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SODIUM POLYSTYRENE SULFONATE

Classification   |    Detailed evidence-based information

Therapeutic Toxic Class

    A) Sodium polystyrene sulfonate (SPS) is a cation-exchange resin that reduces serum potassium when administered either as an enema, orally or by nasogastric tube.

Specific Substances

    1) AEP 1
    2) Flexan 500
    3) Oligo Z
    4) Poly(styrenesulfonate) sodium salt
    5) Versa TL 400
    6) Versa TL 500
    7) Versa TL 71
    8) Kayexalate
    9) Poly(sodium 4-styrenesulfonate)
    10) Poly(sodium p-styrenesulfonate)
    11) Molecular Formula: (C8-H8-O3-S)x.xNa
    12) CAS 9003-59-2
    13) CAS 9080-79-9
    14) CAS 25704-18-1

Available Forms Sources

    A) FORMS
    1) Sodium polystyrene sulfonate (Kayexalate) is available as a cream to light brown, finely ground powder in jars of 1 pound (453.6 g) (Prod Info KAYEXALATE(R) oral powder for suspension rectal powder for suspension, 2010).
    a) One gram of Kayexalate contains 4.1 mEq of sodium; one level teaspoon contains approximately 3.5 g of Kayexalate and 15 mEq of sodium (a heaping teaspoon may contain as much as 10 g to 12 g of Kayexalate (Prod Info KAYEXALATE(R) oral powder for suspension rectal powder for suspension, 2010).
    B) USES
    1) Sodium polystyrene sulfonate is used to enhance potassium excretion in the treatment of hyperkalemia (Prod Info KAYEXALATE(R) oral powder for suspension rectal powder for suspension, 2010).

Life Support

    A) This overview assumes that basic life support measures have been instituted.

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) USES: Sodium polystyrene sulfonate is used to enhance potassium excretion in the treatment of hyperkalemia.
    B) TOXICOLOGY: The resin passes along the intestine or can be retained in the colon after administration by enema, the sodium ions are partially released and are replaced by potassium ions. Electrolyte imbalances including hypocalcemia, hypokalemia, hypomagnesia and significant sodium retention may occur during therapy with sodium polystyrene sulfonate.
    C) EPIDEMIOLOGY: Sodium polystyrene sulfonate is commonly prescribed for the treatment of hyperkalemia.
    D) WITH THERAPEUTIC USE
    1) ADVERSE EFFECTS: Nausea, vomiting, colonic necrosis, anorexia, diarrhea, constipation, hypokalemia, hypocalcemia, hypomagnesemia, and sodium retention may occur. Intestinal obstruction from aluminum hydroxide concretions has occurred when administered in combination with sodium polystyrene sulfonate. GI necrosis has been documented in both the upper and lower GI tract, and the presence of sorbitol, along with sodium polystyrene sulfonate, may be an important factor in inducing necrosis. Weight gain, hypertension, hypernatremia, and worsening of left ventricular failure with congestive heart failure were reported in 2 patients with renal failure and congestive heart failure, following excessive sodium overload secondary to sodium polystyrene sulfonate therapy.
    E) WITH POISONING/EXPOSURE
    1) OVERDOSE: Sodium polystyrene sulfonate generally has minimal toxicity since it is a cation exchanger and is not absorbed. Medically significant hypokalemia is possible.
    2) MILD TO MODERATE TOXICITY: Sodium polystyrene sulfonate aspiration has been reported in several patients; acute bronchitis and bronchopneumonia were reported in patients who had taken the resin by mouth.

