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 631 records · Page 35Linked to original sources

Neonatal nosocomial infection surveillance: incidences by site and a cluster of necrotizing enterocolitis.

Nosocomial infection (NI) was prospectively studied in hospitalized neonates during a 10-month period. The Centers for Disease Control (CDC) criteria (some specified for neonates) were used for surveillance. Forty-nine of 677 infants experienced 73 episodes of NI. The overall incidence was 10.8 NI/100 patients and 6.5 NI/1,000 patient days. The average monthly NI number did not correlate with patient load. Very low birth weight (VLBW) infants showed a higher NI incidence (81.8 NI/100 patients and 11.1 NI/1,000 patient days), also elevated if adjusted for their inherently longer neonatal intensive care unit (NICU) stay. The most common NI sites in the VLBW stratum were sepsis and necrotizing enterocolitis (NEC), the latter occurring in a seasonal cluster. It can be concluded that surveillance for NIs should focus on VLBW infants and include the evaluation of NEC, as it behaves like a nosocomial disease.

Anti-Bacterial Agents↗

Hemorrhagic necrotizing enterocolitis associated with Clostridium difficile infection in four foals.

Severe hemorrhagic necrotizing enterocolitis was determined to be the cause of death for 4 foals. Toxigenic Clostridium difficile was isolated form the intestine of each foal, and large, gram-positive, rod-shaped bacteria lined the surface of necrotic villi. This finding of toxigenic C difficile associated with enteritis in foals adds another possible cause to the list of infectious agents that should be considered when evaluating foals with enteritis. Definitive diagnosis requires a thorough diagnostic evaluation, including procedures that will identify the organism and demonstrate its toxigenicity.

Animals↗

Enteric glial cells. An upstream target for induction of necrotizing enterocolitis and Crohn's disease?

As a direct consequence of the sophisticated arrangement of its intrinsic neurons, the gastrointestinal tract is unique among peripheral organs, in its ability to mediate its own reflexes. Neurons of the enteric nervous system are intimately associated with enteric glial cells. These supporting cells do not resemble Schwann cells, the glial cell found in all other parts of the peripheral nervous system, but share many similarities with astrocytes of the central nervous system. Ablation of enteric glial cells in adult transgenic mice has demonstrated that these cells are essential to maintain the integrity of the small intestine. Acute loss of enteric glial cells induces massive pathological changes with similarities to necrotizing enterocolitis (NEC) and early Crohn's disease. These human conditions share some mechanistic similarities. Identification of enteric glial cell dysfunction/loss as sufficient to induce necrotic/inflammatory bowel disease may be important to understand the pathogenesis of both NEC and Crohn's disease.

Animals↗

Role of bacterial translocation in necrotizing enterocolitis.

The intestinal mucosa functions as a major local defense barrier preventing bacteria that colonize the gut from invading organs and tissues. Under certain circumstances, bacteria colonizing the gastrointestinal tract can cross the gut mucosal barrier to infect the mesenteric lymph node and systemic organs via a process termed bacterial translocation. Factors that promote the translocation of bacteria or endotoxin from the gut include bacterial overgrowth with gram-negative enteric bacilli, impaired host immune defenses and injury to the gut mucosa resulting in increased intestinal permeability. These same promoting factors are present in patients at increased risk of developing necrotizing enterocolitis. Consequently, this review focuses on the potential role of bacterial and endotoxin translocation from the gut in the pathogenesis of necrotizing enterocolitis.

Animals↗

Necrotizing enterocolitis presenting in the Emergency Department: case report and review of differential considerations for vomiting in the neonate.

Historically, most of the acute complications of prematurity have occurred in the neonatal intensive care unit, not in the Emergency Department (ED). It is becoming increasingly common, however, for premature infants to be discharged from the hospital before they have reached a postconceptual age of 40 weeks. Such infants remain at relatively increased risk for a variety of complications of prematurity and may present to the ED in their first month of life. To highlight its symptomatology and review its management, we present the case of an infant presenting back to the ED with coffee ground emesis and fulminant necrotizing enterocolitis.

Emergency Service, Hospital↗

Acquired ileal atresia and spontaneous reconstitution of intestinal continuity in a premature infant with necrotizing enterocolitis.

