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Tumor Lysis Syndrome

Pathophysiology
Metabolic disturbances associated with bulky treatment-responsive tumors. Intracellular contents

Hyperuricemia
Purines release by cell breakdown are converted to uric acid

Hyperkalemia
Potassium released by cell breakdown

Hyperphosphatemia
Phosphorous released by cell breakdown

Hypocalcemia
Serum calcium is bound by phosphate and calcium phosphate precipitates in tissues

Acute Renal Failure
Due to uric acid nephropathy and calcium phosphate deposition.
Uric acid nephropathy: uric acid precipitates in acidic environments and in the highly concentrated renal tubules

Calcium phosphate deposition: calcium phosphate precipitates in an alkaline environment which can be iatrogenically precipitated

 

Epidemiology
Usually associated with:

  • AML
  • High-grade NHL (Burkitt’s)
  • Solid tumors

Usually within 48-72 hours after initiation of chemotherapy

Presentation

  • Acute renal failure – usually oliguric
    • Bleeding, pericarditis, weakness, fatigue, malaise, nausea, vomiting
    • Fluid overload causeing dyspnea, rales, edema, hypertension
    • Renal colic
  • Cardiac arrhythmia
    • 2/2 hyperkalemia and hypocalcemia
  • Hypercalcemia
    • Paresthesia, weakness, tetany
  • Metabolic acidosis
    • 2/2 acute renal failure and release of intracellular acids

Diagnosis

  • Labs: uric acid, phos, potassium, calcium, AG, pH

 

Treatment

  • Hyperuricemia
    • Allopurinol 600mg/day prophylaxis and 600-900 mg/day treatment. Can be given po or IV
    • Rasburicase 50-100 U/kg/day. Contraindicated in G6PD and pregnancy
    • Hydration
    • Urinary alkalinization with sodium bicarbonate titrated to urinary pH of 7.0 (controversial, d/c bicarb if serum bicarb reaches 30 or urinary pH exceeds 7.5). Acetazolamide is second line for urinary alkalinization.
  • Electrolyte disturbances
    • Hyperkalemia
      • Restrict dietary potassium
      • Glucose, insulin, diuretics, kayexelate
    • Hyperphosphatemia
      • Oral phosphate binders
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