Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Necrotizing enterocolitis”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 91 records · Page 5Linked to original sources
PubMed2002

[Diagnosis and characteristics of the clinical course of necrotizing enterocolitis in children].

Necrotizing enterocolitis (NEC) is a disease of unknown etiology affecting mainly premature newborns and occurring in about 1 to 7% of all admissions to neonatal intensive care units. Among the greatest problems is the early diagnosis and adequate and timely treatment, surgery included. In the last quarter of the century the survival rate of premature infants was gradually increasing in national regions and worldwide and accordingly there is an increasing number of babies with NEC. To date, to treat patients with the diagnosed enterocolitis is a complicated problem. The mortality rate among the children remains high. In the period from 1978 to 2000 432 patients with NEC were admitted to the St. Petersburg Center of Neonatal Surgery in the Children Hospital N 1,300 of them requiring surgical interventions. The author's personal experience with the diagnosis and treatment of the disease allowed three main forms of the clinical course of the disease to be established: superacute, acute and subacute.

Critical Care↗
PubMedDate not supplied

Neonatal necrotizing enterocolitis: a focus on.

Necrotizing enterocolitis (NEC) is a multifactorial worldwide problem, representing the most frequent gastrointestinal emergency in neonates. Extremely common in preterm infants, it is also registered in fullterm low birth weight neonates. Despite extensive research, its etiopathogenesis is not completely understood and this neonatal disease remains associated with high morbidity and mortality rates. This review proposes an interdisciplinary focus on recent developments in NEC etiopathogenesis, diagnosis and management.

Enteral Nutrition↗
PubMed1977

[Necrotizing enterocolitis (pediatric review)].

Necrotizing enterocolitis--a highly letal disease in the newborn period--is diagnosed in about 1--2% of the admissions to a nursery. The marcroscopic lesions are basically necroses predominantly found in the ileum, colon and jejunum. Untreated they lead to perforation, peritonitis and sepsis. The predisposing factors include such as perinatal complications, immaturity and umbilical vein catheterization; the main symptoms are bile stained vomiting and blood-streaked diarrhea, followed by signs of fulminant sepsis and peritonitis. The most typical roentgenographic findings are intramural air (pneumatosis intestinalis) and in more advanced cases pneumoperitoneum (free peritoneal air) and portal vein gas. The current plan of management--consisting of immediate withdrawal of oral feeds, gastric suction, intravenous fluid therapy, treatment of shock and administration of antibiotics--and the indication for operation are discussed. Perinatal stress and secondary bacterial invasion of the intestinal lesions seem to play an important role in the etiology of the disease. An early nutrition of the healthy immature with human breast milk seems to reduce the incidence of necrotizing enterocolitis or at least has a mitigating influence on the later course of the disease. The mortality in our own series--as reported--was high (6 patients: 1 survivor, mortality: 83%) as 4 of the patients were admitted with gross symptoms of intestinal perforation and severely shocked.

Disseminated Intravascular Coagulation↗
PubMed2006

Laparotomy versus peritoneal drainage for necrotizing enterocolitis and perforation.

BACKGROUND: Perforated necrotizing enterocolitis is a major cause of morbidity and mortality in premature infants, and the optimal treatment is uncertain. We designed this multicenter randomized trial to compare outcomes of primary peritoneal drainage with laparotomy and bowel resection in preterm infants with perforated necrotizing enterocolitis. METHODS: We randomly assigned 117 preterm infants (delivered before 34 weeks of gestation) with birth weights less than 1500 g and perforated necrotizing enterocolitis at 15 pediatric centers to undergo primary peritoneal drainage or laparotomy with bowel resection. Postoperative care was standardized. The primary outcome was survival at 90 days postoperatively. Secondary outcomes included dependence on parenteral nutrition 90 days postoperatively and length of hospital stay. RESULTS: At 90 days postoperatively, 19 of 55 infants assigned to primary peritoneal drainage had died (34.5 percent), as compared with 22 of 62 infants assigned to laparotomy (35.5 percent, P=0.92). The percentages of infants who depended on total parenteral nutrition were 17 of 36 (47.2 percent) in the peritoneal-drainage group and 16 of 40 (40.0 percent) in the laparotomy group (P=0.53). The mean (+/-SD) length of hospitalization for the 76 infants who were alive 90 days after operation was similar in the primary peritoneal-drainage and laparotomy groups (126+/-58 days and 116+/-56 days, respectively; P=0.43). Subgroup analyses stratified according to the presence or absence of radiographic evidence of extensive necrotizing enterocolitis (pneumatosis intestinalis), gestational age of less than 25 weeks, and serum pH less than 7.30 at presentation showed no significant advantage of either treatment in any group. CONCLUSIONS: The type of operation performed for perforated necrotizing enterocolitis does not influence survival or other clinically important early outcomes in preterm infants. (ClinicalTrials.gov number, NCT00252681.).

