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 145 records · Page 8Linked to original sources

Necrotizing enterocolitis in very low birth weight infants: biodemographic and clinical correlates. National Institute of Child Health and Human Development Neonatal Research Network.

We studied the occurrence of necrotizing enterocolitis in 2681 very low birth weight infants during an 18-month period to characterize the biodemographic and clinical correlates. Proven necrotizing enterocolitis (Bell stage II and beyond) occurred in 10.1% of study infants; necrotizing enterocolitis was suspected in 17.2% of study infants. Positivity of blood cultures was related to necrotizing enterocolitis staging. The mortality rate increased only for stage III necrotizing enterocolitis (54% died). Logistic regression identified medical center of birth, race, gender, birth weight, maternal hemorrhage, duration of ruptured membranes, and cesarean section as significant risk factors. For one center the odds ratio was 3.7, whereas for another center it was only 0.3. For black boys, the odds ratio was 2.3 relative to nonblack boys; for girls, race did not affect prevalence of necrotizing enterocolitis. Age at onset was related to birth weight and gestational age. Intercenter differences in necrotizing enterocolitis prevalence were related to time required to regain birth weight and other indicators of fluid management. Gram-positive organisms predominated in positive blood cultures for stage I and II necrotizing enterocolitis; enteric bacteria were isolated more frequently in infants with stage III disease. We conclude that necrotizing enterocolitis prevalence varies greatly among centers; this may be related to early clinical practices of neonatal care.

Birth Weight↗

Effect of necrotizing enterocolitis on urinary epidermal growth factor levels.

The pattern of urinary epidermal growth factor/creatinine levels in necrotizing enterocolitis was examined in 75 infants (in 28 infants the diagnosis of necrotizing enterocolitis was considered; 47 infants were studied for effect of surgery or nutrition on epidermal growth factor levels). There was a consistent and significant increase in epidermal growth factor/creatinine values at the time of diagnosis of necrotizing enterocolitis compared with baseline values. Epidermal growth factor levels in infants without necrotizing enterocolitis and in early nutrition remained unchanged. These results suggested that urinary epidermal growth factor/creatinine levels may differentiate stage II and III necrotizing enterocolitis from stage I disease. The increased epidermal growth factor/creatinine levels may be related to the absorption into the circulation of preexisting gastrointestinal tract epidermal growth factor through damaged tissue or to increased synthesis by the gastrointestinal tract in response to the injury caused by necrotizing enterocolitis.

Creatinine↗

Oral immunoglobulin for preventing necrotizing enterocolitis in preterm and low birth-weight neonates.

BACKGROUND: Necrotizing enterocolitis (NEC) is the most common emergency of the gastrointestinal tract occurring in the neonatal period. There have been published reports which suggest that oral immunoglobulins IgA and IgG produce an immunoprotective effect in the gastrointestinal mucosa. This systematic review was undertaken to clarify the issue. OBJECTIVES: To assess whether oral immunoglobulin administered to preterm and low birth-weight neonates reduces the incidence of necrotizing enterocolitis without adverse effects. SEARCH STRATEGY: The databases MEDLINE, CINAHL, EMBASE (1966 to October 26, 2003) and the Cochrane Central Register of Controlled Trials (CENTRAL, The Cochrane Library, Issue 3, 2003) were searched. Proceedings of the Perinatal Society of Australia and New Zealand were hand searched. The computer neonatal discussion site 'Nicu Net' was also used. Additionally, all references in the identified trials were checked and authors were contacted to request any additional published or unpublished data. No new trials were identified. SELECTION CRITERIA: All randomised or quasi-randomised controlled trials where oral immunoglobulins were used as prophylaxis against necrotizing enterocolitis in preterm (<37 weeks gestation) and/or low birth-weight (<2500 gms) neonates. DATA COLLECTION AND ANALYSIS: The procedures of the Cochrane Neonatal Review Group (CNRG) were used. The two reviewers independently assessed the trials for their methodological quality and subsequent inclusion in the review. Relative risk (RR), risk difference (RD), and number needed to treat (NNT) were used in the analysis. MAIN RESULTS: Five studies on oral immunoglobulin for the prevention of necrotizing enterocolitis were identified of which three met the inclusion criteria. In this review of the three eligible trials (including a total of 2095 neonates) the oral administration of IgG or an IgG/IgA combination did not result in a significant reduction in the incidence of definite NEC [RR 0.84 (95% CI 0.57, 1.25), RD -0.01 (95% CI -0.03, 0.01)], suspected NEC [RR 0.84 (95% CI 0.49, 1.46), RD -0.01 (95% CI -0.02, 0.01)], need for surgery [RR 0.21 (95% CI 0.02, 1.75), RD -0.03 (95% CI -0.06, 0.00)] or death from NEC [RR 1.10 (95% CI 0.47, 2.59), RD 0.00 (95% CI -0.01, 0.01)]. REVIEWER'S CONCLUSIONS: Based on the available trials, the evidence does not support the administration of oral immunoglobulin for the prevention of NEC. There are no randomised controlled trials of oral IgA alone for the prevention of NEC.

