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

Cocaine is one of the illicit hallucinogenic drugs which can be conveniently taken without resorting to parenteral administration. Almost all organs systems in the body are affected by its abuse. Complications involving the nervous, cardiovascular and reproduction systems have recently been published. In this report, complications relating to gastrointestinal system are reviewed. Acute ischemic syndromes are the most prominent gastrointestinal complication of cocaine use. Severe ischemia results from intense activation of alpha-adrenergic receptors in the mesentery. This ischemia results in gastropyloric ulcerations, gangrene and perforation of small as well as large intestine and colitis. Sudden collapse and deaths have been reported in "body packers" who swallow cocaine filled condoms in an effort to smuggle the drug through the customs. Several cases of acute hepatotoxicity and hepatocellular necrosis from cocaine use have also been reported.
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PMID:Gastrointestinal manifestations of cocaine addiction. 820 75

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

GI bleeding occurs with prolonged exercise and is probably mediated by visceral ischemia. It may produce acute hemorrhage, more chronic symptoms with anemia, or result in guaiac-positive conversion with little clinical disease. Hemorrhagic gastritis and colitis are the most frequently recognized lesions, and are usually transient and reversible. Acid suppression with cimetidine may be effective in selected patients with recurrent HG, but effective therapy for most patients with this form of GI bleeding is still uncertain. Awareness of the association between GI bleeding and exercise should stimulate further investigations into the pathophysiology and therapy.
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PMID:Gastrointestinal bleeding and the athlete. 830 30

Colon ischemia is a well-recognized clinical entity that often occurs spontaneously in patients over the age of 50 years. Many previous cases of nonspecific colitis are now felt to have been secondary to an ischemic event. In contrast to patients with acute mesenteric ischemia and extensive necrosis of the small bowel, the majority of patients with isolated colon ischemia follow a benign clinical course. Most patients present days, weeks, or months after the initial ischemic insult, and many may not have any recognizable antecedent episode of colon ischemia. However, some patients develop a fulminant form of the disease that causes colon infarction and death if not treated early. A high index of suspicion is necessary to make the diagnosis in the hospitalized patient. Endoscopy is recommended to confirm the diagnosis and the extent of injury and to monitor progression or resolution of disease. Aggressive management is of paramount importance to minimize the damage to the ischemic colon and reduce the otherwise high in-hospital mortality rate. Surgical intervention is indicated for patients with evidence of peritonitis or transmural infarction or perforation of the colon and for patients with chronic symptomatic colitis or stricture.
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PMID:Ischemic colitis. 837 27

Eight tests of hemostasis were measured in 233 horses with colic. Blood samples were obtained at admission and for 4 consecutive days of hospitalization. Data were analyzed retrospectively by outcome, by broad-category diagnosis group, by small intestinal disorder, and by smaller categories for comparing specific diseases. Nonsurviving horses and horses with the most severe forms of intestinal ischemia had changes interpreted as hypercoagulative, the intensity of which was increased on the first and second mornings (sample times 2 and 3) after admission, when most significant differences for results of specific tests were detected. Nonsurvivors had decreased antithrombin III activity and prolonged prothrombin and activated partial thromboplastin times; those with strangulating obstructions also had decreased protein C and plasminogen activities. During hospitalization and with survival, these changes tended to reverse. In most horses, regardless of diagnosis or outcome, concentration of fibrin degradation products and fibrinogen, and alpha 2-antiplasmin activity increased over time. Whether these changes reflected specific effects of colic or of the acute-phase response was not determined. In comparisons of small intestinal disorders (proximal enteritis, strangulations, and impactions), diagnostically distinguishing features were not found. Likewise, in comparisons of specific diseases (small vs large intestinal impaction, proximal enteritis vs colitis, small vs large intestinal obstruction), diagnostically distinguishing features were not found.
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PMID:Analysis of hemostasis in horses with colic. 840 38

We have seen two cases of a segmental ischemic colitis develop during nonsteroidal antiinflammatory drug (NSAID) treatment. No other possible etiologic factors were shown. The short-term clinical course and the follow-up were uneventful. NSAIDs have been reported to cause different lesions in the large bowel, either by worsening preexisting colonic diseases or by inducing a primary pathology. We suggest that ischemia should be considered a possible mechanism of NSAID-associated colitis. Such ischemic colitis, not triggered by severe cardiovascular disease or operation, may be related to NSAIDs more often than currently recognized.
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PMID:Segmental ischemic colitis associated with nonsteroidal antiinflammatory drugs. 842 Nov 41

Ischemic colitis represents the most common form of gastrointestinal ischemia. The presumed etiologies are numerous; however, it typically develops "spontaneously," in the absence of major vasculature occlusion, and in the presence of viable intestine elsewhere. It is most usefully classified into gangrenous and nongangrenous forms, the latter of which may be subdivided into transient and chronic types. Ischemic colitis may develop in people who are otherwise healthy, although a variety of clinical settings, such as shock, predispose to its occurrence. It usually presents as an acute abdominal illness with bloody diarrhea. Diagnosis is confirmed by colonoscopy. Therapy and outcome are dependent on the severity of disease. Nongangrenous colonic ischemia usually requires only medical management and is associated with a good prognosis. The chronic subtype may lead to the sequelae of persistent segmental colitis or colonic strictures, occasionally requiring surgery. Urgent operative intervention and a high morbidity and mortality are the hallmarks of gangrenous colonic ischemia. Special considerations must be given to those patients in whom ischemic colitis develops in the context of colon carcinoma or obstructing colon lesions, after abdominal aortic surgery, and following cardiopulmonary bypass. This review will discuss the clinical spectrum of ischemic colitis.
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PMID:Ischemic colitis. 860 63

