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PubMed1994

Epidemiology of necrotizing enterocolitis.

Necrotizing enterocolitis (NEC) is a worldwide problem that has emerged in the past 25 years as the most common gastrointestinal emergency in neonatal intensive care units (NICU). In the United States the incidence ranges from 1 to 7.7% of NICU admissions. Ninety percent of the patients are premature infants. Mucosal injury, bacterial colonization and formula feeding are the three major pathogenetic factors that have been documented in most infants who have developed NEC. However, NEC may develop only if a threshold of injury, imposed by the coincidence of at least two of three events (intestinal ischemia, pathogenic bacteria, and excess of protein substrate) is exceeded. Immunological immaturity of the gut in premature babies may represent the crucial risk factor.

Enterocolitis, Pseudomembranous↗
PubMed1987

Delta-like toxin produced by coagulase-negative staphylococci is associated with neonatal necrotizing enterocolitis.

Necrotizing enterocolitis (NEC) is a serious neonatal disorder of uncertain cause, although fecal bacteria have been implicated in some outbreaks. We examined coagulase-negative staphylococci (CONS) as possible etiologic agents. In our unit, CONS colonized the bowels of most infants studied, including 46% of 70 NEC cases (mean concentration, 10(9.1) CFU/g of stool). Over 90% of tested isolates produced a hemolysin resembling delta toxin of Staphylococcus aureus. Toxin purified from a NEC-associated isolate of Staphylococcus epidermidis resembled reference delta toxin from S. aureus in size, biologic properties, and antigenicity. This delta-like toxin was enteropathic, causing mucosal necrosis and hemorrhage in injected loops of the bowels of infant rats. Adjacent, nonexposed bowel remained normal, as did loops injected with lecithin-neutralized toxin. Using a new enzyme-linked immunosorbent assay (ELISA), we detected delta-like toxin in the stools of 11 of 35 infants colonized with CONS positive for delta-like toxin (Tox+). Positive tests were strongly associated with NEC. Of 18 cases with Tox+ CONS, 10 were positive (56%), whereas only 1 of 17 control infants so colonized was positive (6%, P = 0.002). In NEC patients, the mean fecal toxin concentration was 1,012 ng/g. Toxicity to fibroblasts was demonstrable in filtrates of each of six ELISA-positive samples tested but was absent in all five ELISA-negative samples tested. We conclude that delta-like toxin is elaborated in the bowels of some infants with Tox+ CONS, and its association with NEC suggests that such CONS are enteropathic. In our unit, this mechanism was apparent in 23% of 44 recent cases of endemic NEC.

Bacterial Toxins↗
PubMed1988

SOD prevents damage and attenuates eicosanoid release in a rabbit model of necrotizing enterocolitis.

Necrotizing enterocolitis (NEC) was produced in anesthetized rabbits by transmural injection of intestinal loops with an acidified solution of casein and calcium gluconate, mimicking the luminal milieu of afflicted neonates. Intravenous infusion of superoxide dismutase (SOD) 15 min after NEC induction prevented intestinal damage. In ex vivo perfused intestinal loops, we determined the sites of eicosanoid release and their contribution to the vascular effects of N-formyl-methionyl-leucyl-phenylalanine (fMLP) and platelet-activating factor (PAF) in damaged and SOD-salvaged intestine. The vascular effluent was the primary site of stimulated eicosanoid release. The vascular responses to fMLP (vasoconstriction) and PAF (vasodilation) were not altered by SOD, although vascular resistance was higher in the SOD group. SOD treatment attenuated 1) transmural fluid shifts in ex vivo perfused intestinal preparations, an index of vascular permeability, 2) fMLP-induced prostaglandin E2, 6-ketoprostaglandin F1 alpha (6-keto-PGF1 alpha), and leukotriene B4 (LTB4) release, and 3) PAF-induced release of 6-keto-PGF1 alpha and LTB4. Stimulated thromboxane B2 release was not altered by SOD. Thus NEC can be established by a luminal insult that causes local generation of free radicals and exaggerated release of prostaglandins and leukotrienes.

6-Ketoprostaglandin F1 alpha↗
PubMed1996

Escherichia coli transcytosis in a Caco-2 cell model: implications in neonatal necrotizing enterocolitis.