Administration, Oral↗

Epidemiologic characteristics of necrotizing enterocolitis: a population-based study.

The authors studied retrospectively the epidemiologic characteristics of necrotizing enterocolitis occurring among Georgia infants born during 1977 and 1978; 148 cases of necrotizing enterocolitis were identified. The highest incidence rate for necrotizing enterocolitis occurred among infants weighing 751-1000 g at birth and declined with increasing birth weight to less than 0.2 cases per 1000 live births among infants weighing more than 2500 g at birth. The overall incidence rate for blacks was significantly greater than that for whites (1.6 vs. 0.5 cases per 1000 live births, p = 0.01). The overall case fatality ratio was 38.5%; there were no differences in these ratios between blacks and whites. Necrotizing enterocolitis accounted for 15% of all deaths after the first week of life for infants weighting 1500 g or less at birth. If Georgia incidence rates and fatality ratios are applied to 1978 US births, it is estimated that 2210 cases of necrotizing enterocolitis with over 900 associated deaths would have occurred.

Birth Weight↗

Perinatal risk factors for necrotizing enterocolitis.

The perinatal histories of 50 very low birthweight infants weighing 1500 g, or less, with necrotizing enterocolitis were compared with those of the remaining 325 very low birthweight infants who were admitted to this hospital during a four year study period. Many factors previously reported to be associated with necrotizing enterocolitis were found with equal frequency in both groups of babies. The only adverse factor which was more frequently present in patients with necrotizing enterocolitis was hypothermia on admission to hospital. Those infants who developed severe necrotizing enterocolitis also had a higher incidence of polycythaemia. A further controlled study which examined feeding practices showed that the timing, type, and volume of milk feeding were not different in infants with necrotizing enterocolitis and matched controls. Prematurity is clearly the greatest risk factor which predisposes to the development of necrotizing enterocolitis and most of the factors previously implicated in the aetiology may simply represent the descriptive characteristics of a population of sick, very low birthweight infants.

Animals↗

Prevention of necrotizing enterocolitis in preterm infants: a 20-year experience.

OBJECTIVE: Diet, indomethacin, and early use of dexamethasone have been implicated as possible causes of necrotizing enterocolitis and intestinal perforation. Because we seldom prescribe indomethacin or early dexamethasone therapy and we follow a special dietary regimen that provides late-onset, slow, continuous drip enteral feeding, we reviewed our 20 years of experience for the incidence of necrotizing enterocolitis and bowel perforation. METHODS: We reviewed data on all 1239 very low birth weight infants (501-1500 g) admitted to our level III unit over a period of 20 years (1986-2005), for morphologic parameters, necrotizing enterocolitis, bowel perforation, use of the late-onset, slow, continuous drip protocol, and indomethacin therapy. Outcome data were also compared with Vermont Oxford Network data for the last 4 years. RESULTS: In 20 years, 1158 infants received the late-onset, slow, continuous drip feeding protocol (group I), whereas 81 infants had either a change in dietary regimen, use of indomethacin, or early use of dexamethasone (group II). The rate of necrotizing enterocolitis in group I of 0.4% was significantly lower than that in group II of 6%. Group I, in comparison with the Vermont Oxford Network, had significantly lower rates of necrotizing enterocolitis (0.4% vs 5.9%), surgical necrotizing enterocolitis (0.4% vs 3.1%), and bowel perforation (0.35% vs 2.2%). CONCLUSIONS: Our 20-year experience with 1239 very low birth weight infants suggests strongly that the late-onset, slow, continuous drip feeding protocol and avoidance of indomethacin and early dexamethasone treatment contribute to the prevention of necrotizing enterocolitis.

