What is the treatment for tumor lysis syndrome?

Treatment of Tumor Lysis Syndrome

All patients with clinical tumor lysis syndrome (TLS) should receive aggressive intravenous hydration through central venous access plus rasburicase immediately to prevent life-threatening complications including acute renal failure, cardiac arrhythmias, seizures, and death. 1

Core Treatment Strategy

Immediate Interventions for Clinical TLS

Hydration is the cornerstone of treatment and must be initiated urgently:

• Start IV hydration at least 48 hours before chemotherapy when possible, though rasburicase allows earlier chemotherapy initiation if needed 1
• Maintain urine output at minimum 100 mL/hour (or 3 mL/kg/hour in children <10 kg) 1
• Use loop diuretics (furosemide) or mannitol to achieve target urine output if needed, except in patients with obstructive uropathy or hypovolemia 1, 2
• Administer fluids through central venous access for reliable delivery 1

Rasburicase Administration

Rasburicase is superior to allopurinol for established TLS:

• Rasburicase reduces uric acid to ≤2 mg/dL within 4 hours in 96% of patients, compared to allopurinol which fails to control uric acid in 11% of cases 3
• Dosing: 0.15-0.2 mg/kg/day IV as a 30-minute infusion 3
• Contraindications: G6PD deficiency (causes severe hemolysis), pregnancy, and history of severe hypersensitivity 3
• The response rate with rasburicase is 87% versus 66% with allopurinol alone 3

Management of Specific Electrolyte Abnormalities

Hyperkalemia Management (Algorithmic Approach)

Mild hyperkalemia (<6 mmol/L):

• Aggressive IV hydration plus loop diuretics (furosemide 40-80 mg IV) 1, 2
• Sodium polystyrene 1 g/kg orally or by enema 1, 2

Severe hyperkalemia (≥6 mmol/L or any ECG changes):

• Calcium gluconate 50-100 mg/kg IV over 2-5 minutes to stabilize myocardial membrane (onset 1-3 minutes, duration 30-60 minutes) 1, 2
• Rapid insulin 0.1 units/kg IV plus 25% dextrose 2 mL/kg (onset 15-30 minutes, duration 4-6 hours) 1, 2
• Calcium carbonate 100-200 mg/kg/dose 1
• Sodium bicarbonate to correct acidosis 1
• Continuous ECG monitoring is mandatory for all hyperkalemic patients 1, 2

Hyperphosphatemia Management

• Mild hyperphosphatemia (<1.62 mmol/L) requires no treatment 1
• Moderate to severe hyperphosphatemia: aluminum hydroxide 50-100 mg/kg/day divided in 4 doses orally or by nasogastric tube 1, 2

Hypocalcemia Management

• Asymptomatic hypocalcemia requires no treatment 1
• Symptomatic hypocalcemia (tetany, seizures): calcium gluconate 50-100 mg/kg IV, repeat cautiously if necessary 1

Critical pitfall: Avoid calcium administration in hyperphosphatemia without symptoms, as this promotes calcium-phosphate precipitation in renal tubules and worsens kidney injury 1

Indications for Dialysis

Initiate hemodialysis urgently when:

• Oliguria or anuria develops despite aggressive hydration 1
• Severe, refractory hyperkalemia (≥6 mmol/L unresponsive to medical management) 1, 2
• Severe hyperphosphatemia with renal failure 1
• Fluid overload despite diuretics 1
• Symptomatic uremia 1

Hemodialysis achieves uric acid clearance of 70-100 mL/min and reduces plasma uric acid by approximately 50% with each 6-hour treatment, often restarting diuresis when uric acid falls to 10 mg/dL 1

Laboratory Monitoring

Critical monitoring parameters:

• Recheck potassium every 2-4 hours after initial treatment 2
• Obtain comprehensive metabolic panel, LDH, and CBC immediately when TLS suspected 4
• Calculate eGFR using MDRD formula to assess renal function 4

Important caveat: Rasburicase causes enzymatic degradation of uric acid in blood samples at room temperature, leading to falsely low readings. Samples must be immediately placed on ice and analyzed within 4 hours to avoid spurious results 3

Treatment for Laboratory TLS

Laboratory TLS (≥2 biochemical abnormalities without clinical complications) requires the same aggressive treatment as clinical TLS in:

• All adults with laboratory TLS 1
• Children at high risk for TLS 1
• Children with rapid worsening of biochemical parameters 1

The evidence strongly supports that treatment of laboratory TLS is superimposable to treatment of clinical TLS, as laboratory abnormalities rapidly progress to life-threatening complications without intervention 1