SEARCH · Search PubMed
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.
Thirteen children, ranging in age from 45 days to 2 years, had severe gastrointestinal illness with the features characteristic of neonatal necrotising enterocolitis. All 13 children had preceding gastroenteritis leading to hypovolaemia. Necrotising enterocolitis can occur in children beyond the neonatal age group and it may occur as a sequel to gastroenteritis.
Neonatologists in 100 special care baby units in the United Kingdom and Ireland collaborated in a four year surveillance study of neonatal necrotising enterocolitis. The average overall annual reporting rate of necrotising enterocolitis for infants in England and Wales was 0.3/1000 live births, but ranged from 9.5/1000 live births in infants weighing less than 1000 g at birth to 0.2/1000 live births in infants weighing 2500 g or more. There were more deaths among girls, infants who weighed less than 1500 g at birth, those whose bleeding was abnormal or who had low peripheral platelet counts, infants with Gram negative bacteraemia, and very low birthweight infants who developed it during the first few days of life. In both boys and girls, and in all birthweight groups, operation was associated with increased mortality.
Absent or reversed end diastolic flow (AREDF) velocities in the umbilical artery were identified in 25 high risk pregnancies. In six pregnancies the fetus was abnormal and all but one of these ended in perinatal death. Of the 19 morphologically normal fetuses, three died in utero and there were four neonatal or infant deaths. The mortality rate was 48% for all pregnancies and 37% for those with morphologically normal fetuses. There was a highly significant increased risk for the development of necrotising enterocolitis in these morphologically normal fetuses with AREDF (53%) compared with controls (6%) who did have umbilical artery end diastolic flow velocities in fetal life. There were no significant differences between the matched pairs for parameters of neonatal outcome chosen to reflect neonatal morbidity. These findings demonstrate the close association between AREDF and necrotising enterocolitis that appears to be independent of other variables such as degree of growth retardation, prematurity, and perinatal asphyxia.
A comparative study of bowel colonisation and incidence of necrotising enterocolitis in neonates admitted to an intensive care unit is reported. Neonates of less than 33 weeks gestational age requiring mechanical ventilation for respiratory distress syndrome were randomised during the first week of life to receive either vancomycin and aztreonam or vancomycin and gentamicin for episodes of suspected sepsis after the first week of life. A higher proportion of neonates who received vancomycin and gentamicin had faecal colonisation with enterobacteriaceae at the end of the second, third, and fourth weeks of life. Treatment with vancomycin and aztreonam was associated with a rapid quantitative reduction in faecal colonisation with enterobacteriaceae, whereas there was no quantitative reduction in colonisation with enterobacteriaceae associated with treatment with vancomycin and gentamicin. There were no differences between the two groups in faecal colonisation with anaerobes, Enterococcus sp, Staphylococcus sp, or yeasts. Six (14.6%) of 41 who received vancomycin and gentamicin compared with 0 of 40 who received vancomycin and aztreonam subsequently developed necrotising enterocolitis.
The morphology of antibiotic-associated enterocolitis in the hamster is described and compared with human antibiotic-associated pseudomembranous colitis. It is shown to be a caecal disease with proliferative mucosal changes and in this respect unlike the human counterpart. The bacteriology and toxicology, however, are identical. In addition, mucosal changes are described in animals on antibiotics but without established enterocolitis. As a result we suggest that there may be a spectrum of human disease ranging from mild antibiotic-associated diarrhoea to established pseudomembranous colitis. Therefore, despite the morphological variation, the hamster remains a good model for investigating the pathogenesis of pseudomembranous colitis and antibiotic-associated enteropathy in general.
An enterocolitis has been induced in guinea pigs by alloimmunisation with a mucosal protein. A single dose of immunogen fails to provoke a synthesis of precipitant antibodies, but a high percentage of animals, injected with two or more doses, develop these antibodies. A specific cell mediated immune response was already detectable 30 days after a single dose of immunogen. At later periods and after multiple doses of immunogen positive results were still found, although in a lesser percentage of the animals. The pathology was characterised by the appearance of multiple mucosal ulcerations, congestion, oedema and localised haemorrhage. The target organs were mainly ileum and descending colon. At later periods a combination of mononuclear cell infiltration, fibrocytic proliferation and granuloma formation appeared together with the other lesions. When an intraluminal challenge was made 48 hours before death, a heavy mononuclear cell infiltration was present in the contact area. The lesions appeared to extend to areas which usually remained unaffected. The characteristic immunopathology of this autoimmune enterocolitis in guinea pigs possesses some of the features of human inflammatory bowel diseases and makes it a useful model for further studies.
