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PubMedDate not supplied

Gastrointestinal adenovirus: an important cause of morbidity in patients with necrotizing enterocolitis and gastrointestinal surgery.

Adenoviruses have recently been recognized as etiologic agents of enteric disease in hospitalized infants and young children. Patients who have undergone surgical procedures related to the complications of neonatal necrotizing enterocolitis constitute a population of infants who are often hospitalized for extended periods of time. We studied the incidence of enteric adenovirus infections in infants with necrotizing enterocolitis who had undergone intestinal surgery resulting in colostomies or ileostomies. These studies revealed that 31.7% of the hospital admissions in such patients were complicated by symptomatic infection with enteric adenoviruses. The rate of adenovirus infection in this population was significantly higher than the rate of such infections encountered in infants undergoing ostomy procedures for other conditions and in age-matched hospitalized infants without prior gastrointestinal surgery. The infections with enteric adenovirus were generally accompanied by an increase in intestinal output which was temporally associated with the excretion of adenovirus in the intestinal fluid. In addition infections with enteric adenoviruses in the infants with necrotizing enterocolitis and ostomies were associated with a marked increase in length of hospitalization as compared to uninfected infants with similar underlying gastrointestinal pathology. Epidemiologic analysis revealed that many of the cases of enteric adenovirus infection in the study population occurred during seasons in which enteric adenovirus infections were prevalent in the hospital population. These studies demonstrate that enteric adenovirus infections are major causes of morbidity in hospitalized patients who have of morbidity in hospitalized patients who have undergone ileostomy or colostomy procedures for necrotizing enterocolitis and that the prevention of enteric adenovirus infections might result in a significant improvement in the hospital care of infants with these conditions.

Adenoviridae Infections↗
PubMed2005

Operative strategies for necrotizing enterocolitis: The prevention and treatment of short-bowel syndrome.

Necrotizing enterocolitis (NEC) is the leading cause of short-bowel syndrome (SBS) in infancy. Studies on the acute medical and surgical management of NEC have traditionally focused on short-term morbidity and mortality, with less emphasis on long-term outcomes. Acute surgical management of NEC involves the often competing priorities of controlling sepsis and preserving bowel length. Bowel-preserving strategies for NEC, designed to limit SBS, are based on peritoneal drainage, limited resection, or a combination of both. Drainage-based strategies are generally favored in smaller neonates, while laparotomy-based strategies are favored in larger patients, especially those with a more limited extent of intestinal injury. Comparisons of drainage-based approaches and resection-based approaches are limited by confounding variables, and neither approach is clearly superior with regard to subsequent SBS. These traditional as well as more creative approaches to bowel preservation have application in NEC, yet they depend on a series of patient and treatment characteristics that include the ability of diseased but viable bowel to recover both absorptive and motility function after acute NEC, the ability of the infant to tolerate appropriately drained intraperitoneal contamination, and the ability of the injured intestine to subsequently undergo intestinal adaptive change. In addition, there are a series of operative options that have been designed to mitigate the impact of SBS once it is established. These procedures are not uniquely applied exclusively for NEC-induced SBS. However, strategies that slow intestinal transit, improve peristaltic function, or enhance mucosal absorptive function each have application in the management of SBS.

Digestive System Surgical Procedures↗
PubMed2006

Neurodevelopmental outcomes of neonates with medically and surgically treated necrotizing enterocolitis.

OBJECTIVES: (1) To characterise neurodevelopmental outcome of neonates with necrotizing enterocolitis (NEC); (2) to define whether NEC increases risk of neurodevelopmental impairment in very low birth weight neonates; (3) to investigate whether stage of disease or need for surgery increase risk of poor outcome. DESIGN: A systematic review was performed. Searches identified 182 relevant papers. Ten studies compared extremely low birthweight neonates with NEC to infants of similar age and gestation who did not develop NEC. Data are reported as OR (95% CIs, p values for test for overall effect) and compared by chi2. RESULTS: 7843 children (821 with NEC) were included in the meta-analysis. Median follow-up was 20 months (range 12 to 156). Overall, 45% of children who had neonatal NEC were neurodevelopmentally impaired. Infants with NEC were significantly more likely than infants of similar age and gestation who did not develop NEC to be neurodevelopmentally impaired (1.6 (1.3 to 2.0), p = 0.0001) including a higher risk of cerebral palsy (1.5 (1.2 to 2.0), p = 0.001), visual (2.3 (1.0 to 5.1), p = 0.04), cognitive (1.7 (1.4 to 2.2), p<0.0001) and psychomotor impairment (1.7 (1.3 to 2.2), p<0.0001). The odds ratio of neurodevelopmental impairment was also 2.3 times higher in neonates with Bell's stage III disease or requiring surgery ((1.5 to 3.6), p = 0.0001). CONCLUSIONS: NEC is associated with significantly worse neurodevelopmental outcome than prematurity alone. Presence of advanced NEC and need for surgery increase the risk of neurological impairment.

