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Tumour lysis syndrome means

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Tumour Lysis Syndrome (TLS)

Definition: Tumour lysis syndrome is a metabolic emergency caused by the rapid breakdown (lysis) of large numbers of malignant cells - either spontaneously or, more commonly, following the start of chemotherapy - releasing their intracellular contents into the bloodstream faster than the body can excrete them. It occurs classically with bulky, rapidly growing, chemosensitive malignancies such as high-grade lymphomas (e.g., Burkitt lymphoma) and leukemias.
What happens biochemically: Massive cell death releases potassium, phosphate, and nucleic acids (purines) into the circulation. The purines are metabolized by xanthine oxidase into uric acid. This produces the characteristic tetrad of electrolyte/metabolic derangements:
  • Hyperkalemia
  • Hyperphosphatemia
  • Hypocalcemia (secondary to calcium-phosphate precipitation)
  • Hyperuricemia
Diagnostic criteria (Cairo-Bishop):
Laboratory TLS - two or more of the following within 3 days before to 7 days after chemotherapy:
  • Uric acid ≥ 8 mg/dL or 25% increase from baseline
  • Potassium ≥ 6.0 mEq/L or 25% increase from baseline
  • Phosphorus ≥ 4.5 mg/dL (adults) / ≥ 6.5 mg/dL (children), or 25% increase from baseline
  • Calcium ≤ 7 mg/dL or 25% decrease from baseline
Clinical TLS = Laboratory TLS plus one or more of:
  • Creatinine > 1.5x the upper limit of the age-adjusted reference range
  • Cardiac dysrhythmia or sudden death
  • Seizure
Why it matters (complications): The uric acid precipitates as insoluble crystals in the renal tubules, causing intratubular obstruction, vasoconstriction, and inflammation, leading to acute kidney injury (uric acid nephropathy). High calcium-phosphate product can cause nephrocalcinosis. The electrolyte swings (especially hyperkalemia and hypocalcemia) can precipitate cardiac arrhythmias, seizures, and sudden death.
Management principles:
  • Risk-stratify before starting chemo in at-risk patients
  • Low risk: oral hydration, avoid nephrotoxins
  • High risk: aggressive IV 0.9% saline hydration to maintain GFR and tubular flow
  • Prophylaxis with a xanthine oxidase inhibitor (allopurinol or febuxostat) to block new uric acid formation
  • Rasburicase (recombinant urate oxidase) for patients with already-elevated uric acid - converts uric acid to soluble allantoin (avoid in G6PD deficiency due to hemolysis/methemoglobinemia risk)
  • Close monitoring of electrolytes and renal function; dialysis if severe AKI/refractory electrolyte derangement
  • Brenner and Rector's The Kidney, 2-Volume Set, p. 1878 (Cairo MS, Bishop M. Br J Haematol. 2004;127(1):3-11, as cited)
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