The importance of early microcirculatory changes in the rat colon after exposure to acetic acid was investigated. Administration of 4% acetic acid for 15 sec into an exteriorized colonic segment induced a marked, transient (starting 2 min after the challenge with acetic acid and persisting for 15 min) decrease in the colonic blood flow as estimated by a laser-Doppler flowmeter. Four days after acetic acid administration, a uniform colitis had developed in the exteriorized colonic segment with a total morphological score (TMS) of 15.1 +/- 0.8, myeloperoxidase activity (MPO) increased more than threefold, and plasma exudation into the colonic lumen increased sevenfold. Administration of hydrochloric acid (HCl) with the same pH as the acetic acid or sodium acetate (pH 7.0) did not affect colonic blood flow or produce colitis. Mechanical colonic ischemia, induced by a controlled increase in the intraluminal pressure, resulted in several pathological features of colitis with a TMS of 7.3 +/- 0.2, combined with a significant increase in MPO activity. The TMS and MPO were further increased when mechanical colonic ischemia was combined with HCl or sodium acetate. Pretreatment with SOD and catalase 5 or 15 min before acetic acid administration did not affect the transient ischemia immediately following acetic acid administration. However, it partially prevented the development of colitis. It is concluded that immediate transient ischemia accompanied by the generation of oxygen free radicals might be of importance in the pathogenesis of acetic acid-induced colitis in the rat.
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PMID:The role of transient mucosal ischemia in acetic acid-induced colitis in the rat. 866 Dec 34

Obstructive colitis is an ulcero-inflammatory and necrotizing condition that occurs in the colon proximal to benign or malignant stenosing lesions. it is the result of ischemia due to impairment of blood supply secondary to elevation of the endoluminal pressure, distension of the colonic wall and other factors which impair adequate perfusion. The incidence among patients with colonic obstruction is reported at between 1 and 7%. Of 50 patients with this condition in this series, 30 female and 20 male, 2/3rds were well over 70 yrs of age. Obstruction was most common in the rectosigmoid. In half the patients this was due to adenocarcinoma, 24 were due to benign obstruction and 15 were caused by diverticular disease. Type, extent and depth of ischemic lesions were highly variable and comprised early mucosal hemorrhage and edema, ulcero-hemorrhagic lesions and transmural necrosis. There was always an abrupt transition between affected and normal bowel. A segment of preserved mucosa was usually present on the proximal side of the stenosis. In 16 patients massive dilatation with stretching and thinning of the bowel wall, associated with a blow-out type of perforation or with transmural necrosis, was observed and was considered to have resulted from a rapid rise of endoluminal pressure to high levels. The microscopic and macroscopic features are described in detail and histological factors discussed in relation to the pathological lesions encountered. Emphasis is placed upon the range of appearances and similarities are shared with other inflammatory colonic diseases, particularly idiopathic inflammatory bowel disease. The importance of recognition of this disease entity, not only by pathologists but by surgeons dealing with the disease at operation, is stressed.
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PMID:Obstructive colitis: an analysis of 50 cases and a review of the literature. 877 Nov 49

Since its introduction into clinical medicine, flexible fiberoptic colonoscopy has had a great impact on diagnosis and management of diseases of the colon and rectum. There are three mechanisms responsible for colonoscopic perforation: specifically, mechanical perforation directly from the colonoscope or a biopsy forceps, barotrauma from overzealous air insufflation, and, finally, perforations that occur during therapeutic procedures. Perforation of the colon, which requires surgical intervention more frequently than bleeding, occurs in less than 1 percent of patients undergoing diagnostic colonoscopy and may be seen in up to 3 percent of patients undergoing therapeutic procedures such as polyp removal, dilation of strictures, or laser ablative procedures. Management of colonic perforation secondary to colonoscopy remains a controversial issue in that it can be effectively managed by operative and nonoperative measures. If a perforation does occur, signs and symptoms that the patient will experience will be related to both the size and site of the perforation, adequacy of the bowel preparation, amount of peritoneal soilage, underlying colonic pathology (where a thin walled colon from colitis or ischemia, for example, may result in a larger perforation than a healthy colon), and, finally, overall clinical condition of the patient. Radiology often establishes diagnosis. Plain films of the abdomen and an upright chest x-ray may reveal extravasated air confined to the bowel wall, free intraperitoneal air, retroperitoneal air, subcutaneous emphysema, or even a pneumothorax. A localized perforation may demonstrate lack of pneumoperitoneum. Some surgeons recommend surgery for all colonoscopic perforations; however, there does appear to be a role for conservative management in a select group of patients such as those with silent asymptomatic perforations and those with localized peritonitis without signs of sepsis that continue to improve clinically with conservative management. Finally, conservative management works well in those patients with postpolypectomy coagulation syndrome. Surgery is most definitely indicated in the presence of a large perforation demonstrated either colonoscopically or radiographically and in the setting of generalized peritonitis or ongoing sepsis. The presence of concomitant pathology at time of colonoscopic perforation such as a large sessile polyp likely to be a carcinoma, unremitting colitis, or perforation proximal to a nearly obstructing distal colonic lesion may force immediate surgery. Finally, in the patient who deteriorates with conservative management, one should proceed to surgery.
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PMID:Colonoscopic perforations. Etiology, diagnosis, and management. 891 45


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