To describe the pathology and clinical features of segmental necrotising enterocolitis (SNE) in children and adults, 22 diarrhoeal patients (median age two years, range two months to 50 years) in Bangladesh with this lesion detected at autopsy were examined and compared with two groups of diarrhoeal control patients. Gross pathology consisted of purplish or black mucosal or transmural discoloration with erosions or ulcerations in segments of the jejunum or ileum of 18 cases and of the colon alone in four cases. Two patients had intestinal perforations. Microscopically all specimens showed coagulation necrosis or haemorrhagic necrosis indicative of mucosal ischaemia. In 20 cases there was submucosal oedema and nine showed pneumatosis of the bowel. From 11, one or more of the invasive diarrhoeal pathogens Shigella, Campylobacter and Entamoeba histolytica were detected. From the comparison with controls significant associations were found for a long duration of diarrhoea, blood and mucus in stool, abdominal distension or tenderness, shock not attributable to hypovolaemia, septicaemia, and low concentration of serum protein (p less than 0.05). These findings indicated that segmental necrotising enterocolitis develops sometimes as a fatal complication of prolonged diarrhoeal illnesses associated with shock and hypoproteinaemia and is caused by ischaemic injury to the intestinal mucosa.
Three cases of neutropenic enterocolitis are described. This unusual condition occurs almost exclusively in neutropenic patients and has a fulminating course which is almost invariably fatal without surgical intervention. The lesion is centered on the caecum and hitherto its pathogenesis has been unclear, partly because most studies have been performed on material obtained at necropsy. In these three patients, all of whom were treated surgically, Clostridium septicum was identified by specific immunofluorescence in the bowel wall of the resected specimens. Two patients also had C septicum septicaemia. Various forms of mucosal damage can be identified which predispose towards invasion of the bowel wall by this organism. These cases provide further confirmation of a primary role for C septicum in the pathogenesis of neutropenic enterocolitis.
A 15 year old boy being treated for relapsed acute lymphoblastic leukaemia developed severe diarrhoea and abdominal pain which worsened despite empirical antibiotic treatment. A right hemicolectomy was performed. The caecum and ascending colon showed changes typical of neutropenic enterocolitis. Clostridium tertium was isolated from faeces, blood cultures, and from the resected gut wall, with no evidence of other organisms capable of causing such a condition. As far as is known, this is the first reported case in which neutropenic enterocolitis has been associated with well documented C tertium infection, an organism previously described as a cause of bacteraemia in neutropenic patients.
In a multicentre case-control study of necrotising enterocolitis risk factors were found to vary with birthweight of cases. In very low birthweight cases the risk factors identified were those associated with prolonged or recurrent hypoxia (recurrent apnoea, respiratory distress, assisted ventilation, and umbilical artery catheterisation). In heavier birthweight infants the risk factors were, in contrast, related to hypoxia at birth (low 1 minute Apgar score and endotracheal intubation at birth) and umbilical vessel catheterisation used in exchange transfusions. Contradictory findings in published case-control studies carried out in the USA may be due to differences in patient populations and management policies. Hypoxia and umbilical vessel catheterisation should still be considered as risk factors for necrotising enterocolitis.
Pneumatosis intestinalis was encountered in association with fatal necrotizing enterocolitis in systemic lupus erythematosus (SLE) and polyarteritis nodosa. The radiologic identification of mottled, bubbly, and linear collections of intramural intestinal gas distinguish this ominous complication from benign pneumatosis cystoides intestinalis. In the setting of intestinal vasculitis due to SLE or polyarteritis nodosa, these characteristic radiologic features indicate necrotizing enterocolitis. Since corticosteroids may mask clinical progression of the intestinal lesion, radiologic evaluation is essential in the overall management of the patient with intestinal vasculitis.
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.
A review of the records and radiographs of 21 newborn infants with necrotizing enterocolitis and 10 control infants was performed to test the significance of the persistent loop sign in necrotizing enterocolitis. Twelve clinical and laboratory variables were compared with the persistent loop sign. None of the control infants and seven of the 21 study infants had a persistent loop sign. Four of the seven infants were proven to have necrotic bowel. All four died. Four of the 14 study patients without the persistent loop sign had necrotic bowel. Two of these four infants died. The findings of this study do not support the use of a persistent segmental loop of bowel as a single criterion for surgical intervention.
Two neonates had unusually rapid development of necrotizing enterocolitis within 24 hours of birth. Both patients had decreased systemic perfusion secondary to aortic atresia. Onset of either clinical or radiographic manifestations of necrotizing enterocolitis in the first day of life should alert one to the possible presence of severe left ventricular outflow obstruction.
Two children presented with ischemic enterocolitis, a prodrome that occurs in 80% or more of patients with the hemolytic-uremic syndrome. When the prodrome precedes the development of characteristic laboratory findings or oliguria, the diagnosis of the hemolytic-uremic syndrome often is delayed. The severity of the enterocolitis itself may overshadow renal impairment. Findings of thumbprinting on plain radiographs or on barium enema examinations allow the radiologist to suggest the hemolytic-uremic syndrome as a possible cause before renal or hematologic abnormalities become manifest.
