Synopsis
Predict, prevent, recognise and treat tumour lysis syndrome before potassium, phosphate, urate and calcium disturbances cause arrhythmia, seizure, acute kidney injury or death.
- TLS releases potassium, phosphate and nucleic acid from malignant cells; phosphate lowers calcium and purines become uric acid, producing arrhythmia, seizure and acute kidney injury.
- Assess risk before treatment from malignancy type, burden, LDH, white-cell count, treatment sensitivity, baseline urate, renal function, hydration, obstruction and nephrotoxic medicines.
- First-line baseline tests are potassium, phosphate, adjusted and preferably ionised calcium when symptomatic, urate, creatinine, urea, bicarbonate, LDH, FBC, ECG and accurate fluid balance.
- Low-risk disease generally receives monitoring and hydration; intermediate risk adds allopurinol, while high risk needs monitored care, vigorous but safe hydration and rasburicase according to the current BSH pathway.
- Allopurinol prevents formation of new uric acid but does not remove existing urate; rasburicase rapidly degrades existing urate and is preferred for high-risk or established TLS.
- Rasburicase is contraindicated in G6PD deficiency because it can cause haemolysis and methaemoglobinaemia; after dosing, urate specimens must be kept cold to prevent falsely low ex-vivo results.
- Do not alkalinise urine routinely, do not add potassium or phosphate to maintenance fluid and do not give calcium for asymptomatic hypocalcaemia while phosphate is high.
- Treat life-threatening potassium immediately and involve renal medicine early for oliguria, fluid overload, refractory hyperkalaemia, severe phosphate burden or persistent metabolic rebound.
Key red flags
ECG change, muscle weakness, bradycardia, ventricular arrhythmia or potassium at a severe threshold needs immediate UK Kidney Association hyperkalaemia treatment while tumour lysis is controlled.
Seizure, tetany, laryngospasm or QT prolongation with low calcium requires monitored calcium treatment, whereas asymptomatic hypocalcaemia during hyperphosphataemia is not routinely corrected.
Falling urine output, rapidly increasing creatinine, fluid overload or biochemical rebound despite rasburicase requires immediate renal review for renal replacement therapy.
Weakness, paraesthesia, bradycardia, broad QRS, loss of P waves, sine-wave change or ventricular arrhythmia is an immediate resuscitation problem.
Perioral tingling, cramp, carpopedal spasm, tetany, seizure, laryngospasm or QT prolongation indicates clinically important ionised calcium reduction.
Nausea, flank discomfort, oliguria, rising creatinine, hypertension, pulmonary oedema or encephalopathy suggests clearance failure and accumulating metabolic burden.
Investigation priorities
Detect the biochemical pattern and immediately dangerous membrane toxicity.
Management branches
A treatment-responsive malignancy is about to receive systemic therapy, corticosteroid prephase or another rapid tumour-reducing intervention.
- Classify tumour and patient risk using diagnosis, burden, LDH, white-cell count, renal reserve, urate, hydration, obstruction and planned treatment.
- Correct volume depletion, stop avoidable nephrotoxins and potassium or phosphate supplements and choose ward, high-dependency or ambulatory monitoring appropriate to risk.
- Use hydration alone for selected low risk, add renal-adjusted allopurinol for intermediate risk and use rasburicase with close monitoring for high risk under the BSH pathway.