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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The ability of external imaging to demonstrate intestinal infarction in neonatal necrotizing enterocolitis (NEC) was prospectively evaluated. The radiopharmaceutical technetium--99m diphosphonate was injected intravenously and the patients subsequently underwent abdominal scanning. Clinical patient care and interpretation of the images were entirely independent throughout the study. Of 33 studies, 7 were positive, 4 were suspicious, and 22 were negative. One false positive study detected ischemia without transmural infarction. The second false positive scan occurred postoperatively and was due to misinterpretation of the hyperactivity along the surgical incision. None of the suspicious cases had damaged bowel. The two false negative studies clearly failed to demonstrate frank intestinal necrosis. The presence of very small areas of infarction, errors in technical settings, subjective interpretation of scans and delayed clearance of the radionuclide in a critically ill neonate may all limit the accuracy of external abdominal scanning. However, in spite of an error rate of 12%, it is likely that this technique will enhance the present clinical, laboratory, and radiologic parameters of patient management in NEC.
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PMID:Prospective evaluation of radionuclide scanning in detection of intestinal necrosis in neonatal necrotizing enterocolitis. 701 10

Necrotizing enterocolitis has been attributed to the use of indomethacin (INDO) for medical closure of patent ductus arteriosus. To study the effect of INDO on cardiac output and mesenteric circulation, INDO was given by rectum (0.25 mg/kg, 0.5 mg/kg, 1.25 mg/kg--3 dogs in each group) and the control group received none. The cardiac output and organ blood flow were measured before and 1 hr after INDO with radioactive microspheres using 4 isotopes (Cr53, Ni95, Co57, Sn113). The blood flow to different parts of the GI tract was measured as percent of cardiac output using a gamma counter. Paired t test was used to calculate percent reduction in organ blood flow. During the experiment, there was no reduction in cardiac output in the entire group. Anesthesia had no effect on the control group. In the three INDO treated groups, percent reduction of mucosal blood flow of the stomach (63%, 32%, 68%, p less than 0.01), mid ileum (19%, 59%, 57%, p less than 0.05) and terminal ileum (57%, 35%, 54%, p less than 0.015) was significant. A strong trend in reduction of organ blood flow was noted in other regions. There was no significant change due to different dosages of INDO. The area of ischemia in this dog model corresponds to clinical pathology noted in necrotizing enterocolitis.
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PMID:Effect of indomethacin on mesenteric circulation in mongrel dogs. 717 30

Perinatal changes in fetal heart rate (FHR) were monitored in infants in whom necrotizing enterocolitis (NEC) developed. Eleven of 16 monitoring strips indicated severe FHR changes consistent with perinatal hypoxia, two indicated mild changes, two indicated tachycardia alone, and only one was normal. Severe variable FHR decelerations indicating umbilical cord compression occurred in four cases, persistent late FHR decelerations occurred in two cases, persistent late and severe variable FHR decelerations occurred in two cases, prolonged bradycardia occurred in two cases, and bradycardia with persistent late FHR decelerations occurred in one case. These findings confirm that NEC does occur in infants with perinatal hypoxia and indicate that intestinal ischemia may occur before delivery and after delivery from hypoxia and acidosis from lung disease, exchange transfusion, or sepsis. Perinatal monitoring may become an important determinant in identifying the infant in whom NEC will develop.
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PMID:Fetal heart rate patterns in infants in whom necrotizing enterocolitis develops: a preliminary report. 719 Dec 46

Necrotizing Enterocolitis (NEC) of the new-born is a serious syndrome characterized by bilious vomiting, gastric retention, abdominal distention and bloody stools. Furthermore, the general condition of the neonate is frequently compromised. The pathogenesis is multi-factorial; however, most authors state that the primary cause of this syndrome is due to ischemia of the intestinal wall. The most serious complication in babies with NEC is perforation of the necrotic bowel, a condition which must always be treated surgically. We present a case of NEC that has a particularly interesting clinical course and, as well, an interesting approach to treatment, which involved the placement of a peritoneal drain. This drain was subsequently utilized for peritoneal lavage once the diagnosis of NEC was confirmed, because we felt that the patient's general condition was so serious that he could not tolerate surgery at this time.
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PMID:[Treatment of necrotizing enteritis using peritoneal drainage. Presentation of a clinical case (author's transl)]. 730 14

It is generally accepted that a circulatory disorder of the bowel during the embryonic stage of development plays an important part in the occurrence of atresias of the small bowel and colon, with the exception of the septal types of atresia. In most cases, the cause of this disorder is not known. An experimental study, making use of chick embryos, is presented and the results are discussed. Two sets of experiments were conducted. In the first set the bowel of the chick embryo was subjected to temporary ischemia. In the second one the chick embryo was subjected to a period of general hypoxia. Temporary ischemia of the bowel frequently resulted in stenosis or atresia. The duration of the vascular occlusion was significant factor. Temporary general hypoxia resulted in serious morphologic changes of the bowel and the liver. Stenosis or atresia did not occur in this case, but there was a strong resemblance to the histopathological picture of neonatal necrotizing enterocolitis.
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PMID:The effects of temporary general hypoxia and local ischemia on the development of the intestines: an experimental study. 736 60

