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At least 19 recordsLinked to original sources
PubMed1989

[Postoperative enterocolitis and current status of MRSA enterocolitis--the result of a questionnaire survey in Japan].

There is a trend of increase in the number of Staphylococcus aureus infection recently, and postoperative enterocolitis due to methicillin resistant strains is appearing. Because of this, a nation wide questionnaire survey on postoperative enterocolitis was conducted to clarify the status since 1980. Of the 875 major surgical institutes to which we sent the questionnaire, 370 (42.3%) replied and 67 case reports were obtained from 25 institutes. Twenty published reports were added to this and a total of 87 cases were evaluable. The number of postoperative enterocolitis increased after the year 1985, and those resulting from MRSA infection were more frequent in the northern half of Japan including the Kanto area. It was more frequent in males and the mean age was 57.9. Their onset was sudden, beginning with diarrhea and/or fever between the second and fifth postoperative days. In most of the cases, the cephalosporin group of antibiotics, especially of the third generation, were administered preceding the enterocolitis. Six of cases (24%) did not survive, and in some of the institutes they were considered to be hospital infections, as they appeared consecutively between a short period of time.

Adult↗
PubMed1992

Mucosal immune defence mechanisms in enterocolitis complicating Hirschsprung's disease.

Enterocolitis remains an important cause of morbidity and mortality in Hirschsprung's disease. The aetiology of enterocolitis is uncertain-ischaemic and bacterial causes and recently, rotavirus infections, have been suggested. Bowel tissue from 12 patients with Hirschsprung's disease who underwent Swenson's operation (five of whom had clinical evidence of enterocolitis) and colon from six controls subjects were examined to investigate possible immunopathological mechanisms associated with the disease. IgA, IgM, and J chain (but not IgG) containing plasma cells were significantly increased in the lamina propria along the entire length of resected bowel in enterocolitis patients, compared with non-enterocolitis patients and controls (p less than 0.01). Luminal secretory component staining of the anganglionic segment of colon from enterocolitis patients was considerably reduced. Lamina propria CD68 positive monocyte/macrophages and CD45RO positive leukocytes were increased in enterocolitis patients compared with non-enterocolitis patients (p less than 0.01). CD57 positive natural killer (NK) cells showed a unique distribution pattern compared with other cell types. Patients with enterocolitis showed a significant increase in CD57 positive NK cells in the lamina propria of ganglionic bowel only (p less than 0.05). NK cell values in ganglionic bowel of non-enterocolitis patients and in aganglionic bowel in all patients were similar to controls. The diversity of altered local immune response seen in this study may reflect a multifactorial microbial aetiology in enterocolitis associated with Hirschsprung's disease.

Antigens, CD↗
PubMed1989

Severity of necrotizing enterocolitis: influence on outcome at 2 years of age.

The long-term outcome of very low birth weight (VLBW) infants with necrotizing enterocolitis has been reported to be similar to that of other VLBW infants. To examine the influence of disease severity on outcome, the growth and neurodevelopment of survivors of necrotizing enterocolitis were evaluated when the babies were 20 months' corrected age. Between 1975 and 1983, 1506 VLBW infants were admitted to the hospital, and necrotizing enterocolitis developed in 84 (5.6%). Forty infants (48%) survived to be 20 months' corrected age, and complete follow-up data were available for 36. Survivors were classified by modified Bell's criteria into four groups by increasing severity of disease; 13 had mild necrotizing enterocolitis (stage IIA, IIB), and 23 had severe necrotizing enterocolitis (stage IIIA, IIIB). The 36 survivors were compared with 766 surviving VLBW infants without necrotizing enterocolitis. There were no perinatal or socioeconomic differences between groups. Compared with infants with stage II necrotizing enterocolitis at 20 months, infants with stage III necrotizing enterocolitis had a higher rate of subnormal body weight (39% vs 15%) and subnormal head circumference (30% vs 0%). Thirty-three percent of necrotizing enterocolitis survivors had significant neurodevelopmental impairment; the majority of impaired infants (10 of 12) were survivors of stage III necrotizing enterocolitis. These findings highlight the importance of continued evaluations for medical and neurodevelopmental sequelae.

Child Development↗
PubMed1991

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↗
PubMed1989

A prospective survey of necrotising enterocolitis in very low birthweight infants.

