medical and neurodevelopmental sequelae.

Child Development↗
PubMedDate not supplied

[Pathogenetic concepts of neonatal necrotizing enterocolitis].

The pathogenesis of neonatal necrotizing enterocolitis is still unknown today. Only prematurity has been confirmed as a primary risk factor. Previous studies demonstrated the special pathophysiological conditions in prematurity. Differences in intestinal permeability, blood flow in anemia and hypoxemia, the uptake, transport, delivery and consumption of oxygen, the digestion of carbohydrates and proteins and in intestinal motility between premature and term infants exist. The diving-reflex too is important for intestinal pathophysiology in these patients. The central key of the pathogenesis is the evident vascular damage. Infectious agents, inflammatory mediators, circulatory insufficiency, feeding excess is followed by the initial mucosal damage. This results in an increased intestinal permeability also for inflammatory mediators, endotoxins, bacteria and gas. Ileus, stasis and gas production cause endotoxinemia and abdominal distension. Increased intraluminal pressure with or without activation of inflammatory mediators leads to an important vascular dysregulation. Consecutively these multiple facts cause the "ischemic looking" hemorrhagic necrosis, we call necrotizing enterocolitis.

Acute-Phase Proteins↗
PubMed2005

Patent ductus arteriosus, indomethacin and necrotizing enterocolitis in very low birth weight infants: a population-based study.

BACKGROUND: Patent ductus arteriosus is a risk factor for the development of necrotizing enterocolitis. The use of indomethacin to treat patent ductus arteriosus in preterm infants may either decrease the incidence of necrotizing enterocolitis by stabilizing or closing the ductus arteriosus or increase its incidence by a direct constricting effect on mesenteric blood vessels. The authors sought to evaluate the interrelationship between patent ductus arteriosus, treatment with indomethacin and the risk of necrotizing enterocolitis in very low birth weight infants. METHOD: The Israel National database includes prospectively collected data on 99% of all very low birth weight infants in Israel. The study population comprised 6146 infants of 24-34 weeks' gestation born between 1995 and 2000. The effect of patent ductus arteriosus on necrotizing enterocolitis was assessed using multiple regression analysis. RESULTS: Necrotizing enterocolitis occurred in 5.5% (n = 343) of all infants, in 9.4% of infants with patent ductus arteriosus and in 8.9% of infants who received indomethacin. The occurrence of necrotizing enterocolitis was independently associated with the presence of patent ductus arteriosus among infants not treated with indomethacin (odds ratio, 1.85) and those who received indomethacin therapy (odds ratio, 1.53). Indomethacin therapy in absence of patent ductus arteriosus was not associated with an increased risk of necrotizing enterocolitis (odds ratio, 0.72). CONCLUSIONS: Patent ductus arteriosus is an independent risk factor for the development of necrotizing enterocolitis in very low birth weight infants. Therapy with indomethacin did not have a significant effect on the risk for necrotizing enterocolitis.

Cardiovascular Agents↗
PubMed1992

Role of delayed feeding and of feeding increments in necrotizing enterocolitis.

In spite of a number of studies on necrotizing enterocolitis, there remains controversy concerning prevention regimens, especially with regard to enteral alimentation. This report is of a matched case-control study of the relationship of necrotizing enterocolitis to timing of first feeding, size of feeding volumes and increments, and a risk factor index in 59 case patients with necrotizing enterocolitis and 59 matched control patients. Comparison with control patients showed that case patients were fed earlier, received full-strength formula sooner, and received larger feeding volumes and increments. More highly stressed infants, as measured by the risk index, were more vulnerable to larger feeding increments. Among case patients there was significant correlation of age at first feeding and age at diagnosis (p < 0.0001) even after control for birth weight and risk index score, indicating that delayed feeding was related to delayed onset of disease. These analyses support the theory that earlier, more rapid feeding places stressed infants at greater risk for the development of necrotizing enterocolitis, and that infants with more severe respiratory problems are more vulnerable to such feeding practices.

Birth Weight↗
PubMed1985

Necrotizing enterocolitis: a chronic colonic disease.

While acute necrotizing enterocolitis is a common neonatal condition, the chronicity of the pathologic process is often overlooked. Between 1979 and 1983 at the Foothills Hospital in Calgary, a diagnosis of acute necrotizing enterocolitis was made in 211 infants. Seventeen infants (8%) required urgent surgical treatment in addition to standard medical management. Overall, 206 (98%) infants survived the acute episode. Long-term survival was 92% (194 children). The 12 late deaths were ascribed to chronic cardiovascular, pulmonary and cerebral diseases and "short gut syndrome". Colonic strictures developed in 9% of those treated medically; strictures distal to the mucous fistula developed in 50% of those requiring urgent resection and exteriorization. None of the strictures, which formed between 14 days and 18 months after the diagnosis was made, resolved spontaneously. They tended to be multiple and to involve longer segments in infants who required surgery. Diarrhea prolonged the morbidity in these children. The time course and varied presentation of strictures in this series suggests a rationale for management of infants who survive acute necrotizing enterocolitis.

Chronic Disease↗
PubMedDate not supplied

[Necrotizing enterocolitis in the preterm infant: etiopathogenic considerations].

Necrotizing enterocolitis (NE) represents the most frequent gastrointestinal emergency encountered in neonatal intensive care units. This necrotic-inflammatory bowel disease affects primarily premature patients and it is recorded as an important cause of neonatal morbidity and mortality. The NE aetiology seems to be multifactorial: prematurity, enteral feeding, hypoxia and micro-organisms toxicity are registered as the most important risk factors, able to trigger the phlogistic and necrotic way at the basis of necrotizing enterocolitis. Despite the NE first report was in the past century, the correct pathogenic sequence of this neonatal disease is still hypothetical.

Enteral Nutrition↗
PubMedDate not supplied

[Necrotizing enterocolitis: a 12-year retrospective study].

UNLABELLED: Necrotizing enterocolitis (NEC) is the most relevant intestinal acquired complication during the neonatal period. Due to the improvements in perinatal medicine during the last decade, we wanted to work out possible differences in the incidence, diagnosis and clinical courses of NEC during a 12 years period. PATIENTS AND METHODS: All premature or term newborns were eligible for the study, if a necrotizing enterocolitis > or = stage 2a according to Bell was diagnosed between January 1980-December 1991. RESULTS: During the study period, 90 preterm or term newborns were treated for necrotizing enterocolitis, 19 infants were admitted to our hospital for therapy of established NEC from other hospitals. Forty-five infants had a birthweight of < or = 1500 g. During the years 1987-1991 there was an increase in the incidence (4-12/year, median 9/year, compared to 0-6, median 3/year during the period 1980-1986). This was paralleled by an increase in very low birthweight infants admitted to the NICU (1980-1986: 35-45/year, 1987-1991: 83-108/year). Prominent clinical signs: abdominal distension (85 infants), increased gastric residuals (72), bright blood from rectum (56). Median time of manifestation in infants < or = 30 weeks was 17 days, for infants of 31-34 weeks 8 days and for infants of > or = 35 weeks of gestation 4 days. Eleven infants were fed parenterally exclusively before NEC, 12 infants received exclusively breast milk, 67 formula. Surgical treatment was indicated in 51 infants (indication: intestinal perforation or peritonitis diagnosed by abdominal paracentesis). Seventy-one infants survived, in 17 infants who died, NEC or secondary disorders were the main cause. CONCLUSION: With increasing numbers of very preterm infants, the relevance of NEC becomes more and more important. Concepts of prevention and early diagnosis further have to be worked out.

Birth Weight↗