Cognition Disorders↗
PubMed1998

Lower incidence of necrotizing enterocolitis in infants fed a preterm formula with egg phospholipids.

Necrotizing enterocolitis (NEC) causes approximately 4000 deaths/y and significant morbidity among U.S.-born preterm infants alone. Various combinations of inadequate tissue oxygenation, bacterial overgrowth, and enteral feeding with immaturity may cause the initial damage to intestinal mucosa that culminates in necrosis. Presently, there is not a way to predict the onset of the disease or to prevent its occurrence. As part of risk-benefit assessment, we compared disease in hospitalized preterm infants fed a commercial (control) preterm formula or an experimental formula with egg phospholipids for a randomized, double-masked, clinical study of diet and infant neurodevelopment. Infants fed the experimental formula developed significantly less stage II and III NEC compared with infants fed the control formula (2.9 versus 17.6%, p < 0.05), but had similar rates of bronchopulmonary dysplasia (23.4 versus 23.5%), septicemia (26 versus 31%), and retinopathy of prematurity (38 versus 40%). Compared with the control formula, the experimental formula provided 7-fold more esterified choline, arachidonic acid (AA, 0.4% of total fatty acids), and docosahexaenoic acid (0.13%). Phospholipids are constituents of mucosal membranes and intestinal surfactant, and their components, AA and choline, are substrates for intestinal vasodilatory and cytoprotective eicosanoids (AA) and the vasodilatory neurotransmitter, acetylcholine (choline), respectively. One or more of these components of egg phospholipids may have enhanced one or more immature intestinal functions to lower the incidence of NEC in this study. Regardless of the potential mechanism, a larger randomized trial designed to test the effect of this egg phospholipid-containing formula on NEC seems warranted.

Adult↗
PubMed1999

Circulating pro- and counterinflammatory cytokine levels and severity in necrotizing enterocolitis.

OBJECTIVES: To evaluate the relationship between the severity of necrotizing enterocolitis (NEC) and circulating concentrations of proinflammatory cytokines interleukin (IL)-1beta and IL-8 and counterinflammatory cytokines IL-1 receptor antagonist (IL-1ra) and IL-10. These cytokines have been associated with bowel injury or inflammation and may be released more slowly or later than previously examined cytokines. Also, to determine if any one of these cytokines will predict the eventual severity of NEC when measured at symptom onset. METHOD: Serial blood samples at onset, 8, 24, 48, and 72 hours were obtained from newborn infants with predefined signs and symptoms of NEC. Normal levels were defined from weight-, gestation-, and age-matched controls. Concentrations of the four cytokines were determined by enzyme-linked immunosorbent assay and compared throughout the time period by stage of NEC, using sepsis as a co-factor. Mean concentrations of each cytokine at onset were compared with the controls. Threshold values were obtained with the best combination of high sensitivity and high specificity for defining stage 1 NEC or for diagnosing stage 3 NEC at onset. RESULTS: There were 12 cases of stage 1, 18 cases of stage 2, and 6 cases of stage 3 NEC included in the study, as well as 20 control infants. Concentrations of IL-8 and IL-10 were significantly higher in infants with stage 3 NEC from onset through 24 hours compared with infants with less severe NEC. At onset, concentrations of all four cytokines were significantly higher in stage 3 NEC. To identify, at onset, the infants with a final diagnosis of stage 3 NEC, an IL-1ra concentration of >130 000 pg/mL had a sensitivity of 100% and a specificity of 92%. At 8 hours, an IL-10 concentration of >250 pg/mL had a sensitivity of 100% and a specificity of 90% in identifying stage 3 NEC in infants with symptoms suggestive of NEC at onset. CONCLUSIONS: The severity of NEC and its systemic signs and symptoms are not due to a deficiency of counterregulatory cytokines. In fact, mean concentrations of IL-1ra in NEC are higher than what has been reported in other populations. The cytokines IL-8, IL-1ra, and IL-10 are released later or more slowly after a stimulus and may be more useful in identifying, within hours of symptom onset, which infant will develop significant NEC.

