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PubMed1983

Clostridial species in the pathogenesis of necrotizing enterocolitis in patients with neutropenia.

The role of gram-negative bacteria in the pathogenesis of necrotizing enterocolitis has been stressed. We describe a 21-year-old woman with chronic neutropenia with cyclic fluctuations who died of necrotizing enterocolitis due to Clostridium septicum. Seven patients with cyclic neutropenia and necrotizing enterocolitis have been described in the literature and in each case in which bacteriologic data were reported, a Clostridial infection was documented. Patients with cyclic neutropenia should be treated with antibiotics effective against Clostridial species when abdominal symptoms complicate neutropenic periods.

Adult↗
PubMed1980

[Antibiotic-associated diarrhoea and enterocolitis (author's transl)].

Many antibiotics, particularly the lincomycins, may cause diarrhoea with or without enterocolitis. The pathogenesis of antibiotic-associated diarrhoea without colitis is uncertain; colloidosmotic water binding in the colon by endogenous glycoproteins undegraded by colonic bacteria is considered. Antibiotic-associated enterocolitis is now known to be due to toxin-producing clostridia, proven for Cl. difficile. Improved methods for the detection of toxin and clostridia are presently being studied. Endoscopically, pseudomembranes are characteristic but not antibiotic-specific, they may be absent or missed diagnostically. A possible role of asymptomatic clostridia-carriers in enterocolitis clustering remains to be determined. The potentially lethal course of the disease requires rapid diagnosis and therapy, with discontinuation of the antibiotic, intensive supportive measures and, at least in severe disease, oral vancomycin.

Adult↗
PubMed1994

Enterocolitis following endorectal pull-through procedure in children with Hirschsprung's disease.

The enterocolitis following a pull-through in Hirschsprung's disease can be life-threatening and difficult to distinguish clinically from gastroenteritis and post-operative complications. We reviewed retrospectively the abdominal radiographs in our series to identify specific radiographic characteristics of this syndrome in this population. A total of 55 episodes of enterocolitis with an abdominal series at presentation were located in the files of 43 patients following pull-through surgery for Hirschsprung's disease. There were 15 abdominal series with other complications of Hirschsprung's disease and surgery (seven cases of small bowel obstruction, one of fistula, one of abscess, six of severe constipation) and 71 surveillance follow-up studies. Radiographs were evaluated for bowel dilatation, air-fluid levels, intestinal cut-off sign, speculation, and pneumatosis. The intestinal cut-off sign with two or more air-fluid levels had sensitivity of 68% and specificity of 83%, with a positive predictive value of 0.71 and overall accuracy of 77%. Our review of enterocolitis following pull-through in children with Hirschsprung's disease concludes that the constellation of an intestinal cut-off sign and at least two air-fluid levels on the abdominal series strongly suggests the diagnosis.

Child↗
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↗
PubMed1995

Toxic megacolon complicating pseudomembranous enterocolitis.

PURPOSE: Toxic megacolon is a rare complication of pseudomembranous enterocolitis. We reviewed our recent experience with this complication. METHODS: The first five patients of the series were studied retrospectively, and six others were followed prospectively. RESULTS: Between June 1992 and May 1994, 11 patients (8 male, 3 female) developed toxic megacolon secondary to pseudomembranous enterocolitis. Mean age was 60.7 +/- 11.8 (range, 40-79) years. Presenting symptoms and signs included diarrhea, 100 percent; malaise, 91 percent; abdominal pain, 82 percent; abdominal distention, 82 percent; abdominal tenderness, 72 percent; anemia less than 12 gm, 72 percent; albumin less than 3 gm, 64 percent; tachycardia greater than 100, 55 percent; fever greater than 38.5 degrees celsius, 45 percent; shock or hypotension, 45 percent. Predisposing factors included antibiotics, 64 percent; immunosuppressants or chemotherapy, 36 percent; antidiarrheals, 27 percent; and barium enema in one patient. Five patients (45 percent) had more than one predisposing factor. X-rays showed transverse colon dilation and loss of haustrations in eight patients (72 percent), with a mean diameter of 9.9 +/- 3.4 cm. Flexible proctosigmoidoscopy showed pseudomembranes in all scoped patients, and toxin assay for Clostridium difficile was positive in all patients. One patient had emergency surgery. Ten patients were initially treated medically with nasogastric suction and intravenous resuscitation (90 percent) and antibiotics (100 percent), usually in the intensive care unit (80 percent). Four patients did not respond and underwent surgery; two others improved, then deteriorated, and also underwent surgery. Altogether, 7 of 11 patients (64 percent) underwent surgery. Three patients (27 percent) responded well to medical treatment. One patient was deemed too ill to undergo surgery and died. Mean delay to surgery was 3.0 +/- 1.3 days. No sealed or overt perforation was found at laparotomy. All patients who underwent surgery had a subtotal colectomy, with either a Hartmann's stump (71 percent) or a mucous fistula (29 percent). Eventually, five of seven patients who were operated on and two of four medically treated patients died (overall mortality, 64 percent). Only one patient underwent closure of ileostomy and anastomosis. CONCLUSION: Toxic megacolon complicating pseudomembranous enterocolitis is a serious problem that carries a high morbidity and mortality rate, regardless of treatment.

