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PubMed2000

Duodenal microflora in very-low-birth-weight neonates and relation to necrotizing enterocolitis.

Necrotizing enterocolitis (NEC) is the most common gastrointestinal emergency in the neonatal period. Small-bowel overgrowth with aerobic gram-negative bacteria has previously been implicated in the development of NEC. This prospective study performed quantitative bacteriology on 422 duodenal aspirates collected from 122 very-low-birth-weight (<1,500-g) newborns, at the time of routine changing of nasogastric tubes. Isolates of Enterobacteriaceae were typed by repetitive extragenic, palindromic PCR and pulsed-field gel electrophoresis. One or more samples from 50% of these infants yielded gram-negative bacteria, predominantly Escherichia coli, Klebsiella spp., and Enterobacter spp., with counts up to 10(8) CFU/g. The proportion of samples with gram-negative bacteria increased with postnatal age, while the percentage of sterile samples declined. Molecular typing revealed marked temporal clustering of indistinguishable strains. All infants had been fed prior to isolation of gram-negative organisms. Antibiotic use had no obvious effect on colonization with Enterobacteriaceae. There were 15 episodes of suspected NEC (stage I) and 8 confirmed cases of NEC (2 stage II and 6 stage III) during the study period. Duodenal aspirates were collected prior to clinical onset in 13 episodes of NEC. Seven of these yielded Enterobacteriaceae, of which five strains were also isolated from infants without NEC. Very-low-birth-weight infants have high levels of duodenal colonization with Enterobacteriaceae, with evidence of considerable cross-colonization with indistinguishable strains. There was no association between duodenal colonization with particular strains of Enterobacteriaceae and development of NEC.

Duodenum↗

PubMed2005

Carbon monoxide protects against the development of experimental necrotizing enterocolitis.

Necrotizing enterocolitis (NEC) is a disease of neonates that is increasing in incidence and often results in significant morbidity and mortality. Carbon monoxide (CO), a byproduct of the catabolism of heme, is known to have anti-inflammatory and antiapoptotic properties. In this study, we aimed to demonstrate that inhaled CO protects against the development of intestinal inflammation in a model of experimental NEC as well as decreases enterocyte cell death in vitro. Additionally, we also aimed to demonstrate that CO decreases enterocyte production of inducible nitric oxide synthase (iNOS) and nitric oxide (NO). Neonatal rats were exposed to intermittent hypoxia exposure and formula feeding to induce experimental NEC. Animals randomized to CO treatment were put in an environment containing 0.025% CO for 1 h/day on days 1-3 of life. All animals were killed on day 4 of life. In vitro experiments were performed with IEC-6 cells, a rat enterocyte cell line. Cells were examined for viability, iNOS production, and elaboration of NO. We found that CO diminished levels of serum inflammatory cytokines and nitrites, protected against intestinal inflammation, and decreased ileal iNOS production and protein nitration in a model of experimental NEC. In vitro, CO decreased cytokine- or hypoxia/endotoxin-induced iNOS and NO production. CO also abrogated TNF-alpha- and actinomycin D-induced apoptosis or hypoxia/endotoxin-induced cell death. In conclusion, 1 h of daily low-dose inhaled CO protected against the development of intestinal inflammation in a model of experimental NEC. iNOS and NO production were decreased by CO both in vivo and in vitro. CO may prove to be a useful clinical adjunct in the treatment of NEC.

Administration, Inhalation↗

PubMed2005

Glucocorticoid responsiveness in developing human intestine: possible role in prevention of necrotizing enterocolitis.