Laboratory Monitoring

    A) Monitor serum electrolytes, particularly sodium and potassium levels, and ECG following a significant ingestion.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) MANAGEMENT OF MILD TO MODERATE TOXICITY
    1) Treat is symptomatic and supportive. Replace potassium as needed.
    B) MANAGEMENT OF SEVERE TOXICITY
    1) Patients with severe abdominal pain, or suspected gut obstruction or GI necrosis (colonic necrosis is a rare finding associated with SPS and the concomitant use of sorbitol; not SPS alone) may require surgical consultation and/or radiology imaging. Supportive treatment may be indicated for congestive heart failure. Replace potassium as needed. If rapid potassium replacement (more than 10 mEq/h in adults) is needed, monitor ECG, urine output, and serial potassium levels closely.
    C) DECONTAMINATION
    1) PREHOSPITAL or HOSPITAL: Gastrointestinal decontamination is generally not indicated as sodium polystyrene sulfonate is not systemically absorbed.
    D) AIRWAY MANAGEMENT
    1) In cases with aspiration or congestive heart failure administer 100% humidified supplemental oxygen, perform endotracheal intubation and provide assisted ventilation as required. Administer inhaled beta 2 adrenergic agonists and/or systemic steroids, if bronchospasm develops.
    E) ANTIDOTE
    1) None.
    F) ENHANCED ELIMINATION
    1) Enhanced elimination is unlikely to be necessary.
    G) PATIENT DISPOSITION
    1) OBSERVATION CRITERIA: Mild symptomatic patients or patients with a known large exposure should be observed for at least 6 hours for signs of toxicity.
    2) ADMISSION CRITERIA: Patients with significant symptoms should be admitted for treatment and monitoring. ECG monitoring is indicated in patients with severe hypokalemia or patients that have received rapid potassium replacement. Patients with respiratory failure should be admitted to an ICU setting.
    3) CONSULT CRITERIA: Contact your local poison center for a toxicology consult for any patient with severe toxicity. Patients with severe abdominal pain, suspected intestinal tract obstruction or GI necrosis may require surgical consultation and/or radiological imaging.
    H) PITFALLS
    1) Failure to recognize aspiration, gut obstruction, or GI necrosis. Inappropriate replacement of potassium (ie, excessive, inadequate or too rapid of replacement).
    I) PHARMACOKINETICS
    1) The resin is excreted from the intestinal tract by the fecal route.
    J) DIFFERENTIAL DIAGNOSIS
    1) Barium toxicity, gut obstruction, mild acute caustic ingestion, congestive heart failure.

Range Of Toxicity

    A) TOXICITY: A minimum toxic dose has not been established. Sodium polystyrene sulfonate (SPS) generally has minimal toxicity since it is a cation exchanger and is not absorbed. On average 1 mEq potassium is adsorbed for each gram of SPS administered, although the rate of potassium adsorption varies. THERAPEUTIC DOSE: ADULT: ORAL: Usual dose is 15 to 60 g, which is usually provided by administering 15 g, 1 to 4 times daily. CHILD: 0.5 to 1 g/kg/dose given every 6 hours orally or every 4 to 6 hours rectally; based on the exchange ratio of about 1 g of resin per mEq of excess serum potassium.

Summary Of Exposure

    A) USES: Sodium polystyrene sulfonate is used to enhance potassium excretion in the treatment of hyperkalemia.
    B) TOXICOLOGY: The resin passes along the intestine or can be retained in the colon after administration by enema, the sodium ions are partially released and are replaced by potassium ions. Electrolyte imbalances including hypocalcemia, hypokalemia, hypomagnesia and significant sodium retention may occur during therapy with sodium polystyrene sulfonate.
    C) EPIDEMIOLOGY: Sodium polystyrene sulfonate is commonly prescribed for the treatment of hyperkalemia.
    D) WITH THERAPEUTIC USE
    1) ADVERSE EFFECTS: Nausea, vomiting, colonic necrosis, anorexia, diarrhea, constipation, hypokalemia, hypocalcemia, hypomagnesemia, and sodium retention may occur. Intestinal obstruction from aluminum hydroxide concretions has occurred when administered in combination with sodium polystyrene sulfonate. GI necrosis has been documented in both the upper and lower GI tract, and the presence of sorbitol, along with sodium polystyrene sulfonate, may be an important factor in inducing necrosis. Weight gain, hypertension, hypernatremia, and worsening of left ventricular failure with congestive heart failure were reported in 2 patients with renal failure and congestive heart failure, following excessive sodium overload secondary to sodium polystyrene sulfonate therapy.
    E) WITH POISONING/EXPOSURE
    1) OVERDOSE: Sodium polystyrene sulfonate generally has minimal toxicity since it is a cation exchanger and is not absorbed. Medically significant hypokalemia is possible.
    2) MILD TO MODERATE TOXICITY: Sodium polystyrene sulfonate aspiration has been reported in several patients; acute bronchitis and bronchopneumonia were reported in patients who had taken the resin by mouth.