An 849-g (26-week gestation) premature infant had pneumoperitoneum on the 20th day of life after having normal stools and accepting partial enteric alimentation. Percutaneous penrose drainage had to be performed on 2 consecutive days at 2 different sites (right lower quadrant, left lower quadrant), at which time she stabilized. Eleven days later, she started to pass stool, and oral feeding was begun (1 to 2 mL every 4 hours). Enteral intake could not be advanced because of repeated bouts of abdominal distension, despite having regular bowel motions. Gastrointestinal contrast radiographic investigation suggested a stricture of the ileum. At laparotomy (at age 2 months) ileal atresia with a "V"-shaped defect in the mesentery was found. Surprisingly, intestinal continuity was established via an ileoileal fistula. After resection and anastomosis, she recovered fully. Mesenteric and enteric vascular ischemia (necrotizing enterocolitis) produced acquired ileal atresia-a rare occurrence. More rare is the reestablishment of intestinal continuity by fistulization.

Drainage↗

Does maternal nicotine exposure during gestation increase the injury severity of small intestine in the newborn rats subjected to experimental necrotizing enterocolitis.

BACKGROUND/PURPOSE: The aim of this study was to evaluate the effects of maternal nicotine exposure during gestation on injury severity of small intestine in the newborn rats subjected to hypoxia-reoxygenation and cold stress. METHODS: A total of 21 Sprague-Dawley pregnant rats were divided into 3 equal groups. The groups were labeled as group 1, control group; group 2, hypoxia-reoxygenation group; and group 3, nicotine-hypoxia-reoxygenation group. The rats of group 3 were exposed to nicotine via subcuticular injection for the last week of gestation (2 mg/kg/d). Newborn rats were collected immediately after birth to prevent suckling of maternal milk (40 rat pups in group 1, 43 rat pups in group 2, and 41 rat pups in group 3). Litters in groups 2 and 3 were stressed twice daily with asphyxia followed by cold (4 degrees C for 10 minutes) stress to induce hypoxic intestinal injury which is relevant to human necrotizing enterocolitis. Breathing 100% CO2 for 10 minutes in a chamber followed by 10-minute 100% O2 breathing was the asphyxia model repeated twice daily. After hypoxia-reoxygenation and cold stress, newborn rats were returned to their mother's cages. This protocol was repeated for the following 2 days, and the rat pups were decapitated on the third day. Using this protocol of asphyxia and cold stress, all of neonatal rats developed clinical and pathological signs of hypoxia-induced intestinal injury. The entire gastrointestinal tract was removed and examined macroscopically. A 2-cm section of distal ileum from each animal was taken for histopathological and biochemical examinations. Histological changes in ileal architecture were scored and graded from 1 to 5. The remaining intestinal tissues of the animals were used for lipid peroxidation analysis. RESULTS: Typical signs of hypoxia-induced intestinal injury were observed in the 2 experimental groups (groups 2 and 3) macroscopically. There were more grades 3 and 4 injuries in group 3 (P < .05). The malondialdehyde levels were elevated in groups 2 and 3 (P < .001). The malondialdehyde levels of the group 3 were also significantly higher than group 2 (P < .01). CONCLUSIONS: Maternal nicotine exposure during gestation results in higher grade histological injury in newborn rats subjected to hypoxia-reoxygenation and cold stress.

Administration, Inhalation↗

Multi-modal approach to prophylaxis of necrotizing enterocolitis: clinical report and review of literature.

For the first time a multimodal approach to NEC prophylaxis is reported, consisting of early trophic feeding with human breast milk, and enteral administration of an antibiotic, an antifungal agent, and probiotics. A retrospective analysis of local protocol of NEC prophylaxis is presented. Included were all VLBWI admitted to the NICU, including transfers within the first 28 days of life. These infants were divided into two groups, an "inborn group" (infants admitted within the first 24 h of life) and an "outborn group" (infants admitted after the onset of their second day of life). Prophylaxis of NEC according to protocol was started at the day of admission, and was continued until discharge. Between 1998 and 2004, 405 VLBWI were admitted, including all transfers within the first 28 days of life. A total of 334 (82%) infants were admitted within the first 24 h of life (inborn group), and 71 (18%) were admitted after 24 h of life (outborn group). Five infants developed clinical features of necrotizing enterocolitis. The inborn group showed a NEC incidence of 0.7% (two infants), whereas the outborn group showed a NEC incidence of 4.5% (three infants), respectively. This difference was significant (P=0.049, Fisher's exact test). A surgical treatment with bowel resection was performed in two infants (both from the outborn group). The present study used a combination of different strategies, all having shown to have some beneficial effect, but not having brought a clinical breakthrough in single administration studies. Combinated were the beneficial effects of human breast milk feeding, oral antiobiotics, oral antifungal agents, and the administration of probiotics. In a homogenous group of preterm infants, using this protocol of multimodal NEC prophylaxis, there was a very low incidence of NEC, when started within the first 24 h of life.

