Dig Dis Sci (2014) 59:1375–1377 DOI 10.1007/s10620-014-3251-y
UNM CLINICAL CASE CONFERENCES
An Unusual Cause of Recurrent Right Lower Quadrant Pain Sarita Gayle • Martin Kistin • Joshua Hanson
Published online: 13 June 2014 Springer Science+Business Media New York 2014
Case Presentation A 61-year-old female was hospitalized for a 3-day history of right lower quadrant abdominal pain, described as sharp, non-radiating, worse with movement and associated with nausea and non-bilious, non-bloody vomiting. She also reported a history of right groin pain of 1–2 days duration. She denied diarrhea, constipation, melena, hematochezia, weight change, fevers, or chills. Past medical history included hyperlipidemia, hypothyroidism, and end-stage renal disease due to hypertension and diabetes requiring hemodialysis. Previous surgical operations included an open cholecystectomy and placement of a left upper extremity arteriovenous fistula. Outpatient medications included pioglitazone, metoprolol, amlodipine, furosemide levothyroxine, simvastatin, calcium acetate, aspirin, and occasional use of oral sodium polystyrene sulfonate potassium-binding resin (Kayexalate). She denied use of tobacco, alcohol or recreational drugs. She had no family history of abdominal malignancy or inflammatory bowel disease. Physical examination revealed an afebrile, normotensive, and mildly hypoxic woman (oxygen saturation of 92 %). A systolic murmur was auscultated at the left sternal border; S. Gayle M. Kistin Division of Gastroenterology and Hepatology, Department of Medicine, University of New Mexico School of Medicine, Albuquerque, NM, USA S. Gayle (&) Department of Gastroenterology and Hepatology, 1 University of New Mexico, MSC10-5550, Albuquerque, NM 87131, USA e-mail:
[email protected] J. Hanson Department of Pathology, University of New Mexico School of Medicine, Albuquerque, NM, USA
moderate tenderness to direct palpation was noted in the right lower quadrant and inguinal regions without any rebound or guarding. Complete blood count and liver function tests were normal. Basic metabolic panel: serum sodium 138 mmol/L, potassium 3.9 mmol/L, chloride 94 mmol/L, bicarbonate 31 mmol/L, blood urea nitrogen 20 mg/dL, and creatinine 4.9 mg/dL. Serum calcium, magnesium, and phosphorus were all within normal limits. Due to concern for the presence of an incarcerated hernia, the patient underwent abdominal and pelvic computerized tomographic (CT) scan, which was reported as showing wall thickening of the distal ileum and ascending colon, with pericolic stranding with fat adjacent to the ascending colon, the appendix appearing normal. Bilateral, fat-containing inguinal hernias were also noted. Over the next few days, the patient continued to have abdominal pain, but with improvement in its severity and frequency. Repeat laboratory studies showed elevated white blood cell count of 11.8 9 103, elevated erythrocyte sedimentation rate 46 mm/h, and C-reactive protein 0.6 mg/dL (nl \ 0.3). Stool culture, examination for C. difficile toxin, and fecal leukocytes were negative. During admission, the patient underwent colonoscopy that showed the presence of a 1.5-cm-deep, firm ulcer just distal to the ileocecal valve, with no loss of vascularity of the surrounding mucosa. Biopsies revealed only ulcerated colonic mucosa with architectural distortion. Radiographic follow-through examination of the small bowel was unremarkable. Her symptoms improved, and she was discharged home. An outpatient colonoscopy 1 month later again showed the right colonic ulcer, with grossly normal surrounding mucosa. Biopsies of the terminal ileum and of the ulcer were negative for any specific or definitive findings. Doppler studies of the abdominal vasculature were normal. Given her history of end-stage renal disease,
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Dig Dis Sci (2014) 59:1375–1377
Fig. 1 Segmental necrosis and ulceration of the ascending colon
Fig. 2 Low-power examination demonstrates mucosal ischemic change in the form of hyalinization of the lamina propria and reactive crypts, with a paucity of active cryptitis. This pattern of injury is typical of Kayexalate-induced colitis. The overlying ulcer (bottom of image) harbors the Kayexalate crystals
hypertension and diabetes, the patient was thought to have localized ischemic colitis of the ascending colon. A few weeks later, the patient was re-admitted with severe right lower quadrant pain. Repeat CT imaging of the abdomen and pelvis showed mildly increased thickening of
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Fig. 3 The Kayexalate crystals are identified by their characteristic basophilic appearance with a mosaic pattern resembling fish scales
the colonic wall and obvious inflammation of the ascending colon. Colonoscopy revealed the preexisting ulcer to be smaller; however, a new area of circumferential ulceration spanning 3 cm was observed in the proximal ascending colon (Fig. 1). Mild acute colitis with focal cryptitis, and ischemic-appearing ulceration with associated striated basophilic crystals were reported histologically (Figs. 2, 3).