Birth Weight↗
PubMed2004

Damage control laparotomy for generalized necrotizing enterocolitis.

Macroscopic generalized necrotizing enterocolitis (G-NEC) is associated with a very high mortality in neonates. In some instances, however, multiple bowel segments are necrotic, with most of the remaining small bowel damaged but viable. In these selected patients morbidity can be reduced and survival increased with an aggressive and early surgical approach. We have termed this approach damage control laparotomy (DCL). Over a 5(1/2)-year period, all neonates with G-NEC with adequate length of viable small bowel were subjected to DCL. The procedure is characterized by a resuscitative period of a few hours followed by laparotomy and resection of dead/perforated bowel. The bowel ends are either anastomosed or tied, and the bowel is returned to the abdomen to allow full tissue demarcation. Re-look laparotomy is performed 3-4 days later, at which time any new necrotic bowel is excised and re-joined, to achieve small bowel continuity. In this prospective study, 104 neonates with G-NEC underwent operation; 27 neonates (26%) were considered to have an adequate potential length of viable bowel and were selected for DCL. Nineteen neonates survived in the follow-up period. Early mortality was due to sepsis syndrome in 6 patients, and late mortality in 2 neonates was secondary to the short bowel syndrome. The DCL procedure is another step toward improving survival in surgical G-NEC; this technique avoids proximal stomas and their complications, and at the same time it preserves the best possible bowel length.

Anastomosis, Surgical↗
PubMed2000

Multiple spontaneous small bowel anastomosis in premature infants with multisegmental necrotizing enterocolitis.

BACKGROUND/PURPOSE: Fulminant necrotizing enterocolitis (NEC) may result in extensive bowel necrosis. Resection of involved segments may result in short bowel syndrome. Multiple stomas result in complications and further loss of intestinal length with closure. METHODS: Two patients with extensive multisegmental NEC were treated with an intraluminal stent without anastomosis. All necrotic intestine was resected and the remaining viable intestine was lined up over a feeding tube without anastomosis of the intestinal segments. One patient had a diverting jejunostomy and mucous fistula with the tube used to orient the defunctionalized intervening intestinal segments. The second patient had the bowel left in continuity with the tube brought into the jejunem proximal to the first area of resection and distally brought out through the tip of the appendix. Both tubes were brought through the abdominal wall and secured in a loop. RESULTS: Contrast study findings showed that the intestinal segments had auto-anastomosed. In the first case the tube was left in place and intestinal continuity was restored. The patient is now 4 years old and takes full enteral feeds. The latter patient had the enterostomy tube removed at the time of the contrast study, but only tolerated partial feedings and died at 1 year of total parenteral nutrition-related liver failure. CONCLUSION: The technique eliminates nonviable bowel, maximizes length, avoids multiple stomas, and may help avoid reoperation.

Digestive System Surgical Procedures↗
PubMed1977

Necrotizing enterocolitis after cardiac surgery: a local ischemic lesion?.

Necrotizing enterocolitis continues to be a perplexing problem in the newborn and, in particular, the premature. Its pathogenesis is controversial, although there are well established clinical risk factors. Three patients had necrotizing enterocolitis while under close clinical observation and monitoring, despite the fact that these patients were not at high risk for necrotizing enterocolitis. All three had necrotizing enterocolitis after hypothermia and total circulatory arrest--a complication which until now has not been reported. Because of the close monitoring, these patients provide a unique clinical setting which eliminates most of the etiologic factors that have been implicated in the pathogenesis of necrotizing enterocolitis. The onset of necrotizing enterocolitis shortly after total circulatory arrest and the selective ischemic organ damage observed suggest local perfusion inadequacy. The authors postulate that splanchnic vasoconstriction as a result of marked sympathetic stimulation contributes to this local ischemia and subsequent necrotizing enterocolitis.

Cardiac Surgical Procedures↗
PubMed2003

Enteral glutamine supplementation and dexamethasone attenuate the local intestinal damage in rats with experimental necrotizing enterocolitis.