Breast Feeding↗

Clinical analysis of necrotizing enterocolitis with intestinal perforation in premature infants.

To identify the prognostic factors correlating with the outcome of the perforated necrotizing enterocolitis (NEC), the charts of 20 premature infants with perforated NEC were reviewed. Eight patients had long-term survival and 12 died. Infants in the survival group had significantly lower incidence of starting to feed before perforation, patent ductus arteriosus, indomethacin use, acidosis, and shock. Sepsis was only found in the group of infants that died The survival group were diagnosed with NEC and intestinal perforation at an earlier age than the infants that died. The time from diagnosis of NEC to intestinal perforation was longer in the infants that died. The localization of necrosis from operativefindings were all confined to the ileum-cecum area in survival group. The infants in the survival group were likely to have a single perforation. In addition, according to the operative management, they were divided into three groups: Group I consisted of six patients who received peritoneal drainage only, group II consisted of three patients who received peritoneal drainage followed by laparotomy, and group In consisted of 11 patients who received primary laparotomy. Infants in groups I and II had significantly lower gestational ages and birth weights than group III. There were no significant differences in mortality rates among infants in groups I, II and III. We concluded that the factors including prior enteral feeding, patent ductus arteriosus, indomethacin use, acidosis, sepsis, shock, delayed onset of NEC and perforation, multiple perforation, and diffuse necrotic changes were significant prognostic factors of poor outcome. Peritoneal drainage was a resuscitative procedure in critical condition and laparotomy should mostly be considered as the final treatment in the infants with perforated NEC.

Enterocolitis, Necrotizing↗

Neonatal necrotizing enterocolitis with intestinal perforation in extremely premature infants receiving early indomethacin treatment for patent ductus arteriosus.

Survival of extremely premature infants (< 27 weeks' gestational age) has improved over the past two decades. Indomethacin prophylaxis was used in these infants, who have the highest mortality and morbidity rates, to reduce the incidence of intraventricular hemorrhage and patent ductus arteriosus (PDA). Medical records of 65 extremely premature infants born at our institution between 1995 and 2001 were reviewed retrospectively to determine whether treatment of PDA with indomethacin in the first 48 hours of life reduces the need for PDA ligation or increases neonatal morbidity, when compared to treatment begun later. Thirty infants in the early treatment group (ETG) were treated during the first 48 hours after birth, and 32 infants in the standard treatment group (STG) were managed expectantly for PDA. Three infants died in the first hours of life and were eliminated from further analysis. ETG infants were 24.9 +/- 1.1 (mean +/- SD) weeks' gestation with a birth weight of 678 +/- 143 g. STG infants were 25.3 +/- 1.1 weeks (NS) and 730 +/- 125 g (NS). Hemodynamically significant PDA was diagnosed or confirmed by echocardiography in 19 ETG patients and 17 STG patients. Of the patients with hemodynamically significant PDA, 1 (5%) ETG patient and 6 (35%) STG patients underwent surgical ligation (p = 0.033). Necrotizing enterocolitis (NEC) with intestinal perforation was the most serious morbidity and occurred in 20% of infants in the ETG, but in no STG infant (p = 0.011). Four of the six infants in the ETG with NEC and intestinal perforation died. The overall mortality rate for all infants studied was 28%. We conclude that in extremely premature infants, use of indomethacin during the first 48 hours of life was associated with a reduced need for PDA ligation, but an increased risk of NEC with intestinal perforation.

Anti-Inflammatory Agents, Non-Steroidal↗

Necrotizing enterocolitis in an infant with Omenn syndrome.