Dexamethasone↗

Gastroenteritis with necrotizing enterocolitis in premature babies.

Eleven premature babies developed necrotizing enterocolitis in an epidemic of gastroenteritis and salmonella infection. This occurred in one of two premature baby wards over a period of 10 weeks. All affected babies had severe gastroenteritis and six had salmonella infection. No cases of necrotizing enterocolitis occurred in the unaffected ward during the same period. All other possible factors which might have predisposed to necrotizing enterocolitis occurred with equal frequency in both wards.There seems little doubt that infection was the significant factor in the pathogenesis.

Black or African American↗

Neonatal necrotizing enterocolitis: clinical considerations and pathogenetic concepts.

Necrotizing enterocolitis (NEC), a disease affecting predominantly premature infants, is a leading cause of morbidity and mortality in neonatal intensive care units. Although several predisposing factors have been identified, such as prematurity, enteral feeding, and infection, its pathogenesis remains elusive. In the past 20 years, we have established several animal models of NEC in rats and found several endogenous mediators, especially platelet-activating factor (PAF), which may play a pivotal role in NEC. Injection of PAF induces intestinal necrosis, and PAF antagonists prevent the bowel injury induced by bacterial endotoxin, hypoxia, or challenge with tumor necrosis factor-a (TNF) plus endotoxin in adult rats. The same is true for lesions induced by hypoxia and enteral feeding in neonatal animals. Human patients with NEC show high levels of PAF and decreased plasma PAF-acetylhydrolase, the enzyme degrading PAF. The initial event in our experimental models of NEC is probably polymorphonuclear leukocyte (PMN) activation and adhesion to venules in the intestine, which initiates a local inflammatory reaction involving proinflammatory mediators including TNF, complement, prostaglandins, and leukotriene C4. Subsequent norepinephrine release and mesenteric vasoconstriction result in splanchnic ischemia and reperfusion. Bacterial products (e.g., endotoxin) enter the intestinal tissue during local mucosal barrier breakdown, and endotoxin synergizes with PAF to amplify the inflammation. Reactive oxygen species produced by the activated leukocytes and by intestinal epithelial xanthine oxidase may be the final pathway for tissue injury. Protective mechanisms include nitric oxide produced by the constitutive (mainly neuronal) nitric oxide synthase, and indigenous probiotics such as Bifidobacteria infantis. The former maintains intestinal perfusion and the integrity of the mucosal barrier, and the latter keep virulent bacteria in check. The development of tissue injury depends on the balance between injurious and protective mechanisms.

Animals↗

Surgical therapy for necrotizing enterocolitis: bringing evidence to the bedside.

Necrotizing enterocolitis is the most common surgical emergency in the neonatal intensive care unit. Despite decades of research that have led to a growing knowledge base about this disease, NEC continues to challenge the pediatric surgeon. In this review, we will examine the development of surgical therapy for NEC in the context of the supportive evidence, or lack thereof, for treatment approaches. We will discuss issues of indications for surgical intervention, primary peritoneal drainage versus laparotomy, enterostomy versus primary anastamosis and issues surrounding NEC totalis.

Anastomosis, Surgical↗

Intestinal barrier failure during experimental necrotizing enterocolitis: protective effect of EGF treatment.