Adult↗
PubMed1981

Pseudomembranous enterocolitis: a historical and clinical review.

Pseudomembranous enterocolitis (PMEC) was first documented in 1893. Since this initial description, confusion has reigned in the medical literature concerning its nature and differentiation from such entities as necrotizing enterocolitis and staphylococcal enterocolitis. Since the 1950s, volumes have been written on PMEC and its association with a multitude of different antibiotics. PMEC has generally been used as somewhat of a "wastebasket" designation, being applied to any postoperative patient who develops significant diarrhea while on broad-spectrum antibiotics. More recently, a resurgence of interest in PMEC has led to its recognition as a specific disease entity and to a greater understanding of its etiology. The current review traces the history of PMEC, distinguishes if from similar disease processes, and describes its clinical presentation, diagnosis, and management. PMEC is particularly distinguished from antibiotic-associated diarrhea and certain forms of antibiotic-associated colitis.

Anti-Bacterial Agents↗
PubMed2001

Dietary protein enterocolitis.

Dietary protein enterocolitis generally presents in the 1st year of life with diarrhea, emesis, and irritability. When there is a delay in diagnosis, persistent exposure to the offending dietary antigen leads to increasing enteric inflammation manifesting as bloody diarrhea, anemia, dehydration, and failure to sustain normal patterns of weight gain and growth. The extent of enteric inflammation may be limited to mild proctitis, pancolitis, or true enterocolitis with esophagitis, gastritis, enteropathy, and colitis. The offending antigen is usually cow's milk protein or soy protein. A significant number of the infants are exclusively breast fed, especially those with proctitis. In older children, a wide variety of dietary proteins have been implicated. The inconsistency between allergists and gastroenterologists in the clinical definition of the syndrome remains a significant problem. To the allergist, the definition is based on clinical criteria, allergy testing, and response to double-blind food challenge, whereas to the gastroenterologist, it is defined by histologic criteria and the response of clinical and histologic manifestations to elimination diets. To further complicate the issue, European studies have emphasized the alterations in enteric permeability noted in both enteropathy and enterocolitis. In an effort to establish a unified approach, the International Life Sciences Institute sponsored a workshop in late 1998, which resulted in a document entitled "Classification of Gastrointestinal Disease of Infants and Children Due to Adverse Immunologic Reactions."

Child Welfare↗
PubMed1979

Changes in the incidence of necrotizing enterocolitis associated with variation of the gastrointestinal microflora in neonates.

The incidence of necrotizing enterocolitis was noted to vary in association with significant variation in the gastrointestinal microflora cultured from infants in the neonatal intensive care unit. Increased colonization with E. coli and K. pneumoniae was associated with an increased incidence of necrotizing enterocolitis, which suggests that these organisms are related to the pathogenesis of necrotizing enterocolitis.

Digestive System↗
PubMed2006

Rice protein-induced enterocolitis syndrome.

BACKGROUND AND AIMS: Food protein-induced enterocolitis syndrome (FPIES) is a non-IgE-mediated allergic reaction, usually to cow's milk or soy protein. The aim is to present a series of infants with enterocolitis syndrome developed after rice ingestion. To our knowledge, the issue has only once been described in patients from Europe. METHODS: Data on five patients were retrospectively analyzed. The patients presented with vomiting, diarrhea and dehydration; therefore, allergy was not considered as a diagnosis and the patients underwent broad diagnostic evaluation. Finally, an open food challenge was performed for suspicion of rice allergy. RESULTS: Detailed clinical and laboratory findings are presented. As all patients had symptoms which could have been indicative of a broad spectrum of diseases, a median of two hospitalizations was needed to establish the diagnosis. When the rice protein-induced enterocolitis syndrome is suspected all patients should undergo open food challenge test, as no other diagnostic procedure can confirm the diagnosis. CONCLUSION: This report shows that even hypoallergenic foods such as rice may cause FPIES and should be considered in the differential diagnosis of profuse vomiting and prostration in infants introduced to some kind of rice protein.

