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PubMed2006

Enteral granulocyte colony-stimulating factor for the treatment of mild (stage I) necrotizing enterocolitis: a placebo-controlled pilot study.

BACKGROUND/PURPOSE: The presence of granulocyte colony-stimulating factor (G-CSF) in human milk and the expression of G-CSF receptors on intestinal villous enterocytes of neonates suggest that G-CSF has a role in the development and integrity of the gastrointestinal tract. We hypothesized that enteral recombinant human G-CSF (rhG-CSF) given to preterm infants with necrotizing enterocolitis (NEC) in the earlier stages could protect against disease progression and complications. METHODS: Preterm infants with mild (stage I) NEC (n = 18) were assigned to receive enteral rhG-CSF (n = 8) or placebo (n = 10) for 5 days from the first day of the diagnosis. Clinical and gastrointestinal parameters were followed during the whole period of hospitalization. RESULTS: In the study group, none of the infants with stage I NEC had a clinical progression to stage II or III, whereas in the control group, 5 (50%) infants with stage I NEC had a disease progression to stage II or III (P < .05). In the study group, the time required for the resolution of clinical and radiological findings of NEC and the total duration of systemic therapy and hospitalization were significantly shorter than the control group (P < .001). CONCLUSION: Enteral rhG-CSF treatment could prevent the progression of mild (stage I) NEC to further stages and decrease the time required for the resolution of clinical and radiological signs of the disease.

Disease Progression↗
PubMed2002

Probiotics feeding in prevention of urinary tract infection, bacterial sepsis and necrotizing enterocolitis in preterm infants. A prospective double-blind study.

BACKGROUND: It has been suggested that probiotics can reduce the overgrowth of pathogens in the bowels of preterm infants and contribute to the reduction of the incidence of nosocomial infections in neonatal intensive care units (NICUs). The purpose of this study was to evaluate the effectiveness of Lactobacillus GG supplementation in reducing the incidence of urinary tract infections (UTIs), bacterial sepsis and necrotizing enterocolitis (NEC) in preterm infants. METHODS: A double-blind study was conducted in 12 Italian NICUs. Newborn infants with a gestational age <33 weeks or birthweight <1,500 g were randomized to receive standard milk feed supplemented with Lactobacillus GG (Dicoflor), Dicofarm, Rome, Italy) in a dose of 6 x 10(9) colony-forming units (cfu) once a day until discharge, starting with the first feed or placebo. RESULTS: Five hundred eighty-five patients were studied. The probiotics group (n = 295) and the placebo group (n = 290) exhibited similar clinical characteristics. The duration of Lactobacillus GG and placebo supplementation was 47.3 +/- 26.0 and 48.2 +/- 24.3 days, respectively. Although UTIs (3.4 vs. 5.8%) and NEC (1.4 vs. 2.7%) were found less frequently in the probiotic group compared to the control group, these differences were not significant. Bacterial sepsis was more frequent in the probiotics group (4.4%, n = 11) than in the placebo group (3.8%, n = 9), but the difference was not significant. CONCLUSION: Seven days of Lactobacillus GG supplementation starting with the first feed is not effective in reducing the incidence of UTIs, NEC and sepsis in preterm infants. Further studies are required to confirm our results in lower birthweight populations.

Bacterial Infections↗
PubMed1984

Clostridium difficile isolation in neonates in a special care unit. Lack of correlation with necrotizing enterocolitis.

The stools of 78% of 45 infants in a Special Care Baby Unit yielded Clostridium difficile on culture, and in 67% of these it was possible to detect C. difficile toxin by means of a tissue culture technique. The stools of six of the seven infants with necrotizing enterocolitis were positive for C. difficile, but neither of the two most severely affected contained C. difficile toxin. The incidence of C. difficile isolation was similar in infants treated by exchange transfusion, those treated with antibiotics, those of low birth weight, and those with respiratory distress. The serum of only 2 of 28 infants and 1 of 20 mothers contained a neutralizing factor to C. difficile toxin. The present study does not support a role for C. difficile in neonatal disorders and in particular necrotizing enterocolitis. The reason for the apparent tolerance of the neonatal bowel to C. difficile toxin remains to be explained.

Antitoxins↗
PubMed1998

Necrotizing enterocolitis and C-KIT.

