β οΈ 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.  
π©Ί Prompt recognition and treatment are essential to prevent acute kidney injury, arrhythmias, and death.
βΉοΈ About
- β‘ Metabolic complication during cytotoxic therapy
- 𧬠Caused by rapid breakdown of tumour cells β release of intracellular contents
- ποΈ Classically seen in haematological malignancies (ALL, AML, high-grade lymphomas)
𧬠Aetiology
- π₯ Rapid tumour cell turnover β release of potassium, phosphate, urate β metabolic derangements
- π§ͺ Results in hyperkalaemia, hyperphosphataemia, hypocalcaemia, hyperuricaemia
β οΈ Risk Factors
- π High tumour burden, high-grade/rapidly dividing tumours
- π©Ί Pre-existing renal impairment or tumour infiltration of kidneys
- π΅ Older age
- π Treatment with highly active, cell-cycle specific agents
- π« Concomitant use of uric acidβraising drugs (see below)
π Drugs to Avoid (increase uric acid)
- πΊ Alcohol, ascorbic acid, aspirin, caffeine
- π Cisplatin, diazoxide, thiazide diuretics
- π Adrenaline, ethambutol, levodopa, methyldopa, nicotinic acid
- π§ͺ Pyrazinamide, phenothiazines, theophylline
π¨ High-Risk Patients
- ποΈ Burkittβs / Burkittβs-like lymphoma
- ποΈ Lymphoblastic lymphoma
- π§ͺ ALL with WCC >100 Γ 10βΉ/L
- π§ͺ AML with WCC >100 Γ 10βΉ/L
- π§ͺ CML in blast crisis with WCC >100 Γ 10βΉ/L
- π High-grade lymphoma with bulky disease (LDH >2 Γ ULN or tumour bulk >10 cm)
π©Ί Clinical Features
- π§Ύ Often overlap with chemo side effects β correlation with labs essential
- β¬οΈ Calcium: cramps, tetany, paraesthesias, arrhythmias, heart block, seizures, confusion
- β¬οΈ Phosphate: nausea, diarrhoea, lethargy, seizures
- β¬οΈ Uric acid: gout, AKI
- β¬οΈ Potassium: arrhythmias, muscle weakness (see Hyperkalaemia)
π Investigations
- π Urea & creatinine β β AKI
- π§ͺ Hyperuricaemia, hyperkalaemia, hyperphosphataemia, raised LDH
- β¬οΈ Hypocalcaemia, reduced eGFR
- β‘ Diagnostic definition often uses Cairo-Bishop criteria (β₯2 lab changes within 3 days before or 7 days after treatment)
π§ͺ Pathology
- π₯ Tumour cell lysis β release of intracellular ions & nucleic acids β crystallisation of uric acid & calcium phosphate in renal tubules β AKI
π‘οΈ Prevention
- π§ Optimise hydration (2β3 L/day; IV fluids should not contain potassium)
- π Allopurinol: 300 mg/day (start 24β48h before chemo, reduce dose if CrCl <20 ml/min)
- π Rasburicase: consider in high-risk patients or deteriorating biochemistry
- π High-risk: hydration + rasburicase prophylaxis
π Management
- π§ Maintain hydration (3β4 L/day IV fluids). Strict fluid balance + hourly urine output + urinary catheter
- βοΈ Daily weights; treat fluid retention with IV furosemide/mannitol if >3 kg gain
- π Rasburicase for 3β7 days guided by clinical & biochemical response (avoid in G6PD deficiency)
- π§ͺ Monitor biochemistry 4-hourly (K, POβ, Ca, Mg, urea, creatinine, urate) + ECG monitoring
- β‘ Hypocalcaemia: treat only if symptomatic with IV calcium gluconate (risk of calcium-phosphate precipitation)
- β¬οΈ Hyperphosphataemia: may require dialysis if uncontrolled
- π Avoid calcium supplements except if severe neuromuscular irritability
π References