Necrotizing enterocolitis (NEC) is the most common intestinal disease of premature infants. Although increased mucosal permeability and altered epithelial structure have been associated with many intestinal disorders, the role of intestinal barrier function in NEC pathogenesis is currently unknown. We investigated the structural and functional changes of the intestinal barrier in a rat model of NEC. In addition, the effect of EGF treatment on intestinal barrier function was evaluated. Premature rats were divided into three groups: dam fed (DF), formula fed (NEC), or fed with formula supplemented with 500 ng/ml EGF (NEC + EGF); all groups were exposed to asphyxia/cold stress to develop NEC. Intestinal permeability, goblet cell density, mucin production, and composition of tight junction (TJ) proteins were evaluated in the terminal ileum, the site of NEC injury, and compared with the proximal jejunum, which was unaffected by NEC. Animals with NEC had significantly increased intestinal paracellular permeability compared with DF pups. Ileal goblet cell morphology, mucin production, and TJ composition were altered in animals with NEC. EGF treatment significantly decreased intestinal paracellular permeability, increased goblet cell density and mucin production, and normalized expression of two major TJ proteins, occludin and claudin-3, in the ileum. In conclusion, experimental NEC is associated with disruption of the intestinal barrier. EGF treatment maintains intestinal integrity at the site of injury by accelerating goblet cell maturation and mucin production and normalizing expression of TJ proteins, leading to improved intestinal barrier function.

Animals↗

Epidermal growth factor reduces the development of necrotizing enterocolitis in a neonatal rat model.

Necrotizing enterocolitis (NEC) is the most common gastrointestinal disease of prematurely born infants. Maternal milk plays an important protective role against NEC development and is the major source of epidermal growth factor (EGF) for neonates. The aim of this study was to examine the effect of orally administered EGF on the incidence of NEC in a neonatal rat model. Newborn rats were artificially fed either with growth factor-free rat milk substitute (RMS) or RMS supplemented with 500 ng/ml of EGF (RMS+EGF). Experimental NEC was induced by exposure to asphyxia and cold stress. Development of NEC was evaluated by gross and histological scoring of damage in the ileum. Ileal EGF receptor (EGF-R), EGF, and transforming growth factor-alpha mRNA expression was assessed by RT competitive-PCR, and the EGF-R was localized by immunohistochemistry. EGF supplementation of formula reduced the incidence and severity of NEC in rats (13/16 RMS vs. 4/13 RMS+EGF). Ileal EGF-R mRNA expression was markedly increased in the RMS group compared with RMS+EGF. Enhanced EGF-R expression in the RMS group was localized predominantly in the epithelial cells of injured ileum. These data suggest a new potential therapeutic approach for the prevention and treatment of NEC.

Animals↗

Reduction of experimental necrotizing enterocolitis with anti-TNF-alpha.

Necrotizing enterocolitis (NEC) is the most common gastrointestinal disease of premature infants. However, despite significant morbidity and mortality, the etiology and pathogenesis of NEC are poorly understood. Evidence suggests that ileal proinflammatory mediators such as IL-18 contribute to the pathology associated with this disease. In addition, we have previously shown that upregulation of TNF-alpha in the liver is correlated with ileal disease severity in a neonatal rat model of NEC. With the use of a neonatal rat model of NEC, we evaluated the incidence and severity of ileal damage along with the production of both hepatic and ileal proinflammatory cytokines in animals injected with (anti-TNF-alpha; n = 23) or without (NEC; n = 25) a monoclonal anti-TNF-alpha antibody. In addition, we assessed changes in apoptosis and ileal permeability in the NEC and anti-TNF-alpha groups. Ileal damage was significantly decreased, and the incidence of NEC was reduced from 80% to 17% in animals receiving anti-TNF-alpha. Hepatic TNF-alpha and hepatic and ileal IL-18 were significantly decreased in pups given anti-TNF-alpha compared with those sham injected. In addition, ileal luminal levels of both TNF-alpha and IL-18 were significantly decreased in the anti-TNF-alpha-injected group. Ileal paracellular permeability and the proapoptotic markers Bax and cleaved caspase-3 were significantly decreased in the anti-TNF-alpha group. These data show that hepatic TNF-alpha is an important component for the development of NEC in the neonatal rat model and suggest that anti-TNF-alpha could be used as a potential therapy for human NEC.

Animals↗

Pentoxifylline reduces the incidence and severity of necrotizing enterocolitis in a neonatal rat model.

