eMedicine Specialties > Pediatrics: General Medicine > Oncology
Tumor Lysis Syndrome: Treatment & Medication
Updated: Sep 26, 2008
- Overview
- Differential Diagnoses & Workup
- Treatment & Medication
- Follow-up
Treatment
Medical Care
- Overview
- Tumor lysis syndrome (TLS) management requires initiation of preventive measures in high-risk patients prior to cancer treatment as well as prompt initiation of supportive care for patients who develop acute tumor lysis syndrome during treatment.
- Patients with evidence of pretreatment acute tumor lysis syndrome should be immediately started on tumor lysis syndrome treatment. Although the correction of all parameters prior to the initiation of chemotherapy is preferable, treatment of the malignancy may be needed sooner. Identify high-risk patients before treatment by assessing the extent of tumor burden, histopathologic findings, and renal function.
- Surveillance
- Severe manifestations of tumor lysis syndrome can be prevented only through meticulous laboratory monitoring and careful clinical observation. Necessary cardiac studies include baseline ECG with follow-up studies or continuous cardiac monitoring during treatment.
- Appropriate renal surveillance and fluid status determinations require baseline and daily weights, regular vital sign checks, and frequent measurements of both fluid intake and urine output.
- High-risk patients and those with evidence of tumor lysis syndrome should have at least thrice-daily laboratory monitoring of BUN, creatinine, uric acid, potassium, calcium, and phosphate levels. Monitoring should continue for the first 48-72 hours after chemotherapy initiation.
- Control of hyperuricemia
- Allopurinol is a competitive inhibitor of xanthine oxidase and is given to reduce the conversion of nucleic acid byproducts to uric acid in order to prevent urate nephropathy and subsequent oliguric renal failure.
- It is usually administered orally at 600 mg/d for prophylaxis and at 600-900 mg/d (maximum of 500 mg/m2/d) for treatment of tumor lysis syndrome.
- Patients unable to take oral medications can be given intravenous allopurinol. The inhibition of uric acid synthesis promotes an increase of xanthine in both plasma and the renal system.
- Although reported to be rare, xanthine has the capacity to precipitate in the renal tubules. Other adverse effects include mild-to-severe rash, xanthine stone-induced urolithiasis, acute interstitial nephritis, pneumopathy, fever, and eosinophilia.
- Dose reduction is necessary in renal insufficiency. Dose reduction is also necessary if concomitantly administered with mercaptopurine, 6-thioguanine, or azathioprine because allopurinol interferes with the metabolism of these agents.
- Rasburicase (recombinant urate oxidase) is a newer therapy that can be used when the uric acid levels cannot be sufficiently lowered by standard approaches. It has been shown to be both safe and effective in pediatric patients, as well as adults.
- Rasburicase has emerged as the preferred choice for treatment of hyperuricemia in tumor lysis syndrome.
- Rasburicase has a more rapid onset of action than allopurinol. Some urate oxidase is absent in primates; urate oxidase catalyses the conversion of poorly soluble uric acid to soluble allantoin. By converting uric acid to water-soluble metabolites, it effectively decreases plasma and urinary uric acid levels.
- Unlike allopurinol, uricase does not increase excretion of xanthine and other purine metabolites; therefore, it does not increase tubule crystallization of these compounds.
- Methemoglobinemia has been reported.4 Hemolytic anemia and methemoglobinemia may be adverse effects caused by the oxidative stress produced by hydrogen peroxide, which is a by product of the breakdown of urate to allantoin.
- Allopurinol is a competitive inhibitor of xanthine oxidase and is given to reduce the conversion of nucleic acid byproducts to uric acid in order to prevent urate nephropathy and subsequent oliguric renal failure.
- Hydration
- Volume depletion is a major risk factor for tumor lysis syndrome and must be vigorously corrected. Aggressive intravenous hydration not only helps correct electrolyte disturbances by diluting extracellular fluid but also increases intravascular volume. Increased volume enhances renal blood flow, glomerular filtration rate, and urine volume to decrease the concentration of solutes in the distal nephron and medullary microcirculation.
- Ideally, intravenous hydration in high-risk patients should begin 24-48 hours prior to initiation of cancer therapy and continue for 48-72 hours after completion of chemotherapy.
- Continuous intravenous infusion rates as high as 4-5 L/d (or 3 L/m2/d) yielding urine volumes of at least 3 L/d should be given unless the patient's cardiovascular status indicates impending volume overload.