Necrotizing enterocolitis (NEC) is a major inflammatory disease of the premature human intestine that can be prevented by glucocorticoids if given prenatally before the 34th wk of gestation. This observation suggests that a finite period of steroid responsiveness exists as has been demonstrated in animal models. Human intestinal xenografts were used to determine whether a glucocorticoid responsive period exists in the developing human intestine. Developmental responsiveness was measured by lactase activity and inflammatory responsiveness by IL-8, IL-6, and monocyte chemotactic protein-1 (MCP-1) induction after an endogenous (IL-1 beta) or exogenous (LPS) proinflammatory stimulus, respectively. Functional development of ileal xenografts were monitored for 30 wk posttransplantation, and the lactase activity recapitulated that predicted by in utero development. Cortisone acetate accelerated the ontogeny of lactase at 20 wk (immature) but the effect was lost by 30 wk (mature) posttransplant. Concomitant with accelerated maturation, the IL-8 response to both IL-1 beta and LPS was significantly dampened (from 6- to 3-fold) by glucocorticoid pretreatment in the immature but not mature xenografts. The induction of IL-8 was reflected at the level of IL-8 mRNA, suggesting transcriptional regulation. The excessive activation of IL-8 in the immature gut was mediated by a prolonged activation of ERK and p38 kinases and nuclear translocation of NF-kappa B due to low levels of I kappa B. Steroid pretreatment in immature intestine dampens activation of all three signaling pathways in response to proinflammatory stimuli. Therefore, accelerating intestinal maturation by glucocorticoids within the responsive period by accelerating functional and inflammatory maturation may provide an effective preventive therapy for NEC.

Animals↗

PubMed2004

Epidermal growth factor reduces intestinal apoptosis in an experimental model of necrotizing enterocolitis.

Necrotizing enterocolitis (NEC) is a devastating intestinal disease of premature infants. Although end-stage NEC is characterized histopathologically as extensive necrosis, apoptosis may account for the initial loss of epithelium before full development of disease. We have previously shown that epidermal growth factor (EGF) reduces the incidence of NEC in a rat model. Although EGF has been shown to protect intestinal enterocytes from apoptosis, the mechanism of EGF-mediated protection against NEC is not known. The aim of this study was to investigate if EGF treatment elicits changes in expression of apoptotic markers in the ileum during the development of NEC. With the use of a well-established neonatal rat model of NEC, rats were divided into the following three experimental groups: dam fed (DF), milk formula fed (NEC), or fed with formula supplemented with 500 ng/ml EGF (NEC+EGF). Changes in ileal morphology, gene and protein expression, and histological localization of apoptotic regulators were evaluated. Anti-apoptotic Bcl-2 mRNA levels were markedly reduced and pro-apoptotic Bax mRNA levels were markedly elevated in the NEC group compared with DF controls. Supplementation of EGF into formula significantly increased anti-apoptotic Bcl-2 mRNA, whereas pro-apoptotic Bax was significantly decreased. The Bax-to-Bcl-2 ratio for mRNA and protein was markedly decreased in NEC+EGF animals compared with the NEC group. The presence of caspase-3-positive epithelial cells was markedly reduced in EGF-treated rats. These data suggest that alteration of the balance between pro-and anti-apoptotic proteins in the site of injury is a possible mechanism by which EGF maintains intestinal integrity and protects intestinal epithelium against NEC injury.

Animals↗

PubMed2003

Hepatic inflammatory mediators contribute to intestinal damage in necrotizing enterocolitis.

Necrotizing enterocolitis (NEC) is a common and devastating gastrointestinal disease of premature infants. Along with pathological effects in the ileum, severe NEC is often accompanied by multisystem organ failure, including liver failure. The aim of this study was to determine the changes in hepatic cytokines and inflammatory mediators in experimental NEC. The well-established neonatal rat model of NEC was used in this study, and changes in liver morphology, numbers of Kupffer cells (KC), gene expression, and histological localization of IL-18, TNF-alpha, and inducible nitric oxide synthase were evaluated. Intestinal luminal TNF-alpha levels were also measured. Production of hepatic IL-18 and TNF-alpha and numbers of KC were increased in rats with NEC and correlated with the progression of intestinal damage during NEC development. Furthermore, increased levels of TNF-alpha in the intestinal lumen of rats with NEC was significantly decreased when KC were inhibited with gadolinium chloride. These results suggest an important role of the liver and the gut-liver axis in NEC pathogenesis.

