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Kayexalate-Induced Esophageal Ulcer in a Patient With Gastroparesis
Image of the Month Kayexalate-Induced Esophageal Ulcer in a Patient With Gastroparesis EMMANUEL C. GOROSPE,* JASON T. LEWIS,‡ and DAVID H. BRUINING* *Division of Gastroenterology and Hepatology and ‡Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, Minnesota
A
53-year-old man presented with an episode of coffee-ground emesis. He had undergone bilateral lung transplantation for idiopathic pulmonary fibrosis 1 month before admission. On presentation, his vital signs were stable (heart rate, 95/min; blood pressure, 106/80 mm Hg), with a hemoglobin of 11.4 g/dL. He was on tacrolimus immunosuppression, with trough levels within the therapeutic range (10–12 ng/mL). His serum potassium level had been elevated (range, 5.5–5.9 mmol/L) for 1 week before admission, for which he was being treated with sodium polystyrene sulfonate in sorbitol (Kayexalate 30 g/d orally). Other pertinent laboratory studies included white blood cell count 3700/L, creatinine 1.1 mg/dL, blood urea nitrogen 28 mg/dL, and sodium 135 mmol/L. On esophagogastroduodenoscopy (EGD), there was a white substance throughout the esophagus that looked like aggregated particulate matter rather than candidal lesions (Figure A). At 35– 40 cm from the incisors, there was a nonbleeding 5 ⫻ 1 cm esophageal ulcer, which was biopsied. Histopathology showed ulcerative esophagitis with basophilic, nonpolarizable, rhomboid-like crystals, consistent with Kayexalate (Figure B). There were no fungal elements. Cytomegalovirus and herpes simplex virus immunohistochemical stains, obtained because of immunocompromised status, were negative. The stomach had retained food that on subsequent EGD did not reveal any additional lesions to account for the patient’s upper gastrointestinal bleeding. Further evaluation with gastric emptying scintigraphy demonstrated severe gastroparesis with 24% emptying (normal, 84%–98%) at 4 hours. Because of these findings, Kayexalate was discontinued, and the patient was initiated on a proton pump inhibitor regimen. He had a follow-up EGD after 3 weeks that showed healing of the esophageal ulcer. The patient was completely asymptomatic at his 2-month follow-up. Esophageal ulceration is a rare complication of Kayexalate usage. Kayexalate, a cation-exchange resin, can be administered orally or as an enema for the treatment of hyperkalemia. It is usually mixed with sorbitol as a laxative to prevent fecal impaction and
constipation. Since Lillemoe et al1 first reported potential gastrointestinal injury in 1987, most of the cases have been in uremic and postoperative patients with intestinal ischemia.2 The usual endoscopic findings are erosions, ulcers, cobblestoning, and aggregation of Kayexalate crystals with mucous secretions. The mechanism of mucosal injury remains unknown, although earlier experiments have implicated the sorbitol component as a potential culprit.1 In the largest series of patients (n ⫽ 11) reported to have Kayexalate-induced upper gastrointestinal injury,2 there were 2 patients with associated findings of retained gastric food contents. However, neither had any confirmed diagnosis of gastroparesis. Gastric outlet obstruction and delayed gastrointestinal transit might predispose patients with prolonged luminal contact time with Kayexalate in sorbitol. This is a case report of Kayexalateinduced esophageal ulcer in a patient with a confirmed diagnosis of gastroparesis. Although Kayexalate-induced gastroesophageal injury is rare, its risks should be considered in patients with bowel dysmotility, uremia, hypotension, and other risk factors for bowel ischemia. References 1. Lillemoe KD, Romolo JL, Hamilton SR, et al. Intestinal necrosis due to sodium polystyrene (Kayexalate) in sorbitol enemas: clinical and experimental support for the hypothesis. Surgery 1987;101:267–272. 2. Abraham SC, Bhagavan BS, Lee LA, et al. Upper gastrointestinal tract injury in patients receiving kayexalate (sodium polystyrene sulfonate) in sorbitol: clinical, endoscopic, and histopathologic findings. Am J Surg Pathol 2001;25:637– 644.