- Urinary alkalinization
- Use of isotonic sodium bicarbonate solutions intravenously to promote alkaline diuresis has the potential benefits of solubilizing, and thus minimizing, intratubular precipitation of uric acid. The goal is to increase urinary pH levels to 7 to maximize uric acid solubility in renal tubules and vessels.
- Drawbacks to systemic alkaline therapy include magnification of clinical hypocalcemia by shifting ionized calcium to its nonionized form. Increased likelihood of calcium phosphate precipitation in renal tubules is an additional drawback. For these reasons, routine urine alkalinization is controversial and, if used, must include close monitoring of urinary pH, serum bicarbonate, and uric acid levels to both guide therapy and avoid overzealous alkalinization. Consider titrating sodium bicarbonate intravenous fluid solutions to keep the urine pH level at 7-8.
- If urinary alkalinization is not achieved with exogenous bicarbonate solutions despite increasing serum bicarbonate levels, intravenous acetazolamide at doses of 250-500 mg/d (5 mg/kg/d) may be added to decrease proximal tubule bicarbonate reabsorption, thereby increasing urinary pH level.
- Control of electrolyte disturbances
- Aggressively treat and monitor hyperkalemia. Immediately restrict dietary potassium and remove potassium from intravenous fluids. Acute treatment modalities include intravenous infusion of glucose plus insulin to promote redistribution of potassium from the extracellular to intracellular space, and intravenous calcium gluconate as cardioprotection for potassium levels greater than 6.5 mmol/L or for those with ECG alterations. Intravenous hydration with alkaline fluid as described above can also increase intracellular uptake of potassium. Potassium-wasting diuretics may be used with caution because they may worsen renal precipitation in patients with volume contraction. Long-term therapy (eg, oral potassium-exchange resins) should be given immediately because of the transient effectiveness of acute treatment modalities. If these measures fail to control serum potassium, dialysis should be promptly initiated.
- Hyperphosphatemia is managed with oral phosphate binders and the same solution of glucose plus insulin used for control of hyperkalemia. Hyperphosphatemia may lead to hypocalcemia, which usually resolves as phosphate levels are corrected. In some cases, depressed serum 1,25-dihydroxycholecalciferol levels contribute to hypocalcemia, and administration of calcitriol may correct calcium levels. Such therapy, however, should not be undertaken until serum phosphate levels have normalized to avoid metastatic calcium phosphate calcifications. As a rule, do not correct hypocalcemia unless evidence of neuromuscular irritability is observed, as indicated by a positive Chvostek or Trousseau sign.
- Use of furosemide or mannitol for osmotic diuresis has not proven to be beneficial as front-line therapy. In fact, these modalities may contribute to uric acid or calcium phosphate precipitation in renal tubules in a volume-contracted patient. Instead, diuretics should be reserved for well-hydrated patients with insufficient diuresis, and furosemide alone should be considered for the normovolemic patient with hyperkalemia or for the patient with evidence of fluid overload.
- If the previously mentioned methods fail, consider early initiation of dialysis. Dialysis avoids irreversible renal failure and other life-threatening complications. Indications for dialysis include persistent hyperkalemia or hyperphosphatemia despite treatment, volume overload, uremia, symptomatic hypocalcemia, and hyperuricemia.
- Hemodialysis is preferred over peritoneal dialysis because of better phosphate and uric acid clearance rates. Continuous hemofiltration also has been used and is effective in correcting electrolyte abnormalities and fluid overload.
- Because hyperkalemia can recur after dialysis is initiated and because of the high phosphate burden in some patients with tumor lysis syndrome, electrolyte levels must be frequently monitored and dialysis must be repeated as needed.
Surgical Care
- Patients with tumor lysis syndrome may need surgical intervention for central venous line placement or the placement of a dialysis catheter in cases of extreme hyperkalemia or renal failure.
Consultations
- Patients with cancer who have acute manifestations of tumor lysis syndrome or those at high risk should be treated by personnel who are experienced with tumor lysis syndrome complications and treatment. An oncology unit or ICU with readily available continuous cardiac monitoring and hemodialysis capabilities is preferable.
- If basic supportive care measures are ineffective in controlling electrolyte disturbances or renal function, nephrology and critical care consultants should be accessible to assist in further management.
- Laboratory turnover time must be rapid so that metabolic derangements can be addressed before life-threatening problems arise.
Diet
- Dietary restrictions highly depend on the status of the individual patient. However, patients who are not restricted to a nothing by mouth diet could theoretically benefit from restricting intake of foods that contain high levels of potassium, phosphorus, or uric acid.