BACKGROUND/PURPOSE: In the gut, C-KIT is important for immune system homeostasis, and C-KIT+ cells are known to increase during inflammation. Recently the authors identified that spontaneous intestinal mucosal erosion develops in C-KIT-depleted W/Wv mice after day 14 of life at a high frequency, whereas genotypically normal litter mates do not. The authors hypothesized that a lack of C-KIT may be implicated in the development of necrotizing enterocolitis (NEC). METHODS: Bowel specimens were taken during surgery or postmortem from nine cases of NEC (mean gestational age, 32.0 weeks), six age-matched cases of enteritis, and 10 age-matched controls. Specimens were formalin fixed, paraffin embedded, and labeled with antibody to C-KIT. The number of C-KIT+ cells from five random fields per specimen were compared under light microscopy (200x). Results were expressed as the mean +/- SD and compared using the analysis of variance (ANOVA) test. RESULTS: In enteritis, the number of C-KIT+ cells in the lamina propria and submucosa was significantly higher than in controls (P<.01) indicative of their involvement in inflammation. However, in NEC, the number of C-KIT+ cells in the lamina propria and submucosa was significantly lower than in controls (P<.05) despite histological evidence of inflammation. CONCLUSION: A lack of C-KIT+ cells may exert a causal influence on the development of NEC.

Analysis of Variance↗
PubMed1984

Necrotizing enterocolitis and hemolysis associated with Clostridium perfringens.

Two newborns had necrotizing enterocolitis (NEC) and severe hemolytic anemia. Clostridium perfringens was identified in the peritoneal fluid of both infants, supporting the previous association of C perfringens with hemolysis reported in adult patients. Infants with NEC and hemolytic anemia should be aggressively treated with surgical debridement and high-dose parenteral penicillin G potassium. Similarly, Gram's stain of peritoneal fluid and resected bowel at laparotomy for NEC may be useful for early identification of the primary organism.

Anemia, Hemolytic↗
PubMed1991

Enteric fistula formation secondary to necrotizing enterocolitis.

We report two cases of enterocolonic fistula formation following necrotizing enterocolitis, and a review of the six previously published cases. Ischemic mechanism is the most likely cause. The fistulas were diagnosed by upper gastrointestinal series and contrast enema.

Colonic Diseases↗
PubMed1988

Late onset bowel stenoses after neonatal necrotizing enterocolitis.

In 14 cases of bowel stenoses occurring after neonatal necrotizing enterocolitis (NEC), eight cases presented early, within 8 weeks from the onset of NEC and three beyond 4 months. In the other three cases the stenoses occurred in defunctionalized loops. The late onset stenoses remained undiagnosed until they presented with acute, life-threatening complications, and one of these patients died. We draw attention to these late onset stenoses which could be missed in early contrast studies, and recommend a study at 4 months rather than at 4 weeks, as previously recommended. Those presenting early should not be missed, as all of our cases presented with acute and obvious intestinal obstructions, and they were all still in hospital or undergoing frequent review.

Barium Sulfate↗
PubMed1994

A study of pre-antibiotic bacteriology in 125 patients with necrotizing enterocolitis.

Over a five-year period, 125 newborns with necrotizing enterocolitis (NEC) were managed by us. Their mean birthweight was 1700 g and mean maturity was 32 weeks. Before commencement of antibiotics, routine septic work-up was done in order to define the bacterial spectrum and antibiotic sensitivity. The study includes aerobic and anaerobic cultures of gastric and pharyngeal aspirates, blood cultures, umbilical swabs and culture of umbilical catheter tips in relevant cases. Peritoneal swab results were also analyzed if laparatomy was performed. Positive cultures were present in 45 patients (36%) with 55 positive specimens. Fifteen types of organism were isolated: the commonest was Enterobacter (29%), followed by E. coli (14.5%) and Klebsiella (13%). They were resistant to ampicillin and first-generation cephalosporin. These organisms were usually opportunistic pathogens. Overgrowth of them may be the cause of NEC. Regular review of the antibiotic sensitivity of these organisms allows prompt and appropriate choice of antibiotics. At the same time, antibiotic sensitivity for these organisms was analyzed to guide us in the choice of antibiotic therapy.

Ampicillin Resistance↗
PubMedDate not supplied

Necrotizing enterocolitis: a review of pathogenetic mechanisms and implications for prevention.

Necrotizing enterocolitis (NEC) is a devastating gastrointestinal disease of premature neonates that accounts for 3000 to 4000 deaths each year in the United States. The pathogenesis is not well understood, however theories suggest that prematurity, enteral feeding, bacterial colonization, and intestinal ischemia contribute to the intestinal injury. Furthermore, recent studies have shown that platelet activating factor and perhaps other inflammatory mediators mediate bowel necrosis in animals and possibly in humans. Although no specific intervention for NEC treatment exists, preventive therapy using either enteral IgA supplementation, breast milk feeding, antibiotic prophylaxis, or exogenous steroid administration have reduced the incidence of this overwhelming disease in small randomized trials. These modalities and perhaps PAF antagonists or other inflammatory mediator inhibitors may reduce the incidence or severity of NEC in the next several years.