The pathogenesis of necrotizing enterocolitis (NEC) presumptively is due to an inappropriate intestinal epithelial immunologic response of immature gut to luminal stimuli. Glutamine is essential for intestinal crypt cell proliferation and enhances the cellular response to growth factors. We aimed to test the hypothesis that the supplementation of enteral feedings with glutamine may stimulate an immature intestine and decrease the intestinal inflammatory change in NEC. Immediately after birth, the neonatal rats were weighed and randomized into one of four treatment groups. Group 1 consisted of rats whom were breast-fed. Group 2 (NEC group) consisted of neonates whom were fed with a special rodent formula. Rats in groups 3 and 4 were fed in a similar fashion to those in group 2, and glutamine 0.3 mg/kg per day and dexamethasone 0.5 mg/kg per day were added to their formula, respectively. The neonatal rats were weighed and killed on day 4: the last 4 cm of terminal ileum was harvested for morphological studies and detection of nitrite and nitrate levels in tissue. The animals in the NEC group showed various degrees of inflammatory changes similar to clinical NEC. The inflammatory changes of the intestine appeared to be attenuated in both glutamine- and steroid-treated animals compared to those in the NEC group. Only steroid treatment decreased the tissue levels of these nitrogen oxides that were increased in rats in the NEC group. We herein provide evidence that maturational agents such as glutamine and dexametasone can attenuate the local intestinal inflammatory damage in experimental NEC. These findings support the hypothesis that the gut immaturity in premature infants represents a risk factor for NEC.

Amino Acids↗
PubMed2003

Early full blood count and severity of disease in neonates with necrotizing enterocolitis.

Thrombocytopaenia occurs during necrotizing enterocolitis (NEC), and nadir platelet count is associated with extent of disease. In paediatric meningococcal disease, the product of neutrophil and platelet count at admission is prognostically useful. We therefore aimed to determine whether the first full blood count (FBC) after diagnosis of NEC is useful as a score for poor outcome and severity of disease. Between 1987 to 2001, neutrophils (N), platelets (P) and their product (PN) was available in 187 neonates treated for NEC at our institution. Neonates with NEC were grouped according to the extent of disease (no gangrene, focal, multifocal and pan-intestinal). Data were not normally distributed so Mann-Whitney U test or analysis of variance (ANOVA) on logged data were used ( p<0.05 was considered significant). Receiver operating characteristics (ROC) curves were used to examine the relationship between specificity and sensitivity. A perfect test would have an ROC curve area of 1. Initial P count and PN product of non-survivors were both significantly lower than in survivors ( p<0.0001), whereas N was not different ( p<0.08). Low Log(10)PN was significantly associated with greater extent of disease (ANOVA; no gangrene vs multifocal, p<0.01, vs panintestinal, p<0.0005), suggesting that the initial FBC could be prognostically useful. Area under the ROC survival curve for neutrophils was 0.58, for platelets 0.75 and for PN product 0.71; thus, although no test performed extremely well, initial platelet count and NP product could be useful in evaluating disease severity in neonates with NEC and for further monitoring.

Blood Cell Count↗
PubMed2003

Hematologic abnormalities in severe neonatal necrotizing enterocolitis: 25 years later.

Necrotizing enterocolitis (NEC), the most common surgical emergency in newborns, remains a therapeutic challenge for clinicians. The hematological manifestations associated with NEC were first described 25 years ago. This review discusses current knowledge of the pathophysiology involved in disturbances in megakaryocytopoiesis, coagulation, leukopoiesis, and erythropoiesis that accompany the clinical entity NEC. The discussion includes current understanding of and potential strategies for treating the hematopoietic disturbances that occur secondary to NEC.

Enterocolitis, Necrotizing↗
PubMed2005

Intestinal innate immunity: how does it relate to the pathogenesis of necrotizing enterocolitis.

The pathogenesis of necrotizing enterocolitis (NEC) is poorly understood, but appears to be multifactorial and highly associated with immaturity of the gastrointestinal tract, colonization of the intestinal microbiota, and immature innate immune system. The goal of this review is to provide an overview of some of these risk factors and how they might lead to the genesis of NEC. A better understanding of these factors should help us prevent and treat this devastating disease.

Enterocolitis, Necrotizing↗
PubMedDate not supplied

Necrotizing enterocolitis: pathophysiology and prevention.

