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At least 19 recordsLinked to original sources

PubMed1991

Cocaine: a risk factor for necrotizing enterocolitis.

Necrotizing enterocolitis occurs most often in the small preterm infant, usually with birthweight less than 1.5 kg. Necrotizing enterocolitis has also been described in more mature infants, however, often the result of reduced gastrointestinal blood flow. We describe four relatively large infants from our nursery with varying severity of necrotizing enterocolitis. None had any of the known risk factors; all had a history of maternal cocaine use. Two were initially cared for in the term nursery. All four presented with abdominal distention, bloody stools, vomiting, or residuals. One infant presented with fulminant deterioration and subsequently died; the other three infants were treated medically and survived. It is suggested that a high index of suspicion be maintained for the possibility of necrotizing enterocolitis and feeding intolerance in term and near-term infants exposed in utero to cocaine.

Cocaine↗

PubMed2001

New concepts in necrotizing enterocolitis.

Necrotizing enterocolitis is an overwhelming gastrointestinal emergency that primarily afflicts premature infants born weighing less than 1500 g. Despite years of investigation, the etiology remains unclear, and accepted prevention and treatment strategies are lacking. Studies published over the last year have provided new insight into several aspects of this complex disease. In this review, novel information is presented on (1) the epidemiology; (2) methods of early diagnosis, such as abdominal magnetic resonance imaging; (3) the importance of risk factors, including assessment of feeding strategies and role of bacterial colonization; (4) the pathophysiology, highlighting experimental and clinical trials evaluating the role of inflammatory mediators and growth factors on the disease; (5) preventive strategies, such as anaerobic bacterial supplementation; and (6) surgical interventions, including peritoneal drainage. Understanding some of these important aspects of necrotizing enterocolitis may help improve the outlook of patients with this dreaded disease. Although the incidence of neonatal necrotizing enterocolitis (NEC) and the mortality stemming from this disease have not significantly improved over the last 30 years, there is exciting new information that may significantly improve the outlook of patients with this overwhelming intestinal emergency in the near future.

Enterocolitis, Necrotizing↗

PubMed1998

Necrotizing enterocolitis.

Necrotizing enterocolitis is a relatively common disorder of unknown etiology that primarily affects premature newborns. The majority of babies with necrotizing enterocolitis respond to nonsurgical management, and, despite an increase in the number of premature infants, the surgical mortality rate has improved. This review provides an overview of the current literature covering new developments in etiology, risk factors, pathogenesis, diagnosis, therapy, outcome, and preventable measures related to necrotizing enterocolitis.

Animals↗

PubMed2000

Inflammation in the developing human intestine: A possible pathophysiologic contribution to necrotizing enterocolitis.

Necrotizing enterocolitis (NEC), a major cause of morbidity and mortality in premature infants, occurs after the introduction of oral feedings in conjunction with initial bacterial colonization of the gut and is hypothesized to be due to an immature (inappropriate) enterocyte response to bacterial stimuli. To test this hypothesis, we compared the enterocyte IL-8 response to inflammatory stimuli [lipopolysaccharide (LPS) and IL-1beta] in immature vs. mature human small intestine. Initial in vitro studies comparing confluent Caco-2 cells, a model for mature human enterocytes, with a primary human fetal intestinal cell line (H4 cells) demonstrated that after inflammatory stimulation fetal cells secreted more IL-8 (LPS, 8-fold; IL-1beta, 20-fold) than Caco-2 cells. IL-8 mRNA activity in fetal compared to Caco-2 cells was proportionately increased by the same magnitude with both stimuli. To validate the in vitro observations, small intestinal organ cultures from fetuses vs. older children were exposed to LPS and IL-1beta. Again in human organ cultures from fetuses compared to older children, IL-8 secretion was greater (LPS, 2.5-fold; IL-1beta, 200-fold) and mRNA activity after stimulation was comparably higher, suggesting that increased transcription of the IL-8 gene may account for the excessive response. Using immunohistochemical staining to identify the cellular source of IL-8, activity was noted predominantly in villous and crypt epithelium but also in a few immunoresponsive lymphoid cells. The observation that immature human enterocytes react with excessive pro-inflammatory cytokine production after inflammatory stimulation may help in part explain why prematures exposed to initial colonizing bacteria develop necrotizing enterocolitis.

Adenocarcinoma↗

PubMed2000

Inflammatory polyps after necrotizing enterocolitis.

Necrotizing enterocolitis (NEC) is the most common gastrointestinal emergency in the neonatal period. NEC causes ulceration of the intestinal mucosa and may lead to perforation or a stricture. To the best of the authors' knowledge intestinal inflammatory polyps after NEC have not been described previously. The authors report on a 17-week-old boy with pseudopolyps at the site of a colonic stricture after NEC.

Colonic Polyps↗

PubMed1999

Necrotizing enterocolitis.

Necrotizing enterocolitis (NEC) is the most serious and frequently acquired gastrointestinal disorder in neonates. The pathogenesis of NEC is unknown, but it may result from a disturbance of the delicate balance among gastrointestinal perfusion, enteric organisms, and enteral feeding. Risk factors for NEC include prematurity, hypoxic-ischemic insult, and formula or breast milk feedings. The clinical spectrum of NEC is multifactoral and ranges from temperature instability, apnea, lethargy, abdominal distention, bilious residuals, and guaiac-positive stools to septic shock, disseminated intravascular coagulation, and death. Medical management is usually adequate treatment for NEC. Surgical treatment is considered if medical management is inadequate to control the spread of the disease. Health care team members must be constantly alert to the presentation of NEC. Expeditious treatment will positively influence the outcome of the disease.

Colectomy↗

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↗

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↗

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↗

PubMed1994

Epidemiology of necrotizing enterocolitis.

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

Enterocolitis, Pseudomembranous↗

PubMed1987

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

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

Bacterial Toxins↗

PubMed1988

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

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

6-Ketoprostaglandin F1 alpha↗