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

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.
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PMID:Neonatal necrotizing enterocolitis: implications for an infectious disease. 37 77

Apparently there are different causes for necrotizing enterocolitis (NEC) in the newborn infant. Besides it may be that NEC only is caused by the interaction of several factors such as perinatal complications, medical measures, an aggressive oral alimentation and an adverse colonization of the bowel and that a critical degree of stress is required to initiate enterocolitis. This assumption would help to explain, why one newborn infant can stand an episode of perinatal stress without falling ill, while the other develops the disease a short time later. Probably NEC starts with an intestinal mucosa damage caused by ischemia or local noxae, and only subsequent invasion by the bowel flora into the damaged tissue and gas formation within the bowel wall lead to the picture of necrotizing inflammation and pneumatosis intestinalis.
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PMID:[The etiology of necrotizing enterocolitis in the newborn]. 43 60

About one case of necrotising enterocolitis following an extra-peritoneal and aseptic operation, it seems that a post-operative ileus, by the ischemia of mucous membrane and the swarming of anerobics that it involves, seems to be responsable of this dreadful complication. The macroscopic and deceiver aspect of intestine to an early re-operation can impeed this diagnosis. The hyperbaric oxygenotherapy seems to be a perceptible adjuvant treatment.
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PMID:[Post-operative necrotising enterocolitis. One case cured by hyperbaric oxygenotherapy (author's transl)]. 48 77

In this review the author's opinion regarding the etiology of most cases of perinatal and neonatal bowel ischemia has been stated. It is recognized that the changes brough about by hypoxia (splanchnic shutdown, bowel ischemia) represent the "soil" on which other "seeds" can prosper. In its simplest form following acute ischemia, the processes of repair take over, leading to functional recovery and a presumably normal bowel. In those patients with more extensive initial damage, degrees of stenosis and even atresia may be expected as a result of the healing of the bowel. Rapidly evolving ischemia may produce perforations; these may be restricted and involve only very small areas of bowel or may be part of a more generalized involvement, possibly even with multiple perforations. In other infants, alterations of bacterial flora could contribute to the clinical picture of "necrotizing enterocolitis," and gas may or may not be present in the bowel wall. If the process of ischemia has been relatively mild, or bacterial overgrowth not particularly marked, some of the more obscure functional syndromes may be noted. The persistence of these obscure syndromes may in turn be related to incomplete phases of regeneration of the bowel that fall short of producing stenosis but lead to a mucosa that is not optimally functional.
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PMID:The spectrum of ischemic bowel disease in the newborn. 78 16

Three cases of double left colic stenosis revealed at one month of age by subobstruction are reported. Recovery was obtained by surgery. The evolution of radiological data in one case, and of histological changes observed on the resected sigmoid colon in the two other cases favor the assumption that cicatricial stenosis occurred likewise. These cases also confirm the existence of a benign expression of necrotising enterocolitis, most common with a colonic localization. Such stenosis due to submucous connective sclerosis strengthens the hypothesis that a transitory mesenteric ischemia is responsible for the necrotizing enterocolitis in newborns.
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PMID:[Colonic stenosis following necrotizing enterocolitis in newborn infants. Apropos of 3 cases]. 93 13

The feasibility of the use of indium 111 oxine-labeled autologous leukocytes for the diagnosis of ischemic enterocolitis in vivo was examined in an experimental model of ischemia in dogs. A 30-cm segment of small intestine was devascularized by ligating the arteries and veins from the last arcade in 7 dogs. A sham operation was performed in 3 control dogs. 111In oxine-labeled autologous white blood cells were infused 3.5 hours after operation. Anterior and lateral nuclear scanning was performed at 6 and 24 hours postinfusion with a gamma camera equipped with a low-energy magnifying multihole collimator. The animals were killed after 24 hours. The gross and microscopic appearance of the bowel was evaluated. The radioactivity in the serial specimens of the bowel was measured. In vivo scans were positive (ie, increased uptake in the bowel loop) in all dogs with intestinal ischemia at 6 and 24 hours. No significant uptake was noted in control dogs. Rectilinear scan of the bowel removed at autopsy showed a correlation between the area of infarction and tracer accumulation. In addition, there was a progressive decrease in uptake of 111In oxine from the center of the ischemic lesions to the periphery. Forty percent of the total radioactivity was measured at the center of the lesion, whereas only 6.5% was present at 22.5 cm from the center. Thus the ratio between the ischemic and normal tissue was 10:1 (range, 6.5 to 16). These studies demonstrate that 111In oxine-labeled autologous white blood cells can be used for the diagnosis of ischemic enterocolitis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Indium 111 oxine-labeled leukocytes for early diagnosis of ischemic enterocolitis. 194 80