Animals↗

PubMed2003

Pump implantation for intrathecal baclofen infusion after laparotomy for necrotizing enterocolitis.

Necrotizing enterocolitis (NEC) and spastic cerebral palsy are both familiar complications of prematurity. Children who are otherwise candidates for intrathecal baclofen infusion occasionally have long, transverse, right midabdominal laparotomy incisions from past management of NEC, and these incisions may interfere with selection of a site for pump implantation. Successful pump implantation immediately beneath a laparotomy incision was accomplished using a modification of the popular subfascial technique.

Baclofen↗

PubMed2002

The cost-effectiveness of using banked donor milk in the neonatal intensive care unit: prevention of necrotizing enterocolitis.

Necrotizing enterocolitis (NEC) adds significantly to the cost of care for premature infants and to negative long-term and short-term outcomes for these infants. It is thus in the best interest of the health care system to prevent the occurrence of NEC through feeding protocols that foster NEC prevention (i.e., use of breast milk in the neonatal intensive care unit). Banked donor milk has been shown to be as effective in preventing NEC as mother's milk. Three models of cost analysis are presented to show savings that could accrue to a health care system or individual family if banked donor milk were provided as first feedings when mother's milk is not available. The cost of using banked donor milk to feed premature infants is inconsequential when compared to the savings from NEC prevention.

Cost-Benefit Analysis↗

PubMed2002

Up-regulation of IL-18 and IL-12 in the ileum of neonatal rats with necrotizing enterocolitis.

Necrotizing enterocolitis (NEC) is a common and devastating gastrointestinal disease of premature infants. Because the proinflammatory cytokines IL-18, IL-12, and interferon (IFN)-gamma have been implicated in other diseases of the small intestine, we hypothesized that these cytokines would play an important role in NEC pathogenesis. NEC was induced in newborn rats via enteral feeding with rat milk substitute and asphyxia and cold stress (RMS). Dam-fed, asphyxia- and cold-stressed littermates were used as controls (DF). After 96 h, the distal ileum was removed from all animals and processed to determine expression and localization of IL-18, IL-12, and IFN-gamma using real-time reverse transcriptase PCR and immunohistology. IL-18 and IL-12 mRNA from the RMS group were increased (p < or = 0.05) compared with DF controls, and there was a correlation between increasing IL-18 and IL-12 mRNA levels and progression of tissue damage (r = 0.629 and 0.588, respectively; p < or = 0.05). Immunohistology revealed IL-18 in the cytoplasm of villi and crypt enterocytes and IL-12-positive monocytes/macrophages were increased with disease progression (r = 0.503, p < or = 0.05). No differences in the number of IFN-gamma-positive cells were observed between groups. These data demonstrate up-regulation of IL-18 and IL-12 in experimental NEC and a correlation between production of these proinflammatory cytokines and progression of tissue damage.

Animals↗

PubMedDate not supplied

Pathophysiology and current management of necrotizing enterocolitis.

Necrotizing enterocolitis continues to be a common and life-threatening gastrointestinal emergency in the low birth weight infant. Prematurity, ischemia, enteral feeding, and infectious disease have been identified as common risk factors, however the exact cause of NEC other than prematurity is yet to be identified. Good assessment skills by the nurse are imperative, because clinical signs of NEC can be both subtle and catastrophic. Frequent radiographs are essential for the diagnosis of NEC and ongoing assessment of neonates diagnosed with NEC. Radiographs including an abdominal flat plate examination and a left lateral decubitus film to evaluate for free air should be obtained every 6-8 hours in the neonates with Stages II and III NEC.

Enteral Nutrition↗

PubMed1995

Surgical management of pediatric necrotizing enterocolitis.