Cardiovascular

    3.5.2) CLINICAL EFFECTS
    A) CONGESTIVE HEART FAILURE
    1) WITH THERAPEUTIC USE
    a) SUMMARY: Because of significant sodium retention, especially in patients with impaired renal function, severe congestive heart failure and severe edema may occur (Prod Info sodium polystyrene sulfonate oral suspension, rectal suspension, 2012).
    b) One report describes 2 renal failure patients with left ventricular failure, and one with associated right-sided failure, following excessive sodium overload secondary to sodium polystyrene sulfonate therapy. Total sodium load was estimated to be 590 to 1000 mEq over a 4 to 10 day period and resulted in weight gain, hypertension, hypernatremia, and worsening of left ventricular failure with congestive heart failure. In the case of a 19-year-old man, the sequelae were severe enough to contribute to the patient's death (Berlyne et al, 1966).
    B) HYPERTENSIVE EPISODE
    1) WITH THERAPEUTIC USE
    a) SUMMARY: Because of significant sodium retention, severe hypertension may occur in patients at risk (Prod Info sodium polystyrene sulfonate oral suspension, rectal suspension, 2012).
    b) CASE REPORT: A 25-year-old woman with chronic glomerulonephritis and pyelonephritis developed gross peripheral edema and an increase in blood pressure to 190/130 mmHg from a baseline of 110/70 mmHg within 2 weeks of resin therapy. The patient experienced severe headaches and hypertensive encephalopathy with the elevated blood pressure (Berlyne et al, 1966).

Respiratory

    3.6.2) CLINICAL EFFECTS
    A) SUFFOCATING
    1) WITH POISONING/EXPOSURE
    a) Two cases of sodium polystyrene sulfonate aspiration were reported, occurring in a 3-day-old neonate and a 4-year-old girl. Both patients had been administered sodium polystyrene sulfonate for hyperkalemia. The crystalline, plate-like particles in the alveoli showed a characteristic basophilic polygonal pattern without associated inflammation of the tissues. Fourier transform infrared microspectrophotometry confirmed the identity of the foreign-body material as sodium polystyrene sulfonate (Fenton et al, 1996).
    b) Acute bronchitis and bronchopneumonia were reported in 3 patients who had taken the resin by mouth. At autopsy, particles of sodium polystyrene sulfonate were found in the lungs. Aspiration was not observed as a direct cause of death in these cases (Haupt & Hutchins, 1982).
    B) ACUTE LUNG INJURY
    1) WITH THERAPEUTIC USE
    a) CASE REPORT: An elderly, debilitated woman, with a history of COPD and heart disease, developed acute respiratory distress syndrome following the aspiration of a single dose (30 g) of sodium polystyrene sulfonate. Shortly after this episode, the patient had a sudden onset of hypoxemia and cardiac arrest followed. Cardiopulmonary resuscitation efforts were successful. There was also radiographic evidence of new pulmonary infiltrates and polystyrene sulfonate crystals in the alveoli. Despite supportive respiratory measures, the patient continued to be hypoxic (ie, oxygen saturation remained at 80 to 85%) and symptoms progressed to multiorgan failure and refractory shock. At this time, a decision was made to provide supportive care only with no further resuscitation efforts; the patient died a short time later (Duggal et al, 2014).

Neurologic

    3.7.2) CLINICAL EFFECTS
    A) CENTRAL NERVOUS SYSTEM FINDING
    1) WITH THERAPEUTIC USE
    a) CASE REPORT: A 25-year-old woman with chronic glomerulonephritis and pyelonephritis developed gross peripheral edema and an increase in blood pressure to 190/130 mmHg from a baseline of 110/70 mmHg within 2 weeks of resin therapy. The patient experienced severe headaches and hypertensive encephalopathy with the elevated blood pressure (Berlyne et al, 1966).
    b) RARE: Grand mal seizure has been reported in a patient with chronic hypocalcemia of renal failure given sodium polystyrene sulfonate with magnesium hydroxide (Prod Info sodium polystyrene sulfonate oral suspension, rectal suspension, 2012).

