ICU · oncology

Acute Severe Tumour Lysis Syndrome — Comprehensive ICU Management

Also known as Tumour lysis syndrome (TLS) · Acute tumour lysis syndrome (ATLS) · Tumor lysis syndrome · Hyperuricaemia of malignancy · Rasburicase · Cairo-Bishop classification · Laboratory tumour lysis syndrome · Clinical tumour lysis syndrome · Oncology metabolic emergency · Urate nephropathy

Acute severe tumour lysis syndrome (TLS) = a metabolic oncological emergency from rapid lysis of malignant cells releasing intracellular contents into the extracellular space: HYPERKALAEMIA (intracellular K+ dumped — most dangerous, causes fatal arrhythmia), HYPERPHOSPHATAEMIA (tumour cells carry ~4x normal phosphate), HYPOCALCAEMIA (secondary — Ca2+ precipitates with phosphate as calcium-phosphate crystals), and HYPERURICAEMIA (nucleic acid breakdown → purines → xanthine → uric acid via xanthine oxidase). Uric acid and calcium-phosphate precipitate in renal tubules → acute kidney injury (AKI), which then reduces K+ and phosphate excretion → a self-amplifying vicious cycle. Onset 12-72h after cytotoxic therapy (occasionally spontaneous before therapy in high-burden disease). Highest risk: Burkitt lymphoma, lymphoblastic lymphoma, acute lymphoblastic leukaemia (ALL, WBC high), high-grade non-Hodgkin lymphoma (bulky), AML with high WBC, and rapidly responding tumours treated with venetoclax/rituximab/steroids. Cairo-Bishop definition: laboratory TLS (≥2 abnormal values — urate ≥475 µmol/L/8 mg/dL, K+ ≥6.0 mmol/L, phosphate ≥1.45 mmol/L, Ca2+ ≤1.75 mmol/L or 25% change from baseline within 3 days before to 7 days after therapy) vs clinical TLS (LTLS PLUS AKI, arrhythmia/sudden death, or seizure). Prevention (cornerstone): aggressive IV hydration (3 L/m2/day or ~2-3 L/day, goal urine output 100 mL/m2/h) + urate-lowering therapy stratified by risk — rasburicase 0.15-0.2 mg/kg IV for HIGH risk (recombinant urate oxidase, converts EXISTING uric acid → soluble allantoin, acts within hours; CONTRAINDICATED in G6PD deficiency — haemolysis/methaemoglobinaemia), allopurinol 300 mg/day for INTERMEDIATE risk (xanthine oxidase inhibitor, prevents NEW uric acid only). Treatment of established TLS: aggressive hydration, rasburicase 0.15-0.2 mg/kg, treat hyperkalaemia per standard protocol (calcium gluconate for ECG changes → insulin/dextrose → salbutamol → potassium binders), do NOT routinely treat asymptomatic hypocalcaemia (calcium worsens Ca-P deposition), renal replacement therapy (CRRT preferred) for refractory hyperkalaemia/hyperphosphataemia or AKI. Alkalinisation of urine is NOT recommended (worsens calcium-phosphate precipitation).