Necrotizing enterocolitis is one of the most common gastrointestinal emergencies observed in neonatal intensive care units. Despite extensive research efforts, the etiology and pathogenesis of necrotizing enterocolitis remain unclear. Investigators have attempted to identify various laboratory and clinical factors that would serve as criteria for surgical intervention. Unfortunately, the most sensitive and specific tests detect only advanced disease and perforation. The mainstay of surgical treatment is resection with enterostomy, although resection and primary anastomosis is useful in selected cases. In addition, some neonates may benefit from peritoneal drainage, second look procedures, or proximal diversion.

Anastomosis, Surgical↗

PubMed1976

Changing clinical and roentgenographic patterns of necrotizing enterocolitis.

Necrotizing enterocolitis (NEC) occasionally deviates from the classical presentation of the disease. Small bowel dilatation and pneumatosis are frequently present prior to the actual onset of the clinical presentation. Pneumatosis intestinalis, an important diagnostic sign of NEC, is quite variable; it may be present, persist, worsen, or disappear; or at times it may not be present at all. A severe complication of necrotizing enterocolitis is perforation which in 50 percent of the cases presented without obvious free intra-abdominal air. Accumulation of fluid in the abdomen is stressed as strong evidence for perforation and a strong indication for surgery. The varying features indicate that NEC has a clinical spectrum that extends from benign to severe, and recognition of all these variations will lead to better diagnosis and to a better understanding of the disease. The clinical and roentgenologic variations make classification difficult but the variety most likely represents the combination of a great number of susceptible children and a greater recognition of the disease.

Air↗

PubMed2002

[Surgical treatment of children with necrotizing enterocolitis].

Necrotizing enterocolitis is an acute neonatal disease. It affects in particular premature neonates with a birth weight lower than 1500 g. Despite extensive research the etiology of the disease remains obscure. The majority of authors assume multifactorial causes. Research workers try to detect various laboratory and clinical factors which could serve as criteria for surgical intervention. The sensitivity and specificity of these tests and laboratory examinations detect the disease only in an advanced stage and in the stage of perforation of the gastrointestinal tract (GIT). The main surgical approach to the treatment of this disease remains laparotomy and resection of the necrotic portion of the gut with enterostomy. In a limited number of children resection of a portion of the necrotic gut with primary anastomosis is possible. In some very serious conditions and in infants with a birth weight below 1000 g peritoneal drainage and subsequent "second look" surgery should be sufficient. It is a disease with calls for a maximum individual approach and there are no accurate defined instructions for surgical treatment. The surgeon's experience and the standard of preoperative and postoperative care are decisive.

Enterocolitis, Necrotizing↗

PubMed1996

Resection and primary anastomosis in necrotizing enterocolitis.

Necrotizing enterocolitis (NEC) is the most common surgical emergency in the newborn. Up to half of babies with NEC develop advanced disease requiring surgical intervention. Options include peritoneal drainage under local anaesthetic, enterostomy only, resection and enterostomies, and resection with primary anastomosis. Resection with enterostomies is favoured by many paediatric surgeons but management of neonatal enterostomies can be difficult. The outcome of 26 infants undergoing surgery for advanced NEC over a 2-year period is reviewed. Resection and primary anastomosis was possible in 18 infants of whom two (11%) died. Recurrent NEC developed in four (22%) and strictures in three (17%) of these infants. An initial enterostomy was fashioned in eight infants, three following resection of necrotic intestine and five as a proximal diverting stoma in infants with pan-intestinal involvement. Five of these eight infants died (63%), giving an overall mortality of 27%. Primary anastomosis is an effective procedure following resection of grossly involved intestine in infants with NEC. The mortality and morbidity in this series compared well with those reported for staged procedures.

Anastomosis, Surgical↗

PubMed1988

Use of the barium enema in the diagnosis of necrotizing enterocolitis.