Gastrointestinal

    3.8.2) CLINICAL EFFECTS
    A) NAUSEA AND VOMITING
    1) WITH THERAPEUTIC USE
    a) Nausea and vomiting may occur with therapeutic use (Prod Info sodium polystyrene sulfonate oral suspension, rectal suspension, 2012).
    B) CONSTIPATION
    1) WITH THERAPEUTIC USE
    a) Constipation (Prod Info sodium polystyrene sulfonate oral suspension, rectal suspension, 2012) and fecal impaction are not uncommon, and may be minimized by use of a laxative (Scherr et al, 1961).
    C) DIARRHEA
    1) WITH THERAPEUTIC USE
    a) Diarrhea may occur occasionally during treatment with sodium polystyrene sulfonate (Prod Info sodium polystyrene sulfonate oral suspension, rectal suspension, 2012).
    D) NECROSIS
    1) WITH THERAPEUTIC USE
    a) Necrosis of the gastrointestinal tract caused by sodium polystyrene sulfonate in sorbitol is well documented in uremic patients (Daram et al, 2012; Rogers & Li, 2001; Dardik et al, 2000; Scott et al, 1993) (Gerstman et al, 1992) (Wootton, 1989) (Lillemoe et al, 1987). In some cases, this effect can lead to death, and is thought to be under recognized and under reported (Rashid & Hamilton, 1997). Necrosis has been documented in both the upper and lower GI tract, and the presence of sorbitol, along with sodium polystyrene sulfonate, is apparently an important factor in inducing necrosis (Rashid & Hamilton, 1997).
    b) UPPER GI NECROSIS
    1) CASE REPORT: A 59-year-old woman with end-stage renal disease on chronic hemodialysis and receiving Kayexalate(R) oral suspension presented with coffee-ground emesis. Endoscopy revealed that the mucosa of the gastric body was ulcerated with oozing of fresh blood. Acid-fast staining revealed dark purple crystals consistent with Kayexalate(R) crystals. Long-term opiates in this case may have contributed (ie, a decrease in gastric motility) to an increase in mucosal contact time with Kayexalate(R) (Daram et al, 2012).
    2) MIXED NECROSIS: Roy-Chaudhury et al (1997) reported combined gastric and ileocecal toxicity (serpiginous ulcers) following the oral use of sodium polystyrene sulfonate in sorbitol. The authors suggested that sorbitol rather than Kayexalate is toxic to bowel mucosa, causing colonic necrosis.
    c) COLONIC NECROSIS
    1) COLONIC NECROSIS was described in 5 uremic patients who received sodium polystyrene sulfonate (Kayexalate(R)) in sorbitol enemas, with 4 of these patients eventually dying. Extensive ischemic necrosis was present in all specimens as well as Kayexalate(R) crystals in the intestinal lumen (Lillemoe et al, 1987).
    2) CASE REPORT: A case of colonic necrosis associated with the administration of Kayexalate(R) and sorbitol enemas in a 48-year-old white man with end-stage renal disease, secondary to rapidly progressive glomerulonephritis, has been reported. The patient had been given a Kayexalate(R) enema (50 mg in 200 mL 20% sorbitol) upon admission to the hospital to lower his serum potassium (6.1 mmol/L) prior to kidney transplant surgery. The procedure was uneventful, however, the serum potassium had remained elevated at 6.7 mmol/L necessitating the administration of 3 additional resin enemas. Complications led to the removal of a 58 cm of colon. After a difficult hospital course, the patient was eventually discharged (Wootton et al, 1989). A similar case was reported by other authors (Scott et al, 1993).
    3) In one case report, the colonic necrosis extended down to the anal verge, a richly vascularized area of the colon usually not prone to ischemia (Rogers & Li, 2001).
    E) INTESTINAL OBSTRUCTION
    1) WITH THERAPEUTIC USE
    a) CASE REPORT: A 54-year-old man was successfully resuscitated following a history of constrictive effusive metastatic pericarditis secondary to lung cancer, but developed acute renal failure. Hyperkalemia was treated with insulin, beta agonists, and 30 g of sodium polystyrene sulfonate (sorbitol free) 3 to 4 times daily for 10 days via a nasogastric tube. Hemodialysis was considered but it was determined that the patient was too hemodynamically unstable. On day 12, the patient died. Upon postmortem examination, a huge nonobstructive bezoar was found in the stomach (ie, the stomach was dilated but not damaged) and diagnosed as a sodium polystyrene sodium bezoar. Although the exact mechanism remained unknown, decreased gastric mobility secondary to mesenteric ischemia, reduced gastric secretions leading to crystallization, high dose of therapy, and redissolution of sodium polystyrene solution were suggested as possible causes of upper gastrointestinal injury in a critically ill patient (Croitoru et al, 2015).
    b) CASE REPORT: Intestinal obstruction due to a medication bezoar has been reported in a 27-year-old woman receiving a total of 200 g of sodium polystyrene resin and 30 to 60 mL of aluminum hydroxide suspension every hour for 5 days. Surgical removal of the solid concretion in the small bowel was required in the management of this patient (Townsend et al, 1973).
    F) LOSS OF APPETITE
    1) WITH THERAPEUTIC USE
    a) Anorexia may occur with therapeutic use (Prod Info sodium polystyrene sulfonate oral suspension, rectal suspension, 2012).