Epidemiologic studies have identified enteral feedings as a risk factor for necrotizing enterocolitis (NEC). Enteral feedings provide the substrate for colonization of the newborn gut with gram-negative bacteria with endotoxin production, which may trigger the production of endogenous inflammatory mediators, including platelet-activating factor (PAF). In this prospective study, we examined the effect of enteral feeding on PAF concentration in the stool of preterm and full-term human newborns. The concentration of PAF levels in stool was measured at the following times: at passage of first meconium, within 24 h prior to the onset of feedings, at the 3rd and 14th day of feeding and at any time confirmed NEC developed. Stool samples also were analyzed for levels of acetylhydrolase, the PAF breakdown enzyme. Stool PAF concentration rose significantly following the start of enteral feedings. The mean PAF concentration for day 14 samples was significantly higher than the mean concentration of meconium samples (4.90 +/- 1.03 vs. 1.81 +/- 0.38 ng/g, p < 0.05) and day 0 samples (4.90 +/- 1.03 vs. 1.79 +/- 0.39 ng/g, p < 0.05). For the 7 patients diagnosed with definite NEC, the mean stool PAF concentration was 12.42 +/- 0.77 ng/g, significantly elevated compared to the mean PAF levels in stool from healthy infants at all sampling times (p < 0.01). There was no significant change in acetylhydrolase activity at any of the sampling times. Stool PAF concentration increases with the provision of enteral feedings and rises further with the development of NEC. Since stool acetylhydrolase activity remained unchanged, we speculate the increase of PAF in stool likely represents increased PAF production at the local level following the provision of enteral feedings or the development of neonatal necrotizing enterocolitis.
ANAMNESIS: A 60-year-old patient underwent breast-preserving surgery for breast cancer of TNM stage pTla (m), pN2a (8/12), G2, pMO. After the operation, she received 4 cycles of epirubicin/cyclophosphamide (90/600 mg/m2), followed by 2 cycles of docetaxel (100 mg/m2). Four days after the second cycle of docetaxel, the patient presented with abdominal pain, nausea, vomiting and obstipation of 3 days' duration. FINDINGS: The physical examination showed a distended abdomen, absence of peristaltic sounds and pressure pain in the lower left abdomen. The laboratory examination was conspicuous for granulocytopenia of NCI grade Ill and an increased CRP concentration of 7.7 mg/dl. DIAGNOSIS: The main diagnosis was suspected chemotherapy-associated enterocolitis with signs of paralytic ileus; the latter was confirmed by computer tomography and laparotomy. THERAPY AND COURSE: Primary treatment consisted of placing a stomach tube, infusion therapy, broad-spectrum antibiotics and G-CSF. Later on, 5 explorative laparotomies with abdominal lavage were performed due to deterioration of the general condition and suspicion of intra-abdominal compartment syndrome. After a temporary improvement, the patient died of protracted multi-organ failure 8 weeks after hospitalization. CONCLUSION: Chemotherapy-associated enterocolitis is a very rare but potentially lethal side effect of cytostatic therapy. Therefore, gastrointestinal symptoms should be carefully noted in order to minimize the mortality risk by a timely therapeutic intervention.
Administration of an elemental diet to rats given methotrexate (MTX), 20 mg/kg intraperitoneally (ip), results in 100% mortality from severe enterocolitis. Previous studies indicate that glutamine (GLN), which is not present in elemental diets, is the preferred oxidative substrate for the gut and may facilitate intestinal recovery after injury. This study investigated the effects of a glutamine-supplemented elemental diet (GLN-ED) on nutritional status, intestinal morphometry, bacterial translocation and survival in this lethal model of intestinal injury. Three experiments were performed. In the first experiment, rats received an intragastric elemental diet supplemented with either 2% GLN or an equivalent amount of glycine (Control). After 4 days animals received either MTX, 20 mg/kg ip, or saline ip and were killed 3 days later. The GLN-ED resulted in significantly decreased weight loss, improved nitrogen retention, and increased mucosal weight, protein, and DNA content of the jejunum and colon. In the second experiment rats were assigned to diet as in the first experiment, but all animals received MTX. Control diet animals died within 120 hrs of MTX administration. The GLN-ED group had significantly longer survival time and decreased mortality. In the third experiment animals were assigned to diet and MTX as in the first experiment. Ninety-six hrs later aortic blood cultures revealed enteric bacteremia in animals administered MTX. GLN-ED resulted in a significant reduction in the incidence of bacteremia. These experiments showed that a GLN-ED significantly improved nutritional status, decreased intestinal injury, decreased bacterial translocation, and resulted in improved survival in a lethal model of enterocolitis.