Conflicts of interest The authors disclose no conflicts © 2012 by the AGA Institute 1542-3565/$36.00 doi:10.1016/j.cgh.2011.12.026 CLINICAL GASTROENTEROLOGY AND HEPATOLOGY 2012;10:xxviii
A
53-year-old man presented with an episode of coffee-ground emesis. He had undergone bilateral lung transplantation for idiopathic pulmonary fibrosis 1 month before admission. On presentation, his vital signs were stable (heart rate, 95/min; blood pressure, 106/80 mm Hg), with a hemoglobin of 11.4 g/dL. He was on tacrolimus immunosuppression, with trough levels within the therapeutic range (10–12 ng/mL). His serum potassium level had been elevated (range, 5.5–5.9 mmol/L) for 1 week before admission, for which he was being treated with sodium polystyrene sulfonate in sorbitol (Kayexalate 30 g/d orally). Other pertinent laboratory studies included white blood cell count 3700/L, creatinine 1.1 mg/dL, blood urea nitrogen 28 mg/dL, and sodium 135 mmol/L. On esophagogastroduodenoscopy (EGD), there was a white substance throughout the esophagus that looked like aggregated particulate matter rather than candidal lesions (Figure A). At 35– 40 cm from the incisors, there was a nonbleeding 5 ⫻ 1 cm esophageal ulcer, which was biopsied. Histopathology showed ulcerative esophagitis with basophilic, nonpolarizable, rhomboid-like crystals, consistent with Kayexalate (Figure B). There were no fungal elements. Cytomegalovirus and herpes simplex virus immunohistochemical stains, obtained because of immunocompromised status, were negative. The stomach had retained food that on subsequent EGD did not reveal any additional lesions to account for the patient’s upper gastrointestinal bleeding. Further evaluation with gastric emptying scintigraphy demonstrated severe gastroparesis with 24% emptying (normal, 84%–98%) at 4 hours. Because of these findings, Kayexalate was discontinued, and the patient was initiated on a proton pump inhibitor regimen. He had a follow-up EGD after 3 weeks that showed healing of the esophageal ulcer. The patient was completely asymptomatic at his 2-month follow-up. Esophageal ulceration is a rare complication of Kayexalate usage. Kayexalate, a cation-exchange resin, can be administered orally or as an enema for the treatment of hyperkalemia. It is usually mixed with sorbitol as a laxative to prevent fecal impaction and
constipation. Since Lillemoe et al1 first reported potential gastrointestinal injury in 1987, most of the cases have been in uremic and postoperative patients with intestinal ischemia.2 The usual endoscopic findings are erosions, ulcers, cobblestoning, and aggregation of Kayexalate crystals with mucous secretions. The mechanism of mucosal injury remains unknown, although earlier experiments have implicated the sorbitol component as a potential culprit.1 In the largest series of patients (n ⫽ 11) reported to have Kayexalate-induced upper gastrointestinal injury,2 there were 2 patients with associated findings of retained gastric food contents. However, neither had any confirmed diagnosis of gastroparesis. Gastric outlet obstruction and delayed gastrointestinal transit might predispose patients with prolonged luminal contact time with Kayexalate in sorbitol. This is a case report of Kayexalateinduced esophageal ulcer in a patient with a confirmed diagnosis of gastroparesis. Although Kayexalate-induced gastroesophageal injury is rare, its risks should be considered in patients with bowel dysmotility, uremia, hypotension, and other risk factors for bowel ischemia. References 1. Lillemoe KD, Romolo JL, Hamilton SR, et al. Intestinal necrosis due to sodium polystyrene (Kayexalate) in sorbitol enemas: clinical and experimental support for the hypothesis. Surgery 1987;101:267–272. 2. Abraham SC, Bhagavan BS, Lee LA, et al. Upper gastrointestinal tract injury in patients receiving kayexalate (sodium polystyrene sulfonate) in sorbitol: clinical, endoscopic, and histopathologic findings. Am J Surg Pathol 2001;25:637– 644.
Conflicts of interest The authors disclose no conflicts © 2012 by the AGA Institute 1542-3565/$36.00 doi:10.1016/j.cgh.2011.12.026 CLINICAL GASTROENTEROLOGY AND HEPATOLOGY 2012;10:xxviii