Necrotizing enterocolitis (NEC) is the most common gastrointestinal emergency in the neonatal intensive care unit. It is a disease of medical progress in that more very low-birth-weight neonates are surviving than ever before and are thus susceptible to this potentially devastating disease. NEC received very little attention in the literature before the 1970s but now is well known to all neonatologists and pediatric surgeons. The 1500 to 2000 infants that die every year from this disease in the United States and the large number of infants who develop short gut syndrome from this disease only represent the tip of the iceberg of the problems NEC causes. The widespread fear of NEC among neonatologists and pediatric surgeons has contributed in large part to the use of the IV route rather than the gastrointestinal tract for nourishing these infants for relatively long periods. The consequences of this include a high incidence of sepsis, high hospital costs, and potential long-term neurodevelopmental disability because of poor nutrition during a very vulnerable period of growth and development. The purpose of this review is to provide a brief overview of the clinical presentation and current treatment for NEC, then provide a discussion of the pathophysiology on which strategies for prevention can be formulated.

Enteral Nutrition↗
PubMed2003

Serum cytosolic beta-glucosidase activity in a rat model of necrotizing enterocolitis.

The diagnosis of necrotizing enterocolitis (NEC) is made from a combination of clinical and radiographic findings. There are no useful screening biochemical markers of intestinal injury. The serum concentration of cytosolic beta-glucosidase (CBG), an enzyme found primarily in enterocytes, is markedly elevated in animal models of ischemia and bowel obstruction. We hypothesized that in a rat model of NEC, serum CBG activity would significantly increase before microscopic evidence of severe intestinal injury. Cohorts of 2-wk-old Sprague-Dawley rats (n = 10/cohort) were anesthetized and underwent laparotomy with occlusion of the superior mesenteric artery (SMA). Platelet-activating factor (200 microg/animal) was injected in the proximal duodenum. Serum and intestinal samples were obtained at time 0 (control) and 30, 60, and 90 min of ischemia (I) and after 90 min of I followed by 60 min of reperfusion (I/R). Histopathologic injury was categorized as either no or minimal injury or mural necrosis by two masked investigators and CBG activity was measured by ELISA. Data were analyzed with Fisher's exact test and ANOVA. Only the I/R group had significantly greater mural necrosis compared with the control group (90% versus 0%, respectively, p < 0.001). In contrast, CBG activity was significantly elevated after only 90 min of I and after I/R (15.1 +/- 5.6 and 16.4 +/- 4.3 units/mL, respectively, p < 0.05). We conclude that serum CBG is elevated before transmural intestinal injury in this model and may have utility as an early marker of ischemia in patients at risk for NEC.

Animals↗
PubMed2004

Intestinal epithelial apoptosis initiates gross bowel necrosis in an experimental rat model of neonatal necrotizing enterocolitis.

The histopathology of necrotizing enterocolitis (NEC) is characterized by destruction of the mucosal layer in initial stages and by transmural necrosis of the intestinal wall in advanced stages of the disease. To test the hypothesis that enhanced epithelial apoptosis is an initial event underlying the gross histologic changes, we analyzed epithelial apoptosis and tissue morphology in an animal model of NEC and evaluated the effect of caspase inhibition on the incidence of experimental NEC in this model. Apoptosis was analyzed with terminal deoxynucleotidyltransferase-mediated dUTP-FITC nick end labeling (TUNEL) staining in intestinal sections and by measuring caspase 3 activity from intestinal lysates of neonatal rats subjected to formula feeding and cold/asphyxia stress (FFCAS) and from mother-fed (MF) controls. Morphologic evaluation was based on hematoxylin and eosin staining of intestinal sections. FFCAS resulted in histologic changes consistent with NEC, which were absent from MF animals. FFCAS was also associated with a significantly increased rate of nuclear DNA fragmentation in the small intestinal epithelium compared with MF. Elevated tissue caspase 3 activity confirmed the presence of apoptosis in samples with increased DNA fragmentation. Analysis of the coincidence of morphologic damage and apoptosis in corresponding tissue sections indicated that apoptosis precedes gross morphologic changes in this model. Furthermore, supplementation of formula with 8 boc-aspartyl(OMe)-fluoromethylketone, a pan-caspase inhibitor, significantly reduced the incidences of apoptosis and experimental NEC. These findings indicate that in neonatal rats FFCAS induces epithelial apoptosis that serves as an underlying cause for subsequent gross tissue necrosis.

Animal Nutritional Physiological Phenomena↗
PubMedDate not supplied

Role of bacterial colonization in neonatal necrotizing enterocolitis and its prevention.

