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Tumor Lysis Syndrome

University of Michigan Pediatric Hematology/Oncology Tumor Lysis Guidelines

Definition

  • Oncologic emergency due to tumor lysis with release of intracellular potassium, phosphate, and nucleic acids (source of uric acid) into the bloodstream
  • Uric acid can precipitate in the kidneys leading to renal failure
  • Hyperphosphatemia can lead to calcium phosphate deposition, which can lead to both hypocalcemia and acute kidney injury

Pathophysiology



Figure 1: Tumor Lysis Syndrome Overview


  • Generally occurs with a high tumor burden and with initiation of cytotoxic therapy (i.e. induction chemotherapy)
  • Can also occur spontaneously with high tumor burden (i.e. hyperleukocytosis)
  • The risk of developing tumor lysis syndrome (TLS) varies with the type of leukemia/lymphoma:
    • Extremely high risk: Burkitt Lympoma (bulky or advanced stage)/Leukemia
    • High Risk: T cell Leukemia/lymphoma, ALL with WBC >100K, AML with WBC >50K
    • Intermediate Risk: Stage III/IV Non-Burkitt NHL, Burkitt lymphoma (not bulky or advanced)/Leukemia, ALL with WBC 50-100K, AML with WBC 10-50K
    • Low Risk: All other patients not meeting above criteria

Treatment

  • Monitoring of electrolytes and urine output/urine pH. Generally q6-8hr electrolytes
  • Hydration: Generally 2x maintenance fluids with D5 1/4 to 1/2 NS (can develop SIADH and hyponatremia). Do not add potassium to the fluids. Generally do not add bicarbonate to the fluids unless urine pH <6.5 as high urine pH can precipitate Ca-Phos deposition and uropathy
  • Lasix 1-2 mg/kg/dose as clinically indicated (loop diuretics can also worsen hypocalcemia)
  • Rasburicase when uric acid >8 mg/dL (contraindicated with G6PD deficiency as can cause hemolysis and methemoglobinemia- i.e. male African/Mediterranean/SE asian ancestry)
  • Allopurinol not used routinely at University of Michigan but can be utilized (along with urinary alkalinization as hypoxanthine/xanthine can accumulate and is excreted more easily with a higher urinary pH)
  • Urinary alkalnization NOT indicated as it can worsen Ca-Phos nephropathy and in the setting of rasburicase, hypoxanthine/xanthine excretion with allopurinol is no longer a significant concern
  • Hyperkalemia can be treated with judicious use of calcium (again trying to avoid a CaXPhos product of 60 or more), Lasix, Dextrose/insulin, and sodium bicarbonate. Longer term therapies include Kayexalate.
  • Renal replacement therapy may be necessary for prolonged hyperkalemia or uropathy related to hyperuricemia (rare now with rasburicase) or Ca-Phos deposition
  • Can treat hyperphosphatemia with binding agent such as sevelamer or in more refractory cases, renal replacement therapy

References

1. J Clin Oncol. 2008 Jun 1;26(16):2767-78
2. Eur J Haematol. 2008 Apr;80(4):331-6.
3. Bone Marrow Transplant. 2006 Jun;37(11):997-1001