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

From 1977 to 1991, we encountered 67 patients with Hirschsprung's disease and 14 of them developed enterocolitis, with 3 cases being fatal. Enterocolitis occurred preoperatively in 12 infants, as well as after ileostomy in one and after a pull-through procedure in another. Seven infants had severe enterocolitis, including three with pseudomembranous enterocolitis and four with hemorrhagic necrotizing enterocolitis. Enterocolitis in Hirschsprung's disease mainly occurs due to intestinal obstruction and ischemia; however, in some cases, Clostridium difficile overgrowth and its toxin also appears to be related to severe pseudomembranous enterocolitis. In severe enterocolitis, antibiotics and enterostomy often prove to be ineffective, and thus an early resection of the affected bowel appears to be necessary. Moreover, when the aganglionic segment extends to the small bowel, severe enterocolitis tends to occur in the aganglionic intestine even after performing an enterostomy, and a resection of the aganglionic bowel is therefore recommended to allow for adequate lavage of the segment distal to the enterostomy site.
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PMID:Pseudomembranous enterocolitis and hemorrhagic necrotizing enterocolitis in Hirschsprung's disease. 800 64

Early descriptions of necrotizing enterocolitis (NEC) proposed gut ischemia as a primary factor in pathogenesis. Subsequent laboratory and clinical investigations have failed to support these theories, relegating most to positions of historical significance. Presently, the role of the circulation in the pathogenesis of NEC is unclear; however, several lines of ongoing investigation have begun to provide novel insight into the means by which circulatory aberration may initiate or contribute to the development of bowel necrosis.
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PMID:The role of the circulation in the pathogenesis of necrotizing enterocolitis. 807 Feb 23

Necrotizing enterocolitis (NEC) is a worldwide problem that has emerged in the past 25 years as the most common gastrointestinal emergency in neonatal intensive care units (NICU). In the United States the incidence ranges from 1 to 7.7% of NICU admissions. Ninety percent of the patients are premature infants. Mucosal injury, bacterial colonization and formula feeding are the three major pathogenetic factors that have been documented in most infants who have developed NEC. However, NEC may develop only if a threshold of injury, imposed by the coincidence of at least two of three events (intestinal ischemia, pathogenic bacteria, and excess of protein substrate) is exceeded. Immunological immaturity of the gut in premature babies may represent the crucial risk factor.
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PMID:Epidemiology of necrotizing enterocolitis. 808 75

The pathogenesis of necrotizing enterocolitis remains unknown, but various factors have been postulated including, but not limited to, mesenteric ischemia, enteral alimentation, and infection. Since an understanding of circulatory physiology in developing intestine may provide insight into the role of mesenteric ischemia in the etiology of necrotizing enterocolitis, this review summarizes what is currently known about the regulation of blood flow and oxygenation in developing intestine and how it differs from that in adult intestine. The discussion is divided into intrinsic versus extrinsic factors. Phenomena which may be used to evaluate the capacity for intrinsic vasoregulation include pressure-flow autoregulation, reactive hyperemia, venous hypertension, arterial hypoxemia, and postprandial hyperemia. Extrinsic factors include neurologic and hormonal influences. Additionally, the susceptibility for tissue hypoxia as a function of age and the correlation with subsequent development of mucosal injury are discussed.
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PMID:Regulation of hemodynamics and oxygenation in developing intestine: insight into the pathogenesis of necrotizing enterocolitis. 808 91

Besides classical necrotizing enterocolitis (in neonates), which is seen in India as elsewhere in the world, we observe sporadic cases of tropical enterocolitis, i.e. segmental jejunitis, ileitis or colitis and rarely duodenitis. This is a distinct clinico-pathological entity presenting as "acute abdomen", with pain, bilious vomiting, constipation or bloody diarrhoea. The clinical course is not as fulminating as neonatal necrotizing enterocolitis. Most cases are salvaged by conservative treatment especially after the confidence brought by laparoscopic vision of the abdomen, thus excluding perforation or gangrene of the bowel involved. Without laparoscopy, most of the cases end up in laparotomy. The pathology appears to be a kind of local hyperimmune reaction in the segment of bowel involved, ranging from punctate haemorrhages in the seromuscular layer of the bowel to a generalized red fiery look or perforation due to mucosal ulceration. Whatever the causative agent, the pathogenesis is of local vasculitis leading to ischemia and various patterns of disease.
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PMID:Tropical enterocolitis in children. 808 96

Although medication-induced colonotoxicity is uncommon, it is important that it be recognized, because the initial therapy for this condition is medication discontinuation. This review categorizes the association between the listed medications and colonotoxicity as "well-established" or "probable," according to the following criteria: number of clinical studies by independent clinical investigators, total number of reported cases, plausibility of an association based on experimental and pharmacologic studies, and validity of an association in each reported case. Medications associated with colonic ischemia include cocaine, ergotamine, estrogen, amphetamines, digitalis, methysergide, and vasopressin. Medications associated with colonic pseudoobstruction include narcotics, phenothiazines, vincristine, atropine or other anticholinergics, ganglionic blocking agents, and tricyclic antidepressants. Medications promoting infectious or necrotizing enterocolitis include numerous antibiotics associated with pseudomembranous colitis, deferoxamine associated with Yersinia enterocolitis, chemotherapy associated with neutropenic colitis, and hyperosmolar medications or formulas in infants. Medications associated with an allergic, inflammatory, or cytotoxic colitis include gold compounds, nonsteroidal antiinflammatory drugs, alpha-methyldopa, flucytosine, methotrexate, salicylates, and sulfasalazine. Potassium chloride, administered in slow-release wax matrices, can cause intestinal ulcers. Chronic cathartic use leads to colonic hypomotility and abdominal distention. Methysergide can cause a colonic stricture due to retroperitoneal fibrosis. Intrarectally administered compounds that have produced a toxic colitis include powerful acids, bases, and other corrosives. Enemas using hypertonic radiographic contrast agents have been associated with colitis in patients with colonic obstruction.
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PMID:Colonic toxicity of administered medications and chemicals. 812 79

