Contents

1. 1 University of Michigan Pediatric Hematology/Oncology Tumor Lysis Guidelines
2. 2 Definition
3. 3 Pathophysiology
4. 4 Treatment
5. 5 References

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

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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