Medication
Management of tumor lysis syndrome (TLS), other than hydration and alkalinization, necessitates the use of drugs to correct metabolic disturbances. Use of medications must be instituted before the start of chemotherapy; the goal is to achieve optimal metabolic stability.
An alternative to allopurinol for decreasing uric acid load is rasburicase (urate oxidase), which controls hyperuricemia by converting uric acid to water-soluble allantoin.5,6,7,8 This drug is widely used in Europe and was approved by the Food and Drug Administration (FDA) in the United States.
Xanthine oxidase inhibitors
Allopurinol is used to inhibit xanthine oxidase, thereby reducing uric acid. The intravenous form (Aloprim) may be used for patients unable to tolerate oral administration.
Caution is necessary because of the high uric acid concentration in the urine. In 1986, Andreoli and associates explained some cases of renal failure on the basis of effects of allopurinol in altering purine excretion.9 In the presence of allopurinol, the excretion of uric acid, xanthine, and hypoxanthine increases several hundred folds, enough to exceed their solubility limit in the renal tubules even at a urinary pH level of 7. Also, at a urinary pH level higher than 7.5, crystallization of hypoxanthine may occur, which necessitates withdrawal of bicarbonate from intravenous fluids.
Allopurinol (Aloprim, Zyloprim)
Inhibits xanthine oxidase, the enzyme that synthesizes uric acid from hypoxanthine and xanthine, thus decreasing production and excretion of uric acid and increasing the levels of more soluble xanthine and hypoxanthine. Reduces the synthesis of uric acid without disrupting the biosynthesis of vital purines.
Adult
Oral prophylaxis: 200-600 mg/d PO
Oral treatment: 600-900 mg/d PO; not to exceed 500 mg/m2/d
If unable to take PO: 200-400 mg/m2/d IV; not to exceed 600 mg/d
Pediatric
300-500 mg/m2/d PO divided q8h
200 mg/m2/d IV
Alcohol decreases effects; incidence of rash increased when used concurrently with ampicillin and amoxicillin; large amounts of vitamin C acidify urine and may cause kidney stone formation; allopurinol inhibits metabolism of azathioprine and mercaptopurine; increases serum theophylline level
Documented hypersensitivity
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Diffuse, erythematous, maculopapular rash; not for use in asymptomatic hyperuricemia; reduce dose in renal insufficiency; monitor liver function and perform CBC counts before initiating therapy and periodically thereafter
Uric acid oxidizers
These agents metabolize uric acid to a soluble form, thus preventing acute renal failure (ARF).
Rasburicase (Elitek)
Recombinant form of the enzyme urate oxidase that oxidizes uric acid to allantoin. Used in management and prophylaxis of severe hyperuricemia associated with treatment of malignancy. Hyperuricemia causes a precipitant in kidneys, which leads to acute renal failure. Unlike uric acid, allantoin is soluble and easily excreted by kidneys.
Adult
0.15-0.2 mg/kg/d IV infused over 30 min for 5-7 d
Pediatric
Administer as in adults
None reported
Documented hypersensitivity; G-6-PD deficiency
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
May cause hemolytic anemia secondary to hydrogen peroxide produced during uric acid oxidation; may cause methemoglobinemia; other adverse effects include fever, nausea, and vomiting; children <2 y may experience more vomiting, diarrhea, fever, and rash; avoid shaking or vortexing during product reconstitution; highly antigenic, multiple administration may produce allergic reaction, anaphylaxis, or death; produces false low uric acid levels, accurate levels obtained by collecting blood into prechilled, heparin containing tubes kept at 4 º C and centrifuged at that temperature, maintain resultant plasma at 4 º C and analyze within 4 h of collection; do not administer as IV bolus
Minerals
Calcium is used to treat arrhythmias due to hyperkalemia or hypocalcemia. Frank or impending renal failure requires additional therapeutic measures. Hyperkalemia is the most common life-threatening emergency. Chemotherapy may have to be discontinued temporarily. The entire potassium intake should be immediately discontinued. The use of calcium does not lower serum potassium levels. It is primarily used to protect the myocardium from the deleterious effects of hyperkalemia (ie, arrhythmias) by antagonizing the membrane actions of potassium.