Enterocolitis, Necrotizing↗
PubMed2006

[Evaluation of an experimental model of necrotizing enterocolitis in rats].

OBJECTIVE: To evaluate an experimental model of necrotizing enterocolitis in rats proposed by OKUR e col. in 1995. METHODS: On their first day of life, 28 EPM-Wistar rats weighing between 4 and 6 grams were submitted to hypoxia (H) by placing them in a CO2 gas chamber for rodents' sacrifice, where they received a 100% CO2 air flow for 5 minutes. After the hypoxia the animals were reanimated (R) with a 100% O2 air flow, also for 5 minutes. The animals were allocated in two groups: G1: control (n=12): rats not submitted to H-R; G2: (n=16): rats submitted to H-R. Segments of the small intestine and colon were prepared for histological analysis. The remaining intestine was used to measure tissular malondialdehyde. RESULTS: Mean malondialdehyde dosages were 1.05 (0.44-2.03) and 2.60 (0.59- 6.4) nmol MDA/mg protein for G1 and G2, respectively. G2's mean value was significantly higher than in the control group (p<0.002). Significant statistical difference between the studied groups was found in relation the level of injury, with G1 presenting significantly lower levels than G2. CONCLUSIONS: The model showed that neonatal hypoxia may cause intestinal wall injury in rats. Despite the discreet histological injuries found, the method is suitable for evaluation of tissular free radicals.

Animals↗
PubMed2006

The roles of bacteria and TLR4 in rat and murine models of necrotizing enterocolitis.

Bacteria are thought to contribute to the pathogenesis of necrotizing enterocolitis (NEC), but it is unknown whether their interaction with the epithelium can participate in the initiation of mucosal injury or they can act only following translocation across a damaged intestinal barrier. Our aims were to determine whether bacteria and intestinal epithelial TLR4 play roles in a well-established neonatal rat model and a novel neonatal murine model of NEC. Neonatal rats, C57BL/6J, C3HeB/FeJ (TLR4 wild type), and C3H/HeJ (TLR4 mutant) mice were delivered by Cesarean section and were subjected to formula feeding and cold asphyxia stress or were delivered naturally and were mother-fed. NEC incidence was evaluated by histological scoring, and gene expression was quantified using quantitative real-time PCR from cDNA generated from intestinal total RNA or from RNA obtained by laser capture microdissection. Spontaneous feeding catheter colonization or supplementation of cultured bacterial isolates to formula increased the incidence of experimental NEC. During the first 72 h of life, i.e., the time frame of NEC development in this model, intestinal TLR4 mRNA gradually decreases in mother-fed but increases in formula feeding and cold asphyxia stress, correlating with induced inducible NO synthase. TLR4, inducible NO synthase, and inflammatory cytokine induction occurred in the intestinal epithelium but not in the submucosa. NEC incidence was diminished in C3H/HeJ mice, compared with C3HeB/FeJ mice. In summary, bacteria and TLR4 play significant roles in experimental NEC, likely via an interaction of intraluminal bacteria and aberrantly overexpressed TLR4 in enterocytes.

Animal Feed↗
PubMed2000

Necrotizing enterocolitis: experience of 27 cases from a single Korean institution.

Necrotizing enterocolitis (NEC) can involve any site in the gastrointestinal tract and is a fatal complication of immunosuppression. To characterize NEC, clinical and radiological characteristics were analyzed. A total of 27 cases of NEC were identified from January 1993 to August 1998, and medical records were reviewed. NEC was diagnosed by clinical and radiological criteria, and other mimicking conditions were excluded. Of the NEC cases, 22 (81.5%) occurred in patients with underlying hematologic malignancy. All patients complained of abdominal pain and fever at the time of inclusion. Escherichia coli was the most common pathogen identified. The most common finding by computed tomography was single-layered diffuse bowel wall thickening with variable density. Other findings were ascites, fascial thickening, pneumatosis, and mesenteric lymphadenopathy. Of the patients, 25 were treated with antimicrobials with or without recombinant hematopoietic growth factors, and 2 were treated with surgery because of perforation and profound bleeding. Among the 12 patients who died, NEC was the direct cause of death in 7 patients. In conclusion, computed tomography is an effective tool for early diagnosis of NEC. Bowel rest, broad-spectrum antimicrobials, and recombinant hematopoietic growth factors are important aspects of treatment. Surgery should be reserved for complicated cases.