After resolution of acute necrotizing enterocolitis (NEC), six of 31 surviving infants (19%) developed late ischemic stricture of the colon. Stricture occurred after both medical and surgical treatment for NEC, and in both functional and defunctionalized bowel. In medically-treated infants, the symptoms of intestinal obstruction usually began six to eight weeks after NEC. Surgically-treated infants developed asymptomatic strictures distal to an enterostomy. Barium enema was the appropriate diagnostic study for both groups. Operative management consisted of segmental colonic resection with frequent use of enterostomy. On histopathologic examination, resected strictures showed a spectrum of the reparative process after intestinal ischemia, ranging from obliterative scar to near-normal colon. Because delayed diagnosis led to the death of one of our infants, we recommend a barium enema for early diagnosis of stricture about six weeks after NEC, whether initial treatment was medical or surgical. In a recent infant, two colonic strictures were thus diagnosed and resected prior to development of symptoms of intestinal obstruction.
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PMID:Intestinal obstruction due to colonic stricture following neonatal necrotizing enterocolitis. 740 75

Changes in mucosal permeability may be important in the etiology of necrotizing enterocolitis. The authors have previously shown that subclinical ischemia-reperfusion injury results in increased permeability in the rat intestine, and have partially characterized this phenomenon. In the present study the authors attempt to determine the mechanism by which these changes occur. Six-week-old rats underwent 10-minute superior mesenteric artery occlusion (SMAO) or sham, and mucosal permeability to 51CrEDTA was measured after 30 minutes. Rats were pretreated with saline, inhibitors of oxygen free radicals (superoxide dismutase+catalase, vitamin E, allopurinol, alpha-phenyl-N-tert butyl-nitrone), inhibitors of eicosanoids (indomethacin, quinacrine, diethylcarbamazine, 13-azaprostanoic acid), the putative cytoprotective agent prostaglandin E2, or the inhibitor of neutrophil free radical production fructose 1-6 diphosphate. None of the agents significantly attenuated the increase in mucosal permeability caused by SMAO, although indomethacin and prostaglandin E2 significantly exacerbated the permeability changes. To further explore the role of neutrophils, tissue myeloperoxidase was measured 30 minutes after SMAO. There was no significant difference in myeloperoxidase levels between sham and SMAO animals. These data suggest that the early increase in mucosal permeability after subclinical ischemia-reperfusion injury is not mediated by oxygen free radicals, eicosanoids, or neutrophils. The deleterious effect of indomethacin and prostaglandin E2 suggests a possible protective role for the cyclooxygenase system, but further studies are necessary to elucidate this possibility.
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PMID:Mucosal permeability after subclinical intestinal ischemia-reperfusion injury: an exploration of possible mechanisms. 759 36

Necrotizing enterocolitis (NEC) is a disease characterized by ischemia and necrosis of the gastrointestinal tract frequently leading to perforation of the intestine. It occurs primarily in the premature infant and is a major cause of mortality and morbidity in the low birth weight infant. Careful nursing and medical care can greatly reduce the incidence and severity of this disease, thus decreasing both the associated morbidity and mortality. This article reviews the pathophysiology, diagnosis, and treatment of NEC; presents a case study; and provides a nursing care plan for treatment of this disease.
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PMID:Necrotizing enterocolitis. 765 62

Reactive oxygen metabolites are implicated in gastrointestinal disease and enterocyte injury associated with ischemia-reperfusion, bacterial translocation, inflammatory bowel disease, and necrotizing enterocolitis. The ileal-like, human colon carcinoma cell line, Caco-2, was used to investigate oxidative damage. After challenging Caco-2 cells with reactive oxygen metabolites, the permeability, viability, and energy charge of Caco-2 cells were assessed. Permeability was determined by transepithelial electrical potential and flux of small molecules. Viability was determined by release of 51Cr. Cell energy was evaluated by determining adenylate energy charge. The source of reactive oxygen metabolites, with the exception of menadione, did not affect viability of Caco-2 cells; cell permeability was increased. The increased varied with the source and location of the reactive oxygen metabolite. There was no change in energy charge. This study suggests that reactive oxygen metabolites could cause enterocyte damage and that the source of the reactive oxygen metabolite is an important variable in determining the extent of damage. Antioxidants might prevent injury.
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PMID:Polarized Caco-2 cells. Effect of reactive oxygen metabolites on enterocyte barrier function. 789 34

A case of full-thickness necrosis of the small bowel, and colon, which required partial resection of the jejunum and total resection of the ileum and colon is reported. The case gives the chance for a review of the Literature on intestinal necrosis not caused by vascular occlusion. Nonocclusive intestinal ischemia, acute neonatal necrotizing enterocolitis and adult necrotizing enterocolitis including the Pig-bel disease, common in Papua-New Guinea, are examined. Resemblances and differences in etiology, pathophysiology and clinical findings are discussed. The hypothesis that the process of "bacterial translocation" plays a central role in the pathogenesis of bowel infarction, representing therefore a possible link between infective and vascular mechanisms, is emphasized. Important suggestions on massive intestinal necrosis management are also reported.
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PMID:[Nonocclusive intestinal infarct and necrotizing enterocolitis in the adult]. 794 88


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