Calcium
Administer IV calcium gluconate or calcium chloride to stabilize myocardial conduction in a patient with cardiac arrhythmias. Also moderates nerve and muscle performance by regulating action potential excitation threshold. IV calcium indicated in all cases of severe hyperkalemia (ie, >6 mEq/L), especially when accompanied by ECG changes. Calcium chloride contains about 3 times more elemental calcium than an equal volume of calcium gluconate. Therefore, when hyperkalemia is accompanied by hemodynamic compromise, calcium chloride is preferred over calcium gluconate.
Administration of calcium should be accompanied by the use of other therapies that actually help lower the serum levels of potassium. Other calcium salts (eg, glubionate, gluceptate) have even less elemental calcium than calcium gluconate and are not generally recommended for the therapy of hyperkalemia.
Calcium chloride 1 g = 270 mg (13.5 mEq) of elemental calcium.
Calcium gluconate 1 g = 90 mg (4.5 mEq) of elemental calcium.
Adult
Calcium chloride 10% IV solution:
Hyperkalemia: 2-4 mg/kg slow IV q6-8h prn
Hypocalcemia: 0.5-1 g (7-14 mEq) slow IV; may repeat q1-3d prn
Pediatric
Calcium gluconate: 50 mg/kg slow IV q6-8h prn
Calcium chloride: 10-30 mg/kg slow IV q6-8h prn
Coadministration with digoxin may cause arrhythmias; coadministration with thiazides may induce hypercalcemia; may antagonize effects of calcium channel blockers, atenolol, and sodium polystyrene sulfonate; do not administer with bicarbonate because precipitation in the IV tubing or catheter may occur
Ventricular fibrillation not associated with hyperkalemia; digitalis toxicity; hypercalcemia; renal insufficiency; cardiac disease
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Administer slowly (not to exceed 0.5-1 mL/min) to avoid extravasation; hypercalcemia may occur in renal failure
Intracellular potassium transporters
Sodium bicarbonate, insulin, and glucose cause a transcellular shift of potassium into muscle cells, thereby lowering (temporarily) serum levels of potassium.
Sodium bicarbonate
Intracellularly shifts potassium. May be considered in the treatment of hyperkalemia, even in the absence of metabolic acidosis.
Adult
1 mEq/kg IV; can be administered as a continuous IV infusion by mixing 50-100 mEq/L of IV solution
Pediatric
Administer as in adults
Urinary alkalinization induced by increased sodium bicarbonate concentrations may cause decreased levels of lithium, tetracyclines, chlorpropamide, methotrexate, and salicylates; increases levels of amphetamines, pseudoephedrine, flecainide, anorexiants, mecamylamine, ephedrine, quinidine, and quinine; do not admix calcium and sodium bicarbonate (precipitant forms)
Alkalosis; hypernatremia; hypocalcemia; severe pulmonary edema; unknown abdominal pain
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Sodium bicarbonate should only be used to treat documented hyperkalemia; can cause alkalosis, decreased plasma potassium, hypocalcemia, and hypernatremia; caution in electrolyte imbalances (eg, CHF, cirrhosis, edema, corticosteroid use, renal failure); when administering, avoid extravasation because tissue necrosis can occur
Insulin and dextrose, IV (Novolin, Humulin, Lente Iletin)
Induces intracellular flux of potassium. Presence of insulin results in the intracellular movement of glucose, followed by entry of potassium into muscle cells. Effect is almost immediate, but temporary, and should therefore be followed by therapy that actually enhances potassium clearance (eg, sodium polystyrene sulfonate).
Adult
10 U IV and 50 mL dextrose 50% IV bolus or 500 mL dextrose 10% over 1 h; may be administered prn or by continuous IV infusion
Pediatric
1 U/kg of regular insulin with 2 mL/kg IV bolus of dextrose 25%; may be administered prn or as a continuous IV infusion
Medications that may decrease hypoglycemic effects of insulin include acetazolamide, AIDS antivirals, asparaginase, phenytoin, nicotine, isoniazid, diltiazem, diuretics, corticosteroids, thiazide diuretics, thyroid estrogens, ethacrynic acid, calcitonin, PO contraceptives, diazoxide, dobutamine, phenothiazines, cyclophosphamide, dextrothyroxine, lithium carbonate, epinephrine, morphine sulfate, and niacin; medications that may increase hypoglycemic effects of insulin include calcium, ACE inhibitors, alcohol, tetracyclines, beta-blockers, lithium carbonate, anabolic steroids, pyridoxine, salicylates, MAOIs, mebendazole, sulfonamides, phenylbutazone, chloroquine, clofibrate, fenfluramine, guanethidine, octreotide, pentamidine, and sulfinpyrazone
Documented hypersensitivity; hypoglycemia
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Hyperthyroidism may increase renal clearance of insulin, necessitating more insulin to treat hyperkalemia; hypothyroidism may delay insulin turnover, requiring less insulin to treat hyperkalemia; monitor glucose carefully; dose adjustments of insulin may be necessary in patients diagnosed with renal and hepatic dysfunction
Exchange resins
Sodium polystyrene sulfonate is an exchange resin that can be used to treat mild-to-moderate hyperkalemia. Each mEq of potassium is exchanged for 1 mEq of sodium.