Sixty-three patients with biopsy-proven Hirschsprung's disease were diagnosed at LeBonheur Children's Medical Center, Memphis, TN between 1955 and 1980. Fifty-eight of these patients had pull-through procedures performed by three similarly trained pediatric surgeons. The follow-up was 100 percent, averaging 8 years from initial diagnosis. Demographics, surgical procedures performed, and complications are reviewed. Significant findings are (1) anastomotic strictures occurred most frequently when the level of aganglionosis was at the sigmoid colon; (2) postoperative encopresis was most likely when the endorectal pull-through procedures were performed before the age of 10 months; and (3) with selective use of colostomies or enterostomies performed prior to the pull-through procedure, the incidence of enterocolitis was low, with 0% mortality. On the basis of these findings, we recommend that, when the most proximal level of aganglionosis is the sigmoid colon, it is important to critically inspect the angulation of mesenteric blood vessels and viability of the splenic flexure pull-through colon segment to prevent ischemia and therefore anastomotic strictures. The endorectal pull-through procedure should be delayed until after 10 months of age. Infants with Hirschsprung's disease should have a colostomy or enterostomy prior to a pull-through procedure. Patients diagnosed at 10 months of age or more, who have not had earlier bouts of enterocolitis, are not low percentile weight, and are without signs of severe obstruction, are candidates for pull-through without a prior fecal diversion procedure.
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PMID:Twenty-five years' experience with Hirschsprung's disease. 235 87

An experimental model of ischemia of the distal part of the small intestine has been realized in rats. This experimental study realizes a moderate ischemia of the distal part of ileum loops, by vascular ligations. An important decreasing of the intestinal motility is observed 2 days after the operation, by in vitro study. The motility became normal 7 days after. During this time a microbiological evaluation revealed an important increasing of anaerobic germ in the distal ileum. Total parenteral nutrition preserves the intestinal motility and the endoluminal flora. Ischemia of the small bowel is an important component of enterocolitis by modification of the peristalsis. The total Parenteral Nutrition in such condition seems to protect the intestinal flora.
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PMID:[Consequences of ischemia of the terminal ileum in the rat: influence of exclusive parenteral nutrition]. 312 84

An animal model was proposed to clarify the difference in occurrence of enterocolitis in congenital aganglionosis. When gaseous distention of the colon was localized to the rectosigmoid area, enterocolitis never occurred. On the contrary, when it involved the left colon, enterocolitis occurred in 13 of 15 patients. Intestinal blood flow rates were simultaneously measured in the left colon and rectum of six dogs by using labeled microspheres and expressed in function of the intraluminal pressure. Results show that for elevated values of intraluminal pressure, blood flow was significantly lower in the left colon than in the rectum. These results may explain why ischemia and necrosis occurred more frequently in the left colon than in the rectum.
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PMID:Relationship between parietal blood flow studies in the left colon and the rectum in dogs. Colonic pressure and blood flow. 336 28

The authors report a case of necrotizing enterocolitis which appeared in the first hours of life of a full-term neonate without signs of sepsis. This neonate presented with a severe hypoplasia of the horizontal aorta and very tight coarctation responsible for hepatic, renal and mesenteric ischemia. Reports of enterocolitis as a complication of congenital heart disease are rare and related most often to hypoplastic left heart than to coarctation of the aorta.
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PMID:[A rare cause of neonatal ulcero-necrotizing enterocolitis: aortic coarctation syndrome]. 361 70


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