Omenn syndrome (OS) is a rare disorder within the combined immunodeficiency family that is characterized by a diffuse exudative, erythematous rash, lymphadenopathy, hepatosplenomegaly, alopecia, and failure to thrive. Specific lab findings unique to OS include hypereosinophilia, elevated IgE, excess production of oligoclonal T-cells and near-to-absent B-cells. Much remains elucidated about the underlying genetic cause of OS. Until recently, it was felt that the disease was primarily caused by mutations of the RAG1 or RAG2 genes. The type of mutation of the RAG1 and RAG2 genes in patients with OS affects the degree of functioning variable (diversity) joining [V(D)J] recombination activity, which is critical to the development of lymphoid cell receptor diversity. New work has also shown that thymic tissue in OS patients demonstrates a severe defect in the expression of the autoimmune regulator element. This may contribute to the development of autoreactive T-cells that are felt to be the causative agent of a number of the clinical hallmarks unique to OS. The genetic spectrum of OS was further expanded when a patient with clinical and immunologic features consistent with OS, without RAG mutation, was found to have mutations in both alleles coding for ARTEMIS, a key V(D)J recombination/DNA repair factor. Regardless of the underlying cause, early recognition is critical because patients die at a very young age without bone marrow transplantation. We describe an infant diagnosed with OS post-mortem in which death was directly related to the development of necrotizing enterocolitis.

Enterocolitis, Necrotizing↗

Epidemic occurrence of neonatal necrotizing enterocolitis.

In case-control studies of three epidemics of neonatal necrotizing enterocolitis (NEC) in three different high-risk nurseries in three states, no particular risk factor was associated with affected infants or their mothers. Epidemic cases had higher birth weights and Apgar scores and fewer perinatal difficulties than those previously reported for sporadic cases. Seven infants fed primarily breast milk were not protected against disease. Early antibiotic therapy was associated with a significantly decreased risk of disease in one outbreak. In two hospitals, affected infants who received antibiotic therapy during the first three days of life had a significantly later disease onset. The occurrence of the disease in epidemics and the decreased risk or modification of disease with antibiotic therapy support an infectious etiology for NEC.

Ampicillin↗

Necrotizing enterocolitis in a term infant with coarctation of the aorta complex.

Necrotizing enterocolitis (NEC) sometimes occurs in term infants with congenital heart disease. This article reports a rare case of a term infant with coarctation of the aorta complex who developed NEC on the 8th day after birth. Spontaneous closure of the ductus arteriosus in the 1st week of life may cause intestinal ischemia and hypoxia with resultant NEC.

Aortic Coarctation↗

Recurrent necrotizing enterocolitis.

In the decade 1981 to 1991, 16 infants developed recurrent necrotizing enterocolitis (NEC). They comprised 12 (6%) of 196 neonates referred for further management of NEC and four others referred with major congenital anomalies. Their median gestational age was 32 weeks (range, 27 to 40), median birth weight was 1,260 g (range, 790 to 3,230), and the sex distribution was equal. Recurrent NEC occurred after a median interval of 37 days (range, 11 to 163) from the onset of the initial episode. All but one of the 16 infants were either premature (n = 10) or mature with major congenital anomalies (n = 5). Nine patients had previously undergone surgery for NEC. Medical treatment was successful in 11 patients with recurrent NEC. Two infants died, both of liver failure related to parenteral nutrition; one of whom had suffered four separate episodes of NEC and was found to have a superior mesenteric artery occlusion. There was no consistent association between recurrent NEC and the type or timing of enteral feeds or the anatomical site or method of management of the original attack. The mortality of 12.5% was similar to that for primary NEC.

Child↗

Bacterial contaminated breast milk and necrotizing enterocolitis in preterm twins.

A pair of preterm twins developed fatal necrotizing enterocolitis (NEC) in association with Staphylococcus epidermidis septicaemia after receiving contaminated expressed breast milk (EBM). S. epidermidis NEC can be associated with severe bowel inflammation, high morbidity and mortality. Breast milk is the most suitable nutrient for preterm infants but EBM should undergo regular screening for bacterial overgrowth. We urge caution before administering EBM found to be heavily contaminated with S. epidermidis to preterm infants.

Bacteremia↗

A bacteriologic basis for the clinical presentations of necrotizing enterocolitis.

A study to identify putative bacterial pathogens in infants with necrotizing enterocolitis (NEC) was begun in 1976. Cultures of blood and of peritoneal fluid obtained by paracentesis were carried out in 25 infants with NEC. Segments of intestine excised at operation were Gram stained. Of the 25 infants, 8 recovered with medical management and 17 required operations. The 8 medically treated infants had sterile peritoneal fluid and, with 2 exceptions, sterile blood cultures. Of the 17 operated infants, 16 had bacteria in their blood and/or peritoneal fluid. The majority of resected bowel specimens from these infants contained a confirmatory morphologic type of bacterium within the wall. The clinical course of 8 infants with clostridia was compared to that of 8 infants with gram-negative enteric bacteria (Klebsiella, E. coli, or Bacteroides fragilis). The infants with clostridia were sicker. They had more extensive pneumatosis intestinalis, a higher incidence of portal venous gas, more rapid progression to gangrene, and more extensive gangrene. Infants with gram-negative rods had lower birth weights and lower platelet counts than the clostridial group. The difference in mortality between the two groups was not significant. The inherent pathogenicity of the gut flora may influence the clinical course of NEC. Among infants who develop intestinal gangrene, the clostridia appear to be more virulent than gram-negative enteric bacteria.