Enterocolitis, Pseudomembranous↗
PubMed1987

[A rare cause of neonatal ulcero-necrotizing enterocolitis: aortic coarctation syndrome].

The authors report a case of necrotizing enterocolitis which appeared in the first hours of life of a full-term neonate without signs of sepsis. This neonate presented with a severe hypoplasia of the horizontal aorta and very tight coarctation responsible for hepatic, renal and mesenteric ischemia. Reports of enterocolitis as a complication of congenital heart disease are rare and related most often to hypoplastic left heart than to coarctation of the aorta.

Aorta, Thoracic↗
PubMed1985

Reconstitution of intestinal continuity after resection for neonatal necrotizing enterocolitis.

Thirty-five infants were treated surgically for neonatal necrotizing enterocolitis during the past eight years. Twenty-five of these, managed by resection and exteriorization, later underwent reconstitution of the intestinal tract. Eleven infants (69 per cent) with ileostomy and three (100 per cent) with jejunostomy exhibited stenosis or severe dehydration, electrolyte loss and acidosis requiring closure to achieve positive caloric balance. Fewer serious postoperative complications were observed after reanastomosis by Roux-en-Y enteroenterostomy and single limb ileostomy (Bishop Koop) versus end to end anastomosis. Operative mortality for small intestinal stoma closure was 10 per cent. Complications from colostomy formation occurred in 67 per cent. However, fluid and electrolyte loss was not observed and adequate weight gain was achieved in four of six patients allowing for elective closure by end to end anastomosis. Operative mortality for colostomy closure was nil.

Colon↗
PubMed1994

Total parenteral nutrition in necrotizing enterocolitis.

Total parenteral nutrition (TPN) is used both to prevent necrotizing enterocolitis (NEC) and to treat infants who develop the disease. Evidence for the efficacy of the technique in both settings is discussed. Several practical aspects of TPN also are discussed, as are a variety of theoretical considerations relevant to use of TPN either to prevent NEC or as an adjunct to treatment of the infant with the disease.

Enterocolitis, Pseudomembranous↗
PubMed1994

Prevention of neonatal necrotizing enterocolitis.

There are a number of promising strategies to prevent necrotizing enterocolitis (NEC). These included induction of intestinal maturation with prenatal or postnatal steroids, passive immunization with oral immunoglobulin, modification of enteral feedings, administration of oral antibiotics to decrease bacterial overgrowth while avoiding the development of resistant strains, and acidification of oral fluids to prevent bacterial overgrowth. The initial results need to be confirmed, but it is likely that one or more of these prevention measures will lower the incidence of NEC in the future.

Aminoglycosides↗
PubMed2003

Late graft loss after intestinal transplantation in an adult patient as a result of necrotizing enterocolitis.

A 50-year-old recipient of an intestinal and coecal graft with sudden onset of abdominal distention and pain, lack of bowel movements, and vomiting after closure of the diagnostic ostomy 7 months after transplantation is reported. A plain abdominal radiograph revealed pneumatosis intestinalis. An angiography excluded obstruction of large vessels, however, with absent microcirculation of the intestine. Upper gastrointestinal endoscopy showed extensive ulcerative enteritis with several spontaneous perforations. The patient underwent exploration demonstrating a nonviable intestine. The entire necrotic intestine was removed. Vascular thrombosis was excluded. Clinical data, and macroscopic and histologic features of the intestinal graft were diagnostic for necrotizing enterocolitis (NEC). Though there has been evidence for the occurrence of NEC not only in premature infants but even in older infants, children and adolescents, the presented case is, to our knowledge, the first report of NEC as etiology of late graft loss after intestinal transplantation in an adult recipient.

Enterocolitis, Necrotizing↗
PubMed1994

An animal model of necrotizing enterocolitis induced by infant formula and ischemia in developing piglets.