Acid-Base

    3.11.2) CLINICAL EFFECTS
    A) ALKALOSIS
    1) WITH THERAPEUTIC USE
    a) CASE REPORT: A 49-year-old man with chronic glomerulonephritis became severely alkalotic after the administration of magnesium hydroxide and sodium polystyrene sulfonate combination therapy. While on magnesium hydroxide alone, the patient's acid-base balance was stable, but 1 day following initiation of resin therapy, the CO2 content rose greater than 40 mEq/L. Magnesium hydroxide was discontinued and serum CO2 content values returned to near baseline. It was suggested that the metabolic disturbance was due to magnesium binding to the resin resulting in excess sodium bicarbonate being reabsorbed, thus leading to metabolic alkalosis (Zeissman, 1976).

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) Monitor serum electrolytes, particularly sodium and potassium levels, and ECG following a significant ingestion.

Life Support

    A) Support respiratory and cardiovascular function.

Patient Disposition

    6.3.1) DISPOSITION/ORAL EXPOSURE
    6.3.1.1) ADMISSION CRITERIA/ORAL
    A) Patients with significant symptoms should be admitted for treatment and monitoring. ECG monitoring is indicated in patients with severe hypokalemia or patients that have received rapid potassium replacement. Patients with respiratory failure should be admitted to an ICU setting.
    6.3.1.3) CONSULT CRITERIA/ORAL
    A) Contact your local poison center for a toxicology consult for any patient with severe toxicity. Patients with severe abdominal pain, suspected intestinal tract obstruction or GI necrosis may require surgical consultation and/or radiology imaging.
    6.3.1.5) OBSERVATION CRITERIA/ORAL
    A) Mild symptomatic patients or patients with a known large exposure should be observed for at least 6 hours for signs of toxicity.

Monitoring

    A) Monitor serum electrolytes, particularly sodium and potassium levels, and ECG following a significant ingestion.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) SUMMARY
    1) Prehospital gastrointestinal decontamination is generally not indicated as sodium polystyrene sulfonate (SPS) is not systemically absorbed.
    6.5.2) PREVENTION OF ABSORPTION
    A) SUMMARY
    1) Gastrointestinal decontamination is generally not indicated as sodium polystyrene sulfonate is not systemically absorbed.
    6.5.3) TREATMENT
    A) SUPPORT
    1) MANAGEMENT OF MILD TO MODERATE TOXICITY
    a) Treat is symptomatic and supportive. Replace potassium as needed.
    2) MANAGEMENT OF SEVERE TOXICITY
    a) Patients with severe abdominal pain, or suspected gut obstruction or GI necrosis (colonic necrosis is a rare finding associated with SPS and the concomitant use of sorbitol; not SPS alone (Watson et al, 2012)) may require surgical consultation and/or radiology imaging. Supportive treatment may be indicated for congestive heart failure. Replace potassium as needed. If rapid potassium replacement (more than 10 mEq/h in adults) is needed, monitor ECG, urine output, and serial potassium levels closely.
    B) MONITORING OF PATIENT
    1) Monitor fluid status and serum electrolytes, particularly sodium and potassium levels following a significant ingestion. Monitor ECG in patients with hypokalemia.