Adolescent↗
PubMed2002

Gut hormones in preterm infants with necrotizing enterocolitis during starvation and reintroduction of enteral nutrition.

OBJECTIVES: Gastrointestinal hormones control gut functions in response to enteral nutrition. Diseases involving the gastrointestinal tract, such as necrotizing enterocolitis, may affect gut hormone secretion and therefore influence gut functions. Because bowel rest is an important part of the treatment, infants with this disease are especially at risk for an altered gut hormone secretion and thus for compromised gut functions. METHODS: In the current study, the gastrointestinal hormone profiles of eight preterm infants with an ileostomy after necrotizing enterocolitis (Bell stages 2 and 3) were evaluated during starvation and reintroduction of enteral nutrition. Basal and postprandial plasma concentrations of gastrin, cholecystokinin, and peptide YY were measured with sensitive and specific radioimmunoassays. The results were compared with those of 11 controls. RESULTS: In the patients and the controls, plasma concentrations of all hormones were higher postprandially. The increases in cholecystokinin and peptide YY were significant in the patients. Compared with the controls, all concentrations were higher in the patients, and changes were significant for basal and postprandial cholecystokinin and postprandial peptide YY. CONCLUSIONS: Enteral nutrition stimulates the secretion of gastrointestinal hormones, also in premature infants with a diseased distal small bowel and colon, as in necrotizing enterocolitis. The postprandial increase of peptide YY in patients with an ileostomy indicates that enteral substrate in the colon is not necessary for stimulation of peptide YY secretion.

Cholecystokinin↗
PubMed2001

[An extremely low birth weight infant with pulmonary atresia complicated with necrotizing enterocolitis].

We experienced an extremely low birth weight (ELBW) infant complicated with pulmonary atresia and necrotizing enterocolitis. She was born at 25 weeks of gestation with a birth weight of 752 g. Five hours after birth, she manifested cyanosis and was diagnosed as having pulmonary atresia with intact ventricular septum (PAIVS). Infusion of lipo-prostaglandin E1 (PGE1) was started to keep the ductus open along with infusion of dopamine and dobutamine. At 8 days of life she developed hypotension and metabolic acidosis, and the diagnosis of intestinal perforation was made by free air in the abdomen. The excessive shunt flow to the pulmonary vasculature via the ductus was suspected to have caused an inadequate systemic flow leading to the intestinal ischemia and necrotizing enterocolitis. Lipo-PGE1 was discontinued to decrease the shunt flow through the ductus. Brock's operation (closed transventricular pulmonary valvotomy) was performed at the age of 8 and 11 days and the ligation of the ductus arteriosus was performed at the age of 13 days. Propranolol was administered to inhibit the pulmonary outflow tract constriction along with catecholamines to stabilize hemodynamics. She recovered slowly and her trachea was extubated at 58 days of life.

Anesthesia↗
PubMed1978

The persistent loop sign in neonatal necrotizing enterocolitis: a new indication for surgical intervention?

A new radiographic sign in neonatal necrotizing enterocolitis is described. Five patients with necrotizing enterocolitis exhibited an unchanging dilated loop of small bowel, which was followed by perforation in 3 infants; the other 2 had surgical and/or autopsy corroboration of profound bowel-wall necrosis. It is suggested that infants with a "persistent loop" be considered candidates for laparotomy.

Enterocolitis, Pseudomembranous↗
PubMed1995

Neonatal necrotizing enterocolitis. A 12-year review at a county hospital.