Necrotizing enterocolitis (NEC) is a serious gastrointestinal disorder of preterm infants. Other than an association with prematurity and gastrointestinal feeding, no single factor or mechanism has been consistently linked to this disease. We have previously demonstrated that Escherichia coli isolates obtained from the stool of infants with NEC caused NEC-like injury in a weanling rabbit ileal loop model; this injury, in turn, could be blocked by coinfection with selected Gram(+) bacteria (Enterococcus faecium) isolated from asymptomatic controls. Using Caco-2 cells in a trans-well system, we now demonstrate that the same E. coli isolates can cross epithelial cell monolayers in the absence of ultrastructural change or damage. These results with E. coli contrast with those seen with Salmonella typhimurium, which passed through the monolayer at a higher rate and were associated with striking ultrastructural damage. Transcytosis of E. coli was reduced 3-5-fold in the presence of E. faecium previously shown to block NEC-like injury in the loop model. There was a mild increase in the rate of E. coli transcytosis when studies were conducted with younger, undifferentiated cells; these immature cells had no brush border, had decreased production of brush border-specific enzymes, but retained well defined tight junctions, as demonstrated by transepithelial electrical resistance and electron microscopy. A further reduction/ complete blockage of E. coli transcytosis was observed when E. faecium was used as the coinfectant in studies with these undifferentiated cells. We hypothesize that the ability of E. coli to cross epithelial cell layer is a critical initial step in the cascade of events which lead ultimately to NEC; blockage or reduction in E. coli transcytosis in the presence of certain Gram(+) organisms may play a significant role in prevention of NEC.

Analysis of Variance↗
PubMedDate not supplied

Role of asphyxia and feeding in a neonatal rat model of necrotizing enterocolitis.

Necrotizing enterocolitis (NEC) is a common gastrointestinal disorder affecting premature infants. To investigate critically the importance of the purported risk factors of NEC (formula feeding, asphyxia, bacteria, and prematurity), we developed a neonatal rat model that closely mimics the human disease. Full-term and premature newborn rats were stressed with formula feeding, asphyxia, and/or exogenous bacterial colonization and subsequently evaluated grossly and histologically for the development of intestinal injury. We found that most animals treated with asphyxia, formula feeding, and bacteria developed NEC (77%) and died (86%) by 96 h. All maternally fed animals treated with asphyxia and bacterial colonization survived and had normal intestinal histology. Furthermore, asphyxia was a critical instigating factor, because formula and bacterial exposure without asphyxia resulted in normal intestine and minimal mortality (12%). Enteral bacterial colonization was not a significant determinant of NEC in this model. We conclude that the neonatal rat model is an excellent test system for the study of NEC. As in the human disease, asphyxia and formula feeding play an important role in the pathophysiology of experimental NEC.

Animal Nutritional Physiological Phenomena↗
PubMedDate not supplied

[Neonatal necrotizing enterocolitis].

Necrotizing enterocolitis (NEC) is an extremely severe clinical entity in whose pathogenesis at least two of the following factors are involved: intestinal ischaemia, pathogenic bacterial colonization and excessive substrate in the intestinal contents. Common risk factors are prematurity, rapid increase of feeding volume, polycythemia and perinatal asphyxia. Clinical features are abdominal distention, gastric retention, bloody stools and intestinal wall pneumatosis; while its complications are bowel perforation, peritonitis and shock. Early diagnosis allows prompt medical treatment based upon intestinal rest, no oral feeding, parenteral hydration and nutrition, nasogastric intubation, broad spectrum antibiotics and close surveillance. Surgery is kept to treat complications. Prevention includes feeding with human milk in prematures with slow increase of partial and total volumes, early initial fastening in cases of asphyxia and careful and close surveillance of high-risk newborns.

Enterocolitis, Pseudomembranous↗
PubMed1988

[Etiopathogenic factors in neonatal necrotizing enterocolitis].

Necrotizing enterocolitis is the most common digestive emergency in neonatal units. Several factors are involved in their pathogenesis: intestinal ischemia, bacterial colonization and feeding. To analyse these factors, 25 cases of NEC are compared to a control group of 48 newborns. Results showed an incidence of NEC about 1.6 0/00 live newborns, without a greater mortality in respect to other pathologic newborns. Ischemic factors influence significatively in appearance of ECN (p less than 0.001). None of them received maternal feeding. By this reason it seems to be a protective factor against bottle feeding (p less than 0.05). Enteral feeding its main influence upon mature newborns. No common bacterial findings have been found, but 68% of children developed clinical findings compatible with sepsis. Severity of abdominal sings in clinical examination in the acute phase of NEC is positively correlated with the presence of complications. Individual considerations are needed in sight to the different severity and prognosis of NEC.

