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Pagina 1 a partire dal 203 risultati
Intestinal necrosis following Calcium Resonium-sorbitol administration in a premature uraemic infant.
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Sodium polystyrene sulphonate (Resonium A) in sorbitol given as an enema or orally to treat hyperkalaemia has been described to induce intestinal necrosis in uraemic patients. We report a case of a premature infant with acute renal insufficiency who developed focal transmural necrosis and
The anti-necrosis role of hypoxic preconditioning after acute anoxia is mediated by aldose reductase and sorbitol pathway in PC12 cells.
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It has been demonstrated that hypoxic preconditioning (HP) enhances the survival ability of the organism against the subsequent acute anoxia (AA). However, it is not yet clear whether necrosis induced by AA can be prevented by HP, and what are the underlying mechanisms. In this study, we examined
Colonic necrosis following sodium polystyrene sulfonate (Kayexalate)-sorbitol enema in a renal transplant patient. Report of a case and review of the literature.
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The authors present the case of a patient who developed near total colonic necrosis shortly after renal transplantation. The onset of symptoms was temporally related to the administration of sodium polystyrene (Kayexalate; Sanofi Winthrop Pharmaceuticals, New York, NY)-sorbitol enemas for treatment
Colonic necrosis due to calcium polystyrene sulfonate (Kalimate) not suspended in sorbitol.
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Cation-exchange resins are used in the management of hyperkalemia, particularly in patients with end-stage renal disease. These resins were associated with gastrointestinal tract lesions, especially sodium polystyrene sulfonate (Kayexalate) mixed with sorbitol. We present a case of colonic necrosis
Intestinal Necrosis Associated with Orally Administered Calcium Polystyrene Sulfonate Without Sorbitol.
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OBJECTIVE
To describe a case of extensive intestinal necrosis with oral intake of calcium polystyrene sulfonate without sorbitol.
METHODS
A 73-year-old woman was admitted to the emergency department with abdominal pain. Abdominal computed tomography (CT) scan showed widespread dilatation of the
Colon Necrosis Due to Sodium Polystyrene Sulfonate with and without Sorbitol: An Experimental Study in Rats.
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BACKGROUND
Based on a single rat study by Lillemoe et al, the consensus has been formed to implicate sorbitol rather than sodium polystyrene sulfonate (SPS) as the culprit for colon necrosis in humans treated with SPS and sorbitol. We tested the hypothesis that colon necrosis by sorbitol in the
Intestinal necrosis associated with postoperative orally administered sodium polystyrene sulfonate in sorbitol.
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We estimated the incidence of intestinal necrosis in 752 hospitalized patients who had received sodium polystyrene sulfonate (SPS). Of these 752 patients, 117 were exposed within 1 week of surgery. Two cases of intestinal necrosis were discovered, both in patients who had received orally
Intestinal necrosis related to administration of cation exchange resin without sorbitol: A retrospective analysis of 61 patients with end-stage renal diseases.
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Intestinal necrosis associated with cation exchange resin (CER) is considered related to sorbitol, but it has been reported even in patients receiving CER alone. This study was performed to identify the risk factors of CER-related intestinal necrosis. The pathological database of 61 end-stage renal
Kayexalate (sodium polystyrene sulphonate) in sorbitol associated with intestinal necrosis in uremic patients.
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BACKGROUND
Kayexalate (sodium polystyrene sulphonate) in sorbitol is commonly used to treat hyperkalemia in patients with renal insufficiency. Isolated case reports and one recent large series have documented intestinal necrosis following administration of kayexalate in sorbitol.
METHODS
Two
Intestinal necrosis due to sodium polystyrene (Kayexalate) in sorbitol enemas: clinical and experimental support for the hypothesis.
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Five patients who suffered catastrophic colonic necrosis are presented. All patients were uremic and received sodium polystyrene (Kayexalate) in sorbitol enemas for the treatment of hyperkalemia shortly before the development of signs and symptoms of colonic necrosis. In all specimens extensive
Association of prescription of oral sodium polystyrene sulfonate with sorbitol in an inpatient setting with colonic necrosis: a retrospective cohort study.
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BACKGROUND
Colonic necrosis has been reported after sodium polystyrene sulfonate (SPS)/sorbitol use, but the incidence and relative risk (RR) are not established.
METHODS
Retrospective cohort study.
METHODS
123,391 adult inpatients at a tertiary medical center.
METHODS
Receipt of SPS prescriptions
Acute abdomen with colonic necrosis induced by Kayexalate-sorbitol.
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Colonic necrosis is an unusual complication after treatment of hyperkalemia with sodium polystyrene sulfonate (SPS, Kayexalate) in sorbitol. To increase awareness of this complication, we report a case of necrosis of the transverse colon in a patient given oral and rectal SPS-sorbitol for
Necrosis of the gastrointestinal tract in uremic patients as a result of sodium polystyrene sulfonate (Kayexalate) in sorbitol: an underrecognized condition.
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Sodium polystyrene sulfonate (Kayexalate) in sorbitol given as an enema or orally to treat hyperkalemia has been reported to induce intestinal necrosis in uremic patients. We studied the clinical and pathologic features of 15 patients in whom Kayexalate crystals were observed in specimens from
Intestinal necrosis due to sodium polystyrene sulfonate (Kayexalate) in sorbitol.
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BACKGROUND
Sodium polystyrene sulfonate (SPS, Kayexalate) has been implicated in the development of intestinal necrosis. Sorbitol, added as a cathartic agent, may be primarily responsible. Previous studies have documented bowel necrosis primarily in postoperative, dialysis, and transplant patients.
Colonic necrosis in a young patient receiving oral kayexalate in sorbitol: case report and literature review.
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Kayexalate (sodium polystyrene sulfonate) is a cation-exchange resin used to treat patients with hyperkalemia. Concomitant administration of kayexalate and sorbitol may induce gastrointestinal injury, which is potentially lethal. However, this well-documented complication is often underrecognized
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