Allergens↗
PubMed2004

Epidermal growth factor and necrotizing enterocolitis.

As the number of extremely low-birth-weight infants increases,necrotizing enterocolitis remains a critical eminent problem. Supplementation of enteral feeds with biologically active substances normally present in breast milk, such as epidermal growth factor, seems to be a logical and safe way to reduce the incidence of intestinal inflammation and necrotizing enterocolitis. Continuing basic research and clinical studies are essential before epidermal growth factor can be introduced as an efficient therapeutic approach in the treatment of neonatal necrotizing enterocolitis.

Animals↗
PubMed2004

Severity of enterocolitis is predicted by IL-8 in paediatric oncology patients.

Enterocolitis in oncology patients remains an important complication, but there is a lack of insight into its likely severity from microbial, pathological and inflammatory aspects. Paediatric oncology patients admitted with neutropenic fever, who developed abdominal pain and diarrhoea, were monitored by the takers of rectal biopsies, cultures, and inflammatory marker measurements. Twenty-five patients were included (mean age 7.1 years). 8 patients (32%) needed intensive care treatment, 3 (12%) patients died. Gram-positive bacteraemia was diagnosed in 4 patients (16%). Most patients had negative blood and stool cultures. Predictors of a severe clinical course of the enterocolitis were an increased serum interleukin-8 (IL-8) (>1000 pg/ml) level and an increased serum C-reactive protein level (CRP) (>150 mg/l) level, both measured on the first day of clinical illness. Relative risks (RR) for admission to an Intensive Care Unit (ICU) were 11.3 (95% Confidence Interval (CI) 1.6-77.9) for elevated IL-8 levels and 6.4 (95% (CI) 0.92-45.1) for increased CRP levels. Rectal biopsies and pathology could not predict outcome (P=0.22). IL-8 analysis at the onset of enterocolitis symptoms can identify high-risk patients, which might be used clinically to design future intervention trials.

Abdominal Pain↗
PubMed2006

Intestinal immune defences and the inflammatory response in necrotising enterocolitis.

Necrotising enterocolitis is a devastating neonatal gastrointestinal emergency predominantly affecting low birth weight, premature infants and is accompanied by significant mortality and morbid sequelae. The pathophysiology remains obscure and the management of infants with necrotising enterocolitis has not changed since the recognition of this disease. Necrotising enterocolitis is most likely the clinical culmination of multiple different risk factors interacting with each other to produce bowel injury through a final, common inflammatory pathway. Here, we review intestinal immunity and the specific inflammatory mediators involved in this disease process.

Enterocolitis, Necrotizing↗
PubMed1979

Transcutaneous oxygen (tcPO2) measurements as an aid to fluid therapy in necrotizing enterocolitis.

Impaired peripheral perfusion is a major problem in necrotizing enterocolitis with delayed recognition and definite documentation being primary factors. While blood pressure and other clinical measurements may improperly estimate the severity of the problem, changes in transcutaneous oxygen measurements and their relationship to arterial oxygen (the tcPO2/PaO2 ratio) potentially afford a sensitive measurement of peripheral perfusion. Experience in our unit confirms a close relationship between tcPO2/ and PaO2 being 0.97 +/- 0.04 (SE). Ten infants with birth weights of 640 to 1380 g, who subsequently developed necrotizing enterocolitis, had strikingly lower ratios initially (0.00, 0.00, 0.00, 0.17, 0.21, 0.43, 0.44, 0.48, and 0.56). Use of the tcPO2/PaO2 ratio to monitor fluid therapy was related to outcome, suggesting that this ratio is important in managing necrotizing enterocolitis.

Enterocolitis, Pseudomembranous↗
PubMed1981

A histochemical study of the mucosubstances of the colon in cases of Hirschsprung's disease with and without enterocolitis.

From the histochemical studies of the mucus factor in normal controls and 10 cases with Hirschsprung's disease including 5 with enterocolitis, using Alcian blue-PAS method, we concluded that ganglionosis had no effect on the secretion of mucus. The presence of qualitative changes in the type of mucopolysaccharides, demonstrated as an increase in the sulphated group especially in cases with enterocolitis, was secondary to the chronic obstruction. These nonspecific changes might diminish the protecting mechanism of the mucous membrane. Quantitative changes were seen to be related to the severity of the enterocolitis.