Breast Feeding↗
PubMed1986

The role of paracentesis in the management of infants with necrotizing enterocolitis.

Necrotizing enterocolitis (NEC) is the single most common surgical emergency of the newborn. Yet the indications for surgery in NEC are still not clearly established. Pneumoperitoneum is an absolute indication for surgery. A paracentesis indicative of intestinal gangrene, prior to intestinal perforation, has also been proposed as an indication for surgery. A prospective study was conducted to answer two questions: 1) How accurate and safe is paracentesis in detecting bowel necrosis in neonates with NEC? and 2) Do infants with NEC who are operated on for a positive paracentesis have a decreased morbidity and mortality over those operated on for pneumoperitoneum? Between July 1980 through June 1984, 39 infants with definite NEC and without pneumoperitoneum underwent a paracentesis because of suspected bowel necrosis. There were no false "positive" taps. There were 34 "positive" taps in 36 infants who were proven to have bowel necrosis, for an accuracy of 94 per cent. There were two false "negative" taps (40%) and three true "negative" taps (60%). There were no complications related to the procedure. During this same time period, 68 infants with NEC were operated upon. The indication for surgery was pneumoperitoneum in 29, a "positive" paracentesis in 34, and other reasons in 5. A comparison was made between those operated upon for pneumoperitoneum and those operated upon for a "positive" paracentesis. There was no significant difference in survival between the two groups (76% versus 71%). The early and late complications and the causes of death in each group were similar. A positive paracentesis is a valid objective indication for operation in infants with NEC.(ABSTRACT TRUNCATED AT 250 WORDS)

Abdomen↗
PubMed1984

Surgical treatment of necrotizing enterocolitis.

Necrotizing enterocolitis (NEC) is a serious problem in nurseries for premature infants and neonatal intensive care units, with a high incidence of morbidity and mortality. During the 5-year period 1973-77, 86 infants with NEC were treated at the University of Iowa Hospitals and Clinics; 43 of them underwent surgery and 43 were treated medically. The surgical candidates were more seriously ill, and their survival rate was 42% compared with 63% for those treated conventionally. Early diagnosis and aggressive surgical treatment of NEC may decrease or even prevent the severity of life-threatening complications.

Abdomen↗
PubMed1995

Necrotizing enterocolitis.

Necrotizing enterocolitis (NEC) is a disease characterized by ischemia and necrosis of the gastrointestinal tract frequently leading to perforation of the intestine. It occurs primarily in the premature infant and is a major cause of mortality and morbidity in the low birth weight infant. Careful nursing and medical care can greatly reduce the incidence and severity of this disease, thus decreasing both the associated morbidity and mortality. This article reviews the pathophysiology, diagnosis, and treatment of NEC; presents a case study; and provides a nursing care plan for treatment of this disease.

Enterocolitis, Pseudomembranous↗
PubMed1993

[Necrotizing enterocolitis].

Necrotizing enterocolitis (NEC) is an important cause of neonatal morbidity and mortality. During the last few years, there was an increase in the incidence of this disease, associated with a better knowledge of NEC, and an increase in survival rate, associated with the development, even from a technological point of view, of neonatal intensive care units. In this study, the authors first perform the diagnostic procedures and describe the anatomical and clinical characteristics of NEC, then evaluate by standard criteria a series of patients observed during the last 5 years, revising the various surgical treatments adopted and the results obtained.

Colon↗
PubMed1996

A review of evidence for a role of magnesium and possibly copper deficiency in necrotizing enterocolitis.