Necrotizing enterocolitis (NEC) is a potentially fatal illness in premature neonates. Tumor necrosis factor alpha (TNF-alpha) has been shown to play a central role in the inflammatory cascade leading to the development of NEC. Published evidence points to a significant role of pentoxifylline in inhibition of TNF-alpha and in reducing mucosal injury and improving healing in ischemia-reperfusion experiments. Our aim was to investigate the effect of pentoxifylline on the incidence of NEC in a neonatal rat model. Newborn Sprague-Dawley rat pups originating from eight separate litters were delivered by cesarean section at 21.5 d and were formula fed from birth by orogastric gavage. The rat pups were randomized to receive either intraperitoneal pentoxifylline (15 mg/kg/dose) or placebo, given every 8 h beginning at 24 h of age, in a blinded fashion. Experimental NEC was induced by exposure to hypoxia for 60 s followed by cold stress at 4 degrees C for 10 min. The animals were euthanized at development of NEC or at 96 h and intestinal tissue was processed and examined for histologic changes of NEC. The incidence of NEC was significantly lower in the pentoxifylline group [pentoxifylline 5/38 versus placebo 15/36; p = 0.008, odds ratio (OR) = 0.21 95% confidence interval (CI) 0.07-0.67]. Among the pups developing NEC, significantly fewer rat pups treated with pentoxifylline had severe (>or=3) intestinal injury scores [pentoxifylline 1/5 versus placebo 10/15; p = 0.031, OR 0.06, 95% CI 0.01-0.79]. We conclude that intraperitoneal administration of pentoxifylline significantly reduced the incidence and severity of NEC in our experimental animal model.

Animals↗

Current prognosis in necrotizing enterocolitis with portal vein gas.

OBJECTIVE: To investigate anecdotal reports that portal vein gas in necrotizing enterocolitis is no longer associated with a poor prognosis. PATIENTS AND METHODS: Twelve cases of neonatal necrotizing enterocolitis with portal vein gas from 1988 to 1994 were identified retrospectively from the radiology dictation system in a large university hospital. RESULTS: Two distinct groups of patients with portal vein gas in necrotizing enterocolitis were identified. In 3 of the 12 children, portal vein gas was identified on abdominal films after the diagnosis of necrotizing enterocolitis. These infants had no serious sequelae. By contrast, in 8 of the 9 infants with portal vein gas seen on the initial film at presentation, emergent surgery was required. Four of these infants died from complications of necrotizing enterocolitis and 2 died from sepsis related to total parenteral nutrition. The remaining 2 children have short bowel syndrome, 1 is dependent on total parenteral nutrition and 1 requires continuous gastrostomy tube feedings. CONCLUSION: The children with portal vein gas on the initial abdominal film continue to have a guarded prognosis.

Enterocolitis, Pseudomembranous↗

Enhanced urinary immunoreactive thromboxane in neonatal necrotizing enterocolitis. A diagnostic indicator of thrombotic activity.

Urinary thromboxane B2 levels increased threefold to 20-fold in infants with neonatal necrotizing enterocolitis compared with healthy infants and infants with benign causes of heme-positive stools. Increased urinary thromboxane B2 levels were detected coincidently with the initial signs of necrotizing enterocolitis, and values paralleled the course of the illness. Infants with serious illnesses other than necrotizing enterocolitis had increased urinary thromboxane B2 levels but with lower values than those of infants with necrotizing enterocolitis. Indomethacin therapy appeared to reduce urinary thromboxane B2 levels and reduce their usefulness as a marker of illness. Another product of platelet activation, beta-thromboglobulin, was increased in the urine of infants with necrotizing enterocolitis. Decreased platelet counts in infants with necrotizing enterocolitis correlated inversely with urinary thromboxane. Results of beta-thromboglobulin and platelet studies are consistent with the concept that platelet consumption due to ischemic thrombosis was the source of enhanced thromboxane excretion.

Enterocolitis, Pseudomembranous↗

Neonatal metrizamide gastrointestinal series in suspected necrotizing enterocolitis.