Enhanced Elimination

    A) SUMMARY
    1) DIALYSIS and forced diuresis are NOT of use to remove the toxin.

Summary

    A) TOXICITY: A minimum toxic dose has not been established. Sodium polystyrene sulfonate (SPS) generally has minimal toxicity since it is a cation exchanger and is not absorbed. On average 1 mEq potassium is adsorbed for each gram of SPS administered, although the rate of potassium adsorption varies. THERAPEUTIC DOSE: ADULT: ORAL: Usual dose is 15 to 60 g, which is usually provided by administering 15 g, 1 to 4 times daily. CHILD: 0.5 to 1 g/kg/dose given every 6 hours orally or every 4 to 6 hours rectally; based on the exchange ratio of about 1 g of resin per mEq of excess serum potassium.

Therapeutic Dose

    7.2.1) ADULT
    A) ORAL: The recommended dose is 15 to 60 g 1 to 4 times daily (Prod Info sodium polystyrene sulfonate oral suspension, rectal suspension, 2012).
    B) ORAL SUSPENSION (powdered formula): Each dose should be given as a suspension in water; the amount of fluid usually ranges from 20 to 100 mL, depending on the dose, or 3 to 4 mL/gram resin (Prod Info KAYEXALATE(R) oral powder for suspension rectal powder for suspension, 2010).
    C) ENEMA: The recommended dose is 30 to 50 g (120 to 200 mL) rectally every 6 hours (Prod Info sodium polystyrene sulfonate oral suspension, rectal suspension, 2012; Prod Info KAYEXALATE(R) oral powder for suspension rectal powder for suspension, 2010).
    7.2.2) PEDIATRIC
    A) The effectiveness of sodium polystyrene sulfonate in pediatric patients has not been established. Its use is contraindicated in neonates and especially in premature infants. If given the child should be closely monitored to avoid excessive dosage that could result in impaction of the resin (Prod Info sodium polystyrene sulfonate oral suspension, rectal suspension, 2012).
    B) In smaller children and infants, lower doses are suggested using as a guide a rate of 1 mEq of potassium per gram of resin to calculate the dose (Prod Info KAYEXALATE(R) oral powder for suspension rectal powder for suspension, 2010).

Toxicity Information

    7.7.1) TOXICITY VALUES
    A) ANIMAL DATA
    1) LD50- (INTRAPERITONEAL)MOUSE:
    a) >6750 mg/kg (RTECS, 2002)
    2) LD50- (ORAL)MOUSE:
    a) >10 g/kg (RTECS, 2002)
    3) LD50- (SUBCUTANEOUS)MOUSE:
    a) >15 g/kg (RTECS, 2002)
    4) LD50- (INTRAPERITONEAL)RAT:
    a) >6 g/kg (RTECS, 2002)
    5) LD50- (ORAL)RAT:
    a) >8 g/kg (RTECS, 2002)
    6) LD50- (SUBCUTANEOUS)RAT:
    a) >15 g/kg (RTECS, 2002)

Pharmacologic Mechanism

    A) The resin passes along the intestine or can be retained in the colon after administration by enema, the sodium ions are partially released and are replaced by potassium ions. In general, this action occurs in the large intestine, which excretes potassium ions to a greater degree than does the small intestine. This process can be limited and unpredictable. It usually approximates the order of 33%, but the range is so large that electrolyte balance (eg, potassium, magnesium and calcium) must be frequently monitored (Prod Info KAYEXALATE(R) oral powder for suspension rectal powder for suspension, 2010).

Physical Characteristics

    A) A light brown to brown (golden brown), fine, odorless powder, containing not more than 10% of water (S Sweetman , 2002; Prod Info Kayexalate(R), sodium polystyrene sulfonate, 2001).