Necrotizing enterocolitis (NEC) is a neonatal disorder of unknown cause characterized by rapid necrosis of the bowel, primarily the ileum and colon. It is a worldwide problem. NEC is the most common gastrointestinal emergency in the neonatal intensive care unit, and ranks second as a cause of neonatal death. The incidence of NEC is inversely proportional to the birth weight and the degree of maturity. Infants born at or before 28 weeks gestational age have not received 80 per cent of the magnesium and 67 per cent of the copper found at term. Congenital deficiencies of these essential minerals may be compounded by high renal or gastrointestinal losses and high metabolic demand during the preterm infant's accelerated growth. Platelet thrombi appear early in the intestinal microvasculature in NEC. Platelet thrombosis and release of vasoconstrictor, platelet aggregating thromboxane A2 (TXA2) in human NEC appears to potentiate the intestinal ischaemia and necrosis in neonates who develop NEC. Magnesium and copper deficiency each enhance the synthesis of TXA2. Plasma levels of the inflammatory cytokines tumour necrosis factor (TNF) and interleukin-6 (IL-6) are increased in NEC and in magnesium deficiency; these experimentally produce shock and tissue injury, especially of the intestine. The synthesis of the potent vasoconstrictor endothelin is increased in magnesium deficiency. NEC has been regarded as a luminal insult that causes local generation of destructive oxygen free radicals. Tissues from animals deficient in magnesium are more susceptible to oxidative injury and lipid peroxidation than tissues from normal animals. Magnesium and copper deficiency impair antioxidant defence through decreased synthesis of glutathione and reduced activity of Cu/Zn superoxide dismutase, respectively. Although the aetiology of NEC is unknown, there appears to be sufficient data to implicate magnesium and possibly copper deficiencies in the pathogenesis. Consequences of deficiency of one or both minerals may include increased synthesis or activity of injurious mediators: IL-1, IL-6, TNF, TXA2, endothelin, and oxygen free radicals. A prospective trial of magnesium supplementation, but not copper supplementation, in very premature neonates can be recommended, with NEC as one of the outcome measures.

Copper↗
PubMed1994

Pseudomembranous enterocolitis and hemorrhagic necrotizing enterocolitis in Hirschsprung's disease.

From 1977 to 1991, we encountered 67 patients with Hirschsprung's disease and 14 of them developed enterocolitis, with 3 cases being fatal. Enterocolitis occurred preoperatively in 12 infants, as well as after ileostomy in one and after a pull-through procedure in another. Seven infants had severe enterocolitis, including three with pseudomembranous enterocolitis and four with hemorrhagic necrotizing enterocolitis. Enterocolitis in Hirschsprung's disease mainly occurs due to intestinal obstruction and ischemia; however, in some cases, Clostridium difficile overgrowth and its toxin also appears to be related to severe pseudomembranous enterocolitis. In severe enterocolitis, antibiotics and enterostomy often prove to be ineffective, and thus an early resection of the affected bowel appears to be necessary. Moreover, when the aganglionic segment extends to the small bowel, severe enterocolitis tends to occur in the aganglionic intestine even after performing an enterostomy, and a resection of the aganglionic bowel is therefore recommended to allow for adequate lavage of the segment distal to the enterostomy site.

Enterocolitis, Pseudomembranous↗
PubMed1995

[A pathological comparison between Hirschsprung's enterocolitis and neonate necrotizing enterocolitis].

Autopsy records of 9 cases of neonate Hirschsprung's enterocolitis (HD) and 16 cases of neonate necrotizing enterocolitis (NEC) were analysed. It was found that the NEC lesions were more extensive than HD lesions, the bleeding and inflammation in NEC were also more serious than in HD. From our 21 animal experiments in which we tried to clarify the pathogenesis of Hirschsprung's enterocolitis and NEC, our preliminary hypothesis fro the development of Hirschsprung's enterocolitis being: the distal segment was first obstructed, causing the proximal segment to expand, the increase of pressure within the bowel resulted in ischemia of the intestines, increased bacterial multiplication in the retained feces and bacterial infiltration of the intestinal mucosa. The above being the major cause of HD. When the neonate is in asphyxia or shock, ischemia of the intestines and immunoallergic reactions occur, due to the lack of IgA in the mucosa, the multiplication and infiltration of pathogenic enterobacteria in the intestinal wall results in NEC.

Animals↗
PubMed2005

Sonographic evaluation of neonates with early-stage necrotizing enterocolitis.

BACKGROUND: Necrotizing enterocolitis (NEC) is the most common gastrointestinal emergency in neonatal intensive care units. Ultrasonographic findings in early-stage NEC have not been described. OBJECTIVE: To assess the diagnostic value of ultrasonography for the diagnosis and monitoring of patients with NEC. MATERIALS AND METHODS: We evaluated the sonographic findings of early stages of NEC in 40 neonates who were clinically diagnosed with NEC when they were 2-28 days old. Their average gestational age was 32 weeks, and their mean weight was 1,850 g. All of the patients showed signs of bowel distention on abdominal radiography, with no evidence of pneumatosis intestinalis. We performed bowel sonography in all patients (n = 40), as well as in ten healthy neonates who served as a control group. The studies were conducted with a 10-MHz linear transducer from February 2003 to January 2004. We evaluated the echogenicity of the bowel wall, involved region, ascites, and portal venous gas at both initial and follow-up examinations. We divided the patients into two groups according to the bowel wall echogenicity pattern, group I with echogenic dots in the bowel wall and group II with dense granular echogenicities in the bowel wall. In order to identify any correlations between the ultrasonography and clinical findings, we evaluated the duration of parenteral feeding (NPO) in each group and compared two groups by means of a statistical analysis (Mann-Whitney test). RESULTS: All of the neonates in the control group (n = 10) presented normal bowel wall echogenicity; the patients with NEC presented echogenic dots in 16 patients (40%) and dense granular echogenicities in 24 patients (60%). Portal venous gas was absent in all patients. On the follow-up examinations, the echogenicity of the bowel wall and ascites decreased in 37 patients (93%). The duration of NPO was 11.1 +/- 6.6 days in group I and 16.5 +/- 7.2 days in group II (P < 0.05). CONCLUSION: Echogenic dots or dense granular echogenicities in the bowel wall can be seen in patients with early-stage NEC. Bowel sonography can be helpful for the early diagnosis and monitoring of patients with NEC.