Necrotizing enterocolitis (NEC) is the most common gastrointestinal emergency in premature infants. A major component of the pathophysiology of NEC is the nature of the interaction of bacteria with the premature gut. Intestine microflora are important to the host in resistance to bacterial infections. Diet and environmental conditions can influence this ecosystem. A breast-fed full-term infant has a preferred intestine microbiota in which bifidobacteria predominate over the potentially harmful bacteria, whereas in formula-fed infants coliforms, enterococci and bacteroides predominate. The pattern of bacterial colonization in the premature neonate gut is quite different from that in the gut of the healthy full-term infant. Those infants requiring intensive care acquire intestinal organisms slowly, and the establishment of bifidobacterial flora is retarded. A delayed bacterial colonization of the gut with a limited number of bacterial species tends to be virulent. Bacterial overgrowth is one of major factors promoting bacterial translocation. The aberrant colonization of the premature infant may contribute to the development of NEC. Breast feeding protects infants against NEC. Oligosaccharides and glycoconjugates, natural components in human milk, may prevent intestinal attachment of enteropathogens by acting as receptor homologues. Probiotics and prebiotics modulate the composition of human intestine microflora to the benefit of the host. The beneficial effects may result in the suppression of colonization of harmful microoganisms and/or the stimulation of bifidobacterial growth. In the future, control and manipulation of bacterial colonization in the neonate gut may be a new approach to the prevention and treatment of bacterial intestinal disease of various etiologies.

Bacteria↗
PubMed2000

Enteral antibiotics for preventing necrotising enterocolitis in low birthweight or preterm infants.

BACKGROUND: Necrotising enterocolitis continues to be a problem, particularly in preterm neonates. There have been reports published suggesting that the use of enteral antibiotics may be effective as prophylaxis. This systematic review was undertaken to clarify the issue. OBJECTIVES: To evaluate the benefits and harms of enteral antibiotic prophylaxis for necrotising enterocolitis in low birth weight and preterm infants. SEARCH STRATEGY: Searches were made of the Oxford Database of Perinatal trials, MEDLINE (search terms: necrotizing enterocolitis, antibiotics; LIMITS: newborn infant), previous reviews with cross references, abstracts, conference and symposia proceedings, expert informants and journal handsearching in the fields of Neonatal Pediatrics and Microbiology. SELECTION CRITERIA: All randomized or quasi-randomized controlled trials where enteral antibiotics were used as prophylaxis against NEC in LBW (<2500g) and/or preterm (<37 weeks gestation) infants. DATA COLLECTION AND ANALYSIS: The standard method of the Cochrane Collaboration and its Neonatal Review Group was used. The methodological quality of each trial was reviewed by the second author who was blinded to the trial authors and institutions. Each author extracted data separately before comparison and resolution of differences. Relative risk (RR), risk difference (RD), and number needed to treat were used in the analysis. MAIN RESULTS: The administration of prophylactic enteral antibiotics resulted in a statistically significant reduction in NEC [RR 0.47 (0.23, 0.98); RD -0.072 (-0.136, -0.008); NNT 13.9 (7.4, 125)]. There was a reduction in NEC-related deaths which was of borderline statistical significance [RR 0.16 (0.02, 1.26); RD -0.097 (-0.183, -0.010); NNT 10.3 (5.46, 100)]. There were no significant differences in all deaths (one trial only) or in NEC-like enteropathies (one trial only). There was a statistically significant increase in the incidence of colonisation with resistant bacteria [RR 1.73 (1.00, 2. 97); RD 0.123 (0.008, 0.238); NNT 8.1 (4.2, 125)]. REVIEWER'S CONCLUSIONS: There is insufficient evidence to support the use of enteral antibiotic prophylaxis for NEC in clinical practice. To address this question further, a large trial would be required with a sample size sufficient to examine all the important benefits and harms. Adverse outcomes associated with infection, particularly with resistant bacteria, should be evaluated.

Anti-Bacterial Agents↗
PubMed1979

Necrotizing enterocolitis in the neonate.

Necrotizing enterocolitis has become the most common condition requiring emergency surgical treatment in the newborn infant, far surpassing all major congenital anomalies in number of presentations and in deaths after surgical treatment. No single cause for the disease is known. Necrotizing enterocolitis is characterized by ischemic necrosis of the intestine, with minimal inflammation. In 25 of 50 per cent of patients, surgical resection of gangrenous bowel is necessary. Operation is reserved for infants with intestinal perforation or grangrene. Recent refinements of indications for operation often permit surgical intervention to coincide with the advent of intestinal gangrene. At operation, expeditious resection of frankly necrotic bowel and exteriorization of the marginally viable ends is all that should be attempted. Special problems postoperatively consist of management of sepsis, maintenance of nutrition and vigilant observation for early and late complications, particularly the development of ischemic intestinal stricture.

Animals↗