Sodium polystyrene sulfonate (Kayexalate)
Exchanges sodium for potassium and binds it in the gut, primarily in the large intestine and decreases total-body potassium. Onset of action after PO administration is 2-12 h and is longer when administered rectally. Used in the second stage of therapy to reduce total-body potassium.
Adult
25-50 g PO/PR q6h prn; mix in 25-50 mL of sorbitol
Pediatric
1 g/kg PO q6h prn; mix with 50% sorbitol
Systemic alkalosis may occur if administered concurrently with magnesium hydroxide, aluminum carbonate or similar antacids, and laxatives
Documented hypersensitivity; hypernatremia
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Caution when administering to patients who can be adversely affected by a small increase in sodium loads (eg, severe hypertension, severe congestive heart failure, marked edema); constipation with the possibility of fecal impaction may occur; constipation should be treated with 10-20 mL of 70% sorbitol q2h or prn to produce at least 1-2 watery stools daily
Phosphate Binder
These agents are used to treat hyperphosphatemia.
Aluminum hydroxide (AlternaGEL, Alu-Cap, Amphojel, Dialume)
Has been shown to be an effective phosphate binder. However, aluminum salts are not first-line because of their potential for toxicity.
Adult
2 cap or tab or 10 mL of regular susp PO (in water or fruit juice) as often as q2h, as many as 12 times/d
Pediatric
50-150 mg/kg/d PO divided q4-6h, titrate to maintain serum phosphorus levels within reference range
Decreases effects of tetracyclines, ranitidine, ketoconazole, benzodiazepines, penicillamine, phenothiazines, digoxin, indomethacin, and isoniazid; corticosteroids decrease effects of aluminum in hyperphosphatemia
Documented hypersensitivity
Pregnancy
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Precautions
Use is controversial, onset of action is slow, and response is erratic; caution in recent massive upper GI hemorrhage; renal failure may cause aluminum toxicity
Sevelamer hydrochloride (Renagel)
Polymeric phosphate binder for PO administration. Does not contain aluminum and, thus, aluminum intoxication is not a concern.
Adult
2-4 cap PO pc; adjust based on serum phosphorus concentrations to lower serum phosphorus to <6 mg/dL.
>6 mg/dL and <7.5 mg/dL 2 caps PO tid
>7.5 mg/dL and <9 mg/dL 3 caps PO tid
>9 mg/dL 4 caps PO tid
not to exceed 30 caps/d
Pediatric
Not established. In one study, the most commonly used dosing was 400 mg (1 cap) PO bid in patients aged 2.7-17.9 years old.
May reduce absorption of drugs co-administered with sevelamer
Documented hypersensitivity; bowel obstruction, hypophosphatemia
Pregnancy
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Precautions
Caution in patients with dysphagia, severe GI motility disorders, or swallowing disorders; can cause hypophosphatemia in patients with low or normal serum phosphate levels; when changes in absorption of oral medications may have clinical consequences (eg, antiseizure or antiarrhythmic drugs), medications should be taken 1 h before or 3 h after a dose of sevelamer
More on Tumor Lysis Syndrome |
| Overview: Tumor Lysis Syndrome |
| Differential Diagnoses & Workup: Tumor Lysis Syndrome |
 Treatment & Medication: Tumor Lysis Syndrome |
| Follow-up: Tumor Lysis Syndrome |
| References |
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References
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Further Reading
Keywords
tumor lysis syndrome, TLS, acute tumor lysis syndrome, ATLS, hyperkalemia, hyperuricemia, hyperphosphatemia, hypocalcemia, acute renal failure, ARF, Burkitt lymphoma, T-cell acute lymphoblastic leukemia, hepatoblastoma, neuroblastoma, obstructive uropathy, pericarditis, uremia, renal colic, arthralgia, arthritis, hypertension