Enterocolitis, Necrotizing↗
PubMed2004

Too much short chain fatty acids cause neonatal necrotizing enterocolitis.

Nenatal necrotizing enterocolitis (NEC) is a disease mainly affects premature infants. It is well known that prematurity, enteral formula feeding, and bacterial colonization are three major risk factors for NEC. Acetic acid, propionic acid and butyric acid are short chain fatty acids (SCFAs), which are produced mainly in the colon by bacterial fermentation of undigested carbohydrates. Although luminal production of modest quantities of SCFAs is essential for normal colonic mucosal function, excessive production/accumulation of SCFAs may arise in premature infants due to increased luminal carbohydrates malabsorption and poor gastrointestinal motility, and may have deleterious effects on mucosal integrity. Therefore, it is proposed that too much luminal short chain fatty acids cause neonatal NEC.

Animals↗
PubMed2005

Severe thrombocytopenia predicts outcome in neonates with necrotizing enterocolitis.

OBJECTIVE: Necrotizing enterocolitis (NEC) is a common and serious gastrointestinal disorder that predominately affects premature infants. Few prognostic indices are available to guide physicians through the expected course of the disease. We hypothesized that the degree and timing of onset of severe thrombocytopenia (platelet count <100,000/mm(3)) would be a predictor of adverse outcome and an indication for surgical intervention in infants with NEC. STUDY DESIGN: The clinical presentation and outcome of all infants with Bell stage II or III NEC treated at Texas Children's Hospital between 1997 and 2001 were retrospectively reviewed. Patients were stratified into two groups based on the presence (Group1) or absence (Group 2) of severe thrombocytopenia (platelet count <100,000/mm(3)) within 3 days of a diagnosis of NEC. Differences between groups were compared using logistic regression to estimate adjusted odds ratios. RESULTS: A total of 91 infants met inclusion criteria (average birth weight 1288+/-135 g; average gestational age 29.0+/-3.0 weeks). Compared to infants in Group 2, infants in Group 1 were more premature (28.0+/-4.1 vs 30.0+/-4.2 weeks; p=0.02), more likely to have received postnatal steroids (42.5% vs 20.4%; p=0.02), and more likely to require laparotomy for gangrenous bowel (adjusted OR 16.33; p<0. 001). The presence of severe thrombocytopenia was also a predictor of mortality (adjusted OR 6.39; p=0.002) and NEC-related gastrointestinal complications including cholestatic liver disease and short bowel syndrome (adjusted OR 5.47; p=0.006). CONCLUSION: Severe thrombocytopenia within the first 3 days after a diagnosis of NEC suggests a higher likelihood of bowel gangrene, morbidity, and mortality. Prospective studies of infants with early and severe thrombocytopenia may help determine the optimal timing of laparotomy in infants with NEC.

Enterocolitis, Necrotizing↗
PubMed2005

Role of epidermal growth factor in the pathogenesis of neonatal necrotizing enterocolitis.

Neonatal necrotizing enterocolitis (NEC) is an increasingly frequent condition encountered in premature infants for which the etiology is not well understood. Epidermal growth factor (EGF) is abundant in many fluids bathing the fetal and neonatal gastrointestinal tract, including amniotic fluid, saliva, and breast milk. EGF is acknowledged to be important for normal intestinal development as well as repair following injury to the gastrointestinal mucosa. There appears to be mounting evidence to support a possible link between deficient EGF production and the development of NEC. The relevant evidence for the role of EGF in intestinal development and mucosal repair, as well as its potential involvement in the genesis of NEC will be reviewed.

Animals↗