Necrotizing enterocolitis (NEC) is associated with considerable morbidity and mortality in infants. The diagnosis relies heavily upon radiographic and clinical features. Failure to accurately diagnose NEC is associated with a risk of complications and death, however overdiagnosis also causes both morbidity and mortality as well as excessive medical costs. This report documents the use of barium enema to evaluate suspected clinical or radiographic NEC in 31 premature infants with ambiguous clinical and radiographic signs. The enema was normal in 26 infants and no treatment for NEC was given. Only one of these infants developed signs of NEC subsequent to the examination. Five infants had radiographic evidence of colitis including small ulcerations, spasm, intramural extravasation of barium and mucosal irregularity. Two of the five positive cases are pathologically documented. The barium enema can represent a significant improvement in the specificity of the diagnosis of NEC. Its greatest value is in the exclusion of NEC in ambiguous cases.

Barium Sulfate↗

PubMed1991

Hypoxia, PAF, and necrotizing enterocolitis.

Necrotizing enterocolitis (NEC) is an important neonatal disease with a high mortality rate. The pathophysiology is unclear but epidemiologic studies suggest that hypoxia and infection are important risk factors. In this review we discuss the effect of hypoxia and platelet-activating factor (PAF) on intestinal blood flow and intestinal necrosis, and implicate PAF as an important mediator in hypoxia-induced intestinal injury. Finally we provide evidence that PAF may be important in neonatal NEC.

Animals↗

PubMed1981

Early operation with intestinal diversion for necrotizing enterocolitis.

Necrotizing enterocolitis (NEC) remains a highly lethal disorder despite significant advances in management during the past decade. Increased mortality with perforation and the frequent finding of massive intestinal necrosis have hampered efforts to improve survival. A recent experience with early operation and intestinal diversion in selected patients with clinical features suggesting impending intestinal gangrene suggests a place in the management of infants with rapidly progressive NEC.

Enterocolitis, Pseudomembranous↗

PubMed1987

Hypertonicity of intestinal smooth muscle as a factor of intestinal ischemia in necrotizing enterocolitis.

Necrotizing enterocolitis (NEC) is thought to be secondary to mucosal ischemia. Because blood flow to the submucosal plexus is derived from vessels traversing three separate layers of visceral smooth muscle (longitudinal, circular, and muscularis mucosa), we investigated whether an increase in their tone might elicit mucosal ischemia. The intestinal intraluminal pressure (IIP) and the superior mesenteric artery (SMA) blood flow were evaluated in 23 dogs before and after either ligation of the SMA or neostigmine infusion into the SMA. Changes in vascularity were assessed by silicone rubber casting, India ink, or arteriography. Ten minutes after ligation of the SMA, there was a considerable increase in peristalsis, IIP, and inability to fill the intestinal microcirculation by the three methods described. Mucosal necrosis was present three hours later. In the neostigmine infusion group after a transient increase in mesenteric flow, the IIP rose 750%, while the mesenteric flow fell by 40%, mucosal necrosis occurred in one hour. When myotomy was performed on the antimesenteric border, mucosal necrosis was prevented. In a third group, neostigmine infused (femoral artery) in the hind limb demonstrated vasodilating effects. The data indicate that an increase in the myogenic tone and frequency of contraction of intestinal smooth muscle can produce mucosal ischemia, thus, intestinal hypertonicity may be an important factor in the pathogenesis of intestinal ischemia and possibly NEC. The effects of neostigmine in these experiments raise questions regarding its use during anesthesia in neonates with intestinal low flow states.

Animals↗

PubMed1994

Ostomy care for infants with necrotizing enterocolitis.

Necrotizing Enterocolitis, a disease that affects the gastrointestinal tract of some premature neonates, often results in a temporary stoma. The fragile skin of these neonates, the small surface area of their abdomens, and the limited ostomy supplies available in appropriate sizes can cause difficult pouching situations. The use of a flexible skin barrier with the smallest available pouch maintains the principles of ostomy care, protecting the skin and containing the effluent.

Enterocolitis, Pseudomembranous↗