PURPOSE: A retrospective, 12-year review of neonatal necrotizing enterocolitis was undertaken at a county hospital, with emphasis on presentation signs and symptoms. METHODS: Eight-two patients with presence of intramural air were included in the study. The following signs and symptoms were studied: evidence of respiratory distress, use of umbilical catheters, white blood cell count and temperature at presentation, time interval from birth to diagnosis and time interval from diagnosis to operative intervention, presence of intramural air, air in biliary tree or free air, changes in abdominal girth, and presence of occult or gross blood in stools. Comparison was done among infants who had surgical or medical treatment, premature and full-term infants, and infants who had neonatal necrotizing enterocolitis less than or more than 20 days after birth. RESULTS: Eleven patients had a fatal outcome, with an overall survival of 87 percent. Sixty-four patients were treated medically and 18 had operative treatment. Mortality of the surgically treated group was 44 percent. Neonates who had surgical intervention had a left shift of the white blood cell count more commonly present, and all had documented abdominal distention. There were 62 premature and 20 full-term neonates in the group. Full-term neonates developed neonatal necrotizing enterocolitis earlier after birth (5.3 days compared with 15.3 days in the premature neonate group). Full-term neonates had a better prognosis in our series. Presentation of symptoms more than 20 days after birth did not change outcome. CONCLUSION: Our results reflect the experience of a community-based hospital. Clinical acumen remains the cornerstone of diagnosis and management.

Abdomen↗
PubMed1982

Age at onset of necrotizing enterocolitis: an epidemiologic analysis.

We studied the epidemiologic interrelationships among birth weight, gestational age, and age at onset of necrotizing enterocolitis of the newborn. As birth weight increased, the range of ages at onset and the mean age at onset both decreased. Weekly birth weight-specific attack rates for necrotizing enterocolitis declined sharply in all birth weight groups when the equivalent of 35-36 wk gestational age was reached. Our data are consistent with the hypothesis that the risk period for necrotizing enterocolitis is determined primarily by the maturity of the gastrointestinal tract of the newborn.

Age Factors↗
PubMed1988

Prevention of necrotizing enterocolitis in low-birth-weight infants by IgA-IgG feeding.

In a randomized clinical trial, we evaluated the efficacy of an oral immunoglobulin preparation (73 percent IgA and 26 percent IgG) in reducing the incidence of necrotizing enterocolitis in infants of low birth weight for whom breast milk from their mothers was not available. A total of 434 infants weighing between 800 and 2000 g were eligible for entry in the study. Of these, 255 were withdrawn - 234 during the first week of the study because breast milk from their mothers became available (123 in the treatment group and 111 in the control group), and 21 because of violations of protocol or because breast milk became available after the first week. The duration of follow-up was 28 days. Among the infants for whom breast milk did not become available during the study, there were no cases of necrotizing enterocolitis among the 88 receiving oral IgA-IgG, as compared with six cases among the 91 control infants (P = 0.0143). Of the infants withdrawn from the study, two assigned to the control group had necrotizing enterocolitis. We conclude that the oral administration of IgA-IgG may prevent the development of necrotizing enterocolitis in low-birth-weight infants.

Administration, Oral↗
PubMed2004

Nucleated red blood cells in preterm infants who have necrotizing enterocolitis.

Absolute nucleated red blood cell counts for 23 preterm newborn infants who subsequently had development of necrotizing enterocolitis were significantly higher than for 23 control infants. These infants may have been exposed to relative intrauterine hypoxemia, a possible risk factor for the development of necrotizing enterocolitis.

Case-Control Studies↗
PubMed2003

Systemic arterial pneumatosis in a neonate with necrotizing enterocolitis.

Ultrasound is exquisitely sensitive for the identification of portal vein pneumatosis, which in neonates is commonly caused by necrotizing enterocolitis. We describe the ultrasound finding of systemic arterial pneumatosis in a case of necrotizing enterocolitis associated with congenital heart disease. A combination of a patent ductus venosus and an extracardiac right-to-left shunt via the great vessels through a patent ductus arteriosus provided a pathway for the pneumatosis from the portal vein to the abdominal aorta.

Abnormalities, Multiple↗
PubMed1993

[Risk factors in neonatal necrotizing enterocolitis].

In this case controls prospective study, risk factors for necrotizing enterocolitis from a neonatal intensive care unit, were investigated. In 34 cases and 69 controls, were found; the fetal distress, Apgar score < or = 5 at one minute, < or = 6 at five minutes, gestational age < or = 34 weeks and birth weight < or = 1500 g, like risk factors for necrotizing enterocolitis. The investigation of a new risk factor, abdominal distention with plentiful intestinal gas documented in X ray at initial hours of life, by energetic reanimation at birth, showed that it is not a risk factor.

Case-Control Studies↗