Necrotising enterocolitis is the most common gastrointestinal complication of pre-term infants. In order to determine the strength of the association of hypoxia/ischaemia and infection as causative factors in necrotising enterocolitis, we evaluated all liveborn pre-term infants with a birthweight less than 1500 g and/or gestational age less than 32 weeks in The Netherlands in 1983. The factors related to hypoxia/ischaemia included: asphyxia, respiratory distress syndrome, ventilatory assistance, persistent fetal circulation, persistent ductus arteriosus, apnoea, bradycardia, exchange transfusion and peri/intraventricular haemorrhage; those related to infection were: congenital infections, pneumonia, sepsis and meningitis. Of the 1338 infants enrolled, 1187 survived for more than 24 hours and had complete data. Mean (+/- s.d.) birthweight was 1278 (+/- 297) g and mean (+/- s.d.) gestational age 30.7 (+/- 2.6) weeks. Seventy-three (6.1%) infants developed necrotising enterocolitis: 46 (63.0%) stage I disease (clinically very suspect), 11 (15.1%) stage II (pneumatosis intestinalis) and 16 (21.9%) stage III (intestinal perforation). Mean +/- s.d. birthweight of the infants with necrotising enterocolitis (1197 +/- 284 g) was lower (P less than 0.02) than in those without necrotising enterocolitis (1283 +/- 297 g). Gestational ages were comparable. Mortality in the group with necrotising enterocolitis was 21.9% versus 15.8% in the non-necrotising enterocolitis group (NS). Stepwise logistic regression analysis indicated that among those factors studied, only sepsis and birthweight were truly associated with the occurrence of necrotising enterocolitis.

Enterocolitis, Pseudomembranous↗
PubMed1977

Necrotizing enterocolitis after cardiac surgery: a local ischemic lesion?.

Necrotizing enterocolitis continues to be a perplexing problem in the newborn and, in particular, the premature. Its pathogenesis is controversial, although there are well established clinical risk factors. Three patients had necrotizing enterocolitis while under close clinical observation and monitoring, despite the fact that these patients were not at high risk for necrotizing enterocolitis. All three had necrotizing enterocolitis after hypothermia and total circulatory arrest--a complication which until now has not been reported. Because of the close monitoring, these patients provide a unique clinical setting which eliminates most of the etiologic factors that have been implicated in the pathogenesis of necrotizing enterocolitis. The onset of necrotizing enterocolitis shortly after total circulatory arrest and the selective ischemic organ damage observed suggest local perfusion inadequacy. The authors postulate that splanchnic vasoconstriction as a result of marked sympathetic stimulation contributes to this local ischemia and subsequent necrotizing enterocolitis.

Cardiac Surgical Procedures↗
PubMed1987

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↗
PubMed1986

Ischemic enterocolitis as a complication of Hirschsprung's disease.

Enterocolitis is a recognized complication of Hirschsprung's disease. However, little distinction has been made in the literature between inflammatory enterocolitis and ischemic (necrotizing) enterocolitis when seen with Hirschsprung's disease. We report on four cases of ischemic enterocolitis complicating Hirschsprung's disease. The characteristics of ischemic enterocolitis are compared to those of inflammatory enterocolitis.

Enterocolitis, Pseudomembranous↗
PubMed1990

Role of platelet activating factor and tumor necrosis factor-alpha in neonatal necrotizing enterocolitis.

Because previous investigations have suggested that platelet activating factor and tumor necrosis factor-alpha (TNF-alpha) are important mediators of experimental necrotizing enterocolitis in the rat, we measured platelet activating factor, acetylhydrolase (the platelet activating factor breakdown enzyme), and TNF-alpha in the plasma of 12 human neonates with necrotizing enterocolitis and eight age-matched control subjects with similar gestational ages, postnatal ages, and weights. Almost all patients with necrotizing enterocolitis had elevated plasma platelet activating factor values (18.1 +/- 3.6 ng/ml vs. 3.1 +/- 0.9 ng/ml in control subjects, p less than 0.01). Plasma acetylhydrolase activity was lower in patients than in control subjects (10.6 +/- 0.7 nmol/ml/min vs 23.0 +/- 1.4 nmol/ml/min, p less than 0.01). Plasma TNF-alpha concentration was significantly elevated in patients with necrotizing enterocolitis (136 +/- 75 U/ml vs 1.5 +/- 0.8 U/ml, p less than 0.05), although the individual variation was high. There was no correlation between individual TNF-alpha and platelet activating factor levels. We conclude that platelet activating factor and TNF-alpha are elevated in patients with necrotizing enterocolitis and that suppressed platelet activating factor degradation contributes to the increased platelet activating factor levels; platelet activating factor and TNF-alpha may contribute to the pathophysiology of necrotizing enterocolitis.

1-Alkyl-2-acetylglycerophosphocholine Esterase↗
PubMed1986

Staphylococcus epidermidis-associated enterocolitis.