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It was concluded that the patient likely had necrotic colonic ulceration due to oral Kayexalate-sorbitol treatment, which had been previously administered the patient to control hyperkalemia.
Discussion Kayexalate is a cation exchange resin used orally or as an enema for the treatment of hyperkalemia. In the lumen of the gastrointestinal tract, the sodium ions of the compound are exchanged for potassium ions, with subsequent increased potassium loss in the stool, which consequently increases potassium secretion by the gut, lowering serum potassium. Since Kayexalate also binds calcium ions in the intestine, constipation or even fecal impaction may occur. To avoid these unwelcome adverse effects, Kayexalate is often administered with the osmotic laxative hypertonic sorbitol [1]. Colonic or ileocolonic necrosis is a rare complication, occurring in up to 1 % of patients receiving Kayexalatesorbitol therapy [2]. The exact mechanism of the ensuing mucosal damage is unclear. In 1987, Lillimoe et al. [3] reported colonic necrosis in five uremic patients thought due to the sorbitol suspension rather than the Kayexalate. In non-uremic rats, transmural necrosis was noted in seven of ten rats receiving sorbitol enemas and in six of ten rats receiving Kayexalate in sorbitol enemas. In uremic rats, extensive transmural necrosis was reported in all rats receiving sorbitol or Kayexalate-sorbitol enemas. Nevertheless, a recent review reported that patients using sodium polystyrene sulfonate in the absence of sorbitol also experienced similar gastrointestinal adverse events [4]. Kayexalate in sorbitol is thought to injure the colonic mucosa by altering the mucosal microcirculation and by the release of prostaglandins [5]. Angiotensin-mediated mesenteric vasoconstriction due to hyperreninemia, hypotension, and uremia may also contribute to ischemic injury [5, 6]. Sorbitol is soluble and thus is invisible histologically, though Kayexalate crystals are visible, serving as a marker of prior Kayexalate administration. Patients typically report abdominal pain, nausea, diarrhea or hematochezia. Endoscopic and pathologic findings include mucosal edema, ulceration, pseudomembrane formation, and transmural necrosis. Diagnosis, made within hours to several days after Kayexalate administration, is reliant on the finding of typical basophilic angulated striated crystals of Kayexalate in ischemic-appearing ulcerations. The differential diagnosis of segmental colitis includes inflammatory bowel disease, ischemia, infections,
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diverticulitis, and radiation [7]. Numerous drugs and other medications have also been implicated in causing severe colitis indistinguishable from IBD or ischemic colitis [8, 9]. In this patient, the pattern of symptoms recurring at home and resolving in the hospital suggested that an outpatient treatment or environmental factor was causative. The identity of this problem was confirmed by histologic examination of the colonic biopsies. Physicians should be aware of the rare but lethal side effects of Kayexalate use. The use of Kayexalate in the treatment of acute or chronic hyperkalemia should be reserved to severe cases, where other methods of lowering serum potassium were already tried and unsuccessful.
Key Points • • •
Numerous drugs and medications should be part of the differential diagnosis of severe colitis. Kayexalate use is associated with a rare but lethal complication of intestinal necrosis. Physicians should limit the use of Kayexalate in the treatment of hyperkalemia and look for other agents when possible.
References 1. Chou YH, Wang HY, Hsieh MS. Colonic necrosis in a young patient receiving oral kayexalate in sorbitol: case report and literature review. Kaohsiung J of Med Sci. 2011;27:155–158. 2. Gardiner GW. Kayexalate (sodium polystyrene sulphonate) in sorbitol associated with intestinal necrosis in uremic patients. Can J Gastroenterol. 1997;11:573–577. 3. Lillimoe KD, Romolo JL, Hamilton SR, Pennington LR, et al. Intestinal necrosis due to sodium polystyrene (Kayexalate) in sorbitol enemas: clinical and experimental support for the hypothesis. Surgery. 1987;101:266–272. 4. Harel Z, Harel S, Shah PS, et al. Gastrointestinal adverse events with sodium polystyrene sulfonate (kayexalate) use: a systematic review. Am J Med. 2013;126:264. 5. Thomas A, James BR, Landsberg D. Colonic necrosis due to oral kayexalate in a critically ill patient. Am J Med Sci. 2009;337:305–306. 6. Abraham SC, Bhagavan BS, Lee LA, Rashid A, et al. Upper gastrointestinal tract injury in patients receiving kayexalate in sorbitol. Am J of Surg Pathol. 2001;25:637–644. 7. Eng SC, Surawicz CM. Differential diagnosis of colitis. In: Targan S, Shanahan F, Karp LC, eds. Inflammatory Bowel Disease: From Bench to bedside (Chapter 21). 2nd ed. London: Kluwer Academic Publishers; 2003:431–455. 8. Cappell MS. Colonic toxicity of administered drugs and chemicals. Am J Gastroenterol. 2004;99:1175–11909. 9. Linder JD, Monkemuller KE, Raijman I, et al. Cocaine-associated ischemic colitis. South Med J. 2000;93:909–913.
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