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This is a clinician-written, evidence-based summary aligned to the 2026 MLA Content Map. It is intended for medical students and junior doctors preparing for the UKMLA. Always cross-reference with NICE guidance, local protocols, and clinical judgement.
The Bottom Line
- Occurs when rapid destruction of tumour cells releases intracellular contents (potassium, phosphate, nucleic acids) into the bloodstream faster than renal excretion
- Classic metabolic derangements: HYPERkalaemia, HYPERuricaemia, HYPERphosphataemia, HYPOcalcaemia (secondary to hyperphosphataemia)
- Highest risk: haematological malignancies with high tumour burden and high proliferation rate — Burkitt lymphoma, ALL, AML with high WCC
- Prevention: aggressive IV hydration (3 L/m²/day), rasburicase (high risk) or allopurinol (moderate risk) BEFORE starting chemotherapy
- Treatment: correct electrolytes, aggressive hydration, rasburicase, manage AKI (may need renal replacement therapy)
Overview
Tumour lysis syndrome (TLS) is a potentially fatal oncological emergency that occurs when large numbers of tumour cells are destroyed rapidly — either spontaneously or (more commonly) after initiation of cytotoxic treatment. The massive release of intracellular contents overwhelms normal homeostatic mechanisms. Potassium release causes life-threatening hyperkalaemia. Purine metabolism generates uric acid, which precipitates in renal tubules causing acute urate nephropathy. Phosphate release binds calcium, causing hyperphosphataemia and secondary hypocalcaemia. The resulting AKI further worsens all metabolic derangements.
Epidemiology
TLS occurs most frequently with haematological malignancies: Burkitt lymphoma (highest risk — extremely rapid tumour proliferation), ALL, AML with high WCC (>50 × 10⁹/L), and aggressive NHL. Solid tumour TLS is uncommon but can occur with highly chemo-sensitive tumours (small cell lung cancer, germ cell tumours). The incidence of laboratory TLS is 5-25% in high-risk haematological malignancies; clinical TLS (with organ dysfunction) occurs in 3-10%. Mortality from clinical TLS is approximately 15-30%.
Clinical Features
Symptoms
Nausea, vomiting, diarrhoea
Muscle cramps, tetany (hypocalcaemia)
Palpitations, weakness (hyperkalaemia)
Oliguria or anuria (AKI)
Seizures (hypocalcaemia, uraemia)
May be asymptomatic with only laboratory abnormalities (laboratory TLS)
Signs
Cardiac arrhythmia (hyperkalaemia — peaked T waves, wide QRS, sine wave on ECG)
Tetany, Chvostek and Trousseau signs (hypocalcaemia)
Reduced urine output
Peripheral and pulmonary oedema (fluid overload from aggressive hydration + AKI)
Investigations
First-line
U&Es, potassiumHYPERkalaemia — the most immediately life-threatening derangement. Monitor 6-8 hourly in high-risk patients
UrateHYPERuricaemia — uric acid crystals precipitate in renal tubules causing AKI. Raised urate is often the earliest marker
Phosphate and calciumHYPERphosphataemia causes secondary HYPOcalcaemia (calcium-phosphate precipitation)
CreatinineRising creatinine = AKI. May need renal replacement therapy
LDHMarkedly raised — reflects tumour cell lysis. A marker of tumour burden
Second-line
ECGMonitor for hyperkalaemia changes: peaked T waves → flattened P waves → wide QRS → sine wave → VF/asystole
Urine output monitoringHourly — maintain >100 mL/hour if possible with aggressive hydration
Specialist
Cairo-Bishop criteriaLaboratory TLS: ≥2 metabolic abnormalities (urate >476, K+ >6, PO4 >1.45, Ca2+ <1.75) within 3 days before or 7 days after chemo. Clinical TLS: laboratory TLS + organ dysfunction (AKI, arrhythmia, seizure)
1
Prevention — start BEFORE chemotherapy
- Aggressive IV hydration: 3 L/m²/day (or 200 mL/hour) starting 24-48 hours before chemotherapy
- High risk (Burkitt, ALL, AML with WCC >50): rasburicase 0.2 mg/kg IV single dose — recombinant urate oxidase, rapidly converts uric acid to allantoin (soluble)
- Moderate risk: allopurinol 300-600 mg/day — xanthine oxidase inhibitor, prevents NEW uric acid formation (does not break down existing urate)
- Do NOT alkalinise urine if rasburicase given (controversial and can cause calcium-phosphate precipitation)
2
Treatment of established TLS
- Continue aggressive IV hydration — aim urine output >100 mL/hour
- Hyperkalaemia: insulin-dextrose, calcium gluconate (cardiac protection), salbutamol nebuliser, calcium resonium. Urgent haemodialysis if refractory
- Hyperuricaemia: rasburicase if not already given
- Hyperphosphataemia: phosphate binders (sevelamer, calcium carbonate), IV hydration
- Hypocalcaemia: only treat if symptomatic (tetany, seizures) — IV calcium gluconate. Asymptomatic hypocalcaemia should NOT be aggressively corrected (risk of calcium-phosphate precipitation)
3
Renal replacement therapy
- Indications: refractory hyperkalaemia, severe AKI (oliguria/anuria), refractory metabolic derangements, fluid overload
- Continuous veno-venous haemofiltration (CVVHF) or intermittent haemodialysis — early nephrology input essential
Complications
- Cardiac arrest: From hyperkalaemia — the most immediately life-threatening complication
- Acute kidney injury: From urate and calcium-phosphate crystal deposition in renal tubules. May require dialysis
- Seizures: From hypocalcaemia or uraemia
- DIC: May coexist, particularly in AML with high WCC
UKMLA Exam Tips
- 1The mnemonic for TLS metabolic derangements: 3 HYPER + 1 HYPO → HYPERkalaemia, HYPERuricaemia, HYPERphosphataemia, HYPOcalcaemia
- 2Rasburicase converts uric acid to allantoin (soluble). Allopurinol prevents new urate formation but does not clear existing urate — rasburicase is faster and more effective
- 3Burkitt lymphoma has the HIGHEST risk of TLS — doubling time 24-48 hours, massive tumour burden
- 4Do NOT aggressively treat asymptomatic hypocalcaemia — calcium infusion risks calcium-phosphate precipitation in tissues
- 5Aggressive hydration (3 L/m²/day) is the single most important preventive measure
- 6Rasburicase is contraindicated in G6PD deficiency (produces hydrogen peroxide → haemolysis)
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