Molecular Weight

    A) Varies

General Bibliography

    1) Angelo-Nielsen K & Ringsted C: Resonium A-induced hypocalcaemic tetany. Dan Med Bull 1983; 30:348-349.
    2) Berlyne GM, Janabi K, & Shaw AB: Dangers of resonium A in the treatment of hyperkalemia in renal failure. Lancet 1966; 1:167-169.
    3) Croitoru M, Shouval A, Chepurov D, et al: Giant intragastric sodium polystyrene sulfonate bezoar. Kidney Int 2015; 88(2):415.
    4) Daram SR, Reddy R, & Tang SJ: Sodium polystyrene sulfate-associated gastric ulceration (with video). Gastrointest Endosc 2012; 76(1):220-222.
    5) Dardik A, Moesinger RC, & Efron G: Acute abdomen with colonic necrosis induced by Kayexalate-sorbitol. South Med J 2000; 93(5):511-513.
    6) Duggal A, Salam S, & Mehta A: Refractory hypoxemia due to sodium polystyrene sulfonate (kayexalate) aspiration. Ann Am Thorac Soc 2014; 11(6):993-995.
    7) Fenton JJ, Johnson FB, & Przygodzki RM: Sodium polystyrene sulfonate (Kayexalate) aspiration; histologic appearance and infrared microspectrophotometric analysis of two cases. Arch Pathol Lab Med 1996; 120:967-969.
    8) Gales MA, Gales BJ, & Dyer ME: Rectally administered sodium polystyrene sulfonate. Am J Health-Syst Pharm 1995; 52:2813-2815.
    9) Haupt HM & Hutchins GM: Sodium polystyrene sulfonate pneumonitis. Arch Intern Med 1982; 142:379-381.
    10) Lillemoe KD, Romolo JL, & Hamilton SR: Intestinal necrosis due to sodium polystyrene (Kayexalate) in sorbitol enemas: clinical and experimental support of the hypothesis. Surgery 1987; 101:267-272.
    11) Nepal M, Bucaloiu ID, & Norfolk ER: Hypernatremia in a patient treated with sodium polystyrene sulfonate. Int J Nephrol Renovasc Dis 2010; 3:141-143.
    12) Product Information: KAYEXALATE(R) oral powder for suspension rectal powder for suspension, sodium polystyrene sulfonate oral powder for suspension rectal powder for suspension. Sanofi-Aventis, US, LLC, Bridgewater, NJ, 2010.
    13) Product Information: Kayexalate(R), sodium polystyrene sulfonate. Sanofi-Synthelabo, Inc, New York, NY, 2001.
    14) Product Information: sodium polystyrene sulfonate oral suspension, rectal suspension, sodium polystyrene sulfonate oral suspension, rectal suspension. Roxane Laboratories, Inc. (per DailyMed), Columbus, OH, 2012.
    15) Rashid A & Hamilton SR: Necrosis of the gastrointestinal tract in uremic patients as result of sodium polystyrene sulfonate (Kayexalate) in sorbitol; an underrecognized condition. Am J Surg Path 1997; 21:60-69.
    16) Rogers FB & Li SC: Acute colonic necrosis associated with sodium polystyrene sulfonate (Kayexalate) enemas in a critically ill patient: case report and review of the literature. J Trauma 2001; 51:395-397.
    17) S Sweetman : Martindale: The Complete Drug Reference. London: Pharmaceutical Press (Internet Version). The Pharmaceutical Press. London, UK (Internet Version). Edition expires 2002; provided by Truven Health Analytics Inc., Greenwood Village, CO.
    18) Scherr L, Ogden DA, & Mead AW: Management of hyperkalemia with a cation-exchange resin. N Engl J Med 1961; 264:115-119.
    19) Scott T, Graham S, & Schweitzer E: Colonic necrosis following sodium polystyrene sulfonate (Kayexalate(R))-sorbitol enema in a renal transplant patient. Dis Colon Rectum 1993; 36:607-609.
    20) Townsend CM Jr, Remmers AR Jr, & Sarles HE: Intestinal obstruction from medication bezoar in patients with renal failure. N Engl J Med 1973; 288:1058-1059.
    21) Watson MA, Baker TP, Nguyen A, et al: Association of prescription of oral sodium polystyrene sulfonate with sorbitol in an inpatient setting with colonic necrosis: a retrospective cohort study. Am J Kidney Dis 2012; 60(3):409-416.
    22) Wootton FT, Rhodes DF, & Lee WM: Colonic necrosis with Kayexalate-sorbitol enemas after renal transplantation. Ann Intern Med 1989; 111:947-949.