Tumour Lysis Syndrome
⚠️ Tumour Lysis Syndrome (TLS) is a life-threatening metabolic emergency that can occur during chemotherapy or radiotherapy, particularly in haematological malignancies.
Very rarely, it can occur in bulky or rapidly proliferating solid tumours.
🩺 Prompt recognition and treatment are essential to prevent acute kidney injury, arrhythmias, and death.
ℹ️ About
- ⚡ Metabolic complication during cytotoxic therapy
- 🧬 Caused by rapid breakdown of tumour cells → release of intracellular contents
- 🎗️ Classically seen in haematological malignancies (ALL, AML, high-grade lymphomas)
🧬 Aetiology
- 💥 Rapid tumour cell turnover → release of potassium, phosphate, urate → metabolic derangements
- 🧪 Results in hyperkalaemia, hyperphosphataemia, hypocalcaemia, hyperuricaemia
⚠️ Risk Factors
- 📈 High tumour burden, high-grade/rapidly dividing tumours
- 🩺 Pre-existing renal impairment or tumour infiltration of kidneys
- 👵 Older age
- 💊 Treatment with highly active, cell-cycle specific agents
- 🚫 Concomitant use of uric acid–raising drugs (see below)
💊 Drugs to Avoid (increase uric acid)
- 🍺 Alcohol, ascorbic acid, aspirin, caffeine
- 💉 Cisplatin, diazoxide, thiazide diuretics
- 💊 Adrenaline, ethambutol, levodopa, methyldopa, nicotinic acid
- 🧪 Pyrazinamide, phenothiazines, theophylline
🚨 High-Risk Patients
- 🎗️ Burkitt’s / Burkitt’s-like lymphoma
- 🎗️ Lymphoblastic lymphoma
- 🧪 ALL with WCC >100 × 10⁹/L
- 🧪 AML with WCC >100 × 10⁹/L
- 🧪 CML in blast crisis with WCC >100 × 10⁹/L
- 📊 High-grade lymphoma with bulky disease (LDH >2 × ULN or tumour bulk >10 cm)
🩺 Clinical Features
- 🧾 Often overlap with chemo side effects → correlation with labs essential
- ⬇️ Calcium: cramps, tetany, paraesthesias, arrhythmias, heart block, seizures, confusion
- ⬆️ Phosphate: nausea, diarrhoea, lethargy, seizures
- ⬆️ Uric acid: gout, AKI
- ⬆️ Potassium: arrhythmias, muscle weakness (see Hyperkalaemia)
🔎 Investigations
- 📈 Urea & creatinine ↑ → AKI
- 🧪 Hyperuricaemia, hyperkalaemia, hyperphosphataemia, raised LDH
- ⬇️ Hypocalcaemia, reduced eGFR
- ⚡ Diagnostic definition often uses Cairo-Bishop criteria (≥2 lab changes within 3 days before or 7 days after treatment)
🧪 Pathology
- 💥 Tumour cell lysis → release of intracellular ions & nucleic acids → crystallisation of uric acid & calcium phosphate in renal tubules → AKI
🛡️ Prevention
- 💧 Optimise hydration (2–3 L/day; IV fluids should not contain potassium)
- 💊 Allopurinol: 300 mg/day (start 24–48h before chemo, reduce dose if CrCl <20 ml/min)
- 💉 Rasburicase: consider in high-risk patients or deteriorating biochemistry
- 📊 High-risk: hydration + rasburicase prophylaxis
💊 Management
- 💧 Maintain hydration (3–4 L/day IV fluids). Strict fluid balance + hourly urine output + urinary catheter
- ⚖️ Daily weights; treat fluid retention with IV furosemide/mannitol if >3 kg gain
- 💉 Rasburicase for 3–7 days guided by clinical & biochemical response (avoid in G6PD deficiency)
- 🧪 Monitor biochemistry 4-hourly (K, PO₄, Ca, Mg, urea, creatinine, urate) + ECG monitoring
- ⚡ Hypocalcaemia: treat only if symptomatic with IV calcium gluconate (risk of calcium-phosphate precipitation)
- ⬆️ Hyperphosphataemia: may require dialysis if uncontrolled
- 💊 Avoid calcium supplements except if severe neuromuscular irritability
📚 References