Increased mucosal permeability may represent an important factor in the etiology of necrotizing enterocolitis (NEC). In the present study we used an immature rat model to assess the permeability effects of a number of stresses commonly seen in infants with NEC. In 10-day-old rats, mucosal permeability to 51Cr EDTA was measured after subjecting the animals to 10-minute ischemia-reperfusion injury, 30 minutes of hypoxia (14% oxygen), cold stress (4 degree C for 4 minutes), and intraperitoneal indomethacin (0.2 or 2.0 mg/kg) or theophylline (40 or 200 mg/kg). When compared with appropriate controls, mucosal permeability was found to be significantly increased by ischemia-reperfusion injury, hypoxia, and high-dose indomethacin, but not by cold, theophylline, or low-dose indomethacin. Renal clearance studies confirmed that elevated blood levels of 51Cr EDTA were due to increased permeability rather than decreased renal excretion of the probe. These studies confirm that mucosal permeability in the immature rat is increased by a variety of insults, and may represent a "common pathway" in the etiology of NEC.
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PMID:Mucosal permeability in the immature rat intestine: effects of ischemia-reperfusion, cold stress, hypoxia, and drugs. 826 5

Indomethacin (IND), widely used in premature infants to effect nonoperative closure of patent ductus arteriosus (PDA), has been implicated in gastrointestinal tract (GI) perforations and necrotizing enterocolitis (NEC). The vasoactive effects of IND could simultaneously affect regional blood flow distribution, specifically a decrease in intestinal blood flow. This study determined blood pressure (BP), heart rate (HR), cardiac output (CO), total peripheral resistance (TPR) and regional blood flows (mL/min/g) at baseline, 15, 60, and 120 minutes after intravenous infusion of IND (0.4 mg/kg) in three groups: preterm piglets delivered 7 to 10 days before term; 1- to 2-day-old piglets; and 7- to 14-day-old piglets. IND did not significantly affect hemodynamic parameters (BP, HR, CO, TPR) or regional blood flows to the heart, central nervous system, kidney or GI tract in the premature animals. In 1- to 2-day-old animals, a significant increase in BP and TPR occurred at 120 minutes, with significant decreases in blood flow to the GI tract in the esophagus, stomach, and rectosigmoid. In the 7- to 14-day group CO significantly decreased while TPR increased. Significant decreases in blood flow occurred throughout the GI tract, most pronounced in the small intestine and colon, essentially due to decreased mucosal blood flow. Our study indicates that indomethacin can cause selective GI tract mucosal ischemia, and that the effect is increased in the more developed animal. This effect on mucosal blood flow suggests the GI tract disturbances seen after IND administration are due to an ischemic injury to mucosa previously affected by ischemia-reperfusion injury from other stresses.
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PMID:Indomethacin-induced blood flow distribution in premature and full-term piglets. 826 8

From January 1984 to March 1992, there were 19 infants admitted to our hospital with gastrointestinal perforation not associated with necrotizing enterocolitis. Seven patients (37%) were premature. Six patients (32%) had their perforations located in the stomach, 9 (47%) in the small intestine, and 3 (16%) in the colon. The most common clinical presentation was abdominal distention (95%). Pneumoperitoneum was noted only in 12 (63%) patients. About 60% of the patients had the perforation occur before 4 days of age. The predominant cause of perforation was unknown, so called spontaneous perforation (8/19, 42%), followed by ischemia or infarction (5/19, 26%). The overall mortality rate was 32%. The non-survivors had more severe metabolic acidosis than the survivors, but there were no differences in the birthweight and gestational ages of these two groups. Sepsis accounted for 83% of the deaths. Early diagnosis and treatment are the best ways to promote survival.
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PMID:Gastrointestinal perforation in infants: cases unrelated to necrotizing enterocolitis. 829 54

Free radical-mediated reperfusion injury has been demonstrated in ischemic neonatal bowel necrosis, but the mechanism of injury remains elusive. To determine whether such an injury can be prevented, 76 weaning rats were studied to test the effects of deferoxamine, an iron chelator, in postischemic injury. Group I (N = 20) had a sham laparotomy without vascular occlusion. Group II (N = 21) was subjected to 90 min of superior mesenteric artery occlusion prior to reperfusion. Group III (N = 35) received deferoxamine 15 mg/kg intravenous prereperfusion, in addition to ischemia and reperfusion as in group II. Survival profiles for each group were determined and a scale of pathologic severity was applied and compared. Group I had 100% long-term survival and group II, 14%. Group III had an overall survival of 28% and demonstrated a prolonged postreperfusion survival profile (P < 0.002) compared to group II. Histology was nearly identical to human necrotizing enterocolitis in degrees of bowel wall destruction and relative paucity of neutrophils. Group III showed a significant reduction in severity of injury compared to group II (P < 0.003). We conclude that neonatal bowel ischemia conditions such as necrotizing enterocolitis may be reperfusion injuries wherein free iron plays an important role in tissue injury. Administration of an iron chelating agent under such conditions has a beneficial effect on survival and histology.
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PMID:Prevention of postischemic injury in immature intestine by deferoxamine. 842 36


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