Clostridium↗

The role of inflammatory cytokines and nitric oxide in the pathogenesis of necrotizing enterocolitis.

PURPOSE: The role of inflammatory cytokines in the pathogenesis of necrotizing enterocolitis (NEC) is still undefined. Elevated levels of interleukin (IL)-6 and tumor necrosis factor (TNF)-alpha have been measured in infants with NEC, while elevated levels of nitric oxide (NO) have been reported in newborn infants with clinical sepsis. However, the cellular source of the NO or cytokines is unknown. The authors hypothesized that local intestinal production of NO induced by cytokines may contribute to the pathogenesis of bowel necrosis in NEC by inducing apoptosis (programmed cell death) or necrosis of the enterocytes. We examined the levels of inflammatory cytokines and NO in the intestine of infants undergoing surgical resection for NEC, and the cellular localization of human inducible NO synthase (NOS-2) in the inflamed gut. METHODS: We compared 15 patients undergoing bowel resection for NEC, with six infants (of similar age) undergoing intestinal resection for ileal atresia or stricture, meconium peritonitis, intussusception, or cecal perforation (control). Diagnosis of NEC was confirmed histologically. Representative segments of the surgical specimen were examined for messenger RNA (mRNA) for NOS-2 by Northern blotting and in situ hybridization. Cytokine mRNA was measured by polymerase chain reaction (PCR) because mRNA could not be detected by Northern blotting. The site of NO production was determined by in situ hybridization and immunohistochemistry. Apoptosis was measured using in situ DNA strand break extension (TUNEL). Nitrotyrosine immunoreactivity was assessed to determine if NO mediates cellular injury via peroxynitrite formation. RESULTS: Messenger RNA for NOS-2 was detected in nearly all patients with NEC except for one infant who underwent proximal diverting jejunostomy alone, and who did not have histological evidence of NEC at that site. NOS-2 mRNA was detected less frequently in control patients. In situ hybridization and immunohistochemistry showed that the enterocytes were the predominant source of NOS-2 activity in the intestine of NEC patients. Extensive apoptosis was seen in enterocytes in the apical villi of infants with NEC, and correlated with nitrotyrosine staining. NOS-2 activity was markedly diminished at the time of stoma closure, but remained elevated in infants who died from progressive disease. PCR showed variable cytokine mRNA expression in the intestine. Transforming growth factor (TGF)-beta expression was nearly identical in NEC and control. However, interferon (IFN)-gamma was present in 9 of 10 NEC, but only in one of six control patients. CONCLUSION: The data show that NO is produced in large quantity by enterocytes in the intestinal wall of infants with NEC and leads to apoptosis of enterocytes in apical villi through peroxynitrite formation.

Cytokines↗

Multisystem organ failure and capillary leak syndrome in severe necrotizing enterocolitis of very low birth weight infants.

BACKGROUND: Classification systems for necrotizing enterocolitis (NEC) in preterm infants have been developed to define severity grades relevant for treatment and prognosis. Multisystem organ failure (MSOF) and capillary leak syndrome (CLS) also have prognostic value in these patients. The aim of this retrospective study was to investigate the incidence and predictive value of MSOF and CLS according to the classification criteria. METHODS: The records of 1,022 very low birth weight infants admitted from 1982 to 1996 were reviewed for diagnosis of NEC stage IIA or higher (classification of Walsh and Kliegman). Among those patients (n = 50) the incidence of MSOF and CLS was determined, separately for surgical or conservative treatment. RESULTS: Twelve patients were assigned to stage II, 22 to stage IIIa, and 16 to stage IIIb; 31 infants underwent operation. Mortality rate was not influenced by the grade. In eight patients only gastrointestinal symptoms were found, whereas in 23 patients, up to three organ systems and in 19 patients, four or more organ systems were affected. Mortality depended on the number of involved organ systems. CLS occurred postoperatively in 10 of the 31 infants; eight of them died. CONCLUSION: The prognostic values of MSOF and CLS are higher than that of classification criteria in NEC of VLBW infants.

Capillary Leak Syndrome↗