BACKGROUND/AIMS: The lipid component of piglet formula (0.5% fat) causes increased mucosal permeability in 1-day-old piglets after ischemia/reperfusion. The present study examined if luminal exposure to infant formulas (3.5% fat) and ischemia/reperfusion result in an animal model of necrotizing enterocolitis and if injury is dependent on the formula fat composition. METHODS: Plasma-to-lumen clearance of 51Cr-ethylenediamine-tetraacetic acid was measured, and morphology was evaluated during luminal perfusion with preterm, term, and delipidated preterm cow milk-based infant formulas before and after ischemia/reperfusion in 1-day-old and 1-month-old piglet jejunoileum. In a separate set of experiments, a 1-2-cm segment of ileum was exteriorized and opened to expose the mucosal surface, and the villi were superfused with the above formulas (no ischemia). RESULTS: Before ischemia, clearances were markedly higher for intestinal loops perfused with preterm formula than for loops perfused with term and delipidated formulas in 1-day-old animals. After ischemia, clearances in loops perfused with preterm formula were significantly greater and grossly hemorrhagic and histologically necrotic compared with loops perfused with delipidated formula (minimal injury). Superfusion with preterm formula caused diffuse hyperemia and hemorrhage into intestinal villi. CONCLUSIONS: Luminal perfusion of 1-day-old piglet jejunoileum with predigested and bile acid-solubilized preterm infant formula, in combination with ischemia/reperfusion, produces an animal model of necrotizing enterocolitis, but only if the lipid fraction of the formula is present.

Animal Feed↗
PubMed1999

Conservative intestinal surgery to avoid short-bowel syndrome in multiple intestinal atresias and necrotizing enterocolitis: 6 cases treated by multiple anastomoses and Santulli-type enterostomy.

Neonates with multiple sites of intestinal atresia (MIA) may be predisposed to short-gut syndrome. Anastomoses of the intervening segments may prevent this complication. 5 neonates with MIA, one of them with a gastroschisis, were operated on: a proximal enterostomy was constructed, a side-to-end anastomosis as described by Santulli and several end-to-end anastomoses between the intervening intestinal segments (n = 3 to 7) were performed. An additional infant, initially operated on for a necrotizing enterocolitis (NEC) was managed with the same surgical procedure. Without use of this technique, the remaining length of small intestine would have been 28, 27, 40, 58, 70 and 7 cm. This technique enabled an intestinal length of 49, 54, 96, 107, 92 and 93 cm respectively to be achieved. Ileocecal valve was present in all 5 cases with MIA, but resected in the case with NEC. The enterostomy was reversed 7 weeks later. The initial outcome (delay of enteral feeding, duration of parenteral nutrition) was good: the babies were weaned from parenteral nutrition (PN) after a mean time of 90 days (48 to 163 days). The prognosis (mean follow-up: 31 months, range 14 to 57) was good with regards to growth and development and length of time required before adaptation to normal enteral feedings and stools. This surgical method allows complete decompression of the proximal jejunum so that nutriment can pass into the distal bowel allowing it to enlarge. In cases of MIA, a long tapering proximal enteroplasty is a better procedure than resecting more than 5-10 cm of the proximal distended and hypertrophied bowel. We prefer to perform an enterostomy in association with multiple anastomoses between intervening intestinal segments. The enterostomy is preserved for long enough waiting period to enable the reversion of the histochemical and morphological changes that may have taken place in the bowel.

Anastomosis, Surgical↗
PubMed2000

Graft failure secondary to necrotizing enterocolitis in multi-visceral transplantation recipients: two case reports.

We report on two recipients of multi-visceral grafts who exhibited sudden onset of acute abdomen discomfort 2 weeks post-transplantation after a fairly uneventful immediate post-operative course. Both patients were shown to have pneumatosis intestinalis and one had air in the portal vein. Both patients underwent exploration, which showed non-viable intestine (terminal ileum and colon in the first patient and the entire small intestine distal to the ligament of Treitz in the second patient). There was no vascular thrombosis. The necrotic intestine was resected in both cases. The first patient developed sepsis and died 15 days later despite the rescue efforts. The second patient was re-transplanted twice and is doing well. The histopathology of the segments involved revealed cryptitis, vasculitis, and features of transmural necrosis. Accordingly, both clinical and pathologic features are diagnostic of necrotizing enterocolitis. To our knowledge this is the first report of this complication following intestinal or multi-visceral transplantation.

Adolescent↗
PubMed2000

[Necrotizing enterocolitis: a historical and current review].

Enteritis necroticans, locally called "Darmbrand", is a severe and life threatening infectious disease which was epidemic in Northern Germany after World War II. Darmbrand had a limited appearance, occurring only for a few years. In Lübeck many cases were diagnosed in 1946/1948 and the book "Darmbrand, Enteritis necroticans" was published in 1949 by clinicians and pathologists. Enteritis necroticans is also known as a tropical cause of bloody diarrhea and is caused by Clostridium perfringens Type C (type beta-toxin). The disease is related to pig feasts in Papua New Guinea. Although necrotizing enterocolitis is now a rather rare disease we must be aware of the appearance of this fulminant entity. This paper represents a review on the historic and current aspects of enteritis necroticans and discusses the epidemiology, pathogenesis and treatment of this disease.

Clostridium Infections↗