The diagnosis of necrotizing enterocolitis (NEC) in neonates may be made by clinical presentation, roentgenographic findings, or a combination of both. Diagnosis leads to immediate treatment including nasogastric suction, parenteral antibiotics, plasma, and close monitoring of clinical, roentgenographic, and laboratory findings. Occasionally, neither the clinical nor plain roentgenographic appearance of an infant allows the diagnosis of NEC to be made or excluded with confidence. In such infants portable isotonic metrizamide gastrointestinal (GI) series were used to help make the decision of whether to begin treatment for NEC or to continue feeding the patient. Of 15 patients examined, two exhibited signs of NEC and were successfully treated medically without GI (tract) sequelae. Twelve neonates had normal results of metrizamide GI series and ten were immediately fed with no GI complication. One of these 12 infants had feedings withheld for several days as a result of a positive blood culture. One infant with severe cardiac and pulmonary disease had profound adynamic ileus and could not be fed. We have found the metrizamide GI series to be a useful study in neonates suspected of having NEC.

Bacteriological Techniques↗

Indications for operation in necrotizing enterocolitis revisited.

Operation for necrotizing enterocolitis (NEC) is reserved for infants with intestinal gangrene or perforation. It should not be undertaken until gangrene is present, but ideally should be performed before intestinal perforation occurs. To characterize the onset of intestinal gangrene, data were analyzed for 147 infants with documented NEC, 94 of whom had gangrene. Twelve criteria were evaluated as predictors of intestinal gangrene, using standard epidemiological measures for diagnostic tests. Sensitivity, specificity, positive predictive value, negative predictive value, and prevalence were calculated for each of the proposed operative criteria. The best indications were those whose specificity and positive predictive value approached 100%, and whose prevalence was greater than 10%. These were pneumoperitoneum, positive paracentesis, and portal venous gas. Good indications were those whose specificity and positive predictive value approached 100%, but whose prevalence was less than 10%. These were fixed intestinal loop noted on x-ray, erythema of the abdominal wall, and a palpable abdominal mass. A fair indication for operation--with 91% specificity, 94% positive predictive value, and prevalence of 20%--was "severe" pneumatosis intestinalis, graded by a radiographic system. Poorer indications for operation (and their predictive value for the presence of gangrene) were clinical deterioration (78%), platelet count below 100,000/mm3 (73%), abdominal tenderness (58%), severe gastrointestinal hemorrhage (50%), and gasless abdomen with ascites (0%). No test had a high sensitivity for intestinal gangrene. Portal venous gas should be acknowledged as an indication for operation. Probability analysis may provide a more scientific basis for clinical decision-making.

Enterocolitis, Pseudomembranous↗

Complications after surgical intervention for necrotizing enterocolitis: a multicenter review.

Necrotizing enterocolitis (NEC) is a serious condition affecting predominantly the premature infant. The purpose of this study is to report a multicenter experience of complications in 252 infants requiring surgical therapy for NEC. Data from eight institutions for the years 1980 through 1990 were collected and analyzed for infants undergoing surgical therapy for NEC. Records were reviewed for gestational age, birth weight, age at operation, indications for operation, degree of intestinal involvement, operation(s) performed, complications, and 30-day mortality rates. A total of 264 infants underwent surgical intervention for NEC during the study period. Complete information was available for 252 patients. The mean gestational age was 31 +/- 5 weeks and the mean birth weight was 1,552 +/- 823 g. The mean age at operation was 18 +/- 35 days. Pneumoperitoneum was the most common indication for operation (42%). The 30-day survival rate was 72%. Eighty-one percent of patients underwent primary laparotomy, whereas peritoneal drainage was performed in 48 (19%) patients. Postoperative complications were identified in 119 (47%) patients. The most common postoperative complications were sepsis (9%), intestinal strictures (9%), and short gut (9%). Wound infections occurred in 6%, and the incidence of intraabdominal abscess formation was only 2.3%. Gestational age < 27 weeks (P < .005) and birth weight < 1,000 g (P < .005) were associated with significantly increased mortality but no increase in postoperative morbidity. The incidence of complications was similar in the very low birth weight (< 1,000 g) infants (51%) compared with infants > or = 1,000 g (46%).(ABSTRACT TRUNCATED AT 250 WORDS)

Age Factors↗