Alcian Blue↗
PubMed1988

The role of coagulase-negative Staphylococcus in neonatal necrotizing enterocolitis.

Coagulase-negative Staphylococcus has emerged as a prominent pathogen in the neonatal intensive care unit and a recent report has implicated this organism in necrotizing enterocolitis (NEC). This same study suggests that Staphylococcus epidermidis is most commonly associated with a "mild form of enterocolitis." This prompted a review of the role of coagulase-negative Staphylococcus in the surgical complications of NEC. Between 1982 and 1986, 86 newborns underwent operation for perforation or intestinal necrosis secondary to NEC. Blood cultures, obtained within 72 hours of surgery, were positive in nine of 71 infants (13%). One third of these grew coagulase-negative Staphylococcus. Peritoneal cultures obtained at the time of operation were positive in 71 neonates. The incidence of Staphylococcus epidermidis was 30%. In a third of these cases, coagulase-negative Staphylococcus was the only organism covered. Overall mortality within the group was 33%. Coagulase-negative Staphylococcus was the single most frequent organism recovered from those infants who expired (35%). This data clearly indicates that Staphylococcus epidermidis must be considered as a significant pathogen in NEC. It is associated with both morbidity and mortality and, therefore, warrants appropriate aggressive therapy when recovered from the neonate with enterocolitis.

Enterocolitis, Pseudomembranous↗
PubMed1990

Pathology of neonatal necrotizing enterocolitis: a ten-year experience.

We reviewed pathology specimens from 84 patients seen during a 10-year period with neonatal necrotizing enterocolitis, and these findings were correlated with clinical features. Coagulation (ischemic) necrosis, inflammation, and bacterial overgrowth were all present in the intestine of nearly all patients but with individual variability in the severity of these findings. Overall, coagulation necrosis was more severe than any other finding in most infants, indicating the importance of ischemia in the pathophysiology of necrotizing enterocolitis. Reparative tissue changes such as epithelial regeneration, granulation tissue formation, and fibrosis, found in two thirds of cases, suggested ongoing tissue injury of at least several days' duration. Birth weight, Apgar score, age, feeding status, and the presence of respiratory distress syndrome were not correlated with any particular histologic feature. The pathologic changes of necrotizing enterocolitis suggest that its cause is multifactorial, with ischemia, inflammation, bacterial overgrowth, and reparative tissue changes all playing important roles.

Apgar Score↗
PubMed1978

Relationships of mesenteric thromboembolism, oral feeding, and necrotizing enterocolitis.

Mesenteric blood vessels were examined in postmortem specimens of 30 selected infants. The infants had had necrotizing enterocolitis (16 cases) or other lesions (14 cases). Mesenteric thromboemboli were observed in 12 of the infants with necrotizing enterocolitis (P less than 0.001). Umbilical vessel catheters were apparently responsible for the emboli. Multiple instances of thrombosis and thromboembolism were detected in other organs. Ninety-four percent of infants with necrotizing enterocolitis were orally fed (P less than 0.001). Mesenteric thromboemboli were more frequent in infants who were fed via the digestive route while an umbilical arterial catheter was in place. Mesenteric thromboembolism in these infants was postulated to have been attributable to increased postprandial blood flow in the mesenteric vessels.

Catheterization↗
PubMed1988

Neonatal rotavirus-associated necrotizing enterocolitis: case control study and prospective surveillance during an outbreak.

After the death of a premature infant from rotavirus-associated necrotizing enterocolitis, we instituted prospective surveillance for this disease in our neonatal intensive care unit. During the 4-month study period an additional six cases of necrotizing enterocolitis and eight cases of hemorrhagic gastroenteritis occurred. Rotavirus infection was documented in 11 of these 15 symptomatic infants, in comparison with only eight rotavirus infections in 147 asymptomatic or minimally symptomatic babies (P less than 0.0001). Stools from 110 nursery personnel tested during the outbreak did not contain rotavirus. However, 12 of 59 staff members had serum IgM antibody against rotavirus, suggesting recent infection. In a case-control study we compared babies with severe gastrointestinal illness with a control group randomly selected from asymptomatic babies in the nursery during the time of the outbreak. Univariate analysis found six categorical variables and nine continuous variables that were significantly associated with disease. Multivariate logistic regression analysis, however, found only birth weight (P less than 0.0001), rotavirus infection (P less than 0.0001), and age at time of first nonwater feeding (P less than 0.02) to be associated with gastrointestinal illness. This study provides further evidence for the role of infection in some cases of neonatal necrotizing enterocolitis and hemorrhagic gastroenteritis.

Colorado↗