Nineteen infants (mean +/- SD gestational age 30 +/- 2 weeks, birth weight 1.28 +/- 0.53 kg) with Staphylococcus epidermidis bacteremia were found on retrospective chart review to have had signs and symptoms of acute enterocolitis. This S. epidermidis-associated enterocolitis constituted 37% of the 51 cases of enterocolitis and 23% of the 81 cases of S. epidermidis sepsis during the study period. S. epidermidis-associated enterocolitis was relatively mild compared with other forms of enterocolitis. Although abdominal radiographs showed markedly abnormal bowel gas patterns with distended bowel loops and bowel wall edema, only one infant had pneumatosis intestinalis and none had portal venous or free intraperitoneal gas. Only three infants had neutropenia, and five had thrombocytopenia. None of these infants required surgical intervention. Although bloody stools often persisted for weeks, none of the neonates had prolonged feeding intolerance or development of a stricture. We conclude that S. epidermidis infection is commonly associated with a mild form of enterocolitis in the neonate and that this association should be considered when selecting antibiotics for therapy.

Enterocolitis↗
PubMed1979

Neonatal necrotizing enterocolitis: implications for an infectious disease.

There is a broad spectrum of presentations and severity of necrotizing enterocolitis. Because it may have several different causes, ncerotizing enterocolitis may be a syndrome rather than a specific disease. The triad of formula feeding, intestinal ischemia, and bacterial growth may be part of the pathogenesis of necrotizing enterocolitis. Bacteria are of central importance for the production of pneumatosis, a prerequisite of which is formula feeding. Bacteria may also contribute to the intestinal injury seen after ischemia. However, the disease in the low risk patient seen during an epidemic associated with a single organism is probably caused by a primary gastrointestinal infection. On the other hand, in the stressed newborn infant with mucosal injury the presence of the appropriate bacteria may be all that is needed to initiate the chain of events leading to necrotizing enterocolitis. Figure 2 illustrates the importance of bacteria in all the causes proposed to be involved in the pathogenesis of necrotizing enterocolitis. Whether bacteria are primary or secondary agents, necrotizing enterocolitis should always be approached therapeutically as an infectious disease.

Bacterial Infections↗
PubMed1988

Hirschsprung's disease. Identification of risk factors for enterocolitis.

From 1975 to 1985, 80 infants and children were treated at a major pediatric hospital for Hirschsprung's disease, 19 (24%) of whom developed enterocolitis. In 9 neonates (18%) and 4 infants (29%) enterocolitis was present at diagnosis of Hirschsprung's disease, while 4 children acquired enterocolitis following a pull-through procedure. Significant risk factors for development of Hirschsprung's-associated enterocolitis (HAEC) were delay in diagnosis beyond 1 week of age and the presence of trisomy 21. HAEC did not occur more frequently in patients with long-segment aganglionosis, nor did an initial episode of HAEC confer a higher risk of recurrent enterocolitis. HAEC following a pull-through procedure was correlated with an anorectal stricture in three of four cases. Although neonates with HAEC had a low mortality rate (5%), their morbidity rate was 30% and their hospitalization was twice as long as neonates without enterocolitis.

Age Factors↗
PubMedDate not supplied

Bacteremia in infants with Salmonella enterocolitis.

In order to determine the incidence of Salmonella bacteremia in children with Salmonella enterocolitis and to predict the risk factors of bacteremia, we conducted a prospective study on 264 infants and children with Salmonella enterocolitis from January 1, 1988 to December 31, 1989. They were admitted to the Pediatric Department of Mackay Memorial Hospital with the chief problem of diarrhea. The rectal swab cultures were all positive for nontyphoidal Salmonella. Blood cultures were done immediately when Salmonella enterocolitis was confirmed. Clinical features including age, clinical symptoms, laboratory data, and serogroup were all recorded and analyzed to predict the risk factors of bacteremia in Salmonella enterocolitis. Twenty patients had bacteremia. Among them, 4 had meningitis simultaneously. There was one death, resulting in a 5% mortality in the bacteremia group. The overall rate of bacteremia was 7.6%. For those less than 3 months of age, it was 11.5%. We were unable to find any relationship between the bacteremia and the risk factors such as age, body temperature, clinical symptoms, white blood cell counts and differential counts. Interestingly, it was noted that Salmonella serogroup D1, a highly virulent and invasive Salmonella serogroup, was more closely related to the occurrence of bacteremia. It accounted for 40% of all cases of bacteremia. In conclusion, this study showed that the incidence of bacteremia in cases of Salmonella enterocolitis was 7.6% and the only risk factor of bacteremia was a culture of Salmonella serogroup D1. Therefore, in cases of Salmonella serogroup D1 enterocolitis, antibiotics treatment may be considerable.

Adolescent↗
PubMed1991

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↗